PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
3074944-2	1988	The allelic gene with BgIII site in the first intron codes for faster p53 protein variant, the other allelic gene coding for slower p53 protein variant (according to the mobility in SDS-PAAG).	Sodium Dodecyl Sulfate	182-185	P53	Homo sapiens	132-135
3280124-3	1988	We find that these retinoic acid-induced changes are accompanied by a marked decrease in the levels of p53 and p53 mRNA.	Tretinoin	19-32	P53	Homo sapiens	103-106
2905688-4	1988	Molecular cloning and sequencing of both the alleles of p53 gene revealed a base-pair change in codon 72 causing arginine----proline substitution in the allele with the additional BglII site.	Arginine	113-121	P53	Homo sapiens	56-59
2978869-5	1988	Data obtained from SDS-PAGE show that the HOS-SL cells expressed two forms of p53 with distinct molecular weights.	Sodium Dodecyl Sulfate	19-22	P53	Homo sapiens	78-81
2978869-7	1988	The data obtained from both 1D and 2D gel analyses consistently show that the p53 proteins involved in the association with hsp72/hsc73 were mainly the species that migrated with the slower mobility in the SDS dimension.	Sodium Dodecyl Sulfate	206-209	P53	Homo sapiens	78-81
3280124-3	1988	We find that these retinoic acid-induced changes are accompanied by a marked decrease in the levels of p53 and p53 mRNA.	Tretinoin	19-32	P53	Homo sapiens	111-114
2981174-0	1985	Lack of correlation between loss of anchorage-independent growth and levels of transformation-specific p53 protein in retinoic acid-treated F9 embryonal carcinoma cells.	Tretinoin	118-131	P53	Homo sapiens	103-106
3025664-10	1986	This sequence difference resulted in an arginine being coded for in clone p53-H-1 and a proline being coded for at the equivalent position in clone p53-H-19.	Arginine	40-48	P53	Homo sapiens	74-77
33934760-8	2021	Then, p53-antigen was immobilized on the nanocomposite and used in an indirect immunoassay with horseradish peroxidase (HRP)-conjugated secondary antibody and H2O2 as the substrate, following the typical Michaelis-Menten kinetics.	Hydrogen Peroxide	159-163	P53	Homo sapiens	6-9
6088530-2	1984	Analysis of the immunocomplexes on sodium dodecyl sulfate-polyacrylamide gell electrophoresis revealed that p53, p28, and p19 of adult T-cell leukemia-associated antigens were phosphorylated in vivo.	Sodium Dodecyl Sulfate	35-57	P53	Homo sapiens	108-111
6740945-4	1984	The reticulocyte lysates, however, acquired the ability to produce structural proteins (p53 at least) after addition of purified membranes isolated from the rough endoplasmic reticulum of Krebs-2 cells.	krebs	188-193	P53	Homo sapiens	88-91
6318442-4	1983	Human p53 proteins of at least five different apparent molecular-weight classes in SDS-polyacrylamide gels have been detected.	Sodium Dodecyl Sulfate	83-86	P53	Homo sapiens	6-9
33887260-6	2021	BBR treatment induced DNA replication defects and cell cycle arrest, resulting in apoptosis or cell senescence, depending on p53 status, in BCa cells.	Berberine	0-3	P53	Homo sapiens	125-128
33964346-10	2021	Moreover, overexpression of miR-130a in D-galactose (D-gal)-induced SH-SY5Y cell senescence model attenuated D-gal-induced impaired autophagy and cell senescence, demonstrated by decreased levels of LC3, Ac-p53, p21 and increased p62, suggesting that voluntary wheel running can alleviate brain aging in natural aging rats by up-regulating miR-130a-mediated autophagy.	Galactose	40-51	P53	Homo sapiens	207-210
33964346-10	2021	Moreover, overexpression of miR-130a in D-galactose (D-gal)-induced SH-SY5Y cell senescence model attenuated D-gal-induced impaired autophagy and cell senescence, demonstrated by decreased levels of LC3, Ac-p53, p21 and increased p62, suggesting that voluntary wheel running can alleviate brain aging in natural aging rats by up-regulating miR-130a-mediated autophagy.	Galactose	40-45	P53	Homo sapiens	207-210
33982778-0	2021	Isoquercitrin protects HUVECs against high glucose-induced apoptosis through regulating p53 proteasomal degradation.	Glucose	43-50	P53	Homo sapiens	88-91
33744756-6	2021	Pt/MgO nanoparticles downregulated Bcl-2 and upregulated Bax and p53 tumor suppressor proteins in the cancer cells.	Platinum	0-2	P53	Homo sapiens	65-68
33744756-6	2021	Pt/MgO nanoparticles downregulated Bcl-2 and upregulated Bax and p53 tumor suppressor proteins in the cancer cells.	mgo	3-6	P53	Homo sapiens	65-68
33725366-1	2021	PPM1D is a serine/threonine phosphatase that inactivates the p53 pathway.	Serine	11-17	P53	Homo sapiens	61-64
33968195-1	2021	Wild-type (wt) p53-induced phosphatase 1 (Wip1), encoded by the protein phosphatase, Mg2+/Mn2+ dependent 1D (PPM1D) gene, is a serine/threonine phosphatase induced upon genotoxic stress in a p53-dependent manner.	Serine	127-133	P53	Homo sapiens	15-18
33358075-9	2021	Metformin has been demonstrated to reduce cell-viability post-radiotherapy in both rectal and prostate cancer cell lines, with an enhanced effect in tumours with a p53 mutation and increased apoptosis post-radiotherapy for cervical cancer.	Metformin	0-9	P53	Homo sapiens	164-167
33423323-7	2021	Kyoto Encyclopedia of Genes and Genomes pathway results indicated that most DEGs caused by SCRV infection were identified in the immune system (retinoic acid-inducible gene-I-like receptor/Toll-like receptor/nucleotide-binding oligomerization domain-like receptor/C-type lectin receptor signalling pathway), cellular processes, cell growth and death (p53 signalling pathway, cellular senescence, apoptosis and phagosome), and metabolism.	Tretinoin	144-157	P53	Homo sapiens	351-354
32705438-7	2021	There was a significant increase in the percentage of pSmad2/3L-Thr-positive cells in the p53-positive neoplastic cell population with development of esophageal neoplasia.	Threonine	64-67	P53	Homo sapiens	90-93
33857626-0	2021	Sodium fluoride activates the extrinsic apoptosis via regulating NOX4/ROS-mediated p53/DR5 signaling pathway in lung cells both in vitro and in vivo.	Reactive Oxygen Species	70-73	P53	Homo sapiens	83-86
33857626-8	2021	Specifically, NOX4 knockdown inhibited NaF-induced the activation of p53/DR5 axis by reducing NOX4-derived ROS production.	Reactive Oxygen Species	107-110	P53	Homo sapiens	69-72
33968195-1	2021	Wild-type (wt) p53-induced phosphatase 1 (Wip1), encoded by the protein phosphatase, Mg2+/Mn2+ dependent 1D (PPM1D) gene, is a serine/threonine phosphatase induced upon genotoxic stress in a p53-dependent manner.	magnesium ion	85-89	P53	Homo sapiens	15-18
33906076-16	2021	CONCLUSION: TG potentiated 5-FU"s inhibitory activity to human colorectal cancer through arresting cell cycle progression and inducing p53-mediated apoptosis, which may present a novel strategy in CRC therapies and contribute to the optimizing clinical application of 5-FU.	Thioguanine	12-14	P53	Homo sapiens	135-138
33906076-15	2021	The underlying mechanisms involved in the synergistic effects were probably included: (1) increased activation of caspase cascade; (2) enhancement of DNA damage degree and (3) induction of p53 phosphorylation at Serine 46.	Serine	212-218	P53	Homo sapiens	189-192
33906076-16	2021	CONCLUSION: TG potentiated 5-FU"s inhibitory activity to human colorectal cancer through arresting cell cycle progression and inducing p53-mediated apoptosis, which may present a novel strategy in CRC therapies and contribute to the optimizing clinical application of 5-FU.	Fluorouracil	27-31	P53	Homo sapiens	135-138
33781788-0	2021	T-17, a spirostanol saponin, inhibits p53-independent proliferation and p53-dependent migration of gastric cancer cells.	t-17	0-4	P53	Homo sapiens	38-41
33631201-6	2021	Although BLECs were still undergoing transcriptional changes over time, a targeted transcriptome analysis (TempO-Seq) indicated a time and concentration dependent activation of ATF4, XBP1, Nrf2 and p53 stress response pathways under CsA treatment.	Cyclosporine	233-236	P53	Homo sapiens	198-201
33781788-0	2021	T-17, a spirostanol saponin, inhibits p53-independent proliferation and p53-dependent migration of gastric cancer cells.	t-17	0-4	P53	Homo sapiens	72-75
33781788-6	2021	Pre-treatment with N-acetylcysteine (NAC, a ROS scavenger) demonstrated that reactive oxygen species (ROS) mediated T-17-induced p53-independent apoptosis.	Acetylcysteine	19-35	P53	Homo sapiens	129-132
33781788-6	2021	Pre-treatment with N-acetylcysteine (NAC, a ROS scavenger) demonstrated that reactive oxygen species (ROS) mediated T-17-induced p53-independent apoptosis.	Acetylcysteine	37-40	P53	Homo sapiens	129-132
34053323-1	2021	PURPOSE: The mechanism of cytotoxicity of silibinin on two human hepatocellular carcinoma (HCC) cell lines, HepG2 (p53 wild-type) and Hep3B cells (p53 null), is examined in relation with the induction of autophagy and phosphorylation of AMP-activated protein kinase (p-AMPK).	Silybin	42-51	P53	Homo sapiens	115-118
33781788-6	2021	Pre-treatment with N-acetylcysteine (NAC, a ROS scavenger) demonstrated that reactive oxygen species (ROS) mediated T-17-induced p53-independent apoptosis.	Reactive Oxygen Species	77-100	P53	Homo sapiens	129-132
34053323-1	2021	PURPOSE: The mechanism of cytotoxicity of silibinin on two human hepatocellular carcinoma (HCC) cell lines, HepG2 (p53 wild-type) and Hep3B cells (p53 null), is examined in relation with the induction of autophagy and phosphorylation of AMP-activated protein kinase (p-AMPK).	Silybin	42-51	P53	Homo sapiens	147-150
33781788-6	2021	Pre-treatment with N-acetylcysteine (NAC, a ROS scavenger) demonstrated that reactive oxygen species (ROS) mediated T-17-induced p53-independent apoptosis.	Reactive Oxygen Species	102-105	P53	Homo sapiens	129-132
33781788-6	2021	Pre-treatment with N-acetylcysteine (NAC, a ROS scavenger) demonstrated that reactive oxygen species (ROS) mediated T-17-induced p53-independent apoptosis.	t-17	116-120	P53	Homo sapiens	129-132
34047175-0	2021	A Pin1/PML/P53 axis activated by retinoic acid in NPM-1c-acute myeloid leukemia.	Tretinoin	33-46	P53	Homo sapiens	11-14
34057209-11	2021	Long-term exposure of HGFs to nicotine or CSC significantly suppressed their cellular proliferation and migration and upregulated type I collagen, type III collagen, interleukin (IL)-6, IL-8, p16, p21, and p53 mRNA expression, and IL-6 and IL-8 protein expression.	Nicotine	30-38	P53	Homo sapiens	206-209
34047175-2	2021	We reported that ex vivo, RA triggers NPM-1c degradation, P53 activation and growth arrest.	Tretinoin	26-28	P53	Homo sapiens	58-61
34044006-4	2021	Herein, by proposing a mathematical model of glucose-mediated Nanog regulation, we showed that the differential proliferation behavior of CSCs and cell-type similar to CSCs can be explained by considering the experimentally observed varied expression levels of key positive (STAT3) and negative (p53) regulators of Nanog.	Glucose	45-52	P53	Homo sapiens	296-299
34037422-10	2021	Hyperoside could antagonize N protein-induced S-phase arrest by interfering with interaction between N protein and p53 and inhibit viral replication (P < 0.05).	hyperoside	0-10	P53	Homo sapiens	115-118
34028595-6	2021	In turn, metal-induced inhibition of SIRT was shown to affect deacetylation of target proteins including FOXO, PGC1alpha, p53 and NF-kB.	Metals	9-14	P53	Homo sapiens	122-125
34031188-0	2021	TP53 null mutations identify lung cancer cell lines with highest sensitivity to the non-taxane microtubule inhibitor, eribulin.	taxane	88-94	P53	Homo sapiens	0-4
34028092-0	2021	The p53/p21/p16 and PI3K/Akt signaling pathways are involved in the ameliorative effects of maltol on D-galactose-induced liver and kidney aging and injury.	Galactose	102-113	P53	Homo sapiens	4-7
34014550-11	2021	GSEA demonstrated that various cell cycle pathways along with RB-1 pathway, interleukin-10 signaling, regulation of TP53 activity, and P53 downstream pathway were differentially enriched in NOP58 high expression phenotype.	gsea	0-4	P53	Homo sapiens	116-120
32743640-0	2021	Irinotecan and vandetanib create synergies for treatment of pancreatic cancer patients with concomitant TP53 and KRAS mutations.	Irinotecan	0-10	P53	Homo sapiens	104-108
33992677-7	2021	TF footprinting analysis of our ATAC-seq experiments identified 5 TFs or TF families with evidence for ROS-responsive changes in DNA binding: NRF2, AP-1, p53, NFY, and SP/KLF.	Reactive Oxygen Species	103-106	P53	Homo sapiens	154-157
32743640-0	2021	Irinotecan and vandetanib create synergies for treatment of pancreatic cancer patients with concomitant TP53 and KRAS mutations.	vandetanib	15-25	P53	Homo sapiens	104-108
32743640-8	2021	Irinotecan and vandetanib are prospective drugs for PAAD patients with KRASG12Dmutation and TP53 mutation.	Irinotecan	0-10	P53	Homo sapiens	92-96
32743640-8	2021	Irinotecan and vandetanib are prospective drugs for PAAD patients with KRASG12Dmutation and TP53 mutation.	vandetanib	15-25	P53	Homo sapiens	92-96
33857585-0	2021	Anti-Proliferative and Apoptotic Effect of Gemini Curcumin in p53-Wild Type and p53-Mutant Colorectal Cancer Cell Lines.	Curcumin	50-58	P53	Homo sapiens	62-65
33857585-0	2021	Anti-Proliferative and Apoptotic Effect of Gemini Curcumin in p53-Wild Type and p53-Mutant Colorectal Cancer Cell Lines.	Curcumin	50-58	P53	Homo sapiens	80-83
33990641-0	2021	trans-Fatty acids promote p53-dependent apoptosis triggered by cisplatin-induced DNA interstrand crosslinks via the Nox-RIP1-ASK1-MAPK pathway.	Cisplatin	63-72	P53	Homo sapiens	26-29
33990641-5	2021	However, here we found that in the case of CDDP-induced apoptosis, EA-mediated pro-apoptotic action was reversed by knockout of either p53 or ASK1, despite no increase in p53 apoptotic activity.	Cisplatin	43-47	P53	Homo sapiens	135-138
33990641-7	2021	These results demonstrate that in response to CDDP ICLs, TFAs promote p53-dependent apoptosis through the enhancement of the Nox-RIP1-ASK1-MAPK pathway activation, providing insight into the diverse pathogenetic mechanisms of TFAs according to the types of DNA damage.	Cisplatin	46-50	P53	Homo sapiens	70-73
33984544-0	2021	The protective effect of zinc on morphine-induced testicular toxicity via p53 and Akt pathways: An in vitro and in vivo approach.	Morphine	33-41	P53	Homo sapiens	74-77
34004477-8	2021	gamma-Fe2O3 and Fe3O4 NPs could also cause mitochondrial fusion and fission dysregulation, activate lipid peroxidation and iron metabolism-related genes in a P53-dependent manner.	Iron	123-127	P53	Homo sapiens	158-161
33449813-3	2021	METHODS: This was a phase Ib/II study to determine the safety, recommended phase II dose, and efficacy of eprenetapopt administered in combination with azacitidine in patients with TP53-mutant MDS or acute myeloid leukemia (AML) with 20%-30% marrow blasts (ClinicalTrials.gov identifier: NCT03072043).	eprenetapopt	106-118	P53	Homo sapiens	181-185
33449813-13	2021	CONCLUSION: Combination treatment with eprenetapopt and azacitidine is well-tolerated yielding high rates of clinical response and molecular remissions in patients with TP53-mutant MDS and oligoblastic AML.	eprenetapopt	39-51	P53	Homo sapiens	169-173
33970400-0	2021	The Role of p53 Expression in Patients with RAS/BRAF Wild-Type Metastatic Colorectal Cancer Receiving Irinotecan and Cetuximab as Later Line Treatment.	Irinotecan	102-112	P53	Homo sapiens	12-15
33970400-3	2021	OBJECTIVE: In our study, we evaluated the role of p53 expression in patients with RAS/BRAF wild-type metastatic colorectal cancer (mCRC) receiving irinotecan/cetuximab in an exploratory and a validation cohort.	Irinotecan	147-157	P53	Homo sapiens	50-53
33970400-4	2021	PATIENTS AND METHODS: p53 expression was analysed in patients with RAS/BRAF wild-type mCRC receiving second-line or third-line irinotecan/cetuximab.	Irinotecan	127-137	P53	Homo sapiens	22-25
33966047-1	2021	Role of p53 lysine 120 NEDDylation.	Lysine	12-18	P53	Homo sapiens	8-11
33984544-9	2021	CONCLUSION: The present data indicated the protective effect of zinc against morphine-induced testicular (Sertoli) cell toxicity via p53/Akt pathways in both in vivo and in vitro models and suggested the clinical importance of zinc on infertility among chronic opioid users and addicted men.	Morphine	77-85	P53	Homo sapiens	133-136
33927351-4	2021	Mechanistically, RT-mediated p53 activation antagonizes RT-induced SLC7A11 expression and represses glutathione synthesis, thereby promoting RT-induced lipid peroxidation and ferroptosis.	Glutathione	100-111	P53	Homo sapiens	29-32
33377976-0	2021	Sirt3 is critical for p53-mediated ferroptosis upon ROS-induced stress.	ros	52-55	P53	Homo sapiens	22-25
33662352-5	2021	The use of 5-FU and L-OHP, either alone or in combination, strongly suppressed Akt activation, Survivin, Bcl-2, and Bcl-xL expression, and enhanced Puma, phospho-p53, and p53 expression in Caco-2 cells than in DLD-1 cells.	Fluorouracil	11-15	P53	Homo sapiens	162-165
33662352-5	2021	The use of 5-FU and L-OHP, either alone or in combination, strongly suppressed Akt activation, Survivin, Bcl-2, and Bcl-xL expression, and enhanced Puma, phospho-p53, and p53 expression in Caco-2 cells than in DLD-1 cells.	Fluorouracil	11-15	P53	Homo sapiens	171-174
33987018-12	2021	GSEA showed that high CENPN expression was linked to the following pathways: liver cancer subclass proliferation, cell cycle, p53 signaling pathway, Rb1 pathway, positive regulation of cell cycle G1/S phase transition, and DNA damage response signal transduction by p53 class moderators.	gsea	0-4	P53	Homo sapiens	126-129
33987018-12	2021	GSEA showed that high CENPN expression was linked to the following pathways: liver cancer subclass proliferation, cell cycle, p53 signaling pathway, Rb1 pathway, positive regulation of cell cycle G1/S phase transition, and DNA damage response signal transduction by p53 class moderators.	gsea	0-4	P53	Homo sapiens	266-269
33625525-0	2021	P53-mediated in vitro inhibition of PhIP-induced oxidative damage by myricetin bulk and nano forms in healthy lymphocytes.	myricetin	69-78	P53	Homo sapiens	0-3
33325610-0	2021	Butein induces cellular senescence through reactive oxygen species-mediated p53 activation in osteosarcoma U-2 OS cells.	Oxygen	52-58	P53	Homo sapiens	76-79
33325610-9	2021	Co-administration of the ROS inhibitor NAC largely abolished the up-regulated p53 protein level, and rescued the suppressed viability and colony formation ability in butein-exposed U-2 OS cells.	Reactive Oxygen Species	25-28	P53	Homo sapiens	78-81
33325610-10	2021	Taken together, our data proposed the increased ROS by butein exposure activated p53, and the activated p53 was involved in the anti-proliferative effect of butein via inducing senescence in U-2 OS cells.	Reactive Oxygen Species	48-51	P53	Homo sapiens	81-84
33791017-11	2021	Perp and phorbol-12-myristate-13-acetate-induced protein 1 were demonstrated to have vital roles in the p53 signaling pathway which was indicated in the interaction network.	Tetradecanoylphorbol Acetate	9-40	P53	Homo sapiens	104-107
33713969-8	2021	Futhermore, the ferritinophagy-mediated ROS production triggered p53 activation.	Reactive Oxygen Species	40-43	P53	Homo sapiens	65-68
33350292-0	2021	Metformin promotes apoptosis in primary breast cancer cells by downregulation of cyclin D1 and upregulation of P53 through an AMPK-alpha independent mechanism.	Metformin	0-9	P53	Homo sapiens	111-114
33966732-13	2021	GSEA revealed that 4 pathways exhibited significant differential enrichment in the CLCA2 high-expression phenotype, including the P53 signaling pathway, the ERBB signaling pathway, the NOTCH signaling pathway, and the ubiquitin-mediated proteolysis.	gsea	0-4	P53	Homo sapiens	130-133
33350292-1	2021	AIM: In the present study we aimed to figure out the effect of metformin on the expression of AMPK-alpha, cyclin D1 and Tp53, and apoptosis in primary breast cancer cells (PBCCs).	Metformin	63-72	P53	Homo sapiens	120-124
33350292-8	2021	25mM dose of metformin increased p53 expression significantly compared with the non-treated group.	Metformin	13-22	P53	Homo sapiens	33-36
33350292-10	2021	CONCLUSION: Metformin can modulate cyclin D1 and p53 expression through AMPK-alpha independent mechanism in breast cancer cells, leading to cell proliferation inhibition and apoptosis induction.	Metformin	12-21	P53	Homo sapiens	49-52
33952795-9	2021	Moreover, co-administration of Cisplatin and APS was more efficacious for the antitumor effect than either agent alone, as evidenced by the significant decrease in MMP-9 level and increase in p53.	Cisplatin	31-40	P53	Homo sapiens	192-195
33925065-7	2021	6-Gingerol induced cellular and mitochondrial ROS that elevated DDR through ataxia-telangiectasia mutated and p53 activation.	Reactive Oxygen Species	46-49	P53	Homo sapiens	110-113
33952795-9	2021	Moreover, co-administration of Cisplatin and APS was more efficacious for the antitumor effect than either agent alone, as evidenced by the significant decrease in MMP-9 level and increase in p53.	aps	45-48	P53	Homo sapiens	192-195
33907694-5	2021	Knowing that bladder cancer cell lines that lack TP53 are more resistant to cisplatin and because the tumor lacked any other DNA mutation, this patient may have been a candidate for upfront surgery without neoadjuvant chemotherapy.	Cisplatin	76-85	P53	Homo sapiens	49-53
33925586-4	2021	We used a chromatin-directed proteomic approach and identified ZNF84 as a novel regulator of p21 in various p53-deficient cell lines treated with cytostatic dose of doxorubicin.	Doxorubicin	165-176	P53	Homo sapiens	108-111
33965862-6	2021	Furthermore, the HMGB1/p62/LC3II/LC3I and p53/SSAT/beta-catenin pathways were mainly involved in the inhibition of 13b-induced HCC metastasis by targeting polyamine transporters (PTs) overexpressed in HCC.	CHEMBL3741121	115-118	P53	Homo sapiens	42-45
33923162-1	2021	S100P, a small calcium-binding protein, associates with the p53 protein with micromolar affinity.	Calcium	15-22	P53	Homo sapiens	60-63
33995069-7	2021	More importantly, compounds M1, 6b, and 6d could resist high glucose-induced apoptosis of HK-2 cells by activating SIRT1 and deacetylation of p53.	Glucose	61-68	P53	Homo sapiens	142-145
33922989-8	2021	Targeting p53-mediated DNA damage signaling provides another therapeutic strategy to circumvent cisplatin resistance.	Cisplatin	96-105	P53	Homo sapiens	10-13
33968980-10	2021	RSV significantly ameliorated the release of apoptosis-related cytokines, namely P53, cleaved caspase-3, cytochrome c, and BAX, leading to the amelioration of neuronal apoptosis, brain edema, and neurological impairment 24 h after SAH.	Resveratrol	0-3	P53	Homo sapiens	81-84
33860865-5	2021	The study also reveals that treatment of TSC mutant cells with the drug candidate Proxison combined with reduced concentration of rapamycin can increase production of reactive oxygen species (ROS), can modify miRNA expression pattern associated with p53 regulation and can reduce cell viability.	Sirolimus	130-139	P53	Homo sapiens	250-253
33937075-11	2021	Curcumin-mediated covalent binding of MYC to TRRAP reduces the protein amounts of both interaction partners but does not downregulate TP53, so that the growth-arresting effect of wild type TP53 could prevail.	Curcumin	0-8	P53	Homo sapiens	189-193
33827148-7	2021	DNA damage response and apoptosis including the relationship between FOXOs and ATM-Chk2-p53 are essential for platinum resistance of ovarian cancer.	Platinum	110-118	P53	Homo sapiens	88-91
33906321-10	2021	EGCG combined with DDP treatment caused cell cycle arrest in G1 phase in BGC-823 cells, increase of apoptosis (21.3%) vs EGCG (7.25%) and DDP (3.86%) single-use group (p <0.01), up-regulated gene and protein expressions of p19Arf, p53, p21Cip1 (p <0.01).	Cisplatin	19-22	P53	Homo sapiens	231-234
32845162-1	2021	Abraxas brother protein 1 (ABRO1) is a subunit of the deubiquitinating enzyme BRCC36-containing isopeptidase complex and plays important roles in cellular responses to stress by interacting with its binding partners, such as ubiquitin-specific peptidase 7, p53, activating transcription factor 4, THAP-domain containing 5, and serine hydroxymethyltransferase.	Serine	327-333	P53	Homo sapiens	257-260
32715386-0	2021	A natural flavonoid, apigenin isolated from Clerodendrum viscosum leaves, induces G2/M phase cell cycle arrest and apoptosis in MCF-7 cells through the regulation of p53 and caspase-cascade pathway.	Apigenin	21-29	P53	Homo sapiens	166-169
32715386-10	2021	The results revealed the vital role of p53 in apigenin-induced apoptosis in MCF-7 cells.	Apigenin	46-54	P53	Homo sapiens	39-42
32715386-11	2021	CONCLUSIONS: In the present findings, treatment of apigenin-induced intracellular ROS in MCF-7 cells followed by induction of G2/M phase cell cycle arrest and further apoptosis through the regulation of p53 and caspase-cascade signaling pathway.	Apigenin	51-59	P53	Homo sapiens	203-206
33732332-0	2021	MicroRNA-874-3p promotes testosterone-induced granulosa cell apoptosis by suppressing HDAC1-mediated p53 deacetylation.	Testosterone	25-37	P53	Homo sapiens	101-104
33732332-14	2021	Furthermore, compared with the control group, testosterone treatment notably increased p53 expression and acetylation.	Testosterone	46-58	P53	Homo sapiens	87-90
33732332-17	2021	Collectively, the results of the present study indicated that miR-874-3p was upregulated in PCOS and promoted testosterone-induced GC apoptosis by suppressing HDAC1-mediated p53 deacetylation.	Testosterone	110-122	P53	Homo sapiens	174-177
33868388-12	2021	Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment.	Cisplatin	240-249	P53	Homo sapiens	8-11
33868388-0	2021	Interplay Between Thiamine and p53/p21 Axes Affects Antiproliferative Action of Cisplatin in Lung Adenocarcinoma Cells by Changing Metabolism of 2-Oxoglutarate/Glutamate.	Cisplatin	80-89	P53	Homo sapiens	31-34
33868388-13	2021	Cellular thiamine deficiency may interfere with antiproliferative action of cisplatin due to their common modulation of the p53/p21-dependent metabolic switch between the glutamate oxidation and transamination.	Cisplatin	76-85	P53	Homo sapiens	124-127
33868388-0	2021	Interplay Between Thiamine and p53/p21 Axes Affects Antiproliferative Action of Cisplatin in Lung Adenocarcinoma Cells by Changing Metabolism of 2-Oxoglutarate/Glutamate.	Glutamic Acid	160-169	P53	Homo sapiens	31-34
33868388-13	2021	Cellular thiamine deficiency may interfere with antiproliferative action of cisplatin due to their common modulation of the p53/p21-dependent metabolic switch between the glutamate oxidation and transamination.	Glutamic Acid	171-180	P53	Homo sapiens	124-127
33868388-5	2021	Our work focuses on dependence of the action of the DNA damaging anticancer drug cisplatin on metabolic regulation through p53/p21 axes and cellular thiamine status in human lung adenocarcinoma cells A549.	Cisplatin	81-90	P53	Homo sapiens	123-126
33576462-7	2021	Through downregulating SIRT1 and activating p53 signaling, miR-138-5p induced apoptosis in H2O2-induced AC-16 and HCM cells.	Hydrogen Peroxide	91-95	P53	Homo sapiens	44-47
33868388-12	2021	Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment.	Glutamic Acid	56-65	P53	Homo sapiens	8-11
33915913-0	2021	Heterogeneities in Cell Cycle Checkpoint Activation Following Doxorubicin Treatment Reveal Targetable Vulnerabilities in TP53 Mutated Ultra High-Risk Neuroblastoma Cell Lines.	Doxorubicin	62-73	P53	Homo sapiens	121-125
33915913-3	2021	Here, a comprehensive analysis of cell cycle checkpoint activation following doxorubicin (doxo) treatment was performed using flow cytometry, immunofluorescence and live-cell imaging in a panel of TP53 mutated ultra high-risk neuroblastoma (NB) cell lines, SK-N-DZ, Kelly, SK-N-AS, SK-N-FI, and BE(2)-C.	Doxorubicin	77-88	P53	Homo sapiens	197-201
33534927-10	2021	The top 3 enriched reactome pathway ID are RAB GEFs exchange GTP for GDP on RABs, Regulation of TP53 Degradation and Regulation of TP53 Expression and Degradation.	Guanosine Triphosphate	61-64	P53	Homo sapiens	96-100
33534927-10	2021	The top 3 enriched reactome pathway ID are RAB GEFs exchange GTP for GDP on RABs, Regulation of TP53 Degradation and Regulation of TP53 Expression and Degradation.	Guanosine Triphosphate	61-64	P53	Homo sapiens	131-135
33994742-12	2021	p53 was overexpressed in smokers (80.95%) and those consuming alcohol (60%).	Alcohols	62-69	P53	Homo sapiens	0-3
33611211-15	2021	Oxocrebanine led to the mitotic arrest, and these effects occurred through both p53-dependent and p53-independent pathways.	Oxocrebanine	0-12	P53	Homo sapiens	80-83
33915902-9	2021	In addition, metformin treatment increased the expression of monophosphate (AMP)-activated protein kinase (AMPK) and p53 in both HCT116 xenografts and colorectal cancer cell lines and decreased the expression of the urea cycle enzymes, including carbamoyl phosphate synthase 1 (CPS1), arginase 1 (ARG1), ornithine trans-carbamylase (OTC), and ODC.	Metformin	13-22	P53	Homo sapiens	117-120
33915902-11	2021	These results demonstrate that metformin inhibited CRC cell proliferation via activating AMPK/p53 and that there was an association between metformin, urea cycle inhibition and a reduction in putrescine generation.	Metformin	31-40	P53	Homo sapiens	94-97
33611211-15	2021	Oxocrebanine led to the mitotic arrest, and these effects occurred through both p53-dependent and p53-independent pathways.	Oxocrebanine	0-12	P53	Homo sapiens	98-101
33181285-0	2021	Antrodia camphorata extract (ACE)-induced apoptosis is associated with BMP4 expression and p53-dependent ROS generation in human colon cancer cells.	Reactive Oxygen Species	105-108	P53	Homo sapiens	91-94
34053485-15	2021	Functional annotation and enrichment analysis demonstrated that there might be a crosstalk mechanism on functionally related genes such as nuclear receptor activity, ligand-activated transcription factor activity, and steroid hormone receptor activity, and played a role in the occurrence and development of diseases through forkhead box transcription factor O (FoxO) signaling pathway, Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathway, p53 signaling pathway, and phosphateidylinositol 3-kinase (PI3K)/Akt signaling pathway.	Steroids	218-225	P53	Homo sapiens	481-484
33842535-13	2021	Eventually, GSEA showed that the signaling pathways of the cell cycle, ubiquitin-mediated proteolysis, mismatch repair and p53 were enriched in the GNPNAT1 overexpression group.	gsea	12-16	P53	Homo sapiens	123-126
33869031-10	2021	In PDX models with mutated p53 status, there was significant tumor growth inhibition from the combination of AZD1775 with irinotecan or capecitabine (P <= 0.03), while PDX models with wild type p53 did not show anti-tumor synergy from the same combinations (P >= 0.08).	Irinotecan	122-132	P53	Homo sapiens	27-30
33785447-7	2021	In this review, we will summarize the roles of p53 in the regulation of glucose, lipid, amino acid, nucleotide, iron metabolism, and ROS production.	Glucose	72-79	P53	Homo sapiens	47-50
33785447-7	2021	In this review, we will summarize the roles of p53 in the regulation of glucose, lipid, amino acid, nucleotide, iron metabolism, and ROS production.	Iron	112-116	P53	Homo sapiens	47-50
33785447-7	2021	In this review, we will summarize the roles of p53 in the regulation of glucose, lipid, amino acid, nucleotide, iron metabolism, and ROS production.	ros	133-136	P53	Homo sapiens	47-50
33181285-14	2021	We found that cell death is reversible via inactivation or knockdown of p53 gene and reduction of reactive oxygen species (ROS) generation in response to ACE exposure, indicating that p53 plays an important role in ROS generation induced by ACE.	Reactive Oxygen Species	98-121	P53	Homo sapiens	184-187
33181285-14	2021	We found that cell death is reversible via inactivation or knockdown of p53 gene and reduction of reactive oxygen species (ROS) generation in response to ACE exposure, indicating that p53 plays an important role in ROS generation induced by ACE.	Reactive Oxygen Species	123-126	P53	Homo sapiens	184-187
33181285-14	2021	We found that cell death is reversible via inactivation or knockdown of p53 gene and reduction of reactive oxygen species (ROS) generation in response to ACE exposure, indicating that p53 plays an important role in ROS generation induced by ACE.	Reactive Oxygen Species	215-218	P53	Homo sapiens	72-75
33181285-14	2021	We found that cell death is reversible via inactivation or knockdown of p53 gene and reduction of reactive oxygen species (ROS) generation in response to ACE exposure, indicating that p53 plays an important role in ROS generation induced by ACE.	Reactive Oxygen Species	215-218	P53	Homo sapiens	184-187
33181285-16	2021	CONCLUSION: Our findings demonstrate that ACE has potential as an anticancer agent that induces apoptosis through BMP4 and p53-dependent response to ROS in human colon cancer.	Reactive Oxygen Species	149-152	P53	Homo sapiens	123-126
33742136-7	2021	SNORD50A/B deletion in p53 wild-type breast cancer cells will release GMPS and induce the translocation of GMPS into the nucleus, where GMPS can recruit USP7 and form a complex with p53, thereby decreasing p53 ubiquitination, stabilizing p53 proteins, and inhibiting malignant phenotypes of cancer cells.	guanosine 5'-monophosphorothioate	70-74	P53	Homo sapiens	23-26
33705152-6	2021	The mechanism underling the synergism of JQ1 with CDDP in PGP-CDDP/JQ1 was uncovered to be inhibiting Plk1-mutant Trp53 axis.	Cisplatin	50-54	P53	Homo sapiens	114-119
33833992-14	2021	GSEA revealed that PCBP1-AS1 is closely correlated with cell biological function via the p53 and notch signaling pathways.	gsea	0-4	P53	Homo sapiens	89-92
33619536-4	2021	DeltaNp63 acts as a dominant-negative inhibitor to block the function of p53 and TAp63.	deltanp63	0-9	P53	Homo sapiens	73-76
33738852-6	2021	Notably, results of the SPiDER-beta-Gal analysis suggested that glycine alleviated NaF-induced cellular senescence and downregulated P53, P21, HMGA2, and P16INK4a gene expression in the porcine testicular Sertoli cell line.	Glycine	64-71	P53	Homo sapiens	133-136
33656867-2	2021	DMSe has been recently revealed as a precursor of secondary organic aerosol (SOA), and its resultant SOA possesses strong oxidizing capability toward thiol groups that can perturb several major biological pathways in human airway epithelial cells and is linked to genotoxicity, DNA damage, and p53-mediated stress responses.	Sulfhydryl Compounds	150-155	P53	Homo sapiens	294-297
33685467-11	2021	GSEA results showed that samples highly expressing three core genes were all enriched in the p53 signaling pathway in a validation dataset (P < 0.0001).	gsea	0-4	P53	Homo sapiens	93-96
33713860-4	2021	NC loaded with omega 3 polyunsaturated fatty acid (NC-EPA:DHA 6:1) were more effective than native EPA:DHA 6:1 to prevent Ang II-induced VCAM-1 and p53 upregulation, and SA-beta- galactosidase activity in coronary artery segments.	dehydroacetic acid	58-61	P53	Homo sapiens	148-151
33653952-4	2021	We report that the p53 mutant R248Q (R, arginine; Q, glutamine) forms, both in cancer cells and in solutions, a condensate with unique properties, mesoscopic protein-rich clusters.	Arginine	40-48	P53	Homo sapiens	19-22
33676890-7	2021	ROS significantly increase the expression of TRAIL death receptor 5 (DR5) via the p53 and C/EBP homologous protein pathways.	ros	0-3	P53	Homo sapiens	82-85
33503543-3	2021	As the p53/Mdm2 interaction is alleviated by the phosphorylation of the serine-15 (S15) residue of p53, Wip1, which can directly dephosphorylate phospho-S15, facilitates the Mdm2-mediated degradation of p53.	Serine	72-78	P53	Homo sapiens	7-10
33503543-3	2021	As the p53/Mdm2 interaction is alleviated by the phosphorylation of the serine-15 (S15) residue of p53, Wip1, which can directly dephosphorylate phospho-S15, facilitates the Mdm2-mediated degradation of p53.	Serine	72-78	P53	Homo sapiens	99-102
33503543-3	2021	As the p53/Mdm2 interaction is alleviated by the phosphorylation of the serine-15 (S15) residue of p53, Wip1, which can directly dephosphorylate phospho-S15, facilitates the Mdm2-mediated degradation of p53.	Serine	72-78	P53	Homo sapiens	99-102
33663585-0	2021	First in class dual MDM2/MDMX inhibitor ALRN-6924 enhances antitumor efficacy of chemotherapy in TP53 wild-type hormone receptor-positive breast cancer models.	alrn-6924	40-49	P53	Homo sapiens	97-101
33663585-3	2021	METHODS: Three hundred two cell lines representing multiple tumor types were screened to confirm the role of TP53 status in ALRN-6924 efficacy.	alrn-6924	124-133	P53	Homo sapiens	109-113
33663585-7	2021	RESULTS: ALRN-6924 was active in wild-type TP53 (WT-TP53) cancer cell lines, but not mutant TP53.	alrn-6924	9-18	P53	Homo sapiens	43-47
33663585-7	2021	RESULTS: ALRN-6924 was active in wild-type TP53 (WT-TP53) cancer cell lines, but not mutant TP53.	alrn-6924	9-18	P53	Homo sapiens	52-56
33663585-7	2021	RESULTS: ALRN-6924 was active in wild-type TP53 (WT-TP53) cancer cell lines, but not mutant TP53.	alrn-6924	9-18	P53	Homo sapiens	52-56
33786423-3	2021	GVITMB were found in 7 genes using a pan-cancer approach (APC, FANCL, SLC25A13, ERCC3, MSH6, PMS2, and TP53) and 38 gene sets (e.g., those involved in DNA repair and programmed cell death).	gvitmb	0-6	P53	Homo sapiens	103-107
33738256-0	2021	Chidamide Combined With Doxorubicin Induced p53-Driven Cell Cycle Arrest and Cell Apoptosis Reverse Multidrug Resistance of Breast Cancer.	Doxorubicin	24-35	P53	Homo sapiens	44-47
33653340-12	2021	By performing GSEA, we found that TUBA1C is closely correlated to cell cycle, p53 signaling pathway, glycolysis, and gluconeogenesis.	gsea	14-18	P53	Homo sapiens	78-81
33754023-16	2021	Conclusion: In summary, Rap1 may link telomere biology to fatty acid metabolism and aging-related cardiac pathologies via modulating the p53/PPARalpha signaling pathway, which could represent a therapeutic target in preventing/attenuating cardiac aging.	Fatty Acids	58-68	P53	Homo sapiens	137-140
33747931-12	2021	And GSEA analysis also showed that the risk score was closely related with P53 signaling pathway, pancreatic cancer and T cell receptor signaling pathway.	gsea	4-8	P53	Homo sapiens	75-78
33289076-7	2021	We also confirmed by the increased protein levels of proapoptotic factors such as caspase 3, caspase 9, p53, and Bax after treatment with RGD-PAMAM-FP nanoaggregates and also downregulates antiapoptotic factors.	rgd-pamam-fp	138-150	P53	Homo sapiens	104-107
33892537-14	2021	GSEA analysis found that CENPF was significantly enriched in the cell cycle, P53 signaling pathway, MAPK signaling pathway, DNA replication, spliceosome, ubiquitin-mediated proteolysis, focal adhesion, pathway in cancer, glioma, which was highly consistent with previous studies.	gsea	0-4	P53	Homo sapiens	77-80
33850897-12	2021	Our results finally showed that high-risk cases were associated with cell proliferation and cell cycle related gene sets, high tumor protein P53 (TP53) mutation rate, suppressive immunity and increased sensitivity to cisplatin, gemcitabine and docetaxel.	Cisplatin	217-226	P53	Homo sapiens	141-144
33375991-7	2021	Multivariate logistic regression was used to analyze the effects of TP53 mutation type on platinum resistance.	Platinum	90-98	P53	Homo sapiens	68-72
33648519-10	2021	GSEA indicated that high CDCA7 expression was related to the apoptosis pathway, cell cycle pathway, JAK-STAT pathway, NOD like receptor pathway, P53 pathway, T cell receptor pathway and toll like receptor pathway, etc.	gsea	0-4	P53	Homo sapiens	145-148
33347603-0	2021	Quercetin Induces p53-independent Cancer Cell Death via TFEB-mediated Lysosome Activation and ROS-dependent Ferroptosis.	ros	94-97	P53	Homo sapiens	18-21
33375991-11	2021	TP53 mutations were associated with platinum sensitivity, even after adjusting for BRCA mutation status (OR 0.41, p = 0.048).	Platinum	36-44	P53	Homo sapiens	0-4
33375991-14	2021	After adjusting for BRCA mutations, TP53 mutations are associated with platinum sensitivity, and this effect is not dependent on TP53 mutation type.	Platinum	71-79	P53	Homo sapiens	36-40
33582407-5	2021	ERK1/2- and CDK9-kinases are required to upregulate ATF4 by PG3-Oc which restores p53 transcriptomic-targets in cells without functional-p53.	pg3-oc	60-66	P53	Homo sapiens	82-85
33300245-0	2021	Specifications of the ACMG/AMP variant interpretation guidelines for germline TP53 variants.	Adenosine Monophosphate	27-30	P53	Homo sapiens	78-82
33300245-8	2021	The ClinGen TP53 VCEP recommends the use of these TP53-specific ACMG/AMP guidelines as the standard strategy for TP53 germline variant classification.	Adenosine Monophosphate	69-72	P53	Homo sapiens	12-16
33300245-8	2021	The ClinGen TP53 VCEP recommends the use of these TP53-specific ACMG/AMP guidelines as the standard strategy for TP53 germline variant classification.	Adenosine Monophosphate	69-72	P53	Homo sapiens	50-54
33300245-8	2021	The ClinGen TP53 VCEP recommends the use of these TP53-specific ACMG/AMP guidelines as the standard strategy for TP53 germline variant classification.	Adenosine Monophosphate	69-72	P53	Homo sapiens	50-54
33271245-0	2021	Methoxyeugenol regulates the p53/p21 pathway and suppresses human endometrial cancer cell proliferation.	4-allyl-2,6-dimethoxyphenol	0-14	P53	Homo sapiens	29-32
33271245-9	2021	Probably triggered by the higher ROS levels and mitochondrial dysfunction, the gene expression of p53 and p21 increased and the gene expression of CDK4/6 decreased in response to the methoxyeugenol treatment.	Reactive Oxygen Species	33-36	P53	Homo sapiens	98-101
33271245-9	2021	Probably triggered by the higher ROS levels and mitochondrial dysfunction, the gene expression of p53 and p21 increased and the gene expression of CDK4/6 decreased in response to the methoxyeugenol treatment.	4-allyl-2,6-dimethoxyphenol	183-197	P53	Homo sapiens	98-101
33582407-2	2021	A novel small-molecule, PG3-Oc, restores p53 pathway-signaling in tumor cells with mutant-p53, independently of p53/p73.	pg3-oc	24-30	P53	Homo sapiens	41-44
33418206-9	2021	The genes most relevant to ethanol-induced microtia pathogenesis included FGFR-2, FGFR-3, FGF-8, TP53, IGF1, SHH, CTNNB1, and PAX6, among others.	Ethanol	27-34	P53	Homo sapiens	97-101
33418206-13	2021	We propose that mechanisms involving FGF-family genes, TP53, IGF1 and SHH contribute significantly to ethanol-induced microtia and the accompanying malformation of other structures.	Ethanol	102-109	P53	Homo sapiens	55-59
33582407-2	2021	A novel small-molecule, PG3-Oc, restores p53 pathway-signaling in tumor cells with mutant-p53, independently of p53/p73.	pg3-oc	24-30	P53	Homo sapiens	90-93
33613715-0	2021	p53 expression confers sensitivity to 5-fluorouracil via distinct chromatin accessibility dynamics in human colorectal cancer.	Fluorouracil	38-52	P53	Homo sapiens	0-3
33582407-2	2021	A novel small-molecule, PG3-Oc, restores p53 pathway-signaling in tumor cells with mutant-p53, independently of p53/p73.	pg3-oc	24-30	P53	Homo sapiens	90-93
33582407-3	2021	PG3-Oc partially upregulates the p53-transcriptome (13.7% of public p53 target-gene dataset; 15.2% of in-house dataset) and p53-proteome (18%, HT29; 16%, HCT116-p53-/-).	pg3-oc	0-6	P53	Homo sapiens	33-36
33582407-3	2021	PG3-Oc partially upregulates the p53-transcriptome (13.7% of public p53 target-gene dataset; 15.2% of in-house dataset) and p53-proteome (18%, HT29; 16%, HCT116-p53-/-).	pg3-oc	0-6	P53	Homo sapiens	68-71
33582407-3	2021	PG3-Oc partially upregulates the p53-transcriptome (13.7% of public p53 target-gene dataset; 15.2% of in-house dataset) and p53-proteome (18%, HT29; 16%, HCT116-p53-/-).	pg3-oc	0-6	P53	Homo sapiens	68-71
33582407-3	2021	PG3-Oc partially upregulates the p53-transcriptome (13.7% of public p53 target-gene dataset; 15.2% of in-house dataset) and p53-proteome (18%, HT29; 16%, HCT116-p53-/-).	pg3-oc	0-6	P53	Homo sapiens	68-71
33582407-4	2021	Bioinformatic analysis indicates critical p53-effectors of growth-arrest (p21), apoptosis (PUMA, DR5, Noxa), autophagy (DRAM1), and metastasis-suppression (NDRG1) are induced by PG3-Oc.	pg3-oc	178-184	P53	Homo sapiens	42-45
33650658-0	2021	Circadian clock protein CRY1 prevents paclitaxel-induced senescence of bladder cancer cells by promoting p53 degradation.	Paclitaxel	38-48	P53	Homo sapiens	105-108
33650658-11	2021	These data suggested that the accumulated CRY1 in cisplatin-resistant cells could prevent PTX-induced senescence by promoting p53 degradation.	Cisplatin	50-59	P53	Homo sapiens	126-129
33613715-7	2021	Notably, while treatment with 5-FU mediated global increases in chromatin accessibility, chromatin organization in several genomic regions differed depending on the expression status of p53.	Fluorouracil	30-34	P53	Homo sapiens	186-189
33650658-11	2021	These data suggested that the accumulated CRY1 in cisplatin-resistant cells could prevent PTX-induced senescence by promoting p53 degradation.	Paclitaxel	90-93	P53	Homo sapiens	126-129
33613715-8	2021	Since the occupancy of p53 does not overlap with accessible chromatin regions, the 5-FU-mediated changes in chromatin accessibility were not regulated by direct binding of p53.	Fluorouracil	83-87	P53	Homo sapiens	23-26
33613715-9	2021	In the p53-expressing condition, the 5-FU-mediated accessible chromatin region was primarily associated with genes encoding cell death pathways.	Fluorouracil	37-41	P53	Homo sapiens	7-10
33613715-11	2021	In conclusion, expression of p53 may confer 5-FU sensitivity by regulating chromatin accessibility of distinct genes associated with cell apoptosis in a transcription-independent manner.	Fluorouracil	44-48	P53	Homo sapiens	29-32
33538587-0	2021	Benzothiazolyl and Benzoxazoyl Hydrazones Function as Zinc Metallochaperones to Reactivate Mutant p53.	benzoxazoyl hydrazones	19-41	P53	Homo sapiens	98-101
33747905-5	2021	The RNA-seq analysis results demonstrated that genes affected by RSV treatment were mainly involved in apoptosis and the p53 signaling pathway.	Resveratrol	65-68	P53	Homo sapiens	121-124
33538587-1	2021	We identified a set of thiosemicarbazone (TSC) metal ion chelators that reactivate specific zinc-deficient p53 mutants using a mechanism called zinc metallochaperones (ZMCs) that restore zinc binding by shuttling zinc into cells.	Metals	47-52	P53	Homo sapiens	107-110
33538587-7	2021	We conclude that the benzothiazoyl, benzoxazoyl, and benzimidazoyl hydrazones can function as ZMCs to reactivate mutant p53 in vitro and in vivo.	benzoxazoyl	36-47	P53	Homo sapiens	120-123
33754057-17	2021	The in vitro and in vivo findings further demonstrated that high glucose may promote plakoglobin-dependent cooperation of p53 with HIF-1alpha and Smad3, subsequently increasing the expression of TGF-beta1 and the pro-EndMT target genes of the TGF-beta1/Smad signaling pathway in a KLK8-dependent manner.	Glucose	65-72	P53	Homo sapiens	122-125
33658794-13	2021	Furthermore, the transcriptome sequencing demonstrated that p53 and MAPK signaling pathway might play important roles in the inhibitory effects of ouabain.	Ouabain	147-154	P53	Homo sapiens	60-63
33627632-8	2021	The interaction between RCP and P-gp was verified endogenously and loss of RCP or mutant p53 rendered cells more sensitive to cisplatin and etoposide.	Cisplatin	126-135	P53	Homo sapiens	89-92
33073884-2	2021	Alongside clinical platinum drugs, these bimetallic ruthenium-iron complexes have been screened for their cytotoxicity against MIA PaCa-2 (human pancreatic carcinoma), HCT116 p53+/+ (human colon carcinoma, p53-wild type) and ARPE-19 (human retinal pigment epithelial) cell lines.	Iron	62-66	P53	Homo sapiens	175-178
33669781-7	2021	In addition, downregulation of p53 and/or cyclin D1 may also impact the responsiveness of HEC-1-A and KLE cells to cisplatin.	Cisplatin	115-124	P53	Homo sapiens	31-34
33594332-7	2021	To further determine whether the p53-xCT (the substrate-specific subunit of system Xc-)-glutathione (GSH) axis is involved in HG and IL-1beta induced ferroptosis, HUVECs were transiently transfected with p53 small interfering ribonucleic acid or NC small interfering ribonucleic acid and then treated with HG and IL-1beta.	Glutathione	101-104	P53	Homo sapiens	33-36
33671256-0	2021	Identification and Characterization of MortaparibPlus-A Novel Triazole Derivative That Targets Mortalin-p53 Interaction and Inhibits Cancer-Cell Proliferation by Wild-Type p53-Dependent and -Independent Mechanisms.	Triazoles	62-70	P53	Homo sapiens	104-107
33671256-6	2021	By four rounds of visual assays for mortalin and p53, we identified a novel synthetic small-molecule triazole derivative (4-[(1E)-2-(2-phenylindol-3-yl)-1-azavinyl]-1,2,4-triazole, henceforth named MortaparibPlus).	Triazoles	101-109	P53	Homo sapiens	49-52
33671256-6	2021	By four rounds of visual assays for mortalin and p53, we identified a novel synthetic small-molecule triazole derivative (4-[(1E)-2-(2-phenylindol-3-yl)-1-azavinyl]-1,2,4-triazole, henceforth named MortaparibPlus).	(4-[(1e)-2-(2-phenylindol-3-yl)-1-azavinyl]-1,2,4-triazole	121-179	P53	Homo sapiens	49-52
33628636-12	2021	The P53 signaling pathway was significantly enriched in the gene set GSEA enrichment analysis and differential gene KEGG enrichment analysis.	gsea	69-73	P53	Homo sapiens	4-7
33670160-2	2021	Today we know that p53 plays a role in different biological processes such as proliferation, invasion, pluripotency, metabolism, cell cycle control, ROS (reactive oxygen species) production, apoptosis, inflammation and autophagy.	Reactive Oxygen Species	149-152	P53	Homo sapiens	19-22
33580595-1	2021	The present study sought to evaluate the effect of resveratrol supplementation on mRNA expression levels of peroxisome proliferator-activated receptor alpha (PPARalpha), p53, p21, p16, and serum levels of cluster of differentiation 163 (CD163) to TNF-like weak inducer of apoptosis (TWEAK) ratio in patients with type 2 diabetes.	Resveratrol	51-62	P53	Homo sapiens	170-173
33580595-4	2021	Resveratrol supplementation significantly increased mRNA expression levels of p53 and p21 genes, compared with the placebo group (fold change of p53 = 1.29, p = .04; fold change of p21 = 1.46, p = .006).	Resveratrol	0-11	P53	Homo sapiens	78-81
33580595-4	2021	Resveratrol supplementation significantly increased mRNA expression levels of p53 and p21 genes, compared with the placebo group (fold change of p53 = 1.29, p = .04; fold change of p21 = 1.46, p = .006).	Resveratrol	0-11	P53	Homo sapiens	145-148
33580595-7	2021	Resveratrol supplementation resulted in significant changes in p53 and p21 genes expression, while serum levels of sCD163/sTWEAK ratio also improved in the resveratrol group, without any significant change in adjusted sCD163 levels.	Resveratrol	0-11	P53	Homo sapiens	63-66
33670160-2	2021	Today we know that p53 plays a role in different biological processes such as proliferation, invasion, pluripotency, metabolism, cell cycle control, ROS (reactive oxygen species) production, apoptosis, inflammation and autophagy.	Reactive Oxygen Species	154-177	P53	Homo sapiens	19-22
33566220-0	2021	Novel lnc-HZ03 and miR-hz03 promote BPDE-induced human trophoblastic cell apoptosis and induce miscarriage by upregulating p53/SAT1 pathway.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	36-40	P53	Homo sapiens	123-126
33566220-11	2021	All together, the p53/SAT1 pathway upregulated by lnc-HZ03 and miR-hz03 could promote BPDE-induced human trophoblastic cell apoptosis and the occurrence of miscarriage, shedding novel light on the causes of miscarriage.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	86-90	P53	Homo sapiens	18-21
33566220-17	2021	After exposure to BPDE, lnc-HZ03/miR-hz03 and p53/SAT1 pathways are upregulated and finally induce miscarriage.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	18-22	P53	Homo sapiens	46-49
33357454-3	2021	Here we report the identification of small molecules, including arsenic trioxide (ATO), an established agent in treating acute promyelocytic leukemia, as cysteine-reactive compounds that rescue structural p53 mutations.	Cysteine	154-162	P53	Homo sapiens	205-208
33560536-4	2021	TP53 mutations are highly prevalent in OPSCC driven by mutagens in tobacco and alcohol.	Alcohols	79-86	P53	Homo sapiens	0-4
33564015-0	2021	Retraction Note: JNK confers 5-fluorouracil resistance in p53-deficient and mutant p53-expressing colon cancer cells by inducing survival autophagy.	Fluorouracil	29-43	P53	Homo sapiens	58-61
33564015-0	2021	Retraction Note: JNK confers 5-fluorouracil resistance in p53-deficient and mutant p53-expressing colon cancer cells by inducing survival autophagy.	Fluorouracil	29-43	P53	Homo sapiens	83-86
33357454-4	2021	Crystal structures of arsenic-bound p53 mutants reveal a cryptic allosteric site involving three arsenic-coordinating cysteines within the DNA-binding domain, distal to the zinc-binding site.	Cysteine	118-127	P53	Homo sapiens	36-39
33546743-7	2021	Through integrated data analysis, we obtained five significant p53-dependent metabolic pathways including phenylalanine, glyoxylate, dicarboxylate, and linoleic acid metabolism, and the citrate cycle.	malonic acid	133-146	P53	Homo sapiens	63-66
33314700-0	2021	A thiol-bound drug reservoir enhances APR-246-induced mutant p53 tumor cell death.	Sulfhydryl Compounds	2-7	P53	Homo sapiens	61-64
33314700-6	2021	Due to the reversibility of MQ conjugation, GS-MQ forms an intracellular drug reservoir that increases availability of MQ for targeting mutant p53.	memoquin	28-30	P53	Homo sapiens	143-146
33314700-6	2021	Due to the reversibility of MQ conjugation, GS-MQ forms an intracellular drug reservoir that increases availability of MQ for targeting mutant p53.	gs-mq	44-49	P53	Homo sapiens	143-146
33546743-7	2021	Through integrated data analysis, we obtained five significant p53-dependent metabolic pathways including phenylalanine, glyoxylate, dicarboxylate, and linoleic acid metabolism, and the citrate cycle.	Linoleic Acid	152-165	P53	Homo sapiens	63-66
33592864-3	2021	METHODS: Pubmed, Web of Science, EMBASE, CNKI, China Wanfang databases were searched for studies on the relationship between the p53 expression and the chemosensitivity to platinum drugs in patients with NSCLC.	Platinum	172-180	P53	Homo sapiens	129-132
33562817-6	2021	At the protein level, myricetin-induced upregulation of PARP-1 and decreased expression of Bcl-2, whereas copper-induced changes in the expression of p53, p73, Bax and NME1 were not further affected by myricetin.	Copper	106-112	P53	Homo sapiens	150-153
33614662-0	2021	Rapamycin Protects Skin Fibroblasts From UVA-Induced Photoaging by Inhibition of p53 and Phosphorylated HSP27.	Sirolimus	0-9	P53	Homo sapiens	81-84
33614662-5	2021	In addition, treatment with rapamycin significantly increased cell autophagy levels, decreased the expression of p53 and phosphorylated HSP27, and reduced genotoxic and oxidative cellular stress levels in UVA-induced HDFs.	Sirolimus	28-37	P53	Homo sapiens	113-116
33592864-10	2021	CONCLUSION: Patients with p53 negative expression is more sensitive to platinum-based chemotherapy than those with p53 positive expression in NSCLC, especially in advanced NSCLC.	Platinum	71-79	P53	Homo sapiens	26-29
33592864-0	2021	Meta-analysis of P53 expression and sensitivity to platinum-based chemotherapy in patients with non-small cell lung cancer.	Platinum	51-59	P53	Homo sapiens	17-20
33592864-2	2021	This study aims to explore the correlation between p53 expression and sensitivity to platinum-based chemotherapy in patients with NSCLC.	Platinum	85-93	P53	Homo sapiens	51-54
33530952-9	2021	INI-43 pre-treatment resulted in moderately stabilized p53 and induced p53 reporter activity, which translated to increased p21 and decreased Mcl-1 upon cisplatin combination treatment.	Cisplatin	153-162	P53	Homo sapiens	71-74
33546767-7	2021	We found that inhibition of NAMPT or SIRT2 in iPS cells induces p53 protein by promoting its lysine acetylation.	Lysine	93-99	P53	Homo sapiens	64-67
33542214-2	2021	In response to low-level ROS stress, the expression of Delta133p53, a human p53 isoform, is upregulated to promote cell survival and protect cells from senescence by enhancing the expression of antioxidant genes.	Reactive Oxygen Species	25-28	P53	Homo sapiens	63-66
33546421-5	2021	Frequent genetic alterations observed in pancreatic ductal adenocarcinoma (PDAC) affect KRAS and p53 proteins, which have a role in ROS production and control, respectively.	Reactive Oxygen Species	132-135	P53	Homo sapiens	97-100
33528639-0	2021	Correction to: Nutlin-3 cooperates with doxorubicin to induce apoptosis of human hepatocellular carcinoma cells through p53 or p73 signaling pathways.	Doxorubicin	40-51	P53	Homo sapiens	120-123
33278547-5	2021	RESULTS: Our results showed that the Curcumin binds p53Y220C with Kd = 3.169 +- 0.257 muM and it increases the DNA binding affinity of the mutant by 4-fold with Kd = 851.29 +- 186.27 nM.	Curcumin	37-45	P53	Homo sapiens	52-55
33326188-4	2021	Therefore, a CD44-targeted delivery system is designed and constructed by self-assembly of tyrosine (Tyr)-hyaluronic acid (HA)-polyethyleneimine (PEI), which can radiolabel 131/125 I and load a p53 mutant restoring regent, Prima-1.	Tyrosine	91-99	P53	Homo sapiens	194-197
33326188-4	2021	Therefore, a CD44-targeted delivery system is designed and constructed by self-assembly of tyrosine (Tyr)-hyaluronic acid (HA)-polyethyleneimine (PEI), which can radiolabel 131/125 I and load a p53 mutant restoring regent, Prima-1.	tyr)-hyaluronic acid	101-121	P53	Homo sapiens	194-197
33517274-5	2021	Flow cytometry, western blotting, and caspase-3/7 assays revealed that CCL299 induced G1-phase cell-cycle arrest followed by apoptosis that was associated with up-regulation of p-p53 (Ser15) and p21 expression and the down-regulation of p-CDK2 (Thr160) expression.	ccl299	71-77	P53	Homo sapiens	179-182
33278547-7	2021	By caspase and Annexin V assays, we could demonstrate Curcumin at 3 muM to 8 muM concentration could initiate p53 mediated apoptosis in BxPC-3 cell lines.	Curcumin	54-62	P53	Homo sapiens	110-113
33505114-0	2021	Encorafenib enhances TRAIL-induced apoptosis of colorectal cancer cells dependent on p53/PUMA signaling.	encorafenib	0-11	P53	Homo sapiens	85-88
32458023-3	2021	Following treatment with a platinum-based chemotherapeutic, there is a reduction in global levels of H2Bub1 accompanied by an increase in levels of the tumor suppressor p53.	Platinum	27-35	P53	Homo sapiens	169-172
32458023-6	2021	H2Bub1-enriched genes encompassed fifteen p53 target genes including PPM1D, BTG2, PLK2, MDM2, CDKN1A and BBC3, genes related to ERK/MAPK signalling, those participating in nucleotide excision repair including XPC, and genes involved in the immune response and platinum drug resistance including POLH.	Platinum	260-268	P53	Homo sapiens	42-45
33505114-13	2021	This study indicates that encorafenib stimulates TRAIL-induced apoptosis of CRC cells dependent on p53/PUMA signaling, which may provide instructions for the treatment of CRC.	encorafenib	26-37	P53	Homo sapiens	99-102
33505114-11	2021	Besides, encorafenib administration promoted the expression levels of p53 and PUMA in TRAIL-induced CRC cells.	encorafenib	9-20	P53	Homo sapiens	70-73
33505114-12	2021	Furthermore, p53 knockdown attenuated the expression of PUMA and DR5 in TRAIL-induced CRC cells treated with encorafenib.	encorafenib	109-120	P53	Homo sapiens	13-16
33484475-4	2021	Previously, serine deprivation has been connected to the action of the tumor suppressor p53, and we have previously published on a role for p53 regulating sphingosine kinase 1 (SK1), an enzyme that phosphorylates sphingosine to form sphingosine-1-phosphate (S1P).	Serine	12-18	P53	Homo sapiens	88-91
33629325-7	2021	CONCLUSIONS: Nano-ZnO induced autophagy, upregulated the p53 gene, and facilitated the apoptosis of liver cancer cells, indicating that nano-ZnO might be a therapeutic approach for the treatment of liver cancer patients.	nano-zno	13-21	P53	Homo sapiens	57-60
33629325-7	2021	CONCLUSIONS: Nano-ZnO induced autophagy, upregulated the p53 gene, and facilitated the apoptosis of liver cancer cells, indicating that nano-ZnO might be a therapeutic approach for the treatment of liver cancer patients.	nano-zno	136-144	P53	Homo sapiens	57-60
33717544-13	2021	The results of GSEA enrichment analysis showed that the genes in the high-risk group were mainly enriched in cell cycle and p53 signaling pathways.	gsea	15-19	P53	Homo sapiens	124-127
33525943-11	2022	Conclusion: GSEA revealed that PSMD6 and PSMD11 play a role in PDAC through various biological processes and signaling pathways, including TP53, CDKN2A, MYC pathway, DNA repair, KRAS, cell cycle checkpoint, NIK, NF-kappaB signaling pathway, and proteasomes.	gsea	12-16	P53	Homo sapiens	139-143
33002289-0	2021	Gallic acid potentiates the apoptotic effect of paclitaxel and carboplatin via overexpression of Bax and P53 on the MCF-7 human breast cancer cell line.	Paclitaxel	48-58	P53	Homo sapiens	105-108
33183422-0	2021	Effect of Nano-Platinum on Proliferation and Apoptosis of Non-Small Cell Lung Cancer Cells via P53 Pathway.	Platinum	15-23	P53	Homo sapiens	95-98
33183422-12	2021	The p53-related signaling pathway may participate in the process of apoptosis and reverse the process of cisplatin resistance, but the specific mechanism and whether there are other signaling pathways involved Further research is needed.	Cisplatin	105-114	P53	Homo sapiens	4-7
33372419-10	2021	Interestingly, p53 and EGFR exon 19 deletion mutations were more frequent in patients with hOGG1 Ser/Cys + Cys/Cys hOGG1-Cys variants than with the hOGG1 Ser/Ser genotype (P = 0.010 for p53, P = 0.032 for EGFR).	Cysteine	107-110	P53	Homo sapiens	15-18
33376540-12	2021	GSEA demonstrated the p53, cell cycle, DNA replication, mismatch repair, nucleotide excision repair and PC pathways were associated with low expression of ANLN.	gsea	0-4	P53	Homo sapiens	22-25
33372419-0	2021	Association of hOGG1-Cys variants with occurrence of p53 and EGFR deletion mutations in non-small cell lung cancer.	Cysteine	21-24	P53	Homo sapiens	53-56
33154093-6	2021	A BET inhibitor INCB057643 effectively inhibited cell viability and induced apoptosis in DLBCL/HGBCL cells regardless of MYC/BCL2/TP53 status.	INCB-057643	16-26	P53	Homo sapiens	130-134
33372419-10	2021	Interestingly, p53 and EGFR exon 19 deletion mutations were more frequent in patients with hOGG1 Ser/Cys + Cys/Cys hOGG1-Cys variants than with the hOGG1 Ser/Ser genotype (P = 0.010 for p53, P = 0.032 for EGFR).	Cysteine	107-110	P53	Homo sapiens	15-18
33372419-10	2021	Interestingly, p53 and EGFR exon 19 deletion mutations were more frequent in patients with hOGG1 Ser/Cys + Cys/Cys hOGG1-Cys variants than with the hOGG1 Ser/Ser genotype (P = 0.010 for p53, P = 0.032 for EGFR).	Serine	97-100	P53	Homo sapiens	15-18
33372419-10	2021	Interestingly, p53 and EGFR exon 19 deletion mutations were more frequent in patients with hOGG1 Ser/Cys + Cys/Cys hOGG1-Cys variants than with the hOGG1 Ser/Ser genotype (P = 0.010 for p53, P = 0.032 for EGFR).	Cysteine	101-104	P53	Homo sapiens	15-18
33372419-10	2021	Interestingly, p53 and EGFR exon 19 deletion mutations were more frequent in patients with hOGG1 Ser/Cys + Cys/Cys hOGG1-Cys variants than with the hOGG1 Ser/Ser genotype (P = 0.010 for p53, P = 0.032 for EGFR).	Cysteine	107-110	P53	Homo sapiens	15-18
33372419-12	2021	KEY POINTS: SIGNIFICANT FINDINGS OF THE STUDY: NSCLC patients with hOGG1-Cys variants may have a higher risk of p53 and EGFR deletion mutations than with hOGG1 Ser/Ser genotype.	Cysteine	73-76	P53	Homo sapiens	112-115
33509226-7	2021	Metabolomics microarray analysis and transcriptome sequencing analysis revealed that GOLPH3L promotes central carbon metabolism in breast cancer by stabilizing the p53 suppressor SERPINE1.	Carbon	110-116	P53	Homo sapiens	164-167
33075425-7	2021	Moreover, combining F-Se-Ara-C with cabozantinib, an anticancer drug currently in clinical use, induced synergistic antitumor activity in p53-deficient prostate cancer cells.	cabozantinib	36-48	P53	Homo sapiens	138-141
33054537-9	2021	The time dependent induction of DNA breaks demonstrated in PC3 cells treated with MPO safe concentration stimulated ROS generation and apoptotic DNA damage through increased expression of tumor suppressor p53 and Bax genes and decreased expression of Bcl2 and MDM2 genes.	ros	116-119	P53	Homo sapiens	205-208
33500399-7	2021	Furthermore, immunoprecipitation analysis unveiled that 4DPG prevents complex formation between Vimentin and p53 resulting in the rescue of p53 and its nuclear localization in aggressive 5-FU-R cells.	Fluorouracil	187-191	P53	Homo sapiens	109-112
33396077-8	2021	ROS induced alteration in p53 regulation and some mitogen/ oncogenic functions determine the transformation outcome influencing cyclin-cdk complexes.	ros	0-3	P53	Homo sapiens	26-29
33498875-6	2021	Particularly, basal-like TNBC cells characterized by inactivated BRCA1 and mutated TP53 produce high ROS levels and rely on ROS signaling for their survival and malignant progression.	Reactive Oxygen Species	101-104	P53	Homo sapiens	83-87
33473103-9	2021	This was most evident when the p53-deficient neurons were globally exposed to cisplatin.	Cisplatin	78-87	P53	Homo sapiens	31-34
33356180-11	2021	Taken together, DFS triggered p53-dependent apoptosis in HCEP cells via ROS-mediated crosstalk between the extrinsic and intrinsic pathways.	Reactive Oxygen Species	72-75	P53	Homo sapiens	30-33
33039869-11	2021	These results indicated that Cr(VI)-induced apoptosis of Hep3B cells (p53-null) was closely associated with calcium overload, and was accompanied by the activation of Ca2+/CaM/CaMKII signaling pathway.	Calcium	108-115	P53	Homo sapiens	70-73
33520115-7	2021	In addition to this, iron chelators stimulate apoptotic and ER stress signalling pathways inducing cell death even in cells lacking a functional p53 gene.	Iron	21-25	P53	Homo sapiens	145-148
33039867-0	2021	ROS-mediated genotoxic stress is involved in NaAsO2-induced cell cycle arrest, stemness enhancement and chemoresistance of prostate cancer cells in a p53-independent manner.	ros	0-3	P53	Homo sapiens	150-153
33039867-13	2021	These results suggest that ROS-mediated genotoxic stress is involved in NaAsO2-induced cell cycle arrest, stemness enhancement and chemoresistance of prostate cancer cells in a p53-independent manner.	ros	27-30	P53	Homo sapiens	177-180
33441834-7	2021	GSEA analysis indicated that the most involved hallmarks pathways were P53 pathway, KRAS signaling, estrogen response early and estrogen response late.	gsea	0-4	P53	Homo sapiens	71-74
33520705-0	2020	TIPE1 Promotes Cervical Cancer Cell Chemoresistance to Cisplatin in a Wild-Type p53-Dependent Manner.	Cisplatin	55-64	P53	Homo sapiens	80-83
33446200-11	2021	Interestingly, VP treated protein lysates showed a ROS-dependent high molecular weight (HMW) band when probed for P62 and P53 protein.	Reactive Oxygen Species	51-54	P53	Homo sapiens	122-125
33486250-5	2021	We hypothesized that curcumin attenuates fluoride toxicity through modulation of Ac-p53.	Curcumin	21-29	P53	Homo sapiens	84-87
33505358-5	2020	We found that p53 was upregulated during cellular senescence and osteogenic differentiation of MSCs respectively induced by H2O2 and BMP9.	Hydrogen Peroxide	124-128	P53	Homo sapiens	14-17
33486250-6	2021	Here we investigated how curcumin affects the p53-p21 pathway in fluoride toxicity.	Curcumin	25-33	P53	Homo sapiens	46-49
33486250-13	2021	However, curcumin itself significantly increased Ac-p53 and upregulated p21 protein levels to suppress cell proliferation in a dose-dependent manner.	Curcumin	9-17	P53	Homo sapiens	52-55
33486250-16	2021	These results suggest that curcumin-induced Ac-p53 and p21 led to cell cycle arrest, while curcumin attenuated fluoride-mediated apoptosis via activation of Akt and suppressed fluoride-mediated DNA damage.	Curcumin	27-35	P53	Homo sapiens	47-50
33413604-3	2021	The most potent nutraceutical compound was capsaicin and it exerted its highest cytotoxicity against HCT 116 p53-/- with IC50 value of 19.67 +- 0.06 microM.	Capsaicin	43-52	P53	Homo sapiens	109-112
33641653-8	2021	Mechanistically, we found that ADP could downregulate HIF1A in MDS clones through upregulation of VHL, P53 and MDM2, which is involved in two parallel pathways to downregulate HIF1A.	Adenosine Diphosphate	31-34	P53	Homo sapiens	103-106
33406814-1	2022	APR-246 is a promising new therapeutic agent that targets p53 mutated proteins in myelodysplastic syndromes and in acute myeloid leukemia.	eprenetapopt	0-7	P53	Homo sapiens	58-61
33404935-7	2021	LIPUFU were more cytotoxic than LIP, LIFU, and LIPU in both LS174T (p53+/+, bax-/-) and HT-29 (p53-/0, bax+/+) cell lines.	lipufu	0-6	P53	Homo sapiens	68-71
33404935-7	2021	LIPUFU were more cytotoxic than LIP, LIFU, and LIPU in both LS174T (p53+/+, bax-/-) and HT-29 (p53-/0, bax+/+) cell lines.	lipufu	0-6	P53	Homo sapiens	95-98
33456714-0	2021	Correction: Cepharanthine hydrochloride reverses the mdr1 (P-glycoprotein)-mediated esophageal squamous cell carcinoma cell cisplatin resistance through JNK and p53 signals.	Cisplatin	124-133	P53	Homo sapiens	161-164
33489866-0	2020	BRAF AMP Frequently Co-occurs With IDH1/2, TP53, and ATRX Mutations in Adult Patients With Gliomas and Is Associated With Poorer Survival Than That of Patients Harboring BRAF V600E.	Adenosine Monophosphate	5-8	P53	Homo sapiens	43-47
33489866-5	2020	The BRAF AMP group had significantly more patients with the mutant isocitrate dehydrogenase 1 and 2 (IDH1/2) (73.68% vs. 18.00%; P = 0.000), tumor protein p53 (TP53) (73.68% vs. 30.00%; P = 0.002), and alpha thalassemia/mental retardation syndrome X linked (ATRX) (63.16% vs. 18.00%; P = 0.001) than the mutation group.	Adenosine Monophosphate	9-12	P53	Homo sapiens	155-158
33489866-5	2020	The BRAF AMP group had significantly more patients with the mutant isocitrate dehydrogenase 1 and 2 (IDH1/2) (73.68% vs. 18.00%; P = 0.000), tumor protein p53 (TP53) (73.68% vs. 30.00%; P = 0.002), and alpha thalassemia/mental retardation syndrome X linked (ATRX) (63.16% vs. 18.00%; P = 0.001) than the mutation group.	Adenosine Monophosphate	9-12	P53	Homo sapiens	160-164
33489866-8	2020	Our findings indicate that BRAF AMP frequently occurs with IDH1/2, TP53, and ATRX mutations.	Adenosine Monophosphate	32-35	P53	Homo sapiens	67-71
33749640-7	2021	Concomitantly, Salidorside increased the protein level and activity of PKR and increased the expression of its downstream targets, p-eIF2alpha (Ser51), p53 MAPK, and p53.	salidorside	15-26	P53	Homo sapiens	152-155
32838724-8	2021	Furthermore, C4-treated cells demonstrated marked overexpression of the pro-apoptotic proteins Bax and caspase-3 as well as the tumor suppressor p53.	imciromab pentetate	13-15	P53	Homo sapiens	145-148
33128380-6	2021	A significant increase in intracellular reactive oxygen species level was also observed, suggesting that regulation of apoptotic proteins triggered by myricetin exposure in lymphocytes from myeloma patients occurred through P53 and oxidative stress-dependent pathways.	Reactive Oxygen Species	40-63	P53	Homo sapiens	224-227
33128380-6	2021	A significant increase in intracellular reactive oxygen species level was also observed, suggesting that regulation of apoptotic proteins triggered by myricetin exposure in lymphocytes from myeloma patients occurred through P53 and oxidative stress-dependent pathways.	myricetin	151-160	P53	Homo sapiens	224-227
33310183-6	2021	Furthermore, only the C-terminal domain participates in the jump of p53 along DNA at a high salt concentration.	Salts	92-96	P53	Homo sapiens	68-71
32723262-11	2021	RESULTS: Among Se-DHPM, 49H was selectively cytotoxic to HepG2 cells, reduced cell proliferation and increased BAX (80%) and p53 (66%) causing apoptosis.	49H	24-27	P53	Homo sapiens	125-128
33321290-0	2021	Autophagy-mediated cytoplasmic accumulation of p53 leads to apoptosis through DRAM-BAX in cadmium-exposed human proximal tubular cells.	Cadmium	90-97	P53	Homo sapiens	47-50
33321290-1	2021	The tumor suppressor p53 is involved in cadmium (Cd)-induced apoptosis and autophagy.	Cadmium	40-47	P53	Homo sapiens	21-24
33321290-1	2021	The tumor suppressor p53 is involved in cadmium (Cd)-induced apoptosis and autophagy.	Cadmium	49-51	P53	Homo sapiens	21-24
33321290-2	2021	However, the regulatory mechanisms of p53 in Cd-induced kidney injury are not well established.	Cadmium	45-47	P53	Homo sapiens	38-41
33321290-3	2021	Here, we report the role of autophagy in Cd-induced p53 induction in human proximal tubular cells (HK-2).	Cadmium	41-43	P53	Homo sapiens	52-55
33321290-4	2021	HK-2 cells treated with Cd induced the expression of p53, DNA damage autophagy modulator (DRAM), and Bcl-2-associated X protein (BAX), as well as caused poly [ADP-ribose] polymerase 1 (PARP-1) cleavage.	Cadmium	24-26	P53	Homo sapiens	53-56
33321290-11	2021	Collectively, Cd induces apoptosis through p53-mediated DRAM-BAX signaling, which can be regulated by autophagy.	Cadmium	14-16	P53	Homo sapiens	43-46
33191800-5	2021	Metformin treatment was negatively associated with p53-AP in T2DM patients.	Metformin	0-9	P53	Homo sapiens	51-54
33137455-1	2021	The manner in which p53 maintains redox homeostasis and the means by which two key metabolic elements, glucose and glutamine, contribute to p53-dependent redox stability remain unclear.	Glucose	103-110	P53	Homo sapiens	140-143
33137455-2	2021	To elucidate the manner in which p53 deals with glucose-deprived, reactive oxygen species (ROS)-prone conditions in this regard, two isogenic cancer subclones (HN3R-A and HN3R-B) bearing distinct p53 mutations as an in vitro model of intratumoral p53 heterogeneity were identified.	Glucose	48-55	P53	Homo sapiens	33-36
33137455-2	2021	To elucidate the manner in which p53 deals with glucose-deprived, reactive oxygen species (ROS)-prone conditions in this regard, two isogenic cancer subclones (HN3R-A and HN3R-B) bearing distinct p53 mutations as an in vitro model of intratumoral p53 heterogeneity were identified.	Reactive Oxygen Species	66-89	P53	Homo sapiens	33-36
33137455-2	2021	To elucidate the manner in which p53 deals with glucose-deprived, reactive oxygen species (ROS)-prone conditions in this regard, two isogenic cancer subclones (HN3R-A and HN3R-B) bearing distinct p53 mutations as an in vitro model of intratumoral p53 heterogeneity were identified.	Reactive Oxygen Species	91-94	P53	Homo sapiens	33-36
33137455-5	2021	However, in glucose-deprived and ROS-prone conditions, HN3R-B, the subclone with the original p53 increased the utilization of glutamine by GLS2, thereby maintaining redox homeostasis and ATP.	Reactive Oxygen Species	33-36	P53	Homo sapiens	94-97
33137455-5	2021	However, in glucose-deprived and ROS-prone conditions, HN3R-B, the subclone with the original p53 increased the utilization of glutamine by GLS2, thereby maintaining redox homeostasis and ATP.	Adenosine Triphosphate	188-191	P53	Homo sapiens	94-97
33631963-6	2021	Next-generation sequencing (NGS) was performed on formalin-fixed paraffin-embedded tumor tissue, revealing one mutation in exon 5, TP53: p.A159 V, which may be associated with chemo-resistance.	Paraffin	65-73	P53	Homo sapiens	131-135
33137455-6	2021	Conversely, HN3R-A, the p53-deficient radioresistant subclone displayed an impairment in glutamine usage and high susceptibility to metabolic stresses as well as ROS-inducing agents despite the increased ROS scavenging system.	Reactive Oxygen Species	162-165	P53	Homo sapiens	24-27
33137455-6	2021	Conversely, HN3R-A, the p53-deficient radioresistant subclone displayed an impairment in glutamine usage and high susceptibility to metabolic stresses as well as ROS-inducing agents despite the increased ROS scavenging system.	Reactive Oxygen Species	204-207	P53	Homo sapiens	24-27
33137455-7	2021	Collectively, our findings suggest that p53 governs the alternative utilization of metabolic ingredients, such as glucose and glutamine, in ROS-prone conditions.	Glucose	114-121	P53	Homo sapiens	40-43
33137455-7	2021	Collectively, our findings suggest that p53 governs the alternative utilization of metabolic ingredients, such as glucose and glutamine, in ROS-prone conditions.	Reactive Oxygen Species	140-143	P53	Homo sapiens	40-43
33137455-8	2021	Thus, p53 status may be an important biomarker for selecting cancer treatment strategies, including metabolic drugs and ROS-inducing agents, for recurrent cancers after radiotherapy.	Reactive Oxygen Species	120-123	P53	Homo sapiens	6-9
32128678-10	2021	Eight biological pathways significantly related to ER were identified by GSEA, such as "cell cycle", "homologous recombination" and "p53 signaling pathway."	gsea	73-77	P53	Homo sapiens	133-136
32505732-14	2021	GSEA identified that the FEN1 expression was related to DNA replication, cell cycle, cytosolic and sensing pathways, oocyte meiosis, and the P53 signalling pathway.	gsea	0-4	P53	Homo sapiens	141-144
32631113-0	2021	Fusaric acid decreases p53 expression by altering promoter methylation and m6A RNA methylation in human hepatocellular carcinoma (HepG2) cells.	Fusaric Acid	0-12	P53	Homo sapiens	23-26
33390811-16	2021	Conclusions: LncRNA XIST competitively bound to miRNA 520 in the regulation of cisplatin resistance by BAX, participating apoptosis in the p53 signaling pathway.	Cisplatin	79-88	P53	Homo sapiens	139-142
33320772-0	2021	Influence of common dietary supplements (curcumin, andrographolide, and d-limonene) on the radiobiological responses of p53-competent colonic cancer epithelial cells.	Curcumin	41-49	P53	Homo sapiens	120-123
33320772-0	2021	Influence of common dietary supplements (curcumin, andrographolide, and d-limonene) on the radiobiological responses of p53-competent colonic cancer epithelial cells.	Limonene	72-82	P53	Homo sapiens	120-123
33320772-1	2021	PURPOSE: The main goal of the research was to determine whether commercially available common dietary phytochemical supplements (curcumin, andrographolide, and d-limonene) have radiomodulatory effects on p53-competent human colonic epithelial cells.	Curcumin	129-137	P53	Homo sapiens	204-207
33320772-1	2021	PURPOSE: The main goal of the research was to determine whether commercially available common dietary phytochemical supplements (curcumin, andrographolide, and d-limonene) have radiomodulatory effects on p53-competent human colonic epithelial cells.	Limonene	160-170	P53	Homo sapiens	204-207
32864863-0	2021	Curcumin induced apoptosis is mediated through oxidative stress in mutated p53 and wild type p53 colon adenocarcinoma cell lines.	Curcumin	0-8	P53	Homo sapiens	75-78
32864863-0	2021	Curcumin induced apoptosis is mediated through oxidative stress in mutated p53 and wild type p53 colon adenocarcinoma cell lines.	Curcumin	0-8	P53	Homo sapiens	93-96
32864863-3	2021	This study evaluates the role of p53 in curcumin mediated ROS generation and cell death.	Curcumin	40-48	P53	Homo sapiens	33-36
32864863-3	2021	This study evaluates the role of p53 in curcumin mediated ROS generation and cell death.	Reactive Oxygen Species	58-61	P53	Homo sapiens	33-36
32864863-5	2021	ROS generation occurs within 1 hour of 40 microM curcumin treatment and a reduction was observed by third hour in HCT-116 insinuating p53 involvement.	Reactive Oxygen Species	0-3	P53	Homo sapiens	134-137
32864863-8	2021	Total p53 protein level increase was observed by 24 hours in HCT-116 upon NAC pre-treatment.	Acetylcysteine	74-77	P53	Homo sapiens	6-9
32864863-9	2021	Our results indicate that curcumin induces ROS mediated cell death in colon adenocarcinoma cell lines and may be mediated via p53.	Curcumin	26-34	P53	Homo sapiens	126-129
33187870-10	2021	Metformin treatment reverted LMNA, LMNC, and p53 expression levels to normal levels.	Metformin	0-9	P53	Homo sapiens	45-48
32851589-6	2021	In addition, myricetin treatment intensified the expression of P53 and relegated the expression of EGFR in A549 cells.	myricetin	13-22	P53	Homo sapiens	63-66
33160987-0	2021	SIRT3 protects endothelial cells from high glucose-induced senescence and dysfunction via the p53 pathway.	Glucose	43-50	P53	Homo sapiens	94-97
33160987-5	2021	However, transfection with adenoviral construct including SIRT3 significantly inhibited HG-induced SA-gal activity, decreased p53 acetylation level at the site Lys 320 (k320), and overexpression of SIRT3 antagonized high glucose-induced angiogenic dysfunction.	Lysine	160-163	P53	Homo sapiens	126-129
32851589-8	2021	In silico experiments were carried out against human EGFR and P53 tumor suppressor protein to gain more insights into the binding mode of the myricetin may act as significant potential for anticancer therapy.	myricetin	142-151	P53	Homo sapiens	62-65
33040459-7	2021	In Ba/F3 cells transformed by NPM-ALK and Ki-JK cells, p53 activation induced by knockdown of EBP2 was significantly inhibited by Akt inhibitor GDC-0068, mTORC1 inhibitor rapamycin, and knockdown of Raptor, an essential component of mTORC1.	Sirolimus	171-180	P53	Homo sapiens	55-58
32420759-11	2021	Combination of quercetin and curcumin was effective on genes that were particularly related to p53, NF-kappaB and TGF-alpha pathways.	Curcumin	29-37	P53	Homo sapiens	95-98
33238842-7	2021	Mutant p53 reactivation with a new class of zinc metallochaperones (ZMC) that restore WT p53 structure and function by restoring Zn2+ to Zn2+ deficient mutant p53.	zmc	68-71	P53	Homo sapiens	7-10
33238842-7	2021	Mutant p53 reactivation with a new class of zinc metallochaperones (ZMC) that restore WT p53 structure and function by restoring Zn2+ to Zn2+ deficient mutant p53.	zmc	68-71	P53	Homo sapiens	89-92
33238842-7	2021	Mutant p53 reactivation with a new class of zinc metallochaperones (ZMC) that restore WT p53 structure and function by restoring Zn2+ to Zn2+ deficient mutant p53.	zmc	68-71	P53	Homo sapiens	89-92
33238842-7	2021	Mutant p53 reactivation with a new class of zinc metallochaperones (ZMC) that restore WT p53 structure and function by restoring Zn2+ to Zn2+ deficient mutant p53.	Zinc	129-133	P53	Homo sapiens	7-10
33238842-7	2021	Mutant p53 reactivation with a new class of zinc metallochaperones (ZMC) that restore WT p53 structure and function by restoring Zn2+ to Zn2+ deficient mutant p53.	Zinc	129-133	P53	Homo sapiens	89-92
33238842-7	2021	Mutant p53 reactivation with a new class of zinc metallochaperones (ZMC) that restore WT p53 structure and function by restoring Zn2+ to Zn2+ deficient mutant p53.	Zinc	129-133	P53	Homo sapiens	89-92
33238842-7	2021	Mutant p53 reactivation with a new class of zinc metallochaperones (ZMC) that restore WT p53 structure and function by restoring Zn2+ to Zn2+ deficient mutant p53.	Zinc	137-141	P53	Homo sapiens	7-10
33238842-7	2021	Mutant p53 reactivation with a new class of zinc metallochaperones (ZMC) that restore WT p53 structure and function by restoring Zn2+ to Zn2+ deficient mutant p53.	Zinc	137-141	P53	Homo sapiens	89-92
33238842-7	2021	Mutant p53 reactivation with a new class of zinc metallochaperones (ZMC) that restore WT p53 structure and function by restoring Zn2+ to Zn2+ deficient mutant p53.	Zinc	137-141	P53	Homo sapiens	89-92
32657143-8	2021	In the metformin treated group, the expression of Bax and PUMA genes was enhanced while the expression of Bcl-2, hTERT, mTOR, and p53 genes declined.	Metformin	7-16	P53	Homo sapiens	130-133
33179088-4	2021	The present study demonstrated that reactive oxygen species induced by H<sub>2</sub>O<sub>2</sub> resulted in human granulosa COV434 cell apoptosis via the regulation of sirtuin 1 (SIRT1)-mediated p53 activity.	Reactive Oxygen Species	36-59	P53	Homo sapiens	197-200
33391528-0	2021	Retraction of "MICAL2 Mediates p53 Ubiquitin Degradation through Oxidating p53 Methionine 40 and 160 and Promotes Colorectal Cancer Malignance".	Methionine	79-89	P53	Homo sapiens	31-34
33240430-9	2021	5-FU induced apoptosis through p53-p21 activity, while chrysin arrested the cell cycle in the G2/M phase.	Fluorouracil	0-4	P53	Homo sapiens	31-34
33240412-0	2021	Blockade of TRIM59 enhances esophageal cancer cell chemosensitivity to cisplatin by upregulating p53.	Cisplatin	71-80	P53	Homo sapiens	97-100
33240412-5	2021	At the molecular level, TRIM59 was indicated to be an E3 putative ubiquitin ligase that targeted the p53 protein, leading to increased degradation of p53, which resulted in decreased chemosensitivity to cisplatin.	Cisplatin	203-212	P53	Homo sapiens	101-104
33240412-5	2021	At the molecular level, TRIM59 was indicated to be an E3 putative ubiquitin ligase that targeted the p53 protein, leading to increased degradation of p53, which resulted in decreased chemosensitivity to cisplatin.	Cisplatin	203-212	P53	Homo sapiens	150-153
33240412-8	2021	The results indicated a relationship between TRIM59, p53 and the chemosensitivity of cisplatin.	Cisplatin	85-94	P53	Homo sapiens	53-56
33603536-11	2021	The mRNA of tumor suppressors P53 and ERalpha were downregulated in the mammosphere, but were significantly upregulated upon naringenin treatment.	naringenin	125-135	P53	Homo sapiens	30-33
33603536-12	2021	By modulating the P53 and ERalpha mRNA, naringenin has the potential of inhibiting BCSCs.	naringenin	40-50	P53	Homo sapiens	18-21
32987137-7	2020	Conversely, the sensitivity of GCN5-AIB1-overexpressing MCF7 cells to tamoxifen was restored by forced p53 expression.	Tamoxifen	70-79	P53	Homo sapiens	103-106
33396303-8	2020	We also found that a fraction of p53 in stress-adapted cells was translocated to the nucleus, and that these cells exhibited a significant decline in the level of cisplatin-DNA damage.	Cisplatin	163-172	P53	Homo sapiens	33-36
33425912-0	2020	EGCG Enhanced the Anti-tumor Effect of Doxorubicine in Bladder Cancer via NF-kappaB/MDM2/p53 Pathway.	Doxorubicin	39-51	P53	Homo sapiens	89-92
33425404-0	2020	Efficacy of Venetoclax and Dexamethasone in Refractory IgM Primary Plasma Cell Leukemia with t(11;14) and TP53 Mutation: A Case Report and Literature Review.	Dexamethasone	27-40	P53	Homo sapiens	106-110
33374288-0	2020	S-Adenosyl-l-Methionine Overcomes uL3-Mediated Drug Resistance in p53 Deleted Colon Cancer Cells.	S-Adenosylmethionine	0-23	P53	Homo sapiens	66-69
33374288-1	2020	PURPOSE: In order to study novel therapeutic approaches taking advantage of natural compounds showing anticancer and anti-proliferative effects, we focused our interest on S-adenosyl-l-methionine, a naturally occurring sulfur-containing nucleoside synthesized from adenosine triphosphate and methionine by methionine adenosyltransferase, and its potential in overcoming drug resistance in colon cancer cells devoid of p53.	S-Adenosylmethionine	172-195	P53	Homo sapiens	418-421
33374288-2	2020	RESULTS: In the present study, we demonstrated that S-adenosyl-l-methionine overcomes uL3-mediated drug resistance in p53 deleted colon cancer cells.	S-Adenosylmethionine	52-75	P53	Homo sapiens	118-121
33374288-4	2020	CONCLUSIONS: Results reported in this paper led us to propose S-adenosyl-l-methionine as a potential promising agent for cancer therapy by examining p53 and uL3 profiles in tumors to yield a better clinical outcomes.	S-Adenosylmethionine	62-85	P53	Homo sapiens	149-152
33426081-7	2020	Molecular docking and SPR analyses suggested direct binding of berberine with AKT1 and TP53; quercetin with EGFR and VEGF165; and ginkgetin, isoginkgetin, and daucosterol with VEGF165 with weak affinities.	Berberine	63-72	P53	Homo sapiens	87-91
33425912-12	2020	EGCG enhanced the anti-tumor effect of DOX in bladder cancer via NF-kappaB/MDM2/p53 pathway, suggesting the potential clinical application against bladder cancer patients.	Doxorubicin	39-42	P53	Homo sapiens	80-83
33425912-8	2020	Further mechanistic studies determined that the combination of DOX and EGCG inhibited phosphorylated NF-kappaB and MDM2 expression, and up-regulated p53 expression in tumor, as assessed by western blot and immunohistochemistry.	Doxorubicin	63-66	P53	Homo sapiens	149-152
33425912-9	2020	Western blot in SW780 cells also confirmed that the combined use of EGCG and DOX caused significant increase in p53, p21, and cleaved-PARP expression, and induced significant inhibition in phosphorylated NF-kappaB and MDM2.	Doxorubicin	77-80	P53	Homo sapiens	112-115
33409152-9	2020	Treatment with DSF/Cu induced oxidative stress and DNA damage response by elevating the reactive oxygen species levels; increasing the expression of P53, P21, and gamma-H2AX proteins; and inhibiting Wnt/beta-catenin signaling in vitro and in vivo.	Copper	19-21	P53	Homo sapiens	149-152
33389946-0	2020	Combined Effects of Protocatechuic Acid and 5-Fluorouracil on p53 Gene Expression and Apoptosis in Gastric Adenocarcinoma Cells.	protocatechuic acid	20-39	P53	Homo sapiens	62-65
33389946-0	2020	Combined Effects of Protocatechuic Acid and 5-Fluorouracil on p53 Gene Expression and Apoptosis in Gastric Adenocarcinoma Cells.	Fluorouracil	44-58	P53	Homo sapiens	62-65
33389946-4	2020	Moreover, the combined 5-FU/PCA exposure led to upregulation of p53 and downregulation of Bcl-2 protein when compared to the untreated control cells.	Fluorouracil	23-27	P53	Homo sapiens	64-67
33389946-6	2020	The mechanisms by which the combined 5-FU/PCA exposure exerts its effects are associated with upregulation of p53 gene expression and downregulation of Bcl-2 level.	Fluorouracil	37-41	P53	Homo sapiens	110-113
33389946-7	2020	Therefore, the combination of 5-FU with PCA not only could be a promising approach to potentially reduce the dose requirements of 5-FU but also could promote apoptosis via p53 and Bcl-2 signaling pathways.	Fluorouracil	30-34	P53	Homo sapiens	172-175
33327383-6	2020	The Azurin copper protein and specific antibodies of p53 were used as a capture element for p53 (wild-type and its mutants).	Copper	11-17	P53	Homo sapiens	92-95
33411689-13	2020	GSEA revealed that the cell cycle, p53 signaling pathway, DNA replication, small cell lung cancer, apoptosis, and pathways in cancer were differentially enriched in patients with high expression of RRM2.	gsea	0-4	P53	Homo sapiens	35-38
33381272-7	2020	The cell model in vitro further demonstrated that p53 knockout or knockdown in the HCT116 cell and L02 cell significantly inhibited cell apoptosis and increased cell viability, presented by suppressing ROS production, oxidative stress, and the Nrf2/HO-1 pathway.	ros	202-205	P53	Homo sapiens	50-53
33339442-1	2020	The histone methyltransferase SETD8, which methylates the lysine 20 of histone H4 (H4K20), is reportedly involved in human carcinogenesis along with nonhistone proteins such as p53.	Lysine	58-64	P53	Homo sapiens	177-180
33363381-15	2020	Furthermore, reversed regulation of Fos and P53 based on UBE2N reduction could reverse paclitaxel sensitivity, respectively.	Paclitaxel	87-97	P53	Homo sapiens	44-47
33012506-0	2020	Pharmacological activation of the p53 pathway by a new compound CYZ2017 exerts anti-tumor effects.	cyz2017	64-71	P53	Homo sapiens	34-37
33012506-2	2020	In this study, we report a new p53-MDM2 interaction inhibitor, CYZ2017, which could induce p53 nuclear translocation and possess p53-dependent anti-proliferation activity in a range of cancer cells.	cyz2017	63-70	P53	Homo sapiens	31-34
33012506-2	2020	In this study, we report a new p53-MDM2 interaction inhibitor, CYZ2017, which could induce p53 nuclear translocation and possess p53-dependent anti-proliferation activity in a range of cancer cells.	cyz2017	63-70	P53	Homo sapiens	91-94
33012506-2	2020	In this study, we report a new p53-MDM2 interaction inhibitor, CYZ2017, which could induce p53 nuclear translocation and possess p53-dependent anti-proliferation activity in a range of cancer cells.	cyz2017	63-70	P53	Homo sapiens	91-94
33012506-3	2020	CYZ2017 treatment led to increase of p53 levels and induced the transactivation of its target genes p21.	cyz2017	0-7	P53	Homo sapiens	37-40
33012506-6	2020	These results support that CYZ2017 might be a promising p53-MDM2 interaction inhibitor with good anti-tumor activity.	cyz2017	27-34	P53	Homo sapiens	56-59
33363381-0	2020	UBE2N Regulates Paclitaxel Sensitivity of Ovarian Cancer via Fos/P53 Axis.	Paclitaxel	16-26	P53	Homo sapiens	65-68
33363381-16	2020	Conclusion: Our study suggests that UBE2N could be used as a therapeutic agent for paclitaxel-resistant ovarian cancer through Fos/P53 pathway.	Paclitaxel	83-93	P53	Homo sapiens	131-134
33302580-7	2020	We demonstrated that the temporal treatment of HCT116 and MCF-7 cancer cells (both p53 wild-type) with DPI caused induction of senescence, that was correlated with decreased level of ROS and upregulation of p53/p21 proteins.	ros	183-186	P53	Homo sapiens	83-86
33322746-2	2020	The ATM-CHEK2-p53 axis has been documented as a backbone for DDR and hypothesized as a barrier against cancer initiation.	ddr	61-64	P53	Homo sapiens	14-17
33317179-3	2020	METHOD: We conjugated p53-specific antibodies to metal tags for detection by mass cytometry, allowing the detection of proteins and their post-translational modifications in single cells.	Metals	49-54	P53	Homo sapiens	22-25
33297931-13	2020	Further investigation showed that p53 protein levels had been increased during ROCK1-mediated apoptosis in response to H2O2.	Hydrogen Peroxide	119-123	P53	Homo sapiens	34-37
33302475-4	2020	We found that phenanthriplatin may regulate the genes GPRC5a, TFF1, and TNFRSF10D, which act through p53 to control apoptosis, differently or to a greater extent than cisplatin, and that it, unlike cisplatin, could upregulate ATP5MD, a gene which signals through the Wnt/beta catenin pathway.	phenanthriplatin	14-30	P53	Homo sapiens	101-104
33302475-4	2020	We found that phenanthriplatin may regulate the genes GPRC5a, TFF1, and TNFRSF10D, which act through p53 to control apoptosis, differently or to a greater extent than cisplatin, and that it, unlike cisplatin, could upregulate ATP5MD, a gene which signals through the Wnt/beta catenin pathway.	Cisplatin	198-207	P53	Homo sapiens	101-104
33316776-0	2020	Postprandial triglyceride-rich lipoproteins-induced premature senescence of adipose-derived mesenchymal stem cells via the SIRT1/p53/Ac-p53/p21 axis through oxidative mechanism.	Triglycerides	13-25	P53	Homo sapiens	129-132
33369470-0	2020	Myricetin Apoptotic Effects on T47D Breast Cancer Cells is a P53-Independent Approach.	myricetin	0-9	P53	Homo sapiens	61-64
33488754-14	2020	Conclusion: Taken together, our results revealed that YSQHP likely exerts its antitumor effects by binding to CASP8, GSK3B, PRKCA, and VEGFR2 and by regulating the apoptosis, p53, and PI3K/AKT pathways.	ysqhp	54-59	P53	Homo sapiens	175-178
33293849-5	2020	Conversely, low-level local ROS play an important role both as redox-signaling molecules in a wide spectrum of pathways involved in the maintenance of cellular homeostasis (MAPK/ERK, PTK/PTP, PI3K-AKT-mTOR), and regulating key transcription factors (NFkappaB/IkappaB, Nrf2/KEAP1, AP-1, p53, HIF-1).	Reactive Oxygen Species	28-31	P53	Homo sapiens	286-289
32013613-0	2020	Tanshinone I induces cell apoptosis by reactive oxygen species-mediated endoplasmic reticulum stress and by suppressing p53/DRAM-mediated autophagy in human hepatocellular carcinoma.	tanshinone	0-12	P53	Homo sapiens	120-123
33287884-10	2020	Furthermore, we confirm interactions between circCDYL and RBPs in bladder cancer cells and demonstrate that circCDYL depletion affects hallmarks of cancer and perturbs the expression of key cancer genes, e.g., TP53.	circcdyl	108-116	P53	Homo sapiens	210-214
33091670-5	2020	The results revealed an increase of 15-27 in p53 level compared to the test cells and that p53 protein level of 3b, 3c and 3d was significantly inductive (1419, 571 and 787 pg/mL, respectively) in relation to doxorubicin (1263 pg/mL).	Doxorubicin	209-220	P53	Homo sapiens	91-94
32992248-1	2020	Anthracycline anticancer drugs show multiple strategies of action on gene functioning by regulation of telomerase enzyme by apoptotic factors, e.g. ceramide level, p53 activity, bcl-2 protein levels, besides inhibiting DNA/RNA synthesis and topoisomerase-II action.	Anthracyclines	0-13	P53	Homo sapiens	164-167
32372016-4	2020	By combing with CDC14A and P53, UNC5B dephosphorylated P53 at Ser-315 site.	Serine	62-65	P53	Homo sapiens	27-30
33137557-7	2020	The results revealed an increase of 12-19 in p53 level compared to the test cells and that p53 protein level of 5a and 5b was significantly inductive (991, and 639 pg/mL, respectively) in relation to doxorubicin (1263 pg/mL).	Doxorubicin	200-211	P53	Homo sapiens	91-94
32958825-5	2020	RESULTS: CB11 causes cell death via ROS-mediated ATM-p53-GADD45alpha signalling in human NSCLC cells, and diphenyleneiodonium (DPI), an NADPH oxidase inhibitor, decreases cell death by inhibiting CB11-mediated ATM signalling.	Reactive Oxygen Species	36-39	P53	Homo sapiens	53-56
32372016-4	2020	By combing with CDC14A and P53, UNC5B dephosphorylated P53 at Ser-315 site.	Serine	62-65	P53	Homo sapiens	55-58
33290139-9	2020	Conclusion: The p53 rs1042522 arg allele together with tobacco smoking and alcohol drinking, was associated with an increased risk, for gastric cancer and EC, but not the survival among northwestern Chinese patients.	Arginine	30-33	P53	Homo sapiens	16-19
33254717-8	2020	ASD children had significantly higher serum levels of 15 elements, among which arsenic, silicon, strontium, and vanadium were positively associated with both Hipk2 and p53.	Vanadium	112-120	P53	Homo sapiens	168-171
33290139-9	2020	Conclusion: The p53 rs1042522 arg allele together with tobacco smoking and alcohol drinking, was associated with an increased risk, for gastric cancer and EC, but not the survival among northwestern Chinese patients.	Alcohols	75-82	P53	Homo sapiens	16-19
32985761-6	2020	Mechanistically, TCDD treatment increased the protein levels of cell growth suppressors, including p53, Rb, p21 and regucalcin, and caspase-3 implicated in apoptotic cell death, and decreased the levels of Stat3, mitogen-activated protein kinase (MAPK/Erk1/2) and phospho-MAPK/Erk1/2.	Polychlorinated Dibenzodioxins	17-21	P53	Homo sapiens	99-102
32985761-10	2020	Treatment with both TCDD and PUFAs collaboratively enhanced the levels of AHR, CYP1A1, p53, p21, Rb and regucalcin.	Polychlorinated Dibenzodioxins	20-24	P53	Homo sapiens	87-90
31897925-10	2020	Neoadjuvant chemotherapy with cisplatin, 5-fluorouracil and leucovorin may offer high response rates and long-term control in a subgroup of patients affected by intestinal-type adenocarcinoma, and in particular in those whose tumors harbor a functional p53 protein.	Cisplatin	30-39	P53	Homo sapiens	253-256
33080414-11	2020	GSEA analysis indicated that PABPC1 expression was associated with P53 signaling pathway.	gsea	0-4	P53	Homo sapiens	67-70
31897925-10	2020	Neoadjuvant chemotherapy with cisplatin, 5-fluorouracil and leucovorin may offer high response rates and long-term control in a subgroup of patients affected by intestinal-type adenocarcinoma, and in particular in those whose tumors harbor a functional p53 protein.	Fluorouracil	41-55	P53	Homo sapiens	253-256
32919690-7	2020	Furthermore, results of real-time quantitative PCR (RT-qPCR) and western blot analysis further validated the anticancer effect of FA-Ce6/DOX/BNPs, as evidenced by elevated gene/protein expression levels of apoptotic biomarkers p53, BID, caspase-3, cleaved poly(ADP-ribose) polymerase 1 (PARP-1), and BAX, contrary to levels of the anti-apoptotic marker Bcl-2.	Doxorubicin	137-140	P53	Homo sapiens	227-230
31875760-8	2020	ROS-mediated DNA damage was observed as reflected by the activation of ATM/ATR, p53 and histone.	Reactive Oxygen Species	0-3	P53	Homo sapiens	80-83
33174043-9	2020	Cisplatin increased the expression of genes related to the p53 and FoxO pathways, such as Fas, p21/CDKN1A, and Bcl-2 binding component 3, but decreased the expression of insulin-like growth factor 1 (IGF1), as well as genes in the histone (Hist)1 and Hist2 clusters.	Cisplatin	0-9	P53	Homo sapiens	59-62
32976933-5	2020	These groups also exhibited positive correlations between high metal concentrations and the average p53 expression levels, but negative correlations with the mean p-Akt cascade protein levels in sperm cells.	Metals	63-68	P53	Homo sapiens	100-103
33361854-10	2020	Expression of TP53 and GSTM1 (gene, associated with the glutathione system) was significantlyupregulated in the group of individuals with chronic bronchitis, whereas in patients with chronic obstructive pulmonary disease, no increase was detected; the expression of SERPINB9 and MCF2L genes was downregulated.	Glutathione	56-67	P53	Homo sapiens	14-18
32093585-6	2020	Previous studies have also shown that p53 reduces intracellular ROS.	Reactive Oxygen Species	64-67	P53	Homo sapiens	38-41
32976933-7	2020	Therefore, our findings may suggest that graded levels of metal exposure significantly influence the relative fluctuation in the levels of p53 and Akt cascade proteins in the sperm cells of infertile subjects.	Metals	58-63	P53	Homo sapiens	139-142
33160274-4	2020	Collectively, our study reveals the indispensable role of p53 in orchestrating both glucose and lipid metabolism to maintain proper hESC identity.	Glucose	84-91	P53	Homo sapiens	58-61
33601000-9	2020	Myricetin-mediated SIRT1 activation was further evidenced by the decreased acetylation of NF-kappaB p65 and p53.	myricetin	0-9	P53	Homo sapiens	108-111
33160274-0	2020	p53 coordinates glucose and choline metabolism during the mesendoderm differentiation of human embryonic stem cells.	Glucose	16-23	P53	Homo sapiens	0-3
33256840-5	2020	Moreover, MEG3 increases the methylation modification of histone H3 at the 27th lysine via P53.	Lysine	80-86	P53	Homo sapiens	91-94
33496141-10	2020	FPS and VE could both ameliorate the changes of SA-beta-gal staining characteristics and klotho, P53 and P21 protein expression levels in the HK-2 cells exposed to D-gal.	Galactose	164-169	P53	Homo sapiens	97-100
33256128-8	2020	The regulation of p53 by GRK2 is due to phosphorylative events in Thr-55, which induce the degradation of p53.	Threonine	66-69	P53	Homo sapiens	18-21
33256128-8	2020	The regulation of p53 by GRK2 is due to phosphorylative events in Thr-55, which induce the degradation of p53.	Threonine	66-69	P53	Homo sapiens	106-109
33299882-12	2020	GSEA showed many cancer-related pathways, such as the p53 signaling pathway and the Wnt signaling pathway, were enriched in the high-GJA1-expression group.	gsea	0-4	P53	Homo sapiens	54-57
33245719-3	2020	We observed that anti-apoA-1 antibodies induce growth arrest (in G2/M phase) and cell apoptosis through caspase 3 activation, accompanied by a selective p53 phosphorylation on serine 15.	Serine	176-182	P53	Homo sapiens	153-156
33262612-0	2020	Berberine Inhibits Cell Proliferation by Interfering with Wild-Type and Mutant P53 in Human Glioma Cells.	Berberine	0-9	P53	Homo sapiens	79-82
33239893-13	2020	High expression of TIMP1 was related to p53 pathway by GSEA and short overall survival time.	gsea	55-59	P53	Homo sapiens	40-43
33139577-4	2020	As a result, Akt3-expressing cells activate the DNA damage response pathway, express high levels of p53 and its direct transcriptional target miR-34, and exhibit a proliferation defect, which is rescued by the antioxidant N-acetylcysteine.	Acetylcysteine	222-238	P53	Homo sapiens	100-103
33244272-0	2020	Biomolecular Factors Represented by Bcl-2, p53, and Tumor-Infiltrating Lymphocytes Predict Response for Adjuvant Anthracycline Chemotherapy in Patients with Early Triple-Negative Breast Cancer.	Anthracyclines	113-126	P53	Homo sapiens	43-46
33217815-13	2020	GSEA identified that the expression of BEX4 was related to DNA replication, RNA polymerase, cell cycle, and P53 signaling pathway.	gsea	0-4	P53	Homo sapiens	108-111
32860803-8	2020	Exogenous H2S from sodium hydrosulfide, attenuated the efficacy of DIM in cancer cells by reducing the activation level of p38-p53 axis.	sodium bisulfide	19-38	P53	Homo sapiens	127-130
33047953-3	2020	Additionally, with the assistance of Nt.BstNBI enzyme-assisted target cycling process, a limited amount of target DNA (a fragment of p53 gene) could be converted into extensive output DNA, which could hybridize with capture DNA to yield abundant DNA duplex for loading mimetic enzyme manganese porphyrin (MnPP).	mnpp	305-309	P53	Homo sapiens	133-136
33148342-7	2020	Expression of Mut-p53 confers resistance to selinexor treatment, which can be overcome by combined INCB057643 treatment in HGBCL-DH cells.	INCB-057643	99-109	P53	Homo sapiens	18-21
33281882-16	2020	GSEA revealed that MYC, androgen, and KRAS were relatively activated and p53 was relatively suppressed in high-risk subtype, compared with the levels in the low-risk subtype.	gsea	0-4	P53	Homo sapiens	73-76
33177647-4	2020	Coffee decoction cooperated with tamoxifen to induce cell-cycle arrest and apoptotic cell death, which may have been mediated by decreases in cyclin D1 expression and the activation of p53 tumor suppressor.	Tamoxifen	33-42	P53	Homo sapiens	185-188
33177647-6	2020	The activation of p53 through the cooperative effects of these unidentified component(s), caffeine, and tamoxifen appeared to be due to the suppression of the ERK and Akt pathways.	Tamoxifen	104-113	P53	Homo sapiens	18-21
33177647-7	2020	Although the mechanisms by which the suppression of these pathways induces p53-mediated apoptotic cell death remain unclear, the combination of decaffeinated coffee, caffeine, and tamoxifen also caused cell-cycle arrest and apoptotic cell death, suggesting that unknown compound(s) present in decaffeinated coffee cooperate with caffeine and tamoxifen.	Tamoxifen	180-189	P53	Homo sapiens	75-78
32886745-0	2020	p53 deficiency triggers dysregulation of diverse cellular processes in physiological oxygen.	Oxygen	85-91	P53	Homo sapiens	0-3
33165811-7	2021	Consistent with the previous results, sodium cantharidinate treatment decreased Bcl-2 and mitochondrial cytochrome-c protein expression, as well as phosphorylation of MDM2; meanwhile, it increased the levels of cleaved-caspase-3, cleaved-caspase-9, cleaved-PARP, Bax, and phosphorylated p53, thus inducing the apoptosis of pancreatic cancer cells.	Sodium	38-44	P53	Homo sapiens	287-290
32886745-4	2020	Analysis of mouse and human oncogene-expressing wild-type and p53-deficient cells in physiological oxygen conditions revealed that p53 loss concurrently impacts numerous distinct cellular processes, including apoptosis, genome stabilization, DNA repair, metabolism, migration, and invasion.	Oxygen	99-105	P53	Homo sapiens	62-65
32886745-4	2020	Analysis of mouse and human oncogene-expressing wild-type and p53-deficient cells in physiological oxygen conditions revealed that p53 loss concurrently impacts numerous distinct cellular processes, including apoptosis, genome stabilization, DNA repair, metabolism, migration, and invasion.	Oxygen	99-105	P53	Homo sapiens	131-134
32947166-8	2020	Moreover, the acetazolamide/cisplatin combination could decrease the level of PCNA but increase the level of p53; decrease the ratio of Bcl-2/Bax and increase the expression of caspase-3 compared with the single drug treated group.	Cisplatin	28-37	P53	Homo sapiens	109-112
32805233-1	2020	S100A4 is a small calcium-binding protein that exerts its biological functions by interacting with nonmuscle myosin IIA (NMIIA) and p53.	Calcium	18-25	P53	Homo sapiens	132-135
33294260-0	2020	Chiauranib selectively inhibits colorectal cancer with KRAS wild-type by modulation of ROS through activating the p53 signaling pathway.	chiauranib	0-10	P53	Homo sapiens	114-117
33294260-7	2020	Mechanistically, Chiauranib inhibits KRAS wild-type CRC cells by triggering ROS production via activating the p53 signaling pathway.	chiauranib	17-27	P53	Homo sapiens	110-113
32934683-6	2020	Combined rAd-p53 and curcumin treatment resulted in higher p53 (P<0.01) and p21 (P<0.01) expression compared with rAd-p53 or curcumin were added alone, suggesting an additive effect on TP53 expression.	Curcumin	21-29	P53	Homo sapiens	59-62
33073770-3	2020	Treatment with MHY2256 inhibited the growth of the HCT116 (TP53 wild-type), HT-29 (TP53 mutant), and DLD-1 (TP53 mutant) human colorectal cancer cell lines.	mhy2256	15-22	P53	Homo sapiens	59-63
33073770-3	2020	Treatment with MHY2256 inhibited the growth of the HCT116 (TP53 wild-type), HT-29 (TP53 mutant), and DLD-1 (TP53 mutant) human colorectal cancer cell lines.	mhy2256	15-22	P53	Homo sapiens	83-87
33073770-3	2020	Treatment with MHY2256 inhibited the growth of the HCT116 (TP53 wild-type), HT-29 (TP53 mutant), and DLD-1 (TP53 mutant) human colorectal cancer cell lines.	mhy2256	15-22	P53	Homo sapiens	83-87
32780285-9	2020	Eventually, the relative proteins expression levels of p53, cleaved caspase-9/3, cytochrome c, Fas-L, Fas, FADD and caspase-8 were substantially up-regulated in H2O2-triggered HepG2 cells, and Bax/Bcl-2 ratio and the relative protein expression levels of PARP were dramatically down-regulated.	Hydrogen Peroxide	161-165	P53	Homo sapiens	55-58
32530119-3	2020	As results, quercetin showed contrasting dose-response to cellular behaviors dependent on the ROS-regulated p53 signaling pathways.	ros	94-97	P53	Homo sapiens	108-111
32934683-8	2020	These results indicated that the combination of rAd-p53 with curcumin synergistically potentiates apoptosis and inhibit EMT compared with either rAd-p53 or curcumin treatment alone via the regulation of TP53 regulation.	Curcumin	61-69	P53	Homo sapiens	203-207
32934683-8	2020	These results indicated that the combination of rAd-p53 with curcumin synergistically potentiates apoptosis and inhibit EMT compared with either rAd-p53 or curcumin treatment alone via the regulation of TP53 regulation.	Curcumin	156-164	P53	Homo sapiens	203-207
32934683-6	2020	Combined rAd-p53 and curcumin treatment resulted in higher p53 (P<0.01) and p21 (P<0.01) expression compared with rAd-p53 or curcumin were added alone, suggesting an additive effect on TP53 expression.	Curcumin	21-29	P53	Homo sapiens	59-62
32961616-2	2020	Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM.	Irinotecan	46-56	P53	Homo sapiens	91-94
32961616-2	2020	Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM.	Irinotecan	58-73	P53	Homo sapiens	91-94
32934683-6	2020	Combined rAd-p53 and curcumin treatment resulted in higher p53 (P<0.01) and p21 (P<0.01) expression compared with rAd-p53 or curcumin were added alone, suggesting an additive effect on TP53 expression.	Curcumin	21-29	P53	Homo sapiens	185-189
32961616-2	2020	Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM.	Irinotecan	75-81	P53	Homo sapiens	91-94
32961616-2	2020	Here, we explore enhancement of the effect of irinotecan [camptothecin-11 (CPT-11)] by the p53-dependent induction of carboxylesterase 2 (CES2), a CPT-11-activating enzyme, in MM.	Irinotecan	147-153	P53	Homo sapiens	91-94
32934683-6	2020	Combined rAd-p53 and curcumin treatment resulted in higher p53 (P<0.01) and p21 (P<0.01) expression compared with rAd-p53 or curcumin were added alone, suggesting an additive effect on TP53 expression.	Curcumin	125-133	P53	Homo sapiens	13-16
33000203-11	2020	Upregulation of miR-125a-5p expression inhibited cell viability, migration, invasion and colony formation of SK-Hep1 cells and reduced the expression of HAX1, VEGF, N-cadherin and vimentin, but increased cell apoptosis and the expression of p53 and E-cadherin.	mir-125a-5p	16-27	P53	Homo sapiens	241-244
33000203-14	2020	In conclusion, miR-125a-5p suppresses liver cancer growth via targeting HAX1 and concurrently modulating the expression of p53 and VEGF and EMT-related markers.	mir-125a-5p	15-26	P53	Homo sapiens	123-126
32901866-4	2020	Co-treatment with the TOPK inhibitor, OTS514, in combination with H2O2 increased p53 acetylation and its expression, whereas it decreased Sirtuin 1 (SIRT1) expression, contributing to the promotion of apoptosis.	Hydrogen Peroxide	66-70	P53	Homo sapiens	81-84
32901866-6	2020	Furthermore, the p53 inhibitor, Pifithrin-mu, diminished the augmentation in poly(ADP-ribose) polymerase (PARP) cleavage induced by OTS514 plus H2O2, while the Mdm2 antagonist, Nutlin 3, increased PARP cleavage.	Hydrogen Peroxide	144-148	P53	Homo sapiens	17-20
32901866-7	2020	Moreover, OTS514 further decreased the SIRT1 transcriptional activity decreased by H2O2, but promoted the H2O2-induced p53 or p21 transcriptional activity.	Hydrogen Peroxide	106-110	P53	Homo sapiens	119-122
32956986-11	2020	CONCLUSION: Concurrent aspirin use with osimertinib in EGFR-mutant NSCLC patients was associated with improved survival, regardless of lines of therapy, CNS metastatic status, EGFR mutation type, age, gender, TP53, and PD-L1 status.	Aspirin	23-30	P53	Homo sapiens	209-213
32901866-9	2020	Taken together, the findings of the present study demonstrate that TOPK inhibition promotes p53-mediated granulosa cell apoptosis through SIRT1 downregulation in response to H2O2.	Hydrogen Peroxide	174-178	P53	Homo sapiens	92-95
32901866-10	2020	Therefore, it can be concluded that TOPK suppresses H2O2-induced apoptosis through the modulation of the p53/SIRT1 axis, suggesting a potential role of TOPK in the regulation of human granulosa cell apoptosis, leading to the promotion of abnormal follicular development.	Hydrogen Peroxide	52-56	P53	Homo sapiens	105-108
33051086-0	2020	Metformin inhibits the inflammatory and oxidative stress response induced by skin UVB-irradiation and provides 4-hydroxy-2-nonenal and nitrotyrosine formation and p53 protein activation.	Metformin	0-9	P53	Homo sapiens	163-166
32440821-6	2020	The results showed that the downregulated genes were mainly enriched in synaptic vesicle cycle, nicotine addiction, and GABAergic synapse, whereas the upregulated genes were enriched in the cell cycle, p53 signaling pathway, and cellular senescence.	Nicotine	96-104	P53	Homo sapiens	202-205
33014154-17	2020	GSEA showed that high expression of UBE2T was associated with the Kyoto Encyclopedia of Genes and Genomes pathways "cell cycle", "oxidative phosphorylation", "DNA replication", "p53 signaling pathway", "ubiquitin mediated proteolysis" and "pentose phosphate pathway".	gsea	0-4	P53	Homo sapiens	178-181
33000191-7	2020	Furthermore, it was also demonstrated that the activation of p53/p21 and nuclear factor-kappaB (NF-kappaB) signaling, and downregulation of SIRT1/6 may be involved in IMR-90 cells, in D-gal-induced aging and ICA may effectively prevent IMR-90 cells from these changes induced by D-gal.	Galactose	184-189	P53	Homo sapiens	61-64
32572277-4	2020	Using chemoproteomic platforms, we show that members of the manumycin family of polyketides, which bear multiple potentially reactive sites, target C374 of the putative E3 ligase UBR7 in breast cancer cells, and engage in molecular glue interactions with the neosubstrate tumor-suppressor TP53, leading to p53 transcriptional activation and cell death.	Polyketides	80-91	P53	Homo sapiens	289-293
32572277-4	2020	Using chemoproteomic platforms, we show that members of the manumycin family of polyketides, which bear multiple potentially reactive sites, target C374 of the putative E3 ligase UBR7 in breast cancer cells, and engage in molecular glue interactions with the neosubstrate tumor-suppressor TP53, leading to p53 transcriptional activation and cell death.	Polyketides	80-91	P53	Homo sapiens	306-309
33115417-11	2020	GSEA disclosed that cell circle, RNA degradation, pyrimidine metabolism, base excision repair, aminoacyl tRNA biosynthesis, DNA replication, p53 signaling pathway, nucleotide excision repair, ubiquitin-mediated proteolysis, citrate cycle TCA cycle were notably enriched in E2F2 high expression phenotype.	gsea	0-4	P53	Homo sapiens	141-144
32905825-0	2020	4-Aminobiphenyl suppresses homologous recombination repair by a reactive oxygen species-dependent p53/miR-513a-5p/p53 loop.	Reactive Oxygen Species	64-87	P53	Homo sapiens	98-101
32905825-0	2020	4-Aminobiphenyl suppresses homologous recombination repair by a reactive oxygen species-dependent p53/miR-513a-5p/p53 loop.	Reactive Oxygen Species	64-87	P53	Homo sapiens	114-117
32905825-5	2020	On the other hand, the levels of p53, miR-513a-5p, and gammaH2AX were attenuated by 5 mM N-acetyl-l-cysteine (NAC) pretreatment, indicating that the reactive oxygen species (ROS)-dependent p53-miR-513a-5p was involved in DSB repair in 4-ABP-treated cells.	Acetylcysteine	89-108	P53	Homo sapiens	33-36
32905825-5	2020	On the other hand, the levels of p53, miR-513a-5p, and gammaH2AX were attenuated by 5 mM N-acetyl-l-cysteine (NAC) pretreatment, indicating that the reactive oxygen species (ROS)-dependent p53-miR-513a-5p was involved in DSB repair in 4-ABP-treated cells.	Acetylcysteine	89-108	P53	Homo sapiens	189-192
32905825-5	2020	On the other hand, the levels of p53, miR-513a-5p, and gammaH2AX were attenuated by 5 mM N-acetyl-l-cysteine (NAC) pretreatment, indicating that the reactive oxygen species (ROS)-dependent p53-miR-513a-5p was involved in DSB repair in 4-ABP-treated cells.	Acetylcysteine	110-113	P53	Homo sapiens	33-36
32905825-5	2020	On the other hand, the levels of p53, miR-513a-5p, and gammaH2AX were attenuated by 5 mM N-acetyl-l-cysteine (NAC) pretreatment, indicating that the reactive oxygen species (ROS)-dependent p53-miR-513a-5p was involved in DSB repair in 4-ABP-treated cells.	Acetylcysteine	110-113	P53	Homo sapiens	189-192
32905825-5	2020	On the other hand, the levels of p53, miR-513a-5p, and gammaH2AX were attenuated by 5 mM N-acetyl-l-cysteine (NAC) pretreatment, indicating that the reactive oxygen species (ROS)-dependent p53-miR-513a-5p was involved in DSB repair in 4-ABP-treated cells.	Reactive Oxygen Species	149-172	P53	Homo sapiens	33-36
32905825-5	2020	On the other hand, the levels of p53, miR-513a-5p, and gammaH2AX were attenuated by 5 mM N-acetyl-l-cysteine (NAC) pretreatment, indicating that the reactive oxygen species (ROS)-dependent p53-miR-513a-5p was involved in DSB repair in 4-ABP-treated cells.	Reactive Oxygen Species	149-172	P53	Homo sapiens	189-192
32905825-5	2020	On the other hand, the levels of p53, miR-513a-5p, and gammaH2AX were attenuated by 5 mM N-acetyl-l-cysteine (NAC) pretreatment, indicating that the reactive oxygen species (ROS)-dependent p53-miR-513a-5p was involved in DSB repair in 4-ABP-treated cells.	Reactive Oxygen Species	174-177	P53	Homo sapiens	33-36
32905825-6	2020	These findings indicated that the ROS/p53/miR-513a-5p/p53 loop axis plays a relevant role in regulating HR repair which may facilitate our understanding of molecular mechanisms regarding how miR-513a-5p impacts DSB repair in 4-ABP-treated cells.	Reactive Oxygen Species	34-37	P53	Homo sapiens	38-41
32905825-6	2020	These findings indicated that the ROS/p53/miR-513a-5p/p53 loop axis plays a relevant role in regulating HR repair which may facilitate our understanding of molecular mechanisms regarding how miR-513a-5p impacts DSB repair in 4-ABP-treated cells.	Reactive Oxygen Species	34-37	P53	Homo sapiens	54-57
33163850-7	2020	TP53 pathway alterations were identified in nine cisplatin-resistant patients and had the highest degree of concordance in primary and metastatic specimens, consistent with their association with this treatment-resistant phenotype.	Cisplatin	49-58	P53	Homo sapiens	0-4
33111621-7	2022	Cmpd-4 and Cmpd-8 demonstrated binding with mutated p53 at cysteine 124, similar to the mutant p53 reactivating compound APR-246 (PRIMA-1Met) for functional restoration of the mutant p53.	Cysteine	59-67	P53	Homo sapiens	52-55
33001126-6	2020	The PCL-ss-P(PEGMA-co-GHA) amphiphilic copolymer could self-assemble into nanoparticles, which could be used to encapsulate anticancer drug doxorubicin (DOX) and compress the p53 gene to form the DOX-loaded PCL-ss-P(PEGMA-co-GHA)/p53 complex (abbreviated as DPGHAP/p53).	Doxorubicin	140-151	P53	Homo sapiens	175-178
33001126-6	2020	The PCL-ss-P(PEGMA-co-GHA) amphiphilic copolymer could self-assemble into nanoparticles, which could be used to encapsulate anticancer drug doxorubicin (DOX) and compress the p53 gene to form the DOX-loaded PCL-ss-P(PEGMA-co-GHA)/p53 complex (abbreviated as DPGHAP/p53).	Doxorubicin	140-151	P53	Homo sapiens	230-233
33001126-6	2020	The PCL-ss-P(PEGMA-co-GHA) amphiphilic copolymer could self-assemble into nanoparticles, which could be used to encapsulate anticancer drug doxorubicin (DOX) and compress the p53 gene to form the DOX-loaded PCL-ss-P(PEGMA-co-GHA)/p53 complex (abbreviated as DPGHAP/p53).	Doxorubicin	140-151	P53	Homo sapiens	258-269
33001126-6	2020	The PCL-ss-P(PEGMA-co-GHA) amphiphilic copolymer could self-assemble into nanoparticles, which could be used to encapsulate anticancer drug doxorubicin (DOX) and compress the p53 gene to form the DOX-loaded PCL-ss-P(PEGMA-co-GHA)/p53 complex (abbreviated as DPGHAP/p53).	Doxorubicin	153-156	P53	Homo sapiens	175-178
33001126-6	2020	The PCL-ss-P(PEGMA-co-GHA) amphiphilic copolymer could self-assemble into nanoparticles, which could be used to encapsulate anticancer drug doxorubicin (DOX) and compress the p53 gene to form the DOX-loaded PCL-ss-P(PEGMA-co-GHA)/p53 complex (abbreviated as DPGHAP/p53).	Doxorubicin	153-156	P53	Homo sapiens	230-233
33001126-6	2020	The PCL-ss-P(PEGMA-co-GHA) amphiphilic copolymer could self-assemble into nanoparticles, which could be used to encapsulate anticancer drug doxorubicin (DOX) and compress the p53 gene to form the DOX-loaded PCL-ss-P(PEGMA-co-GHA)/p53 complex (abbreviated as DPGHAP/p53).	Doxorubicin	153-156	P53	Homo sapiens	258-269
33001126-8	2020	MTT assay showed that the DPGHAP/p53 complex had a significant antitumor effect on A549 cells and H1299 cells compared with free DOX or/and p53 gene therapy alone.	Doxorubicin	129-132	P53	Homo sapiens	33-36
33001126-9	2020	Furthermore, the test results from live cell imaging systems revealed that the DPGHAP/p53 complexes could effectively deliver DOX and the p53 gene into A549 cells.	Doxorubicin	126-129	P53	Homo sapiens	86-89
33108147-0	2020	Resveratrol enhances apoptosis induced by the heterocyclic aromatic amines in p53-wt LoVo cells, but not in p53-deficient HaCaT cells.	Resveratrol	0-11	P53	Homo sapiens	78-81
33195700-10	2020	This study highlights that miR-122 overexpression may restore H2O2-induced HUVEC injury by regulating the expression of p53.	Hydrogen Peroxide	62-66	P53	Homo sapiens	120-123
33083850-0	2020	Determination of p53 biomarker using an electrochemical immunoassay based on layer-by-layer films with NiFe2O4 nanoparticles.	nickel ferrite	103-110	P53	Homo sapiens	17-20
33083850-1	2020	A disposable electrochemical immunosensors is presented suitable to detect cancer biomarker p53 using screen-printed carbon electrodes modified with a layer-by-layer (LbL) matrix of carboxylated NiFe2O4 nanoparticles and polyethyleneimine, onto which anti-p53 antibodies were adsorbed.	Carbon	117-123	P53	Homo sapiens	92-95
33083850-1	2020	A disposable electrochemical immunosensors is presented suitable to detect cancer biomarker p53 using screen-printed carbon electrodes modified with a layer-by-layer (LbL) matrix of carboxylated NiFe2O4 nanoparticles and polyethyleneimine, onto which anti-p53 antibodies were adsorbed.	nickel ferrite	195-202	P53	Homo sapiens	92-95
32151151-0	2020	ROS induced p53 activation: DNA damage, redox signaling or both?	Reactive Oxygen Species	0-3	P53	Homo sapiens	12-15
32151151-4	2020	It is therefore not clear whether the observed activation of p53 by ROS is mediated through the DNA damage response, redox signaling or both.	Reactive Oxygen Species	68-71	P53	Homo sapiens	61-64
33082354-10	2020	Lipid raft/caveolae disruptors (methyl-beta-cyclodextrin (MCD) and Nystatin) and Ang II stimulation variably increased O2- generation and phosphorylation of MLC20, Ezrin-Radixin-Moesin (ERM) and p53 but not ERK1/2, effects recapitulated in Cav-1 silenced (siRNA) VSMCs.	methyl-beta-cyclodextrin	32-56	P53	Homo sapiens	195-198
33086658-3	2020	Thus, a better understanding of the molecular changes of epithelial ovarian cancer cells with wild-type p53 in response to treatment with cisplatin could reveal novel mechanisms of chemoresistance.	Cisplatin	138-147	P53	Homo sapiens	104-107
33086658-4	2020	METHODS: Gene expression profiling was performed on an ovarian cancer cell line A2780 with wild-type p53 treated with cisplatin.	Cisplatin	118-127	P53	Homo sapiens	101-104
33121131-4	2020	However, the combination of DOX with OSMI-1 in HepG2 cells synergistically increased apoptotic cell death through the activation of both the p53 and mitochondrial Bcl2 pathways compared to DOX alone.	Doxorubicin	28-31	P53	Homo sapiens	141-144
33055209-0	2020	Functional interplay among thiol-based redox signaling, metabolism, and ferroptosis unveiled by a genetic variant of TP53.	Sulfhydryl Compounds	27-32	P53	Homo sapiens	117-121
33055209-2	2020	The P47S variant of TP53, which exists primarily in African-descent populations, associates with an elevated abundance of low molecular weight (LMW) thiols, including glutathione (GSH) and coenzyme A (CoA).	Sulfhydryl Compounds	149-155	P53	Homo sapiens	20-24
33055209-2	2020	The P47S variant of TP53, which exists primarily in African-descent populations, associates with an elevated abundance of low molecular weight (LMW) thiols, including glutathione (GSH) and coenzyme A (CoA).	Glutathione	167-178	P53	Homo sapiens	20-24
33055209-2	2020	The P47S variant of TP53, which exists primarily in African-descent populations, associates with an elevated abundance of low molecular weight (LMW) thiols, including glutathione (GSH) and coenzyme A (CoA).	Glutathione	180-183	P53	Homo sapiens	20-24
33497945-6	2020	Combined treatment with Cd and Z-YVAD-FMK remarkably elevated Bcl-2 mRNA and protein levels, inhibited p53, Bax, Bak-1, Cyt C, Caspase-9 and Caspase-3 mRNA levels and p53, Bax, Bak-1, Caspase-9/cleaved Caspase-9 and Caspase-3/cleaved Caspase-3 protein levels, increased mitochondrial membrane potential (MMP), decreased apoptosis ratio and cell damage compared to treatment with Cd alone.	Cadmium	24-26	P53	Homo sapiens	103-106
33497945-6	2020	Combined treatment with Cd and Z-YVAD-FMK remarkably elevated Bcl-2 mRNA and protein levels, inhibited p53, Bax, Bak-1, Cyt C, Caspase-9 and Caspase-3 mRNA levels and p53, Bax, Bak-1, Caspase-9/cleaved Caspase-9 and Caspase-3/cleaved Caspase-3 protein levels, increased mitochondrial membrane potential (MMP), decreased apoptosis ratio and cell damage compared to treatment with Cd alone.	Cadmium	24-26	P53	Homo sapiens	167-170
33087710-0	2020	5-FU promotes stemness of colorectal cancer via p53-mediated WNT/beta-catenin pathway activation.	Fluorouracil	0-4	P53	Homo sapiens	48-51
33087710-6	2020	These findings indicate p53 as a critical mediator of 5-FU-induced CSC activation via the WNT/beta-catenin signaling pathway and highlight the significance of combinatorial treatment of WNT inhibitor and 5-FU as a compelling therapeutic strategy to improve the poor outcomes of current 5-FU-based therapies for CRC patients.	Fluorouracil	54-58	P53	Homo sapiens	24-27
33087710-6	2020	These findings indicate p53 as a critical mediator of 5-FU-induced CSC activation via the WNT/beta-catenin signaling pathway and highlight the significance of combinatorial treatment of WNT inhibitor and 5-FU as a compelling therapeutic strategy to improve the poor outcomes of current 5-FU-based therapies for CRC patients.	Fluorouracil	204-208	P53	Homo sapiens	24-27
33087710-6	2020	These findings indicate p53 as a critical mediator of 5-FU-induced CSC activation via the WNT/beta-catenin signaling pathway and highlight the significance of combinatorial treatment of WNT inhibitor and 5-FU as a compelling therapeutic strategy to improve the poor outcomes of current 5-FU-based therapies for CRC patients.	Fluorouracil	204-208	P53	Homo sapiens	24-27
33078306-9	2021	A total of 74 DElncRNAs were obtained in cadmium group compared with the control group, which were enriched in the GO terms, including intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator, branched-chain amino acid biosynthetic process.	Cadmium	41-48	P53	Homo sapiens	202-205
33101585-8	2020	Phillyrin treatment upregulated the expressions of cyclin E, cyclin-dependent kinase 2 (CDK2), and cyclin A and downregulated the expressions of p21 and p-p53, thereby reversing the G0/G1 cell cycle arrest in H2O2-treated RPE cells.	phillyrin	0-9	P53	Homo sapiens	155-158
33178028-8	2020	Further study disclosed that UDCA significantly inhibited As(III)-induced apoptosis through increasing the expression of Bcl-2 and decreasing the expression of Bax, p53, Cyt C, Cleaved caspase-3 and 9.	as(iii)	58-65	P53	Homo sapiens	165-168
33081324-0	2020	Deferasirox-Dependent Iron Chelation Enhances Mitochondrial Dysfunction and Restores p53 Signaling by Stabilization of p53 Family Members in Leukemic Cells.	Iron	22-26	P53	Homo sapiens	85-88
33081324-0	2020	Deferasirox-Dependent Iron Chelation Enhances Mitochondrial Dysfunction and Restores p53 Signaling by Stabilization of p53 Family Members in Leukemic Cells.	Iron	22-26	P53	Homo sapiens	119-122
32749686-17	2020	The results of the current study have highlighted the clinical value of EGFR and TP53 as predictive biomarkers of platinum-resistant recurrent and/or metastatic ESCC for afatinib sensitivity.	Platinum	114-122	P53	Homo sapiens	81-85
33046085-0	2020	Cyclosporin A protects JEG-3 cells against oxidative stress-induced apoptosis by inhibiting the p53 and JNK/p38 signaling pathways.	Cyclosporine	0-13	P53	Homo sapiens	96-99
33046085-13	2020	CsA also attenuated the activation of p53, decreased the expression of Bax and cleavage of PARP, and increased the expression of Bcl-2 and pro-caspase-3 in the JEG-3 treated with H2O2.	Cyclosporine	0-3	P53	Homo sapiens	38-41
33046085-13	2020	CsA also attenuated the activation of p53, decreased the expression of Bax and cleavage of PARP, and increased the expression of Bcl-2 and pro-caspase-3 in the JEG-3 treated with H2O2.	Hydrogen Peroxide	179-183	P53	Homo sapiens	38-41
33110364-9	2020	Furthermore, CAPE treatment increased the Serine 15 (Ser15) and Serine 46 (Ser46) phosphorylation of p53, while decreased the survivin expression.	Serine	42-48	P53	Homo sapiens	101-104
33110364-9	2020	Furthermore, CAPE treatment increased the Serine 15 (Ser15) and Serine 46 (Ser46) phosphorylation of p53, while decreased the survivin expression.	Serine	64-70	P53	Homo sapiens	101-104
33046085-16	2020	CONCLUSIONS: These results suggested that CsA protected trophoblast cells from OS-induced apoptosis via the inhibition of the p53 and JNK/p38 signaling pathways.	Cyclosporine	42-45	P53	Homo sapiens	126-129
31983282-7	2020	Taken together, our data suggest that PRKDC-mediated phosphorylation of PRKAG1 primes AMPK complex to the lysosomal activation by STK11 in cancer cells thereby linking DNA damage response to autophagy and cellular metabolism.Abbreviations: AXIN1: axin 1; 3-MA: 3-methyladenine; 5-FU: 5-fluorouracil; AA mutant: double alanine mutant (S192A, T284A) of PRKAG1; ACACA: acetyl-CoA carboxylase alpha; AICAR: 5-Aminoimidazole-4-carboxamide ribonucleotide; AMPK: AMP-activated protein kinase; ATG: autophagy-related; ATM: ataxia telangiectasia mutated; ATR: ATM serine/threonine kinase; AV: autophagic vacuole; AVd: degradative autophagic vacuole; AVi: initial autophagic vacuole; BECN1: beclin 1; BSA: bovine serum albumin; CBS: cystathionine beta-synthase; CDK7: cyclin dependent kinase 7; CDKN1A: cyclin dependent kinase inhibitor 1A; EGFP: enhanced green fluorescent protein; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GST: glutathione S transferase; H2AX/H2AFX: H2A.X variant histone; HBSS: Hanks balanced salt solution; IP: immunopurification; IR: ionizing radiation; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAP3K9: mitogen-activated protein kinase kinase kinase 9; mRFP: monomeric red fluorescent protein; mCh: mCherry; MCM7: minichromosome maintenance complex component 7; MTORC1: mechanistic target of rapamycin kinase complex 1; NHEJ: non-homologous end joining; NRBP2: nuclear receptor binding protein 2; NTC: non-targeting control; NUAK1: NUAK family kinase 1; PBS: phosphate-buffered saline; PIK3AP1: phosphoinositide-3-kinase adaptor protein 1; PIK3CA: phosphatidylinositol-4,5-biphosphate 3-kinase catalytic subunit alpha; PIKK: phosphatidylinositol 3-kinase-related kinase; PRKAA: protein kinase AMP-activated catalytic subunit alpha; PRKAB: protein kinase AMP-activated non-catalytic subunit beta; PRKAG: protein kinase AMP-activated non-catalytic subunit gamma; PRKDC: protein kinase, DNA-activated, catalytic subunit; RLuc: Renilla luciferase; RPS6KB1: ribosomal protein S6 kinase B1; SQSTM1: sequestosome 1; STK11/LKB1: serine/threonine kinase 11; TP53: tumor protein p53; TSKS: testis specific serine kinase substrate; ULK1: unc-51 like autophagy activating kinase 1; WIPI2: WD repeat domain, phosphoinositide interacting 2; WT: wild type.	Adenosine Monophosphate	86-89	P53	Homo sapiens	2088-2092
33028529-3	2020	Here, we found that DSBs in oxygen/glucose-deprived (OGD) neurons spatiotemporally correlated with the up-regulation of WRAP53 (WD40-encoding p53-antisense RNA), which translocated to the nucleus to activate the DSB repair response.	Oxygen	28-34	P53	Homo sapiens	142-145
33028529-3	2020	Here, we found that DSBs in oxygen/glucose-deprived (OGD) neurons spatiotemporally correlated with the up-regulation of WRAP53 (WD40-encoding p53-antisense RNA), which translocated to the nucleus to activate the DSB repair response.	Glucose	35-42	P53	Homo sapiens	142-145
33036164-10	2020	The most significantly enriched pathways of target genes controlled by these miRNAs comprise p53 tumor suppressor protein (TP53)-regulated metabolic genes, and those involved in regulation of methyl-CpG-binding protein 2 (MECP2) expression, phosphatase and tensin homolog (PTEN) messenger RNA (mRNA) translation and copper homeostasis.	Copper	316-322	P53	Homo sapiens	123-127
31983282-7	2020	Taken together, our data suggest that PRKDC-mediated phosphorylation of PRKAG1 primes AMPK complex to the lysosomal activation by STK11 in cancer cells thereby linking DNA damage response to autophagy and cellular metabolism.Abbreviations: AXIN1: axin 1; 3-MA: 3-methyladenine; 5-FU: 5-fluorouracil; AA mutant: double alanine mutant (S192A, T284A) of PRKAG1; ACACA: acetyl-CoA carboxylase alpha; AICAR: 5-Aminoimidazole-4-carboxamide ribonucleotide; AMPK: AMP-activated protein kinase; ATG: autophagy-related; ATM: ataxia telangiectasia mutated; ATR: ATM serine/threonine kinase; AV: autophagic vacuole; AVd: degradative autophagic vacuole; AVi: initial autophagic vacuole; BECN1: beclin 1; BSA: bovine serum albumin; CBS: cystathionine beta-synthase; CDK7: cyclin dependent kinase 7; CDKN1A: cyclin dependent kinase inhibitor 1A; EGFP: enhanced green fluorescent protein; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GST: glutathione S transferase; H2AX/H2AFX: H2A.X variant histone; HBSS: Hanks balanced salt solution; IP: immunopurification; IR: ionizing radiation; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAP3K9: mitogen-activated protein kinase kinase kinase 9; mRFP: monomeric red fluorescent protein; mCh: mCherry; MCM7: minichromosome maintenance complex component 7; MTORC1: mechanistic target of rapamycin kinase complex 1; NHEJ: non-homologous end joining; NRBP2: nuclear receptor binding protein 2; NTC: non-targeting control; NUAK1: NUAK family kinase 1; PBS: phosphate-buffered saline; PIK3AP1: phosphoinositide-3-kinase adaptor protein 1; PIK3CA: phosphatidylinositol-4,5-biphosphate 3-kinase catalytic subunit alpha; PIKK: phosphatidylinositol 3-kinase-related kinase; PRKAA: protein kinase AMP-activated catalytic subunit alpha; PRKAB: protein kinase AMP-activated non-catalytic subunit beta; PRKAG: protein kinase AMP-activated non-catalytic subunit gamma; PRKDC: protein kinase, DNA-activated, catalytic subunit; RLuc: Renilla luciferase; RPS6KB1: ribosomal protein S6 kinase B1; SQSTM1: sequestosome 1; STK11/LKB1: serine/threonine kinase 11; TP53: tumor protein p53; TSKS: testis specific serine kinase substrate; ULK1: unc-51 like autophagy activating kinase 1; WIPI2: WD repeat domain, phosphoinositide interacting 2; WT: wild type.	Adenosine Monophosphate	86-89	P53	Homo sapiens	2108-2111
32431164-0	2020	Apoptotic and cell cycle response to homoharringtonine and harringtonine in wild and mutant p53 hepatocarcinoma cells.	harringtonin	41-54	P53	Homo sapiens	92-95
32818504-0	2020	Aconitase 2 sensitizes MCF-7 cells to cisplatin eliciting p53-mediated apoptosis in a ROS-dependent manner.	Cisplatin	38-47	P53	Homo sapiens	58-61
32818504-0	2020	Aconitase 2 sensitizes MCF-7 cells to cisplatin eliciting p53-mediated apoptosis in a ROS-dependent manner.	Reactive Oxygen Species	86-89	P53	Homo sapiens	58-61
32818504-5	2020	This response was driven by the accumulation of reactive oxygen species (ROS) following both ACO2 overexpression and CDDP exposure that permit the stabilization/activation of p53 in nuclear and mitochondrial compartments.	Reactive Oxygen Species	48-71	P53	Homo sapiens	175-178
32818504-5	2020	This response was driven by the accumulation of reactive oxygen species (ROS) following both ACO2 overexpression and CDDP exposure that permit the stabilization/activation of p53 in nuclear and mitochondrial compartments.	Reactive Oxygen Species	73-76	P53	Homo sapiens	175-178
32818504-5	2020	This response was driven by the accumulation of reactive oxygen species (ROS) following both ACO2 overexpression and CDDP exposure that permit the stabilization/activation of p53 in nuclear and mitochondrial compartments.	Cisplatin	117-121	P53	Homo sapiens	175-178
32780509-7	2020	GSEA of the risk score suggests that high risk score phenotype was significantly enriched in cell cycle-related biological processes, protein SUMOylation, DNA replication, p53 binding, regulation of DNA repair, and DNA methylation, as well as Myc, Wnt, RB1, E2F, and TEL pathways.	gsea	0-4	P53	Homo sapiens	172-175
31938994-1	2020	AIMS: Inhibitor for the apoptosis-stimulating protein of p53 (iASPP) has been reported to be correlated with 5-fluorouracil (5-Fu) resistance in renal cell carcinoma.	Fluorouracil	109-123	P53	Homo sapiens	57-60
31938994-1	2020	AIMS: Inhibitor for the apoptosis-stimulating protein of p53 (iASPP) has been reported to be correlated with 5-fluorouracil (5-Fu) resistance in renal cell carcinoma.	Fluorouracil	125-129	P53	Homo sapiens	57-60
32621200-12	2020	E2 treatment reduced mRNA expression and protein level of maspin and p53, and elevated Bcl-2 expression.	Estradiol	0-2	P53	Homo sapiens	69-72
32533982-6	2020	In contrast, deactivating MAPK pathway by ZXF1 silencing enhanced cisplatin-induced cell cycle arrest and apoptosis by activating p53/p21 axis.	Cisplatin	66-75	P53	Homo sapiens	130-133
32583165-3	2020	Here were report 1H, 13C, and 15N resonance assignments for the intrinsically disordered BRCA1 fragment 219-504, which contains important interaction sites for the proto-oncogenic transcription factor MYC as well as for p53.	Hydrogen	17-19	P53	Homo sapiens	220-223
32738659-5	2020	Meanwhile, the intracellular ROS-P53 crosstalk can be upregulated by diallyl disulfide (up to 8-fold increase of ROS) and valproate (up to 18-fold increase of P53) to enhance early apoptosis.	ros	29-32	P53	Homo sapiens	33-36
32738659-5	2020	Meanwhile, the intracellular ROS-P53 crosstalk can be upregulated by diallyl disulfide (up to 8-fold increase of ROS) and valproate (up to 18-fold increase of P53) to enhance early apoptosis.	ros	29-32	P53	Homo sapiens	159-162
32738659-5	2020	Meanwhile, the intracellular ROS-P53 crosstalk can be upregulated by diallyl disulfide (up to 8-fold increase of ROS) and valproate (up to 18-fold increase of P53) to enhance early apoptosis.	ros	113-116	P53	Homo sapiens	33-36
32738659-6	2020	The synchronization of enhanced G2/M arrest and ROS-P53 crosstalk devotes to reverse the cisplatin resistance with a high level of resistance reversion index (50.22).	ros	48-51	P53	Homo sapiens	52-55
32738659-6	2020	The synchronization of enhanced G2/M arrest and ROS-P53 crosstalk devotes to reverse the cisplatin resistance with a high level of resistance reversion index (50.22).	Cisplatin	89-98	P53	Homo sapiens	52-55
32942193-7	2020	Further study revealed that ROS-related mitochondrial translocation of p53 was also involved in 1f-induced mitochondrial apoptotic pathway.	Reactive Oxygen Species	28-31	P53	Homo sapiens	71-74
32431164-1	2020	This study aimed to evaluate the modes of action of harringtonine (HT) and homoharringtonine (HHT) alkaloids in cell with wild (HepG2/C3A) and mutant p53 (HuH-7.5).	harringtonin	52-65	P53	Homo sapiens	150-153
32431164-1	2020	This study aimed to evaluate the modes of action of harringtonine (HT) and homoharringtonine (HHT) alkaloids in cell with wild (HepG2/C3A) and mutant p53 (HuH-7.5).	harringtonin	67-69	P53	Homo sapiens	150-153
32945383-0	2020	Resveratrol modulates the apoptosis and autophagic death of human lung adenocarcinoma A549 cells via a p53-dependent pathway: Integrated bioinformatics analysis and experimental validation.	Resveratrol	0-11	P53	Homo sapiens	103-106
32945383-7	2020	By bioinformatics analysis, a total of 1,031 DEGs were identified in the RSV-treated A549 cells, which were enriched in apoptosis-, or autophagy-related biological functions and the p53 signaling pathway.	Resveratrol	73-76	P53	Homo sapiens	182-185
33149857-9	2020	Generally, metabolic memory increased p53 and acetyl-P53 and decreased SIRT1 proteins in HUVECs, which were reversed by alpha-mangostin and metformin.	Metformin	140-149	P53	Homo sapiens	38-41
32945383-12	2020	RSV elevated the p53 levels and decreased the phosphorylated (p-)Mdm2 and p-Akt levels.	Resveratrol	0-3	P53	Homo sapiens	17-20
32945383-13	2020	Pifithrin-alpha, an inhibitor of p53, partially reduced RSV-induced apoptosis and autophagy.	Resveratrol	56-59	P53	Homo sapiens	33-36
32945383-14	2020	On the whole, the results of the present study demonstrated that RSV initiates the apoptosis and autophagic death of A549 cells via the activation of the p53 signaling pathway, further highlighting the potential of RSV for the treatment of NSCLC.	Resveratrol	65-68	P53	Homo sapiens	154-157
32578917-0	2020	A synthetic coumarin derivative (4-flourophenylacetamide-acetyl coumarin) impedes cell cycle at G0/G1 stage, induces apoptosis, and inhibits metastasis via ROS-mediated p53 and AKT signaling pathways in A549 cells.	4-flourophenylacetamide-acetyl coumarin	33-72	P53	Homo sapiens	169-172
32578917-0	2020	A synthetic coumarin derivative (4-flourophenylacetamide-acetyl coumarin) impedes cell cycle at G0/G1 stage, induces apoptosis, and inhibits metastasis via ROS-mediated p53 and AKT signaling pathways in A549 cells.	Reactive Oxygen Species	156-159	P53	Homo sapiens	169-172
32945383-14	2020	On the whole, the results of the present study demonstrated that RSV initiates the apoptosis and autophagic death of A549 cells via the activation of the p53 signaling pathway, further highlighting the potential of RSV for the treatment of NSCLC.	Resveratrol	215-218	P53	Homo sapiens	154-157
32881246-10	2020	These results implied PIO attenuated cisplatin nephrotoxicity by suppressing mitochondria-mediated apoptosis through regulating SIRT1/p53 signalling.	Cisplatin	37-46	P53	Homo sapiens	134-137
33209494-9	2020	Furthermore, eight biological pathways (including the DNA replication, cell cycle and p53 pathways) related to ERCC6L upregulation in HCC were found to be enriched by GSEA, and ERCC6L upregulation was positively correlated with PLK1 (polo-like kinase 1) expression and TP53 mutation in HCC, which preliminarily shed light on the roles of ERCC6L in HCC.	gsea	167-171	P53	Homo sapiens	86-89
32881246-0	2020	Pioglitazone alleviates cisplatin nephrotoxicity by suppressing mitochondria-mediated apoptosis via SIRT1/p53 signalling.	Cisplatin	24-33	P53	Homo sapiens	106-109
33209494-9	2020	Furthermore, eight biological pathways (including the DNA replication, cell cycle and p53 pathways) related to ERCC6L upregulation in HCC were found to be enriched by GSEA, and ERCC6L upregulation was positively correlated with PLK1 (polo-like kinase 1) expression and TP53 mutation in HCC, which preliminarily shed light on the roles of ERCC6L in HCC.	gsea	167-171	P53	Homo sapiens	269-273
33046993-8	2020	Our results showed that curcumin induced ROS accumulation, apoptosis, autophagy, cell cycle arrest, and cellular senescence accompanied by upregulation of p53 and p21 proteins in SiHa cells.	Curcumin	24-32	P53	Homo sapiens	155-158
32451170-4	2020	MATERIALS AND METHODS: TP53 was PCR amplified using the genomic DNA extracted from peripheral blood mononuclear cells and formalin-fixed, paraffin-embedded tissue sections from the tumor site of the patient, and was sequenced.	Paraffin	138-146	P53	Homo sapiens	23-27
32649952-5	2020	In the current study, based on 1H-15N HSQC NMR experiments and HADDOCK results, S100A4 interacts with the intrinsically unstructured transactivation domain (TAD) of the protein p53 and the pentamidine molecules in the presence of calcium ions.	Hydrogen	31-33	P53	Homo sapiens	177-180
33061616-10	2020	GSEA demonstrated that high GTSE1 expression was mainly enriched in the cell cycle (P<0.001), DNA replication (P<0.001), mismatch repair (P<0.001), and p53 signaling pathway (P<0.001).	gsea	0-4	P53	Homo sapiens	152-155
32978368-8	2020	Importantly, the antioxidant N-acetyl-cysteine and the p53 inhibitor pifithrin-alpha attenuated A1874-induced cell death and apoptosis in colon cancer cells.	A1874	96-101	P53	Homo sapiens	55-58
32978368-10	2020	BRD4 degradation and p53 protein elevation, as well as apoptosis induction and oxidative stress were detected in A1874-treated colon cancer tissues.	A1874	113-118	P53	Homo sapiens	21-24
32781074-10	2020	The inhibition of the PRDX1 activity with H7 promoted MPP+-induced cell death, as evidenced by decreased cell viability, increased apoptotic nuclei, increased the DHE signal, and increased p53.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	42-44	P53	Homo sapiens	189-192
32269290-11	2020	Further missense or frameshift mutations were observed in the KRAS, APC, TP53, and CTNNB1 genes in the PGA group.	Folic Acid	103-106	P53	Homo sapiens	73-77
32712543-12	2020	The FUC and DOX combination increased the levels and activity of caspases (CASP3, CASP8) and p53, while decreased the levels and activity of CYP3A4, GST, and PXR in resistant cancer cells.	Doxorubicin	12-15	P53	Homo sapiens	93-96
33089100-2	2020	We show that matrix metalloproteinase-7 (MMP-7) shedding MUC-1 SEA domain releases MUC-1 C-ter, facilitating the nucleolus trafficking of p53 in gefitinib-resistant lung CSCs.	Gefitinib	145-154	P53	Homo sapiens	138-141
33089100-3	2020	The nucleolus colocalizations of p53, MUC-1 C-ter, MMP-7 and nucleolin were observed in the CD34+ CXADR+ CD44v3 + gefitinib-resistant EGFRL858R/T790M CSC colonies.	Gefitinib	114-123	P53	Homo sapiens	33-36
32820905-0	2020	Nicotine promotes WRL68 cells proliferation due to the mutant p53 gain-of-function by activating CDK6-p53-RS-PIN1-STAT1 signaling pathway.	Nicotine	0-8	P53	Homo sapiens	62-65
32820905-0	2020	Nicotine promotes WRL68 cells proliferation due to the mutant p53 gain-of-function by activating CDK6-p53-RS-PIN1-STAT1 signaling pathway.	Nicotine	0-8	P53	Homo sapiens	102-105
32960902-0	2020	Doxorubicin-induced p53 interferes with mitophagy in cardiac fibroblasts.	Doxorubicin	0-11	P53	Homo sapiens	20-23
32820905-6	2020	Also remarkably, nicotine induced the level of p53 mutation at Ser249 (p53-RS).	Nicotine	17-25	P53	Homo sapiens	47-50
32960902-7	2020	Interestingly, these doxorubicin-induced changes were completely or partially restored in p53-/- cardiac fibroblasts.	Doxorubicin	21-32	P53	Homo sapiens	90-93
32960902-10	2020	Interactions between p53 and Parkin increased in doxorubicin-treated cardiac fibroblasts (p = 0.0003).	Doxorubicin	49-60	P53	Homo sapiens	21-24
32820905-6	2020	Also remarkably, nicotine induced the level of p53 mutation at Ser249 (p53-RS).	Nicotine	17-25	P53	Homo sapiens	71-74
32820905-8	2020	Furthermore, it suggested that CDK6-dependent binding between phosphorylation of p53-RS at Ser249 and PIN1 by nicotine treatment leads to the nucleus translocation, followed by interacting with STAT1 and subsequent activation of STAT1 via the improvement of its stability, which is involved in cellular growth and colony formation after nicotine treatment.	Nicotine	110-118	P53	Homo sapiens	81-84
32820905-8	2020	Furthermore, it suggested that CDK6-dependent binding between phosphorylation of p53-RS at Ser249 and PIN1 by nicotine treatment leads to the nucleus translocation, followed by interacting with STAT1 and subsequent activation of STAT1 via the improvement of its stability, which is involved in cellular growth and colony formation after nicotine treatment.	Nicotine	337-345	P53	Homo sapiens	81-84
32820905-9	2020	Simply put, these findings indicated that nicotine induces mutant p53 gain-of function (GOF), activating CDK6-p53-RS-PIN1-STAT1 signaling pathway and promoting cell proliferation, which could contribute to HCC for smokers.	Nicotine	42-50	P53	Homo sapiens	66-69
32820905-9	2020	Simply put, these findings indicated that nicotine induces mutant p53 gain-of function (GOF), activating CDK6-p53-RS-PIN1-STAT1 signaling pathway and promoting cell proliferation, which could contribute to HCC for smokers.	Nicotine	42-50	P53	Homo sapiens	110-113
32611648-0	2020	A biomarker-enriched, randomized Phase II trial of adavosertib (AZD1775) plus paclitaxel and carboplatin for women with platinum-sensitive TP53-mutant ovarian cancer.	Platinum	120-128	P53	Homo sapiens	139-143
33036527-8	2020	After c-myc silenced cells were treated with PM2.5 water soluble solution, The mRNA levels of c-myc, c-fos, and k-ras decreased by 84.1%, 45.4%, and 54.6% (P<0.05) , p53 increased by 192.9% (P<0.05) , and the expression of Caspase-3, Caspase-8, and Caspase-9 decreased by 24.4%, 36.1%, 60.9% (P<0.05) .	Water	51-56	P53	Homo sapiens	166-169
33041795-10	2020	Furthermore, TQ-stimulated increase of reactive oxygen species (ROS) in p53-depleted cells was more pronounced than that in cells with intact p53.	Reactive Oxygen Species	39-62	P53	Homo sapiens	72-75
33041795-10	2020	Furthermore, TQ-stimulated increase of reactive oxygen species (ROS) in p53-depleted cells was more pronounced than that in cells with intact p53.	Reactive Oxygen Species	64-67	P53	Homo sapiens	72-75
32942535-2	2020	In addition to loss of tumor suppressor functions, mutations in TP53 promote cancer progression by altering cellular iron acquisition and metabolism.	Iron	117-121	P53	Homo sapiens	64-68
32942535-3	2020	A newly identified role for TP53 in the coordination of iron homeostasis and cancer cell survival lies in the ability for TP53 to protect against ferroptosis, a form of iron-mediated cell death.	Iron	56-60	P53	Homo sapiens	28-32
32942535-3	2020	A newly identified role for TP53 in the coordination of iron homeostasis and cancer cell survival lies in the ability for TP53 to protect against ferroptosis, a form of iron-mediated cell death.	Iron	56-60	P53	Homo sapiens	122-126
32942535-3	2020	A newly identified role for TP53 in the coordination of iron homeostasis and cancer cell survival lies in the ability for TP53 to protect against ferroptosis, a form of iron-mediated cell death.	Iron	169-173	P53	Homo sapiens	28-32
33005290-4	2020	Different mechanisms including microsatellite instability, increased expression level of key enzyme thymidylate synthase and its polymorphism, increased level of 5-FU-activating enzymes and mutation of TP53 are proposed as the main determinants of resistance to 5-FU in CRC cells.	Fluorouracil	262-266	P53	Homo sapiens	202-206
32942535-3	2020	A newly identified role for TP53 in the coordination of iron homeostasis and cancer cell survival lies in the ability for TP53 to protect against ferroptosis, a form of iron-mediated cell death.	Iron	169-173	P53	Homo sapiens	122-126
32942535-7	2020	As iron-mediated lipid peroxidation is critical for ferroptosis induction, we hypothesized that iron acquisition pathways would be upregulated in mutant TP53-expressing cells.	Iron	3-7	P53	Homo sapiens	153-157
32942535-7	2020	As iron-mediated lipid peroxidation is critical for ferroptosis induction, we hypothesized that iron acquisition pathways would be upregulated in mutant TP53-expressing cells.	Iron	96-100	P53	Homo sapiens	153-157
32942546-8	2020	Results emphasize the importance of active oxygen species in inducing nucleotide lesions at a p53 mutational hotspot in HCV-HCC patients living in geographical areas without dietary exposure to aflatoxin B1.	Oxygen	43-49	P53	Homo sapiens	94-97
32899699-6	2020	We also demonstrate that DHA sensitizes HCT116 cells to DHER-induced apoptosis via P53 regulated DR5 expression in P53 knockdown assays.	dher	56-60	P53	Homo sapiens	83-86
32925794-8	2020	Functional enrichment analysis revealed that these genes are related to pathways such as "glutathione metabolism," "p53 signaling pathway," and "focal adhesion."	Glutathione	90-101	P53	Homo sapiens	116-119
32899699-6	2020	We also demonstrate that DHA sensitizes HCT116 cells to DHER-induced apoptosis via P53 regulated DR5 expression in P53 knockdown assays.	dher	56-60	P53	Homo sapiens	115-118
32687844-0	2020	The vicious cycle between ferritinophagy and ROS production triggered EMT inhibition of gastric cancer cells was through p53/AKT/mTor pathway.	ferritinophagy	26-40	P53	Homo sapiens	121-124
32384200-1	2020	BACKGROUND: Testicular Germ Cell Tumors (TGCTs) are highly sensitive to platinum-based chemotherapy, and wild-type p53 seems to play a pivotal role in this susceptibility.	Platinum	72-80	P53	Homo sapiens	115-118
32867831-0	2020	Boswellic acid sensitizes gastric cancer cells to Cisplatin-induced apoptosis via p53-mediated pathway.	Cisplatin	50-59	P53	Homo sapiens	82-85
32867831-1	2020	BACKGROUND: Cisplatin (CDDP) is an effective anticancer drug for Gastric cancer (GC) that induces apoptosis by altering pro- (p53) and anti-apoptotic (Akt and NFkB) proteins; however, chemoresistance remains a big challenge.	Cisplatin	12-21	P53	Homo sapiens	126-129
32867831-1	2020	BACKGROUND: Cisplatin (CDDP) is an effective anticancer drug for Gastric cancer (GC) that induces apoptosis by altering pro- (p53) and anti-apoptotic (Akt and NFkB) proteins; however, chemoresistance remains a big challenge.	Cisplatin	23-27	P53	Homo sapiens	126-129
32867831-4	2020	This study aimed to examine the effectiveness of AKBA on p53-mediated, CDDP-induced apoptosis in GC cells.	Cisplatin	71-75	P53	Homo sapiens	57-60
32867831-12	2020	CONCLUSIONS: Altogether, our findings suggest that AKBA enhances GC cell sensitivity to CDDP-induced apoptosis via the p53 pathway.	Cisplatin	88-92	P53	Homo sapiens	119-122
32869837-0	2020	Metformin inhibits the growth of ovarian cancer cells by promoting the Parkin-induced p53 ubiquitination.	Metformin	0-9	P53	Homo sapiens	86-89
32869837-10	2020	Further, up-regulated Parkin expression promoted the ubiquitination and degradation of p53, and metformin inhibited the expression of p53 to suppress the proliferation of chemo-resistant ovarian cancer cells.	Metformin	96-105	P53	Homo sapiens	134-137
32869837-11	2020	Mechanistically, metformin could inhibit the growth of ovarian cancer cells by promoting the Parkin-induced p53 ubiquitination.	Metformin	17-26	P53	Homo sapiens	108-111
32869837-12	2020	Altogether, our study demonstrated an inhibitory role of metformin in the growth of chemo-resistant cancer cells through promoting the Parkin-induced p53 ubiquitination, which provides a novel mechanism of metformin for treating ovarian cancer.	Metformin	57-66	P53	Homo sapiens	150-153
32869837-12	2020	Altogether, our study demonstrated an inhibitory role of metformin in the growth of chemo-resistant cancer cells through promoting the Parkin-induced p53 ubiquitination, which provides a novel mechanism of metformin for treating ovarian cancer.	Metformin	206-215	P53	Homo sapiens	150-153
33205006-0	2020	Gb3-cSrc complex in glycosphingolipid-enriched microdomains contributes to the expression of p53 mutant protein and cancer drug resistance via beta-catenin-activated RNA methylation.	Glycosphingolipids	20-37	P53	Homo sapiens	93-96
33205006-8	2020	Genz-161 effectively inhibited GCS activity, and substantially suppressed the elevated Gb3 levels seen in GEMs of p53-mutant cells exposed to doxorubicin.	Doxorubicin	142-153	P53	Homo sapiens	114-117
33072537-0	2020	Restoring of miR-193a-5p Sensitizes Breast Cancer Cells to Paclitaxel through P53 Pathway.	Paclitaxel	59-69	P53	Homo sapiens	78-81
33072537-4	2020	Therefore, the aim of this study was to evaluate the potential function of miR-193a-5p and paclitaxel in the apoptosis induction by targeting P53 in BC cells.	Paclitaxel	91-101	P53	Homo sapiens	142-145
32687844-12	2020	In addition to upregulation of p53, its down-stream targets, AKT/mTor were also downregulated, supporting that DpdtC induced EMT inhibition was achieved through ferritinophagy-ROS vicious cycle mediated p53/AKT/mTor pathway.	ros	176-179	P53	Homo sapiens	203-206
32687844-0	2020	The vicious cycle between ferritinophagy and ROS production triggered EMT inhibition of gastric cancer cells was through p53/AKT/mTor pathway.	ros	45-48	P53	Homo sapiens	121-124
32687844-9	2020	In addition, ferritinophagy triggers Fenton reaction, resulting in ROS production which give rise of p53 response, thus the role of p53 was further investigated.	ros	67-70	P53	Homo sapiens	101-104
32649943-4	2020	Nicotine inhibited the proliferation of SKOV3 and TOV112D OC cells, which have TP53 mutation and wild-type KRAS, but did not inhibit the proliferation of TOV21G or HEY OC cells, which have KRAS mutation and wild-type TP53.	Nicotine	0-8	P53	Homo sapiens	79-83
32272509-14	2020	Conclusion: Dexamethasone increased cell survival in p53 mutated malignant glioma cells and increased autophagy in PTEN-mutant malignant glioma cell but not in PTEN-wildtype cell.	Dexamethasone	12-25	P53	Homo sapiens	53-56
32741018-0	2020	Novel evidence for retinoic acid-induced G (Rig-G) as a tumor suppressor by activating p53 signaling pathway in lung cancer.	Tretinoin	19-32	P53	Homo sapiens	87-90
32485079-0	2020	Suggested application of HER2+ breast tumor phenotype for germline TP53 variant classification within ACMG/AMP guidelines.	Adenosine Monophosphate	107-110	P53	Homo sapiens	67-71
31547774-8	2020	All synthesized molecules (K1-K12) dock at junction p53-DNA and make hydrogen bonded with residues of p53 protein as per docking study.	Hydrogen	69-77	P53	Homo sapiens	102-105
32878253-7	2020	These ROS-mediated responses induce caspase-dependent apoptosis via the activation of B-cell lymphoma 2 (Bcl2), Bcl2-associated X protein (Bax), CCAAT/enhancer-binding protein homologous protein (chop), and phosphoprotein p53 gene expressions.	Reactive Oxygen Species	6-9	P53	Homo sapiens	207-225
32705219-8	2020	Moreover, by using western blot analysis, we determined that EA increased the protein expression of the p53 target proteins p21, p53 upregulated modulator of apoptosis (PUMA) [also known as Bcl-2-binding component 3 (BBC3)] and Phorbol-12-myristate-13-acetate-induced protein 1 (NOXA).	Tetradecanoylphorbol Acetate	228-259	P53	Homo sapiens	104-107
32705219-8	2020	Moreover, by using western blot analysis, we determined that EA increased the protein expression of the p53 target proteins p21, p53 upregulated modulator of apoptosis (PUMA) [also known as Bcl-2-binding component 3 (BBC3)] and Phorbol-12-myristate-13-acetate-induced protein 1 (NOXA).	Tetradecanoylphorbol Acetate	228-259	P53	Homo sapiens	129-132
32863216-6	2020	Site-directed mutations of serine 392 completely blocked the binding of BRD7 to p53, and, in turn, prevented p53 mitochondrial translocation and HSC ferroptosis.	Serine	27-33	P53	Homo sapiens	80-83
32863216-6	2020	Site-directed mutations of serine 392 completely blocked the binding of BRD7 to p53, and, in turn, prevented p53 mitochondrial translocation and HSC ferroptosis.	Serine	27-33	P53	Homo sapiens	109-112
32863216-7	2020	Importantly, mitochondrial p53 interacted with solute carrier family 25 member 28 (SLC25A28) to form complex and enhanced the activity of SLC25A28, which could lead to the abnormal accumulation of redox-active iron and hyperfunction of electron transfer chain (ETC).	Iron	210-214	P53	Homo sapiens	27-30
32502622-0	2020	P53 activation suppresses irinotecan metabolite SN-38-induced cell damage in non-malignant but not malignant epithelial colonic cells.	Irinotecan	26-36	P53	Homo sapiens	0-3
32502622-0	2020	P53 activation suppresses irinotecan metabolite SN-38-induced cell damage in non-malignant but not malignant epithelial colonic cells.	Irinotecan	48-53	P53	Homo sapiens	0-3
32502622-5	2020	SN-38 treatment induced significant apoptosis in all cell lines after 48 h. Nutlin-3a unexpectedly increased cell death in the p53 wild-type CRC cell line, HCT116+/+, while Nutlin-3a pre-treatment provided protection from SN-38 in the p53 wild-type normal cell line, FHS 74.	Irinotecan	0-5	P53	Homo sapiens	127-130
32502622-5	2020	SN-38 treatment induced significant apoptosis in all cell lines after 48 h. Nutlin-3a unexpectedly increased cell death in the p53 wild-type CRC cell line, HCT116+/+, while Nutlin-3a pre-treatment provided protection from SN-38 in the p53 wild-type normal cell line, FHS 74.	Irinotecan	0-5	P53	Homo sapiens	235-238
32679123-5	2020	The treatment of nifedipine dose-dependently suppressed H2O2-induced senescence by reducing Ca2+ entry, autophagy impairment and mTOR signaling, and this suppression was found to be related to senescence-associated beta-galactosidase (SA-beta-gal) activity and the expressions of senescence marker protein 30 (SMP30), p53, and p21.	Hydrogen Peroxide	56-60	P53	Homo sapiens	318-321
32782527-0	2020	Konjac glucomannan reverses multi-drug resistance of HepG2/5-FU cells by suppressing AKT signaling and increasing p53 expression.	Fluorouracil	59-63	P53	Homo sapiens	114-117
32478947-3	2020	The results revealed that doxorubicin (Adriamycin [ADR]) concentrations 10 to 40 times less than commonly used in previous studies induced the DNA damage-dependent G2-checkpoint and completed apoptosis within the same time frame, regardless of the presence or absence of p53, p21, and PUMA.	Doxorubicin	26-37	P53	Homo sapiens	271-274
32478947-3	2020	The results revealed that doxorubicin (Adriamycin [ADR]) concentrations 10 to 40 times less than commonly used in previous studies induced the DNA damage-dependent G2-checkpoint and completed apoptosis within the same time frame, regardless of the presence or absence of p53, p21, and PUMA.	Doxorubicin	39-49	P53	Homo sapiens	271-274
32872665-5	2020	In addition, CD treatment led to cell cycle arrest at the G0/G1 phase and inhibited expression of cyclin D1 and cyclin-dependent kinases 2 and 4 and led to increased levels of p21, p27Kip1 and p53.	Cadmium	13-15	P53	Homo sapiens	193-196
32807076-0	2020	Correction to: Regulation of GAD65 expression by SMAR1 and p53 upon Streptozotocin treatment.	Streptozocin	68-82	P53	Homo sapiens	59-62
32921957-12	2020	PLK1 inhibitors (volasertib and GSK461364) or a BIRC5 inhibitor (YM155) selectively targeted Huh7 cells with mutated p53, but not HepG2 cells with wild-type p53.	GSK 461364	32-41	P53	Homo sapiens	117-120
32921957-12	2020	PLK1 inhibitors (volasertib and GSK461364) or a BIRC5 inhibitor (YM155) selectively targeted Huh7 cells with mutated p53, but not HepG2 cells with wild-type p53.	YM 155	65-70	P53	Homo sapiens	117-120
32922194-9	2020	Furthermore, sesamin induced p53 phosphorylation at serine-46 and serine-15 and upregulated the levels of PUMA, Bax, and PTEN, while inhibiting AKT phosphorylation at serine-473.	Serine	52-58	P53	Homo sapiens	29-32
32884270-9	2020	Upregulation of TP53-gene transcripts was also detected in both nGO- and mGO-treated cells compared to the control, especially at 200 mug/mL.	mgo	73-76	P53	Homo sapiens	16-20
32776119-0	2020	Tanshinone IIA induces ferroptosis in gastric cancer cells through p53 mediated-SLC7A11 down-regulation.	tanshinone	0-14	P53	Homo sapiens	67-70
32974127-0	2020	p53 Affects PGC1alpha Stability Through AKT/GSK-3beta to Enhance Cisplatin Sensitivity in Non-Small Cell Lung Cancer.	Cisplatin	65-74	P53	Homo sapiens	0-3
32825184-4	2020	As a follow-up study of our previous findings, here we have identified that the pharmacological substances, leptomycin B and doxorubicin, can improve the sensitivity of cervical cancer cells to cisplatin inducing HP1gamma-mediated elevation of p53.	Doxorubicin	125-136	P53	Homo sapiens	244-247
32825184-4	2020	As a follow-up study of our previous findings, here we have identified that the pharmacological substances, leptomycin B and doxorubicin, can improve the sensitivity of cervical cancer cells to cisplatin inducing HP1gamma-mediated elevation of p53.	Cisplatin	194-203	P53	Homo sapiens	244-247
32825184-5	2020	Leptomycin B, which inhibits the nuclear export of HP1gamma, increased cisplatin-dependent apoptosis induction by promoting the activation of p53 signaling.	Cisplatin	71-80	P53	Homo sapiens	142-145
32825184-6	2020	We also found that doxorubicin, which induces the DNA damage response, promotes HP1gamma-mediated silencing of UBE2L3 and increases p53 stability.	Doxorubicin	19-30	P53	Homo sapiens	132-135
32825184-8	2020	Doxorubicin sensitized the cisplatin-resistant cervical cancer cells, enhancing their p53 levels and rate of apoptosis when administered together with cisplatin.	Doxorubicin	0-11	P53	Homo sapiens	86-89
32825184-8	2020	Doxorubicin sensitized the cisplatin-resistant cervical cancer cells, enhancing their p53 levels and rate of apoptosis when administered together with cisplatin.	Cisplatin	27-36	P53	Homo sapiens	86-89
32825184-9	2020	Our findings reveal a therapeutic strategy to target a specific molecular pathway that contributes to p53 degradation for the treatment of patients with cervical cancer, particularly with cisplatin resistance.	Cisplatin	188-197	P53	Homo sapiens	102-105
32831651-11	2020	Results: Here, using a panel of OSCC cell lines with wild type or mutant p53, we show that p33ING1b expression is correlated to acetylation of p53 at lysine 382 residue.	Lysine	150-156	P53	Homo sapiens	143-146
32489012-2	2020	The sixteen resulting architectures are water-stable and optically pure, and exhibit improved antiproliferative selectivity against colon cancer cells (HCT116 p53 +/+ ) with respect to the non-cancerous ARPE-19 cell line.	Water	40-45	P53	Homo sapiens	159-162
32505665-1	2020	Doxorubicin is a leading chemotherapeutic halting cellular replication and inducing p53-dependent apoptosis in cancerous tissue.	Doxorubicin	0-11	P53	Homo sapiens	84-87
32445778-9	2020	Further, we found that curcumin promoted the PTEN and p53 expression, as the tumor suppressor genes.	Curcumin	23-31	P53	Homo sapiens	54-57
32806555-8	2020	The upregulation of p-ERK occurred due to mitochondrial translocation of p53, which resulted in increased production of reactive oxygen species, causing the activation of receptor tyrosine kinases (RTKs).	Oxygen	129-135	P53	Homo sapiens	73-76
32824273-0	2020	Sinensetin Induces Autophagic Cell Death through p53-Related AMPK/mTOR Signaling in Hepatocellular Carcinoma HepG2 Cells.	sinensetin	0-10	P53	Homo sapiens	49-52
32824273-7	2020	p53 translocation led to SIN-induced autophagy, whereas p53 translocation inhibited SIN-induced apoptosis.	sinensetin	25-28	P53	Homo sapiens	0-3
32824273-7	2020	p53 translocation led to SIN-induced autophagy, whereas p53 translocation inhibited SIN-induced apoptosis.	sinensetin	84-87	P53	Homo sapiens	56-59
32824273-9	2020	Molecular docking simulation of the p53 core domain showed effective binding with SIN, which was found significant compared with the known p53 activator, RITA.	RITA	154-158	P53	Homo sapiens	36-39
32824273-9	2020	Molecular docking simulation of the p53 core domain showed effective binding with SIN, which was found significant compared with the known p53 activator, RITA.	RITA	154-158	P53	Homo sapiens	139-142
32792545-3	2020	We characterized the target search dynamics of the tumor suppressor p53 along nonspecific DNA at physiological salt concentrations.	Salts	111-115	P53	Homo sapiens	68-71
32792545-5	2020	Both the jumps and the one-dimensional diffusion of p53 along DNA were accelerated at higher salt concentrations, suggesting the rotation-uncoupled movement of p53 along DNA grooves and conformational changes in the p53/DNA complex.	Salts	93-97	P53	Homo sapiens	52-55
32792545-5	2020	Both the jumps and the one-dimensional diffusion of p53 along DNA were accelerated at higher salt concentrations, suggesting the rotation-uncoupled movement of p53 along DNA grooves and conformational changes in the p53/DNA complex.	Salts	93-97	P53	Homo sapiens	160-163
32792545-5	2020	Both the jumps and the one-dimensional diffusion of p53 along DNA were accelerated at higher salt concentrations, suggesting the rotation-uncoupled movement of p53 along DNA grooves and conformational changes in the p53/DNA complex.	Salts	93-97	P53	Homo sapiens	160-163
32801360-5	2020	Then, autophagy improves intracellular H2O2 via promoting p53-mediated depletion of GSH and cysteine and downregulation of xCT.	Hydrogen Peroxide	39-43	P53	Homo sapiens	58-61
32801360-5	2020	Then, autophagy improves intracellular H2O2 via promoting p53-mediated depletion of GSH and cysteine and downregulation of xCT.	Glutathione	84-87	P53	Homo sapiens	58-61
32801360-5	2020	Then, autophagy improves intracellular H2O2 via promoting p53-mediated depletion of GSH and cysteine and downregulation of xCT.	Cysteine	92-100	P53	Homo sapiens	58-61
32784977-8	2020	Furthermore, the anthraquinone-rich dichloromethane fraction displayed the highest anticancer activity when evaluated in a human hepatoma cancer cell line (HepG2), in which it induced increased apoptosis mediated by p53 and caspase activation.	Anthraquinones	17-30	P53	Homo sapiens	216-219
32782440-16	2020	GSEA results indicated that DLGAP5 had significantly enriched into signaling pathways such as the cell cycle, the p53 signaling pathway, and oocyte meiosis.	gsea	0-4	P53	Homo sapiens	114-117
32757802-7	2021	The synergistic antitumor effect of API and CDDP was blocked by addition of the p53 inhibitor Pifithrin-alpha, and siRNA targeting the p53 gene in A549R cells.	Apigenin	36-39	P53	Homo sapiens	80-83
32757802-7	2021	The synergistic antitumor effect of API and CDDP was blocked by addition of the p53 inhibitor Pifithrin-alpha, and siRNA targeting the p53 gene in A549R cells.	Apigenin	36-39	P53	Homo sapiens	135-138
32757802-7	2021	The synergistic antitumor effect of API and CDDP was blocked by addition of the p53 inhibitor Pifithrin-alpha, and siRNA targeting the p53 gene in A549R cells.	Cisplatin	44-48	P53	Homo sapiens	80-83
32757802-7	2021	The synergistic antitumor effect of API and CDDP was blocked by addition of the p53 inhibitor Pifithrin-alpha, and siRNA targeting the p53 gene in A549R cells.	Cisplatin	44-48	P53	Homo sapiens	135-138
32757802-8	2021	Furthermore, API eliminates CDDP-induced CSC via p53, since A549R cells lacking p53 and Pifithrin-alpha addition derepressed the decrease in CD 133 positive cells after API treatment in CDDP-treated A549 and A549R cells.	Cisplatin	28-32	P53	Homo sapiens	49-52
32757802-8	2021	Furthermore, API eliminates CDDP-induced CSC via p53, since A549R cells lacking p53 and Pifithrin-alpha addition derepressed the decrease in CD 133 positive cells after API treatment in CDDP-treated A549 and A549R cells.	Apigenin	13-16	P53	Homo sapiens	49-52
32632453-4	2020	Here, we established two paclitaxel (PTX)-resistant TNBC cancer cell lines using an intermittent and stepwise method and found that long non-coding RNA long intergenic non-protein-coding RNA p53-induced transcript (LINC-PINT) was significantly decreased in PTX-resistant cancer cells.	Paclitaxel	25-35	P53	Homo sapiens	191-194
32632453-4	2020	Here, we established two paclitaxel (PTX)-resistant TNBC cancer cell lines using an intermittent and stepwise method and found that long non-coding RNA long intergenic non-protein-coding RNA p53-induced transcript (LINC-PINT) was significantly decreased in PTX-resistant cancer cells.	Paclitaxel	37-40	P53	Homo sapiens	191-194
32757802-8	2021	Furthermore, API eliminates CDDP-induced CSC via p53, since A549R cells lacking p53 and Pifithrin-alpha addition derepressed the decrease in CD 133 positive cells after API treatment in CDDP-treated A549 and A549R cells.	Cisplatin	186-190	P53	Homo sapiens	49-52
32757802-9	2021	The findings indicate that API might eliminate cancer stem cells and enhance the antitumor effects of CDDP in NSCLC via p53.	Cisplatin	102-106	P53	Homo sapiens	120-123
32742376-5	2020	In HCT116 cells expressing wild-type (wt) TP53, SIRT inhibitors were found to act antagonistically with multiple chemotherapeutic agents (cisplatin, 5-fluorouracil, oxaliplatin, gefitinib, LY294002 and metformin), and decreased the anti-tumor effects of these agents.	Cisplatin	138-147	P53	Homo sapiens	42-46
32460965-0	2020	Corrigendum to "Vitexin protects against ethanol-induced liver injury through Sirt1/p53 signaling pathway" [Eur.	Ethanol	41-48	P53	Homo sapiens	84-87
32750288-0	2020	p53-Mediated Repression of the PGC1A (PPARG Coactivator 1alpha) and APLNR (Apelin Receptor) Signaling Pathways Limits Fatty Acid Oxidation Energetics: Implications for Cardio-oncology.	Fatty Acids	118-128	P53	Homo sapiens	0-3
32397868-0	2020	Expression of Concern: Resveratrol displays converse dose-related effects on 5-fluorouracil-evoked colon cancer cell apoptosis: The roles of caspase-6 and p53.	Resveratrol	23-34	P53	Homo sapiens	155-158
32910383-0	2020	Association of Molecular Genetic Markers of TP53, MDM2, and CDKN1A Genes with Progression-Free Survival of Patients with Ovarian Cancer after Platinum-Based Chemotherapy.	Platinum	142-150	P53	Homo sapiens	44-48
32450254-0	2020	Oxygen-releasing Manganese clay Hybrid Complex triggers p53-mediated cancer cell death in hypoxia.	Oxygen	0-6	P53	Homo sapiens	56-59
32450254-5	2020	In hypoxia, the oxygen from MHC releases cells from S-phase arrest thus causing p53-dependent apoptosis.	Oxygen	16-22	P53	Homo sapiens	80-83
32450254-7	2020	The released oxygen from MHC triggers apoptosis via p53 activation through its enhanced homo-oligomerization, post-translational modifications and nuclear localization.	Oxygen	13-19	P53	Homo sapiens	52-55
32742376-5	2020	In HCT116 cells expressing wild-type (wt) TP53, SIRT inhibitors were found to act antagonistically with multiple chemotherapeutic agents (cisplatin, 5-fluorouracil, oxaliplatin, gefitinib, LY294002 and metformin), and decreased the anti-tumor effects of these agents.	Fluorouracil	149-163	P53	Homo sapiens	42-46
32742376-5	2020	In HCT116 cells expressing wild-type (wt) TP53, SIRT inhibitors were found to act antagonistically with multiple chemotherapeutic agents (cisplatin, 5-fluorouracil, oxaliplatin, gefitinib, LY294002 and metformin), and decreased the anti-tumor effects of these agents.	Gefitinib	178-187	P53	Homo sapiens	42-46
32742376-5	2020	In HCT116 cells expressing wild-type (wt) TP53, SIRT inhibitors were found to act antagonistically with multiple chemotherapeutic agents (cisplatin, 5-fluorouracil, oxaliplatin, gefitinib, LY294002 and metformin), and decreased the anti-tumor effects of these agents.	Metformin	202-211	P53	Homo sapiens	42-46
32558266-8	2020	The up-regulated DEGs were related to "p53 signaling pathway", "FoxO signaling pathway", and "cGMP-PKG signaling pathway" terms, while the down-regulated DEGs were significantly enriched in seven terms including "protein processing in endoplasmic reticulum".	Cyclic GMP	94-98	P53	Homo sapiens	39-42
32141677-2	2020	Curcumin is considered to play a role in the regulation of T-lymphocytes function in the lymphoid tissue of the large intestine, apoptosis of the human papilloma and the activity of the 26S proteasome, and p53 level.	Curcumin	0-8	P53	Homo sapiens	206-209
32727562-6	2020	Based on the data from different approaches, we identified three anticancer compounds, RITA (Reactivation of p53 and Induction of Tumor cell Apoptosis), aminoflavone (AF), and oncrasin-1 (ONC-1), whose tumor cell inhibition activity is dependent on SULT1A1.	RITA	87-91	P53	Homo sapiens	109-112
32727419-8	2020	CONCLUSIONS: This pilot study suggests that both the Arg/Arg and Arg/Pro genotypes of p53 codon 72 polymorphism may have value as independent prognostic or predictive parameters for bevacizumab treatment response and failure.	Arginine	53-56	P53	Homo sapiens	86-89
32243890-6	2020	Gene expression analysis showed that c-MYC level was decreased and TP53 was increased after SB-245392 treatment.	CHEMBL13868	92-101	P53	Homo sapiens	67-71
32792943-6	2020	Further study of the underlying mechanism revealed that the two drugs in combination caused ROS aggregation in NSCLC cells, leading to DNA double-strand breaks and increased expression of the tumor suppressor factor p53.	ros	92-95	P53	Homo sapiens	216-219
32731591-6	2020	Furthermore, N-SNPs triggered apoptosis via the activation of caspase 3 and p53, and suppressed the mTOR signaling pathway via downregulating apoptosis-evading proteins in MCF-7, HCT-116, and HepG2 cells.	n-snps	13-19	P53	Homo sapiens	76-79
32718025-3	2020	Recently, several studies have identified intricate and complicated interplay between ferroptosis, ionizing radiation (IR), ATM (ataxia-telangiectasia mutated)/ATR (ATM and Rad3-related), and tumor suppressor p53, which signifies the participation of the DNA damage response (DDR) in iron-related cell death.	Iron	284-288	P53	Homo sapiens	209-212
32722075-8	2020	In addition, LY and TAM combination induced the apoptotic genes Caspase-3, Caspase-7, and p53, as well as p21 as cell cycle promotor, and significantly downregulated the anti-apoptotic genes Bcl-2 and survivin.	Tamoxifen	20-23	P53	Homo sapiens	90-93
32722340-0	2020	TP53 Mutation Analysis in Gastric Cancer and Clinical Outcomes of Patients with Metastatic Disease Treated with Ramucirumab/Paclitaxel or Standard Chemotherapy.	Paclitaxel	124-134	P53	Homo sapiens	0-4
32722340-6	2020	In the Ramucirumab/Paclitaxel group, 29/48 (60.4%) patients had TP53 mutations.	Paclitaxel	19-29	P53	Homo sapiens	64-68
32390036-0	2020	Diarylethene moiety as an enthalpy-entropy switch: photoisomerizable stapled peptides for modulating p53/MDM2 interaction.	diarylethene	0-12	P53	Homo sapiens	101-104
32390036-1	2020	Analogs of the known inhibitor (peptide pDI) of the p53/MDM2 protein-protein interaction are reported, which are stapled by linkers bearing a photoisomerizable diarylethene moiety.	diarylethene	160-172	P53	Homo sapiens	52-55
32475643-4	2020	Berberine increased the level of p53 protein and of its target p21 both time- and dose-dependently in MCF7 cells.	Berberine	0-9	P53	Homo sapiens	33-36
32774710-0	2020	Downregulation of LINC01021 by curcumin analog Da0324 inhibits gastric cancer progression through activation of P53.	Curcumin	31-39	P53	Homo sapiens	112-115
32657624-10	2021	Curcumin induces apoptosis in Pre B- ALL and T- ALL cells by decreased NF-kB levels, increased p53 levels, PARP-1 cleavage.	Curcumin	0-8	P53	Homo sapiens	95-98
32475643-7	2020	Therefore, we evaluated the possibility of berberine-induced nucleolar stress and observed the disappearance of ribosomal protein (RP)L5 from the nucleolus and accumulation of p53 protein in the nucleus after treatment with 10 or 100 muM berberine in MCF7 cells.	Berberine	238-247	P53	Homo sapiens	176-179
32475643-9	2020	Moreover, downregulation of RPL5 inhibited berberine-driven induction of p53 and p21 and cell death in MCF7 cells.	Berberine	43-52	P53	Homo sapiens	73-76
32475643-11	2020	These results indicated that cell growth inhibition and cell death induced by higher doses (>10 muM) of berberine in MCF7 cells were due to the upregulation of p53 under the nucleolar stress response caused by a significant accumulation of berberine in the nucleoli.	Berberine	104-113	P53	Homo sapiens	160-163
32475643-11	2020	These results indicated that cell growth inhibition and cell death induced by higher doses (>10 muM) of berberine in MCF7 cells were due to the upregulation of p53 under the nucleolar stress response caused by a significant accumulation of berberine in the nucleoli.	Berberine	240-249	P53	Homo sapiens	160-163
32453417-6	2020	Phosphorylation on serine 395 following DNA damage instead regulates p53 mRNA binding to its RING domain and prevents the E2F1 mRNA interaction.	Serine	19-25	P53	Homo sapiens	69-72
32733640-5	2020	Western blot analysis revealed that quercetin reduced copper-induced increase in p53 upregulated modulator of apoptosis (PUMA) expression and promoted upregulation of nucleoside diphosphate kinase NME1.	Copper	54-60	P53	Homo sapiens	81-84
32753889-6	2020	Nonsynonymous variants in EGFR, TTN, TP53 and KRAS, and copy number variations (SCNVs) in chromosome 8q24.3 and 22q11.21 were identified to be associated with platinum response.	Platinum	159-167	P53	Homo sapiens	37-41
32641008-7	2020	Immunoprecipitation was further employed to reveal the molecular interaction of APE1, p53, and LC3 when A549 cells were exposed to cisplatin.	Cisplatin	131-140	P53	Homo sapiens	86-89
32641008-11	2020	Immunoprecipitation results revealed the triple complex of APE1-p53-LC3 in response to cisplatin plus CQ in A549 cells.	Cisplatin	87-96	P53	Homo sapiens	64-67
32641008-13	2020	CONCLUSIONS: Dual inhibition of APE1 and autophagy greatly enhances apoptosis in parental KRASG12S-mutant A549 cells and cisplatin-resistant A549 cells via regulation of APE1-p53-LC3 complex assembly, providing therapeutic vulnerability to overcome cisplatin resistance in the context of KRASG12S-mutant lung cancer.	Cisplatin	121-130	P53	Homo sapiens	175-178
32641008-13	2020	CONCLUSIONS: Dual inhibition of APE1 and autophagy greatly enhances apoptosis in parental KRASG12S-mutant A549 cells and cisplatin-resistant A549 cells via regulation of APE1-p53-LC3 complex assembly, providing therapeutic vulnerability to overcome cisplatin resistance in the context of KRASG12S-mutant lung cancer.	Cisplatin	249-258	P53	Homo sapiens	175-178
32650545-0	2020	Potential Metabolite Nymphayol Isolated from Water Lily (Nymphaea stellata) Flower Inhibits MCF-7 Human Breast Cancer Cell Growth via Upregulation of Cdkn2a, pRb2, p53 and Downregulation of PCNA mRNA Expressions.	Water	45-50	P53	Homo sapiens	164-167
32631421-11	2020	In addition, metformin upregulated the expression of DDR-1 and p53 in human cervical cancer cells.	Metformin	13-22	P53	Homo sapiens	63-66
32630700-0	2020	The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis.	Cisplatin	57-66	P53	Homo sapiens	130-133
32630700-10	2020	ROS act as upstream signaling molecules to initiate apoptosis via p53/p21waf1 axis.	ros	0-3	P53	Homo sapiens	66-69
32695207-10	2020	Conclusion: Ginsenoside Rh1 alleviated HK-2 apoptosis in a cisplatin-induced injury model by inhibiting ROS production and the JNK/p53 pathway.	Cisplatin	59-68	P53	Homo sapiens	131-134
32711437-12	2020	Significant increased risk of lung cancer was found with Arg/Pro genotypes of TP53, Lys/Gln and Gln/Gln variants of XPD in individuals with family history of cancer (OR=3.44; 95% CI=1.36-8.72; p=0.011; OR=3.17; 95% CI=1.20-8.39; p=0.024; OR=16.35; 95% CI=0.92-289.5; p=0.007, respectively).	Arginine	57-60	P53	Homo sapiens	78-82
32044796-9	2020	The combination of C61-LNP and CDDP changed in alterations of the cell cycle regulatory proteins p53, p21, p27, cyclin D1 and cyclin E levels.	Cisplatin	31-35	P53	Homo sapiens	97-100
32342131-6	2020	To briefly determine the cellular pathways involved in the protective role of myricetin against PhIP, we studied gene expression of P53 and ATR kinase (ATM- and Rad3-related), using the real-time PCR technique.	myricetin	78-87	P53	Homo sapiens	132-150
32407985-0	2020	Tumor suppressor p53 independent apoptosis in HT-29 cells by auransterol from Penicillium aurantiacobrunneum.	Auransterol	61-72	P53	Homo sapiens	17-20
33040724-5	2020	The predictions were validated by studying cell metabolic response to the p53 inducer cisplatin.	Cisplatin	86-95	P53	Homo sapiens	74-77
33040724-6	2020	Expression of p53 and its known target, p21, has been evaluated in cisplatin-treated and control human lung adenocarcinoma A549 cells that possess functional p53 pathway.	Cisplatin	67-76	P53	Homo sapiens	14-17
33040724-6	2020	Expression of p53 and its known target, p21, has been evaluated in cisplatin-treated and control human lung adenocarcinoma A549 cells that possess functional p53 pathway.	Cisplatin	67-76	P53	Homo sapiens	158-161
33040724-8	2020	Along with upregulating the expression of p53 and p21, cisplatin affected the activities of metabolic enzymes, whose genes were predicted as carrying the p53-binding sites.	Cisplatin	55-64	P53	Homo sapiens	42-45
33040724-8	2020	Along with upregulating the expression of p53 and p21, cisplatin affected the activities of metabolic enzymes, whose genes were predicted as carrying the p53-binding sites.	Cisplatin	55-64	P53	Homo sapiens	154-157
33040724-10	2020	Simultaneously, the activities of NAD+-dependent IDH, mitochondrial aspartate aminotransferase, and two malate dehydrogenase isoenzymes, whose genes were not predicted to have the p53-binding sequences near the transcription starting points, were upregulated by cisplatin.	NAD	34-37	P53	Homo sapiens	180-183
32407985-11	2020	The cytotoxic effect of auransterol in HT-29 colon cancer cells is mediated by mitochondrial apoptosis independent of p53 activation, cell cycle G1 phase arrest, and inhibition of cell migration.	Auransterol	24-35	P53	Homo sapiens	118-121
32721020-8	2020	Conclusions: Reduced steady-state ATP levels and subsequent activation of the AMPK-p53 pathway provide a link between the metabolic functional deficit and transcriptome alterations, as well as evidence of insufficient ATP to maintain the Na+/K+-ATPase corneal endothelial pump as the cause of the edema that characterizes SLC4A11-associated corneal endothelial dystrophies.	Adenosine Triphosphate	34-37	P53	Homo sapiens	83-86
32229792-11	2020	Moreover, GSEA showed that MAPK and apoptosis pathways induced by TP53 mutation were possibly associated with TACE failure/refractoriness.	gsea	10-14	P53	Homo sapiens	66-70
32377734-9	2020	Of these agents, it was found that resveratrol increased p53 expression by 4.1-fold, decreased SIRT1 expression by 0.2-fold, and it was the most potent inducer of apoptosis.	Resveratrol	35-46	P53	Homo sapiens	57-60
32394497-5	2020	Neferine was shown to downregulate the expression of Bcl-2 and CDK4, and upregulate caspase 3, clePARP, p21, p27, and p53.	neferine	0-8	P53	Homo sapiens	118-121
32561851-0	2020	NEK10 tyrosine phosphorylates p53 and controls its transcriptional activity.	Tyrosine	6-14	P53	Homo sapiens	30-33
32377740-2	2020	Rsv induces expression of the human TP53 and HELB genes, which are involved in the regulation of DNA maintenance.	Resveratrol	0-3	P53	Homo sapiens	36-40
32561851-4	2020	Here, we describe a function for NEK10 in the regulation of p53 transcriptional activity through tyrosine phosphorylation.	Tyrosine	97-105	P53	Homo sapiens	60-63
32605658-0	2020	A ruthenium(II)-curcumin compound modulates NRF2 expression balancing the cancer cell death/survival outcome according to p53 status.	Curcumin	16-24	P53	Homo sapiens	122-125
32412177-6	2020	RESULTS: A significantly higher rate of TP53 mutations was detected in the GDPH cohort (51.3%) compared with the METABRIC cohort (34.4%) (P < 0.01).	gdph	75-79	P53	Homo sapiens	40-44
32412177-7	2020	In the GDPH cohort, 77.8% of the mutations were located in the conserved areas across exons 5-8 of TP53; among these, 112 were identified as missense mutations and mainly clustered in the DNA-binding region.	gdph	7-11	P53	Homo sapiens	99-103
32412177-9	2020	Logistic regression multivariate analysis showed that histological grade III, ki-67 > = 25%, HR- and Her2+ in breast cancer had higher mutation probability of TP53 (P < 0.001 in the GDPH cohort).	gdph	182-186	P53	Homo sapiens	159-163
32605658-6	2020	RESULTS: We found that the curcumin compound induced a certain degree of cell death in all tested cancer cell lines, independently of the p53 status.	Curcumin	27-35	P53	Homo sapiens	138-141
32605658-8	2020	Pharmacologic or genetic NRF2 inhibition further increased the curcumin-induced cell death in both mutp53- and wtp53-carrying cancer cell lines while it did not increase cell death in p53 null cells, suggesting a cytoprotective role for NRF2 and a critical role for functional p53 to achieve an efficient cancer cell response to therapy.	Curcumin	63-71	P53	Homo sapiens	102-105
32617134-8	2020	Further, curcumin-induced DNA demethylation of hGCCs was mediated by the damaged DNA repair-p53-p21/GADD45A-cyclin/CDK-Rb/E2F-DNMT1 axis.	Curcumin	9-17	P53	Homo sapiens	92-95
32605658-8	2020	Pharmacologic or genetic NRF2 inhibition further increased the curcumin-induced cell death in both mutp53- and wtp53-carrying cancer cell lines while it did not increase cell death in p53 null cells, suggesting a cytoprotective role for NRF2 and a critical role for functional p53 to achieve an efficient cancer cell response to therapy.	Curcumin	63-71	P53	Homo sapiens	113-116
32606605-0	2020	Metformin Decreases Insulin Resistance in Type 1 Diabetes Through Regulating p53 and RAP2A in vitro and in vivo.	Metformin	0-9	P53	Homo sapiens	77-80
32606605-8	2020	Metformin could effectively improve insulin resistance and inflammatory response while down-regulating p53 and up-regulating RAP2A.	Metformin	0-9	P53	Homo sapiens	103-106
32606605-10	2020	Conclusion: Metformin improves T1D insulin resistance and inflammatory response through p53/RAP2A pathway, and the regulation of p53/RAP2A pathway is conducive to improving the efficacy of metformin in the treatment of insulin resistance.	Metformin	12-21	P53	Homo sapiens	88-91
32606605-10	2020	Conclusion: Metformin improves T1D insulin resistance and inflammatory response through p53/RAP2A pathway, and the regulation of p53/RAP2A pathway is conducive to improving the efficacy of metformin in the treatment of insulin resistance.	Metformin	189-198	P53	Homo sapiens	129-132
32527012-4	2020	Hypo- or hyperacetylation mutations of STRAP at lysines 147, 148, and 156 (3KR or 3KQ) influence its activation and stabilization of p53.	Lysine	48-55	P53	Homo sapiens	133-136
32402583-9	2020	Additionally, an intracellular calcium rise and subsequent mitochondrial membrane potential collapse, P53 phosphorylation, reduced BcL-2/Bax ratio in the mitochondrial membrane, release cytochrome c from mitochondria, leading to the subsequent activation of caspase 3 activation by H2O2 were all markedly suppressed in the presence of luteolin.	Calcium	31-38	P53	Homo sapiens	102-105
32402583-9	2020	Additionally, an intracellular calcium rise and subsequent mitochondrial membrane potential collapse, P53 phosphorylation, reduced BcL-2/Bax ratio in the mitochondrial membrane, release cytochrome c from mitochondria, leading to the subsequent activation of caspase 3 activation by H2O2 were all markedly suppressed in the presence of luteolin.	Hydrogen Peroxide	282-286	P53	Homo sapiens	102-105
32522803-3	2020	Here, we show that the p53-independent metabolic functions of chromatin-bound MDM2 are exacerbated in LPS and mediate an addiction to serine metabolism that sustains nucleotide synthesis and tumor growth.	Serine	134-140	P53	Homo sapiens	23-26
32592343-1	2020	BACKGROUND: A transversion missense polymorphism of the TP53 tumor suppressor gene at the codon 72 codes proline instead of arginine causes an altered p53 protein expression and has been found to be associated with an elevated risk of various cancer; especially breast and lung cancer.	Arginine	124-132	P53	Homo sapiens	56-60
32512936-0	2020	A Co-Delivery System of Curcumin and p53 for Enhancing the Sensitivity of Drug-Resistant Ovarian Cancer Cells to Cisplatin.	Cisplatin	113-122	P53	Homo sapiens	37-40
32528731-0	2020	Interleukin-6 derived from cancer-associated fibroblasts attenuates the p53 response to doxorubicin in prostate cancer cells.	Doxorubicin	88-99	P53	Homo sapiens	72-75
32528731-2	2020	We have investigated the effect of CAFs on the p53 response to doxorubicin in prostate cancer cells.	Doxorubicin	63-74	P53	Homo sapiens	47-50
32528731-3	2020	We show that CAFs produce interleukin-6 (IL-6), and that IL-6 attenuates p53 induction and upregulation of the pro-apoptotic p53 target Bax upon treatment with doxorubicin.	Doxorubicin	160-171	P53	Homo sapiens	73-76
32528731-3	2020	We show that CAFs produce interleukin-6 (IL-6), and that IL-6 attenuates p53 induction and upregulation of the pro-apoptotic p53 target Bax upon treatment with doxorubicin.	Doxorubicin	160-171	P53	Homo sapiens	125-128
32237195-5	2020	This compound is found to be highly cytotoxic: 5 to 60 times more potent than cisplatin towards ovarian (A2780 and A2780cisR), colon (HCT116 p53+/+ and HCT116 p53-/-), and non-small lung H460 cancer cell lines.	Cisplatin	78-87	P53	Homo sapiens	141-144
32237195-5	2020	This compound is found to be highly cytotoxic: 5 to 60 times more potent than cisplatin towards ovarian (A2780 and A2780cisR), colon (HCT116 p53+/+ and HCT116 p53-/-), and non-small lung H460 cancer cell lines.	Cisplatin	78-87	P53	Homo sapiens	159-162
32294550-11	2020	ROS might contribute to ER stress and further induce apoptosis via the JNK/p53/p21 pathway.	Reactive Oxygen Species	0-3	P53	Homo sapiens	75-78
31993850-7	2020	In VSMCs, lactate increased NR4A1 expression, leading to activation of DNA-PKcs and p53.	Lactic Acid	10-17	P53	Homo sapiens	84-87
31993850-12	2020	Mechanistically, lactate enhanced fission but halted mitophagy via activation of the NR4A1/DNA-PKcs/p53 pathway, evoking apoptosis, finally accelerating osteoblastic phenotype transition of VSMC and calcium deposition.	Lactic Acid	17-24	P53	Homo sapiens	100-103
31993850-13	2020	This study suggests that the NR4A1/DNA-PKcs/p53 pathway is involved in the mechanism by which lactate accelerates vascular calcification, partly through excessive Drp-mediated mitochondrial fission and BNIP3-related mitophagy deficiency.	Lactic Acid	94-101	P53	Homo sapiens	44-47
32592343-1	2020	BACKGROUND: A transversion missense polymorphism of the TP53 tumor suppressor gene at the codon 72 codes proline instead of arginine causes an altered p53 protein expression and has been found to be associated with an elevated risk of various cancer; especially breast and lung cancer.	Arginine	124-132	P53	Homo sapiens	151-154
32179199-7	2020	In human study, the OS sections resulted in reduced expressions of tumor protein p53 (TP53), Caspase-3 (CASP3), and elevated X-linked inhibitor of apoptosis protein (XIAP) expression in comparison with OS-free controls.	Osmium	20-22	P53	Homo sapiens	81-84
32124141-2	2020	The results show that all-trans retinoic acid enhances the effect of Fra-1 on inhibiting cervical cancer proliferation and the glucose consumption, its effect on the loss of mitochondrial membrane potential, on the decreasing of lactic acid as well as ATP, and also influences the expression of MDM2/P53/P21 and LDHA.	Tretinoin	32-45	P53	Homo sapiens	300-303
32124141-7	2020	CONCLUSION: The overall results of the study strongly suggest that all-trans retinoic acid enhances the effect of Fra-1 on inhibiting cervical cancer proliferation and metabolism in vitro, and also influences the expression of MDM2/P53/P21 and LDHA.	Tretinoin	77-90	P53	Homo sapiens	232-235
32179199-7	2020	In human study, the OS sections resulted in reduced expressions of tumor protein p53 (TP53), Caspase-3 (CASP3), and elevated X-linked inhibitor of apoptosis protein (XIAP) expression in comparison with OS-free controls.	Osmium	20-22	P53	Homo sapiens	86-90
32152233-7	2020	Given the prevalence of mutations in p53 and the PI3K pathways in HNSCC in conjunction with loss of p16 genetically or epigenetically, this universal increased sensitivity to cisplatin and BYL719 combination therapy in cancer cells with PIK3CA mutation represents an opportunity to a subset of HNSCC patients.	Cisplatin	175-184	P53	Homo sapiens	37-40
32436611-16	2020	Interestingly, in the taxane combination group, patients with TP53 mutations exhibited longer PFS than those without TP53 mutations (hazard ratio = 0.08, 95% CI = 0.02-0.30, P < 0.001).	taxane	22-28	P53	Homo sapiens	62-66
32436611-16	2020	Interestingly, in the taxane combination group, patients with TP53 mutations exhibited longer PFS than those without TP53 mutations (hazard ratio = 0.08, 95% CI = 0.02-0.30, P < 0.001).	taxane	22-28	P53	Homo sapiens	117-121
32436611-17	2020	However, in the non-taxane combination group, patients with TP53 mutations displayed shorter PFS than those with wild-type TP53 (hazard ratio = 4.84, 95% CI = 1.60-14.66, P = 0.005).	taxane	20-26	P53	Homo sapiens	60-64
32436611-17	2020	However, in the non-taxane combination group, patients with TP53 mutations displayed shorter PFS than those with wild-type TP53 (hazard ratio = 4.84, 95% CI = 1.60-14.66, P = 0.005).	taxane	20-26	P53	Homo sapiens	123-127
32436611-19	2020	TP53 mutations had opposite effects on trastuzumab-treated patients treated with and without taxanes.	Taxoids	93-100	P53	Homo sapiens	0-4
31792920-7	2020	Moreover, high glucose increased the protein levels of p53, acetyl-p53 and p21.	Glucose	15-22	P53	Homo sapiens	55-58
31792920-7	2020	Moreover, high glucose increased the protein levels of p53, acetyl-p53 and p21.	Glucose	15-22	P53	Homo sapiens	67-70
32297368-6	2020	The biomarker p53 (K373) was able to distinguish genotoxicants from non-genotoxicants (2/4), while the induction of reactive oxygen species (ROS), potentially causing DNA damage, was associated with a positive Nrf2 (S40) response (2/2).	Reactive Oxygen Species	141-144	P53	Homo sapiens	14-17
32217375-0	2020	Bromocoumarinplatin, targeting simultaneously mitochondria and nuclei with p53 apoptosis pathway to overcome cisplatin resistance.	Cisplatin	109-118	P53	Homo sapiens	75-78
32217375-3	2020	Moreover, 1 promoted the expression of p53 gene and protein more effectively than cisplatin, leading to the increased anticancer activity of 1 through p53 pathway.	Cisplatin	82-91	P53	Homo sapiens	39-42
32217375-3	2020	Moreover, 1 promoted the expression of p53 gene and protein more effectively than cisplatin, leading to the increased anticancer activity of 1 through p53 pathway.	Cisplatin	82-91	P53	Homo sapiens	151-154
32468080-8	2020	This correlated with differential upregulation of p53/p21 pathway, with S and G2/M arrests by cisplatin and satraplatin in contrast to G1 arrest by oxaliplatin and DAP.	Cisplatin	94-103	P53	Homo sapiens	50-53
32508052-11	2020	RNA-seq analysis identified p53 activation and other signatures accompanying this transdifferentiation; however, the p53 stabilizer nutlin-3 induced alphaSMA expression through reactive oxygen species generation but not through the p53 transcription/mitochondria-dependent pathway, whereas the p38 inhibitor SB203580 could partially inhibit alphaSMA expression.	Reactive Oxygen Species	177-200	P53	Homo sapiens	117-120
32508052-11	2020	RNA-seq analysis identified p53 activation and other signatures accompanying this transdifferentiation; however, the p53 stabilizer nutlin-3 induced alphaSMA expression through reactive oxygen species generation but not through the p53 transcription/mitochondria-dependent pathway, whereas the p38 inhibitor SB203580 could partially inhibit alphaSMA expression.	Reactive Oxygen Species	177-200	P53	Homo sapiens	117-120
32238452-0	2020	Duloxetine attenuates paclitaxel-induced peripheral nerve injury by inhibiting p53-related pathways.	Paclitaxel	22-32	P53	Homo sapiens	79-82
32297602-2	2020	As a DNA damage-inducing agent, doxorubicin could reactivate the transcriptional activity of p53 and modulate the p21 protein level.	Doxorubicin	32-43	P53	Homo sapiens	93-96
32424519-5	2020	The results indicate that the TP53 Arg/Pro heterozygosity (adjusted OR   2.32, 95% CI  1.28-4.34, p = 0.01), Pro/Pro mutant homozygosity (adjusted OR  4.15, 95% CI  1.75-9.86, p = 0.001), along with the combined genotype (Arg/Pro + Pro/Pro) (adjusted OR  2.83, 95% CI  1.61-4.97, p < 0.001) significantly increases the risk of cervical cancer.	Arginine	35-38	P53	Homo sapiens	30-34
32424519-5	2020	The results indicate that the TP53 Arg/Pro heterozygosity (adjusted OR   2.32, 95% CI  1.28-4.34, p = 0.01), Pro/Pro mutant homozygosity (adjusted OR  4.15, 95% CI  1.75-9.86, p = 0.001), along with the combined genotype (Arg/Pro + Pro/Pro) (adjusted OR  2.83, 95% CI  1.61-4.97, p < 0.001) significantly increases the risk of cervical cancer.	Arginine	222-225	P53	Homo sapiens	30-34
31971313-4	2020	alpha-Conidendrin significantly induced apoptosis in breast cancer cells via reactive oxygen species generation, upregulation of p53 and Bax, downregulation of Bcl-2, depolarization of mitochondrial membrane potential (MMP), release of cytochrome c from mitochondria, and activation of caspases-3 and -9.	conidendrin	0-17	P53	Homo sapiens	129-132
31971313-5	2020	alpha-Conidendrin remarkably inhibited the proliferation of breast cancer cells through induction of cell cycle arrest by upregulating p53 and p21 and downregulating cyclin D1 and CDK4.	conidendrin	0-17	P53	Homo sapiens	135-138
32552932-8	2020	CONCLUSION: DHA can induce ROS production in Jurkat cells, which can cause DNA damage, activate the P53 apoptotic pathway, and promote apoptosis of cells.	Reactive Oxygen Species	27-30	P53	Homo sapiens	100-103
32466567-0	2020	Activation of Mitochondrial 2-Oxoglutarate Dehydrogenase by Cocarboxylase in Human Lung Adenocarcinoma Cells A549 Is p53/p21-Dependent and Impairs Cellular Redox State, Mimicking the Cisplatin Action.	Cisplatin	183-192	P53	Homo sapiens	117-120
32459661-0	2020	Resveratrol promotes osteogenesis and alleviates osteoporosis by inhibiting p53.	Resveratrol	0-11	P53	Homo sapiens	76-79
32459661-6	2020	In vitro experiments indicated that MDM2-mediated p53 degradation induced osteoblast differentiation, and resveratrol could partially reverse p53-dependent inhibition of osteogenic differentiation.	Resveratrol	106-117	P53	Homo sapiens	142-145
32459661-7	2020	These findings suggest resveratrol may alleviate osteoporosis at least in part by modulating the MDM2/p53 signaling pathway.	Resveratrol	23-34	P53	Homo sapiens	102-105
31112603-6	2020	We provide in silico, molecular dynamics and experimental data to support that CucWi-N (i) possesses high capability to target mortalin-p53 interaction and hnRNP-K proteins, (ii) triggers replicative senescence and inhibits metastatic potential of the cancer cells, and (iii) inhibits tumor progression and metastasis in vivo.	Nitrogen	85-86	P53	Homo sapiens	136-139
32297602-7	2020	The treatment of MCF-7 breast cancer cells with wild-type p53 by various doses of doxorubicin leads to differences in the extent of DNA damage.	Doxorubicin	82-93	P53	Homo sapiens	58-61
32382022-11	2020	By contrast, Lenvatinib and Cabozantinib appeared more effective in moderately to poorly differentiated cells with mutated p53 and low mitochondrial respiration.	cabozantinib	28-40	P53	Homo sapiens	123-126
32477008-10	2020	KEGG analysis showed that the 28 differently expressed autophagy-related genes were related to platinum drug resistance, apoptosis and p53 signaling pathway.	Platinum	95-103	P53	Homo sapiens	135-138
32489467-9	2020	We observed that cisplatin regulates p53 stability through the depletion of ubiquitination following SIRT1 downregulation.	Cisplatin	17-26	P53	Homo sapiens	37-40
32382008-0	2020	The USP10-HDAC6 axis confers cisplatin resistance in non-small cell lung cancer lacking wild-type p53.	Cisplatin	29-38	P53	Homo sapiens	98-101
32382008-6	2020	Furthermore, reintroducing either USP10 or HDAC6 into a USP10-knockdown NSCLC H1299 cell line with null-p53 renders cisplatin resistance.	Cisplatin	116-125	P53	Homo sapiens	104-107
32457882-0	2020	beta-Elemene Reverses the Resistance of p53-Deficient Colorectal Cancer Cells to 5-Fluorouracil by Inducing Pro-death Autophagy and Cyclin D3-Dependent Cycle Arrest.	Fluorouracil	81-95	P53	Homo sapiens	40-43
32457882-2	2020	5-fluorouracil remains a widely used chemotherapeutic drug in the treatment of advanced colorectal cancer, but chemotherapy drugs are prone to develop drug resistance, p53 deletion or mutation is an important reason for the resistance of colorectal cancer cells to 5-fluorouracil.	Fluorouracil	0-14	P53	Homo sapiens	168-171
32457882-2	2020	5-fluorouracil remains a widely used chemotherapeutic drug in the treatment of advanced colorectal cancer, but chemotherapy drugs are prone to develop drug resistance, p53 deletion or mutation is an important reason for the resistance of colorectal cancer cells to 5-fluorouracil.	Fluorouracil	265-279	P53	Homo sapiens	168-171
32457882-4	2020	This study aimed to investigate the effect of beta-elemene to 5-fluorouracil in drug-resistant p53-deficient colorectal cancer cells HCT116p53-/-, and determine the possible molecular mechanism of beta-elemene to reverse 5-fluorouracil resistance.	Fluorouracil	62-76	P53	Homo sapiens	95-98
32457882-12	2020	Conclusion: beta-elemene enhances the sensitivity of p53 wild-type cells to 5-fluorouracil, beta-elemene can reverse the resistance of HCT116p53-/- to 5-fluorouracil by inducing pro-death autophagy and Cyclin D3-dependent cycle arrest in p53-deficient colorectal cancer, which will provide a new method for the treatment of p53 deletion colorectal cancer patients.	Fluorouracil	76-90	P53	Homo sapiens	53-56
32382008-10	2020	Overall, our studies suggest that USP10 could be a potential biomarker for predicting patient response to platinum, and that targeting USP10 could sensitize lung cancer patients lacking wild-type p53 to platinum-based therapy.	Platinum	203-211	P53	Homo sapiens	196-199
32382022-8	2020	Lenvatinib and Cabozantinib were particularly effective in moderately to poorly differentiated cells with mutated or lacking p53 that have lower basal oxygen consumption rate (OCR), ATP, and maximal respiration capacity than observed in differentiated HCC cells.	cabozantinib	15-27	P53	Homo sapiens	125-128
32382022-8	2020	Lenvatinib and Cabozantinib were particularly effective in moderately to poorly differentiated cells with mutated or lacking p53 that have lower basal oxygen consumption rate (OCR), ATP, and maximal respiration capacity than observed in differentiated HCC cells.	Oxygen	151-157	P53	Homo sapiens	125-128
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	Irinotecan	50-55	P53	Homo sapiens	15-18
32457871-0	2020	Hybrid Molecular Dynamics for Elucidating Cooperativity Between Halogen Bond and Water Molecules During the Interaction of p53-Y220C and the PhiKan5196 Complex.	Water	81-86	P53	Homo sapiens	123-126
32457871-3	2020	In this study, the Y220C-PhiKan5196 complex of p53 protein was adopted as a model, and the functions of three water molecules that formed hydrogen bonds with halogen atoms were analyzed by the simulation method governed by the hybrid quantum mechanical/molecular mechanical molecular dynamics.	Water	110-115	P53	Homo sapiens	47-50
32457871-3	2020	In this study, the Y220C-PhiKan5196 complex of p53 protein was adopted as a model, and the functions of three water molecules that formed hydrogen bonds with halogen atoms were analyzed by the simulation method governed by the hybrid quantum mechanical/molecular mechanical molecular dynamics.	Hydrogen	138-146	P53	Homo sapiens	47-50
32088177-5	2020	Mechanistically, BDMC attenuates cisplatin-induced apoptosis of renal tubular epithelial cells by inhibiting cisplatin-induced up-regulation of p53.	Cisplatin	33-42	P53	Homo sapiens	144-147
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	Irinotecan	272-277	P53	Homo sapiens	15-18
32088177-5	2020	Mechanistically, BDMC attenuates cisplatin-induced apoptosis of renal tubular epithelial cells by inhibiting cisplatin-induced up-regulation of p53.	Cisplatin	109-118	P53	Homo sapiens	144-147
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	Irinotecan	272-277	P53	Homo sapiens	148-151
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	Irinotecan	272-277	P53	Homo sapiens	148-151
32371497-0	2020	p53 is regulated by aerobic glycolysis in cancer cells by the CtBP family of NADH-dependent transcriptional regulators.	NAD	77-81	P53	Homo sapiens	0-3
32371497-3	2020	Here, using human breast cancer cell models, we identified a pathway in which changes in the extramitochondrial-free NADH:NAD+ ratio signaled through the CtBP family of NADH-sensitive transcriptional regulators to control the abundance and activity of p53.	NAD	117-121	P53	Homo sapiens	252-255
32371497-3	2020	Here, using human breast cancer cell models, we identified a pathway in which changes in the extramitochondrial-free NADH:NAD+ ratio signaled through the CtBP family of NADH-sensitive transcriptional regulators to control the abundance and activity of p53.	NAD	122-126	P53	Homo sapiens	252-255
31932645-2	2020	Although previous studies have revealed that some sophoridine derivatives could induce DNA breakage, the underlying mechanisms of inhibition of DNA damage repair (ATR inactivation) and the apoptosis independent of p53, have not been elucidated.	matrine	50-61	P53	Homo sapiens	214-217
32371497-3	2020	Here, using human breast cancer cell models, we identified a pathway in which changes in the extramitochondrial-free NADH:NAD+ ratio signaled through the CtBP family of NADH-sensitive transcriptional regulators to control the abundance and activity of p53.	NAD	169-173	P53	Homo sapiens	252-255
32371497-4	2020	NADH-free forms of CtBPs cooperated with the p53-binding partner HDM2 to suppress p53 function, and loss of these forms in highly glycolytic cells resulted in p53 accumulation.	NAD	0-4	P53	Homo sapiens	82-85
32371497-4	2020	NADH-free forms of CtBPs cooperated with the p53-binding partner HDM2 to suppress p53 function, and loss of these forms in highly glycolytic cells resulted in p53 accumulation.	NAD	0-4	P53	Homo sapiens	82-85
32371497-5	2020	We propose that this pathway represents a "glycolytic stress response" in which the initiation of a protective p53 response by an increased NADH:NAD+ ratio enables cells to avoid cellular damage caused by mismatches between metabolic supply and demand.	NAD	140-144	P53	Homo sapiens	111-114
32371497-5	2020	We propose that this pathway represents a "glycolytic stress response" in which the initiation of a protective p53 response by an increased NADH:NAD+ ratio enables cells to avoid cellular damage caused by mismatches between metabolic supply and demand.	NAD	145-149	P53	Homo sapiens	111-114
32135156-8	2020	Taken together, our current studies provide evidence that nonprotective autophagy in p53wt non-small cell lung cancer cells can be "switched" to protective autophagy in isogenic crp53 cells, and furthermore that inhibition of cytoprotective autophagy is sufficient to restore cisplatin sensitivity in the crp53 cells, largely through the increased promotion of apoptosis, despite the absence of functional p53.	Cisplatin	276-285	P53	Homo sapiens	85-88
32135156-2	2020	The current work provides further evidence of an autophagic switch, in this case in response to the antitumor drug, cisplatin, in non-small cell lung cancer cells that are either wild-type (p53wt) or functionally null in p53 (crp53), the latter generated using CRISPR/Cas9 technology.	Cisplatin	116-125	P53	Homo sapiens	190-193
32032660-12	2020	Moreover, cells exposed to A + N can influence neighboring cells in paracrine fashion, for instance, they shed ectodomain of COL17A1 protein and induce, in p53-dependent mode, the expression of gene for interleukin-7.	Nitrogen	31-32	P53	Homo sapiens	156-159
32135156-5	2020	Specifically, autophagy inhibition in the crp53 cells converts the temporal profile for the loss of cell viability in response to cisplatin to essentially parallel that observed in the p53wt cells.	Cisplatin	130-139	P53	Homo sapiens	44-47
32317087-1	2020	Protein kinase CK2 downregulation induces premature senescence in various human cell types via activation of the reactive oxygen species (ROS)-p53-p21Cip1/WAF1 pathway.	Reactive Oxygen Species	113-136	P53	Homo sapiens	143-146
32317087-1	2020	Protein kinase CK2 downregulation induces premature senescence in various human cell types via activation of the reactive oxygen species (ROS)-p53-p21Cip1/WAF1 pathway.	Reactive Oxygen Species	138-141	P53	Homo sapiens	143-146
32504383-1	2020	The effect of inhibition of the tumor suppressor p53 on the antioxidant system genes expression under the influence of cytotoxic compounds of the platinum group was studied.	Platinum	146-154	P53	Homo sapiens	49-52
32504383-2	2020	It was found that the action of platinum(II) and platinum(IV) complexes induced accumulation of p53 protein with a maximum in 12 h, which was confirmed by an increase in the expression of the P21 gene, the target gene of the p53 protein.	Platinum	32-40	P53	Homo sapiens	96-99
32504383-2	2020	It was found that the action of platinum(II) and platinum(IV) complexes induced accumulation of p53 protein with a maximum in 12 h, which was confirmed by an increase in the expression of the P21 gene, the target gene of the p53 protein.	Platinum	32-40	P53	Homo sapiens	225-228
32504383-2	2020	It was found that the action of platinum(II) and platinum(IV) complexes induced accumulation of p53 protein with a maximum in 12 h, which was confirmed by an increase in the expression of the P21 gene, the target gene of the p53 protein.	Platinum	49-57	P53	Homo sapiens	96-99
32504383-2	2020	It was found that the action of platinum(II) and platinum(IV) complexes induced accumulation of p53 protein with a maximum in 12 h, which was confirmed by an increase in the expression of the P21 gene, the target gene of the p53 protein.	Platinum	49-57	P53	Homo sapiens	225-228
32504383-4	2020	Suppression of p53 protein functions with specific inhibitor alpha-piphitrin under the action of platinum complexes reduced the expression of catalase and superoxide dismutase 2 genes and the target gene P21, which attested to the p53-dependent regulation of these genes.	Platinum	97-105	P53	Homo sapiens	15-18
32504383-4	2020	Suppression of p53 protein functions with specific inhibitor alpha-piphitrin under the action of platinum complexes reduced the expression of catalase and superoxide dismutase 2 genes and the target gene P21, which attested to the p53-dependent regulation of these genes.	Platinum	97-105	P53	Homo sapiens	231-234
32483402-9	2020	While perifosine+vitamin D combinations increased P53 mRNA expression in HEC-1A cells we did not find any significant change in BCL2, BAX mRNA expression levels.	Vitamin D	17-26	P53	Homo sapiens	50-53
32032660-1	2020	Actinomycin D and nutlin-3a (A + N) activate p53, partly through induction of phosphorylation on Ser392.	Nitrogen	33-34	P53	Homo sapiens	45-48
32237067-0	2020	PBK attenuates paclitaxel-induced autophagic cell death by suppressing p53 in H460 non-small cell lung cancer cells.	Paclitaxel	15-25	P53	Homo sapiens	71-74
31904905-8	2020	Coexposure of Si NPs and Cd also augmented mitochondria-mediated apoptosis in HepG2 cells indicated by altered regulation of apoptotic genes (p53, bax, bcl-2, caspase-3, and caspase-9) along with reduced mitochondrial membrane potential.	Cadmium	25-27	P53	Homo sapiens	142-145
32237067-5	2020	Moreover, p53 expression facilitated an increase in the LC3-II/ LC3-I ratio in response to paclitaxel, and PBK knockdown augmented paclitaxel-mediated p53 transcriptional activity.	Paclitaxel	91-101	P53	Homo sapiens	10-13
32237067-5	2020	Moreover, p53 expression facilitated an increase in the LC3-II/ LC3-I ratio in response to paclitaxel, and PBK knockdown augmented paclitaxel-mediated p53 transcriptional activity.	Paclitaxel	131-141	P53	Homo sapiens	151-154
32237067-6	2020	Meanwhile, paclitaxel induced PBK-mediated p53 nuclear export and its subsequent ubiquitination in control cells, but not in PBK knockdown cells.	Paclitaxel	11-21	P53	Homo sapiens	43-46
32237067-7	2020	We conclude that PBK hampers paclitaxel-induced autophagic cell death by suppressing p53, suggesting a potential role of PBK in p53-mediated H460 cell death.	Paclitaxel	29-39	P53	Homo sapiens	85-88
32237067-7	2020	We conclude that PBK hampers paclitaxel-induced autophagic cell death by suppressing p53, suggesting a potential role of PBK in p53-mediated H460 cell death.	Paclitaxel	29-39	P53	Homo sapiens	128-131
32227572-6	2020	Gene set enrichment analysis (GSEA) revealed that P53 and cell cycle signalling pathway-related genes were enriched in patients with high TRIM23 expression levels.	gsea	30-34	P53	Homo sapiens	50-53
32391458-10	2020	Experimental data suggest that CeO2 treatment causes DNA fragmentation through enhanced generation of ROS, which ultimately leads to cellular apoptosis through the p53-dependent mitochondrial signaling pathway.	Reactive Oxygen Species	102-105	P53	Homo sapiens	164-167
32266639-6	2020	Moreover, GSPE was able to avoid mitochondria dysfunction and the increased in p53 and poly-(ADP-ribose) polymerase expression induced by high glucose exposition.	Glucose	143-150	P53	Homo sapiens	79-82
32211658-2	2020	Consequently, cisplatin inhibits the MDM2-mediated ubiquitination, which is the molecular basis of p53 activation.	Cisplatin	14-23	P53	Homo sapiens	99-102
32211658-3	2020	This work provides insight into the cisplatin-induced p53-elevation that is involved in cell apoptosis.	Cisplatin	36-45	P53	Homo sapiens	54-57
32065645-0	2020	Expression of Concern: "Cadmium Induces Intracellular Ca2+- and H2O2-Dependent Apoptosis through JNK- and p53-Mediated Pathways in Skin Epidermal Cell line".	Cadmium	24-31	P53	Homo sapiens	106-109
32065645-0	2020	Expression of Concern: "Cadmium Induces Intracellular Ca2+- and H2O2-Dependent Apoptosis through JNK- and p53-Mediated Pathways in Skin Epidermal Cell line".	Calcium	54-58	P53	Homo sapiens	106-109
32065645-0	2020	Expression of Concern: "Cadmium Induces Intracellular Ca2+- and H2O2-Dependent Apoptosis through JNK- and p53-Mediated Pathways in Skin Epidermal Cell line".	Water	64-68	P53	Homo sapiens	106-109
32266931-2	2020	Both c-Jun and p53 are phosphorylated at Ser63 and Thr18, respectively, in response to low glucose (40 mg/dL of medium) but not high glucose (140 mg/dL of medium) in human hepatoma-derived Huh-7 cells.	UNII-PYZ33YLR8A	51-56	P53	Homo sapiens	15-18
32266931-2	2020	Both c-Jun and p53 are phosphorylated at Ser63 and Thr18, respectively, in response to low glucose (40 mg/dL of medium) but not high glucose (140 mg/dL of medium) in human hepatoma-derived Huh-7 cells.	Glucose	91-98	P53	Homo sapiens	15-18
32266931-2	2020	Both c-Jun and p53 are phosphorylated at Ser63 and Thr18, respectively, in response to low glucose (40 mg/dL of medium) but not high glucose (140 mg/dL of medium) in human hepatoma-derived Huh-7 cells.	Glucose	133-140	P53	Homo sapiens	15-18
32266931-6	2020	A correlation of this low glucose response phosphorylation of Thr386 with the phosphorylation of c-Jun and p53 suggests that VRK1 phosphorylated at Thr386 catalyzes this phosphorylation.	Glucose	26-33	P53	Homo sapiens	107-110
32325827-0	2020	Tumor-Targeted Delivery of the p53-Activating Peptide VIP116 with PEG-Stabilized Lipodisks.	Polyethylene Glycols	66-69	P53	Homo sapiens	31-34
32344513-7	2020	Second, we show that our siRNA-carrying nanoparticles enhanced platinum sensitivity in a p53 wildtype model of non-small cell lung cancer in vitro.	Platinum	63-71	P53	Homo sapiens	89-92
32313004-5	2020	While PTEN and RB1 loss are acquired in CTCs, evolutionary analysis suggest that a PT subclone harboring TP53 loss is the driver of the metastatic event leading to the CDX.	Cefadroxil	168-171	P53	Homo sapiens	105-109
32357518-2	2020	Findings from one YM155-adapted subline of the neuroblastoma cell line UKF-NB-3 had suggested that increased ABCB1 (mediates YM155 efflux) levels, decreased SLC35F2 (mediates YM155 uptake) levels, decreased survivin levels, and TP53 mutations indicate YM155 resistance.	YM 155	18-23	P53	Homo sapiens	228-232
32330121-6	2020	The findings were reproduced in the doxorubicin-induced senescence of young fs-HDF and WI-38 cells via the PKCzeta-LKB1-AMPK signaling pathway, which was regulated by the p53-p21WAF1 pathway when p16INK4a was silenced.	Doxorubicin	36-47	P53	Homo sapiens	171-174
32061389-2	2020	Lysine acetylation is required to mediate activation of p53.	Lysine	0-6	P53	Homo sapiens	56-59
32061389-6	2020	We found that not all lysine residues are equally capable of promoting p53"s functions.	Lysine	22-28	P53	Homo sapiens	71-74
32355541-12	2020	Protein levels of the cell cycle regulators and senescence markers p21 and p53 showed opposite expression patterns in cisplatin-resistant compared with cisplatin sensitive cells.	Cisplatin	118-127	P53	Homo sapiens	75-78
32015093-0	2020	MiR-30e-3p Influences Tumor Phenotype through MDM2/TP53 Axis and Predicts Sorafenib Resistance in Hepatocellular Carcinoma.	mir-30e-3p	0-10	P53	Homo sapiens	51-55
32355541-12	2020	Protein levels of the cell cycle regulators and senescence markers p21 and p53 showed opposite expression patterns in cisplatin-resistant compared with cisplatin sensitive cells.	Cisplatin	152-161	P53	Homo sapiens	75-78
32318262-9	2020	By integrated analysis of both omic data, we found that in response to radiation insult, nitrogen metabolism, glutathione metabolism, arachidonic acid metabolism, and glycolysis or gluconeogenesis may be dysregulated due to p53.	Nitrogen	89-97	P53	Homo sapiens	224-227
32045602-0	2020	Vitexin protects against ethanol-induced liver injury through Sirt1/p53 signaling pathway.	Ethanol	25-32	P53	Homo sapiens	68-71
32045602-12	2020	Vitexin has a protective effect against ethanol-induced liver damage, and the underlying mechanism is probably through Sirt1/p53 mediated mitochondrial apoptotic pathway.	Ethanol	40-47	P53	Homo sapiens	125-128
32318262-9	2020	By integrated analysis of both omic data, we found that in response to radiation insult, nitrogen metabolism, glutathione metabolism, arachidonic acid metabolism, and glycolysis or gluconeogenesis may be dysregulated due to p53.	Glutathione	110-121	P53	Homo sapiens	224-227
32318262-9	2020	By integrated analysis of both omic data, we found that in response to radiation insult, nitrogen metabolism, glutathione metabolism, arachidonic acid metabolism, and glycolysis or gluconeogenesis may be dysregulated due to p53.	Arachidonic Acid	134-150	P53	Homo sapiens	224-227
32337406-9	2020	The simulation results highlight the importance of hydrogen bonds and the salt bridge between Lys94 of MDM2 and Glu17 of p53 in the stability of the p53-MDM2 complex.	Hydrogen	51-59	P53	Homo sapiens	149-152
32287321-0	2020	CCNB2 and AURKA overexpression may cause atypical mitosis in Japanese cortisol-producing adrenocortical carcinoma with TP53 somatic variant.	Hydrocortisone	70-78	P53	Homo sapiens	119-123
32277808-11	2020	Western blotting of HKULC2 cells showed that betulinic acid nanoparticles promoted the expression of p21 and p53 and downregulated CD133, ALDH, BCL2, MCL1, and c-Myc expression.	betulinic acid	45-59	P53	Homo sapiens	109-112
31942711-7	2020	Moreover, nTiO2 potentiated the Cd-induced apoptosis in both cells suggested by altered expression of p53, bax, and bcl-2 genes along with low mitochondrial membrane potential.	Titanium	10-15	P53	Homo sapiens	102-105
32035620-2	2020	Here we report an unexpected finding of a short chain fatty acid modification of p53 in human cells.	Fatty Acids	54-64	P53	Homo sapiens	81-84
32017938-6	2020	By measuring the level of reactive oxygen species, glutathione, superoxide dismutase, and malondialdehyde, the product of lipid peroxidation, we further demonstrated that oxidative stress was a potential factor for both the activation of P53 expression and the increase in long non-coding RNA ROR expression.	Malondialdehyde	90-105	P53	Homo sapiens	238-241
32368398-0	2020	Cisplatin sensitivity mediated by NKX2-1 in lung adenocarcinoma is dependent on p53 mutational status via modulating TNFSF10 expression.	Cisplatin	0-9	P53	Homo sapiens	80-83
32368398-3	2020	We hypothesized that NKX2-1 may confer cisplatin resistance in p53-mutated (p53-MT) lung adenocarcinoma cells but may enhance cisplatin sensitivity in wild-type (p53-WT) cells.	Cisplatin	39-48	P53	Homo sapiens	63-66
32064753-7	2020	The outcomes depicted that target genes were correlated with calcium, as well as cell proliferation, circadian entrainment, EGFR, PI3K-Akt-mTOR, and P53 signaling pathways.	Calcium	61-68	P53	Homo sapiens	149-152
31935430-8	2020	Moreover, GATA3 acted as a regulator for macrophage polarization and interactions between TAMs and HGSOC to support proliferation, motility, and cisplatin chemoresistance in mutant TP53 HGSOC cell lines.	Cisplatin	145-154	P53	Homo sapiens	181-185
32241181-1	2021	The aim of this study was to analyse the antitumor effect of the Cymbopogon densiflorus essential oil in silico and in vitro on bladder cancer cells RT4 and T24, with different TP53 status.	cymbopogon densiflorus essential oil	65-101	P53	Homo sapiens	177-181
31942711-7	2020	Moreover, nTiO2 potentiated the Cd-induced apoptosis in both cells suggested by altered expression of p53, bax, and bcl-2 genes along with low mitochondrial membrane potential.	Cadmium	32-34	P53	Homo sapiens	102-105
31823284-9	2020	Axotomy-induced apoptosis of remote glial cells increased in the presence of p53 activators WR-1065 and nutlin-3 but reduced by pifithrin-alpha that inhibits transcriptional activity of p53.	nutlin 2	104-110	P53	Homo sapiens	77-80
31838664-4	2020	Our observations suggest that P53 suppression by LPS, pifithrin, or small interfering RNA increased the expression of the redox marker malondialdehyde.	Malondialdehyde	135-150	P53	Homo sapiens	30-33
31838664-5	2020	In contrast, P53 induction by Nutlin or the Hsp90 inhibitor AUY922 exerted the opposite effects, namely, suppressed that lipid oxidation marker.	nutlin 2	30-36	P53	Homo sapiens	13-16
31838664-6	2020	The direct measurement of the reactive oxygen species by 2,7-Dichlorodihydrofluorescein diacetate confirmed the antioxidant activity of P53 in the vasculature.	Oxygen	39-45	P53	Homo sapiens	136-139
31838664-7	2020	Furthermore, the increased reactive oxygen species production due to P53 suppression was associated with lung hyperpermeability responses.	Oxygen	36-42	P53	Homo sapiens	69-72
31838664-8	2020	In conclusion, P53 supports endothelial barrier function, at least in part, via the modulation of the reactive oxygen species.	Oxygen	111-117	P53	Homo sapiens	15-18
30693808-0	2020	Cepharanthine combined with 5-fluorouracil inhibits the growth of p53-mutant human colorectal cancer cells.	cepharanthine	0-13	P53	Homo sapiens	66-69
30693808-0	2020	Cepharanthine combined with 5-fluorouracil inhibits the growth of p53-mutant human colorectal cancer cells.	Fluorouracil	28-42	P53	Homo sapiens	66-69
30693808-2	2020	The present study showed that cepharanthine alone or combined with 5-fluorouracil effectively controlled the growth of HT-29 human colorectal cancer cells harboring mutant p53 both in vitro and in vivo.	cepharanthine	30-43	P53	Homo sapiens	172-175
30693808-2	2020	The present study showed that cepharanthine alone or combined with 5-fluorouracil effectively controlled the growth of HT-29 human colorectal cancer cells harboring mutant p53 both in vitro and in vivo.	Fluorouracil	67-81	P53	Homo sapiens	172-175
30693808-6	2020	These findings suggest that cepharanthine is a promising agent for treating patients with colorectal cancer containing p53 mutation.	cepharanthine	28-41	P53	Homo sapiens	119-122
32052927-0	2020	LncRNA MST1P2/miR-133b axis affects the chemoresistance of bladder cancer to cisplatin-based therapy via Sirt1/p53 signaling.	Cisplatin	77-86	P53	Homo sapiens	111-114
32048269-0	2020	Synergistic effects of tanshinone IIA and andrographolide on the apoptosis of cancer cells via crosstalk between p53 and reactive oxygen species pathways.	tanshinone	23-37	P53	Homo sapiens	113-116
32063580-2	2020	Cisplatin-resistant cells, however, can demonstrate increased binding of both MDM2 and MDM4 to p53 but in absence of cellular overexpression.	Cisplatin	0-9	P53	Homo sapiens	95-98
32063580-10	2020	In conclusion, Nutlin-3 fully destabilizes the p53-MDM2-MDM4 complex and synergizes with cisplatin to intensify p53 function, which then downregulates Rad51 through a bimodal mechanism.	Cisplatin	89-98	P53	Homo sapiens	112-115
32048269-9	2020	Tan IIA triggered p53 responses and apoptosis by binding to the DNA of cancer cells.	tanshinone	0-7	P53	Homo sapiens	18-21
32048269-11	2020	CONCLUSION: The combination of Tan IIA and Andro showed significant synergistic effects on cancer cell apoptosis by promoting crosstalk between ROS and p53, providing a novel and effective combination that has the potential to be applied in clinical anticancer therapy.	tanshinone	31-38	P53	Homo sapiens	152-155
32034480-5	2020	CHIP assay was applied to analyze the combined characteristics of JUN and TP53 promoter.	dichlorobis(isopropylamine) dihydroxyplatinum IV-hydrogen peroxide	0-4	P53	Homo sapiens	74-78
31638087-7	2020	H2S exerts its antioxidant effect by limiting free radical reactions through the activation of antioxidant enzymes, including superoxide dismutase, catalase, and glutathione peroxidase, which protect against the effects of aging by regulating apoptosis-related genes, including p53, Bax, and Bcl-2.	Superoxides	126-136	P53	Homo sapiens	278-281
32151917-0	2020	Ethanol extract of Magnoliae cortex (EEMC) limits teratoma formation of pluripotent stem cells by selective elimination of undifferentiated cells through the p53-dependent mitochondrial apoptotic pathway.	Ethanol	0-7	P53	Homo sapiens	158-161
32300484-3	2020	The aim of this study is to investigate the impact of BMI and serum estradiol level on expression of PAX-2, H-TERT, P16, Ki-67, and P53 in studied ETM in reference to benign endometrium and EC.	Estradiol	68-77	P53	Homo sapiens	132-135
32265985-11	2020	GSEA revealed that homologous recombination, p53 signaling pathway, cell cycle, DNA replication, apoptosis, and toll-like receptor signaling were highly enriched upon STEAP1 upregulation.	gsea	0-4	P53	Homo sapiens	45-48
32300484-6	2020	Results: The relation between BMI and serum estradiol level in group 1 and PAX-2, H-TERT, P16, and p53 was statistically significant, while their relation with atypia and ki67 expression was insignificant.	Estradiol	44-53	P53	Homo sapiens	99-102
32156076-7	2020	Binding of Scp53BSF to the SCS and MDM2 oligonucleotides was strongly competed by unlabeled oligonucleotides containing mammalian p53 sites, but very little by a mutated site oligonucleotide.	Oligonucleotides	40-55	P53	Homo sapiens	13-16
32193389-0	2020	Author Correction: African-centric TP53 variant increases iron accumulation and bacterial pathogenesis but improves response to malaria toxin.	Iron	58-62	P53	Homo sapiens	35-39
32256964-9	2020	In addition, autophagy inhibitors or NAC could counteract the effect of DpdtC and restore the level of p53 to the control group, indicating that the upregulation of p53 was caused by ferritinophagy-mediated ROS production.	ros	207-210	P53	Homo sapiens	103-106
32256964-9	2020	In addition, autophagy inhibitors or NAC could counteract the effect of DpdtC and restore the level of p53 to the control group, indicating that the upregulation of p53 was caused by ferritinophagy-mediated ROS production.	ros	207-210	P53	Homo sapiens	165-168
32256964-10	2020	In conclusion, our data demonstrated that the inhibition of EMT induced by DpdtC was realized through ferritinophagy-mediated ROS/p53 pathway, which supported that the activation of ferritinophagic flux was the main driving force in EMT inhibition in gastric cancer cells, and further strengthening the concept that NCOA4 participates in EMT process.	ros	126-129	P53	Homo sapiens	130-133
32138726-8	2020	CONCLUSION: MDA,8-OHdG and wildtype p53 can be used as genotoxic biomarkers in the metal exposed group, since they can accurately reflect the degree of Oxidative damage.	Metals	83-88	P53	Homo sapiens	36-39
32160908-5	2020	Further, we observed the increased p53 Ser 15 phosphorylation in the MDC1 depleted cells.	Serine	39-42	P53	Homo sapiens	35-38
32156076-3	2020	Electrophoretic mobility shift analyses revealed the formation of specific DNA-protein complexes consisting of S. cerevisiae nuclear protein(s) and oligonucleotides containing p53 DNA binding sites.	Oligonucleotides	148-164	P53	Homo sapiens	176-179
32156076-6	2020	Like mammalian p53, the affinity of Scp53BSF for the SCS oligonucleotide was higher than for the MDM2 oligonucleotide.	Oligonucleotides	57-72	P53	Homo sapiens	15-18
32150881-2	2020	The ROS damage biomolecules such as DNA (including p53 gene), RNA, and lipids, and activate inflammatory, angiogenic, and extracellular matrix (ECM) remodeling proteins; which collectively facilitate carcinogenesis.	Reactive Oxygen Species	4-7	P53	Homo sapiens	51-54
32156076-6	2020	Like mammalian p53, the affinity of Scp53BSF for the SCS oligonucleotide was higher than for the MDM2 oligonucleotide.	Oligonucleotides	102-117	P53	Homo sapiens	15-18
32156076-7	2020	Binding of Scp53BSF to the SCS and MDM2 oligonucleotides was strongly competed by unlabeled oligonucleotides containing mammalian p53 sites, but very little by a mutated site oligonucleotide.	Oligonucleotides	40-56	P53	Homo sapiens	13-16
32156076-7	2020	Binding of Scp53BSF to the SCS and MDM2 oligonucleotides was strongly competed by unlabeled oligonucleotides containing mammalian p53 sites, but very little by a mutated site oligonucleotide.	Oligonucleotides	92-108	P53	Homo sapiens	13-16
32144153-0	2020	Withdrawal: Tumor suppressor SMAR1 activates and stabilizes p53 through its arginine-serine-rich motif.	Arginine	76-84	P53	Homo sapiens	60-63
32144153-0	2020	Withdrawal: Tumor suppressor SMAR1 activates and stabilizes p53 through its arginine-serine-rich motif.	Serine	85-91	P53	Homo sapiens	60-63
32150881-5	2020	Vitamin D inhibited oxidative DNA/RNA damage and membrane damage; and stimulated superoxide dismutase expression and p53 promoter activity in melanoma cells.	Vitamin D	0-9	P53	Homo sapiens	117-120
32150881-7	2020	We conclude that vitamin D is beneficial to melanoma cells through the inhibition of oxidative DNA/RNA damage, membrane damage, and the expression of inflammatory, angiogenic and ECM remodeling proteins; and the stimulation of superoxide dismutase expression and p53 promoter activity.	Vitamin D	17-26	P53	Homo sapiens	263-266
32391420-0	2020	Protective role of p53 in doxorubicin-induced cardiomyopathy as a mitochondrial disease.	Doxorubicin	26-37	P53	Homo sapiens	19-22
32122297-10	2020	Interestingly, changes in the p53 pathway, ECM-receptor interactions, and cytokine-cytokine receptor interactions were induced by cisplatin only in Sirt2-deficient cells.	Cisplatin	130-139	P53	Homo sapiens	30-33
32001831-8	2020	Furthermore, prolonged nicotine exposure interferes with p53 function triggered by sodium arsenite.	Nicotine	23-31	P53	Homo sapiens	57-60
32001831-10	2020	CONCLUSION: The data suggest that nicotine treatment, by perturbing intracellular redox state and altering p53 function, can create a pro-tumorigenic environment in lung epithelium.	Nicotine	34-42	P53	Homo sapiens	107-110
31734182-0	2020	Prostaglandin E2 Induces MIR675-5p to Promote Colorectal Tumor Metastasis via Modulation of p53 Expression.	Dinoprostone	0-16	P53	Homo sapiens	92-95
31734182-15	2020	PGE2 downregulates expression of p53 by increasing expression of MIR675-5p, which binds to and prevents translation of TP53 mRNA.	Dinoprostone	0-4	P53	Homo sapiens	33-36
31734182-15	2020	PGE2 downregulates expression of p53 by increasing expression of MIR675-5p, which binds to and prevents translation of TP53 mRNA.	Dinoprostone	0-4	P53	Homo sapiens	119-123
31923958-7	2020	Importantly, the cytotoxicity and cell apoptosis assays confirmed that co-delivery of 5-FU and p53 gene by the cross-linked MSN-g-PCAAMC-b-PDMAEMA@5-FU/p53 induced enhanced chemotherapeutic efficacy as compared to 5-FU delivery alone.	Fluorouracil	86-90	P53	Homo sapiens	152-155
31923958-7	2020	Importantly, the cytotoxicity and cell apoptosis assays confirmed that co-delivery of 5-FU and p53 gene by the cross-linked MSN-g-PCAAMC-b-PDMAEMA@5-FU/p53 induced enhanced chemotherapeutic efficacy as compared to 5-FU delivery alone.	Fluorouracil	147-151	P53	Homo sapiens	95-98
31923958-7	2020	Importantly, the cytotoxicity and cell apoptosis assays confirmed that co-delivery of 5-FU and p53 gene by the cross-linked MSN-g-PCAAMC-b-PDMAEMA@5-FU/p53 induced enhanced chemotherapeutic efficacy as compared to 5-FU delivery alone.	Fluorouracil	147-151	P53	Homo sapiens	95-98
32063101-6	2020	The anticancer effects of Pd/MgO nanoparticles were accentuated by the upregulation of Bax and p53 and downregulation of Bcl-2 protein expressions.	Palladium	26-28	P53	Homo sapiens	95-98
32194724-5	2020	In vitro assays demonstrated that RPL11 knockdown in gastric cancer cell lines carrying the TP53 wild-type gene attenuated 5-FU-induced cell growth suppression and activation of the P53 pathway, but not in cells carrying mutated TP53, suggesting that 5-FU suppresses tumor progression via RPL11-mediated activation of the P53 pathway in gastric cancer.	Fluorouracil	123-127	P53	Homo sapiens	92-96
32194724-5	2020	In vitro assays demonstrated that RPL11 knockdown in gastric cancer cell lines carrying the TP53 wild-type gene attenuated 5-FU-induced cell growth suppression and activation of the P53 pathway, but not in cells carrying mutated TP53, suggesting that 5-FU suppresses tumor progression via RPL11-mediated activation of the P53 pathway in gastric cancer.	Fluorouracil	123-127	P53	Homo sapiens	93-96
32194724-5	2020	In vitro assays demonstrated that RPL11 knockdown in gastric cancer cell lines carrying the TP53 wild-type gene attenuated 5-FU-induced cell growth suppression and activation of the P53 pathway, but not in cells carrying mutated TP53, suggesting that 5-FU suppresses tumor progression via RPL11-mediated activation of the P53 pathway in gastric cancer.	Fluorouracil	123-127	P53	Homo sapiens	182-185
32111081-0	2020	Mutant p53-Associated Molecular Mechanisms of ROS Regulation in Cancer Cells.	Reactive Oxygen Species	46-49	P53	Homo sapiens	7-10
32111081-4	2020	Several studies reported that in contrast with the wild type protein, mutant p53 isoforms fail to exert antioxidant activities and rather increase intracellular ROS, driving a pro-tumorigenic survival.	Reactive Oxygen Species	161-164	P53	Homo sapiens	77-80
32111081-5	2020	These pro-oxidant oncogenic abilities of GOF mutant p53 include signaling and metabolic rewiring, as well as the modulation of critical ROS-related transcription factors and antioxidant systems, which lead ROS unbalance linked to tumor progression.	Reactive Oxygen Species	136-139	P53	Homo sapiens	52-55
32111081-5	2020	These pro-oxidant oncogenic abilities of GOF mutant p53 include signaling and metabolic rewiring, as well as the modulation of critical ROS-related transcription factors and antioxidant systems, which lead ROS unbalance linked to tumor progression.	Reactive Oxygen Species	206-209	P53	Homo sapiens	52-55
32111081-6	2020	The studies summarized here highlight that GOF mutant p53 isoforms might constitute major targets for selective therapeutic intervention against several types of tumors and that ROS enhancement driven by mutant p53 might represent an "Achilles heel" of cancer cells, suggesting pro-oxidant drugs as a therapeutic approach for cancer patients bearing the mutant TP53 gene.	Reactive Oxygen Species	178-181	P53	Homo sapiens	211-214
32092796-12	2020	These results indicated that increased miR-34c mediated synaptic and memory deficits by targeting SYT1 through ROS-JNK-p53 pathway and the miR-34c/SYT1 pathway could be considered as a promising novel therapeutic target for patients with AD.	ros	111-114	P53	Homo sapiens	119-122
31841768-7	2020	We specifically discuss the roles of p53 in the development of chemoresistance to classical cytotoxic agents including for example cisplatin, doxorubicin, 5-fluorouracil, temozolomide, and paclitaxel.	Cisplatin	131-140	P53	Homo sapiens	37-40
31841768-7	2020	We specifically discuss the roles of p53 in the development of chemoresistance to classical cytotoxic agents including for example cisplatin, doxorubicin, 5-fluorouracil, temozolomide, and paclitaxel.	Doxorubicin	142-153	P53	Homo sapiens	37-40
31923941-2	2020	For the first time, MDM2-mediated p53 degradation was identified as a critical factor for developing acquired resistance of doxorubicin (DOX) in HepG2 tumor spheroids, which could be effectively reversed by MDM2 inhibitor MI-773, thereby improving anticancer effects.	Doxorubicin	124-135	P53	Homo sapiens	34-37
31923941-2	2020	For the first time, MDM2-mediated p53 degradation was identified as a critical factor for developing acquired resistance of doxorubicin (DOX) in HepG2 tumor spheroids, which could be effectively reversed by MDM2 inhibitor MI-773, thereby improving anticancer effects.	Doxorubicin	137-140	P53	Homo sapiens	34-37
31923941-3	2020	Therefore, a pH-sensitive liposomal formulation of DOX and MI-773 (LipD/M@CMCS) were developed for recovering p53-mediated DOX resistance in hepatocellular carcinoma.	Doxorubicin	51-54	P53	Homo sapiens	110-113
31923941-3	2020	Therefore, a pH-sensitive liposomal formulation of DOX and MI-773 (LipD/M@CMCS) were developed for recovering p53-mediated DOX resistance in hepatocellular carcinoma.	Doxorubicin	123-126	P53	Homo sapiens	110-113
31923958-2	2020	To this end, we constructed a novel UV-light cross-linked and pH de-cross-linked coumarin-decorated cationic copolymer functionalized mesoporous silica nanoparticles (MSN) for co-delivery of chemotherapeutic agent 5-FU and tumor suppresser p53 gene.	mesoporous silica	134-151	P53	Homo sapiens	240-243
31894323-13	2020	Knockdown of p53 significantly decreased the expression levels of miR-335-5p in JEG-3 cells and in H2O2-treated cells.	Hydrogen Peroxide	99-103	P53	Homo sapiens	13-16
31894323-14	2020	The present results suggested that miR-335-5p expression levels in trophoblast cells could be increased by ROS in a p53-dependent manner, leading to the downregulation of Sp1 and subsequent inhibition of epithelial to mesenchymal transition and cell migration.	Reactive Oxygen Species	107-110	P53	Homo sapiens	116-119
32098292-7	2020	Our results suggest that germline variants in PDEs and other regulators of the cAMP-signaling pathway may contribute to pediatric adrenocortical tumorigenesis, perhaps by cooperating with germline hypomorphic mutant TP53 alleles and uniparental disomy of chromosome 11p15 (Beckwith-Wiedemann syndrome).	Cyclic AMP	79-83	P53	Homo sapiens	216-220
32391420-2	2020	Using genetic models, our recent study demonstrates that mitochondrial genomic DNA regulation by tumor protein p53 (TP53, best known as p53) prevents the cardiotoxicity of low dose doxorubicin which does not activate the p53-dependent cell death pathway.	Doxorubicin	181-192	P53	Homo sapiens	111-114
32391420-2	2020	Using genetic models, our recent study demonstrates that mitochondrial genomic DNA regulation by tumor protein p53 (TP53, best known as p53) prevents the cardiotoxicity of low dose doxorubicin which does not activate the p53-dependent cell death pathway.	Doxorubicin	181-192	P53	Homo sapiens	116-120
32391420-2	2020	Using genetic models, our recent study demonstrates that mitochondrial genomic DNA regulation by tumor protein p53 (TP53, best known as p53) prevents the cardiotoxicity of low dose doxorubicin which does not activate the p53-dependent cell death pathway.	Doxorubicin	181-192	P53	Homo sapiens	136-139
32391420-2	2020	Using genetic models, our recent study demonstrates that mitochondrial genomic DNA regulation by tumor protein p53 (TP53, best known as p53) prevents the cardiotoxicity of low dose doxorubicin which does not activate the p53-dependent cell death pathway.	Doxorubicin	181-192	P53	Homo sapiens	136-139
32062612-2	2020	BBR can induce apoptosis of acute lymphoblastic leukemia (ALL) cells through the MDM2/p53 pathway.	Berberine	0-3	P53	Homo sapiens	86-89
32093281-7	2020	Additionally, the protein stability and transcriptional activity of p53 in TFAM knockdown tumor cells was attenuated, and this was associated with decreased acetylation, especially the acetylation of lysine 382 of p53.	Lysine	200-206	P53	Homo sapiens	68-71
32093281-7	2020	Additionally, the protein stability and transcriptional activity of p53 in TFAM knockdown tumor cells was attenuated, and this was associated with decreased acetylation, especially the acetylation of lysine 382 of p53.	Lysine	200-206	P53	Homo sapiens	214-217
32093281-9	2020	This led to the upregulation of Sirtuin1 (SIRT1), a NAD-dependent protein deacetylase, to deacetylate p53 and attenuated its transcriptional activation on PISD.	NAD	52-55	P53	Homo sapiens	102-105
32093041-9	2020	Both exogenous p53 overexpression and adriamycin-mediated endogenous p53 activation result in the transcriptional upregulation of BTG4.	Doxorubicin	38-48	P53	Homo sapiens	69-72
31945496-0	2020	Thiol antioxidants sensitize malabaricone C induced cancer cell death via reprogramming redox sensitive p53 and NF-kappaB proteins in vitro and in vivo.	Sulfhydryl Compounds	0-5	P53	Homo sapiens	104-107
31945496-0	2020	Thiol antioxidants sensitize malabaricone C induced cancer cell death via reprogramming redox sensitive p53 and NF-kappaB proteins in vitro and in vivo.	malabaricone A	29-41	P53	Homo sapiens	104-107
31945496-0	2020	Thiol antioxidants sensitize malabaricone C induced cancer cell death via reprogramming redox sensitive p53 and NF-kappaB proteins in vitro and in vivo.	Carbon	42-43	P53	Homo sapiens	104-107
31945496-8	2020	Secondly, thiol antioxidants cause rapid glutathionylation of transcription factors [p53, p65 (NF-kappaB) etc.	Sulfhydryl Compounds	10-15	P53	Homo sapiens	85-88
31945496-11	2020	Interestingly, mutation of redox sensitive cysteine residues at 124, 141 and 182 position in p53 significantly reduces mal C plus NAC mediated sensitization of cancer cells.	Cysteine	43-51	P53	Homo sapiens	93-96
31945496-11	2020	Interestingly, mutation of redox sensitive cysteine residues at 124, 141 and 182 position in p53 significantly reduces mal C plus NAC mediated sensitization of cancer cells.	malabaricone C	119-124	P53	Homo sapiens	93-96
31945496-11	2020	Interestingly, mutation of redox sensitive cysteine residues at 124, 141 and 182 position in p53 significantly reduces mal C plus NAC mediated sensitization of cancer cells.	Acetylcysteine	130-133	P53	Homo sapiens	93-96
32062612-4	2020	RESULTS: We found that BBR reduced ALL cell viability and induced apoptosis in p53-null EU-4 and p53-mutant EU-6 cells by downregulating X-linked inhibitor of apoptosis protein (XIAP), which is increased in ALL tissues and cells.	Berberine	23-26	P53	Homo sapiens	79-82
32062612-4	2020	RESULTS: We found that BBR reduced ALL cell viability and induced apoptosis in p53-null EU-4 and p53-mutant EU-6 cells by downregulating X-linked inhibitor of apoptosis protein (XIAP), which is increased in ALL tissues and cells.	Berberine	23-26	P53	Homo sapiens	97-100
32062612-10	2020	CONCLUSIONS: miR-24-3p/PIM-2/XIAP signaling contributes to BBR-mediated leukemia mitigation in p53-defect ALL, which should be further developed as a treatment strategy in ALL patients with p53 deficiency.	Berberine	59-62	P53	Homo sapiens	95-98
32062612-10	2020	CONCLUSIONS: miR-24-3p/PIM-2/XIAP signaling contributes to BBR-mediated leukemia mitigation in p53-defect ALL, which should be further developed as a treatment strategy in ALL patients with p53 deficiency.	Berberine	59-62	P53	Homo sapiens	190-193
32670818-7	2020	Silibinin protects against UVB-induced thymine dimer formation and in turn promotes DNA repair and/or initiates apoptosis in damaged cells via an increase in p53 levels.	Silybin	0-9	P53	Homo sapiens	158-161
31952808-7	2020	[R273C]p53 aggregation is disulfide mediated, leading to cross-beta, thioflavin-T-positive aggregates, whereas hydrophobic interactions dominate self-assembly in [R273L]p53, leading to a mixture of amyloid and amorphous aggregates.	Disulfides	26-35	P53	Homo sapiens	7-10
31952808-7	2020	[R273C]p53 aggregation is disulfide mediated, leading to cross-beta, thioflavin-T-positive aggregates, whereas hydrophobic interactions dominate self-assembly in [R273L]p53, leading to a mixture of amyloid and amorphous aggregates.	Disulfides	26-35	P53	Homo sapiens	169-172
31691131-6	2020	It facilitates p53-mediated apoptosis through the production of reactive oxygen species, nitric oxide and inflammatory cytokines in Mtb-infected M1 macrophages.	Reactive Oxygen Species	64-87	P53	Homo sapiens	15-18
31691131-6	2020	It facilitates p53-mediated apoptosis through the production of reactive oxygen species, nitric oxide and inflammatory cytokines in Mtb-infected M1 macrophages.	Nitric Oxide	89-101	P53	Homo sapiens	15-18
31518438-0	2020	BTK inhibitors synergize with 5-FU to treat drug-resistant TP53-null colon cancers.	Fluorouracil	30-34	P53	Homo sapiens	59-63
32175417-11	2020	Gene regulation network suggested that GPX1 mainly involved in pathways including the glutathione metabolism, ferroptosis, TP53 regulates metabolic genes, reactive oxygen species (ROS) metabolic process, and several other signaling pathways.	Reactive Oxygen Species	155-178	P53	Homo sapiens	123-127
32175417-11	2020	Gene regulation network suggested that GPX1 mainly involved in pathways including the glutathione metabolism, ferroptosis, TP53 regulates metabolic genes, reactive oxygen species (ROS) metabolic process, and several other signaling pathways.	Reactive Oxygen Species	180-183	P53	Homo sapiens	123-127
31871108-0	2020	Effect of Vitamin D on Relapse-Free Survival in a Subgroup of Patients with p53 Protein-Positive Digestive Tract Cancer: A Post Hoc Analysis of the AMATERASU Trial.	Vitamin D	10-19	P53	Homo sapiens	76-79
31871108-7	2020	In a subgroup of patients with p53-positive cancer (n = 226), 5-year RFS was 79% in the vitamin D group, which was significantly higher than the 57% in the placebo group (HR, 0.52; 95% confidence interval, 0.31-0.88; P = 0.02).	Vitamin D	88-97	P53	Homo sapiens	31-34
31871108-8	2020	In the subgroup of patients with p53-negative cancer, 5-year RFS in the vitamin D group versus placebo group was 72% versus 84% (not significantly different), respectively.	Vitamin D	72-81	P53	Homo sapiens	33-36
31871108-11	2020	CONCLUSIONS: These results generate a hypothesis that vitamin D supplementation may improve RFS in patients with p53-positive digestive tract cancer.	Vitamin D	54-63	P53	Homo sapiens	113-116
31712394-6	2020	Our mechanistic analyses revealed that combined treatment with RORgamma antagonists and taxane elicited a robust synergy in killing the resistant cells, which involves a coordinated alteration of p53, Myc and E2F-controlled programs critical for both intrinsic and extrinsic apoptosis, survival and cell growth.	taxane	88-94	P53	Homo sapiens	196-199
32111491-1	2020	Resveratrol modulates the transcription factor NF-kappaB, cytochrome P450 isoenzyme CYP1A1, expression and activity of cyclooxygenase (COX) enzymes, Fas/Fas ligand mediated apoptosis, p53, mTOR and cyclins and various phospho-diesterases resulting in an increase in cytosolic cAMP levels.	Resveratrol	0-11	P53	Homo sapiens	184-187
31706019-5	2020	In fact, the expression levels of the above- mentioned proteins were significantly altered at both mRNA and protein levels after treating the cells with 20 microM Nutlin-3 for 24 h. Additionally, the pro-apoptotic proteins including p53, p21, and Bax were elevated with the concomitant decrease in the key anti-apoptotic proteins following MDM2 inhibitor treatment.	nutlin 2	163-169	P53	Homo sapiens	233-236
31566298-6	2020	Furthermore, aging markers such as senescence-associated beta-galactosidase p53, p21Cip1/WAF1 , and p16INK4A were upregulated under H2 O2 exposure and galangin could reverse its effects.	Water	132-137	P53	Homo sapiens	76-79
31626714-0	2020	Voltage-gated sodium channels beta3 subunit promotes tumorigenesis in hepatocellular carcinoma by facilitating p53 degradation.	Sodium	14-20	P53	Homo sapiens	111-114
31908078-5	2020	p53-induced mitochondrial elongation resulted in mitochondrial dysfunction and subsequent increases in intracellular reactive oxygen species (ROS) levels, an important mediator of cellular senescence.	Oxygen	126-132	P53	Homo sapiens	0-3
31518438-4	2020	Using drug-resistant TP53-null colon cancer cells as a model we demonstrated that p65BTK silencing or chemical inhibition overcame the 5-fluorouracil resistance of CRC cell lines and patient-derived organoids and significantly reduced the growth of xenografted tumours.	Fluorouracil	135-149	P53	Homo sapiens	21-25
31464976-7	2020	Mechanistically, LY treatment elevated ROS generation that activates the p38 mitogen-activated protein kinases (MAPKs) and p53-dependent apoptotic program.	ros	39-42	P53	Homo sapiens	123-126
31112799-6	2020	A role of cytoplasmic p53 in autophagy, pentose phosphate pathway, fatty acid synthesis and oxidation, and drug response has been proposed.	Fatty Acids	67-77	P53	Homo sapiens	22-25
31464976-8	2020	Inhibition of ROS generation by NAC or p38 MAPK signaling by SB203580 attenuated the p53-mediated cell cycle arrest and apoptosis induced by LY.	ros	14-17	P53	Homo sapiens	85-88
31995555-8	2020	Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC).	Acetylcysteine	215-218	P53	Homo sapiens	87-90
31898732-8	2020	Moreover, SRPK2, Numb and p53 coimmunoprecipitated into a triple complex without or with the treatment of 5-fluorouracil in HCT116 cells, and p53 knockdown reversed the upregulation of wtp53 induced by SRPK2 silencing with chemical agent treatment.	Fluorouracil	106-120	P53	Homo sapiens	26-29
31898732-10	2020	Conversely, SRPK2 silencing decreased cell migration and invasion and increased chemosensitivity to 5-fluorouracil or cisplatin, yet these effects could be reversed by p53 knockdown under chemical agent treatment.	Cisplatin	118-127	P53	Homo sapiens	168-171
32083004-7	2020	Screening and validation confirms that ZBTB7A is able to modulate expression of the death receptors TRAIL-R1, TRAIL-R2, Fas and p53 phosphorylated at serine-15.	Serine	150-156	P53	Homo sapiens	128-131
31995555-8	2020	Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC).	Reactive Oxygen Species	181-184	P53	Homo sapiens	87-90
31995555-8	2020	Notably, the triple treatment-induced cytotoxic effects and the elevated expression of p53 and p21 proteins as well as the increased Bax/Bcl-2 ratio, all could be alleviated by the ROS scavenger, N-acetyl-cysteine (NAC).	Acetylcysteine	196-213	P53	Homo sapiens	87-90
31995555-9	2020	These findings indicate that the combination of CGA, TC-HT, and LIPEF may be a promising modality for cancer treatment, as it can induce p53-dependent cell cycle arrest and apoptosis through accumulation of ROS in PANC-1 cells.	Reactive Oxygen Species	207-210	P53	Homo sapiens	137-140
32076462-11	2020	p53 played a key role in inhibiting ROS generation in GC cells, thereby inhibiting apoptosis.	Reactive Oxygen Species	36-39	P53	Homo sapiens	0-3
32012669-7	2020	Furthermore, melatonin supplementation not only significantly enhanced mitochondrial distribution and relative abundances of BMP15 and CAT mRNA, but also decreased intracellular level of ROS and relative abundances of P53 and BAX mRNA of the oocytes.	Melatonin	13-22	P53	Homo sapiens	218-221
31986125-5	2020	RPPA analysis demonstrated expression of tumor promoting proteins in cells that lacked WT-TP53; and this feature could be reversed significantly when the cells were transfected with vector encoding WT-TP53 or treated with berberine or a modified berberine (BBR).	Berberine	222-231	P53	Homo sapiens	90-94
31986125-5	2020	RPPA analysis demonstrated expression of tumor promoting proteins in cells that lacked WT-TP53; and this feature could be reversed significantly when the cells were transfected with vector encoding WT-TP53 or treated with berberine or a modified berberine (BBR).	Berberine	222-231	P53	Homo sapiens	201-205
31991834-7	2020	Carvedilol"s activity was further confirmed in full thickness 3D human reconstituted skin, where carvedilol attenuated UV-mediated epidermal thickening, the number of Ki-67 and p53 positive cells as well as CPD formation.	Carvedilol	0-10	P53	Homo sapiens	177-180
31986125-5	2020	RPPA analysis demonstrated expression of tumor promoting proteins in cells that lacked WT-TP53; and this feature could be reversed significantly when the cells were transfected with vector encoding WT-TP53 or treated with berberine or a modified berberine (BBR).	Berberine	246-255	P53	Homo sapiens	201-205
31991834-7	2020	Carvedilol"s activity was further confirmed in full thickness 3D human reconstituted skin, where carvedilol attenuated UV-mediated epidermal thickening, the number of Ki-67 and p53 positive cells as well as CPD formation.	Carvedilol	97-107	P53	Homo sapiens	177-180
32023774-0	2020	[The influence of TP53 mutation on the therapeutic effect of EGFR tyrosine kinase inhibitor and prognosis of EGFR mutant non-small cell lung cancer patients].	Tyrosine	66-74	P53	Homo sapiens	18-22
31980600-0	2020	African-centric TP53 variant increases iron accumulation and bacterial pathogenesis but improves response to malaria toxin.	Iron	39-43	P53	Homo sapiens	16-20
31690451-1	2020	The p53 protein plays a number of roles in protecting organisms from different genotoxic stresses and this includes DNA damage induced by acetaldehyde, a metabolite of alcohol.	Ethanol	168-175	P53	Homo sapiens	4-7
31959744-0	2020	P53 and Parkin co-regulate mitophagy in bone marrow mesenchymal stem cells to promote the repair of early steroid-induced osteonecrosis of the femoral head.	Steroids	106-113	P53	Homo sapiens	0-3
31759082-4	2020	Further, nuclear accumulation of GluA2 and GAPDH have been studied in neurological disorders like epilepsy and multiple sclerosis, and disruption of this complex rescued neurological symptoms such as astrogliosis, AMPA mediated excitotoxicity and p53 phosphorylation.	alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid	214-218	P53	Homo sapiens	247-250
31973118-6	2020	By comparing the phosphoprotein content, phosphorylation status and phosphorylation sites of exposed cells with that of control cells, our results show that by affecting the phosphoproteome, TiO2-NPs affect cellular processes such as apoptosis, linked with cell cycle and the DNA damage response, TP53 being central to these pathways.	Titanium	191-195	P53	Homo sapiens	297-301
31742997-0	2020	Adoption of a Turn Conformation Drives the Binding Affinity of p53 C-Terminal Domain Peptides to 14-3-3sigma.	Carbon	19-20	P53	Homo sapiens	63-66
31742997-2	2020	A phosphorylated motif within the C-terminal domain (CTD) of p53 is key for binding to the amphipathic groove of 14-3-3.	Carbon	34-35	P53	Homo sapiens	61-64
31953488-4	2020	Truncated p53 mutants modulated droplet formation, suggesting the importance of multivalent electrostatic interactions among the N-terminal and C-terminal domains.	Nitrogen	129-130	P53	Homo sapiens	10-13
31953488-4	2020	Truncated p53 mutants modulated droplet formation, suggesting the importance of multivalent electrostatic interactions among the N-terminal and C-terminal domains.	Carbon	144-145	P53	Homo sapiens	10-13
31953488-5	2020	Second, FRET efficiency measurements for the dimer mutants of p53 revealed that distances between the core domains and between the C-terminal domains were modulated in an opposite manner within the droplets.	Carbon	131-132	P53	Homo sapiens	62-65
31753697-0	2020	Upregulation of p53 through induction of MDM2 degradation: Amino acid prodrugs of anthraquinone analogs.	Anthraquinones	82-95	P53	Homo sapiens	16-19
31690451-2	2020	Since the common tree shrew ingests high levels of alcohol as part of its normal diet, this suggests that its p53 protein may possess unique properties.	Ethanol	51-58	P53	Homo sapiens	110-113
31119730-4	2020	TP53 mutation carriers were significantly more likely to have early onset cancer (p < 0.001) and bilateral breast cancer (p = 0.03), they and were significantly more likely to respond to carboplatin-based neoadjuvant chemotherapy compared to anthracycline- or taxane-based regimen in terms of pathologic complete response (50% vs. 0%, p = 0.006).	Anthracyclines	242-255	P53	Homo sapiens	0-4
31812668-4	2020	We demonstrate that mutant p53 induces MnSOD expression, which is recovered by the ROS scavenger N-acetyl-l-cysteine.	Acetylcysteine	97-116	P53	Homo sapiens	27-30
31812668-6	2020	We also demonstrate that mutant p53 induces the expression of Sirtuin3 (SIRT3), a major mitochondrial NAD+-dependent deacetylase, stimulating MnSOD deacetylation and enzymatic activity.	NAD	102-105	P53	Homo sapiens	32-35
31119730-4	2020	TP53 mutation carriers were significantly more likely to have early onset cancer (p < 0.001) and bilateral breast cancer (p = 0.03), they and were significantly more likely to respond to carboplatin-based neoadjuvant chemotherapy compared to anthracycline- or taxane-based regimen in terms of pathologic complete response (50% vs. 0%, p = 0.006).	taxane	260-266	P53	Homo sapiens	0-4
32010620-0	2019	Involvement of Glutathione Depletion in Selective Cytotoxicity of Oridonin to p53-Mutant Esophageal Squamous Carcinoma Cells.	Glutathione	15-26	P53	Homo sapiens	78-81
31761381-5	2020	10ah-treatment in MGC-803 cells increased the expression of p53, phosphorylated p53 (p-p53), CDK4, p21 to cause cell cycle arrest at G2/M phase, significantly up-regulated the levels of pro-apoptosis proteins Bak, Bax, Bim while down-regulated the anti-apoptosis proteins Bcl-2, Bcl-xL and the levels of cyclin B1, fluctuated the intracellular reactive oxygen species (ROS), Ca2+ and mitochondrial membrane potential, activated Caspase-9 and Caspase-3 to induce apoptosis.	Oxygen	353-359	P53	Homo sapiens	60-63
31761381-5	2020	10ah-treatment in MGC-803 cells increased the expression of p53, phosphorylated p53 (p-p53), CDK4, p21 to cause cell cycle arrest at G2/M phase, significantly up-regulated the levels of pro-apoptosis proteins Bak, Bax, Bim while down-regulated the anti-apoptosis proteins Bcl-2, Bcl-xL and the levels of cyclin B1, fluctuated the intracellular reactive oxygen species (ROS), Ca2+ and mitochondrial membrane potential, activated Caspase-9 and Caspase-3 to induce apoptosis.	Oxygen	353-359	P53	Homo sapiens	80-83
31761381-5	2020	10ah-treatment in MGC-803 cells increased the expression of p53, phosphorylated p53 (p-p53), CDK4, p21 to cause cell cycle arrest at G2/M phase, significantly up-regulated the levels of pro-apoptosis proteins Bak, Bax, Bim while down-regulated the anti-apoptosis proteins Bcl-2, Bcl-xL and the levels of cyclin B1, fluctuated the intracellular reactive oxygen species (ROS), Ca2+ and mitochondrial membrane potential, activated Caspase-9 and Caspase-3 to induce apoptosis.	Oxygen	353-359	P53	Homo sapiens	80-83
31761381-5	2020	10ah-treatment in MGC-803 cells increased the expression of p53, phosphorylated p53 (p-p53), CDK4, p21 to cause cell cycle arrest at G2/M phase, significantly up-regulated the levels of pro-apoptosis proteins Bak, Bax, Bim while down-regulated the anti-apoptosis proteins Bcl-2, Bcl-xL and the levels of cyclin B1, fluctuated the intracellular reactive oxygen species (ROS), Ca2+ and mitochondrial membrane potential, activated Caspase-9 and Caspase-3 to induce apoptosis.	Calcium	375-379	P53	Homo sapiens	60-63
31761381-5	2020	10ah-treatment in MGC-803 cells increased the expression of p53, phosphorylated p53 (p-p53), CDK4, p21 to cause cell cycle arrest at G2/M phase, significantly up-regulated the levels of pro-apoptosis proteins Bak, Bax, Bim while down-regulated the anti-apoptosis proteins Bcl-2, Bcl-xL and the levels of cyclin B1, fluctuated the intracellular reactive oxygen species (ROS), Ca2+ and mitochondrial membrane potential, activated Caspase-9 and Caspase-3 to induce apoptosis.	Calcium	375-379	P53	Homo sapiens	80-83
31761381-5	2020	10ah-treatment in MGC-803 cells increased the expression of p53, phosphorylated p53 (p-p53), CDK4, p21 to cause cell cycle arrest at G2/M phase, significantly up-regulated the levels of pro-apoptosis proteins Bak, Bax, Bim while down-regulated the anti-apoptosis proteins Bcl-2, Bcl-xL and the levels of cyclin B1, fluctuated the intracellular reactive oxygen species (ROS), Ca2+ and mitochondrial membrane potential, activated Caspase-9 and Caspase-3 to induce apoptosis.	Calcium	375-379	P53	Homo sapiens	80-83
32010177-8	2019	Suppression of SOCS1-STAT3-Bcl-2 pathway and activation of p53-Pten signaling both contribute to anti-miR-221/222-induced sensitivity to cisplatin in MDA-MB-231 cells.	Cisplatin	137-146	P53	Homo sapiens	59-62
31676069-8	2020	PMFs also induced the nuclear retention of the tumor suppressor protein p53, a known XPO1 cargo protein, resulting in KHYG-1 cell cycle arrest.	flavone	0-4	P53	Homo sapiens	72-75
31984273-3	2020	Herein, we report the synthesis of new substituted variants of Sondheimer dialkyne and their application in the stapling of p53-based diazido peptides to generate potent stapled peptide-based inhibitors of the oncogenic p53-MDM2 interaction.	dialkyne	74-82	P53	Homo sapiens	124-127
31984273-3	2020	Herein, we report the synthesis of new substituted variants of Sondheimer dialkyne and their application in the stapling of p53-based diazido peptides to generate potent stapled peptide-based inhibitors of the oncogenic p53-MDM2 interaction.	dialkyne	74-82	P53	Homo sapiens	220-223
31984273-3	2020	Herein, we report the synthesis of new substituted variants of Sondheimer dialkyne and their application in the stapling of p53-based diazido peptides to generate potent stapled peptide-based inhibitors of the oncogenic p53-MDM2 interaction.	2,8-diazidoadenosine 5'-triphosphate	134-141	P53	Homo sapiens	124-127
31984273-3	2020	Herein, we report the synthesis of new substituted variants of Sondheimer dialkyne and their application in the stapling of p53-based diazido peptides to generate potent stapled peptide-based inhibitors of the oncogenic p53-MDM2 interaction.	2,8-diazidoadenosine 5'-triphosphate	134-141	P53	Homo sapiens	220-223
31935835-5	2020	Furthermore, we found that the antitumor activity of DSF/Cu against NPC cells occurred through ROS/MAPK and p53-mediated ferroptosis pathways, and that the ROS scavenger N-acetyl-l-cysteine (NAC) could reverse the cellular and lipid ROS levels.	Copper	57-59	P53	Homo sapiens	108-111
31735212-4	2020	We present here the development of an electrochemical immunosensor based on nanostructured screen-printed carbon electrodes for the quantification of unfolded p53 in plasma samples.	Carbon	106-112	P53	Homo sapiens	159-162
33166854-14	2020	CONCLUSION: Our study has identified that TP53 confers worse survival and response to platinum chemotherapy compared to BAP1.	Platinum	86-94	P53	Homo sapiens	42-46
32731241-5	2020	Intestinal-type adenocarcinoma carrying a functional p53 protein may be treated with preoperative cisplatin, 5-fluorouracil, and leucovorin.	Cisplatin	98-107	P53	Homo sapiens	53-56
32731241-5	2020	Intestinal-type adenocarcinoma carrying a functional p53 protein may be treated with preoperative cisplatin, 5-fluorouracil, and leucovorin.	Fluorouracil	109-123	P53	Homo sapiens	53-56
32668972-0	2020	Cryptotanshinone-Induced p53-Dependent Sensitization of Colon Cancer Cells to Apoptotic Drive by Regulation of Calpain and Calcium Homeostasis.	Calcium	123-130	P53	Homo sapiens	25-28
31173893-7	2020	The de novo synthesised PI undergoes remodelling to acquire its characteristic fatty acid profile, which is altered in p53-mutated cancer cells.	Fatty Acids	79-89	P53	Homo sapiens	119-122
31786674-6	2020	This increased risk of death observed for alcohol consumers was more evident in patients with normal p53 expression, GLUT-1 positive or CD-8 positive tumors.	Alcohols	42-49	P53	Homo sapiens	101-104
31368879-4	2020	RESULTS: New water soluble derivatives showed a micromolar cytotoxicity for cultured human tumor cell lines in the dark, including the subline with an altered drug response due to p53 inactivation.	Water	13-18	P53	Homo sapiens	180-183
32357825-12	2020	CONCLUSION: Epirubicin induced apoptosis in human bladder cancer cells by up-regulating the expression of pro-apoptotic factors (caspase-3, p53 and Bax) and down-regulating the expression of anti-apoptotic factor (Bcl-2).	Epirubicin	12-22	P53	Homo sapiens	140-143
31734849-7	2020	Arsenic trioxide (As2O3; 1-5 muM) significantly induced senescence in human articular chondrocytes by increasing senescence-associated beta-galactosidase (SA-beta-Gal) activity and protein expression of p16, p53, and p21.	Superoxides	18-23	P53	Homo sapiens	208-211
32401925-4	2020	Results demonstrated that beta-elemene+paclitaxel induced apoptosis of SKOV3 cells, down-regulated anti-apoptotic Bcl-2 and Bcl-xl gene expression and up-regulated pro-apoptotic P53 and Apaf1 gene expression in SKOV3 cells.	Paclitaxel	39-49	P53	Homo sapiens	178-181
32907379-0	2020	8-Chloro-Adenosine Inhibits Proliferation of MDA-MB-231 and SK-BR-3 Breast Cancer Cells by Regulating ADAR1/p53 Signaling Pathway.	Adenosine	9-18	P53	Homo sapiens	108-111
32951572-3	2020	In 2003, the first anti-tumor gene therapy drug rAd-p53 (recombinant human p53 adenovirus), trade name Gendicine , was approved by the China Food and Drug Administration (CFDA) for treatment of head and neck squamous cell carcinoma (HNSCC) in combination with radiotherapy.	gendicine	103-112	P53	Homo sapiens	52-55
32233998-10	2020	GO analysis showed that DEGs were classified into three groups and DEGs mainly enriched in Steroid biosynthesis, Ubiquitin mediated proteolysis and p53 signaling pathway.	Steroids	91-98	P53	Homo sapiens	148-151
32951572-3	2020	In 2003, the first anti-tumor gene therapy drug rAd-p53 (recombinant human p53 adenovirus), trade name Gendicine , was approved by the China Food and Drug Administration (CFDA) for treatment of head and neck squamous cell carcinoma (HNSCC) in combination with radiotherapy.	gendicine	103-112	P53	Homo sapiens	75-78
31648639-7	2020	Furthermore, Ag@PTX enhanced the anti-canceractivity of A549 cells through ROS-mediated p53 and AKT signalling pathways.	Paclitaxel	16-19	P53	Homo sapiens	88-91
31648639-7	2020	Furthermore, Ag@PTX enhanced the anti-canceractivity of A549 cells through ROS-mediated p53 and AKT signalling pathways.	ros	75-78	P53	Homo sapiens	88-91
31959867-7	2020	NAC treatment prolonged the lifespan and ameliorated pulmonary dysfunction and SAPF by downregulating TIME signaling more than p16INK4a deletion by inhibiting oxidative stress and DNA damage and promoting ubiquitin-proteasome degradation of p16INK4a and p53.	Acetylcysteine	0-3	P53	Homo sapiens	254-257
31804169-5	2020	It has been observed that nickel exposure induces the generation of reactive oxygen species which leads to the increased expression of p53, NF-kbeta, AP-1, and MAPK.	Oxygen	77-83	P53	Homo sapiens	135-138
32054357-3	2020	Doxorubicin (Dox) induces senescence by a p53-dependent pathway and telomere dysfunction of numerous cancers.	Doxorubicin	0-11	P53	Homo sapiens	42-45
31863291-6	2020	The immune infiltration-miRNA functional network analysis showed that the resting mast cell-associated miRNAs are mainly involved in the enrichment of development, mRNA metabolic process, myeloid cell differentiation, Wnt, calcium modulating, interferon, p53 pathways.	Calcium	223-230	P53	Homo sapiens	255-258
31073076-10	2020	In a pre-clinical model of patient-derived TP53 mutant acute lymphoblastic leukemia, APR-246 reduced leukemia burden and strongly synergized with the genotoxic agent doxorubicin leading to superior leukemia-free survival in vivo.	Doxorubicin	166-177	P53	Homo sapiens	43-47
32054357-3	2020	Doxorubicin (Dox) induces senescence by a p53-dependent pathway and telomere dysfunction of numerous cancers.	Doxorubicin	0-3	P53	Homo sapiens	42-45
32098913-8	2020	We further identified Ser15, Thr18 and Ser20 of p53 are critical to the beta-actin: p53 interaction, which upon mutation into alanine abrogates the binding.	UNII-PYZ33YLR8A	29-34	P53	Homo sapiens	84-87
31892967-2	2020	p53-induced glycolysis and apoptosis regulator (TIGAR) is a protein regulates glycolytic activity and glucose metabolism.	Glucose	102-109	P53	Homo sapiens	0-3
31892970-0	2020	Recombinant Dual-target MDM2/MDMX Inhibitor Reverses Doxorubicin Resistance through Activation of the TAB1/TAK1/p38 MAPK Pathway in Wild-type p53 Multidrug-resistant Breast Cancer Cells.	Doxorubicin	53-64	P53	Homo sapiens	142-145
31892970-10	2020	Therefore, the recombinant dual-target MDM2/MDMX inhibitor could reverse doxorubicin resistance via the activation of the TAB1/TAK1/p38 MAPK pathway in wild-type p53 multidrug-resistant BC.	Doxorubicin	73-84	P53	Homo sapiens	162-165
32098913-8	2020	We further identified Ser15, Thr18 and Ser20 of p53 are critical to the beta-actin: p53 interaction, which upon mutation into alanine abrogates the binding.	Alanine	126-133	P53	Homo sapiens	48-51
32098913-8	2020	We further identified Ser15, Thr18 and Ser20 of p53 are critical to the beta-actin: p53 interaction, which upon mutation into alanine abrogates the binding.	Alanine	126-133	P53	Homo sapiens	84-87
31657880-2	2020	p53 is activated by glucose limitation and maintains cell survival via triggering metabolic checkpoint.	Glucose	20-27	P53	Homo sapiens	0-3
33184243-8	2020	GSEA showed that high DSCC1 expression had a positive correlation with p53, and Wnt signaling-related molecules.	gsea	0-4	P53	Homo sapiens	71-74
31657880-5	2020	The current study demonstrated that glucose limitation transcriptionally suppressed BAG3 expression in a p53-dependent manner.	Glucose	36-43	P53	Homo sapiens	105-108
32238696-0	2020	Pro-apoptotic functions of TRAF2 in p53-mediated apoptosis induced by cisplatin.	Cisplatin	70-79	P53	Homo sapiens	36-39
32238696-4	2020	In this study, we assessed the function of TRAF2 in DDR induced by cisplatin, a representative DNA-damaging agent, and found that TRAF2 exerts pro-apoptotic activity through p53-dependent mechanisms at least in human fibrosarcoma cell line HT1080.	Cisplatin	67-76	P53	Homo sapiens	174-177
32238696-6	2020	Moreover, cisplatin-induced JNK activation was attenuated in TRAF2-deficient cells, and pharmacological inhibition of JNK signaling suppressed p53 stabilization.	Cisplatin	10-19	P53	Homo sapiens	143-146
32126555-14	2020	Resveratrol, an activator of sirtuin-1, postponed the IL-1beta-induced senescence through blocking the NF-kappaB/p53/p21 pathway and attenuated the osteoblastic transition and calcification in VSMCs.	Resveratrol	0-11	P53	Homo sapiens	113-116
31738976-5	2020	Cadmium confirmed its recognized carcinogenicity even on neuronal cells by activating the p53 signaling pathway and genes involved in tumor initiation and cancer cell proliferation, and by down-regulating genes coding for tumor suppressors and for DNA repair enzymes.	Cadmium	0-7	P53	Homo sapiens	90-93
31558785-0	2020	Natural history of ovarian high-grade serous carcinoma from time effects of ovulation inhibition and progesterone clearance of p53-defective lesions.	Progesterone	101-113	P53	Homo sapiens	127-130
31558785-5	2020	In accordance with the proposed cleansing effect of progesterone from studies on oral contraceptive use or term pregnancy, a recent study indicated that the p53-null tubal epithelial cells are selectively cleared by progesterone depending on its progesterone receptor.	Progesterone	52-64	P53	Homo sapiens	157-160
31558785-5	2020	In accordance with the proposed cleansing effect of progesterone from studies on oral contraceptive use or term pregnancy, a recent study indicated that the p53-null tubal epithelial cells are selectively cleared by progesterone depending on its progesterone receptor.	Progesterone	216-228	P53	Homo sapiens	157-160
31908576-5	2020	In cultured VSMCs, hydrogen peroxide (H2O2) dose-dependently induced senescence, which was associated with increased numbers of senescence-associated beta-galactosidase-positive cells, decreased expression of SMP30, and activation of p53-p21 and p16 pathways.	Hydrogen Peroxide	19-36	P53	Homo sapiens	234-237
31908576-5	2020	In cultured VSMCs, hydrogen peroxide (H2O2) dose-dependently induced senescence, which was associated with increased numbers of senescence-associated beta-galactosidase-positive cells, decreased expression of SMP30, and activation of p53-p21 and p16 pathways.	Water	38-42	P53	Homo sapiens	234-237
31597953-0	2020	Dichloroacetate restores colorectal cancer chemosensitivity through the p53/miR-149-3p/PDK2-mediated glucose metabolic pathway.	Glucose	101-108	P53	Homo sapiens	72-75
31990243-1	2020	Beryllium ion elicits p53-mediated cell cycle arrest in some types of human cancer cells, and it is a potent inhibitor of GSK3 kinase activity.	Beryllium	0-9	P53	Homo sapiens	22-25
31526948-9	2020	Collectively, our findings showed that curcumin is necessary to promote the protein interaction of NQO1 with p53, therefore, it increases the half-life of p53, and permits the cytotoxic effect of curcumin in cancer cells containing wild type p53.	Curcumin	39-47	P53	Homo sapiens	109-112
31642121-5	2020	Using this tool, we have identified a putative domain enriched in hydrophilic and disorder-promoting residues (Pro, Ser, and Thr) and depleted in positive charges (Arg and Lys) bordering the folded DNA-binding domains of several transcription factors (p53, GCR, NAC46, MYB28, and MYB29).	Serine	116-119	P53	Homo sapiens	252-255
32065108-7	2020	In Sodium sulphite and boric acid treated cells, expression levels of p53 was up-regulated, while that of the Bcl2 was significantly down-regulated.	sodium sulfite	3-18	P53	Homo sapiens	70-73
31642121-5	2020	Using this tool, we have identified a putative domain enriched in hydrophilic and disorder-promoting residues (Pro, Ser, and Thr) and depleted in positive charges (Arg and Lys) bordering the folded DNA-binding domains of several transcription factors (p53, GCR, NAC46, MYB28, and MYB29).	Arginine	164-167	P53	Homo sapiens	252-255
31642121-5	2020	Using this tool, we have identified a putative domain enriched in hydrophilic and disorder-promoting residues (Pro, Ser, and Thr) and depleted in positive charges (Arg and Lys) bordering the folded DNA-binding domains of several transcription factors (p53, GCR, NAC46, MYB28, and MYB29).	Lysine	172-175	P53	Homo sapiens	252-255
31526948-0	2020	Curcumin stabilizes p53 by interaction with NAD(P)H:quinone oxidoreductase 1 in tumor-derived cell lines.	Curcumin	0-8	P53	Homo sapiens	20-23
31526948-1	2020	Curcumin is a natural phytochemical with potent anti-neoplastic properties including modulation of p53.	Curcumin	0-8	P53	Homo sapiens	99-102
31526948-3	2020	The purpose of this study was to describe a mechanism by which curcumin restores p53 levels in human cancer cell lines.	Curcumin	63-71	P53	Homo sapiens	81-84
31526948-5	2020	Here we showed that curcumin increases the half-life of p53 by a physical interaction between p53-NQO1 (p53 - NAD(P)H:quinone oxidoreductase 1) proteins after treatment with curcumin.	Curcumin	20-28	P53	Homo sapiens	56-59
31526948-9	2020	Collectively, our findings showed that curcumin is necessary to promote the protein interaction of NQO1 with p53, therefore, it increases the half-life of p53, and permits the cytotoxic effect of curcumin in cancer cells containing wild type p53.	Curcumin	39-47	P53	Homo sapiens	155-158
31526948-5	2020	Here we showed that curcumin increases the half-life of p53 by a physical interaction between p53-NQO1 (p53 - NAD(P)H:quinone oxidoreductase 1) proteins after treatment with curcumin.	Curcumin	20-28	P53	Homo sapiens	94-97
31526948-5	2020	Here we showed that curcumin increases the half-life of p53 by a physical interaction between p53-NQO1 (p53 - NAD(P)H:quinone oxidoreductase 1) proteins after treatment with curcumin.	Curcumin	20-28	P53	Homo sapiens	94-97
31526948-9	2020	Collectively, our findings showed that curcumin is necessary to promote the protein interaction of NQO1 with p53, therefore, it increases the half-life of p53, and permits the cytotoxic effect of curcumin in cancer cells containing wild type p53.	Curcumin	39-47	P53	Homo sapiens	155-158
31526948-5	2020	Here we showed that curcumin increases the half-life of p53 by a physical interaction between p53-NQO1 (p53 - NAD(P)H:quinone oxidoreductase 1) proteins after treatment with curcumin.	Curcumin	174-182	P53	Homo sapiens	56-59
31526948-5	2020	Here we showed that curcumin increases the half-life of p53 by a physical interaction between p53-NQO1 (p53 - NAD(P)H:quinone oxidoreductase 1) proteins after treatment with curcumin.	Curcumin	174-182	P53	Homo sapiens	94-97
31526948-9	2020	Collectively, our findings showed that curcumin is necessary to promote the protein interaction of NQO1 with p53, therefore, it increases the half-life of p53, and permits the cytotoxic effect of curcumin in cancer cells containing wild type p53.	Curcumin	196-204	P53	Homo sapiens	109-112
31526948-5	2020	Here we showed that curcumin increases the half-life of p53 by a physical interaction between p53-NQO1 (p53 - NAD(P)H:quinone oxidoreductase 1) proteins after treatment with curcumin.	Curcumin	174-182	P53	Homo sapiens	94-97
31526948-6	2020	Interestingly, the cell viability assay after treatment with curcumin showed that the cytotoxic activity was selectively higher in cervical cancer cells contained wild type p53 but not in breast cancer cells contained mutated p53.	Curcumin	61-69	P53	Homo sapiens	173-176
31526948-10	2020	Our findings suggest that the use of curcumin may reactivate the p53 pathway in cancer cells with p53 wild-type.	Curcumin	37-45	P53	Homo sapiens	65-68
31526948-6	2020	Interestingly, the cell viability assay after treatment with curcumin showed that the cytotoxic activity was selectively higher in cervical cancer cells contained wild type p53 but not in breast cancer cells contained mutated p53.	Curcumin	61-69	P53	Homo sapiens	226-229
31526948-7	2020	The cytotoxic effect of curcumin in cervical cancer cells was related to the complex p53-NQO1 that avoids the interaction between p53 and its negative regulator ubiquitin ligase E6-associated protein (E6AP).	Curcumin	24-32	P53	Homo sapiens	85-88
31526948-10	2020	Our findings suggest that the use of curcumin may reactivate the p53 pathway in cancer cells with p53 wild-type.	Curcumin	37-45	P53	Homo sapiens	98-101
31526948-7	2020	The cytotoxic effect of curcumin in cervical cancer cells was related to the complex p53-NQO1 that avoids the interaction between p53 and its negative regulator ubiquitin ligase E6-associated protein (E6AP).	Curcumin	24-32	P53	Homo sapiens	130-133
32691668-7	2020	In addition, knockdown of protein phosphatase, Mg2+/Mn2+ dependent 1D enhanced the expressions of p-p38 and p53 in AML-193 cells and KG-1 cells.	magnesium ion	47-51	P53	Homo sapiens	108-111
32515564-8	2020	CONCLUSION: In Namalva cells that do not produce EBV antigens the treatment of CA results in suppression of ROS generation and activation of the expression of genes ISG15 and P53 (TP53); in P3HR-1 cells producing EBV antigens, the opposite picture is observed - the formation of ROS and the expression of the IFN-alpha and IFN-lambda genes are activated and the activity of the ISG15 and P53 (TP53) genes is suppressed.	Reactive Oxygen Species	279-282	P53	Homo sapiens	180-184
31903119-9	2020	Further in vitro and in vivo models demonstrated that PiHL was crucial in maintaining cell proliferation and inducing 5-FU chemoresistance through a p53-dependent manner.	Fluorouracil	118-122	P53	Homo sapiens	149-152
32691668-8	2020	The above observation suggested that protein phosphatase, Mg2+/Mn2+ dependent 1D knockdown suppressed cell proliferation, promoted cell apoptosis, and activated p38 MAPK/p53 signaling pathway in acute myeloid leukemia cells.	magnesium ion	58-62	P53	Homo sapiens	170-173
31002112-10	2019	Further analysis confirmed that lysines 381, 382, 386 of p53 are the key sites for the ubiquitination modification of SMYD3 to p53.	Lysine	32-39	P53	Homo sapiens	57-60
31976328-0	2019	Dihydroartemisinin Sensitizes Mutant p53 (R248Q)-Expressing Hepatocellular Carcinoma Cells to Doxorubicin by Inhibiting P-gp Expression.	Doxorubicin	94-105	P53	Homo sapiens	37-40
31976328-1	2019	Mutant p53 (R248Q) induces doxorubicin (ADM) resistance in hepatocellular carcinoma (HCC).	Doxorubicin	27-38	P53	Homo sapiens	7-10
31976328-1	2019	Mutant p53 (R248Q) induces doxorubicin (ADM) resistance in hepatocellular carcinoma (HCC).	Doxorubicin	40-43	P53	Homo sapiens	7-10
31976328-3	2019	However, whether DHA could increase therapeutic efficacy of ADM in p53 (R248Q)-expressing HCC cells remains unknown.	Doxorubicin	60-63	P53	Homo sapiens	67-70
31976328-6	2019	As a result, cells expressing p53 (R248Q) displayed higher cell viability and lower cell apoptosis level upon ADM treatment.	Doxorubicin	110-113	P53	Homo sapiens	30-33
31002112-10	2019	Further analysis confirmed that lysines 381, 382, 386 of p53 are the key sites for the ubiquitination modification of SMYD3 to p53.	Lysine	32-39	P53	Homo sapiens	127-130
31976328-8	2019	However, combination of DHA and ADM treatment decreased cell viability and elevated cell apoptosis level in p53 (R248Q)-expressing Hep3B cells.	Doxorubicin	32-35	P53	Homo sapiens	108-111
31976328-11	2019	Finally, DHA treatment could significantly reduce ADM efflux in p53 (R248Q)-expressing cells.	Doxorubicin	50-53	P53	Homo sapiens	64-67
31884961-0	2019	Correction to: Oroxylin A promotes PTEN-mediated negative regulation of MDM2 transcription via SIRT3-mediated deacetylation to stabilize p53 and inhibit glycolysis in wt-p53 cancer cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	15-25	P53	Homo sapiens	137-140
31976328-12	2019	Our results indicate that DHA could decrease P-gp expression via inhibiting the p53 (R248Q)-ERK1/2-NF-kappaB signaling pathway, which eventually confers sensitization of p53 (R248Q)-expressing HCC cells to ADM. Our study provides evidence for the potential application of DHA and ADM combination in treatment of mutant p53 (R248Q)-harbored HCC.	Doxorubicin	206-209	P53	Homo sapiens	80-83
31969973-0	2020	Inhibition of protein FAK enhances 5-FU chemosensitivity to gastric carcinoma via p53 signaling pathways.	Fluorouracil	35-39	P53	Homo sapiens	82-85
31884961-0	2019	Correction to: Oroxylin A promotes PTEN-mediated negative regulation of MDM2 transcription via SIRT3-mediated deacetylation to stabilize p53 and inhibit glycolysis in wt-p53 cancer cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	15-25	P53	Homo sapiens	170-173
31866582-0	2019	Overexpressed methyltransferase-like 1 (METTL1) increased chemosensitivity of colon cancer cells to cisplatin by regulating miR-149-3p/S100A4/p53 axis.	Cisplatin	100-109	P53	Homo sapiens	142-145
31984217-4	2019	More recently, we demonstrated that the SRC family of non-receptor tyrosine kinases (SFK) can phosphorylate SOCS1 leading to its homodimerization and inhibiting its interaction with p53.	Tyrosine	67-75	P53	Homo sapiens	182-185
31866582-10	2019	Taken together, overexpression of METTL1 sensitized CR-CC cells to cisplatin by modulating miR-149-3p/S100A4/p53 axis.	Cisplatin	67-76	P53	Homo sapiens	109-112
31877751-0	2019	Identification and Characterization of a New Platinum-Induced TP53 Mutation in MDAH Ovarian Cancer Cells.	Platinum	45-53	P53	Homo sapiens	62-66
31568878-3	2019	PAMSPF was able to condense DNA and encapsulate RG7388 to form spherical nanoparticles (PAMSPF/p53/RG) with particle sizes of around 200 nm, and remain stable in the presence of heparin and nuclease.	Heparin	178-185	P53	Homo sapiens	95-98
31877751-7	2019	Interestingly, we found that PT-resistant MDAH cells acquired in the TP53 gene a novel secondary mutation (i.e., S185G) that accompanied the R273H typical of MDAH cells.	Platinum	29-31	P53	Homo sapiens	69-73
31877751-8	2019	The double p53S185G/R273H mutant increases the resistance to PT in a TP53 null EOC cellular model.	Platinum	61-63	P53	Homo sapiens	11-14
31877751-8	2019	The double p53S185G/R273H mutant increases the resistance to PT in a TP53 null EOC cellular model.	Platinum	61-63	P53	Homo sapiens	69-73
31877751-9	2019	Overall, we show how the selective pressure of PT is able to induce additional mutation in an already mutant TP53 gene in EOC and how this event could contribute to the acquisition of novel cellular phenotypes.	Platinum	47-49	P53	Homo sapiens	109-113
31920721-4	2019	This metabolic shift leads to increased AMP/ATP and ADP/ATP ratios, to the subsequent AMPK activation, and ultimately to p53-mediated growth arrest.	Adenosine Monophosphate	40-43	P53	Homo sapiens	121-124
31920721-4	2019	This metabolic shift leads to increased AMP/ATP and ADP/ATP ratios, to the subsequent AMPK activation, and ultimately to p53-mediated growth arrest.	Adenosine Triphosphate	44-47	P53	Homo sapiens	121-124
31920721-4	2019	This metabolic shift leads to increased AMP/ATP and ADP/ATP ratios, to the subsequent AMPK activation, and ultimately to p53-mediated growth arrest.	Adenosine Diphosphate	52-55	P53	Homo sapiens	121-124
31871844-8	2019	Three drugs, mitomycin-C, doxorubicin and gemcitabine, were especially more sensitive to bladder cancer with the TP53 mutation.	Doxorubicin	26-37	P53	Homo sapiens	113-117
31891063-5	2019	Chlorido drugs showed similar behavior to cisplatin; they both required p53 to induce apoptosis but only cis-ipa showed DNA damage requirement for apoptosis induction.	Cisplatin	42-51	P53	Homo sapiens	72-75
32237321-9	2020	Further studies showed that after combined use, the number of clonogen formation in A549 cells was significantly reduced(P<0.01); ROS production was increased; the expression of apoptosis-related protein p53 was up-regulated, and the ratio of Bcl-2/Bax was decreased.	Reactive Oxygen Species	130-133	P53	Homo sapiens	204-207
31605953-10	2019	The overexpression of GSTM1 in the above cell lines led to a significant decrease in ROS and an increase in GSH concentration and TP53 levels, suggesting that the controversial role of GSTM1 resulted from the TP53 genotype of HCC cells.	Reactive Oxygen Species	85-88	P53	Homo sapiens	209-213
31621101-3	2019	One posttranslational modification of p53, phosphorylation at Serine 46, selectively occurs after severe DNA damage and is envisioned as a marker of the cell death response.	Serine	62-68	P53	Homo sapiens	38-41
31621101-5	2019	In this essay, the current body of evidence on the molecular function of this deadly p53 mark, its evolutionary conservation, and the regulation of the key players of this response, the p53 Serine 46 kinases, are reviewed and dissected.	Serine	190-196	P53	Homo sapiens	85-88
31098781-0	2019	ASO Author Reflections: Precise p53 Analysis in Formalin-Fixed Paraffin-Embedded Specimens Can Predict Head and Neck Squamous Cell Carcinoma Outcomes.	Paraffin	63-71	P53	Homo sapiens	32-35
31237151-6	2019	Mechanistically, we show that TC-G 1008 mitigates IL-1beta-induced cell cycle arrest at G1 phase by suppressing the expression of p53, p21, PAI-1, and K382 acetylation of p53.	GPR39-C3	30-39	P53	Homo sapiens	130-133
31237151-6	2019	Mechanistically, we show that TC-G 1008 mitigates IL-1beta-induced cell cycle arrest at G1 phase by suppressing the expression of p53, p21, PAI-1, and K382 acetylation of p53.	GPR39-C3	30-39	P53	Homo sapiens	171-174
31237151-7	2019	Moreover, we show that TC-G 1008 treatment restores IL-1beta-induced inhibition of SIRT1 and the silencing of SIRT1 abolishes the function of TC-G 1008 on p53 acetylation and senescence, suggesting that the function of GPR39 signaling is mediated by SIRT1 in chondrocytes.	GPR39-C3	142-151	P53	Homo sapiens	155-158
31605953-10	2019	The overexpression of GSTM1 in the above cell lines led to a significant decrease in ROS and an increase in GSH concentration and TP53 levels, suggesting that the controversial role of GSTM1 resulted from the TP53 genotype of HCC cells.	Glutathione	108-111	P53	Homo sapiens	209-213
31605953-13	2019	GSTM1 also regulates tumor progression by disrupting the ROS-TP53 axis in HCC cells with different genetic backgrounds.	Reactive Oxygen Species	57-60	P53	Homo sapiens	61-65
31549646-9	2019	Immunofluorescence of TCP exposed cells showed activation of p53, caspase3, caspase9 reaffirming the involvement of mitochondrial-dependent intrinsic apoptotic signaling.	Tritolyl Phosphates	22-25	P53	Homo sapiens	61-64
30739221-0	2019	The sodium pump alpha1 subunit regulates bufalin sensitivity of human glioblastoma cells through the p53 signaling pathway.	Sodium	4-10	P53	Homo sapiens	101-104
31706153-2	2019	It is well established that cisplatin alters the expression of many genes involved in several cellular processes and pathways including transcription, p53 signaling pathway, and apoptosis.	Cisplatin	28-37	P53	Homo sapiens	151-154
31726940-6	2019	In conclusion, our findings demonstrate mutant p53 may cause chemo-resistance of tumor because of inactivating PUMA transcription, which prompts some new insights for clinical therapy of cancer patients with mutant p53.Abbreviations: CRC: Colorectal cancer; CDKs: Cyclin-dependent kinases; PUMA: p53 up-regulated modulator of apoptosis; PDGF: the platelet-derived growth factor; WT p53: wild-type p53 protein; mutp53: mutant p53 proteins; BAX: Bcl-2-associated X protein; NOXA: Phorbol-12-myristate-13-acetate-induced protein 1.	Tetradecanoylphorbol Acetate	478-509	P53	Homo sapiens	47-50
31726940-6	2019	In conclusion, our findings demonstrate mutant p53 may cause chemo-resistance of tumor because of inactivating PUMA transcription, which prompts some new insights for clinical therapy of cancer patients with mutant p53.Abbreviations: CRC: Colorectal cancer; CDKs: Cyclin-dependent kinases; PUMA: p53 up-regulated modulator of apoptosis; PDGF: the platelet-derived growth factor; WT p53: wild-type p53 protein; mutp53: mutant p53 proteins; BAX: Bcl-2-associated X protein; NOXA: Phorbol-12-myristate-13-acetate-induced protein 1.	Tetradecanoylphorbol Acetate	478-509	P53	Homo sapiens	215-218
31726940-6	2019	In conclusion, our findings demonstrate mutant p53 may cause chemo-resistance of tumor because of inactivating PUMA transcription, which prompts some new insights for clinical therapy of cancer patients with mutant p53.Abbreviations: CRC: Colorectal cancer; CDKs: Cyclin-dependent kinases; PUMA: p53 up-regulated modulator of apoptosis; PDGF: the platelet-derived growth factor; WT p53: wild-type p53 protein; mutp53: mutant p53 proteins; BAX: Bcl-2-associated X protein; NOXA: Phorbol-12-myristate-13-acetate-induced protein 1.	Tetradecanoylphorbol Acetate	478-509	P53	Homo sapiens	215-218
31726940-6	2019	In conclusion, our findings demonstrate mutant p53 may cause chemo-resistance of tumor because of inactivating PUMA transcription, which prompts some new insights for clinical therapy of cancer patients with mutant p53.Abbreviations: CRC: Colorectal cancer; CDKs: Cyclin-dependent kinases; PUMA: p53 up-regulated modulator of apoptosis; PDGF: the platelet-derived growth factor; WT p53: wild-type p53 protein; mutp53: mutant p53 proteins; BAX: Bcl-2-associated X protein; NOXA: Phorbol-12-myristate-13-acetate-induced protein 1.	Tetradecanoylphorbol Acetate	478-509	P53	Homo sapiens	215-218
31726940-6	2019	In conclusion, our findings demonstrate mutant p53 may cause chemo-resistance of tumor because of inactivating PUMA transcription, which prompts some new insights for clinical therapy of cancer patients with mutant p53.Abbreviations: CRC: Colorectal cancer; CDKs: Cyclin-dependent kinases; PUMA: p53 up-regulated modulator of apoptosis; PDGF: the platelet-derived growth factor; WT p53: wild-type p53 protein; mutp53: mutant p53 proteins; BAX: Bcl-2-associated X protein; NOXA: Phorbol-12-myristate-13-acetate-induced protein 1.	Tetradecanoylphorbol Acetate	478-509	P53	Homo sapiens	215-218
31726940-6	2019	In conclusion, our findings demonstrate mutant p53 may cause chemo-resistance of tumor because of inactivating PUMA transcription, which prompts some new insights for clinical therapy of cancer patients with mutant p53.Abbreviations: CRC: Colorectal cancer; CDKs: Cyclin-dependent kinases; PUMA: p53 up-regulated modulator of apoptosis; PDGF: the platelet-derived growth factor; WT p53: wild-type p53 protein; mutp53: mutant p53 proteins; BAX: Bcl-2-associated X protein; NOXA: Phorbol-12-myristate-13-acetate-induced protein 1.	Tetradecanoylphorbol Acetate	478-509	P53	Homo sapiens	215-218
31638225-11	2019	Function enrichment analysis revealed the genes in the ceRNA network that participated in the p53 signaling pathway [cyclin E2 (CCNE2), ribonucleotide reductase M2 subunit (RRM2)] and nitrogen metabolism [carbonic anhydrase 2 (CA2)], which were also included in the pathways of the CTD.	Nitrogen	184-192	P53	Homo sapiens	94-97
31798724-2	2019	The aim of this study was to determine how curcumin (CRM) used as an adjuvant supports the apoptotic process induced by a single chemical agent treatment (cisplatin-CisPT) on two head and neck squamous cell carcinoma cell lines (FaDu and PE/CA-PJ49) and the involvement of ERK1/2 and/or p53 activation in this process.	Curcumin	43-51	P53	Homo sapiens	287-290
31798724-2	2019	The aim of this study was to determine how curcumin (CRM) used as an adjuvant supports the apoptotic process induced by a single chemical agent treatment (cisplatin-CisPT) on two head and neck squamous cell carcinoma cell lines (FaDu and PE/CA-PJ49) and the involvement of ERK1/2 and/or p53 activation in this process.	Curcumin	53-56	P53	Homo sapiens	287-290
31798724-4	2019	CRM induced an increase of p53 protein phosphorylation in both cell lines.	Curcumin	0-3	P53	Homo sapiens	27-30
31798724-5	2019	CisPt decreased p53 protein phosphorylation in FaDu cells, but increased it in PE/CA-PJ49 cells.	Platinum	0-5	P53	Homo sapiens	16-19
31798724-8	2019	Our data suggest that p53 phosphorylation in the apoptotic process induced by CRM treatment might require the involvement of ERK1/2.	Curcumin	78-81	P53	Homo sapiens	22-25
31798724-9	2019	In this regard the CisPt treatment suggested that p53 phosphorylation is ERK1/2 independent in FaDu cells having a p53 gene deletion and ERK1/2 dependent in PE/CA-PJ49 cells having a p53 gene amplification.	Platinum	19-24	P53	Homo sapiens	50-53
31798724-9	2019	In this regard the CisPt treatment suggested that p53 phosphorylation is ERK1/2 independent in FaDu cells having a p53 gene deletion and ERK1/2 dependent in PE/CA-PJ49 cells having a p53 gene amplification.	Platinum	19-24	P53	Homo sapiens	115-118
31798724-9	2019	In this regard the CisPt treatment suggested that p53 phosphorylation is ERK1/2 independent in FaDu cells having a p53 gene deletion and ERK1/2 dependent in PE/CA-PJ49 cells having a p53 gene amplification.	Platinum	19-24	P53	Homo sapiens	115-118
31798724-10	2019	Moreover, in both tumor cell lines our results support the involvement of p53 phosphorylation-ERK1/2 activation-dependent in the apoptosis induced by combined treatments (CisPt and CRM).	Platinum	171-176	P53	Homo sapiens	74-77
31798724-10	2019	Moreover, in both tumor cell lines our results support the involvement of p53 phosphorylation-ERK1/2 activation-dependent in the apoptosis induced by combined treatments (CisPt and CRM).	Curcumin	181-184	P53	Homo sapiens	74-77
31541355-8	2019	Cisplatin + compound 4 significantly enhanced p53 phosphorylation, induced Bax amount, reduced Bcl2 protein levels, enhanced PARP cleavage and modulated miRNAs expression profile in TNBCs, with a particular overexpression of miR-125a-5p and miR-181a-5p.	Cisplatin	0-9	P53	Homo sapiens	46-49
31885199-7	2019	Instead, we provide evidence that the time-varying acetylation state of p53"s C-terminal lysine residues is critical for gene-specific regulation of stochastic bursting.	Lysine	89-95	P53	Homo sapiens	72-75
31807178-12	2019	The 11 hub genes were primarily enriched in the cell cycle, oocyte meiosis, progesterone-mediated oocyte maturation, the p53 signaling pathway and viral carcinogenesis.	Progesterone	76-88	P53	Homo sapiens	121-124
31807162-13	2019	The results demonstrated that combined treatment of radiation and cisplatin exhibited superior therapeutic effects on osteosarcoma MG-63 cells compared with radiation or cisplatin treatment alone, which may be mediated by the BRCA1-p53 signaling pathway.	Cisplatin	170-179	P53	Homo sapiens	232-235
31418618-7	2019	FCW fume particles were also the most potent in causing ROS and DNA damage and they furthermore activated reporters related to DNA double- strand breaks and p53 signaling.	fcw fume	0-8	P53	Homo sapiens	157-160
31807162-0	2019	The inhibitory effects of cisplatin-radiation combination treatment on malignant osteosarcoma MG-63 cells and BRCA1-p53 pathways are more efficient than single treatments.	Cisplatin	26-35	P53	Homo sapiens	116-119
31807162-10	2019	Furthermore, combined treatment with radiation and cisplatin decreased the mRNA and protein expression levels of BRCA1 and p53.	Cisplatin	51-60	P53	Homo sapiens	123-126
31807162-11	2019	Additionally, combined treatment with radiation and cisplatin had a more potent inhibitory effect on p53 expression than on BRCA1 expression.	Cisplatin	52-61	P53	Homo sapiens	101-104
31970141-3	2019	We evaluated the effects of ectopic expression of p53 on the biological functions of ibuprofen and diclofenac.	Ibuprofen	85-94	P53	Homo sapiens	50-53
31807162-13	2019	The results demonstrated that combined treatment of radiation and cisplatin exhibited superior therapeutic effects on osteosarcoma MG-63 cells compared with radiation or cisplatin treatment alone, which may be mediated by the BRCA1-p53 signaling pathway.	Cisplatin	66-75	P53	Homo sapiens	232-235
31720601-0	2019	The hydrophobically-tagged MDM2-p53 interaction inhibitor Nutlin-3a-HT is more potent against tumor cells than Nutlin-3a.	nutlin 2	58-64	P53	Homo sapiens	32-35
31668020-16	2019	TP53, EGFR and KRAS mutations are associated with expression of glucose and glutamine metabolism-related markers in NSCLC.	Glucose	64-71	P53	Homo sapiens	0-4
31438780-4	2019	Results: Cell senescence, characterized by senescence beta-galactosidase staining and senescence-related genes (p16, p21, and p53) expression, was attenuated by resveratrol.	Resveratrol	161-172	P53	Homo sapiens	126-129
31617338-4	2019	Here, we present evidence that the PI3K-AKTmTOR-reactive oxygen species-p53 pathway is necessary for CK2 downregulation-mediated H3K9me3 and SAHFs formation.	Oxygen	57-63	P53	Homo sapiens	72-75
31779710-7	2019	RESULTS: In vitro treatment of bone marrow-derived macrophages with APG-115 resulted in activation of p53 and p21, and a decrease in immunosuppressive M2 macrophage population through downregulation of c-Myc and c-Maf.	AA-115	68-75	P53	Homo sapiens	102-105
31779710-13	2019	CONCLUSION: Our results demonstrate that p53 activation mediated by APG-115 promotes antitumor immunity in the tumor microenvironment (TME) regardless of the Trp53 status of tumors per se.	AA-115	68-75	P53	Homo sapiens	41-44
31779710-15	2019	Based on the data, a phase 1b clinical trial has been launched for the evaluation of APG-115 in combination with pembrolizumab in solid tumor patients including those with TP53mut tumors.	AA-115	85-92	P53	Homo sapiens	172-176
31720601-2	2019	Nutlin-3a-HT, created by fusing the hydrophobic tag HyT13 to the MDM2-p53 interaction inhibitor Nutlin-3a, prevented cellular accumulation of MDM2 upon p53 reactivation, and had a stronger effect on cell viability and the induction of apoptosis than Nutlin-3a.	nutlin 2	0-6	P53	Homo sapiens	70-73
31720601-2	2019	Nutlin-3a-HT, created by fusing the hydrophobic tag HyT13 to the MDM2-p53 interaction inhibitor Nutlin-3a, prevented cellular accumulation of MDM2 upon p53 reactivation, and had a stronger effect on cell viability and the induction of apoptosis than Nutlin-3a.	nutlin 2	0-6	P53	Homo sapiens	152-155
31720601-2	2019	Nutlin-3a-HT, created by fusing the hydrophobic tag HyT13 to the MDM2-p53 interaction inhibitor Nutlin-3a, prevented cellular accumulation of MDM2 upon p53 reactivation, and had a stronger effect on cell viability and the induction of apoptosis than Nutlin-3a.	nutlin 2	96-102	P53	Homo sapiens	70-73
31744518-0	2019	TPP-related mitochondrial targeting copper (II) complex induces p53-dependent apoptosis in hepatoma cells through ROS-mediated activation of Drp1.	Copper	36-42	P53	Homo sapiens	64-67
31519237-0	2019	Ratiometric fluorescence strategy for p53 gene assay by using nitrogen doped graphene quantum dots and berberine as fluorescence reporters.	Nitrogen	62-70	P53	Homo sapiens	38-41
31519237-0	2019	Ratiometric fluorescence strategy for p53 gene assay by using nitrogen doped graphene quantum dots and berberine as fluorescence reporters.	Berberine	103-112	P53	Homo sapiens	38-41
31519237-2	2019	Nitrogen doped graphene quantum dots (NGQDs) were firstly bound with a single-stranded DNA (P1 DNA), which contains berberine aptamer sequence and p53 gene complementary sequence (Cp53 DNA).	Nitrogen	0-8	P53	Homo sapiens	147-150
31519237-4	2019	P1 DNA can be hydrolyzed by Exonuclease I (Exo I) when target p53 gene was absent, resulting in the release of berberine and the decrease of fluorescence intensity at 537 nm.	Berberine	111-120	P53	Homo sapiens	62-65
31758050-4	2019	First, the redox activities of different p53 redox products were qualitatively investigated on carbon-based electrodes.	Carbon	95-101	P53	Homo sapiens	41-44
31545555-3	2019	These complexes are 12 to 34x more potent than cisplatin against HCT116 p53+/+ and HCT116 p53-/- cells.	Cisplatin	47-56	P53	Homo sapiens	72-75
31772160-6	2019	Furthermore, we show that cytotoxic PNU-159682-P1C1TM drug conjugates specifically inhibit growth of mutant p53 expressing cells in vitro and in vivo.	3'-deamino-3'',4'-anhydro-(2''-methoxy-3''-oxy-4''-morpholinyl)doxorubicin	36-46	P53	Homo sapiens	108-111
20301488-16	1993	Agents/circumstances to avoid: People with germline TP53 pathogenic variants should: (1) avoid known carcinogens including sun exposure, tobacco use, occupational exposures, and excessive alcohol use; and (2) minimize exposure to diagnostic and therapeutic radiation.	Alcohols	188-195	P53	Homo sapiens	52-56
31819616-0	2019	Low-Concentration PTX And RSL3 Inhibits Tumor Cell Growth Synergistically By Inducing Ferroptosis In Mutant p53 Hypopharyngeal Squamous Carcinoma.	Paclitaxel	18-21	P53	Homo sapiens	108-111
31819616-3	2019	Recent findings showed low-concentration paclitaxel (PTX) could inhibit cell death by upregulating p53 expression; downregulating glutaminolysis-related genes.	Paclitaxel	41-51	P53	Homo sapiens	99-102
31819616-3	2019	Recent findings showed low-concentration paclitaxel (PTX) could inhibit cell death by upregulating p53 expression; downregulating glutaminolysis-related genes.	Paclitaxel	53-56	P53	Homo sapiens	99-102
31752383-11	2019	Furthermore, NAC could alleviate p53 and the p53 upregulated modulator of apoptosis (PUMA) expression induced by TRAIL and ASH.	Acetylcysteine	13-16	P53	Homo sapiens	33-36
31752383-11	2019	Furthermore, NAC could alleviate p53 and the p53 upregulated modulator of apoptosis (PUMA) expression induced by TRAIL and ASH.	Acetylcysteine	13-16	P53	Homo sapiens	45-48
31752383-15	2019	In conclusion, the above data suggested that ROS could induce DNA damage and activating p53/PUMA/Bax signaling, and thus, this resulted in the permeabilization of mitochondrial outer membrane and activating caspases as well as sensitizing the HCC cell to apoptosis induced by TRAIL and ASH treatment.	Reactive Oxygen Species	45-48	P53	Homo sapiens	88-91
31652301-6	2019	Here we have used different approaches to show that this event is accompanied by a specific change in the HDM2 structure that affects the HDM2 interactome, such as the N-termini HDM2 - p53 protein-protein interaction.	Nitrogen	168-169	P53	Homo sapiens	185-188
31752145-0	2019	Curcumin Nicotinate Selectively Induces Cancer Cell Apoptosis and Cycle Arrest through a P53-Mediated Mechanism.	Curcumin	0-19	P53	Homo sapiens	89-92
31752145-4	2019	In cancer cells, CN induced apoptosis and cell cycle arrest at G2/M phase through a p53-mediated mechanism, where p53 was activated, p21 and pro-apoptotic proteins Bid and Bak were upregulated, and PARP was cleaved.	Curcumin	17-19	P53	Homo sapiens	84-87
31752145-4	2019	In cancer cells, CN induced apoptosis and cell cycle arrest at G2/M phase through a p53-mediated mechanism, where p53 was activated, p21 and pro-apoptotic proteins Bid and Bak were upregulated, and PARP was cleaved.	Curcumin	17-19	P53	Homo sapiens	114-117
31752145-5	2019	In non-transformed human mammary epithelial cells MCF10A, CN at 50 microM had no cytotoxicity and p53 was not activated, but curcumin at 12.5 microM activated p53 and p21 and inhibited MCF10A cell growth.	Curcumin	125-133	P53	Homo sapiens	159-162
31752145-6	2019	These data suggest that CN inhibits cell growth and proliferation through p53-mediated apoptosis and cell cycle arrest with cancer cell selectivity.	Curcumin	24-26	P53	Homo sapiens	74-77
31703394-0	2019	HDAC4 Levels Control Sensibility toward Cisplatin in Gastric Cancer via the p53-p73/BIK Pathway.	Cisplatin	40-49	P53	Homo sapiens	76-79
31698450-2	2019	We previously showed that the cyclooxygenase (COX) inhibitor indomethacin prevents the ability of stromal cells to diminish p53-mediated killing of cocultured ALL cells in vitro, possibly by blocking the production of prostaglandin E2 (PGE2).	Dinoprostone	218-234	P53	Homo sapiens	124-127
31698450-2	2019	We previously showed that the cyclooxygenase (COX) inhibitor indomethacin prevents the ability of stromal cells to diminish p53-mediated killing of cocultured ALL cells in vitro, possibly by blocking the production of prostaglandin E2 (PGE2).	Dinoprostone	236-240	P53	Homo sapiens	124-127
31698450-6	2019	The indomethacin treatment increased the level of p53 in the leukemic cells, implying that COX inhibition might reduce progression of ALL by attenuating protective paracrine PGE2 signaling from bone marrow stroma to leukemic cells.	Dinoprostone	174-178	P53	Homo sapiens	50-53
31699971-3	2019	One such agent is RITA (reactivation of p53 and induction of tumor cell apoptosis), which restores p53 expression in cells with hyperactive HDM2 and induces apoptosis.	RITA	18-22	P53	Homo sapiens	40-43
31699971-3	2019	One such agent is RITA (reactivation of p53 and induction of tumor cell apoptosis), which restores p53 expression in cells with hyperactive HDM2 and induces apoptosis.	RITA	18-22	P53	Homo sapiens	99-102
31699971-8	2019	Collectively, these findings demonstrate that the translational machinery plays a major role in determining the antineoplastic activity of RITA, and suggest that combining p53 activators and translation modulators may be beneficial.	RITA	139-143	P53	Homo sapiens	172-175
31781509-9	2019	Interestingly, the combination of PJ-1 or PJ-9 with SOR exhibited restoring cell viability of normal cells via controlling Raf-1 and P53 genes expression.	3beta-methoxyserrat-14-en-21beta-ol	34-38	P53	Homo sapiens	133-136
33405676-4	2019	Its anticancer mechanism has been fully demonstrated through apoptosis assays; herein CeAC induced high-level apoptosis (16%), which promoted the expression of proapoptotic proteins (Bax, p53, and caspase 9) in tumor cells.	ceac	86-90	P53	Homo sapiens	188-191
31703394-10	2019	This was further confirmed by silencing of HDAC4, which favored cisplatin-induced apoptosis characterized by cleavage of caspase 3 and induction of proapoptotic genes, such as BIK, in part via a p53-dependent mechanism.	Cisplatin	64-73	P53	Homo sapiens	195-198
31441212-0	2019	Conjugated Physiological Resveratrol Metabolites Induce Senescence in Breast Cancer Cells: Role of p53/p21 and p16/Rb Pathways, and ABC Transporters.	Resveratrol	25-36	P53	Homo sapiens	99-102
31430465-0	2019	The Inability of the Choroid to Revascularize in Oxygen-Induced Retinopathy Results from Increased p53/miR-Let-7b Activity.	Oxygen	49-55	P53	Homo sapiens	99-102
31503014-6	2019	Moreover, the short peptide might have the potentials of reversing FGF2-induced resistance to the doxorubicin via downregulation of the antiapoptotic proteins and counteracting of the antiapoptotic effects of FGF2 on p53-null EOC cells.	Doxorubicin	98-109	P53	Homo sapiens	217-220
31470108-9	2019	An extra-nuclear pathway involved in the proliferation inhibition induced by AR activation in vascular endothelial cells was confirmed by showing that membrane-impermeable testosterone-bovine serum albumin (BSA) treatment significantly increased the levels of p53, p27 and p21 protein and reduced cell proliferation.	Testosterone	172-184	P53	Homo sapiens	260-263
31339188-0	2019	CDK4/6 inhibitor protects chemerin-induced human granulosa-lutein cells from apoptosis by inhibiting the p53/p21 waf pathway.	chemerin	26-34	P53	Homo sapiens	105-108
31908895-13	2019	ATRX and TP53 are important nodes in the network and have potential links with the blood oxygen imbalance.	Oxygen	89-95	P53	Homo sapiens	9-13
31442557-10	2019	It was also shown that KB promoted cytoprotective autophagy by a calcium dependent-p53 downregulation pathway.	Calcium	65-72	P53	Homo sapiens	83-86
30990221-10	2019	Tamoxifen increased ESR2-mutant TP53 interaction leading to reactivation of TP73 and apoptosis.	Tamoxifen	0-9	P53	Homo sapiens	32-36
30990221-13	2019	Our study suggests that ESR2-mutant TP53 combination prognosticates survival in TNBC revealing a novel strategy to stratify TNBC for therapeutic intervention potentially by repurposing tamoxifen.	Tamoxifen	185-194	P53	Homo sapiens	36-40
31441212-7	2019	Senescence is induced through the p53/p21Cip1/Waf1 and p16INK4a /Rb pathways, depending on the RSV metabolite, and requires ABC transporters, but not estrogen receptors.	Resveratrol	95-98	P53	Homo sapiens	34-37
31486135-5	2019	We demonstrated that cisplatin (CDDP)-induced p53-mediated HKII downregulation is a determinant of chemosensitivity in OVCA.	Cisplatin	21-30	P53	Homo sapiens	46-49
31486135-5	2019	We demonstrated that cisplatin (CDDP)-induced p53-mediated HKII downregulation is a determinant of chemosensitivity in OVCA.	Cisplatin	32-36	P53	Homo sapiens	46-49
31358486-4	2019	Transcriptional levels of the senescence markers p15, p53, Rb1 and beta-galactosidase were increased when BPA was combined with metabolic stress.	bisphenol A	106-109	P53	Homo sapiens	54-57
31328874-4	2019	Lysine-to-methionine point mutations at amino acid 27 (H3K27M) co-occur with alterations in signaling genes, including the receptor tyrosine kinases (PDGFR/KIT/VEGFR/MET/EGFR), activin A receptor (ACVR1), intracellular kinases (PI3K/AKT/mTOR), cyclin-dependent kinases (CDKs1/4/6), transcriptional regulators (MYCN), and tumor suppressors (PTEN/TP53).	Lysine	0-6	P53	Homo sapiens	345-349
31328874-4	2019	Lysine-to-methionine point mutations at amino acid 27 (H3K27M) co-occur with alterations in signaling genes, including the receptor tyrosine kinases (PDGFR/KIT/VEGFR/MET/EGFR), activin A receptor (ACVR1), intracellular kinases (PI3K/AKT/mTOR), cyclin-dependent kinases (CDKs1/4/6), transcriptional regulators (MYCN), and tumor suppressors (PTEN/TP53).	Methionine	10-20	P53	Homo sapiens	345-349
31681507-8	2019	Western blot analysis revealed that BPA caused an increase in the cellular protein p53 in a concentration-dependent manner.	bisphenol A	36-39	P53	Homo sapiens	83-86
31781681-0	2019	Mutated p53 Promotes the Symmetric Self-Renewal of Cisplatin-Resistant Lung Cancer Stem-Like Cells and Inhibits the Recruitment of Macrophages.	Cisplatin	51-60	P53	Homo sapiens	8-11
31681507-0	2019	Hormone-Like Effects of Bisphenol A on p53 and Estrogen Receptor Alpha in Breast Cancer Cells.	bisphenol A	24-35	P53	Homo sapiens	39-42
31681507-2	2019	In this study, we analyzed the estrogen-like effects of BPA on the expression of estrogen receptor (ER)alpha and p53 with hormonal and antihormonal treatments in T-47D and MCF-7 cells.	bisphenol A	56-59	P53	Homo sapiens	113-116
31681507-7	2019	Laser confocal microscopy was performed to determine the cytolocalization of p53 and ERalpha upon treatment with BPA.	bisphenol A	113-116	P53	Homo sapiens	77-80
31781681-4	2019	Cisplatin-resistant lung cancer cells with different TP53 backgrounds were generated in vitro by exposing A549, H460, and H661 lung cancer cell lines repeatedly to cisplatin.	Cisplatin	0-9	P53	Homo sapiens	53-57
31601779-0	2019	Correction: APR-246 reactivates mutant p53 by targeting cysteines 124 and 277.	2-amino-10-(3'-(1-methyl-4-piperazinyl)propyl)phenothiazine	12-15	P53	Homo sapiens	39-42
31652494-4	2019	Copper sulfate also increased the levels of apoptosis, senescence, mitochondrial dysfunction, autophagy, ROS, and the expression of several stress proteins, including ATF3, c-Fos, DEC1 (differentiated embryonic chondrocyte gene 1), p21, p53, and HIF-1alpha (hypoxia-inducible factor 1 alpha).	Copper Sulfate	0-14	P53	Homo sapiens	237-240
31652494-6	2019	Selective induction of HIF-1alpha, p53, and phosphorylated ERK proteins by copper was blocked by the knockdown of the transcription factor DEC1, suggesting copper"s effects are mediated by DEC1.	Copper	75-81	P53	Homo sapiens	35-38
31652494-6	2019	Selective induction of HIF-1alpha, p53, and phosphorylated ERK proteins by copper was blocked by the knockdown of the transcription factor DEC1, suggesting copper"s effects are mediated by DEC1.	Copper	156-162	P53	Homo sapiens	35-38
31427086-7	2019	All-trans-retinoic acid (ATRA) treatment of MYCN/NCYM-amplified neuroblastoma CHP134 cells induced TAp63 and reduced p53 expressions, accompanied by downregulation of MYCN/NCYM expressions.	Tretinoin	0-23	P53	Homo sapiens	117-120
31427086-7	2019	All-trans-retinoic acid (ATRA) treatment of MYCN/NCYM-amplified neuroblastoma CHP134 cells induced TAp63 and reduced p53 expressions, accompanied by downregulation of MYCN/NCYM expressions.	Tretinoin	25-29	P53	Homo sapiens	117-120
31492752-4	2019	Mass spectrometry and biochemical analysis of the reaction products identified lysine residues as p53 ubiquitination sites.	Lysine	79-85	P53	Homo sapiens	98-101
31492752-5	2019	A p53 mutant with arginine substitutions of its 18 lysine residues was not ubiquitinated.	Arginine	18-26	P53	Homo sapiens	2-5
31492752-5	2019	A p53 mutant with arginine substitutions of its 18 lysine residues was not ubiquitinated.	Lysine	51-57	P53	Homo sapiens	2-5
31601779-0	2019	Correction: APR-246 reactivates mutant p53 by targeting cysteines 124 and 277.	Cysteine	56-65	P53	Homo sapiens	39-42
31703757-0	2019	Inhibitory effects of polyphyllins I and VII on human cisplatin-resistant NSCLC via p53 upregulation and CIP2A/AKT/mTOR signaling axis inhibition.	Cisplatin	54-63	P53	Homo sapiens	84-87
31601253-10	2019	We then showed that combination treatment with Cl-amidine and docetaxel enhanced p53 nuclear accumulation, which synergistically induced cell cycle arrest and apoptosis.	N-alpha-benzoyl-N5-(2-chloro-1-iminoethyl)-L-ornithine amide	47-57	P53	Homo sapiens	81-84
31597912-0	2019	The crosstalk between STAT3 and p53/RAS signaling controls cancer cell metastasis and cisplatin resistance via the Slug/MAPK/PI3K/AKT-mediated regulation of EMT and autophagy.	Cisplatin	86-95	P53	Homo sapiens	32-35
31597912-7	2019	Thus, our data provide strong evidence that the crosstalk between STAT3 and p53/RAS signaling controls ovarian cancer cell metastasis and cisplatin resistance via the Slug/MAPK/PI3K/AKT-mediated regulation of EMT and autophagy.	Cisplatin	138-147	P53	Homo sapiens	76-79
31783991-2	2019	METHODS: To describe topological features of the MTAs networks associated to intrinsic apoptosis induction in p53-null prostate cancer cells, we predicted and compared the interactomes and topological properties of Paclitaxel and Vincristine, and thus, the essential nodes corresponding with the pro- and anti-apoptotic proteins and their kinetics were subjected to experimental analysis in PC-3 cell line.	Paclitaxel	215-225	P53	Homo sapiens	110-113
31783991-3	2019	RESULTS: The essential nodes of the apoptotic pathways, TP53, and CASP3, were identified in both, Paclitaxel and Vincristine networks, but the intrinsic pathway markers BCL2, BAX, and BCL2L1 were identified as hub nodes only in the Paclitaxel network.	Paclitaxel	98-108	P53	Homo sapiens	56-60
31783991-3	2019	RESULTS: The essential nodes of the apoptotic pathways, TP53, and CASP3, were identified in both, Paclitaxel and Vincristine networks, but the intrinsic pathway markers BCL2, BAX, and BCL2L1 were identified as hub nodes only in the Paclitaxel network.	Paclitaxel	232-242	P53	Homo sapiens	56-60
30721374-6	2019	L-Serine increased intracellular NAD+ content and led to the activation of SIRT1 as determined by p53 luciferase assay and western blot analysis of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1alpha) acetylation.	Serine	2-8	P53	Homo sapiens	98-101
31581548-7	2019	This study showed that (i) the splice mutation in TP53 was present as an early driver mutation at diagnosis; (ii) the mutational profile was shared in pre- and post-NACT tumor samples; (iii) the complete expansion of a single dominant mutant clone through loss of heterozygosity (LOH) had occurred, suggesting a possible mechanism of platinum-resistance in HGSOC under the pressure of NACT.	Platinum	334-342	P53	Homo sapiens	50-54
30949905-12	2019	GSEA revealed that "cell cycle," "HR," "DNA replication," and "p53 signaling" pathways were enriched in high PARPBP expression group.	gsea	0-4	P53	Homo sapiens	63-66
31095781-0	2019	Antiproliferative and toxicogenomic effects of resveratrol in bladder cancer cells with different TP53 status.	Resveratrol	47-58	P53	Homo sapiens	98-102
31095781-3	2019	The aim of this study was to evaluate resveratrol antitumor activity (12.5, 25, 50, 100, 150, 200, and 250 muM) and its possible mechanisms of action in bladder tumor cells with different TP53 gene status (RT4, grade 1, TP53 wild type; 5637-grade 2 and T24-grade 3, TP53 mutated).	Resveratrol	38-49	P53	Homo sapiens	220-224
31095781-3	2019	The aim of this study was to evaluate resveratrol antitumor activity (12.5, 25, 50, 100, 150, 200, and 250 muM) and its possible mechanisms of action in bladder tumor cells with different TP53 gene status (RT4, grade 1, TP53 wild type; 5637-grade 2 and T24-grade 3, TP53 mutated).	Resveratrol	38-49	P53	Homo sapiens	220-224
31095781-8	2019	In addition, the resveratrol antiproliferative effects in wild type TP53 cells were accompanied by modulation of the DNMT1 gene.	Resveratrol	17-28	P53	Homo sapiens	68-72
31095781-11	2019	In conclusion, resveratrol has antiproliferative activity in bladder tumor cells; however, the mechanisms of action are dependent on TP53 status.	Resveratrol	15-26	P53	Homo sapiens	133-137
31102418-0	2019	Impact of p53 function on the sulfotransferase-mediated bioactivation of the alkylated polycyclic aromatic hydrocarbon 1-hydroxymethylpyrene in vitro.	polycyclic aromatic hydrocarbon 1-hydroxymethylpyrene	87-140	P53	Homo sapiens	10-13
31148231-0	2019	p53 induces miR-199a-3p to suppress mechanistic target of rapamycin activation in cisplatin-induced acute kidney injury.	Cisplatin	82-91	P53	Homo sapiens	0-3
31236854-0	2019	MicroRNA-1246 regulates the radio-sensitizing effect of curcumin in bladder cancer cells via activating P53.	Curcumin	56-64	P53	Homo sapiens	104-107
31236854-12	2019	CONCLUSION: miR-1246 is involved in the anti-cancer effects of curcumin and irradiation through targeting the inhibition of p53 gene translation in bladder cancer cells.	Curcumin	63-71	P53	Homo sapiens	124-127
31119778-13	2019	P53 antagonist also inhibited the glucose-induced senescence of cardiac c-kit positive cells.	Glucose	34-41	P53	Homo sapiens	0-3
31119778-14	2019	In conclusion, bradykinin prevents the glucose-induced premature senescence of cardiac c-kit positive cells through the B2R/PI3K/AKT/mTOR/P53 signal pathways.	Glucose	39-46	P53	Homo sapiens	138-141
31336132-4	2019	Moreover, resveratrol increases nuclear inducible cyclooxygenase (COX)-2 accumulation, complexes with p53, and induces p53-dependent anti-proliferation.	Resveratrol	10-21	P53	Homo sapiens	102-105
31336132-4	2019	Moreover, resveratrol increases nuclear inducible cyclooxygenase (COX)-2 accumulation, complexes with p53, and induces p53-dependent anti-proliferation.	Resveratrol	10-21	P53	Homo sapiens	119-122
31336132-12	2019	By inhibiting the T4-activated STAT3 signal transduction axis with S31-201, resveratrol was able to sequentially reestablish COX-2/p53-dependent gene expressions and anti-proliferation.	Resveratrol	76-87	P53	Homo sapiens	131-134
31337255-5	2019	We identified a hitherto-unknown FBXW7-interacting protein, p53, which is phosphorylated by glycogen synthase kinase 3 at serine 33 and then ubiquitylated by SCF(FBXW7) and degraded.	Serine	122-128	P53	Homo sapiens	60-63
31155771-0	2019	Magnolol induces apoptosis in osteosarcoma cells via G0/G1 phase arrest and p53-mediated mitochondrial pathway.	magnolol	0-8	P53	Homo sapiens	76-79
31155771-7	2019	Additionally, under the pretreatment of pifithrin-a (PFT-a, a p53 inhibitor), the magnolol-induced apoptosis was significantly reversed.	magnolol	82-90	P53	Homo sapiens	62-65
31148231-2	2019	For this issue, it is important to probe into the role of p53 in cisplatin-induced AKI.	Cisplatin	65-74	P53	Homo sapiens	58-61
31155771-8	2019	The results above indicated that magnolol induces apoptosis in osteosarcoma cells may via G0/G1 phase arrest and p53-mediated mitochondrial pathway.	magnolol	33-41	P53	Homo sapiens	113-116
31172579-0	2019	Stimulating DDX3 expression by serotonin 5-HT receptor 7 through phosphorylation of p53 via the AC-PKA-ERK signaling pathway.	Serotonin	31-40	P53	Homo sapiens	84-87
31148231-8	2019	In conclusion, our findings reveal that p53, upregulating the expression of miR-199a-3p affects the progress of cisplatin-induced AKI, which might provide a promising therapeutic target of AKI.	Cisplatin	112-121	P53	Homo sapiens	40-43
31144295-5	2019	Mechanistically, there was increased expression in the dopamine neurons of FBXO7-interacting protein, RPL23, which is a sensor of ribosomal stress that inhibits MDM2, the negative regulator of p53.	Dopamine	55-63	P53	Homo sapiens	193-196
31569395-6	2019	Moreover, in FBXW7- and TP53-wild type cells, N6-isopentenyladenosine strongly synergizes with 5-Fluorouracil to inhibit colon cancer growth in vitro.	Isopentenyladenosine	46-69	P53	Homo sapiens	24-28
31326626-0	2019	Differential response of lung cancer cell lines to vitamin D derivatives depending on EGFR, KRAS, p53 mutation status and VDR polymorphism.	Vitamin D	51-60	P53	Homo sapiens	98-101
31326626-5	2019	The goal of our study was to establish if cells differing in EGFR, KRAS, p53 mutation status and VDR polymorphism were sensitive to antiproliferative activity of selected vitamin D derivatives (VDDs).	Vitamin D	171-180	P53	Homo sapiens	73-76
31294899-10	2019	miR-34a-5p was identified as a novel repressor of DAPK acting downstream of p53.	mir-34a-5p	0-10	P53	Homo sapiens	76-79
31569395-6	2019	Moreover, in FBXW7- and TP53-wild type cells, N6-isopentenyladenosine strongly synergizes with 5-Fluorouracil to inhibit colon cancer growth in vitro.	Fluorouracil	95-109	P53	Homo sapiens	24-28
31527453-12	2019	p53 signaling and cell cycle checkpoints were regulated by DOX while ErbB/PI3K-Akt, integrin and focal adhesion signaling were regulated by RM upon combination.	Doxorubicin	59-62	P53	Homo sapiens	0-3
31488712-9	2019	Given a similar mtDNA protection role of p53 in doxorubicin-treated human induced pluripotent stem cell (iPSC)-derived cardiomyocytes, the mitochondrial markers associated with cardiomyopathy development observed in blood and skeletal muscle cells may have prognostic utility.	Doxorubicin	48-59	P53	Homo sapiens	41-44
31546731-5	2019	Furthermore, I3M remarkably increased the production of reactive oxygen species (ROS), which were reduced in transient p53 knockdown, indicating that I3M-mediated apoptosis was promoted by p53-mediated ROS production.	Oxygen	65-71	P53	Homo sapiens	119-122
31546731-5	2019	Furthermore, I3M remarkably increased the production of reactive oxygen species (ROS), which were reduced in transient p53 knockdown, indicating that I3M-mediated apoptosis was promoted by p53-mediated ROS production.	Oxygen	65-71	P53	Homo sapiens	189-192
31571866-7	2019	Pronounced anti-migratory activity, DNA fragmentation, decrease in expression of procaspase-3 and enhancement of p53 expression were further identified upon exposure to surface-coated IONs with tethered doxorubicin and ellipticine.	Doxorubicin	203-214	P53	Homo sapiens	113-116
31319070-7	2019	DOX markedly increased reactive oxygen species production, p53 expression, caspase-3 activity, cleaved caspase-3 levels, and TUNEL-positive cell numbers but reduced Bcl-2 expression and intracellular antioxidant enzyme levels; these effects were effectively antagonized through nicorandil (3 muM, 12 h) pretreatment, which resulted in HUVECs being protected from DOX-induced apoptosis.	Doxorubicin	0-3	P53	Homo sapiens	59-62
31308060-10	2019	Combination of COTI-2 with cisplatin or radiation may be highly relevant in treating patients with HNSCC harboring TP53 mutations.	Cisplatin	27-36	P53	Homo sapiens	115-119
31391192-0	2019	6-Phosphofructo-2-Kinase/Fructose-2,6-Biphosphatase-2 Regulates TP53-Dependent Paclitaxel Sensitivity in Ovarian and Breast Cancers.	Paclitaxel	79-89	P53	Homo sapiens	64-68
31511498-0	2019	Intrinsic adriamycin resistance in p53-mutated breast cancer is related to the miR-30c/FANCF/REV1-mediated DNA damage response.	Doxorubicin	10-20	P53	Homo sapiens	35-38
31283929-0	2019	ROS -mediated p53 activation by juglone enhances apoptosis and autophagy in vivo and in vitro.	ros	0-3	P53	Homo sapiens	14-17
31283929-10	2019	Overall, our results illustrated that JG caused apoptosis and autophagy via activating the ROS-mediated p53 pathway in human liver cancer cells in vitro and in vivo, which provided basic scientific evidence that JG serves as a potential anti-cancer agent.	ros	91-94	P53	Homo sapiens	104-107
31498788-4	2019	The model"s predictions, that a combination treatment of cisplatin and TRAIL would enhance cancer cell death and exhibit a "two-wave killing" temporal pattern, was validated by measuring the dynamics of p53 accumulation, cell fate, and cell death in single cells.	Cisplatin	57-66	P53	Homo sapiens	203-206
31163195-6	2019	Moreover, SG significantly inhibited HCC cell proliferation in a p53-dependent manner by inducing cell cycle arrest and reactive oxygen species (ROS)-associated apoptosis.	Reactive Oxygen Species	120-143	P53	Homo sapiens	65-68
32123852-7	2019	Moreover, aspirin reduced p53 and p21 accumulation in DOX-treated human and mouse fibroblasts.	Aspirin	10-17	P53	Homo sapiens	26-29
32123852-7	2019	Moreover, aspirin reduced p53 and p21 accumulation in DOX-treated human and mouse fibroblasts.	Doxorubicin	54-57	P53	Homo sapiens	26-29
31511540-3	2019	Here, we show that DNA damage-induced SMG7-p53 binding requires phosphorylated Ser15 on p53, and that substitution of the conserved lysine residue K66 in the SMG7 14-3-3-like domain with the glutamic acid (E) abolishes interactions with its client proteins p53 and UPF1.	Glutamic Acid	191-204	P53	Homo sapiens	43-46
31500399-5	2019	Depending on the GnRH isoform and the presence of 4Lys(Bu), the conjugates could regulate the expression of several apoptosis-related genes, especially tumor necrosis factor (TNF), tumor protein p53 (TP53) and the members of growth-factor signaling.	Busulfan	55-57	P53	Homo sapiens	195-198
31500399-5	2019	Depending on the GnRH isoform and the presence of 4Lys(Bu), the conjugates could regulate the expression of several apoptosis-related genes, especially tumor necrosis factor (TNF), tumor protein p53 (TP53) and the members of growth-factor signaling.	Busulfan	55-57	P53	Homo sapiens	200-204
31500399-6	2019	The stronger cytotoxicity of GnRH-I and GnRH-III conjugates containing 4Lys(Bu) was associated with a stronger inhibitory effect on the expression of growth-factor signaling elements in comparison with their 4Ser counterparts, in which the upregulation of TP53 and caspases (e.g., CASP9) seemed to play a more important role.	Busulfan	76-78	P53	Homo sapiens	256-260
31500291-0	2019	Distinct TP53 Mutation Subtypes Differentially Influence Cellular Iron Metabolism.	Iron	66-70	P53	Homo sapiens	9-13
31500291-1	2019	The most commonly mutated gene in all human cancers is the tumor suppressor gene TP53; however, in addition to the loss of tumor suppressor functions, mutations in TP53 can also promote cancer progression by altering cellular iron acquisition and metabolism.	Iron	226-230	P53	Homo sapiens	81-85
31500291-1	2019	The most commonly mutated gene in all human cancers is the tumor suppressor gene TP53; however, in addition to the loss of tumor suppressor functions, mutations in TP53 can also promote cancer progression by altering cellular iron acquisition and metabolism.	Iron	226-230	P53	Homo sapiens	164-168
31500291-2	2019	The primary objective of this work was to determine how TP53 mutation status influences the molecular control of iron homeostasis.	Iron	113-117	P53	Homo sapiens	56-60
31500291-4	2019	The introduction of distinct TP53 mutation types alone was sufficient to disrupt cellular iron metabolism.	Iron	90-94	P53	Homo sapiens	29-33
31500291-7	2019	In response to changes in iron availability, cells harboring either a wild-type TP53 or R273H TP53 mutation displayed canonical IRP-mediated responses, but neither IRP1 RNA binding activity nor IRP2 protein levels were affected by changes in iron status in cells harboring the R175H mutation type.	Iron	26-30	P53	Homo sapiens	80-84
31500291-7	2019	In response to changes in iron availability, cells harboring either a wild-type TP53 or R273H TP53 mutation displayed canonical IRP-mediated responses, but neither IRP1 RNA binding activity nor IRP2 protein levels were affected by changes in iron status in cells harboring the R175H mutation type.	Iron	26-30	P53	Homo sapiens	94-98
31500291-9	2019	These findings suggest a novel, IRP-independent mode of iron regulation in cells expressing distinct TP53 mutations.	Iron	56-60	P53	Homo sapiens	101-105
31346036-6	2019	The polyubiquitylation of p53 occurred via Lys-48 linkage and involved phosphorylation on p53 at Ser-33 and Ser-37 by glycogen synthase kinase 3beta (GSK3beta) and DNA-dependent protein kinase (DNA-PK), respectively.	Lysine	43-46	P53	Homo sapiens	26-29
32042215-7	2019	While ZnO-NPs caused depletion of both wild-type and gain-of-function (GOF) mutant p53 protein in ovarian cancer cells, their ability to induce apoptosis was found to be independent of the p53-mutation status in these cells.	Zinc	6-9	P53	Homo sapiens	83-86
31346036-6	2019	The polyubiquitylation of p53 occurred via Lys-48 linkage and involved phosphorylation on p53 at Ser-33 and Ser-37 by glycogen synthase kinase 3beta (GSK3beta) and DNA-dependent protein kinase (DNA-PK), respectively.	Serine	97-100	P53	Homo sapiens	26-29
31346036-6	2019	The polyubiquitylation of p53 occurred via Lys-48 linkage and involved phosphorylation on p53 at Ser-33 and Ser-37 by glycogen synthase kinase 3beta (GSK3beta) and DNA-dependent protein kinase (DNA-PK), respectively.	Serine	97-100	P53	Homo sapiens	90-93
31346036-6	2019	The polyubiquitylation of p53 occurred via Lys-48 linkage and involved phosphorylation on p53 at Ser-33 and Ser-37 by glycogen synthase kinase 3beta (GSK3beta) and DNA-dependent protein kinase (DNA-PK), respectively.	Serine	108-111	P53	Homo sapiens	26-29
31346036-7	2019	These phosphorylation events created a phosphodegron that enhanced p53 binding to FBW7alpha, allowing for the attachment of polyubiquitin moieties at Lys-132 in p53.	Lysine	150-153	P53	Homo sapiens	67-70
31346036-7	2019	These phosphorylation events created a phosphodegron that enhanced p53 binding to FBW7alpha, allowing for the attachment of polyubiquitin moieties at Lys-132 in p53.	Lysine	150-153	P53	Homo sapiens	161-164
31346036-8	2019	FBW7alpha-dependent p53 polyubiquitylation apparently occurred during and immediately after DNA double-strand breaks induced by either doxorubicin or ionizing radiation.	Doxorubicin	135-146	P53	Homo sapiens	20-23
31346036-10	2019	Phosphodegron-mediated polyubiquitylation of p53 on Lys-132 had functional consequences, with cells in which FBW7alpha-mediated p53 degradation was abrogated exhibiting enhancement of their tumorigenic potential.	Lysine	52-55	P53	Homo sapiens	45-48
31324361-4	2019	Metformin"s main antineoplastic mechanism of action is thought to be mediated through inhibition of mammalian target of rapamycin, inhibition of hypoxia-inducible factor 1 (HIF-1) alpha, and activation of p53.	Metformin	0-9	P53	Homo sapiens	205-208
31598361-4	2019	In addition, hydrogen peroxide-induced p53 activation and BH3 interacting-domain death agonist (BID) expression were higher in CsA-treated cells than those in non-treated cells, whereas hydrogen peroxide-induced activation of mitogen-activated protein kinases including p38, c-Jun N-terminal kinase, and extracellular signal-regulated kinase and activation of protein kinase B were not significantly altered by treatment with CsA.	Hydrogen Peroxide	13-30	P53	Homo sapiens	39-42
31598361-4	2019	In addition, hydrogen peroxide-induced p53 activation and BH3 interacting-domain death agonist (BID) expression were higher in CsA-treated cells than those in non-treated cells, whereas hydrogen peroxide-induced activation of mitogen-activated protein kinases including p38, c-Jun N-terminal kinase, and extracellular signal-regulated kinase and activation of protein kinase B were not significantly altered by treatment with CsA.	Cyclosporine	127-130	P53	Homo sapiens	39-42
31598361-4	2019	In addition, hydrogen peroxide-induced p53 activation and BH3 interacting-domain death agonist (BID) expression were higher in CsA-treated cells than those in non-treated cells, whereas hydrogen peroxide-induced activation of mitogen-activated protein kinases including p38, c-Jun N-terminal kinase, and extracellular signal-regulated kinase and activation of protein kinase B were not significantly altered by treatment with CsA.	Hydrogen Peroxide	186-203	P53	Homo sapiens	39-42
31598361-8	2019	Taken together, these data suggest that CsA can aggravate hydrogen peroxide-induced cell death through p53 activation, BID expression, and ROS production.	Cyclosporine	40-43	P53	Homo sapiens	103-106
31598361-8	2019	Taken together, these data suggest that CsA can aggravate hydrogen peroxide-induced cell death through p53 activation, BID expression, and ROS production.	Hydrogen Peroxide	58-75	P53	Homo sapiens	103-106
31339234-5	2019	In our research, it was also found that the reactivation of p53 induced by oridonin was closely related with the generation of ROS (reactive oxygen species).	Reactive Oxygen Species	127-130	P53	Homo sapiens	60-63
31317586-0	2019	Resveratrol modulates epigenetic regulators of promoter histone methylation and acetylation that restores BRCA1, p53, p21CIP1 in human breast cancer cell lines.	Resveratrol	0-11	P53	Homo sapiens	113-116
31317586-2	2019	Resveratrol (RVT) a much studied anti-cancer natural molecule is known for restoration of BRCA1, p53, and p21 in cancer cells.	Resveratrol	0-11	P53	Homo sapiens	97-100
31324563-0	2019	Upregulation of p53 through induction of MDM2 degradation: Anthraquinone analogs.	Anthraquinones	59-72	P53	Homo sapiens	16-19
31324563-1	2019	In a previous study, a novel anthraquinone analog BW-AQ-101 was identified as a potent inducer of MDM2 degradation, leading to upregulation of p53 and apoptosis in cell culture studies.	Anthraquinones	29-42	P53	Homo sapiens	143-146
31324563-1	2019	In a previous study, a novel anthraquinone analog BW-AQ-101 was identified as a potent inducer of MDM2 degradation, leading to upregulation of p53 and apoptosis in cell culture studies.	bw-aq-101	50-59	P53	Homo sapiens	143-146
31339234-5	2019	In our research, it was also found that the reactivation of p53 induced by oridonin was closely related with the generation of ROS (reactive oxygen species).	Reactive Oxygen Species	132-155	P53	Homo sapiens	60-63
31340166-8	2019	KEY FINDINGS: Based on the results, the highest doses of Dox and Ldox (0.75 and 0.1 mg/kg/BW respectively) significantly increased the level of inflammatory markers and according to other factors especially p53 and SA beta-gal expression, both were able to induce senescence but the changes in Ldox were less tangible than the Dox.	Doxorubicin	57-60	P53	Homo sapiens	207-210
31253693-3	2019	Our previous efforts to identify novel radiosensitizers, using high-throughput screening targeting p53 and Nrf2 revealed a promising N-phenylpyrimidin-2-amine (PPA) lead compound.	N-phenylpyrimidin-2-amine	133-158	P53	Homo sapiens	99-102
31607444-3	2019	P53 reduction by LPS, siRNA for P53 and Pifithrin increased the expression levels of malondialdehyde, a marker of oxidative stress and lipid peroxidation.	Malondialdehyde	85-100	P53	Homo sapiens	0-3
31607444-3	2019	P53 reduction by LPS, siRNA for P53 and Pifithrin increased the expression levels of malondialdehyde, a marker of oxidative stress and lipid peroxidation.	Malondialdehyde	85-100	P53	Homo sapiens	32-35
31998813-4	2019	Here, we report novel data on p53 activating Isatin-based Cu(II) complex exhibiting cytotoxic properties towards HCT116 and MCF7 tumor cell lines, as confirmed by cell viability assay and flow cytometry analysis of apoptosis.	Copper	58-64	P53	Homo sapiens	30-33
31376399-0	2019	The synergistic action of phosphate and interleukin-6 enhances senescence-associated calcification in vascular smooth muscle cells depending on p53.	Phosphates	26-35	P53	Homo sapiens	144-147
31376399-5	2019	Our findings show that p53 plays a major role in senescence-associated vascular calcification induced by phosphate overload.	Phosphates	105-114	P53	Homo sapiens	23-26
31376399-7	2019	We demonstrate that the synergistic action of phosphate overload and IL-6 enhances senescence-associated calcification in a p53-dependent manner and is inhibited by an anti-aging agent (resveratrol) in a dose-dependent manner.	Phosphates	46-55	P53	Homo sapiens	124-127
31376399-7	2019	We demonstrate that the synergistic action of phosphate overload and IL-6 enhances senescence-associated calcification in a p53-dependent manner and is inhibited by an anti-aging agent (resveratrol) in a dose-dependent manner.	Resveratrol	186-197	P53	Homo sapiens	124-127
31480541-4	2019	We found that, in response to DNA-damaging agent doxorubicin, expression of myotonic dystrophy protein kinase (DMPK), which is known to upregulate actomyosin contraction, was increased in a p53-dependent manner.	Doxorubicin	49-60	P53	Homo sapiens	190-193
31480541-6	2019	Furthermore, we found that doxorubicin treatment induced p73 expression, which was significantly attenuated by downregulation of p53.	Doxorubicin	27-38	P53	Homo sapiens	129-132
31538075-7	2019	In the CaSki cells, the p-ERK1/2 level decreased by 37%, the p53 expression level increased by 304%, and the cleaved caspase 3 level increased by 115% in the cisplatin+genistein group compared to that in the cisplatin group.	Cisplatin	158-167	P53	Homo sapiens	61-64
31129972-0	2019	Association between p53 protein phosphorylated at serine 20 expression and ovarian carcinoma stem cells phenotype: correlation with clinicopathological parameters of ovarian cancer.	Serine	50-56	P53	Homo sapiens	20-23
31129972-2	2019	We examined correlation between p53 protein phosphorylated at serine 20 (p-p53(Ser20)) and CD133, SOX2, Notch1 expression in order to reveal p-p53(Ser20) stemness function in ovarian cancer.	Serine	62-68	P53	Homo sapiens	32-35
31462218-10	2019	ROSC treatment also leads to p53 stabilization, which coincides with site-specific phosphorylation at serine 46 and decreased levels of Mdm2.	Serine	102-108	P53	Homo sapiens	29-32
31452810-0	2019	Tanshinone IIA inhibits proliferation and induces apoptosis of human nasopharyngeal carcinoma cells via p53-cyclin B1/CDC2.	tanshinone	0-14	P53	Homo sapiens	104-107
31452810-3	2019	The present study aimed to investigate whether tanshinone IIA inhibits proliferation and induces apoptosis of human nasopharyngeal carcinoma cells via p53-cyclin B1/cell division cycle gene 2 (CDC2).	tanshinone	47-61	P53	Homo sapiens	151-154
31296660-5	2019	ChIP and oligonucleotide pulldown assays further disclosed that p53 binds to the p53RE1 and p53RE3 sites.	Oligonucleotides	9-24	P53	Homo sapiens	64-67
31296660-6	2019	Moreover, ataxia telangiectasia mutated (ATM) or ATM-Rad3-related (ATR) kinase-mediated p53 phosphorylation at Ser-15 or Ser-37 residues activated KAISO transcription by binding its p53RE1 or p53RE3 sites during early DDR.	Serine	111-114	P53	Homo sapiens	88-91
31544060-0	2019	Activation of p53 Gene Expression and Synergistic Antiproliferative Effects of 5-Fluorouracil and beta-escin on MCF7 Cells.	Fluorouracil	79-93	P53	Homo sapiens	14-17
31544060-8	2019	The expression of p53 and apoptosis increased in the combination of 5-FU and beta-escin on MCF7 cells compared to that of control group (P &lt; 0.05).	Fluorouracil	68-72	P53	Homo sapiens	18-21
31544060-10	2019	The combination of 5-FU and beta-escin not only has synergistic effects by increasing cell apoptosis and p53 gene expression but also decreases Bcl-2 signaling protein in MCF7 cell lines.	Fluorouracil	19-23	P53	Homo sapiens	105-108
31452796-9	2019	In summary, shikonin can sensitize esophageal cancer cells to paclitaxel-treatment by promoting cell mitotic arrest and reinforcing the susceptibility of esophageal cancer cells to apoptosis induced by paclitaxel, which is potentially associated with altered levels of Bcl-2 and p53.	Paclitaxel	62-72	P53	Homo sapiens	279-282
31470629-8	2019	The effects of FUS were more potent than those of AFU, with FUS up-regulating p21 expression in a p53-dependent manner, as detected by Western blot analyses, likely the consequence of decreased ERK phosphorylation and increased p38 expression (both of which increase p21 stability).	anhydrofusarubin	50-53	P53	Homo sapiens	98-101
31462222-0	2019	Ethanol extract of asiasari radix preferentially induces apoptosis in G361 human melanoma cells by differential regulation of p53.	Ethanol	0-7	P53	Homo sapiens	126-129
31462222-9	2019	ARE induced cell death in G361 cells through the reactive oxygen species (ROS)-dependent regulation of p53 and p21 in G361 cells.	Reactive Oxygen Species	49-72	P53	Homo sapiens	103-106
31462222-9	2019	ARE induced cell death in G361 cells through the reactive oxygen species (ROS)-dependent regulation of p53 and p21 in G361 cells.	Reactive Oxygen Species	74-77	P53	Homo sapiens	103-106
31462222-11	2019	CONCLUSION: The treatment of ARE preferentially induces apoptosis in melanoma cells by the ROS-dependent differential regulation of p53 level.	Reactive Oxygen Species	91-94	P53	Homo sapiens	132-135
31391058-10	2019	Moreover, Jinfukang induces apoptosis in CTC-TJH-01 cells through the ROS-mediated ATM/ATR-p53 pathway and DNA damage.	ros	70-73	P53	Homo sapiens	91-94
31482012-1	2019	We previously reported that p53-mediated apoptosis is determined by severity of DNA damage, not by the level of p53, in doxorubicin-treated prostate cancer cells.	Doxorubicin	120-131	P53	Homo sapiens	28-31
31482012-4	2019	By using dominant negative p53 to compete with wild-type p53 in transcription activity, we demonstrated that p53-mediated apoptosis in response to doxorubicin- or camptothecin-induced genotoxic stress is transcription-independent.	Doxorubicin	147-158	P53	Homo sapiens	27-30
31482012-4	2019	By using dominant negative p53 to compete with wild-type p53 in transcription activity, we demonstrated that p53-mediated apoptosis in response to doxorubicin- or camptothecin-induced genotoxic stress is transcription-independent.	Doxorubicin	147-158	P53	Homo sapiens	57-60
31482012-4	2019	By using dominant negative p53 to compete with wild-type p53 in transcription activity, we demonstrated that p53-mediated apoptosis in response to doxorubicin- or camptothecin-induced genotoxic stress is transcription-independent.	Doxorubicin	147-158	P53	Homo sapiens	57-60
31482012-6	2019	Interestingly, we also found that doxorubicin-induced p21 expression is activated by p53 in transcription-dependent manner, while camptothecin-induced p21 expression is p53-independent.	Doxorubicin	34-45	P53	Homo sapiens	85-88
31482012-7	2019	We then investigated the p53 ratio of nucleus to cytosol corresponding to low and high dose doxorubicin, camptothecin, or bortezomib treatment.	Doxorubicin	92-103	P53	Homo sapiens	25-28
31441737-0	2019	[Prognostic role of p53 gene polymorphism in risk assessment of anthracycline-induced cardiotoxicity].	Anthracyclines	64-77	P53	Homo sapiens	20-23
31241338-5	2019	The results suggest that p53 can be effectively targeted to the mitochondria by controlling the phosphorylation of pro-apoptotic Bad, which can only localize to the mitochondria when Ser-112 and Ser-136 of Bad are unphosphorylated.	Serine	183-186	P53	Homo sapiens	25-28
31592145-7	2019	We found 0.5 mmol/L of ALA and 3 J/cm2 of red light did not affect the vitality of cells, and could reduce UVB induced apoptosis, accelerate the clearance of CPDs, inhibit proliferation and activate p53.	Alanine	23-26	P53	Homo sapiens	199-202
31388677-9	2019	A weak transcription activity of Cr(VI)-upregulated p53 was associated with its low lysine acetylation in the regulatory C-terminal domain, resulting from the inability of Cr(VI) to activate ATM in ascorbate-restored cells.	Lysine	84-90	P53	Homo sapiens	52-55
31241338-5	2019	The results suggest that p53 can be effectively targeted to the mitochondria by controlling the phosphorylation of pro-apoptotic Bad, which can only localize to the mitochondria when Ser-112 and Ser-136 of Bad are unphosphorylated.	Serine	195-198	P53	Homo sapiens	25-28
31047842-12	2019	Upon restoration of WT-TP53 activity in MIA-PaCa-2 cells, an altered sensitivity to the combination of certain NAX compounds and metformin was observed compared to the parental cells which normally lack WT-TP53.	Metformin	129-138	P53	Homo sapiens	23-27
31047842-12	2019	Upon restoration of WT-TP53 activity in MIA-PaCa-2 cells, an altered sensitivity to the combination of certain NAX compounds and metformin was observed compared to the parental cells which normally lack WT-TP53.	Metformin	129-138	P53	Homo sapiens	206-210
31047842-13	2019	Certain NAX compounds may interact with WT-TP53 and metformin treatment to alter the expression of key molecules involved in cell growth.	Carbonic Acid	8-11	P53	Homo sapiens	43-47
31497354-0	2019	Wild-type TP53 defined gamma-secretase inhibitor sensitivity and synergistic activity with doxorubicin in GSCs.	Doxorubicin	91-102	P53	Homo sapiens	10-14
31592435-0	2019	Synergetic Impact of Combined 5-Fluorouracil and Rutin on Apoptosis in PC3 Cancer Cells through the Modulation of P53 Gene Expression.	Fluorouracil	30-44	P53	Homo sapiens	114-117
31592435-9	2019	Combination of 5-FU/rutin enhanced apoptosis and p53 gene expression in PC3 cells.	Fluorouracil	15-19	P53	Homo sapiens	49-52
31592435-11	2019	Conclusion: Synergistic effects of 5-FU/rutin combination on PC3 cells line enhanced apoptosis, p53 gene expression, and down-regulation of Bcl-2 protein, compared to control separate application.	Fluorouracil	35-39	P53	Homo sapiens	96-99
31497354-9	2019	Finally, GSIs (targeting NOTCH signaling) synergized with doxorubicin (activating wt-p53) to inhibit proliferation and induce apoptosis in wt-p53 GSCs.	Doxorubicin	58-69	P53	Homo sapiens	85-88
31497354-11	2019	Combining GSI with doxorubicin synergistically inhibited the proliferation and survival of GSCs harboring wt-p53.	Doxorubicin	19-30	P53	Homo sapiens	109-112
31289894-0	2019	Functional mismatch repair and inactive p53 drive sensitization of colorectal cancer cells to irinotecan via the IAP antagonist BV6.	Irinotecan	94-104	P53	Homo sapiens	40-43
31073781-0	2019	Copper-imidazo[1,2-a]pyridines induce intrinsic apoptosis and modulate the expression of mutated p53, haem-oxygenase-1 and apoptotic inhibitory proteins in HT-29 colorectal cancer cells.	copper-imidazo[1,2-a]pyridines	0-30	P53	Homo sapiens	97-100
31073781-7	2019	Proteomic analysis revealed that copper-imidazo[1,2-a]pyridines decreased the expression of phosphorylated forms of p53 [phospho-p53(S15), phospho-p53(S46) and phospho-p53(S392)].	copper-imidazo[1,2-a]pyridines	33-63	P53	Homo sapiens	116-119
31073781-7	2019	Proteomic analysis revealed that copper-imidazo[1,2-a]pyridines decreased the expression of phosphorylated forms of p53 [phospho-p53(S15), phospho-p53(S46) and phospho-p53(S392)].	copper-imidazo[1,2-a]pyridines	33-63	P53	Homo sapiens	129-132
31073781-7	2019	Proteomic analysis revealed that copper-imidazo[1,2-a]pyridines decreased the expression of phosphorylated forms of p53 [phospho-p53(S15), phospho-p53(S46) and phospho-p53(S392)].	copper-imidazo[1,2-a]pyridines	33-63	P53	Homo sapiens	129-132
31289894-2	2019	The purpose of this study was to analyze the cytostatic/cytotoxic response of colorectal carcinoma (CRC) cells to irinotecan, depending on the mismatch repair (MMR) and p53 status and to examine the impact of BV6, a bivalent antagonist of inhibitors of apoptosis c-IAP1/c-IAP2, alone or combined with irinotecan.	Irinotecan	114-124	P53	Homo sapiens	169-172
31073781-7	2019	Proteomic analysis revealed that copper-imidazo[1,2-a]pyridines decreased the expression of phosphorylated forms of p53 [phospho-p53(S15), phospho-p53(S46) and phospho-p53(S392)].	copper-imidazo[1,2-a]pyridines	33-63	P53	Homo sapiens	129-132
31289894-4	2019	Upon irinotecan, MMR-deficient/p53-mutated lines repaired DNA double-strand breaks by homologous recombination less efficiently than MMR-proficient/p53-mutated lines and underwent elevated caspase-9-dependent apoptosis.	Irinotecan	5-15	P53	Homo sapiens	31-34
31289894-8	2019	Therefore, the particular MMR+/p53mt signature, often found in non-metastasizing (stage II) CRC might be used as a prognostic factor for an adjuvant therapy using low-dose irinotecan combined with a bivalent IAP antagonist.	Irinotecan	172-182	P53	Homo sapiens	31-34
31183995-0	2019	Modulated electro-hyperthermia induced p53 driven apoptosis and cell cycle arrest additively support doxorubicin chemotherapy of colorectal cancer in vitro.	Doxorubicin	101-112	P53	Homo sapiens	39-42
31078603-6	2019	Furthermore, exposure to the Fe(II) complex led to excessive reactive oxygen species (ROS) accumulation by thioredoxin reductase (TrxR) inhibition and DNA double-strand breaks (DSBs), which in turn sequentially activated ATM, CHK1/2 and p53.	Reactive Oxygen Species	61-84	P53	Homo sapiens	237-240
31078603-6	2019	Furthermore, exposure to the Fe(II) complex led to excessive reactive oxygen species (ROS) accumulation by thioredoxin reductase (TrxR) inhibition and DNA double-strand breaks (DSBs), which in turn sequentially activated ATM, CHK1/2 and p53.	Reactive Oxygen Species	86-89	P53	Homo sapiens	237-240
31196889-3	2019	Zinc metallochaperones (ZMC) are a new class of mutant p53 reactivators that restore WT structure and function to zinc-deficient p53 mutants.	zmc	24-27	P53	Homo sapiens	55-58
31018701-0	2019	Curcumin induces p53-independent inactivation of Nrf2 during oxidative stress-induced apoptosis.	Curcumin	0-8	P53	Homo sapiens	17-20
31018701-6	2019	Interestingly, at early times of exposure to a proapoptotic dose of curcumin (15 muM), we observed nuclear accumulation of Nrf2 and the expression of Nrf2 target genes, whereas at late exposure times we found a reduction of total and nuclear protein levels of Nrf2 as well as downregulation of Nrf2 target genes in the absence of p53 activation.	Curcumin	68-76	P53	Homo sapiens	330-333
30918974-3	2019	COL17 was induced upon p53 activation by cisplatin in SAS; however, this effect was more limited in NA and hardly in Ca9-22 and Sa3, with mutated p53.	Cisplatin	41-50	P53	Homo sapiens	23-26
30912145-6	2019	Then, we found that the pretreatment with nicotine and PNU-282987 showed the neuroprotective antiapoptotic effects via activating the alpha7-nAChRs/MAPK/p53 axis.	Nicotine	42-50	P53	Homo sapiens	153-156
30623450-9	2019	Curcumin can also upregulate the expression and activity of p53 that inhibits tumor cell proliferation and increases apoptosis.	Curcumin	0-8	P53	Homo sapiens	60-63
31088907-1	2019	We discovered that 90.3% of patients with angiomyolipomas, lymphangioleiomyomatosis (LAM), and tuberous sclerosis complex (TSC) carry the arginine variant of codon 72 (R72) of TP53 and that R72 increases the risk for angiomyolipoma.	Arginine	138-146	P53	Homo sapiens	176-180
31088908-0	2019	HIF Inactivation of p53 in Ovarian Cancer Can Be Reversed by Topotecan, Restoring Cisplatin and Paclitaxel Sensitivity.	Cisplatin	82-91	P53	Homo sapiens	20-23
31088908-0	2019	HIF Inactivation of p53 in Ovarian Cancer Can Be Reversed by Topotecan, Restoring Cisplatin and Paclitaxel Sensitivity.	Paclitaxel	96-106	P53	Homo sapiens	20-23
31196889-3	2019	Zinc metallochaperones (ZMC) are a new class of mutant p53 reactivators that restore WT structure and function to zinc-deficient p53 mutants.	zmc	24-27	P53	Homo sapiens	129-132
31196889-6	2019	We explored the mechanism of this and found the reactive oxygen species (ROS) activity of ZMC1 negates the signal on p53 that is generated with chemotherapy and radiation.	Reactive Oxygen Species	48-71	P53	Homo sapiens	117-120
31196889-6	2019	We explored the mechanism of this and found the reactive oxygen species (ROS) activity of ZMC1 negates the signal on p53 that is generated with chemotherapy and radiation.	Reactive Oxygen Species	73-76	P53	Homo sapiens	117-120
31366086-5	2019	Depletion of p53 coincided with a moderate, LA-dependent ROS production, but was not rescued by antioxidant treatment.	ros	57-60	P53	Homo sapiens	13-16
31423257-4	2019	CDS-1548 administration significantly elevated the transcriptional activity of p53 and its downstream target genes in a dose-dependent manner.	cds-1548	0-8	P53	Homo sapiens	79-82
31369573-5	2019	RESULTS: The allele frequency of TP53 codon 72 in our cohort was 37, 42, and 21% for Arg/Arg, Arg/Pro, and Pro/Pro, respectively.	Arginine	85-88	P53	Homo sapiens	33-37
31369573-5	2019	RESULTS: The allele frequency of TP53 codon 72 in our cohort was 37, 42, and 21% for Arg/Arg, Arg/Pro, and Pro/Pro, respectively.	Arginine	89-92	P53	Homo sapiens	33-37
31369573-5	2019	RESULTS: The allele frequency of TP53 codon 72 in our cohort was 37, 42, and 21% for Arg/Arg, Arg/Pro, and Pro/Pro, respectively.	Arginine	89-92	P53	Homo sapiens	33-37
31069753-2	2019	High-dose Meth induces degeneration of dopaminergic neurons through p53-mediated apoptosis.	Methamphetamine	10-14	P53	Homo sapiens	68-71
31366086-10	2019	Intriguingly, the combination of LA and anticancer drugs (doxorubicin, 5-fluorouracil) attenuated p53-mediated stabilization of p21 and resulted in synergistic killing in CRC cells in a p53-dependant manner.	Doxorubicin	58-69	P53	Homo sapiens	98-101
31366086-10	2019	Intriguingly, the combination of LA and anticancer drugs (doxorubicin, 5-fluorouracil) attenuated p53-mediated stabilization of p21 and resulted in synergistic killing in CRC cells in a p53-dependant manner.	Doxorubicin	58-69	P53	Homo sapiens	186-189
31366086-10	2019	Intriguingly, the combination of LA and anticancer drugs (doxorubicin, 5-fluorouracil) attenuated p53-mediated stabilization of p21 and resulted in synergistic killing in CRC cells in a p53-dependant manner.	Fluorouracil	71-85	P53	Homo sapiens	98-101
31366086-10	2019	Intriguingly, the combination of LA and anticancer drugs (doxorubicin, 5-fluorouracil) attenuated p53-mediated stabilization of p21 and resulted in synergistic killing in CRC cells in a p53-dependant manner.	Fluorouracil	71-85	P53	Homo sapiens	186-189
31360122-0	2019	p53 sensitizes chemoresistant non-small cell lung cancer via elevation of reactive oxygen species and suppression of EGFR/PI3K/AKT signaling.	Reactive Oxygen Species	74-97	P53	Homo sapiens	0-3
31336611-10	2019	Activation of DNA damage/repair factors (gammaH2AX, p53, and GADD45) in response to cisplatin was measured.	Cisplatin	84-93	P53	Homo sapiens	52-55
31331008-4	2019	Melatonin-stimulated an increase in p21 which was correlated with a pronounced nuclear translocation of thioredoxin 1 and thioredoxin reductase 1, both of which are known to induce p21 via promoting p53 trans-activation.	Melatonin	0-9	P53	Homo sapiens	199-202
31428569-0	2019	Lobaplatin-Induced Apoptosis Requires p53-Mediated p38MAPK Activation Through ROS Generation in Non-Small-Cell Lung Cancer.	lobaplatin	0-10	P53	Homo sapiens	38-41
31428569-0	2019	Lobaplatin-Induced Apoptosis Requires p53-Mediated p38MAPK Activation Through ROS Generation in Non-Small-Cell Lung Cancer.	Reactive Oxygen Species	78-81	P53	Homo sapiens	38-41
31428569-10	2019	Apoptosis of A549 cells was decreased after transfected with p53 shRNA or treated with reactive oxygen species inhibitor NAC and p38MAPK inhibitor SB203580, suggesting that the p53/ROS/p38MAPK pathway appeared to mediate the LBP-induced apoptosis of A549 cells.	Reactive Oxygen Species	87-110	P53	Homo sapiens	61-64
31428569-10	2019	Apoptosis of A549 cells was decreased after transfected with p53 shRNA or treated with reactive oxygen species inhibitor NAC and p38MAPK inhibitor SB203580, suggesting that the p53/ROS/p38MAPK pathway appeared to mediate the LBP-induced apoptosis of A549 cells.	Reactive Oxygen Species	87-110	P53	Homo sapiens	177-180
31428569-10	2019	Apoptosis of A549 cells was decreased after transfected with p53 shRNA or treated with reactive oxygen species inhibitor NAC and p38MAPK inhibitor SB203580, suggesting that the p53/ROS/p38MAPK pathway appeared to mediate the LBP-induced apoptosis of A549 cells.	Reactive Oxygen Species	181-184	P53	Homo sapiens	61-64
31428569-10	2019	Apoptosis of A549 cells was decreased after transfected with p53 shRNA or treated with reactive oxygen species inhibitor NAC and p38MAPK inhibitor SB203580, suggesting that the p53/ROS/p38MAPK pathway appeared to mediate the LBP-induced apoptosis of A549 cells.	Reactive Oxygen Species	181-184	P53	Homo sapiens	177-180
31360122-2	2019	Somatic mutation of TP53 (36%) and epidermal growth factor receptor (EGFR; &gt; 30%) are major contributors to cisplatin (CDDP) resistance.	Cisplatin	111-120	P53	Homo sapiens	20-24
31282934-5	2019	Meanwhile, other PTMs like sumoylation, neddylation, O-GlcNAcylation, adenosine diphosphate (ADP)-ribosylation, hydroxylation, and beta-hydroxybutyrylation are also shown to play various roles in p53 regulation.	Adenosine	70-79	P53	Homo sapiens	196-199
31323026-9	2019	The CDDP-induced cleavage of caspase-3 was increased during the early phase in Group MG (+), and cleaved caspase-3 was detected even in Group MG (+) with constitutive expression of a mutant type of p53 (hereafter, "+" indicates CDDP treatment).	Cisplatin	228-232	P53	Homo sapiens	198-201
31323026-10	2019	These results interestingly indicate that microgravity altered CDDP sensitivity through activation of caspase-3 by p53-independent mechanism.	Cisplatin	63-67	P53	Homo sapiens	115-118
31360122-2	2019	Somatic mutation of TP53 (36%) and epidermal growth factor receptor (EGFR; &gt; 30%) are major contributors to cisplatin (CDDP) resistance.	Cisplatin	122-126	P53	Homo sapiens	20-24
31323026-0	2019	Simulated microgravity enhances CDDP-induced apoptosis signal via p53-independent mechanisms in cancer cells.	Cisplatin	32-36	P53	Homo sapiens	66-69
31360122-6	2019	In this study, we investigated the role of p53 in regulation of ROS production and EGFR signaling, and the chemosensitivity of NSCLC.	Reactive Oxygen Species	64-67	P53	Homo sapiens	43-46
31323026-4	2019	Therefore, we aimed to clarify the molecular mechanisms of modified cis-diamminedichloroplatinum (CDDP)-sensitivity under simulated microgravity by focusing on p53-related cell death mechanisms.	Cisplatin	68-96	P53	Homo sapiens	160-163
31360122-10	2019	Results: We have demonstrated for the first time that activation of p53 sensitizes chemoresistant NSCLC cells to CDDP by down-regulating EGFR signaling pathway and promoting intracellular ROS production.	Cisplatin	113-117	P53	Homo sapiens	68-71
31323026-4	2019	Therefore, we aimed to clarify the molecular mechanisms of modified cis-diamminedichloroplatinum (CDDP)-sensitivity under simulated microgravity by focusing on p53-related cell death mechanisms.	Cisplatin	98-102	P53	Homo sapiens	160-163
31360122-10	2019	Results: We have demonstrated for the first time that activation of p53 sensitizes chemoresistant NSCLC cells to CDDP by down-regulating EGFR signaling pathway and promoting intracellular ROS production.	Reactive Oxygen Species	188-191	P53	Homo sapiens	68-71
31323026-5	2019	Immunoblotting analyses indicated that, under microgravity, CDDP-induced ATM/p53 signaling increased and caspase-3 was cleaved earlier.	Cisplatin	60-64	P53	Homo sapiens	77-80
31360122-12	2019	Our findings suggest that CDDP-induced apoptosis in chemosensitive NSCLC cells involves p53 activation, leading to suppressed EGFR signaling and ROS production.	Cisplatin	26-30	P53	Homo sapiens	88-91
31323026-9	2019	The CDDP-induced cleavage of caspase-3 was increased during the early phase in Group MG (+), and cleaved caspase-3 was detected even in Group MG (+) with constitutive expression of a mutant type of p53 (hereafter, "+" indicates CDDP treatment).	Cisplatin	4-8	P53	Homo sapiens	198-201
31360122-12	2019	Our findings suggest that CDDP-induced apoptosis in chemosensitive NSCLC cells involves p53 activation, leading to suppressed EGFR signaling and ROS production.	Reactive Oxygen Species	145-148	P53	Homo sapiens	88-91
31360122-14	2019	Conclusion: Collectively, our study reveals that the interaction of the p53 and Akt feedback loops determine the fate of NSCLC cells and their CDDP sensitivity.	Cisplatin	143-147	P53	Homo sapiens	72-75
30902332-0	2019	Detection of p53 DNA using commercially available personal glucose meters based on rolling circle amplification coupled with nicking enzyme signal amplification.	Glucose	59-66	P53	Homo sapiens	13-16
31109646-7	2019	Furthermore, H2O2 triggers p53 activation and promotes p21 expression, indicating a role for the p53/p21 signaling pathway in oxidative stress-induced senescence in BCSCs.	Hydrogen Peroxide	13-17	P53	Homo sapiens	27-30
31109646-7	2019	Furthermore, H2O2 triggers p53 activation and promotes p21 expression, indicating a role for the p53/p21 signaling pathway in oxidative stress-induced senescence in BCSCs.	Hydrogen Peroxide	13-17	P53	Homo sapiens	97-100
30959047-6	2019	On the contrary, resveratrol promoted the accumulation of SIRT-1, PCNA, caspase 3, and p53.	Resveratrol	17-28	P53	Homo sapiens	87-90
31331066-0	2019	Effect of Vasicinone against Paraquat-Induced MAPK/p53-Mediated Apoptosis via the IGF-1R/PI3K/AKT Pathway in a Parkinson"s Disease-Associated SH-SY5Y Cell Model.	vasicinone	10-20	P53	Homo sapiens	51-54
31059712-11	2019	The obtained results confirmed that the anti-proliferative mechanism and increased reactive oxygen species level of DS was associated with down-regulation of TrxR1 pathway which triggers the p53 mediated intrinsic apoptotic mode of cell death in NSCLC cells.	Reactive Oxygen Species	83-106	P53	Homo sapiens	191-194
31295913-9	2019	Moreover, p53 and its family members (p63 and p73) might also be used as predictors of platinum response.	Platinum	87-95	P53	Homo sapiens	10-13
31278094-6	2019	We will aim to evaluate the effects of resveratrol supplementation on mRNA expression of PPARalpha, p53, p21 and p16 in patients with T2D.	Resveratrol	39-50	P53	Homo sapiens	100-103
30902332-2	2019	Herein, on the basis of rolling circle amplification (RCA) coupled with nicking endonuclease-assisted signal amplification (NESA), a simple, sensitive and portable biosensor was developed for the determination of p53 DNA by using the personal glucose meter (PGM) as readout.	Glucose	243-250	P53	Homo sapiens	213-216
31379992-10	2019	Also, the analysis correlated with induced cell death elucidated that concurrent treatment of polysaccharide plus paclitaxel had a further anti-cancer effect against A2780cp cells mainly through restoration of p53 and mitochondrial apoptosis cell death induction.	Paclitaxel	114-124	P53	Homo sapiens	210-213
30896089-8	2019	Alterations within the TP53-MDM2 signal transduction pathway appear to be enriched among patients with platinum-resistant disease.	Platinum	103-111	P53	Homo sapiens	23-27
30508396-5	2019	Fetal ASM exposed to 40% O2 for 7 days exhibited elevated concentrations of senescence-associated markers, including beta-galactosidase; cell cycle checkpoint proteins p16, p21, and p-p53; and the DNA damage marker p-gammaH2A.X (phosphorylated gamma-histone family member X).	Oxygen	25-27	P53	Homo sapiens	184-187
31056264-2	2019	In this study, we present a new mechanism of Irinotecan which inhibits the activities of MDM2, an E3 ligase of tumour suppressor p53, and Bcl-xL, an anti-apoptotic protein, through direct binding.	Irinotecan	45-55	P53	Homo sapiens	129-132
31101761-3	2019	We report here that the ability of SOCS1 to interact with p53 and regulate cellular senescence depends on a structural motif that includes tyrosine (Y)80 in the SH2 domain of SOCS1.	Tyrosine	139-147	P53	Homo sapiens	58-61
30981936-10	2019	These results suggest that aryl-PFRs (e.g., BDP, MDPP, CDP) cause oxidative stress-mediated DNA damage and mitochondrial impairment, and p53-dependent pathway was involved in the aryl-PFRs-induced DNA damage and cell cycle arrest.	Beclomethasone	44-47	P53	Homo sapiens	137-140
30633343-10	2019	KEGG analysis results showed that DEGs were particularly enriched in the cell cycle, the p53 signaling pathway, the Wnt signaling pathway, the Ras signaling pathway, the Rap1 signaling pathway, and tyrosine metabolism.	Tyrosine	198-206	P53	Homo sapiens	89-92
31379409-8	2019	In addition, sublethal treatment with PAM induced phosphorylation of ATM kinase, accumulation of p53 protein, and expression of p21 and GADD45A, which are known p53 target genes, in a Zn2+-dependent manner.	Zinc	184-188	P53	Homo sapiens	97-100
31379409-8	2019	In addition, sublethal treatment with PAM induced phosphorylation of ATM kinase, accumulation of p53 protein, and expression of p21 and GADD45A, which are known p53 target genes, in a Zn2+-dependent manner.	Zinc	184-188	P53	Homo sapiens	161-164
31379409-9	2019	These results suggest that the induction of growth arrest and cellular senescence by sublethal PAM treatment is mediated by Zn2+-dependent activation of the ATM/p53 pathway.	Zinc	124-128	P53	Homo sapiens	161-164
31105124-5	2019	p53 is also involved in the regulation of other cellular metabolism and energy production systems: amino acid metabolism, fatty acid metabolism, nucleic acid metabolism, anti-oxidation, mitochondrial quality control, and autophagy.	Fatty Acids	122-132	P53	Homo sapiens	0-3
31022596-6	2019	RESULTS: Sal-B (10 muM) treatment significantly ameliorated LPS injury to MH7 A cells, as cell viability was increased, expression of p53 and p21 was repressed, apoptosis was inhibited, and the release of MCP-1, IL-6 and TNF-alpha was reduced.	salvianolic acid B	9-14	P53	Homo sapiens	134-137
30254375-10	2019	In addition, downregulated TC2N is involved in the apoptosis of lung cancer cells induced by doxorubicin, leading to p53 pathway activation.	Doxorubicin	93-104	P53	Homo sapiens	117-120
31045925-5	2019	Sensitivity to cisplatin-based chemotherapy likely relies on intact TP53, reciprocal loss of heterozygosity, and high mitochondrial priming.	Cisplatin	15-24	P53	Homo sapiens	68-72
31062473-5	2019	Furthermore, we proved that knockdown of TFAM enhanced the interaction between p53 and MDM2, resulting in decreased expression of p53 and the downstream target TIGAR, and thus leading to elevated level of mitochondrial superoxide and DNA double-strand break (DSB) which were exacerbated when treated the cell with ionizing radiation.	Superoxides	219-229	P53	Homo sapiens	79-82
31075046-1	2019	PURPOSE: Anthracycline-associated risk for subsequent breast cancer in childhood cancer survivors is hypothesized to be mediated by TP53 mutation-related gene-environment interactions.	Anthracyclines	9-22	P53	Homo sapiens	132-136
31049827-9	2019	The Ser 392 phosphorylation level of p53 varied among tumours, and correlation analysis revealed an age-dependent phosphorylation pattern.	Serine	4-7	P53	Homo sapiens	37-40
31049827-11	2019	Moreover, Ser 392 phosphorylation contributed to a nuclear accumulation of p53 in schwannona cultures with TP53 mutation.	Serine	10-13	P53	Homo sapiens	75-78
31049827-11	2019	Moreover, Ser 392 phosphorylation contributed to a nuclear accumulation of p53 in schwannona cultures with TP53 mutation.	Serine	10-13	P53	Homo sapiens	107-111
31348244-10	2019	Additionally, GSEA found that LINC01614 might be involved in TGF-beta-, P53-, IGF-IR-mediated, Wnt and RTK/Ras/MAPK signaling pathways.lncRNAs may play key roles in the development of NSCLC.	gsea	14-18	P53	Homo sapiens	72-75
31056264-5	2019	We further showed that Irinotecan increased the amount of p53 only in the presence of MDM2 and inhibited the physical interaction of Bcl-xL with Bim, a core pro-apoptotic protein.	Irinotecan	23-33	P53	Homo sapiens	58-61
31056264-7	2019	Collectively, we suggest a new mechanism of action for Irinotecan as a dual target inhibitor of MDM2 and Bcl-xL facilitating the anticancer activities mediated by p53 and Bcl-xL interaction partners.	Irinotecan	55-65	P53	Homo sapiens	163-166
31417274-17	2019	Additionally, inducing p53 by doxorubicin (Dox) promoted LINC-PINT expression.	Doxorubicin	30-41	P53	Homo sapiens	23-26
31417274-17	2019	Additionally, inducing p53 by doxorubicin (Dox) promoted LINC-PINT expression.	Doxorubicin	43-46	P53	Homo sapiens	23-26
31235998-18	2019	Western blotting showed that upregulation of miR-34a combined with treatment with doxorubicin caused significant changes in the expression levels of p-p53, SIRT1, cyclin D1, CDK4, CDK6, BCL-2, MDR1/P-gp and AXL proteins (P &lt; 0.01).	Doxorubicin	82-93	P53	Homo sapiens	151-154
31004705-4	2019	The present study aims to examine whether SN affects cell viability, cell cycle, redox balance, genomic stability, and expression of the DNA damage response (DDR)-related genes ATM, ATR, CHEK1, CHECK2, TP53, and SIRT1 in HepG2 cells - used as in vitro hepatocyte model.	Synephrine	42-44	P53	Homo sapiens	202-206
31235998-19	2019	CONCLUSION: MiR-34a may enhance the inhibitory effect of doxorubicin by downregulating MDR1/P-gp and AXL, which may be related to p53 expression.	Doxorubicin	57-68	P53	Homo sapiens	130-133
30445600-4	2019	In addition, TIPE1 promoted cell proliferation and suppressed cisplatin susceptibility in a p53-dependent manner, indicating that TIPE1 facilitates cervical cancer progression primarily through the p53 pathway.	Cisplatin	62-71	P53	Homo sapiens	92-95
31231550-0	2019	Transcriptomic profiling reveals p53 as a key regulator of doxorubicin-induced cardiotoxicity.	Doxorubicin	59-70	P53	Homo sapiens	33-36
31231550-5	2019	Analyses of predicted upstream regulators identified the p53 protein as a key regulator of transcriptomic changes induced by doxorubicin.	Doxorubicin	125-136	P53	Homo sapiens	57-60
31244779-0	2019	Liver and Steroid Hormones-Can a Touch of p53 Make a Difference?	Steroids	10-26	P53	Homo sapiens	42-45
31244779-7	2019	Moreover, p53 was shown to be involved in steroid hormones regulation.	Steroids	42-49	P53	Homo sapiens	10-13
31244779-8	2019	In this review, we discuss the bi-directional regulation of the liver and the steroid hormones pointing to p53 as a novel regulator in this axis.	Steroids	78-85	P53	Homo sapiens	107-110
29808718-3	2019	Results: We observed that high glucose (HG), via activation of nuclear phosphatase PP2Cdelta, suppresses p53 function, and consequently promotes BC cell proliferation, migration, and invasion.	Glucose	31-38	P53	Homo sapiens	105-108
31000199-1	2019	Glucose limitation activates p53, which functions as an adaptive response to maintain cell survival.	Glucose	0-7	P53	Homo sapiens	29-32
31239671-1	2019	Purpose: The objective of this work was to formulate a delivery system of pDNA encoded p53 gene-loaded chitosan-sodium deoxycholate (CS-DS) nanoparticles, and to evaluate their influence on in vitro cytotoxicity and transfection efficiency of p53 gene.	Cadmium	133-138	P53	Homo sapiens	87-90
31239671-1	2019	Purpose: The objective of this work was to formulate a delivery system of pDNA encoded p53 gene-loaded chitosan-sodium deoxycholate (CS-DS) nanoparticles, and to evaluate their influence on in vitro cytotoxicity and transfection efficiency of p53 gene.	Cadmium	133-138	P53	Homo sapiens	243-246
30991050-4	2019	It was observed that CoQ10 suppressed p53/POMC, alpha-MSH production as well as inhibited ROS generation in UVA-irradiated keratinocyte HaCaT cells.	coenzyme Q10	21-26	P53	Homo sapiens	38-41
31171918-6	2019	Results: Our results revealed that the highest cytotoxic effect, the highest induction of apoptosis and significant elevation in P53 and Caspase 3 levels was seen in Paclitaxel/Gallic acid combination.	Paclitaxel	166-176	P53	Homo sapiens	129-132
30861422-5	2019	To antagonize intracellular MDM2/MDMX for p53 activation, we extended this protein, PMIBcr/Abl, by a C-terminal Arg-repeating hexapeptide to facilitate its cellular uptake.	Arginine	112-115	P53	Homo sapiens	42-45
31244286-0	2019	Metformin Modulates Cyclin D1 and P53 Expression to Inhibit Cell Proliferation and to Induce Apoptosis in Cervical Cancer Cell Lines.	Metformin	0-9	P53	Homo sapiens	34-37
31244286-12	2019	Moreover, 30 mM or higher doses of metformin increase significantly p53 expression (p< 0.001).	Metformin	35-44	P53	Homo sapiens	68-71
31244286-14	2019	Conclusion: Metformin can modulate cyclin D1 and p53 expression in HeLa cancer cell line, leadingto inhibition of cell proliferation and induction of apoptosis.	Metformin	12-21	P53	Homo sapiens	49-52
31089945-4	2019	RESULTS: High glucose led to premature senescence of HGMCs, as evident from the increase in the percentage of SA-beta-gal-positive cells, decrease in telomere length, cell cycle arrest at G1 phase,decrease in the expression of miR-126 and p-Akt and increase in the expression of p53, p21 and Rb proteins in the HG group.	Glucose	14-21	P53	Homo sapiens	279-282
31081062-5	2019	Similarly, INKA2 was induced in a p53-dependent manner at both the mRNA and protein level in human cells treated with adriamycin.	Doxorubicin	118-128	P53	Homo sapiens	34-37
30921731-3	2019	Here, we describe the design, via assembly of a p53-activating peptide termed PMI, functionalized PEG and fluorescent lanthanide oxyfluoride nanocrystals, of a novel nanotheranostic shaped in flexible rods.	Polyethylene Glycols	98-101	P53	Homo sapiens	48-51
31095448-6	2019	In addition, the results demonstrated that capsaicin induced the activation of adenosine 5"-monophosphate-activated protein kinase (AMPK), p53 and C-jun N-terminal kinase (JNK).	Capsaicin	43-52	P53	Homo sapiens	139-142
31095448-8	2019	Taken together, the present study suggests that capsaicin effectively causes cell death in human osteosarcoma MG63 cells via the activation of TRPV1-dependent (mitochondrial dysfunction, and overproduction of ROS and JNK) and TRPV1-independent (AMPK-p53) pathways.	Capsaicin	48-57	P53	Homo sapiens	250-253
31089945-6	2019	CONCLUSIONS: High glucose induces the senescence of HGMCs in vitro via the miR-126 and Akt-p53-p21 signaling pathways.	Glucose	18-25	P53	Homo sapiens	91-94
30367486-1	2019	The objective was to investigate the upstream mechanisms of apoptosis which were triggered by a novel antimicrotubule drug, ABT-751, in a tumor protein p53 ( TP53)-deficient hepatocellular carcinoma-derived Hep-3B cells.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	124-127	P53	Homo sapiens	152-155
30367486-1	2019	The objective was to investigate the upstream mechanisms of apoptosis which were triggered by a novel antimicrotubule drug, ABT-751, in a tumor protein p53 ( TP53)-deficient hepatocellular carcinoma-derived Hep-3B cells.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	124-127	P53	Homo sapiens	158-162
30367486-7	2019	Pharmacological inhibition of autophagosome (early autophagy) but not autolysosome (late autophagy) enhanced ABT-751-induced apoptosis in TP53-deficient Hep-3B cells.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	109-112	P53	Homo sapiens	138-142
30367486-8	2019	Our study provided a new strategy to augment ABT-751-induced apoptosis in TP53-deficient cells.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	45-48	P53	Homo sapiens	74-78
30771522-5	2019	RESULTS: Inhibition of Chk1 synergized with cisplatin to induce mitotic cell death in the p53-deficeint SCLC cells.	Cisplatin	44-53	P53	Homo sapiens	90-93
30913453-0	2019	Dihydrosanguinarine suppresses pancreatic cancer cells via regulation of mut-p53/WT-p53 and the Ras/Raf/Mek/Erk pathway.	dihydrosanguinarine	0-19	P53	Homo sapiens	77-80
31042625-10	2019	Our data suggest that PCAF-mediated p53 acetylation is an essential regulatory mechanism for increasing the susceptibility of CRC to 5-FU.	Fluorouracil	133-137	P53	Homo sapiens	36-39
30913453-0	2019	Dihydrosanguinarine suppresses pancreatic cancer cells via regulation of mut-p53/WT-p53 and the Ras/Raf/Mek/Erk pathway.	dihydrosanguinarine	0-19	P53	Homo sapiens	84-87
30913453-3	2019	PURPOSE: To reveal the inhibition of Dihydrosanguinarine on pancreatic cancer cells (PANC-1 and SW1990) proliferation by inducing G0/G1 and G2/M phase arrest via the downregulation of mut-p53 protein, inducing apoptosis and inhibiting invasiveness through the Ras/Mek/Erk signaling pathway.	dihydrosanguinarine	37-56	P53	Homo sapiens	188-191
30913453-12	2019	CONCLUSIONS: Our findings offer the novel perspective that DHSA inhibits pancreatic cancer cells through a bidirectional regulation between mut-p53/-Ras and WT-p53/-Ras to restore the dynamic balance by Ras and p53 proteins.	dihydrosanguinarine	59-63	P53	Homo sapiens	144-147
30913453-12	2019	CONCLUSIONS: Our findings offer the novel perspective that DHSA inhibits pancreatic cancer cells through a bidirectional regulation between mut-p53/-Ras and WT-p53/-Ras to restore the dynamic balance by Ras and p53 proteins.	dihydrosanguinarine	59-63	P53	Homo sapiens	160-163
30913453-12	2019	CONCLUSIONS: Our findings offer the novel perspective that DHSA inhibits pancreatic cancer cells through a bidirectional regulation between mut-p53/-Ras and WT-p53/-Ras to restore the dynamic balance by Ras and p53 proteins.	dihydrosanguinarine	59-63	P53	Homo sapiens	160-163
31138778-4	2019	Ectopic expression of ZCCHC10 in lung cancer cells harboring wild-type p53 dramatically suppresses cell proliferation, colony formation, migration, invasion and cisplatin resistance in vitro, as well as tumor growth and metastasis in vivo.	Cisplatin	161-170	P53	Homo sapiens	71-74
31039479-11	2019	The treatment also stimulated the phosphorylation of p53 at Ser-15, increased its concentration in the nucleus and enhanced Nrf2 translocation into the nucleus.	Serine	60-63	P53	Homo sapiens	53-56
31128065-0	2019	TP53 Gene 72 Arg/Pro (rs1042522) Single Nucleotide Polymorphism Contribute to Increase the Risk of B-Chronic Lymphocytic Leukemia in the Sudanese Population Objective: This study aimed at exploring the association of TP53 72Arg/Pro polymorphism and Risk of ChronicLymphocytic Leukemia and to assess the correlation between TP53 72Arg/Pro polymorphism and clinical parameter,hematological profile and some biological prognostic markers among Sudanese patients with chronic lymphocyticleukemia.	Arginine	13-16	P53	Homo sapiens	0-4
31258748-0	2019	Role of p53 Family Proteins in Metformin Anti-Cancer Activities.	Metformin	31-40	P53	Homo sapiens	8-11
31258748-7	2019	We also aimed to discuss the role of p53 family proteins in metformin-mediated suppression of cancer growth and survival.	Metformin	60-69	P53	Homo sapiens	37-40
30935902-6	2019	The inhibitory effect of curcumin, piperine and vitamin E on cell proliferation involves different markers, and in particular inhibits beta-catenin, cyclinD1 and p53, making them candidates for a possible use in alternative therapies although further studies are needed.	Curcumin	25-33	P53	Homo sapiens	162-165
31128065-0	2019	TP53 Gene 72 Arg/Pro (rs1042522) Single Nucleotide Polymorphism Contribute to Increase the Risk of B-Chronic Lymphocytic Leukemia in the Sudanese Population Objective: This study aimed at exploring the association of TP53 72Arg/Pro polymorphism and Risk of ChronicLymphocytic Leukemia and to assess the correlation between TP53 72Arg/Pro polymorphism and clinical parameter,hematological profile and some biological prognostic markers among Sudanese patients with chronic lymphocyticleukemia.	Arginine	13-16	P53	Homo sapiens	217-221
31128065-0	2019	TP53 Gene 72 Arg/Pro (rs1042522) Single Nucleotide Polymorphism Contribute to Increase the Risk of B-Chronic Lymphocytic Leukemia in the Sudanese Population Objective: This study aimed at exploring the association of TP53 72Arg/Pro polymorphism and Risk of ChronicLymphocytic Leukemia and to assess the correlation between TP53 72Arg/Pro polymorphism and clinical parameter,hematological profile and some biological prognostic markers among Sudanese patients with chronic lymphocyticleukemia.	Arginine	13-16	P53	Homo sapiens	217-221
31027879-3	2019	We found that Hsp70, together with Hsp40, unfolds p53 in an ATP-dependent reaction.	Adenosine Triphosphate	60-63	P53	Homo sapiens	50-53
31113906-11	2019	Our results show that a) oxygen and the targets of SV40LT (e.g. p53) modulate epigenetic aging rates and b) the chronological age of donor cells determines the speed of mitosis-associated DNAm age progression in daughter cells.	Oxygen	25-31	P53	Homo sapiens	64-67
31027879-5	2019	However, when Hsp90 and the adaptor protein Hop are present, p53 is transferred from Hsp70 to Hsp90, allowing restoration of the native state upon ATP hydrolysis.	Adenosine Triphosphate	147-150	P53	Homo sapiens	61-64
31223280-7	2019	The anticancer effects of curcumin are mainly mediated through its regulation of multiple cellular signaling pathways, including Wnt/beta-catenin, PI3K/Akt, JAK/STAT, MAPK, p53 and NF-kB signaling pathways.	Curcumin	26-34	P53	Homo sapiens	173-176
31244936-0	2019	Lgr5-mediated p53 Repression through PDCD5 leads to doxorubicin resistance in Hepatocellular Carcinoma.	Doxorubicin	52-63	P53	Homo sapiens	14-17
31244936-16	2019	Moreover, Lgr5 suppressed Dox-induced apoptosis via the p53 pathway and attenuated the cytotoxicity of Dox to HCC.	Doxorubicin	26-29	P53	Homo sapiens	56-59
31096598-4	2019	EEP augmented copper-induced up-regulation of p53 and Bax mRNA expressions.	Copper	14-20	P53	Homo sapiens	46-49
31096598-8	2019	Our data indicates a pro-oxidative and apoptotic mode of EEP action in the presence of excess copper, wherein ROS/p53/p38 interactions play an important role in death cascades.	Reactive Oxygen Species	110-113	P53	Homo sapiens	114-117
31002510-5	2019	Compound 14 arrested the cell cycle at S and G2 phases and up-regulated thymidylate synthase and p53, consistent with the results of the combination, suggesting 14 adopted a collaborative mode of 5-FU and oxaliplatin to kill cancer cells.	Fluorouracil	196-200	P53	Homo sapiens	97-100
31191795-2	2019	It has shown that wild-type p53 can reverse EMT back to epithelial characteristics, and iron chelator acting as a p53 inducer has been demonstrated.	Iron	88-92	P53	Homo sapiens	114-117
31092438-2	2019	The aim of this study was to investigate the relationship between p53 and IGF1 signaling pathway in young, senescent and H2O2-treated cells.	Hydrogen Peroxide	121-125	P53	Homo sapiens	66-69
31092438-6	2019	The gene expression levels of PI3K, TP53 and catalase (CAT) in senescent and H2O2-treated cells were increased compared to young cells.	Hydrogen Peroxide	77-81	P53	Homo sapiens	36-40
30898612-6	2019	Interestingly, co-treatment with nutlin-3a and certain chemotherapeutic drug such as irinotecan and oxaliplatin resulted in antagonistic effects in cells both lacking and containing WT-TP53 activity.	Irinotecan	85-95	P53	Homo sapiens	185-189
30050056-4	2019	p300 activity toward p53 is negatively regulated by the NAD-dependent deacetylase SIRT1, which deacetylates p53 preventing its transcriptional activation and the induction of p53-dependent apoptosis.	NAD	56-59	P53	Homo sapiens	21-24
30802707-5	2019	Molecular modeling revealed that the compound 4d binds through hydrophobic-hydrophobic interactions with the essential amino acids (LEU: 57, GLY: 58, ILE: 61, and HIS: 96) in the p53-binding cleft, as a standard p53-MDM2 inhibitor (6SJ).	Glycine	141-144	P53	Homo sapiens	179-182
30802707-5	2019	Molecular modeling revealed that the compound 4d binds through hydrophobic-hydrophobic interactions with the essential amino acids (LEU: 57, GLY: 58, ILE: 61, and HIS: 96) in the p53-binding cleft, as a standard p53-MDM2 inhibitor (6SJ).	Histidine	163-166	P53	Homo sapiens	179-182
30050056-4	2019	p300 activity toward p53 is negatively regulated by the NAD-dependent deacetylase SIRT1, which deacetylates p53 preventing its transcriptional activation and the induction of p53-dependent apoptosis.	NAD	56-59	P53	Homo sapiens	108-111
30050056-4	2019	p300 activity toward p53 is negatively regulated by the NAD-dependent deacetylase SIRT1, which deacetylates p53 preventing its transcriptional activation and the induction of p53-dependent apoptosis.	NAD	56-59	P53	Homo sapiens	108-111
30972978-6	2019	Both zinc and p53 can lead to an increase in ROS.	Reactive Oxygen Species	45-48	P53	Homo sapiens	14-17
30972978-0	2019	Zinc cooperates with p53 to inhibit the activity of mitochondrial aconitase through reactive oxygen species accumulation.	Reactive Oxygen Species	84-107	P53	Homo sapiens	21-24
30862715-4	2019	We then performed a genome-wide CRISPR/Cas9 knockout screen in the TP53-null hESC in the presence and absence of sublethal concentrations of cisplatin and identified 137 genes whose loss selectively resensitized the p53-null cells to this chemotherapeutic agent.	Cisplatin	141-150	P53	Homo sapiens	216-219
30862715-6	2019	Moreover, we confirmed that targeting ZNF207/BuGZ sensitizes p53-null hESC to cisplatin.	Cisplatin	78-87	P53	Homo sapiens	61-64
30865562-6	2019	Blocking ROS generation by N-acetylcysteine (NAC) or overexpressing constitutively active AKT vector (CA-AKT) inhibited HMS-incurred p53 mitochondrial translocation and promoted its nuclear targeting.	Acetylcysteine	45-48	P53	Homo sapiens	133-136
30770327-2	2019	The Lung Adjuvant Cisplatin Evaluation Biological Program group found adjuvant chemotherapy to be deleterious in patients with coexisting KRAS/TP53 mutations.	Cisplatin	18-27	P53	Homo sapiens	143-147
31007746-0	2019	miRNA-766 induces apoptosis of human colon cancer cells through the p53/Bax signaling pathway by MDM4.	mirna-766	0-9	P53	Homo sapiens	68-71
31007746-9	2019	These results demonstrated that miRNA-766 induced cell apoptosis in human colon cancer through MDM4/p53.	mirna-766	32-41	P53	Homo sapiens	100-103
30865562-0	2019	Stretching magnitude-dependent inactivation of AKT by ROS led to enhanced p53 mitochondrial translocation and myoblast apoptosis.	Reactive Oxygen Species	54-57	P53	Homo sapiens	74-77
30924710-2	2019	Recent studies, however, have indicated that Nrf2 induction stimulates the development of pre-existing tumors and confers resistance to chemotherapy by elevating drug metabolism and by efficient scavenging of ROS produced by the Warburg effect, which is regulated, in turn, by the p53 tumor suppressor.	Reactive Oxygen Species	209-212	P53	Homo sapiens	281-284
30865562-5	2019	Furthermore, we demonstrated that overaccumulation of reactive oxygen species (ROS) during HMS-inactivated AKT that was activated in LMS-treated cells, which accounted for the distinct p53 subcellular localizations under HMS and LMS.	Reactive Oxygen Species	54-77	P53	Homo sapiens	185-188
30865562-8	2019	Finally, we found that Ser389 phosphorylation of p53 was a downstream event of ROS-inactivated AKT pathway, which was critical to p53 mitochondrial trafficking during HMS stimuli.	Reactive Oxygen Species	79-82	P53	Homo sapiens	49-52
30865562-5	2019	Furthermore, we demonstrated that overaccumulation of reactive oxygen species (ROS) during HMS-inactivated AKT that was activated in LMS-treated cells, which accounted for the distinct p53 subcellular localizations under HMS and LMS.	Reactive Oxygen Species	79-82	P53	Homo sapiens	185-188
30865562-6	2019	Blocking ROS generation by N-acetylcysteine (NAC) or overexpressing constitutively active AKT vector (CA-AKT) inhibited HMS-incurred p53 mitochondrial translocation and promoted its nuclear targeting.	Reactive Oxygen Species	9-12	P53	Homo sapiens	133-136
30865562-8	2019	Finally, we found that Ser389 phosphorylation of p53 was a downstream event of ROS-inactivated AKT pathway, which was critical to p53 mitochondrial trafficking during HMS stimuli.	Reactive Oxygen Species	79-82	P53	Homo sapiens	130-133
30865562-6	2019	Blocking ROS generation by N-acetylcysteine (NAC) or overexpressing constitutively active AKT vector (CA-AKT) inhibited HMS-incurred p53 mitochondrial translocation and promoted its nuclear targeting.	Acetylcysteine	27-43	P53	Homo sapiens	133-136
30865562-10	2019	Altogether, our study uncovered that mitochondrial localization of p53, resulting from p53 Ser389 phosphorylation through ROS-inactivated AKT pathway, prompted C2C12 myoblast apoptosis during HMS stimulation.	Reactive Oxygen Species	122-125	P53	Homo sapiens	67-70
30865562-10	2019	Altogether, our study uncovered that mitochondrial localization of p53, resulting from p53 Ser389 phosphorylation through ROS-inactivated AKT pathway, prompted C2C12 myoblast apoptosis during HMS stimulation.	Reactive Oxygen Species	122-125	P53	Homo sapiens	87-90
30962574-3	2019	Instead, ALOX12 inactivation diminishes p53-mediated ferroptosis induced by reactive oxygen species stress and abrogates p53-dependent inhibition of tumour growth in xenograft models, suggesting that ALOX12 is critical for p53-mediated ferroptosis.	Reactive Oxygen Species	76-99	P53	Homo sapiens	40-43
30651598-2	2019	Human epidemiological studies reveal that a p53 single-nucleotide polymorphism (SNP) at codon 72, encoding proline (P72) or arginine (R72), is associated with differential risk of several cancers, including BrCa.	Arginine	124-132	P53	Homo sapiens	44-47
31091555-11	2019	Metformin stimulates p53- and AMPK-dependent pathways whereas CO can selectively trigger the PERK-dependent signaling pathway.	Metformin	0-9	P53	Homo sapiens	21-24
31086338-0	2019	Publisher Correction: p53 regulation of ammonia metabolism through urea cycle controls polyamine biosynthesis.	Urea	67-71	P53	Homo sapiens	22-25
30664690-3	2019	Isogenic p53-null radioresistant cancer cells established through cumulative irradiation showed decreased oxygen consumption and increased glycolysis with compromised mitochondria, corresponding with their enhanced sensitivity to drugs that target glycolysis.	Oxygen	106-112	P53	Homo sapiens	9-12
30885437-5	2019	Most importantly, in the cisplatin-resistance A549/DDP cells, this kind of agents could enter the nucleus obviously, and emerged a superior inhibitory and apoptotic effects than A549 via activating p53 protein and the related signaling pathways.	Cisplatin	25-34	P53	Homo sapiens	198-201
31183372-8	2019	Then, we found that the TRVP1 agonist capsaicin treatment inhibited CRC growth and induced apoptosis by activating P53.	Capsaicin	38-47	P53	Homo sapiens	115-118
29790387-5	2019	Results: In a set of in vivo studies, renal IR was found to cause severe impairment in renal tissues with massive ROS generation, which occurred contemporaneously with activation of NF-kappaB/p53/p53 upregulated modulator of apoptosis (PUMA)-mediated mitochondrial apoptosis pathways.	Reactive Oxygen Species	114-117	P53	Homo sapiens	192-195
31023317-16	2019	CONCLUSION: Our findings demonstrate for the first time that Fn14 overcomes cisplatin resistance through modulation of the degradation of p53-R248Q and restoration of Fn14 expression might be a novel strategy for the treatment of HGSOC.	Cisplatin	76-85	P53	Homo sapiens	138-141
31106145-7	2019	On the contrary, the sensitivity of cells to cisplatin was decreased after knockdown p53 or in p53 deletion NSCLC cells.	Cisplatin	45-54	P53	Homo sapiens	85-88
31106145-7	2019	On the contrary, the sensitivity of cells to cisplatin was decreased after knockdown p53 or in p53 deletion NSCLC cells.	Cisplatin	45-54	P53	Homo sapiens	95-98
31106145-9	2019	Taken together, our results demonstrate SMYD2 is involved into cisplatin resistance through regulating p53 pathway, and might become a promising therapeutic target for cisplatin resistance in NSCLC.	Cisplatin	63-72	P53	Homo sapiens	103-106
31022952-0	2019	p53-Dependent Apoptotic Effect of Puromycin via Binding of Ribosomal Protein L5 and L11 to MDM2 and its Combination Effect with RITA or Doxorubicin.	RITA	128-132	P53	Homo sapiens	0-3
31022952-0	2019	p53-Dependent Apoptotic Effect of Puromycin via Binding of Ribosomal Protein L5 and L11 to MDM2 and its Combination Effect with RITA or Doxorubicin.	Doxorubicin	136-147	P53	Homo sapiens	0-3
31022952-9	2019	These findings suggest that puromycin induces p53-dependent apoptosis via upregulation of RPL5 or RPL11 for binding with MDM2, and so can be used more effectively in p53 wild-type cancers by combination with RITA or doxorubicin.	RITA	208-212	P53	Homo sapiens	46-49
31022952-9	2019	These findings suggest that puromycin induces p53-dependent apoptosis via upregulation of RPL5 or RPL11 for binding with MDM2, and so can be used more effectively in p53 wild-type cancers by combination with RITA or doxorubicin.	Doxorubicin	216-227	P53	Homo sapiens	46-49
29790387-5	2019	Results: In a set of in vivo studies, renal IR was found to cause severe impairment in renal tissues with massive ROS generation, which occurred contemporaneously with activation of NF-kappaB/p53/p53 upregulated modulator of apoptosis (PUMA)-mediated mitochondrial apoptosis pathways.	Reactive Oxygen Species	114-117	P53	Homo sapiens	196-199
30833076-2	2019	Recent findings suggested that the mutation of tumor suppressor gene p53 promoted lipids synthesis and mutant p53 (mutp53) was essential for regulating mevalonate pathway for cholesterol synthesis.	Cholesterol	175-186	P53	Homo sapiens	69-72
31114366-4	2019	Metformin can activate p53 by activating AMPK and thereby ultimately stop the cell cycle.	Metformin	0-9	P53	Homo sapiens	23-26
30827507-8	2019	Mechanistic analysis corroborated that depression of PACT notably enhanced cisplatin-induced p53 expression, concomitant with the increases in p53-downstream Bax, p21 expression and decrease in Bcl-2 expression.	Cisplatin	75-84	P53	Homo sapiens	93-96
30827507-9	2019	Intriguingly, blocking the p53 pathway notably reversed PACT inhibition-increased cell sensitivity to cisplatin in A2780 cells by elevating cell viability and depressing cell apoptosis.	Cisplatin	102-111	P53	Homo sapiens	27-30
30833076-2	2019	Recent findings suggested that the mutation of tumor suppressor gene p53 promoted lipids synthesis and mutant p53 (mutp53) was essential for regulating mevalonate pathway for cholesterol synthesis.	Cholesterol	175-186	P53	Homo sapiens	110-113
30827507-10	2019	Additionally, abrogation of p53 signaling also blunts PACT suppression-overcomed chemotherapy resistance to cisplatin in A2780/CP cells.	Cisplatin	108-117	P53	Homo sapiens	28-31
30538112-5	2019	RESULTS: We observe that loss of ERCC1 hypersensitizes cells to cisplatin when wild-type (WT) p53 is retained, whereas there is only modest sensitivity in cell lines that are p53mutant/null.	Cisplatin	64-73	P53	Homo sapiens	94-97
30538112-6	2019	In addition, when p53 is disrupted by CRISPR-Cas9 (p53*) in ERCC1Delta/p53WT cells, there is reduced apoptosis and increased viability after platinum treatment.	Platinum	141-149	P53	Homo sapiens	18-21
30538112-6	2019	In addition, when p53 is disrupted by CRISPR-Cas9 (p53*) in ERCC1Delta/p53WT cells, there is reduced apoptosis and increased viability after platinum treatment.	Platinum	141-149	P53	Homo sapiens	51-54
30728154-2	2019	It has now been revealed that p53 mutation status should be considered concomitantly with ERCC1 to predict cisplatin efficacy.See related article by Heyza et al., p. 2523.	Cisplatin	107-116	P53	Homo sapiens	30-33
30538112-10	2019	CONCLUSIONS: Our findings implicate p53 as a potential confounding variable in clinical assessments of ERCC1 as a platinum biomarker via promoting an environment in which error-prone mechanisms of ICL-R may be able to partially compensate for loss of ERCC1.See related commentary by Friboulet et al., p. 2369.	Platinum	114-122	P53	Homo sapiens	36-39
30905619-6	2019	However, functional impairment was reversible when DDR burden was low and could be overcome by transient p53 inhibition.	ddr	51-54	P53	Homo sapiens	105-108
30553920-7	2019	Our results indicate that the combined effect of pairwise PAHs of BaP with Benzo[b]fluoranthene (BbF) and Benz[a]anthracene (BaA) is synergistic on p53 pathway, and that the health risk of the such mixtures increases compared to that of the individual ones.	benz(a)anthracene	106-123	P53	Homo sapiens	148-151
30553920-7	2019	Our results indicate that the combined effect of pairwise PAHs of BaP with Benzo[b]fluoranthene (BbF) and Benz[a]anthracene (BaA) is synergistic on p53 pathway, and that the health risk of the such mixtures increases compared to that of the individual ones.	benz(a)anthracene	125-128	P53	Homo sapiens	148-151
31149366-7	2019	Furthermore, TFAC was the only extract that significantly upregulated the expression of caspase 3, caspase 8 and P53.	tfac	13-17	P53	Homo sapiens	113-116
30988280-6	2019	H2O2 activated AMPK, which then phosphorylated SIRT1 and inhibited its deacetylation activity toward p53 in A549 cells or FOXO1 in NCI-H1299 cells.	Hydrogen Peroxide	0-4	P53	Homo sapiens	101-104
30971831-4	2019	The DOX-res group presented increased thiols and reduced lipoperoxidation, increased levels of nitric oxide, nuclear NF-kB and Nrf2, and reduced nuclear p53 labelling.	Doxorubicin	4-7	P53	Homo sapiens	153-156
30971831-7	2019	The Met-DOX group was more sensitive to DOX-induced OS, presented lower levels of nitric oxide, nuclear NF-kB and Nrf2, and increased nuclear p53.	Doxorubicin	8-11	P53	Homo sapiens	142-145
30755485-10	2019	The 5"-iodotubercidin treatment also suppressed beta-catenin, lymphoid enhancer-binding factor 1 (LEF-1), cyclin D1, N-Myc, and INSM1 levels, ultimately leading to apoptosis via caspase-3 and p53 activation.	5-iodotubercidin	4-21	P53	Homo sapiens	192-195
30623565-4	2019	Based on the reported prerequisite role of nucleolar stress response in stress-induced p53 protein accumulation, we have also provided evidence suggesting that Sirt1-mediated inhibition on nucleolar stress response may represent a novel mechanism by which Sirt1 can modulate intracellular p53 accumulation independent of lysine deacetylation.	Lysine	321-327	P53	Homo sapiens	87-90
30939155-6	2019	The curative effect repositioning of digoxin, a cardiovascular medication, was combined with fluvastatin and lovastatin, and the results further implied that p21 induction is involved in a p53-dependent and p53-independent manner.	Digoxin	37-44	P53	Homo sapiens	189-192
30939155-6	2019	The curative effect repositioning of digoxin, a cardiovascular medication, was combined with fluvastatin and lovastatin, and the results further implied that p21 induction is involved in a p53-dependent and p53-independent manner.	Digoxin	37-44	P53	Homo sapiens	207-210
30939155-7	2019	Digoxin modified the effects of statins on ATF3, p21, p53, and cyclin D1 expression, while fluvastatin boosted its DNA damage effect and lovastatin impeded its DNA damage effect.	Digoxin	0-7	P53	Homo sapiens	54-57
30623565-4	2019	Based on the reported prerequisite role of nucleolar stress response in stress-induced p53 protein accumulation, we have also provided evidence suggesting that Sirt1-mediated inhibition on nucleolar stress response may represent a novel mechanism by which Sirt1 can modulate intracellular p53 accumulation independent of lysine deacetylation.	Lysine	321-327	P53	Homo sapiens	289-292
31109596-9	2019	GSEA showed the enrichment of cell cycle, apoptosis, p53-dependent G1 DNA damage response, S-phase, mitotic M-M G1 phases, and FA-mediated cell death in the CDC25C high-expression phenotype.	gsea	0-4	P53	Homo sapiens	53-56
30748015-2	2019	The present study tests the hypothesis that the EtOH-induced DNA damage response is mediated through p53 pathways and influenced by growth factor signals.	Ethanol	48-52	P53	Homo sapiens	101-104
30748015-7	2019	Treatment with p53 siRNA potentiated EtOH- and TGFbeta1-induced changes in the numbers of proliferating NSCs and increased the proportion of NSCs expressing the apoptotic marker annexin V.	Ethanol	37-41	P53	Homo sapiens	15-18
30748015-8	2019	CONCLUSIONS: Thus, it appears that EtOH and TGFbeta1 affect proliferation, DNA repair, and survival of NSCs via p53-mediated activities.	Ethanol	35-39	P53	Homo sapiens	112-115
30456590-5	2019	H2O2 treated cells showed characteristic senescence-associated features including increased cell size, senescence-associated beta-galactosidase activity (SA-beta-gal), development of senescence-associated secretory phenotype (SASP), activation of reactive oxygen species (ROS) and pathways, DNA damage as well as induction of cell cycle inhibitors (p53/p21WAF1/p16INK4a).	Hydrogen Peroxide	0-4	P53	Homo sapiens	349-352
30748015-0	2019	p53-Mediated Activities in NS-5 Neural Stem Cells: Effects of Ethanol.	Ethanol	62-69	P53	Homo sapiens	0-3
30720065-10	2019	Notably, TCDD treatment increased the levels of p53, retinoblastoma, p21 and regucalcin, which are depressors of carcinogenesis.	Polychlorinated Dibenzodioxins	9-13	P53	Homo sapiens	48-51
30683654-3	2019	Here, we show TGFbeta induces p38-mediated FH phosphorylation at Thr 90, which leads to a FH/CSL (also known as RBP-Jkappa)/p53 complex formation and FH accumulation at p21 promoter under concomitant activation of Notch signaling; in turn, FH inhibits histone H3 Lys 36 demethylation and thereby promotes p21 transcription and cell growth arrest.	Threonine	65-68	P53	Homo sapiens	124-127
30683654-3	2019	Here, we show TGFbeta induces p38-mediated FH phosphorylation at Thr 90, which leads to a FH/CSL (also known as RBP-Jkappa)/p53 complex formation and FH accumulation at p21 promoter under concomitant activation of Notch signaling; in turn, FH inhibits histone H3 Lys 36 demethylation and thereby promotes p21 transcription and cell growth arrest.	Lysine	263-266	P53	Homo sapiens	124-127
30683654-4	2019	In addition, FH is massively phosphorylated at the Ser 46 by PAK4 in non-small cell lung cancer (NSCLC) cells, and PAK4-phosphorylated FH binds to 14-3-3, resulting in cytosolic detention of FH and prohibition of FH/CSL/p53 complex formation.	Serine	51-54	P53	Homo sapiens	220-223
31020875-8	2019	In particular, our study provides the mechanistic foundation that OMA reduces the expression and secretion of MMP-9 through LKB1-mediated PEA3 degradation via the ROS-dependent ATM-Chk2-p53 signalling axis, resulting from inhibition of IDH enzymes.	Reactive Oxygen Species	163-166	P53	Homo sapiens	186-189
30387173-6	2019	Through binding to the 3"-untranslated region of WIP1, miR-590 inhibited WIP1 expression and, therefore, enhanced the effect of Dox on OS cell proliferation and apoptosis through downstream ATM-p53 signaling.	Doxorubicin	128-131	P53	Homo sapiens	194-197
30387173-9	2019	Taken together, these results showed that p65-mediated miR-590/WIP1/ATM-p53 modulation might be a novel target to enhance the cellular effect of Dox on OS cell lines.	Doxorubicin	145-148	P53	Homo sapiens	72-75
30144378-8	2019	Both ADP and cisplatin increased p53 protein, but ADP was also able to enhance p53 messenger RNA.	Adenosine Diphosphate	5-8	P53	Homo sapiens	33-36
30710424-9	2019	The marked reduction in SIRT1 expression by combination of metformin and tenovin-6 increased acetylation of p53 at lysine 382 and enhanced p53 stability in LKB1-deficient A549 cells.	Metformin	59-68	P53	Homo sapiens	108-111
30710424-9	2019	The marked reduction in SIRT1 expression by combination of metformin and tenovin-6 increased acetylation of p53 at lysine 382 and enhanced p53 stability in LKB1-deficient A549 cells.	Metformin	59-68	P53	Homo sapiens	139-142
30710424-9	2019	The marked reduction in SIRT1 expression by combination of metformin and tenovin-6 increased acetylation of p53 at lysine 382 and enhanced p53 stability in LKB1-deficient A549 cells.	Lysine	115-121	P53	Homo sapiens	108-111
30144378-8	2019	Both ADP and cisplatin increased p53 protein, but ADP was also able to enhance p53 messenger RNA.	Cisplatin	13-22	P53	Homo sapiens	33-36
30144378-8	2019	Both ADP and cisplatin increased p53 protein, but ADP was also able to enhance p53 messenger RNA.	Cisplatin	13-22	P53	Homo sapiens	79-82
30144378-8	2019	Both ADP and cisplatin increased p53 protein, but ADP was also able to enhance p53 messenger RNA.	Adenosine Diphosphate	50-53	P53	Homo sapiens	79-82
30144378-9	2019	P53 silencing resulted in a very large decrement of cell death induced by ADP or by cisplatin and reverted ADP effects on mTOR/S6K phosphorylation, suggesting that activated p53 may act as a negative regulator of mTOR.	Adenosine Diphosphate	74-77	P53	Homo sapiens	0-3
30144378-9	2019	P53 silencing resulted in a very large decrement of cell death induced by ADP or by cisplatin and reverted ADP effects on mTOR/S6K phosphorylation, suggesting that activated p53 may act as a negative regulator of mTOR.	Adenosine Diphosphate	74-77	P53	Homo sapiens	174-177
30144378-9	2019	P53 silencing resulted in a very large decrement of cell death induced by ADP or by cisplatin and reverted ADP effects on mTOR/S6K phosphorylation, suggesting that activated p53 may act as a negative regulator of mTOR.	Cisplatin	84-93	P53	Homo sapiens	0-3
30144378-9	2019	P53 silencing resulted in a very large decrement of cell death induced by ADP or by cisplatin and reverted ADP effects on mTOR/S6K phosphorylation, suggesting that activated p53 may act as a negative regulator of mTOR.	Cisplatin	84-93	P53	Homo sapiens	174-177
30144378-9	2019	P53 silencing resulted in a very large decrement of cell death induced by ADP or by cisplatin and reverted ADP effects on mTOR/S6K phosphorylation, suggesting that activated p53 may act as a negative regulator of mTOR.	Adenosine Diphosphate	107-110	P53	Homo sapiens	0-3
30144378-9	2019	P53 silencing resulted in a very large decrement of cell death induced by ADP or by cisplatin and reverted ADP effects on mTOR/S6K phosphorylation, suggesting that activated p53 may act as a negative regulator of mTOR.	Adenosine Diphosphate	107-110	P53	Homo sapiens	174-177
30678901-8	2019	Further, the comparative relative expression profiling of the candidate genes were showed significant (p &lt; 0.05) down-regulation of IL6, BCL2, p53, and MMP9 in the BRM270 NPs treated cells, compared to the free BRM270 and doxorubicin.	Doxorubicin	225-236	P53	Homo sapiens	146-149
30892598-6	2019	The DNA-binding core domain of p53 has 10 cysteine residues, three of which participate in holding a zinc atom that is critical for p53 structure and function.	Cysteine	42-50	P53	Homo sapiens	31-34
30892598-6	2019	The DNA-binding core domain of p53 has 10 cysteine residues, three of which participate in holding a zinc atom that is critical for p53 structure and function.	Cysteine	42-50	P53	Homo sapiens	132-135
30892598-7	2019	Several novel compounds that refold and reactivate missense mutant p53 bind to specific p53 cysteine residues.	Cysteine	92-100	P53	Homo sapiens	67-70
30892598-7	2019	Several novel compounds that refold and reactivate missense mutant p53 bind to specific p53 cysteine residues.	Cysteine	92-100	P53	Homo sapiens	88-91
30350304-0	2019	AG1031 induces apoptosis through suppressing SIRT1/p53 pathway in human neuroblastoma cells.	N-Acetylhexosamine	0-6	P53	Homo sapiens	51-54
30350304-7	2019	Moreover, AG1031 treatment could down-regulate SIRT1 in a dose-dependent manner and up-regulate p53 acetylation, while overexpression of SIRT1 significantly attenuated the anti-tumor effect of AG1031 in SH-SY5Y cells.	N-Acetylhexosamine	10-16	P53	Homo sapiens	96-99
30844644-6	2019	The effects of TRIM69 overexpression in UVB-induced cell apoptosis and ROS production was clearly weakened by p53 overexpression, thus suggesting a role for p53 in TRIM69 functions.	Reactive Oxygen Species	71-74	P53	Homo sapiens	110-113
30881498-0	2019	Resveratrol induces p53 in colorectal cancer through SET7/9.	Resveratrol	0-11	P53	Homo sapiens	20-23
30881498-5	2019	Additionally, resveratrol enhanced the expression of tumour protein p53 (p53) and p53 target genes, including Bcl2 associated X, apoptosis regulator and Bcl2 binding component 3 that have a pivotal role in p53-dependent apoptosis.	Resveratrol	14-25	P53	Homo sapiens	68-71
30881498-5	2019	Additionally, resveratrol enhanced the expression of tumour protein p53 (p53) and p53 target genes, including Bcl2 associated X, apoptosis regulator and Bcl2 binding component 3 that have a pivotal role in p53-dependent apoptosis.	Resveratrol	14-25	P53	Homo sapiens	73-76
30881498-5	2019	Additionally, resveratrol enhanced the expression of tumour protein p53 (p53) and p53 target genes, including Bcl2 associated X, apoptosis regulator and Bcl2 binding component 3 that have a pivotal role in p53-dependent apoptosis.	Resveratrol	14-25	P53	Homo sapiens	73-76
30881498-5	2019	Additionally, resveratrol enhanced the expression of tumour protein p53 (p53) and p53 target genes, including Bcl2 associated X, apoptosis regulator and Bcl2 binding component 3 that have a pivotal role in p53-dependent apoptosis.	Resveratrol	14-25	P53	Homo sapiens	73-76
30881498-6	2019	Furthermore, treating cells with resveratrol upregulated SET domain containing lysine methyltransferase 7/9 (SET7/9) expression, which positively regulates p53 through its mono-methylation at lysine 372, compared with untreated cells.	Resveratrol	33-44	P53	Homo sapiens	156-159
30881498-6	2019	Furthermore, treating cells with resveratrol upregulated SET domain containing lysine methyltransferase 7/9 (SET7/9) expression, which positively regulates p53 through its mono-methylation at lysine 372, compared with untreated cells.	Lysine	79-85	P53	Homo sapiens	156-159
30881498-8	2019	However, the genetic knockdown of SET7/9 by short hairpin RNA attenuated the resveratrol-driven overexpression of p53, cleaved caspase-3 and PARP.	Resveratrol	77-88	P53	Homo sapiens	114-117
30881498-9	2019	Collectively, these results reveal the molecular mechanisms by which resveratrol induces p53 stability in colon cancer that results in the activation of p53-mediated apoptosis.	Resveratrol	69-80	P53	Homo sapiens	89-92
30881498-9	2019	Collectively, these results reveal the molecular mechanisms by which resveratrol induces p53 stability in colon cancer that results in the activation of p53-mediated apoptosis.	Resveratrol	69-80	P53	Homo sapiens	153-156
30844644-6	2019	The effects of TRIM69 overexpression in UVB-induced cell apoptosis and ROS production was clearly weakened by p53 overexpression, thus suggesting a role for p53 in TRIM69 functions.	Reactive Oxygen Species	71-74	P53	Homo sapiens	157-160
30925159-7	2019	Finally, lysine residue 358 was the key site for p53 K63-linked ubiquitination by the N and P proteins.	Lysine	9-15	P53	Homo sapiens	49-52
30883017-7	2019	In addition, delanzomib enhanced the Dox-induced phosphorylation of p38/JNK and the expression of transcriptional target proteins of p53, such as p21, p27, NOXA, and PUMA.	Doxorubicin	37-40	P53	Homo sapiens	133-136
31068300-10	2019	RRM1 silencing significantly inhibited the proliferation (P &amp;lt; 0.01) and enhanced the apoptosis-inducing effect of paclitaxel in MCF-7/R cells (P &amp;lt; 0.001); RRM1 silencing also resulted in obviously reduced Akt phosphorylation, suppressed Bcl-2 expression and promoted the expression of p53 protein in MCF-7/R cells.	Paclitaxel	121-131	P53	Homo sapiens	299-302
31019655-0	2019	Hsp90 Inhibitor SNX-2112 Enhances TRAIL-Induced Apoptosis of Human Cervical Cancer Cells via the ROS-Mediated JNK-p53-Autophagy-DR5 Pathway.	Reactive Oxygen Species	97-100	P53	Homo sapiens	114-117
30910997-4	2019	DYRK1A (dual-specificity tyrosine-phosphorylated and tyrosine-regulated kinase 1A), an EGFR-stabilizing kinase, is downregulated by p53 and, when ectopically expressed, can attenuate p53 activation-induced EGFR reduction and cellular senescence.	Tyrosine	25-33	P53	Homo sapiens	132-135
30910997-4	2019	DYRK1A (dual-specificity tyrosine-phosphorylated and tyrosine-regulated kinase 1A), an EGFR-stabilizing kinase, is downregulated by p53 and, when ectopically expressed, can attenuate p53 activation-induced EGFR reduction and cellular senescence.	Tyrosine	25-33	P53	Homo sapiens	183-186
31019655-8	2019	ROS scavenger NAC rescued SNX-2112/TRAIL-induced apoptosis and suppressed SNX-2112-induced p-JNK and p53.	Reactive Oxygen Species	0-3	P53	Homo sapiens	101-104
30841620-0	2019	Cisplatin Synergistically Enhances Antitumor Potency of Conditionally Replicating Adenovirus via p53 Dependent or Independent Pathways in Human Lung Carcinoma.	Cisplatin	0-9	P53	Homo sapiens	97-100
30885251-10	2019	The phosphorylation of CCDC106 at Ser-130 and Ser-147 is required for its interaction with p53 and nuclear localization, respectively.	Serine	34-37	P53	Homo sapiens	91-94
30885251-10	2019	The phosphorylation of CCDC106 at Ser-130 and Ser-147 is required for its interaction with p53 and nuclear localization, respectively.	Serine	46-49	P53	Homo sapiens	91-94
30886745-6	2019	Here we demonstrate that PpIX is a dual inhibitor of p53/MDM2 and p53/MDM4 interactions and activates apoptosis in B-cell chronic lymphocytic leukemia cells without illumination and without affecting normal cells.	protoporphyrin IX	25-29	P53	Homo sapiens	66-69
30886745-7	2019	PpIX stabilizes p53 and TAp73 proteins, induces p53-downstream apoptotic targets and provokes cancer cell death at doses non-toxic to normal cells.	protoporphyrin IX	0-4	P53	Homo sapiens	16-19
30886745-7	2019	PpIX stabilizes p53 and TAp73 proteins, induces p53-downstream apoptotic targets and provokes cancer cell death at doses non-toxic to normal cells.	protoporphyrin IX	0-4	P53	Homo sapiens	48-51
30886745-8	2019	Our findings open up new opportunities for repurposing PpIX for treating lymphoblastic leukemia with wild-type TP53.	protoporphyrin IX	55-59	P53	Homo sapiens	111-115
30602570-2	2019	p53 reactivation with induction of massive apoptosis-1 (PRIMA-1) and its primary active metabolite, 2-methylene-3-quinuclidinone (MQ), can restore unfolded p53 mutants to a native conformation that induces apoptosis and activates several p53 target genes.	memoquin	130-132	P53	Homo sapiens	0-3
30602570-2	2019	p53 reactivation with induction of massive apoptosis-1 (PRIMA-1) and its primary active metabolite, 2-methylene-3-quinuclidinone (MQ), can restore unfolded p53 mutants to a native conformation that induces apoptosis and activates several p53 target genes.	memoquin	130-132	P53	Homo sapiens	156-159
30602570-2	2019	p53 reactivation with induction of massive apoptosis-1 (PRIMA-1) and its primary active metabolite, 2-methylene-3-quinuclidinone (MQ), can restore unfolded p53 mutants to a native conformation that induces apoptosis and activates several p53 target genes.	memoquin	130-132	P53	Homo sapiens	156-159
30721669-9	2019	The anti-proliferation effects of bepridil and azelastine on the cell lines with mutated and deleted p53 implied some p53-independent anti-proliferation effects.	azelastine	47-57	P53	Homo sapiens	101-104
30721669-9	2019	The anti-proliferation effects of bepridil and azelastine on the cell lines with mutated and deleted p53 implied some p53-independent anti-proliferation effects.	azelastine	47-57	P53	Homo sapiens	118-121
30865893-0	2019	p53 Promotes Cancer Cell Adaptation to Glutamine Deprivation by Upregulating Slc7a3 to Increase Arginine Uptake.	Arginine	96-104	P53	Homo sapiens	0-3
30865893-6	2019	We also show that increased intracellular arginine levels following glutamine deprivation are dependent on p53.	Arginine	42-50	P53	Homo sapiens	107-110
30886745-0	2019	Protoporphyrin IX is a dual inhibitor of p53/MDM2 and p53/MDM4 interactions and induces apoptosis in B-cell chronic lymphocytic leukemia cells.	protoporphyrin IX	0-17	P53	Homo sapiens	41-44
30886745-0	2019	Protoporphyrin IX is a dual inhibitor of p53/MDM2 and p53/MDM4 interactions and induces apoptosis in B-cell chronic lymphocytic leukemia cells.	protoporphyrin IX	0-17	P53	Homo sapiens	54-57
30886745-5	2019	PpIX induces p53-dependent and TAp73-dependent apoptosis and inhibits TAp73/MDM2 and TAp73/MDM4 interactions.	protoporphyrin IX	0-4	P53	Homo sapiens	13-16
30886745-6	2019	Here we demonstrate that PpIX is a dual inhibitor of p53/MDM2 and p53/MDM4 interactions and activates apoptosis in B-cell chronic lymphocytic leukemia cells without illumination and without affecting normal cells.	protoporphyrin IX	25-29	P53	Homo sapiens	53-56
30866414-7	2019	Moreover, we showed that p53 family member DeltaNp63alpha transcriptionally suppressed integrin beta1 expression and is responsible for metformin-mediated upregulation of integrin beta1.	Metformin	136-145	P53	Homo sapiens	25-28
30895171-1	2019	Prima-1Met (APR-246) was previously shown to be dependent on glutathione inhibition and on ROS induction in cancer cells with mutated or deleted TP53.	ros	91-94	P53	Homo sapiens	145-149
30841620-8	2019	In conclusion, cisplatin synergistically increased the tumor-killing of CRAd by (1) increasing CRAd transduction via enhanced CAR expression and (2) increasing p53 dependent or independent apoptosis of lung cancer cell lines.	Cisplatin	15-24	P53	Homo sapiens	160-163
30639360-5	2019	Mechanistically, our findings showed that OMA activated p53-mediated apoptosis through ROS-dependent ATM-Chk2 signaling and reduced the expression of vascular endothelial growth factor through ROS-dependent E2F1-mediated hypoxia inducible factor-1alpha degradation.	Reactive Oxygen Species	87-90	P53	Homo sapiens	56-59
30483907-9	2019	Among the proteins related to apoptosis, abundances of CHOP and p53 were reduced, whereas those of Bcl-2 and Bcl-xL were enhanced in the jejunum of 100-200% glycine-supplemented piglets.	Glycine	157-164	P53	Homo sapiens	64-67
30723117-6	2019	Depletion of EZH2 by antisense oligonucleotides inhibited p53 GOF mutant-mediated cancer growth.	Oligonucleotides	31-47	P53	Homo sapiens	58-61
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	Polyethylene Glycols	0-3	P53	Homo sapiens	80-83
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	Polyethylene Glycols	0-3	P53	Homo sapiens	99-102
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	Disulfides	172-181	P53	Homo sapiens	80-83
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	Disulfides	172-181	P53	Homo sapiens	99-102
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	Glutathione	321-332	P53	Homo sapiens	80-83
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	Glutathione	321-332	P53	Homo sapiens	99-102
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	Glutathione	334-337	P53	Homo sapiens	80-83
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	Glutathione	334-337	P53	Homo sapiens	99-102
30660931-5	2019	A diazonium modified screen-printed carbon electrode immobilized with a DNA sequence related to the p53 tumour suppressor gene, the most commonly affected gene in human UV-induced skin cancer, was applied as an electrochemical DNA sensor.	Carbon	36-42	P53	Homo sapiens	100-103
30690027-9	2019	In this study, we observed an enhanced DNA damage and cellular apoptosis via the ATM/CHK2/P53 pathway(s) in HeLa and SiHa cells treated with cisplatin combined with DAPT of Notch1 inhibitor.	Cisplatin	141-150	P53	Homo sapiens	90-93
30448218-5	2019	The tumors in IPG VII with HNF1beta+/p53+/ARID1A+ immunophenotype demonstrated a significantly worse overall survival and progression-free survival as compared with the other IPGs.	2-Isopropoxyethanol	14-17	P53	Homo sapiens	37-40
30842655-4	2019	Here we report that the tumour suppressor p53, the most frequently mutated gene in human tumours, regulates ammonia metabolism by repressing the urea cycle.	Urea	145-149	P53	Homo sapiens	42-45
30594071-6	2019	PDR3 also upregulated serine phosphorylation of p53, which subsequently mediated apoptosis through the death receptors: tumor necrosis factor (TNF)-related apoptosis-inducing ligand receptors 1/2 (TRAIL-R1/R2), Fas-associated via death domain (FADD), and Fas.	Serine	22-28	P53	Homo sapiens	48-51
30778219-8	2019	HMGA proteins and NAMPT promote the proinflammatory SASP through NAD+-mediated suppression of AMPK kinase, which suppresses the p53-mediated inhibition of p38 MAPK to enhance NF-kappaB activity.	NAD	65-69	P53	Homo sapiens	128-131
30936596-3	2019	The AMP-activated protein kinase (AMPK), as a metabolic sensor, could be activated with metformin and it can also launch a p53-dependent metabolic checkpoint and might inhibit cancer cell growth.	Metformin	88-97	P53	Homo sapiens	123-126
30936596-8	2019	Real-time PCR revealed that metformin induced apoptosis in TE8 and TE11 cells by activating p53, down-regulating Bcl-2 expression.	Metformin	28-37	P53	Homo sapiens	92-95
30936596-10	2019	Conclusion: Metformin induced apoptosis in ESCC by down-regulating Bcl-2 expression, and up-regulating p53 and induced apoptosis increased by 2-deoxy-d-glucose.	Metformin	12-21	P53	Homo sapiens	103-106
30252118-5	2019	Here we show that the binding of MDM2 to the p53 mRNA brings ATM to the p53 polysome where it phosphorylates the nascent p53 at serine 15 and prevents MDM2-mediated degradation of p53.	Serine	128-134	P53	Homo sapiens	45-48
30252118-5	2019	Here we show that the binding of MDM2 to the p53 mRNA brings ATM to the p53 polysome where it phosphorylates the nascent p53 at serine 15 and prevents MDM2-mediated degradation of p53.	Serine	128-134	P53	Homo sapiens	72-75
30252118-5	2019	Here we show that the binding of MDM2 to the p53 mRNA brings ATM to the p53 polysome where it phosphorylates the nascent p53 at serine 15 and prevents MDM2-mediated degradation of p53.	Serine	128-134	P53	Homo sapiens	72-75
30252118-5	2019	Here we show that the binding of MDM2 to the p53 mRNA brings ATM to the p53 polysome where it phosphorylates the nascent p53 at serine 15 and prevents MDM2-mediated degradation of p53.	Serine	128-134	P53	Homo sapiens	72-75
30667081-7	2019	Moreover, drug sensitivity to doxorubicin was increased in these TP53 knock-out osteosarcoma cells.	Doxorubicin	30-41	P53	Homo sapiens	65-69
30615941-4	2019	Next, we generated IN for HepG2 cells, identified reporter transcription factors based on IN and found that the modulation of these genes affects key metabolic pathways associated with lipid metabolism (steroid biosynthesis, PPAR signalling pathway, fatty acid synthesis and oxidation) and cancer development (DNA replication, cell cycle and p53 signalling) involved in the progression of NAFLD and HCC.	Steroids	203-210	P53	Homo sapiens	342-345
30615941-4	2019	Next, we generated IN for HepG2 cells, identified reporter transcription factors based on IN and found that the modulation of these genes affects key metabolic pathways associated with lipid metabolism (steroid biosynthesis, PPAR signalling pathway, fatty acid synthesis and oxidation) and cancer development (DNA replication, cell cycle and p53 signalling) involved in the progression of NAFLD and HCC.	Fatty Acids	250-260	P53	Homo sapiens	342-345
30842655-0	2019	p53 regulation of ammonia metabolism through urea cycle controls polyamine biosynthesis.	Urea	45-49	P53	Homo sapiens	0-3
30778058-4	2019	Mechanistically, miR-135 accumulates specifically in response to glutamine deprivation and requires ROS-dependent activation of mutant p53, which directly promotes miR-135 expression.	ros	100-103	P53	Homo sapiens	135-138
30628717-8	2019	Further experiments validated that p53 enhanced the sensitivity of NCI-H1299 cells to Taxol through initiating the caspase-3 and -9 intrinsic death pathways, and resulted in cell cycle arrest at the G1/S phases.	Paclitaxel	86-91	P53	Homo sapiens	35-38
30562828-6	2019	Furthermore, damulin B activated the following: both intrinsic and extrinsic apoptosis pathways along with early G1 phase arrest via the upregulation of the Bax, Bid, tBid, cleaved caspase-8, and p53 expression levels; downregulation of the procaspase-8/-9, CDK4, CDK6, and cyclin D1 expression levels; and more release of cytochrome c in the cytoplasm.	damulin B	13-22	P53	Homo sapiens	196-199
30813936-10	2019	However, p53 was phosphorylated at serine 15 only in CCRF-CEM and MOLT-4 but not in SUP-B15 cells.	Serine	35-41	P53	Homo sapiens	9-12
30813936-12	2019	CONCLUSIONS: The delay in DSB repair and lower sensitivity to daunorubicin seen in the B lymphocyte derived SUP-B15 cells could be due to loss of function of p53 that may be correlated to increased expression of SOD2 and lower ROS production.	Reactive Oxygen Species	227-230	P53	Homo sapiens	158-161
30873235-4	2019	Screening of the library for p53-MDM2 inhibition by fluorescence polarization and 1H,15N HSQC NMR measurements confirm MDM2 binding.	Hydrogen	82-84	P53	Homo sapiens	29-32
30778138-10	2019	Spheroids from the p53 mutant STS 117 cell line were more resistant to RT and doxorubicin.	Doxorubicin	78-89	P53	Homo sapiens	19-22
30834235-5	2019	When we combined IO with the Chk1 inhibitor UCN-01, we successfully abrogated IO-induced G2/M arrest regardless of the underlying p53 status, indicating that the DNA damage response triggered by IO is also modulated by p53-independent mechanisms.	io	17-19	P53	Homo sapiens	219-222
30834235-5	2019	When we combined IO with the Chk1 inhibitor UCN-01, we successfully abrogated IO-induced G2/M arrest regardless of the underlying p53 status, indicating that the DNA damage response triggered by IO is also modulated by p53-independent mechanisms.	io	78-80	P53	Homo sapiens	219-222
30834235-5	2019	When we combined IO with the Chk1 inhibitor UCN-01, we successfully abrogated IO-induced G2/M arrest regardless of the underlying p53 status, indicating that the DNA damage response triggered by IO is also modulated by p53-independent mechanisms.	io	78-80	P53	Homo sapiens	219-222
30834235-9	2019	Furthermore, co-treatment with IO and UCN-01 significantly increased cell death in primary cells expressing mutant p53.	io	31-33	P53	Homo sapiens	115-118
30591552-5	2019	Importantly, Pep8 alone or together with a low dose of doxorubicin potently induced p53 expression and suppressed colony and tumor sphere formation and xenograft tumors in Rbm38- and p53-dependent manners.	Doxorubicin	55-66	P53	Homo sapiens	84-87
30591552-5	2019	Importantly, Pep8 alone or together with a low dose of doxorubicin potently induced p53 expression and suppressed colony and tumor sphere formation and xenograft tumors in Rbm38- and p53-dependent manners.	Doxorubicin	55-66	P53	Homo sapiens	183-186
30770552-7	2019	Furthermore, 5-FU combined with LEP-2a also resulted in p53 activation and NF-kappaB inhibition, and cell cycle arrest in the S phase as well as cell metastasis stagnation.	Fluorouracil	13-17	P53	Homo sapiens	56-59
29631413-6	2019	Augmented PPARalpha in hypertrophied myocytes revealed downregulated p53 acetylation (lys 382), leading to reduced apoptosis.	Lysine	86-89	P53	Homo sapiens	69-72
30863051-0	2019	A chemoenzymatically synthesized cholesterol-g-poly(amine-co-ester)-mediated p53 gene delivery for achieving antitumor efficacy in prostate cancer.	Cholesterol	33-44	P53	Homo sapiens	77-80
30755224-0	2019	PRIMA-1MET-induced neuroblastoma cell death is modulated by p53 and mycn through glutathione level.	eprenetapopt	0-10	P53	Homo sapiens	60-63
30755224-0	2019	PRIMA-1MET-induced neuroblastoma cell death is modulated by p53 and mycn through glutathione level.	Glutathione	81-92	P53	Homo sapiens	60-63
30755224-12	2019	Variations of MYCN and p53 modulated intracellular levels of GSH and resulted in increased/decreased sensitivity of PRIMA-1MET.	Glutathione	61-64	P53	Homo sapiens	23-26
30755224-12	2019	Variations of MYCN and p53 modulated intracellular levels of GSH and resulted in increased/decreased sensitivity of PRIMA-1MET.	eprenetapopt	116-126	P53	Homo sapiens	23-26
30755224-15	2019	Although p53 is involved in PRIMA-1MET-mediated cell death, our results suggest that direct interaction with p53 has a limited role in neuroblastoma but rather acts through modulation of GSH levels.	Glutathione	187-190	P53	Homo sapiens	109-112
29631413-7	2019	Such cells showed increased binding of PPARalpha with p53 that in turn reduced interaction of p53 with glycogen synthase kinase-3beta (GSK3beta), which upregulated inactive phospho-GSK3beta (serine [Ser]9) expression within mitochondrial protein fraction.	Serine	191-197	P53	Homo sapiens	54-57
29631413-7	2019	Such cells showed increased binding of PPARalpha with p53 that in turn reduced interaction of p53 with glycogen synthase kinase-3beta (GSK3beta), which upregulated inactive phospho-GSK3beta (serine [Ser]9) expression within mitochondrial protein fraction.	Serine	191-197	P53	Homo sapiens	94-97
29631413-7	2019	Such cells showed increased binding of PPARalpha with p53 that in turn reduced interaction of p53 with glycogen synthase kinase-3beta (GSK3beta), which upregulated inactive phospho-GSK3beta (serine [Ser]9) expression within mitochondrial protein fraction.	Serine	199-202	P53	Homo sapiens	54-57
29631413-7	2019	Such cells showed increased binding of PPARalpha with p53 that in turn reduced interaction of p53 with glycogen synthase kinase-3beta (GSK3beta), which upregulated inactive phospho-GSK3beta (serine [Ser]9) expression within mitochondrial protein fraction.	Serine	199-202	P53	Homo sapiens	94-97
30728290-0	2019	Tissue-specific regulation of p53 by PKM2 is redox dependent and provides a therapeutic target for anthracycline-induced cardiotoxicity.	Anthracyclines	99-112	P53	Homo sapiens	30-33
30881947-0	2019	Phosphorylation of p53 Serine 15 Is a Predictor of Survival for Patients with Hepatocellular Carcinoma.	Serine	23-29	P53	Homo sapiens	19-22
30881947-3	2019	Aim: To evaluate the prognostic value of p53 and p53 phosphorylation at serine 15 (p53 Ser15-P) in patients with HCC.	Serine	72-78	P53	Homo sapiens	49-52
30881947-3	2019	Aim: To evaluate the prognostic value of p53 and p53 phosphorylation at serine 15 (p53 Ser15-P) in patients with HCC.	Serine	72-78	P53	Homo sapiens	49-52
30728290-2	2019	Many chemotherapeutics (including anthracyclines, such as doxorubicin) induce the proapoptotic transcription factor p53 in the tumor and nonspecifically in the heart, promoting heart failure.	Anthracyclines	34-48	P53	Homo sapiens	116-119
30728290-2	2019	Many chemotherapeutics (including anthracyclines, such as doxorubicin) induce the proapoptotic transcription factor p53 in the tumor and nonspecifically in the heart, promoting heart failure.	Doxorubicin	58-69	P53	Homo sapiens	116-119
30728290-6	2019	We show by coimmunoprecipitation and mass spectrometry that the redox-regulated pyruvate kinase muscle 2 (PKM2) directly binds with p53 and that the redox status of cysteine-423 of tetrameric (but not monomeric) PKM2 is critical for the differential regulation of p53 transcriptional activity.	Cysteine	165-173	P53	Homo sapiens	132-135
30728290-6	2019	We show by coimmunoprecipitation and mass spectrometry that the redox-regulated pyruvate kinase muscle 2 (PKM2) directly binds with p53 and that the redox status of cysteine-423 of tetrameric (but not monomeric) PKM2 is critical for the differential regulation of p53 transcriptional activity.	Cysteine	165-173	P53	Homo sapiens	264-267
30718466-3	2019	Our preliminary study revealed heat stress (HS)-induced apoptosis of vascular endothelial cells was associated with reactive oxygen species (ROS)-induced p53 translocation into mitochondria.	Reactive Oxygen Species	116-139	P53	Homo sapiens	154-157
30455251-6	2019	The mutant p53-MDM2 complex is deficient in catalyzing ubiquitin release from the activated E2 conjugating enzyme.	Estradiol	92-94	P53	Homo sapiens	11-14
30838093-3	2019	Wild type (WT) p53 contains a proline at amino acid 47, but approximately 1% of African-Americans express a p53 allele with a serine at amino acid 47 (Pro47Ser, hereafter S47).	Serine	126-132	P53	Homo sapiens	108-111
30718466-3	2019	Our preliminary study revealed heat stress (HS)-induced apoptosis of vascular endothelial cells was associated with reactive oxygen species (ROS)-induced p53 translocation into mitochondria.	Reactive Oxygen Species	141-144	P53	Homo sapiens	154-157
30718466-5	2019	Based on these studies, we presumed Pin1 is a key intermediate in regulation of mitochondrial p53 translocation through a HS-induced ROS-p53 transcription-independent apoptosis pathway.	Reactive Oxygen Species	133-136	P53	Homo sapiens	94-97
30718466-5	2019	Based on these studies, we presumed Pin1 is a key intermediate in regulation of mitochondrial p53 translocation through a HS-induced ROS-p53 transcription-independent apoptosis pathway.	Reactive Oxygen Species	133-136	P53	Homo sapiens	137-140
30718466-8	2019	Furthermore, we also found ROS production was a critical mediator in HS-induced Pin1/p53 signaling and was involved in regulating mitochondrial apoptosis pathway activation.	Reactive Oxygen Species	27-30	P53	Homo sapiens	85-88
30578766-4	2019	Methylation of the transited adenosine was catalyzed by methyltransferase like 3 (METTL3), and this m6A-RNA promoted a preferential pre-mRNA splicing; consequently, the produced p53 R273H mutant protein resulted in acquired multidrug resistance in colon cancer cells.	Adenosine	29-38	P53	Homo sapiens	178-181
29773887-7	2019	On the other hand, VCA-1 treatment enhanced intracellular ROS (reactive oxygen species) generation also in a p53-independent manner, and consequently promoted caspase activation.	Reactive Oxygen Species	58-61	P53	Homo sapiens	109-112
29773887-7	2019	On the other hand, VCA-1 treatment enhanced intracellular ROS (reactive oxygen species) generation also in a p53-independent manner, and consequently promoted caspase activation.	Reactive Oxygen Species	63-86	P53	Homo sapiens	109-112
30419285-3	2019	METHODS: Fluorescence and Forster resonance energy transfer (FRET) were used to determine both the binding affinity and the distance between the lone tryptophan (FRET donor) of DNA Binding Domain (DBD) of p53 and the Iaedens dye (FRET acceptor) bound to the p28 peptide.	Tryptophan	150-160	P53	Homo sapiens	205-208
30325501-6	2019	Furthermore, combined treatment with progesterone plus mifepristone (PG+MIFE) gave an enhanced anti-proliferative effect in comparison with hydrocortisone plus mifepristone (HC+MIFE) by significantly reducing markers of proliferation (BrdU+ and Ki67 expression) and tumor suppressors (PTEN, TP53), and increasing the percentage of pro-apoptotic cells.	Progesterone	37-49	P53	Homo sapiens	291-295
30578766-5	2019	Furthermore, glycosphingolipids (particularly globotriaosylceramide) generated from serial ceramide glycosylation were seen to activate cSrc and beta-catenin signaling so as to upregulate METTL3 expression, in turn promoting expression of p53 R273H mutant protein, with consequent drug resistance.	Glycosphingolipids	13-31	P53	Homo sapiens	239-242
30760381-8	2019	Consistently, adriamycin-induced (ADR) activation of endogenous p53 also caused significant repression of the PRR11 and SKA2 gene pair expression.	Doxorubicin	14-24	P53	Homo sapiens	64-67
30388553-1	2019	An ultrahigh sensitive, simple and reliable Electrochemiluminescence (ECL) immunosensor for selective quantification of p53 protein was designed according to the enhancement effects of AuNPs on ECL emission of CdS nanocrystals (CdS NCs).	Cadmium	210-213	P53	Homo sapiens	120-123
30388553-2	2019	CdS NCs were immobilized on the glassy carbon electrode and AuNPs introduced to the process through formation of a sandwich-type immunocomplex between first anti-p53/p53/ secondary anti-p53.	Cadmium	0-3	P53	Homo sapiens	162-165
30388553-2	2019	CdS NCs were immobilized on the glassy carbon electrode and AuNPs introduced to the process through formation of a sandwich-type immunocomplex between first anti-p53/p53/ secondary anti-p53.	Cadmium	0-3	P53	Homo sapiens	166-169
30388553-2	2019	CdS NCs were immobilized on the glassy carbon electrode and AuNPs introduced to the process through formation of a sandwich-type immunocomplex between first anti-p53/p53/ secondary anti-p53.	Cadmium	0-3	P53	Homo sapiens	166-169
30465996-1	2019	We have successfully encapsulated two proteins, bovine serum albumin (BSA) and p53, in chitosan-tripolyphosphate (TPP) nanoparticles at various pH values from 5.5 to 6.5 and delivered the particles to human melanoma cells.	triphosphoric acid	96-112	P53	Homo sapiens	79-82
30488540-5	2019	In the present study, MDM4/MDM2 double knockdown with the siRNAs enhanced 5-fluorouracil (5-FU)-induced p53 activation, arrested the cell cycle at G1 phase, and potentiated the antitumor effect of 5-FU in wtTP53/highMDM4 human colon (HCT116 and LoVo) and gastric (SNU-1 and NUGC-4) cancer cells.	Fluorouracil	74-88	P53	Homo sapiens	104-107
30488540-5	2019	In the present study, MDM4/MDM2 double knockdown with the siRNAs enhanced 5-fluorouracil (5-FU)-induced p53 activation, arrested the cell cycle at G1 phase, and potentiated the antitumor effect of 5-FU in wtTP53/highMDM4 human colon (HCT116 and LoVo) and gastric (SNU-1 and NUGC-4) cancer cells.	Fluorouracil	90-94	P53	Homo sapiens	104-107
30488540-6	2019	Exposure to 5-FU alone induced MDM2 as well as p21 and PUMA by p53 activation.	Fluorouracil	12-16	P53	Homo sapiens	63-66
30488540-7	2019	As p53-MDM2 forms a negative feedback loop, enhancement of the antitumor effect of 5-FU by MDM4/MDM2 double knockdown could be attributed to blocking of the feedback mechanism in addition to direct suppression of these p53 antagonists.	Fluorouracil	83-87	P53	Homo sapiens	3-6
30488540-7	2019	As p53-MDM2 forms a negative feedback loop, enhancement of the antitumor effect of 5-FU by MDM4/MDM2 double knockdown could be attributed to blocking of the feedback mechanism in addition to direct suppression of these p53 antagonists.	Fluorouracil	83-87	P53	Homo sapiens	219-222
30400061-2	2019	This tumor suppression system is based upon the kill switch being triggered in cells in which p53 has been inactivated; such kill switch consisting of a rapid, catastrophic increase in ROS caused by the induction of irreversible uncompetitive inhibition of glucose-6- phosphate dehydrogenase (G6PD), which requires high concentrations of both inhibitor (DHEA) and G6P substrate.	ros	185-188	P53	Homo sapiens	94-97
30483736-3	2019	The current study identified a potential pathway by revealing that TRAIL and 6-sho or chloroquine acted together to trigger reactive oxygen species (ROS) production, to upregulate tumor-suppressor protein 53 (p53) expression and to change the mitochondrial transmembrane potential (MTP).	Reactive Oxygen Species	149-152	P53	Homo sapiens	209-212
30133149-5	2019	In this review, we will discuss the role of p53 tumor suppressor in iron homeostasis.	Iron	68-72	P53	Homo sapiens	44-47
30431068-5	2019	Investigating the mechanism, it was revealed that necroptosis may be induced in HCT116 p53+/+ cells by significantly increasing reactive oxygen species (ROS) and decreasing mitochondrial membrane potential (MMP), whereas little alterations were detected in HCT116 p53-/- cells.	Reactive Oxygen Species	128-151	P53	Homo sapiens	87-90
30431068-5	2019	Investigating the mechanism, it was revealed that necroptosis may be induced in HCT116 p53+/+ cells by significantly increasing reactive oxygen species (ROS) and decreasing mitochondrial membrane potential (MMP), whereas little alterations were detected in HCT116 p53-/- cells.	Reactive Oxygen Species	153-156	P53	Homo sapiens	87-90
30431068-6	2019	Unexpectedly, a much lower level of ATP was detected in HCT116 p53-/- cells compared with in HCT116 p53+/+ cells.	Adenosine Triphosphate	36-39	P53	Homo sapiens	63-66
30431068-8	2019	Furthermore, western blot analysis and ROS measurements indicated that AMPK inhibition, using dorsomorphin dihydrochloride, accelerated necroptosis by increasing ROS generation in HCT116 p53-/- cells.	Reactive Oxygen Species	162-165	P53	Homo sapiens	187-190
30431068-10	2019	In conclusion, these data strongly suggested that AMPK activation may be enhanced in HCT116 p53-/- cells under serum-depleted conditions via a drop in cellular ATP levels.	Adenosine Triphosphate	160-163	P53	Homo sapiens	92-95
31933859-5	2019	Finally, c-MYC, OCT4 and p53 were determined to contribute to the transcriptional regulation of NEAT1.1 under cisplatin using ChIP assay.	Cisplatin	110-119	P53	Homo sapiens	25-28
31933864-12	2019	CONCLUSION: Our study clarified that OGF inhibits cell migration and proliferation of HCC in animal experiments and that exogenous OGF enhances the anti-tumor activity of cisplatin on HCC by upregulating p21 and p53.	Cisplatin	171-180	P53	Homo sapiens	212-215
30483736-4	2019	Treatment with N-acetyl-L-cysteine reversed these effects, restoring the MTP and attenuated ROS production and p53 expression.	Acetylcysteine	15-34	P53	Homo sapiens	111-114
30675226-0	2019	MicroRNA-504 modulates osteosarcoma cell chemoresistance to cisplatin by targeting p53.	Cisplatin	60-69	P53	Homo sapiens	83-86
30478746-1	2019	The purpose of this study was to evaluate the synergistic apoptotic effect of CKD-602 in combination with cisplatin on different p53 statuses of oral squamous cell carcinoma (OSCC) cell lines, YD-8, YD-9, and YD-38.	Cisplatin	106-115	P53	Homo sapiens	129-132
30535478-0	2019	TP53 upregulates alpha-smooth muscle actin expression in tamoxifen-resistant breast cancer cells.	Tamoxifen	57-66	P53	Homo sapiens	0-4
30675226-12	2019	These results indicate that miR-504 contributes to cisplatin resistance in MG63 osteosarcoma cells by suppressing p53.	Cisplatin	51-60	P53	Homo sapiens	114-117
30766866-6	2019	Among the tested spirooxindoles, spiropyrazoline oxindole 1a was selective against the cancer cell line expressing wild-type p53 and presented low cytotoxicity.	spiropyrazoline oxindole	33-57	P53	Homo sapiens	125-128
30592172-14	2019	CONCLUSION: Paclitaxel can significantly repress cell proliferation and induce apoptosis of HS 737.T cells through activating Caspase-3, PARP1, p53, and TP53INP1.	Paclitaxel	12-22	P53	Homo sapiens	144-147
30272249-0	2019	Nicotine Promotes Human Papillomavirus (HPV)-Immortalized Cervical Epithelial Cells (H8) Proliferation by Activating RPS27a-Mdm2-P53 Pathway In Vitro.	Nicotine	0-8	P53	Homo sapiens	129-132
30272249-5	2019	Moreover, nicotine decreased the level of P53, resulted from a shortened P53 half-life.	Nicotine	10-18	P53	Homo sapiens	42-45
30272249-5	2019	Moreover, nicotine decreased the level of P53, resulted from a shortened P53 half-life.	Nicotine	10-18	P53	Homo sapiens	73-76
30272249-7	2019	It suggested that reduction in stabilization of P53 induced by nicotine may be negative regulator for P53/P21 signaling pathway that acts to prevent the growth of cells.	Nicotine	63-71	P53	Homo sapiens	48-51
30272249-7	2019	It suggested that reduction in stabilization of P53 induced by nicotine may be negative regulator for P53/P21 signaling pathway that acts to prevent the growth of cells.	Nicotine	63-71	P53	Homo sapiens	102-105
30272249-8	2019	In addition, reduction of RPS27a expression in nicotine treatment H8 cells up-regulated phosphorylation of Mdm2 at serine residue 166, followed by facilitating Mdm2-mediated ubiquitination of P53.	Nicotine	47-55	P53	Homo sapiens	192-195
30272249-9	2019	Simply put, these findings suggest that nicotine promotes H8 cell lines proliferation by activating RPS27a-Mdm2-P53 pathway in vitro.	Nicotine	40-48	P53	Homo sapiens	112-115
30834051-10	2019	Status of p53 was investigated to see their association with the result of the H. pylori, age and sex, tumor status, smoking and extra salt intake of the patients.	Salts	135-139	P53	Homo sapiens	10-13
30592172-9	2019	RNA-seq and bioinformatics analysis showed that apoptosis, death receptor signaling pathway, TNF signaling pathway, and TP53 regulated transcription of cell death genes pathway were closely associated with paclitaxel in the treatment of GCTB.	Paclitaxel	206-216	P53	Homo sapiens	120-124
30592172-10	2019	Western bolt results revealed that paclitaxel induced cleavage of Caspase-3 and PARP1, and increased the phosphorylation level of p53 in HS 737.T cells.	Paclitaxel	35-45	P53	Homo sapiens	130-133
30867818-0	2019	Interaction between p53 and Ras signaling controls cisplatin resistance via HDAC4- and HIF-1alpha-mediated regulation of apoptosis and autophagy.	Cisplatin	51-60	P53	Homo sapiens	20-23
30868056-4	2019	Anti-cancer drug adriamycin (ADR) treatment induced cell death in p53-wild-type human osteosarcoma U2OS cells, and this was accompanied by a remarkable accumulation of p53 and gammaH2AX.	Doxorubicin	17-27	P53	Homo sapiens	66-69
30868056-4	2019	Anti-cancer drug adriamycin (ADR) treatment induced cell death in p53-wild-type human osteosarcoma U2OS cells, and this was accompanied by a remarkable accumulation of p53 and gammaH2AX.	Doxorubicin	17-27	P53	Homo sapiens	168-171
30643005-3	2019	These characteristics are typically associated with regulation through chromatin acetylation by binding histone H3 trimethylated at lysine 4 (H3K4me3) and through transcriptional activity of transcription factor P53 and NF-kappaB.	Lysine	132-138	P53	Homo sapiens	212-215
30867818-15	2019	Conclusion: HIF-1alpha and HDAC4 may mediate the interaction between p53 and RAS signaling to actively control ovarian cancer cisplatin resistance through dysregulation of apoptosis and autophagy.	Cisplatin	126-135	P53	Homo sapiens	69-72
31459462-5	2019	Dialkyne 3 was successfully employed for "peptide stapling" of a p53-based diazido peptide, whereby two azides are bridged to give a product with a stabilized conformation.	dialkyne	0-8	P53	Homo sapiens	65-68
30696035-10	2019	All these results proved that p53 was involved in apoptosis via mitochondria-mediated pathway and the process was regulated by ROS.	Reactive Oxygen Species	127-130	P53	Homo sapiens	30-33
30683849-7	2019	SETD3 binds p53 in cells in response to doxorubicin treatment and positively regulates p53 target genes activation under these conditions.	Doxorubicin	40-51	P53	Homo sapiens	12-15
30573364-9	2019	Further analyses suggested that magnolol-induced apoptosis was related to the abnormal expression of p53, Bax, Bcl-2, cytochrome c and caspase activation.	magnolol	32-40	P53	Homo sapiens	101-104
30666159-0	2019	Peptidylarginine deiminase 4 overexpression resensitizes MCF-7/ADR breast cancer cells to adriamycin via GSK3beta/p53 activation.	Doxorubicin	90-100	P53	Homo sapiens	114-117
30733851-5	2019	Using a human skin cell model, a transient phosphorylation and nuclear translocation of p53, preceded by the phosphorylation of upstream serine- (ATM) and serine/threonine-protein kinase (ATR), was detected after CAP treatment.	Serine	137-143	P53	Homo sapiens	88-91
30655613-5	2019	The Arg variant of TP53 is more efficient at inducing apoptosis, whereas the Pro variant is a more potent inductor of cell cycle arrest and DNA repair.	Arginine	4-7	P53	Homo sapiens	19-23
30723502-0	2019	Autophagy Regulated by Gain of Function Mutant p53 Enhances Proteasomal Inhibitor-Mediated Cell Death through Induction of ROS and ERK in Lung Cancer Cells.	ros	123-126	P53	Homo sapiens	47-50
30622244-3	2019	In this study, we found that EPO suppresses p53-dependent apoptosis induced by genotoxic (daunorubicin, doxorubicin, and gamma-radiation) and non-genotoxic (nutlin-3a) agents and induces a senescence-like state in myeloid leukemia cells.	Doxorubicin	104-115	P53	Homo sapiens	44-47
30407667-7	2019	Also, the proposed protocol provided a smart strategy to monitor the relationship between nitric oxide and p53 protein activity in living cells.	Nitric Oxide	90-102	P53	Homo sapiens	107-110
30723502-5	2019	The presence of R273H-P53 conferred the cancer cells with drug resistance not only against the widely used chemotherapeutic agents like cisplatin (CDDP) or 5-flurouracil (5-FU) but also against potent alternative modes of therapy like proteasomal inhibition.	Fluorouracil	171-175	P53	Homo sapiens	22-25
30723502-5	2019	The presence of R273H-P53 conferred the cancer cells with drug resistance not only against the widely used chemotherapeutic agents like cisplatin (CDDP) or 5-flurouracil (5-FU) but also against potent alternative modes of therapy like proteasomal inhibition.	Cisplatin	136-145	P53	Homo sapiens	22-25
30723502-5	2019	The presence of R273H-P53 conferred the cancer cells with drug resistance not only against the widely used chemotherapeutic agents like cisplatin (CDDP) or 5-flurouracil (5-FU) but also against potent alternative modes of therapy like proteasomal inhibition.	Cisplatin	147-151	P53	Homo sapiens	22-25
30960044-4	2019	Doxorubicin (DOX) could be loaded into the cavity of CD polymers to form DOX-loaded nanoparticles (DOX-NPs) and the p53 gene could be subsequently condensed by DOX-NPs.	Doxorubicin	0-11	P53	Homo sapiens	116-119
30409904-3	2019	Here, using Bcl6 -/- knockout mice, HEK293A and HCT116 p53 -/- cells, and site-directed mutagenesis, we found that BCL6 interacts with p53 and thereby inhibits acetylation of Lys-132 in p53 by E1A-binding protein p300 (p300), a modification that normally occurs upon DNA damage-induced cellular stress and whose abrogation by BCL6 diminished transcriptional activation of p53 target genes, including that encoding caspase-1.	Lysine	175-178	P53	Homo sapiens	135-138
30409904-3	2019	Here, using Bcl6 -/- knockout mice, HEK293A and HCT116 p53 -/- cells, and site-directed mutagenesis, we found that BCL6 interacts with p53 and thereby inhibits acetylation of Lys-132 in p53 by E1A-binding protein p300 (p300), a modification that normally occurs upon DNA damage-induced cellular stress and whose abrogation by BCL6 diminished transcriptional activation of p53 target genes, including that encoding caspase-1.	Lysine	175-178	P53	Homo sapiens	135-138
30409904-3	2019	Here, using Bcl6 -/- knockout mice, HEK293A and HCT116 p53 -/- cells, and site-directed mutagenesis, we found that BCL6 interacts with p53 and thereby inhibits acetylation of Lys-132 in p53 by E1A-binding protein p300 (p300), a modification that normally occurs upon DNA damage-induced cellular stress and whose abrogation by BCL6 diminished transcriptional activation of p53 target genes, including that encoding caspase-1.	Lysine	175-178	P53	Homo sapiens	135-138
30960044-4	2019	Doxorubicin (DOX) could be loaded into the cavity of CD polymers to form DOX-loaded nanoparticles (DOX-NPs) and the p53 gene could be subsequently condensed by DOX-NPs.	Doxorubicin	13-16	P53	Homo sapiens	116-119
30960044-7	2019	As a result, enhanced cell growth inhibition, with decreased DOX dosage was achieved due to the synergistic effect of co-delivery of DOX and the p53 gene.	Doxorubicin	61-64	P53	Homo sapiens	145-148
30755813-4	2019	Cisplatin, a DNA damaging agent, induced cleavages of PARP and caspase-3 without increase of p53 levels, indicating that the p53 down-stream pathway was disrupted in these cells.	Cisplatin	0-9	P53	Homo sapiens	125-128
31544704-0	2019	The Pharmacogenomics "Side-effect" of TP53/EGFR in Non-small Cell Lung Cancer Accompanied with Atorvastatin Therapy: A Functional Network Analysis.	Atorvastatin	95-107	P53	Homo sapiens	38-42
31544704-12	2019	CONCLUSION: Gene-phenotype connectivity for atorvastatin in non-small cell lung cancer was identified using functional/activity network analysis method, and our findings demonstrated that TP53 and EGFR could be the potential targets in cancer patients with atorvastatin therapy.	Atorvastatin	44-56	P53	Homo sapiens	188-192
31544704-12	2019	CONCLUSION: Gene-phenotype connectivity for atorvastatin in non-small cell lung cancer was identified using functional/activity network analysis method, and our findings demonstrated that TP53 and EGFR could be the potential targets in cancer patients with atorvastatin therapy.	Atorvastatin	257-269	P53	Homo sapiens	188-192
30261716-0	2019	Cis-3-O-p-hydroxycinnamoyl Ursolic Acid Induced ROS-Dependent p53-Mediated Mitochondrial Apoptosis in Oral Cancer Cells.	Reactive Oxygen Species	48-51	P53	Homo sapiens	62-65
30370860-0	2019	Hydroxyl Group Difference between Anthraquinone Derivatives Regulate Different Cell Death Pathways via Nucleo-Cytoplasmic Shuttling of p53.	Anthraquinones	34-47	P53	Homo sapiens	135-138
30697266-12	2019	Co-treatment with captopril and the AKT inhibitor MK-2206 reduced the H2O2-induced P53 and ICAM-1 protein expression (p &lt; 0.05).	Hydrogen Peroxide	70-74	P53	Homo sapiens	83-86
30482390-2	2019	The present study identified a novel pathway of p53 accumulation by SIRT2 suppression in HCT116(p53+/+) cells in which SIRT2 suppression led to escape from mitotic cell death caused by spindle assembly checkpoint activation induced by microtubule inhibitors such as nocodazole but not apoptosis or G1 or G2 arrest.	Nocodazole	266-276	P53	Homo sapiens	48-51
30482390-2	2019	The present study identified a novel pathway of p53 accumulation by SIRT2 suppression in HCT116(p53+/+) cells in which SIRT2 suppression led to escape from mitotic cell death caused by spindle assembly checkpoint activation induced by microtubule inhibitors such as nocodazole but not apoptosis or G1 or G2 arrest.	Nocodazole	266-276	P53	Homo sapiens	96-99
30482390-6	2019	Thus, the P/CAF-MDM2-p53-p21 axis enables the escape from mitotic cell death and confers resistance to nocodazole in HCT116(p53+/+) cells with SIRT2 suppression.	Nocodazole	103-113	P53	Homo sapiens	21-24
30482390-6	2019	Thus, the P/CAF-MDM2-p53-p21 axis enables the escape from mitotic cell death and confers resistance to nocodazole in HCT116(p53+/+) cells with SIRT2 suppression.	Nocodazole	103-113	P53	Homo sapiens	124-127
30391673-9	2019	In addition, berberine inhibited p38-p53 mediated BAX activation, mitochondrial dysfunction and platelet apoptosis induced by HG.	Berberine	13-22	P53	Homo sapiens	37-40
30813877-13	2019	Among all formula of REE, the inhibition of proliferation rates and expression of E6 and L1, and the increase in expression of p53 and Rb in HFK-HPV18 was highest in ethanol-extracted compound REE group.	Ethanol	166-173	P53	Homo sapiens	127-130
30537571-6	2019	Moreover, cadmium suppressed astrocytic proliferation by inducing S and G2/M phase cell cycle arrest and promoting p53, p21, and p27 expression.	Cadmium	10-17	P53	Homo sapiens	115-118
30339780-3	2019	This organometallic complex induced p53-independent cytotoxicity and reduced size and vascularization of patients-derived tumor explants that are resistant to platinum drugs.	Platinum	159-167	P53	Homo sapiens	36-39
30318011-10	2019	CONCLUSION: The combination treatment of p53-null HL-60 cells with DNA-damaging agent CLB and HDACIs NaBu and TSA triggered additive to synergistic effects on apoptosis and upregulated BCL6 and p21 expression.	sethoxydim	101-105	P53	Homo sapiens	41-44
29842822-0	2019	Biosynthesized composites of Au-Ag nanoparticles using Trapa peel extract induced ROS-mediated p53 independent apoptosis in cancer cells.	Reactive Oxygen Species	82-85	P53	Homo sapiens	95-98
29842822-9	2019	Mechanistically, Au-AgNPs derived with Trapa peel extract significantly enhance ROS which trigger p53-independent apoptosis in various cancer cells effectively.	Reactive Oxygen Species	80-83	P53	Homo sapiens	98-101
30414976-10	2019	Overall, the work reveals that andrographolide through modulation of p53 and HNF4A, regulates miRNAs leading to upregulation of HO-1, glutathione and thioredoxin systems.	Glutathione	134-145	P53	Homo sapiens	69-72
30387805-7	2019	Additionally, resveratrol treatment decreased the protein expression levels of cyclin D1, cyclin E2 and BCL2 apoptosis regulator, while it increased BCL2 associated X and tumor protein p53, all of which are involved in the regulation of cell cycle and apoptosis.	Resveratrol	14-25	P53	Homo sapiens	185-188
30447351-0	2019	N-acetylcysteine ameliorates cisplatin-induced renal senescence and renal interstitial fibrosis through sirtuin1 activation and p53 deacetylation.	Acetylcysteine	0-16	P53	Homo sapiens	128-131
30447351-0	2019	N-acetylcysteine ameliorates cisplatin-induced renal senescence and renal interstitial fibrosis through sirtuin1 activation and p53 deacetylation.	Cisplatin	29-38	P53	Homo sapiens	128-131
30447351-10	2019	N-acetylcysteine (NAC), an antioxidant, attenuated premature senescence and decreased renal fibrosis, and its effects were dependent on sirtuin1 (SIRT1) activation and p53 deacetylation.	Acetylcysteine	0-16	P53	Homo sapiens	168-171
30447351-10	2019	N-acetylcysteine (NAC), an antioxidant, attenuated premature senescence and decreased renal fibrosis, and its effects were dependent on sirtuin1 (SIRT1) activation and p53 deacetylation.	Acetylcysteine	18-21	P53	Homo sapiens	168-171
30389549-7	2019	Using primary samples from acute leukemia patients, we show that the combination of Nutlin-3 plus Tanshinone IIA synergistically induces cytotoxicity by activating p53 and inhibiting the AKT/mTOR pathway.	tanshinone	98-112	P53	Homo sapiens	164-167
30656973-0	2019	MDM2 antagonist-loaded targeted micelles in combination with doxorubicin: effective synergism against human glioblastoma via p53 re-activation.	Doxorubicin	61-72	P53	Homo sapiens	125-128
31089357-0	2019	Sensitization of Resistance Ovarian Cancer Cells to Cisplatin by Biogenic Synthesized Silver Nanoparticles through p53 Activation.	Cisplatin	52-61	P53	Homo sapiens	115-118
31089357-12	2019	The combined use of cAgNPs and cisplatin resulted in upregulated expression of p53 gene and downregulated expression of MPP-9 gene.	Cisplatin	31-40	P53	Homo sapiens	79-82
30145226-1	2019	We previously demonstrated that progesterone (P4) up-regulated p53 expression, which in turn increased p21 and p27 expression, and finally resulted in proliferation inhibition in human umbilical vein endothelial cells (HUVEC).	Progesterone	32-44	P53	Homo sapiens	63-66
31168030-5	2019	Interestingly, the effects of gefitinib were observed in EGFR or p53 knockout (KO) cells.	Gefitinib	30-39	P53	Homo sapiens	65-68
30535690-5	2019	Using these protocols, we recently detected a metabolic alteration that occurs during aging by the monitoring the lactate/pyruvate ratio in a long-lived mutant of the mammalian tumor suppressor p53 ortholog CEP-1 in C. elegans.	Lactic Acid	114-121	P53	Homo sapiens	194-197
30467244-9	2019	CONCLUSIONS: The TP53 codon 72 Arg allele and XRCC1 codon 399 Gln allele are likely to have a protective effect against lung adenocarcinoma, especially in individuals older than 50 years of age.	Arginine	31-34	P53	Homo sapiens	17-21
31087303-3	2019	Much like nucleosomal histones, the tumor suppressor protein p53 is acetylated on a number of distinct lysine residues, often with distinct functional consequences.	Lysine	103-109	P53	Homo sapiens	61-64
30446350-14	2019	We conclude that in fibroblasts RSV stimulates the PGC-1alpha and p53 pathways, and up-regulates genes affecting the glucose metabolism, mitochondrial beta-oxidation, and mitochondrial biogenesis.	Resveratrol	32-35	P53	Homo sapiens	66-69
30301863-7	2019	Corroborating the basis of sensitivity, transcriptional profiling of platinum-resistant ARID1A-mutated HT1197 cells treated with panobinostat reveals negative enrichment for both cyto-proliferative (MYC and E2F targets) and DNA repair gene sets, and positive enrichment for TP53 and inflammatory gene sets.	Platinum	69-77	P53	Homo sapiens	274-278
30655810-0	2019	Rotundic acid induces Cas3-MCF-7 cell apoptosis through the p53 pathway.	rotundic acid	0-13	P53	Homo sapiens	60-63
30483727-5	2019	Curcumin targets numerous signaling pathways associated with cancer therapy, including pathways mediated by p53, Ras, phosphatidylinositol-3-kinase, protein kinase B, Wnt-beta catenin and mammalian target of rapamycin.	Curcumin	0-8	P53	Homo sapiens	108-111
30655810-3	2019	The results from an MTT assay demonstrated that RA effectively inhibited Cas3-MCF-7 cell viability in a dose-dependent manner and induced cell apoptosis via caspase-3 activity within 12 to 48 h. Western blotting and fluorescence-activated cell sorting demonstrated that RA initiated Cas3-MCF-7 cell apoptosis via p53 activation.	rotundic acid	48-50	P53	Homo sapiens	313-316
30655755-0	2019	Puerarin in inducing apoptosis of bladder cancer cells through inhibiting SIRT1/p53 pathway.	puerarin	0-8	P53	Homo sapiens	80-83
30655810-4	2019	The silencing of the p53 gene in the Cas3-MCF-7 cell line led to decreased RA-induced Cas3-MCF-7 cell caspase-3 activity and cell apoptosis.	rotundic acid	75-77	P53	Homo sapiens	21-24
30655755-9	2019	Compared with those in the puerarin group, the apoptosis rate in the combination group was decreased, and the expression level of apoptosis-related protein Bax was also significantly decreased, but the expression level of Bcl-2 was increased, and SIRT1 and p53 protein expression levels were also remarkably increased.	puerarin	27-35	P53	Homo sapiens	257-260
31597834-4	2019	Moreover, clinical trials of alvocidib (flavopiridol), an inhibitor of the CDK9, pevonedistat, an inhibitor of NEDD8, and APR-246, a reactivator of mutant p53, are in progress.	2-amino-10-(3'-(1-methyl-4-piperazinyl)propyl)phenothiazine	122-125	P53	Homo sapiens	155-158
30655755-10	2019	Puerarin can inhibit the proliferation of bladder cancer T24 cells and induce apoptosis, and the possible mechanism is related to the inhibition of SIRT1/p53 signaling pathway.	puerarin	0-8	P53	Homo sapiens	154-157
30591679-8	2018	RNA sequencing analysis suggested that sFRP4-mediated apoptosis is via the Fas-p53 pathway by activating the Wnt calcium and reactive oxygen species pathways.	Calcium	113-120	P53	Homo sapiens	79-82
30480671-5	2018	The complexes that were most active, with sub-micromolar IC50 (72 h) values against HCT116wt cells, that is 8b, 9b, 10a-c, worked by a mode of action that was dependent on the functional p53, yet were still far more active than cisplatin in both of the HCT116wt and HCT116-/- variants.	Cisplatin	228-237	P53	Homo sapiens	187-190
30593585-10	2018	GSEA showed that BC patients with high expression of KIF15, KIF20A, KIF23, KIF2C and KIF4A were enriched in the cell cycle process, P53 regulation pathway and mismatch repair.	gsea	0-4	P53	Homo sapiens	132-135
30591679-8	2018	RNA sequencing analysis suggested that sFRP4-mediated apoptosis is via the Fas-p53 pathway by activating the Wnt calcium and reactive oxygen species pathways.	Reactive Oxygen Species	125-148	P53	Homo sapiens	79-82
30643427-11	2019	Hypoxia supernatants significantly increased MRP, P-gp, p53 and Beclin-1 proteins in SKOV3 cells, which were significantly reduced by tBoc.	tboc	134-138	P53	Homo sapiens	56-59
30603043-3	2018	Results: By employing a drug repurposing approach, we found that protoporphyrin IX (PpIX), a metabolite of aminolevulinic acid applied in photodynamic therapy of cancer, stabilizes TAp73 and activates TAp73-dependent apoptosis in cancer cells lacking p53.	protoporphyrin IX	65-82	P53	Homo sapiens	251-254
30603043-3	2018	Results: By employing a drug repurposing approach, we found that protoporphyrin IX (PpIX), a metabolite of aminolevulinic acid applied in photodynamic therapy of cancer, stabilizes TAp73 and activates TAp73-dependent apoptosis in cancer cells lacking p53.	protoporphyrin IX	84-88	P53	Homo sapiens	251-254
30029111-10	2018	Simultaneously, ROS induced persistent DNA-damage (Comet-assay) that stimulated G2/M arrest for p53-mediated damage-repair, aided by checkpoint-promoter (Chk1) activation and mitotic-inducers (i.e. Cdc-25, Cdk1, cyclinB1) inhibition.	ros	16-19	P53	Homo sapiens	96-99
30577494-5	2018	Furthermore, suppression of DUSP6 by siRNA, or inhibition with the small molecule inhibitor, BCI, at a dose without cytotoxicity, potentiated the effect of MDM2 inhibitors through increased ATM-dependent p53 phosphorylation, as demonstrated by complete reversal with the ATM inhibitor, KU55933.	(E)-2-Benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one	93-96	P53	Homo sapiens	204-207
30316750-3	2018	We succeeded in detecting an attenuation in the affinity of p53 towards Mdm2 caused by the phosphorylation at Thr18.	UNII-PYZ33YLR8A	110-115	P53	Homo sapiens	60-63
30607176-8	2018	The genotypic distribution at codon 72 of TP53 in control group was 20%, 62.4% and 16.6% for Arg (wildtype), Arg/Pro (heterozygous) and Pro (homozygous variant) respectively.	Arginine	93-96	P53	Homo sapiens	42-46
30607176-8	2018	The genotypic distribution at codon 72 of TP53 in control group was 20%, 62.4% and 16.6% for Arg (wildtype), Arg/Pro (heterozygous) and Pro (homozygous variant) respectively.	Arginine	109-112	P53	Homo sapiens	42-46
30010803-0	2018	Selective killing of human breast cancer cells by the styryl lactone (R)-goniothalamin is mediated by glutathione conjugation, induction of oxidative stress and marked reactivation of the R175H mutant p53 protein.	goniothalamin	69-86	P53	Homo sapiens	201-204
30607176-10	2018	The absence of Arg at codon 72 of TP53 is relevant with age higher than 40 years and metastasis to other organs.	Arginine	15-18	P53	Homo sapiens	34-38
30010803-6	2018	We hypothesized that the redox imbalance induced by GON may affect the structure of the R175H mutant p53 protein, and account for greater cytotoxicity.	goniothalamin	52-55	P53	Homo sapiens	101-104
30588012-8	2018	Results: In the present study, we found that resveratrol dramatically inhibited melanoma cell proliferation and induced cell apoptosis through upregulation of p53 in a concentration-dependent manner.	Resveratrol	45-56	P53	Homo sapiens	159-162
30252476-6	2018	In both complexes, we observe significant changes in the water local density as the two proteins approach, supporting the existence of a clear dewetting transition in the case of MDM2-p53, with an onset distance of 5.6-7.6 A.	Water	57-62	P53	Homo sapiens	184-187
30230059-2	2018	The common p53 mutation Y220C causes local protein unfolding, aggregation, and can result in a loss of Zn in the DNA-binding domain.	Zinc	103-105	P53	Homo sapiens	11-14
30387987-5	2018	The ARPI-derived bioactive peptides exhibit synergistic anticancer effect with DOX by regulating pro- and antiapoptotic-relevant proteins ( p53, Bax, Bcl-2, pro-caspase-3) at mitochondria.	Doxorubicin	79-82	P53	Homo sapiens	140-143
30521558-5	2018	Additionally, Patched-1 protein expression was associated with worse DFS, while p53 overexpression was associated with worse OS.	Osmium	125-127	P53	Homo sapiens	80-83
30563120-3	2018	After D2O treatment, the p53-cyclin-dependent kinase (CDK) pathway was stimulated, leading to inhibition of the proliferation of HSCs and an increase in the [ATP]/[ADP] ratio.	Adenosine Triphosphate	158-161	P53	Homo sapiens	25-28
30563120-3	2018	After D2O treatment, the p53-cyclin-dependent kinase (CDK) pathway was stimulated, leading to inhibition of the proliferation of HSCs and an increase in the [ATP]/[ADP] ratio.	Adenosine Diphosphate	164-167	P53	Homo sapiens	25-28
30230059-5	2018	Their Zn-binding affinity was characterized using spectroscopic methods and demonstrate the ability of compounds L4 and L5 to increase intracellular levels of Zn2+ in a p53-Y220C-mutant cell line.	Zinc	159-163	P53	Homo sapiens	169-172
30524726-0	2018	p53-mediated adaptation to serine starvation is retained by a common tumour-derived mutant.	Serine	27-33	P53	Homo sapiens	0-3
30524726-5	2018	Results: We show that a commonly occurring p53 mutant, R248W, retains wild-type ability to support survival under serine starvation.	Serine	114-120	P53	Homo sapiens	43-46
30091208-8	2018	This implied that the deactivated Akt caused by MC/DMC was p53-dependent.	10-decarbamoylmitomycin C	51-54	P53	Homo sapiens	59-62
30524726-9	2018	Conclusion: Our work shows that mutant p53s can selectively retain wild-type p53 functions that allow adaptation to serine starvation through the activation of antioxidant defence pathways.	Serine	116-122	P53	Homo sapiens	39-42
30524726-9	2018	Conclusion: Our work shows that mutant p53s can selectively retain wild-type p53 functions that allow adaptation to serine starvation through the activation of antioxidant defence pathways.	Serine	116-122	P53	Homo sapiens	77-80
30524726-10	2018	Tumours containing this p53 mutation are resistant to serine-limited conditions and less responsive to therapy.	Serine	54-60	P53	Homo sapiens	24-27
29871517-16	2018	Treatment with rapamycin decreased p53 accumulation, and 3-MA inhibited the decrease in p53 induced by HPC.	Sirolimus	15-24	P53	Homo sapiens	35-38
30091208-2	2018	MC analog, 10-decarbamoyl mitomycin C (DMC), unlike MC, has stronger effects on cancer with p53 mutation.	10-decarbamoylmitomycin C	11-37	P53	Homo sapiens	92-95
30091208-13	2018	In summary, MC/DMC regulate Akt activation in a p53-dependent manner.	10-decarbamoylmitomycin C	15-18	P53	Homo sapiens	48-51
30091208-2	2018	MC analog, 10-decarbamoyl mitomycin C (DMC), unlike MC, has stronger effects on cancer with p53 mutation.	10-decarbamoylmitomycin C	39-42	P53	Homo sapiens	92-95
30414472-6	2018	Further, we identified top 50 overexpressed genes of SCLC by Oncomine, and the interconnected genes with the 4 aspirin DPTs in SCLC (IKBKB, NFKBIA, PTGS2 and TP53) by STRING.	Aspirin	111-118	P53	Homo sapiens	158-162
30091208-3	2018	We previously demonstrated that MC/DMC could activate p21WAF 1/ CIP 1 in MCF-7 (p53-proficient) and K562 (p53-deficient) cells in a p53-independent mode.	10-decarbamoylmitomycin C	35-38	P53	Homo sapiens	80-83
30091208-3	2018	We previously demonstrated that MC/DMC could activate p21WAF 1/ CIP 1 in MCF-7 (p53-proficient) and K562 (p53-deficient) cells in a p53-independent mode.	10-decarbamoylmitomycin C	35-38	P53	Homo sapiens	106-109
30091208-3	2018	We previously demonstrated that MC/DMC could activate p21WAF 1/ CIP 1 in MCF-7 (p53-proficient) and K562 (p53-deficient) cells in a p53-independent mode.	10-decarbamoylmitomycin C	35-38	P53	Homo sapiens	106-109
30221683-10	2018	Bioinformatics prediction revealed that aspirin was closely associated with cell proliferation and apoptosis, including the p53 and NF-kappaB signaling pathways.	Aspirin	40-47	P53	Homo sapiens	124-127
30286548-10	2018	Identified 386 genes which exhibited both differential methylation and expression were functionally associated with pathways including cardiovascular system development, regulation of blood vessel size, vasculature development, p53 pathway, AC-modulating/inhibiting GPCRs pathway and cellular response to metal ion/inorganic substance.	Metals	305-310	P53	Homo sapiens	228-231
30399406-0	2018	17beta-estradiol inhibits human umbilical vascular endothelial cell senescence by regulating autophagy via p53.	Estradiol	0-16	P53	Homo sapiens	107-110
30415163-0	2018	A novel all-trans retinoic acid derivative inhibits proliferation and induces apoptosis of myelodysplastic syndromes cell line SKM-1 cells via up-regulating p53.	Tretinoin	18-31	P53	Homo sapiens	157-160
30539860-9	2018	Moreover, 3-MA inhibited while rapamycin facilitated 5-FU-induced p53 protein expression.	Fluorouracil	53-57	P53	Homo sapiens	66-69
29633022-6	2018	Moreover, mutant IDH1 can drive the immortalization and transformation of p53-/pRb-deficient astrocytes by reactivating telomerase and stabilizing telomeres in combination with increased histone lysine methylation and c-Myc/Max binding at the TERT promoter.	Lysine	195-201	P53	Homo sapiens	74-77
30539860-11	2018	Especially, Beclin1 overexpression increased while Beclin1 knockdown decreased 5-FU-induced p53 expression.	Fluorouracil	79-83	P53	Homo sapiens	92-95
30274043-7	2018	Furthermore, doxorubicin released from biomaterials with cyclodextrin moderately induced the expression of tumor suppressor protein p53 whereas p21 expression was similar to control cells.	Doxorubicin	13-24	P53	Homo sapiens	132-135
30274043-7	2018	Furthermore, doxorubicin released from biomaterials with cyclodextrin moderately induced the expression of tumor suppressor protein p53 whereas p21 expression was similar to control cells.	Cyclodextrins	57-69	P53	Homo sapiens	132-135
30507074-0	2018	Comparative transcriptomic analysis reveals adriamycin-induced apoptosis via p53 signaling pathway in retinal pigment epithelial cells.	Doxorubicin	44-54	P53	Homo sapiens	77-80
30275526-7	2018	Compared with wild-type, OS was significantly reduced among CCR-treated patients with TP53 or NRAS mutations and azacitidine-treated patients with FLT3 or TET2 mutations.	Osmium	25-27	P53	Homo sapiens	86-90
30467317-6	2018	Ganetespib decreased growth of endogenous Pten/Tp53 null tumors, confirming therapeutic activity in situ.	STA 9090	0-10	P53	Homo sapiens	47-51
30143976-7	2018	Intriguingly, dietary curcumin supplementation modulated autophagy through the activation of beclin-1, ATG5, Dynein, LC3a, LC3b-I/II and downregulation of p53 &amp; mTOR expression level.	Curcumin	22-30	P53	Homo sapiens	155-158
30196236-0	2018	The Mutant p53-Targeting Compound APR-246 Induces ROS-Modulating Genes in Breast Cancer Cells.	ros	50-53	P53	Homo sapiens	11-14
30568488-0	2018	Role of curcumin in regulating p53 in breast cancer: an overview of the mechanism of action.	Curcumin	8-16	P53	Homo sapiens	31-34
30568488-11	2018	This review summarizes the effects of curcumin as a regulator of p53 in BC and the key molecular mechanisms of this regulation.	Curcumin	38-46	P53	Homo sapiens	65-68
30380295-0	2018	Evaluation of Maltose Binding Protein-Tagged hATR Kinase Domain Catalytic Activity with p53 Ser-15 Phosphorylation.	Serine	92-95	P53	Homo sapiens	88-91
30591797-5	2018	Histone H2AX phosphorylation and expression of Myt1, cyclin A2, cyclin B1 and p53 were increased in HCT8 and HT29 cells on treatment with matrine for 48 h. Matrine treatment also increased the phosphorylation of cdc2 significantly compared to control cells at 48 h (P &lt; 0.05).	matrine	138-145	P53	Homo sapiens	78-81
30504836-6	2018	CXCR4 upregulation in radioresistant tumour ECs was highly associated with SDF-1+ TAM recruitment and M2 polarization of TAMs, which was suppressed by Trp53 deletion.	Tamoxifen	121-125	P53	Homo sapiens	151-156
30265530-0	2018	N-O Reduction and ROS-Mediated AKT/FOXO1 and AKT/P53 Pathways Are Involved in Growth Promotion and Cytotoxicity of Cyadox.	ros	18-21	P53	Homo sapiens	49-52
30453545-10	2018	In addition, RA modulated the protein expression of intrinsic mitochondrial apoptotic pathway-related genes, such as Bax, Bcl-2, caspase-3 and poly (ADP-ribose) polymerase 1 (PARP-1) (cleaved) via the upregulation of p53 derived from HDAC2 downregulation, leading to the increased apoptosis of PC-3 and DU145 cells.	rosmarinic acid	13-15	P53	Homo sapiens	217-220
30265530-10	2018	Thus, the present study revealed that N-O reduction of cyadox and ROS-mediated AKT/FOXO1 and AKT/P53 pathways were involved in growth promotion and cytotoxicity of cyadox.	ros	66-69	P53	Homo sapiens	97-100
30446605-0	2018	Withdrawal: Inhibition of AMP-activated protein kinase sensitizes cancer cells to cisplatin-induced apoptosis via hyper-induction of p53.	Cisplatin	82-91	P53	Homo sapiens	133-136
30318526-0	2018	Spice-derived phenolic, malabaricone B induces mitochondrial damage in lung cancer cells via a p53-independent pathway.	malabaricone B	24-38	P53	Homo sapiens	95-98
30442142-0	2018	Metformin causes cancer cell death through downregulation of p53-dependent differentiated embryo chondrocyte 1.	Metformin	0-9	P53	Homo sapiens	61-64
30442142-5	2018	We later clarified the effect of metformin on p53 protein stability using transient transfection and cycloheximide chase analyses.	Metformin	33-42	P53	Homo sapiens	46-49
30442142-6	2018	RESULTS: We observed that metformin represses cell cycle progression, thereby inducing subG1 populations, and had induced apoptosis through downregulation of p53 protein and a target gene, differentiated embryo chondrocyte 1 (DEC1).	Metformin	26-35	P53	Homo sapiens	158-161
30442142-9	2018	Examination of the mechanisms underlying metformin-induced HeLa cell death revealed that reduced stability of p53 in metformin-treated cells leads to decreases in DEC1 and induction of apoptosis.	Metformin	41-50	P53	Homo sapiens	110-113
30442142-9	2018	Examination of the mechanisms underlying metformin-induced HeLa cell death revealed that reduced stability of p53 in metformin-treated cells leads to decreases in DEC1 and induction of apoptosis.	Metformin	117-126	P53	Homo sapiens	110-113
30442142-10	2018	CONCLUSION: The involvement of DEC1 provides new insight into the positive or negative functional roles of p53 in the metformin-induced cytotoxicity in tumor cells.	Metformin	118-127	P53	Homo sapiens	107-110
30257366-13	2018	The anticancer effect of parthenolide is mediated by angiogenesis inhibition and activation of P53- dependent apoptosis.	parthenolide	25-37	P53	Homo sapiens	95-98
30362715-5	2018	Our results show that NMR order parameter-derived conformational entropy is linearly correlated with the change in free energy of urea-mediated denaturation, the latter being a well-established reporter of stability in p53 core domain mutants.	Urea	130-134	P53	Homo sapiens	219-222
28884602-13	2018	Expression analysis by real-time PCR showed the significant up-regulation of two tumour suppressor genes, P53 and P21 in response to combination of silibinin and paclitaxel.	Silybin	148-157	P53	Homo sapiens	106-109
28884602-13	2018	Expression analysis by real-time PCR showed the significant up-regulation of two tumour suppressor genes, P53 and P21 in response to combination of silibinin and paclitaxel.	Paclitaxel	162-172	P53	Homo sapiens	106-109
30257366-0	2018	Parthenolide inhibits tumor-promoting effects of nicotine in lung cancer by inducing P53 - dependent apoptosis and inhibiting VEGF expression.	parthenolide	0-12	P53	Homo sapiens	85-88
30257366-0	2018	Parthenolide inhibits tumor-promoting effects of nicotine in lung cancer by inducing P53 - dependent apoptosis and inhibiting VEGF expression.	Nicotine	49-57	P53	Homo sapiens	85-88
30483050-7	2018	We found that treatment of 400 muM GM elicited the formation of ROS, which, in turn, led to PINK1 degradation, parkin recruitment, autophagy formation, an increase of p53 and cleaved-caspase 3 in HEI-OC1 cells and murine HCs.	Reactive Oxygen Species	64-67	P53	Homo sapiens	167-170
30483050-8	2018	In contrast, co-treatment with ROS scavenger N-acetyl-L-cysteine (NAC) inhibited parkin recruitment, alleviated autophagy and p53 pathway-related damaged-cell elimination.	Reactive Oxygen Species	31-34	P53	Homo sapiens	126-129
30400903-0	2018	Porcine reproductive and respiratory syndrome virus inhibits MARC-145 proliferation via inducing apoptosis and G2/M arrest by activation of Chk/Cdc25C and p53/p21 pathway.	marc-145	61-69	P53	Homo sapiens	155-158
30450337-3	2018	Recent studies have found that p53 acts as a positive regulator of ferroptosis by promoting ROS production.	Reactive Oxygen Species	92-95	P53	Homo sapiens	31-34
30450337-4	2018	p53 directly regulates the metabolic versatility of cells by favoring mitochondrial respiration, leading to ROS-mediated ferroptosis.	Reactive Oxygen Species	108-111	P53	Homo sapiens	0-3
30450337-5	2018	In mild stress, p53 protects cell survival via eliminating ROS; additionally, in human colorectal cancer, p53 antagonizes ferroptosis by formation of the DPP4-p53 complex.	Reactive Oxygen Species	59-62	P53	Homo sapiens	16-19
30450337-5	2018	In mild stress, p53 protects cell survival via eliminating ROS; additionally, in human colorectal cancer, p53 antagonizes ferroptosis by formation of the DPP4-p53 complex.	Reactive Oxygen Species	59-62	P53	Homo sapiens	106-109
30450337-5	2018	In mild stress, p53 protects cell survival via eliminating ROS; additionally, in human colorectal cancer, p53 antagonizes ferroptosis by formation of the DPP4-p53 complex.	Reactive Oxygen Species	59-62	P53	Homo sapiens	106-109
30450337-6	2018	In short, the mechanisms of p53-mediated ROS production underlying cellular response are poorly understood.	Reactive Oxygen Species	41-44	P53	Homo sapiens	28-31
30450337-7	2018	In the context of recent research results, the indistinct roles of p53 on ROS-mediated ferroptosis are scrutinized to understand the mechanism underlying p53-mediated tumor suppression.	Reactive Oxygen Species	74-77	P53	Homo sapiens	67-70
30450337-7	2018	In the context of recent research results, the indistinct roles of p53 on ROS-mediated ferroptosis are scrutinized to understand the mechanism underlying p53-mediated tumor suppression.	Reactive Oxygen Species	74-77	P53	Homo sapiens	154-157
30098371-3	2018	Activation of AMPK by the reduced ATP levels can induce inhibition of reactive oxygen species (ROS) production and activate p53-mediated DNA repair.	Adenosine Triphosphate	34-37	P53	Homo sapiens	124-127
30098371-7	2018	In our project we aim to understand the effects of metformin on p53 and DNA-BER system based on the oxidative status in type 2 diabetes patients.	Metformin	51-60	P53	Homo sapiens	64-67
30098371-10	2018	Although the increase in DNA pol beta was not significant, XRCC1 and p53 levels were significantly upregulated with metformin treatment in type 2 diabetes patients.	Metformin	116-125	P53	Homo sapiens	69-72
30103170-0	2018	Metronomic oral doxorubicin in combination of Chk1 inhibitor MK-8776 for p53-deficient breast cancer treatment.	Doxorubicin	16-27	P53	Homo sapiens	73-76
30103170-3	2018	In this light, within the limits of p53-deficient breast cancer, we demonstrate the enhanced anticancer effect of metronomic chemotherapy using doxorubicin when combined with Chk1 inhibitor MK-8776 by specifically augmenting the direct cytotoxic effect on cancer cells.	Doxorubicin	144-155	P53	Homo sapiens	36-39
30103170-5	2018	MK-8776 selectively enhanced the cytotoxic effect of low-concentration doxorubicin in p53-deficient breast cancer cells by abrogating the Chk1-dependent cell cycle arrest in vitro.	Doxorubicin	71-82	P53	Homo sapiens	86-89
30103170-6	2018	Consistently, combining MK-8776 significantly improved the anticancer effect of the daily administered oral doxorubicin in p53-deficient breast cancer xenografts especially in a lower dose of doxorubicin without evident systemic toxicities.	Doxorubicin	108-119	P53	Homo sapiens	123-126
30103170-7	2018	Combination therapy of MK-8776 and metronomic oral doxorubicin would be thus promising in the treatment of p53-deficient breast cancer benefited from the augmented direct cytotoxic effect and low risk of toxicities.	Doxorubicin	51-62	P53	Homo sapiens	107-110
30257366-10	2018	The real time PCR assay demonstrated that parthenolide down-regulated the expression of Bcl-2 and up-regulated the expression of E2F1, P53, GADD45, BAX, BIM, and CASP 3,7,8,9, which indicates an activation of P53- dependent apoptosis pathway in response to parthenolide.	parthenolide	42-54	P53	Homo sapiens	135-138
30257366-10	2018	The real time PCR assay demonstrated that parthenolide down-regulated the expression of Bcl-2 and up-regulated the expression of E2F1, P53, GADD45, BAX, BIM, and CASP 3,7,8,9, which indicates an activation of P53- dependent apoptosis pathway in response to parthenolide.	parthenolide	42-54	P53	Homo sapiens	209-212
29334793-6	2018	Moreover, Ru@MSNs induced ROS overproduction in cancer cells, leading to DNA damage and p53 phosphorylation, consequently promoting cancer cells apoptosis.	ros	26-29	P53	Homo sapiens	88-91
30366906-1	2018	Mutations in Trp53, prevalent in human cancer, are reported to drive tumorigenesis through dominant-negative effects (DNEs) over wild-type TRP53 function as well as neomorphic gain-of-function (GOF) activity.	dnes	118-122	P53	Homo sapiens	13-18
29941676-2	2018	We have detected a primate-specific adrenal androgen-mediated tumor suppression system in which circulating DHEAS is converted to DHEA specifically in cells in which TP53 has been inactivated DHEA is an uncompetitive inhibitor of glucose-6-phosphate dehydrogenase (G6PD), an enzyme indispensable for maintaining reactive oxygen species within limits survivable by the cell.	Reactive Oxygen Species	312-335	P53	Homo sapiens	166-170
29941676-6	2018	The triggering of these enzymes in the TP53-affected cell combines with the primate-specific G6PC promoter sequence motif that enables G6P substrate accumulation, driving uncompetitive inhibition of G6PD to irreversibility and ROS-mediated cell death.	Reactive Oxygen Species	227-230	P53	Homo sapiens	39-43
30132535-0	2018	Resveratrol inhibited the progression of human hepatocellular carcinoma by inducing autophagy via regulating p53 and the phosphoinositide 3-kinase/protein kinase B pathway.	Resveratrol	0-11	P53	Homo sapiens	109-112
30226600-0	2018	Rotundic acid enhances the impact of radiological toxicity on MCF-7 cells through the ATM/p53 pathway.	rotundic acid	0-13	P53	Homo sapiens	90-93
30226600-7	2018	Using western blotting, it was demonstrated that radiation induced the expression of ataxia-telangiectasia mutated (ATM) and p53 protein, and that RA enhanced this effect.	rotundic acid	147-149	P53	Homo sapiens	125-128
30226600-10	2018	These results suggest that the ATM/p53 pathway directly participates in radiation and RA-induced apoptosis in MCF-7 cells.	rotundic acid	86-88	P53	Homo sapiens	35-38
29970902-2	2018	P53-like muscle-invasive bladder cancers are generally resistant to cisplatin-based chemotherapy, but exhibit heterogeneous clinical outcomes with a prognosis intermediate to that of the luminal and basal subtypes.	Cisplatin	68-77	P53	Homo sapiens	0-3
30132535-7	2018	It was revealed that resveratrol upregulated the expression of p53 while decreasing the ratio of phosphorylated protein kinase B (p-Akt)/Akt in HCC cells.	Resveratrol	21-32	P53	Homo sapiens	63-66
30132535-8	2018	Treatment with p53 inhibitor pifithrin-alpha and Akt activator insulin-like growth factor-1 decreased the expression of Beclin1 while significantly promoting cell proliferation, invasion and migration compared with the resveratrol treatment group.	Resveratrol	219-230	P53	Homo sapiens	15-18
30132535-9	2018	Taken together, the results of the present study revealed that resveratrol inhibited the proliferation and mobility of HCC cells through inducing autophagy via activating p53 and inhibiting phosphoinositide 3-kinase/Akt.	Resveratrol	63-74	P53	Homo sapiens	171-174
30333875-0	2018	Antitumorigenic effect of damnacanthal on melanoma cell viability through p53 and NF-kappaB/caspase-3 signaling pathways.	damnacanthal	26-38	P53	Homo sapiens	74-77
30374014-10	2018	Transfection of wild-type p53 plasmid or treatments with cytotoxic reagents including irradiation and 5-FU all induced miR-492 overexpression.	Fluorouracil	102-106	P53	Homo sapiens	26-29
30333875-5	2018	Damnacanthal treatment increased caspase-3/8 and 9 activity, and promoted B-cell lymphoma 2-associated X protein, tumor protein p53 (p53) and p21 protein expression levels in melanoma cells.	damnacanthal	0-12	P53	Homo sapiens	128-131
30333875-5	2018	Damnacanthal treatment increased caspase-3/8 and 9 activity, and promoted B-cell lymphoma 2-associated X protein, tumor protein p53 (p53) and p21 protein expression levels in melanoma cells.	damnacanthal	0-12	P53	Homo sapiens	133-136
30375398-0	2018	The cisplatin-induced lncRNA PANDAR dictates the chemoresistance of ovarian cancer via regulating SFRS2-mediated p53 phosphorylation.	Cisplatin	4-13	P53	Homo sapiens	113-116
30375398-3	2018	In this study, we report that PANDAR serves as a negative regulator of cisplatin sensitivity in human ovarian cancer via PANDAR-SRFS2-p53 feedback regulation in nuclear.	Cisplatin	71-80	P53	Homo sapiens	134-137
30405800-7	2018	Furthermore, DOX resulted in increased alterations in DNA damage-related proteins such as p-ATM, p-Chk2, p-p53, p21 and gammaH2AX, but not p16.	Doxorubicin	13-16	P53	Homo sapiens	107-110
30405800-8	2018	Notably, the combination of dinaciclib and DOX inhibited cell growth and promoted senescence by transforming the suppressive effects of the ATM/Chk2/p53/p21 signaling pathway and enhancing the p16 signaling pathway.	Doxorubicin	43-46	P53	Homo sapiens	149-152
30375398-7	2018	Further investigation revealed that PANDAR-reduced cisplatin sensitivity was likely or partly due to the PANDAR-binding protein SFRS2 (arginine/serine-rich 2), a splicing factor with the ability to negative regulate p53 and its phosphorylation at Serine 15 (Ser15).	Cisplatin	51-60	P53	Homo sapiens	216-219
30375398-7	2018	Further investigation revealed that PANDAR-reduced cisplatin sensitivity was likely or partly due to the PANDAR-binding protein SFRS2 (arginine/serine-rich 2), a splicing factor with the ability to negative regulate p53 and its phosphorylation at Serine 15 (Ser15).	Arginine	135-143	P53	Homo sapiens	216-219
30375398-7	2018	Further investigation revealed that PANDAR-reduced cisplatin sensitivity was likely or partly due to the PANDAR-binding protein SFRS2 (arginine/serine-rich 2), a splicing factor with the ability to negative regulate p53 and its phosphorylation at Serine 15 (Ser15).	Serine	144-150	P53	Homo sapiens	216-219
30375398-7	2018	Further investigation revealed that PANDAR-reduced cisplatin sensitivity was likely or partly due to the PANDAR-binding protein SFRS2 (arginine/serine-rich 2), a splicing factor with the ability to negative regulate p53 and its phosphorylation at Serine 15 (Ser15).	Serine	247-253	P53	Homo sapiens	216-219
30375398-9	2018	In addition, in platinum-treated patients with relapsed ovarian cancer, resistant period was positively correlated with the expression of PANDAR and SFRS2, and inversely associated with expression of p53-Ser15 and PUMA in these clinical tissues.	Platinum	16-24	P53	Homo sapiens	200-203
30375484-3	2018	In cells with glucocorticoid receptor-alpha (GR) expression corresponding to higher clinical tumor levels, Dex-induced growth arrest was followed by marked cell expansion, beta-galactosidase expression and Ki67 negativity, despite variable p53 and K-RAS status.	Dexamethasone	107-110	P53	Homo sapiens	240-243
30555547-0	2018	MICAL2 Mediates p53 Ubiquitin Degradation through Oxidating p53 Methionine 40 and 160 and Promotes Colorectal Cancer Malignance.	Methionine	64-74	P53	Homo sapiens	16-19
30348672-7	2018	These events act in concert with a modest upregulation of p53 activity to limit the levels of reactive oxygen species (ROS).	Reactive Oxygen Species	94-117	P53	Homo sapiens	58-61
30348672-7	2018	These events act in concert with a modest upregulation of p53 activity to limit the levels of reactive oxygen species (ROS).	Reactive Oxygen Species	119-122	P53	Homo sapiens	58-61
30410974-6	2018	This signal was identified as norepinephrine, which was confirmed to stimulate invasion of ovarian cancer cells lacking wild-type p53.	Norepinephrine	30-44	P53	Homo sapiens	130-133
30555547-0	2018	MICAL2 Mediates p53 Ubiquitin Degradation through Oxidating p53 Methionine 40 and 160 and Promotes Colorectal Cancer Malignance.	Methionine	64-74	P53	Homo sapiens	60-63
30555547-14	2018	MICAL2 was also found to oxidize p53 at methionine 40 and 160, which mediated p53 ubiquitin degradation.	Methionine	40-50	P53	Homo sapiens	33-36
30555547-14	2018	MICAL2 was also found to oxidize p53 at methionine 40 and 160, which mediated p53 ubiquitin degradation.	Methionine	40-50	P53	Homo sapiens	78-81
30555549-6	2018	Results: AuNP-DPA were effectively enriched in tumor sites and subsequently internalized by cancer cells, thereby suppressing tumor growth via reactivating p53 signaling.	aunp-dpa	9-17	P53	Homo sapiens	156-159
30443171-7	2018	In addition, cisplatin significantly upregulated ATF3, phospho-P53(ser46), and cleaved caspase 3 expression in lung cancer cells, but overexpression of NDRG1 in the presence of cisplatin reduced the level of these proteins elevated by cisplatin (P &lt; 0.05).	Cisplatin	13-22	P53	Homo sapiens	63-66
30555549-7	2018	More importantly, through a series of in vivo experiments, AuNP-DPA showed excellent biosafety without the common side effects that hinder p53 therapies in clinic trials.	aunp-dpa	59-67	P53	Homo sapiens	139-142
30555549-8	2018	Conclusion: The present study not only sheds light on the development of AuNP-DPA as a novel class of antitumor agents for drugging the p53 pathway in vivo, but also supplies a new strategy to use D-peptides as intracellular PPI inhibitors for cancer-targeted therapy.	aunp-dpa	73-81	P53	Homo sapiens	136-139
30057300-0	2018	Role of Thiol Reactivity for Targeting Mutant p53.	Sulfhydryl Compounds	8-13	P53	Homo sapiens	46-49
30057300-2	2018	Recent studies have identified several mutant p53-reactivating compounds that target thiol groups in mutant p53.	Sulfhydryl Compounds	85-90	P53	Homo sapiens	46-49
30057300-2	2018	Recent studies have identified several mutant p53-reactivating compounds that target thiol groups in mutant p53.	Sulfhydryl Compounds	85-90	P53	Homo sapiens	108-111
30057300-4	2018	Analysis of the National Cancer Institute database revealed that Michael acceptors show the highest selectivity for mutant p53-expressing cells among analyzed thiol-reactive compounds.	Sulfhydryl Compounds	159-164	P53	Homo sapiens	123-126
30057300-5	2018	Further experimental testing demonstrated that Michael acceptors, aldehydes, imines, and primary alcohols can promote thermodynamic stabilization of mutant p53.	Alcohols	97-105	P53	Homo sapiens	156-159
30057300-6	2018	Moreover, mild thiol reactivity, often coupled with combined chemical functional groups, such as in imines, aldehydes, and primary alcohols, can stimulate mutant p53 refolding.	Sulfhydryl Compounds	15-20	P53	Homo sapiens	162-165
30057300-6	2018	Moreover, mild thiol reactivity, often coupled with combined chemical functional groups, such as in imines, aldehydes, and primary alcohols, can stimulate mutant p53 refolding.	Alcohols	131-139	P53	Homo sapiens	162-165
30217444-0	2018	ALDH2 mediates the dose-response protection of chronic ethanol against endothelial senescence through SIRT1/p53 pathway.	Ethanol	55-62	P53	Homo sapiens	108-111
30410558-4	2018	We found that the combined use of A549/DDP cells with SFI and cisplatin enhanced cell cycle arrested in the G2/M phase, which was accompanied by upregulation of p53 and p21 protein expression and induced mitochondrial apoptosis in conjunction with the upregulation of Bax and the downregulation of Bcl-2 protein expression.	Cisplatin	62-71	P53	Homo sapiens	161-164
30217444-5	2018	Furthermore, ALDH2 deficiency impairs the dose-response protection of ethanol against endothelial senescence by promoting the accumulation of 4-HNE, the formation of 4-HNE-SIRT1 protein adducts and the subsequent decrease in SIRT1-dependent p53 deacetylation.	Ethanol	70-77	P53	Homo sapiens	241-244
30405856-7	2018	The upregulated genes were enriched in cell cycle, ECM-receptor interaction, and p53 signaling pathway, while the downregulated genes were enriched in retrograde endocannabinoid signaling, glutamatergic synapse, morphine addiction, GABAergic synapse, and calcium signaling pathway.	Morphine	212-220	P53	Homo sapiens	81-84
30217444-6	2018	Collectively, our data indicate that ALDH2 mediates the protection of appropriate ethanol by modulating SIRT1/p53-dependent endothelial senescence.	Ethanol	82-89	P53	Homo sapiens	110-113
30217455-0	2018	4-Hydroxybenzoic acid (4-HBA) enhances the sensitivity of human breast cancer cells to adriamycin as a specific HDAC6 inhibitor by promoting HIPK2/p53 pathway.	Doxorubicin	87-97	P53	Homo sapiens	147-150
30217455-7	2018	4-HBA significantly promoted the anticancer effect of ADM on apoptosis induction, as evidenced by the increased expressions of Caspase-3 and PARP cleavage, which was associated with the promotion p53 and homeodomain interacting protein kinase-2 (HIPK2) expressions in ADM-resistant breast cancer cells.	Doxorubicin	54-57	P53	Homo sapiens	196-199
30215795-0	2018	The impact of p53 function on the metabolic activation of the carcinogenic air pollutant 3-nitrobenzanthrone and its metabolites 3-aminobenzanthrone and N-hydroxy-3-aminobenzanthrone in human cells.	3-aminobenzanthrone	129-148	P53	Homo sapiens	14-17
30215795-5	2018	Bioactivation of both metabolites 3-ABA and N-OH-3-ABA on the other hand was WT-TP53 dependent.	3-aminobenzanthrone	34-39	P53	Homo sapiens	80-84
30215795-5	2018	Bioactivation of both metabolites 3-ABA and N-OH-3-ABA on the other hand was WT-TP53 dependent.	n-oh-3-aba	44-54	P53	Homo sapiens	80-84
30215795-6	2018	Lower 3-ABA- and N-OH-3-ABA-DNA adduct levels were found in TP53(+/-) and TP53(-/-) cells compared to TP53(+/+) cells, and p53"s impact was attributed to differences in cytochrome P450 (CYP) 1A1 expression for 3-ABA whereas for N-OH-3-ABA, an impact of this tumour suppressor on sulphotransferase (SULT) 1A1/3 expression was detected.	3-aminobenzanthrone	6-11	P53	Homo sapiens	60-64
30215795-6	2018	Lower 3-ABA- and N-OH-3-ABA-DNA adduct levels were found in TP53(+/-) and TP53(-/-) cells compared to TP53(+/+) cells, and p53"s impact was attributed to differences in cytochrome P450 (CYP) 1A1 expression for 3-ABA whereas for N-OH-3-ABA, an impact of this tumour suppressor on sulphotransferase (SULT) 1A1/3 expression was detected.	3-aminobenzanthrone	6-11	P53	Homo sapiens	74-78
30215795-6	2018	Lower 3-ABA- and N-OH-3-ABA-DNA adduct levels were found in TP53(+/-) and TP53(-/-) cells compared to TP53(+/+) cells, and p53"s impact was attributed to differences in cytochrome P450 (CYP) 1A1 expression for 3-ABA whereas for N-OH-3-ABA, an impact of this tumour suppressor on sulphotransferase (SULT) 1A1/3 expression was detected.	3-aminobenzanthrone	6-11	P53	Homo sapiens	74-78
30215795-6	2018	Lower 3-ABA- and N-OH-3-ABA-DNA adduct levels were found in TP53(+/-) and TP53(-/-) cells compared to TP53(+/+) cells, and p53"s impact was attributed to differences in cytochrome P450 (CYP) 1A1 expression for 3-ABA whereas for N-OH-3-ABA, an impact of this tumour suppressor on sulphotransferase (SULT) 1A1/3 expression was detected.	n-oh-3-aba	17-27	P53	Homo sapiens	60-64
30215795-6	2018	Lower 3-ABA- and N-OH-3-ABA-DNA adduct levels were found in TP53(+/-) and TP53(-/-) cells compared to TP53(+/+) cells, and p53"s impact was attributed to differences in cytochrome P450 (CYP) 1A1 expression for 3-ABA whereas for N-OH-3-ABA, an impact of this tumour suppressor on sulphotransferase (SULT) 1A1/3 expression was detected.	n-oh-3-aba	17-27	P53	Homo sapiens	74-78
30215795-6	2018	Lower 3-ABA- and N-OH-3-ABA-DNA adduct levels were found in TP53(+/-) and TP53(-/-) cells compared to TP53(+/+) cells, and p53"s impact was attributed to differences in cytochrome P450 (CYP) 1A1 expression for 3-ABA whereas for N-OH-3-ABA, an impact of this tumour suppressor on sulphotransferase (SULT) 1A1/3 expression was detected.	n-oh-3-aba	17-27	P53	Homo sapiens	74-78
30215795-6	2018	Lower 3-ABA- and N-OH-3-ABA-DNA adduct levels were found in TP53(+/-) and TP53(-/-) cells compared to TP53(+/+) cells, and p53"s impact was attributed to differences in cytochrome P450 (CYP) 1A1 expression for 3-ABA whereas for N-OH-3-ABA, an impact of this tumour suppressor on sulphotransferase (SULT) 1A1/3 expression was detected.	n-oh-3-aba	17-27	P53	Homo sapiens	123-126
30215795-6	2018	Lower 3-ABA- and N-OH-3-ABA-DNA adduct levels were found in TP53(+/-) and TP53(-/-) cells compared to TP53(+/+) cells, and p53"s impact was attributed to differences in cytochrome P450 (CYP) 1A1 expression for 3-ABA whereas for N-OH-3-ABA, an impact of this tumour suppressor on sulphotransferase (SULT) 1A1/3 expression was detected.	3-aminobenzanthrone	22-27	P53	Homo sapiens	60-64
30215795-6	2018	Lower 3-ABA- and N-OH-3-ABA-DNA adduct levels were found in TP53(+/-) and TP53(-/-) cells compared to TP53(+/+) cells, and p53"s impact was attributed to differences in cytochrome P450 (CYP) 1A1 expression for 3-ABA whereas for N-OH-3-ABA, an impact of this tumour suppressor on sulphotransferase (SULT) 1A1/3 expression was detected.	3-aminobenzanthrone	22-27	P53	Homo sapiens	74-78
30215795-6	2018	Lower 3-ABA- and N-OH-3-ABA-DNA adduct levels were found in TP53(+/-) and TP53(-/-) cells compared to TP53(+/+) cells, and p53"s impact was attributed to differences in cytochrome P450 (CYP) 1A1 expression for 3-ABA whereas for N-OH-3-ABA, an impact of this tumour suppressor on sulphotransferase (SULT) 1A1/3 expression was detected.	3-aminobenzanthrone	22-27	P53	Homo sapiens	74-78
30215795-6	2018	Lower 3-ABA- and N-OH-3-ABA-DNA adduct levels were found in TP53(+/-) and TP53(-/-) cells compared to TP53(+/+) cells, and p53"s impact was attributed to differences in cytochrome P450 (CYP) 1A1 expression for 3-ABA whereas for N-OH-3-ABA, an impact of this tumour suppressor on sulphotransferase (SULT) 1A1/3 expression was detected.	n-oh-3-aba	228-238	P53	Homo sapiens	60-64
30215795-6	2018	Lower 3-ABA- and N-OH-3-ABA-DNA adduct levels were found in TP53(+/-) and TP53(-/-) cells compared to TP53(+/+) cells, and p53"s impact was attributed to differences in cytochrome P450 (CYP) 1A1 expression for 3-ABA whereas for N-OH-3-ABA, an impact of this tumour suppressor on sulphotransferase (SULT) 1A1/3 expression was detected.	n-oh-3-aba	228-238	P53	Homo sapiens	74-78
30215795-6	2018	Lower 3-ABA- and N-OH-3-ABA-DNA adduct levels were found in TP53(+/-) and TP53(-/-) cells compared to TP53(+/+) cells, and p53"s impact was attributed to differences in cytochrome P450 (CYP) 1A1 expression for 3-ABA whereas for N-OH-3-ABA, an impact of this tumour suppressor on sulphotransferase (SULT) 1A1/3 expression was detected.	n-oh-3-aba	228-238	P53	Homo sapiens	74-78
30215795-6	2018	Lower 3-ABA- and N-OH-3-ABA-DNA adduct levels were found in TP53(+/-) and TP53(-/-) cells compared to TP53(+/+) cells, and p53"s impact was attributed to differences in cytochrome P450 (CYP) 1A1 expression for 3-ABA whereas for N-OH-3-ABA, an impact of this tumour suppressor on sulphotransferase (SULT) 1A1/3 expression was detected.	n-oh-3-aba	228-238	P53	Homo sapiens	123-126
30303965-4	2018	Biological methods demonstrated the oxidative damage of P19 neurons and showed that quercetin improved neuronal survival by preventing H2O2-induced p53 and Bcl-2 down-regulation and modulated Akt and ERK1/2 signalling pathways.	Hydrogen Peroxide	135-139	P53	Homo sapiens	148-151
30405856-7	2018	The upregulated genes were enriched in cell cycle, ECM-receptor interaction, and p53 signaling pathway, while the downregulated genes were enriched in retrograde endocannabinoid signaling, glutamatergic synapse, morphine addiction, GABAergic synapse, and calcium signaling pathway.	Calcium	255-262	P53	Homo sapiens	81-84
30241011-4	2018	Cu complexes exerted chemotherapeutic effects via activating p53 and inducing production of reactive oxygen species to regulate expression of the B-cell lymphoma-2 family of proteins, causing a change in the mitochondrial membrane potential and release of cytochrome c to form a dimer with apoptosis protease activating factor-1, resulting in activation of caspase-9/3 to induce apoptosis.	Copper	0-2	P53	Homo sapiens	61-64
30205260-0	2018	Novel tacrine platinum(II) complexes display high anticancer activity via inhibition of telomerase activity, dysfunction of mitochondria, and activation of the p53 signaling pathway.	Platinum	14-22	P53	Homo sapiens	160-163
30003648-7	2018	Moreover, we observe that ROS produced by MAO-A lead to the accumulation of p53 in the cytosol where it inhibits parkin, an important regulator of mitophagy, resulting in mitochondrial dysfunction.	Reactive Oxygen Species	26-29	P53	Homo sapiens	76-79
30305801-1	2018	Background: p16 and p53 genes are frequently mutated in triple negative breast cancer &amp; prognostic value of these mutations have been shown; however, their role as immunohistochemical overexpression has not been fully validated.	Adenosine Monophosphate	87-90	P53	Homo sapiens	20-23
30283098-2	2018	ROS and RNS can influence tumor cell malignancy via the redox-regulated transcription factor NF-kappaB, whose activation is further regulated by the mutation status of p53.	Reactive Oxygen Species	0-3	P53	Homo sapiens	168-171
30283098-5	2018	Nanoparticle activity was related to the decreased level of intracellular ROS and RNS, which downregulated NF-kappaB signaling depending on the p53 status of the cell line.	Reactive Oxygen Species	74-77	P53	Homo sapiens	144-147
30349639-0	2018	Unfolding the roles of resveratrol in p53 regulation.	Resveratrol	23-34	P53	Homo sapiens	38-41
30318520-0	2018	Mutant p53 blocks SESN1/AMPK/PGC-1alpha/UCP2 axis increasing mitochondrial O2-  production in cancer cells.	Oxygen	75-77	P53	Homo sapiens	7-10
30120489-0	2018	Replica to the Opinion Letter regarding the article "Sensitization of colorectal cancer cells to irinotecan by the Survivin inhibitor LLP3 depends on XAF1 proficiency in the context of mutated p53" (Arch Toxicol https://doi.org/10.1007/s00204-018-240-x).	Irinotecan	97-107	P53	Homo sapiens	193-196
30096294-4	2018	We found that strong activation of p53, marked by serine 46 and 392 phosphorylation, was associated with inactivating phosphorylation of proapoptotic BAD protein on serine 136.	Serine	50-56	P53	Homo sapiens	35-38
30096294-4	2018	We found that strong activation of p53, marked by serine 46 and 392 phosphorylation, was associated with inactivating phosphorylation of proapoptotic BAD protein on serine 136.	Serine	165-171	P53	Homo sapiens	35-38
30096294-6	2018	The accumulation of PIM2 following treatment with A + N was suppressed in p53-knockdown cells.	Ethanol	50-55	P53	Homo sapiens	74-77
30096294-9	2018	Moreover, we found that in A549 cells, the treatment with A + N stimulated in p53-dependent fashion the expression of other high cooperativity p53 target genes, DRAXIN and H19.	Ethanol	58-63	P53	Homo sapiens	78-81
30096294-9	2018	Moreover, we found that in A549 cells, the treatment with A + N stimulated in p53-dependent fashion the expression of other high cooperativity p53 target genes, DRAXIN and H19.	Ethanol	58-63	P53	Homo sapiens	143-146
30059758-4	2018	Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-).	Fluorouracil	104-118	P53	Homo sapiens	43-46
30059758-4	2018	Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-).	Fluorouracil	104-118	P53	Homo sapiens	261-264
30059758-4	2018	Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-).	Fluorouracil	104-118	P53	Homo sapiens	261-264
30059758-4	2018	Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-).	Fluorouracil	120-124	P53	Homo sapiens	43-46
30059758-4	2018	Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-).	Fluorouracil	120-124	P53	Homo sapiens	261-264
30059758-4	2018	Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-).	Fluorouracil	120-124	P53	Homo sapiens	261-264
30059758-10	2018	In conclusion, in p53wt colon cancer cells chemosensitivity against oxaliplatin or 5-FU could be enhanced by downregulation of CerS5 expression leading to reduced autophagy and mitochondrial respiration.	Fluorouracil	83-87	P53	Homo sapiens	18-21
30318520-5	2018	We also show a correlation between the decrease of reduced thiols with a poorer clinical outcome of CLL patients bearing mutant TP53 gene.	Sulfhydryl Compounds	59-65	P53	Homo sapiens	128-132
30318520-6	2018	The restoration of the mitochondrial uncoupling protein 2 (UCP2) expression, as well as the addition of the radical scavenger N-acetyl-L-cysteine, reversed the oncogenic effects of mutant p53 as cellular hyper-proliferation, antiapoptotic effect, and resistance to drugs.	Acetylcysteine	126-145	P53	Homo sapiens	188-191
30285883-7	2018	Testing this, we found that estrogen receptor-positive, TP53 wild-type breast cancer cells that were made senescent by doxorubicin treatment were sensitive to tamoxifen.	Doxorubicin	119-130	P53	Homo sapiens	56-60
30285883-7	2018	Testing this, we found that estrogen receptor-positive, TP53 wild-type breast cancer cells that were made senescent by doxorubicin treatment were sensitive to tamoxifen.	Tamoxifen	159-168	P53	Homo sapiens	56-60
30341510-15	2018	High glucose led to high expression of p53, p21, Rb, p-stat1 and p-stat3 and premature senescence of HGMCs by activating the telomere-p53-p21-Rb and JAK/STAT signaling pathways.	Glucose	5-12	P53	Homo sapiens	39-42
29334602-7	2018	The combination of TMZ and metformin enhanced AMPK phosphorylation and inhibited mammalian target of rapamycin phosphorylation, AKT phosphorylation, and p53 expression.	Metformin	27-36	P53	Homo sapiens	153-156
30076608-3	2018	EXPERIMENTAL APPROACH: Anti-proliferative activity of the (R)-tryptophanol-derived bicyclic lactam SYNAP was evaluated in a range of human cancer cells with different p53 status.	D-Tryptophanol	58-74	P53	Homo sapiens	167-170
30341510-15	2018	High glucose led to high expression of p53, p21, Rb, p-stat1 and p-stat3 and premature senescence of HGMCs by activating the telomere-p53-p21-Rb and JAK/STAT signaling pathways.	Glucose	5-12	P53	Homo sapiens	134-137
29405768-5	2018	The MEK inhibitor PD98059 and ERK1/2 siRNA significantly inhibited apoptosis, ERK1/2 activation, as well as p53 and phospho-p53 (serine-15) levels in human lymphoblasts undergoing DEB-induced apoptosis.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	18-25	P53	Homo sapiens	124-127
30056083-3	2018	Compared to 5-FU alone, MH synergistically enhanced the chemotherapeutic effects of 5-FU, by reducing cell proliferation through the suppression of EGFR, HER2, p-Akt and p-mTOR expression, and promoting apoptosis by the modulation pro-apoptotic (p53, Bax, Cyto c, FasL caspase-3, -8, -9 and cleave-PARP) and anti-apoptotic (Bcl-2) markers.	Fluorouracil	84-88	P53	Homo sapiens	246-249
30066859-8	2018	The results of western blot analysis revealed that TCDD increased the protein levels of p53, Rb, p21, and regucalcin, which are suppressors of the growth of tumor cells.	Polychlorinated Dibenzodioxins	51-55	P53	Homo sapiens	88-91
30236029-2	2018	The results showed that matrine (&gt;=10 muM) caused a significant inhibition on cell viability and 10 and 100 muM matrine induced cell apoptosis via influencing p53, bax, casp3, and bcl-2 expressions in A549 cells.	matrine	24-31	P53	Homo sapiens	162-165
30085332-0	2018	Radiosensitization by irinotecan is attributed to G2/M phase arrest, followed by enhanced apoptosis, probably through the ATM/Chk/Cdc25C/Cdc2 pathway in p53-mutant colorectal cancer cells.	Irinotecan	22-32	P53	Homo sapiens	153-156
30085332-4	2018	In the present study, we examined the radiosensitizing effects of irinotecan on the p53-mutant colorectal cancer cell lines, HT29 and SW620, and explored the potential underlying mechanisms.	Irinotecan	66-76	P53	Homo sapiens	84-87
29405768-5	2018	The MEK inhibitor PD98059 and ERK1/2 siRNA significantly inhibited apoptosis, ERK1/2 activation, as well as p53 and phospho-p53 (serine-15) levels in human lymphoblasts undergoing DEB-induced apoptosis.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	18-25	P53	Homo sapiens	108-111
29803744-5	2018	SIRT1 protein level in ADSCs was increased by the treatment with H2O2, meanwhile, H2O2 activated p53-depended apoptosis in high concentration.	Hydrogen Peroxide	65-69	P53	Homo sapiens	97-100
29803744-5	2018	SIRT1 protein level in ADSCs was increased by the treatment with H2O2, meanwhile, H2O2 activated p53-depended apoptosis in high concentration.	Hydrogen Peroxide	82-86	P53	Homo sapiens	97-100
30085332-11	2018	In addition, the expression of Ser216p-Cdc25C was also increased in the combined group, indicating that irinotecan likely radiosensitized the p53-mutant HT29 and SW620 cells through the ATM/Chk/Cdc25C/Cdc2 pathway.	Irinotecan	104-114	P53	Homo sapiens	142-145
29665004-0	2018	Thiostrepton degrades mutant p53 by eliciting an autophagic response in SW480 cells.	Thiostrepton	0-12	P53	Homo sapiens	29-32
29665004-4	2018	In order to elucidate the mechanism of thiostrepton triggered mutant p53 degradation, we explored the impact of proteasome inhibition on activation of autophagy.	Thiostrepton	39-51	P53	Homo sapiens	69-72
29665004-5	2018	Combined treatment of thiostrepton and cycloheximide/chloroquine prevented the degradation of mutant p53 protein, reinforcing autophagy as the means of mutant p53 destabilization.	Thiostrepton	22-34	P53	Homo sapiens	101-104
29665004-5	2018	Combined treatment of thiostrepton and cycloheximide/chloroquine prevented the degradation of mutant p53 protein, reinforcing autophagy as the means of mutant p53 destabilization.	Thiostrepton	22-34	P53	Homo sapiens	159-162
29665004-7	2018	Subsequent interactome analysis performed post thiostrepton treatment revealed an association of p53 with autophagosome complex associated proteins such as BAG3, p62 and HSC70.	Thiostrepton	47-59	P53	Homo sapiens	97-100
29665004-8	2018	Reaccumulation of p53 was seen in BAG3 silenced cells treated with thiostrepton, thereby confirming the role of BAG3 in destabilization of this molecule.	Thiostrepton	67-79	P53	Homo sapiens	18-21
29580868-6	2018	We then proved that TRPV1 overexpression or its agonist capsaicin treatment inhibited melanoma growth by activating p53 and inducing cell apoptosis.	Capsaicin	56-65	P53	Homo sapiens	116-119
30774789-2	2018	Our research was aimed to study p53 protein codon 72 polymorphism, a single base pair change of either arginine (Arg; CGC) or proline (Pro; CCC) that creates 3 distinct genotypes in reticular oral lichen planus (OLP) in comparison to oral SCC which is the most common oral mucosal malignancy as positive control and inflammatory fibrous hyperplasia (IFH) lesion as negative control.	Arginine	103-111	P53	Homo sapiens	32-35
30774789-2	2018	Our research was aimed to study p53 protein codon 72 polymorphism, a single base pair change of either arginine (Arg; CGC) or proline (Pro; CCC) that creates 3 distinct genotypes in reticular oral lichen planus (OLP) in comparison to oral SCC which is the most common oral mucosal malignancy as positive control and inflammatory fibrous hyperplasia (IFH) lesion as negative control.	Arginine	113-116	P53	Homo sapiens	32-35
30197676-2	2018	RBEL1A may block the transcriptional activity of p53, which is important in the induction of cisplatin sensitivity.	Cisplatin	93-102	P53	Homo sapiens	49-52
29974318-2	2018	In the present study, we investigated the preventive effects of curcumin against AFB1-induced apoptosis through the molecular regulation of p53, caspase-3, Bax, caspase-9, Bcl-2 and cytochrome-C associated with mitochondrial pathway.	Curcumin	64-72	P53	Homo sapiens	140-143
30106452-7	2018	Platinum increased p53 and p-p53 (ser15) in a time-dependent manner in 3D cultures.	Platinum	0-8	P53	Homo sapiens	19-22
30197676-6	2018	Consistent with previous studies, the present study demonstrated that cisplatin treatment and RBEL1A overexpression blocked the oligomerization of p53 in MCF-7 cells and led to a decrease of the transcriptional activity of p53 and its downstream target gene p21.	Cisplatin	70-79	P53	Homo sapiens	147-150
30106452-7	2018	Platinum increased p53 and p-p53 (ser15) in a time-dependent manner in 3D cultures.	Platinum	0-8	P53	Homo sapiens	29-32
30197676-6	2018	Consistent with previous studies, the present study demonstrated that cisplatin treatment and RBEL1A overexpression blocked the oligomerization of p53 in MCF-7 cells and led to a decrease of the transcriptional activity of p53 and its downstream target gene p21.	Cisplatin	70-79	P53	Homo sapiens	223-226
30106452-9	2018	Under 3D culture condition, knockdown of integrin beta4 did not detectably change the basal p53 protein level but increased p53 and p-p53 (ser15) protein accumulation induced by platinum.	Platinum	178-186	P53	Homo sapiens	124-127
30106452-9	2018	Under 3D culture condition, knockdown of integrin beta4 did not detectably change the basal p53 protein level but increased p53 and p-p53 (ser15) protein accumulation induced by platinum.	Platinum	178-186	P53	Homo sapiens	124-127
30197676-11	2018	Taken together, these results suggest that the induction of RBEL1A following cisplatin treatment may partially inhibit chemosensitivity in a p53-dependent manner.	Cisplatin	77-86	P53	Homo sapiens	141-144
30106452-11	2018	Knockdown of wild-type p53 decreased sensitivity to platinum in 3D cultures.	Platinum	52-60	P53	Homo sapiens	23-26
30173893-0	2018	Paclitaxel promotes lung cancer cell apoptosis via MEG3-P53 pathway activation.	Paclitaxel	0-10	P53	Homo sapiens	56-59
30106452-12	2018	Since it has been proven that platinum damages DNA to kill cells and p53 plays a key role in the DNA damage response, our results indicated that integrin beta4 reduced DNA damage-induced p53 activation to decrease chemosensitivity in CRC.	Platinum	30-38	P53	Homo sapiens	187-190
30355102-11	2018	Moreover, oxygen and glucose deprivation promoted MDM2 binding with p53 in neurons.	Oxygen	10-16	P53	Homo sapiens	68-71
30355102-12	2018	Disruption of the MDM2-p53 interaction with nutlin-3a, or MDM2 knockdown by siRNA, triggered p53 accumulation, which increased neuronal susceptibility to oxygen and glucose deprivation-induced apoptosis.	Oxygen	154-160	P53	Homo sapiens	23-26
30355102-12	2018	Disruption of the MDM2-p53 interaction with nutlin-3a, or MDM2 knockdown by siRNA, triggered p53 accumulation, which increased neuronal susceptibility to oxygen and glucose deprivation-induced apoptosis.	Oxygen	154-160	P53	Homo sapiens	93-96
30173893-10	2018	PTX significantly inhibited the proliferation of NSCLC cells and increased the expressions of MEG3 and P53.	Paclitaxel	0-3	P53	Homo sapiens	103-106
30173893-13	2018	Our results suggest that the MEG3-P53 pathway is involved in the apoptosis of A549 cells induced by PTX.	Paclitaxel	100-103	P53	Homo sapiens	34-37
30121551-3	2018	In human renal proximal tubule (human kidney 2 [HK-2]) cells, inhibition of p53 by PIF reduced the high glucose (HG)-induced extracellular matrix (ECM) accumulation and reversed the inhibitory effect of HG on mRNA expression levels of lncRNA zinc finger E-box binding homeobox1-antisense RNA 1 (ZEB1-AS1) and ZEB1.	Glucose	104-111	P53	Homo sapiens	76-79
30258081-5	2018	Metabolome profiling reveals that niclosamide induces mitochondrial uncoupling, which renders mutant p53 cells susceptible to mitochondrial-dependent apoptosis through preferential accumulation of arachidonic acid (AA), and represents a first-in-class inhibitor of p53 mutant tumors.	Arachidonic Acid	197-213	P53	Homo sapiens	101-104
30141807-10	2018	Our data indicate that lipin1 overexpression may cause reduction of intracellular iron content, which could activate the p53-p21-p27 signaling pathways, leading to cell cycle arrest at the G0/G1 phase in the hepatic carcinoma cells.	Iron	82-86	P53	Homo sapiens	121-124
30217020-0	2018	A New Synthetic Histone Deacetylase Inhibitor, MHY2256, Induces Apoptosis and Autophagy Cell Death in Endometrial Cancer Cells via p53 Acetylation.	mhy2256	47-54	P53	Homo sapiens	131-134
30217020-1	2018	We previously discovered a novel sirtuin (SIRT) inhibitor, MHY2256, that exerts anticancer activity through p53 acetylation in MCF-7 human breast cancer cells.	mhy2256	59-66	P53	Homo sapiens	108-111
30245854-11	2018	After doxorubicin treatment, Thr454-phosphorylation of DBC1, required to inhibit deacetylation of p53 by SIRT1, was decreased and therefore acetylation of p53 was also decreased with KLLN knockdown.	Doxorubicin	6-17	P53	Homo sapiens	98-101
30245854-11	2018	After doxorubicin treatment, Thr454-phosphorylation of DBC1, required to inhibit deacetylation of p53 by SIRT1, was decreased and therefore acetylation of p53 was also decreased with KLLN knockdown.	Doxorubicin	6-17	P53	Homo sapiens	155-158
30280037-9	2018	Analysis using the cBio portal indicated that aspirin might have effects on multiple tumor suppressors, such as TP53, PTEN, and RB1 and that TP53 might play a central role in aspirin-associated genes.	Aspirin	46-53	P53	Homo sapiens	112-116
30280037-9	2018	Analysis using the cBio portal indicated that aspirin might have effects on multiple tumor suppressors, such as TP53, PTEN, and RB1 and that TP53 might play a central role in aspirin-associated genes.	Aspirin	175-182	P53	Homo sapiens	141-145
30257423-4	2018	Nano-TQ effectively augments the anticancer roles of doxorubicin by upregulation of P53 and downregulation of Bcl2 and potentiates paclitaxel"s apoptosis in MCF-7 breast cancer cells.	Doxorubicin	53-64	P53	Homo sapiens	84-87
30237857-3	2018	TX-induced stress signal was transmitted by protein kinase (ATM &amp; ATR) and phosphorylation of its downstream targets CHK1, CHK2, ATM, and ATR, respectively at the Ser 345, Thr68, Ser1981 and Ser 428 residues involved in complex disruption and p53 up-regulation.	Serine	167-170	P53	Homo sapiens	247-250
30282320-0	2018	Dimetallic Ru(II) arene complexes appended on bis-salicylaldimine induce cancer cell death and suppress invasion via p53-dependent signaling.	bis-salicylaldimine	46-65	P53	Homo sapiens	117-120
30282320-13	2018	Taken together, we demonstrated that bis-salicylaldimine based dimetallic Ru-(p-cymene) complexes exerts anticancer effects by p53 pathway, suggesting the promising chemotherapeutic potentials of these Ru(II) complexes for the treatment of cancer.	bis-salicylaldimine	37-56	P53	Homo sapiens	127-130
30237857-3	2018	TX-induced stress signal was transmitted by protein kinase (ATM &amp; ATR) and phosphorylation of its downstream targets CHK1, CHK2, ATM, and ATR, respectively at the Ser 345, Thr68, Ser1981 and Ser 428 residues involved in complex disruption and p53 up-regulation.	Serine	183-186	P53	Homo sapiens	247-250
30211098-7	2018	Expression of mutant p53 protein from NPC tissue paraffin block with immunohistochemical cracking technique was using monoclonal rabbit Anti Human p53 clone 318-6-11 (Dako, North America, Inc., 6392 Via Real Carpinteria, CA 93013 USA), microscope light binoculars was assessed visually by an Anatomical Pathology Consultant.	Paraffin	49-57	P53	Homo sapiens	21-24
29775409-5	2018	Exposure to a low dose of doxorubicin (Doxo) induced similar DNA damage and DNA damage response (DDR) as measured by RAD50 and MRE11 expression, checkpoint kinase 2 activation, and gammaH2A.X recruitment at DNA strand breaks in both cell groups, indicating that silence of p53-TAD does not affect the DDR mechanism upstream of p53.	Doxorubicin	26-37	P53	Homo sapiens	273-276
29775409-5	2018	Exposure to a low dose of doxorubicin (Doxo) induced similar DNA damage and DNA damage response (DDR) as measured by RAD50 and MRE11 expression, checkpoint kinase 2 activation, and gammaH2A.X recruitment at DNA strand breaks in both cell groups, indicating that silence of p53-TAD does not affect the DDR mechanism upstream of p53.	Doxorubicin	26-37	P53	Homo sapiens	327-330
29775409-5	2018	Exposure to a low dose of doxorubicin (Doxo) induced similar DNA damage and DNA damage response (DDR) as measured by RAD50 and MRE11 expression, checkpoint kinase 2 activation, and gammaH2A.X recruitment at DNA strand breaks in both cell groups, indicating that silence of p53-TAD does not affect the DDR mechanism upstream of p53.	Doxorubicin	39-43	P53	Homo sapiens	273-276
29775409-5	2018	Exposure to a low dose of doxorubicin (Doxo) induced similar DNA damage and DNA damage response (DDR) as measured by RAD50 and MRE11 expression, checkpoint kinase 2 activation, and gammaH2A.X recruitment at DNA strand breaks in both cell groups, indicating that silence of p53-TAD does not affect the DDR mechanism upstream of p53.	Doxorubicin	39-43	P53	Homo sapiens	327-330
29482350-7	2018	Knowing that TP53 is an antioncogene protein that acts as a tumor suppressor and regulator of apoptosis, the lowest frequency of Arg/Arg genotype observed in these high-risk patients may indicate lower protection from the atherosclerosis process.	Arginine	129-132	P53	Homo sapiens	13-17
29482350-7	2018	Knowing that TP53 is an antioncogene protein that acts as a tumor suppressor and regulator of apoptosis, the lowest frequency of Arg/Arg genotype observed in these high-risk patients may indicate lower protection from the atherosclerosis process.	Arginine	133-136	P53	Homo sapiens	13-17
30280787-11	2018	RESULTS: Growing levels of DUSP, aging proteins P53 and P16, with inhibition of TLR4 signal pathway were found in the H2O2-induced aging model of myeloma cell line RPMI8226.	Hydrogen Peroxide	118-122	P53	Homo sapiens	48-51
30194148-2	2018	Here, the effect of vitamin D on p53-positive DU4475 cells and its ability to decrease the IC50 of PTX in these cells were investigated.	Vitamin D	20-29	P53	Homo sapiens	33-36
29777905-10	2018	Moreover, changes in ADI1 (biosynthetic) and SAT1 (catabolic) partially depended on the iron-regulated changes in c-Myc and/or p53.	Iron	88-92	P53	Homo sapiens	127-130
29185360-0	2018	Role of metformin on base excision repair pathway in p53 wild-type H2009 and HepG2 cancer cells.	Metformin	8-17	P53	Homo sapiens	53-56
29185360-3	2018	The understanding of the participation of oxidative stress in the action mechanism of metformin and its related effects on p53 and on DNA base excision repair (BER) system can help us to get closer to solve metformin puzzle in cancer.	Metformin	86-95	P53	Homo sapiens	123-126
29964297-13	2018	P53 expression followed by LPS-induced inflammation was also be restricted by suppressing ROS generation.	Reactive Oxygen Species	90-93	P53	Homo sapiens	0-3
30317268-0	2018	Evaluation of correlation between expression of P53 and Malondialdehyde levels in prostate cancer patients.	Malondialdehyde	56-71	P53	Homo sapiens	48-51
30317268-1	2018	The analytical study was conducted at the National University of Sciences and Technology, Islamabad, Pakistan from Nov 2012 to Nov 2013 to find out, correlate and assess negative correlation of serum malondialdehyde (MDA) with expression of p53 gene, and comprised 32 samples.	Malondialdehyde	200-215	P53	Homo sapiens	241-244
29916532-8	2018	Resveratrol induced the ROS-p38-p53 pathway by increasing the gene expression of phosphorylated p38 mitogen-activated protein kinase, while it induced the p53 and ER stress pathway by increasing the gene expression levels of phosphorylated eukaryotic initiation factor 2alpha and C/EBP homologous protein.	Resveratrol	0-11	P53	Homo sapiens	32-35
29916532-8	2018	Resveratrol induced the ROS-p38-p53 pathway by increasing the gene expression of phosphorylated p38 mitogen-activated protein kinase, while it induced the p53 and ER stress pathway by increasing the gene expression levels of phosphorylated eukaryotic initiation factor 2alpha and C/EBP homologous protein.	Resveratrol	0-11	P53	Homo sapiens	155-158
29916532-8	2018	Resveratrol induced the ROS-p38-p53 pathway by increasing the gene expression of phosphorylated p38 mitogen-activated protein kinase, while it induced the p53 and ER stress pathway by increasing the gene expression levels of phosphorylated eukaryotic initiation factor 2alpha and C/EBP homologous protein.	Reactive Oxygen Species	24-27	P53	Homo sapiens	32-35
29916532-9	2018	The enhanced ROS-p38-p53 and ER stress pathways promoted apoptosis by downregulating B-cell lymphoma-2 (Bcl-2) expression and upregulating Bcl-2-associated X protein expression.	Reactive Oxygen Species	13-16	P53	Homo sapiens	21-24
29702749-3	2018	The topical application of melatonin, AFMK, or NAS protected epidermal cells against UVB-induced 8-OHdG formation and apoptosis with a further increase in p53ser15 expression, especially after application of melatonin or AFMK but not after NAS use.	Melatonin	27-36	P53	Homo sapiens	155-158
29702749-3	2018	The topical application of melatonin, AFMK, or NAS protected epidermal cells against UVB-induced 8-OHdG formation and apoptosis with a further increase in p53ser15 expression, especially after application of melatonin or AFMK but not after NAS use.	Melatonin	208-217	P53	Homo sapiens	155-158
29964297-14	2018	CONCLUSIONS: The present study shows that LPS-induced inflammation in HGFs is partially dependent on P53 modulating ROS and ROS stimulating P53, which suggests that P53 and ROS may form a feedback loop.	Reactive Oxygen Species	116-119	P53	Homo sapiens	101-104
29964297-14	2018	CONCLUSIONS: The present study shows that LPS-induced inflammation in HGFs is partially dependent on P53 modulating ROS and ROS stimulating P53, which suggests that P53 and ROS may form a feedback loop.	Reactive Oxygen Species	124-127	P53	Homo sapiens	101-104
29964297-14	2018	CONCLUSIONS: The present study shows that LPS-induced inflammation in HGFs is partially dependent on P53 modulating ROS and ROS stimulating P53, which suggests that P53 and ROS may form a feedback loop.	Reactive Oxygen Species	124-127	P53	Homo sapiens	101-104
29464864-8	2018	A further case study in breast invasive carcinoma (BRCA) found that DRCE expression was consistent with the drug response pattern and the aberrant expression of the two NEAT1-related DRCEs may lead to poor response to tamoxifen therapy for patients with TP53 mutations.	Tamoxifen	218-227	P53	Homo sapiens	254-258
30031063-0	2018	Resveratrol sensitizes lung cancer cell to TRAIL by p53 independent and suppression of Akt/NF-kappaB signaling.	Resveratrol	0-11	P53	Homo sapiens	52-55
30031063-10	2018	FINDINGS: Resveratrol is a polyphenolic compound capable of activation of tumor suppressor p53 and its pro-apoptotic modulator PUMA.	Resveratrol	10-21	P53	Homo sapiens	91-94
29853027-7	2018	The sensitive for specific p53 detection was achieved due to the facile magnetic separation from the complex condition, and the reduced non-specific absorption effect by dextran.	Dextrans	170-177	P53	Homo sapiens	27-30
30154459-0	2018	Tolerance to sustained activation of the cAMP/Creb pathway activity in osteoblastic cells is enabled by loss of p53.	Cyclic AMP	41-45	P53	Homo sapiens	112-115
30154459-5	2018	Normal osteoblasts (p53 WT) rapidly underwent apoptosis in response to acute elevation of cAMP levels or activity, whereas p53-deficient osteoblasts tolerated this aberrant cAMP/Creb level and activity.	Cyclic AMP	173-177	P53	Homo sapiens	123-126
30154459-6	2018	Using the p53 activating small-molecule Nutlin-3a and cAMP/Creb1 activator forskolin, we addressed the question of how p53 responds to the activation of cAMP.	Cyclic AMP	153-157	P53	Homo sapiens	119-122
30154459-7	2018	We observed that p53 acts dominantly to protect cells from excessive cAMP accumulation.	Cyclic AMP	69-73	P53	Homo sapiens	17-20
30154459-10	2018	This highlights the cAMP/Creb axis as a potentially actionable therapeutic vulnerability in p53-deficient tumors such as OS.	Cyclic AMP	20-24	P53	Homo sapiens	92-95
30154459-11	2018	These results define a mechanism through which p53 protects normal osteoblasts from excessive or abnormal cAMP accumulation, which becomes fundamentally compromised in OS.	Cyclic AMP	106-110	P53	Homo sapiens	47-50
30142917-0	2018	Induction of p53 Phosphorylation at Serine 20 by Resveratrol Is Required to Activate p53 Target Genes, Restoring Apoptosis in MCF-7 Cells Resistant to Cisplatin.	Serine	36-42	P53	Homo sapiens	13-16
30142917-6	2018	We have shown that Resv induces sensitivity to CDDP in MCF-7 and MCF-7R cells and that the downregulation of p53 protein expression and inhibition of p53 protein activity enhances resistance to CDDP in both cell lines.	Cisplatin	194-198	P53	Homo sapiens	109-112
29954944-4	2018	We further reveal that mutant p53 forms physiological associations and direct interactions with MLL4 and promotes the enhancer binding of MLL4, which is required for TNFalpha-inducible H3K4me1 and histone H3 lysine 27 acetylation (H3K27ac) levels, enhancer-derived transcript (eRNA) synthesis, and mutant p53-dependent target gene activation.	Lysine	208-214	P53	Homo sapiens	30-33
29954944-4	2018	We further reveal that mutant p53 forms physiological associations and direct interactions with MLL4 and promotes the enhancer binding of MLL4, which is required for TNFalpha-inducible H3K4me1 and histone H3 lysine 27 acetylation (H3K27ac) levels, enhancer-derived transcript (eRNA) synthesis, and mutant p53-dependent target gene activation.	Lysine	208-214	P53	Homo sapiens	305-308
30140002-6	2018	APR-246/MQ also inhibits Trxs in mutant p53-expressing Saos-2 His-273 cells, showing modification of Trx1 and mitochondrial Trx2.	Histidine	62-65	P53	Homo sapiens	40-43
30142917-6	2018	We have shown that Resv induces sensitivity to CDDP in MCF-7 and MCF-7R cells and that the downregulation of p53 protein expression and inhibition of p53 protein activity enhances resistance to CDDP in both cell lines.	Cisplatin	194-198	P53	Homo sapiens	150-153
30142917-0	2018	Induction of p53 Phosphorylation at Serine 20 by Resveratrol Is Required to Activate p53 Target Genes, Restoring Apoptosis in MCF-7 Cells Resistant to Cisplatin.	Resveratrol	49-60	P53	Homo sapiens	13-16
30142917-7	2018	On the other hand, we found that Resv induces serine 20 (S20) phosphorylation in chemoresistant cells to activate p53 target genes such as PUMA and BAX, restoring apoptosis.	Serine	46-52	P53	Homo sapiens	114-117
30142917-9	2018	Interestingly, Resv attenuates CDDP-induced p53 phosphorylation in serine 15 (S15) and serine 46 (S46) probably through dephosphorylation and deactivation of ATM.	Cisplatin	31-35	P53	Homo sapiens	44-47
30142917-0	2018	Induction of p53 Phosphorylation at Serine 20 by Resveratrol Is Required to Activate p53 Target Genes, Restoring Apoptosis in MCF-7 Cells Resistant to Cisplatin.	Resveratrol	49-60	P53	Homo sapiens	85-88
30142917-9	2018	Interestingly, Resv attenuates CDDP-induced p53 phosphorylation in serine 15 (S15) and serine 46 (S46) probably through dephosphorylation and deactivation of ATM.	Serine	67-73	P53	Homo sapiens	44-47
30142917-0	2018	Induction of p53 Phosphorylation at Serine 20 by Resveratrol Is Required to Activate p53 Target Genes, Restoring Apoptosis in MCF-7 Cells Resistant to Cisplatin.	Cisplatin	151-160	P53	Homo sapiens	13-16
30142917-10	2018	It also activates different kinases, such as CK1, CHK2, and AMPK to induce phosphorylation of p53 in S20, suggesting a novel mechanism of p53 activation and chemosensitization to CDDP.	Cisplatin	179-183	P53	Homo sapiens	94-97
30142917-10	2018	It also activates different kinases, such as CK1, CHK2, and AMPK to induce phosphorylation of p53 in S20, suggesting a novel mechanism of p53 activation and chemosensitization to CDDP.	Cisplatin	179-183	P53	Homo sapiens	138-141
30142917-4	2018	Resveratrol (Resv) is a natural compound representing a promising chemosensitizer for cancer treatment that has been shown to sensitize tumor cells through upregulation and phosphorylation of p53 and inhibition of RAD51.	Resveratrol	0-11	P53	Homo sapiens	192-195
30142917-4	2018	Resveratrol (Resv) is a natural compound representing a promising chemosensitizer for cancer treatment that has been shown to sensitize tumor cells through upregulation and phosphorylation of p53 and inhibition of RAD51.	Resveratrol	0-4	P53	Homo sapiens	192-195
30197757-8	2018	Cross-talk between Zac1, IL-11, p53, and suppressor of cytokine signaling 3 was differentially affected by copper sulfate, digoxin, and caffeine.	Copper Sulfate	107-121	P53	Homo sapiens	32-35
30197757-8	2018	Cross-talk between Zac1, IL-11, p53, and suppressor of cytokine signaling 3 was differentially affected by copper sulfate, digoxin, and caffeine.	Digoxin	123-130	P53	Homo sapiens	32-35
30093705-5	2018	Simultaneously, it caused mitochondrial translocation of p53 and effectively inhibited glucose uptake, expression of GLUT transporters as well as hexokinase (HK II) - a key glycolytic enzyme that most cancer cells thrive on.	Glucose	87-94	P53	Homo sapiens	57-60
30126368-6	2018	Flow cytometry results revealed inhibition of ultraviolet radiation (UV)- and ionizing radiation (IR)- induced apoptosis and disruption of TP53-mediated cell cycle arrest after UV, IR and Nocodazole treatment.	Nocodazole	188-198	P53	Homo sapiens	139-143
30116169-7	2018	The results demonstrate that the bile acids, ursodeoxycholate and tauroursodeoxycholate, exhibit selective cytotoxicity toward nonfunctional p53 cell lines suggesting a p53-mediated role in inhibition of cell clonogenicity and potential chemopreventative properties.	Bile Acids and Salts	33-43	P53	Homo sapiens	141-144
30116169-7	2018	The results demonstrate that the bile acids, ursodeoxycholate and tauroursodeoxycholate, exhibit selective cytotoxicity toward nonfunctional p53 cell lines suggesting a p53-mediated role in inhibition of cell clonogenicity and potential chemopreventative properties.	Bile Acids and Salts	33-43	P53	Homo sapiens	169-172
30111797-5	2018	A microarray analysis revealed that the suppression of the checkpoint kinase 1 (CHK1) pathway explained the resistance to 5-FU, especially in p53 wild-type cancer cells such as HCT-8.	Fluorouracil	122-126	P53	Homo sapiens	142-145
29980405-5	2018	Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisplatin, irinotecan, oxaliplatin, and paclitaxel increased significantly.	Fluorouracil	172-184	P53	Homo sapiens	28-32
30072621-0	2018	Inhibitor of CBP Histone Acetyltransferase Downregulates p53 Activation and Facilitates Methylation at Lysine 27 on Histone H3.	Lysine	103-109	P53	Homo sapiens	57-60
29980405-5	2018	Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisplatin, irinotecan, oxaliplatin, and paclitaxel increased significantly.	Fluorouracil	186-189	P53	Homo sapiens	28-32
29947891-0	2018	Sensitization of colorectal cancer cells to irinotecan by the Survivin inhibitor LLP3 depends on XAF1 proficiency in the context of mutated p53.	Irinotecan	44-54	P53	Homo sapiens	140-143
29980405-5	2018	Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisplatin, irinotecan, oxaliplatin, and paclitaxel increased significantly.	Cisplatin	192-201	P53	Homo sapiens	28-32
29980405-5	2018	Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisplatin, irinotecan, oxaliplatin, and paclitaxel increased significantly.	Irinotecan	203-213	P53	Homo sapiens	28-32
29980405-5	2018	Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisplatin, irinotecan, oxaliplatin, and paclitaxel increased significantly.	Paclitaxel	232-242	P53	Homo sapiens	28-32
29980405-6	2018	Likewise, the sensitivity to drugs used to treat other cancers such as: doxorubicin, mitoxantrone, and 4 hydroxy tamoxifen (4HT) also increased upon introduction of WT-TP53 into MIA-PaCa-2 cells.	Doxorubicin	72-83	P53	Homo sapiens	168-172
29980405-6	2018	Likewise, the sensitivity to drugs used to treat other cancers such as: doxorubicin, mitoxantrone, and 4 hydroxy tamoxifen (4HT) also increased upon introduction of WT-TP53 into MIA-PaCa-2 cells.	4'-hydroxytamoxifen	124-127	P53	Homo sapiens	168-172
29980405-7	2018	Furthermore, the sensitivity to certain inhibitors which target: PI3K/mTORC1, PDK1, SRC, GSK-3, and biochemical processes such as proteasomal degradation and the nutraceutical berberine as increased upon introduction of WT-TP53.	Berberine	176-185	P53	Homo sapiens	223-227
29923368-10	2018	Pharmacologic or genetic manipulation of the reactive oxygen species (ROS)/ATM/Chk2/TP53 pathway efficiently blocked L5-induced endothelial senescence.	Reactive Oxygen Species	45-68	P53	Homo sapiens	84-88
29923368-10	2018	Pharmacologic or genetic manipulation of the reactive oxygen species (ROS)/ATM/Chk2/TP53 pathway efficiently blocked L5-induced endothelial senescence.	Reactive Oxygen Species	70-73	P53	Homo sapiens	84-88
29726704-9	2018	In contrast, zafirlukast showed a greater antiproliferative effect than montelukast and induced G0/G1 cell cycle arrest by upregulating p53 and p21 expression.	zafirlukast	13-24	P53	Homo sapiens	136-139
30065615-3	2018	Results: p53 heterozygous arginine variant was associated with decreased risk of breast cancer in total cohort.	Arginine	26-34	P53	Homo sapiens	9-12
29702192-8	2018	Moreover, PAB depleted intracellular GSH via p53-mediated xCT pathway, which further exacerbated accumulation of H2O2 and lipid peroxides.	pseudolaric acid B	10-13	P53	Homo sapiens	45-48
29702192-8	2018	Moreover, PAB depleted intracellular GSH via p53-mediated xCT pathway, which further exacerbated accumulation of H2O2 and lipid peroxides.	Glutathione	37-40	P53	Homo sapiens	45-48
29702192-8	2018	Moreover, PAB depleted intracellular GSH via p53-mediated xCT pathway, which further exacerbated accumulation of H2O2 and lipid peroxides.	Hydrogen Peroxide	113-117	P53	Homo sapiens	45-48
29660403-10	2018	In contrast, both metformin and fulvene-5, inhibitors of NOX4, facilitated the reversal of TP53 WT and Mut adaptive responses from pro-survival to radio-sensitization and vice versa, respectively.	Metformin	18-27	P53	Homo sapiens	91-95
28797827-0	2018	Interaction between mTOR pathway inhibition and autophagy induction attenuates adriamycin-induced vascular smooth muscle cell senescence through decreased expressions of p53/p21/p16.	Doxorubicin	79-89	P53	Homo sapiens	170-173
28797827-7	2018	Results of further experiments showed that mTOR pathway inhibition regulates adriamycin-induced expression of senescence markers (p53/p21/p16), which plays an important role in different aspects of cellular aging.	Doxorubicin	77-87	P53	Homo sapiens	130-133
29660403-13	2018	Under these conditions NOX4 expression was inhibited by about 50%, resulting in a reversal in the expression of the TP53 WT and Mut survivin-associated adaptive responses as was observed following metformin and fulvene-5 treatment.	Metformin	197-206	P53	Homo sapiens	116-120
29749471-9	2018	Furthermore, blockade of temozolomide (TMZ)-induced autophagy by 3-methyladenine (3-MA) resulted in enhanced activation of apoptotic markers, as well as tumor suppresor protein p53 (p53) expression in U87MG cells.	3-methyladenine	82-86	P53	Homo sapiens	177-180
29749471-9	2018	Furthermore, blockade of temozolomide (TMZ)-induced autophagy by 3-methyladenine (3-MA) resulted in enhanced activation of apoptotic markers, as well as tumor suppresor protein p53 (p53) expression in U87MG cells.	3-methyladenine	82-86	P53	Homo sapiens	182-185
29786746-0	2018	Luteolin induces myelodysplastic syndrome-derived cell apoptosis via the p53-dependent mitochondrial signaling pathway mediated by reactive oxygen species.	Reactive Oxygen Species	131-154	P53	Homo sapiens	73-76
29786746-11	2018	The increased intracellular level of ROS appeared to induce the activation of p53 and elevate the B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2 ratio, which modulates DeltaPsim and triggers the release of cytochrome c, and may increase the activities of apoptotic protease activating factor 1, caspase-3, -8 and -9 to further trigger the destruction of structural and specific proteins and thereby cell apoptosis.	Reactive Oxygen Species	37-40	P53	Homo sapiens	78-81
30288482-4	2018	Objective: This study was designed to examine associations of TP53 72 Arg&gt;Pro (rs1042522), and MDM2 309 T&gt;G (rs937283) polymorphisms with spermatogenetic failure in Iranian population.	Arginine	70-73	P53	Homo sapiens	62-66
29786746-13	2018	These data suggested that luteolin exerts its pro-apoptotic action partly through the p53-dependent mitochondrial signaling pathway mediated by intracellular ROS, which provides a promising therapeutic candidate for patients with MDS.	Reactive Oxygen Species	158-161	P53	Homo sapiens	86-89
30128492-8	2018	Results: Expression levels of ANGPTL3, IL-1beta, IL-6, Bax, P53, VEGF, and integrin alphaVbeta3 were found to be upregulated after high-glucose stimulation or ANGPTL3 overexpression in HRMECs or diabetic retinal tissue.	Glucose	136-143	P53	Homo sapiens	60-63
29668110-8	2018	Pre-incubation with ROS scavenger N-acetyl-l-cysteine preserved AR and PSA abundance, markedly reduced ISC-4-induced apoptosis and attenuated p53 Ser phosphorylation, p21Cip1, and p-H2A.X.	Reactive Oxygen Species	20-23	P53	Homo sapiens	142-145
28679068-2	2018	In present study, berberine hydrochloride (BER) triggered proliferative inhibition and G2/M arrest in AGS cells, down-regulated protein expression of cyclin B1, Bcl-2, up-regulated expression of p21, p53 and cleaved caspase 3, but showed no effect on protein expression of CHOP, Bip, and caspase 4.	Berberine	43-46	P53	Homo sapiens	200-203
29665051-5	2018	Mechanistic studies revealed that the sensitizing effect of hyperbaric oxygen is due to decreased ratio of Bcl-2/Bax, increased level of p53, cleaved Caspase3, GRP78, CHOP, and LC3.	Oxygen	71-77	P53	Homo sapiens	137-140
29668110-0	2018	Phenylbutyl isoselenocyanate induces reactive oxygen species to inhibit androgen receptor and to initiate p53-mediated apoptosis in LNCaP prostate cancer cells.	Reactive Oxygen Species	37-60	P53	Homo sapiens	106-109
29855544-6	2018	Moreover, resveratrol, a HDAC inhibitor, controlled not only acetylated p53 status but also DNTTIP1 expression, leading to a similar phenotype of siDNTTIP1 cells.	Resveratrol	10-21	P53	Homo sapiens	72-75
29668110-8	2018	Pre-incubation with ROS scavenger N-acetyl-l-cysteine preserved AR and PSA abundance, markedly reduced ISC-4-induced apoptosis and attenuated p53 Ser phosphorylation, p21Cip1, and p-H2A.X.	Acetylcysteine	34-53	P53	Homo sapiens	142-145
29668110-8	2018	Pre-incubation with ROS scavenger N-acetyl-l-cysteine preserved AR and PSA abundance, markedly reduced ISC-4-induced apoptosis and attenuated p53 Ser phosphorylation, p21Cip1, and p-H2A.X.	Serine	146-149	P53	Homo sapiens	142-145
29574239-4	2018	Considering the antitumor activity of benzothiazolic derivatives, this study aimed to demonstrate the action of benzothiazolic (E)-2-((2-(benzo[d]thiazol-2-yl)hydrazono)methyl)-4-nitrophenol (AFN01) against three established human melanoma cell lines that recapitulate the molecular landscape of the disease in terms of its genetic alterations and mutations, such as the TP53, NRAS and B-RAF genes.	benzothiazolic	38-52	P53	Homo sapiens	371-375
30124118-0	2018	TP53-dependence on the effect of doxorubicin and Src inhibitor combination therapy.	Doxorubicin	33-44	P53	Homo sapiens	0-4
29859204-6	2018	Zolpidem prevented death of P19 neurons exposed to glutamate, and abolished the glutamate-induced increase in ROS production, p53 and Bax expression, and caspase-3/7 activity.	Glutamic Acid	80-89	P53	Homo sapiens	126-129
30124118-2	2018	This study found an association between alterations in the TP53 gene and the synergy score for combination treatment with doxorubicin and an Src kinase inhibitor using human osteosarcoma cell lines (MG63 and U2OS) and human colon cancer cell line.	Doxorubicin	122-133	P53	Homo sapiens	59-63
30124118-3	2018	Doxorubicin was found to activate signal transducer and activator of transcription 3 via Src kinase in cancer cells harboring alterations in TP53.	Doxorubicin	0-11	P53	Homo sapiens	141-145
30124118-4	2018	A drug combination study using patient-derived cells confirmed that an Src kinase inhibitor synergizes with doxorubicin in cancer cells harboring alterations in TP53, while antagonizing its effect in cancer cells expressing wild-type TP53.	Doxorubicin	108-119	P53	Homo sapiens	161-165
30124118-5	2018	Our findings suggest that genetic alterations in TP53 are a critical factor in determining the use of a combination treatment of doxorubicin and Src inhibitors.	Doxorubicin	129-140	P53	Homo sapiens	49-53
29853637-6	2018	Fluorescence experiments revealed conformational changes of the single Trp and Tyr residues before p53 unfolding and the presence of MG conformers, some of which were highly prone to aggregation.	Tryptophan	71-74	P53	Homo sapiens	99-102
30060357-9	2018	Oxygen consumption rate of siTimeless-1 and siTimeless-2 group were 3.686+-0.389 and 3.955+-0.431, respectively, significantly higher than 1.690+-0.297 of control group (P&lt;0.05); Oxygen consumption rate of Timeless overexpressed group was 1.302+-0.336, significantly lower than 3.185+-0.262 of vector transfected group (P&lt;0.05) Timeless inhibited the expression of p53.	Oxygen	0-6	P53	Homo sapiens	371-374
30064446-15	2018	shRNA p53 reversed TNFAIP8 shRNA-mediated regulation of cell proliferation, cell cycle, cisplatin sensitivity, and expression levels of RAD51, a DNA repair gene.	Cisplatin	88-97	P53	Homo sapiens	6-9
30064446-16	2018	CONCLUSION: Our work uncovers a hitherto unappreciated role of TNFAIP8 in NSCLC proliferation and cisplatin chemoresistance that is mediated through the MDM2/p53 pathway.	Cisplatin	98-107	P53	Homo sapiens	158-161
30057418-13	2018	Instead, p53 acetylation at lysine 382 was unexpectedly upregulated.	Lysine	28-34	P53	Homo sapiens	9-12
29853637-6	2018	Fluorescence experiments revealed conformational changes of the single Trp and Tyr residues before p53 unfolding and the presence of MG conformers, some of which were highly prone to aggregation.	Tyrosine	79-82	P53	Homo sapiens	99-102
29853637-9	2018	Our findings support the use of single-Trp fluorescence as a probe for evaluating p53 stability, effects of mutations, and the efficacy of therapeutics designed to stabilize p53.	Tryptophan	39-42	P53	Homo sapiens	82-85
29853637-9	2018	Our findings support the use of single-Trp fluorescence as a probe for evaluating p53 stability, effects of mutations, and the efficacy of therapeutics designed to stabilize p53.	Tryptophan	39-42	P53	Homo sapiens	174-177
30029680-0	2018	Regulation of tNOX expression through the ROS-p53-POU3F2 axis contributes to cellular responses against oxaliplatin in human colon cancer cells.	ros	42-45	P53	Homo sapiens	46-49
29750510-0	2018	Pathways of Metabolite-Related Damage to a Synthetic p53 Gene Exon 7 Oligonucleotide Using Magnetic Enzyme Bioreactor Beads and LC-MS/MS Sequencing.	Oligonucleotides	69-84	P53	Homo sapiens	53-56
30029680-10	2018	Further experiments revealed that in p53-wild-type cells, oxaliplatin enhanced ROS generation and p53 transcriptional activation, leading to down-regulation of the transcriptional factor, POU3F2, which enhances the expression of tNOX.	ros	79-82	P53	Homo sapiens	37-40
30029680-11	2018	Moreover, the addition of a ROS scavenger reversed the p53 activation, POU3F2 down-regulation, and apoptosis induced by oxaliplatin in p53-wild-type cells.	ros	28-31	P53	Homo sapiens	55-58
30029680-11	2018	Moreover, the addition of a ROS scavenger reversed the p53 activation, POU3F2 down-regulation, and apoptosis induced by oxaliplatin in p53-wild-type cells.	ros	28-31	P53	Homo sapiens	135-138
30029680-12	2018	In the p53-null line, on the other hand, oxaliplatin treatment triggered less ROS generation and no p53 protein, such that POU3F2 and tNOX were not down-regulated and oxaliplatin-mediated cytotoxicity was attenuated.	ros	78-81	P53	Homo sapiens	7-10
30100998-0	2018	cAMP-mediated autophagy inhibits DNA damage-induced death of leukemia cells independent of p53.	Cyclic AMP	0-4	P53	Homo sapiens	91-94
30100998-2	2018	We have previously utilized an in vitro model of the most common form of childhood cancer, B cell precursor acute lymphoblastic leukemia (BCP-ALL), to show that activation of the cAMP signaling pathway inhibits p53-mediated apoptosis in response to DNA damage in both cell lines and primary leukemic cells.	Cyclic AMP	179-183	P53	Homo sapiens	211-214
30100998-3	2018	The present study reveals that cAMP-mediated survival of BCP-ALL cells exposed to DNA damaging agents, involves a critical and p53-independent enhancement of autophagy.	Cyclic AMP	31-35	P53	Homo sapiens	127-130
30100998-6	2018	Stimulation of the cAMP signaling pathway further augments autophagy and inhibits the DNA damage-induced cell death concomitant with reduced nuclear levels of p53.	Cyclic AMP	19-23	P53	Homo sapiens	159-162
30029680-13	2018	CONCLUSION: Our results show that oxaliplatin mediates differential cellular responses in colon cancer cells depending on their p53 status, and demonstrate that the ROS-p53 axis is important for regulating POU3F2 and its downstream target, tNOX.	ros	165-168	P53	Homo sapiens	169-172
30011295-6	2018	Pre-treatment with the antioxidant, N-acetylcysteine, prevented the actions of arecoline on cell viability, G2/M growth arrest, reactive oxygen species (ROS) production, and the levels of CDK1, p21, p27, p53, cyclin B1, and phospho-AMPK proteins.	Acetylcysteine	36-52	P53	Homo sapiens	204-207
30050469-9	2018	Of the 2,713 genes that were significantly upregulated following a 48 h incubation with 250 muM tamoxifen, most were categorized as either growth-related or pro-apoptotic intermediates that fit into the Tp53 and/or MAPK signaling pathways.	Tamoxifen	96-105	P53	Homo sapiens	203-207
30050469-10	2018	Collectively, our results display that the effects of tamoxifen on the breast cancer MCF-7 cell line are mediated by the activation of important signaling pathways including Tp53 and MAPKs to induce apoptosis.	Tamoxifen	54-63	P53	Homo sapiens	174-178
29970880-2	2018	Importantly, several genes involved in the "Central carbon metabolism pathway in cancer", as reported in the Kyoto Encyclopedia of Genes and Genomes, were either up- (ACLY, ERBB2, GCK, MYC, PGM, PKFB2, SLC1A5, SLC7A5, SLC16A3,) or down- (IDH, MDH1, OGDH, P53, PDK) regulated in response to the drug association.	Carbon	52-58	P53	Homo sapiens	255-258
29920999-6	2018	Interestingly, p53 pathway proteins and mitogen-activated protein kinase (MAPK) signalling pathway components were up-regulated by H2 O2 but exhibited a downward trend in MSCs co-cultured with ADASs.	Hydrogen Peroxide	131-136	P53	Homo sapiens	15-18
29740674-5	2018	Deacetylmycoepoxydiene (DA-MED), a cytotoxic natural polyketide, functions as a Rac1 agonist in p53-null NSCLC H1299 cells.	Polyketides	53-63	P53	Homo sapiens	96-99
29680675-5	2018	Short-time (8-min) light irradiation produced non-lethal amount of ROS to disrupt the endosomal membranes and facilitate p53 gene release via degradation of TK-PEI, which collectively enhanced p53 expression levels toward anti-cancer gene therapy.	ros	67-70	P53	Homo sapiens	121-124
29680675-5	2018	Short-time (8-min) light irradiation produced non-lethal amount of ROS to disrupt the endosomal membranes and facilitate p53 gene release via degradation of TK-PEI, which collectively enhanced p53 expression levels toward anti-cancer gene therapy.	ros	67-70	P53	Homo sapiens	193-196
29680675-6	2018	Long-time (30-min) light irradiation at the post-transfection state generated lethal amount of ROS, which cooperatively killed cancer cells to strengthen p53 gene therapy.	ros	95-98	P53	Homo sapiens	154-157
29684853-0	2018	Naringenin improve hepatitis C virus infection induced insulin resistance by increase PTEN expression via p53-dependent manner.	naringenin	0-10	P53	Homo sapiens	106-109
29941169-8	2018	CSE did not increase p53 phosphorylation in any of the cells; however, AMCs showed constitutive P-p53 expression.	amcs	71-75	P53	Homo sapiens	98-101
29593028-9	2018	Altered expression of heme-synthetic enzymes (coproporphyrinogen oxidase and ferrochelatase) and induction of p53 were observed, probably accounting for increased PpIX and subsequent cancer cell death.	protoporphyrin IX	163-167	P53	Homo sapiens	110-113
29250709-6	2018	We showed that folic acid increased cell viability and decreased apoptosis in a dose-dependent manner, and that this effect was mediated by decreased caspase-3/7 activity, upregulated BCL2/BAX ratio, and downregulated TP53, CASP3, and CASP8 expressions.	Folic Acid	15-25	P53	Homo sapiens	218-222
29963152-6	2018	Expression of the apoptosis-related gene TP53 and caspase 3 activation were enhanced in cisplatin-treated U251 cells.	Cisplatin	88-97	P53	Homo sapiens	41-45
29782646-3	2018	In our present study, we report that KCTD5 may physically interact with DeltaNp63alpha, which is a member of the p53 family.	deltanp63alpha	72-86	P53	Homo sapiens	113-116
29727353-11	2018	Only paclitaxel-treated ovarian cancer cells showed decrease in expression of p53.	Paclitaxel	5-15	P53	Homo sapiens	78-81
29667777-7	2018	The results showed that iPS-CM significantly reduced H2 O2 -induced ILC apoptosis through down-regulation of autophagic and apoptotic proteins LC3-I/II, Beclin-1, P62, P53 and BAX as well as up-regulation of BCL-2, which could be inhibited by LY294002 (25 mumol/L).	Hydrogen Peroxide	53-58	P53	Homo sapiens	168-171
29971135-0	2018	Hypoxia exposure induced cisplatin resistance partially via activating p53 and hypoxia inducible factor-1alpha in non-small cell lung cancer A549 cells.	Cisplatin	25-34	P53	Homo sapiens	71-74
29971135-4	2018	In the present study, the effects of hypoxia on the response of the NSCLC A549 cell line to the clinically relevant cytotoxic cisplatin were evaluated via regulating hypoxia inducible facor-1alpha (HIF-1alpha) and p53.	Cisplatin	126-135	P53	Homo sapiens	214-217
29971135-8	2018	As a result, activated p53 desensitized A549 cells to cisplatin potentially through increasing the non-proliferation status of A549 cells and therefore minimizing the influence of cisplatin.	Cisplatin	54-63	P53	Homo sapiens	23-26
29971135-8	2018	As a result, activated p53 desensitized A549 cells to cisplatin potentially through increasing the non-proliferation status of A549 cells and therefore minimizing the influence of cisplatin.	Cisplatin	180-189	P53	Homo sapiens	23-26
29971135-9	2018	Taken together, these results identified the exact effects of HIF-1alpha and p53 induced by hypoxia and potentially elucidated their protective effects on A549 cells against cisplatin.	Cisplatin	174-183	P53	Homo sapiens	77-80
29966311-2	2018	FAK has been shown to interact with p14ARF (alternative reading frame)&amp;mdash;a well-established tumor suppressor&amp;mdash;and functions in the negative regulation of cancer through both p53-dependent and -independent pathways.	Adenosine Monophosphate	71-74	P53	Homo sapiens	191-194
29675670-5	2018	We report an intensity-dependent regulation of exercise-induced increases in nuclear peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha) protein content, nuclear phosphorylation of p53 (serine 15), and PGC-1alpha messenger RNA (mRNA), as well as training-induced increases in PGC-1alpha and p53 protein content.	Serine	215-221	P53	Homo sapiens	210-213
29717634-7	2018	Notch signaling was also involved in glucose metabolism through p53 inactivation.	Glucose	37-44	P53	Homo sapiens	64-67
29966311-2	2018	FAK has been shown to interact with p14ARF (alternative reading frame)&amp;mdash;a well-established tumor suppressor&amp;mdash;and functions in the negative regulation of cancer through both p53-dependent and -independent pathways.	Adenosine Monophosphate	117-120	P53	Homo sapiens	191-194
29966255-0	2018	The Curcumin Analog CH-5 Exerts Anticancer Effects in Human Osteosarcoma Cells via Modulation of Transcription Factors p53/Sp1.	Curcumin	4-12	P53	Homo sapiens	119-122
30018734-6	2018	Gene set enrichment analysis (GSEA) identified p53 signaling, Notch, Wnt, VEGF, and MEK gene sets enriched in recurrent GBM.	gsea	30-34	P53	Homo sapiens	47-50
29966255-8	2018	These results suggest that CH-5 has potentially higher anticancer activity than curcumin, which is associated with the expression of apoptosis-associated genes regulated by the transcription factors Sp1 and p53.	Curcumin	80-88	P53	Homo sapiens	207-210
29738772-5	2018	Interestingly, co-treatment with DHA could effectively restore the anticancer effect of 5-FU against HCT116 TP53-/- cells, which manifested as the inhibition of proliferation and induction of reactive oxygen species (ROS)-mediated apoptosis and was accompanied by the upregulation of B-cell lymphoma 2 (BCL-2) and downregulation of the BCL-2-associated X protein (BAX).	Fluorouracil	88-92	P53	Homo sapiens	108-112
29988358-8	2018	Treatment of compound-1H could arrest cell cycle in S phase through up-regulating P21 and P53, and down-regulating cyclin A and E in a dose-dependent manner.	Hydrogen	22-24	P53	Homo sapiens	90-93
30018739-0	2018	Resveratrol prevents p53 aggregation in vitro and in breast cancer cells.	Resveratrol	0-11	P53	Homo sapiens	21-24
30018739-3	2018	We tested the potential of resveratrol, a naturally occurring polyphenol, to interact and prevent the aggregation of wild-type and mutant p53 in vitro using fluorescence spectroscopy techniques and in human breast cancer cells (MDA-MB-231, HCC-70 and MCF-7) using immunofluorescence co-localization assays.	Resveratrol	27-38	P53	Homo sapiens	138-141
30018739-4	2018	Based on our data, an interaction occurs between resveratrol and the wild-type p53 core domain (p53C).	Resveratrol	49-60	P53	Homo sapiens	79-82
30018739-6	2018	Additionally, resveratrol reduces mutant p53 protein aggregation in MDA-MB-231 and HCC-70 cells but not in the wild-type p53 cell line MCF-7.	Resveratrol	14-25	P53	Homo sapiens	41-44
30018739-9	2018	Our study provides evidence that resveratrol directly modulates p53, enhancing our understanding of the mechanisms involved in p53 aggregation and its potential as a therapeutic strategy for cancer treatment.	Resveratrol	33-44	P53	Homo sapiens	64-67
30018739-9	2018	Our study provides evidence that resveratrol directly modulates p53, enhancing our understanding of the mechanisms involved in p53 aggregation and its potential as a therapeutic strategy for cancer treatment.	Resveratrol	33-44	P53	Homo sapiens	127-130
29983877-0	2018	Mutations of p53 decrease sensitivity to the anthracycline treatments in bladder cancer cells.	Anthracyclines	45-58	P53	Homo sapiens	13-16
29872820-6	2018	Furthermore, the reduction of the cellular iron content induced alterations of p53-p27-p21 signaling to arrest the cell cycle at S phase in SMMC7721 cells treated by chemerin.	Iron	43-47	P53	Homo sapiens	79-82
29743236-0	2018	IDH1 Arg-132 mutant promotes tumor formation through down-regulating p53.	Arginine	5-8	P53	Homo sapiens	69-72
29743236-5	2018	Rescue expression of p53 can inhibit the proliferation rate and impair the resistance of apoptosis induced by doxorubicin in IDH1 R132Q mouse embryonic fibroblast cells.	Doxorubicin	110-121	P53	Homo sapiens	21-24
29983877-2	2018	In this study, we assessed the efficacy and mechanisms of anthracyclines-induced apoptosis and inhibition of cell viability in human bladder cancer cells expressing wild-type (wt) p53 (RT4 and SW780) and mutated (mt) p53 (UM-UC-3, 5637, T-24, J82, and TCCSUP) protein.	Anthracyclines	58-72	P53	Homo sapiens	180-183
29702091-5	2018	Significantly, MALAT1 deletion sensitized HepG2 cells to 5-FU-induced cell cycle arrest in G1 phase, as evidenced by the significant reduction in Cyclin D1 and CDK4 and increase in p53, p21 and p27 protein levels.	Fluorouracil	57-61	P53	Homo sapiens	181-184
29983877-2	2018	In this study, we assessed the efficacy and mechanisms of anthracyclines-induced apoptosis and inhibition of cell viability in human bladder cancer cells expressing wild-type (wt) p53 (RT4 and SW780) and mutated (mt) p53 (UM-UC-3, 5637, T-24, J82, and TCCSUP) protein.	Anthracyclines	58-72	P53	Homo sapiens	217-220
29983877-3	2018	Anthracyclines inhibited cell viability in tested TCC cells, but were less effective in mt-p53 TCC cells, especially in the drug-resistant J82 and TCCSUP cells.	Anthracyclines	0-14	P53	Homo sapiens	91-94
29983877-4	2018	Anthracyclines upregulated the expression of wt p53 protein in RT4 and SW780 cells, but had no effect on expression of mt p53 protein in UM-UC-3, 5637, T-24, J82, and TCCSUP cells.	Anthracyclines	0-14	P53	Homo sapiens	48-51
29983877-5	2018	The anthracyclines activated caspase 3/7 and cleavage of PARP in wt-p53 RT4 and SW780 cells, and mt-p53 5637, UM-UC-3, and T-24, but not in mt-p53 J82 and TCCSUP cells.	Anthracyclines	4-18	P53	Homo sapiens	68-71
29983877-6	2018	The anthracyclines-induced cleavage of PARP was blocked by p53 siRNA in wt-p53 RT4 cells.	Anthracyclines	4-18	P53	Homo sapiens	59-62
29983877-6	2018	The anthracyclines-induced cleavage of PARP was blocked by p53 siRNA in wt-p53 RT4 cells.	Anthracyclines	4-18	P53	Homo sapiens	75-78
29983877-9	2018	In conclusion, our results demonstrated that the anthracycline-induced resistance in bladder cancer cells positively correlated with TP53 mutations in the tetramerization domain in J82 and TCCSUP cells.	Anthracyclines	49-62	P53	Homo sapiens	133-137
29963241-3	2018	Here we demonstrate that CPT-11 stalls such cells in the G2/M phase of the cell cycle, induces an accumulation of the tumor suppressor p53, the replicative stress/DNA damage marker gammaH2AX, phosphorylation of the checkpoint kinases ATM and ATR, and an ATR-dependent accumulation of the pro-survival molecule survivin.	Irinotecan	25-31	P53	Homo sapiens	135-138
29898731-13	2018	PC-3 cells lacking p53 and PTEN with reduced ROS levels showed significant activation of Akt and NF-kappaB pathway.	ros	45-48	P53	Homo sapiens	19-22
29895782-2	2018	EtOH increased senescence activity, levels of reactive oxygen species (ROS) and the expression of cell cycle regulators (p53, p21 and p16) and senescence-associated secretory phenotype (SASP) genes (interleukin [IL]-1beta, IL-6, IL-8 and tumor necrosis factor-alpha) in HPDLCs and cementoblasts.	Ethanol	0-4	P53	Homo sapiens	121-124
29890668-4	2018	A cell-based screening method with a p53-responsive luciferase-reporter assay system revealed that an ethanol extract of Oroxylum indicum bark increased p53 transcriptional activity.	Ethanol	102-109	P53	Homo sapiens	37-40
29890631-5	2018	The tumor suppressor protein p53 is emerging as a key regulator of metabolic processes and metabolic reprogramming in cancer cells&amp;mdash;balancing the pendulum between cell death and survival.	Adenosine Monophosphate	131-134	P53	Homo sapiens	29-32
29890668-4	2018	A cell-based screening method with a p53-responsive luciferase-reporter assay system revealed that an ethanol extract of Oroxylum indicum bark increased p53 transcriptional activity.	Ethanol	102-109	P53	Homo sapiens	153-156
29580374-0	2018	Mitochondrial dysfunction suppresses p53 expression via calcium-mediated nuclear factor-kB signaling in HCT116 human colorectal carcinoma cells.	Calcium	56-63	P53	Homo sapiens	37-40
29867024-6	2018	As a result, the oncogenic characteristics of miR-483-3p are linked to the effect of some of the most relevant cancer-related genes, TP53 and CTNNB1, as well as to one of the most important cancer hallmark: the aberrant glucose metabolism of tumor cells.	Glucose	220-227	P53	Homo sapiens	133-137
29754265-0	2018	Resveratrol analogue, (E)-N-(2-(4-methoxystyryl) phenyl) furan-2-carboxamide induces G2/M cell cycle arrest through the activation of p53-p21CIP1/WAF1 in human colorectal HCT116 cells.	Resveratrol	0-11	P53	Homo sapiens	134-137
29660338-7	2018	It was found that TPA induced interaction between the transcriptional factors Sp1 and P53 producing Sp1-p53 complex which strongly interacted with c-Jun only after short exposure to TPA.	Tetradecanoylphorbol Acetate	18-21	P53	Homo sapiens	86-89
29660338-7	2018	It was found that TPA induced interaction between the transcriptional factors Sp1 and P53 producing Sp1-p53 complex which strongly interacted with c-Jun only after short exposure to TPA.	Tetradecanoylphorbol Acetate	18-21	P53	Homo sapiens	104-107
29660338-7	2018	It was found that TPA induced interaction between the transcriptional factors Sp1 and P53 producing Sp1-p53 complex which strongly interacted with c-Jun only after short exposure to TPA.	Tetradecanoylphorbol Acetate	182-185	P53	Homo sapiens	86-89
29660338-7	2018	It was found that TPA induced interaction between the transcriptional factors Sp1 and P53 producing Sp1-p53 complex which strongly interacted with c-Jun only after short exposure to TPA.	Tetradecanoylphorbol Acetate	182-185	P53	Homo sapiens	104-107
29660338-8	2018	In addition, TPA treatment highly induced the expression of CREB which attached to the Sp1-p53 complex mainly after a long exposure to TPA.	Tetradecanoylphorbol Acetate	13-16	P53	Homo sapiens	91-94
29660338-8	2018	In addition, TPA treatment highly induced the expression of CREB which attached to the Sp1-p53 complex mainly after a long exposure to TPA.	Tetradecanoylphorbol Acetate	135-138	P53	Homo sapiens	91-94
29660338-9	2018	A strong binding of sp1, p53 and CREB proteins with HTLV-1 LTR and strong binding of NF-kappaB with HIV-1 LTR were observed after long (24 h) and short (6 h) exposures to TPA respectively by Chip assay.	Tetradecanoylphorbol Acetate	171-174	P53	Homo sapiens	25-28
29660338-10	2018	These results support the possibility that sp1, p53 and CREB are involved in the TPA induced HTLV-1 LTR expression while TPA activation of HIV-1 LTR seems to be dependent on PKC activity through the NF-kappaB pathway.	Tetradecanoylphorbol Acetate	81-84	P53	Homo sapiens	48-51
29580374-5	2018	The p53 expression was reduced by activation of nuclear factor-kappaB that depended on elevated levels of free calcium in HCT116/rho0 cells.	Calcium	111-118	P53	Homo sapiens	4-7
29698619-8	2018	Moreover, inhibition of p53 increased the inhibitory effect in p53-wild hepatocarcinoma cells, as well as apoptotic cells and ROS generation.	Reactive Oxygen Species	126-129	P53	Homo sapiens	24-27
29492901-11	2018	CONCLUSIONS: From our results we conclude that DENSpm-induced apoptotic cell death is increased when autophagy is inhibited by 3-MA or Beclin-1 siRNA through PA depletion and PA catabolic activation in colon cancer cells, regardless p53 mutation status.	3-methyladenine	127-131	P53	Homo sapiens	233-236
29575058-1	2018	The absolute configurations of the diastereomers of novel amino acid ester derivatives of 2,3-substituted isoindolinones, which are known as apoptosis activators due to their ability to inhibit the MDM2-p53 PPI, were assigned using NMR and computational methods.	2,3-substituted isoindolinones	90-120	P53	Homo sapiens	203-206
29602546-10	2018	GSEA show that p53/hypoxia pathway, androgen response, notch signaling, fatty acid metabolism, glycolysis and estrogen response late are differentially enriched in TFAP2B high expression phenotype.	gsea	0-4	P53	Homo sapiens	15-18
29772519-2	2018	The mechanisms underlying resistance to doxorubicin, cisplatin, and 5-fluorouracil involve p53 and P-glycoprotein (P-gp).	Doxorubicin	40-51	P53	Homo sapiens	91-94
29772519-2	2018	The mechanisms underlying resistance to doxorubicin, cisplatin, and 5-fluorouracil involve p53 and P-glycoprotein (P-gp).	Cisplatin	53-62	P53	Homo sapiens	91-94
29772519-2	2018	The mechanisms underlying resistance to doxorubicin, cisplatin, and 5-fluorouracil involve p53 and P-glycoprotein (P-gp).	Fluorouracil	68-82	P53	Homo sapiens	91-94
28926094-0	2018	Curcumin regulates proliferation, autophagy, and apoptosis in gastric cancer cells by affecting PI3K and P53 signaling.	Curcumin	0-8	P53	Homo sapiens	105-108
28926094-1	2018	In this study, we aimed to investigate the effects of curcumin on cell activities of gastric cancer (GC), and the connection between curcumin and P53, as well as, PI3K signaling.	Curcumin	133-141	P53	Homo sapiens	146-149
28926094-4	2018	Western blot assay was also employed to detect impacts of curcumin on tophosphatidylinositol-3 kinase (PI3K) and P53 signaling pathways-related proteins.	Curcumin	58-66	P53	Homo sapiens	113-116
28926094-8	2018	Western blot results showed that curcumin activated P53 signaling pathway and inhibited PI3K signaling pathway.	Curcumin	33-41	P53	Homo sapiens	52-55
28926094-10	2018	Additionally, curcumin activated the P53 signaling pathway by up-regulating P53 and P21, which also inhibited PI3K pathway through down-regulating PI3K, p-Akt, and p-mTOR.	Curcumin	14-22	P53	Homo sapiens	37-40
28926094-10	2018	Additionally, curcumin activated the P53 signaling pathway by up-regulating P53 and P21, which also inhibited PI3K pathway through down-regulating PI3K, p-Akt, and p-mTOR.	Curcumin	14-22	P53	Homo sapiens	76-79
29779937-11	2018	CONCLUSION: Our results suggest that CSCs in the ER+ cells escape the effect of DOX treatment by the elevation of p53 expression.	Doxorubicin	80-83	P53	Homo sapiens	114-117
29436749-0	2018	HOXA13 contributes to gastric carcinogenesis through DHRS2 interacting with MDM2 and confers 5-FU resistance by a p53-dependent pathway.	Fluorouracil	93-97	P53	Homo sapiens	114-117
29352505-0	2018	p53-independent Noxa induction by cisplatin is regulated by ATF3/ATF4 in head and neck squamous cell carcinoma cells.	Cisplatin	34-43	P53	Homo sapiens	0-3
29352505-5	2018	Here, we show that the upregulation of Noxa is critical for cisplatin-induced apoptosis in p53-null HNSCC cells.	Cisplatin	60-69	P53	Homo sapiens	91-94
29436749-9	2018	Furthermore, HOXA13 conferred 5-FU resistance through MRP1 by a p53-dependent pathway.	Fluorouracil	30-34	P53	Homo sapiens	64-67
29352505-11	2018	In conclusion, ATF3 and ATF4 are important regulators that induce Noxa by cisplatin treatment in a p53-independent manner.	Cisplatin	74-83	P53	Homo sapiens	99-102
29928326-0	2018	Miltirone-induced apoptosis in cisplatin-resistant lung cancer cells through upregulation of p53 signaling pathways.	Cisplatin	31-40	P53	Homo sapiens	93-96
29928358-0	2018	Resveratrol suppresses human cervical carcinoma cell proliferation and elevates apoptosis via the mitochondrial and p53 signaling pathways.	Resveratrol	0-11	P53	Homo sapiens	116-119
29658603-10	2018	Finally, we demonstrated that the marked changes in the A549/DDP cell response to NaHS may be triggered by the activation of p53, and overexpression of p21, caspase-3, Bax and MMP-2, as well as the downregulation of Bcl-xL.	sodium bisulfide	82-86	P53	Homo sapiens	125-128
29684847-5	2018	RESULTS: Cell lines and tumor cells p53+, p53- revealed a significant decrease in cell survival after camptothecin, paclitaxel, cisplatin treatment, compared to the control group (p &lt; 0.01).	Paclitaxel	116-126	P53	Homo sapiens	42-45
29928326-8	2018	The results of the present study demonstrated that miltirone induces apoptosis in cisplatin-resistant lung cancer cells through ROS-p53, AIF, PARP and MMP2/9 signaling pathways.	Cisplatin	82-91	P53	Homo sapiens	132-135
29928326-8	2018	The results of the present study demonstrated that miltirone induces apoptosis in cisplatin-resistant lung cancer cells through ROS-p53, AIF, PARP and MMP2/9 signaling pathways.	Reactive Oxygen Species	128-131	P53	Homo sapiens	132-135
29620221-0	2018	CT-1042, a novel anticancer agent, exhibits effects by activating p53 and inhibiting survivin.	ct-1042	0-7	P53	Homo sapiens	66-69
29620221-9	2018	In addition, CT-1042 induced mitochondrial-mediated apoptosis by activating p53 and Bax, as well as inhibiting Bcl-2 and survivin.	ct-1042	13-20	P53	Homo sapiens	76-79
29928358-7	2018	In addition, p53, a protein that is essential for cell survival and cell cycle progression, exhibited elevated expression levels in resveratrol-treated HeLa cells.	Resveratrol	132-143	P53	Homo sapiens	13-16
29684847-0	2018	The association between p53 protein phosphorylation at serine 15, serine 20 and sensitivity of cells isolated from patients with ovarian cancer and cell lines to chemotherapy in in vitro study.	Serine	55-61	P53	Homo sapiens	24-27
29684847-0	2018	The association between p53 protein phosphorylation at serine 15, serine 20 and sensitivity of cells isolated from patients with ovarian cancer and cell lines to chemotherapy in in vitro study.	Serine	66-72	P53	Homo sapiens	24-27
29684847-5	2018	RESULTS: Cell lines and tumor cells p53+, p53- revealed a significant decrease in cell survival after camptothecin, paclitaxel, cisplatin treatment, compared to the control group (p &lt; 0.01).	Cisplatin	128-137	P53	Homo sapiens	36-39
29684847-1	2018	BACKGROUND: The association between p53 protein phosphorylated at serine 15 (Ser15), serine 20 (Ser20) and ovarian tumor cell sensitivity after chemotherapy was analyzed in order to define the influence of p53 activation on tumor cell sensitivity to chemotherapy.	Serine	66-72	P53	Homo sapiens	36-39
29684847-5	2018	RESULTS: Cell lines and tumor cells p53+, p53- revealed a significant decrease in cell survival after camptothecin, paclitaxel, cisplatin treatment, compared to the control group (p &lt; 0.01).	Paclitaxel	116-126	P53	Homo sapiens	36-39
29684847-5	2018	RESULTS: Cell lines and tumor cells p53+, p53- revealed a significant decrease in cell survival after camptothecin, paclitaxel, cisplatin treatment, compared to the control group (p &lt; 0.01).	Cisplatin	128-137	P53	Homo sapiens	42-45
29684847-6	2018	In p53+ group, the expression of Ser20 significantly increased after camptothecin and paclitaxel (p &lt; 0.05).	Paclitaxel	86-96	P53	Homo sapiens	3-6
29716766-4	2018	In the present study, ATF3, p53, and p53 target gene Bax expression increased in CD patients; a mouse 2, 4, 6-trinitrobenzenesulfonic acid (TNBS)-induced CD model; and a TNF-alpha-treated HT29 cell colitis model.	Trinitrobenzenesulfonic Acid	102-138	P53	Homo sapiens	37-40
29697201-0	2018	Mir-1307 regulates cisplatin resistance by targeting Mdm4 in breast cancer expressing wild type P53.	Cisplatin	19-28	P53	Homo sapiens	96-99
29544765-1	2018	PURPOSE: The heavy subunit of the iron storage protein ferritin (FHC) is essential for the intracellular iron metabolism and, at the same time, it represents a central hub of iron-independent pathways, such as cell proliferation, angiogenesis, p53 regulation, chemokine signalling, stem cell expansion, miRNAs expression.	Iron	34-38	P53	Homo sapiens	244-247
29795190-4	2018	Enforced miR-181a expression enhanced 5-FU-induced p53-dependent mitochondrial apoptosis, including declined Bcl-2/Bax ratio, loss of mitochondrial membrane potential, cytochrome c release, and caspase-9 and caspase-3 activation.	Fluorouracil	38-42	P53	Homo sapiens	51-54
29848325-14	2018	RESULTS: Under high glucose conditions, miR-155 was detected in HK-2 cells in concentration gradient, increased expression of p53 and down-regulated expression of sirt1 and autophagy-associated proteins LC3II, ATG5 and ATG7.	Glucose	20-27	P53	Homo sapiens	126-129
32254384-5	2018	After that, the prodrug and the gene vector copolymers were mixed in an aqueous solution in order to self-assemble into hybrid micelles, which could then condense the p53 gene and finally form DOX prodrug/p53 co-loaded nanoparticles.	Doxorubicin	193-196	P53	Homo sapiens	167-170
32254384-5	2018	After that, the prodrug and the gene vector copolymers were mixed in an aqueous solution in order to self-assemble into hybrid micelles, which could then condense the p53 gene and finally form DOX prodrug/p53 co-loaded nanoparticles.	Doxorubicin	193-196	P53	Homo sapiens	205-208
32254384-9	2018	Furthermore, the results from the live cell imaging system revealed that the hybrid micelle/p53 gene nanoparticles could effectively deliver and release DOX and the p53 genes into A549 cells.	Doxorubicin	153-156	P53	Homo sapiens	92-95
29899847-5	2018	Furthermore, the inhibitors increased the endogenous p53 levels that were induced by cisplatin.	Cisplatin	85-94	P53	Homo sapiens	53-56
29843463-6	2018	ZMCs reactivate mutant p53 using a novel two-part mechanism that involves restoring the wild-type structure by reestablishing zinc binding and activating p53 through post-translational modifications induced by cellular reactive oxygen species (ROS).	Reactive Oxygen Species	219-242	P53	Homo sapiens	23-26
29843463-6	2018	ZMCs reactivate mutant p53 using a novel two-part mechanism that involves restoring the wild-type structure by reestablishing zinc binding and activating p53 through post-translational modifications induced by cellular reactive oxygen species (ROS).	Reactive Oxygen Species	244-247	P53	Homo sapiens	23-26
29843463-6	2018	ZMCs reactivate mutant p53 using a novel two-part mechanism that involves restoring the wild-type structure by reestablishing zinc binding and activating p53 through post-translational modifications induced by cellular reactive oxygen species (ROS).	Reactive Oxygen Species	244-247	P53	Homo sapiens	154-157
29795190-5	2018	However, inhibition of miR-181a was associated with reduced p53-mediated mitochondrial apoptosis induced by 5-FU.	Fluorouracil	108-112	P53	Homo sapiens	60-63
29795190-9	2018	In conclusion, these results demonstrate that miR-181a increases p53 protein expression and transcriptional activity by targeting BIRC6 and promotes 5-FU-induced apoptosis in mesangial cells.	Fluorouracil	149-153	P53	Homo sapiens	65-68
29887958-9	2018	The top 10 hub genes were identified to be hub genes from the PPI network, and the model revealed that these genes were enriched in various pathways, including neuroactive ligand-receptor interaction, p53 and glutathione metabolism signaling pathways.	Glutathione	209-220	P53	Homo sapiens	201-204
30003124-1	2018	Background &amp; Aims: Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).	Adenosine Monophosphate	12-15	P53	Homo sapiens	81-84
29783665-3	2018	Here, a commercial NGS cancer panel comprising 26 genes, including TP53, was used to identify new genetic markers of platinum resistance and patient prognosis in a retrospective set of patients diagnosed with epithelial ovarian cancer.	Platinum	117-125	P53	Homo sapiens	67-71
29783665-4	2018	Six novel TP53 somatic mutations in untreated tumors from six distinct patients diagnosed with HGSOC were identified: TP53 c.728_739delTGGGCGGCATGA (p.Met243_Met247del, in-frame insertion or deletion (INDEL); TP53 c.795_809delGGGACGGAACAGCTT (p.Gly266_Phe270del, in-frame INDEL); TP53 c.826_827GC&gt;AT (p.Ala276Ile, missense); TP53 c.1022insT (p.Arg342Profs*5, frameshift INDEL); TP53 c.1180delT (p.Ter394Aspfs*28, frameshift INDEL); and TP53 c.573insT (p.Gln192Serfs*17, frameshift INDEL).	arg342profs	347-358	P53	Homo sapiens	10-14
29783665-4	2018	Six novel TP53 somatic mutations in untreated tumors from six distinct patients diagnosed with HGSOC were identified: TP53 c.728_739delTGGGCGGCATGA (p.Met243_Met247del, in-frame insertion or deletion (INDEL); TP53 c.795_809delGGGACGGAACAGCTT (p.Gly266_Phe270del, in-frame INDEL); TP53 c.826_827GC&gt;AT (p.Ala276Ile, missense); TP53 c.1022insT (p.Arg342Profs*5, frameshift INDEL); TP53 c.1180delT (p.Ter394Aspfs*28, frameshift INDEL); and TP53 c.573insT (p.Gln192Serfs*17, frameshift INDEL).	arg342profs	347-358	P53	Homo sapiens	118-122
29783665-4	2018	Six novel TP53 somatic mutations in untreated tumors from six distinct patients diagnosed with HGSOC were identified: TP53 c.728_739delTGGGCGGCATGA (p.Met243_Met247del, in-frame insertion or deletion (INDEL); TP53 c.795_809delGGGACGGAACAGCTT (p.Gly266_Phe270del, in-frame INDEL); TP53 c.826_827GC&gt;AT (p.Ala276Ile, missense); TP53 c.1022insT (p.Arg342Profs*5, frameshift INDEL); TP53 c.1180delT (p.Ter394Aspfs*28, frameshift INDEL); and TP53 c.573insT (p.Gln192Serfs*17, frameshift INDEL).	arg342profs	347-358	P53	Homo sapiens	118-122
29783665-4	2018	Six novel TP53 somatic mutations in untreated tumors from six distinct patients diagnosed with HGSOC were identified: TP53 c.728_739delTGGGCGGCATGA (p.Met243_Met247del, in-frame insertion or deletion (INDEL); TP53 c.795_809delGGGACGGAACAGCTT (p.Gly266_Phe270del, in-frame INDEL); TP53 c.826_827GC&gt;AT (p.Ala276Ile, missense); TP53 c.1022insT (p.Arg342Profs*5, frameshift INDEL); TP53 c.1180delT (p.Ter394Aspfs*28, frameshift INDEL); and TP53 c.573insT (p.Gln192Serfs*17, frameshift INDEL).	arg342profs	347-358	P53	Homo sapiens	118-122
29783665-4	2018	Six novel TP53 somatic mutations in untreated tumors from six distinct patients diagnosed with HGSOC were identified: TP53 c.728_739delTGGGCGGCATGA (p.Met243_Met247del, in-frame insertion or deletion (INDEL); TP53 c.795_809delGGGACGGAACAGCTT (p.Gly266_Phe270del, in-frame INDEL); TP53 c.826_827GC&gt;AT (p.Ala276Ile, missense); TP53 c.1022insT (p.Arg342Profs*5, frameshift INDEL); TP53 c.1180delT (p.Ter394Aspfs*28, frameshift INDEL); and TP53 c.573insT (p.Gln192Serfs*17, frameshift INDEL).	arg342profs	347-358	P53	Homo sapiens	118-122
29783665-4	2018	Six novel TP53 somatic mutations in untreated tumors from six distinct patients diagnosed with HGSOC were identified: TP53 c.728_739delTGGGCGGCATGA (p.Met243_Met247del, in-frame insertion or deletion (INDEL); TP53 c.795_809delGGGACGGAACAGCTT (p.Gly266_Phe270del, in-frame INDEL); TP53 c.826_827GC&gt;AT (p.Ala276Ile, missense); TP53 c.1022insT (p.Arg342Profs*5, frameshift INDEL); TP53 c.1180delT (p.Ter394Aspfs*28, frameshift INDEL); and TP53 c.573insT (p.Gln192Serfs*17, frameshift INDEL).	arg342profs	347-358	P53	Homo sapiens	118-122
29783665-4	2018	Six novel TP53 somatic mutations in untreated tumors from six distinct patients diagnosed with HGSOC were identified: TP53 c.728_739delTGGGCGGCATGA (p.Met243_Met247del, in-frame insertion or deletion (INDEL); TP53 c.795_809delGGGACGGAACAGCTT (p.Gly266_Phe270del, in-frame INDEL); TP53 c.826_827GC&gt;AT (p.Ala276Ile, missense); TP53 c.1022insT (p.Arg342Profs*5, frameshift INDEL); TP53 c.1180delT (p.Ter394Aspfs*28, frameshift INDEL); and TP53 c.573insT (p.Gln192Serfs*17, frameshift INDEL).	arg342profs	347-358	P53	Homo sapiens	118-122
29753331-1	2018	TIGAR is a p53 target gene that is known to protect cells from ROS-induced apoptosis by promoting the pentose phosphate pathway.	ros	63-66	P53	Homo sapiens	11-14
29872500-5	2018	Here we show that resveratrol controls breast cancer cell proliferation by inducing tumor-suppressive miRNAs (miR-34a, miR-424, and miR-503) via the p53 pathway and then by suppressing heterogeneous nuclear ribonucleoprotein A1 (HNRNPA1), which is associated with tumorigenesis and tumor progression.	Resveratrol	18-29	P53	Homo sapiens	149-152
29805774-8	2018	Conversely, induction of p53 expression may regulate differently the tumor cell metabolism, inducing senescence, autophagy and apoptosis, which are dependent on the regulation of the PI3K/AKT/mTOR pathway and/or ROS induction.	Reactive Oxygen Species	212-215	P53	Homo sapiens	25-28
29476819-2	2018	SIRT1 deacetylates p53 in a NAD+-dependent manner to inhibit transcription activity of p53, in turn modulate pathways that are implicated in regulation of tissue homoeostasis and many disease states.	NAD	28-32	P53	Homo sapiens	19-22
29476819-2	2018	SIRT1 deacetylates p53 in a NAD+-dependent manner to inhibit transcription activity of p53, in turn modulate pathways that are implicated in regulation of tissue homoeostasis and many disease states.	NAD	28-32	P53	Homo sapiens	87-90
29323455-0	2018	Selenocysteine inhibits human osteosarcoma cells growth through triggering mitochondrial dysfunction and ROS-mediated p53 phosphorylation.	Reactive Oxygen Species	105-108	P53	Homo sapiens	118-121
29788155-14	2018	Among patients treated with GDC-0575 and gemcitabine, there were four confirmed partial responses, three occurring in patients with tumors harboring TP53 mutation.	GDC-0575	28-36	P53	Homo sapiens	149-153
29229990-8	2018	These results suggest that p53 mediates DDR and exerts its tumor suppressive role in part by regulating the expression of ACER2, which in turn regulates the bioactive sphingolipid lipids.	sphingolipid lipids	167-186	P53	Homo sapiens	27-30
29323455-7	2018	Moreover, SeC triggered p53 phosphorylation by inducing reactive oxygen species (ROS) overproduction.	Reactive Oxygen Species	56-79	P53	Homo sapiens	24-27
29323455-7	2018	Moreover, SeC triggered p53 phosphorylation by inducing reactive oxygen species (ROS) overproduction.	Reactive Oxygen Species	81-84	P53	Homo sapiens	24-27
29323455-8	2018	ROS inhibition effectively blocked SeC-induced cytotoxicity and p53 phosphorylation.	Reactive Oxygen Species	0-3	P53	Homo sapiens	64-67
29323455-10	2018	These results indicated that SeC had the potential to inhibit human osteosarcoma cells growth in vitro and in vivo through triggering mitochondrial dysfunction and ROS-mediated p53 phosphorylation, which validated the potential application of Se-containing compounds in treatment of human osteosarcoma.	Reactive Oxygen Species	164-167	P53	Homo sapiens	177-180
29723979-6	2018	Phosphatase and tensin homologue deleted on chromosome 10/Protein kinase B, PKB (PTEN/AKT) and the tumor suppressor p53 pathway have been proven to play a pivotal role in regulating cell apoptosis by regulating the oxidative stress and/or ROS quenching.	Reactive Oxygen Species	239-242	P53	Homo sapiens	116-119
29670092-0	2018	APR-246 reactivates mutant p53 by targeting cysteines 124 and 277.	Cysteine	44-53	P53	Homo sapiens	27-30
29670092-5	2018	APR-246 is converted to the reactive electrophile methylene quinuclidinone (MQ), which binds covalently to p53 core domain.	eprenetapopt	0-7	P53	Homo sapiens	107-110
29670092-5	2018	APR-246 is converted to the reactive electrophile methylene quinuclidinone (MQ), which binds covalently to p53 core domain.	memoquin	76-78	P53	Homo sapiens	107-110
29670092-6	2018	We identified cysteine 277 as a prime binding target for MQ in p53.	Cysteine	14-22	P53	Homo sapiens	63-66
29723979-7	2018	In this review, we summarize the current research and our view of how PTEN/AKT and p53 with their partners transduce signals downstream, and what the implications are for MSCs&amp;rsquo; biology.	Adenosine Monophosphate	176-179	P53	Homo sapiens	83-86
29700097-7	2018	In addition, PGE2/sulprostone was able to stimulate the expression of Gi1, phosphorylated-extracellular signal-regulated kinases 1/2 (p-ERK1/2) and p53.	Dinoprostone	13-17	P53	Homo sapiens	148-151
30027149-7	2018	In the Calligonum extract+H2O2 group, apoptosis, as well as expression of apoptotic genes (Bax and P53), was significantly lower than the group treated with H2O2 alone.	Hydrogen Peroxide	26-30	P53	Homo sapiens	99-102
29555649-2	2018	In contrast, resveratrol binds to integrin alphavbeta3 at a discrete site and induces p53-dependent antiproliferation in malignant neoplastic cells.	Resveratrol	13-24	P53	Homo sapiens	86-89
29521142-3	2018	Melatonin pre-treatment prior to ionizing radiation was associated with a decrease in cell proliferation and an increase in p53 mRNA expression, leading to an increase in the radiosensitivity of breast cancer cells.	Melatonin	0-9	P53	Homo sapiens	124-127
29555649-6	2018	Knockdown of PD-L1 by small hairpin RNA (shRNA) relieved the inhibitory effect of T4 on resveratrol-induced nuclear accumulation of COX-2- and COX-2/p53-dependent gene expression.	Resveratrol	88-99	P53	Homo sapiens	149-152
31938352-0	2018	High glucose concentration induces retinal endothelial cell apoptosis by activating p53 signaling pathway.	Glucose	5-12	P53	Homo sapiens	84-87
31938352-10	2018	Further research indicated that the protein levels of p53, pro-apoptotic cleaved-caspase-3, and bax were significantly upregulated, and the level of bcl-2 was decreased after treating with glucose at 30 mmol/L.	Glucose	189-196	P53	Homo sapiens	54-57
31938352-12	2018	In conclusion, high glucose concentration induces apoptosis in retinal endothelial cells by activating p53 signaling pathway.	Glucose	20-27	P53	Homo sapiens	103-106
29542252-7	2018	We subsequently showed that USP4 regulated cisplatin-induced cell apoptosis via p53 signalling.	Cisplatin	43-52	P53	Homo sapiens	80-83
29231257-0	2018	Halofuginone-induced autophagy suppresses the migration and invasion of MCF-7 cells via regulation of STMN1 and p53.	halofuginone	0-12	P53	Homo sapiens	112-115
29565448-3	2018	Our previous study revealed that kaempferol triggered apoptosis in human umbilical vein endothelial cells (HUVECs) by ROS-mediated p53/ATM/death receptor signaling.	ros	118-121	P53	Homo sapiens	131-134
29568929-9	2018	Mechanistic studies demonstrated that KNDC1 triggered a p53-ROS positive feedback loop, which serves a crucial role in regulating senescence.	Reactive Oxygen Species	60-63	P53	Homo sapiens	56-59
29511347-0	2018	PARP-1 inhibition with or without ionizing radiation confers reactive oxygen species-mediated cytotoxicity preferentially to cancer cells with mutant TP53.	Reactive Oxygen Species	61-84	P53	Homo sapiens	150-154
29662081-0	2018	A quantitative LumiFluo assay to test inhibitory compounds blocking p53 degradation induced by human papillomavirus oncoprotein E6 in living cells.	lumifluo	15-23	P53	Homo sapiens	68-71
29291545-8	2018	Impaired PPP disturbed redox-cycling, generated reactive oxygen species (ROS), which triggered cell cycle arrest and caused the switch to Chk2/p53/NF-kappaB pathway-mediated P-gp induction.	Reactive Oxygen Species	48-71	P53	Homo sapiens	143-146
29291545-8	2018	Impaired PPP disturbed redox-cycling, generated reactive oxygen species (ROS), which triggered cell cycle arrest and caused the switch to Chk2/p53/NF-kappaB pathway-mediated P-gp induction.	Reactive Oxygen Species	73-76	P53	Homo sapiens	143-146
29854627-0	2018	Neuro- and nephroprotective effect of grape seed proanthocyanidin extract against carboplatin and thalidomide through modulation of inflammation, tumor suppressor protein p53, neurotransmitters, oxidative stress and histology.	proanthocyanidin	49-65	P53	Homo sapiens	171-174
29690507-0	2018	Hypoxia-Induced Cisplatin Resistance in Non-Small Cell Lung Cancer Cells Is Mediated by HIF-1alpha and Mutant p53 and Can Be Overcome by Induction of Oxidative Stress.	Cisplatin	16-25	P53	Homo sapiens	110-113
29690507-1	2018	The compound APR-246 (PRIMA-1MET) is a known reactivator of (mutant) p53 and inducer of oxidative stress which can sensitize cancer cells to platinum-based chemotherapeutics.	Platinum	141-149	P53	Homo sapiens	69-72
29690507-3	2018	This study focusses on the role of hypoxia-inducible factor-1&amp;alpha; (HIF-1&amp;alpha;) and the p53 tumor suppressor protein in hypoxia-induced cisplatin resistance in non-small cell lung cancer (NSCLC) cells and the potential of APR-246 to overcome this resistance.	Cisplatin	148-157	P53	Homo sapiens	100-103
29690507-4	2018	We observed that hypoxia-induced cisplatin resistance only occurred in the p53 mutant NCI-H2228Q331* cell line, and not in the wild type A549 and mutant NCI-H1975R273H cell lines.	Cisplatin	33-42	P53	Homo sapiens	75-78
29690507-5	2018	Cisplatin reduced HIF-1&amp;alpha; protein levels in NCI-H2228Q331* cells, leading to a shift in expression from HIF-1&amp;alpha;-dependent to p53-dependent transcription targets under hypoxia.	Cisplatin	0-9	P53	Homo sapiens	143-146
29690507-8	2018	Our data further support the rationale of combining APR-246 with cisplatin in NSCLC, since their synergistic interaction is retained or enforced under hypoxic conditions in the presence of mutant p53.	Cisplatin	65-74	P53	Homo sapiens	196-199
29662081-6	2018	We validated the assay by testing two small molecules, SAHA and RITA, reported to impair the E6-mediated p53 degradation.	RITA	64-68	P53	Homo sapiens	105-108
29662081-8	2018	The possibility to specifically and quantitatively monitor the ability of a selected compound to rescue p53 in a cellular context through our LumiFluo assay could represent an important step towards the successful development of anti-HPV drugs.	lumifluo	142-150	P53	Homo sapiens	104-107
29774081-10	2018	G9a dimethylated p53 at lysine 373, which in turn increased Plk1 expression and promoted CRC cell growth.	Lysine	24-30	P53	Homo sapiens	17-20
29373839-5	2018	NgBR knockdown enhanced paclitaxel-induced cell apoptosis by modulating expression of p53 and survivin in ERalpha positive breast cancer cells via NgBR-mediated PI3K/Akt and MAPK/ERK signaling pathways.	Paclitaxel	24-34	P53	Homo sapiens	86-89
29731965-10	2018	In this study, the presence of both TP53 mutation and 17p/TP53 deletion, but not the individual variants, was associated with poor prognosis in DLBCL patients after treatment with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) or similar regimens.	Doxorubicin	209-220	P53	Homo sapiens	36-40
29731965-10	2018	In this study, the presence of both TP53 mutation and 17p/TP53 deletion, but not the individual variants, was associated with poor prognosis in DLBCL patients after treatment with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) or similar regimens.	Doxorubicin	209-220	P53	Homo sapiens	58-62
29695998-3	2018	However, p53 has a number of other functions that recent data strongly implicate in tumor suppression, particularly with regard to the control of metabolism and ferroptosis (iron- and lipid-peroxide-mediated cell death) by p53.	Iron	174-178	P53	Homo sapiens	9-12
29695998-3	2018	However, p53 has a number of other functions that recent data strongly implicate in tumor suppression, particularly with regard to the control of metabolism and ferroptosis (iron- and lipid-peroxide-mediated cell death) by p53.	Iron	174-178	P53	Homo sapiens	223-226
29619114-0	2018	Omega-3 fatty acid DHA modulates p53, survivin, and microRNA-16-1 expression in KRAS-mutant colorectal cancer stem-like cells.	dehydroacetic acid	19-22	P53	Homo sapiens	33-36
28550687-0	2018	Tanshinone Suppresses Arecoline-Induced Epithelial-Mesenchymal Transition in Oral Submucous Fibrosis by Epigenetically Reactivating the p53 Pathway.	tanshinone	0-10	P53	Homo sapiens	136-139
28550687-7	2018	In addition, p53 and its downstream molecules were decreased by arecoline treatment in oral mucosal fibroblasts, which was reversed by treatment with TSN in a dose-dependent manner.	tanshinone	150-153	P53	Homo sapiens	13-16
28550687-8	2018	Our results also revealed that arecoline stimulation resulted in hypermethylation of the promoter of TP53 and subsequent downregulation of p53 levels, which was reversed by TSN.	tanshinone	173-176	P53	Homo sapiens	101-105
28550687-8	2018	Our results also revealed that arecoline stimulation resulted in hypermethylation of the promoter of TP53 and subsequent downregulation of p53 levels, which was reversed by TSN.	tanshinone	173-176	P53	Homo sapiens	139-142
27819521-4	2018	Moreover, we found that combination treatment of miR-326 and curcumin caused significant inhibition of the SHH/GLI1 pathway in glioma cells compared with either treatment alone, independent of p53 status.	Curcumin	61-69	P53	Homo sapiens	193-196
29619114-4	2018	Here, we investigated whether in vitro concentrations of DHA equal to human plasma levels, are able to modulate, Wt-p53, survivin, and microRNA-16-1 in CRC cells with stem cell-like properties.	dehydroacetic acid	57-60	P53	Homo sapiens	116-119
29619114-9	2018	Treatment with 100 and 150 muM/L DHA increased microRNA-16-1 expression levels by 1.3- to 1.7-fold and enhanced the microRNA-16-1/survivin mRNA, p53/survivin, and caspase-3/survivin protein ratios by 1.7- to 1.8-, 1.3- to 2.6-, and 1.3- to 2-fold increases respectively.	dehydroacetic acid	33-36	P53	Homo sapiens	145-148
29619114-11	2018	Conclusion: Wt-p53, survivin, and microRNA-16-1 appear to be promising molecular targets of DHA.	dehydroacetic acid	92-95	P53	Homo sapiens	15-18
29409053-7	2018	Clinical activity of GDC-0575 combined with chemotherapy in patients with TP53-mutated and TP53 wild-type STS was also assessed.	GDC-0575	21-29	P53	Homo sapiens	74-78
29351612-10	2018	This alcohol consumption signature was also observed in liver cancer and head and neck squamous cell carcinoma, and its mutational activity was substantially higher in samples with mutations in TP53.	Alcohols	5-12	P53	Homo sapiens	194-198
29409053-7	2018	Clinical activity of GDC-0575 combined with chemotherapy in patients with TP53-mutated and TP53 wild-type STS was also assessed.	GDC-0575	21-29	P53	Homo sapiens	91-95
29409053-9	2018	Moreover, we observed a synergistic or additive effect of GDC-0575 together with gemcitabine in vitro and in vivo in TP53-proficient but not TP53-deficient sarcoma models.	GDC-0575	58-66	P53	Homo sapiens	117-121
29409053-10	2018	In a phase I study of GDC-0575 in combination with gemcitabine, two patients with metastatic TP53-mutated STS had an exceptional, long-lasting response despite administration of a very low dose of gemcitabine whereas one patient with wild-type TP53 STS had no clinical benefit.	GDC-0575	22-30	P53	Homo sapiens	93-97
29409053-10	2018	In a phase I study of GDC-0575 in combination with gemcitabine, two patients with metastatic TP53-mutated STS had an exceptional, long-lasting response despite administration of a very low dose of gemcitabine whereas one patient with wild-type TP53 STS had no clinical benefit.	GDC-0575	22-30	P53	Homo sapiens	244-248
29484412-12	2018	Upstream regulators of the above proteins, MDM2, phospho-MDM2 (at Ser166) and AKT, phospho-AKT (at Thr308) were all attenuated by melatonin, which led to an increase in p53.	Melatonin	130-139	P53	Homo sapiens	169-172
29393335-5	2018	Additionally, the mechanism underlying the cis-DDP-induced apoptosis was indicated to involve the activation of p53, c-Jun-N-terminal kinase (JNK) and p38 signaling.	Cisplatin	43-50	P53	Homo sapiens	112-115
29275510-0	2018	Bisphenol A induces DSB-ATM-p53 signaling leading to cell cycle arrest, senescence, autophagy, stress response, and estrogen release in human fetal lung fibroblasts.	bisphenol A	0-11	P53	Homo sapiens	28-31
29360968-8	2018	Using the p53-specific pharmacological inhibitor (pifithrin-alpha) and siRNA could partially attenuate PPV-induced Bax upregulation, caspase-3 activation, apoptosis, and the reduction of progesterone production in primary porcine SLCs.	Progesterone	187-199	P53	Homo sapiens	10-13
29579543-8	2018	Furthermore, the expression levels of p300, Ac-p53, p53, p-p21 and p16 were significantly increased in senescent and H2O2-induced cells compared to young cells.	Hydrogen Peroxide	117-121	P53	Homo sapiens	47-50
29579543-8	2018	Furthermore, the expression levels of p300, Ac-p53, p53, p-p21 and p16 were significantly increased in senescent and H2O2-induced cells compared to young cells.	Hydrogen Peroxide	117-121	P53	Homo sapiens	52-55
29471006-5	2018	Astilbin significantly decreased reactive oxygen species (ROS) accumulation and alleviated ROS-induced activation of p53, MAPKs and AKT signaling cascades, which in turn attenuated cisplatin-induced HEK-293 cell apoptosis.	Reactive Oxygen Species	91-94	P53	Homo sapiens	117-120
29471006-5	2018	Astilbin significantly decreased reactive oxygen species (ROS) accumulation and alleviated ROS-induced activation of p53, MAPKs and AKT signaling cascades, which in turn attenuated cisplatin-induced HEK-293 cell apoptosis.	Cisplatin	181-190	P53	Homo sapiens	117-120
29261364-1	2018	BACKGROUND: The TP53 codon 72 Proline-Arginine polymorphism (TP53 P72R) is the most widely studied candidate among those evaluated for a putative association between impaired apoptosis and glaucoma.	Arginine	38-46	P53	Homo sapiens	16-20
29261364-1	2018	BACKGROUND: The TP53 codon 72 Proline-Arginine polymorphism (TP53 P72R) is the most widely studied candidate among those evaluated for a putative association between impaired apoptosis and glaucoma.	Arginine	38-46	P53	Homo sapiens	61-65
29261364-2	2018	Considering the earlier findings about enhanced apoptotic potential by the Arg variant of TP53 P72R and the conflicting results about its association with glaucoma, we initiated a hospital-based case-control association study in a north Indian cohort to investigate the association of TP53 P72R with glaucoma.	Arginine	75-78	P53	Homo sapiens	90-94
28982275-5	2018	Besides, BPA induces Michigan Cancer Foundation-7 breast cancer cells proliferation by dysregulating PTEN/serine/threonine kinase/p53 axis.	bisphenol A	9-12	P53	Homo sapiens	130-133
28577130-0	2018	Gemcitabine/Cisplatin Treatment Induces Concomitant SERTAD1, CDKN2B and GADD45A Modulation and Cellular Changes in Bladder Cancer Cells Regardless of the Site of TP53 Mutation.	Cisplatin	12-21	P53	Homo sapiens	162-166
29552226-7	2018	These results indicated that dietary flavone may potentiate breast cancer cell apoptosis induced by metformin, and PI3K/AKT is involved in regulating MDMX/p53 signaling.	flavone	37-44	P53	Homo sapiens	155-158
29557783-3	2018	In humans, single nucleotide polymorphism (SNP) with either arginine (R72) or proline (P72) at codon 72 influences p53 activity; the P72 allele has a weaker p53 activity and function in tumor suppression.	Arginine	60-68	P53	Homo sapiens	115-118
29471073-0	2018	The impact of chemotherapeutic drugs on the CYP1A1-catalysed metabolism of the environmental carcinogen benzo[a]pyrene: Effects in human colorectal HCT116 TP53(+/+), TP53(+/-) and TP53(-/-) cells.	pyrene	112-118	P53	Homo sapiens	155-159
29590203-0	2018	Reprogramming of the estrogen responsive transcriptome contributes to tamoxifen-dependent protection against tumorigenesis in the p53 null mammary epithelial cells.	Tamoxifen	70-79	P53	Homo sapiens	130-133
29382728-0	2018	The curcumin analog HO-3867 selectively kills cancer cells by converting mutant p53 protein to transcriptionally active wildtype p53.	Curcumin	4-12	P53	Homo sapiens	80-83
29382728-0	2018	The curcumin analog HO-3867 selectively kills cancer cells by converting mutant p53 protein to transcriptionally active wildtype p53.	Curcumin	4-12	P53	Homo sapiens	129-132
29382728-5	2018	Here, we report on the effects of a curcumin analog, HO-3867, on p53 activity in cancer cells from different origins.	Curcumin	36-44	P53	Homo sapiens	65-68
29471073-4	2018	We found that etoposide and ellipticine induced CYP1A1 in TP53(+/+) cells but not in TP53(-/-) cells, demonstrating that the mechanism of CYP1A1 induction is p53-dependent; cisplatin had no such effect.	Cisplatin	173-182	P53	Homo sapiens	158-161
29572435-9	2018	Up-regulated beta-arrestin 1/2 promoted podocyte apoptosis and p53 pathway by increasing Bax, cleaved caspase-3, and p-p53 levels in high-glucose-induced podocytes.	Glucose	138-145	P53	Homo sapiens	63-66
29572435-9	2018	Up-regulated beta-arrestin 1/2 promoted podocyte apoptosis and p53 pathway by increasing Bax, cleaved caspase-3, and p-p53 levels in high-glucose-induced podocytes.	Glucose	138-145	P53	Homo sapiens	119-122
29499113-6	2018	In vitro responses to 13e vary significantly and interestingly based on cell type: in p53 wild-type MV4-11 cells, 13e induced cell death via apoptosis and G1/S cell cycle arrest, which is likely mediated by a p53-dependent pathway, while in p53-null PC-3 cells, 13e caused G2/M arrest and inhibited cell proliferation without inducing caspase-3-dependent apoptosis.	CHEMBL3741879	22-25	P53	Homo sapiens	86-89
29568320-3	2018	The enzymes responsible for arginine methylation, protein arginine methyltransferases (PRMTs), have been shown to methylate or associate with important regulatory proteins of the cell cycle and DNA damage repair pathways, such as cyclin D1, p53, p21 and the retinoblastoma protein.	Arginine	28-36	P53	Homo sapiens	241-244
29557783-3	2018	In humans, single nucleotide polymorphism (SNP) with either arginine (R72) or proline (P72) at codon 72 influences p53 activity; the P72 allele has a weaker p53 activity and function in tumor suppression.	Arginine	60-68	P53	Homo sapiens	157-160
29358327-8	2018	Low-level overexpression of p53 in pAVICs via an adenovirus vector did not affect pAVIC apoptosis but promoted warfarin-induced calcium deposition and expression of osteogenic markers.	Calcium	128-135	P53	Homo sapiens	28-31
29301826-0	2018	p53-Reactive T Cells Are Associated with Clinical Benefit in Patients with Platinum-Resistant Epithelial Ovarian Cancer After Treatment with a p53 Vaccine and Gemcitabine Chemotherapy.	Platinum	75-83	P53	Homo sapiens	0-3
29301826-0	2018	p53-Reactive T Cells Are Associated with Clinical Benefit in Patients with Platinum-Resistant Epithelial Ovarian Cancer After Treatment with a p53 Vaccine and Gemcitabine Chemotherapy.	Platinum	75-83	P53	Homo sapiens	143-146
29358327-11	2018	Of note, overexpression of Slug increased osteogenic marker Runx2 expression, but not pAVIC calcium deposition, and Slug knockdown attenuated pAVIC calcification and p53-mediated pAVIC calcium deposition and expression of osteogenic markers.	Calcium	185-192	P53	Homo sapiens	166-169
29358327-9	2018	shRNA-mediated p53 knockdown attenuated the pAVIC calcium deposition and osteogenic marker expression.	Calcium	50-57	P53	Homo sapiens	15-18
29178461-2	2018	However, culminating from seminal findings in rodents more than a decade ago, several studies have demonstrated that p53 is required to maintain basal mitochondrial function [ie, respiration and reactive oxygen species (ROS) homeostasis].	Reactive Oxygen Species	195-218	P53	Homo sapiens	117-120
29518119-10	2018	When p53 expression was inhibited with siRNA in parental HT-29 cells, ROS production and apoptosis increased to levels seen in the NAT1 knockout cells.	Reactive Oxygen Species	70-73	P53	Homo sapiens	5-8
29429877-7	2018	Furthermore, we provide evidence that haemanthamine and other Amaryllidaceae alkaloids also inhibit specifically ribosome biogenesis, triggering nucleolar stress response and leading to p53 stabilization in cancer cells.	hemanthamine	38-51	P53	Homo sapiens	186-189
29178461-2	2018	However, culminating from seminal findings in rodents more than a decade ago, several studies have demonstrated that p53 is required to maintain basal mitochondrial function [ie, respiration and reactive oxygen species (ROS) homeostasis].	Reactive Oxygen Species	220-223	P53	Homo sapiens	117-120
29644009-7	2018	Especially, this study revealed for the first time that pomalidomide enhances p53 on pancreatic cancer cells.	pomalidomide	56-68	P53	Homo sapiens	78-81
29285847-0	2018	2-anilino-4-amino-5-aroylthiazole-type compound AS7128 inhibits lung cancer growth through decreased iASPP and p53 interaction.	2-anilino-4-amino-5-aroylthiazole	0-33	P53	Homo sapiens	111-114
29185024-7	2018	However, fluoride-induced Ac-p53 was suppressed by the SIRT1 activator resveratrol (50 microM).	Resveratrol	71-82	P53	Homo sapiens	29-32
29196192-7	2018	Moreover, macrovipecetin alone or combined with cisplatin induced the expression of TRADD, p53, Bax, Bim and Bad and down-regulated the Bcl-2 expression and ROS levels in SK-MEL-28 cells.	Cisplatin	48-57	P53	Homo sapiens	91-94
29392716-5	2018	Antioxidant (N-acetyl-L-cysteine, NAC) treatment in vitro not only quantitatively and functionally improved BM MSCs derived from PT patients through down-regulation of the p38 (also termed MAPK14) and p53 (also termed TP53) pathways but also partially rescued the impaired ability of BM MSCs to support megakaryocytopoiesis.	Acetylcysteine	13-32	P53	Homo sapiens	201-204
29392716-5	2018	Antioxidant (N-acetyl-L-cysteine, NAC) treatment in vitro not only quantitatively and functionally improved BM MSCs derived from PT patients through down-regulation of the p38 (also termed MAPK14) and p53 (also termed TP53) pathways but also partially rescued the impaired ability of BM MSCs to support megakaryocytopoiesis.	Acetylcysteine	13-32	P53	Homo sapiens	218-222
29233839-9	2018	Thus, somatic mutations of cAMP/PKA pathway genes, mainly PRKACA, coding for the catalytic alpha-subunit of PKA, are found in cortisol-secreting adenomas, whereas IGF-II overexpression and alterations of p53 signaling pathway are observed in ACC.	Cyclic AMP	27-31	P53	Homo sapiens	204-207
29233839-9	2018	Thus, somatic mutations of cAMP/PKA pathway genes, mainly PRKACA, coding for the catalytic alpha-subunit of PKA, are found in cortisol-secreting adenomas, whereas IGF-II overexpression and alterations of p53 signaling pathway are observed in ACC.	Hydrocortisone	126-134	P53	Homo sapiens	204-207
29331588-9	2018	Notably, montelukast reduced expression of the senescence markers p53, p21 and PAI-1.	montelukast	9-20	P53	Homo sapiens	66-69
29331588-10	2018	In addition, montelukast ameliorated TNF-alpha-induced K382 acetylation of p53 by promoting the expression of SIRT1.	montelukast	13-24	P53	Homo sapiens	75-78
29331588-11	2018	Silencing of SIRT1 using SIRT1 siRNA broke the inhibitory effects of montelukast on K382 acetylation of p53.	montelukast	69-80	P53	Homo sapiens	104-107
29255096-2	2018	Resveratrol - the polyphenolic phytoalexin - binds to integrin alphavbeta3 to induce apoptosis in cancer cells via cyclooxygenase 2 (COX-2) nuclear accumulation and p53-dependent apoptosis.	Resveratrol	0-11	P53	Homo sapiens	165-168
29286156-0	2018	Metformin-induced activation of AMPK inhibits the proliferation and migration of human aortic smooth muscle cells through upregulation of p53 and IFI16.	Metformin	0-9	P53	Homo sapiens	138-141
29286156-8	2018	In addition, metformin was able to activate p53, IFI16 and AMPK, in order to inhibit proliferation and migration of HASMCs.	Metformin	13-22	P53	Homo sapiens	44-47
29286156-9	2018	Furthermore, siRNA-mediated knockdown of p53 and IFI16 attenuated AMPK activation and reversed the suppressive effects of metformin.	Metformin	122-131	P53	Homo sapiens	41-44
29286156-11	2018	These results indicated that metformin-induced activation of AMPK suppresses the proliferation and migration of HASMCs by upregulating p53 and IFI16.	Metformin	29-38	P53	Homo sapiens	135-138
29402413-0	2018	Inhibition of CREPT restrains gastric cancer growth by regulation of cycle arrest, migration and apoptosis via ROS-regulated p53 pathway.	Reactive Oxygen Species	111-114	P53	Homo sapiens	125-128
29629344-10	2018	The induced expression of cytochrome c, p53, p21 and p27, and down-regulated CDK2 and CDK4 may be the underlying molecular mechanisms of esculetin effect.	esculetin	137-146	P53	Homo sapiens	40-43
28777435-6	2018	Cell treatment with ADP or 2-MeS-ADP also provokes the activation of p53, causing an accumulation of the G1 cyclin-dependent kinase inhibitors p21WAF1 and p27Kip .	Adenosine Diphosphate	20-23	P53	Homo sapiens	69-72
28777435-6	2018	Cell treatment with ADP or 2-MeS-ADP also provokes the activation of p53, causing an accumulation of the G1 cyclin-dependent kinase inhibitors p21WAF1 and p27Kip .	methylthio-ADP	27-36	P53	Homo sapiens	69-72
29673545-0	2018	Curcumin induces apoptosis and cell cycle arrest via the activation of reactive oxygen species-independent mitochondrial apoptotic pathway in Smad4 and p53 mutated colon adenocarcinoma HT29 cells.	Curcumin	0-8	P53	Homo sapiens	152-155
29673545-0	2018	Curcumin induces apoptosis and cell cycle arrest via the activation of reactive oxygen species-independent mitochondrial apoptotic pathway in Smad4 and p53 mutated colon adenocarcinoma HT29 cells.	Reactive Oxygen Species	71-94	P53	Homo sapiens	152-155
29673545-4	2018	To test this hypothesis, the apoptosis-inducing potential and cell cycle inhibition effect of ROS induced by curcumin was investigated in Smd4 and p53 mutated HT-29 colon adenocarcinoma cells.	Reactive Oxygen Species	94-97	P53	Homo sapiens	147-150
29673545-12	2018	In conclusion, our data provide the first evidence that curcumin induces ROS independent apoptosis and cell cycle arrest in colon cancer cells that carry mutation on Smad4 and p53.	Curcumin	56-64	P53	Homo sapiens	176-179
30250886-1	2018	We have recently reported a TP53 (known as p53) regulated long noncoding RNA named TRINGS (Tp53-regulated inhibitor of necrosis under glucose starvation).	Glucose	134-141	P53	Homo sapiens	28-32
30250886-1	2018	We have recently reported a TP53 (known as p53) regulated long noncoding RNA named TRINGS (Tp53-regulated inhibitor of necrosis under glucose starvation).	Glucose	134-141	P53	Homo sapiens	43-46
30250886-1	2018	We have recently reported a TP53 (known as p53) regulated long noncoding RNA named TRINGS (Tp53-regulated inhibitor of necrosis under glucose starvation).	Glucose	134-141	P53	Homo sapiens	91-95
30250886-2	2018	With the aid of TRINGS, p53 was shown to prevent cancer cells against necroptosis under glucose starvation.	Glucose	88-95	P53	Homo sapiens	24-27
29485619-9	2018	Resveratrol and to a greater extent pterostilbene downregulates the HPV oncoprotein E6, induces caspase-3 activation, and upregulates p53 protein levels.	Resveratrol	0-11	P53	Homo sapiens	134-137
29397938-4	2018	In human osteosarcoma cell line U2OS cells, DRAK1 was mainly localized in the nucleus and translocated outside the nucleus through Ser395 phosphorylation by protein kinase C. In the nucleus, DRAK1 associated with tumor suppressor p53 and positively regulated p53 transcriptional activity in response to DNA-damaging agent cisplatin.	Cisplatin	322-331	P53	Homo sapiens	230-233
29431732-5	2018	Specifically, blocking AhR redirected IFN-beta signaling to STAT3 phosphorylation through both tyrosine and serine sites, which subsequently facilitated STAT3 nuclear translocation and subsequent binding to the p53 promoter in the nucleus.	Tyrosine	95-103	P53	Homo sapiens	211-214
29431732-5	2018	Specifically, blocking AhR redirected IFN-beta signaling to STAT3 phosphorylation through both tyrosine and serine sites, which subsequently facilitated STAT3 nuclear translocation and subsequent binding to the p53 promoter in the nucleus.	Serine	108-114	P53	Homo sapiens	211-214
29431732-6	2018	Upregulation of p53 in turn disrupted the pentose phosphate pathway, leading to excessive ROS production and dormant TRC death.	ros	90-93	P53	Homo sapiens	16-19
29223572-0	2018	Curcumin ameliorates the in vitro efficacy of carfilzomib in human multiple myeloma U266 cells targeting p53 and NF-kappaB pathways.	Curcumin	0-8	P53	Homo sapiens	105-108
29223572-0	2018	Curcumin ameliorates the in vitro efficacy of carfilzomib in human multiple myeloma U266 cells targeting p53 and NF-kappaB pathways.	carfilzomib	46-57	P53	Homo sapiens	105-108
29223572-8	2018	Our results confirmed the induction of p53/p21 axis and G0/G1 cell cycle arrest in anticancer activities of both drugs, an effect more pronounced for the CFZ-curcumin tested combinations.	carfilzomib	154-157	P53	Homo sapiens	39-42
29223572-8	2018	Our results confirmed the induction of p53/p21 axis and G0/G1 cell cycle arrest in anticancer activities of both drugs, an effect more pronounced for the CFZ-curcumin tested combinations.	Curcumin	158-166	P53	Homo sapiens	39-42
29440484-0	2018	Synergistic and additive effect of retinoic acid in circumventing resistance to p53 restoration.	Tretinoin	35-48	P53	Homo sapiens	80-83
29643975-4	2018	In this study, we found that physiological hypoxia (10% O2) enhanced the stemness properties and promoted the proliferation ability of iHepSCs by accelerating G1/S transition via p53-p21 signaling pathway.	Oxygen	56-58	P53	Homo sapiens	179-182
29466247-8	2018	Collectively, down-regulation of ZEB1 caused by UVA induced ROS could transcriptionally inhibit DNMT1, leading to low methylation level of senescence related proteins p53 and increase its expression, eventually result in cellar senescence.	Reactive Oxygen Species	60-63	P53	Homo sapiens	167-170
29556360-1	2018	Over 70% of head &amp; neck squamous cell carcinoma (HNSCC) patients carry TP53 oncogenic mutations.	Adenosine Monophosphate	18-21	P53	Homo sapiens	75-79
29334216-2	2018	The particle size and the zeta potential of PTX-DODAB/p53-rHDL nanoparticles were 177.2 nm and -20.06 mV, respectively.	Paclitaxel	44-47	P53	Homo sapiens	54-57
29432478-0	2018	Correction: Apoptosis by [Pt(O,O"-acac)(gamma-acac)(DMS)] requires PKC-delta mediated p53 activation in malignant pleural mesothelioma.	dms	52-55	P53	Homo sapiens	86-89
29487530-0	2018	Scutellarin Increases Cisplatin-Induced Apoptosis and Autophagy to Overcome Cisplatin Resistance in Non-small Cell Lung Cancer via ERK/p53 and c-met/AKT Signaling Pathways.	Cisplatin	22-31	P53	Homo sapiens	135-138
29487530-5	2018	Mechanistic analyses indicated that cisplatin-induced caspase-3-dependent apoptosis was elevated in the presence of scutellarin through activating extracellular signal-regulated kinases (ERK)-mediated p53 pathway.	Cisplatin	36-45	P53	Homo sapiens	201-204
29472838-9	2018	Pharmacological inhibition of p53 increased lymphocyte survival in Ca&amp;AD patients, contrary to the effect previously reported in HC and AD.	Adenosine Monophosphate	70-73	P53	Homo sapiens	30-33
29472838-11	2018	In all, these results show that cancer imprints an increased resistance to H2O2-induced death in lymphocytes that persists after AD development, and is dependent on both PARP-1 and p53.	Hydrogen Peroxide	75-79	P53	Homo sapiens	181-184
29472838-12	2018	p53 inhibition showed a differential role in cancer and Ca&amp;AD compared to HC and AD lymphocytes, that could explain the inverse susceptibility to oxidative death in cancer and AD.	Adenosine Monophosphate	59-62	P53	Homo sapiens	0-3
29434452-1	2018	AIM: To investigate the predictive value of PIK3CA and TP53 mutation status in colorectal cancer (CRC) patients treated with 5-fluorouracil-based chemotherapy.	Fluorouracil	125-139	P53	Homo sapiens	55-59
29434452-12	2018	CONCLUSION: Double mutation of PIK3CA and TP53 is correlated with a shorter OS in stage II/III CRC patients treated with 5-fluorouracil-based therapy.	Fluorouracil	121-135	P53	Homo sapiens	42-46
29162510-8	2018	CONCLUSION: MMP9, OPN, TP53 and CDKN2A were the identified markers that were expressed in a similar pattern in early embryonic development and cancer development &amp; invasion suggesting that these genes are activated during embryogenesis and might be re-expressed in cancer metastasis.	Adenosine Monophosphate	163-166	P53	Homo sapiens	23-27
29568365-7	2018	Taken together, our results suggested amiodarone caused cancer cell death might be through increased SRSF3-PTC and miR-224 reduction in a p53-independent manner.	Amiodarone	38-48	P53	Homo sapiens	138-141
29242151-2	2018	However, resveratrol-induced nuclear accumulation of COX-2 enhances p53-dependent anti-proliferation in different types of cancers.	Resveratrol	9-20	P53	Homo sapiens	68-71
29130578-8	2018	Notably, mitochondrially targeted p53 (mito-p53) directly reduced mitochondria DNA-encoded ND2 and ND4 gene expression resulting in increased reactive oxygen species (ROS) and reduced mitochondrial oxygen consumption.	Reactive Oxygen Species	142-165	P53	Homo sapiens	34-37
29130578-8	2018	Notably, mitochondrially targeted p53 (mito-p53) directly reduced mitochondria DNA-encoded ND2 and ND4 gene expression resulting in increased reactive oxygen species (ROS) and reduced mitochondrial oxygen consumption.	Reactive Oxygen Species	142-165	P53	Homo sapiens	44-47
29130578-8	2018	Notably, mitochondrially targeted p53 (mito-p53) directly reduced mitochondria DNA-encoded ND2 and ND4 gene expression resulting in increased reactive oxygen species (ROS) and reduced mitochondrial oxygen consumption.	Reactive Oxygen Species	167-170	P53	Homo sapiens	34-37
29130578-8	2018	Notably, mitochondrially targeted p53 (mito-p53) directly reduced mitochondria DNA-encoded ND2 and ND4 gene expression resulting in increased reactive oxygen species (ROS) and reduced mitochondrial oxygen consumption.	Reactive Oxygen Species	167-170	P53	Homo sapiens	44-47
29130578-8	2018	Notably, mitochondrially targeted p53 (mito-p53) directly reduced mitochondria DNA-encoded ND2 and ND4 gene expression resulting in increased reactive oxygen species (ROS) and reduced mitochondrial oxygen consumption.	Oxygen	151-157	P53	Homo sapiens	34-37
29130578-8	2018	Notably, mitochondrially targeted p53 (mito-p53) directly reduced mitochondria DNA-encoded ND2 and ND4 gene expression resulting in increased reactive oxygen species (ROS) and reduced mitochondrial oxygen consumption.	Oxygen	151-157	P53	Homo sapiens	44-47
29225132-0	2018	Ginsenoside Rh4 induces apoptosis and autophagic cell death through activation of the ROS/JNK/p53 pathway in colorectal cancer cells.	Reactive Oxygen Species	86-89	P53	Homo sapiens	94-97
29329830-1	2018	The CBP (CREB (cAMP responsive element binding protein) binding protein) bromodomain (BRD) could recognize and bind with acetyl K382 of human tumor suppressor protein p53 which the mutation of encoding gene might cause human cancers.	Cyclic AMP	15-19	P53	Homo sapiens	167-170
29274324-7	2018	The results demonstrate that two AHR antagonists, alpha-naphthoflavone (alpha-NF) and resveratrol, decreased cell proliferation, arrested cells in the gap 1/synthesis (G1/S) phases, and increased p53 levels and apoptosis.	Resveratrol	86-97	P53	Homo sapiens	196-199
29144987-6	2018	In the mechanism, BPDE significantly increased pro-apoptosis protein (P53 and Bak1) and decreased anti-apoptosis protein (Bcl-2).	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	18-22	P53	Homo sapiens	70-73
29189925-0	2018	Overexpression of Sirtuin2 prevents high glucose-induced vascular endothelial cell injury by regulating the p53 and NF-kappaB signaling pathways.	Glucose	41-48	P53	Homo sapiens	108-111
29285650-10	2018	Furthermore, gemigliptin augments the inhibitory effect of metformin on proliferation and migration through involvement of matrix metalloproteinase-2, matrix metalloproteinase-9, p53, p21, VCAM-1, and ERK in thyroid carcinoma cells.	Metformin	59-68	P53	Homo sapiens	179-182
29242151-3	2018	Treatment with resveratrol leads to phosphorylation and nuclear translocation of mitogen-activated protein kinase (ERK1/2), and accumulation of nuclear COX-2 to complex with pERK1/2 and p53.	Resveratrol	15-26	P53	Homo sapiens	186-189
29242151-4	2018	The consequence is Ser-15 phosphorylation of p53 (pSer15-p53), and induction of anti-proliferation in cancer cells.	Serine	19-22	P53	Homo sapiens	45-48
29242151-4	2018	The consequence is Ser-15 phosphorylation of p53 (pSer15-p53), and induction of anti-proliferation in cancer cells.	Serine	19-22	P53	Homo sapiens	57-60
29242151-5	2018	We investigated the mechanisms by which resveratrol-inducible COX-2 facilitates p53-dependent anti-proliferation in prostate cancer LNCaP cells.	Resveratrol	40-51	P53	Homo sapiens	80-83
29242151-6	2018	Resveratrol treatment caused nuclear accumulation and complexing of ERK1/2, pSer15-p53 and COX-2 which was activated ERK1/2-dependent.	Resveratrol	0-11	P53	Homo sapiens	83-86
29242151-11	2018	In summary, these results demonstrate that inducible COX-2 associates with phosphorylated ERK1/2 to induce the phosphorylation of Ser-15 in p53 and then complexes with p53 and SUMO-1 which binds to p53-responsive pro-apoptotic genes to enhance their expression.	Serine	130-133	P53	Homo sapiens	140-143
29345296-10	2018	The decrease in the VEGF-A level following incubation with cisplatin correlated with a higher p53 protein expression, while no such correlation was observed following treatment of the A549 cells with sunitinib.	Cisplatin	59-68	P53	Homo sapiens	94-97
29281902-19	2018	Local application of rAd-p53 combined with local injection of bleomycin and intravenous infusion of cisplatin, epirubicin and isocyclophosphamide was effective for treatment of uterine sarcoma, especially for patients with liver metastases.	Epirubicin	111-121	P53	Homo sapiens	25-28
29338444-1	2018	Gendicine (recombinant human p53 adenovirus), developed by Shenzhen SiBiono GeneTech Co. Ltd., was approved in 2003 by the China Food and Drug Administration (CFDA) as a first-in-class gene therapy product to treat head and neck cancer, and entered the commercial market in 2004.	gendicine	0-9	P53	Homo sapiens	29-32
29528476-3	2018	This study investigated the effects of ultramolecular dilution of the taxane anti-cancer drugs, which are not commonly used in homeopathic medicines, on mRNA expression profiles of five key genes (p53, p21, COX-2, TUBB2A and TUBB3) in the breast cancer cell line MCF-7.	taxane	70-76	P53	Homo sapiens	197-200
28833404-7	2018	The ERK inhibitor PD98059 and siRNA-mediated ERK silencing induced G1 arrest and p21WAF1/CIP1 expression by downregulating c-Myc in p53-deficient cells.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	18-25	P53	Homo sapiens	132-135
29479097-9	2018	CONCLUSIONS: In Pakistani women the association of TP53 gene codon 72 arginine/proline polymorphism was present..	Arginine	70-78	P53	Homo sapiens	51-55
28902433-14	2018	Curcumin also regulated the BLM and IL-17A mediated changes in p53-PAI-1 expression.	Curcumin	0-8	P53	Homo sapiens	63-66
28902433-15	2018	Curcumin has the ability to regulate inflammatory cytokines during BLM-induced injury and their effect on p53-PAI-1 expression.	Curcumin	0-8	P53	Homo sapiens	106-109
28902433-0	2018	Curcumin alleviates IL-17A-mediated p53-PAI-1 expression in bleomycin-induced alveolar basal epithelial cells.	Curcumin	0-8	P53	Homo sapiens	36-39
29257266-0	2018	Wee1 inhibition can suppress tumor proliferation and sensitize p53 mutant colonic cancer cells to the anticancer effect of irinotecan.	Irinotecan	123-133	P53	Homo sapiens	63-66
29207086-7	2018	Notably, a combination of Tan IIA and doxorubicin (DOX) exposure resulted in further MDM4 overexpression in H1299 cells, indicating that Tan IIA sensitized p53-deficient and MDM4-overexpressing H1299 cells to DOX-induced apoptosis.	Doxorubicin	38-49	P53	Homo sapiens	156-159
29207086-7	2018	Notably, a combination of Tan IIA and doxorubicin (DOX) exposure resulted in further MDM4 overexpression in H1299 cells, indicating that Tan IIA sensitized p53-deficient and MDM4-overexpressing H1299 cells to DOX-induced apoptosis.	Doxorubicin	51-54	P53	Homo sapiens	156-159
29207090-7	2018	Dox-induced cardiac senescence was accompanied by decreased cellular proliferation and viability, increased expression of p53 and p16, and decreased telomere length and telomerase activity, while these effects were relieved by silencing endogenous lincRNA-p21.	Doxorubicin	0-3	P53	Homo sapiens	122-125
29207130-0	2018	Ethanol extract from Cnidium monnieri (L.) Cusson induces cell cycle arrest and apoptosis via regulation of the p53-independent pathway in HepG2 and Hep3B hepatocellular carcinoma cells.	Ethanol	0-7	P53	Homo sapiens	112-115
29434958-0	2018	Anticancer effects of 10-hydroxycamptothecin induce apoptosis of human osteosarcoma through activating caspase-3, p53 and cytochrome c pathways.	10-hydroxycamptothecin	22-44	P53	Homo sapiens	114-117
29290620-2	2018	We hypothesized that the pharmacological activation of p53 with low-dose doxorubicin, which is widely used to treat several types of cancer, may have beneficial effects on nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH).	Doxorubicin	73-84	P53	Homo sapiens	55-58
29290620-0	2018	Pharmacological stimulation of p53 with low-dose doxorubicin ameliorates diet-induced nonalcoholic steatosis and steatohepatitis.	Doxorubicin	49-60	P53	Homo sapiens	31-34
29434992-2	2018	Salvianolic acid B suppressed osteosarcoma cell proliferation and induced apoptosis in the osteosarcoma MG63 cell line, and activated the expressions of cleaved caspase-3, phosphorylated-tumor protein (p)38 mitogen-activated protein kinase (p-p38 MAPK) and phosphorylated-p53 (p-p53) proteins in the MG63 cells.	salvianolic acid B	0-18	P53	Homo sapiens	272-275
29434958-6	2018	The anticancer effects of HCPT were demonstrated to significantly activate the protein expression of p53, PARP-1 and cytochrome c, and suppress Bcl-2 protein expression and promote the activity of caspase-9 and caspase-3 in human osteosarcoma cells.	10-hydroxycamptothecin	26-30	P53	Homo sapiens	101-104
29434992-2	2018	Salvianolic acid B suppressed osteosarcoma cell proliferation and induced apoptosis in the osteosarcoma MG63 cell line, and activated the expressions of cleaved caspase-3, phosphorylated-tumor protein (p)38 mitogen-activated protein kinase (p-p38 MAPK) and phosphorylated-p53 (p-p53) proteins in the MG63 cells.	salvianolic acid B	0-18	P53	Homo sapiens	279-282
29434992-4	2018	The silencing of p38 expression inhibited the anticancer effect of salvianolic acid B on the levels of cell proliferation, p-p53 protein expression and ROS generation level in the MG63 cells.	salvianolic acid B	67-85	P53	Homo sapiens	125-128
29434958-7	2018	In conclusion, the anticancer effects of HCPT appear to induce the apoptosis of human osteosarcoma cells through the activation of the caspase-3, p53 and cytochrome c pathways.	10-hydroxycamptothecin	41-45	P53	Homo sapiens	146-149
29391550-2	2018	Pulsed Hill-type dynamics involves the binding of multiple signal molecules to a receptor and occurs e.g., when transcription factor p53 orchestrates cancer prevention, during calcium signaling, and during circadian rhythms.	Calcium	176-183	P53	Homo sapiens	133-136
29600625-1	2018	This study aimed to investigate the effect of notoginsenoside R1 in delaying H2O2-induced vascular endothelial cell senescence through microRNA-34a/SIRT1/p53 signal pathway.	Hydrogen Peroxide	77-81	P53	Homo sapiens	154-157
29429512-12	2018	RESULTS: The saline-treated HCC group (with prior 15 week DEN exposure) showed higher levels of wnt4 and p53 gene expression (1.59 and 1.36 fold, respectively) and increased percentage in OV6+ progenitor cells (+4.9% in absolute terms) compared to saline-treated controls (p &lt; 0.01, ANOVA).	Sodium Chloride	13-19	P53	Homo sapiens	105-108
29600625-14	2018	The possible mechanism is that notoginsenoside R1 can delay the senescence process of vascular endothelial cells induced by H2O2 by regulating microRNA-34a/SIRT1/p53 signal pathway.	Hydrogen Peroxide	124-128	P53	Homo sapiens	162-165
29422776-8	2018	p53 transcriptional activity was assayed by qPCR, apoptosis by flow cytometry and glycolysis by glucose and lactate measurements, with quantification of glycolytic enzymes expression.	Glucose	96-103	P53	Homo sapiens	0-3
29422776-8	2018	p53 transcriptional activity was assayed by qPCR, apoptosis by flow cytometry and glycolysis by glucose and lactate measurements, with quantification of glycolytic enzymes expression.	Lactic Acid	108-115	P53	Homo sapiens	0-3
29307819-0	2018	Absence of REV3L promotes p53-regulated cancer cell metabolism in cisplatin-treated lung carcinoma cells.	Cisplatin	66-75	P53	Homo sapiens	26-29
29378575-6	2018	DHA, Omegaven  and oxaliplatin were associated with significant downregulation of VEGF and p53 protein, and upregulation of p21 protein.	dehydroacetic acid	0-3	P53	Homo sapiens	91-94
29568362-6	2018	The antitumor activity was partly due to NO-cGMP dependent pathway, contributing to reduced cell number and apoptosis, and partly to the salicylaldehyde moiety and reactive oxygen species (ROS) activated ERK1/2 signaling converging on p53 dependent caspase-3 cleavage.	Reactive Oxygen Species	164-187	P53	Homo sapiens	235-238
29568362-6	2018	The antitumor activity was partly due to NO-cGMP dependent pathway, contributing to reduced cell number and apoptosis, and partly to the salicylaldehyde moiety and reactive oxygen species (ROS) activated ERK1/2 signaling converging on p53 dependent caspase-3 cleavage.	Reactive Oxygen Species	189-192	P53	Homo sapiens	235-238
31508193-6	2018	The presence of the R337H TP53 mutation suggests a mechanism for the observed response to metformin.	Metformin	90-99	P53	Homo sapiens	26-30
29378575-8	2018	CONCLUSION: DHA, Omegaven  and oxaliplatin were associated with downregulation of p53 and VEGF in both cells.	dehydroacetic acid	12-15	P53	Homo sapiens	82-85
29307819-2	2018	The use of low fidelity DNA polymerases in the translesional synthesis (TLS) DNA damage response pathway that repairs lesions caused by cisplatin also presents a mutational carcinogenic burden on cells that needs to be regulated by the tumor suppressor protein p53.	Cisplatin	136-145	P53	Homo sapiens	261-264
29307819-4	2018	In this study, the fluorescence lifetime of the metabolic coenzyme NADH reveals that the absence of REV3L can promote the p53-mediated upregulation of oxidative phosphorylation in cisplatin-treated H1299 lung carcinoma cells and increases cancer cell sensitivity to this platinum-based chemotherapy.	NAD	67-71	P53	Homo sapiens	122-125
29307819-4	2018	In this study, the fluorescence lifetime of the metabolic coenzyme NADH reveals that the absence of REV3L can promote the p53-mediated upregulation of oxidative phosphorylation in cisplatin-treated H1299 lung carcinoma cells and increases cancer cell sensitivity to this platinum-based chemotherapy.	Cisplatin	180-189	P53	Homo sapiens	122-125
29307819-4	2018	In this study, the fluorescence lifetime of the metabolic coenzyme NADH reveals that the absence of REV3L can promote the p53-mediated upregulation of oxidative phosphorylation in cisplatin-treated H1299 lung carcinoma cells and increases cancer cell sensitivity to this platinum-based chemotherapy.	Platinum	271-279	P53	Homo sapiens	122-125
29307819-5	2018	These results demonstrate a previously unrecognized relationship between p53 and REV3L in cancer cell metabolism and may lead to improvements in chemotherapy treatment plans that reduce cisplatin resistance in lung cancer.	Cisplatin	186-195	P53	Homo sapiens	73-76
29346757-5	2018	This delay requires the p53 transcriptional target CDKN1A (encoding p21) and is associated with both slower depletion of intracellular glutathione and a reduced accumulation of toxic lipid-reactive oxygen species (ROS).	Glutathione	135-146	P53	Homo sapiens	24-27
29268127-0	2018	Design, synthesis and biological evaluation of 1, 4-dihydro indeno[1,2-c] pyrazole linked oxindole analogues as potential anticancer agents targeting tubulin and inducing p53 dependent apoptosis.	2-oxindole	90-98	P53	Homo sapiens	171-174
29348517-4	2018	In this study, we investigated the role of NDRG2 in chemo-sensitivity, focusing on cisplatin in U937 histiocytic lymphoma, which has the loss-of-functional mutation in p53.	Cisplatin	83-92	P53	Homo sapiens	168-171
29260852-17	2018	Molecular dynamics (MD) and phasor analysis of single Trp fluorescence signals point toward the presence of preamyloidogenic conformations of p53, which are not observed for p63 or p73.	Tryptophan	54-57	P53	Homo sapiens	142-145
29260852-19	2018	Protection of backbone hydrogen bonds (BHBs) has been shown to be an important factor for the stability of amyloidogenic proteins and was employed to identify and stabilize the structural defect resulting from the p53 Y220C mutation.	Hydrogen	23-31	P53	Homo sapiens	214-217
29367587-0	2018	Long non-coding RNA and microRNA-675/let-7a mediates the protective effect of melatonin against early brain injury after subarachnoid hemorrhage via targeting TP53 and neural growth factor.	Melatonin	78-87	P53	Homo sapiens	159-163
29367587-8	2018	H2O2 obviously upregulated expressions of H19, miR-675, and NGF, and downregulated let-7a and TP53 levels; however, MT treatment reduced expressions of H19, miR-675, and NGF, and improved let-7a and TP53 levels.	Hydrogen Peroxide	0-4	P53	Homo sapiens	94-98
29367587-8	2018	H2O2 obviously upregulated expressions of H19, miR-675, and NGF, and downregulated let-7a and TP53 levels; however, MT treatment reduced expressions of H19, miR-675, and NGF, and improved let-7a and TP53 levels.	Hydrogen Peroxide	0-4	P53	Homo sapiens	199-203
29352261-8	2018	We showed that doxorubicin induced cell senescence in both p53+/+ and p53-/- HCT116 cells, proving that this process is p53-independent.	Doxorubicin	15-26	P53	Homo sapiens	59-62
29352261-8	2018	We showed that doxorubicin induced cell senescence in both p53+/+ and p53-/- HCT116 cells, proving that this process is p53-independent.	Doxorubicin	15-26	P53	Homo sapiens	70-73
29352261-8	2018	We showed that doxorubicin induced cell senescence in both p53+/+ and p53-/- HCT116 cells, proving that this process is p53-independent.	Doxorubicin	15-26	P53	Homo sapiens	70-73
29346757-5	2018	This delay requires the p53 transcriptional target CDKN1A (encoding p21) and is associated with both slower depletion of intracellular glutathione and a reduced accumulation of toxic lipid-reactive oxygen species (ROS).	ros	214-217	P53	Homo sapiens	24-27
29233643-4	2018	Here, we report that SIRT6 deacetylates lysine 382 of p53 in short synthetic peptide sequence and in full length p53.	Lysine	40-46	P53	Homo sapiens	113-116
30613833-6	2018	Results: Significant resistance to 5-FU resulted from p53-loss or from gain-of-function (GOF) mutation (R248W) and was greatest when GOF mutation was coupled with loss of wild-type p53.	Fluorouracil	35-39	P53	Homo sapiens	54-57
29233643-4	2018	Here, we report that SIRT6 deacetylates lysine 382 of p53 in short synthetic peptide sequence and in full length p53.	Lysine	40-46	P53	Homo sapiens	54-57
29433671-8	2018	The three phytochemicals activated the ROS-p38-p53 apoptotic pathway by increasing the level of phosphorylated p38 MAPK and p53, and they activated the ER stress-mediated apoptotic pathway by increasing the level of phosphorylated eIF2alpha and C/EBP homologous protein (CHOP).	Reactive Oxygen Species	39-42	P53	Homo sapiens	47-50
29433671-8	2018	The three phytochemicals activated the ROS-p38-p53 apoptotic pathway by increasing the level of phosphorylated p38 MAPK and p53, and they activated the ER stress-mediated apoptotic pathway by increasing the level of phosphorylated eIF2alpha and C/EBP homologous protein (CHOP).	Reactive Oxygen Species	39-42	P53	Homo sapiens	124-127
29433671-9	2018	Both the ROS-p38-p53 and ER stress-mediated pathway induced the mitochondrial apoptotic pathway by attenuating Bcl-2 expression and upregulating BAX.	Reactive Oxygen Species	9-12	P53	Homo sapiens	17-20
29483824-5	2018	Mechanistically, dioscin may down-regulate the expression of SH2 domain-containing phosphatase-2 (SHP2) at the transcription level by increasing p53 binding to the SHP2 promoter due to reactive oxygen species (ROS).	Reactive Oxygen Species	185-208	P53	Homo sapiens	145-148
29541415-2	2018	We found that NSAIDs including celecoxib (CCB) and ibuprofen (IBU) significantly potentiated the cytotoxicity of Hsp90 inhibitors in human multidrug-resistant (MDR) cells expressing high levels of mutant p53 (mutp53) protein and P-glycoprotein (P-gp), and reversed Hsp90 inhibitor resistance caused by activation of heat shock factor 1 (HSF1) and by up-regulation of heat shock proteins (Hsps) and P-gp.	Ibuprofen	51-60	P53	Homo sapiens	204-207
29541415-2	2018	We found that NSAIDs including celecoxib (CCB) and ibuprofen (IBU) significantly potentiated the cytotoxicity of Hsp90 inhibitors in human multidrug-resistant (MDR) cells expressing high levels of mutant p53 (mutp53) protein and P-glycoprotein (P-gp), and reversed Hsp90 inhibitor resistance caused by activation of heat shock factor 1 (HSF1) and by up-regulation of heat shock proteins (Hsps) and P-gp.	Ibuprofen	62-65	P53	Homo sapiens	204-207
30205806-7	2018	Several studies have demonstrated that silibinin exerts its protective potential partly through interacting with the tumor suppressor gene p53.	Silybin	39-48	P53	Homo sapiens	139-142
28918503-8	2018	The activation of p-GSK3beta expression, cyclophilin D inhibition, and p53 activation through ROS are involved in CoQ0-induced HL-60 apoptotic cell death.	ros	94-97	P53	Homo sapiens	71-74
29174981-7	2018	Excitingly, Lys-104 (K104), a previously identified lysine acetylation site of TIP60 with unknown function, was observed to be indispensable for inducing p53-mediated apoptosis under low glucose condition.	Lysine	12-15	P53	Homo sapiens	154-157
29174981-7	2018	Excitingly, Lys-104 (K104), a previously identified lysine acetylation site of TIP60 with unknown function, was observed to be indispensable for inducing p53-mediated apoptosis under low glucose condition.	Lysine	52-58	P53	Homo sapiens	154-157
29174981-7	2018	Excitingly, Lys-104 (K104), a previously identified lysine acetylation site of TIP60 with unknown function, was observed to be indispensable for inducing p53-mediated apoptosis under low glucose condition.	Glucose	187-194	P53	Homo sapiens	154-157
29331104-2	2018	The present study aimed to investigate whether microRNA-34a (miR-34a), which is a downstream target of P53, is involved in H2O2-induced MSC cell death.	Hydrogen Peroxide	123-127	P53	Homo sapiens	103-106
29185755-3	2018	Furthermore, the expression of p27, a crucial cell cycle control protein, was regulated by binding of progesterone on progesterone receptor B, thus leading to antiproliferative signaling via multiple signaling pathways including p53, PTEN, and antioxidant systems.	Progesterone	102-114	P53	Homo sapiens	229-232
29416929-5	2018	By performing next-generation sequencing on the patient and subsequent verification by Sanger sequencing among other family members, a new germ-line P53 replication error, a trinucleotide repeat mutation in the coding region, was identified in two generations of this Li-Fraumeni family.	trinucleotide	174-187	P53	Homo sapiens	149-152
29493466-8	2018	Drug interactions showed dissimilar results with antagonistic effects with any drug combination in MCF-7 and clear synergic interactions between both PLK1 inhibitors and cisplatin, temozolomide or doxorubicin in Hs578T, which is TP53 mutated.	Cisplatin	170-179	P53	Homo sapiens	229-233
28593498-10	2018	As expected, BPDE activated DNA damage signaling, p53 and AP-1 dependent signaling, oxidative stress response, and apoptosis.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	13-17	P53	Homo sapiens	50-53
29228154-9	2018	Significant changes in gene expression in molecular networks related to Tumor Protein 53 and phosphatidylinositol signaling were identified using DIRAC.	dirac	146-151	P53	Homo sapiens	72-88
29111347-7	2018	N6L toxicity appears to be p53 dependent but interestingly, the leukemic cell line harbouring the mutated form of NPM1 is more resistant to treatment, suggesting that NPM1 cytoplasmic delocalization confers protection from p53 activation.	CHEMBL2152433	0-3	P53	Homo sapiens	27-30
30613833-6	2018	Results: Significant resistance to 5-FU resulted from p53-loss or from gain-of-function (GOF) mutation (R248W) and was greatest when GOF mutation was coupled with loss of wild-type p53.	Fluorouracil	35-39	P53	Homo sapiens	181-184
30488759-4	2018	Here we mathematically modeled the recently dual-phase p53 dynamics under doxorubicin treatment.	Doxorubicin	74-85	P53	Homo sapiens	55-58
30613833-7	2018	F10 is much more potent than 5-FU (137-314-fold depending on TP53 mutational status).	Fluorouracil	29-33	P53	Homo sapiens	61-65
30488759-5	2018	We found that p53 could perform sequential pulses followed by a high-amplitude terminal pulse at relatively low doxorubicin treatment, whereas p53 became steadily accumulated when damage level was high.	Doxorubicin	112-123	P53	Homo sapiens	14-17
30488759-8	2018	Furthermore, lower binding affinity and degradation rate of p53 target genes could favorably discriminate high and low dose doxorubicin treatment.	Doxorubicin	124-135	P53	Homo sapiens	60-63
30198376-0	2018	P53 enhances apoptosis induced by doxorubicin only under conditions of severe DNA damage.	Doxorubicin	34-45	P53	Homo sapiens	0-3
28843007-6	2018	Western blot analysis indicated that ABT-737 combined with HQ increased the levels of cleaved PARP and gamma-H2AX, but significantly decreased the level of P53.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	37-40	P53	Homo sapiens	156-159
30198376-2	2018	However, the comparison of doxorubicin treatment between LNCaP cells carrying p53-wild type and PC3 cells carrying p53-null suggested that p53 might be essential for maximizing apoptosis.	Doxorubicin	27-38	P53	Homo sapiens	78-81
30198376-5	2018	These results advocated that doxorubicin-induced DNA damage controls p53 function for intensifying apoptosis.	Doxorubicin	29-40	P53	Homo sapiens	69-72
30198376-6	2018	Indeed, overexpression of p53 only enhanced apoptosis under conditions of severe DNA damage induced by high concentrations of doxorubicin in LNCaP cells.	Doxorubicin	126-137	P53	Homo sapiens	26-29
28937686-0	2018	Serine 392 phosphorylation modulates p53 mitochondrial translocation and transcription-independent apoptosis.	Serine	0-6	P53	Homo sapiens	37-40
28937686-7	2018	In this study, we focused on the role of serine 392 phosphorylation in the control of p53-dependent apoptosis.	Serine	41-47	P53	Homo sapiens	86-89
28937686-12	2018	Our observations support the premise that serine 392 phosphorylation of p53 influences its mitochondrial translocation and transcription-independent apoptotic function.	Serine	42-48	P53	Homo sapiens	72-75
28287251-0	2018	Cisplatin induced apoptosis of ovarian cancer A2780s cells by activation of ERK/p53/PUMA signals.	Cisplatin	0-9	P53	Homo sapiens	80-83
29307398-6	2018	TP53 codon 72 (arginine) exhibits higher rates of apoptosis and leukemia inhibitory factor expression, whereas the C allele (proline) reduces leukemia inhibitory factor expression.	Arginine	15-23	P53	Homo sapiens	0-4
28287251-9	2018	Inhibition of ERK1/2 using PD98059, a selective MEK inhibitor, blocked the apoptotic cell death but prevented CDDP-induced accumulation of p53 and PUMA.	Cisplatin	110-114	P53	Homo sapiens	139-142
28287251-10	2018	Knockdown of P53 by siRNA transfection also blocked CDDP-induced accumulation of PUMA.	Cisplatin	52-56	P53	Homo sapiens	13-16
28287251-7	2018	The results shown that treatment of A2780s cells with CDDP (3 mug/ml) for 6-24h induced apoptosis, resulting in the activation of extracellular signal-regulated kinase 1/2 (ERK1/2) and accumulation of p53 and PUMA (p53 upregulated modulator of apoptosis) protein.	Cisplatin	54-58	P53	Homo sapiens	201-204
28287251-11	2018	We therefore concluded that CDDP activated ERK1/2 and induced-p53-dependent PUMA upregulation, resulting in triggering apoptosis in A2780s cells.	Cisplatin	28-32	P53	Homo sapiens	62-65
28287251-12	2018	Our study clearly demonstrates that the ERK1/2/p53/PUMA axis is related to CDDP-induced cell death in A2780s cells.	Cisplatin	75-79	P53	Homo sapiens	47-50
28287251-7	2018	The results shown that treatment of A2780s cells with CDDP (3 mug/ml) for 6-24h induced apoptosis, resulting in the activation of extracellular signal-regulated kinase 1/2 (ERK1/2) and accumulation of p53 and PUMA (p53 upregulated modulator of apoptosis) protein.	Cisplatin	54-58	P53	Homo sapiens	215-218
28287251-8	2018	Knockdown of P53 or PUMA by siRNA transfection blocked CDDP-induced apoptosis.	Cisplatin	55-59	P53	Homo sapiens	13-16
28287251-9	2018	Inhibition of ERK1/2 using PD98059, a selective MEK inhibitor, blocked the apoptotic cell death but prevented CDDP-induced accumulation of p53 and PUMA.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	27-34	P53	Homo sapiens	139-142
28860061-6	2018	In addition, porphyran significantly affected the p53-p21 pathways in H2O2-treated WI-38 cells.	Hydrogen Peroxide	70-74	P53	Homo sapiens	50-53
28884474-3	2018	Specifically suboptimal doses of iPA (0.1 and 1 microM) control the selective upregulation of UL16-binding protein 2 on p53wt-expressing U343MG and that of MICA/B on p53mut-expressing U251MG cells.	Isopentenyladenosine	33-36	P53	Homo sapiens	120-123
28884474-3	2018	Specifically suboptimal doses of iPA (0.1 and 1 microM) control the selective upregulation of UL16-binding protein 2 on p53wt-expressing U343MG and that of MICA/B on p53mut-expressing U251MG cells.	Isopentenyladenosine	33-36	P53	Homo sapiens	166-169
28884479-8	2018	Moreover, the p53-HDAC1-mSin3a repressive complex also involved in the inhibition of Aurora-A gene expression upon cisplatin treatment.	Cisplatin	115-124	P53	Homo sapiens	14-17
28981157-10	2018	Mechanistically, melatonin halted fission but recovered mitophagy via blockade of NR4A1/DNA-PKcs/p53 pathway, finally improving mitochondrial and liver function in the setting of NAFLD.	Melatonin	17-26	P53	Homo sapiens	97-100
29094329-8	2018	Allopurinol reduced p53 and p-p53 levels induced by high glucose suggesting an axis of xanthine oxidase-derived ROS, DNA damage, p53 stabilization and endothelial dysfunction that may contribute to the pathogenesis of diabetic nephropathy.	Glucose	57-64	P53	Homo sapiens	20-23
29094329-8	2018	Allopurinol reduced p53 and p-p53 levels induced by high glucose suggesting an axis of xanthine oxidase-derived ROS, DNA damage, p53 stabilization and endothelial dysfunction that may contribute to the pathogenesis of diabetic nephropathy.	Glucose	57-64	P53	Homo sapiens	30-33
29094329-8	2018	Allopurinol reduced p53 and p-p53 levels induced by high glucose suggesting an axis of xanthine oxidase-derived ROS, DNA damage, p53 stabilization and endothelial dysfunction that may contribute to the pathogenesis of diabetic nephropathy.	Glucose	57-64	P53	Homo sapiens	30-33
28981157-12	2018	Meanwhile, we also confirm that melatonin has the ability to cut off the NR4A1/DNA-PKcs/p53 pathway, which confers a protective advantage to hepatocytes and mitochondria.	Melatonin	32-41	P53	Homo sapiens	88-91
28981157-13	2018	The manipulation of NR4A1/DNA-PKcs/p53 pathway by melatonin highlights a new entry point for treating NAFLD.	Melatonin	50-59	P53	Homo sapiens	35-38
28780388-1	2018	In a recent study, we found that blocking the protein kinase ataxia telangiectasia mutated (ATM) with the small molecule inhibitor (SMI) KU-55933 can completely abrogate Mn-induced phosphorylation of p53 at serine 15 (p-p53) in human induced pluripotent stem cell (hiPSC)-differentiated striatal neuroprogenitors.	Serine	207-213	P53	Homo sapiens	200-203
29203914-2	2018	Our objective was to engender synthetic lethality to paclitaxel (PTX), the frontline treatment for endometrial cancer, in tumours with mutant p53 and enhance the therapeutic efficacy using polymeric nanoparticles (NPs).	Paclitaxel	53-63	P53	Homo sapiens	142-145
29203914-2	2018	Our objective was to engender synthetic lethality to paclitaxel (PTX), the frontline treatment for endometrial cancer, in tumours with mutant p53 and enhance the therapeutic efficacy using polymeric nanoparticles (NPs).	Paclitaxel	65-68	P53	Homo sapiens	142-145
29203914-6	2018	Together, our data provide compelling evidence for future studies of BIBF- and PTX-loaded NPs as a therapeutic opportunity for LOF p53 cancers.	Paclitaxel	79-82	P53	Homo sapiens	131-134
30518708-1	2018	SIRT1, an NAD+-dependent deacetylase, causes deacetylation and down-regulation of its target p53.	NAD	10-13	P53	Homo sapiens	93-96
29115429-0	2018	Resveratrol-mediated apoptosis in renal cell carcinoma via the p53/AMP-activated protein kinase/mammalian target of rapamycin autophagy signaling pathway.	Resveratrol	0-11	P53	Homo sapiens	63-66
29115429-8	2018	Resveratrol also promoted the expression of p53 and activated phospho-AMP-activated protein kinase (AMPK).	Resveratrol	0-11	P53	Homo sapiens	44-47
29115429-10	2018	In conclusion, resveratrol suppressed RCC viability and migration, and promoted RCC apoptosis via the p53/AMPK/mTOR-induced autophagy signaling pathway.	Resveratrol	15-26	P53	Homo sapiens	102-105
27871087-0	2018	The HDM2 (MDM2) Inhibitor NVP-CGM097 Inhibits Tumor Cell Proliferation and Shows Additive Effects with 5-Fluorouracil on the p53-p21-Rb-E2F1 Cascade in the p53wild type Neuroendocrine Tumor Cell Line GOT1.	Fluorouracil	103-117	P53	Homo sapiens	125-128
27871087-0	2018	The HDM2 (MDM2) Inhibitor NVP-CGM097 Inhibits Tumor Cell Proliferation and Shows Additive Effects with 5-Fluorouracil on the p53-p21-Rb-E2F1 Cascade in the p53wild type Neuroendocrine Tumor Cell Line GOT1.	Fluorouracil	103-117	P53	Homo sapiens	156-159
27871087-10	2018	NVP-CGM097 and 5-fluorouracil increased p53 and p21 expression in an additive manner.	Fluorouracil	15-29	P53	Homo sapiens	40-43
29343974-6	2018	Results: GSEA suggested that TP53 mutations were significantly associated with cell differentiation, proliferation, cell adhesion biological processes, and MAPK pathway.	gsea	9-13	P53	Homo sapiens	29-33
29138869-0	2018	Cepharanthine exhibits a potent anticancer activity in p53-mutated colorectal cancer cells through upregulation of p21Waf1/Cip1.	cepharanthine	0-13	P53	Homo sapiens	55-58
29138869-3	2018	Mutated p53 in CRC was reported to be associated with resistance to commonly used chemotherapeutic agents including, 5-fluorouracil, oxaliplatin and irinotecan.	Fluorouracil	117-131	P53	Homo sapiens	8-11
29138869-3	2018	Mutated p53 in CRC was reported to be associated with resistance to commonly used chemotherapeutic agents including, 5-fluorouracil, oxaliplatin and irinotecan.	Irinotecan	149-159	P53	Homo sapiens	8-11
29949804-1	2018	BACKGROUND: The purpose of our case control study is to explore the potential association of tumor protein 53 (TP53) c.215G&amp;gt;C, p. (Arg72Pro) polymorphism (rs1042522) with the risk of breast cancer (BC) development in the Moroccan population.	Adenosine Monophosphate	124-127	P53	Homo sapiens	93-109
29949804-1	2018	BACKGROUND: The purpose of our case control study is to explore the potential association of tumor protein 53 (TP53) c.215G&amp;gt;C, p. (Arg72Pro) polymorphism (rs1042522) with the risk of breast cancer (BC) development in the Moroccan population.	Adenosine Monophosphate	124-127	P53	Homo sapiens	111-115
29949804-7	2018	CONCLUSION: Our results suggest that TP53 c.215G&amp;gt;C, p. (Arg72Pro) polymorphism may be considered as a genetic marker for predisposition to BC in Moroccan population.	Adenosine Monophosphate	49-52	P53	Homo sapiens	37-41
29756546-8	2018	Moreover, sinomenine inhibited the growth of U87 xenograft tumors in vivo and raised the p53 protein expression.	sinomenine	10-20	P53	Homo sapiens	89-92
29756546-9	2018	Collectively, sinomenine shows antiproliferative effects against glioma cells which is mediated through downregulation of sirtuin 1 and induction of p53 activity.	sinomenine	14-24	P53	Homo sapiens	149-152
29254796-6	2018	Our results revealed that 22 of 41 (54%) VINs showed novel accentuated wild type (WT) staining with non-linear basal staining for p53, including 12 (52%) cases histologically suggestive of DVIN and 10 (56%) described as UVIN.	vins	41-45	P53	Homo sapiens	130-133
29756546-0	2018	Sinomenine Induces G1-Phase Cell Cycle Arrest and Apoptosis in Malignant Glioma Cells Via Downregulation of Sirtuin 1 and Induction of p53 Acetylation.	sinomenine	0-10	P53	Homo sapiens	135-138
29756546-6	2018	Mechanistically, sinomenine promoted p53 expression and acetylation and reduced the expression of sirtuin 1.	sinomenine	17-27	P53	Homo sapiens	37-40
29756546-7	2018	Ectopic expression of sirtuin 1 significantly prevented sinomenine-induced p53 acetylation and growth suppression in glioma cells.	sinomenine	56-66	P53	Homo sapiens	75-78
29233996-5	2017	However, the PEPD-p53 complex is critical for p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve robust p53 activation, which is mediated by reactive oxygen species.	Doxorubicin	88-99	P53	Homo sapiens	18-21
29951436-0	2017	Association of p53 codon 72 Arg&gt;Pro polymorphism and risk of cancer in Iranian population: A systematic review and meta-analysis.	Arginine	28-31	P53	Homo sapiens	15-18
29951436-1	2017	Background: Different studies have investigated the association between p53 codon 72 Arg&gt;Pro polymorphism and cancer risk.	Arginine	85-88	P53	Homo sapiens	72-75
29951436-12	2017	Conclusion: Our study revealed that p53 codon 72 Arg&gt;Pro polymorphism was not associated with overall cancer odds in Iranian population.	Arginine	49-52	P53	Homo sapiens	36-39
29225033-0	2017	Mutant p53 Gains Its Function via c-Myc Activation upon CDK4 Phosphorylation at Serine 249 and Consequent PIN1 Binding.	Serine	80-86	P53	Homo sapiens	7-10
29383186-0	2017	Bisphenol A induces cell cycle arrest in primary and prostate cancer cells through EGFR/ERK/p53 signaling pathway activation.	bisphenol A	0-11	P53	Homo sapiens	92-95
29383186-7	2017	Altogether, these findings show a novel signaling pathway in which EGFR activation plays a key role on BPA-induced cell cycle inhibition through a pathway involving AR and ERbeta/EGFR complexes, ERK and p53.	bisphenol A	103-106	P53	Homo sapiens	203-206
29061672-9	2017	Further, they resensitized mutant p53-expressing cell lines resistant to 5-fluorouracil.	Fluorouracil	73-87	P53	Homo sapiens	34-37
29416744-7	2018	Western blotting showed that PDOX caused much higher expressions of P53, P21, Aparf-1, pro- and cleaved-caspase 3, compared with DOX.	Doxorubicin	30-33	P53	Homo sapiens	68-71
29021323-8	2017	Mechanistically, doxorubicin-induced DNA damage in c-kit+ cells resulted in expression of p53.	Doxorubicin	17-28	P53	Homo sapiens	90-93
29021323-9	2017	Inhibition of p53 blocked cardiomyocyte differentiation in response to doxorubicin, whereas stabilization of p53 was sufficient to increase c-kit-derived cardiomyocyte differentiation.	Doxorubicin	71-82	P53	Homo sapiens	14-17
29242407-4	2017	By RNA-sequencing, transcriptome changes were analyzed in human ECs exposed to H2O2, highlighting a pivotal role of p53-signaling.	Hydrogen Peroxide	79-83	P53	Homo sapiens	116-119
29242407-6	2017	Among microRNAs (miRNAs), miR-192-5p was the most induced by H2O2 treatment, in a p53-dependent manner.	Hydrogen Peroxide	61-65	P53	Homo sapiens	82-85
29242407-9	2017	A central role of the p53-pathway was also confirmed by the analysis of differential exon usage: Upon H2O2 treatment, the expression of p53-dependent 5"-isoforms of MDM2 and PVT1 increased selectively.	Hydrogen Peroxide	102-106	P53	Homo sapiens	22-25
29242407-9	2017	A central role of the p53-pathway was also confirmed by the analysis of differential exon usage: Upon H2O2 treatment, the expression of p53-dependent 5"-isoforms of MDM2 and PVT1 increased selectively.	Hydrogen Peroxide	102-106	P53	Homo sapiens	136-139
29371974-0	2017	Novel proteasome inhibitor delanzomib sensitizes cervical cancer cells to doxorubicin-induced apoptosis via stabilizing tumor suppressor proteins in the p53 pathway.	Doxorubicin	74-85	P53	Homo sapiens	153-156
29233996-5	2017	However, the PEPD-p53 complex is critical for p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve robust p53 activation, which is mediated by reactive oxygen species.	Doxorubicin	88-99	P53	Homo sapiens	46-49
29371974-7	2017	Additionally, delanzomib worked synergistically with Dox to further upregulate p53 and its downstream targets and enhanced Dox-induced p38 phosphorylation.	Doxorubicin	53-56	P53	Homo sapiens	79-82
29233996-5	2017	However, the PEPD-p53 complex is critical for p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve robust p53 activation, which is mediated by reactive oxygen species.	Doxorubicin	88-99	P53	Homo sapiens	46-49
29233996-5	2017	However, the PEPD-p53 complex is critical for p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve robust p53 activation, which is mediated by reactive oxygen species.	Doxorubicin	88-99	P53	Homo sapiens	46-49
29233996-5	2017	However, the PEPD-p53 complex is critical for p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve robust p53 activation, which is mediated by reactive oxygen species.	Hydrogen Peroxide	104-108	P53	Homo sapiens	18-21
29233996-5	2017	However, the PEPD-p53 complex is critical for p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve robust p53 activation, which is mediated by reactive oxygen species.	Hydrogen Peroxide	104-108	P53	Homo sapiens	46-49
29233996-5	2017	However, the PEPD-p53 complex is critical for p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve robust p53 activation, which is mediated by reactive oxygen species.	Hydrogen Peroxide	104-108	P53	Homo sapiens	46-49
29233996-5	2017	However, the PEPD-p53 complex is critical for p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve robust p53 activation, which is mediated by reactive oxygen species.	Hydrogen Peroxide	104-108	P53	Homo sapiens	46-49
29233996-5	2017	However, the PEPD-p53 complex is critical for p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve robust p53 activation, which is mediated by reactive oxygen species.	Reactive Oxygen Species	202-225	P53	Homo sapiens	18-21
29233996-5	2017	However, the PEPD-p53 complex is critical for p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve robust p53 activation, which is mediated by reactive oxygen species.	Reactive Oxygen Species	202-225	P53	Homo sapiens	46-49
29233996-5	2017	However, the PEPD-p53 complex is critical for p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve robust p53 activation, which is mediated by reactive oxygen species.	Reactive Oxygen Species	202-225	P53	Homo sapiens	46-49
29233996-5	2017	However, the PEPD-p53 complex is critical for p53 response to stress, as stress signals doxorubicin and H2O2 each must free p53 from PEPD in order to achieve robust p53 activation, which is mediated by reactive oxygen species.	Reactive Oxygen Species	202-225	P53	Homo sapiens	46-49
29054408-3	2017	Here, we show HDAC6 negatively regulates pro-apoptotic acetylation of p53 at lysine residue 120 (K120) in mesenchymal stem cells (MSCs).	Lysine	77-83	P53	Homo sapiens	70-73
29292794-6	2017	Moreover, knockdown of p53 resulted in higher non-transferrin-bound iron uptake, which was mediated by increased ZIP14 levels.	Iron	68-72	P53	Homo sapiens	23-26
29333130-3	2017	Here, curcumin, flavokawain B, and alpinetin were docked against the crystal structure of R273H mutant p53 in silico.	Curcumin	6-14	P53	Homo sapiens	103-106
29333130-4	2017	Consequently, all the compounds bind to the cavity of R273H mutant p53 with a dissociation constant estimated to have 36.57, 70.77, and 75.11 microM for curcumin, flavokawain B, and alpinetin, respectively.	Curcumin	153-161	P53	Homo sapiens	67-70
29292794-7	2017	Our study highlights a role for p53 in regulating nutrient metabolism and provides insight into how iron and possibly other metals such as zinc and manganese could be regulated in p53-inactivated tumor cells.	Iron	100-104	P53	Homo sapiens	32-35
29292794-7	2017	Our study highlights a role for p53 in regulating nutrient metabolism and provides insight into how iron and possibly other metals such as zinc and manganese could be regulated in p53-inactivated tumor cells.	Iron	100-104	P53	Homo sapiens	180-183
29110611-13	2017	Further study showed curcumin induced cell cycle arrest by activating G2 checkpoint through p53 pathway.	Curcumin	21-29	P53	Homo sapiens	92-95
28989024-3	2017	Forced inhibition of cPKC or aPKC induced the activation of senescence markers, including senescence-associated beta-galactosidase activity and reactive oxygen species (ROS)-p53-p21Cip1/WAF1 axis in HCT116 and HEK293 cells.	Reactive Oxygen Species	144-167	P53	Homo sapiens	174-177
28989024-3	2017	Forced inhibition of cPKC or aPKC induced the activation of senescence markers, including senescence-associated beta-galactosidase activity and reactive oxygen species (ROS)-p53-p21Cip1/WAF1 axis in HCT116 and HEK293 cells.	Reactive Oxygen Species	169-172	P53	Homo sapiens	174-177
28989024-7	2017	Therefore, this study suggests for the first time that downregulation of PKC induces senescence through the AKT-FoxO3a-ROS-p53-p21Cip1/WAF1 pathway in HCT116 and HEK293 cells.	Reactive Oxygen Species	119-122	P53	Homo sapiens	123-126
29423021-0	2018	Association of p53 and mitochondrial gene with chemosensitization by metformin in ovarian cancer.	Metformin	69-78	P53	Homo sapiens	15-18
29423021-1	2018	Objective: This study aims to investigate the association of p53 and D-loop gene with drug resistance and sensitization induced by metformin in ovarian cancer.	Metformin	131-140	P53	Homo sapiens	61-64
29074256-6	2017	Additionally, the molecular docking studies between the tumour suppressor protein p53 with the lead compound 3h, which exhibited better anticancer activity against HeLa cells was examined.	Tritium	109-111	P53	Homo sapiens	82-85
29089230-1	2017	A series of novel amino acid ester derivatives of 2,3-substituted isoindolinones was synthesized and evaluated for p53-mediated apoptotic activity.	2,3-substituted isoindolinones	50-80	P53	Homo sapiens	115-118
29191192-11	2017	Furthermore, the expression of the apoptosis-inducing proteins, p53 and caspase-3, significantly increased in response to ETBO, whereas the expression of the anti-apoptotic protein, Bcl-2, decreased.	etbo	122-126	P53	Homo sapiens	64-67
29191192-12	2017	These data imply that ETBO induces apoptosis by caspase activation through the modulation of pro-apoptotic and anti-apoptotic gene, p53 and Bcl-2, respectively.	etbo	22-26	P53	Homo sapiens	132-135
29046333-0	2017	The p53-inducible long noncoding RNA TRINGS protects cancer cells from necrosis under glucose starvation.	Glucose	86-93	P53	Homo sapiens	4-7
28421464-6	2017	Somatic gene sequencing revealed a novel TP53 mutation in DNA extracted from paraffin-embedded tissue, a deletion of 8bp in exon 8 (c.811_818del8; GAGGTGCG/-) in homo or hemizygosis causing a subsequent frameshift and premature stop codon at position 302.	Paraffin	77-85	P53	Homo sapiens	41-45
28835450-5	2017	At early precancerous and neoplastic stages, antioxidant activity decreases and ROS appear to promote cancer initiation via inducing oxidative damage and base pair substitution mutations in pro-oncogenes and tumor suppressor genes, such as RAS and TP53, respectively.	Reactive Oxygen Species	80-83	P53	Homo sapiens	248-252
29043595-11	2017	Cortisol increased the Bcl2L12 expression in HCC to inhibit p53 expression.	Hydrocortisone	0-8	P53	Homo sapiens	60-63
29043595-12	2017	CONCLUSIONS: Stress hormone cortisol suppresses p53 in HCC via enhancing Bcl2L12 expression in HCC.	Hydrocortisone	28-36	P53	Homo sapiens	48-51
29046333-4	2017	Here, we show that under glucose starvation condition, p53 directly upregulates a novel lncRNA named TRINGS (Tp53-regulated inhibitor of necrosis under glucose starvation) in human tumor cells.	Glucose	25-32	P53	Homo sapiens	55-58
29039478-0	2017	Phosphorylation of eIF2alpha suppresses cisplatin-induced p53 activation and apoptosis by attenuating oxidative stress via ATF4-mediated HO-1 expression in human renal proximal tubular cells.	Cisplatin	40-49	P53	Homo sapiens	58-61
29039462-0	2017	Antiproliferative activity of di-2-pyridylhydrazone dithiocarbamate acetate partly involved in p53 mediated apoptosis and autophagy.	di-2-pyridylhydrazone dithiocarbamate acetate	30-75	P53	Homo sapiens	95-98
29039478-6	2017	Cisplatin induced eIF2alpha phosphorylation as well as p53 activation.	Cisplatin	0-9	P53	Homo sapiens	55-58
29039478-3	2017	It has been suggested that oxidative stress and p53 activation play important roles in cisplatin-induced nephrotoxicity.	Cisplatin	87-96	P53	Homo sapiens	48-51
29039478-8	2017	Of note, Sal003-mediated upregulation of eIF2alpha phosphorylation suppressed cisplatin-induced p53 activation.	Cisplatin	78-87	P53	Homo sapiens	96-99
29039478-9	2017	Furthermore, reduction of eIF2alpha phosphorylation by PERK knockdown enhanced cisplatin-induced p53 activation and apoptosis.	Cisplatin	79-88	P53	Homo sapiens	97-100
29039558-0	2017	Insulin in combination with cisplatin induces the apoptosis of ovarian cancer cells via p53 and JNK activation.	Cisplatin	28-37	P53	Homo sapiens	88-91
29039478-12	2017	Taken together, these results suggest that phosphorylation of eIF2alpha suppresses cisplatin-induced p53 activation and apoptosis by attenuating oxidative stress via ATF4-mediated HO-1 expression in HK-2 cells, as ATF4 expression is usually dependent on the phosphorylation of eIF2alpha and may also transcriptionally induce the expression of HO-1 in response to oxidative stress.	Cisplatin	83-92	P53	Homo sapiens	101-104
28802253-0	2017	The Combination of Metformin and Valproic Acid Induces Synergistic Apoptosis in the Presence of p53 and Androgen Signaling in Prostate Cancer.	Metformin	19-28	P53	Homo sapiens	96-99
29302583-3	2017	The HPV oncoprotein E6 binds to the tumor suppressor gene product p53, promoting its degradation; the Arg allele of TP53 R72P polymorphism binds more ardently with HPV E6 than the Pro variant.	Arginine	102-105	P53	Homo sapiens	66-69
29302583-3	2017	The HPV oncoprotein E6 binds to the tumor suppressor gene product p53, promoting its degradation; the Arg allele of TP53 R72P polymorphism binds more ardently with HPV E6 than the Pro variant.	Arginine	102-105	P53	Homo sapiens	116-120
29039537-10	2017	In conclusion, juglone potentiated TRAIL-induced apoptosis in melanoma cells, and these effects were partially mediated through the ROS-p38-p53 pathway.	Reactive Oxygen Species	132-135	P53	Homo sapiens	140-143
29070518-8	2017	Digoxin treatment combined with IR allowed the damaged cell to progress through the cell cycle via suppression of cell cycle-related proteins (p53, cyclin D1, cyclin B1, CDK4, and p-cdc2).	Digoxin	0-7	P53	Homo sapiens	143-146
29179721-7	2017	Mechanistically, apigenin activated p53 that induced catalase, a ROS scavenger enzyme, and inhibited STAT3, the most important pro-survival pathway in PEL, as assessed by p53 silencing.	ros	65-68	P53	Homo sapiens	36-39
29167573-3	2017	We studied the anti-cancer activity of metformin on colorectal cancer (CRC) by using the drug to treat HT29, HCT116 and HCT116 p53-/- CRC cells.	Metformin	39-48	P53	Homo sapiens	127-130
29175850-5	2017	We demonstrate the use of INDRA and natural language to model three biological processes of increasing scope: (i) p53 dynamics in response to DNA damage, (ii) adaptive drug resistance in BRAF-V600E-mutant melanomas, and (iii) the RAS signaling pathway.	indra	26-31	P53	Homo sapiens	114-117
28967197-7	2017	Furthermore, inactivation of mitochondria and activation of p53 protein are observed during MGNP treatment, which provides evidence for metformin-induced cell apoptosis pathways.	mgnp	92-96	P53	Homo sapiens	60-63
28967197-7	2017	Furthermore, inactivation of mitochondria and activation of p53 protein are observed during MGNP treatment, which provides evidence for metformin-induced cell apoptosis pathways.	Metformin	136-145	P53	Homo sapiens	60-63
29290977-3	2017	We have previously reported that expression of Bruton"s Tyrosine Kinase (BTK) induces phosphorylation of p53 at the N-terminus, including Serine 15, and increases its protein levels and activity.	Serine	138-144	P53	Homo sapiens	105-108
29161238-0	2017	Downregulation of Inhibition of Apoptosis-Stimulating Protein of p53 (iASPP) Suppresses Cisplatin-Resistant Gastric Carcinoma In Vitro.	Cisplatin	88-97	P53	Homo sapiens	65-68
28942112-4	2017	Further investigations on mechanism of action of this class of compound demonstrated that the representative compound 8k could trigger p53/Bax-independent colorectal cancer cell apoptosis via inducing ROS accumulation.	ros	201-204	P53	Homo sapiens	135-138
29296177-0	2017	ISG15 silencing increases cisplatin resistance via activating p53-mediated cell DNA repair.	Cisplatin	26-35	P53	Homo sapiens	62-65
28981686-8	2017	Physiologically relevant nucleolar stress induction with reactive oxygen species reaffirms a p53-independent p27kip1 response pathway and leads to nascent pre-rRNA reduction.	Reactive Oxygen Species	57-80	P53	Homo sapiens	93-96
28928082-0	2017	miR-338-3p confers 5-fluorouracil resistance in p53 mutant colon cancer cells by targeting the mammalian target of rapamycin.	Fluorouracil	19-33	P53	Homo sapiens	48-51
28928082-1	2017	Evidence demonstrate that p53 mutations and microRNAs (miRs) are important components of 5-FU resistance in colorectal cancer (CRC).	Fluorouracil	89-93	P53	Homo sapiens	26-29
28928082-8	2017	Moreover, inhibition of miR-338-3p in HT29 and HCT116 p53-/- cells increased their sensitivity to 5-FU treatment.	Fluorouracil	98-102	P53	Homo sapiens	54-57
28928082-10	2017	Our results reveal a critical and novel role of miR-338-3p in the correlation of 5-FU resistance with p53 status.	Fluorouracil	81-85	P53	Homo sapiens	102-105
28928082-11	2017	Moreover, the miR-338-3p inhibitor has the potential to overcome 5-FU resistance in p53 mutant colon cancer cells.	Fluorouracil	65-69	P53	Homo sapiens	84-87
29033244-4	2017	Here, we demonstrate that iASPP, a known p53 inhibitor, lowers ROS independently of p53.	Reactive Oxygen Species	63-66	P53	Homo sapiens	41-44
29131834-7	2017	Pathway analysis of potential mRNAs targets of these miRNA revealed in the DLBCL group potential up-regulation of STAT3, IL8, p13k/AKT and TGF-B signaling, and potential down-regulation of the PTEN and p53 pathways; while in the HL group we have found the cAMP-mediated pathway and p53 pathway to be potentially down-regulated.	Cyclic AMP	256-260	P53	Homo sapiens	202-205
28869866-3	2017	In order to overcome these limitations, an oncolytic Ad expressing a p53 variant (oAd-vp53) that is resistant to p53 inactivation in the tumor microenvironment was complexed with PEGylated and PTX-conjugated polymeric micelle (APP).	Paclitaxel	193-196	P53	Homo sapiens	69-72
29127423-6	2017	We demonstrate that, in the cells with active p53, ectopic expression of NPRL2 induces NOX2-dependent production of reactive oxygen species and DNA damage.	Reactive Oxygen Species	116-139	P53	Homo sapiens	46-49
28931625-0	2017	PML is a ROS sensor activating p53 upon oxidative stress.	Reactive Oxygen Species	9-12	P53	Homo sapiens	31-34
29126407-7	2017	RESULTS: Patients with Arg/Arg and Arg/Pro at codon 72 of TP53 had a higher complete response rate (61% vs. 44%, P = 0.007) than those with Pro/Pro.	Arginine	23-26	P53	Homo sapiens	58-62
28867193-7	2017	Our results indicate that TRIM25 is associated with cisplatin resistance and 14-3-3sigma-MDM2-p53 signaling pathway is involved in this process, suggesting targeting TRIM25 may be a potential strategy for the reversal of cisplatin resistance.	Cisplatin	221-230	P53	Homo sapiens	94-97
28696156-4	2017	In this study we isolated cisplatin-resistant clones from MHM cells, an MDM2-amplified and p53 wild-type osteosarcoma cell line.	Cisplatin	26-35	P53	Homo sapiens	91-94
28760703-7	2017	p53 was upregulated by DOX, and appeared to be a direct target of Sirt3, suggesting that Sirt3-mediated protection against cell death could be related to this protein.	Doxorubicin	23-26	P53	Homo sapiens	0-3
28801242-8	2017	H2O2 contributed to T/B-mediated ERK1/2 activation that mediated p53 phosphorylation at serine 15 (Ser15) and increased p21 expression.	Hydrogen Peroxide	0-4	P53	Homo sapiens	65-68
28801242-8	2017	H2O2 contributed to T/B-mediated ERK1/2 activation that mediated p53 phosphorylation at serine 15 (Ser15) and increased p21 expression.	Serine	88-94	P53	Homo sapiens	65-68
28888620-6	2017	In addition, p53-overexpressing cells accumulated intracellular ROS via cytochrome c release mediated by the BH3-only protein Noxa induction.	Reactive Oxygen Species	64-67	P53	Homo sapiens	13-16
28387973-0	2017	Fusaric Acid Induces DNA Damage and Post-Translational Modifications of p53 in Human Hepatocellular Carcinoma (HepG2 ) Cells.	Fusaric Acid	0-12	P53	Homo sapiens	72-75
28425621-0	2017	p53-competent cells and p53-deficient cells display different susceptibility to oxygen functionalized graphene cytotoxicity and genotoxicity.	Oxygen	80-86	P53	Homo sapiens	0-3
28425621-0	2017	p53-competent cells and p53-deficient cells display different susceptibility to oxygen functionalized graphene cytotoxicity and genotoxicity.	Oxygen	80-86	P53	Homo sapiens	24-27
28425621-5	2017	Here, we show that p53 functional status correlates with oxygen functionalized graphene (f-G) cytotoxicity and genotoxicity in vitro.	Oxygen	57-63	P53	Homo sapiens	19-22
28425621-6	2017	The f-G exposed p53-competent cells, but not p53-deficient cells, initiated G0 /G1 phase cell cycle arrest, suppressed reactive oxygen species, and entered apoptosis.	Reactive Oxygen Species	119-142	P53	Homo sapiens	16-19
28387973-8	2017	FA decreased the protein expression of p53 (0.24-fold, P = 0.0004) and increased the expression of p-Ser-15-p53 (12.74-fold, P = 0.0126) and a-K382-p53 (2.24-fold, P = 0.0096).	Serine	101-104	P53	Homo sapiens	108-111
28387973-8	2017	FA decreased the protein expression of p53 (0.24-fold, P = 0.0004) and increased the expression of p-Ser-15-p53 (12.74-fold, P = 0.0126) and a-K382-p53 (2.24-fold, P = 0.0096).	Serine	101-104	P53	Homo sapiens	108-111
29068287-1	2017	All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to activate p14 expression via promoter hypermethylation to induce p53-dependent apoptosis in human hepatocytes.	Tretinoin	0-23	P53	Homo sapiens	162-165
29068287-1	2017	All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to activate p14 expression via promoter hypermethylation to induce p53-dependent apoptosis in human hepatocytes.	Tretinoin	25-29	P53	Homo sapiens	162-165
27989010-0	2017	Effect of curcumin on the expression of p53, transforming growth factor-beta, and inducible nitric oxide synthase in oral submucous fibrosis: A pilot study.	Curcumin	10-18	P53	Homo sapiens	40-43
29068287-2	2017	In this study, we found that the oncogenic hepatitis B virus (HBV) X protein (HBx) of HBV, derived from both overexpression and 1.2-mer replicon systems, suppresses ATRA-induced apoptosis in p53-positive human hepatocytes.	Tretinoin	165-169	P53	Homo sapiens	191-194
27989010-6	2017	After therapy with curcumin, a decrease in the expression of p53, TGF-beta, and iNOS was seen in 25%, 32.1%, and 32.1% of the samples, respectively; however, the difference in pretreatment and post-treatment expressions was not found to be statistically significant.	Curcumin	19-27	P53	Homo sapiens	61-64
27989010-7	2017	CONCLUSION: The present finding suggest that curcumin could have an effect on the expression of p53, iNOS, and TGF-beta in OSMF, and thus, could prove to be an effective chemopreventive agent for its management.	Curcumin	45-53	P53	Homo sapiens	96-99
29068287-4	2017	As a result, HBx was able to impair the potential of ATRA to activate apoptosis-related molecules, including Bax, p53-upregulated modulator of apoptosis, caspase-9, caspase-3 and poly (ADP-ribose) polymerase.	Tretinoin	53-57	P53	Homo sapiens	114-117
29068287-5	2017	In conclusion, the present study provides a new oncogenic action mechanism of HBx, namely by suppressing the anticancer potential of ATRA to induce p53-dependent apoptosis in HBV-infected hepatocytes.	Tretinoin	133-137	P53	Homo sapiens	148-151
28543759-11	2017	In conclusion, we established a connection among ROS, ATM and p73 in AGG-induced apoptosis, which might be useful in enhancing the therapeutic targeting of p53 deficient oral squamous cell carcinoma.	Reactive Oxygen Species	49-52	P53	Homo sapiens	156-159
29093644-0	2017	Synergistic anticancer effect of combined crocetin and cisplatin on KYSE-150 cells via p53/p21 pathway.	Cisplatin	55-64	P53	Homo sapiens	87-90
28618116-1	2017	Mutations in the tumor suppressor p53 are highly prevalent in cancers and are known to influence the sensitivity of cells to various chemotherapeutics including the anti-cancer candidates 1,25-dihydrovitamin D3 [1,25D3] and metformin.	Metformin	224-233	P53	Homo sapiens	34-37
29035366-0	2017	Cytoplasmic p53 couples oncogene-driven glucose metabolism to apoptosis and is a therapeutic target in glioblastoma.	Glucose	40-47	P53	Homo sapiens	12-15
29035366-3	2017	Mechanistic studies revealed that after attenuated glucose consumption, Bcl-xL blocks cytoplasmic p53 from triggering intrinsic apoptosis.	Glucose	51-58	P53	Homo sapiens	98-101
29035366-7	2017	Together, these studies identify a crucial link among oncogene signaling, glucose metabolism, and cytoplasmic p53, which may potentially be exploited for combination therapy in GBM and possibly other malignancies.	Glucose	74-81	P53	Homo sapiens	110-113
29093644-15	2017	Conclusions: We concluded that crocetin combined with cisplatin exerts a synergistic anticancer effect by up-regulating the p53/p21 pathway.	Cisplatin	54-63	P53	Homo sapiens	124-127
28944886-0	2017	Sulforaphane induces p53-deficient SW480 cell apoptosis via the ROS-MAPK signaling pathway.	Reactive Oxygen Species	64-67	P53	Homo sapiens	21-24
28944886-9	2017	In addition, the results demonstrated that even at the lowest concentrations (5 microM), SFN increased the sensitivity of p53-proficient HCT-116 cells to cisplatin.	Cisplatin	154-163	P53	Homo sapiens	122-125
28813624-11	2017	All mixed confluent cultures expressed enhanced radio-sensitization (P &lt;= 0.047) characteristic of TP53 Mut cells, which could be inhibited by their exposure to the antioxidant N-acetyl-l-cysteine (NAC) indicating a role for intercellular signaling by reactive oxygen species (ROS).	Reactive Oxygen Species	255-278	P53	Homo sapiens	102-106
28813624-11	2017	All mixed confluent cultures expressed enhanced radio-sensitization (P &lt;= 0.047) characteristic of TP53 Mut cells, which could be inhibited by their exposure to the antioxidant N-acetyl-l-cysteine (NAC) indicating a role for intercellular signaling by reactive oxygen species (ROS).	Reactive Oxygen Species	280-283	P53	Homo sapiens	102-106
29093644-14	2017	The wild-type p53 inhibitor, PFT-alpha suppressed the overexpression of p53/p21 and the synergistic effect induced by the combination of crocetin and cisplatin.	Cisplatin	150-159	P53	Homo sapiens	72-75
29093644-14	2017	The wild-type p53 inhibitor, PFT-alpha suppressed the overexpression of p53/p21 and the synergistic effect induced by the combination of crocetin and cisplatin.	Cisplatin	150-159	P53	Homo sapiens	14-17
28945070-8	2017	Detailed molecular studies on MCF7 cells also established that upon exposure to Se@CMHA-DOX NPs, MCF7 cells endure G2/M cell cycle arrest and p53-mediated caspase-independent apoptosis.	Doxorubicin	88-91	P53	Homo sapiens	142-145
29073244-5	2017	We found that 10 muM resveratrol improved the proliferation of porcine PSCs, increased the expression of A-beta-catenin (active beta-catenin), Pcna, C-Myc, Bcl-2 and sirtuin-1 (Sirt1), and decreased the expression of P53, Caspase3.	Resveratrol	21-32	P53	Homo sapiens	217-220
29031295-0	2017	Competitive amperometric immunosensor for determination of p53 protein in urine with carbon nanotubes/gold nanoparticles screen-printed electrodes: A potential rapid and noninvasive screening tool for early diagnosis of urinary tract carcinoma.	Carbon	85-91	P53	Homo sapiens	59-62
29031295-2	2017	Here we report the first study on the development and validation of a novel disposable competitive amperometric immunosensor for determination of p53 protein at subnanomolar levels, based on p53 immobilization on gold nanoparticles/carbon nanotubes modified screen-printed carbon electrodes.	Carbon	232-238	P53	Homo sapiens	146-149
29031295-2	2017	Here we report the first study on the development and validation of a novel disposable competitive amperometric immunosensor for determination of p53 protein at subnanomolar levels, based on p53 immobilization on gold nanoparticles/carbon nanotubes modified screen-printed carbon electrodes.	Carbon	273-279	P53	Homo sapiens	191-194
29031295-2	2017	Here we report the first study on the development and validation of a novel disposable competitive amperometric immunosensor for determination of p53 protein at subnanomolar levels, based on p53 immobilization on gold nanoparticles/carbon nanotubes modified screen-printed carbon electrodes.	Carbon	273-279	P53	Homo sapiens	146-149
29048401-5	2017	Treating cells with a genotoxic drug doxorubicin at various doses and durations, we found that a mild and prolonged challenge triggered sequential p53 pulses and ultimately resulted in a terminal pulse enacting apoptosis in a comparable rate with that induced by an acute and high-dose treatment.	Doxorubicin	37-48	P53	Homo sapiens	147-150
29033320-5	2017	However, when mitophagy is inhibited, p53 is phosphorylated at serine-392 by PINK1, a kinase associated with mitophagy, on mitochondria and translocated into the nucleus, where it binds to the NANOG promoter to prevent OCT4 and SOX2 transcription factors from activating the expression of NANOG, a transcription factor critical for maintaining the stemness and the self-renewal ability of CSCs, resulting in the reduction of hepatic CSC populations.	Serine	63-69	P53	Homo sapiens	38-41
29228612-0	2017	MiR-204 enhances mitochondrial apoptosis in doxorubicin-treated prostate cancer cells by targeting SIRT1/p53 pathway.	Doxorubicin	44-55	P53	Homo sapiens	105-108
29228612-6	2017	Furthermore, we found that restore of miR-204 dramatically enhanced the cytotoxicity of doxorubicin (DOX) against prostate cancer cell lines C4-2 and LNCaP carrying wild type (WT) p53.	Doxorubicin	88-99	P53	Homo sapiens	180-183
29228612-6	2017	Furthermore, we found that restore of miR-204 dramatically enhanced the cytotoxicity of doxorubicin (DOX) against prostate cancer cell lines C4-2 and LNCaP carrying wild type (WT) p53.	Doxorubicin	101-104	P53	Homo sapiens	180-183
29228612-8	2017	As the results, acetylated p53 induced by DOX upregulates the expression of Noxa and Puma followed by induction of mitochondrial apoptosis.	Doxorubicin	42-45	P53	Homo sapiens	27-30
29228612-9	2017	These data demonstrate that restore of miR-204 in prostate cancer cells enhances the mitochondrial apoptosis induced by doxorubicin by targeting the SIRT1/p53 pathway.	Doxorubicin	120-131	P53	Homo sapiens	155-158
28892622-6	2017	As Au-NPFe2O3NC possess high peroxidase-like activity for the oxidation of TMB in the presence of H2O2 [TMB is a common chromogenic substrate for HRP in enzyme-linked immunosorbent assays (ELISAs)], we envisage that our assay could find a wide range of application in developing ELISA-based sensing approaches in the fields of medicine (i.e., detection of other biomarkers the same as p53 autoantibody), biotechnology, and environmental sciences.	au-npfe2o3nc	3-15	P53	Homo sapiens	385-388
29051574-7	2017	Furthermore, FLO also induces G0/G1 cell cycle arrest via increase of p21 levels through activating ROS/p53/p21 pathway.	Reactive Oxygen Species	100-103	P53	Homo sapiens	104-107
28892622-6	2017	As Au-NPFe2O3NC possess high peroxidase-like activity for the oxidation of TMB in the presence of H2O2 [TMB is a common chromogenic substrate for HRP in enzyme-linked immunosorbent assays (ELISAs)], we envisage that our assay could find a wide range of application in developing ELISA-based sensing approaches in the fields of medicine (i.e., detection of other biomarkers the same as p53 autoantibody), biotechnology, and environmental sciences.	Hydrogen Peroxide	98-102	P53	Homo sapiens	385-388
28673807-8	2017	In addition, ROS induced by walsuronoid B upregulated p53 levels; conversely, p53 stimulated ROS.	Reactive Oxygen Species	13-16	P53	Homo sapiens	54-57
29042481-6	2017	At the molecular level, TSP1 increased Nox1-dependent generation of reactive oxygen species (ROS), leading to the increased abundance of the transcription factor p53.	Reactive Oxygen Species	68-91	P53	Homo sapiens	162-165
29042481-6	2017	At the molecular level, TSP1 increased Nox1-dependent generation of reactive oxygen species (ROS), leading to the increased abundance of the transcription factor p53.	Reactive Oxygen Species	93-96	P53	Homo sapiens	162-165
29085821-7	2017	Additionally, metformin increased the expression levels of p53, Bax, Bad while it reduced expression levels of Akt, Bcl-2, and Mdm2.	Metformin	14-23	P53	Homo sapiens	59-62
28673807-8	2017	In addition, ROS induced by walsuronoid B upregulated p53 levels; conversely, p53 stimulated ROS.	Reactive Oxygen Species	93-96	P53	Homo sapiens	78-81
28971953-8	2017	Further analysis indicated that inhibition of the mammalian target of rapamycin allows efficient cardiomyocyte differentiation through overcoming p53-dependent apoptosis of human pluripotent stem cells during high-density monolayer culture via blunting p53 translation and mitochondrial reactive oxygen species production.	Reactive Oxygen Species	287-310	P53	Homo sapiens	146-149
29020632-3	2017	Here, we show that p53 activation by 5-fluorouracil or nutlin-3 synergizes with a reversible Cdk7as inhibitor to induce cell death.	Fluorouracil	37-51	P53	Homo sapiens	19-22
28981110-0	2017	Overaccumulation of p53-mediated autophagy protects against betulinic acid-induced apoptotic cell death in colorectal cancer cells.	betulinic acid	60-74	P53	Homo sapiens	20-23
28981110-6	2017	Moreover, we found that p53 was firstly activated by short exposure to BA and then was rapidly degraded via the ubiquitin-mediated degradation pathway in both wtp53 and mutp53 CRC cells.	betulinic acid	71-73	P53	Homo sapiens	24-27
29051813-0	2017	Differential impact of various reactive oxygen species (ROS) on HIF-1alpha/p53 direct interaction in SK-N-MC neuroblastoma cells.	Reactive Oxygen Species	31-54	P53	Homo sapiens	75-78
29051813-0	2017	Differential impact of various reactive oxygen species (ROS) on HIF-1alpha/p53 direct interaction in SK-N-MC neuroblastoma cells.	Reactive Oxygen Species	56-59	P53	Homo sapiens	75-78
29051813-2	2017	Aside from its transcriptional regulation, other mechanisms, such as post translational modifications and protein-protein interactions, the interaction between HIF-1alpha and p53 has attracted more attention mainly due to simultaneous enhancement in the protein levels of these two anti- and pro-apoptotic vital transcriptional factors within the ROS-stressed cells.	Reactive Oxygen Species	347-350	P53	Homo sapiens	175-178
29051813-5	2017	Then, the effect of different ROS on interaction between HIF-1alpha and p53 proteins was examined by co-immunoprecipitation.	Reactive Oxygen Species	30-33	P53	Homo sapiens	72-75
29051813-8	2017	It appeared that direct communication between HIF-1alpha and p53 proteins by ROS stresses, under both normoxic and hypoxic conditions, was governed by HIF-1alpha at a certain induced level.	Reactive Oxygen Species	77-80	P53	Homo sapiens	61-64
29051731-14	2017	In addition, deregulations of the p53 pathway seem to contribute to the H2O2-induced death in MCI and AD lymphocytes, which show increased p53 expression.	Hydrogen Peroxide	72-76	P53	Homo sapiens	34-37
29051731-14	2017	In addition, deregulations of the p53 pathway seem to contribute to the H2O2-induced death in MCI and AD lymphocytes, which show increased p53 expression.	Hydrogen Peroxide	72-76	P53	Homo sapiens	139-142
28968425-11	2017	Among these molecules, the protein levels of STAT3 were greatly enhanced in all hepatocyte nuclei and further elevated in the cytoplasm in HCC tissue samples at 18 months, and the levels of phosphorylated TP53 (p-p53-Ser 6 and -Ser 15) were increased in liver tissues.	Serine	217-220	P53	Homo sapiens	205-209
28691365-9	2017	The mechanistic analysis revealed that Akt increased ROS levels through NOX4 induction, and increased Akt-dependent NF-kappaB binding to the NOX4 promoter is responsible for NOX4 induction upon p53 expression.	Reactive Oxygen Species	53-56	P53	Homo sapiens	194-197
28968425-11	2017	Among these molecules, the protein levels of STAT3 were greatly enhanced in all hepatocyte nuclei and further elevated in the cytoplasm in HCC tissue samples at 18 months, and the levels of phosphorylated TP53 (p-p53-Ser 6 and -Ser 15) were increased in liver tissues.	Serine	228-231	P53	Homo sapiens	205-209
28649131-10	2017	In p53 wild-type A549 cells, PAB (20 mumol/L) caused senescence, and time-dependently increased glucose utilization; knockdown of p53 or p21 significantly decreased the uptake and metabolism of glucose but elevated PAB-induced apoptosis.	pseudolaric acid B	215-218	P53	Homo sapiens	130-133
28649131-12	2017	Similar results were observed in another p53 wild-type H460 cells treated with PAB.	pseudolaric acid B	79-82	P53	Homo sapiens	41-44
28649131-2	2017	Our previous study showed that PAB mainly induced senescence via p53-p21 activation rather than apoptosis in suppression of the growth of human lung cancer A549 cells (p53 wild-type).	pseudolaric acid B	31-34	P53	Homo sapiens	65-68
28649131-2	2017	Our previous study showed that PAB mainly induced senescence via p53-p21 activation rather than apoptosis in suppression of the growth of human lung cancer A549 cells (p53 wild-type).	pseudolaric acid B	31-34	P53	Homo sapiens	168-171
28649131-10	2017	In p53 wild-type A549 cells, PAB (20 mumol/L) caused senescence, and time-dependently increased glucose utilization; knockdown of p53 or p21 significantly decreased the uptake and metabolism of glucose but elevated PAB-induced apoptosis.	pseudolaric acid B	29-32	P53	Homo sapiens	3-6
28649131-10	2017	In p53 wild-type A549 cells, PAB (20 mumol/L) caused senescence, and time-dependently increased glucose utilization; knockdown of p53 or p21 significantly decreased the uptake and metabolism of glucose but elevated PAB-induced apoptosis.	Glucose	194-201	P53	Homo sapiens	130-133
28291626-7	2017	Mus81 knockdown also induced S phase arrest and elevated apoptosis in CDDP treated HCT116 cells through activating CHK1/CDC25A/CDK2 and CHK1/p53/Bax pathways, while these effects could be counteracted by CHK1 inhibition.	Cisplatin	70-74	P53	Homo sapiens	141-144
28756530-0	2017	Intricatinol synergistically enhances the anticancerous activity of cisplatin in human A549 cells via p38 MAPK/p53 signalling.	Cisplatin	68-77	P53	Homo sapiens	111-114
28755014-2	2017	Dexamethasone, one of the premedications of pemetrexed, may downregulate p53 through the glucocorticoid receptor (GR).	Dexamethasone	0-13	P53	Homo sapiens	73-76
28656647-9	2017	In contrast, ASPP1 knockdown promoted cell growth and prevent 5-FU-induced p53 activation and apoptosis.	Fluorouracil	62-66	P53	Homo sapiens	75-78
28886471-0	2017	DNA damage by 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced p53-mediated apoptosis through activation of cytochrome P450/aryl hydrocarbon receptor.	Polychlorinated Dibenzodioxins	14-49	P53	Homo sapiens	58-61
28886471-9	2017	Moreover, TCDD increased expression of p53 and PUMA and our data showed that TCDD induced DNA damage followed by p53-mediated apoptosis.	Polychlorinated Dibenzodioxins	10-14	P53	Homo sapiens	39-42
28886471-9	2017	Moreover, TCDD increased expression of p53 and PUMA and our data showed that TCDD induced DNA damage followed by p53-mediated apoptosis.	Polychlorinated Dibenzodioxins	10-14	P53	Homo sapiens	113-116
28886471-9	2017	Moreover, TCDD increased expression of p53 and PUMA and our data showed that TCDD induced DNA damage followed by p53-mediated apoptosis.	Polychlorinated Dibenzodioxins	77-81	P53	Homo sapiens	39-42
28886471-9	2017	Moreover, TCDD increased expression of p53 and PUMA and our data showed that TCDD induced DNA damage followed by p53-mediated apoptosis.	Polychlorinated Dibenzodioxins	77-81	P53	Homo sapiens	113-116
29308362-6	2017	Molecular analysis of p53 codon 72 gene polymorphism was performed by polymerase chain reaction - restriction fragment length polymorphism for Arg/Arg, Arg/Pro, and Pro/Pro.	Arginine	143-146	P53	Homo sapiens	22-25
29308362-6	2017	Molecular analysis of p53 codon 72 gene polymorphism was performed by polymerase chain reaction - restriction fragment length polymorphism for Arg/Arg, Arg/Pro, and Pro/Pro.	Arginine	147-150	P53	Homo sapiens	22-25
29308362-6	2017	Molecular analysis of p53 codon 72 gene polymorphism was performed by polymerase chain reaction - restriction fragment length polymorphism for Arg/Arg, Arg/Pro, and Pro/Pro.	Arginine	147-150	P53	Homo sapiens	22-25
29308362-8	2017	Results: Genotype frequencies of 35 carcinoma cases of p53 Arg/Arg, Arg/Pro, and Pro/Pro were 23%, 57%, and 20%, respectively, and six leukoplakia cases of p53 Arg/Arg and Arg/Pro genotype were 50% and 50%, respectively.	Arginine	59-62	P53	Homo sapiens	55-58
28831795-9	2017	Further, the result depicted a direct correlation between the generations of ROS with mitochondrial-dependent apoptosis through the involvement of p53 phosphorylation upon EDTFP-1 induction, suggesting this COF material is a novel chemotherapeutic agent for cancer treatment.	ros	77-80	P53	Homo sapiens	147-150
28675767-0	2017	Sirtuin7 is involved in protecting neurons against oxygen-glucose deprivation and reoxygenation-induced injury through regulation of the p53 signaling pathway.	Oxygen	51-57	P53	Homo sapiens	137-140
28843398-5	2017	Compared to the E6/E7 SP alone, E6/E7 SP with cisplatin treatment effectively restored TP53 and RB/E2F signaling and contributes to differences in cell fate, such as apoptosis or cell cycle arrest.	Cisplatin	46-55	P53	Homo sapiens	87-91
28765903-5	2017	To examine the mechanism underlying the relationship between p53 and FN expression, we treated MCF7 breast cancer cells with the tumor promoter TPA (12-O-tetradecanoylphorbol-13-acetate).	Tetradecanoylphorbol Acetate	144-147	P53	Homo sapiens	61-64
28765903-7	2017	In contrast, the level of p53 expression was decreased by TPA treatment.	Tetradecanoylphorbol Acetate	58-61	P53	Homo sapiens	26-29
28765903-9	2017	Furthermore, the alterations in FN and p53 expression in response to TPA were prevented by a specific MEK inhibitor, UO126.	Tetradecanoylphorbol Acetate	69-72	P53	Homo sapiens	39-42
28765903-10	2017	Finally, we demonstrated that TPA triggers degradation of p53 through the proteasomal pathway in MCF7 cells.	Tetradecanoylphorbol Acetate	30-33	P53	Homo sapiens	58-61
28950914-9	2017	CONCLUSIONS: Our results provide in vitro evidence that RSV produces anti-tumor effect by activating DDR pathway in an ATM/Chk2/p53 dependent manner.	Resveratrol	56-59	P53	Homo sapiens	128-131
28500782-11	2017	Further study uncovered that melatonin inhibited the upregulation of p53, ERK and p38 protein expressions in BMSCs with iron overload.	Melatonin	29-38	P53	Homo sapiens	69-72
28500782-11	2017	Further study uncovered that melatonin inhibited the upregulation of p53, ERK and p38 protein expressions in BMSCs with iron overload.	Iron	120-124	P53	Homo sapiens	69-72
28500782-12	2017	Collectively, melatonin plays a protective role in iron overload-induced osteogenic differentiation dysfunction and senescence through blocking ROS accumulation and p53/ERK/p38 activation.	Melatonin	14-23	P53	Homo sapiens	165-168
28500782-12	2017	Collectively, melatonin plays a protective role in iron overload-induced osteogenic differentiation dysfunction and senescence through blocking ROS accumulation and p53/ERK/p38 activation.	Iron	51-55	P53	Homo sapiens	165-168
28888100-5	2017	In contrast to their wt counterparts, the p53- or p21-deficient cells treated with SCH900776 and cisplatin or LA-12 enter mitosis and become polyploid, and the senescence phenotype is strongly suppressed.	Cisplatin	97-106	P53	Homo sapiens	42-45
28791403-10	2017	Among DLBCL cases, the TP53 mutations shortened both OS and PFS of patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) and decreased both OS and PFS of patients with secondary DLBCL disease.	Doxorubicin	126-137	P53	Homo sapiens	23-27
28710679-6	2017	Thereafter, either free p53 liberated from the fusion protein through thrombin treatment or Histidine-tagged p53 were recognized efficiently by the selected phage.	Histidine	92-101	P53	Homo sapiens	109-112
28937626-0	2017	Aspalathin Reverts Doxorubicin-Induced Cardiotoxicity through Increased Autophagy and Decreased Expression of p53/mTOR/p62 Signaling.	Doxorubicin	19-30	P53	Homo sapiens	110-113
28937626-3	2017	Increasing evidence indicates that tumour protein p53 (p53), adenosine monophosphate-activated protein kinase (AMPK), nucleoporin p62 (p62), and the mammalian target of rapamycin (mTOR) are critical mediators of Dox-induced apoptosis, and subsequent dysregulation of autophagy.	Doxorubicin	212-215	P53	Homo sapiens	50-53
28927457-2	2017	All-trans retinoic acid (ATRA) and isotretinoin (13-cis retinoic acid) enhance p53 expression.	Tretinoin	0-23	P53	Homo sapiens	79-82
28926586-6	2017	Further analysis unambiguously showed that SOX14 triggered posttranslational modification of p53 protein, as detected by the significantly increased level of phospho-p53 (Ser-15) in SOX14-overexpressing HeLa cells.	Serine	171-174	P53	Homo sapiens	93-96
28926586-6	2017	Further analysis unambiguously showed that SOX14 triggered posttranslational modification of p53 protein, as detected by the significantly increased level of phospho-p53 (Ser-15) in SOX14-overexpressing HeLa cells.	Serine	171-174	P53	Homo sapiens	166-169
28927457-2	2017	All-trans retinoic acid (ATRA) and isotretinoin (13-cis retinoic acid) enhance p53 expression.	Tretinoin	25-29	P53	Homo sapiens	79-82
28927457-4	2017	Benzoyl peroxide and hydrogen peroxide elicit oxidative stress, which upregulates p53.	Hydrogen Peroxide	21-38	P53	Homo sapiens	82-85
28927457-5	2017	Azelaic acid leads to mitochondrial damage associated with increased release of reactive oxygen species inducing p53.	Reactive Oxygen Species	80-103	P53	Homo sapiens	113-116
28886730-0	2017	Annexin A2 contributes to cisplatin resistance by activation of JNK-p53 pathway in non-small cell lung cancer cells.	Cisplatin	26-35	P53	Homo sapiens	68-71
28703385-8	2017	A CsA-sensitive induction of p53 mRNA expression was also detected.	Cyclosporine	2-5	P53	Homo sapiens	29-32
28886730-11	2017	CONCLUSIONS: These data suggested that Annexin A2 induces cisplatin resistance of NSCLCs via regulation of JNK/c-Jun/p53 signaling, and provided an evidence that blockade of Annexin A2 could serve as a novel therapeutic approach for overcoming drug resistance in NSCLCs.	Cisplatin	58-67	P53	Homo sapiens	117-120
28878400-7	2017	Moreover, pretreatment of the cells with a decoy oligonucleotide carrying wild-type p53-response element markedly attenuated OT-induced THTR1, PDHB and OGDH gene expression suggesting an important role of p53 in transactivation of these genes.	Oligonucleotides	49-64	P53	Homo sapiens	84-87
28886153-2	2017	Although SUVmax reflects increased glucose uptake and metabolism possibly induced by activation of growth factor signaling or TP53 dysfunction, tumor characteristics of SUVmax-high breast cancers remain to be elucidated.	Glucose	35-42	P53	Homo sapiens	126-130
28878262-0	2017	Hyper-O-GlcNAcylation induces cisplatin resistance via regulation of p53 and c-Myc in human lung carcinoma.	Cisplatin	30-39	P53	Homo sapiens	69-72
28878262-7	2017	Gene manipulation studies revealed that O-GlcNAcylation of p53/c-Myc is in part a regulator of CDDP-induced apoptosis.	Cisplatin	95-99	P53	Homo sapiens	59-62
28878262-8	2017	Accordingly, we classified CDDP resistance by hyper-O-GlcNAcylation in lung carcinoma cells as either p53 or c-Myc dependence based on their molecular targets.	Cisplatin	27-31	P53	Homo sapiens	102-105
28878400-7	2017	Moreover, pretreatment of the cells with a decoy oligonucleotide carrying wild-type p53-response element markedly attenuated OT-induced THTR1, PDHB and OGDH gene expression suggesting an important role of p53 in transactivation of these genes.	Oligonucleotides	49-64	P53	Homo sapiens	205-208
28874603-6	2017	An Arg-to-His, but not Arg-to-Lys, mutation in the transcription factor p53 (p53-R273H) decreased its transcriptional activity and attenuated the DNA damage response in fibroblasts and breast cancer cells with high pHi.	Arginine	3-6	P53	Homo sapiens	72-75
28874603-6	2017	An Arg-to-His, but not Arg-to-Lys, mutation in the transcription factor p53 (p53-R273H) decreased its transcriptional activity and attenuated the DNA damage response in fibroblasts and breast cancer cells with high pHi.	Arginine	3-6	P53	Homo sapiens	77-80
28874603-6	2017	An Arg-to-His, but not Arg-to-Lys, mutation in the transcription factor p53 (p53-R273H) decreased its transcriptional activity and attenuated the DNA damage response in fibroblasts and breast cancer cells with high pHi.	Histidine	10-13	P53	Homo sapiens	72-75
28874603-6	2017	An Arg-to-His, but not Arg-to-Lys, mutation in the transcription factor p53 (p53-R273H) decreased its transcriptional activity and attenuated the DNA damage response in fibroblasts and breast cancer cells with high pHi.	Histidine	10-13	P53	Homo sapiens	77-80
28979810-5	2017	It was found that chemotherapy drugs, such as epirubicin (EPB) and mitomycin C (MMC), effectively blocked expression of PcG in p53-wild-type HepG2 cells but not in PLC/PRF5 and Hep3B cells with p53 mutation or deletion.	Epirubicin	46-56	P53	Homo sapiens	127-130
28709868-0	2017	Protective effect of p53 on the viability of intervertebral disc nucleus pulposus cells under low glucose condition.	Glucose	98-105	P53	Homo sapiens	21-24
28709868-4	2017	In this study, we found that p53 decreased and leaked to the cytoplasm in NP cells as the glucose level decreases, in contrast to cancer cells in which p53 increases and concentrates to the nuclei.	Glucose	90-97	P53	Homo sapiens	29-32
28979810-5	2017	It was found that chemotherapy drugs, such as epirubicin (EPB) and mitomycin C (MMC), effectively blocked expression of PcG in p53-wild-type HepG2 cells but not in PLC/PRF5 and Hep3B cells with p53 mutation or deletion.	Epirubicin	46-56	P53	Homo sapiens	194-197
28816773-5	2017	In our study, combined 3-BP and 5-FU treatment upregulated p53 and p21, whereas cyclin-dependent kinase CDK4 and CDK2 were downregulated, which led to G0/G1 phase arrest.	bromopyruvate	23-27	P53	Homo sapiens	59-62
28628491-0	2017	Calcein-acetoxymethy ester enhances the antitumor effects of doxorubicin in nonsmall cell lung cancer by regulating the TopBP1/p53RR pathway.	Doxorubicin	61-72	P53	Homo sapiens	127-130
28628491-5	2017	Furthermore, we found that TopBP1, which we previously showed was involved in doxorubicin resistance through upregulation of aberrant p53, was involved in calcein-AM-mediated increased doxorubicin sensitivity.	Doxorubicin	78-89	P53	Homo sapiens	134-137
28628491-5	2017	Furthermore, we found that TopBP1, which we previously showed was involved in doxorubicin resistance through upregulation of aberrant p53, was involved in calcein-AM-mediated increased doxorubicin sensitivity.	Doxorubicin	185-196	P53	Homo sapiens	134-137
28759712-6	2017	Hormones inhibit resveratrol-stimulated phosphorylation of p53 on Ser15, resveratrol-induced nuclear COX-2 accumulation, and formation of p53-COX-2 nuclear complexes.	Resveratrol	17-28	P53	Homo sapiens	59-62
28759712-6	2017	Hormones inhibit resveratrol-stimulated phosphorylation of p53 on Ser15, resveratrol-induced nuclear COX-2 accumulation, and formation of p53-COX-2 nuclear complexes.	Resveratrol	17-28	P53	Homo sapiens	138-141
28759712-7	2017	Subsequently, hormones impair resveratrol-induced COX-2-/p53-dependent gene expression.	Resveratrol	30-41	P53	Homo sapiens	57-60
28628491-6	2017	Doxorubicin upregulated the expression of aberrant p53.	Doxorubicin	0-11	P53	Homo sapiens	51-54
28816773-5	2017	In our study, combined 3-BP and 5-FU treatment upregulated p53 and p21, whereas cyclin-dependent kinase CDK4 and CDK2 were downregulated, which led to G0/G1 phase arrest.	Fluorouracil	32-36	P53	Homo sapiens	59-62
28870897-6	2017	Detailed analyses revealed that the mTORC1 and p53 signaling pathways are main targets of curcumin.	Curcumin	90-98	P53	Homo sapiens	47-50
28633436-5	2017	Testosterone treatment of croaker G/T cells increased intracellular zinc levels, mitogen-activated protein (MAP) kinase activity, caspase 3 activity, messenger RNA levels of proapoptotic members Bax, p53, and c-Jun N-terminal kinase, and the incidence of apoptosis, similar to findings in mammalian cancer cells, but also increased cyclic adenosine monophosphate concentrations.	Testosterone	0-12	P53	Homo sapiens	200-203
28673515-0	2017	High glucose-induced p53 phosphorylation contributes to impairment of endothelial antioxidant system.	Glucose	5-12	P53	Homo sapiens	21-24
28710022-3	2017	The cholesterol oxidation products also induced a decrease in the levels of Bid and Bcl-2, increase in the levels of p53 and Bax, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), production of reactive oxygen species, depletion of GSH and cell death in both cell lines.	Cholesterol	4-15	P53	Homo sapiens	117-120
28633436-6	2017	Transfection with small interfering RNA targeting croaker ZIP9 blocked testosterone-induced increase in bax, p53, and jnk expression.	Testosterone	71-83	P53	Homo sapiens	109-112
28799801-0	2017	Cross-generational effects of alcohol dependence in humans on HRAS and TP53 methylation in offspring.	Alcohols	30-37	P53	Homo sapiens	71-75
28799801-1	2017	AIM: We hypothesized that cross-generational effects of alcohol exposure could alter DNA methylation and expression of the HRAS oncogene and TP53 tumor suppressor gene that drive cancer development.	Alcohols	56-63	P53	Homo sapiens	141-145
28799801-4	2017	CONCLUSION: The results suggest that ancestral exposure to alcohol can have enduring effects that impact epigenetic processes such as DNA methylation that controls expression of genes that drive cancer development such as HRAS and TP53.	Alcohols	59-66	P53	Homo sapiens	231-235
28214344-5	2017	Furthermore our results revealed that neferine combined with cisplatin down regulate the expression of Bcl-2 and up regulate the expression of Bax, Bad, Bak, release of cytochrome c, p53 levels, then activated cleavage forms of caspase-9, caspase-3, and PARP.	neferine	38-46	P53	Homo sapiens	183-186
28677808-6	2017	Additionally, IMBP potentiated the therapeutic efficacy of doxorubicin-based breast cancer chemotherapy via the activation of cell cycle arrest and cell apoptosis pathway genes including p53, p21, CDK2, cyclin A, caspase 9, Bcl-2 and Bax.	Doxorubicin	59-70	P53	Homo sapiens	187-190
28214344-5	2017	Furthermore our results revealed that neferine combined with cisplatin down regulate the expression of Bcl-2 and up regulate the expression of Bax, Bad, Bak, release of cytochrome c, p53 levels, then activated cleavage forms of caspase-9, caspase-3, and PARP.	Cisplatin	61-70	P53	Homo sapiens	183-186
28857739-7	2017	Moreover, p53 arg/arg patients infected by an HPV16 prototype strain were associated with an increased risk of more severe lesions, while a significant relationship between the p53 arg/arg genotype in patients with T350G sequence variation and the risk of high-grade squamous intraepithelial lesions (HSILs) was revealed.	Arginine	14-17	P53	Homo sapiens	10-13
28857739-7	2017	Moreover, p53 arg/arg patients infected by an HPV16 prototype strain were associated with an increased risk of more severe lesions, while a significant relationship between the p53 arg/arg genotype in patients with T350G sequence variation and the risk of high-grade squamous intraepithelial lesions (HSILs) was revealed.	Arginine	18-21	P53	Homo sapiens	10-13
28857739-8	2017	CONCLUSION: The oncogenic potential of the virus is increased by the presence of the p53 arg/arg genotype in the Greek population in such a way that the specific protein interaction E6 (L83V)-p53 (Arg-72) can modify an individual"s susceptibility to cervical disease.	Arginine	93-96	P53	Homo sapiens	192-195
28857739-8	2017	CONCLUSION: The oncogenic potential of the virus is increased by the presence of the p53 arg/arg genotype in the Greek population in such a way that the specific protein interaction E6 (L83V)-p53 (Arg-72) can modify an individual"s susceptibility to cervical disease.	Arginine	197-200	P53	Homo sapiens	85-88
28857739-8	2017	CONCLUSION: The oncogenic potential of the virus is increased by the presence of the p53 arg/arg genotype in the Greek population in such a way that the specific protein interaction E6 (L83V)-p53 (Arg-72) can modify an individual"s susceptibility to cervical disease.	Arginine	197-200	P53	Homo sapiens	192-195
28857739-7	2017	Moreover, p53 arg/arg patients infected by an HPV16 prototype strain were associated with an increased risk of more severe lesions, while a significant relationship between the p53 arg/arg genotype in patients with T350G sequence variation and the risk of high-grade squamous intraepithelial lesions (HSILs) was revealed.	Arginine	18-21	P53	Homo sapiens	10-13
28857739-7	2017	Moreover, p53 arg/arg patients infected by an HPV16 prototype strain were associated with an increased risk of more severe lesions, while a significant relationship between the p53 arg/arg genotype in patients with T350G sequence variation and the risk of high-grade squamous intraepithelial lesions (HSILs) was revealed.	Arginine	18-21	P53	Homo sapiens	10-13
28857739-8	2017	CONCLUSION: The oncogenic potential of the virus is increased by the presence of the p53 arg/arg genotype in the Greek population in such a way that the specific protein interaction E6 (L83V)-p53 (Arg-72) can modify an individual"s susceptibility to cervical disease.	Arginine	89-92	P53	Homo sapiens	85-88
28857739-8	2017	CONCLUSION: The oncogenic potential of the virus is increased by the presence of the p53 arg/arg genotype in the Greek population in such a way that the specific protein interaction E6 (L83V)-p53 (Arg-72) can modify an individual"s susceptibility to cervical disease.	Arginine	89-92	P53	Homo sapiens	192-195
28857739-8	2017	CONCLUSION: The oncogenic potential of the virus is increased by the presence of the p53 arg/arg genotype in the Greek population in such a way that the specific protein interaction E6 (L83V)-p53 (Arg-72) can modify an individual"s susceptibility to cervical disease.	Arginine	93-96	P53	Homo sapiens	85-88
28575972-4	2017	After irradiation, the obtained curcumin loaded micelle showed a better transfection, and the p53 protein expression in Hela cells was higher.	Curcumin	32-40	P53	Homo sapiens	94-97
27048255-6	2017	RESULTS: Treatment with high concentrations of glucose induced GMC senescence accompanied by shortened telomere length and increase of beta-galactosidase staining as well as P53 protein, which was abrogated after application of caveolin-1-siRNA.	Glucose	47-54	P53	Homo sapiens	174-177
28575972-5	2017	The apoptosis assay showed that the complex could induce a more significant apoptosis to Hela cells than that of curcumin or p53 used alone, and the curcumin loaded micelle inducing apoptosis was best after irradiation.	Curcumin	149-157	P53	Homo sapiens	125-128
28912678-6	2017	These findings demonstrated that ROS might be located upstream of IL-17A and HMGB1 so that ROS can regulate HMGB1/IL-17A expression to affect the p53 and PI3K/Akt signaling pathways and therefore promote the occurrence of apoptosis in microglial cells.	ros	33-36	P53	Homo sapiens	146-149
28527113-7	2017	Higher level of GTP-Cdc42 was correlated with increase expression of mutant p53 and reduced ARHGAP44.	Guanosine Triphosphate	16-19	P53	Homo sapiens	76-79
27644130-8	2017	The transcriptional activation of p21 was shown to be dependent on p53, as it can be blocked by PFT-alpha, and correlated with the increased phosphorylation of p53 at Serine 15.	Serine	167-173	P53	Homo sapiens	67-70
27644130-8	2017	The transcriptional activation of p21 was shown to be dependent on p53, as it can be blocked by PFT-alpha, and correlated with the increased phosphorylation of p53 at Serine 15.	Serine	167-173	P53	Homo sapiens	160-163
29084683-8	2017	The treatment of crocin plus cisplatin significantly increased the expression of p53 and Bax (p&lt; 0.05), and significantly decreased the Bcl-2 expression (p&lt;0.05).	Cisplatin	29-38	P53	Homo sapiens	81-84
28912678-6	2017	These findings demonstrated that ROS might be located upstream of IL-17A and HMGB1 so that ROS can regulate HMGB1/IL-17A expression to affect the p53 and PI3K/Akt signaling pathways and therefore promote the occurrence of apoptosis in microglial cells.	ros	91-94	P53	Homo sapiens	146-149
28851987-2	2017	Here we describe p53-dependent control of the rate-limiting enzyme in the pyrimidine catabolic pathway, dihydropyrimidine dehydrogenase (DPYD) and its effect on pharmacokinetics of and response to 5-fluorouracil (5-FU).	Fluorouracil	197-211	P53	Homo sapiens	17-20
28851987-2	2017	Here we describe p53-dependent control of the rate-limiting enzyme in the pyrimidine catabolic pathway, dihydropyrimidine dehydrogenase (DPYD) and its effect on pharmacokinetics of and response to 5-fluorouracil (5-FU).	Fluorouracil	213-217	P53	Homo sapiens	17-20
28851987-3	2017	Using in silico/chromatin-immunoprecipitation (ChIP) analysis we identify a conserved p53 DNA-binding site (p53BS) downstream of the DPYD gene with increased p53 occupancy following 5-FU treatment of cells.	Fluorouracil	182-186	P53	Homo sapiens	86-89
28851987-3	2017	Using in silico/chromatin-immunoprecipitation (ChIP) analysis we identify a conserved p53 DNA-binding site (p53BS) downstream of the DPYD gene with increased p53 occupancy following 5-FU treatment of cells.	Fluorouracil	182-186	P53	Homo sapiens	108-111
28851987-6	2017	In-vivo, liver specific Tp53 loss increases the conversion of 5-FU to 5-FUH2 in plasma and elicits a diminished 5-FU therapeutic response in a syngeneic colorectal tumor model consistent with increased DPYD-activity.	Fluorouracil	62-66	P53	Homo sapiens	24-28
28851987-6	2017	In-vivo, liver specific Tp53 loss increases the conversion of 5-FU to 5-FUH2 in plasma and elicits a diminished 5-FU therapeutic response in a syngeneic colorectal tumor model consistent with increased DPYD-activity.	Fluorouracil	70-74	P53	Homo sapiens	24-28
28819136-9	2017	In addition, BPA caused DNA damage through the p53-p21 signaling pathway.	bisphenol A	13-16	P53	Homo sapiens	47-50
28837147-12	2017	In keeping, p21 mRNA, that is induced by p53 and inhibited by ZEB1, is induced by DOXO treatment and is decreased by SDF1 administration.	Doxorubicin	82-86	P53	Homo sapiens	41-44
28803777-3	2017	We found that p53 transcriptionally represses paraoxonase 2 (PON2), which regulates GLUT1-mediated glucose transport via stomatin.	Glucose	99-106	P53	Homo sapiens	14-17
28666330-4	2017	All oligonucleotides investigated have shown a noteworthy antiproliferative activity against lung cancer cell line Calu 6 and colorectal cancer cell line HCT-116 p53-/-.	Oligonucleotides	4-20	P53	Homo sapiens	162-165
29156743-1	2017	All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells.	Tretinoin	0-23	P53	Homo sapiens	174-177
29156743-1	2017	All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells.	Tretinoin	0-23	P53	Homo sapiens	220-223
29156743-1	2017	All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells.	Tretinoin	25-29	P53	Homo sapiens	174-177
29156743-1	2017	All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells.	Tretinoin	25-29	P53	Homo sapiens	220-223
29156743-2	2017	In the present study, we found that hepatitis C virus (HCV) Core derived from ectopic expression or HCV infection overcomes ATRA-induced apoptosis in p53-positive hepatoma cells.	Tretinoin	124-128	P53	Homo sapiens	150-153
29156743-6	2017	Based on these observations, we conclude that HCV Core executes its oncogenic potential by suppressing the p53-dependent apoptosis induced by ATRA in human hepatoma cells.	Tretinoin	142-146	P53	Homo sapiens	107-110
28655792-4	2017	C646 treatment blocked acetylation of specific lysine residues that regulate p53 activity.	Lysine	47-53	P53	Homo sapiens	77-80
28696098-0	2017	Enhanced Binding Affinity via Destabilization of the Unbound State: A Millisecond Hydrogen-Deuterium Exchange Study of the Interaction between p53 and a Pleckstrin Homology Domain.	Hydrogen	82-90	P53	Homo sapiens	143-146
28814292-7	2017	Resveratrol also regulated Sirt1 and acetylated p53 expression perturbed by irradiation in the small intestine.	Resveratrol	0-11	P53	Homo sapiens	48-51
28655792-5	2017	Exploitation of differential p53 genetic backgrounds between human hematopoietic and colorectal cancer cells improved the therapeutic index of doxorubicin with C646 cotreatment.	Doxorubicin	143-154	P53	Homo sapiens	29-32
28109089-0	2017	Betulinic Acid Inhibits Cell Proliferation in Human Oral Squamous Cell Carcinoma via Modulating ROS-Regulated p53 Signaling.	betulinic acid	0-14	P53	Homo sapiens	110-113
28789701-7	2017	Ad5/F11p-PSCAE-UPII-E1A plus cisplatin could upregulate the proteins expression of p53, Bax, and cleaved caspase-3, and downregulated Bcl-2 protein expression in T24, EJ and 5637 cells.	Cisplatin	29-38	P53	Homo sapiens	83-86
28796811-4	2017	Nonetheless, early single peak of ROS formation along with lysosomal membrane permeabilization and cathepsin activation regulated cisplatin- and UV-induced necrosis in p53-null HCT-116 cells.	ros	34-37	P53	Homo sapiens	168-171
28796811-4	2017	Nonetheless, early single peak of ROS formation along with lysosomal membrane permeabilization and cathepsin activation regulated cisplatin- and UV-induced necrosis in p53-null HCT-116 cells.	Cisplatin	130-139	P53	Homo sapiens	168-171
28790461-5	2017	CAPE-pNO2 induced apoptosis in HT-29 cells by up-regulating P53, cleaved-caspase-3, Bax, P38 and CytoC; CAPE-pNO2 also up-regulated P21Cip1 and P27Kip1 and down-regulated CDK2 and c-Myc to promote cell cycle arrest in G0/G1.	cape-pno2	0-9	P53	Homo sapiens	60-63
28109089-0	2017	Betulinic Acid Inhibits Cell Proliferation in Human Oral Squamous Cell Carcinoma via Modulating ROS-Regulated p53 Signaling.	ros	96-99	P53	Homo sapiens	110-113
28109089-8	2017	BA dose-dependently increased p53 expression in KB cells and implanted tumors.	betulinic acid	0-2	P53	Homo sapiens	30-33
28109089-10	2017	Knockdown of p53 blocked BA-induced increase in apoptosis, cell cycle arrest, and inhibition of cell proliferation.	betulinic acid	25-27	P53	Homo sapiens	13-16
28109089-11	2017	NAC treatment suppressed BA-induced increase in p53 expression.	betulinic acid	25-27	P53	Homo sapiens	48-51
28109089-13	2017	Taken together, the data demonstrated that ROS-p53 signaling was crucial for BA-exhibited antitumor effect in OSCC.	ros	43-46	P53	Homo sapiens	47-50
28109089-13	2017	Taken together, the data demonstrated that ROS-p53 signaling was crucial for BA-exhibited antitumor effect in OSCC.	betulinic acid	77-79	P53	Homo sapiens	47-50
28785074-7	2017	In addition, treatment of PD98059 reversed low-dose arsenite-induced MDM2 expression, and the inhibition of ERK2 expression could significantly block MDM2 expression as a consequence, and p53 expression automatically was increased.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	26-33	P53	Homo sapiens	188-191
28767065-4	2017	Herein we report similar observations with cancer cell lines expressing wild-type p53 (A549 lung carcinoma) or mutant p53 (MDA-MB-231 breast carcinoma) after treatment with the chemotherapeutic drug cisplatin.	Cisplatin	199-208	P53	Homo sapiens	82-85
28686074-4	2017	Increased levels of phosphorylated ATM (p-ATM) and its downstream molecules, CHK2, p-CHK2, p-53, and p-p53 were also detected in cisplatin-resistant cells, suggesting an activation of ATM signaling in these cells.	Cisplatin	129-138	P53	Homo sapiens	91-95
28686074-4	2017	Increased levels of phosphorylated ATM (p-ATM) and its downstream molecules, CHK2, p-CHK2, p-53, and p-p53 were also detected in cisplatin-resistant cells, suggesting an activation of ATM signaling in these cells.	Cisplatin	129-138	P53	Homo sapiens	103-106
28932295-4	2017	RESULTS: MDM2mRNA overexpression correlated with low grade low stage non invasive tumors, while P53 &gt; 40% &amp; p16 &lt; 10% cut offs correlated with high grade high stage invasive carcinomas &amp; bilharzial tumors (P=0.000).	Adenosine Monophosphate	110-113	P53	Homo sapiens	96-99
28932295-4	2017	RESULTS: MDM2mRNA overexpression correlated with low grade low stage non invasive tumors, while P53 &gt; 40% &amp; p16 &lt; 10% cut offs correlated with high grade high stage invasive carcinomas &amp; bilharzial tumors (P=0.000).	Adenosine Monophosphate	196-199	P53	Homo sapiens	96-99
28767065-4	2017	Herein we report similar observations with cancer cell lines expressing wild-type p53 (A549 lung carcinoma) or mutant p53 (MDA-MB-231 breast carcinoma) after treatment with the chemotherapeutic drug cisplatin.	Cisplatin	199-208	P53	Homo sapiens	118-121
27927016-0	2017	Inhibition of Cathepsin S Induces Mitochondrial ROS That Sensitizes TRAIL-Mediated Apoptosis Through p53-Mediated Downregulation of Bcl-2 and c-FLIP.	Reactive Oxygen Species	48-51	P53	Homo sapiens	101-104
27927016-5	2017	ZFL downregulated Bcl-2 expression at the transcriptional level in a p53-dependent manner, and overexpression of Bcl-2 also markedly blocked apoptosis induced by combined treatment with ZFL and TRAIL.	zfl	0-3	P53	Homo sapiens	69-72
27927016-7	2017	Moreover, ZFL increased the expression of Cbl, an E3 ligase of c-FLIP, in a p53-dependent manner, and knockdown of Cbl markedly prevented c-FLIP downregulation and the apoptosis induced by ZFL plus TRAIL.	zfl	10-13	P53	Homo sapiens	76-79
27927016-8	2017	Interestingly, ZFL induced p53 expression via production of mitochondrial reactive oxygen species (ROS).	zfl	15-18	P53	Homo sapiens	27-30
27927016-8	2017	Interestingly, ZFL induced p53 expression via production of mitochondrial reactive oxygen species (ROS).	Reactive Oxygen Species	74-97	P53	Homo sapiens	27-30
27927016-8	2017	Interestingly, ZFL induced p53 expression via production of mitochondrial reactive oxygen species (ROS).	Reactive Oxygen Species	99-102	P53	Homo sapiens	27-30
27927016-11	2017	CONCLUSION: Our results indicated that inhibition of cathepsin S stimulates TRAIL-induced apoptosis through downregulation of Bcl-2 and Cbl-mediated c-FLIP by ROS-mediated p53 expression.	Reactive Oxygen Species	159-162	P53	Homo sapiens	172-175
28609685-9	2017	CONCLUSIONS: Our results suggest that palmitate-induced apoptosis depends on the activation of the TLR4/ROS/p53 signaling pathway, and that TLR4 may be a potential therapeutic target for the prevention and treatment of atherosclerosis.	Reactive Oxygen Species	104-107	P53	Homo sapiens	108-111
28608259-9	2017	CONCLUSIONS: JS-K enhances the anti-cancer activity of Doxorubicin in renal carcinoma cells by upregulating p53 expression and prevents cardiac myocytes toxicity of Doxorubicin by decreasing oxidative stress.	Doxorubicin	55-66	P53	Homo sapiens	108-111
28436014-3	2017	We assessed the extent to which the pharmacokinetic characteristics are a function of the staple for a peptide inhibiting the interaction of p53 with the human double minute 2 (Hdm2) protein and differ from those of the standard cationic cell-penetrating peptide nona-arginine.	Arginine	268-276	P53	Homo sapiens	141-144
28608259-4	2017	Effect of p53 on the combination of JS-K and Doxorubicin was determined using p53 inhibitor Pifithrin-alpha and p53 activator III.	Doxorubicin	45-56	P53	Homo sapiens	10-13
28845527-0	2017	Extracellular NAMPT/visfatin causes p53 deacetylation via NAD production and SIRT1 activation in breast cancer cells.	NAD	58-61	P53	Homo sapiens	36-39
28608259-4	2017	Effect of p53 on the combination of JS-K and Doxorubicin was determined using p53 inhibitor Pifithrin-alpha and p53 activator III.	Doxorubicin	45-56	P53	Homo sapiens	78-81
28608259-4	2017	Effect of p53 on the combination of JS-K and Doxorubicin was determined using p53 inhibitor Pifithrin-alpha and p53 activator III.	Doxorubicin	45-56	P53	Homo sapiens	78-81
28608259-7	2017	Additionally, Pifithrin-alpha reversed the promoting effect of JS-K on Doxorubicin-induced renal carcinoma cell apoptosis; conversely, the p53 activator III exacerbated the promoting effect of JS-K on Doxorubicin-induced renal carcinoma cell apoptosis.	Doxorubicin	201-212	P53	Homo sapiens	139-142
28528452-5	2017	RESULTS: Overexpression of wild-type p53 as a transgene or pharmacological activation by doxorubicin drug treatment shows significant suppression of NIS transcription in multiple BC cell types which also results in lowered NIS protein content and cellular iodide intake.	Doxorubicin	89-100	P53	Homo sapiens	37-40
28845527-10	2017	In conclusion, the results show that extracellular visfatin produces NAD that causes upregulation of SIRT1 activity and p53 deacetylation.	NAD	69-72	P53	Homo sapiens	120-123
28571773-6	2017	In addition, DATS enhances TRAIL-induced apoptosis through the downregulation of anti-apoptotic protein (Mcl-1) and the upregulation of DR5 receptors through actions on the ROS- induced-p53.	ros	173-176	P53	Homo sapiens	186-189
28714573-8	2017	Furthermore, 53 chemical substructures associated with genotoxicity were enriched in certain classes of p53 actives, for example, anthracyclines (antineoplastics) and vinca alkaloids (tubulin disruptors).	Anthracyclines	130-144	P53	Homo sapiens	104-107
28646291-9	2017	Two resveratrol-associated genes, adenomatous polyposis coli (APC) and TP53, found in CRC were further mined, using cBio portal and Colorectal Cancer Atlas which predicted a mechanistic link to exist between resveratrol QR2/TP53 CIN.	Resveratrol	4-15	P53	Homo sapiens	71-75
28646291-9	2017	Two resveratrol-associated genes, adenomatous polyposis coli (APC) and TP53, found in CRC were further mined, using cBio portal and Colorectal Cancer Atlas which predicted a mechanistic link to exist between resveratrol QR2/TP53 CIN.	Resveratrol	4-15	P53	Homo sapiens	224-228
28646291-9	2017	Two resveratrol-associated genes, adenomatous polyposis coli (APC) and TP53, found in CRC were further mined, using cBio portal and Colorectal Cancer Atlas which predicted a mechanistic link to exist between resveratrol QR2/TP53 CIN.	Resveratrol	208-219	P53	Homo sapiens	71-75
28627630-9	2017	Exogenous melatonin positively influenced quality of blastocysts, which may be mediated via upregulation of p53 signaling and correcting DNA methylation changes caused by "rescue IVM".	Melatonin	10-19	P53	Homo sapiens	108-111
28714518-3	2017	Mass spectrometric analysis of HCT116 p53+/+ and HCT116 p53-/- cells treated with adriamycin identified 124 proteins increased by DNA damage in a p53-dependent manner.	Doxorubicin	82-92	P53	Homo sapiens	38-41
28714518-3	2017	Mass spectrometric analysis of HCT116 p53+/+ and HCT116 p53-/- cells treated with adriamycin identified 124 proteins increased by DNA damage in a p53-dependent manner.	Doxorubicin	82-92	P53	Homo sapiens	56-59
28714518-3	2017	Mass spectrometric analysis of HCT116 p53+/+ and HCT116 p53-/- cells treated with adriamycin identified 124 proteins increased by DNA damage in a p53-dependent manner.	Doxorubicin	82-92	P53	Homo sapiens	56-59
29067453-0	2017	Inhibitory effect of hyperoside isolated from Zanthoxylum bungeanum leaves on SW620 human colorectal cancer cells via induction of the p53 signaling pathway and apoptosis.	hyperoside	21-31	P53	Homo sapiens	135-138
29265025-12	2017	INTERPRETATION &amp; CONCLUSIONS: Our results suggest that TP53 may be linked with T2DM.	Adenosine Monophosphate	16-19	P53	Homo sapiens	59-63
27967292-5	2017	P53 antagonism by lenalidomide or other therapeutics such as antisense oligonucleotides, repopulates erythroid precursors and enhances effective erythropoiesis.	Oligonucleotides	71-87	P53	Homo sapiens	0-3
28656213-6	2017	BMH-21 also decreased MDM2 proto-oncogene expression and increased protein levels of the tumor suppressor p53 and p53 phosphorylated at serine 15 (p-p53-Ser15), which contributed to increased expression of the downstream apoptosis-related protein BCL2 associated X (BAX) and activation of caspase-3.	Serine	136-142	P53	Homo sapiens	106-109
28656213-6	2017	BMH-21 also decreased MDM2 proto-oncogene expression and increased protein levels of the tumor suppressor p53 and p53 phosphorylated at serine 15 (p-p53-Ser15), which contributed to increased expression of the downstream apoptosis-related protein BCL2 associated X (BAX) and activation of caspase-3.	Serine	136-142	P53	Homo sapiens	114-117
28656213-6	2017	BMH-21 also decreased MDM2 proto-oncogene expression and increased protein levels of the tumor suppressor p53 and p53 phosphorylated at serine 15 (p-p53-Ser15), which contributed to increased expression of the downstream apoptosis-related protein BCL2 associated X (BAX) and activation of caspase-3.	Serine	136-142	P53	Homo sapiens	114-117
28789369-5	2017	Notably, the Pro72 allele was significantly enriched in patients with ESCC compared with its abundance in the healthy control group, and the genotype of Pro/Arg on p53 codon 72 was confirmed to exhibit a significant correlation with ESCC in Mongolian patients.	Arginine	157-160	P53	Homo sapiens	164-167
28789369-7	2017	Mongolian patients who carry the partocular genotype of Arg/Pro or Pro/Pro on p53 codon 72 may be more likely to develop ESCC.	Arginine	56-59	P53	Homo sapiens	78-81
28450532-8	2017	Breast cancer treatment by doxorubicin, an anti-cancer drug, involves induction of apoptosis by p53; we thus wanted to check whether miR-191-5p affects doxorubicin sensitivity.	Doxorubicin	27-38	P53	Homo sapiens	96-99
28258023-4	2017	Additionally, excessive ROS caused by physapubescin B also induced p53-dependent apoptotic cell death.	Reactive Oxygen Species	24-27	P53	Homo sapiens	67-70
28450532-10	2017	Overall, this work highlights the importance of the p53-miR-191-SOX4 axis in the regulation of apoptosis and drug resistance in breast cancer and offers a preclinical proof-of-concept for use of an Anti-miR-191 and doxorubicin combination as a rational approach to pursue for better breast cancer treatment.	Doxorubicin	215-226	P53	Homo sapiens	52-55
28754018-2	2017	Metal ions, such as magnesium and zinc ions, have important influences on p53-DNA interactions for stabilizing the structure of the protein and enhancing its affinity to DNA.	Metals	0-5	P53	Homo sapiens	74-77
28446729-0	2017	WP1130 attenuates cisplatin resistance by decreasing P53 expression in non-small cell lung carcinomas.	Cisplatin	18-27	P53	Homo sapiens	53-56
28446729-4	2017	After being combined with WP1130, cisplatin sensitivity was significantly increased in A549 and HCC827 cells with decreased p53 expression, inhibiting their proliferation, but not in p53-deficient NCI-H1299 cells.	Cisplatin	34-43	P53	Homo sapiens	124-127
28446729-5	2017	The synergistic cytotoxicity of the cisplatin and WP1130 co-treatment was abolished in p53-knockdown cells.	Cisplatin	36-45	P53	Homo sapiens	87-90
28446729-6	2017	Western blotting verified the decreased p53 expression in A549 and HCC827 cells treated with cisplatin and WP1130.	Cisplatin	93-102	P53	Homo sapiens	40-43
28446729-8	2017	Taken together, our findings confirm that the inclusion of WP1130 is potentially contributes to better therapeutic effects of cisplatin-based chemotherapy of NSCLCs in a manner dependent on the USP9X-p53 ubiquitination-mediated degradation pathway.	Cisplatin	126-135	P53	Homo sapiens	200-203
28366708-7	2017	Moreover, the simultaneous treatment of leukemia cells with ABT-737 and resveratrol resulted in a reduction in mitochondrial membrane potential, an increase of p53 protein level and up-regulation of the Bax/Bcl-2 ratio.	Resveratrol	72-83	P53	Homo sapiens	160-163
28346428-7	2017	The ROS-p53-positive feedback loop is an essential mechanism of this synergistic cytotoxicity.	Reactive Oxygen Species	4-7	P53	Homo sapiens	8-11
28915555-4	2017	Consequently, 28 genes were designated as the p53-repressed gene module, whose gene components were simultaneously suppressed in breast cancer cells treated with Adriamycin.	Doxorubicin	162-172	P53	Homo sapiens	46-49
28536076-6	2017	Here in this study we focus on the inhibitory effects of polyarginine and its analogues polyornithine, canavanine, and citrulline on the inhibition of p53 mutant peptide aggregation, and p53 mutant cancer cell proliferation inhibition in vitro.	Canavanine	103-113	P53	Homo sapiens	151-154
28536076-6	2017	Here in this study we focus on the inhibitory effects of polyarginine and its analogues polyornithine, canavanine, and citrulline on the inhibition of p53 mutant peptide aggregation, and p53 mutant cancer cell proliferation inhibition in vitro.	Canavanine	103-113	P53	Homo sapiens	187-190
28754018-3	2017	In the present study, we systematically investigated the interaction of full length human protein p53 with DNA in metal ion solution by atomic force microscopy (AFM).	Metals	114-119	P53	Homo sapiens	98-101
28159923-2	2017	SHH-TP53-mutated as well as MYC-amplified Non-WNT/Non-SHH medulloblastoma show the worst prognosis.Here we present evidence that single application of the multi-kinase inhibitor Vandetanib displays anti-neoplastic efficacy against cell lines derived from high-risk SHH-TP53-mutated and MYC-amplified Non-WNT/Non-SHH medulloblastoma.	vandetanib	178-188	P53	Homo sapiens	4-8
28159923-2	2017	SHH-TP53-mutated as well as MYC-amplified Non-WNT/Non-SHH medulloblastoma show the worst prognosis.Here we present evidence that single application of the multi-kinase inhibitor Vandetanib displays anti-neoplastic efficacy against cell lines derived from high-risk SHH-TP53-mutated and MYC-amplified Non-WNT/Non-SHH medulloblastoma.	vandetanib	178-188	P53	Homo sapiens	269-273
28159923-4	2017	In this context our investigation documents that Vandetanib in combination with the clinically available PI3K inhibitor GDC-0941 leads to enhanced cytotoxicity against MYC-amplified and SHH-TP53-mutated medulloblastoma.	vandetanib	49-59	P53	Homo sapiens	190-194
28159923-7	2017	Of note, the combination of Vandetanib, GDC-0941 and Etoposide results in MYC-amplified and SHH-TP53-mutated cell lines in complete loss of cell viability.	vandetanib	28-38	P53	Homo sapiens	96-100
28660943-7	2017	Mechanistically, UA@M-CS-FA induced cancer cell apoptosis and inhibited migration via cell cycle arrest in the G0/G1 stage, regulating the PARP/Bcl-2/MMP-9/CD44/PTEN/P53.	m-cs-fa	20-27	P53	Homo sapiens	166-169
28704484-0	2017	Apoptosis by [Pt(O,O"-acac)(gamma-acac)(DMS)] requires PKC-delta mediated p53 activation in malignant pleural mesothelioma.	dms	40-43	P53	Homo sapiens	74-77
28684738-8	2017	Moreover, chrysin attenuated DOX-induced apoptosis via decreasing expression of p53, Bax, Puma, Noxa, cytochrome c and caspase-3 while increasing expression of Bcl-2.	Doxorubicin	29-32	P53	Homo sapiens	80-83
28684422-0	2017	WITHDRAWN: Curcumin shifts RAS-induced pro-proliferative MEK/ERK-signaling toward pro-apoptotic p38MAPK/JNK1-signaling, triggering p53 activation and apoptosis.	Curcumin	11-19	P53	Homo sapiens	131-134
28744147-8	2017	Transinfection of p53 serine could inhibit the expression of p53 in uveal melanoma and the invasion ability of the cells.	Serine	22-28	P53	Homo sapiens	18-21
28744147-8	2017	Transinfection of p53 serine could inhibit the expression of p53 in uveal melanoma and the invasion ability of the cells.	Serine	22-28	P53	Homo sapiens	61-64
28247504-7	2017	Co-treated cells had greater reductions in gefitinib-induced CYP1A1/CYB1B1, EGFR, cyclin D1, p-Akt (Ser473), and survivin mRNA/protein expression, as well as an increase in p-p53 (Ser15).	Gefitinib	43-52	P53	Homo sapiens	175-178
29057306-0	2017	Inhibiting system xC- and glutathione biosynthesis - a potential Achilles" heel in mutant-p53 cancers.	Glutathione	26-37	P53	Homo sapiens	90-93
28594550-0	2017	Methylseleninic Acid Prevents Patulin-Induced Hepatotoxicity and Nephrotoxicity via the Inhibition of Oxidative Stress and Inactivation of p53 and MAPKs.	methylselenic acid	0-20	P53	Homo sapiens	139-142
29057306-2	2017	We found that mutant p53 impairs the function of nuclear factor (erythroid-derived 2)-like 2 (NFE2L2, commonly known as NRF2), suppresses solute carrier family 7 member 11 (SLC7A11) expression, and diminishes cellular glutamate/cystine exchange.	Glutamic Acid	218-227	P53	Homo sapiens	21-24
29057306-4	2017	Mutant p53 tumors are thus inherently susceptible to further perturbations of the SLC7A11/glutathione axis.	Glutathione	90-101	P53	Homo sapiens	7-10
28671612-6	2017	The extraordinary loss of arginine may be attributed to some extent to composition of its codons as well as to the importance of arginine in the functioning of prominent tumor suppressor proteins like p53.	Arginine	26-34	P53	Homo sapiens	201-204
28574838-1	2017	Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration.	Reactive Oxygen Species	190-193	P53	Homo sapiens	54-57
28574838-1	2017	Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration.	Reactive Oxygen Species	190-193	P53	Homo sapiens	150-153
28574838-1	2017	Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration.	Reactive Oxygen Species	82-105	P53	Homo sapiens	54-57
28574838-1	2017	Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration.	Reactive Oxygen Species	82-105	P53	Homo sapiens	150-153
28574838-1	2017	Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration.	Reactive Oxygen Species	82-105	P53	Homo sapiens	150-153
28574838-1	2017	Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration.	Reactive Oxygen Species	107-110	P53	Homo sapiens	54-57
28574838-1	2017	Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration.	Reactive Oxygen Species	107-110	P53	Homo sapiens	150-153
28574838-1	2017	Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration.	Reactive Oxygen Species	190-193	P53	Homo sapiens	150-153
28671612-6	2017	The extraordinary loss of arginine may be attributed to some extent to composition of its codons as well as to the importance of arginine in the functioning of prominent tumor suppressor proteins like p53.	Arginine	129-137	P53	Homo sapiens	201-204
28574838-1	2017	Previously, we showed wild-type (WT) and mutant (mut) p53 differentially regulate reactive oxygen species (ROS) generation by NADPH oxidase-4 (NOX4): p53-WT suppresses TGFbeta-induced NOX4, ROS and cell migration, whereas tumor-associated mut-p53 proteins enhance NOX4 expression and cell migration.	Reactive Oxygen Species	107-110	P53	Homo sapiens	150-153
28918747-0	2017	Omega-3 Polyunsaturated Fatty Acids Eicosapentaenoic Acid and Docosahexaenoic Acid Enhance Dexamethasone Sensitivity in Multiple Myeloma Cells by the p53/miR-34a/Bcl-2 Axis.	Dexamethasone	91-104	P53	Homo sapiens	150-153
28475405-3	2017	A common coding region variant at amino acid 72 of p53 encodes either proline (P72) or arginine (R72).	Arginine	87-95	P53	Homo sapiens	51-54
28918747-7	2017	In addition, we observed that PUFAs induced p53 protein expression in MM cells under dexamethasone administration.	Dexamethasone	85-98	P53	Homo sapiens	44-47
28918747-8	2017	Furthermore, suppressing p53 by its inhibitor, Pifithrin-alpha, regulated the miR-34a expression and modulated the sensitivity to dexamethasone in U266 cells.	Dexamethasone	130-143	P53	Homo sapiens	25-28
28918747-9	2017	In summary, these results suggest that PUFAs enhance dexamethasone sensitivity to MM cells through the p53/miR-34a axis with a likely contribution of Bcl-2 suppression.	Dexamethasone	53-66	P53	Homo sapiens	103-106
28539160-0	2017	Phosphorylation of p53 at threonine 155 is required for Jab1-mediated nuclear export of p53.	Threonine	26-35	P53	Homo sapiens	19-22
28539160-0	2017	Phosphorylation of p53 at threonine 155 is required for Jab1-mediated nuclear export of p53.	Threonine	26-35	P53	Homo sapiens	88-91
28539160-2	2017	Here, we show that phosphorylation at the threonine 155 residue is essential for Jab1-mediated p53 nuclear export.	Threonine	42-51	P53	Homo sapiens	95-98
28539160-3	2017	Jab1 stimulated phosphorylation of p53 at T155 was inhibited by curcumin, an inhibitor of COP9 signalosome (CSN)-associated kinases.	Curcumin	64-72	P53	Homo sapiens	35-38
28714848-3	2017	For this effect, HBx sequentially activated ataxia telangiectasia mutated kinase and checkpoint kinase 2 via phosphorylation at the Ser-1981 and Thr-68 residues, respectively, which led to the activation of p53 via phosphorylation at the Ser-15 and Ser-20 residues.	Serine	132-135	P53	Homo sapiens	207-210
28288992-4	2017	RPL26, in turn, is required for the recruitment of the serine/arginine-rich splicing factor SRSF7 to p53 pre-mRNA and generation of alternatively spliced p53beta RNA.	Serine	55-61	P53	Homo sapiens	101-104
28431961-6	2017	Then, senescence under these conditions showed persistent activation of p53 pathway and mitochondrial dysfunctions, characterized by O2 - generation, inhibition of respiratory complex II activity and over-expression of SOD2 and GPX1 detoxification enzymes.	Superoxides	133-135	P53	Homo sapiens	72-75
28417340-10	2017	The absence of tryptophan increased p53, although its effect on p53"s transcriptional targets was heterogeneous.	Tryptophan	15-25	P53	Homo sapiens	36-39
28417340-13	2017	Considering the decreased apoptosis, it is likely that tryptophan depletion enhances autophagy through a p53-mediated increase of BNIP3L.	Tryptophan	55-65	P53	Homo sapiens	105-108
28819369-14	2017	Ganetespib reduced the phosphorylation of p53, Akt1/2/3 and PRAS40, as well as of WNK1, a kinase which regulates intracellular chloride concentrations.	STA 9090	0-10	P53	Homo sapiens	42-45
28498637-4	2017	Catecholamines inhibited doxorubicin (DOX)-induced p53 acetylation and transcription-activation activities by inducing the expression of Sirt1.	Doxorubicin	25-36	P53	Homo sapiens	51-54
28498637-4	2017	Catecholamines inhibited doxorubicin (DOX)-induced p53 acetylation and transcription-activation activities by inducing the expression of Sirt1.	Doxorubicin	38-41	P53	Homo sapiens	51-54
28498637-5	2017	Knockdown of the Sirt1 expression by the specific siRNA remarkably blocked the inhibitory effects of ISO on DOX-induced p53 acetylation.	Doxorubicin	108-111	P53	Homo sapiens	120-123
28405933-1	2017	P53 mutation was detected through the application of a biosensing approach based on the decrease in the fluorescence of oligonucleotide-templated silver nanoclusters (DNA-AgNCs).	Oligonucleotides	120-135	P53	Homo sapiens	0-3
28714848-3	2017	For this effect, HBx sequentially activated ataxia telangiectasia mutated kinase and checkpoint kinase 2 via phosphorylation at the Ser-1981 and Thr-68 residues, respectively, which led to the activation of p53 via phosphorylation at the Ser-15 and Ser-20 residues.	Threonine	145-148	P53	Homo sapiens	207-210
28714848-3	2017	For this effect, HBx sequentially activated ataxia telangiectasia mutated kinase and checkpoint kinase 2 via phosphorylation at the Ser-1981 and Thr-68 residues, respectively, which led to the activation of p53 via phosphorylation at the Ser-15 and Ser-20 residues.	Serine	238-241	P53	Homo sapiens	207-210
28714848-3	2017	For this effect, HBx sequentially activated ataxia telangiectasia mutated kinase and checkpoint kinase 2 via phosphorylation at the Ser-1981 and Thr-68 residues, respectively, which led to the activation of p53 via phosphorylation at the Ser-15 and Ser-20 residues.	Serine	238-241	P53	Homo sapiens	207-210
28502718-0	2017	Mitochondrial ND5 mutation mediated elevated ROS regulates apoptotic pathway epigenetically in a P53 dependent manner for generating pro-cancerous phenotypes.	Reactive Oxygen Species	45-48	P53	Homo sapiens	97-100
28502718-5	2017	Cells over-expressing mtND5 variant produced both peroxide as well as super-oxide ROS; the generation of which was dependent on the functional status of P53; modulating epigenetically the expression of key apoptosis pathway genes.	Superoxides	70-81	P53	Homo sapiens	153-156
28502718-5	2017	Cells over-expressing mtND5 variant produced both peroxide as well as super-oxide ROS; the generation of which was dependent on the functional status of P53; modulating epigenetically the expression of key apoptosis pathway genes.	Reactive Oxygen Species	82-85	P53	Homo sapiens	153-156
28502718-7	2017	We propose that somatic mutation in mtND5 resulting in down-regulated complex I enzyme activity, elevated ROS and up-regulation of a set of nuclear anti-apoptotic genes epigenetically in the P53 dysfunctional cellular background, has provided a unique understanding of the molecular mechanism of mitochondrial mutation; and the concomitant existence of somatically acquired mitochondrial and nuclear p53 mutations, in cancer progression and promotion.	Reactive Oxygen Species	106-109	P53	Homo sapiens	191-194
28661480-5	2017	The reason for this may be an increase in the level of cellular ROS after knockdown of Prdx2, which may subsequently lead to an increase in the expression of phosphorylated p53 (p-p53) and p38-MAPK/p21.	Reactive Oxygen Species	64-67	P53	Homo sapiens	173-176
28560439-13	2017	Taken together, the present study provides the first report that ISL induces apoptosis in Caki cells via generation of ROS, which causes induction of p53 and inhibition of the STAT3 signaling pathway.	Reactive Oxygen Species	119-122	P53	Homo sapiens	150-153
29137250-4	2017	This chaperone-mediated mutated p53-TAp73alpha complex induced chemoresistance to DNA damaging reagents, like Cisplatin, Doxorubicin, Etoposide or Camptothecin.	Cisplatin	110-119	P53	Homo sapiens	32-35
29137250-4	2017	This chaperone-mediated mutated p53-TAp73alpha complex induced chemoresistance to DNA damaging reagents, like Cisplatin, Doxorubicin, Etoposide or Camptothecin.	Doxorubicin	121-132	P53	Homo sapiens	32-35
28661480-5	2017	The reason for this may be an increase in the level of cellular ROS after knockdown of Prdx2, which may subsequently lead to an increase in the expression of phosphorylated p53 (p-p53) and p38-MAPK/p21.	Reactive Oxygen Species	64-67	P53	Homo sapiens	180-183
28658321-3	2017	HTR-8/SVneo cells were treated with doxorubicin to activate p53; STMN1 and TTP levels were detected by quantitative reverse transcription-PCR and western blotting.	Doxorubicin	36-47	P53	Homo sapiens	60-63
28092678-4	2017	Depletion of PFKFB4 from p53-deficient cancer cells increased levels of the allosteric regulator fructose-2,6-bisphosphate, leading to increased glycolytic activity but decreased routing of metabolites through the oxidative arm of the pentose-phosphate pathway.	Phosphates	113-122	P53	Homo sapiens	25-28
28416637-8	2017	SJSA cells treated with 5-fluorouracil, which induces metabolic and genotoxic stress and activates p53, further implicated CDK19 in p53 target gene expression.	Fluorouracil	24-38	P53	Homo sapiens	99-102
28416637-8	2017	SJSA cells treated with 5-fluorouracil, which induces metabolic and genotoxic stress and activates p53, further implicated CDK19 in p53 target gene expression.	Fluorouracil	24-38	P53	Homo sapiens	132-135
28604612-4	2017	Although there are no data linking the loss of p53 function and melatonin synthesis or signaling in cancer, melatonin does activate the p53 tumor-suppressor pathway in this disease.	Melatonin	108-117	P53	Homo sapiens	136-139
28601088-7	2017	Notably, keratinocytes exposed to UVB plus heat in the presence of the SIRT1 inhibitor, Ex-527, showed a similar phenotype to those exposed to UV alone; i.e. an increase in p53 acetylation, increased apoptosis and low levels of Survivin.	6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide	88-94	P53	Homo sapiens	173-176
28535155-7	2017	The continued expression of APOBEC3B in p53-defective cells not only caused a kataegic mutational signature but also caused hypersensitivity to small-molecule DDR inhibitors (ATR, CHEK1, CHEK2, PARP, WEE1 inhibitors) as well as cisplatin/ATR inhibitor and ATR/PARP inhibitor combinations.	Cisplatin	228-237	P53	Homo sapiens	40-43
28644127-5	2017	These phenotypes are caused by induction of p53 and accumulation of the glycolytic intermediate fructose 6-phosphate, leading to engagement of the hexosamine biosynthetic pathway (HBP), increased O-GlcNAcylation, and p53 stabilization.	Hexosamines	147-157	P53	Homo sapiens	44-47
28629161-0	2017	Cancer Chemoprevention by Resveratrol: The p53 Tumor Suppressor Protein as a Promising Molecular Target.	Resveratrol	26-37	P53	Homo sapiens	43-46
28629161-4	2017	The aim of this review is to collect and present recent evidence from the literature regarding resveratrol and its effects on cancer prevention, molecular signaling (especially regarding the involvement of p53 protein), and therapeutic perspectives with an emphasis on clinical trial results to date.	Resveratrol	95-106	P53	Homo sapiens	206-209
28155807-11	2017	In conclusion, cisplatin affects the viability, proliferation, and differentiation of ADSCs both in vitro and in vivo via certain signaling pathways, such as p53 and Fas/FasL.	Cisplatin	15-24	P53	Homo sapiens	158-161
28591603-2	2017	To elucidate how p53 maintains efficient target search at different concentrations of divalent cations such as Ca2+ and Mg2+, we prepared two mutants of p53, each possessing one of its two DNA-binding domains, the CoreTet mutant having the structured core domain plus the tetramerization (Tet) domain, and the TetCT mutant having Tet plus the disordered C-terminal domain.	magnesium ion	120-124	P53	Homo sapiens	17-20
28591603-7	2017	The disordered C-terminal domain can associate with DNA irrespective of [Mg2+], and can maintain an equilibrium balance of the two search modes and the p53 search distance.	magnesium ion	73-77	P53	Homo sapiens	152-155
28591603-8	2017	These results suggest that p53 modulates the quaternary structure of the complex between p53 and DNA under different [Mg2+] and that it maintains the target search along DNA.	magnesium ion	118-122	P53	Homo sapiens	27-30
28591603-8	2017	These results suggest that p53 modulates the quaternary structure of the complex between p53 and DNA under different [Mg2+] and that it maintains the target search along DNA.	magnesium ion	118-122	P53	Homo sapiens	89-92
28400230-0	2017	Investigation of the inhibitory mechanism of apomorphine against MDM2-p53 interaction.	Apomorphine	45-56	P53	Homo sapiens	70-73
29774995-2	2017	Method:Immunohistochemical staining of MCT-1 and p53 was carried out in 41 cases of laryngeal squamous cell carcinoma embedded in paraffin, and the relationship between positive expression and clinicopathological data was evaluated.	Paraffin	130-138	P53	Homo sapiens	49-52
28322991-4	2017	The molecular basis showed that thyroxine receptor stimulation triggers Phosphatidyl Inositol 3-kinase (PI3K)/Akt signaling activation leading to the E3 ligase MDM2 phosphorylation at serine 166, which directly interacted with p53 for degradation.	Serine	184-190	P53	Homo sapiens	227-230
28494179-10	2017	p53 family members and molecular subtypes of TNBC are also important alternative considerations for predicting platinum response based on the preclinical trials.	Platinum	111-119	P53	Homo sapiens	0-3
28400230-3	2017	In addition, both enantiomers of apomorphine showed potent inhibitory activity against the native MDM2-p53 interaction.	Apomorphine	33-44	P53	Homo sapiens	103-106
28400230-4	2017	In this study, we investigated the inhibitory mechanism of both enantiomers of apomorphine against the MDM2-p53 interaction.	Apomorphine	79-90	P53	Homo sapiens	108-111
28400230-2	2017	During the course of our screening study for novel MDM2-p53 interaction inhibitors, we identified that NPD6878 (R-(-)-apomorphine) inhibited both the native l-MDM2-l-p53 interaction and the mirror-image d-MDM2-d-p53 interaction at equipotent doses.	Apomorphine	112-129	P53	Homo sapiens	56-59
28400230-5	2017	Achiral oxoapomorphine, which was converted from chiral apomorphines under aerobic conditions, served as the reactive species to form a covalent bond at Cys77 of MDM2, leading to the inhibitory effect against the binding to p53.	Apomorphine	56-68	P53	Homo sapiens	224-227
28400230-2	2017	During the course of our screening study for novel MDM2-p53 interaction inhibitors, we identified that NPD6878 (R-(-)-apomorphine) inhibited both the native l-MDM2-l-p53 interaction and the mirror-image d-MDM2-d-p53 interaction at equipotent doses.	Apomorphine	112-129	P53	Homo sapiens	166-169
28400230-2	2017	During the course of our screening study for novel MDM2-p53 interaction inhibitors, we identified that NPD6878 (R-(-)-apomorphine) inhibited both the native l-MDM2-l-p53 interaction and the mirror-image d-MDM2-d-p53 interaction at equipotent doses.	Apomorphine	112-129	P53	Homo sapiens	166-169
28656004-9	2017	But the downstream of HIF-1alpha occurred the bifurcation dependent on the dosage of berberine: AMPK-HIF-1alpha-P-gp inactivation played a crucial role on the DOX chemosensitivity of low-dose berberine, while AMPK-HIF-1alpha downregulaton inducing p53 activation led to apoptosis in high-dose berberine.	Berberine	85-94	P53	Homo sapiens	248-251
28678322-0	2017	Downregulated long non-coding RNA TRPM2-AS inhibits cisplatin resistance of non-small cell lung cancer cells via activation of p53- p66shc pathway.	Cisplatin	52-61	P53	Homo sapiens	127-130
28656004-9	2017	But the downstream of HIF-1alpha occurred the bifurcation dependent on the dosage of berberine: AMPK-HIF-1alpha-P-gp inactivation played a crucial role on the DOX chemosensitivity of low-dose berberine, while AMPK-HIF-1alpha downregulaton inducing p53 activation led to apoptosis in high-dose berberine.	Doxorubicin	159-162	P53	Homo sapiens	248-251
28477877-0	2017	TP53 mutations in p53-negative dysplastic urothelial cells from Belgian AAN patients: New evidence for aristolochic acid-induced molecular pathogenesis and carcinogenesis.	aristolochic acid I	103-120	P53	Homo sapiens	0-4
28440512-0	2017	Astemizole protects against human umbilical vein endothelial cell injury induced by hydrogen peroxide via the p53 signaling pathway.	Hydrogen Peroxide	84-101	P53	Homo sapiens	110-113
28440512-8	2017	In conclusion, astemizole effectively protected endothelial cells against oxidative stress induced by H2O2, a function that may involve ROS/p53/p21Cip1/Waf1/ p16INK4a signaling pathways.	Hydrogen Peroxide	102-106	P53	Homo sapiens	140-143
28232385-4	2017	Although the expression of most A3 genes (including A3C and A3H) was stimulated by the activation of p53, treatment with the DNA-damaging agent doxorubicin or the p53 stabilizer Nutlin led to repression of the A3B gene.	Doxorubicin	144-155	P53	Homo sapiens	101-104
28477877-0	2017	TP53 mutations in p53-negative dysplastic urothelial cells from Belgian AAN patients: New evidence for aristolochic acid-induced molecular pathogenesis and carcinogenesis.	aristolochic acid I	103-120	P53	Homo sapiens	18-21
29029401-2	2017	Lysine methylation of histones such as H4K20 and non-histone proteins including p53 has been shown to be essential for the mounting of the DDR.	Lysine	0-6	P53	Homo sapiens	80-83
28588727-11	2017	The expression of p53 was increased in the combined PE and CDDP treatment group.	Cisplatin	59-63	P53	Homo sapiens	18-21
28588727-12	2017	Upregulation of p53-dependent apoptosis-associated proteins, including Bcl-2-associated X protein and cleaved caspases-9 and -3, was observed in the combined PE and CDDP treatment group.	Cisplatin	165-169	P53	Homo sapiens	16-19
28238728-6	2017	According to the analysis of KEGG pathway and Cytoscape gene network, this study identified that BPA exposure reduced miR-149 expression to down-regulate DNA repair gene ARF6 (ADP-ribosylation factor 6) and tumor protein p53 (TP53), and up-regulate CCNE2 (cyclin E2) potentially to interrupt cell cycle.	bisphenol A	97-100	P53	Homo sapiens	221-224
28238728-6	2017	According to the analysis of KEGG pathway and Cytoscape gene network, this study identified that BPA exposure reduced miR-149 expression to down-regulate DNA repair gene ARF6 (ADP-ribosylation factor 6) and tumor protein p53 (TP53), and up-regulate CCNE2 (cyclin E2) potentially to interrupt cell cycle.	bisphenol A	97-100	P53	Homo sapiens	226-230
28653879-5	2017	In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells.	Reactive Oxygen Species	35-58	P53	Homo sapiens	228-232
28653879-5	2017	In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells.	Doxorubicin	143-154	P53	Homo sapiens	122-126
28653879-5	2017	In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells.	Doxorubicin	143-154	P53	Homo sapiens	228-232
28653879-5	2017	In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells.	Doxorubicin	143-154	P53	Homo sapiens	228-232
28653879-5	2017	In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells.	Acetylcysteine	207-223	P53	Homo sapiens	122-126
28653879-5	2017	In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells.	Acetylcysteine	207-223	P53	Homo sapiens	228-232
28653879-5	2017	In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells.	Acetylcysteine	207-223	P53	Homo sapiens	228-232
28653879-6	2017	N-acetylcysteine prevented phosphorylation of P53 protein that had been induced by doxorubicin.	Acetylcysteine	0-16	P53	Homo sapiens	46-49
28653879-6	2017	N-acetylcysteine prevented phosphorylation of P53 protein that had been induced by doxorubicin.	Doxorubicin	83-94	P53	Homo sapiens	46-49
28653879-10	2017	In conclusion, TP53 genetic alteration is a critical factor that determines the use of antioxidant supplements during doxorubicin treatment.	Doxorubicin	118-129	P53	Homo sapiens	15-19
28580174-0	2017	Effects of concomitant inactivation of p53 and pRb on response to doxorubicin treatment in breast cancer cell lines.	Doxorubicin	66-77	P53	Homo sapiens	39-42
28580174-2	2017	We inactivated TP53 and/or RB1 by siRNA mediated knockdown in breast cancer cell lines varying with respect to ER/PgR and Her-2 status as well as TP53 and RB1 mutation status (MCF-7, T47D, HTB-122 and CRL2324) and determined effects on cell cycle arrest, apoptosis and senescence with or without concomitant treatment with doxorubicin.	Doxorubicin	323-334	P53	Homo sapiens	15-19
28580174-5	2017	While no significant change was observed for the CRL2324 cells upon doxorubicin treatment, MCF-7, T47D as well as HTB-122 cells responded to knockdown of TP53 and RB1 in concert, with a decrease in the fraction of cells in G1/G0-phase (P=0.042, 0.021 and 0.027, respectively).	Doxorubicin	68-79	P53	Homo sapiens	154-158
28580174-8	2017	Interestingly, upon doxorubicin treatment, concomitant inactivation of TP53 and RB1 caused a decrease in senescence in MCF-7 cells (P=0.027).	Doxorubicin	20-31	P53	Homo sapiens	71-75
28653879-0	2017	TP53 alteration determines the combinational cytotoxic effect of doxorubicin and an antioxidant NAC.	Doxorubicin	65-76	P53	Homo sapiens	0-4
28653879-5	2017	In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells.	Doxorubicin	15-26	P53	Homo sapiens	122-126
28653879-5	2017	In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells.	Doxorubicin	15-26	P53	Homo sapiens	228-232
28653879-5	2017	In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells.	Doxorubicin	15-26	P53	Homo sapiens	228-232
28653879-5	2017	In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells.	Reactive Oxygen Species	35-58	P53	Homo sapiens	122-126
28653879-5	2017	In this study, doxorubicin-induced reactive oxygen species was shown to differentially affect cancer cells based on their TP53 genetic status; doxorubicin-induced apoptosis was attenuated by an antioxidant, N-acetylcysteine, in TP53 wild cells; however, N-acetylcysteine caused a synergistic increase in the apoptosis rate in TP53-altered cells.	Reactive Oxygen Species	35-58	P53	Homo sapiens	228-232
28412363-7	2017	We also observe that WDR5 is required for p53 induction in response to cisplatin treatment.	Cisplatin	71-80	P53	Homo sapiens	42-45
28542145-7	2017	TRIM45 conjugates K63-linked polyubiquitin chain to the C-terminal six lysine residues of p53, thereby inhibiting the availability of these residues to the K48-linked polyubiquitination that targets p53 for degradation.	Lysine	71-77	P53	Homo sapiens	90-93
28542145-7	2017	TRIM45 conjugates K63-linked polyubiquitin chain to the C-terminal six lysine residues of p53, thereby inhibiting the availability of these residues to the K48-linked polyubiquitination that targets p53 for degradation.	Lysine	71-77	P53	Homo sapiens	199-202
29029384-2	2017	In order to identify novel p53 target genes, we utilized an unbiased microarray approach and identified Rap2B as a robust candidate, which belongs to the Ras-related GTP-binding protein superfamily and exhibits increased expression in various human cancers.	Guanosine Triphosphate	166-169	P53	Homo sapiens	27-30
28580174-10	2017	We found concomitant inactivation of TP53 and RB1 to affect various routes of response to doxorubicin treatment in breast cancer cells.	Doxorubicin	90-101	P53	Homo sapiens	37-41
28529565-0	2017	Prodelphinidins isolated from Chinese bayberry leaves induces apoptosis via the p53-dependent signaling pathways in OVCAR-3 human ovarian cancer cells.	prodelphinidins	0-15	P53	Homo sapiens	80-83
28415717-5	2017	In the presence of wild-type p53, cells exposed to C-1311 entered senescence.	Carbon	51-52	P53	Homo sapiens	29-32
28522974-11	2017	Up-regulation of p53 and p21 in colorectal carcinoma cells treated with low-dose PTX also contributed to inhibition of tumor cell growth.	Paclitaxel	81-84	P53	Homo sapiens	17-20
28464864-0	2017	Metformin produces growth inhibitory effects in combination with nutlin-3a on malignant mesothelioma through a cross-talk between mTOR and p53 pathways.	Metformin	0-9	P53	Homo sapiens	139-142
28476801-12	2017	CONCLUSION: AzaC significantly increases the sensitivity of MCF7 cells to Dox via activation of ERK1/2, P53, BAX and caspase-3.	Doxorubicin	74-77	P53	Homo sapiens	104-107
28189587-7	2017	In addition, deacetylation of p53 is required to make lysine residues accessible to ubiquitin ligases.	Lysine	54-60	P53	Homo sapiens	30-33
28427506-6	2017	Response to adjuvant cisplatin-based chemotherapy appears to be related to basal, luminal, and p53-like intrinsic subtypes.	Cisplatin	21-30	P53	Homo sapiens	95-98
27633574-8	2017	Carbon ions caused larger increase in the quantity of p53 and p21 compared to therapeutic protons.	Carbon	0-6	P53	Homo sapiens	54-57
27606834-7	2017	In a dose-dependent manner, naringenin decreased phosphorylation of ERK1/2, P70S6K, S6, and P38 in PC3 cells, and reduced phosphorylation of ERK1/2, P53, P38, and JNK proteins in LNCaP cells.	naringenin	28-38	P53	Homo sapiens	149-152
28730758-6	2017	This paper summarizes data about platinum derivatives through a multidisciplinary approach, starting from a chemical point of view and on to their mechanism of action, mechanism of cellular resistance, predictive factors for the outcome of chemotherapy such as micro RNAs (miRNAs), tumor suppressor protein p53, and the excision repair cross-complementing 1 protein (ERCC1).	Platinum	33-41	P53	Homo sapiens	307-310
28529594-8	2017	Western blot analyses were then performed, and the results revealed an increase in tumor protein 53 and cleaved caspase 9, and a decrease in B-cell lymphoma 2 protein expressions in PsA and PsA + 5-FU treated colon cancer cells compared with the vehicle-treated (PBS) cells.	Fluorouracil	196-200	P53	Homo sapiens	83-99
28214592-4	2017	We found that the polymorphism rs1042522:C &gt; G in codon 72 of exon 4 of the TP53 gene, whose C variant produces a proline and is more common in most ethnicities, has a G variant producing an arginine in 79.8% of NFPAs (n = 42; p &lt; 1.411 x 10-18 vs. 1000 Genomes database), causing patients to present a decade earlier with symptomatic NFPAs.	Arginine	194-202	P53	Homo sapiens	79-83
28476801-8	2017	These observations were accompanied by activation of ERK1/2 and p38MAPK, as well as up-regulation of BAX and P53 in the AzaC/Dox group.	Doxorubicin	125-128	P53	Homo sapiens	109-112
30345409-9	2017	The putative toxicity pathway for cytotoxicity of these metals and metal mixtures identified by LASSO is composed of phospho-RPS6KB1, phospho-p53, cleaved CASP3, phospho-MAPK8, IL-10, and Hif-1alpha.	Metals	56-61	P53	Homo sapiens	142-145
27419830-0	2017	Resveratrol targeting of AKT and p53 in glioblastoma and glioblastoma stem-like cells to suppress growth and infiltration.	Resveratrol	0-11	P53	Homo sapiens	33-36
27419830-4	2017	METHODS Resveratrol"s effects on cell proliferation, sphere-forming ability, and invasion were tested using multiple patient-derived GBM stem-like cell (GSC) lines and established U87 glioma cells, and changes in oncogenic AKT and tumor suppressive p53 were analyzed.	Resveratrol	8-19	P53	Homo sapiens	249-252
27419830-10	2017	In U87 glioma cells and GSCs, resveratrol reduced AKT phosphorylation and induced p53 expression and activation that led to transcription of downstream p53 target genes.	Resveratrol	30-41	P53	Homo sapiens	82-85
27419830-10	2017	In U87 glioma cells and GSCs, resveratrol reduced AKT phosphorylation and induced p53 expression and activation that led to transcription of downstream p53 target genes.	Resveratrol	30-41	P53	Homo sapiens	152-155
27419830-13	2017	CONCLUSIONS Resveratrol potently inhibited GBM and GSC growth and infiltration, acting partially via AKT deactivation and p53 induction, and suppressed glioblastoma growth in vivo.	Resveratrol	12-23	P53	Homo sapiens	122-125
27419830-14	2017	The ability of resveratrol to modulate AKT and p53, as well as reportedly many other antitumorigenic pathways, is attractive for therapy against a genetically heterogeneous tumor such as GBM.	Resveratrol	15-26	P53	Homo sapiens	47-50
28447756-8	2017	The mRNA expression levels of p53 and p21 in the group treated with 240 mg/l matrine were significantly higher compared with the control group.	matrine	77-84	P53	Homo sapiens	30-33
28447756-10	2017	The protein expression levels of p53 and p21 were significantly higher in the 240 mg/l matrine group compared with the control group.	matrine	87-94	P53	Homo sapiens	33-36
28529576-7	2017	As expected, MIR31HG lncRNA knockdown sensitized PC9-R cells to gefitinib, and further experiments revealed that turning off the EGFR/PI3K/AKT signaling pathway activated expression of p53 in PC9-R cells transfected with si-MIR31HG.	Gefitinib	64-73	P53	Homo sapiens	185-188
28315428-0	2017	p53 modulates the effect of ribosomal protein S6 kinase1 (S6K1) on cisplatin toxicity in chronic myeloid leukemia cells.	Cisplatin	67-76	P53	Homo sapiens	0-3
28111262-6	2017	DHA promoted reactive oxygen species production and activated p53 in two glioma cell lines, U87 and U251.	dehydroacetic acid	0-3	P53	Homo sapiens	62-65
28111262-10	2017	In conclusion, DHA inhibited the migration and invasion of human glioma cells with different types of p53 via different pathways.	dehydroacetic acid	15-18	P53	Homo sapiens	102-105
28315428-4	2017	To our surprise, S6K1 inhibition decreased cisplatin-induced DNA damage and cell death only in p53-/- BC CML cells but not in p53+/+ BC CML cells.	Cisplatin	43-52	P53	Homo sapiens	95-98
28315428-7	2017	Our results confirmed that S6K1 inhibition reversed cisplatin toxicity is dependent on p53 expression in CML cells.	Cisplatin	52-61	P53	Homo sapiens	87-90
28315428-10	2017	Taken together, our results suggest that p53/PDK1/S6K1 is a novel pathway regulating cisplatin toxicity in BC CML cells.	Cisplatin	85-94	P53	Homo sapiens	41-44
28513299-0	2017	Anti-tumor effect of cisplatin in human oral squamous cell carcinoma was enhanced by andrographolide via upregulation of phospho-p53 in vitro and in vivo.	Cisplatin	21-30	P53	Homo sapiens	129-132
28638272-7	2017	Furthermore, ETCH-induced apoptosis was mediated by increase in pro-apoptotic proteins including cleaved caspase-3 and p53, and by decrease in anti-apoptotic protein, Bcl-2 in ETCH-treated cancer cells.	etch	13-17	P53	Homo sapiens	119-122
29082697-9	2017	The protein expressions of Caspase-3, PTEN and p53 were all increased after being treated with resveratrol, while the expression of p-AKT was decreased after the treatment.	Resveratrol	95-106	P53	Homo sapiens	47-50
28453502-11	2017	Moreover, some GO terms (regulation of programmed cell death and regulation of cell death) and pathways (p53 signaling pathway, methane metabolism, and viral myocarditis) might be involved.	Methane	128-135	P53	Homo sapiens	105-108
28458631-0	2017	Inhibition of Mitochondrial p53 Accumulation by PFT-mu Prevents Cisplatin-Induced Peripheral Neuropathy.	Cisplatin	64-73	P53	Homo sapiens	28-31
28455491-5	2017	Melatonin and its metabolites enhanced the DNA repair in melanocytes exposed to UVB and stimulated expression of p53 phosphorylated at Ser-15.	Melatonin	0-9	P53	Homo sapiens	113-116
28455491-5	2017	Melatonin and its metabolites enhanced the DNA repair in melanocytes exposed to UVB and stimulated expression of p53 phosphorylated at Ser-15.	Serine	135-138	P53	Homo sapiens	113-116
28187856-0	2017	Corrigendum to "PCB153, TCDD and estradiol compromise the benzo[a]pyrene-induced p53-response via FoxO3a" [Chem.	Estradiol	33-42	P53	Homo sapiens	81-84
28187856-0	2017	Corrigendum to "PCB153, TCDD and estradiol compromise the benzo[a]pyrene-induced p53-response via FoxO3a" [Chem.	pyrene	66-72	P53	Homo sapiens	81-84
28423695-0	2017	NDRG2 promotes adriamycin sensitivity through a Bad/p53 complex at the mitochondria in breast cancer.	Doxorubicin	15-25	P53	Homo sapiens	52-55
28487608-7	2017	With respect to the other p53 isoforms, mRNA level of Delta133p53 was significantly reduced in a dose-dependent manner by treatment with only PDTC or PTDC in combination with cisplatin (P &lt; 0.01), whereas p53beta mRNA expression was not altered by PDTC treatment (P &gt; 0.05).	Cisplatin	175-184	P53	Homo sapiens	26-29
28881766-4	2017	We showed that As4S4 inhibited the expression of NFATc1, NFATc3, and NFATc4, and modulated the expression of NFATc2 accompanying with p53.	as4s4	15-20	P53	Homo sapiens	134-137
28458631-4	2017	We hypothesized that cisplatin acts as a cellular stressor that triggers p53 accumulation at mitochondria, leading to mitochondrial dysfunction and CIPN.	Cisplatin	21-30	P53	Homo sapiens	73-76
28458631-6	2017	We show here for the first time that in vivo cisplatin rapidly increases mitochondrial accumulation of p53 in dorsal root ganglia (DRG), spinal cord, and peripheral nerve without evidence for apoptosis.	Cisplatin	45-54	P53	Homo sapiens	103-106
28458631-8	2017	Pre-treatment with PFT-mu prevented the early cisplatin-induced increase in mitochondrial p53 and the reduction in mitochondrial membrane potential.	Cisplatin	46-55	P53	Homo sapiens	90-93
28458631-9	2017	Inhibition of the early mitochondrial p53 accumulation by PFT-mu also prevented the abnormalities in mitochondrial morphology and mitochondrial bioenergetics (reduced oxygen consumption rate, maximum respiratory capacity, and adenosine triphosphate synthesis) that develop in DRG and peripheral nerve after cisplatin-treatment.	Oxygen	167-173	P53	Homo sapiens	38-41
28458631-9	2017	Inhibition of the early mitochondrial p53 accumulation by PFT-mu also prevented the abnormalities in mitochondrial morphology and mitochondrial bioenergetics (reduced oxygen consumption rate, maximum respiratory capacity, and adenosine triphosphate synthesis) that develop in DRG and peripheral nerve after cisplatin-treatment.	Adenosine Triphosphate	226-248	P53	Homo sapiens	38-41
28458631-9	2017	Inhibition of the early mitochondrial p53 accumulation by PFT-mu also prevented the abnormalities in mitochondrial morphology and mitochondrial bioenergetics (reduced oxygen consumption rate, maximum respiratory capacity, and adenosine triphosphate synthesis) that develop in DRG and peripheral nerve after cisplatin-treatment.	Cisplatin	307-316	P53	Homo sapiens	38-41
28458631-11	2017	In conclusion, PFT-mu is a potential neuroprotective agent that prevents cisplatin-induced mitochondrial dysfunction in DRG and peripheral nerves thereby protecting against CIPN through blockade of the early cisplatin-induced increase in mitochondrial p53.	Cisplatin	208-217	P53	Homo sapiens	252-255
28406482-7	2017	Interestingly, cisplatin treatment also contributed to the increasement of HDAC, the interaction of TRIB1 with HDAC, and inactivation of p53.	Cisplatin	15-24	P53	Homo sapiens	137-140
28153791-0	2017	HDAC6 deacetylates p53 at lysines 381/382 and differentially coordinates p53-induced apoptosis.	Lysine	26-33	P53	Homo sapiens	19-22
28881600-0	2017	Curcumin induces G2/M cell cycle arrest and apoptosis of head and neck squamous cell carcinoma in vitro and in vivo through ATM/Chk2/p53-dependent pathway.	Curcumin	0-8	P53	Homo sapiens	133-136
28153791-4	2017	Interestingly, HDAC6 levels inversely correlated with p53 acetylation at lysines 381/382 associated with p53 functional activation.	Lysine	73-80	P53	Homo sapiens	54-57
28153791-4	2017	Interestingly, HDAC6 levels inversely correlated with p53 acetylation at lysines 381/382 associated with p53 functional activation.	Lysine	73-80	P53	Homo sapiens	105-108
28216618-5	2017	The signaling pathways involved in DAG-caused cell cycle arrest was further analyzed in LN229 cells, which revealed that DAG dose-dependently activated two parallel signaling cascades, ie, the p53-p21 cascade and the CDC25C-CDK1 cascade.	Dianhydrogalactitol	35-38	P53	Homo sapiens	193-196
28186994-7	2017	Gene set enrichment analysis (GSEA) revealed that cancer-related process and pathways, including p53-cell cycle and NFkappaB-epithelial mesenchymal transition (EMT) pathway, were significantly correlated with TRIM47 expression.	gsea	30-34	P53	Homo sapiens	97-100
28369097-0	2017	p53 pathway determines the cellular response to alcohol-induced DNA damage in MCF-7 breast cancer cells.	Alcohols	48-55	P53	Homo sapiens	0-3
28369097-2	2017	Alcohol is known to induce oxidative stress and DNA damage; likewise, p53 is a critical modulator of the DNA repair pathway and ensures genomic integrity.	Alcohols	0-7	P53	Homo sapiens	70-73
28369097-4	2017	The impact of alcohol on p53 is recognized, yet the role of p53 in alcohol-induced mammary carcinogenesis remains poorly defined.	Alcohols	67-74	P53	Homo sapiens	60-63
28369097-6	2017	p53 activity and target gene expression after alcohol exposure were determined using p53 luciferase reporter assay, qPCR, and Western blotting.	Alcohols	46-53	P53	Homo sapiens	0-3
28369097-6	2017	p53 activity and target gene expression after alcohol exposure were determined using p53 luciferase reporter assay, qPCR, and Western blotting.	Alcohols	46-53	P53	Homo sapiens	85-88
28369097-9	2017	A p53-dependent signaling cascade was stimulated by alcohol-induced DNA damage.	Alcohols	52-59	P53	Homo sapiens	2-5
28369097-10	2017	Moderate to high concentrations of alcohol (0.1-0.8% v/v) induced p53 activation, as indicated by increased p53 phosphorylation, reporter gene activity, and p21/Bax gene expression, which led to G0/G1 cell cycle arrest.	Alcohols	35-42	P53	Homo sapiens	66-69
28369097-10	2017	Moderate to high concentrations of alcohol (0.1-0.8% v/v) induced p53 activation, as indicated by increased p53 phosphorylation, reporter gene activity, and p21/Bax gene expression, which led to G0/G1 cell cycle arrest.	Alcohols	35-42	P53	Homo sapiens	108-111
28369097-13	2017	Our study suggests that functional p53 plays a critical role in cellular responses to alcohol-induced DNA damage, which protects the cells from DNA damage associated with breast cancer risk.	Alcohols	86-93	P53	Homo sapiens	35-38
28216618-5	2017	The signaling pathways involved in DAG-caused cell cycle arrest was further analyzed in LN229 cells, which revealed that DAG dose-dependently activated two parallel signaling cascades, ie, the p53-p21 cascade and the CDC25C-CDK1 cascade.	Dianhydrogalactitol	121-124	P53	Homo sapiens	193-196
28216621-0	2017	Dual anti-ischemic effects of rosmarinic acid n-butyl ester via alleviation of DAPK-p53-mediated neuronal damage and microglial inflammation.	rosmarinic acid n-butyl ester	30-59	P53	Homo sapiens	84-87
28107698-11	2017	The combination of the IC50 doses of apigenin (15muM) and cisplatin (7.5muM) for 48h significantly enhanced cisplatin"s cytotoxic and apoptotic effects through downregulation of Bcl-2, sharpin and survivin; and upregulation of caspase-8, Apaf-1 and p53 mRNA expression.	Apigenin	37-45	P53	Homo sapiens	249-252
28131915-0	2017	ROCK1/p53/NOXA signaling mediates cardiomyocyte apoptosis in response to high glucose in vitro and vivo.	Glucose	78-85	P53	Homo sapiens	6-9
28547941-6	2017	Suppression of E6 associated proteins by RITA induces accumulation of tumor suppressant p53.	RITA	41-45	P53	Homo sapiens	88-91
28107698-11	2017	The combination of the IC50 doses of apigenin (15muM) and cisplatin (7.5muM) for 48h significantly enhanced cisplatin"s cytotoxic and apoptotic effects through downregulation of Bcl-2, sharpin and survivin; and upregulation of caspase-8, Apaf-1 and p53 mRNA expression.	Cisplatin	58-67	P53	Homo sapiens	249-252
28110188-7	2017	The complex 1 and 2 treated cells show increased level of intracellular ROS generation which was preceded by p53 activation.	ros	72-75	P53	Homo sapiens	109-112
28152473-0	2017	Combination of arabinogalactan and curcumin induces apoptosis in breast cancer cells in vitro and inhibits tumor growth via overexpression of p53 level in vivo.	Curcumin	35-43	P53	Homo sapiens	142-145
28264987-0	2017	Nuclear retention of the lncRNA SNHG1 by doxorubicin attenuates hnRNPC-p53 protein interactions.	Doxorubicin	41-52	P53	Homo sapiens	71-74
28258507-7	2017	Herein we report on the effect of unmodified and neutron activated phosphine ruthenium II complexes on glioblastoma cell lines carrying wild-type and mutated p53 tumor suppressor gene.	ruthenium ii	77-89	P53	Homo sapiens	158-161
28258507-9	2017	The phosphine ruthenium II complexes tested were highly active against glioblastoma cell lines inducing cell death both through apoptosis and autophagy in a p53 independent fashion.	ruthenium ii	14-26	P53	Homo sapiens	157-160
28264987-5	2017	Upon doxorubicin treatment, the lncRNA SNHG1 is retained in the nucleus through its binding with nucleolin and it competes with p53 for hnRNPC binding, which upregulates p53 levels and promotes p53-dependent apoptosis by impairing hnRNPC regulation of p53 activity.	Doxorubicin	5-16	P53	Homo sapiens	170-173
28264987-5	2017	Upon doxorubicin treatment, the lncRNA SNHG1 is retained in the nucleus through its binding with nucleolin and it competes with p53 for hnRNPC binding, which upregulates p53 levels and promotes p53-dependent apoptosis by impairing hnRNPC regulation of p53 activity.	Doxorubicin	5-16	P53	Homo sapiens	170-173
28264987-5	2017	Upon doxorubicin treatment, the lncRNA SNHG1 is retained in the nucleus through its binding with nucleolin and it competes with p53 for hnRNPC binding, which upregulates p53 levels and promotes p53-dependent apoptosis by impairing hnRNPC regulation of p53 activity.	Doxorubicin	5-16	P53	Homo sapiens	170-173
28264987-6	2017	Our results indicate that a balance between lncRNA SNHG1 and hnRNPC regulates p53 activity and p53-dependent apoptosis upon doxorubicin treatment, and further indicate that a change in lncRNA subcellular localization under specific circumstances is biologically significant.	Doxorubicin	124-135	P53	Homo sapiens	78-81
28027428-4	2017	We found that the water extract of P. koraiensis pinecones exhibits significant cytotoxic activity, with IC50 values ranging from 0.62 to 1.73 mg/ml in four human lung cancer cell lines, A549, H1264, H1299, and Calu-6, irrespective of their p53 status.	Water	18-23	P53	Homo sapiens	241-244
28384067-0	2017	miR-101 Enhances Cisplatin-Induced DNA Damage Through Decreasing Nicotinamide Adenine Dinucleotide Phosphate Levels by Directly Repressing Tp53-Induced Glycolysis and Apoptosis Regulator Expression in Prostate Cancer Cells.	Cisplatin	17-26	P53	Homo sapiens	139-143
28264987-5	2017	Upon doxorubicin treatment, the lncRNA SNHG1 is retained in the nucleus through its binding with nucleolin and it competes with p53 for hnRNPC binding, which upregulates p53 levels and promotes p53-dependent apoptosis by impairing hnRNPC regulation of p53 activity.	Doxorubicin	5-16	P53	Homo sapiens	128-131
28130753-7	2017	Our data indicated that up-regulation of intracellular ROS induced by H2O2 significantly inhibited proliferation and induced apoptosis accompanying G1 cell cycle arrest and elevated expression of p53.	Reactive Oxygen Species	55-58	P53	Homo sapiens	196-199
28264987-6	2017	Our results indicate that a balance between lncRNA SNHG1 and hnRNPC regulates p53 activity and p53-dependent apoptosis upon doxorubicin treatment, and further indicate that a change in lncRNA subcellular localization under specific circumstances is biologically significant.	Doxorubicin	124-135	P53	Homo sapiens	95-98
28130753-7	2017	Our data indicated that up-regulation of intracellular ROS induced by H2O2 significantly inhibited proliferation and induced apoptosis accompanying G1 cell cycle arrest and elevated expression of p53.	Hydrogen Peroxide	70-74	P53	Homo sapiens	196-199
28130753-9	2017	Our results suggested that up-regulation of intracellular ROS inhibited proliferation by promoting expression of p53 and induced G1 cycle arrest and apoptosis.	Reactive Oxygen Species	58-61	P53	Homo sapiens	113-116
27431052-6	2017	Moreover, effects of coumestrol on cell signaling pathways were investigated and it increased phosphorylation of ERK1/2, JNK, P90RSK, and P53 proteins in a dose- and time-dependent manner whereas phosphorylation of AKT was reduced by coumestrol under the same conditions for culture of PC3 and LNCaP cells.	Coumestrol	21-31	P53	Homo sapiens	138-141
28471195-13	2017	CONCLUSION: During development of PLA method for detection of protein complexes between p53 family members we detected interactions of p53 and p63 with T-antigen and mut-p53 and DeltaNp63 with TAp73 tumour suppressor in tumour cell lines and p53 tetramers in paraffin sections of colorectal cancer tissue.	Paraffin	259-267	P53	Homo sapiens	88-91
28471195-13	2017	CONCLUSION: During development of PLA method for detection of protein complexes between p53 family members we detected interactions of p53 and p63 with T-antigen and mut-p53 and DeltaNp63 with TAp73 tumour suppressor in tumour cell lines and p53 tetramers in paraffin sections of colorectal cancer tissue.	Paraffin	259-267	P53	Homo sapiens	135-138
28471195-13	2017	CONCLUSION: During development of PLA method for detection of protein complexes between p53 family members we detected interactions of p53 and p63 with T-antigen and mut-p53 and DeltaNp63 with TAp73 tumour suppressor in tumour cell lines and p53 tetramers in paraffin sections of colorectal cancer tissue.	Paraffin	259-267	P53	Homo sapiens	135-138
28471195-13	2017	CONCLUSION: During development of PLA method for detection of protein complexes between p53 family members we detected interactions of p53 and p63 with T-antigen and mut-p53 and DeltaNp63 with TAp73 tumour suppressor in tumour cell lines and p53 tetramers in paraffin sections of colorectal cancer tissue.	Paraffin	259-267	P53	Homo sapiens	135-138
28284059-0	2017	Reactivating p53 and Inducing Tumor Apoptosis (RITA) Enhances the Response of RITA-Sensitive Colorectal Cancer Cells to Chemotherapeutic Agents 5-Fluorouracil and Oxaliplatin.	Fluorouracil	144-158	P53	Homo sapiens	13-16
28089541-7	2017	The expression of p53, enhancer of zeste homolog 2, IMP3, and DNA methyltransferase-1 was significantly weaker in noninvasive Pap-BTs than in invasive Pap-BTs (P&lt;.01).	pap-bts	126-133	P53	Homo sapiens	18-21
28348409-0	2017	Inhibiting the system xC-/glutathione axis selectively targets cancers with mutant-p53 accumulation.	Glutathione	26-37	P53	Homo sapiens	83-86
28193839-3	2017	In this study, we report that, under glucose deprivation, metformin inhibited expression of DeltaNp63alpha, a p53 family member involved in cell adhesion pathways, resulting in disruption of cell matrix adhesion and subsequent apoptosis in human squamous carcinoma cells.	Metformin	58-67	P53	Homo sapiens	110-113
28096517-5	2017	We demonstrate that clitocine can induce the production of p53 protein in cells harboring p53 nonsense-mutated alleles.	clitocine	20-29	P53	Homo sapiens	59-62
28096517-5	2017	We demonstrate that clitocine can induce the production of p53 protein in cells harboring p53 nonsense-mutated alleles.	clitocine	20-29	P53	Homo sapiens	90-93
28096517-6	2017	In these cells, clitocine restored production of full-length and functional p53 as evidenced by induced transcriptional activation of downstream p53 target genes, progression of cells into apoptosis, and impeded growth of nonsense-containing human ovarian cancer tumors in xenograft tumor models.	clitocine	16-25	P53	Homo sapiens	76-79
28096517-6	2017	In these cells, clitocine restored production of full-length and functional p53 as evidenced by induced transcriptional activation of downstream p53 target genes, progression of cells into apoptosis, and impeded growth of nonsense-containing human ovarian cancer tumors in xenograft tumor models.	clitocine	16-25	P53	Homo sapiens	145-148
28348409-4	2017	This diminishes glutathione synthesis, rendering mutant-p53 tumours susceptible to oxidative damage.	Glutathione	16-27	P53	Homo sapiens	56-59
28348409-6	2017	Moreover, we demonstrate that SLC7A11 expression is a novel and robust predictive biomarker for APR-246, a first-in-class mutant-p53 reactivator that also binds and depletes glutathione in tumours, triggering lipid peroxidative cell death.	Glutathione	174-185	P53	Homo sapiens	129-132
28348409-8	2017	We propose a new paradigm for targeting cancers that accumulate mutant-p53 protein by inhibiting the SLC7A11-glutathione axis.	Glutathione	109-120	P53	Homo sapiens	71-74
28349922-5	2017	Pharmacological inhibition of PIKKs abrogated S009-131 induced phosphorylation of p53 at Ser 15.	Serine	89-92	P53	Homo sapiens	82-85
28356713-0	2017	Artonin E induces p53-independent G1 cell cycle arrest and apoptosis through ROS-mediated mitochondrial pathway and livin suppression in MCF-7 cells.	Reactive Oxygen Species	77-80	P53	Homo sapiens	18-21
27617579-5	2017	The endogenous MDM2, when it was induced by p53 subjecting to DNA-damaging stimuli such as treatment with doxorubicin, was also significantly inhibited by FKBP12.	Doxorubicin	106-117	P53	Homo sapiens	44-47
27617579-8	2017	The FKBP12-mediated downregulation of MDM2 in response to doxorubicin or nutlin-3 results in continuing and constitutive activation of p53, inhibition of XIAP and sensitization of cancer cells to apoptosis.	Doxorubicin	58-69	P53	Homo sapiens	135-138
28348485-0	2017	ECRG2 enhances the anti-cancer effects of cisplatin in cisplatin-resistant esophageal cancer cells via upregulation of p53 and downregulation of PCNA.	Cisplatin	42-51	P53	Homo sapiens	119-122
28119452-8	2017	Blockade of P53 or NF-kappaB attenuated cisplatin-induced miR-375 expression, supporting a role of P53 and NF-kappaB in miR-375 induction.	Cisplatin	40-49	P53	Homo sapiens	12-15
28119452-8	2017	Blockade of P53 or NF-kappaB attenuated cisplatin-induced miR-375 expression, supporting a role of P53 and NF-kappaB in miR-375 induction.	Cisplatin	40-49	P53	Homo sapiens	99-102
28119452-11	2017	Together, these results suggest that upon cisplatin exposure, P53 and NF-kappaB collaboratively induce miR-375 expression, which, in turn, represses HNF-1beta activity, resulting in renal tubular cell apoptosis and nephrotoxicity.	Cisplatin	42-51	P53	Homo sapiens	62-65
28303973-0	2017	E6/E7-P53-POU2F1-CTHRC1 axis promotes cervical cancer metastasis and activates Wnt/PCP pathway.	pcp	83-86	P53	Homo sapiens	6-9
28303009-0	2017	Resveratrol sequentially induces replication and oxidative stresses to drive p53-CXCR2 mediated cellular senescence in cancer cells.	Resveratrol	0-11	P53	Homo sapiens	77-80
28303009-9	2017	We also demonstrated a critical role of the p53-CXCR2 axis in mediating RSV-induced senescence.	Resveratrol	72-75	P53	Homo sapiens	44-47
28297660-3	2017	Because ovulation is frequent and HGSOC is rare, we hypothesized that luteal-phase progesterone (P4) could eliminate p53-defective FT cells.	Progesterone	83-95	P53	Homo sapiens	117-120
28294157-0	2017	Alkaline ceramidase 2 is a novel direct target of p53 and induces autophagy and apoptosis through ROS generation.	ros	98-101	P53	Homo sapiens	50-53
28178647-0	2017	Enhancement of TRAIL-induced apoptosis by 5-fluorouracil requires activating Bax and p53 pathways in TRAIL-resistant lung cancers.	Fluorouracil	42-56	P53	Homo sapiens	85-88
28178647-5	2017	Interestingly, 5-fluorouracil treatment markedly increased Bax and p53 levels and 5-fluorouracil and TRAIL cotreatment increased Ac-cas3 and Ac-cas8 levels compared with those in control cells.	Fluorouracil	15-29	P53	Homo sapiens	67-70
28178647-6	2017	Taken together, the present study demonstrated that 5-fluorouracil enhances TRAIL-induced apoptosis in TRAIL-resistant lung adenocarcinoma cells by activating Bax and p53, and also suggest that TRAIL and 5-fluorouracil cotreatment can be used as an adequate therapeutic strategy for TRAIL-resistant human cancers.	Fluorouracil	52-66	P53	Homo sapiens	167-170
28348485-0	2017	ECRG2 enhances the anti-cancer effects of cisplatin in cisplatin-resistant esophageal cancer cells via upregulation of p53 and downregulation of PCNA.	Cisplatin	55-64	P53	Homo sapiens	119-122
28179588-5	2017	For SNPs interacting with anthracycline treatment, siRNA knockdown experiments were carried out to validate candidate genes.In the test for interaction between SNP genotype and TP53 status, we identified one locus, represented by rs10916264 (p(interaction) = 3.44 x 10-5; FDR-adjusted p = 0.0011) in estrogen receptor (ER) positive cases.	Anthracyclines	26-39	P53	Homo sapiens	177-181
28082445-1	2017	p53-related protein kinase (TP53RK, also known as PRPK) is an upstream kinase that phosphorylates (serine residue Ser15) and mediates p53 activity.	Serine	99-105	P53	Homo sapiens	0-3
28184025-6	2017	The magnitude of this effect on lactate production correlated with the differential sensitivity of HNSCC cells to Pt compounds (CDDP vs CBP) and p53-driven Pt chemotherapy resistance.	Lactic Acid	32-39	P53	Homo sapiens	145-148
28187375-0	2017	A comparative study of nuclear 8-hydroxyguanosine expression in Autoimmune Thyroid Diseases and Papillary Thyroid Carcinoma and its relationship with p53, Bcl-2 and Ki-67 cancer related proteins.	8-hydroxyguanosine	31-49	P53	Homo sapiens	150-153
28212547-0	2017	Resveratrol induces cell cycle arrest and apoptosis with docetaxel in prostate cancer cells via a p53/ p21WAF1/CIP1 and p27KIP1 pathway.	Resveratrol	0-11	P53	Homo sapiens	98-101
28104581-0	2017	High glucose stimulates proliferation and inhibits apoptosis of non-small-cell lung cancer cells by JNK-mediated downregulation of p53 pathway.	Glucose	5-12	P53	Homo sapiens	131-134
28150492-4	2017	This antiangiogenesis effect was derived from the particle size dependent uptake and production of intracellular reactive oxygen species (ROS) that directly interfered with p53 tumor suppressor pathway.	Reactive Oxygen Species	113-136	P53	Homo sapiens	173-176
28150492-4	2017	This antiangiogenesis effect was derived from the particle size dependent uptake and production of intracellular reactive oxygen species (ROS) that directly interfered with p53 tumor suppressor pathway.	Reactive Oxygen Species	138-141	P53	Homo sapiens	173-176
28274247-7	2017	RESULTS: We observed that gossypol inhibited expression of both MDM2 and VEGF in human breast cancer cells with either wild-type or mutant p53.	Gossypol	26-34	P53	Homo sapiens	139-142
28000054-11	2017	Furthermore, 5-FU retains its ability to cause nuclear accumulation of p53 in the presence of irinotecan or topotecan.	Fluorouracil	13-17	P53	Homo sapiens	71-74
28000054-11	2017	Furthermore, 5-FU retains its ability to cause nuclear accumulation of p53 in the presence of irinotecan or topotecan.	Irinotecan	94-104	P53	Homo sapiens	71-74
28131902-9	2017	Altogether, all results suggested that CQ synergistically sensitized human CRC cells with WT p53 to SN-38 through lysosomal and mitochondrial apoptotic pathway via p53-ROS cross-talk.	Reactive Oxygen Species	168-171	P53	Homo sapiens	164-167
28146458-13	2017	Phosphokinase arrays revealed that different O2 concentrations activated distinct sets of cytoprotective and cell death-associated kinases, including mitogen-activated protein kinases, Src kinases, p53, Akt, mitogen-activated and stress-activated kinase, Lyn, Lck, p70S6, signal transducers and activators of transcription 5b and 6, glycogen synthase kinase 3a/b and 5" AMP-activated protein kinases 1/2.	Oxygen	45-47	P53	Homo sapiens	198-201
28611978-6	2017	KEY MESSAGE: High rates of tumor suppressor gene p53 mutations, particularly p53 arginine mutations, were detected in pancreatic cancer patients.	Arginine	81-89	P53	Homo sapiens	49-52
28131902-0	2017	CQ synergistically sensitizes human colorectal cancer cells to SN-38/CPT-11 through lysosomal and mitochondrial apoptotic pathway via p53-ROS cross-talk.	Irinotecan	63-68	P53	Homo sapiens	134-137
28131902-0	2017	CQ synergistically sensitizes human colorectal cancer cells to SN-38/CPT-11 through lysosomal and mitochondrial apoptotic pathway via p53-ROS cross-talk.	Irinotecan	69-75	P53	Homo sapiens	134-137
28131902-4	2017	Notably, another autophagy inhibitor chloroquine (CQ) synergistically enhanced the anti-tumor activity of SN-38 in CRC cells with wild type (WT) p53.	Irinotecan	106-111	P53	Homo sapiens	145-148
28131902-5	2017	Subsequently, we identified a potential mechanism of this cooperative interaction by showing that CQ and SN-38 acted together to trigger reactive oxygen species (ROS) burst, upregulate p53 expression, elicit the loss of lysosomal membrane potential (LMP) and mitochondrial membrane potential ( psim).	Irinotecan	105-110	P53	Homo sapiens	185-188
28131902-6	2017	In addition, ROS induced by CQ plus SN-38 upregulated p53 levels by activating p38, conversely, p53 stimulated ROS.	Reactive Oxygen Species	13-16	P53	Homo sapiens	54-57
28131902-6	2017	In addition, ROS induced by CQ plus SN-38 upregulated p53 levels by activating p38, conversely, p53 stimulated ROS.	Irinotecan	36-41	P53	Homo sapiens	54-57
28131902-6	2017	In addition, ROS induced by CQ plus SN-38 upregulated p53 levels by activating p38, conversely, p53 stimulated ROS.	Reactive Oxygen Species	111-114	P53	Homo sapiens	96-99
28131902-9	2017	Altogether, all results suggested that CQ synergistically sensitized human CRC cells with WT p53 to SN-38 through lysosomal and mitochondrial apoptotic pathway via p53-ROS cross-talk.	Irinotecan	100-105	P53	Homo sapiens	93-96
28199187-8	2017	Interestingly, the combined treatment with curcumin and docetaxel modulates the expression of RTKs, PI3K, phospho-AKT, NF-kappa B, p53, and COX-2.	Curcumin	43-51	P53	Homo sapiens	131-134
28611978-6	2017	KEY MESSAGE: High rates of tumor suppressor gene p53 mutations, particularly p53 arginine mutations, were detected in pancreatic cancer patients.	Arginine	81-89	P53	Homo sapiens	77-80
28611978-8	2017	Oral bacteria peptidylarginine deiminases might lead to the p53 and K-ras point mutations by degrading arginine.	Arginine	22-30	P53	Homo sapiens	60-63
28024576-6	2017	We have found that apoptosis induced by RSV-DF was associated with the higher expression of p53, caspase-3, and BAX than the free RSV.	Resveratrol	40-43	P53	Homo sapiens	92-95
28229963-0	2017	Constitutively activated ERK sensitizes cancer cells to doxorubicin: Involvement of p53-EGFR-ERK pathway.	Doxorubicin	56-67	P53	Homo sapiens	84-87
28280421-1	2017	The p53-inducible gene 3 (PIG3), initially identified as a gene downstream of p53, plays an important role in the apoptotic process triggered by p53-mediated reactive oxygen species (ROS) production.	Reactive Oxygen Species	158-181	P53	Homo sapiens	4-7
28280421-1	2017	The p53-inducible gene 3 (PIG3), initially identified as a gene downstream of p53, plays an important role in the apoptotic process triggered by p53-mediated reactive oxygen species (ROS) production.	Reactive Oxygen Species	158-181	P53	Homo sapiens	78-81
28280421-1	2017	The p53-inducible gene 3 (PIG3), initially identified as a gene downstream of p53, plays an important role in the apoptotic process triggered by p53-mediated reactive oxygen species (ROS) production.	Reactive Oxygen Species	183-186	P53	Homo sapiens	4-7
28280421-1	2017	The p53-inducible gene 3 (PIG3), initially identified as a gene downstream of p53, plays an important role in the apoptotic process triggered by p53-mediated reactive oxygen species (ROS) production.	Reactive Oxygen Species	183-186	P53	Homo sapiens	78-81
28229968-0	2017	Cytotoxic and toxicogenomic effects of silibinin in bladder cancer cells with different TP53 status.	Silybin	39-48	P53	Homo sapiens	88-92
28229968-3	2017	Therefore, in this study we investigated the cytotoxic and toxicogenetic activity of silibinin in bladder cancer cells with different TP53 statuses.	Silybin	85-94	P53	Homo sapiens	134-138
28229968-6	2017	Silibinin promoted decreased proliferation and increased late apoptosis in TP53 mutated cells.	Silybin	0-9	P53	Homo sapiens	75-79
28229968-10	2017	In conclusion, despite the reduction of clone formation in both cell lines, the toxicogenomic effect of silibinin on FRAP/mTOR, AKT2, FGFR3, DNMT1 and miR100 was dependent on the TP53 status.	Silybin	104-113	P53	Homo sapiens	179-183
28229968-11	2017	Taken together, the data confirmed the role of silibinin as an antiproliferative compound, whose mechanism of action was related to the TP53 status.	Silybin	47-56	P53	Homo sapiens	136-140
28031409-3	2017	The current study demonstrates that, unlike cisplatin, platinum analogues oxaliplatin and DACH-diacetato-dichloro-Pt(IV) (DAP) strongly stabilize and activate p53v172F in resistant cells, as indicated by prolonged p53 half-life and transactivation of targets p21 (CDKN1A) and MDM2.	dach-diacetato-dichloro-pt	90-116	P53	Homo sapiens	159-162
28012015-0	2017	Modulation of cell death in human colorectal and breast cancer cells through a manganese chelate by involving GSH with intracellular p53 status.	Glutathione	110-113	P53	Homo sapiens	133-136
28012015-5	2017	Present study discloses that MnNG targets specifically wild-type-p53 expressing Hct116 and MCF-7 cells by significantly depleting both cytosolic, mitochondrial GSH, and modulating nuclear GSH through Glutathione reductase and Glutamate-cysteine ligase depletion that may in turn induce p53-mediated intrinsic apoptosis in them.	Glutathione	160-163	P53	Homo sapiens	65-68
28012015-6	2017	Thus GSH addition abrogates p53-mediated apoptosis in wild-type-p53 expressing cells.	Glutathione	5-8	P53	Homo sapiens	28-31
28012015-6	2017	Thus GSH addition abrogates p53-mediated apoptosis in wild-type-p53 expressing cells.	Glutathione	5-8	P53	Homo sapiens	64-67
28012015-8	2017	However, GSH addition partially replenishes the down-regulated or modulated GSH pool in cytosol, mitochondria, and nucleus, and relatively abrogates MnNG-induced intrinsic apoptosis in p53-mutated MDA-MB-468 cells.	Glutathione	9-12	P53	Homo sapiens	185-188
28012015-10	2017	Thus p53 status with intracellular GSH is critical for the modulation of MnNG-induced apoptosis.	Glutathione	35-38	P53	Homo sapiens	5-8
28031409-0	2017	Functional Activation of Mutant p53 by Platinum Analogues in Cisplatin-Resistant Cells Is Dependent on Phosphorylation.	Platinum	39-47	P53	Homo sapiens	32-35
28031409-0	2017	Functional Activation of Mutant p53 by Platinum Analogues in Cisplatin-Resistant Cells Is Dependent on Phosphorylation.	Cisplatin	61-70	P53	Homo sapiens	32-35
28031409-3	2017	The current study demonstrates that, unlike cisplatin, platinum analogues oxaliplatin and DACH-diacetato-dichloro-Pt(IV) (DAP) strongly stabilize and activate p53v172F in resistant cells, as indicated by prolonged p53 half-life and transactivation of targets p21 (CDKN1A) and MDM2.	Platinum	55-63	P53	Homo sapiens	159-162
28031409-3	2017	The current study demonstrates that, unlike cisplatin, platinum analogues oxaliplatin and DACH-diacetato-dichloro-Pt(IV) (DAP) strongly stabilize and activate p53v172F in resistant cells, as indicated by prolonged p53 half-life and transactivation of targets p21 (CDKN1A) and MDM2.	Platinum	55-63	P53	Homo sapiens	214-217
28031409-3	2017	The current study demonstrates that, unlike cisplatin, platinum analogues oxaliplatin and DACH-diacetato-dichloro-Pt(IV) (DAP) strongly stabilize and activate p53v172F in resistant cells, as indicated by prolonged p53 half-life and transactivation of targets p21 (CDKN1A) and MDM2.	dach-diacetato-dichloro-pt	90-116	P53	Homo sapiens	214-217
28231799-5	2017	METHODS: We aimed to compare the cytotoxic effects of cisplatin and a trans-sulfonamide-platinum-complex (TSPC), in two human melanoma cell lines that differ in their TP53 status: SK-MEL-5, TP53 wild type, and SK-MEL-28, TP53 mutated.	Cisplatin	54-63	P53	Homo sapiens	167-171
28347251-8	2017	Meanwhile, knockdown of methyl methanesulfonate and ultraviolet-sensitive gene clone 81 activated the p53/Bcl-2 pathway in response to cisplatin.	Cisplatin	135-144	P53	Homo sapiens	102-105
28118603-7	2017	This constitutive cholesterol synthesis is controlled by the cell cycle, as it can be turned off by cyclin-dependent kinase inhibitors and it correlates with disabled cell cycle control though loss of p53 and RB.	Cholesterol	18-29	P53	Homo sapiens	201-204
28152424-1	2017	BACKGROUND &amp; AIM: p53 activation by cellular stresses induces the transcription of hundreds of its target genes.	Adenosine Monophosphate	12-15	P53	Homo sapiens	22-25
28152424-2	2017	To elucidate the entire picture of its downstream pathway, we screened a cDNA microarray dataset of adriamycin-treated HCT116 p53-/- or p53+/+ cells and identified EPSIN 3 as a novel p53 target.	Doxorubicin	100-110	P53	Homo sapiens	126-129
28152424-2	2017	To elucidate the entire picture of its downstream pathway, we screened a cDNA microarray dataset of adriamycin-treated HCT116 p53-/- or p53+/+ cells and identified EPSIN 3 as a novel p53 target.	Doxorubicin	100-110	P53	Homo sapiens	136-139
28152424-2	2017	To elucidate the entire picture of its downstream pathway, we screened a cDNA microarray dataset of adriamycin-treated HCT116 p53-/- or p53+/+ cells and identified EPSIN 3 as a novel p53 target.	Doxorubicin	100-110	P53	Homo sapiens	136-139
28069986-5	2017	When compared with control, ethanol exposure led to a 43% decrease in blastocyst rate and activated pathways associated with oxidative stress and nervous system damage, such as TP53 and TGF.	Ethanol	28-35	P53	Homo sapiens	177-181
28230866-0	2017	Oridonin induces autophagy via inhibition of glucose metabolism in p53-mutated colorectal cancer cells.	Glucose	45-52	P53	Homo sapiens	67-70
28095394-7	2017	RESULTS: Selection of HCT116 cells for trabectedin resistance resulted in p53-independent hypersensitivity of the selected subline against cisplatin.	Cisplatin	139-148	P53	Homo sapiens	74-77
28038466-0	2017	Drug-dependent functionalization of wild-type and mutant p53 in cisplatin-resistant human ovarian tumor cells.	Cisplatin	64-73	P53	Homo sapiens	57-60
28038466-1	2017	Cisplatin (cis-Pt) resistance in tumor cells from p53 dysfunction is a significant clinical problem.	Cisplatin	0-9	P53	Homo sapiens	50-53
28038466-1	2017	Cisplatin (cis-Pt) resistance in tumor cells from p53 dysfunction is a significant clinical problem.	Cisplatin	11-17	P53	Homo sapiens	50-53
28038466-3	2017	Therefore, we examined the status of p53 in cisplatin-resistant ovarian tumor models and its functional response to cis-Pt and the mechanistically-distinct non-cross-resistant oxaliplatin (oxali-Pt).	Cisplatin	44-53	P53	Homo sapiens	37-40
28038466-3	2017	Therefore, we examined the status of p53 in cisplatin-resistant ovarian tumor models and its functional response to cis-Pt and the mechanistically-distinct non-cross-resistant oxaliplatin (oxali-Pt).	Cisplatin	116-122	P53	Homo sapiens	37-40
28038466-5	2017	Mutant p53 in 2780CP/Cl-16 (p53V172F) and OVCAR-10 (p53V172F and p53G266R) cells, predicted as non-functional in p53 database, displayed attenuated response to cis-Pt, as did the polymorphic p53P72R (functionally equivalent to wild-type p53) in HEY and OVCA-433 cell lines.	Cisplatin	160-166	P53	Homo sapiens	7-10
27894814-0	2017	Tanshinone IIA induced cell death via miR30b-p53-PTPN11/SHP2 signaling pathway in human hepatocellular carcinoma cells.	tanshinone	0-10	P53	Homo sapiens	45-48
28246474-8	2017	CONCLUSION: ST ethanol extracts induced the apoptosis of hepatocellular carcinoma SMMC-7721 cells through up-regulated Fas, caspase-8, caspse-3 and p53, and down-regulated FasL and Bcl-2 in the mitochondrial pathway.	Ethanol	15-22	P53	Homo sapiens	148-151
28208611-0	2017	Betulinic Acid-Mediated Apoptosis in Human Prostate Cancer Cells Involves p53 and Nuclear Factor-Kappa B (NF-kappaB) Pathways.	betulinic acid	0-14	P53	Homo sapiens	74-77
28208611-7	2017	BA treatment resulted in stabilization of p53 through increase in phosphorylation at Ser15 in LNCaP cells, but not in DU145 cells, and induction of cyclin kinase inhibitor p21/Waf1 in both cell types.	betulinic acid	0-2	P53	Homo sapiens	42-45
28208611-9	2017	We demonstrate that BA may induce apoptosis by stabilizing p53 and downregulating NF-kappaB pathway in human prostate cancer cells, irrespective of the androgen association, and therefore can potentially be developed as a molecule of interest in cancer chemoprevention.	betulinic acid	20-22	P53	Homo sapiens	59-62
27894814-6	2017	Further, we screened that PTPN11 and Tp53 are the two critical genomes involved in the pharmacology of Tanshinone IIA.	tanshinone	103-117	P53	Homo sapiens	37-41
27894814-12	2017	This study confirmed that Tanshinone IIA may induce hepatoma cell death through the miR30b-p53- PTPN11/SHP2 pathway.	tanshinone	26-40	P53	Homo sapiens	91-94
28028695-9	2017	An increase in p53 levels was detected following 5-FU treatment; pifithrin-alpha, an inhibitor of p53 activation, reversed 5-FU-induced SESN2 expression.	Fluorouracil	123-127	P53	Homo sapiens	15-18
27270636-0	2017	Up-regulation of Siah1 by ethanol triggers apoptosis in neural crest cells through p38 MAPK-mediated activation of p53 signaling pathway.	Ethanol	26-33	P53	Homo sapiens	115-118
27270636-2	2017	This study was designed to test the hypothesis that Siah1 mediates ethanol-induced apoptosis in NCCs through p38 MAPK-mediated activation of the p53 signaling pathway.	Ethanol	67-74	P53	Homo sapiens	145-148
27270636-3	2017	We found that exposure of NCCs to ethanol resulted in the increases in the total protein levels of p53 and the phosphorylation of p53 at serine 15.	Ethanol	34-41	P53	Homo sapiens	99-102
27270636-3	2017	We found that exposure of NCCs to ethanol resulted in the increases in the total protein levels of p53 and the phosphorylation of p53 at serine 15.	Ethanol	34-41	P53	Homo sapiens	130-133
27270636-3	2017	We found that exposure of NCCs to ethanol resulted in the increases in the total protein levels of p53 and the phosphorylation of p53 at serine 15.	Serine	137-143	P53	Homo sapiens	130-133
27270636-6	2017	Knock-down of Siah1 by siRNA or down-regulation of p38 MAPK by either siRNA or inhibitor significantly diminished ethanol-induced accumulations of p53 and the phosphorylation of p53.	Ethanol	114-121	P53	Homo sapiens	147-150
27270636-6	2017	Knock-down of Siah1 by siRNA or down-regulation of p38 MAPK by either siRNA or inhibitor significantly diminished ethanol-induced accumulations of p53 and the phosphorylation of p53.	Ethanol	114-121	P53	Homo sapiens	178-181
27270636-7	2017	In addition, ethanol exposure resulted in a significant increase in the expression of p53 downstream targets and apoptosis in NCCs, which can be significantly diminished by down-regulation of Siah1 with siRNA.	Ethanol	13-20	P53	Homo sapiens	86-89
27270636-9	2017	These results demonstrate that Siah1 plays a crucial role in ethanol-induced apoptosis in NCCs, and that the up-regulation of Siah1 by ethanol can trigger apoptosis through p38 MAPK-mediated activation of the p53 signaling pathway.	Ethanol	61-68	P53	Homo sapiens	209-212
28028695-9	2017	An increase in p53 levels was detected following 5-FU treatment; pifithrin-alpha, an inhibitor of p53 activation, reversed 5-FU-induced SESN2 expression.	Fluorouracil	49-53	P53	Homo sapiens	15-18
28028695-9	2017	An increase in p53 levels was detected following 5-FU treatment; pifithrin-alpha, an inhibitor of p53 activation, reversed 5-FU-induced SESN2 expression.	Fluorouracil	123-127	P53	Homo sapiens	98-101
27270636-9	2017	These results demonstrate that Siah1 plays a crucial role in ethanol-induced apoptosis in NCCs, and that the up-regulation of Siah1 by ethanol can trigger apoptosis through p38 MAPK-mediated activation of the p53 signaling pathway.	Ethanol	135-142	P53	Homo sapiens	209-212
28028695-11	2017	Taken together, our results suggest that 5-FU increases SESN2 levels via a p53-dependent pathway, which contributes to inhibition of cancer cell migration in vitro.	Fluorouracil	41-45	P53	Homo sapiens	75-78
28357076-5	2017	The distribution frequency of p53 sites of arginine (Arg)/Arg, Arg/proline (Pro), Pro/Pro were 18.4, 48.8 and 32.8% in the control group, as compared with 18.7, 49.9 and 31.4% in the case group, which indicated that there was no difference between two groups (chi2=0.14; P=0.93).	Arginine	43-51	P53	Homo sapiens	30-33
28357076-5	2017	The distribution frequency of p53 sites of arginine (Arg)/Arg, Arg/proline (Pro), Pro/Pro were 18.4, 48.8 and 32.8% in the control group, as compared with 18.7, 49.9 and 31.4% in the case group, which indicated that there was no difference between two groups (chi2=0.14; P=0.93).	Arginine	53-56	P53	Homo sapiens	30-33
28357076-7	2017	However, interactions between p53 codon 72 SNP and smoking, alcohol consumption and HBV infection may increase the risk of HCC [smoking odds ratio (OR), 2.00; 95% confidence interval (CI), 1.21-3.29; alcohol consumption OR, 1.87; 95% CI, 1.08-3.26; HBV infection OR, 1.84; 95% CI, 1.10-3.08].	Alcohols	200-207	P53	Homo sapiens	30-33
28357076-5	2017	The distribution frequency of p53 sites of arginine (Arg)/Arg, Arg/proline (Pro), Pro/Pro were 18.4, 48.8 and 32.8% in the control group, as compared with 18.7, 49.9 and 31.4% in the case group, which indicated that there was no difference between two groups (chi2=0.14; P=0.93).	Arginine	58-61	P53	Homo sapiens	30-33
28357076-5	2017	The distribution frequency of p53 sites of arginine (Arg)/Arg, Arg/proline (Pro), Pro/Pro were 18.4, 48.8 and 32.8% in the control group, as compared with 18.7, 49.9 and 31.4% in the case group, which indicated that there was no difference between two groups (chi2=0.14; P=0.93).	Arginine	58-61	P53	Homo sapiens	30-33
28272690-15	2017	CONCLUSIONS: These results suggest that LE and GA ameliorate cisplatin-induced apoptosis through reduction of ROS-mediating p53 activation and promotion of p21 expression in HK-2 cells.	Reactive Oxygen Species	110-113	P53	Homo sapiens	124-127
28163043-5	2017	With doxorubicin, a larger fraction of CPCs carrying an extra-copy of the p53 allele recruited gammaH2A.X reestablishing DNA integrity.	Doxorubicin	5-16	P53	Homo sapiens	74-77
28272690-0	2017	Licorice and its active compound glycyrrhizic acid ameliorates cisplatin-induced nephrotoxicity through inactivation of p53 by scavenging ROS and overexpression of p21 in human renal proximal tubular epithelial cells.	Cisplatin	63-72	P53	Homo sapiens	120-123
28272690-0	2017	Licorice and its active compound glycyrrhizic acid ameliorates cisplatin-induced nephrotoxicity through inactivation of p53 by scavenging ROS and overexpression of p21 in human renal proximal tubular epithelial cells.	Reactive Oxygen Species	138-141	P53	Homo sapiens	120-123
28050764-1	2017	Cutaneous melanoma (CM) cells are resistant to apoptosis, and steroid hormones are involved in this process through regulation of TP53, MDM2, BAX, and BCL2 expression.	Steroids	62-78	P53	Homo sapiens	130-134
28272690-2	2017	Cisplatin-induced apoptosis in renal cells is associated with reactive oxygen species (ROS)-mediated p53 activation.	Cisplatin	0-9	P53	Homo sapiens	101-104
28272690-2	2017	Cisplatin-induced apoptosis in renal cells is associated with reactive oxygen species (ROS)-mediated p53 activation.	Reactive Oxygen Species	62-85	P53	Homo sapiens	101-104
28272690-2	2017	Cisplatin-induced apoptosis in renal cells is associated with reactive oxygen species (ROS)-mediated p53 activation.	Reactive Oxygen Species	87-90	P53	Homo sapiens	101-104
28272690-15	2017	CONCLUSIONS: These results suggest that LE and GA ameliorate cisplatin-induced apoptosis through reduction of ROS-mediating p53 activation and promotion of p21 expression in HK-2 cells.	Cisplatin	61-70	P53	Homo sapiens	124-127
28119262-0	2017	Silibinin induces hepatic stellate cell cycle arrest via enhancing p53/p27 and inhibiting Akt downstream signaling protein expression.	Silybin	0-9	P53	Homo sapiens	67-70
28119262-9	2017	RESULTS: Silibinin inhibits LX-2 cell proliferation in dose- and time-dependent manner; we showed that silibinin upregulated the protein expressions of p27 and p53.	Silybin	103-112	P53	Homo sapiens	160-163
28352348-10	2017	5-FU+GA further decreased P53, survivin and TS mRNA and protein levels in the two CRC cell lines compared with single drugs, whereas increased P53 protein levels were observed in HCT116 cells.	Fluorouracil	0-4	P53	Homo sapiens	26-29
28352348-10	2017	5-FU+GA further decreased P53, survivin and TS mRNA and protein levels in the two CRC cell lines compared with single drugs, whereas increased P53 protein levels were observed in HCT116 cells.	Fluorouracil	0-4	P53	Homo sapiens	143-146
27128966-4	2017	Metformin promoted cytotoxic effects only in the cancer cells irrespective of the p53 status and not in the normal primary-cultured cells.	Metformin	0-9	P53	Homo sapiens	82-85
28356995-0	2017	Apigenin enhances the cisplatin cytotoxic effect through p53-modulated apoptosis.	Cisplatin	22-31	P53	Homo sapiens	57-60
27959444-5	2017	In addition, western blot analysis indicated that gigantol enhanced the activities of caspase-3, PARP and p53 and downregulated the expression of p-Akt/Akt.	gigantol	50-58	P53	Homo sapiens	106-109
28356995-6	2017	Treatment with apigenin increased cisplatin-induced DNA damage and the apoptosis of tumor cells in a p53-dependent manner.	Cisplatin	34-43	P53	Homo sapiens	101-104
27637603-0	2017	The Presence of Serum p53 Antibody Predicts the Pathological Tumor Response to Neoadjuvant Chemotherapy with Docetaxel, Cisplatin and Fluorouracil (DCF) in Esophageal Squamous Cell Carcinoma.	Cisplatin	120-129	P53	Homo sapiens	22-25
27637603-0	2017	The Presence of Serum p53 Antibody Predicts the Pathological Tumor Response to Neoadjuvant Chemotherapy with Docetaxel, Cisplatin and Fluorouracil (DCF) in Esophageal Squamous Cell Carcinoma.	Fluorouracil	134-146	P53	Homo sapiens	22-25
27888811-3	2017	Overexpression of mutated p53 with reduced or abolished function is often connected to resistance to standard medications, including cisplatin, alkylating agents (temozolomide), anthracyclines, (doxorubicin), antimetabolites (gemcitabine), antiestrogenes (tamoxifen) and EGFR-inhibitors (cetuximab).	Cisplatin	133-142	P53	Homo sapiens	26-29
28143445-11	2017	RESULTS: The combination of AUY922 with cisplatin, radiation and CCRT was found to be synergistic in p53 mutant HNSCC.	Cisplatin	40-49	P53	Homo sapiens	101-104
28052008-8	2017	Taken together, combination of metformin and 2-deoxyglucose reverses MDR of MCF-7/Dox cells by recovering p53 function and increasing doxorubicin accumulation.	Metformin	31-40	P53	Homo sapiens	106-109
27888811-3	2017	Overexpression of mutated p53 with reduced or abolished function is often connected to resistance to standard medications, including cisplatin, alkylating agents (temozolomide), anthracyclines, (doxorubicin), antimetabolites (gemcitabine), antiestrogenes (tamoxifen) and EGFR-inhibitors (cetuximab).	Anthracyclines	178-192	P53	Homo sapiens	26-29
27888811-3	2017	Overexpression of mutated p53 with reduced or abolished function is often connected to resistance to standard medications, including cisplatin, alkylating agents (temozolomide), anthracyclines, (doxorubicin), antimetabolites (gemcitabine), antiestrogenes (tamoxifen) and EGFR-inhibitors (cetuximab).	Doxorubicin	195-206	P53	Homo sapiens	26-29
27888811-3	2017	Overexpression of mutated p53 with reduced or abolished function is often connected to resistance to standard medications, including cisplatin, alkylating agents (temozolomide), anthracyclines, (doxorubicin), antimetabolites (gemcitabine), antiestrogenes (tamoxifen) and EGFR-inhibitors (cetuximab).	Tamoxifen	256-265	P53	Homo sapiens	26-29
28052008-0	2017	Targeting P-glycoprotein function, p53 and energy metabolism: Combination of metformin and 2-deoxyglucose reverses the multidrug resistance of MCF-7/Dox cells to doxorubicin.	Metformin	77-86	P53	Homo sapiens	35-38
28052008-8	2017	Taken together, combination of metformin and 2-deoxyglucose reverses MDR of MCF-7/Dox cells by recovering p53 function and increasing doxorubicin accumulation.	Doxorubicin	82-85	P53	Homo sapiens	106-109
28116660-0	2017	Salvianolic acid B attenuates oxidized low-density lipoprotein-induced endothelial cell apoptosis through inhibition of oxidative stress, p53, and caspase-3 pathways.	salvianolic acid B	0-18	P53	Homo sapiens	138-141
27836734-0	2017	Doxorubicin anti-tumor mechanisms include Hsp60 post-translational modifications leading to the Hsp60/p53 complex dissociation and instauration of replicative senescence.	Doxorubicin	0-11	P53	Homo sapiens	102-105
28116660-10	2017	CONCLUSION: Sal B exhibited anti-apoptotic effects in ox-LDL-induced endothelial cell injury by suppressing oxidative stress, p53, and caspase-3.	salvianolic acid B	12-17	P53	Homo sapiens	126-129
28071670-2	2017	Using a phosphoprotein-screening array, we found that Benzyl Isothiocynate, (BITC) increases p53 phosphorylation in breast cancer cells and reveal an important role of ERK and PRAS40/MDM2 in BITC-mediated p53 activation.	benzyl isothiocynate	54-74	P53	Homo sapiens	93-96
28102315-3	2017	Here we describe the first restriction-enzyme-assisted LC-MS/MS sequencing study of the influence of methyl cytosines (MeC) on kinetics of p53 gene adduction by model metabolite benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE), using methodology applicable to correlate gene damage sites for drug and pollutant metabolites with mutation sites.	methyl cytosines	101-117	P53	Homo sapiens	139-142
28102315-3	2017	Here we describe the first restriction-enzyme-assisted LC-MS/MS sequencing study of the influence of methyl cytosines (MeC) on kinetics of p53 gene adduction by model metabolite benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE), using methodology applicable to correlate gene damage sites for drug and pollutant metabolites with mutation sites.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	178-221	P53	Homo sapiens	139-142
28102315-3	2017	Here we describe the first restriction-enzyme-assisted LC-MS/MS sequencing study of the influence of methyl cytosines (MeC) on kinetics of p53 gene adduction by model metabolite benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE), using methodology applicable to correlate gene damage sites for drug and pollutant metabolites with mutation sites.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	223-227	P53	Homo sapiens	139-142
28102315-8	2017	Conformational and hydrophobicity changes in the MeC-p53 exon 7 fragment revealed by CD spectra and molecular modeling increase the BPDE binding constant to G in codon 248 consistent with a pathway in which preceding reactant binding greatly facilitates the rate of covalent SN2 coupling.	Cadmium	85-87	P53	Homo sapiens	53-56
28102315-8	2017	Conformational and hydrophobicity changes in the MeC-p53 exon 7 fragment revealed by CD spectra and molecular modeling increase the BPDE binding constant to G in codon 248 consistent with a pathway in which preceding reactant binding greatly facilitates the rate of covalent SN2 coupling.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	132-136	P53	Homo sapiens	53-56
27238838-9	2017	Collectively, these results suggest that Foxp3 is a downstream target of p53 that is sufficient to induce p21 expression, ROS production and p53-mediated senescence.	Reactive Oxygen Species	122-125	P53	Homo sapiens	73-76
27911860-3	2017	Recently, studies have focused on physiological mechanisms such as acetylation of lysine residues to rescue the wild type activity of mutant p53.	Lysine	82-88	P53	Homo sapiens	141-144
28071670-2	2017	Using a phosphoprotein-screening array, we found that Benzyl Isothiocynate, (BITC) increases p53 phosphorylation in breast cancer cells and reveal an important role of ERK and PRAS40/MDM2 in BITC-mediated p53 activation.	benzyl isothiocynate	54-74	P53	Homo sapiens	205-208
28081228-9	2017	However, upon hypoxia the cisplatin-induced cell cycle arrest and expression of p53 and p21 were abrogated.	Cisplatin	26-35	P53	Homo sapiens	80-83
27935863-9	2017	For instance, cisplatin triggered preferentially p53 and folate biosynthesis while the ruthenium complex induced endoplasmic reticulum stress and trans-sulfuration pathways.	Cisplatin	14-23	P53	Homo sapiens	49-52
28044934-5	2017	Results &amp;amp; Conclusion: Studies on cells revealed that 2 (i) demonstrated a high antiproliferative effect, which was higher toward HeLa and C6 cancer cells than toward healthy Vero cells; (ii) impaired the migration of HeLa cells; (iii) altered the P53-Bcl-2 ratio in favor of apoptosis; (iv) strongly bound to DNA/BSA macromolecules; and (v) inhibited human topoisomerase I and KpnI or BamHI restriction endonucleases.	Adenosine Monophosphate	13-16	P53	Homo sapiens	255-258
28068434-9	2017	Given that modulation of calcium signaling has been demonstrated to change sensitivity of chemotherapeutic agents to apoptotic signals, in principle, we explored the paradigm of how p53 modulation of calcium regulators in ER+ breast cancer patients impacts and influences therapeutic outcomes.	Calcium	200-207	P53	Homo sapiens	182-185
27901482-3	2017	Recently, hyperglycemia has been shown to reduce p53 phosphorylation at serine 46 (Ser46), the target residue of HIPK2, thus impairing p53 apoptotic function.	Serine	72-78	P53	Homo sapiens	49-52
27901482-3	2017	Recently, hyperglycemia has been shown to reduce p53 phosphorylation at serine 46 (Ser46), the target residue of HIPK2, thus impairing p53 apoptotic function.	Serine	72-78	P53	Homo sapiens	135-138
29147905-4	2017	Considering oxidative stress response and dopamine synthesis, the regulation of Nrf2, p53, and PSF by DJ-1 is especially important.	Dopamine	42-50	P53	Homo sapiens	86-89
27604683-0	2017	Antiproliferative and Apoptotic Effect of Dendrosomal Curcumin Nanoformulation in P53 Mutant and Wide-Type Cancer Cell Lines.	Curcumin	54-62	P53	Homo sapiens	82-85
27270439-2	2017	Here we identified that the lysine-specific demethylase KDM3A played a dual role in breast cancer cell invasion and apoptosis by demethylating histone and the non-histone protein p53, respectively.	Lysine	28-34	P53	Homo sapiens	179-182
28081741-0	2017	Depletion of NFBD1/MDC1 Induces Apoptosis in Nasopharyngeal Carcinoma Cells Through the p53-ROS-Mitochondrial Pathway.	Reactive Oxygen Species	92-95	P53	Homo sapiens	88-91
28081741-6	2017	Further analysis showed that loss of NFBD1 resulted in increased production of intracellular reactive oxygen species (ROS) depending on p53, which subsequently triggered the mitochondrial apoptotic pathway.	Reactive Oxygen Species	93-116	P53	Homo sapiens	136-139
28081741-6	2017	Further analysis showed that loss of NFBD1 resulted in increased production of intracellular reactive oxygen species (ROS) depending on p53, which subsequently triggered the mitochondrial apoptotic pathway.	Reactive Oxygen Species	118-121	P53	Homo sapiens	136-139
28231749-0	2017	Flavonoids and Tannins from Smilax china L. Rhizome Induce Apoptosis Via Mitochondrial Pathway and MDM2-p53 Signaling in Human Lung Adenocarcinoma Cells.	Tannins	15-22	P53	Homo sapiens	104-107
28231749-9	2017	Finally, cleaved-caspase-3 protein levels in the total flavonoids or total tannins-treated H1299 (p53 null) and p53-knockdown A549 cells were increased.	Tannins	75-82	P53	Homo sapiens	98-101
27834950-5	2017	In response to the chemotherapeutic agent doxorubicin, p53 regulates v2 through binding to an intragenic enhancer, together indicating that p53 and v2 engage in complex reciprocal regulation.	Doxorubicin	42-53	P53	Homo sapiens	55-58
27729002-12	2017	In conclusion, we identified that miR-30 functioned as a potential oncomiR through P53/ROS-mediated regulation of mitochondrial apoptotic pathway.	ros	87-90	P53	Homo sapiens	83-86
27836543-0	2017	miR-34a sensitizes lung cancer cells to cisplatin via p53/miR-34a/MYCN axis.	Cisplatin	40-49	P53	Homo sapiens	54-57
27836543-6	2017	In addition, p53 was found to monitor the expression of miR-34a in NSCLC cells after cisplatin treatment.	Cisplatin	85-94	P53	Homo sapiens	13-16
27836543-7	2017	Therefore, the sensitivity of cisplatin in NSCLC cells was modulated via p53/miR-34a/MYCN axis.	Cisplatin	30-39	P53	Homo sapiens	73-76
28191463-0	2017	Substrate Stiffness Influences Doxorubicin-Induced p53 Activation via ROCK2 Expression.	Doxorubicin	31-42	P53	Homo sapiens	51-54
28191463-3	2017	Here, we show that, in MCF-7 breast cancer cells, extracellular stiffness influences p53 activation induced by the antitumor drug doxorubicin.	Doxorubicin	130-141	P53	Homo sapiens	85-88
28191463-4	2017	Cell growth inhibition by doxorubicin was increased in response to ECM rigidity in a p53-dependent manner.	Doxorubicin	26-37	P53	Homo sapiens	85-88
28191463-6	2017	Knockdown of ROCK2 expression or pharmacological inhibition of ROCK decreased doxorubicin-induced p53 activation.	Doxorubicin	78-89	P53	Homo sapiens	98-101
28347732-0	2017	Association between the p53 arginine/arginine homozygous genotype at codon 72 and human papillomavirus E6/E7 mRNA expression.	Arginine	28-36	P53	Homo sapiens	24-27
28347732-0	2017	Association between the p53 arginine/arginine homozygous genotype at codon 72 and human papillomavirus E6/E7 mRNA expression.	Arginine	37-45	P53	Homo sapiens	24-27
28347732-9	2017	CONCLUSION: The presence of the p53 arginine/arginine homozygous genotype at codon 72 was significantly associated with the positive HPV E6/E7 mRNA expression.	Arginine	36-44	P53	Homo sapiens	32-35
28347732-9	2017	CONCLUSION: The presence of the p53 arginine/arginine homozygous genotype at codon 72 was significantly associated with the positive HPV E6/E7 mRNA expression.	Arginine	45-53	P53	Homo sapiens	32-35
27768124-5	2017	The human Tp53 gene harbors a common single-nucleotide polymorphism (SNP) at codon 72, which yields an arginine-to-proline amino-acidic substitution (Arg72Pro) that modulates the apoptotic activity of the p53 protein.	Arginine	103-111	P53	Homo sapiens	10-14
27768124-5	2017	The human Tp53 gene harbors a common single-nucleotide polymorphism (SNP) at codon 72, which yields an arginine-to-proline amino-acidic substitution (Arg72Pro) that modulates the apoptotic activity of the p53 protein.	Arginine	103-111	P53	Homo sapiens	11-14
28296564-3	2017	AZD1775 significantly improved the cytotoxicity of 5-FU in a p53-mutated colorectal cancer cell line (HT29 cells), decreasing the IC50 from 9.3 muM to 3.5 muM.	Fluorouracil	51-55	P53	Homo sapiens	61-64
27834950-5	2017	In response to the chemotherapeutic agent doxorubicin, p53 regulates v2 through binding to an intragenic enhancer, together indicating that p53 and v2 engage in complex reciprocal regulation.	Doxorubicin	42-53	P53	Homo sapiens	140-143
28957796-0	2017	Wild-Type P53 Induces Sodium/Iodide Symporter Expression Allowing Radioiodide Therapy in Anaplastic Thyroid Cancer.	Sodium	22-28	P53	Homo sapiens	10-13
28746938-9	2017	We also found treatment with NSCLC cells with Magnolol resulted in apoptosis activation through a p53-independent pathway, and autophgy induction via down-regulation of the Akt/mTOR pathway.	magnolol	46-54	P53	Homo sapiens	98-101
27768124-9	2017	Patients harboring the Pro allele of the Tp53 Arg72Pro SNP showed higher levels of circulating EPC-containing CD34+ cells, EPC-mobilizing cytokines - vascular endothelial growth factor and stromal cell-derived factor-1alpha - and good functional outcome following ICH, when compared with the homozygous Arg allele patients, which is compatible with increased neovascularization.	Arginine	46-49	P53	Homo sapiens	41-45
27913286-6	2017	Coumestrol treatment induced ROS generation coupled to DNA fragmentation, up-regulation of p53/p21, cell cycle arrest at G1/S phase, mitochondrial membrane depolarization and caspases 9/3 activation.	Coumestrol	0-10	P53	Homo sapiens	91-94
27794029-0	2017	Reversible p53 inhibition prevents cisplatin ototoxicity without blocking chemotherapeutic efficacy.	Cisplatin	35-44	P53	Homo sapiens	11-14
27794029-3	2017	We found activation of the ATM-Chk2-p53 pathway to be a major determinant of cisplatin ototoxicity.	Cisplatin	77-86	P53	Homo sapiens	36-39
28749708-2	2017	The suppressor of morphogenesis of genitalia (SMG-1) kinase is activated during hyperoxia and promotes cell survival by phosphorylating the tumor suppressor p53 on serine 15.	Serine	164-170	P53	Homo sapiens	157-160
28749708-3	2017	Here, we investigate whether SMG-1 and p53 blunt this vicious cycle of progressive ROS production and decline in mitochondrial respiration seen during hyperoxia.	Reactive Oxygen Species	83-86	P53	Homo sapiens	39-42
28749708-9	2017	Genetic depletion of p53 in A549 cells and ablation of the p53 gene in H1299 or HCT116 cells revealed that SMG-1 influences mitochondrial ROS through activation of p53.	Reactive Oxygen Species	138-141	P53	Homo sapiens	59-62
28749708-9	2017	Genetic depletion of p53 in A549 cells and ablation of the p53 gene in H1299 or HCT116 cells revealed that SMG-1 influences mitochondrial ROS through activation of p53.	Reactive Oxygen Species	138-141	P53	Homo sapiens	59-62
28749708-10	2017	CONCLUSIONS: Our findings show that hyperoxia does not promote a vicious cycle of progressive mitochondrial ROS and dysfunction because SMG-1-p53 signaling attenuates production of mitochondrial ROS without preserving respiration.	Reactive Oxygen Species	195-198	P53	Homo sapiens	142-145
28769986-0	2017	Curcumin Induces p53-Null Hepatoma Cell Line Hep3B Apoptosis through the AKT-PTEN-FOXO4 Pathway.	Curcumin	0-8	P53	Homo sapiens	17-20
28769986-2	2017	This study explored the mechanism by which curcumin induces p53-null hepatoma cell apoptosis.	Curcumin	43-51	P53	Homo sapiens	60-63
27919208-10	2017	Metformin reduces tumour cell growth and metastasis by activating the p53 tumour suppressor gene.	Metformin	0-9	P53	Homo sapiens	70-73
27584029-8	2017	Analysis of cisplatin-resistant cases has identified high rates of alterations within the TP53-MDM2 axis and a high proportion of patients with potentially actionable targets, including TP53-MDM2, PI3 kinase, and MAPK signaling pathway alterations.	Cisplatin	12-21	P53	Homo sapiens	90-94
27584029-8	2017	Analysis of cisplatin-resistant cases has identified high rates of alterations within the TP53-MDM2 axis and a high proportion of patients with potentially actionable targets, including TP53-MDM2, PI3 kinase, and MAPK signaling pathway alterations.	Cisplatin	12-21	P53	Homo sapiens	186-190
27866093-0	2017	NSCA-1-a novel N-substituted coumalamide derivative-increases Adriamycin sensitivity in HepG2/adriamycin cells through modulating Akt/GSK-3beta signaling and p53-dependant apoptotic pathway.	Doxorubicin	62-72	P53	Homo sapiens	158-161
27866093-10	2017	In addition, we found that combined treatment with NSCA-1 enhance cell apoptosis induced by Adriamycin via p53-dependant apoptotic pathway.	Doxorubicin	92-102	P53	Homo sapiens	107-110
29333597-2	2017	TP53 codon 72 polymorphism (P72R) results in proline (P) or arginine (R) at 72 amino acid position, which causes synthesis of proteins with distinct functions.	Arginine	60-68	P53	Homo sapiens	0-4
27913286-6	2017	Coumestrol treatment induced ROS generation coupled to DNA fragmentation, up-regulation of p53/p21, cell cycle arrest at G1/S phase, mitochondrial membrane depolarization and caspases 9/3 activation.	ros	29-32	P53	Homo sapiens	91-94
27913286-10	2017	In conclusion, copper targeted ROS-mediated p53-dependent mechanism better explains the cytotoxic action of coumestrol in MCF-7 cells.	Copper	15-21	P53	Homo sapiens	44-47
27913286-10	2017	In conclusion, copper targeted ROS-mediated p53-dependent mechanism better explains the cytotoxic action of coumestrol in MCF-7 cells.	ros	31-34	P53	Homo sapiens	44-47
27976481-5	2017	Accumulation of ROS and subsequent activation of NRF2, p53, AP-1 and NF-kappaB-dependent pathways, with downstream activation of antioxidant mechanisms (e.g., SOD2 and HMOX1 expression), is observed in the UV-treated cells.	Reactive Oxygen Species	16-19	P53	Homo sapiens	55-58
27913286-10	2017	In conclusion, copper targeted ROS-mediated p53-dependent mechanism better explains the cytotoxic action of coumestrol in MCF-7 cells.	Coumestrol	108-118	P53	Homo sapiens	44-47
28477117-7	2017	Ser46 on p53 is directly phosphorylated by ATM in a p53 conformation-dependent manner using the ATP analogue-accepting ATM mutant (ATM-AS) system.	Adenosine Triphosphate	96-99	P53	Homo sapiens	9-12
27902328-4	2017	For this effect, HCV core sequentially activated ataxia telangiectasia mutated and checkpoint kinase 2 via phosphorylation at Ser-1981 and Thr-68 residues, respectively, resulting in stabilization of p53 via phosphorylation at Ser-15 and Ser-20 residues and subsequent transcriptional activation of PA28gamma expression.	Serine	126-129	P53	Homo sapiens	200-203
27902328-4	2017	For this effect, HCV core sequentially activated ataxia telangiectasia mutated and checkpoint kinase 2 via phosphorylation at Ser-1981 and Thr-68 residues, respectively, resulting in stabilization of p53 via phosphorylation at Ser-15 and Ser-20 residues and subsequent transcriptional activation of PA28gamma expression.	Threonine	139-142	P53	Homo sapiens	200-203
27902328-4	2017	For this effect, HCV core sequentially activated ataxia telangiectasia mutated and checkpoint kinase 2 via phosphorylation at Ser-1981 and Thr-68 residues, respectively, resulting in stabilization of p53 via phosphorylation at Ser-15 and Ser-20 residues and subsequent transcriptional activation of PA28gamma expression.	Serine	227-230	P53	Homo sapiens	200-203
27902328-4	2017	For this effect, HCV core sequentially activated ataxia telangiectasia mutated and checkpoint kinase 2 via phosphorylation at Ser-1981 and Thr-68 residues, respectively, resulting in stabilization of p53 via phosphorylation at Ser-15 and Ser-20 residues and subsequent transcriptional activation of PA28gamma expression.	Serine	227-230	P53	Homo sapiens	200-203
27770912-8	2017	More excitedly, in comparison with single DOX or p53 delivery, the co-delivery of DOX and gene p53 using PDP micelles displayed higher cytotoxicity, induced higher apoptosis rate of tumor cells and blocked more effectively the migration of cancer cells in vitro.	Doxorubicin	42-45	P53	Homo sapiens	95-98
27770912-8	2017	More excitedly, in comparison with single DOX or p53 delivery, the co-delivery of DOX and gene p53 using PDP micelles displayed higher cytotoxicity, induced higher apoptosis rate of tumor cells and blocked more effectively the migration of cancer cells in vitro.	Doxorubicin	82-85	P53	Homo sapiens	49-52
28477117-7	2017	Ser46 on p53 is directly phosphorylated by ATM in a p53 conformation-dependent manner using the ATP analogue-accepting ATM mutant (ATM-AS) system.	Adenosine Triphosphate	96-99	P53	Homo sapiens	52-55
29081884-7	2017	These results indicate that SIRT1 activation by either RSV or overexpression of SIRT1 can exert neuroprotective effects partly by inhibiting p53 acetylation in NMDA-induced neurotoxicity.	Resveratrol	55-58	P53	Homo sapiens	141-144
27959389-3	2017	The present study aimed to assess anticancer effects of matrine in p53-deficient human Hep3B hepatoma cells.	matrine	56-63	P53	Homo sapiens	67-70
27959389-8	2017	Finally, combination therapy of matrine with 100 microM epotoside successfully killed more Hep3B cells, suggesting that matrine can sensitize p53-deficient Hep3B cells to epotoside-induced apoptosis.	epotoside	56-65	P53	Homo sapiens	142-145
27959389-8	2017	Finally, combination therapy of matrine with 100 microM epotoside successfully killed more Hep3B cells, suggesting that matrine can sensitize p53-deficient Hep3B cells to epotoside-induced apoptosis.	matrine	120-127	P53	Homo sapiens	142-145
27959389-8	2017	Finally, combination therapy of matrine with 100 microM epotoside successfully killed more Hep3B cells, suggesting that matrine can sensitize p53-deficient Hep3B cells to epotoside-induced apoptosis.	epotoside	171-180	P53	Homo sapiens	142-145
28043143-9	2017	Annexin V-FITC/PI staining showed a significant dose-dependent induction of apoptosis by ALA-PDT in H8 cells, associated with accumulation of the tumor suppressor protein p53 and the cyclin-dependent kinase inhibitor p21.	Alanine	89-92	P53	Homo sapiens	171-174
28123519-9	2017	Furthermore, the overexpression of Bax, and the downregulation of P-gP, P53 and Bcl-2 observed demonstrated the potential mechanism(s) of NaI131 and GA intervention.	nai131	138-144	P53	Homo sapiens	72-75
28694916-6	2017	The H2O2-mediated increased expression of the proapoptotic genes, BAX and p53, was attenuated by IAA treatment, while IAA treatment increased antiapoptotic genes, BCL-2 and ATF5 expression.	Hydrogen Peroxide	4-8	P53	Homo sapiens	74-77
28216878-7	2017	CONCLUSIONS: The present data demonstrated that NJet regulated the growth of IMR-32 and SK-N-MC through reduction in MYCN expression that lead to down regulation of MDM2 protein and increase in p53 expression.	sk-n-mc	88-95	P53	Homo sapiens	194-197
28193070-4	2016	After magnetic capture of the modified MBs onto screen-printed carbon working electrodes, the amperometric signal using the system hydroquinone/H2O2 was related to the levels of p53-autoantibodies in the sample.	Carbon	63-69	P53	Homo sapiens	178-181
30460048-5	2017	p53 was transcriptionally down regulated in all the three cell lines, but with different extents, in response to increasing concentration of cadmium.	Cadmium	141-148	P53	Homo sapiens	0-3
30460048-7	2017	The p53 knock out cell line was highly sensitive to cadmium-induced toxicity; so was the cell line in which p53 mRNA expression was highly down regulated.	Cadmium	52-59	P53	Homo sapiens	4-7
30460048-7	2017	The p53 knock out cell line was highly sensitive to cadmium-induced toxicity; so was the cell line in which p53 mRNA expression was highly down regulated.	Cadmium	52-59	P53	Homo sapiens	108-111
30460048-8	2017	This might implicate an unknown protective role of p53 signaling during heavy metal toxicity and that one of the possible mechanisms by which cadmium manifests its cytotoxic effect is through the transcriptional down regulation of p53 gene.	Cadmium	142-149	P53	Homo sapiens	231-234
28117010-0	2017	Inhibition of p53 Mutant Peptide Aggregation In Vitro by Cationic Osmolyte Acetylcholine Chloride.	Acetylcholine	75-97	P53	Homo sapiens	14-17
28117010-3	2017	Here in this study we focus on the inhibitory effects of cationic osmolyte molecules acetylcholine chloride, and choline on an aggregation prone 10 amino acid p53 mutant peptide WRPILTIITL, and the corresponding wildtype peptide RRPILTIITL in vitro.	Acetylcholine	85-107	P53	Homo sapiens	159-162
28117010-5	2017	The results show that acetylcholine chloride in micromolar concentrations significantly inhibit p53 mutant peptide aggregation in vitro, and could be promising candidate for p53 mutant/ misfolded protein aggregation inhibition.	Acetylcholine	22-44	P53	Homo sapiens	96-99
28117010-5	2017	The results show that acetylcholine chloride in micromolar concentrations significantly inhibit p53 mutant peptide aggregation in vitro, and could be promising candidate for p53 mutant/ misfolded protein aggregation inhibition.	Acetylcholine	22-44	P53	Homo sapiens	174-177
28003030-6	2016	Immunohistochemical staining for p53 was performed on paraffin-embedded 5-mum sections using mouse anti-human tumor protein p53 monoclonal antibody (DO-7, Dako, Denmark).	Paraffin	54-62	P53	Homo sapiens	33-36
28025407-3	2016	We demonstrated a requirement of nuclear p53 S-nitrosylation in inducing a nitric oxide/PGC-1alpha-mediated antioxidant pathway in skeletal muscle.	Nitric Oxide	75-87	P53	Homo sapiens	41-44
28193070-4	2016	After magnetic capture of the modified MBs onto screen-printed carbon working electrodes, the amperometric signal using the system hydroquinone/H2O2 was related to the levels of p53-autoantibodies in the sample.	Hydrogen Peroxide	144-148	P53	Homo sapiens	178-181
27912880-15	2016	CONCLUSION: HCPT and BA, a new and effective combination therapy, synergistically target Topo I and up-regulate p53 to induce cell apoptosis and cell cycle arrest.	10-hydroxycamptothecin	12-16	P53	Homo sapiens	112-115
27998224-3	2016	We conducted a proof-of-principle phase II study in patients with p53 tumor suppressor gene ( TP53)-mutated ovarian cancer refractory or resistant (&lt; 3 months) to first-line platinum-based therapy to determine overall response rate, progression-free and overall survival, pharmacokinetics, and modulation of phosphorylated cyclin-dependent kinase (CDK1) in skin biopsies.	Platinum	177-185	P53	Homo sapiens	66-69
27998224-3	2016	We conducted a proof-of-principle phase II study in patients with p53 tumor suppressor gene ( TP53)-mutated ovarian cancer refractory or resistant (&lt; 3 months) to first-line platinum-based therapy to determine overall response rate, progression-free and overall survival, pharmacokinetics, and modulation of phosphorylated cyclin-dependent kinase (CDK1) in skin biopsies.	Platinum	177-185	P53	Homo sapiens	94-98
27591972-5	2016	The p53(del) cells was more sensitive to cisplatin (PDD) and 5-fluorouracil (5FU) than p53(wt) cells but there was not significant difference.	Cisplatin	41-50	P53	Homo sapiens	4-7
27591972-5	2016	The p53(del) cells was more sensitive to cisplatin (PDD) and 5-fluorouracil (5FU) than p53(wt) cells but there was not significant difference.	Fluorouracil	61-75	P53	Homo sapiens	4-7
27591972-5	2016	The p53(del) cells was more sensitive to cisplatin (PDD) and 5-fluorouracil (5FU) than p53(wt) cells but there was not significant difference.	Fluorouracil	77-80	P53	Homo sapiens	4-7
27997533-5	2016	Patient-specific TP53 assays were developed for 31 unique mutations identified in formalin-fixed paraffin-embedded tumour DNA from these patients.	Paraffin	97-105	P53	Homo sapiens	17-21
27709883-0	2016	A Unique Mdm2-Binding Mode of the 3-Pyrrolin-2-one- and 2-Furanone-Based Antagonists of the p53-Mdm2 Interaction.	3-pyrroline-2-one	34-50	P53	Homo sapiens	92-95
27709883-3	2016	Here, we present the syntheses, activities, and crystal structures of two novel classes of Mdm2-p53 inhibitors that are based on the 3-pyrrolin-2-one and 2-furanone scaffolds.	3-pyrroline-2-one	133-149	P53	Homo sapiens	96-99
27984128-3	2016	In cisplatin-induced AKI or nephrotoxicity, the DDR pathway of ATR/Chk2/p53 is activated and contributes to renal tubular cell apoptosis.	Cisplatin	3-12	P53	Homo sapiens	72-75
27810895-7	2016	In addition, PKM2 interferes with phosphorylation of P53 at serine 15, known to stimulate P53 activity by the ATM serine/threonine kinase.	Serine	60-66	P53	Homo sapiens	53-56
27777309-0	2016	Human epidermal growth factor receptor 4 (Her4) Suppresses p53 Protein via Targeting the MDMX-MDM2 Protein Complex: IMPLICATION OF A NOVEL MDMX SER-314 PHOSPHOSITE.	Serine	144-147	P53	Homo sapiens	59-62
27810895-7	2016	In addition, PKM2 interferes with phosphorylation of P53 at serine 15, known to stimulate P53 activity by the ATM serine/threonine kinase.	Serine	60-66	P53	Homo sapiens	90-93
27777309-0	2016	Human epidermal growth factor receptor 4 (Her4) Suppresses p53 Protein via Targeting the MDMX-MDM2 Protein Complex: IMPLICATION OF A NOVEL MDMX SER-314 PHOSPHOSITE.	phosphosite	152-163	P53	Homo sapiens	59-62
27994465-7	2016	Furthermore, Ag@PEI@PTX enhanced cytotoxic effects on HepG2 cells and triggered intracellular reactive oxygen species; the signaling pathways of AKT, p53, and MAPK were activated to advance cell apoptosis.	Paclitaxel	20-23	P53	Homo sapiens	150-153
27777309-5	2016	Remarkably, inhibition of Ser-314 phosphorylation either with Ser-to-Ala substitution or with a specific inhibitor of CDK4/6 kinase blocked Her4-induced stabilization of MDMX-MDM2 and rescued p53 activity.	Serine	26-29	P53	Homo sapiens	192-195
27777309-5	2016	Remarkably, inhibition of Ser-314 phosphorylation either with Ser-to-Ala substitution or with a specific inhibitor of CDK4/6 kinase blocked Her4-induced stabilization of MDMX-MDM2 and rescued p53 activity.	Alanine	69-72	P53	Homo sapiens	192-195
27994465-7	2016	Furthermore, Ag@PEI@PTX enhanced cytotoxic effects on HepG2 cells and triggered intracellular reactive oxygen species; the signaling pathways of AKT, p53, and MAPK were activated to advance cell apoptosis.	Reactive Oxygen Species	94-117	P53	Homo sapiens	150-153
27994519-0	2016	Anticancer Effects of a New SIRT Inhibitor, MHY2256, against Human Breast Cancer MCF-7 Cells via Regulation of MDM2-p53 Binding.	mhy2256	44-51	P53	Homo sapiens	116-119
27924828-0	2016	rpL3 promotes the apoptosis of p53 mutated lung cancer cells by down-regulating CBS and NFkappaB upon 5-FU treatment.	Fluorouracil	102-106	P53	Homo sapiens	31-34
27924828-6	2016	Our results suggest that combination of rpL3 and 5-FU is a promising strategy for chemotherapy of lung cancers lacking functional p53 that are resistant to 5-FU.	Fluorouracil	49-53	P53	Homo sapiens	130-133
27994519-11	2016	A significant increase in acetylated p53, a target protein of SIRT, was observed in MCF-7 cells after MHY2256 treatment.	mhy2256	102-109	P53	Homo sapiens	37-40
27994519-14	2016	These results suggest that a new SIRT inhibitor, MHY2256, has anticancer activity through p53 acetylation in MCF-7 human breast cancer cells.	mhy2256	49-56	P53	Homo sapiens	90-93
27735058-1	2016	The C-terminal domain (CTD) of tumor suppressor protein p53 is an intrinsically disordered region that binds to various partner proteins, where lysine of CTD is acetylated/nonacetylated and histidine neutralized/non-neutralized.	Lysine	144-150	P53	Homo sapiens	56-59
27735058-1	2016	The C-terminal domain (CTD) of tumor suppressor protein p53 is an intrinsically disordered region that binds to various partner proteins, where lysine of CTD is acetylated/nonacetylated and histidine neutralized/non-neutralized.	Histidine	190-199	P53	Homo sapiens	56-59
27654922-6	2016	Compared to untreated glioblastoma cells TPEN treatment or expression of ZIP9 results in activation of the tumor suppressor p53 by phosphorylation at serine residue 46 (Ser46) and in inactivation of the migration relevant glycogen synthase kinase 3 beta (GSK-3beta) by phosphorylation at serine residue 9 (Ser9).	Serine	150-156	P53	Homo sapiens	124-127
28033105-6	2016	Multivariate analysis showed a significant association with NSCLC for the combination between the TP53 codon72 Arg/Pro and the Pro/Pro genotypes (OR 2.21, 95 % CI 1.390-3.51; p=0.001).	Arginine	111-114	P53	Homo sapiens	98-102
28149884-7	2016	So, mutant p53 has been reported to supply the cancer cells of glucose and nutrients, and, to avoid reactive oxygen species (ROS) mediated damage during oxidative stress.	Glucose	63-70	P53	Homo sapiens	11-14
28149884-7	2016	So, mutant p53 has been reported to supply the cancer cells of glucose and nutrients, and, to avoid reactive oxygen species (ROS) mediated damage during oxidative stress.	Reactive Oxygen Species	100-123	P53	Homo sapiens	11-14
28149884-7	2016	So, mutant p53 has been reported to supply the cancer cells of glucose and nutrients, and, to avoid reactive oxygen species (ROS) mediated damage during oxidative stress.	Reactive Oxygen Species	125-128	P53	Homo sapiens	11-14
27657825-12	2016	The apoptosis related protein p53 expression was increased, and apoptosis suppressor Bcl-2 was inhibited in DU-145 after curcumin treatment.	Curcumin	121-129	P53	Homo sapiens	30-33
27654922-6	2016	Compared to untreated glioblastoma cells TPEN treatment or expression of ZIP9 results in activation of the tumor suppressor p53 by phosphorylation at serine residue 46 (Ser46) and in inactivation of the migration relevant glycogen synthase kinase 3 beta (GSK-3beta) by phosphorylation at serine residue 9 (Ser9).	Serine	288-294	P53	Homo sapiens	124-127
27611480-0	2016	p53-dependent up-regulation of CDKN1A and down-regulation of CCNE2 in response to beryllium.	Beryllium	82-91	P53	Homo sapiens	0-3
27611480-3	2016	This study sought to determine the role of p53, the tumour-suppressing transcription factor, in mediating beryllium-induced cytostasis.	Beryllium	106-115	P53	Homo sapiens	43-46
27906186-8	2016	More precisely, sPIF (i) decreases the phosphorylation of p53 at Ser-15, (ii) enhances the B-cell lymphoma-2 (BCL2) expression and (iii) reduces the BCL2-associated X protein (BAX) and BCL2 homologous antagonist killer (BAK) mRNA expression levels.	Serine	65-68	P53	Homo sapiens	58-61
27764550-0	2016	Paclitaxel-induced aberrant mitosis and mitotic slippage efficiently lead to proliferative death irrespective of canonical apoptosis and p53.	Paclitaxel	0-10	P53	Homo sapiens	137-140
27611480-6	2016	Key elements of the beryllium-response were compared in normal and p53-knockdown A172 cells using RT-PCR and Western blotting.	Beryllium	20-29	P53	Homo sapiens	67-70
27611480-13	2016	CONCLUSIONS: Beryllium elicited p53-dependent changes in mRNA levels of key determinants of cell proliferation such as p21 and cyclin E2.	Beryllium	13-22	P53	Homo sapiens	32-35
27613187-0	2016	Vitamin C in synergism with cisplatin induces cell death in cervical cancer cells through altered redox cycling and p53 upregulation.	Cisplatin	28-37	P53	Homo sapiens	116-119
27701048-10	2016	Overall, we observed that CIO NPs induced cytotoxicity and apoptosis in HepG2 cells through ROS via p53 pathway.	Reactive Oxygen Species	92-95	P53	Homo sapiens	100-103
28096969-9	2016	CONCLUSION: The findings of the current study suggest that our combination strategy, which merges two detached gene (p53) and drug (curcumin) delivery systems into an integrated platform, may represent huge potential as a novel and efficient modality for glioblastoma treatment.	Curcumin	132-140	P53	Homo sapiens	117-120
28053964-7	2016	p53 gene polymorphism at codon 72 is statistically significant in Arg/Arg and Pro/Pro genotypes.	Arginine	66-69	P53	Homo sapiens	0-3
28053964-7	2016	p53 gene polymorphism at codon 72 is statistically significant in Arg/Arg and Pro/Pro genotypes.	Arginine	70-73	P53	Homo sapiens	0-3
27050716-11	2016	CONCLUSION: In patients who had received adjuvant TPF for node-positive penile squamous cell carcinoma, p53 IHC expression seemed to be associated with a poorer outcome, and further study is warranted in larger data sets to confirm these findings.	TPF	50-53	P53	Homo sapiens	104-107
28105142-8	2016	In the rAd/p53 + 5-Fu group, the tumor necrosis ratio, and Smad4 and Brca1 expression levels also significantly increased at various time points (P&lt;0.05).	Fluorouracil	17-21	P53	Homo sapiens	11-14
27779649-5	2016	Results indicated that curcumin combined with paclitaxel decreased c-Ha-Ras, Rho-A, p53 and Bcl-xL gene expression in comparison to control and substances alone in MCF-7 cell line.	Curcumin	23-31	P53	Homo sapiens	84-87
27779649-5	2016	Results indicated that curcumin combined with paclitaxel decreased c-Ha-Ras, Rho-A, p53 and Bcl-xL gene expression in comparison to control and substances alone in MCF-7 cell line.	Paclitaxel	46-56	P53	Homo sapiens	84-87
27779649-11	2016	Curcumin alone and combined with paclitaxel increased p53, Bid, caspase-3, caspase-8 and Bax gene expression in MDA-MB-231, whereas Bcl-xL decreased such expression in MDA-MB-231 cells.	Curcumin	0-8	P53	Homo sapiens	54-57
27779649-11	2016	Curcumin alone and combined with paclitaxel increased p53, Bid, caspase-3, caspase-8 and Bax gene expression in MDA-MB-231, whereas Bcl-xL decreased such expression in MDA-MB-231 cells.	Paclitaxel	33-43	P53	Homo sapiens	54-57
27613187-8	2016	RESULTS: Our results clearly demonstrated that CDDP and VC treatment exhibited ameliorative effect on induction of cell death by p53 overexpression and generation of hydrogen peroxide in SiHa cells, thereby reducing the dosage of CDDP required to induce cell death in cancer cells.	Cisplatin	47-51	P53	Homo sapiens	129-132
27613187-8	2016	RESULTS: Our results clearly demonstrated that CDDP and VC treatment exhibited ameliorative effect on induction of cell death by p53 overexpression and generation of hydrogen peroxide in SiHa cells, thereby reducing the dosage of CDDP required to induce cell death in cancer cells.	Cisplatin	230-234	P53	Homo sapiens	129-132
26756900-0	2016	COX-2 inhibitor NS-398 suppresses doxorubicin-induced p53 accumulation through inhibition of ROS-mediated Jnk activation.	Doxorubicin	34-45	P53	Homo sapiens	54-57
28053903-0	2016	The influence of p53 mutation status on the anti-cancer effect of cisplatin in oral squamous cell carcinoma cell lines.	Cisplatin	66-75	P53	Homo sapiens	17-20
28053903-1	2016	OBJECTIVES: The purpose of this study was to evaluate the anti-cancer activity of cisplatin by studying its effects on cell viability and identifying the mechanisms underlying the induction of cell cycle arrest and apoptosis on oral squamous cell carcinoma (OSCC) cell lines with varying p53 mutation status.	Cisplatin	82-91	P53	Homo sapiens	288-291
28053903-10	2016	Also, immunoblotting analysis indicated that p53 and p21 were detected only in YD-8 and YD-9 cell lines after cisplatin treatment.	Cisplatin	110-119	P53	Homo sapiens	45-48
27614750-0	2016	Association of p53 codon 72 polymorphism and survival of North Indian lung cancer patients treated with platinum-based chemotherapy.	Platinum	104-112	P53	Homo sapiens	15-18
26756900-0	2016	COX-2 inhibitor NS-398 suppresses doxorubicin-induced p53 accumulation through inhibition of ROS-mediated Jnk activation.	Reactive Oxygen Species	93-96	P53	Homo sapiens	54-57
26756900-4	2016	In this study, we investigated the effect of NS-398, a COX-2 inhibitor, on modulation of doxorubicin (DOX)-induced p53 accumulation.	Doxorubicin	89-100	P53	Homo sapiens	115-118
26756900-4	2016	In this study, we investigated the effect of NS-398, a COX-2 inhibitor, on modulation of doxorubicin (DOX)-induced p53 accumulation.	Doxorubicin	102-105	P53	Homo sapiens	115-118
26756900-6	2016	Nutlin-3alpha or MG132 abolished the suppressive effect of a COX-2 inhibitor on DOX-induced p53 increase.	Doxorubicin	80-83	P53	Homo sapiens	92-95
26756900-8	2016	DOX-induced accumulation of p53 was attenuated by a specific inhibitor or knockdown of Jun-N-terminal kinase (Jnk).	Doxorubicin	0-3	P53	Homo sapiens	28-31
26756900-9	2016	In addition, DOX-induced Jnk activation was decreased in COX-2 KO MEFs or by COX-2 inhibition, suggesting that Jnk stabilizes p53 by a mechanism that involves COX-2.	Doxorubicin	13-16	P53	Homo sapiens	126-129
26756900-10	2016	Pre-treatment with a reactive oxygen species (ROS) scavenger, N-acetylcysteine, attenuated DOX-induced Jnk activation and subsequent p53 accumulation.	Reactive Oxygen Species	21-44	P53	Homo sapiens	133-136
26756900-10	2016	Pre-treatment with a reactive oxygen species (ROS) scavenger, N-acetylcysteine, attenuated DOX-induced Jnk activation and subsequent p53 accumulation.	Reactive Oxygen Species	46-49	P53	Homo sapiens	133-136
26756900-10	2016	Pre-treatment with a reactive oxygen species (ROS) scavenger, N-acetylcysteine, attenuated DOX-induced Jnk activation and subsequent p53 accumulation.	Acetylcysteine	62-78	P53	Homo sapiens	133-136
26756900-10	2016	Pre-treatment with a reactive oxygen species (ROS) scavenger, N-acetylcysteine, attenuated DOX-induced Jnk activation and subsequent p53 accumulation.	Doxorubicin	91-94	P53	Homo sapiens	133-136
27779703-6	2016	In addition, resveratrol was observed to arrest cell cycle progression in G1/S phase by increasing the protein expression levels of p53 and p21, and concurrently reducing the protein expression levels of CDK2, cyclin A and cyclin E. Furthermore, resveratrol treatment significantly induced apoptosis in eosinophils, likely through the upregulation of Bim and Bax protein expression levels and the downregulation of Bcl-2 protein expression.	Resveratrol	13-24	P53	Homo sapiens	132-135
26756900-12	2016	These results suggest that COX-2 activates Jnk through modulation of ROS levels, leading to accumulation of p53.	Reactive Oxygen Species	69-72	P53	Homo sapiens	108-111
28105206-0	2016	Curcumin enhances temsirolimus-induced apoptosis in human renal carcinoma cells through upregulation of YAP/p53.	Curcumin	0-8	P53	Homo sapiens	108-111
28105206-5	2016	Co-treatment with temsirolimus and curcumin led to the activation of cleaved poly ADP-ribose polymerase and caspase 3, upregulation of p53 expression and nuclear translocation, and downregulation of B-cell lymphoma 2 protein expression.	Curcumin	35-43	P53	Homo sapiens	135-138
28105222-10	2016	Furthermore, while curcumin induced cell apoptosis and enhanced the expression ratio of Bax/Bcl-2, which are downstream molecules of p53, ectopic expression of H19 inhibited curcumin-induced cell apoptosis.	Curcumin	19-27	P53	Homo sapiens	133-136
28105206-6	2016	Furthermore, curcumin treatment was demonstrated to increase Yes-associated protein (YAP) expression in a time-dependent manner, which was concurrent with the curcumin-induced expression pattern of p53 after 2 h. In addition, knockdown of YAP by small interfering RNA caused the attenuation of curcumin-induced increased p53 expression in RCC cells.	Curcumin	13-21	P53	Homo sapiens	198-201
28105206-6	2016	Furthermore, curcumin treatment was demonstrated to increase Yes-associated protein (YAP) expression in a time-dependent manner, which was concurrent with the curcumin-induced expression pattern of p53 after 2 h. In addition, knockdown of YAP by small interfering RNA caused the attenuation of curcumin-induced increased p53 expression in RCC cells.	Curcumin	13-21	P53	Homo sapiens	321-324
28105206-6	2016	Furthermore, curcumin treatment was demonstrated to increase Yes-associated protein (YAP) expression in a time-dependent manner, which was concurrent with the curcumin-induced expression pattern of p53 after 2 h. In addition, knockdown of YAP by small interfering RNA caused the attenuation of curcumin-induced increased p53 expression in RCC cells.	Curcumin	159-167	P53	Homo sapiens	198-201
28105206-6	2016	Furthermore, curcumin treatment was demonstrated to increase Yes-associated protein (YAP) expression in a time-dependent manner, which was concurrent with the curcumin-induced expression pattern of p53 after 2 h. In addition, knockdown of YAP by small interfering RNA caused the attenuation of curcumin-induced increased p53 expression in RCC cells.	Curcumin	159-167	P53	Homo sapiens	321-324
28105206-6	2016	Furthermore, curcumin treatment was demonstrated to increase Yes-associated protein (YAP) expression in a time-dependent manner, which was concurrent with the curcumin-induced expression pattern of p53 after 2 h. In addition, knockdown of YAP by small interfering RNA caused the attenuation of curcumin-induced increased p53 expression in RCC cells.	Curcumin	159-167	P53	Homo sapiens	198-201
28105206-6	2016	Furthermore, curcumin treatment was demonstrated to increase Yes-associated protein (YAP) expression in a time-dependent manner, which was concurrent with the curcumin-induced expression pattern of p53 after 2 h. In addition, knockdown of YAP by small interfering RNA caused the attenuation of curcumin-induced increased p53 expression in RCC cells.	Curcumin	159-167	P53	Homo sapiens	321-324
28105167-0	2016	Cisplatin induces HepG2 cell cycle arrest through targeting specific long noncoding RNAs and the p53 signaling pathway.	Cisplatin	0-9	P53	Homo sapiens	97-100
28105206-7	2016	In conclusion, the present results indicate that combined curcumin and temsirolimus treatment has a synergistic effect on apoptosis in human RCC cells, through the activation of p53.	Curcumin	58-66	P53	Homo sapiens	178-181
28105167-14	2016	The results suggested that the lncRNAs RP11-134G8.8, RP11-363E7.4 and RP1-193H18.2, and their co-expression genes, which annotated into the p53 signaling pathway, could be potential targets for cisplatin treatment.	Cisplatin	194-203	P53	Homo sapiens	140-143
28105206-8	2016	Mechanistically, YAP is essential in the induction of p53 expression by curcumin.	Curcumin	72-80	P53	Homo sapiens	54-57
28105222-1	2016	Curcumin, a major phytochemical in turmeric, inhibits the proliferation of many types of solid cancer cells by enhancing p53 expression.	Curcumin	0-8	P53	Homo sapiens	121-124
28105222-7	2016	The protein expression of p53, B-cell lymphoma (Bcl)-2, Bcl-2-associated X protein (Bax) and c-Myc in curcumin-treated cells was detected by western blotting.	Curcumin	102-110	P53	Homo sapiens	26-29
27823629-9	2016	However, the O-methyl ester increased p53 acetylation better than javamide-I in monocytic THP-1 cells.	o-methyl ester	13-27	P53	Homo sapiens	38-41
27816507-5	2016	Additionally, depletion of NAD+ causes sensitization of cancer cells to oxidative damage by disruption of the anti-oxidant defense system, decreased cell proliferation, and initiation of cell death through manipulation of cell signaling pathways (e.g., SIRT1 and p53).	NAD	27-31	P53	Homo sapiens	263-266
27823629-10	2016	Since caspase 3/7 activation is often followed by the p53 activation, we investigated their effects on caspase 3/7, and found that O-methyl ester again activated caspase 3/7 greater than javamide-I in the cells, eventually leading to apoptotic cell death.	o-methyl ester	131-145	P53	Homo sapiens	54-57
27879682-8	2016	CONCLUSION: Our study suggested that ziyuglycoside I-triggered MDA-MB-231 cell cycle arrest and apoptosis were probably mediated by p53.	ziyuglycoside	37-50	P53	Homo sapiens	132-135
27835895-0	2016	Enhancement of 5-FU sensitivity by the proapoptotic rpL3 gene in p53 null colon cancer cells through combined polymer nanoparticles.	Fluorouracil	15-19	P53	Homo sapiens	65-68
27775892-1	2016	Scaffold modification based on Wang"s pioneering MDM2-p53 inhibitors led to novel, chemically stable spiro-oxindole compounds bearing a spiro[3H-indole-3,2"-pyrrolidin]-2(1H)-one scaffold that are not prone to epimerization as observed for the initial spiro[3H-indole-3,3"-pyrrolidin]-2(1H)-one scaffold.	spiro[3h-indole-3,3"-pyrrolidin]-2(1h)-one	252-294	P53	Homo sapiens	54-57
31051014-5	2016	We further tested the impact of PPIP5K1 overexpression on an array of apoptosis markers and observed that PPIP5K1 decreased p53 phosphorylation on key residues, including Ser-15, -46, and -392.	Serine	171-174	P53	Homo sapiens	124-127
27863474-2	2016	Recently, we demonstrated increased resistance to 3-BrPA in wt p53 tumor cells compared to those with p53 silencing or mutation.	bromopyruvate	50-56	P53	Homo sapiens	63-66
27646943-7	2016	Results TP53 alterations were present exclusively in cisplatin-resistant tumors and were particularly prevalent among primary mediastinal nonseminomas (72%).	Cisplatin	53-62	P53	Homo sapiens	8-12
27646943-11	2016	Conclusion In GCT, TP53 and MDM2 alterations were associated with cisplatin resistance and inferior outcomes, independent of the IGCCCG model.	Cisplatin	66-75	P53	Homo sapiens	19-23
27769050-7	2016	A series of biochemical experiments using nicotine-treated cells suggested that the dephosphorylation of p53 (Ser-20) and BAX (Ser-184) by PPM1F is a critical posttranslational modification, as observed in breast cancer patients who were heavy smokers.	Nicotine	42-50	P53	Homo sapiens	105-108
27769050-7	2016	A series of biochemical experiments using nicotine-treated cells suggested that the dephosphorylation of p53 (Ser-20) and BAX (Ser-184) by PPM1F is a critical posttranslational modification, as observed in breast cancer patients who were heavy smokers.	Serine	110-113	P53	Homo sapiens	105-108
27863474-9	2016	CONCLUSIONS: This report is the first to show that Prima-1 kills hypoxic wt p53 KRAS-mutant cells resistant to 3-BrPA, partly by decreasing GLUT-1 expression and exacerbating pro-oxidant stress.	bromopyruvate	111-117	P53	Homo sapiens	76-79
27904675-4	2016	Real-time quantitative PCR showed that HOTAIR, p21 and p53 mRNA expressions in doxorubicin (DOX)-treated or gamma-ray-irradiated Tca8113 cells were up-regulated.	Doxorubicin	79-90	P53	Homo sapiens	55-58
27904675-4	2016	Real-time quantitative PCR showed that HOTAIR, p21 and p53 mRNA expressions in doxorubicin (DOX)-treated or gamma-ray-irradiated Tca8113 cells were up-regulated.	Doxorubicin	92-95	P53	Homo sapiens	55-58
27904675-5	2016	Knockdown of p53 expression inhibited DOX-induced HOTAIR up-regulation, suggesting that DNA damage-induced HOTAIR expression may be associated with p53.	Doxorubicin	38-41	P53	Homo sapiens	13-16
27904675-5	2016	Knockdown of p53 expression inhibited DOX-induced HOTAIR up-regulation, suggesting that DNA damage-induced HOTAIR expression may be associated with p53.	Doxorubicin	38-41	P53	Homo sapiens	148-151
27841296-6	2016	The expressions of p53 and Bax genes were markedly elevated in HCT 116 cells after exposure to DOX/DID.	Doxorubicin	95-98	P53	Homo sapiens	19-22
27833134-6	2016	The Gene Set Enrichment Analysis (GSEA) revealed that genes associated with cell adhesion molecules, cell cycle, P53 signaling pathway and JAK/STAT signaling pathway were remarkably enriched in lower-LINC00271 versus higher-LINC00271 tumors.	gsea	34-38	P53	Homo sapiens	113-116
27891503-4	2016	In this study, we have optimized the protocol for Sanger sequencing of TP53 using DNA extracted from archival paraffin-embedded biopsies.	Paraffin	110-118	P53	Homo sapiens	71-75
27122200-2	2016	In this work, p53/BPEI-beta-CD/AD-dox complex was fabricated and employed to investigate the interaction manner between p53 and doxorubicin (Dox).	Doxorubicin	128-139	P53	Homo sapiens	14-17
27832134-0	2016	Comparison of the QuantiGene 2.0 Assay and Real-Time RT-PCR in the Detection of p53 Isoform mRNA Expression in Formalin-Fixed Paraffin-Embedded Tissues- A Preliminary Study.	Paraffin	126-134	P53	Homo sapiens	80-83
27832134-4	2016	However, there are serious limitations when detecting p53 isoforms using this method, particularly for formalin-fixed paraffin-embedded (FFPE) tissues.	Paraffin	118-126	P53	Homo sapiens	54-57
27122200-2	2016	In this work, p53/BPEI-beta-CD/AD-dox complex was fabricated and employed to investigate the interaction manner between p53 and doxorubicin (Dox).	Doxorubicin	128-139	P53	Homo sapiens	120-123
27122200-2	2016	In this work, p53/BPEI-beta-CD/AD-dox complex was fabricated and employed to investigate the interaction manner between p53 and doxorubicin (Dox).	Doxorubicin	141-144	P53	Homo sapiens	14-17
27122200-2	2016	In this work, p53/BPEI-beta-CD/AD-dox complex was fabricated and employed to investigate the interaction manner between p53 and doxorubicin (Dox).	Doxorubicin	141-144	P53	Homo sapiens	120-123
27122200-3	2016	Briefly, branched polyethylenimine (BPEI) was conjugated with beta-cyclodextrin hydrate (beta-CD) to form BPEI-beta-CD backbone, and p53 plasmid was condensed by positively charged BPEI via electrostatic interaction, while Dox was first conjugated with adamantine (AD) and then assembled with BPEI-beta-CD backbone via the host-guest interaction.	Doxorubicin	223-226	P53	Homo sapiens	133-136
27122200-5	2016	Moreover, p53/BPEI-beta-CD/AD-dox complex released Dox and enabled the expression of p53 gene in a sequential manner, and the released Dox and expressed p53 gene showed successive inhibition of the growth of HeLa cells in vitro.	Doxorubicin	30-33	P53	Homo sapiens	10-13
27122200-5	2016	Moreover, p53/BPEI-beta-CD/AD-dox complex released Dox and enabled the expression of p53 gene in a sequential manner, and the released Dox and expressed p53 gene showed successive inhibition of the growth of HeLa cells in vitro.	Doxorubicin	30-33	P53	Homo sapiens	85-88
27122200-5	2016	Moreover, p53/BPEI-beta-CD/AD-dox complex released Dox and enabled the expression of p53 gene in a sequential manner, and the released Dox and expressed p53 gene showed successive inhibition of the growth of HeLa cells in vitro.	Doxorubicin	30-33	P53	Homo sapiens	85-88
27122200-5	2016	Moreover, p53/BPEI-beta-CD/AD-dox complex released Dox and enabled the expression of p53 gene in a sequential manner, and the released Dox and expressed p53 gene showed successive inhibition of the growth of HeLa cells in vitro.	Doxorubicin	51-54	P53	Homo sapiens	10-13
27122200-5	2016	Moreover, p53/BPEI-beta-CD/AD-dox complex released Dox and enabled the expression of p53 gene in a sequential manner, and the released Dox and expressed p53 gene showed successive inhibition of the growth of HeLa cells in vitro.	Doxorubicin	51-54	P53	Homo sapiens	85-88
27122200-5	2016	Moreover, p53/BPEI-beta-CD/AD-dox complex released Dox and enabled the expression of p53 gene in a sequential manner, and the released Dox and expressed p53 gene showed successive inhibition of the growth of HeLa cells in vitro.	Doxorubicin	51-54	P53	Homo sapiens	85-88
27634759-0	2016	Posttranscriptional Upregulation of p53 by Reactive Oxygen Species in Chronic Lymphocytic Leukemia.	Reactive Oxygen Species	43-66	P53	Homo sapiens	36-39
27543608-3	2016	Here, we report a rationally synthesized chalcone-based pyrido[ b ]indole, CPI-7c, as a unique small-molecule inhibitor of MDM2, which not only inhibited MDM2-p53 interaction but also promoted MDM2 degradation.	cpi-7c	75-81	P53	Homo sapiens	159-162
27543608-6	2016	Collectively, we identified CPI-7c as a novel small-molecule inhibitor of MDM2 with a unique two-prong mechanism of action that sensitized TRAIL-resistant cancer cells to apoptosis by modulating the MDM2-p53-DR4/DR5 pathway.	cpi-7c	28-34	P53	Homo sapiens	204-207
27634759-8	2016	p53 induction relied on the increase in intracellular reactive oxygen species observed after CD154 and IL4 stimulation.	Reactive Oxygen Species	54-77	P53	Homo sapiens	0-3
27514406-8	2016	IMPLICATIONS: This study provides a solid rationale for the stratification of lung adenocarcinoma patients according to the functional ERCC1- and mutational TP53 status, where functionally ERCC1-incompetent patients could benefit from sequential cisplatin and etoposide chemotherapy.	Cisplatin	246-255	P53	Homo sapiens	157-161
27666201-0	2016	Mitomycin C and decarbamoyl mitomycin C induce p53-independent p21WAF1/CIP1 activation.	10-decarbamoylmitomycin C	16-39	P53	Homo sapiens	47-50
27666201-5	2016	In addition, DMC can provoke strong p53-independent cell death.	10-decarbamoylmitomycin C	13-16	P53	Homo sapiens	36-39
27666201-6	2016	Our hypothesis is that the stereochemistry of the major unique beta-ICL generated by DMC is responsible for this p53-independent cell death signaling.	10-decarbamoylmitomycin C	85-88	P53	Homo sapiens	113-116
27514406-0	2016	Ercc1 Deficiency Promotes Tumorigenesis and Increases Cisplatin Sensitivity in a Tp53 Context-Specific Manner.	Cisplatin	54-63	P53	Homo sapiens	81-85
26486567-11	2016	CONCLUSION: In this study, p53 expression was found to be predictive of prevalent advanced neoplasia and progression to advanced neoplasia in patients with BE-IND.	be-ind	156-162	P53	Homo sapiens	27-30
27789249-0	2016	Ang-(1-7) inhibited mitochondrial fission in high-glucose-induced podocytes by upregulation of miR-30a and downregulation of Drp1 and p53.	Glucose	50-57	P53	Homo sapiens	134-137
27775703-3	2016	Here, through high-throughput screening we identify statins, cholesterol-lowering drugs, as degradation inducers for conformational or misfolded p53 mutants with minimal effects on wild-type p53 (wtp53) and DNA contact mutants.	Cholesterol	61-72	P53	Homo sapiens	145-148
27748864-2	2016	The antitumor pharmacological effects of BA consist of triggering apoptosis via the mitochondrial pathway, regulating the cell cycle and the angiogenic pathway via factors, including specificity protein transcription factors, cyclin D1 and epidermal growth factor receptor, inhibiting the signal transducer and activator of transcription 3 and nuclear factor-kappaB signaling pathways, preventing the invasion and metastasis of tumor cells, and affecting the expression of topoisomerase I, p53 and lamin B1.	betulinic acid	41-43	P53	Homo sapiens	490-493
27895723-0	2016	Cisplatin-induced regulation of signal transduction pathways and transcription factors in p53-mutated subclone variants of hepatoma cells: Potential application for therapeutic targeting.	Cisplatin	0-9	P53	Homo sapiens	90-93
27626169-0	2016	The putative oncotarget CSN5 controls a transcription-uncorrelated p53-mediated autophagy implicated in cancer cell survival under curcumin treatment.	Curcumin	131-139	P53	Homo sapiens	67-70
28053293-0	2016	Correction: 5-Fluorouracil-induced RNA stress engages a TRAIL-DISC-dependent apoptosis axis facilitated by p53.	Fluorouracil	12-26	P53	Homo sapiens	107-110
30641628-33	2016	05) , the expressions of PPAR-gamma and P53 protein were up-regulated in the FKR combined gefitinib group (P &lt;0.	Gefitinib	90-99	P53	Homo sapiens	40-43
27554639-7	2016	A reduction in TAZ can also enhance the sensitivity of tumor cells to vitamin D by regulating the p53/CYP24A1 pathway.	Vitamin D	70-79	P53	Homo sapiens	98-101
27843742-1	2016	To compare clinical curative effects and toxicity of recombinant human adenovirus-p53 injection (rAd-p53, Gendicine) combining chemoradiotherapy (CRT)/radiotherapy (RT) with those obtained with CRT/RT alone in nasopharyngeal carcinoma (NPC).	gendicine	106-115	P53	Homo sapiens	82-85
27626308-11	2016	Interestingly, GSK2830371 sensitized MCL cells to bortezomib and doxorubicin in p53 wild-type and mutant cells; p38 signaling appeared to be involved in the GSK2830371/bortezomib lethality.	Doxorubicin	65-76	P53	Homo sapiens	80-83
27708247-0	2016	Scriptaid overcomes hypoxia-induced cisplatin resistance in both wild-type and mutant p53 lung cancer cells.	Cisplatin	36-45	P53	Homo sapiens	86-89
27708247-6	2016	Addition of scriptaid also overcomes the cisplatin resistance exhibited in lung cancer cells with stabilized hypoxia inducible factor 1 (HIF1)-alpha (mutant) and mutant p53.	Cisplatin	41-50	P53	Homo sapiens	169-172
27708247-8	2016	Together, our results suggest that the combination of low dose cisplatin and scriptaid is cytotoxic to NSCLC lines, can overcome hypoxia induced resistance and mutant p53- induced instability often associated with this cancer, and has the potential to be an effective therapeutic modality.	Cisplatin	63-72	P53	Homo sapiens	167-170
27626169-2	2016	The COP9 signalosome (CSN) component CSN5, a known specific target for curcumin, can control p53 stability by increasing its degradation through ubiquitin system.	Curcumin	71-79	P53	Homo sapiens	93-96
27626169-3	2016	But the correlation of CSN5-controlled p53 to anticancer therapeutic effect of curcumin is currently unknown.	Curcumin	79-87	P53	Homo sapiens	39-42
27626169-4	2016	Here we showed that CSN5-controlled p53 was transcriptional inactive and responsible for autophagy in human normal BJ cells and cancer HepG2 cells under curcumin treatment.	Curcumin	153-161	P53	Homo sapiens	36-39
27626169-5	2016	Of note, CSN5-initiated cellular autophagy by curcumin treatment was abolished in p53-null HCT116p53-/- cancer cells, which could be rescued by reconstitution with wild-type p53 or transcription inactive p53 mutant p53R273H.	Curcumin	46-54	P53	Homo sapiens	82-85
27626169-5	2016	Of note, CSN5-initiated cellular autophagy by curcumin treatment was abolished in p53-null HCT116p53-/- cancer cells, which could be rescued by reconstitution with wild-type p53 or transcription inactive p53 mutant p53R273H.	Curcumin	46-54	P53	Homo sapiens	97-100
27626169-5	2016	Of note, CSN5-initiated cellular autophagy by curcumin treatment was abolished in p53-null HCT116p53-/- cancer cells, which could be rescued by reconstitution with wild-type p53 or transcription inactive p53 mutant p53R273H.	Curcumin	46-54	P53	Homo sapiens	97-100
27626169-6	2016	Furthermore, CSN5-controlled p53 conferred a pro-survival autophagy in diverse cancer cells response to curcumin.	Curcumin	104-112	P53	Homo sapiens	29-32
27626169-7	2016	Genetic p53 deletion, as well as autophagy pharmacological inhibition by chloroquine, significantly enhanced the therapeutic effect of curcumin on cancer cells in vitro and in vivo, but not normal cells.	Curcumin	135-143	P53	Homo sapiens	8-11
27626169-9	2016	The p53 expression state is a useful biomarker for predicting the anticancer therapeutic effect of curcumin.	Curcumin	99-107	P53	Homo sapiens	4-7
27777210-1	2016	OBJECTIVE: To observe the effect of RITA, a small molecule that targets p53, combined with temozolomide (TMZ) on proliferation, colony formation and apoptosis of human glioblastoma U87 cells and explore the underlying mechanism.	RITA	36-40	P53	Homo sapiens	72-75
27792778-1	2016	We study the dynamic propensity of the backbone hydrogen bonds of the protein MDM2 (the natural regulator of the tumor suppressor p53) in order to determine its binding properties.	Hydrogen	48-56	P53	Homo sapiens	130-133
27792778-2	2016	This approach is fostered by the observation that certain backbone hydrogen bonds at the p53-binding site exhibit a dynamical propensity in simulations that differs markedly form their state-value (that is, formed/not formed) in the PDB structure of the apo protein.	Hydrogen	67-75	P53	Homo sapiens	89-92
27780269-0	2016	Comparative Assessment of Vitamin-B12, Folic Acid and Homocysteine Levels in Relation to p53 Expression in Megaloblastic Anemia.	Folic Acid	39-49	P53	Homo sapiens	89-92
27780269-7	2016	Next, we have measured the p53 expression in the paraffin embedded blocks prepared from bone marrow biopsy, using immunohistochemistry, and the expression levels correlated with VB9 and VB12 levels.	Paraffin	49-57	P53	Homo sapiens	27-30
27777210-8	2016	Both RITA and TMZ, especially the latter, significantly increased the expressions of p53, p21, puma, and other apoptosis-associated genes to accelerate apoptosis and inhibit the growth and colony formation of U87 cells, and the effect was more obvious with a combined treatment.	RITA	5-9	P53	Homo sapiens	85-88
27777210-9	2016	CONCLUSION: RITA inhibits the growth of human glioblastoma cells and enhance their sensitivity to TMZ by up-regulating p53 expression, and when combined, RITA and TMZ show a synergistic effect to cause a stronger cell inhibition.	RITA	12-16	P53	Homo sapiens	119-122
27520484-5	2016	Importantly, in breast cancer specimens from patients with neoadjuvant anthracycline-based or taxane-based chemotherapy, tumor-derived endothelial microvessels, lined by EGFR-amplified or/and TP53+-CD31+ endothelial cells, was significantly higher in patients with progressive or stable disease (PD/SD) than in those with a partial or complete response (PR/CR).	taxane	94-100	P53	Homo sapiens	192-196
27777774-7	2016	RESULTS: B7-H1 expression in human HCT 116 p53+/+ and HCT 116 p53-/- CRC cells lines, while low at baseline, can be induced by treatment with 5-FU.	Fluorouracil	142-146	P53	Homo sapiens	43-46
27777774-7	2016	RESULTS: B7-H1 expression in human HCT 116 p53+/+ and HCT 116 p53-/- CRC cells lines, while low at baseline, can be induced by treatment with 5-FU.	Fluorouracil	142-146	P53	Homo sapiens	62-65
27611952-0	2016	Role of TP53 mutations in triple negative and HER2-positive breast cancer treated with neoadjuvant anthracycline/taxane-based chemotherapy.	Anthracyclines	99-112	P53	Homo sapiens	8-12
27611952-0	2016	Role of TP53 mutations in triple negative and HER2-positive breast cancer treated with neoadjuvant anthracycline/taxane-based chemotherapy.	taxane	113-119	P53	Homo sapiens	8-12
27611952-3	2016	TP53 status was correlated to response to neoadjuvant anthracycline/taxane-based chemotherapy with or without carboplatin and trastuzumab/lapatinib in HER2-positive and bevacizumab in TNBC.	Anthracyclines	54-67	P53	Homo sapiens	0-4
27611952-3	2016	TP53 status was correlated to response to neoadjuvant anthracycline/taxane-based chemotherapy with or without carboplatin and trastuzumab/lapatinib in HER2-positive and bevacizumab in TNBC.	taxane	68-74	P53	Homo sapiens	0-4
27404761-6	2016	The cells treated with 50microM of curcumin, 30.91microM (NEC-1), 20.70microM (NEC-2) and 16.86microM (NEC-3) showed enhanced activation of p53 and elevated bax/Bcl2 expression (NEC-3), increased cytochrome-c in cytosol (NEC-2) confirming the enhanced cytotoxicity.	Curcumin	35-43	P53	Homo sapiens	140-143
27760664-0	2016	[Interferon alpha sensitizes human osteosarcoma cells to doxorubicin-induced apoptosis through p53-dependent pathway].	Doxorubicin	57-68	P53	Homo sapiens	95-98
27568863-6	2016	We observed an increase in p53 levels, which was dependent on ROS production.	ros	62-65	P53	Homo sapiens	27-30
27556514-8	2016	The anti-apoptotic activity of Y-27632 correlated with a reduction in p53 serine 15 phosphorylation and the consequent reduction in the expression of downstream target genes p21 and DAPK1, two genes involved in the induction of cell death.	Serine	74-80	P53	Homo sapiens	70-73
27760664-15	2016	Conclusion: IFNalpha sensitizes human osteosarcoma cells to doxorubicin-induced apoptosis through p53-dependent pathway.	Doxorubicin	60-71	P53	Homo sapiens	98-101
27735941-9	2016	MDM2 inhibitor-induced p53 activation further enhanced YM155 activity.	YM 155	55-60	P53	Homo sapiens	23-26
27582538-8	2016	Applying metabolic inhibitors in the presence and absence of D-glucose and L-glutamine in cell culture experiments resulted in higher glycolytic and mitochondrial activity in TP53 mutant breast cancer cell lines.	Glucose	61-70	P53	Homo sapiens	175-179
27760664-7	2016	Results: IFNalpha treatment for 72 h did not induce cytotoxicity but greatly enhanced doxorubicin-induced cytotoxicity and apoptosis in p53-wild U2OS cells but not p53-mutant MG63 cells.	Doxorubicin	86-97	P53	Homo sapiens	136-139
27760664-10	2016	The expression of p53, Bax, Mdm2 and p21 was up-regulated by doxorubicin and further increased in response to combination.	Doxorubicin	61-72	P53	Homo sapiens	18-21
27529569-0	2016	Hypertonic Saline Primes Activation of the p53-p21 Signaling Axis in Human Small Airway Epithelial Cells That Prevents Inflammation Induced by Pro-inflammatory Cytokines.	Sodium Chloride	11-17	P53	Homo sapiens	43-46
27616194-10	2016	Finally, we found that the extracellular signal-regulated kinase 1/2 (ERK1/2) signal was regulated by p53 whose expression was induced by rapamycin.	Sirolimus	138-147	P53	Homo sapiens	102-105
27616194-11	2016	Overall, this study demonstrates that rapamycin inhibited the proliferation of Huh7 cells by up-regulating the expression of p53 and down-regulating the ERK1/2 signal, indicating that p53 is a useful biomarker for anti-cancer therapy using the specific inhibitor of mTOR signal, rapamycin, against hepatocellular carcinoma cells.	Sirolimus	38-47	P53	Homo sapiens	125-128
27616194-11	2016	Overall, this study demonstrates that rapamycin inhibited the proliferation of Huh7 cells by up-regulating the expression of p53 and down-regulating the ERK1/2 signal, indicating that p53 is a useful biomarker for anti-cancer therapy using the specific inhibitor of mTOR signal, rapamycin, against hepatocellular carcinoma cells.	Sirolimus	38-47	P53	Homo sapiens	184-187
27616194-11	2016	Overall, this study demonstrates that rapamycin inhibited the proliferation of Huh7 cells by up-regulating the expression of p53 and down-regulating the ERK1/2 signal, indicating that p53 is a useful biomarker for anti-cancer therapy using the specific inhibitor of mTOR signal, rapamycin, against hepatocellular carcinoma cells.	Sirolimus	279-288	P53	Homo sapiens	184-187
27620489-0	2016	Heme oxygenase-1-mediated apoptosis under cadmium-induced oxidative stress is regulated by autophagy, which is sensitized by tumor suppressor p53.	Cadmium	42-49	P53	Homo sapiens	142-145
27620489-4	2016	Here we show that the role of HO-1 under Cd-induced oxidative stress is dependent upon autophagy, which is sensitized by the tumor suppressor p53.	Cadmium	41-43	P53	Homo sapiens	142-145
27620489-5	2016	The sensitivity to Cd was 3.5- and 14-fold higher in p53-expressing YD8 and H460 cells than in p53-null YD10B and H1299 cells, respectively.	Cadmium	19-21	P53	Homo sapiens	53-56
27620489-5	2016	The sensitivity to Cd was 3.5- and 14-fold higher in p53-expressing YD8 and H460 cells than in p53-null YD10B and H1299 cells, respectively.	Cadmium	19-21	P53	Homo sapiens	95-98
27620489-6	2016	The levels of p53 in YD8 and H460 cells decreased in a Cd concentration-dependent manner, which was inhibited by pretreatment with N-acetylcysteine.	Cadmium	55-57	P53	Homo sapiens	14-17
27620489-6	2016	The levels of p53 in YD8 and H460 cells decreased in a Cd concentration-dependent manner, which was inhibited by pretreatment with N-acetylcysteine.	Acetylcysteine	131-147	P53	Homo sapiens	14-17
27620489-8	2016	Cd exposure to p53-overexpressing YD10B cells enhanced Cd-induced HO-1 and LC3-II levels, whereas genetic knockdown of p53 in YD8 cells resulted in the suppression of Cd-induced levels of HO-1 and LC3-II, indicating that p53 is required in the sensing of HO-1 and induction of autophagy.	Cadmium	0-2	P53	Homo sapiens	15-18
27774504-1	2016	This article contains raw and processed data related to a research, "Honokiol induces autophagic cell death in malignant glioma through reactive oxygen species-mediated regulation of the p53/PI3K/Akt/mTOR signaling pathway" (C.J.	Reactive Oxygen Species	136-159	P53	Homo sapiens	187-190
27620489-8	2016	Cd exposure to p53-overexpressing YD10B cells enhanced Cd-induced HO-1 and LC3-II levels, whereas genetic knockdown of p53 in YD8 cells resulted in the suppression of Cd-induced levels of HO-1 and LC3-II, indicating that p53 is required in the sensing of HO-1 and induction of autophagy.	Cadmium	55-57	P53	Homo sapiens	15-18
27542250-2	2016	Recently, we have reported that increased mitochondrial fission promotes autophagy and apoptosis resistance in hepatocellular carcinoma (HCC) cell through ROS-mediated coordinated regulation of NF-kappaB and p53 pathways.	ros	155-158	P53	Homo sapiens	208-211
27620489-8	2016	Cd exposure to p53-overexpressing YD10B cells enhanced Cd-induced HO-1 and LC3-II levels, whereas genetic knockdown of p53 in YD8 cells resulted in the suppression of Cd-induced levels of HO-1 and LC3-II, indicating that p53 is required in the sensing of HO-1 and induction of autophagy.	Cadmium	55-57	P53	Homo sapiens	15-18
27633119-7	2016	Finally, we found that pretreatment with NAC prevented the JNK, p53, caspase-9 and -3 protein phosphorylation induced by the polysaccharide, however, pretreatment with SP600125 did not affect the generation of ROS, suggesting that ROS is upstream of JNK.	Acetylcysteine	41-44	P53	Homo sapiens	64-67
27698449-0	2016	Cr(VI) induces premature senescence through ROS-mediated p53 pathway in L-02 hepatocytes.	Reactive Oxygen Species	44-47	P53	Homo sapiens	57-60
27698449-6	2016	By applying antioxidant Trolox, we also confirmed that ROS mediated p53 activation.	Reactive Oxygen Species	55-58	P53	Homo sapiens	68-71
27698449-8	2016	We found p53 could inhibit pro-survival genes B-cell lymphoma-2 (Bcl-2), myeloid leukemia-1 (Mcl-1) and S phase related cell cycle proteins cyclin-dependent kinase 2 (CDK2), Cyclin E to induce premature senescence, and the functional role of ROS in Cr(VI)-induced premature senescence is depend on p53.	Reactive Oxygen Species	242-245	P53	Homo sapiens	9-12
27698449-9	2016	The results suggest that Cr(VI) has a role in premature senescence by promoting ROS-dependent p53 activation in L-02 hepatocytes.	Reactive Oxygen Species	80-83	P53	Homo sapiens	94-97
27431785-8	2016	This study demonstrates that the combination of NCS and PTX can potentiate the effect on survival and apoptosis of glioma cells via suppression of Akt, bcl-2, and activations of p53; Meanwhile, the in vivo studies also confirmed that the combination of NCS and PTX synergistically inhibit the gliom growth.	Paclitaxel	56-59	P53	Homo sapiens	178-181
27520561-5	2016	p53-deficient cancer cells produced reactive oxygen species, which activated fibroblasts to mediate angiogenesis by secreting vascular endothelial growth factor (VEGF) both in vivo and in vitro Activated fibroblasts significantly contributed to tumor progression.	Reactive Oxygen Species	36-59	P53	Homo sapiens	0-3
27567443-7	2016	Zn supplementation (IC50=15muM), increased significantly CDKN2A, pRB1 &amp; p53 and markedly reduced mdm2 expression; also protein expression levels of CDKN2A and pRb1 was significantly increased.	Zinc	0-2	P53	Homo sapiens	76-79
27498709-6	2016	The H2O2-exposed hMSCs showed cellular senescence with significantly increased protein levels of acetyl-p53 and p21 in comparison with the untreated hMSCs, and these effects were prevented by pre-treatment with EGCG.	Hydrogen Peroxide	4-8	P53	Homo sapiens	104-107
28357198-1	2016	Elevated cAMP levels in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) cells attenuate the doxorubicin-induced p53 accumulation and protect cells against apoptosis.	Doxorubicin	100-111	P53	Homo sapiens	120-123
28357198-7	2016	p53 protein expression was reduced in cells treated with combination of cAMP-elevating agents and doxorubicin in contrast to cells treated with doxorubicin alone even in CREB-knocked down cells.	Cyclic AMP	72-76	P53	Homo sapiens	0-3
28357198-7	2016	p53 protein expression was reduced in cells treated with combination of cAMP-elevating agents and doxorubicin in contrast to cells treated with doxorubicin alone even in CREB-knocked down cells.	Doxorubicin	98-109	P53	Homo sapiens	0-3
27419887-0	2016	The preventive effects of hyperoside on lung cancer in vitro by inducing apoptosis and inhibiting proliferation through Caspase-3 and P53 signaling pathway.	hyperoside	26-36	P53	Homo sapiens	134-137
27496712-0	2016	PAK4 Phosphorylates p53 at Serine 215 to Promote Liver Cancer Metastasis.	Serine	27-33	P53	Homo sapiens	20-23
28357198-0	2016	Cyclic AMP-Induced p53 Destabilization is Independent of CREB in Pre-B Acute Lymphoblastic Leukemia Cells.	Cyclic AMP	0-10	P53	Homo sapiens	19-22
28357198-1	2016	Elevated cAMP levels in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) cells attenuate the doxorubicin-induced p53 accumulation and protect cells against apoptosis.	Cyclic AMP	9-13	P53	Homo sapiens	120-123
27302019-4	2016	Specifically, HBx attenuated p53-TBP-RB1 transcription complex recruitment and interaction and this was associated with hyper-phosphorylation of p53 at serine 315 by HBx.	Serine	152-158	P53	Homo sapiens	29-32
27401370-3	2016	Cisplatin, a widely used cytotoxic drug represses PIK3CA promoter activity and attenuates PI3K/AKT cell survival pathway through p53 activation in sensitive cells.	Cisplatin	0-9	P53	Homo sapiens	129-132
27401370-4	2016	However, very little is understood about the overall mechanism of p53-PIK3CA interaction and influence of p53 on the transcriptional status of PIK3CA during cisplatin resistance.	Cisplatin	157-166	P53	Homo sapiens	106-109
26497030-5	2016	Interestingly, an increase in phosphorylation of p53 was paralleled with p-Erk, and PD98059 also blocked the level of p-p53.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	84-91	P53	Homo sapiens	49-52
26497030-5	2016	Interestingly, an increase in phosphorylation of p53 was paralleled with p-Erk, and PD98059 also blocked the level of p-p53.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	84-91	P53	Homo sapiens	120-123
26497030-8	2016	Moreover, PD98059 significantly decreased the levels of p-Erk and p-p53; however, p53 siRNA had little effect on the level of p-Erk.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	10-17	P53	Homo sapiens	68-71
27401370-10	2016	Non-invasive real time imaging using two different luciferase reporters showed that cisplatin could simultaneously induce PIK3CA attenuation and p53 activation with growth regression in sensitive tumours but not in the resistant tumours where only low level of p53 activation and sustained growth was observed.	Cisplatin	84-93	P53	Homo sapiens	261-264
27401370-5	2016	Here we showed that cisplatin could dynamically alter p53 occupancy between the p53 binding sequences present in PIK3CA promoter in ovarian and breast cancer cells.	Cisplatin	20-29	P53	Homo sapiens	54-57
27401370-5	2016	Here we showed that cisplatin could dynamically alter p53 occupancy between the p53 binding sequences present in PIK3CA promoter in ovarian and breast cancer cells.	Cisplatin	20-29	P53	Homo sapiens	80-83
27401370-11	2016	This is the first report on phosphorylation of p53 serine 46 as a modulator of p53-PIK3CA promoter interaction which influences altered binding of p53 at different consensus sequences in the same promoter in response to chemotherapeutic stress.	Serine	51-57	P53	Homo sapiens	47-50
27401370-7	2016	Interestingly, cisplatin resistant cells when challenged with cisplatin demonstrated abolished PIK3CA promoter attenuation, low level of p53 binding, and loss of p53 serine 46 phosphorylation.	Cisplatin	15-24	P53	Homo sapiens	137-140
27401370-11	2016	This is the first report on phosphorylation of p53 serine 46 as a modulator of p53-PIK3CA promoter interaction which influences altered binding of p53 at different consensus sequences in the same promoter in response to chemotherapeutic stress.	Serine	51-57	P53	Homo sapiens	79-82
27302019-4	2016	Specifically, HBx attenuated p53-TBP-RB1 transcription complex recruitment and interaction and this was associated with hyper-phosphorylation of p53 at serine 315 by HBx.	Serine	152-158	P53	Homo sapiens	145-148
27401370-11	2016	This is the first report on phosphorylation of p53 serine 46 as a modulator of p53-PIK3CA promoter interaction which influences altered binding of p53 at different consensus sequences in the same promoter in response to chemotherapeutic stress.	Serine	51-57	P53	Homo sapiens	79-82
27401370-7	2016	Interestingly, cisplatin resistant cells when challenged with cisplatin demonstrated abolished PIK3CA promoter attenuation, low level of p53 binding, and loss of p53 serine 46 phosphorylation.	Cisplatin	15-24	P53	Homo sapiens	162-165
27401370-7	2016	Interestingly, cisplatin resistant cells when challenged with cisplatin demonstrated abolished PIK3CA promoter attenuation, low level of p53 binding, and loss of p53 serine 46 phosphorylation.	Cisplatin	62-71	P53	Homo sapiens	137-140
27401370-7	2016	Interestingly, cisplatin resistant cells when challenged with cisplatin demonstrated abolished PIK3CA promoter attenuation, low level of p53 binding, and loss of p53 serine 46 phosphorylation.	Cisplatin	62-71	P53	Homo sapiens	162-165
27401370-7	2016	Interestingly, cisplatin resistant cells when challenged with cisplatin demonstrated abolished PIK3CA promoter attenuation, low level of p53 binding, and loss of p53 serine 46 phosphorylation.	Serine	166-172	P53	Homo sapiens	162-165
27599894-8	2016	H2O2-induced ROS production increased the levels of phosphorylated-p38 mitogen activated protein kinase, c-Jun N-terminal kinase, ataxia telangiectasia mutated and p53; these increases were inhibited by pretreatment with C. setidens.	Hydrogen Peroxide	0-4	P53	Homo sapiens	164-167
27401370-10	2016	Non-invasive real time imaging using two different luciferase reporters showed that cisplatin could simultaneously induce PIK3CA attenuation and p53 activation with growth regression in sensitive tumours but not in the resistant tumours where only low level of p53 activation and sustained growth was observed.	Cisplatin	84-93	P53	Homo sapiens	145-148
27599894-8	2016	H2O2-induced ROS production increased the levels of phosphorylated-p38 mitogen activated protein kinase, c-Jun N-terminal kinase, ataxia telangiectasia mutated and p53; these increases were inhibited by pretreatment with C. setidens.	Reactive Oxygen Species	13-16	P53	Homo sapiens	164-167
27298278-0	2016	Naphthohydroquinones, naphthoquinones, anthraquinones, and a naphthohydroquinone dimer isolated from the aerial parts of Morinda parvifolia and their cytotoxic effects through up-regulation of p53.	1,4-naphthohydroquinone	0-20	P53	Homo sapiens	193-196
27229883-8	2016	These data provide the first evidence that beta-Ecd protects SH-SY5Y cells against 6-OHDA-induced apoptosis, possibly through mitochondria protection and p53 modulation via ROS-dependent ASK1-p38(MAPK) pathways.	Reactive Oxygen Species	173-176	P53	Homo sapiens	154-157
27499152-1	2016	PURPOSE: p53, widely known as a tumor-suppressing gene, has recently been reported to regulate glucose metabolism in human cancers through the synthesis of cytochrome c oxidase 2 (SCO2), cytochrome c oxidase complex (COX), and TP53-induced glycolysis and apoptosis regulator (TIGAR).	Glucose	95-102	P53	Homo sapiens	9-12
27298278-0	2016	Naphthohydroquinones, naphthoquinones, anthraquinones, and a naphthohydroquinone dimer isolated from the aerial parts of Morinda parvifolia and their cytotoxic effects through up-regulation of p53.	1,4-naphthohydroquinone	61-80	P53	Homo sapiens	193-196
27708748-3	2016	Both patients were resistant to anthracycline therapy, resembling what has been observed for TP53 mutations.	Anthracyclines	32-45	P53	Homo sapiens	93-97
27468716-4	2016	In particular, extensive studies have demonstrated that curcumin targets numerous therapeutically important cancer signaling pathways such as p53, Ras, PI3K, AKT, Wnt-beta catenin, mTOR and so on.	Curcumin	56-64	P53	Homo sapiens	142-145
27689798-12	2016	Collectively, our findings demonstrate, for the first time, that 1800MHz EMR induces apoptosis-related events such as ROS burst and more oxidative DNA damage, which in turn promote p53-dependent caspase-3 activation through release of cytochrome c from mitochondrion.	Reactive Oxygen Species	118-121	P53	Homo sapiens	181-184
32263487-4	2016	The internalized BSeC@MSNs-RGD triggered mitochondrial dysfunction and intracellular ROS overproduction, which subsequently activated the p53 and MAPKs pathways.	ros	85-88	P53	Homo sapiens	138-141
27711766-6	2016	An intimate relationship between p53, ROS production and extent of cell death has also been established using p53 wild, null and mutant type cancer cells.	ros	38-41	P53	Homo sapiens	110-113
27729767-6	2016	In addition, TopBP1 knockdown with specific small interfering RNA in NCI-H1299 cells enhanced the doxorubicin chemosensitivity and decreased the expression of p53 in the presence of doxorubicin.	Doxorubicin	182-193	P53	Homo sapiens	159-162
27564099-9	2016	Moreover, pretreatment with U0126 suppressed curcumin and cisplatin-induced upregulation of p53, p21, and p-STAT3 and downregulation of survival proteins in both cells.	Curcumin	45-53	P53	Homo sapiens	92-95
27564099-9	2016	Moreover, pretreatment with U0126 suppressed curcumin and cisplatin-induced upregulation of p53, p21, and p-STAT3 and downregulation of survival proteins in both cells.	Cisplatin	58-67	P53	Homo sapiens	92-95
27729767-4	2016	We found that p53-deficient lung cancer cells (NCI-H1299) displayed the greatest resistance to doxorubicin compared with NCI-H358, A549, and HCC827 cells with p53 expression.	Doxorubicin	95-106	P53	Homo sapiens	14-17
27564099-7	2016	In addition, when 253J-Bv cells were co-treated with curcumin and cisplatin, p53 and p21 expression levels were markedly increased when compared to controls.	Curcumin	53-61	P53	Homo sapiens	77-80
27564099-7	2016	In addition, when 253J-Bv cells were co-treated with curcumin and cisplatin, p53 and p21 expression levels were markedly increased when compared to controls.	Cisplatin	66-75	P53	Homo sapiens	77-80
27673332-12	2016	CDDP increased the expression of p53 and p21 indicating cell cycle arrest.	Cisplatin	0-4	P53	Homo sapiens	33-36
27664064-0	2016	Multiple cyclin kinase inhibitors promote bile acid-induced apoptosis and autophagy in primary hepatocytes via p53-CD95-dependent signaling.	Bile Acids and Salts	42-51	P53	Homo sapiens	111-114
27729767-7	2016	After doxorubicin administration, co-immunoprecipitation assay showed that TopBP1 promoted the expression of p53 in NCI-H1299 cells.	Doxorubicin	6-17	P53	Homo sapiens	109-112
27428610-7	2016	Based on our data, we propose that regulation of triacylglycerols at the molecular level happens downstream of p53 activation and potentially is a mechanism to prevent lipid oxidation during apoptosis.	Triglycerides	49-65	P53	Homo sapiens	111-114
27479485-4	2016	The modified DNA efficiently cross-linked with p53 protein through alkylation of cysteine and showed potential for cross-linking with histidine (in C277H mutant of p53).	Cysteine	81-89	P53	Homo sapiens	47-50
27479485-4	2016	The modified DNA efficiently cross-linked with p53 protein through alkylation of cysteine and showed potential for cross-linking with histidine (in C277H mutant of p53).	Histidine	134-143	P53	Homo sapiens	47-50
27479485-4	2016	The modified DNA efficiently cross-linked with p53 protein through alkylation of cysteine and showed potential for cross-linking with histidine (in C277H mutant of p53).	Histidine	134-143	P53	Homo sapiens	164-167
27688818-2	2016	Lysine residues of non-histone proteins including proliferating cell nuclear antigen (PCNA) and p53 are also monomethylated.	Lysine	0-6	P53	Homo sapiens	96-99
27517620-7	2016	Inhibition of glucosylceramide synthase with d-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) sensitized p53-R273H cancer cells and tumor xenografts to doxorubicin treatments.	Doxorubicin	167-178	P53	Homo sapiens	120-123
27639846-9	2016	In a doxorubicin (Dox)-induced DNA damage assay we show that eEF1Bgamma depletion significantly decreases p53 protein accumulation and slightly impacts on Che-1 accumulation.	Doxorubicin	18-21	P53	Homo sapiens	106-109
27695348-8	2016	Mechanistic studies revealed that HOTAIR modified the promoter of p53 and enhanced histone H3 lysine 27 trimethylation (H3K27me3).	Lysine	94-100	P53	Homo sapiens	66-69
27538679-0	2016	Apple Polyphenol Phloretin Inhibits Colorectal Cancer Cell Growth via Inhibition of the Type 2 Glucose Transporter and Activation of p53-Mediated Signaling.	polyphenol phloretin	6-26	P53	Homo sapiens	133-136
27517620-9	2016	This study demonstrated that p53-R273H promotes EMT and induced pluripotency of CSCs in cancer cells exposed to doxorubicin, mainly through Zeb1 and beta-catenin transcription factors.	Doxorubicin	112-123	P53	Homo sapiens	29-32
27422604-0	2016	miR-214 promotes apoptosis and sensitizes breast cancer cells to doxorubicin by targeting the RFWD2-p53 cascade.	Doxorubicin	65-76	P53	Homo sapiens	100-103
27609465-6	2016	Interestingly, enzyme immunoassays, TOPFlash/FOPFlash reporter activity assays and western blotting analysis demonstrated oxaliplatin-mediated downregulation of PGE2 and Wnt/beta-catenin signaling in a manner dependent on p53.	Dinoprostone	161-165	P53	Homo sapiens	222-225
27470586-1	2016	We previously showed that protein kinase CK2 downregulation mediates senescence through the reactive oxygen species (ROS)-p53-p21(Cip1/WAF1) pathway in various human cells.	Reactive Oxygen Species	92-115	P53	Homo sapiens	122-125
27470586-1	2016	We previously showed that protein kinase CK2 downregulation mediates senescence through the reactive oxygen species (ROS)-p53-p21(Cip1/WAF1) pathway in various human cells.	Reactive Oxygen Species	117-120	P53	Homo sapiens	122-125
27600721-0	2016	Aggregation tendencies in the p53 family are modulated by backbone hydrogen bonds.	Hydrogen	67-75	P53	Homo sapiens	30-33
26876197-5	2016	The analogous cisplatin-resistant 2780CP/Cl-24 cells, which express loss of p53 heterozygosity, retained the p53(V172F) mutation and high p53-MDM4 binding, but demonstrated lower p53-bound MDM2 that was associated with reduced p53 ubiquitination and enhanced p53 stability.	Cisplatin	14-23	P53	Homo sapiens	109-112
26876197-5	2016	The analogous cisplatin-resistant 2780CP/Cl-24 cells, which express loss of p53 heterozygosity, retained the p53(V172F) mutation and high p53-MDM4 binding, but demonstrated lower p53-bound MDM2 that was associated with reduced p53 ubiquitination and enhanced p53 stability.	Cisplatin	14-23	P53	Homo sapiens	109-112
26876197-5	2016	The analogous cisplatin-resistant 2780CP/Cl-24 cells, which express loss of p53 heterozygosity, retained the p53(V172F) mutation and high p53-MDM4 binding, but demonstrated lower p53-bound MDM2 that was associated with reduced p53 ubiquitination and enhanced p53 stability.	Cisplatin	14-23	P53	Homo sapiens	109-112
26876197-7	2016	However, downregulation of MDM2 or MDM4 by small interfering RNA in either resistant cell line induced p53 and restored p21 transactivation at 37  C, as did cisplatin-induced DNA damage at 32.5  C that coincided with reduced p53-MDM4 binding and cisplatin resistance.	Cisplatin	157-166	P53	Homo sapiens	225-228
26876197-8	2016	These results demonstrate that cisplatin-mediated p53(V172F) mutation regulates p53 stability at the normothermic temperature, but it is the increased recruitment of MDM4 by the homomeric or heteromeric mutant p53(V172F) complex that inhibits p53-dependent transactivation.	Cisplatin	31-40	P53	Homo sapiens	50-55
26876197-8	2016	These results demonstrate that cisplatin-mediated p53(V172F) mutation regulates p53 stability at the normothermic temperature, but it is the increased recruitment of MDM4 by the homomeric or heteromeric mutant p53(V172F) complex that inhibits p53-dependent transactivation.	Cisplatin	31-40	P53	Homo sapiens	50-53
26876197-8	2016	These results demonstrate that cisplatin-mediated p53(V172F) mutation regulates p53 stability at the normothermic temperature, but it is the increased recruitment of MDM4 by the homomeric or heteromeric mutant p53(V172F) complex that inhibits p53-dependent transactivation.	Cisplatin	31-40	P53	Homo sapiens	80-83
26876197-8	2016	These results demonstrate that cisplatin-mediated p53(V172F) mutation regulates p53 stability at the normothermic temperature, but it is the increased recruitment of MDM4 by the homomeric or heteromeric mutant p53(V172F) complex that inhibits p53-dependent transactivation.	Cisplatin	31-40	P53	Homo sapiens	80-83
26876197-9	2016	This represents a novel cellular mechanism of p53 inhibition, and, thereby, induction of cisplatin resistance.	Cisplatin	89-98	P53	Homo sapiens	46-49
26876197-0	2016	Heterozygous p53(V172F) mutation in cisplatin-resistant human tumor cells promotes MDM4 recruitment and decreases stability and transactivity of p53.	Cisplatin	36-45	P53	Homo sapiens	13-18
26876197-0	2016	Heterozygous p53(V172F) mutation in cisplatin-resistant human tumor cells promotes MDM4 recruitment and decreases stability and transactivity of p53.	Cisplatin	36-45	P53	Homo sapiens	13-16
26876197-3	2016	In the present study, cisplatin-resistant 2780CP/Cl-16 ovarian tumor cells expressed a heterozygous, temperature-sensitive p53(V172F) mutation, which reduced p53 half-life by two- to threefold compared with homozygous wild-type (wt) p53 in parental A2780 cells.	Cisplatin	22-31	P53	Homo sapiens	123-128
26876197-3	2016	In the present study, cisplatin-resistant 2780CP/Cl-16 ovarian tumor cells expressed a heterozygous, temperature-sensitive p53(V172F) mutation, which reduced p53 half-life by two- to threefold compared with homozygous wild-type (wt) p53 in parental A2780 cells.	Cisplatin	22-31	P53	Homo sapiens	123-126
26876197-3	2016	In the present study, cisplatin-resistant 2780CP/Cl-16 ovarian tumor cells expressed a heterozygous, temperature-sensitive p53(V172F) mutation, which reduced p53 half-life by two- to threefold compared with homozygous wild-type (wt) p53 in parental A2780 cells.	Cisplatin	22-31	P53	Homo sapiens	158-161
26876197-5	2016	The analogous cisplatin-resistant 2780CP/Cl-24 cells, which express loss of p53 heterozygosity, retained the p53(V172F) mutation and high p53-MDM4 binding, but demonstrated lower p53-bound MDM2 that was associated with reduced p53 ubiquitination and enhanced p53 stability.	Cisplatin	14-23	P53	Homo sapiens	76-79
26876197-5	2016	The analogous cisplatin-resistant 2780CP/Cl-24 cells, which express loss of p53 heterozygosity, retained the p53(V172F) mutation and high p53-MDM4 binding, but demonstrated lower p53-bound MDM2 that was associated with reduced p53 ubiquitination and enhanced p53 stability.	Cisplatin	14-23	P53	Homo sapiens	109-114
26876197-5	2016	The analogous cisplatin-resistant 2780CP/Cl-24 cells, which express loss of p53 heterozygosity, retained the p53(V172F) mutation and high p53-MDM4 binding, but demonstrated lower p53-bound MDM2 that was associated with reduced p53 ubiquitination and enhanced p53 stability.	Cisplatin	14-23	P53	Homo sapiens	109-112
27600721-6	2016	Molecular Dynamics (MD) simulations indicated specific regions of structural heterogeneity unique to p53, which may be promoted by elevated incidence of exposed backbone hydrogen bonds (BHBs).	Hydrogen	170-178	P53	Homo sapiens	101-104
27601274-4	2016	Histidine-tag pull-down assay using purified p53(1-393)-His and G-actin confirms direct physical association between p53 and monomeric G-actin.	Histidine	0-9	P53	Homo sapiens	45-48
27339904-6	2016	In addition, we investigated an increased level of intracellular ROS (reactive oxygen species), which was preceded by p53 activation.	Reactive Oxygen Species	65-68	P53	Homo sapiens	118-121
27601274-4	2016	Histidine-tag pull-down assay using purified p53(1-393)-His and G-actin confirms direct physical association between p53 and monomeric G-actin.	Histidine	0-9	P53	Homo sapiens	117-120
27339904-6	2016	In addition, we investigated an increased level of intracellular ROS (reactive oxygen species), which was preceded by p53 activation.	Reactive Oxygen Species	70-93	P53	Homo sapiens	118-121
27601274-4	2016	Histidine-tag pull-down assay using purified p53(1-393)-His and G-actin confirms direct physical association between p53 and monomeric G-actin.	Histidine	0-3	P53	Homo sapiens	45-48
27601274-4	2016	Histidine-tag pull-down assay using purified p53(1-393)-His and G-actin confirms direct physical association between p53 and monomeric G-actin.	Histidine	0-3	P53	Homo sapiens	117-120
27341700-8	2016	This concentration did not seem to cause inhibition of DNA DSB repair but induced a significant G2/M arrest, which was particularly emphasized in p53-null H1299 cells treated with NU7441 and carbon ions.	Carbon	191-197	P53	Homo sapiens	146-149
27599722-0	2016	Reactivation of mutant p53 by capsaicin, the major constituent of peppers.	Capsaicin	30-39	P53	Homo sapiens	23-26
27599722-6	2016	Capsaicin (CPS) is the major constituent of peppers and show antitumor activity by targeting several molecular pathway, however, its effect on mutant p53 reactivation has not been assessed yet.	Capsaicin	0-9	P53	Homo sapiens	150-153
27599722-7	2016	In this study we aimed at investigating whether mutant p53 could be a new target of capsaicin-induced cell death and the underlying mechanisms.	Capsaicin	84-93	P53	Homo sapiens	55-58
27599722-8	2016	METHODS: p53 levels were analysed by western blot upon capsaicin treatment in the presence of the autophagy inhibitor chloroquine.	Capsaicin	55-64	P53	Homo sapiens	9-12
27599722-11	2016	RESULTS: Here, we show that capsaicin induced autophagy that was, at least in part, responsible of mutant p53 protein degradation.	Capsaicin	28-37	P53	Homo sapiens	106-109
27599722-12	2016	Abrogation of mutant p53 by capsaicin restored wild-type p53 activities over mutant p53 functions, contributing to cancer cell death.	Capsaicin	28-37	P53	Homo sapiens	21-24
27599722-12	2016	Abrogation of mutant p53 by capsaicin restored wild-type p53 activities over mutant p53 functions, contributing to cancer cell death.	Capsaicin	28-37	P53	Homo sapiens	57-60
27599722-12	2016	Abrogation of mutant p53 by capsaicin restored wild-type p53 activities over mutant p53 functions, contributing to cancer cell death.	Capsaicin	28-37	P53	Homo sapiens	57-60
27599722-14	2016	CONCLUSION: These findings demonstrate for the first time that capsaicin may reduce mutant p53 levels and reactivate wild-type p53 protein in mutant p53-carrying cells and the p53 reactivation contributes to capsaicin-induced cell death.	Capsaicin	63-72	P53	Homo sapiens	91-94
27599722-14	2016	CONCLUSION: These findings demonstrate for the first time that capsaicin may reduce mutant p53 levels and reactivate wild-type p53 protein in mutant p53-carrying cells and the p53 reactivation contributes to capsaicin-induced cell death.	Capsaicin	63-72	P53	Homo sapiens	127-130
27599722-14	2016	CONCLUSION: These findings demonstrate for the first time that capsaicin may reduce mutant p53 levels and reactivate wild-type p53 protein in mutant p53-carrying cells and the p53 reactivation contributes to capsaicin-induced cell death.	Capsaicin	63-72	P53	Homo sapiens	127-130
27599722-14	2016	CONCLUSION: These findings demonstrate for the first time that capsaicin may reduce mutant p53 levels and reactivate wild-type p53 protein in mutant p53-carrying cells and the p53 reactivation contributes to capsaicin-induced cell death.	Capsaicin	63-72	P53	Homo sapiens	127-130
27477115-8	2016	Moreover, the expression of BCL-2, CYP17A1, CYP19A1, SOD1, and GPX4 were up-regulated by 0.01ng/mL melatonin or combined with IIK7, but decreased for the mRNA levels of BAX, P53, and CASPASE-3, as compared with control or groups treated with Luzindole or 4P-PDOT in the presence of melatonin.	Melatonin	99-108	P53	Homo sapiens	174-177
27422117-4	2016	Further, p53 strongly favors G-quadruplexes folded in potassium over those formed in sodium, thus indicating the telomeric G-quadruplex conformational selectivity of p53.	Sodium	85-91	P53	Homo sapiens	9-12
27422117-4	2016	Further, p53 strongly favors G-quadruplexes folded in potassium over those formed in sodium, thus indicating the telomeric G-quadruplex conformational selectivity of p53.	Sodium	85-91	P53	Homo sapiens	166-169
27418282-3	2016	By quantifying the number of hydrate water molecules, we provide a microscopic description for the interactions of water with a wild-type p53 TAD and two p53 TAD peptides.	Water	37-42	P53	Homo sapiens	138-141
27418282-3	2016	By quantifying the number of hydrate water molecules, we provide a microscopic description for the interactions of water with a wild-type p53 TAD and two p53 TAD peptides.	Water	37-42	P53	Homo sapiens	154-157
27418282-3	2016	By quantifying the number of hydrate water molecules, we provide a microscopic description for the interactions of water with a wild-type p53 TAD and two p53 TAD peptides.	Water	115-120	P53	Homo sapiens	138-141
27418282-3	2016	By quantifying the number of hydrate water molecules, we provide a microscopic description for the interactions of water with a wild-type p53 TAD and two p53 TAD peptides.	Water	115-120	P53	Homo sapiens	154-157
27419353-5	2016	Together, the Hippo and p53 signaling pathways cooperate on multiple levels to fine-tune SREPB activity and regulate cholesterol/lipid levels.	Cholesterol	117-128	P53	Homo sapiens	24-27
27551077-5	2016	PK11007 stabilized p53 in vitro via selective alkylation of two surface-exposed cysteines without compromising its DNA binding activity.	Cysteine	80-89	P53	Homo sapiens	19-22
27208501-4	2016	The TIS21-mediated switch of senescence to apoptosis was accompanied by nuclear translocation of p53 protein and its modifications on Ser-15 and Ser-46 phosphorylation and acetylations on Lys-120, -320, -373 and -382 residues.	Serine	134-137	P53	Homo sapiens	97-100
25268149-9	2016	The level of the tumor suppressor protein p53 in HeLa cells increased significantly upon treatment with free epirubicin, but remained relatively unchanged when cells were treated with equivalent dose of nanoparticle-loaded drug, suggesting a possible shift from p53-dependent DNA/RNA intercalation-based induction of cytotoxicity by free epirubicin to a caspase 3-induced cell death by the epirubicin-loaded PBCA formulation.	Epirubicin	109-119	P53	Homo sapiens	42-45
25268149-9	2016	The level of the tumor suppressor protein p53 in HeLa cells increased significantly upon treatment with free epirubicin, but remained relatively unchanged when cells were treated with equivalent dose of nanoparticle-loaded drug, suggesting a possible shift from p53-dependent DNA/RNA intercalation-based induction of cytotoxicity by free epirubicin to a caspase 3-induced cell death by the epirubicin-loaded PBCA formulation.	Epirubicin	338-348	P53	Homo sapiens	42-45
25268149-9	2016	The level of the tumor suppressor protein p53 in HeLa cells increased significantly upon treatment with free epirubicin, but remained relatively unchanged when cells were treated with equivalent dose of nanoparticle-loaded drug, suggesting a possible shift from p53-dependent DNA/RNA intercalation-based induction of cytotoxicity by free epirubicin to a caspase 3-induced cell death by the epirubicin-loaded PBCA formulation.	Epirubicin	338-348	P53	Homo sapiens	42-45
28139534-1	2016	BACKGROUND &amp; OBJECTIVES: The Arg&gt;Pro polymorphism in codon 72 of p53 gene is known to affect the susceptibility of cervical cancer differently in different population worldwide although information regarding its role in determining survival status and disease outcome in patients is lacking.	Adenosine Monophosphate	12-15	P53	Homo sapiens	72-75
27414741-0	2016	ROS-mediated apoptosis of HAPI microglia through p53 signaling following PFOS exposure.	ros	0-3	P53	Homo sapiens	49-52
27414741-6	2016	Interestingly, NAC, a ROS inhibitor, inhibited p53 expression, and decreased the apoptosis of HAPI microglia.	ros	22-25	P53	Homo sapiens	47-50
27414741-7	2016	Taken together, these findings suggest that upregulated production of ROS plays a vital role in PFOS-mediated apoptosis in HAPI microglia via the modulation of p53 signaling.	ros	70-73	P53	Homo sapiens	160-163
28139534-1	2016	BACKGROUND &amp; OBJECTIVES: The Arg&gt;Pro polymorphism in codon 72 of p53 gene is known to affect the susceptibility of cervical cancer differently in different population worldwide although information regarding its role in determining survival status and disease outcome in patients is lacking.	Arginine	33-36	P53	Homo sapiens	72-75
28139534-2	2016	The present study was conducted to determine the genotype frequency and prognostic role of p53 codon 72 Arg&gt;Pro polymorphism in patients with advanced stage cervical cancer in India.	Arginine	104-107	P53	Homo sapiens	91-94
27385486-5	2016	Herein, we report that GOF mutant R175H and R273H p53 proteins trigger PKM2 phosphorylation on Tyr 105 through the involvement of mTOR signaling.	Tyrosine	95-98	P53	Homo sapiens	50-53
27485825-9	2016	Further analysis indicated that co-expression of VHL and P53 inhibited cell proliferation by completely inhibiting the cell cycle at the G0/G1 phase, and promoted apoptosis following treatment with ADM or sunitinib.	Doxorubicin	198-201	P53	Homo sapiens	57-60
27484725-11	2016	This suggested that the enhanced cisplatin chemosensitivity with Ad-ING4-P53 gene therapy in hypopharyngeal cancer xenografts may be associated with apoptosis induction through upregulation of Bax expression and downregulation of Bcl-2.	Cisplatin	33-42	P53	Homo sapiens	73-76
27484725-0	2016	Co-expression of ING4 and P53 enhances hypopharyngeal cancer chemosensitivity to cisplatin in vivo.	Cisplatin	81-90	P53	Homo sapiens	26-29
27484725-3	2016	The current study investigated the effects of co-expression of inhibitor of growth protein 4 (ING4) and P53, a tumor suppressor gene, on chemosensitivity to cisplatin in human hypopharyngeal cancer xenografts in vivo, and the potential molecular mechanisms involved.	Cisplatin	157-166	P53	Homo sapiens	104-107
27621580-0	2016	Synergistic anticancer effect of exogenous wild-type p53 gene combined with 5-FU in human colon cancer resistant to 5-FU in vivo.	Fluorouracil	116-120	P53	Homo sapiens	53-56
27484725-10	2016	The results of immunohistochemistry analysis demonstrated that Bax expression was increased and Bcl-2 was decreased in the Ad-ING4-P53 + cisplatin group.	Cisplatin	137-146	P53	Homo sapiens	131-134
27602127-13	2016	In conclusion, PHB is an adriamycin resistance-associated gene, which may inhibit the proliferation of human osteosarcoma MG-63 cells by interacting with the oncogenes or tumor suppressor genes, c-myc, c-fos, p53 and Rb.	Doxorubicin	25-35	P53	Homo sapiens	209-212
27030122-4	2016	Human endothelial cells, with increased extracellular ATP concentration in cell proximity, were more resistant to irradiation or chemically induced DNA damage evaluated with the DNA damage markers gammaH2AX and phosphorylated p53.	Adenosine Triphosphate	54-57	P53	Homo sapiens	226-229
27494891-6	2016	Mechanistic studies suggested that treatment of cells with PHPO or with PHPO + cisplatin differentially inhibited the PI3K/Akt, MAPK and ATM/Chk2 pathways, which consequently suppressed the anti-apoptotic factors Bcl-xL, Bcl-2 and XIAP, but activated the pro-apoptotic factors Bad, Bax, p53, caspase 9, caspase 8, caspase 7 and PARP.	phpo	59-63	P53	Homo sapiens	287-290
27494891-6	2016	Mechanistic studies suggested that treatment of cells with PHPO or with PHPO + cisplatin differentially inhibited the PI3K/Akt, MAPK and ATM/Chk2 pathways, which consequently suppressed the anti-apoptotic factors Bcl-xL, Bcl-2 and XIAP, but activated the pro-apoptotic factors Bad, Bax, p53, caspase 9, caspase 8, caspase 7 and PARP.	phpo	72-76	P53	Homo sapiens	287-290
27494891-6	2016	Mechanistic studies suggested that treatment of cells with PHPO or with PHPO + cisplatin differentially inhibited the PI3K/Akt, MAPK and ATM/Chk2 pathways, which consequently suppressed the anti-apoptotic factors Bcl-xL, Bcl-2 and XIAP, but activated the pro-apoptotic factors Bad, Bax, p53, caspase 9, caspase 8, caspase 7 and PARP.	Cisplatin	79-88	P53	Homo sapiens	287-290
27621580-8	2016	In the rAd/p53 + 5-FU group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups (P &lt; 0.05), and the expression of PKC was lower than that of the control, 5-FU and rAd/p53 groups at more than 48 h (P &lt; 0.05).	Fluorouracil	17-21	P53	Homo sapiens	11-14
27621580-8	2016	In the rAd/p53 + 5-FU group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups (P &lt; 0.05), and the expression of PKC was lower than that of the control, 5-FU and rAd/p53 groups at more than 48 h (P &lt; 0.05).	Fluorouracil	17-21	P53	Homo sapiens	197-200
27621580-8	2016	In the rAd/p53 + 5-FU group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups (P &lt; 0.05), and the expression of PKC was lower than that of the control, 5-FU and rAd/p53 groups at more than 48 h (P &lt; 0.05).	Fluorouracil	95-99	P53	Homo sapiens	11-14
27621580-8	2016	In the rAd/p53 + 5-FU group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups (P &lt; 0.05), and the expression of PKC was lower than that of the control, 5-FU and rAd/p53 groups at more than 48 h (P &lt; 0.05).	Fluorouracil	95-99	P53	Homo sapiens	11-14
27621580-9	2016	In the rAd/p53 group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups at more than 48 h (P &lt; 0.05), and the expression of PKC was lower than that of the control and 5-FU groups at more than 120 h (P &lt; 0.05).	Fluorouracil	88-92	P53	Homo sapiens	11-14
27621580-1	2016	AIM: To investigate the anticancer effect of a recombinant adenovirus-mediated p53 (rAd-p53) combined with 5-fluorouracil (5-FU) in human colon cancer resistant to 5-FU in vivo and the mechanism of rAd-p53 in reversal of 5-FU resistance.	Fluorouracil	164-168	P53	Homo sapiens	79-82
27621580-9	2016	In the rAd/p53 group, the expression of P-gp and MRP1 was lower that of the control and 5-FU groups at more than 48 h (P &lt; 0.05), and the expression of PKC was lower than that of the control and 5-FU groups at more than 120 h (P &lt; 0.05).	Fluorouracil	198-202	P53	Homo sapiens	11-14
27621580-1	2016	AIM: To investigate the anticancer effect of a recombinant adenovirus-mediated p53 (rAd-p53) combined with 5-fluorouracil (5-FU) in human colon cancer resistant to 5-FU in vivo and the mechanism of rAd-p53 in reversal of 5-FU resistance.	Fluorouracil	164-168	P53	Homo sapiens	88-91
27621580-10	2016	CONCLUSION: 5-FU combined with rAd-p53 has a synergistic anticancer effect in SW480/5-FU (5-FU resistance), which contributes to reversal of 5-FU resistance.	Fluorouracil	84-88	P53	Homo sapiens	35-38
27621580-1	2016	AIM: To investigate the anticancer effect of a recombinant adenovirus-mediated p53 (rAd-p53) combined with 5-fluorouracil (5-FU) in human colon cancer resistant to 5-FU in vivo and the mechanism of rAd-p53 in reversal of 5-FU resistance.	Fluorouracil	164-168	P53	Homo sapiens	88-91
27621580-10	2016	CONCLUSION: 5-FU combined with rAd-p53 has a synergistic anticancer effect in SW480/5-FU (5-FU resistance), which contributes to reversal of 5-FU resistance.	Fluorouracil	84-88	P53	Homo sapiens	35-38
27621580-1	2016	AIM: To investigate the anticancer effect of a recombinant adenovirus-mediated p53 (rAd-p53) combined with 5-fluorouracil (5-FU) in human colon cancer resistant to 5-FU in vivo and the mechanism of rAd-p53 in reversal of 5-FU resistance.	Fluorouracil	164-168	P53	Homo sapiens	79-82
27621580-10	2016	CONCLUSION: 5-FU combined with rAd-p53 has a synergistic anticancer effect in SW480/5-FU (5-FU resistance), which contributes to reversal of 5-FU resistance.	Fluorouracil	84-88	P53	Homo sapiens	35-38
27621580-1	2016	AIM: To investigate the anticancer effect of a recombinant adenovirus-mediated p53 (rAd-p53) combined with 5-fluorouracil (5-FU) in human colon cancer resistant to 5-FU in vivo and the mechanism of rAd-p53 in reversal of 5-FU resistance.	Fluorouracil	164-168	P53	Homo sapiens	88-91
27621580-1	2016	AIM: To investigate the anticancer effect of a recombinant adenovirus-mediated p53 (rAd-p53) combined with 5-fluorouracil (5-FU) in human colon cancer resistant to 5-FU in vivo and the mechanism of rAd-p53 in reversal of 5-FU resistance.	Fluorouracil	164-168	P53	Homo sapiens	88-91
27621580-6	2016	The p53 expression was higher in the rAd/p53 and the rAd/p53 + 5-FU groups than that of the control and 5-FU groups (P &lt; 0.05), and were higher in the rAd/p53 + 5-FU group than that of the rAd/p53 group (P &lt; 0.05).	Fluorouracil	63-67	P53	Homo sapiens	4-7
27621580-6	2016	The p53 expression was higher in the rAd/p53 and the rAd/p53 + 5-FU groups than that of the control and 5-FU groups (P &lt; 0.05), and were higher in the rAd/p53 + 5-FU group than that of the rAd/p53 group (P &lt; 0.05).	Fluorouracil	104-108	P53	Homo sapiens	4-7
27621580-6	2016	The p53 expression was higher in the rAd/p53 and the rAd/p53 + 5-FU groups than that of the control and 5-FU groups (P &lt; 0.05), and were higher in the rAd/p53 + 5-FU group than that of the rAd/p53 group (P &lt; 0.05).	Fluorouracil	104-108	P53	Homo sapiens	4-7
27477846-7	2016	This concentration gradually decreased, and H2was almost undetectable in medium after 12 h. At 24 h after TCDD exposure, HUVECs treated with TCDD exhibited increased 8OHdG and acetyl-p53 expression, decreased nicotinamide adenine dinucleotide (NAD(+))/NADH ratio, impaired Sirt1 activity, and enhanced senescence-associated beta-galactosidase.	Polychlorinated Dibenzodioxins	141-145	P53	Homo sapiens	183-186
27235580-4	2016	Moreover, we found that 17beta-estradiol treatment protects neurons from the Abeta-peptide induced neurotoxicity by increasing miR-125b expression that, in turn, decreased the expression, both at gene and protein levels, of the pro-apoptopic proteins Bak1 and p53.	Estradiol	24-40	P53	Homo sapiens	260-263
27576884-11	2016	However, only p53 overexpression was associated with predicting CSS independently of tumor stage.&amp;nbsp.	Adenosine Monophosphate	98-101	P53	Homo sapiens	14-17
27486986-6	2016	Here, we demonstrate for the first time that TAp73beta, a p53-family protein, is implicated in Cisplatin-induced apoptosis of Bone Sarcomas".	Cisplatin	95-104	P53	Homo sapiens	58-61
27545131-13	2016	(7) The expression of P53 was significantly higher in GSNO group than in the blank control group (P&lt; 0.05), which could be significantly down regulated by pretreatment with high, medium and low concentration ICA in a concentration-dependent manner, above effects could be blocked by LY294002(all P&lt;0.05).	S-Nitrosoglutathione	54-58	P53	Homo sapiens	22-25
27556439-7	2016	Curcumin pre-treatment consistently and markedly down-regulated the mRNA expression levels of p53, Bax, caspase-9 and -3 and up-regulated the mRNA expression level of Bcl-2.	Curcumin	0-8	P53	Homo sapiens	94-97
27535933-0	2016	Lysine methylation represses p53 activity in teratocarcinoma cancer cells.	Lysine	0-6	P53	Homo sapiens	29-32
27535933-3	2016	Here we report that in the teratocarcinoma cell line NTera2, p53 is subject to lysine methylation at its carboxyl terminus, which has been shown to repress p53"s transcriptional activity.	Lysine	79-85	P53	Homo sapiens	61-64
27535933-3	2016	Here we report that in the teratocarcinoma cell line NTera2, p53 is subject to lysine methylation at its carboxyl terminus, which has been shown to repress p53"s transcriptional activity.	Lysine	79-85	P53	Homo sapiens	156-159
27535933-6	2016	Our results provide evidence that lysine methylation of endogenous wild-type p53 represses its activity in cancer cells and suggest new therapeutic possibilities of targeting testicular teratocarcinoma.	Lysine	34-40	P53	Homo sapiens	77-80
27545325-3	2016	Intriguingly, the expression of ISG15, UBE1L and UBCH8 is induced by DNA-damaging agents, such as ultraviolet and doxorubicin, which are known to induce p53.	Doxorubicin	114-125	P53	Homo sapiens	153-156
27496966-0	2016	Nimbolide sensitizes human colon cancer cells to TRAIL through reactive oxygen species- and ERK-dependent up-regulation of death receptors, p53, and Bax.	nimbolide	0-9	P53	Homo sapiens	140-143
27267810-9	2016	Taken together, the optimized carbazole scaffold provides a promising starting point for the development of high-affinity ligands to reactivate the tumor suppressor function of the p53 mutant Y220C in cancer cells.	carbazole	30-39	P53	Homo sapiens	181-184
26776159-5	2016	We demonstrate the requirement of linc-475 for the proper induction of a p53-dependent cell cycle inhibitory response.	linc-475	34-42	P53	Homo sapiens	73-76
26776159-6	2016	We further confirm the functional importance of linc-475 in the maintenance of CDKN1A/p21 levels, a cell cycle inhibitor and a major p53 target gene, following p53 activation.	linc-475	48-56	P53	Homo sapiens	133-136
26776159-6	2016	We further confirm the functional importance of linc-475 in the maintenance of CDKN1A/p21 levels, a cell cycle inhibitor and a major p53 target gene, following p53 activation.	linc-475	48-56	P53	Homo sapiens	160-163
27527606-7	2016	RESULTS: Upon treatment with 5-fluorouracil (5-FU), apoptosis was increased in latently infected ACH2 cells encoding competent p53 compared with uninfected parent A3.01 cells, while the apoptosis of latently infected p53 null J1.1 cells was less than that of uninfected cells.	Fluorouracil	45-49	P53	Homo sapiens	127-130
27527606-7	2016	RESULTS: Upon treatment with 5-fluorouracil (5-FU), apoptosis was increased in latently infected ACH2 cells encoding competent p53 compared with uninfected parent A3.01 cells, while the apoptosis of latently infected p53 null J1.1 cells was less than that of uninfected cells.	Fluorouracil	45-49	P53	Homo sapiens	217-220
27527606-10	2016	Furthermore, the activation levels of p53 in both cells were further increased upon 5-FU treatment.	Fluorouracil	84-88	P53	Homo sapiens	38-41
27527606-11	2016	Consistent with p53 status, apoptosis was markedly increased in ACH2 and NCHA2 cells compared with uninfected and latently infected J1.1 cells upon treatment with other anticancer drugs such as doxorubicin and etoposide.	Doxorubicin	194-205	P53	Homo sapiens	16-19
27527606-12	2016	Inhibition of p53 in cells with latent HIV-1 infection diminished apoptosis upon 5-FU treatment.	Fluorouracil	81-85	P53	Homo sapiens	14-17
27511909-4	2016	The induced oxidative stress was associated with phosphorylation of p53 on serine 15, a marker of DNA damage, induction of the cyclin-cyclin dependent kinase inhibitors p21(Waf1) and p27(Kip1), and perturbations in cell cycle progression (p &lt; .001).	Serine	75-81	P53	Homo sapiens	68-71
27302066-1	2016	Our previous study suggested that ceramide synthase 6 (CerS6), an enzyme in sphingolipid biosynthesis, is regulated by p53: CerS6 was elevated in several cell lines in response to transient expression of p53 or in response to folate stress, which is known to activate p53.	Folic Acid	226-232	P53	Homo sapiens	119-122
27302066-1	2016	Our previous study suggested that ceramide synthase 6 (CerS6), an enzyme in sphingolipid biosynthesis, is regulated by p53: CerS6 was elevated in several cell lines in response to transient expression of p53 or in response to folate stress, which is known to activate p53.	Folic Acid	226-232	P53	Homo sapiens	204-207
27302066-1	2016	Our previous study suggested that ceramide synthase 6 (CerS6), an enzyme in sphingolipid biosynthesis, is regulated by p53: CerS6 was elevated in several cell lines in response to transient expression of p53 or in response to folate stress, which is known to activate p53.	Folic Acid	226-232	P53	Homo sapiens	204-207
27374783-5	2016	In addition, the good antitumor effects of CHO-PGEA and PI-PGEA were confirmed with suppressor tumor gene p53 systems in vitro and in vivo.	Cholesterol	43-46	P53	Homo sapiens	106-109
27527606-7	2016	RESULTS: Upon treatment with 5-fluorouracil (5-FU), apoptosis was increased in latently infected ACH2 cells encoding competent p53 compared with uninfected parent A3.01 cells, while the apoptosis of latently infected p53 null J1.1 cells was less than that of uninfected cells.	Fluorouracil	29-43	P53	Homo sapiens	127-130
27527606-7	2016	RESULTS: Upon treatment with 5-fluorouracil (5-FU), apoptosis was increased in latently infected ACH2 cells encoding competent p53 compared with uninfected parent A3.01 cells, while the apoptosis of latently infected p53 null J1.1 cells was less than that of uninfected cells.	Fluorouracil	29-43	P53	Homo sapiens	217-220
27021787-4	2016	The cells were then incubated for another 24h with or without doxorubicin (DOX, 1muM), an anthracyclin antitumor antibiotic that promotes p53-mediated apoptosis.	Doxorubicin	62-73	P53	Homo sapiens	138-141
27021787-4	2016	The cells were then incubated for another 24h with or without doxorubicin (DOX, 1muM), an anthracyclin antitumor antibiotic that promotes p53-mediated apoptosis.	Doxorubicin	75-78	P53	Homo sapiens	138-141
27288732-11	2016	Its intensity is cell type- and p53-independent, but predicted by the inhibition of autophagic flux and by the liposolubility of individual drugs and alleviated by cholesterol ablation.	Cholesterol	164-175	P53	Homo sapiens	32-35
27506388-8	2016	RSV-GSE also induced mitochondrial-mediated apoptosis in colon CSCs characterized by elevated p53, Bax/Bcl-2 ratio and cleaved PARP.	Resveratrol	0-3	P53	Homo sapiens	94-97
27501149-4	2016	Cell death was attributed to dysfunction of mitochondrial bioenergetics in p53-deficient cells, which was characterized by decreased mitochondrial respiration, steady-state ATP level and membrane potential, but augmented reactive oxygen species (ROS).	Adenosine Triphosphate	173-176	P53	Homo sapiens	75-78
27501149-4	2016	Cell death was attributed to dysfunction of mitochondrial bioenergetics in p53-deficient cells, which was characterized by decreased mitochondrial respiration, steady-state ATP level and membrane potential, but augmented reactive oxygen species (ROS).	Reactive Oxygen Species	221-244	P53	Homo sapiens	75-78
27501149-4	2016	Cell death was attributed to dysfunction of mitochondrial bioenergetics in p53-deficient cells, which was characterized by decreased mitochondrial respiration, steady-state ATP level and membrane potential, but augmented reactive oxygen species (ROS).	Reactive Oxygen Species	246-249	P53	Homo sapiens	75-78
27496966-0	2016	Nimbolide sensitizes human colon cancer cells to TRAIL through reactive oxygen species- and ERK-dependent up-regulation of death receptors, p53, and Bax.	Reactive Oxygen Species	63-86	P53	Homo sapiens	140-143
27608947-1	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in converting nicotinamide to NAD(+), essential for a number of enzymes and regulatory proteins involved in a variety of cellular processes, including deacetylation enzyme SIRT1 which modulates several tumor suppressors such as p53 and FOXO.	NAD	116-122	P53	Homo sapiens	314-317
27409664-6	2016	Furthermore, downregulation of CTBP1 by miR-644a upregulates wild type- or mutant-p53 which acts as a "molecular switch" between G1-arrest and apoptosis by inducing cyclin-dependent kinase inhibitor 1 (p21, CDKN1A, CIP1) or pro-apoptotic phorbol-12-myristate-13-acetate-induced protein 1 (Noxa, PMAIP1), respectively.	Tetradecanoylphorbol Acetate	238-269	P53	Homo sapiens	82-85
27062045-5	2016	Here, we found that the melatonin treatment markedly inhibited the senescent characteristics of CPCs after exposed to sublethal concentration of H2 O2 , including the increase in senescence-associated beta-galactosidase (SA-beta-gal)-positive CPCs, senescence-associated heterochromatin loci (SAHF), secretory IL-6 level, and the upregulation of p53 and p21 proteins.	Melatonin	24-33	P53	Homo sapiens	346-349
27260513-3	2016	We detected a significant "in vitro" generation of 8-oxodG between the codons 163 and 175, corresponding to a TP53 region with high mutation prevalence, after treatment with xanthine plus xanthine oxidase, a ROS-generating system.	Xanthine	174-182	P53	Homo sapiens	110-114
27260513-3	2016	We detected a significant "in vitro" generation of 8-oxodG between the codons 163 and 175, corresponding to a TP53 region with high mutation prevalence, after treatment with xanthine plus xanthine oxidase, a ROS-generating system.	Reactive Oxygen Species	208-211	P53	Homo sapiens	110-114
29894073-12	2016	They may therefore, conclude that detection of allelic polymorphisms of codon 72 of the p53 gene including arginine/arginine could be a risk factor predisposition for breast cancer and valuable tool for determining prognosis, progress, and treatment purposes.	Arginine	107-115	P53	Homo sapiens	88-91
29894073-12	2016	They may therefore, conclude that detection of allelic polymorphisms of codon 72 of the p53 gene including arginine/arginine could be a risk factor predisposition for breast cancer and valuable tool for determining prognosis, progress, and treatment purposes.	Arginine	116-124	P53	Homo sapiens	88-91
27446244-8	2016	Oxycodone induced a dose-dependent increase in the expression levels of p53 and Bax apoptosis-related genes, whereas it decreased the gene expression levels of Bcl-2.	Oxycodone	0-9	P53	Homo sapiens	72-75
27233942-5	2016	Stronger intracellular TrxR inhibition and higher accumulation of ROS (O2( -) and H2O2) are responsible for more effective S-phase arrest and mitochondria-mediated apoptotic induction of A549 cells by PL-CL than PLvia p53-p21-cyclinA/CDK2 and ASK1-JNK/p38 signaling cascade pathways, respectively.	Reactive Oxygen Species	66-69	P53	Homo sapiens	218-221
26370097-0	2016	Extremely low frequency electromagnetic field sensitizes cisplatin-resistant human ovarian adenocarcinoma cells via P53 activation.	Cisplatin	57-66	P53	Homo sapiens	116-119
26370097-12	2016	Semi-quantitative RT-PCR showed that in synergistic groups of cisplatin and EL-EMF, expression of P53 was increased but the expression level of MPP-2 gene decreased.	Cisplatin	62-71	P53	Homo sapiens	98-101
27279458-0	2016	Tanshinone I induces human colorectal cancer cell apoptosis: The potential roles of Aurora A-p53 and survivin-mediated signaling pathways.	tanshinone	0-12	P53	Homo sapiens	93-96
27279458-6	2016	Tanshinone I markedly inhibited CRC cell growth and induced apoptosis in CRC cells with functional p53 protein.	tanshinone	0-12	P53	Homo sapiens	99-102
27279458-8	2016	In tse cells with wild-type p53, data showed that Tanshinone I mediated Aurora A inhibition results in p53 upregulation, which is required for cell apoptosis.	tanshinone	50-62	P53	Homo sapiens	28-31
27279458-8	2016	In tse cells with wild-type p53, data showed that Tanshinone I mediated Aurora A inhibition results in p53 upregulation, which is required for cell apoptosis.	tanshinone	50-62	P53	Homo sapiens	103-106
27279458-11	2016	These observations were further substantiated by the pivotal role of survivin in Tanshinone I mediated apoptosis in CRC cells with p53 mutant.	tanshinone	81-93	P53	Homo sapiens	131-134
27279458-12	2016	Tanshinone I, a novel natural compound, exerts significant inhibitory effect on CRC cell growth via a mechanism involving either Aurora A-p53 axis or survivin-involving mechanism depending on different intrinsic characteristics of tumor cells.	tanshinone	0-12	P53	Homo sapiens	138-141
27422544-6	2016	ROS promotes p53 inducing MALM (Mieap-induced accumulation of lysosome-like organelles within mitochondria) to repair dysfunctional mitochondria and MIV (Mieap-induced vacuole) to accomplish damaged mitochondria degradation.	ros	0-3	P53	Homo sapiens	13-16
27347849-5	2016	In cancer cells, p53 missense mutants cooperate with Nrf2 (NFE2L2) to activate proteasome gene transcription, resulting in resistance to the proteasome inhibitor carfilzomib.	carfilzomib	162-173	P53	Homo sapiens	17-20
27347849-6	2016	Combining the mutant p53-inactivating agent APR-246 (PRIMA-1MET) with the proteasome inhibitor carfilzomib is effective in overcoming chemoresistance in triple-negative breast cancer cells, creating a therapeutic opportunity for treatment of solid tumours and metastasis with mutant p53.	carfilzomib	95-106	P53	Homo sapiens	283-286
27215386-3	2016	This involves phosphorylation by ATM on serine residues HDM2(S395) and HDMX(S403), promoting their respective interaction with the p53 mRNA.	Serine	40-46	P53	Homo sapiens	131-134
27113042-11	2016	These findings demonstrated that folic acid protected neuronal cells against Al-malt-induced apoptosis by preventing the downregulation of miR-19 and modulation of miR-19 related downstream PTEN/AKT/p53 pathway.	Folic Acid	33-43	P53	Homo sapiens	199-202
27236003-0	2016	Honokiol induces autophagic cell death in malignant glioma through reactive oxygen species-mediated regulation of the p53/PI3K/Akt/mTOR signaling pathway.	Reactive Oxygen Species	67-90	P53	Homo sapiens	118-121
27236003-13	2016	Taken together, our data indicated that honokiol induced ROS-mediated autophagic cell death through regulating the p53/PI3K/Akt/mTOR signaling pathway.	Reactive Oxygen Species	57-60	P53	Homo sapiens	115-118
27090187-2	2016	AEF effectively antagonized the senescence-associated beta-galactosidase staining and upregulation of p53 and p21(Cip1/WAF1) induced by UVB or H2O2 treatment in HS68 cells.	Hydrogen Peroxide	143-147	P53	Homo sapiens	102-105
27483224-1	2016	We previously reported that prenylated chalcone 2 (PC2), the O-prenyl derivative (2) of 2"-hydroxy-3,4,4",5,6"-pentamethoxychalcone (1), induced cytotoxicity of tumor cells via disruption of p53-MDM2 interaction.	2"-hydroxy-3,4,4",5,6"-pentamethoxychalcone	88-131	P53	Homo sapiens	191-194
27323408-2	2016	Cellular stressors such as reactive oxygen species can promote translocation of p53 into mitochondria where it acts to protect mitochondrial genome or trigger cell death via transcription-independent manner.	Reactive Oxygen Species	27-50	P53	Homo sapiens	80-83
27191893-6	2016	However, when stratified by chemotherapy regimen, patients whose tumors had TP53 and HR mutations demonstrated a marked survival advantage when treated with platinum and paclitaxel vs. platinum +/- cyclophosphamide (median OS of 90 months (95% CI 50-NA) vs. 29.5 months (95% CI 17.7-50.5), p = 0.0005).	Platinum	157-165	P53	Homo sapiens	76-80
27191893-6	2016	However, when stratified by chemotherapy regimen, patients whose tumors had TP53 and HR mutations demonstrated a marked survival advantage when treated with platinum and paclitaxel vs. platinum +/- cyclophosphamide (median OS of 90 months (95% CI 50-NA) vs. 29.5 months (95% CI 17.7-50.5), p = 0.0005).	Paclitaxel	170-180	P53	Homo sapiens	76-80
27323853-7	2016	Finally, we show that NF-YA loss sensitizes HPV18-positive cells toward the DNA damaging agent Doxorubicin, via p53-mediated transcriptional response.	Doxorubicin	95-106	P53	Homo sapiens	112-115
27191893-6	2016	However, when stratified by chemotherapy regimen, patients whose tumors had TP53 and HR mutations demonstrated a marked survival advantage when treated with platinum and paclitaxel vs. platinum +/- cyclophosphamide (median OS of 90 months (95% CI 50-NA) vs. 29.5 months (95% CI 17.7-50.5), p = 0.0005).	Platinum	185-193	P53	Homo sapiens	76-80
27291286-7	2016	Control of TRP upon activation, as demonstrated here for p53, might be a general activation mechanism of transcription factors.	Tryptophan	11-14	P53	Homo sapiens	57-60
27154500-10	2016	Finally, the co-delivery of Dox and p53-pDNA using the copolymer displayed greater cytotoxic effect compared with the Dox-loaded nanoparticle counterpart as revealed by cell viability and Caspase 3 expression assay.	Doxorubicin	118-121	P53	Homo sapiens	36-39
27154500-16	2016	In addition, the co-delivery of doxorubicin and p53 plasmid DNA using the new copolymer displayed greater cytotoxic effect compared with single agent (i.e. Dox) loaded counterpart, which indicated the significance of rapid dissociation of therapeutic agents from the carrier for synergistic cytotoxic effects on cancer cells.	Doxorubicin	156-159	P53	Homo sapiens	48-51
27416811-0	2016	Metabonomics applied in exploring the antitumour mechanism of physapubenolide on hepatocellular carcinoma cells by targeting glycolysis through the Akt-p53 pathway.	physapubenolide	62-77	P53	Homo sapiens	152-155
27185882-4	2016	Nitric oxide suppresses activation of the DDR (as measured by gammaH2AX formation and the phosphorylation of KAP1 and p53) in response to multiple genotoxic agents, including camptothecin, H2O2, and nitric oxide itself, despite the presence of DNA damage.	Nitric Oxide	0-12	P53	Homo sapiens	118-121
26936915-8	2016	Western blots demonstrated that MI-773 potently induced expression of p53 and its downstream targets p21, MDM2, and induced phosphorylation of p53 (serine 392) in low passage primary human ACC cells.	Serine	148-154	P53	Homo sapiens	143-146
27416811-7	2016	These results confirm that PB exhibits anti-cancer activities through the Akt-p53 pathway.	physapubenolide	27-29	P53	Homo sapiens	78-81
32263394-4	2016	Furthermore, the nanosystem (Bio-PLGA@Ru) was efficiently internalized by cancer cells by the lipid raft-mediated endocytosis pathway, triggered ROS overproduction and activated p53-mediated apoptosis in cancer cells.	ros	145-148	P53	Homo sapiens	178-181
27383270-0	2016	Inactivation of oncogenic cAMP-specific phosphodiesterase 4D by miR-139-5p in response to p53 activation.	Cyclic AMP	26-30	P53	Homo sapiens	90-93
27471396-3	2016	The aim of this study was to determine the therapeutic efficacy of lobaplatin on p53-mutant lung squamous cancer cells SK-MES-1.	lobaplatin	67-77	P53	Homo sapiens	81-84
27226597-4	2016	We used the genetic code expansion concept to produce natively folded, site-specific, and lysine-acetylated Sirt1-3 substrate proteins, namely Ras-related nuclear, p53, PEPCK1, superoxide dismutase, cyclophilin D, and Hsp10, and analyzed the deacetylation reaction.	Lysine	90-96	P53	Homo sapiens	164-167
27462151-13	2016	Moreover, Se@PEI@siRNA exhibited enhanced cytotoxic effects on cancer cells and triggered intracellular reactive oxygen species, and the signaling pathways of p53 and AKT were activated to advance cell apoptosis.	Reactive Oxygen Species	104-127	P53	Homo sapiens	159-162
27174050-5	2016	In the present study, we identified 9 Ru (II)-Arene Schiff-base (RAS) complexes able to induce p53-independent cytotoxicity and discuss structural features that are required for their p53-independent activity.	9 ru (ii)-arene	36-51	P53	Homo sapiens	95-98
27174050-5	2016	In the present study, we identified 9 Ru (II)-Arene Schiff-base (RAS) complexes able to induce p53-independent cytotoxicity and discuss structural features that are required for their p53-independent activity.	9 ru (ii)-arene	36-51	P53	Homo sapiens	184-187
27304668-0	2016	Glaucarubinone sensitizes KB cells to paclitaxel by inhibiting ABC transporters via ROS-dependent and p53-mediated activation of apoptotic signaling pathways.	Paclitaxel	38-48	P53	Homo sapiens	102-105
27304668-9	2016	Importantly, GLU and/or PTX triggered apoptosis through the activation of pro-apoptotic proteins such as p53, Bax, and caspase-9.	Paclitaxel	24-27	P53	Homo sapiens	105-108
27261574-0	2016	Curcumin and Ellagic acid synergistically induce ROS generation, DNA damage, p53 accumulation and apoptosis in HeLa cervical carcinoma cells.	Curcumin	0-8	P53	Homo sapiens	77-80
27063514-3	2016	DDR-induced signaling in cells activates the ATM-p53 and ATM-IKKalpha/beta-interferon (IFN)-beta signaling pathways, thus leading to an induction of the p53 and IFN-inducible IFI16 gene.	ddr	0-3	P53	Homo sapiens	49-52
27063514-3	2016	DDR-induced signaling in cells activates the ATM-p53 and ATM-IKKalpha/beta-interferon (IFN)-beta signaling pathways, thus leading to an induction of the p53 and IFN-inducible IFI16 gene.	ddr	0-3	P53	Homo sapiens	153-156
27399772-7	2016	It generated a distinct response in reactive oxygen species (ROS) generation and p53 levels depending on the p53 cell line status (wild type or mutant).	Reactive Oxygen Species	36-59	P53	Homo sapiens	109-112
27399772-7	2016	It generated a distinct response in reactive oxygen species (ROS) generation and p53 levels depending on the p53 cell line status (wild type or mutant).	Reactive Oxygen Species	61-64	P53	Homo sapiens	109-112
27041461-0	2016	Activation of p53 contributes to pseudolaric acid B-induced senescence in human lung cancer cells in vitro.	pseudolaric acid B	33-51	P53	Homo sapiens	14-17
27041461-12	2016	Knockdown of p53 expression with siRNA significantly suppressed PAB-induced senescence in A549 cells (p53 wild).	pseudolaric acid B	64-67	P53	Homo sapiens	13-16
27041461-12	2016	Knockdown of p53 expression with siRNA significantly suppressed PAB-induced senescence in A549 cells (p53 wild).	pseudolaric acid B	64-67	P53	Homo sapiens	102-105
27041461-13	2016	Furthermore, PAB-induced senescence was also observed in human lung cancer H460 cells (p53 wild), but not in human lung cancer H1299 cells (p53 null).	pseudolaric acid B	13-16	P53	Homo sapiens	87-90
27261574-5	2016	Besides this, Curcumin and Ellagic acid also restore p53, induce ROS formation and DNA damage.	Curcumin	14-22	P53	Homo sapiens	53-56
27046389-0	2016	Copper induced apoptosis in Caco-2 and Hep-G2 cells: Expression of caspases 3, 8 and 9, AIF and p53.	Copper	0-6	P53	Homo sapiens	96-99
27109893-10	2016	Pre-mature senescence induced due to limited glucose availability was found to be regulated by nuclear translocated p53 which, in turn, induced p21, pAkt and pERK.	Glucose	45-52	P53	Homo sapiens	116-119
27371670-4	2016	Similarly, during oxygen stress, p53 facilitates redirection of cellular metabolism toward energy generation through nonoxidative means, the suppression of reactive oxygen species (ROS) generation, and ROS detoxification-promoting cell survival.	Oxygen	18-24	P53	Homo sapiens	33-36
27371670-4	2016	Similarly, during oxygen stress, p53 facilitates redirection of cellular metabolism toward energy generation through nonoxidative means, the suppression of reactive oxygen species (ROS) generation, and ROS detoxification-promoting cell survival.	Reactive Oxygen Species	156-179	P53	Homo sapiens	33-36
27371670-4	2016	Similarly, during oxygen stress, p53 facilitates redirection of cellular metabolism toward energy generation through nonoxidative means, the suppression of reactive oxygen species (ROS) generation, and ROS detoxification-promoting cell survival.	Reactive Oxygen Species	181-184	P53	Homo sapiens	33-36
27371670-4	2016	Similarly, during oxygen stress, p53 facilitates redirection of cellular metabolism toward energy generation through nonoxidative means, the suppression of reactive oxygen species (ROS) generation, and ROS detoxification-promoting cell survival.	Reactive Oxygen Species	202-205	P53	Homo sapiens	33-36
27369359-2	2016	Paraffin tumors of all clinical subtypes from 1661 patients with operable breast cancer who were treated within 4 adjuvant trials with anthracycline-taxanes chemotherapy were informative for TP53 and PIK3CA mutation status (semiconductor sequencing genotyping) and for stromal TILs density.	Paraffin	0-8	P53	Homo sapiens	191-195
26896489-9	2016	In A549 cells with functional p53, the repair of cisplatin/DNA adducts is determined by a complex action of HMGB1 and p53 as an increase of DNA repair capacity was registered only after silencing of both proteins.	Cisplatin	49-58	P53	Homo sapiens	30-33
27382207-0	2016	Differential Expressions of p53, p53R2, hRRM2 and PBR in Chronic Lymphocytic Leukemia: A Correlation with Intracellular Cholesterol.	Cholesterol	120-131	P53	Homo sapiens	28-31
26896489-9	2016	In A549 cells with functional p53, the repair of cisplatin/DNA adducts is determined by a complex action of HMGB1 and p53 as an increase of DNA repair capacity was registered only after silencing of both proteins.	Cisplatin	49-58	P53	Homo sapiens	118-121
27129209-8	2016	We further explored that DNA damage-induced wild-type p53 leads to spindle assembly checkpoint arrest by repressing UBE2C, whereas mutant p53 causes premature anaphase exit by increasing UBE2C expression in the presence of 5-fluorouracil.	Fluorouracil	223-237	P53	Homo sapiens	138-141
27482284-7	2016	All of the studies indicated that curcumin decreased glioblastoma cell viability through various pathways (i.e. decrease in prosurvival proteins such as nuclear factor kappaB, activator protein 1, and phosphoinositide 3 kinase, and upregulation of apoptotic pathways like p21, p53, and executor caspase 3).	Curcumin	34-42	P53	Homo sapiens	277-280
27177208-0	2016	A novel all-trans retinoic acid derivative 4-amino-2-trifluoromethyl-phenyl retinate inhibits the proliferation of human hepatocellular carcinoma HepG2 cells by inducing G0/G1 cell cycle arrest and apoptosis via upregulation of p53 and ASPP1 and downregulation of iASPP.	Tretinoin	18-31	P53	Homo sapiens	228-231
27177208-14	2016	Moreover, the fluorescent density of p53 was higher in the nuclei after exposure to ATPR than that in the ATRA group.	Tretinoin	106-110	P53	Homo sapiens	37-40
27390612-4	2016	This chimeric protein, M3-p53-R12, can be expressed in E. coli and purified using immobilized metal ion chromatography followed by serial refolding dialysis.	Metals	94-99	P53	Homo sapiens	26-29
27446805-9	2016	The interplay between the IGF1 and p53 pathways is also of major relevance in terms of metabolic regulation, including glucose transport and glycolysis.	Glucose	119-126	P53	Homo sapiens	35-38
27223080-7	2016	Median-drug-effect analysis showed Nutlin-3 or RG7388 combination with cisplatin was additive to, or synergistic in a p53-dependent manner, resulting in increased p53 activation, cell cycle arrest and apoptosis, associated with increased p21WAF1 protein and/or caspase-3/7 activity compared to cisplatin alone.	Cisplatin	71-80	P53	Homo sapiens	118-121
27223080-7	2016	Median-drug-effect analysis showed Nutlin-3 or RG7388 combination with cisplatin was additive to, or synergistic in a p53-dependent manner, resulting in increased p53 activation, cell cycle arrest and apoptosis, associated with increased p21WAF1 protein and/or caspase-3/7 activity compared to cisplatin alone.	Cisplatin	71-80	P53	Homo sapiens	163-166
27223080-7	2016	Median-drug-effect analysis showed Nutlin-3 or RG7388 combination with cisplatin was additive to, or synergistic in a p53-dependent manner, resulting in increased p53 activation, cell cycle arrest and apoptosis, associated with increased p21WAF1 protein and/or caspase-3/7 activity compared to cisplatin alone.	Cisplatin	294-303	P53	Homo sapiens	118-121
27346053-5	2016	Cleavage-associated HCO3(-)-dependent events, including increase of intracellular pH, upregulation of miR-125b and downregulation of p53, also required Cl(-).	Bicarbonates	20-24	P53	Homo sapiens	133-136
27351203-0	2016	miR-24-3p Suppresses Malignant Behavior of Lacrimal Adenoid Cystic Carcinoma by Targeting PRKCH to Regulate p53/p21 Pathway.	mir-24-3p	0-9	P53	Homo sapiens	108-111
27351203-8	2016	These results suggest that miR-24-3p promotes the p53/p21 pathway by down-regulating PRKCH expression in lacrimal adenoid cystic carcinoma cells.	mir-24-3p	27-36	P53	Homo sapiens	50-53
27232943-7	2016	Refined analysis of KEGG pathways showed that 2 - one linked to p53 and a second to prostate cancer - have functional connectivity to resveratrol and its four direct protein targets.	Resveratrol	134-145	P53	Homo sapiens	64-67
27336364-16	2016	The interaction of MDM2-p53 was maintained in infected RPS14 knockdown cells despite emetine treatment, confirming a unique mechanism by which emetine exploits RPS14 to disrupt MDM2-p53 interaction.	Emetine	85-92	P53	Homo sapiens	24-27
27336364-16	2016	The interaction of MDM2-p53 was maintained in infected RPS14 knockdown cells despite emetine treatment, confirming a unique mechanism by which emetine exploits RPS14 to disrupt MDM2-p53 interaction.	Emetine	143-150	P53	Homo sapiens	24-27
27336364-16	2016	The interaction of MDM2-p53 was maintained in infected RPS14 knockdown cells despite emetine treatment, confirming a unique mechanism by which emetine exploits RPS14 to disrupt MDM2-p53 interaction.	Emetine	143-150	P53	Homo sapiens	182-185
27336364-9	2016	HCMV inhibition by emetine depended on ribosomal processing S14 (RPS14) binding to MDM2, leading to disruption of HCMV-induced MDM2-p53 and MDM2-IE2 interactions.	Emetine	19-26	P53	Homo sapiens	132-135
27420953-0	2016	Borax-induced apoptosis in HepG2 cells involves p53, Bcl-2, and Bax.	borax	0-5	P53	Homo sapiens	48-51
27420953-10	2016	The apoptotic process triggered by borax involved the upregulation of p53 and Bax and the downregulation of Bcl-2, which was confirmed by a change in the mitochondrial membrane potential.	borax	35-40	P53	Homo sapiens	70-73
27420953-11	2016	These results elucidate a borax-induced apoptotic pathway in HepG2 cells that involves the upregulation of p53 and Bax and the downregulation of Bcl-2.	borax	26-31	P53	Homo sapiens	107-110
27058630-9	2016	The log10IC50 values for two out of 14 selected phytochemicals from these plants (acovenoside A and ouabain) of 60 tumor cell lines were correlated to the expression of ABC-transporters (ABCB1, ABCB5, ABCC1, ABCG2), oncogenes (EGFR, RAS) and tumor suppressors (TP53).	Ouabain	100-107	P53	Homo sapiens	261-265
27283735-3	2016	Curcumin is known to activate 20S proteasome and promotes the degradation of intrinsically unfolded p53 tumor suppressor protein.	Curcumin	0-8	P53	Homo sapiens	100-103
27270209-6	2016	In p53-expressing cells, citral increases phosphorylation of serine-15 of p53.	Serine	61-67	P53	Homo sapiens	74-77
27228201-9	2016	Finally, we have shown that the inclusion complex of alpha-CD and curcumin (CCC) preferentially enters into the human lung cancer cell (A549) as compared to the normal lung fibroblast cell (WI38), causes apoptotic death, activates tumor suppressor protein (p53) and cyclin-dependent kinase inhibitor 1 (p21), and inhibits 3D spheroid growth of cancer cell.	Curcumin	66-74	P53	Homo sapiens	257-260
27228201-9	2016	Finally, we have shown that the inclusion complex of alpha-CD and curcumin (CCC) preferentially enters into the human lung cancer cell (A549) as compared to the normal lung fibroblast cell (WI38), causes apoptotic death, activates tumor suppressor protein (p53) and cyclin-dependent kinase inhibitor 1 (p21), and inhibits 3D spheroid growth of cancer cell.	Chlormequat	76-79	P53	Homo sapiens	257-260
27270209-9	2016	Citral increases intracellular oxygen radicals and this leads to activation of p53.	Reactive Oxygen Species	31-46	P53	Homo sapiens	79-82
27270209-11	2016	Pretreatment with N-acetylcysteine decreases phosphorylation of p53 in citral-treated ECC-1 and OVCAR-3.	Acetylcysteine	18-34	P53	Homo sapiens	64-67
32263321-4	2016	In this system, Doxorubicin-loaded aptamer duplex and plasmid DNA (p53) can be bound by PEI by electronic interactions to form stable complexes which effectively protect the aptamer and p53 from DNase degradation.	Doxorubicin	16-27	P53	Homo sapiens	67-70
32263321-4	2016	In this system, Doxorubicin-loaded aptamer duplex and plasmid DNA (p53) can be bound by PEI by electronic interactions to form stable complexes which effectively protect the aptamer and p53 from DNase degradation.	Doxorubicin	16-27	P53	Homo sapiens	186-189
32263321-9	2016	Moreover, the apoptosis percentage of HeLa cells treated with PEI/ARAD/Dox/p53 complex increased to 40.8%, compared to 24.7% for PEI/ARAD/Dox complex and 11.5% for PEI/ARAD/p53, respectively.	Doxorubicin	71-74	P53	Homo sapiens	75-78
27144434-0	2016	MEK5/ERK5 signaling inhibition increases colon cancer cell sensitivity to 5-fluorouracil through a p53-dependent mechanism.	Fluorouracil	74-88	P53	Homo sapiens	99-102
32263321-9	2016	Moreover, the apoptosis percentage of HeLa cells treated with PEI/ARAD/Dox/p53 complex increased to 40.8%, compared to 24.7% for PEI/ARAD/Dox complex and 11.5% for PEI/ARAD/p53, respectively.	Doxorubicin	71-74	P53	Homo sapiens	173-176
32263321-9	2016	Moreover, the apoptosis percentage of HeLa cells treated with PEI/ARAD/Dox/p53 complex increased to 40.8%, compared to 24.7% for PEI/ARAD/Dox complex and 11.5% for PEI/ARAD/p53, respectively.	Doxorubicin	138-141	P53	Homo sapiens	75-78
27147566-7	2016	Moreover, JNK2 phosphorylated p53 at Thr-81, thus protecting p53 from MDM2-induced proteasome degradation.	Threonine	37-40	P53	Homo sapiens	30-33
27147566-7	2016	Moreover, JNK2 phosphorylated p53 at Thr-81, thus protecting p53 from MDM2-induced proteasome degradation.	Threonine	37-40	P53	Homo sapiens	61-64
27129302-4	2016	Strikingly, this single phosphorylation event controls HEY1 stability and function: simulation of HEY1 Ser-68 phosphorylation increases HEY1 protein stability but inhibits its ability to enhance p53 transcriptional activity.	Serine	103-106	P53	Homo sapiens	195-198
27129302-12	2016	Simulation of HEY1 Ser-68 phosphorylation prevents its interaction with p53, RPL11 and MDM2 and abolishes HEY1 migration to nucleolar caps upon ribosomal stress.	Serine	19-22	P53	Homo sapiens	72-75
27124102-0	2016	Increased mitochondrial fission promotes autophagy and hepatocellular carcinoma cell survival through the ROS-modulated coordinated regulation of the NFKB and TP53 pathways.	ros	106-109	P53	Homo sapiens	159-163
27358718-7	2016	The combined network shows that glycolytic enzymes are linked to miRs via p53, c-MYC, HIF1alpha, whereas the genes in serine, glycine and one carbon metabolism are regulated via the c-MYC, as well as other regulatory organization that cannot be observed by investigating individual miRs, TFs, and target genes.	Glycine	126-133	P53	Homo sapiens	74-77
27358718-7	2016	The combined network shows that glycolytic enzymes are linked to miRs via p53, c-MYC, HIF1alpha, whereas the genes in serine, glycine and one carbon metabolism are regulated via the c-MYC, as well as other regulatory organization that cannot be observed by investigating individual miRs, TFs, and target genes.	Carbon	142-148	P53	Homo sapiens	74-77
27210019-0	2016	Lysines in the tetramerization domain of p53 selectively modulate G1 arrest.	Lysine	0-7	P53	Homo sapiens	41-44
27124102-7	2016	We further demonstrated that the survival-promoting role of increased mitochondrial fission was mediated via elevated ROS production and subsequent activation of AKT, which facilitated MDM2-mediated TP53 degradation, and NFKBIA- and IKK-mediated transcriptional activity of NFKB in HCC cells.	ros	118-121	P53	Homo sapiens	199-203
27210019-4	2016	By changing lysines 351 and 357 to arginine, thereby blocking all post-translational modifications of these residues, DNA binding and transcriptional regulation by p53 remain virtually unchanged.	Lysine	12-19	P53	Homo sapiens	164-167
26876578-4	2016	DNA damaging agents such as doxorubicin also induced STAT5A expression in a p53 dependent manner.	Doxorubicin	28-39	P53	Homo sapiens	76-79
27210019-4	2016	By changing lysines 351 and 357 to arginine, thereby blocking all post-translational modifications of these residues, DNA binding and transcriptional regulation by p53 remain virtually unchanged.	Arginine	35-43	P53	Homo sapiens	164-167
27210019-5	2016	On the other hand, by changing these lysines to glutamine (2KQ-p53), thereby neutralizing their positive charge and potentially mimicking acetylation, p53 is impaired in the induction of cell cycle arrest and yet can still effectively induce cell death.	Lysine	37-44	P53	Homo sapiens	63-66
27210019-5	2016	On the other hand, by changing these lysines to glutamine (2KQ-p53), thereby neutralizing their positive charge and potentially mimicking acetylation, p53 is impaired in the induction of cell cycle arrest and yet can still effectively induce cell death.	Lysine	37-44	P53	Homo sapiens	151-154
27210019-7	2016	Our findings show that strong induction of p21 is not sufficient to block H1299 cells in G1, and imply that modification of one or both of the lysines within the tetramerization domain may serve as a mechanism to shunt p53 from inducing cell cycle arrest.	Lysine	143-150	P53	Homo sapiens	219-222
26984736-0	2016	Downregulation of LRRC8A protects human ovarian and alveolar carcinoma cells against Cisplatin-induced expression of p53, MDM2, p21Waf1/Cip1, and Caspase-9/-3 activation.	Cisplatin	85-94	P53	Homo sapiens	117-120
26984736-2	2016	In Cisplatin-sensitive cells Cisplatin treatment increases p53-protein level as well as downstream signaling, e.g., expression of p21(Waf1/Cip1), Bax, Noxa, MDM2, and activation of Caspase-9/-3.	Cisplatin	3-12	P53	Homo sapiens	59-62
26984736-2	2016	In Cisplatin-sensitive cells Cisplatin treatment increases p53-protein level as well as downstream signaling, e.g., expression of p21(Waf1/Cip1), Bax, Noxa, MDM2, and activation of Caspase-9/-3.	Cisplatin	29-38	P53	Homo sapiens	59-62
26984736-3	2016	In contrast, Cisplatin-resistant cells do not enter apoptosis, i.e., their p53 and downstream signaling are reduced and caspase activity unaltered following Cisplatin exposure.	Cisplatin	13-22	P53	Homo sapiens	75-78
26984736-3	2016	In contrast, Cisplatin-resistant cells do not enter apoptosis, i.e., their p53 and downstream signaling are reduced and caspase activity unaltered following Cisplatin exposure.	Cisplatin	157-166	P53	Homo sapiens	75-78
26984736-4	2016	Reduced LRRC8A expression and VSOAC activity are previously shown to correlate with Cisplatin resistance, and here we demonstrate that pharmacological inhibition and transient knockdown of LRRC8A reduce the protein level of p53, MDM2, and p21(Waf1/Cip1) as well as Caspase-9/-3 activation in Cisplatin-sensitive cells.	Cisplatin	84-93	P53	Homo sapiens	224-227
26984736-4	2016	Reduced LRRC8A expression and VSOAC activity are previously shown to correlate with Cisplatin resistance, and here we demonstrate that pharmacological inhibition and transient knockdown of LRRC8A reduce the protein level of p53, MDM2, and p21(Waf1/Cip1) as well as Caspase-9/-3 activation in Cisplatin-sensitive cells.	Cisplatin	292-301	P53	Homo sapiens	224-227
26984736-7	2016	Our data indicate 1) that expression/activity of LRRC8A is essential for Cisplatin-induced increase in p53 protein level and its downstream signaling, i.e., Caspase-9/-3 activation, expression of p21(Waf1/Cip1) and MDM2; and 2) that downregulation of LRRC8A-dependent osmolyte transporters contributes to acquirement of Cisplatin resistance in ovarian and lung carcinoma cells.	Cisplatin	73-82	P53	Homo sapiens	103-106
26984736-7	2016	Our data indicate 1) that expression/activity of LRRC8A is essential for Cisplatin-induced increase in p53 protein level and its downstream signaling, i.e., Caspase-9/-3 activation, expression of p21(Waf1/Cip1) and MDM2; and 2) that downregulation of LRRC8A-dependent osmolyte transporters contributes to acquirement of Cisplatin resistance in ovarian and lung carcinoma cells.	Cisplatin	320-329	P53	Homo sapiens	103-106
27272838-0	2016	Immunohistochemical Evaluation of the Role of p53 Mutation in Cervical Cancer: Ser-20 p53-Mutant Correlates with Better Prognosis.	Serine	79-82	P53	Homo sapiens	46-49
27272838-0	2016	Immunohistochemical Evaluation of the Role of p53 Mutation in Cervical Cancer: Ser-20 p53-Mutant Correlates with Better Prognosis.	Serine	79-82	P53	Homo sapiens	86-89
27031930-2	2016	In this study, a dual responsive co-delivery system RHD/p53 was fabricated to enhance the antitumor efficacy with a low dose of doxorubicin (DOX).	Doxorubicin	128-139	P53	Homo sapiens	56-59
27031930-2	2016	In this study, a dual responsive co-delivery system RHD/p53 was fabricated to enhance the antitumor efficacy with a low dose of doxorubicin (DOX).	Doxorubicin	141-144	P53	Homo sapiens	56-59
27031930-9	2016	Due to the cleavage of disulfide bonds triggered by the high-content GSH in cytoplasm, the complexes would be degraded and released p53 for co-therapy to improve antitumor efficacy.	Disulfides	23-32	P53	Homo sapiens	132-135
27031930-9	2016	Due to the cleavage of disulfide bonds triggered by the high-content GSH in cytoplasm, the complexes would be degraded and released p53 for co-therapy to improve antitumor efficacy.	Glutathione	69-72	P53	Homo sapiens	132-135
27383327-8	2016	Water-solvable vitamin E Trolox significantly promoted MCF7 cell proliferation in vitro, while reducing intracellular ROS level and p53 expression.	Water	0-5	P53	Homo sapiens	132-135
27163202-6	2016	However, it inhibited Chk1 activation and G2/M arrest with combination of cisplatin treatment, resulting in p53-independent apoptosis.	Cisplatin	74-83	P53	Homo sapiens	108-111
27304453-10	2016	The results revealed that (1) homozygosity of the Pro72 variant of p53 was present in 26 laryngeal carcinoma patients (65%), (2) heterozygosity for the Pro/Arg genotype was present in 13 patients (32.5%), and (3) the Arg72 variant of the p53 allele was present in 1 patient (2.5%) before treatment.	Arginine	156-159	P53	Homo sapiens	67-70
27075929-11	2016	Mechanistically, proapoptotic WW domain-containing oxidoreductase and p53 block the protective TNF receptor adaptor factor 2 that allows nitric oxide synthase 2 to synthesize nitric oxide and bubble formation.	Nitric Oxide	137-149	P53	Homo sapiens	70-73
27082635-0	2016	Theaflavin-3, 3"-digallate induces apoptosis and G2 cell cycle arrest through the Akt/MDM2/p53 pathway in cisplatin-resistant ovarian cancer A2780/CP70 cells.	Cisplatin	106-115	P53	Homo sapiens	91-94
27082017-7	2016	Results indicated that curcumin decreased expression of EMT-related genes in Tumor2 cell line when compared to its counterpart as E-cadherin, N-cadherin, ZEB2, Twist1, Slug, Axl, vimentin, STAT-3, fibronectin; and genes p53 and caveolin-1, as well as apoptotic genes caspase-3, caspase-8, and others such as cyclin D1 and NFkappaB.	Curcumin	23-31	P53	Homo sapiens	220-223
26935926-0	2016	p53 determines prognostic significance of the carbohydrate stem cell marker TF1 (CD176) in ovarian cancer.	Carbohydrates	46-58	P53	Homo sapiens	0-3
26688517-9	2016	p53 expression was increased in BSM from asthmatic patients both ex vivo and in vitro, with a decreased interaction with mouse double minute 2 homolog (Mdm2) and an increased phosphorylation of serine 20.	Serine	194-200	P53	Homo sapiens	0-3
27035231-9	2016	Knockdown of ISYNA1 caused resistance to adriamycin treatment, demonstrating the role of ISYNA1 in p53-mediated growth suppression.	Doxorubicin	41-51	P53	Homo sapiens	99-102
27032906-7	2016	Furthermore, NF-kappaB/p53 pathway was activated during the process of autophagy induced by TCS and the ROS generation was mediated by it in MKN-45 cells.	Reactive Oxygen Species	104-107	P53	Homo sapiens	23-26
27376811-2	2016	The change from an arginine (Arg) to a proline (Pro) at codon 72 can influence the biological activity of p53, which predisposes to an increased risk of recurrent spontaneous abortion (RSA).	Arginine	19-27	P53	Homo sapiens	106-109
27376811-2	2016	The change from an arginine (Arg) to a proline (Pro) at codon 72 can influence the biological activity of p53, which predisposes to an increased risk of recurrent spontaneous abortion (RSA).	Arginine	29-32	P53	Homo sapiens	106-109
27376811-7	2016	There was a significant association between p53 polymorphism at codon 72 and RSA in recessive model (Pro/Pro vs. Pro/Arg+Arg/Arg; OR=1.60, 95% CI: 1.14-2.24) and co-dominant model (Pro/Pro vs. Arg/Arg; OR=1.47, 95% CI: 1.02-2.12) whether the study that was deviated from HWE was eliminated or not.	Arginine	117-120	P53	Homo sapiens	44-47
27376811-7	2016	There was a significant association between p53 polymorphism at codon 72 and RSA in recessive model (Pro/Pro vs. Pro/Arg+Arg/Arg; OR=1.60, 95% CI: 1.14-2.24) and co-dominant model (Pro/Pro vs. Arg/Arg; OR=1.47, 95% CI: 1.02-2.12) whether the study that was deviated from HWE was eliminated or not.	Arginine	121-124	P53	Homo sapiens	44-47
27376811-7	2016	There was a significant association between p53 polymorphism at codon 72 and RSA in recessive model (Pro/Pro vs. Pro/Arg+Arg/Arg; OR=1.60, 95% CI: 1.14-2.24) and co-dominant model (Pro/Pro vs. Arg/Arg; OR=1.47, 95% CI: 1.02-2.12) whether the study that was deviated from HWE was eliminated or not.	Arginine	121-124	P53	Homo sapiens	44-47
27376811-7	2016	There was a significant association between p53 polymorphism at codon 72 and RSA in recessive model (Pro/Pro vs. Pro/Arg+Arg/Arg; OR=1.60, 95% CI: 1.14-2.24) and co-dominant model (Pro/Pro vs. Arg/Arg; OR=1.47, 95% CI: 1.02-2.12) whether the study that was deviated from HWE was eliminated or not.	Arginine	121-124	P53	Homo sapiens	44-47
27376811-7	2016	There was a significant association between p53 polymorphism at codon 72 and RSA in recessive model (Pro/Pro vs. Pro/Arg+Arg/Arg; OR=1.60, 95% CI: 1.14-2.24) and co-dominant model (Pro/Pro vs. Arg/Arg; OR=1.47, 95% CI: 1.02-2.12) whether the study that was deviated from HWE was eliminated or not.	Arginine	121-124	P53	Homo sapiens	44-47
26152521-9	2016	Pretreatment of cells with ROS scavenger N-acetyl cysteine abrogated the inhibitory effect of CA on the JAK2-STAT3/Src-STAT3 signaling and rescued cells from CA-induced apoptosis by blocking the induction of p53 and the cleavage of caspase-3 and PARP in HCT116 cells.	ros	27-30	P53	Homo sapiens	208-211
26899019-0	2016	Prognostic and Predictive Effect of TP53 Mutations in Patients with Non-Small Cell Lung Cancer from Adjuvant Cisplatin-Based Therapy Randomized Trials: A LACE-Bio Pooled Analysis.	Cisplatin	109-118	P53	Homo sapiens	36-40
26152521-9	2016	Pretreatment of cells with ROS scavenger N-acetyl cysteine abrogated the inhibitory effect of CA on the JAK2-STAT3/Src-STAT3 signaling and rescued cells from CA-induced apoptosis by blocking the induction of p53 and the cleavage of caspase-3 and PARP in HCT116 cells.	Acetylcysteine	41-58	P53	Homo sapiens	208-211
27221738-2	2016	We investigated role of microRNAs in regulating p53-p21 pathway in high glucose (HG)-induced cardiomyocyte hypertrophy and apoptosis.	Glucose	72-79	P53	Homo sapiens	48-51
27238720-9	2016	Phosphorylation of the Ser 46 residue on p53, the expression of P53AIP1, Mdm2, p21, as well as caspase-3 and CK-18 were significantly increased in explants at 40  C and 42  C. Conversely, these effects were significantly attenuated by leptin 10 nM at both 40  C and 42  C. The BCL2/BAX ratio was also significantly decreased in explants at 40  C and 42  C compared with explants incubated at 37  C, which was prevented by leptin stimulation.	Serine	23-26	P53	Homo sapiens	41-44
27109601-9	2016	However, resveratrol displayed synergism when combined with metformin as shown by the downregulation of p53/gammaH2AX/p-chk2.	Resveratrol	9-20	P53	Homo sapiens	104-107
27109601-9	2016	However, resveratrol displayed synergism when combined with metformin as shown by the downregulation of p53/gammaH2AX/p-chk2.	Metformin	60-69	P53	Homo sapiens	104-107
27109601-5	2016	We found that metformin inhibited UVC-induced upregulation of p53, as well as downregulated the expression of two DNA damage markers: gammaH2AX and p-chk2.	Metformin	14-23	P53	Homo sapiens	62-65
27168162-11	2016	The cisplatin-induced expression of pAkt was not affected by LCN2; however, the expression of p53 and p21 was increased by LCN2-silencing.	Cisplatin	4-13	P53	Homo sapiens	94-97
27195669-11	2016	Despite similar p53 activation profiles, these data revealed widespread dampening of p53 and NRF2-related genes as early as 4 h after exposure at higher, unrecoverable Zn2+ exposures.	Zinc	168-172	P53	Homo sapiens	85-88
27179933-7	2016	RESULTS: We observed strong synergy with APR-246 and cisplatin in all tumor samples carrying a TP53 missense mutation, while synergistic or additive effects were found in cells with wild type or TP53 nonsense mutations.	Cisplatin	53-62	P53	Homo sapiens	95-99
27179933-9	2016	Moreover, APR-246 sensitized TP53 mutant primary ovarian cancer cells, isolated from a clinically platinum-resistant patient, to cisplatin; the IC50 value of cisplatin decreased 3.6 fold from 6.5 to 1.8 muM in the presence of clinically relevant concentration of APR-246.	Cisplatin	129-138	P53	Homo sapiens	29-33
27059084-8	2016	We demonstrate that low oxygen stimulates a complex signaling network involving PI3K/Akt, Notch, and canonical Wnt pathways, which mediate the observed increase in nuclear Oct4a and REST, with simultaneous decrease in p53, AIF, and Bak.	Oxygen	24-30	P53	Homo sapiens	218-221
27034006-7	2016	Reduction of cellular levels of p53 stimulates hBD3 expression, while activation of p53 by doxorubicin inhibits its expression in primary oral keratinocytes and CaSki cells, suggesting that p53 represses hBD3 expression.	Doxorubicin	91-102	P53	Homo sapiens	84-87
27034006-7	2016	Reduction of cellular levels of p53 stimulates hBD3 expression, while activation of p53 by doxorubicin inhibits its expression in primary oral keratinocytes and CaSki cells, suggesting that p53 represses hBD3 expression.	Doxorubicin	91-102	P53	Homo sapiens	84-87
27050276-0	2016	Crosstalk between the IGF-1R/AKT/mTORC1 pathway and the tumor suppressors p53 and p27 determines cisplatin sensitivity and limits the effectiveness of an IGF-1R pathway inhibitor.	Cisplatin	97-106	P53	Homo sapiens	74-77
27050276-5	2016	Cisplatin (CP) activated the IGF-1R/AKT/mTORC1 pathway and stabilized p53 in osteosarcoma (OS) cells.	Cisplatin	0-9	P53	Homo sapiens	70-73
27534737-0	2016	Correction: 5-Fluorouracil-induced RNA stress engages a TRAIL-DISC-dependent apoptosis axis facilitated by p53.	Fluorouracil	12-26	P53	Homo sapiens	107-110
27159678-0	2016	Association of p53 codon72 Arg&gt;Pro polymorphism with susceptibility to nasopharyngeal carcinoma: evidence from a case-control study and meta-analysis.	Arginine	27-30	P53	Homo sapiens	15-18
27159678-3	2016	Single-nucleotide polymorphism of p53 at codon72 leading to substitution of proline (Pro) in place of arginine (Arg) has been identified as a risk factor for development of many cancers, including nasopharyngeal carcinoma (NPC).	Arginine	102-110	P53	Homo sapiens	34-37
27159678-3	2016	Single-nucleotide polymorphism of p53 at codon72 leading to substitution of proline (Pro) in place of arginine (Arg) has been identified as a risk factor for development of many cancers, including nasopharyngeal carcinoma (NPC).	Arginine	112-115	P53	Homo sapiens	34-37
27159678-5	2016	We aimed to conduct a case-control study for a possible relation of p53 codon72 Arg&gt;Pro polymorphism with NPC risk in underdeveloped states of India, combine the result with previously available records from different databases and perform a meta-analysis to draw a more definitive conclusion.	Arginine	80-83	P53	Homo sapiens	68-71
27159678-7	2016	The p53 codon72 Arg&gt;Pro polymorphism was typed by polymerase chain reaction, which showed an association with NPC risk.	Arginine	16-19	P53	Homo sapiens	4-7
27159678-11	2016	The outcome of the study indicated that both allele frequency and genotype distribution of p53 codon72 Arg&gt;Pro polymorphism were significantly associated with NPC risk.	Arginine	103-106	P53	Homo sapiens	91-94
27009858-9	2016	P53 is strongly accumulated in response to 5-FU-induced dormant cells through the activation of ubiquitin ligase anaphase-promoting complex (APC/C) and TGF-beta/Smad signaling.	Fluorouracil	43-47	P53	Homo sapiens	0-3
27274280-5	2016	Moreover, the phosphorylation of AMP-activated protein kinase (AMPK) and the expression of p53 were increased upon metformin treatment, and the inhibition of p53 abrogated the induction of miR-23a by metformin, suggesting that AMPK/p53 signaling axis is responsible for the induction of miR-23a by metformin.	Metformin	200-209	P53	Homo sapiens	91-94
27274280-5	2016	Moreover, the phosphorylation of AMP-activated protein kinase (AMPK) and the expression of p53 were increased upon metformin treatment, and the inhibition of p53 abrogated the induction of miR-23a by metformin, suggesting that AMPK/p53 signaling axis is responsible for the induction of miR-23a by metformin.	Metformin	200-209	P53	Homo sapiens	158-161
27274280-5	2016	Moreover, the phosphorylation of AMP-activated protein kinase (AMPK) and the expression of p53 were increased upon metformin treatment, and the inhibition of p53 abrogated the induction of miR-23a by metformin, suggesting that AMPK/p53 signaling axis is responsible for the induction of miR-23a by metformin.	Metformin	200-209	P53	Homo sapiens	158-161
27274280-6	2016	In summary, we unraveled a novel AMPK/p53/miR-23a/FOXA1 axis in the regulation of apoptosis in HCC, and the application of metformin could, therefore, be effective in the treatment of HCC.	Metformin	123-132	P53	Homo sapiens	38-41
27148686-3	2016	Costunolide induced an ROS-dependent increase in p53 abrogated telomerase activity.	Reactive Oxygen Species	23-26	P53	Homo sapiens	49-52
27274280-0	2016	Metformin induces apoptosis of human hepatocellular carcinoma HepG2 cells by activating an AMPK/p53/miR-23a/FOXA1 pathway.	Metformin	0-9	P53	Homo sapiens	96-99
27274280-5	2016	Moreover, the phosphorylation of AMP-activated protein kinase (AMPK) and the expression of p53 were increased upon metformin treatment, and the inhibition of p53 abrogated the induction of miR-23a by metformin, suggesting that AMPK/p53 signaling axis is responsible for the induction of miR-23a by metformin.	Metformin	115-124	P53	Homo sapiens	91-94
27274280-5	2016	Moreover, the phosphorylation of AMP-activated protein kinase (AMPK) and the expression of p53 were increased upon metformin treatment, and the inhibition of p53 abrogated the induction of miR-23a by metformin, suggesting that AMPK/p53 signaling axis is responsible for the induction of miR-23a by metformin.	Metformin	115-124	P53	Homo sapiens	158-161
27274280-5	2016	Moreover, the phosphorylation of AMP-activated protein kinase (AMPK) and the expression of p53 were increased upon metformin treatment, and the inhibition of p53 abrogated the induction of miR-23a by metformin, suggesting that AMPK/p53 signaling axis is responsible for the induction of miR-23a by metformin.	Metformin	115-124	P53	Homo sapiens	158-161
27274280-5	2016	Moreover, the phosphorylation of AMP-activated protein kinase (AMPK) and the expression of p53 were increased upon metformin treatment, and the inhibition of p53 abrogated the induction of miR-23a by metformin, suggesting that AMPK/p53 signaling axis is responsible for the induction of miR-23a by metformin.	Metformin	200-209	P53	Homo sapiens	91-94
27274280-5	2016	Moreover, the phosphorylation of AMP-activated protein kinase (AMPK) and the expression of p53 were increased upon metformin treatment, and the inhibition of p53 abrogated the induction of miR-23a by metformin, suggesting that AMPK/p53 signaling axis is responsible for the induction of miR-23a by metformin.	Metformin	200-209	P53	Homo sapiens	158-161
27274280-5	2016	Moreover, the phosphorylation of AMP-activated protein kinase (AMPK) and the expression of p53 were increased upon metformin treatment, and the inhibition of p53 abrogated the induction of miR-23a by metformin, suggesting that AMPK/p53 signaling axis is responsible for the induction of miR-23a by metformin.	Metformin	200-209	P53	Homo sapiens	158-161
26965143-4	2016	Interestingly, mutant p53 ubiquitination status was regulated by ataxia-telangectasia mutated (ATM) activation and downstream phosphorylation of mutant p53 (serine 15), both in resting and in genotoxin-treated lung cancer cells.	Serine	157-163	P53	Homo sapiens	22-25
26984266-11	2016	Based on these results, kaempferol-induced HUVEC apoptosis was involved in an ROS-mediated p53/ATM/death receptor signaling.	Reactive Oxygen Species	78-81	P53	Homo sapiens	91-94
26984670-1	2016	In the present study, we investigated the effects and molecular mechanism of 5-caffeoylquinic acid (5-CQA), a natural phenolic compound isolated from Ligularia fischeri, on cell invasion, proliferation and adhesion in p53 wild-type A549 and p53-deficient H1299 non-small cell lung cancer (NSCLC) cells.	Chlorogenic Acid	100-105	P53	Homo sapiens	218-221
26728272-0	2016	Neuropeptide Y protects kidney against cisplatin-induced nephrotoxicity by regulating p53-dependent apoptosis pathway.	Cisplatin	39-48	P53	Homo sapiens	86-89
26965143-4	2016	Interestingly, mutant p53 ubiquitination status was regulated by ataxia-telangectasia mutated (ATM) activation and downstream phosphorylation of mutant p53 (serine 15), both in resting and in genotoxin-treated lung cancer cells.	Serine	157-163	P53	Homo sapiens	152-155
26936454-7	2016	Furthermore, CA generated reactive oxygen species (ROS), and pretreatment with ROS scavenger N-acetyl cysteine (NAC) abrogated CA-induced cleavage of PARP and expression of p53.	Reactive Oxygen Species	79-82	P53	Homo sapiens	173-176
26892272-5	2016	Co-treatment with lupeol and 5-Fu induced apoptosis through up-regulating the expressions of Bax and p53 and down-regulating the expressions of survivin and Bcl-2.	Fluorouracil	29-33	P53	Homo sapiens	101-104
26987028-10	2016	The results showed that both GA and cisplatin changed the morphology, inhibited the growth and induced apoptosis in the H446 cells by inducing generation of ROS, disruption of MMP, downregulation of XIAP expression, and upregulation of Bax, Apaf-1, DIABLO and p53 expression.	Cisplatin	36-45	P53	Homo sapiens	260-263
26936454-7	2016	Furthermore, CA generated reactive oxygen species (ROS), and pretreatment with ROS scavenger N-acetyl cysteine (NAC) abrogated CA-induced cleavage of PARP and expression of p53.	Acetylcysteine	93-110	P53	Homo sapiens	173-176
26936454-7	2016	Furthermore, CA generated reactive oxygen species (ROS), and pretreatment with ROS scavenger N-acetyl cysteine (NAC) abrogated CA-induced cleavage of PARP and expression of p53.	Acetylcysteine	112-115	P53	Homo sapiens	173-176
26662955-6	2016	However, Notch1 mRNA high expression is significantly associated with worsen OS in TP53 wild-type ovarian cancer patients, while it is significantly associated with better OS in TP53 mutation-type ovarian cancer patients.	Osmium	77-79	P53	Homo sapiens	83-87
27313779-5	2016	Platinum increased p53 in a dose-dependent and time-dependent manner.	Platinum	0-8	P53	Homo sapiens	19-22
27125496-5	2016	This approach yielded yet-undescribed guinea pig monoclonal antibodies against threonine 18-phosphorylated p53 and threonine 68-phosphorylated CHK2 with high affinity and specificity.	Threonine	79-88	P53	Homo sapiens	107-110
26596838-0	2016	Aspirin acetylates wild type and mutant p53 in colon cancer cells: identification of aspirin acetylated sites on recombinant p53.	Aspirin	0-7	P53	Homo sapiens	40-43
26596838-0	2016	Aspirin acetylates wild type and mutant p53 in colon cancer cells: identification of aspirin acetylated sites on recombinant p53.	Aspirin	0-7	P53	Homo sapiens	125-128
26596838-0	2016	Aspirin acetylates wild type and mutant p53 in colon cancer cells: identification of aspirin acetylated sites on recombinant p53.	Aspirin	85-92	P53	Homo sapiens	125-128
26596838-2	2016	We previously demonstrated that aspirin acetylated the tumor suppressor protein p53 at lysine 382 in MDA-MB-231 human breast cancer cells.	Aspirin	32-39	P53	Homo sapiens	80-83
26596838-2	2016	We previously demonstrated that aspirin acetylated the tumor suppressor protein p53 at lysine 382 in MDA-MB-231 human breast cancer cells.	Lysine	87-93	P53	Homo sapiens	80-83
26596838-4	2016	We demonstrate that aspirin induced acetylation of p53 in both cell lines in a concentration-dependent manner.	Aspirin	20-27	P53	Homo sapiens	51-54
26596838-5	2016	Aspirin-acetylated p53 was localized to the nucleus.	Aspirin	0-7	P53	Homo sapiens	19-22
26596838-7	2016	Aspirin also acetylated recombinant p53 (rp53) in vitro suggesting that it occurs through a non-enzymatic chemical reaction.	Aspirin	0-7	P53	Homo sapiens	36-39
26596838-10	2016	Our results suggest that aspirin"s anti-cancer effect may involve acetylation and activation of wild type and mutant p53 and induction of target gene expression.	Aspirin	25-32	P53	Homo sapiens	117-120
26596838-11	2016	This is the first report attempting to characterize p53 acetylation sites targeted by aspirin.	Aspirin	86-93	P53	Homo sapiens	52-55
26996126-0	2016	Cisplatin-induced apoptosis in non-small-cell lung cancer cells is dependent on Bax- and Bak-induction pathway and synergistically activated by BH3-mimetic ABT-263 in p53 wild-type and mutant cells.	Cisplatin	0-9	P53	Homo sapiens	167-170
26996126-0	2016	Cisplatin-induced apoptosis in non-small-cell lung cancer cells is dependent on Bax- and Bak-induction pathway and synergistically activated by BH3-mimetic ABT-263 in p53 wild-type and mutant cells.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	156-159	P53	Homo sapiens	167-170
26996126-2	2016	Accumulating evidence has shown that cisplatin activates the p53-dependent apoptotic pathway, but it also induces apoptosis in p53-mutated cancer cells.	Cisplatin	37-46	P53	Homo sapiens	61-64
26996126-2	2016	Accumulating evidence has shown that cisplatin activates the p53-dependent apoptotic pathway, but it also induces apoptosis in p53-mutated cancer cells.	Cisplatin	37-46	P53	Homo sapiens	127-130
26996126-4	2016	In contrast, the expression of proapoptotic multidomain Bcl-2-family members, Bak and Bax, was induced by cisplatin in p53-dependent and -independent manners, respectively.	Cisplatin	106-115	P53	Homo sapiens	119-122
26996126-5	2016	Moreover, in wild-type p53-expressing cells, cisplatin mainly used the Bak-dependent apoptotic pathway, but this apoptotic pathway shifted to the Bax-dependent pathway by loss-of-function of p53.	Cisplatin	45-54	P53	Homo sapiens	23-26
26996126-7	2016	From this result, we tested the effect of ABT-263 (Navitoclax), the specific inhibitor of Bcl-2 and Bcl-XL, but not Mcl-1, and found that ABT-263 synergistically enhanced cisplatin-induced apoptosis in NSCLC cells in the presence or absence of p53.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	138-141	P53	Homo sapiens	244-247
27313779-6	2016	There was no detectable difference in basal p53 levels between 3D cultures and 2D cultures but cisplatin induced less p53 in both HCT116 3D cultures and LoVo 3D cultures.	Cisplatin	95-104	P53	Homo sapiens	118-121
27313779-8	2016	Knockdown of p53 significantly decreased sensitivity to platinum in 3D cultures.	Platinum	56-64	P53	Homo sapiens	13-16
27313779-9	2016	Knockdown of p53 decreased cleaved caspase 3 and apoptosis induced by cisplatin.	Cisplatin	70-79	P53	Homo sapiens	13-16
27313779-11	2016	Knockdown of p53 decreased cisplatin"s induction of c-Jun N-terminal kinase 1/2 (JNK1/2) activation, whereas inhibition of JNK1/2 activation increased chemosensitivity.	Cisplatin	27-36	P53	Homo sapiens	13-16
27313779-12	2016	Inhibition of p38 activation decreased cisplatin"s induction of p53, but no difference in p38 activation by cisplatin was observed between 2D cultures and 3D cultures.	Cisplatin	39-48	P53	Homo sapiens	64-67
27313779-13	2016	Taken together, our results suggest that p53 is involved in a 3D architecture-mediated decrease in chemosensitivity to platinum in colon cancer.	Platinum	119-127	P53	Homo sapiens	41-44
27012201-7	2016	Notably, chemotherapeutic reagent cisplatin induction of p53 is markedly attenuated in response to ectopic expression of TRIM65.	Cisplatin	34-43	P53	Homo sapiens	57-60
27128904-0	2016	Protective Effect of Tyrosol and S-Adenosylmethionine against Ethanol-Induced Oxidative Stress of Hepg2 Cells Involves Sirtuin 1, P53 and Erk1/2 Signaling.	4-hydroxyphenylethanol	21-28	P53	Homo sapiens	130-133
27128904-0	2016	Protective Effect of Tyrosol and S-Adenosylmethionine against Ethanol-Induced Oxidative Stress of Hepg2 Cells Involves Sirtuin 1, P53 and Erk1/2 Signaling.	S-Adenosylmethionine	33-53	P53	Homo sapiens	130-133
27128904-0	2016	Protective Effect of Tyrosol and S-Adenosylmethionine against Ethanol-Induced Oxidative Stress of Hepg2 Cells Involves Sirtuin 1, P53 and Erk1/2 Signaling.	Ethanol	62-69	P53	Homo sapiens	130-133
27097159-8	2016	AK301 selectively targeted APC-mutant colonocytes and promoted TNF-induced apoptosis in p53-mutant colon cancer cells.	MLS000061043	0-5	P53	Homo sapiens	88-91
27102814-13	2016	The increased ROS production up-regulated the p53 protein level, which led to the up-regulation of Bax and down-regulation of Bcl-2.	Reactive Oxygen Species	14-17	P53	Homo sapiens	46-49
27547448-7	2016	Consistent with the inhibitory effect of PXR on p53, elevated PXR levels decreased doxorubicin- or nutlin-3a-mediated toxicity and promoted malignant transformation in colon cancer cells.	Doxorubicin	83-94	P53	Homo sapiens	48-51
26967060-6	2016	This appears to be related to reduced phosphorylation of serine residues in both N-terminal and C-terminal regions of the p53 molecule.	Serine	57-63	P53	Homo sapiens	122-125
27104558-9	2016	Pre-treating hepatocytes with insulin significantly stimulated phosphorylated-Akt and reversed SFA-induced up-regulation of p53.	Fatty Acids	95-98	P53	Homo sapiens	124-127
27104558-14	2016	Our study demonstrated that insulin strongly protected against SFA-induced lipotoxicity in hepatocytes mechanistically through alleviating ER stress via a PI3K/Akt/p53 involved pathway but independently from autophagy.	Fatty Acids	63-66	P53	Homo sapiens	164-167
26764206-6	2016	Extending our observation of p53 inhibition on proximal tubule glucose tracer uptake, we demonstrated by intravital MPM that pharmacological inhibition of p53 diminishes mitochondrial potential difference.	Glucose	63-70	P53	Homo sapiens	29-32
26764206-6	2016	Extending our observation of p53 inhibition on proximal tubule glucose tracer uptake, we demonstrated by intravital MPM that pharmacological inhibition of p53 diminishes mitochondrial potential difference.	Glucose	63-70	P53	Homo sapiens	155-158
27077811-5	2016	Another criterion of the screen was increased sensitivity of p53-negative tumor cells to cisplatin (CDDP) in a Wip1-dependent manner.	Cisplatin	89-98	P53	Homo sapiens	61-64
26982372-3	2016	Linking benzamide substrates with a rotatable C-N bond, we constructed a novel semirigid pyramid-like scaffold that could support its two-turn alpha-helix mimicry without aromatic stacking interactions and could adopt the different dihedral angles of the key residues of p53 and BH3-only peptides.	benzamide	8-17	P53	Homo sapiens	271-274
26982372-3	2016	Linking benzamide substrates with a rotatable C-N bond, we constructed a novel semirigid pyramid-like scaffold that could support its two-turn alpha-helix mimicry without aromatic stacking interactions and could adopt the different dihedral angles of the key residues of p53 and BH3-only peptides.	Carbon	46-47	P53	Homo sapiens	271-274
26982372-3	2016	Linking benzamide substrates with a rotatable C-N bond, we constructed a novel semirigid pyramid-like scaffold that could support its two-turn alpha-helix mimicry without aromatic stacking interactions and could adopt the different dihedral angles of the key residues of p53 and BH3-only peptides.	Nitrogen	48-49	P53	Homo sapiens	271-274
27077811-5	2016	Another criterion of the screen was increased sensitivity of p53-negative tumor cells to cisplatin (CDDP) in a Wip1-dependent manner.	Cisplatin	100-104	P53	Homo sapiens	61-64
27077811-6	2016	We have found that a treatment with a low dose (75 nM) of MK-1775, a recently described specific chemical inhibitor of Wee1, decreases CDDP-induced H2AX phosphorylation in p53-negative cells and enhances the Wip1-sensitization of p53-negative tumors.	Cisplatin	135-139	P53	Homo sapiens	172-175
27077811-6	2016	We have found that a treatment with a low dose (75 nM) of MK-1775, a recently described specific chemical inhibitor of Wee1, decreases CDDP-induced H2AX phosphorylation in p53-negative cells and enhances the Wip1-sensitization of p53-negative tumors.	Cisplatin	135-139	P53	Homo sapiens	230-233
32263194-12	2016	In conclusion, GNP-(PHA-E)-GEM could induce growth inhibition and cytotoxicity, which was mediated through inhibition of EGFR phosphorylation and the switching on of p53 that causes cell apoptosis of NSCLC cells A-549 and H292.	gnp-(pha-e)-gem	15-30	P53	Homo sapiens	166-169
26840531-5	2016	Moreover, Tf-NGO@HPIP effectively induced cancer-cell apoptosis through activation of superoxide-mediated p53 and MAPK pathways along with inactivation of ERK and AKT.	Superoxides	86-96	P53	Homo sapiens	106-109
26967561-1	2016	We have previously shown that melatonin exerts tumor suppressor activities by inducing the p38-p53 axis.	Melatonin	30-39	P53	Homo sapiens	95-98
27067391-6	2016	Custom oligonucleotide baits spanning the complete coding, non-coding, and intergenic regions 10 kb up- and downstream of ATM, BRCA1, BRCA2, CDH1, CHEK2, PALB2, and TP53 were synthesized for solution hybridization enrichment.	Oligonucleotides	7-22	P53	Homo sapiens	165-169
26148235-3	2016	Interestingly, RNF31 decreased p53 stability, whereas depletion of RNF31 in breast cancer cells caused cell cycle arrest and cisplatin-induced apoptosis in a p53-dependent manner.	Cisplatin	125-134	P53	Homo sapiens	158-161
26148237-7	2016	Comparative X-ray crystallographic analyses of MDMX and of pTyr99 MDMX in complex with PMI as well as modeling studies reveal that the phosphate group of pTyr99 imposes extensive steric clashes with the C-terminus of PMI or p53 peptide and induces a significant lateral shift of the peptide ligand, contributing to the dramatic decrease in the binding affinity of MDMX for p53.	Phosphates	135-144	P53	Homo sapiens	224-227
26148237-7	2016	Comparative X-ray crystallographic analyses of MDMX and of pTyr99 MDMX in complex with PMI as well as modeling studies reveal that the phosphate group of pTyr99 imposes extensive steric clashes with the C-terminus of PMI or p53 peptide and induces a significant lateral shift of the peptide ligand, contributing to the dramatic decrease in the binding affinity of MDMX for p53.	Phosphates	135-144	P53	Homo sapiens	373-376
26942697-0	2016	Repeated PM2.5 exposure inhibits BEAS-2B cell P53 expression through ROS-Akt-DNMT3B pathway-mediated promoter hypermethylation.	ros	69-72	P53	Homo sapiens	46-49
26942697-8	2016	In conclusion, our results strongly suggest that repeated exposure to PM2.5 induces epigenetic silencing of P53 through ROS-Akt-DNMT3B pathway-mediated promoter hypermethylation, which not only provides a possible explanation for PM-induced lung cancer, but also may help to identify specific interventions to prevent PM-induced lung carcinogenesis.	ros	120-123	P53	Homo sapiens	108-111
27070592-5	2016	In addition, suppression of mTOR activity by rapamycin decreased the level of activity of p70S6K, induced upregulation of p53 and caspase 3, and led to increase of apoptosis in K562R(IMT) cells.	Sirolimus	45-54	P53	Homo sapiens	122-125
27044825-14	2016	sCD40L in combination with cisplatin decreased the expression levels of GST-pi, LRP, Survivin, p53 and Bcl-2 in both epithelial ovarian cancer cell lines.	Cisplatin	27-36	P53	Homo sapiens	95-98
26842845-5	2016	This inhibition was due to the Profilin mediated attenuation of IkappaBalpha degradation, thereby preventing p65 nuclear translocation and low NF-kappaB DNA binding activity.Moreover, Profilin increases level of p53 in the presence of known inducers, such as doxorubicin, vinblastine, and benzofuran.	Doxorubicin	259-270	P53	Homo sapiens	212-215
26704388-11	2016	A role for p53 appears important as GCS-100 induces p53 expression and shRNA knockdown of p53 protected OCI-AML3 cells from the cytotoxic effects of the GCS-100/ABT-737 treatment combination.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	161-164	P53	Homo sapiens	11-14
26704388-11	2016	A role for p53 appears important as GCS-100 induces p53 expression and shRNA knockdown of p53 protected OCI-AML3 cells from the cytotoxic effects of the GCS-100/ABT-737 treatment combination.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	161-164	P53	Homo sapiens	52-55
26704388-11	2016	A role for p53 appears important as GCS-100 induces p53 expression and shRNA knockdown of p53 protected OCI-AML3 cells from the cytotoxic effects of the GCS-100/ABT-737 treatment combination.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	161-164	P53	Homo sapiens	52-55
27044842-0	2016	The novel anthraquinone derivative IMP1338 induces death of human cancer cells by p53-independent S and G2/M cell cycle arrest.	Anthraquinones	10-23	P53	Homo sapiens	82-85
27044825-15	2016	The protein expression level of GST-pi, LRP and P53 protein was also decreased upon sCD40L in combination with cisplatin although the expression level of Bcl-2 and survivin protein had no significant difference.	Cisplatin	111-120	P53	Homo sapiens	48-51
27044842-7	2016	In addition, IMP1338 markedly induced the phosphorylation of histone H2AX and Chk1 in both cell lines while the combination of 5-fluorouracil (5-FU) and radiation inhibited the viability of HCT116, HCT116 p53(-/-), and HT29 cells compared to 5-FU or radiation alone.	Fluorouracil	127-141	P53	Homo sapiens	205-208
26851235-2	2016	Although gene association network analysis demonstrated gene expression profile changes in the liver of human TP53 knock-in mice after acute AAI exposure, to date, whether AAI causes hepatic tumorigenesis is still not confirmed.	aristolochic acid I	141-144	P53	Homo sapiens	110-114
27044842-7	2016	In addition, IMP1338 markedly induced the phosphorylation of histone H2AX and Chk1 in both cell lines while the combination of 5-fluorouracil (5-FU) and radiation inhibited the viability of HCT116, HCT116 p53(-/-), and HT29 cells compared to 5-FU or radiation alone.	Fluorouracil	143-147	P53	Homo sapiens	205-208
26851285-0	2016	Acetylation of p53 Protein at Lysine 120 Up-regulates Apaf-1 Protein and Sensitizes the Mitochondrial Apoptotic Pathway.	Lysine	30-36	P53	Homo sapiens	15-18
26851285-3	2016	Here we demonstrate that acetylation of p53 at Lys-120 up-regulates its transcriptional activity toward Apaf-1, a core component in the mitochondrial apoptotic pathway, and thus sensitizes caspase activation and apoptosis.	Lysine	47-50	P53	Homo sapiens	40-43
26851285-7	2016	Therefore, HDAC inhibitors can induce p53 acetylation at lysine 120, which in turn enhances mitochondrion-mediated apoptosis through transcriptional up-regulation of Apaf-1.	Lysine	57-63	P53	Homo sapiens	38-41
26851285-4	2016	We found that histone deacetylase (HDAC) inhibitors, including butyrate, augment Lys-120 acetylation of p53 and thus Apaf-1 expression by inhibiting HDAC1.	Lysine	81-84	P53	Homo sapiens	104-107
26684585-2	2016	It has recently been reported that p53 regulates glucose metabolism and that an increase in p53 protein level is induced after serum deprivation or treatments with a natural compound,trans-Resveratrol (Rsv).	Resveratrol	183-200	P53	Homo sapiens	35-38
26684585-2	2016	It has recently been reported that p53 regulates glucose metabolism and that an increase in p53 protein level is induced after serum deprivation or treatments with a natural compound,trans-Resveratrol (Rsv).	Resveratrol	183-200	P53	Homo sapiens	92-95
26826118-0	2016	Sequential Combination Therapy of CDK Inhibition and Doxorubicin Is Synthetically Lethal in p53-Mutant Triple-Negative Breast Cancer.	Doxorubicin	53-64	P53	Homo sapiens	92-95
26936104-0	2016	Paeoniflorin attenuates ultraviolet B-induced apoptosis in human keratinocytes by inhibiting the ROS-p38-p53 pathway.	Reactive Oxygen Species	97-100	P53	Homo sapiens	105-108
26936104-6	2016	The present study evaluated the protective effects of PF on UV-induced skin damage in vitro, and demonstrated that the effects were mediated via the ROS-p38-p53 pathway.	Reactive Oxygen Species	149-152	P53	Homo sapiens	157-160
26936104-11	2016	Notably, these effects were shown to be mediated, at least in part, via inhibition of the ROS-p38-p53 pathway.	Reactive Oxygen Species	90-93	P53	Homo sapiens	98-101
26936104-9	2016	Treatment with PF markedly reduced the production of ROS, and inhibited the activation of p38 and p53 in human keratinocytes, thus suggesting that the ROS-p38-p53 pathway has a role in UV-B-induced skin damage.	Reactive Oxygen Species	151-154	P53	Homo sapiens	98-101
26891889-5	2016	Sublytic concentrations of hydrogen peroxide (H2O2) plus NO donor S-nitroso-N-acetyl-D, L-penicillamine (SNAP) enabled to induce a toxic oxidative/nitrosative stress through activating both p38 MAPK and p53 cascades, and cause DNA damage and protein tyrosine nitration in primary neuronal cultures.	Hydrogen Peroxide	27-44	P53	Homo sapiens	203-206
26891889-5	2016	Sublytic concentrations of hydrogen peroxide (H2O2) plus NO donor S-nitroso-N-acetyl-D, L-penicillamine (SNAP) enabled to induce a toxic oxidative/nitrosative stress through activating both p38 MAPK and p53 cascades, and cause DNA damage and protein tyrosine nitration in primary neuronal cultures.	Hydrogen Peroxide	46-50	P53	Homo sapiens	203-206
26508031-10	2016	Moreover, esculetin increased the percentage of cells in G2/M phase and regulated the expressions of p53, p21, CDK1, and cyclin B1.	esculetin	10-19	P53	Homo sapiens	101-104
27073477-1	2016	The Ras family small guanosine 5"-triphosphate (GTP)-binding protein Rap2B is is a member of the Ras oncogene family and a novel target of p53 that regulates the p53-mediated pro-survival function of cells.	Guanosine Triphosphate	21-46	P53	Homo sapiens	139-142
27073477-1	2016	The Ras family small guanosine 5"-triphosphate (GTP)-binding protein Rap2B is is a member of the Ras oncogene family and a novel target of p53 that regulates the p53-mediated pro-survival function of cells.	Guanosine Triphosphate	21-46	P53	Homo sapiens	162-165
27073477-1	2016	The Ras family small guanosine 5"-triphosphate (GTP)-binding protein Rap2B is is a member of the Ras oncogene family and a novel target of p53 that regulates the p53-mediated pro-survival function of cells.	Guanosine Triphosphate	48-51	P53	Homo sapiens	139-142
27073477-1	2016	The Ras family small guanosine 5"-triphosphate (GTP)-binding protein Rap2B is is a member of the Ras oncogene family and a novel target of p53 that regulates the p53-mediated pro-survival function of cells.	Guanosine Triphosphate	48-51	P53	Homo sapiens	162-165
27030982-4	2016	However, the cellular response encompassing ataxia-telangiectasia mutated kinase activation and p53 phosphorylation both on serine 15 as well as on serine 46 resulted very similar among the aforementioned cell types.	Serine	124-130	P53	Homo sapiens	96-99
27031960-7	2016	In addition to the increase in p53 stability due to TGase 2 inhibition, the administration of a DNA-damaging anti-cancer drug such as doxorubicin-induced apoptosis in RCC cell lines and synergistically reduced tumor volume in a xenograft model.	Doxorubicin	134-145	P53	Homo sapiens	31-34
27030982-4	2016	However, the cellular response encompassing ataxia-telangiectasia mutated kinase activation and p53 phosphorylation both on serine 15 as well as on serine 46 resulted very similar among the aforementioned cell types.	Serine	148-154	P53	Homo sapiens	96-99
26909605-8	2016	Furthermore, in cell culture models, ERalpha positively regulates MDM4 and MDM2 expression via p53-independent mechanisms, and these effects can be blocked by the clinically-relevant endocrine therapies fulvestrant and tamoxifen.	Tamoxifen	219-228	P53	Homo sapiens	95-98
26883108-7	2016	In addition, combined treatment with GSK2830371 and doxorubicin or nutlin-3 potentiated cell death through a strong induction of p53 pathway and activation of caspase 9.	Doxorubicin	52-63	P53	Homo sapiens	129-132
26976603-1	2016	An important component of the activity of p53 as a tumor suppressor is its interaction with the transcriptional coactivators cyclic-AMP response element-binding protein (CREB)-binding protein (CBP) and p300, which activate transcription of p53-regulated stress response genes and stabilize p53 against ubiquitin-mediated degradation.	Cyclic AMP	125-135	P53	Homo sapiens	42-45
26976603-1	2016	An important component of the activity of p53 as a tumor suppressor is its interaction with the transcriptional coactivators cyclic-AMP response element-binding protein (CREB)-binding protein (CBP) and p300, which activate transcription of p53-regulated stress response genes and stabilize p53 against ubiquitin-mediated degradation.	Cyclic AMP	125-135	P53	Homo sapiens	240-243
26976603-1	2016	An important component of the activity of p53 as a tumor suppressor is its interaction with the transcriptional coactivators cyclic-AMP response element-binding protein (CREB)-binding protein (CBP) and p300, which activate transcription of p53-regulated stress response genes and stabilize p53 against ubiquitin-mediated degradation.	Cyclic AMP	125-135	P53	Homo sapiens	240-243
26812210-10	2016	A p53-derived peptide binds with high affinity (Kd value of 150nM) and causes the formation of an extensive network of hydrogen bonds within MdmX; this constitutes the induction of order within MdmX through ligand binding.	Hydrogen	119-127	P53	Homo sapiens	2-5
26934645-7	2016	Moreover, N-acetylcysteine (reactive oxygen species scavenger) blocked the SK inhibitor-induced increase in p21 and p53 expression but had no effect on the proteasomal degradation of SK1a.	Acetylcysteine	10-26	P53	Homo sapiens	116-119
26934645-7	2016	Moreover, N-acetylcysteine (reactive oxygen species scavenger) blocked the SK inhibitor-induced increase in p21 and p53 expression but had no effect on the proteasomal degradation of SK1a.	Reactive Oxygen Species	28-51	P53	Homo sapiens	116-119
26958937-0	2016	Oroxylin A modulates mitochondrial function and apoptosis in human colon cancer cells by inducing mitochondrial translocation of wild-type p53.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	0-10	P53	Homo sapiens	139-142
26958937-5	2016	We determined that oroxylin A induces p53 mitochondrial translocation and inhibits SOD2 activity.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	19-29	P53	Homo sapiens	38-41
26958937-6	2016	Additionally, our studies demonstrate that oroxylin A promotes the formation and mitochondrial translocation of the p53-Recql4 complex in HCT-116 cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	43-53	P53	Homo sapiens	116-119
26958937-7	2016	Finally, we showed that oroxylin A triggers cytosolic p53 activation, thereby promoting apoptosis.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	24-34	P53	Homo sapiens	54-57
26958937-9	2016	Thus, oroxylin A induces mitochondrial translocation of p53 and leads to mitochondrial dysfunction in human colon cancer cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	6-16	P53	Homo sapiens	56-59
26986569-13	2016	In the same cells, the amide also increased the acetylation of lysine (K382) in p53, but not (K305).	Lysine	63-69	P53	Homo sapiens	80-83
26575022-5	2016	We demonstrate for the first time that DOX-induced cell detachment is associated with p73 cleavage and caspase activation, independently of the p53 status.	Doxorubicin	39-42	P53	Homo sapiens	144-147
26982218-7	2016	We experimentally verify that prolonged exposure to low doses of BPA results in a delayed response to UV-C-induced DNA damage, due to impairment of p21-Tp53 axis, with the BPA-treated cells more prone to cell death and DNA damage accumulation.	bisphenol A	65-68	P53	Homo sapiens	152-156
26982218-7	2016	We experimentally verify that prolonged exposure to low doses of BPA results in a delayed response to UV-C-induced DNA damage, due to impairment of p21-Tp53 axis, with the BPA-treated cells more prone to cell death and DNA damage accumulation.	bisphenol A	172-175	P53	Homo sapiens	152-156
26974436-12	2016	Treatment with DMDP-1 &amp; -2 also showed up-regulation of total and phosphorylated p53 levels in a time dependent manner.	Adenosine Monophosphate	23-26	P53	Homo sapiens	85-88
26969379-2	2016	PURPOSE: In this study the effects of naturally occurring homochelidonine in comparison to chelidonine on cell cycle progression and cell death in leukemic T-cells with different p53 status are described.	homochelidonine	58-73	P53	Homo sapiens	179-182
26974552-0	2016	Correction: Curcumin Significantly Enhances Dual PI3K/Akt and mTOR Inhibitor NVP-BEZ235-Induced Apoptosis in Human Renal Carcinoma Caki Cells through Down-Regulation of p53-Dependent Bcl-2 Expression and Inhibition of Mcl-1 Protein Stability.	Curcumin	12-20	P53	Homo sapiens	169-172
26883465-0	2016	Meeting Organocatalysis with Drug Discovery: Asymmetric Synthesis of 3,3"-Spirooxindoles Fused with Tetrahydrothiopyrans as Novel p53-MDM2 Inhibitors.	3,3"-spirooxindoles	69-88	P53	Homo sapiens	130-133
26800624-11	2016	The TPP-BLM treatment synergistically induced apoptosis through caspase-3, caspase-8 and caspase-9 activation, Bcl-2 upregulation and p53 overexpression.	tpp-blm	4-11	P53	Homo sapiens	134-137
26909609-5	2016	Furthermore, co-suppression of RelB or p53 with ARNT isoform 1 prevented cell cycle arrest and blocked doxorubicin induced apoptosis.	Doxorubicin	103-114	P53	Homo sapiens	39-42
26874277-2	2016	Pin1 binds phosphorylated p53 and stabilizes p53 to cause cell cycle arrest and apoptosis quickly in response to doxorubicin.	Doxorubicin	113-124	P53	Homo sapiens	26-29
26874277-2	2016	Pin1 binds phosphorylated p53 and stabilizes p53 to cause cell cycle arrest and apoptosis quickly in response to doxorubicin.	Doxorubicin	113-124	P53	Homo sapiens	45-48
26646755-0	2016	TP53 mutational status is predictive of pazopanib response in advanced sarcomas.	pazopanib	40-49	P53	Homo sapiens	0-4
26872218-5	2016	2alpha-Hydroxyursolic acid significantly down-regulated expressions of TRAF2, PCNA, cyclin D1, and CDK4 and up-regulated the expressions of p-ASK1, p-p38, p-p53, and p-21.	2-hydroxyursolic acid	0-26	P53	Homo sapiens	157-160
26358154-4	2016	In this study, we utilized our microarray data to identify and characterize novel p53 target genes expressed in human liver cells and associated with steroid hormones processing and transfer.	Steroids	150-166	P53	Homo sapiens	82-85
26427013-4	2016	All the three copper complexes can effectively induce apoptosis of the three human tumor cells, which was accompanied with upregulation of the expression of p53 and Bax, while Bcl-2 decreased.	Copper	14-20	P53	Homo sapiens	157-160
26739061-0	2016	Astemizole-Histamine induces Beclin-1-independent autophagy by targeting p53-dependent crosstalk between autophagy and apoptosis.	Histamine	11-20	P53	Homo sapiens	73-76
26358154-5	2016	We identified the steroid hormones binding factors, sex hormone-binding globulin (SHBG), corticosteroid-binding globulin (CBG) and cytochrome P450 family 21 subfamily A polypeptide 2, as novel p53 target genes.	Steroids	18-25	P53	Homo sapiens	193-196
26358154-8	2016	We demonstrated that the induction of the steroid hormones binding factors can be mediated by binding to specific p53 responsive elements within their promoters.	Steroids	42-49	P53	Homo sapiens	114-117
26775629-5	2016	Using BCC/KMC1 cell line as a model, the upstream signaling of p53 activation was dissected by over-expression of TLR7/8, the addition of ROS scavenger, ATM/ATR inhibitors and pan-caspase inhibitor.	ros	138-141	P53	Homo sapiens	63-66
26757339-5	2016	We showed that cathepsin L activity was decreased in HCT116 p53(+/+) cells after adriamycin treatment, but not in HCT116 p53(-/-) cells.	Doxorubicin	81-91	P53	Homo sapiens	60-63
26341473-6	2016	We provide evidence that the decreases in SIRT1 activity and expression facilitated by increasing poly(ADP-ribose) polymerase-1 (PARP-1) activation and microRNA-34a levels through cisplatin-mediated p53 activation aggravate the associated ototoxicity.	Cisplatin	180-189	P53	Homo sapiens	199-202
26794443-7	2016	In contrast, NADPH oxidase and p53 (especially acetylation-defective mutant p53) act as positive regulators of ferroptosis by promotion of ROS production and inhibition of expression of SLC7A11 (a specific light-chain subunit of the cystine/glutamate antiporter), respectively.	Reactive Oxygen Species	139-142	P53	Homo sapiens	31-34
26794443-7	2016	In contrast, NADPH oxidase and p53 (especially acetylation-defective mutant p53) act as positive regulators of ferroptosis by promotion of ROS production and inhibition of expression of SLC7A11 (a specific light-chain subunit of the cystine/glutamate antiporter), respectively.	Reactive Oxygen Species	139-142	P53	Homo sapiens	76-79
26794443-7	2016	In contrast, NADPH oxidase and p53 (especially acetylation-defective mutant p53) act as positive regulators of ferroptosis by promotion of ROS production and inhibition of expression of SLC7A11 (a specific light-chain subunit of the cystine/glutamate antiporter), respectively.	Glutamic Acid	241-250	P53	Homo sapiens	31-34
26794443-7	2016	In contrast, NADPH oxidase and p53 (especially acetylation-defective mutant p53) act as positive regulators of ferroptosis by promotion of ROS production and inhibition of expression of SLC7A11 (a specific light-chain subunit of the cystine/glutamate antiporter), respectively.	Glutamic Acid	241-250	P53	Homo sapiens	76-79
26479129-5	2016	RESULTS: Carvedilol decreased the protein levels of p53, Bax and cytochrome c and increased that of Bcl-2 in HL-1 cells expressing E334K MyBPC.	Carvedilol	9-19	P53	Homo sapiens	52-55
26775629-8	2016	In BCC/KMC1 cells, the induction of p53 by IMQ was achieved through increased ROS production to stimulate the ATM/ATR-Chk1/Chk2 axis but was not mediated by inducing DNA damage.	ros	78-81	P53	Homo sapiens	36-39
26824641-6	2016	Both AMPA supplementation and elevated glycine decreased the mRNA abundance of SHMT2 and tumor protein p53 (TP53), which is activated in response to cellular stress, compared to controls (P &lt;= 0.02).	Glycine	39-46	P53	Homo sapiens	103-106
26576483-9	2016	Pathway analysis revealed that elevated c-myc expression and ethanol uptake synergistically lead to strong AKT activation, Mdm2 phosphorylation and as a consequence to inhibition of p53.	Ethanol	61-68	P53	Homo sapiens	182-185
26576483-10	2016	CONCLUSIONS: Expression of c-myc and EtOH-uptake synergistically accelerate the progression of ALD most likely due to loss of p53-dependent protection.	Ethanol	37-41	P53	Homo sapiens	126-129
26824641-6	2016	Both AMPA supplementation and elevated glycine decreased the mRNA abundance of SHMT2 and tumor protein p53 (TP53), which is activated in response to cellular stress, compared to controls (P &lt;= 0.02).	Glycine	39-46	P53	Homo sapiens	108-112
26490992-0	2016	Curcumin induces apoptosis in p53-null Hep3B cells through a TAp73/DNp73-dependent pathway.	Curcumin	0-8	P53	Homo sapiens	30-33
26675982-1	2016	The TP53-induced glycolysis and apoptosis regulator (TIGAR) is a p53 target gene known to regulate glycolysis by acting as fructose bis-phosphatase (FBPase) and modulate reactive oxygen species.	Reactive Oxygen Species	170-193	P53	Homo sapiens	65-68
26581877-6	2016	Our results indicate that confinement of p53 in the cytoplasm is one of the potential mechanisms by which TPA interferes with the process of radiation-induced apoptosis in human lymphocytes.	Tetradecanoylphorbol Acetate	106-109	P53	Homo sapiens	41-44
26909997-5	2016	In TP53*11, there was 100% homozygous Glu distribution in both groups.	Glutamic Acid	38-41	P53	Homo sapiens	3-7
25961931-4	2016	In the present study we exposed a series of p53 wild-type human cancer cell lines to drugs such as actinomycin D (ActD), doxorubicin, 5-fluorouracil and CX-5461, which hinder ribosomal RNA (rRNA) synthesis.	Doxorubicin	121-132	P53	Homo sapiens	44-47
25961931-4	2016	In the present study we exposed a series of p53 wild-type human cancer cell lines to drugs such as actinomycin D (ActD), doxorubicin, 5-fluorouracil and CX-5461, which hinder ribosomal RNA (rRNA) synthesis.	Fluorouracil	134-148	P53	Homo sapiens	44-47
26912277-0	2016	Accumulation of p53 via down-regulation of UBE2D family genes is a critical pathway for cadmium-induced renal toxicity.	Cadmium	88-95	P53	Homo sapiens	16-19
26912277-2	2016	In Cd renal toxicity, p53 is thought to be involved.	Cadmium	3-5	P53	Homo sapiens	22-25
26912277-4	2016	Here, we aimed to define the association between UBE2D family members and p53-dependent apoptosis in human proximal tubular cells (HK-2 cells) treated with Cd.	Cadmium	156-158	P53	Homo sapiens	74-77
26912277-6	2016	Double knockdown of UBE2D2 and UBE2D4 caused an increase in p53 protein levels, and knockdown of p53 attenuated not only Cd-induced apoptosis, but also Cd-induced apoptosis-related gene expression (BAX and PUMA).	Cadmium	121-123	P53	Homo sapiens	97-100
26912277-6	2016	Double knockdown of UBE2D2 and UBE2D4 caused an increase in p53 protein levels, and knockdown of p53 attenuated not only Cd-induced apoptosis, but also Cd-induced apoptosis-related gene expression (BAX and PUMA).	Cadmium	152-154	P53	Homo sapiens	97-100
26912277-8	2016	These findings suggest that down-regulation of UBE2D family genes followed by accumulation of p53 in proximal tubular cells is an important mechanism for Cd-induced renal toxicity.	Cadmium	154-156	P53	Homo sapiens	94-97
26840457-5	2016	In addition, NgBR suppresses p53 protein levels through activation of the PI3K/Akt/MDM2 pathway, which promotes p53 degradation via the ubiquitin proteasome pathway and thus increases the resistance of human hepatocellular cancer cells to 5-FU.	Fluorouracil	239-243	P53	Homo sapiens	29-32
26840457-5	2016	In addition, NgBR suppresses p53 protein levels through activation of the PI3K/Akt/MDM2 pathway, which promotes p53 degradation via the ubiquitin proteasome pathway and thus increases the resistance of human hepatocellular cancer cells to 5-FU.	Fluorouracil	239-243	P53	Homo sapiens	112-115
26909997-6	2016	TP53*72 showed genotypic distribution: in the control group, there was 16.10% homozygous Pro, and 42.44% heterozygous and 41.46% homozygous Arg; in the BC group, there was 15.43% homozygous Pro, and 42.55% heterozygous and 42.02% homozygous Arg.	Arginine	140-143	P53	Homo sapiens	0-4
26909997-6	2016	TP53*72 showed genotypic distribution: in the control group, there was 16.10% homozygous Pro, and 42.44% heterozygous and 41.46% homozygous Arg; in the BC group, there was 15.43% homozygous Pro, and 42.55% heterozygous and 42.02% homozygous Arg.	Arginine	241-244	P53	Homo sapiens	0-4
26909997-10	2016	In TP53*248, there was 100% homozygous Arg distribution in both groups.	Arginine	39-42	P53	Homo sapiens	3-7
26937175-7	2016	Depletion of p53 or HIF1alpha impaired both antagonist-elicited apoptoses to differential extents, corresponding to their expression changes responding to chemical treatments, and double knockdown of p53 and HIF1alpha remarkably hindered MI-319- or rapamycin-induced apoptosis, suggesting that both p53 and HIF1alpha are involved in MDM2 or mTOR antagonist-induced apoptosis.	MI 319	238-244	P53	Homo sapiens	200-203
26937175-7	2016	Depletion of p53 or HIF1alpha impaired both antagonist-elicited apoptoses to differential extents, corresponding to their expression changes responding to chemical treatments, and double knockdown of p53 and HIF1alpha remarkably hindered MI-319- or rapamycin-induced apoptosis, suggesting that both p53 and HIF1alpha are involved in MDM2 or mTOR antagonist-induced apoptosis.	Sirolimus	249-258	P53	Homo sapiens	13-16
26937175-7	2016	Depletion of p53 or HIF1alpha impaired both antagonist-elicited apoptoses to differential extents, corresponding to their expression changes responding to chemical treatments, and double knockdown of p53 and HIF1alpha remarkably hindered MI-319- or rapamycin-induced apoptosis, suggesting that both p53 and HIF1alpha are involved in MDM2 or mTOR antagonist-induced apoptosis.	MI 319	238-244	P53	Homo sapiens	13-16
26937175-7	2016	Depletion of p53 or HIF1alpha impaired both antagonist-elicited apoptoses to differential extents, corresponding to their expression changes responding to chemical treatments, and double knockdown of p53 and HIF1alpha remarkably hindered MI-319- or rapamycin-induced apoptosis, suggesting that both p53 and HIF1alpha are involved in MDM2 or mTOR antagonist-induced apoptosis.	Sirolimus	249-258	P53	Homo sapiens	200-203
26937175-7	2016	Depletion of p53 or HIF1alpha impaired both antagonist-elicited apoptoses to differential extents, corresponding to their expression changes responding to chemical treatments, and double knockdown of p53 and HIF1alpha remarkably hindered MI-319- or rapamycin-induced apoptosis, suggesting that both p53 and HIF1alpha are involved in MDM2 or mTOR antagonist-induced apoptosis.	MI 319	238-244	P53	Homo sapiens	200-203
26937175-7	2016	Depletion of p53 or HIF1alpha impaired both antagonist-elicited apoptoses to differential extents, corresponding to their expression changes responding to chemical treatments, and double knockdown of p53 and HIF1alpha remarkably hindered MI-319- or rapamycin-induced apoptosis, suggesting that both p53 and HIF1alpha are involved in MDM2 or mTOR antagonist-induced apoptosis.	Sirolimus	249-258	P53	Homo sapiens	200-203
26799187-0	2016	p38 MAPK-induced MDM2 degradation confers paclitaxel resistance through p53-mediated regulation of EGFR in human lung cancer cells.	Paclitaxel	42-52	P53	Homo sapiens	72-75
26886852-0	2016	Comprehensive Expression Profiling and Functional Network Analysis of p53-Regulated MicroRNAs in HepG2 Cells Treated with Doxorubicin.	Doxorubicin	122-133	P53	Homo sapiens	70-73
26886852-5	2016	Here, 33 miRNAs significantly regulated by p53 (12 up-regulated and 21 down-regulated) were detected between the doxorubicin-treated and untreated HepG2 cells in two biological replicates for small RNA sequencing and 8 miRNAs have been reported previously to be associated with HCC.	Doxorubicin	113-124	P53	Homo sapiens	43-46
26799187-9	2016	These results suggest for the first time that the p38 MAPK/p53/EGFR axis is crucial for the facilitation of PTX resistance in NSCLCs.	Paclitaxel	108-111	P53	Homo sapiens	59-62
26799187-11	2016	These results provide a foundation for the future development of potential therapeutic strategies to regulate the p38 MAPK/p53/EGFR pathway for the treatment of lung cancer patients with PTX resistance.	Paclitaxel	187-190	P53	Homo sapiens	123-126
25961932-2	2016	Despite the absence of detectable DNA damage, severe hypoxia (&lt;0.1% O2) induces a DNA damage response, including the activation of p53 and subsequent induction of p53-dependent apoptosis.	Oxygen	71-73	P53	Homo sapiens	134-137
26875667-7	2016	Repression of ATMIN in hypoxia is mediated by both p53 and HIF-1alpha in an oxygen dependent manner.	Oxygen	76-82	P53	Homo sapiens	51-54
25961932-2	2016	Despite the absence of detectable DNA damage, severe hypoxia (&lt;0.1% O2) induces a DNA damage response, including the activation of p53 and subsequent induction of p53-dependent apoptosis.	Oxygen	71-73	P53	Homo sapiens	166-169
26865836-11	2015	ICC analysis for bcl2 and p53 also confirmed our results; in treated samples for the dose of LD50 in 24 and 48 h of cisplatin and hypercin, more cells expressed p53 (guardian of cells in front of tumor formation/progression) and less expressed bcl2 (which has anti apoptotic activity) compared to untreated samples.	Cisplatin	116-125	P53	Homo sapiens	26-29
26865836-11	2015	ICC analysis for bcl2 and p53 also confirmed our results; in treated samples for the dose of LD50 in 24 and 48 h of cisplatin and hypercin, more cells expressed p53 (guardian of cells in front of tumor formation/progression) and less expressed bcl2 (which has anti apoptotic activity) compared to untreated samples.	Cisplatin	116-125	P53	Homo sapiens	161-164
26768586-0	2016	miR214-regulated p53-NOX4/p66shc pathway plays a crucial role in the protective effect of Ginkgolide B against cisplatin-induced cytotoxicity in HEI-OC1 cells.	Cisplatin	111-120	P53	Homo sapiens	17-20
26859482-12	2016	DC cell culture supplemented with N-acetylcysteine, or alternatively grown in low oxygen, afforded significant proliferative benefits (proliferation: maximum 2-fold increase; NAC: 5-fold p53 decrease; low oxygen: maximum 3.5-fold p53 decrease).	Acetylcysteine	34-50	P53	Homo sapiens	187-190
26859482-12	2016	DC cell culture supplemented with N-acetylcysteine, or alternatively grown in low oxygen, afforded significant proliferative benefits (proliferation: maximum 2-fold increase; NAC: 5-fold p53 decrease; low oxygen: maximum 3.5-fold p53 decrease).	Acetylcysteine	34-50	P53	Homo sapiens	230-233
26859482-12	2016	DC cell culture supplemented with N-acetylcysteine, or alternatively grown in low oxygen, afforded significant proliferative benefits (proliferation: maximum 2-fold increase; NAC: 5-fold p53 decrease; low oxygen: maximum 3.5-fold p53 decrease).	Acetylcysteine	175-178	P53	Homo sapiens	187-190
26859482-12	2016	DC cell culture supplemented with N-acetylcysteine, or alternatively grown in low oxygen, afforded significant proliferative benefits (proliferation: maximum 2-fold increase; NAC: 5-fold p53 decrease; low oxygen: maximum 3.5-fold p53 decrease).	Oxygen	205-211	P53	Homo sapiens	230-233
26768586-10	2016	Over-expression of p53 suppressed the inhibitory effects of GB on NOX4 and p66(shc) expression and superoxide generation and the protective effects of GB on loss of cell viability and apoptosis associated with cisplatin.	Superoxides	99-109	P53	Homo sapiens	19-22
26768586-8	2016	Moreover, p53 expression was increased by cisplatin.	Cisplatin	42-51	P53	Homo sapiens	10-13
26768586-10	2016	Over-expression of p53 suppressed the inhibitory effects of GB on NOX4 and p66(shc) expression and superoxide generation and the protective effects of GB on loss of cell viability and apoptosis associated with cisplatin.	Cisplatin	210-219	P53	Homo sapiens	19-22
26768586-13	2016	We demonstrate that GB decreases superoxide generation and the subsequent apoptosis through reduction of p53-mediated NOX4/p66(shc) pathway via up-regulation of miR214, resulting in attenuation of cisplatin-induced cytotoxicity.	Superoxides	33-43	P53	Homo sapiens	105-108
26700961-7	2016	Third, transfection of mutp53-specific siRNAs in cancer cells expressing both wtp53 and mutp53 also reduced cell proliferation and migration with increased transcripts of p53 downstream target genes, which became further profound when cells were treated with an MDM2 inhibitor Nutlin-3a or a chemotherapeutic agent doxorubicin.	Doxorubicin	315-326	P53	Homo sapiens	26-29
26768586-13	2016	We demonstrate that GB decreases superoxide generation and the subsequent apoptosis through reduction of p53-mediated NOX4/p66(shc) pathway via up-regulation of miR214, resulting in attenuation of cisplatin-induced cytotoxicity.	Cisplatin	197-206	P53	Homo sapiens	105-108
26870698-7	2016	One of these molecules, APR-246, is a prodrug that is converted to the Michael acceptor methylene quinuclidinone (MQ) that binds covalently to cysteines in p53, leading to refolding and restoration of wild type p53 function.	memoquin	114-116	P53	Homo sapiens	156-159
26870698-7	2016	One of these molecules, APR-246, is a prodrug that is converted to the Michael acceptor methylene quinuclidinone (MQ) that binds covalently to cysteines in p53, leading to refolding and restoration of wild type p53 function.	memoquin	114-116	P53	Homo sapiens	211-214
26870698-7	2016	One of these molecules, APR-246, is a prodrug that is converted to the Michael acceptor methylene quinuclidinone (MQ) that binds covalently to cysteines in p53, leading to refolding and restoration of wild type p53 function.	Cysteine	143-152	P53	Homo sapiens	156-159
26870698-7	2016	One of these molecules, APR-246, is a prodrug that is converted to the Michael acceptor methylene quinuclidinone (MQ) that binds covalently to cysteines in p53, leading to refolding and restoration of wild type p53 function.	Cysteine	143-152	P53	Homo sapiens	211-214
26956973-5	2016	Metformin induces the expression of tristetraprolin (TTP) in breast cancer cells in a p53-independent manner.	Metformin	0-9	P53	Homo sapiens	86-89
26796280-2	2016	Cisplatin may initiate p73-dependent apoptosis in p53 mutant cell lines through Fas trimerization and Caspase-8 activation and Bax up regulation and subsequent Caspase-9 activation.	Cisplatin	0-9	P53	Homo sapiens	50-53
25398514-6	2016	Bypass of the need for metabolic activation by treating cells with the corresponding reactive PAH-diol-epoxide metabolites resulted in similar adduct levels in all cell lines, which confirms that the influence of p53 is on the metabolism of the parent PAHs.	diol	98-102	P53	Homo sapiens	213-216
26781309-17	2016	Western blot analysis revealed dephosphorylation of Akt (Ser 473) with activation of p53, Bax, Bak, Bid and reduction in Bcl-2 and Bcl-xL levels.	Serine	57-60	P53	Homo sapiens	85-88
26956973-3	2016	p53 wild-type and p53 mutant breast cancer cells were treated with metformin, and expression of TTP and c-Myc was analyzed by semi-quantitative RT-PCR, Western blots, and promoter activity assay.	Metformin	67-76	P53	Homo sapiens	0-3
26174106-11	2016	We also report that AdoMet consistently causes an increase of p53 and p21 cell-cycle inhibitor, a decrease of cyclin A and cyclin E protein levels, and a marked increase of pro-apoptotic Bax/Bcl-2 ratio, with caspase-3 activation and PARP cleavage.	S-Adenosylmethionine	20-26	P53	Homo sapiens	62-65
26751966-4	2016	Tumor suppressor protein p53 activation and G1/G0 cell cycle arrest support cell survival upon prolonged arginine starvation.	Arginine	105-113	P53	Homo sapiens	25-28
26751966-5	2016	Cells with the mutant or deleted TP53 fail to stop cell cycle progression at defined cell cycle checkpoints which appears to be associated with reduced recovery after durable metabolic stress triggered by arginine withdrawal.	Arginine	205-213	P53	Homo sapiens	33-37
26893664-8	2016	Naringenin and ABT-737 also decreased Akt activation and increased p53 expression, suggesting the involvement of these pathways in the inhibition of gastric cell growth.	naringenin	0-10	P53	Homo sapiens	67-70
26893664-8	2016	Naringenin and ABT-737 also decreased Akt activation and increased p53 expression, suggesting the involvement of these pathways in the inhibition of gastric cell growth.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	15-18	P53	Homo sapiens	67-70
26924930-6	2016	Increased p21 and reduced p53 in high glucose conditioned cells were changed by agmatine.	Glucose	38-45	P53	Homo sapiens	26-29
26691054-1	2016	The TP53-induced glycolysis and apoptosis regulator (TIGAR) is a p53 target gene, which functions to suppress reactive oxygen species (ROS) damage and protect cells from apoptosis.	Reactive Oxygen Species	110-133	P53	Homo sapiens	65-68
26691054-1	2016	The TP53-induced glycolysis and apoptosis regulator (TIGAR) is a p53 target gene, which functions to suppress reactive oxygen species (ROS) damage and protect cells from apoptosis.	Reactive Oxygen Species	135-138	P53	Homo sapiens	65-68
26691280-12	2016	Results indicated that 5-FU decreased H-ras, Rho-A, p53, Stat1 and increased Bax gene expression in Tumor2 and decreased Rac1, Rho-A, NF-kappaB and increased Bax and caspase-3 protein expression in Tumor2.	Fluorouracil	23-27	P53	Homo sapiens	52-55
26699757-3	2016	Exposure of J/Neo cells to kaempeferol caused cytotoxicity and activation of the ATM/ATR-Chk1/Chk2 pathway, activating the phosphorylation of p53 (Ser-15), inhibitory phosphorylation of Cdc25C (Ser-216), and inactivation of cyclin-dependent kinase 1 (Cdk1), with resultant G2- arrest of the cell cycle.	Serine	147-150	P53	Homo sapiens	142-145
26985323-1	2016	A new subseries of substituted piperidines as p53-HDM2 inhibitors exemplified by 21 has been developed from the initial lead 1.	Piperidines	31-42	P53	Homo sapiens	46-49
26718886-9	2016	The patients with a proline (Pro) polymorphism in SNP72 of TP53 showed significantly higher PrP-positive rates than those with arginine (Arg).	Arginine	137-140	P53	Homo sapiens	59-63
26727270-1	2016	The drug pentamidine inhibits calcium-dependent complex formation with p53 ((Ca)S100B p53) in malignant melanoma (MM) and restores p53 tumor suppressor activity in vivo.	Calcium	30-37	P53	Homo sapiens	71-74
26727270-1	2016	The drug pentamidine inhibits calcium-dependent complex formation with p53 ((Ca)S100B p53) in malignant melanoma (MM) and restores p53 tumor suppressor activity in vivo.	Calcium	30-37	P53	Homo sapiens	86-89
26727270-1	2016	The drug pentamidine inhibits calcium-dependent complex formation with p53 ((Ca)S100B p53) in malignant melanoma (MM) and restores p53 tumor suppressor activity in vivo.	Calcium	30-37	P53	Homo sapiens	86-89
26706021-1	2016	Flavonoid resveratrol modulates the transcription factor NF-kappaB; inhibits the cytochrome P450 isoenzyme CYP1 A1; suppresses the expression and activity of cyclooxygenase enzymes; and modulates Fas/Fas-ligand-mediated apoptosis, p53, mammalian target of rapamycin, and cyclins and various phosphodiesterases.	Resveratrol	10-21	P53	Homo sapiens	231-234
26673821-0	2016	UBE4B targets phosphorylated p53 at serines 15 and 392 for degradation.	Serine	36-43	P53	Homo sapiens	29-32
26630137-8	2016	TP53 participated in ROS- and DNA damage-induced cell death differently.	Reactive Oxygen Species	21-24	P53	Homo sapiens	0-4
26673821-6	2016	We show that UBE4B coimmunoprecipitates with phosphorylated p53 at serines 15 and 392.	Serine	67-74	P53	Homo sapiens	60-63
26694802-5	2016	RA induced the increment of p53 levels, caspase-3 activation, and poly-ADP-ribose polymerase cleavage and the reduction of the procaspase-3 and Bcl2.	rosmarinic acid	0-2	P53	Homo sapiens	28-31
26655813-7	2016	Further investigation revealed that CREB blockade by decoy oligonucleotides functionally inhibited transactivation of CREB, and significantly increased radiosensitivity of multiple human cancer cell lines including TP53- and/or RB-mutated cells with minimal effects on normal cells.	Oligonucleotides	59-75	P53	Homo sapiens	215-219
26692350-0	2016	Actin-binding doliculide causes premature senescence in p53 wild type cells.	doliculide	14-24	P53	Homo sapiens	56-59
26692350-4	2016	In this work we used p53 wild-type cells to dissect the reaction of these cells towards subtoxic doses of doliculide.	doliculide	106-116	P53	Homo sapiens	21-24
26238069-0	2016	TP53 mutations are associated with higher rates of pathologic complete response to anthracycline/cyclophosphamide-based neoadjuvant chemotherapy in operable primary breast cancer.	Anthracyclines	83-96	P53	Homo sapiens	0-4
26711147-5	2016	In addition, ASA could led to a loss in the mitochondrial out membrane potential, up-regulate p53, phosphorylated p53 and Bax, down-regulate Bcl-2, release cytochrome c from the mitochondria to the cytoplasm, and activate caspase-9 and caspase-3 in A549 cells, which revealed that ASA could also induce apoptosis through the mitochondria mediated pathway.	Aspirin	13-16	P53	Homo sapiens	94-97
26711147-5	2016	In addition, ASA could led to a loss in the mitochondrial out membrane potential, up-regulate p53, phosphorylated p53 and Bax, down-regulate Bcl-2, release cytochrome c from the mitochondria to the cytoplasm, and activate caspase-9 and caspase-3 in A549 cells, which revealed that ASA could also induce apoptosis through the mitochondria mediated pathway.	Aspirin	13-16	P53	Homo sapiens	114-117
26238069-7	2016	Our results suggested that patients with TP53 mutations are more likely to respond to anthracycline/ cyclophosphamide-based neoadjuvant chemotherapy and have a favorable survival.	Anthracyclines	86-99	P53	Homo sapiens	41-45
26712469-5	2016	As sirtuins deacetylate non-histone targets including FoxO1/3a and p53, berberine increased the acetylation load of FoxO1/3a and p53 proteins.	Berberine	72-81	P53	Homo sapiens	67-70
26712469-0	2016	Concurrent acetylation of FoxO1/3a and p53 due to sirtuins inhibition elicit Bim/PUMA mediated mitochondrial dysfunction and apoptosis in berberine-treated HepG2 cells.	Berberine	138-147	P53	Homo sapiens	39-42
26712469-2	2016	The current study aimed to decode the impact of acetylation/deacetylation of non-histone targets i.e. FoxO1/3a and p53 of sirtuins (NAD(+) dependent enzymes with lysine deacetylase activity) in berberine treated human hepatoma cells.	NAD	132-138	P53	Homo sapiens	115-118
26712469-5	2016	As sirtuins deacetylate non-histone targets including FoxO1/3a and p53, berberine increased the acetylation load of FoxO1/3a and p53 proteins.	Berberine	72-81	P53	Homo sapiens	129-132
26712469-2	2016	The current study aimed to decode the impact of acetylation/deacetylation of non-histone targets i.e. FoxO1/3a and p53 of sirtuins (NAD(+) dependent enzymes with lysine deacetylase activity) in berberine treated human hepatoma cells.	Berberine	194-203	P53	Homo sapiens	115-118
26712469-11	2016	Thus, our findings suggest that berberine mediated sirtuins inhibition resulting into FoxO1/3a and p53 acetylation followed by BH3-only protein Bim/PUMA activation may in part be responsible for mitochondria-mediated apoptosis.	Berberine	32-41	P53	Homo sapiens	99-102
26712469-4	2016	Combination of nicotinamide (sirtuin inhibitor) with berberine potentiated sirtuins inhibition and increased the expression of FoxO1/3a and phosphorylation of p53 tumor suppressor protein.	Berberine	53-62	P53	Homo sapiens	159-162
26696550-0	2016	TP53 Codon 72 Polymorphism Predicts Efficacy of Paclitaxel Plus Capecitabine Chemotherapy in Advanced Gastric Cancer Patients.	Paclitaxel	48-58	P53	Homo sapiens	0-4
26517689-0	2016	Novel p53-dependent anticancer strategy by targeting iron signaling and BNIP3L-induced mitophagy.	Iron	53-57	P53	Homo sapiens	6-9
26517689-7	2016	Altogether, targeting BNIP3L in wild-type p53 colon cancer cells is a novel anticancer strategy activating iron depletion signaling and the mitophagy-related cell death pathway.	Iron	107-111	P53	Homo sapiens	42-45
27099787-1	2016	This study was performed in order to reveal the effect of Noopept (ethyl ester of N-phenylacetyl-Lprolylglycine, GVS-111) on the DNA-binding activity of transcriptional factors (TF) in HEK293 cells transiently transfected with luciferase reporter constructs containing sequences for CREB, NFAT, NF-kappaB, p53, STAT1, GAS, VDR, HSF1, and HIF-1.	n-phenylacetyl-lprolylglycine	82-111	P53	Homo sapiens	306-309
26743233-0	2016	CPUY201112, a novel synthetic small-molecule compound and inhibitor of heat shock protein Hsp90, induces p53-mediated apoptosis in MCF-7 cells.	CPUY201112	0-10	P53	Homo sapiens	105-108
26743233-10	2016	These results demonstrate that CPUY201112 is a novel Hsp90 inhibitor with potential use in treating wild-type p53 related cancers.	CPUY201112	31-41	P53	Homo sapiens	110-113
26727575-7	2016	Knockdown of p53, Mieap or BNIP3 in LS174T cells severely impaired the hypoxia-activated function, leading to the accumulation of unhealthy mitochondria and increase of mitochondrial reactive oxygen species generation.	Reactive Oxygen Species	183-206	P53	Homo sapiens	13-16
26727575-8	2016	The mitochondrial reactive oxygen species generated by unhealthy mitochondria in the p53/Mieap/BNIP3-deficient cells remarkably enhanced cancer cell migration and invasion under hypoxic condition.	Reactive Oxygen Species	18-41	P53	Homo sapiens	85-88
26696550-1	2016	BACKGROUND AND AIMS: The present study analyzed the relationship between TP53 codon 72 polymorphisms and the clinical outcome of advanced gastric cancer patients receiving capecitabine plus paclitaxel chemotherapy.	Paclitaxel	190-200	P53	Homo sapiens	73-77
26696550-5	2016	RESULTS: The Pro/Pro genotypes of TP53 codon 72 were significantly correlated with a lower response rate to capecitabine plus paclitaxel chemotherapy in patients with gastric cancer when compared to the Arg/Arg genotype (30.6 vs. 63.2%, p value 0.000).	Paclitaxel	126-136	P53	Homo sapiens	34-38
26696550-5	2016	RESULTS: The Pro/Pro genotypes of TP53 codon 72 were significantly correlated with a lower response rate to capecitabine plus paclitaxel chemotherapy in patients with gastric cancer when compared to the Arg/Arg genotype (30.6 vs. 63.2%, p value 0.000).	Arginine	203-206	P53	Homo sapiens	34-38
26696550-5	2016	RESULTS: The Pro/Pro genotypes of TP53 codon 72 were significantly correlated with a lower response rate to capecitabine plus paclitaxel chemotherapy in patients with gastric cancer when compared to the Arg/Arg genotype (30.6 vs. 63.2%, p value 0.000).	Arginine	207-210	P53	Homo sapiens	34-38
26696550-7	2016	CONCLUSIONS: TP53 codon 72 polymorphisms was effective in predicting the response to chemotherapy and correlate with PFS and OS in patients with advanced gastric cancer treated with paclitaxel and capecitabine chemotherapy.	Paclitaxel	182-192	P53	Homo sapiens	13-17
26694174-6	2016	We proved that the differential response of LNCaP and PC3 to doxorubicin was p53-independent by introducing wild-type or dominant negative p53 into PC3 or LNCaP cells, respectively.	Doxorubicin	61-72	P53	Homo sapiens	77-80
26599622-0	2016	A surface charge-switchable and folate modified system for co-delivery of proapoptosis peptide and p53 plasmid in cancer therapy.	Folic Acid	32-38	P53	Homo sapiens	99-102
26599622-2	2016	The FK/p53/PEG-PLL(DA) complexes were fabricated by coating the folate incorporated positively charged FK/p53 complexes with charge-switchable PEG-shield (PEG-PLL(DA)) through electrostatic interaction.	Polyethylene Glycols	11-14	P53	Homo sapiens	7-10
26599622-2	2016	The FK/p53/PEG-PLL(DA) complexes were fabricated by coating the folate incorporated positively charged FK/p53 complexes with charge-switchable PEG-shield (PEG-PLL(DA)) through electrostatic interaction.	Polyethylene Glycols	11-14	P53	Homo sapiens	106-109
26599622-2	2016	The FK/p53/PEG-PLL(DA) complexes were fabricated by coating the folate incorporated positively charged FK/p53 complexes with charge-switchable PEG-shield (PEG-PLL(DA)) through electrostatic interaction.	peg-pll	11-18	P53	Homo sapiens	7-10
26599622-2	2016	The FK/p53/PEG-PLL(DA) complexes were fabricated by coating the folate incorporated positively charged FK/p53 complexes with charge-switchable PEG-shield (PEG-PLL(DA)) through electrostatic interaction.	peg-pll	11-18	P53	Homo sapiens	106-109
26599622-3	2016	At the physiological pH 7.4 in the bloodstream, PEG-PLL(DA) could extend the circulating time by shielding the positively charged FK/p53 complexes.	peg-pll	48-55	P53	Homo sapiens	133-136
26599622-4	2016	After the accumulation of the FK/p53/PEG-PLL(DA) complexes in tumor sites, tumor-acidity-triggered charge switch led to the detachment of PEG-PLL(DA) from the FK/p53 complexes, and resulted in efficient tumor cell entry by folate-mediated uptake and electrostatic attraction.	peg-pll	37-44	P53	Homo sapiens	33-36
26599622-4	2016	After the accumulation of the FK/p53/PEG-PLL(DA) complexes in tumor sites, tumor-acidity-triggered charge switch led to the detachment of PEG-PLL(DA) from the FK/p53 complexes, and resulted in efficient tumor cell entry by folate-mediated uptake and electrostatic attraction.	peg-pll	37-44	P53	Homo sapiens	162-165
26599622-4	2016	After the accumulation of the FK/p53/PEG-PLL(DA) complexes in tumor sites, tumor-acidity-triggered charge switch led to the detachment of PEG-PLL(DA) from the FK/p53 complexes, and resulted in efficient tumor cell entry by folate-mediated uptake and electrostatic attraction.	peg-pll	138-145	P53	Homo sapiens	33-36
26599622-4	2016	After the accumulation of the FK/p53/PEG-PLL(DA) complexes in tumor sites, tumor-acidity-triggered charge switch led to the detachment of PEG-PLL(DA) from the FK/p53 complexes, and resulted in efficient tumor cell entry by folate-mediated uptake and electrostatic attraction.	peg-pll	138-145	P53	Homo sapiens	162-165
26599622-4	2016	After the accumulation of the FK/p53/PEG-PLL(DA) complexes in tumor sites, tumor-acidity-triggered charge switch led to the detachment of PEG-PLL(DA) from the FK/p53 complexes, and resulted in efficient tumor cell entry by folate-mediated uptake and electrostatic attraction.	Folic Acid	223-229	P53	Homo sapiens	33-36
26599622-4	2016	After the accumulation of the FK/p53/PEG-PLL(DA) complexes in tumor sites, tumor-acidity-triggered charge switch led to the detachment of PEG-PLL(DA) from the FK/p53 complexes, and resulted in efficient tumor cell entry by folate-mediated uptake and electrostatic attraction.	Folic Acid	223-229	P53	Homo sapiens	162-165
26599622-5	2016	Stimulated by the high content glutathione (GSH) in cytoplasm, the cleavage of disulfide bond resulted in the liberation of proapoptosis peptide C-KLA(TPP) and the p53 gene, which exerted the combined tumor therapy by regulating both intrinsic and extrinsic apoptotic pathways.	Glutathione	31-42	P53	Homo sapiens	164-167
26599622-5	2016	Stimulated by the high content glutathione (GSH) in cytoplasm, the cleavage of disulfide bond resulted in the liberation of proapoptosis peptide C-KLA(TPP) and the p53 gene, which exerted the combined tumor therapy by regulating both intrinsic and extrinsic apoptotic pathways.	Glutathione	44-47	P53	Homo sapiens	164-167
26599622-5	2016	Stimulated by the high content glutathione (GSH) in cytoplasm, the cleavage of disulfide bond resulted in the liberation of proapoptosis peptide C-KLA(TPP) and the p53 gene, which exerted the combined tumor therapy by regulating both intrinsic and extrinsic apoptotic pathways.	Disulfides	79-88	P53	Homo sapiens	164-167
26773176-11	2016	In paclitaxel-resistant cells, there was a significant increase in Six1 and BCL-2 mRNA levels (p = 0.0007) with a marked decrease in pro-apoptotic Bax mRNA expression level (p = 0.03); however, there was no significant change in P53 expression (p = 0.025).	Paclitaxel	3-13	P53	Homo sapiens	229-232
26592665-3	2016	Exposure of H460 cells to radiation induced a marked accumulation of cell death-promoting reactive oxygen species, but this effect was blocked in radiation-treated H460 PSMC5-knockdown cells through downregulation of the p53-p21 pathway.	Reactive Oxygen Species	90-113	P53	Homo sapiens	221-224
26497762-7	2016	Melatonin 1 nM induced a 2-fold change in p53 expression as compared to radiation alone.	Melatonin	0-9	P53	Homo sapiens	42-45
26497762-8	2016	The regulatory action of melatonin on p53 could be a link between melatonin and its modulatory action on the sensitivity of breast cancer cells to ionizing radiation.	Melatonin	25-34	P53	Homo sapiens	38-41
26497762-8	2016	The regulatory action of melatonin on p53 could be a link between melatonin and its modulatory action on the sensitivity of breast cancer cells to ionizing radiation.	Melatonin	66-75	P53	Homo sapiens	38-41
26636375-4	2016	ATM or p53 down regulation was shown to modulate differently the cellular fate of H(2)O(2)-treated hMESCs.	Hydrogen Peroxide	82-90	P53	Homo sapiens	7-10
26636375-5	2016	ATM inhibition allowed H(2)O(2)-stimulated hMESCs to escape the permanent cell cycle arrest due to loss of the functional ATM/p53/p21/Rb pathway, and induced bypass of mitosis and re-entry into S phase, resulting in tetraploid cells.	Hydrogen Peroxide	23-31	P53	Homo sapiens	126-129
26636375-6	2016	On the contrary, suppression of the p53 transcriptional activity caused a pronounced cell death of H(2)O(2)-treated hMESCs via autophagy induction.	Hydrogen Peroxide	99-107	P53	Homo sapiens	36-39
26507802-4	2016	H-RuBmp demonstrated a higher interaction potency with the cell membrane and induced higher levels of ROS overproduction in cancer cells to regulate the AKT, MAPK, and p53 signaling pathways.	h-rubmp	0-7	P53	Homo sapiens	168-171
27010918-0	2016	Heat Killed Attenuated Leishmania Induces Apoptosis of HepG2 Cells Through ROS Mediated p53 Dependent Mitochondrial Pathway.	ros	75-78	P53	Homo sapiens	88-91
27010918-11	2016	In conclusion, Leishmania donovani UR6 efficiently induces apoptosis in HepG2 cells through ROS mediated p53 dependent mitochondrial pathway.	ros	92-95	P53	Homo sapiens	105-108
27010918-13	2016	From our study we found that Leishmania donovani UR6 efficiently induced apoptosis in HepG2 cells through ROS mediated p53 dependent mitochondrial pathway.	ros	106-109	P53	Homo sapiens	119-122
26900800-5	2016	We found that both Tennovin-1 and BI2536 increased the anti-neoplastic activity of metformin, an inhibitor of oxidative phosphorylation, in a p53 dependent manner.	Metformin	83-92	P53	Homo sapiens	142-145
27825169-9	2016	Importantly, the rapamycin resistant cells demonstrated attenuated accumulation of p53 in the nucleus in response to rapamycin treatment.	Sirolimus	17-26	P53	Homo sapiens	83-86
27825169-10	2016	Moreover, the inhibition of MDM2 by siMDM2 sensitizes A498 cells to rapamycin through the activation of p53.	Sirolimus	68-77	P53	Homo sapiens	104-107
26507802-4	2016	H-RuBmp demonstrated a higher interaction potency with the cell membrane and induced higher levels of ROS overproduction in cancer cells to regulate the AKT, MAPK, and p53 signaling pathways.	ros	102-105	P53	Homo sapiens	168-171
27385051-2	2016	A low level of melatonin is associated with an increased risk of cancer, possibly by decreasing the expression of tumor-suppressor genes, such as p53.	Melatonin	15-24	P53	Homo sapiens	146-149
26721407-2	2016	As a non-enzymatic function, it is involved in the stabilization of several tumour suppressors such as p53, p33 and p73&amp;amp;#945;.	Adenosine Monophosphate	120-123	P53	Homo sapiens	103-106
26209050-10	2016	The gene-gene interaction of these polymorphisms increased EOC risk in a more than additive manner (ORs for the presence of both BAX AA and TP53 Arg/Pro genotypes = 8.7, 95 % CI = 1.66-45.48).	Arginine	145-148	P53	Homo sapiens	140-144
26721407-2	2016	As a non-enzymatic function, it is involved in the stabilization of several tumour suppressors such as p53, p33 and p73&amp;amp;#945;.	Adenosine Monophosphate	124-127	P53	Homo sapiens	103-106
26590797-9	2016	Moreover, IAZP augmented the doxorubicin-induced degradation of p21, activation of p53, CDK2, caspase 3/7 and phosphorylation of Rb protein.	Doxorubicin	29-40	P53	Homo sapiens	83-86
26884717-12	2016	Taken together, these suggested that CsA could suppress ROS-mediated p53 mitochondrial distribution and cell apoptosis depended on its inhibition effect to mitochondrial permeability transition.	ros	56-59	P53	Homo sapiens	69-72
26738694-7	2016	Moreover, genotype analysis revealed a statistically significant association between Pro/Pro genotype of p53 Arg72Pro polymorphism and increased frequencies of MN both spontaneous and AFB1-induced cultures when compared Arg/Arg genotype (0.69 +- 0.19 versus 0.46 +- 0.13, p &lt; 0.001; 1.59 +- 0.65 versus 1.01 +- 0.41 p &lt; 0.001; respectively).	Arginine	109-112	P53	Homo sapiens	105-108
26738694-7	2016	Moreover, genotype analysis revealed a statistically significant association between Pro/Pro genotype of p53 Arg72Pro polymorphism and increased frequencies of MN both spontaneous and AFB1-induced cultures when compared Arg/Arg genotype (0.69 +- 0.19 versus 0.46 +- 0.13, p &lt; 0.001; 1.59 +- 0.65 versus 1.01 +- 0.41 p &lt; 0.001; respectively).	Arginine	220-223	P53	Homo sapiens	105-108
26669907-0	2016	The presence of carbon nanostructures in bakery products induces metabolic stress in human mesenchymal stem cells through CYP1A and p53 gene expression.	Carbon	16-22	P53	Homo sapiens	132-135
26241176-1	2016	Combination therapy of carbon-ion beam with the far upstream element-binding protein (FBP)-interacting repressor, FIR, which interferes with DNA damage repair proteins, was proposed as an approach for esophageal cancer treatment with low side effects regardless of TP53 status.	Carbon	23-29	P53	Homo sapiens	265-269
26572087-13	2016	Taken together, these findings indicate that the expression of del p53 in MCF-7/del p53 cells enables the cells to partially acquire doxorubicin resistance characteristics of the MCF-7/adr cells.	Doxorubicin	133-144	P53	Homo sapiens	84-87
26572087-2	2016	However, in our previous study, we demonstrated that a deletion spanning codons 127-133 in the p53 gene (designated as del p53) was detected in doxorubicin-resistant MCF-7 cell lines following various induction processes.	Doxorubicin	144-155	P53	Homo sapiens	95-98
26887694-0	2016	Effect of oxygen pressure during incubation with a (10)B-carrier on (10)B uptake capacity of cultured p53 wild-type and mutated tumor cells: dependency on p53 status of tumor cells and types of (10)B-carriers.	Oxygen	10-16	P53	Homo sapiens	102-105
26572087-2	2016	However, in our previous study, we demonstrated that a deletion spanning codons 127-133 in the p53 gene (designated as del p53) was detected in doxorubicin-resistant MCF-7 cell lines following various induction processes.	Doxorubicin	144-155	P53	Homo sapiens	123-126
26572087-7	2016	The MCF-7/del p53 cells acquired resistance to doxorubicin with increased P-gp efflux function.	Doxorubicin	47-58	P53	Homo sapiens	14-17
26572087-9	2016	The inhibition of nuclear factor (NF)-kappaB by cyclosporine sensitized the MCF-7/del p53 cells to doxorubicin toxicity.	Cyclosporine	48-60	P53	Homo sapiens	86-89
26572087-9	2016	The inhibition of nuclear factor (NF)-kappaB by cyclosporine sensitized the MCF-7/del p53 cells to doxorubicin toxicity.	Doxorubicin	99-110	P53	Homo sapiens	86-89
26572087-13	2016	Taken together, these findings indicate that the expression of del p53 in MCF-7/del p53 cells enables the cells to partially acquire doxorubicin resistance characteristics of the MCF-7/adr cells.	Doxorubicin	133-144	P53	Homo sapiens	67-70
28203651-6	2016	SNP analysis of p53 codon 72 demonstrated the highest prevalence of the Arg/Arg (56%) phenotype, followed by Arg/Pro (33%) and Pro/Pro (11%).	Arginine	72-75	P53	Homo sapiens	16-19
27323551-6	2016	Immuno-histochemical staining for P53 performed on paraffin blocks and quantified with 12- point weighted score proposed by W.Y chan.	Paraffin	51-59	P53	Homo sapiens	34-37
28203651-6	2016	SNP analysis of p53 codon 72 demonstrated the highest prevalence of the Arg/Arg (56%) phenotype, followed by Arg/Pro (33%) and Pro/Pro (11%).	Arginine	76-79	P53	Homo sapiens	16-19
28203651-6	2016	SNP analysis of p53 codon 72 demonstrated the highest prevalence of the Arg/Arg (56%) phenotype, followed by Arg/Pro (33%) and Pro/Pro (11%).	Arginine	76-79	P53	Homo sapiens	16-19
26471831-5	2016	RESULTS: mTOR inhibitors AZD8055, RAD-001, rapamycin and BEZ235 induced synergistic cytotoxicity with the Chk1 inhibitor V158411 in p53 mutant colon cancer cells.	Sirolimus	43-52	P53	Homo sapiens	132-135
27992315-7	2016	The best choice of two molecules were obtained by docking in specific solvent for 6 nanoseconds at a temperature of 310 K. Out of a library of compounds, acetamido-2-carboxy-4-dimethylamino-2- hydroxybenzophenone satisfied the ADMET and was found to be a potential target for mutant p53.	acetamido-2-carboxy-4-dimethylamino-2- hydroxybenzophenone	154-212	P53	Homo sapiens	283-286
26585176-0	2016	An anthraquinone derivative from Luffa acutangula induces apoptosis in human lung cancer cell line NCI-H460 through p53-dependent pathway.	Anthraquinones	3-16	P53	Homo sapiens	116-119
26585176-9	2016	In silico studies demonstrate that DHMA formed hydrogen bond interaction with key residues Trp26, Phe55 and Lys24 by which it disrupt the binding of p53 with MDM2 receptor.	Hydrogen	47-55	P53	Homo sapiens	149-152
25465239-0	2016	Gene Expression Profile of NF-kappaB, Nrf2, Glycolytic, and p53 Pathways During the SH-SY5Y Neuronal Differentiation Mediated by Retinoic Acid.	Tretinoin	129-142	P53	Homo sapiens	60-63
26774139-8	2016	In addition, chidamide alone or in combination with 5-Fu increased the p53, phosphorylated-p53 (p-p53), p21 and gammaH2AX levels, but suppressed cyclin dependent kinase 4 (CDK4) expression in tumor cells.	Fluorouracil	52-56	P53	Homo sapiens	71-74
26774139-8	2016	In addition, chidamide alone or in combination with 5-Fu increased the p53, phosphorylated-p53 (p-p53), p21 and gammaH2AX levels, but suppressed cyclin dependent kinase 4 (CDK4) expression in tumor cells.	Fluorouracil	52-56	P53	Homo sapiens	91-94
26639236-0	2016	10-Hydroxycamptothecin induces apoptosis in human neuroblastoma SMS-KCNR cells through p53, cytochrome c and caspase 3 pathways.	10-hydroxycamptothecin	0-22	P53	Homo sapiens	87-90
26774139-8	2016	In addition, chidamide alone or in combination with 5-Fu increased the p53, phosphorylated-p53 (p-p53), p21 and gammaH2AX levels, but suppressed cyclin dependent kinase 4 (CDK4) expression in tumor cells.	Fluorouracil	52-56	P53	Homo sapiens	91-94
27185980-11	2016	CONCLUSION: Since p53 is known as an important inhibitory trigger for proliferative cycle of cells, in current study it was concluded that p53 inhibitory role decreases as malignancy potential increases, also tumors dependence on steroids via steroid receptors decreases as malignancy potential increases.	Steroids	230-238	P53	Homo sapiens	18-21
27185980-11	2016	CONCLUSION: Since p53 is known as an important inhibitory trigger for proliferative cycle of cells, in current study it was concluded that p53 inhibitory role decreases as malignancy potential increases, also tumors dependence on steroids via steroid receptors decreases as malignancy potential increases.	Steroids	230-238	P53	Homo sapiens	139-142
26977261-0	2016	Different Regulation of p53 Expression by Cadmium Exposure in Kidney, Liver, Intestine, Vasculature, and Brain Astrocytes.	Cadmium	42-49	P53	Homo sapiens	24-27
26498391-6	2016	Furthermore, we showed that resveratrol enhanced glioblastoma-initiating cells to temozolomide-induced apoptosis through DNA double-stranded breaks/pATM/pATR/p53 pathway activation, and promoted glioblastoma-initiating cell differentiation involving p-STAT3 inactivation.	Resveratrol	28-39	P53	Homo sapiens	158-161
26785263-1	2016	BACKGROUND: In human papillomavirus (HPV)-induced carcinogenesis, the arginine (Arg) allele of the TP53 codon 72 polymorphism binds more efficiently to the HPV E6 oncoprotein than the proline (Pro) allele.	Arginine	70-78	P53	Homo sapiens	99-103
26785263-1	2016	BACKGROUND: In human papillomavirus (HPV)-induced carcinogenesis, the arginine (Arg) allele of the TP53 codon 72 polymorphism binds more efficiently to the HPV E6 oncoprotein than the proline (Pro) allele.	Arginine	80-83	P53	Homo sapiens	99-103
26785263-8	2016	Most OPSCC patients had the TP53 Arg/Arg or Arg/Pro genotype.	Arginine	33-36	P53	Homo sapiens	28-32
27703600-0	2016	Cholesterol Retards Senescence in Bone Marrow Mesenchymal Stem Cells by Modulating Autophagy and ROS/p53/p21Cip1/Waf1 Pathway.	Cholesterol	0-11	P53	Homo sapiens	101-104
27703600-4	2016	CH prevented the increase in SA-beta-gal positive cells induced by RITA (reactivation of p53 and induction of tumor cell apoptosis, a p53 activator) or 3-MA (3-methyladenine, an autophagy inhibitor).	RITA	67-71	P53	Homo sapiens	89-92
27703600-4	2016	CH prevented the increase in SA-beta-gal positive cells induced by RITA (reactivation of p53 and induction of tumor cell apoptosis, a p53 activator) or 3-MA (3-methyladenine, an autophagy inhibitor).	RITA	67-71	P53	Homo sapiens	134-137
27703600-5	2016	Our results indicate that CH not only is a structural component of cell membrane but also functionally contributes to regulating cellular senescence by modulating cell cycle, autophagy, and the ROS/p53/p21Cip1/Waf1 signaling pathway.	ros	194-197	P53	Homo sapiens	198-201
27457236-3	2016	At the molecular level, inhibition of NF-kB, Akt/PI3K, and MAPK pathways and enhancement of p53 are among the most important anticancer alterations induced by curcumin.	Curcumin	159-167	P53	Homo sapiens	92-95
27375834-5	2016	H2O2 produces both nuclear and mitochondrial DNA lesions, increases the expression of cell adhesion molecules, and increases p53 activity and other transcription factors orchestrating cancer cell death.	Hydrogen Peroxide	0-4	P53	Homo sapiens	125-128
29707645-4	2016	It then discusses emerging concepts, especially the topoisomerase IIb-p53-mitochondrion axis that may lead to the development of mechanistically based novel strategies to protect against cardiotoxicity and enhance the effectiveness of doxorubicin therapy.	Doxorubicin	235-246	P53	Homo sapiens	70-73
26977261-2	2016	Our previous studies indicated that Cd induces p53-dependent apoptosis by inhibiting gene expression of the ubiquitin-conjugating enzyme (Ube) 2d family in both human and rat proximal tubular cells.	Cadmium	36-38	P53	Homo sapiens	47-50
26977261-8	2016	In human brain microvascular endothelial cells (HBMECs), Cd did not suppress gene expression of the Ube2d family, but increased the p53 protein level.	Cadmium	57-59	P53	Homo sapiens	132-135
26977261-10	2016	These results suggest that Cd-induced apoptosis through p53 protein is associated with renal toxicity but not hepatic toxicity, and the modification of p53 protein by Cd may vary depending on cell type.	Cadmium	27-29	P53	Homo sapiens	56-59
26977261-10	2016	These results suggest that Cd-induced apoptosis through p53 protein is associated with renal toxicity but not hepatic toxicity, and the modification of p53 protein by Cd may vary depending on cell type.	Cadmium	167-169	P53	Homo sapiens	152-155
26540344-0	2015	Ell3 stabilizes p53 following CDDP treatment via its effects on ubiquitin-dependent and -independent proteasomal degradation pathways in breast cancer cells.	Cisplatin	30-34	P53	Homo sapiens	16-19
26540344-3	2015	Here, we report that the transcription elongation factor Ell3 sensitizes luminal type-cancer cell line, MCF7, which have wild-type p53, to the chemotherapeutic agent cis-diamminedichloroplatinum(II) (CDDP) by stabilizing p53.	Cisplatin	166-198	P53	Homo sapiens	221-224
26782376-10	2015	Analysis of p53 gene polymorphisms showed a higher frequency for the genotype Arg/Pro (66%) and a lower frequency for the Arg/Arg (23%) and Pro/Pro (11%) genotypes.	Arginine	78-81	P53	Homo sapiens	12-15
25450742-7	2015	Cisplatin affected several pathways including, p53 signalling, Nrf2 mediated oxidative stress response, mitochondrial processes, mTOR and AMPK signalling.	Cisplatin	0-9	P53	Homo sapiens	47-50
26782376-10	2015	Analysis of p53 gene polymorphisms showed a higher frequency for the genotype Arg/Pro (66%) and a lower frequency for the Arg/Arg (23%) and Pro/Pro (11%) genotypes.	Arginine	122-125	P53	Homo sapiens	12-15
26782376-10	2015	Analysis of p53 gene polymorphisms showed a higher frequency for the genotype Arg/Pro (66%) and a lower frequency for the Arg/Arg (23%) and Pro/Pro (11%) genotypes.	Arginine	122-125	P53	Homo sapiens	12-15
26384430-0	2015	CITED2 silencing sensitizes cancer cells to cisplatin by inhibiting p53 trans-activation and chromatin relaxation on the ERCC1 DNA repair gene.	Cisplatin	44-53	P53	Homo sapiens	68-71
27073729-5	2016	In this study, p53-wild type U2OS and p53-null MG-63 osteosarcoma-derived cells were used to investigate the mechanism of doxorubicin-induced cytotoxicity.	Doxorubicin	122-133	P53	Homo sapiens	15-18
27073729-6	2016	In cell viability assays, doxorubicin effectively induced apoptosis in U2OS cells via the p53 signaling pathway, evidenced by elevated PUMA and p21 protein levels and activated caspase 3 cleavage.	Doxorubicin	26-37	P53	Homo sapiens	90-93
27073729-7	2016	In contrast, p53-null MG-63 cells were resistant to doxorubicin-induced apoptosis, while exogenous expression of p53 increased drug sensitivity in those cells.	Doxorubicin	52-63	P53	Homo sapiens	13-16
27073729-10	2016	Knockdown of Smad3 expression by small hairpin RNA (shRNA) showed that Smad3 was required for p53-mediated TGF-beta signaling in response to doxorubicin treatment in U2OS and MG-63 cells.	Doxorubicin	141-152	P53	Homo sapiens	94-97
27073729-11	2016	Taken together, these data demonstrate that p53 and TGF-beta/Smad3 signaling pathways are both essential for doxorubicin-induced cytotoxicity in osteosarcoma cells.	Doxorubicin	109-120	P53	Homo sapiens	44-47
27073729-0	2016	P53 is required for Doxorubicin-induced apoptosis via the TGF-beta signaling pathway in osteosarcoma-derived cells.	Doxorubicin	20-31	P53	Homo sapiens	0-3
26384430-7	2015	These results demonstrate that CITED2/p300 can be recruited by p53 at the promoter of the repair gene ERCC1 in response to cisplatin-induced DNA damage.	Cisplatin	123-132	P53	Homo sapiens	63-66
26384430-8	2015	The CITED2/p300/p53/ERCC1 pathway is thus involved in the cell response to cisplatin and represents a potential target for cancer therapy.	Cisplatin	75-84	P53	Homo sapiens	16-19
26497680-2	2015	Here, we hypothesized that mutant p53 could upregulate Nrf2 expression at the transcriptional level, thereby conferring cisplatin resistance in non-small cell lung cancer (NSCLC).	Cisplatin	120-129	P53	Homo sapiens	34-37
26450832-2	2015	It is interesting to find for the first time that DOX@NT-MSNs down-regulate the expression of apoptosis suppressor genes and inhibit DNA repair process by disturbing the p53 pathway.	Doxorubicin	50-53	P53	Homo sapiens	170-173
26497680-5	2015	The MTT assay indicated that an increase in Nrf2 expression by mutant p53 is responsible for cisplatin resistance.	Cisplatin	93-102	P53	Homo sapiens	70-73
26497680-8	2015	The prognostic significance of Nrf2 mRNA levels on OS and RFS was also observed in patients who have received cisplatin-based chemotherapy, particularly in p53-mutant patients.	Cisplatin	110-119	P53	Homo sapiens	156-159
26391003-1	2015	This work describes cytotoxic effect of non-platinum metal-based compounds on the human T-leukemic cells with different p53 status (p53 wild-type MOLT-4 and p53-deficient Jurkat cells).	Metals	53-58	P53	Homo sapiens	132-135
26497680-9	2015	Collectively, mutant p53 may confer cisplatin resistance via upregulation of Nrf2 expression, and Nrf2 mRNA level may predict chemotherapeutic response and outcomes in NSCLC.	Cisplatin	36-45	P53	Homo sapiens	21-24
26677765-5	2015	Specifically, we show that metformin enhances adult NPC proliferation and self-renewal dependent upon the p53 family member and transcription factor TAp73, while it promotes neuronal differentiation of these cells by activating the AMPK-aPKC-CBP pathway.	Metformin	27-36	P53	Homo sapiens	106-109
26465677-0	2015	A Novel Platinum-Maurocalcine Conjugate Induces Apoptosis of Human Glioblastoma Cells by Acting through the ROS-ERK/AKT-p53 Pathway.	ros	108-111	P53	Homo sapiens	120-123
26391003-1	2015	This work describes cytotoxic effect of non-platinum metal-based compounds on the human T-leukemic cells with different p53 status (p53 wild-type MOLT-4 and p53-deficient Jurkat cells).	Metals	53-58	P53	Homo sapiens	132-135
26391003-6	2015	In case of the p53 wild-type MOLT-4 cells, the expression of the tumor-suppressor protein p53 and its form phosphorylated at the serine 15 increased after both V1 and Mo1 treatment, similar to the effect of cis-DDP.	Serine	129-135	P53	Homo sapiens	15-18
26391003-6	2015	In case of the p53 wild-type MOLT-4 cells, the expression of the tumor-suppressor protein p53 and its form phosphorylated at the serine 15 increased after both V1 and Mo1 treatment, similar to the effect of cis-DDP.	Serine	129-135	P53	Homo sapiens	90-93
26629991-0	2015	Metformin and Resveratrol Inhibited High Glucose-Induced Metabolic Memory of Endothelial Senescence through SIRT1/p300/p53/p21 Pathway.	Metformin	0-9	P53	Homo sapiens	119-122
26629991-0	2015	Metformin and Resveratrol Inhibited High Glucose-Induced Metabolic Memory of Endothelial Senescence through SIRT1/p300/p53/p21 Pathway.	Resveratrol	14-25	P53	Homo sapiens	119-122
26629991-9	2015	Furthermore, we found that RSV or MET treatment prevented senescent "memory" by modulating SIRT1/p300/p53/p21 pathway.	Resveratrol	27-30	P53	Homo sapiens	102-105
26629991-11	2015	In conclusion, short-term high glucose stimulation could induce sustained endothelial senescence via SIRT1/p300/p53/p21 pathway.	Glucose	31-38	P53	Homo sapiens	112-115
26573797-7	2015	It goes further by demonstrating that an important regulator of aromatase, the obesity-associated and tumor-derived factor prostaglandin E2, inhibits p53 in the breast adipose stroma.	Dinoprostone	123-139	P53	Homo sapiens	150-153
26605532-9	2015	Analysis of the DHS sequences uncovers one mutation (chr18: 52417839G&gt;C) in the tumour cells of a patient with follicular thyroid carcinoma, which affects the binding of the tumour suppressor protein p53 and correlates with decreased expression of its target gene TXNL1.	dhs	16-19	P53	Homo sapiens	203-206
26404525-7	2015	Blocking oxidized phospholipid-rich LMPs with a specific antibody significantly prevented LMP-induced Rb apoptosis and reversed the expression patterns of SYK, p53, p21.	Phospholipids	18-30	P53	Homo sapiens	160-163
26438057-0	2015	Core domain mutant Y220C of p53 protein has a key role in copper homeostasis in case of free fatty acids overload.	Copper	58-64	P53	Homo sapiens	28-31
26438057-8	2015	Here we provide evidence on the role of p53 in the modulation of copper homeostasis, in an experimental model of NAFLD.	Copper	65-71	P53	Homo sapiens	40-43
26438057-10	2015	Interestingly, p53 activation correlated with the intracellular copper level maintenance.	Copper	64-70	P53	Homo sapiens	15-18
26438057-11	2015	We demonstrated that, in hepatoma cell lines, core domain mutant Y220C of p53 affects the modulation of SCO2 and Copper transporter 1 (CTR1), influencing, in this way, intracellular copper homeostasis in presence of FFAs accumulation, and that the 220 residue of the protein is crucial for such control.	Copper	182-188	P53	Homo sapiens	74-77
26438057-12	2015	The role of p53 we highlighted may have deep implications in clinical conditions where copper homeostasis is deregulated.	Copper	87-93	P53	Homo sapiens	12-15
25736303-8	2015	The combination of 5-FU and Res significantly increased the percentage of apoptotic cells and the level of activated caspase-3, cleaved PARP and p53 proteins as well as increased the Bax/Bcl-2 ratio.	Fluorouracil	19-23	P53	Homo sapiens	145-148
26459801-0	2015	Targeting the  133p53 isoform can restore chemosensitivity in 5-fluorouracil-resistant cholangiocarcinoma cells.	Fluorouracil	62-76	P53	Homo sapiens	18-21
26459801-9	2015	Increased  133p53 was correlated with 5-FU in a dose-dependent manner.	Fluorouracil	38-42	P53	Homo sapiens	14-17
25713051-1	2015	We study transition of the temporal behaviours of p53 and MDM2 in a stress p53-MDM2-NO regulatory network induced by a bioactive molecule NO (Nitric Oxide).	Nitric Oxide	142-154	P53	Homo sapiens	50-53
26041389-5	2015	The expressions of p53 and p21 were decreased in H2O2-treated RTEF-1 o/e human umbilical vein endothelial cells.	Hydrogen Peroxide	49-53	P53	Homo sapiens	19-22
26520021-8	2015	The support l-tyrosine Sepharose used in chromatographic experiments promotes the separation of native pVAX1-LacZ and pcDNA3-FLAG-p53 samples (oc+sc) by decreasing the salt concentration.	Tyrosine	12-22	P53	Homo sapiens	130-133
26520021-8	2015	The support l-tyrosine Sepharose used in chromatographic experiments promotes the separation of native pVAX1-LacZ and pcDNA3-FLAG-p53 samples (oc+sc) by decreasing the salt concentration.	Salts	168-172	P53	Homo sapiens	130-133
26467393-4	2015	Human aortic smooth muscle cells treated with beta-Glycerophosphate (BGP, 10mM) suffered cellular senescence by increasing p53, p21 and p16 expression and the senescence associated beta-galactosidase activity.	beta-glycerophosphoric acid	46-67	P53	Homo sapiens	123-126
25713051-1	2015	We study transition of the temporal behaviours of p53 and MDM2 in a stress p53-MDM2-NO regulatory network induced by a bioactive molecule NO (Nitric Oxide).	Nitric Oxide	142-154	P53	Homo sapiens	75-78
26350565-0	2015	The cholesterol metabolite 27-hydroxycholesterol regulates p53 activity and increases cell proliferation via MDM2 in breast cancer cells.	Cholesterol	4-15	P53	Homo sapiens	59-62
25400040-6	2015	Moreover, overexpression of p28(GANK) attenuated the capability of NF-kappaB binding to the target gene IkappaBalpha promoter, but also weakened adriamycin-induced NF-kappaB pro-apoptotic gene Fas and FasL expression, which subsequently made p53-deficient tumor cells resistance to adriamycin.	Doxorubicin	145-155	P53	Homo sapiens	242-245
26496980-8	2015	Numerous pathways, including p53, c-Jun N-terminal kinases (JNK), Akt and extracellular signal-regulated kinases (ERK)1/2 pathways were markedly altered following treatment of THP-1 cells with curcumin and naringenin.	Curcumin	193-201	P53	Homo sapiens	29-32
26376962-10	2015	Mutant TP53 cells and cells in which p53 activity was abrogated (shRNA) demonstrated a blunted lactate response to irradiation, consistent with a radioresistant phenotype.	Lactic Acid	95-102	P53	Homo sapiens	37-40
26496980-8	2015	Numerous pathways, including p53, c-Jun N-terminal kinases (JNK), Akt and extracellular signal-regulated kinases (ERK)1/2 pathways were markedly altered following treatment of THP-1 cells with curcumin and naringenin.	naringenin	206-216	P53	Homo sapiens	29-32
26496980-9	2015	These results indicated that naringenin may enhance curcumin-induced apoptosis through inhibiting the Akt and ERK pathways, and promoting the JNK and p53 pathways.	naringenin	29-39	P53	Homo sapiens	150-153
26496980-9	2015	These results indicated that naringenin may enhance curcumin-induced apoptosis through inhibiting the Akt and ERK pathways, and promoting the JNK and p53 pathways.	Curcumin	52-60	P53	Homo sapiens	150-153
26503508-6	2015	In addition, berberine increased the expression of the tumor suppressor p53 in FaDu cells.	Berberine	13-22	P53	Homo sapiens	72-75
26486083-4	2015	We hypothesized that cisplatin induces cytotoxicity through DNA adduct formation, oxidative stress, transcriptional factors (p53 and AP-1), cell cycle regulation, stress signaling and apoptosis in APL cells.	Cisplatin	21-30	P53	Homo sapiens	125-128
26486083-7	2015	Cisplatin also activated p53 and phosphorylated activator protein (AP-1) component, c-Jun at serine (63, 73) residue simultaneously leading to cell cycle arrest through stimulation of p21 and down regulation of cyclins and cyclin dependent kinases in APL cell lines.	Cisplatin	0-9	P53	Homo sapiens	25-28
26486083-7	2015	Cisplatin also activated p53 and phosphorylated activator protein (AP-1) component, c-Jun at serine (63, 73) residue simultaneously leading to cell cycle arrest through stimulation of p21 and down regulation of cyclins and cyclin dependent kinases in APL cell lines.	Serine	93-99	P53	Homo sapiens	25-28
25823026-2	2015	RBM38 RNA-binding protein, also called RNPC1 and a target of p53, inhibits p53 messenger RNA (mRNA) translation, which can be reversed by GSK3 protein kinase via phosphorylation of RBM38 at serine 195.	Serine	190-196	P53	Homo sapiens	61-64
25823026-2	2015	RBM38 RNA-binding protein, also called RNPC1 and a target of p53, inhibits p53 messenger RNA (mRNA) translation, which can be reversed by GSK3 protein kinase via phosphorylation of RBM38 at serine 195.	Serine	190-196	P53	Homo sapiens	75-78
26579714-12	2015	This parameter has been observed to be able to mimic the binding affinity of the p53 ts-mutants at 300 K and 310 K. Thus the correlation between MM-GBSA free energy of binding and hydrogen bonds formed by the interface residues between p53 and DNA has revealed the temperature dependent nature of these mutants.	Hydrogen	180-188	P53	Homo sapiens	81-84
26703569-9	2015	Furthermore, by using genechip analysis, we observed that linalool can promote p53, p21, p27, p16, and p18 gene expression.	linalool	58-66	P53	Homo sapiens	79-82
26447614-0	2015	Silibinin enhances the repair of ultraviolet B-induced DNA damage by activating p53-dependent nucleotide excision repair mechanism in human dermal fibroblasts.	Silybin	0-9	P53	Homo sapiens	80-83
26447614-6	2015	In UVB exposed fibroblasts, silibinin treatment also increased p53 and GADD45alpha expression; the key regulators of the NER pathway and DNA repair.	Silybin	28-37	P53	Homo sapiens	63-66
26447614-9	2015	Moreover, in the presence of pifithrin-alpha, an inhibitor of p53, the DNA repair efficacy of silibinin was compromised associated with a reduction in XPA and GADD45alpha transcripts.	Silybin	94-103	P53	Homo sapiens	62-65
26447614-10	2015	Together, these findings suggest that silibinin"s efficacy against UVB-induced photodamage is primarily by inhibiting NER and p53; and these findings further support silibinin"s usage as a potential inexpensive, effective, and non-toxic agent for skin cancer chemoprevention.	Silybin	38-47	P53	Homo sapiens	126-129
26599019-0	2015	Metformin Radiosensitizes p53-Deficient Colorectal Cancer Cells through Induction of G2/M Arrest and Inhibition of DNA Repair Proteins.	Metformin	0-9	P53	Homo sapiens	26-29
26599019-1	2015	The present study addressed whether the combination of metformin and ionizing radiation (IR) would show enhanced antitumor effects in radioresistant p53-deficient colorectal cancer cells, focusing on repair pathways for IR-induced DNA damage.	Metformin	55-64	P53	Homo sapiens	149-152
26599019-2	2015	Metformin caused a higher reduction in clonogenic survival as well as greater radiosensitization and inhibition of tumor growth of p53-/- than of p53+/+ colorectal cancer cells and xenografts.	Metformin	0-9	P53	Homo sapiens	131-134
26599019-2	2015	Metformin caused a higher reduction in clonogenic survival as well as greater radiosensitization and inhibition of tumor growth of p53-/- than of p53+/+ colorectal cancer cells and xenografts.	Metformin	0-9	P53	Homo sapiens	146-149
26599019-5	2015	In conclusion, metformin enhanced radiosensitivity by inducing G2/M arrest and reducing the expression of DNA repair proteins even in radioresistant HCT116 p53-/- colorectal cancer cells and tumors.	Metformin	15-24	P53	Homo sapiens	156-159
26579714-12	2015	This parameter has been observed to be able to mimic the binding affinity of the p53 ts-mutants at 300 K and 310 K. Thus the correlation between MM-GBSA free energy of binding and hydrogen bonds formed by the interface residues between p53 and DNA has revealed the temperature dependent nature of these mutants.	Hydrogen	180-188	P53	Homo sapiens	236-239
26505788-1	2015	Lysine acetyltransferase 8 (KAT8) is a histone acetyltransferase (HAT) responsible for acetylating lysine 16 on histone H4 (H4K16) and plays a role in cell cycle progression as well as acetylation of the tumor suppressor protein p53.	Lysine	99-105	P53	Homo sapiens	229-232
26472020-11	2015	These findings suggest that ROS and p53 mutations may trigger a series of events, beginning with overexpressing miR-182 by ROS and beta-catenin, impairing the DNA damage response, promoting DNA instability, bypassing senescence and eventually leading to DNA instable tumors in FTSE cells.	Reactive Oxygen Species	123-126	P53	Homo sapiens	36-39
26885449-5	2015	In association with the reduction of MYC onco-protein, metformin significantly restored p53 tumor suppressor gene expression.	Metformin	55-64	P53	Homo sapiens	88-91
26885449-6	2015	The distinctive effects of metformin and PP242 on MYC reduction and P53 restoration suggested that metformin inhibited cell growth through a different pathway from PP242 in salivary carcinoma cells.	Metformin	99-108	P53	Homo sapiens	68-71
26885117-8	2015	Tumor protein 53 (P=0.015) and TRIB3 (P=0.045) expressions increased markedly in 80-mg atorvastatin group.	Atorvastatin	87-99	P53	Homo sapiens	0-16
26408200-5	2015	We present evidence that, as perinuclear aggresomes accumulate, they are associated with abnormal nuclear morphology and DNA double-strand breaks, resulting in cell cycle arrest via the phosphorylated p53 (Ser-15)-dependent pathway.	Serine	206-209	P53	Homo sapiens	201-204
26456774-3	2015	Resveratrol induces p53-dependent apoptosis via plasma membrane integrin alphavbeta3.	Resveratrol	0-11	P53	Homo sapiens	20-23
26491887-5	2015	We confirmed that ouabain induced chromosome segregation disorder and S-cell cycle block by decreasing the expression of AURKA, SMC2, Cyclin D, and p-CDK1 as well as increasing the expression of p53.	Ouabain	18-25	P53	Homo sapiens	195-198
26421917-3	2015	Here we consider an IDR of the tumor suppressor p53 protein, p53CTD, as an important example related to carcinogenesis and analyze its binding to four targets accompanying the formation of target-dependent structures (i.e., helix, sheet, and two different coils) using our statistical-mechanical method combined with molecular models for water.	Water	338-343	P53	Homo sapiens	48-51
26456774-6	2015	DHT inhibited resveratrol-stimulated phosphorylation of Ser-15 of p53 in a concentration-dependent manner.	Resveratrol	14-25	P53	Homo sapiens	66-69
26456774-6	2015	DHT inhibited resveratrol-stimulated phosphorylation of Ser-15 of p53 in a concentration-dependent manner.	Serine	56-59	P53	Homo sapiens	66-69
26456774-8	2015	DHT inhibited resveratrol-induced nuclear complex of p53-COX-2 formation which is required p53-dependent apoptosis.	Resveratrol	14-25	P53	Homo sapiens	53-56
26456774-8	2015	DHT inhibited resveratrol-induced nuclear complex of p53-COX-2 formation which is required p53-dependent apoptosis.	Resveratrol	14-25	P53	Homo sapiens	91-94
26456774-9	2015	ChIP studies of COX-2/p53 binding to DNA and expression of p53-responsive genes indicated that DHT inhibited resveratrol-induced p53-directed transcriptional activity.	Resveratrol	109-120	P53	Homo sapiens	22-25
26456774-9	2015	ChIP studies of COX-2/p53 binding to DNA and expression of p53-responsive genes indicated that DHT inhibited resveratrol-induced p53-directed transcriptional activity.	Resveratrol	109-120	P53	Homo sapiens	59-62
26456774-9	2015	ChIP studies of COX-2/p53 binding to DNA and expression of p53-responsive genes indicated that DHT inhibited resveratrol-induced p53-directed transcriptional activity.	Resveratrol	109-120	P53	Homo sapiens	59-62
26456774-10	2015	In addition, DHT did inhibit resveratrol-induced COX-2/p53-dependent gene expression.	Resveratrol	29-40	P53	Homo sapiens	55-58
26040007-7	2015	Additionally, p38 MAPK and p53 were activated in response to NaHS.	sodium bisulfide	61-65	P53	Homo sapiens	27-30
26115576-0	2015	Identification of a new p53/MDM2 inhibitor motif inspired by studies of chlorofusin.	chlorofusin	72-83	P53	Homo sapiens	24-27
26115576-1	2015	Previous studies on the natural product chlorofusin have shown that the full peptide and azaphilone structure are required for inhibition of the interaction between MDM2 and p53.	chlorofusin	40-51	P53	Homo sapiens	174-177
26115576-3	2015	From this small library the first ever non-azaphilone containing chlorofusin analog with MDM2/p53 activity was identified.	chlorofusin	65-76	P53	Homo sapiens	94-97
26522181-5	2015	DOX initiated DNA damage response (DDR) and upregulated PARP1 and p53 expression, resulting in morphological changes similar to those observed during necrosis.	Doxorubicin	0-3	P53	Homo sapiens	66-69
26040007-10	2015	p38 MAPK and p53 play an important role in NaHS-induced apoptosis in C6 cells.	sodium bisulfide	43-47	P53	Homo sapiens	13-16
26363031-7	2015	When p53 and Rb were turned down, the FF-exposed secretory cells overcame apoptosis and expanded the population carrying ROS and DSB.	Reactive Oxygen Species	121-124	P53	Homo sapiens	5-8
26227335-4	2015	We will use p53 and nuclear receptors, especially estrogen receptor alpha, as examples to discuss the dynamic nature of non-histone protein lysine methylation, the writers, erasers, and readers of these modifications, and the crosstalk between lysine methylation and other PTMs in regulating the functions of the modified proteins.	Lysine	140-146	P53	Homo sapiens	12-15
26535076-5	2015	H2O2-induced ROS increased the levels of phosphorylated p38 mitogen activated protein kinase (MAPK), Jun-N-terminal kinase (JNK), ataxia telangiectasia mutated (ATM), and p53, which were inhibited by lycopene pretreatment.	Hydrogen Peroxide	0-4	P53	Homo sapiens	171-174
26535076-5	2015	H2O2-induced ROS increased the levels of phosphorylated p38 mitogen activated protein kinase (MAPK), Jun-N-terminal kinase (JNK), ataxia telangiectasia mutated (ATM), and p53, which were inhibited by lycopene pretreatment.	Reactive Oxygen Species	13-16	P53	Homo sapiens	171-174
26363031-11	2015	The study revealed ROS and mitogens in mature ovarian follicles could initiate the transformation of fimbria epithelium in the context of p53 loss and melatonin is a potent preventive agent.	Reactive Oxygen Species	19-22	P53	Homo sapiens	138-141
26397233-3	2015	In the present study, adriamycin and nutlin-3 were used to activate p53, which induced both miR-203 and Puma expression in HCT116 cells.	Doxorubicin	22-32	P53	Homo sapiens	68-71
26205328-5	2015	Here, we describe recent work defining a new class of drugs termed zinc metallochaperones that restore WT p53 structure and function by restoring Zn(2+) to Zn(2+)-deficient mutant p53.	Zinc	146-148	P53	Homo sapiens	106-109
26205328-5	2015	Here, we describe recent work defining a new class of drugs termed zinc metallochaperones that restore WT p53 structure and function by restoring Zn(2+) to Zn(2+)-deficient mutant p53.	Zinc	146-148	P53	Homo sapiens	180-183
26205328-5	2015	Here, we describe recent work defining a new class of drugs termed zinc metallochaperones that restore WT p53 structure and function by restoring Zn(2+) to Zn(2+)-deficient mutant p53.	Zinc	156-158	P53	Homo sapiens	106-109
26205328-5	2015	Here, we describe recent work defining a new class of drugs termed zinc metallochaperones that restore WT p53 structure and function by restoring Zn(2+) to Zn(2+)-deficient mutant p53.	Zinc	156-158	P53	Homo sapiens	180-183
26494712-9	2015	This newly evolved function is achieved by the binding of the PCL1 N-terminal PHD domain to the C-terminal domain of p53 through two unique serine residues, which were acquired during recent vertebrate evolution.	Serine	140-146	P53	Homo sapiens	117-120
26287402-10	2015	Phosphorylated AMPK is involved in the regulation of 17beta-estradiol-mediated inhibition of SC viability through increasing p53 and p27 expression and inhibiting mTOR and Skp2 expression.	Estradiol	53-69	P53	Homo sapiens	125-128
26519823-0	2015	Cadmium treatment suppresses DNA polymerase delta catalytic subunit gene expression by acting on the p53 and Sp1 regulatory axis.	Cadmium	0-7	P53	Homo sapiens	101-104
26519823-7	2015	Our results indicated that Cd-mediated impairment of BER pathway, besides acting on the enzymatic functions of some key proteins, is also exerted at the gene expression level of Poldelta by acting on the p53-Sp1 regulatory axis.	Cadmium	27-29	P53	Homo sapiens	204-207
26365581-11	2015	Synergistic effect with tamoxifen was observed in terms of increased p53 protein level.	Tamoxifen	24-33	P53	Homo sapiens	69-72
26386653-7	2015	We also found that under serum deprivation condition, leptin decreases p53 levels and the inhibitory leptin effect is lost when cells were pretreated with 50 muM PD98059 or 10 muM LY29004; or were transfected with dominant negative mutants of intermediates of these pathways, suggesting that MAPK and PI3K signaling pathways are necessaries for leptin action.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	162-169	P53	Homo sapiens	71-74
25154814-4	2015	We have established that Protein Phosphatase Magnesium-dependent 1 D (PPM1D) confers CDDP resistance in gynecological cancer cells by deactivating p53.	cddp	85-89	P53	Homo sapiens	147-150
26460892-0	2015	Curcumin induces p53-independent necrosis in H1299 cells via a mitochondria-associated pathway.	Curcumin	0-8	P53	Homo sapiens	17-20
26460892-1	2015	Curcumin has been shown to have various therapeutic and/or adjuvant therapeutic effects on human cancers, as it inhibits cancer cell proliferation and induces apoptosis through p53-dependent molecular pathways.	Curcumin	0-8	P53	Homo sapiens	177-180
26460892-2	2015	However, numerous cancer cell types bear a mutant p53 gene, and whether curcumin has any therapeutic effects on p53-deficient/mutant cancer cells has remained elusive.	Curcumin	72-80	P53	Homo sapiens	112-115
26460892-7	2015	In conclusion, the present study suggested that curcumin-induced necrotic cell death was mediated via a p53-independent molecular pathway, which was associated with Bax and Bak translocation, caspase activation and cytochrome c release.	Curcumin	48-56	P53	Homo sapiens	104-107
26170095-5	2015	It was observed that p53 binds at the CsA-binding site of CypD.	Cyclosporine	38-41	P53	Homo sapiens	21-24
26386653-8	2015	Additionally, leptin diminished Ser-46 p53 phosphorylation and this effect in placental explants was mediated by the activation of MAPK and PI3K pathways.	Serine	32-35	P53	Homo sapiens	39-42
26259609-5	2015	Mitochondrial biogenesis and cytosolic production of reactive oxygen species were also reduced after p53 inhibition; the latter change induced mitochondrial superoxide accumulation and mitochondrial damage, which triggered the activation of caspase 3.	Reactive Oxygen Species	53-76	P53	Homo sapiens	101-104
26259609-5	2015	Mitochondrial biogenesis and cytosolic production of reactive oxygen species were also reduced after p53 inhibition; the latter change induced mitochondrial superoxide accumulation and mitochondrial damage, which triggered the activation of caspase 3.	Superoxides	157-167	P53	Homo sapiens	101-104
26341291-0	2015	Natural products induce a G protein-mediated calcium pathway activating p53 in cancer cells.	Calcium	45-52	P53	Homo sapiens	72-75
26586936-9	2015	As4S4 and cisplatin synergistically stimulated p53, phosphor-p38 (p-p38), and increased cleaved caspase 3 (c-caspase 3).	as4s4	0-5	P53	Homo sapiens	47-50
26341291-5	2015	Further, we demonstrate that this elevation of intracellular calcium modulates p53 activity and the subsequent transcription of several pro-apoptotic genes encoding PIG8, CD95, PIDD, TP53INP, RRM2B, Noxa, p21 and PUMA.	Calcium	61-68	P53	Homo sapiens	79-82
26586936-9	2015	As4S4 and cisplatin synergistically stimulated p53, phosphor-p38 (p-p38), and increased cleaved caspase 3 (c-caspase 3).	Cisplatin	10-19	P53	Homo sapiens	47-50
26400171-3	2015	Benzo[a]pyrene,diol epoxide (BPDE) is a potent cigarette smoke carcinogen that forms guanine adducts at TP53 CpG mutation hotspot sites including codons 157, 158, 245, 248 and 273.	diol epoxide	15-27	P53	Homo sapiens	104-108
26400171-3	2015	Benzo[a]pyrene,diol epoxide (BPDE) is a potent cigarette smoke carcinogen that forms guanine adducts at TP53 CpG mutation hotspot sites including codons 157, 158, 245, 248 and 273.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	29-33	P53	Homo sapiens	104-108
26400171-4	2015	We performed molecular modelling of BPDE-adducted TP53 duplex sequences to determine the degree of local distortion caused by adducts which could influence the ability of nucleotide excision repair.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	36-40	P53	Homo sapiens	50-54
26400171-6	2015	Using TP53 trinucleotide mutation signatures for lung cancer in smokers and non-smokers we further show that codons 157 and 273 have the highest mutation probability in smokers.	trinucleotide	11-24	P53	Homo sapiens	6-10
26513723-0	2015	The Role of Structural Elements of the 5"-Terminal Region of p53 mRNA in Translation under Stress Conditions Assayed by the Antisense Oligonucleotide Approach.	Oligonucleotides	134-149	P53	Homo sapiens	61-64
26193055-8	2015	Furthermore, the increase in expression of phosphorylated p53 induced by cisplatin is markedly attenuated by pretreatment with erdosteine in the mitochondrial fraction.	Cisplatin	73-82	P53	Homo sapiens	58-61
26512957-0	2015	P53-dependent upregulation of neutral sphingomyelinase-2: role in doxorubicin-induced growth arrest.	Doxorubicin	66-77	P53	Homo sapiens	0-3
26439986-0	2015	Estradiol induces apoptosis via activation of miRNA-23a and p53: implication for gender difference in liver cancer development.	Estradiol	0-9	P53	Homo sapiens	60-63
26493598-6	2015	We then show that U87- p53 inactivity can be rescued by zinc (Zn).	Zinc	62-64	P53	Homo sapiens	23-26
26492315-4	2015	Our results suggest that combined treatment with rosiglitazone and LA-12 might be promising anticancer strategy in colon-derived tumours regardless of their p53 status, and also favourable in those defective in PTEN function.	Rosiglitazone	49-62	P53	Homo sapiens	157-160
25619836-0	2015	Three-dimensional microenvironment confers enhanced sensitivity to doxorubicin by reducing p53-dependent induction of autophagy.	Doxorubicin	67-78	P53	Homo sapiens	91-94
25619836-6	2015	Moreover, in the monolayer-cultured cells, DOXO treatment led to increases in p53 and DRAM-1 expression, which is a p53-dependent activator of autophagy that functions in response to DNA damage.	Doxorubicin	43-47	P53	Homo sapiens	78-81
25619836-6	2015	Moreover, in the monolayer-cultured cells, DOXO treatment led to increases in p53 and DRAM-1 expression, which is a p53-dependent activator of autophagy that functions in response to DNA damage.	Doxorubicin	43-47	P53	Homo sapiens	116-119
25619836-8	2015	The knockdown of p53 by shRNA blocked DRAM-1 activation, impaired autophagy induction and sensitized only those cells maintained under 2D conditions to DOXO.	Doxorubicin	152-156	P53	Homo sapiens	17-20
25619836-9	2015	In addition, 2D-cultured MDA-MB-231 cells (a p53-mutated breast cancer cell line) not only showed increased sensitivity to DOXO compared with MCF-7 cells but also failed to induce DRAM-1 expression or autophagy.	Doxorubicin	123-127	P53	Homo sapiens	45-48
25619836-11	2015	These results suggest that the 3D tissue microenvironment controls tumor cell sensitivity to DOXO treatment by preventing p53-DRAM-autophagy axis activation.	Doxorubicin	93-97	P53	Homo sapiens	122-125
26459859-8	2015	All these parameters conclude that elevated unconjugated bilirubin causes thrombocytopenia by stimulating platelet apoptosis via mitochondrial ROS-induced p38 and p53 activation.	Reactive Oxygen Species	143-146	P53	Homo sapiens	163-166
26334096-0	2015	A phase 1/2 study combining gemcitabine, Pegintron and p53 SLP vaccine in patients with platinum-resistant ovarian cancer.	Platinum	88-96	P53	Homo sapiens	55-58
26505347-7	2015	Interestingly, in the kidney, cisplatin treatment can activate AMP-activated protein kinase (AMPK), a signaling molecule that is also critical for p53-mediated inactivation of mammalian target of rapamycin (mTOR) pathways.	Cisplatin	30-39	P53	Homo sapiens	147-150
26540407-5	2015	Surprisingly, the genetic or chemical silencing of p53 significantly enhanced the cytotoxic effects of both VMY and the DNA damaging drug, doxorubicin.	Doxorubicin	139-150	P53	Homo sapiens	51-54
26505347-10	2015	Given the fact that p53 can regulate autophagy by inactivating mTOR via AMPK, our results suggest that the p53 pathway may also play a critical role in the pathogenesis of cisplatin-induced renal damage.	Cisplatin	172-181	P53	Homo sapiens	20-23
26505347-10	2015	Given the fact that p53 can regulate autophagy by inactivating mTOR via AMPK, our results suggest that the p53 pathway may also play a critical role in the pathogenesis of cisplatin-induced renal damage.	Cisplatin	172-181	P53	Homo sapiens	107-110
26431317-7	2015	Further analysis revealed that TPA+UVC co-exposure caused synergistic perturbation of specific genes associated with p53, AP-1 and inflammatory pathways important in carcinogenesis.	Tetradecanoylphorbol Acetate	31-34	P53	Homo sapiens	117-120
26025680-7	2015	Depletion of JMJD5 inhibited cell proliferation and enhanced adriamycin-induced cell growth suppression in the presence of p53.	Doxorubicin	61-71	P53	Homo sapiens	123-126
26264138-2	2015	P53 overproduction led to transcriptional downregulation of some yeast genes, such as the TRX1/2 thioredoxin system, which plays a key role in cell protection against various oxidative stresses induced by reactive oxygen species (ROS).	Reactive Oxygen Species	205-228	P53	Homo sapiens	0-3
26264138-2	2015	P53 overproduction led to transcriptional downregulation of some yeast genes, such as the TRX1/2 thioredoxin system, which plays a key role in cell protection against various oxidative stresses induced by reactive oxygen species (ROS).	Reactive Oxygen Species	230-233	P53	Homo sapiens	0-3
26264138-5	2015	Furthermore, measurements of ROS amounts by flow cytometry and fluorescence microscopy indicated that the TRX2 protein acted probably through its increased detoxifying activity on the P53-generated ROS.	Reactive Oxygen Species	29-32	P53	Homo sapiens	184-187
26264138-5	2015	Furthermore, measurements of ROS amounts by flow cytometry and fluorescence microscopy indicated that the TRX2 protein acted probably through its increased detoxifying activity on the P53-generated ROS.	Reactive Oxygen Species	198-201	P53	Homo sapiens	184-187
26264138-7	2015	The growth inhibitory effect of P53 was partially reversed by the antioxidant N-acetylcysteine.	Acetylcysteine	78-94	P53	Homo sapiens	32-35
26264138-8	2015	Our data strengthen the idea that overexpression of a single gene (trx2) decreases the p53-mediated cell death by decreasing ROS accumulation.	Reactive Oxygen Species	125-128	P53	Homo sapiens	87-90
26408691-4	2015	Treatment of tumor cells with the antioxidant N-acetylcysteine was able to prevent Zn(2+)-induced apoptosis, as well as the increase of p53 and FAS ligand protein induced by zinc.	Acetylcysteine	46-62	P53	Homo sapiens	136-139
26408691-5	2015	Zinc induces apoptosis in melanoma cells by increasing ROS and this effect may be mediated by the ROS-dependent induction of p53 and FAS/FAS ligand.	Reactive Oxygen Species	98-101	P53	Homo sapiens	125-128
26408696-2	2015	This study was performed to investigate the anticancer properties of alpha-santalol associated with the induction of apoptosis in cultured MCF-7 [estrogen receptor (ER)-positive, and wild-type p53)] and MDA-MB-231 (ER-negative and mutant p53) breast cancer cells.	a-santalol	69-83	P53	Homo sapiens	193-196
26408696-2	2015	This study was performed to investigate the anticancer properties of alpha-santalol associated with the induction of apoptosis in cultured MCF-7 [estrogen receptor (ER)-positive, and wild-type p53)] and MDA-MB-231 (ER-negative and mutant p53) breast cancer cells.	a-santalol	69-83	P53	Homo sapiens	238-241
26250568-5	2015	When cells were pretreated with a p53 inhibitor (pifithrin-a), followed by magnolol treatment, pifithrin-a blocked magnolol-induced apoptosis and G0 /G1 arrest.	magnolol	115-123	P53	Homo sapiens	34-37
26250568-0	2015	Magnolol inhibits growth of gallbladder cancer cells through the p53 pathway.	magnolol	0-8	P53	Homo sapiens	65-68
26231140-4	2015	In the resting neutrophils resveratrol and to lesser extent other polyphenols increased DNA damage and increased the level of p53.	Resveratrol	27-38	P53	Homo sapiens	126-129
26250568-4	2015	Magnolol also blocked cell cycle progression at G0 /G1 phase and induced mitochondrial-related apoptosis by upregulating p53 and p21 protein levels and by downregulating cyclin D1, CDC25A, and Cdk2 protein levels.	magnolol	0-8	P53	Homo sapiens	121-124
26231140-7	2015	These compounds appeared the most effective inducers of p53 in the TPA-challenged neutrophils, what may suggest that pro-apoptotic activity of these stilbenes might be related to p53 activation.	Tetradecanoylphorbol Acetate	67-70	P53	Homo sapiens	56-59
26231140-7	2015	These compounds appeared the most effective inducers of p53 in the TPA-challenged neutrophils, what may suggest that pro-apoptotic activity of these stilbenes might be related to p53 activation.	Tetradecanoylphorbol Acetate	67-70	P53	Homo sapiens	179-182
26205069-5	2015	The typical mechanism of cisplatin action involves DNA damage, activation of p53 protein and induction of cell death, as previously described for titanium ions.	Cisplatin	25-34	P53	Homo sapiens	77-80
26187504-11	2015	Importantly, APR-246 synergistically enhanced the inhibitory effects of cisplatin and 5-fluorouracil through p53 accumulation.	Cisplatin	72-81	P53	Homo sapiens	109-112
26187504-11	2015	Importantly, APR-246 synergistically enhanced the inhibitory effects of cisplatin and 5-fluorouracil through p53 accumulation.	Fluorouracil	86-100	P53	Homo sapiens	109-112
25971460-9	2015	Finally, we showed that the induction of Sestrin-2 by Sevoflurane was mediated by p53.	Sevoflurane	54-65	P53	Homo sapiens	82-85
26314369-0	2015	Zn(II)-curc targets p53 in thyroid cancer cells.	Zinc	0-6	P53	Homo sapiens	20-23
26314369-5	2015	Here, we investigated whether Zn(II)-curc could affect p53 in thyroid cancer cells with both p53 mutation (R273H) and wild-type p53.	Zinc	30-36	P53	Homo sapiens	55-58
26314369-8	2015	In addition, Zn(II)-curc triggered p53 target gene expression in wild-type p53-carrying cells.	Zinc	13-19	P53	Homo sapiens	35-38
26314369-8	2015	In addition, Zn(II)-curc triggered p53 target gene expression in wild-type p53-carrying cells.	Zinc	13-19	P53	Homo sapiens	75-78
26314369-10	2015	Taken together, our data indicate that Zn(II)-curc promotes the reactivation of p53 in thyroid cancer cells, providing in vitro evidence for a potential therapeutic approach in thyroid cancers.	Zinc	39-45	P53	Homo sapiens	80-83
26315556-0	2015	Myricetin inhibits proliferation of cisplatin-resistant cancer cells through a p53-dependent apoptotic pathway.	myricetin	0-9	P53	Homo sapiens	79-82
26315556-0	2015	Myricetin inhibits proliferation of cisplatin-resistant cancer cells through a p53-dependent apoptotic pathway.	Cisplatin	36-45	P53	Homo sapiens	79-82
26383681-7	2015	Interestingly, metformin may enhance radiation response specifically in certain genetic backgrounds, such as in cells with loss of the tumor suppressors p53 and LKB1, giving rise to a therapeutic ratio and potential predictive biomarkers.	Metformin	15-24	P53	Homo sapiens	153-156
25762091-5	2015	RESULTS: Here, we show that expression of Rap2B was induced by nocodazole in a p53-dependent manner.	Nocodazole	63-73	P53	Homo sapiens	79-82
25929783-5	2015	Cell death was accompanied by a significant increase in phosphorylated p53 at serine 15 and accumulation of PTEN.	Serine	78-84	P53	Homo sapiens	71-74
25659586-6	2015	We report here the ability of p73 to upregulate the expression of the A2B receptor, a recently characterized p53 target that effectively promotes cell death in response to extracellular adenosine--a metabolite that accumulates during various forms of cellular stress.	Adenosine	186-195	P53	Homo sapiens	109-112
24798859-5	2015	Here, we report that the environmental carcinogen benzo[a]pyrene (BaP) upregulated the expression of seven p53-targeting miRNAs (miR-25, miR-15a, miR-16, miR-92, miR-125b, miR-141, and miR-200a), while 2,3,7,8-tetrachlorodibenzo-rho-dioxin (TCDD) upregulated two of them (miR-25 and miR-92) in MM cells.	Polychlorinated Dibenzodioxins	241-245	P53	Homo sapiens	107-110
26208523-11	2015	These data indicate that the DACH carrier ligand in oxaliplatin triggers signaling via the p53-miR-34a-E2F axis, leading to transcriptional regulation that ultimately results in accumulation of dUTP and reduced dTTP biosynthesis, potentially enhancing 5-FU cytotoxicity.	Fluorouracil	252-256	P53	Homo sapiens	91-94
25959925-4	2015	Cisplatin-resistant A549R cells treated with Ru@L-SeNPs-siRNA demonstrated significant downregulation of P-glycoprotein (P-gp) expression, resulting in unprecedented enhanced cytotoxicity through the induction of apoptosis with the involvement of phosphorylation of p53, MAPK and PI3K/Akt signaling pathways.	Cisplatin	0-9	P53	Homo sapiens	266-269
26004085-10	2015	Our findings strongly indicate that concomitant inactivation of the p53- and pRB- pathways predict resistance towards anthracyclines and mitomycin in breast cancer in vivo.	Anthracyclines	118-132	P53	Homo sapiens	68-71
25659586-9	2015	Moreover, treatment of p53-null cancer cells with the chemotherapeutic drug adriamycin (doxorubicin) induces A2B in a p73-dependent manner and, in combination with an A2B agonist, substantially enhances apoptotic death.	Doxorubicin	76-86	P53	Homo sapiens	23-26
25659586-9	2015	Moreover, treatment of p53-null cancer cells with the chemotherapeutic drug adriamycin (doxorubicin) induces A2B in a p73-dependent manner and, in combination with an A2B agonist, substantially enhances apoptotic death.	Doxorubicin	88-99	P53	Homo sapiens	23-26
25659586-10	2015	We therefore propose an alternate and distinct p53-independent pathway to stimulate programmed cell death involving p73-mediated engagement of adenosine signalling.	Adenosine	143-152	P53	Homo sapiens	47-50
26317157-0	2015	Depletion of the cisplatin targeted HMGB-box factor UBF selectively induces p53-independent apoptotic death in transformed cells.	Cisplatin	17-26	P53	Homo sapiens	76-79
26313152-8	2015	Expression of anti-apoptotic proteins Bcl-2 and Mcl-1 and DNA repair associated molecules ATM, CHK1, TP73, p53, and ERCC1 were significantly up regulated in cisplatin-treated A549sc and H157sc cells, but no increase was detected in A549IL-6si and H157IL-6si cells.	Cisplatin	157-166	P53	Homo sapiens	107-110
26302161-7	2015	This study shows that p53 is activated in astrocytes during ischemia and that inhibition of the activity of this molecule prevents not only OGD-induced neuronal and astrocytic death but also astrocyte activation and impaired glutamate uptake.	Glutamic Acid	225-234	P53	Homo sapiens	22-25
26420962-0	2015	TP53 codon 72 Arg/Arg polymorphism is associated with a higher risk for inflammatory bowel disease development.	Arginine	14-17	P53	Homo sapiens	0-4
26406246-4	2015	Hypoxia induced translocation of p53 was investigated by using mitochondrial membrane permeability transition pore blocker cyclosporin A (blocks entry of p53 to mitochondria) and confirmed by western blot and immunofluorescence.	Cyclosporine	123-136	P53	Homo sapiens	33-36
26406246-4	2015	Hypoxia induced translocation of p53 was investigated by using mitochondrial membrane permeability transition pore blocker cyclosporin A (blocks entry of p53 to mitochondria) and confirmed by western blot and immunofluorescence.	Cyclosporine	123-136	P53	Homo sapiens	154-157
26342198-9	2015	Furthermore, blockage of the beta1-integrin/FAK/PI3K/AKT/mTOR pathway by siRNA or specific chemical inhibitors, or rescue of p53 activation can partially reverse the switch of glucose metabolism and inhibit the migration of Twist-overexpressing MCF10A cells and Twist-positive breast cancer cells.	Glucose	176-183	P53	Homo sapiens	125-128
26342198-10	2015	Thus, our data suggest that Twist promotes reprogramming of glucose metabolism in MCF10A-Twist cells and Twist-positive breast cancer cells via activation of the beta1-integrin/FAK/PI3K/AKT/mTOR pathway and inhibition of the p53 pathway.	Glucose	60-67	P53	Homo sapiens	225-228
26309162-7	2015	Moreover, h-R3-dendriplexes for p53 delivery indicated efficient cell growth inhibition and potentiated paclitaxel-induced cell death.	Paclitaxel	104-114	P53	Homo sapiens	32-35
26387611-0	2015	The energy blockers bromopyruvate and lonidamine lead GL15 glioblastoma cells to death by different p53-dependent routes.	bromopyruvate	20-33	P53	Homo sapiens	100-103
26387611-6	2015	In addition, Akt(Ser(473)) and p53(Ser(15)/Ser(315)) dephosphorylation occurred.	Serine	35-38	P53	Homo sapiens	31-34
26387611-6	2015	In addition, Akt(Ser(473)) and p53(Ser(15)/Ser(315)) dephosphorylation occurred.	Serine	35-38	P53	Homo sapiens	31-34
26420962-0	2015	TP53 codon 72 Arg/Arg polymorphism is associated with a higher risk for inflammatory bowel disease development.	Arginine	18-21	P53	Homo sapiens	0-4
26420962-4	2015	A single nucleotide polymorphism (SNP) in the TP53 gene resulting in the presence of either arginine (Arg) or proline (Pro) or both at codon 72 was shown to alter TP53 tumor-suppressor properties.	Arginine	92-100	P53	Homo sapiens	46-50
26420962-4	2015	A single nucleotide polymorphism (SNP) in the TP53 gene resulting in the presence of either arginine (Arg) or proline (Pro) or both at codon 72 was shown to alter TP53 tumor-suppressor properties.	Arginine	92-100	P53	Homo sapiens	163-167
26420962-4	2015	A single nucleotide polymorphism (SNP) in the TP53 gene resulting in the presence of either arginine (Arg) or proline (Pro) or both at codon 72 was shown to alter TP53 tumor-suppressor properties.	Arginine	102-105	P53	Homo sapiens	46-50
26420962-4	2015	A single nucleotide polymorphism (SNP) in the TP53 gene resulting in the presence of either arginine (Arg) or proline (Pro) or both at codon 72 was shown to alter TP53 tumor-suppressor properties.	Arginine	102-105	P53	Homo sapiens	163-167
26420962-8	2015	RESULTS: The most frequent TP53 genotype in IBD patients was Arg/Arg occurring in 54%-64% of cases (and in only 32% of controls).	Arginine	61-64	P53	Homo sapiens	27-31
26420962-8	2015	RESULTS: The most frequent TP53 genotype in IBD patients was Arg/Arg occurring in 54%-64% of cases (and in only 32% of controls).	Arginine	65-68	P53	Homo sapiens	27-31
26420962-11	2015	CONCLUSION: The data suggests that the TP53 codon 72 Arg/Arg genotype is associated with increased risk for IBD development.	Arginine	53-56	P53	Homo sapiens	39-43
26420962-11	2015	CONCLUSION: The data suggests that the TP53 codon 72 Arg/Arg genotype is associated with increased risk for IBD development.	Arginine	57-60	P53	Homo sapiens	39-43
26368019-10	2015	Gyp was also found to up-regulate 5-Fu-caused phospho-p53 expression and thus augment 5-Fu-induced G0/G1 phase arrest.	Fluorouracil	34-38	P53	Homo sapiens	54-57
26188124-8	2015	3) Finally, VTD or its modified analogs offer a valuable adjuvant chemotherapy strategy to improve the efficacy of 5-FU-based chemotherapy for colon cancer patients harboring WT-p53.	Fluorouracil	115-119	P53	Homo sapiens	178-181
26337205-7	2015	In contrast, in apoptosis sensitive cells activated p53 increased superoxide levels and inhibited glycolysis through repression of glycolytic pathway genes.	Superoxides	66-76	P53	Homo sapiens	52-55
26337205-12	2015	Specifically, the findings indicate 1) that glycolysis plays an essential role in autophagy by limiting superoxide levels and maintaining expression of ATG genes required for autophagic vesicle maturation, 2) that p53 can promote or inhibit autophagy depending on the status of glycolysis, and 3) that inhibiting protective autophagy can expand the breadth of cells susceptible to Nutlin-3a induced apoptosis.	Superoxides	104-114	P53	Homo sapiens	214-217
26815194-0	2015	[p14ARF enhances cisplatin-induced apoptosis in human osteosarcoma cells in p53-independent pathway].	Cisplatin	17-26	P53	Homo sapiens	76-79
26815194-16	2015	CONCLUSION: p14ARF enhances cisplatin-induced apoptosis in human osteosarcoma MG63 cells in p53-independent caspase-9-dependent pathway, in which the intrinsic mitochondrial apoptotic pathway is involved.	Cisplatin	28-37	P53	Homo sapiens	92-95
26368019-12	2015	Inhibition of ROS and p53 respectively reversed the cell death induced by 5-Fu + Gyp, suggesting the key roles of ROS and p53 in the process.	ros	14-17	P53	Homo sapiens	122-125
26368019-12	2015	Inhibition of ROS and p53 respectively reversed the cell death induced by 5-Fu + Gyp, suggesting the key roles of ROS and p53 in the process.	Fluorouracil	74-78	P53	Homo sapiens	22-25
26368019-12	2015	Inhibition of ROS and p53 respectively reversed the cell death induced by 5-Fu + Gyp, suggesting the key roles of ROS and p53 in the process.	Fluorouracil	74-78	P53	Homo sapiens	122-125
26368019-12	2015	Inhibition of ROS and p53 respectively reversed the cell death induced by 5-Fu + Gyp, suggesting the key roles of ROS and p53 in the process.	ros	114-117	P53	Homo sapiens	22-25
26225749-5	2015	Treatment of MCF-7 cells with metformin or phenformin induced increase in p53 protein levels and the transcription of its downstream target genes, Bax and p21, in a dose-dependent manner.	Metformin	30-39	P53	Homo sapiens	74-77
26208454-3	2015	Exogenous H2O2 tended to promote SIRT1 expression and induce more autophagy through mTOR pathway in control ph ESCs, by contrast more apoptosis via activation of p53 and caspase-3 in SIRT1-knockdown ph ESCs.	Hydrogen Peroxide	10-14	P53	Homo sapiens	162-165
26211519-2	2015	It is found that in the presence of p53, the strong interaction between the wild-type p53 and its consensus DNA sequence on the electrode surface can block the electron transfer from the BOD to the electrode, thus providing a good opportunity for reducing the electrocatalytic activity of oxygen reduction in the biocathode.	Oxygen	289-295	P53	Homo sapiens	36-39
26211519-2	2015	It is found that in the presence of p53, the strong interaction between the wild-type p53 and its consensus DNA sequence on the electrode surface can block the electron transfer from the BOD to the electrode, thus providing a good opportunity for reducing the electrocatalytic activity of oxygen reduction in the biocathode.	Oxygen	289-295	P53	Homo sapiens	86-89
26211519-3	2015	This in combination with the glucose oxidation at the carbon nanotube/Meldola"s blue/glucose dehydrogenase bioanode can result in a current/or power decrease of BFC in the presence of wild-type p53.	Glucose	29-36	P53	Homo sapiens	194-197
26211519-3	2015	This in combination with the glucose oxidation at the carbon nanotube/Meldola"s blue/glucose dehydrogenase bioanode can result in a current/or power decrease of BFC in the presence of wild-type p53.	Carbon	54-60	P53	Homo sapiens	194-197
26225749-0	2015	p53 is required for metformin-induced growth inhibition, senescence and apoptosis in breast cancer cells.	Metformin	20-29	P53	Homo sapiens	0-3
26225749-2	2015	The tumor inhibitory effect of metformin on p53-mutated breast cancer cells remains unclear.	Metformin	31-40	P53	Homo sapiens	44-47
26225749-6	2015	Moreover, we demonstrated that AMPK-mTOR signaling played a role in metformin-induced p53 up-regulation.	Metformin	68-77	P53	Homo sapiens	86-89
26225749-3	2015	Data from the present study demonstrated that p53 knockdown or mutation has a negative effect on metformin or phenformin-induced growth inhibition, senescence and apoptosis in breast cancer cells.	Metformin	97-106	P53	Homo sapiens	46-49
26225749-4	2015	We also found that p53 reactivating agent nutlin-3alpha and CP/31398 promoted metformin-induced growth inhibition, senescence and apoptosis in MCF-7 (wt p53) and MDA-MB-231 (mt p53) cells, respectively.	Metformin	78-87	P53	Homo sapiens	19-22
26225749-4	2015	We also found that p53 reactivating agent nutlin-3alpha and CP/31398 promoted metformin-induced growth inhibition, senescence and apoptosis in MCF-7 (wt p53) and MDA-MB-231 (mt p53) cells, respectively.	Metformin	78-87	P53	Homo sapiens	153-156
26225749-4	2015	We also found that p53 reactivating agent nutlin-3alpha and CP/31398 promoted metformin-induced growth inhibition, senescence and apoptosis in MCF-7 (wt p53) and MDA-MB-231 (mt p53) cells, respectively.	Metformin	78-87	P53	Homo sapiens	153-156
26225749-7	2015	The present study showed that p53 is required for metformin or phenformin-induced growth inhibition, senescence and apoptosis in breast cancer cells.	Metformin	50-59	P53	Homo sapiens	30-33
26225749-8	2015	The combination of metformin with p53 reactivating agents, like nutlin-3alpha and CP/31398, is a promising strategy for improving metformin-mediated anti-cancer therapy, especially for tumors with p53 mutations.	Metformin	19-28	P53	Homo sapiens	197-200
26225749-8	2015	The combination of metformin with p53 reactivating agents, like nutlin-3alpha and CP/31398, is a promising strategy for improving metformin-mediated anti-cancer therapy, especially for tumors with p53 mutations.	Metformin	130-139	P53	Homo sapiens	34-37
26225749-8	2015	The combination of metformin with p53 reactivating agents, like nutlin-3alpha and CP/31398, is a promising strategy for improving metformin-mediated anti-cancer therapy, especially for tumors with p53 mutations.	Metformin	130-139	P53	Homo sapiens	197-200
26375862-3	2015	In gynecologic cancers, p53 is a pivotal determinant of cisplatin sensitivity, while BCL-2 family members are associated with taxane sensitivity.	Cisplatin	56-65	P53	Homo sapiens	24-27
26405550-6	2015	Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P&lt;0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC.	Arginine	368-371	P53	Homo sapiens	40-43
26183023-2	2015	Previously, we found that p53 interacts with KAISO, and acetylation of p53 lysine residues by p300 is modulated by KAISO.	Lysine	75-81	P53	Homo sapiens	71-74
26405550-6	2015	Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P&lt;0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC.	Arginine	368-371	P53	Homo sapiens	40-43
26405550-6	2015	Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P&lt;0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC.	Arginine	247-255	P53	Homo sapiens	40-43
26405550-6	2015	Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P&lt;0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC.	Arginine	257-260	P53	Homo sapiens	40-43
25989210-0	2015	Actinomycin D and nutlin-3a synergistically promote phosphorylation of p53 on serine 46 in cancer cell lines of different origin.	Serine	78-84	P53	Homo sapiens	71-74
25989210-7	2015	Indeed, co-treatment of various cell lines with actinomycin D and nutlin-3a resulted in a synergistic increase of p53 phosphorylation on serine 46.	Serine	137-143	P53	Homo sapiens	114-117
26472972-9	2015	Curcumin and citral generated ROS and activated p53 and poly (ADP-ribose) polymerase-1 mediated apoptotic pathways.	Curcumin	0-8	P53	Homo sapiens	48-51
26617937-6	2015	Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, and Treponema denticola possess the PAD enzyme, and p53 arginine mutations have been detected in patients with pancreatic cancer.	Arginine	127-135	P53	Homo sapiens	123-126
26617937-9	2015	The hypothesis in question can be tested if the DNA of P. gingivalis or the antibodies against P. gingivalis can be detected in patients with the p53 arginine mutation.If this hypothesis is true, it could reveal the real cause of pancreatic cancer, which is a fatal disease.	Arginine	150-158	P53	Homo sapiens	146-149
26036622-0	2015	Curcumin Inhibits Invasiveness and Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma Through Reducing Matrix Metalloproteinase 2, 9 and Modulating p53-E-Cadherin Pathway.	Curcumin	0-8	P53	Homo sapiens	163-166
26036622-5	2015	RESULTS: Our data showed that curcumin treatment not only decreased the expression of MMP-2 and MMP-9 to inhibit invasiveness in oral cancer but also modulated the expression of EMT markers, such as Snail, Twist, and E-cadherin, and induced p53 expression that is crucial to EMT repression.	Curcumin	30-38	P53	Homo sapiens	241-244
25633717-0	2015	The tubulysin analogue KEMTUB10 induces apoptosis in breast cancer cells via p53, Bim and Bcl-2.	kemtub10	23-31	P53	Homo sapiens	77-80
25633717-8	2015	KEMTUB10-induced apoptosis involves p53 and Bim, and to some extent Bcl-2 phosphorylation.	kemtub10	0-8	P53	Homo sapiens	36-39
26133772-1	2015	The p53-inducible gene 3 (PIG3 or TP53I3) is a downstream gene of p53, which can be involved in the process of apoptosis induced by p53 via the production of reactive oxygen species (ROS).	Reactive Oxygen Species	158-181	P53	Homo sapiens	4-7
26205253-5	2015	Internalized nanoparticles trigger glioma cell apoptosis by activation of ROS-mediated p53 phosphorylation.	ros	74-77	P53	Homo sapiens	87-90
26133772-1	2015	The p53-inducible gene 3 (PIG3 or TP53I3) is a downstream gene of p53, which can be involved in the process of apoptosis induced by p53 via the production of reactive oxygen species (ROS).	Reactive Oxygen Species	158-181	P53	Homo sapiens	66-69
26133772-1	2015	The p53-inducible gene 3 (PIG3 or TP53I3) is a downstream gene of p53, which can be involved in the process of apoptosis induced by p53 via the production of reactive oxygen species (ROS).	Reactive Oxygen Species	158-181	P53	Homo sapiens	66-69
26133772-1	2015	The p53-inducible gene 3 (PIG3 or TP53I3) is a downstream gene of p53, which can be involved in the process of apoptosis induced by p53 via the production of reactive oxygen species (ROS).	Reactive Oxygen Species	183-186	P53	Homo sapiens	4-7
26177745-3	2015	Paclitaxel and other microtubule inhibitors can inhibit the growth of different types of cancer cells and induce apoptosis which is believed to be p53-independent.	Paclitaxel	0-10	P53	Homo sapiens	147-150
26133772-1	2015	The p53-inducible gene 3 (PIG3 or TP53I3) is a downstream gene of p53, which can be involved in the process of apoptosis induced by p53 via the production of reactive oxygen species (ROS).	Reactive Oxygen Species	183-186	P53	Homo sapiens	66-69
26133772-1	2015	The p53-inducible gene 3 (PIG3 or TP53I3) is a downstream gene of p53, which can be involved in the process of apoptosis induced by p53 via the production of reactive oxygen species (ROS).	Reactive Oxygen Species	183-186	P53	Homo sapiens	66-69
25916210-4	2015	According to flow cytometric analysis, nimbolide treatment resulted in G2/M arrest in 786-O and A-498 cells accompanied with an increase in the phosphorylation status of p53, cdc2, cdc25c, and decreased expressions of cyclin A, cyclin B, cdc2, and cdc25c.	nimbolide	39-48	P53	Homo sapiens	170-173
26425661-3	2015	Recent studies suggest that PRMT5, which is frequently elevated in human cancers, cooperates with oncogenic cyclin D1 and leaves marks on p53 by way of arginine methylation, promoting the bypass of wild-type p53, and in doing so, evade apoptosis.	Arginine	152-160	P53	Homo sapiens	138-141
26255724-4	2015	In MRC-5 human fetal lung cells, capsaicin augmented silent mating type information regulation 1 (SIRT1) deacetylase activity and the intracellular NAD(+)/NADH ratio, decreasing acetylation of p53 and inducing autophagy.	Capsaicin	33-42	P53	Homo sapiens	193-196
26061814-0	2015	p53 attenuates AKT signaling by modulating membrane phospholipid composition.	Phospholipids	52-64	P53	Homo sapiens	0-3
26061814-2	2015	Here we report a previously unrecognized role of p53 in membrane phospholipids composition.	Phospholipids	65-78	P53	Homo sapiens	49-52
26061814-3	2015	By repressing the expression of stearoyl-CoA desaturase 1, SCD, the enzyme that converts saturated to mono-unsaturated fatty acids, p53 causes a shift in the content of phospholipids with mono-unsaturated acyl chains towards more saturated phospholipid species, particularly of the phosphatidylinositol headgroup class.	Phospholipids	169-182	P53	Homo sapiens	132-135
26061814-3	2015	By repressing the expression of stearoyl-CoA desaturase 1, SCD, the enzyme that converts saturated to mono-unsaturated fatty acids, p53 causes a shift in the content of phospholipids with mono-unsaturated acyl chains towards more saturated phospholipid species, particularly of the phosphatidylinositol headgroup class.	Phospholipids	169-181	P53	Homo sapiens	132-135
26061814-4	2015	This shift affects levels of phosphatidylinositol phosphates, attenuates the oncogenic AKT pathway, and contributes to the p53-mediated control of cell survival.	Phosphatidylinositol Phosphates	29-60	P53	Homo sapiens	123-126
26061814-5	2015	These findings expand the p53 network to phospholipid metabolism and uncover a new molecular pathway connecting p53 to AKT signaling.	Phospholipids	41-53	P53	Homo sapiens	26-29
26312160-5	2015	Functional studies on TP53 mutant cells demonstrated an impaired p53-mediated response, resistance to ex vivo doxorubicin administration, overexpression of DNA damage response (DDR) activation markers and high sensitivity to pharmacologic DDR inhibition.	Doxorubicin	110-121	P53	Homo sapiens	22-26
26255724-5	2015	In contrast, capsaicin decreased the intracellular NAD(+)/NADH ratio, possibly through inhibition of tumor-associated NADH oxidase (tNOX), and diminished SIRT1 expression leading to enhanced p53 acetylation and apoptosis.	Capsaicin	13-22	P53	Homo sapiens	191-194
26305257-3	2015	Our previous studies and those of others on Chinese medicinal herbs and miRNAs in various cancer models have provided a possibility of new cancer therapies, for example, up-regulating the expression of miR-23a may activate the positive regulatory network of p53 and miR-23a involved in the mechanism underlying the anti-tumor effect of berberine in hepatocellular carcinoma (HCC).	Berberine	336-345	P53	Homo sapiens	258-261
26297485-0	2015	The beneficial effect of Zinc(II) on low-dose chemotherapeutic sensitivity involves p53 activation in wild-type p53-carrying colorectal cancer cells.	Zinc	25-33	P53	Homo sapiens	84-87
26297485-0	2015	The beneficial effect of Zinc(II) on low-dose chemotherapeutic sensitivity involves p53 activation in wild-type p53-carrying colorectal cancer cells.	Zinc	25-33	P53	Homo sapiens	112-115
26297485-11	2015	CONCLUSIONS: These results provide evidence that ZnCl2 might be a valuable adjuvant in chemotherapeutic regimens of colorectal cancer harboring wild-type p53, able to both activate p53 and reduce the amount of drugs for antitumor purposes.	zinc chloride	49-54	P53	Homo sapiens	154-157
26297485-11	2015	CONCLUSIONS: These results provide evidence that ZnCl2 might be a valuable adjuvant in chemotherapeutic regimens of colorectal cancer harboring wild-type p53, able to both activate p53 and reduce the amount of drugs for antitumor purposes.	zinc chloride	49-54	P53	Homo sapiens	181-184
26327815-5	2015	Furthermore, SH-SY5Y apoptosis via the mitochondria-dependent p53 pathway and cell cycle arrest caused by ROP16 dealt with direct serine 15/37 phosphorylation of p53.	Serine	130-136	P53	Homo sapiens	162-165
26113084-7	2015	[18F]-FDG PET-CT scans revealed a relative increase in glucose uptake in mutant TP53 versus WT TP53 tumors, with FX11 administration downregulating metabolic activity only in mutant TP53 tumors.	Glucose	55-62	P53	Homo sapiens	80-84
26113084-7	2015	[18F]-FDG PET-CT scans revealed a relative increase in glucose uptake in mutant TP53 versus WT TP53 tumors, with FX11 administration downregulating metabolic activity only in mutant TP53 tumors.	Glucose	55-62	P53	Homo sapiens	95-99
26113084-7	2015	[18F]-FDG PET-CT scans revealed a relative increase in glucose uptake in mutant TP53 versus WT TP53 tumors, with FX11 administration downregulating metabolic activity only in mutant TP53 tumors.	Glucose	55-62	P53	Homo sapiens	95-99
26143716-0	2015	One-Dimensional Sliding of p53 Along DNA Is Accelerated in the Presence of Ca(2+) or Mg(2+) at Millimolar Concentrations.	magnesium ion	85-91	P53	Homo sapiens	27-30
26143716-2	2015	To address how the search process of p53 is affected by the changes in the concentration of Mg(2+) and Ca(2+) after the cell damages, we investigated its sliding dynamics at different concentrations of the divalent cations.	magnesium ion	92-98	P53	Homo sapiens	37-40
26143716-4	2015	The averaged diffusion coefficient calculated from the mean square displacement of p53 on DNA increased significantly at the higher concentration of Mg(2+) or Ca(2+), indicating that the divalent cations accelerate the sliding likely by weakening the DNA-p53 interaction.	magnesium ion	149-155	P53	Homo sapiens	83-86
26143716-4	2015	The averaged diffusion coefficient calculated from the mean square displacement of p53 on DNA increased significantly at the higher concentration of Mg(2+) or Ca(2+), indicating that the divalent cations accelerate the sliding likely by weakening the DNA-p53 interaction.	magnesium ion	149-155	P53	Homo sapiens	255-258
26269716-6	2015	We found that IL6, TNF, CXCL8, IL1B and ERK1/2 were the top genes in terms of the number of connections in platinum-induced neuropathy and TP53, MYC, PARP1, P38 MAPK and TNF for combined taxane-platinum-induced neuropathy.	Platinum	107-115	P53	Homo sapiens	139-143
26269716-6	2015	We found that IL6, TNF, CXCL8, IL1B and ERK1/2 were the top genes in terms of the number of connections in platinum-induced neuropathy and TP53, MYC, PARP1, P38 MAPK and TNF for combined taxane-platinum-induced neuropathy.	taxane	187-193	P53	Homo sapiens	139-143
26269716-6	2015	We found that IL6, TNF, CXCL8, IL1B and ERK1/2 were the top genes in terms of the number of connections in platinum-induced neuropathy and TP53, MYC, PARP1, P38 MAPK and TNF for combined taxane-platinum-induced neuropathy.	Platinum	194-202	P53	Homo sapiens	139-143
27551445-2	2015	Recently, we have described that RUNX2 attenuates p53/TAp73-dependent cell death of human osteosarcoma U2OS cells bearing wild-type p53 in response to adriamycin.	Doxorubicin	151-161	P53	Homo sapiens	50-53
27551445-2	2015	Recently, we have described that RUNX2 attenuates p53/TAp73-dependent cell death of human osteosarcoma U2OS cells bearing wild-type p53 in response to adriamycin.	Doxorubicin	151-161	P53	Homo sapiens	132-135
25944617-7	2015	In addition, in low ERCC1 expression NSCLC cell lines, knockdown of GOF mutant p53 enhanced cisplatin sensitivity.	Cisplatin	92-101	P53	Homo sapiens	79-82
26231043-4	2015	Clinically relevant, low concentrations of doxorubicin synergize in vitro and in vivo with DCA to further enhance p53 activation and to block tumor progression.	Doxorubicin	43-54	P53	Homo sapiens	114-117
25944617-8	2015	Further double knockdown of ERCC1 and GOF mutant p53 but not ERCC1 knockdown alone increased the cisplatin sensitivity of cells with both high ERCC1 expression and GOF p53 mutations.	Cisplatin	97-106	P53	Homo sapiens	49-52
26345853-7	2015	According to gene ontology analysis, these genes are involved in lung development, respiratory system development, cell cycle, histidine metabolism, the Wnt signaling pathway, and the p53 signaling pathway.	Histidine	127-136	P53	Homo sapiens	184-187
25944617-8	2015	Further double knockdown of ERCC1 and GOF mutant p53 but not ERCC1 knockdown alone increased the cisplatin sensitivity of cells with both high ERCC1 expression and GOF p53 mutations.	Cisplatin	97-106	P53	Homo sapiens	168-171
25944617-9	2015	Therefore, this study demonstrated that ERCC1 expression combined with p53 mutation status may determine the efficacy of cisplatin and HDACi combined therapy and guide the development of future NSCLC therapies.	Cisplatin	121-130	P53	Homo sapiens	71-74
25944617-0	2015	The predictive value of ERCC1 and p53 for the effect of panobinostat and cisplatin combination treatment in NSCLC.	Cisplatin	73-82	P53	Homo sapiens	34-37
26148435-4	2015	Importantly, it has been reported that arsenic induces reactive oxygen species (ROS), a process counteracted by p53.	Reactive Oxygen Species	55-78	P53	Homo sapiens	112-115
25997894-7	2015	H9c2 cardiomyoblasts cultured in the galactose-modified media showed lower DOX-induced activation of the apoptotic pathway, measured by decreased caspase-3 and -9 activation, and lower p53 expression, although ultimately loss of cells was not prevented.	Galactose	37-46	P53	Homo sapiens	185-188
26148435-4	2015	Importantly, it has been reported that arsenic induces reactive oxygen species (ROS), a process counteracted by p53.	Reactive Oxygen Species	80-83	P53	Homo sapiens	112-115
26148435-7	2015	Furthermore, for the first time, we demonstrate that arsenic activates p53-dependent transcription of ROS detoxification genes, such as SESN1, and by an indirect mechanism involving ATF3, genes that could be responsible for the S phase cell cycle arrest, such as CDC25A.	Reactive Oxygen Species	102-105	P53	Homo sapiens	71-74
25912478-0	2015	P53-dependent miRNAs mediate nitric oxide-induced apoptosis in colonic carcinogenesis.	Nitric Oxide	29-41	P53	Homo sapiens	0-3
26112218-6	2015	Knocking-down of PKM2 significantly enhanced gemcitabine-induced cell apoptosis through the activation of caspase 3/7 and PARP cleavage, and this inhibitory activity was associated with p38-mediated activation of p53 phosphorylation at serine 46.	Serine	236-242	P53	Homo sapiens	213-216
26070487-3	2015	Through an unbiased genome-wide ChIP-seq analysis, we have found that 5-lipoxygenase (ALOX5, 5-LO) which is a key enzyme of leukotriene (LT) biosynthesis, is a direct target gene of p53 and its expression is induced by genotoxic stress via actinomycin D (Act.D) or etoposide (Eto) treatment.	Leukotrienes	124-135	P53	Homo sapiens	182-185
26035065-10	2015	In summary, the results of our present study demonstrate that HSCs protect HepG2 cells against cisplatin-induced apoptosis and its protective effects occur via inhibiting the activation of p53, which is of critical importance for enhanced understanding of fundamental cancer biology.	Cisplatin	95-104	P53	Homo sapiens	189-192
26114728-6	2015	ROS production by LFBL mediated p53-dependent apoptosis and recovery was suppressed by promoting G1/S phase arrest and failure of cellular tight junctions.	Reactive Oxygen Species	0-3	P53	Homo sapiens	32-35
26114728-6	2015	ROS production by LFBL mediated p53-dependent apoptosis and recovery was suppressed by promoting G1/S phase arrest and failure of cellular tight junctions.	lfbl	18-22	P53	Homo sapiens	32-35
26202022-4	2015	As a sensor of cellular stress, p53 is a relevant messenger of cell death signaling in ROS-driven photodynamic therapy (PDT) of cancer.	ros	87-90	P53	Homo sapiens	32-35
25991017-4	2015	Pre-treatment with resveratrol, a SIRT1 activator, could attenuate rotenone-induced cell injury and p53 expression, whereas down-regulation of SIRT1 directly increased p53 expression.	Resveratrol	19-30	P53	Homo sapiens	100-103
26055447-8	2015	Norepinephrine markedly increased p53 expression in endothelial cells and macrophages.	Norepinephrine	0-14	P53	Homo sapiens	34-37
25991017-9	2015	Resveratrol activated SIRT1 can target H3K9 and regulate p53 gene expression at the transcriptional level, thus inhibiting p53 transcription to enhance neuroprotection, alleviating rotenone induced dopaminergic neurodegeneration.	Resveratrol	0-11	P53	Homo sapiens	57-60
25991017-9	2015	Resveratrol activated SIRT1 can target H3K9 and regulate p53 gene expression at the transcriptional level, thus inhibiting p53 transcription to enhance neuroprotection, alleviating rotenone induced dopaminergic neurodegeneration.	Resveratrol	0-11	P53	Homo sapiens	123-126
25952326-0	2015	Resveratrol induces DNA damage in colon cancer cells by poisoning topoisomerase II and activates the ATM kinase to trigger p53-dependent apoptosis.	Resveratrol	0-11	P53	Homo sapiens	123-126
25952326-5	2015	We show that the tumor suppressor p53 is activated in response to RSV and participates to the apoptotic process.	Resveratrol	66-69	P53	Homo sapiens	34-37
25952326-6	2015	Additionally, we show that HCT-116 p53 wt colon carcinoma cells are significantly more sensitive than HCT-116 p53-/- cells to RSV.	Resveratrol	126-129	P53	Homo sapiens	35-38
25952326-6	2015	Additionally, we show that HCT-116 p53 wt colon carcinoma cells are significantly more sensitive than HCT-116 p53-/- cells to RSV.	Resveratrol	126-129	P53	Homo sapiens	110-113
26025927-8	2015	In addition, mitophagy was induced by deletion of p53, with this effect being weakened by Parkin knockdown at a low oxygen tension.	Oxygen	116-122	P53	Homo sapiens	50-53
25362853-10	2015	miR-34a-5p induced cell apoptosis, cell cycle arrest at G1 phase and p53 transcription activity in HCT116 cells, but not in the HCT116 p53 knockout (p53(-/-)) cells.	mir-34a-5p	0-10	P53	Homo sapiens	69-72
25362853-11	2015	miR-34a-5p significantly suppressed the HCT116 growth in vivo, whereas it showed no effect on the HCT116 p53(-/-) xenograft, indicating that the growth-inhibiting effect by miR-34a-5p was dependent on p53.	mir-34a-5p	173-183	P53	Homo sapiens	201-204
26198749-6	2015	RESULTS: 3-BrPA could activate dose-dependent apoptosis (type 1 PCD) and regulated necrosis (type 3 PCD) of T24 (grade III; H-Ras(G12V); p53(DeltaY126)), but not RT4 (grade I), cells, with PARP, MLKL, Drp1 and Nec-7-targeted components critically orchestrating necrotic death.	bromopyruvate	9-15	P53	Homo sapiens	137-140
26196392-7	2015	Most importantly, the up-regulation of AMPK, p53, p21CIP1, p27KIP1 and the down-regulation of cyclinD1 are involved in the anti-tumor action of metformin in vivo.	Metformin	144-153	P53	Homo sapiens	45-48
26196392-9	2015	AMPK, p53, p21CIP1, p27KIP1 and cyclinD1 are involved in the inhibition of tumor growth that is induced by metformin and cell cycle arrest in ESCC.	Metformin	107-116	P53	Homo sapiens	6-9
26107995-7	2015	Interestingly, RuPOP@MWCNTs significantly enhanced the anticancer efficacy of clinically used X-ray against R-HepG2 cells through induction of apoptosis and G0/G1 cell cycle arrest, with the involvement of ROS overproduction, which activated several downstream signaling pathways, including DNA damage-mediated p53 phosphorylation, activation of p38, and inactivation of AKT and ERK.	ros	206-209	P53	Homo sapiens	311-314
25840356-8	2015	However, overexpression of SIRT1 through resveratrol treatment or transfection clearly attenuated the NiONPs-induced apoptosis and activation of p53 and Bax.	Resveratrol	41-52	P53	Homo sapiens	145-148
26209226-12	2015	Also, loss of GTSE1 expression caused a significant increase in P53 mediated apoptosis in cisplatin treated cells.	Cisplatin	90-99	P53	Homo sapiens	64-67
25982682-2	2015	Rare p53 mutations may be associated with cisplatin resistance.	Cisplatin	42-51	P53	Homo sapiens	5-8
26051007-0	2015	Proteomic Analysis of G2/M Arrest Triggered by Natural Borneol/Curcumin in HepG2 Cells, the Importance of the Reactive Oxygen Species-p53 Pathway.	Reactive Oxygen Species	110-133	P53	Homo sapiens	134-137
26162681-7	2015	Downstream events, measured by time-series reverse-phase protein microarrays, high-content imaging, and flow cytometry, showed a dramatic increase in mitochondrially produced reactive oxygen species (ROS) and subsequent DNA damage with up-regulation of ATM, p53, and p21 proteins.	Reactive Oxygen Species	175-198	P53	Homo sapiens	258-261
26162681-7	2015	Downstream events, measured by time-series reverse-phase protein microarrays, high-content imaging, and flow cytometry, showed a dramatic increase in mitochondrially produced reactive oxygen species (ROS) and subsequent DNA damage with up-regulation of ATM, p53, and p21 proteins.	Reactive Oxygen Species	200-203	P53	Homo sapiens	258-261
25980497-11	2015	In addition to the genomic regulation of TRPM8 by AR and p53, our findings indicate that the testosterone-induced PMTRPM8 activity elicits Ca2+ uptake, subsequently causing apoptotic cell death.	Testosterone	93-105	P53	Homo sapiens	57-60
26217671-4	2015	RITA binds N-terminal transactivation domain of p53 (Np53) weakly, preventing direct observation of the complex in the gas phase.	RITA	0-4	P53	Homo sapiens	48-51
26146988-7	2015	In addition, CDK5 knockdown alone and in combination with paclitaxel induced G1 cell cycle arrest and caspase 3 dependent apoptotic cell death associated with post-translational upregulation and nuclear translocation of TP53 and p27(Kip1) as well as TP53-dependent transcriptional induction of p21(Cip1) in wild type TP53 cancer cells.	Paclitaxel	58-68	P53	Homo sapiens	250-254
25912556-1	2015	This letter illustrates the significant chemosensitizing effects of chrysin to resistance cancer cells and refers to the article on "Combination of chrysin and cisplatin promotes the apoptosis of Hep G2 cells by up-regulating p53" by Li et al., published in your journal recently.	Cisplatin	160-169	P53	Homo sapiens	226-229
26146988-7	2015	In addition, CDK5 knockdown alone and in combination with paclitaxel induced G1 cell cycle arrest and caspase 3 dependent apoptotic cell death associated with post-translational upregulation and nuclear translocation of TP53 and p27(Kip1) as well as TP53-dependent transcriptional induction of p21(Cip1) in wild type TP53 cancer cells.	Paclitaxel	58-68	P53	Homo sapiens	220-224
26146988-7	2015	In addition, CDK5 knockdown alone and in combination with paclitaxel induced G1 cell cycle arrest and caspase 3 dependent apoptotic cell death associated with post-translational upregulation and nuclear translocation of TP53 and p27(Kip1) as well as TP53-dependent transcriptional induction of p21(Cip1) in wild type TP53 cancer cells.	Paclitaxel	58-68	P53	Homo sapiens	250-254
26124332-7	2015	Curcumin also increased phosphorylation of p53 and Histone H2A.X (S140) in the nuclei of NCI-H460 cells.	Curcumin	0-8	P53	Homo sapiens	43-46
25944899-4	2015	c-Abl and HIPK2 synergized in activating p53 on apoptotic promoters in a reporter assay, and c-Abl was required for endogenous HIPK2 accumulation and phosphorylation of p53 at Ser(46) in response to DNA damage by gamma- and UV radiation.	Serine	176-179	P53	Homo sapiens	41-44
25944899-4	2015	c-Abl and HIPK2 synergized in activating p53 on apoptotic promoters in a reporter assay, and c-Abl was required for endogenous HIPK2 accumulation and phosphorylation of p53 at Ser(46) in response to DNA damage by gamma- and UV radiation.	Serine	176-179	P53	Homo sapiens	169-172
25944899-7	2015	Under this condition, DNA damage-induced HIPK2 accumulation, phosphorylation of p53 at Ser(46), and apoptosis were attenuated.	Serine	87-90	P53	Homo sapiens	80-83
25754581-1	2015	We previously showed that progesterone (P4) could inhibit the proliferation of human umbilical venous endothelial cells (HUVECs) through the p53-dependent pathway.	Progesterone	26-38	P53	Homo sapiens	141-144
26049746-4	2015	This apparently irreversible EPHOSS phenomenon results from increased mitochondrial reactive oxygen species, mediated by a p53-cyclophilin D-mitochondrial permeability transition pore axis, and involves hypoxia inducing factor-1alpha and micro-RNA 210.	Reactive Oxygen Species	84-107	P53	Homo sapiens	123-126
25576341-9	2015	H2O2 upregulated p53 and miR-143, but downregulated ATG2B, Bcl-2, and LC3-I expression in U2OS cells (wild-type p53) but not in SAOS-2 (p53-null) cells.	Hydrogen Peroxide	0-4	P53	Homo sapiens	17-20
25576341-9	2015	H2O2 upregulated p53 and miR-143, but downregulated ATG2B, Bcl-2, and LC3-I expression in U2OS cells (wild-type p53) but not in SAOS-2 (p53-null) cells.	Hydrogen Peroxide	0-4	P53	Homo sapiens	112-115
25576341-9	2015	H2O2 upregulated p53 and miR-143, but downregulated ATG2B, Bcl-2, and LC3-I expression in U2OS cells (wild-type p53) but not in SAOS-2 (p53-null) cells.	Hydrogen Peroxide	0-4	P53	Homo sapiens	112-115
25232917-8	2015	Patients with homozygous Arg/arg at codon 72 of P53 had a better median OS months than Arg/Pro and Pro/Pro (13.4 vs. 8.4 vs. 1.5 months, respectively; P = 0.045).	Arginine	25-28	P53	Homo sapiens	48-51
25232917-8	2015	Patients with homozygous Arg/arg at codon 72 of P53 had a better median OS months than Arg/Pro and Pro/Pro (13.4 vs. 8.4 vs. 1.5 months, respectively; P = 0.045).	Arginine	29-32	P53	Homo sapiens	48-51
25232917-8	2015	Patients with homozygous Arg/arg at codon 72 of P53 had a better median OS months than Arg/Pro and Pro/Pro (13.4 vs. 8.4 vs. 1.5 months, respectively; P = 0.045).	Arginine	87-90	P53	Homo sapiens	48-51
25232917-9	2015	P53/p21 combination had a better median OS and disease-free survival (DFS) of 12.1 and 13.7 months for wild type cases (GG + Ser/ser) and 20.3 and 20.7 months for patients with either variant genes (GC + Ser/arg) compared with 1.1 and 1.9 months for patients with both variant genes (CC + arg/arg), (P = 0.037 and 0.004).	Serine	125-128	P53	Homo sapiens	0-3
25232917-9	2015	P53/p21 combination had a better median OS and disease-free survival (DFS) of 12.1 and 13.7 months for wild type cases (GG + Ser/ser) and 20.3 and 20.7 months for patients with either variant genes (GC + Ser/arg) compared with 1.1 and 1.9 months for patients with both variant genes (CC + arg/arg), (P = 0.037 and 0.004).	Serine	129-132	P53	Homo sapiens	0-3
25232917-9	2015	P53/p21 combination had a better median OS and disease-free survival (DFS) of 12.1 and 13.7 months for wild type cases (GG + Ser/ser) and 20.3 and 20.7 months for patients with either variant genes (GC + Ser/arg) compared with 1.1 and 1.9 months for patients with both variant genes (CC + arg/arg), (P = 0.037 and 0.004).	Serine	204-207	P53	Homo sapiens	0-3
25232917-9	2015	P53/p21 combination had a better median OS and disease-free survival (DFS) of 12.1 and 13.7 months for wild type cases (GG + Ser/ser) and 20.3 and 20.7 months for patients with either variant genes (GC + Ser/arg) compared with 1.1 and 1.9 months for patients with both variant genes (CC + arg/arg), (P = 0.037 and 0.004).	Arginine	208-211	P53	Homo sapiens	0-3
25232917-9	2015	P53/p21 combination had a better median OS and disease-free survival (DFS) of 12.1 and 13.7 months for wild type cases (GG + Ser/ser) and 20.3 and 20.7 months for patients with either variant genes (GC + Ser/arg) compared with 1.1 and 1.9 months for patients with both variant genes (CC + arg/arg), (P = 0.037 and 0.004).	Arginine	289-292	P53	Homo sapiens	0-3
25232917-9	2015	P53/p21 combination had a better median OS and disease-free survival (DFS) of 12.1 and 13.7 months for wild type cases (GG + Ser/ser) and 20.3 and 20.7 months for patients with either variant genes (GC + Ser/arg) compared with 1.1 and 1.9 months for patients with both variant genes (CC + arg/arg), (P = 0.037 and 0.004).	Arginine	289-292	P53	Homo sapiens	0-3
25858091-5	2015	We show that Emp53 binds specifically to oligonucleotides containing conventional p53 binding sites, indicating that it exhibits a function as a DNA binding transcription factor.	Oligonucleotides	41-57	P53	Homo sapiens	15-18
26123760-10	2015	However, a significant association between p53 Arg72Pro polymorphism and the risk of oral cancer with HPV infection was detected in the Arg/Arg vs. Arg/Pro + Pro/Pro model.	Arginine	47-50	P53	Homo sapiens	43-46
25695150-5	2015	The mRNA expression levels of p53, p53beta and B-cell lymphoma 2-associated X protein (Bax) were detected in the MKN45 and SGC-7901 cells following treatment with cisplatin by reverse transcription-PCR.	Cisplatin	163-172	P53	Homo sapiens	30-33
25695150-10	2015	In the MKN45 cells, p53beta, p53 and Bax mRNA expression levels gradually increased with the dose of cisplatin, and the expression of p53beta was positively correlated with the expression of p53 (tr=6.358, P&lt;0.05) and Bax (tr=8.023, P&lt;0.05).	Cisplatin	101-110	P53	Homo sapiens	20-23
25695150-10	2015	In the MKN45 cells, p53beta, p53 and Bax mRNA expression levels gradually increased with the dose of cisplatin, and the expression of p53beta was positively correlated with the expression of p53 (tr=6.358, P&lt;0.05) and Bax (tr=8.023, P&lt;0.05).	Cisplatin	101-110	P53	Homo sapiens	29-32
26122615-3	2015	p53 regulates various metabolic pathways, helping to balance glycolysis and oxidative phosphorylation, limiting the production of reactive oxygen species, and contributing to the ability of cells to adapt to and survive mild metabolic stresses.	Reactive Oxygen Species	130-153	P53	Homo sapiens	0-3
25263447-0	2015	p53 protein aggregation promotes platinum resistance in ovarian cancer.	Platinum	33-41	P53	Homo sapiens	0-3
26123760-10	2015	However, a significant association between p53 Arg72Pro polymorphism and the risk of oral cancer with HPV infection was detected in the Arg/Arg vs. Arg/Pro + Pro/Pro model.	Arginine	136-139	P53	Homo sapiens	43-46
26123760-10	2015	However, a significant association between p53 Arg72Pro polymorphism and the risk of oral cancer with HPV infection was detected in the Arg/Arg vs. Arg/Pro + Pro/Pro model.	Arginine	136-139	P53	Homo sapiens	43-46
25827071-4	2015	The potential of ATRA to stabilize p53 was almost completely abolished by knock-down of p14 in HepG2 cells and was not observed in p14-negative A549 cells.	Tretinoin	17-21	P53	Homo sapiens	35-38
25827071-7	2015	Ectopic expression of DNA methyltransferase 1 almost completely abolished the potential of ATRA to activate the p14-MDM2-p53 pathway and induce p53-dependent apoptosis.	Tretinoin	91-95	P53	Homo sapiens	121-124
25827071-0	2015	All-trans retinoic acid induces p53-depenent apoptosis in human hepatocytes by activating p14 expression via promoter hypomethylation.	Tretinoin	10-23	P53	Homo sapiens	32-35
25827071-2	2015	Here we found that ATRA induces apoptosis in p53-positive HepG2 cells, but not in p53-negative Hep3B cells.	Tretinoin	19-23	P53	Homo sapiens	45-48
25827071-7	2015	Ectopic expression of DNA methyltransferase 1 almost completely abolished the potential of ATRA to activate the p14-MDM2-p53 pathway and induce p53-dependent apoptosis.	Tretinoin	91-95	P53	Homo sapiens	144-147
26030124-5	2015	Here, we examined the effect of a novel protein assembly modulator, the lysine (Lys)-specific molecular tweezer, CLR01, on different aggregation stages of misfolded mutant p53 in vitro and on the cytotoxicity of the resulting p53 aggregates in cell culture.	Lysine	72-78	P53	Homo sapiens	172-175
26110921-6	2015	Mechanistic studies suggested that As4S4 acted synergistically with As3+ to down-regulate Bcl-2 and nuclear factor-kappaB expression, up-regulate Bax and p53 expression, and induce activation of caspase-12 and caspase-3.	as4s4	35-40	P53	Homo sapiens	154-157
26181367-2	2015	Previously, an increased expression of Sin3B and tumour suppressor protein, p53 has been established upon adriamycin treatment.	Doxorubicin	106-116	P53	Homo sapiens	76-79
26181367-5	2015	This increase in Sin3B expression upon stress is found to be p53-dependent and is associated with enhanced interaction of Sin3B with Ser(15) phosphorylated p53.	Serine	133-136	P53	Homo sapiens	61-64
26181367-5	2015	This increase in Sin3B expression upon stress is found to be p53-dependent and is associated with enhanced interaction of Sin3B with Ser(15) phosphorylated p53.	Serine	133-136	P53	Homo sapiens	156-159
26030124-6	2015	We found that CLR01 induced rapid formation of beta-sheet-rich, intermediate-size p53 aggregates yet inhibited further p53 aggregation and reduced the cytotoxicity of the resulting aggregates.	clr01	14-19	P53	Homo sapiens	82-85
26030124-6	2015	We found that CLR01 induced rapid formation of beta-sheet-rich, intermediate-size p53 aggregates yet inhibited further p53 aggregation and reduced the cytotoxicity of the resulting aggregates.	clr01	14-19	P53	Homo sapiens	119-122
26030124-7	2015	Our data suggest that aggregation modulators, such as CLR01, could prevent the formation of toxic p53 aggregates.	clr01	54-59	P53	Homo sapiens	98-101
26030124-5	2015	Here, we examined the effect of a novel protein assembly modulator, the lysine (Lys)-specific molecular tweezer, CLR01, on different aggregation stages of misfolded mutant p53 in vitro and on the cytotoxicity of the resulting p53 aggregates in cell culture.	Lysine	80-83	P53	Homo sapiens	172-175
26086967-1	2015	Two main causes of platinum resistance are mutation in the tumor suppressor gene TP53 and drug-induced increase in intracellular glutathione concentration.	Platinum	19-27	P53	Homo sapiens	81-85
26041883-2	2015	Among the mechanisms of anti-apoptosis activated by the hormone are interference with the Ser-15 phosphorylation (activation) of p53 and with TNFalpha/Fas-induced apoptosis.	Serine	90-93	P53	Homo sapiens	129-132
26041883-5	2015	Tetraiodothyroacetic acid (tetrac) is a T4 derivative that, in a model of resveratrol-induced p53-dependent apoptosis in glioma cells, blocks the anti-apoptotic action of thyroid hormone, permitting specific serine phosphorylation of p53 and apoptosis to proceed.	Resveratrol	74-85	P53	Homo sapiens	94-97
26105784-5	2015	Taken together, our results indicate that heat stress induces apoptosis through the mitochondrial pathway with ROS dependent mitochondrial p53 translocation and Ca(2+) dyshomeostasis, and the ensuing intro Bax mitochondrial translocation as the upstream events involved in triggering the apoptotic process observed upon cellular exposure to heat stress.	Reactive Oxygen Species	111-114	P53	Homo sapiens	139-142
26073944-5	2015	We linked ROS production and induction of the mitochondrial permeability transition pore (MPTP) via cyclophilin D and p53 as mechanisms of EPHOSS.	ros	10-13	P53	Homo sapiens	118-121
26086967-4	2015	APR-246 is a prodrug that is converted to the active compound methylene quinuclidinone (MQ), a Michael acceptor that binds to cysteine residues in mutant p53 and restores its wild-type conformation.	memoquin	88-90	P53	Homo sapiens	154-157
26086967-4	2015	APR-246 is a prodrug that is converted to the active compound methylene quinuclidinone (MQ), a Michael acceptor that binds to cysteine residues in mutant p53 and restores its wild-type conformation.	Cysteine	126-134	P53	Homo sapiens	154-157
26086967-6	2015	We also show that treatment with APR-246 completely restores the cisplatin and doxorubicin sensitivity to p53-mutant drug-resistant ovarian cancer cells.	Cisplatin	65-74	P53	Homo sapiens	106-109
26086967-6	2015	We also show that treatment with APR-246 completely restores the cisplatin and doxorubicin sensitivity to p53-mutant drug-resistant ovarian cancer cells.	Doxorubicin	79-90	P53	Homo sapiens	106-109
26086967-7	2015	We propose that this unique ability of APR-246/MQ to bind to cysteines in both mutant p53 and glutathione has a key role in the resensitization as well as in the outstanding synergistic effects observed with APR-246 in combination with platinum compounds in ovarian cancer cell lines and primary cancer cells.	Cysteine	61-70	P53	Homo sapiens	86-89
26086967-7	2015	We propose that this unique ability of APR-246/MQ to bind to cysteines in both mutant p53 and glutathione has a key role in the resensitization as well as in the outstanding synergistic effects observed with APR-246 in combination with platinum compounds in ovarian cancer cell lines and primary cancer cells.	Platinum	236-244	P53	Homo sapiens	86-89
26086967-10	2015	Our results provide a strong rationale for the ongoing clinical study with APR-246 in combination with platinum-based therapy in patients with p53-mutant recurrent high-grade serous (HGS) ovarian cancer.	Platinum	103-111	P53	Homo sapiens	143-146
26086967-12	2015	Combined treatment with APR-246 and platinum or other DNA-damaging drugs could allow dramatically improved therapy of a wide range of therapy refractory p53 mutant tumors.	Platinum	36-44	P53	Homo sapiens	153-156
25939861-0	2015	Efficient one-pot synthesis of trans-Pt(II)(salicylaldimine)(4-picoline)Cl complexes: effective agents for enhanced expression of p53 tumor suppressor genes.	salicylaldehyde imine	44-59	P53	Homo sapiens	130-133
26425688-1	2015	We investigated the hypothesis that the varying treatment efficacy of adjuvant 5-fluorouracil (5FU) in stage III colon cancer is linked to the TP53 mutational status.	Fluorouracil	79-93	P53	Homo sapiens	143-147
26425688-1	2015	We investigated the hypothesis that the varying treatment efficacy of adjuvant 5-fluorouracil (5FU) in stage III colon cancer is linked to the TP53 mutational status.	Fluorouracil	95-98	P53	Homo sapiens	143-147
26425688-11	2015	The biomarker TP53 independently predicted effect of adjuvant 5FU in N1 colon cancer patients.	Fluorouracil	62-65	P53	Homo sapiens	14-18
25965911-4	2015	Our results show 5-FU induced cell apoptosis through p53/PUMA pathway, with aberrant Akt activation, which may well explain the mechanism of 5-FU resistance.	Fluorouracil	17-21	P53	Homo sapiens	53-56
26024660-0	2015	ROS-p53-cyclophilin-D signaling mediates salinomycin-induced glioma cell necrosis.	Reactive Oxygen Species	0-3	P53	Homo sapiens	4-7
25749422-0	2015	WP1130 increases doxorubicin sensitivity in hepatocellular carcinoma cells through usp9x-dependent p53 degradation.	Doxorubicin	17-28	P53	Homo sapiens	99-102
25749422-6	2015	Downregulation of p53 abolished the synergistic cytotoxicity of doxorubicin and WP1130 on HCC cells.	Doxorubicin	64-75	P53	Homo sapiens	18-21
25749422-7	2015	Mechanistically, we found that combined treatment with WP1130 suppressed doxorubicin-mediated upregulation of p53 via promoting its ubiquitin-proteasome dependent degradation, whereas knockdown of DUB usp9x abolished this effect.	Doxorubicin	73-84	P53	Homo sapiens	110-113
25749422-8	2015	Taken together, these results demonstrate that combined treatment with WP1130 sensitized HCC cells to doxorubicin via usp9x-depedent p53 degradation.	Doxorubicin	102-113	P53	Homo sapiens	133-136
25818185-11	2015	Finally, pretreatment of cells with DMY prior to H2O2 exposure resulted in the inhibition of p53 activation, followed by the regulation of the expression of Bcl-2 and Bax, the release of cytochrome c, the cleavage (activation) of caspase-9 and caspase-3, and then the suppression of PARP cleavage in H2O2-induced HUVECs.	Hydrogen Peroxide	49-53	P53	Homo sapiens	93-96
25947292-0	2015	PLGA-Loaded Gold-Nanoparticles Precipitated with Quercetin Downregulate HDAC-Akt Activities Controlling Proliferation and Activate p53-ROS Crosstalk to Induce Apoptosis in Hepatocarcinoma Cells.	Reactive Oxygen Species	135-138	P53	Homo sapiens	131-134
25947292-9	2015	NQ induced apoptosis in HepG2 cells by activating p53-ROS crosstalk and induces epigenetic modifications leading to inhibited proliferation and cell cycle arrest.	nq	0-2	P53	Homo sapiens	50-53
25947292-9	2015	NQ induced apoptosis in HepG2 cells by activating p53-ROS crosstalk and induces epigenetic modifications leading to inhibited proliferation and cell cycle arrest.	Reactive Oxygen Species	54-57	P53	Homo sapiens	50-53
26029824-3	2015	Human p53-TAD contains seven serine and two threonine residues, all of which can be phosphorylated.	Serine	29-35	P53	Homo sapiens	6-9
26029824-3	2015	Human p53-TAD contains seven serine and two threonine residues, all of which can be phosphorylated.	Threonine	44-53	P53	Homo sapiens	6-9
26024660-9	2015	Reactive oxygen species (ROS) production was required for salinomycin-induced p53 mitochondrial translocation, mPTP opening and necrosis, and anti-oxidants n-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) inhibited p53 translocation, mPTP opening and glioma cell death.	Reactive Oxygen Species	0-23	P53	Homo sapiens	78-81
26024660-9	2015	Reactive oxygen species (ROS) production was required for salinomycin-induced p53 mitochondrial translocation, mPTP opening and necrosis, and anti-oxidants n-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) inhibited p53 translocation, mPTP opening and glioma cell death.	Reactive Oxygen Species	0-23	P53	Homo sapiens	228-231
26024660-9	2015	Reactive oxygen species (ROS) production was required for salinomycin-induced p53 mitochondrial translocation, mPTP opening and necrosis, and anti-oxidants n-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) inhibited p53 translocation, mPTP opening and glioma cell death.	Reactive Oxygen Species	25-28	P53	Homo sapiens	78-81
26116417-4	2015	Based on our results, the major effect from plasma exposure was found to be the activation of MAPK and p53 signaling pathways, resulting in changes in gene expression of MEKK, GADD, FOS and JUN.	gadd	176-180	P53	Homo sapiens	103-106
25088203-7	2015	Furthermore, the phosphorylation of ATM targets, including gammaH2AX, threonine 68 (T68) on CHK2 (CHK2 pT68) and serine 15 (S15) on p53 were decreased in overexpression and increased in knockdown BMI1 cells in response to ETOP.	Serine	113-119	P53	Homo sapiens	132-135
25698149-4	2015	Based on this finding, we explored the contribution of p53 status in predicting the response to adjuvant CMF or CMF followed doxorubicin chemotherapy of a group of TNBC patients.	Doxorubicin	125-136	P53	Homo sapiens	55-58
25698149-5	2015	Results indicated that TNBC patients with a p53-positive tumor had a shorter relapse-free and overall survival than patients carrying a p53-negative TNBC, corroborating our hypothesis about the relationship between TNBC phenotype (basal-like versus normal-like) and p53 status as predictor of response to anthracycline/CMF-based chemotherapy.	Anthracyclines	305-318	P53	Homo sapiens	44-47
26097804-8	2015	Molecular studies have identified that silibinin targets pleotropic signaling pathways including mitogenic, cell cycle, apoptosis, autophagy, p53, NF-kappaB, etc.	Silybin	39-48	P53	Homo sapiens	142-145
26024660-9	2015	Reactive oxygen species (ROS) production was required for salinomycin-induced p53 mitochondrial translocation, mPTP opening and necrosis, and anti-oxidants n-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) inhibited p53 translocation, mPTP opening and glioma cell death.	Reactive Oxygen Species	25-28	P53	Homo sapiens	228-231
25992654-10	2015	These findings demonstrate that MEG3 is significantly downregulated in LAD and partially regulates the cisplatin resistance of LAD cells through the control of p53 and Bcl-xl expression.	Cisplatin	103-112	P53	Homo sapiens	160-163
25825497-8	2015	LLY-507 is active in cells as measured by reduction of SMYD2-induced monomethylation of p53 Lys(370) at submicromolar concentrations.	LLY-507	0-7	P53	Homo sapiens	88-91
25825497-8	2015	LLY-507 is active in cells as measured by reduction of SMYD2-induced monomethylation of p53 Lys(370) at submicromolar concentrations.	Lysine	92-95	P53	Homo sapiens	88-91
27314071-2	2016	We have uncovered a novel function of p53 that contributes to tumor suppression through regulation of cystine metabolism, reactive oxygen species responses, and ferroptosis.	Reactive Oxygen Species	122-145	P53	Homo sapiens	38-41
25797115-0	2015	Induction of cell cycle arrest and apoptosis by betulinic acid-rich fraction from Dillenia suffruticosa root in MCF-7 cells involved p53/p21 and mitochondrial signalling pathway.	betulinic acid	48-62	P53	Homo sapiens	133-136
25839657-4	2015	Intracellular ROS levels were increased in hBM-MSCs; this was accompanied by a decrease in the expression of the antioxidant enzymes catalase and superoxide dismutase (SOD)1 and 2 and of phosphorylated forkhead box O1 (p-FOXO1) as well as an increase in the expression of p53 and p16, along with a reduction in differentiation potential.	Reactive Oxygen Species	14-17	P53	Homo sapiens	272-275
25993660-9	2015	Cells expressing SBP1 also demonstrated a robust induction in the phosphorylation of the p53 tumor suppressor at serine 15.	Serine	113-119	P53	Homo sapiens	89-92
25839657-5	2015	When the antioxidant ascorbic acid was used to eliminate excess ROS, the levels of antioxidant enzymes (catalase, SOD1 and 2, p-FOXO1, and p53) were partly restored.	Reactive Oxygen Species	64-67	P53	Homo sapiens	139-142
25981919-0	2015	Sensitivity of apoptosis-resistant colon cancer cells to tanshinones is mediated by autophagic cell death and p53-independent cytotoxicity.	tanshinone	57-68	P53	Homo sapiens	110-113
25981919-12	2015	Besides, the cytotoxic actions of the two tanshinones were p53-independent, which could be useful in inhibiting the growth of apoptosis-resistant cancer cells with p53 defects.	tanshinone	42-53	P53	Homo sapiens	59-62
25981919-12	2015	Besides, the cytotoxic actions of the two tanshinones were p53-independent, which could be useful in inhibiting the growth of apoptosis-resistant cancer cells with p53 defects.	tanshinone	42-53	P53	Homo sapiens	164-167
25824034-3	2015	Elevated p53 is involved in mitochondrial mediated apoptosis of neuronal cells in Parkinson"s patients who are folate deficient as well.	Folic Acid	111-117	P53	Homo sapiens	9-12
24998844-1	2015	Resveratrol (trans-3,5,4"-truhydroxystilbene) possesses a strong anticancer activity exhibited as the induction of apoptosis through p53 activation.	Resveratrol	0-11	P53	Homo sapiens	133-136
24998844-1	2015	Resveratrol (trans-3,5,4"-truhydroxystilbene) possesses a strong anticancer activity exhibited as the induction of apoptosis through p53 activation.	trans-3,5,4"-truhydroxystilbene	13-44	P53	Homo sapiens	133-136
24998844-2	2015	However, the molecular mechanism and direct target(s) of resveratrol-induced p53 activation remain elusive.	Resveratrol	57-68	P53	Homo sapiens	77-80
24998844-4	2015	Depletion of G3BP1 significantly diminishes resveratrol-induced p53 expression and apoptosis.	Resveratrol	44-55	P53	Homo sapiens	64-67
24998844-7	2015	Resveratrol, on the other hand, directly binds to G3BP1 and prevents the G3BP1/USP10 interaction, resulting in enhanced USP10-mediated deubiquitination of p53, and consequently increased p53 expression.	Resveratrol	0-11	P53	Homo sapiens	155-158
24998844-7	2015	Resveratrol, on the other hand, directly binds to G3BP1 and prevents the G3BP1/USP10 interaction, resulting in enhanced USP10-mediated deubiquitination of p53, and consequently increased p53 expression.	Resveratrol	0-11	P53	Homo sapiens	187-190
24998844-8	2015	These findings disclose a novel mechanism of resveratrol-induced p53 activation and resveratrol-induced apoptosis by direct targeting of G3BP1.	Resveratrol	45-56	P53	Homo sapiens	65-68
24998852-6	2015	These findings expand our understanding of the function of TPL2 as a negative regulator of carcinogenesis by defining a nuclear role for this kinase in the topological sequestration of NPM, linking p53 signaling to the generation of threonine 199-phosphorylated NPM.	Threonine	233-242	P53	Homo sapiens	198-201
25955698-7	2015	Doxorubicin also dose-dependently induced p53, which is known to repress the transcription of IGF1R and induce that of IGFBP3.	Doxorubicin	0-11	P53	Homo sapiens	42-45
25955698-8	2015	Pre-treatment with the p53 inhibitor, pifithrin-alpha, prevented apoptosis and the changes in IGF-1R and IGFBP-3 elicited by doxorubicin.	Doxorubicin	125-136	P53	Homo sapiens	23-26
25876645-9	2015	The present study suggests capsaicin and DIM work synergistically to inhibit cell proliferation and induce apoptosis in colorectal cancer through modulating transcriptional activity of NF-kappaB, p53, and target genes associated with apoptosis.	Capsaicin	27-36	P53	Homo sapiens	196-199
25955843-8	2015	While recent studies showed that treatment with only TRAIL was not effective against pancreatic cancer cells, the present data showed that metformin sensitized p53-mutated pancreatic cancer cells to TRAIL.	Metformin	139-148	P53	Homo sapiens	160-163
25854514-0	2015	Efficient co-delivery of a Pt(IV) prodrug and a p53 activator to enhance the anticancer activity of cisplatin.	Cisplatin	100-109	P53	Homo sapiens	48-51
25854514-3	2015	Once inside cells, cisplatin is released to attack genomic DNA and kill cancer cells; simultaneously, the p53 activator results in active p53, a key protein involved in the apoptotic pathways initiated by platinum drugs.	Cisplatin	19-28	P53	Homo sapiens	106-109
25854514-3	2015	Once inside cells, cisplatin is released to attack genomic DNA and kill cancer cells; simultaneously, the p53 activator results in active p53, a key protein involved in the apoptotic pathways initiated by platinum drugs.	Cisplatin	19-28	P53	Homo sapiens	138-141
25770930-0	2015	Combination of chrysin and cisplatin promotes the apoptosis of Hep G2 cells by up-regulating p53.	Cisplatin	27-36	P53	Homo sapiens	93-96
25882531-1	2015	We have published p53-MDM2 interaction inhibitors possessing a novel dihydroimidazothiazole scaffold.	dihydroimidazothiazole	69-91	P53	Homo sapiens	18-21
25770930-4	2015	Combination of chrysin and cisplatin increased the phosphorylation and accumulation of p53 through activating ERK1/2 in Hep G2 cells, which led to the overexpression of the pro-apoptotic proteins Bax and DR5 and the inhibition of the anti-apoptotic protein Bcl-2.	chrysin	15-22	P53	Homo sapiens	87-90
25770930-4	2015	Combination of chrysin and cisplatin increased the phosphorylation and accumulation of p53 through activating ERK1/2 in Hep G2 cells, which led to the overexpression of the pro-apoptotic proteins Bax and DR5 and the inhibition of the anti-apoptotic protein Bcl-2.	Cisplatin	27-36	P53	Homo sapiens	87-90
25942498-0	2015	8-Triazolylpurines: Towards Fluorescent Inhibitors of the MDM2/p53 Interaction.	8-triazolylpurines	0-18	P53	Homo sapiens	63-66
25669829-0	2015	Phase I study of pazopanib and vorinostat: a therapeutic approach for inhibiting mutant p53-mediated angiogenesis and facilitating mutant p53 degradation.	pazopanib	17-26	P53	Homo sapiens	88-91
25669829-0	2015	Phase I study of pazopanib and vorinostat: a therapeutic approach for inhibiting mutant p53-mediated angiogenesis and facilitating mutant p53 degradation.	pazopanib	17-26	P53	Homo sapiens	138-141
26222594-2	2015	The obtained xPolyR8-KLA(TPP) could not only initiate tumor cell apoptosis by C-KLA(TPP) with improved cell penetrating ability, but was also capable of loading and delivering the tumor cell suppressing p53 gene.	tetraphenylporphine sulfonate	25-28	P53	Homo sapiens	203-206
26222594-2	2015	The obtained xPolyR8-KLA(TPP) could not only initiate tumor cell apoptosis by C-KLA(TPP) with improved cell penetrating ability, but was also capable of loading and delivering the tumor cell suppressing p53 gene.	tetraphenylporphine sulfonate	84-87	P53	Homo sapiens	203-206
26222594-3	2015	It was found that, after internalization by cancer cells, the xPolyR8-KLA(TPP)/p53 complex released the C-KLA(TPP) moiety and the p53 gene in the cytoplasm due to its reducible disulfide bonds.	tetraphenylporphine sulfonate	74-77	P53	Homo sapiens	79-82
26222594-3	2015	It was found that, after internalization by cancer cells, the xPolyR8-KLA(TPP)/p53 complex released the C-KLA(TPP) moiety and the p53 gene in the cytoplasm due to its reducible disulfide bonds.	tetraphenylporphine sulfonate	74-77	P53	Homo sapiens	130-133
26222594-3	2015	It was found that, after internalization by cancer cells, the xPolyR8-KLA(TPP)/p53 complex released the C-KLA(TPP) moiety and the p53 gene in the cytoplasm due to its reducible disulfide bonds.	tetraphenylporphine sulfonate	110-113	P53	Homo sapiens	79-82
26222594-3	2015	It was found that, after internalization by cancer cells, the xPolyR8-KLA(TPP)/p53 complex released the C-KLA(TPP) moiety and the p53 gene in the cytoplasm due to its reducible disulfide bonds.	tetraphenylporphine sulfonate	110-113	P53	Homo sapiens	130-133
26222594-3	2015	It was found that, after internalization by cancer cells, the xPolyR8-KLA(TPP)/p53 complex released the C-KLA(TPP) moiety and the p53 gene in the cytoplasm due to its reducible disulfide bonds.	Disulfides	177-186	P53	Homo sapiens	79-82
26222594-3	2015	It was found that, after internalization by cancer cells, the xPolyR8-KLA(TPP)/p53 complex released the C-KLA(TPP) moiety and the p53 gene in the cytoplasm due to its reducible disulfide bonds.	Disulfides	177-186	P53	Homo sapiens	130-133
26222594-4	2015	By regulating both the intrinsic and extrinsic apoptotic pathways, the xPolyR8-KLA(TPP)/p53 complex performed as a synergetic system and lead to a more efficient cancer cell death.	tetraphenylporphine sulfonate	83-86	P53	Homo sapiens	88-91
25829127-0	2015	N-Isopropylacrylamide-modified polyethylenimine-mediated p53 gene delivery to prevent the proliferation of cancer cells.	N-isopropylacrylamide	0-21	P53	Homo sapiens	57-60
25823563-8	2015	These observations collectively strongly suggest that both endoplasmic reticulum stress-mediated calcium release and Bax targeting might be altering mitochondrion membrane potential which in turn could induce secondary apoptotic signals; subsequently, endoplasmic reticulum stress can also lead to nuclear localization of Nuclear factor-kappaB (NF-kappaB) which in turn favors p53 mediated apoptotic signals.	Calcium	97-104	P53	Homo sapiens	377-380
25683911-2	2015	Treatment of p53 wild-type melanoma cells with the genotoxic agent doxorubicin induces G2-M arrest, inhibitory phosphorylation of cell cycle kinase Cdc2 (CDK1) and enhanced expression of p53/p21.	Doxorubicin	67-78	P53	Homo sapiens	13-16
25683911-2	2015	Treatment of p53 wild-type melanoma cells with the genotoxic agent doxorubicin induces G2-M arrest, inhibitory phosphorylation of cell cycle kinase Cdc2 (CDK1) and enhanced expression of p53/p21.	Doxorubicin	67-78	P53	Homo sapiens	187-190
25683911-9	2015	In line with this, the p53-mutant SK-Mel-28 melanoma cells do not mount a significant G0-G1 arrest under combined doxorubicin and Chk1 inhibitor treatment but rather show extensive apoptosis.	Doxorubicin	114-125	P53	Homo sapiens	23-26
25683911-13	2015	Combined treatment with chemotherapeutic agents such as doxorubicin and Chk1 inhibitors may help to overcome apoptosis resistance of p53-proficient melanoma cells.	Doxorubicin	56-67	P53	Homo sapiens	133-136
25713207-1	2015	We recently reported induction of UGT2B7 by its substrate epirubicin, a cytotoxic anthracycline anticancer drug, via activation of p53 and subsequent recruitment of p53 to the UGT2B7 promoter in hepatocellular carcinoma HepG2 cells.	Epirubicin	58-68	P53	Homo sapiens	131-134
25713207-1	2015	We recently reported induction of UGT2B7 by its substrate epirubicin, a cytotoxic anthracycline anticancer drug, via activation of p53 and subsequent recruitment of p53 to the UGT2B7 promoter in hepatocellular carcinoma HepG2 cells.	Epirubicin	58-68	P53	Homo sapiens	165-168
25713207-1	2015	We recently reported induction of UGT2B7 by its substrate epirubicin, a cytotoxic anthracycline anticancer drug, via activation of p53 and subsequent recruitment of p53 to the UGT2B7 promoter in hepatocellular carcinoma HepG2 cells.	Anthracyclines	82-95	P53	Homo sapiens	165-168
25840605-10	2015	Currently, the chemokine receptor inhibitor CCX140 holds promise for CKD and the p53 inhibitor QPI-1002 for AKI.	qpi-1002	95-103	P53	Homo sapiens	81-84
25583641-7	2015	Further, the expression of two important cell cycle inhibitory proteins, p21 and p53, in the curcumin- and culture medium-treated cells without curcumin was evaluated by intracellular flow cytometry.	Curcumin	93-101	P53	Homo sapiens	81-84
25583641-10	2015	Flow cytometry analysis showed a twofold increase in the expression of both p21 and p53 in curcumin-treated cells as compared to the medium-treated cells, suggesting that curcumin inhibits EPC growth by mainly inhibiting the G1 to S phase transition in the cell cycle.	Curcumin	91-99	P53	Homo sapiens	84-87
25583641-10	2015	Flow cytometry analysis showed a twofold increase in the expression of both p21 and p53 in curcumin-treated cells as compared to the medium-treated cells, suggesting that curcumin inhibits EPC growth by mainly inhibiting the G1 to S phase transition in the cell cycle.	Curcumin	171-179	P53	Homo sapiens	84-87
26191131-10	2015	In addition, GQP significantly affected the p53-p21 and p16-pRb pathways in H2O2-treated WI-38 cells.	Hydrogen Peroxide	76-80	P53	Homo sapiens	44-47
25767119-5	2015	Silencing Smad2, inhibition of ERK, or introducing a phosphorylation-defective mutation at Ser-392 in p53 abrogates the R175H mutant p53-dependent regulation of these TGF-beta target genes.	Serine	91-94	P53	Homo sapiens	102-105
25878193-3	2015	Because DOX in cells activates a DNA damage response involving ataxia telangiectasia-mutated (ATM)-mediated activation of p53, we investigated whether the activation of the p53 in cells by DNA-damaging agents such as DOX or bleomycin could regulate the AhR levels.	Doxorubicin	8-11	P53	Homo sapiens	122-125
25878193-3	2015	Because DOX in cells activates a DNA damage response involving ataxia telangiectasia-mutated (ATM)-mediated activation of p53, we investigated whether the activation of the p53 in cells by DNA-damaging agents such as DOX or bleomycin could regulate the AhR levels.	Doxorubicin	8-11	P53	Homo sapiens	173-176
25878193-3	2015	Because DOX in cells activates a DNA damage response involving ataxia telangiectasia-mutated (ATM)-mediated activation of p53, we investigated whether the activation of the p53 in cells by DNA-damaging agents such as DOX or bleomycin could regulate the AhR levels.	Doxorubicin	217-220	P53	Homo sapiens	173-176
25767119-5	2015	Silencing Smad2, inhibition of ERK, or introducing a phosphorylation-defective mutation at Ser-392 in p53 abrogates the R175H mutant p53-dependent regulation of these TGF-beta target genes.	Serine	91-94	P53	Homo sapiens	133-136
25710967-1	2015	p53 is a Zn(2+)-dependent tumor suppressor inactivated in &gt;50% of human cancers.	Zinc	9-11	P53	Homo sapiens	0-3
25710967-2	2015	The most common mutation, R175H, inactivates p53 by reducing its affinity for the essential zinc ion, leaving the mutant protein unable to bind the metal in the low [Zn(2+)]free environment of the cell.	Metals	148-153	P53	Homo sapiens	45-48
25755280-8	2015	Significantly, treatment with the DNA damage-inducing drug doxorubicin results in the loss of the PATZ1 transcription factor as p53 accumulates.	Doxorubicin	59-70	P53	Homo sapiens	128-131
25710967-6	2015	These [Zn(2+)]free levels are predicted to result in ~90% saturation of p53-R175H, thus accounting for its observed reactivation.	Zinc	7-13	P53	Homo sapiens	72-75
25985628-8	2015	Met deprivation results in a rapid decrease in intracellular S-adenosyl-methionine (SAM), triggering the activation of p53 signaling, reducing pluripotent marker gene NANOG expression, and poising human ES/iPS cells for differentiation, follow by potentiated differentiation into all three germ layers.	S-Adenosylmethionine	84-87	P53	Homo sapiens	119-122
25814188-8	2015	It was also shown that OXAZ-1 potently triggered a p53-dependent mitochondria-mediated apoptosis, characterized by reactive oxygen species generation, mitochondrial membrane potential dissipation, Bax translocation to mitochondria, and cytochrome c release, and exhibited a p53-dependent synergistic effect with conventional chemotherapeutic drugs.	Reactive Oxygen Species	115-138	P53	Homo sapiens	51-54
25860929-8	2015	In vitro and in vivo assessments demonstrated aberrant induction of phosphorylated p53 at Serine 15 [phospho-p53(Ser15)] in human FBXW7-deficient CRC cells as compared to their FBXW7-wild-type counterparts.	Serine	90-96	P53	Homo sapiens	109-112
25542229-6	2015	Real-time RT-PCR showed that ibuprofen altered the expression of several genes including Akt, P53, PCNA, Bax, and Bcl2 in the AGS cells.	Ibuprofen	29-38	P53	Homo sapiens	94-97
25888625-10	2015	The biological effects of miR-29c may be mediated by its target WIP1 which regulates p53 activity via dephosphorylation at Ser-15.	Serine	123-126	P53	Homo sapiens	85-88
25744307-9	2015	We show that 10(-8)M levels of CdCl2 activate ERK1/2 (Tyr 204) and the p53 specific ubiquitin ligase Mdm2 (Ser 166) via Raf and MEK by acting through the epidermal growth factor receptor (EGFR).	Serine	107-110	P53	Homo sapiens	71-74
25902914-0	2015	Oroxylin A promotes PTEN-mediated negative regulation of MDM2 transcription via SIRT3-mediated deacetylation to stabilize p53 and inhibit glycolysis in wt-p53 cancer cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	0-10	P53	Homo sapiens	122-125
25902914-0	2015	Oroxylin A promotes PTEN-mediated negative regulation of MDM2 transcription via SIRT3-mediated deacetylation to stabilize p53 and inhibit glycolysis in wt-p53 cancer cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	0-10	P53	Homo sapiens	155-158
25902914-9	2015	RESULTS: Here, we analyzed the underlying mechanisms that oroxylin A regulated p53 level and glycolytic metabolism in wt-p53 cancer cells, and found that oroxylin A inhibited glycolysis through upregulating p53 level.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	58-68	P53	Homo sapiens	79-82
25902914-9	2015	RESULTS: Here, we analyzed the underlying mechanisms that oroxylin A regulated p53 level and glycolytic metabolism in wt-p53 cancer cells, and found that oroxylin A inhibited glycolysis through upregulating p53 level.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	58-68	P53	Homo sapiens	121-124
25902914-9	2015	RESULTS: Here, we analyzed the underlying mechanisms that oroxylin A regulated p53 level and glycolytic metabolism in wt-p53 cancer cells, and found that oroxylin A inhibited glycolysis through upregulating p53 level.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	58-68	P53	Homo sapiens	121-124
25902914-9	2015	RESULTS: Here, we analyzed the underlying mechanisms that oroxylin A regulated p53 level and glycolytic metabolism in wt-p53 cancer cells, and found that oroxylin A inhibited glycolysis through upregulating p53 level.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	154-164	P53	Homo sapiens	79-82
25902914-9	2015	RESULTS: Here, we analyzed the underlying mechanisms that oroxylin A regulated p53 level and glycolytic metabolism in wt-p53 cancer cells, and found that oroxylin A inhibited glycolysis through upregulating p53 level.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	154-164	P53	Homo sapiens	121-124
25902914-9	2015	RESULTS: Here, we analyzed the underlying mechanisms that oroxylin A regulated p53 level and glycolytic metabolism in wt-p53 cancer cells, and found that oroxylin A inhibited glycolysis through upregulating p53 level.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	154-164	P53	Homo sapiens	121-124
25902914-10	2015	Oroxylin A did not directly affect the transcription of wt-p53, but suppressed the MDM2-mediated degradation of p53 via downregulating MDM2 transcription in wt-p53 cancer cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	0-10	P53	Homo sapiens	112-115
25902914-10	2015	Oroxylin A did not directly affect the transcription of wt-p53, but suppressed the MDM2-mediated degradation of p53 via downregulating MDM2 transcription in wt-p53 cancer cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	0-10	P53	Homo sapiens	112-115
25902914-14	2015	CONCLUSIONS: These results provide a p53-independent mechanism of MDM2 transcription and reveal the potential of oroxylin A on glycolytic regulation in both wt-p53 and mut-p53 cancer cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	113-123	P53	Homo sapiens	160-163
25902914-14	2015	CONCLUSIONS: These results provide a p53-independent mechanism of MDM2 transcription and reveal the potential of oroxylin A on glycolytic regulation in both wt-p53 and mut-p53 cancer cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	113-123	P53	Homo sapiens	160-163
25894969-8	2015	One patient with lymphoid BC/Ph+ ALL who harbored a T315I ABL mutation and was treated with ponatinib was found to have developed a newly acquired V216M TP53 mutation (12% of transcripts) when becoming resistant to ponatinib.	ponatinib	92-101	P53	Homo sapiens	153-157
25894969-8	2015	One patient with lymphoid BC/Ph+ ALL who harbored a T315I ABL mutation and was treated with ponatinib was found to have developed a newly acquired V216M TP53 mutation (12% of transcripts) when becoming resistant to ponatinib.	ponatinib	215-224	P53	Homo sapiens	153-157
25894969-9	2015	Ponatinib led to a decrease of ABL T315I positive transcripts from 47% before ponatinib treatment to 16% at the time of ponatinib resistance in this patient, suggesting that both TP53 and ABL mutations were present in the same clone and that the newly acquired TP53 mutation might have caused ponatinib resistance in this patient.	ponatinib	0-9	P53	Homo sapiens	179-183
25894969-9	2015	Ponatinib led to a decrease of ABL T315I positive transcripts from 47% before ponatinib treatment to 16% at the time of ponatinib resistance in this patient, suggesting that both TP53 and ABL mutations were present in the same clone and that the newly acquired TP53 mutation might have caused ponatinib resistance in this patient.	ponatinib	0-9	P53	Homo sapiens	261-265
25910231-4	2015	Treatment of cells with curcumin induced both p53 and the related protein p73 in head and neck and lung cancer cell lines.	Curcumin	24-32	P53	Homo sapiens	46-49
25860929-0	2015	FBXW7-mutated colorectal cancer cells exhibit aberrant expression of phosphorylated-p53 at Serine-15.	Serine	91-97	P53	Homo sapiens	84-87
25860929-8	2015	In vitro and in vivo assessments demonstrated aberrant induction of phosphorylated p53 at Serine 15 [phospho-p53(Ser15)] in human FBXW7-deficient CRC cells as compared to their FBXW7-wild-type counterparts.	Serine	90-96	P53	Homo sapiens	83-86
25825738-5	2015	Mutation of two critical tryptophan residues in the hydrophobic peptide disrupted the intramolecular interaction and increased p53 binding, providing further evidence for mechanistic mimicry.	Tryptophan	25-35	P53	Homo sapiens	127-130
26015807-9	2015	This signature includes the GTPBP4 gene coding for a GTP-binding protein that interacts with p53.	Guanosine Triphosphate	28-31	P53	Homo sapiens	93-96
25706509-3	2015	The dynamics of water in the interdomain region between an E3 ubiquitin ligase (MDM2) and three different peptides derived from the tumor suppressor protein p53 are studied using molecular dynamics.	Water	16-21	P53	Homo sapiens	157-160
25665036-9	2015	Resveratrol also ameliorated the augmentation of pro-apoptotic markers including p53, Bax, caspase 3 activity and apoptotic DNA fragmentation induced by doxorubicin in hearts from aged animals, whereas these reductions were diminished by combined treatment with SIRT1 inhibitors.	Resveratrol	0-11	P53	Homo sapiens	81-84
25644651-1	2015	Complexation of cisplatin with a p53 activator as a single anticancer agent resulted in synergistically improved cytotoxicity in p53 wild-type but not p53 null human cancer cells.	Cisplatin	16-25	P53	Homo sapiens	33-36
25644651-1	2015	Complexation of cisplatin with a p53 activator as a single anticancer agent resulted in synergistically improved cytotoxicity in p53 wild-type but not p53 null human cancer cells.	Cisplatin	16-25	P53	Homo sapiens	129-132
25644651-1	2015	Complexation of cisplatin with a p53 activator as a single anticancer agent resulted in synergistically improved cytotoxicity in p53 wild-type but not p53 null human cancer cells.	Cisplatin	16-25	P53	Homo sapiens	129-132
25644651-4	2015	Chalcoplatin significantly induced p53 activation as well as the subsequent apoptosis pathways.	chalcoplatin	0-12	P53	Homo sapiens	35-38
26131172-10	2015	Interestingly, in the subgroup analysis regarding P53 codon 72 polymorphism, increased HCC risk could be observed in the Pro/Pro+Pro/Arg subgroup under a recessive model (OR=1.78; 95% CI=1.29-2.44).	Arginine	133-136	P53	Homo sapiens	50-53
24858040-6	2015	We identified the uric acid transporter SLC2A9 (also known as GLUT9) as a direct p53 target gene and a key downstream effector in the reduction of reactive oxygen species (ROS) through transporting uric acid as a source of antioxidant.	Reactive Oxygen Species	147-170	P53	Homo sapiens	81-84
24858040-9	2015	The increased production of ROS because of p53 loss was rescued by SLC2A9 expression.	Reactive Oxygen Species	28-31	P53	Homo sapiens	43-46
25596561-1	2015	Paclitaxel is an alternative chemotherapeutic agent for chronic myelogenous leukemia (CML) when primary or secondary resistance of tyrosine kinase inhibitors (TKI) is emerging, because paclitaxel could bypass the apoptotic deficiencies linked to p53 and fas ligand pathways in CML.	Paclitaxel	0-10	P53	Homo sapiens	246-249
24858040-6	2015	We identified the uric acid transporter SLC2A9 (also known as GLUT9) as a direct p53 target gene and a key downstream effector in the reduction of reactive oxygen species (ROS) through transporting uric acid as a source of antioxidant.	Reactive Oxygen Species	172-175	P53	Homo sapiens	81-84
24858040-11	2015	Our findings suggest that the p53-SLC2A9 pathway is a novel antioxidant mechanism that uses uric acid to maintain ROS homeostasis and prevent accumulation of ROS-associated damage that potentially contributes to cancer development.	Reactive Oxygen Species	114-117	P53	Homo sapiens	30-33
24858040-11	2015	Our findings suggest that the p53-SLC2A9 pathway is a novel antioxidant mechanism that uses uric acid to maintain ROS homeostasis and prevent accumulation of ROS-associated damage that potentially contributes to cancer development.	Reactive Oxygen Species	158-161	P53	Homo sapiens	30-33
25799988-2	2015	Here we show that p53 inhibits cystine uptake and sensitizes cells to ferroptosis, a non-apoptotic form of cell death, by repressing expression of SLC7A11, a key component of the cystine/glutamate antiporter.	Glutamic Acid	187-196	P53	Homo sapiens	18-21
24858040-7	2015	Oxidative stress induced SLC2A9 expression in a p53-dependent manner, and inhibition of SLC2A9 by small interfering RNA (siRNA) or anti-gout drugs such as probenecid significantly increased ROS levels in an uric acid-dependent manner and greatly sensitized cancer cells to chemotherapeutic drugs.	Reactive Oxygen Species	190-193	P53	Homo sapiens	48-51
25799988-3	2015	Notably, p53(3KR), an acetylation-defective mutant that fails to induce cell-cycle arrest, senescence and apoptosis, fully retains the ability to regulate SLC7A11 expression and induce ferroptosis upon reactive oxygen species (ROS)-induced stress.	Reactive Oxygen Species	202-225	P53	Homo sapiens	9-12
25799988-3	2015	Notably, p53(3KR), an acetylation-defective mutant that fails to induce cell-cycle arrest, senescence and apoptosis, fully retains the ability to regulate SLC7A11 expression and induce ferroptosis upon reactive oxygen species (ROS)-induced stress.	Reactive Oxygen Species	227-230	P53	Homo sapiens	9-12
25799988-6	2015	Our findings uncover a new mode of tumour suppression based on p53 regulation of cystine metabolism, ROS responses and ferroptosis.	Reactive Oxygen Species	101-104	P53	Homo sapiens	63-66
25495168-1	2015	The aim of this proof-of-concept study was to determine the effects of three-month Metformin therapy on the expression of tumor-regulatory genes (p53, cyclin D2 and BCL-2) in the endometrium of women with polycystic ovary syndrome (PCOS).	Metformin	83-92	P53	Homo sapiens	146-149
25889455-8	2015	In vitro experiments in cell lines indicated that enzymes controlling DNA methylation were differentially regulated by codon 72 Arg or Pro isoforms of p53.	Arginine	128-131	P53	Homo sapiens	151-154
25670618-7	2015	Higher p53 expression was observed in HsiI cells compared with H-vector after exposure with CIB.	cib	92-95	P53	Homo sapiens	7-10
25670618-10	2015	CIB irradiation further intensified both intrinsic and extrinsic pathways of apoptosis synergistically along with up-regulation of p53 in HsiI cells resulting overall higher apoptosis in HsiI than H-vector.	cib	0-3	P53	Homo sapiens	131-134
25430047-1	2015	This study aimed to clarify the association between the TP53 rs1625895 polymorphism and the efficiency of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) therapy in 106 patients with diffuse large B cell lymphoma (DLBCL).	Doxorubicin	143-154	P53	Homo sapiens	56-60
25691460-0	2015	Evolutionary Action Score of TP53 Coding Variants Is Predictive of Platinum Response in Head and Neck Cancer Patients.	Platinum	67-75	P53	Homo sapiens	29-33
25691460-1	2015	TP53 is the most frequently altered gene in head and neck squamous cell carcinoma (HNSCC), with mutations occurring in over two thirds of cases; however, the predictive response of these mutations to cisplatin-based therapy remains elusive.	Cisplatin	200-209	P53	Homo sapiens	0-4
25691460-3	2015	The EAp53 approach clearly identifies a subset of high-risk TP53 mutations associated with decreased sensitivity to cisplatin both in vitro and in vivo in preclinical models of HNSCC.	Cisplatin	116-125	P53	Homo sapiens	60-64
25780454-0	2015	Curcumin improves the paclitaxel-induced apoptosis of HPV-positive human cervical cancer cells via the NF-kappaB-p53-caspase-3 pathway.	Curcumin	0-8	P53	Homo sapiens	113-116
25780454-0	2015	Curcumin improves the paclitaxel-induced apoptosis of HPV-positive human cervical cancer cells via the NF-kappaB-p53-caspase-3 pathway.	Paclitaxel	22-32	P53	Homo sapiens	113-116
25780454-8	2015	The expression levels of p53 protein and cleaved caspase-3 were increased significantly in the curcumin plus paclitaxel-treated HeLa and CaSki cells compared with those in the cells treated with paclitaxel alone (P&lt;0.01).	Curcumin	95-103	P53	Homo sapiens	25-28
25780454-8	2015	The expression levels of p53 protein and cleaved caspase-3 were increased significantly in the curcumin plus paclitaxel-treated HeLa and CaSki cells compared with those in the cells treated with paclitaxel alone (P&lt;0.01).	Paclitaxel	109-119	P53	Homo sapiens	25-28
25780454-8	2015	The expression levels of p53 protein and cleaved caspase-3 were increased significantly in the curcumin plus paclitaxel-treated HeLa and CaSki cells compared with those in the cells treated with paclitaxel alone (P&lt;0.01).	Paclitaxel	195-205	P53	Homo sapiens	25-28
25780454-10	2015	This suggests that the combined effect of curcumin and paclitaxel was associated with the NF-kappaB-p53-caspase-3 pathway.	Curcumin	42-50	P53	Homo sapiens	100-103
25780454-10	2015	This suggests that the combined effect of curcumin and paclitaxel was associated with the NF-kappaB-p53-caspase-3 pathway.	Paclitaxel	55-65	P53	Homo sapiens	100-103
25780454-11	2015	In conclusion, curcumin has the ability to improve the paclitaxel-induced apoptosis of HPV-positive human cervical cancer cell lines via the NF-kappaB-p53-caspase-3 pathway.	Curcumin	15-23	P53	Homo sapiens	151-154
25780454-11	2015	In conclusion, curcumin has the ability to improve the paclitaxel-induced apoptosis of HPV-positive human cervical cancer cell lines via the NF-kappaB-p53-caspase-3 pathway.	Paclitaxel	55-65	P53	Homo sapiens	151-154
25495168-8	2015	Tumor suppressor gene (p53) was significantly up-regulated after Metformin (10 out of 14 women), with p value 0.016.	Metformin	65-74	P53	Homo sapiens	23-26
25495168-10	2015	In conclusion, Metformin therapy improved clinical and metabolic parameters in women with PCOS and up-regulated p53 tumor suppressor gene significantly.	Metformin	15-24	P53	Homo sapiens	112-115
25489053-3	2015	We found that p53 phosphorylation at serine 15 is the most responsive cell signaling event to manganese exposure (of 18 tested) in human neuroprogenitors and a mouse striatal cell line.	Serine	37-43	P53	Homo sapiens	14-17
25548100-7	2015	Concurrent Bcl-xL antagonism by the BH3 mimetic ABT-263 combined with carfilzomib synergistically enhanced apoptosis that was dependent on Bax or p53, and was attenuated by Noxa or Bik shRNA.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	48-51	P53	Homo sapiens	146-149
25660211-8	2015	Western blotting analysis indicated that the Cu complex activates the p53 dependent pathway of apoptosis.	Copper	45-47	P53	Homo sapiens	70-73
25617667-9	2015	Using immunofluorescent staining we observed that the secosteroids reduced the generation cyclobutane pyrimidine dimers in response to UVB and enhanced expression of p53 phosphorylated at Ser-15, but not at Ser-46.	Serine	188-191	P53	Homo sapiens	166-169
25515619-0	2015	Resveratrol induces cell cycle arrest via a p53-independent pathway in A549 cells.	Resveratrol	0-11	P53	Homo sapiens	44-47
25515619-6	2015	The immunofluorescence and western blot analysis results revealed that resveratrol upregulated the nuclear expression of p53 in A549 cells.	Resveratrol	71-82	P53	Homo sapiens	121-124
25515619-9	2015	The present study may offer a scientific basis for the further in-depth evaluation of resveratrol in the association of p53 and cell cycle arrest.	Resveratrol	86-97	P53	Homo sapiens	120-123
26261798-0	2015	Elevation of cAMP Levels Inhibits Doxorubicin-Induced Apoptosis in Pre- B ALL NALM- 6 Cells Through Induction of BAD Phosphorylation and Inhibition of P53 Accumulation.	Cyclic AMP	13-17	P53	Homo sapiens	151-154
26261798-0	2015	Elevation of cAMP Levels Inhibits Doxorubicin-Induced Apoptosis in Pre- B ALL NALM- 6 Cells Through Induction of BAD Phosphorylation and Inhibition of P53 Accumulation.	Doxorubicin	34-45	P53	Homo sapiens	151-154
26261798-5	2015	Protein expression of p53, BAD and phoshorylated BAD was detected by western blotting analysis.cAMP-increasing agents diminished the doxorubicin-mediated cytotoxicity in NALM-6 cells as indicated by the viability assays.	Cyclic AMP	95-99	P53	Homo sapiens	22-25
26261798-8	2015	Western blot results revealed the reduced expression of p53 protein in cells treated with combination of cAMP-elevating agents and doxorubicin in contrast to cells treated with doxorubicin alone.	Cyclic AMP	105-109	P53	Homo sapiens	56-59
26261798-8	2015	Western blot results revealed the reduced expression of p53 protein in cells treated with combination of cAMP-elevating agents and doxorubicin in contrast to cells treated with doxorubicin alone.	Doxorubicin	131-142	P53	Homo sapiens	56-59
26261798-8	2015	Western blot results revealed the reduced expression of p53 protein in cells treated with combination of cAMP-elevating agents and doxorubicin in contrast to cells treated with doxorubicin alone.	Doxorubicin	177-188	P53	Homo sapiens	56-59
26261798-11	2015	Our study suggests that elevated cAMP levels inhibit doxorubicin-induced apoptosis in pre-B ALL cells through induction of BAD phosphorylation and abrogation of p53 accumulation.	Cyclic AMP	33-37	P53	Homo sapiens	161-164
26261798-11	2015	Our study suggests that elevated cAMP levels inhibit doxorubicin-induced apoptosis in pre-B ALL cells through induction of BAD phosphorylation and abrogation of p53 accumulation.	Doxorubicin	53-64	P53	Homo sapiens	161-164
25535325-4	2015	In the present study, we found that H2O2 induced apoptotic cell death in p53-positive human hepatocytes, but not in p53-negative human hepatocytes.	Hydrogen Peroxide	36-40	P53	Homo sapiens	73-76
25548100-7	2015	Concurrent Bcl-xL antagonism by the BH3 mimetic ABT-263 combined with carfilzomib synergistically enhanced apoptosis that was dependent on Bax or p53, and was attenuated by Noxa or Bik shRNA.	carfilzomib	70-81	P53	Homo sapiens	146-149
25647149-7	2015	Paclitaxel increased p53 protein expression in 10A, 10AT, 10ATG3B and 10CA1a cells, by 87, 102, 812 and 84%, respectively.	Paclitaxel	0-10	P53	Homo sapiens	21-24
25633416-9	2015	FOXM1 effector genes such as CDK4, p53 and cyclin D1 were downregulated in gastric cancer cells by combination treatment with DIM and paclitaxel.	Paclitaxel	134-144	P53	Homo sapiens	35-38
25647149-13	2015	The decreased responsiveness to paclitaxel observed in 10CA1a tumor cells was likely due, in part, to activation of the Akt signaling pathway and a high expression of wild-type p53 with lack of p21Waf1/Cip1.	Paclitaxel	32-42	P53	Homo sapiens	177-180
25821946-9	2015	Furthermore, phosphorylation of ATM targets, including gammaH2AX and serine 15 (S15) on p53, were increased in Rap1 silencing cells in response to etoposide.	Serine	69-75	P53	Homo sapiens	88-91
25359126-0	2015	The Apoptotic Effect of Plant Based Nanosilver in Colon Cancer Cells is a p53 Dependent Process Involving ROS and JNK Cascade.	ros	106-109	P53	Homo sapiens	74-77
25359126-5	2015	PD-AgNP-mediated apoptosis in CRCs is a p53 dependent process involving ROS and JNK cascade.	ros	72-75	P53	Homo sapiens	40-43
25938156-2	2015	METHODS: Immunohistochemical SP staining method was used to quantify the protein expression levels of Ki-67 and p53 protein in 10 cases of normal oral mucosa, 16 cases of oral leukoplakia (OLK) tissue, and 48 cases of oral squamous cell carcinoma.	TFF2 protein, human	29-31	P53	Homo sapiens	112-115
25789029-0	2015	A preliminary study of the effect of curcumin on the expression of p53 protein in a human multiple myeloma cell line.	Curcumin	37-45	P53	Homo sapiens	67-70
25789029-5	2015	The expression of p53 protein in the MM RPMI 8226 cells following treatment with curcumin was detected by western blotting and ELISA.	Curcumin	81-89	P53	Homo sapiens	18-21
25789029-7	2015	In the MM RPMI 8226 cells treated with curcumin, the expression of the p53 and Bax genes was upregulated, while the expression of the MDM2 gene was downregulated.	Curcumin	39-47	P53	Homo sapiens	71-74
25789029-8	2015	p53 protein expression was higher in the curcumin experimental group compared with the control group.	Curcumin	41-49	P53	Homo sapiens	0-3
25789029-10	2015	In the MM RPMI 8226 cells treated with curcumin, p53 protein levels were upregulated, which suggested that curcumin may promote the apoptosis of MM cells by upregulating p53 protein expression.	Curcumin	39-47	P53	Homo sapiens	49-52
25789029-10	2015	In the MM RPMI 8226 cells treated with curcumin, p53 protein levels were upregulated, which suggested that curcumin may promote the apoptosis of MM cells by upregulating p53 protein expression.	Curcumin	39-47	P53	Homo sapiens	170-173
25789029-10	2015	In the MM RPMI 8226 cells treated with curcumin, p53 protein levels were upregulated, which suggested that curcumin may promote the apoptosis of MM cells by upregulating p53 protein expression.	Curcumin	107-115	P53	Homo sapiens	49-52
25789029-10	2015	In the MM RPMI 8226 cells treated with curcumin, p53 protein levels were upregulated, which suggested that curcumin may promote the apoptosis of MM cells by upregulating p53 protein expression.	Curcumin	107-115	P53	Homo sapiens	170-173
25704882-11	2015	Accordingly, inhibitors of NF-kappaB and of the NF-kappaB/p53-regulated anti-apoptotic protein survivin significantly sensitize colon carcinoma cells expressing wild-type HDAC2 to apoptosis induced by the genotoxin doxorubicin.	Doxorubicin	215-226	P53	Homo sapiens	58-61
25742468-9	2015	Functional tests demonstrated that truncating mutation Arg458X causes enhancement of dephosphorylation activity of PPM1D toward serine 15 of p53, whereas Lys469Glu version is equivalent to the wild-type.	Serine	128-134	P53	Homo sapiens	141-144
32262124-7	2015	Furthermore, the intracellular nanosystem triggered the overproduction of reactive oxygen species (ROS) as early as 25 min after treatment, which activated various downstream signaling pathways such as p53, AKT and MAPKs to induce the cell death.	Reactive Oxygen Species	74-97	P53	Homo sapiens	202-205
32262124-7	2015	Furthermore, the intracellular nanosystem triggered the overproduction of reactive oxygen species (ROS) as early as 25 min after treatment, which activated various downstream signaling pathways such as p53, AKT and MAPKs to induce the cell death.	Reactive Oxygen Species	99-102	P53	Homo sapiens	202-205
25691063-8	2015	Further, we determined the Ser 215 residue of p53 is critical for functional regulation by AK-B and EBNA3C and that the kinase domain of AK-B which includes amino acid residues 106, 111 and 205 was important for p53 regulation.	Serine	27-30	P53	Homo sapiens	46-49
25605022-0	2015	p53 activates G1 checkpoint following DNA damage by doxorubicin during transient mitotic arrest.	Doxorubicin	52-63	P53	Homo sapiens	0-3
25774791-4	2015	RESULTS: The pooled data by a fixed-effects model suggested an increased risk of CM associated with p53 Arg72Pro polymorphism under the genetic model of Arg/Pro vs. Pro/Pro without heterogeneity (ORArg/Pro vs. Pro/Pro = 1.76, 95% CI = 1.55-1.99, Pheterogeneity = 0.075).	Arginine	104-107	P53	Homo sapiens	100-103
26064201-1	2015	BACKGROUND: The polymorphism of TP53 codon 72, a transversion of G to C (Arg to Pro), has been demonstrated to be associated with the risk for lung cancer.	Arginine	73-76	P53	Homo sapiens	32-36
26064201-3	2015	Thus, we performed a meta-analysis by pooling all currently available case-control studies to estimate the effect of TP53 codon 72 Arg/Pro polymorphism on the development of lung cancer in the Chinese population.	Arginine	131-134	P53	Homo sapiens	117-121
25837273-4	2015	It is also identified that the modulation of p53 by scopoletin are related to the induction of autophagy.	Scopoletin	52-62	P53	Homo sapiens	45-48
25837273-9	2015	Therefore, these findings suggest that scopoletin could exert a positive effect on anti-aging related to autophagy through modulation of p53 in human lung fibroblasts.	Scopoletin	39-49	P53	Homo sapiens	137-140
25766317-0	2015	Reactive oxygen species and p21Waf1/Cip1 are both essential for p53-mediated senescence of head and neck cancer cells.	Reactive Oxygen Species	0-23	P53	Homo sapiens	64-67
25766317-4	2015	DNA-damaging reactive oxygen species (ROS) are a by-product of ionizing radiation that lead to the activation of p53, transcription of p21(cip1/waf1) and, in the case of wild-type TP53 HNSCC cells, cause senescence.	Reactive Oxygen Species	13-36	P53	Homo sapiens	113-116
25766317-4	2015	DNA-damaging reactive oxygen species (ROS) are a by-product of ionizing radiation that lead to the activation of p53, transcription of p21(cip1/waf1) and, in the case of wild-type TP53 HNSCC cells, cause senescence.	Reactive Oxygen Species	13-36	P53	Homo sapiens	180-184
25766317-4	2015	DNA-damaging reactive oxygen species (ROS) are a by-product of ionizing radiation that lead to the activation of p53, transcription of p21(cip1/waf1) and, in the case of wild-type TP53 HNSCC cells, cause senescence.	Reactive Oxygen Species	38-41	P53	Homo sapiens	113-116
25766317-4	2015	DNA-damaging reactive oxygen species (ROS) are a by-product of ionizing radiation that lead to the activation of p53, transcription of p21(cip1/waf1) and, in the case of wild-type TP53 HNSCC cells, cause senescence.	Reactive Oxygen Species	38-41	P53	Homo sapiens	180-184
25766317-6	2015	For the first time, we show that persistent exposure to low levels of the ROS, hydrogen peroxide, leads to the long-term expression of p21 in HNSCC cells with a partially functional TP53, resulting in senescence.	Reactive Oxygen Species	74-77	P53	Homo sapiens	182-186
25766317-6	2015	For the first time, we show that persistent exposure to low levels of the ROS, hydrogen peroxide, leads to the long-term expression of p21 in HNSCC cells with a partially functional TP53, resulting in senescence.	Hydrogen Peroxide	79-96	P53	Homo sapiens	182-186
25766317-7	2015	We conclude that the level of ROS is crucial in initiating p53"s transcription of p21 leading to senescence.	Reactive Oxygen Species	30-33	P53	Homo sapiens	59-62
25766317-8	2015	It is p21"s ability to sustain elevated levels of ROS, in turn, that allows for a long-term oxidative stress, and ensures an active p53-p21-ROS signaling loop.	Reactive Oxygen Species	50-53	P53	Homo sapiens	132-135
25766317-8	2015	It is p21"s ability to sustain elevated levels of ROS, in turn, that allows for a long-term oxidative stress, and ensures an active p53-p21-ROS signaling loop.	Reactive Oxygen Species	140-143	P53	Homo sapiens	132-135
25806354-0	2015	p53 Calls upon CIA (Calcium Induced Apoptosis) to Counter Stress.	Calcium	20-27	P53	Homo sapiens	0-3
25616665-6	2015	Inhibition of miR-520g in p53(-/-) cells increased their sensitivity to 5-FU treatment.	Fluorouracil	72-76	P53	Homo sapiens	26-29
25575314-4	2015	Although 1, 2 and pifithrin-alpha caused serious inhibition on p53, 1 and 2 significantly cause the loss of mitochondrial membrane potential and increase of the reactive oxygen species level, cytochrome c, apaf-1 and caspase-3/9 ratio in BEL-7404 cells.	Reactive Oxygen Species	161-184	P53	Homo sapiens	63-75
25767399-2	2015	METHODS: The expression level of p53 protein was detected by immunohistochemistry in primary early-stage ER-positive breast tumor specimens from 293 postmenopausal breast cancer patients who received first-line AI treatment (letrozole, anastrozole, or exemestane) until relapse, and analysis was performed to determine whether expression of p53 protein affected the response to endocrine therapy.	Anastrozole	236-247	P53	Homo sapiens	33-36
25741709-7	2015	DAVID and KEGG pathway analysis suggested that the target genes were generally involved in cell apoptosis, p53, neurotrophin, calcium, chemokine and Jak-STAT signalling pathways.	Calcium	126-133	P53	Homo sapiens	107-110
25750273-0	2015	The effect of silibinin in enhancing toxicity of temozolomide and etoposide in p53 and PTEN-mutated resistant glioma cell lines.	Silybin	14-23	P53	Homo sapiens	79-82
25750273-4	2015	In this project, we evaluated the effects of silibinin, a natural plant component of milk thistle seeds, to potentiate toxic effects of chemotherapy drugs such as temozolomide, etoposide and irinotecan on LN229, U87 and A172 (P53 and phosphatase and tensin homolog (PTEN) -tumor suppressor-mutated) glioma cell lines.	Silybin	45-54	P53	Homo sapiens	226-229
25750305-8	2015	Patients with positive nuclear p53 had significantly lower vitamin D levels (4.18 ng/ml), compared to patients without nuclear p53 expression.	Vitamin D	59-68	P53	Homo sapiens	31-34
25582697-5	2015	Molecular analysis of lymphomas revealed that arginine methylation of p53 selectively suppresses expression of crucial proapoptotic and antiproliferative target genes, thereby sustaining tumor cell self-renewal and proliferation and bypassing the need for the acquisition of inactivating p53 mutations.	Arginine	46-54	P53	Homo sapiens	70-73
25750340-1	2015	BACKGROUND/AIM: We undertook a case-control and a case-case study to examine the possible association of p53 codon72 polymorphism with the breast cancer risk and resistance to anthracycline-based chemotherapy.	Anthracyclines	176-189	P53	Homo sapiens	105-108
25776512-11	2015	CONCLUSIONS: Taken together, the results of our study clearly suggested that the cell death induced by the combination of RSV-GNPs would involve alteration in expression of p53, p21, caspase-3, Bax, Bcl-2 and NF-kappaB, indicating oxidative mechanism in NCI-H460 cells.	Resveratrol	122-125	P53	Homo sapiens	173-176
26222289-10	2015	Finally, gene expression studies suggested triggering of the p53 mediated caspase signalling gene cascade in 5-FU@DsAgNC treated cells.	Fluorouracil	109-113	P53	Homo sapiens	61-64
25776512-9	2015	Moreover, Western blotting analysis showed that apoptosis induced by RSV-GNPs is associated with the increased Bax, p53, p21, caspase-3 protein levels, and decreased Bcl-2 and NF-kappaB proteins expression, which indicates the involvement of mitochondria-dependent apoptosis in the anticancer efficacy of RSV-GNPs in NCI-H460 cells.	Resveratrol	69-72	P53	Homo sapiens	116-119
25582697-5	2015	Molecular analysis of lymphomas revealed that arginine methylation of p53 selectively suppresses expression of crucial proapoptotic and antiproliferative target genes, thereby sustaining tumor cell self-renewal and proliferation and bypassing the need for the acquisition of inactivating p53 mutations.	Arginine	46-54	P53	Homo sapiens	288-291
25667616-10	2015	Furthermore, in the naringenin-treated K562 cells, the labeling index of proliferating cell nuclear antigen was observed to be increased by immunochemical staining, the mRNA and protein expression levels of p21/WAF1 were strongly upregulated in reverse transcription-polymerase chain reaction and western blot analyses, whereas p53 gene expression was not significantly changed.	naringenin	20-30	P53	Homo sapiens	328-331
25595558-7	2015	Consistent with this observation in SK-MEL28 cells, Sp1 was necessary for the tamoxifen-regulated  Raf-1:ER to induce p21(CIP1) transcription in U251 cells, in which TP53 is mutated.	Tamoxifen	78-87	P53	Homo sapiens	166-170
25226867-7	2015	TP53 sequence analysis of the index patient revealed the germline mutation c.1025G &gt; C in a heterozygous state, resulting in an amino acid exchange from arginine to proline (p.Arg342Pro) in the tetramerization domain of p53.	Arginine	156-164	P53	Homo sapiens	0-4
25226867-7	2015	TP53 sequence analysis of the index patient revealed the germline mutation c.1025G &gt; C in a heterozygous state, resulting in an amino acid exchange from arginine to proline (p.Arg342Pro) in the tetramerization domain of p53.	Arginine	156-164	P53	Homo sapiens	223-226
25667616-16	2015	Cell cycle arrest and apoptosis-inducing effects, achieved through p53-independent p21/WAF1 upregulation, are likely to be the mechanism of the antileukemic effects of naringenin, and the protective effect against ADM chemotherapy-induced damage in PMNs may be due to the antioxidant capability of this agent at low concentrations.	naringenin	168-178	P53	Homo sapiens	67-70
26005978-9	2015	Indians compared to control population presented: - TP53 super representation of Arg/Arg haplotype, 74.5% versus 42.5%, p&lt;0.0001.	Arginine	81-84	P53	Homo sapiens	52-56
25537301-9	2015	Moreover, studies also found that ROS acted as an upstream mediator in NB/BDCur-induced HepG2 cell growth inhibition and led to DNA damage with up-regulation of the expression level of phosphorylated ATM and p53.	ros	34-37	P53	Homo sapiens	208-211
26005978-9	2015	Indians compared to control population presented: - TP53 super representation of Arg/Arg haplotype, 74.5% versus 42.5%, p&lt;0.0001.	Arginine	85-88	P53	Homo sapiens	52-56
25563581-8	2015	The Gene Ontology and KEGG pathway analysis revealed that the target genes of co-expressed miRNAs were highly involved in the cell cycle process, metal ion binding, modification of plasma membrane, and the p53 signal pathway.	Metals	146-151	P53	Homo sapiens	206-209
25594146-5	2015	RESULTS: In FSECs treated with catalytic iron for up to 6 days, we observed an increase in cell viability, NO production, and p53, pan-Ras, ERK/MAPK, PI3K/Akt, Ki67, and c-Myc activations (P &lt; 0.05) in a dose-dependent and time-dependent manner.	Iron	41-45	P53	Homo sapiens	126-129
25922718-5	2015	RESULTS: We found that CK could significantly enhance cisplatin-induced p53 expression and activity in two lung cancer cell lines, H460 and A549.	Cisplatin	54-63	P53	Homo sapiens	72-75
25639717-0	2015	CR389, a benzoimidazolyl pyridinone analog, induces cell cycle arrest and apoptosis via p53 activation in human ovarian cancer PA-1 cells.	cr389	0-5	P53	Homo sapiens	88-91
25639717-3	2015	In addition, activation of p53 via phosphorylation at Ser15 and subsequent up-regulation of p21(CIP1) showed that CR389 also induces p53-dependent-p21(CIP1)-mediated cell cycle arrest.	cr389	114-119	P53	Homo sapiens	27-30
25639717-3	2015	In addition, activation of p53 via phosphorylation at Ser15 and subsequent up-regulation of p21(CIP1) showed that CR389 also induces p53-dependent-p21(CIP1)-mediated cell cycle arrest.	cr389	114-119	P53	Homo sapiens	133-136
25639717-6	2015	Therefore, we conclude that CR389 is a candidate therapeutic agent for the treatment of human ovarian cancer via the activation of p53.	cr389	28-33	P53	Homo sapiens	131-134
25637534-6	2015	Interestingly, p53 and p53 phosphorylation (Ser-15), as well as the cyclin-dependent kinase inhibitors p21 and p27, were induced similarly in both proliferating and quiescent cells after irradiation.	Serine	44-47	P53	Homo sapiens	23-26
25607831-8	2015	Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells.	Acetylcysteine	18-35	P53	Homo sapiens	163-166
25607831-8	2015	Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells.	Acetylcysteine	37-40	P53	Homo sapiens	163-166
25490952-10	2015	Furthermore, Cd-induced superoxide and lipid peroxidation mediated activation of proapoptotic markers p21 and p53 in the developing embryo.	Cadmium	13-15	P53	Homo sapiens	110-113
25490952-10	2015	Furthermore, Cd-induced superoxide and lipid peroxidation mediated activation of proapoptotic markers p21 and p53 in the developing embryo.	Superoxides	24-34	P53	Homo sapiens	110-113
25499080-3	2015	Silencing of p53 or KRAS in A549 or H358 cells either enhanced or attenuated the resistance of cells to cisplatin and taxol through promotion or suppression of the NF-kappaB p65 nuclear translocation.	Cisplatin	104-113	P53	Homo sapiens	13-16
25499080-3	2015	Silencing of p53 or KRAS in A549 or H358 cells either enhanced or attenuated the resistance of cells to cisplatin and taxol through promotion or suppression of the NF-kappaB p65 nuclear translocation.	Paclitaxel	118-123	P53	Homo sapiens	13-16
25499080-4	2015	Introduction of a wild type p53 into p53 null lung cancer cell lines H1299 and H358 inhibited NF-kappaB activity, leading to the enhanced response to chemotherapeutic drugs.	ZINC78587988	79-83	P53	Homo sapiens	28-31
25499080-4	2015	Introduction of a wild type p53 into p53 null lung cancer cell lines H1299 and H358 inhibited NF-kappaB activity, leading to the enhanced response to chemotherapeutic drugs.	ZINC78587988	79-83	P53	Homo sapiens	37-40
26065288-3	2015	A-T transversion of the p53 gene is now considered to be a mutational "signature" of aristolochic acid, which is a cause of endemic nephropathy.	aristolochic acid I	85-102	P53	Homo sapiens	24-27
25847421-0	2015	TP53 mutations induced by BPDE in Xpa-WT and Xpa-Null human TP53 knock-in (Hupki) mouse embryo fibroblasts.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	26-30	P53	Homo sapiens	0-4
25847421-0	2015	TP53 mutations induced by BPDE in Xpa-WT and Xpa-Null human TP53 knock-in (Hupki) mouse embryo fibroblasts.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	26-30	P53	Homo sapiens	60-64
25704813-4	2015	Here, we show that in oncogenic-Ras-expressing cells, p53 promotes oxidative phosphorylation (OXPHOS) and cell survival upon glucose starvation.	Glucose	125-132	P53	Homo sapiens	54-57
25611347-1	2015	Quinofuracins A-E, novel anthraquinone derivatives containing beta-D-galactofuranose that were isolated from the fungus Staphylotrichum boninense PF1444, induced p53-dependent cell death in human tumor cells.	Anthraquinones	25-38	P53	Homo sapiens	162-165
25704813-6	2015	Using gene expression profiling and ChIP-seq analysis, we identify several p53-inducible fatty acid metabolism-related genes.	Fatty Acids	89-99	P53	Homo sapiens	75-78
25634217-0	2015	Prostaglandin E2 inhibits p53 in human breast adipose stromal cells: a novel mechanism for the regulation of aromatase in obesity and breast cancer.	Dinoprostone	0-16	P53	Homo sapiens	26-29
25584700-4	2015	Altered spectral characteristics of the Trp53 residue suggest that the core of the protein attains a CH-pi interaction at a low concentration of the salt, with an increase in the packing density.	Salts	149-153	P53	Homo sapiens	40-45
25519225-0	2015	Genetic mutation of p53 and suppression of the miR-17~92 cluster are synthetic lethal in non-small cell lung cancer due to upregulation of vitamin D Signaling.	Vitamin D	139-148	P53	Homo sapiens	20-23
25634217-6	2015	Therefore, it was hypothesized that p53 is regulated by PGE2 and involved in the PGE2-mediated regulation of aromatase.	Dinoprostone	56-60	P53	Homo sapiens	36-39
25634217-6	2015	Therefore, it was hypothesized that p53 is regulated by PGE2 and involved in the PGE2-mediated regulation of aromatase.	Dinoprostone	81-85	P53	Homo sapiens	36-39
25634217-7	2015	Results demonstrate that PGE2 causes a significant decrease in p53 transcript and nuclear protein expression, as well as phosphorylation at Ser15 in primary human breast ASCs.	Dinoprostone	25-29	P53	Homo sapiens	63-66
25634217-8	2015	Stabilization of p53 with RITA leads to a significant decrease in the PGE2-stimulated aromatase mRNA expression and activity, and PII activity.	Dinoprostone	70-74	P53	Homo sapiens	17-20
25634217-9	2015	Interaction of p53 with PII was demonstrated and this interaction is decreased in the presence of PGE2.	Dinoprostone	98-102	P53	Homo sapiens	15-18
25634217-13	2015	Overall, our results demonstrate that p53 is a negative regulator of aromatase in the breast and its inhibition by PGE2 provides a novel mechanism for aromatase regulation in obesity and breast cancer.	Dinoprostone	115-119	P53	Homo sapiens	38-41
25444916-8	2015	Conditional knockdown of p53 by tetracycline inducible expression system significantly abrogated curcumin-induced miR-192-5p/215 upregulation in the p53 wild-type H460, A427 and A549 cells.	Curcumin	97-105	P53	Homo sapiens	149-152
25658320-7	2015	To a different extent, either the antioxidant N-acetyl-cysteine or the p53 inhibitor, Pifithrin-alpha, recover cell viability and decrease ROS formation.	Reactive Oxygen Species	139-142	P53	Homo sapiens	71-74
25658463-9	2015	Treatment of wild-type TP53 neuroblastoma cell lines with both GSK2830371 and either doxorubicin or carboplatin resulted in enhanced cell death, mediated through caspase 3/7 induction, as compared to either agent alone.	Doxorubicin	85-96	P53	Homo sapiens	23-27
25567764-1	2015	We report in this work that the Abeta peptide directly interacts with tubulin close to the vinblastine and GTP/GDP binding site, inhibits the tubulin polymerization rate, induces tubulin aggregation, causes cell shrinking, enhances Mad2, BubR1, p53, and p21 activation in MCF7 cells and induces the apoptotic death of A549, HeLa and MCF7 cells.	Guanosine Triphosphate	107-110	P53	Homo sapiens	245-248
24469051-4	2015	Interestingly, p53 promotes miR-506 expression level, indicating that miR-506 mediates cross talk between p53, NF-kappaB p65 and ROS.	Reactive Oxygen Species	129-132	P53	Homo sapiens	15-18
24469051-4	2015	Interestingly, p53 promotes miR-506 expression level, indicating that miR-506 mediates cross talk between p53, NF-kappaB p65 and ROS.	Reactive Oxygen Species	129-132	P53	Homo sapiens	106-109
25651062-5	2015	Biochemical and nuclear magnetic resonance analyses show that other surrounding PTMs, including phosphorylation of serine/threonine residues of p53, affect association with TTD.	Serine	115-121	P53	Homo sapiens	144-147
25651062-5	2015	Biochemical and nuclear magnetic resonance analyses show that other surrounding PTMs, including phosphorylation of serine/threonine residues of p53, affect association with TTD.	Threonine	122-131	P53	Homo sapiens	144-147
25502560-5	2015	When the level of miR-96 increased, the expression of the anti-apoptotic regulator XIAP and p53 stability regulator UBE2N decreased, resulting in increased apoptosis and growth inhibition following 5-FU exposure.	Fluorouracil	198-202	P53	Homo sapiens	92-95
25444916-0	2015	Curcumin promotes apoptosis by activating the p53-miR-192-5p/215-XIAP pathway in non-small cell lung cancer.	Curcumin	0-8	P53	Homo sapiens	46-49
25444916-7	2015	Curcumin also promoted miR-192-5p/215 expressions in A549 cells (p53 wild type) but not in H1299 cells (p53-null).	Curcumin	0-8	P53	Homo sapiens	65-68
25444916-8	2015	Conditional knockdown of p53 by tetracycline inducible expression system significantly abrogated curcumin-induced miR-192-5p/215 upregulation in the p53 wild-type H460, A427 and A549 cells.	Curcumin	97-105	P53	Homo sapiens	25-28
25444916-9	2015	Conversely, ectopic expression of exogenous wild-type but not R273H mutant p53 in the p53-null H1299 cells enabled miR-192-5p/215 response to curcumin treatment.	Curcumin	142-150	P53	Homo sapiens	75-78
25503558-4	2015	Here, we report that after systemic injection of tamoxifen, the vast majority of Pax7-expressing cells remain quiescent despite mutation of p53 and Kras.	Tamoxifen	49-58	P53	Homo sapiens	140-143
25444916-9	2015	Conversely, ectopic expression of exogenous wild-type but not R273H mutant p53 in the p53-null H1299 cells enabled miR-192-5p/215 response to curcumin treatment.	Curcumin	142-150	P53	Homo sapiens	86-89
25444916-12	2015	Taken together, this study highlights that the proapoptotic effects of curcumin depend on miR-192-5p/215 induction and the p53-miR-192-5p/215-XIAP pathway is an important therapeutic target for non-small cell lung cancer.	Curcumin	71-79	P53	Homo sapiens	123-126
25445786-6	2015	SIRT7 overexpressing cells when treated with low dose of doxorubicin (0.25 microM) showed delayed onset of senescence, lesser accumulation of DNA damage marker gammaH2AX and lowered levels of growth arrest markers viz., p53 and p21 when compared to doxorubicin treated control GFP expressing cells.	Doxorubicin	57-68	P53	Homo sapiens	220-223
25613365-9	2015	Depletion of TACC3 up-regulated the phosphorylation of p53 at Serine 33, a site known to be phosphorylated by p38 under cellular stress and further induced the accumulation of phosphorylated p53 to the centrosome.	Serine	62-68	P53	Homo sapiens	55-58
25445786-8	2015	When treated with higher dose of doxorubicin (&gt;1 microM), SIRT7 conferred resistance to apoptosis by attenuating stress activated kinases (SAPK viz., p38 and JNK) and p53 response thereby shifting the cellular fate towards senescence.	Doxorubicin	33-44	P53	Homo sapiens	170-173
25445786-10	2015	SIRT7 mediated resistance to doxorubicin induced apoptosis and senescence was lost when p53 level was restored by nutlin treatment.	Doxorubicin	29-40	P53	Homo sapiens	88-91
25385265-0	2015	TP53 oncomorphic mutations predict resistance to platinum- and taxane-based standard chemotherapy in patients diagnosed with advanced serous ovarian carcinoma.	Platinum	49-57	P53	Homo sapiens	0-4
25464270-0	2015	CUL4B impedes stress-induced cellular senescence by dampening a p53-reactive oxygen species positive feedback loop.	Reactive Oxygen Species	68-91	P53	Homo sapiens	64-67
25464270-1	2015	Tumor suppressor p53 is known to regulate the level of intracellular reactive oxygen species (ROS).	Reactive Oxygen Species	69-92	P53	Homo sapiens	17-20
25464270-1	2015	Tumor suppressor p53 is known to regulate the level of intracellular reactive oxygen species (ROS).	Reactive Oxygen Species	94-97	P53	Homo sapiens	17-20
25464270-3	2015	We here report that a p53-ROS positive feedback loop drives a senescence program in normal human fibroblasts (NHFs) and this senescence-driving loop is negatively regulated by CUL4B.	Reactive Oxygen Species	26-29	P53	Homo sapiens	22-25
25464270-5	2015	We observed that p53-dependent ROS production was significantly augmented and stress-induced senescence was greatly enhanced when CUL4B was absent or depleted.	Reactive Oxygen Species	31-34	P53	Homo sapiens	17-20
25464270-8	2015	Together, our results established a critical role of CUL4B in negatively regulating the p53-ROS positive feedback loop that drives cellular senescence.	Reactive Oxygen Species	92-95	P53	Homo sapiens	88-91
25483438-12	2015	This attenuated high-glucose-induced ROS generation, ER stress signaling, and p53 expression.	Glucose	21-28	P53	Homo sapiens	78-81
25483438-14	2015	Such a decrease generates intracellular ROS, which increases ER stress-mediated p53 expression, and subsequently causes apoptosis by increasing Bax promoter activity.	Reactive Oxygen Species	40-43	P53	Homo sapiens	80-83
25385265-0	2015	TP53 oncomorphic mutations predict resistance to platinum- and taxane-based standard chemotherapy in patients diagnosed with advanced serous ovarian carcinoma.	taxane	63-69	P53	Homo sapiens	0-4
25385265-9	2015	Patients with oncomorphic TP53 mutations demonstrated significantly worse PFS, a 60% higher risk of recurrence (HR=1.60, 95% confidence intervals 1.09, 2.33, p=0.015), and higher rates of platinum resistance (chi(2) test p=0.0024) when compared with single nucleotide mutations not categorized as oncomorphic.	Platinum	188-196	P53	Homo sapiens	26-30
25504633-0	2015	Wee-1 kinase inhibition overcomes cisplatin resistance associated with high-risk TP53 mutations in head and neck cancer through mitotic arrest followed by senescence.	Cisplatin	34-43	P53	Homo sapiens	81-85
25256710-2	2015	Several genetic polymorphisms exist in TP53, including a proline to arginine variant at amino acid 72 (P72 and R72, respectively); this polymorphism alters p53 function.	Arginine	68-76	P53	Homo sapiens	39-43
25256710-2	2015	Several genetic polymorphisms exist in TP53, including a proline to arginine variant at amino acid 72 (P72 and R72, respectively); this polymorphism alters p53 function.	Arginine	68-76	P53	Homo sapiens	156-159
25504633-2	2015	We found that cisplatin treatment of HNSCC cells with mutant TP53 leads to arrest of cells in the G2 phase of the cell cycle, leading us to hypothesize that the wee-1 kinase inhibitor MK-1775 would abrogate the cisplatin-induced G2 block and thereby sensitize isogenic HNSCC cells with mutant TP53 or lacking p53 expression to cisplatin.	Cisplatin	14-23	P53	Homo sapiens	61-65
25504633-2	2015	We found that cisplatin treatment of HNSCC cells with mutant TP53 leads to arrest of cells in the G2 phase of the cell cycle, leading us to hypothesize that the wee-1 kinase inhibitor MK-1775 would abrogate the cisplatin-induced G2 block and thereby sensitize isogenic HNSCC cells with mutant TP53 or lacking p53 expression to cisplatin.	Cisplatin	14-23	P53	Homo sapiens	293-297
25404486-0	2015	Selective ROS-dependent p53-associated anticancer effects of the hypoxoside derivative rooperol on human teratocarcinomal cancer stem-like cells.	Reactive Oxygen Species	10-13	P53	Homo sapiens	24-27
25351378-0	2015	Biological characteristics of Taxol-resistant ovarian cancer cells and reversal of Taxol resistance by adenovirus expressing p53.	Paclitaxel	83-88	P53	Homo sapiens	125-128
25504633-2	2015	We found that cisplatin treatment of HNSCC cells with mutant TP53 leads to arrest of cells in the G2 phase of the cell cycle, leading us to hypothesize that the wee-1 kinase inhibitor MK-1775 would abrogate the cisplatin-induced G2 block and thereby sensitize isogenic HNSCC cells with mutant TP53 or lacking p53 expression to cisplatin.	Cisplatin	14-23	P53	Homo sapiens	309-312
25504633-2	2015	We found that cisplatin treatment of HNSCC cells with mutant TP53 leads to arrest of cells in the G2 phase of the cell cycle, leading us to hypothesize that the wee-1 kinase inhibitor MK-1775 would abrogate the cisplatin-induced G2 block and thereby sensitize isogenic HNSCC cells with mutant TP53 or lacking p53 expression to cisplatin.	Cisplatin	211-220	P53	Homo sapiens	61-65
25504633-2	2015	We found that cisplatin treatment of HNSCC cells with mutant TP53 leads to arrest of cells in the G2 phase of the cell cycle, leading us to hypothesize that the wee-1 kinase inhibitor MK-1775 would abrogate the cisplatin-induced G2 block and thereby sensitize isogenic HNSCC cells with mutant TP53 or lacking p53 expression to cisplatin.	Cisplatin	211-220	P53	Homo sapiens	61-65
25504633-4	2015	We also used a novel TP53 mutation classification scheme to identify which TP53 mutations are associated with limited tumor responses to cisplatin treatment.	Cisplatin	137-146	P53	Homo sapiens	21-25
25504633-4	2015	We also used a novel TP53 mutation classification scheme to identify which TP53 mutations are associated with limited tumor responses to cisplatin treatment.	Cisplatin	137-146	P53	Homo sapiens	75-79
25504633-6	2015	Consistent with its ability to chemosensitize, MK-1775 abrogated the cisplatin-induced G2 block in p53-defective cells leading to mitotic arrest associated with a senescence-like phenotype.	Cisplatin	69-78	P53	Homo sapiens	99-102
25504633-7	2015	Furthermore, MK-1775 enhanced the efficacy of cisplatin in vivo in tumors harboring TP53 mutations.	Cisplatin	46-55	P53	Homo sapiens	84-88
25504633-8	2015	These results indicate that HNSCC cells expressing high-risk p53 mutations are significantly sensitized to cisplatin therapy by the selective wee-1 kinase inhibitor, supporting the clinical evaluation of MK-1775 in combination with cisplatin for the treatment of patients with TP53 mutant HNSCC.	Cisplatin	107-116	P53	Homo sapiens	61-64
25501339-0	2015	Ad-p53 enhances the sensitivity of triple-negative breast cancer MDA-MB-468 cells to the EGFR inhibitor gefitinib.	Gefitinib	104-113	P53	Homo sapiens	3-6
25501339-8	2015	Importantly, wild-type p53 was able to reverse the drug resistance of MDA-MB-468 cells to gefitinib through inactivation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway.	Gefitinib	90-99	P53	Homo sapiens	23-26
25304379-0	2015	Chaetoglobosin K induces apoptosis and G2 cell cycle arrest through p53-dependent pathway in cisplatin-resistant ovarian cancer cells.	chaetoglobosins	0-16	P53	Homo sapiens	68-71
25092068-8	2015	Delivered cisplatin cooperated with piroxicam in modulating cell cycle regulators as caspase-3, p53 and p21.	Cisplatin	10-19	P53	Homo sapiens	96-99
25647416-0	2015	Differential salt-induced dissociation of the p53 protein complexes with circular and linear plasmid DNA substrates suggest involvement of a sliding mechanism.	Salts	13-17	P53	Homo sapiens	46-49
25647416-2	2015	Salt concentrations above 200 mM strongly affected association of the p53 protein to any plasmid DNA substrate.	Salts	0-4	P53	Homo sapiens	70-73
25647416-3	2015	Strikingly different behavior was observed when dissociation of pre-formed p53-DNA complexes in increased salt concentrations was studied.	Salts	106-110	P53	Homo sapiens	75-78
24374014-5	2015	p53 regulates many different aspects of metabolism, including glycolysis, mitochondrial oxidative phosphorylation, pentose phosphate pathway, fatty acid synthesis and oxidation, to maintain the homeostasis of cellular metabolism, which contributes to the role of p53 in tumor suppression.	Fatty Acids	142-152	P53	Homo sapiens	0-3
25304379-0	2015	Chaetoglobosin K induces apoptosis and G2 cell cycle arrest through p53-dependent pathway in cisplatin-resistant ovarian cancer cells.	Cisplatin	93-102	P53	Homo sapiens	68-71
25444910-6	2015	By contrast, arsenic trioxide, which by inhibiting wild-type p53-induced phosphatase-1 that serves responses downstream of p53, and by depolymerizing tubulin, synergistically enhanced cisplatin cytotoxicity including loss of SP cells.	Cisplatin	184-193	P53	Homo sapiens	61-64
25444910-6	2015	By contrast, arsenic trioxide, which by inhibiting wild-type p53-induced phosphatase-1 that serves responses downstream of p53, and by depolymerizing tubulin, synergistically enhanced cisplatin cytotoxicity including loss of SP cells.	TFF2 protein, human	225-227	P53	Homo sapiens	61-64
25478729-0	2015	Alternation of adriamycin penetration kinetics in MCF-7 cells from 2D to 3D culture based on P-gp expression through the Chk2/p53/NF-kappaB pathway.	Doxorubicin	15-25	P53	Homo sapiens	126-129
25584637-0	2015	Oxidation of p53 through DNA charge transport involves a network of disulfides within the DNA-binding domain.	Disulfides	68-78	P53	Homo sapiens	13-16
25584637-6	2015	Differential thiol labeling was used to determine the oxidation states of cysteine residues within p53 after DNA-mediated oxidation.	Sulfhydryl Compounds	13-18	P53	Homo sapiens	99-102
25584637-6	2015	Differential thiol labeling was used to determine the oxidation states of cysteine residues within p53 after DNA-mediated oxidation.	Cysteine	74-82	P53	Homo sapiens	99-102
25584637-9	2015	A distinct shift in peptide labeling toward (13)C2D2-iodoacetamide-labeled cysteines is observed in oxidized samples, confirming that chemical oxidation of p53 occurs at long range.	Iodoacetamide	53-66	P53	Homo sapiens	156-159
25584637-9	2015	A distinct shift in peptide labeling toward (13)C2D2-iodoacetamide-labeled cysteines is observed in oxidized samples, confirming that chemical oxidation of p53 occurs at long range.	Cysteine	75-84	P53	Homo sapiens	156-159
25584637-11	2015	On the basis of these data, it is proposed that disulfide formation involving C275 is critical for inducing oxidative dissociation of p53 from DNA.	Disulfides	48-57	P53	Homo sapiens	134-137
25623255-0	2015	Bone marrow stroma-derived PGE2 protects BCP-ALL cells from DNA damage-induced p53 accumulation and cell death.	Dinoprostone	27-31	P53	Homo sapiens	79-82
25623255-3	2015	We have recently demonstrated that the second messenger cyclic adenosine monophosphate (cAMP) through activation of protein kinase A (PKA) has the ability to inhibit DNA damage-induced p53 accumulation and thereby promote survival of the leukaemic blasts.	Cyclic AMP	56-86	P53	Homo sapiens	185-188
25623255-3	2015	We have recently demonstrated that the second messenger cyclic adenosine monophosphate (cAMP) through activation of protein kinase A (PKA) has the ability to inhibit DNA damage-induced p53 accumulation and thereby promote survival of the leukaemic blasts.	Cyclic AMP	88-92	P53	Homo sapiens	185-188
25623255-13	2015	CONCLUSIONS: Our findings support our hypothesis that BM-derived PGE(2), through activation of cAMP-PKA signalling in BCP-ALL blasts, can inhibit the tumour suppressive activity of wild type p53, thereby promoting leukaemogenesis and protecting against therapy-induced leukaemic cell death.	Cyclic AMP	95-99	P53	Homo sapiens	191-194
25505174-3	2015	Furthermore, we also provide evidence that Plk1 inhibition makes PCa cells carrying WT p53 much more sensitive to low-dose metformin treatment.	Metformin	123-132	P53	Homo sapiens	87-90
25505174-4	2015	Mechanistically, we found that co-treatment with BI2536 and metformin induced p53-dependent apoptosis and further activated the p53/Redd-1 pathway.	Metformin	60-69	P53	Homo sapiens	78-81
25505174-4	2015	Mechanistically, we found that co-treatment with BI2536 and metformin induced p53-dependent apoptosis and further activated the p53/Redd-1 pathway.	Metformin	60-69	P53	Homo sapiens	128-131
25461314-5	2015	Additionally, N9 also potentiates the production of the pro-apoptotic markers Bax and p53 via inhibition of MDM2.	Nonoxynol	14-16	P53	Homo sapiens	86-89
25583481-7	2015	p53 genetic inactivation in ETC-impaired neural stem cells is caused by increased reactive oxygen species and associated oxidative DNA damage.	Reactive Oxygen Species	82-105	P53	Homo sapiens	0-3
28962365-6	2015	Alternatively, in TP53- and RB1-negative Hep-3B cells, GTN increased CDKN1C transcription and its subsequent translation by acting as a histone deacetylase inhibitor.	goniothalamin	55-58	P53	Homo sapiens	18-22
25615717-7	2015	Moreover, low oxygen tension significantly up-regulated VEGF and bFGF mRNA expression and protein secretion while reducing the expression level of tumour suppressor genes p16, p21, p53, and pRb.	Oxygen	14-20	P53	Homo sapiens	181-184
25510514-4	2015	The interaction of 9 OPFRs with p53 DNA fragment under simulated physiological conditions (phosphate buffer solution of pH 7.40), was explored by UV absorption spectroscopy, fluorescence spectroscopy and molecular modeling method.	Phosphates	91-100	P53	Homo sapiens	32-35
25524737-3	2015	The present authors have previously shown that an increased intracellular level of cAMP disrupts p53-mediated apoptosis in human pre-B NALM-6 cells and inhibition of NF-kappaB prevents prosurvival effect of cAMP during DNA damage.	Cyclic AMP	83-87	P53	Homo sapiens	97-100
25524737-6	2015	The results of present study showed that cAMP disrupted DNA damage/p53-mediated apoptosis through AKT and subsequent NF-kappaB activation.	Cyclic AMP	41-45	P53	Homo sapiens	67-70
25785018-4	2015	Sophoridine also triggered significant down-regulated the expression of p27, CDK2, Survivin, Livin, Bcl-2, E2F1 and the transcriptional activity of FoxM1, NF-kappab and AP-1, meanwhile, up-regulated the expression of caspase-3/8, p53, Smac, c-JNK and p38-MAPK.	matrine	0-11	P53	Homo sapiens	230-233
25407898-0	2015	Nucleolar targeting by platinum: p53-independent apoptosis follows rRNA inhibition, cell-cycle arrest, and DNA compaction.	Platinum	23-31	P53	Homo sapiens	33-36
25511708-0	2015	Sigma 1 Receptor antagonist potentiates the anti-cancer effect of p53 by regulating ER stress, ROS production, Bax levels, and caspase-3 activation.	ros	95-98	P53	Homo sapiens	66-69
25543136-5	2015	We find that mutation of Trp53 results in PIs containing reduced-length fatty acid moieties.	Fatty Acids	72-82	P53	Homo sapiens	25-30
25543136-6	2015	Our results suggest that the anchoring tails of lipid second messengers form an additional layer of PIP signaling in cancer that operates independently of PTEN/PI3-kinase activity but is instead linked to p53.	Phosphatidylinositol Phosphates	100-103	P53	Homo sapiens	205-208
25404730-0	2015	p53 Protein-mediated regulation of phosphoglycerate dehydrogenase (PHGDH) is crucial for the apoptotic response upon serine starvation.	Serine	117-123	P53	Homo sapiens	0-3
25404730-2	2015	Here we report that PHGDH, the key metabolic enzyme that catalyzes the rate-limiting step of the serine biosynthesis pathway, is a target of p53 in human melanoma cells.	Serine	97-103	P53	Homo sapiens	141-144
25404730-3	2015	p53 suppresses PHGDH expression and inhibits de novo serine biosynthesis.	Serine	53-59	P53	Homo sapiens	0-3
25446071-3	2015	Here we report for the first time that cadmium, nickel and cobalt, which have already been shown to disturb various DNA repair mechanisms, can also influence p63 and p73 sequence-specific DNA binding activity and transactivation of p53 family target genes.	Cadmium	39-46	P53	Homo sapiens	232-235
25446071-4	2015	Based on results of electrophoretic mobility shift assay and luciferase reporter assay, we conclude that cadmium inhibits sequence-specific binding of all three core domains to p53 consensus sequences and abolishes transactivation of several promoters (e.g. BAX and MDM2) by 50muM concentrations.	Cadmium	105-112	P53	Homo sapiens	177-180
25446071-5	2015	In the presence of specific DNA, all p53 family core domains were partially protected against loss of DNA binding activity due to cadmium treatment.	Cadmium	130-137	P53	Homo sapiens	37-40
25446071-6	2015	Effective cadmium concentration to abolish DNA-protein interactions was about two times higher for p63 and p73 proteins than for p53.	Cadmium	10-17	P53	Homo sapiens	129-132
25404730-4	2015	Notably, upon serine starvation, p53-mediated cell death is enhanced dramatically in response to Nutlin-3 treatment.	Serine	14-20	P53	Homo sapiens	33-36
25404730-7	2015	These results demonstrate an important role of p53 in regulating the serine biosynthesis pathway through suppressing PHGDH expression and reveal serine deprivation as a novel approach to sensitize p53-mediated apoptotic responses in human melanoma cells.	Serine	69-75	P53	Homo sapiens	47-50
25404730-7	2015	These results demonstrate an important role of p53 in regulating the serine biosynthesis pathway through suppressing PHGDH expression and reveal serine deprivation as a novel approach to sensitize p53-mediated apoptotic responses in human melanoma cells.	Serine	145-151	P53	Homo sapiens	197-200
25446071-7	2015	Furthermore, we detected partial reversibility of cadmium inhibition for all p53 family members by EDTA.	Cadmium	50-57	P53	Homo sapiens	77-80
26745097-4	2015	DOX and 2DG treatments resulted in altered radiation-induced expression levels of p53 and PTEN genes in T47D as well as SKBR3 cells.	Doxorubicin	0-3	P53	Homo sapiens	82-85
25446071-8	2015	DTT was able to reverse cadmium inhibition only for p53 and p73.	Cadmium	24-31	P53	Homo sapiens	52-55
25446071-10	2015	In summary, cadmium strongly inhibits p53, p63 and p73 DNA binding in vitro and in cells in comparison to nickel and cobalt.	Cadmium	12-19	P53	Homo sapiens	38-41
25446071-11	2015	The role of cadmium inhibition of p53 tumor suppressor family in carcinogenesis is discussed.	Cadmium	12-19	P53	Homo sapiens	34-37
25824785-8	2015	OIT3 possibly correlated with calcium binding revealed by the annotation analyses and was regulated by a large number of transcription factors including STAT, SOX9, CREB, NF-kB, PPARG and p53.	Calcium	30-37	P53	Homo sapiens	188-191
25427901-4	2015	Changes in cancer genes and in signaling pathways (MAPK, RAS, Rb, TGFbeta, p53, PTEN, ECM, osteopontin, Wnt) may also contribute to ethanol-mediated mechanisms in carcinogenesis.	Ethanol	132-139	P53	Homo sapiens	75-78
25773855-0	2015	Silibilin-induces apoptosis in breast cancer cells by modulating p53, p21, Bak and Bcl-XL pathways.	silibilin	0-9	P53	Homo sapiens	65-68
25773855-7	2015	Taken together, the results suggest that silibinin inhibits the proliferation and induces apoptosis of MCF-7 cells by down-regulating Bak, P53, P21, BRCA1, BCL-Xl and thus may be considered as an effective adjuvant drug to produce a better chemopreventive response for the cancer therapy.	Silybin	41-50	P53	Homo sapiens	139-142
26320467-0	2015	Treatment with a Small Synthetic Compound, KMU-193, induces Apoptosis in A549 Human Lung Carcinoma Cells through p53 Up-Regulation.	kmu	43-46	P53	Homo sapiens	113-116
25921167-1	2015	OBJECTIVE: To assess associations between codon 72 polymorphisms (Pro or B and Arg or b alleles) of the TP53 gene and lung cancer risk among Bangladeshis.	Arginine	79-82	P53	Homo sapiens	104-108
26434906-3	2015	The aim of the study was to elucidate the role of p53 in the induction of apoptosis by eugenol and capsaicin in a human gastric cancer cell line, AGS.	Capsaicin	99-108	P53	Homo sapiens	50-53
26320467-9	2015	Collectively, these results for the first time demonstrate that KMU-193 has strong apoptotic effects on A549 cells and these are largely mediated through caspase-3- and p53-dependent pathways.	kmu	64-67	P53	Homo sapiens	169-172
26434906-6	2015	RESULTS: In the presence of p53, capsaicin was a more potent pro-apoptotic agent than eugenol.	Capsaicin	33-42	P53	Homo sapiens	28-31
26320432-1	2015	BACKGROUND: Earlier studies on the association between p53 codon 72 Arg&gt;Pro polymorphism and cancer risk were inconclusive and conflicting for the Saudi population.	Arginine	68-71	P53	Homo sapiens	55-58
26434906-7	2015	However, silencing of p53 significantly abrogated apoptosis induced by capsaicin but not that by eugenol.	Capsaicin	71-80	P53	Homo sapiens	22-25
26700591-3	2015	Here, we show that a branched-chain C-20 polyunsaturated fatty acid, geranylgeranoic acid (GGA), induces upregulation of the cellular protein levels of TP53-induced glycolysis and apoptosis regulator (TIGAR) and synthesis of cytochrome c oxidase 2 (SCO2) in human hepatoma-derived HuH-7cells harboring the mutant TP53 gene, suggesting that GGA may shift an energetic state of the tumor cells from aerobic glycolysis to mitochondrial respiration.	Carbon	36-37	P53	Homo sapiens	152-156
26320432-9	2015	CONCLUSIONS: The current meta-analysis suggests that the codon 72 Arg&gt;Pro polymorphism of the p53 gene might not contribute to cancer susceptibility in Saudi population.	Arginine	66-69	P53	Homo sapiens	97-100
26021729-8	2015	3-MA and Atg5 siRNA increased the ox-LDL-induced increases of the p53 protein level and the annexin V-positive staining, which was decreased by z-vad-fmk.	3-methyladenine	0-4	P53	Homo sapiens	66-69
26252178-0	2015	Decrease of mitochondrial p53 during late apoptosis is linked to its dephosphorylation on serine 20.	Serine	90-96	P53	Homo sapiens	26-29
26252178-2	2015	We determined the kinetics of the mitochondrial translocation of p53 in HCT-116 and PA-1 cells exposed to different genotoxic stresses (doxorubicin, camptothecin, UVB).	Doxorubicin	136-147	P53	Homo sapiens	65-68
26252178-4	2015	We show that the serine 20 phosphorylated form of p53 is present at the mitochondria and that the decrease of p53 mitochondrial level during late apoptosis correlates with a decrease of Ser-20 phosphorylation.	Serine	17-23	P53	Homo sapiens	50-53
26252178-4	2015	We show that the serine 20 phosphorylated form of p53 is present at the mitochondria and that the decrease of p53 mitochondrial level during late apoptosis correlates with a decrease of Ser-20 phosphorylation.	Serine	17-23	P53	Homo sapiens	110-113
26252178-4	2015	We show that the serine 20 phosphorylated form of p53 is present at the mitochondria and that the decrease of p53 mitochondrial level during late apoptosis correlates with a decrease of Ser-20 phosphorylation.	Serine	186-189	P53	Homo sapiens	50-53
26252178-4	2015	We show that the serine 20 phosphorylated form of p53 is present at the mitochondria and that the decrease of p53 mitochondrial level during late apoptosis correlates with a decrease of Ser-20 phosphorylation.	Serine	186-189	P53	Homo sapiens	110-113
26252178-7	2015	We propose here that the level of serine 20 phosphorylation is influential on p53 mitochondrial localization during late apoptosis.	Serine	34-40	P53	Homo sapiens	78-81
25565400-0	2015	Decarbamoyl mitomycin C (DMC) activates p53-independent ataxia telangiectasia and rad3 related protein (ATR) chromatin eviction.	10-decarbamoylmitomycin C	0-23	P53	Homo sapiens	40-43
25483068-0	2015	ATM regulates cell fate choice upon p53 activation by modulating mitochondrial turnover and ROS levels.	Reactive Oxygen Species	92-95	P53	Homo sapiens	36-39
25565400-0	2015	Decarbamoyl mitomycin C (DMC) activates p53-independent ataxia telangiectasia and rad3 related protein (ATR) chromatin eviction.	10-decarbamoylmitomycin C	25-28	P53	Homo sapiens	40-43
25565400-3	2015	We previously reported that the novel DMC induced beta-interstrand DNA crosslinks induce a p53-independent form of cell death.	10-decarbamoylmitomycin C	38-41	P53	Homo sapiens	91-94
25715001-0	2015	Inside the tumor: p53 modulates calcium homeostasis.	Calcium	32-39	P53	Homo sapiens	18-21
25565400-4	2015	The p53-independent DMC cytotoxicity associates with the activation, and subsequent depletion, of Chk1.	10-decarbamoylmitomycin C	20-23	P53	Homo sapiens	4-7
25565400-10	2015	Our results suggest that DMC induces a p53-independent disassociation of ATR from chromatin that facilitates Chk1 checkpoint activation and Rad51 chromatin recruitment.	10-decarbamoylmitomycin C	25-28	P53	Homo sapiens	39-42
25331851-3	2015	Upon adriamycin (ADR) exposure, human osteosarcoma-derived U2OS cells underwent cell death in association with an upregulation of TAp73 and various p53/TAp73-target gene products together with RUNX2.	Doxorubicin	5-15	P53	Homo sapiens	148-151
25880696-0	2015	p53 orchestrates calcium signaling in vivo.	Calcium	17-24	P53	Homo sapiens	0-3
26218928-0	2015	Dynamic roles of p53-mediated metabolic activities in ROS-induced stress responses.	Reactive Oxygen Species	54-57	P53	Homo sapiens	17-20
26218928-5	2015	Here, we report that wild type p53 can induce both apoptosis and ferroptosis upon reactive oxygen species (ROS)-induced stress.	Reactive Oxygen Species	82-105	P53	Homo sapiens	31-34
26218928-5	2015	Here, we report that wild type p53 can induce both apoptosis and ferroptosis upon reactive oxygen species (ROS)-induced stress.	Reactive Oxygen Species	107-110	P53	Homo sapiens	31-34
26218928-7	2015	Notably, activated p53 dynamically modulates intracellular ROS, causing an initial reduction and a subsequent increase of ROS levels.	Reactive Oxygen Species	59-62	P53	Homo sapiens	19-22
26218928-7	2015	Notably, activated p53 dynamically modulates intracellular ROS, causing an initial reduction and a subsequent increase of ROS levels.	Reactive Oxygen Species	122-125	P53	Homo sapiens	19-22
26004413-5	2015	Here we review the current knowledge on COX-independent effects of ibuprofen, which affect changes in gene expression or alternative splicing and act through various cell cycle- and apoptosis-regulating pathways, including beta-catenin, NF-kappaB, PPARgamma and p53.	Ibuprofen	67-76	P53	Homo sapiens	262-265
25789565-7	2015	Here, we show that p53 phosphorylation at Ser 33 contributes to H2O2-induced miR-200s transcription.	Serine	42-45	P53	Homo sapiens	19-22
25789565-7	2015	Here, we show that p53 phosphorylation at Ser 33 contributes to H2O2-induced miR-200s transcription.	Hydrogen Peroxide	64-68	P53	Homo sapiens	19-22
25789565-8	2015	In addition, we show that p38alpha can directly phosphorylate p53 at serine 33 upon H2O2 exposure.	Serine	69-75	P53	Homo sapiens	62-65
25789565-8	2015	In addition, we show that p38alpha can directly phosphorylate p53 at serine 33 upon H2O2 exposure.	Hydrogen Peroxide	84-88	P53	Homo sapiens	62-65
25463242-7	2015	Data revealed that high glucose, FFA, and hypoxia down-regulated hCdc14A expression remarkably, and also affected the expression of other cell cycle-related proteins such as cyclin B, cyclin D, cyclin E, and p53.	Glucose	24-31	P53	Homo sapiens	208-211
25353185-0	2015	Progesterone receptor-NFkappaB complex formation is required for progesterone-induced NFkappaB nuclear translocation and binding onto the p53 promoter.	Progesterone	65-77	P53	Homo sapiens	138-141
26089934-3	2015	Cisplatin was known to exhibit cytotoxic effect to renal cells by inducing apoptosis through activation of p53.	Cisplatin	0-9	P53	Homo sapiens	107-110
26089934-9	2015	Apigenin reduced cisplatin-induced phosphorylation and expression of p53, with no significant influence on production of ROS that is known to induce p53 activation.	Cisplatin	17-26	P53	Homo sapiens	69-72
26089934-11	2015	Taken together, these results suggest that apigenin ameliorates cisplatin-induced apoptosis through reduction of p53 activation and promotion of PI3K/Akt pathway in HK-2 cells.	Cisplatin	64-73	P53	Homo sapiens	113-116
26333122-6	2015	The p53 protein was activated and phosphorylated at serines 15 and 392 and accumulated in the nucleus after 24 and 48 h. The Mdm2 protein was present in the cytoplasm with its maximal level after 8 and 16 h. The p21 protein was detected in the nucleus after 24 and 48 h. Increased levels of phosphorylated Chk2 at threonine 68 were observed in the cytoplasmic fraction after 24 and 48 h of mitoxantrone treatment.	Serine	52-59	P53	Homo sapiens	4-7
26333122-6	2015	The p53 protein was activated and phosphorylated at serines 15 and 392 and accumulated in the nucleus after 24 and 48 h. The Mdm2 protein was present in the cytoplasm with its maximal level after 8 and 16 h. The p21 protein was detected in the nucleus after 24 and 48 h. Increased levels of phosphorylated Chk2 at threonine 68 were observed in the cytoplasmic fraction after 24 and 48 h of mitoxantrone treatment.	Threonine	314-323	P53	Homo sapiens	4-7
26441204-6	2015	The changes in the levels of key proteins show that benfluron provoked activation of p53 and induced phosphorylation of p53 on serine 15 and serine 392.	Serine	127-133	P53	Homo sapiens	120-123
25971446-9	2015	CAP metabolites preferentially caused double base lesion, the G and C of the ACG sequence complementary to codon 273 of the p53 gene, in the presence of NADH and Cu(II).	NAD	153-157	P53	Homo sapiens	124-127
26333122-9	2015	p53 was phosphorylated at serines 15 and 392 and accumulated in the nucleus.	Serine	26-33	P53	Homo sapiens	0-3
25553088-0	2015	Upregulation of Acetylcholinesterase Mediated by p53 Contributes to Cisplatin-Induced Apoptosis in Human Breast Cancer Cell.	Cisplatin	68-77	P53	Homo sapiens	49-52
25473754-4	2015	Immunohistochemistry for p53 was performed on all paraffin blocks of fallopian tube and non-neoplastic endometrium.	Paraffin	50-58	P53	Homo sapiens	25-28
25310526-7	2015	p53 and Bax were upregulated and Bcl2 was downregulated in the EB1-depleted PTX-treated MCF-7 cells, indicating that the apoptosis occurs via a p53-dependent pathway.	Paclitaxel	76-79	P53	Homo sapiens	0-3
25310526-7	2015	p53 and Bax were upregulated and Bcl2 was downregulated in the EB1-depleted PTX-treated MCF-7 cells, indicating that the apoptosis occurs via a p53-dependent pathway.	Paclitaxel	76-79	P53	Homo sapiens	144-147
25310623-0	2015	5-FU resistance abrogates the amplified cytotoxic effects induced by inhibiting checkpoint kinase 1 in p53-mutated colon cancer cells.	Fluorouracil	0-4	P53	Homo sapiens	103-106
26098630-7	2015	Moreover, RMSD, RMSF, hydrogen bonds, salt bridge, and secondary structure analyses revealed that the NBD protein had a strong bond with p53 motif and the protein-ligand complex was stable.	Hydrogen	22-30	P53	Homo sapiens	137-140
25310623-6	2015	In contrast, in p53-deficient, 5-FU-resistant (5FUR) colon cancer cells that we developed, 5-FU enhanced DNA damage but did not induce Chk1/ATM activation or cell cycle arrest.	Fluorouracil	31-35	P53	Homo sapiens	16-19
25310623-6	2015	In contrast, in p53-deficient, 5-FU-resistant (5FUR) colon cancer cells that we developed, 5-FU enhanced DNA damage but did not induce Chk1/ATM activation or cell cycle arrest.	Fluorouracil	91-95	P53	Homo sapiens	16-19
25553088-9	2015	CONCLUSION: Taken together, these results suggested that AChE expression could be upregulated by the activation of p53 during apoptosis induced by cisplatin in MCF-7 cells.	Cisplatin	147-156	P53	Homo sapiens	115-118
25252686-4	2015	In this study, we show that virus-mediated ROS upregulation activates the protein kinase, ataxia telangiectasia mutated, which in turn phosphorylates serine 15 on p53.	Reactive Oxygen Species	43-46	P53	Homo sapiens	163-166
25464291-7	2015	Firstly, reactive oxygen species (ROS) is generated induced by MnO@SiO2 NPs, then p53 is activated followed by an increase in the bax and a decrease in the bcl-2, ultimately leading to G2/M phase arrest, increasing the activity of caspase-3 and inducing apoptosis.	Reactive Oxygen Species	9-32	P53	Homo sapiens	82-85
25464291-7	2015	Firstly, reactive oxygen species (ROS) is generated induced by MnO@SiO2 NPs, then p53 is activated followed by an increase in the bax and a decrease in the bcl-2, ultimately leading to G2/M phase arrest, increasing the activity of caspase-3 and inducing apoptosis.	Reactive Oxygen Species	34-37	P53	Homo sapiens	82-85
25131770-11	2015	Metformin, an AMPK activator, more strongly suppressed cell growth in p53-mutant cell lines with inactive SIRT1 than in p53-mutant cell lines with active SIRT1.	Metformin	0-9	P53	Homo sapiens	70-73
25131770-11	2015	Metformin, an AMPK activator, more strongly suppressed cell growth in p53-mutant cell lines with inactive SIRT1 than in p53-mutant cell lines with active SIRT1.	Metformin	0-9	P53	Homo sapiens	120-123
25131770-13	2015	Metformin could be a therapeutic drug for HCC in patients with mutated p53, inactivated SIRT1, and AMPK expression.	Metformin	0-9	P53	Homo sapiens	71-74
25252686-4	2015	In this study, we show that virus-mediated ROS upregulation activates the protein kinase, ataxia telangiectasia mutated, which in turn phosphorylates serine 15 on p53.	Serine	150-156	P53	Homo sapiens	163-166
25252686-6	2015	Rather p53 appears to be involved in suppressing intracellular ROS levels in astrocytes under oxidative stress.	Reactive Oxygen Species	63-66	P53	Homo sapiens	7-10
25252686-7	2015	The activated p53 appears to delay retroviral gene expression by suppressing NADPH oxidase, a superoxide-producing enzyme.	Superoxides	94-104	P53	Homo sapiens	14-17
25262359-11	2015	Curcumin treatment also altered the expressions of apoptosis associated proteins NF-kappaB, p38 and p53.	Curcumin	0-8	P53	Homo sapiens	100-103
25143433-4	2015	Cisplatin treatment elicited apoptosis, ATM phosphorylation, upregulation of p53, Noxa (PMAIP1), and PUMA (BBC3), and cleavage of caspase-9, -7, fodrin, and PARP-1 in MCF-7 cells.	Cisplatin	0-9	P53	Homo sapiens	77-80
24975171-3	2015	Accumulation of Cu causes necrosis that looks to be facilitated by DNA damage, followed by activation of P53.	Copper	16-18	P53	Homo sapiens	105-108
25502079-3	2015	A common polymorphism of the p53 codon 72 in exon 4 with two alleles encoding arginine or proline is known at this locus.	Arginine	78-86	P53	Homo sapiens	29-32
25143433-5	2015	Inducible DeltaNErbB2 expression strongly reduced cisplatin-induced ATM- and p53-phosphorylation, augmented Noxa upregulation and caspase-9 and -7 cleavage, doubled p21(WAF1/Cip1) (CDKN1A) expression, and nearly abolished Bcl-2 expression.	Cisplatin	50-59	P53	Homo sapiens	77-80
25348361-9	2015	In conclusion, DNA-PKcs suppression had complementary effects in combination with CDDP and 5-Fu treatment in HepG2 cells, which was associated with suppression of NF-kappaB signaling pathway cascade, activation of caspase-3 and p53, as well as down-regulation of Bcl-2 and GSH.	Cisplatin	82-86	P53	Homo sapiens	228-231
25333296-2	2015	In the present study, the antiproliferative effects of IS on A375 human melanoma cells were examined in vitro and a possible mechanism through the ROS-p38-p53 pathway is discussed.	Reactive Oxygen Species	147-150	P53	Homo sapiens	155-158
25333296-8	2015	Crucially, it was confirmed that these effects were mediated at least in part by activating the ROS-p38-p53 pathway.	Reactive Oxygen Species	96-99	P53	Homo sapiens	104-107
25348361-9	2015	In conclusion, DNA-PKcs suppression had complementary effects in combination with CDDP and 5-Fu treatment in HepG2 cells, which was associated with suppression of NF-kappaB signaling pathway cascade, activation of caspase-3 and p53, as well as down-regulation of Bcl-2 and GSH.	Fluorouracil	91-95	P53	Homo sapiens	228-231
25815376-1	2015	SIRT1 regulates p53 transcriptional activation in response to genotoxic insult by deacetylating key lysine residues.	Lysine	100-106	P53	Homo sapiens	16-19
25384972-6	2015	The blockade of basal (adenosine-free) signaling from A2a inhibits protein kinase A (PKA) activity, thereby recruiting cytosolic p53, which opens the mitochondrial permeability transition pore and impairs mitochondrial respiration, resulting in apoptosis.	Adenosine	23-32	P53	Homo sapiens	129-132
25738310-12	2015	Sorafenib suppressed p53 expression at both mRNA and protein levels, which might contribute to cell cycle arrest and sensitize tumor cells to irinotecan.	Irinotecan	142-152	P53	Homo sapiens	21-24
25164962-4	2015	Sequential treatment of Taxol or cisplatin, followed by MK-2206, induced a synergistic inhibition of cell proliferation and effectively promoted cell death, either by inhibiting the phosphorylation of Akt and its downstream effectors 4E-BP1 and p70S6K in SKOV3 cells or by restoring p53 levels, which were downregulated after Taxol or cisplatin treatment, in ES2 cells.	Paclitaxel	24-29	P53	Homo sapiens	283-286
25164962-4	2015	Sequential treatment of Taxol or cisplatin, followed by MK-2206, induced a synergistic inhibition of cell proliferation and effectively promoted cell death, either by inhibiting the phosphorylation of Akt and its downstream effectors 4E-BP1 and p70S6K in SKOV3 cells or by restoring p53 levels, which were downregulated after Taxol or cisplatin treatment, in ES2 cells.	Cisplatin	33-42	P53	Homo sapiens	283-286
24986024-7	2015	The less effectiveness could be due to the induction of ROS and p53 by UVB because removing ROS by L-NAC (10 mm) in p53 null cells could lead to alternative splicing of hdm2 upon UVB irradiation.	ros	56-59	P53	Homo sapiens	116-119
25436001-10	2015	The PDCD5 transfected cells showed higher sensitivity to cisplatin treatment than the HepG2-Neo cells, with a higher p53 protein expression level.	Cisplatin	57-66	P53	Homo sapiens	117-120
26180584-6	2015	This decrease seemed to be the main signal responsible for maintaining the intracellular redox homeostasis hindering the activation of p53 induced by ROS, p38MAPK, and PKCdelta.	ros	150-153	P53	Homo sapiens	135-138
25289524-8	2015	Parthenolide-treated cells showed up-regulation of p53, Bax, caspase-3, -6, and -3 genes and down-regulation of Bcl-2 gene (p &lt;= 0.008).	parthenolide	0-12	P53	Homo sapiens	51-54
25833236-2	2015	The present study investigated the anticancer effect of irinotecan on p53-negative Caco-2 and p53-positive CW2 human colorectal cancer cell lines.	Irinotecan	56-66	P53	Homo sapiens	70-73
24986024-7	2015	The less effectiveness could be due to the induction of ROS and p53 by UVB because removing ROS by L-NAC (10 mm) in p53 null cells could lead to alternative splicing of hdm2 upon UVB irradiation.	ros	92-95	P53	Homo sapiens	64-67
24986024-7	2015	The less effectiveness could be due to the induction of ROS and p53 by UVB because removing ROS by L-NAC (10 mm) in p53 null cells could lead to alternative splicing of hdm2 upon UVB irradiation.	ros	92-95	P53	Homo sapiens	116-119
26123305-5	2015	In heart, RGS6-dependent reactive oxygen species (ROS) production promotes doxorubicin (Dox)-induced cardiomyopathy, while in cancer cells RGS6/ROS signaling is necessary for activation of the ataxia telangiectasia mutated/p53/apoptosis pathway required for the chemotherapeutic efficacy of Dox.	Reactive Oxygen Species	144-147	P53	Homo sapiens	223-226
27012093-1	2015	Human endometrium-derived mesenchymal stem cells (hMESC) under the sublethal oxidative stress induced by H2O2 activate both p53/p21/Rb and p38MAPK/MAPKAPK-2 pathways that are responsible for the induction of hMESC premature senescence (Borodkina et al., 2014).	Hydrogen Peroxide	105-109	P53	Homo sapiens	124-127
26021170-3	2015	We compared the effect of the NaBu treatment on the human cell line with different TP53 mutation profile, including: wild-type TP53, single nucleotide substitutions, and the complete absence of TP53 gene.	sethoxydim	30-34	P53	Homo sapiens	83-87
26021170-3	2015	We compared the effect of the NaBu treatment on the human cell line with different TP53 mutation profile, including: wild-type TP53, single nucleotide substitutions, and the complete absence of TP53 gene.	sethoxydim	30-34	P53	Homo sapiens	127-131
26021170-3	2015	We compared the effect of the NaBu treatment on the human cell line with different TP53 mutation profile, including: wild-type TP53, single nucleotide substitutions, and the complete absence of TP53 gene.	sethoxydim	30-34	P53	Homo sapiens	127-131
26021170-4	2015	NaBu activated the TP53 protein via hyper acetylation at lysine residue K382, without significant changes in the level of protein expression.	sethoxydim	0-4	P53	Homo sapiens	19-23
26021170-4	2015	NaBu activated the TP53 protein via hyper acetylation at lysine residue K382, without significant changes in the level of protein expression.	Lysine	57-63	P53	Homo sapiens	19-23
26021170-5	2015	Western blotting demonstrated that the addition of NaBu triggers a significant increase in the p21/Waf1 protein level in both the TP53 wild-type cells and in the cells with single nucleotide substitutions in the domain responsible for the binding of TP53 protein to DNA.	sethoxydim	51-55	P53	Homo sapiens	130-134
26021170-5	2015	Western blotting demonstrated that the addition of NaBu triggers a significant increase in the p21/Waf1 protein level in both the TP53 wild-type cells and in the cells with single nucleotide substitutions in the domain responsible for the binding of TP53 protein to DNA.	sethoxydim	51-55	P53	Homo sapiens	250-254
26021170-8	2015	Overall, our results suggest that the NaBu-dependent induction of p21/Waf1 does require the presence of TP53 protein but unexpectedly it can occur regardless of mutational changes in the domain responsible for the TP53 binding to DNA.	sethoxydim	38-42	P53	Homo sapiens	104-108
26021170-8	2015	Overall, our results suggest that the NaBu-dependent induction of p21/Waf1 does require the presence of TP53 protein but unexpectedly it can occur regardless of mutational changes in the domain responsible for the TP53 binding to DNA.	sethoxydim	38-42	P53	Homo sapiens	214-218
26349243-3	2015	It has been suggested that DOX induces death of cancer cells via p53-dependent apoptosis, however, the information regarding the role of p73 protein, a member of p53 tumor suppressor family, is scanty.	Doxorubicin	27-30	P53	Homo sapiens	65-68
25436977-6	2014	Resveratrol-induced gene expression, including transcription of the most up-regulated genes and pro-apoptotic p53-dependent genes, was not affected by culture pH changes.	Resveratrol	0-11	P53	Homo sapiens	110-113
26021170-9	2015	One of the hypothetical explanations is that NaBu increases the level of TP53 acetylation, and the modified protein is able to establish a new network of protein-protein interactions or trigger some conformational changes affecting the TP53-dependent transcriptional machinery even when its DNA binding ability is impaired.	sethoxydim	45-49	P53	Homo sapiens	73-77
26021170-9	2015	One of the hypothetical explanations is that NaBu increases the level of TP53 acetylation, and the modified protein is able to establish a new network of protein-protein interactions or trigger some conformational changes affecting the TP53-dependent transcriptional machinery even when its DNA binding ability is impaired.	sethoxydim	45-49	P53	Homo sapiens	236-240
25179905-5	2014	Following 2-MeO-E2 treatment, only HCT116 (p53(+/+)) cells exhibited an enhancement in the levels of p53, p-p53 (Ser-15), p21(WAF1/CIP1), and Bax; however, the Bak level remained relatively constant in both cell types, and the Bcl-2 level decreased only in HCT116 (p53(+/+)) cells.	Serine	113-116	P53	Homo sapiens	43-46
25521755-7	2014	Rg3 also decreased the expression of HDAC3 and increased the acetylation of p53 on lysine (k373/k382).	Lysine	83-89	P53	Homo sapiens	76-79
25526208-6	2014	The p53 codon 72 Pro/Pro genotype was associated with a longer median PFS time of 30.3 months compared with 18.2 months for patients with Arg/Arg variants.	Arginine	138-141	P53	Homo sapiens	4-7
25526208-6	2014	The p53 codon 72 Pro/Pro genotype was associated with a longer median PFS time of 30.3 months compared with 18.2 months for patients with Arg/Arg variants.	Arginine	142-145	P53	Homo sapiens	4-7
25526208-7	2014	Moreover, the p53 codon 72 Pro/ Pro genotype was associated with a longer median OS time of 31.6 months compared with 25.8 months for those with Arg/Arg variants; the P value was marginally significant.	Arginine	145-148	P53	Homo sapiens	14-17
25526208-7	2014	Moreover, the p53 codon 72 Pro/ Pro genotype was associated with a longer median OS time of 31.6 months compared with 25.8 months for those with Arg/Arg variants; the P value was marginally significant.	Arginine	149-152	P53	Homo sapiens	14-17
25531293-0	2014	Carbon-ion beam irradiation kills X-ray-resistant p53-null cancer cells by inducing mitotic catastrophe.	Carbon	0-6	P53	Homo sapiens	50-53
25531293-1	2014	BACKGROUND AND PURPOSE: To understand the mechanisms involved in the strong killing effect of carbon-ion beam irradiation on cancer cells with TP53 tumor suppressor gene deficiencies.	Carbon	94-100	P53	Homo sapiens	143-147
25531293-4	2014	X-ray and carbon-ion beam irradiations predominantly induced apoptosis of the p53+/+ cells but not the p53-/- cells.	Carbon	10-16	P53	Homo sapiens	78-81
25531293-5	2014	In the p53-/- cells, carbon-ion beam irradiation, but not X-ray irradiation, markedly induced mitotic catastrophe that was associated with premature mitotic entry with harboring long-retained DSBs at 24 h post-irradiation.	Carbon	21-27	P53	Homo sapiens	7-10
25531293-6	2014	CONCLUSIONS: Efficient induction of mitotic catastrophe in apoptosis-resistant p53-deficient cells implies a strong cancer cell-killing effect of carbon-ion beam irradiation that is independent of the p53 status, suggesting its biological advantage over X-ray treatment.	Carbon	146-152	P53	Homo sapiens	79-82
25565771-11	2015	CONCLUSION: As4S4 is a potent cytotoxic agent for gastric cancer cells, as it induced apoptosis both in vitro and in vivo through a p53-dependent pathway.	as4s4	12-17	P53	Homo sapiens	132-135
25449279-8	2014	In conclusion, we report for the first time that COH-203, one compound in the combretastatin family, promotes anti-proliferative activity through the induction of p-53 dependent senescence.	combretastatin	78-92	P53	Homo sapiens	163-167
25466181-6	2014	Here we showed that combination treatment with PPM1D-specific inhibitor SPI-001 and doxorubicin suppressed cell viability of HCT-116 cells overexpressing C-terminal truncated PPM1D through p53 activation compared with doxorubicin alone.	Doxorubicin	84-95	P53	Homo sapiens	189-192
25401416-7	2014	Transcriptome data were confirmed for 12 of 15 selected genes and seven (PLK3, LAMP3, ETV7, UNC5B, NTN1, DUSP5, SNAI1) were synergistically up-regulated after Doxo+TNFalpha and dependent both on p53 and NFkappaB.	Doxorubicin	159-163	P53	Homo sapiens	195-198
25401416-6	2014	A panel of genes was examined by qPCR coupled to p53 activation by Doxo, 5-Fluoruracil and Nutlin-3a, or to p53 or NFkappaB inhibition.	Doxorubicin	67-71	P53	Homo sapiens	49-52
25401416-6	2014	A panel of genes was examined by qPCR coupled to p53 activation by Doxo, 5-Fluoruracil and Nutlin-3a, or to p53 or NFkappaB inhibition.	Fluorouracil	73-86	P53	Homo sapiens	49-52
25495224-3	2014	RESULTS: The effect of IL-1beta, but not of TNF-alpha, on glutamate-mediated excitatory postsynaptic currents was blocked by pifithrin-alpha (PFT), inhibitor of p53.	Glutamic Acid	58-67	P53	Homo sapiens	161-164
25516654-6	2014	RESULTS: Lobaplatin inhibited the proliferation of human gastric cancer cells and induced apoptosis, which may be associated with the up-regulation of Bax expression, poly(ADP-ribose) polymerase (PARP) cleavage, p53 expression and the reduction of Bcl-2 expression.	lobaplatin	9-19	P53	Homo sapiens	212-215
25482151-1	2014	BACKGROUND: PA28gamma (also known as Ki, REG gamma, PMSE3), a member of the ubiquitin-and ATP-independent proteasome activator family 11S, has been proved to show proteasome-dependent and -independent effects on several proteins including tumor suppressor p53, cyclin-dependent kinase inhibitor p21 and steroid receptor co-activator 3 (SCR-3).	Adenosine Triphosphate	90-93	P53	Homo sapiens	256-259
25087850-9	2014	Excess ROS amplified apoptotic signals by activating many downstream pathways such as p53 and MAPK pathways to promote cell apoptosis.	ros	7-10	P53	Homo sapiens	86-89
25064493-0	2014	Indoleamine 2,3-dioxygenase increases p53 levels in alloreactive human T cells, and both indoleamine 2,3-dioxygenase and p53 suppress glucose uptake, glycolysis and proliferation.	Glucose	134-141	P53	Homo sapiens	121-124
24994538-5	2014	A poorer response to purine nucleoside analogues (PNAs) is observed in patients with more marked leukocytosis, bulky splenomegaly, an unmutated immunoglobulin variable heavy chain (IgVH) gene profile, use of VH4-34 or with TP53 mutations.	Purine Nucleosides	21-38	P53	Homo sapiens	223-227
25220870-0	2014	Promotion of p53 expression and reactive oxidative stress production is involved in zerumbone-induced cisplatin sensitization of non-small cell lung cancer cells.	Cisplatin	102-111	P53	Homo sapiens	13-16
25311616-6	2014	Under these same conditions, we also found that resveratrol altered the phosphorylation of several proteins involved in various biological processes, most notably transcriptional modulators, represented by p53, FOXA1, and AATF.	Resveratrol	48-59	P53	Homo sapiens	206-209
24313628-4	2014	We observed that p53 protein residue at Ser 15 was phosphorylated after cryopreservation.	Serine	40-43	P53	Homo sapiens	17-20
25220870-13	2014	Combinational treatment with zerumbone and cisplatin significantly accelerated apoptosis and promoted p53 expression and ROS production in NSCLC cells, compared with each alone.	Cisplatin	43-52	P53	Homo sapiens	102-105
25216733-9	2014	In a dose-dependent manner copper also provoked transcriptional changes of genes involved in intracellular signaling and induction of apoptosis (p53, c-fos, Bcl-2 and Bax).	Copper	27-33	P53	Homo sapiens	145-148
25344835-5	2014	We have identified an acridine derivative (PubChem CID-765471) previously known for its capacity to activate p53 independently of DNA damage, although the molecular mechanism underlying p53 activation had remained uncharacterized.	Acridines	22-30	P53	Homo sapiens	109-112
25344835-5	2014	We have identified an acridine derivative (PubChem CID-765471) previously known for its capacity to activate p53 independently of DNA damage, although the molecular mechanism underlying p53 activation had remained uncharacterized.	Acridines	22-30	P53	Homo sapiens	186-189
24115240-1	2014	BACKGROUND: The TP53 single nucleotide polymorphism (SNP) rs1042522 encodes arginine (Arg) or proline (Pro).	Arginine	76-84	P53	Homo sapiens	16-20
24115240-1	2014	BACKGROUND: The TP53 single nucleotide polymorphism (SNP) rs1042522 encodes arginine (Arg) or proline (Pro).	Arginine	86-89	P53	Homo sapiens	16-20
25302047-2	2014	Evidence showed that tumor suppressor p53 plays an important role in regulating the generation of cellular ROS, either by reducing oxidative stress under physiological and mildly stressed conditions, or by promoting oxidative stress under highly stressed conditions.	Reactive Oxygen Species	107-110	P53	Homo sapiens	38-41
25302047-6	2014	Depletion of p53-regulated antioxidant gene SESN1 by RNA interference also resulted in an elevation of MN-gamma-H2AX (+).	gamma-h2ax	106-116	P53	Homo sapiens	13-16
25269486-3	2014	Resveratrol inhibited proliferation and induced apoptosis in HepG2 cells via activation of caspase-9 and caspase-3, upregulation of the Bax/Bcl-2 ratio and induction of p53 expression.	Resveratrol	0-11	P53	Homo sapiens	169-172
25426548-0	2014	Targeting of mutant p53-induced FoxM1 with thiostrepton induces cytotoxicity and enhances carboplatin sensitivity in cancer cells.	Thiostrepton	43-55	P53	Homo sapiens	20-23
25244701-4	2014	Using the intrinsically disordered N-terminal region of the p53 protein as an experimental model, a set of proline (PRO) and alanine (ALA) to glycine (GLY) substitution variants were designed to modulate backbone conformational propensities without introducing non-native intramolecular interactions.	Alanine	125-132	P53	Homo sapiens	60-63
25244701-4	2014	Using the intrinsically disordered N-terminal region of the p53 protein as an experimental model, a set of proline (PRO) and alanine (ALA) to glycine (GLY) substitution variants were designed to modulate backbone conformational propensities without introducing non-native intramolecular interactions.	Glycine	142-149	P53	Homo sapiens	60-63
25244701-4	2014	Using the intrinsically disordered N-terminal region of the p53 protein as an experimental model, a set of proline (PRO) and alanine (ALA) to glycine (GLY) substitution variants were designed to modulate backbone conformational propensities without introducing non-native intramolecular interactions.	Glycine	151-154	P53	Homo sapiens	60-63
25474278-9	2014	The post-progression survival (PPS) of p53-positive patients undergoing 2nd and/or 3rd line chemotherapy with irinotecan and/or cetuximab was significantly longer compared to p53-negative patients.	Irinotecan	110-120	P53	Homo sapiens	39-42
25474278-11	2014	mCRC patients with p53 overexpression undergoing an irinotecan containing second- or third-line chemotherapy after oxaliplatin failure have a significantly longer post-progression survival compared to patients without p53 overexpression.	Irinotecan	52-62	P53	Homo sapiens	19-22
25474278-12	2014	To validate the clinical impact of p53 in patients with mCRC treated with irinotecan- and/or cetuximab further studies are needed.	Irinotecan	74-84	P53	Homo sapiens	35-38
25448679-5	2014	Finally, HEPN1 overexpression increases the expression of p53, p21, and Bax, all of which are ROS-upregulated proteins.	Reactive Oxygen Species	94-97	P53	Homo sapiens	58-61
25623760-8	2014	RESULTS: The MTT assay showed a stronger inhibitory effect of gefitinib on MDA-MB-468 cells infected with Ad-p53 than on the control cells.	Gefitinib	62-71	P53	Homo sapiens	109-112
25623760-16	2014	CONCLUSIONS: Wild-type p53 may reverse the sensitivity of MDA-MB-468 cells to gefitinib through down-regulation of the PI3K/Akt pathway.	Gefitinib	78-87	P53	Homo sapiens	23-26
25623760-1	2014	OBJECTIVE: To observe the impact of concurrent administration of recombinant human p53 adenovirus (Ad-p53) with EGFR inhibitor gefitinib on breast cancer MDA-MB-468 cells.	Gefitinib	127-136	P53	Homo sapiens	83-86
25623760-1	2014	OBJECTIVE: To observe the impact of concurrent administration of recombinant human p53 adenovirus (Ad-p53) with EGFR inhibitor gefitinib on breast cancer MDA-MB-468 cells.	Gefitinib	127-136	P53	Homo sapiens	102-105
25451271-5	2014	We found that treatment with thapsigargin, a stimulator of p53 expression and an inducer of ER stress, decreased Pin1 expression in HCT116 cells.	Thapsigargin	29-41	P53	Homo sapiens	59-62
25429397-5	2014	Accordingly, more mucous cells are present in primary human airway cultures with p53(Arg) compared with p53(Pro).	Arginine	85-88	P53	Homo sapiens	81-84
25429619-0	2014	ROS inhibit autophagy by downregulating ULK1 mediated by the phosphorylation of p53 in selenite-treated NB4 cells.	Reactive Oxygen Species	0-3	P53	Homo sapiens	80-83
25469035-10	2014	Our results showed that treatment with 17beta-estradiol and/or ER agonists in human LoVo colorectal cancer cells activated p53 and then up-regulated p21 and p27 protein levels, subsequently inhibiting the downstream target gene, cyclin D1, which regulates cell proliferation.	Estradiol	39-55	P53	Homo sapiens	123-126
25469035-12	2014	These results demonstrate that 17beta-estradiol and/or ER agonists downregulate migration-related proteins through the p53 signaling pathway in human LoVo colorectal cancer cells.	Estradiol	31-47	P53	Homo sapiens	119-122
25469035-13	2014	These findings suggest that p53 plays a critical role in the 17beta-estradiol and/or ER agonist-mediated protective activity against colorectal cancer progression.	Estradiol	61-77	P53	Homo sapiens	28-31
25429619-6	2014	Collectively, our results show that ROS inhibited autophagy by downregulating the p70S6K/p53/ULK1 axis in selenite-treated NB4 cells.	Reactive Oxygen Species	36-39	P53	Homo sapiens	89-92
25071015-9	2014	In the early setting, data suggested longer disease free survival in p53 negative patients in the lowest glucose category (p=0.053).	Glucose	105-112	P53	Homo sapiens	69-72
25279998-9	2014	Evaluation of the mutagenicity of anti-B[a]P-diol epoxide with B[a]P-7,8-dione on p53 showed that the o-quinone produced by AKRs was the more potent mutagen, provided that it was permitted to redox cycle, and that the mutations observed were G to T transversions, reminiscent of those observed in human lung cancer.	diol epoxide	45-57	P53	Homo sapiens	82-85
25622680-12	2014	Cisplatin up-regulated p53, Mdm2 and p21 in both cell lines.	Cisplatin	0-9	P53	Homo sapiens	23-26
25622680-17	2014	CONCLUSION: p14ARF enhances the chemosensitivity to cisplatin in human osteosarcoma U2OS cells through p53 apoptotic pathway.	Cisplatin	52-61	P53	Homo sapiens	103-106
25411964-8	2014	FOXM1 knockdown significantly inhibited migration and invasion of ovarian cancer cells and enhanced paclitaxel-mediated cell death and mitotic catastrophe in a p53-independent manner.	Paclitaxel	100-110	P53	Homo sapiens	160-163
25071015-0	2014	p53 status as effect modifier of the association between pre-treatment fasting glucose and breast cancer outcomes in non diabetic, HER2 positive patients treated with trastuzumab.	Glucose	79-86	P53	Homo sapiens	0-3
25367122-12	2014	We also found that both wtgal-7 and R74S inhibited dox-induced PARP-1 cleavage and p53 protein expression.	Doxorubicin	51-54	P53	Homo sapiens	83-86
25369051-9	2014	Crucially, administration of N-acetylcysteine, a ROS scavenger, abrogated the effect of PA-2 on p53 acetylation and mitochondria translocation, thus identifying RONS as proximal molecules mediating the anticancer effect of PA-2.	Acetylcysteine	29-45	P53	Homo sapiens	96-99
25217696-5	2014	Normal hematopoietic cells showed elevated ROS levels through increased intracellular iron levels when treated with lipocalin-2, which led to p53 pathway activation, increased apoptosis, and decreased cellular proliferation.	Reactive Oxygen Species	43-46	P53	Homo sapiens	142-145
25217696-5	2014	Normal hematopoietic cells showed elevated ROS levels through increased intracellular iron levels when treated with lipocalin-2, which led to p53 pathway activation, increased apoptosis, and decreased cellular proliferation.	Iron	86-90	P53	Homo sapiens	142-145
24896104-9	2014	miR-125a-5p inhibited the expression of tumour protein 53 (TP53), and curcumin treatment up-regulated the expression of TP53.	Curcumin	70-78	P53	Homo sapiens	120-124
25014164-4	2014	Here we show that the histone 3 lysine 4- and lysine 36-specific methyltransferase Smyd2 acts as an endogenous antagonistic player of p53-dependent cardiomyocyte apoptosis.	Lysine	32-38	P53	Homo sapiens	134-137
25014164-4	2014	Here we show that the histone 3 lysine 4- and lysine 36-specific methyltransferase Smyd2 acts as an endogenous antagonistic player of p53-dependent cardiomyocyte apoptosis.	Lysine	46-52	P53	Homo sapiens	134-137
25193633-5	2014	In this study, we showed that the depletion of p53 proteins by digoxin involved not only inhibition of protein synthesis but also inhibition at the post-transcriptional level.	Digoxin	63-70	P53	Homo sapiens	47-50
25193633-7	2014	Digoxin also modulated G2/M arrest, DNA damage and apoptosis through the p53-dependent pathway in HeLa cells.	Digoxin	0-7	P53	Homo sapiens	73-76
24845152-6	2014	These results suggest that psoralen induces apoptosis in cancer cells via mechanisms that involve caspase-3, p53, Bax, and Bcl-2 pathway.	Ficusin	27-35	P53	Homo sapiens	109-112
24749765-8	2014	H2O2 increased the expression of BAX, BAD, p53 and caspase-3 in a time-dependent manner, those of which anthocyanin significantly decreased.	Hydrogen Peroxide	0-4	P53	Homo sapiens	43-46
27308524-0	2016	The heme-p53 interaction: Linking iron metabolism to p53 signaling and tumorigenesis.	Iron	34-38	P53	Homo sapiens	9-12
27308524-0	2016	The heme-p53 interaction: Linking iron metabolism to p53 signaling and tumorigenesis.	Iron	34-38	P53	Homo sapiens	53-56
25135223-8	2014	Excessive ROS triggered DNA damage and activated downstream signaling pathways, including the phosphorylation of p53 and p38MAPK, and down-regulation of phosphorylated AKT and ERK, finally resulted in increase of radiosensitivity and inhibition of tumor reproduction.	ros	10-13	P53	Homo sapiens	113-116
24896104-10	2014	Taken together, these results indicate that curcumin exerted inhibitory effects on NPC by inhibiting the expression of miR-125a-5p and, subsequently, enhancing the expression of TP53.	Curcumin	44-52	P53	Homo sapiens	178-182
25014355-6	2014	Testosterone treatment caused up-regulation of proapoptotic genes Bax (Bcl-2-associated X protein), p53 (tumor protein p53), and JNK (c-Jun N-terminal kinases) in both cell lines and increased expression of Bax, Caspase 3, and cytochrome C proteins.	Testosterone	0-12	P53	Homo sapiens	100-103
25014355-7	2014	Treatment with a zinc chelator or a MAPK inhibitor blocked testosterone-induced increases in Bax, p53, and JNK mRNA expression.	Testosterone	59-71	P53	Homo sapiens	98-101
25014355-6	2014	Testosterone treatment caused up-regulation of proapoptotic genes Bax (Bcl-2-associated X protein), p53 (tumor protein p53), and JNK (c-Jun N-terminal kinases) in both cell lines and increased expression of Bax, Caspase 3, and cytochrome C proteins.	Testosterone	0-12	P53	Homo sapiens	119-122
25412667-8	2014	Pretreatment with TJ-10 inhibited H2O2-induced up-regulation of p53 and enhanced AMPKalpha1 expression.	Hydrogen Peroxide	34-38	P53	Homo sapiens	64-67
25158131-0	2014	p53 directly regulates the transcription of the human frataxin gene and its lack of regulation in tumor cells decreases the utilization of mitochondrial iron.	Iron	153-157	P53	Homo sapiens	0-3
25208472-9	2014	The Beclin-1-p53 interaction was also disrupted by exposure to cisplatin-induced stress resulting in higher level of Beclin-1 because of lesser ubiquitination.	Cisplatin	63-72	P53	Homo sapiens	13-16
25316267-4	2014	There were significant differences in the frequency of TP53 and MDM2 genotypes in EC patients-increased EC occurrence was observed with the presence of MDM2 G/G and TP53 Arg/Arg genotypes, while allele Pro of TP53 decreased cancer risk.	Arginine	170-173	P53	Homo sapiens	55-59
25135238-7	2014	The TP53 genotype was assessed from paraffin-embedded diagnostic tumor biopsies using a standardized gene-specific TP53 sequencing protocol (mark53 kit; mark53 Ltd, Vienna, Austria).	Paraffin	36-44	P53	Homo sapiens	4-8
25135238-13	2014	CONCLUSIONS: The biomarker TP53 divides esophageal cancer patients into 2 categories with markedly different outcomes: patients with a normal TP53 marker status may experience notable benefits from neoadjuvant chemotherapy with cisplatin/fluorouracil, whereas those with a mutant TP53 marker status appear to be at risk for lack of response.	Cisplatin	228-237	P53	Homo sapiens	27-31
25135238-13	2014	CONCLUSIONS: The biomarker TP53 divides esophageal cancer patients into 2 categories with markedly different outcomes: patients with a normal TP53 marker status may experience notable benefits from neoadjuvant chemotherapy with cisplatin/fluorouracil, whereas those with a mutant TP53 marker status appear to be at risk for lack of response.	Fluorouracil	238-250	P53	Homo sapiens	27-31
25172633-10	2014	Between 2 and 4 h following curcumin treatment, p53 levels increased with maximum levels reached by 8 h. Thus, curcumin homing to the nucleolus induces redistribution of p14(ARF) to the nucleoplasm where interaction with MDM2 leads to stabilization of p53, with subsequent initiation of apoptosis.	Curcumin	28-36	P53	Homo sapiens	48-51
25172633-10	2014	Between 2 and 4 h following curcumin treatment, p53 levels increased with maximum levels reached by 8 h. Thus, curcumin homing to the nucleolus induces redistribution of p14(ARF) to the nucleoplasm where interaction with MDM2 leads to stabilization of p53, with subsequent initiation of apoptosis.	Curcumin	28-36	P53	Homo sapiens	252-255
25172633-10	2014	Between 2 and 4 h following curcumin treatment, p53 levels increased with maximum levels reached by 8 h. Thus, curcumin homing to the nucleolus induces redistribution of p14(ARF) to the nucleoplasm where interaction with MDM2 leads to stabilization of p53, with subsequent initiation of apoptosis.	Curcumin	111-119	P53	Homo sapiens	48-51
25172633-10	2014	Between 2 and 4 h following curcumin treatment, p53 levels increased with maximum levels reached by 8 h. Thus, curcumin homing to the nucleolus induces redistribution of p14(ARF) to the nucleoplasm where interaction with MDM2 leads to stabilization of p53, with subsequent initiation of apoptosis.	Curcumin	111-119	P53	Homo sapiens	252-255
25316267-4	2014	There were significant differences in the frequency of TP53 and MDM2 genotypes in EC patients-increased EC occurrence was observed with the presence of MDM2 G/G and TP53 Arg/Arg genotypes, while allele Pro of TP53 decreased cancer risk.	Arginine	170-173	P53	Homo sapiens	165-169
25316267-4	2014	There were significant differences in the frequency of TP53 and MDM2 genotypes in EC patients-increased EC occurrence was observed with the presence of MDM2 G/G and TP53 Arg/Arg genotypes, while allele Pro of TP53 decreased cancer risk.	Arginine	170-173	P53	Homo sapiens	165-169
25316267-4	2014	There were significant differences in the frequency of TP53 and MDM2 genotypes in EC patients-increased EC occurrence was observed with the presence of MDM2 G/G and TP53 Arg/Arg genotypes, while allele Pro of TP53 decreased cancer risk.	Arginine	174-177	P53	Homo sapiens	55-59
25316267-4	2014	There were significant differences in the frequency of TP53 and MDM2 genotypes in EC patients-increased EC occurrence was observed with the presence of MDM2 G/G and TP53 Arg/Arg genotypes, while allele Pro of TP53 decreased cancer risk.	Arginine	174-177	P53	Homo sapiens	165-169
25316267-4	2014	There were significant differences in the frequency of TP53 and MDM2 genotypes in EC patients-increased EC occurrence was observed with the presence of MDM2 G/G and TP53 Arg/Arg genotypes, while allele Pro of TP53 decreased cancer risk.	Arginine	174-177	P53	Homo sapiens	165-169
25316267-5	2014	Analysis of combined MDM2/TP53 polymorphisms revealed that T/T-Pro/Arg genotype decreased EC risk, whereas G/G-Arg/Arg genotype increased it.	Arginine	67-70	P53	Homo sapiens	26-30
25316267-6	2014	Association of these genetic polymorphisms with histological grading showed increased MDM2 G/G homozygote and TP53 Arg/Arg homozygote frequencies in grading 2 as well as allele G overrepresentation in G1 and G3 EC patients.	Arginine	115-118	P53	Homo sapiens	110-114
25316267-6	2014	Association of these genetic polymorphisms with histological grading showed increased MDM2 G/G homozygote and TP53 Arg/Arg homozygote frequencies in grading 2 as well as allele G overrepresentation in G1 and G3 EC patients.	Arginine	119-122	P53	Homo sapiens	110-114
25316267-7	2014	Finally, with clinical FIGO staging under evaluation, an increase in MDM2 G/G and TP53 Arg/Arg homozygote frequencies in staging I and TP53 Arg/Arg homozygote frequencies in staging II were observed.	Arginine	87-90	P53	Homo sapiens	82-86
25316267-7	2014	Finally, with clinical FIGO staging under evaluation, an increase in MDM2 G/G and TP53 Arg/Arg homozygote frequencies in staging I and TP53 Arg/Arg homozygote frequencies in staging II were observed.	Arginine	91-94	P53	Homo sapiens	82-86
25316267-7	2014	Finally, with clinical FIGO staging under evaluation, an increase in MDM2 G/G and TP53 Arg/Arg homozygote frequencies in staging I and TP53 Arg/Arg homozygote frequencies in staging II were observed.	Arginine	91-94	P53	Homo sapiens	82-86
25316267-7	2014	Finally, with clinical FIGO staging under evaluation, an increase in MDM2 G/G and TP53 Arg/Arg homozygote frequencies in staging I and TP53 Arg/Arg homozygote frequencies in staging II were observed.	Arginine	91-94	P53	Homo sapiens	82-86
25313037-5	2014	XAF1 stimulates homeodomain-interacting protein kinase 2 (HIPK2)-mediated Ser-46 phosphorylation of p53 by blocking E3 ubiquitin ligase Siah2 interaction with and ubiquitination of HIPK2.	Serine	74-77	P53	Homo sapiens	100-103
25688502-12	2014	After irradiation with carbon ions and temozolomide, cell survival rates depended on p53 status, with a decreased survival rate in wildtype cells.	Carbon	23-29	P53	Homo sapiens	85-88
25688502-13	2014	CONCLUSIONS: Irinotecan and paclitaxel are an effective treatment for HCT 116 wt cells, whereas HCT 116 cells with p53 deficiency can be treated successfully with paclitaxel and gemcitabine.	Paclitaxel	163-173	P53	Homo sapiens	115-118
25356874-5	2014	In that sense, enhanced DNA repair, high glutathione levels and functional p53 have a critical role on cisplatin resistance.	Cisplatin	103-112	P53	Homo sapiens	75-78
25258113-9	2014	SIGNIFICANCE: This is the first study demonstrating that vanadium complexes could induce a p53 dependent apoptotic mechanism in high risk HPV16-positive cervical cancers.	Vanadium	57-65	P53	Homo sapiens	91-94
25319447-8	2014	It was also observed that the expression levels of p53 and the phospho-p53 were enhanced in the presence of additive oxygen flow compared with those from the pure helium plasma treatment.	Oxygen	117-123	P53	Homo sapiens	51-54
25350363-1	2014	2-Acetylpyridine acetylhydrazone (H2AcMe), 2-benzoylpyridine acetylhydrazone (H2BzMe) and complexes [Cu(H2AcMe)Cl2] (1) and [Cu(H2BzMe)Cl2] (2) were assayed for their cytotoxicity against wild type p53 U87 and mutant p53 T98 glioma cells, and against MRC-5 fibroblast cells.	cu(h2acme)cl2	101-114	P53	Homo sapiens	198-201
25350363-1	2014	2-Acetylpyridine acetylhydrazone (H2AcMe), 2-benzoylpyridine acetylhydrazone (H2BzMe) and complexes [Cu(H2AcMe)Cl2] (1) and [Cu(H2BzMe)Cl2] (2) were assayed for their cytotoxicity against wild type p53 U87 and mutant p53 T98 glioma cells, and against MRC-5 fibroblast cells.	cu(h2acme)cl2	101-114	P53	Homo sapiens	217-220
25350363-6	2014	The cytotoxic effect of 1 in U87 cells could be related to its ability to provoke the release of ROS, suggesting that the cytotoxicity of 1 might be somehow p53 dependent.	ros	97-100	P53	Homo sapiens	157-160
25288756-6	2014	Ras signaling selectively inactivates p53-mediated induction of p21Cip1 expression by inhibiting acetylation of specific lysine residues in the p53 DNA binding domain.	Lysine	121-127	P53	Homo sapiens	38-41
25288756-6	2014	Ras signaling selectively inactivates p53-mediated induction of p21Cip1 expression by inhibiting acetylation of specific lysine residues in the p53 DNA binding domain.	Lysine	121-127	P53	Homo sapiens	144-147
25288756-7	2014	Proliferation of cells lacking both Ras proteins and p53 can be prevented by reexpression of the human p53 ortholog, provided that it retains an active DNA binding domain and an intact lysine residue at position 164.	Lysine	185-191	P53	Homo sapiens	53-56
25288756-7	2014	Proliferation of cells lacking both Ras proteins and p53 can be prevented by reexpression of the human p53 ortholog, provided that it retains an active DNA binding domain and an intact lysine residue at position 164.	Lysine	185-191	P53	Homo sapiens	103-106
25319447-8	2014	It was also observed that the expression levels of p53 and the phospho-p53 were enhanced in the presence of additive oxygen flow compared with those from the pure helium plasma treatment.	Oxygen	117-123	P53	Homo sapiens	71-74
25219883-2	2014	Proteasome inhibitors and melatonin are both intimately involved in the regulation of major signal transduction proteins including p53, cyclin p27, transcription factor NF-kappaB, apoptotic factors Bax and Bim, caspase 3, caspase 9, anti-apoptotic factor Bcl-2, TRAIL, NRF2 and transcription factor beta-catenin.	Melatonin	26-35	P53	Homo sapiens	131-134
25294809-6	2014	The pharmacologic delivery of a metal ion to restore proper folding of a mutant protein is unique to medicinal chemistry and represents a new pathway to drug mutant p53.	Metals	32-37	P53	Homo sapiens	165-168
25305377-7	2014	ROS further led to symptoms of early apoptosis by deregulating Akt (Protein Kinase B) and activating c-Jun N-terminal Kinase (JNK), p38 Mitogen Activated Protein Kinase (MAPK), p53, and autophagy starting from ~8h of incubation.	ros	0-3	P53	Homo sapiens	177-180
25080334-10	2014	The synergistic use of AVPIR8/p53 significantly increased the sensitivity of the resistant tumor cells to the cytotoxic agent doxorubicin by inducing apoptosis, as demonstrated in the cellular studies.	Doxorubicin	126-137	P53	Homo sapiens	30-33
25080334-12	2014	Coadministration of AVPIR8/p53 enabled a full arrest of tumor growth combined with a reduced DOX dose, yielding a productive and safe cancer treatment.	Doxorubicin	93-96	P53	Homo sapiens	27-30
25275589-5	2014	The G-1 treatment increased expression of p53 and its phosphorylation levels at Serine 15, promoted its nuclear translocation, and inhibited its ubiquitylation, which mediated the growth arrest effects on cell proliferation.	Serine	80-86	P53	Homo sapiens	42-45
24930072-6	2014	Up-regulation of p38 MAPK activity in responding the ROS stabilize p53 and activate p21 transcription, the critical regulatory in G1/S checkpoint.	Reactive Oxygen Species	53-56	P53	Homo sapiens	67-70
25139326-4	2014	This process is characterized by an early generation of reactive oxygen species (ROS) resulting in p53 up-regulation.	Reactive Oxygen Species	56-79	P53	Homo sapiens	99-102
25064805-5	2014	The combination of Nano Se and irinotecan showed increased cytotoxic effect with HCT-8 tumor cells likely by p53 mediated apoptosis.	Irinotecan	31-41	P53	Homo sapiens	109-112
25139326-4	2014	This process is characterized by an early generation of reactive oxygen species (ROS) resulting in p53 up-regulation.	Reactive Oxygen Species	81-84	P53	Homo sapiens	99-102
25139326-9	2014	On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES.	Reactive Oxygen Species	56-59	P53	Homo sapiens	63-66
25139326-9	2014	On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES.	Reactive Oxygen Species	56-59	P53	Homo sapiens	111-114
25139326-9	2014	On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES.	Reactive Oxygen Species	56-59	P53	Homo sapiens	111-114
25139326-9	2014	On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES.	Reactive Oxygen Species	151-154	P53	Homo sapiens	63-66
25139326-9	2014	On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES.	Reactive Oxygen Species	151-154	P53	Homo sapiens	111-114
25139326-9	2014	On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES.	Reactive Oxygen Species	151-154	P53	Homo sapiens	111-114
24499675-6	2014	p21 and p53 siRNA consistently decreased H3TMK9 foci formation in U87M G-neo but not in U87MG-E6 cells after arsenite treatment.	g-neo	71-76	P53	Homo sapiens	8-11
25139326-9	2014	On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES.	Reactive Oxygen Species	151-154	P53	Homo sapiens	63-66
25139326-9	2014	On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES.	Reactive Oxygen Species	151-154	P53	Homo sapiens	111-114
25139326-9	2014	On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES.	Reactive Oxygen Species	151-154	P53	Homo sapiens	111-114
25139326-10	2014	In sum, p53 up-regulation by ROS triggers a positive feedback loop responsible of further increasing ROS production and reinforcing PES-driven non-necroptotic necrosis.	Reactive Oxygen Species	29-32	P53	Homo sapiens	8-11
25139326-10	2014	In sum, p53 up-regulation by ROS triggers a positive feedback loop responsible of further increasing ROS production and reinforcing PES-driven non-necroptotic necrosis.	Reactive Oxygen Species	101-104	P53	Homo sapiens	8-11
24926617-2	2014	To investigate post-transcriptional controls as an additional dimension of p53-directed gene expression responses, we performed a translatome analysis through polysomal profiling on MCF7 cells upon 16 hours of doxorubicin or nutlin-3a treatment.	Doxorubicin	210-221	P53	Homo sapiens	75-78
25082753-3	2014	The particles" surface porous morphology and distributions of doxorubicin and p53 were systematically characterized by scanning electron microscopy, flow cytometry, fluorescence microscopy and confocal laser scanning microscopy, revealing that doxorubicin and the plasmid were successfully co-encapsulated.	Doxorubicin	244-255	P53	Homo sapiens	78-81
25019212-2	2014	We evaluated the cytotoxicity of BA in two breast cancer cell lines MCF-7 and T47D differing in their p53 status.	betulinic acid	33-35	P53	Homo sapiens	102-105
25153662-8	2014	Moreover, this association was enhanced when combined with HPV-16 seropositivity and p53 Arg/Arg or Arg/Pro genotypes.	Arginine	89-92	P53	Homo sapiens	85-88
25153662-8	2014	Moreover, this association was enhanced when combined with HPV-16 seropositivity and p53 Arg/Arg or Arg/Pro genotypes.	Arginine	93-96	P53	Homo sapiens	85-88
25153662-8	2014	Moreover, this association was enhanced when combined with HPV-16 seropositivity and p53 Arg/Arg or Arg/Pro genotypes.	Arginine	93-96	P53	Homo sapiens	85-88
25070648-5	2014	Furthermore, western blot analysis revealed that curcumin induced p53 and p21(WAF1/CIP1) expression with a concomitant decrease in proliferating cell nuclear antigen protein levels (P&lt;0.05).	Curcumin	49-57	P53	Homo sapiens	66-69
25086499-3	2014	Furthermore, while p53R2, a p53-inducible peptide involved in the synthesis of dNTPs normally works toward suppression of cancer through elimination of reactive oxygen species (ROS), inhibition of MAPK/ERK pathway and providing dNTPs for DNA repair, the overexpression of p53R2 is reported to be associated with cancer progression and resistance to therapy.	Reactive Oxygen Species	177-180	P53	Homo sapiens	19-22
25086499-3	2014	Furthermore, while p53R2, a p53-inducible peptide involved in the synthesis of dNTPs normally works toward suppression of cancer through elimination of reactive oxygen species (ROS), inhibition of MAPK/ERK pathway and providing dNTPs for DNA repair, the overexpression of p53R2 is reported to be associated with cancer progression and resistance to therapy.	Reactive Oxygen Species	152-175	P53	Homo sapiens	19-22
25070648-6	2014	Curcumin effectively inhibited primary hRPE cell proliferation, which may be mediated by the p53 pathway.	Curcumin	0-8	P53	Homo sapiens	93-96
24734887-7	2014	Furthermore, NAC significantly decreased cleaved caspase 3, p53 and renal epithelial tubular cell apoptosis.	Acetylcysteine	13-16	P53	Homo sapiens	60-63
24801417-8	2014	CD147 facilitated the cell surface expression of MCT1 and lactate export, which led to activation of the PI3K/Akt/MDM2 pathway and thus increased p53 degradation.	Lactic Acid	58-65	P53	Homo sapiens	146-149
24913304-0	2014	A cisplatin-resistant head and neck cancer cell line with cytoplasmic p53(mut) exhibits ATP-binding cassette transporter upregulation and high glutathione levels.	Cisplatin	2-11	P53	Homo sapiens	70-73
24913304-0	2014	A cisplatin-resistant head and neck cancer cell line with cytoplasmic p53(mut) exhibits ATP-binding cassette transporter upregulation and high glutathione levels.	Glutathione	143-154	P53	Homo sapiens	70-73
24913304-1	2014	PURPOSE: Head and neck squamous cell carcinoma (HNSCC) cell lines with cytoplasmically sequestered mutant p53 (p53(mut_c)) are frequently more resistant to cisplatin (CDDP) than cells with mutant but nuclear p53 (p53(mut_n)).	Cisplatin	156-165	P53	Homo sapiens	106-109
24913304-1	2014	PURPOSE: Head and neck squamous cell carcinoma (HNSCC) cell lines with cytoplasmically sequestered mutant p53 (p53(mut_c)) are frequently more resistant to cisplatin (CDDP) than cells with mutant but nuclear p53 (p53(mut_n)).	Cisplatin	156-165	P53	Homo sapiens	111-114
24913304-1	2014	PURPOSE: Head and neck squamous cell carcinoma (HNSCC) cell lines with cytoplasmically sequestered mutant p53 (p53(mut_c)) are frequently more resistant to cisplatin (CDDP) than cells with mutant but nuclear p53 (p53(mut_n)).	Cisplatin	156-165	P53	Homo sapiens	111-114
24913304-1	2014	PURPOSE: Head and neck squamous cell carcinoma (HNSCC) cell lines with cytoplasmically sequestered mutant p53 (p53(mut_c)) are frequently more resistant to cisplatin (CDDP) than cells with mutant but nuclear p53 (p53(mut_n)).	Cisplatin	156-165	P53	Homo sapiens	111-114
24913304-1	2014	PURPOSE: Head and neck squamous cell carcinoma (HNSCC) cell lines with cytoplasmically sequestered mutant p53 (p53(mut_c)) are frequently more resistant to cisplatin (CDDP) than cells with mutant but nuclear p53 (p53(mut_n)).	Cisplatin	167-171	P53	Homo sapiens	106-109
24913304-2	2014	The aim of the study was to identify underlying mechanisms implicated in CDDP resistance of HNSCC cells carrying cytoplasmic p53(mut).	Cisplatin	73-77	P53	Homo sapiens	125-128
24913304-3	2014	METHODS: Microarray analysis, quantitative reverse transcription polymerase chain reaction, Western blot analysis and immunocytochemistry were used to identify and evaluate candidate genes involved in CDDP resistance of p53(mut_c) cells.	Cisplatin	201-205	P53	Homo sapiens	220-223
24913304-10	2014	CONCLUSIONS: The observations in this study point to a major role of p53(mut_c) in conferring a stem cell like phenotype to HNSCC cells that is associated with ABCC2/G2 overexpression, high GSH and metabolic activity levels as well as CDDP resistance.	Glutathione	190-193	P53	Homo sapiens	69-72
24913304-10	2014	CONCLUSIONS: The observations in this study point to a major role of p53(mut_c) in conferring a stem cell like phenotype to HNSCC cells that is associated with ABCC2/G2 overexpression, high GSH and metabolic activity levels as well as CDDP resistance.	Cisplatin	235-239	P53	Homo sapiens	69-72
25051299-6	2014	In relation to treatment options, TP53 mutations were associated with poor response to anthracyclines and radiotherapy.	Anthracyclines	87-101	P53	Homo sapiens	34-38
25113166-3	2014	By examining the interactions of estradiol (E2) and progesterone (P4) in women, we propose that changes in physiologic reproductive hormone templates of exposure and timing can affect fertility and even cancer through the silencing or amplification of gene products; such as P53 and Bcl-2 in women.	Estradiol	33-42	P53	Homo sapiens	275-278
25113166-3	2014	By examining the interactions of estradiol (E2) and progesterone (P4) in women, we propose that changes in physiologic reproductive hormone templates of exposure and timing can affect fertility and even cancer through the silencing or amplification of gene products; such as P53 and Bcl-2 in women.	Progesterone	52-64	P53	Homo sapiens	275-278
25103241-8	2014	Moreover, ATP-induced apoptosis and signaling-p53 increase, AMPK activation, and PARP cleavage-as well as autophagy induction were also inhibited by dipyridamole.	Adenosine Triphosphate	10-13	P53	Homo sapiens	46-49
25202347-6	2014	In addition, immunohistochemistry (IHC) was performed to detect the p53 expression level in specimens from 118 paraffin-embedded cancerous tissues.	Paraffin	111-119	P53	Homo sapiens	68-71
25268131-10	2014	U-II downregulated p53 expression in DOX-induced HUVECs apoptosis, and it rapidly activated extracellular signal-regulated protein kinase (ERK) and Akt.	Doxorubicin	37-40	P53	Homo sapiens	19-22
24831732-0	2014	Curcumin modulates miR-19/PTEN/AKT/p53 axis to suppress bisphenol A-induced MCF-7 breast cancer cell proliferation.	Curcumin	0-8	P53	Homo sapiens	35-38
24831732-0	2014	Curcumin modulates miR-19/PTEN/AKT/p53 axis to suppress bisphenol A-induced MCF-7 breast cancer cell proliferation.	bisphenol A	56-67	P53	Homo sapiens	35-38
24831732-6	2014	Meanwhile, BPA-induced upregulation of oncogenic miR-19a and miR-19b, and the dysregulated expression of miR-19-related downstream proteins, including PTEN, p-AKT, p-MDM2, p53, and proliferating cell nuclear antigen, were reversed by curcumin.	bisphenol A	11-14	P53	Homo sapiens	172-175
24831732-8	2014	These results suggest for the first time that curcumin modulates miR-19/PTEN/AKT/p53 axis to exhibit its protective effects against BPA-associated breast cancer promotion.	Curcumin	46-54	P53	Homo sapiens	81-84
25034526-6	2014	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in lung cancer were 25.5, 37.7, and 36.8 %, respectively; frequencies in the controls were 53.4, 30.2, and 16.4 %, respectively (p &lt; 0.01).	Arginine	47-50	P53	Homo sapiens	19-22
25034526-6	2014	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in lung cancer were 25.5, 37.7, and 36.8 %, respectively; frequencies in the controls were 53.4, 30.2, and 16.4 %, respectively (p &lt; 0.01).	Arginine	51-54	P53	Homo sapiens	19-22
25034526-6	2014	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in lung cancer were 25.5, 37.7, and 36.8 %, respectively; frequencies in the controls were 53.4, 30.2, and 16.4 %, respectively (p &lt; 0.01).	Arginine	51-54	P53	Homo sapiens	19-22
25115399-2	2014	Here, we show that cytoplasmic p53 suppresses cell invasion by reducing mitochondrial reactive oxygen species (ROS) levels.	Reactive Oxygen Species	86-109	P53	Homo sapiens	31-34
25115399-2	2014	Here, we show that cytoplasmic p53 suppresses cell invasion by reducing mitochondrial reactive oxygen species (ROS) levels.	Reactive Oxygen Species	111-114	P53	Homo sapiens	31-34
25115399-3	2014	Analysis revealed that this function is mediated by Bcl-2 family proteins: Cytoplasmic p53 binds Bcl-w, liberating Bax, which then binds ND5, a subunit of respiratory complex-I, thereby suppressing complex-I activity and thus ROS production.	Reactive Oxygen Species	226-229	P53	Homo sapiens	87-90
25115399-7	2014	This study demonstrates a link between p53 and Bcl-2 proteins as regulators of ROS production and cellular invasiveness, and reveals complex-I, especially ND5, as their functional target.	Reactive Oxygen Species	79-82	P53	Homo sapiens	39-42
24831732-8	2014	These results suggest for the first time that curcumin modulates miR-19/PTEN/AKT/p53 axis to exhibit its protective effects against BPA-associated breast cancer promotion.	bisphenol A	132-135	P53	Homo sapiens	81-84
25149542-8	2014	Finally, we showed that Cisplatin could restrain the invasion of ESCC cells by inducing the expression of ATF3 via P53 signaling.	Cisplatin	24-33	P53	Homo sapiens	115-118
25268131-11	2014	The DOX induced change of p53 was not affected by U-II antagonist (urantide) under ATF-3 knockdown.	Doxorubicin	4-7	P53	Homo sapiens	26-29
25260780-0	2014	High glucose dephosphorylates serine 46 and inhibits p53 apoptotic activity.	Glucose	5-12	P53	Homo sapiens	53-56
25112877-0	2014	p53 is required for cisplatin-induced processing of the mitochondrial fusion protein L-Opa1 that is mediated by the mitochondrial metallopeptidase Oma1 in gynecologic cancers.	Cisplatin	20-29	P53	Homo sapiens	0-3
25112877-5	2014	The requirements of Oma1 and p53 for CDDP-induced L-Opa1 processing, mitochondrial fragmentation, and apoptosis were examined by siRNA or cDNA.	Cisplatin	37-41	P53	Homo sapiens	29-32
25112877-9	2014	Silencing p53 expression attenuated the effects of CDDP in Oma1 (40 kDa) increase, L-Opa1 processing, mitochondrial fragmentation, and apoptosis in chemosensitive OVCA cells, whereas reconstitution of p53 in p53 mutant or null chemoresistant OVCA cells induced Oma1 (40 kDa) increase, L-Opa1 processing, mitochondrial fragmentation, and apoptosis irrespective of the presence of CDDP.	Cisplatin	51-55	P53	Homo sapiens	10-13
25112877-9	2014	Silencing p53 expression attenuated the effects of CDDP in Oma1 (40 kDa) increase, L-Opa1 processing, mitochondrial fragmentation, and apoptosis in chemosensitive OVCA cells, whereas reconstitution of p53 in p53 mutant or null chemoresistant OVCA cells induced Oma1 (40 kDa) increase, L-Opa1 processing, mitochondrial fragmentation, and apoptosis irrespective of the presence of CDDP.	Cisplatin	51-55	P53	Homo sapiens	201-204
25112877-9	2014	Silencing p53 expression attenuated the effects of CDDP in Oma1 (40 kDa) increase, L-Opa1 processing, mitochondrial fragmentation, and apoptosis in chemosensitive OVCA cells, whereas reconstitution of p53 in p53 mutant or null chemoresistant OVCA cells induced Oma1 (40 kDa) increase, L-Opa1 processing, mitochondrial fragmentation, and apoptosis irrespective of the presence of CDDP.	Cisplatin	51-55	P53	Homo sapiens	201-204
25112877-9	2014	Silencing p53 expression attenuated the effects of CDDP in Oma1 (40 kDa) increase, L-Opa1 processing, mitochondrial fragmentation, and apoptosis in chemosensitive OVCA cells, whereas reconstitution of p53 in p53 mutant or null chemoresistant OVCA cells induced Oma1 (40 kDa) increase, L-Opa1 processing, mitochondrial fragmentation, and apoptosis irrespective of the presence of CDDP.	Cisplatin	379-383	P53	Homo sapiens	10-13
25112877-10	2014	Prohibitin 1 (Phb1) dissociates from Opa1-Phb1 complex and binds phosphorylated p53 (serine 15) in response to CDDP in chemosensitive but not chemoresistant CECA cells.	Serine	85-91	P53	Homo sapiens	80-83
25112877-10	2014	Prohibitin 1 (Phb1) dissociates from Opa1-Phb1 complex and binds phosphorylated p53 (serine 15) in response to CDDP in chemosensitive but not chemoresistant CECA cells.	Cisplatin	111-115	P53	Homo sapiens	80-83
25112877-11	2014	These findings demonstrate that (a) p53 and Oma1 mediate L-Opa1 processing, (b) mitochondrial fragmentation is involved in CDDP-induced apoptosis in OVCA and CECA cells, and (c) dysregulated mitochondrial dynamics may in part be involved in the pathophysiology of CDDP resistance.	Cisplatin	264-268	P53	Homo sapiens	36-39
25260780-5	2014	However, whether high glucose might modify p53Ser46 phosphorylation has never been addressed.	Glucose	22-29	P53	Homo sapiens	43-46
25260780-7	2014	Analyses of p53 posttranslational modifications showed that drug-induced p53Ser46 phosphorylation was reduced by high glucose.	Glucose	118-125	P53	Homo sapiens	12-15
25260780-7	2014	Analyses of p53 posttranslational modifications showed that drug-induced p53Ser46 phosphorylation was reduced by high glucose.	Glucose	118-125	P53	Homo sapiens	73-76
25260780-8	2014	Such reduction depended by high glucose-induced calyculin A-sensitive phosphatase(s), able to specifically target p53Ser46 phosphorylation.	Glucose	32-39	P53	Homo sapiens	114-117
25260780-10	2014	In agreement, a constitutively phosphorylated Ser46D p53 mutant was resistant to high glucose.	ser46d	46-52	P53	Homo sapiens	53-56
25260780-10	2014	In agreement, a constitutively phosphorylated Ser46D p53 mutant was resistant to high glucose.	Glucose	86-93	P53	Homo sapiens	53-56
25260780-13	2014	CONCLUSIONS: These data indicate that high glucose specifically inhibited Ser46 phosphorylation thus reducing p53 apoptotic activity.	Glucose	43-50	P53	Homo sapiens	110-113
25108166-4	2014	Our results revealed that H2O2 reduced viability of cells through up-regulation of p53 followed by increase in Bax/Bcl2 ratio.	Hydrogen Peroxide	26-30	P53	Homo sapiens	83-86
25142144-6	2014	Genotype data for the TP53-Arg72Pro polymorphism, which is associated with responses to platinum-based doublet chemotherapy, were subsequently incorporated into the prediction analysis.	Platinum	88-96	P53	Homo sapiens	22-26
25108166-9	2014	These results collectively suggest that ROS are involved in activation of both the defensive and pro-apoptotic pathways encompassing HIF-1alpha and p53, respectively.	Reactive Oxygen Species	40-43	P53	Homo sapiens	148-151
24929187-0	2014	ATM-p53 pathway causes G2/M arrest, but represses apoptosis in pseudolaric acid B-treated HeLa cells.	pseudolaric acid B	63-81	P53	Homo sapiens	4-7
24929187-6	2014	The expressions of p-ATM and p-p53 that were involved in G2/M arrest increased at 12h after treatment with PAB.	pseudolaric acid B	107-110	P53	Homo sapiens	31-34
25018059-9	2014	We determined that oxLDL triggered the phosphorylation of ERK and, in turn, the activation of p53 and other apoptosis-related events, including calcium accumulation, destabilization of the mitochondrial permeability and disruption of the balance between pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins.	Calcium	144-151	P53	Homo sapiens	94-97
24942805-7	2014	The up-regulation of miR-23a by berberine is p53-dependent.	Berberine	32-41	P53	Homo sapiens	45-48
24995577-8	2014	Treatments with progressively increasing concentrations (from 100 muM to 500 muM) of esculetin produced a reduction of Bcl2/Bax ratio in NB4 cells at 19 h, without affecting p53 levels.	esculetin	85-94	P53	Homo sapiens	174-177
25181509-6	2014	When MI-63 was combined with the BH3 mimetic ABT-737, enhanced activity was seen in both wild-type and mutant p53 models.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	45-48	P53	Homo sapiens	110-113
24814195-8	2014	Furthermore, activation of FOXO3a induced cell apoptosis irrespective of p53 status, whereas p53 may act as FOXO3a downstream molecules involved in cisplatin-induced cell apoptosis.	Cisplatin	148-157	P53	Homo sapiens	93-96
24942805-0	2014	Berberine-induced tumor suppressor p53 up-regulation gets involved in the regulatory network of MIR-23a in hepatocellular carcinoma.	Berberine	0-9	P53	Homo sapiens	35-38
24942805-1	2014	AIM OF THE STUDY: To investigate the involvement of p53 in the regulatory network of microRNA-23a (miR-23a) in berberine-treated hepatocellular carcinoma (HCC) cells.	Berberine	111-120	P53	Homo sapiens	52-55
32261761-7	2014	Internalized FAC@CurP-SeNPs triggers intracellular ROS overproduction, thus activates p53, MAPKs pathways and inhibits NFkappaB and to promote cell apoptosis.	ros	51-54	P53	Homo sapiens	86-89
24726874-0	2014	Aspirin-induced inhibition of adipogenesis was p53-dependent and associated with inactivation of pentose phosphate pathway.	Aspirin	0-7	P53	Homo sapiens	47-50
24726874-3	2014	The present study aims at evaluating the possible existence of a putative p53-dependent pathway underlying the aspirin-induced inhibition of adipogenesis.	Aspirin	111-118	P53	Homo sapiens	74-77
24726874-10	2014	It indicated that aspirin induced adipocyte differentiation through p53-p21 pathway.	Aspirin	18-25	P53	Homo sapiens	68-71
24726874-17	2014	We demonstrated that aspirin-induced inhibition of adipogenesis was p53-dependent and associated with inactivation of PPP.	Aspirin	21-28	P53	Homo sapiens	68-71
24726874-19	2014	Moreover, when use aspirin in therapeutic strategy, the p53 status should be considered.	Aspirin	19-26	P53	Homo sapiens	56-59
25184754-1	2014	In the Balkan and Taiwan, the relationship between exposure to aristolochic acid and risk of urothelial neoplasms was inferred from the A&gt;T genetic hallmark in TP53 gene from malignant cells.	aristolochic acid I	63-80	P53	Homo sapiens	163-167
25184754-2	2014	This study aimed to characterize the TP53 mutational spectrum in urothelial cancers consecutive to Aristolochic Acid Nephropathy in Belgium.	aristolochic acid I	99-116	P53	Homo sapiens	37-41
25056872-0	2014	Electrochemical detection of DNA binding by tumor suppressor p53 protein using osmium-labeled oligonucleotide probes and catalytic hydrogen evolution at the mercury electrode.	Osmium	79-85	P53	Homo sapiens	61-64
25056872-0	2014	Electrochemical detection of DNA binding by tumor suppressor p53 protein using osmium-labeled oligonucleotide probes and catalytic hydrogen evolution at the mercury electrode.	Oligonucleotides	94-109	P53	Homo sapiens	61-64
25056872-0	2014	Electrochemical detection of DNA binding by tumor suppressor p53 protein using osmium-labeled oligonucleotide probes and catalytic hydrogen evolution at the mercury electrode.	Hydrogen	131-139	P53	Homo sapiens	61-64
25056872-2	2014	We show that double-stranded ONs bearing a dT20 tail labeled with Os,bipy are specifically recognized by the tumor suppressor p53 protein according to the presence or absence of a specific binding site (p53CON) in the double-stranded segment.	Osmium	66-68	P53	Homo sapiens	126-129
25056872-4	2014	To detect the p53-bound osmium-labeled probes, we took advantage of a catalytic peak yielded by Os,bipy-modified DNA at the mercury-based electrodes, allowing facile determination of subnanogram quantities of the labeled oligonucleotides.	Osmium	24-30	P53	Homo sapiens	14-17
25056872-4	2014	To detect the p53-bound osmium-labeled probes, we took advantage of a catalytic peak yielded by Os,bipy-modified DNA at the mercury-based electrodes, allowing facile determination of subnanogram quantities of the labeled oligonucleotides.	Osmium	96-98	P53	Homo sapiens	14-17
25056872-4	2014	To detect the p53-bound osmium-labeled probes, we took advantage of a catalytic peak yielded by Os,bipy-modified DNA at the mercury-based electrodes, allowing facile determination of subnanogram quantities of the labeled oligonucleotides.	Oligonucleotides	221-237	P53	Homo sapiens	14-17
25069803-3	2014	Ni(II)-induced toxicogenomic change has been associated with altered activity of HIF, p53, c-MYC, NFkappaB and iron and 2-oxoglutarate-dependent dioxygenases.	Nickel(2+)	0-6	P53	Homo sapiens	86-89
25069803-4	2014	Advancing high-throughput technology has indicated the toxicogenome of Ni(II) involves crosstalk between HIF, p53, c-MYC, NFkappaB and dioxygenases.	Nickel(2+)	71-77	P53	Homo sapiens	110-113
24942805-8	2014	Inhibition of p53 expression and activity could block the up-regulation of miR-23a induced by berberine.	Berberine	94-103	P53	Homo sapiens	14-17
24942805-9	2014	Furthermore, berberine-induced miR-23a expression may mediate the transcription activation of p53-related tumor suppressive genes p21 and GADD45alpha.	Berberine	13-22	P53	Homo sapiens	94-97
24942805-14	2014	CONCLUSION: Our study reveals that miR-23a may be involved in regulating the anti-HCC effect of berberine by mediating the regulation of p53.	Berberine	96-105	P53	Homo sapiens	137-140
24970682-0	2014	Metformin induces microRNA-34a to downregulate the Sirt1/Pgc-1alpha/Nrf2 pathway, leading to increased susceptibility of wild-type p53 cancer cells to oxidative stress and therapeutic agents.	Metformin	0-9	P53	Homo sapiens	131-134
25025520-2	2014	The arginine allele at codon 72 in p53 tumor suppressor gene has been reported to be a risk-factor in different ethnic groups.	Arginine	4-12	P53	Homo sapiens	35-38
25217394-6	2014	Western blotting detected the protein expression of p21 and p53 increased and PCNA, CDK1, cyclin B decreased in GCV+rAAV+Dox group.	Doxorubicin	121-124	P53	Homo sapiens	60-63
24568186-8	2014	We speculated that iron, a by-product of HO-1-catalyzed reactions, could mediate 15d-PGJ2-induced p53 expression.	Iron	19-23	P53	Homo sapiens	98-101
24568186-9	2014	Upregulation of p53 expression by 15d-PGJ2 was abrogated by the iron chelator desferrioxamine in MCF-7 cells.	Iron	64-68	P53	Homo sapiens	16-19
24568186-13	2014	In conclusion, upregulation of p53 and p21 via HO-1 induction and subsequent release of iron with accumulation of H-ferritin may confer resistance to oxidative damage in cancer cells frequently challenged by redox-cycling anticancer drugs.	Iron	88-92	P53	Homo sapiens	31-34
24970682-11	2014	Furthermore, upregulation of death receptor 5 by metformin-mediated Sirt1 downregulation enhanced the sensitivity of wild-type p53 cancer cells to TRAIL-induced apoptosis.	Metformin	49-58	P53	Homo sapiens	127-130
24970682-4	2014	Using human cancer cell lines that exhibit differential expression of p53, we found that metformin reduced Sirt1 protein levels in cancer cells bearing wild-type p53, but did not affect Sirt1 protein levels in cancer cell lines harboring mutant forms of p53.	Metformin	89-98	P53	Homo sapiens	70-73
24970682-12	2014	Our results demonstrated that metformin induces miR-34a to suppress the Sirt1/Pgc-1alpha/Nrf2 pathway and increases susceptibility of wild-type p53 cancer cells to oxidative stress and TRAIL-induced apoptosis.	Metformin	30-39	P53	Homo sapiens	144-147
24970682-4	2014	Using human cancer cell lines that exhibit differential expression of p53, we found that metformin reduced Sirt1 protein levels in cancer cells bearing wild-type p53, but did not affect Sirt1 protein levels in cancer cell lines harboring mutant forms of p53.	Metformin	89-98	P53	Homo sapiens	162-165
24970682-4	2014	Using human cancer cell lines that exhibit differential expression of p53, we found that metformin reduced Sirt1 protein levels in cancer cells bearing wild-type p53, but did not affect Sirt1 protein levels in cancer cell lines harboring mutant forms of p53.	Metformin	89-98	P53	Homo sapiens	162-165
24970682-5	2014	Metformin-induced p53 protein levels in wild-type p53 cancer cells resulted in upregulation of microRNA (miR)-34a.	Metformin	0-9	P53	Homo sapiens	18-21
24970682-5	2014	Metformin-induced p53 protein levels in wild-type p53 cancer cells resulted in upregulation of microRNA (miR)-34a.	Metformin	0-9	P53	Homo sapiens	50-53
24839208-2	2014	Reactive oxygen species (ROS) and reactive nitrogen species generations have been proposed to be an important mechanism of DOX-induced cardiotoxicity and cardiomyocyte apoptosis, which may be mediated by p53 protein.	Doxorubicin	123-126	P53	Homo sapiens	204-207
24968890-13	2014	Co-administration of CFZ and CPT-11 induced G2/M arrest, increased p21WAF1/CIP, and decreased mutant p53 and cdc25c expression.	Irinotecan	29-35	P53	Homo sapiens	101-104
25092778-6	2014	After adjustment for clinical variables associated with these end points, mutations in TP53 (HR, 2.30; P = .027), TET2 (HR, 2.40; P = .033), and DNMT3A (HR, 2.08; P = .049) were associated with decreased OS.	Osmium	204-206	P53	Homo sapiens	87-91
24839208-2	2014	Reactive oxygen species (ROS) and reactive nitrogen species generations have been proposed to be an important mechanism of DOX-induced cardiotoxicity and cardiomyocyte apoptosis, which may be mediated by p53 protein.	Reactive Oxygen Species	0-23	P53	Homo sapiens	204-207
24839208-2	2014	Reactive oxygen species (ROS) and reactive nitrogen species generations have been proposed to be an important mechanism of DOX-induced cardiotoxicity and cardiomyocyte apoptosis, which may be mediated by p53 protein.	Reactive Oxygen Species	25-28	P53	Homo sapiens	204-207
25177931-4	2014	TP53 11 presented the following genotypic distribution: the control group was 98.28% homozygous wild-type (Glu) and 1.72% homozygous variant (Gln/Lys), and the heterozygous genotype was not identified.	Glutamic Acid	107-110	P53	Homo sapiens	0-4
25536560-2	2014	To set of p53-mediated apoptosis gene polymorphisms (TP53 codon 72 Arg/Pro, r21 codon 31 Ser/Arg, MDM2 SNP309) for the occurrence of CLL in patients who were exposed to ionizing radiation (IR) from the Chornobyl accident.	Arginine	67-70	P53	Homo sapiens	10-13
25536560-2	2014	To set of p53-mediated apoptosis gene polymorphisms (TP53 codon 72 Arg/Pro, r21 codon 31 Ser/Arg, MDM2 SNP309) for the occurrence of CLL in patients who were exposed to ionizing radiation (IR) from the Chornobyl accident.	Serine	89-92	P53	Homo sapiens	10-13
25536560-2	2014	To set of p53-mediated apoptosis gene polymorphisms (TP53 codon 72 Arg/Pro, r21 codon 31 Ser/Arg, MDM2 SNP309) for the occurrence of CLL in patients who were exposed to ionizing radiation (IR) from the Chornobyl accident.	Arginine	93-96	P53	Homo sapiens	10-13
25536560-7	2014	The distribution of genotypes in patients with CLL did not differ from controls, except for reduced the frequency of homozygotes Arg/Arg TP53 among patients with CLL (p = 0.01).	Arginine	129-132	P53	Homo sapiens	137-141
25536560-7	2014	The distribution of genotypes in patients with CLL did not differ from controls, except for reduced the frequency of homozygotes Arg/Arg TP53 among patients with CLL (p = 0.01).	Arginine	133-136	P53	Homo sapiens	137-141
24411723-0	2014	The interaction between organic phosphate ester and p53: an integrated experimental and in silico approach.	organic phosphate ester	24-47	P53	Homo sapiens	52-55
24112103-3	2014	METHODS: TP53 mutations were determined with direct sequencing on paraffin-embedded carcinoma tissue from 31 young patients and compared with two older age OSCC reference groups: one from the same institute (N = 87) and an independent one (N = 675).	Paraffin	66-74	P53	Homo sapiens	9-13
24561640-8	2014	By contrast, expression of p53 was upregulated by L-Arg.	Arginine	50-55	P53	Homo sapiens	27-30
24548268-8	2014	Melanoma cell lines cultured on dermal equivalent showed decreased expression of p53 after Dox treatment, and this outcome was accompanied by induction of interleukin IL-6, IL-8, and matrix metalloproteinases 2 and 9.	Doxorubicin	91-94	P53	Homo sapiens	81-84
25064843-0	2014	Phospholipase D2 downregulation induces cellular senescence through a reactive oxygen species-p53-p21Cip1/WAF1 pathway.	Reactive Oxygen Species	70-93	P53	Homo sapiens	94-97
25064843-7	2014	Taken together, these results show that PLD2 downregulation causes senescence through the p53-p21(Cip1/WAF1) pathway by stimulating ROS production, which is induced by CK2 inhibition.	Reactive Oxygen Species	132-135	P53	Homo sapiens	90-93
25177931-6	2014	TP53 72 showed the following genotypic distribution: the control group was 29.75% homozygous wild-type (Arg), 47.11% heterozygous (Arg-Pro), and 23.14% homozygous variant (Pro).	Arginine	104-107	P53	Homo sapiens	0-4
25156493-4	2014	ArhGAP30 binds to p53 C-terminal domain and P300, facilitating P300-mediated acetylation of p53 at lysine 382.	Lysine	99-105	P53	Homo sapiens	18-21
25177931-6	2014	TP53 72 showed the following genotypic distribution: the control group was 29.75% homozygous wild-type (Arg), 47.11% heterozygous (Arg-Pro), and 23.14% homozygous variant (Pro).	Arginine	131-134	P53	Homo sapiens	0-4
25156493-4	2014	ArhGAP30 binds to p53 C-terminal domain and P300, facilitating P300-mediated acetylation of p53 at lysine 382.	Lysine	99-105	P53	Homo sapiens	92-95
25177931-8	2014	Only one patient had the homozygous TP53 248 genotype (Arg-Trp/Gln); all other patients were homozygous wild-type in both the control and endometriosis groups (P = 0.51; NS).	Arginine	55-58	P53	Homo sapiens	36-40
25177931-8	2014	Only one patient had the homozygous TP53 248 genotype (Arg-Trp/Gln); all other patients were homozygous wild-type in both the control and endometriosis groups (P = 0.51; NS).	Tryptophan	59-62	P53	Homo sapiens	36-40
24960055-9	2014	Taken together, HBCD and PCBs at low concentrations could increase the resistance of HCC cells to cisplatin through modulation on NF-kappaB pathway activation and p53 function, which is associated with the activity of PI3K/Akt pathway.	Cisplatin	98-107	P53	Homo sapiens	163-166
25221773-0	2014	In silico study of fragile histidine triad interaction domains with MDM2 and p53.	Histidine	27-36	P53	Homo sapiens	77-80
25221773-1	2014	BACKGROUND: Fragile histidine triad (FHIT) is considered as a member of the histidine triad (HIT) nucleotide-binding protein superfamily regarded as a putative tumor suppressor executing crucial role in inhibiting p53 degradation by MDM2.	Histidine	20-29	P53	Homo sapiens	214-217
25221773-1	2014	BACKGROUND: Fragile histidine triad (FHIT) is considered as a member of the histidine triad (HIT) nucleotide-binding protein superfamily regarded as a putative tumor suppressor executing crucial role in inhibiting p53 degradation by MDM2.	Histidine	76-85	P53	Homo sapiens	214-217
24862437-0	2014	Selective purification of supercoiled p53-encoding pDNA with L-methionine-agarose matrix.	Methionine	61-73	P53	Homo sapiens	38-41
24944268-3	2014	Magnesium deficiency significantly increased cisplatin-associated weight loss and markers of renal damage (plasma blood urea nitrogen and creatinine), histological changes, inflammation, and renal cell apoptosis and modulated signaling pathways (e.g., ERK1/2, p53, and STAT3).	Cisplatin	45-54	P53	Homo sapiens	260-263
24960060-6	2014	In addition, analysis of p53 target genes in TPA-pre-treated TK6 cells revealed a significant modulation of UVC-induced gene expression that supported a shift toward a pro-apoptotic phenotype.	Tetradecanoylphorbol Acetate	45-48	P53	Homo sapiens	25-28
25337187-8	2014	FoxM1 inhibition by thiostrepton induced apoptosis of NPC cells by down-regulation of bcl-2, up-regulation of bax and p53, and inducing release of cytochrome c accompanied by activation of caspase-9, cleaved caspase-3 and cleaved PARP.	Thiostrepton	20-32	P53	Homo sapiens	118-121
25118938-11	2014	These results suggest that cadmium exposure induces the activation of Notch1 signaling in renal proximal tubular cells with cooperative activation by the p53 and PI3K/Akt signaling pathways; the resultant expression of Snail, a repressor of E-cadherin expression, might lead to cellular damage by decreasing cell-cell adhesion.	Cadmium	27-34	P53	Homo sapiens	154-157
24954032-0	2014	PCB153, TCDD and estradiol compromise the benzo[a]pyrene-induced p53-response via FoxO3a.	Polychlorinated Dibenzodioxins	8-12	P53	Homo sapiens	65-68
24954032-0	2014	PCB153, TCDD and estradiol compromise the benzo[a]pyrene-induced p53-response via FoxO3a.	Estradiol	17-26	P53	Homo sapiens	65-68
24954032-3	2014	We have studied the effect of TCDD, PCB153 and estradiol on p53 signaling induced by PAHs.	Polychlorinated Dibenzodioxins	30-34	P53	Homo sapiens	60-63
24954032-3	2014	We have studied the effect of TCDD, PCB153 and estradiol on p53 signaling induced by PAHs.	Estradiol	47-56	P53	Homo sapiens	60-63
24954032-9	2014	Our data indicate interplay between p53, FoxO3a and 14-3-3 leading to an attenuated BaP induced apoptosis in cells co-exposed to TCDD, PCB 153 or estradiol.	Polychlorinated Dibenzodioxins	129-133	P53	Homo sapiens	36-39
24712391-5	2014	The improvements in therapeutic response over either PTX-VE or 5-FU-TPGS therapy alone were demonstrated by the ability to effectively induce the apoptosis of tumor cells via up-regulation of tumor suppressor p53 and beta-tubulin and by the significant inhibition of cell cycle progression.	Paclitaxel	53-56	P53	Homo sapiens	209-212
24712391-5	2014	The improvements in therapeutic response over either PTX-VE or 5-FU-TPGS therapy alone were demonstrated by the ability to effectively induce the apoptosis of tumor cells via up-regulation of tumor suppressor p53 and beta-tubulin and by the significant inhibition of cell cycle progression.	Fluorouracil	63-67	P53	Homo sapiens	209-212
24954032-9	2014	Our data indicate interplay between p53, FoxO3a and 14-3-3 leading to an attenuated BaP induced apoptosis in cells co-exposed to TCDD, PCB 153 or estradiol.	Estradiol	146-155	P53	Homo sapiens	36-39
24801133-9	2014	Array comparative genomic hybridization detected a 1.36 Mb deletion in 8q22.3 that encompassed RRM2B and NCALD, which encode the small subunit of p53-inducible ribonucleotide reductase and neurocalcin delta in the neuronal calcium sensor family of calcium-binding proteins, respectively.	Calcium	223-230	P53	Homo sapiens	146-149
24801133-9	2014	Array comparative genomic hybridization detected a 1.36 Mb deletion in 8q22.3 that encompassed RRM2B and NCALD, which encode the small subunit of p53-inducible ribonucleotide reductase and neurocalcin delta in the neuronal calcium sensor family of calcium-binding proteins, respectively.	Calcium	248-255	P53	Homo sapiens	146-149
25002230-4	2014	We report herein on the radioprotective activity of 8-hydroxyquinoline (8HQ) derivatives that were initially designed so as to interact with the Zn(2+) in p53.	Zinc	145-147	P53	Homo sapiens	155-158
24830845-6	2014	Six dual-point mutants were found to have moderate or high activities with their IC50 values ranging from 16.3 to 137.0 muM, which are better than that of wild-type p53 peptide (IC50 = 182.6 muM) and close to that of classical anticancer agent cis-platin (IC50 = 4.3 muM).	Cisplatin	244-254	P53	Homo sapiens	165-168
24801380-0	2014	Doxorubicin and 5-fluorouracil induced accumulation and transcriptional activity of p53 are independent of the phosphorylation at serine 15 in MCF-7 breast cancer cells.	Doxorubicin	0-11	P53	Homo sapiens	84-87
24801380-0	2014	Doxorubicin and 5-fluorouracil induced accumulation and transcriptional activity of p53 are independent of the phosphorylation at serine 15 in MCF-7 breast cancer cells.	Fluorouracil	16-30	P53	Homo sapiens	84-87
24801380-0	2014	Doxorubicin and 5-fluorouracil induced accumulation and transcriptional activity of p53 are independent of the phosphorylation at serine 15 in MCF-7 breast cancer cells.	Serine	130-136	P53	Homo sapiens	84-87
24801380-4	2014	But contrary to some reports, we observed minimal phosphorylation of p53 at serine 15 in MCF-7 cells after drug treatment.	Serine	76-82	P53	Homo sapiens	69-72
24867259-0	2014	Nutlin-3 induces BCL2A1 expression by activating ELK1 through the mitochondrial p53-ROS-ERK1/2 pathway.	ros	84-87	P53	Homo sapiens	80-83
24867259-3	2014	However, we previously demonstrated that the nutlin-3-induced mitochondrial translocation of p53 stimulates ERK1/2 activation, an anti-apoptosis signal, via mitochondrial ROS generation.	ros	171-174	P53	Homo sapiens	93-96
24839007-9	2014	Together, the findings suggested that GTP-induced necroptosis was modulated by the p53-independent pathway, which was related to the translocation of Bax and Bak to mitochondria, release of cytochrome c, and activation of caspases.	Guanosine Triphosphate	38-41	P53	Homo sapiens	83-86
24412988-5	2014	An increasing number of cytosolic and mitochondrial proteins involved in mitochondrial metabolism and respiration are regulated by p53, which influences mitochondrial ROS production as well.	ros	167-170	P53	Homo sapiens	131-134
25135721-6	2014	Both PDOX and DOX caused an up-regulation of the P53/P21-related signal pathway, and PDOX significantly increased expression of P53 and caspase 3, and arrested the cell cycle at the G1/G2 phase.	Doxorubicin	6-9	P53	Homo sapiens	49-52
24867336-8	2014	Finally, melatonin and its metabolites further enhanced expression of p53 phosphorylated at Ser-15 but not at Ser-46 or its nonphosphorylated form.	Melatonin	9-18	P53	Homo sapiens	70-73
24867336-8	2014	Finally, melatonin and its metabolites further enhanced expression of p53 phosphorylated at Ser-15 but not at Ser-46 or its nonphosphorylated form.	Serine	92-95	P53	Homo sapiens	70-73
23475592-2	2014	This SNP encodes either an arginine or proline at position 72 (R72P) of the p53 protein, which can alter the apoptotic activity of p53 via transcriptional and non-transcriptional mechanisms.	Arginine	27-35	P53	Homo sapiens	76-79
23475592-2	2014	This SNP encodes either an arginine or proline at position 72 (R72P) of the p53 protein, which can alter the apoptotic activity of p53 via transcriptional and non-transcriptional mechanisms.	Arginine	27-35	P53	Homo sapiens	131-134
24782034-9	2014	The most frequent genotype in both CIN(+) and CIN(-) patients was Arg/Pro TP53 codon 72 and A1A1 for 16-bp Del in intron 3.	Arginine	66-69	P53	Homo sapiens	74-78
24920214-0	2014	Melatonin down-regulates MDM2 gene expression and enhances p53 acetylation in MCF-7 cells.	Melatonin	0-9	P53	Homo sapiens	59-62
24920214-1	2014	Compelling evidence demonstrated that melatonin increases p53 activity in cancer cells.	Melatonin	38-47	P53	Homo sapiens	58-61
24920214-12	2014	Consequently, melatonin-treated cells display significantly higher values of both p53 and acetylated p53.	Melatonin	14-23	P53	Homo sapiens	82-85
24920214-12	2014	Consequently, melatonin-treated cells display significantly higher values of both p53 and acetylated p53.	Melatonin	14-23	P53	Homo sapiens	101-104
24920214-14	2014	Our results provide evidence that melatonin enhances p53 acetylation by modulating the MDM2/MDMX/p300 pathway, disclosing new insights for understanding its anticancer effect.	Melatonin	34-43	P53	Homo sapiens	53-56
25220593-5	2014	We also observed induction of LCE1 expressions by DNA damage, which was caused by treatment with adriamycin or UV irradiation in a wild-type p53-dependent manner.	Doxorubicin	97-107	P53	Homo sapiens	141-144
24833091-0	2014	Novel p53 codon 240 Ser &gt; Thr coding region mutation in the patients of oral squamous cell carcinoma (OSCC).	Serine	20-23	P53	Homo sapiens	6-9
24833091-0	2014	Novel p53 codon 240 Ser &gt; Thr coding region mutation in the patients of oral squamous cell carcinoma (OSCC).	Threonine	29-32	P53	Homo sapiens	6-9
24839007-1	2014	Green tea polyphenol (GTP) is one of the most promising chemopreventive agent for cancer; it can inhibit cancer cell proliferation and induce apoptosis through p53-dependent cell signaling pathways.	Guanosine Triphosphate	22-25	P53	Homo sapiens	160-163
29259398-9	2015	Conclusions: We conclude: the p53 codon 72*Arg/*Arg genotype, with its strong apoptotic effects, negatively influences spermatozoa motility and male fertility.	Arginine	43-46	P53	Homo sapiens	30-33
24839007-2	2014	Unfortunately, many tumor cells lack the functional p53, and little is known about the effect of GTP on the p53-deficient/mutant cancer cells.	Guanosine Triphosphate	97-100	P53	Homo sapiens	108-111
24839007-3	2014	To understand the p53-independent mechanisms in GTP-treated p53-dificient/mutant cancer cells, we have now examined GTP-induced cytotoxicity in human hepatoma Hep3B cells (p53-deficient).	Guanosine Triphosphate	48-51	P53	Homo sapiens	60-63
24839007-3	2014	To understand the p53-independent mechanisms in GTP-treated p53-dificient/mutant cancer cells, we have now examined GTP-induced cytotoxicity in human hepatoma Hep3B cells (p53-deficient).	Guanosine Triphosphate	48-51	P53	Homo sapiens	60-63
29259398-9	2015	Conclusions: We conclude: the p53 codon 72*Arg/*Arg genotype, with its strong apoptotic effects, negatively influences spermatozoa motility and male fertility.	Arginine	48-51	P53	Homo sapiens	30-33
24946211-9	2014	The anti-oxidant N-acetylcysteine (NAC), the P53 inhibitor pifithrin-alpha (PFTalpha) as well as P53 siRNA knockdown suppressed berberine-induced P53 mitochondrial translocation and Cyp-D association, thus inhibiting mitochondrial membrane potential (MMP) decrease and prostate cancer cell necrosis.	Berberine	128-137	P53	Homo sapiens	45-48
24934571-0	2014	Diphenylpyrroles: Novel p53 activators.	diphenylpyrroles	0-16	P53	Homo sapiens	24-27
24934571-5	2014	Herein, diphenylpyrroles were introduced and evaluated as a novel scaffold in the field of p53 activators.	diphenylpyrroles	8-24	P53	Homo sapiens	91-94
25009184-1	2014	In mammalian cells, tumor suppressor p53 plays critical roles in the regulation of glucose metabolism, including glycolysis and oxidative phosphorylation, but whether and how p53 also regulates gluconeogenesis is less clear.	Glucose	83-90	P53	Homo sapiens	37-40
24946211-8	2014	Our data found that in prostate cancer cells, berberine induced reactive oxygen species (ROS) production, which dictated P53 translocation to mitochondria, where it physically interacted with Cyp-D to open mitochondrial permeability transition pore (mPTP).	Berberine	46-55	P53	Homo sapiens	121-124
24946211-9	2014	The anti-oxidant N-acetylcysteine (NAC), the P53 inhibitor pifithrin-alpha (PFTalpha) as well as P53 siRNA knockdown suppressed berberine-induced P53 mitochondrial translocation and Cyp-D association, thus inhibiting mitochondrial membrane potential (MMP) decrease and prostate cancer cell necrosis.	Berberine	128-137	P53	Homo sapiens	97-100
24946211-8	2014	Our data found that in prostate cancer cells, berberine induced reactive oxygen species (ROS) production, which dictated P53 translocation to mitochondria, where it physically interacted with Cyp-D to open mitochondrial permeability transition pore (mPTP).	Reactive Oxygen Species	89-92	P53	Homo sapiens	121-124
24946211-9	2014	The anti-oxidant N-acetylcysteine (NAC), the P53 inhibitor pifithrin-alpha (PFTalpha) as well as P53 siRNA knockdown suppressed berberine-induced P53 mitochondrial translocation and Cyp-D association, thus inhibiting mitochondrial membrane potential (MMP) decrease and prostate cancer cell necrosis.	Berberine	128-137	P53	Homo sapiens	97-100
25788859-11	2014	Decreased Survivin, Cyclin D, Bcl-2, and increased Caspase-3, P53 expression level were aslo confirmed by western blot in 5-fluorouracil combine with myricetin groups in vitro.	myricetin	150-159	P53	Homo sapiens	62-65
25788859-11	2014	Decreased Survivin, Cyclin D, Bcl-2, and increased Caspase-3, P53 expression level were aslo confirmed by western blot in 5-fluorouracil combine with myricetin groups in vitro.	Fluorouracil	122-136	P53	Homo sapiens	62-65
24144307-5	2014	[Flu + Clo + Bu + SAHA] resulted in synergistic cytotoxicity, which can be attributed to (1) activated DNA-damage response and cell cycle checkpoint activation through the ATM-CHK2-P53 (or P73) pathway or ATM-CHK2-cdc25-cdc2 pathway, (2) histone modifications and (3) activated apoptosis pathway.	Busulfan	13-15	P53	Homo sapiens	181-184
25033896-6	2014	Immunohistochemistry SP staining was used to measure the expression of p53 protein.	TFF2 protein, human	21-23	P53	Homo sapiens	71-74
24918814-7	2014	RESULTS: Ionising radiation induced a dramatic reactive oxygen species (ROS)-mediated inhibition of GI, leading to AP-modified Hsp27 protein accumulation that, in a mechanism involving p53 and NF-kappaB, triggered an apoptotic mitochondrial pathway.	Reactive Oxygen Species	47-70	P53	Homo sapiens	185-188
24918814-7	2014	RESULTS: Ionising radiation induced a dramatic reactive oxygen species (ROS)-mediated inhibition of GI, leading to AP-modified Hsp27 protein accumulation that, in a mechanism involving p53 and NF-kappaB, triggered an apoptotic mitochondrial pathway.	Reactive Oxygen Species	72-75	P53	Homo sapiens	185-188
24974868-0	2014	DNA impedance biosensor for detection of cancer, TP53 gene mutation, based on gold nanoparticles/aligned carbon nanotubes modified electrode.	Carbon	105-111	P53	Homo sapiens	49-53
24974868-1	2014	For the first time, a new platform based on electrochemical growth of Au nanoparticles on aligned multi-walled carbon nanotubes (A-MWCNT) was developed for sensitive lable-free DNA detection of the TP53 gene mutation, one of the most popular genes in cancer research.	Carbon	111-117	P53	Homo sapiens	198-202
23727633-7	2014	Increased levels of acetylated p53 as well as increased RNA levels of its pro-senescence effector p21 were evident in dexamethasone-treated tenocytes.	Dexamethasone	118-131	P53	Homo sapiens	31-34
23727633-8	2014	Levels of the p53 deacetylase sirtuin 1 were lower in dexamethasone-treated cells compared with controls.	Dexamethasone	54-67	P53	Homo sapiens	14-17
23727633-9	2014	Knockdown of p53 or inhibition of p53 activity prevented dexamethasone-induced senescence.	Dexamethasone	57-70	P53	Homo sapiens	13-16
23727633-9	2014	Knockdown of p53 or inhibition of p53 activity prevented dexamethasone-induced senescence.	Dexamethasone	57-70	P53	Homo sapiens	34-37
25221641-0	2014	PTEN deficiency and mutant p53 confer glucose-addiction to thyroid cancer cells: impact of glucose depletion on cell proliferation, cell survival, autophagy and cell migration.	Glucose	38-45	P53	Homo sapiens	27-30
25221641-8	2014	Genetic silencing of either wild-type PTEN or p53 in WRO cells resulted in increased uptake of glucose, whereas the ectopic expression of PTEN in FTC133 cells resulted in diminished glucose uptake.	Glucose	95-102	P53	Homo sapiens	46-49
25221641-11	2014	We propose that concurrent PTEN deficiency and mutant p53 leads to a glucose-addiction state that renders the cancer cell more sensitive to glucose restriction.	Glucose	69-76	P53	Homo sapiens	54-57
24806432-0	2014	Extracellular signal-regulated kinase signaling-mediated induction and interaction of FOXO3a and p53 contribute to the inhibition of nasopharyngeal carcinoma cell growth by curcumin.	Curcumin	173-181	P53	Homo sapiens	97-100
24806432-4	2014	To further explore the potential mechanism, we showed that curcumin increased the phosphorylation of ERK1/2 but not p38 MAPK in a time-dependent manner, and induced protein expression of the tumor suppressors FOXO3a and p53 in a dose-dependent manner, which were not observed in the presence of PD98059, an inhibitor of ERK1/2.	Curcumin	59-67	P53	Homo sapiens	220-223
24806432-5	2014	Furthermore, silencing of FOXO3a and p53 genes by siRNAs overcame the inhibitory effect of curcumin on cell proliferation.	Curcumin	91-99	P53	Homo sapiens	37-40
24806432-6	2014	Silencing or blockade of p53 using siRNA or chemical inhibitor abrogated the effect of curcumin on expression of FOXO3a protein; silencing or overexpression of FOXO3a had no further effect on curcumin-induced p53 protein expression.	Curcumin	87-95	P53	Homo sapiens	25-28
24806432-8	2014	Together, our studies show that curcumin inhibits growth and induces apoptosis of NPC cells through ERK1/2-mediated increase in the protein expression and interaction of p53 and FOXO3a.	Curcumin	32-40	P53	Homo sapiens	170-173
24806432-9	2014	p53 is upstream of FOXO3a, which form a regulatory loop that mediates the effect of curcumin.	Curcumin	84-92	P53	Homo sapiens	0-3
25033286-1	2014	Up-regulated sirtuin 1 (SIRT1), an NAD+-dependent class III histone deacetylase, deacetylates p53 and inhibits its transcriptional activity, leading to cell survival.	NAD	35-39	P53	Homo sapiens	94-97
24913980-3	2014	Our findings indicate that sublethal doses of doxorubicin and melphalan initiate a DNA damage response (DDR) controlling ligand upregulation on MM cell lines and patient-derived malignant plasma cells in Chk1/2-dependent and p53-independent manner.	Doxorubicin	46-57	P53	Homo sapiens	225-228
25025378-8	2014	Moreover, combined positive expression of p53 and pAkt led to significantly increased PFS in subgroups carrying the XRCC1 Gln allele (HR 7.057; 95% CI 2.073-24.021; P = 0.002) or the ERCC1 Cys allele (HR 2.568; 95% CI 1.056-6.248; P = 0.038).	Cysteine	189-192	P53	Homo sapiens	42-45
24859470-0	2014	As a novel p53 direct target, bidirectional gene HspB2/alphaB-crystallin regulates the ROS level and Warburg effect.	Reactive Oxygen Species	87-90	P53	Homo sapiens	11-14
24859470-9	2014	The ROS level and the Warburg effect are affected after the depletion of p53, HspB2 and alphaB-crystallin respectively.	Reactive Oxygen Species	4-7	P53	Homo sapiens	73-76
24859470-11	2014	These findings provide novel insights into the role of p53 as a regulator of bidirectional gene pair HspB2/alphaB-crystallin-mediated ROS and the Warburg effect.	Reactive Oxygen Species	134-137	P53	Homo sapiens	55-58
25276192-10	2014	Evidence of apoptosis and protein expression of p53 and Bcl-2 indicated that both single applications and combinations of CPE and doxorubicin are able to increase apoptotic bodies of MCF-7 cells by increasing the proteins expression.	Doxorubicin	130-141	P53	Homo sapiens	48-51
24158762-8	2014	CONCLUSIONS: Our results support a beneficial effect of Mediterranean diet and Mediterranean diet supplemented with Coenzyme Q10 on DNA damage as compared to the detrimental action of a saturated fatty acid-rich diet, which triggers the p53-dependent DNA repair machinery.	Fatty Acids	186-206	P53	Homo sapiens	237-240
24915467-0	2014	Rapamycin prevents strong phosphorylation of p53 on serine 46 and attenuates activation of the p53 pathway in A549 lung cancer cells exposed to actinomycin D.	Sirolimus	0-9	P53	Homo sapiens	45-48
24915467-0	2014	Rapamycin prevents strong phosphorylation of p53 on serine 46 and attenuates activation of the p53 pathway in A549 lung cancer cells exposed to actinomycin D.	Sirolimus	0-9	P53	Homo sapiens	95-98
24915467-0	2014	Rapamycin prevents strong phosphorylation of p53 on serine 46 and attenuates activation of the p53 pathway in A549 lung cancer cells exposed to actinomycin D.	Serine	52-58	P53	Homo sapiens	45-48
24915467-1	2014	The activation of the p53 pathway by 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), a molecule that mimics metabolic stress, is attenuated by rapamycin, an inhibitor of mTOR kinase, immunosuppressant, and cancer drug.	Sirolimus	150-159	P53	Homo sapiens	22-25
24915467-5	2014	Rapamycin inhibited the accumulation of phospho-Ser46 p53, attenuated upregulation of some p53 target genes, and altered cell-cycle progression.	Sirolimus	0-9	P53	Homo sapiens	54-57
24915467-5	2014	Rapamycin inhibited the accumulation of phospho-Ser46 p53, attenuated upregulation of some p53 target genes, and altered cell-cycle progression.	Sirolimus	0-9	P53	Homo sapiens	91-94
24798868-7	2014	Silybin treatment also downregulated SIRT1 and upregulated p53 acetylation.	Silybin	0-7	P53	Homo sapiens	59-62
24743655-7	2014	Several novel RNAi suppressors of Tp53 were identified, one of which, PRDM1beta (BLIMP-1), was confirmed to be an Arg-specific transcript.	Arginine	114-117	P53	Homo sapiens	34-38
25151759-1	2014	INTRODUCTION: Malignant transformation of sex-steroid dependent tissues is associated with the loss of expression of sex steroid receptors as well as of the tumor suppression gene p53.	Steroids	46-53	P53	Homo sapiens	180-183
24928858-0	2014	Critical role for p53-serine 15 phosphorylation in stimulating transactivation at p53-responsive promoters.	Serine	22-28	P53	Homo sapiens	18-21
24816189-6	2014	In consequence, p53 OD mutants interfere with the capacity of WT p53 tetramers to be properly ubiquitylated and result in changes of p53-dependent protein expression patterns, including the pro-apoptotic proteins Bax and PUMA under basal and adriamycin-induced conditions.	Doxorubicin	242-252	P53	Homo sapiens	16-19
24816189-6	2014	In consequence, p53 OD mutants interfere with the capacity of WT p53 tetramers to be properly ubiquitylated and result in changes of p53-dependent protein expression patterns, including the pro-apoptotic proteins Bax and PUMA under basal and adriamycin-induced conditions.	Doxorubicin	242-252	P53	Homo sapiens	65-68
24816189-6	2014	In consequence, p53 OD mutants interfere with the capacity of WT p53 tetramers to be properly ubiquitylated and result in changes of p53-dependent protein expression patterns, including the pro-apoptotic proteins Bax and PUMA under basal and adriamycin-induced conditions.	Doxorubicin	242-252	P53	Homo sapiens	65-68
24928858-0	2014	Critical role for p53-serine 15 phosphorylation in stimulating transactivation at p53-responsive promoters.	Serine	22-28	P53	Homo sapiens	82-85
24928858-2	2014	Some stimuli, such as DNA damage, lead to rapid and substantial multisite phosphorylation of p53, nucleated initially through phosphorylation of serine 15.	Serine	145-151	P53	Homo sapiens	93-96
24981574-0	2014	Cisplatin modulates B-cell translocation gene 2 to attenuate cell proliferation of prostate carcinoma cells in both p53-dependent and p53-independent pathways.	Cisplatin	0-9	P53	Homo sapiens	116-119
24691905-5	2014	By employing homologous recombination, we introduced various combinations of missense mutations (lysine to arginine) into eight acetylation sites of the endogenous p53 gene in human embryonic stem cells (hESCs).	Lysine	97-103	P53	Homo sapiens	164-167
24691905-5	2014	By employing homologous recombination, we introduced various combinations of missense mutations (lysine to arginine) into eight acetylation sites of the endogenous p53 gene in human embryonic stem cells (hESCs).	Arginine	107-115	P53	Homo sapiens	164-167
24981574-0	2014	Cisplatin modulates B-cell translocation gene 2 to attenuate cell proliferation of prostate carcinoma cells in both p53-dependent and p53-independent pathways.	Cisplatin	0-9	P53	Homo sapiens	134-137
24981574-5	2014	Cisplatin treatments enhanced p53 and BTG2 expression, repressed AR and PSA expression, and blocked the activation of androgen on the PSA secretion in LNCaP cells.	Cisplatin	0-9	P53	Homo sapiens	30-33
24981574-9	2014	Our results indicated that cisplatin attenuates prostate cancer cell proliferation partly mediated by upregulation of BTG2 through the p53-dependent pathway or p53-independent NFkappaB pathway.	Cisplatin	27-36	P53	Homo sapiens	135-138
24981574-9	2014	Our results indicated that cisplatin attenuates prostate cancer cell proliferation partly mediated by upregulation of BTG2 through the p53-dependent pathway or p53-independent NFkappaB pathway.	Cisplatin	27-36	P53	Homo sapiens	160-163
24932684-7	2014	Finally, increased p53 activation was found to be independent of aberrantly activated AMP-activated protein kinase (AMPK) that occurs in response to MIF/D-DT-deficiency but is dependent on reactive oxygen species (ROS) that mediate aberrant AMPK activation in these cells.	Reactive Oxygen Species	189-212	P53	Homo sapiens	19-22
24952595-0	2014	Histone deacetylase 2 and N-Myc reduce p53 protein phosphorylation at serine 46 by repressing gene transcription of tumor protein 53-induced nuclear protein 1.	Serine	70-76	P53	Homo sapiens	39-42
24952595-0	2014	Histone deacetylase 2 and N-Myc reduce p53 protein phosphorylation at serine 46 by repressing gene transcription of tumor protein 53-induced nuclear protein 1.	Serine	70-76	P53	Homo sapiens	116-132
24952595-3	2014	Tumor protein 53-induced nuclear protein 1 (TP53INP1) phosphorylates p53 protein at serine 46, leading to enhanced p53 activity, transcriptional activation of p53 target genes and programmed cell death.	Serine	84-90	P53	Homo sapiens	69-72
24952595-3	2014	Tumor protein 53-induced nuclear protein 1 (TP53INP1) phosphorylates p53 protein at serine 46, leading to enhanced p53 activity, transcriptional activation of p53 target genes and programmed cell death.	Serine	84-90	P53	Homo sapiens	115-118
24952595-3	2014	Tumor protein 53-induced nuclear protein 1 (TP53INP1) phosphorylates p53 protein at serine 46, leading to enhanced p53 activity, transcriptional activation of p53 target genes and programmed cell death.	Serine	84-90	P53	Homo sapiens	115-118
24474455-8	2014	The Arg72Pro-p53 polymorphism showed for the genotypes Arg/Pro and Pro/Pro, and for the Pro allele, a significant association only to the risk for CIN (p&lt;0.03).	Arginine	4-7	P53	Homo sapiens	13-16
24737586-3	2014	In this current study, we found low expression of UNC5A in bladder cancer, an effective induction of UNC5A by cisplatin in bladder cancer cell lines with wt p53, and a significant reduction of cisplatin-mediated cell death following silencing the endogenous UNC5A.	Cisplatin	110-119	P53	Homo sapiens	157-160
24952595-6	2014	HDAC2 and N-Myc reduced TP53INP1 gene expression by direct binding to the TP53INP1 gene promoter, leading to transcriptional repression of TP53INP1, p53 protein de-phosphorylation at serine 46, neuroblastoma cell proliferation and survival.	Serine	183-189	P53	Homo sapiens	149-152
24932684-7	2014	Finally, increased p53 activation was found to be independent of aberrantly activated AMP-activated protein kinase (AMPK) that occurs in response to MIF/D-DT-deficiency but is dependent on reactive oxygen species (ROS) that mediate aberrant AMPK activation in these cells.	Reactive Oxygen Species	214-217	P53	Homo sapiens	19-22
24939878-0	2014	Caveolin-1 regulates lung cancer stem-like cell induction and p53 inactivation in carbon nanotube-driven tumorigenesis.	Carbon	82-88	P53	Homo sapiens	62-65
24841907-7	2014	These results demonstrated for the first time that ISO simultaneously induced apoptosis and autophagy by ROS-related p53, PI3K/Akt, JNK, and p38 signaling pathways.	Reactive Oxygen Species	105-108	P53	Homo sapiens	117-120
24922076-6	2014	We provide evidence that the decrease in SIRT1 activity and expression facilitated by increasing poly(ADP-ribose) transferase (PARP)-1 activation and microRNA-34a through p53 activation aggravates cisplatin-mediated ototoxicity.	Cisplatin	197-206	P53	Homo sapiens	171-174
24841907-0	2014	Isoorientin induces apoptosis and autophagy simultaneously by reactive oxygen species (ROS)-related p53, PI3K/Akt, JNK, and p38 signaling pathways in HepG2 cancer cells.	Reactive Oxygen Species	62-85	P53	Homo sapiens	100-103
24841907-0	2014	Isoorientin induces apoptosis and autophagy simultaneously by reactive oxygen species (ROS)-related p53, PI3K/Akt, JNK, and p38 signaling pathways in HepG2 cancer cells.	Reactive Oxygen Species	87-90	P53	Homo sapiens	100-103
24927813-11	2014	In total, targeting the atypical kinase Wee1 with an siRNA-based therapeutic or a selective ATP competitive small molecule inhibitor would be a feasible approach to targeting p53 inactive tumors in the clinic.	Adenosine Triphosphate	92-95	P53	Homo sapiens	175-178
24926985-0	2014	Capsaicin-induced activation of p53-SMAR1 auto-regulatory loop down-regulates VEGF in non-small cell lung cancer to restrain angiogenesis.	Capsaicin	0-9	P53	Homo sapiens	32-35
24926985-4	2014	Capsaicin-treatment re-activated p53-SMAR1 positive feed-back loop in these cells to persuade p53-mediated HIF-1alpha degradation and SMAR1-induced repression of Cox-2 expression that restrained HIF-1alpha nuclear localization.	Capsaicin	0-9	P53	Homo sapiens	33-36
24926985-4	2014	Capsaicin-treatment re-activated p53-SMAR1 positive feed-back loop in these cells to persuade p53-mediated HIF-1alpha degradation and SMAR1-induced repression of Cox-2 expression that restrained HIF-1alpha nuclear localization.	Capsaicin	0-9	P53	Homo sapiens	94-97
24922063-18	2014	On the other hand, we determined that leptin reduced the phosphorylation of Ser-46 p53 that plays a pivotal role for apoptotic signaling by p53.	Serine	76-79	P53	Homo sapiens	83-86
24922063-18	2014	On the other hand, we determined that leptin reduced the phosphorylation of Ser-46 p53 that plays a pivotal role for apoptotic signaling by p53.	Serine	76-79	P53	Homo sapiens	140-143
24738879-0	2014	Inhibition enhancer of zeste homologue 2 promotes senescence and apoptosis induced by doxorubicin in p53 mutant gastric cancer cells.	Doxorubicin	86-97	P53	Homo sapiens	101-104
24853176-0	2014	MGMT promoter hypermethylation and K-RAS, PTEN and TP53 mutations in tamoxifen-exposed and non-exposed endometrial cancer cases.	Tamoxifen	69-78	P53	Homo sapiens	51-55
24853816-5	2014	The DNA sequence dependence of p53 oxidative dissociation was examined by electrophoretic mobility shift assays using oligonucleotides containing both synthetic and human p53 consensus sequences with an appended photooxidant, anthraquinone.	Anthraquinones	226-239	P53	Homo sapiens	31-34
24922640-3	2014	RESULTS: Significant differences were observed in the p53 expression between the different groups: NN and CIN I (p=0.010); NN and CIN II (p&lt;0.00001); CIN II and CIN III (p=0.02); CIN II and CIS (p=0.0220); CIN II and CEC (p=0.010).	cin iii	164-171	P53	Homo sapiens	54-57
24648042-7	2014	High-dose steroids with anti-CD52 appeared to improve the response rate in 17p-/TP53 mutated cases and allogeneic transplantation achieved prolonged disease control irrespective of high-risk disease.	Steroids	10-18	P53	Homo sapiens	80-84
25061640-0	2014	Reply to Liu: Amino acid 104 asparagine/glutamic acid of p53 is an adaptively selected site for extreme environments in mammals of the Tibet plateau.	Glutamic Acid	40-53	P53	Homo sapiens	57-60
24668897-7	2014	Array comparative genomic hybridization (array CGH) detected a 3.2 Mb duplication of 17p13.1-p13.2 encompassing TP53, FXR2, NLGN2, and SLC2A4, which encodes the insulin-responsive glucose transporter 4 (GLUT4) associated with insulin-stimulated glucose uptake in adipocytes and muscle.	Glucose	180-187	P53	Homo sapiens	112-116
24668897-7	2014	Array comparative genomic hybridization (array CGH) detected a 3.2 Mb duplication of 17p13.1-p13.2 encompassing TP53, FXR2, NLGN2, and SLC2A4, which encodes the insulin-responsive glucose transporter 4 (GLUT4) associated with insulin-stimulated glucose uptake in adipocytes and muscle.	Glucose	245-252	P53	Homo sapiens	112-116
24710610-2	2014	A common polymorphism of the encoding TP53 gene (codon 72, Pro &gt; Arg, rs1042522) is associated with susceptibility to virus-related and other cancers.	Arginine	68-71	P53	Homo sapiens	38-42
24710610-5	2014	The allele frequency of TP53 codon 72 Arg was 0.30 among 314 Ghanaian primiparae and 0.31 among 545 Rwandan children, respectively, and it was not associated with infection prevalence or parasite density.	Arginine	38-41	P53	Homo sapiens	24-28
24684237-5	2014	The predicted targets of these miRNAs are clearly enriched in genes involved in heparan-sulfate biosynthesis, extracellular matrix-receptor interaction, carbohydrate digestion and absorption, p53 signaling, and cytokine-cytokine-receptor interaction.	Carbohydrates	153-165	P53	Homo sapiens	192-195
24151879-1	2014	Protein lysine methyltransferase G9a, which catalyzes methylation of lysine 9 of histone H3 (H3K9) and lysine 373 (K373) of p53, is overexpressed in human cancers.	Lysine	8-14	P53	Homo sapiens	124-127
24469921-5	2014	Furthermore HIV-Tat and morphine exposure increased activation of extracellular signal-regulated kinase-1/2 (ERK1/2), enhanced levels of p53 and p21, and decreased cyclin D1 and Akt levels in NPCs.	Morphine	24-32	P53	Homo sapiens	137-140
24469921-6	2014	Regulated by ERK1/2 and p53, p21 was found to be indispensible for Tat and morphine mediated cell cycle arrest.	Morphine	75-83	P53	Homo sapiens	24-27
24151879-1	2014	Protein lysine methyltransferase G9a, which catalyzes methylation of lysine 9 of histone H3 (H3K9) and lysine 373 (K373) of p53, is overexpressed in human cancers.	Lysine	69-75	P53	Homo sapiens	124-127
24625390-6	2014	In the event of pairwise combinations of the single nucleotide polymorphisms, a risk elevation was shown for MDM2 GG homozygotes/p53 wild-type Arg in hereditary melanoma (P=0.01).	Arginine	143-146	P53	Homo sapiens	129-132
24823795-5	2014	We demonstrate that cisplatin and adriamycin elicit distinct effects on TP53 and TP63 binding events, through which TP53 can induce or repress transcription of an extensive network of genes by direct binding and/or modulation of TP63 activity.	Cisplatin	20-29	P53	Homo sapiens	72-76
24691657-10	2014	During adriamycin-mediated apoptosis, Unc5D was significantly induced in p53-proficient SH-SY5Y cells but not in p53-deficient SK-N-BE cells.	Doxorubicin	7-17	P53	Homo sapiens	73-76
24691657-13	2014	Notably, Unc5D expression also induced phosphorylation of p53 at serine-15.	Serine	65-71	P53	Homo sapiens	58-61
24691657-14	2014	Unc5D is thus a newly identified transcriptional target of pro-apoptotic p53 and may also act upstream of p53 to induce p53-dependent apoptosis by phosphorylation at ser-15.	Serine	166-169	P53	Homo sapiens	73-76
24691657-14	2014	Unc5D is thus a newly identified transcriptional target of pro-apoptotic p53 and may also act upstream of p53 to induce p53-dependent apoptosis by phosphorylation at ser-15.	Serine	166-169	P53	Homo sapiens	106-109
24691657-14	2014	Unc5D is thus a newly identified transcriptional target of pro-apoptotic p53 and may also act upstream of p53 to induce p53-dependent apoptosis by phosphorylation at ser-15.	Serine	166-169	P53	Homo sapiens	106-109
24710632-8	2014	DNA damage induced p53 stabilization and p21 induction by cisplatin treatment confirmed that wt-AGR2 expression suppressed the p53 pathway.	Cisplatin	58-67	P53	Homo sapiens	127-130
24823795-5	2014	We demonstrate that cisplatin and adriamycin elicit distinct effects on TP53 and TP63 binding events, through which TP53 can induce or repress transcription of an extensive network of genes by direct binding and/or modulation of TP63 activity.	Cisplatin	20-29	P53	Homo sapiens	116-120
24823795-5	2014	We demonstrate that cisplatin and adriamycin elicit distinct effects on TP53 and TP63 binding events, through which TP53 can induce or repress transcription of an extensive network of genes by direct binding and/or modulation of TP63 activity.	Doxorubicin	34-44	P53	Homo sapiens	72-76
24823795-5	2014	We demonstrate that cisplatin and adriamycin elicit distinct effects on TP53 and TP63 binding events, through which TP53 can induce or repress transcription of an extensive network of genes by direct binding and/or modulation of TP63 activity.	Doxorubicin	34-44	P53	Homo sapiens	116-120
24756776-5	2014	Forced overexpression of GRP78 protected the cisplatin-sensitive A2780 cells from cisplatin-induced senescence through P53 and CDC2.	Cisplatin	45-54	P53	Homo sapiens	119-122
24756776-5	2014	Forced overexpression of GRP78 protected the cisplatin-sensitive A2780 cells from cisplatin-induced senescence through P53 and CDC2.	Cisplatin	82-91	P53	Homo sapiens	119-122
24886669-5	2014	RESULTS: Doxorubicin treatment segregated organotypic human breast tumors into distinct Responder or Non Responder groups, characterized by differential proliferative index, stabilization of p53, and induction of apoptosis.	Doxorubicin	9-20	P53	Homo sapiens	191-194
24504677-3	2014	The biomolecular characteristics of tumors, such as appropriate expression of organic cation transporters or genetic alterations including p53, K-ras, LKB1, and PI3K may impact metformin"s anticancer efficiency.	Metformin	177-186	P53	Homo sapiens	139-142
24929515-0	2014	[Blueberry anthocyanins induce G2/M cell cycle arrest and apoptosis of oral cancer KB cells through down-regulation methylation of p53].	blueberry anthocyanins	1-23	P53	Homo sapiens	131-134
24833526-9	2014	We further demonstrate that an activation of the oncologically relevant transcription factor p53 in lung cancer cells induces SIAH2, depletes TYK2, and abrogates the tyrosine phosphorylation of STAT1 and STAT3.	Tyrosine	166-174	P53	Homo sapiens	93-96
24874727-4	2014	We have previously reported that Zn(II) restores a folded conformation from mutp53 misfolding, rescuing wild-type (wt) p53/DNA-binding and transcription activities.	Zinc	33-39	P53	Homo sapiens	79-82
24874727-9	2014	Mechanistically, Zn(II) restored the wtp53 ability to induce the expression of the p53 target gene DRAM (damage-regulated autophagy modulator), a key regulator of autophagy, leading to autophagic induction.	Zinc	17-23	P53	Homo sapiens	39-42
24875531-8	2014	Our data suggest that RP loss promotes the aberrant activation of both S6 kinase and p53 by increasing intracellular ROS levels.	Reactive Oxygen Species	117-120	P53	Homo sapiens	85-88
24831807-0	2014	Interactions between exosomes from breast cancer cells and primary mammary epithelial cells leads to generation of reactive oxygen species which induce DNA damage response, stabilization of p53 and autophagy in epithelial cells.	Reactive Oxygen Species	115-138	P53	Homo sapiens	190-193
24845634-10	2014	RESULTS: Pulsed H2O2 exposure triggered the acetylation of p53 at lysine 382 (K382) and subsequent increase in its target p21(Waf1/Cip1).	Hydrogen Peroxide	16-20	P53	Homo sapiens	59-62
24845634-10	2014	RESULTS: Pulsed H2O2 exposure triggered the acetylation of p53 at lysine 382 (K382) and subsequent increase in its target p21(Waf1/Cip1).	Lysine	66-72	P53	Homo sapiens	59-62
24835245-6	2014	We also found that HIF-1alpha does not contribute to the protection against DNA damage that can be observed in low oxygen environments, and that there are certain DNA damaging agents, such as doxorubicin and actinomycin D, that prevent HIF-1alpha induction independently of p53.	Doxorubicin	192-203	P53	Homo sapiens	274-277
24940547-3	2014	From the Arrhenius behavior, we find the energy barrier to unzipping introduced by p53 to be 2 x 10(-20) J, whereas cys135ser mutant p53 does not show suppression of unzipping, which gives clues to its functional inability to suppress tumor growth.	cys135ser	116-125	P53	Homo sapiens	133-136
24657665-3	2014	The G to T transversion at the third position of codon 249 (AGG) of the TP53 gene, substituting arginine to serine, is the most common aflatoxin-induced mutation linked to HCC.	Arginine	96-104	P53	Homo sapiens	72-76
24657665-3	2014	The G to T transversion at the third position of codon 249 (AGG) of the TP53 gene, substituting arginine to serine, is the most common aflatoxin-induced mutation linked to HCC.	Serine	108-114	P53	Homo sapiens	72-76
24831807-10	2014	Under these conditions, phosphorylation of p53 at serine 15 was also observed.	Serine	50-56	P53	Homo sapiens	43-46
24714748-10	2014	RESULTS: We found that WT-p53 is a potent suppressor of TGF-beta-induced Nox4, ROS production, and cell migration in p53-null lung epithelial (H1299) cells.	Reactive Oxygen Species	79-82	P53	Homo sapiens	26-29
24819061-6	2014	Unexpectedly, however, we uncovered a novel role for p53 in the regulation of cancer cell NAD(+) and its reduced form NADH.	NAD	90-96	P53	Homo sapiens	53-56
24829158-4	2014	CDDP induced apoptosis within cells through the generation of reactive oxygen species (ROS), regulated the ROS-mediated expression of Bax, Bcl-2, and p53, and induced the degradation of the poly (ADP-ribosyl) polymerase (PARP).	Cisplatin	0-4	P53	Homo sapiens	150-153
24829158-4	2014	CDDP induced apoptosis within cells through the generation of reactive oxygen species (ROS), regulated the ROS-mediated expression of Bax, Bcl-2, and p53, and induced the degradation of the poly (ADP-ribosyl) polymerase (PARP).	Reactive Oxygen Species	107-110	P53	Homo sapiens	150-153
24819061-6	2014	Unexpectedly, however, we uncovered a novel role for p53 in the regulation of cancer cell NAD(+) and its reduced form NADH.	NAD	118-122	P53	Homo sapiens	53-56
24819061-7	2014	Thus, LDH-A silencing by RNAi, or its inhibition using a small-molecule inhibitor, resulted in a p53-dependent increase in the cancer cell ratio of NADH:NAD(+).	NAD	148-152	P53	Homo sapiens	97-100
24819061-7	2014	Thus, LDH-A silencing by RNAi, or its inhibition using a small-molecule inhibitor, resulted in a p53-dependent increase in the cancer cell ratio of NADH:NAD(+).	NAD	153-159	P53	Homo sapiens	97-100
24819061-8	2014	This effect was specific for p53(+/+) cancer cells and correlated with (i) reduced activity of NAD(+)-dependent deacetylase sirtuin 1 (SIRT1) and (ii) an increase in acetylated p53, a known target of SIRT1 deacetylation activity.	NAD	95-101	P53	Homo sapiens	29-32
24819061-11	2014	Our results identify a unique strategy by which the NADH/NAD(+) cellular redox status can be modulated in a cancer-specific, p53-dependent manner and we show that this can impact upon the activity of important NAD(H)-dependent enzymes.	NAD	52-56	P53	Homo sapiens	125-128
24819061-11	2014	Our results identify a unique strategy by which the NADH/NAD(+) cellular redox status can be modulated in a cancer-specific, p53-dependent manner and we show that this can impact upon the activity of important NAD(H)-dependent enzymes.	NAD	57-63	P53	Homo sapiens	125-128
24819061-11	2014	Our results identify a unique strategy by which the NADH/NAD(+) cellular redox status can be modulated in a cancer-specific, p53-dependent manner and we show that this can impact upon the activity of important NAD(H)-dependent enzymes.	NAD	210-216	P53	Homo sapiens	125-128
24632713-3	2014	The present results demonstrate that GO-203 and BTZ synergistically downregulate expression of the p53-inducible regulator of glycolysis and apoptosis (TIGAR), which promotes shunting of glucose-6-phosphate into the pentose phosphate pathway to generate reduced glutathione (GSH).	Glutathione	262-273	P53	Homo sapiens	99-102
24810057-3	2014	Particularly, the phosphorylation at serine-46 of p53 is indispensable in promoting pro-apoptotic genes that are, however, poorly determined.	Serine	37-43	P53	Homo sapiens	50-53
24632713-3	2014	The present results demonstrate that GO-203 and BTZ synergistically downregulate expression of the p53-inducible regulator of glycolysis and apoptosis (TIGAR), which promotes shunting of glucose-6-phosphate into the pentose phosphate pathway to generate reduced glutathione (GSH).	Glutathione	275-278	P53	Homo sapiens	99-102
24810057-4	2014	In the current study, we identified palmdelphin as a pro-apoptotic gene induced by p53 in a phosphorylated serine-46-specific manner.	Serine	107-113	P53	Homo sapiens	83-86
24810057-10	2014	These findings define palmdelphin as a target of serine-46-phosphorylated p53 that controls cell death in response to DNA damage.	Serine	49-55	P53	Homo sapiens	74-77
24843801-7	2014	There is a statistically significant association between p53 codon 72 polymorphism and allergic asthma: Arg/Arg genotype is more represented in asthmatic patients than in controls (P=0.018).	Arginine	104-107	P53	Homo sapiens	57-60
24746804-4	2014	Met deprivation results in a rapid decrease in intracellular S-adenosylmethionine (SAM), triggering the activation of p53-p38 signaling, reducing NANOG expression, and poising human iPSC/ESCs for differentiation, follow by potentiated differentiation into all three germ layers.	S-Adenosylmethionine	83-86	P53	Homo sapiens	118-121
24813712-3	2014	Here, we show that following phosphorylation by the ataxia telangiectasia mutated (ATM) kinase at serine 403, the C-terminal RING domain of HDMX binds the nascent p53 mRNA to promote a conformation that supports the p53 mRNA-HDM2 interaction and the induction of p53 synthesis.	Serine	98-104	P53	Homo sapiens	163-166
24813712-3	2014	Here, we show that following phosphorylation by the ataxia telangiectasia mutated (ATM) kinase at serine 403, the C-terminal RING domain of HDMX binds the nascent p53 mRNA to promote a conformation that supports the p53 mRNA-HDM2 interaction and the induction of p53 synthesis.	Serine	98-104	P53	Homo sapiens	216-219
24813712-3	2014	Here, we show that following phosphorylation by the ataxia telangiectasia mutated (ATM) kinase at serine 403, the C-terminal RING domain of HDMX binds the nascent p53 mRNA to promote a conformation that supports the p53 mRNA-HDM2 interaction and the induction of p53 synthesis.	Serine	98-104	P53	Homo sapiens	216-219
24843801-7	2014	There is a statistically significant association between p53 codon 72 polymorphism and allergic asthma: Arg/Arg genotype is more represented in asthmatic patients than in controls (P=0.018).	Arginine	108-111	P53	Homo sapiens	57-60
24480460-5	2014	Treatment of cells overexpressing Aurora-A and ATM/Chk2 with the ATM specific inhibitor KU-55933 increased the cell sensitivity to cisplatin and irradiation through increasing the phosphorylation of p53 at Ser15 and inhibiting the expression of Chk2, gammaH2AX (Ser319), and RAD51.	Cisplatin	131-140	P53	Homo sapiens	199-202
24368645-5	2014	Mutational analysis of p53 and EGFR was performed on DNA extracted from paraffin-embedded tumors.	Paraffin	72-80	P53	Homo sapiens	23-26
24462821-0	2014	Inhibition of p53 increases chemosensitivity to 5-FU in nutrient-deprived hepatocarcinoma cells by suppressing autophagy.	Fluorouracil	48-52	P53	Homo sapiens	14-17
24462821-3	2014	In this study, we show that inhibition of p53 enhanced apoptosis and increased chemosensitivity to 5-fluorouracil (5-FU) in nutrient-deprived hepatocarcinoma cells (HCC).	Fluorouracil	99-113	P53	Homo sapiens	42-45
24462821-3	2014	In this study, we show that inhibition of p53 enhanced apoptosis and increased chemosensitivity to 5-fluorouracil (5-FU) in nutrient-deprived hepatocarcinoma cells (HCC).	Fluorouracil	115-119	P53	Homo sapiens	42-45
24462821-7	2014	Furthermore, combining p53 inhibition and nutrient deprivation or 5-FU treatment resulted in a marked increase in reactive oxygen species generation and mitochondrial damage.	Reactive Oxygen Species	114-137	P53	Homo sapiens	23-26
24462821-8	2014	Antioxidants reduced nutrient deprivation or 5-FU-induced cell death of HCC after p53 inhibition.	Fluorouracil	45-49	P53	Homo sapiens	82-85
24843889-0	2014	Berberine induces apoptosis in human multiple myeloma cell line U266 through hypomethylation of p53 promoter.	Berberine	0-9	P53	Homo sapiens	96-99
24633296-5	2014	We describe here an MHC class II binding peptide from the tumor protein p53, which possesses an acetylated lysine at position 120 (p53110-124/AcK120) that is effective in eliciting CD4(+) T cell responses specific for the acetylated peptide.	Lysine	107-113	P53	Homo sapiens	72-75
24843889-6	2014	By using epigenetic chromatin modification enzymes PCR Array, gene expression microarray, RT-PCR and Bisulphite sequencing, the results show that berberine can repress the expression of DNMT1 and DNMT3B, which triggers hypomethylation of TP53 by changing the DNA methylation level and the alteration of p53 dependent signal pathway in human multiple melanoma cell U266.	Berberine	146-155	P53	Homo sapiens	238-242
24787013-6	2014	EBV sensitized TP53-mutated BL cells to all spindle poisons tested, including vincristine and taxol, an effect that was systematically downmodulated by pretreatment of cells with inhibitors of p38 and c-Jun N-terminal kinase (JNK) mitogen-activated protein kinases.	Paclitaxel	94-99	P53	Homo sapiens	15-19
24843889-6	2014	By using epigenetic chromatin modification enzymes PCR Array, gene expression microarray, RT-PCR and Bisulphite sequencing, the results show that berberine can repress the expression of DNMT1 and DNMT3B, which triggers hypomethylation of TP53 by changing the DNA methylation level and the alteration of p53 dependent signal pathway in human multiple melanoma cell U266.	Berberine	146-155	P53	Homo sapiens	303-306
24765160-0	2014	Damnacanthal is a potent inducer of apoptosis with anticancer activity by stimulating p53 and p21 genes in MCF-7 breast cancer cells.	damnacanthal	0-12	P53	Homo sapiens	86-89
24528089-6	2014	By employing the quantitative chromatin immunoprecipitation assay in detecting specific histone modifications in senescence-related genes including p53 and p16, it was demonstrated that the mRNA expression of p53 was associated with increased H4 acetylation in replicative senescence and increased H4 acetylation and trimethylation of histone H3 at lysine 4 (H3K4me3) in premature senescence.	Lysine	349-355	P53	Homo sapiens	148-151
24528089-6	2014	By employing the quantitative chromatin immunoprecipitation assay in detecting specific histone modifications in senescence-related genes including p53 and p16, it was demonstrated that the mRNA expression of p53 was associated with increased H4 acetylation in replicative senescence and increased H4 acetylation and trimethylation of histone H3 at lysine 4 (H3K4me3) in premature senescence.	Lysine	349-355	P53	Homo sapiens	209-212
24626522-5	2014	This flavone also suppressed the expression of both cyclin B1 and its activating partners, Cdc2 and Cdc25c, whereas the expression of cell cycle inhibitors, such as p53 and p53-dependent p21(CIP1/WAF1), was increased after apigenin treatment.	flavone	5-12	P53	Homo sapiens	173-176
24548601-1	2014	BACKGROUND: Together with p53, the NAD-dependent lysine deacetylase SIRT1 and the microRNA miR-34a form a feedback loop which self-regulates SIRT1 expression and modulates p53-dependent responses.	NAD	35-38	P53	Homo sapiens	26-29
24548601-1	2014	BACKGROUND: Together with p53, the NAD-dependent lysine deacetylase SIRT1 and the microRNA miR-34a form a feedback loop which self-regulates SIRT1 expression and modulates p53-dependent responses.	NAD	35-38	P53	Homo sapiens	172-175
24727577-12	2014	These findings show that CPF induced hNPCs death in part through NF-kappaB activation via ROS generation, enabling the interaction of p53 with Bcl-2 and Bax and subsequent release of cytochrome c.	Reactive Oxygen Species	90-93	P53	Homo sapiens	134-137
24765160-7	2014	Furthermore, damnacanthal-mediated apoptosis involves the sustained activation of p21, leading to the transcription of p53 and the Bax gene.	damnacanthal	13-25	P53	Homo sapiens	119-122
24765160-8	2014	Overall, the present study provided significant evidence demonstrating that p53-mediated damnacanthal induced apoptosis through the activation of p21 and caspase-7.	damnacanthal	89-101	P53	Homo sapiens	76-79
23999197-8	2014	Accordingly, the improvement of insulin sensitivity with surgery-induced weight loss (+51%, P=0.01) and metformin (+42%, P=0.02) led to increased adipose p53.	Metformin	104-113	P53	Homo sapiens	154-157
23999197-9	2014	While the glucose-intolerant GLP-1R KO mice showed decreased mesenteric p53 (-45.4%, P=0.017), high glucose led to decreased p53 in pre-adipocytes (-27%, P&lt;0.0001).	Glucose	10-17	P53	Homo sapiens	72-75
23999197-9	2014	While the glucose-intolerant GLP-1R KO mice showed decreased mesenteric p53 (-45.4%, P=0.017), high glucose led to decreased p53 in pre-adipocytes (-27%, P&lt;0.0001).	Glucose	100-107	P53	Homo sapiens	125-128
24634414-2	2014	In this article, we show that overexpression of the MT1G isoform sensitizes colorectal cell lines to the chemotherapeutic agents oxaliplatin (OXA) and 5-fluorouracil (5-FU), in part through enhancing p53 and repressing NF-kappaB activity.	Fluorouracil	151-165	P53	Homo sapiens	200-203
24634414-6	2014	We show for the first time that OXA and 5-FU induce higher levels of intracellular labile zinc, as measured using the fluorescent probe FLUOZIN-3, and that such zinc contributes to the activation of p53 and repression of NF-kappaB.	Fluorouracil	40-44	P53	Homo sapiens	199-202
24495481-0	2014	Significance of TP53 mutations as predictive markers of adjuvant cisplatin-based chemotherapy in completely resected non-small-cell lung cancer.	Cisplatin	65-74	P53	Homo sapiens	16-20
24604218-10	2014	Immunoblotting revealed the Bid and Bcl-2 proteins to be downregulated, and truncated-Bid, Bax and p53 proteins to be upregulated by curcumin and EF-24.	Curcumin	133-141	P53	Homo sapiens	99-102
24491546-6	2014	PEITC enhances TRAIL-induced apoptosis through the downregulation of cell survival proteins and the upregulation of DR5 receptors through actions on the ROS-induced-p53.	ros	153-156	P53	Homo sapiens	165-168
24399651-0	2014	The impact of arsenic trioxide and all-trans retinoic acid on p53 R273H-codon mutant glioblastoma.	Tretinoin	45-58	P53	Homo sapiens	62-65
24399651-6	2014	The results showed that U87-p53(R273H) cells generated more rapid neurosphere growth than U87-p53(wt) but inhibition of neurosphere proliferation was seen with both ATO and ATRA.	Tretinoin	173-177	P53	Homo sapiens	28-31
24399651-7	2014	U87-p53(R273H) neurospheres showed resistance to differentiation into glial cells and neuronal cells with ATO and ATRA exposure.	Tretinoin	114-118	P53	Homo sapiens	4-7
24399651-8	2014	ATO was able to generate apoptosis at high doses and proliferation of U87-p53(wt) and U87-p53(R273H) cells was reduced with ATO and ATRA in a dose-dependent manner.	Tretinoin	132-136	P53	Homo sapiens	74-77
24399651-8	2014	ATO was able to generate apoptosis at high doses and proliferation of U87-p53(wt) and U87-p53(R273H) cells was reduced with ATO and ATRA in a dose-dependent manner.	Tretinoin	132-136	P53	Homo sapiens	90-93
24399651-9	2014	Elevated pERK1/2 and p53 expression was seen in U87-p53(R273H) neurospheres, which could be reduced with ATO and ATRA treatment.	Tretinoin	113-117	P53	Homo sapiens	21-24
24399651-9	2014	Elevated pERK1/2 and p53 expression was seen in U87-p53(R273H) neurospheres, which could be reduced with ATO and ATRA treatment.	Tretinoin	113-117	P53	Homo sapiens	52-55
24810255-9	2014	Obviously, p53 protects cells from the cytotoxicity of Enzastaurin in combination with SBE13.	SBE13	87-92	P53	Homo sapiens	11-14
24799992-9	2014	Melatonin reduced cisplatin-induced cell death, decreasing phosphorylated p53 apoptotic protein, cleaved caspase 3 and Bax levels but increasing anti-apoptotic Bcl-2 gene and protein expression.	Melatonin	0-9	P53	Homo sapiens	74-77
24759730-0	2014	Non-thermal atmospheric pressure plasma preferentially induces apoptosis in p53-mutated cancer cells by activating ROS stress-response pathways.	Reactive Oxygen Species	115-118	P53	Homo sapiens	76-79
24759730-5	2014	The apoptotic effect of NTAPP was greater for p53-mutated cancer cells; artificial p53 expression in p53-negative HT29 cells decreased the pro-apoptotic effect of NTAPP.	Plasma Gases	24-29	P53	Homo sapiens	46-49
24759730-5	2014	The apoptotic effect of NTAPP was greater for p53-mutated cancer cells; artificial p53 expression in p53-negative HT29 cells decreased the pro-apoptotic effect of NTAPP.	Plasma Gases	163-168	P53	Homo sapiens	83-86
24759730-5	2014	The apoptotic effect of NTAPP was greater for p53-mutated cancer cells; artificial p53 expression in p53-negative HT29 cells decreased the pro-apoptotic effect of NTAPP.	Plasma Gases	163-168	P53	Homo sapiens	83-86
24759730-10	2014	Collectively, these results strongly support the potential of NTAPP as a selective anticancer treatment, especially for p53-mutated cancer cells.	Plasma Gases	62-67	P53	Homo sapiens	120-123
24519527-3	2014	We recently demonstrated that a combination of sodium arsenite (NaAsO2) and hyperthermia sensitizes p53-expressing ovarian cancer cells to cisplatin by modulating DNA repair pathway and enhancing platinum accumulation.	Cisplatin	139-148	P53	Homo sapiens	100-103
24766860-0	2014	p38alpha MAPK-mediated induction and interaction of FOXO3a and p53 contribute to the inhibited-growth and induced-apoptosis of human lung adenocarcinoma cells by berberine.	Berberine	162-171	P53	Homo sapiens	63-66
24766860-9	2014	Interestingly, inhibition of p53 using one specific inhibitor (Pifithrin-alpha) and silencing of p53 using siRNAs overcome the inhibitory effect of BBR on cell growth.	Berberine	148-151	P53	Homo sapiens	97-100
24743574-15	2014	Taken together, combined treatment with NVP-BEZ235 and curcumin induces apoptosis through p53-dependent Bcl-2 mRNA down-regulation at the transcriptional level and Mcl-1 protein down-regulation at the post-transcriptional level.	Curcumin	55-63	P53	Homo sapiens	90-93
24747975-0	2014	Evaluating the association between p53 codon 72 Arg&gt;pro polymorphism and risk of ovary cancer: a meta-analysis.	Arginine	48-51	P53	Homo sapiens	35-38
24747975-3	2014	Therefore, we performed this meta-analysis to investigate the relation between p53 codon 72 Arg&gt;Pro polymorphism and overall OC susceptibility.	Arginine	92-95	P53	Homo sapiens	79-82
24747975-4	2014	METHODS: We searched all eligible published studies based on the association between codon 72 of the p53 Arg&gt;Pro polymorphism and risk of OC.	Arginine	105-108	P53	Homo sapiens	101-104
24747975-10	2014	CONCLUSIONS: This meta-analysis suggested that codon 72 of the p53 Arg&gt;Pro polymorphism may not significantly contribute in ovary cancer susceptibility.	Arginine	67-70	P53	Homo sapiens	63-66
24743574-0	2014	Curcumin significantly enhances dual PI3K/Akt and mTOR inhibitor NVP-BEZ235-induced apoptosis in human renal carcinoma Caki cells through down-regulation of p53-dependent Bcl-2 expression and inhibition of Mcl-1 protein stability.	Curcumin	0-8	P53	Homo sapiens	157-160
24743574-11	2014	Combined treatment with NVP-BEZ235 and curcumin reduced Bcl-2 expression in wild-type p53 HCT116 human colon carcinoma cells but not p53-null HCT116 cells.	Curcumin	39-47	P53	Homo sapiens	86-89
24656661-0	2014	Core modification of substituted piperidines as novel inhibitors of HDM2-p53 protein-protein interaction.	Piperidines	33-44	P53	Homo sapiens	73-76
24733045-0	2014	JNK confers 5-fluorouracil resistance in p53-deficient and mutant p53-expressing colon cancer cells by inducing survival autophagy.	Fluorouracil	12-26	P53	Homo sapiens	41-44
24733045-6	2014	Inhibition of JNK by the compound SP600125 or JNK siRNA suppressed autophagy and phosphorylation of c-Jun and Bcl-2 but increased 5-FU-induced apoptosis in both HCT116 p53(-/-) and HT29 cells.	Fluorouracil	130-134	P53	Homo sapiens	168-171
24733045-0	2014	JNK confers 5-fluorouracil resistance in p53-deficient and mutant p53-expressing colon cancer cells by inducing survival autophagy.	Fluorouracil	12-26	P53	Homo sapiens	66-69
24733045-7	2014	Taken together, our results suggest that JNK activation confers 5-FU resistance in HCT116 p53(-/-) and HT29 cells by promoting autophagy as a pro-survival effect, likely via inducing Bcl-2 phosphorylation.	Fluorouracil	64-68	P53	Homo sapiens	90-93
24733045-8	2014	These results provide a promising strategy to improve the efficacy of 5-FU-based chemotherapy for colorectal cancer patients harboring a p53 gene mutation.	Fluorouracil	70-74	P53	Homo sapiens	137-140
24733045-3	2014	Here we report that 5-FU treatment causes aberrant autophagosome accumulation in HCT116 p53(-/-) and HT-29 cancer cells.	Fluorouracil	20-24	P53	Homo sapiens	88-91
24601644-0	2014	Novel inhibitors of the MDM2-p53 interaction featuring hydrogen bond acceptors as carboxylic acid isosteres.	Hydrogen	55-63	P53	Homo sapiens	29-32
24601644-1	2014	We previously reported the discovery of potent and selective morpholinone and piperidinone inhibitors of the MDM2-p53 interaction.	Morpholin-3-one	61-73	P53	Homo sapiens	114-117
24685134-0	2014	Iron metabolism regulates p53 signaling through direct heme-p53 interaction and modulation of p53 localization, stability, and function.	Iron	0-4	P53	Homo sapiens	26-29
24717393-5	2014	Our results further demonstrated that this antitumor activity was caused by the activation of the p53-dependent apoptosis pathway via p53 phosphorylation at serine (15Ser).	Serine	157-163	P53	Homo sapiens	98-101
24685134-0	2014	Iron metabolism regulates p53 signaling through direct heme-p53 interaction and modulation of p53 localization, stability, and function.	Iron	0-4	P53	Homo sapiens	60-63
24685134-0	2014	Iron metabolism regulates p53 signaling through direct heme-p53 interaction and modulation of p53 localization, stability, and function.	Iron	0-4	P53	Homo sapiens	60-63
24685134-3	2014	Here, we report that the tumor suppressor protein p53 is downregulated during iron excess.	Iron	78-82	P53	Homo sapiens	50-53
24685134-5	2014	Moreover, in a tumorigenicity assay, iron deprivation suppressed wild-type p53-dependent tumor growth, suggesting that upregulation of wild-type p53 signaling underlies the selective efficacy of iron deprivation.	Iron	37-41	P53	Homo sapiens	75-78
24685134-5	2014	Moreover, in a tumorigenicity assay, iron deprivation suppressed wild-type p53-dependent tumor growth, suggesting that upregulation of wild-type p53 signaling underlies the selective efficacy of iron deprivation.	Iron	37-41	P53	Homo sapiens	145-148
24685134-5	2014	Moreover, in a tumorigenicity assay, iron deprivation suppressed wild-type p53-dependent tumor growth, suggesting that upregulation of wild-type p53 signaling underlies the selective efficacy of iron deprivation.	Iron	195-199	P53	Homo sapiens	75-78
24685134-5	2014	Moreover, in a tumorigenicity assay, iron deprivation suppressed wild-type p53-dependent tumor growth, suggesting that upregulation of wild-type p53 signaling underlies the selective efficacy of iron deprivation.	Iron	195-199	P53	Homo sapiens	145-148
24685134-6	2014	Our findings thus identify a direct link between iron/heme homeostasis and the regulation of p53 signaling, which not only provides mechanistic insights into iron-excess-associated tumorigenesis but may also help predict and improve outcomes in iron-deprivation-based chemotherapy.	Iron	49-53	P53	Homo sapiens	93-96
24685134-6	2014	Our findings thus identify a direct link between iron/heme homeostasis and the regulation of p53 signaling, which not only provides mechanistic insights into iron-excess-associated tumorigenesis but may also help predict and improve outcomes in iron-deprivation-based chemotherapy.	Iron	158-162	P53	Homo sapiens	93-96
24685134-6	2014	Our findings thus identify a direct link between iron/heme homeostasis and the regulation of p53 signaling, which not only provides mechanistic insights into iron-excess-associated tumorigenesis but may also help predict and improve outcomes in iron-deprivation-based chemotherapy.	Iron	158-162	P53	Homo sapiens	93-96
24748790-1	2014	p28 is an anionic, amphipathic, cell-penetrating peptide derived from the cupredoxin azurin that binds to the DNA-binding domain (DBD) of the tumor suppressor protein, p53, and induces a post-translational increase in the level of wild type and mutated p53 in a wide variety of human cancer cells.	cupredoxin azurin	74-91	P53	Homo sapiens	168-171
24748790-1	2014	p28 is an anionic, amphipathic, cell-penetrating peptide derived from the cupredoxin azurin that binds to the DNA-binding domain (DBD) of the tumor suppressor protein, p53, and induces a post-translational increase in the level of wild type and mutated p53 in a wide variety of human cancer cells.	cupredoxin azurin	74-91	P53	Homo sapiens	253-256
24782773-4	2014	METHODS: The ability of adenosine to regulate p53 and Rb protein levels, proliferation, apoptosis and senescence was tested in the human HSC cell line LX-2 and rat primary HSC.	Adenosine	24-33	P53	Homo sapiens	46-49
24657168-3	2014	The inositol pyrophosphates, such as 5-diphosphoinositol pentakisphosphate (IP7), are generated by a family of inositol hexakisphosphate kinases (IP6Ks), of which IP6K2 has been implicated in p53-associated cell death.	ip7	76-79	P53	Homo sapiens	192-195
24657168-6	2014	This process stimulates p53 phosphorylation at serine 15 to activate the cell death program in human cancer cells and in murine B cells.	Serine	47-53	P53	Homo sapiens	24-27
24717393-5	2014	Our results further demonstrated that this antitumor activity was caused by the activation of the p53-dependent apoptosis pathway via p53 phosphorylation at serine (15Ser).	Serine	157-163	P53	Homo sapiens	134-137
24555485-0	2014	Synergistic induction of apoptosis by methylseleninic acid and cisplatin, the role of ROS-ERK/AKT-p53 pathway.	methylselenic acid	38-58	P53	Homo sapiens	98-101
24555485-0	2014	Synergistic induction of apoptosis by methylseleninic acid and cisplatin, the role of ROS-ERK/AKT-p53 pathway.	ros	86-89	P53	Homo sapiens	98-101
24381013-6	2014	p53 affects many aspects of cellular metabolism including catabolism, anabolism and reactive oxygen species levels.	Reactive Oxygen Species	84-107	P53	Homo sapiens	0-3
24692714-4	2014	TMC caused DNA double-strand breaks, and enhanced expression of caspase-3 and -9, poly (ADP-ribose) polymerase, cytochrome c, calpain-1 and -2, phosphorylation of histone H2AX, phosphorylation of checkpoint kinases 2, p53, BCL2-antagonist/killer and BCL2-associated x protein, while reducing the mitochondrial membrane potential, and expression of B-cell lymphoma-2.	tmc	0-3	P53	Homo sapiens	218-221
24384472-8	2014	Through this study, we have provided the first evidence on the pivotal role of arginine 213 that determines the p53 mediated functions of p21 in human cancer cells.	Arginine	79-87	P53	Homo sapiens	112-115
24736075-3	2014	As dexamethasone strongly regulates many genes including p53 through the glucocorticoid receptor (GR), we hypothesized that dexamethasone influences tumor response to pemetrexed.	Dexamethasone	3-16	P53	Homo sapiens	57-60
24535669-0	2014	Quercetin regulates the sestrin 2-AMPK-p38 MAPK signaling pathway and induces apoptosis by increasing the generation of intracellular ROS in a p53-independent manner.	Reactive Oxygen Species	134-137	P53	Homo sapiens	143-146
24959493-3	2014	In chronic hypoxia, there is a liberation of Reactive Oxygen Species (ROS) due to tissue injury as a result of ischemia and induction of hypoxia inducible factor - 1HIF-1 and p53 which in turn activates pro-apoptotic factors leading to alteration in the regulation of pro-apoptotic gene Blc-2 to be involved in causing the DNA damage.	Reactive Oxygen Species	45-68	P53	Homo sapiens	175-178
24959493-3	2014	In chronic hypoxia, there is a liberation of Reactive Oxygen Species (ROS) due to tissue injury as a result of ischemia and induction of hypoxia inducible factor - 1HIF-1 and p53 which in turn activates pro-apoptotic factors leading to alteration in the regulation of pro-apoptotic gene Blc-2 to be involved in causing the DNA damage.	Reactive Oxygen Species	70-73	P53	Homo sapiens	175-178
24521534-6	2014	Although p53 mutations were associated with tobacco smoking and alcohol drinking, this association disappeared in virus-unrelated HNSCC.	Alcohols	64-71	P53	Homo sapiens	9-12
24413150-0	2014	ROS-dependent activation of JNK converts p53 into an efficient inhibitor of oncogenes leading to robust apoptosis.	Reactive Oxygen Species	0-3	P53	Homo sapiens	41-44
24413150-4	2014	Here, we report that concurrent pharmacological activation of p53 and inhibition of thioredoxin reductase followed by generation of reactive oxygen species (ROS), result in the synthetic lethality in cancer cells.	Reactive Oxygen Species	132-155	P53	Homo sapiens	62-65
24413150-4	2014	Here, we report that concurrent pharmacological activation of p53 and inhibition of thioredoxin reductase followed by generation of reactive oxygen species (ROS), result in the synthetic lethality in cancer cells.	Reactive Oxygen Species	157-160	P53	Homo sapiens	62-65
24413150-5	2014	ROS promote the activation of c-Jun N-terminal kinase (JNK) and DNA damage response, which establishes a positive feedback loop with p53.	Reactive Oxygen Species	0-3	P53	Homo sapiens	133-136
24413150-10	2014	Further, our results may enable new pharmacological strategy to exploit abnormally high ROS level, often linked with higher aggressiveness in cancer, to selectively kill cancer cells upon pharmacological reactivation of p53.	Reactive Oxygen Species	88-91	P53	Homo sapiens	220-223
26005655-3	2014	Although some studies have indicated an association between the TP53 Arg/Arg variant and an increased risk for prostate cancer, other studies have shown a positive correlation between the TP53 Pro/Pro genotype instead.	Arginine	69-72	P53	Homo sapiens	64-68
26005655-3	2014	Although some studies have indicated an association between the TP53 Arg/Arg variant and an increased risk for prostate cancer, other studies have shown a positive correlation between the TP53 Pro/Pro genotype instead.	Arginine	73-76	P53	Homo sapiens	64-68
24736075-3	2014	As dexamethasone strongly regulates many genes including p53 through the glucocorticoid receptor (GR), we hypothesized that dexamethasone influences tumor response to pemetrexed.	Dexamethasone	124-137	P53	Homo sapiens	57-60
24504010-7	2014	Genes with expression changed by drugs were related to GO term "extracellular region" and "p53 signaling pathway" in both 5-FU- and CDDP-treated cells.	Fluorouracil	122-126	P53	Homo sapiens	91-94
24473091-11	2014	The decrease in CAK activity was determined by observing the intensity of Ser(392) phosphorylation in p53, in vitro, which decreased with an increase in arsenic dose.	Serine	74-77	P53	Homo sapiens	102-105
24615009-7	2014	Notably, patients with TP53 mutation and the Pro72 allele experienced a 23.7-fold increase in hazard ratio (95% CI 3.38-165.9; P = 0.001) for OS compared with patients with wild-type p53 and those with the Arg/Arg genotype.	Arginine	206-209	P53	Homo sapiens	23-27
24615009-7	2014	Notably, patients with TP53 mutation and the Pro72 allele experienced a 23.7-fold increase in hazard ratio (95% CI 3.38-165.9; P = 0.001) for OS compared with patients with wild-type p53 and those with the Arg/Arg genotype.	Arginine	210-213	P53	Homo sapiens	23-27
24343341-0	2014	The mitochondrial cyclophilin D/p53 complexation mediates doxorubicin-induced non-apoptotic death of A549 lung cancer cells.	Doxorubicin	58-69	P53	Homo sapiens	32-35
24343341-2	2014	In the current study, we provided evidence to show that mitochondrial p53 and cyclophilin D (Cyp-D) complexation is required for doxorubicin-induced death of lung cancer A549 cells.	Doxorubicin	129-140	P53	Homo sapiens	70-73
24343341-5	2014	In A549 cells, doxorubicin-activated p53, the latter translocated to mitochondria and physically interacted with Cyp-D.	Doxorubicin	15-26	P53	Homo sapiens	37-40
24343341-8	2014	Together, these data suggested that Dox-induced non-apoptotic death of A549 cells requires mitochondrial Cyp-D-p53 complexation.	Doxorubicin	36-39	P53	Homo sapiens	111-114
24504010-7	2014	Genes with expression changed by drugs were related to GO term "extracellular region" and "p53 signaling pathway" in both 5-FU- and CDDP-treated cells.	Cisplatin	132-136	P53	Homo sapiens	91-94
24787294-2	2014	Genetic changes in the carcinoma cells, such as alterations to TP53, NOTCH1, and specific gene expression profiles, contribute to derangements in cancer and microenvironment cells such as increased ROS, overproduction of cytokines, and epithelial to mesenchymal transition (EMT).	ros	198-201	P53	Homo sapiens	63-67
24691158-0	2014	Uncovering the basis of ATP hydrolysis activity in purified human p53 protein: a reinvestigation.	Adenosine Triphosphate	24-27	P53	Homo sapiens	66-69
24691158-3	2014	ATP binding/hydrolysis by p53 had been implicated in its DNA binding functions.	Adenosine Triphosphate	0-3	P53	Homo sapiens	26-29
24691158-4	2014	However, till date, no ATP binding/hydrolysis domains have been mapped in p53.	Adenosine Triphosphate	23-26	P53	Homo sapiens	74-77
24691158-5	2014	In the current study, we have reinvestigated the ATP hydrolysis activity associated with recombinant human p53 protein expressed and purified from E.coli.	Adenosine Triphosphate	49-52	P53	Homo sapiens	107-110
24565839-0	2014	p53 down-regulates SETDB1 gene expression during paclitaxel induced-cell death.	Paclitaxel	49-59	P53	Homo sapiens	0-3
24326769-0	2014	The association between polymorphism of P53 Codon72 Arg/Pro and hepatocellular carcinoma susceptibility: evidence from a meta-analysis of 15 studies with 3,704 cases.	Arginine	52-55	P53	Homo sapiens	40-43
24326769-2	2014	Polymorphism of p53 gene codon72 arginine (Arg)/proline (Pro) (rs1042522) may influence the function of p53 protein and then affect the processing of carcinogenesis.	Arginine	33-41	P53	Homo sapiens	16-19
24326769-2	2014	Polymorphism of p53 gene codon72 arginine (Arg)/proline (Pro) (rs1042522) may influence the function of p53 protein and then affect the processing of carcinogenesis.	Arginine	33-41	P53	Homo sapiens	104-107
24326769-2	2014	Polymorphism of p53 gene codon72 arginine (Arg)/proline (Pro) (rs1042522) may influence the function of p53 protein and then affect the processing of carcinogenesis.	Arginine	43-46	P53	Homo sapiens	16-19
24326769-2	2014	Polymorphism of p53 gene codon72 arginine (Arg)/proline (Pro) (rs1042522) may influence the function of p53 protein and then affect the processing of carcinogenesis.	Arginine	43-46	P53	Homo sapiens	104-107
24326769-3	2014	It has been suggested that p53 codon72 Arg/Pro polymorphism is associated with susceptibility to hepatocellular carcinoma (HCC).	Arginine	39-42	P53	Homo sapiens	27-30
24326769-10	2014	This meta-analysis suggests that p53 codon72 Arg/Pro polymorphism may be associated with the risk of HCC, especially in subgroup analysis of Asian and Caucasian population, hospital-based population, the female, and the individuals infected with hepatitis virus.	Arginine	45-48	P53	Homo sapiens	33-36
24548297-0	2014	Selective and potent morpholinone inhibitors of the MDM2-p53 protein-protein interaction.	Morpholin-3-one	21-33	P53	Homo sapiens	57-60
26432589-10	2014	These results clearly demonstrate that the bystander effect is p53-dependent for low LET irradiation, but it is p53-independent for high LET irradiation which may be because of p53-independent ROS generation due to mitochondrial dysfunction.	ros	193-196	P53	Homo sapiens	112-115
26432589-10	2014	These results clearly demonstrate that the bystander effect is p53-dependent for low LET irradiation, but it is p53-independent for high LET irradiation which may be because of p53-independent ROS generation due to mitochondrial dysfunction.	ros	193-196	P53	Homo sapiens	112-115
24476809-6	2014	The piPEI-mediated delivery of native anti-E6 antibodies or anti-E6 antibodies equipped with a nuclear localization signal (NLS), led to regeneration of the p53 tumor suppression protein in E6-transformed CaSki cells.	pipei	4-9	P53	Homo sapiens	157-160
24565839-5	2014	PTX treatment induces the p53 protein, but down-regulates expression of SETDB1 at the transcriptional level as well as the protein level.	Paclitaxel	0-3	P53	Homo sapiens	26-29
24565839-10	2014	This result demonstrates that PTX down-regulates SETDB1 gene expression in a p53 dependent manner, and p53 might participate in heterochromatic repression on the promoter regions of SETDB1.	Paclitaxel	30-33	P53	Homo sapiens	77-80
24440808-3	2014	We observed that silibinin significantly induced the expression of the non-steroidal anti-inflammatory drug-activated gene-1 (NAG-1) in both p53 wild-type and p53-null cancer cell lines, suggesting that silibinin-induced NAG-1 up-regulation is p53-independent manner.	Silybin	17-26	P53	Homo sapiens	141-144
24440808-3	2014	We observed that silibinin significantly induced the expression of the non-steroidal anti-inflammatory drug-activated gene-1 (NAG-1) in both p53 wild-type and p53-null cancer cell lines, suggesting that silibinin-induced NAG-1 up-regulation is p53-independent manner.	Silybin	17-26	P53	Homo sapiens	159-162
24440808-3	2014	We observed that silibinin significantly induced the expression of the non-steroidal anti-inflammatory drug-activated gene-1 (NAG-1) in both p53 wild-type and p53-null cancer cell lines, suggesting that silibinin-induced NAG-1 up-regulation is p53-independent manner.	Silybin	17-26	P53	Homo sapiens	159-162
24440808-3	2014	We observed that silibinin significantly induced the expression of the non-steroidal anti-inflammatory drug-activated gene-1 (NAG-1) in both p53 wild-type and p53-null cancer cell lines, suggesting that silibinin-induced NAG-1 up-regulation is p53-independent manner.	Silybin	203-212	P53	Homo sapiens	141-144
24063548-5	2014	The reduction of PTEN in the nucleus, in turn, decreased p53 acetylation and transcription, reduced the expression of the p53 target gene glutathione peroxidase-1 (GPX1), resulting in reactive oxygen species (ROS) accumulation and endothelial damage.	Reactive Oxygen Species	209-212	P53	Homo sapiens	122-125
24667842-4	2014	Here, we aimed to determine the effect of SFN on ROS levels and to identify key biomarkers leading to ROS unbalance and apoptosis in the p53-null MG-63 osteosarcoma cell line.	Reactive Oxygen Species	102-105	P53	Homo sapiens	137-140
24664296-7	2014	Moreover, the level of activated p53 and PARP-1 were significantly induced by BaP, whereas this induction was markedly reduced after curcumin and VE co-treatment.	Curcumin	133-141	P53	Homo sapiens	33-36
24667498-5	2014	We found that p53 indeed exists as a hydroxylated protein in vivo and that the hydroxylation occurs mainly on lysine 382 of p53.	Lysine	110-116	P53	Homo sapiens	14-17
24667498-5	2014	We found that p53 indeed exists as a hydroxylated protein in vivo and that the hydroxylation occurs mainly on lysine 382 of p53.	Lysine	110-116	P53	Homo sapiens	124-127
24464582-13	2014	Lastly, we show that this Pu-27-mediated sensitivity is p53-independent.	Plutonium	26-28	P53	Homo sapiens	56-59
24063548-5	2014	The reduction of PTEN in the nucleus, in turn, decreased p53 acetylation and transcription, reduced the expression of the p53 target gene glutathione peroxidase-1 (GPX1), resulting in reactive oxygen species (ROS) accumulation and endothelial damage.	Reactive Oxygen Species	184-207	P53	Homo sapiens	122-125
24576095-1	2014	TIGAR [TP53 (tumour protein 53)-induced glycolysis and apoptosis regulator] protein is known for its ability to inhibit glycolysis, shifting glucose consumption towards the pentose phosphate pathway to promote antioxidant protection of cancer cells.	Glucose	141-148	P53	Homo sapiens	7-11
24637639-5	2014	Besides these interactions on the principal side, we observe a cation-pi interaction between acetylcholine and Trp53 on the complementary side and a water-mediated hydrogen bond from acetylcholine to backbone atoms of Leu102 and Met114, both of importance for anchoring acetylcholine to the complementary side.	Acetylcholine	93-106	P53	Homo sapiens	111-116
24486524-0	2014	p53 inactivation decreases dependence on estrogen/ERK signalling for proliferation but promotes EMT and susceptility to 3-bromopyruvate in ERalpha+ breast cancer MCF-7 cells.	bromopyruvate	120-135	P53	Homo sapiens	0-3
24486524-7	2014	p53 siRNA silencing by electroporation in wt TP53 MCF-7 cells also decreased estrogen dependence and response to MEK inhibition, while also conferring susceptibility to 3-BrPA.	bromopyruvate	169-175	P53	Homo sapiens	0-3
24602316-15	2014	MiR-125a-5p also increased p53 protein expression in HNE-1 cells, and decreased Her2 protein expression in HNE-1 and HK-1 cells.	mir-125a-5p	0-11	P53	Homo sapiens	27-30
24260774-8	2014	The experimental results confirmed the association rule identified for the p53 pathway and mitochondrial superoxide levels (via MitoSox reagent) and further revealed that blocking of the transcriptional activity of p53 lowered the MitoSox signal.	Superoxides	105-115	P53	Homo sapiens	75-78
24260774-8	2014	The experimental results confirmed the association rule identified for the p53 pathway and mitochondrial superoxide levels (via MitoSox reagent) and further revealed that blocking of the transcriptional activity of p53 lowered the MitoSox signal.	Superoxides	105-115	P53	Homo sapiens	215-218
24182986-5	2014	The primary objectives of the current study were to investigate the effects of haemanthamine and haemanthidine on the induction of apoptosis and the cell cycle regulatory pathway in p53-null Jurkat cells.	hemanthamine	79-92	P53	Homo sapiens	182-185
25101185-0	2014	Cadmium Impairs p53 Activity in HepG2 Cells.	Cadmium	0-7	P53	Homo sapiens	16-19
25101185-4	2014	The present work is designed to gain an insight into the mechanism of p53 impairment at gene and protein level to understand Cd-induced resistance to apoptosis.	Cadmium	125-127	P53	Homo sapiens	70-73
24603648-5	2014	Resveratrol induced cell cycle arrest in the S- and G2/M- phase and apoptosis was mediated by activation of p53 and caspase-3 in HepG2 cells.	Resveratrol	0-11	P53	Homo sapiens	108-111
24603648-6	2014	In contrast to primary hepatocytes, resveratrol treated HepG2 cells showed a reduction of NAMPT enzymatic activity and increased p53 acetylation (K382).	Resveratrol	36-47	P53	Homo sapiens	129-132
24361399-14	2014	SIGNIFICANCE: These results demonstrate that tamoxifen promotes senescence through a ROS-p53-p21(Cip1/WAF1) dependent pathway by inhibiting CK2 activity in breast cancer and colon cancer cells.	Tamoxifen	45-54	P53	Homo sapiens	89-92
24361399-14	2014	SIGNIFICANCE: These results demonstrate that tamoxifen promotes senescence through a ROS-p53-p21(Cip1/WAF1) dependent pathway by inhibiting CK2 activity in breast cancer and colon cancer cells.	Reactive Oxygen Species	85-88	P53	Homo sapiens	89-92
24361399-13	2014	Finally, experiments using T47D (wild-type p53) and MDA-MB-435 (mutant p53) cell lines suggested that tamoxifen induces p53-independent ROS production as well as p53-dependent senescence in breast cancer cells.	Tamoxifen	102-111	P53	Homo sapiens	43-46
24361399-13	2014	Finally, experiments using T47D (wild-type p53) and MDA-MB-435 (mutant p53) cell lines suggested that tamoxifen induces p53-independent ROS production as well as p53-dependent senescence in breast cancer cells.	Tamoxifen	102-111	P53	Homo sapiens	71-74
24361399-13	2014	Finally, experiments using T47D (wild-type p53) and MDA-MB-435 (mutant p53) cell lines suggested that tamoxifen induces p53-independent ROS production as well as p53-dependent senescence in breast cancer cells.	Tamoxifen	102-111	P53	Homo sapiens	71-74
24492002-4	2014	UV-induced DNA damage activates VRK1, and is accompanied by phosphorylation of p53 at Thr-18 before it accumulates.	Threonine	86-89	P53	Homo sapiens	79-82
24011472-6	2014	Significant progresses have been made with a new p53 encoding pDNA microgel that is suitable for the loading and release of pDNA and doxorubicin.	Doxorubicin	133-144	P53	Homo sapiens	49-52
24361399-13	2014	Finally, experiments using T47D (wild-type p53) and MDA-MB-435 (mutant p53) cell lines suggested that tamoxifen induces p53-independent ROS production as well as p53-dependent senescence in breast cancer cells.	Tamoxifen	102-111	P53	Homo sapiens	71-74
24596382-10	2014	In vivo 100-IU hCG injections for 5 weeks elevated serum estradiol levels (35.7 vs. 23.5 pg/ml); thus, the mechanisms of hCG action may be directly coordinated via the p53-mediated mitochondrial apoptotic pathway and indirectly through ovarian steroid secretion that elevates estrogen levels.	Estradiol	57-66	P53	Homo sapiens	168-171
24366574-8	2014	These findings, together with significantly elevated MT, decreased p53 and Bax indicate PC-3 to be cisplatin-resistant.	Cisplatin	99-108	P53	Homo sapiens	67-70
24463159-0	2014	TP53 K351N mutation-associated platinum resistance after neoadjuvant chemotherapy in patients with advanced ovarian cancer.	Platinum	31-39	P53	Homo sapiens	0-4
24463159-1	2014	OBJECTIVE: TP53 K351N mutation is associated with acquired cisplatin resistance in ovarian cancer cells following exposure to cisplatin.	Cisplatin	59-68	P53	Homo sapiens	11-15
24463159-1	2014	OBJECTIVE: TP53 K351N mutation is associated with acquired cisplatin resistance in ovarian cancer cells following exposure to cisplatin.	Cisplatin	126-135	P53	Homo sapiens	11-15
24463159-10	2014	CONCLUSIONS: TP53 K351N mutation may be associated with induction of platinum resistance after NACT in advanced EOC.	Platinum	69-77	P53	Homo sapiens	13-17
24365999-0	2014	A novel oxiranylchromenone derivative, MHY336, induces apoptosis and cell cycle arrest via a p53- and p21-dependent pathway in HCT116 human colon cancer cells.	MHY336	39-45	P53	Homo sapiens	93-96
24365999-2	2014	Using these three isogenic variants, the roles of p53 and p21 in the cellular response to treatment with MHY336, a novel topoisomerase IIalpha inhibitor, were investigated.	MHY336	105-111	P53	Homo sapiens	50-53
24486404-4	2014	Interestingly, NTP induced a sub-G(1) arrest in p53 wild-type OSCCs, but not in p53-mutated OSCCs.	Plasma Gases	15-18	P53	Homo sapiens	48-51
24486404-5	2014	In addition, NTP increased the expression levels of ATM, p53 (Ser 15, 20 and 46), p21, and cyclin D1.	Serine	62-65	P53	Homo sapiens	57-60
24486404-6	2014	A comet assay, Western blotting and immunocytochemistry of gammaH2AX suggested that NTP-induced apoptosis and sub-G(1) arrest were associated with DNA damage and the ATM/p53 signaling pathway in SCC25 cells.	Plasma Gases	84-87	P53	Homo sapiens	170-173
24486404-8	2014	Taken together, these results indicate that NTP induced apoptotic cell death in p53 wild-type OSCCs through a novel mechanism involving DNA damage and triggering of sub-G(1) arrest via the ATM/p53 pathway.	Plasma Gases	44-47	P53	Homo sapiens	80-83
24486404-8	2014	Taken together, these results indicate that NTP induced apoptotic cell death in p53 wild-type OSCCs through a novel mechanism involving DNA damage and triggering of sub-G(1) arrest via the ATM/p53 pathway.	Plasma Gases	44-47	P53	Homo sapiens	193-196
24702801-10	2014	CONCLUSION: The anti-colon cancer activity of tanshinone I was more potent and selective than tanshinone IIA, and is p53 dependent.	tanshinone	46-56	P53	Homo sapiens	117-120
22223508-5	2014	Our data reaffirms the oncogenic capability of MIC with elevated DNA damage response proteins pATM and gamma-H2AX, deregulation of DNA damage check point genes CHK1 and CHK2, altered expression of p53 and p21 proteins involved in cell cycle arrest with perturbation in GADD-45 expression in the treated cells.	gadd	269-273	P53	Homo sapiens	197-200
24365999-5	2014	However, p53-null and p21-null cells were more resistant to the antiproliferative and apoptotic effects of MHY336 than p53-wt cells.	MHY336	107-113	P53	Homo sapiens	9-12
24365999-6	2014	The same result was achieved by knocking down p53 and p21 with siRNA in p53-wt cells, indicating that p53 and p21 play a crucial role in MHY336-induced cell cycle arrest and apoptosis.	MHY336	137-143	P53	Homo sapiens	46-49
24365999-6	2014	The same result was achieved by knocking down p53 and p21 with siRNA in p53-wt cells, indicating that p53 and p21 play a crucial role in MHY336-induced cell cycle arrest and apoptosis.	MHY336	137-143	P53	Homo sapiens	72-75
24365999-6	2014	The same result was achieved by knocking down p53 and p21 with siRNA in p53-wt cells, indicating that p53 and p21 play a crucial role in MHY336-induced cell cycle arrest and apoptosis.	MHY336	137-143	P53	Homo sapiens	72-75
24365999-3	2014	Our results showed that MHY336 treatment increased the expression of p53 over time in cells with wild-type p53 status.	MHY336	24-30	P53	Homo sapiens	69-72
24365999-3	2014	Our results showed that MHY336 treatment increased the expression of p53 over time in cells with wild-type p53 status.	MHY336	24-30	P53	Homo sapiens	107-110
24366007-8	2014	Notably, the levels of nutlin-3-induced ROS were correlated with the mitochondrial translocation of p53 and this induction was prevented by PFT-mu, an inhibitor of the mitochondrial translocation of p53.	ros	40-43	P53	Homo sapiens	100-103
25337571-9	2014	Ethanol also increased the phosphorylation of p53 and p53 activation was followed by an increase in the p21 tumor suppressor protein accompanied by a gradual decrease in phospho-Rb protein.	Ethanol	0-7	P53	Homo sapiens	46-49
24366007-8	2014	Notably, the levels of nutlin-3-induced ROS were correlated with the mitochondrial translocation of p53 and this induction was prevented by PFT-mu, an inhibitor of the mitochondrial translocation of p53.	ros	40-43	P53	Homo sapiens	199-202
24366007-11	2014	Collectively, these results suggest that nutlin-3 induces HO-1 expression via the activation of both JNK which is dependent on ROS generated by p53 translocated to the mitochondria and p38 MAPK which appears to be stimulated by a ROS-independent mechanism, and this HO-1 induction may inhibit nutlin-3-induced apoptosis, constituting a negative feedback loop of p53-induced apoptosis.	ros	127-130	P53	Homo sapiens	144-147
24445997-0	2014	Roles of Atox1 and p53 in the trafficking of copper-64 to tumor cell nuclei: implications for cancer therapy.	Copper	45-51	P53	Homo sapiens	19-22
24445997-9	2014	In cells treated with cisplatin, the uptake of (64)Cu in the nucleus of HCT 116 p53(+/+) cells was greater than that in HCT 116 p53(-/-) cells.	Cisplatin	22-31	P53	Homo sapiens	80-83
24445997-9	2014	In cells treated with cisplatin, the uptake of (64)Cu in the nucleus of HCT 116 p53(+/+) cells was greater than that in HCT 116 p53(-/-) cells.	Cisplatin	22-31	P53	Homo sapiens	128-131
24445997-9	2014	In cells treated with cisplatin, the uptake of (64)Cu in the nucleus of HCT 116 p53(+/+) cells was greater than that in HCT 116 p53(-/-) cells.	Copper	51-53	P53	Homo sapiens	80-83
25337571-9	2014	Ethanol also increased the phosphorylation of p53 and p53 activation was followed by an increase in the p21 tumor suppressor protein accompanied by a gradual decrease in phospho-Rb protein.	Ethanol	0-7	P53	Homo sapiens	54-57
25337571-10	2014	CONCLUSION: Our results suggest that ethanol mediates apoptosis of neuroblastoma cells by stimulating p53-related cell cycle arrest mediated through activation of the JNK-related pathway.	Ethanol	37-44	P53	Homo sapiens	102-105
24435975-7	2014	However, in a multivariate analysis adjusted for alcohol consumption, smoking, ethnicity, and number of pregnancies, the interaction between the genotypes TP53 Arg/Arg (rs1042522) and MDM2 TT (rs2279744) showed to be associated to RPL, increasing the risk for this condition (OR = 2.58, 95% CI: 1.31-5.07, p = 0.006).	Alcohols	49-56	P53	Homo sapiens	155-159
24445997-10	2014	Atox1 expression increased in HCT 116 p53(+/+) and p53(-/-) cells treated with cisplatin; however, Atox1 localized to the nuclei of p53(+/+) cells more than in the p53(-/-) cells.	Cisplatin	79-88	P53	Homo sapiens	38-41
24445997-10	2014	Atox1 expression increased in HCT 116 p53(+/+) and p53(-/-) cells treated with cisplatin; however, Atox1 localized to the nuclei of p53(+/+) cells more than in the p53(-/-) cells.	Cisplatin	79-88	P53	Homo sapiens	51-54
24445997-10	2014	Atox1 expression increased in HCT 116 p53(+/+) and p53(-/-) cells treated with cisplatin; however, Atox1 localized to the nuclei of p53(+/+) cells more than in the p53(-/-) cells.	Cisplatin	79-88	P53	Homo sapiens	51-54
24445997-10	2014	Atox1 expression increased in HCT 116 p53(+/+) and p53(-/-) cells treated with cisplatin; however, Atox1 localized to the nuclei of p53(+/+) cells more than in the p53(-/-) cells.	Cisplatin	79-88	P53	Homo sapiens	51-54
24246002-8	2014	Univariate analyses showed overexpression of p53 to be a significant prognostic indicator in patients with UEA (P &lt; 0.02).	uea	107-110	P53	Homo sapiens	45-48
24421392-2	2014	We have shown that ursodeoxycholic acid, a hydrophilic bile acid, counteracts the miR-34a/sirtuin 1 (SIRT1)/p53 pathway, activated in the liver of nonalcoholic steatohepatitis (NASH) patients.	Bile Acids and Salts	55-64	P53	Homo sapiens	108-111
24435975-7	2014	However, in a multivariate analysis adjusted for alcohol consumption, smoking, ethnicity, and number of pregnancies, the interaction between the genotypes TP53 Arg/Arg (rs1042522) and MDM2 TT (rs2279744) showed to be associated to RPL, increasing the risk for this condition (OR = 2.58, 95% CI: 1.31-5.07, p = 0.006).	Arginine	160-163	P53	Homo sapiens	155-159
24435975-7	2014	However, in a multivariate analysis adjusted for alcohol consumption, smoking, ethnicity, and number of pregnancies, the interaction between the genotypes TP53 Arg/Arg (rs1042522) and MDM2 TT (rs2279744) showed to be associated to RPL, increasing the risk for this condition (OR = 2.58, 95% CI: 1.31-5.07, p = 0.006).	Arginine	164-167	P53	Homo sapiens	155-159
24435975-8	2014	In conclusion, our study indicates that the combination of TP53 Arg/Arg (rs1042522) and MDM2 TT (rs2279744) genotypes may be a risk factor for RPL.	Arginine	64-67	P53	Homo sapiens	59-63
24435975-8	2014	In conclusion, our study indicates that the combination of TP53 Arg/Arg (rs1042522) and MDM2 TT (rs2279744) genotypes may be a risk factor for RPL.	Arginine	68-71	P53	Homo sapiens	59-63
24161623-0	2014	Murine double minute 2 siRNA and wild-type p53 gene therapy enhances sensitivity of the SKOV3/DDP ovarian cancer cell line to cisplatin chemotherapy in vitro and in vivo.	Cisplatin	126-135	P53	Homo sapiens	43-46
24366026-2	2014	The polymorphism in the p53 72nd codon involves a proline to arginine substitution, leading to changes in gene transcription activity, interaction with other proteins and modulation of apoptosis.	Arginine	61-69	P53	Homo sapiens	24-27
24380814-8	2014	Nuclear accumulation and ATM-dependent phosphorylation of p53 on serine 15 were also observed.	Serine	65-71	P53	Homo sapiens	58-61
24868967-5	2014	RESULTS: After inhibition of p53 using PFT-alpha or siRNA, the high levels of p53, p53-ser 20 and p21 induced by B [a] P were markedly decreased.	Serine	87-90	P53	Homo sapiens	29-32
24161623-2	2014	Here we show a critical role for cisplatin combined with gene therapy, using transfection of a p53 gene/MDM2-siRNA plasmid, in improving cisplatin sensitivity of SKOV3/DDP cells with a strong inhibition of tumor cell growth in vitro and in vivo.	Cisplatin	33-42	P53	Homo sapiens	95-98
24161623-2	2014	Here we show a critical role for cisplatin combined with gene therapy, using transfection of a p53 gene/MDM2-siRNA plasmid, in improving cisplatin sensitivity of SKOV3/DDP cells with a strong inhibition of tumor cell growth in vitro and in vivo.	Cisplatin	137-146	P53	Homo sapiens	95-98
24161623-5	2014	These results indicate that cisplatin chemotherapy combined with targeting the MDM2/p53 axis is an attractive strategy to treat SKOV3/DDP cancer.	Cisplatin	28-37	P53	Homo sapiens	84-87
24634836-1	2014	The regulatory mechanisms by which hydrogen peroxide (H2O2) modulates the activity of transcription factors in bacteria (OxyR and PerR), lower eukaryotes (Yap1, Maf1, Hsf1 and Msn2/4) and mammalian cells (AP-1, NRF2, CREB, HSF1, HIF-1, TP53, NF-kappaB, NOTCH, SP1 and SCREB-1) are reviewed.	Hydrogen Peroxide	35-52	P53	Homo sapiens	236-240
24643130-6	2014	Through suppressing the interaction between p53 and MDM2, MDM2-mediated p53 ubiquitination was remarkably decreased after capsaicin treatment, which resulted in the stabilization and accumulation of p53.	Capsaicin	122-131	P53	Homo sapiens	72-75
24491565-2	2014	Here, we report that in CdCl2-exposed human bronchial epithelial cells (BEAS-2B), the level of p53 is dramatically decreased in a time- and dose-dependent manner, suggesting that the observed Cd-induced cytotoxicity is not likely due to the pro-apoptotic function of p53.	Cadmium	24-26	P53	Homo sapiens	95-98
24491565-2	2014	Here, we report that in CdCl2-exposed human bronchial epithelial cells (BEAS-2B), the level of p53 is dramatically decreased in a time- and dose-dependent manner, suggesting that the observed Cd-induced cytotoxicity is not likely due to the pro-apoptotic function of p53.	Cadmium	24-26	P53	Homo sapiens	267-270
24587255-0	2014	A compensatory role of NF-kappaB to p53 in response to 5-FU-based chemotherapy for gastric cancer cell lines.	Fluorouracil	55-59	P53	Homo sapiens	36-39
24587255-5	2014	Seven genes induced by 5-FU treatment in an NF-kappaB-dependent manner were identified, five of which are known p53 targets.	Fluorouracil	23-27	P53	Homo sapiens	112-115
24587255-8	2014	We also demonstrated that cell lines bearing Pro/Pro homozygosity in codon72 of p53 exon4, which is important for NF-kappaB binding to p53, are more resistant to 5-FU than those with Arg/Arg homozygosity.	Fluorouracil	162-166	P53	Homo sapiens	80-83
24587255-8	2014	We also demonstrated that cell lines bearing Pro/Pro homozygosity in codon72 of p53 exon4, which is important for NF-kappaB binding to p53, are more resistant to 5-FU than those with Arg/Arg homozygosity.	Arginine	183-186	P53	Homo sapiens	80-83
24587255-8	2014	We also demonstrated that cell lines bearing Pro/Pro homozygosity in codon72 of p53 exon4, which is important for NF-kappaB binding to p53, are more resistant to 5-FU than those with Arg/Arg homozygosity.	Arginine	187-190	P53	Homo sapiens	80-83
24587255-9	2014	We conclude that NF-kappaB plays an important role in the response to 5-FU treatment in gastric cancer cell lines, with a possible compensatory function of p53.	Fluorouracil	70-74	P53	Homo sapiens	156-159
24587255-10	2014	These results suggest that NF-kappaB is a potential 5-FU-chemosensitivity prediction marker that may reflect 5-FU-induced stress-response pathways, including p53.	Fluorouracil	52-56	P53	Homo sapiens	158-161
24587255-10	2014	These results suggest that NF-kappaB is a potential 5-FU-chemosensitivity prediction marker that may reflect 5-FU-induced stress-response pathways, including p53.	Fluorouracil	109-113	P53	Homo sapiens	158-161
24643130-6	2014	Through suppressing the interaction between p53 and MDM2, MDM2-mediated p53 ubiquitination was remarkably decreased after capsaicin treatment, which resulted in the stabilization and accumulation of p53.	Capsaicin	122-131	P53	Homo sapiens	72-75
24643130-7	2014	The results of p53-shRNA experiment further demonstrated that p53 knockdown severely impaired the sensitivity of tested cells to capsaicin, G0/G1 phase arrest and the apoptosis induced by capsaicin in p53-knockdown cells was also dramatically decreased, implicating the important role of p53 played in capsaicin"s antitumor activity.	Capsaicin	129-138	P53	Homo sapiens	15-18
24643130-7	2014	The results of p53-shRNA experiment further demonstrated that p53 knockdown severely impaired the sensitivity of tested cells to capsaicin, G0/G1 phase arrest and the apoptosis induced by capsaicin in p53-knockdown cells was also dramatically decreased, implicating the important role of p53 played in capsaicin"s antitumor activity.	Capsaicin	129-138	P53	Homo sapiens	62-65
24643130-7	2014	The results of p53-shRNA experiment further demonstrated that p53 knockdown severely impaired the sensitivity of tested cells to capsaicin, G0/G1 phase arrest and the apoptosis induced by capsaicin in p53-knockdown cells was also dramatically decreased, implicating the important role of p53 played in capsaicin"s antitumor activity.	Capsaicin	129-138	P53	Homo sapiens	62-65
24643130-7	2014	The results of p53-shRNA experiment further demonstrated that p53 knockdown severely impaired the sensitivity of tested cells to capsaicin, G0/G1 phase arrest and the apoptosis induced by capsaicin in p53-knockdown cells was also dramatically decreased, implicating the important role of p53 played in capsaicin"s antitumor activity.	Capsaicin	129-138	P53	Homo sapiens	62-65
24643130-7	2014	The results of p53-shRNA experiment further demonstrated that p53 knockdown severely impaired the sensitivity of tested cells to capsaicin, G0/G1 phase arrest and the apoptosis induced by capsaicin in p53-knockdown cells was also dramatically decreased, implicating the important role of p53 played in capsaicin"s antitumor activity.	Capsaicin	188-197	P53	Homo sapiens	15-18
24643130-7	2014	The results of p53-shRNA experiment further demonstrated that p53 knockdown severely impaired the sensitivity of tested cells to capsaicin, G0/G1 phase arrest and the apoptosis induced by capsaicin in p53-knockdown cells was also dramatically decreased, implicating the important role of p53 played in capsaicin"s antitumor activity.	Capsaicin	188-197	P53	Homo sapiens	62-65
24643130-7	2014	The results of p53-shRNA experiment further demonstrated that p53 knockdown severely impaired the sensitivity of tested cells to capsaicin, G0/G1 phase arrest and the apoptosis induced by capsaicin in p53-knockdown cells was also dramatically decreased, implicating the important role of p53 played in capsaicin"s antitumor activity.	Capsaicin	188-197	P53	Homo sapiens	62-65
24643130-7	2014	The results of p53-shRNA experiment further demonstrated that p53 knockdown severely impaired the sensitivity of tested cells to capsaicin, G0/G1 phase arrest and the apoptosis induced by capsaicin in p53-knockdown cells was also dramatically decreased, implicating the important role of p53 played in capsaicin"s antitumor activity.	Capsaicin	188-197	P53	Homo sapiens	62-65
24643130-7	2014	The results of p53-shRNA experiment further demonstrated that p53 knockdown severely impaired the sensitivity of tested cells to capsaicin, G0/G1 phase arrest and the apoptosis induced by capsaicin in p53-knockdown cells was also dramatically decreased, implicating the important role of p53 played in capsaicin"s antitumor activity.	Capsaicin	188-197	P53	Homo sapiens	15-18
24643130-7	2014	The results of p53-shRNA experiment further demonstrated that p53 knockdown severely impaired the sensitivity of tested cells to capsaicin, G0/G1 phase arrest and the apoptosis induced by capsaicin in p53-knockdown cells was also dramatically decreased, implicating the important role of p53 played in capsaicin"s antitumor activity.	Capsaicin	188-197	P53	Homo sapiens	62-65
24643130-7	2014	The results of p53-shRNA experiment further demonstrated that p53 knockdown severely impaired the sensitivity of tested cells to capsaicin, G0/G1 phase arrest and the apoptosis induced by capsaicin in p53-knockdown cells was also dramatically decreased, implicating the important role of p53 played in capsaicin"s antitumor activity.	Capsaicin	188-197	P53	Homo sapiens	62-65
24643130-7	2014	The results of p53-shRNA experiment further demonstrated that p53 knockdown severely impaired the sensitivity of tested cells to capsaicin, G0/G1 phase arrest and the apoptosis induced by capsaicin in p53-knockdown cells was also dramatically decreased, implicating the important role of p53 played in capsaicin"s antitumor activity.	Capsaicin	188-197	P53	Homo sapiens	62-65
24375404-5	2014	We found that MYBBP1A has two regions that directly bind to lysine residues of the p53 C-terminal regulatory domain.	Lysine	60-66	P53	Homo sapiens	83-86
24634836-1	2014	The regulatory mechanisms by which hydrogen peroxide (H2O2) modulates the activity of transcription factors in bacteria (OxyR and PerR), lower eukaryotes (Yap1, Maf1, Hsf1 and Msn2/4) and mammalian cells (AP-1, NRF2, CREB, HSF1, HIF-1, TP53, NF-kappaB, NOTCH, SP1 and SCREB-1) are reviewed.	Hydrogen Peroxide	54-58	P53	Homo sapiens	236-240
24643130-0	2014	Capsaicin mediates cell cycle arrest and apoptosis in human colon cancer cells via stabilizing and activating p53.	Capsaicin	0-9	P53	Homo sapiens	110-113
24643130-4	2014	The underlying mechanism of capsaicin"s antitumor potency was mainly attributed to the stabilization and activation of p53.	Capsaicin	28-37	P53	Homo sapiens	119-122
24643130-5	2014	Capsaicin substantially prolonged the half-life of p53 and significantly elevated the transcriptional activity of p53.	Capsaicin	0-9	P53	Homo sapiens	51-54
24643130-5	2014	Capsaicin substantially prolonged the half-life of p53 and significantly elevated the transcriptional activity of p53.	Capsaicin	0-9	P53	Homo sapiens	114-117
24643130-6	2014	Through suppressing the interaction between p53 and MDM2, MDM2-mediated p53 ubiquitination was remarkably decreased after capsaicin treatment, which resulted in the stabilization and accumulation of p53.	Capsaicin	122-131	P53	Homo sapiens	44-47
24403071-8	2014	Adding either Lys-59 or Lys-109 back to the Otub1(K0) mutant restores the monoubiquitination of Otub1 and its function to stabilize and activate p53.	Lysine	14-17	P53	Homo sapiens	145-148
24403071-8	2014	Adding either Lys-59 or Lys-109 back to the Otub1(K0) mutant restores the monoubiquitination of Otub1 and its function to stabilize and activate p53.	Lysine	24-27	P53	Homo sapiens	145-148
24586407-5	2014	DNA damage was induced by ultraviolet type C (UVC) radiation, or 10-decarbamoyl mitomycin C (DMC, an agent known to induce mammalian p53-independent cell death).	10-decarbamoylmitomycin C	65-91	P53	Homo sapiens	133-136
24556689-7	2014	The activities of both forkhead box O (FOXO1) and p53 were required for upregulation of bim RNA expression in high glucose.	Glucose	115-122	P53	Homo sapiens	50-53
24556689-9	2014	High glucose coupled with oxidative stress resulted in upregulation of miR28-5p, which directly inhibited expression of the p53 deacetylase sirtuin 3, resulting in increased levels of acetylated p53.	Glucose	5-12	P53	Homo sapiens	124-127
24556689-9	2014	High glucose coupled with oxidative stress resulted in upregulation of miR28-5p, which directly inhibited expression of the p53 deacetylase sirtuin 3, resulting in increased levels of acetylated p53.	Glucose	5-12	P53	Homo sapiens	195-198
24586533-7	2014	Transient gene expression assays suggested that CPT or DOX"s attenuation of PSA promoter activity is dependent on both the androgen and p53 response elements within of the PSA promoter.	Doxorubicin	55-58	P53	Homo sapiens	136-139
24586533-8	2014	Our results indicated that CPT and DOX attenuate cell proliferation via upregulation of BTG2 gene expression through the p53-dependent pathway.	Doxorubicin	35-38	P53	Homo sapiens	121-124
24586533-9	2014	The CPT and DOX block the PSA gene expression by upregulation of p53 activity and downregulation of androgen receptor activity.	Doxorubicin	12-15	P53	Homo sapiens	65-68
24586407-5	2014	DNA damage was induced by ultraviolet type C (UVC) radiation, or 10-decarbamoyl mitomycin C (DMC, an agent known to induce mammalian p53-independent cell death).	10-decarbamoylmitomycin C	93-96	P53	Homo sapiens	133-136
24586407-9	2014	Consistent with DMC inducing p53-independent cell death in mammalian cells DMC induced a C. elegans p53-independent germline cell death pathway.	10-decarbamoylmitomycin C	16-19	P53	Homo sapiens	29-32
24586407-9	2014	Consistent with DMC inducing p53-independent cell death in mammalian cells DMC induced a C. elegans p53-independent germline cell death pathway.	10-decarbamoylmitomycin C	75-78	P53	Homo sapiens	29-32
24586407-9	2014	Consistent with DMC inducing p53-independent cell death in mammalian cells DMC induced a C. elegans p53-independent germline cell death pathway.	10-decarbamoylmitomycin C	75-78	P53	Homo sapiens	100-103
24446736-0	2014	Induction of lung cancer cell apoptosis through a p53 pathway by [6]-shogaol and its cysteine-conjugated metabolite M2.	Cysteine	85-93	P53	Homo sapiens	50-53
24269727-0	2014	ROS and RNS induced apoptosis through p53 and iNOS mediated pathway by a dibasic hydroxamic acid molecule in leukemia cells.	ros	0-3	P53	Homo sapiens	38-41
24269727-0	2014	ROS and RNS induced apoptosis through p53 and iNOS mediated pathway by a dibasic hydroxamic acid molecule in leukemia cells.	dibasic hydroxamic acid	73-96	P53	Homo sapiens	38-41
24269727-9	2014	Therefore OBPHA, having a structurally relevant pharmacophore provides important insight into the development of new ROS and RNS generating chemicals inducing p53 dependent apoptosis.	ros	117-120	P53	Homo sapiens	159-162
24525822-0	2014	Transactivation of bad by vorinostat-induced acetylated p53 enhances doxorubicin-induced cytotoxicity in cervical cancer cells.	Doxorubicin	69-80	P53	Homo sapiens	56-59
24525822-6	2014	Moreover, a chromatin immunoprecipitation analysis showed that the co-treatment of HeLa cells with VOR and DOX increased the recruitment of acetylated p53 to the bad promoter, with consequent bad transactivation.	Doxorubicin	107-110	P53	Homo sapiens	151-154
24525822-7	2014	Conversely, C33A cervical cancer cells containing mutant p53 co-treated with VOR and DOX did not exhibit Bad upregulation, acetylated p53 induction or consequent synergistic growth inhibition.	Doxorubicin	85-88	P53	Homo sapiens	57-60
24525822-8	2014	Together, the synergistic growth inhibition of cervical cancer cell lines induced by co-treatment with VOR and DOX can be attributed to the upregulation of Bad, which is induced by acetylated p53.	Doxorubicin	111-114	P53	Homo sapiens	192-195
24525822-9	2014	These results show for the first time that the acetylation of p53, rather than histones, is a mechanism for the synergistic growth inhibition induced by VOR and DOX co-treatments.	Doxorubicin	161-164	P53	Homo sapiens	62-65
24553354-0	2014	Hydrogen peroxide/ATR-Chk2 activation mediates p53 protein stabilization and anti-cancer activity of cheliensisin A in human cancer cells.	Hydrogen Peroxide	0-17	P53	Homo sapiens	47-50
24444609-2	2014	Here, we show that capsaicin-induced oxidative DNA damage culminates in p53 activation to up-regulate expression of miR-34a in non-small cell lung carcinoma (NSCLC) cells.	Capsaicin	19-28	P53	Homo sapiens	72-75
24525232-5	2014	p53-like MIBCs were consistently resistant to neoadjuvant methotrexate, vinblastine, doxorubicin and cisplatin chemotherapy, and all chemoresistant tumors adopted a p53-like phenotype after therapy.	Doxorubicin	85-96	P53	Homo sapiens	0-3
24525232-5	2014	p53-like MIBCs were consistently resistant to neoadjuvant methotrexate, vinblastine, doxorubicin and cisplatin chemotherapy, and all chemoresistant tumors adopted a p53-like phenotype after therapy.	Cisplatin	101-110	P53	Homo sapiens	0-3
24457472-4	2014	The patients in the treatment group were given arterial infusion of p53 gene (Gendicine, Shenzhen Sibiono GeneTech Co, Ltd) with Gendicine (10vp) combined with hydroxycamptothecin (20 mg), once a week, for a course continuously for 3 weeks.	gendicine	78-87	P53	Homo sapiens	68-71
24507760-3	2014	METHOD: We have developed a redox-responsive thiolated gelatin based nanoparticle system that efficiently delivers its payload in the presence of glutathione-mediated reducing intra-cellular environment and could be successfully used for site-specific wt-p53 expressing plasmid DNA as well as gemcitabine delivery by targeting epidermal growth factor receptor (EGFR).	Glutathione	146-157	P53	Homo sapiens	255-258
24457472-4	2014	The patients in the treatment group were given arterial infusion of p53 gene (Gendicine, Shenzhen Sibiono GeneTech Co, Ltd) with Gendicine (10vp) combined with hydroxycamptothecin (20 mg), once a week, for a course continuously for 3 weeks.	gendicine	129-138	P53	Homo sapiens	68-71
24343843-0	2014	Associations between cigarette smoking, hormone therapy, and folate intake with incident colorectal cancer by TP53 protein expression level in a population-based cohort of older women.	Folic Acid	61-67	P53	Homo sapiens	110-114
24268202-0	2014	p53 mediated apoptosis by reduction sensitive shielding ternary complexes based on disulfide linked PEI ternary complexes.	Disulfides	83-92	P53	Homo sapiens	0-3
24277474-0	2014	Thymidylate synthase expression and p21(WAF1)/p53 phenotype of colon cancers identify patients who may benefit from 5-fluorouracil based therapy.	Fluorouracil	116-130	P53	Homo sapiens	46-49
24126240-10	2014	Some of the differences in the effects of methionine between cell lines may be related to disparate p53 status.	Methionine	42-52	P53	Homo sapiens	100-103
24177958-5	2014	When human cancer cells were treated with DNA damaging agent, adriamycin (0.08 mug/ml), p21 was induced following p53 induction.	Doxorubicin	62-72	P53	Homo sapiens	114-117
24177958-7	2014	When these cells were simultaneously treated with a c-ABL kinase inhibitor, STI571, or a c-ABL-specific siRNA along with adriamycin, the p53-dependent p21 induction was dramatically diminished, even though p53 is substantially induced.	Doxorubicin	121-131	P53	Homo sapiens	137-140
24177958-7	2014	When these cells were simultaneously treated with a c-ABL kinase inhibitor, STI571, or a c-ABL-specific siRNA along with adriamycin, the p53-dependent p21 induction was dramatically diminished, even though p53 is substantially induced.	Doxorubicin	121-131	P53	Homo sapiens	206-209
24324033-6	2014	Moreover, by modulating the p53 axis, miR-221 impacts cell-cycle progression and apoptotic response to doxorubicin in hepatocellular carcinoma-derived cell lines.	Doxorubicin	103-114	P53	Homo sapiens	28-31
24333670-7	2014	Serine/arginine-rich splicing factor 3 was a promising candidate for the serine/arginine-rich splicing factors responsible for the alternative splicing of p53 in response to caffeine treatment.	Serine	73-79	P53	Homo sapiens	155-158
24333670-7	2014	Serine/arginine-rich splicing factor 3 was a promising candidate for the serine/arginine-rich splicing factors responsible for the alternative splicing of p53 in response to caffeine treatment.	Arginine	7-15	P53	Homo sapiens	155-158
24333671-6	2014	Meanwhile, we observed p53 mRNA at the peak in 10(-6)mol/L 17beta-estradiol treated cells for 24h via enhancing its core promoter activity.	Estradiol	59-75	P53	Homo sapiens	23-26
24248600-6	2014	Here, we show that vIRF-3 associates with the DNA-binding domain of p53, inhibits p53 phosphorylation on serine residues S15 and S20, and antagonizes p53 oligomerization and the DNA-binding affinity.	Serine	105-111	P53	Homo sapiens	68-71
24248600-6	2014	Here, we show that vIRF-3 associates with the DNA-binding domain of p53, inhibits p53 phosphorylation on serine residues S15 and S20, and antagonizes p53 oligomerization and the DNA-binding affinity.	Serine	105-111	P53	Homo sapiens	82-85
24248600-6	2014	Here, we show that vIRF-3 associates with the DNA-binding domain of p53, inhibits p53 phosphorylation on serine residues S15 and S20, and antagonizes p53 oligomerization and the DNA-binding affinity.	Serine	105-111	P53	Homo sapiens	82-85
24145719-0	2014	Effects of prostaglandin E2 on p53 mRNA transcription and p53 mutagenesis during T-cell-independent human B-cell clonal expansion.	Dinoprostone	11-27	P53	Homo sapiens	31-34
24356923-4	2014	The resultant p53 suppresses cell growth and induces a shorter cellular lifespan, and also compromises mitochondrial biogenesis leading to the overproduction of reactive oxygen species (ROS) causing multiple aging phenotypes.	Reactive Oxygen Species	161-184	P53	Homo sapiens	14-17
24356923-4	2014	The resultant p53 suppresses cell growth and induces a shorter cellular lifespan, and also compromises mitochondrial biogenesis leading to the overproduction of reactive oxygen species (ROS) causing multiple aging phenotypes.	Reactive Oxygen Species	186-189	P53	Homo sapiens	14-17
24324033-10	2014	IMPLICATIONS: These findings reveal a novel miR-221-sustained regulatory loop that determines a p53-context-specific response to doxorubicin treatment in hepatocellular carcinoma.	Doxorubicin	129-140	P53	Homo sapiens	96-99
24465521-2	2014	We have previously shown that 17beta-estradiol (E2) protects cardiomyocytes exposed to hypoxia-reoxygenation (H/R) by inhibiting p38alpha - p53 signaling in apoptosis and activating pro-survival p38beta mitogen activated protein kinase (p38beta MAPK), leading to suppression of reactive oxygen species (ROS) post H/R.	Estradiol	30-46	P53	Homo sapiens	140-143
24640606-5	2014	Further studies indicated that kirenol treatment triggered the arrest of cell cycle S period which might resulted from the up-regulation of phosphorylation of p53 (Ser 6 and Ser 37) and expression of p21 protein.	Serine	164-167	P53	Homo sapiens	159-162
24477002-9	2014	Because somatic mutations in p53 occur late in tumor progression, antioxidants may accelerate the growth of early tumors or precancerous lesions in high-risk populations such as smokers and patients with chronic obstructive pulmonary disease who receive NAC to relieve mucus production.	Acetylcysteine	254-257	P53	Homo sapiens	29-32
24461075-3	2014	METHODS: The human breast cancer cell lines MCF-7 (p53 wildtype) and MDA-MB-231 (p53 mutant) were treated with DCQ under normoxia or hypoxia.	Decylubiquinol	111-114	P53	Homo sapiens	81-84
24452144-2	2014	Recently, we have shown that Roslin 2 or R2 (1-benzyl-15,3,5,7-tetraazatricyclo[3.3.1.1~3,7~]decane) compound disrupts FAK and p53 proteins, activates p53 transcriptional activity, and blocks tumor growth.	1-benzyl-15,3,5,7-tetraazatricyclo	45-79	P53	Homo sapiens	127-130
24452144-2	2014	Recently, we have shown that Roslin 2 or R2 (1-benzyl-15,3,5,7-tetraazatricyclo[3.3.1.1~3,7~]decane) compound disrupts FAK and p53 proteins, activates p53 transcriptional activity, and blocks tumor growth.	1-benzyl-15,3,5,7-tetraazatricyclo	45-79	P53	Homo sapiens	151-154
24418562-0	2014	Reactive oxygen species activate NFkappaB (p65) and p53 and induce apoptosis in RVFV infected liver cells.	Reactive Oxygen Species	0-23	P53	Homo sapiens	52-55
24418562-5	2014	Increased ROS levels correlated with activation of NFkappaB (p65) and p53 responses, which in conjunction with infection, was also reflected as macromolecular rearrangements observed using size fractionation of protein lysates.	Reactive Oxygen Species	10-13	P53	Homo sapiens	70-73
24344116-0	2014	Deficiency in p53 is required for doxorubicin induced transcriptional activation of NF-kB target genes in human breast cancer.	Doxorubicin	34-45	P53	Homo sapiens	14-17
24344116-3	2014	We studied NF-kB-dependent gene expression induced by doxorubicin in breast cancer cells and fresh human cancer specimens with different genetic backgrounds focusing on their p53 status.	Doxorubicin	54-65	P53	Homo sapiens	175-178
24344116-7	2014	Doxorubicin treatment in the p53-mutated MDA-MB-231 cells resulted in NF-kB driven-gene transcription signature.	Doxorubicin	0-11	P53	Homo sapiens	29-32
24344116-10	2014	Furthermore, restoration of p53WT in the mutant p53 MDA-MB-231 cells impaired NF-kB driven transcription induced by doxorubicin.	Doxorubicin	116-127	P53	Homo sapiens	28-31
24344116-10	2014	Furthermore, restoration of p53WT in the mutant p53 MDA-MB-231 cells impaired NF-kB driven transcription induced by doxorubicin.	Doxorubicin	116-127	P53	Homo sapiens	48-51
24344116-12	2014	This study supports that p53 deficiency is necessary for a doxorubicin driven NF-kB-response that limits doxorubicin cytotoxicity in breast cancer and is linked to an aggressive clinical behavior.	Doxorubicin	59-70	P53	Homo sapiens	25-28
24344116-12	2014	This study supports that p53 deficiency is necessary for a doxorubicin driven NF-kB-response that limits doxorubicin cytotoxicity in breast cancer and is linked to an aggressive clinical behavior.	Doxorubicin	105-116	P53	Homo sapiens	25-28
23996892-4	2014	By adjustment for oxidative risk factors of HCC, the compound CT and TT genotypes in relative to the CC wild-type were associated with 83% reduced lymphocytic p53 oxidative lesions of HCC patients with RBC folate lower than 688 ng/mL (OR: 0.17, 95%CI: 0.07-0.43).	Folic Acid	206-212	P53	Homo sapiens	159-162
23996892-10	2014	CONCLUSION: Our data demonstrated that reduced MTHFR activities associated with the MTHFR T allele may interact with RBC folate as the risk modifiers of lymphocytic p53 oxidative lesions of HCC patients.	Folic Acid	121-127	P53	Homo sapiens	165-168
24317338-9	2014	These results suggest that ABCA1, ABCA3, ABCA7 and ABCB10 are candidate genes for the cisplatin efflux transporter that is involved in the cisplatin resistance of KCP-4 cells, and that the mutation at codon 72 of p53 may contribute to the development of cisplatin resistance.	Cisplatin	86-95	P53	Homo sapiens	213-216
24317338-9	2014	These results suggest that ABCA1, ABCA3, ABCA7 and ABCB10 are candidate genes for the cisplatin efflux transporter that is involved in the cisplatin resistance of KCP-4 cells, and that the mutation at codon 72 of p53 may contribute to the development of cisplatin resistance.	Cisplatin	139-148	P53	Homo sapiens	213-216
24317338-9	2014	These results suggest that ABCA1, ABCA3, ABCA7 and ABCB10 are candidate genes for the cisplatin efflux transporter that is involved in the cisplatin resistance of KCP-4 cells, and that the mutation at codon 72 of p53 may contribute to the development of cisplatin resistance.	Cisplatin	139-148	P53	Homo sapiens	213-216
24434508-0	2014	The traditional Chinese medical compound Rocaglamide protects nonmalignant primary cells from DNA damage-induced toxicity by inhibition of p53 expression.	rocaglamide	41-52	P53	Homo sapiens	139-142
24434508-6	2014	Investigation of the molecular mechanism of Roc-A-mediated protection revealed that Roc-A specifically blocks DNA damage-induced upregulation of the transcription factor p53 by inhibiting its protein synthesis.	rocaglamide	44-49	P53	Homo sapiens	170-173
24434508-9	2014	Our data suggest that Roc-A may be used as an adjuvant to reduce the side effects of chemotherapy in patients with p53-deficient or -mutated tumors.	rocaglamide	22-27	P53	Homo sapiens	115-118
24289924-5	2014	As cellular ATP levels recover, TAF1 is able to phosphorylate p53 on Thr55, which leads to dissociation of p53 from the p21 promoter.	Adenosine Triphosphate	12-15	P53	Homo sapiens	62-65
24275138-2	2014	Others subsequently indicated that mutant p53 tumor cells undergo p53 degradation and cell death under aerobic glucose-free conditions.	Glucose	111-118	P53	Homo sapiens	42-45
24314664-6	2014	Doxorubicin, a commonly used chemotherapeutic agent, induces apoptosis through p53 and p73 signaling such that the lowDeltaNp73 level promotes the p73-mediated intrinsic pathway of apoptosis.	Doxorubicin	0-11	P53	Homo sapiens	79-82
24275138-2	2014	Others subsequently indicated that mutant p53 tumor cells undergo p53 degradation and cell death under aerobic glucose-free conditions.	Glucose	111-118	P53	Homo sapiens	66-69
24275138-4	2014	p53 Silencing decreased survival of glucose-starved C8161 melanoma with pyruvate supplementation under hypoxia (&lt;=1% oxygen), but increased resistance to glycolytic inhibitors oxamate and 2-deoxyglucose in 5mM glucose, preferentially under normoxia.	Glucose	36-43	P53	Homo sapiens	0-3
24275138-4	2014	p53 Silencing decreased survival of glucose-starved C8161 melanoma with pyruvate supplementation under hypoxia (&lt;=1% oxygen), but increased resistance to glycolytic inhibitors oxamate and 2-deoxyglucose in 5mM glucose, preferentially under normoxia.	Oxygen	120-126	P53	Homo sapiens	0-3
24275138-4	2014	p53 Silencing decreased survival of glucose-starved C8161 melanoma with pyruvate supplementation under hypoxia (&lt;=1% oxygen), but increased resistance to glycolytic inhibitors oxamate and 2-deoxyglucose in 5mM glucose, preferentially under normoxia.	Glucose	198-205	P53	Homo sapiens	0-3
24052409-3	2014	We demonstrated that mahanine-induced apoptosis involved reactive oxygen species (ROS)-mediated nuclear accumulation of PTEN and its interaction with p53/p73.	Reactive Oxygen Species	57-80	P53	Homo sapiens	150-153
24403501-10	2014	Cisplatin produced a similar profile, with increased p53 protein.	Cisplatin	0-9	P53	Homo sapiens	53-56
24052409-3	2014	We demonstrated that mahanine-induced apoptosis involved reactive oxygen species (ROS)-mediated nuclear accumulation of PTEN and its interaction with p53/p73.	Reactive Oxygen Species	82-85	P53	Homo sapiens	150-153
24052409-0	2014	Mahanine synergistically enhances cytotoxicity of 5-fluorouracil through ROS-mediated activation of PTEN and p53/p73 in colon carcinoma.	Fluorouracil	50-64	P53	Homo sapiens	109-112
24052409-0	2014	Mahanine synergistically enhances cytotoxicity of 5-fluorouracil through ROS-mediated activation of PTEN and p53/p73 in colon carcinoma.	Reactive Oxygen Species	73-76	P53	Homo sapiens	109-112
25422197-11	2014	The analysis of p53 72 SNP revealed that p53 (Arg/Arg), (Pro /Arg) variant are higher (40.59% and 33.66%) as compared to p53 pro/pro variant (25.74%) in the healthy population.	Arginine	46-49	P53	Homo sapiens	16-19
25520084-0	2014	Roles of p53 and caspases in induction of apoptosis in MCF- 7 breast cancer cells treated with a methanolic extract of Nigella sativa seeds.	methanolic	97-107	P53	Homo sapiens	9-12
24998560-6	2014	DAPI and TUNEL staining showed that parthenolide could increase the number of apoptotic nuclei, while reducing the expression of the anti-apoptotic protein Bcl-2 and elevating the expression of related proteins, like p53, Bax, cleaved caspase9 and cleaved caspase3.	parthenolide	36-48	P53	Homo sapiens	217-220
24935359-10	2014	The combined p53 with p16(INK4a) profiles were significantly correlated with alcohol consumption in younger patients (p=0.006).	Alcohols	77-84	P53	Homo sapiens	13-16
25422197-11	2014	The analysis of p53 72 SNP revealed that p53 (Arg/Arg), (Pro /Arg) variant are higher (40.59% and 33.66%) as compared to p53 pro/pro variant (25.74%) in the healthy population.	Arginine	46-49	P53	Homo sapiens	41-44
25422197-11	2014	The analysis of p53 72 SNP revealed that p53 (Arg/Arg), (Pro /Arg) variant are higher (40.59% and 33.66%) as compared to p53 pro/pro variant (25.74%) in the healthy population.	Arginine	46-49	P53	Homo sapiens	41-44
25422197-11	2014	The analysis of p53 72 SNP revealed that p53 (Arg/Arg), (Pro /Arg) variant are higher (40.59% and 33.66%) as compared to p53 pro/pro variant (25.74%) in the healthy population.	Arginine	50-53	P53	Homo sapiens	16-19
25422197-11	2014	The analysis of p53 72 SNP revealed that p53 (Arg/Arg), (Pro /Arg) variant are higher (40.59% and 33.66%) as compared to p53 pro/pro variant (25.74%) in the healthy population.	Arginine	50-53	P53	Homo sapiens	41-44
25422197-11	2014	The analysis of p53 72 SNP revealed that p53 (Arg/Arg), (Pro /Arg) variant are higher (40.59% and 33.66%) as compared to p53 pro/pro variant (25.74%) in the healthy population.	Arginine	50-53	P53	Homo sapiens	41-44
24606472-0	2014	Expression of bcl-2 and p53 in induction of esophageal cancer cell apoptosis by ECRG2 in combination with cisplatin.	Cisplatin	106-115	P53	Homo sapiens	24-27
25422197-11	2014	The analysis of p53 72 SNP revealed that p53 (Arg/Arg), (Pro /Arg) variant are higher (40.59% and 33.66%) as compared to p53 pro/pro variant (25.74%) in the healthy population.	Arginine	50-53	P53	Homo sapiens	16-19
24606473-4	2014	Curcumin inhibited HDACs, HPV expression and differentially increased acetylation and up-regulation of p53 in SiHa and SiHaR, leading to cell cycle arrest at G1-S phase.	Curcumin	0-8	P53	Homo sapiens	103-106
25422197-11	2014	The analysis of p53 72 SNP revealed that p53 (Arg/Arg), (Pro /Arg) variant are higher (40.59% and 33.66%) as compared to p53 pro/pro variant (25.74%) in the healthy population.	Arginine	50-53	P53	Homo sapiens	41-44
24716981-4	2014	Expression of p53 protein was evaluated immunohistochemically in sections of paraffin- embedded tissue.	Paraffin	77-85	P53	Homo sapiens	14-17
25422197-11	2014	The analysis of p53 72 SNP revealed that p53 (Arg/Arg), (Pro /Arg) variant are higher (40.59% and 33.66%) as compared to p53 pro/pro variant (25.74%) in the healthy population.	Arginine	50-53	P53	Homo sapiens	41-44
23073516-1	2014	BACKGROUND: Investigation of p53 immunoreactivity in formalin-fixed paraffin-embedded tissues of normal renal tissue and renal cell carcinoma with respect to histopathologic subtype and nuclear grade of RCC.	Paraffin	68-76	P53	Homo sapiens	29-32
23983146-8	2014	In addition, neferine could induce p53 and its effector protein p21 and downregulation of cell cycle regulatory protein cyclin D1 thereby inducing G1 cell cycle arrest.	neferine	13-21	P53	Homo sapiens	35-38
24761888-6	2014	Further, significant differences were observed in the p53 exon 8 mutations for the genetic polymorphisms of Lys/Arg for AhR (p=0.02, 95%CI: 0.70-15.86), Val/Val for CYP1A1 (p=0.04, 95%CI: 0.98-19.09) and null for GSTM1 (p=0.02, 95%CI: 1.19-6.26), respectively.	Lysine	108-111	P53	Homo sapiens	54-57
24761888-6	2014	Further, significant differences were observed in the p53 exon 8 mutations for the genetic polymorphisms of Lys/Arg for AhR (p=0.02, 95%CI: 0.70-15.86), Val/Val for CYP1A1 (p=0.04, 95%CI: 0.98-19.09) and null for GSTM1 (p=0.02, 95%CI: 1.19-6.26), respectively.	Arginine	112-115	P53	Homo sapiens	54-57
23583620-0	2014	Dipeptide analysis of p53 mutations and evolution of p53 family proteins.	Dipeptides	0-9	P53	Homo sapiens	22-25
23583620-5	2014	We analyze the amino acid and dipeptide composition of p53/p63/p73 proteins across evolution and compare them with the gain/loss of amino acids and dipeptides in human p53 following cancer-related somatic mutations.	Dipeptides	30-39	P53	Homo sapiens	55-58
23583620-5	2014	We analyze the amino acid and dipeptide composition of p53/p63/p73 proteins across evolution and compare them with the gain/loss of amino acids and dipeptides in human p53 following cancer-related somatic mutations.	Dipeptides	148-158	P53	Homo sapiens	168-171
23583620-7	2014	The dipeptide mutational gain/loss ratios are inversely correlated with those observed over p53 evolution but tend to follow the increasing p63/p73-like dipeptide propensities.	Dipeptides	4-13	P53	Homo sapiens	92-95
23583620-8	2014	We successfully simulated the p53 cancer mutation spectrum using the dipeptide composition across the p53 family accounting for the likelihood of mutations in p53 codons.	Dipeptides	69-78	P53	Homo sapiens	30-33
23583620-8	2014	We successfully simulated the p53 cancer mutation spectrum using the dipeptide composition across the p53 family accounting for the likelihood of mutations in p53 codons.	Dipeptides	69-78	P53	Homo sapiens	102-105
23583620-8	2014	We successfully simulated the p53 cancer mutation spectrum using the dipeptide composition across the p53 family accounting for the likelihood of mutations in p53 codons.	Dipeptides	69-78	P53	Homo sapiens	102-105
24189097-1	2014	For developing a multifunctional bioreducible targeted and synergistic co-delivery system for anticancer drug paclitaxel (PTX) and p53 gene for potential cancer therapy, supramolecular self-assembled inclusion complex was prepared from PTX and star-shaped cationic polymer containing gamma-cyclodextrin (gamma-CD) and multiple oligoethylenimine (OEI) arms with folic acid (FA) conjugated via a disulfide linker.	Paclitaxel	236-239	P53	Homo sapiens	131-134
24189097-8	2014	Therefore, the multifunctional gamma-CD-OEI-SS-FA/PTX self-assembly system with the synergistic effects of redox-sensitive FA-targeted and PTX-enhanced p53 gene delivery may be promising for cancer therapeutic application.	Paclitaxel	50-53	P53	Homo sapiens	152-155
24189097-8	2014	Therefore, the multifunctional gamma-CD-OEI-SS-FA/PTX self-assembly system with the synergistic effects of redox-sensitive FA-targeted and PTX-enhanced p53 gene delivery may be promising for cancer therapeutic application.	Paclitaxel	139-142	P53	Homo sapiens	152-155
25215298-6	2014	Moreover, we conducted p53 mutation analysis and revealed a mutation at codon 273 which led to the replacement of arginine by histidine.	Arginine	114-122	P53	Homo sapiens	23-26
24211075-0	2014	A cationic cholesterol based nanocarrier for the delivery of p53-EGFP-C3 plasmid to cancer cells.	Cholesterol	11-22	P53	Homo sapiens	61-64
25215298-6	2014	Moreover, we conducted p53 mutation analysis and revealed a mutation at codon 273 which led to the replacement of arginine by histidine.	Histidine	126-135	P53	Homo sapiens	23-26
24967384-6	2014	Our further studies demonstrated that ERR alpha suppressed ROS induction of tumor suppressor P53 and its target genes NOXA and XAF1 which are mediators of P53-dependent apoptosis.	Reactive Oxygen Species	59-62	P53	Homo sapiens	93-96
25250341-5	2014	RESULTS: ERCC1 118C and TP53 72Arg polymorphisms were associated with increased risks of platinum-induced nephrotoxicity.	Platinum	89-97	P53	Homo sapiens	24-28
25013761-9	2014	Our results also demonstrated that p53 was activated followed by generation of reactive oxygen species (ROS) and activation of c-Jun N-terminal kinase (JNK).	Reactive Oxygen Species	79-102	P53	Homo sapiens	35-38
25013761-9	2014	Our results also demonstrated that p53 was activated followed by generation of reactive oxygen species (ROS) and activation of c-Jun N-terminal kinase (JNK).	Reactive Oxygen Species	104-107	P53	Homo sapiens	35-38
24967384-6	2014	Our further studies demonstrated that ERR alpha suppressed ROS induction of tumor suppressor P53 and its target genes NOXA and XAF1 which are mediators of P53-dependent apoptosis.	Reactive Oxygen Species	59-62	P53	Homo sapiens	155-158
24967384-7	2014	In conclusion, this study demonstrated that ERR alpha plays an important role in the development of MTX resistance through blocking MTX-induced ROS production and attenuating the activation of p53 mediated apoptosis signaling pathway, and points to ERR alpha as a novel target for improving osteosarcoma therapy.	Reactive Oxygen Species	144-147	P53	Homo sapiens	193-196
25482940-2	2014	In this study, we investigated the role of the p53 and MDM2 genes in predicting adverse events in NSCLC patients treated with platinum-based chemotherapy.	Platinum	126-134	P53	Homo sapiens	47-50
24434574-8	2014	Ad-mda-7 treatments upregulated Akt phosphorylation but suppressed IkappaB-alpha levels, whereas 5-FU treatments induced phosphorylation of p53 and extracellular signal-regulated protein kinases 1 and 2.	Fluorouracil	97-101	P53	Homo sapiens	140-143
25482947-6	2014	We found that inhibitors of the mTOR pathway including rapamycin, wortmannin, and caffeine blunted the p53 response to nucleolar stress induced by actinomycin D.	Sirolimus	55-64	P53	Homo sapiens	103-106
25482947-10	2014	We found that rapamycin mimicked the effect of RPL11 depletion in terms of blunting the p53 response to nucleolar stress.	Sirolimus	14-23	P53	Homo sapiens	88-91
24552824-0	2014	The NAD+ synthesizing enzyme nicotinamide mononucleotide adenylyltransferase 2 (NMNAT-2) is a p53 downstream target.	NAD	4-7	P53	Homo sapiens	94-97
24846461-9	2014	We here show that this temporal separation of pro- and anti-apoptotic signaling induced by inhibition of Dicer1 is synergistic and synthetic lethal to low-dose 5-FU chemotherapy in p53-mutated HACAT cells.	Fluorouracil	160-164	P53	Homo sapiens	181-184
24621507-3	2014	Conversely, Tip60 activates p53 through direct association on target promoters as well as acetylation of p53 at lysine 120 (K120).	Lysine	112-118	P53	Homo sapiens	105-108
24552824-4	2014	This notion led us to examine whether p53 can regulate NAD(+) biosynthesis in the cell.	NAD	55-61	P53	Homo sapiens	38-41
24552824-8	2014	Furthermore, knockdown of NMNAT-2 significantly reduces cellular NAD(+) levels and protects cells from p53-dependent cell death upon DNA damage, suggesting an important functional role of NMNAT-2 in p53-mediated signaling.	NAD	65-71	P53	Homo sapiens	199-202
24552824-9	2014	Our demonstration that p53 modulates cellular NAD(+) synthesis is congruent with p53"s emerging role as a key regulator of metabolism and related cell fate.	NAD	46-52	P53	Homo sapiens	23-26
24552824-9	2014	Our demonstration that p53 modulates cellular NAD(+) synthesis is congruent with p53"s emerging role as a key regulator of metabolism and related cell fate.	NAD	46-52	P53	Homo sapiens	81-84
24169561-9	2014	Furthermore, CRT knock-down suppressed the ovarian steroid-stimulated PRL and IGFBP1 expression and morphological differentiation, and silencing of EPAC2 or CRT significantly increased senescence-associated beta-galactosidase activity with enhanced p21 expression and decreased p53 expression.	Steroids	51-58	P53	Homo sapiens	278-281
24240108-9	2014	The activation of HDM2 by AURKA led to induction of P53 ubiquitination and attenuation of cisplatin-induced activation of P53 in gastric cancer cells.	Cisplatin	90-99	P53	Homo sapiens	122-125
24899917-1	2014	The latest experimental evidence indicates that acetylation of p53 at K164 (lysine 164) and K120 may induce directly cell apoptosis under severe DNA damage.	Lysine	76-82	P53	Homo sapiens	63-66
24239893-0	2014	Resveratrol contributes to chemosensitivity of malignant mesothelioma cells with activation of p53.	Resveratrol	0-11	P53	Homo sapiens	95-98
25070816-0	2014	L-arginine enhances arginine deiminase induced human lymphoma cell growth inhibition through NF-kBp65 and p53 expression in vitro.	Arginine	0-10	P53	Homo sapiens	106-109
25070816-6	2014	RESULTS AND CONCLUSIONS: L-arginine enhanced ADI-induced inhibited cell growth through expression of NF-kappaBp65 and p53 in a dose-dependent manner.	Arginine	25-35	P53	Homo sapiens	118-121
25431609-5	2014	In addition, H2O2 produced transcriptional changes in p53, JNK, p38 MAPK, AKT, BAX, and CDK4 that were inclined towards apoptosis, while GBR-extracts showed some transcriptional changes (upregulation of BAX and p53) that suggested an inclination for apoptosis although other changes (upregulation of antioxidant genes, AKT, JNK, and p38 MAPK) suggested that GBR-extracts favored survival of the HepG2 cells.	Hydrogen Peroxide	13-17	P53	Homo sapiens	54-57
25431609-5	2014	In addition, H2O2 produced transcriptional changes in p53, JNK, p38 MAPK, AKT, BAX, and CDK4 that were inclined towards apoptosis, while GBR-extracts showed some transcriptional changes (upregulation of BAX and p53) that suggested an inclination for apoptosis although other changes (upregulation of antioxidant genes, AKT, JNK, and p38 MAPK) suggested that GBR-extracts favored survival of the HepG2 cells.	Hydrogen Peroxide	13-17	P53	Homo sapiens	211-214
24239893-4	2014	Resveratrol, in combination with clofarabine, time-dependently induced a strong cytotoxic effect with the nuclear accumulation of phospho-p53 (p-p53) in MSTO-211H cells, but not in normal mesothelial MeT-5A cells.	Resveratrol	0-11	P53	Homo sapiens	138-141
24239893-4	2014	Resveratrol, in combination with clofarabine, time-dependently induced a strong cytotoxic effect with the nuclear accumulation of phospho-p53 (p-p53) in MSTO-211H cells, but not in normal mesothelial MeT-5A cells.	Resveratrol	0-11	P53	Homo sapiens	145-148
24239893-10	2014	Taken together, these results demonstrate that resveratrol and clofarabine synergistically elicit apoptotic signal via a p53-dependent pathway, and provide a scientific rationale for clinical evaluation of resveratrol as a promising chemopotentiator in MM.	Resveratrol	47-58	P53	Homo sapiens	121-124
24239893-10	2014	Taken together, these results demonstrate that resveratrol and clofarabine synergistically elicit apoptotic signal via a p53-dependent pathway, and provide a scientific rationale for clinical evaluation of resveratrol as a promising chemopotentiator in MM.	Resveratrol	206-217	P53	Homo sapiens	121-124
24391441-1	2014	Oligonucleotides homologous to 3"-telomere overhang (T-oligos) trigger inherent telomere-based DNA damage responses mediated by p53 and/or ATM and induce senescence or apoptosis in various cancerous cells.	Oligonucleotides	0-16	P53	Homo sapiens	128-131
25693294-8	2014	There is clear evidence that the carbon-ion irradiation enables the enhanced cell killing in cells with wild-type P53 gene via gap-junction mediated bystander effect.	Carbon	33-39	P53	Homo sapiens	114-117
24173829-0	2014	S(+)-ibuprofen destabilizes MYC/MYCN and AKT, increases p53 expression, and induces unfolded protein response and favorable phenotype in neuroblastoma cell lines.	Ibuprofen	1-14	P53	Homo sapiens	56-59
24173829-9	2014	Gene expression profile and Ingenuity pathway analyses using TP53-mutated SKNAS cells further revealed that S(+)-ibuprofen suppressed molecular pathways associated with cell growth and conversely enhanced those of cell cycle arrest and the unfolded protein response.	Ibuprofen	109-122	P53	Homo sapiens	61-65
24190633-7	2014	MHY218 also caused an increase in the expression levels of p21(WAF1/CIP1), a G2/M phase inhibitor, in a p53-independent pathway.	N1-hydroxy-N8-(4-phenoxyphenyl)octanediamide	0-6	P53	Homo sapiens	104-107
24218165-7	2014	The presence of gammaH2AX foci and phosphorylation of TP53(ser15) and CHK1(ser317) were shown in U343 cells, compatible with cisplatin-induced DNA damage.	Cisplatin	125-134	P53	Homo sapiens	54-58
24724504-3	2014	In addition, drug Gliotoxin (GTX) and targeting molecules (Lysozyme, p53 and Folic acid) have been incorporated into f-SWNT-COS. f-SWNTs-COS-GTX-p53, f-SWNTs-COS-GTX-lysozyme, f-SWNTs-COS-GTX-FA have been physiochemically characterized for DDS.	Folic Acid	77-87	P53	Homo sapiens	145-148
24724504-3	2014	In addition, drug Gliotoxin (GTX) and targeting molecules (Lysozyme, p53 and Folic acid) have been incorporated into f-SWNT-COS. f-SWNTs-COS-GTX-p53, f-SWNTs-COS-GTX-lysozyme, f-SWNTs-COS-GTX-FA have been physiochemically characterized for DDS.	carbonyl sulfide	124-127	P53	Homo sapiens	69-72
24724504-3	2014	In addition, drug Gliotoxin (GTX) and targeting molecules (Lysozyme, p53 and Folic acid) have been incorporated into f-SWNT-COS. f-SWNTs-COS-GTX-p53, f-SWNTs-COS-GTX-lysozyme, f-SWNTs-COS-GTX-FA have been physiochemically characterized for DDS.	carbonyl sulfide	124-127	P53	Homo sapiens	145-148
24724504-3	2014	In addition, drug Gliotoxin (GTX) and targeting molecules (Lysozyme, p53 and Folic acid) have been incorporated into f-SWNT-COS. f-SWNTs-COS-GTX-p53, f-SWNTs-COS-GTX-lysozyme, f-SWNTs-COS-GTX-FA have been physiochemically characterized for DDS.	carbonyl sulfide	137-140	P53	Homo sapiens	69-72
24724504-3	2014	In addition, drug Gliotoxin (GTX) and targeting molecules (Lysozyme, p53 and Folic acid) have been incorporated into f-SWNT-COS. f-SWNTs-COS-GTX-p53, f-SWNTs-COS-GTX-lysozyme, f-SWNTs-COS-GTX-FA have been physiochemically characterized for DDS.	carbonyl sulfide	137-140	P53	Homo sapiens	145-148
24056736-4	2014	These forms of p53 were purified from whole cell lysates by means of immunoaffinity chromatography and SDS-PAGE, and peptides derived from them were subjected to nano-ultra-high-performance LC-MS and MS/MS analyses on a high-resolution accurate-mass MS platform (data available via ProteomeXchange, PXD000464).	Sodium Dodecyl Sulfate	103-106	P53	Homo sapiens	15-18
25393968-4	2014	The results show that berberine is able to arrest cell cycle and activate apoptotic pathway as shown in both cell lines by deoxyribonucleic acid fragmentation, caspase-3 cleavage, p53 and p27 protein overexpression.	Berberine	22-31	P53	Homo sapiens	180-183
24190973-8	2014	The activation of p53 through AMPK-mediated MDMX phosphorylation and inactivation was further confirmed by using cell and animal model systems with two AMPK activators, metformin and salicylate (the active form of aspirin).	Metformin	169-178	P53	Homo sapiens	18-21
24190973-8	2014	The activation of p53 through AMPK-mediated MDMX phosphorylation and inactivation was further confirmed by using cell and animal model systems with two AMPK activators, metformin and salicylate (the active form of aspirin).	Aspirin	214-221	P53	Homo sapiens	18-21
24012657-0	2014	Acetyl-L-carnitine rescues scopolamine-induced memory deficits by restoring insulin-like growth factor II via decreasing p53 oxidation.	Acetylcarnitine	0-18	P53	Homo sapiens	121-124
24445528-9	2014	Phosphorylation of p53 at serine-15 and of Sp1 at serines appears to be involved.	Serine	26-32	P53	Homo sapiens	19-22
24012657-5	2014	The beneficial effects of acetyl-L-carnitine may occur through amelioration of oxidative stress because it effectively decreases the levels of oxidative products and increases the activity of superoxide dismutase; this leads to a recovery in the suppressed activity of p53 caused oxidative stimuli, which in turn restores levels of insulin-like growth factor II, an important hormone for learning and memory.	Acetylcarnitine	26-44	P53	Homo sapiens	269-272
24121312-0	2014	Correlation of (18)F-fluoromisonidazole PET findings with HIF-1alpha and p53 expressions in head and neck cancer: comparison with (18)F-FDG PET.	fluoromisonidazole	21-39	P53	Homo sapiens	73-76
24173110-4	2014	Three SNPs in the p53 pathway were identified using the Sanger sequencing method from retrospectively collected paraffin-embedded biopsy specimens.	Paraffin	112-120	P53	Homo sapiens	18-21
24173208-0	2014	Autophagy induction by low-dose cisplatin: the role of p53 in autophagy.	Cisplatin	32-41	P53	Homo sapiens	55-58
24173208-13	2014	Following 3-MA pretreatment, cisplatin-induced autophagy was found to be markedly reduced (a 3-fold reduction) in wild-type p53 compared to null-type p53 cells.	3-methyladenine	10-14	P53	Homo sapiens	124-127
24173208-13	2014	Following 3-MA pretreatment, cisplatin-induced autophagy was found to be markedly reduced (a 3-fold reduction) in wild-type p53 compared to null-type p53 cells.	Cisplatin	29-38	P53	Homo sapiens	124-127
24173208-13	2014	Following 3-MA pretreatment, cisplatin-induced autophagy was found to be markedly reduced (a 3-fold reduction) in wild-type p53 compared to null-type p53 cells.	Cisplatin	29-38	P53	Homo sapiens	150-153
24173208-14	2014	However, cisplatin-induced apoptosis increased in wild-type p53 compared to null-type p53 cells.	Cisplatin	9-18	P53	Homo sapiens	60-63
24173208-14	2014	However, cisplatin-induced apoptosis increased in wild-type p53 compared to null-type p53 cells.	Cisplatin	9-18	P53	Homo sapiens	86-89
24173208-15	2014	Autophagy induction and apoptotic shift after autophagy inhibition may be mediated by p53 activation in lung cancer cells treated with low-dose cisplatin.	Cisplatin	144-153	P53	Homo sapiens	86-89
25140197-5	2014	Therefore, combination of ATRA with DAC and SAHA represents promising tool for therapy of leukemic disease with nonfunctional p53 signalization.	Tretinoin	26-30	P53	Homo sapiens	126-129
24038750-3	2014	We further discovered that the silencing of Oct4 significantly reduces the expression of Sirt1, a deacetylase known to inhibit p53 activity and the differentiation of ESCs, leading to increased acetylation of p53 at lysine 120 and 164.	Lysine	216-222	P53	Homo sapiens	209-212
24038750-5	2014	In addition, using knock-in approach, we revealed that the acetylation of p53 at lysine 120 and 164 is required for both stabilization and activity of p53 in hESCs.	Lysine	81-87	P53	Homo sapiens	74-77
24038750-5	2014	In addition, using knock-in approach, we revealed that the acetylation of p53 at lysine 120 and 164 is required for both stabilization and activity of p53 in hESCs.	Lysine	81-87	P53	Homo sapiens	151-154
24078252-2	2014	We performed genome-wide profiling of p53 chromatin interactions and target gene expression in human embryonic stem cells (hESCs) in response to early differentiation, induced by retinoic acid, versus DNA damage, caused by adriamycin.	Tretinoin	179-192	P53	Homo sapiens	38-41
24078252-2	2014	We performed genome-wide profiling of p53 chromatin interactions and target gene expression in human embryonic stem cells (hESCs) in response to early differentiation, induced by retinoic acid, versus DNA damage, caused by adriamycin.	Doxorubicin	223-233	P53	Homo sapiens	38-41
24712372-6	2014	Meanwhile, as a critical regulator in the cisplatin-induced apoptosis, p53 was elevated by silencing of hsa-miR-98-5p.	Cisplatin	42-51	P53	Homo sapiens	71-74
24712372-7	2014	These results suggested that EGCG inhibited the expression of hsa-miR-98-5p, followed by an increase of p53, thus the efficacy of cisplatin was enhanced.	Cisplatin	130-139	P53	Homo sapiens	104-107
24348832-11	2014	In addition, VX680 and cisplatin increased the expression of the p53 protein.	Cisplatin	23-32	P53	Homo sapiens	65-68
24732641-0	2014	MDM2 rs2279744 and TP53 rs1042522 polymorphisms associated with etoposide- and cisplatin-induced grade III/IV neutropenia in Chinese extensive-stage small-cell lung cancer patients.	Cisplatin	79-88	P53	Homo sapiens	19-23
26168133-7	2014	Berberine induced cell cycle arrest at the G2/M phase by upregulation of p53 and p21 expression and suppressed cyclin B1, cyclin-dependent kinase 1 (cdc2), cdc25c, and phosphorylated retinoblastoma tumor-suppressor protein (pRb) expression.	Berberine	0-9	P53	Homo sapiens	73-76
26168133-9	2014	Inhibition of phosphatidylinositol 3-kinase (PI3K)/Akt with LY294002 (LY) and p38 kinase with SB203580 (SB), respectively, decreased berberine-induced p53 and p21 expression and restored cell proliferation and expression of cyclin B1, cdc2, cdc25c, and pRb cell cycle progression proteins.	Berberine	133-142	P53	Homo sapiens	151-154
25140197-0	2014	Decitabine and SAHA-induced apoptosis is accompanied by survivin downregulation and potentiated by ATRA in p53-deficient cells.	Tretinoin	99-103	P53	Homo sapiens	107-110
25140197-1	2014	While p53-dependent apoptosis is triggered by combination of methyltransferase inhibitor decitabine (DAC) and histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) in leukemic cell line CML-T1, reactive oxygen species (ROS) generation as well as survivin and Bcl-2 deregulation participated in DAC + SAHA-induced apoptosis in p53-deficient HL-60 cell line.	Reactive Oxygen Species	209-232	P53	Homo sapiens	6-9
25140197-1	2014	While p53-dependent apoptosis is triggered by combination of methyltransferase inhibitor decitabine (DAC) and histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) in leukemic cell line CML-T1, reactive oxygen species (ROS) generation as well as survivin and Bcl-2 deregulation participated in DAC + SAHA-induced apoptosis in p53-deficient HL-60 cell line.	Reactive Oxygen Species	234-237	P53	Homo sapiens	6-9
25147862-4	2014	Further results indicated that Vit C caused the dysregulation of some stress responses factors (SIRT1, p53 and FOXO3) in ARPE-19 cells response to H2O2.	Hydrogen Peroxide	147-151	P53	Homo sapiens	103-106
25201196-0	2014	Crosstalk between Mdm2, p53 and HIF1-alpha: distinct responses to oxygen stress and implications for tumour hypoxia.	Oxygen	66-72	P53	Homo sapiens	24-27
24900784-0	2014	Discovery of Potent and Orally Active p53-MDM2 Inhibitors RO5353 and RO2468 for Potential Clinical Development.	ro5353	58-64	P53	Homo sapiens	38-41
24900784-4	2014	Here we report two new potent, selective, and orally active p53-MDM2 antagonists, RO5353 and RO2468, as follow-ups with promising potential for clinical development.	ro5353	82-88	P53	Homo sapiens	60-63
24376578-10	2013	In the MDM2 SNP309-TP53 R72P interaction analysis, we found that subjects with MDM2 309TT and TP53 Pro/Pro genotype, MDM2 309 TG and TP53 Arg/Pro genotype, and MDM2 309 GG and TP53 Pro/Pro genotype were associated with significantly increased risk of developing HCC as compared with the reference MDM2 309TT and TP53 Arg/Arg genotype.	Arginine	138-141	P53	Homo sapiens	19-23
24359630-14	2013	Collectively, these data reveal a role for p53 in cellular metabolic reprogramming under acidosis, in order to permit increased bioenergetic capacity and ROS neutralization.	Reactive Oxygen Species	154-157	P53	Homo sapiens	43-46
24163369-8	2013	Chromatin immunoprecipitation demonstrated direct and specific association of p53 with the distal NEK2 promoter, which was enhanced by doxorubicin.	Doxorubicin	135-146	P53	Homo sapiens	78-81
24376853-10	2013	Moreover, the p53 was phosphorylated, translocated into nucleus, and bound to Rp following ROS stimulation.	Reactive Oxygen Species	91-94	P53	Homo sapiens	14-17
24376853-11	2013	The results suggest ROS play an important role in initiation of EBV reactivation by MNNG through a p53-dependent mechanism.	Reactive Oxygen Species	20-23	P53	Homo sapiens	99-102
24163369-7	2013	Stabilization of endogenous p53 by doxorubicin or ectopic expression of p53, but not a p53 DNA-binding mutant, decreased NEK2 expression.	Doxorubicin	35-46	P53	Homo sapiens	28-31
24099794-1	2013	The successful clinical management of lung cancer is limited by frequent loss-of-function mutations in p53 which cooperates with chronic oxidant-stress induced adaptations in mercapturic acid pathway (MAP) which in turn regulates critical intracellular signaling cascades that determine therapeutic refractoriness.	Acetylcysteine	175-191	P53	Homo sapiens	103-106
24330748-5	2013	Immuno-precipitation/-blot studies were performed to demonstrate interactions between Id4, p53 and CBP/p300 and acetylation of specific lysine residues within p53.	Lysine	136-142	P53	Homo sapiens	159-162
24076372-5	2013	PLK1 was downregulated in cisplatin exposed HCT116p53(+/+) but not HCT116p53(-/-) cells, indicating p53-suppressed PLK1 upon DNA damage.	Cisplatin	26-35	P53	Homo sapiens	50-53
32261335-7	2013	Furthermore, Se@Trolox effectively blocked the cisplatin-induced reactive oxygen species (ROS) accumulation, activation of AKT and MAPK signaling and DNA damage-mediated p53 phosphorylation in HK-2 cells.	Cisplatin	47-56	P53	Homo sapiens	170-173
32261335-7	2013	Furthermore, Se@Trolox effectively blocked the cisplatin-induced reactive oxygen species (ROS) accumulation, activation of AKT and MAPK signaling and DNA damage-mediated p53 phosphorylation in HK-2 cells.	Reactive Oxygen Species	65-88	P53	Homo sapiens	170-173
32261335-7	2013	Furthermore, Se@Trolox effectively blocked the cisplatin-induced reactive oxygen species (ROS) accumulation, activation of AKT and MAPK signaling and DNA damage-mediated p53 phosphorylation in HK-2 cells.	Reactive Oxygen Species	90-93	P53	Homo sapiens	170-173
24336073-3	2013	We identified two abundantly expressed microRNAs, miR-16 and miR-26a, whose expression is regulated by p53 during the checkpoint arrest induced by the genotoxic drug, doxorubicin.	Doxorubicin	167-178	P53	Homo sapiens	103-106
24139845-0	2013	Trisubstituted and tetrasubstituted pyrazolines as a novel class of cell-growth inhibitors in tumor cells with wild type p53.	pyrazolines	36-47	P53	Homo sapiens	121-124
24309939-10	2013	Molecular docking analysis suggested that WA could bind to HRas-GTP, causing accumulation of Ras-GTP and excessive activation of Raf/ERK/p53-p21.	Guanosine Triphosphate	64-67	P53	Homo sapiens	137-140
24002658-0	2013	Role of p53 in cAMP/PKA pathway mediated apoptosis.	Cyclic AMP	15-19	P53	Homo sapiens	8-11
24145670-3	2013	In a recent issue of Genes &amp; Development, we demonstrated that blocking macroautophagy under nutritional stress condition leads to the degradation of mutant TP53 through activating the chaperone-mediated autophagy (CMA) pathway in nonproliferating cancer cells.	Adenosine Monophosphate	28-31	P53	Homo sapiens	161-165
23999236-5	2013	Protection by EHT1864 was observed in both p53 wildtype (HepG2) and p53 deficient (Hep3B) human hepatoma cells and, furthermore, remained unaffected upon pharmacological inhibition of p53 in HepG2.	EHT 1864	14-21	P53	Homo sapiens	43-46
23999236-5	2013	Protection by EHT1864 was observed in both p53 wildtype (HepG2) and p53 deficient (Hep3B) human hepatoma cells and, furthermore, remained unaffected upon pharmacological inhibition of p53 in HepG2.	EHT 1864	14-21	P53	Homo sapiens	68-71
23999236-5	2013	Protection by EHT1864 was observed in both p53 wildtype (HepG2) and p53 deficient (Hep3B) human hepatoma cells and, furthermore, remained unaffected upon pharmacological inhibition of p53 in HepG2.	EHT 1864	14-21	P53	Homo sapiens	68-71
24090840-4	2013	At low level of ZnO NMs induced ROS, p53 triggers expression of antioxidant genes such as SOD2, GPX1, SESN1, SESN2 and ALDH4A1 to restore oxidative homeostasis while at high concentration of ZnO NMs, the elevated level of intracellular ROS activated the apoptotic pathway through p53.	Reactive Oxygen Species	32-35	P53	Homo sapiens	37-40
24090840-4	2013	At low level of ZnO NMs induced ROS, p53 triggers expression of antioxidant genes such as SOD2, GPX1, SESN1, SESN2 and ALDH4A1 to restore oxidative homeostasis while at high concentration of ZnO NMs, the elevated level of intracellular ROS activated the apoptotic pathway through p53.	Reactive Oxygen Species	236-239	P53	Homo sapiens	37-40
24090840-6	2013	p53 deficient cells cancer cells such as DLD-1 and SW480 are more susceptible to ZnO induced cell death compared to p53 proficient cells such as colon epithelial cells NCM460 and HCT116 cells in a ROS dependent manner.	Reactive Oxygen Species	197-200	P53	Homo sapiens	0-3
24090840-6	2013	p53 deficient cells cancer cells such as DLD-1 and SW480 are more susceptible to ZnO induced cell death compared to p53 proficient cells such as colon epithelial cells NCM460 and HCT116 cells in a ROS dependent manner.	Reactive Oxygen Species	197-200	P53	Homo sapiens	116-119
24032643-8	2013	Melatonin in the nanomolar range activates the intrinsic and/or the extrinsic apoptotic pathway in cancer cells, namely through an increase in the p53/MDM2p ratio and downregulation of Sirt1.	Melatonin	0-9	P53	Homo sapiens	147-150
23983135-10	2013	Heme iron intake was associated with an increased risk of colorectal tumors harboring G&gt;A transitions in KRAS and APC and overexpression of P53.	Iron	5-9	P53	Homo sapiens	143-146
23983135-9	2013	Heme iron intake was positively associated with the risk of P53 overexpressed tumors but not with tumors without P53 overexpression (Pheterogeneity = 0.12).	Iron	5-9	P53	Homo sapiens	60-63
24293316-4	2013	This netrin-1 upregulation which appears to be p53-dependent is a survival mechanism as netrin-1 silencing by siRNA is associated with a potentiation of cancer cell death upon Doxorubicin treatment.	Doxorubicin	176-187	P53	Homo sapiens	47-50
23837948-4	2013	This study demonstrates that SeC acts as an effective enhancer of 5-FU-induced apoptosis in A375 human melanoma cells through induction of mitochondria-mediated apoptosis with the involvement of DNA damage-mediated p53 phosphorylation and ERK inactivation.	Fluorouracil	66-70	P53	Homo sapiens	215-218
23792775-5	2013	We found that NAC displayed a broad-spectrum chemoprotective activity against all three metals, including suppression of cytotoxicity, apoptosis, p53 activation, and HSP72 and HIF-1alpha upregulation.	Acetylcysteine	14-17	P53	Homo sapiens	146-149
24141649-11	2013	SNU-1528 had an in-frame deletion of 42 base pairs of p53 gene and showed over 20-fold resistance for taxol compared to the other cell lines.	Paclitaxel	102-107	P53	Homo sapiens	54-57
23786650-0	2013	Alpha particle-induced bystander effect is mediated by ROS via a p53-dependent SCO2 pathway in hepatoma cells.	Reactive Oxygen Species	55-58	P53	Homo sapiens	65-68
24253321-11	2013	The keys residues which contribute to the binding of p53 to DNA by forming crucial hydrogen bonds have also been discussed in detail.	Hydrogen	83-91	P53	Homo sapiens	53-56
23625774-11	2013	p53 levels were inversely associated with the expression of Oct4, Sox2, and Nanog in response to cisplatin.	Cisplatin	97-106	P53	Homo sapiens	0-3
24231356-9	2013	Furthermore, P110-TAT treatment suppressed mtHtt-induced association of p53 with mitochondria in multiple HD models.	mthtt	43-48	P53	Homo sapiens	72-75
23897043-2	2013	The goal of the trial was to determine whether p53 status could be used to select patients who would benefit from inclusion of taxanes in anthracycline-based chemotherapy.	Taxoids	127-134	P53	Homo sapiens	47-50
23897043-2	2013	The goal of the trial was to determine whether p53 status could be used to select patients who would benefit from inclusion of taxanes in anthracycline-based chemotherapy.	Anthracyclines	138-151	P53	Homo sapiens	47-50
24210632-9	2013	Therefore, we hypothesize that conjugation of hydrophilic vitamin folic acid or its analogs to these drugs (termed "FOLICation") may provide them with the much-needed hydrophilic cover and make them suitable for investigation as potentially novel p53-MDM2 inhibitors.	vitamin folic acid	58-76	P53	Homo sapiens	247-250
24280450-0	2013	Evaluation of zinc (II) chelators for inhibiting p53-mediated apoptosis.	Zinc	14-23	P53	Homo sapiens	49-52
24005536-6	2013	Capsaicin administration induced p53 activation, mitochondrial translocation and Bcl-2 killer association, such effects were dependent on AMPK activation.	Capsaicin	0-9	P53	Homo sapiens	33-36
24280450-9	2013	Our findings indicate that the use of zinc (II) chelators represent a new approach for protecting against radiation-induced p53-dependent apoptosis through the inhibition of p53-dependent apoptotic pathways.	Zinc	38-47	P53	Homo sapiens	124-127
24280450-9	2013	Our findings indicate that the use of zinc (II) chelators represent a new approach for protecting against radiation-induced p53-dependent apoptosis through the inhibition of p53-dependent apoptotic pathways.	Zinc	38-47	P53	Homo sapiens	174-177
24188375-8	2013	Hydrogen peroxide generation by oxidation of 2",7"-dichlorodihydrofluorescein diacetate to the fluorescent compound 2",7"-dichlorfluorescein assay, acridine orange/ethidium bromide staining, flow cytometry analysis of annexin-V/7-amino-actinomycin, mitochondrial membrane potential and immunocytochemistry detection of transcription factor p53, caspase-3 and apoptosis-inducing factor (AIF) were evaluated.	Hydrogen Peroxide	0-17	P53	Homo sapiens	340-343
24256616-6	2013	Chromatin Immuno-Precipitation (ChIP) assays conducted in doxorubicin-treated MCF7 cells and HCT116 p53+/+ revealed moderate induction of p53 occupancy at the miR-202, -1204, -1206, -10b RE-containing sites, while weak occupancy was observed for the miR-23b-associated RE only in MCF7 cells.	Doxorubicin	58-69	P53	Homo sapiens	138-141
24256616-7	2013	RT-qPCR analyses cells showed modest doxorubicin- and/or Nutlin-dependent induction of the levels of mature miR-10b, -23b, -151a in HCT116 p53+/+ and MCF7 cells.	Doxorubicin	37-48	P53	Homo sapiens	139-142
24278348-0	2013	Human serum albumin and p53-activating peptide fusion protein is able to promote apoptosis and deliver fatty acid-modified molecules.	Fatty Acids	103-113	P53	Homo sapiens	24-27
24348903-5	2013	In addition to p53 mediated apoptotic signatures, GSEA and pathway analysis identified a set of p53-repressed genes that were reciprocally over-expressed in neuroblastoma patients with the worst overall outcome in multiple clinical cohorts.	gsea	50-54	P53	Homo sapiens	96-99
24136147-9	2013	Addition of the chemotherapeutic drug cisplatin to the combination further increased p53 and DR5 levels and rhTRAIL- and D269H/E195R-induced apoptosis.	Cisplatin	38-47	P53	Homo sapiens	85-88
24244623-8	2013	In addition we observed that the combined exposure to Cyclosporine A + nerve growth factor promoted an up-regulation of p75 (NTR) and its target genes, p53 and BAD leading to the activation of intrinsic apoptosis.	Cyclosporine	54-68	P53	Homo sapiens	152-155
23954456-7	2013	Catechin downregulated Bcl-2, initiated the release of cytochrome c into the cytosol and upregulated Bax, caspase-3,-9 and p53 in the HepG2 cells.	Catechin	0-8	P53	Homo sapiens	123-126
24244378-3	2013	Recently, antisense oligonucleotides have been used to reduce the p53 level in tumour cells which facilitates their radiation-induced apoptosis.	Oligonucleotides	20-36	P53	Homo sapiens	66-69
24191930-3	2013	The NAPA (protein) Napsin A was described to promote resistance to cisplatin by degradation of the tumor suppressor p53.	Cisplatin	67-76	P53	Homo sapiens	116-119
24000115-6	2013	Real-time PCR analyses showed that berberine, NAX012 and NAX014 compounds increased the expression of some cell-cycle checkpoint molecules involved in cell senescence such as p53, p21(WAF1) , p16(INK4a) , and PAI-1, already after 24 h of 50 microM treatments.	Berberine	35-44	P53	Homo sapiens	175-178
23949254-7	2013	GSK461364 has shown a greater sensitive antitumor effect in p53-mutated cancer compared with that of p53-wild type cancer cells in a preclinical study.	GSK 461364	0-9	P53	Homo sapiens	60-63
23911866-5	2013	The resulting accumulation of p53 proteins from phosphorylation at Ser-15 and Ser-392 correlated with an increase in p21 and caspase activation.	Serine	67-70	P53	Homo sapiens	30-33
23911866-5	2013	The resulting accumulation of p53 proteins from phosphorylation at Ser-15 and Ser-392 correlated with an increase in p21 and caspase activation.	Serine	78-81	P53	Homo sapiens	30-33
23703322-0	2013	p53 regulates a non-apoptotic death induced by ROS.	Reactive Oxygen Species	47-50	P53	Homo sapiens	0-3
23494264-3	2013	In addition, our findings revealed that the sequential activity of Foxo3a by guanosine 5"-triphosphate can impede cellular proliferation and suppress p73 expression as oncoprotein in K562 cells; thus identifying Foxo3a as a tumor suppressor in these p53 null cells.	Guanosine Triphosphate	77-102	P53	Homo sapiens	250-253
23703322-1	2013	DNA damage induced by reactive oxygen species and several chemotherapeutic agents promotes both p53 and poly (ADP-ribose) polymerase (PARP) activation.	Reactive Oxygen Species	22-45	P53	Homo sapiens	96-99
24096875-6	2013	The inhibition of Lys(118) acetylation promoted the generation of NOS3-promoting prosurvival form of p53.	Lysine	18-21	P53	Homo sapiens	101-104
23872073-6	2013	Reactive oxygen species (ROS)-dependent mechanisms initiated by TGF-beta1 were critical for EGFR(Y845) and p53(Ser15) phosphorylation and target gene expression.	Reactive Oxygen Species	0-23	P53	Homo sapiens	107-110
23872073-6	2013	Reactive oxygen species (ROS)-dependent mechanisms initiated by TGF-beta1 were critical for EGFR(Y845) and p53(Ser15) phosphorylation and target gene expression.	Reactive Oxygen Species	25-28	P53	Homo sapiens	107-110
24096875-0	2013	p53"s choice of myocardial death or survival: Oxygen protects infarct myocardium by recruiting p53 on NOS3 promoter through regulation of p53-Lys(118) acetylation.	Oxygen	46-52	P53	Homo sapiens	0-3
24096875-8	2013	Understanding this novel oxygen-p53 survival pathway will open new avenues in cardioprotection molecular therapy.	Oxygen	25-31	P53	Homo sapiens	32-35
24096875-0	2013	p53"s choice of myocardial death or survival: Oxygen protects infarct myocardium by recruiting p53 on NOS3 promoter through regulation of p53-Lys(118) acetylation.	Oxygen	46-52	P53	Homo sapiens	95-98
24096875-0	2013	p53"s choice of myocardial death or survival: Oxygen protects infarct myocardium by recruiting p53 on NOS3 promoter through regulation of p53-Lys(118) acetylation.	Oxygen	46-52	P53	Homo sapiens	95-98
24096875-0	2013	p53"s choice of myocardial death or survival: Oxygen protects infarct myocardium by recruiting p53 on NOS3 promoter through regulation of p53-Lys(118) acetylation.	Lysine	142-145	P53	Homo sapiens	0-3
23603746-4	2013	Resveratrol treatment (150-250 micromol/l) for 48 h increased cell cycle arrest at the G1 phase in C33A (with mutation in p53) and HeLa cells (HPV18 positive), as well as in CaSki and SiHa cell lines (HPV16 positive).	Resveratrol	0-11	P53	Homo sapiens	122-125
24096875-0	2013	p53"s choice of myocardial death or survival: Oxygen protects infarct myocardium by recruiting p53 on NOS3 promoter through regulation of p53-Lys(118) acetylation.	Lysine	142-145	P53	Homo sapiens	95-98
24096875-0	2013	p53"s choice of myocardial death or survival: Oxygen protects infarct myocardium by recruiting p53 on NOS3 promoter through regulation of p53-Lys(118) acetylation.	Lysine	142-145	P53	Homo sapiens	95-98
24096875-4	2013	p53 exhibited a differential DNA-binding, namely, BAX-p53RE in the infarct heart or NOS3-p53RE in the oxygenated heart, which was regulated by oxygen-induced, post-translational modification of p53.	Oxygen	102-108	P53	Homo sapiens	0-3
24096875-5	2013	In the infarct heart, p53 was heavily acetylated at Lys(118) residue, which was exclusively reversed in the oxygenated heart, apparently regulated by oxygen-dependent expression of TIP60.	Lysine	52-55	P53	Homo sapiens	22-25
24096875-5	2013	In the infarct heart, p53 was heavily acetylated at Lys(118) residue, which was exclusively reversed in the oxygenated heart, apparently regulated by oxygen-dependent expression of TIP60.	Oxygen	108-114	P53	Homo sapiens	22-25
23929259-7	2013	Cisplatin-induced nephropathy is also mediated through the p53 and protein kinase-Cdelta (PKCdelta) signalling pathways.	Cisplatin	0-9	P53	Homo sapiens	59-62
24100270-0	2013	Mechanism of cadmium induced apoptosis in human peripheral blood lymphocytes: the role of p53, Fas and Caspase-3.	Cadmium	13-20	P53	Homo sapiens	90-93
24100270-11	2013	Cd induced p53-dependent apoptosis through cooperation between Bak upregulation without changing the Bcl-2 and Bax expression.	Cadmium	0-2	P53	Homo sapiens	11-14
23603746-8	2013	Interestingly, after resveratrol treatment, the expression of p53 was decreased in HPV18-positive cell lines (CaLo and HeLa) and increased in HPV16-positive cell lines (CaSki and SiHa) and C33A cells.	Resveratrol	21-32	P53	Homo sapiens	62-65
23768371-5	2013	Coumestrol promoted senescence through the p53-p21(Cip1/WAF1) pathway by inducing reactive oxygen species (ROS) production in MCF-7 and HCT116 cells.	Coumestrol	0-10	P53	Homo sapiens	43-46
23735541-10	2013	Decrease of p53 and Bcl-2, fragmentation of DNA, increase of Bax and, finally, activation of caspases 3 and 9 in NB4 leukaemia cells make the apoptotic process induced by Ptx irreversible.	Paclitaxel	171-174	P53	Homo sapiens	12-15
23768371-5	2013	Coumestrol promoted senescence through the p53-p21(Cip1/WAF1) pathway by inducing reactive oxygen species (ROS) production in MCF-7 and HCT116 cells.	Reactive Oxygen Species	82-105	P53	Homo sapiens	43-46
23875998-3	2013	In the present work, we show that p53-expressing cells are more susceptible to cell death after an apoptotic stimulus such as H2O2.	Hydrogen Peroxide	126-130	P53	Homo sapiens	34-37
23768371-5	2013	Coumestrol promoted senescence through the p53-p21(Cip1/WAF1) pathway by inducing reactive oxygen species (ROS) production in MCF-7 and HCT116 cells.	Reactive Oxygen Species	107-110	P53	Homo sapiens	43-46
23970333-0	2013	p53 restoration can overcome cisplatin resistance through inhibition of Akt as well as induction of Bax.	Cisplatin	29-38	P53	Homo sapiens	0-3
23263852-5	2013	In addition, decreasing c-Myc level and increasing of phosphorylated p53 (Ser 15) and WAF1/p21 were also taken part in Mn-mediated lung toxicity.	Serine	74-77	P53	Homo sapiens	69-72
23982736-0	2013	Low concentration of metformin induces a p53-dependent senescence in hepatoma cells via activation of the AMPK pathway.	Metformin	21-30	P53	Homo sapiens	41-44
23982736-8	2013	In addition, p53 siRNA transfection attenuated metformin-induced SA-beta-gal staining.	Metformin	47-56	P53	Homo sapiens	13-16
23970333-12	2013	The induction of wild-type p53 can enhance CDDP-induced apoptosis not only by inducing Bax protein but also by suppressing anti-apoptotic proteins through inhibition of Akt.	Cisplatin	43-47	P53	Homo sapiens	27-30
23982736-9	2013	Intriguingly, co-expression of SIRT1 and p53 dramatically reduced the levels of Ac-p53, however, low doses of metformin treatment partially reversed the effect of SIRT1 on p53 acetylation and elevated SA-beta-gal activity.	Metformin	110-119	P53	Homo sapiens	83-86
23982736-9	2013	Intriguingly, co-expression of SIRT1 and p53 dramatically reduced the levels of Ac-p53, however, low doses of metformin treatment partially reversed the effect of SIRT1 on p53 acetylation and elevated SA-beta-gal activity.	Metformin	110-119	P53	Homo sapiens	83-86
23970333-13	2013	In conclusion, this study suggests that the primary contributor to resistance to CDDP in SNU-16 cells may well be a failure of induction of apoptosis due to a lack of induction of pro-apoptotic proteins rather than suppression of anti-apoptotic proteins, and that restoration of p53 function can overcome the resistance to CDDP not only by augmenting the pro-apoptotic drive through p53-mediated transcriptional activation but also by inhibiting the anti-apoptotic drive through inhibition of Akt activity.	Cisplatin	81-85	P53	Homo sapiens	279-282
23982736-10	2013	These observations indicate that activation of the AMPK pathway promotes senescence in hepatoma cells exposed to low concentrations of metformin in a p53-dependent manner.	Metformin	135-144	P53	Homo sapiens	150-153
23970333-13	2013	In conclusion, this study suggests that the primary contributor to resistance to CDDP in SNU-16 cells may well be a failure of induction of apoptosis due to a lack of induction of pro-apoptotic proteins rather than suppression of anti-apoptotic proteins, and that restoration of p53 function can overcome the resistance to CDDP not only by augmenting the pro-apoptotic drive through p53-mediated transcriptional activation but also by inhibiting the anti-apoptotic drive through inhibition of Akt activity.	Cisplatin	81-85	P53	Homo sapiens	383-386
24102557-3	2013	KEY FINDINGS: More recently, major biomarkers such as AMPK, p53 and Bcl-2 have been identified as important to apoptosis induction by doxorubicin.	Doxorubicin	134-145	P53	Homo sapiens	60-63
23529952-5	2013	Results indicate that PEG2000-DPSE-QUE-NPS showed dose-dependent cytotoxicity to C6 glioma cells and enhanced ROS accumulation induced upregulation of p53 protein, which was accompanied with an increase in cytochrome c and caspase-3 protein levels.	ros	110-113	P53	Homo sapiens	151-154
24032713-6	2013	Enhancer of zeste homologue 2 (EZH2), an important histone-modifying enzyme, is able to trimethylate histone 3 on lysine 27 (H3K27Me3), consequently leading to gene silencing, especially silencing of tumor suppressor genes such as p53.	Lysine	114-120	P53	Homo sapiens	231-234
24012792-7	2013	Further, the DeltaE6 in GST-DeltaE6 seemed to retain the binding ability to p53 as determined by the glutathione-GST capture ELISA.	Glutathione	101-112	P53	Homo sapiens	76-79
23875779-1	2013	BACKGROUND &amp; AIMS: Apoptosis mediated by p53 plays a pathological role in the progression of hepatosteatosis.	Adenosine Monophosphate	12-15	P53	Homo sapiens	45-48
23955846-5	2013	The results reveal that H2 O2 can induce apoptosis effectively by regulating the activity of apoptosis-related biomolecules, including pro-apoptotic factors p53 and Bax, and anti-apoptotic factor Bcl-2.	Hydrogen Peroxide	24-29	P53	Homo sapiens	157-160
24101517-0	2013	Mitochondrial disulfide relay mediates translocation of p53 and partitions its subcellular activity.	Disulfides	14-23	P53	Homo sapiens	56-59
25606382-0	2013	The association between polymorphism of P53 codon 72 Arg/Pro and hepatocellular carcinoma susceptibility: evidence from a meta-analysis of 15 studies with 3704 cases.	Arginine	53-56	P53	Homo sapiens	40-43
25606382-2	2013	Polymorphism of p53 gene codon 72 Arg/Pro (rs1042522) may influence the function of p53 protein and then affect the processing of carcinogenesis.	Arginine	34-37	P53	Homo sapiens	16-19
25606382-2	2013	Polymorphism of p53 gene codon 72 Arg/Pro (rs1042522) may influence the function of p53 protein and then affect the processing of carcinogenesis.	Arginine	34-37	P53	Homo sapiens	84-87
25606382-3	2013	It has been suggested that p53 codon 72 Arg/Pro polymorphism is associated with susceptibility to hepatocellular carcinoma (HCC).	Arginine	40-43	P53	Homo sapiens	27-30
25606382-10	2013	CONCLUSIONS/SIGNIFICANCE: This meta-analysis suggests that p53 codon 72 Arg/Pro polymorphism may be associated with the risk of HCC, especially in subgroup analysis of Asian and Caucasian population, hospital-based population, the female, and the individuals infected with hepatitis virus.	Arginine	72-75	P53	Homo sapiens	59-62
24157877-4	2013	Compound C did not induce the phosphorylation of p53 but dramatically increased the protein level of p53 similar to some other transcriptional inhibitors, including 5,6-dichloro-1-beta-D-ribobenzimidazole (DRB).	Dichlororibofuranosylbenzimidazole	206-209	P53	Homo sapiens	101-104
24194938-0	2013	Acetylation of lysine 382 and phosphorylation of serine 392 in p53 modulate the interaction between p53 and MDC1 in vitro.	Lysine	15-21	P53	Homo sapiens	100-103
24101517-2	2013	Here we report that the mammalian homolog of the yeast mitochondrial disulfide relay protein Mia40 (CHCHD4) is necessary for the respiratory-dependent translocation of p53 into the mitochondria.	Disulfides	69-78	P53	Homo sapiens	168-171
24194938-0	2013	Acetylation of lysine 382 and phosphorylation of serine 392 in p53 modulate the interaction between p53 and MDC1 in vitro.	Serine	49-55	P53	Homo sapiens	63-66
24194938-0	2013	Acetylation of lysine 382 and phosphorylation of serine 392 in p53 modulate the interaction between p53 and MDC1 in vitro.	Serine	49-55	P53	Homo sapiens	100-103
24101517-5	2013	Thus, the mitochondrial disulfide relay system allows p53 to regulate two spatially segregated genomes depending on oxidative metabolic activity.	Disulfides	24-33	P53	Homo sapiens	54-57
24194938-5	2013	We further show that both acetylation of lysine 382 and phosphorylation of serine 392 in p53 enhance the interaction between p53 and MDC1.	Lysine	41-47	P53	Homo sapiens	125-128
24051088-2	2013	However, in this study we found that adenosine treatment results in cellular senescence in A549 lung cancer cells both in vitro and in vivo; adenosine induces cell cycle arrest and senescence in a p53/p21 dependent manner; adenosine elevates the level of phosphor-gammaH2AX, pCHK2 and pBRCA1, the markers for prolonged DNA damage response which are likely responsible for initiating the cellular senescence.	Adenosine	37-46	P53	Homo sapiens	197-200
24194938-5	2013	We further show that both acetylation of lysine 382 and phosphorylation of serine 392 in p53 enhance the interaction between p53 and MDC1.	Serine	75-81	P53	Homo sapiens	89-92
24194938-5	2013	We further show that both acetylation of lysine 382 and phosphorylation of serine 392 in p53 enhance the interaction between p53 and MDC1.	Serine	75-81	P53	Homo sapiens	125-128
24194938-7	2013	Our data suggests a new role for acetylation of lysine 382 and phosphorylation of serine 392 in p53 in the cellular stress response and offers the first evidence for an interaction involving MDC1 that is modulated by acetylation.	Serine	82-88	P53	Homo sapiens	96-99
24138843-8	2013	ZD6474 inhibited cyclin E expression and induced p53 expression when combined with UV-B.	vandetanib	0-6	P53	Homo sapiens	49-52
24147064-9	2013	Finally, doxorubicin caused a significant elevation in the levels of signalling proteins p-Akt, p-Erk 1/2, p-Drp1 and p-p53.	Doxorubicin	9-20	P53	Homo sapiens	120-123
24055188-2	2013	The ability of resveratrol to enhance anti-proliferative effects of etoposide in wild type p53 liver carcinoma (HepG2) and colon cancer (HCT-116) cells was investigated with focusing on p53 activation.	Resveratrol	15-26	P53	Homo sapiens	91-94
24055188-7	2013	P53 expression was up-regulated by resveratrol and etoposide and pre-incubation of both cells with resveratrol increased levels of etoposide-induced p53 expression.	Resveratrol	35-46	P53	Homo sapiens	0-3
24055188-7	2013	P53 expression was up-regulated by resveratrol and etoposide and pre-incubation of both cells with resveratrol increased levels of etoposide-induced p53 expression.	Resveratrol	99-110	P53	Homo sapiens	0-3
24055188-7	2013	P53 expression was up-regulated by resveratrol and etoposide and pre-incubation of both cells with resveratrol increased levels of etoposide-induced p53 expression.	Resveratrol	99-110	P53	Homo sapiens	149-152
24055188-9	2013	It seems that resveratrol exerts differential synergistic effect with etoposide on proliferation of cancer cells from different origin which is mainly accompanied by p53 activation.	Resveratrol	14-25	P53	Homo sapiens	166-169
24051088-2	2013	However, in this study we found that adenosine treatment results in cellular senescence in A549 lung cancer cells both in vitro and in vivo; adenosine induces cell cycle arrest and senescence in a p53/p21 dependent manner; adenosine elevates the level of phosphor-gammaH2AX, pCHK2 and pBRCA1, the markers for prolonged DNA damage response which are likely responsible for initiating the cellular senescence.	Adenosine	141-150	P53	Homo sapiens	197-200
24051088-2	2013	However, in this study we found that adenosine treatment results in cellular senescence in A549 lung cancer cells both in vitro and in vivo; adenosine induces cell cycle arrest and senescence in a p53/p21 dependent manner; adenosine elevates the level of phosphor-gammaH2AX, pCHK2 and pBRCA1, the markers for prolonged DNA damage response which are likely responsible for initiating the cellular senescence.	Adenosine	141-150	P53	Homo sapiens	197-200
23973939-4	2013	To examine the response of the p53 signaling pathway to stimulation with different concentrations of sulfite, a time course study of p53, Mdm2, and Bcl-2 expression was conducted in an immortalized hepatic cell line, HL-7702.	Sulfites	101-108	P53	Homo sapiens	31-34
24113589-5	2013	Pretreatment with nitric oxide (NO) scavengers suppressed the apoptotic biochemical changes induced by 20 muM emodin, and attenuated emodin-induced p53 and p21 expression involved in apoptotic signaling.	Nitric Oxide	18-30	P53	Homo sapiens	148-151
23964676-5	2013	Additionally, similar tumor suppressor activities of p53-CC and wt-p53 were detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), annexin-V, 7-aminoactinomycin D (7-AAD), and colony-forming assays.	7-aminoactinomycin D	191-196	P53	Homo sapiens	53-56
23632965-7	2013	Moreover, 1 muM ghrelin induced apoptosis in colorectal adenocarcinoma cells by inhibiting the ubiquitin-proteasome system and by activating autophagy, with p53 having an "interactive" role.	Ghrelin	16-23	P53	Homo sapiens	157-160
24088713-3	2013	SET7/9 (Setd7, KMT7) is a protein methyltransferase that catalyses lysine monomethylation of histones, but also methylates many non-histone target proteins such as p53 or DNMT1.	Lysine	67-73	P53	Homo sapiens	164-167
23837945-8	2013	RESULTS: Patients carrying p53 Arg/Arg or Arg/Pro had a higher risk of esophageal SCC (P&lt;0.001, Odds ratio [OR] 4.98, 95% confidential interval [CI] 3.46-7.17), however, not found in MDM2 rs937283.	Arginine	31-34	P53	Homo sapiens	27-30
23837945-8	2013	RESULTS: Patients carrying p53 Arg/Arg or Arg/Pro had a higher risk of esophageal SCC (P&lt;0.001, Odds ratio [OR] 4.98, 95% confidential interval [CI] 3.46-7.17), however, not found in MDM2 rs937283.	Arginine	35-38	P53	Homo sapiens	27-30
23837945-8	2013	RESULTS: Patients carrying p53 Arg/Arg or Arg/Pro had a higher risk of esophageal SCC (P&lt;0.001, Odds ratio [OR] 4.98, 95% confidential interval [CI] 3.46-7.17), however, not found in MDM2 rs937283.	Arginine	35-38	P53	Homo sapiens	27-30
23837945-9	2013	The risk of esophageal SCC increased significantly among patients carrying p53 Arg/Arg, or Arg/Pro and HPV16-seropositivity (P&lt;0.001, OR 9.33, 95% CI 5.44-16.0), but not for MDM2 rs937283.	Arginine	79-82	P53	Homo sapiens	75-78
23837945-11	2013	CONCLUSION: HPV16 seropositivity synergized with p53 Arg/Arg or Arg/Pro and increased ESCC risk, especially in smokers or drinkers.	Arginine	53-56	P53	Homo sapiens	49-52
23740383-5	2013	While the beta blocker carvedilol (1 muM) normalized the level of p53 and Bcl-2 and the calcium channel blocker (CCB) bepridil (0.5 muM) normalized that of Bcl-2, both the CCB azelnidipine (1 muM) and the angiotensin receptor blocker (ARB) olmesartan (10 muM) normalized those of p53, Bax, cytochrome c, and Bcl-XL.	Carvedilol	23-33	P53	Homo sapiens	66-69
23807739-6	2013	Ghrelin signaling promotes the oncogene CDK6 gene expression and represses the tumor suppressor gene P53 gene expression in gastric cancer.	Ghrelin	0-7	P53	Homo sapiens	101-104
23851445-8	2013	Furthermore, the ability of ATRA to induce senescence is reduced in p14(ARF)-depleted melanocytes, and we provide proof-of-concept that ATRA can induce irreversible growth arrest in melanoma cells with an intact RARbeta-p14(ARF) signaling axis, independent of p16(INK4A) and p53 status.	Tretinoin	136-140	P53	Homo sapiens	275-278
23225645-5	2013	The proof-of-concept for rapid immuno-SERS microscopy with 30 msec acquisition time per pixel for selective imaging of the p53 family member p63 in prostate tissue sections is demonstrated.	Serine	38-42	P53	Homo sapiens	123-126
23807740-0	2013	Condurango-glycoside-A fraction of Gonolobus condurango induces DNA damage associated senescence and apoptosis via ROS-dependent p53 signalling pathway in HeLa cells.	Reactive Oxygen Species	115-118	P53	Homo sapiens	129-132
23807740-9	2013	Expression profiles of certain relevant genes and proteins like p53, Akt, Bcl-2, Bax, cytochrome c and caspase 3 also provided evidence of ROS mediated p53 up-regulation and further boost in Bax expression and followed by cytochrome c release and activation of caspase 3.	Reactive Oxygen Species	139-142	P53	Homo sapiens	64-67
23807740-9	2013	Expression profiles of certain relevant genes and proteins like p53, Akt, Bcl-2, Bax, cytochrome c and caspase 3 also provided evidence of ROS mediated p53 up-regulation and further boost in Bax expression and followed by cytochrome c release and activation of caspase 3.	Reactive Oxygen Species	139-142	P53	Homo sapiens	152-155
24298606-0	2013	Lysine-specific modifications of p53: a matter of life and death?	Lysine	0-6	P53	Homo sapiens	33-36
23561593-0	2013	MGMT repletion after treatment of glioblastoma cells with temozolomide and O6-benzylguanine implicates NFkappaB and mutant p53.	O(6)-benzylguanine	75-91	P53	Homo sapiens	123-126
24137434-7	2013	However, pre-treatment of the cells with tanshinone IIA inhibited p65/NF-kappaB nuclear translocation and p53/p21 pathway activation.	tanshinone	41-55	P53	Homo sapiens	106-109
23561593-4	2013	In this study we investigated the potential mechanisms of resistance to combination treatment with TMZ and BG in the MGMT-proficient, p53-mutated (mt p53) T98G glioblastoma (GBM) cell line, looking for an effect on nuclear factor kappa B (NFkappaB) and mt p53, which are both transcriptional regulators of MGMT.	O(6)-benzylguanine	107-109	P53	Homo sapiens	134-137
23561593-4	2013	In this study we investigated the potential mechanisms of resistance to combination treatment with TMZ and BG in the MGMT-proficient, p53-mutated (mt p53) T98G glioblastoma (GBM) cell line, looking for an effect on nuclear factor kappa B (NFkappaB) and mt p53, which are both transcriptional regulators of MGMT.	O(6)-benzylguanine	107-109	P53	Homo sapiens	150-153
23561593-4	2013	In this study we investigated the potential mechanisms of resistance to combination treatment with TMZ and BG in the MGMT-proficient, p53-mutated (mt p53) T98G glioblastoma (GBM) cell line, looking for an effect on nuclear factor kappa B (NFkappaB) and mt p53, which are both transcriptional regulators of MGMT.	O(6)-benzylguanine	107-109	P53	Homo sapiens	150-153
23863845-1	2013	A p53 hot-spot mutation found frequently in human cancer is the replacement of R273 by histidine or cysteine residues resulting in p53 loss of function as a tumor suppressor.	Histidine	87-96	P53	Homo sapiens	2-5
23863845-1	2013	A p53 hot-spot mutation found frequently in human cancer is the replacement of R273 by histidine or cysteine residues resulting in p53 loss of function as a tumor suppressor.	Histidine	87-96	P53	Homo sapiens	131-134
23863845-1	2013	A p53 hot-spot mutation found frequently in human cancer is the replacement of R273 by histidine or cysteine residues resulting in p53 loss of function as a tumor suppressor.	Cysteine	100-108	P53	Homo sapiens	2-5
23863845-1	2013	A p53 hot-spot mutation found frequently in human cancer is the replacement of R273 by histidine or cysteine residues resulting in p53 loss of function as a tumor suppressor.	Cysteine	100-108	P53	Homo sapiens	131-134
23863845-6	2013	Contrary to our previously studied wild-type (wt) p53-DNA complexes showing non-canonical Hoogsteen A/T base pairs of the DNA helix that lead to local minor-groove narrowing and enhanced electrostatic interactions with p53, the current structures display Watson-Crick base pairs associated with direct or water-mediated hydrogen bonds with p53 at the minor groove.	Water	305-310	P53	Homo sapiens	50-53
23863845-6	2013	Contrary to our previously studied wild-type (wt) p53-DNA complexes showing non-canonical Hoogsteen A/T base pairs of the DNA helix that lead to local minor-groove narrowing and enhanced electrostatic interactions with p53, the current structures display Watson-Crick base pairs associated with direct or water-mediated hydrogen bonds with p53 at the minor groove.	Hydrogen	320-328	P53	Homo sapiens	50-53
24298606-3	2013	In this review, we focus on the role of recently discovered lysine-specific modifications of p53, methylation and acetylation in particular, and their effects on p53 activity in damaged cells.	Lysine	60-66	P53	Homo sapiens	93-96
24298606-3	2013	In this review, we focus on the role of recently discovered lysine-specific modifications of p53, methylation and acetylation in particular, and their effects on p53 activity in damaged cells.	Lysine	60-66	P53	Homo sapiens	162-165
23965518-5	2013	ERK1/2 related p53 activation, but not reactive oxygen species, was responsible for Doxorubicin induced caspase-3 cleavage.	Doxorubicin	84-95	P53	Homo sapiens	15-18
23661153-7	2013	Naringenin induced a rapid accumulation of p53, which might account for the naringenin-induced G0/G1 and G2/M phase arrests in Hep G2 cells.	naringenin	0-10	P53	Homo sapiens	43-46
23860773-0	2013	P53 codon 72 Arg/Pro polymorphism and glioma risk: an updated meta-analysis.	Arginine	13-16	P53	Homo sapiens	0-3
23812725-0	2013	P53 codon 72 Arg/Pro polymorphism and lung cancer risk in Asians: an updated meta-analysis.	Arginine	13-16	P53	Homo sapiens	0-3
23812725-1	2013	The polymorphism of p53 codon 72, a transversion of G to C (Arg to Pro), has been demonstrated to be associated with the risk for lung cancer.	Arginine	60-63	P53	Homo sapiens	20-23
23715779-9	2013	Concerning the histological types of lung cancer, the p53 codon 72 variant exerts risk effect on the lung carcinogenesis in patients with adenocarcinoma (OR Arg/Pro vs. Arg/Arg = 1.10, 95 % CI = 1.00-1.22, P OR = 0.048).	Arginine	157-160	P53	Homo sapiens	54-57
23715779-9	2013	Concerning the histological types of lung cancer, the p53 codon 72 variant exerts risk effect on the lung carcinogenesis in patients with adenocarcinoma (OR Arg/Pro vs. Arg/Arg = 1.10, 95 % CI = 1.00-1.22, P OR = 0.048).	Arginine	169-172	P53	Homo sapiens	54-57
23715779-9	2013	Concerning the histological types of lung cancer, the p53 codon 72 variant exerts risk effect on the lung carcinogenesis in patients with adenocarcinoma (OR Arg/Pro vs. Arg/Arg = 1.10, 95 % CI = 1.00-1.22, P OR = 0.048).	Arginine	169-172	P53	Homo sapiens	54-57
23715779-10	2013	Additionally, subgroup analysis by the smoking status demonstrated that the p53 codon 72 variant seemed to play a protective role in lung carcinogenesis among the non-smokers but not the smokers in the contrast model of Arg/Pro vs. Arg/Arg (OR Arg/Pro vs. Arg/Arg = 0.71, 95 % CI = 0.50-1.00, P OR = 0.049).	Arginine	232-235	P53	Homo sapiens	76-79
23860773-1	2013	P53 codon 72 Arg/Pro is a C/G variation upstream of the p53 gene on human chromosome 17p13.	Arginine	13-16	P53	Homo sapiens	0-3
23715779-10	2013	Additionally, subgroup analysis by the smoking status demonstrated that the p53 codon 72 variant seemed to play a protective role in lung carcinogenesis among the non-smokers but not the smokers in the contrast model of Arg/Pro vs. Arg/Arg (OR Arg/Pro vs. Arg/Arg = 0.71, 95 % CI = 0.50-1.00, P OR = 0.049).	Arginine	232-235	P53	Homo sapiens	76-79
23715779-10	2013	Additionally, subgroup analysis by the smoking status demonstrated that the p53 codon 72 variant seemed to play a protective role in lung carcinogenesis among the non-smokers but not the smokers in the contrast model of Arg/Pro vs. Arg/Arg (OR Arg/Pro vs. Arg/Arg = 0.71, 95 % CI = 0.50-1.00, P OR = 0.049).	Arginine	232-235	P53	Homo sapiens	76-79
23715779-10	2013	Additionally, subgroup analysis by the smoking status demonstrated that the p53 codon 72 variant seemed to play a protective role in lung carcinogenesis among the non-smokers but not the smokers in the contrast model of Arg/Pro vs. Arg/Arg (OR Arg/Pro vs. Arg/Arg = 0.71, 95 % CI = 0.50-1.00, P OR = 0.049).	Arginine	232-235	P53	Homo sapiens	76-79
23715779-10	2013	Additionally, subgroup analysis by the smoking status demonstrated that the p53 codon 72 variant seemed to play a protective role in lung carcinogenesis among the non-smokers but not the smokers in the contrast model of Arg/Pro vs. Arg/Arg (OR Arg/Pro vs. Arg/Arg = 0.71, 95 % CI = 0.50-1.00, P OR = 0.049).	Arginine	232-235	P53	Homo sapiens	76-79
23812725-3	2013	Thus, we performed a meta-analysis by pooling all currently available case-control studies to estimate the effect of p53 codon 72 Arg/Pro polymorphism on the development of lung cancer.	Arginine	130-133	P53	Homo sapiens	117-120
23812725-6	2013	The overall OR for the dominant genetic model indicated that the p53 codon 72 Arg/Pro variant was positively correlated with lung cancer risk (ORArg/Pro + Pro/Pro vs. Arg/Arg = 1.14, 95 %CI 1.07-1.23, P OR &lt; 0.001).	Arginine	78-81	P53	Homo sapiens	65-68
23812725-6	2013	The overall OR for the dominant genetic model indicated that the p53 codon 72 Arg/Pro variant was positively correlated with lung cancer risk (ORArg/Pro + Pro/Pro vs. Arg/Arg = 1.14, 95 %CI 1.07-1.23, P OR &lt; 0.001).	Arginine	145-148	P53	Homo sapiens	65-68
23812725-6	2013	The overall OR for the dominant genetic model indicated that the p53 codon 72 Arg/Pro variant was positively correlated with lung cancer risk (ORArg/Pro + Pro/Pro vs. Arg/Arg = 1.14, 95 %CI 1.07-1.23, P OR &lt; 0.001).	Arginine	145-148	P53	Homo sapiens	65-68
23812725-10	2013	The updated meta-analysis suggests that the p53 codon 72 Arg/Pro polymorphism is a risk factor for lung cancer in the Asian population.	Arginine	57-60	P53	Homo sapiens	44-47
23860773-1	2013	P53 codon 72 Arg/Pro is a C/G variation upstream of the p53 gene on human chromosome 17p13.	Arginine	13-16	P53	Homo sapiens	56-59
23860773-2	2013	Many case-control studies have investigated the association between p53 codon 72 Arg/Pro polymorphism and glioma risk but provided inconsistent findings.	Arginine	81-84	P53	Homo sapiens	68-71
23860773-5	2013	The pooled odds ratio (OR) with 95 % confidence interval (95 % CI) was calculated to estimate the effect of p53 codon 72 Arg/Pro variant on the development of glioma.	Arginine	121-124	P53	Homo sapiens	108-111
23860773-9	2013	Our study suggests that the polymorphism of p53 codon 72 Arg/Pro may play a protective role in the development of glioblastoma.	Arginine	57-60	P53	Homo sapiens	44-47
23860773-10	2013	The relationship of p53 codon 72 Arg/Pro polymorphism with the susceptibility to glioma needs further estimation by more individual studies with high quality across ethnicities.	Arginine	33-36	P53	Homo sapiens	20-23
23796514-1	2013	S100A6 is a calcium binding protein that, like some other members of the S100 protein family, is able to bind p53.	Calcium	12-19	P53	Homo sapiens	110-113
24433772-2	2013	METHODS: The expression of Gli1, MDM2 and p53 proteins in 57 paired paraffin embedded pancreatic ductal adenocarcinoma (PDAC) specimens and adjacent non-cancerous pancreatic tissues was detected by immunohistochemistry.	Paraffin	68-76	P53	Homo sapiens	42-45
24198727-4	2013	Both H2O2 treatment and AdRas12V infection induced senescence in VECs, as assessed by senescence-associated beta-Gal activity and the expression of proteins such as p53 and p21(CIP1).	Hydrogen Peroxide	5-9	P53	Homo sapiens	165-168
24074238-5	2013	The frequent presence of wild-type TP53 and the low levels of p53 in complex with the p53 negative feed-back regulator MDM2 contribute to cisplatin sensitivity.	Cisplatin	138-147	P53	Homo sapiens	35-39
24074238-5	2013	The frequent presence of wild-type TP53 and the low levels of p53 in complex with the p53 negative feed-back regulator MDM2 contribute to cisplatin sensitivity.	Cisplatin	138-147	P53	Homo sapiens	62-65
24074238-5	2013	The frequent presence of wild-type TP53 and the low levels of p53 in complex with the p53 negative feed-back regulator MDM2 contribute to cisplatin sensitivity.	Cisplatin	138-147	P53	Homo sapiens	86-89
23830811-10	2013	With the increase in the dose of DES, p53 levels first increased (0.5-4.0mM) and then decreased (8.0mM).	diethyl sulfate	33-36	P53	Homo sapiens	38-41
23830811-11	2013	Down-regulation of p53 by RNA interference increased 4.0mM of DES-induced apoptosis but did not affect 2.0mM DES-induced cell cycle arrest.	diethyl sulfate	62-65	P53	Homo sapiens	19-22
23830811-15	2013	p53 might play an important role in the transition between evoking cell cycle arrest/pro-survival and apoptosis programs upon DES exposure.	diethyl sulfate	126-129	P53	Homo sapiens	0-3
23108402-0	2013	5-Fluorouracil signaling through a calcium-calmodulin-dependent pathway is required for p53 activation and apoptosis in colon carcinoma cells.	Fluorouracil	0-14	P53	Homo sapiens	88-91
24086535-3	2013	Akt and p53 are determinants of cisplatin sensitivity.	Cisplatin	32-41	P53	Homo sapiens	8-11
24086535-5	2013	However, the precise role of rictor and the relationship between rictor and p53 in cisplatin resistance remains poorly understood.	Cisplatin	83-92	P53	Homo sapiens	76-79
23108402-3	2013	Current knowledge states that in certain cell types, 5-FU-induced stress is signaling through a p53-dependent induction of tumor necrosis factor-receptor oligomerization required for death-inducing signaling complex formation and caspase-8 activation.	Fluorouracil	53-57	P53	Homo sapiens	96-99
23108402-4	2013	Here we establish a role of calcium (Ca(2+)) as a messenger for p53 activation in response to 5-FU.	Calcium	28-35	P53	Homo sapiens	64-67
24052075-8	2013	Doxorubicin strongly induces p53 and p73 binding to the NIS promoter, leading to an increased expression of endogenous NIS mRNA and protein in HCC and CCA cells, but not in PHH.	Doxorubicin	0-11	P53	Homo sapiens	29-32
23108402-4	2013	Here we establish a role of calcium (Ca(2+)) as a messenger for p53 activation in response to 5-FU.	Fluorouracil	94-98	P53	Homo sapiens	64-67
23108402-5	2013	Using a combination of pharmacological and genetic approaches, we show that treatment of colon carcinoma cells stimulates entry of extracellular Ca(2+) through long lasting-type plasma membrane channels, which further directs posttranslational phosphorylation of at least three p53 serine residues (S15, S33 and S37) by means of calmodulin (CaM) activity.	Serine	282-288	P53	Homo sapiens	278-281
24052075-9	2013	Silencing NIS expression reduced doxorubicin-induced apoptosis in HCC cells, pointing to a possible role of a p53-family-dependent expression of NIS in apoptotic cell death.	Doxorubicin	33-44	P53	Homo sapiens	110-113
23108402-7	2013	Moreover, ectopic expression of p53 S15A in HCT116 p53(-/-) cells confirmed the importance of a Ca(2+)-CaM-p53 axis in 5-FU-induced extrinsic apoptosis.	Fluorouracil	119-123	P53	Homo sapiens	32-35
23819990-7	2013	In the absence of UCP2, endothelial growth stimulation provoked mitochondrial network fragmentation and premature senescence via a mechanism involving superoxide-mediated p53 activation.	Superoxides	151-161	P53	Homo sapiens	171-174
23456958-11	2013	In vitro, inhibition of GRP78 reduces apoptosis in response to 5-FU in p53 wild-type cells.	Fluorouracil	63-67	P53	Homo sapiens	71-74
23922104-0	2013	Src kinases in chondrosarcoma chemoresistance and migration: dasatinib sensitises to doxorubicin in TP53 mutant cells.	Doxorubicin	85-96	P53	Homo sapiens	100-104
24040102-7	2013	p53-knockdown experiment in C2C12 cells and experiment using p53-deficient HCT116 cells showed that splitomicin and resveratrol modulated apoptosis by p53-dependent and p53-independent pathways.	Resveratrol	116-127	P53	Homo sapiens	61-64
24040102-7	2013	p53-knockdown experiment in C2C12 cells and experiment using p53-deficient HCT116 cells showed that splitomicin and resveratrol modulated apoptosis by p53-dependent and p53-independent pathways.	Resveratrol	116-127	P53	Homo sapiens	61-64
24040102-8	2013	In p53-independent cell protective pathway, we found that FOXO1, FOXO3a, and FOXO4 were involved in SOD2"s upregulation by resveratrol.	Resveratrol	123-134	P53	Homo sapiens	3-6
24039769-5	2013	To this end, the C2IN-p53 fusion construct was overexpressed in E. coli with good solubility, purified by heparin affinity chromatography and protein identity was confirmed by immunoblotting.	Heparin	106-113	P53	Homo sapiens	22-25
23726949-6	2013	Additionally, melatonin treatment down-regulated SIRT1 and up-regulated acetylated-p53.	Melatonin	14-23	P53	Homo sapiens	83-86
24040083-6	2013	Either overexpression of wild-type p53 or induction of the endogenous p53 by the genotoxic agent doxorubicin repressed SALL2 promoter activity in various cell lines.	Doxorubicin	97-108	P53	Homo sapiens	70-73
23772810-12	2013	Excessive iron could also induce apoptosis, arrest cell cycle, and decrease function of BMMNC and UC-MSC, which was accompanied by increased ROS level and stimulated p38MAPK, p53 signaling pathway.	Iron	10-14	P53	Homo sapiens	175-178
24019961-2	2013	We previously reported that the proline 72 polymorphic variant of p53 (P72) demonstrates increased ability to transactivate a subset of genes, relative to arginine 72 (R72); one of these genes is macrophage colony stimulating factor (CSF1).	Arginine	155-163	P53	Homo sapiens	66-69
23852422-0	2013	Cheliensisin A inhibits EGF-induced cell transformation with stabilization of p53 protein via a hydrogen peroxide/Chk1-dependent axis.	Hydrogen Peroxide	96-113	P53	Homo sapiens	78-81
23852422-9	2013	Finally, increased hydrogen peroxide was found to mediate Chk1 phosphorylation at Ser345, p53 protein induction, cell apoptotic induction, and transformation inhibition following Chel A treatment.	Hydrogen Peroxide	19-36	P53	Homo sapiens	90-93
23852422-9	2013	Finally, increased hydrogen peroxide was found to mediate Chk1 phosphorylation at Ser345, p53 protein induction, cell apoptotic induction, and transformation inhibition following Chel A treatment.	chel	179-183	P53	Homo sapiens	90-93
24005866-4	2013	Accumulation of reactive oxygen species (ROS) was observed in the progression of cell cycle arrest, which was associated with the increased expression of cell cycle regulating factors, p53 and p21.	Reactive Oxygen Species	16-39	P53	Homo sapiens	185-188
24005866-4	2013	Accumulation of reactive oxygen species (ROS) was observed in the progression of cell cycle arrest, which was associated with the increased expression of cell cycle regulating factors, p53 and p21.	Reactive Oxygen Species	41-44	P53	Homo sapiens	185-188
23483183-1	2013	PURPOSE: It was shown that individuals homozygous for the Arg-encoding allele of codon 72 TP53 gene may have an increased risk to human papillomavirus (HPV)-related cervical carcinomas.	Arginine	58-61	P53	Homo sapiens	90-94
23483183-9	2013	RESULTS: The distribution of Arg/Arg, Arg/Pro, and Pro/Pro genotypes of codon 72 of TP53 gene was: 63.3, 34.7, and 2.0 % in the cervical carcinomas and 58.1, 33.8, and 8.1 % in the control group.	Arginine	29-32	P53	Homo sapiens	84-88
23483183-9	2013	RESULTS: The distribution of Arg/Arg, Arg/Pro, and Pro/Pro genotypes of codon 72 of TP53 gene was: 63.3, 34.7, and 2.0 % in the cervical carcinomas and 58.1, 33.8, and 8.1 % in the control group.	Arginine	33-36	P53	Homo sapiens	84-88
23483183-9	2013	RESULTS: The distribution of Arg/Arg, Arg/Pro, and Pro/Pro genotypes of codon 72 of TP53 gene was: 63.3, 34.7, and 2.0 % in the cervical carcinomas and 58.1, 33.8, and 8.1 % in the control group.	Arginine	33-36	P53	Homo sapiens	84-88
23483183-11	2013	CONCLUSIONS: The results indicate that carriers of Arg allele of codon 72 TP53 gene have an increased risk for development of cervical carcinoma in Serbian women.	Arginine	51-54	P53	Homo sapiens	74-78
23966169-4	2013	Of note, unstressed HCT116 p53(+/+) cells simultaneously show increased O2 consumption and decreased mitochondrial superoxide production compared with their p53-null counterpart.	Superoxides	72-74	P53	Homo sapiens	27-30
23966169-4	2013	Of note, unstressed HCT116 p53(+/+) cells simultaneously show increased O2 consumption and decreased mitochondrial superoxide production compared with their p53-null counterpart.	Superoxides	115-125	P53	Homo sapiens	27-30
23966169-9	2013	Taking into account that deregulations of mitochondrial respiration and reactive oxygen species production are tightly linked to cancer development, we suggest that mitochondrial p53 may be an important regulator of normal mitochondrial and cellular physiology, potentially exerting tumor suppression activity inside mitochondria.	Reactive Oxygen Species	72-95	P53	Homo sapiens	179-182
23678008-7	2013	Pull down assays demonstrated the occurrence of complex comprising of all three proteins and DNA, where p53 tends to compete out hRAD51 and BRCA2(BRC1-8), leading to not only the decline in ATP hydrolysis but also the strand exchange function of hRAD51 that was stimulated by BRCA2(BRC1-8).	Adenosine Triphosphate	190-193	P53	Homo sapiens	104-107
23810214-6	2013	By contrast, 5-fluorouracil induced G2 cell-cycle arrest and apoptosis that may be associated with p53 activation and p21 up-regulation.	Fluorouracil	13-27	P53	Homo sapiens	99-102
23873478-7	2013	RESULTS: Experiments with HCT116 cells that are p53 +/+ (p53 wild-type) and -/- (p53 null) grown in cell culture demonstrated that preincubation with cisplatin increased expression of p53 and subsequently enhanced localization of (64)Cu from (64)Cu-acetate and (64)Cu-DOTA-cetuximab to the tumor cell nuclei.	Cisplatin	150-159	P53	Homo sapiens	48-51
23873478-7	2013	RESULTS: Experiments with HCT116 cells that are p53 +/+ (p53 wild-type) and -/- (p53 null) grown in cell culture demonstrated that preincubation with cisplatin increased expression of p53 and subsequently enhanced localization of (64)Cu from (64)Cu-acetate and (64)Cu-DOTA-cetuximab to the tumor cell nuclei.	Cisplatin	150-159	P53	Homo sapiens	57-60
23873478-7	2013	RESULTS: Experiments with HCT116 cells that are p53 +/+ (p53 wild-type) and -/- (p53 null) grown in cell culture demonstrated that preincubation with cisplatin increased expression of p53 and subsequently enhanced localization of (64)Cu from (64)Cu-acetate and (64)Cu-DOTA-cetuximab to the tumor cell nuclei.	Cisplatin	150-159	P53	Homo sapiens	57-60
23873478-7	2013	RESULTS: Experiments with HCT116 cells that are p53 +/+ (p53 wild-type) and -/- (p53 null) grown in cell culture demonstrated that preincubation with cisplatin increased expression of p53 and subsequently enhanced localization of (64)Cu from (64)Cu-acetate and (64)Cu-DOTA-cetuximab to the tumor cell nuclei.	Cisplatin	150-159	P53	Homo sapiens	57-60
24067199-0	2013	Cisplatin induces cell cycle arrest and senescence via upregulating P53 and P21 expression in HepG2 cells.	Cisplatin	0-9	P53	Homo sapiens	68-71
23088850-8	2013	Mechanistic analysis revealed that Beclin-1 did not interact with proapoptotic proteins Bax and Bak; however, Beclin-1 was found to interact with p53 in the cytosol and mitochondria upon resveratrol treatment.	Resveratrol	187-198	P53	Homo sapiens	146-149
23839309-0	2013	Chk1/2 inhibition overcomes the cisplatin resistance of head and neck cancer cells secondary to the loss of functional p53.	Cisplatin	32-41	P53	Homo sapiens	119-122
23839309-2	2013	TP53 is the most commonly mutated gene in HNSCC, and the impact of p53 mutation on response to cisplatin treatment is poorly understood.	Cisplatin	95-104	P53	Homo sapiens	67-70
23839309-3	2013	Here, we show unambiguously that wild-type TP53 (wtp53) is associated with sensitivity of HNSCC cells to cisplatin treatment, whereas mutation or loss of TP53 is associated with cisplatin resistance.	Cisplatin	105-114	P53	Homo sapiens	43-47
23839309-3	2013	Here, we show unambiguously that wild-type TP53 (wtp53) is associated with sensitivity of HNSCC cells to cisplatin treatment, whereas mutation or loss of TP53 is associated with cisplatin resistance.	Cisplatin	178-187	P53	Homo sapiens	154-158
23839309-4	2013	We also show that senescence is the major cellular response to cisplatin in wtp53 HNSCC cells and that cisplatin resistance in p53-null or -mutant TP53 cells is due to their lack of senescence.	Cisplatin	63-72	P53	Homo sapiens	78-81
23839309-4	2013	We also show that senescence is the major cellular response to cisplatin in wtp53 HNSCC cells and that cisplatin resistance in p53-null or -mutant TP53 cells is due to their lack of senescence.	Cisplatin	103-112	P53	Homo sapiens	147-151
23839309-6	2013	Treatment of p53-deficient HNSCC cells with the Chk inhibitor AZD7762 sensitizes them to cisplatin through induction of mitotic cell death.	Cisplatin	89-98	P53	Homo sapiens	13-16
23839309-7	2013	This is the first report showing the ability of a Chk kinase inhibitor to sensitize TP53-deficient HNSCC to cisplatin in a synthetic lethal manner, which has significance given the frequency of TP53 mutations in this disease and because cisplatin has become part of standard therapy for aggressive HNSCC tumors.	Cisplatin	108-117	P53	Homo sapiens	84-88
23839309-7	2013	This is the first report showing the ability of a Chk kinase inhibitor to sensitize TP53-deficient HNSCC to cisplatin in a synthetic lethal manner, which has significance given the frequency of TP53 mutations in this disease and because cisplatin has become part of standard therapy for aggressive HNSCC tumors.	Cisplatin	108-117	P53	Homo sapiens	194-198
23839309-7	2013	This is the first report showing the ability of a Chk kinase inhibitor to sensitize TP53-deficient HNSCC to cisplatin in a synthetic lethal manner, which has significance given the frequency of TP53 mutations in this disease and because cisplatin has become part of standard therapy for aggressive HNSCC tumors.	Cisplatin	237-246	P53	Homo sapiens	84-88
24067199-9	2013	Western blotting confirmed P53 and P21 expression changes similar to their mRNA expressions during cisplatin-induced cellular senescence in HepG2 cells.	Cisplatin	99-108	P53	Homo sapiens	27-30
23891087-8	2013	Loss of AMPK sensitized cells to the anti-proliferative effects of metformin, while loss of p53 promoted both the growth inhibitory and toxic effects of metformin.	Metformin	153-162	P53	Homo sapiens	92-95
24228232-3	2013	The aim of the present study was to evaluate whether zinc dichloride (ZnCl2), which was known to re-establish the chemosensitivity of cancer cells by reactivating p53, promotes immunogenic instances of cell death.	zinc chloride	53-68	P53	Homo sapiens	163-166
24228232-3	2013	The aim of the present study was to evaluate whether zinc dichloride (ZnCl2), which was known to re-establish the chemosensitivity of cancer cells by reactivating p53, promotes immunogenic instances of cell death.	zinc chloride	70-75	P53	Homo sapiens	163-166
23670255-2	2013	Previously, we identified GADD153 as a target of BRCA1 protein, which increases doxorubicin sensitivity in human p53 -/- PCa cells (PC3).	Doxorubicin	80-91	P53	Homo sapiens	113-116
23881456-6	2013	SIRT1 activator, resveratrol, dose-dependently attenuated the growth-inhibitory and apoptosis-inducing effect of cudraflavone B and blocked cudraflavone B-induced regulatory protein expressions in the mitochondrial pathway such as p53, p21, p27, Bax, caspase-3, and cytochrome-c. Conversely, treatment with SIRT1 inhibitor sirtinol caused opposite effects.	Resveratrol	17-28	P53	Homo sapiens	231-234
23891087-0	2013	Contributions of AMPK and p53 dependent signaling to radiation response in the presence of metformin.	Metformin	91-100	P53	Homo sapiens	26-29
23891087-10	2013	CONCLUSIONS: The anti-proliferative activity of metformin may confer benefit in combination with radiotherapy, and this benefit is intensified upon loss of AMPK or p53 signaling.	Metformin	48-57	P53	Homo sapiens	164-167
23891087-2	2013	Metformin activates AMPK that in turn can launch a p53-dependent metabolic checkpoint.	Metformin	0-9	P53	Homo sapiens	51-54
23891087-4	2013	Since radiation-induced signaling also involves AMPK and p53, we investigated their importance in mediating responses to metformin and radiation.	Metformin	121-130	P53	Homo sapiens	57-60
23843462-7	2013	The activated AKT phosphorylated MDM2 at Ser(166) and promoted degradation of the tumor suppressor p53.	Serine	41-44	P53	Homo sapiens	99-102
23976973-3	2013	Here we have shown that in cancer cells treated with anti-neoplastic drug GaQ3, p53, there is an increase in intracellular calcium levels by transcriptional regulation of a novel calcium channel gene TRPC6.	Calcium	123-130	P53	Homo sapiens	80-83
23976973-0	2013	p53 increases intra-cellular calcium release by transcriptional regulation of calcium channel TRPC6 in GaQ3-treated cancer cells.	Calcium	29-36	P53	Homo sapiens	0-3
23977343-8	2013	These data demonstrated firstly to our knowledge that IFN-beta produced synergistic anti-tumor effects with cisplatin or pemetrexed on mesothelioma through up-regulated p53 expression.	Cisplatin	108-117	P53	Homo sapiens	169-172
23976973-6	2013	This research work shows that p53 and its transcriptional activity is critical in regulation of calcium signaling and an increase in the intracellular calcium level might be one of the anti-cancer strategies to induce apoptosis in cancer cells.	Calcium	96-103	P53	Homo sapiens	30-33
23976973-6	2013	This research work shows that p53 and its transcriptional activity is critical in regulation of calcium signaling and an increase in the intracellular calcium level might be one of the anti-cancer strategies to induce apoptosis in cancer cells.	Calcium	151-158	P53	Homo sapiens	30-33
23845906-0	2013	Cisplatin-induced non-apoptotic death of pancreatic cancer cells requires mitochondrial cyclophilin-D-p53 signaling.	Cisplatin	0-9	P53	Homo sapiens	102-105
23934659-0	2013	Cisplatin causes cell death via TAB1 regulation of p53/MDM2/MDMX circuitry.	Cisplatin	0-9	P53	Homo sapiens	51-54
23680455-3	2013	In normal conditions, ROS have an important role in signal transduction and gene transcription, nevertheless, ROS may act as a trigger for carcinogenesis via persistent DNA injuries as well as mutations in p53 such as conditions observed in skin, hepatocellular, and colon cancers.	Reactive Oxygen Species	22-25	P53	Homo sapiens	206-209
23845906-3	2013	Here, we found that cisplatin mainly induced non-apoptotic death of the pancreatic cancer cells (AsPC-1 and Capan-2), which was associated with a significant p53 activation (phosphorylation and accumulation).	Cisplatin	20-29	P53	Homo sapiens	158-161
23845906-11	2013	Together, these data suggested that cisplatin-induced non-apoptotic death requires mitochondria Cyp-D-p53 signaling in pancreatic cancer cells.	Cisplatin	36-45	P53	Homo sapiens	102-105
23845906-5	2013	We provided evidences to support that mitochondrial Cyp-D/p53 complexation might be critical for cisplatin-induced non-apoptotic death of pancreatic cancer cells.	Cisplatin	97-106	P53	Homo sapiens	58-61
23845906-7	2013	Both CsA and Cyp-D knockdown also disrupted the Cyp-D/p53 complex formation in mitochondria.	Cyclosporine	5-8	P53	Homo sapiens	54-57
23845906-8	2013	Meanwhile, the pancreatic cancer cells with p53 knockdown were resistant to cisplatin.	Cisplatin	76-85	P53	Homo sapiens	44-47
23950944-6	2013	Moreover, p53 activator doxorubicin significantly enhanced GR 1-9/10 promoter activity in HepG2 cells at 100 nM, which was associated with significantly higher protein content of p53 and GR.	Doxorubicin	24-35	P53	Homo sapiens	10-13
23848581-0	2013	In vivo activation of the p53 tumor suppressor pathway by an engineered cyclotide.	Cyclotides	72-81	P53	Homo sapiens	26-29
23848581-6	2013	The resulting cyclotide MCo-PMI was able to bind with low nanomolar affinity to both Hdm2 and HdmX, showed high stability in human serum, and was cytotoxic to wild-type p53 cancer cell lines by activating the p53 tumor suppressor pathway both in vitro and in vivo.	Cyclotides	14-23	P53	Homo sapiens	169-172
23848581-6	2013	The resulting cyclotide MCo-PMI was able to bind with low nanomolar affinity to both Hdm2 and HdmX, showed high stability in human serum, and was cytotoxic to wild-type p53 cancer cell lines by activating the p53 tumor suppressor pathway both in vitro and in vivo.	Cyclotides	14-23	P53	Homo sapiens	209-212
23950944-6	2013	Moreover, p53 activator doxorubicin significantly enhanced GR 1-9/10 promoter activity in HepG2 cells at 100 nM, which was associated with significantly higher protein content of p53 and GR.	Doxorubicin	24-35	P53	Homo sapiens	179-182
23898080-8	2013	Doxorubicin induced activity of p53 and NF-kappaB.	Doxorubicin	0-11	P53	Homo sapiens	32-35
23897481-7	2013	Pro184 makes a ring-to-ring interaction with Trp53 of Cul5, which is substituted by alanine in Cul2.	Alanine	84-91	P53	Homo sapiens	45-50
23652278-10	2013	Ser-15 of p53 was phosphorylated after 24 h of treatment of the cancer cells with OSU-03012.	Serine	0-3	P53	Homo sapiens	10-13
23898080-9	2013	Parthenolide markedly reduced the constitutive and doxorubicin-induced NF-kappaB activity measured as the nuclear NF-kappaB, and expression of matrix metalloproteinase-9 (MMP9) and it had no effect on p53.	parthenolide	0-12	P53	Homo sapiens	201-204
23898080-9	2013	Parthenolide markedly reduced the constitutive and doxorubicin-induced NF-kappaB activity measured as the nuclear NF-kappaB, and expression of matrix metalloproteinase-9 (MMP9) and it had no effect on p53.	Doxorubicin	51-62	P53	Homo sapiens	201-204
23859017-4	2013	Cytotoxic concentrations of the nitric oxide donor sodium nitroprusside activated several proapoptotic mechanisms, including stimulation of the stress kinase pathways mediated by c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), inhibition of the translation initiation factor eIF2alpha, induction and phosphorylation of the p53 protein, and inhibited Akt-mediated antiapoptotic signaling, independent of Ras function.	Nitric Oxide	32-44	P53	Homo sapiens	354-357
24074787-8	2013	We reported that TP53 mutated non inflammatory locally advanced breast carcinomas had a high rate of complete pathological response to dose-dense doxorubicin-cyclophosphamide chemotherapy, while TP53 wild-type (WT) tumors never achieved complete response.	Doxorubicin	146-157	P53	Homo sapiens	17-21
23725219-7	2013	Additionally, functional silencing of MIR21 and MIR30D in L428 cells showed increased sensitivity to doxorubicin-induced apoptosis, pointing towards abnormalities of mitochondrial intrinsic and TP53-CDKN1A pathways as related to miRNA deregulation in cHL.	Doxorubicin	101-112	P53	Homo sapiens	194-198
24074787-10	2013	A recent work confirmed these findings in MMTV-Wnt1 mammary tumors, showing that growth arrest and senescent phenotype, not apoptosis, were induced in TP53 WT tumors following doxorubicin treatment, while lack of arrest in mutant tumors resulted in aberrant mitoses, cell death and a superior clinical response.	Doxorubicin	176-187	P53	Homo sapiens	151-155
24074787-12	2013	Taken together, these data can help to better understand p53-mediated response to doxorubicin-based chemotherapy in breast cancer: in ER(+) TP53 WT breast cancers, ER-induced inhibition of p53 apoptotic response would lead preferentially to tumor cell senescence and subsequent resistance to treatment.	Doxorubicin	82-93	P53	Homo sapiens	57-60
24074787-12	2013	Taken together, these data can help to better understand p53-mediated response to doxorubicin-based chemotherapy in breast cancer: in ER(+) TP53 WT breast cancers, ER-induced inhibition of p53 apoptotic response would lead preferentially to tumor cell senescence and subsequent resistance to treatment.	Doxorubicin	82-93	P53	Homo sapiens	140-144
24074787-12	2013	Taken together, these data can help to better understand p53-mediated response to doxorubicin-based chemotherapy in breast cancer: in ER(+) TP53 WT breast cancers, ER-induced inhibition of p53 apoptotic response would lead preferentially to tumor cell senescence and subsequent resistance to treatment.	Doxorubicin	82-93	P53	Homo sapiens	189-192
24156017-7	2013	In p53 knockdown cells, KBrO3 did not suppress BubR1 and Mad2 expression and increased both binucleated cells and cells with &gt;4N DNA content.	kbro3	24-29	P53	Homo sapiens	3-6
23708884-9	2013	Taken together, these findings indicate that the DNA damage-dependent p53-regulated mitochondrial pathway as well as the extrinsic pathway play a crucial role in C110g-induced apoptosis, which provide a better understanding of the molecular mechanisms of trifluoromethyl benzopyrans in cervical cancer.	trifluoromethyl benzopyrans	255-282	P53	Homo sapiens	70-73
23607751-10	2013	On the contrary, doxorubicin abolished p21 activation and elicited p53 induction both in SSc- and HC-MSCs.	Doxorubicin	17-28	P53	Homo sapiens	67-70
23495037-4	2013	Blockade of cyclooxygenase-2 (COX-2) activity by siRNA or NS398 correspondingly inhibited ceramide-induced p53 Ser-15 phosphorylation and apoptosis; thus COX-2 appears at the apex of the p38 kinase-mediated signaling cascade induced by ceramide.	Serine	111-114	P53	Homo sapiens	107-110
23495037-8	2013	In summary, resveratrol and ceramide converge on an endocytosis-requiring, ERK1/2-dependent signal transduction pathway and induction of COX-expression as an essential molecular antecedent for subsequent p53-dependent apoptosis.	Resveratrol	12-23	P53	Homo sapiens	204-207
24009628-1	2013	BACKGROUND: Silent mating type information regulation 2 homolog 1 (SIRT1), an NAD+-dependent deacetylase, might act as a tumor promoter by inhibiting p53, but may also as a tumor suppressor by inhibiting several oncogenes such as beta-catenin and survivin.	NAD	78-81	P53	Homo sapiens	150-153
23677787-4	2013	We observed that TGEV infection decreased p300/CBP, downregulated MDM2 and promoted p53 phosphorylation at serines 15, 20 and 46, resulting in accumulation and activation of p53 in PK-15 cells.	Serine	107-114	P53	Homo sapiens	84-87
23946688-0	2013	Mutant p53-Notch1 Signaling Axis Is Involved in Curcumin-Induced Apoptosis of Breast Cancer Cells.	Curcumin	48-56	P53	Homo sapiens	7-10
23946688-3	2013	The present study aimed to determine whether the mutant p53 can be a potent transcriptional activator of the Notch1 in MDA-MB-231 cells, and explore the role of this mutant p53-Notch1 axis in curcumin-induced apoptosis.	Curcumin	192-200	P53	Homo sapiens	56-59
23946688-3	2013	The present study aimed to determine whether the mutant p53 can be a potent transcriptional activator of the Notch1 in MDA-MB-231 cells, and explore the role of this mutant p53-Notch1 axis in curcumin-induced apoptosis.	Curcumin	192-200	P53	Homo sapiens	173-176
23946688-6	2013	We confirmed the suppressive effect of curcumin on Notch1 transcription by performing a Notch1 promoter-driven reporter assay and identified a putative p53-binding site in the Notch1 promoter by EMSA and chromatin immunoprecipitation analysis.	Curcumin	39-47	P53	Homo sapiens	152-155
23666059-0	2013	Nutlin-3a, an MDM2 antagonist and p53 activator, helps to preserve the replicative potential of cancer cells treated with a genotoxic dose of resveratrol.	Resveratrol	142-153	P53	Homo sapiens	34-37
23946688-8	2013	Moreover, curcumin-induced apoptosis was further enhanced by the knockdown of Notch1 or mutant p53, but it was decreased by the overexpression of active Notch1.	Curcumin	10-18	P53	Homo sapiens	95-98
23946688-9	2013	Taken together, our results demonstrate, for the first time, that Notch1 is a transcriptional target of mutant p53 in breast cancer cells and suggest that the targeting of mutant p53 and/or Notch1 may be combined with a chemotherapeutic strategy to improve the response of breast cancer cells to curcumin.	Curcumin	296-304	P53	Homo sapiens	111-114
23946688-9	2013	Taken together, our results demonstrate, for the first time, that Notch1 is a transcriptional target of mutant p53 in breast cancer cells and suggest that the targeting of mutant p53 and/or Notch1 may be combined with a chemotherapeutic strategy to improve the response of breast cancer cells to curcumin.	Curcumin	296-304	P53	Homo sapiens	179-182
23649769-1	2013	The close relationship between aflatoxins and 249ser TP53 gene mutation (AGG to AGT, Arg to Ser) in hepatocellular carcinoma (HCC) makes this mutation an indirect indicator of dietary contamination with this toxin.	Arginine	85-88	P53	Homo sapiens	53-57
23649769-1	2013	The close relationship between aflatoxins and 249ser TP53 gene mutation (AGG to AGT, Arg to Ser) in hepatocellular carcinoma (HCC) makes this mutation an indirect indicator of dietary contamination with this toxin.	Serine	92-95	P53	Homo sapiens	53-57
23649769-9	2013	TP53 exon 7 mutations, which are related to aflatoxins exposure, were found at 14.6% (249ser), 7.3% (250leu) and 2.4% (250ser) in 41 cases of HCC and 1.4% in 74 liver cirrhosis (without HCC) cases, suggesting a moderate dietary exposure to aflatoxins in the Espirito Santo State, Brazil.	249ser	86-92	P53	Homo sapiens	0-4
23666059-10	2013	Thus, the hyperactivation of p53 by nutlin-3a helps to preserve the replicative potential of cells exposed to resveratrol.	Resveratrol	110-121	P53	Homo sapiens	29-32
23683469-5	2013	The p53 gene contains a single nucleotide polymorphism at codon 72 of exon 4 which encodes either proline (Pro) or arginine (Arg).	Arginine	115-123	P53	Homo sapiens	4-7
23796712-0	2013	p53 regulates glucose metabolism by miR-34a.	Glucose	14-21	P53	Homo sapiens	0-3
23796712-3	2013	p53 has been emphasized as a metabolic regulator involved in glucose, glutamine, and purine metabolism.	Glucose	61-68	P53	Homo sapiens	0-3
23796712-8	2013	The results suggest that p53 has a miR-34a-dependent integrated mechanism to regulate glucose metabolism.	Glucose	86-93	P53	Homo sapiens	25-28
23775793-3	2013	Human osteosarcoma U2OS cells treated with anti-cancer drugs Doxorubicin (DXR) or Nutlin-3 (Nutlin) led to strikingly different p53 gene binding patterns based on chromatin immunoprecipitation with high-throughput sequencing experiments.	Doxorubicin	61-72	P53	Homo sapiens	128-131
23775793-8	2013	Furthermore, both p53 binding and transactivation were associated with increased active histone modification histone H3 lysine 4 trimethylation.	Lysine	120-126	P53	Homo sapiens	18-21
23936455-10	2013	We observed that cells with complete loss of wild-type TP53 alleles ((-/-) or (-/mut)) were resistant to CRT following treatment with 5-fluorouracil and radiation.	Fluorouracil	134-148	P53	Homo sapiens	55-59
23817040-2	2013	TIGAR (TP53-induced glycolysis and apoptosis regulator), which is a p53-inducible gene, functions in the suppression of ROS (reactive oxygen species) and protects U2OS cells from undergoing cell death.	Reactive Oxygen Species	120-123	P53	Homo sapiens	68-71
23817040-2	2013	TIGAR (TP53-induced glycolysis and apoptosis regulator), which is a p53-inducible gene, functions in the suppression of ROS (reactive oxygen species) and protects U2OS cells from undergoing cell death.	Reactive Oxygen Species	125-148	P53	Homo sapiens	68-71
23683469-5	2013	The p53 gene contains a single nucleotide polymorphism at codon 72 of exon 4 which encodes either proline (Pro) or arginine (Arg).	Arginine	125-128	P53	Homo sapiens	4-7
23867003-8	2013	NAC induced p53 and reduced p65 protein expression through activation of PPARalpha.	Acetylcysteine	0-3	P53	Homo sapiens	12-15
23632240-6	2013	The miR-34b/c CC-TP53 Arg/Arg combination significantly increased the risk of HCC (AOR: 13.644; 95% CI: 1.451-128.301).	Arginine	22-25	P53	Homo sapiens	17-21
23632240-6	2013	The miR-34b/c CC-TP53 Arg/Arg combination significantly increased the risk of HCC (AOR: 13.644; 95% CI: 1.451-128.301).	Arginine	26-29	P53	Homo sapiens	17-21
23632240-8	2013	CONCLUSIONS: Our findings suggest that loss of the T allele in miR-34b/c T&gt;C, and the miR-34b/c CC-TP53 Arg/Arg combination increases the risk of HCC in the Korean population.	Arginine	107-110	P53	Homo sapiens	102-106
23632240-8	2013	CONCLUSIONS: Our findings suggest that loss of the T allele in miR-34b/c T&gt;C, and the miR-34b/c CC-TP53 Arg/Arg combination increases the risk of HCC in the Korean population.	Arginine	111-114	P53	Homo sapiens	102-106
23399702-6	2013	The p53 band in Figure 3C is very similar to the Caspase 9 blot in Figure 4B and is cropped and duplicated in Figure 6A as p-NFKB by cisplatin in SiHa cells.	Cisplatin	133-142	P53	Homo sapiens	4-7
23621494-0	2013	MPK-09, a small molecule inspired from bioactive styryllactone restores the wild-type function of mutant p53.	styryllactone	49-62	P53	Homo sapiens	105-108
23806001-0	2013	Template-directed fluorogenic oligonucleotide ligation using "click" chemistry: detection of single nucleotide polymorphism in the human p53 tumor suppressor gene.	Oligonucleotides	30-45	P53	Homo sapiens	137-140
23806001-5	2013	Wild-type and mutant p53 alleles were used to demonstrate that template-directed fluorogenic oligonucleotide ligation is sequence-specific and is capable of single nucleotide discrimination under mild conditions, even without the removal of unreacted probes.	Oligonucleotides	93-108	P53	Homo sapiens	21-24
23874455-4	2013	Pharmacologic targeting of STAT3 expression in cervical cancer cell lines either by STAT3-specific siRNA or blocking its tyrosine phosphorylation by AG490 or curcumin led to dose-dependent accumulation of p53 and pRb in cervical cancer cells.	Tyrosine	121-129	P53	Homo sapiens	205-208
23867003-9	2013	Silencing of p53 and overexpression of p65 blocked the effect of NAC on PDK1 promoter activity and protein expression.	Acetylcysteine	65-68	P53	Homo sapiens	13-16
23874455-4	2013	Pharmacologic targeting of STAT3 expression in cervical cancer cell lines either by STAT3-specific siRNA or blocking its tyrosine phosphorylation by AG490 or curcumin led to dose-dependent accumulation of p53 and pRb in cervical cancer cells.	Curcumin	158-166	P53	Homo sapiens	205-208
23867003-10	2013	CONCLUSION: Our results show that NAC inhibits PDK1 expression through PPARalpha-mediated induction of p53 and inhibition of p65 protein expression.	Acetylcysteine	34-37	P53	Homo sapiens	103-106
23684722-12	2013	CONCLUSIONS: Physalin A induced apoptotic cell death via p53-Noxa-mediated ROS generation, and autophagy played a protective role against apoptosis through up-regulating the p38-NF-kappaB survival pathway in A375-S2 cells.	Reactive Oxygen Species	75-78	P53	Homo sapiens	57-60
23729362-8	2013	Cell death of 5-fluorouracil (5FU)-treated p53-null GSK3B-silenced colon carcinoma cells occurred via PARP1-dependent and AIF-mediated but RIP1-independent necroptosis.	Fluorouracil	14-28	P53	Homo sapiens	43-46
23729362-8	2013	Cell death of 5-fluorouracil (5FU)-treated p53-null GSK3B-silenced colon carcinoma cells occurred via PARP1-dependent and AIF-mediated but RIP1-independent necroptosis.	Fluorouracil	30-33	P53	Homo sapiens	43-46
25206494-7	2013	Ethanol also increased p53 phosphorylation, followed by an increase in p21 tumor suppressor protein and a decrease in phospho-Rb (retinoblastoma) protein, leading to alterations in the expressions and activity of cyclin dependent protein kinases.	Ethanol	0-7	P53	Homo sapiens	23-26
25206494-8	2013	Our results suggest that ethanol mediates apoptosis of SK-N-SH neuroblastoma cells by activating p53-related cell cycle arrest possibly through activation of the c-Jun N-terminal protein kinase-related cell death pathway.	Ethanol	25-32	P53	Homo sapiens	97-100
22789708-1	2013	Herein we propose the benzimidazole-2-one substructure as a suitable tryptophan mimic and thus a reasonable starting point for the design of p53 Mdm2 antagonists.	Tryptophan	69-79	P53	Homo sapiens	141-144
23685175-1	2013	We have discovered and reported potent p53-MDM2 interaction inhibitors possessing dihydroimidazothiazole scaffold.	dihydroimidazothiazole	82-104	P53	Homo sapiens	39-42
23684722-0	2013	Physalin A induces apoptosis via p53-Noxa-mediated ROS generation, and autophagy plays a protective role against apoptosis through p38-NF-kappaB survival pathway in A375-S2 cells.	Reactive Oxygen Species	51-54	P53	Homo sapiens	33-36
23578555-7	2013	Overall, the combined Dox and chi-p53 treatment exhibited enhanced cytotoxicity as compared to either Dox or chi-p53 treatments alone.	Doxorubicin	22-25	P53	Homo sapiens	113-116
23861960-11	2013	This supports a deeper link between proteins of the p53-family and metabolic pathways, as PRODH modulates the balance of proline and glutamate levels and those of their derivative alpha-keto-glutarate (alpha-KG) under normal and pathological (tumor) conditions.	Glutamic Acid	133-142	P53	Homo sapiens	52-55
23692869-6	2013	BPDE-induced cdc2 down-regulation is p53 dependent, although there is no correspondence between p53 accumulation and cdc2 down-regulation.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	0-4	P53	Homo sapiens	37-40
23692869-7	2013	BPDE-induced cdc2 down-regulation corresponded with accumulation of the cell cycle inhibitor protein p21 (transactivation product of p53).	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	0-4	P53	Homo sapiens	133-136
23844043-11	2013	Our study demonstrates that UVB irradiation results in ROS accumulation and ERK activation, which causes the nuclear p53 accumulation and TM promoter binding to inhibit TM expression.	Reactive Oxygen Species	55-58	P53	Homo sapiens	117-120
23578555-7	2013	Overall, the combined Dox and chi-p53 treatment exhibited enhanced cytotoxicity as compared to either Dox or chi-p53 treatments alone.	Doxorubicin	102-105	P53	Homo sapiens	34-37
23759586-5	2013	Dexamethasone also induced expression of miR-34a, which acts to suppress SIRT1 deacetylase, and thus allows maintained acetylation and inactivation of p53.	Dexamethasone	0-13	P53	Homo sapiens	151-154
23793604-7	2013	The P53 Arg/Pro genotype or Pro/Pro genotype was significantly associated with an increased risk of developing breast cancer, compared to the P53 Arg/Arg genotype in both the case-control sets (all P &lt; 0.05).	Arginine	8-11	P53	Homo sapiens	4-7
23815892-10	2013	In contrast, the expression of the apoptotic-related gene - P53, apoptotic executer - caspase 3 and apoptotic initiator - caspase 9 were downregulated after geniposide treatment.	geniposide	157-167	P53	Homo sapiens	60-131
23815892-11	2013	CONCLUSIONS: Our results indicate that geniposide can protect SH-SY5Y cells against formaldehyde stress through modulating the expression of Bcl-2, P53, caspase 3 and caspase 9, and by increasing the activity of intracellular superoxide dismutase and glutathione peroxidase.	geniposide	39-49	P53	Homo sapiens	148-151
23417568-6	2013	We also observed that menadione induced JNK-dependent p53 expression and apoptotic death in SK-N-MC cells while H2O2-induced JNK activation was p53 independent.	sk-n-mc	92-99	P53	Homo sapiens	54-57
23417568-6	2013	We also observed that menadione induced JNK-dependent p53 expression and apoptotic death in SK-N-MC cells while H2O2-induced JNK activation was p53 independent.	Hydrogen Peroxide	112-116	P53	Homo sapiens	144-147
23759586-7	2013	Reporter assays showed that both these dexamethasone-induced miRNAs act downstream of their target genes to prevent p53 tumor suppressor actions and, ultimately, resist cytotoxic responses in MM.	Dexamethasone	39-52	P53	Homo sapiens	116-119
23759586-10	2013	In summary, dexamethasone-induced miR-125b induces cell death resistance mechanisms in MM cells via the p53/miR-34a/SIRT1 signaling network and provides these cells with an enhanced level of resistance to cytotoxic chemotherapeutics.	Dexamethasone	12-25	P53	Homo sapiens	104-107
23653048-6	2013	In the MLH1-proficient cells SN-38, the active metabolite of irinotecan, induced lower levels of DNA damage than in MLH1-deficient cells, as shown by the weaker induction of gamma-H2AX and p53 phosphorylation.	Irinotecan	29-34	P53	Homo sapiens	189-192
23673340-7	2013	Expanding roles for MYC, PI3K and TP53 in regulating reactive oxygen production, glycolysis and glutaminolysis in lymphoma cells have been described.	Oxygen	62-68	P53	Homo sapiens	34-38
23612020-0	2013	Two p53-related metabolic regulators, TIGAR and SCO2, contribute to oroxylin A-mediated glucose metabolism in human hepatoma HepG2 cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	68-78	P53	Homo sapiens	4-7
23612020-0	2013	Two p53-related metabolic regulators, TIGAR and SCO2, contribute to oroxylin A-mediated glucose metabolism in human hepatoma HepG2 cells.	Glucose	88-95	P53	Homo sapiens	4-7
23612020-6	2013	Moreover, oroxylin A could increase protein and mRNA expression of TP53-induced glycolysis and apoptosis regulator (TIGAR) and synthesis of cytochrome c oxidase 2 (SCO2), which are the key metabolic modulators regulated by p53.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	10-20	P53	Homo sapiens	223-226
23612020-8	2013	Oroxylin A and adriamycin also modulated the stability and activity of p53 through inducing phosphorylation of p53 at Ser15 and suppressing the expression of MDM2.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	0-10	P53	Homo sapiens	71-74
23612020-8	2013	Oroxylin A and adriamycin also modulated the stability and activity of p53 through inducing phosphorylation of p53 at Ser15 and suppressing the expression of MDM2.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	0-10	P53	Homo sapiens	111-114
23653048-6	2013	In the MLH1-proficient cells SN-38, the active metabolite of irinotecan, induced lower levels of DNA damage than in MLH1-deficient cells, as shown by the weaker induction of gamma-H2AX and p53 phosphorylation.	Irinotecan	61-71	P53	Homo sapiens	189-192
23612020-8	2013	Oroxylin A and adriamycin also modulated the stability and activity of p53 through inducing phosphorylation of p53 at Ser15 and suppressing the expression of MDM2.	Doxorubicin	15-25	P53	Homo sapiens	71-74
23612020-8	2013	Oroxylin A and adriamycin also modulated the stability and activity of p53 through inducing phosphorylation of p53 at Ser15 and suppressing the expression of MDM2.	Doxorubicin	15-25	P53	Homo sapiens	111-114
23098692-5	2013	1,25(OH)2D3 augmented the effect of cisplatin in an embryonal carcinoma-derived cell line (NTera2), possibly through downregulation of pluripotency genes and simultaneous upregulation of the cell cycle regulators p21, p27, p53, p73 and FOXO1, while no significant effects were found in TCam-2 and 2102Ep cell lines (derived from seminoma and embryonal carcinoma, respectively).	Cisplatin	36-45	P53	Homo sapiens	223-226
23612020-9	2013	Furthermore, p53 siRNA and p53 inhibitor assay in wild-type p53 HepG2 cells both revealed the key role of p53 in oroxylin A and adriamycin-mediated glycolytic metabolism regulation.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	113-123	P53	Homo sapiens	13-16
23612020-9	2013	Furthermore, p53 siRNA and p53 inhibitor assay in wild-type p53 HepG2 cells both revealed the key role of p53 in oroxylin A and adriamycin-mediated glycolytic metabolism regulation.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	113-123	P53	Homo sapiens	27-30
23612020-9	2013	Furthermore, p53 siRNA and p53 inhibitor assay in wild-type p53 HepG2 cells both revealed the key role of p53 in oroxylin A and adriamycin-mediated glycolytic metabolism regulation.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	113-123	P53	Homo sapiens	27-30
23612020-9	2013	Furthermore, p53 siRNA and p53 inhibitor assay in wild-type p53 HepG2 cells both revealed the key role of p53 in oroxylin A and adriamycin-mediated glycolytic metabolism regulation.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	113-123	P53	Homo sapiens	27-30
23612020-9	2013	Furthermore, p53 siRNA and p53 inhibitor assay in wild-type p53 HepG2 cells both revealed the key role of p53 in oroxylin A and adriamycin-mediated glycolytic metabolism regulation.	Doxorubicin	128-138	P53	Homo sapiens	13-16
23612020-9	2013	Furthermore, p53 siRNA and p53 inhibitor assay in wild-type p53 HepG2 cells both revealed the key role of p53 in oroxylin A and adriamycin-mediated glycolytic metabolism regulation.	Doxorubicin	128-138	P53	Homo sapiens	27-30
23612020-9	2013	Furthermore, p53 siRNA and p53 inhibitor assay in wild-type p53 HepG2 cells both revealed the key role of p53 in oroxylin A and adriamycin-mediated glycolytic metabolism regulation.	Doxorubicin	128-138	P53	Homo sapiens	27-30
23612020-9	2013	Furthermore, p53 siRNA and p53 inhibitor assay in wild-type p53 HepG2 cells both revealed the key role of p53 in oroxylin A and adriamycin-mediated glycolytic metabolism regulation.	Doxorubicin	128-138	P53	Homo sapiens	27-30
23612020-10	2013	Transfecting wt p53 plasmid to p53-deficient H1299 cells could inverse some of the metabolic characteristics regulated by oroxylin A.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	122-132	P53	Homo sapiens	16-19
23612020-10	2013	Transfecting wt p53 plasmid to p53-deficient H1299 cells could inverse some of the metabolic characteristics regulated by oroxylin A.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	122-132	P53	Homo sapiens	31-34
23606744-6	2013	In the study reported here we found that cytoplasmic DGKzeta attenuates p53-mediated cytotoxicity against doxorubicin-induced DNA damage by facilitating cytoplasmic anchoring and degradation of p53 through a ubiquitin-proteasome system.	Doxorubicin	106-117	P53	Homo sapiens	72-75
23606744-6	2013	In the study reported here we found that cytoplasmic DGKzeta attenuates p53-mediated cytotoxicity against doxorubicin-induced DNA damage by facilitating cytoplasmic anchoring and degradation of p53 through a ubiquitin-proteasome system.	Doxorubicin	106-117	P53	Homo sapiens	194-197
23401182-0	2013	The effect of zinc and the role of p53 in copper-induced cellular stress responses.	Copper	42-48	P53	Homo sapiens	35-38
23401182-2	2013	A number of previous studies have shown that zinc (Zn) modulates mitogenic activity via several signalling pathways, such as AKT, mitogen-activated protein kinase (MAPK), nuclear factor-kappa B (NF -kappaB), AP-1 and p53.	Zinc	51-53	P53	Homo sapiens	217-220
23401182-4	2013	Intracellular free Zn modulates p53 activity and stability, and excess Zn alters the p53 protein structure and down-regulates p53"s binding to DNA.	Zinc	71-73	P53	Homo sapiens	85-88
23401182-4	2013	Intracellular free Zn modulates p53 activity and stability, and excess Zn alters the p53 protein structure and down-regulates p53"s binding to DNA.	Zinc	71-73	P53	Homo sapiens	85-88
23401182-5	2013	Copper (Cu) accumulation causes apoptosis that seems to be mediated by DNA damage and subsequent p53 activation.	Copper	0-6	P53	Homo sapiens	97-100
23401182-5	2013	Copper (Cu) accumulation causes apoptosis that seems to be mediated by DNA damage and subsequent p53 activation.	Copper	8-10	P53	Homo sapiens	97-100
23401182-6	2013	Cu can also displace Zn from its normal binding site on p53, resulting in abnormal protein folding and disruption of p53 function.	Copper	0-2	P53	Homo sapiens	56-59
23401182-6	2013	Cu can also displace Zn from its normal binding site on p53, resulting in abnormal protein folding and disruption of p53 function.	Copper	0-2	P53	Homo sapiens	117-120
23401182-6	2013	Cu can also displace Zn from its normal binding site on p53, resulting in abnormal protein folding and disruption of p53 function.	Zinc	21-23	P53	Homo sapiens	56-59
23401182-6	2013	Cu can also displace Zn from its normal binding site on p53, resulting in abnormal protein folding and disruption of p53 function.	Zinc	21-23	P53	Homo sapiens	117-120
23401182-12	2013	This review discusses the central role of p53 and the redox-inert metal Zn in the cellular stress responses induced by the redox active biometal Cu.	Copper	145-147	P53	Homo sapiens	42-45
23499753-2	2013	H2O2 exposure reduced cellular proliferation similarly in both p53-290 and vector cells, and p53-290 cells demonstrating decreased cell viability at 1mM H2O2 (~85% viable).	Hydrogen Peroxide	0-4	P53	Homo sapiens	63-66
23499753-2	2013	H2O2 exposure reduced cellular proliferation similarly in both p53-290 and vector cells, and p53-290 cells demonstrating decreased cell viability at 1mM H2O2 (~85% viable).	Hydrogen Peroxide	153-157	P53	Homo sapiens	93-96
23814485-8	2013	Moreover, modification of the p53 serine 46 residue was critical for RKIP induction and ERK suppression as well as cellular senescence.	Serine	34-40	P53	Homo sapiens	30-33
23422071-0	2013	Analysis of TP53 mutation spectra reveals the fingerprint of the potent environmental carcinogen, aristolochic acid.	aristolochic acid I	98-115	P53	Homo sapiens	12-16
23946774-7	2013	Even at low doses of radiation from iron ions, global genome profiling of the irradiated cells revealed the upregulation of genes associated with the activation of stress-related signaling pathways (ubiquitin-mediated proteolysis, p53 signaling, cell cycle and apoptosis), which occurred in a dose-dependent manner.	Iron	36-40	P53	Homo sapiens	231-234
23422071-2	2013	Here we review the pieces of evidence that support the role of aristolochic acid (AA) in inducing a mutational fingerprint in the tumor suppressor gene TP53 in urothelial carcinomas of the upper urinary tract (UUT).	aristolochic acid I	63-80	P53	Homo sapiens	152-156
23486648-6	2013	We showed that curcumin-treated Jurkat cells and resting T cells showed neither DNA lesions nor did they activate key proteins in the DDR signalling pathway, such as phospho-ATM and phospho-p53.	Curcumin	15-23	P53	Homo sapiens	190-193
23624782-9	2013	The combination of SNP309 GG + TG and TP53 codon 72 Arg/Arg significantly increased endometrial cancer risk.	Arginine	52-55	P53	Homo sapiens	38-42
23624782-9	2013	The combination of SNP309 GG + TG and TP53 codon 72 Arg/Arg significantly increased endometrial cancer risk.	Arginine	56-59	P53	Homo sapiens	38-42
23624782-11	2013	This result was supported by in vitro data showing that endometrial cancer cell lines with the SNP309 G allele failed to show growth inhibition by treatment with RITA, which reduces p53-MDM2 binding.	RITA	162-166	P53	Homo sapiens	182-185
23807219-5	2013	The natural product and putative BH3 mimetic gossypol enhanced the cytotoxicity of BRD4770 in a synergistic manner in p53-mutant PANC-1 cells but not in immortalized non-tumorigenic pancreatic cells.	Gossypol	45-53	P53	Homo sapiens	118-121
23624782-12	2013	The presence of the SNP309 G allele and TP53 codon 72 Arg/Arg genotype is associated with an increased risk of endometrial cancer in Japanese women.	Arginine	54-57	P53	Homo sapiens	40-44
23624782-12	2013	The presence of the SNP309 G allele and TP53 codon 72 Arg/Arg genotype is associated with an increased risk of endometrial cancer in Japanese women.	Arginine	58-61	P53	Homo sapiens	40-44
23727578-3	2013	p53 activation by 5-fluorouracil significantly increased hGBP1 expression in wild-type p53 cells, but not in p53-null cells.	Fluorouracil	18-32	P53	Homo sapiens	0-3
23727578-3	2013	p53 activation by 5-fluorouracil significantly increased hGBP1 expression in wild-type p53 cells, but not in p53-null cells.	Fluorouracil	18-32	P53	Homo sapiens	87-90
23727578-3	2013	p53 activation by 5-fluorouracil significantly increased hGBP1 expression in wild-type p53 cells, but not in p53-null cells.	Fluorouracil	18-32	P53	Homo sapiens	87-90
23727578-4	2013	Knockdown of p53 expression remarkably impaired hGBP1 expression induced by 5-fluorouracil, type I interferon treatment, or influenza A virus infection.	Fluorouracil	76-90	P53	Homo sapiens	13-16
23651583-0	2013	Resveratrol promotes proteasome-dependent degradation of Nanog via p53 activation and induces differentiation of glioma stem cells.	Resveratrol	0-11	P53	Homo sapiens	67-70
23651583-6	2013	p53 activation is an important factor in Nanog suppression and treatment with resveratrol was also found to activate the p53/p21 pathway.	Resveratrol	78-89	P53	Homo sapiens	0-3
23651583-6	2013	p53 activation is an important factor in Nanog suppression and treatment with resveratrol was also found to activate the p53/p21 pathway.	Resveratrol	78-89	P53	Homo sapiens	121-124
23651583-9	2013	Our results also suggest that targeting GSCs via the p53-Nanog axis, with resveratrol for instance, could be a therapeutic strategy against glioblastoma.	Resveratrol	74-85	P53	Homo sapiens	53-56
23826318-2	2013	Here we show that MDM2 can inhibit Axin-stimulated p53-dependent apoptosis by suppressing p53 phosphorylation at Ser 46 and apoptosis-related p53 transactivational activity.	Serine	113-116	P53	Homo sapiens	51-54
22824800-4	2013	In this study, we characterized p53 isoform expression patterns in glioblastoma, gliosis, non-tumor brain and neural progenitor cells by SDS-PAGE, immunoblot, mass spectrometry and reverse transcription-PCR.	Sodium Dodecyl Sulfate	137-140	P53	Homo sapiens	32-35
23826318-2	2013	Here we show that MDM2 can inhibit Axin-stimulated p53-dependent apoptosis by suppressing p53 phosphorylation at Ser 46 and apoptosis-related p53 transactivational activity.	Serine	113-116	P53	Homo sapiens	90-93
22869143-3	2013	Doxorubicin, a common chemotherapeutic agent, is known to promote PML-mediated p53 activation in part by promoting PML-dependent MDM2 nucleolar sequestration.	Doxorubicin	0-11	P53	Homo sapiens	79-82
23826318-2	2013	Here we show that MDM2 can inhibit Axin-stimulated p53-dependent apoptosis by suppressing p53 phosphorylation at Ser 46 and apoptosis-related p53 transactivational activity.	Serine	113-116	P53	Homo sapiens	90-93
22869143-4	2013	We discovered that BMK1 deactivation coupled with doxorubicin synergistically enhanced MDM2 nucleolar sequestration and, consequently, promoted PML-mediated p53 upregulation leading to tumor cell apoptosis in vitro and tumor regression in vivo.	Doxorubicin	50-61	P53	Homo sapiens	157-160
23566959-0	2013	p53 activation by Ni(II) is a HIF-1alpha independent response causing caspases 9/3-mediated apoptosis in human lung cells.	Nickel(2+)	18-24	P53	Homo sapiens	0-3
23576563-2	2013	p53 is acetylated at lysine 120 (K120) by acetyltranferases Tip60 (KAT5) and hMOF (KAT8) in response to DNA damage.	Lysine	21-27	P53	Homo sapiens	0-3
23676219-7	2013	By phosphorylating p53 on its serine-15, HIPK1 favored its transactivation potential, which led to a rise in p21 protein level and a decline in cell proliferation.	Serine	30-36	P53	Homo sapiens	19-22
23566959-2	2013	We examined whether Ni(II) elicits a toxicologically significant activation of the tumor suppressor p53, which is typically associated with genotoxic responses.	Nickel(2+)	20-26	P53	Homo sapiens	100-103
23566959-11	2013	Knockdown of p53 also led to derepression of antiapoptotic MCL1 in Ni(II)-treated cells.	Nickel(2+)	67-73	P53	Homo sapiens	13-16
23566959-4	2013	Confirming the activation of p53, its knockdown suppressed the ability of Ni(II) to upregulate MDM2 and p21 (CDKN1A).	Nickel(2+)	74-80	P53	Homo sapiens	29-32
23566959-12	2013	Overall, our results indicate that p53 plays a major role in apoptotic death of human lung cells by Ni(II).	Nickel(2+)	100-106	P53	Homo sapiens	35-38
23566959-5	2013	Unlike DNA damage, induction of GADD45A by Ni(II) was p53-independent.	Nickel(2+)	43-49	P53	Homo sapiens	54-57
23566959-13	2013	Chronic exposure to Ni(II) may promote selection of resistant cells with inactivated p53, providing an explanation for the origin of p53 mutations by this epigenetic carcinogen.	Nickel(2+)	20-26	P53	Homo sapiens	85-88
23566959-6	2013	Ni(II) also increased p53-Ser15 phosphorylation and p21 expression in normal human lung fibroblasts.	Nickel(2+)	0-6	P53	Homo sapiens	22-25
23566959-13	2013	Chronic exposure to Ni(II) may promote selection of resistant cells with inactivated p53, providing an explanation for the origin of p53 mutations by this epigenetic carcinogen.	Nickel(2+)	20-26	P53	Homo sapiens	133-136
23566959-8	2013	Ni(II)-treated H460 cells showed no evidence of necrosis and their apoptosis and clonogenic death were suppressed by p53 knockdown.	Nickel(2+)	0-6	P53	Homo sapiens	117-120
23360684-4	2013	The cleavage of caspases and PARP, activation of p53 and mitochondrial-mediated apoptosis pathways induced by cisplatin were effectively blocked by cyanidin.	Cisplatin	110-119	P53	Homo sapiens	49-52
23612976-6	2013	Most of the effects of Wip1 may be attributed to its ability to dephosphorylate p53 at Ser(15) and to inhibit DNA damage response.	Serine	87-90	P53	Homo sapiens	80-83
23612976-7	2013	However, we also uncover a regulatory pathway whereby suppression of p53 Ser(15) phosphorylation is associated with enhanced phosphorylation at Ser(46), increased p53 protein levels, and induction of Noxa expression.	Serine	73-76	P53	Homo sapiens	69-72
23612976-7	2013	However, we also uncover a regulatory pathway whereby suppression of p53 Ser(15) phosphorylation is associated with enhanced phosphorylation at Ser(46), increased p53 protein levels, and induction of Noxa expression.	Serine	73-76	P53	Homo sapiens	163-166
23612976-7	2013	However, we also uncover a regulatory pathway whereby suppression of p53 Ser(15) phosphorylation is associated with enhanced phosphorylation at Ser(46), increased p53 protein levels, and induction of Noxa expression.	Serine	144-147	P53	Homo sapiens	69-72
22721392-0	2013	The role of autophagic cell death and apoptosis in irinotecan-treated p53 null colon cancer cells.	Irinotecan	51-61	P53	Homo sapiens	70-73
22721392-1	2013	The roles of autophagic cell death and apoptosis induced by topoisomerase inhibitor irinotecan in colon cancer cells with deleted p53 were investigated during 48 h. We report that irinotecan-dependent cytotoxicity and proapoptotic activity were reduced in the present model while autophagy levels significantly increased.	Irinotecan	180-190	P53	Homo sapiens	130-133
22721392-4	2013	These results suggest that different modes of cell death in p53 null colon cancer cells treated with cytostatics (irinotecan) may be activated simultaneously.	Irinotecan	114-124	P53	Homo sapiens	60-63
23601819-0	2013	Design, synthesis and biological evaluation of novel 3,4,5-trisubstituted aminothiophenes as inhibitors of p53-MDM2 interaction.	3,4,5-trisubstituted aminothiophenes	53-89	P53	Homo sapiens	107-110
23601819-2	2013	A series of 3,4,5-trisubstituted aminothiophenes were designed, synthesized, and evaluated for their p53-MDM2 binding inhibitory potency and anti-proliferation activities against A549 and PC3 tumor cell lines.	3,4,5-trisubstituted aminothiophenes	12-48	P53	Homo sapiens	101-104
23601819-4	2013	Meanwhile, most of the 3,4,5-trisubstituted aminothiophenes displayed better or equivalent anti-proliferation activities against wild-type p53 cell line A549 compared to that of Nutlin-3.	3,4,5-trisubstituted aminothiophenes	23-59	P53	Homo sapiens	139-142
23799024-4	2013	In the present study, we revealed that high glucose could induce GDF15 expression and secretion in cultured human umbilical vein endothelial cells in a ROS- and p53-dependent manner.	Glucose	44-51	P53	Homo sapiens	161-164
23611770-0	2013	Design, synthesis and biological evaluation of novel 3,4,5-trisubstituted aminothiophenes as inhibitors of p53-MDM2 interaction.	3,4,5-trisubstituted aminothiophenes	53-89	P53	Homo sapiens	107-110
23843848-6	2013	METHODS: We have studied the effect of 1, 1.5, and 2 Gy doses of 9 MV X-rays along with 1 microM doxorubicin on inducing cell death, apoptosis and also p53 and PTEN gene expression in T47D and SKBR3 breast cancer cells.	Doxorubicin	97-108	P53	Homo sapiens	152-155
23571142-0	2013	Prognostic role of p53 messenger ribonucleic acid expression in patients after curative resection for stage I to III colorectal cancer: association with colon cancer stem cell markers.	ribonucleic	33-44	P53	Homo sapiens	19-22
23563592-3	2013	In particular, the association of p53 with the mechanism(s) of taxane-mediated cell death is still controversial.	taxane	63-69	P53	Homo sapiens	34-37
23843848-7	2013	RESULTS: Doxorubicin treatment resulted in upregulation of radiation-induced levels of p53 and downregulation of PTEN at 1 and 1.5 Gy in T47D breast cancer cells, as well as downregulation of p53 mRNA level of expression and upregulation of PTEN mRNA level of expression in SKBR3 breast cancer cell line.	Doxorubicin	9-20	P53	Homo sapiens	87-90
23843848-7	2013	RESULTS: Doxorubicin treatment resulted in upregulation of radiation-induced levels of p53 and downregulation of PTEN at 1 and 1.5 Gy in T47D breast cancer cells, as well as downregulation of p53 mRNA level of expression and upregulation of PTEN mRNA level of expression in SKBR3 breast cancer cell line.	Doxorubicin	9-20	P53	Homo sapiens	192-195
23030661-13	2013	Total p53 activity and particularly phosphorylated p53 at serine 46, were significantly enhanced compared with controls (47.11 +- 9.84 units/mL vs. 1.5 +- 0 units/mL and 32.22 +- 10.23 units/mL vs. 0.15 +- 0 units/mL, respectively, at 48 h).	Serine	58-64	P53	Homo sapiens	51-54
23588680-0	2013	All-trans retinoic acid upregulates the expression of p53 via Axin and inhibits the proliferation of glioma cells.	Tretinoin	10-23	P53	Homo sapiens	54-57
23588680-2	2013	In the present study, we demonstrated that ATRA activated the expression of p53 via Axin and induced cell cycle arrest at the G1/S phase and apoptosis of glioma cells.	Tretinoin	43-47	P53	Homo sapiens	76-79
23588680-6	2013	Furthermore, loss-of-function of Axin in glioma cells by RNAi blocked ATRA-induced cell cycle phase arrest and apoptosis via downregulation of p53.	Tretinoin	70-74	P53	Homo sapiens	143-146
23798621-6	2013	DACH1 phosphorylation at serine residue (S439) inhibited p53 binding and phosphorylation at p53 amino-terminal sites (S15, S20) enhanced DACH1 binding.	Serine	25-31	P53	Homo sapiens	92-95
23798621-7	2013	DACH1 binding to p53 was inhibited by NAD-dependent deacetylation via DACH1 K628.	NAD	38-41	P53	Homo sapiens	17-20
23512991-0	2013	Preclinical evaluation of a novel ATM inhibitor, KU59403, in vitro and in vivo in p53 functional and dysfunctional models of human cancer.	KU59403	49-56	P53	Homo sapiens	82-85
23686430-0	2013	Curcumin induces apoptosis in human colorectal carcinoma (HCT-15) cells by regulating expression of Prp4 and p53.	Curcumin	0-8	P53	Homo sapiens	109-112
23686430-6	2013	Western blot analysis revealed that curcumin treatment activated caspase-3 and decreased expression of p53 and Prp4B in a time-dependent manner.	Curcumin	36-44	P53	Homo sapiens	103-106
23595149-4	2013	We here demonstrate that p53 stimulated by the DNA-damaging agent doxorubicin (DOX) induced the expression of TTP in cancer cells.	Doxorubicin	66-77	P53	Homo sapiens	25-28
23595149-4	2013	We here demonstrate that p53 stimulated by the DNA-damaging agent doxorubicin (DOX) induced the expression of TTP in cancer cells.	Doxorubicin	79-82	P53	Homo sapiens	25-28
23030661-16	2013	CONCLUSION: Following incubation with H2 S , OKSCs express multiple p53-associated genes, including programmed cell death, cell-cycle control and DNA-repair genes.	Hydrogen	38-40	P53	Homo sapiens	68-71
23632475-4	2013	Metformin (i) activated the ataxia telengiectasia-mutated (ATM)-AMPK-p53/p21(cip1) and inhibited the Akt-mammalian target of rapamycin (mTOR)-eIF4E-binding protein 1 (4EBP1) pathways, (ii) induced G1 cycle arrest and (iii) enhanced apoptosis.	Metformin	0-9	P53	Homo sapiens	69-72
23564481-0	2013	Association between the p53 codon 72 Arg/Pro polymorphism and hepatocellular carcinoma risk.	Arginine	37-40	P53	Homo sapiens	24-27
23564481-1	2013	Previous studies regarding the association of p53 codon 72 Arg/Pro polymorphism with hepatocellular carcinoma (HCC) risk have provided conflicting and inconclusive findings.	Arginine	59-62	P53	Homo sapiens	46-49
23564481-4	2013	The strength of the association of p53 codon 72 Arg/Pro polymorphism with HCC risk was estimated by the pooled odds ratio (OR) with its corresponding 95 % confidence interval (95 % CI).	Arginine	48-51	P53	Homo sapiens	35-38
23564481-9	2013	This meta-analysis suggests that the p53 codon 72 Arg/Pro polymorphism may play a critical role in the development of HCC, and gender and family history of HCC may not modulate the effect of p53 codon 72 Arg/Pro in HCC risk.	Arginine	50-53	P53	Homo sapiens	37-40
23504554-5	2013	The gene-gene interaction of miR-34b/c rs4938723 and TP-53 Arg72-Pro showed that the combined genotypes of rs4938723CT/CC and TP-53CG/CC increased the risk of NPC (rs4938723CT/CC + TP-53CG/CC vs. rs4938723 TT+TP-53 CG/CC: OR=1.58, 95 % CI 1.04-2.42, p=0.03).	neotetrazolium	53-55	P53	Homo sapiens	126-131
23599430-5	2013	Here, we show that p53 was transiently phosphorylated at Ser-15 in epithelial cells treated with an imperceptible voltage (1 V/cm) and a 0.1-ms pulse width.	Serine	57-60	P53	Homo sapiens	19-22
23597064-1	2013	Structural analysis of both the MDM2-p53 protein-protein interaction and several small molecules bound to MDM2 led to the design and synthesis of tetrasubstituted morpholinone 10, an MDM2 inhibitor with a biochemical IC50 of 1.0 muM.	Morpholin-3-one	163-175	P53	Homo sapiens	37-40
23470866-7	2013	In conclusion, we suggested that oroxylin A reversed MDR by G2/M arrest and the underlying mechanism attributed to the suppression of P-gp expression via Chk2/P53/NF-kappaB signaling pathway.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	33-41	P53	Homo sapiens	159-162
23717592-0	2013	Proinflammatory cytokines and bile acids upregulate DeltaNp73 protein, an inhibitor of p53 and p73 tumor suppressors.	Bile Acids and Salts	30-40	P53	Homo sapiens	87-90
23706821-5	2013	Conversely, the Numb-p53 interaction and Numb-mediated apoptosis are significantly enhanced by depletion of Set8 from cancer cells or by treating the cells with doxorubicin, a chemotherapeutic drug that causes a reduction in the mRNA and protein levels of Set8.	Doxorubicin	161-172	P53	Homo sapiens	21-24
23564911-6	2013	CRM1 inhibitor KPT-185 induced mainly full-length p53 and apoptosis in a p53-dependent manner, whereas inhibition of proliferation was p53 independent.	KPT-185	15-22	P53	Homo sapiens	73-76
23704974-7	2013	The DEABM reproduced cellular population dynamics seen during the menstrual cycle and pregnancy, and demonstrated the oncogenic effect of known genetic factors associated with breast cancer, namely TP53 and Myc, in simulations spanning ~40 years of simulated time.	deabm	4-9	P53	Homo sapiens	198-202
23564911-6	2013	CRM1 inhibitor KPT-185 induced mainly full-length p53 and apoptosis in a p53-dependent manner, whereas inhibition of proliferation was p53 independent.	KPT-185	15-22	P53	Homo sapiens	50-53
23564911-6	2013	CRM1 inhibitor KPT-185 induced mainly full-length p53 and apoptosis in a p53-dependent manner, whereas inhibition of proliferation was p53 independent.	KPT-185	15-22	P53	Homo sapiens	73-76
23663243-1	2013	BACKGROUND: Codon 72 (Arg/Pro), the most frequently studied single nucleotide polymorphism (SNP) of p53 to date, is associated with the ability of the gene to induce cell apoptosis.	Arginine	22-25	P53	Homo sapiens	100-103
23672670-11	2013	After taxane application, p21WAF1/CIP1 expression was only induced in MCF-7 cells with functional p53.	taxane	6-12	P53	Homo sapiens	98-101
23583237-4	2013	Here we demonstrate that MYBBP1A interacts with lysine residues in the C-terminal regulatory domain region of p53.	Lysine	48-54	P53	Homo sapiens	110-113
23603988-2	2013	We recently demonstrated that through their physical interaction, cdk9 phosphorylates p53 on Ser-392, leading to p53 stability and accumulation.	Serine	93-96	P53	Homo sapiens	86-89
23603988-2	2013	We recently demonstrated that through their physical interaction, cdk9 phosphorylates p53 on Ser-392, leading to p53 stability and accumulation.	Serine	93-96	P53	Homo sapiens	113-116
23603988-5	2013	Using western blot analysis, we found that cdk9 promotes inhibition and phosphorylation of Mdm2 on Ser-395, thus preventing degradation of p53, a protein that is directly involved in promoting p53 ubiquitination.	Serine	99-102	P53	Homo sapiens	139-142
23603988-5	2013	Using western blot analysis, we found that cdk9 promotes inhibition and phosphorylation of Mdm2 on Ser-395, thus preventing degradation of p53, a protein that is directly involved in promoting p53 ubiquitination.	Serine	99-102	P53	Homo sapiens	193-196
23589839-4	2013	Here, we show that Myc-induced altered glutamine metabolism involves ATP depletion and activation of the energy sensor AMP-activated protein kinase (AMPK), which induces stabilizing phosphorylation of p53 at Ser15.	Adenosine Triphosphate	69-72	P53	Homo sapiens	201-204
23717325-3	2013	In association with homeodomain-interacting protein kinase-2 (HIPK2), TP53INP1 phosphorylates p53 protein at Serine-46.	Serine	109-115	P53	Homo sapiens	94-97
23663243-5	2013	The p53 codon 72 SNP was identified from retrospectively collected paraffin-embedded biopsy specimens using Sanger sequencing.	Paraffin	67-75	P53	Homo sapiens	4-7
23428467-3	2013	Using this approach, in association with a yeast p53 transactivation assay, the pyranoxanthone (3,4-dihydro-12-hydroxy-2,2-dimethyl-2H,6H-pyrano[3,2-b]xanthen-6-one) (1) was identified as a putative small-molecule inhibitor of p53-MDM2 interaction.	pyranoxanthone	80-94	P53	Homo sapiens	227-230
23667851-5	2013	Germline TP53 mutation c.566C&gt;T results in the missense mutation GCC (Ala) to GTC (Val) at codon 189 (A189V) and has been reported in a case of multiple primary colon tumors.	Alanine	73-76	P53	Homo sapiens	9-13
23428467-4	2013	The activity of the pyranoxanthone 1 as inhibitor of p53-MDM2 interaction was further investigated in human tumor cells with wild-type p53 and overexpressed MDM2.	pyranoxanthone	20-34	P53	Homo sapiens	53-56
23428467-4	2013	The activity of the pyranoxanthone 1 as inhibitor of p53-MDM2 interaction was further investigated in human tumor cells with wild-type p53 and overexpressed MDM2.	pyranoxanthone	20-34	P53	Homo sapiens	135-138
23428467-5	2013	Notably, the pyranoxanthone 1 mimicked the activity of known p53 activators, leading to p53 stabilization and activation of p53-dependent transcriptional activity.	pyranoxanthone	13-27	P53	Homo sapiens	61-64
23664374-1	2013	In this issue of Molecular Cell,Long and Crighton (2013) report a cell death priming mechanism activated by p53 that senses extracellular adenosine accumulated following chemotherapy or hypoxia, providing a novel connection between adenosine signaling and apoptosis.	Adenosine	138-147	P53	Homo sapiens	108-111
23664374-1	2013	In this issue of Molecular Cell,Long and Crighton (2013) report a cell death priming mechanism activated by p53 that senses extracellular adenosine accumulated following chemotherapy or hypoxia, providing a novel connection between adenosine signaling and apoptosis.	Adenosine	232-241	P53	Homo sapiens	108-111
23608226-9	2013	Induction of T-bet in YT cells up-regulated p53, leading to increased sensitivity in response to doxorubicin.	Doxorubicin	97-108	P53	Homo sapiens	44-47
23428467-5	2013	Notably, the pyranoxanthone 1 mimicked the activity of known p53 activators, leading to p53 stabilization and activation of p53-dependent transcriptional activity.	pyranoxanthone	13-27	P53	Homo sapiens	88-91
23354308-0	2013	Degradation of NF-kappaB, p53 and other regulatory redox-sensitive proteins by thiol-conjugating and -nitrosylating drugs in human tumor cells.	Sulfhydryl Compounds	79-84	P53	Homo sapiens	26-29
23428467-5	2013	Notably, the pyranoxanthone 1 mimicked the activity of known p53 activators, leading to p53 stabilization and activation of p53-dependent transcriptional activity.	pyranoxanthone	13-27	P53	Homo sapiens	88-91
23428467-7	2013	By computational docking studies, it was predicted that, like nutlin-3a, a known small-molecule inhibitor of p53-MDM2 interaction, pyranoxanthone 1 binds to the p53-binding site of MDM2.	pyranoxanthone	131-145	P53	Homo sapiens	109-112
23428467-7	2013	By computational docking studies, it was predicted that, like nutlin-3a, a known small-molecule inhibitor of p53-MDM2 interaction, pyranoxanthone 1 binds to the p53-binding site of MDM2.	pyranoxanthone	131-145	P53	Homo sapiens	161-164
23428467-9	2013	Besides its potential use as molecular probe and possible lead to develop anticancer agents, the pyranoxanthone 1 will pave the way for the structure-based design of a new class of p53-MDM2 inhibitors.	pyranoxanthone	97-111	P53	Homo sapiens	181-184
23354308-5	2013	DSF and copper-chelated DSF at concentrations of 50-200 microM induced the disappearance of wild-type p53, mutant p53, NF-kappaB subunit p50 and the ubiquitin-activating enzyme E1 (UBE1) in tumor cell lines.	Copper	8-14	P53	Homo sapiens	102-105
23354308-5	2013	DSF and copper-chelated DSF at concentrations of 50-200 microM induced the disappearance of wild-type p53, mutant p53, NF-kappaB subunit p50 and the ubiquitin-activating enzyme E1 (UBE1) in tumor cell lines.	Copper	8-14	P53	Homo sapiens	114-117
23354312-2	2013	We have recently shown that melatonin induces p38-dependent phosphorylation of both p53 and histone H2AX.	Melatonin	28-37	P53	Homo sapiens	84-87
23354312-4	2013	In addition, the inhibition of p38 activities impairs melatonin"s capability to induce a p53-dependent DNA damage response and thus its ability to maintain genome integrity.	Melatonin	54-63	P53	Homo sapiens	89-92
23354312-5	2013	Since melatonin-induced p53 phosphorylation requires an intact p38 phosphorylation cascade and p38 can be activated by G proteins, we supposed that melatonin"s activities could be mediated by its G-protein-coupled membrane receptors, MT1 and MT2.	Melatonin	6-15	P53	Homo sapiens	24-27
23354312-5	2013	Since melatonin-induced p53 phosphorylation requires an intact p38 phosphorylation cascade and p38 can be activated by G proteins, we supposed that melatonin"s activities could be mediated by its G-protein-coupled membrane receptors, MT1 and MT2.	Melatonin	148-157	P53	Homo sapiens	24-27
23574722-7	2013	siRNA-mediated depletion of GLS2 sensitizes cells to ROS-induced apoptosis, suggesting that the TAp63/GLS2 axis can be functionally important as a cellular antioxidant pathway in the absence of p53.	ros	53-56	P53	Homo sapiens	194-197
23354312-6	2013	Here, we show that the activation of the p53-dependent DNA damage response by melatonin is indeed mediated by MT1 and MT2.	Melatonin	78-87	P53	Homo sapiens	41-44
23483263-4	2013	The combined inhibition of the HDAC and SIRT1 deacetylases abolished the cAMP-mediated deacetylation of p53, implying that cAMP-mediated deacetylation of p53 is dependent on the activity of these two classes of histone deacetylases.	Cyclic AMP	123-127	P53	Homo sapiens	154-157
23483263-5	2013	Importantly, diminishing the activity of HDACs and SIRT1 was also found to reverse the inhibitory effect of cAMP on the DNA damage-induced p53 stabilization and apoptosis, suggesting the involvement of the p53 acetylation pathway in the anti-apoptotic effect of cAMP signalling.	Cyclic AMP	108-112	P53	Homo sapiens	139-142
23483119-4	2013	In the present study, we show that, in addition to these well-studied molecular mechanisms, the treatment of wild-type TP53 MCF-7 and mutant TP53 MDA-MB-231 human breast cancer cells with desferrioxamine (DFO), a model iron chelator, causes significant epigenetic alterations at the global and gene-specific levels.	Iron	219-223	P53	Homo sapiens	119-123
23483119-4	2013	In the present study, we show that, in addition to these well-studied molecular mechanisms, the treatment of wild-type TP53 MCF-7 and mutant TP53 MDA-MB-231 human breast cancer cells with desferrioxamine (DFO), a model iron chelator, causes significant epigenetic alterations at the global and gene-specific levels.	Iron	219-223	P53	Homo sapiens	141-145
23483263-0	2013	cAMP signalling inhibits p53 acetylation and apoptosis via HDAC and SIRT deacetylases.	Cyclic AMP	0-4	P53	Homo sapiens	25-28
23483263-1	2013	Activation of cAMP signalling potently inhibits DNA damage-induced apoptosis in acute lymphoblastic leukemia cells by promoting the turnover of p53 protein.	Cyclic AMP	14-18	P53	Homo sapiens	144-147
23483263-2	2013	Recently, we showed that the cAMP-induced destabilization of p53 in DNA-damaged cells occurs as a result of enhanced interaction between p53 and HDM2.	Cyclic AMP	29-33	P53	Homo sapiens	61-64
23483263-2	2013	Recently, we showed that the cAMP-induced destabilization of p53 in DNA-damaged cells occurs as a result of enhanced interaction between p53 and HDM2.	Cyclic AMP	29-33	P53	Homo sapiens	137-140
23483263-5	2013	Importantly, diminishing the activity of HDACs and SIRT1 was also found to reverse the inhibitory effect of cAMP on the DNA damage-induced p53 stabilization and apoptosis, suggesting the involvement of the p53 acetylation pathway in the anti-apoptotic effect of cAMP signalling.	Cyclic AMP	108-112	P53	Homo sapiens	206-209
23483263-3	2013	In this report, we present results showing that increased levels of cAMP in cells with DNA damage enhances the deacetylation of p53, an event that facilitates the interaction of p53 with HDM2, thus annulling the stabilizing effect of DNA damage on p53.	Cyclic AMP	68-72	P53	Homo sapiens	128-131
23483263-3	2013	In this report, we present results showing that increased levels of cAMP in cells with DNA damage enhances the deacetylation of p53, an event that facilitates the interaction of p53 with HDM2, thus annulling the stabilizing effect of DNA damage on p53.	Cyclic AMP	68-72	P53	Homo sapiens	178-181
23483263-5	2013	Importantly, diminishing the activity of HDACs and SIRT1 was also found to reverse the inhibitory effect of cAMP on the DNA damage-induced p53 stabilization and apoptosis, suggesting the involvement of the p53 acetylation pathway in the anti-apoptotic effect of cAMP signalling.	Cyclic AMP	262-266	P53	Homo sapiens	139-142
23483263-3	2013	In this report, we present results showing that increased levels of cAMP in cells with DNA damage enhances the deacetylation of p53, an event that facilitates the interaction of p53 with HDM2, thus annulling the stabilizing effect of DNA damage on p53.	Cyclic AMP	68-72	P53	Homo sapiens	178-181
23483263-4	2013	The combined inhibition of the HDAC and SIRT1 deacetylases abolished the cAMP-mediated deacetylation of p53, implying that cAMP-mediated deacetylation of p53 is dependent on the activity of these two classes of histone deacetylases.	Cyclic AMP	73-77	P53	Homo sapiens	104-107
23483263-5	2013	Importantly, diminishing the activity of HDACs and SIRT1 was also found to reverse the inhibitory effect of cAMP on the DNA damage-induced p53 stabilization and apoptosis, suggesting the involvement of the p53 acetylation pathway in the anti-apoptotic effect of cAMP signalling.	Cyclic AMP	262-266	P53	Homo sapiens	206-209
23483263-4	2013	The combined inhibition of the HDAC and SIRT1 deacetylases abolished the cAMP-mediated deacetylation of p53, implying that cAMP-mediated deacetylation of p53 is dependent on the activity of these two classes of histone deacetylases.	Cyclic AMP	73-77	P53	Homo sapiens	154-157
23483263-4	2013	The combined inhibition of the HDAC and SIRT1 deacetylases abolished the cAMP-mediated deacetylation of p53, implying that cAMP-mediated deacetylation of p53 is dependent on the activity of these two classes of histone deacetylases.	Cyclic AMP	123-127	P53	Homo sapiens	104-107
23639512-3	2013	The wild-type p53 codon has two common polymorphic variants from a single-base-pair substitution at codon 72, where either C-C-C encodes proline (p53-p72) or C-G-C encodes arginine (p53-R72).	Carbon	123-124	P53	Homo sapiens	14-17
24325731-8	2013	We conclude that exogenous melatonin enhances the development of porcine cloned embryos and improves embryo quality by inhibiting p53-mediated apoptotic pathway.	Melatonin	27-36	P53	Homo sapiens	130-133
23545901-8	2013	Taken together, our results indicate that GABARBP can regulate the pro-apoptotic activity of cisplatin via the upregulation of p53 expression.	Cisplatin	93-102	P53	Homo sapiens	127-130
23129176-0	2013	Notch pathway is involved in high glucose-induced apoptosis in podocytes via Bcl-2 and p53 pathways.	Glucose	34-41	P53	Homo sapiens	87-90
23129176-2	2013	Here we demonstrated that high glucose (HG) upregulated Notch pathway in podocytes accompanied with the alteration of Bcl-2 and p53 pathways, subsequently leading to podocytes apoptosis.	Glucose	31-38	P53	Homo sapiens	128-131
22752506-6	2013	Moreover, co-expressions of CK2alpha and PrPs induced phosphorylation on p53 at the position of serine 6 (p53-Ser6), although much weaker than that in the cells expressing CK2alpha and CK2beta, while expressions of either PrPs or CK2 subunits did not change the cellular p53 level or induce phosphorylation on p53 at Ser9.	Serine	96-102	P53	Homo sapiens	73-76
22752506-6	2013	Moreover, co-expressions of CK2alpha and PrPs induced phosphorylation on p53 at the position of serine 6 (p53-Ser6), although much weaker than that in the cells expressing CK2alpha and CK2beta, while expressions of either PrPs or CK2 subunits did not change the cellular p53 level or induce phosphorylation on p53 at Ser9.	Serine	96-102	P53	Homo sapiens	106-109
22752506-6	2013	Moreover, co-expressions of CK2alpha and PrPs induced phosphorylation on p53 at the position of serine 6 (p53-Ser6), although much weaker than that in the cells expressing CK2alpha and CK2beta, while expressions of either PrPs or CK2 subunits did not change the cellular p53 level or induce phosphorylation on p53 at Ser9.	Serine	96-102	P53	Homo sapiens	106-109
22752506-6	2013	Moreover, co-expressions of CK2alpha and PrPs induced phosphorylation on p53 at the position of serine 6 (p53-Ser6), although much weaker than that in the cells expressing CK2alpha and CK2beta, while expressions of either PrPs or CK2 subunits did not change the cellular p53 level or induce phosphorylation on p53 at Ser9.	Serine	96-102	P53	Homo sapiens	106-109
23639512-3	2013	The wild-type p53 codon has two common polymorphic variants from a single-base-pair substitution at codon 72, where either C-C-C encodes proline (p53-p72) or C-G-C encodes arginine (p53-R72).	Carbon	123-124	P53	Homo sapiens	146-149
23639512-3	2013	The wild-type p53 codon has two common polymorphic variants from a single-base-pair substitution at codon 72, where either C-C-C encodes proline (p53-p72) or C-G-C encodes arginine (p53-R72).	Carbon	123-124	P53	Homo sapiens	146-149
23639512-3	2013	The wild-type p53 codon has two common polymorphic variants from a single-base-pair substitution at codon 72, where either C-C-C encodes proline (p53-p72) or C-G-C encodes arginine (p53-R72).	c-g-c	158-163	P53	Homo sapiens	14-17
23639512-3	2013	The wild-type p53 codon has two common polymorphic variants from a single-base-pair substitution at codon 72, where either C-C-C encodes proline (p53-p72) or C-G-C encodes arginine (p53-R72).	Arginine	172-180	P53	Homo sapiens	14-17
22963136-6	2013	Most of the p53 negative cases with Maspin nuclear predominance, which seems to respond to 5-Fluorouracil, were microsatellite instability (MSI) cases.	Fluorouracil	91-105	P53	Homo sapiens	12-15
22290509-11	2013	We conclude that p53 independent apoptosis induced by combining curcumin and TSA involves JNK activation.	Curcumin	64-72	P53	Homo sapiens	17-20
23633924-6	2013	We found that compared with any single treatment, combination of lower doses of INZ and CIS or DOX significantly promoted apoptosis and cell growth inhibition in human non-small lung cancer and colon cancer cell lines in a p53-dependent fashion.	Doxorubicin	95-98	P53	Homo sapiens	223-226
23336807-0	2013	Ambient UVA-induced expression of p53 and apoptosis in human skin melanoma A375 cell line by quinine.	Quinine	93-100	P53	Homo sapiens	34-37
23446517-6	2013	Previously, we showed that Pi inhibits proliferation and aggressiveness of U2OS human osteosarcoma cells and that Pi is capable of inducing sensitization of osteosarcoma cells to doxorubicin in a p53-dependent manner.	Doxorubicin	179-190	P53	Homo sapiens	196-199
22963136-10	2013	CONCLUSIONS: Maspin nuclear expression, associated with p53 ones, might be used either to select the high-risk microsatellite stable (MSS) colorectal carcinomas diagnosed in Stage II or those MSI cases which can respond to 5-Fluorouracil.	Fluorouracil	223-237	P53	Homo sapiens	56-59
23618908-3	2013	On DNA damage mediated by adriamycin (ADR) exposure, p53 as well as RUNX2 was induced at protein and mRNA level in human osteosarcoma-derived U2OS cells in association with a significant upregulation of various p53-target genes.	Doxorubicin	26-36	P53	Homo sapiens	53-56
23430247-3	2013	After EtOH exposure, cells produce excessive reactive oxygen species formation, p53 expression, and most importantly, caspase-2 activation.	Ethanol	6-10	P53	Homo sapiens	80-83
23376608-4	2013	In the c-Myc siRNA-transfected and apigenin-treated cells, compared with the apigenin-treated control cells, apoptosis and phosphorylation of p38 and p53 were ameliorated.	Apigenin	35-43	P53	Homo sapiens	150-153
23376608-6	2013	In conclusion, our results indicate that apigenin induces apoptosis mediated via c-Myc with concomitant phosphorylation of p53 and p38 in FRO ATC cells.	Apigenin	41-49	P53	Homo sapiens	123-126
23618908-3	2013	On DNA damage mediated by adriamycin (ADR) exposure, p53 as well as RUNX2 was induced at protein and mRNA level in human osteosarcoma-derived U2OS cells in association with a significant upregulation of various p53-target genes.	Doxorubicin	26-36	P53	Homo sapiens	211-214
23618908-10	2013	Of note, HDAC6-specific chemical inhibitor tubacin treatment enhanced ADR-mediated upregulation of p53-target gene expression, indicating that deacetylase activity of HDAC6 is required for RUNX2-mediated downregulation of p53-target gene.	tubacin	43-50	P53	Homo sapiens	99-102
23618908-10	2013	Of note, HDAC6-specific chemical inhibitor tubacin treatment enhanced ADR-mediated upregulation of p53-target gene expression, indicating that deacetylase activity of HDAC6 is required for RUNX2-mediated downregulation of p53-target gene.	tubacin	43-50	P53	Homo sapiens	222-225
23620761-0	2013	Metformin downregulates the insulin/IGF-I signaling pathway and inhibits different uterine serous carcinoma (USC) cells proliferation and migration in p53-dependent or -independent manners.	Metformin	0-9	P53	Homo sapiens	151-154
23499005-4	2013	Moreover, B55alpha is specifically induced upon glutamine deprivation in a ROS-dependent manner to activate p53 and promote cell survival.	ros	75-78	P53	Homo sapiens	108-111
23501101-1	2013	Cysteine oxidation and covalent modification of redox sensitive transcription factors including p53 are known, among others, as important events in cell response to oxidative stress.	Cysteine	0-8	P53	Homo sapiens	96-99
23620761-8	2013	Our results show that metformin interacts with the IGF pathway, and induces apoptosis and inhibition of proliferation and migration of USC cell lines with both wild type and mutant p53.	Metformin	22-31	P53	Homo sapiens	181-184
23423487-0	2013	Effect of TP53 codon 72 and MDM2 SNP309 polymorphisms on survival of gastric cancer among patients who receiving 5-fluorouracil-based postoperative adjuvant chemotherapy.	Fluorouracil	113-127	P53	Homo sapiens	10-14
23423487-5	2013	However, the TP53 codon 72 polymorphism had a prominent correlation with clinical outcome of patients receiving 5-fluorouracil (5-Fu)-based postoperative chemotherapy [Arg/Arg + Arg/Pro vs. Pro/Pro, adjusted hazard ratio (HR) = 1.63, 95 % confidence interval (CI) = 1.08-2.44].	Arginine	172-175	P53	Homo sapiens	13-17
23462712-8	2013	Similarly to cisplatin this compound interacts with nuclear DNA and induces both p53 and p21(waf), and thus it represents an interesting starting point for future optimisation of new Pt(II) complexes forming DNA adducts.	Cisplatin	13-22	P53	Homo sapiens	81-84
23522190-5	2013	The frequency of p53 protein degradation was also much higher in HPV 16/18 E6-positive/Arg/Arg lung tumors than in the other 3 groups.	Arginine	87-90	P53	Homo sapiens	17-20
23125026-0	2013	Targeted nitric oxide delivery preferentially induces glioma cell chemosensitivity via altered p53 and O(6) -methylguanine-DNA methyltransferase activity.	Nitric Oxide	9-21	P53	Homo sapiens	95-98
23373735-0	2013	Regulation of carboxylesterase-2 expression by p53 family proteins and enhanced anti-cancer activities among 5-fluorouracil, irinotecan and doxazolidine prodrug.	Irinotecan	125-135	P53	Homo sapiens	47-50
23423487-5	2013	However, the TP53 codon 72 polymorphism had a prominent correlation with clinical outcome of patients receiving 5-fluorouracil (5-Fu)-based postoperative chemotherapy [Arg/Arg + Arg/Pro vs. Pro/Pro, adjusted hazard ratio (HR) = 1.63, 95 % confidence interval (CI) = 1.08-2.44].	Arginine	172-175	P53	Homo sapiens	13-17
23423487-5	2013	However, the TP53 codon 72 polymorphism had a prominent correlation with clinical outcome of patients receiving 5-fluorouracil (5-Fu)-based postoperative chemotherapy [Arg/Arg + Arg/Pro vs. Pro/Pro, adjusted hazard ratio (HR) = 1.63, 95 % confidence interval (CI) = 1.08-2.44].	Fluorouracil	112-126	P53	Homo sapiens	13-17
23423487-8	2013	CONCLUSIONS: Our findings showed that TP53 codon 72 polymorphism was associated with survival of gastric cancer patients treated with 5-Fu-based postoperative chemotherapy.	Fluorouracil	134-138	P53	Homo sapiens	38-42
23423487-5	2013	However, the TP53 codon 72 polymorphism had a prominent correlation with clinical outcome of patients receiving 5-fluorouracil (5-Fu)-based postoperative chemotherapy [Arg/Arg + Arg/Pro vs. Pro/Pro, adjusted hazard ratio (HR) = 1.63, 95 % confidence interval (CI) = 1.08-2.44].	Fluorouracil	128-132	P53	Homo sapiens	13-17
23430755-6	2013	By double labeling of senescent cells, first by SA-beta-Gal and then by antibodies against genes related to cellular senescence, we found that p21, p16, and RARbeta, but not p53, were upregulated by bexarotene in mammary tumors and in breast cancer cell lines, suggesting involvement of multiple signaling pathways in mediating the senescence program of rexinoids.	Bexarotene	199-209	P53	Homo sapiens	174-177
23423487-5	2013	However, the TP53 codon 72 polymorphism had a prominent correlation with clinical outcome of patients receiving 5-fluorouracil (5-Fu)-based postoperative chemotherapy [Arg/Arg + Arg/Pro vs. Pro/Pro, adjusted hazard ratio (HR) = 1.63, 95 % confidence interval (CI) = 1.08-2.44].	Arginine	168-171	P53	Homo sapiens	13-17
23450781-8	2013	Sulphathiazole treatment was followed by higher expression of p53/DRAM and downregulation of Akt/mTOR pathway resulting in death autophagy.	Sulfathiazole	0-14	P53	Homo sapiens	62-65
23462184-8	2013	Our results suggest a specific function of p19(INK4D), but not p16(INK4A), in sensitizing MYCN-amplified cells with a functional p53 pathway to doxorubicin-induced cell death.	Doxorubicin	144-155	P53	Homo sapiens	129-132
23462184-10	2013	Additional chromosomal aberrations affecting the p53-p21 and CDK4-pRB axes compound the effects of MYCN on the G(1) checkpoint and reduce sensitivity to cell death after doxorubicin treatment.	Doxorubicin	170-181	P53	Homo sapiens	49-52
23462184-11	2013	CDK4 inhibition partly restores G(1)-S arrest and sensitizes cells to doxorubicin-mediated cell death in MYCN-amplified cells with an intact p53 pathway.	Doxorubicin	70-81	P53	Homo sapiens	141-144
23466706-4	2013	We have recently shown that macroautophagy (autophagy) provides a route for p53 mutant degradation during restriction of glucose.	Glucose	121-128	P53	Homo sapiens	76-79
23557559-14	2013	No p53 gene mutation was detected on the exon 4 - 9, and Pro/Arg SNPs on p53 codon 72 were detected in the cutaneous NK/T-cell lymphoma.	Arginine	61-64	P53	Homo sapiens	73-76
23241309-5	2013	In response to hydrogen peroxide (H2O2), we measured an increase in PtdIns5P in cells derived from human osteosarcoma, U2OS (5-fold); breast tumors, MDA-MB-468 (2-fold); and fibrosarcoma, HT1080 (3-fold); and in p53-null murine embryonic fibroblasts (8-fold).	Hydrogen Peroxide	15-32	P53	Homo sapiens	212-215
23241309-5	2013	In response to hydrogen peroxide (H2O2), we measured an increase in PtdIns5P in cells derived from human osteosarcoma, U2OS (5-fold); breast tumors, MDA-MB-468 (2-fold); and fibrosarcoma, HT1080 (3-fold); and in p53-null murine embryonic fibroblasts (8-fold).	Hydrogen Peroxide	34-38	P53	Homo sapiens	212-215
23194110-8	2013	Importantly, immunocytochemistry of the diabetic ulcer-derived fibroblasts proved nuclear over expression of potent proliferation inhibitors and pro-senescence proteins as p53 phosphorylated on serine-15 and p21(Cip) (1).	Serine	194-200	P53	Homo sapiens	172-175
22773548-9	2013	Cell line studies showed that metformin inhibits hepatocyte proliferation and induces cell cycle arrest at G0/G1 phase via AMP-activated protein kinase and its upstream kinase LKB1 to upregulate p21/Cip1 and p27/Kip1 and downregulate cyclin D1 in a dose-dependent manner, but independent of p53.	Metformin	30-39	P53	Homo sapiens	291-294
22961628-0	2013	Mdm2 antagonists induce apoptosis and synergize with cisplatin overcoming chemoresistance in TP53 wild-type ovarian cancer cells.	Cisplatin	53-62	P53	Homo sapiens	93-97
22961628-4	2013	Cisplatin is a genotoxic drug that leads cells to apoptosis through the activation of the p53 pathway.	Cisplatin	0-9	P53	Homo sapiens	90-93
22961628-7	2013	The wild-type p53 cisplatin-resistant ovarian cancer cell-line A2780cis was used to test the effect of Nutlin-3a (Nut3a) on apoptosis response.	Cisplatin	18-27	P53	Homo sapiens	14-17
22961628-9	2013	Increased apoptosis was also induced in wild-type TP53 primary OVCa cultures by double cisplatin-Nut3a treatment.	Cisplatin	87-96	P53	Homo sapiens	50-54
22961628-11	2013	As increased response was generalized in primary tumors, this cisplatin-Nut3a combination could be useful for the treatment of patients harboring wild-type TP53 who do not respond to standard chemotherapy.	Cisplatin	62-71	P53	Homo sapiens	156-160
22809997-6	2013	We demonstrated using HPV16(+) SiHa cervical cancer cells that E6-Ru-ASO induces after illumination, a reactivation of p53, the most important target of E6, as well as the inhibition of cell proliferation with a selective repression of E6 at the protein level.	e6-ru-aso	63-72	P53	Homo sapiens	119-122
23188704-5	2013	From among a panel of apoptosis-related factors (p53, Bcl-2, Bcl-XL, BAX, and survivin), the expression of Livin was upregulated after cisplatin treatment in a dose-dependent manner.	Cisplatin	135-144	P53	Homo sapiens	49-52
23388716-6	2013	These results indicated that the mutations created by substitution of residues 443 to 448 for alanine (Sub19) impair repression of transcription of IFN-inducible genes, by the E1B, 55-kDa protein, consistent with their location in a segment required for repression of p53-dependent transcription.	Alanine	94-101	P53	Homo sapiens	268-271
23416275-1	2013	Acetylation of C-terminal lysine residues in the p53 tumor suppressor is associated with increased stability and transcription factor activity.	Lysine	26-32	P53	Homo sapiens	49-52
23416275-3	2013	Here, we show that p14(ARF) increases the level of p53 acetylated at lysine 382 in a nuclear chromatin-rich fraction.	Lysine	69-75	P53	Homo sapiens	51-54
23376438-7	2013	Use of an inhibitor specific to c-Jun N-terminal kinase (JNK), p38 kinase or p53, but not pan-caspase or caspase-8, decreased the toxin-induced generation of reactive oxygen species (ROS) and also attenuated the alpha-ZOL- or beta-ZOL-induced decrease of cell viability.	Reactive Oxygen Species	158-181	P53	Homo sapiens	77-80
23376438-7	2013	Use of an inhibitor specific to c-Jun N-terminal kinase (JNK), p38 kinase or p53, but not pan-caspase or caspase-8, decreased the toxin-induced generation of reactive oxygen species (ROS) and also attenuated the alpha-ZOL- or beta-ZOL-induced decrease of cell viability.	Reactive Oxygen Species	183-186	P53	Homo sapiens	77-80
22841540-1	2013	Colorectal carcinomas (CRCs) with P53 mutations have been shown to be resistant to chemotherapy with 5-fluorouracil (5-FU), the most widely used chemotherapeutic drug for CRC treatment.	Fluorouracil	101-115	P53	Homo sapiens	34-37
22841540-1	2013	Colorectal carcinomas (CRCs) with P53 mutations have been shown to be resistant to chemotherapy with 5-fluorouracil (5-FU), the most widely used chemotherapeutic drug for CRC treatment.	Fluorouracil	117-121	P53	Homo sapiens	34-37
23376438-10	2013	Collectively, these results suggest that the activation of p53, JNK or p38 kinase by ZEN metabolites is the main upstream signal required for the mitochondrial alteration of Bcl-2/Bax signaling pathways and intracellular ROS generation, while MMP loss and nuclear translocation of AIF are the critical downstream events for ZEN metabolite-mediated apoptosis in macrophages.	Reactive Oxygen Species	221-224	P53	Homo sapiens	59-62
23530619-0	2013	p53-independent early and late apoptosis is mediated by ceramide after exposure of tumor cells to photon or carbon ion irradiation.	Carbon	108-114	P53	Homo sapiens	0-3
23313430-3	2013	Calcium-dependent binding of dimeric S100B(betabeta) to p53-NRD blocks access to these PTM sites and disrupts the p53 tetramer to inhibit p53 activation.	Calcium	0-7	P53	Homo sapiens	56-59
23313430-3	2013	Calcium-dependent binding of dimeric S100B(betabeta) to p53-NRD blocks access to these PTM sites and disrupts the p53 tetramer to inhibit p53 activation.	Calcium	0-7	P53	Homo sapiens	114-117
23313430-3	2013	Calcium-dependent binding of dimeric S100B(betabeta) to p53-NRD blocks access to these PTM sites and disrupts the p53 tetramer to inhibit p53 activation.	Calcium	0-7	P53	Homo sapiens	114-117
23863680-6	2013	And the ROS related signaling factors of p-p38MAPK, p38 MAPK, P53 were measured by Western blot.	Reactive Oxygen Species	8-11	P53	Homo sapiens	62-65
23863680-15	2013	And ROS stimulates the signaling pathways of p-p38MAPK and P53.	Reactive Oxygen Species	4-7	P53	Homo sapiens	59-62
23382381-4	2013	Cellular responses to DNA damage induced by etoposide or doxorubicin include down-regulation of endogenous supervillin coincident with increases in p53.	Doxorubicin	57-68	P53	Homo sapiens	148-151
23364526-0	2013	Reduced carbohydrate availability enhances exercise-induced p53 signaling in human skeletal muscle: implications for mitochondrial biogenesis.	Carbohydrates	8-20	P53	Homo sapiens	60-63
23526248-0	2013	Ras puts the brake on doxorubicin-mediated cell death in p53-expressing cells.	Doxorubicin	22-33	P53	Homo sapiens	57-60
23321474-4	2013	Nitric oxide activates the unfolded protein and heat shock responses and MAPK kinase signaling, whereas H2O2 stimulates p53 stabilization and poly(ADP-ribose) polymerase (PARP) activation but fails to induce the unfolded protein or heat shock responses or MAPK activation.	Hydrogen Peroxide	104-108	P53	Homo sapiens	120-123
23492768-7	2013	We will also introduce several pivotal ROS-sensitive molecules, such as hypoxia-inducible factors, p38 mitogen-activated protein kinase (p38) and p53, involved in the redox-regulated stem cell self-renewal.	Reactive Oxygen Species	39-42	P53	Homo sapiens	146-149
23482764-7	2013	Moreover, beta-elemene plus docetaxel induced elevated levels of caspase-9 and p53 proteins in A2780/CP70 cells, and the combination of beta-elemene plus a taxane caused marked cell-cycle arrest at the G2/M phase in these cells.	taxane	156-162	P53	Homo sapiens	79-82
23299313-4	2013	By studying primary cells collected from pediatric BCP-ALL patients and healthy controls, we found that cAMP profoundly decreased basal and DNA damage-induced p53 levels and cell death in malignant cells, whereas normal BCP counterparts displayed slightly augmented cell death when exposed to cAMP-increasing agents.	Cyclic AMP	104-108	P53	Homo sapiens	159-162
23299313-5	2013	We did not find evidence for a selection process involving generation of increased basal cAMP levels in BCP-ALL cells, but we demonstrate that paracrine signaling involving prostaglandin E2-induced cAMP generation has the potential to suppress p53 activation and cell death induction.	Dinoprostone	173-189	P53	Homo sapiens	244-247
23299313-5	2013	We did not find evidence for a selection process involving generation of increased basal cAMP levels in BCP-ALL cells, but we demonstrate that paracrine signaling involving prostaglandin E2-induced cAMP generation has the potential to suppress p53 activation and cell death induction.	Cyclic AMP	198-202	P53	Homo sapiens	244-247
23316052-7	2013	Taken together with the mutagenesis, isothermal titration calorimetry, and paramagnetic relaxation enhancement data, our structural comparisons provided the structural basis of p53TAD2-mediated interaction with the anti-apoptotic proteins, revealing that Bcl-X(L)/Bcl-2, MDM2, and cAMP-response element-binding protein-binding protein/p300 share highly similar modes of binding to the dual p53TAD motifs, p53TAD1 and p53TAD2.	Cyclic AMP	281-285	P53	Homo sapiens	177-180
23497256-6	2013	The concurrent administration of MI-319 markedly increased the antitumor and anti-angiogenic activities of sunitinib and led to sustained p53-dependent gene expression.	MI 319	33-39	P53	Homo sapiens	138-141
23497288-8	2013	When miR-125b was knocked down in EWS cells, both the Dox-resistant and parental cells showed an enhanced sensitivity to doxorubicin, which was associated with the upregulation of the pro-apoptotic molecules, p53 and Bak.	Doxorubicin	54-57	P53	Homo sapiens	209-212
23187459-5	2013	However, the upregulation of the p53-mediated protein p53 upregulated modulator of apoptosis (PUMA) by nutlin-3 is likely to be ROS independent because antioxidants failed to block PUMA upregulation.	Reactive Oxygen Species	128-131	P53	Homo sapiens	33-36
23187459-5	2013	However, the upregulation of the p53-mediated protein p53 upregulated modulator of apoptosis (PUMA) by nutlin-3 is likely to be ROS independent because antioxidants failed to block PUMA upregulation.	Reactive Oxygen Species	128-131	P53	Homo sapiens	54-57
23482786-6	2013	RESULTS: p53 expression was significantly correlated with patients who were undergoing hemodialysis (p=0.005) and had increased serum creatinine levels (p=0.001).	Creatinine	134-144	P53	Homo sapiens	9-12
23302226-4	2013	We previously showed that p53 is a major player in cisplatin hypersensitivity and therefore investigated whether Oct-4 may directly affect p53 activity.	Cisplatin	51-60	P53	Homo sapiens	26-29
23238993-3	2013	Here, we show that two of these compounds, CP-31398 and RITA, induce cell growth inhibition, apoptosis, and autophagy by activating p53/DNA binding and p53 phosphorylation (Ser15), without affecting the total p53 amount.	RITA	56-60	P53	Homo sapiens	132-135
23238993-3	2013	Here, we show that two of these compounds, CP-31398 and RITA, induce cell growth inhibition, apoptosis, and autophagy by activating p53/DNA binding and p53 phosphorylation (Ser15), without affecting the total p53 amount.	RITA	56-60	P53	Homo sapiens	152-155
23238993-3	2013	Here, we show that two of these compounds, CP-31398 and RITA, induce cell growth inhibition, apoptosis, and autophagy by activating p53/DNA binding and p53 phosphorylation (Ser15), without affecting the total p53 amount.	RITA	56-60	P53	Homo sapiens	152-155
23238993-6	2013	The protective role of autophagy in cell growth inhibition by CP-31398 and RITA is supported by the finding that the AMPK inhibitor compound C or the autophagy inhibitors chloroquine or 3-methyladenine sensitize both pancreatic adenocarcinoma cell lines to the apoptotic response induced by p53-reactivating molecules.	3-methyladenine	186-201	P53	Homo sapiens	291-294
23246812-0	2013	Functional characterisation of p53 mutants identified in breast cancers with suboptimal responses to anthracyclines or mitomycin.	Anthracyclines	101-115	P53	Homo sapiens	31-34
23246812-2	2013	TP53 mutations, in particular those affecting the L2/L3 domains, are associated with resistance to anthracycline or mitomycin treatment in breast cancer patients.	Anthracyclines	99-112	P53	Homo sapiens	0-4
23246812-13	2013	GENERAL SIGNIFICANCE: Our data add further information characterising the effects of somatic TP53 mutations on p53 protein function and anthracycline resistance in breast cancer.	Anthracyclines	136-149	P53	Homo sapiens	93-97
23433851-0	2013	Arginine homozygosity in codon 72 of p53 correlates with failure to imatinib response in chronic myeloid leukemia.	Arginine	0-8	P53	Homo sapiens	37-40
23165797-7	2013	Interestingly, there was a trend toward longer time to progression after chemotherapy for tumors with the apoptosis-prone p53 variant R72 (P = .07), which was strongest with doxorubicin/ifosfamide-based regimens (P = .01).	Doxorubicin	174-185	P53	Homo sapiens	122-125
23222814-0	2013	Bisphenol-A-induced inactivation of the p53 axis underlying deregulation of proliferation kinetics, and cell death in non-malignant human breast epithelial cells.	bisphenol A	0-11	P53	Homo sapiens	40-43
23161404-3	2013	In this study, we demonstrated that lithium and SB216763, which are pharmacological inhibitors of GSK3, attenuated p53 accumulation and caspase-3 activation, as shown by PARP cleavage induced by the DNA-damaging agents doxorubicin, etoposide and camptothecin.	Doxorubicin	219-230	P53	Homo sapiens	115-118
23161404-7	2013	GSK3 inhibition also reduced the phosphorylation of wild-type p53 at serine 33, which is induced by doxorubicin, etoposide and camptothecin in the mitochondria.	Serine	69-75	P53	Homo sapiens	62-65
23161404-7	2013	GSK3 inhibition also reduced the phosphorylation of wild-type p53 at serine 33, which is induced by doxorubicin, etoposide and camptothecin in the mitochondria.	Doxorubicin	100-111	P53	Homo sapiens	62-65
23314357-8	2013	Of note, nutlin-3 caused the accumulation of mitochondrial reactive oxygen species (ROS) and this correlated with the mitochondrial translocation of p53.	Reactive Oxygen Species	59-82	P53	Homo sapiens	149-152
23434523-7	2013	DNA damage induced by AAI led to an arrest of cells in the S-phase which was associated with the increased expression of p53 and p21 proteins.	aristolochic acid I	22-25	P53	Homo sapiens	121-124
22833338-4	2013	Here we show that RSV, at both concentration ranges, leads to a marked increase in p53, while a decrease of SIRT1 expression level, as well as enzyme activity, only occurred at the higher concentration range.	Resveratrol	18-21	P53	Homo sapiens	83-86
23314357-8	2013	Of note, nutlin-3 caused the accumulation of mitochondrial reactive oxygen species (ROS) and this correlated with the mitochondrial translocation of p53.	Reactive Oxygen Species	84-87	P53	Homo sapiens	149-152
23360948-0	2013	Switching p53 states by calcium: dynamics and interaction of stress systems.	Calcium	24-31	P53	Homo sapiens	10-13
23184052-7	2013	Subgroup analyses by ethnicity showed that TP53 Arg72Pro polymorphism contributed to bladder cancer risk in East Asians in three genetic models (For Pro vs. Arg, Fixed-effects OR 1.18, 95 % CI 1.05-1.32; For ProPro vs. ArgArg, Fixed-effects OR 1.40, 95 % CI 1.11-1.77; For ProPro vs. ArgPro/ArgArg, Fixed-effects OR 1.32, 95 % CI 1.07-1.62).	Arginine	48-51	P53	Homo sapiens	43-47
23192612-1	2013	Among many alterations within the TP53 gene the rs1042522 (C72G, p.Pro72Arg) has been associated with numerous cancers , however the results differ between populations for opposite Pro or Arg alleles.	Arginine	72-75	P53	Homo sapiens	34-38
23808158-7	2013	Moreover, EGCG suppressed the high glucose-induced expression of c-fos, c-myc and p53.	Glucose	35-42	P53	Homo sapiens	82-85
23360948-2	2013	The high dose of calcium in the system activates the nitric oxide synthase, synthesizing nitric oxide which then downregulates Mdm2 and influences drastically the p53-Mdm2 network regulation, lifting the system from a normal to a stressed state.	Calcium	17-24	P53	Homo sapiens	163-166
23360948-2	2013	The high dose of calcium in the system activates the nitric oxide synthase, synthesizing nitric oxide which then downregulates Mdm2 and influences drastically the p53-Mdm2 network regulation, lifting the system from a normal to a stressed state.	Nitric Oxide	53-65	P53	Homo sapiens	163-166
23360948-3	2013	The increase in calcium level switches the system to different states, as identified by the different behaviours of the p53 temporal dynamics, i.e. oscillation death to sustain the oscillation state via a mixed state of dampened and oscillation death states.	Calcium	16-23	P53	Homo sapiens	120-123
22619007-6	2013	In addition, Silibinin caused an increase in p53 and p21 protein level as well as mRNA levels.	Silybin	13-22	P53	Homo sapiens	45-48
22628241-8	2013	Furthermore, western blotting analysis indicated that curcumin induced the release of cytochrome c, a significant increase of Bax and p53 and a marked reduction of Bcl-2 and survivin in LoVo cells.	Curcumin	54-62	P53	Homo sapiens	134-137
23395165-2	2013	A new study shows that, upon serine starvation, the tumor suppressor p53 activates p21 to shift metabolic flux from purine biosynthesis to glutathione production, which enhances cellular proliferation and viability by combating ROS (Maddocks et al., 2013).	ros	228-231	P53	Homo sapiens	69-72
23149124-5	2013	Stable silencing of STAT3 expression sensitized A549 cells to DNA damaging chemotherapeutics doxorubicin and cisplatin in a p53-independent manner.	Cisplatin	109-118	P53	Homo sapiens	124-127
23368735-0	2013	The contrasting activity of iodido versus chlorido ruthenium and osmium arene azo- and imino-pyridine anticancer complexes: control of cell selectivity, cross-resistance, p53 dependence, and apoptosis pathway.	azo- and imino-pyridine	78-101	P53	Homo sapiens	171-174
22469985-6	2013	Moreover, viral reactivation compromised p53-dependent apoptosis in PEL cells treated with genotoxic anti-cancer agents doxorubicin and etoposide.	Doxorubicin	120-131	P53	Homo sapiens	41-44
22815158-6	2013	Activation of p53 by FK866 involved increased acetylation of p53 at lysine 382 with subsequent increase in the expression of p21 and BAX.	Lysine	68-74	P53	Homo sapiens	14-17
22815158-6	2013	Activation of p53 by FK866 involved increased acetylation of p53 at lysine 382 with subsequent increase in the expression of p21 and BAX.	Lysine	68-74	P53	Homo sapiens	61-64
23274516-4	2013	The changes of p53 status were dependent on DNA damage which was caused by compound C induced reactive oxygen species (ROS) generation and associated with activated ataxia-telangiectasia mutated (ATM) protein.	Reactive Oxygen Species	94-117	P53	Homo sapiens	15-18
23274516-4	2013	The changes of p53 status were dependent on DNA damage which was caused by compound C induced reactive oxygen species (ROS) generation and associated with activated ataxia-telangiectasia mutated (ATM) protein.	Reactive Oxygen Species	119-122	P53	Homo sapiens	15-18
23395165-0	2013	The Hunger Games: p53 regulates metabolism upon serine starvation.	Serine	48-54	P53	Homo sapiens	18-21
23395165-2	2013	A new study shows that, upon serine starvation, the tumor suppressor p53 activates p21 to shift metabolic flux from purine biosynthesis to glutathione production, which enhances cellular proliferation and viability by combating ROS (Maddocks et al., 2013).	Serine	29-35	P53	Homo sapiens	69-72
23395165-2	2013	A new study shows that, upon serine starvation, the tumor suppressor p53 activates p21 to shift metabolic flux from purine biosynthesis to glutathione production, which enhances cellular proliferation and viability by combating ROS (Maddocks et al., 2013).	Glutathione	139-150	P53	Homo sapiens	69-72
23178654-1	2013	Previously, our in vivo studies demonstrated that folic acid (FA) could inhibit angiogenesis and in vitro studies showed that FA reduced vascular endothelial cell proliferation through activating the cSrc/ERK-2/NFkappaB/p53 pathway mediated by FA receptor (FR).	Folic Acid	50-60	P53	Homo sapiens	220-223
24280180-4	2013	A gene expression microarray screen followed by constraint-based modeling (CBM) predicting metabolic changes imposed by the transcriptomic changes suggested a role for p53 in enhancing gluconeogenesis (de novo synthesis of glucose).	Glucose	223-230	P53	Homo sapiens	168-171
24280180-7	2013	CONCLUSIONS: These findings portray p53 as a novel regulator of glucose production.	Glucose	64-71	P53	Homo sapiens	36-39
24280180-8	2013	By facilitating glucose export, p53 may prevent it from being shunted to pro-cancerous pathways such as glycolysis and the PPP.	Glucose	16-23	P53	Homo sapiens	32-35
23088536-2	2013	Human ASPPs (apoptosis-stimulating proteins of p53) comprise three family members: ASPP1, ASPP2 and iASPP (inhibitory ASPP), which is uniquely overexpressed in many cancers.	aspps	6-11	P53	Homo sapiens	47-50
24280180-0	2013	p53 promotes the expression of gluconeogenesis-related genes and enhances hepatic glucose production.	Glucose	82-89	P53	Homo sapiens	0-3
24280180-2	2013	p53 represses metabolic pathways that support tumor development (such as glycolysis and the pentose phosphate pathway (PPP)) and enhances metabolic pathways that are considered counter-tumorigenic such as fatty acid oxidation.	Fatty Acids	205-215	P53	Homo sapiens	0-3
22861165-4	2013	RESULTS: We found that upon GSH shortage, induced either by its chemical depletion or by metabolic stress (i.e., fasting), p53 binds to the PPARGC1A promoter of both human and mouse genes, and this event is positively related to increased PGC-1alpha expression.	Glutathione	28-31	P53	Homo sapiens	123-126
23201008-5	2013	Upon treatment with 5-Aza-CdR, ATM activation was clearly associated with P53 phosphorylation at Ser(15), which was directly responsible for 5-Aza-CdR modified P21(Waf1/Cip1) expression.	Serine	97-100	P53	Homo sapiens	74-77
23448605-3	2013	The aim of our study was to detect the level of apoptosis, expression bcl-2 and p53, associated with the different doses of CsA.	Cyclosporine	124-127	P53	Homo sapiens	80-83
23201157-5	2013	EXPERIMENTAL DESIGN: In vitro phosphorylation of p53 by Aurora-A was performed and the phosphorylated protein was then digested with trypsin and enriched for phosphopeptides by immobilized metal affinity chromatography.	Metals	189-194	P53	Homo sapiens	49-52
23201157-8	2013	RESULTS: Ser-106 of p53 was identified as a novel site phosphorylated by Aurora-A.	Serine	9-12	P53	Homo sapiens	20-23
23201157-10	2013	In addition, phosphate-sensitive Phos-tag SDS-PAGE was used to confirm that the Ser-106 of p53 is in vivo phosphorylated by Aurora-A.	Phosphates	13-22	P53	Homo sapiens	91-94
23201157-10	2013	In addition, phosphate-sensitive Phos-tag SDS-PAGE was used to confirm that the Ser-106 of p53 is in vivo phosphorylated by Aurora-A.	Sodium Dodecyl Sulfate	42-45	P53	Homo sapiens	91-94
23201157-10	2013	In addition, phosphate-sensitive Phos-tag SDS-PAGE was used to confirm that the Ser-106 of p53 is in vivo phosphorylated by Aurora-A.	Serine	80-83	P53	Homo sapiens	91-94
23201157-11	2013	Finally, co-immunoprecipitation studies suggested that Ser-106 phosphorylation of p53 decreases its interaction with MDM2 and prolongs the half-life of p53.	Serine	55-58	P53	Homo sapiens	82-85
23201157-11	2013	Finally, co-immunoprecipitation studies suggested that Ser-106 phosphorylation of p53 decreases its interaction with MDM2 and prolongs the half-life of p53.	Serine	55-58	P53	Homo sapiens	152-155
22955948-6	2013	IKK-beta and p85 S6K1 contributed to H(2)O(2)-induced phosphorylation of Mdm2 (S166) and p53 accumulation.	Hydrogen Peroxide	37-45	P53	Homo sapiens	89-92
23036084-4	2013	Using quantitative RT-PCR analysis, we found that miR-34a was highly upregulated in the p53 wild-type A549 human lung cancer cell line when treated with the DNA damaging agent adriamycin (ADR), but not in the SBC-5 cells harboring mutated p53.	Doxorubicin	176-186	P53	Homo sapiens	88-91
23306062-3	2013	Here, we show that E2F1 overexpression, due to p53 or p21 inactivation, promotes expression of human oncoprotein CIP2A, which in turn, by inhibiting PP2A activity, increases stabilizing serine 364 phosphorylation of E2F1.	Serine	186-192	P53	Homo sapiens	47-50
22855178-3	2013	It has been shown that methylation of CpG dinucleotides located in the promoter region of p53 is associated with low expression levels of this gene.	cytidylyl-3'-5'-guanosine	38-55	P53	Homo sapiens	90-93
23076534-6	2013	Periostin-overexpressing cells treated with cisplatin or 5-FU showed significantly (p &lt; 0.05) decreased expression of Bax and p53 proteins and increased expression of Bcl-2 protein, when compared to drug-treated mock counterparts.	Cisplatin	44-53	P53	Homo sapiens	129-132
23252827-4	2013	Furthermore, inhibition of the miR-183/96/182 cluster induced ROS-mediated AKT/survival independent of three target genes FGF9, CPEB1, and FOXO1, and inhibition of the miRNA cluster induced p53/apoptosis signaling, which was dependent on these same genes.	ros	62-65	P53	Homo sapiens	190-193
23076534-6	2013	Periostin-overexpressing cells treated with cisplatin or 5-FU showed significantly (p &lt; 0.05) decreased expression of Bax and p53 proteins and increased expression of Bcl-2 protein, when compared to drug-treated mock counterparts.	Fluorouracil	57-61	P53	Homo sapiens	129-132
23124852-5	2013	After scavenging ROS with N-acetylcysteine, Wnt/beta-catenin signaling-induced MSC aging was significantly attenuated and the DNA damage and the expression of p16(INK4A), p53, and p21 were reduced in MSCs.	Reactive Oxygen Species	17-20	P53	Homo sapiens	171-174
23124852-5	2013	After scavenging ROS with N-acetylcysteine, Wnt/beta-catenin signaling-induced MSC aging was significantly attenuated and the DNA damage and the expression of p16(INK4A), p53, and p21 were reduced in MSCs.	Acetylcysteine	26-42	P53	Homo sapiens	171-174
23076534-10	2013	Taken together, our data indicate that periostin confers protection against cisplatin or 5-FU-induced apoptosis in SGC-7901 cells, likely through modulating the Akt/p53 pathway, and thus represents a potential therapeutic target in gastric cancer.	Fluorouracil	89-93	P53	Homo sapiens	165-168
23192640-1	2013	The genetic polymorphism of p53 codon 72 Arg/Pro has been implicated in oral cancer risk, but the results of previous studies remain controversial and ambiguous.	Arginine	41-44	P53	Homo sapiens	28-31
22926048-3	2013	HEDS is rapidly detoxified in normal glucose but triggered a p53-independent metabolic stress in glucose depleted state that caused loss of NADPH, protein and non-protein thiol homeostasis and Ku function, and enhanced sensitivity of both p53 wild type and mutant cells to radiation induced oxidative stress.	Glucose	97-104	P53	Homo sapiens	61-64
22926048-3	2013	HEDS is rapidly detoxified in normal glucose but triggered a p53-independent metabolic stress in glucose depleted state that caused loss of NADPH, protein and non-protein thiol homeostasis and Ku function, and enhanced sensitivity of both p53 wild type and mutant cells to radiation induced oxidative stress.	Sulfhydryl Compounds	171-176	P53	Homo sapiens	61-64
27481281-7	2013	It was found that the pi-pi stacking between Tyr 51 of MDM2 and ligands is the critical event in MDM2-p53 dissociation.	Tyrosine	45-48	P53	Homo sapiens	102-105
23192640-2	2013	To estimate the effect of the p53 codon 72 Arg/Pro polymorphism on the risk of oral cancer, a meta-analysis was performed.	Arginine	43-46	P53	Homo sapiens	30-33
23192640-3	2013	Based on a comprehensive search in PubMed, Embase, Web of Science, and China National Knowledge Infrastructure (CNKI) databases, we identified all available publications assessing the association between p53 codon 72 Arg/Pro polymorphism and oral cancer risk.	Arginine	217-220	P53	Homo sapiens	204-207
23356739-0	2013	Differential effects of garcinol and curcumin on histone and p53 modifications in tumour cells.	Curcumin	37-45	P53	Homo sapiens	61-64
23469783-8	2013	CONCLUSION: Iron overload can inhibit the proliferation of MSCs and induce their apoptosis through the generation of ROS, which is probably due to the stimulation of p38MAPK- p53 signaling pathway.	Iron	12-16	P53	Homo sapiens	175-178
23469783-8	2013	CONCLUSION: Iron overload can inhibit the proliferation of MSCs and induce their apoptosis through the generation of ROS, which is probably due to the stimulation of p38MAPK- p53 signaling pathway.	Reactive Oxygen Species	117-120	P53	Homo sapiens	175-178
23434831-3	2013	Moreover, asperolide A significantly activated MAP kinases (ERK1/2, JNK and p38 MAP kinase) by phosphorylation, and only the inhibition of ERK activation by PD98059 reversed downregulation of G2/M regulatory proteins CDC2, and suppressed upregulation of p21 and p-p53 levels.	asperolide	10-20	P53	Homo sapiens	264-267
23356739-4	2013	In this study we assessed the effects of the phytocompounds garcinol and curcumin on histone and p53 modification in cancer cells, focussing on the breast tumour cell line MCF7.	Curcumin	73-81	P53	Homo sapiens	97-100
23351152-0	2013	PRIMA-1 increases cisplatin sensitivity in chemoresistant ovarian cancer cells with p53 mutation: a requirement for Akt down-regulation.	Cisplatin	18-27	P53	Homo sapiens	84-87
23356234-6	2013	We also used the MTT assay and flow cytometry to investigate if silencing of mutant p53 by knockdown with small interfering (si)RNA would change the sensitivity to cisplatin treatment.	Cisplatin	164-173	P53	Homo sapiens	84-87
23356234-8	2013	Moreover, our study also showed that the p53-targeting siRNA cooperated with cisplatin in the inhibition of bladder cancer cells.	Cisplatin	77-86	P53	Homo sapiens	41-44
23351152-5	2013	Apoptosis in cells treated with PRIMA-1 (0.156 muM) and CDDP treatment (10 muM) was significantly suppressed by p53-siRNA.	Cisplatin	56-60	P53	Homo sapiens	112-115
23351152-6	2013	PRIMA-1 increased phospho-p53 (Ser15) content in Akt down-regulated cells treated with CDDP.	Cisplatin	87-91	P53	Homo sapiens	26-29
23351152-8	2013	Our findings raise the possibility that PRIMA-1 may be useful candidate for adjuvant therapy with CDDP in chemoresistant ovarian cancer with p53 mutation when Akt is down-regulated.	Cisplatin	98-102	P53	Homo sapiens	141-144
23244159-0	2013	Electrochemical study on the effects of epigenetic cytosine methylation on anti-benzo[a]pyrene diol epoxide damage at TP53 oligomers.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	80-107	P53	Homo sapiens	118-122
23343191-5	2013	RESULTS: The combination of 100 nM doxorubicin followed by 1200 nM P276-00 showed synergistic effect in the p53-positive and p53-mutated cell lines H-460 and H23 respectively as compared to the p53-null cell line H1299.	Doxorubicin	35-46	P53	Homo sapiens	108-111
23343191-5	2013	RESULTS: The combination of 100 nM doxorubicin followed by 1200 nM P276-00 showed synergistic effect in the p53-positive and p53-mutated cell lines H-460 and H23 respectively as compared to the p53-null cell line H1299.	Doxorubicin	35-46	P53	Homo sapiens	125-128
23343191-5	2013	RESULTS: The combination of 100 nM doxorubicin followed by 1200 nM P276-00 showed synergistic effect in the p53-positive and p53-mutated cell lines H-460 and H23 respectively as compared to the p53-null cell line H1299.	Doxorubicin	35-46	P53	Homo sapiens	125-128
23287470-0	2013	A novel link between p53 and ROS.	ros	29-32	P53	Homo sapiens	21-24
23242140-0	2013	Serine starvation induces stress and p53-dependent metabolic remodelling in cancer cells.	Serine	0-6	P53	Homo sapiens	37-40
23242140-5	2013	Transient p53-p21 (also known as CDKN1A) activation and cell-cycle arrest promoted cell survival by efficiently channelling depleted serine stores to glutathione synthesis, thus preserving cellular anti-oxidant capacity.	Serine	133-139	P53	Homo sapiens	10-13
23242140-5	2013	Transient p53-p21 (also known as CDKN1A) activation and cell-cycle arrest promoted cell survival by efficiently channelling depleted serine stores to glutathione synthesis, thus preserving cellular anti-oxidant capacity.	Glutathione	150-161	P53	Homo sapiens	10-13
23242140-6	2013	Cells lacking p53 failed to complete the response to serine depletion, resulting in oxidative stress, reduced viability and severely impaired proliferation.	Serine	53-59	P53	Homo sapiens	14-17
23242140-7	2013	The role of p53 in supporting cancer cell proliferation under serine starvation was translated to an in vivo model, indicating that serine depletion has a potential role in the treatment of p53-deficient tumours.	Serine	62-68	P53	Homo sapiens	12-15
23242140-7	2013	The role of p53 in supporting cancer cell proliferation under serine starvation was translated to an in vivo model, indicating that serine depletion has a potential role in the treatment of p53-deficient tumours.	Serine	132-138	P53	Homo sapiens	12-15
23255126-0	2013	Wild-type and mutant p53 mediate cisplatin resistance through interaction and inhibition of active caspase-9.	Cisplatin	33-42	P53	Homo sapiens	21-24
23255126-9	2013	In a p53-null background, the high-level expression of both exogenous WT and mutant p53 increased the resistance of these cells to cisplatin, and the data showed a correlation between high p53 expression and caspase-9 inhibition.	Cisplatin	131-140	P53	Homo sapiens	84-87
23255126-9	2013	In a p53-null background, the high-level expression of both exogenous WT and mutant p53 increased the resistance of these cells to cisplatin, and the data showed a correlation between high p53 expression and caspase-9 inhibition.	Cisplatin	131-140	P53	Homo sapiens	84-87
23239315-1	2013	RATIONALE: The efficiency of Sirtuin1, a major target for the treatment of various metabolic disorders such as inflammation and type 2 diabetes mellitus, can be modulated via low molecular mass SIRT1 activators (e.g. resveratrol, SRT1720, and SRT2104).The administration of such compounds results in increased deacetylation of substrates including p53, FOXO1, and PGC1alpha, potentially leading to an improved physical performance.	Resveratrol	217-228	P53	Homo sapiens	348-351
23148227-3	2013	Upon adriamycin (ADR) exposure, p53 as well as RUNX1 were strongly induced in p53-proficient HCT116 and U2OS cells, which were closely associated with significant transactivation of p53 target genes, such as p21(WAF)(1), BAX, NOXA, and PUMA.	Doxorubicin	5-15	P53	Homo sapiens	32-35
23536002-0	2013	Tumor suppressor protein Pdcd4 interacts with Daxx and modulates the stability of Daxx and the Hipk2-dependent phosphorylation of p53 at serine 46.	Serine	137-143	P53	Homo sapiens	130-133
23148227-3	2013	Upon adriamycin (ADR) exposure, p53 as well as RUNX1 were strongly induced in p53-proficient HCT116 and U2OS cells, which were closely associated with significant transactivation of p53 target genes, such as p21(WAF)(1), BAX, NOXA, and PUMA.	Doxorubicin	5-15	P53	Homo sapiens	78-81
23536002-6	2013	Daxx has previously been shown to serve as a scaffold for protein kinase Hipk2 and tumor suppressor protein p53 and to stimulate the phosphorylation of p53 at serine 46 (Ser-46) in response to genotoxic stress.	Serine	159-165	P53	Homo sapiens	152-155
23148227-3	2013	Upon adriamycin (ADR) exposure, p53 as well as RUNX1 were strongly induced in p53-proficient HCT116 and U2OS cells, which were closely associated with significant transactivation of p53 target genes, such as p21(WAF)(1), BAX, NOXA, and PUMA.	Doxorubicin	5-15	P53	Homo sapiens	78-81
23536002-6	2013	Daxx has previously been shown to serve as a scaffold for protein kinase Hipk2 and tumor suppressor protein p53 and to stimulate the phosphorylation of p53 at serine 46 (Ser-46) in response to genotoxic stress.	Serine	170-173	P53	Homo sapiens	152-155
23148227-8	2013	Furthermore, RUNX1 was associated with p300 histone acetyltransferase, and ADR-dependent acetylation of p53 at Lys-373/382 was markedly inhibited in RUNX1 knockdown cells.	Lysine	111-114	P53	Homo sapiens	104-107
23303309-3	2013	Also key to better understanding is why and how the anti-diabetic drug metformin (the world"s most prescribed pharmaceutical product) preferentially kills oxidant-deficient mesenchymal p53(- -) cells.	Metformin	71-80	P53	Homo sapiens	185-188
24024154-5	2013	Using soluble guanylyl cyclase (sGC) and p53 as model  NO-sensitive proteins, we demonstrate that their concentration-dependent responses to  NO are a function of the O2 concentration.	Oxygen	167-169	P53	Homo sapiens	41-44
24024154-6	2013	p53 requires relatively high steady-state  NO concentrations (&gt;600 nM) to induce its phosphorylation (P-ser-15), whereas sGC responds to low  NO concentrations (&lt;100 nM).	Serine	107-110	P53	Homo sapiens	0-3
23804139-0	2013	p53 expression in pretreatment specimen predicts response to neoadjuvant chemotherapy including anthracycline and taxane in patients with primary breast cancer.	Anthracyclines	96-109	P53	Homo sapiens	0-3
23804139-0	2013	p53 expression in pretreatment specimen predicts response to neoadjuvant chemotherapy including anthracycline and taxane in patients with primary breast cancer.	taxane	114-120	P53	Homo sapiens	0-3
24289605-7	2013	First, we evaluated whether the genotoxic potential of cisplatin/gemcitabine was dependent on TP53 status.	Cisplatin	55-64	P53	Homo sapiens	94-98
28976149-5	2013	The results indicate that the oligonucleotide G13494A substitution in intron 6 proapoptotic gene TP53 in older individuals may have a modulating effect on the risk of indolent lymphoma.	Oligonucleotides	30-45	P53	Homo sapiens	97-101
24289605-13	2013	However, cisplatin was the most effective, causing the highest level of DNA damage in both wild-type and mutated TP53 cells.	Cisplatin	9-18	P53	Homo sapiens	113-117
22767080-5	2013	Expression and activation of p53 by phosphorylation at serine 15 and 37 were studied using Western blot assay immediately after three independent exposures of cell cultures provided from three different donors.	Serine	55-61	P53	Homo sapiens	29-32
24335178-14	2013	CONCLUSION: These findings not only indicate NAC as a rational approach for better treatment of cervical cancer with improved therapeutic outcomes, due partly to the ability of cisplatin to promote the p53:miR-34a:E2F1 positive feed-forward loop and the p53:miR-605:Mdm2 positive feedback loop.	Cisplatin	177-186	P53	Homo sapiens	202-205
23161364-5	2013	p53 was upregulated upon Taxol treatment in p53 wild type cells and deletion of p53 diminished Taxol-induced apoptosis.	Paclitaxel	25-30	P53	Homo sapiens	44-47
23161364-5	2013	p53 was upregulated upon Taxol treatment in p53 wild type cells and deletion of p53 diminished Taxol-induced apoptosis.	Paclitaxel	25-30	P53	Homo sapiens	44-47
23161364-5	2013	p53 was upregulated upon Taxol treatment in p53 wild type cells and deletion of p53 diminished Taxol-induced apoptosis.	Paclitaxel	95-100	P53	Homo sapiens	0-3
23161364-6	2013	p53 target proteins including MDM2, p21, BAX, and beta-isoform of PUMA were also upregulated by Taxol in p53 wild type cells.	Paclitaxel	96-101	P53	Homo sapiens	0-3
23161364-6	2013	p53 target proteins including MDM2, p21, BAX, and beta-isoform of PUMA were also upregulated by Taxol in p53 wild type cells.	Paclitaxel	96-101	P53	Homo sapiens	105-108
23161364-7	2013	Conversely, when the wild type p53 was re-introduced into two different p53 null cancer cell lines, Taxol-induced apoptosis was enhanced.	Paclitaxel	100-105	P53	Homo sapiens	31-34
23161364-7	2013	Conversely, when the wild type p53 was re-introduced into two different p53 null cancer cell lines, Taxol-induced apoptosis was enhanced.	Paclitaxel	100-105	P53	Homo sapiens	72-75
23161364-8	2013	Among post-translational modifications that affect p53 stability and function, p53 acetylation, rather than phosphorylation, increased significantly in Taxol-treated cells.	Paclitaxel	152-157	P53	Homo sapiens	51-54
23161364-8	2013	Among post-translational modifications that affect p53 stability and function, p53 acetylation, rather than phosphorylation, increased significantly in Taxol-treated cells.	Paclitaxel	152-157	P53	Homo sapiens	79-82
23161364-9	2013	When acetylation was enhanced by anti-Sirt1 siRNA or an HDAC inhibitor, Taxol-induced apoptosis was enhanced, which was not observed in p53 null cells.	Paclitaxel	72-77	P53	Homo sapiens	136-139
23161364-11	2013	Thus, p53 plays a pro-apoptotic role in Taxol-induced apoptosis and acetylation of p53 contributes to this pro-apoptotic function in response to Taxol in several human cancer cell lines, suggesting that enhancing acetylation of p53 could have potential implication for increasing the sensitivity of cancer cells to Taxol.	Paclitaxel	40-45	P53	Homo sapiens	6-9
23161364-11	2013	Thus, p53 plays a pro-apoptotic role in Taxol-induced apoptosis and acetylation of p53 contributes to this pro-apoptotic function in response to Taxol in several human cancer cell lines, suggesting that enhancing acetylation of p53 could have potential implication for increasing the sensitivity of cancer cells to Taxol.	Paclitaxel	145-150	P53	Homo sapiens	83-86
23161364-11	2013	Thus, p53 plays a pro-apoptotic role in Taxol-induced apoptosis and acetylation of p53 contributes to this pro-apoptotic function in response to Taxol in several human cancer cell lines, suggesting that enhancing acetylation of p53 could have potential implication for increasing the sensitivity of cancer cells to Taxol.	Paclitaxel	145-150	P53	Homo sapiens	83-86
23161364-11	2013	Thus, p53 plays a pro-apoptotic role in Taxol-induced apoptosis and acetylation of p53 contributes to this pro-apoptotic function in response to Taxol in several human cancer cell lines, suggesting that enhancing acetylation of p53 could have potential implication for increasing the sensitivity of cancer cells to Taxol.	Paclitaxel	145-150	P53	Homo sapiens	83-86
23161364-11	2013	Thus, p53 plays a pro-apoptotic role in Taxol-induced apoptosis and acetylation of p53 contributes to this pro-apoptotic function in response to Taxol in several human cancer cell lines, suggesting that enhancing acetylation of p53 could have potential implication for increasing the sensitivity of cancer cells to Taxol.	Paclitaxel	145-150	P53	Homo sapiens	83-86
23841076-5	2013	Similarly, pretreatment with the antioxidant N-acetyl-cysteine (NAC) markedly inhibited both the autophagy and the apoptosis triggered by DHA, indicating that mitochondrial ROS mediate the cytotoxicity of DHA in mutant p53 cells.	Acetylcysteine	45-62	P53	Homo sapiens	219-222
23841076-5	2013	Similarly, pretreatment with the antioxidant N-acetyl-cysteine (NAC) markedly inhibited both the autophagy and the apoptosis triggered by DHA, indicating that mitochondrial ROS mediate the cytotoxicity of DHA in mutant p53 cells.	Acetylcysteine	64-67	P53	Homo sapiens	219-222
23841076-5	2013	Similarly, pretreatment with the antioxidant N-acetyl-cysteine (NAC) markedly inhibited both the autophagy and the apoptosis triggered by DHA, indicating that mitochondrial ROS mediate the cytotoxicity of DHA in mutant p53 cells.	Reactive Oxygen Species	173-176	P53	Homo sapiens	219-222
23841076-7	2013	Collectively, these findings present a novel mechanism of ROS-regulated apoptosis and autophagy that involves Akt-mTOR signaling in prostate cancer cells with mutant p53 exposed to DHA.	Reactive Oxygen Species	58-61	P53	Homo sapiens	166-169
23054612-6	2013	Importantly, when p53 was activated following the administration of either of three different anticancer chemotherapeutic agents (cisplatin, etoposide or doxorubicin), it was able to induce CYP3A genes, which are the main factors in systemic clearance of these agents.	Cisplatin	130-139	P53	Homo sapiens	18-21
23054612-6	2013	Importantly, when p53 was activated following the administration of either of three different anticancer chemotherapeutic agents (cisplatin, etoposide or doxorubicin), it was able to induce CYP3A genes, which are the main factors in systemic clearance of these agents.	Doxorubicin	154-165	P53	Homo sapiens	18-21
22918438-1	2013	The tumor suppressor p53 is an important regulator of intracellular reactive oxygen species (ROS) levels, although downstream mediators of p53 remain to be elucidated.	Reactive Oxygen Species	68-91	P53	Homo sapiens	21-24
22918438-1	2013	The tumor suppressor p53 is an important regulator of intracellular reactive oxygen species (ROS) levels, although downstream mediators of p53 remain to be elucidated.	Reactive Oxygen Species	93-96	P53	Homo sapiens	21-24
22918438-2	2013	Here, we show that p53 and its downstream targets, p53-inducible ribonucleotide reductase (p53R2) and p53-inducible gene 3 (PIG3), physically and functionally interact with catalase for efficient regulation of intracellular ROS, depending on stress intensity.	Reactive Oxygen Species	224-227	P53	Homo sapiens	19-22
22918438-2	2013	Here, we show that p53 and its downstream targets, p53-inducible ribonucleotide reductase (p53R2) and p53-inducible gene 3 (PIG3), physically and functionally interact with catalase for efficient regulation of intracellular ROS, depending on stress intensity.	Reactive Oxygen Species	224-227	P53	Homo sapiens	51-54
22918438-3	2013	Under physiological conditions, the antioxidant functions of p53 are mediated by p53R2, which maintains increased catalase activity and thereby protects against endogenous ROS.	Reactive Oxygen Species	172-175	P53	Homo sapiens	61-64
22918438-5	2013	These results highlight the essential role of catalase in p53-mediated ROS regulation and suggest that the p53/p53R2-catalase and p53/PIG3-catalase pathways are critically involved in intracellular ROS regulation under physiological conditions and during the response to DNA damage, respectively.	Reactive Oxygen Species	71-74	P53	Homo sapiens	58-61
22918438-5	2013	These results highlight the essential role of catalase in p53-mediated ROS regulation and suggest that the p53/p53R2-catalase and p53/PIG3-catalase pathways are critically involved in intracellular ROS regulation under physiological conditions and during the response to DNA damage, respectively.	Reactive Oxygen Species	71-74	P53	Homo sapiens	107-110
22918438-5	2013	These results highlight the essential role of catalase in p53-mediated ROS regulation and suggest that the p53/p53R2-catalase and p53/PIG3-catalase pathways are critically involved in intracellular ROS regulation under physiological conditions and during the response to DNA damage, respectively.	Reactive Oxygen Species	71-74	P53	Homo sapiens	107-110
22918438-5	2013	These results highlight the essential role of catalase in p53-mediated ROS regulation and suggest that the p53/p53R2-catalase and p53/PIG3-catalase pathways are critically involved in intracellular ROS regulation under physiological conditions and during the response to DNA damage, respectively.	Reactive Oxygen Species	198-201	P53	Homo sapiens	58-61
22918438-5	2013	These results highlight the essential role of catalase in p53-mediated ROS regulation and suggest that the p53/p53R2-catalase and p53/PIG3-catalase pathways are critically involved in intracellular ROS regulation under physiological conditions and during the response to DNA damage, respectively.	Reactive Oxygen Species	198-201	P53	Homo sapiens	107-110
22918438-5	2013	These results highlight the essential role of catalase in p53-mediated ROS regulation and suggest that the p53/p53R2-catalase and p53/PIG3-catalase pathways are critically involved in intracellular ROS regulation under physiological conditions and during the response to DNA damage, respectively.	Reactive Oxygen Species	198-201	P53	Homo sapiens	107-110
24217648-0	2013	Doxorubicin caused apoptosis of mesenchymal stem cells via p38, JNK and p53 pathway.	Doxorubicin	0-11	P53	Homo sapiens	72-75
24217648-9	2013	Also, the phosphorylated and total p53 proteins were increased in doxorubicin-treated BMSCs.	Doxorubicin	66-77	P53	Homo sapiens	35-38
24217648-12	2013	CONCLUSION: Taken together, doxorubicin caused BMSCs apoptosis associated with p38, JNK and p53 pathways.	Doxorubicin	28-39	P53	Homo sapiens	92-95
23161364-0	2013	p53 acetylation enhances Taxol-induced apoptosis in human cancer cells.	Paclitaxel	25-30	P53	Homo sapiens	0-3
23161364-4	2013	Here we investigated the function of p53 in Taxol-induced apoptosis using p53 wild type and p53 null cancer cell lines.	Paclitaxel	44-49	P53	Homo sapiens	37-40
23161364-5	2013	p53 was upregulated upon Taxol treatment in p53 wild type cells and deletion of p53 diminished Taxol-induced apoptosis.	Paclitaxel	25-30	P53	Homo sapiens	0-3
23841076-0	2013	The omega-3 polyunsaturated fatty acid DHA induces simultaneous apoptosis and autophagy via mitochondrial ROS-mediated Akt-mTOR signaling in prostate cancer cells expressing mutant p53.	Reactive Oxygen Species	106-109	P53	Homo sapiens	181-184
23022267-0	2013	Tyrosine phosphatase inhibitors combined with retinoic acid can enhance differentiation of neuroblastoma cells and trigger ERK- and AKT-dependent, p53-independent senescence.	Tretinoin	46-59	P53	Homo sapiens	147-150
23063463-5	2013	Recent findings suggest a novel role for p53 in TGF-beta1-induced PAI-1 transcription that involves ROS generation and p53/SMAD interactions.	Reactive Oxygen Species	100-103	P53	Homo sapiens	41-44
24335168-6	2013	In addition, we found USP7, a positive regulator of tumor suppressor p53, as a new molecular target of metformin.	Metformin	103-112	P53	Homo sapiens	69-72
24335171-0	2013	Berberine induces apoptosis in p53-null leukemia cells by down-regulating XIAP at the post-transcriptional level.	Berberine	0-9	P53	Homo sapiens	31-34
24335171-2	2013	However, the underlying molecular mechanisms of berberine induced p53-independent apoptosis remain unclear.	Berberine	48-57	P53	Homo sapiens	66-69
24335171-3	2013	METHODS: The p53-null leukemia cell line EU-4 cells were exposed to berberine.	Berberine	68-77	P53	Homo sapiens	13-16
24335171-7	2013	RESULTS: Berberine induced p53-independent, XIAP-mediated apoptotic cell death in p53-null leukemia cells.	Berberine	9-18	P53	Homo sapiens	27-30
24335171-7	2013	RESULTS: Berberine induced p53-independent, XIAP-mediated apoptotic cell death in p53-null leukemia cells.	Berberine	9-18	P53	Homo sapiens	82-85
24335171-11	2013	CONCLUSION: Our findings characterize the molecular mechanisms of berberine-induced caspase activation and subsequent apoptosis, and berberine may be a novel candidate inducer of apoptosis in leukemia cells, which normally lack p53 expression.	Berberine	133-142	P53	Homo sapiens	228-231
24335178-12	2013	Among the three anti-cancer drugs included in NAC, cisplatin was found to be the main component that caused increases in p53 protein levels, miR-34a and miR-605 miRNA levels, and decreases in Mdm2 and E2F1 protein levels.	Cisplatin	51-60	P53	Homo sapiens	121-124
24335178-14	2013	CONCLUSION: These findings not only indicate NAC as a rational approach for better treatment of cervical cancer with improved therapeutic outcomes, due partly to the ability of cisplatin to promote the p53:miR-34a:E2F1 positive feed-forward loop and the p53:miR-605:Mdm2 positive feedback loop.	Cisplatin	177-186	P53	Homo sapiens	254-257
22201594-3	2013	In addition, as the byproducts of metabolism, reactive oxygen species (ROS) generated in the mitochondria can serve as signaling molecules to regulate p53 function.	Reactive Oxygen Species	46-69	P53	Homo sapiens	151-154
24112172-7	2013	The p53 expression was markedly increased in a concentration dependent manner in both iron treatment groups.	Iron	86-90	P53	Homo sapiens	4-7
24112172-8	2013	CONCLUSION: The soluble divalent iron and, to a greater degree trivalent iron, inhibited HASMC proliferation in a dosedependent manner, which may be attributed to reduction of PCNA expression and increase of p53 expression.	Iron	33-37	P53	Homo sapiens	208-211
24112172-8	2013	CONCLUSION: The soluble divalent iron and, to a greater degree trivalent iron, inhibited HASMC proliferation in a dosedependent manner, which may be attributed to reduction of PCNA expression and increase of p53 expression.	Iron	73-77	P53	Homo sapiens	208-211
23165143-10	2013	Sertraline and thioridazine interfere with this repressive feedback by targeting directly TPT1/TCTP and inhibiting its binding to MDM2, restoring wildtype p53 function.	Sertraline	0-10	P53	Homo sapiens	155-158
22201594-3	2013	In addition, as the byproducts of metabolism, reactive oxygen species (ROS) generated in the mitochondria can serve as signaling molecules to regulate p53 function.	Reactive Oxygen Species	71-74	P53	Homo sapiens	151-154
23210739-3	2013	The frequencies of GG genotype at 309 position in the second promoter (P2) of MDM2 and Arginine in codon72 of p53 were found to be 3.5 (odds ratio [OR]=3.51; 95% confidence interval [CI]=1.93-6.4; p&lt;0.0001) and 5 (OR=4.978; 95% CI=2.7-9.2; p&lt;0.0001) fold higher, respectively, in cases than in the control.	Arginine	87-95	P53	Homo sapiens	110-113
23394088-10	2013	More recently, we demonstrated that Pi is capable also of inducing sensitization of osteosarcoma cells to doxorubicin in a p53-dependent manner and through a mechanism involving ERK1/2 down-regulation.	Doxorubicin	106-117	P53	Homo sapiens	123-126
23210739-4	2013	On gene-gene interactions between MDM2 and p53 polymorphisms, the frequency of MDM2 G/G and p53 Arg/Arg together was found to be 6.5-fold higher in cervical cancer patients compared with healthy controls (OR=6.497; 95% CI=2.987-14.13; p&lt;0.0001).	Arginine	96-99	P53	Homo sapiens	43-46
23210739-4	2013	On gene-gene interactions between MDM2 and p53 polymorphisms, the frequency of MDM2 G/G and p53 Arg/Arg together was found to be 6.5-fold higher in cervical cancer patients compared with healthy controls (OR=6.497; 95% CI=2.987-14.13; p&lt;0.0001).	Arginine	96-99	P53	Homo sapiens	92-95
23210739-4	2013	On gene-gene interactions between MDM2 and p53 polymorphisms, the frequency of MDM2 G/G and p53 Arg/Arg together was found to be 6.5-fold higher in cervical cancer patients compared with healthy controls (OR=6.497; 95% CI=2.987-14.13; p&lt;0.0001).	Arginine	100-103	P53	Homo sapiens	43-46
23210739-4	2013	On gene-gene interactions between MDM2 and p53 polymorphisms, the frequency of MDM2 G/G and p53 Arg/Arg together was found to be 6.5-fold higher in cervical cancer patients compared with healthy controls (OR=6.497; 95% CI=2.987-14.13; p&lt;0.0001).	Arginine	100-103	P53	Homo sapiens	92-95
23210739-5	2013	We found an association of p53 codon72 arginine and MDM2 SNP309 GG genotype with different clinical and histological grades, human papillomavirus (HPV) infection, and age at the time of diagnosis of cervical cancer.	Arginine	39-47	P53	Homo sapiens	27-30
23210739-6	2013	In conclusion, Arginine at codon72 of p53 and GG genotype at 309 in P2 of MDM2 together reveal a direct proportionality with the tumor grade of cervical cancer along with HPV infection in postmenopausal women.	Arginine	15-23	P53	Homo sapiens	38-41
23781585-8	2013	Western blotting demonstrated that the expression of P53 protein increased and the expression of HPV E6 survivin protein decreased in HeLa cells treated with MIF at low concentrations (&lt; or = 10 micromol/l) combined with cisplatin.	Cisplatin	224-233	P53	Homo sapiens	53-56
23781585-10	2013	The strengthening effect of growth inhibition and chemosensitivity to cisplatin of mifepristone are associated with down-regulating HPV E6 survivin protein and upregulating p53 protein.	Cisplatin	70-79	P53	Homo sapiens	173-176
24601052-6	2013	p53 positive expression and Ki67 high expression were associated with high PTX (p = 0.01 and p &lt; 0.01, respectively) and CBDCA (p = 0.03 and p &lt; 0.01, respectively) sensitivity.	Paclitaxel	75-78	P53	Homo sapiens	0-3
23092908-7	2013	RESULTS: The distribution of Arg/Arg, Arg/Pro and Pro/Pro genotypes of codon 72 of the TP53 gene was: 46.8%, 46.8% and 6.4%, respectively in the ovarian carcinomas and 64.3%, 31.4% and 4.3%, respectively in the control group.	Arginine	29-32	P53	Homo sapiens	87-91
23092908-7	2013	RESULTS: The distribution of Arg/Arg, Arg/Pro and Pro/Pro genotypes of codon 72 of the TP53 gene was: 46.8%, 46.8% and 6.4%, respectively in the ovarian carcinomas and 64.3%, 31.4% and 4.3%, respectively in the control group.	Arginine	33-36	P53	Homo sapiens	87-91
23092908-7	2013	RESULTS: The distribution of Arg/Arg, Arg/Pro and Pro/Pro genotypes of codon 72 of the TP53 gene was: 46.8%, 46.8% and 6.4%, respectively in the ovarian carcinomas and 64.3%, 31.4% and 4.3%, respectively in the control group.	Arginine	33-36	P53	Homo sapiens	87-91
23128467-0	2013	N-acetylcysteine potentiates doxorubicin-induced ATM and p53 activation             in ovarian cancer cells.	Acetylcysteine	0-16	P53	Homo sapiens	57-60
23533526-5	2013	The elevated ROS triggered the activation of ataxia-telangiectasia mutation (ATM), which further enhanced the ATF3 upregulation and subsequently enhanced p53 function by phosphorylation at Serine 15 and Serine 392.	Reactive Oxygen Species	13-16	P53	Homo sapiens	154-157
23533526-5	2013	The elevated ROS triggered the activation of ataxia-telangiectasia mutation (ATM), which further enhanced the ATF3 upregulation and subsequently enhanced p53 function by phosphorylation at Serine 15 and Serine 392.	Serine	189-195	P53	Homo sapiens	154-157
23533526-5	2013	The elevated ROS triggered the activation of ataxia-telangiectasia mutation (ATM), which further enhanced the ATF3 upregulation and subsequently enhanced p53 function by phosphorylation at Serine 15 and Serine 392.	Serine	203-209	P53	Homo sapiens	154-157
23784838-6	2013	In this review, building on recent findings of p53-induced apoptosis and DNA-repair mechanisms in TGCTs, we will discuss the molecular bases that drive tumor sensitivity to cisplatin, emphasizing the new therapeutic approaches proposed to eventually constrain tumor recurrence, and target TGCTs which are unresponsive to standard therapies.	Cisplatin	173-182	P53	Homo sapiens	47-50
23128378-9	2013	Furthermore,             iNOS gene-mediated enhancement of cisplatin-mediated antitumor effects in lung             cancer may be related to the attenuation of p-mTOR, MMP2 and the activation of             p-p53.	Cisplatin	59-68	P53	Homo sapiens	209-212
24141202-4	2013	The resulting accumulation of p53 proteins from phosphorylation at serine-15 and serine-392 was correlated with an increase in p21 and caspase activation.	Serine	67-73	P53	Homo sapiens	30-33
24141202-4	2013	The resulting accumulation of p53 proteins from phosphorylation at serine-15 and serine-392 was correlated with an increase in p21 and caspase activation.	Serine	81-87	P53	Homo sapiens	30-33
23737838-0	2013	Resveratrol Impedes the Stemness, Epithelial-Mesenchymal Transition, and Metabolic Reprogramming of Cancer Stem Cells in Nasopharyngeal Carcinoma through p53 Activation.	Resveratrol	0-11	P53	Homo sapiens	154-157
23737838-6	2013	We found that resveratrol impeded CSC properties through the activation of p53 and this effect could be reversed by knockdown of p53.	Resveratrol	14-25	P53	Homo sapiens	75-78
23737838-6	2013	We found that resveratrol impeded CSC properties through the activation of p53 and this effect could be reversed by knockdown of p53.	Resveratrol	14-25	P53	Homo sapiens	129-132
23737838-7	2013	Furthermore, resveratrol suppressed the stemness and EMT through reactivating p53 and inducing miR-145 and miR-200c, which were downregulated in NPC CSCs.	Resveratrol	13-24	P53	Homo sapiens	78-81
23737838-8	2013	In conclusion, we demonstrated that resveratrol employed the p53 pathway in regulating stemness, EMT, and metabolic reprogramming.	Resveratrol	36-47	P53	Homo sapiens	61-64
23737838-9	2013	Further investigation of the molecular mechanism of p53 activation by resveratrol may provide useful information for the development of novel therapies for cancer treatment through targeting to CSCs.	Resveratrol	70-81	P53	Homo sapiens	52-55
23216904-6	2013	This suggests that Nox-generated ROS transduce senescence signals by activating the p53 and p16Ink4a pathway.	nicotine 1-N-oxide	19-22	P53	Homo sapiens	84-87
23216904-6	2013	This suggests that Nox-generated ROS transduce senescence signals by activating the p53 and p16Ink4a pathway.	Reactive Oxygen Species	33-36	P53	Homo sapiens	84-87
23128467-10	2013	Collectively, we conclude that doxorubicin induces ATM/p53 activation             leading to reorganization of cytoskeletal networks, inhibition of mTOR activity,             and inhibition of cell proliferation and migration.	Doxorubicin	31-42	P53	Homo sapiens	55-58
23128467-0	2013	N-acetylcysteine potentiates doxorubicin-induced ATM and p53 activation             in ovarian cancer cells.	Doxorubicin	29-40	P53	Homo sapiens	57-60
23128467-6	2013	Doxorubicin induces             phosphorylation of p53 at Ser15 and 20, acetylation of p53 and ATM activation.	Doxorubicin	0-11	P53	Homo sapiens	51-54
23128467-6	2013	Doxorubicin induces             phosphorylation of p53 at Ser15 and 20, acetylation of p53 and ATM activation.	Doxorubicin	0-11	P53	Homo sapiens	87-90
23128467-9	2013	Pretreatment of CaOV3 cells with antioxidant N-acetylcysteine (NAC),             but not pyrrolidine dithiocarbamate (PDTC) potentiates doxorubicin-induced phosphorylation             of p53 and ATM.	Acetylcysteine	45-61	P53	Homo sapiens	187-190
23128467-9	2013	Pretreatment of CaOV3 cells with antioxidant N-acetylcysteine (NAC),             but not pyrrolidine dithiocarbamate (PDTC) potentiates doxorubicin-induced phosphorylation             of p53 and ATM.	Acetylcysteine	63-66	P53	Homo sapiens	187-190
23128467-9	2013	Pretreatment of CaOV3 cells with antioxidant N-acetylcysteine (NAC),             but not pyrrolidine dithiocarbamate (PDTC) potentiates doxorubicin-induced phosphorylation             of p53 and ATM.	Doxorubicin	136-147	P53	Homo sapiens	187-190
22803791-0	2013	The substitutions G245C and G245D in the Zn(2+)-binding pocket of the p53 protein result in differences of conformational flexibility of the DNA-binding domain.	Zinc	41-47	P53	Homo sapiens	70-73
22674530-0	2013	Inorganic phosphate enhances sensitivity of human osteosarcoma U2OS cells to doxorubicin via a p53-dependent pathway.	Phosphates	0-19	P53	Homo sapiens	95-98
22674530-0	2013	Inorganic phosphate enhances sensitivity of human osteosarcoma U2OS cells to doxorubicin via a p53-dependent pathway.	Doxorubicin	77-88	P53	Homo sapiens	95-98
22674530-8	2013	Remarkably, Pi/doxorubicin combination-induced cytotoxicity was accompanied by an increase of p53 protein levels and of p53 target genes mdm2, p21 and Bax, and was significantly reduced by the p53 inhibitor pifithrine-alpha.	Doxorubicin	15-26	P53	Homo sapiens	94-97
22674530-8	2013	Remarkably, Pi/doxorubicin combination-induced cytotoxicity was accompanied by an increase of p53 protein levels and of p53 target genes mdm2, p21 and Bax, and was significantly reduced by the p53 inhibitor pifithrine-alpha.	Doxorubicin	15-26	P53	Homo sapiens	120-123
22674530-8	2013	Remarkably, Pi/doxorubicin combination-induced cytotoxicity was accompanied by an increase of p53 protein levels and of p53 target genes mdm2, p21 and Bax, and was significantly reduced by the p53 inhibitor pifithrine-alpha.	Doxorubicin	15-26	P53	Homo sapiens	120-123
23991369-2	2013	In human populations, the p53 gene contains a common single nucleotide polymorphism (SNP) affecting codon 72 that determines whether a proline (P72) or an arginine (R72) is present at this amino acid position of the polypeptide.	Arginine	155-163	P53	Homo sapiens	26-29
23124863-1	2013	The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene in association with human papillomavirus (HPV) 16 E6 variants has been implicated as a risk marker in cervical neoplasia.	Arginine	4-7	P53	Homo sapiens	66-69
23124863-1	2013	The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene in association with human papillomavirus (HPV) 16 E6 variants has been implicated as a risk marker in cervical neoplasia.	Arginine	8-11	P53	Homo sapiens	66-69
23124863-1	2013	The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene in association with human papillomavirus (HPV) 16 E6 variants has been implicated as a risk marker in cervical neoplasia.	Arginine	8-11	P53	Homo sapiens	66-69
23124863-4	2013	The data obtained showed statistically significant different distribution of p53 genotypes between healthy controls and precursor lesions, with the p53 arginine homozygous increased in high-grade squamous intraepithelial lesions.	Arginine	152-160	P53	Homo sapiens	77-80
23124863-4	2013	The data obtained showed statistically significant different distribution of p53 genotypes between healthy controls and precursor lesions, with the p53 arginine homozygous increased in high-grade squamous intraepithelial lesions.	Arginine	152-160	P53	Homo sapiens	148-151
23124863-7	2013	In conclusion, p53 arginine homozygous was found to be increased in high-grade lesions, supporting the results of previous investigations indicating that HPV-positive patients with p53 Arg/Arg have an increased risk of developing pre-cancerous lesions.	Arginine	19-27	P53	Homo sapiens	15-18
23124863-7	2013	In conclusion, p53 arginine homozygous was found to be increased in high-grade lesions, supporting the results of previous investigations indicating that HPV-positive patients with p53 Arg/Arg have an increased risk of developing pre-cancerous lesions.	Arginine	19-27	P53	Homo sapiens	181-184
23124863-7	2013	In conclusion, p53 arginine homozygous was found to be increased in high-grade lesions, supporting the results of previous investigations indicating that HPV-positive patients with p53 Arg/Arg have an increased risk of developing pre-cancerous lesions.	Arginine	185-188	P53	Homo sapiens	15-18
23124863-7	2013	In conclusion, p53 arginine homozygous was found to be increased in high-grade lesions, supporting the results of previous investigations indicating that HPV-positive patients with p53 Arg/Arg have an increased risk of developing pre-cancerous lesions.	Arginine	185-188	P53	Homo sapiens	181-184
23124863-7	2013	In conclusion, p53 arginine homozygous was found to be increased in high-grade lesions, supporting the results of previous investigations indicating that HPV-positive patients with p53 Arg/Arg have an increased risk of developing pre-cancerous lesions.	Arginine	189-192	P53	Homo sapiens	15-18
23124863-7	2013	In conclusion, p53 arginine homozygous was found to be increased in high-grade lesions, supporting the results of previous investigations indicating that HPV-positive patients with p53 Arg/Arg have an increased risk of developing pre-cancerous lesions.	Arginine	189-192	P53	Homo sapiens	181-184
23124863-8	2013	In addition, T350G HPV 16 variant was over-represented in p53 Arg homozygous women with cervical lesions.	Arginine	62-65	P53	Homo sapiens	58-61
22803791-3	2013	We have previously obtained an evidence that amino acid substitutions in the p53 Zn(2+)-binding pocket can presumably exert an influence on Zn(2+) position in the Zn(2+)-p53 complex and thereby affect p53 binding to DNA.	Zinc	81-87	P53	Homo sapiens	77-80
22803791-3	2013	We have previously obtained an evidence that amino acid substitutions in the p53 Zn(2+)-binding pocket can presumably exert an influence on Zn(2+) position in the Zn(2+)-p53 complex and thereby affect p53 binding to DNA.	Zinc	81-87	P53	Homo sapiens	170-173
22803791-3	2013	We have previously obtained an evidence that amino acid substitutions in the p53 Zn(2+)-binding pocket can presumably exert an influence on Zn(2+) position in the Zn(2+)-p53 complex and thereby affect p53 binding to DNA.	Zinc	81-87	P53	Homo sapiens	170-173
22803791-3	2013	We have previously obtained an evidence that amino acid substitutions in the p53 Zn(2+)-binding pocket can presumably exert an influence on Zn(2+) position in the Zn(2+)-p53 complex and thereby affect p53 binding to DNA.	Zinc	81-83	P53	Homo sapiens	77-80
22803791-3	2013	We have previously obtained an evidence that amino acid substitutions in the p53 Zn(2+)-binding pocket can presumably exert an influence on Zn(2+) position in the Zn(2+)-p53 complex and thereby affect p53 binding to DNA.	Zinc	81-83	P53	Homo sapiens	170-173
22803791-3	2013	We have previously obtained an evidence that amino acid substitutions in the p53 Zn(2+)-binding pocket can presumably exert an influence on Zn(2+) position in the Zn(2+)-p53 complex and thereby affect p53 binding to DNA.	Zinc	81-83	P53	Homo sapiens	170-173
22803791-3	2013	We have previously obtained an evidence that amino acid substitutions in the p53 Zn(2+)-binding pocket can presumably exert an influence on Zn(2+) position in the Zn(2+)-p53 complex and thereby affect p53 binding to DNA.	Zinc	140-142	P53	Homo sapiens	77-80
22803791-3	2013	We have previously obtained an evidence that amino acid substitutions in the p53 Zn(2+)-binding pocket can presumably exert an influence on Zn(2+) position in the Zn(2+)-p53 complex and thereby affect p53 binding to DNA.	Zinc	140-142	P53	Homo sapiens	170-173
22803791-3	2013	We have previously obtained an evidence that amino acid substitutions in the p53 Zn(2+)-binding pocket can presumably exert an influence on Zn(2+) position in the Zn(2+)-p53 complex and thereby affect p53 binding to DNA.	Zinc	140-142	P53	Homo sapiens	170-173
22803791-4	2013	With these background considerations, our aim was to estimate the effect of the putative changes in the Zn(2+) position in its binding pocket due to the G245C and G245D substitutions on the conformation of the p53 DNA-binding motif.	Zinc	104-106	P53	Homo sapiens	210-213
22803791-6	2013	MD simulations demonstrated that (1) the two substitutions in the Zn(2+)-binding pocket caused changes in the conformation of the p53 DNA-binding motif, as compared with the wild-type (WT) p53; (2) binding of Zn(2+) to the p53 mutant forms reduced the effect of the substitutions on conformational change; and (3) Zn(2+) binding in the normal position compensated the effect of the mutations on the conformation in comparison to the altered Zn(2+) position.	Zinc	66-68	P53	Homo sapiens	130-133
22803791-6	2013	MD simulations demonstrated that (1) the two substitutions in the Zn(2+)-binding pocket caused changes in the conformation of the p53 DNA-binding motif, as compared with the wild-type (WT) p53; (2) binding of Zn(2+) to the p53 mutant forms reduced the effect of the substitutions on conformational change; and (3) Zn(2+) binding in the normal position compensated the effect of the mutations on the conformation in comparison to the altered Zn(2+) position.	Zinc	66-68	P53	Homo sapiens	189-192
22803791-6	2013	MD simulations demonstrated that (1) the two substitutions in the Zn(2+)-binding pocket caused changes in the conformation of the p53 DNA-binding motif, as compared with the wild-type (WT) p53; (2) binding of Zn(2+) to the p53 mutant forms reduced the effect of the substitutions on conformational change; and (3) Zn(2+) binding in the normal position compensated the effect of the mutations on the conformation in comparison to the altered Zn(2+) position.	Zinc	66-68	P53	Homo sapiens	189-192
22803791-6	2013	MD simulations demonstrated that (1) the two substitutions in the Zn(2+)-binding pocket caused changes in the conformation of the p53 DNA-binding motif, as compared with the wild-type (WT) p53; (2) binding of Zn(2+) to the p53 mutant forms reduced the effect of the substitutions on conformational change; and (3) Zn(2+) binding in the normal position compensated the effect of the mutations on the conformation in comparison to the altered Zn(2+) position.	Zinc	209-211	P53	Homo sapiens	130-133
22803791-6	2013	MD simulations demonstrated that (1) the two substitutions in the Zn(2+)-binding pocket caused changes in the conformation of the p53 DNA-binding motif, as compared with the wild-type (WT) p53; (2) binding of Zn(2+) to the p53 mutant forms reduced the effect of the substitutions on conformational change; and (3) Zn(2+) binding in the normal position compensated the effect of the mutations on the conformation in comparison to the altered Zn(2+) position.	Zinc	209-211	P53	Homo sapiens	130-133
22803791-6	2013	MD simulations demonstrated that (1) the two substitutions in the Zn(2+)-binding pocket caused changes in the conformation of the p53 DNA-binding motif, as compared with the wild-type (WT) p53; (2) binding of Zn(2+) to the p53 mutant forms reduced the effect of the substitutions on conformational change; and (3) Zn(2+) binding in the normal position compensated the effect of the mutations on the conformation in comparison to the altered Zn(2+) position.	Zinc	209-211	P53	Homo sapiens	130-133
23116945-2	2013	Chronic inflammatory processes share a common mechanism in which increased production of reactive oxygen species activates p53 and NF-kappaB signaling, leading to up-regulation of pro-inflammatory cytokine expression and impairment of glucose metabolism.	Reactive Oxygen Species	89-112	P53	Homo sapiens	123-126
23665932-12	2013	Taken together, the findings of the present study suggest that MSC partially induces p53-mediated apoptosis through ROS generation in human lung epithelial cells and this may have broader implications for our understanding of pulmonary diseases.	Reactive Oxygen Species	116-119	P53	Homo sapiens	85-88
23445829-0	2013	Variation in presentation and presence of DNA adducts and p53 mutations in patients with endemic nephropathy--an environmental form of the aristolochic acid nephropathy.	aristolochic acid I	139-156	P53	Homo sapiens	58-61
23677569-0	2013	Oligonucleotide suppression of bcl-2 in LNCaP cells is compensated by increased androgen sensitivity, p53 and oncogene activity, and suppressed caspase-3.	Oligonucleotides	0-15	P53	Homo sapiens	102-105
23441616-0	2013	Nobiletin induces apoptosis and potentiates the effects of the anticancer drug 5-fluorouracil in p53-mutated SNU-16 human gastric cancer cells.	Fluorouracil	79-93	P53	Homo sapiens	97-100
23065251-5	2013	We found that resveratrol treatment alone dose-dependently increased caspase-3 cleavage, as well as the levels of Bax, p53 and acetylated-p53.	Resveratrol	14-25	P53	Homo sapiens	119-122
23065251-5	2013	We found that resveratrol treatment alone dose-dependently increased caspase-3 cleavage, as well as the levels of Bax, p53 and acetylated-p53.	Resveratrol	14-25	P53	Homo sapiens	138-141
23441616-5	2013	The expression of p53 protein increased after treatment with 5-FU, but not nobiletin, whereas the expression of p21 (WAF1/CIP1)  protein increased after treatment with nobiletin, but not 5-FU.	Fluorouracil	61-65	P53	Homo sapiens	18-21
23530648-4	2013	The objective of the present study was to determine the effect of natural isothiocyanate (phenethyl isothiocyanate; PEITC) on different HSPs (27, 70, and 90) and HSF1 in 2 breast cancer cell lines, namely breast adenocarcinoma MCF-7 (with wild type p53) and highly metastatic breast cancer cell MDA-MB-231 (with mutated p53).	isothiocyanic acid	74-88	P53	Homo sapiens	249-252
23530648-4	2013	The objective of the present study was to determine the effect of natural isothiocyanate (phenethyl isothiocyanate; PEITC) on different HSPs (27, 70, and 90) and HSF1 in 2 breast cancer cell lines, namely breast adenocarcinoma MCF-7 (with wild type p53) and highly metastatic breast cancer cell MDA-MB-231 (with mutated p53).	isothiocyanic acid	74-88	P53	Homo sapiens	320-323
23441616-7	2013	The results of this study suggest the potential application of nobiletin to the enhancement of 5-FU efficiency in p53 mutant tumors.	Fluorouracil	95-99	P53	Homo sapiens	114-117
23117293-7	2013	Pre-treatment with curcumin at a low concentration of 2 micromol/l increased IR-induced G2/M arrest in the cell cycle and increased the expression of cyclin-dependent kinase inhibitors, p21cip1 and p53.	Curcumin	19-27	P53	Homo sapiens	198-201
23744428-5	2013	The levels of P21, P-P27 and P53/P-P53 reached their peaks 4 h after anisomycin treatment, presenting a positive correlation with anisomycin concentration, and P16, P-P21, P27, P57, P73/P-P73 and P-Rb changed little with the prolonged exposure time or increased concentrations of anisomycin.	Anisomycin	69-79	P53	Homo sapiens	29-32
23064281-7	2013	In addition, sequential or concomitant treatment of bortezomib and cisplatin             stimulated the expression of p53, hScrib and p21 and the stimulation was markedly             influenced by the order of drugs in HeLa cells.	Cisplatin	67-76	P53	Homo sapiens	118-121
24381593-3	2013	We hypothesized that synthetic lethality can be achieved in endometrial cancer cells with mutant p53 by combining paclitaxel with agents to overcome G2/M arrest and induce mitotic catastrophe.	Paclitaxel	114-124	P53	Homo sapiens	97-100
24381593-4	2013	The combination of BIBF1120, an investigational VEGFR, PDGFR, and FGFR multityrosine kinase inhibitor with established anti-angiogenic activity, with paclitaxel abrogated the G2/M checkpoint in p53-null endometrial cancer cells via modulation of G2/M checkpoint regulators followed by induction of mitotic cell death.	Paclitaxel	150-160	P53	Homo sapiens	194-197
24381593-5	2013	In endometrial cancer cells harboring an oncogenic gain-of-function p53 mutation, synthetic lethality was created by combining paclitaxel with BIBF1120 and a histone deacetylase inhibitor, which serves to destabilize mutant p53.	Paclitaxel	127-137	P53	Homo sapiens	68-71
24381593-5	2013	In endometrial cancer cells harboring an oncogenic gain-of-function p53 mutation, synthetic lethality was created by combining paclitaxel with BIBF1120 and a histone deacetylase inhibitor, which serves to destabilize mutant p53.	Paclitaxel	127-137	P53	Homo sapiens	224-227
23950593-10	2013	CONCLUSIONS: These results suggested that BDMC-induced ROS accumulation may contribute to its inhibitory effect on MCF-7 cell viability through regulation of p53/p21 and p16/Rb pathways.	ros	55-58	P53	Homo sapiens	158-161
24512730-1	2013	It has been reported that upregulated SIRT1 (NAD(+)-dependent class III histone deacetylase) deacetylates the p53 protein, represses its function, and allows for tumor cell growth in various cancers.	NAD	45-51	P53	Homo sapiens	110-113
23744428-5	2013	The levels of P21, P-P27 and P53/P-P53 reached their peaks 4 h after anisomycin treatment, presenting a positive correlation with anisomycin concentration, and P16, P-P21, P27, P57, P73/P-P73 and P-Rb changed little with the prolonged exposure time or increased concentrations of anisomycin.	Anisomycin	69-79	P53	Homo sapiens	35-38
23744428-5	2013	The levels of P21, P-P27 and P53/P-P53 reached their peaks 4 h after anisomycin treatment, presenting a positive correlation with anisomycin concentration, and P16, P-P21, P27, P57, P73/P-P73 and P-Rb changed little with the prolonged exposure time or increased concentrations of anisomycin.	Anisomycin	130-140	P53	Homo sapiens	29-32
23744428-5	2013	The levels of P21, P-P27 and P53/P-P53 reached their peaks 4 h after anisomycin treatment, presenting a positive correlation with anisomycin concentration, and P16, P-P21, P27, P57, P73/P-P73 and P-Rb changed little with the prolonged exposure time or increased concentrations of anisomycin.	Anisomycin	130-140	P53	Homo sapiens	35-38
23744428-5	2013	The levels of P21, P-P27 and P53/P-P53 reached their peaks 4 h after anisomycin treatment, presenting a positive correlation with anisomycin concentration, and P16, P-P21, P27, P57, P73/P-P73 and P-Rb changed little with the prolonged exposure time or increased concentrations of anisomycin.	Anisomycin	130-140	P53	Homo sapiens	29-32
23744428-5	2013	The levels of P21, P-P27 and P53/P-P53 reached their peaks 4 h after anisomycin treatment, presenting a positive correlation with anisomycin concentration, and P16, P-P21, P27, P57, P73/P-P73 and P-Rb changed little with the prolonged exposure time or increased concentrations of anisomycin.	Anisomycin	130-140	P53	Homo sapiens	35-38
23744428-9	2013	Furthermore, the level of P21 and P53 mRNA was increased with the enhanced concentrations of anisomycin.	Anisomycin	93-103	P53	Homo sapiens	34-37
23744428-10	2013	CONCLUSION: The results indicate that anisomycin may activate the P53/P21/P27 signaling to decrease the expression of ICBP90, inhibit expression of P-CDK2 to block the cells into S and G2/M phases, and finally result in proliferation inhibition of Jurkat T cells.	Anisomycin	38-48	P53	Homo sapiens	66-69
23469172-8	2013	Testing our method on models for the arginine catabolism and the negative feedback loop of the p53 signalling pathway, we found that it estimated the parameters with high accuracy and within a reasonable computation time compared to well-known approaches, including Particle Swarm Optimization, Nelder-Mead, and Firefly Algorithm.	Arginine	37-45	P53	Homo sapiens	95-98
23555949-0	2013	Zoledronic acid produces combinatory anti-tumor effects with cisplatin on mesothelioma by increasing p53 expression levels.	Cisplatin	61-70	P53	Homo sapiens	101-104
23555949-5	2013	ZOL-treated cells as well as CDDP-treated cells induced p53 phosphorylation at Ser 15, a marker of p53 activation, and up-regulated p53 protein expression levels.	Cisplatin	29-33	P53	Homo sapiens	56-59
23555949-5	2013	ZOL-treated cells as well as CDDP-treated cells induced p53 phosphorylation at Ser 15, a marker of p53 activation, and up-regulated p53 protein expression levels.	Cisplatin	29-33	P53	Homo sapiens	99-102
23555949-5	2013	ZOL-treated cells as well as CDDP-treated cells induced p53 phosphorylation at Ser 15, a marker of p53 activation, and up-regulated p53 protein expression levels.	Cisplatin	29-33	P53	Homo sapiens	99-102
23555949-5	2013	ZOL-treated cells as well as CDDP-treated cells induced p53 phosphorylation at Ser 15, a marker of p53 activation, and up-regulated p53 protein expression levels.	Serine	79-82	P53	Homo sapiens	56-59
23555949-6	2013	Down-regulation of p53 levels with siRNA however did not influence the ZOL-mediated cytotoxicity but negated the combinatory effects by ZOL and CDDP.	Cisplatin	144-148	P53	Homo sapiens	19-22
22862424-0	2013	The p53-dependent expression of frataxin controls 5-aminolevulinic acid-induced accumulation of protoporphyrin IX and photo-damage in cancerous cells.	protoporphyrin IX	96-113	P53	Homo sapiens	4-7
22862424-5	2013	Thus, the decrease of the expression of frataxin unregulated by p53 in tumor cells enhances ALA-induced photo-damage, by down-regulation of mitochondrial functions.	Alanine	92-95	P53	Homo sapiens	64-67
23555731-1	2013	The transactivation domain (TAD) of tumor suppressor p53 can bind with the nuclear coactivator binding domain (NCBD) of cyclic-AMP response element binding protein (CBP) and activate transcription.	Cyclic AMP	120-130	P53	Homo sapiens	53-56
23469203-4	2013	We identified resveratrol as a regulator of MTA1/NuRD complex and re-activator of p53 acetylation in prostate cancer (PCa).	Resveratrol	14-25	P53	Homo sapiens	82-85
23469203-5	2013	In the current study, we addressed whether resveratrol analogues also possess the ability to inhibit MTA1 and to reverse p53 deacetylation.	Resveratrol	43-54	P53	Homo sapiens	121-124
23468845-0	2013	Prediction of P53 mutants (multiple sites) transcriptional activity based on structural (2D&amp;3D) properties.	Adenosine Monophosphate	92-95	P53	Homo sapiens	14-17
23451128-6	2013	An up-regulated expression of CDK inhibitor p21 along with suppressed expression of mutated p53 was observed in MDA-MB-231 cells treated with alpha-santalol.	a-santalol	142-156	P53	Homo sapiens	92-95
23405080-5	2013	Cd also increased intracellular reactive oxygen species (ROS) generation and malondialdehyde (MDA) production and induced mitochondrial dysfunction (the loss of mitochondrial membrane potential (MMP) and the increase of cytosolic cytochrome c release), the decreased Bcl-2 expression, increased p53 expression, poly (ADP-ribose) polymerase (PARP) cleavage, and caspase cascades, which accompanied with intracellular Cd accumulation.	Cadmium	0-2	P53	Homo sapiens	295-298
23308284-4	2013	Data derived from experiments in colon cancer cells indicate that Cl-amidine causes a G1 arrest, and that this was p53-dependent.	N-alpha-benzoyl-N5-(2-chloro-1-iminoethyl)-L-ornithine amide	66-76	P53	Homo sapiens	115-118
23359652-8	2013	In cells expressing wild-type p53 (OV2008 and C13*), SB225002 increased total and phospho-Ser p53 levels, and p53 knock-down decreased SB225002-induced apoptosis, without affecting premature mitosis.	Serine	90-93	P53	Homo sapiens	30-33
23308284-5	2013	In a separate set of experiments, we found that Cl-amidine caused a significant increase in microRNA-16 (miRNA-16), and that this increase was also p53-dependent.	N-alpha-benzoyl-N5-(2-chloro-1-iminoethyl)-L-ornithine amide	48-58	P53	Homo sapiens	148-151
23200181-6	2013	Furthermore, the expression of p53, Fas, Bax and activated caspase-3 protein was significantly upregulated in cells treated with HMME-SDT and DOX, whereas Bcl-2 protein was downregulated.	Doxorubicin	142-145	P53	Homo sapiens	31-34
23534290-5	2013	Thus, in ATC cells the ionizing radiation and Ptx exhibited competitive effects upon phosphorylation of cell cycle controllers: p53, pRb, CHK2, cAbl and expression of Bax.	Paclitaxel	46-49	P53	Homo sapiens	128-131
22178897-6	2012	The first is that of ROS producer linked to p53 induced apoptosis.	Reactive Oxygen Species	21-24	P53	Homo sapiens	44-47
22982566-4	2012	However, hypoxia further increased the susceptibility of mutant p53 breast cancer SKBR3 cells to lower PRIMA-1 levels, possibly through oxidative stress since this was counteracted by N-acetylcysteine.	Acetylcysteine	184-200	P53	Homo sapiens	64-67
22885806-1	2012	We have examined the relationship between chemotherapy-induced mitotic catastrophe and cell death by apoptosis in both wild-type and p53(-/-) HCT116 human colon carcinoma cells treated with nanomolar concentrations of paclitaxel (PTX), a drug that acts on tubulin altering the normal development of mitosis.	Paclitaxel	218-228	P53	Homo sapiens	133-136
22885806-3	2012	In the presence of PTX, the percentage of polyploid cells observed was higher in p53-deficient cells, indicating that mitotic slippage was favored compared to wild-type cells, with the presence of large multinucleate cells.	Paclitaxel	19-22	P53	Homo sapiens	81-84
22885806-5	2012	Lack of p53 facilitated endoreduplication and polyploidy in PTX-treated cells, but cells were still killed with similar efficacy through the same apoptotic-like mechanism in the absence of caspase activity.	Paclitaxel	60-63	P53	Homo sapiens	8-11
23151607-0	2012	Efficient synthesis of RITA and its analogues: derivation of analogues with improved antiproliferative activity via modulation of p53/miR-34a pathway.	RITA	23-27	P53	Homo sapiens	130-133
23652223-9	2012	Cadmium has also been shown to replace Zn in the tumor suppressor protein, p53 thereby impairing p53"s DNA binding activity and associated repair processes.	Cadmium	0-7	P53	Homo sapiens	75-78
23652223-9	2012	Cadmium has also been shown to replace Zn in the tumor suppressor protein, p53 thereby impairing p53"s DNA binding activity and associated repair processes.	Cadmium	0-7	P53	Homo sapiens	97-100
23652223-9	2012	Cadmium has also been shown to replace Zn in the tumor suppressor protein, p53 thereby impairing p53"s DNA binding activity and associated repair processes.	Zinc	39-41	P53	Homo sapiens	75-78
23652223-9	2012	Cadmium has also been shown to replace Zn in the tumor suppressor protein, p53 thereby impairing p53"s DNA binding activity and associated repair processes.	Zinc	39-41	P53	Homo sapiens	97-100
23652223-10	2012	The expression of the p53 protein is significantly depressed by cadmium.	Cadmium	64-71	P53	Homo sapiens	22-25
22559194-3	2012	Under low levels of reactive oxygen species (ROS), "normal" amounts of p53 upregulates expression of antioxidant genes, protecting macromolecules from ROS-induced damage.	Reactive Oxygen Species	20-43	P53	Homo sapiens	71-74
22559194-3	2012	Under low levels of reactive oxygen species (ROS), "normal" amounts of p53 upregulates expression of antioxidant genes, protecting macromolecules from ROS-induced damage.	Reactive Oxygen Species	45-48	P53	Homo sapiens	71-74
22559194-3	2012	Under low levels of reactive oxygen species (ROS), "normal" amounts of p53 upregulates expression of antioxidant genes, protecting macromolecules from ROS-induced damage.	Reactive Oxygen Species	151-154	P53	Homo sapiens	71-74
22559194-4	2012	However, at high levels or extended exposure of ROS, p53 expression is enhanced, activating pro-oxidant genes and resulting in p53-dependent apoptosis.	Reactive Oxygen Species	48-51	P53	Homo sapiens	53-56
22559194-4	2012	However, at high levels or extended exposure of ROS, p53 expression is enhanced, activating pro-oxidant genes and resulting in p53-dependent apoptosis.	Reactive Oxygen Species	48-51	P53	Homo sapiens	127-130
23165211-7	2012	Downregulation of p53 with siRNA lowered cisplatin-induced apoptosis in Tera and Tera-CP, which was associated with a diminished Fas membrane expression.	Cisplatin	41-50	P53	Homo sapiens	18-21
23165211-0	2012	Pro- and anti-apoptotic effects of p53 in cisplatin-treated human testicular cancer are cell context-dependent.	Cisplatin	42-51	P53	Homo sapiens	35-38
23165211-8	2012	In contrast, p53 suppression augmented cisplatin-induced apoptosis in Scha and 2102EP and concomitantly strongly suppressed MDM2 and p21 mRNA and protein expression.	Cisplatin	39-48	P53	Homo sapiens	13-16
23165211-3	2012	We analyzed functionality of wild-type p53 in cisplatin sensitivity in the human TC setting using a p53 short interfering (si)RNA approach.	Cisplatin	46-55	P53	Homo sapiens	39-42
23165211-9	2012	Our results indicate that p53 is involved in transactivation of pro- and anti-apoptotic genes in untreated and cisplatin-treated TC cells, but subtle differences are present between TC cell lines.	Cisplatin	111-120	P53	Homo sapiens	26-29
23165211-6	2012	Following cisplatin exposure, expression levels of p53 increased, with a subsequent increase in MDM2 and p21 mRNA and protein levels and Fas cell membrane levels.	Cisplatin	10-19	P53	Homo sapiens	51-54
23165211-10	2012	The opposite role of p53 in cisplatin-induced apoptosis among TC cell lines demonstrates the importance of the cellular context for the p53 transactivation phenotype in TC cells.	Cisplatin	28-37	P53	Homo sapiens	21-24
23165211-10	2012	The opposite role of p53 in cisplatin-induced apoptosis among TC cell lines demonstrates the importance of the cellular context for the p53 transactivation phenotype in TC cells.	Cisplatin	28-37	P53	Homo sapiens	136-139
23235459-4	2012	In this study, we showed that under DNA damage conditions induced by chemotherapeutic drugs, gamma irradiation and hydrogen peroxide, p53 upregulates a novel protein, proline-rich acidic protein 1 (PRAP1).	Hydrogen Peroxide	115-132	P53	Homo sapiens	134-137
23137536-9	2012	Therefore, the present results show that miR-186, miR-216b, miR-337-3p, and miR-760 cooperatively promote cellular senescence through the p53-p21(Cip1/WAF1) pathway by CKII downregulation-mediated ROS production in HCT116 cells.	Reactive Oxygen Species	197-200	P53	Homo sapiens	138-141
23235459-6	2012	The induction of PRAP1 expression by p53 may promote resistance of cancer cells to chemotherapeutic drugs such as 5-fluorouracil (5-FU), as knockdown of PRAP1 increases apoptosis in cancer cells after 5-FU treatment.	Fluorouracil	114-128	P53	Homo sapiens	37-40
23235459-6	2012	The induction of PRAP1 expression by p53 may promote resistance of cancer cells to chemotherapeutic drugs such as 5-fluorouracil (5-FU), as knockdown of PRAP1 increases apoptosis in cancer cells after 5-FU treatment.	Fluorouracil	130-134	P53	Homo sapiens	37-40
23235459-6	2012	The induction of PRAP1 expression by p53 may promote resistance of cancer cells to chemotherapeutic drugs such as 5-fluorouracil (5-FU), as knockdown of PRAP1 increases apoptosis in cancer cells after 5-FU treatment.	Fluorouracil	201-205	P53	Homo sapiens	37-40
22286760-3	2012	The MTA1 promoter contains two putative p53 response elements (p53REs), which were repressed by the p53-inducing drug 5-fluorouracil (5-FU).	Fluorouracil	118-132	P53	Homo sapiens	40-43
23185017-1	2012	The p53-inducible protein TIGAR (Tp53-induced Glycolysis and Apoptosis Regulator) functions as a fructose-2,6-bisphosphatase (Fru-2,6-BPase), and through promotion of the pentose phosphate pathway, increases NADPH production to help limit reactive oxygen species (ROS).	Reactive Oxygen Species	239-262	P53	Homo sapiens	4-7
23185017-1	2012	The p53-inducible protein TIGAR (Tp53-induced Glycolysis and Apoptosis Regulator) functions as a fructose-2,6-bisphosphatase (Fru-2,6-BPase), and through promotion of the pentose phosphate pathway, increases NADPH production to help limit reactive oxygen species (ROS).	Reactive Oxygen Species	264-267	P53	Homo sapiens	4-7
22286760-3	2012	The MTA1 promoter contains two putative p53 response elements (p53REs), which were repressed by the p53-inducing drug 5-fluorouracil (5-FU).	Fluorouracil	118-132	P53	Homo sapiens	63-66
22286760-3	2012	The MTA1 promoter contains two putative p53 response elements (p53REs), which were repressed by the p53-inducing drug 5-fluorouracil (5-FU).	Fluorouracil	134-138	P53	Homo sapiens	40-43
22286760-3	2012	The MTA1 promoter contains two putative p53 response elements (p53REs), which were repressed by the p53-inducing drug 5-fluorouracil (5-FU).	Fluorouracil	134-138	P53	Homo sapiens	63-66
22286760-4	2012	Notably, 5-FU treatment decreased MTA1 expression only in p53 wild-type cells.	Fluorouracil	9-13	P53	Homo sapiens	58-61
22286760-5	2012	p53 and histone deacetylases 1/2 were recruited, and acetylation of H3K9 was decreased on the promoter region including the p53REs after 5-FU treatment.	Fluorouracil	137-141	P53	Homo sapiens	0-3
23177934-6	2012	PYGL depletion and the consequent glycogen accumulation led to increased reactive oxygen species (ROS) levels that contributed to a p53-dependent induction of senescence and markedly impaired tumorigenesis in vivo.	Reactive Oxygen Species	73-96	P53	Homo sapiens	132-135
22286760-5	2012	p53 and histone deacetylases 1/2 were recruited, and acetylation of H3K9 was decreased on the promoter region including the p53REs after 5-FU treatment.	Fluorouracil	137-141	P53	Homo sapiens	124-127
23177934-6	2012	PYGL depletion and the consequent glycogen accumulation led to increased reactive oxygen species (ROS) levels that contributed to a p53-dependent induction of senescence and markedly impaired tumorigenesis in vivo.	Reactive Oxygen Species	98-101	P53	Homo sapiens	132-135
22843228-0	2012	Folic acid inhibits endothelial cell proliferation through activating the cSrc/ERK 2/NF-kappaB/p53 pathway mediated by folic acid receptor.	Folic Acid	0-10	P53	Homo sapiens	95-98
22750268-3	2012	In the present work, we focused on reviewing the current knowledge about the dysregulation of the proteins/enzymes involved in the key regulatory steps of glucose transport, glycolysis, TCA cycle and glutaminolysis by several oncogenes including c-Myc and hypoxia inducible factor-1 (HIF-1) and tumor suppressor, p53, in cancer cells.	Glucose	155-162	P53	Homo sapiens	313-316
22790872-3	2012	Our analysis of genome-wide chromatin occupancy by p53 using chromatin immunoprecipitation (ChIP)-seq revealed "p53 default program", that is, the pattern of major p53-bound sites that is similar upon p53 activation by nutlin3a, reactivation of p53 and induction of tumor cell apoptosis (RITA) or 5-fluorouracil in breast cancer cells, despite different biological outcomes.	Fluorouracil	297-311	P53	Homo sapiens	51-54
22634494-0	2012	The p53-reactivating small-molecule RITA enhances cisplatin-induced cytotoxicity and apoptosis in head and neck cancer.	Cisplatin	50-59	P53	Homo sapiens	4-7
22634494-1	2012	We evaluated whether the restoration of p53 function by the p53-reactivating small molecule RITA (reactivation of p53 and induction of tumor cell apoptosis enhances cisplatin-induced cytotoxicity and apoptosis in head-and-neck cancer (HNC).	Cisplatin	165-174	P53	Homo sapiens	40-43
22634494-1	2012	We evaluated whether the restoration of p53 function by the p53-reactivating small molecule RITA (reactivation of p53 and induction of tumor cell apoptosis enhances cisplatin-induced cytotoxicity and apoptosis in head-and-neck cancer (HNC).	Cisplatin	165-174	P53	Homo sapiens	60-63
22634494-1	2012	We evaluated whether the restoration of p53 function by the p53-reactivating small molecule RITA (reactivation of p53 and induction of tumor cell apoptosis enhances cisplatin-induced cytotoxicity and apoptosis in head-and-neck cancer (HNC).	Cisplatin	165-174	P53	Homo sapiens	60-63
22634494-4	2012	RITA promoted apoptosis in association with upregulation of p21, BAX, and cleaved caspase-3; notably, the apoptotic response was blocked by pifithrin-alpha, demonstrating its p53 dependence.	RITA	0-4	P53	Homo sapiens	175-178
22634494-7	2012	Our data suggest that the restoration of p53 tumor-suppressive function by RITA enhances the cytotoxicity and apoptosis of cisplatin, an action that may offer an attractive strategy for treating HNC.	RITA	75-79	P53	Homo sapiens	41-44
22634494-7	2012	Our data suggest that the restoration of p53 tumor-suppressive function by RITA enhances the cytotoxicity and apoptosis of cisplatin, an action that may offer an attractive strategy for treating HNC.	Cisplatin	123-132	P53	Homo sapiens	41-44
23682426-11	2012	We also found that berberine-induced apoptosis was associated with an upregulated expressions of p53 and prohibitin (PHB), and decreased vimentin expression.	Berberine	19-28	P53	Homo sapiens	97-100
22790872-3	2012	Our analysis of genome-wide chromatin occupancy by p53 using chromatin immunoprecipitation (ChIP)-seq revealed "p53 default program", that is, the pattern of major p53-bound sites that is similar upon p53 activation by nutlin3a, reactivation of p53 and induction of tumor cell apoptosis (RITA) or 5-fluorouracil in breast cancer cells, despite different biological outcomes.	Fluorouracil	297-311	P53	Homo sapiens	112-115
22790872-3	2012	Our analysis of genome-wide chromatin occupancy by p53 using chromatin immunoprecipitation (ChIP)-seq revealed "p53 default program", that is, the pattern of major p53-bound sites that is similar upon p53 activation by nutlin3a, reactivation of p53 and induction of tumor cell apoptosis (RITA) or 5-fluorouracil in breast cancer cells, despite different biological outcomes.	Fluorouracil	297-311	P53	Homo sapiens	112-115
22790872-3	2012	Our analysis of genome-wide chromatin occupancy by p53 using chromatin immunoprecipitation (ChIP)-seq revealed "p53 default program", that is, the pattern of major p53-bound sites that is similar upon p53 activation by nutlin3a, reactivation of p53 and induction of tumor cell apoptosis (RITA) or 5-fluorouracil in breast cancer cells, despite different biological outcomes.	Fluorouracil	297-311	P53	Homo sapiens	112-115
22790872-3	2012	Our analysis of genome-wide chromatin occupancy by p53 using chromatin immunoprecipitation (ChIP)-seq revealed "p53 default program", that is, the pattern of major p53-bound sites that is similar upon p53 activation by nutlin3a, reactivation of p53 and induction of tumor cell apoptosis (RITA) or 5-fluorouracil in breast cancer cells, despite different biological outcomes.	Fluorouracil	297-311	P53	Homo sapiens	112-115
22640875-10	2012	METHODS: To analyze DNA in complex with p53, we incorporated (125)I-dCTP in two different positions of synthetic duplexes containing the consensus p53-binding site.	2'-deoxycytidine 5'-triphosphate	68-72	P53	Homo sapiens	40-43
23151455-0	2012	Dietary downregulation of mutant p53 levels via glucose restriction: mechanisms and implications for tumor therapy.	Glucose	48-55	P53	Homo sapiens	33-36
23151455-3	2012	We report here that glucose restriction (GR) induces p53 mutant deacetylation, routing it for degradation via autophagy.	Glucose	20-27	P53	Homo sapiens	53-56
23151455-5	2012	Furthermore, we found that a carbohydrate-free dietetic regimen that lowers the fasting glucose levels blunts p53 mutant expression and oncogenic activity relative to a normal diet in several animal model systems.	Carbohydrates	29-41	P53	Homo sapiens	110-113
23151455-5	2012	Furthermore, we found that a carbohydrate-free dietetic regimen that lowers the fasting glucose levels blunts p53 mutant expression and oncogenic activity relative to a normal diet in several animal model systems.	Glucose	88-95	P53	Homo sapiens	110-113
23151455-6	2012	These findings indicate that the stability of mutant forms of p53 is influenced by the levels of glucose and by dietetic habits.	Glucose	97-104	P53	Homo sapiens	62-65
22270257-10	2012	Conversely potency of PP242 and the combination index for PP242 + irinotecan were unrelated, but synergy exists across all dose levels in PP242 and irinotecan sensitive, p53 wild-type cell lines.	Irinotecan	148-158	P53	Homo sapiens	170-173
22944355-0	2012	Determination of cellular uptake and intracellular levels of Cenersen (Aezea( ), EL625), a p53 antisense oligonucleotide in acute myeloid leukemia cells.	Oligonucleotides	105-120	P53	Homo sapiens	91-94
23053979-0	2012	p53 Codon 72 arginine/proline polymorphism and cancer in Sudan.	Arginine	13-21	P53	Homo sapiens	0-3
23053979-1	2012	The aim of this report is to determine frequencies and associations of p53 codon 72 arg/pro polymorphism with different types of cancer in Sudan.	Arginine	84-87	P53	Homo sapiens	71-74
23053979-2	2012	p53 codon72 arg/pro polymorphism distribution and allele frequencies in 264 samples of different types of cancers were investigated using PCR.	Arginine	12-15	P53	Homo sapiens	0-3
23053979-8	2012	We concluded that p53 arg/pro polymorphism has different pattern of frequency in different types of cancer among Sudanese patients, indicating perhaps different etiology and biology of these tumours.	Arginine	22-25	P53	Homo sapiens	18-21
22910273-3	2012	We explored synergistic efficacy of a low dose of curcumin (CCM) and a low dose of paclitaxel (PTX) in HBTSC and human glioblastoma LN18 (p53 mutant and PTEN proficient) and U138MG (p53 mutant and PTEN mutant) cells.	Curcumin	50-58	P53	Homo sapiens	138-141
23023313-3	2012	In this study, we used MCF-7 and MDA-MB-231 human breast carcinoma cells which             have different estrogen receptor (ER) and tumor suppressor p53 statuses to examine             the mechanisms of taxol-induced growth inhibition and apoptosis.	Paclitaxel	204-209	P53	Homo sapiens	150-153
22886373-9	2012	In summary, the present study provides experimental evidence that Cr(VI) leads to energy metabolism disturbance and p53-dependent cell cycle arrest via ROS in L-02 hepatocytes.	Reactive Oxygen Species	152-155	P53	Homo sapiens	116-119
22886373-0	2012	Hexavalent chromium induces energy metabolism disturbance and p53-dependent cell cycle arrest via reactive oxygen species in L-02 hepatocytes.	Reactive Oxygen Species	98-121	P53	Homo sapiens	62-65
22886373-8	2012	ROS-mediated p53 activation was found to involve in Cr(VI)-induced cell cycle arrest, and p53 inhibitor Pifithrin-alpha (PFT-alpha) rescued Cr(VI)-induced reduction of check point proteins Mrc1 and BubR1, thus inhibiting cell cycle arrest.	Reactive Oxygen Species	0-3	P53	Homo sapiens	13-16
23023313-9	2012	These findings             suggest that taxol-induced G2/M arrest and apoptosis in human breast carcinoma             cells is mediated through the ER- and p53-independent upregulation of p21.	Paclitaxel	40-45	P53	Homo sapiens	156-159
23192191-2	2012	In this work, the interactions of two selected pyrene derivatives (1-OHP and 1-PBO) and human tumor-related DNA (p53 DNA and C-myc DNA) are investigated by spectroscopic and non-native polyacrylamide gel electrophoresis (PAGE) methods.	pyrene	47-53	P53	Homo sapiens	113-116
22954457-2	2012	When DNA is damaged, phosphorylation of p53 at its Ser 15 residue induces p53R2 production.	Serine	51-54	P53	Homo sapiens	40-43
23131771-7	2012	Interestingly, in the presence of calcium ions Annexin A2 showed increased binding with p53 IRES.	Calcium	34-41	P53	Homo sapiens	88-91
23257465-5	2012	The roles of p53-p21 and p16-Rb pathways can induce hematopoietic dysfunction and lead to ROS-induced HSC senescence.	Reactive Oxygen Species	90-93	P53	Homo sapiens	13-16
23192191-2	2012	In this work, the interactions of two selected pyrene derivatives (1-OHP and 1-PBO) and human tumor-related DNA (p53 DNA and C-myc DNA) are investigated by spectroscopic and non-native polyacrylamide gel electrophoresis (PAGE) methods.	1-pbo	77-82	P53	Homo sapiens	113-116
23351311-0	2012	Genistein abrogates G2 arrest induced by curcumin in p53 deficient T47D cells.	Curcumin	41-49	P53	Homo sapiens	53-56
23351311-10	2012	RESULTS: In this study curcumin induced G2 arrest on p53 deficient T47D cells at the concentration of 10 muM.	Curcumin	23-31	P53	Homo sapiens	53-56
23036742-8	2012	These results suggest that phycocyanin might suppress d-galactose-induced hLEC apoptosis through two pathways: mitochondrial pathway, involving p53 and Bcl-2 family protein expression, and unfolded protein response pathway, involving GRP78 and CHOP expression.	Galactose	54-65	P53	Homo sapiens	144-147
23192191-6	2012	Besides, the binding of pyrene derivatives to p53 DNA is stronger than that for C-myc DNA.	pyrene	24-30	P53	Homo sapiens	46-49
23203124-8	2012	This impairment of p53 suppressed the hydrogen peroxide-induced apoptotic response in hepatocytes.	Hydrogen Peroxide	38-55	P53	Homo sapiens	19-22
22868134-0	2012	Suillus collinitus methanolic extract increases p53 expression and causes cell cycle arrest and apoptosis in a breast cancer cell line.	methanolic	19-29	P53	Homo sapiens	48-51
22868134-9	2012	Particularly, its methanolic extract appears to have a p53-mediated effect on the normal cell cycle distribution and apoptosis induction in a human breast tumor cell line.	methanolic	18-28	P53	Homo sapiens	55-58
22962266-5	2012	Unexpectedly, when CAFs were analyzed, p53 accumulation and induction of p21 was observed only in tumors with constitutively low p53 protein and accumulation upon cisplatin treatment.	Cisplatin	163-172	P53	Homo sapiens	39-42
23046248-3	2012	The nanomolar inhibitor 5 possessed good p53-MDM2 inhibitory activity (K(i) = 780 nM) due to its hydrophobic and hydrogen bonding interactions with MDM2.	Hydrogen	113-121	P53	Homo sapiens	41-44
22962266-0	2012	Cancer cells cue the p53 response of cancer-associated fibroblasts to cisplatin.	Cisplatin	70-79	P53	Homo sapiens	21-24
22899716-5	2012	Herein, we examine the effect of p53(R273H), a commonly occurring mutated p53 form, on the expression of phase 2 ROS-detoxifying enzymes and on the ability of cells to readopt a reducing environment after exposure to oxidative stress.	Reactive Oxygen Species	113-116	P53	Homo sapiens	33-36
22899716-5	2012	Herein, we examine the effect of p53(R273H), a commonly occurring mutated p53 form, on the expression of phase 2 ROS-detoxifying enzymes and on the ability of cells to readopt a reducing environment after exposure to oxidative stress.	Reactive Oxygen Species	113-116	P53	Homo sapiens	74-77
22899716-8	2012	This effect of mutant p53 is manifested by decreased expression of phase 2 detoxifying enzymes NQO1 and HO-1 and high ROS levels.	Reactive Oxygen Species	118-121	P53	Homo sapiens	22-25
22955915-1	2012	TP53 mutation is an independent marker of poor prognosis in patients with diffuse large B-cell lymphoma (DLBCL) treated with cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone (CHOP) therapy.	Doxorubicin	143-162	P53	Homo sapiens	0-4
23079576-6	2012	RESULTS: The most strongly differentially enriched pathways between breast cancers stratified by TP53 mutation status include in addition to TP53 signalling, several known cancer pathways involved in renal, prostate, pancreatic, colorectal, lung and other cancers, and signalling pathways such as calcium signalling, MAPK, ERBB and vascular endothelial growth factor (VEGF) signalling pathways.	Calcium	297-304	P53	Homo sapiens	97-101
22583696-9	2012	Since H4 and p53 both contain the target lysine in an unstructured part of the protein, we conclude that the long recognition sequence of SET8 makes it difficult to methylate a lysine in a folded region of a protein, because amino acid side chains essential for recognition will be buried.	Lysine	41-47	P53	Homo sapiens	13-16
23163657-1	2012	Artemis phosphorylation at serine 516 (Ser516) has important regulatory functions in the repair of radiation-induced DNA damage, V(D)J recombination, p53-dependent apoptosis and cell cycle control.	Serine	27-33	P53	Homo sapiens	150-153
22892830-1	2012	The Arg and Pro variants in p53 codon 72 were shown to have different regulation properties of p53-dependent DNA repair target genes that can affect various levels of cytogenetic aberrations in chronic hepatitis B patients.	Arginine	4-7	P53	Homo sapiens	28-31
22892830-1	2012	The Arg and Pro variants in p53 codon 72 were shown to have different regulation properties of p53-dependent DNA repair target genes that can affect various levels of cytogenetic aberrations in chronic hepatitis B patients.	Arginine	4-7	P53	Homo sapiens	95-98
22750558-9	2012	p53 knock-down abrogated H(2)O(2)-induced premature senescence of vector control- and IkappaBalphaSR-expressing HDFs functionally linking canonical NF-kappaB-dependent control of p53 levels to ROS-induced HDF senescence.	Hydrogen Peroxide	25-33	P53	Homo sapiens	0-3
22750558-9	2012	p53 knock-down abrogated H(2)O(2)-induced premature senescence of vector control- and IkappaBalphaSR-expressing HDFs functionally linking canonical NF-kappaB-dependent control of p53 levels to ROS-induced HDF senescence.	Hydrogen Peroxide	25-33	P53	Homo sapiens	179-182
22750558-9	2012	p53 knock-down abrogated H(2)O(2)-induced premature senescence of vector control- and IkappaBalphaSR-expressing HDFs functionally linking canonical NF-kappaB-dependent control of p53 levels to ROS-induced HDF senescence.	Reactive Oxygen Species	193-196	P53	Homo sapiens	0-3
22610972-7	2012	Finally, phosphorylation of TAX1BP2 at serine-763 by cyclin-dependent kinase (CDK)2 abolished the TAX1BP2-mediated p38 activation and tumor-suppressive activity, indicating that TAX1BP2 can adapt CDK2 signaling to the p38/p53/p21 pathway.	Serine	39-45	P53	Homo sapiens	222-225
22576474-0	2012	Variant 1 of KIAA0101, overexpressed in hepatocellular carcinoma, prevents doxorubicin-induced apoptosis by inhibiting p53 activation.	Doxorubicin	75-86	P53	Homo sapiens	119-122
22576474-4	2012	Semiquantitative RT-PCR, real-time quantitative RT-PCR, and western blot analysis demonstrated that doxorubicin (Adriamycin, ADR) treatment down-regulated expression of the KIAA0101 tv1, whereas it increased the acetylation of the p53 protein.	Doxorubicin	100-111	P53	Homo sapiens	231-234
22576474-4	2012	Semiquantitative RT-PCR, real-time quantitative RT-PCR, and western blot analysis demonstrated that doxorubicin (Adriamycin, ADR) treatment down-regulated expression of the KIAA0101 tv1, whereas it increased the acetylation of the p53 protein.	Doxorubicin	113-123	P53	Homo sapiens	231-234
22951418-7	2012	Inactivation of p53 impairs aerobic mitochondrial functions and causes greater dependence on anaerobic glycolysis, elevates lactate levels, reduces mitochondrial density in skeletal muscle and reduces endurance during physical exercise.	Lactic Acid	124-131	P53	Homo sapiens	16-19
23146670-5	2012	Whereas doxorubicin treatment in early-passaged cells results in nucleosome density changes near the p53 binding sites of the p21 promoter, our studies show that senescent cells with a high p21 transcription activity had a comparable nucleosome distribution as unstressed young cells.	Doxorubicin	8-19	P53	Homo sapiens	101-104
22454142-8	2012	NS-cultured cells exposed to H(2)O(2) showed significantly reduced cell viability (~50 %), increased p53 and caspase-3, and DNA fragmentation, without affecting ADNP expression.	Hydrogen Peroxide	29-37	P53	Homo sapiens	101-104
22951418-8	2012	Lowered p53 and increased NF-kappaB are associated with elevated reactive oxygen species.	Reactive Oxygen Species	65-88	P53	Homo sapiens	8-11
23077249-6	2012	Interestingly, both ER agonists such as estradiol and the selective ER modulator (SERM) tamoxifen promote p53 antagonism.	Estradiol	40-49	P53	Homo sapiens	106-109
23077249-6	2012	Interestingly, both ER agonists such as estradiol and the selective ER modulator (SERM) tamoxifen promote p53 antagonism.	Tamoxifen	88-97	P53	Homo sapiens	106-109
23086311-6	2012	To investigate the gene and drug co-delivery property, p53 expression plasmid and doxorubicin hydrochloride (DOX) were loaded in CaCO(3)-KALA-p53-DOX nanoparticles.	Doxorubicin	82-107	P53	Homo sapiens	142-145
22892142-6	2012	p53-dependent enhancement of ascorbate cytotoxicity is caused by increased reactive oxygen species generation via a differentially regulated p53 transcriptional network.	Reactive Oxygen Species	75-98	P53	Homo sapiens	0-3
23086311-6	2012	To investigate the gene and drug co-delivery property, p53 expression plasmid and doxorubicin hydrochloride (DOX) were loaded in CaCO(3)-KALA-p53-DOX nanoparticles.	Doxorubicin	146-149	P53	Homo sapiens	55-58
23086311-6	2012	To investigate the gene and drug co-delivery property, p53 expression plasmid and doxorubicin hydrochloride (DOX) were loaded in CaCO(3)-KALA-p53-DOX nanoparticles.	Doxorubicin	146-149	P53	Homo sapiens	142-145
23086311-7	2012	The in vitro cell growth inhibition effect of CaCO(3)-KALA-p53-DOX nanoparticles was evaluated by MTT assay.	Doxorubicin	63-66	P53	Homo sapiens	59-62
23086311-8	2012	Compared with CaCO(3)-p53-DOX nanoparticles, CaCO(3)-KALA-p53-DOX nanoparticles exhibited enhanced delivery efficiency, which led to a stronger inhibition effect on HeLa cells.	Doxorubicin	26-29	P53	Homo sapiens	22-25
23086311-8	2012	Compared with CaCO(3)-p53-DOX nanoparticles, CaCO(3)-KALA-p53-DOX nanoparticles exhibited enhanced delivery efficiency, which led to a stronger inhibition effect on HeLa cells.	Doxorubicin	26-29	P53	Homo sapiens	58-61
23086311-8	2012	Compared with CaCO(3)-p53-DOX nanoparticles, CaCO(3)-KALA-p53-DOX nanoparticles exhibited enhanced delivery efficiency, which led to a stronger inhibition effect on HeLa cells.	Doxorubicin	62-65	P53	Homo sapiens	58-61
22981564-7	2012	The encapsulation efficiency of Dox was significantly higher when it was encapsulated alone compared to co-encapsulation with chi-p53 nanoparticles.	Doxorubicin	32-35	P53	Homo sapiens	130-133
22951905-1	2012	Tumor protein (TP)-p53 family members (TP63, TP63 and TP73) are guardians of the genome and key players in orchestrating the cellular response to cisplatin treatment.	Cisplatin	146-155	P53	Homo sapiens	19-22
23095216-2	2012	Previous work from our group and that of others suggests that one mechanism underlying these changes is alteration of cell proliferation, apoptosis, and DNA-repair in neural stem cells (NSCs) produced as a consequence of ethanol-induced effects on the expression of genes related to p53-signaling.	Ethanol	221-228	P53	Homo sapiens	283-286
22948151-6	2012	Induction of p53 can be achieved by several means, such as UV radiation and treatment with anti-cancer agents (including doxorubicin, etoposide, roscovitine, flavopiridol, and nutlin-3).	Doxorubicin	121-132	P53	Homo sapiens	13-16
22892142-6	2012	p53-dependent enhancement of ascorbate cytotoxicity is caused by increased reactive oxygen species generation via a differentially regulated p53 transcriptional network.	Reactive Oxygen Species	75-98	P53	Homo sapiens	141-144
22983008-9	2012	In addition, CREBZF expression confers sensitivity to 5-fluorouracil, a p53-activating chemotherapeutic drug.	Fluorouracil	54-68	P53	Homo sapiens	72-75
22872685-6	2012	Treatment with low doses of Peg IFN-alpha 2a combined with Nutlin-3 increased phospho-p53 and p21 protein levels in PV CD34(+) cells and increased the degree of apoptosis.	Polyethylene Glycols	28-31	P53	Homo sapiens	86-89
22995624-0	2012	Discovery of novel dihydroimidazothiazole derivatives as p53-MDM2 protein-protein interaction inhibitors: synthesis, biological evaluation and structure-activity relationships.	dihydroimidazothiazole	19-41	P53	Homo sapiens	57-60
22683437-2	2012	Other individual reports identified lysine acetylation as a PTM regulating transcription factors and co-activators including p53, c-Myc, PGC1alpha and Ku70.	Lysine	36-42	P53	Homo sapiens	125-128
22898888-6	2012	Further analyses showed that CPT-11 induced in both types of cells DNA damage and activated stress response pathways including p53 and p16 but with varying activity of stress kinase p38 and selected stress-associated microRNAs.	Irinotecan	29-35	P53	Homo sapiens	127-130
22796259-0	2012	Mycoepoxydiene, a fungal polyketide inhibits MCF-7 cells through simultaneously targeting p53 and NF-kappaB pathways.	Polyketides	25-35	P53	Homo sapiens	90-93
23031740-2	2012	Loss of p53 results in increased expression of CD44, a cancer stem cell (CSC) marker, which is involved in the scavenging of reactive oxygen species (ROS).	Reactive Oxygen Species	125-148	P53	Homo sapiens	8-11
23031740-2	2012	Loss of p53 results in increased expression of CD44, a cancer stem cell (CSC) marker, which is involved in the scavenging of reactive oxygen species (ROS).	Reactive Oxygen Species	150-153	P53	Homo sapiens	8-11
22796259-4	2012	The present results show that MED induces DNA damage through the production of reactive oxygen species (ROS), which resulted in the phosphorylation of H2AX and the activation of the Ataxia telangiectasia mutated kinase (ATM) and p53 signaling pathways.	Reactive Oxygen Species	79-102	P53	Homo sapiens	229-232
22796259-4	2012	The present results show that MED induces DNA damage through the production of reactive oxygen species (ROS), which resulted in the phosphorylation of H2AX and the activation of the Ataxia telangiectasia mutated kinase (ATM) and p53 signaling pathways.	Reactive Oxygen Species	104-107	P53	Homo sapiens	229-232
22746287-8	2012	Treatment with CuB induced the differentiation of DCs cocultured with tumor cells 16HBE/BPDE and enhanced the sensitivity of 16HBE/BPDE cells to p53-specific CTL by inhibiting the JAK2/STAT3 activation, but also enhancing the interferon-gamma-related STAT1 activation in 16HBE/BPDE cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	131-135	P53	Homo sapiens	145-148
21898049-0	2012	1H, 13C, and 15N backbone and side-chain chemical shift assignments for the 31 kDa human galectin-7 (p53-induced gene 1) homodimer, a pro-apoptotic lectin.	Hydrogen	0-2	P53	Homo sapiens	101-104
22746287-8	2012	Treatment with CuB induced the differentiation of DCs cocultured with tumor cells 16HBE/BPDE and enhanced the sensitivity of 16HBE/BPDE cells to p53-specific CTL by inhibiting the JAK2/STAT3 activation, but also enhancing the interferon-gamma-related STAT1 activation in 16HBE/BPDE cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	131-135	P53	Homo sapiens	145-148
22747580-6	2012	In addition, ATP attenuated p53 accumulation, DNA damage (assessed by poly(ADP-ribose) formation and the comet assay) and topoisomerase II inhibition after doxorubicin treatment, and doxorubicin cytotoxicity was diminished by the p53 inhibitor pifithrin-alpha.	Adenosine Triphosphate	13-16	P53	Homo sapiens	28-31
22747580-6	2012	In addition, ATP attenuated p53 accumulation, DNA damage (assessed by poly(ADP-ribose) formation and the comet assay) and topoisomerase II inhibition after doxorubicin treatment, and doxorubicin cytotoxicity was diminished by the p53 inhibitor pifithrin-alpha.	Adenosine Triphosphate	13-16	P53	Homo sapiens	230-233
22765290-3	2012	In this review, we focus on highlighting several representative plant natural compounds such as curcumin, resveratrol, paclitaxel, oridonin, quercetin and plant lectin - that may lead to cancer cell death - for regulation of some core autophagic pathways, involved in Ras-Raf signalling, Beclin-1 interactome, BCR-ABL, PI3KCI/Akt/mTOR, FOXO1 signalling and p53.	Curcumin	96-104	P53	Homo sapiens	357-360
22747580-6	2012	In addition, ATP attenuated p53 accumulation, DNA damage (assessed by poly(ADP-ribose) formation and the comet assay) and topoisomerase II inhibition after doxorubicin treatment, and doxorubicin cytotoxicity was diminished by the p53 inhibitor pifithrin-alpha.	Doxorubicin	156-167	P53	Homo sapiens	230-233
22765290-3	2012	In this review, we focus on highlighting several representative plant natural compounds such as curcumin, resveratrol, paclitaxel, oridonin, quercetin and plant lectin - that may lead to cancer cell death - for regulation of some core autophagic pathways, involved in Ras-Raf signalling, Beclin-1 interactome, BCR-ABL, PI3KCI/Akt/mTOR, FOXO1 signalling and p53.	Resveratrol	106-117	P53	Homo sapiens	357-360
22747580-6	2012	In addition, ATP attenuated p53 accumulation, DNA damage (assessed by poly(ADP-ribose) formation and the comet assay) and topoisomerase II inhibition after doxorubicin treatment, and doxorubicin cytotoxicity was diminished by the p53 inhibitor pifithrin-alpha.	Doxorubicin	183-194	P53	Homo sapiens	230-233
22765290-3	2012	In this review, we focus on highlighting several representative plant natural compounds such as curcumin, resveratrol, paclitaxel, oridonin, quercetin and plant lectin - that may lead to cancer cell death - for regulation of some core autophagic pathways, involved in Ras-Raf signalling, Beclin-1 interactome, BCR-ABL, PI3KCI/Akt/mTOR, FOXO1 signalling and p53.	Paclitaxel	119-129	P53	Homo sapiens	357-360
23193415-0	2012	Lobaplatin inhibits the proliferation of hepatollular carcinoma through p53 apoptosis axis.	lobaplatin	0-10	P53	Homo sapiens	72-75
22252971-9	2012	We propose that RSV exerts its chondroprotective functions, in part, by deactivating p53-induced apoptosis in human primary chondrocytes, but not human chondrosarcoma.	Resveratrol	16-19	P53	Homo sapiens	85-88
23168703-6	2012	Mutational analysis of TP53 was done in DNA extracted from formalin fixed paraffin embedded tissue of 80 CaP and 24 BPH cases.	Paraffin	74-82	P53	Homo sapiens	23-27
23168703-13	2012	INTERPRETATION &amp; CONCLUSIONS: The results of the present study demonstrate that TP53 codon 72 polymorphism plays significant role in the pathogenesis and susceptibility to CaP and BPH.	Adenosine Monophosphate	16-19	P53	Homo sapiens	84-88
23168703-13	2012	INTERPRETATION &amp; CONCLUSIONS: The results of the present study demonstrate that TP53 codon 72 polymorphism plays significant role in the pathogenesis and susceptibility to CaP and BPH.	cap	176-179	P53	Homo sapiens	84-88
23168708-11	2012	INTERPRETATION &amp; CONCLUSIONS: Our results show that p53 gene mutation may be associated with gastric carcinogenesis independent to H. pylori infection and absence of K-ras gene mutation questions its role in the pathogenesis of GC and PUD in Indian patients.	Adenosine Monophosphate	16-19	P53	Homo sapiens	56-59
22803606-6	2012	Added serotonin (100 ng/ml) led to a bystander effectin HCT116 p53(-/-) cells recipient of ICCM from 0.5 Gy gamma-irradiated HCT116 p53(+/+) cells, but had no effect when the ICCM was from gamma-irradiated HCT116 P53(-/-) cells.	Serotonin	6-15	P53	Homo sapiens	63-66
22803606-6	2012	Added serotonin (100 ng/ml) led to a bystander effectin HCT116 p53(-/-) cells recipient of ICCM from 0.5 Gy gamma-irradiated HCT116 p53(+/+) cells, but had no effect when the ICCM was from gamma-irradiated HCT116 P53(-/-) cells.	Serotonin	6-15	P53	Homo sapiens	132-135
22803606-6	2012	Added serotonin (100 ng/ml) led to a bystander effectin HCT116 p53(-/-) cells recipient of ICCM from 0.5 Gy gamma-irradiated HCT116 p53(+/+) cells, but had no effect when the ICCM was from gamma-irradiated HCT116 P53(-/-) cells.	Serotonin	6-15	P53	Homo sapiens	213-216
21931970-5	2012	L: -pipecolic acid as-APF and/or as-APF significantly inhibited proliferation of each cell line in a dose-dependent manner with IC(50)"s in the nanomolar range, regardless of tissue origin, cell type (carcinoma vs. melanoma), or p53 or ras mutation status.	pipecolic acid	0-18	P53	Homo sapiens	229-232
22982226-8	2012	Moreover, NaHS markedly suppressed radiation-induced phosphorylation of P53, decrease of Bcl-2/Bax, and activity of nuclear factor kappaB (NF-kappaB).	sodium bisulfide	10-14	P53	Homo sapiens	72-75
22641095-7	2012	In primary cultured hepatocytes, transforming growth factor (TGF)-beta treatment increased p53 and p66Shc signaling, leading to exaggerated reactive oxygen species (ROS) accumulation and apoptosis.	Reactive Oxygen Species	140-163	P53	Homo sapiens	91-94
22641095-7	2012	In primary cultured hepatocytes, transforming growth factor (TGF)-beta treatment increased p53 and p66Shc signaling, leading to exaggerated reactive oxygen species (ROS) accumulation and apoptosis.	Reactive Oxygen Species	165-168	P53	Homo sapiens	91-94
22641095-8	2012	Deficient p53 signaling inhibited TGF-beta-induced p66Shc signaling, ROS accumulation, and hepatocyte apoptosis.	Reactive Oxygen Species	69-72	P53	Homo sapiens	10-13
22641095-12	2012	CONCLUSIONS: p53 in hepatocytes regulates steatohepatitis progression by controlling p66Shc signaling, ROS levels, and apoptosis, all of which may be regulated by TGF-beta.	Reactive Oxygen Species	103-106	P53	Homo sapiens	13-16
22735644-1	2012	Human DBC1 (deleted in breast cancer-1; KIAA1967) is a nuclear protein that, in response to DNA damage, competitively inhibits the NAD(+)-dependent deacetylase SIRT1, a regulator of p53 apoptotic functions in response to genotoxic stress.	NAD	131-137	P53	Homo sapiens	182-185
22799769-2	2012	We proposed PTHLH-activated network that upstream included the regulation of apoptosis, signal transduction resulting in induction of apoptosis, signal transduction by p53 class mediator resulting in transcription of p21 class mediator, negative regulation of centriole replication, negative regulation of fatty acid biosynthesis, negative regulation of Wnt receptor signaling pathway, anaphase-promoting complex-dependent proteasomal ubiquitin-dependent protein catabolism, apoptosis, induction of apoptosis, and negative regulation of phosphorylation.	Fatty Acids	306-316	P53	Homo sapiens	168-171
22593008-3	2012	For this purpose, a amonafide analogue, 7-d (2-(3-(2-(Dimethylamino)ethylamino)propyl)-6-(dodecylamino)-1H-benzo[de]isoquinoline-1,3(2H)-dione) was screened, which exhibited high antitumor activity against p53-deficient human Chronic Myelogenous Leukemia (CML) K562 cells.	7-d	40-43	P53	Homo sapiens	206-209
22641095-1	2012	BACKGROUND &amp; AIMS: The tumor suppressor p53 is a primary sensor of stressful stimuli, controlling a number of biologic processes.	Adenosine Monophosphate	12-15	P53	Homo sapiens	44-47
22493095-3	2012	Sumoylation of HDAC2 at lysine 462 allows binding of HDAC2 to p53.	Lysine	24-30	P53	Homo sapiens	62-65
22493095-5	2012	Deacetylation of p53 at lysine 320 by sumoylated HDAC2 blocks recruitment of p53 into promoter-associated complexes and p53-dependent expression of genes for cell cycle control and apoptosis.	Lysine	24-30	P53	Homo sapiens	17-20
22493095-5	2012	Deacetylation of p53 at lysine 320 by sumoylated HDAC2 blocks recruitment of p53 into promoter-associated complexes and p53-dependent expression of genes for cell cycle control and apoptosis.	Lysine	24-30	P53	Homo sapiens	77-80
22493095-5	2012	Deacetylation of p53 at lysine 320 by sumoylated HDAC2 blocks recruitment of p53 into promoter-associated complexes and p53-dependent expression of genes for cell cycle control and apoptosis.	Lysine	24-30	P53	Homo sapiens	77-80
22287315-4	2012	Cortisol induced HPV-E6 expression and suppressed p53 and miR-145 in cervical cancer cells.	Hydrocortisone	0-8	P53	Homo sapiens	50-53
22841759-0	2012	Metabolic regulation of oxygen and redox homeostasis by p53: lessons from evolutionary biology?	Oxygen	24-30	P53	Homo sapiens	56-59
22549273-0	2012	Microvessel density and status of p53 protein as potential prognostic factors for adjuvant anthracycline chemotherapy in retrospective analysis of early breast cancer patients group.	Anthracyclines	91-104	P53	Homo sapiens	34-37
22549273-2	2012	The aim of this retrospective study was to investigate the effect of microvessel density (MVD) and status of p53 protein on 5-year disease free survival (DFS) in the group of breast cancer patients treated with anthracyclines in adjuvant setting.	Anthracyclines	211-225	P53	Homo sapiens	109-112
23017148-1	2012	BACKGROUND: Nucleoside analogs used in the chemotherapy of solid tumors, such as the capecitabine catabolite 5"-deoxy-5-fluorouridine (5"-DFUR) trigger a transcriptomic response that involves the aquaglyceroporin aquaporin 3 along with other p53-dependent genes.	capecitabine catabolite	85-108	P53	Homo sapiens	242-245
22549660-6	2012	Our findings indicated that by synergism with anticancer drugs, FLX modulation of apoptosis via targeting p53 and Bcl-2 expression, FLX reverse the breast cancer cell"s resistance and enhance the chemosensitivity to ADM and PTX.	Doxorubicin	216-219	P53	Homo sapiens	106-109
22549660-6	2012	Our findings indicated that by synergism with anticancer drugs, FLX modulation of apoptosis via targeting p53 and Bcl-2 expression, FLX reverse the breast cancer cell"s resistance and enhance the chemosensitivity to ADM and PTX.	Paclitaxel	224-227	P53	Homo sapiens	106-109
22880817-3	2012	Here, we performed molecular simulations of p53 at various salt concentrations finding that, at physiological salt concentration, p53 diffuses along nonspecific DNA via rotation-uncoupled sliding with its CTD, whereas the core domain repeats dissociation and association.	Salts	59-63	P53	Homo sapiens	44-47
22913742-3	2012	Previously, peptides derived from CapZ, p53, NDR, HDM2, and HDM4 have been shown to interact with S100B in a calcium-dependent manner.	Calcium	109-116	P53	Homo sapiens	40-43
22963678-0	2012	Ethanol extract of paeonia suffruticosa Andrews (PSE) induced AGS human gastric cancer cell apoptosis via fas-dependent apoptosis and MDM2-p53 pathways.	Ethanol	0-7	P53	Homo sapiens	139-142
22880817-3	2012	Here, we performed molecular simulations of p53 at various salt concentrations finding that, at physiological salt concentration, p53 diffuses along nonspecific DNA via rotation-uncoupled sliding with its CTD, whereas the core domain repeats dissociation and association.	Salts	59-63	P53	Homo sapiens	130-133
22880817-3	2012	Here, we performed molecular simulations of p53 at various salt concentrations finding that, at physiological salt concentration, p53 diffuses along nonspecific DNA via rotation-uncoupled sliding with its CTD, whereas the core domain repeats dissociation and association.	Salts	110-114	P53	Homo sapiens	44-47
22880817-3	2012	Here, we performed molecular simulations of p53 at various salt concentrations finding that, at physiological salt concentration, p53 diffuses along nonspecific DNA via rotation-uncoupled sliding with its CTD, whereas the core domain repeats dissociation and association.	Salts	110-114	P53	Homo sapiens	130-133
22880817-5	2012	In the simulation of tetrameric full-length p53, two DNA binding domains both bound to nonspecific DNA in a characteristic form at low salt concentration, whereas at physiological salt concentration, only CTD kept bound to DNA and the core domain frequently hopped on DNA.	Salts	135-139	P53	Homo sapiens	44-47
22880817-5	2012	In the simulation of tetrameric full-length p53, two DNA binding domains both bound to nonspecific DNA in a characteristic form at low salt concentration, whereas at physiological salt concentration, only CTD kept bound to DNA and the core domain frequently hopped on DNA.	Salts	180-184	P53	Homo sapiens	44-47
22696202-0	2012	Increased acetylation of lysine 317/320 of p53 caused by BCR-ABL protects from cytoplasmic translocation of p53 and mitochondria-dependent apoptosis in response to DNA damage.	Lysine	25-31	P53	Homo sapiens	43-46
22446899-12	2012	ROS production was partially dependent on the upregulation of p53 upon shikonin treatment.	Reactive Oxygen Species	0-3	P53	Homo sapiens	62-65
22696202-0	2012	Increased acetylation of lysine 317/320 of p53 caused by BCR-ABL protects from cytoplasmic translocation of p53 and mitochondria-dependent apoptosis in response to DNA damage.	Lysine	25-31	P53	Homo sapiens	108-111
22696202-6	2012	In this study we have investigated whether the expression of BCR-ABL could influence the acetylation of p53, specifically at lysine 317/320 (K317/K320), which has been shown to regulate nuclear export and transcription-independent apoptotic activity of p53.	Lysine	125-131	P53	Homo sapiens	104-107
24009836-10	2012	Resveratrol-induced p53 expression strongly correlated with the enhancement of cytotoxicity observed upon combination of resveratrol with DMS or 4-HPR.	Resveratrol	0-11	P53	Homo sapiens	20-23
24009836-10	2012	Resveratrol-induced p53 expression strongly correlated with the enhancement of cytotoxicity observed upon combination of resveratrol with DMS or 4-HPR.	Resveratrol	121-132	P53	Homo sapiens	20-23
24009836-10	2012	Resveratrol-induced p53 expression strongly correlated with the enhancement of cytotoxicity observed upon combination of resveratrol with DMS or 4-HPR.	dms	138-141	P53	Homo sapiens	20-23
22607092-0	2012	P53-mediated GSH depletion enhanced the cytotoxicity of NO in silibinin-treated human cervical carcinoma HeLa cells.	Glutathione	13-16	P53	Homo sapiens	0-3
23019099-6	2012	This finding excluded that the individual p53 spots in 2D gels reflect charge isomers generated by phosphorylation, but rather suggest that they are due to conformational flexibility of urea-denatured monomeric p53 molecules or deamidation of asparagine and glutamine residues.	Urea	186-190	P53	Homo sapiens	42-45
23019099-6	2012	This finding excluded that the individual p53 spots in 2D gels reflect charge isomers generated by phosphorylation, but rather suggest that they are due to conformational flexibility of urea-denatured monomeric p53 molecules or deamidation of asparagine and glutamine residues.	Urea	186-190	P53	Homo sapiens	211-214
22607092-0	2012	P53-mediated GSH depletion enhanced the cytotoxicity of NO in silibinin-treated human cervical carcinoma HeLa cells.	Silybin	62-71	P53	Homo sapiens	0-3
22607092-10	2012	JNK and p53 have been shown to mediate the depletion of GSH [ 2 , 3 ], and we previously demonstrated the existence of a ROS-JNK-p53 cycle in silibinin-treated HeLa cells [ 4 ].	Reactive Oxygen Species	121-124	P53	Homo sapiens	129-132
22607092-10	2012	JNK and p53 have been shown to mediate the depletion of GSH [ 2 , 3 ], and we previously demonstrated the existence of a ROS-JNK-p53 cycle in silibinin-treated HeLa cells [ 4 ].	Silybin	142-151	P53	Homo sapiens	8-11
22607092-10	2012	JNK and p53 have been shown to mediate the depletion of GSH [ 2 , 3 ], and we previously demonstrated the existence of a ROS-JNK-p53 cycle in silibinin-treated HeLa cells [ 4 ].	Silybin	142-151	P53	Homo sapiens	129-132
22607092-11	2012	Thus, we speculated that p53 also plays a crucial role in the silibinin-induced GSH depletion.	Silybin	62-71	P53	Homo sapiens	25-28
22607092-11	2012	Thus, we speculated that p53 also plays a crucial role in the silibinin-induced GSH depletion.	Glutathione	80-83	P53	Homo sapiens	25-28
22607092-15	2012	Cumulatively, these findings support the idea that the silibinin-induced GSH depletion, which is mediated by p53, enhances the cytotoxicity of NO in HeLa cells.	Silybin	55-64	P53	Homo sapiens	109-112
22607092-15	2012	Cumulatively, these findings support the idea that the silibinin-induced GSH depletion, which is mediated by p53, enhances the cytotoxicity of NO in HeLa cells.	Glutathione	73-76	P53	Homo sapiens	109-112
22796327-3	2012	PRODH expression is inducible by p53, leading to increased proline oxidation, reactive oxygen species formation, and induction of apoptosis.	Reactive Oxygen Species	78-101	P53	Homo sapiens	33-36
22815059-5	2012	The anthracycline anticancer drug epirubicin (EPB) synergizes the cytotoxicity of HMCAZ5 in cancer cells by upregulating DR5 expression on the cell surfaces, enhancing p53 expression, Bid cleavage, and JNK phosphorylation and downregulating c-FLIP expression and Akt phosphorylation.	Epirubicin	34-44	P53	Homo sapiens	168-171
22684338-5	2012	We found that 5-FU profoundly induces             ER stress in Sk-Hep1 cells and upregulates p53 and activates CHOP/GADD153 and             caspase-12.	Fluorouracil	14-18	P53	Homo sapiens	93-96
22864287-0	2012	PHF20 is an effector protein of p53 double lysine methylation that stabilizes and activates p53.	Lysine	43-49	P53	Homo sapiens	32-35
22531959-3	2012	Compared with the p53 wildtype U2OS cells, miR-34a expression was much lower in p53 deficient Saos2 cells upon cisplatin treatment.	Cisplatin	111-120	P53	Homo sapiens	80-83
22763759-6	2012	However, the growth-inhibitory activity of vincristine, doxorubicin, carboplatin, etoposide, and temozolomide was significantly impaired by silencing of TP53.	Doxorubicin	56-67	P53	Homo sapiens	153-157
22692183-7	2012	p53 allele frequency             for Arg/Arg was 43.6% (34/78), for Arg/Pro 37.2% (29/78) and for Pro/Pro 19.2%             (15/78).	Arginine	37-40	P53	Homo sapiens	0-3
22692183-7	2012	p53 allele frequency             for Arg/Arg was 43.6% (34/78), for Arg/Pro 37.2% (29/78) and for Pro/Pro 19.2%             (15/78).	Arginine	41-44	P53	Homo sapiens	0-3
22692183-7	2012	p53 allele frequency             for Arg/Arg was 43.6% (34/78), for Arg/Pro 37.2% (29/78) and for Pro/Pro 19.2%             (15/78).	Arginine	41-44	P53	Homo sapiens	0-3
22692183-10	2012	Although the p53 arginine allele is itself             an important risk factor for cervical cancer, the combined risk with LOH of Rb,             which appears to be greater, might indicate a possible epistatic effect of the             two genes/polymorphisms.	Arginine	17-25	P53	Homo sapiens	13-16
22864287-0	2012	PHF20 is an effector protein of p53 double lysine methylation that stabilizes and activates p53.	Lysine	43-49	P53	Homo sapiens	92-95
23077460-11	2012	The p53 and ER/PR status may predict tumour response on rHuEpo and cDDP treatment.	Cisplatin	67-71	P53	Homo sapiens	4-7
22710790-0	2012	Rapamycin induces p53-independent apoptosis through the mitochondrial             pathway in non-small cell lung cancer cells.	Sirolimus	0-9	P53	Homo sapiens	18-21
22710790-7	2012	We found that rapamycin induced             apoptosis in NSCLC cell lines with p53 mutations.	Sirolimus	14-23	P53	Homo sapiens	79-82
22766626-6	2012	We found that zinc(II) ions caused elevated expression             of Ki-67, a marker of proliferation, extremely low expression of p53, high expression             of Bcl-2 and no changes in the expression of p53.	Zinc	14-22	P53	Homo sapiens	132-135
22773829-4	2012	Specifically, GR agonists hydrocortisone or dexamethasone inhibited p53-dependent apoptosis induced by cisplatin, ionizing radiation, or the MDM2 antagonist Nutlin-3.	Hydrocortisone	26-40	P53	Homo sapiens	68-71
22773829-4	2012	Specifically, GR agonists hydrocortisone or dexamethasone inhibited p53-dependent apoptosis induced by cisplatin, ionizing radiation, or the MDM2 antagonist Nutlin-3.	Dexamethasone	44-57	P53	Homo sapiens	68-71
22773829-4	2012	Specifically, GR agonists hydrocortisone or dexamethasone inhibited p53-dependent apoptosis induced by cisplatin, ionizing radiation, or the MDM2 antagonist Nutlin-3.	Cisplatin	103-112	P53	Homo sapiens	68-71
22120717-4	2012	Here we report that short hairpin RNA-mediated gene suppression of wild-type p53 or ectopic expression of mutant temperature-sensitive dominant-negative p53(V135A) increased glucose consumption and lactate production, decreased oxygen consumption and enhanced hypoxia-induced cell death in p53 wild-type human glioblastoma cells.	Lactic Acid	198-205	P53	Homo sapiens	77-80
22561451-7	2012	In addition, resveratrol suppressed Ang II-induced induction of p53 and its downstream target gene p21, both of which play an important role in the induction of senescence.	Resveratrol	13-24	P53	Homo sapiens	64-67
22561451-8	2012	Resveratrol suppressed senescence of VSMC possibly through inhibition of AT1R-dependent induction of p53/p21.	Resveratrol	0-11	P53	Homo sapiens	101-104
22561451-8	2012	Resveratrol suppressed senescence of VSMC possibly through inhibition of AT1R-dependent induction of p53/p21.	vsmc	37-41	P53	Homo sapiens	101-104
22561451-9	2012	Suppression of p53 induction may be involved in the longevity by resveratrol.	Resveratrol	65-76	P53	Homo sapiens	15-18
22869710-4	2012	EDTA removes Zn(2+) to generate apo-p53, which aggregated faster than holo-p53.	Zinc	13-15	P53	Homo sapiens	36-39
22869710-6	2012	Apo-p53 was not an obligatory intermediate in the aggregation of holo-p53, but affords a parallel pathway that may be relevant to oncogenic mutants with impaired Zn(2+) binding.	Zinc	162-168	P53	Homo sapiens	4-7
22120717-4	2012	Here we report that short hairpin RNA-mediated gene suppression of wild-type p53 or ectopic expression of mutant temperature-sensitive dominant-negative p53(V135A) increased glucose consumption and lactate production, decreased oxygen consumption and enhanced hypoxia-induced cell death in p53 wild-type human glioblastoma cells.	Lactic Acid	198-205	P53	Homo sapiens	153-156
22120717-4	2012	Here we report that short hairpin RNA-mediated gene suppression of wild-type p53 or ectopic expression of mutant temperature-sensitive dominant-negative p53(V135A) increased glucose consumption and lactate production, decreased oxygen consumption and enhanced hypoxia-induced cell death in p53 wild-type human glioblastoma cells.	Lactic Acid	198-205	P53	Homo sapiens	153-156
22120717-4	2012	Here we report that short hairpin RNA-mediated gene suppression of wild-type p53 or ectopic expression of mutant temperature-sensitive dominant-negative p53(V135A) increased glucose consumption and lactate production, decreased oxygen consumption and enhanced hypoxia-induced cell death in p53 wild-type human glioblastoma cells.	Oxygen	228-234	P53	Homo sapiens	77-80
22120717-4	2012	Here we report that short hairpin RNA-mediated gene suppression of wild-type p53 or ectopic expression of mutant temperature-sensitive dominant-negative p53(V135A) increased glucose consumption and lactate production, decreased oxygen consumption and enhanced hypoxia-induced cell death in p53 wild-type human glioblastoma cells.	Oxygen	228-234	P53	Homo sapiens	153-156
22120717-4	2012	Here we report that short hairpin RNA-mediated gene suppression of wild-type p53 or ectopic expression of mutant temperature-sensitive dominant-negative p53(V135A) increased glucose consumption and lactate production, decreased oxygen consumption and enhanced hypoxia-induced cell death in p53 wild-type human glioblastoma cells.	Oxygen	228-234	P53	Homo sapiens	153-156
22730327-2	2012	SEPW1 depletion increases phosphorylation of Ser-33 in p53, which is associated with decreased p53 ubiquitination and stabilization of p53.	Serine	45-48	P53	Homo sapiens	55-58
22706202-4	2012	Depletion of elevated CAV1 led to AMPK activation followed by a p53-dependent G1 cell-cycle arrest and autophagy, suggesting that elevated CAV1 may contribute to ATP generation.	Adenosine Triphosphate	162-165	P53	Homo sapiens	64-67
22888789-0	2012	Interferon regulatory factor 4 binding protein is a novel p53 target gene and suppresses cisplatin-induced apoptosis of breast cancer cells.	Cisplatin	89-98	P53	Homo sapiens	58-61
22888789-4	2012	IBP expression was negatively regulated by wild-type p53 and was p53 dependently suppressed by DNA damage agent cisplatin.	Cisplatin	112-121	P53	Homo sapiens	65-68
22888789-5	2012	Furthermore, high levels of IBP were found to decrease cisplatin-induced growth suppression and apoptotic cell death, which was associated with decreased p53 activity and imbalanced Bcl-2 family member expression.	Cisplatin	55-64	P53	Homo sapiens	154-157
21932419-3	2012	HIPK2 modulates wild-type p53 activity toward proapoptotic transcription and tumor suppression by the phosphorylation of serine 46.	Serine	121-127	P53	Homo sapiens	26-29
21932419-5	2012	Combined administration of adriamycin and zinc restores activity of misfolded p53 and enables the induction of its proapoptotic and tumor suppressor functions in vitro and in vivo.	Doxorubicin	27-37	P53	Homo sapiens	78-81
21932419-9	2012	The combined treatment of adriamycin and zinc also restores wild-type p53 conformation and induces proapoptotic transcription activity.	Doxorubicin	26-36	P53	Homo sapiens	70-73
22888789-6	2012	CONCLUSIONS: IBP is a novel p53 target gene which suppresses cisplatin-mediated apoptosis of breast cancer cells via negative feedback regulation of the p53 signalling pathway, suggesting IBP may serve as a target for pharmacologic intervention of breast cancer resistant to cisplatin therapy.	Cisplatin	61-70	P53	Homo sapiens	28-31
22888789-6	2012	CONCLUSIONS: IBP is a novel p53 target gene which suppresses cisplatin-mediated apoptosis of breast cancer cells via negative feedback regulation of the p53 signalling pathway, suggesting IBP may serve as a target for pharmacologic intervention of breast cancer resistant to cisplatin therapy.	Cisplatin	61-70	P53	Homo sapiens	153-156
22888789-6	2012	CONCLUSIONS: IBP is a novel p53 target gene which suppresses cisplatin-mediated apoptosis of breast cancer cells via negative feedback regulation of the p53 signalling pathway, suggesting IBP may serve as a target for pharmacologic intervention of breast cancer resistant to cisplatin therapy.	Cisplatin	275-284	P53	Homo sapiens	28-31
22888789-6	2012	CONCLUSIONS: IBP is a novel p53 target gene which suppresses cisplatin-mediated apoptosis of breast cancer cells via negative feedback regulation of the p53 signalling pathway, suggesting IBP may serve as a target for pharmacologic intervention of breast cancer resistant to cisplatin therapy.	Cisplatin	275-284	P53	Homo sapiens	153-156
22730327-2	2012	SEPW1 depletion increases phosphorylation of Ser-33 in p53, which is associated with decreased p53 ubiquitination and stabilization of p53.	Serine	45-48	P53	Homo sapiens	95-98
22730327-2	2012	SEPW1 depletion increases phosphorylation of Ser-33 in p53, which is associated with decreased p53 ubiquitination and stabilization of p53.	Serine	45-48	P53	Homo sapiens	95-98
22875003-3	2012	We have profiled ABT-737 specificity for all six pro-survival Bcl-2 proteins, in p53 wild-type or p53-mutant human T-leukemic cells.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	17-20	P53	Homo sapiens	81-84
22875003-3	2012	We have profiled ABT-737 specificity for all six pro-survival Bcl-2 proteins, in p53 wild-type or p53-mutant human T-leukemic cells.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	17-20	P53	Homo sapiens	98-101
22730327-7	2012	These results imply that SEPW1 silencing increases MKK4, which activates p38gamma, p38delta, and JNK2 to phosphorylate p53 on Ser-33 and cause a transient G(1) arrest.	Serine	126-129	P53	Homo sapiens	119-122
22862878-8	2012	Antp-p21 killed cancer cells selectively that were malignant as a result of mutations or nuclear exclusion of the p53 and p21 genes and over-expression of MDM2.	antp	0-4	P53	Homo sapiens	114-117
22505655-5	2012	These modifications, especially phosphorylation of serine and threonine residues in the N-terminal transactivation domain, affect p53 stability and activity by modulating the affinity of protein-protein interactions.	Serine	51-57	P53	Homo sapiens	130-133
22607196-6	2012	The synergistic effect of 5-FU induced by oroxylin A was also found in the suppression of Bcl-2 and in the activation of P53, Bax, PARP, and procaspase-3 proteins in HT-29 cells.	Fluorouracil	26-30	P53	Homo sapiens	121-124
22607196-6	2012	The synergistic effect of 5-FU induced by oroxylin A was also found in the suppression of Bcl-2 and in the activation of P53, Bax, PARP, and procaspase-3 proteins in HT-29 cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	42-52	P53	Homo sapiens	121-124
22594855-7	2012	In HCL-variant, adverse prognostic factors for survival were older age (P = 0 04), anaemia (P = 0 01) and TP 53 mutations (P = 0 02).	Hydrochloric Acid	3-6	P53	Homo sapiens	106-111
22785210-7	2012	This is evident in G 2 arrest and increases in levels of cleaved caspase 3 and p53 phosphorylated at serine 20.	Serine	101-107	P53	Homo sapiens	79-82
22785213-0	2012	The DNA binding and accumulation of p53 from breast cancer cell lines and the link with serine 15 phosphorylation.	Serine	88-94	P53	Homo sapiens	36-39
22785213-4	2012	Treatment of MCF-7 cells with H2O2 caused an increase in this binding affinity while this same treatment of ZR-75-1 cells caused the p53 protein to lose binding affinity to several genes.	Hydrogen Peroxide	30-34	P53	Homo sapiens	133-136
22785213-5	2012	The mutant p53 proteins from all cell lines had minimal to weak binding to these sequences even after treatment with H2O2.	Hydrogen Peroxide	117-121	P53	Homo sapiens	11-14
22785213-6	2012	The p53 protein from the ZR-75-1 cells and three cell lines with mutant p53 showed serine 15 phosphorylated protein, but we found no correlation between that modification and the levels or localization of this protein although DNA binding affinity of wild-type protein might be affected by this modification.	Serine	83-89	P53	Homo sapiens	4-7
22505655-5	2012	These modifications, especially phosphorylation of serine and threonine residues in the N-terminal transactivation domain, affect p53 stability and activity by modulating the affinity of protein-protein interactions.	Threonine	62-71	P53	Homo sapiens	130-133
22528789-5	2012	The polyarginine11R as a PTD, nuclear localization sequence (NLS), and laminin (Ln) fused to the p53 peptide corresponding to the MDM2 binding site (p53-NLS-Ln-11R) effectively penetrated the plasma membrane of the glioma cells and was translocated into the nucleus.	polyarginine11r	4-19	P53	Homo sapiens	149-152
22564437-7	2012	Pretreatment with ACF enhanced the induction of p53 protein expression and phosphorylation on serine 15 by gamma-irradiation.	Serine	94-100	P53	Homo sapiens	48-51
21633925-3	2012	In the present study, we show that retinoic acid enhances the cytostatic and apoptogenic properties of the novel adamantyl retinoid ST1926 in a panel of neuroblastoma cells with different p53 status and caspase 8 expression, resulting in synergistic effects as assessed by Combination Index and Isobologram analysis.	Tretinoin	35-48	P53	Homo sapiens	188-191
21633925-8	2012	Although not modulated, p53 appeared to enhance cells responsiveness to retinoid/ATRA combination.	Tretinoin	81-85	P53	Homo sapiens	24-27
22415970-6	2012	The sensitization by RSV involved the enhancement of p53 levels, the decrease of procaspase 8 and the activation of caspases 7 and 9.	Resveratrol	21-24	P53	Homo sapiens	53-56
22797300-7	2012	Our identification of HCLK2 as a substrate of PHD3 reveals the mechanism through which hypoxia inhibits the DDR, suggesting hydroxylation of HCLK2 is a potential therapeutic target for regulating the ATR/CHK1/p53 pathway.	ddr	108-111	P53	Homo sapiens	209-212
22852466-4	2012	The highest level of gene inhibition was observed in the cases treated with p53 siRNA gene; in the case of transfection with siPort, the NeoFX value was 33.8%, while in the case of SWNTC-COOH as delivery system for p53 siRNA was 37.5%.	Carbonic Acid	187-191	P53	Homo sapiens	76-79
22711357-3	2012	In the presence of histone deacetylase inhibitor (HDACi), p53 is a prerequisite for the initiation of the EBV lytic cycle by facilitating the expression of Zta.	zta	156-159	P53	Homo sapiens	58-61
21605570-4	2012	The predominantly indirect genotoxic carcinogen cadmium inhibits the BER pathway and potentially interferes with zinc binding proteins such as p53.	Cadmium	48-55	P53	Homo sapiens	143-146
21605570-8	2012	Here, a direct involvement of p53 was only observed with respect to APE1 gene expression contributing to an altered APE activity, while OGG activity was presumably affected indirectly due to a stronger accumulation of cadmium in HCT116 p53(+/+) cells.	Cadmium	218-225	P53	Homo sapiens	236-239
21605570-5	2012	Therefore, this study was accomplished to investigate whether p53 is involved in the cadmium-induced inhibition of BER activity.	Cadmium	85-92	P53	Homo sapiens	62-65
21605570-9	2012	In summary, p53 indeed affects the BER pathway directly and indirectly in response to cadmium treatment.	Cadmium	86-93	P53	Homo sapiens	12-15
21605570-7	2012	We present evidence that p53 is not essential for hOGG1 and APE1 gene expression as well as OGG and APE activity in unstressed HCT116 cells; however, it plays an important role in the cellular response to cadmium treatment.	Cadmium	205-212	P53	Homo sapiens	25-28
22653969-5	2012	The Chk1/2 inhibitor AZD7762 potentiated the antiproliferative effects of bendamustine, melphalan, and doxorubicin but not bortezomib in multiple myeloma cell lines that were p53-deficient.	Doxorubicin	103-114	P53	Homo sapiens	175-178
21837762-5	2012	The results showed that cisplatin decreased the protein expression levels of DeltaNp73beta in a dose-dependent manner, and both TAp73 and p53 were upregulated after cisplatin treatment.	Cisplatin	24-33	P53	Homo sapiens	138-141
21837762-5	2012	The results showed that cisplatin decreased the protein expression levels of DeltaNp73beta in a dose-dependent manner, and both TAp73 and p53 were upregulated after cisplatin treatment.	Cisplatin	165-174	P53	Homo sapiens	138-141
22576881-3	2012	DNA damage induced the phosphorylation of p53 at Ser 15 (p-p53) and the phosphorylation of ERK (p-ERK).	Serine	49-52	P53	Homo sapiens	42-45
22576881-3	2012	DNA damage induced the phosphorylation of p53 at Ser 15 (p-p53) and the phosphorylation of ERK (p-ERK).	Serine	49-52	P53	Homo sapiens	59-62
22665525-1	2012	The topoisomerase I inhibitor irinotecan is used to treat advanced colorectal cancer and has been shown to have p53-independent anticancer activity.	Irinotecan	30-40	P53	Homo sapiens	112-115
22653969-8	2012	In summary, the cytotoxic effects of bendamustine, melphalan and doxorubicin on p53-deficient multiple myeloma cell lines were enhanced by the coadministration of AZD7762.	Doxorubicin	65-76	P53	Homo sapiens	80-83
22665525-2	2012	The aim of this study was to identify the p53-independent signaling mechanisms activated by irinotecan.	Irinotecan	92-102	P53	Homo sapiens	42-45
22665525-3	2012	Transcriptional profiling of isogenic HCT116 p53 wild-type and p53 null cells was carried out following treatment with the active metabolite of irinotecan, SN38.	Irinotecan	144-154	P53	Homo sapiens	45-48
22689577-11	2012	Overall, these results suggest for the first time that Sirt-1 can regulate p53 and NF-kappaB signaling via deacetylation, demonstrating a novel role for resveratrol in the treatment of tendinitis/tendinopathy.	Resveratrol	153-164	P53	Homo sapiens	75-78
22665525-3	2012	Transcriptional profiling of isogenic HCT116 p53 wild-type and p53 null cells was carried out following treatment with the active metabolite of irinotecan, SN38.	Irinotecan	144-154	P53	Homo sapiens	63-66
22052810-2	2012	A single nucleotide polymorphism of TP53 encoding either arginine or proline at codon 72 is suggested to alter in vitro p53 behavior.	Arginine	57-65	P53	Homo sapiens	36-40
22052810-2	2012	A single nucleotide polymorphism of TP53 encoding either arginine or proline at codon 72 is suggested to alter in vitro p53 behavior.	Arginine	57-65	P53	Homo sapiens	120-123
22707142-7	2012	Our study suggests that, among Asians, the p53 codon 72 Arg/Arg genotype is associated with a modestly decreased risk of gastric cancer, and that this difference in genotype distribution may be associated with cancer stage, location, differentiation and metastasis.	Arginine	56-59	P53	Homo sapiens	43-46
22707142-7	2012	Our study suggests that, among Asians, the p53 codon 72 Arg/Arg genotype is associated with a modestly decreased risk of gastric cancer, and that this difference in genotype distribution may be associated with cancer stage, location, differentiation and metastasis.	Arginine	60-63	P53	Homo sapiens	43-46
22445862-0	2012	Docetaxel and 5-fluorouracil induce human p53 tumor suppressor gene transcription via a short sequence at core promoter element.	Fluorouracil	14-28	P53	Homo sapiens	42-45
22445862-3	2012	Docetaxel (DOC), a member of the taxanes family that is widely used in cancer chemotherapy, activates p53 at the transcriptional level.	Taxoids	33-40	P53	Homo sapiens	102-105
22445862-9	2012	The same mutations also inhibited 5-fluorouracil (5-FU)-inducible p53 expression.	Fluorouracil	34-48	P53	Homo sapiens	66-69
22445862-9	2012	The same mutations also inhibited 5-fluorouracil (5-FU)-inducible p53 expression.	Fluorouracil	50-54	P53	Homo sapiens	66-69
22249977-0	2012	Impact of codon 72 Arg &gt; Pro single nucleotide polymorphism in TP53 gene in the risk of kangri cancer: a case control study in Kashmir.	Arginine	19-22	P53	Homo sapiens	66-70
22621920-0	2012	ATP depletion triggers acute myeloid leukemia differentiation through an ATR/Chk1 protein-dependent and p53 protein-independent pathway.	Adenosine Triphosphate	0-3	P53	Homo sapiens	104-107
22245200-7	2012	Activation of p53 by phosphorylation at serine 315 and serine 37 was monitored by Western blotting.	Serine	40-46	P53	Homo sapiens	14-17
22245200-7	2012	Activation of p53 by phosphorylation at serine 315 and serine 37 was monitored by Western blotting.	Serine	55-61	P53	Homo sapiens	14-17
22245200-11	2012	In agreement with this finding, phosphorylation of p53 at serine 315 involved in PAI-1 expression was similar with high and low LET radiation, whereas phosphorylation of p53 at serine 37, involved in apoptosis induction, was much higher after high LET irradiation.	Serine	58-64	P53	Homo sapiens	51-54
22245200-11	2012	In agreement with this finding, phosphorylation of p53 at serine 315 involved in PAI-1 expression was similar with high and low LET radiation, whereas phosphorylation of p53 at serine 37, involved in apoptosis induction, was much higher after high LET irradiation.	Serine	177-183	P53	Homo sapiens	170-173
22442140-1	2012	Focus on "A novel inverse relationship between metformin-triggered AMPK-SIRT1 signaling and p53 protein abundance in high glucose-exposed HepG2 cells".	Metformin	47-56	P53	Homo sapiens	92-95
22378745-0	2012	A novel inverse relationship between metformin-triggered AMPK-SIRT1 signaling and p53 protein abundance in high glucose-exposed HepG2 cells.	Metformin	37-46	P53	Homo sapiens	82-85
22442140-1	2012	Focus on "A novel inverse relationship between metformin-triggered AMPK-SIRT1 signaling and p53 protein abundance in high glucose-exposed HepG2 cells".	Glucose	122-129	P53	Homo sapiens	92-95
22378745-0	2012	A novel inverse relationship between metformin-triggered AMPK-SIRT1 signaling and p53 protein abundance in high glucose-exposed HepG2 cells.	Glucose	112-119	P53	Homo sapiens	82-85
22378745-5	2012	Metformin induced activation of AMPK and SIRT1 and decreased p53 protein abundance.	Metformin	0-9	P53	Homo sapiens	61-64
22716215-11	2012	The combination of 5-FU and chloroquine induced G1 arrest, up-regulation of p27 and p53, and down-regulation of CDK2 and cyclin D1.	Fluorouracil	19-23	P53	Homo sapiens	84-87
22378745-8	2012	In addition, overexpression of p53 decreased SIRT1 gene expression and protein abundance, as well as AMPK activity in metformin-treated cells.	Metformin	118-127	P53	Homo sapiens	31-34
22576699-7	2012	Further studies indicated that LKB1-enhancing cisplatin-mediated antitumor effects might be associated with the upregulation of p-p53 and p-JNK, and downregulation of p-mammalian target of rapamycin, matrix metalloproteinase (MMP)-2 and MMP-9.	Cisplatin	46-55	P53	Homo sapiens	130-133
22647487-0	2012	MAPK14/p38alpha confers irinotecan resistance to TP53-defective cells by inducing survival autophagy.	Irinotecan	24-34	P53	Homo sapiens	49-53
22576012-0	2012	Autophagy is induced through the ROS-TP53-DRAM1 pathway in response to mitochondrial protein synthesis inhibition.	Reactive Oxygen Species	33-36	P53	Homo sapiens	37-41
22576012-6	2012	The ROS elevation resulting from mitochondrial protein synthesis inhibition induced TP53 expression at transcriptional levels by enhancing TP53 promoter activity, and increased TP53 protein stability by suppressing TP53 ubiquitination through MAPK14/p38 MAPK-mediated TP53 phosphorylation.	Reactive Oxygen Species	4-7	P53	Homo sapiens	84-88
22576012-6	2012	The ROS elevation resulting from mitochondrial protein synthesis inhibition induced TP53 expression at transcriptional levels by enhancing TP53 promoter activity, and increased TP53 protein stability by suppressing TP53 ubiquitination through MAPK14/p38 MAPK-mediated TP53 phosphorylation.	Reactive Oxygen Species	4-7	P53	Homo sapiens	139-143
22576012-6	2012	The ROS elevation resulting from mitochondrial protein synthesis inhibition induced TP53 expression at transcriptional levels by enhancing TP53 promoter activity, and increased TP53 protein stability by suppressing TP53 ubiquitination through MAPK14/p38 MAPK-mediated TP53 phosphorylation.	Reactive Oxygen Species	4-7	P53	Homo sapiens	139-143
22576012-6	2012	The ROS elevation resulting from mitochondrial protein synthesis inhibition induced TP53 expression at transcriptional levels by enhancing TP53 promoter activity, and increased TP53 protein stability by suppressing TP53 ubiquitination through MAPK14/p38 MAPK-mediated TP53 phosphorylation.	Reactive Oxygen Species	4-7	P53	Homo sapiens	139-143
22576012-6	2012	The ROS elevation resulting from mitochondrial protein synthesis inhibition induced TP53 expression at transcriptional levels by enhancing TP53 promoter activity, and increased TP53 protein stability by suppressing TP53 ubiquitination through MAPK14/p38 MAPK-mediated TP53 phosphorylation.	Reactive Oxygen Species	4-7	P53	Homo sapiens	139-143
22576012-8	2012	Altogether, these data indicate that autophagy is induced through the ROS-TP53-DRAM1 pathway in response to mitochondrial protein synthesis inhibition.	Reactive Oxygen Species	70-73	P53	Homo sapiens	74-78
23705067-5	2012	FoxOs, sirtuins and the p53/p66shc signaling cascade alter osteoblast number and bone formation via ROS-dependent and -independent mechanisms.	Reactive Oxygen Species	100-103	P53	Homo sapiens	24-27
22434045-6	2012	Knock-down of Fer also increased the level of Reactive-Oxygen Species (ROS) in CC cells, and subjection of Fer depleted cells to ROS neutralizing scavengers significantly decreased the induced phosphorylation and activation of ATM and p53.	Reactive Oxygen Species	129-132	P53	Homo sapiens	235-238
22434045-7	2012	Notably, over-expression of Fer opposed the Doxorubicin driven activation of ATM and p53, which can be mediated by ROS.	Doxorubicin	44-55	P53	Homo sapiens	85-88
22434045-7	2012	Notably, over-expression of Fer opposed the Doxorubicin driven activation of ATM and p53, which can be mediated by ROS.	Reactive Oxygen Species	115-118	P53	Homo sapiens	85-88
22722496-11	2012	Overall, our findings indicate that S-phase-specific, TopBP1-independent activation of the ATR-p53 axis is a critical stress response to FA-DPC, which has implications for understanding of FA carcinogenesis.	fa-dpc	137-143	P53	Homo sapiens	95-98
22565279-8	2012	Furthermore, our data also indicate that the formation of reactive oxygen species (ROS), decline of mitochondrial membrane potential (DeltaPsi(m)), increasing p53 and decreasing c-Myc levels play important roles in response to BPDE toxicity.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	227-231	P53	Homo sapiens	159-162
22359193-9	2012	The stable transfection of PDCD5 demonstrated G2/M cell cycle arrest, increased apoptosis and nuclear translocation of PDCD5 and p53 after cisplatin treatment.	Cisplatin	139-148	P53	Homo sapiens	129-132
22381680-11	2012	The transcription of these genes correlates with TP53 activation as documented by p21 messenger RNA elevation, a surrogate for TP53 activation and by using TP53 temperature-sensitive cells treated with adriamycin.	Doxorubicin	202-212	P53	Homo sapiens	49-53
22565279-9	2012	In conclusion, these results suggest that BPDE-mediated apoptosis occurs via caspase-9 dependent mitochondria pathway associated with ROS formation, loss of DeltaPsi(m), up-regulation of p53 and down-regulation of c-Myc, but independent of the opening of mPTP in 16HBE cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	42-46	P53	Homo sapiens	187-190
22534478-4	2012	RESULTS: p53 expression were associated with the significantly shorter disease-free survival (DFS) (p&lt;0.001) and overall survival (OS) (p=0.012) in the curatively resected advanced gastric cancer patients receiving capecitabine plus paclitaxel.	Paclitaxel	236-246	P53	Homo sapiens	9-12
22534478-6	2012	CONCLUSIONS: p53 expression positive might predict prognosis in gastric cancer patients who underwent curative surgery followed by adjuvant capecitabine plus paclitaxel chemotherapy.	Paclitaxel	158-168	P53	Homo sapiens	13-16
22534478-7	2012	A favorable effect of capecitabine plus paclitaxel might therefore be expected in patients that do not express p53.	Paclitaxel	40-50	P53	Homo sapiens	111-114
22552582-1	2012	Acetylation of the tumor suppressor gene p53 at the carboxy-terminal lysine (Lys) residues enhances its transcriptional activity associated with cell cycle arrest and apoptosis.	Lysine	69-75	P53	Homo sapiens	41-44
22552582-1	2012	Acetylation of the tumor suppressor gene p53 at the carboxy-terminal lysine (Lys) residues enhances its transcriptional activity associated with cell cycle arrest and apoptosis.	Lysine	77-80	P53	Homo sapiens	41-44
22427690-5	2012	Furthermore, the Zn(+2) region conformational p53 mutants (p53(R175H) and p53(H179R)) induced the CGS by elevating H-Ras activity.	Zinc	17-19	P53	Homo sapiens	46-49
22427690-5	2012	Furthermore, the Zn(+2) region conformational p53 mutants (p53(R175H) and p53(H179R)) induced the CGS by elevating H-Ras activity.	Zinc	17-19	P53	Homo sapiens	59-62
22427690-5	2012	Furthermore, the Zn(+2) region conformational p53 mutants (p53(R175H) and p53(H179R)) induced the CGS by elevating H-Ras activity.	Zinc	17-19	P53	Homo sapiens	59-62
22706304-5	2012	Treatment of a human mammary epithelial cell line with doxorubicin resulted in ISGylation of the p53 family protein p63.	Doxorubicin	55-66	P53	Homo sapiens	97-100
22356895-2	2012	To seek predictive biomarkers, we analysed single nucleotide polymorphisms (SNPs) in the p53 and MDM2 genes in LAHNSCC patients treated with cisplatin-based CRT.	Cisplatin	141-150	P53	Homo sapiens	89-92
22356895-9	2012	In contrast, the predictive utility of the 72 Arg/Pro SNP in p53 requires mutational analysis of p53, limiting its routine clinical use.	Arginine	46-49	P53	Homo sapiens	97-100
22356895-9	2012	In contrast, the predictive utility of the 72 Arg/Pro SNP in p53 requires mutational analysis of p53, limiting its routine clinical use.	Arginine	46-49	P53	Homo sapiens	61-64
22717582-4	2012	In proof-of-principle studies, betulinic acid, doxorubicin and vincristine induced cell death in a p53- and NOXA-independent pathway involving mitochondrial pore formation, release of cytochrome c and caspase activation.	betulinic acid	31-45	P53	Homo sapiens	99-102
22717582-4	2012	In proof-of-principle studies, betulinic acid, doxorubicin and vincristine induced cell death in a p53- and NOXA-independent pathway involving mitochondrial pore formation, release of cytochrome c and caspase activation.	Doxorubicin	47-58	P53	Homo sapiens	99-102
22570471-0	2012	Inhibition of nicotinamide phosphoribosyltransferase (NAMPT) activity by small molecule GMX1778 regulates reactive oxygen species (ROS)-mediated cytotoxicity in a p53- and nicotinic acid phosphoribosyltransferase1 (NAPRT1)-dependent manner.	Reactive Oxygen Species	106-129	P53	Homo sapiens	163-166
22570471-10	2012	GMX1778-mediated ROS induction is p53-dependent, suggesting that the status of both p53 and NAPRT1 might affect tumor apoptosis, as determined by annexin-V staining.	Reactive Oxygen Species	17-20	P53	Homo sapiens	34-37
22570471-10	2012	GMX1778-mediated ROS induction is p53-dependent, suggesting that the status of both p53 and NAPRT1 might affect tumor apoptosis, as determined by annexin-V staining.	Reactive Oxygen Species	17-20	P53	Homo sapiens	84-87
22570471-0	2012	Inhibition of nicotinamide phosphoribosyltransferase (NAMPT) activity by small molecule GMX1778 regulates reactive oxygen species (ROS)-mediated cytotoxicity in a p53- and nicotinic acid phosphoribosyltransferase1 (NAPRT1)-dependent manner.	Reactive Oxygen Species	131-134	P53	Homo sapiens	163-166
22717582-5	2012	In contrast, when betulinic acid was combined with either doxorubicine or vincristine, cell death signaling changed considerably; the drug combinations clearly depended on both p53 and NOXA.	betulinic acid	18-32	P53	Homo sapiens	177-180
22717582-5	2012	In contrast, when betulinic acid was combined with either doxorubicine or vincristine, cell death signaling changed considerably; the drug combinations clearly depended on both p53 and NOXA.	Doxorubicin	58-70	P53	Homo sapiens	177-180
22428663-0	2012	Cell cycle regulation by carboxylated multiwalled carbon nanotubes through p53-independent induction of p21 under the control of the BMP signaling pathway.	Carbon	50-56	P53	Homo sapiens	75-78
22428663-1	2012	This report describes how carboxylated multiwalled carbon nanotubes (MWCNTs) induce p53-independent p21 expression and cell cycle arrest.	Carbon	51-57	P53	Homo sapiens	84-87
22469513-3	2012	Treatment of the cells with DOX induced reactive oxygen species (ROS) generation and a concomitant increase in apoptotic cell death through the mitochondrial death pathway independent of p53.	Doxorubicin	28-31	P53	Homo sapiens	187-190
22414726-5	2012	Although p53 was phosphorylated at Serine 15 in response to adducts, long term growth inhibition of mammalian cells was not affected by p53 status.	Serine	35-41	P53	Homo sapiens	9-12
22672905-0	2012	Global tumor protein p53/p63 interactome: making a case for cisplatin chemoresistance.	Cisplatin	60-69	P53	Homo sapiens	21-24
22672905-6	2012	Using quantitative mass-spectrometry of protein complexes labeled with isobaric tags, we showed that TP53 and DeltaNp63alpha are involved in numerous protein-protein interactions, which are likely to be implicated in the response of tumor cells to cisplatin exposure.	Cisplatin	248-257	P53	Homo sapiens	101-105
22672905-9	2012	Overall, our studies provide an integrated proteomic platform in making a case for the role of the p53/p63 interactome in cisplatin chemoresistance.	Cisplatin	122-131	P53	Homo sapiens	99-102
22469844-5	2012	When MTS-p53 cells were treated with the nucleoside reverse transcriptase inhibitor (NRTI), 2",3"-dideoxycytidine or 2",3"-dideoxyinosine, mtDNA depletion that resembled untransfected controls was observed in both instances.	Zalcitabine	92-113	P53	Homo sapiens	9-12
22002314-0	2012	Melatonin triggers p53Ser phosphorylation and prevents DNA damage accumulation.	Melatonin	0-9	P53	Homo sapiens	19-22
22002314-2	2012	This paper illustrates that melatonin induces phosphorylation of p53 at Ser-15 inhibiting cell proliferation and preventing DNA damage accumulation of both normal and transformed cells.	Melatonin	28-37	P53	Homo sapiens	65-68
22002314-2	2012	This paper illustrates that melatonin induces phosphorylation of p53 at Ser-15 inhibiting cell proliferation and preventing DNA damage accumulation of both normal and transformed cells.	Serine	72-75	P53	Homo sapiens	65-68
22002314-3	2012	This activity requires p53 and promyelocytic leukemia (PML) expression and efficient phosphorylation of p53 at Ser-15 residue.	Serine	111-114	P53	Homo sapiens	23-26
22002314-3	2012	This activity requires p53 and promyelocytic leukemia (PML) expression and efficient phosphorylation of p53 at Ser-15 residue.	Serine	111-114	P53	Homo sapiens	104-107
22002314-4	2012	Melatonin-induced p53 phosphorylation at Ser-15 residue does not require ataxia telangiectasia-mutated activity, whereas it is severely impaired upon chemical inhibition of p38 mitogen-activated protein kinase activity.	Melatonin	0-9	P53	Homo sapiens	18-21
22002314-4	2012	Melatonin-induced p53 phosphorylation at Ser-15 residue does not require ataxia telangiectasia-mutated activity, whereas it is severely impaired upon chemical inhibition of p38 mitogen-activated protein kinase activity.	Serine	41-44	P53	Homo sapiens	18-21
22002314-5	2012	By and large, these findings imply that the activation of the p53 tumor-suppressor pathway is a critical mediator of melatonin and its anticancer effects.	Melatonin	117-126	P53	Homo sapiens	62-65
22611237-8	2012	DNA damage is a likely trigger for p53-dependent AICD because susceptible lymphoblasts expressed significantly elevated levels of both phosphorylated ataxia telangiectasia mutated-Ser(1980) and phospho-H2AX-Ser(139).	Serine	180-183	P53	Homo sapiens	35-38
22611237-8	2012	DNA damage is a likely trigger for p53-dependent AICD because susceptible lymphoblasts expressed significantly elevated levels of both phosphorylated ataxia telangiectasia mutated-Ser(1980) and phospho-H2AX-Ser(139).	Serine	207-210	P53	Homo sapiens	35-38
22698404-3	2012	Doxorubicin-treated p53 mutant tumors failed to arrest proliferation, leading to abnormal mitoses and cell death, whereas p53 wild-type tumors arrested, avoiding mitotic catastrophe.	Doxorubicin	0-11	P53	Homo sapiens	20-23
22258307-11	2012	CONCLUSION: This meta-analysis suggests that p53 codon 72 Pro/Pro + Arg/Pro genotypes are associated with increased risk of endometriosis in Asian.	Arginine	68-71	P53	Homo sapiens	45-48
22117613-6	2012	FUTURE DIRECTIONS: In this review, we describe how ROS production regulates p53 activity and how p53 can, in turn, influence cellular ROS production.	Reactive Oxygen Species	134-137	P53	Homo sapiens	97-100
22614867-9	2012	In conclusion, ROS-mediated oxidative stress, the activation of p53, Bax, caspase-3 and oxidative DNA damage are involved in the mechanistic pathways of nano-TiO(2)-induced apoptosis in HEK-293 cells.	Reactive Oxygen Species	15-18	P53	Homo sapiens	64-67
22465335-6	2012	p53 fused with 3R (3R-p53) was delivered into glioma cells without pyrenebutyrate but could not be translocated into the nucleus.	pyrenebutyrate	67-81	P53	Homo sapiens	0-3
22465335-7	2012	In contrast, 3R-p53 was observed in nuclei of glioma cells when co-applied with pyrenebutyrate.	pyrenebutyrate	80-94	P53	Homo sapiens	16-19
22634534-4	2012	The objective of the present study was to clarify the role of the expression status of proteins involved in the Rb and p53 tumour suppressor pathways in sensitivity and resistance of GCTs to cisplatin-based chemotherapy.	Cisplatin	191-200	P53	Homo sapiens	119-122
22117613-2	2012	Redox-sensitive proteins, such as the tumor suppressor protein p53, are susceptible to ROS-dependent modifications, which could impact their activities and/or biological functions.	Reactive Oxygen Species	87-90	P53	Homo sapiens	63-66
22117613-5	2012	CRITICAL ISSUES: Recent studies present evidence that ROS function upstream of p53 in some model systems, while in others ROS production could be a downstream effect of p53 activation.	Reactive Oxygen Species	54-57	P53	Homo sapiens	79-82
22117613-5	2012	CRITICAL ISSUES: Recent studies present evidence that ROS function upstream of p53 in some model systems, while in others ROS production could be a downstream effect of p53 activation.	Reactive Oxygen Species	54-57	P53	Homo sapiens	169-172
22117613-5	2012	CRITICAL ISSUES: Recent studies present evidence that ROS function upstream of p53 in some model systems, while in others ROS production could be a downstream effect of p53 activation.	Reactive Oxygen Species	122-125	P53	Homo sapiens	169-172
22117613-6	2012	FUTURE DIRECTIONS: In this review, we describe how ROS production regulates p53 activity and how p53 can, in turn, influence cellular ROS production.	Reactive Oxygen Species	51-54	P53	Homo sapiens	76-79
22397410-0	2012	Golgi-SNARE GS28 potentiates cisplatin-induced apoptosis by forming GS28-MDM2-p53 complexes and by preventing the ubiquitination and degradation of p53.	Cisplatin	29-38	P53	Homo sapiens	78-81
22397410-0	2012	Golgi-SNARE GS28 potentiates cisplatin-induced apoptosis by forming GS28-MDM2-p53 complexes and by preventing the ubiquitination and degradation of p53.	Cisplatin	29-38	P53	Homo sapiens	148-151
22397410-6	2012	Conversely, GS28 overexpression induced the accumulation of p53 and Bax as well as the pro-apoptotic phosphorylation of p53 on Ser(46).	Serine	127-130	P53	Homo sapiens	120-123
22397410-9	2012	As expected, ectopic expression of p53 in H1299 cells restored the modulatory effects of GS28 on sensitivity to cisplatin.	Cisplatin	112-121	P53	Homo sapiens	35-38
22404155-9	2012	Enhanced level of phosphorylated-p53 (Ser-15) was observed after gamma-irradiation but not after carbon-ion irradiation.	Serine	38-41	P53	Homo sapiens	33-36
22417066-6	2012	The antiproliferative effect of XRT/RSV treatment correlated with increased expression of p15, p21, and mutant p53 and decreased expression of cyclin B, cyclin D, and cdk2.	Resveratrol	36-39	P53	Homo sapiens	111-114
22555805-7	2012	Intriguingly, AKR1A1 depletion induced phosphorylation of p53 at serine 15 and G 2/M transition in response to irradiation.	Serine	65-71	P53	Homo sapiens	58-61
22304673-4	2012	The six reviews in this Forum showcase the up-to-date knowledge on how ROS modulate or interact with the p53 protein, epithelial-mesenchymal transition, tumor stromal cells, angiogenesis, and cancer stem cells, which are essential factors in cancer development and metastasis.	Reactive Oxygen Species	71-74	P53	Homo sapiens	105-108
23360043-4	2012	Immunohistochemical staining for p53 was performed on formalin fixed paraffin embedded tissue sections with appropriate positive and negative control.	Paraffin	69-77	P53	Homo sapiens	33-36
21826651-10	2012	Furthermore, increased levels of wild-type GRK2 induced upregulation of phosphor-Ser(15) p53 and cyclin B1 in a dose-dependent manner.	Serine	81-84	P53	Homo sapiens	89-92
21477265-9	2012	An increased risk was also associated with the TP53 Pro/Pro genotype (OR = 2.19, 95% CI = 1.54-3.06) compared with the Arg/Arg genotype.	Arginine	119-122	P53	Homo sapiens	47-51
21477265-9	2012	An increased risk was also associated with the TP53 Pro/Pro genotype (OR = 2.19, 95% CI = 1.54-3.06) compared with the Arg/Arg genotype.	Arginine	123-126	P53	Homo sapiens	47-51
22522053-8	2012	In addition, p53 involved in curcumin-mediated Fas, FasL, and DR5 expression and cell apoptosis in chondrosarcoma cells.	Curcumin	29-37	P53	Homo sapiens	13-16
21494837-5	2012	We found that a C-1 acetoxymethyl derivative of 7-deoxypancratistatin, JC-TH-acetate-4 (JCTH-4), was effective in inducing apoptosis in both p53 positive (HCT 116) and p53 negative (HT-29) human CRC cell lines, demonstrating similar efficacy to that of natural PST.	jc-th-acetate	71-84	P53	Homo sapiens	141-144
21494837-5	2012	We found that a C-1 acetoxymethyl derivative of 7-deoxypancratistatin, JC-TH-acetate-4 (JCTH-4), was effective in inducing apoptosis in both p53 positive (HCT 116) and p53 negative (HT-29) human CRC cell lines, demonstrating similar efficacy to that of natural PST.	jc-th-acetate	71-84	P53	Homo sapiens	168-171
21308489-8	2012	The present study indicates that p53 null osteosarcoma MG63 cells are susceptible to the ATO; the inhibition of catalase and the resulted intracellular ROS accumulation are an important molecular mechanism under which ATO induces apoptosis of p53-deficient osteosarcoma cells.	ros	152-155	P53	Homo sapiens	33-36
21308489-8	2012	The present study indicates that p53 null osteosarcoma MG63 cells are susceptible to the ATO; the inhibition of catalase and the resulted intracellular ROS accumulation are an important molecular mechanism under which ATO induces apoptosis of p53-deficient osteosarcoma cells.	ros	152-155	P53	Homo sapiens	243-246
22441128-4	2012	In the present study, the early therapeutic response of rAd/p53, combined with 5-fluorouracil (5-FU) or with iodized oil, was observed in a human colon cancer model.	Fluorouracil	79-93	P53	Homo sapiens	60-63
22622028-6	2012	We show that activation of the MC1R by alpha-MSH contributes to phosphorylation of p53 on serine 15, a known requirement for stabilization and activation of p53, a major sensor of DNA damage.	Serine	90-96	P53	Homo sapiens	83-86
22622028-6	2012	We show that activation of the MC1R by alpha-MSH contributes to phosphorylation of p53 on serine 15, a known requirement for stabilization and activation of p53, a major sensor of DNA damage.	Serine	90-96	P53	Homo sapiens	157-160
22711025-1	2012	Cyclotherapy is a promising endeavor to improve cancer treatment by tackling the dose-limiting side effects of chemotherapy, especially for cancers harboring mutations in the TP53 tumor suppressor.	cyclotherapy	0-12	P53	Homo sapiens	175-179
22342995-4	2012	Consistent with these observations, the apoptotic pathway activated upon H2O2 treatment relies upon Trx1 oxidation, and is mediated by the p38(MAPK)/p53 signaling axis.	Hydrogen Peroxide	73-77	P53	Homo sapiens	149-152
22441128-8	2012	p53 expression reached its peak at 120 h in the rAd/p53 group, at 72 h in the rAd/p53+5-FU group, and at 48 h in the rAd/p53+iodized oil group.	Fluorouracil	86-90	P53	Homo sapiens	0-3
22441128-10	2012	The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect.	Fluorouracil	22-26	P53	Homo sapiens	125-128
22441128-10	2012	The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect.	Fluorouracil	22-26	P53	Homo sapiens	125-128
22441128-10	2012	The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect.	Fluorouracil	66-70	P53	Homo sapiens	18-21
22441128-10	2012	The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect.	Fluorouracil	66-70	P53	Homo sapiens	125-128
22441128-10	2012	The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect.	Fluorouracil	66-70	P53	Homo sapiens	125-128
22441128-10	2012	The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect.	Fluorouracil	66-70	P53	Homo sapiens	18-21
22441128-10	2012	The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect.	Fluorouracil	66-70	P53	Homo sapiens	125-128
22441128-10	2012	The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect.	Fluorouracil	66-70	P53	Homo sapiens	125-128
22493143-5	2012	An activation of p53 (TP53) transcriptional activity in Dox- or Dox+TSA-treated cells was revealed by the increased expression levels of p53 mRNA/protein as well as p53-driven luciferase activities.	Doxorubicin	56-59	P53	Homo sapiens	17-20
22493143-5	2012	An activation of p53 (TP53) transcriptional activity in Dox- or Dox+TSA-treated cells was revealed by the increased expression levels of p53 mRNA/protein as well as p53-driven luciferase activities.	Doxorubicin	56-59	P53	Homo sapiens	22-26
22493143-5	2012	An activation of p53 (TP53) transcriptional activity in Dox- or Dox+TSA-treated cells was revealed by the increased expression levels of p53 mRNA/protein as well as p53-driven luciferase activities.	Doxorubicin	56-59	P53	Homo sapiens	137-140
22493143-5	2012	An activation of p53 (TP53) transcriptional activity in Dox- or Dox+TSA-treated cells was revealed by the increased expression levels of p53 mRNA/protein as well as p53-driven luciferase activities.	Doxorubicin	56-59	P53	Homo sapiens	137-140
22493143-5	2012	An activation of p53 (TP53) transcriptional activity in Dox- or Dox+TSA-treated cells was revealed by the increased expression levels of p53 mRNA/protein as well as p53-driven luciferase activities.	Doxorubicin	64-67	P53	Homo sapiens	17-20
22493143-5	2012	An activation of p53 (TP53) transcriptional activity in Dox- or Dox+TSA-treated cells was revealed by the increased expression levels of p53 mRNA/protein as well as p53-driven luciferase activities.	Doxorubicin	64-67	P53	Homo sapiens	22-26
22493143-5	2012	An activation of p53 (TP53) transcriptional activity in Dox- or Dox+TSA-treated cells was revealed by the increased expression levels of p53 mRNA/protein as well as p53-driven luciferase activities.	Doxorubicin	64-67	P53	Homo sapiens	137-140
22493143-5	2012	An activation of p53 (TP53) transcriptional activity in Dox- or Dox+TSA-treated cells was revealed by the increased expression levels of p53 mRNA/protein as well as p53-driven luciferase activities.	Doxorubicin	64-67	P53	Homo sapiens	137-140
22043989-11	2012	The apoptotic effect of both extracts, especially GTPs, seems to be mediated by both P 53 and Bcl-2.	Guanosine Triphosphate	50-54	P53	Homo sapiens	85-89
22510407-8	2012	These results indicate that HBx impacts p53-mediated transcription of Mfn2, providing insight into the negative effect of HBx against p53-dependent chemotherapeutic agents, such as doxorubicin, used in the treatment of HCC.	Doxorubicin	181-192	P53	Homo sapiens	40-43
22510407-8	2012	These results indicate that HBx impacts p53-mediated transcription of Mfn2, providing insight into the negative effect of HBx against p53-dependent chemotherapeutic agents, such as doxorubicin, used in the treatment of HCC.	Doxorubicin	181-192	P53	Homo sapiens	134-137
22559167-7	2012	The effects of rapamycin and/or bortezomib on the mRNA expression levels of p53, p27, p21 and Bcl-2 family in HCCLM3 cells were evaluated by RT-PCR.	Sirolimus	15-24	P53	Homo sapiens	76-79
22552282-11	2012	These data demonstrate that oxygen regulates Mcl-1 and p53 stability during placentation via HIF-1-controlled MULE expression.	Oxygen	28-34	P53	Homo sapiens	55-58
22465181-5	2012	In the OVCAR-3 and SK-OV-3 cell lines, licochalocone A induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels; an increase in Bax levels; loss of the mitochondrial transmembrane potential; cytochrome c release; activation of caspases (-8, -9 and -3); cleavage of PARP-1; and an increase in the tumor suppressor p53 levels.	licochalocone a	39-54	P53	Homo sapiens	325-328
21963854-6	2012	p53 pre-methylated at lysine-372 (p53K372 mono-methylation) by SET7 protects p53 from E6-induced degradation.	Lysine	22-28	P53	Homo sapiens	0-3
21963854-6	2012	p53 pre-methylated at lysine-372 (p53K372 mono-methylation) by SET7 protects p53 from E6-induced degradation.	Lysine	22-28	P53	Homo sapiens	34-37
22551440-0	2012	Prognostic and predictive value of TP53 mutations in node-positive breast cancer patients treated with anthracycline- or anthracycline/taxane-based adjuvant therapy: results from the BIG 02-98 phase III trial.	Anthracyclines	103-116	P53	Homo sapiens	35-39
22551440-0	2012	Prognostic and predictive value of TP53 mutations in node-positive breast cancer patients treated with anthracycline- or anthracycline/taxane-based adjuvant therapy: results from the BIG 02-98 phase III trial.	Anthracyclines	121-134	P53	Homo sapiens	35-39
22551440-0	2012	Prognostic and predictive value of TP53 mutations in node-positive breast cancer patients treated with anthracycline- or anthracycline/taxane-based adjuvant therapy: results from the BIG 02-98 phase III trial.	taxane	135-141	P53	Homo sapiens	35-39
22551440-1	2012	INTRODUCTION: Pre-clinical data suggest p53-dependent anthracycline-induced apoptosis and p53-independent taxane activity.	Anthracyclines	54-67	P53	Homo sapiens	40-43
22551440-1	2012	INTRODUCTION: Pre-clinical data suggest p53-dependent anthracycline-induced apoptosis and p53-independent taxane activity.	taxane	106-112	P53	Homo sapiens	90-93
22546652-8	2012	Up regulation of p53 gene expression provides cue for apoptotic activity of hyoscyamine.	Hyoscyamine	76-87	P53	Homo sapiens	17-20
22288499-6	2012	Serial mutations at serine and threonine residues in the NTD confirm that p53(Ser15) phosphorylation induces dissociation of the p53-RPA70 complex in hypoxia.	Serine	20-26	P53	Homo sapiens	74-77
22288499-6	2012	Serial mutations at serine and threonine residues in the NTD confirm that p53(Ser15) phosphorylation induces dissociation of the p53-RPA70 complex in hypoxia.	Serine	20-26	P53	Homo sapiens	129-132
22288499-6	2012	Serial mutations at serine and threonine residues in the NTD confirm that p53(Ser15) phosphorylation induces dissociation of the p53-RPA70 complex in hypoxia.	Threonine	31-40	P53	Homo sapiens	74-77
22644859-3	2012	In adriamycin-resistant MCF-7 human breast cancer (MCF-7/ADR) cells, which express a mutant form of p53, 3-GAP induced significant apoptosis, which was accompanied by no change in p53 transcriptional activity, but an increase in Bax expression, cyt c release, and activation of caspase-9, 7, and 3.	Doxorubicin	3-13	P53	Homo sapiens	100-103
22644859-11	2012	These effects are mediated through p53-independent caspase-3 activation and reduction of the capacity for cellular antioxidants, such as GSTpi and GSH.	Glutathione	147-150	P53	Homo sapiens	35-38
22074401-10	2012	p53 induced higher intracellular Ca(2+)  release and ROS followed by activation of p53 downstream genes including those for the micro RNA mir34a.	Reactive Oxygen Species	53-56	P53	Homo sapiens	0-3
22074401-11	2012	In p53(-/-)  and p53 mutant cells, GaQ(3) -induced Ca(2+) -signalling generated ROS.	Reactive Oxygen Species	80-83	P53	Homo sapiens	17-20
22074401-8	2012	Ca(2+)  signalling, p53, p300 and ROS were serially knocked down to study Ca(2+) -p53-ROS ineractions in GaQ(3) -induced apoptosis.	Reactive Oxygen Species	86-89	P53	Homo sapiens	82-85
22394450-1	2012	S100A2 is an EF-hand calcium ion (Ca(2+))-binding protein that activates the tumour suppressor p53.	Calcium	21-28	P53	Homo sapiens	95-98
22489661-0	2012	Radiation/paclitaxel treatment of p53-abnormal non-small cell lung cancer xenograft tumor and associated mechanism.	Paclitaxel	10-20	P53	Homo sapiens	34-37
22551548-6	2012	RESULTS: The analysis revealed a germline nonsense mutation in exon 8 at codon 306 of the codified region of the TP53 gene, causing a change of CGA to TGA (Arg Stop) in the proband, her mother, her cousin and her maternal uncle.	Arginine	156-159	P53	Homo sapiens	113-117
22509835-0	2012	Quercetin enhancement of arsenic-induced apoptosis via stimulating ROS-dependent p53 protein ubiquitination in human HaCaT keratinocytes.	Reactive Oxygen Species	67-70	P53	Homo sapiens	81-84
22509835-4	2012	A decrease in the p53 protein with increased protein ubiquitination was detected in QUE/As(+3)-treated HaCaT cells, and this was prevented by the addition of NAC.	Acetylcysteine	158-161	P53	Homo sapiens	18-21
22509835-7	2012	Additionally, QUE and BSO enhanced the cytotoxic effects of monomethylarsonous acid (MMA(+3)) but not other arsenic compounds in accordance with increased p53 protein ubiquitination in HaCaT cells.	monomethylarsonous acid	60-83	P53	Homo sapiens	155-158
22509835-8	2012	QUE plus As(+3) stimulation of apoptosis in human HaCaT keratinocytes via activating ROS-dependent p53 protein ubiquitination may offer a rationale for the use of QUE to improve the clinical efficacy of arsenics in treating psoriasis.	Reactive Oxygen Species	85-88	P53	Homo sapiens	99-102
22783341-3	2012	Therefore, it has been suggested as a potential target for the treatment of hepatitis C. However, recent evidence shows that miR-122 decreases HBV replication through the inhibitory effect of p53 on HBV transcription, and consequently it acts as a tumor-suppressor through both a decrease in HBV replication and by directly targeting cyclin G1, as well as Wnt/beta-catenin, and NDRG3 pathways.	wnt	356-359	P53	Homo sapiens	192-195
22348537-6	2012	The activation of tumor suppressor protein 53 (p53) and its phosphorylations on serines 15 and 392 were detected from the first day after irradiation by 20 Gy and remained elevated to day 13.	Serine	80-87	P53	Homo sapiens	47-50
22142405-11	2012	The exposure of DPSCs and HDFs to cisplatin provoked an increase in p53 and p21 expression and p53 phosphorylation of serine 15.	Cisplatin	34-43	P53	Homo sapiens	68-71
22142405-11	2012	The exposure of DPSCs and HDFs to cisplatin provoked an increase in p53 and p21 expression and p53 phosphorylation of serine 15.	Cisplatin	34-43	P53	Homo sapiens	95-98
22142405-11	2012	The exposure of DPSCs and HDFs to cisplatin provoked an increase in p53 and p21 expression and p53 phosphorylation of serine 15.	Serine	118-124	P53	Homo sapiens	95-98
22331493-0	2012	Sodium arsenite +- hyperthermia sensitizes p53-expressing human ovarian cancer cells to cisplatin by modulating platinum-DNA damage responses.	Cisplatin	88-97	P53	Homo sapiens	43-46
22858706-5	2012	Paraffin-embebeded sections were immunostained for p53 and p21WAF1.	Paraffin	0-8	P53	Homo sapiens	51-54
21684138-5	2012	Cisplatin triggered marked activation of stress signaling pathways [p53, Jun N-terminal kinase (JNK), and p38-alpha mitogen-activated protein kinase (MAPK)] and promoted cell death in the kidneys (increased DNA fragmentation, caspases-3/7 activity, terminal deoxynucleotidyl transferase-mediated uridine triphosphate nick-end labeling), associated with attenuation of various prosurvival signaling pathways [e.g., extracellular signal-regulated kinase (ERK) and p38-beta MAPK].	Cisplatin	0-9	P53	Homo sapiens	68-71
21684138-8	2012	Thus, the cisplatin-induced nephropathy is associated with activation of various cell death and proinflammatory pathways (p53, JNK, p38-alpha, TNF-alpha and NF-kappaB) and impairments of key prosurvival signaling mechanisms (ERK and p38-beta).	Cisplatin	10-19	P53	Homo sapiens	122-125
22534715-7	2012	Interestingly, direct DNA sequencing of the paraffin-embedded tumor sample identified a novel R248Q mutation in the TP53 gene.	Paraffin	44-52	P53	Homo sapiens	116-120
22328720-7	2012	At the molecular level, cisplatin treatment resulted in elevated p53 levels, enhanced caspase-3 activation, and reduced p21 levels in E6-suppressed cells.	Cisplatin	24-33	P53	Homo sapiens	65-68
21997969-5	2012	Furthermore, tanshinone IIA activated the phosphorylation of p53 at Ser 15 residue and its downstream p21 and p27.	Serine	68-71	P53	Homo sapiens	61-64
21997969-7	2012	Conversely, silencing p53 using its specific siRNA reversed cyclin D1 expression inhibited by tanshinone IIA.	tanshinone	94-108	P53	Homo sapiens	22-25
22369716-3	2012	Melatonin"s SERM actions include modulation of estrogen-regulated cell proliferation, invasiveness and expression of proteins, growth factors and proto-oncogenes (hTERT, p53, p21, TGFbeta, E-cadherin, etc.).	Melatonin	0-9	P53	Homo sapiens	170-173
22331493-11	2012	Hyperthermia +- sodium arsenite enhanced cellular and DNA accumulation of platinum in wild-type p53-expressing cells.	Platinum	74-82	P53	Homo sapiens	96-99
22331493-12	2012	Only hyperthermia enhanced platinum accumulation in p53-null cells.	Platinum	27-35	P53	Homo sapiens	52-55
22331493-13	2012	In conclusion, sodium arsenite +- hyperthermia sensitizes wild-type p53-expressing EOC cells to cisplatin by suppressing DNA repair protein XPC and increasing cellular and DNA platinum accumulation.	Cisplatin	96-105	P53	Homo sapiens	68-71
21766316-0	2012	Effects of SiO2 nanoparticles on HFL-I activating ROS-mediated apoptosis via p53 pathway.	Reactive Oxygen Species	50-53	P53	Homo sapiens	77-80
22331493-0	2012	Sodium arsenite +- hyperthermia sensitizes p53-expressing human ovarian cancer cells to cisplatin by modulating platinum-DNA damage responses.	Platinum	112-120	P53	Homo sapiens	43-46
22331493-3	2012	P53 plays a critical role in cellular response to DNA damage and has been implicated in EOC response to platinum chemotherapy.	Platinum	104-112	P53	Homo sapiens	0-3
22331493-4	2012	In this study, we examined the role of p53 status in EOC response to a novel combination of cisplatin, sodium arsenite, and hyperthermia.	Cisplatin	92-101	P53	Homo sapiens	39-42
22331493-5	2012	Human EOC cells were treated with cisplatin +- 20muM sodium arsenite at 37 C or 39 C for 1 h. Sodium arsenite +- hyperthermia sensitized wild-type p53-expressing (A2780, A2780/CP70, OVCA 420, OVCA 429, and OVCA 433) EOC cells to cisplatin.	Cisplatin	34-43	P53	Homo sapiens	147-150
22331493-6	2012	Hyperthermia sensitized p53-null SKOV-3 and p53-mutant (OVCA 432 and OVCAR-3) cells to cisplatin.	Cisplatin	87-96	P53	Homo sapiens	24-27
22331493-6	2012	Hyperthermia sensitized p53-null SKOV-3 and p53-mutant (OVCA 432 and OVCAR-3) cells to cisplatin.	Cisplatin	87-96	P53	Homo sapiens	44-47
22564603-8	2012	CsA induced p27 and p53, as well as degradation of 116-kd PARP into an 89-kd fragment.	Cyclosporine	0-3	P53	Homo sapiens	20-23
22331493-8	2012	XPC, a critical DNA damage recognition protein in global genome repair pathway, was induced by cisplatin only in wild-type p53-expressing cells.	Cisplatin	95-104	P53	Homo sapiens	123-126
22331493-9	2012	Cotreatment with sodium arsenite +- hyperthermia attenuated cisplatin-induced XPC in wild-type p53-expressing cells.	Cisplatin	60-69	P53	Homo sapiens	95-98
22723163-2	2012	METHODS: Recombinant plasmid of mutant p53 gene-targeting siRNA was transfected into gastric cancer SGC7901 cells by Lipofectamine(TM)2000.	Thulium	131-133	P53	Homo sapiens	39-42
22331493-10	2012	XPC siRNA transfection sensitized wild-type p53-expressing cells to cisplatin, suggesting that sodium arsenite +- hyperthermia attenuation of XPC is a mechanism by which wild-type p53-expressing cells are sensitized to cisplatin.	Cisplatin	68-77	P53	Homo sapiens	44-47
21927021-0	2012	The oncogenic phosphatase PPM1D confers cisplatin resistance in ovarian carcinoma cells by attenuating checkpoint kinase 1 and p53 activation.	Cisplatin	40-49	P53	Homo sapiens	127-130
21927021-6	2012	Our findings establish for the first time that PPM1D confers CDDP resistance in OVCA cells through attenuating CDDP-induced, Chk1-mediated, p53-dependent apoptosis.	Cisplatin	111-115	P53	Homo sapiens	140-143
22480684-3	2012	In the present study, we found that E2F-1 has an inhibitory effect on p53 during adriamycin (ADR)-mediated DNA damage response.	Doxorubicin	81-91	P53	Homo sapiens	70-73
22537194-8	2012	We show that an increment of the intracellular reactive oxygen species (ROS) and p53 is required for MTA-induced cytotoxicity by utilizing N-Acetyl-L-Cysteine (NAC) to blockage of ROS and p53-defective H1299 NSCLC cell line.	Reactive Oxygen Species	47-70	P53	Homo sapiens	188-191
22537194-8	2012	We show that an increment of the intracellular reactive oxygen species (ROS) and p53 is required for MTA-induced cytotoxicity by utilizing N-Acetyl-L-Cysteine (NAC) to blockage of ROS and p53-defective H1299 NSCLC cell line.	Reactive Oxygen Species	72-75	P53	Homo sapiens	188-191
22537194-8	2012	We show that an increment of the intracellular reactive oxygen species (ROS) and p53 is required for MTA-induced cytotoxicity by utilizing N-Acetyl-L-Cysteine (NAC) to blockage of ROS and p53-defective H1299 NSCLC cell line.	Acetylcysteine	139-158	P53	Homo sapiens	81-84
22537194-8	2012	We show that an increment of the intracellular reactive oxygen species (ROS) and p53 is required for MTA-induced cytotoxicity by utilizing N-Acetyl-L-Cysteine (NAC) to blockage of ROS and p53-defective H1299 NSCLC cell line.	Acetylcysteine	139-158	P53	Homo sapiens	188-191
22537194-8	2012	We show that an increment of the intracellular reactive oxygen species (ROS) and p53 is required for MTA-induced cytotoxicity by utilizing N-Acetyl-L-Cysteine (NAC) to blockage of ROS and p53-defective H1299 NSCLC cell line.	Reactive Oxygen Species	180-183	P53	Homo sapiens	81-84
22537194-8	2012	We show that an increment of the intracellular reactive oxygen species (ROS) and p53 is required for MTA-induced cytotoxicity by utilizing N-Acetyl-L-Cysteine (NAC) to blockage of ROS and p53-defective H1299 NSCLC cell line.	Reactive Oxygen Species	180-183	P53	Homo sapiens	188-191
21927021-3	2012	A determinant of CDDP sensitivity in OVCA, p53, is activated by checkpoint kinase 1 (Chk1) in response to DNA damage.	Cisplatin	17-21	P53	Homo sapiens	43-46
21927021-6	2012	Our findings establish for the first time that PPM1D confers CDDP resistance in OVCA cells through attenuating CDDP-induced, Chk1-mediated, p53-dependent apoptosis.	Cisplatin	61-65	P53	Homo sapiens	140-143
22513874-6	2012	ROS accumulation in turn triggers p53-dependent cell cycle arrest and apoptosis.	Reactive Oxygen Species	0-3	P53	Homo sapiens	34-37
22237799-6	2012	We show here that metanephric p53 is phosphorylated and acetylated on key serine and lysine residues, respectively, in a temporal profile which correlates with the maturational changes in total p53 levels and DNA-binding activity.	Serine	74-80	P53	Homo sapiens	30-33
22237799-6	2012	We show here that metanephric p53 is phosphorylated and acetylated on key serine and lysine residues, respectively, in a temporal profile which correlates with the maturational changes in total p53 levels and DNA-binding activity.	Lysine	85-91	P53	Homo sapiens	30-33
22521640-0	2012	WITHDRAWN: Hexavalent chromium induces premature senescence through reactive oxygen species-mediated p53 pathway in L-02 hepatocytes.	Reactive Oxygen Species	68-91	P53	Homo sapiens	101-104
22052190-9	2012	These results suggest that PATZ1 may have an important role in the regulation of EC senescence through an ROS-mediated p53-dependent pathway and contribute to vascular diseases associated with aging.	ros	106-109	P53	Homo sapiens	119-122
22471785-6	2012	CONCLUSION: Our findings suggest that S. crispus ethanol extract induced apoptosis and DNA fragmentation on hormone dependent breast cancer cell line MCF-7 via mitochondria dependent p53 apoptosis pathway.	Ethanol	49-56	P53	Homo sapiens	183-186
21404051-2	2012	We explored whether the quality of dietary fat alters postprandial oxidative DNA damage and whether supplementation with CoQ improves antioxidant capacity by modifying the activation/stabilization of p53 in elderly subjects.	coenzyme Q10	121-124	P53	Homo sapiens	200-203
21404051-8	2012	Moreover, Med+CoQ diet induced a postprandial decrease of cytoplasmatic p53, nuclear p-p53 (Ser20), and nuclear and cytoplasmatic monoubiquitinated p53 protein (p &lt; 0.05).	coenzyme Q10	14-17	P53	Homo sapiens	72-75
21404051-8	2012	Moreover, Med+CoQ diet induced a postprandial decrease of cytoplasmatic p53, nuclear p-p53 (Ser20), and nuclear and cytoplasmatic monoubiquitinated p53 protein (p &lt; 0.05).	coenzyme Q10	14-17	P53	Homo sapiens	87-90
21404051-8	2012	Moreover, Med+CoQ diet induced a postprandial decrease of cytoplasmatic p53, nuclear p-p53 (Ser20), and nuclear and cytoplasmatic monoubiquitinated p53 protein (p &lt; 0.05).	coenzyme Q10	14-17	P53	Homo sapiens	87-90
22493354-1	2012	BACKGROUND/AIM: This study specifies a strategy to improve radiotherapy by partial synchronization of p53-deficient cancer cells (FaDu and H1299) in mitosis using taxol, with protecting p53 wild-type cells (A549) by the prior administration of cytostatic compounds.	Paclitaxel	163-168	P53	Homo sapiens	102-105
21706156-0	2012	MDM2 SNP309 and TP53 R72P associated with severe and febrile neutropenia in breast cancer patients treated with 5-FU/epirubicin/cyclophosphamide.	Fluorouracil	112-116	P53	Homo sapiens	16-20
21706156-1	2012	The aim of this study was to investigate the association of two genetic polymorphisms, MDM2 SNP309 and TP53 R72P, with incidence of neutropenia in breast cancer patients treated with 5-FU/epirubicin/cyclophosphamide (FEC).	Fluorouracil	183-187	P53	Homo sapiens	103-107
22298641-1	2012	Curcumin can induce p53-independent apoptosis.	Curcumin	0-8	P53	Homo sapiens	20-23
22298641-3	2012	Here, we show that curcumin-induced apoptosis in a panel of tumor cells with mutant p53.	Curcumin	19-27	P53	Homo sapiens	84-87
22298641-10	2012	The results suggest that curcumin induction of ROS activates MAPKs, at least partially by inhibiting PP2A and PP5, thereby leading to p53-independent apoptosis in tumor cells.	Curcumin	25-33	P53	Homo sapiens	134-137
22298641-10	2012	The results suggest that curcumin induction of ROS activates MAPKs, at least partially by inhibiting PP2A and PP5, thereby leading to p53-independent apoptosis in tumor cells.	Reactive Oxygen Species	47-50	P53	Homo sapiens	134-137
22314264-0	2012	Effects of lobaplatin as a single agent and in combination with TRAIL on the growth of triple-negative p53-mutated breast cancers in vitro.	lobaplatin	11-21	P53	Homo sapiens	103-106
22314264-8	2012	Lobaplatin showed substantial cytotoxic effects in two in-vitro models of p53-mutated TNBC.	lobaplatin	0-10	P53	Homo sapiens	74-77
22425181-6	2012	In addition, lobaplatin increased p53, Bax expression, caspase-3 and poly (ADP-ribose) polymerase (PARP) cleavage, and reduced Bcl-2 expression, which contributed to the apoptosis of CCA cells.	lobaplatin	13-23	P53	Homo sapiens	34-37
22382680-8	2012	Western blot analysis confirmed that p53 proteins were phosphorylated by nicotine.	Nicotine	73-81	P53	Homo sapiens	37-40
22294162-5	2012	N-acetylcysteine, a reactive oxygen species scavenger, not only blocked the oridonin-induced increase in hydrogen peroxide and glutathione depletion, but also blocked apoptosis and senescence induced by oridonin, as evidenced by the decrease in Annexin V and senescence-associated beta-galactosidase- positive cells and the inhibition of oridonin-induced upregulation of p53 and p16 and downregulation of c-Myc.	Acetylcysteine	0-16	P53	Homo sapiens	371-374
22421154-4	2012	ssRNAs containing an adenosine and uridine-rich (ARE) element are permissive targets for p53-mediated degradation.	Adenosine	21-30	P53	Homo sapiens	89-92
22421154-7	2012	Ribonuclease activity is enhanced in cytoplasmic extracts of HCT116 (p53+/+) cells exposed to gamma-irradiation or treated by the non-genotoxic drug AS101 but decreased following treatment by genotoxic (e.g., doxorubicin) or non-genotoxic (e.g., DFMO) agents, thus indicating that p53 exonuclease activity is dependent on the specific stress and nature of the substrate.	Doxorubicin	209-220	P53	Homo sapiens	69-72
22421154-7	2012	Ribonuclease activity is enhanced in cytoplasmic extracts of HCT116 (p53+/+) cells exposed to gamma-irradiation or treated by the non-genotoxic drug AS101 but decreased following treatment by genotoxic (e.g., doxorubicin) or non-genotoxic (e.g., DFMO) agents, thus indicating that p53 exonuclease activity is dependent on the specific stress and nature of the substrate.	Eflornithine	246-250	P53	Homo sapiens	69-72
22421157-0	2012	MiRNA-34 intrinsically links p53 tumor suppressor and Wnt signaling.	mirna-34	0-8	P53	Homo sapiens	29-32
21935692-8	2012	Expression of PARP, p53 and OGG1 measured by western blotting was increased in Zn-depleted cells indicating that DNA repair mechanisms are activated.	Zinc	79-81	P53	Homo sapiens	20-23
23543587-6	2012	The effect of TP53 mutations were studied on the chemosensitivity of two new drugs AZD115 and RHPS4, an Aurora Kinase B inhibitor and Telomerase inhibitor respectively.	azd115	83-89	P53	Homo sapiens	14-18
20960027-6	2012	In this study sensitivity to the inhibitor ZM447439 was tested on a panel of 15 non-malignant and malignant epithelial cell lines that differed with respect to BRCA2 and p53 status and related to level of Aurora kinase expression.	4-(4-(N-benzoylamino)anilino)-6-methoxy-7-(3-(1-morpholino)propoxy)quinazoline	43-51	P53	Homo sapiens	170-173
20978925-8	2012	CG200745 increased acetylation of p53 lysine residues K320, K373, and K382.	Lysine	38-44	P53	Homo sapiens	34-37
20978925-8	2012	CG200745 increased acetylation of p53 lysine residues K320, K373, and K382.	5-Bromo-2-fluoropyridine	54-58	P53	Homo sapiens	34-37
22134899-3	2012	Chromatin immunoprecipitation assays demonstrated that JMJD2A was recruited together with p53 to the promoter of the p21 cell cycle inhibitor upon stimulation with the DNA damaging agent, adriamycin.	Doxorubicin	188-198	P53	Homo sapiens	90-93
22323293-10	2012	In agreement with this, increased p53 levels are necessary for a calcium-induced increase in neurons.	Calcium	65-72	P53	Homo sapiens	34-37
22382680-9	2012	Under various doses of nicotine, a decrease in the anti-apoptotic protein Bcl-2, but an increase in p53 and cleaved caspase-3 protein levels, was detected in a dose-dependent manner.	Nicotine	23-31	P53	Homo sapiens	100-103
22198295-3	2012	Treatment with actin- damaging agents including pectenotoxin-2 (PTX-2) increases phosphorylation of Ser-15 and Ser-37 residues of p53, but not Ser-20 residue.	Serine	100-103	P53	Homo sapiens	130-133
22198295-3	2012	Treatment with actin- damaging agents including pectenotoxin-2 (PTX-2) increases phosphorylation of Ser-15 and Ser-37 residues of p53, but not Ser-20 residue.	Serine	111-114	P53	Homo sapiens	130-133
22315229-2	2012	Earlier studies suggest that upon DNA damage, a specific B subunit, B56gamma, bridges the PP2A AC core to p53, leading to dephosphorylation of p53 at Thr-55, induction of the p53 transcriptional target p21, and the inhibition of cell proliferation and transformation.	Threonine	150-153	P53	Homo sapiens	106-109
22315229-2	2012	Earlier studies suggest that upon DNA damage, a specific B subunit, B56gamma, bridges the PP2A AC core to p53, leading to dephosphorylation of p53 at Thr-55, induction of the p53 transcriptional target p21, and the inhibition of cell proliferation and transformation.	Threonine	150-153	P53	Homo sapiens	143-146
22198295-3	2012	Treatment with actin- damaging agents including pectenotoxin-2 (PTX-2) increases phosphorylation of Ser-15 and Ser-37 residues of p53, but not Ser-20 residue.	Serine	111-114	P53	Homo sapiens	130-133
22315229-2	2012	Earlier studies suggest that upon DNA damage, a specific B subunit, B56gamma, bridges the PP2A AC core to p53, leading to dephosphorylation of p53 at Thr-55, induction of the p53 transcriptional target p21, and the inhibition of cell proliferation and transformation.	Threonine	150-153	P53	Homo sapiens	143-146
22387547-4	2012	By using RT-PCR and Western blotting, the expression levels of XPD, P53, phospho-P53 (ser-15), P21, Bax, Bcl-2 and HBx were detected.	Serine	86-89	P53	Homo sapiens	81-84
22401965-0	2012	Activation of the BRCA1/Chk1/p53/p21(Cip1/Waf1) pathway by nitric oxide and cell cycle arrest in human neuroblastoma NB69 cells.	Nitric Oxide	59-71	P53	Homo sapiens	29-32
22361354-4	2012	We find that stabilization of Mdm2, and correspondingly p53 downregulation in unstressed cells, is accomplished by a specific isoform of USP7 (USP7S), which is phosphorylated at serine 18 by the protein kinase CK2.	Serine	178-184	P53	Homo sapiens	56-59
22226932-3	2012	Capsaicin treatment of MCF-7 cells induced S-phase arrest and autophagy through the AMPKalpha-mTOR signaling pathway and the accumulation of p53 in the nucleus and cytosol, including a change in mitochondrial membrane potential.	Capsaicin	0-9	P53	Homo sapiens	141-144
22226932-6	2012	ATM inhibitors, including Ku55933 and caffeine, and the genetic or pharmacological inhibition of p53 prevented capsaicin-induced DNA-PKcs phosphorylation and stimulated PARP-1 cleavage, but had no effect on microtubule-associated protein light chain 3 (LC3)-II levels.	Capsaicin	111-120	P53	Homo sapiens	97-100
22230478-7	2012	On the other hand, the expression of exogenous p53 in H1299 and Hep3B cells was decreased following overexpression of HURP, and these cells showed decreased sensitivity to cisplatin-induced apoptosis.	Cisplatin	172-181	P53	Homo sapiens	47-50
22227273-12	2012	These results were also supported by our therapeutic study, where curcumin induced apoptosis both by p53 dependent and independent manner, while celecoxib followed only p53 independent pathway.	Curcumin	66-74	P53	Homo sapiens	101-104
22226932-8	2012	In M059K cells, but not M059J cells, capsaicin induced ATM and DNA-PKcs phosphorylation, p53 accumulation, and the stimulation of LC3II production, all of which were attenuated by knockdown of the autophagy-related gene atg5.	Capsaicin	37-46	P53	Homo sapiens	89-92
22420423-8	2012	Analyzing the ATM-chk2-p53 cascade, low ATM levels (defined as the lower 5 to 50% percentiles) or mutations inactivating TP53 or CHEK2 robustly predicted anthracycline resistance (P-values varying between 0.001 and 0.027 depending on the percentile used to define "low" ATM levels).	Anthracyclines	154-167	P53	Homo sapiens	23-26
22419115-7	2012	The oxygen-mediated rescue of mutant p53 followed by its trans-activation is responsible for the induction of p53-downstream apoptotic, cell-cycle arrest and DNA-repair genes.	Oxygen	4-10	P53	Homo sapiens	37-40
22419115-7	2012	The oxygen-mediated rescue of mutant p53 followed by its trans-activation is responsible for the induction of p53-downstream apoptotic, cell-cycle arrest and DNA-repair genes.	Oxygen	4-10	P53	Homo sapiens	110-113
22419115-9	2012	We have thus concluded that oxygen therapy without pressure, as opposed to HBO therapy, may be ideal for hypoxic tumor regression, which functions through oxygen-mediated rescue of mutant p53 followed by induction of apoptosis.	Oxygen	28-34	P53	Homo sapiens	188-191
22419115-9	2012	We have thus concluded that oxygen therapy without pressure, as opposed to HBO therapy, may be ideal for hypoxic tumor regression, which functions through oxygen-mediated rescue of mutant p53 followed by induction of apoptosis.	Oxygen	155-161	P53	Homo sapiens	188-191
22307140-4	2012	Specifically, we focus on the functions of p53 in regulating aerobic glycolysis, oxidative phosphorylation, the pentose phosphate pathway, fatty acid synthesis and oxidation, and glutamine metabolism, and we discuss the therapeutic strategy whereby p53 helps to prevent malignant progression.	Fatty Acids	139-149	P53	Homo sapiens	43-46
22420423-8	2012	Analyzing the ATM-chk2-p53 cascade, low ATM levels (defined as the lower 5 to 50% percentiles) or mutations inactivating TP53 or CHEK2 robustly predicted anthracycline resistance (P-values varying between 0.001 and 0.027 depending on the percentile used to define "low" ATM levels).	Anthracyclines	154-167	P53	Homo sapiens	121-125
22420423-11	2012	CONCLUSIONS: Our data indicate loss of function of the ATM-Chk2-p53 cascade to be strongly associated with resistance to anthracycline/mitomycin-containing chemotherapy in breast cancer.	Anthracyclines	121-134	P53	Homo sapiens	64-67
22223137-0	2012	Upregulated p53 expression activates apoptotic pathways in wild-type p53-bearing mesothelioma and enhances cytotoxicity of cisplatin and pemetrexed.	Cisplatin	123-132	P53	Homo sapiens	12-15
22410253-6	2012	Cisplatin induced apoptosis of TYST cells through the activation of p53 expression and down-regulation of Bcl- expression.	Cisplatin	0-9	P53	Homo sapiens	68-71
22166495-5	2012	In mechanistic studies, UVB-irradiated cells showed a transient upregulation of both phosphorylated (Ser-15 and Ser-392) and total p53, whereas silibinin pretreatment led to a more sustained upregulation and stronger nuclear localization of p53.	Silybin	144-153	P53	Homo sapiens	241-244
22166495-6	2012	Silibinin also caused a marked upregulation of GADD45alpha, a downstream target of p53, implicated in DNA repair and cell cycle regulation.	Silybin	0-9	P53	Homo sapiens	83-86
22166495-7	2012	Importantly, under p53 and GADD45alpha knockdown conditions, cells were more susceptible to UVB-induced apoptosis without any significant S phase arrest, and protective effects of silibinin were compromised.	Silybin	180-189	P53	Homo sapiens	19-22
22420423-0	2012	Low expression levels of ATM may substitute for CHEK2 /TP53 mutations predicting resistance towards anthracycline and mitomycin chemotherapy in breast cancer.	Anthracyclines	100-113	P53	Homo sapiens	55-59
22285752-4	2012	In other cells without adenovirus expression, the C-terminal domain of WTX binds to the DNA-binding domain of p53, enhances its binding to CBP, and increases CBP/p300-mediated acetylation of p53 at Lys 373/382.	Lysine	198-201	P53	Homo sapiens	191-194
22362889-0	2012	The p53 cofactor Strap exhibits an unexpected TPR motif and oligonucleotide-binding (OB)-fold structure.	Oligonucleotides	60-75	P53	Homo sapiens	4-7
22166495-9	2012	Together, our results show for the first time that p53-mediated GADD45alpha upregulation is the key mechanism by which silibinin protects against UVB-induced photodamage and provides a strong rationale to investigate silibinin in reducing the risk and/or preventing early onset of NMSC.	Silybin	119-128	P53	Homo sapiens	51-54
22166495-9	2012	Together, our results show for the first time that p53-mediated GADD45alpha upregulation is the key mechanism by which silibinin protects against UVB-induced photodamage and provides a strong rationale to investigate silibinin in reducing the risk and/or preventing early onset of NMSC.	Silybin	217-226	P53	Homo sapiens	51-54
22223137-2	2012	We examined whether forced expression of p53 inhibited growth of mesothelioma cells and produced anti-tumor effects by a combination of cisplatin (CDDP) or pemetrexed (PEM), the first-line drugs for mesothelioma treatments.	Cisplatin	136-145	P53	Homo sapiens	41-44
22223137-6	2012	Transduction with Ad-p53 suppressed viability of mesothelioma cells and augmented the growth inhibition by CDDP or PEM mostly in a synergistic manner.	Cisplatin	107-111	P53	Homo sapiens	21-24
22223137-2	2012	We examined whether forced expression of p53 inhibited growth of mesothelioma cells and produced anti-tumor effects by a combination of cisplatin (CDDP) or pemetrexed (PEM), the first-line drugs for mesothelioma treatments.	Cisplatin	147-151	P53	Homo sapiens	41-44
22333583-0	2012	Retained platinum uptake and indifference to p53 status make novel transplatinum agents active in platinum-resistant cells compared to cisplatin and oxaliplatin.	Platinum	72-80	P53	Homo sapiens	45-48
22283740-5	2012	Pifithrin-alpha (PFT-alpha), a specific inhibitor of p53, reduced ROS production and reversed silibinin"s growth-inhibitory effect.	Silybin	94-103	P53	Homo sapiens	53-56
22421763-13	2012	As for 8 adenocarcinoma patients, the inhibition rate of CDDP of p53-overexpressed patients(59+-8%)was significantly(p=0.	Cisplatin	57-61	P53	Homo sapiens	65-68
22421763-15	2012	p53 overexpression may be a predictive marker for chemotherapy using CDDP in lung adenocarcinoma.	Cisplatin	69-73	P53	Homo sapiens	0-3
22421763-16	2012	CONCLUSION: p53 overexpression may be a possible predictive marker for adjuvant chemotherapy using CDDP in NSCLC.	Cisplatin	99-103	P53	Homo sapiens	12-15
22283740-0	2012	P53 activation plays a crucial role in silibinin induced ROS generation via PUMA and JNK.	Silybin	39-48	P53	Homo sapiens	0-3
22283740-6	2012	The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS.	Reactive Oxygen Species	4-7	P53	Homo sapiens	90-93
22283740-0	2012	P53 activation plays a crucial role in silibinin induced ROS generation via PUMA and JNK.	Reactive Oxygen Species	57-60	P53	Homo sapiens	0-3
22283740-6	2012	The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS.	Reactive Oxygen Species	4-7	P53	Homo sapiens	122-125
22283740-4	2012	Silibinin promoted the expression phosphorylated-p53 (p-p53) in a dose-dependent manner.	Silybin	0-9	P53	Homo sapiens	49-52
22283740-4	2012	Silibinin promoted the expression phosphorylated-p53 (p-p53) in a dose-dependent manner.	Silybin	0-9	P53	Homo sapiens	56-59
22283740-6	2012	The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS.	Acetylcysteine	18-35	P53	Homo sapiens	90-93
22283740-6	2012	The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS.	Acetylcysteine	18-35	P53	Homo sapiens	122-125
22283740-6	2012	The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS.	Acetylcysteine	37-40	P53	Homo sapiens	90-93
22283740-6	2012	The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS.	Acetylcysteine	37-40	P53	Homo sapiens	122-125
22283740-6	2012	The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS.	Silybin	53-62	P53	Homo sapiens	90-93
22283740-6	2012	The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS.	Silybin	53-62	P53	Homo sapiens	122-125
22283740-6	2012	The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS.	Reactive Oxygen Species	148-151	P53	Homo sapiens	122-125
22283740-6	2012	The ROS scavenger N-acetyl cysteine (NAC) attenuated silibinin-induced up-regulation of p-p53 expression, suggesting that p53 might be regulated by ROS and forms a positive feedback loop with ROS.	Reactive Oxygen Species	148-151	P53	Homo sapiens	122-125
22283740-10	2012	Activation of p53 was suppressed by SP600125 and expression of p-JNK was inhibited by PFT-alpha, therefore silibinin might activate a ROS-JNK-p53 cycle to induce cell death.	Silybin	107-116	P53	Homo sapiens	14-17
22283740-10	2012	Activation of p53 was suppressed by SP600125 and expression of p-JNK was inhibited by PFT-alpha, therefore silibinin might activate a ROS-JNK-p53 cycle to induce cell death.	Silybin	107-116	P53	Homo sapiens	142-145
22283740-10	2012	Activation of p53 was suppressed by SP600125 and expression of p-JNK was inhibited by PFT-alpha, therefore silibinin might activate a ROS-JNK-p53 cycle to induce cell death.	Reactive Oxygen Species	134-137	P53	Homo sapiens	14-17
22283740-10	2012	Activation of p53 was suppressed by SP600125 and expression of p-JNK was inhibited by PFT-alpha, therefore silibinin might activate a ROS-JNK-p53 cycle to induce cell death.	Reactive Oxygen Species	134-137	P53	Homo sapiens	142-145
22283740-13	2012	These results showed that p53 could interfere with mitochondrial functions such as MMP via PUMA pathways, thus resulting in ROS generation.	Reactive Oxygen Species	124-127	P53	Homo sapiens	26-29
22283740-14	2012	In order to elucidate the functions of p53 in silibinin induced ROS generation, we have chosen the A431 cells (human epithelial carcinoma) because they lack p53 activity (p53His273 mutation).	Silybin	46-55	P53	Homo sapiens	39-42
22283740-17	2012	p53 activation plays a crucial role in silibinin induced ROS generation.	Silybin	39-48	P53	Homo sapiens	0-3
22283740-17	2012	p53 activation plays a crucial role in silibinin induced ROS generation.	Reactive Oxygen Species	57-60	P53	Homo sapiens	0-3
22421763-11	2012	The inhibition rate of CDDP was 50+-12% for p53- overexpressed patients, and 50+-12% for patients not overexpressed.	Cisplatin	23-27	P53	Homo sapiens	44-47
22223356-7	2012	MCF-10A cells morphologically transformed by long-term exposure to AlCl(3) display strong upregulation of the p53/p21(Waf1) pathway, a key mediator of growth arrest and senescence.	Aluminum Chloride	67-74	P53	Homo sapiens	110-113
22223356-8	2012	These results suggest that aluminium is not generically mutagenic, but similar to an activated oncogene, it induces proliferation stress, DSBs and senescence in normal mammary epithelial cells; and that long-term exposure to AlCl(3) generates and selects for cells able to bypass p53/p21(Waf1) -mediated cellular senescence.	Aluminum Chloride	225-232	P53	Homo sapiens	280-283
22357201-2	2012	Among TP53 gene polymorphisms, the most studied is the G to C transversion in exon 4 at codon 72, which results in three distinct genotypes, Arg/Arg, Pro/Pro and Arg/Pro, each one encoding different p53 isoforms.	Arginine	141-144	P53	Homo sapiens	6-10
21604265-3	2012	High salt and sorbitol were found to activate similar molecular pathways, including the p38 MAPK and the p53-p21(WAF1)-pRb axis, that were not stimulated by high urea.	Salts	5-9	P53	Homo sapiens	105-108
21604265-5	2012	Furthermore, salt- and sorbitol-treated cells were able to phosphorylate histone H2A.X on Ser139, in contrast to cells exposed to urea, indicating a common mechanism for DNA repair, which was achieved by a p53-dependent activation of the G1 checkpoint by both solutes.	Salts	13-17	P53	Homo sapiens	206-209
22357201-2	2012	Among TP53 gene polymorphisms, the most studied is the G to C transversion in exon 4 at codon 72, which results in three distinct genotypes, Arg/Arg, Pro/Pro and Arg/Pro, each one encoding different p53 isoforms.	Arginine	145-148	P53	Homo sapiens	6-10
22357201-2	2012	Among TP53 gene polymorphisms, the most studied is the G to C transversion in exon 4 at codon 72, which results in three distinct genotypes, Arg/Arg, Pro/Pro and Arg/Pro, each one encoding different p53 isoforms.	Arginine	145-148	P53	Homo sapiens	6-10
22357201-7	2012	In our population, p53 genotypes were in Hardy-Weinberg (HW) equilibrium (X2 HM less than 3.84), showing a predominance of arginine allele (total Arg allele frequency of 68%).	Arginine	123-131	P53	Homo sapiens	19-22
22357201-7	2012	In our population, p53 genotypes were in Hardy-Weinberg (HW) equilibrium (X2 HM less than 3.84), showing a predominance of arginine allele (total Arg allele frequency of 68%).	Arginine	146-149	P53	Homo sapiens	19-22
21765463-11	2012	Nutlin-3, RITA and Topotecan lead to comparable p53 activation and growth inhibition under normoxia and hypoxia.	RITA	10-14	P53	Homo sapiens	48-51
22037227-1	2012	BACKGROUND &amp; AIMS: In this study we aimed at characterizing the regulation of hepatic metabolic pathways by the p53 transcription factor.	Adenosine Monophosphate	12-15	P53	Homo sapiens	116-119
22071594-3	2012	Following metabolic activation, aristolochic acid reacts with genomic DNA to form aristolactam-DNA adducts that generate a unique TP53 mutational spectrum in the urothelium.	aristolochic acid I	32-49	P53	Homo sapiens	130-134
22265823-5	2012	We further demonstrated that puerarin protected against MPP(+)-induced p53 nuclear accumulation, Puma (p53-upregulated mediator of apoptosis) and Bax expression and caspase-3-dependent programmed cell death (PCD).	puerarin	29-37	P53	Homo sapiens	71-74
22265823-5	2012	We further demonstrated that puerarin protected against MPP(+)-induced p53 nuclear accumulation, Puma (p53-upregulated mediator of apoptosis) and Bax expression and caspase-3-dependent programmed cell death (PCD).	puerarin	29-37	P53	Homo sapiens	103-106
22265823-8	2012	Collectively, these data suggest that the activation of PI3K/Akt pathway is involved in the protective effect of puerarin against MPP(+)-induced neuroblastoma SH-SY5Y cell death through inhibiting nuclear p53 accumulation and subsequently caspase-3-dependent PCD.	puerarin	113-121	P53	Homo sapiens	205-208
22301190-2	2012	Moreover, p53 regulates glucose metabolism and its mutation results in the metabolic switch to the Warburg effect found in cancer cells.	Glucose	24-31	P53	Homo sapiens	10-13
22172427-5	2012	Furthermore, PGG suppressed PARP cleavage and caspase-3 activation, cytochrome c release, up-regulation of bax and p53 in cisplatin-treated HRCs.	Cisplatin	122-131	P53	Homo sapiens	115-118
22301190-5	2012	Here we demonstrated that p53-inducible microRNA-34a (miR-34a) repressed inosine 5"-monophosphate dehydrogenase (IMPDH), a rate-limiting enzyme of de novo GTP biosynthesis.	Guanosine Triphosphate	155-158	P53	Homo sapiens	26-29
22290291-6	2012	Through endoplasmic reticulum (ER) stress, DIM stimulated the activation of p53 via Ser-15 phosphorylation, leading to increased expression of the BH3-only proapoptotic Bcl-2 members Puma and Noxa.	Serine	84-87	P53	Homo sapiens	76-79
22250642-6	2012	Further studies performed in the cells with wt p53 status show differences between cisplatin and C1 at the level of cell cycle regulation.	Cisplatin	83-92	P53	Homo sapiens	47-50
22184616-0	2012	Regulation of monocarboxylate transporter MCT1 expression by p53 mediates inward and outward lactate fluxes in tumors.	Lactic Acid	93-100	P53	Homo sapiens	61-64
22184616-4	2012	Under hypoxic conditions, p53 loss promoted MCT1 expression and lactate export produced by elevated glycolytic flux, both in vitro and in vivo.	Lactic Acid	64-71	P53	Homo sapiens	26-29
22184616-7	2012	Following glucose deprivation, upregulated MCT1 in p53(-/-) cells promoted lactate import and favored cell proliferation by fuelling mitochondrial respiration.	Lactic Acid	75-82	P53	Homo sapiens	51-54
22184616-9	2012	Together, our findings identify MCT1 as a target for p53 repression and they suggest that MCT1 elevation in p53-deficient tumors allows them to adapt to metabolic needs by facilitating lactate export or import depending on the glucose availability.	Lactic Acid	185-192	P53	Homo sapiens	53-56
22184616-9	2012	Together, our findings identify MCT1 as a target for p53 repression and they suggest that MCT1 elevation in p53-deficient tumors allows them to adapt to metabolic needs by facilitating lactate export or import depending on the glucose availability.	Lactic Acid	185-192	P53	Homo sapiens	108-111
22184616-9	2012	Together, our findings identify MCT1 as a target for p53 repression and they suggest that MCT1 elevation in p53-deficient tumors allows them to adapt to metabolic needs by facilitating lactate export or import depending on the glucose availability.	Glucose	227-234	P53	Homo sapiens	53-56
22184616-9	2012	Together, our findings identify MCT1 as a target for p53 repression and they suggest that MCT1 elevation in p53-deficient tumors allows them to adapt to metabolic needs by facilitating lactate export or import depending on the glucose availability.	Glucose	227-234	P53	Homo sapiens	108-111
22117079-11	2012	The data presented here implicate the regulation of p53 subcellular localization and apoptosis by PARC as a contributing factor in CDDP resistance in OVCA cells and Ca(2+)/calpain in PARC post-translational processing and chemosensitivity.	Cisplatin	131-135	P53	Homo sapiens	52-55
22117079-1	2012	Resistance to cisplatin (CDDP)-based therapy is a major hurdle to the successful treatment of human ovarian cancer (OVCA), and the chemoresistant phenotype in OVCA cells is associated with Akt-attenuated p53-mediated apoptosis.	Cisplatin	14-23	P53	Homo sapiens	204-207
22305266-11	2012	More, we present evidence that over-expression of p53 or p53/p65 in the PANC1 cells were more sensitive to DOX treatment, correlated with activation of caspase-3 and clear elevation of nuclear p21 level.	Doxorubicin	107-110	P53	Homo sapiens	50-53
22117079-1	2012	Resistance to cisplatin (CDDP)-based therapy is a major hurdle to the successful treatment of human ovarian cancer (OVCA), and the chemoresistant phenotype in OVCA cells is associated with Akt-attenuated p53-mediated apoptosis.	Cisplatin	25-29	P53	Homo sapiens	204-207
22117079-6	2012	Here, we present evidence that CDDP promotes calpain-mediated PARC down-regulation, mitochondrial and nuclear p53 accumulation, and apoptosis in chemosensitive but not resistant OVCA cells.	Cisplatin	31-35	P53	Homo sapiens	110-113
22117079-7	2012	Inhibition of Akt is required to sensitize chemoresistant cells to CDDP in a p53-dependent manner, an effect enhanced by PARC down-regulation.	Cisplatin	67-71	P53	Homo sapiens	77-80
22305266-11	2012	More, we present evidence that over-expression of p53 or p53/p65 in the PANC1 cells were more sensitive to DOX treatment, correlated with activation of caspase-3 and clear elevation of nuclear p21 level.	Doxorubicin	107-110	P53	Homo sapiens	57-60
22305266-13	2012	The present findings here reinforced this idea by showing p21"s ability of potentiality of DOX-induced cell death correlated with its inhibition of cell cycle progression after over-expression of p53 or p53/p65.	Doxorubicin	91-94	P53	Homo sapiens	196-199
22305266-13	2012	The present findings here reinforced this idea by showing p21"s ability of potentiality of DOX-induced cell death correlated with its inhibition of cell cycle progression after over-expression of p53 or p53/p65.	Doxorubicin	91-94	P53	Homo sapiens	203-206
22305266-14	2012	CONCLUSION: Our data suggested p65 could increase p53-mediated cell death in response to DOX in PANC1 cells.	Doxorubicin	89-92	P53	Homo sapiens	50-53
21983885-0	2012	Role and interaction of p53, BAX and the stress-activated protein kinases p38 and JNK in benzo(a)pyrene-diolepoxide induced apoptosis in human colon carcinoma cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	89-115	P53	Homo sapiens	24-27
22002102-6	2012	Wild type p53 function inhibits the efficacy of a combined IR and ABT-737 treatment via a p21-dependent G1 cell cycle arrest.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	66-69	P53	Homo sapiens	10-13
22002102-7	2012	Moreover, mutant as well as wild type p53 counteract the pro-apoptotic activity of ABT-737 by maintaining the expression levels of the Mcl-1 protein.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	83-86	P53	Homo sapiens	38-41
22002102-8	2012	Thus, p53 regulates the sensitivity to ABT-737 of glioblastoma cells.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	39-42	P53	Homo sapiens	6-9
22179573-3	2012	The resulting pyr-dba functioned as the enone analogs of curcumin and efficiently inhibited the activation of NF-kappaB and the growth of colorectal carcinoma HCT116 p53+/+ cells as well as the HIV-1 IN-LEDGF/p75 interaction.	pyr-dba	14-21	P53	Homo sapiens	166-169
22179573-3	2012	The resulting pyr-dba functioned as the enone analogs of curcumin and efficiently inhibited the activation of NF-kappaB and the growth of colorectal carcinoma HCT116 p53+/+ cells as well as the HIV-1 IN-LEDGF/p75 interaction.	enone	40-45	P53	Homo sapiens	166-169
22179573-3	2012	The resulting pyr-dba functioned as the enone analogs of curcumin and efficiently inhibited the activation of NF-kappaB and the growth of colorectal carcinoma HCT116 p53+/+ cells as well as the HIV-1 IN-LEDGF/p75 interaction.	Curcumin	57-65	P53	Homo sapiens	166-169
21983885-11	2012	As reported previously, we could reconfirm a critical role of p53 in BPDE-induced apoptosis.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	69-73	P53	Homo sapiens	62-65
21983885-12	2012	Furthermore, induced levels of total p53 and its transcriptional target p21 declined at higher BPDE concentrations correlating with reduced rates of apoptosis.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	95-99	P53	Homo sapiens	37-40
21983885-13	2012	Interestingly, increased phosphorylation of p53 at serine 15 remained elevated at higher BPDE concentrations thus disconnecting p53 phosphorylation from downstream apoptosis.	Serine	51-57	P53	Homo sapiens	44-47
21983885-13	2012	Interestingly, increased phosphorylation of p53 at serine 15 remained elevated at higher BPDE concentrations thus disconnecting p53 phosphorylation from downstream apoptosis.	Serine	51-57	P53	Homo sapiens	128-131
21983885-13	2012	Interestingly, increased phosphorylation of p53 at serine 15 remained elevated at higher BPDE concentrations thus disconnecting p53 phosphorylation from downstream apoptosis.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	89-93	P53	Homo sapiens	44-47
21983885-13	2012	Interestingly, increased phosphorylation of p53 at serine 15 remained elevated at higher BPDE concentrations thus disconnecting p53 phosphorylation from downstream apoptosis.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	89-93	P53	Homo sapiens	128-131
21983885-14	2012	Hence, phosphorylation of p53 seems not only to be a more sensitive biomarker of BPDE exposure but might serve other functions unrelated to apoptosis.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	81-85	P53	Homo sapiens	26-29
22114073-3	2012	Exposure of human prostate cancer LNCaP cells (harboring wild-type p53) and PC-3 cells (lacking p53) with 10-80 mug/ml of GTP for 24 h resulted in dose-dependent inhibition of class I HDAC enzyme activity and its protein expression.	Guanosine Triphosphate	122-125	P53	Homo sapiens	67-70
22114073-3	2012	Exposure of human prostate cancer LNCaP cells (harboring wild-type p53) and PC-3 cells (lacking p53) with 10-80 mug/ml of GTP for 24 h resulted in dose-dependent inhibition of class I HDAC enzyme activity and its protein expression.	Guanosine Triphosphate	122-125	P53	Homo sapiens	96-99
22085531-8	2012	Importantly, the ROS scavenger N-acetylcysteine (NAC) could inhibited LPS-induced autophagy and knockdown of p8 by RNA interference inhibited the autophagy, p53 protein level increase, the translocation of p53 into nuclei and the ROS level increase induced by LPS in HUVECs.	Acetylcysteine	49-52	P53	Homo sapiens	157-160
22593641-10	2012	Upregulation of proline dehydrogenase by the tumor suppressor, p53, leads to enhanced mitochondrial reactive oxygen species that induce the intrinsic apoptotic pathway.	Reactive Oxygen Species	100-123	P53	Homo sapiens	63-66
22112863-6	2012	Upon treatment with depsipeptide, p53 phosphorylation at threonine 18 (Thr18) was specifically induced.	Threonine	57-66	P53	Homo sapiens	34-37
22112863-6	2012	Upon treatment with depsipeptide, p53 phosphorylation at threonine 18 (Thr18) was specifically induced.	UNII-PYZ33YLR8A	71-76	P53	Homo sapiens	34-37
22112863-7	2012	Furthermore, we also demonstrated that phosphorylation of p53 at Thr18 is required for p53 acetylation at lysine 373/382 and for p21 expression in response to depsipeptide treatment.	UNII-PYZ33YLR8A	65-70	P53	Homo sapiens	58-61
22112863-7	2012	Furthermore, we also demonstrated that phosphorylation of p53 at Thr18 is required for p53 acetylation at lysine 373/382 and for p21 expression in response to depsipeptide treatment.	UNII-PYZ33YLR8A	65-70	P53	Homo sapiens	87-90
22112863-7	2012	Furthermore, we also demonstrated that phosphorylation of p53 at Thr18 is required for p53 acetylation at lysine 373/382 and for p21 expression in response to depsipeptide treatment.	Lysine	106-112	P53	Homo sapiens	58-61
22112863-7	2012	Furthermore, we also demonstrated that phosphorylation of p53 at Thr18 is required for p53 acetylation at lysine 373/382 and for p21 expression in response to depsipeptide treatment.	Lysine	106-112	P53	Homo sapiens	87-90
22112863-8	2012	Our results demonstrate that depsipeptide plays an anti-neoplastic role by generating ROS to elicit p53/p21 pathway activation.	Reactive Oxygen Species	86-89	P53	Homo sapiens	100-103
22093905-5	2012	Interestingly, human p53 induces cell death in recombinant strains Mut(s)  with characteristic markers of apoptosis such as DNA fragmentation, exposure of phosphatidylserine, and reactive oxygen species generation.	Reactive Oxygen Species	179-202	P53	Homo sapiens	21-24
22103682-7	2012	We further demonstrate that the C-terminal glycine-arginine rich domain of nucleolin serves as the predominant binding domain for direct interaction with p53.	Glycine	43-50	P53	Homo sapiens	154-157
22103682-7	2012	We further demonstrate that the C-terminal glycine-arginine rich domain of nucleolin serves as the predominant binding domain for direct interaction with p53.	Arginine	51-59	P53	Homo sapiens	154-157
22103682-9	2012	Conversely, the adjacent glycine-arginine rich domain of nucleolin interacted with p53 causing a modest stimulatory effect on p53 ubiquitination.	Glycine	25-32	P53	Homo sapiens	83-86
22103682-9	2012	Conversely, the adjacent glycine-arginine rich domain of nucleolin interacted with p53 causing a modest stimulatory effect on p53 ubiquitination.	Glycine	25-32	P53	Homo sapiens	126-129
22103682-9	2012	Conversely, the adjacent glycine-arginine rich domain of nucleolin interacted with p53 causing a modest stimulatory effect on p53 ubiquitination.	Arginine	33-41	P53	Homo sapiens	83-86
22103682-9	2012	Conversely, the adjacent glycine-arginine rich domain of nucleolin interacted with p53 causing a modest stimulatory effect on p53 ubiquitination.	Arginine	33-41	P53	Homo sapiens	126-129
22197648-0	2012	Water"s potential role: Insights from studies of the p53 core domain.	Water	0-5	P53	Homo sapiens	53-56
20686816-1	2012	Unlike its cytotoxicity in p53-functional cell lines, Nutlin-1, the small-molecule inhibitor of murine double minute (MDM2), significantly enhanced the differentiation-inducing activity of all-trans retinoic acid (ATRA) in HL60 and NB4 cells (p53-nonfunctional) but not in U937 cells (p53 wild-type).	Tretinoin	214-218	P53	Homo sapiens	243-246
20686816-1	2012	Unlike its cytotoxicity in p53-functional cell lines, Nutlin-1, the small-molecule inhibitor of murine double minute (MDM2), significantly enhanced the differentiation-inducing activity of all-trans retinoic acid (ATRA) in HL60 and NB4 cells (p53-nonfunctional) but not in U937 cells (p53 wild-type).	Tretinoin	214-218	P53	Homo sapiens	243-246
20686816-2	2012	Moreover, we demonstrated that the synergistic differentiation-inducing activity of Nutlin-1 combined with ATRA appeared in a p53-independent manner.	Tretinoin	107-111	P53	Homo sapiens	126-129
21827374-2	2012	Cenersen, an oligonucleotide targeting TP53, has been shown to abrogate the activity of TP53 gain-of-function mutants and to increase sensitivity of lymphoma cells to cytotoxic chemotherapy in vitro.	Oligonucleotides	13-28	P53	Homo sapiens	39-43
22197648-5	2012	We examined seven wild/mutant X-ray structures and observed two types of water-network hydration in three "hot hydration centers" (DNA- or small molecule- binding surfaces of the p53 core domain).	Water	73-78	P53	Homo sapiens	179-182
21827374-2	2012	Cenersen, an oligonucleotide targeting TP53, has been shown to abrogate the activity of TP53 gain-of-function mutants and to increase sensitivity of lymphoma cells to cytotoxic chemotherapy in vitro.	Oligonucleotides	13-28	P53	Homo sapiens	88-92
22197648-9	2012	The particular environment created by different water molecules around the p53 core domain also partly explains the structural vulnerabilities of this protein.	Water	48-53	P53	Homo sapiens	75-78
21607615-2	2012	A guanine (G)/cytosine (C) common single nucleotide polymorphism (SNP) at second position of codon 72 in exon 4 of p53 gene determines a arginine (Arg) to proline (Pro) (Arg72Pro) aminoacidic substitution within the proline-rich domain of p53 protein.	Arginine	137-145	P53	Homo sapiens	115-118
21607615-2	2012	A guanine (G)/cytosine (C) common single nucleotide polymorphism (SNP) at second position of codon 72 in exon 4 of p53 gene determines a arginine (Arg) to proline (Pro) (Arg72Pro) aminoacidic substitution within the proline-rich domain of p53 protein.	Arginine	137-145	P53	Homo sapiens	239-242
21607615-2	2012	A guanine (G)/cytosine (C) common single nucleotide polymorphism (SNP) at second position of codon 72 in exon 4 of p53 gene determines a arginine (Arg) to proline (Pro) (Arg72Pro) aminoacidic substitution within the proline-rich domain of p53 protein.	Arginine	147-150	P53	Homo sapiens	115-118
21607615-2	2012	A guanine (G)/cytosine (C) common single nucleotide polymorphism (SNP) at second position of codon 72 in exon 4 of p53 gene determines a arginine (Arg) to proline (Pro) (Arg72Pro) aminoacidic substitution within the proline-rich domain of p53 protein.	Arginine	147-150	P53	Homo sapiens	239-242
22056254-2	2012	Here we determine the effect of the tumor suppressor protein, p53, on trafficking (64)Cu to tumor cell nuclei from DOTA vs. CB-TE2A-conjugated agonist Y3-TATE and the antagonist (64)Cu-CB-TE2A-sst2-ANT in cell lines that are positive or negative for p53.	Copper	86-88	P53	Homo sapiens	62-65
22184063-7	2012	Moreover, phosphorylation of VprBP at serine 895 impairs the ability of VprBP to bind H3 tails and to repress p53 transactivation.	Serine	38-44	P53	Homo sapiens	110-113
22515118-0	2012	Geranylgeranylacetone attenuates cisplatin-induced reductions in cell viability by suppressing the elevation of intracellular p53 content without heat shock protein induction.	Cisplatin	33-42	P53	Homo sapiens	126-129
22515118-7	2012	We found that GGA suppressed the CDDP-induced elevation of intracellular p53 content.	Cisplatin	33-37	P53	Homo sapiens	73-76
22515118-8	2012	In conclusion, GGA attenuates viability reductions and caspase-3 activation in CDDP-treated cells by suppressing the elevation of intracellular p53 content without HSP induction.	Cisplatin	79-83	P53	Homo sapiens	144-147
22056254-7	2012	The (64)Cu from agonists (64)Cu-DOTA-Y3-TATE and (64)Cu-CB-TE2A-Y3-TATE showed greater nuclear localization at 24 h in p53 +/+ vs. -/- cells; however, there was no difference in the levels of (64)Cu from the antagonist based on p53 status.	Copper	8-10	P53	Homo sapiens	119-122
22056254-7	2012	The (64)Cu from agonists (64)Cu-DOTA-Y3-TATE and (64)Cu-CB-TE2A-Y3-TATE showed greater nuclear localization at 24 h in p53 +/+ vs. -/- cells; however, there was no difference in the levels of (64)Cu from the antagonist based on p53 status.	Copper	8-10	P53	Homo sapiens	228-231
22056254-7	2012	The (64)Cu from agonists (64)Cu-DOTA-Y3-TATE and (64)Cu-CB-TE2A-Y3-TATE showed greater nuclear localization at 24 h in p53 +/+ vs. -/- cells; however, there was no difference in the levels of (64)Cu from the antagonist based on p53 status.	Copper	29-31	P53	Homo sapiens	119-122
22056254-2	2012	Here we determine the effect of the tumor suppressor protein, p53, on trafficking (64)Cu to tumor cell nuclei from DOTA vs. CB-TE2A-conjugated agonist Y3-TATE and the antagonist (64)Cu-CB-TE2A-sst2-ANT in cell lines that are positive or negative for p53.	Copper	86-88	P53	Homo sapiens	250-253
22176582-3	2012	We investigated segmental chain motions in p53-TAD using fluorescence quenching of an extrinsic label by tryptophan in combination with fluorescence correlation spectroscopy (PET-FCS).	Tryptophan	105-115	P53	Homo sapiens	43-46
22020547-11	2012	Taken together, we             suggest that TPA reciprocally regulates the level of p21 and p53 expression via             a MEK/ERK-dependent pathway.	Tetradecanoylphorbol Acetate	44-47	P53	Homo sapiens	92-95
22020547-12	2012	The up-regulation of p21 in response to TPA is mediated             through a p53-independent mechanism in breast cancer cells.	Tetradecanoylphorbol Acetate	40-43	P53	Homo sapiens	78-81
22391175-2	2012	Using fluorescence in situ hybridization (FISH), the P53 gene was detected in paraffin-embedded tonsil tissues from 50 cases of DLBCL, while all the peripheral blood of patients was collected for detecting P53 protein in serum by using enzyme-linked immunosorbent assay (ELISA).	Paraffin	78-86	P53	Homo sapiens	53-56
22020547-0	2012	TPA-induced p21 expression augments G2/M arrest through a p53-independent             mechanism in human breast cancer cells.	Tetradecanoylphorbol Acetate	0-3	P53	Homo sapiens	58-61
22020547-4	2012	Our results showed that TPA increased the level of p21 expression             in MCF-7 cells with wild-type p53 and MDA-MB-231 cells with mutant p53 in a dose-dependent             manner.	Tetradecanoylphorbol Acetate	24-27	P53	Homo sapiens	108-111
22020547-4	2012	Our results showed that TPA increased the level of p21 expression             in MCF-7 cells with wild-type p53 and MDA-MB-231 cells with mutant p53 in a dose-dependent             manner.	Tetradecanoylphorbol Acetate	24-27	P53	Homo sapiens	145-148
22020547-5	2012	In contrast, TPA decreased the expression of p53 in MCF-7 cells, but did             not affect MDA-MB-231 cells.	Tetradecanoylphorbol Acetate	13-16	P53	Homo sapiens	45-48
22020547-6	2012	We next examined the regulatory mechanism of TPA             on p21 and p53 expression.	Tetradecanoylphorbol Acetate	45-48	P53	Homo sapiens	72-75
22020547-7	2012	Our results showed that the TPA-induced up-regulation             of p21 and down-regulation of p53 was reversed by UO126 (a MEK1/2 inhibitor),             but not by SP600125 (a JNK inhibitor) or SB203580 (a p38 inhibitor), although             TPA increased the phosphorylation of ERK and JNK in MCF-7 cells.	Tetradecanoylphorbol Acetate	28-31	P53	Homo sapiens	96-99
21979946-0	2012	Germline SDHx variants modify breast and thyroid cancer risks in Cowden and Cowden-like syndrome via FAD/NAD-dependant destabilization of p53.	NAD	105-108	P53	Homo sapiens	138-141
22147694-4	2012	WT p53 exists in mutant conformation in hypoxic core of MCF-7 solid tumors, and its conformation is oxygen-dependent.	Oxygen	100-106	P53	Homo sapiens	3-6
22117045-4	2012	The MUC1-C inhibitor-induced increases in ROS were also associated with down-regulation of the p53-inducible regulator of glycolysis and apoptosis (TIGAR).	Reactive Oxygen Species	42-45	P53	Homo sapiens	95-98
22166212-6	2012	Recently, RITA was shown to induce apoptosis by promoting p53Ser46 phosphorylation.	RITA	10-14	P53	Homo sapiens	58-61
22192357-0	2012	14-3-3sigma regulation by p53 mediates a chemotherapy response to 5-fluorouracil in MCF-7 breast cancer cells via Akt inactivation.	Fluorouracil	66-80	P53	Homo sapiens	26-29
22192357-5	2012	Meanwhile, initial treatments with high concentrations of 5-Fu clearly induced 14-3-3sigma and p53 expression in a time-dependent manner.	Fluorouracil	58-62	P53	Homo sapiens	95-98
21979946-11	2012	This loss of p53 was regulated by MDM2-independent NADH quinone oxidoreductase 1-mediated protein degradation, likely due to the imbalance of flavin adenine dinucleotide/nicotinamide adenine dinucleotide in SDH(var+) cells.	NAD	170-203	P53	Homo sapiens	13-16
22194015-1	2012	During the last decade, we saw an explosion of studies investigating the role of lysine methylation/demethylation of histones and non-histone proteins, such as p53, NF-kappaB, and E2F1.	Lysine	81-87	P53	Homo sapiens	160-163
22123926-6	2012	Thus, wild-type p53 limited lactate production in cancer cells unless Pdk2 could be elevated.	Lactic Acid	28-35	P53	Homo sapiens	16-19
22214662-3	2012	Here, we report that RAX/PACT interacts with the SUMO E2 ligase Ubc9 to stimulate p53-Ubc9 association and reversible p53 sumoylation on lysine 386.	Lysine	137-143	P53	Homo sapiens	118-121
22214662-8	2012	Significantly, p53 stability is decreased in cells with reduced RAX/PACT or PKR following doxorubicin treatment, and expression of exogenous RAX/ PACT promotes phosphorylation of wild-type but not p53(K386R) on serine 392.	Doxorubicin	90-101	P53	Homo sapiens	15-18
22214662-8	2012	Significantly, p53 stability is decreased in cells with reduced RAX/PACT or PKR following doxorubicin treatment, and expression of exogenous RAX/ PACT promotes phosphorylation of wild-type but not p53(K386R) on serine 392.	Serine	211-217	P53	Homo sapiens	15-18
22053912-9	2012	In addition, both anti-BPDE and B[a]P-7,8-trans-dihydrodiol induced p53 expression ~6 h post-treatment at concentrations as low as 1 muM consistent with extensive DNA damage.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	23-27	P53	Homo sapiens	68-71
22065775-6	2012	The overexpression of Wip1 in normal tissues provided protection from cisplatin-induced apoptosis through decreased strength of upstream signaling to p53.	Cisplatin	70-79	P53	Homo sapiens	150-153
22289634-1	2012	Human TP53 gene is characterised by a polymorphism at codon 72 leading to an Arginine-to-Proline (R/P) substitution.	Arginine	77-85	P53	Homo sapiens	6-10
22525470-9	2012	The differential responses to 5-FU between these cell lines appeared to be due to the difference in the TP53 gene status, thus providing a molecular basis for the bioassays using these cell lines in the toxicology field.	Fluorouracil	30-34	P53	Homo sapiens	104-108
22525470-10	2012	Our results indicate that the clinical efficacy of 5-FU chemotherapy may depend on the TP53 genotype.	Fluorouracil	51-55	P53	Homo sapiens	87-91
23227799-7	2012	Our results show that HUVECs incubated with 200 muM H(2)O(2) had significantly decreased the viability of endothelial cells, which was accompanied with apparent cell apoptosis, the activation of caspase-3 and the upregulation of p53 expression, which was known to play a key role in H(2)O(2) -induced cell apoptosis.	Hydrogen Peroxide	52-60	P53	Homo sapiens	229-232
22679561-8	2012	In addition, single cisplatin treatment was combined with the silencing of E6AP or p53.	Cisplatin	20-29	P53	Homo sapiens	83-86
22679561-9	2012	The comparison to HeLa and SiHa cells revealed a higher sensitivity of the novel cell lines to cisplatin treatment, which caused p53 accumulation and transcriptional induction of p21.	Cisplatin	95-104	P53	Homo sapiens	129-132
22213289-6	2012	In p53-null cells, the combination of low dose 5-FU with up to 6 muM quercetin promoted clonogenic survival.	Fluorouracil	47-51	P53	Homo sapiens	3-6
22901123-7	2012	RESULTS: Overall, a significant association was detected between the p53 Arg72Pro polymorphism and GC risk (Pro-allele vs. Arg-allele: OR=1.05, 95%CI=1.01-1.08; Pro/Pro vs. Arg/Arg: OR=1.13, 95%CI=1.04-1.22).	Arginine	73-76	P53	Homo sapiens	69-72
22502699-2	2012	A common single nucleotide polymorphism located within the proline rich region of TP53 gene at codon 72 in exon 4 encodes either proline or arginine.	Arginine	140-148	P53	Homo sapiens	82-86
22502699-3	2012	TP53 Arg 72 is more active than TP53 Pro 72 in inducing apoptosis.	Arginine	5-8	P53	Homo sapiens	0-4
22901123-7	2012	RESULTS: Overall, a significant association was detected between the p53 Arg72Pro polymorphism and GC risk (Pro-allele vs. Arg-allele: OR=1.05, 95%CI=1.01-1.08; Pro/Pro vs. Arg/Arg: OR=1.13, 95%CI=1.04-1.22).	Arginine	123-126	P53	Homo sapiens	69-72
22901123-7	2012	RESULTS: Overall, a significant association was detected between the p53 Arg72Pro polymorphism and GC risk (Pro-allele vs. Arg-allele: OR=1.05, 95%CI=1.01-1.08; Pro/Pro vs. Arg/Arg: OR=1.13, 95%CI=1.04-1.22).	Arginine	123-126	P53	Homo sapiens	69-72
22901126-2	2012	Ser/Cys polymorphism in hOGG1 and Arg/Pro polymorphism in p53 among 124 patients with lung cancer and 128 normal people were detected using PCR-RFLP.	Serine	0-3	P53	Homo sapiens	58-61
22901126-2	2012	Ser/Cys polymorphism in hOGG1 and Arg/Pro polymorphism in p53 among 124 patients with lung cancer and 128 normal people were detected using PCR-RFLP.	Arginine	34-37	P53	Homo sapiens	58-61
22104152-0	2012	Hoiamide D, a marine cyanobacteria-derived inhibitor of p53/MDM2 interaction.	hoiamide D	0-10	P53	Homo sapiens	56-59
23167335-13	2012	CONCLUSION: We suggest that SNPs in the P53 pathway, especially the P21 ser31arg polymorphism and combined polymorphisms especially the P21/ MDM2 might be genetic susceptibility factors in the pathogenesis of AML.	ser31arg	72-80	P53	Homo sapiens	40-43
22829740-6	2012	The strategy of the research work was to target the site of interaction of Rb1 -E7 &amp; p53-E6.	Adenosine Monophosphate	84-87	P53	Homo sapiens	89-92
23464484-1	2012	Recently, we reported that an ethanol extract of Iris nertschinskia induces p53-dependent apoptosis in the MCF7 human breast cancer cell line.	Ethanol	30-37	P53	Homo sapiens	76-79
22975518-11	2012	Magnolol downregulated expression of the antiapoptotic protein Bcl2, upregulated expression of pro-apoptotic protein p53 and Bax, and caused the release of mitochondrial cytochrome c.	magnolol	0-8	P53	Homo sapiens	117-120
22975518-12	2012	Magnolol-induced p53 and Bcl2 expression was abolished in the presence of compound C. Magnolol inhibited migration and invasion of HCT-116 cells through AMPK activation.	magnolol	0-8	P53	Homo sapiens	17-20
22975518-12	2012	Magnolol-induced p53 and Bcl2 expression was abolished in the presence of compound C. Magnolol inhibited migration and invasion of HCT-116 cells through AMPK activation.	magnolol	86-94	P53	Homo sapiens	17-20
22104152-3	2012	Hoiamide D displayed inhibitory activity against p53/MDM2 interaction (EC(50)=4.5 muM), an attractive target for anticancer drug development.	hoiamide D	0-10	P53	Homo sapiens	49-52
22090360-6	2012	The effect of the drug metformin on overcoming mutant p53-associated radiation resistance was examined in vitro as well as in vivo, using an orthotopic xenograft model.	Metformin	23-32	P53	Homo sapiens	54-57
21713761-9	2012	In addition, FBI-1 could inhibit cell death induced by 5-fluorouracil or doxorubicin through suppressing the activation of p53.	Fluorouracil	55-69	P53	Homo sapiens	123-126
21713761-9	2012	In addition, FBI-1 could inhibit cell death induced by 5-fluorouracil or doxorubicin through suppressing the activation of p53.	Doxorubicin	73-84	P53	Homo sapiens	123-126
22759968-4	2012	RESULTS: Extracellular adenosine induces Lu-65 cell apoptosis in a concentration (0.01-10 mM)-dependent manner, and the effect was inhibited by the A(3) adenosine receptor inhibitor MRS1191 or by knocking-down A(3) adenosine receptor or p53.	Adenosine	23-32	P53	Homo sapiens	237-240
22759968-6	2012	Adenosine upregulated expression of p53 and Noxa mRNAs and activated caspase-3 and -9, but not caspase-8.	Adenosine	0-9	P53	Homo sapiens	36-39
22759968-7	2012	Those adenosine effects were still inhibited by knocking-down A(3) adenosine receptor or p53.	Adenosine	6-15	P53	Homo sapiens	89-92
22759968-8	2012	CONCLUSION: The results of the present study show that adenosine upregulates p53 expression via A(3) adenosine receptor, to promote p53-dependent Noxa gene transcription, causing activation of caspase-9 and the effector caspase-3 to induce Lu-65 cell apoptosis.	Adenosine	55-64	P53	Homo sapiens	77-80
22759968-8	2012	CONCLUSION: The results of the present study show that adenosine upregulates p53 expression via A(3) adenosine receptor, to promote p53-dependent Noxa gene transcription, causing activation of caspase-9 and the effector caspase-3 to induce Lu-65 cell apoptosis.	Adenosine	55-64	P53	Homo sapiens	132-135
21895873-0	2012	Retracted: Modulation of p53 /Akt / phosphatase and tensin homolog expression by esculetin potentiates the anticancer activity of cisplatin and prevents its nephrotoxicity.	esculetin	81-90	P53	Homo sapiens	25-28
21895873-0	2012	Retracted: Modulation of p53 /Akt / phosphatase and tensin homolog expression by esculetin potentiates the anticancer activity of cisplatin and prevents its nephrotoxicity.	Cisplatin	130-139	P53	Homo sapiens	25-28
22759956-0	2012	AMP converted from intracellularly transported adenosine upregulates p53 expression to induce malignant pleural mesothelioma cell apoptosis.	Adenosine Monophosphate	0-3	P53	Homo sapiens	69-72
22759956-0	2012	AMP converted from intracellularly transported adenosine upregulates p53 expression to induce malignant pleural mesothelioma cell apoptosis.	Adenosine	47-56	P53	Homo sapiens	69-72
22759956-5	2012	Adenosine upregulated expression of the p53 mRNA and protein, that is abolished by ABT-702, but not by knocking-down A(3) adenosine receptor.	Adenosine	0-9	P53	Homo sapiens	40-43
22759956-5	2012	Adenosine upregulated expression of the p53 mRNA and protein, that is abolished by ABT-702, but not by knocking-down A(3) adenosine receptor.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	83-86	P53	Homo sapiens	40-43
22759956-6	2012	Adenosine-induced apoptosis in NCI-H28 cells was significantly inhibited by knocking-down p53 and in part by knocking-down A(3) adenosine receptor.	Adenosine	0-9	P53	Homo sapiens	90-93
22759956-7	2012	CONCLUSION: The results of the present study show that AMP converted from intracellularly transported adenosine upregulates p53 expression to induce caspase-independent apoptosis in malignant pleural mesothelioma cells and that A(3) adenosine receptor also participates partially in the apoptosis by the different mechanism.	Adenosine Monophosphate	55-58	P53	Homo sapiens	124-127
22759956-7	2012	CONCLUSION: The results of the present study show that AMP converted from intracellularly transported adenosine upregulates p53 expression to induce caspase-independent apoptosis in malignant pleural mesothelioma cells and that A(3) adenosine receptor also participates partially in the apoptosis by the different mechanism.	Adenosine	102-111	P53	Homo sapiens	124-127
22090360-9	2012	Expression of disruptive TP53 mutations significantly decreased radiation-induced senescence, as measured by SA-beta-gal staining, p21 expression, and release of ROS.	Reactive Oxygen Species	162-165	P53	Homo sapiens	25-29
22090360-10	2012	The mitochondrial agent metformin potentiated the effects of radiation in the presence of a disruptive TP53 mutation partially via senescence.	Metformin	24-33	P53	Homo sapiens	103-107
22090360-13	2012	Metformin can serve as a radiosensitizer for HNSCC with disruptive TP53, presaging the possibility of personalizing HNSCC treatment.	Metformin	0-9	P53	Homo sapiens	67-71
22915839-6	2012	Doxorubicin induced senescence signaling was mediated by p53-p21(CIP/WAF-1) and was accelerated in the absence of functional Hsp90.	Doxorubicin	0-11	P53	Homo sapiens	57-60
22123233-4	2012	Genetic connections are being made between p53 and an increasing number of metabolic activities such as oxidative phosphorylation, glycolysis and fatty acid oxidation.	Fatty Acids	146-156	P53	Homo sapiens	43-46
22019631-2	2012	In this review the tumor suppressor genes p53, FoxO, retinoblastoma (RB), p21, p16, and breast cancer susceptibility genes 1 and 2 (BRCA1 and BRCA2) and their roles in oxidative stress are summarized with a focus on the links and interplay between their pathways and reactive oxygen species (ROS).	Reactive Oxygen Species	267-290	P53	Homo sapiens	42-45
22007260-4	2012	Rhein induced dose- and time-dependent manners increase in caspase-9-mediated apoptosis correlating with activation of ROS-mediated activation of NF-kappaB- and p53-signaling pathways in both cell types.	ros	119-122	P53	Homo sapiens	161-164
22019631-2	2012	In this review the tumor suppressor genes p53, FoxO, retinoblastoma (RB), p21, p16, and breast cancer susceptibility genes 1 and 2 (BRCA1 and BRCA2) and their roles in oxidative stress are summarized with a focus on the links and interplay between their pathways and reactive oxygen species (ROS).	Reactive Oxygen Species	292-295	P53	Homo sapiens	42-45
22019631-4	2012	On the other hand, recent studies have revealed a pro-oxidant role for p53 by which cellular ROS are increased by enhanced transcription of proapoptotic genes.	Reactive Oxygen Species	93-96	P53	Homo sapiens	71-74
22393286-9	2012	CONCLUSION: Overall, our data demonstrated that ZnO NPs selectively induce apoptosis in cancer cells, which is likely to be mediated by reactive oxygen species via p53 pathway, through which most of the anticancer drugs trigger apoptosis.	Reactive Oxygen Species	136-159	P53	Homo sapiens	164-167
22210716-9	2012	Our study indicated that a high prevalence of the genotype Arg/Pro at the p53 codon 72 may contribute to susceptibility to OSCC, especially in combination with the use of carcinogenic tobacco-specific nitrosamine (TSNA)-rich toombak.	Arginine	59-62	P53	Homo sapiens	74-77
22210716-9	2012	Our study indicated that a high prevalence of the genotype Arg/Pro at the p53 codon 72 may contribute to susceptibility to OSCC, especially in combination with the use of carcinogenic tobacco-specific nitrosamine (TSNA)-rich toombak.	tsna	214-218	P53	Homo sapiens	74-77
23049256-6	2012	Under the same conditions, LMWP-SOD1 abolished activation of the cell cycle regulator proteins, p53 and p21(Cip1), induced by hydrogen peroxide.	Hydrogen Peroxide	126-143	P53	Homo sapiens	96-99
21918844-6	2012	The desipramine/cisplatin combination resulted in increased levels of p53 as well as mitochondrial damage, caspase activation, and poly(ADP ribose) polymerase cleavage, suggesting that desipramine may synergize with cisplatin more than with other platinum chemotherapeutics partly by activating distinct apoptotic pathways.	Cisplatin	16-25	P53	Homo sapiens	70-73
22778941-2	2012	Cisplatin forms inter- and intrastrand crosslinked DNA adducts and its cytotoxicity is mediated by propagation of DNA damage recognition signals to downstream pathways involving ATR, p53, p73, and mitogen-activated protein kinases, ultimately resulting in apoptosis.	Cisplatin	0-9	P53	Homo sapiens	183-186
23113120-8	2012	A positive correlation was found between survivin level and total human p53 level in children with ALL (r=0.501 &amp; P&lt;0.0001).	Adenosine Monophosphate	113-116	P53	Homo sapiens	72-75
22583615-5	2012	Ataxia telangiectasia mutated protein kinase (ATM) was activated by GL331 through its autophosphorylation at Ser1981, which led to the activation of DNA damage signaling pathways including p53/p21 and Chk2/Cdc25A cascades.	GL 331	68-73	P53	Homo sapiens	189-192
22466960-8	2012	Interruption of ERK and p53 activities decreased SU11274-induced autophagy, and blocking of ERK by the specific inhibitor PD98059 suppressed SU11274-induced p53 activation.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	122-129	P53	Homo sapiens	157-160
23038158-10	2012	The risk of p53 mutation was also higher in participants with APE1 Asp/Asp plus hOGG1-Cys than in those with APE1-Glu plus hOGG1 Ser/Ser (OR, 3.72; 95% CI, 1.33-10.40; P = 0.012).	Serine	133-136	P53	Homo sapiens	12-15
23038158-11	2012	CONCLUSIONS: These results suggest that the APE1 Asp/Asp genotype and the combination of the APE1 Asp/Asp and hOGG1-Cys variants are associated with increased risk of p53 mutation in non-small cell lung cancer.	Cysteine	116-119	P53	Homo sapiens	167-170
22124122-6	2012	Wnt5a and calcium ionophore activate NFATc1, NFATc2, NF-kappaB, and B cell lymphoma 6 (BCL-6) promptly and upregulate CD40 expression in GC B and Ramos cells, whereas p53 and JNK are not upregulated or activated.	Calcium	10-17	P53	Homo sapiens	167-170
23216635-0	2012	Reactive oxygen species mediate Cr(VI)-induced S phase arrest through p53 in human colon cancer cells.	Reactive Oxygen Species	0-23	P53	Homo sapiens	70-73
23038158-0	2012	The APE1 Asp/Asp genotype and the combination of APE1 Asp/Asp and hOGG1-Cys variants are associated with increased p53 mutation in non-small cell lung cancer.	Cysteine	72-75	P53	Homo sapiens	115-118
23038158-9	2012	However, a higher risk of p53 mutation was found in participants with the APE1 Asp/Asp genotype than in those with the APE1-Glu allele (OR, 2.15; 95% CI, 1.19-3.87; P = 0.011).	Glutamic Acid	124-127	P53	Homo sapiens	26-29
23038158-10	2012	The risk of p53 mutation was also higher in participants with APE1 Asp/Asp plus hOGG1-Cys than in those with APE1-Glu plus hOGG1 Ser/Ser (OR, 3.72; 95% CI, 1.33-10.40; P = 0.012).	Cysteine	86-89	P53	Homo sapiens	12-15
23038158-10	2012	The risk of p53 mutation was also higher in participants with APE1 Asp/Asp plus hOGG1-Cys than in those with APE1-Glu plus hOGG1 Ser/Ser (OR, 3.72; 95% CI, 1.33-10.40; P = 0.012).	Glutamic Acid	114-117	P53	Homo sapiens	12-15
23038158-10	2012	The risk of p53 mutation was also higher in participants with APE1 Asp/Asp plus hOGG1-Cys than in those with APE1-Glu plus hOGG1 Ser/Ser (OR, 3.72; 95% CI, 1.33-10.40; P = 0.012).	Serine	129-132	P53	Homo sapiens	12-15
21964832-12	2012	Taken together, we suggest that BBR may be used as an effective             ingredient for anticancer products, which trigger the transcriptional activity             and the inhibition of the degradation of p53, a tumor suppressor gene, in human             breast cancer.	Berberine	32-35	P53	Homo sapiens	208-211
22613405-1	2012	OBJECTIVE: The association between codon 72 polymorphism of the tumour protein p53 (TP53) gene - which results in a missense mutation of arginine (R) to proline (P) - and susceptibility to hepatocellular carcinoma (HCC) is controversial.	Arginine	137-145	P53	Homo sapiens	79-82
22613405-1	2012	OBJECTIVE: The association between codon 72 polymorphism of the tumour protein p53 (TP53) gene - which results in a missense mutation of arginine (R) to proline (P) - and susceptibility to hepatocellular carcinoma (HCC) is controversial.	Arginine	137-145	P53	Homo sapiens	84-88
23936624-1	2012	A texaphyrin-oxaliplatin conjugate, oxaliTEX, was designed to test the concept that a platinum analog can overcome defects in drug accumulation and p53-dependent DNA damage response in a tumor model expressing multifactorial mechanisms of cisplatin resistance.	Platinum	86-94	P53	Homo sapiens	148-151
23936624-3	2012	Unlike cisplatin, oxaliTEX accumulated and formed DNA adducts, stabilized and activated p53 at similar levels in both sensitive and resistant cells, and induced apoptosis in both models.	oxalitex	18-26	P53	Homo sapiens	88-91
22876131-0	2012	Involvement of Smac, p53, and caspase pathways in induction of apoptosis by gossypol in human retinoblastoma cells.	Gossypol	76-84	P53	Homo sapiens	21-24
21964832-0	2012	Effect of berberine on p53 expression by TPA in breast cancer cells.	Berberine	10-19	P53	Homo sapiens	23-26
22760199-8	2012	Phospho-p53 and phospho-H2Ax Western blot indicate subsequent DNA damage as an important effector of doxorubicin-induced death.	Doxorubicin	101-112	P53	Homo sapiens	8-11
22389628-4	2012	In response to retinoic acid, CBP/p300 acetylates p53 at lysine 373, which leads to dissociation from E3-ubiquitin ligases HDM2 and TRIM24.	Tretinoin	15-28	P53	Homo sapiens	50-53
22589701-4	2012	The upregulation of NOX is also consistently observed in cancer cells with compromised mitochondria due to the activation of oncogenic Ras or loss of p53, and in primary pancreatic cancer tissues.	nicotine 1-N-oxide	20-23	P53	Homo sapiens	150-153
22737085-5	2012	Foxa1-only sites are enriched for p53 binding sites and are frequently found near genes important to cell cycle regulation, while Foxa2-restricted sites show only a limited match to the forkhead consensus and are found in genes involved in steroid and lipid metabolism.	Steroids	240-247	P53	Homo sapiens	34-37
23285001-6	2012	Furthermore, patients with high p53 expression in tumors acquired remarkable survival benefit from adjuvant first-line platinum-based-chemotherapy.	Platinum	119-127	P53	Homo sapiens	32-35
23285001-8	2012	Thus, p53 expression is a potent prognostic and predictive factor for resectable gastric cancer with adjuvant platinum-based chemotherapy.	Platinum	110-118	P53	Homo sapiens	6-9
23285096-4	2012	Here we investigated the mechanisms of GTP-induced apoptosis in human prostate cancer LNCaP cells stably-transfected with short hairpin-RNA against p53 (LNCaPshp53) and control vector (LNCaPshV).	Guanosine Triphosphate	39-42	P53	Homo sapiens	148-151
23285096-5	2012	GTP treatment induced p53 stabilization and activation of downstream targets p21/waf1 and Bax in a dose-dependent manner specifically in LNCaPshV cells.	Guanosine Triphosphate	0-3	P53	Homo sapiens	22-25
23259030-7	2012	Furthermore, EGCG was found to prevent serial passage- and H(2)O(2)-induced senescence in HDFs by suppressing p53 acetylation, but the Sirt1 activity was unaffected.	Hydrogen Peroxide	59-67	P53	Homo sapiens	110-113
23300887-11	2012	Ser-15 of p53 was phosphorylated after 15 min treatment of the cancer cells with SDGE.	Serine	0-3	P53	Homo sapiens	10-13
23300887-11	2012	Ser-15 of p53 was phosphorylated after 15 min treatment of the cancer cells with SDGE.	sdge	81-85	P53	Homo sapiens	10-13
23300887-13	2012	Inhibitor of p53, pifithrin-alpha, attenuated the anti-cancer effects of SDGE and apoptosis was also not observed in the p53(neg) SKOV-3 cells.	sdge	73-77	P53	Homo sapiens	13-16
23272171-0	2012	Dexamethasone reduces sensitivity to cisplatin by blunting p53-dependent cellular senescence in non-small cell lung cancer.	Dexamethasone	0-13	P53	Homo sapiens	59-62
23272171-0	2012	Dexamethasone reduces sensitivity to cisplatin by blunting p53-dependent cellular senescence in non-small cell lung cancer.	Cisplatin	37-46	P53	Homo sapiens	59-62
23272171-6	2012	DEX co-treatment cells exhibited the decrease of DNA damage signaling pathway proteins, the lower expression of p53 and p21(CIP1), the lower cellular secretory program and down-regulation of NF-kappaB and its signaling cascade.	Dexamethasone	0-3	P53	Homo sapiens	112-115
23272171-8	2012	CONCLUSIONS: Our results underscore that DEX reduces chemotherapy sensitivity by blunting therapy induced cellular senescence after chemotherapy in NSCLC, which may, at least in part, in a p53-dependent manner.	Dexamethasone	41-44	P53	Homo sapiens	189-192
22389628-4	2012	In response to retinoic acid, CBP/p300 acetylates p53 at lysine 373, which leads to dissociation from E3-ubiquitin ligases HDM2 and TRIM24.	Lysine	57-63	P53	Homo sapiens	50-53
22389628-7	2012	Induction of p53 levels is a key step: RNA-interference-mediated knockdown of p53 delays differentiation, whereas depletion of negative regulators of p53 or ectopic expression of p53 yields spontaneous differentiation of hESCs, independently of retinoic acid.	Tretinoin	245-258	P53	Homo sapiens	13-16
23152782-11	2012	Western blot analysis suggested that pretreatment with Ki-67-7 sensitized bladder cancer cells to curcumin-mediated apoptosis and cell cycle arrest by p53- and p21-independent mechanisms.	Curcumin	98-106	P53	Homo sapiens	151-154
23152798-0	2012	Transient transfection of a wild-type p53 gene triggers resveratrol-induced apoptosis in cancer cells.	Resveratrol	56-67	P53	Homo sapiens	38-41
23133614-8	2012	Moreover, the enhanced doxorubicin resistance is independent of DNA damage related p53 pathway, but at least partially through the ERK1/2 pathway.	Doxorubicin	23-34	P53	Homo sapiens	83-86
23152798-2	2012	p53 has been suggested to play a role in the anticancer properties of resveratrol.	Resveratrol	70-81	P53	Homo sapiens	0-3
23152798-3	2012	We investigated resveratrol-induced cytotoxicity in H1299 cells, which are non-small lung cancer cells that have a partial deletion of the gene that encodes the p53 protein.	Resveratrol	16-27	P53	Homo sapiens	161-164
23152798-7	2012	Resveratrol also increased the p53 protein levels in MCF-7 cells without altering the p53 mRNA levels, suggesting a post-translational modulation of the protein.	Resveratrol	0-11	P53	Homo sapiens	31-34
23152798-8	2012	The resveratrol-induced cytotoxicity in these cells was partially mediated by p53 and involved the activation of caspases 9 and 7 and the cleavage of PARP.	Resveratrol	4-15	P53	Homo sapiens	78-81
23152798-11	2012	The transient transfection of a wild-type p53-GFP gene caused H1299 cells to become more responsive to the pro-apoptotic properties of resveratrol, similarly to findings in the p53-positive MCF-7 cells.	Resveratrol	135-146	P53	Homo sapiens	42-45
23152798-12	2012	Our results suggest a possible therapeutic strategy based on the use of resveratrol for the treatment of tumors that are typically unresponsive to conventional therapies because of the loss of normal p53 function.	Resveratrol	72-83	P53	Homo sapiens	200-203
23133524-0	2012	Gatifloxacin induces S and G2-phase cell cycle arrest in pancreatic cancer cells via p21/p27/p53.	Gatifloxacin	0-12	P53	Homo sapiens	93-96
23133524-5	2012	However, Gatifloxacin mediated G(2)-phase cell cycle arrest was found to be p53 dependent in both the cell lines.	Gatifloxacin	9-21	P53	Homo sapiens	76-79
23071787-6	2012	The frequency of somatic TP53 inactivation was 25.4% in Arg/Arg, 20.9% in Arg/Pro, and 16.7% in Pro/Pro patients, which may reflect a higher selective pressure to mutate the Arg-allele.	Arginine	56-59	P53	Homo sapiens	25-29
23071787-6	2012	The frequency of somatic TP53 inactivation was 25.4% in Arg/Arg, 20.9% in Arg/Pro, and 16.7% in Pro/Pro patients, which may reflect a higher selective pressure to mutate the Arg-allele.	Arginine	60-63	P53	Homo sapiens	25-29
23071787-6	2012	The frequency of somatic TP53 inactivation was 25.4% in Arg/Arg, 20.9% in Arg/Pro, and 16.7% in Pro/Pro patients, which may reflect a higher selective pressure to mutate the Arg-allele.	Arginine	60-63	P53	Homo sapiens	25-29
23071787-6	2012	The frequency of somatic TP53 inactivation was 25.4% in Arg/Arg, 20.9% in Arg/Pro, and 16.7% in Pro/Pro patients, which may reflect a higher selective pressure to mutate the Arg-allele.	Arginine	60-63	P53	Homo sapiens	25-29
23049825-3	2012	In this study we evaluate the association between a p53 variant functionally known to influence apoptosis (codon 72 Pro/Arg) and the subset of primary open angle glaucoma (POAG) patients with early loss of central visual field.	Arginine	120-123	P53	Homo sapiens	52-55
23049825-4	2012	METHODS: Genotypes for the p53 codon 72 polymorphism (Pro/Arg) were obtained for 264 POAG patients and 400 controls from the U.S. and in replication studies for 308 POAG patients and 178 controls from Australia (GIST).	Arginine	58-61	P53	Homo sapiens	27-30
23056530-1	2012	Current evidence suggests that ghrelin, a stomach derived peptide, exerts its orexigenic action through specific modulation of Sirtuin1 (SIRT1)/p53 and AMP-activated protein kinase (AMPK) pathways, which ultimately increase the expression of agouti-related protein (AgRP) and neuropeptide Y (NPY) in the arcuate nucleus of the hypothalamus (ARC).	Ghrelin	31-38	P53	Homo sapiens	144-147
22911849-9	2012	Over-expression of the dominant negative p53 mutant DeltaTAp53, which inhibits p53 activity, prevented the TPA-induced K14 down-regulation in C9 cells.	Tetradecanoylphorbol Acetate	107-110	P53	Homo sapiens	41-44
22905229-10	2012	Pharmacologic inhibition of the p53 E3 ligase MDM2 resulted in increased p53 levels and improved response to doxorubicin in vitro.	Doxorubicin	109-120	P53	Homo sapiens	32-35
22911849-9	2012	Over-expression of the dominant negative p53 mutant DeltaTAp53, which inhibits p53 activity, prevented the TPA-induced K14 down-regulation in C9 cells.	Tetradecanoylphorbol Acetate	107-110	P53	Homo sapiens	59-62
22911849-11	2012	Finally, we found that TPA induces the phosphorylation of p53 at residue 378, which enhances the affinity of p53 to bind to Sp1 and repress K14 expression.	Tetradecanoylphorbol Acetate	23-26	P53	Homo sapiens	58-61
22911849-11	2012	Finally, we found that TPA induces the phosphorylation of p53 at residue 378, which enhances the affinity of p53 to bind to Sp1 and repress K14 expression.	Tetradecanoylphorbol Acetate	23-26	P53	Homo sapiens	109-112
22859938-7	2012	We found p53 nuclear localization, activity, and phosphorylation at serine 15 on p53 increased during ER stress.	Serine	68-74	P53	Homo sapiens	9-12
22848731-0	2012	An NQO1-initiated and p53-independent apoptotic pathway determines the anti-tumor effect of tanshinone IIA against non-small cell lung cancer.	tanshinone	92-106	P53	Homo sapiens	22-25
22859938-7	2012	We found p53 nuclear localization, activity, and phosphorylation at serine 15 on p53 increased during ER stress.	Serine	68-74	P53	Homo sapiens	81-84
22848731-8	2012	TSA activated a ROS triggered, p53 independent and caspase dependent mitochondria apoptotic cell death pathway that is characterized with increased ratio of Bax to Bcl-xl, mitochondrial membrane potential disruption, cytochrome c release, and subsequent caspase activation and PARP-1 cleavage.	tanshinone	0-3	P53	Homo sapiens	31-34
22590594-2	2012	Deregulation of p53 and/or p73-associated apoptotic pathways contribute to the platinum-based resistance in ovarian cancer.	Platinum	79-87	P53	Homo sapiens	16-19
22574148-5	2012	These results show an up-regulation of p53 phosphorylation at several serine sites after RVFV MP-12 infection that is highly dependent on the viral protein NSs.	Serine	70-76	P53	Homo sapiens	39-42
22662219-9	2012	RITA induced p53 in GIST48B, followed by antiproliferative effects and a strong induction of apoptosis.	RITA	0-4	P53	Homo sapiens	13-16
22590594-4	2012	In this study, we found that genetic variants of Bcl-2 proteins exist among cisplatin-sensitive and -resistant ovarian cancer cells, and the responses of NOXA and Bax to cisplatin are regulated mainly by p53.	Cisplatin	170-179	P53	Homo sapiens	204-207
22514710-3	2012	The increase in SA-gal staining was preceded by increases in both p53 phosphorylation (S15) (1 h) and transactivation (6 h) and the abundance of the cyclin inhibitor p21(CIP1) (16 h).	sa-gal	16-22	P53	Homo sapiens	66-69
22606351-6	2012	Since p53 and p16 are homozygously deleted in the K562 cells, the DOX-induced senescence in K562 cells ought to be independent of p53 and p16-pRb pathways.	Doxorubicin	66-69	P53	Homo sapiens	6-9
22606351-6	2012	Since p53 and p16 are homozygously deleted in the K562 cells, the DOX-induced senescence in K562 cells ought to be independent of p53 and p16-pRb pathways.	Doxorubicin	66-69	P53	Homo sapiens	130-133
22514710-9	2012	In conclusion, the results indicate that H(2)O(2) at low concentrations causes premature senescence in human keratinocytes by activating p53-p21(CIP1) signaling and that these effects can be prevented by acute AMPK activation and enhanced by AMPK downregulation.	Hydrogen Peroxide	41-49	P53	Homo sapiens	137-140
22448262-0	2012	Cadmium induces p53-dependent apoptosis in human prostate epithelial cells.	Cadmium	0-7	P53	Homo sapiens	16-19
22448262-6	2012	Subsequently, cellular response to cadmium was evaluated after siRNA-mediated p53 silencing in wild type p53-expressing RWPE-1 and LNCaP cells, and after adenoviral p53 overexpression in p53-deficient DU145 and PC-3 cell lines.	Cadmium	35-42	P53	Homo sapiens	78-81
22448262-6	2012	Subsequently, cellular response to cadmium was evaluated after siRNA-mediated p53 silencing in wild type p53-expressing RWPE-1 and LNCaP cells, and after adenoviral p53 overexpression in p53-deficient DU145 and PC-3 cell lines.	Cadmium	35-42	P53	Homo sapiens	105-108
22448262-6	2012	Subsequently, cellular response to cadmium was evaluated after siRNA-mediated p53 silencing in wild type p53-expressing RWPE-1 and LNCaP cells, and after adenoviral p53 overexpression in p53-deficient DU145 and PC-3 cell lines.	Cadmium	35-42	P53	Homo sapiens	105-108
22448262-6	2012	Subsequently, cellular response to cadmium was evaluated after siRNA-mediated p53 silencing in wild type p53-expressing RWPE-1 and LNCaP cells, and after adenoviral p53 overexpression in p53-deficient DU145 and PC-3 cell lines.	Cadmium	35-42	P53	Homo sapiens	105-108
22448262-8	2012	On the other hand, p53 silencing was able to suppress cadmium-induced apoptosis.	Cadmium	54-61	P53	Homo sapiens	19-22
22448262-9	2012	Our results demonstrate that cadmium can induce p53-dependent apoptosis in human prostate epithelial cells and suggest p53 mutation as a possible contributing factor for the acquisition of apoptotic resistance in cadmium prostatic carcinogenesis.	Cadmium	29-36	P53	Homo sapiens	48-51
22448262-9	2012	Our results demonstrate that cadmium can induce p53-dependent apoptosis in human prostate epithelial cells and suggest p53 mutation as a possible contributing factor for the acquisition of apoptotic resistance in cadmium prostatic carcinogenesis.	Cadmium	213-220	P53	Homo sapiens	119-122
22242180-9	2012	Thus this study suggests that ROS/RNS contributed to change of p53 tertiary structure and that unfolded p53 can be considered as an early marker of oxidative imbalance in these patients.	ros	30-33	P53	Homo sapiens	63-66
22412944-7	2012	In comparison with control groups, the levels of p53, phospho-p53 (ser15), and p21 proteins were significantly increased while phospho-p53 (Thr55) and survivin were significantly decreased after treatments of pre-DOX and LMB (P&lt;0.05).	Doxorubicin	213-216	P53	Homo sapiens	49-52
22412944-7	2012	In comparison with control groups, the levels of p53, phospho-p53 (ser15), and p21 proteins were significantly increased while phospho-p53 (Thr55) and survivin were significantly decreased after treatments of pre-DOX and LMB (P&lt;0.05).	Doxorubicin	213-216	P53	Homo sapiens	62-65
22412944-7	2012	In comparison with control groups, the levels of p53, phospho-p53 (ser15), and p21 proteins were significantly increased while phospho-p53 (Thr55) and survivin were significantly decreased after treatments of pre-DOX and LMB (P&lt;0.05).	Doxorubicin	213-216	P53	Homo sapiens	62-65
22412944-9	2012	In conclusion, our results suggest that drug-resistant lung cancer cells with p53 wild type could be sensitized to cell death by scheduled combination treatment of DOX and LMB through activating and restoring p53 as well as potentially other signaling pathway(s) involving sequestosome 1.	Doxorubicin	164-167	P53	Homo sapiens	78-81
22412944-9	2012	In conclusion, our results suggest that drug-resistant lung cancer cells with p53 wild type could be sensitized to cell death by scheduled combination treatment of DOX and LMB through activating and restoring p53 as well as potentially other signaling pathway(s) involving sequestosome 1.	Doxorubicin	164-167	P53	Homo sapiens	209-212
22299029-1	2012	We have previously shown that TPA activates HTLV-1 LTR in Jurkat T-cells by inducing the binding of Sp1-p53 complex to the Sp1 site residing within the Ets responsive region 1 (ERR-1) of the LTR and that this activation is inhibited by PKCalpha and PKCepsilon.	Tetradecanoylphorbol Acetate	30-33	P53	Homo sapiens	104-107
23139858-6	2012	This phenotypic change was completely reversed by p53 reactivation via treatment with proteasome inhibitor MG132 or co-knockdown of E3 ligase HDM2 and partially suppressed by ATP treatment.	Adenosine Triphosphate	175-178	P53	Homo sapiens	50-53
22395499-10	2012	Frequency of Arg/Arg genotype of p53 gene was higher among cases (43%) compared with controls (33.3%), but the difference was not statistically significant (p=0.75).	Arginine	13-16	P53	Homo sapiens	33-36
22395499-10	2012	Frequency of Arg/Arg genotype of p53 gene was higher among cases (43%) compared with controls (33.3%), but the difference was not statistically significant (p=0.75).	Arginine	17-20	P53	Homo sapiens	33-36
22160723-7	2011	These cells exhibited a high yield of ROS-induced DNA single- and double-strand breaks and activation of the ATR-Chk1-ATM-Chk2-p53 pathway that led to Fas and caspase-8, -3, and -7 activation, whereas macrophages and DCs derived from them were protected.	Reactive Oxygen Species	38-41	P53	Homo sapiens	127-130
23350039-7	2012	O-linked attachment of GlcNAc to Ser and Thr residues regulates a variety of intracellular proteins, including transcription factors such as NFkappaB, c-myc and p53.	Serine	33-36	P53	Homo sapiens	161-164
23350039-7	2012	O-linked attachment of GlcNAc to Ser and Thr residues regulates a variety of intracellular proteins, including transcription factors such as NFkappaB, c-myc and p53.	Threonine	41-44	P53	Homo sapiens	161-164
22044530-6	2011	In the presence of nutlin-3, an HDM2 inhibitor, TCDD was still able to suppress 1-NP-induced p53 expression.	Polychlorinated Dibenzodioxins	48-52	P53	Homo sapiens	93-96
22044530-0	2011	2,3,7,8-Tetrachlorodibenzo-p-dioxin"s suppression of 1-nitropyrene-induced p53 expression is mediated by cytochrome P450 1A1.	Polychlorinated Dibenzodioxins	0-35	P53	Homo sapiens	75-78
22044530-6	2011	In the presence of nutlin-3, an HDM2 inhibitor, TCDD was still able to suppress 1-NP-induced p53 expression.	1-nitropyrene	80-84	P53	Homo sapiens	93-96
22044530-8	2011	Accordingly, TCDD"s suppression of 1-NP-induced p53 expression was compound-specific, and the contribution of HDM2 to the abolition of 1-NP-induced p53 was limited.	Polychlorinated Dibenzodioxins	13-17	P53	Homo sapiens	48-51
22044530-0	2011	2,3,7,8-Tetrachlorodibenzo-p-dioxin"s suppression of 1-nitropyrene-induced p53 expression is mediated by cytochrome P450 1A1.	1-nitropyrene	53-66	P53	Homo sapiens	75-78
22044530-8	2011	Accordingly, TCDD"s suppression of 1-NP-induced p53 expression was compound-specific, and the contribution of HDM2 to the abolition of 1-NP-induced p53 was limited.	1-nitropyrene	35-39	P53	Homo sapiens	48-51
22044530-2	2011	TCDD was shown to suppress p53 expression in response to genotoxic stress and hypoxic conditions.	Polychlorinated Dibenzodioxins	0-4	P53	Homo sapiens	27-30
22044530-8	2011	Accordingly, TCDD"s suppression of 1-NP-induced p53 expression was compound-specific, and the contribution of HDM2 to the abolition of 1-NP-induced p53 was limited.	1-nitropyrene	135-139	P53	Homo sapiens	148-151
22044530-9	2011	beta-Naphthoflavon (beta-NF), an aryl hydrocarbon receptor (AHR) agonist, mimicked TCDD"s action and abolished 1-NP-induced p53 expression.	1-nitropyrene	111-115	P53	Homo sapiens	124-127
22044530-11	2011	Results indicate that activation of the AHR is required for TCDD"s suppression of 1-NP"s induction of p53.	Polychlorinated Dibenzodioxins	60-64	P53	Homo sapiens	102-105
21861192-7	2011	ROS inhibition prevented p73 and Noxa expression but not p53 and p21 expression, suggesting a role for Noxa in p53-independent apoptosis in melanoma cells.	ros	0-3	P53	Homo sapiens	111-114
21982800-6	2011	Subjects with the p53 Arg/Pro + Pro/Pro genotype or MDM2 SNP309 TG+GG genotype, in conjunction with high urinary total arsenic (&gt;=14.02mug/L), had a signicantly higher RCC risk than those with the p53 Arg/Arg or MDM2 SNP309 TT genotypes and low urinary total arsenic.	Arginine	22-25	P53	Homo sapiens	18-21
21862591-4	2011	Furthermore, p53-mediated repression of transcription factors c-Myc and HIF1alpha, key drivers of ATP-generating pathways in tumors, contributed to ATP production block.	Adenosine Triphosphate	98-101	P53	Homo sapiens	13-16
21862591-4	2011	Furthermore, p53-mediated repression of transcription factors c-Myc and HIF1alpha, key drivers of ATP-generating pathways in tumors, contributed to ATP production block.	Adenosine Triphosphate	148-151	P53	Homo sapiens	13-16
22155925-7	2011	The proliferation defects induced by silencing LB1 are accompanied by a p53-dependent reduction in mitochondrial reactive oxygen species (ROS), which can be rescued by growth under hypoxic conditions.	Reactive Oxygen Species	113-136	P53	Homo sapiens	72-75
22155925-7	2011	The proliferation defects induced by silencing LB1 are accompanied by a p53-dependent reduction in mitochondrial reactive oxygen species (ROS), which can be rescued by growth under hypoxic conditions.	Reactive Oxygen Species	138-141	P53	Homo sapiens	72-75
22157150-1	2011	The serine/threonine protein kinase Aurora A is known to interact with and phosphorylate tumor suppressor p53 at Serine 215 (S215), inhibiting the transcriptional activity of p53.	Serine	113-119	P53	Homo sapiens	106-109
22157150-1	2011	The serine/threonine protein kinase Aurora A is known to interact with and phosphorylate tumor suppressor p53 at Serine 215 (S215), inhibiting the transcriptional activity of p53.	Serine	113-119	P53	Homo sapiens	175-178
22013068-0	2011	Curcumin enhances the efficacy of chemotherapy by tailoring p65NFkappaB-p300 cross-talk in favor of p53-p300 in breast cancer.	Curcumin	0-8	P53	Homo sapiens	100-103
21903092-5	2011	Expression of exogenous p53 in H1299 cells was increased following knockdown of NAPA and these cells showed increased sensitivity to cisplatin-induced apoptosis.	Cisplatin	133-142	P53	Homo sapiens	24-27
21889927-6	2011	An M2 induced DDR in p53-defective MDA-MB-231 cells was abrogated by UCN-01, a ubiquitous inhibitor of kinases including Chk1, in a response associated with substantial mitotic catastrophe and strong synergy.	ddr	14-17	P53	Homo sapiens	21-24
21903092-10	2011	These results indicate that NAPA promotes resistance to cisplatin through synoviolin and the ERAD complex which together induce the degradation of p53 and thus prevent apoptosis.	Cisplatin	56-65	P53	Homo sapiens	147-150
21903092-11	2011	Based on these findings, we propose that the combination of cisplatin and knockdown of NAPA represents a novel and attractive strategy to eradicate p53-sensitive cancer cells.	Cisplatin	60-69	P53	Homo sapiens	148-151
21479885-0	2011	Quercetin enhances 5-fluorouracil-induced apoptosis in MSI colorectal cancer cells through p53 modulation.	Fluorouracil	19-33	P53	Homo sapiens	91-94
21833626-8	2011	Our findings support experimental data implicating combined effects of MDM2 protein and the p53-mediated pathway in breast carcinogenesis, and suggest that soy isoflavones may exert protective effect via down-regulation of the MDM2 protein.	Isoflavones	160-171	P53	Homo sapiens	92-95
21856437-0	2011	Different roles of p53 in the regulation of DNA damage caused by 1,2-heteroannelated anthraquinones and doxorubicin.	Anthraquinones	85-99	P53	Homo sapiens	19-22
21597459-5	2011	Hades polyubiquitinates p53 in vitro independent of Mdm2 and targets a critical lysine residue in p53 (lysine 24) distinct from those targeted by Mdm2.	Lysine	80-86	P53	Homo sapiens	24-27
21597459-5	2011	Hades polyubiquitinates p53 in vitro independent of Mdm2 and targets a critical lysine residue in p53 (lysine 24) distinct from those targeted by Mdm2.	Lysine	80-86	P53	Homo sapiens	98-101
21597459-5	2011	Hades polyubiquitinates p53 in vitro independent of Mdm2 and targets a critical lysine residue in p53 (lysine 24) distinct from those targeted by Mdm2.	Lysine	103-109	P53	Homo sapiens	24-27
21597459-5	2011	Hades polyubiquitinates p53 in vitro independent of Mdm2 and targets a critical lysine residue in p53 (lysine 24) distinct from those targeted by Mdm2.	Lysine	103-109	P53	Homo sapiens	98-101
21983037-6	2011	In this report, we examined the role of oncogenes, DNA damage, and reactive oxygen species, signals that stabilize wild-type p53, on the stabilization of mutant p53 in vivo and the consequences of this expression on tumor formation and survival.	Reactive Oxygen Species	67-90	P53	Homo sapiens	161-164
21225623-0	2011	Regulation of p53 and cell proliferation by resveratrol and its derivatives in breast cancer cells: an in silico and biochemical approach targeting integrin alphavbeta3.	Resveratrol	44-55	P53	Homo sapiens	14-17
21479885-6	2011	RESULTS: CO115 p53-wt cells are more sensitive to 5-FU than the p53-mutated HCT15.	Fluorouracil	50-54	P53	Homo sapiens	15-18
22101337-3	2011	Using gene expression microarray analysis, we find that DNA damage response (DDR) pathways elicited by veliparib (ABT-888), a PARP inhibitor, plus topotecan comprise the G1/S checkpoint, ATM, and p53 signaling pathways in p53-wildtype cancer cell lines and BRCA1, BRCA2 and ATR pathway in p53-mutant lines.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	114-117	P53	Homo sapiens	196-199
22101337-3	2011	Using gene expression microarray analysis, we find that DNA damage response (DDR) pathways elicited by veliparib (ABT-888), a PARP inhibitor, plus topotecan comprise the G1/S checkpoint, ATM, and p53 signaling pathways in p53-wildtype cancer cell lines and BRCA1, BRCA2 and ATR pathway in p53-mutant lines.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	114-117	P53	Homo sapiens	222-225
22101337-3	2011	Using gene expression microarray analysis, we find that DNA damage response (DDR) pathways elicited by veliparib (ABT-888), a PARP inhibitor, plus topotecan comprise the G1/S checkpoint, ATM, and p53 signaling pathways in p53-wildtype cancer cell lines and BRCA1, BRCA2 and ATR pathway in p53-mutant lines.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	114-117	P53	Homo sapiens	222-225
21225623-8	2011	Further, stilbene-elicited signaling cascade leading to p53 activation was examined in MCF-7 cells and results showed that resveratrol and triacetyl-resveratrol induced both ERK and p38 phosphorylation, whereas only marginal changes in state of phosphorylation in these two kinases were observed in trimethoxy-resveratrol-treated cells.	Resveratrol	123-134	P53	Homo sapiens	56-59
21856437-0	2011	Different roles of p53 in the regulation of DNA damage caused by 1,2-heteroannelated anthraquinones and doxorubicin.	Doxorubicin	104-115	P53	Homo sapiens	19-22
22248668-0	2011	Regulation of glucose metabolism by p53: emerging new roles for the tumor suppressor.	Glucose	14-21	P53	Homo sapiens	36-39
21952947-9	2011	Accordingly, DNA damage induced by doxorubicin also induced increased expression of cyclin B1 and cyclin A in cells that express p53$^{\rm{R172H} }$.	Doxorubicin	35-46	P53	Homo sapiens	129-132
21875941-3	2011	We have shown previously that the presence of excess R2 subunits protects p53-deficient human colon cancer cells from cisplatin-induced DNA damage and replication stress.	Cisplatin	118-127	P53	Homo sapiens	74-77
21602882-2	2011	Phosphorylation of p53 at S46, an apoptosis-specific p53 posttranslational modification, is the most characterized HIPK2 function in response to lethal doses of ultraviolet (UV), ionizing radiation or different anticancer drugs, such as cisplatin, roscovitine and doxorubicin (DOX).	Cisplatin	237-246	P53	Homo sapiens	19-22
21602882-2	2011	Phosphorylation of p53 at S46, an apoptosis-specific p53 posttranslational modification, is the most characterized HIPK2 function in response to lethal doses of ultraviolet (UV), ionizing radiation or different anticancer drugs, such as cisplatin, roscovitine and doxorubicin (DOX).	Cisplatin	237-246	P53	Homo sapiens	53-56
21602882-2	2011	Phosphorylation of p53 at S46, an apoptosis-specific p53 posttranslational modification, is the most characterized HIPK2 function in response to lethal doses of ultraviolet (UV), ionizing radiation or different anticancer drugs, such as cisplatin, roscovitine and doxorubicin (DOX).	Doxorubicin	264-275	P53	Homo sapiens	19-22
21602882-2	2011	Phosphorylation of p53 at S46, an apoptosis-specific p53 posttranslational modification, is the most characterized HIPK2 function in response to lethal doses of ultraviolet (UV), ionizing radiation or different anticancer drugs, such as cisplatin, roscovitine and doxorubicin (DOX).	Doxorubicin	264-275	P53	Homo sapiens	53-56
21602882-2	2011	Phosphorylation of p53 at S46, an apoptosis-specific p53 posttranslational modification, is the most characterized HIPK2 function in response to lethal doses of ultraviolet (UV), ionizing radiation or different anticancer drugs, such as cisplatin, roscovitine and doxorubicin (DOX).	Doxorubicin	277-280	P53	Homo sapiens	19-22
21196432-4	2011	Two pathways are proposed for exploiting tyrosinase expression: (a) a p53-dependent pathway leading to apoptosis or arrest and (b) a reactive oxygen species-mediated induction of endoplasmic reticulum stress in p53 mutant tumors.	Reactive Oxygen Species	133-156	P53	Homo sapiens	211-214
21344396-11	2011	p53-related suppression of LRP expression was completely reversed by doxorubicin treatment and Adr, whereas CP and VP-16 treatment induced LRP expression increased significantly.	Doxorubicin	69-80	P53	Homo sapiens	0-3
21602882-2	2011	Phosphorylation of p53 at S46, an apoptosis-specific p53 posttranslational modification, is the most characterized HIPK2 function in response to lethal doses of ultraviolet (UV), ionizing radiation or different anticancer drugs, such as cisplatin, roscovitine and doxorubicin (DOX).	Doxorubicin	277-280	P53	Homo sapiens	53-56
20548326-6	2011	Genes involved in the "biological oxidation" and "G(1)/S checkpoint" pathways were the most significantly represented at 24 h, whereas genes involved in the "cell cycle" and "DNA replication" pathways were represented at 48 and 72 h. Genes associated with the "apoptosis" pathway were also significantly represented at 72 h. Modulation of the expression of p53 and p53-induced genes (CDKN1A/p21 and GADD45), which are involved in the G(1)/S transition, suggested an effect of ibuprofen on cell-cycle progression.	Ibuprofen	476-485	P53	Homo sapiens	357-360
22077725-3	2011	We have examined potential alterations in p53 in response to 2-ME(2), E(2) and the microtubule disruptor taxol in T47D breast cancer cells.	Paclitaxel	105-110	P53	Homo sapiens	42-45
20548326-6	2011	Genes involved in the "biological oxidation" and "G(1)/S checkpoint" pathways were the most significantly represented at 24 h, whereas genes involved in the "cell cycle" and "DNA replication" pathways were represented at 48 and 72 h. Genes associated with the "apoptosis" pathway were also significantly represented at 72 h. Modulation of the expression of p53 and p53-induced genes (CDKN1A/p21 and GADD45), which are involved in the G(1)/S transition, suggested an effect of ibuprofen on cell-cycle progression.	Ibuprofen	476-485	P53	Homo sapiens	365-368
20548326-9	2011	Ibuprofen induced ROS, which resulted in cellular alterations that promoted a p53-dependent G(1) blockade.	Ibuprofen	0-9	P53	Homo sapiens	78-81
20548326-9	2011	Ibuprofen induced ROS, which resulted in cellular alterations that promoted a p53-dependent G(1) blockade.	Reactive Oxygen Species	18-21	P53	Homo sapiens	78-81
22312705-7	2011	Accordingly, P53 protein expression showed a significant up-regulation; MTT results showed that after incubation with 5-FU, miR-122 transfectants had higher cell inhibitory rates than negative miRNA or untreated cells; flow cytometry results demonstrated that apoptosis rate increased in miR-122 transfected cells, compared with negative miRNA or untreated cells.	Fluorouracil	118-122	P53	Homo sapiens	13-16
22312705-9	2011	MiR-122 can specifically down-regulate the expression of Bcl-2 and Bcl-XL, and increase P53 activity in BEL-7402/5-FU cells, which increased cells spontaneous apoptosis and sensitize cells to 5-FU.	Fluorouracil	113-117	P53	Homo sapiens	88-91
22077725-8	2011	The observed upregulation of p53 induced by 2-ME(2) is inhibited by concurrent treatment with 1 microM taxol.	Paclitaxel	103-108	P53	Homo sapiens	29-32
22340787-11	2011	CONCLUSIONS: Melatonin can inhibit proliferation and induce apoptosis of fibroblasts in hypertrophic scar through regulating the gene expressions of cyclin E, p53, and Fas.	Melatonin	13-22	P53	Homo sapiens	159-162
22340095-2	2011	METHODS: Wild-type p53 ovarian carcinoma cell line A2780 cells were treated with genotoxic agent adriamycin.	Doxorubicin	97-107	P53	Homo sapiens	19-22
21911080-0	2011	Benzo(a)pyrene-induced mitochondrial dysfunction and cell death in p53-null Hep3B cells.	pyrene	8-14	P53	Homo sapiens	67-70
22041887-8	2011	In coculture, tamoxifen induces the upregulation of TIGAR (TP53-induced glycolysis and apoptosis regulator), a p53 regulated gene that simultaneously inhibits glycolysis, autophagy and apoptosis and reduces ROS generation, thereby promoting oxidative mitochondrial metabolism.	Tamoxifen	14-23	P53	Homo sapiens	111-114
21855885-6	2011	As predicted, use of poly-SUS allowed separation of the His-tagged tumor suppressor protein, p53, at sample buffer concentrations as low as 0.08% w/v (2.9 mM), which is 24 times lower than required for SDS in the standard reducing PAGE protocol.	Sodium Dodecyl Sulfate	202-205	P53	Homo sapiens	93-96
21953469-3	2011	Here we characterize the mechanisms accounting for the nuclear accumulation of a new point mutation (Lys-351 to Asn) in the nuclear export sequence of p53 identified in a cisplatin-resistant ovarian carcinoma cell line (A2780 CIS).	Cisplatin	171-180	P53	Homo sapiens	151-154
21953469-5	2011	As a consequence, cells expressing p53 K351N mutant showed defects in cisplatin-induced translocation of p53 to mitochondria, Bax oligomerization, and mitochondrial membrane depolarization.	Cisplatin	70-79	P53	Homo sapiens	35-38
21953469-5	2011	As a consequence, cells expressing p53 K351N mutant showed defects in cisplatin-induced translocation of p53 to mitochondria, Bax oligomerization, and mitochondrial membrane depolarization.	Cisplatin	70-79	P53	Homo sapiens	105-108
21953469-6	2011	These data identify K351N as a critical mutation of p53 that contributes to the development and maintenance of resistance to cisplatin.	Cisplatin	125-134	P53	Homo sapiens	52-55
22071691-4	2011	Finally, miR-885-3p modulated the cisplatin-induced TP53-dependent mitochondrial apoptosis by up regulation of MDM4 levels and down regulation of BCL2 levels in mitochondria.	Cisplatin	34-43	P53	Homo sapiens	52-56
22041887-8	2011	In coculture, tamoxifen induces the upregulation of TIGAR (TP53-induced glycolysis and apoptosis regulator), a p53 regulated gene that simultaneously inhibits glycolysis, autophagy and apoptosis and reduces ROS generation, thereby promoting oxidative mitochondrial metabolism.	ros	207-210	P53	Homo sapiens	111-114
22075440-8	2011	CONCLUSIONS: It appears that TP53 status determines the clinical importance of nuclear survivin expression in taxane-platinum treated ovarian cancer patients.	taxane	110-116	P53	Homo sapiens	29-33
22075440-8	2011	CONCLUSIONS: It appears that TP53 status determines the clinical importance of nuclear survivin expression in taxane-platinum treated ovarian cancer patients.	Platinum	117-125	P53	Homo sapiens	29-33
21880715-10	2011	Meanwhile, mutation of EDEE residues impairs both the binding and the enzymatic activity of SMYD2 to p53 Lys-370.	Lysine	105-108	P53	Homo sapiens	101-104
21880715-2	2011	Here we report that SMYD2 prefers to methylate p53 Lys-370 over histone substrates in vitro.	Lysine	51-54	P53	Homo sapiens	47-50
21973212-4	2011	In MRC-5 cells treated with methylseleninic acid (MSeA, 0-10 muM), depletion of p53 hampers senescence-associated expression of beta-galactosidase, disrupts the otherwise S and G2/M cell cycle arrest, desensitizes such cells to MSeA treatment, and increases genome instability.	methylselenic acid	28-48	P53	Homo sapiens	80-83
21880715-11	2011	These data together reveal the molecular basis of SMYD2 in specifically recognizing and regulating functions of p53 tumor suppressor through Lys-370 monomethylation.	Lysine	141-144	P53	Homo sapiens	112-115
21880715-3	2011	Consistently, the level of endogenous p53 Lys-370 monomethylation is significantly elevated when SMYD2 is overexpressed in vivo.	Lysine	42-45	P53	Homo sapiens	38-41
21880715-7	2011	In addition, a unique EDEE motif between the loop of anti-parallel beta7 and beta8 sheets of the SET core not only interacts with p53 substrate but also forms a hydrogen bond network with residues from CTD.	Hydrogen	161-169	P53	Homo sapiens	130-133
21927014-0	2011	Platinum-(IV)-derivative satraplatin induced G2/M cell cycle perturbation via p53-p21(waf1/cip1)-independent pathway in human colorectal cancer cells.	Platinum	0-8	P53	Homo sapiens	78-81
22055193-7	2011	Lpin1 expression in response to nutritional stress is controlled through the ROS-ATM-p53 pathway and is conserved in human cells.	ros	77-80	P53	Homo sapiens	85-88
21552291-6	2011	Both mouse and human cells lacking p53 are hypersensitive to hydrogen peroxide (H(2)O(2))-induced cell death compared with their isogenic wild-type counterparts.	Hydrogen Peroxide	61-78	P53	Homo sapiens	35-38
21552291-6	2011	Both mouse and human cells lacking p53 are hypersensitive to hydrogen peroxide (H(2)O(2))-induced cell death compared with their isogenic wild-type counterparts.	Hydrogen Peroxide	80-88	P53	Homo sapiens	35-38
22037398-8	2011	In hMSCs isolated from a chronic lymphocytic leukemia (CLL) patient, p53 and p21 were induced by cisplatin and gamma-irradiation, while RPA2 was phosphorylated on serine4/8 in particular following cisplatin.	Cisplatin	197-206	P53	Homo sapiens	69-72
21552291-7	2011	By contrast, p53(-/-) cells are expectedly resistant to cell death upon exposure to DNA-damaging agents such as cisplatin (CDDP) and etoposide.	Cisplatin	112-121	P53	Homo sapiens	13-16
21552291-7	2011	By contrast, p53(-/-) cells are expectedly resistant to cell death upon exposure to DNA-damaging agents such as cisplatin (CDDP) and etoposide.	Cisplatin	123-127	P53	Homo sapiens	13-16
21552291-8	2011	Although p53 and its classical targets such as p21 and Mdm2 are activated by both H(2)O(2) and CDDP, we found that the expression of haeme-oxygenase-1 (HO-1)-an antioxidant and antiapoptotic protein-was directly induced only upon H(2)O(2) treatment in a p53-dependent manner.	Hydrogen Peroxide	82-90	P53	Homo sapiens	9-12
21552291-8	2011	Although p53 and its classical targets such as p21 and Mdm2 are activated by both H(2)O(2) and CDDP, we found that the expression of haeme-oxygenase-1 (HO-1)-an antioxidant and antiapoptotic protein-was directly induced only upon H(2)O(2) treatment in a p53-dependent manner.	Cisplatin	95-99	P53	Homo sapiens	9-12
21552291-8	2011	Although p53 and its classical targets such as p21 and Mdm2 are activated by both H(2)O(2) and CDDP, we found that the expression of haeme-oxygenase-1 (HO-1)-an antioxidant and antiapoptotic protein-was directly induced only upon H(2)O(2) treatment in a p53-dependent manner.	Hydrogen Peroxide	230-238	P53	Homo sapiens	9-12
21552291-11	2011	Finally, H(2)O(2)-mediated cell death was rescued significantly in p53-deficient cells by antioxidant treatment, as well as by bilirubin, a by-product of HO-1 metabolism.	Hydrogen Peroxide	9-17	P53	Homo sapiens	67-70
22009531-6	2011	Exposure to DMBA and TPA activated p53 and decreased MnSOD expression via p53-mediated suppression of Sp1 binding to the MnSOD promoter in normal-appearing skin and benign papillomas.	Tetradecanoylphorbol Acetate	21-24	P53	Homo sapiens	35-38
22009531-6	2011	Exposure to DMBA and TPA activated p53 and decreased MnSOD expression via p53-mediated suppression of Sp1 binding to the MnSOD promoter in normal-appearing skin and benign papillomas.	Tetradecanoylphorbol Acetate	21-24	P53	Homo sapiens	74-77
22032922-8	2011	The increase in CGB7 levels upon doxorubicin treatment is lost after siRNA-directed knockdown of p53.	Doxorubicin	33-44	P53	Homo sapiens	97-100
21191649-0	2011	P53 genotype as a determinant of ER expression and tamoxifen response in the MMTV-Wnt-1 model of mammary carcinogenesis.	Tamoxifen	51-60	P53	Homo sapiens	0-3
21191649-9	2011	These data demonstrate that p53 regulates ER expression in vivo, and affects response to tamoxifen.	Tamoxifen	89-98	P53	Homo sapiens	28-31
21726628-2	2011	We have previously shown that induction of p21(Waf1) by p53 is responsible for protection of cells against adriamycin-induced polyploidy formation and mitotic catastrophe.	Doxorubicin	107-117	P53	Homo sapiens	56-59
21726628-3	2011	Here we show that adriamycin treatment suppressed Plk1 expression in a p53- and p21(Waf1)-dependent manner.	Doxorubicin	18-28	P53	Homo sapiens	71-74
21726628-4	2011	Ablation of p21(Waf1) inhibited the adriamycin-induced p53 activation, and this inhibition was alleviated by knockdown of Plk1, suggesting that p21(Waf1)-dependent suppression of Plk1 expression is responsible for maintaining p53 activation during stress response.	Doxorubicin	36-46	P53	Homo sapiens	55-58
21726628-4	2011	Ablation of p21(Waf1) inhibited the adriamycin-induced p53 activation, and this inhibition was alleviated by knockdown of Plk1, suggesting that p21(Waf1)-dependent suppression of Plk1 expression is responsible for maintaining p53 activation during stress response.	Doxorubicin	36-46	P53	Homo sapiens	226-229
21726628-6	2011	Overexpression of Plk1 inhibited the p53-mediated prevention of caspase-independent mitotic death, but not polyploidy formation, in adriamycin-treated cells.	Doxorubicin	132-142	P53	Homo sapiens	37-40
21726628-7	2011	Together our results indicate that suppression of Plk1 by p21(Waf1) is responsible for p53-dependent protection against adriamycin-induced caspase-independent mitotic death.	Doxorubicin	120-130	P53	Homo sapiens	87-90
21926165-4	2011	Changes in proliferation, mitotic catastrophe, apoptosis, and underlying mechanism in ovarian cancer cells of different p53 status following paclitaxel exposure were also analyzed.	Paclitaxel	141-151	P53	Homo sapiens	120-123
22032989-5	2011	Tandem affinity purification and immunoprecipitations combined with mass spectrometry studies indicate that CSA and CSB associate within a Cullin Ring Ubiquitin Ligase complex responsible, under certain circumstances, for p53 ubiquitination.	Cyclosporine	108-111	P53	Homo sapiens	222-225
22032989-6	2011	This study identifies CSA and CSB as the key elements of a regulatory mechanism that equilibrate beneficial and detrimental effects of p53 activity upon cellular stress.	Cyclosporine	22-25	P53	Homo sapiens	135-138
22033337-4	2011	Our results show that virus infection induces p53 acetylation at lysine 379, and that this modification is absolutely required for p53-dependent transcriptional transactivation of both, pro-apoptotic and IFN-stimulated genes induced by virus infection, and for p53-mediated control of virus replication.	Lysine	65-71	P53	Homo sapiens	46-49
22033337-4	2011	Our results show that virus infection induces p53 acetylation at lysine 379, and that this modification is absolutely required for p53-dependent transcriptional transactivation of both, pro-apoptotic and IFN-stimulated genes induced by virus infection, and for p53-mediated control of virus replication.	Lysine	65-71	P53	Homo sapiens	131-134
22033337-4	2011	Our results show that virus infection induces p53 acetylation at lysine 379, and that this modification is absolutely required for p53-dependent transcriptional transactivation of both, pro-apoptotic and IFN-stimulated genes induced by virus infection, and for p53-mediated control of virus replication.	Lysine	65-71	P53	Homo sapiens	131-134
22037398-4	2011	Cisplatin and gamma-irradiation activated the DNA damage response in hMSCs, including induction of p53 and p21, and activation of PI3 kinase-related protein kinase (PIKK)-dependent phosphorylation of histone H2AX on serine 139, and replication protein A2 on serine4/serine8.	Cisplatin	0-9	P53	Homo sapiens	99-102
22037398-8	2011	In hMSCs isolated from a chronic lymphocytic leukemia (CLL) patient, p53 and p21 were induced by cisplatin and gamma-irradiation, while RPA2 was phosphorylated on serine4/8 in particular following cisplatin.	Cisplatin	97-106	P53	Homo sapiens	69-72
21807113-4	2011	Sirt1, a NAD-dependent class III histone deacetylase, has a paradoxical role in tumorigenesis by deacetylating several transcription factors, including p53, E2F1 and forkhead proteins.	NAD	9-12	P53	Homo sapiens	152-155
21838704-3	2011	The local concentration of the nitric oxide defines its anti- or protumorigenic function by interacting with DNA or DNA repair enzymes and tumor suppressor gene, p53, as well.	Nitric Oxide	31-43	P53	Homo sapiens	162-165
21595775-4	2011	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in EC were 39.4%, 45.6%, and 15.0%, respectively; frequencies in the controls were 43.2%, 45.6%, and 11.2%, respectively.	Arginine	47-50	P53	Homo sapiens	19-22
21595775-4	2011	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in EC were 39.4%, 45.6%, and 15.0%, respectively; frequencies in the controls were 43.2%, 45.6%, and 11.2%, respectively.	Arginine	51-54	P53	Homo sapiens	19-22
21595775-4	2011	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in EC were 39.4%, 45.6%, and 15.0%, respectively; frequencies in the controls were 43.2%, 45.6%, and 11.2%, respectively.	Arginine	51-54	P53	Homo sapiens	19-22
21946130-3	2011	Resveratrol may arrest, among various tumors, cell growth in both papillary and follicular thyroid cancer by activation of the mitogen-activated protein kinase (MAPK) signal transduction pathway as well as increase of p53 and its phosphorylation.	Resveratrol	0-11	P53	Homo sapiens	218-221
21945951-7	2011	In cells with ATM expression silenced by shRNA, AICAR-induced p53 phosphorylation at Ser(15) and Ser(37) was attenuated.	Serine	85-88	P53	Homo sapiens	62-65
21945951-8	2011	Furthermore, p53 activation by AICAR was blocked by rapamycin, a specific inhibitor of the mTOR kinase, which is a crucial regulator of cell growth.	Sirolimus	52-61	P53	Homo sapiens	13-16
21945951-0	2011	The activation of the p53 pathway by the AMP mimetic AICAR is reduced by inhibitors of the ATM or mTOR kinases.	Adenosine Monophosphate	41-44	P53	Homo sapiens	22-25
22057999-9	2011	Meta-analysis results  showed that the Pro allele and Pro carrier (Arg/Pro + Pro/Pro) of p53 codon 72  polymorphism were significantly related with endometrial cancer risk (OR =  1.25, 95%CI = 1.10-1.41, P = 0.0005; OR = 1.34, 95%CI = 1.12-1.59, P = 0.001,  respectively).	Arginine	67-70	P53	Homo sapiens	89-92
21594648-0	2011	Overexpression of miR-22 reverses paclitaxel-induced chemoresistance through activation of PTEN signaling in p53-mutated colon cancer cells.	Paclitaxel	34-44	P53	Homo sapiens	109-112
21594648-4	2011	We further investigated the role of miR-22 on cytotoxicity of paclitaxel in both the p53-mutated and p53 wild-type colon cancer cells.	Paclitaxel	62-72	P53	Homo sapiens	101-104
22260024-0	2011	[Involvement of p38-p53 signal pathway in resveratrol-induced apoptosis in MCF-7 cells].	Resveratrol	42-53	P53	Homo sapiens	20-23
22260024-7	2011	Resveratrol could induce apoptosis and activate p38 and p53 in a time dependent manner in MCF-7 cells.	Resveratrol	0-11	P53	Homo sapiens	56-59
22260024-8	2011	In addition, the cell growth inhibitory ratio and the apoptotic ratio of resveratrol-treated group decreased markedly by the p38 MAPK inhibitor SB203580 or p53 inhibitor pifithrin-alpha.	Resveratrol	73-84	P53	Homo sapiens	156-159
22260024-9	2011	Further experiments confirmed that resveratrol-induced p53 activation was reduced by SB203580 whereas the activation of p38 was not affected by pifithrin-alpha.	Resveratrol	35-46	P53	Homo sapiens	55-58
22260024-10	2011	In conclusion, resveratrol induced apoptosis in MCF-7 cells could be through activating p38-p53 signal pathway.	Resveratrol	15-26	P53	Homo sapiens	92-95
21594648-8	2011	Importantly, miR-22 overexpression enhanced the cytotoxic role of paclitaxel in p53-mutated HT-29 and HCT-15 cells, but not in p53 wild-type HCT-116 cell.	Paclitaxel	66-76	P53	Homo sapiens	80-83
21594648-9	2011	We further demonstrated that the tumor-suppressive role of miR-22 in p53-mutated colon cancer cells was mediated by upregulating PTEN expression, which negatively regulated Akt phosphorylation at Ser(473) and MTDH expression, and subsequently increased Bax and active caspase-3 levels.	Serine	196-199	P53	Homo sapiens	69-72
22041521-9	2011	A functionally relevant p53 missense mutation in codon 273 of exon 8 [CGT (Arg) -&gt; CAT (His)] was confirmed by direct sequencing.	Arginine	75-78	P53	Homo sapiens	24-27
22057999-11	2011	We  concluded that the Pro allele (Arg/Pro + Pro/Pro) of p53 codon 72 polymorphism  is a potential risk factor for endometrial cancer.	Arginine	35-38	P53	Homo sapiens	57-60
21859827-0	2011	Regulator of G protein signaling 6 mediates doxorubicin-induced ATM and p53 activation by a reactive oxygen species-dependent mechanism.	Doxorubicin	44-55	P53	Homo sapiens	72-75
22029423-12	2011	CONCLUSIONS: Our results suggest that RSV arrests cell cycle, promotes apoptosis and sensitizes PrCa cells to IR likely through a desirable dual action to activate the ATM-AMPK-p53-p21(cip1)/p27(kip1) and inhibit the Akt signalling pathways.	Resveratrol	38-41	P53	Homo sapiens	177-180
21859827-0	2011	Regulator of G protein signaling 6 mediates doxorubicin-induced ATM and p53 activation by a reactive oxygen species-dependent mechanism.	Reactive Oxygen Species	92-115	P53	Homo sapiens	72-75
21859827-1	2011	Doxorubicin (DXR), among the most widely used cancer chemotherapy agents, promotes cancer cell death via activation of ataxia telangiectasia mutated (ATM) and the resultant upregulation of tumor suppressor p53.	Doxorubicin	0-11	P53	Homo sapiens	206-209
21859827-1	2011	Doxorubicin (DXR), among the most widely used cancer chemotherapy agents, promotes cancer cell death via activation of ataxia telangiectasia mutated (ATM) and the resultant upregulation of tumor suppressor p53.	Doxorubicin	13-16	P53	Homo sapiens	206-209
21859827-6	2011	RGS6 mediated activation of ATM and p53 by DXR via a reactive oxygen species (ROS)-dependent and DNA damage-independent mechanism.	Reactive Oxygen Species	53-76	P53	Homo sapiens	36-39
21859827-6	2011	RGS6 mediated activation of ATM and p53 by DXR via a reactive oxygen species (ROS)-dependent and DNA damage-independent mechanism.	Reactive Oxygen Species	78-81	P53	Homo sapiens	36-39
21516123-1	2011	Mammalian Ste20-like kinase-1 (MST1) kinase mediates H2O2-induced cell death by anticancer drugs such as cisplatin in a p53-dependent manner.	Hydrogen Peroxide	53-57	P53	Homo sapiens	120-123
21951851-4	2011	In this review, we summarize mitochondrial function and ROS generation, and also highlight ROS-modulated core autophagic pathways involved in ATG4-ATG8/LC3, Beclin-1, p53, PTEN, PI3K-Akt-mTOR and MAPK signaling in cancer.	Reactive Oxygen Species	91-94	P53	Homo sapiens	167-170
21516123-1	2011	Mammalian Ste20-like kinase-1 (MST1) kinase mediates H2O2-induced cell death by anticancer drugs such as cisplatin in a p53-dependent manner.	Cisplatin	105-114	P53	Homo sapiens	120-123
21516123-3	2011	Here we show that peroxiredoxin-I (PRX-I) is an essential intermediate in H2O2-induced MST1 activation and cisplatin-induced cell death through p53.	Cisplatin	107-116	P53	Homo sapiens	144-147
21361874-8	2011	The bcl-2, p53 and cox-2 genes in both cell lines treated with ASA seem to exhibit different patterns of expression.	Aspirin	63-66	P53	Homo sapiens	11-14
21909125-12	2011	H2O2 (100 mumol/L) significantly decreased Sirt1 expression, and induced up-regulation of p53 acetylation and p16(INK4a), which were blocked by pre-treatment with RHL (10 mumol/L).	Hydrogen Peroxide	0-4	P53	Homo sapiens	90-93
21965754-9	2011	These effects were independent of p53 activation because the level of serine-15 phosphorylated p53 was not affected after drug treatment.	Serine	70-76	P53	Homo sapiens	95-98
21361874-4	2011	The mechanism of action of different concentrations of ASA were compared in K562 (non-MDR) and Lucena (MDR) cells by analysing cell viability, apoptosis and necrosis, intracellular ROS (reactive oxygen species) formation and bcl-2, p53 and cox-2 gene expression.	Aspirin	55-58	P53	Homo sapiens	232-235
21286718-6	2011	The effects of cetuximab or irinotecan as single agents or the combination on the expression of p53, p16, and EGFR signaling pathways were also studied.	Irinotecan	28-38	P53	Homo sapiens	96-99
21832879-0	2011	Metabolic utilization of exogenous pyruvate by mutant p53 (R175H) human melanoma cells promotes survival under glucose depletion.	Glucose	111-118	P53	Homo sapiens	54-57
21832879-4	2011	Mutant p53 melanoma were resistant to a comparable metabolic restriction, only showing PARP fragmentation when glucose depletion was accompanied by treatment with diphenylene iodonium (DPI), a NADPH oxidase inhibitor of superoxide (O2*-) generation.	Glucose	111-118	P53	Homo sapiens	7-10
21832879-4	2011	Mutant p53 melanoma were resistant to a comparable metabolic restriction, only showing PARP fragmentation when glucose depletion was accompanied by treatment with diphenylene iodonium (DPI), a NADPH oxidase inhibitor of superoxide (O2*-) generation.	Superoxides	220-230	P53	Homo sapiens	7-10
21832879-4	2011	Mutant p53 melanoma were resistant to a comparable metabolic restriction, only showing PARP fragmentation when glucose depletion was accompanied by treatment with diphenylene iodonium (DPI), a NADPH oxidase inhibitor of superoxide (O2*-) generation.	Superoxides	232-234	P53	Homo sapiens	7-10
21832879-6	2011	Metabolic utilization and survival under glucose depletion was increased by pyruvate in mutant p53 (R175H) cells.	Glucose	41-48	P53	Homo sapiens	95-98
21832879-7	2011	Our results show for the first time that melanoma cells harbouring a p53 (R175H) mutation increase: a) survival under glucose depletion, counteracted by NADPH-oxidase modulators like DPI; b) resistance to DPI when supplemented with exogenous pyruvate.	Glucose	118-125	P53	Homo sapiens	69-72
21455220-4	2011	Met ensures cell survival through a new path in which c-Abl and p38-MAPK are employed to elicit p53 phosphorylation on Ser(392) and Mdm2 upregulation.	Serine	119-122	P53	Homo sapiens	96-99
21737614-0	2011	Resveratrol, through NF-Y/p53/Sin3/HDAC1 complex phosphorylation, inhibits estrogen receptor alpha gene expression via p38MAPK/CK2 signaling in human breast cancer cells.	Resveratrol	0-11	P53	Homo sapiens	26-29
21660051-5	2011	Silencing of GSK-3beta or p53 expression was cardioprotective, indicating that activation of the ERK-GSK-3beta-p53 signaling pathway is involved in Zn(2+)-sensitive myocyte death.	Zinc	148-150	P53	Homo sapiens	26-29
21660051-5	2011	Silencing of GSK-3beta or p53 expression was cardioprotective, indicating that activation of the ERK-GSK-3beta-p53 signaling pathway is involved in Zn(2+)-sensitive myocyte death.	Zinc	148-150	P53	Homo sapiens	111-114
20467885-10	2011	Irinotecan and simvastatin combination treatment of A549 and H460 cells increased G(1) phase arrest, which was associated with up-regulation of p21(WAF1/CIP) and p53 compared with irinotecan alone.	Irinotecan	0-10	P53	Homo sapiens	162-165
20567995-7	2011	However, SN 28049 inhibited HCT116 cell growth in vitro and activated the p53 pathway to induce a state with G(2)/M-phase DNA content, low mitotic index and a high proportion of binucleate cells.	N-(2-(dimethylamino)ethyl)-2,6-dimethyl-1-oxo-1,2-dihydroxybenzo(b)-1,6-naphthyridine-4-carboxamide	9-17	P53	Homo sapiens	74-77
21724641-7	2011	Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370).	Lysine	310-313	P53	Homo sapiens	97-100
22331725-0	2011	TP53 gene status and human papilloma virus infection in response to platinum plus taxane-based chemotherapy of epithelial ovarian carcinomas.	Platinum	68-76	P53	Homo sapiens	0-4
22331725-0	2011	TP53 gene status and human papilloma virus infection in response to platinum plus taxane-based chemotherapy of epithelial ovarian carcinomas.	taxane	82-88	P53	Homo sapiens	0-4
22331725-11	2011	The distribution of codon 72 TP53 genotypes was: Arg/Arg 38.5%, Arg/Pro 50.0%, Pro/Pro 11.5%.	Arginine	49-52	P53	Homo sapiens	29-33
21724641-7	2011	Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370).	Lysine	310-313	P53	Homo sapiens	97-100
21724641-7	2011	Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370).	Lysine	101-104	P53	Homo sapiens	50-53
21724641-7	2011	Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370).	Lysine	101-104	P53	Homo sapiens	97-100
21724641-7	2011	Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370).	Lysine	101-104	P53	Homo sapiens	97-100
21724641-7	2011	Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370).	Lysine	310-313	P53	Homo sapiens	97-100
21724641-7	2011	Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370).	Lysine	101-104	P53	Homo sapiens	97-100
21724641-7	2011	Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370).	Lysine	310-313	P53	Homo sapiens	50-53
21791603-4	2011	Specifically, we show that Pirh2, a target of the p53 tumor suppressor, monoubiquitinates PolH at one of multiple lysine residues.	Lysine	114-120	P53	Homo sapiens	50-53
21724641-7	2011	Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370).	Lysine	310-313	P53	Homo sapiens	97-100
21724641-7	2011	Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370).	Lysine	310-313	P53	Homo sapiens	97-100
21724641-7	2011	Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370).	Lysine	310-313	P53	Homo sapiens	97-100
21724641-7	2011	Further modeling study of Smyd2 in complex with a p53 peptide indicates that mono-methylation of p53-Lys(372) might result in steric conflict of the methyl group with the surrounding residues of Smyd2, providing a structural explanation for the inhibitory effect of the SET7/9-mediated mono-methylation of p53-Lys(372) on the Smyd2-mediated methylation of p53-Lys(370).	Lysine	310-313	P53	Homo sapiens	50-53
21465263-5	2011	We find an increase in phosphorylated p53 at serine 15 (S15), diminished acetylation at lysine 382 (K382), altered ubiquitination pattern, and oligomerization activity as a function of mHtt expression.	Serine	45-51	P53	Homo sapiens	38-41
21743969-8	2011	Moreover, simultaneous treatment with resveratrol and a Notch-1 inhibitor (MRK-003) partially attenuated the apoptosis and completely blocked the activation of Notch-1 and the increase in wild-type p53.	Resveratrol	38-49	P53	Homo sapiens	198-201
22200028-2	2011	Emerging experimental evidence shows that isoflavones could induce cancer cell death by regulating multiple cellular signaling pathways including Akt, NF-kappaB, MAPK, Wnt, androgen receptor (AR), p53 and Notch signaling, all of which have been found to be deregulated in cancer cells.	Isoflavones	42-53	P53	Homo sapiens	197-200
21743969-0	2011	Notch-1 activation-dependent p53 restoration contributes to resveratrol-induced apoptosis in glioblastoma cells.	Resveratrol	60-71	P53	Homo sapiens	29-32
21743969-5	2011	We demonstrated that resveratrol strongly suppressed cell growth and induced apoptosis in A172 and T98G glioblastoma cells, which have low active Notch-1 expression and a heterozygous p53 mutation.	Resveratrol	21-32	P53	Homo sapiens	184-187
21864926-2	2011	The decrease in intracellular ROS levels in response to TIGAR may also play a role in the ability of p53 to protect from the accumulation of genomic lesions.	Reactive Oxygen Species	30-33	P53	Homo sapiens	101-104
21743969-6	2011	Our results suggest that resveratrol significantly activates intracellular Notch-1 and restores wild-type p53 expression in a time-dependent manner.	Resveratrol	25-36	P53	Homo sapiens	106-109
21784846-2	2011	In the present work, we have found that transcriptional activation of the oxidative stress-responsive heat shock factor 1 (HSF-1) and expression of heat shock proteins, including Hsp27, which is normally known to augment proteasomal p53 degradation, are inhibited in Adriamycin (doxorubicin)-resistant MCF-7 cells (MCF-7/adr).	Doxorubicin	267-277	P53	Homo sapiens	233-236
21810437-0	2011	Involvement of phorbol-12-myristate-13-acetate-induced protein 1 in goniothalamin-induced TP53-dependent and -independent apoptosis in hepatocellular carcinoma-derived cells.	goniothalamin	68-81	P53	Homo sapiens	90-94
21810437-1	2011	The objective was to investigate the upstream apoptotic mechanisms that were triggered by a styrylpyrone derivative, goniothalamin (GTN), in tumor protein p53 (TP53)-positive and -negative hepatocellular carcinoma (HCC)-derived cells.	goniothalamin	117-130	P53	Homo sapiens	155-158
21810437-1	2011	The objective was to investigate the upstream apoptotic mechanisms that were triggered by a styrylpyrone derivative, goniothalamin (GTN), in tumor protein p53 (TP53)-positive and -negative hepatocellular carcinoma (HCC)-derived cells.	goniothalamin	117-130	P53	Homo sapiens	160-164
21810437-1	2011	The objective was to investigate the upstream apoptotic mechanisms that were triggered by a styrylpyrone derivative, goniothalamin (GTN), in tumor protein p53 (TP53)-positive and -negative hepatocellular carcinoma (HCC)-derived cells.	goniothalamin	132-135	P53	Homo sapiens	155-158
21810437-1	2011	The objective was to investigate the upstream apoptotic mechanisms that were triggered by a styrylpyrone derivative, goniothalamin (GTN), in tumor protein p53 (TP53)-positive and -negative hepatocellular carcinoma (HCC)-derived cells.	goniothalamin	132-135	P53	Homo sapiens	160-164
21810437-3	2011	Results indicated that GTN triggered phorbol-12-myristate-13-acetate-induced protein 1 (PMAIP1, also known as NOXA)-mediated apoptosis via TP53-dependent and -independent pathways.	goniothalamin	23-26	P53	Homo sapiens	139-143
21810437-4	2011	In TP53-positive SK-Hep1 cells, GTN furthermore induced TP53 transcription-dependent and -independent apoptosis.	goniothalamin	32-35	P53	Homo sapiens	3-7
21810437-4	2011	In TP53-positive SK-Hep1 cells, GTN furthermore induced TP53 transcription-dependent and -independent apoptosis.	goniothalamin	32-35	P53	Homo sapiens	56-60
21784846-2	2011	In the present work, we have found that transcriptional activation of the oxidative stress-responsive heat shock factor 1 (HSF-1) and expression of heat shock proteins, including Hsp27, which is normally known to augment proteasomal p53 degradation, are inhibited in Adriamycin (doxorubicin)-resistant MCF-7 cells (MCF-7/adr).	Doxorubicin	279-290	P53	Homo sapiens	233-236
21872575-11	2011	Furthermore, p53 siRNA and p21 siRNA transfection attenuated adriamycin-induced SA-beta-gal staining.	Doxorubicin	61-71	P53	Homo sapiens	13-16
21875573-8	2011	SEPW1 controls p21 by modulating levels of the p53 transcription factor, and this is associated with changes in phosphorylation of Ser-33 in p53.	Serine	131-134	P53	Homo sapiens	47-50
21875573-8	2011	SEPW1 controls p21 by modulating levels of the p53 transcription factor, and this is associated with changes in phosphorylation of Ser-33 in p53.	Serine	131-134	P53	Homo sapiens	141-144
21742020-5	2011	Upregulation of hHR23 expression by low-dose cisplatin was accompanied by an increase in p53, p21, and XPC protein levels.	Cisplatin	45-54	P53	Homo sapiens	89-92
20712406-4	2011	p53 orchestrates mitochondrial redox signaling by the coordinated control of at least two key effectors: the superoxide scavenger MnSOD, and the ROS generator p66shc.	Superoxides	109-119	P53	Homo sapiens	0-3
20712406-4	2011	p53 orchestrates mitochondrial redox signaling by the coordinated control of at least two key effectors: the superoxide scavenger MnSOD, and the ROS generator p66shc.	Reactive Oxygen Species	145-148	P53	Homo sapiens	0-3
20712410-5	2011	Among the many antioxidant genes activated by p53, Sestrins (Sesns) are critical for suppression of reactive oxygen species (ROS) and protection from oxidative stress, transformation, and genomic instability.	Reactive Oxygen Species	100-123	P53	Homo sapiens	46-49
20712410-5	2011	Among the many antioxidant genes activated by p53, Sestrins (Sesns) are critical for suppression of reactive oxygen species (ROS) and protection from oxidative stress, transformation, and genomic instability.	Reactive Oxygen Species	125-128	P53	Homo sapiens	46-49
20919943-0	2011	Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production.	Reactive Oxygen Species	95-118	P53	Homo sapiens	15-18
20919943-5	2011	Here, it has been considered p53 broad potential contribution through its ability to regulate selected key cancer signaling pathways, where ROS participate as inductors or effectors of the final biological outcome.	Reactive Oxygen Species	140-143	P53	Homo sapiens	29-32
20919943-7	2011	In addition, we have considered potential mechanisms by which p53 could collaborate with signal transduction pathways such as transforming growth factor-beta (TGF-beta) and stress-activated protein kinases (SAPK) that produce ROS, to stop or eliminate uncontrolled proliferating cells.	Reactive Oxygen Species	226-229	P53	Homo sapiens	62-65
21194382-5	2011	We propose that interactions between p53 and its isoforms Delta40p53 or Delta133p53 play critical roles in intracellular signaling by reactive oxygen species.	Reactive Oxygen Species	134-157	P53	Homo sapiens	37-40
21413016-0	2011	TP53 Mutational signature for aristolochic acid: an environmental carcinogen.	aristolochic acid I	30-47	P53	Homo sapiens	0-4
21413016-1	2011	This study was designed to establish the TP53 mutational spectrum of aristolochic acid (AA), examined in the context of endemic (Balkan) nephropathy, an environmental disease associated with transitional cell (urothelial) carcinomas of the upper urinary tract (UUC).	aristolochic acid I	69-86	P53	Homo sapiens	41-45
21892948-10	2011	The mutation results in substitution of arginine for the highly conserved glycine at residue 199 located at the p53 dimer-dimer interface.	Arginine	40-48	P53	Homo sapiens	112-115
21780790-1	2011	Protein lysine methyltransferase G9a plays key roles in the transcriptional repression of a variety of genes via dimethylation of lysine 9 on histone H3 (H3K9me2) of chromatin as well as dimethylation of nonhistone proteins including tumor suppressor p53.	Lysine	8-14	P53	Homo sapiens	251-254
21821029-3	2011	Here we show that Aurora-A phosphorylates hnRNPK, a transcriptional coactivator of p53, on serine 379.	Serine	91-97	P53	Homo sapiens	83-86
21843507-2	2011	Here, we show that ATRA induces promoter hypomethylation of p16 and p21 via down-regulation of DNA methyltransferases 1, 3a, and 3b to facilitate binding of Ets1/2 to the p16 promoter and p53 to the p21 promoter, resulting in up-regulation of their expression and subsequent induction of cellular senescence in HepG2 cells.	Tretinoin	19-23	P53	Homo sapiens	188-191
21892948-10	2011	The mutation results in substitution of arginine for the highly conserved glycine at residue 199 located at the p53 dimer-dimer interface.	Glycine	74-81	P53	Homo sapiens	112-115
21671008-0	2011	Insulin receptor signaling activated by penta-O-galloyl-alpha-D: -glucopyranose induces p53 and apoptosis in cancer cells.	Glucose	66-79	P53	Homo sapiens	88-91
21674128-0	2011	DNA damage signaling in response to 5-fluorouracil in three colorectal cancer cell lines with different mismatch repair and TP53 status.	Fluorouracil	36-50	P53	Homo sapiens	124-128
21880462-0	2011	miR-98 regulates cisplatin-induced A549 cell death by inhibiting TP53 pathway.	Cisplatin	17-26	P53	Homo sapiens	65-69
21880462-8	2011	Moreover, the expression of miR-98 and Bcl-2 was decreased, while miR-34a-c and TP53 was increased after A549 treated with cisplatin.	Cisplatin	123-132	P53	Homo sapiens	80-84
30780881-7	2011	A recent article explored the role of the tumor-suppressor gene TP53 in the response of breast cancer cell lines to tamoxifen and the pure anti-estrogen, fulvestrant.	Tamoxifen	116-125	P53	Homo sapiens	64-68
21869603-6	2011	In drug sensitive MCF-7 cells which have wild-type p53; ERK, p53 and downstream p21 (Cip-1 ) were induced upon exposure to doxorubicin.	Doxorubicin	123-134	P53	Homo sapiens	51-54
21869603-6	2011	In drug sensitive MCF-7 cells which have wild-type p53; ERK, p53 and downstream p21 (Cip-1 ) were induced upon exposure to doxorubicin.	Doxorubicin	123-134	P53	Homo sapiens	61-64
21869603-7	2011	In contrast, in the drug resistant cells which expressed activated Akt-1, much lower levels of p53 and p21 (Cip1) were induced upon exposure to doxorubicin.	Doxorubicin	144-155	P53	Homo sapiens	95-98
21484135-9	2011	CONCLUSIONS: Although serum 249(serine) p53 mutation is rarely found in Taiwanese patients, HBV carriers have a higher prevalence of codon 72 mutants than patients with much severe liver diseases or HCV infection, which implies that codon 72 mutants may affect at an earlier stage of HBV infection.	Serine	32-38	P53	Homo sapiens	40-43
21687937-0	2011	The cell death response to the ROS inducer, cobalt chloride, in neuroblastoma cell lines according to p53 status.	Reactive Oxygen Species	31-34	P53	Homo sapiens	102-105
21687937-5	2011	In SHSY5Y cells, p53 serine-15 phosphorylation appeared early (6 h) in the mitochondria, and also in the nucleus after 12 h. In contrast, in SKNBE(2c) cells, the slight nuclear signal disappeared with CoCl2 treatment.	Serine	21-27	P53	Homo sapiens	17-20
21674128-3	2011	The pattern of DNA damage checkpoint activation in bolus 5-FU-treated HT29 (TP53-deficient/MMR-proficient) cultures suggested SSB formation (CHEK1 activation) followed by DSB formation (CHEK2 activation and increased phospho-H2AX levels), but no cell death suggested that DNA repair capacity was not overwhelmed.	Fluorouracil	57-61	P53	Homo sapiens	76-80
21674128-4	2011	High-dose 5-FU treatment led to activation of ATM/CHEK2/TP53 (not CHEK1) in TP53-proficient and TP53-depleted HCT116 (later CHEK2 activation relative to TP53-proficient) cultures; HCT15 cultures had ATM activation only.	Fluorouracil	10-14	P53	Homo sapiens	56-60
21674128-4	2011	High-dose 5-FU treatment led to activation of ATM/CHEK2/TP53 (not CHEK1) in TP53-proficient and TP53-depleted HCT116 (later CHEK2 activation relative to TP53-proficient) cultures; HCT15 cultures had ATM activation only.	Fluorouracil	10-14	P53	Homo sapiens	76-80
21674128-4	2011	High-dose 5-FU treatment led to activation of ATM/CHEK2/TP53 (not CHEK1) in TP53-proficient and TP53-depleted HCT116 (later CHEK2 activation relative to TP53-proficient) cultures; HCT15 cultures had ATM activation only.	Fluorouracil	10-14	P53	Homo sapiens	76-80
21674128-4	2011	High-dose 5-FU treatment led to activation of ATM/CHEK2/TP53 (not CHEK1) in TP53-proficient and TP53-depleted HCT116 (later CHEK2 activation relative to TP53-proficient) cultures; HCT15 cultures had ATM activation only.	Fluorouracil	10-14	P53	Homo sapiens	76-80
21674128-6	2011	TP53-depleted HCT116 cultures also had DSBs after high-dose 5-FU treatment but experienced a (transient) G1/S cell cycle arrest that protected them from apoptosis.	Fluorouracil	60-64	P53	Homo sapiens	0-4
21674128-9	2011	DNA repair and cell cycle responses to 5-FU-induced DNA damage were distinctly affected by MMR and TP53 (role in BER/NER) functionalities, but MMR deficiency especially seemed to confer less overall sensitivity to 5-FU.	Fluorouracil	39-43	P53	Homo sapiens	99-103
21821009-4	2011	With prolonged exposure to nocodazole, a microtubule-depolymerizing agent, p62-deficient HCT116 cells exhibited an accumulation of a polyploid population with a limited appearance of apoptotic cells, which was attributable to the attenuated stabilization of p53.	Nocodazole	27-37	P53	Homo sapiens	258-261
21810677-1	2011	INTRODUCTION: Retrospective studies suggest that p53 alteration is prognostic for recurrence in patients with urothelial bladder cancer and predictive for benefit from combination methotrexate, vinblastine, doxorubicin, and cisplatin (MVAC) adjuvant chemotherapy.	Doxorubicin	207-218	P53	Homo sapiens	49-52
21810677-1	2011	INTRODUCTION: Retrospective studies suggest that p53 alteration is prognostic for recurrence in patients with urothelial bladder cancer and predictive for benefit from combination methotrexate, vinblastine, doxorubicin, and cisplatin (MVAC) adjuvant chemotherapy.	Cisplatin	224-233	P53	Homo sapiens	49-52
21425328-11	2011	In conclusion, ROS dependent-ATM/p53 signaling pathway is involved in HMJ-30-induced apoptosis in U-2 OS cells.	ros	15-18	P53	Homo sapiens	33-36
21514041-0	2011	Gene expression signature of TP53 but not its mutation status predicts response to sequential paclitaxel and 5-FU/epirubicin/cyclophosphamide in human breast cancer.	Paclitaxel	94-104	P53	Homo sapiens	29-33
21514041-0	2011	Gene expression signature of TP53 but not its mutation status predicts response to sequential paclitaxel and 5-FU/epirubicin/cyclophosphamide in human breast cancer.	Fluorouracil	109-113	P53	Homo sapiens	29-33
21514041-0	2011	Gene expression signature of TP53 but not its mutation status predicts response to sequential paclitaxel and 5-FU/epirubicin/cyclophosphamide in human breast cancer.	Epirubicin	114-124	P53	Homo sapiens	29-33
21514041-1	2011	PURPOSE: The aim of this study was to determine whether TP53 mutation status (MS) can predict response of breast cancer to paclitaxel followed by 5-FU/epirubicin/cyclophosphamide (P-FEC).	Paclitaxel	123-133	P53	Homo sapiens	56-60
21660965-7	2011	Overexpression of CITED2 also decreased sensitivity to cisplatin in p53-defective H1299 cells when exogenous p53 expression was re-introduced.	Cisplatin	55-64	P53	Homo sapiens	68-71
21660965-7	2011	Overexpression of CITED2 also decreased sensitivity to cisplatin in p53-defective H1299 cells when exogenous p53 expression was re-introduced.	Cisplatin	55-64	P53	Homo sapiens	109-112
21660965-9	2011	Notably, the effects of CITED2 knockdown on p53 accumulation and the increase of p53"s target Bax were more pronounced after treatment with cisplatin.	Cisplatin	140-149	P53	Homo sapiens	44-47
21660965-9	2011	Notably, the effects of CITED2 knockdown on p53 accumulation and the increase of p53"s target Bax were more pronounced after treatment with cisplatin.	Cisplatin	140-149	P53	Homo sapiens	81-84
21660965-10	2011	Based on these results, we propose that a combination of cisplatin and CITED2 shRNA may represent an effective treatment against p53-sensitive cancer cells.	Cisplatin	57-66	P53	Homo sapiens	129-132
21616106-1	2011	BACKGROUND &amp; AIMS: Mutations in TP53, a tumor suppressor gene, are associated with prognosis of many cancers.	Adenosine Monophosphate	12-15	P53	Homo sapiens	36-40
21316118-4	2011	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in LC were 37.0%, 46.2%, and 16.7%, respectively; frequencies in the controls were 43.2%, 45.6%, and 11.2%, respectively (p&lt;0.01).	Arginine	47-50	P53	Homo sapiens	19-22
21316118-4	2011	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in LC were 37.0%, 46.2%, and 16.7%, respectively; frequencies in the controls were 43.2%, 45.6%, and 11.2%, respectively (p&lt;0.01).	Arginine	51-54	P53	Homo sapiens	19-22
21316118-4	2011	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in LC were 37.0%, 46.2%, and 16.7%, respectively; frequencies in the controls were 43.2%, 45.6%, and 11.2%, respectively (p&lt;0.01).	Arginine	51-54	P53	Homo sapiens	19-22
21441950-4	2011	We show here that the anthracyclines doxorubicin, daunorubicin and epirubicin further increase the amounts of mutant p53 mRNA and protein in cancer cells.	Anthracyclines	22-36	P53	Homo sapiens	117-120
21705328-6	2011	Our data indicate that TPA-induced MnSOD expression was independent of p53 and most likely mediated by PKC-alpha-, and -epsilon-dependent signaling pathways.	Tetradecanoylphorbol Acetate	23-26	P53	Homo sapiens	71-74
21441950-0	2011	Anthracyclines induce the accumulation of mutant p53 through E2F1-dependent and -independent mechanisms.	Anthracyclines	0-14	P53	Homo sapiens	49-52
21441950-4	2011	We show here that the anthracyclines doxorubicin, daunorubicin and epirubicin further increase the amounts of mutant p53 mRNA and protein in cancer cells.	Doxorubicin	37-48	P53	Homo sapiens	117-120
21441950-4	2011	We show here that the anthracyclines doxorubicin, daunorubicin and epirubicin further increase the amounts of mutant p53 mRNA and protein in cancer cells.	Epirubicin	67-77	P53	Homo sapiens	117-120
21441950-8	2011	Instead, a natural antisense transcript of TP53, WRAP53, was strongly augmented by idarubicin and etoposide, but only less so by the other anthracyclines under study.	Anthracyclines	139-153	P53	Homo sapiens	43-47
21441950-11	2011	Reducing the levels of mutant p53 by small-interfering RNA increased chemosensitivity, and idarubicin prevented cell survival more efficiently than the mutant p53-inducing doxorubicin.	Doxorubicin	172-183	P53	Homo sapiens	159-162
21441950-12	2011	We conclude that even closely related anthracyclines induce the synthesis of different, opposing transcripts from the TP53 locus.	Anthracyclines	38-52	P53	Homo sapiens	118-122
21712378-0	2011	Resveratrol induces p53-independent, X-linked inhibitor of apoptosis protein (XIAP)-mediated Bax protein oligomerization on mitochondria to initiate cytochrome c release and caspase activation.	Resveratrol	0-11	P53	Homo sapiens	20-23
21609781-8	2011	Oxygen beam irradiated cells showed phosphorylation of Chk1, Chk2 and p53.	Oxygen	0-6	P53	Homo sapiens	70-73
21712378-2	2011	Here, we show that resveratrol induced p53-independent, X-linked inhibitor of apoptosis protein (XIAP)-mediated translocation of Bax to mitochondria where it underwent oligomerization to initiate apoptosis.	Resveratrol	19-30	P53	Homo sapiens	39-42
21855805-2	2011	In particular, Set7/9 (KMT7)-mediated monomethylation of human p53 at lysine 372 (p53K372me1) was suggested to be essential for p53 activation in human cell lines.	Lysine	70-76	P53	Homo sapiens	63-66
21855805-2	2011	In particular, Set7/9 (KMT7)-mediated monomethylation of human p53 at lysine 372 (p53K372me1) was suggested to be essential for p53 activation in human cell lines.	Lysine	70-76	P53	Homo sapiens	82-85
21855806-3	2011	Originally defined as a critical layer of p53 regulation in human cell lines, p53 lysine methylation by Set7/9 (also called Setd7) was proposed to fulfill a similar function in vivo in the mouse, promoting p53 acetylation, stabilization, and activation upon DNA damage (Kurash et al., 2008).	Lysine	82-88	P53	Homo sapiens	42-45
21855806-3	2011	Originally defined as a critical layer of p53 regulation in human cell lines, p53 lysine methylation by Set7/9 (also called Setd7) was proposed to fulfill a similar function in vivo in the mouse, promoting p53 acetylation, stabilization, and activation upon DNA damage (Kurash et al., 2008).	Lysine	82-88	P53	Homo sapiens	78-81
21609781-10	2011	The noteworthy finding of this study is the activation of the sensor proteins, ATM and ATR by oxygen irradiation and the significant activation of Chk1, Chk2 and p53 only in the oxygen beam irradiated cells.	Oxygen	178-184	P53	Homo sapiens	162-165
21548882-6	2011	Co-administration of 3BrPA (3-bromopyruvate), a well-known inhibitor of glycolysis, and succinate dehydrogenase, enhanced apoptosis and AMPK/p38(MAPK)/p53 signalling pathway activation.	bromopyruvate	21-26	P53	Homo sapiens	151-154
21843334-1	2011	BACKGROUND: Single-nucleotide polymorphisms within TP53 gene (codon 72 exon 4, rs1042522, encoding either arginine or proline) and MDM2 promoter (SNP309; rs2279744), have been independently associated with increased risk of several cancer types.	Arginine	106-114	P53	Homo sapiens	51-55
21832239-6	2011	This FACT inaccessibility leads to phosphorylation of the p53 Ser(392) by casein kinase 2 and inhibition of NF-kappaB-dependent transcription, which requires FACT activity at the elongation stage.	Serine	62-65	P53	Homo sapiens	58-61
21548882-6	2011	Co-administration of 3BrPA (3-bromopyruvate), a well-known inhibitor of glycolysis, and succinate dehydrogenase, enhanced apoptosis and AMPK/p38(MAPK)/p53 signalling pathway activation.	bromopyruvate	28-43	P53	Homo sapiens	151-154
21482024-7	2011	Ki23057 increased the p53 expression level in OCUM-2M/SN38 and OCUM-2M/PTX, but not in OCUM-2M/VP16.	Paclitaxel	71-74	P53	Homo sapiens	22-25
21440619-6	2011	Furthermore, we found that interaction of PKCdelta and c-Abl played a crucial role in p53 accumulation in the nucleus, which was linked to the apoptosis of NPCs in response to high glucose.	Glucose	181-188	P53	Homo sapiens	86-89
21655990-11	2011	Messenger RNA expression was significantly downregulated by metformin for PDE3B (phosphodiesterase 3B, cGMP-inhibited; a critical regulator of cAMP levels that affect activation of AMP-activated protein kinase, AMPK), confirmed by immunohistochemistry, SSR3, TP53 and CCDC14.	Metformin	60-69	P53	Homo sapiens	259-263
21655990-11	2011	Messenger RNA expression was significantly downregulated by metformin for PDE3B (phosphodiesterase 3B, cGMP-inhibited; a critical regulator of cAMP levels that affect activation of AMP-activated protein kinase, AMPK), confirmed by immunohistochemistry, SSR3, TP53 and CCDC14.	Cyclic AMP	143-147	P53	Homo sapiens	259-263
21655990-13	2011	Gene set analysis additionally revealed that p53, BRCA1 and cell cycle pathways also had reduced expression following metformin.	Metformin	118-127	P53	Homo sapiens	45-48
21514377-5	2011	VRK1 (Vaccinia-related kinase 1) is an early response gene required for cyclin D1 expression, regulates p53 by a specific Thr18 phosphorylation, controls chromatin condensation by histone phosphorylation, nuclear envelope assembly by phosphorylation of BANF1, and participates in signalling required for Golgi fragmentation late in the G2 phase.	UNII-PYZ33YLR8A	122-127	P53	Homo sapiens	104-107
21933600-5	2011	METHODS: The expression of P53 protein and MDM-2 protein was immunohistochemically detected using monoclonal antibodies in 242 paraffin embedded tissues, including 30 normal brain tissues from patients with craniocerebral injury and 212 tissues from patients with primary glioma (grade I - II group: 5 cases of grade I, 119 cases of grade II; and grade III--IV group: 53 cases of grade III, and 35 cases of grade IV).	Paraffin	127-135	P53	Homo sapiens	27-30
21701263-1	2011	DNA damage, stalled replication forks, errors in mRNA splicing, and availability of nutrients activate specific phosphatidylinositiol-3 kinase-like kinases (PIKKs) that in turn phosphorylate downstream targets such as p53 on serine 15.	Serine	225-231	P53	Homo sapiens	218-221
21701263-4	2011	Here, we demonstrate that siRNA oligonucleotides targeting the mRNA surveillance proteins SMG1, Upf1, Upf2, or the PIKK protein ATM attenuated p53 (ser15) phosphorylation in cells damaged by high oxygen (hyperoxia), a model of persistent oxidative stress that damages nucleotides.	Oligonucleotides	32-48	P53	Homo sapiens	143-146
21701263-4	2011	Here, we demonstrate that siRNA oligonucleotides targeting the mRNA surveillance proteins SMG1, Upf1, Upf2, or the PIKK protein ATM attenuated p53 (ser15) phosphorylation in cells damaged by high oxygen (hyperoxia), a model of persistent oxidative stress that damages nucleotides.	Oxygen	196-202	P53	Homo sapiens	143-146
21734451-5	2011	It can trigger G 2/M arrest in wild type p53 containing cells, which was attributed to the decreased Cdc2 kinase activity resulting at least partly from a high level of inhibitory tyrosine phosphorylation on Cdc2 protein at Tyr-15.	Tyrosine	180-188	P53	Homo sapiens	41-44
21734451-5	2011	It can trigger G 2/M arrest in wild type p53 containing cells, which was attributed to the decreased Cdc2 kinase activity resulting at least partly from a high level of inhibitory tyrosine phosphorylation on Cdc2 protein at Tyr-15.	Tyrosine	224-227	P53	Homo sapiens	41-44
21866459-3	2011	MRP4 and P53 protein expression in the paraffin-embedded specimen were detected by immunohistochemistry.	Paraffin	39-47	P53	Homo sapiens	9-12
21529996-4	2011	RESULTS: Use of NSAIDs, particularly aspirin, was associated with a reduced odds ratio (OR) of SCC, especially tumors positive for p53 (OR 0.29; 95% confidence interval 0.11-0.79) or with PTCH loss of heterozygosity (OR 0.35; 95% confidence interval 0.13-0.96).	Aspirin	37-44	P53	Homo sapiens	131-134
21642861-8	2011	Interestingly, p53 acetylation at lysine 382 was significantly increased, and c-myc expression simultaneously down-regulated in cotreated cells.	Lysine	34-40	P53	Homo sapiens	15-18
21642861-10	2011	Furthermore, c-myc down-regulation and apoptotic cell death coinduced by IR and HDACI were suppressed in cells transfected with mutant K382R p53 and C135Y p53 displaying loss of acetylation at lysine 382 and DNA-binding activity, respectively.	Lysine	193-199	P53	Homo sapiens	141-144
21642861-10	2011	Furthermore, c-myc down-regulation and apoptotic cell death coinduced by IR and HDACI were suppressed in cells transfected with mutant K382R p53 and C135Y p53 displaying loss of acetylation at lysine 382 and DNA-binding activity, respectively.	Lysine	193-199	P53	Homo sapiens	155-158
21693655-3	2011	PATIENTS AND METHODS: Epithelial p53 expression was evaluated using two immunohistochemical antibodies (DO7 and 1801) in formalin-fixed, paraffin-embedded tissue from patients with node-positive breast cancer who were randomized to four cycles of cyclophosphamide and one of three doses of doxorubicin (60, 75, or 90 mg/m(2); AC) and to receive four subsequent cycles of paclitaxel (T) or not.	Paraffin	137-145	P53	Homo sapiens	33-36
21693655-3	2011	PATIENTS AND METHODS: Epithelial p53 expression was evaluated using two immunohistochemical antibodies (DO7 and 1801) in formalin-fixed, paraffin-embedded tissue from patients with node-positive breast cancer who were randomized to four cycles of cyclophosphamide and one of three doses of doxorubicin (60, 75, or 90 mg/m(2); AC) and to receive four subsequent cycles of paclitaxel (T) or not.	Doxorubicin	290-301	P53	Homo sapiens	33-36
21693655-3	2011	PATIENTS AND METHODS: Epithelial p53 expression was evaluated using two immunohistochemical antibodies (DO7 and 1801) in formalin-fixed, paraffin-embedded tissue from patients with node-positive breast cancer who were randomized to four cycles of cyclophosphamide and one of three doses of doxorubicin (60, 75, or 90 mg/m(2); AC) and to receive four subsequent cycles of paclitaxel (T) or not.	Paclitaxel	371-381	P53	Homo sapiens	33-36
21693655-4	2011	Prognostic and predictive value of p53 protein expression was assessed, independent of treatment assignment, for escalating doses of doxorubicin or addition of T with endpoints of relapse-free (RFS) and overall survival (OS).	Doxorubicin	133-144	P53	Homo sapiens	35-38
21693655-9	2011	CONCLUSION: Nuclear staining of p53 by immunohistochemistry is associated with worse prognosis in node-positive patients treated with adjuvant doxorubicin-based chemotherapy but is not a useful predictor of benefit from doxorubicin dose escalation or the addition of paclitaxel.	Doxorubicin	143-154	P53	Homo sapiens	32-35
21693655-9	2011	CONCLUSION: Nuclear staining of p53 by immunohistochemistry is associated with worse prognosis in node-positive patients treated with adjuvant doxorubicin-based chemotherapy but is not a useful predictor of benefit from doxorubicin dose escalation or the addition of paclitaxel.	Paclitaxel	267-277	P53	Homo sapiens	32-35
21461655-5	2011	RESULTS: The frequencies of Arg/Arg, Arg/Pro, and Pro/Pro genotypes of the p53 codon 72 polymorphism were 43.3, 42.0, and 13.0% in the gastric cancer patients; 40.5, 45.0, and 14.0% in the colorectal cancer patients; and 43.2, 45.6, and 11.2% in the controls, respectively.	Arginine	28-31	P53	Homo sapiens	75-78
21461655-5	2011	RESULTS: The frequencies of Arg/Arg, Arg/Pro, and Pro/Pro genotypes of the p53 codon 72 polymorphism were 43.3, 42.0, and 13.0% in the gastric cancer patients; 40.5, 45.0, and 14.0% in the colorectal cancer patients; and 43.2, 45.6, and 11.2% in the controls, respectively.	Arginine	32-35	P53	Homo sapiens	75-78
21461655-5	2011	RESULTS: The frequencies of Arg/Arg, Arg/Pro, and Pro/Pro genotypes of the p53 codon 72 polymorphism were 43.3, 42.0, and 13.0% in the gastric cancer patients; 40.5, 45.0, and 14.0% in the colorectal cancer patients; and 43.2, 45.6, and 11.2% in the controls, respectively.	Arginine	32-35	P53	Homo sapiens	75-78
21592546-6	2011	Cisplatin also potently inhibited G1-phase Cdk4/cyclin D1 and Cdk2/cyclin E activities at ~18 h. In agreement, exposure of cisplatin-treated A2780, HCT-116(p53-/-) and HCT-116(p21-/-) tumor cells to nocodazole revealed limited G1-arrest that was dependent on p53 and p21.	Cisplatin	0-9	P53	Homo sapiens	156-159
21592546-6	2011	Cisplatin also potently inhibited G1-phase Cdk4/cyclin D1 and Cdk2/cyclin E activities at ~18 h. In agreement, exposure of cisplatin-treated A2780, HCT-116(p53-/-) and HCT-116(p21-/-) tumor cells to nocodazole revealed limited G1-arrest that was dependent on p53 and p21.	Cisplatin	0-9	P53	Homo sapiens	259-262
21592546-6	2011	Cisplatin also potently inhibited G1-phase Cdk4/cyclin D1 and Cdk2/cyclin E activities at ~18 h. In agreement, exposure of cisplatin-treated A2780, HCT-116(p53-/-) and HCT-116(p21-/-) tumor cells to nocodazole revealed limited G1-arrest that was dependent on p53 and p21.	Cisplatin	123-132	P53	Homo sapiens	156-159
21592546-6	2011	Cisplatin also potently inhibited G1-phase Cdk4/cyclin D1 and Cdk2/cyclin E activities at ~18 h. In agreement, exposure of cisplatin-treated A2780, HCT-116(p53-/-) and HCT-116(p21-/-) tumor cells to nocodazole revealed limited G1-arrest that was dependent on p53 and p21.	Cisplatin	123-132	P53	Homo sapiens	259-262
21600209-4	2011	In addition, some effect of ghrelin 1-8 on some of these parameters (expression of MAPK/ERK1,2, bax, p53) were verified.	Ghrelin	28-35	P53	Homo sapiens	101-104
21792013-1	2011	BACKGROUND: In non-small cell lung cancer, expression of excision repair cross-complementation group 1 (ERCC1) and p53 correlates with platinum resistance and class III beta-tubulin with resistance to taxanes.	Platinum	135-143	P53	Homo sapiens	115-118
21792013-1	2011	BACKGROUND: In non-small cell lung cancer, expression of excision repair cross-complementation group 1 (ERCC1) and p53 correlates with platinum resistance and class III beta-tubulin with resistance to taxanes.	Taxoids	201-208	P53	Homo sapiens	115-118
21457722-0	2011	The ethanol extract of Scutellaria baicalensis and the active compounds induce cell cycle arrest and apoptosis including upregulation of p53 and Bax in human lung cancer cells.	Ethanol	4-11	P53	Homo sapiens	137-140
21457773-5	2011	After BP-treatment the strongest p53 protein induction and phosphorylation at serine 392 was found in ZR-75-1 cells with a wt TP53 gene.	Serine	78-84	P53	Homo sapiens	33-36
21906442-5	2011	The expression levels of caspase-3, -8, -9, c-FLIP, Bcl-2, p53, and p21 in the FLS changed after epirubicin treatment.	Epirubicin	97-107	P53	Homo sapiens	59-62
21906442-6	2011	CONCLUSION: Epirubicin may coordinate with AD5-10 in inducing FLS apoptosis through affecting the levels of p53, p21, c-FLIP, and Bcl-2.	Epirubicin	12-22	P53	Homo sapiens	108-111
21557991-4	2011	We demonstrate that zinc pyrithione-induced cytotoxity in dermal fibroblasts is dose-dependent and it associates with increased intracellular zinc concentrations and activated stress response pathways including p53 and stress kinase p38.	pyrithione zinc	20-35	P53	Homo sapiens	211-214
21802012-0	2011	Cholesterol secosterol aldehydes induce amyloidogenesis and dysfunction of wild-type tumor protein p53.	Cholesterol	0-11	P53	Homo sapiens	99-102
21802012-3	2011	Herein we show that the inflammation-derived cholesterol 5,6-secosterol aldehydes, atheronal-A (KA) and -B (ALD), but not the polyunsaturated fatty acid (PUFA)-derived aldehydes 4-hydroxynonenal (HNE) and 4-hydroxyhexenal (HHE), induce misfolding of wild-type p53 into an amyloidogenic form that binds thioflavin T and Congo red dyes but cannot bind to a consensus DNA sequence.	Cholesterol	45-56	P53	Homo sapiens	260-263
21708134-3	2011	Treatment with the cell cycle inhibitors, aphidicolin or nocodazole also revealed increased NDRG1 phosphorylation in p53-deficient cells.	Nocodazole	57-67	P53	Homo sapiens	117-120
21383696-4	2011	The c-Myc stabilizes p53 by rpL11-mediated HDM2 inhibition, and ASK1/p38 activates p53 by phosphorylation on serine 15 and 33.	Serine	109-115	P53	Homo sapiens	83-86
21669188-0	2011	Glutathione selectively inhibits Doxorubicin induced phosphorylation of p53Ser15, caspase dependent ceramide production and apoptosis in human leukemic cells.	Glutathione	0-11	P53	Homo sapiens	72-75
21746909-0	2011	Tumor suppressor p53 regulates bile acid homeostasis via small heterodimer partner.	Bile Acids and Salts	31-40	P53	Homo sapiens	17-20
21746909-4	2011	Here we demonstrate that p53 lowers bile acid (BA) levels under both normal and stressed conditions primarily through up-regulating expression of small heterodimer partner, a critical inhibitor of BA synthesis.	Bile Acids and Salts	36-45	P53	Homo sapiens	25-28
21746909-4	2011	Here we demonstrate that p53 lowers bile acid (BA) levels under both normal and stressed conditions primarily through up-regulating expression of small heterodimer partner, a critical inhibitor of BA synthesis.	Bile Acids and Salts	47-49	P53	Homo sapiens	25-28
21746909-4	2011	Here we demonstrate that p53 lowers bile acid (BA) levels under both normal and stressed conditions primarily through up-regulating expression of small heterodimer partner, a critical inhibitor of BA synthesis.	Bile Acids and Salts	197-199	P53	Homo sapiens	25-28
21730979-8	2011	In A2780 cells sensitisation to cisplatin was greatest in cells with functional p53 and mismatch repair (MMR) and sensitisation to temozolomide was greatest in p53 mutant cells with functional MMR.	Cisplatin	32-41	P53	Homo sapiens	80-83
21669188-0	2011	Glutathione selectively inhibits Doxorubicin induced phosphorylation of p53Ser15, caspase dependent ceramide production and apoptosis in human leukemic cells.	Doxorubicin	33-44	P53	Homo sapiens	72-75
21669188-5	2011	Glutathione pre-treatment inhibits Doxorubicin-induced p53Ser(15) phosphorylation, caspase dependent ceramide (Cer) generation, Poly (ADP-ribose) polymerase (PARP) cleavage, and DNA fragmentation.	Glutathione	0-11	P53	Homo sapiens	55-58
21669188-5	2011	Glutathione pre-treatment inhibits Doxorubicin-induced p53Ser(15) phosphorylation, caspase dependent ceramide (Cer) generation, Poly (ADP-ribose) polymerase (PARP) cleavage, and DNA fragmentation.	Doxorubicin	35-46	P53	Homo sapiens	55-58
20839263-5	2011	Curcumin in combination with oxaliplatin was able to decrease proliferative capacity of oxaliplatin-resistant p53 wildtype and p53(-/-) cell lines more effectively than oxaliplatin alone.	Curcumin	0-8	P53	Homo sapiens	110-113
21709442-4	2011	DR5, Fas, Bax, Bad, Puma and Bnip3L were induced by 5-FU and adriamycin (ADR) in HCT116 cells in a p53-dependent manner.	Fluorouracil	52-56	P53	Homo sapiens	99-102
21709442-4	2011	DR5, Fas, Bax, Bad, Puma and Bnip3L were induced by 5-FU and adriamycin (ADR) in HCT116 cells in a p53-dependent manner.	Doxorubicin	61-71	P53	Homo sapiens	99-102
21696969-0	2011	18beta-Glycyrrhetinic acid derivatives induced mitochondrial-mediated apoptosis through reactive oxygen species-mediated p53 activation in NTUB1 cells.	Reactive Oxygen Species	88-111	P53	Homo sapiens	121-124
21696969-9	2011	These results suggested that 25 induced a mitochondrial-mediated apoptosis in NTUB1 cells through activation of p53, which are mainly mediated ROS generated by 25.	Reactive Oxygen Species	143-146	P53	Homo sapiens	112-115
20839263-5	2011	Curcumin in combination with oxaliplatin was able to decrease proliferative capacity of oxaliplatin-resistant p53 wildtype and p53(-/-) cell lines more effectively than oxaliplatin alone.	Curcumin	0-8	P53	Homo sapiens	127-130
21586571-0	2011	Peptide-protein interactions suggest that acetylation of lysines 381 and 382 of p53 is important for positive coactivator 4-p53 interaction.	Lysine	57-64	P53	Homo sapiens	80-83
21654191-1	2011	The combined treatment with nanomolar doses of the PPARgamma ligand Rosiglitazone (BRL) and the RXR ligand 9-cis-retinoic acid (9RA) induces a p53-dependent apoptosis in MCF7, SKBR3 and T47D human breast cancer cells.	Rosiglitazone	68-81	P53	Homo sapiens	143-146
21637162-0	2011	Adenovirus-mediated p53 gene therapy reverses resistance of breast cancer cells to adriamycin.	Doxorubicin	83-93	P53	Homo sapiens	20-23
21637162-1	2011	The aim of this study was to determine whether adenovirus-mediated p53 gene (Ad-p53) transfection can enhance adriamycin cytotoxicity and reverse adriamycin resistance in human breast cancer cells and explore its effect on the expression of MDR1 gene and permeability-glycoprotein (P-gp).	Doxorubicin	110-120	P53	Homo sapiens	67-70
21637162-1	2011	The aim of this study was to determine whether adenovirus-mediated p53 gene (Ad-p53) transfection can enhance adriamycin cytotoxicity and reverse adriamycin resistance in human breast cancer cells and explore its effect on the expression of MDR1 gene and permeability-glycoprotein (P-gp).	Doxorubicin	110-120	P53	Homo sapiens	80-83
21637162-1	2011	The aim of this study was to determine whether adenovirus-mediated p53 gene (Ad-p53) transfection can enhance adriamycin cytotoxicity and reverse adriamycin resistance in human breast cancer cells and explore its effect on the expression of MDR1 gene and permeability-glycoprotein (P-gp).	Doxorubicin	146-156	P53	Homo sapiens	67-70
21637162-1	2011	The aim of this study was to determine whether adenovirus-mediated p53 gene (Ad-p53) transfection can enhance adriamycin cytotoxicity and reverse adriamycin resistance in human breast cancer cells and explore its effect on the expression of MDR1 gene and permeability-glycoprotein (P-gp).	Doxorubicin	146-156	P53	Homo sapiens	80-83
21586571-0	2011	Peptide-protein interactions suggest that acetylation of lysines 381 and 382 of p53 is important for positive coactivator 4-p53 interaction.	Lysine	57-64	P53	Homo sapiens	124-127
21637162-9	2011	After transfection with a multiplicity of infection of 50 for Ad-p53, chemosensitivity of MCF-7/ADR cells increased by 18.1 times (P=0.001), and 50% inhibitory concentration (IC50) of adriamycin decreased from 4.54 +- 0.91 to 0.26 +- 0.11 mg/l.	Doxorubicin	184-194	P53	Homo sapiens	65-68
21637162-15	2011	This study suggests that Ad-p53 can reverse MCF-7/MDR cell resistance to adriamycin.	Doxorubicin	73-83	P53	Homo sapiens	28-31
21586571-8	2011	NMR and mutagenesis studies indicated that serine 73 of PC4 is an important residue for recognition of p53.	Serine	43-49	P53	Homo sapiens	103-106
21586571-9	2011	Intermolecular nuclear Overhauser effect placed aspartate 76 in the vicinity of lysine 381, indicating that the region around residues 73-76 of PC4 is important for p53 recognition.	Lysine	80-86	P53	Homo sapiens	165-168
21586571-10	2011	We conclude that the 380-386 region of p53 interacts with the region around residues 73-76 of PC4, and acetylation of lysine 382/381 of p53 may play an important role in modulating p53-PC4 interaction and as a consequence PC4 mediated activation of p53 target genes.	Lysine	118-124	P53	Homo sapiens	39-42
21586571-10	2011	We conclude that the 380-386 region of p53 interacts with the region around residues 73-76 of PC4, and acetylation of lysine 382/381 of p53 may play an important role in modulating p53-PC4 interaction and as a consequence PC4 mediated activation of p53 target genes.	Lysine	118-124	P53	Homo sapiens	136-139
21586571-10	2011	We conclude that the 380-386 region of p53 interacts with the region around residues 73-76 of PC4, and acetylation of lysine 382/381 of p53 may play an important role in modulating p53-PC4 interaction and as a consequence PC4 mediated activation of p53 target genes.	Lysine	118-124	P53	Homo sapiens	136-139
21586571-10	2011	We conclude that the 380-386 region of p53 interacts with the region around residues 73-76 of PC4, and acetylation of lysine 382/381 of p53 may play an important role in modulating p53-PC4 interaction and as a consequence PC4 mediated activation of p53 target genes.	Lysine	118-124	P53	Homo sapiens	136-139
21458064-6	2011	mRNA expression and western blot experiments also proved that co-delivery of Dox with wt p53 plasmid from PC-Dox/wt p53 complexes could promote wt p53 gene expression largely.	Doxorubicin	77-80	P53	Homo sapiens	89-92
21458064-6	2011	mRNA expression and western blot experiments also proved that co-delivery of Dox with wt p53 plasmid from PC-Dox/wt p53 complexes could promote wt p53 gene expression largely.	Doxorubicin	77-80	P53	Homo sapiens	116-119
21458064-6	2011	mRNA expression and western blot experiments also proved that co-delivery of Dox with wt p53 plasmid from PC-Dox/wt p53 complexes could promote wt p53 gene expression largely.	Doxorubicin	77-80	P53	Homo sapiens	116-119
21458064-6	2011	mRNA expression and western blot experiments also proved that co-delivery of Dox with wt p53 plasmid from PC-Dox/wt p53 complexes could promote wt p53 gene expression largely.	Doxorubicin	109-112	P53	Homo sapiens	89-92
21540236-5	2011	We show that metformin increases REDD1 expression in a p53-dependent manner.	Metformin	13-22	P53	Homo sapiens	55-58
21683812-6	2011	In addition, p53 was found to repress Crm1 promoter activity, after induction with doxorubicin, with p53 siRNA blocking the effect.	Doxorubicin	83-94	P53	Homo sapiens	13-16
21516318-9	2011	Recent use of ibuprofen was significantly associated with increased risk of ER+/PR+(OR 1.33, 95% CI: 1.09-1.62), HER2- (OR 1.27, 95% CI: 1.05-1.53), and p53- breast cancers (OR 1.28, 95% CI: 1.04-1.57), as well as luminal A or B breast cancers.	Ibuprofen	14-23	P53	Homo sapiens	153-156
21565979-4	2011	Induction of p21 was inhibited by miR-22 after exposure to the genotoxic agent Adriamycin (doxorubicin; Bedford Laboratories), sensitizing cells to p53-dependent apoptosis.	Doxorubicin	79-89	P53	Homo sapiens	148-151
21540236-8	2011	Finally, we show the contribution of p53 in mediating metformin action in prostate cancer cells.	Metformin	54-63	P53	Homo sapiens	37-40
21565979-4	2011	Induction of p21 was inhibited by miR-22 after exposure to the genotoxic agent Adriamycin (doxorubicin; Bedford Laboratories), sensitizing cells to p53-dependent apoptosis.	Doxorubicin	91-102	P53	Homo sapiens	148-151
21540236-9	2011	These results highlight the p53/REDD1 axis as a new molecular target in anticancer therapy in response to metformin treatment.	Metformin	106-115	P53	Homo sapiens	28-31
21565980-3	2011	SIRT1, the main member of the sirtuin family, inactivates p53 by deacetylating a critical lysine residue.	Lysine	90-96	P53	Homo sapiens	58-61
22207897-5	2011	Knockdown of miR-203 following cisplatin treatment enhances p53, p21, and Bax protein expression.	Cisplatin	31-40	P53	Homo sapiens	60-63
21692052-11	2011	Exploration of 1 such cell line (HN30) suggested that the presence of wild-type p53 can partially protect tumor cells from glucose starvation.	Glucose	123-130	P53	Homo sapiens	80-83
21402718-3	2011	By using human p53 knockin (Hupki) mice carrying a single nucleotide polymorphism (SNP) at codon 72 (arginine/proline), the arginine allele was demonstrated to produce higher uterine LIF levels during implantation than the proline allele.	Arginine	124-132	P53	Homo sapiens	15-18
21402718-4	2011	In humans, the diversity of haplotypes of the p53 gene has decreased during evolution, because the arginine allele, existing in only a subset of haplotypes, is under positive selection.	Arginine	99-107	P53	Homo sapiens	46-49
21561866-5	2011	Knockdown of S27a significantly attenuates the p53 activation in cells in response to treatment with ribosomal stress-inducing agent actinomycin D or 5-fluorouracil.	Fluorouracil	150-164	P53	Homo sapiens	47-50
21756539-0	2011	RITA enhances chemosensivity of pre-B ALL cells to doxorubicin by inducing p53-dependent apoptosis.	RITA	0-4	P53	Homo sapiens	75-78
21756539-0	2011	RITA enhances chemosensivity of pre-B ALL cells to doxorubicin by inducing p53-dependent apoptosis.	Doxorubicin	51-62	P53	Homo sapiens	75-78
21756539-2	2011	Here, we used small-molecule reactivation of p53 and induction of tumor cell apoptosis (RITA) to sensitize leukemic NALM-6 cells to doxorubicin by upregulating p53 protein.	Doxorubicin	132-143	P53	Homo sapiens	45-48
21756539-2	2011	Here, we used small-molecule reactivation of p53 and induction of tumor cell apoptosis (RITA) to sensitize leukemic NALM-6 cells to doxorubicin by upregulating p53 protein.	Doxorubicin	132-143	P53	Homo sapiens	160-163
21750659-0	2011	Activation of cAMP signaling interferes with stress-induced p53 accumulation in ALL-derived cells by promoting the interaction between p53 and HDM2.	Cyclic AMP	14-18	P53	Homo sapiens	60-63
21095038-10	2011	Additionally, treatment with p53 inducer adriamycin (ADR) alone or in combination with DAC increased the expression of IGFBP7 in the 3 cell lines.	Doxorubicin	41-51	P53	Homo sapiens	29-32
21750659-0	2011	Activation of cAMP signaling interferes with stress-induced p53 accumulation in ALL-derived cells by promoting the interaction between p53 and HDM2.	Cyclic AMP	14-18	P53	Homo sapiens	135-138
21750659-4	2011	We have previously shown that the second messenger cAMP can inhibit DNA damage-induced wild-type p53 accumulation in acute lymphoblastic leukemia cells, leading to a profound reduction of their apoptotic response.	Cyclic AMP	51-55	P53	Homo sapiens	97-100
21750659-5	2011	In the present article, we provide a mechanistic insight into the regulation of p53 levels by cAMP.	Cyclic AMP	94-98	P53	Homo sapiens	80-83
21750659-6	2011	We show that increased levels of cAMP augment the binding of p53 to its negative regulator HDM2, overriding the DNA damage-induced dissociation of p53 from HDM2.	Cyclic AMP	33-37	P53	Homo sapiens	61-64
21750659-6	2011	We show that increased levels of cAMP augment the binding of p53 to its negative regulator HDM2, overriding the DNA damage-induced dissociation of p53 from HDM2.	Cyclic AMP	33-37	P53	Homo sapiens	147-150
21750659-8	2011	The apoptosis inhibitory effect of cAMP is further shown to depend on this effect on p53 levels.	Cyclic AMP	35-39	P53	Homo sapiens	85-88
21750659-9	2011	These findings potentially implicate deregulation of cAMP signaling as a candidate mechanism used by transformed cells to quench the p53 response while retaining wild-type p53.	Cyclic AMP	53-57	P53	Homo sapiens	133-136
21750659-9	2011	These findings potentially implicate deregulation of cAMP signaling as a candidate mechanism used by transformed cells to quench the p53 response while retaining wild-type p53.	Cyclic AMP	53-57	P53	Homo sapiens	172-175
21606339-5	2011	Treatment of cells with the DNA-damaging drug doxorubicin or the p53 stabilizing agent Nutlin-3, however, is accompanied by p53-dependent subsequent loss of nucleosomes associated with such p53 REs.	Doxorubicin	46-57	P53	Homo sapiens	124-127
21673677-3	2011	RESULTS: Presence of GMP (21% of the cases) was significantly associated with high-grade tumours and TP53 mutations in addition to the basal-like and HER2 subtypes of breast cancer as defined by gene expression data.	guanosine 5'-monophosphorothioate	21-24	P53	Homo sapiens	101-105
21950100-6	2011	It has been observed, that 6 h after exposure oflymphocytes to hydrogen peroxide and UV-light at doses 1510 and 3020 J/m2, the p53 level of investigated cells raises.	Hydrogen Peroxide	63-80	P53	Homo sapiens	127-130
21950100-9	2011	The authors come to the conclusion about the leading role of receptor-mediated (Fas-dependent) caspase- and p53-dependent ways of realizing apoptosis oflymphocytes induced by UV-light at doses 151 and 1510 J/m2 and active oxygen metabolites.	Oxygen	222-228	P53	Homo sapiens	108-111
21606339-5	2011	Treatment of cells with the DNA-damaging drug doxorubicin or the p53 stabilizing agent Nutlin-3, however, is accompanied by p53-dependent subsequent loss of nucleosomes associated with such p53 REs.	Doxorubicin	46-57	P53	Homo sapiens	124-127
21406194-4	2011	Here, we examined whether S-nitrosylation of the NF-kappaB, p53, and Wnt signaling proteins by NO-ASA might explain, in part, its mechanism of action in colon cancer.	Aspirin	98-101	P53	Homo sapiens	60-63
21339736-14	2011	Although p53-pathway-dependent apoptotic agents could upregulate endogenous hOTAG-12b and p53 in UCI-101/107 OC cells, hOTAG-12b could also induce apoptosis in p53-null and platinum-resistant SKOV3 OC cells and Doxycycline-induced hOTAG-12b did not alter p53.	hotag-12b	76-85	P53	Homo sapiens	9-12
21339736-15	2011	Further study showed that hOTAG-12b increases mRNAs of pro-apoptotic genes such as BAD, GADD45alpha and CIEDB, while inhibiting anti-apoptotic NAIP and Akt1 expression, suggesting that hOTAG-12b-induced apoptosis might be p53-independent.	hotag-12b	26-35	P53	Homo sapiens	222-225
21353507-1	2011	The function of p53 induced by ganoderic acids (GAs) in anti-invasion was unknown, although our previous work reported the inhibition of tumor invasion and metastasis by Ganoderic acid T (GA-T).	ganoderic acid S	31-46	P53	Homo sapiens	16-19
21406194-6	2011	Using a modified biotin switch assay we demonstrated that NO-ASA S-nitrosylates the signaling proteins p53, beta-catenin, and NF-kappaB, in colon cancer cells in a time- and concentration-dependent manner.	Aspirin	61-64	P53	Homo sapiens	103-106
21480648-8	2011	In addition, the distinct p53 activation profile of 1 compared with cisplatin provides an explanation for the activity of this ruthenium drug against cisplatin-resistant cells.	Cisplatin	150-159	P53	Homo sapiens	26-29
21737649-3	2011	We prepared H1299 cells (p53-null) with various mutations of p53 at three sites (serine 15, 20 and 46) and examined the radiosensitivity of the cells.	Serine	81-87	P53	Homo sapiens	61-64
21539808-4	2011	We show that in the absence of PABP, the glycolytic enzyme GAPDH translocated to the cell nucleus and activated the GAPDH mediated apoptotic pathway by enhancing acetylation and serine 46 phosphorylation of p53.	Serine	178-184	P53	Homo sapiens	207-210
21258400-0	2011	ATR mediates cisplatin resistance in a p53 genotype-specific manner.	Cisplatin	13-22	P53	Homo sapiens	39-42
21258400-4	2011	Here, we demonstrate that genetic inhibition of ATR expression selectively enhanced cisplatin sensitivity in human colorectal cancer cells with inactivated p53.	Cisplatin	84-93	P53	Homo sapiens	156-159
21258400-6	2011	Knock-in of functional p53 in ATR-deficient cells restored checkpoint function, suppressed apoptotic pathways and markedly increased clonogenic survival after cisplatin treatment.	Cisplatin	159-168	P53	Homo sapiens	23-26
21489989-0	2011	Serine/threonine kinase 17A is a novel p53 target gene and modulator of cisplatin toxicity and reactive oxygen species in testicular cancer cells.	Reactive Oxygen Species	95-118	P53	Homo sapiens	39-42
21489989-1	2011	Testicular cancer is highly curable with cisplatin-based therapy, and testicular cancer-derived human embryonal carcinoma (EC) cells undergo a p53-dominant transcriptional response to cisplatin.	Cisplatin	184-193	P53	Homo sapiens	143-146
21489989-3	2011	Cisplatin-mediated induction of STK17A in the EC cell line NT2/D1 was prevented with p53 siRNA.	Cisplatin	0-9	P53	Homo sapiens	85-88
21489989-5	2011	A functional p53 response element that binds endogenous p53 in a cisplatin-dependent manner was identified 5 kb upstream of the first coding exon of STK17A.	Cisplatin	65-74	P53	Homo sapiens	13-16
21489989-5	2011	A functional p53 response element that binds endogenous p53 in a cisplatin-dependent manner was identified 5 kb upstream of the first coding exon of STK17A.	Cisplatin	65-74	P53	Homo sapiens	56-59
21737649-4	2011	In three mutant forms of p53--S15A, S20A and S46A--serine was converted to alanine at these sites to prevent phosphorylation, and in two other mutant forms, S15D and S20D, serine was converted to aspartic acid to mimic phosphorylation.	Serine	51-57	P53	Homo sapiens	25-28
21737649-4	2011	In three mutant forms of p53--S15A, S20A and S46A--serine was converted to alanine at these sites to prevent phosphorylation, and in two other mutant forms, S15D and S20D, serine was converted to aspartic acid to mimic phosphorylation.	Alanine	75-82	P53	Homo sapiens	25-28
21737649-4	2011	In three mutant forms of p53--S15A, S20A and S46A--serine was converted to alanine at these sites to prevent phosphorylation, and in two other mutant forms, S15D and S20D, serine was converted to aspartic acid to mimic phosphorylation.	Serine	172-178	P53	Homo sapiens	25-28
21406185-4	2011	In this study, we found that a small molecule, reactivation of p53 and induction of tumor cell apoptosis (RITA), showed anti-cancer activity against gefitinib-resistant H1650 cells through a p53-independent pathway.	Gefitinib	149-158	P53	Homo sapiens	63-66
21406185-4	2011	In this study, we found that a small molecule, reactivation of p53 and induction of tumor cell apoptosis (RITA), showed anti-cancer activity against gefitinib-resistant H1650 cells through a p53-independent pathway.	Gefitinib	149-158	P53	Homo sapiens	191-194
21740780-9	2011	In resveratrol sensitive cells, capan-2 and colo357, the activation of caspase-3 was detected and showed significant caspase-3 activation upon resveratrol treatment; p53 and p21 were also detected up-regulated upon resveratrol treatment.	Resveratrol	143-154	P53	Homo sapiens	166-169
21280026-7	2011	In contrast, the substitution of Cha for Phe341 in the hydrophobic core enhanced the stability of the tetrameric structure with a T(m) value of  100 degrees C. Phe328 and Phe338 interact with each other through pi-interactions, whereas Phe341 is buried in the surrounding alkyl side-chains of the hydrophobic core of the p53 tetramerization domain.	cyclohexylalanine	33-36	P53	Homo sapiens	321-324
21411502-2	2011	Our studies on the drug-resistant p53-mutant as compared with drug-resistant p53 wild-type neuroblastoma revealed a novel mechanism for resistance to apoptosis: a direct role of p53 in regulating the cellular concentration of proapoptotic alkenals by functioning as a specific and saturable allosteric inhibitor of the alkenal-glutathione conjugate transporter, RLIP76.	Glutathione	327-338	P53	Homo sapiens	34-37
21411502-2	2011	Our studies on the drug-resistant p53-mutant as compared with drug-resistant p53 wild-type neuroblastoma revealed a novel mechanism for resistance to apoptosis: a direct role of p53 in regulating the cellular concentration of proapoptotic alkenals by functioning as a specific and saturable allosteric inhibitor of the alkenal-glutathione conjugate transporter, RLIP76.	Glutathione	327-338	P53	Homo sapiens	77-80
21411502-2	2011	Our studies on the drug-resistant p53-mutant as compared with drug-resistant p53 wild-type neuroblastoma revealed a novel mechanism for resistance to apoptosis: a direct role of p53 in regulating the cellular concentration of proapoptotic alkenals by functioning as a specific and saturable allosteric inhibitor of the alkenal-glutathione conjugate transporter, RLIP76.	Glutathione	327-338	P53	Homo sapiens	77-80
21411502-4	2011	Drug transport studies revealed that p53 inhibited both basal and PKCalpha-stimulated transport of glutathione conjugates of 4HNE (GSHNE) and doxorubicin.	Glutathione	99-110	P53	Homo sapiens	37-40
21411502-4	2011	Drug transport studies revealed that p53 inhibited both basal and PKCalpha-stimulated transport of glutathione conjugates of 4HNE (GSHNE) and doxorubicin.	Doxorubicin	142-153	P53	Homo sapiens	37-40
21411502-7	2011	Taken together, these studies provide powerful evidence for a novel mechanism for drug and apoptosis resistance in p53-mutant neuroblastoma, based on a model of regulation of p53-induced apoptosis by RLIP76, where p53 is a saturable and specific allosteric inhibitor of RLIP76, and p53 loss results in overexpression of RLIP76; thus, in the absence of p53, the drug and glutathione-conjugate transport activities of RLIP76 are enhanced.	Glutathione	370-381	P53	Homo sapiens	115-118
21411502-7	2011	Taken together, these studies provide powerful evidence for a novel mechanism for drug and apoptosis resistance in p53-mutant neuroblastoma, based on a model of regulation of p53-induced apoptosis by RLIP76, where p53 is a saturable and specific allosteric inhibitor of RLIP76, and p53 loss results in overexpression of RLIP76; thus, in the absence of p53, the drug and glutathione-conjugate transport activities of RLIP76 are enhanced.	Glutathione	370-381	P53	Homo sapiens	175-178
21411502-7	2011	Taken together, these studies provide powerful evidence for a novel mechanism for drug and apoptosis resistance in p53-mutant neuroblastoma, based on a model of regulation of p53-induced apoptosis by RLIP76, where p53 is a saturable and specific allosteric inhibitor of RLIP76, and p53 loss results in overexpression of RLIP76; thus, in the absence of p53, the drug and glutathione-conjugate transport activities of RLIP76 are enhanced.	Glutathione	370-381	P53	Homo sapiens	175-178
21411502-7	2011	Taken together, these studies provide powerful evidence for a novel mechanism for drug and apoptosis resistance in p53-mutant neuroblastoma, based on a model of regulation of p53-induced apoptosis by RLIP76, where p53 is a saturable and specific allosteric inhibitor of RLIP76, and p53 loss results in overexpression of RLIP76; thus, in the absence of p53, the drug and glutathione-conjugate transport activities of RLIP76 are enhanced.	Glutathione	370-381	P53	Homo sapiens	175-178
21411502-7	2011	Taken together, these studies provide powerful evidence for a novel mechanism for drug and apoptosis resistance in p53-mutant neuroblastoma, based on a model of regulation of p53-induced apoptosis by RLIP76, where p53 is a saturable and specific allosteric inhibitor of RLIP76, and p53 loss results in overexpression of RLIP76; thus, in the absence of p53, the drug and glutathione-conjugate transport activities of RLIP76 are enhanced.	Glutathione	370-381	P53	Homo sapiens	175-178
21740780-9	2011	In resveratrol sensitive cells, capan-2 and colo357, the activation of caspase-3 was detected and showed significant caspase-3 activation upon resveratrol treatment; p53 and p21 were also detected up-regulated upon resveratrol treatment.	Resveratrol	3-14	P53	Homo sapiens	166-169
21463657-5	2011	Overexpression of TRIM29 promoted degradation and changed localization of Tip60 and reduced acetylation of p53 at lysine 120 by Tip60, resulting in enhancement of cell growth and transforming activity.	Lysine	114-120	P53	Homo sapiens	107-110
20623183-4	2011	We report that induction of ERbeta expression causes abrogation of the S-phase, and the Chk1/Cdc25C-mediated G2/M checkpoints after cisplatin and doxorubicin exposure in p53-defective breast cancer cells but not in p53 wild-type mammary cells.	Cisplatin	132-141	P53	Homo sapiens	170-173
20623183-4	2011	We report that induction of ERbeta expression causes abrogation of the S-phase, and the Chk1/Cdc25C-mediated G2/M checkpoints after cisplatin and doxorubicin exposure in p53-defective breast cancer cells but not in p53 wild-type mammary cells.	Doxorubicin	146-157	P53	Homo sapiens	170-173
21416250-7	2011	CDDP marginally induced acetylated p53 within 24 h after administration.	Cisplatin	0-4	P53	Homo sapiens	35-38
21740780-9	2011	In resveratrol sensitive cells, capan-2 and colo357, the activation of caspase-3 was detected and showed significant caspase-3 activation upon resveratrol treatment; p53 and p21 were also detected up-regulated upon resveratrol treatment.	Resveratrol	143-154	P53	Homo sapiens	166-169
21619452-0	2011	Cyclic AMP-induced p53 destabilization is independent of EPAC in pre-B acute lymphoblastic leukemia cells in vitro.	Cyclic AMP	0-10	P53	Homo sapiens	19-22
21826189-0	2011	Regulation of p53 function by lysine methylation.	Lysine	30-36	P53	Homo sapiens	14-17
21826189-2	2011	In addition to histones, several other nuclear factors such as the tumor suppressor and transcription factor p53 undergo lysine methylation, suggesting that this modification may be a common mechanism for modulating protein-protein interactions and key cellular signaling pathways.	Lysine	121-127	P53	Homo sapiens	109-112
21826189-3	2011	This article focuses on how lysine methylation events on the C-terminal tail of p53 are generated, sensed and transduced to modulate p53 functions.	Lysine	28-34	P53	Homo sapiens	80-83
21826189-3	2011	This article focuses on how lysine methylation events on the C-terminal tail of p53 are generated, sensed and transduced to modulate p53 functions.	Lysine	28-34	P53	Homo sapiens	133-136
21547354-9	2011	Although there were no significant differences in PTEN, hMLH1 and hMSH2 expression between the two groups, p53 mutation was more frequent in three out of five cases (60%) in the TAM group compared with 2 of 15 cases in the EMC group (13.3%).	Tamoxifen	178-181	P53	Homo sapiens	107-110
21382959-6	2011	Furthermore, CEDLI activates p53 and Bax, reduces Bcl-2 expression, and causes mitochondrial stress and the release of apoptosis-inducing factor into the cytosol followed by its translocation into the nucleus, resulting in hepatoma cell apoptosis.	cedli	13-18	P53	Homo sapiens	29-32
21357660-8	2011	Physiological concentrations of insulin also reversed high glucose-induced increases in p53 and vascular cell adhesion molecule-1 and decreases in senescence marker protein-30.	Glucose	59-66	P53	Homo sapiens	88-91
21622155-4	2011	In this study, we showed that RSV (~25 micromolar) potentiated GSE (&lt;= 35 microg/mL) induced colon cancer cell apoptosis via activation of p53 dependent pathways.	Resveratrol	30-33	P53	Homo sapiens	142-145
21455577-4	2011	ii) Genome-wide analyses using 44 K Agilent"s whole human arrays followed by Gene Set Enrichment Analysis (GSEA)-based screening of the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway database revealed a differential modulation of the JIMT-1 transcriptome at the level of the cell cycle and p53 pathways.	gsea	107-111	P53	Homo sapiens	298-301
21619452-4	2011	More importantly, we were interested to show through which receptor cAMP acts to promote p53 degradation.	Cyclic AMP	68-72	P53	Homo sapiens	89-92
21619452-9	2011	RESULTS: We show that elevation of cAMP levels in ALL cells exposed to DNA damage attenuates p53 accumulation.	Cyclic AMP	35-39	P53	Homo sapiens	93-96
21619452-10	2011	Inhibition of proteosome function with MG-132 reversed the inhibitory effect of cAMP on p53.	Cyclic AMP	80-84	P53	Homo sapiens	88-91
21619452-13	2011	DISCUSSION AND CONCLUSION: Our studies demonstrate that cAMP-PKA pathway regulates the sensitivity toward DNA-damaging agents via inhibition of a p53-dependent pathway in B-cell precursor ALL (BCP-ALL) cells.	Cyclic AMP	56-60	P53	Homo sapiens	146-149
21619452-3	2011	OBJECTIVE: The aim of this study was to investigate the inhibitory role of cyclic adenosine monophosphate (cAMP) levels on p53 protein in acute lymphoblastic leukemia (ALL) cells.	Cyclic AMP	75-105	P53	Homo sapiens	123-126
21619452-3	2011	OBJECTIVE: The aim of this study was to investigate the inhibitory role of cyclic adenosine monophosphate (cAMP) levels on p53 protein in acute lymphoblastic leukemia (ALL) cells.	Cyclic AMP	107-111	P53	Homo sapiens	123-126
21551225-4	2011	Furthermore, NFBD1 influences p53-mediated transcription in response to adriamycin.	Doxorubicin	72-82	P53	Homo sapiens	30-33
21570352-0	2011	TP53 status for prediction of sensitivity to taxane versus non-taxane neoadjuvant chemotherapy in breast cancer (EORTC 10994/BIG 1-00): a randomised phase 3 trial.	taxane	45-51	P53	Homo sapiens	0-4
21570352-0	2011	TP53 status for prediction of sensitivity to taxane versus non-taxane neoadjuvant chemotherapy in breast cancer (EORTC 10994/BIG 1-00): a randomised phase 3 trial.	taxane	63-69	P53	Homo sapiens	0-4
21570352-2	2011	We therefore tested the hypothesis that taxanes confer a greater advantage than do anthracyclines on breast cancers with mutated TP53 than in those with wild-type TP53.	Taxoids	40-47	P53	Homo sapiens	129-133
21518729-9	2011	In summary, our data show that ATM and p53 coordinately regulate FOXM1 via E2F to modulate epirubicin response and resistance in breast cancer.	Epirubicin	91-101	P53	Homo sapiens	39-42
21599591-10	2011	Dose-dense treatment with HDMP and Rtx is an effective therapy with a favorable safety profile in patients with high-risk CLL, including those with 17p deletion/TP53 mutation.	hdmp	26-30	P53	Homo sapiens	161-165
21518729-0	2011	ATM and p53 regulate FOXM1 expression via E2F in breast cancer epirubicin treatment and resistance.	Epirubicin	63-73	P53	Homo sapiens	8-11
21518729-3	2011	We also established that there is a loss of p53 function in MCF-7-EPI(R) cells and that epirubicin represses FOXM1 expression at transcription and gene promoter levels through activation of p53 and repression of E2F activity in MCF-7 cells.	Epirubicin	88-98	P53	Homo sapiens	190-193
21479363-3	2011	Here, we used MCF-7 and MDA-MB231 breast cancer cells as a model to demonstrate that resveratrol induced the expression of ASPP1, a new member of the ASPP (apoptosis stimulation protein of p53) family, which plays an important role in the regulation of apoptosis.	Resveratrol	85-96	P53	Homo sapiens	189-192
21518729-5	2011	Moreover, transient promoter transfection assays showed that epirubicin and its cellular effectors p53 and E2F1 modulate FOXM1 transcription through an E2F-binding site located within the proximal promoter region.	Epirubicin	61-71	P53	Homo sapiens	99-102
21626334-6	2011	This mutation causes a nonsense mutation (Arg-to-Stop codon) that has been shown to attenuate p53 function.	Arginine	42-45	P53	Homo sapiens	94-97
21624110-7	2011	Interestingly, Nutlin-3a seemed to potentiate the effect of classical drugs as Doxorubicin and Cisplatin in cell lines with mutated TP53, but inhibited the effect of Methotrexate.	Cisplatin	95-104	P53	Homo sapiens	132-136
21576488-5	2011	First, p53 is partially activated by primary modifications such as phosphorylation at Ser-15/20 to induce cell cycle arrest, with its level varying in a series of pulses.	Serine	86-89	P53	Homo sapiens	7-10
21576488-6	2011	If the damage cannot be fixed after a critical number of p53 pulses, then p53 is fully activated by further modifications such as phosphorylation at Ser-46 to trigger apoptosis, with its concentration switching to rather high levels.	Serine	149-152	P53	Homo sapiens	74-77
21624110-6	2011	RESULTS: Clear synergism was observed when Doxorubicin and Nutlin-3a were combined in cell lines with wild-type TP53 and amplified MDM2, or with Methotrexate in both MDM2 normal and amplified sarcoma cell lines, allowing for up to tenfold reduction of cytotoxic drug dose.	Doxorubicin	43-54	P53	Homo sapiens	112-116
21262221-6	2011	Autophagic specific inhibitor 3-methyladenine (3-MA) treatment reversed silibinin-induced p53 suppression as well as NF-kappaB activation, suggesting that there was a positive feedback loop between p53 inhibition-mediated NF-kappaB activation and autophagy.	3-methyladenine	47-51	P53	Homo sapiens	90-93
21471201-4	2011	Treating human squamous cell carcinoma (SCC) cells with the anti-cancer compounds, resveratrol and doxorubicin, triggered p53-independent premature senescence by invoking oxidative stress-mediated DNA damage.	Resveratrol	83-94	P53	Homo sapiens	122-125
21471201-4	2011	Treating human squamous cell carcinoma (SCC) cells with the anti-cancer compounds, resveratrol and doxorubicin, triggered p53-independent premature senescence by invoking oxidative stress-mediated DNA damage.	Doxorubicin	99-110	P53	Homo sapiens	122-125
21549095-3	2011	We found that TopIn (7-phenyl-6H-[1,2,5]oxadiazolo[3,4-e]indole 3-oxide) efficiently activated p53-mediated transcriptional activity and induced phosphorylation of p53 at Ser15, thereby stabilizing the p53 protein.	topin	14-19	P53	Homo sapiens	95-98
21549095-3	2011	We found that TopIn (7-phenyl-6H-[1,2,5]oxadiazolo[3,4-e]indole 3-oxide) efficiently activated p53-mediated transcriptional activity and induced phosphorylation of p53 at Ser15, thereby stabilizing the p53 protein.	topin	14-19	P53	Homo sapiens	164-167
21549095-3	2011	We found that TopIn (7-phenyl-6H-[1,2,5]oxadiazolo[3,4-e]indole 3-oxide) efficiently activated p53-mediated transcriptional activity and induced phosphorylation of p53 at Ser15, thereby stabilizing the p53 protein.	topin	14-19	P53	Homo sapiens	164-167
21262221-2	2011	In the present study it was found that silibinin-induced autophagy through increasing the conversion of LC3 I to LC3 II and up-regulating Beclin-1 expression, which was concomitant with p53 suppression and NF-kappaB activation.	Silybin	39-48	P53	Homo sapiens	186-189
21262221-6	2011	Autophagic specific inhibitor 3-methyladenine (3-MA) treatment reversed silibinin-induced p53 suppression as well as NF-kappaB activation, suggesting that there was a positive feedback loop between p53 inhibition-mediated NF-kappaB activation and autophagy.	3-methyladenine	30-45	P53	Homo sapiens	90-93
21398698-4	2011	DDR1 is functionally activated as determined by its tyrosine phosphorylation, in response to p53-dependent DNA damage.	Tyrosine	52-60	P53	Homo sapiens	93-96
21262221-6	2011	Autophagic specific inhibitor 3-methyladenine (3-MA) treatment reversed silibinin-induced p53 suppression as well as NF-kappaB activation, suggesting that there was a positive feedback loop between p53 inhibition-mediated NF-kappaB activation and autophagy.	3-methyladenine	30-45	P53	Homo sapiens	198-201
21262221-6	2011	Autophagic specific inhibitor 3-methyladenine (3-MA) treatment reversed silibinin-induced p53 suppression as well as NF-kappaB activation, suggesting that there was a positive feedback loop between p53 inhibition-mediated NF-kappaB activation and autophagy.	3-methyladenine	47-51	P53	Homo sapiens	198-201
21262221-6	2011	Autophagic specific inhibitor 3-methyladenine (3-MA) treatment reversed silibinin-induced p53 suppression as well as NF-kappaB activation, suggesting that there was a positive feedback loop between p53 inhibition-mediated NF-kappaB activation and autophagy.	Silybin	72-81	P53	Homo sapiens	90-93
21262221-6	2011	Autophagic specific inhibitor 3-methyladenine (3-MA) treatment reversed silibinin-induced p53 suppression as well as NF-kappaB activation, suggesting that there was a positive feedback loop between p53 inhibition-mediated NF-kappaB activation and autophagy.	Silybin	72-81	P53	Homo sapiens	198-201
21262221-7	2011	In addition, we also found that 3-MA efficiently abrogated silibinin"s cyto-protective effect against mitomycin C-induced cell death, and reversed the suppressive efficacy of silibinin on p53 expression, suggesting that autophagy contributed to silibinin"s cyto-protective effect against mitomycin C-induced cell death in A375-S2 cells.	3-methyladenine	32-36	P53	Homo sapiens	188-191
21262221-7	2011	In addition, we also found that 3-MA efficiently abrogated silibinin"s cyto-protective effect against mitomycin C-induced cell death, and reversed the suppressive efficacy of silibinin on p53 expression, suggesting that autophagy contributed to silibinin"s cyto-protective effect against mitomycin C-induced cell death in A375-S2 cells.	Silybin	175-184	P53	Homo sapiens	188-191
21262221-7	2011	In addition, we also found that 3-MA efficiently abrogated silibinin"s cyto-protective effect against mitomycin C-induced cell death, and reversed the suppressive efficacy of silibinin on p53 expression, suggesting that autophagy contributed to silibinin"s cyto-protective effect against mitomycin C-induced cell death in A375-S2 cells.	Silybin	175-184	P53	Homo sapiens	188-191
21454683-1	2011	The common polymorphism of p53 at codon 72, either encoding proline or arginine, has drawn attention as a genetic factor associated with clinical outcome or cancer risk for the last 2 decades.	Arginine	71-79	P53	Homo sapiens	27-30
21454683-3	2011	The arginine form (p53-72R) shows significantly enhanced phosphorylation at Ser-6 and Ser-20 compared with the proline form (p53-72P).	Arginine	4-12	P53	Homo sapiens	19-22
21525412-0	2011	Acetylation of lysine 120 of p53 endows DNA-binding specificity at effective physiological salt concentration.	Lysine	15-21	P53	Homo sapiens	29-32
21454683-3	2011	The arginine form (p53-72R) shows significantly enhanced phosphorylation at Ser-6 and Ser-20 compared with the proline form (p53-72P).	Arginine	4-12	P53	Homo sapiens	125-128
21454683-3	2011	The arginine form (p53-72R) shows significantly enhanced phosphorylation at Ser-6 and Ser-20 compared with the proline form (p53-72P).	Serine	76-79	P53	Homo sapiens	19-22
21454683-3	2011	The arginine form (p53-72R) shows significantly enhanced phosphorylation at Ser-6 and Ser-20 compared with the proline form (p53-72P).	Serine	86-89	P53	Homo sapiens	19-22
21593792-1	2011	We have recently shown that induction of the p53 tumour suppressor protein by the small-molecule RITA (reactivation of p53 and induction of tumour cell apoptosis; 2,5-bis(5-hydroxymethyl-2-thienyl)furan) inhibits hypoxia-inducible factor-1alpha and vascular endothelial growth factor expression in vivo and induces p53-dependent tumour cell apoptosis in normoxia and hypoxia.	NSC 652287	163-202	P53	Homo sapiens	45-48
21480602-0	2011	Phenolic fraction of tobacco smoke inhibits BPDE-induced apoptosis response and potentiates cell transformation: role of attenuation of p53 response.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	44-48	P53	Homo sapiens	136-139
21480602-6	2011	Increased cell transformation and decreased apoptosis by TSCPhFr were associated with attenuation of BPDE-induced p53 accumulation.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	101-105	P53	Homo sapiens	114-117
21480602-7	2011	JB6 cells transfected with p53 siRNA showed significantly less apoptosis induction by BPDE as compared to control cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	86-90	P53	Homo sapiens	27-30
21480602-9	2011	Also, in p53 null HCT116 p53(-/-) cells, BPDE-induced apoptosis is unresponsive to TSCPhFr.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	41-45	P53	Homo sapiens	9-12
21480602-9	2011	Also, in p53 null HCT116 p53(-/-) cells, BPDE-induced apoptosis is unresponsive to TSCPhFr.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	41-45	P53	Homo sapiens	25-28
21480602-12	2011	Our observations indicate that attenuation of BPDE-induced p53 response has a role in apoptosis inhibition and increased cell transformation by TSCPhFr.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	46-50	P53	Homo sapiens	59-62
21454683-4	2011	We also show diminished Mdm2-mediated degradation of p53-72R compared with p53-72P, which is at least partly brought about by higher levels of phosphorylation at Ser-20 in p53-72R.	Serine	162-165	P53	Homo sapiens	53-56
21454683-4	2011	We also show diminished Mdm2-mediated degradation of p53-72R compared with p53-72P, which is at least partly brought about by higher levels of phosphorylation at Ser-20 in p53-72R.	Serine	162-165	P53	Homo sapiens	75-78
21454683-4	2011	We also show diminished Mdm2-mediated degradation of p53-72R compared with p53-72P, which is at least partly brought about by higher levels of phosphorylation at Ser-20 in p53-72R.	Serine	162-165	P53	Homo sapiens	75-78
21454683-5	2011	Furthermore, enhanced p21 expression in p53-72R-expressing cells, which is dependent on phosphorylation at Ser-6, was demonstrated.	Serine	107-110	P53	Homo sapiens	40-43
21525412-0	2011	Acetylation of lysine 120 of p53 endows DNA-binding specificity at effective physiological salt concentration.	Salts	91-95	P53	Homo sapiens	29-32
21525412-3	2011	We prepared p53 specifically acetylated at Lys120, AcK120p53, by in vivo incorporation of acetylated lysine to study biophysical and structural consequences of acetylation that may shed light on its biological role.	Lysine	101-107	P53	Homo sapiens	12-15
21525412-5	2011	p53 binds DNA randomly in vitro at effective physiological salt concentration and does not bind specifically to DNA or distinguish among its different response elements until higher salt concentrations.	Salts	59-63	P53	Homo sapiens	0-3
21525412-5	2011	p53 binds DNA randomly in vitro at effective physiological salt concentration and does not bind specifically to DNA or distinguish among its different response elements until higher salt concentrations.	Salts	182-186	P53	Homo sapiens	0-3
21398407-4	2011	Moreover, these synergistic effects of vorinostat/ABT-737 were blunted in cells with an inactive p53 pathway or in cells lacking expression of the p53 target gene, noxa.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	50-53	P53	Homo sapiens	97-100
21372224-7	2011	Exposure of cells to the ADC demonstrated signaling pathways leading to PARP cleavage, but differences versus free SN-38 in p53 and p21 upregulation were noted.	Irinotecan	115-120	P53	Homo sapiens	124-127
21398407-4	2011	Moreover, these synergistic effects of vorinostat/ABT-737 were blunted in cells with an inactive p53 pathway or in cells lacking expression of the p53 target gene, noxa.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	50-53	P53	Homo sapiens	147-150
21454715-7	2011	A citrulline-mimicking Arg-NLS-Gln ING4 mutant, which has all Arg residues in the NLS mutated to Gln, loses its affinity for p53, can no longer promote p53 acetylation, and results in repression of downstream p21 expression.	Arginine	23-26	P53	Homo sapiens	125-128
21575166-11	2011	CONCLUSION: Examining almost all known human micro-RNA species confirmed the miR-371-373 cluster as a promising target for explaining cisplatin resistance, potentially by counteracting wild-type P53 induced senescence or linking it with the potency to differentiate.	Cisplatin	134-143	P53	Homo sapiens	195-198
21454715-7	2011	A citrulline-mimicking Arg-NLS-Gln ING4 mutant, which has all Arg residues in the NLS mutated to Gln, loses its affinity for p53, can no longer promote p53 acetylation, and results in repression of downstream p21 expression.	Arginine	23-26	P53	Homo sapiens	152-155
21562496-2	2011	Here, we report that histone deacetylase inhibitors (HDACI), that is, MS-275, valproic acid or SAHA, provide a novel strategy for sensitization of medulloblastoma to DNA-damaging drugs such as Doxorubicin, VP16 and Cisplatin by promoting p53-dependent, mitochondrial apoptosis.	Doxorubicin	193-204	P53	Homo sapiens	238-241
21562496-4	2011	Combined treatment with MS-275 and Doxorubicin or VP16 cooperates to promote binding of p53 to Bax and p53-dependent Bax activation, resulting in enhanced loss of mitochondrial membrane potential, cytochrome c release and caspase-dependent apoptosis.	Doxorubicin	35-46	P53	Homo sapiens	88-91
21562496-4	2011	Combined treatment with MS-275 and Doxorubicin or VP16 cooperates to promote binding of p53 to Bax and p53-dependent Bax activation, resulting in enhanced loss of mitochondrial membrane potential, cytochrome c release and caspase-dependent apoptosis.	Doxorubicin	35-46	P53	Homo sapiens	103-106
21573174-0	2011	IFI16 induction by glucose restriction in human fibroblasts contributes to autophagy through activation of the ATM/AMPK/p53 pathway.	Glucose	19-26	P53	Homo sapiens	120-123
21376033-7	2011	Also, MHY336 significantly down-regulated topoisomerase II alpha expression and up-regulated p53 expression in LNCaP cells (wild-type p53), whereas it up-regulated the topoisomerase II alpha protein in both DU145 and PC3 cells (p53 mutated or deleted).	MHY336	6-12	P53	Homo sapiens	93-96
21376033-7	2011	Also, MHY336 significantly down-regulated topoisomerase II alpha expression and up-regulated p53 expression in LNCaP cells (wild-type p53), whereas it up-regulated the topoisomerase II alpha protein in both DU145 and PC3 cells (p53 mutated or deleted).	MHY336	6-12	P53	Homo sapiens	134-137
21376033-7	2011	Also, MHY336 significantly down-regulated topoisomerase II alpha expression and up-regulated p53 expression in LNCaP cells (wild-type p53), whereas it up-regulated the topoisomerase II alpha protein in both DU145 and PC3 cells (p53 mutated or deleted).	MHY336	6-12	P53	Homo sapiens	134-137
21573174-1	2011	BACKGROUND: Glucose restriction in cells increases the AMP/ATP ratio (energetic stress), which activates the AMPK/p53 pathway.	Glucose	12-19	P53	Homo sapiens	114-117
21573174-1	2011	BACKGROUND: Glucose restriction in cells increases the AMP/ATP ratio (energetic stress), which activates the AMPK/p53 pathway.	Adenosine Monophosphate	55-58	P53	Homo sapiens	114-117
21573174-1	2011	BACKGROUND: Glucose restriction in cells increases the AMP/ATP ratio (energetic stress), which activates the AMPK/p53 pathway.	Adenosine Triphosphate	59-62	P53	Homo sapiens	114-117
21573174-4	2011	METHODOLOGY/PRINCIPAL FINDINGS: We found that glucose restriction or treatment of human diploid fibroblasts (HDFs) with the activators of the AMPK/p53 pathway induced the expression of IFI16 protein.	Glucose	46-53	P53	Homo sapiens	147-150
21573174-7	2011	Importantly, the knockdown of the IFI16 expression in HDFs inhibited the activation of the ATM/AMPK/p53 pathway in response to glucose restriction and also increased the survival of HDFs.	Glucose	127-134	P53	Homo sapiens	100-103
21445010-0	2011	In the right place at the right time: analysis of p53 serine 312 phosphorylation in vivo.	Serine	54-60	P53	Homo sapiens	50-53
21490443-20	2011	Strong and diffuse p53 positivity in SER may be useful in differentiation from UEA.	uea	79-82	P53	Homo sapiens	19-22
21354697-3	2011	Importantly, miR-203 overexpression increased the cytotoxic role of paclitaxel in the p53-mutated colon cancer cells, but not in the p53 wild-type cells.	Paclitaxel	68-78	P53	Homo sapiens	86-89
21428456-0	2011	Electrochemical detection of anti-benzo[a]pyrene diol epoxide DNA damage on TP53 codon 273 oligomers.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	34-61	P53	Homo sapiens	76-80
21428456-1	2011	DNA damage from (+/-)-anti-benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE) at a hotspot TP53 gene sequence was electrochemically detected.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	72-76	P53	Homo sapiens	91-95
21376392-9	2011	With no significant changes in the mRNA levels of p53, the increase in overall p53 protein levels and its post-translational modification by phosphorylation at Ser-15 are induced by CdTe QD treatment.	Serine	160-163	P53	Homo sapiens	79-82
21291320-10	2011	CONCLUSIONS: These data suggest that the p53 codon 72 Arg/Arg genotype and Arg allele are associated with a lower risk of bladder cancer in Chinese population.	Arginine	54-57	P53	Homo sapiens	41-44
21287141-0	2011	Glucose oscillations, more than constant high glucose, induce p53 activation and a metabolic memory in human endothelial cells.	Glucose	46-53	P53	Homo sapiens	62-65
21287141-2	2011	Evaluation of the effects of exposure of HUVECs to oscillating high glucose on the induction of markers of oxidative stress and DNA damage (phospho-gamma-histone H2AX and PKCdelta) and onset of metabolic memory, and the possible role of the tumour suppressor transcriptional factor p53 is of pivotal interest.	Glucose	68-75	P53	Homo sapiens	282-285
21287141-4	2011	Transcriptional activity of p53 was also evaluated in the first 24 h after high glucose exposure.	Glucose	80-87	P53	Homo sapiens	28-31
21287141-8	2011	Transcriptional activity of p53 peaked 6 h after glucose exposure, showing a predicted oscillatory behaviour.	Glucose	49-56	P53	Homo sapiens	28-31
21287141-10	2011	Hyperactivation of p53 during glucose oscillation might be due to the absence of consistent feedback inhibition during each glucose spike and might account for the worse outcome of this condition.	Glucose	30-37	P53	Homo sapiens	19-22
21291320-10	2011	CONCLUSIONS: These data suggest that the p53 codon 72 Arg/Arg genotype and Arg allele are associated with a lower risk of bladder cancer in Chinese population.	Arginine	58-61	P53	Homo sapiens	41-44
21291320-10	2011	CONCLUSIONS: These data suggest that the p53 codon 72 Arg/Arg genotype and Arg allele are associated with a lower risk of bladder cancer in Chinese population.	Arginine	58-61	P53	Homo sapiens	41-44
22087162-8	2011	P53 was expressed by more cells in the Des and cisplatin groups than in the serum-only group (32.6%, 31.5% and 3.3%, respectively; Des vs. serum only, p &lt; 0.05; cisplatin vs. serum only, p &lt; 0.05), with no difference between the Des and cisplatin groups (p &gt; 0.05).	Cisplatin	47-56	P53	Homo sapiens	0-3
22087162-8	2011	P53 was expressed by more cells in the Des and cisplatin groups than in the serum-only group (32.6%, 31.5% and 3.3%, respectively; Des vs. serum only, p &lt; 0.05; cisplatin vs. serum only, p &lt; 0.05), with no difference between the Des and cisplatin groups (p &gt; 0.05).	Cisplatin	164-173	P53	Homo sapiens	0-3
22087162-8	2011	P53 was expressed by more cells in the Des and cisplatin groups than in the serum-only group (32.6%, 31.5% and 3.3%, respectively; Des vs. serum only, p &lt; 0.05; cisplatin vs. serum only, p &lt; 0.05), with no difference between the Des and cisplatin groups (p &gt; 0.05).	Cisplatin	164-173	P53	Homo sapiens	0-3
21468597-7	2011	We found that the TP53 Pro/Pro genotype compared to the Arg/Arg genotype had a profound effect on pancreatic cancer risk among males, particularly among heavy smokers and excessive alcohol drinkers.	Alcohols	181-188	P53	Homo sapiens	18-22
21780454-0	2011	Identification of p53 gene by using CdSe/ZnS conjugation and hybridization.	Zinc	41-44	P53	Homo sapiens	18-21
21780454-2	2011	We have prepared oligonucleotide conjugated to QD as a probe to detect p53 tumor suppressor gene related to hereditary cancer.	Oligonucleotides	17-32	P53	Homo sapiens	71-74
21780454-3	2011	QDs with carboxyl functional group have been conjugated to thiol-modified oligo nucleotides, which have been used as a hybridization probe for p53 gene.	Sulfhydryl Compounds	59-64	P53	Homo sapiens	143-146
21780454-3	2011	QDs with carboxyl functional group have been conjugated to thiol-modified oligo nucleotides, which have been used as a hybridization probe for p53 gene.	Oligonucleotides	74-91	P53	Homo sapiens	143-146
21472523-0	2011	Identification of two reactive cysteine residues in the tumor suppressor protein p53 using top-down FTICR mass spectrometry.	Cysteine	31-39	P53	Homo sapiens	81-84
21472523-2	2011	The discovery of cysteine-targeting compounds that cause re-activation of mutant p53 and the death of tumor cells in vivo has emphasized the functional importance of p53 thiols.	Cysteine	17-25	P53	Homo sapiens	81-84
21472523-2	2011	The discovery of cysteine-targeting compounds that cause re-activation of mutant p53 and the death of tumor cells in vivo has emphasized the functional importance of p53 thiols.	Cysteine	17-25	P53	Homo sapiens	166-169
21472523-2	2011	The discovery of cysteine-targeting compounds that cause re-activation of mutant p53 and the death of tumor cells in vivo has emphasized the functional importance of p53 thiols.	Sulfhydryl Compounds	170-176	P53	Homo sapiens	166-169
21472523-3	2011	Using a combination of top-down and middle-down FTICR mass spectrometry, we show that of the 10 Cys residues in the core domain of wild-type p53, Cys182 and Cys277 exhibit a remarkable preference for modification by the alkylating reagent N-ethylmaleimide.	Cysteine	96-99	P53	Homo sapiens	141-144
21472523-5	2011	Further alkylation of p53 beyond Cys182 and Cys277 was found to trigger co-operative modification of the remaining seven Cys residues and protein unfolding.	Cysteine	33-36	P53	Homo sapiens	22-25
21460846-5	2011	Fluorescence and hydrogen-exchange measurements support a loosening of the structure of p53 in the presence of Hsp90 and its domains.	Hydrogen	17-25	P53	Homo sapiens	88-91
21383020-6	2011	Silencing of EDD induces phosphorylation of p53 at Ser(15) and activates p53 target genes in fibroblasts and some transformed cells without activation of DNA damage response.	Serine	51-54	P53	Homo sapiens	44-47
21383020-8	2011	On the other hand, overexpression of EDD inhibits p53-Ser(15) phosphorylation and suppresses the induction of p53 target genes during DNA damage, and this effect does not require its E3 ligase activity.	Serine	54-57	P53	Homo sapiens	50-53
21513889-3	2011	p53 activation is dependent on lysine acetylation by the lysine acetyltransferase and transcriptional coactivator CREB-binding protein (CBP) and on acetylation-directed CBP recruitment for p53 target gene expression.	Lysine	31-37	P53	Homo sapiens	0-3
21559451-8	2011	Nocodazole-mediated cell-cycle arrest was accompanied by higher rate of apoptosis and upregulation of p53.	Nocodazole	0-10	P53	Homo sapiens	102-105
21556366-0	2011	Predictive and prognostic impact of TP53 mutations and MDM2 promoter genotype in primary breast cancer patients treated with epirubicin or paclitaxel.	Epirubicin	125-135	P53	Homo sapiens	36-40
21556366-0	2011	Predictive and prognostic impact of TP53 mutations and MDM2 promoter genotype in primary breast cancer patients treated with epirubicin or paclitaxel.	Paclitaxel	139-149	P53	Homo sapiens	36-40
21556366-1	2011	BACKGROUND: TP53 mutations have been associated with resistance to anthracyclines but not to taxanes in breast cancer patients.	Anthracyclines	67-81	P53	Homo sapiens	12-16
21556366-8	2011	PRINCIPAL FINDINGS: While TP53 and CHEK2 mutations predicted resistance to epirubicin, MDM2 status did not.	Epirubicin	75-85	P53	Homo sapiens	26-30
21556366-10	2011	Remarkably, TP53 mutations (p = 0.007) but also MDM2 309TG/GG genotype status (p = 0.012) were associated with a poor disease-specific survival among patients having paclitaxel but not patients having epirubicin first-line.	Paclitaxel	166-176	P53	Homo sapiens	12-16
21556366-10	2011	Remarkably, TP53 mutations (p = 0.007) but also MDM2 309TG/GG genotype status (p = 0.012) were associated with a poor disease-specific survival among patients having paclitaxel but not patients having epirubicin first-line.	Epirubicin	201-211	P53	Homo sapiens	12-16
21556366-12	2011	CONCLUSION: TP53 and CHEK2 mutations were associated with lack of response to epirubicin monotherapy.	Epirubicin	78-88	P53	Homo sapiens	12-16
21556366-13	2011	In contrast, TP53 mutations and MDM2 309G allele status conferred poor disease-specific survival among patients treated with primary paclitaxel but not epirubicin monotherapy.	Paclitaxel	133-143	P53	Homo sapiens	13-17
21509038-0	2011	Disruption of the MDM2-p53 interaction strongly potentiates p53-dependent apoptosis in cisplatin-resistant human testicular carcinoma cells via the Fas/FasL pathway.	Cisplatin	87-96	P53	Homo sapiens	23-26
21510868-5	2011	Importantly, pharmacological or genetic ablation of NF-kappaB reversed the inhibitory effect of cAMP on DNA damage-induced apoptosis, demonstrating that, in addition to p53, cAMP relies on the activity of NF-kappaB to provide cells with a survival advantage in the face of DNA damage.	Cyclic AMP	96-100	P53	Homo sapiens	169-172
21509038-0	2011	Disruption of the MDM2-p53 interaction strongly potentiates p53-dependent apoptosis in cisplatin-resistant human testicular carcinoma cells via the Fas/FasL pathway.	Cisplatin	87-96	P53	Homo sapiens	60-63
21509038-3	2011	In the present study, we demonstrate that p53 resides in a complex with MDM2 at higher cisplatin concentrations in cisplatin-resistant human TC cells compared with cisplatin-sensitive TC cells.	Cisplatin	87-96	P53	Homo sapiens	42-45
21509038-3	2011	In the present study, we demonstrate that p53 resides in a complex with MDM2 at higher cisplatin concentrations in cisplatin-resistant human TC cells compared with cisplatin-sensitive TC cells.	Cisplatin	115-124	P53	Homo sapiens	42-45
21509038-3	2011	In the present study, we demonstrate that p53 resides in a complex with MDM2 at higher cisplatin concentrations in cisplatin-resistant human TC cells compared with cisplatin-sensitive TC cells.	Cisplatin	115-124	P53	Homo sapiens	42-45
21509038-4	2011	Inhibition of the MDM2-p53 interaction using either Nutlin-3 or MDM2 RNA interference resulted in hyperactivation of the p53 pathway and a strong induction of apoptosis in cisplatin-sensitive and -resistant TC cells.	Cisplatin	172-181	P53	Homo sapiens	23-26
21510868-2	2011	We have recently shown that p53 is critical for the inhibitory effect of cAMP on genotoxic agents-mediated apoptosis in BCP-ALLs.	Cyclic AMP	73-77	P53	Homo sapiens	28-31
20549698-0	2011	p53 status influences response to tamoxifen but not to fulvestrant in breast cancer cell lines.	Tamoxifen	34-43	P53	Homo sapiens	0-3
21532991-0	2011	p53 hypersensitivity is the predominant mechanism of the unique responsiveness of testicular germ cell tumor (TGCT) cells to cisplatin.	Cisplatin	125-134	P53	Homo sapiens	0-3
21532991-4	2011	Here we show that siRNA-mediated silencing of p53 is sufficient to completely abrogate hypersensitivity not only to Cisplatin but also to non-genotoxic inducers of p53 such as the Mdm2 antagonist Nutlin-3 and the proteasome inhibitor Bortezomib.	Cisplatin	116-125	P53	Homo sapiens	46-49
21446692-4	2011	Via combining an aptamer with a common hairpin DNA probe, we designed a self-blocked fluorescent bifunctional oligonucleotide probe (signaling probe) for the homogeneous parallel detection of two disease markers, PDGF-BB and the p53 gene.	Oligonucleotides	110-125	P53	Homo sapiens	229-232
20549698-5	2011	We show that p53 mutated cells were more resistant to cytotoxic effects of 4-hydroxy-tamoxifen (OHT) compared to p53 wild-type cells.	4'-hydroxytamoxifen	75-94	P53	Homo sapiens	13-16
21459001-3	2011	Through the use of high-throughput screening of 1500 compounds, we have identified a small molecule inhibitor, 15-carboxy-13-isopropylatis-13-ene-17,18-dioic acid (NSC15520), that inhibited both the binding of Rad9-GST and p53-GST fusion proteins to the RPA N-terminal DNA binding domain (DBD), interactions that are essential for robust DNA damage signaling.	17,18-dioic acid	146-162	P53	Homo sapiens	223-226
20549698-7	2011	p53 mutated cells were also hypersensitive to proliferative effects of estradiol.	Estradiol	71-80	P53	Homo sapiens	0-3
21496227-6	2011	Treatment with berberine resulted in repression of E6 and E7 levels and concomitant increase in p53 and Rb expression in both cell types.	Berberine	15-24	P53	Homo sapiens	96-99
21643554-0	2011	Differential DNA damage responses in p53 proficient and deficient cells: cisplatin-induced nuclear import of XPA is independent of ATR checkpoint in p53-deficient lung cancer cells.	Cisplatin	73-82	P53	Homo sapiens	37-40
21489314-16	2011	The inverse effect was observed in the TP53 mutated T24 cell line where TFAP2alpha silencing augmented cisplatin and gemcitabine sensitivity and did not stimulate proliferation.	Cisplatin	103-112	P53	Homo sapiens	39-43
21417280-1	2011	Proteins which bind methylated lysines ("readers" of the histone code) are important components in the epigenetic regulation of gene expression and can also modulate other proteins that contain methyl-lysine such as p53 and Rb.	Lysine	31-38	P53	Homo sapiens	216-219
21185067-0	2011	Expression of gamma-H2AX in endometrial carcinomas: an immunohistochemical study with p53.	gamma-h2ax	14-24	P53	Homo sapiens	86-89
21277958-7	2011	Additionally, 1.7-fold induction of p53 and 5-fold induction of endonuclease G genes involved in CAD-independent DNA fragmentation were noted under the influence of BPA.	bisphenol A	165-168	P53	Homo sapiens	36-39
21323611-9	2011	The exact mechanisms of apoptosis inhibition by TCDD are not fully understood, but both in vivo and in vitro studies consistently showed an involvement of the tumor suppressor p53 in this effect.	Polychlorinated Dibenzodioxins	48-52	P53	Homo sapiens	176-179
21329728-6	2011	Moreover, long-standing LS lesions showed significantly increased expression of p53 when compared to short-standing LS, ELS, and HS.	N-[(2S,3S,4R)-3,4-dihydroxy-8-oxo-8-[(4-pentylphenyl)amino]-1-{[(2S,3R,4S,5R,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]oxy}octan-2-yl]hexacosanamide	120-123	P53	Homo sapiens	80-83
21288478-11	2011	CONCLUSIONS: These data demonstrate that the Flt3-ITD confers sensitivity to Ara-C, but resistance to doxorubicin in a manner that depends on p53.	Doxorubicin	102-113	P53	Homo sapiens	142-145
21779512-7	2011	Furthermore, they discuss the potential mechanisms by which p53 regulates aging and longevity, including the p53 regulation of insulin/TOR signaling, stem/progenitor cells, and reactive oxygen species.	Reactive Oxygen Species	177-200	P53	Homo sapiens	60-63
21598493-3	2011	Different particle size quantum dots fluorescent probes were applied to detect P53 protein and Bcl-2 protein simultaneously in paraffin-embedded tissue section of human tongue squamous cell carcinoma under fluorescent microscope.	Paraffin	127-135	P53	Homo sapiens	79-82
21480327-8	2011	However, association of MYBL2/LINC silencing with doxorubicin-induced DNA damage caused stronger growth restraint in p53(-/-) Huh7 and Hep3B cells than in p53(+/+) Huh6 and HepG2 cells.	Doxorubicin	50-61	P53	Homo sapiens	117-120
21480327-8	2011	However, association of MYBL2/LINC silencing with doxorubicin-induced DNA damage caused stronger growth restraint in p53(-/-) Huh7 and Hep3B cells than in p53(+/+) Huh6 and HepG2 cells.	Doxorubicin	50-61	P53	Homo sapiens	155-158
21598493-6	2011	P53 protein and Bcl-2 protein can be combined with different particle size quantum dots fluorescent probes respectively in the same paraffin-embedded tissue section of human tongue squamous cell carcinoma and two kinds of fluorescene can be observed.	Paraffin	132-140	P53	Homo sapiens	0-3
21480327-9	2011	Doxorubicin triggered LIN9 dissociation from MYBL2 in p53(+/+) cell lines and increased MYBL2-LIN9 complexes in p53(-/-) cells.	Doxorubicin	0-11	P53	Homo sapiens	54-57
21480327-9	2011	Doxorubicin triggered LIN9 dissociation from MYBL2 in p53(+/+) cell lines and increased MYBL2-LIN9 complexes in p53(-/-) cells.	Doxorubicin	0-11	P53	Homo sapiens	112-115
21384097-5	2011	Several studies have demonstrated that inappropriate ROS levels arising from disruption of the Atm, PI3K-Akt, or Mdm2-p53 pathways impair HSC function in vivo.	Reactive Oxygen Species	53-56	P53	Homo sapiens	118-121
21480327-10	2011	Doxorubicin-induced MYBL2 dissociation from LIN9 led to p21(WAF1) up-regulation in p53(+/+) but not in p53(-/-) cell lines.	Doxorubicin	0-11	P53	Homo sapiens	83-86
21480327-11	2011	Suppression of p53 or p21(WAF1) genes abolished DNA damage response, enhanced apoptosis, and inhibited growth in doxorubicin-treated cells harboring p53(+/+) .	Doxorubicin	113-124	P53	Homo sapiens	15-18
21480327-11	2011	Suppression of p53 or p21(WAF1) genes abolished DNA damage response, enhanced apoptosis, and inhibited growth in doxorubicin-treated cells harboring p53(+/+) .	Doxorubicin	113-124	P53	Homo sapiens	149-152
21317290-0	2011	The GAS41-PP2Cbeta complex dephosphorylates p53 at serine 366 and regulates its stability.	Serine	51-57	P53	Homo sapiens	44-47
21258766-4	2011	The dose- and time-dependent effect of H2O2 on Bax, p53 and Bcl-2 expression was assessed by Western blot analysis.	Hydrogen Peroxide	39-43	P53	Homo sapiens	52-55
21258766-5	2011	Treatment of cells with 1 mM H2O2 for 1 h induced an increase in Bax and p53 expression, but the expression of Bcl-2 was not affected by H2O2 treatment.	Hydrogen Peroxide	29-33	P53	Homo sapiens	73-76
20729006-5	2011	RESULTS: We found that the P53 72Arg/Arg genotype was associated with increased RP risk compared with the 72Pro/Pro genotype.	Arginine	33-36	P53	Homo sapiens	27-30
21317290-3	2011	We demonstrate here that the newly identified complex GAS41-PP2Cbeta, and not PP2Cbeta alone, is specifically required for dephosphorylation of serine 366 on p53.	Serine	144-150	P53	Homo sapiens	158-161
21443808-10	2011	The findings indicate that in regions exposed to high levels of depleted uranium, although p53 and HER-2/neu overexpression are both high, correlation of their expression with age, grade, tumor size, recurrence and lymph node involvement is similar to studies that have been conducted on populations not exposed to depleted uranium.	Uranium	73-80	P53	Homo sapiens	91-94
21465572-2	2011	In response to oxidative, nitrosative, and electrophilic insults, p53 undergoes post-translational modifications, such as oxidation and covalent modification of cysteines, nitration of tyrosines, acetylation of lysines, phosphorylation of serine/threonine residues, etc.	Cysteine	161-170	P53	Homo sapiens	66-69
21465572-2	2011	In response to oxidative, nitrosative, and electrophilic insults, p53 undergoes post-translational modifications, such as oxidation and covalent modification of cysteines, nitration of tyrosines, acetylation of lysines, phosphorylation of serine/threonine residues, etc.	Tyrosine	185-194	P53	Homo sapiens	66-69
21465572-2	2011	In response to oxidative, nitrosative, and electrophilic insults, p53 undergoes post-translational modifications, such as oxidation and covalent modification of cysteines, nitration of tyrosines, acetylation of lysines, phosphorylation of serine/threonine residues, etc.	Lysine	211-218	P53	Homo sapiens	66-69
21465572-2	2011	In response to oxidative, nitrosative, and electrophilic insults, p53 undergoes post-translational modifications, such as oxidation and covalent modification of cysteines, nitration of tyrosines, acetylation of lysines, phosphorylation of serine/threonine residues, etc.	Serine	239-245	P53	Homo sapiens	66-69
21465572-2	2011	In response to oxidative, nitrosative, and electrophilic insults, p53 undergoes post-translational modifications, such as oxidation and covalent modification of cysteines, nitration of tyrosines, acetylation of lysines, phosphorylation of serine/threonine residues, etc.	Threonine	246-255	P53	Homo sapiens	66-69
21496427-9	2011	CONCLUSIONS: Cisplatin resistance of lung cancer cells is associated with overexpression of GRP75 gene, which could regulate the expressions of p53 and bcl-2.	Cisplatin	13-22	P53	Homo sapiens	144-147
21451571-6	2011	Phosphorylation of p53 serine residues that interfere with the interaction between p53 and its negative regulator MDM2 and enhance pro-apoptotic gene transcription also occurs subsequent to PERP expression.	Serine	23-29	P53	Homo sapiens	19-22
21451571-6	2011	Phosphorylation of p53 serine residues that interfere with the interaction between p53 and its negative regulator MDM2 and enhance pro-apoptotic gene transcription also occurs subsequent to PERP expression.	Serine	23-29	P53	Homo sapiens	83-86
21308739-8	2011	Concomitantly, wt p53 was strongly activated by phosphorylation at Ser(46).	Serine	67-70	P53	Homo sapiens	18-21
21303901-4	2011	VPA seems to stabilize a specific acetyl modification (lysine 120) of the p53 tumor suppressor protein, resulting in an increase in its proapoptotic function at the mitochondrial membrane.	Lysine	55-61	P53	Homo sapiens	74-77
21364582-11	2011	Similarly, treatment with p53 inducer adriamycin alone or in combination with DAC enhanced DSC3 expression.	Doxorubicin	38-48	P53	Homo sapiens	26-29
21057544-1	2011	Inducible acetylation of p53 at lysine residues has a great impact on regulating the transactivation of this protein, which is associated with cell growth arrest and/or apoptosis under various stress conditions.	Lysine	32-38	P53	Homo sapiens	25-28
21087144-5	2011	The current study demonstrates that DC cells signal a DNA damage response through p53 and its downstream mediator, p21(WAF/CIP), which is accompanied by an elevation in steady-state levels of superoxide and percent glutathione disulfide, both indicators of oxidative stress.	Superoxides	192-202	P53	Homo sapiens	82-85
21087144-7	2011	Further, restoring telomerase activity or inhibiting p53 or p21(WAF/CIP) significantly mitigated growth inhibition as well as caused a significant decrease in steady-state levels of superoxide.	Superoxides	182-192	P53	Homo sapiens	53-56
21087144-8	2011	Our results support a model in which telomerase insufficiency in DC leads to p21(WAF/CIP) signaling, via p53, to cause increased steady-state levels of superoxide, metabolic oxidative stress, and senescence.	Superoxides	152-162	P53	Homo sapiens	105-108
21248071-1	2011	HIPK2 activates the apoptotic arm of the DNA damage response by phosphorylating tumor suppressor p53 at serine 46.	Serine	104-110	P53	Homo sapiens	97-100
21278235-6	2011	We found that GCS silencing sensitized these mutant p53 cells to doxorubicin but did not affect the sensitivity of cells with wild-type p53.	Doxorubicin	65-76	P53	Homo sapiens	52-55
21130866-8	2011	FasL up-regulation; activation of caspases-8, -2, -9, and -3; and chromatin condensation were decreased by the p53 inhibitor pifithrin-alpha, implicating p53 as an upstream factor in the activation of death receptor-mediated apoptosis by H(2)O(2).	Water	238-243	P53	Homo sapiens	111-114
21130866-8	2011	FasL up-regulation; activation of caspases-8, -2, -9, and -3; and chromatin condensation were decreased by the p53 inhibitor pifithrin-alpha, implicating p53 as an upstream factor in the activation of death receptor-mediated apoptosis by H(2)O(2).	Water	238-243	P53	Homo sapiens	154-157
21212274-1	2011	Nitric oxide (NO) is a potent activator of the p53 tumor suppressor protein, thereby inducing cell cycle arrest and apoptosis.	Nitric Oxide	0-12	P53	Homo sapiens	47-50
21194538-7	2011	Further, it reduces the cell viability of MDA-MB-231 breast cancer cells, increases p53 expression in mammary tumors and shows maximum tumor volume reduction, suggesting that tannic acid potentiates the anti-cancer activity of doxorubicin.	Tannins	175-186	P53	Homo sapiens	84-87
21194538-7	2011	Further, it reduces the cell viability of MDA-MB-231 breast cancer cells, increases p53 expression in mammary tumors and shows maximum tumor volume reduction, suggesting that tannic acid potentiates the anti-cancer activity of doxorubicin.	Doxorubicin	227-238	P53	Homo sapiens	84-87
21241697-7	2011	However, mutant p53 blocked doxorubicin-mediated CIP2A down-regulation in HCT116 cells.	Doxorubicin	28-39	P53	Homo sapiens	16-19
21357744-3	2011	The p53 tumor suppressor protein, an important transcriptional regulator of apoptosis, naturally occurs in humans in two variants with single nucleotide polymorphisms resulting in Arg or Pro at residue 72.	Arginine	180-183	P53	Homo sapiens	4-7
21357744-6	2011	In primary cultured neurons, Arg(72)-p53, but not Pro(72)-p53, interacted directly with mitochondrial Bcl-xL and activated the intrinsic apoptotic pathway, increasing vulnerability to ischemia-induced apoptotic cell death.	Arginine	29-32	P53	Homo sapiens	37-40
21357744-7	2011	These results suggest that the Tp53 Arg/Arg genotype governs neuronal vulnerability to apoptosis and can be considered as a genetic marker predicting poor functional outcome after stroke.	Arginine	36-39	P53	Homo sapiens	31-35
21357744-7	2011	These results suggest that the Tp53 Arg/Arg genotype governs neuronal vulnerability to apoptosis and can be considered as a genetic marker predicting poor functional outcome after stroke.	Arginine	40-43	P53	Homo sapiens	31-35
21057547-8	2011	Consistently, knockdown with respective siRNAs revealed that AXIN and PML depend on each other to elevate p53-Ser-46 phosphorylation and to induce apoptosis after treatment with genotoxins.	Serine	110-113	P53	Homo sapiens	106-109
21394211-0	2011	Role of p53 serine 46 in p53 target gene regulation.	Serine	12-18	P53	Homo sapiens	8-11
21156795-0	2011	Ras puts the brake on doxorubicin-mediated cell death in p53-expressing cells.	Doxorubicin	22-33	P53	Homo sapiens	57-60
21156795-2	2011	Contradictory reports often open windows to understand the role of p53 tumor suppressor in doxorubicin-mediated cell death.	Doxorubicin	91-102	P53	Homo sapiens	67-70
21156795-3	2011	In this report, we provide evidences that doxorubicin induced more cell death in p53-negative tumor cells.	Doxorubicin	42-53	P53	Homo sapiens	81-84
21156795-4	2011	Several cells, having p53 basal expression, showed increase in p53 DNA binding upon doxorubicin treatment.	Doxorubicin	84-95	P53	Homo sapiens	22-25
21156795-4	2011	Several cells, having p53 basal expression, showed increase in p53 DNA binding upon doxorubicin treatment.	Doxorubicin	84-95	P53	Homo sapiens	63-66
21156795-5	2011	Doxorubicin induced cell death in p53-positive cells through expression of p53-dependent genes and activation of caspases and caspase-mediated cleavage of cellular proteins.	Doxorubicin	0-11	P53	Homo sapiens	34-37
21156795-5	2011	Doxorubicin induced cell death in p53-positive cells through expression of p53-dependent genes and activation of caspases and caspase-mediated cleavage of cellular proteins.	Doxorubicin	0-11	P53	Homo sapiens	75-78
21156795-6	2011	Surprisingly, in p53-negative cells, doxorubicin-mediated cell death was more aggressive (faster and intense).	Doxorubicin	37-48	P53	Homo sapiens	17-20
21156795-7	2011	Doxorubicin increased the amount of Fas ligand (FasL) by enhancing activator protein (AP) 1 DNA binding in both p53-positive and p53-negative cells, but the basal expression of Fas was higher in p53-negative cells.	Doxorubicin	0-11	P53	Homo sapiens	112-115
21156795-7	2011	Doxorubicin increased the amount of Fas ligand (FasL) by enhancing activator protein (AP) 1 DNA binding in both p53-positive and p53-negative cells, but the basal expression of Fas was higher in p53-negative cells.	Doxorubicin	0-11	P53	Homo sapiens	129-132
21156795-7	2011	Doxorubicin increased the amount of Fas ligand (FasL) by enhancing activator protein (AP) 1 DNA binding in both p53-positive and p53-negative cells, but the basal expression of Fas was higher in p53-negative cells.	Doxorubicin	0-11	P53	Homo sapiens	129-132
21156795-9	2011	Activation of caspases was faster in p53-negative cells upon doxorubicin treatment.	Doxorubicin	61-72	P53	Homo sapiens	37-40
21156795-11	2011	Overexpression of Ras decreased the amount of Fas in p53-negative cells, thereby decreasing doxorubicin-mediated aggressive cell death.	Doxorubicin	92-103	P53	Homo sapiens	53-56
21156795-12	2011	Overall, this study will help to understand the much studied chemotherapeutic drug, doxorubicin-mediated cell signaling cascade, that leads to cell death in p53-positive and -negative cells.	Doxorubicin	84-95	P53	Homo sapiens	157-160
21156795-13	2011	High basal expression of Fas might be an important determinant in doxorubicin-mediated cell death in p53-negative cells.	Doxorubicin	66-77	P53	Homo sapiens	101-104
21394211-0	2011	Role of p53 serine 46 in p53 target gene regulation.	Serine	12-18	P53	Homo sapiens	25-28
21394211-5	2011	To assess the role of post-translational modifications in target gene choice and activation we investigated the genome-wide level of phosphorylation of Serine 46 of p53 bound to DNA (p53-pS46) and of Serine 15 (p53-pS15).	Serine	152-158	P53	Homo sapiens	165-168
21448430-5	2011	Significantly reduced risk of EC was associated with TP53 genotypes for Arg/Arg + Arg/Pro vs Pro/Pro (OR = 0.73, 95% CI: 0.57-0.94, P = 0.014).	Arginine	72-75	P53	Homo sapiens	53-57
21448430-5	2011	Significantly reduced risk of EC was associated with TP53 genotypes for Arg/Arg + Arg/Pro vs Pro/Pro (OR = 0.73, 95% CI: 0.57-0.94, P = 0.014).	Arginine	76-79	P53	Homo sapiens	53-57
21448430-5	2011	Significantly reduced risk of EC was associated with TP53 genotypes for Arg/Arg + Arg/Pro vs Pro/Pro (OR = 0.73, 95% CI: 0.57-0.94, P = 0.014).	Arginine	76-79	P53	Homo sapiens	53-57
21107702-5	2011	Our results demonstrated that mutant p53, like wt p53, was induced upon doxorubicin treatment.	Doxorubicin	72-83	P53	Homo sapiens	50-53
21366897-5	2011	RESULTS: We found that sensitivity to cisplatin correlates significantly with levels of EGR-1 expression in tumors with wild-type p53/INK4a/p16 status.	Cisplatin	38-47	P53	Homo sapiens	130-133
21107702-7	2011	However, Complex I and II activities in the mitochondria were compromised only in wt p53-bearing cells after doxorubicin treatment, but not in mutant p53-bearing cells.	Doxorubicin	109-120	P53	Homo sapiens	85-88
21107702-8	2011	Similarly, doxorubicin treatment caused greater cell death only in wt p53-bearing cells, but not in mutant p53-bearing cells.	Doxorubicin	11-22	P53	Homo sapiens	70-73
21107702-5	2011	Our results demonstrated that mutant p53, like wt p53, was induced upon doxorubicin treatment.	Doxorubicin	72-83	P53	Homo sapiens	37-40
21107702-9	2011	When p53 deficient Ramos cells were transfected with mutant p53 (249S), the cells showed resistance to doxorubicin-induced cell death and decreases in complex activities.	Doxorubicin	103-114	P53	Homo sapiens	5-8
21107702-4	2011	In this study, we used doxorubicin, a chemotherapeutic drug, to treat five human lymphoma cell lines with wt, mutant or deficient in p53, to induce p53 activation and mitochondrial translocation.	Doxorubicin	23-34	P53	Homo sapiens	133-136
21107702-4	2011	In this study, we used doxorubicin, a chemotherapeutic drug, to treat five human lymphoma cell lines with wt, mutant or deficient in p53, to induce p53 activation and mitochondrial translocation.	Doxorubicin	23-34	P53	Homo sapiens	148-151
21107702-9	2011	When p53 deficient Ramos cells were transfected with mutant p53 (249S), the cells showed resistance to doxorubicin-induced cell death and decreases in complex activities.	Doxorubicin	103-114	P53	Homo sapiens	60-63
21107702-11	2011	Ellipticine enhanced p53 mitochondrial translocation, decreased Complex I activity, and sensitized p53 mutant cells to doxorubicin-induced apoptosis.	Doxorubicin	119-130	P53	Homo sapiens	99-102
21324703-2	2011	In an attempt to identify novel p53 inhibitors, a quality collection of compounds structurally related to pifithrin-beta were designed and synthesized as potential inhibitors of p53.	(2-benzoylethyl)trimethylammonium	116-120	P53	Homo sapiens	32-35
21078359-5	2011	The tryptophan environment of the molten globule beta-fragment has been probed by selective modification with N-bromosuccinimide (NBS), which shows that two tryptophans, possibly Trp 53 and Trp 152 are oxidized while the other Trp 128 remains resistant to oxidation.	Tryptophan	4-14	P53	Homo sapiens	179-185
21078359-5	2011	The tryptophan environment of the molten globule beta-fragment has been probed by selective modification with N-bromosuccinimide (NBS), which shows that two tryptophans, possibly Trp 53 and Trp 152 are oxidized while the other Trp 128 remains resistant to oxidation.	Tryptophan	157-168	P53	Homo sapiens	179-185
21324703-2	2011	In an attempt to identify novel p53 inhibitors, a quality collection of compounds structurally related to pifithrin-beta were designed and synthesized as potential inhibitors of p53.	(2-benzoylethyl)trimethylammonium	116-120	P53	Homo sapiens	178-181
21123835-3	2011	Furthermore, prior research suggests that TP53 mutations preferentially occur on the arginine allele to selectively inactivate the p63 pathway.	Arginine	85-93	P53	Homo sapiens	42-46
21429301-0	2011	Vitamin C increases the apoptosis via up-regulation p53 during cisplatin treatment in human colon cancer cells.	Cisplatin	63-72	P53	Homo sapiens	52-55
21429301-4	2011	Cisplatin (CDDP) is a DNA damaging agent and is widely used for treating cancer, while the role of p53 in CDDP-induced cell death has been stressed.	Cisplatin	106-110	P53	Homo sapiens	99-102
21429301-5	2011	Using cell growth assays, morphological methods, Western blotting, flow cytometry, and DNA fragmentation analysis, we measured the expression of p53 level involved in the effect of VC on CDDP-induced apoptosis of HCT116, a human colon cancer cell line.	Cisplatin	187-191	P53	Homo sapiens	145-148
21429301-6	2011	CDDP plus VC treatment resulted in significantly increased apoptosis along with upregulation of p53 compared to untreated cells and/or CDDP-treated cells.	Cisplatin	0-4	P53	Homo sapiens	96-99
21429301-7	2011	These results suggest that VC enhanced CDDP sensitivity and apoptosis via upregulation of p53.	Cisplatin	39-43	P53	Homo sapiens	90-93
21205083-1	2011	We previously reported that mitochondrial transcription factor A (mtTFA) preferentially recognizes cisplatin-damaged DNA via physical interaction with p53 and is upregulated by treatment with cisplatin and fluorouracil (5-FU).	Cisplatin	99-108	P53	Homo sapiens	151-154
21205083-1	2011	We previously reported that mitochondrial transcription factor A (mtTFA) preferentially recognizes cisplatin-damaged DNA via physical interaction with p53 and is upregulated by treatment with cisplatin and fluorouracil (5-FU).	Cisplatin	192-201	P53	Homo sapiens	151-154
21061155-4	2011	Laser confocal microscopy results reveal that PHB colocalized with the expression products of c-myc, c-fos, p53, and Rb, but the colocalization region was altered after RA treatment.	Tretinoin	169-171	P53	Homo sapiens	108-111
21205083-1	2011	We previously reported that mitochondrial transcription factor A (mtTFA) preferentially recognizes cisplatin-damaged DNA via physical interaction with p53 and is upregulated by treatment with cisplatin and fluorouracil (5-FU).	Fluorouracil	206-218	P53	Homo sapiens	151-154
21314329-0	2011	Upregulation of p53 expression in patients with colorectal cancer by administration of curcumin.	Curcumin	87-95	P53	Homo sapiens	16-19
21314329-3	2011	The results showed that curcumin administration increased body weight, decreased serum TNF-alpha levels, increased apoptotic tumor cells, enhanced expression of p53 molecule in tumor tissue, and modulated tumor cell apoptotic pathway.	Curcumin	24-32	P53	Homo sapiens	161-164
21314329-4	2011	We conclude that the curcumin treatment improves the general health of patients with colorectal cancer via the mechanism of increased p53 molecule expression in tumor cells and consequently speeds up tumor cell apoptosis.	Curcumin	21-29	P53	Homo sapiens	134-137
21151202-1	2011	p53, NFkappaB, STAT3, and several other transcription factors are reversibly methylated on lysine residues by enzymes that also modify histones.	Lysine	91-97	P53	Homo sapiens	0-3
21146884-4	2011	The association between BMI and diabetes depends on p53 polymorphism: Odds Ratio shows a high significant association between BMI and diabetes in *Arg/*Arg subjects (p=0.00001).	Arginine	147-150	P53	Homo sapiens	52-55
21043833-10	2011	Interactions of betel quid with p53 genotypes in lung cancer showed significant increase for all the three genotypes, indicating a major role of betel quid (OR=5.90, CI=1.67-20.81, p=0.006; OR=5.44, CI=1.67-17.75, p=0.005; and OR=5.84, CI=1.70-19.97, p=0.005 for Arg/Arg, Arg/Pro, and Pro/Pro, respectively).	Arginine	263-266	P53	Homo sapiens	32-35
21043833-10	2011	Interactions of betel quid with p53 genotypes in lung cancer showed significant increase for all the three genotypes, indicating a major role of betel quid (OR=5.90, CI=1.67-20.81, p=0.006; OR=5.44, CI=1.67-17.75, p=0.005; and OR=5.84, CI=1.70-19.97, p=0.005 for Arg/Arg, Arg/Pro, and Pro/Pro, respectively).	Arginine	267-270	P53	Homo sapiens	32-35
21043833-10	2011	Interactions of betel quid with p53 genotypes in lung cancer showed significant increase for all the three genotypes, indicating a major role of betel quid (OR=5.90, CI=1.67-20.81, p=0.006; OR=5.44, CI=1.67-17.75, p=0.005; and OR=5.84, CI=1.70-19.97, p=0.005 for Arg/Arg, Arg/Pro, and Pro/Pro, respectively).	Arginine	267-270	P53	Homo sapiens	32-35
21146884-4	2011	The association between BMI and diabetes depends on p53 polymorphism: Odds Ratio shows a high significant association between BMI and diabetes in *Arg/*Arg subjects (p=0.00001).	Arginine	152-155	P53	Homo sapiens	52-55
20839231-4	2011	We demonstrate here that G1-phase accumulation was induced by Cd in WI38 (wild-type for p53 and Rb), but not in the SV40 large T antigen-transformed variant WI38-VA13 (p53- and Rb-defective).	Cadmium	62-64	P53	Homo sapiens	88-91
20839231-5	2011	Cd-induced cell-cycle arrest was associated with a decrease in CDK2 protein and with increase in p21 expression and p53 phosphorylation.	Cadmium	0-2	P53	Homo sapiens	116-119
21094160-1	2011	BACKGROUND &amp; AIMS: Mutations in TP53, a tumor suppressor gene, are associated with prognosis of many cancers.	Adenosine Monophosphate	12-15	P53	Homo sapiens	36-40
21340684-2	2011	By transcriptional activation and other means, p53 is able to contribute to the regulation of glycolysis, oxidative phosphorylation, glutaminolysis, insulin sensitivity, nucleotide biosynthesis, mitochondrial integrity, fatty acid oxidation, antioxidant response, autophagy and mTOR signalling.	Fatty Acids	220-230	P53	Homo sapiens	47-50
21240456-0	2011	An ethanol extract of Iris nertschinskia induces p53-dependent apoptosis in the MCF7 human breast cancer cell line.	Ethanol	3-10	P53	Homo sapiens	49-52
21240456-8	2011	Our results suggest that p53 sensitizes tumor cells to the ethanol extract of Iris nertschinskia by Bax protein induction and caspase-dependent apoptosis.	Ethanol	59-66	P53	Homo sapiens	25-28
21091766-5	2011	Concomitantly, melatonin and D3, alone or in combination, caused a significant reduction in Akt phosphorylation and MDM2 values, with a consequent increase of p53/MDM2 ratio.	Melatonin	15-24	P53	Homo sapiens	159-162
21468563-5	2011	Western blot analysis showed that myricetin increased the protein levels of the p53/p21 cascade, and markedly decreased Cdc2 and cyclin B1 protein levels in HepG2 cells.	myricetin	34-43	P53	Homo sapiens	80-83
21106301-9	2011	More specifically, cigarette smoke stimulates metabolism of E(2) into the genotoxic metabolites, 4-OHE(1) and 4-OHE(2,) which interact with DNA in cancer-related genes, including the tumor suppressor gene, p53, and the proto-oncogene K-ras, two genes frequently mutated in patients with lung cancer.	Estradiol	60-64	P53	Homo sapiens	206-209
21239614-1	2011	We previously showed that progesterone (P4) inhibited the proliferation of human umbilical vein endothelial cells (HUVECs) through a p53-dependent pathway.	Progesterone	26-38	P53	Homo sapiens	133-136
21239614-7	2011	Moreover, administration with cSrc antisense oligonucleotide prevented the P4-induced increases of the levels of p53 mRNA and protein.	Oligonucleotides	45-60	P53	Homo sapiens	113-116
21145397-3	2011	We have previously shown that cisplatin induces apoptosis in dorsal root ganglion (DRG) sensory neurons by covalently binding to nuclear DNA (nDNA), resulting in DNA damage, subsequent p53 activation and Bax-mediated apoptosis via the mitochondria.	Cisplatin	30-39	P53	Homo sapiens	185-188
21336302-3	2011	The tumour suppressor p53 has now been reported to block a metabolic pathway (the pentose phosphate pathway) that diverts glucose away from bioenergetic into biosynthetic routes.	Glucose	122-129	P53	Homo sapiens	22-25
21336310-8	2011	Therefore, enhanced PPP glucose flux due to p53 inactivation may increase glucose consumption and direct glucose towards biosynthesis in tumour cells.	Glucose	24-31	P53	Homo sapiens	44-47
21336310-8	2011	Therefore, enhanced PPP glucose flux due to p53 inactivation may increase glucose consumption and direct glucose towards biosynthesis in tumour cells.	Glucose	74-81	P53	Homo sapiens	44-47
21338495-7	2011	Unexpectedly, Nutlin-3 also mediated phosphorylation of p53 at key DNA-damage-specific serine residues (Ser15, 20 and 37).	Serine	87-93	P53	Homo sapiens	56-59
21500551-9	2011	Intra-cellular levels of gamma-H2AX and phosphorylated P53 protein were significantly increased in high glucose groups.	Glucose	104-111	P53	Homo sapiens	55-58
21500551-13	2011	ATM-P53 pathway, the key proteins related to DNA double strain damage repairing mechanisms, may play an important role in high glucose induced cellular senescence and atherosclerosis.	Glucose	127-134	P53	Homo sapiens	4-7
21386967-5	2011	Direct or indirect activation of TP53 pathway with 5-aza-2"-deoxycitidine, Curcumin or Nutlin-3 induced an increase in apoptosis of ALL cells.	Curcumin	75-83	P53	Homo sapiens	33-37
21386980-1	2011	Human VRK1 induces a stabilization and accumulation of p53 by specific phosphorylation in Thr18.	UNII-PYZ33YLR8A	90-95	P53	Homo sapiens	55-58
21386980-6	2011	Induction of DNA damage by UV, IR, etoposide and doxorubicin stabilizes p53 and induces DRAM expression, followed by VRK1 downregulation and a reduction in p53 Thr18 phosphorylation.	Doxorubicin	49-60	P53	Homo sapiens	72-75
21386980-6	2011	Induction of DNA damage by UV, IR, etoposide and doxorubicin stabilizes p53 and induces DRAM expression, followed by VRK1 downregulation and a reduction in p53 Thr18 phosphorylation.	Doxorubicin	49-60	P53	Homo sapiens	156-159
21386980-6	2011	Induction of DNA damage by UV, IR, etoposide and doxorubicin stabilizes p53 and induces DRAM expression, followed by VRK1 downregulation and a reduction in p53 Thr18 phosphorylation.	UNII-PYZ33YLR8A	160-165	P53	Homo sapiens	156-159
21271695-6	2011	The best cyclopeptide of the series exhibited a K(d) of 8.0 muM, representing a 24-fold improvement in affinity over that of the linear lysine 382-acetylated p53 peptide.	Lysine	136-142	P53	Homo sapiens	158-161
20473904-6	2011	Moreover, EBNA-5 was found to inhibit the degradation of p53 in vitro.	N-tert-Butyl-N-ethylnitrosamine	10-14	P53	Homo sapiens	57-60
21216229-0	2011	Aurora-A promotes gefitinib resistance via a NF-kappaB signaling pathway in p53 knockdown lung cancer cells.	Gefitinib	18-27	P53	Homo sapiens	76-79
21216229-12	2011	Our findings also suggest that p53 not only stimulates apoptosis-related event but also inhibits the drug-resistance ability of Aurora-A, and consequently promotes the gefitinib-induced cellular apoptotic process.	Gefitinib	168-177	P53	Homo sapiens	31-34
21148320-7	2011	Specifically, acetylation of p53 at lysine 120, a DNA-binding domain residue mutated in human cancer, is essential for triggering apoptosis.	Lysine	36-42	P53	Homo sapiens	29-32
21216229-3	2011	We have previously demonstrated that p53 is a crucial regulator in mediating gefitinib-induced cell death, which upregulates apoptosis-related molecules.	Gefitinib	77-86	P53	Homo sapiens	37-40
21216229-4	2011	However, the mechanism of p53 involvement in cellular resistance to gefitinib remains unclear.	Gefitinib	68-77	P53	Homo sapiens	26-29
21216229-5	2011	In this study, we found that human non-small cell lung cancer cells, A549, with wild-type p53 exhibited a low level of Aurora-A expression and were sensitive to treatment with gefitinib.	Gefitinib	176-185	P53	Homo sapiens	90-93
21216229-6	2011	p53-knockdown A549 cells exhibited a high level of Aurora-A expression and were resistant to gefitinib-mediated apoptosis induction.	Gefitinib	93-102	P53	Homo sapiens	0-3
21216229-7	2011	In addition, the silencing of Aurora-A expression using an Aurora-A specific siRNA in p53-knockdown cells sensitized the A549 cancer cells to gefitinib-mediated apoptosis, suggesting a role for Aurora-A in gefitinib resistance.	Gefitinib	142-151	P53	Homo sapiens	86-89
21216229-7	2011	In addition, the silencing of Aurora-A expression using an Aurora-A specific siRNA in p53-knockdown cells sensitized the A549 cancer cells to gefitinib-mediated apoptosis, suggesting a role for Aurora-A in gefitinib resistance.	Gefitinib	206-215	P53	Homo sapiens	86-89
21167259-0	2011	Curcumin I protects the dopaminergic cell line SH-SY5Y from 6-hydroxydopamine-induced neurotoxicity through attenuation of p53-mediated apoptosis.	Curcumin	0-10	P53	Homo sapiens	123-126
21167259-9	2011	Taken together, these findings indicate that curcumin I protects dopaminergic neurons from 6-OHDA-induced toxicity via the reduction of ROS production, and subsequent attenuation of p53 phosphorylation and reduction of the Bax/Bcl-2 ratio.	Curcumin	45-55	P53	Homo sapiens	182-185
21378327-5	2011	The effect of zeranol-serum on mRNA expression of cell cycle regulating gene (cyclin D1) and tumor suppressor genes (p53, and p21) was evaluated using real-time RT-PCR.	Zeranol	14-21	P53	Homo sapiens	117-120
21210663-4	2011	After a sandwich immunoreaction, the HRP-p53(392)Ab(2)-GO captured onto the electrode surface produced an amplified electrocatalytic response by the reduction of enzymatically oxidized thionine in the presence of hydrogen peroxide.	Hydrogen Peroxide	213-230	P53	Homo sapiens	41-44
21541041-3	2011	In the current study, pretreatment with nitric oxide (NO) scavengers inhibited PDT-induced mitochondrial membrane potential (MMP) changes, activation of caspase-9, caspase-3, p21-activated protein kinase 2 (PAK2) and c-Jun N-terminal kinase (JNK), and gene expression of p53 and p21 involved in apoptotic signaling.	Nitric Oxide	40-52	P53	Homo sapiens	271-274
21118815-10	2011	However, other DNA damage response markers such as up-regulation and serine 15 phosphorylation of p53 or serine 1524 phosphorylation of BRCA1 were not triggered by LACV infection.	Serine	69-75	P53	Homo sapiens	98-101
20948431-9	2011	Low concentrations of boningmycin led to a senescent phenotype with an increase in senescence-associated beta-galactosidase activity and the time-dependent increase of p21, p27, and p53 expressions from 48 to120 h. Taken together, the results showed that boningmycin exhibits potent antitumor actions through the induction of apoptosis and cellular senescence.	boningmycin	22-33	P53	Homo sapiens	182-185
21378327-7	2011	Zeranol-serum up-regulated cyclin D1 and down-regulated p53 and p21 expression in PCHBECs compared with control serum.	Zeranol	0-7	P53	Homo sapiens	56-59
20959117-3	2011	Using MCF-7 cells, we observed that doxorubicin treatment triggered autophosphorylation of ATM on serine 1981 and the ATM-dependent activation of its downstream effectors p53, Chk2, and SMC1.	Doxorubicin	36-47	P53	Homo sapiens	171-174
20882314-2	2011	Our study proposes to rationally design a p53 antisense oligonucleotide (ASO) repository, which contains a series of ASOs containing single nucleotide differences to discriminate between each mutant and wild type (WT) p53.	Oligonucleotides	56-71	P53	Homo sapiens	42-45
20882314-2	2011	Our study proposes to rationally design a p53 antisense oligonucleotide (ASO) repository, which contains a series of ASOs containing single nucleotide differences to discriminate between each mutant and wild type (WT) p53.	Oligonucleotides	56-71	P53	Homo sapiens	218-221
20882314-3	2011	The Sfold software was used to predict target-accessibility and we designed an initial series of antisense oligonucleotides (ASO) that target the p53 mutants A161T, R175H and R249S.	Oligonucleotides	107-123	P53	Homo sapiens	146-149
20473858-2	2011	At low Dox concentrations, tumor suppressor p53 is activated, which enhances the expression of p21(Waf1/Cip1) (p21).	Doxorubicin	7-10	P53	Homo sapiens	44-47
21134073-6	2011	Combined treatment of isoflavones and curcumin additively suppressed cellular proliferation and induced phosphorylation of ATM, histone H2AX, Chk2 and p53.	Isoflavones	22-33	P53	Homo sapiens	151-154
21134073-6	2011	Combined treatment of isoflavones and curcumin additively suppressed cellular proliferation and induced phosphorylation of ATM, histone H2AX, Chk2 and p53.	Curcumin	38-46	P53	Homo sapiens	151-154
21263216-4	2011	BrdU photolysis resulted in well-controlled, dose- dependent generation of DSBs equivalent to radiation doses between 0.2 - 20 Gy, as determined by pulsed-field gel electrophoresis, and accompanied by dose-dependent ATM (ser-1981), H2AX (ser-139), Chk2 (thr-68), and p53 (ser-15) phosphorylation.	Serine	221-224	P53	Homo sapiens	267-270
20689555-3	2011	We report here that in response to a low dose of doxorubicin (which induces cell cycle arrest without promoting apoptosis), p53 directly transactivates the human p53 internal promoter, inducing Delta133p53alpha protein expression.	Doxorubicin	49-60	P53	Homo sapiens	124-127
20689555-3	2011	We report here that in response to a low dose of doxorubicin (which induces cell cycle arrest without promoting apoptosis), p53 directly transactivates the human p53 internal promoter, inducing Delta133p53alpha protein expression.	Doxorubicin	49-60	P53	Homo sapiens	162-165
20473858-3	2011	At high concentrations, Dox activates p53 leading to apoptosis without enhancing p21 expression.	Doxorubicin	24-27	P53	Homo sapiens	38-41
20473858-5	2011	Here, we report that the DNA methyltransferase (DNMT) DNMT3a was upregulated by Dox especially at concentrations that induced apoptosis in HCT116 colorectal cancer cells, and this process was regulated by p53.	Doxorubicin	80-83	P53	Homo sapiens	205-208
20425122-2	2011	In the present study, we have investigated the effects of 5-FU treatment on apoptosis induction in wild-type and mutant p53 urinary bladder cancer cells.	Fluorouracil	58-62	P53	Homo sapiens	120-123
20419384-4	2011	PCR amplification for the analysis of p53 codon 72 arginine/proline alleles was carried out in a separate reaction.	Arginine	51-59	P53	Homo sapiens	38-41
21360640-0	2011	Heparin plays a key regulatory role via a p53/FAK-dependent signaling in melanoma cell adhesion and migration.	Heparin	0-7	P53	Homo sapiens	42-45
21360640-6	2011	Moreover, heparin stimulated the p53 expression (P &lt;= 0.001) of M5 cells and its increased accumulation in the nucleus.	Heparin	10-17	P53	Homo sapiens	33-36
21360640-8	2011	In conclusion, the results of this study clearly demonstrate that the action of heparin in the regulation of melanoma cell adhesion and migration involves a p53/FAK/signaling pathway, which may be of importance in molecular targeted therapy of the disease.	Heparin	80-87	P53	Homo sapiens	157-160
20665703-6	2011	ZD6474 inhibited cyclin D1 and cyclin E expression and induced p53 expression when combined with paclitaxel.	vandetanib	0-6	P53	Homo sapiens	63-66
20425122-4	2011	RESULTS: In the urothelial bladder cancer cell lines RT4 and T24, 5-FU-induced TS inhibition proved to be associated with cell type-dependent (a) sensitivity to the drug, (b) Caspase-mediated apoptosis, (c) p53 stabilization and activation, as well as Rb phosphorylation and E2F1 expression and (d) transcriptional regulation of p53 target genes and their cognate proteins, while an E2F-dependent transcriptional network did not seem to be critically engaged in such type of responses.	Fluorouracil	66-70	P53	Homo sapiens	207-210
20425122-4	2011	RESULTS: In the urothelial bladder cancer cell lines RT4 and T24, 5-FU-induced TS inhibition proved to be associated with cell type-dependent (a) sensitivity to the drug, (b) Caspase-mediated apoptosis, (c) p53 stabilization and activation, as well as Rb phosphorylation and E2F1 expression and (d) transcriptional regulation of p53 target genes and their cognate proteins, while an E2F-dependent transcriptional network did not seem to be critically engaged in such type of responses.	Fluorouracil	66-70	P53	Homo sapiens	329-332
20425122-5	2011	CONCLUSIONS: We have shown that in the wild-type p53 context of RT4 cells, 5-FU-triggered apoptosis was prominently efficient and mainly regulated by p53-dependent mechanisms, whereas the mutant p53 environment of T24 cells was able to provide notable levels of resistance to apoptosis, basically ascribed to E2F-independent, and still unidentified, pathways.	Fluorouracil	75-79	P53	Homo sapiens	49-52
20425122-5	2011	CONCLUSIONS: We have shown that in the wild-type p53 context of RT4 cells, 5-FU-triggered apoptosis was prominently efficient and mainly regulated by p53-dependent mechanisms, whereas the mutant p53 environment of T24 cells was able to provide notable levels of resistance to apoptosis, basically ascribed to E2F-independent, and still unidentified, pathways.	Fluorouracil	75-79	P53	Homo sapiens	150-153
20425122-5	2011	CONCLUSIONS: We have shown that in the wild-type p53 context of RT4 cells, 5-FU-triggered apoptosis was prominently efficient and mainly regulated by p53-dependent mechanisms, whereas the mutant p53 environment of T24 cells was able to provide notable levels of resistance to apoptosis, basically ascribed to E2F-independent, and still unidentified, pathways.	Fluorouracil	75-79	P53	Homo sapiens	150-153
21051157-8	2011	Morphine induces over-expression of p53 gene that could mediate stem cell apoptosis.	Morphine	0-8	P53	Homo sapiens	36-39
21194611-1	2011	The p53 tumor suppressor protein is one of the key checkpoints in cellular response to a variety of stress mechanisms, including exposure to various toxic metal complexes.	Metals	155-160	P53	Homo sapiens	4-7
21194611-4	2011	Previous studies have shown that uranyl acetate and uranyl nitrate are capable of inducing DNA strand breaks and potentially of inducing oxidative stress through free radical generation, two potential mechanisms for activation of p53.	Uranyl Nitrate	52-66	P53	Homo sapiens	230-233
21194611-5	2011	Based on these studies, we hypothesized that either uranyl acetate or uranyl nitrate could act as an activator of p53.	Uranyl Nitrate	70-84	P53	Homo sapiens	114-117
21194611-7	2011	All of our results demonstrate that there is not a p53-mediated response to either uranyl acetate or uranyl nitrate, demonstrating that any cellular response to uranium exposure likely occurs in a p53-independent fashion under the conditions studied.	Uranium	161-168	P53	Homo sapiens	197-200
21051157-9	2011	Therefore we hypothesized that due to reduction in the testosterone levels, elevation in the DHT levels, and over-expression of p53 gene, morphine could prevent neural stem cell proliferation.	Morphine	138-146	P53	Homo sapiens	128-131
21216935-9	2011	Bid truncation and mitochondrial translocation of Bid and p53 was induced by fisetin in the presence or absence of cisplatin.	Cisplatin	115-124	P53	Homo sapiens	58-61
21047991-10	2011	This phenomenon is associated with p53 activation caused by increasing reactive oxygen species (ROS) levels because of the downregulation of superoxide dismutase expression in si-c-Jun-transfected cells.	Reactive Oxygen Species	71-94	P53	Homo sapiens	35-38
21245319-1	2011	Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53.	NAD	62-95	P53	Homo sapiens	167-170
21245319-1	2011	Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53.	NAD	62-95	P53	Homo sapiens	214-217
21245319-1	2011	Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53.	NAD	97-103	P53	Homo sapiens	167-170
21245319-1	2011	Numerous studies indicate that Sirtuin 1 (SIRT1), a mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylase (HDAC), plays a crucial role in p53-mediated stress responses by deacetylating p53.	NAD	97-103	P53	Homo sapiens	214-217
21047991-10	2011	This phenomenon is associated with p53 activation caused by increasing reactive oxygen species (ROS) levels because of the downregulation of superoxide dismutase expression in si-c-Jun-transfected cells.	Reactive Oxygen Species	96-99	P53	Homo sapiens	35-38
20972827-6	2011	Exposure to resveratrol decreased SIRT1 content, concomitant with an increase in the acetylated form of sirtuin substrates p53 and NFkappa-beta.	Resveratrol	12-23	P53	Homo sapiens	123-126
21071137-6	2011	Here, we have used five estrogen-dependent breast cancer cells lines with different p53 status, including an isogenic model, to show that FAK expression was regulated in a p53-dependent manner in response to estradiol.	Estradiol	208-217	P53	Homo sapiens	172-175
21575475-0	2011	[Relationship between the Akt-regulated direct p53 mitochondrial translocation and the resistance to cisplatin of ovarian cancer cells].	Cisplatin	101-110	P53	Homo sapiens	47-50
21575475-1	2011	OBJECTIVE: To explore Akt-regulated direct p53 mitochondrial translocation in cisplatin-induced apoptosis in ovarian cancer cells and the relationship between this and chemoresistance in ovarian cancer.	Cisplatin	78-87	P53	Homo sapiens	43-46
21575475-3	2011	The p53 accumulation in mitochondria was determined in purified mitochondrial fractions in cisplatin-sensitive and -resistant ovarian cancer cells.	Cisplatin	91-100	P53	Homo sapiens	4-7
21575475-6	2011	RESULTS: Cisplatin induced mitochondrial p53 accumulation and apoptosis in chemosensitive cells (P &lt; 0.05), but not in resistant cells (P &gt; 0.05).	Cisplatin	9-18	P53	Homo sapiens	41-44
21575475-8	2011	CONCLUSIONS: Cisplatin induces direct p53 mitochondrial accumulation in chemosensitive cells, and Akt confers resistance in ovarian cancer cells, in part, by regulating the direct action of p53 in mitochondrial death pathway.	Cisplatin	13-22	P53	Homo sapiens	38-41
21575475-8	2011	CONCLUSIONS: Cisplatin induces direct p53 mitochondrial accumulation in chemosensitive cells, and Akt confers resistance in ovarian cancer cells, in part, by regulating the direct action of p53 in mitochondrial death pathway.	Cisplatin	13-22	P53	Homo sapiens	190-193
21071137-9	2011	ChIP experiment showed that p53 bound to FAK promoter in the presence of estradiol in p53 wild-type but not in mutant p53 cells, suggesting a direct role of p53 in down regulating FAK mRNA expression.	Estradiol	73-82	P53	Homo sapiens	28-31
21071137-9	2011	ChIP experiment showed that p53 bound to FAK promoter in the presence of estradiol in p53 wild-type but not in mutant p53 cells, suggesting a direct role of p53 in down regulating FAK mRNA expression.	Estradiol	73-82	P53	Homo sapiens	86-89
21071137-9	2011	ChIP experiment showed that p53 bound to FAK promoter in the presence of estradiol in p53 wild-type but not in mutant p53 cells, suggesting a direct role of p53 in down regulating FAK mRNA expression.	Estradiol	73-82	P53	Homo sapiens	86-89
21071137-9	2011	ChIP experiment showed that p53 bound to FAK promoter in the presence of estradiol in p53 wild-type but not in mutant p53 cells, suggesting a direct role of p53 in down regulating FAK mRNA expression.	Estradiol	73-82	P53	Homo sapiens	86-89
21076775-0	2011	Predicting the coordination geometry for Mg2+ in the p53 DNA-binding domain: insights from computational studies.	magnesium ion	41-45	P53	Homo sapiens	53-56
20959462-7	2011	Importantly, the Aurora B-mediated phosphorylation on Ser(269) or Thr(284) significantly compromises p53 transcriptional activity.	Serine	54-57	P53	Homo sapiens	101-104
20959462-7	2011	Importantly, the Aurora B-mediated phosphorylation on Ser(269) or Thr(284) significantly compromises p53 transcriptional activity.	Threonine	66-69	P53	Homo sapiens	101-104
21076775-1	2011	Zn(2+) in the tumor-suppressor protein p53 DNA-binding domain (DBD) is essential for its structural stability and DNA-binding specificity.	Zinc	0-2	P53	Homo sapiens	39-42
21076775-2	2011	Mg(2+) has also been recently reported to bind to the p53DBD and influence its DNA-binding activity.	magnesium ion	0-6	P53	Homo sapiens	54-57
21076775-3	2011	In this contribution, the binding geometry of Mg(2+) in the p53DBD and the mechanism of how Mg(2+) affects its DNA-binding activity were investigated using density functional theory (DFT) calculations and molecular dynamics (MD) simulations.	magnesium ion	46-52	P53	Homo sapiens	60-63
21076775-3	2011	In this contribution, the binding geometry of Mg(2+) in the p53DBD and the mechanism of how Mg(2+) affects its DNA-binding activity were investigated using density functional theory (DFT) calculations and molecular dynamics (MD) simulations.	magnesium ion	92-98	P53	Homo sapiens	60-63
21076775-8	2011	The simulation results of the Mg(2+) system and the native Zn(2+) system show that the binding affinity of Mg(2+)to the p53DBD is weaker than that of Zn(2+), in agreement with the DFT calculation results and experiments.	magnesium ion	30-36	P53	Homo sapiens	120-123
21076775-8	2011	The simulation results of the Mg(2+) system and the native Zn(2+) system show that the binding affinity of Mg(2+)to the p53DBD is weaker than that of Zn(2+), in agreement with the DFT calculation results and experiments.	Zinc	59-61	P53	Homo sapiens	120-123
21076775-8	2011	The simulation results of the Mg(2+) system and the native Zn(2+) system show that the binding affinity of Mg(2+)to the p53DBD is weaker than that of Zn(2+), in agreement with the DFT calculation results and experiments.	magnesium ion	107-113	P53	Homo sapiens	120-123
21264228-10	2011	These results suggest that (1) mitochondrial ROS and NIX are essential factors for MALM, (2) MIV is a novel mechanism for lysosomal degradation of mitochondria, and (3) the p53-Mieap pathway plays a pivotal role in MQC by repairing or eliminating unhealthy mitochondria via MALM or MIV generation, respectively.	Reactive Oxygen Species	45-48	P53	Homo sapiens	173-176
21084274-9	2011	By overexpression of a dominant-negative p53 protein, we show that ABT-737-induced cellular senescence is p53-dependent.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	67-70	P53	Homo sapiens	41-44
21084274-9	2011	By overexpression of a dominant-negative p53 protein, we show that ABT-737-induced cellular senescence is p53-dependent.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	67-70	P53	Homo sapiens	106-109
21078664-0	2011	Nimbolide sensitizes human colon cancer cells to TRAIL through reactive oxygen species- and ERK-dependent up-regulation of death receptors, p53, and Bax.	nimbolide	0-9	P53	Homo sapiens	140-143
21127198-11	2011	Induction of receptors by DBA, however, was p53-independent, as deletion of p53 had no effect on receptor induction.	dibenzylidene acetone	26-29	P53	Homo sapiens	44-47
21245169-8	2011	Recruitment of BRCA1 to the p53-binding region of the p21 promoter in response to DNA damage required methylation of Arg 754 of p300 by CARM1.	Arginine	117-120	P53	Homo sapiens	28-31
21078664-9	2011	In addition, nimbolide down-regulated cell survival proteins, including I-FLICE, cIAP-1, cIAP-2, Bcl-2, Bcl-xL, survivin, and X-linked inhibitor of apoptosis protein, and up-regulated the pro-apoptotic proteins p53 and Bax.	nimbolide	13-22	P53	Homo sapiens	211-214
21078664-10	2011	Interestingly, p53 and Bax up-regulation by nimbolide was required for sensitization to TRAIL but not for DR up-regulation.	nimbolide	44-53	P53	Homo sapiens	15-18
21078664-0	2011	Nimbolide sensitizes human colon cancer cells to TRAIL through reactive oxygen species- and ERK-dependent up-regulation of death receptors, p53, and Bax.	Reactive Oxygen Species	63-86	P53	Homo sapiens	140-143
21078664-11	2011	Overall, our results indicate that nimbolide can sensitize colon cancer cells to TRAIL-induced apoptosis through three distinct mechanisms: reactive oxygen species- and ERK-mediated up-regulation of DR5 and DR4, down-regulation of cell survival proteins, and up-regulation of p53 and Bax.	nimbolide	35-44	P53	Homo sapiens	276-279
21040738-13	2011	Our results reveal that up-regulation of the key upstream signaling factor, PTEN, in MCF-7/DOX cells inhibited Akt phosphorylation, which ultimately causes increase in their regulatory p53 levels affecting the induction of G2/M cell cycle arrest and apoptosis.	Doxorubicin	91-94	P53	Homo sapiens	185-188
21223569-3	2011	METHODS: We examined the effect of long-term 17beta-estradiol (E2) treatment (five days) on the p53-Mdm2 pathway in estrogen receptor alpha (ERalpha) positive breast cancer cell lines that contain wild-type p53 (MCF-7 and ZR75-1).	Estradiol	45-61	P53	Homo sapiens	96-99
21223569-3	2011	METHODS: We examined the effect of long-term 17beta-estradiol (E2) treatment (five days) on the p53-Mdm2 pathway in estrogen receptor alpha (ERalpha) positive breast cancer cell lines that contain wild-type p53 (MCF-7 and ZR75-1).	Estradiol	63-65	P53	Homo sapiens	96-99
20951126-4	2011	This is first demonstration that damnacanthal-mediated apoptosis involves the sustained activation of the p38 MAPK pathway, leading to the transcription of the death receptor family genes encoding DR5/TRAIL and TNF-R1/TNF-alpha genes as well as the p53-regulated Bax gene.	damnacanthal	33-45	P53	Homo sapiens	249-252
20951126-9	2011	Taken together, this study provided first evidence demonstrating that TRAIL-, TNF-alpha-, and p53-mediated damnacanthal-induced apoptosis require the activation of p38 MAPK and mitochondrion-mediated caspase-dependent pathways.	damnacanthal	107-119	P53	Homo sapiens	94-97
21117647-2	2011	Through a thiol-based mechanism, APE1 reduces a number of important transcription factors, including AP-1, p53, NF-kappaB, and HIF-1alpha.	Sulfhydryl Compounds	10-15	P53	Homo sapiens	107-110
20951126-0	2011	Activation of p38 MAPK by damnacanthal mediates apoptosis in SKHep 1 cells through the DR5/TRAIL and TNFR1/TNF-alpha and p53 pathways.	damnacanthal	26-38	P53	Homo sapiens	121-124
21261644-3	2011	Resveratrol treatment in vitro causes activation and nuclear translocation of mitogen-activated protein kinase (ERK1/2), consequent phosphorylation of Ser-15 of p53, and apoptosis.	Resveratrol	0-11	P53	Homo sapiens	161-164
21214929-6	2011	Here we report on the reconstitution of the p53 tumor suppressor pathway in a p53-independent manner via p73 with combination treatments of alpha-TEA, a small bioactive lipid, plus DOXO or CDDP.	Doxorubicin	181-185	P53	Homo sapiens	44-47
21214929-6	2011	Here we report on the reconstitution of the p53 tumor suppressor pathway in a p53-independent manner via p73 with combination treatments of alpha-TEA, a small bioactive lipid, plus DOXO or CDDP.	Doxorubicin	181-185	P53	Homo sapiens	78-81
21214929-6	2011	Here we report on the reconstitution of the p53 tumor suppressor pathway in a p53-independent manner via p73 with combination treatments of alpha-TEA, a small bioactive lipid, plus DOXO or CDDP.	Cisplatin	189-193	P53	Homo sapiens	44-47
21214929-8	2011	RESULTS: Combination treatments of alpha-TEA plus DOXO or CDDP act cooperatively to induce apoptosis, caspase-8 and caspase-9 cleavage, p73, phospho-c-Ab1 and phospho-JNK protein expression, and increase expression of p53 downstream mediators; namely, death receptor-5, CD95/APO-1 (Fas), Bax and Noxa, as well as Yap nuclear translocation - plus reduce expression of Bcl-2.	Doxorubicin	50-54	P53	Homo sapiens	218-221
21214929-8	2011	RESULTS: Combination treatments of alpha-TEA plus DOXO or CDDP act cooperatively to induce apoptosis, caspase-8 and caspase-9 cleavage, p73, phospho-c-Ab1 and phospho-JNK protein expression, and increase expression of p53 downstream mediators; namely, death receptor-5, CD95/APO-1 (Fas), Bax and Noxa, as well as Yap nuclear translocation - plus reduce expression of Bcl-2.	Cisplatin	58-62	P53	Homo sapiens	218-221
21139584-8	2011	Treatment with a combination of GUT-70 and bortezomib or doxorubicin had synergistic antiproliferative effects in MCL cells that were independent of p53 status.	Doxorubicin	57-68	P53	Homo sapiens	149-152
21146529-0	2011	Targeting of p53 and its homolog p73 by protoporphyrin IX.	protoporphyrin IX	40-57	P53	Homo sapiens	13-16
21146529-3	2011	Here we show the direct binding of PpIX to the N-terminal domain of p53.	protoporphyrin IX	35-39	P53	Homo sapiens	68-71
21146529-4	2011	Furthermore, we addressed the induction of apoptosis in HCT 116 p53-null cells by PpIX and revealed interactions between PpIX and p73.	protoporphyrin IX	82-86	P53	Homo sapiens	64-67
21146529-4	2011	Furthermore, we addressed the induction of apoptosis in HCT 116 p53-null cells by PpIX and revealed interactions between PpIX and p73.	protoporphyrin IX	121-125	P53	Homo sapiens	64-67
21146529-5	2011	We propose that PpIX disrupts the p53/MDM2 or MDMX and p73/MDM2 complexes and thereby activates the p53- or p73-dependent cancer cell death.	protoporphyrin IX	16-20	P53	Homo sapiens	34-37
21146529-5	2011	We propose that PpIX disrupts the p53/MDM2 or MDMX and p73/MDM2 complexes and thereby activates the p53- or p73-dependent cancer cell death.	protoporphyrin IX	16-20	P53	Homo sapiens	100-103
21214929-10	2011	CONCLUSIONS: Data show that alpha-TEA in combination with DOXO or CDDP synergistically enhances apoptosis in TNBC via targeting p53-mediated genes in a p73-dependent manner, and that p73 responses are downstream of c-Abl, JNK and Yap.	Doxorubicin	58-62	P53	Homo sapiens	128-131
21214929-10	2011	CONCLUSIONS: Data show that alpha-TEA in combination with DOXO or CDDP synergistically enhances apoptosis in TNBC via targeting p53-mediated genes in a p73-dependent manner, and that p73 responses are downstream of c-Abl, JNK and Yap.	Cisplatin	66-70	P53	Homo sapiens	128-131
21224072-4	2011	We found that well-known proteasome inhibitors such as MG132 and bortezomib, as well as the recently discovered proteasome inhibitor thiostrepton, induced p53-independent apoptosis in human cancer cell lines that correlated with p53-independent induction of proapoptotic Noxa but not Puma protein.	Thiostrepton	133-145	P53	Homo sapiens	155-158
21224072-4	2011	We found that well-known proteasome inhibitors such as MG132 and bortezomib, as well as the recently discovered proteasome inhibitor thiostrepton, induced p53-independent apoptosis in human cancer cell lines that correlated with p53-independent induction of proapoptotic Noxa but not Puma protein.	Thiostrepton	133-145	P53	Homo sapiens	229-232
21224072-6	2011	Notably, thiostrepton induced more potent apoptosis in HepG2 cells with p53 knockdown than in parental cells with wild-type p53.	Thiostrepton	9-21	P53	Homo sapiens	72-75
21224072-6	2011	Notably, thiostrepton induced more potent apoptosis in HepG2 cells with p53 knockdown than in parental cells with wild-type p53.	Thiostrepton	9-21	P53	Homo sapiens	124-127
21261644-3	2011	Resveratrol treatment in vitro causes activation and nuclear translocation of mitogen-activated protein kinase (ERK1/2), consequent phosphorylation of Ser-15 of p53, and apoptosis.	Serine	151-154	P53	Homo sapiens	161-164
21261644-5	2011	By a PD98059-inhibitable process, resveratrol causes inducible COX-2 to accumulate in the nucleus where it complexes with pERK1/2 and p53.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	5-12	P53	Homo sapiens	134-137
21261644-5	2011	By a PD98059-inhibitable process, resveratrol causes inducible COX-2 to accumulate in the nucleus where it complexes with pERK1/2 and p53.	Resveratrol	34-45	P53	Homo sapiens	134-137
21261644-7	2011	NS-398, a specific pharmacologic inhibitor of COX-2, prevents resveratrol-induced complexing of nuclear ERK1/2 with COX-2 and with pSer-15-p53 and subsequent apoptosis; cyclooxygenase enzyme activity is not involved.	Resveratrol	62-73	P53	Homo sapiens	139-142
21261644-8	2011	Molecular steps in the pro-apoptotic action of resveratrol in cancer cells include induction of intranuclear COX-2 accumulation relevant to activation of p53.	Resveratrol	47-58	P53	Homo sapiens	154-157
21790217-3	2011	The ERE-linked p53 gene with the proline variant at codon 72 showed lower transfection rates than the gene without ERE or with the arginine variant at codon 72.	Arginine	131-139	P53	Homo sapiens	15-18
22471498-5	2011	Furthermore, transient knockdown of Wrap53 by siRNAs in U-2OS cells treated with 10 muM cisplatin reduced p53 mRNA transcript levels by up to 50% of those of controls.	Cisplatin	88-97	P53	Homo sapiens	39-42
22292621-2	2011	In exon 4 of the gene TP53, a codon 72 polymorphism causing an Arg/Pro substitution has been reported in breast and other cancers.	Arginine	63-66	P53	Homo sapiens	22-26
22393962-7	2011	CONCLUSIONS: Our results suggest that the codon 72 SNP which results in amino acid substitution of Arginine to Proline in cell cycle regulatory gene P53, is associated with sporadic CRC risk and carriers of Pro/Pro genotype and more than 50 years old may have high susceptibility.	Arginine	99-107	P53	Homo sapiens	149-152
21598212-6	2011	PCR amplification of TP53 codon 72 polymorphism: TP53 codon 72 genotypes were detected by PCR using specific primer pairs for amplifying the proline or the arginine Alleles.	Arginine	156-164	P53	Homo sapiens	49-53
21598212-13	2011	In control samples, the genotype distribution for TP53 polymorphism showed 30.4%, 45.2% and 24.4% for the arginine/arginine, arginine/proline and proline/proline genotypes, respectively.	Arginine	106-114	P53	Homo sapiens	50-54
21598212-13	2011	In control samples, the genotype distribution for TP53 polymorphism showed 30.4%, 45.2% and 24.4% for the arginine/arginine, arginine/proline and proline/proline genotypes, respectively.	Arginine	115-123	P53	Homo sapiens	50-54
21598212-13	2011	In control samples, the genotype distribution for TP53 polymorphism showed 30.4%, 45.2% and 24.4% for the arginine/arginine, arginine/proline and proline/proline genotypes, respectively.	Arginine	115-123	P53	Homo sapiens	50-54
21598212-18	2011	Overexpression of p53 was observed in 50.8 percent of cancer specimens which most of them were arginine/arginine genotype (P&lt;0.001).	Arginine	95-103	P53	Homo sapiens	18-21
21598212-18	2011	Overexpression of p53 was observed in 50.8 percent of cancer specimens which most of them were arginine/arginine genotype (P&lt;0.001).	Arginine	104-112	P53	Homo sapiens	18-21
21672450-4	2011	However, only few reports have shown an association between the Arginine (R) variant at position 52 of p53 and increased susceptibility to HPV E6 mediated degradation and thus to increased cancer susceptibility.	Arginine	64-72	P53	Homo sapiens	103-106
21672450-7	2011	This variant seems to be differently segregated in different ethnic/geographical locations; therefore, there might be a possible role of this genetic variant associated with a certain genetic background, which can explain why some studies reveal increased risk of cervical cancer development associated with Arginine p53 variant.	Arginine	308-316	P53	Homo sapiens	317-320
22471498-7	2011	Our findings suggest that cisplatin upregulates the expression of p53 in osteosarcoma cells by upregulating the transcript levels of Wrap53.	Cisplatin	26-35	P53	Homo sapiens	66-69
20875833-4	2011	Analysis of upstream regulators of HNF4alpha expression, including p53 and ATF3, showed that copper caused an increase in the steady-state levels of these proteins.	Copper	93-99	P53	Homo sapiens	67-70
20875833-5	2011	These results support a model for copper-responsive transcription in which the metal affects ATF3 expression and stabilizes p53 resulting in the down-regulation of HNF4alpha expression.	Copper	34-40	P53	Homo sapiens	124-127
21212516-0	2011	Silibinin activated p53 and induced autophagic death in human fibrosarcoma HT1080 cells via reactive oxygen species-p38 and c-Jun N-terminal kinase pathways.	Silybin	0-9	P53	Homo sapiens	20-23
20875833-5	2011	These results support a model for copper-responsive transcription in which the metal affects ATF3 expression and stabilizes p53 resulting in the down-regulation of HNF4alpha expression.	Metals	79-84	P53	Homo sapiens	124-127
21212516-2	2011	Pifithrin-alpha (PFT-alpha), a specific inhibitor of p53, reduced autophagy and reversed silibinin"s growth-inhibitory effect; besides, PFT-alpha decreased the activation of caspase-3, a crucial executor of apoptosis.	Silybin	89-98	P53	Homo sapiens	53-56
21212516-12	2011	These results suggest that silibinin might induce p53-mediated autophagic cell death by activating ROS-p38 and JNK pathways, as well as inhibiting MEK/ERK and PI3K/Akt pathways.	Silybin	27-36	P53	Homo sapiens	50-53
21212516-12	2011	These results suggest that silibinin might induce p53-mediated autophagic cell death by activating ROS-p38 and JNK pathways, as well as inhibiting MEK/ERK and PI3K/Akt pathways.	Reactive Oxygen Species	99-102	P53	Homo sapiens	50-53
21212516-3	2011	Silibinin upregulated expression of p53/phosphorylated-p53 (p-p53) in a time-dependent manner.	Silybin	0-9	P53	Homo sapiens	36-39
20875833-6	2011	In addition, copper may directly affect p53 protein levels.	Copper	13-19	P53	Homo sapiens	40-43
21212516-3	2011	Silibinin upregulated expression of p53/phosphorylated-p53 (p-p53) in a time-dependent manner.	Silybin	0-9	P53	Homo sapiens	55-58
20966084-0	2011	DNA damage, DNA repair rates and mRNA expression levels of cell cycle genes (TP53, p21(CDKN1A), BCL2 and BAX) with respect to occupational exposure to styrene.	Styrene	151-158	P53	Homo sapiens	77-81
21212516-3	2011	Silibinin upregulated expression of p53/phosphorylated-p53 (p-p53) in a time-dependent manner.	Silybin	0-9	P53	Homo sapiens	55-58
21512242-6	2011	PLE and PLEg reduced the phosphorylation of checkpoint proteins such as structural maintenance of chromosomes 1 (SMC1), checkpoint kinase 1 (Chk1), and p53 in DOX-treated cells.	Doxorubicin	159-162	P53	Homo sapiens	152-155
22101376-8	2011	The individuals carrying the heterozygous genotype (Arg/Trp-Arg/Gln) in the p53 codon 248 polymorphism showed high BC risk (p &lt; 0.001).	Arginine	52-55	P53	Homo sapiens	76-79
22101376-8	2011	The individuals carrying the heterozygous genotype (Arg/Trp-Arg/Gln) in the p53 codon 248 polymorphism showed high BC risk (p &lt; 0.001).	Tryptophan	56-59	P53	Homo sapiens	76-79
22101376-8	2011	The individuals carrying the heterozygous genotype (Arg/Trp-Arg/Gln) in the p53 codon 248 polymorphism showed high BC risk (p &lt; 0.001).	Arginine	60-63	P53	Homo sapiens	76-79
22101376-10	2011	The minor allele (Trp/Gln) carriers of the p53 codon 248 demonstrated a 1.7-fold risk for BC.	Tryptophan	18-21	P53	Homo sapiens	43-46
20221692-8	2011	This reduction in p53 protein levels resulted in reduced p53-dependent responses induced by DNA damage in p53 wild-type cells, lowering the capacity of doxorubicine to induce apoptosis.	Doxorubicin	152-164	P53	Homo sapiens	18-21
20221692-8	2011	This reduction in p53 protein levels resulted in reduced p53-dependent responses induced by DNA damage in p53 wild-type cells, lowering the capacity of doxorubicine to induce apoptosis.	Doxorubicin	152-164	P53	Homo sapiens	57-60
20221692-8	2011	This reduction in p53 protein levels resulted in reduced p53-dependent responses induced by DNA damage in p53 wild-type cells, lowering the capacity of doxorubicine to induce apoptosis.	Doxorubicin	152-164	P53	Homo sapiens	57-60
21045015-7	2011	Expression of total and serine-15-phosphorylated p53 and p53-inducible cell cycle regulatory protein p21 and ribonucleotide reductase subunit p53R2 involved in DNA repair were measured by immunobloting and reverse transcription-polymerase chain reaction.	Serine	24-30	P53	Homo sapiens	49-52
21045015-8	2011	Exposure to resveratrol or triacetyl-resveratrol activated p53, increased p21 and p53R2 and decreased PSA expression in LNCaP cells.	Resveratrol	12-23	P53	Homo sapiens	59-62
21045015-12	2011	CWR22Rv1 cells exposed to resveratrol and triacetyl-resveratrol showed a G1S block, concomitant with increased p53 and p21 expression; however, identically treated PC-3 cells showed attenuated progression through the SG2M phases.	Resveratrol	26-37	P53	Homo sapiens	111-114
21166494-2	2011	Results showed that T47D cells were found to be more sensitive to silibinin than MCF7 as observed by proliferation, clonogenic, and apoptotic assays, which was abrogated by pan-caspase inhibitor but remained unaffected by p53 inhibitor.	Silybin	66-75	P53	Homo sapiens	222-225
20966084-5	2011	We found negative correlations between mRNA expression of TP53, BCL2, BAX and styrene exposure (P &lt; 0.001 for all parameters).	Styrene	78-85	P53	Homo sapiens	58-62
20943371-0	2011	Grifolin, a potent antitumour natural product upregulates death-associated protein kinase 1 DAPK1 via p53 in nasopharyngeal carcinoma cells.	grifolin	0-8	P53	Homo sapiens	102-105
21187340-3	2011	Resveratrol also causes nuclear accumulation of the enzyme cyclooxygenase (COX)-2 and of the oncogene suppressor protein, p53.	Resveratrol	0-11	P53	Homo sapiens	122-125
21187340-6	2011	This finding implicates nuclear COX-2 in p53-mediated apoptosis induced by resveratrol.	Resveratrol	75-86	P53	Homo sapiens	41-44
21187340-7	2011	Sumoylation is important to stabilization of p53 and a COX-2-SUMO-1 interaction suggests sumoylation of COX-2 in resveratrol-treated cells and (iv) chromatin immunoprecipitation studies showed binding of induced nuclear COX-2 to the promoter region of PIG3 and Bax, pro-apoptotic gene targets of transcriptionally active p53.	Resveratrol	113-124	P53	Homo sapiens	321-324
21187340-8	2011	Nuclear accumulation of activated ERK1/2 and sumolyated COX-2 are essential to resveratrol-induced pSer-15-p53-mediated apoptosis in human ovarian cancer cells.	Resveratrol	79-90	P53	Homo sapiens	107-110
22212723-4	2011	RESULTS: In subjects with the *Arg/*Arg genotype of p53 codon 72, no association was observed between CAD and PTPN22.	Arginine	31-34	P53	Homo sapiens	52-55
22212723-4	2011	RESULTS: In subjects with the *Arg/*Arg genotype of p53 codon 72, no association was observed between CAD and PTPN22.	Arginine	36-39	P53	Homo sapiens	52-55
22312557-0	2011	The Role of Wild-Type p53 in Cisplatin-Induced Chk2 Phosphorylation and the Inhibition of Platinum Resistance with a Chk2 Inhibitor.	Cisplatin	29-38	P53	Homo sapiens	22-25
22312557-6	2011	Overexpression of p53 by cDNA transfection in wt-p53 (but not p53 deficient) cells doubled the amount of Chk2 phosphorylation 48 hours after cisplatin treatment.	Cisplatin	141-150	P53	Homo sapiens	18-21
22312557-8	2011	We conclude that wild-type p53, in response to cisplatin stimulation, plays a role in the upstream regulation of Chk2 phosphorylation at Thr-68.	Cisplatin	47-56	P53	Homo sapiens	27-30
22312557-8	2011	We conclude that wild-type p53, in response to cisplatin stimulation, plays a role in the upstream regulation of Chk2 phosphorylation at Thr-68.	Threonine	137-140	P53	Homo sapiens	27-30
22312557-9	2011	Cells without normal p53 function survive via an alternative pathway in response to the exogenous influence of cisplatin.	Cisplatin	111-120	P53	Homo sapiens	21-24
21291372-5	2011	Resveratrol impacts on the mitochondrial functions (respiratory chain, oncoproteins, gene expression, etc), in which p53 protein can be involved and its acetylated or phosphorylated forms.	Resveratrol	0-11	P53	Homo sapiens	117-120
21248471-3	2011	To develop an effective and low cytotoxic biological agent for targeted therapy, a p53 fusion protein, which was conjugated with the minimum motif of oxygen-dependent degradation domain (ODD) and the basic domain of TAT of HIV-1 named as TAT-ODD-p53, was evaluated for the treatment of NSCLC established by grafting H1299 cell line in which TP53 is homozygously deleted.	Oxygen	150-156	P53	Homo sapiens	83-86
22178888-0	2011	Adenosine promotes GATA-2-regulated p53 gene transcription to induce HepG2 cell apoptosis.	Adenosine	0-9	P53	Homo sapiens	36-39
22178888-4	2011	RESULTS: Extracellular adenosine upregulated expression of the p53 mRNA and protein in HepG2 human hepatoma cells.	Adenosine	23-32	P53	Homo sapiens	63-66
22178888-5	2011	Adenosine induced apoptosis, disrupted mitochondrial membrane potentials, and activated caspase-3, -8 and -9 in HepG2 cells, and those effects were inhibited by silencing the p53-targetd gene.	Adenosine	0-9	P53	Homo sapiens	175-178
22178888-6	2011	In the assay of transcriptional activity using full-length p53 gene promoter and 5" deletion mutants combined with the luciferase reporter vector, adenosine enhanced transcriptional activity for full-length p53 gene promoter, that was prevented by deleting from -240 to -146 bp on the promoter.	Adenosine	147-156	P53	Homo sapiens	59-62
22178888-6	2011	In the assay of transcriptional activity using full-length p53 gene promoter and 5" deletion mutants combined with the luciferase reporter vector, adenosine enhanced transcriptional activity for full-length p53 gene promoter, that was prevented by deleting from -240 to -146 bp on the promoter.	Adenosine	147-156	P53	Homo sapiens	207-210
22178888-7	2011	In the EMSA using a (32)P-labeled DNA probe to detect binding to the putative GATA-2 biding site on the p53 gene promoter, adenosine produced (32)P-positive signals in nuclear extracts from HepG2 cells.	Adenosine	123-132	P53	Homo sapiens	104-107
22178888-9	2011	In the ChIP assay, adenosine increased PCR products for the p53 gene promoter in chromosomal extracts from HepG2 cells, immunoprecipitated using an anti-GATA-2 antibody.	Adenosine	19-28	P53	Homo sapiens	60-63
22178888-10	2011	Adenosine-induced upregulation of the p53 mRNA expression was suppressed by knocking-down GATA-2.	Adenosine	0-9	P53	Homo sapiens	38-41
22178888-11	2011	CONCLUSION: The results of the present study show that p53 is a transcriptional target of GATA-2 and that adenosine upregulates GATA-2-regulated p53 expression, thereby activating caspase-3, -8, and -9 to induce HepG2 cell apoptosis.	Adenosine	106-115	P53	Homo sapiens	55-58
22178888-11	2011	CONCLUSION: The results of the present study show that p53 is a transcriptional target of GATA-2 and that adenosine upregulates GATA-2-regulated p53 expression, thereby activating caspase-3, -8, and -9 to induce HepG2 cell apoptosis.	Adenosine	106-115	P53	Homo sapiens	145-148
20943371-9	2011	Grifolin induced upregulation of DAPK1 via p53 was also observed in tumour cells derived from human breast cancer and human colon cancer.	grifolin	0-8	P53	Homo sapiens	43-46
21631964-8	2011	It can be concluded that: 1) mitoxantrone- induced phosphorylation of p53 on serine 15 and serine 392 is ATM dependent and MEK1/2-ERK1/2 independent.	Serine	77-83	P53	Homo sapiens	70-73
21144624-5	2011	The anthra[2,3-b]furan-5,10-dione 9 with distal methylamino groups was markedly potent against drug-resistant cell lines with P-glycoprotein overexpression or p53 gene deletion.	anthra[2,3-b]furan-5,10-dione	4-33	P53	Homo sapiens	159-162
20940027-5	2011	Furthermore, western blot analysis of p53, JNK, and caspase-3 showed that ROS generation was accompanied by JNK activation.	ros	74-77	P53	Homo sapiens	38-41
21631964-8	2011	It can be concluded that: 1) mitoxantrone- induced phosphorylation of p53 on serine 15 and serine 392 is ATM dependent and MEK1/2-ERK1/2 independent.	Serine	91-97	P53	Homo sapiens	70-73
21976978-5	2011	The characteristic vibrational bands of the p53-4-ATP nanoparticle system were then used to identify the p53 molecules when they were captured by a recognition substrate comprising a monolayer of azurin in molecules possessing significant affinity for this tumor suppressor.	Adenosine Triphosphate	50-53	P53	Homo sapiens	44-47
21673905-0	2011	Zeranol down-regulates p53 expression in primary cultured human breast cancer epithelial cells through epigenetic modification.	Zeranol	0-7	P53	Homo sapiens	23-26
20926450-0	2011	Naturally occurring germline and tumor-associated mutations within the ATP-binding motifs of PTEN lead to oxidative damage of DNA associated with decreased nuclear p53.	Adenosine Triphosphate	71-74	P53	Homo sapiens	164-167
20926450-8	2011	Our data, thus, reveal a novel mechanism of tumorigenesis in patients with germline or somatic mutations affecting PTEN ATP-binding motifs, i.e. qualitative and quantitative impairment of PTEN due to the loss of its phosphatase activity, and nuclear mislocalization, resulting in rapid PTEN protein degradation, suppression of p53-mediated transcriptional activity, loss of protection against oxidative stress as well as accumulation of spontaneous DNA DSBs.	Adenosine Triphosphate	120-123	P53	Homo sapiens	327-330
20232387-3	2011	We examined gene expression changes in Hupki (human TP53 knock-in) mice after treatment with aristolochic acid I (AAI) by gavage (5 mg/kg body weight).	aristolochic acid I	93-112	P53	Homo sapiens	52-56
21976978-5	2011	The characteristic vibrational bands of the p53-4-ATP nanoparticle system were then used to identify the p53 molecules when they were captured by a recognition substrate comprising a monolayer of azurin in molecules possessing significant affinity for this tumor suppressor.	Adenosine Triphosphate	50-53	P53	Homo sapiens	105-108
21932578-5	2011	A large increase of p53 *Arg/*Arg was observed in T1D patients with age at onset &lt; 6 years.	Arginine	25-28	P53	Homo sapiens	20-23
21275261-3	2011	In the present study we tested the hypothesis that the functional status of p53 in tumour cells might have an impact on the efficiency of C-1305 in experiments with both p53-deficient human HL-60 promyelocytic leukemia cells and human MCF-7 breast cancer cells harboring a functional p53 pathway.	Carbon	138-139	P53	Homo sapiens	76-79
21275261-3	2011	In the present study we tested the hypothesis that the functional status of p53 in tumour cells might have an impact on the efficiency of C-1305 in experiments with both p53-deficient human HL-60 promyelocytic leukemia cells and human MCF-7 breast cancer cells harboring a functional p53 pathway.	Carbon	138-139	P53	Homo sapiens	170-173
21275261-3	2011	In the present study we tested the hypothesis that the functional status of p53 in tumour cells might have an impact on the efficiency of C-1305 in experiments with both p53-deficient human HL-60 promyelocytic leukemia cells and human MCF-7 breast cancer cells harboring a functional p53 pathway.	Carbon	138-139	P53	Homo sapiens	170-173
21275261-9	2011	These observations suggest that C-1305 abrogates the restriction checkpoint and promotes G1/S transition in cells lacking functional p53.	Carbon	32-33	P53	Homo sapiens	133-136
22242209-2	2011	We assessed the immunohistochemical expression of p53 and P-gp using formalin-fixed, paraffin-embedded specimens in 108 patients diagnosed with de novo DLBC.	Paraffin	85-93	P53	Homo sapiens	50-53
21799252-0	2011	Activation of glutathione peroxidase and inhibition of p53-related apoptosis by apomorphine.	Apomorphine	80-91	P53	Homo sapiens	55-58
21932578-5	2011	A large increase of p53 *Arg/*Arg was observed in T1D patients with age at onset &lt; 6 years.	Arginine	30-33	P53	Homo sapiens	20-23
22442608-2	2011	MATERIALS AND METHODS: The standard immunohistochemical method along with MIB-1 and DO-7; DAKO antibodies was used to study the expression of p53 and ki-67 in paraffin-embedded tissue specimens.	Paraffin	159-167	P53	Homo sapiens	142-145
20931131-1	2011	Upon genomic insult, the tumor suppressor p53 is phosphorylated and acetylated at specific serine and lysine residues, increasing its stability and transactivation function.	Serine	91-97	P53	Homo sapiens	42-45
20931131-1	2011	Upon genomic insult, the tumor suppressor p53 is phosphorylated and acetylated at specific serine and lysine residues, increasing its stability and transactivation function.	Lysine	102-108	P53	Homo sapiens	42-45
20941532-9	2011	Furthermore, estradiol-pretreated HPV-negative cell line C33A showed reduction in level of Telomerase, PCNA, p16, and activation of both p53 and p73 tumor suppressor proteins, thus, demonstrating the importance of E6 in estradiol-mediated protective effect.	Estradiol	13-22	P53	Homo sapiens	137-140
21863213-0	2011	The p53 upregulated modulator of apoptosis (PUMA) chemosensitizes intrinsically resistant ovarian cancer cells to cisplatin by lowering the threshold set by Bcl-x(L) and Mcl-1.	Cisplatin	114-123	P53	Homo sapiens	4-7
21863213-3	2011	The p53 mutation correlates significantly with resistance to platinum-based chemotherapy, early relapse and shortened overall survival in ovarian cancer patients.	Platinum	61-69	P53	Homo sapiens	4-7
21863213-5	2011	In this study, we showed that the induction of PUMA by cisplatin was abolished in p53-deficient SKOV3 cells.	Cisplatin	55-64	P53	Homo sapiens	82-85
22180829-1	2011	NAD-dependent Class III histone deacetylase SIRT1 is a multiple functional protein and has been demonstrated critically involved in stress response, cellular metabolism and aging through deacetylating variety of substrates including p53, forkhead transcription factors, PGC-1alpha, NF-kappaB, Ku70 and histones.	NAD	0-3	P53	Homo sapiens	233-236
20817676-6	2011	Comparing activated p53 binding in nuclear extracts from doxorubicin- or ionizing radiation (IR)-treated human cells, we observed little difference in binding profiles.	Doxorubicin	57-68	P53	Homo sapiens	20-23
20817676-9	2011	Chromatin immunoprecipitation-sequencing in lymphoblastoid cells confirmed p53 binding to seven polymorphic p53 REs in response to doxorubicin.	Doxorubicin	131-142	P53	Homo sapiens	75-78
20805247-9	2011	Furthermore, we showed that activation of p53 in doxorubicin-induced senescent cells increased E2F1 and p53 interaction, diminished E2F1 recruitment to MEF promoter and reduced MEF expression.	Doxorubicin	49-60	P53	Homo sapiens	42-45
20817676-9	2011	Chromatin immunoprecipitation-sequencing in lymphoblastoid cells confirmed p53 binding to seven polymorphic p53 REs in response to doxorubicin.	Doxorubicin	131-142	P53	Homo sapiens	108-111
20805247-9	2011	Furthermore, we showed that activation of p53 in doxorubicin-induced senescent cells increased E2F1 and p53 interaction, diminished E2F1 recruitment to MEF promoter and reduced MEF expression.	Doxorubicin	49-60	P53	Homo sapiens	104-107
21776823-5	2011	Metformin induced apoptosis by arresting cells in G1 phase and reducing cyclin D level and increasing the expression of p21 and cyclin E. Molecular and cellular studies indicated that metformin significantly elevated p53 and Bax levels and reduced STAT3 and Bcl-2.	Metformin	0-9	P53	Homo sapiens	217-220
21776823-5	2011	Metformin induced apoptosis by arresting cells in G1 phase and reducing cyclin D level and increasing the expression of p21 and cyclin E. Molecular and cellular studies indicated that metformin significantly elevated p53 and Bax levels and reduced STAT3 and Bcl-2.	Metformin	184-193	P53	Homo sapiens	217-220
21776823-8	2011	Furthermore, MEK inhibitor significantly suppressed metformin-induced p53 and Bax elevation while ERK inhibitor generated a slight reduction in p53 levels.	Metformin	52-61	P53	Homo sapiens	70-73
22194993-3	2011	In the present study we investigated the effect of paclitaxel in combination with two novel HDACi, ST2782 or ST3595, able to induce p53 and tubulin hyperacetylation.	Paclitaxel	51-61	P53	Homo sapiens	132-135
21776823-11	2011	All these results suggested that metformin activated p53, Bax, and induced tumor cell apoptosis through the ERK signaling pathway.	Metformin	33-42	P53	Homo sapiens	53-56
21109480-8	2011	In combination therapy, p53RA small molecules enhanced the anti-tumor activity of cisplatin, 5-fluorouracil, paclitaxel, and erlotinib against HNSCC cells.	Cisplatin	82-91	P53	Homo sapiens	24-27
21109480-8	2011	In combination therapy, p53RA small molecules enhanced the anti-tumor activity of cisplatin, 5-fluorouracil, paclitaxel, and erlotinib against HNSCC cells.	Fluorouracil	93-107	P53	Homo sapiens	24-27
21109480-8	2011	In combination therapy, p53RA small molecules enhanced the anti-tumor activity of cisplatin, 5-fluorouracil, paclitaxel, and erlotinib against HNSCC cells.	Paclitaxel	109-119	P53	Homo sapiens	24-27
22194993-4	2011	A synergistic effect of the paclitaxel/ST2782 (or ST3595) combination was found in wild-type p53 ovarian carcinoma cells, but not in a p53 mutant subline, in spite of a marked tubulin acetylation.	Paclitaxel	28-38	P53	Homo sapiens	93-96
22194993-9	2011	Our results support the relevance of p53 modulation as a major determinant of the synergistic interaction observed between paclitaxel and novel HDACi and emphasize the therapeutic interest of this combination.	Paclitaxel	123-133	P53	Homo sapiens	37-40
22022534-5	2011	METHODOLOGY: During induction of senescence by low levels of endogenous p53 and ectopic p21, cells were co-treated with nocodazole, which eliminated proliferating cells.	Nocodazole	120-130	P53	Homo sapiens	72-75
22110707-4	2011	HIPK2 is an important regulator of apoptosis, which forms a complex with the tumor suppressor p53, mediating p53 phosphorylation at Ser 46 and thus promoting pro-apoptotic gene expression.	Serine	132-135	P53	Homo sapiens	94-97
22110707-4	2011	HIPK2 is an important regulator of apoptosis, which forms a complex with the tumor suppressor p53, mediating p53 phosphorylation at Ser 46 and thus promoting pro-apoptotic gene expression.	Serine	132-135	P53	Homo sapiens	109-112
22110707-8	2011	Functionally, we demonstrate that HPV23 E6 inhibits HIPK2-mediated p53 Ser 46 phosphorylation through enforcing dissociation of the HIPK2/p53 complex.	Serine	71-74	P53	Homo sapiens	67-70
22110707-8	2011	Functionally, we demonstrate that HPV23 E6 inhibits HIPK2-mediated p53 Ser 46 phosphorylation through enforcing dissociation of the HIPK2/p53 complex.	Serine	71-74	P53	Homo sapiens	138-141
22110707-10	2011	Thus, cutaneous HPV23 E6 prevents HIPK2-mediated p53 Ser 46 phosphorylation, which may favour survival of UV-damaged keratinocytes and skin carcinogenesis by apoptosis evasion.	Serine	53-56	P53	Homo sapiens	49-52
22028823-10	2011	Genotoxic stress induced by Adriamycin treatment increases the levels of hSin3B that is recruited to the promoters of p53-target genes (HSPA8, MAD1 and CRYZ).	Doxorubicin	28-38	P53	Homo sapiens	118-121
22028823-11	2011	More importantly recruitment of hSin3B and repression of the three p53-target promoters upon Adriamycin treatment were observed only in p53(+/+) cell lines.	Doxorubicin	93-103	P53	Homo sapiens	67-70
22028823-11	2011	More importantly recruitment of hSin3B and repression of the three p53-target promoters upon Adriamycin treatment were observed only in p53(+/+) cell lines.	Doxorubicin	93-103	P53	Homo sapiens	136-139
21473121-3	2011	Assumption about the leading part of a p53-dependent way in realization apoptosis human lymphocytes in the conditions of influence of UV-light and reactive oxygen species is put forward.	Reactive Oxygen Species	147-170	P53	Homo sapiens	39-42
21980358-1	2011	Phosphorylation at murine Serine 18 (human Serine 15) is a critical regulatory process for the tumor suppressor function of p53.	Serine	26-32	P53	Homo sapiens	124-127
21980358-1	2011	Phosphorylation at murine Serine 18 (human Serine 15) is a critical regulatory process for the tumor suppressor function of p53.	Serine	43-49	P53	Homo sapiens	124-127
21858223-9	2011	However, the down-regulation of FOXM1 by either thiostrepton or U0126 required the presence of p53 in ovarian cancer cells.	Thiostrepton	48-60	P53	Homo sapiens	95-98
21629734-5	2011	Colony formation assay was used to assess the sensitivity of hormone dependent, p53 wt (LNCaP) and hormone independent p53 mutant (PC3) CaP cell lines to the cytotoxic effect of IR and Doxorubicin in the presence or absence of Ku55933 and NU7441 which are small molecule inhibitors of ATM and DNA-PK, respectively.	Doxorubicin	185-196	P53	Homo sapiens	119-122
21603599-7	2011	Our online cell biosensor measurements reveal for the first time the time scale of metabolic response until onset of cell death under cisplatin treatment, which is in good agreement with models of p53-mediated cell fate decision.	Cisplatin	134-143	P53	Homo sapiens	197-200
21857991-6	2011	We find that this downregulation of HR is not only completely dependent on the binding site of p53 with replication protein A but also the ATR/ATM serine 15 phosphorylation site.	Serine	147-153	P53	Homo sapiens	95-98
21887339-0	2011	The chemotherapeutic drug 5-fluorouracil promotes PKR-mediated apoptosis in a p53-independent manner in colon and breast cancer cells.	Fluorouracil	26-40	P53	Homo sapiens	78-81
21887339-5	2011	PKR protein was activated by 5-FU treatment in a p53-independent manner, inducing phosphorylation of the protein synthesis translation initiation factor eIF-2alpha and cell death by apoptosis.	Fluorouracil	29-33	P53	Homo sapiens	49-52
21629658-2	2011	Real-time RT-PCR and Western blot analysis revealed that CALB2 mRNA and protein expression were down-regulated in p53 wild-type and p53 null isogenic HCT116 CRC cell lines following 48 h and 72 h 5-FU treatment.	Fluorouracil	196-200	P53	Homo sapiens	114-117
21673964-6	2011	Mechanistic studies (both in vitro and in vivo) revealed that FBA-TPQ might exert its activity through Reactive Oxygen Species (ROS)-associated activation of the death receptor, p53-MDM2, and PI3K-Akt pathways in OVCAR-3 cells, which is in accordance with in vitro microarray (Human genome microarrays, Agilent) data analysis (GEO accession number: GSE25317).	6-hydroxydopa quinone	66-69	P53	Homo sapiens	178-181
21673964-6	2011	Mechanistic studies (both in vitro and in vivo) revealed that FBA-TPQ might exert its activity through Reactive Oxygen Species (ROS)-associated activation of the death receptor, p53-MDM2, and PI3K-Akt pathways in OVCAR-3 cells, which is in accordance with in vitro microarray (Human genome microarrays, Agilent) data analysis (GEO accession number: GSE25317).	Reactive Oxygen Species	103-126	P53	Homo sapiens	178-181
21673964-6	2011	Mechanistic studies (both in vitro and in vivo) revealed that FBA-TPQ might exert its activity through Reactive Oxygen Species (ROS)-associated activation of the death receptor, p53-MDM2, and PI3K-Akt pathways in OVCAR-3 cells, which is in accordance with in vitro microarray (Human genome microarrays, Agilent) data analysis (GEO accession number: GSE25317).	Reactive Oxygen Species	128-131	P53	Homo sapiens	178-181
21625555-0	2011	Modeling a new water channel that allows SET9 to dimethylate p53.	Water	15-20	P53	Homo sapiens	61-64
21075072-5	2010	The ectopic expression of p53 in p53-deficient cells (Hep3B) reduced TAp63 promoter activity, and knockdown of TAp63 attenuated doxorubicin-induced cell growth arrest by promoting cell cycle progression, leading to an increase in the percentage of G(2)/M cells.	Doxorubicin	128-139	P53	Homo sapiens	26-29
21159183-9	2010	There were indications of p53 aberrations being associated with the combined effect of smoking, alcohol and work history.	Alcohols	96-103	P53	Homo sapiens	26-29
21093410-3	2010	During adriamycin (ADR)-mediated apoptosis, p53 and p73 were induced to stabilize in association with a significant reduction of MDM2 and Itch, suggesting that, in addition to Itch, MDM2 could also be involved in the stability control of p73.	Doxorubicin	7-17	P53	Homo sapiens	44-47
21034746-10	2010	Unlike MDA MB-231, in MCF-7 cells, CC upregulates the level of phospho-p53 (Ser-15) and FasL, suggesting the involvement of extrinsic pathway.	Serine	76-79	P53	Homo sapiens	71-74
21167021-0	2010	Catechin hydrate suppresses MCF-7 proliferation through TP53/Caspase-mediated apoptosis.	Catechin	0-8	P53	Homo sapiens	56-60
21418001-4	2010	Under relatively favorable conditions, p53 helps to maintain intracellular homeostasis by balancing anabolic and catabolic processes and by timely elimination of reactive oxygen species.	Reactive Oxygen Species	162-185	P53	Homo sapiens	39-42
20802529-4	2010	Cisplatin-induced Noxa expression was ERK dependent, but p53 independent, and inhibition of ERK activation markedly attenuated cisplatin-induced cell death, as well as Noxa expression.	Cisplatin	0-9	P53	Homo sapiens	57-60
20708607-10	2010	In addition, oxaliplatin increased the levels of phospho-p53 (Ser-15) and total p53 proteins.	Serine	62-65	P53	Homo sapiens	57-60
20842432-0	2010	RETRACTED ARTICLE: Cytotoxic activities of tubeimoside-2 on human hepatoma HepG2 cells by induction of G2/M phase arrest and apoptosis in a p53-dependent manner.	tubeimoside-2	43-56	P53	Homo sapiens	140-143
20549306-5	2010	BeSO(4) caused phosphorylation of serine-15 of p53, accumulation of p53 protein, and expression of p21, the cyclin-dependent kinase inhibitor that is prominent during senescence.	Serine	34-40	P53	Homo sapiens	47-50
20840860-6	2010	Downregulation of p53 target genes BAX and/or GADD45 alpha led to decreased in PPP1R13L activation after adriamycin and/or etoposide treatments.	Doxorubicin	105-115	P53	Homo sapiens	18-21
20633010-6	2010	5-FU induced p53 and p21 accumulation together with a decrease in cyclin B1 and Bcl-2 levels in treated keloid fibroblasts.	Fluorouracil	0-4	P53	Homo sapiens	13-16
20725098-0	2010	Resveratrol-induced p53-independent apoptosis of human nasopharyngeal carcinoma cells is correlated with the downregulation of DeltaNp63.	Resveratrol	0-11	P53	Homo sapiens	20-23
20573444-2	2010	Moreover, hypoxic cells are less sensitive than normoxic cells to doxorubicin cytotoxicity, a potent activator of the p53 tumor suppressor gene.	Doxorubicin	66-77	P53	Homo sapiens	118-121
20725098-2	2010	Trans-resveratrol (RSV) has been shown to exert proapoptotic activities through a p53-dependent or p53-independent pathway in various cancer cells.	Resveratrol	0-17	P53	Homo sapiens	82-85
20725098-2	2010	Trans-resveratrol (RSV) has been shown to exert proapoptotic activities through a p53-dependent or p53-independent pathway in various cancer cells.	Resveratrol	0-17	P53	Homo sapiens	99-102
20725098-2	2010	Trans-resveratrol (RSV) has been shown to exert proapoptotic activities through a p53-dependent or p53-independent pathway in various cancer cells.	Resveratrol	19-22	P53	Homo sapiens	82-85
20725098-2	2010	Trans-resveratrol (RSV) has been shown to exert proapoptotic activities through a p53-dependent or p53-independent pathway in various cancer cells.	Resveratrol	19-22	P53	Homo sapiens	99-102
20725098-6	2010	The RSV effect was accompanied by the downregulation of DeltaNp63 and the upregulation of p53 protein in a dose-dependent manner.	Resveratrol	4-7	P53	Homo sapiens	90-93
21311676-8	2010	With the co-treatment of PD98059 and melatonin, the expression of p-p53, p21, and MDM2 did not decrease.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	25-32	P53	Homo sapiens	68-71
21099361-7	2010	In addition, p53-induced increases in intracellular levels of ROS were also inhibited in cells overexpressing Nek6.	ros	62-65	P53	Homo sapiens	13-16
21042727-4	2010	2DG significantly inhibits ATP production in p53-deficient lung cancer cells (H358) but not in p53-wt cells (A549).	Adenosine Triphosphate	27-30	P53	Homo sapiens	45-48
21042727-6	2010	In the presence of p53, increased ROS from OXPHOS increases the expression of p53 target genes known to modulate metabolism, including synthesis of cytochrome c oxidase 2 (SCO2) and TP53-induced glycolysis and apoptosis regulator (TIGAR).	ros	34-37	P53	Homo sapiens	19-22
21042727-6	2010	In the presence of p53, increased ROS from OXPHOS increases the expression of p53 target genes known to modulate metabolism, including synthesis of cytochrome c oxidase 2 (SCO2) and TP53-induced glycolysis and apoptosis regulator (TIGAR).	ros	34-37	P53	Homo sapiens	78-81
22432562-8	2010	Overexpression of p53 mRNA was observed in both cancerous cell lines, but it was differentially altered by folic acid administration in only SCC25 cells.	Folic Acid	107-117	P53	Homo sapiens	18-21
22432562-9	2010	These findings suggest folic acid administration may significantly alter growth of oral cancers in vitro via p53-dependent and p53-independent pathways.	Folic Acid	23-33	P53	Homo sapiens	109-112
22432562-9	2010	These findings suggest folic acid administration may significantly alter growth of oral cancers in vitro via p53-dependent and p53-independent pathways.	Folic Acid	23-33	P53	Homo sapiens	127-130
20461443-3	2010	We aimed to comprehensively review the evidence for the prognostic usefulness of p53 immunohistochemical expression in paraffin-embedded tissue specimens from diffusely infiltrating astrocytomas.	Paraffin	119-127	P53	Homo sapiens	81-84
20861261-2	2010	During viral infection, E1B-55K and E4orf6 substitute for the substrate-binding subunits of the host cell cullin 5 class of ubiquitin ligases, resulting in p53 polyubiquitinylation and proteasomal degradation.	cullin 5	106-114	P53	Homo sapiens	156-159
20935061-5	2010	Stratification analyses showed that a reduced risk associated with the -606CC genotype was more pronounced in subgroups of non-smokers, non-drinkers, younger subjects (defined as &lt;=57 years), carriers of the TP53 Arg/Arg (rs1042522) genotype, patients with oropharyngeal cancer or late-stage SCCHN.	Arginine	216-219	P53	Homo sapiens	211-215
20935061-5	2010	Stratification analyses showed that a reduced risk associated with the -606CC genotype was more pronounced in subgroups of non-smokers, non-drinkers, younger subjects (defined as &lt;=57 years), carriers of the TP53 Arg/Arg (rs1042522) genotype, patients with oropharyngeal cancer or late-stage SCCHN.	Arginine	220-223	P53	Homo sapiens	211-215
20935220-3	2010	The proapoptotic effects of berberine were closely associated with both the MDM2 expression levels and p53 status of a set of ALL cell lines.	Berberine	28-37	P53	Homo sapiens	103-106
20935220-4	2010	The most potent apoptosis was induced by berberine in ALL cells with both MDM2 overexpression and a wild-type (wt)-p53, whereas no proapoptotic effect was detected in ALL cells that were negative for MDM2 and wt-p53.	Berberine	41-50	P53	Homo sapiens	115-118
20935220-4	2010	The most potent apoptosis was induced by berberine in ALL cells with both MDM2 overexpression and a wild-type (wt)-p53, whereas no proapoptotic effect was detected in ALL cells that were negative for MDM2 and wt-p53.	Berberine	41-50	P53	Homo sapiens	212-215
20935220-5	2010	In contrast to the conventional chemotherapeutic drug doxorubicin, which induces p53 activation and a subsequent upregulation of MDM2, berberine strongly induced persistent downregulation of MDM2 followed by a steady-state activation of p53.	Doxorubicin	54-65	P53	Homo sapiens	81-84
20935220-5	2010	In contrast to the conventional chemotherapeutic drug doxorubicin, which induces p53 activation and a subsequent upregulation of MDM2, berberine strongly induced persistent downregulation of MDM2 followed by a steady-state activation of p53.	Berberine	135-144	P53	Homo sapiens	81-84
20935220-5	2010	In contrast to the conventional chemotherapeutic drug doxorubicin, which induces p53 activation and a subsequent upregulation of MDM2, berberine strongly induced persistent downregulation of MDM2 followed by a steady-state activation of p53.	Berberine	135-144	P53	Homo sapiens	237-240
21119367-1	2010	This study was undertaken to investigate the expression of p53, Ki-67, and CD31 proteins in endometrial polyps of postmenopausal women treated with tamoxifen (TAM).	Tamoxifen	148-157	P53	Homo sapiens	59-62
21119367-1	2010	This study was undertaken to investigate the expression of p53, Ki-67, and CD31 proteins in endometrial polyps of postmenopausal women treated with tamoxifen (TAM).	Tamoxifen	159-162	P53	Homo sapiens	59-62
20803550-9	2010	Both Nutlin-3a and IR caused a large increase in APBs that was dependent on p53 and p21 expression.	tert-butoxycarbonyl-trimethylsilylalanyl-prolyl-boro-methoxypropylglycine-pinanediol	49-53	P53	Homo sapiens	76-79
21311676-0	2010	Melatonin Induces Apoptotic Cell Death via p53 in LNCaP Cells.	Melatonin	0-9	P53	Homo sapiens	43-46
21311676-1	2010	In this study, we examined whether melatonin promotes apoptotic cell death via p53 in prostate LNCaP cells.	Melatonin	35-44	P53	Homo sapiens	79-82
21311676-6	2010	Melatonin increased the expressions of p53, p21, and p27.	Melatonin	0-9	P53	Homo sapiens	39-42
21311676-8	2010	With the co-treatment of PD98059 and melatonin, the expression of p-p53, p21, and MDM2 did not decrease.	Melatonin	37-46	P53	Homo sapiens	68-71
21311676-10	2010	Together, these results suggest that p53-dependent induction of JNK/p38 MAPK directly participates in apoptosis induced by melatonin.	Melatonin	123-132	P53	Homo sapiens	37-40
20945503-0	2010	Unveiling the methylation status of CpG dinucleotides in the substituted segment of the human p53 knock-in (Hupki) mouse genome.	cytidylyl-3'-5'-guanosine	36-53	P53	Homo sapiens	94-97
20945503-1	2010	Methylated cytosines within CpG dinucleotides (mCpGs) along the DNA-binding domain of the TP53 tumor suppressor gene (exons ~5-8) are the single most significant mutational target in human cancers.	cytidylyl-3'-5'-guanosine	28-45	P53	Homo sapiens	90-94
20878668-0	2010	Stabilization of mutant p53 via alkylation of cysteines and effects on DNA binding.	Cysteine	46-55	P53	Homo sapiens	24-27
21120630-0	2010	Oligonucleotide microarrays with high discriminating power for the detection of single nucleotide variations in the p53 gene.	Oligonucleotides	0-15	P53	Homo sapiens	116-119
20309662-0	2010	R72P polymorphism of TP53 in ulcerative colitis patients is associated with the incidence of colectomy, use of steroids and the presence of a positive family history.	Steroids	111-119	P53	Homo sapiens	21-25
20309662-2	2010	The most commonly and extensively studied single nucleotide polymorphism (SNP) of p53 is Arg&gt;Pro substitution on codon 72 (R72P).	Arginine	89-92	P53	Homo sapiens	82-85
20564491-6	2010	Moreover, inhibition of ERK by treatment of cells with the ERK-specific inhibitor PD98059 blocked WEGS-mediated p53 expression.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	82-89	P53	Homo sapiens	112-115
20878668-3	2010	We have discovered ligands containing an alpha,beta-unsaturated double bond, characteristic of Michael acceptors, that bind covalently to generic cysteine sites in the p53 core domain.	Cysteine	146-154	P53	Homo sapiens	168-171
20840854-0	2010	Non-dioxin-like PCBs interact with benzo[a]pyrene-induced p53-responses and inhibit apoptosis.	pyrene	43-49	P53	Homo sapiens	58-61
20797428-0	2010	Resveratrol induces p53 and suppresses myocardin-mediated vascular smooth muscle cell differentiation.	Resveratrol	0-11	P53	Homo sapiens	20-23
20797428-6	2010	Consistent with previous studies, RSVL induces the nuclear translocation of p53 and the expression of p53-responsive genes such as Cdkn1a, Gadd45a, Gadd45, and Fas.	Resveratrol	34-38	P53	Homo sapiens	76-79
20797428-6	2010	Consistent with previous studies, RSVL induces the nuclear translocation of p53 and the expression of p53-responsive genes such as Cdkn1a, Gadd45a, Gadd45, and Fas.	Resveratrol	34-38	P53	Homo sapiens	102-105
20851891-6	2010	Phospho-Ser(269)-specific monoclonal antibodies were generated and used to demonstrate that p53 phosphorylation is induced at Ser(269) after irradiation with kinetics similar to those of p53 protein induction.	Serine	8-11	P53	Homo sapiens	92-95
20851891-6	2010	Phospho-Ser(269)-specific monoclonal antibodies were generated and used to demonstrate that p53 phosphorylation is induced at Ser(269) after irradiation with kinetics similar to those of p53 protein induction.	Serine	126-129	P53	Homo sapiens	92-95
20851891-7	2010	Phosphomimetic mutation at Ser(269) inactivated the transcription activation function and clonogenic suppressor activity of p53.	Serine	27-30	P53	Homo sapiens	124-127
20847049-9	2010	Molecular dynamics simulations suggest that (i) solvation of phospho-Ser(215) and phospho-Ser(269) by positive charged residues or solvent water leads to local unfolding, which is accompanied by local destabilization of the N-terminal loop and global destabilization of p53, and (ii) the double alanine 215/269 mutation disrupts hydrogen bonding normally stabilized by both Ser(215) and Ser(269).	Serine	90-93	P53	Homo sapiens	270-273
20847049-8	2010	However, the double mutant p53(S215A/S269A) was transcriptionally inactive and more thermally unstable than either individual Ser-Ala loop mutant.	Serine	126-129	P53	Homo sapiens	27-30
21187919-8	2010	Furthermore, the combination of MNP-Fe3O4 with adriamycin or daunorubicin increased p53 protein levels and decreased NF-kappaB protein levels more than adriamycin or daunorubicin alone, indicating that MNP-Fe3O4 could enhance the effect of chemotherapeutic drugs on p53 and NF-kappaB.	Doxorubicin	47-57	P53	Homo sapiens	84-87
20847049-8	2010	However, the double mutant p53(S215A/S269A) was transcriptionally inactive and more thermally unstable than either individual Ser-Ala loop mutant.	Alanine	130-133	P53	Homo sapiens	27-30
20847049-9	2010	Molecular dynamics simulations suggest that (i) solvation of phospho-Ser(215) and phospho-Ser(269) by positive charged residues or solvent water leads to local unfolding, which is accompanied by local destabilization of the N-terminal loop and global destabilization of p53, and (ii) the double alanine 215/269 mutation disrupts hydrogen bonding normally stabilized by both Ser(215) and Ser(269).	Serine	69-72	P53	Homo sapiens	270-273
20847049-9	2010	Molecular dynamics simulations suggest that (i) solvation of phospho-Ser(215) and phospho-Ser(269) by positive charged residues or solvent water leads to local unfolding, which is accompanied by local destabilization of the N-terminal loop and global destabilization of p53, and (ii) the double alanine 215/269 mutation disrupts hydrogen bonding normally stabilized by both Ser(215) and Ser(269).	Water	139-144	P53	Homo sapiens	270-273
20847049-9	2010	Molecular dynamics simulations suggest that (i) solvation of phospho-Ser(215) and phospho-Ser(269) by positive charged residues or solvent water leads to local unfolding, which is accompanied by local destabilization of the N-terminal loop and global destabilization of p53, and (ii) the double alanine 215/269 mutation disrupts hydrogen bonding normally stabilized by both Ser(215) and Ser(269).	Serine	90-93	P53	Homo sapiens	270-273
20847049-9	2010	Molecular dynamics simulations suggest that (i) solvation of phospho-Ser(215) and phospho-Ser(269) by positive charged residues or solvent water leads to local unfolding, which is accompanied by local destabilization of the N-terminal loop and global destabilization of p53, and (ii) the double alanine 215/269 mutation disrupts hydrogen bonding normally stabilized by both Ser(215) and Ser(269).	Serine	90-93	P53	Homo sapiens	270-273
20847049-10	2010	These data indicate that p53 has evolved two serine phosphoacceptor residues within conformationally flexible epitopes that normally stabilize the p53 DNA-binding domain but whose phosphorylation induces a mutant conformation to wild type p53.	Serine	45-51	P53	Homo sapiens	25-28
20847049-10	2010	These data indicate that p53 has evolved two serine phosphoacceptor residues within conformationally flexible epitopes that normally stabilize the p53 DNA-binding domain but whose phosphorylation induces a mutant conformation to wild type p53.	Serine	45-51	P53	Homo sapiens	147-150
20847049-10	2010	These data indicate that p53 has evolved two serine phosphoacceptor residues within conformationally flexible epitopes that normally stabilize the p53 DNA-binding domain but whose phosphorylation induces a mutant conformation to wild type p53.	Serine	45-51	P53	Homo sapiens	147-150
20851891-2	2010	A combinatorial peptide chip used to identify the novel kinase consensus site RXSPhi(K/D) led to the discovery of a homologous phosphorylation site in the S10 beta-strand of p53 at Ser(269).	Serine	181-184	P53	Homo sapiens	174-177
20851891-3	2010	Overlapping peptide libraries confirmed that Ser(269) was a phosphoacceptor site in vitro, and immunochemical approaches evaluated whether p53 is phosphorylated in vivo at Ser(269).	Serine	172-175	P53	Homo sapiens	139-142
20851891-4	2010	Mutation or phosphorylation of p53 at Ser(269) attenuates binding of the p53-specific monoclonal antibody DO-12, identifying an assay for measuring Ser(269) phosphorylation of p53 in vivo.	Serine	38-41	P53	Homo sapiens	31-34
20851891-4	2010	Mutation or phosphorylation of p53 at Ser(269) attenuates binding of the p53-specific monoclonal antibody DO-12, identifying an assay for measuring Ser(269) phosphorylation of p53 in vivo.	Serine	38-41	P53	Homo sapiens	73-76
20851891-4	2010	Mutation or phosphorylation of p53 at Ser(269) attenuates binding of the p53-specific monoclonal antibody DO-12, identifying an assay for measuring Ser(269) phosphorylation of p53 in vivo.	Serine	38-41	P53	Homo sapiens	73-76
20851891-4	2010	Mutation or phosphorylation of p53 at Ser(269) attenuates binding of the p53-specific monoclonal antibody DO-12, identifying an assay for measuring Ser(269) phosphorylation of p53 in vivo.	Serine	148-151	P53	Homo sapiens	31-34
20851891-4	2010	Mutation or phosphorylation of p53 at Ser(269) attenuates binding of the p53-specific monoclonal antibody DO-12, identifying an assay for measuring Ser(269) phosphorylation of p53 in vivo.	Serine	148-151	P53	Homo sapiens	73-76
20851891-4	2010	Mutation or phosphorylation of p53 at Ser(269) attenuates binding of the p53-specific monoclonal antibody DO-12, identifying an assay for measuring Ser(269) phosphorylation of p53 in vivo.	Serine	148-151	P53	Homo sapiens	73-76
20847049-3	2010	A novel phosphorylation site exists within this region at Ser(269), whose phosphomimetic mutation inactivates p53.	Serine	58-61	P53	Homo sapiens	110-113
20847049-4	2010	The phosphomimetic p53 (S269D) exhibits characteristics of mutant p53: stable binding to Hsp70 in vivo, elevated ubiquitination in vivo, inactivity in DNA binding and transcription, increased thermoinstability using thermal shift assays, and lambda(max) of intrinsic tryptophan fluorescence at 403 nm rather than 346 nm, characteristic of wild type p53.	Tryptophan	267-277	P53	Homo sapiens	19-22
20847049-4	2010	The phosphomimetic p53 (S269D) exhibits characteristics of mutant p53: stable binding to Hsp70 in vivo, elevated ubiquitination in vivo, inactivity in DNA binding and transcription, increased thermoinstability using thermal shift assays, and lambda(max) of intrinsic tryptophan fluorescence at 403 nm rather than 346 nm, characteristic of wild type p53.	Tryptophan	267-277	P53	Homo sapiens	66-69
20847049-4	2010	The phosphomimetic p53 (S269D) exhibits characteristics of mutant p53: stable binding to Hsp70 in vivo, elevated ubiquitination in vivo, inactivity in DNA binding and transcription, increased thermoinstability using thermal shift assays, and lambda(max) of intrinsic tryptophan fluorescence at 403 nm rather than 346 nm, characteristic of wild type p53.	Tryptophan	267-277	P53	Homo sapiens	66-69
20940192-6	2010	CONCLUSION: Polymorphisms in the TP53 and PARP1 genes are involved in inter-individual differences in the response to platinum-based doublet chemotherapy in patients with NSCLC.	Platinum	118-126	P53	Homo sapiens	33-37
21187919-8	2010	Furthermore, the combination of MNP-Fe3O4 with adriamycin or daunorubicin increased p53 protein levels and decreased NF-kappaB protein levels more than adriamycin or daunorubicin alone, indicating that MNP-Fe3O4 could enhance the effect of chemotherapeutic drugs on p53 and NF-kappaB.	Doxorubicin	47-57	P53	Homo sapiens	266-269
20816748-6	2010	Using glutathione pull-down methods, we demonstrate that the C-terminal domain of USP7 contains additional binding sites, a.a. 801-1050 and a.a. 880-1050 for mdm2 and p53, respectively.	Glutathione	6-17	P53	Homo sapiens	167-170
21086258-6	2010	The genotype p53Arg Arg was associated with a low risk for thyroid cancer (OR = 0.15; P &lt; 0.0001), indicating that the arginine allele in homozygosis could have a protective effect against carcinogenesis.	Arginine	122-130	P53	Homo sapiens	13-16
20380827-4	2010	Specifically, we focus on the role of asbestos in augmenting AEC apoptosis by the mitochondria- and p53-regulated death pathways that result from the production of iron-derived reactive oxygen species (ROS) and DNA damage.	Reactive Oxygen Species	202-205	P53	Homo sapiens	100-103
21088491-1	2010	Atomistic simulations of a set of stapled peptides derived from the transactivation domain of p53 (designed by Verdine &amp; colleagues, JACS 2007 129:2456) and complexed to MDM2 reveal that the good binders are uniquely characterized by higher helicity and by extensive interactions between the hydrocarbon staples and the MDM2 surface; in contrast the poor binders have reduced helicity and their staples are mostly solvent exposed.	Adenosine Monophosphate	120-123	P53	Homo sapiens	94-97
21088492-3	2010	In here, we showed that over expression of p53 wild type prevented the phosphorylation of serine 2 in the carboxyl terminal domain (CTD) of RNA polymerase II.	Serine	90-96	P53	Homo sapiens	43-46
21078189-11	2010	Exposure of p53+/+ cells to DCQ induced single strand breaks and triggered the activation of the nuclear kinase ATM by phosphorylation at Ser-1981 in all cell cycle phases.	Decylubiquinol	28-31	P53	Homo sapiens	12-15
21078189-11	2010	Exposure of p53+/+ cells to DCQ induced single strand breaks and triggered the activation of the nuclear kinase ATM by phosphorylation at Ser-1981 in all cell cycle phases.	Serine	138-141	P53	Homo sapiens	12-15
21078189-13	2010	CONCLUSIONS: Collectively, our findings indicate that DCQ reduces the colony survival of HCT116 and induces apoptosis even in cells that are null for p53 or p21, which makes it a molecule of clinical significance, since many resistant colon tumors harbor mutations in p53.	Decylubiquinol	54-57	P53	Homo sapiens	150-153
21078189-13	2010	CONCLUSIONS: Collectively, our findings indicate that DCQ reduces the colony survival of HCT116 and induces apoptosis even in cells that are null for p53 or p21, which makes it a molecule of clinical significance, since many resistant colon tumors harbor mutations in p53.	Decylubiquinol	54-57	P53	Homo sapiens	268-271
21078189-0	2010	Cell death by the quinoxaline dioxide DCQ in human colon cancer cells is enhanced under hypoxia and is independent of p53 and p21.	Decylubiquinol	38-41	P53	Homo sapiens	118-121
21078189-8	2010	In p53-/- cells, 10 muM DCQ significantly reduced HIF-1alpha expression, especially under hypoxia, despite the constitutive expression of this protein in control cells.	Decylubiquinol	24-27	P53	Homo sapiens	3-6
21072901-1	2010	AIM: To investigate p53 mutations in esophageal cancer in a high-risk population, and correlate them with smoking, alcohol consumption and betel chewing.	Alcohols	115-122	P53	Homo sapiens	20-23
20810912-6	2010	Compared with 20% oxygen, exposure of syncytiotrophoblasts to &lt;1% oxygen upregulated hypoxia-inducible factor (HIF)-1alpha and rapidly downregulated p53.	Oxygen	69-75	P53	Homo sapiens	152-155
20810912-7	2010	Activity of p53 in hypoxic syncytiotrophoblasts was reduced by the higher expression of the negative p53 regulator MDMX and by the reduction of phosphorylation of p53 at Ser(392), which reduces p53 activity.	Serine	170-173	P53	Homo sapiens	12-15
20727582-8	2010	Moreover, inhibition of ROS attenuated silica nanoparticles-induced apoptosis and inflammation and the activation of JNK, c-Jun, p53 and NF-kappaB.	Reactive Oxygen Species	24-27	P53	Homo sapiens	129-132
20655883-3	2010	Here, we showed the effects of knocking down plk1 gene through small interference RNA (siRNA) on cell cycle progression, proliferation and chemosensitivity of p53 mutant A431 cells to cisplatin (CDDP).	Cisplatin	184-193	P53	Homo sapiens	159-162
20655883-3	2010	Here, we showed the effects of knocking down plk1 gene through small interference RNA (siRNA) on cell cycle progression, proliferation and chemosensitivity of p53 mutant A431 cells to cisplatin (CDDP).	Cisplatin	195-199	P53	Homo sapiens	159-162
21034513-10	2010	For the most sensitive SMMC-7721 cells, lobaplatin arrested cell cycle progression in G1 and G2/M phases time-dependently which might be associated with the down-regulation of cyclin B, CDK1, CDC25C, phosphorylated CDK1 (pCDK1), pCDK4, Rb, E2F, and pRb, and the up-regulation of p53, p21, and p27.	lobaplatin	40-50	P53	Homo sapiens	279-282
20155316-4	2010	Sildenafil enhanced sensitivity to adriamycin markedly in the p53 mutant MDA-MB231 and p53 null MCF-7/E6 cells and moderately in the MCF-7/caspase 3 and 4T1 cell lines.	Doxorubicin	35-45	P53	Homo sapiens	62-65
20155316-4	2010	Sildenafil enhanced sensitivity to adriamycin markedly in the p53 mutant MDA-MB231 and p53 null MCF-7/E6 cells and moderately in the MCF-7/caspase 3 and 4T1 cell lines.	Doxorubicin	35-45	P53	Homo sapiens	87-90
20978201-7	2010	Marked increase in p53, a downstream target of the activated ATM pathway, was detected only in response to camptothecin and doxorubicin.	Doxorubicin	124-135	P53	Homo sapiens	19-22
22993626-7	2010	The mechanisms involved in the MCF-7 cell proliferation stimulated by zeranol-containing sera may include up-regulation of cyclin D1 and down-regulation of p53 and p21 expression at the mRNA and protein levels in the cells.	Zeranol	70-77	P53	Homo sapiens	156-159
20878061-3	2010	NEEP21 expression is inducible in non-neuronal human cancer cell lines by exposure to adriamycin, hydrogen peroxide, UV and gamma-ray in a p53-dependent manner.	Doxorubicin	86-96	P53	Homo sapiens	139-142
20878061-3	2010	NEEP21 expression is inducible in non-neuronal human cancer cell lines by exposure to adriamycin, hydrogen peroxide, UV and gamma-ray in a p53-dependent manner.	Hydrogen Peroxide	98-115	P53	Homo sapiens	139-142
20878126-11	2010	Some CLL cells in which dexamethasone-mediated killing was enhanced were derived from patients with poor prognostic markers, including p53 mutations and unmutated IgVH genes.	Dexamethasone	24-37	P53	Homo sapiens	135-138
20827489-9	2010	Significant immunohistochemical differences could be detected between PGA with and without adenocarcinoma regarding ki67 and p53.	Folic Acid	70-73	P53	Homo sapiens	125-128
20472336-0	2010	Curcumin causes superoxide anion production and p53-independent apoptosis in human colon cancer cells.	Curcumin	0-8	P53	Homo sapiens	48-51
20472336-3	2010	Curcumin killed wild-type p53 HCT-116 cells and mutant p53 HT-29 cells in a dose- and time-dependent manner.	Curcumin	0-8	P53	Homo sapiens	26-29
20472336-3	2010	Curcumin killed wild-type p53 HCT-116 cells and mutant p53 HT-29 cells in a dose- and time-dependent manner.	Curcumin	0-8	P53	Homo sapiens	55-58
20472336-5	2010	Similar results were obtained when the cytotoxic effect of curcumin was assessed in wild-type p53 HCT-116 cells after siRNA-mediated p53 knockdown.	Curcumin	59-67	P53	Homo sapiens	94-97
20472336-5	2010	Similar results were obtained when the cytotoxic effect of curcumin was assessed in wild-type p53 HCT-116 cells after siRNA-mediated p53 knockdown.	Curcumin	59-67	P53	Homo sapiens	133-136
20472336-6	2010	Chromatin condensation, poly (ADP-ribose) polymerase-1 cleavage and reduced pro-caspase-3 levels in curcumin-treated p53(+/+) and p53(-/-) HCT-116 cells suggested that curcumin caused apoptosis.	Curcumin	100-108	P53	Homo sapiens	117-120
20472336-7	2010	In addition, exposure to curcumin resulted in superoxide anion production and phosphorylation of oxidative stress proteins in p53(+/+) and p53(-/-) HCT-116 cells.	Curcumin	25-33	P53	Homo sapiens	126-129
20472336-7	2010	In addition, exposure to curcumin resulted in superoxide anion production and phosphorylation of oxidative stress proteins in p53(+/+) and p53(-/-) HCT-116 cells.	Curcumin	25-33	P53	Homo sapiens	139-142
21051933-5	2010	Super-induction of p53 by either nutlin-3a or high concentrations of DOX (high-DOX) prevented low-DOX-induced senescence, converting it into quiescence.	Doxorubicin	69-72	P53	Homo sapiens	19-22
21051933-5	2010	Super-induction of p53 by either nutlin-3a or high concentrations of DOX (high-DOX) prevented low-DOX-induced senescence, converting it into quiescence.	Doxorubicin	79-82	P53	Homo sapiens	19-22
21051933-5	2010	Super-induction of p53 by either nutlin-3a or high concentrations of DOX (high-DOX) prevented low-DOX-induced senescence, converting it into quiescence.	Doxorubicin	79-82	P53	Homo sapiens	19-22
20727621-5	2010	The Ru(arene) complexes 6a-c were also more efficacious against combretastatin-refractory p53(+) cells of human HT-29 colon carcinoma when compared to their parent 4-(3,4-dimethoxy-5-methoxy/halo-phenyl)-5-(3-hydroxy-4-methoxyphenyl)-oxazoles 4a-c.	combretastatin	64-78	P53	Homo sapiens	90-93
20878066-0	2010	Amifostine enhancement of the anti-cancer effects of paclitaxel in endometrial cancer is TP53-dependent.	Paclitaxel	53-63	P53	Homo sapiens	89-93
20878066-5	2010	In this report, using a cell line with knock-down p53 expression through siRNA, we found that amifostine enhancement of paclitaxel"s anticancer effect is p53 status-dependent.	Paclitaxel	120-130	P53	Homo sapiens	50-53
20878066-5	2010	In this report, using a cell line with knock-down p53 expression through siRNA, we found that amifostine enhancement of paclitaxel"s anticancer effect is p53 status-dependent.	Paclitaxel	120-130	P53	Homo sapiens	154-157
20878066-8	2010	Sensitivity to the therapeutic effect of paclitaxel in combination with amifostine was dependent upon the status of p53.	Paclitaxel	41-51	P53	Homo sapiens	116-119
20878066-9	2010	A tumor with a nonsense TP53 mutation showed increased therapeutic response to paclitaxel and amifostine as measured by tumor weight compared to a tumor with wild- type TP53.	Paclitaxel	79-89	P53	Homo sapiens	24-28
20878066-10	2010	Our study provides a rationale for a clinical trial of combined paclitaxel and amifostine in endometrial cancer patients whose tumors harbor TP53 mutations.	Paclitaxel	64-74	P53	Homo sapiens	141-145
20601193-0	2010	Manganese superoxide dismutase vs. p53: regulation of mitochondrial ROS.	Reactive Oxygen Species	68-71	P53	Homo sapiens	35-38
20601193-3	2010	p53 affect mitochondrial ROS production, in part, by regulating the expression of the mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD).	Reactive Oxygen Species	25-28	P53	Homo sapiens	0-3
20601193-4	2010	Recent evidence suggests mitochondrial regulation of p53 activity through mechanisms that affect ROS production, and a breakdown of communication amongst mitochondria, p53, and the nucleus can have broad implications in disease development.	Reactive Oxygen Species	97-100	P53	Homo sapiens	53-56
21384570-2	2010	The p53 gene is characterized by Arg/Pro polymorphism in codon 72 whose alleles exhibit differential functional activity.	Arginine	33-36	P53	Homo sapiens	4-7
20807809-3	2010	The aim of this study was to examine the expression of NER gene transcripts, p53, and p21 in melanoma cell lines treated with cisplatin compared with melanocytes.	Cisplatin	126-135	P53	Homo sapiens	77-80
20691179-9	2010	Furthermore, immunoblotting results demonstrated that p53 and p27 were up-regulated suggesting that barberine seems to play a pro-apoptotic role in cancer cells.	barberine	100-109	P53	Homo sapiens	54-57
20821791-0	2010	High specificity in protein recognition by hydrogen-bond-surrogate alpha-helices: selective inhibition of the p53/MDM2 complex.	Hydrogen	43-51	P53	Homo sapiens	110-113
20975832-1	2010	BACKGROUND: The NAD-dependent deacetylase SIRT1 is a nutrient-sensitive coordinator of stress-tolerance, multiple homeostatic processes and healthspan, while p53 is a stress-responsive transcription factor and our paramount tumour suppressor.	NAD	16-19	P53	Homo sapiens	158-161
20976134-0	2010	Mitochondrial uncoupling inhibits p53 mitochondrial translocation in TPA-challenged skin epidermal JB6 cells.	Tetradecanoylphorbol Acetate	69-72	P53	Homo sapiens	34-37
20976134-2	2010	In addition to its transcriptional activation, a fraction of p53 translocates to mitochondria at the very early stage of apoptosis, which eventually contributes to the loss of mitochondrial membrane potential, generation of reactive oxygen species (ROS), cytochrome c release, and caspase activation.	Reactive Oxygen Species	224-247	P53	Homo sapiens	61-64
20976134-2	2010	In addition to its transcriptional activation, a fraction of p53 translocates to mitochondria at the very early stage of apoptosis, which eventually contributes to the loss of mitochondrial membrane potential, generation of reactive oxygen species (ROS), cytochrome c release, and caspase activation.	Reactive Oxygen Species	249-252	P53	Homo sapiens	61-64
20976134-5	2010	Our results showed that mitochondrial uncoupling blocked p53 mitochondrial translocation induced by 12-O-tetradecanoylphorbol 13-acetate (TPA), a known tumor promoter to induce p53-mediated apoptosis in skin carcinogenesis.	Tetradecanoylphorbol Acetate	100-136	P53	Homo sapiens	57-60
20976134-5	2010	Our results showed that mitochondrial uncoupling blocked p53 mitochondrial translocation induced by 12-O-tetradecanoylphorbol 13-acetate (TPA), a known tumor promoter to induce p53-mediated apoptosis in skin carcinogenesis.	Tetradecanoylphorbol Acetate	100-136	P53	Homo sapiens	177-180
20976134-5	2010	Our results showed that mitochondrial uncoupling blocked p53 mitochondrial translocation induced by 12-O-tetradecanoylphorbol 13-acetate (TPA), a known tumor promoter to induce p53-mediated apoptosis in skin carcinogenesis.	Tetradecanoylphorbol Acetate	138-141	P53	Homo sapiens	57-60
20976134-5	2010	Our results showed that mitochondrial uncoupling blocked p53 mitochondrial translocation induced by 12-O-tetradecanoylphorbol 13-acetate (TPA), a known tumor promoter to induce p53-mediated apoptosis in skin carcinogenesis.	Tetradecanoylphorbol Acetate	138-141	P53	Homo sapiens	177-180
20952532-4	2010	In the October 1, 2010, issue of Genes &amp; Development, they introduced us to a novel mechanism of p53 translational control, by which a 5"-3" cap-independent, poly(A)-independent, RNA-RNA interaction enhances p53 translation by binding the ribosomal protein RPL26 following DNA damage.	Adenosine Monophosphate	40-43	P53	Homo sapiens	101-104
20952532-4	2010	In the October 1, 2010, issue of Genes &amp; Development, they introduced us to a novel mechanism of p53 translational control, by which a 5"-3" cap-independent, poly(A)-independent, RNA-RNA interaction enhances p53 translation by binding the ribosomal protein RPL26 following DNA damage.	Adenosine Monophosphate	40-43	P53	Homo sapiens	212-215
20952532-5	2010	Oligonucleotides designed against this 5"-3" untranslated region (UTR) duplex disrupted the binding of RPL26 to p53 mRNA and reduced p53 synthesis and, therefore, function.	Oligonucleotides	0-16	P53	Homo sapiens	112-115
20952532-5	2010	Oligonucleotides designed against this 5"-3" untranslated region (UTR) duplex disrupted the binding of RPL26 to p53 mRNA and reduced p53 synthesis and, therefore, function.	Oligonucleotides	0-16	P53	Homo sapiens	133-136
20807809-7	2010	However, induction of p53 was only significant in the melanocytes at 6 and 24 hours after cisplatin treatment.	Cisplatin	90-99	P53	Homo sapiens	22-25
20807809-8	2010	Inhibition of p53 expression significantly decreased the expression of all the GGR transcripts in melanocytes at 6 and 24 hours after cisplatin treatment.	Cisplatin	134-143	P53	Homo sapiens	14-17
20427142-1	2010	A common polymorphism at codon 72 of human TP53 gene determines a proline to arginine aminoacidic substitution within the proline-rich domain of p53 protein.	Arginine	77-85	P53	Homo sapiens	43-47
20688913-0	2010	ATP binding to Hsp90 is sufficient for effective chaperoning of p53 protein.	Adenosine Triphosphate	0-3	P53	Homo sapiens	64-67
20688913-6	2010	Surprisingly, in the case of WT, but also E42A Hsp90beta, the presence of ATP stimulates dissociation of Hsp90-p53 complexes and results in p53 binding to the promoter sequence.	Adenosine Triphosphate	74-77	P53	Homo sapiens	111-114
20688913-6	2010	Surprisingly, in the case of WT, but also E42A Hsp90beta, the presence of ATP stimulates dissociation of Hsp90-p53 complexes and results in p53 binding to the promoter sequence.	Adenosine Triphosphate	74-77	P53	Homo sapiens	140-143
20688913-9	2010	The ATP-dependent dissociation of p53-Hsp90 complex allows further folding of p53 protein to an active conformation, able to bind to the promoter sequence.	Adenosine Triphosphate	4-7	P53	Homo sapiens	34-37
20688913-9	2010	The ATP-dependent dissociation of p53-Hsp90 complex allows further folding of p53 protein to an active conformation, able to bind to the promoter sequence.	Adenosine Triphosphate	4-7	P53	Homo sapiens	78-81
20688913-11	2010	Altogether, our research indicates that ATP binding to Hsp90beta is a sufficient step for effective WT p53 client protein chaperoning.	Adenosine Triphosphate	40-43	P53	Homo sapiens	103-106
20427142-1	2010	A common polymorphism at codon 72 of human TP53 gene determines a proline to arginine aminoacidic substitution within the proline-rich domain of p53 protein.	Arginine	77-85	P53	Homo sapiens	145-148
20427142-9	2010	Because of the presence of arginine, a selective trypsin proteolytic cleavage at R(72), giving rise to two selective shorter peptides, occurred in p53R(72), but was missing in the case of p53P(72) trypsin digest, in which an uncleaved longer peptide was instead identified.	Arginine	27-35	P53	Homo sapiens	147-150
20849851-1	2010	Homeodomain-interacting protein kinase-2 (HIPK2) is a crucial regulator of p53 apoptotic function by phosphorylating serine 46 (Ser46) in response to DNA damage.	Serine	117-123	P53	Homo sapiens	75-78
20577877-1	2010	The TP53 tumor suppressor gene contains a well-studied polymorphism that encodes either proline (P) or arginine (R) at codon 72, and over half of the world"s population is homozygous for R at this codon.	Arginine	103-111	P53	Homo sapiens	4-8
20655369-8	2010	Inhibition of cellular CYP3A4 or CYP1A/1B suppressed the aflatoxin B(1)- and dimethylbenz[a]anthracene-mediated P53 response, respectively, indicating that HepG2 cells are capable of metabolizing these compounds in a CYP1A/B/3A4-dependent manner.	dimethylbenz	77-89	P53	Homo sapiens	112-115
20679889-1	2010	The objective of this study is to explore the safety, efficacy, and administration method of the recombinant adenovirus p53 gene (rAd-p53, or gendicine) in the treatment of pulmonary metastasis tumor from advanced hepatocellular carcinoma (HCC).	gendicine	142-151	P53	Homo sapiens	120-123
21036715-0	2010	Curcumin-altered p53-response genes regulate radiosensitivity in p53-mutant Ewing"s sarcoma cells.	Curcumin	0-8	P53	Homo sapiens	17-20
21036715-0	2010	Curcumin-altered p53-response genes regulate radiosensitivity in p53-mutant Ewing"s sarcoma cells.	Curcumin	0-8	P53	Homo sapiens	65-68
21036715-1	2010	AIM: Curcumin has been demonstrated to have antitumor effects including radiosensitization by modulating many molecular targets including p53.	Curcumin	5-13	P53	Homo sapiens	138-141
21036715-2	2010	Herein, we investigated the radiosensitizing effect of curcumin in p53 mutant Ewing"s sarcoma (ES) cells.	Curcumin	55-63	P53	Homo sapiens	67-70
21036715-8	2010	CONCLUSION: These results suggest that curcumin potentially radiosensitizes p53-mutant ES cells by regulating IR-modulated p53-response genes.	Curcumin	39-47	P53	Homo sapiens	76-79
21036715-8	2010	CONCLUSION: These results suggest that curcumin potentially radiosensitizes p53-mutant ES cells by regulating IR-modulated p53-response genes.	Curcumin	39-47	P53	Homo sapiens	123-126
21036715-9	2010	However, the curcumin-associated p53-independent regulation of downstream targets remains to be explored.	Curcumin	13-21	P53	Homo sapiens	33-36
20390439-5	2010	Furthermore, cadmium induces cell proliferation, inactivates negative growth stimuli, such as the tumor suppressor protein p53, and provokes resistance towards apoptosis.	Cadmium	13-20	P53	Homo sapiens	123-126
20638924-4	2010	CONCLUSION: We introduced new data related to the contribution of p53 codon 72 to toxicity due to 5-fluorouracil and cyclophosphamide-based neoadjuvant chemotherapy in patients with breast cancer.	Fluorouracil	98-112	P53	Homo sapiens	66-69
20622899-4	2010	The PBK-p53 interaction appears to downmodulate p53 transactivation function as indicated by PBK/TOPK knockdown experiments, which show upregulated expression of the key p53 target gene and cyclin-dependent kinase inhibitor p21 in HCT116 cells, particularly after genotoxic damage from doxorubicin.	Doxorubicin	286-297	P53	Homo sapiens	8-11
20622899-4	2010	The PBK-p53 interaction appears to downmodulate p53 transactivation function as indicated by PBK/TOPK knockdown experiments, which show upregulated expression of the key p53 target gene and cyclin-dependent kinase inhibitor p21 in HCT116 cells, particularly after genotoxic damage from doxorubicin.	Doxorubicin	286-297	P53	Homo sapiens	48-51
20622899-4	2010	The PBK-p53 interaction appears to downmodulate p53 transactivation function as indicated by PBK/TOPK knockdown experiments, which show upregulated expression of the key p53 target gene and cyclin-dependent kinase inhibitor p21 in HCT116 cells, particularly after genotoxic damage from doxorubicin.	Doxorubicin	286-297	P53	Homo sapiens	48-51
21036698-2	2010	Previous studies with 5-FU suggest that proapoptotic protein BAX and tumor suppressor protein TP53 are central factors in this process.	Fluorouracil	22-26	P53	Homo sapiens	94-98
21036698-8	2010	Our results demonstrate the activation of alternative death pathways following treatment with 5-FU, despite mutations in the TP53 and BAX genes.	Fluorouracil	94-98	P53	Homo sapiens	125-129
20413215-5	2010	Here, the relationship between p53 activation and its post-translational modifications was investigated in the human cancer cell lines HepG2 and A549 in response to GA or adriamycin treatment.	Doxorubicin	171-181	P53	Homo sapiens	31-34
20532936-3	2010	Polymorphisms at codon 72 of p53 (arginine (Arg72) to proline transition) confers differences in mitochondrial translocation and apoptosis inducing capabilities of p53 in vitro.	Arginine	34-42	P53	Homo sapiens	29-32
20935493-5	2010	We have found that some genotoxic insults, namely, UV light and cisplatin, lead to proteasomal degradation of L37 in the nucleoplasm and to the ensuing L11-dependent stabilization of p53.	Cisplatin	64-73	P53	Homo sapiens	183-186
20532936-3	2010	Polymorphisms at codon 72 of p53 (arginine (Arg72) to proline transition) confers differences in mitochondrial translocation and apoptosis inducing capabilities of p53 in vitro.	Arginine	34-42	P53	Homo sapiens	164-167
20174822-7	2010	Anti-tumoral effects of Nutlin-3/DOX targeting the p53/MDM2 and p73/MDM2 pathways were evaluated in HCC cell lines.	Doxorubicin	33-36	P53	Homo sapiens	51-54
20837656-4	2010	Short, single-strand oligonucleotides that target this 5"-3"-UTR base-pairing region blunt the binding of RPL26 to p53 mRNA in cells and reduce p53 induction and p53-mediated cell death after several different types of DNA damage and cellular stress.	Oligonucleotides	21-37	P53	Homo sapiens	115-118
20837656-4	2010	Short, single-strand oligonucleotides that target this 5"-3"-UTR base-pairing region blunt the binding of RPL26 to p53 mRNA in cells and reduce p53 induction and p53-mediated cell death after several different types of DNA damage and cellular stress.	Oligonucleotides	21-37	P53	Homo sapiens	144-147
20837656-4	2010	Short, single-strand oligonucleotides that target this 5"-3"-UTR base-pairing region blunt the binding of RPL26 to p53 mRNA in cells and reduce p53 induction and p53-mediated cell death after several different types of DNA damage and cellular stress.	Oligonucleotides	21-37	P53	Homo sapiens	144-147
20837656-5	2010	The ability to reduce stress induction of p53 with oligonucleotides or other small molecules has numerous potential therapeutic uses.	Oligonucleotides	51-67	P53	Homo sapiens	42-45
20811722-0	2010	Effect of rapamycin, an mTOR inhibitor, on radiation sensitivity of lung cancer cells having different p53 gene status.	Sirolimus	10-19	P53	Homo sapiens	103-106
20702634-4	2010	We show that the induction of miR-203 observed during calcium-induced differentiation of HFKs is significantly reduced in HFKs expressing E6 and in p53i HFKs.	Calcium	54-61	P53	Homo sapiens	148-151
21063838-4	2010	The expression of apoptosis related p53 and Bcl-2 protein and the second messenger calcium were detected respectively by Western blotting, patch clamp and confocal calcium imaging.	Calcium	164-171	P53	Homo sapiens	36-39
20594980-0	2010	24R,25-Dihydroxyvitamin D3, lysophosphatidic acid, and p53: a signaling axis in the inhibition of phosphate-induced chondrocyte apoptosis.	Phosphates	98-107	P53	Homo sapiens	55-58
20412452-4	2010	Therefore, P53 Arg is an ameloblastoma-susceptible allele [OR (95% CI) = 2.06 (1.28-3.31), P = 0.002].	Arginine	15-18	P53	Homo sapiens	11-14
20567883-3	2010	We find that both SPE B and G308S can stimulate the serine phosphorylation of p53, and p53 phosphorylation is inhibited by the anti-Fas antibody but not by anti-alpha(V)beta(3) antibody.	Serine	52-58	P53	Homo sapiens	78-81
20577896-4	2010	Here we show that this p53 reduction is suppressed by transfecting cells with Mdm2 antisense oligonucleotides or small interfering RNA.	Oligonucleotides	93-109	P53	Homo sapiens	23-26
21103079-3	2010	The level of p27 was decreased by hydrogen peroxide in a dose-dependent manner in human colon carcinoma HCT 116 (p53-positive) cells while it was increased upon exposure to hydrogen peroxide in HT 29 (p53-negative) cells.	Hydrogen Peroxide	34-51	P53	Homo sapiens	113-116
21103079-3	2010	The level of p27 was decreased by hydrogen peroxide in a dose-dependent manner in human colon carcinoma HCT 116 (p53-positive) cells while it was increased upon exposure to hydrogen peroxide in HT 29 (p53-negative) cells.	Hydrogen Peroxide	173-190	P53	Homo sapiens	201-204
20412452-6	2010	Therefore, the increased risk associated with P53 Arg may not be influenced by either the sex of patients or clinical characteristics of the tumours.	Arginine	50-53	P53	Homo sapiens	46-49
20412452-7	2010	Moreover, when compared with homozygous P53 Pro, people who carried the Arg allele had a remarkably high risk of developing ameloblastoma [adjusted OR (95% CI) = 7.26 (2.34-23.41), P &lt; 10(-3)].	Arginine	72-75	P53	Homo sapiens	40-43
20412452-8	2010	CONCLUSION: The Arg allele of P53 gene codon 72 may increase susceptibility, and P53 may be important in the aetiology of ameloblastoma.	Arginine	16-19	P53	Homo sapiens	30-33
20547212-10	2010	Annexin V plays an important role in maintenance of calcium homeostasis which when disturbed can activate a p53-dependent cell death.	Calcium	52-59	P53	Homo sapiens	108-111
20590525-0	2010	p38(MAPK)/p53 signalling axis mediates neuronal apoptosis in response to tetrahydrobiopterin-induced oxidative stress and glucose uptake inhibition: implication for neurodegeneration.	Glucose	122-129	P53	Homo sapiens	10-13
20840120-0	2010	TRP-ing off the p53 apoptotic switch.	Tryptophan	0-3	P53	Homo sapiens	16-19
20562916-5	2010	Inhibiting DUSP26 expression in the IMR-32 neuroblastoma cell line enhanced doxorubicin-induced p53 phosphorylation at Ser20 and Ser37, p21, Puma, Bax expression as well as apoptosis.	Doxorubicin	76-87	P53	Homo sapiens	96-99
21092505-15	2010	Only malignant tumors showed positive immunoreactivity for Ki-67 staining and P53 staining (20% &amp; 34% respectively).	Adenosine Monophosphate	97-100	P53	Homo sapiens	78-81
20624405-1	2010	AIMS: the aims of the study are to investigate the additive effect of exogenous short-carbon chain phospholipids, C(2)-ceramide, on an anti-cancer drug paclitaxel (PTX)-induced senescence of human non-small cell lung cancer (NSCLC) cells deficient in functional p53 and p16, and to examine whether mitogen-activated protein kinase (MAPK) plays a role in ceramide-sensitized senescence of NSCLC cells.	Phospholipids	99-112	P53	Homo sapiens	262-265
20624405-1	2010	AIMS: the aims of the study are to investigate the additive effect of exogenous short-carbon chain phospholipids, C(2)-ceramide, on an anti-cancer drug paclitaxel (PTX)-induced senescence of human non-small cell lung cancer (NSCLC) cells deficient in functional p53 and p16, and to examine whether mitogen-activated protein kinase (MAPK) plays a role in ceramide-sensitized senescence of NSCLC cells.	Paclitaxel	152-162	P53	Homo sapiens	262-265
20624405-1	2010	AIMS: the aims of the study are to investigate the additive effect of exogenous short-carbon chain phospholipids, C(2)-ceramide, on an anti-cancer drug paclitaxel (PTX)-induced senescence of human non-small cell lung cancer (NSCLC) cells deficient in functional p53 and p16, and to examine whether mitogen-activated protein kinase (MAPK) plays a role in ceramide-sensitized senescence of NSCLC cells.	Paclitaxel	164-167	P53	Homo sapiens	262-265
20720205-9	2010	Furthermore, DMBA-3,4-dihydrodiol-1,2-epoxide, a DNA-reactive metabolite of DMBA, was sufficient to upregulate p53, induce caspase-9 cleavage, and initiate B cell apoptosis in the absence of stromal cells, suggesting that production of this metabolite by the stromal cells and transfer to the B cells are proximal events in triggering apoptosis.	dmba-3,4-dihydrodiol-1,2-epoxide	13-45	P53	Homo sapiens	111-114
20562916-6	2010	In contrast, DUSP26 overexpression in the SK-N-SH cell line inhibited doxorubicin-induced p53 phosphorylation at Ser20 and Ser37, p21, Puma, Bax expression and apoptosis.	Doxorubicin	70-81	P53	Homo sapiens	90-93
20945139-8	2010	Importantly, the synergistic effect of CsA or SFA with cisplatin was shown even in p53 defective Hep3B cells.	Cyclosporine	39-42	P53	Homo sapiens	83-86
20732856-4	2010	We observed an increased risk of cervical cancer associated with the p53 Arg/Arg (OR, 2.25; 95% CI, 1.11-4.54) or p21 Ser/Ser (OR, 2.09; 95% CI, 1.04-4.19) genotype, compared with the p53 Pro/Pro or p21 Arg/Arg genotype, respectively.	Arginine	77-80	P53	Homo sapiens	69-72
20732856-4	2010	We observed an increased risk of cervical cancer associated with the p53 Arg/Arg (OR, 2.25; 95% CI, 1.11-4.54) or p21 Ser/Ser (OR, 2.09; 95% CI, 1.04-4.19) genotype, compared with the p53 Pro/Pro or p21 Arg/Arg genotype, respectively.	Arginine	77-80	P53	Homo sapiens	69-72
20732856-5	2010	In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes.	Arginine	208-211	P53	Homo sapiens	41-44
20732856-5	2010	In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes.	Arginine	208-211	P53	Homo sapiens	204-207
20732856-5	2010	In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes.	Arginine	212-215	P53	Homo sapiens	41-44
20732856-5	2010	In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes.	Arginine	212-215	P53	Homo sapiens	204-207
20732856-5	2010	In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes.	Serine	224-227	P53	Homo sapiens	41-44
20732856-5	2010	In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes.	Serine	224-227	P53	Homo sapiens	204-207
20732856-5	2010	In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes.	Serine	228-231	P53	Homo sapiens	41-44
20732856-5	2010	In additional, interaction between these p53 and p21 polymorphisms increased the risk of cervical cancer in a multiplicative manner, with the OR being 3.96 (95% CI, 1.51-10.41) for subjects carrying both p53 Arg/Arg and p21 Ser/Ser genotypes.	Serine	228-231	P53	Homo sapiens	204-207
20944137-0	2010	Increasing p53 protein sensitizes non-small cell lung cancer to paclitaxel and cisplatin in vitro.	Paclitaxel	64-74	P53	Homo sapiens	11-14
20944137-0	2010	Increasing p53 protein sensitizes non-small cell lung cancer to paclitaxel and cisplatin in vitro.	Cisplatin	79-88	P53	Homo sapiens	11-14
20944137-7	2010	A significant positive correlation between p53 protein concentration and cytotoxic response was demonstrated (R(2) for CDDP=0.823; R(2) for PAX=0.909; p&lt;0.001).	Cisplatin	119-123	P53	Homo sapiens	43-46
20944137-7	2010	A significant positive correlation between p53 protein concentration and cytotoxic response was demonstrated (R(2) for CDDP=0.823; R(2) for PAX=0.909; p&lt;0.001).	Paclitaxel	140-143	P53	Homo sapiens	43-46
20944137-8	2010	CONCLUSION: Increasing intracellular p53 protein concentrations can augment the effect of CDDP and PAX in NSCLC, despite the baseline level of p53 protein expression.	Cisplatin	90-94	P53	Homo sapiens	37-40
20944137-8	2010	CONCLUSION: Increasing intracellular p53 protein concentrations can augment the effect of CDDP and PAX in NSCLC, despite the baseline level of p53 protein expression.	Paclitaxel	99-102	P53	Homo sapiens	37-40
20732856-4	2010	We observed an increased risk of cervical cancer associated with the p53 Arg/Arg (OR, 2.25; 95% CI, 1.11-4.54) or p21 Ser/Ser (OR, 2.09; 95% CI, 1.04-4.19) genotype, compared with the p53 Pro/Pro or p21 Arg/Arg genotype, respectively.	Arginine	73-76	P53	Homo sapiens	69-72
20732856-4	2010	We observed an increased risk of cervical cancer associated with the p53 Arg/Arg (OR, 2.25; 95% CI, 1.11-4.54) or p21 Ser/Ser (OR, 2.09; 95% CI, 1.04-4.19) genotype, compared with the p53 Pro/Pro or p21 Arg/Arg genotype, respectively.	Arginine	77-80	P53	Homo sapiens	69-72
20945139-8	2010	Importantly, the synergistic effect of CsA or SFA with cisplatin was shown even in p53 defective Hep3B cells.	Cisplatin	55-64	P53	Homo sapiens	83-86
20945139-10	2010	In conclusion, CsA or SFA synergistically enhances cisplatin-induced apoptosis in HCC cells including the p53-defective Hep3B.	Cyclosporine	15-18	P53	Homo sapiens	106-109
20536385-0	2010	Wild type p53-dependent transcriptional upregulation of cathepsin L expression is mediated by C/EBP&amp;#x03B1; in human glioblastoma cells.	Adenosine Monophosphate	100-103	P53	Homo sapiens	10-13
20945139-10	2010	In conclusion, CsA or SFA synergistically enhances cisplatin-induced apoptosis in HCC cells including the p53-defective Hep3B.	Cisplatin	51-60	P53	Homo sapiens	106-109
20610613-6	2010	RESULTS: Here, we present a manually curated TCDD-mediated AhR signaling pathway including crosstalks with the hypoxia pathway that copes with oxygen deficiency and the p53 pathway that induces a DNA damage response.	Polychlorinated Dibenzodioxins	45-49	P53	Homo sapiens	169-172
20610613-8	2010	Using the mathematical model, we have investigated: (i) TCDD dose-dependent effects on AhR target genes; (ii) the crosstalk effect between AhR and hypoxia signals; and (iii) p53 inhibition effect of TCDD-liganded AhR.	Polychlorinated Dibenzodioxins	199-203	P53	Homo sapiens	174-177
20526748-1	2010	Cisplatin and doxorubicin are widely used anticancer drugs that cause DNA damage, which activates the ATM-Chk2-p53 pathway in cancer cells.	Cisplatin	0-9	P53	Homo sapiens	111-114
20526748-1	2010	Cisplatin and doxorubicin are widely used anticancer drugs that cause DNA damage, which activates the ATM-Chk2-p53 pathway in cancer cells.	Doxorubicin	14-25	P53	Homo sapiens	111-114
20600834-5	2010	Untreated HCT116 cells showed low levels of glut-p53, which increased markedly after H(2)O(2), diamide, cisplatin, and doxorubicin treatments.	Cisplatin	104-113	P53	Homo sapiens	49-52
20630997-9	2010	P53 KDs with lower nontreated BARs were less sensitive to TRAIL and cisplatinum than wild-type.	Cisplatin	68-79	P53	Homo sapiens	0-3
20047843-9	2010	While limited clinical data suggest that p53 mutations are associated with resistance to platinum-based therapies in NSCLC, data on p53 IHC positivity are equivocal.	Platinum	89-97	P53	Homo sapiens	41-44
20600834-0	2010	Cys-141 glutathionylation of human p53: Studies using specific polyclonal antibodies in cancer samples and cell lines.	Cysteine	0-3	P53	Homo sapiens	35-38
20600834-1	2010	Previously, we reported that human p53 is functionally inactivated by S-glutathionylation at Cys-141 during oxidative and DNA-damaging treatments.	Cysteine	93-96	P53	Homo sapiens	35-38
20600834-5	2010	Untreated HCT116 cells showed low levels of glut-p53, which increased markedly after H(2)O(2), diamide, cisplatin, and doxorubicin treatments.	Doxorubicin	119-130	P53	Homo sapiens	49-52
20600834-9	2010	Human prostate and prostate cancer tissues showed an abundant presence of glut-p53 in luminal epithelium, a site well known to generate ROS.	ros	136-139	P53	Homo sapiens	79-82
20827430-4	2010	However, we found that the p53 Arg72Pro was associated with an increased risk of esophageal cancer ((Pro/Arg +Pro/Pro) versus Arg/Arg: OR=1.20, 95%CI=1.06-1.36) without any between-study heterogeneity.	Arginine	31-34	P53	Homo sapiens	27-30
19800779-8	2010	Moreover, resveratrol significantly enhanced p53-dependent transcriptional activity, but slightly reduced NF-kappaB-dependent transcriptional activity.	Resveratrol	10-21	P53	Homo sapiens	45-48
20017137-0	2010	Cooperation of tumor-derived HBx mutants and p53-249(ser) mutant in regulating cell proliferation, anchorage-independent growth and aneuploidy in a telomerase-immortalized normal human hepatocyte-derived cell line.	Serine	53-56	P53	Homo sapiens	45-48
20017137-2	2010	Convincing epidemiological and experimental evidence also links HCC to aflatoxin, a naturally occurring mycotoxin that produces a signature p53-249(ser) mutation.	Serine	148-151	P53	Homo sapiens	140-143
20017137-8	2010	p53-249(ser) rescued CNT-mediated inhibition of colony formation.	Serine	8-11	P53	Homo sapiens	0-3
20017137-9	2010	Although HHT4 cells lacked an anchorage independent growth capability as they did not form any colonies in soft agar, the CT-expressing HHT4 cells could form colonies, which could be significantly enhanced by p53-249(ser).	Serine	217-220	P53	Homo sapiens	209-212
19771536-4	2010	The purpose of this study was to examine whether p53 Arg at the polymorphic position 72 could represents a risk factor for women with high-risk HPV-associated malignant cervical lesions.	Arginine	53-56	P53	Homo sapiens	49-52
20827430-4	2010	However, we found that the p53 Arg72Pro was associated with an increased risk of esophageal cancer ((Pro/Arg +Pro/Pro) versus Arg/Arg: OR=1.20, 95%CI=1.06-1.36) without any between-study heterogeneity.	Arginine	105-108	P53	Homo sapiens	27-30
20827430-4	2010	However, we found that the p53 Arg72Pro was associated with an increased risk of esophageal cancer ((Pro/Arg +Pro/Pro) versus Arg/Arg: OR=1.20, 95%CI=1.06-1.36) without any between-study heterogeneity.	Arginine	105-108	P53	Homo sapiens	27-30
20827430-5	2010	In the stratified analysis by ethnicity, we found that the increased esophageal cancer risk associated with p53 Arg72Pro polymorphism was more evident in Asian group ((Pro/Arg +Pro/Pro) versus Arg/Arg: OR=1.35, 95%CI=1.14-1.60, P=0.09 for heterogeneity test), although we still failed to find any significant association between GSTP1 Ile105Val polymorphism and esophageal cancer risk in different ethnicity.	Arginine	112-115	P53	Homo sapiens	108-111
20827430-5	2010	In the stratified analysis by ethnicity, we found that the increased esophageal cancer risk associated with p53 Arg72Pro polymorphism was more evident in Asian group ((Pro/Arg +Pro/Pro) versus Arg/Arg: OR=1.35, 95%CI=1.14-1.60, P=0.09 for heterogeneity test), although we still failed to find any significant association between GSTP1 Ile105Val polymorphism and esophageal cancer risk in different ethnicity.	Arginine	172-175	P53	Homo sapiens	108-111
20827430-5	2010	In the stratified analysis by ethnicity, we found that the increased esophageal cancer risk associated with p53 Arg72Pro polymorphism was more evident in Asian group ((Pro/Arg +Pro/Pro) versus Arg/Arg: OR=1.35, 95%CI=1.14-1.60, P=0.09 for heterogeneity test), although we still failed to find any significant association between GSTP1 Ile105Val polymorphism and esophageal cancer risk in different ethnicity.	Arginine	172-175	P53	Homo sapiens	108-111
20656010-7	2010	In addition, the increased expression of p53 was also observed in berberine-treated HeLa cells, and as a node point of these different pathways in a protein-protein interaction network constructed by GeneGo software, p53 might be the possible drug-target of berberine"s anti-cancer on HeLa cells, which was predicted by a flexible ligand-protein inverse docking program, INVDOCK.	Berberine	66-75	P53	Homo sapiens	41-44
20525765-0	2010	Levetiracetam enhances p53-mediated MGMT inhibition and sensitizes glioblastoma cells to temozolomide.	Levetiracetam	0-13	P53	Homo sapiens	23-26
20525765-5	2010	Chromatin immunoprecipitation analysis reveals that LEV enhances p53 binding on the MGMT promoter by recruiting the mSin3A/histone deacetylase 1 (HDAC1) corepressor complex.	Levetiracetam	52-55	P53	Homo sapiens	65-68
21103216-5	2010	Proline to alanine substitutions at P53, P481, P484, and P485 in the V42C background, as well as P53, P481, and P484 in the G489C background, exhibited decreased nucleotidase activities.	Alanine	11-18	P53	Homo sapiens	36-39
21103216-6	2010	More importantly, alanine substitutions at P53 and P481 in the V42C background and P481 in the G489C background no longer exhibited the ATP-induced decrease in transmembrane cross-linking efficiency.	Alanine	18-25	P53	Homo sapiens	43-46
21103216-6	2010	More importantly, alanine substitutions at P53 and P481 in the V42C background and P481 in the G489C background no longer exhibited the ATP-induced decrease in transmembrane cross-linking efficiency.	Adenosine Triphosphate	136-139	P53	Homo sapiens	43-46
20656010-7	2010	In addition, the increased expression of p53 was also observed in berberine-treated HeLa cells, and as a node point of these different pathways in a protein-protein interaction network constructed by GeneGo software, p53 might be the possible drug-target of berberine"s anti-cancer on HeLa cells, which was predicted by a flexible ligand-protein inverse docking program, INVDOCK.	Berberine	66-75	P53	Homo sapiens	217-220
20656010-7	2010	In addition, the increased expression of p53 was also observed in berberine-treated HeLa cells, and as a node point of these different pathways in a protein-protein interaction network constructed by GeneGo software, p53 might be the possible drug-target of berberine"s anti-cancer on HeLa cells, which was predicted by a flexible ligand-protein inverse docking program, INVDOCK.	Berberine	258-267	P53	Homo sapiens	41-44
20656010-7	2010	In addition, the increased expression of p53 was also observed in berberine-treated HeLa cells, and as a node point of these different pathways in a protein-protein interaction network constructed by GeneGo software, p53 might be the possible drug-target of berberine"s anti-cancer on HeLa cells, which was predicted by a flexible ligand-protein inverse docking program, INVDOCK.	Berberine	258-267	P53	Homo sapiens	217-220
20643100-2	2010	Previous data indicated that the cytosolic serine peptidase tripeptidyl-peptidase II (TPPII) translocates into the nucleus of most tumor cell lines in response to gamma-irradiation and ROS production; an event that promoted p53 expression as well as caspase-activation.	Reactive Oxygen Species	185-188	P53	Homo sapiens	224-227
20630574-8	2010	However, a significantly decreased risk of bladder cancer was associated with TP53 genotypes for Arg/Arg versus Pro/Pro (odds ratio 0.74, 95% confidence interval 0.55-0.99) and Arg/Arg plus Arg/Pro versus Pro/Pro (odds ratio 0.77, 95% confidence interval 0.59-1.00) in Asians.	Arginine	97-100	P53	Homo sapiens	78-82
20630574-8	2010	However, a significantly decreased risk of bladder cancer was associated with TP53 genotypes for Arg/Arg versus Pro/Pro (odds ratio 0.74, 95% confidence interval 0.55-0.99) and Arg/Arg plus Arg/Pro versus Pro/Pro (odds ratio 0.77, 95% confidence interval 0.59-1.00) in Asians.	Arginine	101-104	P53	Homo sapiens	78-82
20630574-8	2010	However, a significantly decreased risk of bladder cancer was associated with TP53 genotypes for Arg/Arg versus Pro/Pro (odds ratio 0.74, 95% confidence interval 0.55-0.99) and Arg/Arg plus Arg/Pro versus Pro/Pro (odds ratio 0.77, 95% confidence interval 0.59-1.00) in Asians.	Arginine	101-104	P53	Homo sapiens	78-82
20630574-8	2010	However, a significantly decreased risk of bladder cancer was associated with TP53 genotypes for Arg/Arg versus Pro/Pro (odds ratio 0.74, 95% confidence interval 0.55-0.99) and Arg/Arg plus Arg/Pro versus Pro/Pro (odds ratio 0.77, 95% confidence interval 0.59-1.00) in Asians.	Arginine	101-104	P53	Homo sapiens	78-82
20630574-8	2010	However, a significantly decreased risk of bladder cancer was associated with TP53 genotypes for Arg/Arg versus Pro/Pro (odds ratio 0.74, 95% confidence interval 0.55-0.99) and Arg/Arg plus Arg/Pro versus Pro/Pro (odds ratio 0.77, 95% confidence interval 0.59-1.00) in Asians.	Arginine	101-104	P53	Homo sapiens	78-82
20696891-6	2010	While 17beta-estradiol (E2) enhanced ERalpha binding to p53 and inhibited p21 transcription, antiestrogens decreased ERalpha recruitment and induced transcription.	Estradiol	6-22	P53	Homo sapiens	56-59
20696891-10	2010	Furthermore, retrospective studies analyzing response to tamoxifen therapy in a subset of patients with ER-positive breast cancer expressing either wild-type or mutant p53 suggest that the presence of wild-type p53 is an important determinant of positive therapeutic response.	Tamoxifen	57-66	P53	Homo sapiens	168-171
20696891-10	2010	Furthermore, retrospective studies analyzing response to tamoxifen therapy in a subset of patients with ER-positive breast cancer expressing either wild-type or mutant p53 suggest that the presence of wild-type p53 is an important determinant of positive therapeutic response.	Tamoxifen	57-66	P53	Homo sapiens	211-214
20808790-5	2010	The mitochondrial kinase activity of cyclin B1/Cdk1 was found to specifically phosphorylate p53 at Ser-315 residue, leading to enhanced mitochondrial ATP production and reduced mitochondrial apoptosis.	Serine	99-102	P53	Homo sapiens	92-95
20808879-6	2010	We also present NetWalk analysis of microarray gene expression data from MCF7 cells exposed to different doses of doxorubicin, which reveals a switch-like pattern in the p53 regulated network in cell cycle arrest and apoptosis.	Doxorubicin	114-125	P53	Homo sapiens	170-173
20808790-5	2010	The mitochondrial kinase activity of cyclin B1/Cdk1 was found to specifically phosphorylate p53 at Ser-315 residue, leading to enhanced mitochondrial ATP production and reduced mitochondrial apoptosis.	Adenosine Triphosphate	150-153	P53	Homo sapiens	92-95
20808790-7	2010	Enforced translocation of cyclin B1 and Cdk1 into mitochondria with a mitochondrial-targeting-peptide increased levels of Ser-315 phosphorylation on mitochondrial p53, improved ATP production and decreased apoptosis by sequestering p53 from binding to Bcl-2 and Bcl-xL.	Serine	122-125	P53	Homo sapiens	163-166
20808790-7	2010	Enforced translocation of cyclin B1 and Cdk1 into mitochondria with a mitochondrial-targeting-peptide increased levels of Ser-315 phosphorylation on mitochondrial p53, improved ATP production and decreased apoptosis by sequestering p53 from binding to Bcl-2 and Bcl-xL.	Serine	122-125	P53	Homo sapiens	232-235
20435884-3	2010	Losses of TP53 and CDKN2A, observed in 8% and 35% of patients, respectively, were significantly associated with a shorter survival after rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) treatment, independently of the International Prognostic Index and of the cell of origin.	Doxorubicin	166-177	P53	Homo sapiens	10-14
20727180-0	2010	Nicotine-induced survival signaling in lung cancer cells is dependent on their p53 status while its down-regulation by curcumin is independent.	Nicotine	0-8	P53	Homo sapiens	79-82
20727180-3	2010	We observed that the proliferative index of nicotine is different in the lung cancer cell lines H1299 (p53-/-) and A549 (p53+/+) which indicates that the mode of up-regulation of survival signals by nicotine might be different in cells with and without p53.	Nicotine	44-52	P53	Homo sapiens	103-106
20727180-3	2010	We observed that the proliferative index of nicotine is different in the lung cancer cell lines H1299 (p53-/-) and A549 (p53+/+) which indicates that the mode of up-regulation of survival signals by nicotine might be different in cells with and without p53.	Nicotine	44-52	P53	Homo sapiens	121-124
20727180-3	2010	We observed that the proliferative index of nicotine is different in the lung cancer cell lines H1299 (p53-/-) and A549 (p53+/+) which indicates that the mode of up-regulation of survival signals by nicotine might be different in cells with and without p53.	Nicotine	44-52	P53	Homo sapiens	121-124
20727180-3	2010	We observed that the proliferative index of nicotine is different in the lung cancer cell lines H1299 (p53-/-) and A549 (p53+/+) which indicates that the mode of up-regulation of survival signals by nicotine might be different in cells with and without p53.	Nicotine	199-207	P53	Homo sapiens	103-106
20727180-3	2010	We observed that the proliferative index of nicotine is different in the lung cancer cell lines H1299 (p53-/-) and A549 (p53+/+) which indicates that the mode of up-regulation of survival signals by nicotine might be different in cells with and without p53.	Nicotine	199-207	P53	Homo sapiens	121-124
20727180-3	2010	We observed that the proliferative index of nicotine is different in the lung cancer cell lines H1299 (p53-/-) and A549 (p53+/+) which indicates that the mode of up-regulation of survival signals by nicotine might be different in cells with and without p53.	Nicotine	199-207	P53	Homo sapiens	121-124
20727180-7	2010	The hypothesis was confirmed when lower concentrations of nicotine induced NF-kappaB in two more lung cancer cells, Hop-92 and NCI-H522 with mutant p53 status.	Nicotine	58-66	P53	Homo sapiens	148-151
20727180-8	2010	Silencing of p53 in A549 using siRNA made the cells susceptible to nicotine-induced NF-kappaB nuclear translocation as in A549 DN-p53 cells.	Nicotine	67-75	P53	Homo sapiens	13-16
20727180-8	2010	Silencing of p53 in A549 using siRNA made the cells susceptible to nicotine-induced NF-kappaB nuclear translocation as in A549 DN-p53 cells.	Nicotine	67-75	P53	Homo sapiens	130-133
20727180-9	2010	CONCLUSIONS: The present study reveals a detrimental role of nicotine especially in lung cancer patients with impaired p53 status and identifies curcumin as a potential chemopreventive.	Nicotine	61-69	P53	Homo sapiens	119-122
20808790-8	2010	Furthermore, reconstitution of wild-type p53 in p53-deficient HCT116 p53(-/-) cells resulted in an increased mitochondrial ATP production and suppression of apoptosis.	Adenosine Triphosphate	123-126	P53	Homo sapiens	41-44
20808790-8	2010	Furthermore, reconstitution of wild-type p53 in p53-deficient HCT116 p53(-/-) cells resulted in an increased mitochondrial ATP production and suppression of apoptosis.	Adenosine Triphosphate	123-126	P53	Homo sapiens	48-51
20808790-8	2010	Furthermore, reconstitution of wild-type p53 in p53-deficient HCT116 p53(-/-) cells resulted in an increased mitochondrial ATP production and suppression of apoptosis.	Adenosine Triphosphate	123-126	P53	Homo sapiens	48-51
20808790-10	2010	These results demonstrate a unique anti-apoptotic function of mitochondrial p53 regulated by cyclin B1/Cdk1-mediated Ser-315 phosphorylation in p53-wild-type tumor cells, which may provide insights for improving the efficacy of anti-cancer therapy, especially for tumors that retain p53.	Serine	117-120	P53	Homo sapiens	76-79
20808790-10	2010	These results demonstrate a unique anti-apoptotic function of mitochondrial p53 regulated by cyclin B1/Cdk1-mediated Ser-315 phosphorylation in p53-wild-type tumor cells, which may provide insights for improving the efficacy of anti-cancer therapy, especially for tumors that retain p53.	Serine	117-120	P53	Homo sapiens	144-147
20808790-10	2010	These results demonstrate a unique anti-apoptotic function of mitochondrial p53 regulated by cyclin B1/Cdk1-mediated Ser-315 phosphorylation in p53-wild-type tumor cells, which may provide insights for improving the efficacy of anti-cancer therapy, especially for tumors that retain p53.	Serine	117-120	P53	Homo sapiens	144-147
20452410-7	2010	Moreover, DOXO solutions, even at low concentration, cause apoptosis in epithelial cells, through activation of intrinsic pathway p53-independent.	Doxorubicin	10-14	P53	Homo sapiens	130-133
20682800-0	2010	Targeting wild-type and mutant p53 with small molecule CP-31398 blocks the growth of rhabdomyosarcoma by inducing reactive oxygen species-dependent apoptosis.	Reactive Oxygen Species	114-137	P53	Homo sapiens	31-34
20682800-8	2010	Apoptosis induced by CP-31398 occurred with translocation of p53 to mitochondria, leading to altered mitochondrial membrane potential, cytochrome c release, and reactive oxygen species release.	Reactive Oxygen Species	161-184	P53	Homo sapiens	61-64
20514025-4	2010	The tumor suppressor homeodomain-interacting protein kinase-2 (HIPK2) is a crucial regulator of p53 apoptotic function by phosphorylating its N-terminal serine 46 (Ser46) and facilitating Lys382 acetylation at the C-terminus.	Serine	153-159	P53	Homo sapiens	96-99
20703075-4	2010	We previously reported that the highly conserved p53 Arg(R)-174 is substituted by lysine (K) in Spalax, identical to a tumor-associated mutation.	Arginine	53-56	P53	Homo sapiens	49-52
20703075-4	2010	We previously reported that the highly conserved p53 Arg(R)-174 is substituted by lysine (K) in Spalax, identical to a tumor-associated mutation.	Lysine	82-88	P53	Homo sapiens	49-52
20704765-5	2010	When 5-FU and LY were treated in single and sequential combinations, the expression of p-AKT, p-NFkB, p-p53 and bcl-2 was observed on different concentrations by Western blot analysis.	Fluorouracil	5-9	P53	Homo sapiens	104-107
20704765-12	2010	In sequential combination of 5-FU and LY, the expression of p-p53 was increased and bcl-2 expression was diminished compared to 5-FU alone.	Fluorouracil	29-33	P53	Homo sapiens	62-65
20706634-13	2010	Reduced formation of reactive oxygen species in HIF-1alpha-competent cells was identified as the molecular mechanism of HIF-1alpha-mediated inhibition of p53.	Reactive Oxygen Species	21-44	P53	Homo sapiens	154-157
20614940-1	2010	Protein lysine methyltransferase G9a, which catalyzes methylation of lysine 9 of histone H3 (H3K9) and lysine 373 (K373) of p53, is overexpressed in human cancers.	Lysine	8-14	P53	Homo sapiens	124-127
20614940-1	2010	Protein lysine methyltransferase G9a, which catalyzes methylation of lysine 9 of histone H3 (H3K9) and lysine 373 (K373) of p53, is overexpressed in human cancers.	Lysine	69-75	P53	Homo sapiens	124-127
20624391-0	2010	Elevation of cyclic AMP causes an imbalance between NF-kappaB and p53 in NALM-6 cells treated by doxorubicin.	Cyclic AMP	13-23	P53	Homo sapiens	66-69
20624391-0	2010	Elevation of cyclic AMP causes an imbalance between NF-kappaB and p53 in NALM-6 cells treated by doxorubicin.	Doxorubicin	97-108	P53	Homo sapiens	66-69
20624391-1	2010	We previously showed that cAMP can inhibit DNA damage-induced wild type p53 accumulation in human pre-B NALM-6 cells, leading to a profound reduction of their apoptotic response.	Cyclic AMP	26-30	P53	Homo sapiens	72-75
20631301-1	2010	The longevity-promoting NAD+-dependent class III histone deacetylase Sirtuin 1 (SIRT1) is involved in stem cell function by controlling cell fate decision and/or by regulating the p53-dependent expression of NANOG.	NAD	24-28	P53	Homo sapiens	180-183
20729567-3	2010	The control of ROS and senescence by p53 may help to explain how p53 can function to both restrain and promote aging.	ros	15-18	P53	Homo sapiens	37-40
20682067-0	2010	Alpha-santalol, a chemopreventive agent against skin cancer, causes G2/M cell cycle arrest in both p53-mutated human epidermoid carcinoma A431 cells and p53 wild-type human melanoma UACC-62 cells.	a-santalol	0-14	P53	Homo sapiens	99-102
20682067-0	2010	Alpha-santalol, a chemopreventive agent against skin cancer, causes G2/M cell cycle arrest in both p53-mutated human epidermoid carcinoma A431 cells and p53 wild-type human melanoma UACC-62 cells.	a-santalol	0-14	P53	Homo sapiens	153-156
20682067-3	2010	Thus, the objective of this study was to investigate effects of alpha-santalol on cell cycle progression in both p53 mutated human epidermoid carcinoma A431 cells and p53 wild-type human melanoma UACC-62 cells to elucidate the mechanism(s) of action.	a-santalol	64-78	P53	Homo sapiens	113-116
20682067-8	2010	alpha-Santalol treatment up-regulated the expression of p21 and suppressed expressions of mutated p53 in A431 cells; whereas, alpha-santalol treatment increased expressions of wild-type p53 in UACC-62 cells.	a-santalol	0-14	P53	Homo sapiens	98-101
20682067-8	2010	alpha-Santalol treatment up-regulated the expression of p21 and suppressed expressions of mutated p53 in A431 cells; whereas, alpha-santalol treatment increased expressions of wild-type p53 in UACC-62 cells.	a-santalol	126-140	P53	Homo sapiens	186-189
20729567-3	2010	The control of ROS and senescence by p53 may help to explain how p53 can function to both restrain and promote aging.	ros	15-18	P53	Homo sapiens	65-68
20651843-12	2010	We also found that the apoptotic process triggered by adenosine was involved in G0-G1 cell-cycle arrest, enhanced the activity of caspase-3, upregulated p53 and NF-kappaB p65 expression, and downregulated Bcl-2 expression.	Adenosine	54-63	P53	Homo sapiens	153-156
20662736-7	2010	Anthracycline (topoisomerase II inhibitors such as mitoxantrone and ellipticine) and camptothecin (topoisomerase I inhibitor) derivatives including topotecan induce DNA double strand breaks, which activate the p53 pathway through the ataxia telangiectasia mutated-checkpoint kinase 2 (ATM-CHK2) DNA damage response pathway.	Anthracyclines	0-13	P53	Homo sapiens	210-213
19851859-12	2010	All the HPV-positive cases were homozygous for arginine at TP53 codon 72, a genotype associated with HPV-related cancer risk, and the tumors showed p16(INK4A) immunostaining, a marker of HPV-associated cancers.	Arginine	47-55	P53	Homo sapiens	59-63
20471503-1	2010	NAD(+)-dependent Class III histone deacetylase SIRT1 is a multiple function protein critically involved in stress responses, cellular metabolism and aging through deacetylating a variety of substrates including p53, forkhead-box transcription factors, PGC-1alpha, NF-kappaB, Ku70 and histones.	NAD	0-6	P53	Homo sapiens	211-214
20226587-3	2010	Co-treatment of etoposide and KG-135 markedly elevated the expression and phosphorylation at the serine 15 residue of p53 as well as the cellular levels of Bax and p21(Waf1/Cip1).	Serine	97-103	P53	Homo sapiens	118-121
20562210-5	2010	RESULTS: ALC enhanced the sensitivity to cisplatin of tumor cells with functional p53.	Cisplatin	41-50	P53	Homo sapiens	82-85
20466611-11	2010	CONCLUSIONS: Cholesterol and phytosterol treatment differentially regulated the growth of prostate cancer cells and the expression of p53 and cav-1, a gene that regulates androgen-regulated signals.	Cholesterol	13-24	P53	Homo sapiens	134-137
20538734-2	2010	Although its metabolites bind at several positions in TP53, a mutation at codon 249 (AGG to AGT, arginine to serine, p.R249S) accounts for 90% of TP53 mutations in AFB(1)-related HCC.	Arginine	97-105	P53	Homo sapiens	146-150
20538734-2	2010	Although its metabolites bind at several positions in TP53, a mutation at codon 249 (AGG to AGT, arginine to serine, p.R249S) accounts for 90% of TP53 mutations in AFB(1)-related HCC.	Serine	109-115	P53	Homo sapiens	146-150
20562210-9	2010	The in vivo ALC/cisplatin combination caused the activation of p53, associated with protein acetylation and induction of target genes.	Cisplatin	16-25	P53	Homo sapiens	63-66
20562210-10	2010	CONCLUSIONS: ALC was effective in enhancing the antitumor potential of platinum compounds in wild-type p53 tumors.	Platinum	71-79	P53	Homo sapiens	103-106
20845286-7	2010	BRCA1-IRIS abrogation of the homeostatic balance maintained by p38MAPK-p53-WIP1 pathway suppressed cell death induced by a lethal dose of UVC, high dosages of etoposide or H2O2, and allowed cells to survive and proliferate post geno-/cell-toxic stresses.	Hydrogen Peroxide	172-176	P53	Homo sapiens	71-74
20660093-7	2010	These changes were normalized to those observed in ZN by treating ZS cells with Pifitherin, an inhibitor of p53 transactivation activity.	Zinc	51-53	P53	Homo sapiens	108-111
20577264-4	2010	In this study, we show that G2 and S-phase-expressed 1 (GTSE1) protein, a negative regulator of p53, is required for G2 checkpoint recovery and that Plk1 phosphorylation of GTSE1 at Ser 435 promotes its nuclear localization, and thus shuttles p53 out of the nucleus to lead to its degradation during the recovery.	Serine	182-185	P53	Homo sapiens	96-99
20577264-4	2010	In this study, we show that G2 and S-phase-expressed 1 (GTSE1) protein, a negative regulator of p53, is required for G2 checkpoint recovery and that Plk1 phosphorylation of GTSE1 at Ser 435 promotes its nuclear localization, and thus shuttles p53 out of the nucleus to lead to its degradation during the recovery.	Serine	182-185	P53	Homo sapiens	243-246
20716879-7	2010	Interestingly, a pathway analysis revealed that expressions of p53-related genes were up-regulated in the 5-FU-sensitive groups.	Fluorouracil	106-110	P53	Homo sapiens	63-66
20432447-2	2010	This study shows that restriction of tyrosine and phenylalanine (Tyr/Phe), glutamine (Gln), or methionine (Met) differentially modulates glucose metabolism, glycogen synthase kinase 3beta (GSK3beta), p53, and pyruvate dehydrogenase (PDH) in these two cell lines.	Tyrosine	37-45	P53	Homo sapiens	200-203
20596601-10	2010	In the core signaling pathways of glioblastoma, curcumin either significantly influences the p53 pathway by enhancing p53 and p21 and suppressing cdc2 or significantly inhibits the RB pathway by enhancing CDKN2A/p16 and suppressing phosphorylated RB.	Curcumin	48-56	P53	Homo sapiens	93-96
20596601-10	2010	In the core signaling pathways of glioblastoma, curcumin either significantly influences the p53 pathway by enhancing p53 and p21 and suppressing cdc2 or significantly inhibits the RB pathway by enhancing CDKN2A/p16 and suppressing phosphorylated RB.	Curcumin	48-56	P53	Homo sapiens	118-121
20432447-2	2010	This study shows that restriction of tyrosine and phenylalanine (Tyr/Phe), glutamine (Gln), or methionine (Met) differentially modulates glucose metabolism, glycogen synthase kinase 3beta (GSK3beta), p53, and pyruvate dehydrogenase (PDH) in these two cell lines.	Methionine	95-105	P53	Homo sapiens	200-203
20432447-6	2010	Tyr/Phe, Gln and Met restriction increase phosphorylation of GSK3beta-Ser(9), phosphorylation of p53-Ser(15) and reduce the mitochondrial localization of PDH.	Tyrosine	0-3	P53	Homo sapiens	97-100
25961194-1	2010	We have previously shown that presence of estradiol (E2) in the growth medium causes (i) proliferation of T47D breast cancer cells, (ii) elevation of p53 levels, and (iii) hyperphos-phorylation of retinoblastoma protein (pRb).	Estradiol	42-51	P53	Homo sapiens	150-153
19499188-0	2010	The effect of cellular environment and p53 status on the mode of action of the platinum derivative LA-12.	Platinum	79-87	P53	Homo sapiens	39-42
20432447-6	2010	Tyr/Phe, Gln and Met restriction increase phosphorylation of GSK3beta-Ser(9), phosphorylation of p53-Ser(15) and reduce the mitochondrial localization of PDH.	Serine	101-104	P53	Homo sapiens	97-100
20432447-2	2010	This study shows that restriction of tyrosine and phenylalanine (Tyr/Phe), glutamine (Gln), or methionine (Met) differentially modulates glucose metabolism, glycogen synthase kinase 3beta (GSK3beta), p53, and pyruvate dehydrogenase (PDH) in these two cell lines.	Tyrosine	65-68	P53	Homo sapiens	200-203
20432447-8	2010	In p53-null PC3 cells, Tyr/Phe, Gln and Met restriction decreases glucose consumption, reduces phosphorylation of Akt-Ser(473), and increases phosphorylation of GSK3beta-Ser(9).	Tyrosine	23-26	P53	Homo sapiens	3-6
20653475-6	2010	CONCLUSIONS: NAC prevents the increased expression levels of p53 and CASP8 induced by long-term maintained hypoxia.	Acetylcysteine	13-16	P53	Homo sapiens	61-64
20421238-6	2010	We identified a novel germ line variant of the 177 mutant (Pro to Arg; P177R) of p53 by genomic sequencing.	Arginine	66-69	P53	Homo sapiens	81-84
20455200-6	2010	Moreover, expression profiling and Ingenuity pathway analysis results showed that the cytotoxicity of berberine was accompanied with an activation of BRCA1-mediated DNA damage response, G1/S and G2/M cell cycle checkpoint regulation, and P53 signalling pathways.	Berberine	102-111	P53	Homo sapiens	238-241
20639885-1	2010	The p53 tumor suppressor interacts with its negative regulator Mdm2 via the former"s N-terminal region and core domain, yet the extreme p53 C-terminal region contains lysine residues ubiquitinated by Mdm2 and can bear post-translational modifications that inhibit Mdm2-p53 association.	Lysine	167-173	P53	Homo sapiens	136-139
20639885-1	2010	The p53 tumor suppressor interacts with its negative regulator Mdm2 via the former"s N-terminal region and core domain, yet the extreme p53 C-terminal region contains lysine residues ubiquitinated by Mdm2 and can bear post-translational modifications that inhibit Mdm2-p53 association.	Lysine	167-173	P53	Homo sapiens	136-139
20673369-5	2010	Phosphorylation at specific serine residues in p53 is essential for it to cause cell growth inhibition.	Serine	28-34	P53	Homo sapiens	47-50
21090107-7	2010	We further proved fact that resveratrol can specifically promote the activity of sirt1; moreover, activated sirt1 modulates the activity of caspase-3 and bcl-2 family, involving in transcriptional regulation of p53 and NF-kappaB through antagonizing factor-induced acetylation.	Resveratrol	28-39	P53	Homo sapiens	211-214
20868594-5	2010	CONCLUSION: Following introduction of rAd-p53, many genes regulating cell cycle, proliferation and apoptosis expresses up or down which significantly enhance chemosensitivity and killing efficiency of cisplatin on human lung adenocarcinoma A549 cells.	Cisplatin	201-210	P53	Homo sapiens	42-45
20673277-0	2010	TRP-ing off the p53 apoptotic switch.	Tryptophan	0-3	P53	Homo sapiens	16-19
20566882-6	2010	In epithelial carcinoma cells the activation of p53 in response to mitochondrial electron transport chain complex III inhibitors does not require phosphorylation of p53 at Serine 15 or up-regulation of p14(ARF).	Serine	172-178	P53	Homo sapiens	48-51
20798760-5	2010	Specifically, 2,7-DAM is not cytotoxic and does not activate the p53 pathway while MC and DMC are cytotoxic and able to activate the p53 pathway.	10-decarbamoylmitomycin C	90-93	P53	Homo sapiens	133-136
20798760-6	2010	DMC is more cytotoxic than MC and can also kill p53-deficient cells by inducing degradation of Checkpoint 1 protein, which is not seen with MC treatment of the p53-deficient cells.	10-decarbamoylmitomycin C	0-3	P53	Homo sapiens	48-51
20798760-6	2010	DMC is more cytotoxic than MC and can also kill p53-deficient cells by inducing degradation of Checkpoint 1 protein, which is not seen with MC treatment of the p53-deficient cells.	10-decarbamoylmitomycin C	0-3	P53	Homo sapiens	160-163
20536192-0	2010	DNA adducts of decarbamoyl mitomycin C efficiently kill cells without wild-type p53 resulting from proteasome-mediated degradation of checkpoint protein 1.	10-decarbamoylmitomycin C	15-38	P53	Homo sapiens	80-83
20536192-1	2010	The mitomycin derivative 10-decarbamoyl mitomycin C (DMC) more rapidly activates a p53-independent cell death pathway than mitomycin C (MC).	10-decarbamoylmitomycin C	25-51	P53	Homo sapiens	83-86
20536192-1	2010	The mitomycin derivative 10-decarbamoyl mitomycin C (DMC) more rapidly activates a p53-independent cell death pathway than mitomycin C (MC).	10-decarbamoylmitomycin C	53-56	P53	Homo sapiens	83-86
20536192-4	2010	We find the increase in mitosene 1-beta-adduct formation correlates with a condensed nuclear morphology and increased cytotoxicity in human cancer cells with or without p53.	mitosene	24-32	P53	Homo sapiens	169-172
20536192-9	2010	Thus, the mitosene-1-beta stereoisomeric DNA adducts produced by the DMC signal for a p53-independent mode of cell death correlated with reduced nuclear size, persistent DNA damage, increased ubiquitin proteolysis and reduced Chk1 protein.	10-decarbamoylmitomycin C	69-72	P53	Homo sapiens	86-89
20663147-0	2010	DeltaNp63 transcriptionally regulates ATM to control p53 Serine-15 phosphorylation.	Serine	57-63	P53	Homo sapiens	53-56
20663147-4	2010	DeltaNp63alpha depletion by RNAi reduces steady-state ATM mRNA and protein levels, and attenuates p53 Serine-15 phosphorylation.	Serine	102-108	P53	Homo sapiens	98-101
20663147-5	2010	Conversely, ectopic expression of DeltaNp63alpha in p63-null tumour cells stimulates ATM transcription and p53 Serine-15 phosphorylation.	Serine	111-117	P53	Homo sapiens	107-110
21132089-2	2010	In such cancers, S100B binds wild-type p53 in a calcium-dependent manner, sequestering it, and promoting its degradation, resulting in the loss of p53-dependent tumor suppression activities.	Calcium	48-55	P53	Homo sapiens	39-42
20661724-5	2010	The cisplatin treatment significantly down-regulated the p53 and p21 expression level, while up-regulated the p27 expression in the YCC-3/R cells compared to the parental cells.	Cisplatin	4-13	P53	Homo sapiens	57-60
20622265-5	2010	Furthermore, SOCS1 contributes to p53 activation and phosphorylation on serine 15 by forming a ternary complex with ATM or ATR.	Serine	72-78	P53	Homo sapiens	34-37
20649542-7	2010	Manganese superoxide dismutase (MnSOD), a p53-regulated gene that is a vital antioxidant enzyme localized in the matrix of mitochondria, scavenges reactive oxygen species.	Reactive Oxygen Species	147-170	P53	Homo sapiens	42-45
20649542-8	2010	Recent studies suggest that mitochondria can regulate p53 activity and that assaults on the cell that affect mitochondrial ROS production and mitochondrial function can influence p53 activity.	Reactive Oxygen Species	123-126	P53	Homo sapiens	179-182
20581467-1	2010	BACKGROUND &amp; AIMS: p73 belongs to the p53 family of transcription factors known to regulate cell cycle and apoptosis.	Adenosine Monophosphate	12-15	P53	Homo sapiens	42-45
20092938-4	2010	Enhanced phosphorylations of p53 at Ser 15 and Ser 20 and up-regulation of PUMA, a p53 target protein, were observed after X-irradiation in the presence of edaravone.	Serine	36-39	P53	Homo sapiens	29-32
20230799-5	2010	The NAG-1 expression by LYR-8 was not blocked by pifithrin-alpha, a specific p53 inhibitor, which was different from doxorubicin that induced p53-dependent NAG-1 transcriptional activity.	Doxorubicin	117-128	P53	Homo sapiens	142-145
20367642-6	2010	We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway.	Fluorouracil	39-53	P53	Homo sapiens	145-148
20367642-6	2010	We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway.	Fluorouracil	39-53	P53	Homo sapiens	191-194
20367642-6	2010	We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway.	Fluorouracil	39-53	P53	Homo sapiens	191-194
20367642-6	2010	We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway.	Fluorouracil	55-59	P53	Homo sapiens	145-148
20367642-6	2010	We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway.	Fluorouracil	55-59	P53	Homo sapiens	191-194
20367642-6	2010	We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway.	Fluorouracil	55-59	P53	Homo sapiens	191-194
20367642-8	2010	Furthermore, the combination of poly I:C, 5-FU and IFN-alpha induced the highest apoptosis in HCT116 p53(+/+) and p53(-/-) cells.	Fluorouracil	42-46	P53	Homo sapiens	101-104
20367642-8	2010	Furthermore, the combination of poly I:C, 5-FU and IFN-alpha induced the highest apoptosis in HCT116 p53(+/+) and p53(-/-) cells.	Fluorouracil	42-46	P53	Homo sapiens	114-117
20451471-6	2010	Therefore, we investigated whether the serine/threonine wild-type p53-induced phosphatase 1 (WIP1/PPM1D) might regulate NER.	Serine	39-45	P53	Homo sapiens	66-69
20380571-4	2010	The frequencies of Arg/Arg, Arg/Pro, and Pro/Pro genotypes for P53 codon 72 were 51.7%, 41.4%, and 6.9% in patients and 42.6%, 47.3%, and 10.1% in controls, respectively.	Arginine	19-22	P53	Homo sapiens	63-66
20380571-4	2010	The frequencies of Arg/Arg, Arg/Pro, and Pro/Pro genotypes for P53 codon 72 were 51.7%, 41.4%, and 6.9% in patients and 42.6%, 47.3%, and 10.1% in controls, respectively.	Arginine	23-26	P53	Homo sapiens	63-66
20380571-4	2010	The frequencies of Arg/Arg, Arg/Pro, and Pro/Pro genotypes for P53 codon 72 were 51.7%, 41.4%, and 6.9% in patients and 42.6%, 47.3%, and 10.1% in controls, respectively.	Arginine	23-26	P53	Homo sapiens	63-66
20452167-4	2010	Ghrelin promoted proliferation (PCNA, cyclin B1, MAPK) and progesterone secretion but suppressed apoptosis (Bax, caspase 3, p53).	Ghrelin	0-7	P53	Homo sapiens	124-127
20446899-2	2010	This study suggested that G2/M cell cycle arrest was triggered by ROS/NO productions with regulations of p53, p21, cell division cycle 25C (Cdc25C), Cdc2 and cyclin B1, which were able to be prevented by protein tyrosine kinase (PTK) activity inhibitor genistein or JNK inhibitor SP600125.	Reactive Oxygen Species	66-69	P53	Homo sapiens	105-108
20199942-12	2010	Specifically, activation of NF-B up-regulated mot-2 expression, which prevented nuclear translocation of p53 and switched the binding preference of the p53 and NF-B coactivator CBP [cyclic AMP-responsive element binding protein (CREB) binding protein] from p53 to NF-B.	Cyclic AMP	182-192	P53	Homo sapiens	105-108
20199942-12	2010	Specifically, activation of NF-B up-regulated mot-2 expression, which prevented nuclear translocation of p53 and switched the binding preference of the p53 and NF-B coactivator CBP [cyclic AMP-responsive element binding protein (CREB) binding protein] from p53 to NF-B.	Cyclic AMP	182-192	P53	Homo sapiens	152-155
20199942-12	2010	Specifically, activation of NF-B up-regulated mot-2 expression, which prevented nuclear translocation of p53 and switched the binding preference of the p53 and NF-B coactivator CBP [cyclic AMP-responsive element binding protein (CREB) binding protein] from p53 to NF-B.	Cyclic AMP	182-192	P53	Homo sapiens	152-155
20558835-0	2010	Cell cycle arrest and apoptosis in TP53 subtypes of bladder carcinoma cell lines treated with cisplatin and gemcitabine.	Cisplatin	94-103	P53	Homo sapiens	35-39
20558835-8	2010	TP53-wild type cells (RT4) were more sensitive to apoptosis than were mutated TP53 cells when treated with cisplatin or gemcitabine.	Cisplatin	107-116	P53	Homo sapiens	0-4
20558835-8	2010	TP53-wild type cells (RT4) were more sensitive to apoptosis than were mutated TP53 cells when treated with cisplatin or gemcitabine.	Cisplatin	107-116	P53	Homo sapiens	78-82
20233844-4	2010	Using this approach, we quantified the site-specific cysteine oxidation status of endogenous p53 for the first time and found that Cys182 at the dimerization interface of the DNA binding domain is particularly susceptible to diamide oxidation intracellularly.	Cysteine	53-61	P53	Homo sapiens	93-96
21072344-5	2010	The zinc-binding status of p53 in the cell is impacted significantly by the presence of tumorigenic mutations and by metal ion homeostasis.	Metals	117-122	P53	Homo sapiens	27-30
20097305-2	2010	It also directly interacts and stabilizes p53 through phosphorylation at serine-15 residue.	Serine	73-79	P53	Homo sapiens	42-45
20228093-5	2010	We observed significantly higher mean intakes of alcohol, total meat and red meat, in the group with p53 mutations and advanced Dukes" stage disease (daily alcohol intake was 7 and 12 g for p53- and p53+ cases, respectively, P = 0.04; daily total meat intake was 69 and 100 g for p53- and p53+ cases, respectively, P = 0.03 and daily red meat intake was 39 and 75 g for p53- and p53+ cases, respectively, P = 0.01).	Alcohols	49-56	P53	Homo sapiens	101-104
20650775-6	2010	CONCLUSION: Sophoridine can inhibit the growth of transplanted solid tumor of human SW480 cell line, the mechanism of which involves the inhibition of p53 and VEGF expression.	matrine	12-23	P53	Homo sapiens	151-154
20571075-0	2010	Sensitivity of cancer cells to Plk1 inhibitor GSK461364A is associated with loss of p53 function and chromosome instability.	GSK 461364A	46-56	P53	Homo sapiens	84-87
20571075-3	2010	In this assay, cell lines that have lost p53 expression or carry mutations in the TP53 gene tended to be more sensitive to GSK461364A.	GSK 461364A	123-133	P53	Homo sapiens	41-44
20571075-3	2010	In this assay, cell lines that have lost p53 expression or carry mutations in the TP53 gene tended to be more sensitive to GSK461364A.	GSK 461364A	123-133	P53	Homo sapiens	82-86
20571075-5	2010	Further mechanistic studies showed that p53 wild-type (WT) and not mutant cells can activate a postmitotic tetraploidy checkpoint and arrest at pseudo-G(1) state after GSK461364A treatment.	GSK 461364A	168-178	P53	Homo sapiens	40-43
20571075-6	2010	RNA silencing of WT p53 increased the antiproliferative activity of GSK461364A.	GSK 461364A	68-78	P53	Homo sapiens	20-23
20171194-7	2010	NAC subsequently inhibited BEL-induced activation of p38 and p53 in LNCaP cells.	Acetylcysteine	0-3	P53	Homo sapiens	61-64
20514442-5	2010	We report that treatment of the DNA MMR competent/p53 mutant colorectal cancer cell line SW480 with 1 mM aspirin for 48 h caused changes in mRNA expression of several key genes involved in DNA damage signalling pathways, including a significant down-regulation in transcription of the genes ATR, BRCA1 and MAPK12.	Aspirin	105-112	P53	Homo sapiens	50-53
20514446-6	2010	5-FU (400 microM) induced apoptosis in MCF-7 cell monolayer as determined by HO/PI staining, PARP cleavage, p53 induction, Bax induction, and Bcl-2 down-regulation.	Fluorouracil	0-4	P53	Homo sapiens	108-111
20514446-10	2010	Furthermore, most of p53 induced by 5-FU was aggregated in MTS with necrotic core.	Fluorouracil	36-40	P53	Homo sapiens	21-24
20399660-4	2010	p53 shuts down these pathways and refocuses cells to utilize mitochondrial oxidative phosphorylation, thereby maximizing efficient ATP production and minimizing the synthesis of substrates for cell division.	Adenosine Triphosphate	131-134	P53	Homo sapiens	0-3
20499882-0	2010	Nitration of the tumor suppressor protein p53 at tyrosine 327 promotes p53 oligomerization and activation.	Tyrosine	49-57	P53	Homo sapiens	42-45
20499882-0	2010	Nitration of the tumor suppressor protein p53 at tyrosine 327 promotes p53 oligomerization and activation.	Tyrosine	49-57	P53	Homo sapiens	71-74
20499882-1	2010	Previous studies demonstrate that nitric oxide (NO) promotes p53 transcriptional activity by a classical DNA damage responsive mechanism involving activation of ATM/ATR and phosphorylation of p53.	Nitric Oxide	34-46	P53	Homo sapiens	61-64
20499882-1	2010	Previous studies demonstrate that nitric oxide (NO) promotes p53 transcriptional activity by a classical DNA damage responsive mechanism involving activation of ATM/ATR and phosphorylation of p53.	Nitric Oxide	34-46	P53	Homo sapiens	192-195
20418912-6	2010	Further, we found that LY294002 completely abolished the activation of p53 target genes (particularly pro-apoptotic) under adriamycin-high conditions, whereas it only marginally repressed the p53 target genes under adriamycin-low conditions; in fact, it further activated the transcription of NOXA, HRK, APAF1 and CASP5 genes.	Doxorubicin	123-133	P53	Homo sapiens	71-74
20596254-2	2010	BaP 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of benzo(a)pyrene (BaP), attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 gene mutations.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	27-31	P53	Homo sapiens	146-149
20347026-8	2010	Transfection of wild-type p53 using the complexes also significantly increased the sensitivity of BT474 cells to doxorubicin chemotherapy, suggesting the potential of this carrier in cancer gene therapy.	Doxorubicin	113-124	P53	Homo sapiens	26-29
20596254-2	2010	BaP 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of benzo(a)pyrene (BaP), attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 gene mutations.	Deoxyguanosine	90-104	P53	Homo sapiens	146-149
20525364-3	2010	In the two decades since its original discovery, p53 has found a singularly prominent place in our understanding of human gastric cancer and H. pylori cause accumulation of reactive oxygen species in the mucosa compartment.	Reactive Oxygen Species	173-196	P53	Homo sapiens	49-52
20651340-6	2010	The RBE of carbon beam was larger in mutant-type p53 cells than in wild-type p53 cells.	Carbon	11-17	P53	Homo sapiens	49-52
20353787-0	2010	ROS leads to MnSOD upregulation through ERK2 translocation and p53 activation in selenite-induced apoptosis of NB4 cells.	Reactive Oxygen Species	0-3	P53	Homo sapiens	63-66
20431990-6	2010	The switching on of p53 also causes changes in fatty acid metabolism, especially down-regulation of both fatty acid synthase and stearoyl-CoA (delta-9) desaturase.	Fatty Acids	47-57	P53	Homo sapiens	20-23
20651340-6	2010	The RBE of carbon beam was larger in mutant-type p53 cells than in wild-type p53 cells.	Carbon	11-17	P53	Homo sapiens	77-80
20651330-8	2010	p53 status appeared to determine the cell cycle stage at which methionine acts.	Methionine	63-73	P53	Homo sapiens	0-3
20544694-5	2010	Critical proteins in pathways for DNA damage detection/repair signaling, like p53 and ataxia telangiectasia mutated, and DNA repair itself, like oxoguanine glycosylase 1 and Cockayne syndrome B, can often, but not always, protect the embryo from ROS-initiating teratogens.	Reactive Oxygen Species	246-249	P53	Homo sapiens	78-81
20219242-0	2010	Biotinylated transferrin/avidin/biotinylated disulfide containing PEI bioconjugates mediated p53 gene delivery system for tumor targeted transfection.	Disulfides	45-54	P53	Homo sapiens	93-96
20219242-2	2010	In this paper, biotinylated transferrin/avidin/biotinylated disulfide containing PEI bioconjugates (TABP-SS) mediated p53 gene delivery system was formed attributed to the "avidin-biotin bridge".	Disulfides	60-69	P53	Homo sapiens	118-121
20018442-0	2010	Hypoxia suppresses chemotherapeutic drug-induced p53 Serine 46 phosphorylation by triggering HIPK2 degradation.	Serine	53-59	P53	Homo sapiens	49-52
19806450-0	2010	Overexpression of p53 is correlated with poor outcome in premenopausal women with breast cancer treated with tamoxifen after chemotherapy.	Tamoxifen	109-118	P53	Homo sapiens	18-21
19806450-8	2010	The p53-overexpressing patients with breast cancer between 35 and 50 years of age who received tamoxifen following chemotherapy had the greatest adverse effect on outcome.	Tamoxifen	95-104	P53	Homo sapiens	4-7
19806450-9	2010	Overexpression of p53 is significantly associated with tamoxifen resistance in premenopausal women with breast cancer.	Tamoxifen	55-64	P53	Homo sapiens	18-21
20018442-5	2010	Concordantly, hypoxic tumor cells show an impaired p53 Ser46 phosphorylation in response to treatment with the chemotherapeutic Adriamycin.	Doxorubicin	128-138	P53	Homo sapiens	51-54
20018442-6	2010	Remarkably, proteasome-inhibition rescues HIPK2 expression in hypoxic hepatoma cells and restores p53 Ser46 phosphorylation and caspase activity after Adriamycin treatment.	Doxorubicin	151-161	P53	Homo sapiens	98-101
20546244-0	2010	Cell proliferation and cell cycle alterations in oesophageal p53-mutated cancer cells treated with cisplatin in combination with photodynamic therapy.	Cisplatin	99-108	P53	Homo sapiens	61-64
20368736-6	2010	We also found that p53 knockdown or inhibition of mTOR activity by rapamycin cotreatment impairs 6-TG- and 5-FU-induced upregulation of BNIP3 protein levels and autophagy.	Sirolimus	67-76	P53	Homo sapiens	19-22
20368736-6	2010	We also found that p53 knockdown or inhibition of mTOR activity by rapamycin cotreatment impairs 6-TG- and 5-FU-induced upregulation of BNIP3 protein levels and autophagy.	Thioguanine	97-101	P53	Homo sapiens	19-22
20368736-6	2010	We also found that p53 knockdown or inhibition of mTOR activity by rapamycin cotreatment impairs 6-TG- and 5-FU-induced upregulation of BNIP3 protein levels and autophagy.	Fluorouracil	107-111	P53	Homo sapiens	19-22
20368736-8	2010	These findings suggest that BNIP3 mediates 6-TG- and 5-FU-induced autophagy in a p53- and mTOR-dependent manner.	Thioguanine	43-47	P53	Homo sapiens	81-84
20368736-8	2010	These findings suggest that BNIP3 mediates 6-TG- and 5-FU-induced autophagy in a p53- and mTOR-dependent manner.	Fluorouracil	53-57	P53	Homo sapiens	81-84
20382639-0	2010	Benzo[a]pyrene diol epoxide stimulates an inflammatory response in normal human lung fibroblasts through a p53 and JNK mediated pathway.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	0-27	P53	Homo sapiens	107-110
20221783-3	2010	The inhibitory effect of GW501516 on VSMC proliferation was associated with cell cycle arrest at the G1 to S phase transition, which was accompanied by the induction of p21 and p53 along with decreased cyclin-dependent kinase 4 expression.	vsmc	37-41	P53	Homo sapiens	177-180
20598227-0	2010	Role of acetylated p53 in regulating the expression of map2 in retinoic acid-induced P19 cells.	Tretinoin	63-76	P53	Homo sapiens	19-22
20598227-1	2010	OBJECTIVE: To investigate the regulatory mechanisms of acetylated p53 in the expression of microtubule-associated protein-2 (MAP2) in neuronal differentiation of P19 cells induced by all-trans retinoic acid (RA).	Tretinoin	208-210	P53	Homo sapiens	66-69
20546244-5	2010	MATERIALS AND METHODS: p53-mutated KYSE-510 cells were treated with CDDP alone or in combination with PDT.	Cisplatin	68-72	P53	Homo sapiens	23-26
20456495-7	2010	Curcuminoids also promote the phosphorylation of p53 on serine 15 in a dose-dependent and p38-dependent manner, suggesting that these compounds may activate p53.	Serine	56-62	P53	Homo sapiens	49-52
20456495-7	2010	Curcuminoids also promote the phosphorylation of p53 on serine 15 in a dose-dependent and p38-dependent manner, suggesting that these compounds may activate p53.	Serine	56-62	P53	Homo sapiens	157-160
19839049-7	2010	Additionally, disruption of ZEB1-histone deacetylase repressor complexes and down-regulation of SIRT1 histone deacetylase up-regulate proapoptotic genes in the p53 apoptotic pathway resulting in the increased sensitivity of cancer cells to the chemotherapeutic agent doxorubicin.	Doxorubicin	267-278	P53	Homo sapiens	160-163
20429769-3	2010	Both azadirachtin and nimbolide significantly suppressed the viability of HeLa cells in a dose-dependent manner by inducing cell cycle arrest at G0/G1 phase accompanied by p53-dependent p21 accumulation and down-regulation of the cell cycle regulatory proteins cyclin B, cyclin D1 and PCNA.	azadirachtin	5-17	P53	Homo sapiens	172-175
20429769-3	2010	Both azadirachtin and nimbolide significantly suppressed the viability of HeLa cells in a dose-dependent manner by inducing cell cycle arrest at G0/G1 phase accompanied by p53-dependent p21 accumulation and down-regulation of the cell cycle regulatory proteins cyclin B, cyclin D1 and PCNA.	nimbolide	22-31	P53	Homo sapiens	172-175
19948747-0	2010	Study of p53 codon 72 polymorphism and codon 249 mutations in Southern India in relation to age, alcohol drinking and smoking habits.	Alcohols	97-104	P53	Homo sapiens	9-12
19948747-4	2010	Since mutations in the p53 gene are present in approximately 40% of all human lung cancers and are more common in smokers than in nonsmokers, we aimed to detect the status of p53 at codon 72 for Arg/Arg or Arg/Pro or Pro/Pro allele polymorphism and p53 codon 249 mutation in smokers and nonsmokers of South India.	Arginine	195-198	P53	Homo sapiens	23-26
19948747-4	2010	Since mutations in the p53 gene are present in approximately 40% of all human lung cancers and are more common in smokers than in nonsmokers, we aimed to detect the status of p53 at codon 72 for Arg/Arg or Arg/Pro or Pro/Pro allele polymorphism and p53 codon 249 mutation in smokers and nonsmokers of South India.	Arginine	195-198	P53	Homo sapiens	175-178
19948747-4	2010	Since mutations in the p53 gene are present in approximately 40% of all human lung cancers and are more common in smokers than in nonsmokers, we aimed to detect the status of p53 at codon 72 for Arg/Arg or Arg/Pro or Pro/Pro allele polymorphism and p53 codon 249 mutation in smokers and nonsmokers of South India.	Arginine	195-198	P53	Homo sapiens	175-178
19948747-4	2010	Since mutations in the p53 gene are present in approximately 40% of all human lung cancers and are more common in smokers than in nonsmokers, we aimed to detect the status of p53 at codon 72 for Arg/Arg or Arg/Pro or Pro/Pro allele polymorphism and p53 codon 249 mutation in smokers and nonsmokers of South India.	Arginine	199-202	P53	Homo sapiens	175-178
19948747-4	2010	Since mutations in the p53 gene are present in approximately 40% of all human lung cancers and are more common in smokers than in nonsmokers, we aimed to detect the status of p53 at codon 72 for Arg/Arg or Arg/Pro or Pro/Pro allele polymorphism and p53 codon 249 mutation in smokers and nonsmokers of South India.	Arginine	199-202	P53	Homo sapiens	175-178
19948747-4	2010	Since mutations in the p53 gene are present in approximately 40% of all human lung cancers and are more common in smokers than in nonsmokers, we aimed to detect the status of p53 at codon 72 for Arg/Arg or Arg/Pro or Pro/Pro allele polymorphism and p53 codon 249 mutation in smokers and nonsmokers of South India.	Arginine	199-202	P53	Homo sapiens	175-178
19948747-4	2010	Since mutations in the p53 gene are present in approximately 40% of all human lung cancers and are more common in smokers than in nonsmokers, we aimed to detect the status of p53 at codon 72 for Arg/Arg or Arg/Pro or Pro/Pro allele polymorphism and p53 codon 249 mutation in smokers and nonsmokers of South India.	Arginine	199-202	P53	Homo sapiens	175-178
20346999-7	2010	Additionally, bolus (3h) doxorubicin incubation led to phosphorylation of p53 at serine 392, induction of p21, G2 arrest and increase of proapoptotic protein Bax.	Tritium	21-23	P53	Homo sapiens	74-77
20512840-3	2010	Actually, polymorphic variants Arg and Pro were found to have different properties of regulation of TP53-dependent DNA repair target genes, that can effect various levels of chromosome aberrations in cancer patients with these genotypes.	Arginine	31-34	P53	Homo sapiens	100-104
20512840-5	2010	It was shown that the Arg variant of TP53 gene is associated with high frequency of AC and chromatid breaks.	Arginine	22-25	P53	Homo sapiens	37-41
20428827-7	2010	The study demonstrated that cisplatin induces K562 cells to apoptosis by reducing miR-106 which up-regulates RB1 or by inhibiting miR-150 which increases P53 expression.	Cisplatin	28-37	P53	Homo sapiens	154-157
20299546-0	2010	2,3,7,8-tetrachlorodibenzo-p-dioxin counteracts the p53 response to a genotoxicant by upregulating expression of the metastasis marker agr2 in the hepatocarcinoma cell line HepG2.	Polychlorinated Dibenzodioxins	0-35	P53	Homo sapiens	52-55
20299546-2	2010	In this study, we show that TCDD treatment counteracts the p53 activation (phosphorylation and acetylation) elicited by a genotoxic compound, etoposide, in the human hepatocarcinoma cell line HepG2 and we delineated the mechanisms of this interaction.	Polychlorinated Dibenzodioxins	28-32	P53	Homo sapiens	59-62
20299546-9	2010	These results suggest that AhR ligands such as TCDD might contribute to tumor progression by inhibiting p53 regulation (phosphorylation and acetylation) triggered by genotoxicants via the increased expression of the metastasis marker AGR2.	Polychlorinated Dibenzodioxins	47-51	P53	Homo sapiens	104-107
20504344-8	2010	Importantly, inhibition of miR-21 and miR-222 by anti-miRNA oligonucleotides induced a significant increase in caspase activity in fludarabine-treated p53-mutant MEG-01 cells, suggesting that miR-21 and miR-222 up-regulation may be involved in the establishment of fludarabine resistance.	Oligonucleotides	60-76	P53	Homo sapiens	151-154
20504360-0	2010	Resveratrol suppresses IGF-1 induced human colon cancer cell proliferation and elevates apoptosis via suppression of IGF-1R/Wnt and activation of p53 signaling pathways.	Resveratrol	0-11	P53	Homo sapiens	146-149
20504360-8	2010	Resveratrol treatment induced apoptosis by activating tumor suppressor p53 protein, whereas IGF-1R siRNA treatment did not affect apoptosis.	Resveratrol	0-11	P53	Homo sapiens	71-74
20504360-9	2010	Our data suggests that resveratrol not only suppresses cell proliferation by inhibiting IGF-1R and its downstream signaling pathways similar to that of IGF-1R siRNA but also enhances apoptosis via activation of the p53 pathway.	Resveratrol	23-34	P53	Homo sapiens	215-218
20428768-7	2010	The phosphorylations of both p38 MAP kinase and p53 induced by doxorubicin were suppressed by low doses of ionizing radiation.	Doxorubicin	63-74	P53	Homo sapiens	48-51
20428768-10	2010	The results thus suggest that low doses of radiation suppress doxorubicin-induced replicative senescence through the inhibition of p38-dependent phosphorylation of p53 and by activation of ERK1/2, without genomic damage.	Doxorubicin	62-73	P53	Homo sapiens	164-167
20483782-6	2010	We also demonstrate that IFN-gamma treatment, which is used to induce IgG2a switching, increases intracellular ROS levels, and activates p53 in switching B cells, and show that p53 inhibits IgG2a class switching through its antioxidant-regulating function.	Reactive Oxygen Species	111-114	P53	Homo sapiens	177-180
20351180-3	2010	p400, an SWI2/SNF2-related ATPase that serves as an ATP-dependent chromatin remodeling enzyme, exists as an integral subunit of a TIP60 complex but also resides within a distinct complex that presumably lacks TIP60 and appears to be involved in the transcriptional repression of basal p53 target gene expression.	Adenosine Triphosphate	27-30	P53	Homo sapiens	285-288
20368352-7	2010	Mechanistically, ATDC binds p53, and this interaction is potentially fine-tuned by posttranslational acetylation of lysine 116 on ATDC.	Lysine	116-122	P53	Homo sapiens	28-31
20428827-3	2010	We also showed that miR-106 and miR-150 were down-regulated while their target genes (RB1 and P53, respectively) were up-regulated after cisplatin treatment.	Cisplatin	137-146	P53	Homo sapiens	94-97
20058240-1	2010	BACKGROUND: We previously described the identification of a transcriptional inhibitor ARC and FoxM1 inhibitors, thiazole antibiotics, Siomycin A and thiostrepton that were able to induce potent p53-independent apoptosis in cancer cell lines of different origin.	siomycin A	134-144	P53	Homo sapiens	194-197
20058240-1	2010	BACKGROUND: We previously described the identification of a transcriptional inhibitor ARC and FoxM1 inhibitors, thiazole antibiotics, Siomycin A and thiostrepton that were able to induce potent p53-independent apoptosis in cancer cell lines of different origin.	Thiostrepton	149-161	P53	Homo sapiens	194-197
20353948-0	2010	RUNX3 modulates DNA damage-mediated phosphorylation of tumor suppressor p53 at Ser-15 and acts as a co-activator for p53.	Serine	79-82	P53	Homo sapiens	72-75
20353948-2	2010	In this study, we found that RUNX3 is closely involved in DNA damage-dependent phosphorylation of tumor suppressor p53 at Ser-15 and acts as a co-activator for p53.	Serine	122-125	P53	Homo sapiens	115-118
20353948-2	2010	In this study, we found that RUNX3 is closely involved in DNA damage-dependent phosphorylation of tumor suppressor p53 at Ser-15 and acts as a co-activator for p53.	Serine	122-125	P53	Homo sapiens	160-163
20353948-3	2010	The small interference RNA-mediated knockdown of RUNX3 inhibited adriamycin (ADR)-dependent apoptosis in p53-proficient cells but not in p53-deficient cells in association with a significant reduction of p53-target gene expression as well as phosphorylation of p53 at Ser-15.	Doxorubicin	65-75	P53	Homo sapiens	105-108
20353948-8	2010	Additionally, RUNX3 had an ability to induce the phosphorylation of p53 at Ser-15, thereby promoting p53-dependent apoptosis.	Serine	75-78	P53	Homo sapiens	68-71
20353948-8	2010	Additionally, RUNX3 had an ability to induce the phosphorylation of p53 at Ser-15, thereby promoting p53-dependent apoptosis.	Serine	75-78	P53	Homo sapiens	101-104
20353948-11	2010	Thus, our present results strongly suggest that RUNX3 acts as a novel co-activator for p53 through regulating its DNA damage-induced phosphorylation at Ser-15 and also provide a clue to understanding the molecular mechanisms underlying RUNX3-mediated tumor suppression.	Serine	152-155	P53	Homo sapiens	87-90
20504360-10	2010	CONCLUSIONS: For the first time, we report that resveratrol suppresses colon cancer cell proliferation and elevates apoptosis even in the presence of IGF-1 via suppression of IGF-1R/Akt/Wnt signaling pathways and activation of p53, suggesting its potential role as a chemotherapeutic agent.	Resveratrol	48-59	P53	Homo sapiens	227-230
20346999-7	2010	Additionally, bolus (3h) doxorubicin incubation led to phosphorylation of p53 at serine 392, induction of p21, G2 arrest and increase of proapoptotic protein Bax.	Doxorubicin	25-36	P53	Homo sapiens	74-77
20346999-7	2010	Additionally, bolus (3h) doxorubicin incubation led to phosphorylation of p53 at serine 392, induction of p21, G2 arrest and increase of proapoptotic protein Bax.	Serine	81-87	P53	Homo sapiens	74-77
20346999-9	2010	Continuous (24h) treatment with 5 microM doxorubicin resulted in cell cycle arrest in G0/G1 phase that was neither accompanied by phosphorylation and activation of p53 nor enhanced expression of p21.	Doxorubicin	41-52	P53	Homo sapiens	164-167
20225330-8	2010	Furthermore, stratification analyses showed that the risk of SPM associated with p53 variant genotypes (Arg/Pro + Pro/Pro) was more pronounced in several subgroups.	Arginine	104-107	P53	Homo sapiens	81-84
20457898-8	2010	Like rapamycin, which is known to suppress senescence, p53 inhibited the mTOR pathway.	Sirolimus	5-14	P53	Homo sapiens	55-58
20470425-0	2010	Decreased transcription-coupled nucleotide excision repair capacity is associated with increased p53- and MLH1-independent apoptosis in response to cisplatin.	Cisplatin	148-157	P53	Homo sapiens	97-100
20307547-7	2010	The signature HKKme2 motif of p53, which defines specificity, is identified through a combination of NMR resonance perturbations, mutagenesis, measurements of binding affinities and docking simulations, and analysis of the crystal structures of 53BP1 bound to p53 peptides containing other dimethyl-lysine marks, p53K370me2 (p53 dimethylated at Lys370) and p53K372me2 (p53 dimethylated at Lys372).	Lysine	299-305	P53	Homo sapiens	30-33
20307547-7	2010	The signature HKKme2 motif of p53, which defines specificity, is identified through a combination of NMR resonance perturbations, mutagenesis, measurements of binding affinities and docking simulations, and analysis of the crystal structures of 53BP1 bound to p53 peptides containing other dimethyl-lysine marks, p53K370me2 (p53 dimethylated at Lys370) and p53K372me2 (p53 dimethylated at Lys372).	Lysine	299-305	P53	Homo sapiens	260-263
20307547-7	2010	The signature HKKme2 motif of p53, which defines specificity, is identified through a combination of NMR resonance perturbations, mutagenesis, measurements of binding affinities and docking simulations, and analysis of the crystal structures of 53BP1 bound to p53 peptides containing other dimethyl-lysine marks, p53K370me2 (p53 dimethylated at Lys370) and p53K372me2 (p53 dimethylated at Lys372).	Lysine	299-305	P53	Homo sapiens	260-263
20307547-7	2010	The signature HKKme2 motif of p53, which defines specificity, is identified through a combination of NMR resonance perturbations, mutagenesis, measurements of binding affinities and docking simulations, and analysis of the crystal structures of 53BP1 bound to p53 peptides containing other dimethyl-lysine marks, p53K370me2 (p53 dimethylated at Lys370) and p53K372me2 (p53 dimethylated at Lys372).	Lysine	299-305	P53	Homo sapiens	260-263
20470425-3	2010	Cisplatin resistance is multi-factorial but can be associated with increased DNA repair capacity, mutations in p53 or loss of DNA mismatch repair capacity.	Cisplatin	0-9	P53	Homo sapiens	111-114
20470425-7	2010	Decreased TC-NER capacity was associated with an increase in the sensitivity of tumour cells to cisplatin-induced apoptosis, even in p53 null and DNA mismatch repair-deficient cell lines.	Cisplatin	96-105	P53	Homo sapiens	133-136
20406839-7	2010	RESULTS: TRAIL/doxorubicin combination induced marked STS local and metastatic growth inhibition in a p53-independent manner.	Doxorubicin	15-26	P53	Homo sapiens	102-105
20356045-9	2010	Taken together, these data suggested that in addition to the mitochondrial- and Fas receptor-mediated apoptotic pathways involved, ROS-dependent and p53-regulated DR5 expression was also demonstrated to play a pivotal role in the synergistic enhancement of TRAIL-induced apoptosis instigated by 6-DG in Hep G2 cells.	Reactive Oxygen Species	131-134	P53	Homo sapiens	149-152
20646592-5	2010	And the expressions of cell cycle protein P53, P21, CDK2 were detected by Western blot after the treatment of capsaicin.	Capsaicin	110-119	P53	Homo sapiens	42-45
20646592-11	2010	After a 48-hour treatment with capsaicin, the expressions of P53 and P21 were up-regulated in contrary to the expression of CDK2.	Capsaicin	31-40	P53	Homo sapiens	61-64
20646592-12	2010	CONCLUSION: Capsaicin induces the cell cycle arrest of bladder cancer RT4 cells G(0)/G(1) phase and growth inhibition via TRPV1 receptor by modulating the expression of P53, P21 and CDK2.	Capsaicin	12-21	P53	Homo sapiens	169-172
20459745-0	2010	NSC109268 potentiates cisplatin-induced cell death in a p53-independent manner.	Cisplatin	22-31	P53	Homo sapiens	56-59
20459745-7	2010	The objective of the present study is to determine if p53 is responsible for cisplatin sensitization by NSC109268.	Cisplatin	77-86	P53	Homo sapiens	54-57
20459745-10	2010	Cisplatin caused a concentration-dependent increase in p53 in 2008 and 2008/C13* cells, and the induction of p53 correlated with cisplatin-induced apoptosis as determined by the cleavage of PARP.	Cisplatin	0-9	P53	Homo sapiens	55-58
20459745-10	2010	Cisplatin caused a concentration-dependent increase in p53 in 2008 and 2008/C13* cells, and the induction of p53 correlated with cisplatin-induced apoptosis as determined by the cleavage of PARP.	Cisplatin	0-9	P53	Homo sapiens	109-112
20459745-10	2010	Cisplatin caused a concentration-dependent increase in p53 in 2008 and 2008/C13* cells, and the induction of p53 correlated with cisplatin-induced apoptosis as determined by the cleavage of PARP.	Cisplatin	129-138	P53	Homo sapiens	109-112
20459745-11	2010	NSC109268 alone had no effect on p53 but it enhanced p53 level in response to cisplatin.	Cisplatin	78-87	P53	Homo sapiens	53-56
20459757-5	2010	Oxygen tension also affects many mammalian transactivators including AP-1, NFkB, and p53 by affecting the reduced state of critical cysteines in these proteins.	Oxygen	0-6	P53	Homo sapiens	85-88
20459757-5	2010	Oxygen tension also affects many mammalian transactivators including AP-1, NFkB, and p53 by affecting the reduced state of critical cysteines in these proteins.	Cysteine	132-141	P53	Homo sapiens	85-88
20190805-6	2010	Delta133p53 expression is increased in response to DNA damage by doxorubicin in p53 wild-type cell lines, but not in p53-mutated cells.	Doxorubicin	65-76	P53	Homo sapiens	8-11
20190805-6	2010	Delta133p53 expression is increased in response to DNA damage by doxorubicin in p53 wild-type cell lines, but not in p53-mutated cells.	Doxorubicin	65-76	P53	Homo sapiens	80-83
20219657-6	2010	This HY253-induced G(1) phase arrest is associated with decreased expression of cyclin D and up-regulation of p21(CIP1), via p53 phosphorylation at Ser-15, which resulted in increased hypophosphorylated pRb in A549 cells.	Serine	148-151	P53	Homo sapiens	125-128
20658010-1	2010	UNLABELLED: p53 tumoral suppressor gene harbors a functional polymorphism which codes either arginine (Arg) or proline (Pro) in the protein p53 of codon 72.	Arginine	93-101	P53	Homo sapiens	12-15
20658010-1	2010	UNLABELLED: p53 tumoral suppressor gene harbors a functional polymorphism which codes either arginine (Arg) or proline (Pro) in the protein p53 of codon 72.	Arginine	93-101	P53	Homo sapiens	140-143
20658010-1	2010	UNLABELLED: p53 tumoral suppressor gene harbors a functional polymorphism which codes either arginine (Arg) or proline (Pro) in the protein p53 of codon 72.	Arginine	103-106	P53	Homo sapiens	12-15
20658010-1	2010	UNLABELLED: p53 tumoral suppressor gene harbors a functional polymorphism which codes either arginine (Arg) or proline (Pro) in the protein p53 of codon 72.	Arginine	103-106	P53	Homo sapiens	140-143
20404548-4	2010	Identification of guanidinoacetate methyltransferase (GAMT) as a new p53 target connects p53 to creatine metabolism critical in the regulation of ATP homeostasis.	Adenosine Triphosphate	146-149	P53	Homo sapiens	69-72
20404548-4	2010	Identification of guanidinoacetate methyltransferase (GAMT) as a new p53 target connects p53 to creatine metabolism critical in the regulation of ATP homeostasis.	Adenosine Triphosphate	146-149	P53	Homo sapiens	89-92
20404548-5	2010	The involvement of GAMT in both genotoxic and metabolic stressinduced apoptosis, as well as the requirement of p53-dependent upregulation of GAMT in glucose starvation-mediated fatty acid oxidation (FAO), demonstrate a further role of p53 in coordinating stress response with changes in cellular metabolism.	Glucose	149-156	P53	Homo sapiens	111-114
20404548-5	2010	The involvement of GAMT in both genotoxic and metabolic stressinduced apoptosis, as well as the requirement of p53-dependent upregulation of GAMT in glucose starvation-mediated fatty acid oxidation (FAO), demonstrate a further role of p53 in coordinating stress response with changes in cellular metabolism.	Glucose	149-156	P53	Homo sapiens	235-238
20404548-5	2010	The involvement of GAMT in both genotoxic and metabolic stressinduced apoptosis, as well as the requirement of p53-dependent upregulation of GAMT in glucose starvation-mediated fatty acid oxidation (FAO), demonstrate a further role of p53 in coordinating stress response with changes in cellular metabolism.	Fatty Acids	177-187	P53	Homo sapiens	111-114
20421506-3	2010	We found that the transactivation domain of p53 made specific interactions with the C-terminal oligonucleotide/oligosaccharide-binding-fold domains of BRCA2 (BRCA2(CTD)).	Oligonucleotides	95-110	P53	Homo sapiens	44-47
20459648-3	2010	The expressions of IDH1 and p53 in formalin-fixed paraffin-embedded tissue sections from 44 osteosarcoma patients were determined by immunohistochemistry, and the correlation between them and clinicopagthological features were analyzed.	Paraffin	50-58	P53	Homo sapiens	28-31
20425836-4	2010	Array CGH using a 244 K oligonucleotide array showed a homogeneous de novo 17p13.1 microdeletion of 400 kb involving TP53 and 25 other genes, including genes involved in brain function (EFNB3, FXR2).	Oligonucleotides	24-39	P53	Homo sapiens	117-121
20164124-0	2010	Secreted protein acidic and rich in cysteine-induced cellular senescence in colorectal cancers in response to irinotecan is mediated by P53.	Irinotecan	110-120	P53	Homo sapiens	136-139
20019240-0	2010	Differential levels of transcription of p53-regulated genes by the arginine/proline polymorphism: p53 with arginine at codon 72 favors apoptosis.	Arginine	67-75	P53	Homo sapiens	40-43
20403587-2	2010	The results show that the carcinogenic mutation R249S affects the flexibility of L3 loop region in p53, inducing the loss of important hydrogen bonds observed at interaction in the wild-type with DNA, on the other hand the suppressor mutation H168R on the R249S assists in maintaining the wild-type like flexibility of the L3 region in p53 and thus recover the interaction terms lost in the carcinogenic mutation alone.	Hydrogen	135-143	P53	Homo sapiens	99-102
20019240-0	2010	Differential levels of transcription of p53-regulated genes by the arginine/proline polymorphism: p53 with arginine at codon 72 favors apoptosis.	Arginine	67-75	P53	Homo sapiens	98-101
20019240-0	2010	Differential levels of transcription of p53-regulated genes by the arginine/proline polymorphism: p53 with arginine at codon 72 favors apoptosis.	Arginine	107-115	P53	Homo sapiens	40-43
20019240-0	2010	Differential levels of transcription of p53-regulated genes by the arginine/proline polymorphism: p53 with arginine at codon 72 favors apoptosis.	Arginine	107-115	P53	Homo sapiens	98-101
20019240-4	2010	The largest difference between p53-arginine and p53-proline was found with the PERP gene involved in cell-cell adhesion and apoptosis.	Arginine	35-43	P53	Homo sapiens	31-34
20407015-7	2010	At high levels of galactose-induced p53 expression, 12 of 21 mutants that retain transactivation seemed similar to wild-type.	Galactose	18-27	P53	Homo sapiens	36-39
20395957-6	2010	Our findings demonstrate that (i) PKR, Ser/Thr kinase, phosphorylates its new substrate Cdc2 at the Tyr 4 residue, (ii) PKR-mediated Tyr 4-phosphorylation facilitates Cdc2 ubiquitination and proteosomal degradation, (iii) unphosphorylated Tyr 4 prevents Cdc2 ubiquitination, and (iv) downstream from p53, PKR has a crucial role in G2 arrest and triggers Cdc2 downregulation under genotoxic conditions.	Tyrosine	100-103	P53	Homo sapiens	300-303
20395957-6	2010	Our findings demonstrate that (i) PKR, Ser/Thr kinase, phosphorylates its new substrate Cdc2 at the Tyr 4 residue, (ii) PKR-mediated Tyr 4-phosphorylation facilitates Cdc2 ubiquitination and proteosomal degradation, (iii) unphosphorylated Tyr 4 prevents Cdc2 ubiquitination, and (iv) downstream from p53, PKR has a crucial role in G2 arrest and triggers Cdc2 downregulation under genotoxic conditions.	Tyrosine	133-136	P53	Homo sapiens	300-303
20395957-6	2010	Our findings demonstrate that (i) PKR, Ser/Thr kinase, phosphorylates its new substrate Cdc2 at the Tyr 4 residue, (ii) PKR-mediated Tyr 4-phosphorylation facilitates Cdc2 ubiquitination and proteosomal degradation, (iii) unphosphorylated Tyr 4 prevents Cdc2 ubiquitination, and (iv) downstream from p53, PKR has a crucial role in G2 arrest and triggers Cdc2 downregulation under genotoxic conditions.	Tyrosine	133-136	P53	Homo sapiens	300-303
20406950-3	2010	It is known that the interaction of the vitamin D metabolite 1,25-dihydroxyvitamin D(3) (1,25D) with its functional vitamin D receptor leads to differentiation, G(1) arrest, and increased cell survival in p53-null AML cells.	Vitamin D	40-49	P53	Homo sapiens	205-208
20406950-6	2010	We find that 1,25D alone induces monocytic differentiation in these cell lines similar to that seen in p53-null AML cells, suggesting that the presence of wild-type p53 is compatible with activation of vitamin D signaling.	Vitamin D	202-211	P53	Homo sapiens	165-168
20372852-12	2010	Our findings indicate the possible association of the Glu allele of the TP53BP1 Asp353Glu polymorphism with lower risk of lung cancer especially among the Pro allele carriers of the TP53 Arg72Pro polymorphism.	Glutamic Acid	54-57	P53	Homo sapiens	72-76
20338640-4	2010	Analysis of the expression pattern of a key set of cell cycle regulators revealed that the expression of Zta and Rta substantially interfered with the cell cycle regulatory machinery in Raji cells, strongly inhibiting the expression of Rb and p53 and inducing the expression of E2F1.	zta	105-108	P53	Homo sapiens	243-246
20372863-7	2010	Cisplatin treatment induced caspase-3, -9, p53, Bax, NF-kappaB and MAPK expression, and suppressed Bcl-2 and Bcl-xl expression, whereas cells transfected with pcDNA3.1-ARL6IP1 showed lower levels of cisplatin-induced caspase-3, -9, p53, Bax, NF-kappaB and MAPK up-regulation and higher levels of cisplatin-suppressed Bcl-2 and Bcl-xl down-regulation.	Cisplatin	0-9	P53	Homo sapiens	43-46
20372863-7	2010	Cisplatin treatment induced caspase-3, -9, p53, Bax, NF-kappaB and MAPK expression, and suppressed Bcl-2 and Bcl-xl expression, whereas cells transfected with pcDNA3.1-ARL6IP1 showed lower levels of cisplatin-induced caspase-3, -9, p53, Bax, NF-kappaB and MAPK up-regulation and higher levels of cisplatin-suppressed Bcl-2 and Bcl-xl down-regulation.	Cisplatin	0-9	P53	Homo sapiens	232-235
20228054-3	2010	Here, we show that p53-dependent apoptosis in response to different DNA-damaging agents was reduced when normal and cancer cells were cultured at physiological oxygen tensions instead of the usual atmospheric levels.	Oxygen	160-166	P53	Homo sapiens	19-22
20372863-8	2010	These novel findings collectively suggest that ARL6IP1 may play a key role in cisplatin-induced apoptosis in CaSki cervical cancer cells by regulating the expression of apoptosis-associated proteins such as caspase-3, -9, p53, NF-kappaB, MAPK, Bcl-2, Bcl-xl, and Bax.	Cisplatin	78-87	P53	Homo sapiens	222-225
20422012-4	2010	Surprisingly, unlike the case for other p53 target promoters, p53-mediated transactivation of FLT1-T constructs or expression of the endogenous FLT1 gene, as well as binding of p53 and ER at the promoter constructs, was inducible by doxorubicin but not by 5-fluorouracil.	Doxorubicin	233-244	P53	Homo sapiens	62-65
20167603-5	2010	DYRK1A and DYRK3 directly phosphorylate SIRT1 at Thr(522), promoting deacetylation of p53.	Threonine	49-52	P53	Homo sapiens	86-89
20208557-0	2010	15-Deoxy-Delta(12,14)-prostaglandin J(2) stabilizes, but functionally inactivates p53 by binding to the cysteine 277 residue.	Cysteine	104-112	P53	Homo sapiens	82-85
20208557-6	2010	Moreover, by conducting an in vitro [(35)S]-labeled p53 translation assay, we identified cysteine 277 as a putative site of p53 modification by 15d-PGJ(2).	Cysteine	89-97	P53	Homo sapiens	52-55
20208557-6	2010	Moreover, by conducting an in vitro [(35)S]-labeled p53 translation assay, we identified cysteine 277 as a putative site of p53 modification by 15d-PGJ(2).	Cysteine	89-97	P53	Homo sapiens	124-127
20208557-10	2010	In conclusion, 15d-PGJ(2) can undergo nucleophilic addition to p53, presumably at the cysteine 277 residue, rendering this tumor suppressor less susceptible to proteasomal degradation.	Cysteine	86-94	P53	Homo sapiens	63-66
20140020-6	2010	Furthermore, treatment with the non-genotoxic agent Nutlin-3 sensitizes cells for doxorubicin, showing that activation of p53 by targeting its regulators is an efficient strategy to decrease cell viability of breast cancer cells.	Doxorubicin	82-93	P53	Homo sapiens	122-125
20422012-4	2010	Surprisingly, unlike the case for other p53 target promoters, p53-mediated transactivation of FLT1-T constructs or expression of the endogenous FLT1 gene, as well as binding of p53 and ER at the promoter constructs, was inducible by doxorubicin but not by 5-fluorouracil.	Doxorubicin	233-244	P53	Homo sapiens	62-65
20351271-0	2010	Phosphate-activated glutaminase (GLS2), a p53-inducible regulator of glutamine metabolism and reactive oxygen species.	Reactive Oxygen Species	94-117	P53	Homo sapiens	42-45
20422012-4	2010	Surprisingly, unlike the case for other p53 target promoters, p53-mediated transactivation of FLT1-T constructs or expression of the endogenous FLT1 gene, as well as binding of p53 and ER at the promoter constructs, was inducible by doxorubicin but not by 5-fluorouracil.	Fluorouracil	256-270	P53	Homo sapiens	62-65
20351271-1	2010	We identified a p53 target gene, phosphate-activated mitochondrial glutaminase (GLS2), a key enzyme in conversion of glutamine to glutamate, and thereby a regulator of glutathione (GSH) synthesis and energy production.	Phosphates	33-42	P53	Homo sapiens	16-19
20351271-1	2010	We identified a p53 target gene, phosphate-activated mitochondrial glutaminase (GLS2), a key enzyme in conversion of glutamine to glutamate, and thereby a regulator of glutathione (GSH) synthesis and energy production.	Glutamic Acid	130-139	P53	Homo sapiens	16-19
20422012-4	2010	Surprisingly, unlike the case for other p53 target promoters, p53-mediated transactivation of FLT1-T constructs or expression of the endogenous FLT1 gene, as well as binding of p53 and ER at the promoter constructs, was inducible by doxorubicin but not by 5-fluorouracil.	Fluorouracil	256-270	P53	Homo sapiens	62-65
20351271-1	2010	We identified a p53 target gene, phosphate-activated mitochondrial glutaminase (GLS2), a key enzyme in conversion of glutamine to glutamate, and thereby a regulator of glutathione (GSH) synthesis and energy production.	Glutathione	168-179	P53	Homo sapiens	16-19
20227390-0	2010	Rosiglitazone enhances the radiosensitivity of p53-mutant HT-29 human colorectal cancer cells.	Rosiglitazone	0-13	P53	Homo sapiens	47-50
20351271-1	2010	We identified a p53 target gene, phosphate-activated mitochondrial glutaminase (GLS2), a key enzyme in conversion of glutamine to glutamate, and thereby a regulator of glutathione (GSH) synthesis and energy production.	Glutathione	181-184	P53	Homo sapiens	16-19
20351271-4	2010	Further, siRNA down-regulation of either GLS2 or p53 compromises the GSH-dependent antioxidant system and increases intracellular ROS levels.	Glutathione	69-72	P53	Homo sapiens	49-52
20351271-4	2010	Further, siRNA down-regulation of either GLS2 or p53 compromises the GSH-dependent antioxidant system and increases intracellular ROS levels.	Reactive Oxygen Species	130-133	P53	Homo sapiens	49-52
20351271-5	2010	High ROS levels following GLS2 knockdown also coincide with stimulation of p53-induced cell death.	Reactive Oxygen Species	5-8	P53	Homo sapiens	75-78
20351271-6	2010	We propose that GLS2 control of intracellular ROS levels and the apoptotic response facilitates the ability of p53 to protect cells from accumulation of genomic damage and allows cells to survive after mild and repairable genotoxic stress.	Reactive Oxygen Species	46-49	P53	Homo sapiens	111-114
20351271-9	2010	Thus, our results provide evidence for a unique metabolic role for p53, linking glutamine metabolism, energy, and ROS homeostasis, which may contribute to p53 tumor suppressor function.	Reactive Oxygen Species	114-117	P53	Homo sapiens	67-70
20351271-9	2010	Thus, our results provide evidence for a unique metabolic role for p53, linking glutamine metabolism, energy, and ROS homeostasis, which may contribute to p53 tumor suppressor function.	Reactive Oxygen Species	114-117	P53	Homo sapiens	155-158
19922265-4	2010	Expression of the p53-regulated downstream proteins like p21, and DNA-damage-dependent p53 phosphorylation at serine-15 residue also was not elicited by the CUVA treatment, at a low coralyne concentration.	Serine	110-116	P53	Homo sapiens	18-21
19922265-4	2010	Expression of the p53-regulated downstream proteins like p21, and DNA-damage-dependent p53 phosphorylation at serine-15 residue also was not elicited by the CUVA treatment, at a low coralyne concentration.	Serine	110-116	P53	Homo sapiens	87-90
20418953-1	2010	BACKGROUND: Homeodomain interacting protein kinase 2 (HIPK2) is an evolutionary conserved serine/threonine kinase whose activity is fundamental in maintaining wild-type p53 function, thereby controlling the destiny of cells when exposed to DNA damaging agents.	Serine	90-96	P53	Homo sapiens	169-172
20138829-5	2010	In this study we found that curcumin induces apoptotic cell death in MCF-7 cells, as assessed by MTT assay, DNA ladder formation, PARP cleavage, p53 and Bax induction.	Curcumin	28-36	P53	Homo sapiens	145-148
20140014-7	2010	The regulation of the p53 family by S100 is complicated and depends on the target preference of each individual S100 protein, the concentration of the proteins and calcium, as well as the splicing variation of p63 or p73.	Calcium	164-171	P53	Homo sapiens	22-25
20378837-7	2010	Consistent with these functions of GLS2, the activation of p53 increases the levels of glutamate and alpha-ketoglutarate, mitochondrial respiration rate, and GSH levels and decreases reactive oxygen species (ROS) levels in cells.	Glutamic Acid	87-96	P53	Homo sapiens	59-62
20378837-7	2010	Consistent with these functions of GLS2, the activation of p53 increases the levels of glutamate and alpha-ketoglutarate, mitochondrial respiration rate, and GSH levels and decreases reactive oxygen species (ROS) levels in cells.	Glutathione	158-161	P53	Homo sapiens	59-62
20378837-7	2010	Consistent with these functions of GLS2, the activation of p53 increases the levels of glutamate and alpha-ketoglutarate, mitochondrial respiration rate, and GSH levels and decreases reactive oxygen species (ROS) levels in cells.	Reactive Oxygen Species	183-206	P53	Homo sapiens	59-62
20378837-7	2010	Consistent with these functions of GLS2, the activation of p53 increases the levels of glutamate and alpha-ketoglutarate, mitochondrial respiration rate, and GSH levels and decreases reactive oxygen species (ROS) levels in cells.	Reactive Oxygen Species	208-211	P53	Homo sapiens	59-62
20398418-6	2010	An increased risk was also associated with the TP53 Pro/Pro genotype (OR = 2.22, 95% CI = 1.58-3.10) compared to the Arg/Arg genotype.	Arginine	117-120	P53	Homo sapiens	47-51
20398418-6	2010	An increased risk was also associated with the TP53 Pro/Pro genotype (OR = 2.22, 95% CI = 1.58-3.10) compared to the Arg/Arg genotype.	Arginine	121-124	P53	Homo sapiens	47-51
20354524-7	2010	RESULTS: Oncogenic KRAS sensitised colorectal tumour cells to oxaliplatin and 5-FU in a p53-dependent manner and promoted p53 phosphorylation at Ser37 and Ser392, without affecting p53 stabilisation, p21 induction, or cell-cycle arrest.	Fluorouracil	78-82	P53	Homo sapiens	88-91
20354524-11	2010	CONCLUSION: Oncogenic KRAS determines the cellular response to p53 activation by oxaliplatin or 5-FU, by facilitating apoptosis induction through Noxa.	Fluorouracil	96-100	P53	Homo sapiens	63-66
20227390-3	2010	In this study, rosiglitazone treatment significantly reduced the cell viability of p53-wild type HCT116 cells but not p53-mutant HT-29 cells.	Rosiglitazone	15-28	P53	Homo sapiens	83-86
20227390-4	2010	Interestingly, rosiglitazone pretreatment enhanced radiosensitivity in p53-mutant HT-29 cells but not HCT116 cells, and prolonged radiation-induced G(2)/M arrest and enhanced radiation-induced cell growth inhibition in HT-29 cells.	Rosiglitazone	15-28	P53	Homo sapiens	71-74
19882681-7	2010	In contrast, in breast cancer cells transfected with MT1 exposed to 1.2 microT of the 50 Hz EMF, the expression of p53 and c-myc increased significantly after melatonin treatment but for p21(WAF) the increase was not significant.	Melatonin	159-168	P53	Homo sapiens	115-118
20124408-7	2010	Binding of SCH529074 to the p53 DBD is specifically displaced by an oligonucleotide with a sequence derived from the p53-response element.	Oligonucleotides	68-83	P53	Homo sapiens	28-31
20124408-7	2010	Binding of SCH529074 to the p53 DBD is specifically displaced by an oligonucleotide with a sequence derived from the p53-response element.	Oligonucleotides	68-83	P53	Homo sapiens	117-120
19882681-6	2010	Expression of BRCA-1, p53, p21(WAF), and c-myc was increased by estradiol stimulation and subsequently decreased by melatonin treatment in both cell lines, except for p53 expression in the transfected cell line, thereby proving the antiestrogenic effect of melatonin at molecular level.	Estradiol	64-73	P53	Homo sapiens	22-25
19882681-6	2010	Expression of BRCA-1, p53, p21(WAF), and c-myc was increased by estradiol stimulation and subsequently decreased by melatonin treatment in both cell lines, except for p53 expression in the transfected cell line, thereby proving the antiestrogenic effect of melatonin at molecular level.	Melatonin	116-125	P53	Homo sapiens	22-25
20700368-1	2010	PURPOSE: Benzo[a]pyrene 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of benzo[a]pyrene, attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 mutations.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	47-51	P53	Homo sapiens	160-163
20700368-1	2010	PURPOSE: Benzo[a]pyrene 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of benzo[a]pyrene, attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 mutations.	Deoxyguanosine	104-118	P53	Homo sapiens	160-163
20073508-11	2010	Sensitization occurred through a p53 signaling pathway, as indicated by caspase 3/7 upregulation following plk1 knockdown and doxorubicin treatment, and this effect could be abrogated using a p53 inhibitor.	Doxorubicin	126-137	P53	Homo sapiens	33-36
20073508-11	2010	Sensitization occurred through a p53 signaling pathway, as indicated by caspase 3/7 upregulation following plk1 knockdown and doxorubicin treatment, and this effect could be abrogated using a p53 inhibitor.	Doxorubicin	126-137	P53	Homo sapiens	192-195
19810096-0	2010	Combination of p53 codon 72 polymorphism and inactive p53 mutation predicts chemosensitivity to 5-fluorouracil in colorectal cancer.	Fluorouracil	96-110	P53	Homo sapiens	15-18
20447055-9	2010	It was further demonstrated that XCT-790-induced ROS modulated p53 and Rb signalling pathways and suppressed cell replication.	Reactive Oxygen Species	49-52	P53	Homo sapiens	63-66
20107315-5	2010	MK-1775 enhanced the cytotoxic effects of 5-FU in p53-deficient human colon cancer cells.	Fluorouracil	42-46	P53	Homo sapiens	50-53
20068143-13	2010	High glucose and palmitate increased p53 acetylation and JNK phosphorylation; these effects were abolished in siRNA SIRT1-treated cells.	Glucose	5-12	P53	Homo sapiens	37-40
19810096-5	2010	In the Arg/Arg variant, apoptotic cells induced by 5-FU treatment in patients without inactive p53 mutation were more markedly increased than those in patients with inactive p53 mutation (p = 0.037).	Arginine	7-10	P53	Homo sapiens	95-98
19810096-5	2010	In the Arg/Arg variant, apoptotic cells induced by 5-FU treatment in patients without inactive p53 mutation were more markedly increased than those in patients with inactive p53 mutation (p = 0.037).	Arginine	7-10	P53	Homo sapiens	174-177
19810096-0	2010	Combination of p53 codon 72 polymorphism and inactive p53 mutation predicts chemosensitivity to 5-fluorouracil in colorectal cancer.	Fluorouracil	96-110	P53	Homo sapiens	54-57
19810096-5	2010	In the Arg/Arg variant, apoptotic cells induced by 5-FU treatment in patients without inactive p53 mutation were more markedly increased than those in patients with inactive p53 mutation (p = 0.037).	Arginine	11-14	P53	Homo sapiens	95-98
19810096-5	2010	In the Arg/Arg variant, apoptotic cells induced by 5-FU treatment in patients without inactive p53 mutation were more markedly increased than those in patients with inactive p53 mutation (p = 0.037).	Arginine	11-14	P53	Homo sapiens	174-177
19810096-2	2010	We investigated whether p53 polymorphism and mutation were associated with in vitro sensitivity to 5-fluorouracil (5-FU) in patients with colorectal cancer.	Fluorouracil	99-113	P53	Homo sapiens	24-27
19810096-5	2010	In the Arg/Arg variant, apoptotic cells induced by 5-FU treatment in patients without inactive p53 mutation were more markedly increased than those in patients with inactive p53 mutation (p = 0.037).	Fluorouracil	51-55	P53	Homo sapiens	95-98
19810096-5	2010	In the Arg/Arg variant, apoptotic cells induced by 5-FU treatment in patients without inactive p53 mutation were more markedly increased than those in patients with inactive p53 mutation (p = 0.037).	Fluorouracil	51-55	P53	Homo sapiens	174-177
19810096-2	2010	We investigated whether p53 polymorphism and mutation were associated with in vitro sensitivity to 5-fluorouracil (5-FU) in patients with colorectal cancer.	Fluorouracil	115-119	P53	Homo sapiens	24-27
19810096-8	2010	The combination of the p53 codon 72 polymorphism and p53 mutation status is a potential predictive marker of sensitivity to 5-FU in CRC.	Fluorouracil	124-128	P53	Homo sapiens	23-26
19810096-8	2010	The combination of the p53 codon 72 polymorphism and p53 mutation status is a potential predictive marker of sensitivity to 5-FU in CRC.	Fluorouracil	124-128	P53	Homo sapiens	53-56
19810096-4	2010	5-FU sensitivity of tumor cells without inactive p53 mutation in the arginine/arginine (Arg/Arg) variant was significantly higher than that of tumor cells with or without inactive p53 mutation in other variants (p = 0.022), whereas the 5-FU sensitivity of tumor cells with inactive p53 mutation in the Arg/Arg variant was significantly lower than that of tumor cells with or without inactive p53 mutation in other variants (p = 0.002).	Fluorouracil	0-4	P53	Homo sapiens	49-52
19810096-4	2010	5-FU sensitivity of tumor cells without inactive p53 mutation in the arginine/arginine (Arg/Arg) variant was significantly higher than that of tumor cells with or without inactive p53 mutation in other variants (p = 0.022), whereas the 5-FU sensitivity of tumor cells with inactive p53 mutation in the Arg/Arg variant was significantly lower than that of tumor cells with or without inactive p53 mutation in other variants (p = 0.002).	Arginine	69-77	P53	Homo sapiens	49-52
20101229-4	2010	p53delta expression was associated with impaired response to primary platinum-based chemotherapy (P=0.032).	Platinum	69-77	P53	Homo sapiens	0-3
19810103-0	2010	Resveratrol enhances p53 acetylation and apoptosis in prostate cancer by inhibiting MTA1/NuRD complex.	Resveratrol	0-11	P53	Homo sapiens	21-24
19882171-1	2010	OBJECTIVE: The purpose of our study was to evaluate the feasibility and treatment outcomes of recombinant adenovirus-p53 (rAd-p53, trademarked as Gendicine) combined with fractionated stereotactic radiotherapy (fSRT) in treatment of primary hepatocellular carcinoma (HCC).	gendicine	146-155	P53	Homo sapiens	117-120
20308316-4	2010	We show that the quinoline derivative chloroquine activates the p53 pathway and suppresses growth of glioma cells in vitro and in vivo in an orthotopic (U87MG) human glioblastoma mouse model.	quinoline	17-26	P53	Homo sapiens	64-67
20123963-0	2010	Requirement of ATM for rapid p53 phosphorylation at Ser46 without Ser/Thr-Gln sequences.	Serine	52-55	P53	Homo sapiens	29-32
20123963-3	2010	To elucidate the direct phosphorylation of p53 at Ser46 by ATM, an ATM mutant (ATM-AS) sensitive to ATP analogues was engineered.	Adenosine Triphosphate	100-103	P53	Homo sapiens	43-46
20123963-4	2010	In vitro kinase assays revealed that p53 was phosphorylated at Ser46 by ATM-AS, even when ATP analogues were used as phosphate donors, although this phosphorylation site is not in an SQ motif, a consensus ATM site.	Adenosine Triphosphate	90-93	P53	Homo sapiens	37-40
20123963-4	2010	In vitro kinase assays revealed that p53 was phosphorylated at Ser46 by ATM-AS, even when ATP analogues were used as phosphate donors, although this phosphorylation site is not in an SQ motif, a consensus ATM site.	Phosphates	117-126	P53	Homo sapiens	37-40
20123963-7	2010	These results suggest that ATM phosphorylates a noncanonical serine residue on p53 by mechanisms different from those for the phosphorylation of Ser15.	Serine	61-67	P53	Homo sapiens	79-82
20034524-11	2010	These results suggest that p53 plays a pivotal role in decreased integrin-mediated extracellular matrix component expression in cisplatin-induced tubule cell apoptosis, and reveal a novel aspect of PACAP-mediated renoprotection.	Cisplatin	128-137	P53	Homo sapiens	27-30
20034524-5	2010	The damage to HK-2 cells caused by cisplatin involved the activation of p53, caspase-7, and poly (ADP-ribose) polymerase-1 (PARP-1).	Cisplatin	35-44	P53	Homo sapiens	72-75
19918261-5	2010	The molecular mechanism of drug sensitivity with COS has been investigated by microarray gene expressions followed by gene network analysis and it reveals that a cdc42/rac1 guanine exchange factor, ARHGEF6, with p53 and DNA-Pkc (PRKDC) is central to induce apoptosis in Cbl(cos) (Cbl with COS) cells.	carbonyl sulfide	49-52	P53	Homo sapiens	212-215
19918261-5	2010	The molecular mechanism of drug sensitivity with COS has been investigated by microarray gene expressions followed by gene network analysis and it reveals that a cdc42/rac1 guanine exchange factor, ARHGEF6, with p53 and DNA-Pkc (PRKDC) is central to induce apoptosis in Cbl(cos) (Cbl with COS) cells.	carbonyl sulfide	274-277	P53	Homo sapiens	212-215
20491334-4	2010	Comparative analysis of frequency of p53 occurrence in serum in three studied group has been done with respect to nicotine addiction in COPD and NSCLC groups.	Nicotine	114-122	P53	Homo sapiens	37-40
19918261-5	2010	The molecular mechanism of drug sensitivity with COS has been investigated by microarray gene expressions followed by gene network analysis and it reveals that a cdc42/rac1 guanine exchange factor, ARHGEF6, with p53 and DNA-Pkc (PRKDC) is central to induce apoptosis in Cbl(cos) (Cbl with COS) cells.	carbonyl sulfide	289-292	P53	Homo sapiens	212-215
20060462-10	2010	In conclusion, ROS-mediated oxidative stress, the activation of p53 and up-regulation of Bax/Bcl-2 ratio are involved in mechanistic pathways of 21 nm SiO(2) induced apoptosis in L-02 cells.	Reactive Oxygen Species	15-18	P53	Homo sapiens	64-67
20175992-1	2010	Selective binding of the wild type tumor suppressor protein p53 to negatively and positively supercoiled (sc) DNA was studied using intercalative drugs chloroquine (CQ), ethidium bromide, acridine derivatives and doxorubicin as a modulators of the level of DNA supercoiling.	Acridines	188-196	P53	Homo sapiens	60-63
19963248-4	2010	METHODS: The p53 carboxyl-terminal peptides covalently coupled with cell-penetrating peptides were synthesized with D- or L-amino acids.	d- or l-amino acids	116-135	P53	Homo sapiens	13-16
20118233-2	2010	Lysine methylation has recently emerged as a key post-translational modification that alters the activity of p53.	Lysine	0-6	P53	Homo sapiens	109-112
20118233-3	2010	Here, we describe a novel lysine methylation site in p53 that is carried out by two homologous histone methyltransferases, G9a and Glp.	Lysine	26-32	P53	Homo sapiens	53-56
20118233-4	2010	G9a and Glp specifically methylate p53 at Lys(373), resulting mainly in dimethylation.	Lysine	42-45	P53	Homo sapiens	35-38
20118233-5	2010	During DNA damage, the overall level of p53 modified at Lys(373)me2 does not increase, despite the dramatic increase in total p53, indicating that Lys(373)me2 correlates with inactive p53.	Lysine	56-59	P53	Homo sapiens	40-43
20175992-1	2010	Selective binding of the wild type tumor suppressor protein p53 to negatively and positively supercoiled (sc) DNA was studied using intercalative drugs chloroquine (CQ), ethidium bromide, acridine derivatives and doxorubicin as a modulators of the level of DNA supercoiling.	Doxorubicin	213-224	P53	Homo sapiens	60-63
20215500-0	2010	Targeting cancer cell metabolism: the combination of metformin and 2-deoxyglucose induces p53-dependent apoptosis in prostate cancer cells.	Metformin	53-62	P53	Homo sapiens	90-93
20227041-8	2010	Thus, p53 status can determine the biological impact of vitamin D on tumor cells.	Vitamin D	56-65	P53	Homo sapiens	6-9
20036733-7	2010	UVB-irradiated KP provoked an appreciable accumulation of pSer(15)-p53/COX-2 complexes, but this nuclear association of complexes was partially inhibited by PD98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	157-164	P53	Homo sapiens	67-70
20215500-6	2010	At the cellular level, the combination of metformin and 2DG induced p53-dependent apoptosis via the energy sensor pathway AMP kinase, and the reexpression of a functional p53 in p53-deficient prostate cancer cells restored caspase-3 activity.	Metformin	42-51	P53	Homo sapiens	68-71
20215500-6	2010	At the cellular level, the combination of metformin and 2DG induced p53-dependent apoptosis via the energy sensor pathway AMP kinase, and the reexpression of a functional p53 in p53-deficient prostate cancer cells restored caspase-3 activity.	Metformin	42-51	P53	Homo sapiens	171-174
20036271-9	2010	Poly(ADP-ribosyl)ation of P53 is reported to block its activation, DNA binding and its functioning as a transcription factor.	Adenosine Diphosphate	5-8	P53	Homo sapiens	26-29
20215500-7	2010	In addition to apoptosis, the combination of metformin and 2DG arrested prostate cancer cells in G(2)-M. This G(2)-M arrest was independent of p53 and correlated with a stronger decrease in cell viability than obtained with either drug.	Metformin	45-54	P53	Homo sapiens	143-146
19919837-1	2010	BACKGROUND &amp; AIMS: p53 Mutations are very common in human hepatocellular carcinoma, and induction of hepatic p53 expression causes lysis of implanted hepatoblastoma cells in a chimeric mouse.	Adenosine Monophosphate	12-15	P53	Homo sapiens	113-116
20811532-2	2010	Mutation of tumour suppressor gene p53 at codon 249(ser) at exon 7 has been found to contribute significantly to replication of damaged DNA and subsequent tumour progression.	Serine	52-55	P53	Homo sapiens	35-38
20193843-9	2010	Moreover, we identified mutation of TP53 gene in codon 273; triplet CGT coding Arg was changed to CAG coding His.	Arginine	79-82	P53	Homo sapiens	36-40
20193843-9	2010	Moreover, we identified mutation of TP53 gene in codon 273; triplet CGT coding Arg was changed to CAG coding His.	GUANOSINE 5'-TRIPHOSPHATE P3-[1-(2-NITROPHENYL)ETHYL ESTER]	98-101	P53	Homo sapiens	36-40
20193843-9	2010	Moreover, we identified mutation of TP53 gene in codon 273; triplet CGT coding Arg was changed to CAG coding His.	Histidine	109-112	P53	Homo sapiens	36-40
20193851-1	2010	Polymorphism at codon 72 of TP53, resulting in either the arginine (Arg) or proline (Pro) form of p53 (R72P), has been associated with the susceptibility to different cancers.	Arginine	58-66	P53	Homo sapiens	28-32
20193851-1	2010	Polymorphism at codon 72 of TP53, resulting in either the arginine (Arg) or proline (Pro) form of p53 (R72P), has been associated with the susceptibility to different cancers.	Arginine	58-66	P53	Homo sapiens	98-101
20193851-1	2010	Polymorphism at codon 72 of TP53, resulting in either the arginine (Arg) or proline (Pro) form of p53 (R72P), has been associated with the susceptibility to different cancers.	Arginine	68-71	P53	Homo sapiens	28-32
20193851-1	2010	Polymorphism at codon 72 of TP53, resulting in either the arginine (Arg) or proline (Pro) form of p53 (R72P), has been associated with the susceptibility to different cancers.	Arginine	68-71	P53	Homo sapiens	98-101
20119745-5	2010	In addition, the two mentioned compounds inhibit intracellular signalling mechanisms leading to apoptotic cell death, namely those mediated by mitochondria, which was confirmed by their ability to overcome t-BHP-induced morphological changes in the mitochondrial network, loss of mitochondrial membrane potential, increased expression of the pro-apoptotic proteins p53, Bax and AIF and activation of caspases-3 and -9.	tert-Butylhydroperoxide	206-211	P53	Homo sapiens	365-368
22993551-0	2010	Thymoquinone hydrazone derivatives cause cell cycle arrest in p53-competent colorectal cancer cells.	thymoquinone hydrazone	0-22	P53	Homo sapiens	62-65
20075077-4	2010	Treatment with the genotoxic agents, doxorubicin or etoposide, induced Foxp3 expression in p53-positive carcinoma cells, but not in cells lacking p53 function.	Doxorubicin	37-48	P53	Homo sapiens	91-94
20022955-4	2010	In a promoter-specific context, inhibition of H3R17 methylation represses expression of p21, a p53-responsive gene, thus implicating a possible role for H3 Arg-17 methylation in tumor suppressor function.	Arginine	156-159	P53	Homo sapiens	95-98
20393586-5	2010	In terms of transcriptional regulation, ROS affect the phosphorylation, activation, oxidation, and DNA binding of transcription factors such as AP-1, NF-kappaB, p53, and HIF-1alpha, leading to changes in target gene expression.	Reactive Oxygen Species	40-43	P53	Homo sapiens	161-164
19932175-0	2010	Phosphorylation of serine 392 in p53 is a common and integral event during p53 induction by diverse stimuli.	Serine	19-25	P53	Homo sapiens	33-36
19932175-0	2010	Phosphorylation of serine 392 in p53 is a common and integral event during p53 induction by diverse stimuli.	Serine	19-25	P53	Homo sapiens	75-78
20060030-9	2010	Taken together, these results demonstrate that I3C induces cell cycle arrest at G0/G1 through the activation of p-p53 at Ser 15 and induces caspase-8 mediated apoptosis via the Fas death receptor.	Serine	121-124	P53	Homo sapiens	114-117
19965871-3	2010	A previous study has shown that upon exposure to genotoxic stress, DYRK2 translocates into the nucleus and phosphorylates p53 at Ser-46, thereby inducing apoptosis.	Serine	129-132	P53	Homo sapiens	122-125
20100965-10	2010	Factors associated with good cisplatin response include young age (P = .001), low BRCA1 mRNA expression (P = .03), BRCA1 promoter methylation (P = .04), p53 nonsense or frameshift mutations (P = .01), and a gene expression signature of E2F3 activation (P = .03).	Cisplatin	29-38	P53	Homo sapiens	153-156
19856322-6	2010	Mechanistically, this is a cooperative process: key residues, particularly Lys120 and Arg280 acted as sensors; upon finding their hydrogen-bonding partners, they lock in, anchoring p53 into the major groove.	Hydrogen	130-138	P53	Homo sapiens	181-184
19965871-2	2010	Phosphorylation of p53 at Ser-46 is indispensable for the commitment to apoptotic cell death.	Serine	26-29	P53	Homo sapiens	19-22
19808950-6	2010	Only tumor protein 53 was increased in the atorvastatin 80-mg group.	Atorvastatin	43-55	P53	Homo sapiens	5-21
19732952-9	2010	P53 inhibition in B5/Bu250(6) cells using pifithrin-alpha alleviated these effects, suggesting a role for p53 therein; this observation was supported by the relative resistance of p53-null K562 cells to [DAC+Bu] combinations and by the effects of an anti-p53 shRNA on the OCI-AML3 cell line.	Busulfan	21-23	P53	Homo sapiens	0-3
19732952-10	2010	We conclude that the synergistic effects of [DAC+Bu] are p53-dependent and involve cell cycle arrest, apoptosis induction and down-regulation of pro-survival genes.	Busulfan	49-51	P53	Homo sapiens	57-60
20023006-0	2010	Iron chelator-mediated alterations in gene expression: identification of novel iron-regulated molecules that are molecular targets of hypoxia-inducible factor-1 alpha and p53.	Iron	0-4	P53	Homo sapiens	171-174
20023006-0	2010	Iron chelator-mediated alterations in gene expression: identification of novel iron-regulated molecules that are molecular targets of hypoxia-inducible factor-1 alpha and p53.	Iron	79-83	P53	Homo sapiens	171-174
20023006-5	2010	Apart from iron-mediated regulation of expression via hypoxia inducible factor-1 alpha, it was noteworthy that the transcription factor p53 was also involved in iron-regulated gene expression.	Iron	11-15	P53	Homo sapiens	136-139
20025073-1	2010	Recent studies have suggested an association between dietary folate, and related B-vitamins, and risk for cancer, potentially mediated by the p53 tumor suppressor gene.	Folic Acid	61-67	P53	Homo sapiens	142-145
20025073-2	2010	The aim of this study was to explore the effect of dietary folate and vitamin B(6) intake on p53 in the molecular pathogenesis of esophageal adenocarcinoma (EADC).	Folic Acid	59-65	P53	Homo sapiens	93-96
20178585-0	2010	Protection of p53 wild type cells from taxol by nutlin-3 in the combined lung cancer treatment.	Paclitaxel	39-44	P53	Homo sapiens	14-17
20103635-7	2010	The lower cisplatin concentration was also accompanied by reduced induction of p53, which could be restored by downregulation of annexin A3.	Cisplatin	10-19	P53	Homo sapiens	79-82
19944674-7	2010	Curcumin inhibited cell growth, induced apoptosis and upregulated maspin gene expression in MCF-7 cells and these findings were further correlated with the upregulation of p53 protein and downregulation of Bcl-2, suggesting maspin mediated apoptosis in MCF-7 cells.	Curcumin	0-8	P53	Homo sapiens	172-175
19965871-8	2010	Upon exposure to genotoxic stress, ATM phosphorylates DYRK2 at Thr-33 and Ser-369, which enables DYRK2 to escape from degradation by dissociation from MDM2 and to induce the kinase activity toward p53 at Ser-46 in the nucleus.	Threonine	63-66	P53	Homo sapiens	197-200
19965871-8	2010	Upon exposure to genotoxic stress, ATM phosphorylates DYRK2 at Thr-33 and Ser-369, which enables DYRK2 to escape from degradation by dissociation from MDM2 and to induce the kinase activity toward p53 at Ser-46 in the nucleus.	Serine	74-77	P53	Homo sapiens	197-200
19965871-8	2010	Upon exposure to genotoxic stress, ATM phosphorylates DYRK2 at Thr-33 and Ser-369, which enables DYRK2 to escape from degradation by dissociation from MDM2 and to induce the kinase activity toward p53 at Ser-46 in the nucleus.	Serine	204-207	P53	Homo sapiens	197-200
19889954-0	2010	Inhibitors of histone deacetylases suppress cisplatin-induced p53 activation and apoptosis in renal tubular cells.	Cisplatin	44-53	P53	Homo sapiens	62-65
20048189-0	2010	TP53 mutations and pathologic complete response to neoadjuvant cisplatin and fluorouracil chemotherapy in resected oral cavity squamous cell carcinoma.	Cisplatin	63-72	P53	Homo sapiens	0-4
20048189-0	2010	TP53 mutations and pathologic complete response to neoadjuvant cisplatin and fluorouracil chemotherapy in resected oral cavity squamous cell carcinoma.	Fluorouracil	77-89	P53	Homo sapiens	0-4
20048189-9	2010	CONCLUSION The results indicate that the loss of function (transactivation activities) of p53 mutant proteins may predict a significant low pCR rate and suboptimal response to cisplatin-based neoadjuvant chemotherapy in patients with oral cavity SCC.	Cisplatin	176-185	P53	Homo sapiens	90-93
19889954-8	2010	Mechanistically, SAHA inhibited and TSA delayed p53 phosphorylation, acetylation, and activation during cisplatin incubation.	Cisplatin	104-113	P53	Homo sapiens	48-51
19889954-10	2010	Interestingly, in HCT116 colon cancer cells, SAHA suppressed cisplatin-induced p53 activation, but enhanced apoptosis.	Cisplatin	61-70	P53	Homo sapiens	79-82
19889954-11	2010	The results suggest that inhibitors of histone deacetylases can protect against cisplatin nephrotoxicity by attenuating DNA damage response and associated p53 activation.	Cisplatin	80-89	P53	Homo sapiens	155-158
19882354-0	2010	Inhibitory role of cAMP on doxorubicin-induced apoptosis in pre-B ALL cells through dephosphorylation of p53 serine residues.	Cyclic AMP	19-23	P53	Homo sapiens	105-108
20019189-0	2010	Iron-dependent regulation of MDM2 influences p53 activity and hepatic carcinogenesis.	Iron	0-4	P53	Homo sapiens	45-48
20019189-4	2010	Iron dependent regulation of MDM2/p53 was confirmed ex-vivo in human monocytes, by manipulation of iron pool and in a genetic model of iron deficiency, leading to modulation of p53 target genes involved in the antioxidant response and apoptosis.	Iron	0-4	P53	Homo sapiens	34-37
20019189-4	2010	Iron dependent regulation of MDM2/p53 was confirmed ex-vivo in human monocytes, by manipulation of iron pool and in a genetic model of iron deficiency, leading to modulation of p53 target genes involved in the antioxidant response and apoptosis.	Iron	0-4	P53	Homo sapiens	177-180
20019189-4	2010	Iron dependent regulation of MDM2/p53 was confirmed ex-vivo in human monocytes, by manipulation of iron pool and in a genetic model of iron deficiency, leading to modulation of p53 target genes involved in the antioxidant response and apoptosis.	Iron	99-103	P53	Homo sapiens	34-37
20019189-5	2010	Iron status influenced p53 ubiquitination and degradation rate, and the MDM2 inhibitor nutlin increased p53 levels in iron-depleted cells.	Iron	0-4	P53	Homo sapiens	23-26
20019189-5	2010	Iron status influenced p53 ubiquitination and degradation rate, and the MDM2 inhibitor nutlin increased p53 levels in iron-depleted cells.	Iron	118-122	P53	Homo sapiens	104-107
20019189-7	2010	The MDM2 -309T &gt; G promoter polymorphism, determining increased MDM2 and lower p53 activity, was associated with higher risk of hepatocarcinoma in cirrhotic patients with hemochromatosis, and with HFE mutations in patients with hepatocarcinoma without hemochromatosis, suggesting an interaction between MDM2 and iron in the pathogenesis of hepatocarcinoma.	Iron	315-319	P53	Homo sapiens	82-85
20019189-8	2010	In conclusion, iron status influences p53 activity and antioxidant response by modulating MDM2 expression.	Iron	15-19	P53	Homo sapiens	38-41
19941080-3	2010	METHODS: Genomic mutation and protein expression of p53 were investigated retrospectively by polymerase chain reaction (PCR) single-strand conformation polymorphism (SSCP) and immunohistochemistry (IHC) using biopsy specimens from 77 ESCC patients before chemotherapy with 5-fluorouracil, adriamycin, and cisplatin.	Fluorouracil	273-287	P53	Homo sapiens	52-55
19941080-3	2010	METHODS: Genomic mutation and protein expression of p53 were investigated retrospectively by polymerase chain reaction (PCR) single-strand conformation polymorphism (SSCP) and immunohistochemistry (IHC) using biopsy specimens from 77 ESCC patients before chemotherapy with 5-fluorouracil, adriamycin, and cisplatin.	Doxorubicin	289-299	P53	Homo sapiens	52-55
19941080-3	2010	METHODS: Genomic mutation and protein expression of p53 were investigated retrospectively by polymerase chain reaction (PCR) single-strand conformation polymorphism (SSCP) and immunohistochemistry (IHC) using biopsy specimens from 77 ESCC patients before chemotherapy with 5-fluorouracil, adriamycin, and cisplatin.	Cisplatin	305-314	P53	Homo sapiens	52-55
19882354-0	2010	Inhibitory role of cAMP on doxorubicin-induced apoptosis in pre-B ALL cells through dephosphorylation of p53 serine residues.	Doxorubicin	27-38	P53	Homo sapiens	105-108
19882354-0	2010	Inhibitory role of cAMP on doxorubicin-induced apoptosis in pre-B ALL cells through dephosphorylation of p53 serine residues.	Serine	109-115	P53	Homo sapiens	105-108
19882354-1	2010	Exposure of cells to chemotherapeutic drug doxorubicin, a DNA-damaging agent, induces an increase in the levels and activity of the wild-type p53 protein.	Doxorubicin	43-54	P53	Homo sapiens	142-145
19882354-2	2010	Less well appreciated was the effect of cAMP levels on posttranslational modifications of p53 in response to doxorubicin.	Cyclic AMP	40-44	P53	Homo sapiens	90-93
19882354-2	2010	Less well appreciated was the effect of cAMP levels on posttranslational modifications of p53 in response to doxorubicin.	Doxorubicin	109-120	P53	Homo sapiens	90-93
19882354-3	2010	Here we show that elevation of cAMP in pre-B acute lymphoblastic leukemia NALM-6 cells significantly attenuated phosphorylation state of p53 at Ser6, Ser9, Ser15, Ser20, Ser37, Ser46 and Ser392 upon exposure to doxorubicin.	Cyclic AMP	31-35	P53	Homo sapiens	137-140
19882354-3	2010	Here we show that elevation of cAMP in pre-B acute lymphoblastic leukemia NALM-6 cells significantly attenuated phosphorylation state of p53 at Ser6, Ser9, Ser15, Ser20, Ser37, Ser46 and Ser392 upon exposure to doxorubicin.	Doxorubicin	211-222	P53	Homo sapiens	137-140
19882354-5	2010	In conclusion, our results suggest that activation of cAMP-signaling system may repress p53-dependent apoptosis in malignant cells exposed to doxorubicin.	Cyclic AMP	54-58	P53	Homo sapiens	88-91
19882354-5	2010	In conclusion, our results suggest that activation of cAMP-signaling system may repress p53-dependent apoptosis in malignant cells exposed to doxorubicin.	Doxorubicin	142-153	P53	Homo sapiens	88-91
19585117-10	2010	Western blotting assay revealed oroxylin A enhanced 5-FU-induced apoptosis in HepG2 cells by elevating the expressions of apoptotic-inducing proteins P53 and cleaved PARP and decreasing the expression of apoptotic-inhibitory proteins COX-2, Bcl-2, and pro-caspase3.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	32-42	P53	Homo sapiens	150-153
19583730-0	2010	Dicoumarol enhances doxorubicin-induced cytotoxicity in p53 wild-type urothelial cancer cells through p38 activation.	Doxorubicin	20-31	P53	Homo sapiens	56-59
19583730-3	2010	Then, dicoumarol-mediated enhancement of doxorubicin-induced cytotoxicity was screened in urothelial cancer cell lines with different p53 statuses or RT112 stable transfectants with a dominant-negative mutant of p53 (p53DN).	Doxorubicin	41-52	P53	Homo sapiens	212-215
19583730-4	2010	To clarify the importance of the modification of p53 function by dicoumarol to enhance doxorubicin toxicity, the change in the p53-p21 pathway and mitogen-activated protein kinase (MAPK)-mitochondria pathway by the combined treatment were elucidated by Western blot analysis.	Doxorubicin	87-98	P53	Homo sapiens	49-52
19583730-8	2010	The combined treatment with dicoumarol suppressed p53/p21 induction by doxorubicin and resulted in sequential p38 MAPK activation, myeloid cell leukaemia 1 suppression and caspase cleavage.	Doxorubicin	71-82	P53	Homo sapiens	50-53
19583730-10	2010	CONCLUSION: These results suggest that concomitant use of dicoumarol could enhance the cytotoxicity of doxorubicin in urothelial cancer cells with wt-p53 through the p53/p21/p38 MAPK pathways.	Doxorubicin	103-114	P53	Homo sapiens	150-153
19583730-10	2010	CONCLUSION: These results suggest that concomitant use of dicoumarol could enhance the cytotoxicity of doxorubicin in urothelial cancer cells with wt-p53 through the p53/p21/p38 MAPK pathways.	Doxorubicin	103-114	P53	Homo sapiens	166-169
19585117-10	2010	Western blotting assay revealed oroxylin A enhanced 5-FU-induced apoptosis in HepG2 cells by elevating the expressions of apoptotic-inducing proteins P53 and cleaved PARP and decreasing the expression of apoptotic-inhibitory proteins COX-2, Bcl-2, and pro-caspase3.	Fluorouracil	52-56	P53	Homo sapiens	150-153
19927155-7	2010	We find that direct binding of p53 to importin-alpha3 depends on the positive charge contributed by lysine residues 319-321 within NLS I.	Lysine	100-106	P53	Homo sapiens	31-34
19845689-6	2010	Furthermore, heparin inhibited cyclin-dependent kinase inhibitor p21(WAF1/CIP1) and p53 tumour suppressor gene and protein expression up to 2-fold or 1.8-fold, respectively, and stimulated cyclin D1 expression up to 1.8-fold, in these cell lines through a p38-mediated mechanism.	Heparin	13-20	P53	Homo sapiens	84-87
19927155-11	2010	Thus, under normal growth conditions, ubiquitination of Lys 319-321 negatively regulates p53-importin-alpha3 binding, thereby restraining p53 import.	Lysine	56-59	P53	Homo sapiens	89-92
19927155-11	2010	Thus, under normal growth conditions, ubiquitination of Lys 319-321 negatively regulates p53-importin-alpha3 binding, thereby restraining p53 import.	Lysine	56-59	P53	Homo sapiens	138-141
20124455-0	2010	Gossypol induces apoptosis by activating p53 in prostate cancer cells and prostate tumor-initiating cells.	Gossypol	0-8	P53	Homo sapiens	41-44
19950206-10	2010	BBR-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of MAP Kinases (JNK and p38 MAPK), ASK1, Akt, and p53.	Berberine	0-3	P53	Homo sapiens	146-149
19918798-5	2010	PTX/LPC combination acted by favoring p53 stabilization through a lowering in p-Akt levels and in ps166-MDM2, the phosphorylated-MDM2 form that enters the nucleus and induces p53 export and degradation.	Paclitaxel	0-3	P53	Homo sapiens	38-41
19918798-5	2010	PTX/LPC combination acted by favoring p53 stabilization through a lowering in p-Akt levels and in ps166-MDM2, the phosphorylated-MDM2 form that enters the nucleus and induces p53 export and degradation.	Paclitaxel	0-3	P53	Homo sapiens	175-178
19918798-8	2010	PTX/LPC treatment induced a weakness of Akt-MDM2-p53 complex and increased nuclear p53 levels.	Paclitaxel	0-3	P53	Homo sapiens	49-52
19918798-8	2010	PTX/LPC treatment induced a weakness of Akt-MDM2-p53 complex and increased nuclear p53 levels.	Paclitaxel	0-3	P53	Homo sapiens	83-86
20124455-8	2010	These studies show for the first time that gossypol treatment induces DNA damage and activates p53.	Gossypol	43-51	P53	Homo sapiens	95-98
20080565-6	2010	Interestingly, we find that endogenous GRK2 down-regulation is prevented on activation of the G2/M checkpoint by doxorubicin and that stabilized GRK2 levels in such conditions inversely correlate with the p53 response and the induction of apoptosis, suggesting that GRK2 participates in the regulatory network controlling cell cycle arrest and survival in such conditions.	Doxorubicin	113-124	P53	Homo sapiens	205-208
20126473-0	2010	Translocation of p53 to mitochondria is regulated by its lipid binding property to anionic phospholipids and it participates in cell death control.	Phospholipids	91-104	P53	Homo sapiens	17-20
19922762-0	2010	Linalool preferentially induces robust apoptosis of a variety of leukemia cells via upregulating p53 and cyclin-dependent kinase inhibitors.	linalool	0-8	P53	Homo sapiens	97-100
19922762-3	2010	Treatment of leukemia cells by linalool for 12h led to strong activation of p53, cyclin-dependent kinase inhibitors (CDKIs), GADD45alpha, c-jun and phosphorylated-JNK, suggesting that linalool-induced apoptosis might be associated with activation of p53 and CDKIs.	linalool	31-39	P53	Homo sapiens	76-79
19922762-3	2010	Treatment of leukemia cells by linalool for 12h led to strong activation of p53, cyclin-dependent kinase inhibitors (CDKIs), GADD45alpha, c-jun and phosphorylated-JNK, suggesting that linalool-induced apoptosis might be associated with activation of p53 and CDKIs.	linalool	31-39	P53	Homo sapiens	250-253
19940145-8	2010	Further, knockdown of siah-1 prevented high glucose-induced cell death of Muller cells potentially by inhibiting p53 phosphorylation consistent with previous observations, indicating that nuclear GAPDH induces cell death via p53 activation.	Glucose	44-51	P53	Homo sapiens	113-116
19940145-8	2010	Further, knockdown of siah-1 prevented high glucose-induced cell death of Muller cells potentially by inhibiting p53 phosphorylation consistent with previous observations, indicating that nuclear GAPDH induces cell death via p53 activation.	Glucose	44-51	P53	Homo sapiens	225-228
19855432-5	2010	ROS generation was attributed to the suppression of B-cell lymphoma-2 (Bcl-2) phosphorylation, and resulted in DNA damage and p53 activation.	Reactive Oxygen Species	0-3	P53	Homo sapiens	126-129
20038740-3	2010	To test whether the effects of doxorubicin on cardiac anatomy and function were mediated by alterations in cardiac progenitor cells (CPCs), these cells were exposed to the anthracycline, which increased the formation of reactive oxygen species and caused increases in DNA damage, expression of p53, telomere attrition, and apoptosis.	Anthracyclines	172-185	P53	Homo sapiens	294-297
21338227-2	2010	In the tumour suppressor Trp53 gene, a codon 72 polymorphism is frequent in the form of a single nucleotide polymorphism that leads to substitution of an arginine for a proline.	Arginine	154-162	P53	Homo sapiens	25-30
19802016-0	2010	Akt promotes chemoresistance in human ovarian cancer cells by modulating cisplatin-induced, p53-dependent ubiquitination of FLICE-like inhibitory protein.	Cisplatin	73-82	P53	Homo sapiens	92-95
19802016-1	2010	Although Akt is a determinant of cisplatin (cis-diaminedichloroplatinum (CDDP)) resistance in ovarian cancer cells, which is related in part to its inhibitory action on p53 activation, precisely how Akt confers CDDP resistance is unclear.	Cisplatin	33-42	P53	Homo sapiens	169-172
19802016-1	2010	Although Akt is a determinant of cisplatin (cis-diaminedichloroplatinum (CDDP)) resistance in ovarian cancer cells, which is related in part to its inhibitory action on p53 activation, precisely how Akt confers CDDP resistance is unclear.	Cisplatin	44-71	P53	Homo sapiens	169-172
19802016-1	2010	Although Akt is a determinant of cisplatin (cis-diaminedichloroplatinum (CDDP)) resistance in ovarian cancer cells, which is related in part to its inhibitory action on p53 activation, precisely how Akt confers CDDP resistance is unclear.	Cisplatin	73-77	P53	Homo sapiens	169-172
19802016-2	2010	In this study, we show that CDDP induced p53-dependent Fas-associated death domain-like interleukin-1beta-converting enzyme (FLICE)-like inhibitory protein (FLIP) degradation in chemosensitive ovarian cancer cells but not their resistant counterparts.	Cisplatin	28-32	P53	Homo sapiens	41-44
19802016-3	2010	CDDP induced FLIP-p53-Itch interaction, colocalization and FLIP ubiquitination in chemosensitive but not chemoresistant ovarian cancer cells.	Cisplatin	0-4	P53	Homo sapiens	18-21
19802016-6	2010	These results suggest that Akt confers resistance, in part, by modulating CDDP-induced, p53-dependent FLIP ubiquitination.	Cisplatin	74-78	P53	Homo sapiens	88-91
19686703-6	2010	ZM-induced apoptosis was associated with an upregulation of p53, breakdown of the mitochondrial membrane potential (DeltaPsim) and activation of caspase-3.	4-(4-(N-benzoylamino)anilino)-6-methoxy-7-(3-(1-morpholino)propoxy)quinazoline	0-2	P53	Homo sapiens	60-63
20082853-2	2010	To investigate the frequency of proline and arginine alleles of TP53 codon 72, the present study analyzed the DNA from blood samples of 30 Iranian women with endometrial cancer, in comparison with 32 healthy women.	Arginine	44-52	P53	Homo sapiens	64-68
19883646-0	2010	Theaflavins retard human breast cancer cell migration by inhibiting NF-kappaB via p53-ROS cross-talk.	Reactive Oxygen Species	86-89	P53	Homo sapiens	82-85
19883646-2	2010	Our data suggest that p53-dependent reactive oxygen species (ROS) induce p53-phosphorylation via p38MAPK in a feedback loop to inhibit IkappaBalpha-phosphorylation and NF-kappaB/p65 nuclear translocation, thereby down-regulating the metastatic proteins metalloproteinase (MMP)-2 and MMP-9.	Reactive Oxygen Species	36-59	P53	Homo sapiens	22-25
19883646-2	2010	Our data suggest that p53-dependent reactive oxygen species (ROS) induce p53-phosphorylation via p38MAPK in a feedback loop to inhibit IkappaBalpha-phosphorylation and NF-kappaB/p65 nuclear translocation, thereby down-regulating the metastatic proteins metalloproteinase (MMP)-2 and MMP-9.	Reactive Oxygen Species	36-59	P53	Homo sapiens	73-76
19883646-2	2010	Our data suggest that p53-dependent reactive oxygen species (ROS) induce p53-phosphorylation via p38MAPK in a feedback loop to inhibit IkappaBalpha-phosphorylation and NF-kappaB/p65 nuclear translocation, thereby down-regulating the metastatic proteins metalloproteinase (MMP)-2 and MMP-9.	Reactive Oxygen Species	61-64	P53	Homo sapiens	22-25
19883646-2	2010	Our data suggest that p53-dependent reactive oxygen species (ROS) induce p53-phosphorylation via p38MAPK in a feedback loop to inhibit IkappaBalpha-phosphorylation and NF-kappaB/p65 nuclear translocation, thereby down-regulating the metastatic proteins metalloproteinase (MMP)-2 and MMP-9.	Reactive Oxygen Species	61-64	P53	Homo sapiens	73-76
19883646-5	2010	These results indicate that inhibition of NF-kappaB via p53-ROS crosstalk is a pre-requisite for theaflavins to accomplish the anti-migratory effect in breast cancer cells.	Reactive Oxygen Species	60-63	P53	Homo sapiens	56-59
19943112-6	2010	Interestingly, selective inactivation of NF-kappaB using either an NF-kappaB decoy or parthenolide, a blocker of IKK-dependent NF-kappaB activation, reduced, rather then increased, apoptosis and p53 levels in FC1-depleted cells.	parthenolide	86-98	P53	Homo sapiens	195-198
21133638-5	2010	OBJECTIVE: The purpose of this study was to investigate the p53 polymorphism at codon 72 which results in encoding of either proline or arginine.	Arginine	136-144	P53	Homo sapiens	60-63
19913499-3	2010	Pretreatment of 1-LN cancer cells with this agent significantly inhibited antibody or doxorubicin-induced upregulation of p53.	Doxorubicin	86-97	P53	Homo sapiens	122-125
19360465-3	2010	Of the analyzed genes, ERCC2, XRCC1, XRCC2, XRCC3 and Lig4 participate in DNA repair, TP53 in cell cycle check point control, AIB1, AR, COMT, CYP11A1, CYP17A1, CYP19A1, HSD17 and PGR in steroid hormone biosynthesis/metabolism/signaling, TYMS in folate metabolism and HER2, IL6, LRP1, TGFB and TGFBR1 affect cell growth.	Steroids	186-201	P53	Homo sapiens	86-90
20686221-6	2010	In our study curcumin increased the expression of GADD45 and 153 in a p53-independent manner.	Curcumin	13-21	P53	Homo sapiens	70-73
20190405-9	2010	Induction of p53, the activation of caspase-3 by H(2)O(2) which accompanying downregulation of bcl-2, was blocked by CXC195.	Hydrogen Peroxide	49-57	P53	Homo sapiens	13-16
19360465-3	2010	Of the analyzed genes, ERCC2, XRCC1, XRCC2, XRCC3 and Lig4 participate in DNA repair, TP53 in cell cycle check point control, AIB1, AR, COMT, CYP11A1, CYP17A1, CYP19A1, HSD17 and PGR in steroid hormone biosynthesis/metabolism/signaling, TYMS in folate metabolism and HER2, IL6, LRP1, TGFB and TGFBR1 affect cell growth.	Folic Acid	245-251	P53	Homo sapiens	86-90
20557688-9	2010	In conclusion, the release of ROS by PU- or PTFE-treated THP-1 cells may induce iNOS expression and cause apoptosis in HUVECs via the p53, Bax and Bcl-2 proteins.	Reactive Oxygen Species	30-33	P53	Homo sapiens	134-137
20500145-8	2010	Finally, ursodeoxycholic acid (UDCA), an endogenous bile acid used to treat cholestatic liver diseases, was recently described as a fine modulator of the complex control of p53 by Mdm-2.	Bile Acids and Salts	52-61	P53	Homo sapiens	173-176
19854294-2	2010	Our explorative pathway analysis on seven published gene-sets associated with platinum resistance in ovarian cancer reveals TP53 and transforming growth factor beta as key genes.	Platinum	78-86	P53	Homo sapiens	124-128
20130515-5	2010	RESULTS: Women homozygous for the p53 codon 72 Arg genotype were at a 5.6-fold higher risk for developing cervical intraepithelial neoplasia (CIN) 2 or 3 compared with those showing homozygosity for the Pro genotype or heterozygosity for the Pro/Arg genotype.	Arginine	47-50	P53	Homo sapiens	34-37
20130515-5	2010	RESULTS: Women homozygous for the p53 codon 72 Arg genotype were at a 5.6-fold higher risk for developing cervical intraepithelial neoplasia (CIN) 2 or 3 compared with those showing homozygosity for the Pro genotype or heterozygosity for the Pro/Arg genotype.	Arginine	246-249	P53	Homo sapiens	34-37
20809980-9	2010	Higher levels of PGG induced more caspase-mediated apoptosis in MCF-7, in strong association with induction of P53 Ser(15) phosphorylation, than in MDA-MB-231 cells.	Serine	115-118	P53	Homo sapiens	111-114
20339300-8	2010	Real-time PCR indicated that the expression of Bcl-2, Pax3, Bmp4 and Slug was down-regulated in the nicotine group, while the expression of P53, Bax and Msx1 was up-regulated.	Nicotine	100-108	P53	Homo sapiens	140-143
20005456-12	2010	Phosphorylation of p53 at serine 15 as well as the expression of p21(WAF1/CIP1) was induced in NP-2 cells after irradiation.	Serine	26-32	P53	Homo sapiens	19-22
20005456-13	2010	Furthermore, we found that irradiation with C-ions induced cellular senescence in a human glioma cell line lacking functional p53.	Carbon	44-45	P53	Homo sapiens	126-129
20563922-6	2010	The TP53 polymorphism distribution in this population was 64 (21.1%) Arg/Arg, 55 (18.1%) Pro/Pro, and 185 (60.9%) Arg/Pro.	Arginine	69-72	P53	Homo sapiens	4-8
19609560-2	2010	The objective of this study was to explore the value of the p53 mutational status, using four different techniques, in advanced OC patients as a predictive marker for responsiveness to platinum-based chemotherapy.	Platinum	185-193	P53	Homo sapiens	60-63
20010306-3	2010	Mutation analysis of TP53 Exons 4 to 9 on DNA from formalin-fixed, paraffin-embedded specimens was performed by bidirectional DNA sequencing.	Paraffin	67-75	P53	Homo sapiens	21-25
19857530-7	2010	Lys 305 of p53 was identified as one of the Ub acceptor sites using this strategy.	Lysine	0-3	P53	Homo sapiens	11-14
21253477-5	2010	to evaluate whatever inactivation of tumor suppressor gene (p53) increases with the tumor progression from normal salivary tissue to PA and eventually CPA.	cpa	151-154	P53	Homo sapiens	60-63
20505276-7	2010	Furthermore, polymerase chain reaction-single-strand conformation polymorphism and following nucleotide sequencing showed that the p53 gene was mutated at codon 215, leading to an amino acid substitution from Ser to Arg.	Serine	209-212	P53	Homo sapiens	131-134
20505276-7	2010	Furthermore, polymerase chain reaction-single-strand conformation polymorphism and following nucleotide sequencing showed that the p53 gene was mutated at codon 215, leading to an amino acid substitution from Ser to Arg.	Arginine	216-219	P53	Homo sapiens	131-134
20563922-6	2010	The TP53 polymorphism distribution in this population was 64 (21.1%) Arg/Arg, 55 (18.1%) Pro/Pro, and 185 (60.9%) Arg/Pro.	Arginine	73-76	P53	Homo sapiens	4-8
20563922-6	2010	The TP53 polymorphism distribution in this population was 64 (21.1%) Arg/Arg, 55 (18.1%) Pro/Pro, and 185 (60.9%) Arg/Pro.	Arginine	73-76	P53	Homo sapiens	4-8
19629643-5	2010	Here, we show that four of seven types of DNA damage signals we examined (induction by etoposide, doxorubicin, camptothecin and cisplatin treatment) resulted in significant Apak phosphorylation and dissociation of Apak from p53, releasing the inhibition of p53 transcriptional activity.	Doxorubicin	98-109	P53	Homo sapiens	224-227
19608275-8	2010	Furthermore, the synergistically potentiated apoptosis by p38 MAPK inhibition was associated with the attenuation of ATO+bortezomib-mediated activation of Hsp27 as well as the enhancement of ATO+bortezomib-mediated JNK activation, p53 up-regulation, and Bcl-2 down-regulation.	ato+bortezomib	191-205	P53	Homo sapiens	231-234
19676105-10	2010	We conclude that p53-independent curcumin-induced apoptosis in ovarian carcinoma cells involves p38 MAPK activation, ablation of prosurvival Akt signaling, and reduced expression of the antiapoptotic proteins Bcl-2 and survivin.	Curcumin	33-41	P53	Homo sapiens	17-20
19676105-0	2010	Curcumin-induced apoptosis in ovarian carcinoma cells is p53-independent and involves p38 mitogen-activated protein kinase activation and downregulation of Bcl-2 and survivin expression and Akt signaling.	Curcumin	0-8	P53	Homo sapiens	57-60
19629643-5	2010	Here, we show that four of seven types of DNA damage signals we examined (induction by etoposide, doxorubicin, camptothecin and cisplatin treatment) resulted in significant Apak phosphorylation and dissociation of Apak from p53, releasing the inhibition of p53 transcriptional activity.	Doxorubicin	98-109	P53	Homo sapiens	257-260
19676105-3	2010	In this study we show that curcumin exhibited time- and dose-dependent cytotoxicity against monolayer cultures of ovarian carcinoma cell lines with differing p53 status (wild-type p53: HEY, OVCA429; mutant p53: OCC1; null p53: SKOV3).	Curcumin	27-35	P53	Homo sapiens	158-161
19676105-3	2010	In this study we show that curcumin exhibited time- and dose-dependent cytotoxicity against monolayer cultures of ovarian carcinoma cell lines with differing p53 status (wild-type p53: HEY, OVCA429; mutant p53: OCC1; null p53: SKOV3).	Curcumin	27-35	P53	Homo sapiens	180-183
19676105-3	2010	In this study we show that curcumin exhibited time- and dose-dependent cytotoxicity against monolayer cultures of ovarian carcinoma cell lines with differing p53 status (wild-type p53: HEY, OVCA429; mutant p53: OCC1; null p53: SKOV3).	Curcumin	27-35	P53	Homo sapiens	180-183
19676105-3	2010	In this study we show that curcumin exhibited time- and dose-dependent cytotoxicity against monolayer cultures of ovarian carcinoma cell lines with differing p53 status (wild-type p53: HEY, OVCA429; mutant p53: OCC1; null p53: SKOV3).	Curcumin	27-35	P53	Homo sapiens	180-183
19629643-5	2010	Here, we show that four of seven types of DNA damage signals we examined (induction by etoposide, doxorubicin, camptothecin and cisplatin treatment) resulted in significant Apak phosphorylation and dissociation of Apak from p53, releasing the inhibition of p53 transcriptional activity.	Cisplatin	128-137	P53	Homo sapiens	224-227
19629643-5	2010	Here, we show that four of seven types of DNA damage signals we examined (induction by etoposide, doxorubicin, camptothecin and cisplatin treatment) resulted in significant Apak phosphorylation and dissociation of Apak from p53, releasing the inhibition of p53 transcriptional activity.	Cisplatin	128-137	P53	Homo sapiens	257-260
21499441-6	2010	Both, NPM and NCL interact with p53 and hinder its phosphorylation at Serine 15 in response to bleomycin.	Serine	70-76	P53	Homo sapiens	32-35
20661829-0	2010	Protection of p53 wild type cells from taxol by genistein in the combined treatment of lung cancer.	Paclitaxel	39-44	P53	Homo sapiens	14-17
20117988-10	2010	In cells treated with a low concentration of L-Arg, the expressions of VEGF and COX-2 were increased as compared with those in the control cells; higher concentrations of L-Arg obviously decreased the expressions of p53 and bcl-2 and increased the expression of bax.	Arginine	45-50	P53	Homo sapiens	216-219
20117988-10	2010	In cells treated with a low concentration of L-Arg, the expressions of VEGF and COX-2 were increased as compared with those in the control cells; higher concentrations of L-Arg obviously decreased the expressions of p53 and bcl-2 and increased the expression of bax.	Arginine	171-176	P53	Homo sapiens	216-219
20117988-13	2010	The mechanism of L-Arg- induced cell apoptosis may be related to the up-regulation of bax protein and the down-regulation of p53 and bcl-2 proteins.	Arginine	17-22	P53	Homo sapiens	125-128
20025464-0	2010	DNA damage and p53-mediated growth arrest in human cells treated with platinum nanoparticles.	Platinum	70-78	P53	Homo sapiens	15-18
20432164-6	2010	These data support an association between calcium and rectal tumors overall as well as specifically with TP53 mutations.	Calcium	42-49	P53	Homo sapiens	105-109
20661829-1	2010	This study specifies the basic principles to selectively kill p53-deficient cells (H1299, FaDu) by taxol and to protect p53 wild type cells (A549) by the prior administration of structurally related flavonoids (apigenin, genistein, and quercetin).	Paclitaxel	99-104	P53	Homo sapiens	62-65
20661829-7	2010	The proposed therapeutic strategy allows protection of p53 wild type cells from taxol and selectively increases apoptosis in p53-deficient cells.	Paclitaxel	80-85	P53	Homo sapiens	55-58
20661829-7	2010	The proposed therapeutic strategy allows protection of p53 wild type cells from taxol and selectively increases apoptosis in p53-deficient cells.	Paclitaxel	80-85	P53	Homo sapiens	125-128
20228131-0	2010	Cyclophosphamide dose intensification may circumvent anthracycline resistance of p53 mutant breast cancers.	Anthracyclines	53-66	P53	Homo sapiens	81-84
20228131-1	2010	The predictive value of p53 for the efficacy of front-line anthracycline-based chemotherapy regimens has been a matter of significant controversy.	Anthracyclines	59-72	P53	Homo sapiens	24-27
20228131-8	2010	Indeed, when restricting our analysis to patients with ER(-) tumors, we confirmed that a mutant p53 status was associated with anthracycline resistance, but found that p53 inactivation was required for response to the dose-intense alkylating regimen.	Anthracyclines	127-140	P53	Homo sapiens	96-99
20185936-8	2010	CONCLUSIONS: Redox-active iron and copper in pleural fluid and saliva, upon encounter with CS, may be responsible for this carcinogenesis, mediated via alteration of p53 function.	Iron	26-30	P53	Homo sapiens	166-169
20185936-8	2010	CONCLUSIONS: Redox-active iron and copper in pleural fluid and saliva, upon encounter with CS, may be responsible for this carcinogenesis, mediated via alteration of p53 function.	Copper	35-41	P53	Homo sapiens	166-169
20980775-3	2010	RESULTS: The wt-p53 human pancreatic tumor cell line Capan-2 and p53-efficient mouse embryonic fibroblasts (MEFs) were more responsive to treatment with TMZ + BG than mutant p53 Capan-1 and p53-null MEFs.	O(6)-benzylguanine	159-161	P53	Homo sapiens	16-19
20681406-3	2010	Deficient tumor suppressor functions, such as TP53 mutations and p14(ARF)/p16(INK4a) deletions, are characteristic for GBM and can cause resistance to DNA damaging agents such as cisplatin and to HDACi like TSA.	Cisplatin	179-188	P53	Homo sapiens	46-50
20980775-3	2010	RESULTS: The wt-p53 human pancreatic tumor cell line Capan-2 and p53-efficient mouse embryonic fibroblasts (MEFs) were more responsive to treatment with TMZ + BG than mutant p53 Capan-1 and p53-null MEFs.	O(6)-benzylguanine	159-161	P53	Homo sapiens	65-68
20980775-6	2010	The effect of p53 on BG + TMZ toxicity was supported by a marked change in apoptosis when p53 function was restored/inactivated.	O(6)-benzylguanine	21-23	P53	Homo sapiens	14-17
20980775-6	2010	The effect of p53 on BG + TMZ toxicity was supported by a marked change in apoptosis when p53 function was restored/inactivated.	O(6)-benzylguanine	21-23	P53	Homo sapiens	90-93
20699632-5	2010	RESULTS: the oxamic and tartronic acids inhibited aerobic glycolysis, impaired the growth of both cell lines and also induced an increased expression of p53-upregulated modulator of apoptosis, a signal of cell death.	oxamic	13-19	P53	Homo sapiens	153-156
19861417-7	2009	Persistent DHCR24 overexpression did not alter the phosphorylation status of p53 but resulted in decreased acetylation of p53 at lysine residues 373 and 382 in the nucleus after treatment with hydrogen peroxide.	Lysine	129-135	P53	Homo sapiens	122-125
20041757-4	2010	For human cells irradiated with iron ions, cell survival was decreased, and in p53 mutant cells, the levels of mutagenesis were increased when HRR was impaired.	Iron	32-36	P53	Homo sapiens	79-82
20495739-9	2010	We used the monoclonal antibody DO7 that detects the wild and mutant form of p53-protein, by EnVision technique and DAB-visualization.	diazobenzenesulfonic acid	116-119	P53	Homo sapiens	77-80
20023923-2	2009	Azide, a singlet oxygen quencher, greatly reduced the p53 photocrosslinking, consistent with the idea that singlet oxygen is the reactive oxygen species involved in p53 photocrosslinking.	Reactive Oxygen Species	129-152	P53	Homo sapiens	54-57
20023923-2	2009	Azide, a singlet oxygen quencher, greatly reduced the p53 photocrosslinking, consistent with the idea that singlet oxygen is the reactive oxygen species involved in p53 photocrosslinking.	Reactive Oxygen Species	129-152	P53	Homo sapiens	165-168
20530960-6	2010	CONCLUSIONS: These results show that experimental varicocele may induce p53-dependent apoptosis through activation of gamma-H2AX in the primary spermatocytes, and suggest that gamma-H2AX may be related to apoptotic signal transduction in experimental varicocele.	gamma-h2ax	118-128	P53	Homo sapiens	72-75
20530960-6	2010	CONCLUSIONS: These results show that experimental varicocele may induce p53-dependent apoptosis through activation of gamma-H2AX in the primary spermatocytes, and suggest that gamma-H2AX may be related to apoptotic signal transduction in experimental varicocele.	gamma-h2ax	176-186	P53	Homo sapiens	72-75
19861417-7	2009	Persistent DHCR24 overexpression did not alter the phosphorylation status of p53 but resulted in decreased acetylation of p53 at lysine residues 373 and 382 in the nucleus after treatment with hydrogen peroxide.	Hydrogen Peroxide	193-210	P53	Homo sapiens	122-125
19819244-5	2009	Phosphorylation of Ser and Thr residues increased the affinity for the p53 TAD.	Serine	19-22	P53	Homo sapiens	71-74
19833096-4	2009	These effects were associated with decreased 8-iso-prostaglandin F(2alpha) and peroxynitrite formation, enhanced protein expression of NAD(+)-dependent class III histone deacetylase sirtuin (SIRT) 1, and downregulated protein expression of histone senescence factor p53.	NAD	135-141	P53	Homo sapiens	266-269
19995986-10	2009	These results demonstrate that ChREBP plays a key role both in redirecting glucose metabolism to anabolic pathways and suppressing p53 activity.	Glucose	75-82	P53	Homo sapiens	131-134
19819244-5	2009	Phosphorylation of Ser and Thr residues increased the affinity for the p53 TAD.	Threonine	27-30	P53	Homo sapiens	71-74
19954513-0	2009	Identification of colorectal cancer patients with tumors carrying the TP53 mutation on the codon 72 proline allele that benefited most from 5-fluorouracil (5-FU) based postoperative chemotherapy.	Fluorouracil	140-154	P53	Homo sapiens	70-74
19682970-1	2009	Sirtuins are nicotinamide adenine dinucleotide (NAD(+))-dependent deacetylases that catalyze the deacetylation of proteins such as histones and p53.	NAD	13-46	P53	Homo sapiens	144-147
19735649-5	2009	Both phosphorylated-p53 (Ser-15) and gamma-H2AX were up-regulated and accumulated in the nuclei of p53-wild type human colorectal cancer HCT116 cells after exposure to oxaliplatin.	Serine	25-28	P53	Homo sapiens	20-23
19735649-5	2009	Both phosphorylated-p53 (Ser-15) and gamma-H2AX were up-regulated and accumulated in the nuclei of p53-wild type human colorectal cancer HCT116 cells after exposure to oxaliplatin.	Serine	25-28	P53	Homo sapiens	99-102
19816404-7	2009	Blocking MDM2 phosphorylation by alanine substitution of all six phosphorylation sites results in constitutive degradation of p53 after DNA damage.	Alanine	33-40	P53	Homo sapiens	126-129
19934315-0	2009	Imatinib mesylate induces cisplatin hypersensitivity in Bcr-Abl+ cells by differential modulation of p53 transcriptional and proapoptotic activity.	Cisplatin	26-35	P53	Homo sapiens	101-104
19934315-8	2009	As a consequence, phosphorylation of p53 on Ser(15) and its activity as a transcription factor was significantly diminished.	Serine	44-47	P53	Homo sapiens	37-40
19934315-9	2009	Furthermore, p53 accumulated predominantly in the cytoplasm in Bcr-Abl(+) cells treated with imatinib and cisplatin.	Cisplatin	106-115	P53	Homo sapiens	13-16
19934315-10	2009	Silencing of p53 significantly reduced sensitivity to cisplatin in imatinib-treated Bcr-Abl(+) cells, indicating that p53 retains its proapoptotic activity.	Cisplatin	54-63	P53	Homo sapiens	13-16
19934315-10	2009	Silencing of p53 significantly reduced sensitivity to cisplatin in imatinib-treated Bcr-Abl(+) cells, indicating that p53 retains its proapoptotic activity.	Cisplatin	54-63	P53	Homo sapiens	118-121
19934315-11	2009	Simultaneous downregulation of Bcl-x(L) was an additional requirement for cisplatin hypersensitivity, as p53-dependent cell death could be antagonized by exogenous Bcl-x(L).	Cisplatin	74-83	P53	Homo sapiens	105-108
19934326-2	2009	Nocodazole-mediated aneuploidy was increased in p53-defective (p53Mut) cells; however, it was not increased in p53 wild-type (p53WT) cells.	Nocodazole	0-10	P53	Homo sapiens	48-51
19934326-2	2009	Nocodazole-mediated aneuploidy was increased in p53-defective (p53Mut) cells; however, it was not increased in p53 wild-type (p53WT) cells.	Nocodazole	0-10	P53	Homo sapiens	63-66
20005840-2	2009	We report that SOCS1 is required for transcriptional activity, DNA binding, and serine 15 phosphorylation of p53 in the context of STAT5 signaling.	Serine	80-86	P53	Homo sapiens	109-112
19766654-6	2009	In fact, substitution of this Asn to Ala of CHC diminished its ability to interact with p53, leading to reduced activity to transactivate p53.	Alanine	37-40	P53	Homo sapiens	88-91
19766654-6	2009	In fact, substitution of this Asn to Ala of CHC diminished its ability to interact with p53, leading to reduced activity to transactivate p53.	Alanine	37-40	P53	Homo sapiens	138-141
19958544-0	2009	An MDM2 antagonist (MI-319) restores p53 functions and increases the life span of orally treated follicular lymphoma bearing animals.	MI 319	20-26	P53	Homo sapiens	37-40
19958544-1	2009	BACKGROUND: MI-319 is a synthetic small molecule designed to target the MDM2-P53 interaction.	MI 319	12-18	P53	Homo sapiens	77-80
19958544-7	2009	In vitro, MI-319 exhibited the strongest anti-proliferation activity against FSCCL and four patient cells, which all have wild-type p53.	MI 319	10-16	P53	Homo sapiens	132-135
19954513-0	2009	Identification of colorectal cancer patients with tumors carrying the TP53 mutation on the codon 72 proline allele that benefited most from 5-fluorouracil (5-FU) based postoperative chemotherapy.	Fluorouracil	156-160	P53	Homo sapiens	70-74
19954513-2	2009	Previous in vitro and clinical investigations reported that CRC patients with wild-type p53 gene (TP53)-tumors benefit from 5-fluorouracil (5-FU) based chemotherapy, while those with mutated TP53-tumors do not.	Fluorouracil	124-138	P53	Homo sapiens	88-91
19954513-2	2009	Previous in vitro and clinical investigations reported that CRC patients with wild-type p53 gene (TP53)-tumors benefit from 5-fluorouracil (5-FU) based chemotherapy, while those with mutated TP53-tumors do not.	Fluorouracil	124-138	P53	Homo sapiens	98-102
19954513-2	2009	Previous in vitro and clinical investigations reported that CRC patients with wild-type p53 gene (TP53)-tumors benefit from 5-fluorouracil (5-FU) based chemotherapy, while those with mutated TP53-tumors do not.	Fluorouracil	140-144	P53	Homo sapiens	88-91
19954513-2	2009	Previous in vitro and clinical investigations reported that CRC patients with wild-type p53 gene (TP53)-tumors benefit from 5-fluorouracil (5-FU) based chemotherapy, while those with mutated TP53-tumors do not.	Fluorouracil	140-144	P53	Homo sapiens	98-102
19954513-10	2009	We raised a possibility that Dukes" stage C colorectal cancer patients with tumors carrying TP53 mutation, especially the P72 allele, benefited from 5-FU based postoperative chemotherapy.	Fluorouracil	149-153	P53	Homo sapiens	92-96
19930465-1	2009	Tumor suppressor p53 plays a pivotal role in the regulation of cell fate determination in response to a variety of cellular stress including carbon source depletion.	Carbon	141-147	P53	Homo sapiens	17-20
19903847-7	2009	Secondly, it increases p53 transcriptional activity by raising p53 phosphorylation at Ser(46) and decreases p53 protein degradation by reducing p53 phosphorylation at Ser(315).	Serine	86-89	P53	Homo sapiens	23-26
19903847-7	2009	Secondly, it increases p53 transcriptional activity by raising p53 phosphorylation at Ser(46) and decreases p53 protein degradation by reducing p53 phosphorylation at Ser(315).	Serine	86-89	P53	Homo sapiens	63-66
19903847-7	2009	Secondly, it increases p53 transcriptional activity by raising p53 phosphorylation at Ser(46) and decreases p53 protein degradation by reducing p53 phosphorylation at Ser(315).	Serine	86-89	P53	Homo sapiens	63-66
19903847-7	2009	Secondly, it increases p53 transcriptional activity by raising p53 phosphorylation at Ser(46) and decreases p53 protein degradation by reducing p53 phosphorylation at Ser(315).	Serine	86-89	P53	Homo sapiens	63-66
19764997-6	2009	Single nucleotide polymorphisms (SNPs) in TP53 (codon 72, arginine &gt; proline) and MDM2 (SNP309, T &gt; G) were genotyped using PCR-RFLP, and nuclear expression levels of p53 were examined using immunohistochemistry.	Arginine	58-66	P53	Homo sapiens	42-46
19930465-9	2009	Taken together, our present findings suggest that p53 is transcriptionally regulated by CREB/phospho-AMPKalpha complex and thereby contributing to the induction of apoptosis under carbon source depletion.	Carbon	180-186	P53	Homo sapiens	50-53
20050373-7	2009	Melatonin"s blockade of BMAL1 expression is associated with the decreased expression of SIRT1, a member of the Silencing Information Regulator family and a histone and protein deacetylase that inhibits the expression of DNA repair enzymes (p53, BRCA1 &amp; 2, and Ku70) and the expression of apoptosis-associated genes.	Melatonin	0-9	P53	Homo sapiens	240-243
19548002-0	2009	Adenovirally mediated p53 overexpression diversely influence the cell cycle of HEp-2 and CAL 27 cell lines upon cisplatin and methotrexate treatment.	Cisplatin	112-121	P53	Homo sapiens	22-25
19548002-7	2009	RESULTS: In CAL 27 cells overexpression of p53 completely abrogated high S phase content observed in methotrexate-treated cells into a G1 and slight G2 arrest, while it sustained G2 arrest of the cells treated with cisplatin, along with the reduction of DNA synthesis and cyclin B1 expression.	Cisplatin	215-224	P53	Homo sapiens	43-46
19548002-8	2009	On the other hand, in HEp-2 cell line p53 overexpression slightly slowed down the progression through S phase in cells treated with methotrexate, decreased the cyclin B1 expression only after 24 h, and failed to sustain the G2 arrest after treatment with cisplatin alone.	Cisplatin	255-264	P53	Homo sapiens	38-41
19548002-10	2009	CONCLUSIONS: This study demonstrates that adenovirally mediated p53 overexpression at sub-cytotoxic levels enhanced the activity of low doses of cisplatin and methotrexate in HEp-2 and CAL 27 cells through changes in the cell cycle.	Cisplatin	145-154	P53	Homo sapiens	64-67
19544329-0	2009	Activation of p53/p21/PUMA alliance and disruption of PI-3/Akt in multimodal targeting of apoptotic signaling cascades in cervical cancer cells by a pentacyclic triterpenediol from Boswellia serrata.	triterpenediol	161-175	P53	Homo sapiens	14-17
19906512-0	2009	Telomeric DNA induces p53-dependent reactive oxygen species and protects against oxidative damage.	Reactive Oxygen Species	36-59	P53	Homo sapiens	22-25
19906512-3	2009	Telomere homolog oligonucleotides (T-oligos) induce adaptive DNA damage responses including increased DNA repair capacity and these effects are mediated, at least in part, through p53.	Oligonucleotides	17-33	P53	Homo sapiens	180-183
19906512-7	2009	Further, T-oligo increases cellular ROS levels via a p53-dependent pathway, and these increases are abrogated by the NAD(P)H oxidase inhibitor diphenyliodonium chloride.	Reactive Oxygen Species	36-39	P53	Homo sapiens	53-56
19741726-7	2009	In addition, nutlin-3a treatment enhanced doxorubicin cytotoxicity against ALK+ ALCL cells harbouring mt p53, and this was associated with p73 upregulation.	Doxorubicin	42-53	P53	Homo sapiens	105-108
19544329-3	2009	It caused oxidative stress by early generation of nitric oxide and reactive oxygen species that robustly up regulated time-dependent expression of p53/p21/PUMA while conversely abrogating phosphatidylinositol-3-kinase (PI3K)/Akt pathways in parallel.	Nitric Oxide	50-62	P53	Homo sapiens	147-150
19544329-3	2009	It caused oxidative stress by early generation of nitric oxide and reactive oxygen species that robustly up regulated time-dependent expression of p53/p21/PUMA while conversely abrogating phosphatidylinositol-3-kinase (PI3K)/Akt pathways in parallel.	Reactive Oxygen Species	67-90	P53	Homo sapiens	147-150
19626645-0	2009	Involvement of p53 in oroxylin A-induced apoptosis in cancer cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	22-32	P53	Homo sapiens	15-18
19952113-5	2009	However, the anticancer drug cisplatin, known to stabilize and activate p53 and p73, downregulated PDGFRB expression not only in SH-SY5Y but also in IMR-32.	Cisplatin	29-38	P53	Homo sapiens	72-75
19626645-2	2009	In this study, we investigate whether p53 is involved in oroxylin A-triggered viability inhibition and apoptosis induction in cancer cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	57-67	P53	Homo sapiens	38-41
19626645-3	2009	In a panel of different cancer cell lines, more potent inhibitory effects of oroxylin A were observed in wtp53 cells than those in mtp53 or p53-null cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	77-87	P53	Homo sapiens	107-110
19626645-4	2009	Moreover, p53-siRNA-transfected HepG2 cells showed lower levels of apoptosis induced by oroxylin A than control-siRNA-transfected cells.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	88-98	P53	Homo sapiens	10-13
19626645-5	2009	Likewise, after oroxylin A treatment, p53-null K-562 cells displayed promoted apoptosis rate when transfected with wtp53 plasmid.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	16-26	P53	Homo sapiens	38-41
19626645-6	2009	Western blot and real-time RT-PCR assay revealed that oroxylin A markedly upregulated p53 protein expression in HepG2 and p53-overexpressing K-562 cells, but had no influence on p53 mRNA synthesis.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	54-64	P53	Homo sapiens	86-89
19626645-6	2009	Western blot and real-time RT-PCR assay revealed that oroxylin A markedly upregulated p53 protein expression in HepG2 and p53-overexpressing K-562 cells, but had no influence on p53 mRNA synthesis.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	54-64	P53	Homo sapiens	122-125
19626645-6	2009	Western blot and real-time RT-PCR assay revealed that oroxylin A markedly upregulated p53 protein expression in HepG2 and p53-overexpressing K-562 cells, but had no influence on p53 mRNA synthesis.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	54-64	P53	Homo sapiens	122-125
19626645-7	2009	Furthermore, after co-treatment with cycloheximide, oroxylin A still exerted a little effect on p53 expression.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	52-62	P53	Homo sapiens	96-99
19626645-10	2009	Additionally, the antioxidant N-acetyl-L-cysteine could obviously abrogate p53 stabilization triggered by oroxylin A.	Acetylcysteine	30-49	P53	Homo sapiens	75-78
19626645-10	2009	Additionally, the antioxidant N-acetyl-L-cysteine could obviously abrogate p53 stabilization triggered by oroxylin A.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	106-116	P53	Homo sapiens	75-78
19626645-11	2009	Therefore, it is summarized that oroxylin A stabilized p53 expression and induced apoptosis at the posttranslational level via downregulating MDM2 expression and interfering MDM2-modulated proteasome-related p53 degradation.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	33-43	P53	Homo sapiens	55-58
19626645-11	2009	Therefore, it is summarized that oroxylin A stabilized p53 expression and induced apoptosis at the posttranslational level via downregulating MDM2 expression and interfering MDM2-modulated proteasome-related p53 degradation.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	33-43	P53	Homo sapiens	208-211
19952113-6	2009	Chromatin immunoprecipitation showed that cisplatin removed DeltaNp73 from the PDGFRB promoter and recruited p53 and p73, leading to binding of histone deacetylase 4.	Cisplatin	42-51	P53	Homo sapiens	109-112
19925028-3	2009	Treatment of MCF-7 cells having wild-type p53 with hydrogen peroxide increased the binding of p53 to DNA as detected using all three assays, but to different extents.	Hydrogen Peroxide	51-68	P53	Homo sapiens	42-45
20017148-7	2009	Moreover, the decreased expression of GRP78 induced by GRP78siRNA or versipelostatin decreased the formation of high molecular weight p53 complexes and p53 monomer and increased trophoblastic invasion.	versipelostatin	69-84	P53	Homo sapiens	134-137
20017148-7	2009	Moreover, the decreased expression of GRP78 induced by GRP78siRNA or versipelostatin decreased the formation of high molecular weight p53 complexes and p53 monomer and increased trophoblastic invasion.	versipelostatin	69-84	P53	Homo sapiens	152-155
19925028-3	2009	Treatment of MCF-7 cells having wild-type p53 with hydrogen peroxide increased the binding of p53 to DNA as detected using all three assays, but to different extents.	Hydrogen Peroxide	51-68	P53	Homo sapiens	94-97
19843866-5	2009	The PADI4 gene encodes an enzyme catalyzing the citrullination of arginine residues in proteins, and ectopic expression of p53 or PADI4 induced protein citrullination.	Arginine	66-74	P53	Homo sapiens	123-126
19744477-2	2009	Here, we demonstrate that emodin induces apoptosis in human lung adenocarcinoma A549 cells by activating a reactive oxygen species-elicited ATM-p53-Bax signaling pathway.	Reactive Oxygen Species	107-130	P53	Homo sapiens	144-147
19744477-6	2009	Upon emodin treatment, p53 is phosphorylated at Ser(15), which is accompanied by the ATM phosphorylation at Ser(1981).	Serine	48-51	P53	Homo sapiens	23-26
19744477-6	2009	Upon emodin treatment, p53 is phosphorylated at Ser(15), which is accompanied by the ATM phosphorylation at Ser(1981).	Serine	108-111	P53	Homo sapiens	23-26
19744477-9	2009	Taken together, our results demonstrate that emodin-induced reactive oxygen species generation activates an ATM-p53-Bax-dependent signaling pathway, which consequently leads to mitochondria-dependent apoptotic cell death in human lung adenocarcinoma A549 cells.	Reactive Oxygen Species	60-83	P53	Homo sapiens	112-115
19716362-3	2009	The tumor suppressor p53 is induced upon iron depletion, and controls reactive oxygen species level.	Iron	41-45	P53	Homo sapiens	21-24
19716362-3	2009	The tumor suppressor p53 is induced upon iron depletion, and controls reactive oxygen species level.	Reactive Oxygen Species	70-93	P53	Homo sapiens	21-24
19833129-2	2009	Several serine residues within the acidic domain of MDM2 are phosphorylated to maintain its activity but become hypo-phosphorylated following DNA damage, leading to inactivation of MDM2 and induction of p53.	Serine	8-14	P53	Homo sapiens	203-206
19580791-8	2009	A subsequent p53/p21(CIP1/WAF1)-dependent inhibition of G1 to S transition is triggered by Curcumin and DAC as a consequence of the mitotic slippage, preventing post-mitotic cells from re-entering the cell cycle.	Curcumin	91-99	P53	Homo sapiens	13-16
19856920-0	2009	Discovery and optimization of chromenotriazolopyrimidines as potent inhibitors of the mouse double minute 2-tumor protein 53 protein-protein interaction.	chromenotriazolopyrimidines	30-57	P53	Homo sapiens	108-124
19670329-6	2009	The p53 response to cisplatin was also largely confined to peripheral cell layers.	Cisplatin	20-29	P53	Homo sapiens	4-7
19815708-6	2009	Here, we show that sirolimus and paclitaxel differentially induce self-digesting autophagy in vascular endothelial cells with changes in expression of LC3B, p53, and Bcl-2, considerably suppressing re-endothelialization and revascularization.	Sirolimus	19-28	P53	Homo sapiens	157-160
19917243-2	2009	(2009) have identified the enzyme guanidinoacetate methyltransferase (GAMT) that regulates creatine metabolism as a p53 target involved in apoptosis, reactive oxygen species (ROS), and fatty acid metabolism.	Reactive Oxygen Species	150-173	P53	Homo sapiens	116-119
19917243-2	2009	(2009) have identified the enzyme guanidinoacetate methyltransferase (GAMT) that regulates creatine metabolism as a p53 target involved in apoptosis, reactive oxygen species (ROS), and fatty acid metabolism.	Reactive Oxygen Species	175-178	P53	Homo sapiens	116-119
19917243-2	2009	(2009) have identified the enzyme guanidinoacetate methyltransferase (GAMT) that regulates creatine metabolism as a p53 target involved in apoptosis, reactive oxygen species (ROS), and fatty acid metabolism.	Fatty Acids	185-195	P53	Homo sapiens	116-119
19917247-5	2009	Additionally, p53--&gt;GAMT upregulates fatty acid oxidation (FAO) induced by glucose starvation, utilizing this pathway as an alternate ATP-generating energy source.	Fatty Acids	40-50	P53	Homo sapiens	14-17
19917247-5	2009	Additionally, p53--&gt;GAMT upregulates fatty acid oxidation (FAO) induced by glucose starvation, utilizing this pathway as an alternate ATP-generating energy source.	Adenosine Triphosphate	137-140	P53	Homo sapiens	14-17
19815708-6	2009	Here, we show that sirolimus and paclitaxel differentially induce self-digesting autophagy in vascular endothelial cells with changes in expression of LC3B, p53, and Bcl-2, considerably suppressing re-endothelialization and revascularization.	Paclitaxel	33-43	P53	Homo sapiens	157-160
19641144-0	2009	Enhanced DNA binding capacity on up-regulated epidermal wild-type p53 in vitiligo by H2O2-mediated oxidation: a possible repair mechanism for DNA damage.	Hydrogen Peroxide	85-89	P53	Homo sapiens	66-69
18853251-1	2009	The p53 tumor suppressor gene has a central role in the defense against cancer, including breast cancer, and contains a polymorphic variant (Arg/Pro) at codon 72 that has been shown to have different biological properties regarding apoptosis and cell cycle arrest.	Arginine	141-144	P53	Homo sapiens	4-7
19838062-5	2009	Interestingly, a novel approximately 130 kDa form of TrxR1, presumably representing a stable covalently linked dimer, and an increased generation of reactive oxygen species (ROS) were induced by RITA in cancer cells in a p53-dependent manner.	Reactive Oxygen Species	149-172	P53	Homo sapiens	221-224
19838062-5	2009	Interestingly, a novel approximately 130 kDa form of TrxR1, presumably representing a stable covalently linked dimer, and an increased generation of reactive oxygen species (ROS) were induced by RITA in cancer cells in a p53-dependent manner.	Reactive Oxygen Species	174-177	P53	Homo sapiens	221-224
19923910-0	2009	The combination of 5-fluorouracil plus p53 pathway restoration is associated with depletion of p53-deficient or mutant p53-expressing putative colon cancer stem cells.	Fluorouracil	19-33	P53	Homo sapiens	95-98
19923910-0	2009	The combination of 5-fluorouracil plus p53 pathway restoration is associated with depletion of p53-deficient or mutant p53-expressing putative colon cancer stem cells.	Fluorouracil	19-33	P53	Homo sapiens	95-98
19923910-6	2009	We further show that p53-reporter activity is induced in DLD1 putative cancer stem cell side-populations analyzed by their Hoechst dye efflux properties following treatment with the p53 pathway restoring drug ellipticine.	hoechst dye	123-134	P53	Homo sapiens	21-24
19923910-6	2009	We further show that p53-reporter activity is induced in DLD1 putative cancer stem cell side-populations analyzed by their Hoechst dye efflux properties following treatment with the p53 pathway restoring drug ellipticine.	hoechst dye	123-134	P53	Homo sapiens	182-185
19874399-6	2009	Interestingly, the combination of the homozygous Arg/Arg genotype of p53 codon 72 and homozygous GG genotype of MDM2 SNP309 polymorphisms was significantly associated with the risk of endometrial cancer (odds ratio = 3.28, 95% confidence interval = 1.13 to 9.53, P= 0.0212).	Arginine	49-52	P53	Homo sapiens	69-72
19874399-6	2009	Interestingly, the combination of the homozygous Arg/Arg genotype of p53 codon 72 and homozygous GG genotype of MDM2 SNP309 polymorphisms was significantly associated with the risk of endometrial cancer (odds ratio = 3.28, 95% confidence interval = 1.13 to 9.53, P= 0.0212).	Arginine	53-56	P53	Homo sapiens	69-72
19642109-3	2009	The vertical dimension and the bearing volume of the DNA binding domain (DBD) of p53, anchored to functionalized gold substrate through exposed lysine residues, alone and after deposing AZ, have been measured by TM-AFM.	Lysine	144-150	P53	Homo sapiens	81-84
20009884-0	2009	Expression of p53 protein phosphorylated at serine 20 and serine 392 in malignant and benign ovarian neoplasms: correlation with clinicopathological parameters of tumors.	Serine	44-50	P53	Homo sapiens	14-17
20009884-0	2009	Expression of p53 protein phosphorylated at serine 20 and serine 392 in malignant and benign ovarian neoplasms: correlation with clinicopathological parameters of tumors.	Serine	58-64	P53	Homo sapiens	14-17
20009884-2	2009	The study investigated the expression of p53 protein phosphorylated at serine 20 (Ser20) and Ser392 and the association between clinicopathological parameters of ovarian neoplasms with respect to p53 protein overexpression.	Serine	71-77	P53	Homo sapiens	41-44
20024960-6	2009	DEB increased the acetylation of p53 at lys-382, dramatically reduced complex formation between p53 and its regulator protein mdm2 and induced the phosphorylation of p53 at serines 15, 20, 37, 46, and 392 in human lymphoblasts.	Lysine	40-43	P53	Homo sapiens	33-36
20024960-7	2009	A dramatic increase in phosphorylation of p53 at serine 15 in correlation to total p53 levels was observed in DEB-exposed Ataxia Telangiectasia Mutated (ATM) proficient human lymphoblasts as compared to DEB-exposed ATM-deficient human lymphoblasts; this implicates the ATM kinase in the elevation of p53 levels in DEB-exposed cells.	Serine	49-55	P53	Homo sapiens	42-45
20024960-7	2009	A dramatic increase in phosphorylation of p53 at serine 15 in correlation to total p53 levels was observed in DEB-exposed Ataxia Telangiectasia Mutated (ATM) proficient human lymphoblasts as compared to DEB-exposed ATM-deficient human lymphoblasts; this implicates the ATM kinase in the elevation of p53 levels in DEB-exposed cells.	Serine	49-55	P53	Homo sapiens	83-86
20024960-7	2009	A dramatic increase in phosphorylation of p53 at serine 15 in correlation to total p53 levels was observed in DEB-exposed Ataxia Telangiectasia Mutated (ATM) proficient human lymphoblasts as compared to DEB-exposed ATM-deficient human lymphoblasts; this implicates the ATM kinase in the elevation of p53 levels in DEB-exposed cells.	Serine	49-55	P53	Homo sapiens	83-86
19887545-6	2009	MK-1775 abrogates G(2) DNA damage checkpoint, leading to apoptosis in combination with DNA-damaging chemotherapeutic agents such as gemcitabine, carboplatin, and cisplatin selectively in p53-deficient cells.	Cisplatin	162-171	P53	Homo sapiens	187-190
19731257-3	2009	The dependence of p53-mediated chemosensitivity on pRb status was first investigated in a prospective study on the prognostic relevance of p53 in breast cancer patients treated with adjuvant chemotherapy (5-fluorouracil, methotrexate and cyclophosphamide).	Fluorouracil	205-219	P53	Homo sapiens	18-21
19731257-6	2009	We then studied the role of pRb status in the p53-mediated response to 5-fluorouracil and methotrexate or doxorubicin treatment in three human cancer cell lines.	Fluorouracil	71-85	P53	Homo sapiens	46-49
19423162-2	2009	A G-C exchange at p53 codon 72 polymorphism results in a substitution of proline (Pro) for arginine (Arg) in the transactivation domain, which was shown to alter the primary structure of the p53 protein.	Arginine	91-99	P53	Homo sapiens	18-21
19423162-2	2009	A G-C exchange at p53 codon 72 polymorphism results in a substitution of proline (Pro) for arginine (Arg) in the transactivation domain, which was shown to alter the primary structure of the p53 protein.	Arginine	91-99	P53	Homo sapiens	191-194
19423162-2	2009	A G-C exchange at p53 codon 72 polymorphism results in a substitution of proline (Pro) for arginine (Arg) in the transactivation domain, which was shown to alter the primary structure of the p53 protein.	Arginine	101-104	P53	Homo sapiens	18-21
19423162-2	2009	A G-C exchange at p53 codon 72 polymorphism results in a substitution of proline (Pro) for arginine (Arg) in the transactivation domain, which was shown to alter the primary structure of the p53 protein.	Arginine	101-104	P53	Homo sapiens	191-194
19683006-4	2009	Here, we examined the thermodynamic and kinetic stability of p53 DNA binding domains from selected invertebrate and vertebrate species by differential scanning calorimetry and equilibrium urea denaturation.	Urea	188-192	P53	Homo sapiens	61-64
19699254-4	2009	Capsaicin also induced degradation of tumor suppressor p53; this effect was enhanced by the ER stressor tunicamycin.	Capsaicin	0-9	P53	Homo sapiens	55-58
19699254-5	2009	The proteasome inhibitor MG132 completely blocked capsaicin-induced p53 degradation and enhanced apoptotic cell death.	Capsaicin	50-59	P53	Homo sapiens	68-71
19854137-4	2009	Importantly, we demonstrate that while the two MOF complexes have indistinguishable activity on histone H4 K16, they differ dramatically in acetylating nonhistone substrate p53.	nonhistone	152-162	P53	Homo sapiens	173-176
19876867-6	2009	We found a deletion of AAG at position 595-597 of TP53 (exon 6), resulting in the deletion of Glu 199 in the protein and a genomic polymorphism of TP73, identified as an A-to-G change, at position E8/+15 at intron 8 (IVS8-15A&gt;G).	Glutamic Acid	94-97	P53	Homo sapiens	50-54
19822456-3	2009	In addition, recent work has provided new insights into mechanisms underlying the antiapoptotic functions of the endogenous bile acid ursodeoxycholic acid (UDCA), suggesting that the finely tuned, complex control of p53 by Mdm2 is a key step in the UDCA modulation of deregulated, p53-triggered apoptosis.	Bile Acids and Salts	124-133	P53	Homo sapiens	216-219
19822456-3	2009	In addition, recent work has provided new insights into mechanisms underlying the antiapoptotic functions of the endogenous bile acid ursodeoxycholic acid (UDCA), suggesting that the finely tuned, complex control of p53 by Mdm2 is a key step in the UDCA modulation of deregulated, p53-triggered apoptosis.	Bile Acids and Salts	124-133	P53	Homo sapiens	281-284
19749791-0	2009	Repression of SHP-1 expression by p53 leads to trkA tyrosine phosphorylation and suppression of breast cancer cell proliferation.	Tyrosine	52-60	P53	Homo sapiens	34-37
19749791-3	2009	p53 can induce trkA activation and tyrosine phosphorylation in the absence of NGF stimulation.	Tyrosine	35-43	P53	Homo sapiens	0-3
20723345-7	2009	The p53 expression levels were higher in Anip973/CDDP than in Anip973 (P&lt;0.01).	cddp	49-53	P53	Homo sapiens	4-7
19808967-5	2009	MDM2 blocks RUNX3 transcriptional activity by interacting with RUNX3 through an acidic domain adjacent to the p53-binding domain of MDM2 and ubiquitinates RUNX3 on key lysine residues to mediate nuclear export and proteasomal degradation.	Lysine	168-174	P53	Homo sapiens	110-113
19770592-4	2009	The present study demonstrates that cisplatin induces the PIDD (p53 induced protein with a death domain) dependent activation of caspase-2.	Cisplatin	36-45	P53	Homo sapiens	64-67
19806023-4	2009	Here we investigated the properties of a new p53 mutant (Lys 351 to Asn) in the TD identified in a cisplatin-resistant ovarian carcinoma cell line (A2780 CIS).	Cisplatin	99-108	P53	Homo sapiens	45-48
19806023-7	2009	Data obtained from the analysis of p53 subcellular localization revealed that K351N mutation inhibits the nuclear export of p53 and accumulation in the cytoplasm induced by cisplatin treatment.	Cisplatin	173-182	P53	Homo sapiens	35-38
19828073-8	2009	We also found a preliminary evidence that, given a triple-negative profile, the distribution of p53 protein is mostly supported in "zero" and "high" states providing useful information in selecting patients that could benefit from an adjuvant anthracyclines/alkylating agent-based chemotherapy.	Anthracyclines	243-257	P53	Homo sapiens	96-99
19806023-7	2009	Data obtained from the analysis of p53 subcellular localization revealed that K351N mutation inhibits the nuclear export of p53 and accumulation in the cytoplasm induced by cisplatin treatment.	Cisplatin	173-182	P53	Homo sapiens	124-127
19713938-1	2009	The p53-inducible TIGAR protein functions as a fructose-2,6-bisphosphatase, promoting the pentose phosphate pathway and helping to lower intracellular reactive oxygen species (ROS).	Reactive Oxygen Species	151-174	P53	Homo sapiens	4-7
19828042-3	2009	Stress-induced homeodomain-interacting protein kinase-2 (HIPK2) phosphorylates p53 at serine-46 (Ser46) for p53 apoptotic activity; p53 acetylation at different C-terminus lysines including p300-mediated lysine-382 (Lys382) is also required for full activation of p53 transcriptional activity.	Serine	86-92	P53	Homo sapiens	79-82
19828042-5	2009	RESULTS: Knockdown of HIPK2 inhibited both adriamycin-induced Ser46 phosphorylation and Lys382 acetylation in p53 protein; however, while combination of ADR and zinc restored Ser46 phosphorylation it did not recover Lys382 acetylation.	Doxorubicin	43-53	P53	Homo sapiens	110-113
19713938-1	2009	The p53-inducible TIGAR protein functions as a fructose-2,6-bisphosphatase, promoting the pentose phosphate pathway and helping to lower intracellular reactive oxygen species (ROS).	Reactive Oxygen Species	176-179	P53	Homo sapiens	4-7
19572936-14	2009	Although the results obtained may indicate that an anaesthetic gas mixture containing sevoflurane induces p53-dependent apoptosis in the Caco-2 cells, the mechanism of apoptosis induction is unclear and remains to be elucidated.	Sevoflurane	86-97	P53	Homo sapiens	106-109
19648647-7	2009	In contrast, expression of growth arrest and DNA damage (GADD) 45alpha, a DNA repair gene that can be regulated by p53-dependent and p53-independent pathways, is stimulated by nitric oxide in a JNK-dependent manner, and knockdown of GADD45alpha expression attenuates the repair of nitric oxide-induced beta-cell DNA damage.	Nitric Oxide	176-188	P53	Homo sapiens	115-118
18930193-1	2009	OBJECTIVE: To determine whether the p53 codon 72 single nucleotide polymorphism, a change of the amino acid arginine (Arg) to proline (Pro) resulting from a single nucleotide mutation of guanine (G) to cytosine (C), has a clinically significant effect on implantation rate in fresh IVF cycles.	Arginine	118-121	P53	Homo sapiens	36-39
19648647-7	2009	In contrast, expression of growth arrest and DNA damage (GADD) 45alpha, a DNA repair gene that can be regulated by p53-dependent and p53-independent pathways, is stimulated by nitric oxide in a JNK-dependent manner, and knockdown of GADD45alpha expression attenuates the repair of nitric oxide-induced beta-cell DNA damage.	Nitric Oxide	176-188	P53	Homo sapiens	133-136
19648647-7	2009	In contrast, expression of growth arrest and DNA damage (GADD) 45alpha, a DNA repair gene that can be regulated by p53-dependent and p53-independent pathways, is stimulated by nitric oxide in a JNK-dependent manner, and knockdown of GADD45alpha expression attenuates the repair of nitric oxide-induced beta-cell DNA damage.	Nitric Oxide	281-293	P53	Homo sapiens	115-118
19648647-7	2009	In contrast, expression of growth arrest and DNA damage (GADD) 45alpha, a DNA repair gene that can be regulated by p53-dependent and p53-independent pathways, is stimulated by nitric oxide in a JNK-dependent manner, and knockdown of GADD45alpha expression attenuates the repair of nitric oxide-induced beta-cell DNA damage.	Nitric Oxide	281-293	P53	Homo sapiens	133-136
19846903-3	2009	Capsaicin and resveratrol, alone or in combination, inhibited cell growth and promoted apoptosis by the elevation of NO; combined treatment in p53-WT cells was most effective.	Capsaicin	0-9	P53	Homo sapiens	143-146
19846903-3	2009	Capsaicin and resveratrol, alone or in combination, inhibited cell growth and promoted apoptosis by the elevation of NO; combined treatment in p53-WT cells was most effective.	Resveratrol	14-25	P53	Homo sapiens	143-146
19846903-7	2009	These findings provide insight into the mechanism of apoptotic action of capsaicin and resveratrol based on p53 status and indicate manipulation of NO may offer exciting opportunities to improve the effectiveness of colon cancer treatment.	Capsaicin	73-82	P53	Homo sapiens	108-111
19846903-7	2009	These findings provide insight into the mechanism of apoptotic action of capsaicin and resveratrol based on p53 status and indicate manipulation of NO may offer exciting opportunities to improve the effectiveness of colon cancer treatment.	Resveratrol	87-98	P53	Homo sapiens	108-111
19363466-11	2009	The growth of SiHa xenograft tumors was reduced using paclitaxel combined with intronic and exonic siRNA, compared with exonic siRNA alone, confirming the synergistic relationship between p53 restoration and paclitaxel.	Paclitaxel	54-64	P53	Homo sapiens	188-191
20443159-8	2009	Induction of apoptosis and cell cycle arrest, important mechanisms for cancer therapy, are stimulated by resveratrol through different mechanisms, e.g., activation of p53 and modulation of cell cycle proteins.	Resveratrol	105-116	P53	Homo sapiens	167-170
19452524-7	2009	Ibuprofen-type drugs, IL6 polymorphisms (rs1800796) and dietary alpha-tocopherol and lycopene significantly altered likelihood of having a TP53 mutation.	Ibuprofen	0-9	P53	Homo sapiens	139-143
19521721-5	2009	Similarly, the alleles of rs1042522 in TP53 that encode arginine (G-allele) or proline (C-allele) at codon 72, which cause increased pro-apoptotic (G-allele) or cell-cycle arrest activities (C-allele), respectively, may moderate p53"s ability to prevent DNA damage.	Arginine	56-64	P53	Homo sapiens	39-43
19521721-5	2009	Similarly, the alleles of rs1042522 in TP53 that encode arginine (G-allele) or proline (C-allele) at codon 72, which cause increased pro-apoptotic (G-allele) or cell-cycle arrest activities (C-allele), respectively, may moderate p53"s ability to prevent DNA damage.	Arginine	56-64	P53	Homo sapiens	229-232
19452524-8	2009	This was especially true for TP53 transversion mutations and dietary antioxidants (OR for beta-carotene 0.51 95% CI 0.27, 0.97, p trend 0.03; alpha-tocopherol 0.41 95% CI 0.20, 0.84, p trend 0.02) Beta-carotene and ibuprofen significantly altered risk of KRAS2 tumors.	Ibuprofen	215-224	P53	Homo sapiens	29-33
19834285-2	2009	We found that silibinin exhibited a protective effect against chemotherapeutic reagent mitomycin C-induced cell death in A375-S2 cells in a p53-dependent manner, which contradicted the findings of previous studies investigating the anti-neoplastic activity of silibinin and developing silibinin as a potential anti-neoplastic drug in clinical therapy.	Silybin	14-23	P53	Homo sapiens	140-143
20157557-4	2009	Addition of nutlin restored doxorubicin-induced p53 protein and transcriptional activity in senescent cells to the levels in early passage cells but only partially restored its apoptotic activity, suggesting that changes in both upstream and downstream p53 signaling during senescence are responsible for attenuated response to genotoxic stress.	Doxorubicin	28-39	P53	Homo sapiens	48-51
19596268-5	2009	In fact, most of the lymphoma cell lines expressing high levels of galectin-7 did not express any detectable level of p53, although expressed p21(Waf1/Cip1) gene following doxorubicin treatment, indicating that p53 was functional in these cells.	Doxorubicin	172-183	P53	Homo sapiens	211-214
19605487-5	2009	Both HCV core protein and a chemotherapeutic agent for HCC, 5-flouorouracil (5-FU), are known to modulate p53.	5-flouorouracil	60-75	P53	Homo sapiens	106-109
19605487-5	2009	Both HCV core protein and a chemotherapeutic agent for HCC, 5-flouorouracil (5-FU), are known to modulate p53.	Fluorouracil	77-81	P53	Homo sapiens	106-109
19605487-6	2009	We examined here whether an association between core and HAX-1 has any functional relevance to p53 modulation in 5-FU-treated cells.	Fluorouracil	113-117	P53	Homo sapiens	95-98
19605487-9	2009	Further, 5-FU-mediated p53 expression was reduced with concurrent HAX-1 suppression in core- or polyprotein-expressing cells compared to control HepG2 cells, and caspase-2 and -7 activities were diminished.	Fluorouracil	9-13	P53	Homo sapiens	23-26
19605487-11	2009	These observations underscore an association between HCV core and HAX-1, which promotes 5-FU mediated p53-dependent caspase-7 activation and hepatocyte growth inhibition.	Fluorouracil	88-92	P53	Homo sapiens	102-105
19681600-0	2009	Effect of thioredoxin deletion and p53 cysteine replacement on human p53 activity in wild-type and thioredoxin reductase null yeast.	Cysteine	39-47	P53	Homo sapiens	69-72
19681600-7	2009	Substitutions at Zn-coordinating cysteines C176, C238, or C242 resulted in p53 inactivation.	Zinc	17-19	P53	Homo sapiens	75-78
19681600-7	2009	Substitutions at Zn-coordinating cysteines C176, C238, or C242 resulted in p53 inactivation.	Cysteine	33-42	P53	Homo sapiens	75-78
19681600-8	2009	Unexpectedly, substitution at cysteine C275 also inactivated p53, which was the first evidence for a non-zinc-coordinating cysteine being essential for p53 function.	Cysteine	30-38	P53	Homo sapiens	61-64
19681600-8	2009	Unexpectedly, substitution at cysteine C275 also inactivated p53, which was the first evidence for a non-zinc-coordinating cysteine being essential for p53 function.	Cysteine	30-38	P53	Homo sapiens	152-155
19681600-8	2009	Unexpectedly, substitution at cysteine C275 also inactivated p53, which was the first evidence for a non-zinc-coordinating cysteine being essential for p53 function.	Cysteine	123-131	P53	Homo sapiens	61-64
19681600-8	2009	Unexpectedly, substitution at cysteine C275 also inactivated p53, which was the first evidence for a non-zinc-coordinating cysteine being essential for p53 function.	Cysteine	123-131	P53	Homo sapiens	152-155
19681600-9	2009	Cysteine substitutions at six positions (C124, C135, C141, C182, C229, and C277) neither inactivated p53 nor relieved the requirement for thioredoxin reductase.	Cysteine	0-8	P53	Homo sapiens	101-104
19681600-11	2009	The results suggested that p53 dependence on thioredoxin reductase either was indirect, perhaps mediated by an upstream activator of p53, or was due to oxidation of one or more of the four essential cysteines.	Cysteine	199-208	P53	Homo sapiens	27-30
19705844-6	2009	The specific ATM inhibitor caffeine significantly decreased tricetin-mediated G2/M arrest by inhibiting the phosphorylation of p53 (serine 15) and Chk2.	Serine	132-138	P53	Homo sapiens	127-130
20157557-4	2009	Addition of nutlin restored doxorubicin-induced p53 protein and transcriptional activity in senescent cells to the levels in early passage cells but only partially restored its apoptotic activity, suggesting that changes in both upstream and downstream p53 signaling during senescence are responsible for attenuated response to genotoxic stress.	Doxorubicin	28-39	P53	Homo sapiens	253-256
19805293-6	2009	The N-terminal 616 aa of CBP, which includes the conserved Zn(2+)-binding C/H1-TAZ1 domain, was the minimal domain sufficient to destabilize p53 in vivo, and it included within an intrinsic E3 autoubiquitination activity and, in a two-step E4 assay, exhibited robust E4 activity for p53.	Zinc	59-65	P53	Homo sapiens	141-144
19784392-8	2009	CONCLUSIONS: Our preliminary results indicate that the arginine variant of rs1042522 within p53 is associated with increased risk of POAG.	Arginine	55-63	P53	Homo sapiens	92-95
19738071-10	2009	Taken together, our results provide new insights on the mechanism of action of pomalidomide and lenalidomide in the regulation of gene transcription, imply possible efficacy in p53 mutated and deleted cancer, and suggest new potential clinical uses as an epigenetic therapy.	pomalidomide	79-91	P53	Homo sapiens	177-180
19706948-6	2009	Comparing the cell cycle change, Glu-GNPs induced acceleration in the G0/G1 phase and accumulation of cells in the G2/M phase at 29.8% versus 18.4% for controls at 24 h. G2/M arrest was accompanied by decreased expression of p53 and cyclin A, and increased expression of cyclin B1 and cyclin E. In conclusion, Glu-GNPs trigger activation of the CDK kinases leading to cell cycle acceleration in the G0/G1 phase and accumulation in the G2/M phase.	Glutamic Acid	33-36	P53	Homo sapiens	225-228
19581934-2	2009	Drug-resistant KB cells selected with cisplatin or oxaliplatin were found to have increased p53 levels and in oxaliplatin-selected cells, a larger p53 predominantly in the cytoplasm.	Cisplatin	38-47	P53	Homo sapiens	92-95
19561079-4	2009	Gene expression profiling of the human fibrosarcoma HT1080 cells showed that, while cisplatin induced p53 targets, A0 up-regulated genes involved in the unfolded protein response (UPR) and response to heavy metals.	Cisplatin	84-93	P53	Homo sapiens	102-105
19796081-0	2009	Oligonucleotide probe array for p53 gene alteration analysis in DNA from formalin-fixed paraffin-embedded breast cancer tissues.	Paraffin	88-96	P53	Homo sapiens	32-35
19796081-2	2009	We sequenced the p53 gene in DNA extracted from archival paraffin-embedded BC tissues and compared the results obtained from direct sequencing with those obtained by oligonucleotide probe array (OPA).	Paraffin	57-65	P53	Homo sapiens	17-20
19578044-7	2009	Furthermore, p53 promotes cisplatin-induced apoptosis by directly binding and counteracting Bcl-x(L) antiapoptotic function.	Cisplatin	26-35	P53	Homo sapiens	13-16
19184017-0	2009	Doxorubicin-induced mitochondrial dysfunction is secondary to nuclear p53 activation in H9c2 cardiomyoblasts.	Doxorubicin	0-11	P53	Homo sapiens	70-73
19184017-4	2009	RESULTS: Doxorubicin accumulation in the nucleus was detected after 3 h treatment, followed by an increase in p53 and a decrease in mitochondrial membrane potential.	Doxorubicin	9-20	P53	Homo sapiens	110-113
19184017-7	2009	Importantly, pifithrin-alpha, a p53 inhibitor, protected against DOX-induced mitochondrial depolarization, caspase activation and cell death.	Doxorubicin	65-68	P53	Homo sapiens	32-35
19184017-8	2009	CONCLUSION: Mitochondrial dysfunction in H9c2 myoblasts treated with DOX is a consequence of nuclear p53 activation rather than a direct effect of the drug on mitochondria.	Doxorubicin	69-72	P53	Homo sapiens	101-104
19578044-8	2009	In conclusion, our findings suggest a novel mode of action for cisplatin to overcome Bcl-2-mediated protection against apoptosis, which requires preferential activation of Bak and p53-mediated upregulation of Noxa protein levels and lipid peroxidation.	Cisplatin	63-72	P53	Homo sapiens	180-183
19652535-0	2009	Wild-type p53 protects normal cells against apoptosis induced by thiostrepton.	Thiostrepton	65-77	P53	Homo sapiens	10-13
19890497-1	2009	Pin1 specifically catalyzes the cis/trans isomerization of phospho-Ser/Thr-Pro bonds and plays an important role in many cellular events through the effects of conformational change on the function of its biological substrates, including cell division cycle 25 C (Cdc25C), c-Jun and p53.	Serine	67-70	P53	Homo sapiens	283-286
19652535-4	2009	We found that only normal cells that have wild-type p53 were resistant to the thiazole antibiotic, thiostrepton, suggesting that p53 plays an antiapoptotic role in normal cells.	Thiostrepton	99-111	P53	Homo sapiens	52-55
19652535-4	2009	We found that only normal cells that have wild-type p53 were resistant to the thiazole antibiotic, thiostrepton, suggesting that p53 plays an antiapoptotic role in normal cells.	Thiostrepton	99-111	P53	Homo sapiens	129-132
19652535-5	2009	In this case p53 status, but not the transformation of cells per se determines their sensitivity to thiostrepton and possibly to other anticancer drugs.	Thiostrepton	100-112	P53	Homo sapiens	13-16
19652535-6	2009	Since p53 is mutated in 50% of human cancers, thiostrepton may selectively kill cancer, but not normal cells.	Thiostrepton	46-58	P53	Homo sapiens	6-9
19890497-1	2009	Pin1 specifically catalyzes the cis/trans isomerization of phospho-Ser/Thr-Pro bonds and plays an important role in many cellular events through the effects of conformational change on the function of its biological substrates, including cell division cycle 25 C (Cdc25C), c-Jun and p53.	Threonine	71-74	P53	Homo sapiens	283-286
19444912-9	2009	These findings represent a novel strategy that could be exploited to overcome cisplatin resistance in patients regardless of p53 status or ability to perform MMR.	Cisplatin	78-87	P53	Homo sapiens	125-128
19783968-6	2009	The exposure of MCF-7 cells to conventional form of doxorubicin resulted in the decrease of p53 expression and the increase of Bcl-2 expression.	Doxorubicin	52-63	P53	Homo sapiens	92-95
19444912-3	2009	Mismatch-repair (MMR) and p53 have previously been shown to be important determinants of cisplatin resistance and can contribute to cisplatin resistance clinically.	Cisplatin	89-98	P53	Homo sapiens	26-29
19444912-3	2009	Mismatch-repair (MMR) and p53 have previously been shown to be important determinants of cisplatin resistance and can contribute to cisplatin resistance clinically.	Cisplatin	132-141	P53	Homo sapiens	26-29
18681908-0	2009	SIRT1 confers protection against UVB- and H2O2-induced cell death via modulation of p53 and JNK in cultured skin keratinocytes.	Hydrogen Peroxide	42-46	P53	Homo sapiens	84-87
18681908-8	2009	Activation of SIRT1 negatively regulates UV- and H(2)O(2)-induced p53 acetylation, because nicotinamide and sirtinol as well as SIRT1 siRNA enhance UV- and H(2)O(2)-induced p53 acetylation, whereas SIRT1 activator resveratrol inhibits it.	Hydrogen Peroxide	49-57	P53	Homo sapiens	66-69
19633417-8	2009	Interestingly, several of these compounds share the ability to target thiols and affect the redox state of p53, indicating that this is critical for mutant p53 rescue.	Sulfhydryl Compounds	70-76	P53	Homo sapiens	156-159
18681908-8	2009	Activation of SIRT1 negatively regulates UV- and H(2)O(2)-induced p53 acetylation, because nicotinamide and sirtinol as well as SIRT1 siRNA enhance UV- and H(2)O(2)-induced p53 acetylation, whereas SIRT1 activator resveratrol inhibits it.	Hydrogen Peroxide	49-57	P53	Homo sapiens	173-176
18681908-8	2009	Activation of SIRT1 negatively regulates UV- and H(2)O(2)-induced p53 acetylation, because nicotinamide and sirtinol as well as SIRT1 siRNA enhance UV- and H(2)O(2)-induced p53 acetylation, whereas SIRT1 activator resveratrol inhibits it.	Hydrogen Peroxide	156-164	P53	Homo sapiens	66-69
18681908-8	2009	Activation of SIRT1 negatively regulates UV- and H(2)O(2)-induced p53 acetylation, because nicotinamide and sirtinol as well as SIRT1 siRNA enhance UV- and H(2)O(2)-induced p53 acetylation, whereas SIRT1 activator resveratrol inhibits it.	Hydrogen Peroxide	156-164	P53	Homo sapiens	173-176
18681908-8	2009	Activation of SIRT1 negatively regulates UV- and H(2)O(2)-induced p53 acetylation, because nicotinamide and sirtinol as well as SIRT1 siRNA enhance UV- and H(2)O(2)-induced p53 acetylation, whereas SIRT1 activator resveratrol inhibits it.	Resveratrol	214-225	P53	Homo sapiens	66-69
19657586-4	2009	We observed that carrying the Pro/Pro genotype of P53 Arg72Pro was a risk factor with respect to the Pro/Arg + Arg/Arg genotypes [Odds Ratio (OR) = 2.02; 95% Confidence Interval (CI) 1.02-4.00; p = 0.047].	Arginine	54-57	P53	Homo sapiens	50-53
19657586-4	2009	We observed that carrying the Pro/Pro genotype of P53 Arg72Pro was a risk factor with respect to the Pro/Arg + Arg/Arg genotypes [Odds Ratio (OR) = 2.02; 95% Confidence Interval (CI) 1.02-4.00; p = 0.047].	Arginine	105-108	P53	Homo sapiens	50-53
19657586-4	2009	We observed that carrying the Pro/Pro genotype of P53 Arg72Pro was a risk factor with respect to the Pro/Arg + Arg/Arg genotypes [Odds Ratio (OR) = 2.02; 95% Confidence Interval (CI) 1.02-4.00; p = 0.047].	Arginine	105-108	P53	Homo sapiens	50-53
19723892-2	2009	A clear p53-dependent expression pattern of PDF was shown in a panel of colorectal cancer cell lines following acute exposure to oxaliplatin, 5-fluorouracil, and SN38.	Fluorouracil	142-156	P53	Homo sapiens	8-11
19714248-1	2009	BACKGROUND: The tumor suppressor homeodomain-interacting protein kinase-2 (HIPK2) by phosphorylating serine 46 (Ser46) is a crucial regulator of p53 apoptotic function.	Serine	101-107	P53	Homo sapiens	145-148
19542220-7	2009	Treatment of p53 mutant colon cancer cells with 5-FU led to an elongated G1 in a Mirk-dependent manner, as G1 was shortened by ectopic overexpression of cyclin D1 mutated at the Mirk phosphorylation site (T288A), but not by wild-type cyclin D1.	Fluorouracil	48-52	P53	Homo sapiens	13-16
19693275-4	2009	Curcumin predominantly induced mitochondria-mediated ROS formation and stimulated the expression of the redox-sensitive pro-apoptotic factor p53.	Curcumin	0-8	P53	Homo sapiens	141-144
19679550-2	2009	We report here that p53, in multiple lines of human cancer cells, is down-regulated by cardiac glycoside drugs digoxin and ouabain, potent inhibitors of Na(+)/K(+)-ATPase.	Digoxin	111-118	P53	Homo sapiens	20-23
19679550-8	2009	Although lowering extracellular K(+) did not reduce p53 as did ouabain and digoxin, it did potentiate both digoxin- and ouabain-induced p53 reduction in sensitive lines.	Digoxin	107-114	P53	Homo sapiens	136-139
19465072-4	2009	Effectiveness of the Pas segment in the intracellular delivery of bioactive peptides using arginine-rich CPPs was exemplified through the enhanced growth inhibition activity of the malignant glioma cells by a retro-inverso peptide derived from the p53 C-terminal 22-amino-acid segment (positions 361-382).	Arginine	91-99	P53	Homo sapiens	248-251
19555448-8	2009	This reduced apoptosis by melatonin was associated with the increase of Bcl-2 expression and a reduction of Bax/Bcl-2 ratio through a relative decrease of p53 mRNA and protein.	Melatonin	26-35	P53	Homo sapiens	155-158
19555448-13	2009	These differential effects on radiation-induced apoptosis by melatonin might involve the regulation of p53 expression.	Melatonin	61-70	P53	Homo sapiens	103-106
21475903-4	2009	Polymorphisms of TP53 include codon 72 containing either arginine (CGC) or proline (CCC).	Arginine	57-65	P53	Homo sapiens	17-21
21475903-4	2009	Polymorphisms of TP53 include codon 72 containing either arginine (CGC) or proline (CCC).	Chlormequat	84-87	P53	Homo sapiens	17-21
19645506-3	2009	Magnolol treatment decreased the protein levels of cyclins A and D1 and increased p21/Cip1, but not cyclins B and D3, cyclin-dependent kinase (CDK)2, CDK4, CDC25C, Weel, p27/Kip1, and p53.	magnolol	0-8	P53	Homo sapiens	184-187
19706526-7	2009	Moreover, HIF2alpha inhibition promotes p53-mediated responses by disrupting cellular redox homeostasis, thereby permitting reactive oxygen species (ROS) accumulation and DNA damage.	Reactive Oxygen Species	124-147	P53	Homo sapiens	40-43
19706526-7	2009	Moreover, HIF2alpha inhibition promotes p53-mediated responses by disrupting cellular redox homeostasis, thereby permitting reactive oxygen species (ROS) accumulation and DNA damage.	Reactive Oxygen Species	149-152	P53	Homo sapiens	40-43
19672316-4	2009	Here, we report that Siomycin A and thiostrepton stabilize the expression of a variety of proteins, such as p21, Mcl-1, p53 and hdm-2 and also act as proteasome inhibitors in vitro.	siomycin A	21-31	P53	Homo sapiens	120-123
19397966-1	2009	Benzo(a)pyrene (BP) forms benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE)-DNA adducts in human breast adenocarcinoma MCF-7 cells, leading to p53 protein induction and phosphorylation.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	26-69	P53	Homo sapiens	144-147
19397966-1	2009	Benzo(a)pyrene (BP) forms benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE)-DNA adducts in human breast adenocarcinoma MCF-7 cells, leading to p53 protein induction and phosphorylation.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	71-75	P53	Homo sapiens	144-147
19672316-4	2009	Here, we report that Siomycin A and thiostrepton stabilize the expression of a variety of proteins, such as p21, Mcl-1, p53 and hdm-2 and also act as proteasome inhibitors in vitro.	Thiostrepton	36-48	P53	Homo sapiens	120-123
19653336-6	2009	Irinotecan sensitizes p53 wild type, mutant and null cells to Fas-mediated cell apoptosis in CRC cells.	Irinotecan	0-10	P53	Homo sapiens	22-25
19541923-12	2009	Ectopic expression of c-Jun/c-Fos or p300 or treatment of cells with phorbol 12-myristate 13-acetate (PMA) stimulated endogenous TFF2 mRNA expression and promoter activity, and p53 inhibited the effects of AP-1 and PMA on TFF2.	Tetradecanoylphorbol Acetate	69-100	P53	Homo sapiens	177-180
19653336-7	2009	Wild type p53 cells were more sensitive to irinotecan than mutated p53.	Irinotecan	43-53	P53	Homo sapiens	10-13
19653336-10	2009	p53 and VEGF status of the patients" tumour is likely to affect the responsiveness of CRC to irinotecan.	Irinotecan	93-103	P53	Homo sapiens	0-3
19651615-5	2009	JNK phosphorylation of p53 at Threonine 81 occurring on polysomes is required for the dissociation of Ubc13 from p53, leading to p53 multimerization and transcriptional activation.	Threonine	30-39	P53	Homo sapiens	23-26
19651615-5	2009	JNK phosphorylation of p53 at Threonine 81 occurring on polysomes is required for the dissociation of Ubc13 from p53, leading to p53 multimerization and transcriptional activation.	Threonine	30-39	P53	Homo sapiens	113-116
19651615-5	2009	JNK phosphorylation of p53 at Threonine 81 occurring on polysomes is required for the dissociation of Ubc13 from p53, leading to p53 multimerization and transcriptional activation.	Threonine	30-39	P53	Homo sapiens	113-116
19541923-12	2009	Ectopic expression of c-Jun/c-Fos or p300 or treatment of cells with phorbol 12-myristate 13-acetate (PMA) stimulated endogenous TFF2 mRNA expression and promoter activity, and p53 inhibited the effects of AP-1 and PMA on TFF2.	Tetradecanoylphorbol Acetate	102-105	P53	Homo sapiens	177-180
19491654-5	2009	In OVCAR-3 cells, p53 gene therapy inhibited the cell growth and sensitized cells to CPT-11/SN-38, but not to docetaxel.	Irinotecan	85-91	P53	Homo sapiens	18-21
19646678-4	2009	VRK1, one of three members of the mammalian VRK family, is a serine/threonine kinase that phosphorylates p53 and CREB and is essential for nuclear envelope formation.	Serine	61-67	P53	Homo sapiens	105-108
19468031-12	2009	Positive p53 status was related to poorer OS and CSS.	Osmium	42-44	P53	Homo sapiens	9-12
19491654-11	2009	These results support the combination of p53 gene therapy with topoisomerase I inhibitors SN-38/CPT-11 when tumour cells contain mutated p53.	Irinotecan	90-95	P53	Homo sapiens	137-140
19491654-5	2009	In OVCAR-3 cells, p53 gene therapy inhibited the cell growth and sensitized cells to CPT-11/SN-38, but not to docetaxel.	Irinotecan	92-97	P53	Homo sapiens	18-21
19491654-11	2009	These results support the combination of p53 gene therapy with topoisomerase I inhibitors SN-38/CPT-11 when tumour cells contain mutated p53.	Irinotecan	96-102	P53	Homo sapiens	137-140
19661311-5	2009	A number of biological parameters, including less advanced tumors and p53 overexpression, were significantly associated with additive chemosensitivity to HDACIs in combination with FLOX and FLIRI in multivariate analyses (p&lt; or =0.001 to 0.023).	flox	181-185	P53	Homo sapiens	70-73
19661313-1	2009	BACKGROUND: We have reported that resveratrol (RSV) and 5-fluorouracil (5-FU) evoked apoptosis through caspase-6 activation in wild-type (p53+/+) and knockout (p53(-/-)) HCT116 human colon cancer cells.	Resveratrol	34-45	P53	Homo sapiens	138-141
19661313-1	2009	BACKGROUND: We have reported that resveratrol (RSV) and 5-fluorouracil (5-FU) evoked apoptosis through caspase-6 activation in wild-type (p53+/+) and knockout (p53(-/-)) HCT116 human colon cancer cells.	Resveratrol	34-45	P53	Homo sapiens	160-163
19661313-1	2009	BACKGROUND: We have reported that resveratrol (RSV) and 5-fluorouracil (5-FU) evoked apoptosis through caspase-6 activation in wild-type (p53+/+) and knockout (p53(-/-)) HCT116 human colon cancer cells.	Resveratrol	47-50	P53	Homo sapiens	138-141
19661313-1	2009	BACKGROUND: We have reported that resveratrol (RSV) and 5-fluorouracil (5-FU) evoked apoptosis through caspase-6 activation in wild-type (p53+/+) and knockout (p53(-/-)) HCT116 human colon cancer cells.	Resveratrol	47-50	P53	Homo sapiens	160-163
19661313-1	2009	BACKGROUND: We have reported that resveratrol (RSV) and 5-fluorouracil (5-FU) evoked apoptosis through caspase-6 activation in wild-type (p53+/+) and knockout (p53(-/-)) HCT116 human colon cancer cells.	Fluorouracil	56-70	P53	Homo sapiens	138-141
19723057-9	2009	Thus, the electrophilic carbon center located in the alpha,beta-unsaturated carbonyl moiety of the cyclopentenone ring might be critical for the control of DNA-binding activity as well as cellular levels of p53 by 15d-PGJ(2).	Carbon	24-30	P53	Homo sapiens	207-210
19723072-5	2009	Chromatin immunoprecipitation analysis has revealed phenyl butyrate and its combinations with RA and vitamin B3 cause histone H4 acetylation in the p21 promoter regions corresponding to p53 and/or Sp1 sites.	Phenylbutyrates	52-67	P53	Homo sapiens	186-189
19723072-5	2009	Chromatin immunoprecipitation analysis has revealed phenyl butyrate and its combinations with RA and vitamin B3 cause histone H4 acetylation in the p21 promoter regions corresponding to p53 and/or Sp1 sites.	Tretinoin	94-96	P53	Homo sapiens	186-189
19661313-1	2009	BACKGROUND: We have reported that resveratrol (RSV) and 5-fluorouracil (5-FU) evoked apoptosis through caspase-6 activation in wild-type (p53+/+) and knockout (p53(-/-)) HCT116 human colon cancer cells.	Fluorouracil	56-70	P53	Homo sapiens	160-163
19661313-1	2009	BACKGROUND: We have reported that resveratrol (RSV) and 5-fluorouracil (5-FU) evoked apoptosis through caspase-6 activation in wild-type (p53+/+) and knockout (p53(-/-)) HCT116 human colon cancer cells.	Fluorouracil	72-76	P53	Homo sapiens	138-141
19661313-1	2009	BACKGROUND: We have reported that resveratrol (RSV) and 5-fluorouracil (5-FU) evoked apoptosis through caspase-6 activation in wild-type (p53+/+) and knockout (p53(-/-)) HCT116 human colon cancer cells.	Fluorouracil	72-76	P53	Homo sapiens	160-163
19661313-4	2009	RESULTS: SC (100 microM) sensitized RSV- (200 microM) and 5-FU (500 microM)-evoked apoptosis in p53+/+ but not p53(-/-) cells.	Fluorouracil	58-62	P53	Homo sapiens	96-99
19723085-7	2009	DHA and ALA inhibited DNA fragmentation, inhibited the decrease in cell viability, and inhibited the expression of apoptotic genes (p53, Bax, apoptosis-inducing factor) induced by hydrogen peroxide in pancreatic acinar cells.	Hydrogen Peroxide	180-197	P53	Homo sapiens	132-135
19661313-7	2009	CONCLUSION: SC is a novel sensitizing agent for both RSV- and 5-FU-evoked apoptosis, through the enhancement of caspase-6 activation in a p53-dependent manner.	Fluorouracil	62-66	P53	Homo sapiens	138-141
19502594-6	2009	Moreover, we observed that CPS activates ATM kinase that is involved in Ser15, Ser20 and Ser392 p53 phosphorylation as shown by the use of the specific inhibitor KU55933.	Capsaicin	27-30	P53	Homo sapiens	96-99
19397953-4	2009	RESULTS: We show that p53 and damage-specific DNA binding protein 2 (ddb2) genes are up-regulated by morphine in a naloxone-sensitive manner.	Morphine	101-109	P53	Homo sapiens	22-25
19397953-5	2009	Furthermore, the results indicate that DNA damage, quantified by apurinic-apyrimidinic site counting assay and phosphorylation of Ser-15 in P53 protein, is induced in CD3+ T cells by morphine in a naloxone-sensitive manner.	Serine	130-133	P53	Homo sapiens	140-143
19397953-5	2009	Furthermore, the results indicate that DNA damage, quantified by apurinic-apyrimidinic site counting assay and phosphorylation of Ser-15 in P53 protein, is induced in CD3+ T cells by morphine in a naloxone-sensitive manner.	Morphine	183-191	P53	Homo sapiens	140-143
19397953-6	2009	GENERAL SIGNIFICANCE: Because it was shown that only the kappa opioid receptor gene is expressed in CD3+ T cells in the opioid receptor family, the present study suggests that morphine induces DNA damage through the action on the kappa opioid receptor, which leads to immune suppression by activation of P53-mediated signal transduction.	Morphine	176-184	P53	Homo sapiens	304-307
19438509-0	2009	Reactive oxygen species up-regulate p53 and Puma; a possible mechanism for apoptosis during combined treatment with TRAIL and wogonin.	Reactive Oxygen Species	0-23	P53	Homo sapiens	36-39
19438509-5	2009	KEY RESULTS: During combined treatment with wogonin and TRAIL, cytotoxicity, poly(ADP-ribose) polymerase cleavage and caspase activation were associated with up-regulation of p53 through DNA damage and reactive oxygen species (ROS) generation.	Reactive Oxygen Species	202-225	P53	Homo sapiens	175-178
19438509-5	2009	KEY RESULTS: During combined treatment with wogonin and TRAIL, cytotoxicity, poly(ADP-ribose) polymerase cleavage and caspase activation were associated with up-regulation of p53 through DNA damage and reactive oxygen species (ROS) generation.	Reactive Oxygen Species	227-230	P53	Homo sapiens	175-178
19397953-0	2009	Morphine induces DNA damage and P53 activation in CD3+ T cells.	Morphine	0-8	P53	Homo sapiens	32-35
19346293-0	2009	Effect of metal ion on the structural stability of tumour suppressor protein p53 DNA-binding domain.	Metals	10-15	P53	Homo sapiens	77-80
19340872-5	2009	RESULTS: D-allose had inhibitory effects on all 3 cell lines and tended to upregulate mRNA expression of glucose transporters, p21 and p53, and downregulate mRNA expression of cyclin A2, cyclin B1, and CDC2.	allose	9-17	P53	Homo sapiens	135-138
19820363-1	2009	BACKGROUND: The aim of the study was to assess the efficacy of pegylated liposomal doxorubicin (PLD) and oxaliplatin in patients affected by relapsed epithelial ovarian cancer with a family history of BRCA and p53 mutations.	Doxorubicin	83-94	P53	Homo sapiens	210-213
19578756-0	2009	Human bladder cancer cells undergo cisplatin-induced apoptosis that is associated with p53-dependent and p53-independent responses.	Cisplatin	35-44	P53	Homo sapiens	87-90
19578756-0	2009	Human bladder cancer cells undergo cisplatin-induced apoptosis that is associated with p53-dependent and p53-independent responses.	Cisplatin	35-44	P53	Homo sapiens	105-108
19578756-4	2009	In the present study, using MTT-based assays, Western blotting and semi-quantitative RT-PCR, we examined the apoptosis-related cellular responses to cisplatin exposure in two human urinary bladder cancer cell lines characterized by different malignancy grade and p53 genetic status.	Cisplatin	149-158	P53	Homo sapiens	263-266
19578756-5	2009	Both RT4 (grade I; wild-type p53) and T24 (grade III; mutant p53) cell types proved to be vulnerable to cisplatin apoptotic activity, albeit in a grade-dependent and drug dose-specific manner, as demonstrated by the proteolytic processing profiles of Caspase-8, Caspase-9, Caspase-3, and the Caspase repertoire characteristic substrates PARP and Lamin A/C, as well.	Cisplatin	104-113	P53	Homo sapiens	61-64
19578756-6	2009	The differential resistance of RT4 and T24 cells to cisplatin-induced apoptosis was associated with an RT4-specific phosphorylation (Ser15; Ser392) pattern of p53, together with structural amputations of the Akt and XIAP anti-apoptotic regulators.	Cisplatin	52-61	P53	Homo sapiens	159-162
19578757-0	2009	TCDD mediates inhibition of p53 and activation of ERalpha signaling in MCF-7 cells at moderate hypoxic conditions.	Polychlorinated Dibenzodioxins	0-4	P53	Homo sapiens	28-31
19578757-6	2009	Simultaneous exposure to TCDD and hypoxia resulted in a moderate but reproducible inhibition of p53 expression.	Polychlorinated Dibenzodioxins	25-29	P53	Homo sapiens	96-99
19578757-12	2009	The combination of inhibition of functional p53 protein and induction of ERalpha signaling could serve as a model for the operational sequence of TCDD effects to prevent cell death and promote breast tumor progression.	Polychlorinated Dibenzodioxins	146-150	P53	Homo sapiens	44-47
19346293-6	2009	The thermal stability monitored by DSC scans showed that the binding of metal ions to p53DBD increased the thermal stability of the protein.	Metals	72-77	P53	Homo sapiens	86-89
19470675-0	2009	siRNA targeted to p53 attenuates ischemic and cisplatin-induced acute kidney injury.	Cisplatin	46-55	P53	Homo sapiens	18-21
19346293-9	2009	Analysis of acrylamide quenching experiments revealed that the binding of metal ions to p53DBD induced a structural modification of the protein and this change provided significant protection against acrylamide quenching.	Metals	74-79	P53	Homo sapiens	88-91
19470675-5	2009	Following glomerular filtration, endocytic uptake of Cy3-siRNA by PTCs was rapid and extensive, and significantly reduced ischemia-induced p53 upregulation.	cy3	53-56	P53	Homo sapiens	139-142
19470675-10	2009	siRNA to p53 was also effective in a model of cisplatin-induced kidney injury.	Cisplatin	46-55	P53	Homo sapiens	9-12
19346293-10	2009	Overall, the present results indicated that p53DBD underwent a conformational change upon the binding of metal ions, which was characterized by an increased stability of the protein.	Metals	105-110	P53	Homo sapiens	44-47
19559722-8	2009	Moreover, resveratrol induced telomeric instability in U-2 OS cells and the activation of DNA damage signaling in both cell lines, manifested as the phosphorylation of histone H2AX at serine 139 and of p53 at serines 15 and 37.	Resveratrol	10-21	P53	Homo sapiens	202-205
19625214-11	2009	Null results were noted in studies with sound epidemiological design and conduct (1.06 [0.87-1.29] for arginine homozygotes compared with heterozygotes), and studies in which TP53 genotype was determined from white blood cells (1.06 [0.87-1.29] for arginine homozygotes compared with heterozygotes).	Arginine	103-111	P53	Homo sapiens	175-179
19406223-5	2009	By conducting a series of luciferase-based reporter assays, we revealed that the catechin mixture only up-regulates the p53 reporter.	Catechin	81-89	P53	Homo sapiens	120-123
19528227-5	2009	The increase in mitochondrial mass and ROS in response to oncogenic ras depended on intact p53 and Rb tumor suppression pathways.	Reactive Oxygen Species	39-42	P53	Homo sapiens	91-94
19528237-7	2009	Telomere uncapping through either TRF2 shelterin protein knockdown or exposure to telomere G-strand DNA oligonucleotides significantly increases the transcription of TERRA, an effect mediated by the functional cooperation between MLL and the tumor suppressor p53.	Oligonucleotides	104-120	P53	Homo sapiens	259-262
19617712-4	2009	Here we report that human double minute-2 protein (HDM2), a p53-specific E3 ubiquitin ligase, specifically ubiquitinates HEXIM1 through the lysine residues located within the basic region of HEXIM1.	Lysine	140-146	P53	Homo sapiens	60-63
19470404-5	2009	These results suggest that arsenite potentiates the BPDE-induced supF mutation via a p53-independent mechanism.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	52-56	P53	Homo sapiens	85-88
19460356-0	2009	Antiproliferation and apoptosis induced by tamoxifen in human bile duct carcinoma QBC939 cells via upregulated p53 expression.	Tamoxifen	43-52	P53	Homo sapiens	111-114
19460356-5	2009	Increased expression of p53 was observed in TAM-treated cells, indicating that p53 might play an important role in TAM-induced apoptosis in QBC939 cells.	Tamoxifen	44-47	P53	Homo sapiens	24-27
19460356-5	2009	Increased expression of p53 was observed in TAM-treated cells, indicating that p53 might play an important role in TAM-induced apoptosis in QBC939 cells.	Tamoxifen	44-47	P53	Homo sapiens	79-82
19460356-5	2009	Increased expression of p53 was observed in TAM-treated cells, indicating that p53 might play an important role in TAM-induced apoptosis in QBC939 cells.	Tamoxifen	115-118	P53	Homo sapiens	24-27
19460356-5	2009	Increased expression of p53 was observed in TAM-treated cells, indicating that p53 might play an important role in TAM-induced apoptosis in QBC939 cells.	Tamoxifen	115-118	P53	Homo sapiens	79-82
19719971-12	2009	Furthermore, 3-BrPA stimulation decreased the expressions of Bcl-2, c-Myc and mutant p53, which were strongly associated with the programmed cell death signal transduction pathway.	bromopyruvate	13-19	P53	Homo sapiens	85-88
19719971-13	2009	CONCLUSION: 3-BrPA inhibits proliferation, induces S phase and G2/M phase arrest, and promotes apoptosis in MCF-7 cells, which processes might be mediated by the downregulation of the expressions of Bcl-2, c-Myc and mutant p53.	bromopyruvate	12-18	P53	Homo sapiens	223-226
19494119-3	2009	We and others identified acetylation of the p53 DNA binding domain at lysine 120 as a critical event in apoptosis induction.	Lysine	70-76	P53	Homo sapiens	44-47
19494119-4	2009	Although initial studies showed that Lys-120 acetylation plays a role in p53 function in the nucleus, we report here a role for Lys-120 acetylation in transcription-independent apoptosis.	Lysine	37-40	P53	Homo sapiens	73-76
19494119-5	2009	We demonstrate that the Lys-120-acetylated isoform of p53 is enriched at mitochondria.	Lysine	24-27	P53	Homo sapiens	54-57
19494119-9	2009	These data support a model whereby Lys-120 acetylation contributes to both the transcription-dependent and -independent apoptotic pathways induced by p53.	Lysine	35-38	P53	Homo sapiens	150-153
19603033-2	2009	In addition, the mismatch repair protein, hMLH1, has been linked to DNA damage-induced apoptosis by cisplatin by both p53-dependent and -independent mechanisms.	Cisplatin	100-109	P53	Homo sapiens	118-121
19464429-1	2009	HCT116 (p53(+/+)) human colon carcinoma cells treated with nanomolar concentrations of doxorubicin underwent transient senescence, synthesized DNA, showed endopolyploidization, increased their size and became multinucleated without a significant increase in mitosis.	Doxorubicin	87-98	P53	Homo sapiens	8-11
19409072-1	2009	Inhibition of the tumour suppressor p53 by PFT (pifithrin-alpha) promotes p53-mediated apoptosis and protects against doxorubicin-induced apoptosis.	Doxorubicin	118-129	P53	Homo sapiens	36-39
19337030-4	2009	Furthermore, we found that pretreatment with the autophagy inhibitor 3-methyladenine or beclin 1 siRNA further activated p53 and its downstream apoptotic pathways, while the autophagy inducer rapamycin showed the opposite effects.	3-methyladenine	69-84	P53	Homo sapiens	121-124
19505151-5	2009	Here we demonstrate that the interaction with a consensus DNA sequence provides the core domain of p53 with enhanced conformational stability at physiological salt concentrations (0.15 M).	Salts	159-163	P53	Homo sapiens	99-102
19337030-7	2009	Further autophagy induction with rapamycin protects DA neurons from lactacystin-mediated cell death by downregulating p53 and its related apoptotic pathways and by inducing autophagy to degrade aggregated proteins.	Sirolimus	33-42	P53	Homo sapiens	118-121
19655389-4	2009	By regulating metal ions, MT-I+II can control metal-containing transcription factors, zinc-finger proteins and p53.	Metals	14-19	P53	Homo sapiens	111-114
19052714-0	2009	TP53 codon 72 polymorphism associated with prognosis in patients with advanced gastric cancer treated with paclitaxel and cisplatin.	Paclitaxel	107-117	P53	Homo sapiens	0-4
19052714-0	2009	TP53 codon 72 polymorphism associated with prognosis in patients with advanced gastric cancer treated with paclitaxel and cisplatin.	Cisplatin	122-131	P53	Homo sapiens	0-4
19052714-4	2009	RESULTS: The Arg/Pro and Pro/Pro genotypes of TP53 codon 72 were significantly correlated with a lower response rate to the combination chemotherapy when compared to the Arg/Arg genotype (35.7 vs. 66.7%, P-value 0.019) in a logistic regression analysis.	Arginine	13-16	P53	Homo sapiens	46-50
19052714-4	2009	RESULTS: The Arg/Pro and Pro/Pro genotypes of TP53 codon 72 were significantly correlated with a lower response rate to the combination chemotherapy when compared to the Arg/Arg genotype (35.7 vs. 66.7%, P-value 0.019) in a logistic regression analysis.	Arginine	170-173	P53	Homo sapiens	46-50
19432880-4	2009	In addition, the Mdmx mutant cooperates with Mdm2 to induce ubiquitination of p53 at C-terminal lysine residues, and the integrity of the C-terminal lysines was partly required for the cooperative inhibition.	Lysine	96-102	P53	Homo sapiens	78-81
19432880-4	2009	In addition, the Mdmx mutant cooperates with Mdm2 to induce ubiquitination of p53 at C-terminal lysine residues, and the integrity of the C-terminal lysines was partly required for the cooperative inhibition.	Lysine	149-156	P53	Homo sapiens	78-81
19052714-4	2009	RESULTS: The Arg/Pro and Pro/Pro genotypes of TP53 codon 72 were significantly correlated with a lower response rate to the combination chemotherapy when compared to the Arg/Arg genotype (35.7 vs. 66.7%, P-value 0.019) in a logistic regression analysis.	Arginine	170-173	P53	Homo sapiens	46-50
19052714-5	2009	A multivariate survival analysis also showed that the time to progression for the patients with the Arg/Pro and Pro/Pro genotypes of TP53 codon 72 was worse than for the patients with the Arg/Arg genotype (Hazard ratio = 3.056, P-value = 0.047), whereas the overall survival was not significantly different.	Arginine	100-103	P53	Homo sapiens	133-137
19052714-5	2009	A multivariate survival analysis also showed that the time to progression for the patients with the Arg/Pro and Pro/Pro genotypes of TP53 codon 72 was worse than for the patients with the Arg/Arg genotype (Hazard ratio = 3.056, P-value = 0.047), whereas the overall survival was not significantly different.	Arginine	188-191	P53	Homo sapiens	133-137
19432898-7	2009	This observation implies that there is a feedback signaling loop involving p21/ROS/p53 in apoptotic responses.	Reactive Oxygen Species	79-82	P53	Homo sapiens	83-86
19052714-5	2009	A multivariate survival analysis also showed that the time to progression for the patients with the Arg/Pro and Pro/Pro genotypes of TP53 codon 72 was worse than for the patients with the Arg/Arg genotype (Hazard ratio = 3.056, P-value = 0.047), whereas the overall survival was not significantly different.	Arginine	188-191	P53	Homo sapiens	133-137
19052714-6	2009	CONCLUSION: The TP53 codon 72 SNP was found to be predictive of the response to chemotherapy and correlate with the time to progression in patients with advanced gastric cancer treated with paclitaxel and cisplatin chemotherapy.	Paclitaxel	190-200	P53	Homo sapiens	16-20
19052714-6	2009	CONCLUSION: The TP53 codon 72 SNP was found to be predictive of the response to chemotherapy and correlate with the time to progression in patients with advanced gastric cancer treated with paclitaxel and cisplatin chemotherapy.	Cisplatin	205-214	P53	Homo sapiens	16-20
19472297-3	2009	In this study, designed to elucidate the regulation of MVP in young and senescent HDFs, we examined the levels of transcriptional factors for the MVP gene, which revealed that among the putative transcriptional factors, p53 decreased only in young HDFs, but not in senescent HDFs in response to H(2)O(2) treatment in the same mode as the expression of MVP.	Hydrogen Peroxide	295-303	P53	Homo sapiens	220-223
19472297-4	2009	Moreover, the phosphorylation status of p53 increased only in senescent HDFs but not in young HDFs in response to H(2)O(2) treatment.	Hydrogen Peroxide	114-122	P53	Homo sapiens	40-43
19548636-3	2009	We used the Orru three component reaction (O-3CR) along with a rapid and efficient, recently discovered amidation reaction to dramatically improve the water solubility of our recently discovered low molecular weight p53/mdm2 antagonists.	Water	151-156	P53	Homo sapiens	216-219
19297420-8	2009	Based on these results and the fact that Mg(2+) exists at relatively high concentration in the cell, we propose that Mg(2+) is one of potential factors to affect or regulate the transactivation of p53.	magnesium ion	41-47	P53	Homo sapiens	197-200
19297420-8	2009	Based on these results and the fact that Mg(2+) exists at relatively high concentration in the cell, we propose that Mg(2+) is one of potential factors to affect or regulate the transactivation of p53.	magnesium ion	117-123	P53	Homo sapiens	197-200
19434453-8	2009	Notably, stage I patients with p53 mutation and p53 codon 72 Pro/Pro genotype experienced a 2.66-fold hazard ratio (95% CI 1.21-5.85) for overall survival when compared with those with p53 wild-type and Arg/Arg genotype.	Arginine	203-206	P53	Homo sapiens	31-34
19434453-8	2009	Notably, stage I patients with p53 mutation and p53 codon 72 Pro/Pro genotype experienced a 2.66-fold hazard ratio (95% CI 1.21-5.85) for overall survival when compared with those with p53 wild-type and Arg/Arg genotype.	Arginine	203-206	P53	Homo sapiens	48-51
19434453-8	2009	Notably, stage I patients with p53 mutation and p53 codon 72 Pro/Pro genotype experienced a 2.66-fold hazard ratio (95% CI 1.21-5.85) for overall survival when compared with those with p53 wild-type and Arg/Arg genotype.	Arginine	203-206	P53	Homo sapiens	48-51
19434453-8	2009	Notably, stage I patients with p53 mutation and p53 codon 72 Pro/Pro genotype experienced a 2.66-fold hazard ratio (95% CI 1.21-5.85) for overall survival when compared with those with p53 wild-type and Arg/Arg genotype.	Arginine	207-210	P53	Homo sapiens	31-34
19434453-8	2009	Notably, stage I patients with p53 mutation and p53 codon 72 Pro/Pro genotype experienced a 2.66-fold hazard ratio (95% CI 1.21-5.85) for overall survival when compared with those with p53 wild-type and Arg/Arg genotype.	Arginine	207-210	P53	Homo sapiens	48-51
19434453-8	2009	Notably, stage I patients with p53 mutation and p53 codon 72 Pro/Pro genotype experienced a 2.66-fold hazard ratio (95% CI 1.21-5.85) for overall survival when compared with those with p53 wild-type and Arg/Arg genotype.	Arginine	207-210	P53	Homo sapiens	48-51
19242657-0	2009	Tunicamycin suppresses cisplatin-induced HepG2 cell apoptosis via enhancing p53 protein nuclear export.	Cisplatin	23-32	P53	Homo sapiens	76-79
19085001-0	2009	High-efficiency transfer and expression of AdCMV-p53 in human cervix adenocarcinoma cells induced by subclinical-dose carbon beam radiation.	Carbon	118-124	P53	Homo sapiens	49-52
19085001-1	2009	PURPOSE: The aim of this study is to evaluate the effect of carbon-beam irradiation on adenovirus-mediated p53 transfer in human cervix adenocarcinoma.	Carbon	60-66	P53	Homo sapiens	107-110
19158844-2	2009	UVA irradiation of human melanocytes caused generation of reactive oxygen species, which altered the intracellular redox balance and was accompanied by translocation of p53 to mitochondria.	Reactive Oxygen Species	58-81	P53	Homo sapiens	169-172
19347880-5	2009	Additionally, Rad51d (E233G) conferred increased cisplatin resistance of an MCF7 cell line in which p53 expression was stably knocked down by shRNAp53, indicating that the effect of this variant is dependent upon p53 status.	Cisplatin	49-58	P53	Homo sapiens	100-103
19347880-5	2009	Additionally, Rad51d (E233G) conferred increased cisplatin resistance of an MCF7 cell line in which p53 expression was stably knocked down by shRNAp53, indicating that the effect of this variant is dependent upon p53 status.	Cisplatin	49-58	P53	Homo sapiens	147-150
19347880-0	2009	Cisplatin resistance conferred by the RAD51D (E233G) genetic variant is dependent upon p53 status in human breast carcinoma cell lines.	Cisplatin	0-9	P53	Homo sapiens	87-90
19242657-4	2009	In order to further explore the mechanism underlying tumor resistance to cisplatin, we observed that increased nuclear export of endogenous p53 protein by pharmacological inducers of ER stress, such as tunicamycin, was associated with the suppression of cisplatin-induced apoptosis.	Cisplatin	73-82	P53	Homo sapiens	140-143
19347880-3	2009	We describe in this report that the Rad51d (E233G) genetic variant confers increased cisplatin resistance and cell growth phenotypes in human breast carcinoma cell lines with a mutant p53 gene (BT20 and T47D) but not with a wild-type p53 gene (MCF-7).	Cisplatin	85-94	P53	Homo sapiens	184-187
19347880-3	2009	We describe in this report that the Rad51d (E233G) genetic variant confers increased cisplatin resistance and cell growth phenotypes in human breast carcinoma cell lines with a mutant p53 gene (BT20 and T47D) but not with a wild-type p53 gene (MCF-7).	Cisplatin	85-94	P53	Homo sapiens	234-237
19242657-4	2009	In order to further explore the mechanism underlying tumor resistance to cisplatin, we observed that increased nuclear export of endogenous p53 protein by pharmacological inducers of ER stress, such as tunicamycin, was associated with the suppression of cisplatin-induced apoptosis.	Cisplatin	254-263	P53	Homo sapiens	140-143
19242657-5	2009	These results suggested that tumor suppressor p53 protein may play a key role in cisplatin-induced HepG2 cells apoptosis.	Cisplatin	81-90	P53	Homo sapiens	46-49
19584241-6	2009	Concomitant with the increase of proteins at endogenous levels, the in vivo phosphorylation of p53 at residues Ser(46)/Ser(392) and Mdm2 at residue Ser(166) was observed.	Serine	111-114	P53	Homo sapiens	95-98
19584241-6	2009	Concomitant with the increase of proteins at endogenous levels, the in vivo phosphorylation of p53 at residues Ser(46)/Ser(392) and Mdm2 at residue Ser(166) was observed.	Serine	119-122	P53	Homo sapiens	95-98
19531575-13	2009	If confirmed in other models, these results suggest that p16 and p53 status affects the 5-aza-irinotecan interaction.	Irinotecan	94-104	P53	Homo sapiens	65-68
19584241-6	2009	Concomitant with the increase of proteins at endogenous levels, the in vivo phosphorylation of p53 at residues Ser(46)/Ser(392) and Mdm2 at residue Ser(166) was observed.	Serine	119-122	P53	Homo sapiens	95-98
19584233-7	2009	In contrast, inhibition of Aurora-B by ZM447439 also interferes with normal chromosome alignment during mitosis and overrides the mitotic spindle checkpoint but allows a subsequent endoreduplication, although ZM447439 potently activates the p53-dependent postmitotic G(1) checkpoint.	4-(4-(N-benzoylamino)anilino)-6-methoxy-7-(3-(1-morpholino)propoxy)quinazoline	209-217	P53	Homo sapiens	241-244
19513503-5	2009	Interestingly, it was revealed that treatment with exogenous S100A4 protein reduced transcriptional activity of p53 and abrogated the modification of calcium binding affinity of S100A4 protein.	Calcium	150-157	P53	Homo sapiens	112-115
21475861-9	2009	In a recent study using protein-specific anti-acetyl lysine antibodies and immunological methods, we demonstrated the ability of aspirin to acetylate the tumor suppressor protein p53.	Lysine	53-59	P53	Homo sapiens	179-182
21475861-9	2009	In a recent study using protein-specific anti-acetyl lysine antibodies and immunological methods, we demonstrated the ability of aspirin to acetylate the tumor suppressor protein p53.	Aspirin	129-136	P53	Homo sapiens	179-182
19428812-0	2009	Ammonia-induced activation of p53 in cultured astrocytes: role in cell swelling and glutamate uptake.	Glutamic Acid	84-93	P53	Homo sapiens	30-33
19428812-8	2009	We therefore examined the potential role of p53 in the ammonia-induced inhibition of glutamate uptake and found that PFT also reversed the ammonia-induced inhibition of glutamate uptake.	Glutamic Acid	85-94	P53	Homo sapiens	44-47
19428812-9	2009	Our results indicate that a potentially important downstream target of ammonia neurotoxicity is p53, whose activation contributes to astrocyte swelling and glutamate uptake inhibition, processes likely a consequence of ONS derived from the mPT and activation of NF-kappaB.	Glutamic Acid	156-165	P53	Homo sapiens	96-99
19217709-0	2009	Role of p53 in the induction of cyclooxygenase-2 by cisplatin or paclitaxel in non-small cell lung cancer cell lines.	Cisplatin	52-61	P53	Homo sapiens	8-11
19650989-5	2009	METHODS: p53 gene and chromosome 13q14 expression in paraffin sections of 30 cases of primary intestinal lymphoma and 10 cases of lymph node reactive hyperplasia were ascertained using an improved FISH technique.	Paraffin	53-61	P53	Homo sapiens	9-12
20161293-1	2009	Chlorofusin, its seven chromophore diastereomers, and key analogues were comparatively examined for inhibition of MDM2-p53 binding revealing that the chromophore, but not simple replacements, contributes significantly to the natural products properties, and that this contribution is independent of its relative and absolute stereochemistry.	chlorofusin	0-11	P53	Homo sapiens	119-122
19217709-0	2009	Role of p53 in the induction of cyclooxygenase-2 by cisplatin or paclitaxel in non-small cell lung cancer cell lines.	Paclitaxel	65-75	P53	Homo sapiens	8-11
19217709-6	2009	We report herein that lung cancer cell lines expressing wild-type p53, when exposed to cisplatin treatment, induced COX-2 (mRNA and protein), with concurrent synthesis of prostaglandins (PGE(2)).	Cisplatin	87-96	P53	Homo sapiens	66-69
19217709-6	2009	We report herein that lung cancer cell lines expressing wild-type p53, when exposed to cisplatin treatment, induced COX-2 (mRNA and protein), with concurrent synthesis of prostaglandins (PGE(2)).	Prostaglandins	171-185	P53	Homo sapiens	66-69
19217709-8	2009	Further, after silencing of wild-type p53 expressed in A549 cells by RNA interference, cisplatin was no longer able to induce COX-2 expression.	Cisplatin	87-96	P53	Homo sapiens	38-41
19217709-9	2009	Therefore, we suggest that induction of COX-2 by cisplatin in NSCLC cell lines is dependent on p53.	Cisplatin	49-58	P53	Homo sapiens	95-98
19217709-10	2009	For paclitaxel treatment, an increase in COX-2 mRNA expression was observed in H460 and A549 (wild-type p53 cell lines).	Paclitaxel	4-14	P53	Homo sapiens	104-107
19217709-11	2009	Moreover, paclitaxel treatment increased COX-2 expression in ACC-LC-319 cell lines (p53 null), showing a p53-independent effect.	Paclitaxel	10-20	P53	Homo sapiens	84-87
19217709-11	2009	Moreover, paclitaxel treatment increased COX-2 expression in ACC-LC-319 cell lines (p53 null), showing a p53-independent effect.	Paclitaxel	10-20	P53	Homo sapiens	105-108
19369702-4	2009	Although hypoxia has been shown to induce reactive oxygen species (ROS) generation in the mitochondria resulting in enhanced p53 expression, our data demonstrate that hypoxia-induced p53 expression and phosphorylation are independent of ROS.	Reactive Oxygen Species	67-70	P53	Homo sapiens	125-128
19558663-1	2009	BACKGROUND: Ser-249 TP53 mutation (249(Ser)) is a molecular evidence for aflatoxin-related carcinogenesis in Hepatocellular Carcinoma (HCC) and it is frequent in some African and Asian regions, but it is unusual in Western countries.	Serine	12-15	P53	Homo sapiens	20-24
19558663-1	2009	BACKGROUND: Ser-249 TP53 mutation (249(Ser)) is a molecular evidence for aflatoxin-related carcinogenesis in Hepatocellular Carcinoma (HCC) and it is frequent in some African and Asian regions, but it is unusual in Western countries.	Serine	39-42	P53	Homo sapiens	20-24
19470478-3	2009	The p53 allele encoding proline at codon 72 (P72) was found to be significantly enriched over the allele encoding arginine (R72) among in vitro fertilization (IVF) patients.	Arginine	114-122	P53	Homo sapiens	4-7
19328230-0	2009	Cisplatin-induced nitrosylation of p53 prevents its mitochondrial translocation.	Cisplatin	0-9	P53	Homo sapiens	35-38
19328230-5	2009	Cisplatin treatment in the presence of an iNOS inhibitor (1400W) allowed p53 mitochondrial translocation.	Cisplatin	0-9	P53	Homo sapiens	73-76
19328230-5	2009	Cisplatin treatment in the presence of an iNOS inhibitor (1400W) allowed p53 mitochondrial translocation.	N-((3-(aminomethyl)phenyl)methyl)ethanimidamide	58-63	P53	Homo sapiens	73-76
19416725-5	2009	This suggests that acetylation at Lys-120 of p53 negatively regulates a signaling pathway leading to NFAT activation.	Lysine	34-37	P53	Homo sapiens	45-48
19146838-0	2009	Caspase- and p53-dependent apoptosis in breast carcinoma cells induced by a synthetic selenadiazole derivative.	1,2,3-Selenadiazole	86-99	P53	Homo sapiens	13-16
19366707-4	2009	Within 1 h following TPA treatment of skin epithelial (JB6) cells, p53 accumulated in mitochondria.	Tetradecanoylphorbol Acetate	21-24	P53	Homo sapiens	67-70
19253369-3	2009	Ascochlorin specifically induces p53 phosphorylation at ser 392 without affecting ser 15 or 20, whereas DNA damaging agents typically phosphorylate these serines.	Serine	56-59	P53	Homo sapiens	33-36
19366707-6	2009	The suppressive effect of NPM on p53 mitochondrial localization is also observed in TPA-treated primary epithelial cells and in JB6 cells treated with doxorubicin.	Tetradecanoylphorbol Acetate	84-87	P53	Homo sapiens	33-36
19366707-6	2009	The suppressive effect of NPM on p53 mitochondrial localization is also observed in TPA-treated primary epithelial cells and in JB6 cells treated with doxorubicin.	Doxorubicin	151-162	P53	Homo sapiens	33-36
19216720-8	2009	Meanwhile, the use of 3-aminobenzamide, a PARP-1 inhibitor known to prevent AIF (apoptosis-inducing factor) release, significantly decreases staurosporine-induced death in these p53mt carcinoma cells, suggesting a preferential implication of caspase-independent apoptosis.	3-aminobenzamide	22-38	P53	Homo sapiens	178-181
19318914-4	2009	The patient was first treated with adenovirus-mediated wild-type p53 gene (Ad-p53, gendicine) combined with oxaliplatin (200 mg) and transcatheter arterial chemoembolization or transcatheter arterial chemotherapy for two cycles.	gendicine	83-92	P53	Homo sapiens	65-68
19398950-3	2009	We show that depletion of Artemis under typical culture conditions (21% oxygen) leads to a spontaneous phosphorylation and stabilization of p53, and resulting cellular G1 arrest and apoptosis.	Oxygen	72-78	P53	Homo sapiens	140-143
19398950-5	2009	Culturing of cellsat 3% oxygen or treatment with an antioxidant abrogated p53 stabilization, indicating that oxidative stress is the responsible cellular stimulus.	Oxygen	24-30	P53	Homo sapiens	74-77
19398950-7	2009	In addition, we show that p53-inducible genes involved in reducing reactive oxygen species are upregulated by Artemis depletion.	Reactive Oxygen Species	67-90	P53	Homo sapiens	26-29
19528459-4	2009	Moreover, activation of p53, p53-dependent expression of p21 and p21-dependent senescence were observed in sigma-KO, but not parental cells after a treatment with a low cisplatin dose.	Cisplatin	169-178	P53	Homo sapiens	24-27
19528459-4	2009	Moreover, activation of p53, p53-dependent expression of p21 and p21-dependent senescence were observed in sigma-KO, but not parental cells after a treatment with a low cisplatin dose.	Cisplatin	169-178	P53	Homo sapiens	29-32
19342093-11	2009	It was shown that through simultaneous delivery of both p53 gene and DOX using FA32 micelles, an increase in p53 mRNA expression level as well as end point cytotoxicity towards HepG2 cells was achieved.	Doxorubicin	69-72	P53	Homo sapiens	109-112
19528459-5	2009	CONCLUSION: A 14-3-3sigma-dependent mechanism inhibits p53 activation in parental cells treated with a low cisplatin dose, thereby blocking p21 expression that is essential for senescence and consequently conferring to the parental cells a significant degree of resistance to cisplatin.	Cisplatin	107-116	P53	Homo sapiens	55-58
19528459-5	2009	CONCLUSION: A 14-3-3sigma-dependent mechanism inhibits p53 activation in parental cells treated with a low cisplatin dose, thereby blocking p21 expression that is essential for senescence and consequently conferring to the parental cells a significant degree of resistance to cisplatin.	Cisplatin	276-285	P53	Homo sapiens	55-58
19082758-0	2009	p53 and ATF-2 partly mediate the overexpression of COX-2 in H(2)O (2)-induced premature senescence of human fibroblasts.	Hydrogen Peroxide	60-69	P53	Homo sapiens	0-3
19286634-7	2009	Introduction of SIRT1 or disruption of p53 inhibits high glucose-induced endothelial senescence and dysfunction.	Glucose	57-64	P53	Homo sapiens	39-42
19627195-6	2009	Exposure of young HDFs to H(2)O(2) induced G2/M cell cycle arrest, positive senescence-associated (SA) beta-galactosidase (beta-gal) staining, and elevated p53, p21, and p16 protein levels.	Hydrogen Peroxide	26-34	P53	Homo sapiens	156-159
19458054-10	2009	Ad-p53/miR-p21 also significantly increased the chemosensitivity of cancer cells to adriamycin (doxorubicin).	Doxorubicin	84-94	P53	Homo sapiens	3-6
19458054-10	2009	Ad-p53/miR-p21 also significantly increased the chemosensitivity of cancer cells to adriamycin (doxorubicin).	Doxorubicin	96-107	P53	Homo sapiens	3-6
19308457-4	2009	In the TP53 gene, methylated CpG dinucleotides are sequences selectively targeted by endogenous and exogenous mutagenic processes.	cytidylyl-3'-5'-guanosine	29-46	P53	Homo sapiens	7-11
19397590-5	2009	Flow cytometry and fluorescence microscopy revealed that although As(2)O(3) alone caused a moderate level of mitotic arrest, it greatly attenuated paclitaxel-induced mitotic arrest in cells with p53 deficiency.	Paclitaxel	147-157	P53	Homo sapiens	195-198
19235535-5	2009	Expression of the proapoptotic genes bax, bak, bad and p53/Tp53 increased in polymorphonuclear leukocytes exposed to gossypol.	Gossypol	117-125	P53	Homo sapiens	55-58
19235535-5	2009	Expression of the proapoptotic genes bax, bak, bad and p53/Tp53 increased in polymorphonuclear leukocytes exposed to gossypol.	Gossypol	117-125	P53	Homo sapiens	59-63
19343786-10	2009	Finally, immunoprecipitated wild-type p53 from doxorubicin treated U2OS cells can pull-down endogenous alphaB-crystallin and Fbx4.	Doxorubicin	47-58	P53	Homo sapiens	38-41
19627195-7	2009	However, cotreatment with dropwort or Sedum ethanol extract significantly lowered p53, p21, and p16 levels and intracellular reactive oxygen species levels and attenuated the cell cycle arrest compared with H(2)O(2)-alone treatment.	Ethanol	44-51	P53	Homo sapiens	82-85
19627195-10	2009	In conclusion, dropwort showed a potential anti-senescence activity in H(2)O(2)-treated HDFs, which might be mediated by reducing p16, p21, and p53 levels and oxidative stress.	Hydrogen Peroxide	71-79	P53	Homo sapiens	144-147
19155208-0	2009	Identification of new p53 acetylation sites in COS-1 cells.	carbonyl sulfide	47-50	P53	Homo sapiens	22-25
19461130-2	2009	For example, respiration and carbohydrate synthesis are coupled to the circadian clock in cyanobacteria (Ishiura et al 1998 Science 281 1519) and ultradian oscillations with time periods of a few hours have been observed in immune response (NF-kappaB, Hoffmann et al 2002 Science 298 1241, Neson et al 2004 Science 306 704), apoptosis (p53, Lahav et al 2004 Nat.	Carbohydrates	29-41	P53	Homo sapiens	336-339
19332559-0	2009	TTK/hMps1 mediates the p53-dependent postmitotic checkpoint by phosphorylating p53 at Thr18.	UNII-PYZ33YLR8A	86-91	P53	Homo sapiens	23-26
19332559-0	2009	TTK/hMps1 mediates the p53-dependent postmitotic checkpoint by phosphorylating p53 at Thr18.	UNII-PYZ33YLR8A	86-91	P53	Homo sapiens	79-82
19332559-3	2009	p53 has long been known to be activated by spindle poisons, such as nocodazole and Taxol, although the underlying mechanism remains elusive.	Nocodazole	68-78	P53	Homo sapiens	0-3
19332559-3	2009	p53 has long been known to be activated by spindle poisons, such as nocodazole and Taxol, although the underlying mechanism remains elusive.	Paclitaxel	83-88	P53	Homo sapiens	0-3
19332559-5	2009	TTK/hMps1 phoshorylates the N-terminal domain of p53 at Thr18, and this phosphorylation disrupts the interaction with MDM2 and abrogates MDM2-mediated p53 ubiquitination.	UNII-PYZ33YLR8A	56-61	P53	Homo sapiens	49-52
19332559-6	2009	Phosphorylation at Thr18 enhances p53-dependent activation of not only p21 but also Lats2, two mediators of the postmitotic checkpoint.	UNII-PYZ33YLR8A	19-24	P53	Homo sapiens	34-37
19332559-7	2009	Furthermore, a phospho-mimicking substitution at Thr18 (T18D) is more competent than the phospho-deficient mutant (T18A) in rescuing the tetraploid checkpoint defect of p53-depleted cells.	UNII-PYZ33YLR8A	49-54	P53	Homo sapiens	169-172
19580479-0	2009	Transient dephosphorylation of p53 serine 376 as an early response to ionizing radiation.	Serine	35-41	P53	Homo sapiens	31-34
19580479-3	2009	A continuous increase in the nuclear p53 protein was observed in irradiated cells beginning 1 h after irradiation that persisted for 8 h. Surprisingly, immunofluorescence microscopy revealed a transient, rapid and sensitive increase in a radiation-induced nuclear dephosphorylated p53 using antibody PAb421, which detects p53 when serine 376 is dephosphorylated.	Serine	331-337	P53	Homo sapiens	37-40
19580479-5	2009	The results are consistent with a radiation-induced, sensitive and rapid dephosphorylation of p53 at serine 376.	Serine	101-107	P53	Homo sapiens	94-97
19580479-7	2009	The data suggest that dephosphorylation of serine 376 on constitutive nuclear p53 is a sensitive and early signaling event in the response of cells to DNA damage induced by ionizing radiation.	Serine	43-49	P53	Homo sapiens	78-81
19363523-10	2009	Accordingly, phosphorylation of Thr18 and hepta-phosphorylation dramatically shifts the balance towards favouring the binding of p300 with p53, and is thus likely to be an important factor in its regulation.	UNII-PYZ33YLR8A	32-37	P53	Homo sapiens	139-142
19587434-6	2009	Effect of arsenic trioxide and adriamycin on the mutant p53 expression in Raji cells was detected by semi-quantitive RT-PCR.	Doxorubicin	31-41	P53	Homo sapiens	56-59
19587434-12	2009	CONCLUSION: As(2)O(3) and ADM alone or combined can inhibit the proliferation, induce cell apoptosis, and downregulate the expression of mutant p53 in vitro.	Doxorubicin	26-29	P53	Homo sapiens	144-147
19408261-3	2009	Formation of hydrogen bonds upon helix folding could contribute significantly to the enhanced enthalpy observed in binding of the linear peptides.The human double minute 2 protein (HDM2) binds a short peptide derived from the N terminus of the tumor-suppressor protein, p53.	Hydrogen	13-21	P53	Homo sapiens	270-273
19451596-7	2009	Subjects carrying the TP53 Arg72Pro polymorphism were found to have a significantly increased death risk (Pro/Pro versus Arg/Arg; hazard ratio, 2.90; 95% CI, 1.28-6.66).	Arginine	27-30	P53	Homo sapiens	22-26
20719132-2	2009	It has been proven that ERCC1, RRM1, p53 expressions were related to resistance to platinum and prognosis of the patcents with lung cancer.	Platinum	83-91	P53	Homo sapiens	37-40
19451596-7	2009	Subjects carrying the TP53 Arg72Pro polymorphism were found to have a significantly increased death risk (Pro/Pro versus Arg/Arg; hazard ratio, 2.90; 95% CI, 1.28-6.66).	Arginine	121-124	P53	Homo sapiens	22-26
19451596-8	2009	In the subgroup of 130 high-grade osteosarcomas, the TP53 Arg72Pro was an independent marker of EFS (Pro/Pro versus Arg/Arg; hazard ratio, 2.67; 95% CI, 1.17-6.11).	Arginine	58-61	P53	Homo sapiens	53-57
19451596-8	2009	In the subgroup of 130 high-grade osteosarcomas, the TP53 Arg72Pro was an independent marker of EFS (Pro/Pro versus Arg/Arg; hazard ratio, 2.67; 95% CI, 1.17-6.11).	Arginine	116-119	P53	Homo sapiens	53-57
19334741-1	2009	Lysine methylation is an important post-translational modification that affects protein function; for example, the transcriptional activity of the p53 tumor suppressor protein.	Lysine	0-6	P53	Homo sapiens	147-150
19334741-3	2009	The method, which relies on the synthesis of (13)C-enriched alkylating agents, was applied to the production of 15-residue p53 peptides variously methylated at lysine analogue 370.	Lysine	160-166	P53	Homo sapiens	123-126
19411067-4	2009	We show here that PRIMA-1 is converted to compounds that form adducts with thiols in mutant p53.	Sulfhydryl Compounds	75-81	P53	Homo sapiens	92-95
19383811-7	2009	p53 Pro/Pro was strongly associated with shorter survival in the entire cohort (MS of 11.8 versus 29.1 months, P &lt; 0.0001; adjusted hazard ratio for death, 2.05; 95% confidence interval, 1.30-3.24; P = 0.002 for Pro/Pro versus Arg/Arg).	Arginine	230-233	P53	Homo sapiens	0-3
19270508-0	2009	Modulation of thymidilate synthase and p53 expression by HDAC inhibitor vorinostat resulted in synergistic antitumor effect in combination with 5FU or raltitrexed.	Fluorouracil	144-147	P53	Homo sapiens	39-42
19229245-6	2009	Knockdown of MDH1 significantly reduces binding of acetylated-p53 and transcription-active histone codes to the promoter upon glucose depletion.	Glucose	126-133	P53	Homo sapiens	62-65
19442044-7	2009	Eicosanoid-independent pro-apoptotic pathways include enhanced lipid peroxidation, modulation of mitochondrial calcium homeostasis and enhanced production of reactive oxygen species as well as activation of p53.	Eicosanoids	0-10	P53	Homo sapiens	207-210
19413947-0	2009	Loss of p53 causes mitochondrial DNA depletion and altered mitochondrial reactive oxygen species homeostasis.	Reactive Oxygen Species	73-96	P53	Homo sapiens	8-11
19413947-2	2009	Here we demonstrate a new conserved role for p53 in mtDNA copy number maintenance and mitochondrial reactive oxygen species (ROS) homeostasis.	Reactive Oxygen Species	100-123	P53	Homo sapiens	45-48
19413947-2	2009	Here we demonstrate a new conserved role for p53 in mtDNA copy number maintenance and mitochondrial reactive oxygen species (ROS) homeostasis.	Reactive Oxygen Species	125-128	P53	Homo sapiens	45-48
19413947-6	2009	Finally, p53-depleted cells exhibit significant disruption of cellular ROS homeostasis, characterized by reduced mitochondrial and cellular superoxide levels and increased cellular hydrogen peroxide.	Reactive Oxygen Species	71-74	P53	Homo sapiens	9-12
19413947-6	2009	Finally, p53-depleted cells exhibit significant disruption of cellular ROS homeostasis, characterized by reduced mitochondrial and cellular superoxide levels and increased cellular hydrogen peroxide.	Superoxides	140-150	P53	Homo sapiens	9-12
19413947-6	2009	Finally, p53-depleted cells exhibit significant disruption of cellular ROS homeostasis, characterized by reduced mitochondrial and cellular superoxide levels and increased cellular hydrogen peroxide.	Hydrogen Peroxide	181-198	P53	Homo sapiens	9-12
19383811-7	2009	p53 Pro/Pro was strongly associated with shorter survival in the entire cohort (MS of 11.8 versus 29.1 months, P &lt; 0.0001; adjusted hazard ratio for death, 2.05; 95% confidence interval, 1.30-3.24; P = 0.002 for Pro/Pro versus Arg/Arg).	Arginine	234-237	P53	Homo sapiens	0-3
18992840-0	2009	The p53-p66shc-Manganese Superoxide Dismutase (MnSOD) network: a mitochondrial intrigue to generate reactive oxygen species.	Reactive Oxygen Species	100-123	P53	Homo sapiens	4-7
18992840-3	2009	The present short review summarizes recent discoveries on mitochondrial reactive oxygen species regulation by p53, a tumor suppressor protein and p66shc, a protein implicated in the life-span determination.	Reactive Oxygen Species	72-95	P53	Homo sapiens	110-113
19362238-0	2009	Different mechanisms of cell death in radiosensitive and radioresistant p53 mutated head and neck squamous cell carcinoma cell lines exposed to carbon ions and x-rays.	Carbon	144-150	P53	Homo sapiens	72-75
19360335-0	2009	Berberine inhibits p53-dependent cell growth through induction of apoptosis of prostate cancer cells.	Berberine	0-9	P53	Homo sapiens	19-22
19304334-0	2009	Selective ablation of Notch3 in HCC enhances doxorubicin"s death promoting effect by a p53 dependent mechanism.	Doxorubicin	45-56	P53	Homo sapiens	87-90
19360335-4	2009	However, the p53 expressing LNCaP cells were more susceptible against berberine than the p53 lacking PC-3 cells.	Berberine	70-79	P53	Homo sapiens	13-16
19360335-6	2009	Exploration of p53 siRNA or pifithrin-alpha, a p53 inhibitor to the LNCaP cells, suppressed berberine-induced cell death and expression of apoptosis-related proteins.	Berberine	92-101	P53	Homo sapiens	15-18
19360335-6	2009	Exploration of p53 siRNA or pifithrin-alpha, a p53 inhibitor to the LNCaP cells, suppressed berberine-induced cell death and expression of apoptosis-related proteins.	Berberine	92-101	P53	Homo sapiens	47-50
19360335-8	2009	Therefore, these results indicated that berberine inhibited p53-dependent prostate cancer cell death.	Berberine	40-49	P53	Homo sapiens	60-63
19360352-0	2009	The MDM2 antagonist nutlin-3 sensitizes p53-null neuroblastoma cells to doxorubicin via E2F1 and TAp73.	Doxorubicin	72-83	P53	Homo sapiens	40-43
19304334-7	2009	Ablating p53 expression in Notch3 knockdown (KD) cells largely abolished their enhanced doxorubicin sensitivity; and Notch3 KD in p53(-/-) Hep3B cells failed to influence their response to doxorubicin.	Doxorubicin	88-99	P53	Homo sapiens	9-12
19424414-4	2009	Using MAPD we measured sequence-specific p53 binding of doxorubicin-activated or transiently expressed p53 to REs from established p53 target genes and p53 consensus REs.	Doxorubicin	56-67	P53	Homo sapiens	41-44
19357962-0	2009	Simultaneous phosphorylation of p53 at serine 15 and 20 induces apoptosis in human glioma cells by increasing expression of pro-apoptotic genes.	Serine	39-45	P53	Homo sapiens	32-35
19357962-3	2009	Here we test the hypothesis that phosphorylation of serine 15 and/or 20 is causally related to p53-mediated apoptosis in human gliomas.	Serine	52-58	P53	Homo sapiens	95-98
19357962-4	2009	Introduction of p53 plasmids containing alanine mutations at serine 15 or/and serine 20 (which block phosphorylation) or aspartate mutations (which mimic phosphorylation) at the same sites, implicated simultaneous phosphorylation of both sites in the induction of apoptosis.	Serine	61-67	P53	Homo sapiens	16-19
19266268-7	2009	This compound also increased P53 Ser(15) phosphorylation and PARP cleavage in LNCaP cells, but required higher dosage than for suppressing AR-PSA.	Serine	33-36	P53	Homo sapiens	29-32
19199318-8	2009	ARO cells are highly resistant to apoptosis and express both p53 and Gal-3, which are increased upon cisplatin treatment.	Cisplatin	101-110	P53	Homo sapiens	61-64
19424414-4	2009	Using MAPD we measured sequence-specific p53 binding of doxorubicin-activated or transiently expressed p53 to REs from established p53 target genes and p53 consensus REs.	Doxorubicin	56-67	P53	Homo sapiens	103-106
19424414-4	2009	Using MAPD we measured sequence-specific p53 binding of doxorubicin-activated or transiently expressed p53 to REs from established p53 target genes and p53 consensus REs.	Doxorubicin	56-67	P53	Homo sapiens	103-106
19424414-4	2009	Using MAPD we measured sequence-specific p53 binding of doxorubicin-activated or transiently expressed p53 to REs from established p53 target genes and p53 consensus REs.	Doxorubicin	56-67	P53	Homo sapiens	103-106
19265193-1	2009	Acetylation of p53 at carboxyl-terminal lysine residues enhances its transcriptional activity associated with cell cycle arrest and apoptosis.	Lysine	40-46	P53	Homo sapiens	15-18
19251701-8	2009	Furthermore, upon activation by oncogenic ras, p38gamma stimulated the transcriptional activity of p53 by phosphorylating p53 at Ser(33), suggesting that the ability of p38gamma to mediate senescence is at least partly achieved through p53.	Serine	129-132	P53	Homo sapiens	99-102
19251701-8	2009	Furthermore, upon activation by oncogenic ras, p38gamma stimulated the transcriptional activity of p53 by phosphorylating p53 at Ser(33), suggesting that the ability of p38gamma to mediate senescence is at least partly achieved through p53.	Serine	129-132	P53	Homo sapiens	122-125
19251701-8	2009	Furthermore, upon activation by oncogenic ras, p38gamma stimulated the transcriptional activity of p53 by phosphorylating p53 at Ser(33), suggesting that the ability of p38gamma to mediate senescence is at least partly achieved through p53.	Serine	129-132	P53	Homo sapiens	122-125
19265193-2	2009	Here we demonstrate that p53 acetylation at Lys-320/Lys-373/Lys-382 is also required for its transcription-independent functions in BAX activation, reactive oxygen species production, and apoptosis in response to the histone deacetylase inhibitors (HDACi) suberoylanilide hydroxamic acid and LAQ824.	Lysine	44-47	P53	Homo sapiens	25-28
19265193-2	2009	Here we demonstrate that p53 acetylation at Lys-320/Lys-373/Lys-382 is also required for its transcription-independent functions in BAX activation, reactive oxygen species production, and apoptosis in response to the histone deacetylase inhibitors (HDACi) suberoylanilide hydroxamic acid and LAQ824.	Lysine	52-55	P53	Homo sapiens	25-28
19428366-0	2009	p53 mutations as fingerprints for aristolochic acid: an environmental carcinogen in endemic (Balkan) nephropathy.	aristolochic acid I	34-51	P53	Homo sapiens	0-3
19265193-2	2009	Here we demonstrate that p53 acetylation at Lys-320/Lys-373/Lys-382 is also required for its transcription-independent functions in BAX activation, reactive oxygen species production, and apoptosis in response to the histone deacetylase inhibitors (HDACi) suberoylanilide hydroxamic acid and LAQ824.	Lysine	52-55	P53	Homo sapiens	25-28
19265193-2	2009	Here we demonstrate that p53 acetylation at Lys-320/Lys-373/Lys-382 is also required for its transcription-independent functions in BAX activation, reactive oxygen species production, and apoptosis in response to the histone deacetylase inhibitors (HDACi) suberoylanilide hydroxamic acid and LAQ824.	Reactive Oxygen Species	148-171	P53	Homo sapiens	25-28
19386914-3	2009	p53 isoforms recognized by phospho-p53-specific (at Ser-15) or "mutant" conformation-specific antibodies were highly and specifically expressed in axons and axonal growth cones in primary hippocampal neurons.	Serine	52-55	P53	Homo sapiens	0-3
19475715-4	2009	Our results have revealed that reactive oxygen species (ROS) and p21 are involved in cell cycle arrest in a p53 independent manner but late hour apoptotic response was accompanied by the p53 up-regulation, loss of mitochondrial transmembrane potential (MTP), down-regulation of Bcl-xl, activation of caspase-3 and release of cytochrome c (Cyt c).	Reactive Oxygen Species	31-54	P53	Homo sapiens	108-111
19475715-4	2009	Our results have revealed that reactive oxygen species (ROS) and p21 are involved in cell cycle arrest in a p53 independent manner but late hour apoptotic response was accompanied by the p53 up-regulation, loss of mitochondrial transmembrane potential (MTP), down-regulation of Bcl-xl, activation of caspase-3 and release of cytochrome c (Cyt c).	Reactive Oxygen Species	56-59	P53	Homo sapiens	108-111
19475715-8	2009	Taken together, we have demonstrated that cadmium promotes ROS generation, which potently initiates the cell cycle arrest at early hours and finally induces p53-dependent apoptosis at later part of the event.	Cadmium	42-49	P53	Homo sapiens	157-160
19475715-8	2009	Taken together, we have demonstrated that cadmium promotes ROS generation, which potently initiates the cell cycle arrest at early hours and finally induces p53-dependent apoptosis at later part of the event.	Reactive Oxygen Species	59-62	P53	Homo sapiens	157-160
19091459-0	2009	p53 hot-spot mutants increase tumor vascularization via ROS-mediated activation of the HIF1/VEGF-A pathway.	Reactive Oxygen Species	56-59	P53	Homo sapiens	0-3
19454241-3	2009	In this system, we could target only the cells expressing p53 at endogenous levels, as observed in UV- or adriamycin-stimulated A549 cells.	Doxorubicin	106-116	P53	Homo sapiens	58-61
19091459-5	2009	Effect of ROS on angiogenesis in tumors expressing hot-spot p53 mutants was correlated with their ability to increase a content of HIF1 transcriptional factor responsible for up-regulation of VEGF-A mRNAs.	Reactive Oxygen Species	10-13	P53	Homo sapiens	60-63
19097688-0	2009	Andrographolide enhances 5-fluorouracil-induced apoptosis via caspase-8-dependent mitochondrial pathway involving p53 participation in hepatocellular carcinoma (SMMC-7721) cells.	Fluorouracil	25-39	P53	Homo sapiens	114-117
19097688-8	2009	Surprisingly, the addition of ANDRO to 5-FU induces synergistic apoptosis, which could be corroborated to the increased caspase-8, p53 activity and the significant changes of Bax conformation in these cells, resulting in increased losses of mitochondrial membrane potential, increased release of cytochrome c, and activation of caspase-9 and caspase-3.	Fluorouracil	39-43	P53	Homo sapiens	131-134
19248770-4	2009	Introduction of the signal sequence from mIL-31 to human p53 protein failed to secrete the products, but further addition of the N-glycosylation site resulted in constitutive secretion of biologically active p53 protein into the medium in the N-glycosylated form.	Nitrogen	129-130	P53	Homo sapiens	208-211
19248770-4	2009	Introduction of the signal sequence from mIL-31 to human p53 protein failed to secrete the products, but further addition of the N-glycosylation site resulted in constitutive secretion of biologically active p53 protein into the medium in the N-glycosylated form.	Nitrogen	243-244	P53	Homo sapiens	208-211
18462472-8	2009	Multivariate analysis showed that those with TP53 codon 72 Arg/Pro allele had significantly shorter survival than those with Arg/Arg allele (hazard ratio 1.35; 95% CI = 1.07-1.71).	Arginine	59-62	P53	Homo sapiens	45-49
19233169-4	2009	We find that p53 is needed for efficient cell cycle arrest when Aurora kinases are inhibited by either ZM447439 or VE-465.	4-(4-(N-benzoylamino)anilino)-6-methoxy-7-(3-(1-morpholino)propoxy)quinazoline	103-111	P53	Homo sapiens	13-16
19233169-6	2009	ZM447439 induced the localized accumulation of gammaH2A.X indicating that p53 induction by this drug occurs in response to DNA damage.	4-(4-(N-benzoylamino)anilino)-6-methoxy-7-(3-(1-morpholino)propoxy)quinazoline	0-8	P53	Homo sapiens	74-77
19351845-3	2009	Previously, we found that p53 genotype was correlated with ER expression and response to tamoxifen in mammary tumors arising in mouse mammary tumor virus-Wnt-1 transgenic mice.	Tamoxifen	89-98	P53	Homo sapiens	26-29
19351845-5	2009	To test this, MCF-7 cells were treated with doxorubicin or ionizing radiation, both of which stimulated a 5-fold increase in p53 expression.	Doxorubicin	44-55	P53	Homo sapiens	125-128
19351845-7	2009	In cells treated with small interfering RNA (siRNA) targeting p53, expression of both p53 and ER was significantly reduced (&gt;60%) by 24 h. Induction of ER by DNA-damaging agents was p53 dependent as either ionizing radiation or doxorubicin failed to up-regulate ER after treatment with p53-targeting siRNA.	Doxorubicin	231-242	P53	Homo sapiens	62-65
19351845-7	2009	In cells treated with small interfering RNA (siRNA) targeting p53, expression of both p53 and ER was significantly reduced (&gt;60%) by 24 h. Induction of ER by DNA-damaging agents was p53 dependent as either ionizing radiation or doxorubicin failed to up-regulate ER after treatment with p53-targeting siRNA.	Doxorubicin	231-242	P53	Homo sapiens	86-89
19351845-7	2009	In cells treated with small interfering RNA (siRNA) targeting p53, expression of both p53 and ER was significantly reduced (&gt;60%) by 24 h. Induction of ER by DNA-damaging agents was p53 dependent as either ionizing radiation or doxorubicin failed to up-regulate ER after treatment with p53-targeting siRNA.	Doxorubicin	231-242	P53	Homo sapiens	86-89
19351845-7	2009	In cells treated with small interfering RNA (siRNA) targeting p53, expression of both p53 and ER was significantly reduced (&gt;60%) by 24 h. Induction of ER by DNA-damaging agents was p53 dependent as either ionizing radiation or doxorubicin failed to up-regulate ER after treatment with p53-targeting siRNA.	Doxorubicin	231-242	P53	Homo sapiens	86-89
19185564-1	2009	Although the primary response to Adriamycin (doxorubicin) in p53 mutant MDA-MB231 and p53 null MCF-7/E6 breast tumor cells is apoptotic cell death, the residual surviving population appears to be in a state of senescence, based on cell morphology, beta galactosidase staining, induction of p21(waf1/cip1) and down regulation of cdc2/cdk1.	Doxorubicin	33-43	P53	Homo sapiens	61-64
19185564-1	2009	Although the primary response to Adriamycin (doxorubicin) in p53 mutant MDA-MB231 and p53 null MCF-7/E6 breast tumor cells is apoptotic cell death, the residual surviving population appears to be in a state of senescence, based on cell morphology, beta galactosidase staining, induction of p21(waf1/cip1) and down regulation of cdc2/cdk1.	Doxorubicin	45-56	P53	Homo sapiens	61-64
19185564-6	2009	Taken together, these studies suggest that accelerated senescence induced by Adriamycin is similar in cells with wild type p53 and in cells lacking functional p53 with regard to the upregulation of p21(waf1/cip1), down regulation of cdc2 and the involvement of reactive oxygen species.	Doxorubicin	77-87	P53	Homo sapiens	123-126
19331830-4	2009	Two human p14ARF residues (Ala(14) and Thr(31)) were found to destabilize the protein while two others (Val(24) and Ala(41)) promoted more efficient p53 stabilization and activation.	Alanine	116-119	P53	Homo sapiens	149-152
19336515-5	2009	The Adriamycin-induced Twist1 expression and the interaction of Twist1 with p53-Mdm2 were examined by immunoblotting and immunoprecipitation, respectively.	Doxorubicin	4-14	P53	Homo sapiens	76-79
19336515-10	2009	Further, Twist1 reduction in Adriamycin-treated cells promoted p53-dependent p21 induction and disrupted the association of p53 with Mdm2.	Doxorubicin	29-39	P53	Homo sapiens	63-66
19336515-10	2009	Further, Twist1 reduction in Adriamycin-treated cells promoted p53-dependent p21 induction and disrupted the association of p53 with Mdm2.	Doxorubicin	29-39	P53	Homo sapiens	124-127
18989634-3	2009	We defined P53 overexpression through immunohistochemistry of paraffin-embedded tumor tissues, using cutpoints based on percent of cells positive.	Paraffin	62-70	P53	Homo sapiens	11-14
19288022-8	2009	Curcumin increased the protein expressions of p21 and Bax, but decreased the protein expression of p53 and Bcl-2 in MDA-MB-231 cells.	Curcumin	0-8	P53	Homo sapiens	99-102
19704938-0	2009	Effect of nitric oxide donor, a modulator of tumor drug resistance, on cell death and p53 protein expression.	Nitric Oxide	10-22	P53	Homo sapiens	86-89
20126301-6	2009	In particular, we discuss p53-mediated mechanisms that prevent damage caused by reactive oxygen species and the effects of lipotoxicity.	Reactive Oxygen Species	80-103	P53	Homo sapiens	26-29
18765292-4	2009	Here, we report, based on affinity chromatography and co-immunoprecipitation results that S100A6 interacts with p53 in the presence of calcium ions.	Calcium	135-142	P53	Homo sapiens	112-115
19188449-1	2009	The NAD(+)-dependent histone deacetylase hSirT1 regulates cell survival and stress responses by inhibiting p53-, NF-kappaB-, and E2F1-dependent transcription.	NAD	4-10	P53	Homo sapiens	107-110
19139269-4	2009	Exposure to capsaicin or DHC caused induction of p53, p21, and G(0)/G(1) arrest.	Capsaicin	12-21	P53	Homo sapiens	49-52
19304743-2	2009	The prognostic value of p53 in the outcome of adjuvant anthracycline-containing chemotherapy was evaluated according to molecular subclasses defined using the expression of estrogen receptor, progesterone receptor and human epidermal growth factor receptor 2.	Anthracyclines	55-68	P53	Homo sapiens	24-27
19304743-8	2009	CONCLUSIONS: p53 status could be a specific prognostic factor in triple-negative breast cancer patients treated by adjuvant anthracycline-based regimen.	Anthracyclines	124-137	P53	Homo sapiens	13-16
19225536-5	2009	Despite the non-genotoxic mode of nutlin 3A treatment, we show evidence that stabilization of p53 is associated with its phosphorylation at serine 15 residue and activation of AMPK.	Serine	140-146	P53	Homo sapiens	94-97
19642417-0	2009	The isolation, total synthesis and structure elucidation of chlorofusin, a natural product inhibitor of the p53-mDM2 protein-protein interaction.	chlorofusin	60-71	P53	Homo sapiens	108-111
19223463-2	2009	Here, we show that induction of p53 by the small-molecule RITA (reactivation of p53 and induction of tumor cell apoptosis) [2,5-bis(5-hydroxymethyl-2-thienyl) furan] (NSC-652287) inhibits HIF-1alpha and vascular endothelial growth factor expression in vivo and induces significant tumor cell apoptosis in normoxia and hypoxia in p53-positive cells.	NSC 652287	124-164	P53	Homo sapiens	32-35
19223463-2	2009	Here, we show that induction of p53 by the small-molecule RITA (reactivation of p53 and induction of tumor cell apoptosis) [2,5-bis(5-hydroxymethyl-2-thienyl) furan] (NSC-652287) inhibits HIF-1alpha and vascular endothelial growth factor expression in vivo and induces significant tumor cell apoptosis in normoxia and hypoxia in p53-positive cells.	NSC 652287	124-164	P53	Homo sapiens	80-83
19223463-2	2009	Here, we show that induction of p53 by the small-molecule RITA (reactivation of p53 and induction of tumor cell apoptosis) [2,5-bis(5-hydroxymethyl-2-thienyl) furan] (NSC-652287) inhibits HIF-1alpha and vascular endothelial growth factor expression in vivo and induces significant tumor cell apoptosis in normoxia and hypoxia in p53-positive cells.	NSC 652287	124-164	P53	Homo sapiens	80-83
19642417-2	2009	One such interaction between MDM2 (HDM2) and p53, that silences the tumour suppression activities of p53, was found to be inhibited by the recently isolated natural product chlorofusin.	chlorofusin	173-184	P53	Homo sapiens	45-48
19642417-2	2009	One such interaction between MDM2 (HDM2) and p53, that silences the tumour suppression activities of p53, was found to be inhibited by the recently isolated natural product chlorofusin.	chlorofusin	173-184	P53	Homo sapiens	101-104
19153082-2	2009	The p53 residues Leu(26), Trp(23), and Phe(19) are crucial to mediate these interactions.	Tryptophan	26-29	P53	Homo sapiens	4-7
19397439-0	2009	Suppression of NF-kappaB activity by parthenolide induces X-ray sensitivity through inhibition of split-dose repair in TP53 null prostate cancer cells.	parthenolide	37-49	P53	Homo sapiens	119-123
19397439-1	2009	We have shown that parthenolide, a sesquiterpene lactone, is a radiation sensitizer for human CGL1 hybrid cells that have constitutively activated NF-kappaB and wild-type p53.	parthenolide	19-31	P53	Homo sapiens	171-174
19397439-10	2009	We propose that the suppression of radiation-induced NF-kappaB activity by parthenolide leads to X-ray sensitization through inhibition of split-dose repair in p53 null PC-3 prostate cancer cells.	parthenolide	75-87	P53	Homo sapiens	160-163
19139065-3	2009	We show that base adducts caused by a potent carcinogen, benzo[a]pyrene diol epoxide (BPDE), constitute a strong signal for TopBP1-dependent ATR kinase activity on Chk1 and p53.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	57-84	P53	Homo sapiens	173-176
19139065-3	2009	We show that base adducts caused by a potent carcinogen, benzo[a]pyrene diol epoxide (BPDE), constitute a strong signal for TopBP1-dependent ATR kinase activity on Chk1 and p53.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	86-90	P53	Homo sapiens	173-176
19101993-3	2009	Genetic analysis showed a germline TP53 mutation in codon 220 exon 6, which changed TAT --> TGT and resulted in a tyrosine-to-cysteine amino acid substitution (Tyr220Cys).	Tyrosine	114-122	P53	Homo sapiens	35-39
19101993-3	2009	Genetic analysis showed a germline TP53 mutation in codon 220 exon 6, which changed TAT --> TGT and resulted in a tyrosine-to-cysteine amino acid substitution (Tyr220Cys).	Cysteine	126-134	P53	Homo sapiens	35-39
19468318-6	2009	Pretreatment with nitric oxide (NO) scavengers inhibited apoptotic biochemical changes induced by 5 microM MG/15 mM glucose, and increased the gene expression levels of p53 and p21 involved in apoptotic signaling.	Nitric Oxide	18-30	P53	Homo sapiens	169-172
19302811-6	2009	Treatment with 4 mM of H(2)O(2) for 24 or 96 h caused increase in Bax (56%, 227%), cytochrome c (282%, 701%), Smac/DIABLO (155%, 260%), caspase-3 protease activity (51%, 141%), and nuclear and cytosolic p53 (719%, 1581%) levels in the myotubes.	Hydrogen Peroxide	23-31	P53	Homo sapiens	203-206
19323829-4	2009	EBNA-5 associates with p53-hMDM2-p14ARF complexes.	N-tert-Butyl-N-ethylnitrosamine	0-4	P53	Homo sapiens	23-26
19046801-12	2009	Mutations of p53 determined in NHL cases (30%) were of Arg-176 (1/20: 5%), Phe-238 (1/20: 5%), Ser-249 (2/20; 10%), Lys-249 (1/20: 5%) and Phe-250 (1/20: 5%).	Arginine	55-58	P53	Homo sapiens	13-16
19046801-12	2009	Mutations of p53 determined in NHL cases (30%) were of Arg-176 (1/20: 5%), Phe-238 (1/20: 5%), Ser-249 (2/20; 10%), Lys-249 (1/20: 5%) and Phe-250 (1/20: 5%).	Serine	95-98	P53	Homo sapiens	13-16
19046801-12	2009	Mutations of p53 determined in NHL cases (30%) were of Arg-176 (1/20: 5%), Phe-238 (1/20: 5%), Ser-249 (2/20; 10%), Lys-249 (1/20: 5%) and Phe-250 (1/20: 5%).	Lysine	116-119	P53	Homo sapiens	13-16
19221494-0	2009	p53 methylation--the Arg-ument is clear.	Arginine	21-24	P53	Homo sapiens	0-3
19220000-9	2009	Phosphorylation of the p53 TAD at Thr18 or Ser20 increases the KIX binding affinity.	UNII-PYZ33YLR8A	34-39	P53	Homo sapiens	23-26
19081178-5	2009	Co-immunoprecipitation studies showed the presence of high levels of p53-HDM2 complexes in doxorubicin but not nutlin-3 treated cells suggesting that HDM2 association is responsible for the loss of p53 activity.	Doxorubicin	91-102	P53	Homo sapiens	69-72
19221494-4	2009	p53 activity is influenced by post-translational modifications, including phosphorylation and lysine methylation.	Lysine	94-100	P53	Homo sapiens	0-3
19221494-5	2009	Most recently, arginine methylation mediated by PRMT5, has been identified as an additional and important p53 modification.	Arginine	15-23	P53	Homo sapiens	106-109
19221494-6	2009	DNA damage induced p53 arginine methylation impacts on the biochemical properties and functional outcome of the p53 response.	Arginine	23-31	P53	Homo sapiens	19-22
19242108-0	2009	Downregulation of Wip-1 phosphatase expression in MCF-7 breast cancer cells enhances doxorubicin-induced apoptosis through p53-mediated transcriptional activation of Bax.	Doxorubicin	85-96	P53	Homo sapiens	123-126
19221494-6	2009	DNA damage induced p53 arginine methylation impacts on the biochemical properties and functional outcome of the p53 response.	Arginine	23-31	P53	Homo sapiens	112-115
19242108-7	2009	The enhanced apoptotic response was correlated with increased phosphorylation of N-terrninal p53-Ser15 and -Ser46 and increased expression of the pro-apoptotic Bax gene at both the mRNA and protein level.	Nitrogen	81-82	P53	Homo sapiens	93-96
19218339-9	2009	Furthermore, Chk1 silencing sensitized p53-null MM cells to both an S phase block and apoptosis in the presence of doxorubicin.	Doxorubicin	115-126	P53	Homo sapiens	39-42
19159633-0	2009	Berberine induces p53-dependent cell cycle arrest and apoptosis of human osteosarcoma cells by inflicting DNA damage.	Berberine	0-9	P53	Homo sapiens	18-21
19159633-9	2009	Thus, one major mechanism by which berberine exerts its growth-inhibitory effect is to inflict genomic lesions on cells, which in turn trigger the activation of p53 and the p53-dependent cellular responses including cell cycle arrest and apoptosis.	Berberine	35-44	P53	Homo sapiens	161-164
19159633-9	2009	Thus, one major mechanism by which berberine exerts its growth-inhibitory effect is to inflict genomic lesions on cells, which in turn trigger the activation of p53 and the p53-dependent cellular responses including cell cycle arrest and apoptosis.	Berberine	35-44	P53	Homo sapiens	173-176
19202066-2	2009	Recently, we have shown that p53 regulates glucose metabolism through the IKK-NF-kappaB pathway and that, in the absence of p53, the positive feedback loop between IKK-NF-kappaB and glycolysis has an integral role in oncogene-induced cell transformation.	Glucose	43-50	P53	Homo sapiens	29-32
19261747-4	2009	Furthermore, the synergistic effects of p53 and Pten deletion are mediated by deregulation of mammalian target of rapamycin (mTOR) signaling, consistent with the ability of rapamycin to block bladder tumorigenesis in preclinical studies.	Sirolimus	114-123	P53	Homo sapiens	40-43
19010591-5	2009	Moreover, we confirmed that the ROS-p38-p53 pathway was involved in PCL-induced autophagy.	ros	32-35	P53	Homo sapiens	40-43
19265549-5	2009	RESULTS: Significant differential modulation of 151 genes were found at 4 h after start of induction therapy with cytarabine and anthracycline, including significant overexpression of 31 genes associated with p53 regulation.	Anthracyclines	129-142	P53	Homo sapiens	209-212
19202066-4	2009	In p53-deficient cells, the O-GlcNAcylated IKKbeta and the activating phosphorylation of IKK were decreased by p65/NF-kappaB knockdown or glucose depletion.	Glucose	138-145	P53	Homo sapiens	3-6
19202066-8	2009	Taken together, we propose a novel mechanism for the enhancement of NF-kappaB activity by loss of p53, which evokes positive feedback regulation from enhanced glucose metabolism to IKK in oncogenesis.	Glucose	159-166	P53	Homo sapiens	98-101
18575867-4	2009	The H69 cells and resistant cell lines have a p53 mutation and consequently decrease expression of p21 in response to platinum drug treatment, promoting progression of the cell cycle instead of increasing p21 to maintain the arrest.	Platinum	118-126	P53	Homo sapiens	46-49
19067706-0	2009	Bexarotene activates the p53/p73 pathway in human cutaneous T-cell lymphoma.	Bexarotene	0-10	P53	Homo sapiens	25-28
19067706-13	2009	We further found that bexarotene activates p53 by phosphorylation at Ser15, which influences the binding of p53 to promoters for cell cycle arrest, induces p73 upregulation, and, in concordance, also modulates some p53/p73 downstream target genes, such as p21, Bax, survivin and cdc2.	Bexarotene	22-32	P53	Homo sapiens	43-46
19067706-13	2009	We further found that bexarotene activates p53 by phosphorylation at Ser15, which influences the binding of p53 to promoters for cell cycle arrest, induces p73 upregulation, and, in concordance, also modulates some p53/p73 downstream target genes, such as p21, Bax, survivin and cdc2.	Bexarotene	22-32	P53	Homo sapiens	108-111
19067706-13	2009	We further found that bexarotene activates p53 by phosphorylation at Ser15, which influences the binding of p53 to promoters for cell cycle arrest, induces p73 upregulation, and, in concordance, also modulates some p53/p73 downstream target genes, such as p21, Bax, survivin and cdc2.	Bexarotene	22-32	P53	Homo sapiens	108-111
19067706-14	2009	Bexarotene-mediated ataxia telangiectasia mutated protein (ATM) activation in all studied lines suggests that ATM is likely to be the p53/p73 upstream activator.	Bexarotene	0-10	P53	Homo sapiens	134-137
19067706-15	2009	CONCLUSIONS: Our data indicate for the first time that bexarotene exerts its effect in CTCL mainly by triggering the p53/p73-dependent cell cycle inhibition pathway, probably by upstream ATM activation.	Bexarotene	55-65	P53	Homo sapiens	117-120
19264704-0	2009	Induction of cellular senescence by secretory phospholipase A2 in human dermal fibroblasts through an ROS-mediated p53 pathway.	Reactive Oxygen Species	102-105	P53	Homo sapiens	115-118
19197340-7	2009	We show that PLA2R regulates senescence in a reactive oxygen species-DNA damage-p53-dependent manner.	Reactive Oxygen Species	45-68	P53	Homo sapiens	80-83
19086036-1	2009	UNLABELLED: Toxic bile acids induce hepatocyte apoptosis, for which p53 and cyclin D1 have been implicated as underlying mediators.	Bile Acids and Salts	18-28	P53	Homo sapiens	68-71
19296337-7	2009	Similar gel mobility shift of p53-binding oligonucleotide with BMG-1 and Sf9 cell lysates indicated analogous transcriptional activity of Sfp53.	Oligonucleotides	42-57	P53	Homo sapiens	30-33
19471670-7	2009	In p53 deleted SKOV3 cells, cisplatin treatment after Ad-p53 showed higher growth inhibition than the treatment before Ad-p53 transduction, and reverse relationship was observed in p53 mutated OVCAR-3 cells.	Cisplatin	28-37	P53	Homo sapiens	3-6
19471670-7	2009	In p53 deleted SKOV3 cells, cisplatin treatment after Ad-p53 showed higher growth inhibition than the treatment before Ad-p53 transduction, and reverse relationship was observed in p53 mutated OVCAR-3 cells.	Cisplatin	28-37	P53	Homo sapiens	57-60
19471670-7	2009	In p53 deleted SKOV3 cells, cisplatin treatment after Ad-p53 showed higher growth inhibition than the treatment before Ad-p53 transduction, and reverse relationship was observed in p53 mutated OVCAR-3 cells.	Cisplatin	28-37	P53	Homo sapiens	57-60
19471670-7	2009	In p53 deleted SKOV3 cells, cisplatin treatment after Ad-p53 showed higher growth inhibition than the treatment before Ad-p53 transduction, and reverse relationship was observed in p53 mutated OVCAR-3 cells.	Cisplatin	28-37	P53	Homo sapiens	57-60
19471670-9	2009	CONCLUSION: The synergistic growth inhibition by combination of Ad-p53 and cisplatin may depend on the p53 status and the temporal sequence of cisplatin treatment, suggesting judicious selective application of this strategy in clinical trials.	Cisplatin	75-84	P53	Homo sapiens	103-106
19471670-9	2009	CONCLUSION: The synergistic growth inhibition by combination of Ad-p53 and cisplatin may depend on the p53 status and the temporal sequence of cisplatin treatment, suggesting judicious selective application of this strategy in clinical trials.	Cisplatin	143-152	P53	Homo sapiens	67-70
19150257-0	2009	HCT116 cells deficient in p21(Waf1) are hypersensitive to tyrosine kinase inhibitors and adriamycin through a mechanism unrelated to p21 and dependent on p53.	Doxorubicin	89-99	P53	Homo sapiens	154-157
19150257-8	2009	We found that, in HCT116p21(-/-) cells, p53 showed higher stability, higher transcriptional activity and phosphorylation in serines associated with p53 activity.	Serine	124-131	P53	Homo sapiens	40-43
19150257-8	2009	We found that, in HCT116p21(-/-) cells, p53 showed higher stability, higher transcriptional activity and phosphorylation in serines associated with p53 activity.	Serine	124-131	P53	Homo sapiens	148-151
19150257-9	2009	Furthermore, silencing of p53 with siRNA and inactivation of p53 with a dominant negative mutant rescued the hypersensitive response to kinases inhibitors, 5-fluorouracil and adriamycin in HCT116p21(-/-) cells.	Fluorouracil	156-170	P53	Homo sapiens	26-29
19150257-9	2009	Furthermore, silencing of p53 with siRNA and inactivation of p53 with a dominant negative mutant rescued the hypersensitive response to kinases inhibitors, 5-fluorouracil and adriamycin in HCT116p21(-/-) cells.	Fluorouracil	156-170	P53	Homo sapiens	61-64
19150257-9	2009	Furthermore, silencing of p53 with siRNA and inactivation of p53 with a dominant negative mutant rescued the hypersensitive response to kinases inhibitors, 5-fluorouracil and adriamycin in HCT116p21(-/-) cells.	Doxorubicin	175-185	P53	Homo sapiens	26-29
19150257-9	2009	Furthermore, silencing of p53 with siRNA and inactivation of p53 with a dominant negative mutant rescued the hypersensitive response to kinases inhibitors, 5-fluorouracil and adriamycin in HCT116p21(-/-) cells.	Doxorubicin	175-185	P53	Homo sapiens	61-64
19150122-1	2009	OBJECTIVE: The aim of the study was to evaluate the prognostic significance of p53 and PTEN in patients with epithelial ovarian cancer who were treated with taxane and platinum-based chemotherapy.	taxane	157-163	P53	Homo sapiens	79-82
19150122-1	2009	OBJECTIVE: The aim of the study was to evaluate the prognostic significance of p53 and PTEN in patients with epithelial ovarian cancer who were treated with taxane and platinum-based chemotherapy.	Platinum	168-176	P53	Homo sapiens	79-82
19212663-3	2009	For p53 genotype analysis, breast cancer patients presented a significant (p&lt;0.05) over-representation of p53 Arg homozygosity (55.5%) compared with the healthy control group (33.3%).	Arginine	113-116	P53	Homo sapiens	109-112
19212663-6	2009	It is possible that p53 Arg homozygosity is associated with breast cancer and may represent a potential risk factor for breast tumorigenesis.	Arginine	24-27	P53	Homo sapiens	20-23
19212664-2	2009	We hypothesized that the anticancer effects of aspirin may involve acetylation of the tumor suppressor protein p53, a known regulator of apoptosis.	Aspirin	47-54	P53	Homo sapiens	111-114
19212664-3	2009	In the present study, we determined if aspirin at the physiologically achievable concentration of 100 microM acetylates p53 and modulates the expression of p21CIP1, a protein involved in cell cycle arrest, and Bax, a pro-apoptotic protein.	Aspirin	39-46	P53	Homo sapiens	120-123
19212664-4	2009	Using MDA-MB-231 human breast cancer cells, we demonstrate that aspirin at 100 microM concentration markedly acetylated the p53 protein, which was primarily localized to the nucleus.	Aspirin	64-71	P53	Homo sapiens	124-127
19264704-7	2009	These results suggest that sPLA(2) has a role in cellular senescence in HDFs during inflammatory response by promoting ROS-dependent p53 activation and might therefore contribute to inflammatory disorders associated with aging.	Reactive Oxygen Species	119-122	P53	Homo sapiens	133-136
19064630-0	2009	Psoralen-induced DNA interstrand cross-links block transcription and induce p53 in an ataxia-telangiectasia and rad3-related-dependent manner.	Ficusin	0-8	P53	Homo sapiens	76-79
19276167-0	2009	Parthenolide promotes the ubiquitination of MDM2 and activates p53 cellular functions.	parthenolide	0-12	P53	Homo sapiens	63-66
19276167-4	2009	We found that the natural product, small-molecule anti-inflammatory agent parthenolide (PN), which is actively being investigated as a potential therapeutic for many human cancers, induces ubiquitination of MDM2 in treated cells, resulting in the activation of p53 and other MDM2-regulated tumor-suppressor proteins.	parthenolide	74-86	P53	Homo sapiens	261-264
19276167-4	2009	We found that the natural product, small-molecule anti-inflammatory agent parthenolide (PN), which is actively being investigated as a potential therapeutic for many human cancers, induces ubiquitination of MDM2 in treated cells, resulting in the activation of p53 and other MDM2-regulated tumor-suppressor proteins.	parthenolide	88-90	P53	Homo sapiens	261-264
18620780-1	2009	BACKGROUND: In a previously published in vitro study based on top-down proteomics we found that the calcium-binding proteins S100A6 and S100A4 were affected by exposure to ionizing radiation in a p53-dependent fashion.	Calcium	100-107	P53	Homo sapiens	196-199
19064630-6	2009	To better understand the mechanism by which PUVA treatment induces p53, we exposed human skin fibroblasts with PUVA under conditions that differentially produce monoadducts and ICLs and found that psoralen-induced ICLs induced phosphorylation of the Ser-15 site of p53 and apoptosis much more effectively than psoralen-induced monoadducts.	Ficusin	310-318	P53	Homo sapiens	67-70
19064630-6	2009	To better understand the mechanism by which PUVA treatment induces p53, we exposed human skin fibroblasts with PUVA under conditions that differentially produce monoadducts and ICLs and found that psoralen-induced ICLs induced phosphorylation of the Ser-15 site of p53 and apoptosis much more effectively than psoralen-induced monoadducts.	Ficusin	197-205	P53	Homo sapiens	67-70
19064630-6	2009	To better understand the mechanism by which PUVA treatment induces p53, we exposed human skin fibroblasts with PUVA under conditions that differentially produce monoadducts and ICLs and found that psoralen-induced ICLs induced phosphorylation of the Ser-15 site of p53 and apoptosis much more effectively than psoralen-induced monoadducts.	Ficusin	197-205	P53	Homo sapiens	265-268
19201868-8	2009	p53 was processed to three cleavage products of p40, p35, and p13 fragments at Lys(24) and Lys(305).	Lysine	79-82	P53	Homo sapiens	0-3
19030178-0	2009	TP53 mutation signature supports involvement of aristolochic acid in the aetiology of endemic nephropathy-associated tumours.	aristolochic acid I	48-65	P53	Homo sapiens	0-4
19030178-3	2009	Using a novel mutation assay in which we can induce and select mutations in human TP53 sequences in vitro by exposure of cultured cells to a mutagen, we found that A to T mutations were elicited by aristolochic acid at sites in TP53 rarely mutated in human cancers in general, but which were observed in the BEN patients.	aristolochic acid I	198-215	P53	Homo sapiens	82-86
19030178-3	2009	Using a novel mutation assay in which we can induce and select mutations in human TP53 sequences in vitro by exposure of cultured cells to a mutagen, we found that A to T mutations were elicited by aristolochic acid at sites in TP53 rarely mutated in human cancers in general, but which were observed in the BEN patients.	aristolochic acid I	198-215	P53	Homo sapiens	228-232
19212643-1	2009	The impact of a polymorphism of the wild-type human tumour suppressor gene p53(wt) on carcinogenesis is subject of controversy ever since a higher susceptibility of p53 to HPV-E6 mediated degradation when encoding for Arginine at codon 72 (p53Arg) was first reported.	Arginine	218-226	P53	Homo sapiens	75-78
19212643-1	2009	The impact of a polymorphism of the wild-type human tumour suppressor gene p53(wt) on carcinogenesis is subject of controversy ever since a higher susceptibility of p53 to HPV-E6 mediated degradation when encoding for Arginine at codon 72 (p53Arg) was first reported.	Arginine	218-226	P53	Homo sapiens	165-168
19462899-7	2009	Immunohistochemistry test demonstrated that tanshinone A upregulate P53 expression in both cells and also weakly upregulate the CerBb-2 expression in MCF-7 (P &lt; 0.05), whereas no influence on CerBb-2 expression of MDA-MB-231 and on Bcl-2 expression of both cells were demonstrated (P &gt; 0.05).	tanshinone	44-56	P53	Homo sapiens	68-71
19196987-3	2009	Phosphorylation of p53 at serines 362 and 366 by IKK2 leads to its recruitment to and ubiquitination by beta-TrCP1.	Serine	26-33	P53	Homo sapiens	19-22
19196987-6	2009	Substitutions at Ser-362 and 366 of p53 by alanines (p53 AA) result in reduced phosphorylation of p53 by IKK2, decreased association with beta-TrCP1, and thus increased stability of p53 and expression of p53 target genes such as p21, altering the G1 phase of the cell cycle.	Serine	17-20	P53	Homo sapiens	36-39
19196987-6	2009	Substitutions at Ser-362 and 366 of p53 by alanines (p53 AA) result in reduced phosphorylation of p53 by IKK2, decreased association with beta-TrCP1, and thus increased stability of p53 and expression of p53 target genes such as p21, altering the G1 phase of the cell cycle.	Serine	17-20	P53	Homo sapiens	53-56
19196987-6	2009	Substitutions at Ser-362 and 366 of p53 by alanines (p53 AA) result in reduced phosphorylation of p53 by IKK2, decreased association with beta-TrCP1, and thus increased stability of p53 and expression of p53 target genes such as p21, altering the G1 phase of the cell cycle.	Serine	17-20	P53	Homo sapiens	53-56
19196987-6	2009	Substitutions at Ser-362 and 366 of p53 by alanines (p53 AA) result in reduced phosphorylation of p53 by IKK2, decreased association with beta-TrCP1, and thus increased stability of p53 and expression of p53 target genes such as p21, altering the G1 phase of the cell cycle.	Serine	17-20	P53	Homo sapiens	53-56
19196987-6	2009	Substitutions at Ser-362 and 366 of p53 by alanines (p53 AA) result in reduced phosphorylation of p53 by IKK2, decreased association with beta-TrCP1, and thus increased stability of p53 and expression of p53 target genes such as p21, altering the G1 phase of the cell cycle.	Serine	17-20	P53	Homo sapiens	53-56
19196987-6	2009	Substitutions at Ser-362 and 366 of p53 by alanines (p53 AA) result in reduced phosphorylation of p53 by IKK2, decreased association with beta-TrCP1, and thus increased stability of p53 and expression of p53 target genes such as p21, altering the G1 phase of the cell cycle.	Alanine	43-51	P53	Homo sapiens	36-39
19196987-6	2009	Substitutions at Ser-362 and 366 of p53 by alanines (p53 AA) result in reduced phosphorylation of p53 by IKK2, decreased association with beta-TrCP1, and thus increased stability of p53 and expression of p53 target genes such as p21, altering the G1 phase of the cell cycle.	Alanine	43-51	P53	Homo sapiens	53-56
19196987-6	2009	Substitutions at Ser-362 and 366 of p53 by alanines (p53 AA) result in reduced phosphorylation of p53 by IKK2, decreased association with beta-TrCP1, and thus increased stability of p53 and expression of p53 target genes such as p21, altering the G1 phase of the cell cycle.	Alanine	43-51	P53	Homo sapiens	53-56
19196987-6	2009	Substitutions at Ser-362 and 366 of p53 by alanines (p53 AA) result in reduced phosphorylation of p53 by IKK2, decreased association with beta-TrCP1, and thus increased stability of p53 and expression of p53 target genes such as p21, altering the G1 phase of the cell cycle.	Alanine	43-51	P53	Homo sapiens	53-56
19196987-6	2009	Substitutions at Ser-362 and 366 of p53 by alanines (p53 AA) result in reduced phosphorylation of p53 by IKK2, decreased association with beta-TrCP1, and thus increased stability of p53 and expression of p53 target genes such as p21, altering the G1 phase of the cell cycle.	Alanine	43-51	P53	Homo sapiens	53-56
19106109-0	2009	p53 Oligomerization is essential for its C-terminal lysine acetylation.	Lysine	52-58	P53	Homo sapiens	0-3
19106109-1	2009	Acetylation of multiple lysine residues in the p53 plays critical roles in the protein stability and transcriptional activity of p53.	Lysine	24-30	P53	Homo sapiens	47-50
19106109-1	2009	Acetylation of multiple lysine residues in the p53 plays critical roles in the protein stability and transcriptional activity of p53.	Lysine	24-30	P53	Homo sapiens	129-132
19106109-3	2009	We found that p53 mutants that are defective in tetramer formation are also defective in C-terminal lysine residue acetylation.	Lysine	100-106	P53	Homo sapiens	14-17
19106109-4	2009	Consistently, we found that several cancer-derived p53 mutants that bear mutations in the tetramerization domain cannot form oligomers and are defective in C-terminal lysine acetylation, and these mutants are inactive in p21 transactivation.	Lysine	167-173	P53	Homo sapiens	51-54
19166313-6	2009	Using a competitive fluorescence anisotropy assay, we determined that monophosphorylation of p53 at Ser(15) or Thr(18) increased the affinity of p53(1-39) for Taz2, and diphosphorylations at Ser(15) and Ser(37) or Thr(18) and Ser(20) further increased the affinity.	Serine	100-103	P53	Homo sapiens	93-96
19166313-6	2009	Using a competitive fluorescence anisotropy assay, we determined that monophosphorylation of p53 at Ser(15) or Thr(18) increased the affinity of p53(1-39) for Taz2, and diphosphorylations at Ser(15) and Ser(37) or Thr(18) and Ser(20) further increased the affinity.	Serine	100-103	P53	Homo sapiens	145-148
19166313-6	2009	Using a competitive fluorescence anisotropy assay, we determined that monophosphorylation of p53 at Ser(15) or Thr(18) increased the affinity of p53(1-39) for Taz2, and diphosphorylations at Ser(15) and Ser(37) or Thr(18) and Ser(20) further increased the affinity.	Threonine	111-114	P53	Homo sapiens	145-148
19166313-6	2009	Using a competitive fluorescence anisotropy assay, we determined that monophosphorylation of p53 at Ser(15) or Thr(18) increased the affinity of p53(1-39) for Taz2, and diphosphorylations at Ser(15) and Ser(37) or Thr(18) and Ser(20) further increased the affinity.	Serine	191-194	P53	Homo sapiens	93-96
19166313-6	2009	Using a competitive fluorescence anisotropy assay, we determined that monophosphorylation of p53 at Ser(15) or Thr(18) increased the affinity of p53(1-39) for Taz2, and diphosphorylations at Ser(15) and Ser(37) or Thr(18) and Ser(20) further increased the affinity.	Serine	191-194	P53	Homo sapiens	145-148
19166313-6	2009	Using a competitive fluorescence anisotropy assay, we determined that monophosphorylation of p53 at Ser(15) or Thr(18) increased the affinity of p53(1-39) for Taz2, and diphosphorylations at Ser(15) and Ser(37) or Thr(18) and Ser(20) further increased the affinity.	Serine	191-194	P53	Homo sapiens	93-96
19166313-6	2009	Using a competitive fluorescence anisotropy assay, we determined that monophosphorylation of p53 at Ser(15) or Thr(18) increased the affinity of p53(1-39) for Taz2, and diphosphorylations at Ser(15) and Ser(37) or Thr(18) and Ser(20) further increased the affinity.	Serine	191-194	P53	Homo sapiens	145-148
19166313-6	2009	Using a competitive fluorescence anisotropy assay, we determined that monophosphorylation of p53 at Ser(15) or Thr(18) increased the affinity of p53(1-39) for Taz2, and diphosphorylations at Ser(15) and Ser(37) or Thr(18) and Ser(20) further increased the affinity.	Threonine	214-217	P53	Homo sapiens	93-96
19166313-6	2009	Using a competitive fluorescence anisotropy assay, we determined that monophosphorylation of p53 at Ser(15) or Thr(18) increased the affinity of p53(1-39) for Taz2, and diphosphorylations at Ser(15) and Ser(37) or Thr(18) and Ser(20) further increased the affinity.	Threonine	214-217	P53	Homo sapiens	145-148
19166313-6	2009	Using a competitive fluorescence anisotropy assay, we determined that monophosphorylation of p53 at Ser(15) or Thr(18) increased the affinity of p53(1-39) for Taz2, and diphosphorylations at Ser(15) and Ser(37) or Thr(18) and Ser(20) further increased the affinity.	Serine	191-194	P53	Homo sapiens	93-96
19166313-6	2009	Using a competitive fluorescence anisotropy assay, we determined that monophosphorylation of p53 at Ser(15) or Thr(18) increased the affinity of p53(1-39) for Taz2, and diphosphorylations at Ser(15) and Ser(37) or Thr(18) and Ser(20) further increased the affinity.	Serine	191-194	P53	Homo sapiens	145-148
19059205-7	2009	The cell adhesion strength in the presence of SPBE, beta-sitosterol and cholesterol and the observation was that the increase in p53 expression triggered an increase in the intracellular force generation.	Cholesterol	72-83	P53	Homo sapiens	129-132
19201868-8	2009	p53 was processed to three cleavage products of p40, p35, and p13 fragments at Lys(24) and Lys(305).	Lysine	91-94	P53	Homo sapiens	0-3
18929442-6	2009	Western Blot showed that SN-38 down-regulated protein expression of p-Akt and increased protein expression of p53 and p21, but it had no effects on protein expression of Bax, Bcl-2 and Akt.	Irinotecan	25-30	P53	Homo sapiens	110-113
19217391-6	2009	Additionally, they suggest that the increased affinity of Taz2 for p53(1-39) phosphorylated at Thr(18) is due in part to electrostatic interactions of the phosphate with neighboring arginine residues in Taz2.	Threonine	95-98	P53	Homo sapiens	67-70
19217391-6	2009	Additionally, they suggest that the increased affinity of Taz2 for p53(1-39) phosphorylated at Thr(18) is due in part to electrostatic interactions of the phosphate with neighboring arginine residues in Taz2.	Phosphates	155-164	P53	Homo sapiens	67-70
19217391-6	2009	Additionally, they suggest that the increased affinity of Taz2 for p53(1-39) phosphorylated at Thr(18) is due in part to electrostatic interactions of the phosphate with neighboring arginine residues in Taz2.	Arginine	182-190	P53	Homo sapiens	67-70
19217391-7	2009	Thermodynamic experiments revealed the importance of hydrophobic interactions in the complex of Taz2 with p53 phosphorylated at Ser(15) and Thr(18).	Serine	128-131	P53	Homo sapiens	106-109
19217391-7	2009	Thermodynamic experiments revealed the importance of hydrophobic interactions in the complex of Taz2 with p53 phosphorylated at Ser(15) and Thr(18).	Threonine	140-143	P53	Homo sapiens	106-109
19084536-9	2009	However, for a few sequences containing multiple CpG dinucleotides, such as sites in the RB and Met genes, methylation resulted in a four- to sixfold increase in binding of p53.	cytidylyl-3'-5'-guanosine	49-66	P53	Homo sapiens	173-176
19216755-9	2009	In the ATRA-responsive cell lines, ATRA significantly increased the protein expression of Chmp1A, CRBP-1, P53 and phospho-P53 at serine 15 and 37 position.	Serine	129-135	P53	Homo sapiens	106-109
19216755-9	2009	In the ATRA-responsive cell lines, ATRA significantly increased the protein expression of Chmp1A, CRBP-1, P53 and phospho-P53 at serine 15 and 37 position.	Serine	129-135	P53	Homo sapiens	122-125
19216755-11	2009	Also, Chmp1A silencing diminished the increase of Chmp1A, P53 and phospho-P53 protein expression induced by ATRA.	Tretinoin	108-112	P53	Homo sapiens	58-61
18929442-7	2009	Transfection of the full-length Akt cDNA into HeLa and SiHa cells resulted in the reduction of apoptosis induced by SN-38, and Akt kinase activity regulated the p53 pathway, indicating that inhibition of the Akt pathway played an important role in exhibition of SN-38-mediated cytotoxic effect.	Irinotecan	262-267	P53	Homo sapiens	161-164
19216755-11	2009	Also, Chmp1A silencing diminished the increase of Chmp1A, P53 and phospho-P53 protein expression induced by ATRA.	Tretinoin	108-112	P53	Homo sapiens	74-77
18929442-8	2009	Our data suggested that SN-38 could induce apoptosis through a p53 pathway and that activation of p53 in response to S-38 is governed by Akt.	Irinotecan	24-29	P53	Homo sapiens	63-66
18929442-8	2009	Our data suggested that SN-38 could induce apoptosis through a p53 pathway and that activation of p53 in response to S-38 is governed by Akt.	Irinotecan	24-29	P53	Homo sapiens	98-101
18929442-8	2009	Our data suggested that SN-38 could induce apoptosis through a p53 pathway and that activation of p53 in response to S-38 is governed by Akt.	Sulfur-38	117-121	P53	Homo sapiens	98-101
19075013-9	2009	One of these phosphorylations, on tyrosine 99, inhibited Hdmx interaction with p53.	Tyrosine	34-42	P53	Homo sapiens	79-82
19101573-12	2009	Interestingly, 2,3-DHBA and histone peptide-6 caused base damage in the 5"-ACG-3" and 5"-CCG-3" sequences, hotspots of the p53 gene.	2,3-dihydroxybenzoic acid	15-23	P53	Homo sapiens	123-126
18951928-0	2009	Intracellular zinc increase inhibits p53(-/-) pancreatic adenocarcinoma cell growth by ROS/AIF-mediated apoptosis.	Reactive Oxygen Species	87-90	P53	Homo sapiens	37-40
19082896-0	2009	Nonlinear cooperation of p53-ING1-induced bax expression and protein S-nitrosylation in GSNO-induced thymocyte apoptosis: a quantitative approach with cross-platform validation.	S-Nitrosoglutathione	88-92	P53	Homo sapiens	25-28
18951928-5	2009	We show that Zn/PDTC induces p53 proteasomal degradation and that the proteasome inhibitor MG132 further increases fibroblast growth inhibition by Zn/PDTC, suggesting that p53 degradation plays an important role in fibroblast resistance to Zn/PDTC.	Zinc	13-15	P53	Homo sapiens	29-32
19243248-0	2009	Adenovirus-mediated wild-type p53 transfer radiosensitizes H1299 cells to subclinical-dose carbon-ion irradiation through the restoration of p53 function.	Carbon	91-97	P53	Homo sapiens	30-33
18951928-5	2009	We show that Zn/PDTC induces p53 proteasomal degradation and that the proteasome inhibitor MG132 further increases fibroblast growth inhibition by Zn/PDTC, suggesting that p53 degradation plays an important role in fibroblast resistance to Zn/PDTC.	Zinc	13-15	P53	Homo sapiens	172-175
18951928-5	2009	We show that Zn/PDTC induces p53 proteasomal degradation and that the proteasome inhibitor MG132 further increases fibroblast growth inhibition by Zn/PDTC, suggesting that p53 degradation plays an important role in fibroblast resistance to Zn/PDTC.	Zinc	147-149	P53	Homo sapiens	172-175
19095450-4	2009	This HY251-induced G(1) phase arrest is associated with decreased expression of cyclin D3 and up-regulation of p21(CIP1) and p27(KIP1), via p53 phosphorylation at Ser-15 by transcriptional up-regulation of ATM, which resulted in increased hypophosphorylated pRb in HeLa cells.	Serine	163-166	P53	Homo sapiens	140-143
19155291-1	2009	The major determinants of 5-flurouracil (5-FU) response would seem, based on accumulated literature, to be thymidylate synthase (TYMS, TS) expression levels, TS gene modifications, and TP53 status.	Fluorouracil	41-45	P53	Homo sapiens	185-189
19155291-2	2009	We tested 5-FU sensitivity in yeast and human cancer cell models in which TS or TP53 alleles and expression were varied.	Fluorouracil	10-14	P53	Homo sapiens	80-84
19243248-0	2009	Adenovirus-mediated wild-type p53 transfer radiosensitizes H1299 cells to subclinical-dose carbon-ion irradiation through the restoration of p53 function.	Carbon	91-97	P53	Homo sapiens	141-144
19169960-1	2009	Contusugene ladenovec (Advexin; INGN-201; Introgen Therapeutics Inc) is a replication-impaired, non-integrating, serotype 5 adenoviral vector that carries the p53 gene under the control of the CMV promoter.	contusugene	0-11	P53	Homo sapiens	159-162
19188164-8	2009	The combination of Nutlin-3 with doxorubicin or bortezomib was synergistic in wt-TP53 MCL cells.	Doxorubicin	33-44	P53	Homo sapiens	81-85
19179064-0	2009	Modifications of p53: competing for the lysines.	Lysine	40-47	P53	Homo sapiens	17-20
19179064-2	2009	In addition to a multitude of phosphorylated serines and threonines, many of the lysine residues in p53 can be modified to regulate activity, stability and subcellular localization of the protein.	Lysine	81-87	P53	Homo sapiens	100-103
19179064-3	2009	This complexity is amplified by the variety of modifications that can target the same lysine residue - often with opposing effects on p53 function.	Lysine	86-92	P53	Homo sapiens	134-137
19096907-6	2009	This study was designed to evaluate the efficacy of different fixatives, of microwaving and microwave pretreatment method to retrieve p53 immunoreactivity in paraffin-embedded non-lesioned (adjacent normal tissue) human skin samples or pathological human skin samples diagnosed as basal cell carcinoma.	Paraffin	158-166	P53	Homo sapiens	134-137
19243304-6	2009	In light of these new findings, the following review focuses on p53/mitochondria connections, in particular how reactive oxygen species generated at mitochondria regulate p53 activity.	Reactive Oxygen Species	112-135	P53	Homo sapiens	64-67
19243304-6	2009	In light of these new findings, the following review focuses on p53/mitochondria connections, in particular how reactive oxygen species generated at mitochondria regulate p53 activity.	Reactive Oxygen Species	112-135	P53	Homo sapiens	171-174
19085961-8	2009	Moreover, we found that ectopic overexpression of p33(ING1b) or p24(ING1c) significantly induced p53 protein acetylation at Lys-373/Lys-382 residue, but did not alter the phosphorylation status of p53.	Lysine	124-127	P53	Homo sapiens	97-100
19085961-8	2009	Moreover, we found that ectopic overexpression of p33(ING1b) or p24(ING1c) significantly induced p53 protein acetylation at Lys-373/Lys-382 residue, but did not alter the phosphorylation status of p53.	Lysine	132-135	P53	Homo sapiens	97-100
18978812-0	2009	Nitric oxide prodrug JS-K inhibits ubiquitin E1 and kills tumor cells retaining wild-type p53.	Nitric Oxide	0-12	P53	Homo sapiens	90-93
19101635-4	2009	These novel functions of p53 help to align metabolic processes with the proliferation and energy status, to maintain optimal mode of glucose metabolism and to boost the energy efficient mitochondrial respiration in response to ATP deficiency.	Adenosine Triphosphate	227-230	P53	Homo sapiens	25-28
19148534-7	2009	Thus, TACC3 is thought to be the critical molecule in mediating the anticancer mechanisms of paclitaxel in p53 inactivated cells by inducing G2/M arrest and apoptosis.	Paclitaxel	93-103	P53	Homo sapiens	107-110
19595309-5	2009	There are, however, still many open questions regarding, for example, whether sirtuins deacetylate those lysine residues in p53 that are critical for its activity.	Lysine	105-111	P53	Homo sapiens	124-127
19144918-0	2009	The p53-cathepsin axis cooperates with ROS to activate programmed necrotic death upon DNA damage.	Reactive Oxygen Species	39-42	P53	Homo sapiens	4-7
19144918-7	2009	p53 induces cathepsin Q that cooperates with reactive oxygen species (ROS) to execute necrosis.	Reactive Oxygen Species	45-68	P53	Homo sapiens	0-3
19144918-7	2009	p53 induces cathepsin Q that cooperates with reactive oxygen species (ROS) to execute necrosis.	Reactive Oxygen Species	70-73	P53	Homo sapiens	0-3
19103993-0	2009	Acute doxorubicin cardiotoxicity is associated with p53-induced inhibition of the mammalian target of rapamycin pathway.	Doxorubicin	6-17	P53	Homo sapiens	52-55
18824293-5	2009	Transfection of p53 into the Hep3B cell line increased the sensitivity of tumor cells to cisplatin.	Cisplatin	89-98	P53	Homo sapiens	16-19
19224462-7	2009	Patients who had the allele Pro of the TP53 Arg72Pro polymorphism had an increased risk of tumor development (odds ratio, OR = 3.23; confidence interval at 95%, 95%CI = 1.71-6.08; P = 0.003), as did the allele Ser of TP53 Pro47Ser polymorphism (OR = 1.28; 95%CI = 0.03-2.10; P = 0.01).	Serine	210-213	P53	Homo sapiens	39-43
19224462-7	2009	Patients who had the allele Pro of the TP53 Arg72Pro polymorphism had an increased risk of tumor development (odds ratio, OR = 3.23; confidence interval at 95%, 95%CI = 1.71-6.08; P = 0.003), as did the allele Ser of TP53 Pro47Ser polymorphism (OR = 1.28; 95%CI = 0.03-2.10; P = 0.01).	Serine	210-213	P53	Homo sapiens	217-221
18781628-0	2009	Oxidation of methionine residue at hydrophobic core destabilizes p53 tetrameric structure.	Methionine	13-23	P53	Homo sapiens	65-68
19331147-6	2009	The protein levels of Bcl-2 decreased and Bax increased in the mitochondrial fraction while the Bax protein decreased, and p53 and cytochrome c protein levels increased in the cytosolic fraction in HepG2 cells after capsaicin treatment for 24 h by Western blot.	Capsaicin	216-225	P53	Homo sapiens	123-126
18781628-4	2009	A methionine residue (Met340) is located at the hydrophobic core in p53 tetramerization domain.	Methionine	2-12	P53	Homo sapiens	68-71
18781628-5	2009	Here, we demonstrated that Met340 residue can be oxidized to methionine sulfoxide under oxidative conditions and investigated effects of the oxidation of p53 tetramerization domain on its stability and oligomerization state by CD measurement and gel filtration.	Cadmium	227-229	P53	Homo sapiens	154-157
18781628-9	2009	These results taken together suggested that oxidation of methionine residues in the p53 protein might be one of the inactivation mechanisms of p53 transcriptional function under conditions of oxidative stress.	Methionine	57-67	P53	Homo sapiens	84-87
18781628-9	2009	These results taken together suggested that oxidation of methionine residues in the p53 protein might be one of the inactivation mechanisms of p53 transcriptional function under conditions of oxidative stress.	Methionine	57-67	P53	Homo sapiens	143-146
19593673-6	2009	The molecular changes in both cell lines due to DOX treatment could be classified into: (1) the basal level of p53, p21, BRCA1, GST and TOPOIIalpha mRNA was higher in MCF7/DOX than MCF7/WT.	Doxorubicin	48-51	P53	Homo sapiens	111-114
18228136-4	2009	RT(2) Profiler PCR Array was used to identify differentially expressed genes in Dox and/or 2ME treatment groups, based on significance of results 4 genes were selected: MDR1, Bcl2, P53 and Cyclin D1.	Doxorubicin	80-83	P53	Homo sapiens	181-184
18758183-2	2009	P27 and P53 play important roles in the signal transduction leading to neointimal growth inhibition and induction of apoptosis of smooth muscle cells due to rapamycin and paclitaxel.	Sirolimus	157-166	P53	Homo sapiens	8-11
18758183-2	2009	P27 and P53 play important roles in the signal transduction leading to neointimal growth inhibition and induction of apoptosis of smooth muscle cells due to rapamycin and paclitaxel.	Paclitaxel	171-181	P53	Homo sapiens	8-11
19821999-10	2009	Incubation of MDA-MB-231 cells with BU-32 results in the accumulation of cell cycle inhibitor proteins p21 and p27 and stabilization of the tumor suppressor protein p53.	Busulfan	36-38	P53	Homo sapiens	165-168
19118006-8	2009	Mutation of p53 Ser(58) (equivalent to human p53 Ser(46)) abrogates transcription of these genes, indicating that TP53INP1-mediated p53 Ser(58) phosphorylation is implicated in this process.	Serine	16-19	P53	Homo sapiens	12-15
19118006-8	2009	Mutation of p53 Ser(58) (equivalent to human p53 Ser(46)) abrogates transcription of these genes, indicating that TP53INP1-mediated p53 Ser(58) phosphorylation is implicated in this process.	Serine	16-19	P53	Homo sapiens	45-48
19118006-8	2009	Mutation of p53 Ser(58) (equivalent to human p53 Ser(46)) abrogates transcription of these genes, indicating that TP53INP1-mediated p53 Ser(58) phosphorylation is implicated in this process.	Serine	16-19	P53	Homo sapiens	45-48
19118006-8	2009	Mutation of p53 Ser(58) (equivalent to human p53 Ser(46)) abrogates transcription of these genes, indicating that TP53INP1-mediated p53 Ser(58) phosphorylation is implicated in this process.	Serine	49-52	P53	Homo sapiens	12-15
19118006-8	2009	Mutation of p53 Ser(58) (equivalent to human p53 Ser(46)) abrogates transcription of these genes, indicating that TP53INP1-mediated p53 Ser(58) phosphorylation is implicated in this process.	Serine	49-52	P53	Homo sapiens	45-48
19118006-8	2009	Mutation of p53 Ser(58) (equivalent to human p53 Ser(46)) abrogates transcription of these genes, indicating that TP53INP1-mediated p53 Ser(58) phosphorylation is implicated in this process.	Serine	49-52	P53	Homo sapiens	45-48
19118006-8	2009	Mutation of p53 Ser(58) (equivalent to human p53 Ser(46)) abrogates transcription of these genes, indicating that TP53INP1-mediated p53 Ser(58) phosphorylation is implicated in this process.	Serine	49-52	P53	Homo sapiens	12-15
19118006-8	2009	Mutation of p53 Ser(58) (equivalent to human p53 Ser(46)) abrogates transcription of these genes, indicating that TP53INP1-mediated p53 Ser(58) phosphorylation is implicated in this process.	Serine	49-52	P53	Homo sapiens	45-48
19118006-8	2009	Mutation of p53 Ser(58) (equivalent to human p53 Ser(46)) abrogates transcription of these genes, indicating that TP53INP1-mediated p53 Ser(58) phosphorylation is implicated in this process.	Serine	49-52	P53	Homo sapiens	45-48
19669740-5	2009	Western blot revealed that surfactin induced accumulation of the tumor suppressor p53 and cyclin kinase inhibitor p21(waf1/cip1), and inhibited the activity of the G(2)-specific kinase, cyclin B1/p34(cdc2).	surfactin peptide	27-36	P53	Homo sapiens	82-85
19111056-9	2009	The identification of p53 and its potential targets confirms a known role for p53 in the MC-RR response.	microcystin RR	89-94	P53	Homo sapiens	22-25
19111056-9	2009	The identification of p53 and its potential targets confirms a known role for p53 in the MC-RR response.	microcystin RR	89-94	P53	Homo sapiens	78-81
19454177-0	2009	Gamma-radiation-induced phosphorylation of p53 on serine 15 is dose-dependent in MOLT-4 leukaemia cells.	Serine	50-56	P53	Homo sapiens	43-46
19454177-4	2009	Here we employed Western blotting and ELISA assay to investigate the response of post-translationally modified p53 (particularly phosphorylated on serine 15) after gamma-irradiation.	Serine	147-153	P53	Homo sapiens	111-114
19454177-7	2009	The presented data indicate that p53 phosphorylated on serine 15 might be used as a potential biodosimetric marker.	Serine	55-61	P53	Homo sapiens	33-36
20067883-15	2009	beta-carotene, lycopene and all-trans retinoic acid alone and in combination with docetaxel were found to influence the expression of bcl-2 and p53 antigen in the cells examined.	Tretinoin	38-51	P53	Homo sapiens	144-147
18937971-6	2009	Platinum highly sensitive response showed a positive association with TP53 accumulation (p=0.045).	Platinum	0-8	P53	Homo sapiens	70-74
19291875-2	2009	The p53 codon 72 Arg-Pro (CGC to CCC) polymorphism of exon 4 affects various biological properties; recently, it was reported that this polymorphism affects the ability to induce apoptosis in vitro.	Arginine	17-20	P53	Homo sapiens	4-7
19291875-10	2009	We concluded that the p53 codon 72 Arg/Pro polymorphism is not associated with glaucoma in Brazilian patients.	Arginine	35-38	P53	Homo sapiens	22-25
19202565-6	2009	Scavenging of DADS-induced ROS by N-acetyl cysteine or reduced glutathione inhibited cell cycle arrest, apoptosis and p53 activation by DADS.	Reactive Oxygen Species	27-30	P53	Homo sapiens	118-121
19219727-0	2009	Pseudolaric acid B-induced apoptosis through p53-dependent pathway in human gastric carcinoma cells.	pseudolaric acid B	0-18	P53	Homo sapiens	45-48
19202565-6	2009	Scavenging of DADS-induced ROS by N-acetyl cysteine or reduced glutathione inhibited cell cycle arrest, apoptosis and p53 activation by DADS.	Acetylcysteine	34-51	P53	Homo sapiens	118-121
19202565-6	2009	Scavenging of DADS-induced ROS by N-acetyl cysteine or reduced glutathione inhibited cell cycle arrest, apoptosis and p53 activation by DADS.	Glutathione	63-74	P53	Homo sapiens	118-121
19202565-7	2009	These results suggest that ROS trigger the DADS-induced cell cycle arrest and apoptosis and that ROS are involved in stress-induced signaling upstream of p53 activation.	Reactive Oxygen Species	27-30	P53	Homo sapiens	154-157
19202565-7	2009	These results suggest that ROS trigger the DADS-induced cell cycle arrest and apoptosis and that ROS are involved in stress-induced signaling upstream of p53 activation.	Reactive Oxygen Species	97-100	P53	Homo sapiens	154-157
19202565-9	2009	Moreover, DADS-induced apoptosis was also prevented by treatment with oligomycin, which is known to prevent p53-dependent apoptosis by reducing ROS levels in mitochondria.	Reactive Oxygen Species	144-147	P53	Homo sapiens	108-111
19202565-10	2009	These results suggest that mitochondrial ROS may serve as second messengers in DADS-induced apoptosis, which requires activation of p53.	Reactive Oxygen Species	41-44	P53	Homo sapiens	132-135
19414966-6	2009	Presence of homozygous arginine at codon 72 renders p53 about seven times more susceptible to E6-mediated proteolytic degradation.	Arginine	23-31	P53	Homo sapiens	52-55
19240372-0	2009	The p53-induced Siva-1 plays a significant role in cisplatin-mediated apoptosis.	Cisplatin	51-60	P53	Homo sapiens	4-7
19240372-3	2009	METHODS: Cisplatin treated HCT116 colorectal carcinoma cells (p53+/+ and -/-) were used in the study.	Cisplatin	9-18	P53	Homo sapiens	62-65
19240372-6	2009	RESULTS: Treatment with cisplatin induced Siva-1 expression in a p53 dependent manner.	Cisplatin	24-33	P53	Homo sapiens	65-68
19183832-5	2009	The bile duct cancer revealed a well-differentiated adenocarcinoma without mutation of the K-ras gene and with p53 miss-sense mutation of GTG (Val) to GAG (Glu) on codon 272 in exon 8.	Glutamic Acid	156-159	P53	Homo sapiens	111-114
18459128-0	2009	p53 Cooperates berberine-induced growth inhibition and apoptosis of non-small cell human lung cancer cells in vitro and tumor xenograft growth in vivo.	Berberine	15-24	P53	Homo sapiens	0-3
18753126-3	2009	Here we report identification of the first three in vivo non-histone protein substrates of lysine propionylation in eukaryotic cells: p53, p300, and CREB-binding protein.	Lysine	91-97	P53	Homo sapiens	134-137
19263877-4	2009	STUDY DESIGN: In a genetic association study, PD1.5 (7785) C/T, CTLA-4 +49 A/G, and p53 codon 72 Arg/Pro SNPs were genotyped in case-control groups with patient/control ratios of 92:295, 83:84 and 85:150, respectively.	Arginine	97-100	P53	Homo sapiens	84-87
18459128-3	2009	Treatment of A549, which express wild-type p53, and H1299, which are p53-deficient, human lung cancer cells with berberine resulted in inhibition of cell proliferation and an increase in apoptotic cell death; however, A549 cells were more sensitive to the berberine-induced cytotoxic effects than H1299 cells.	Berberine	113-122	P53	Homo sapiens	43-46
18459128-3	2009	Treatment of A549, which express wild-type p53, and H1299, which are p53-deficient, human lung cancer cells with berberine resulted in inhibition of cell proliferation and an increase in apoptotic cell death; however, A549 cells were more sensitive to the berberine-induced cytotoxic effects than H1299 cells.	Berberine	113-122	P53	Homo sapiens	69-72
18459128-4	2009	Further, the treatment of A549 cells with pifithrin-alpha, a specific inhibitor of p53, or transfection of A549 cells with a p53 antisense oligodeoxynucleotide resulted in a reduction in the berberine-induced inhibition of cell proliferation and apoptosis.	Berberine	191-200	P53	Homo sapiens	83-86
18459128-4	2009	Further, the treatment of A549 cells with pifithrin-alpha, a specific inhibitor of p53, or transfection of A549 cells with a p53 antisense oligodeoxynucleotide resulted in a reduction in the berberine-induced inhibition of cell proliferation and apoptosis.	Berberine	191-200	P53	Homo sapiens	125-128
19838927-4	2009	Indeed, the combination of curcumin and resveratrol was found to be more effective in inhibiting growth of p53-positive (wt) and p53-negative colon cancer HCT-116 cells in vitro and in vivo in SCID xenografts of colon cancer HCT-116 (wt) cells than either agent alone.	Curcumin	27-35	P53	Homo sapiens	107-110
19139119-7	2009	Rosiglitazone was also found to stimulate p53, a tumor suppressor known to mediate some of the effects of nicotine.	Rosiglitazone	0-13	P53	Homo sapiens	42-45
19139119-7	2009	Rosiglitazone was also found to stimulate p53, a tumor suppressor known to mediate some of the effects of nicotine.	Nicotine	106-114	P53	Homo sapiens	42-45
19139119-8	2009	Interestingly, p53 up-regulation was needed for rosiglitazone-induced inhibition of alpha4 nAChR.	Rosiglitazone	48-61	P53	Homo sapiens	15-18
19139119-9	2009	Thus, rosiglitazone inhibits alpha4 nAChR expression in NSCLC cells through activation of extracellular signal-regulated kinase and p38 mitogen-activated protein kinase, which triggers induction of p53.	Rosiglitazone	6-19	P53	Homo sapiens	198-201
18820127-9	2009	The combination of SN-38 and 17AAG was shown to be synergistic in p53-null but not in parental HCT116 cells by median effect/combination index analysis.	Irinotecan	19-24	P53	Homo sapiens	66-69
19940524-1	2009	OBJECTIVES: Several studies have examined the association of codon 72 polymorphism of the TP53 gene, encoding either arginine or proline, in several tumor types but none have investigated its role in Kaposi"s sarcoma (KS) development.	Arginine	117-125	P53	Homo sapiens	90-94
19147537-0	2009	Focused PCR screen reveals p53 dependence of nitric oxide-induced apoptosis and up-regulation of maspin and plasminogen activator inhibitor-1 in tumor cells.	Nitric Oxide	45-57	P53	Homo sapiens	27-30
19147537-1	2009	We investigated p53-dependent gene expression in nitric oxide (NO)-induced apoptosis of two tumor cell types.	Nitric Oxide	49-61	P53	Homo sapiens	16-19
19838927-4	2009	Indeed, the combination of curcumin and resveratrol was found to be more effective in inhibiting growth of p53-positive (wt) and p53-negative colon cancer HCT-116 cells in vitro and in vivo in SCID xenografts of colon cancer HCT-116 (wt) cells than either agent alone.	Curcumin	27-35	P53	Homo sapiens	129-132
19838927-4	2009	Indeed, the combination of curcumin and resveratrol was found to be more effective in inhibiting growth of p53-positive (wt) and p53-negative colon cancer HCT-116 cells in vitro and in vivo in SCID xenografts of colon cancer HCT-116 (wt) cells than either agent alone.	Resveratrol	40-51	P53	Homo sapiens	107-110
19838927-4	2009	Indeed, the combination of curcumin and resveratrol was found to be more effective in inhibiting growth of p53-positive (wt) and p53-negative colon cancer HCT-116 cells in vitro and in vivo in SCID xenografts of colon cancer HCT-116 (wt) cells than either agent alone.	Resveratrol	40-51	P53	Homo sapiens	129-132
19399188-9	2009	Additionally, AECHL-1 treatment resulted in the phosphorylation of p53 at serine 15 in B16F10 tumors, which seems to exhibit p53-dependent growth inhibitory responses.	Serine	74-80	P53	Homo sapiens	67-70
20047009-1	2009	An efficient and convergent solution-phase synthesis of the cyclic peptide of the natural product chlorofusin, a reported inhibitor of the MDM2-p53 interaction, is detailed.	chlorofusin	98-109	P53	Homo sapiens	144-147
19421315-6	2009	We used the microtubules damaging agent paclitaxel (PTX), to arrest the cells in the M phase, in a p53 mutated melanoma cell line with modulated Myc level and activity.	Paclitaxel	40-50	P53	Homo sapiens	99-102
19421315-6	2009	We used the microtubules damaging agent paclitaxel (PTX), to arrest the cells in the M phase, in a p53 mutated melanoma cell line with modulated Myc level and activity.	Paclitaxel	52-55	P53	Homo sapiens	99-102
18823952-0	2008	Kinetic stabilization of microtubule dynamic instability by benomyl increases the nuclear transport of p53.	Benomyl	60-67	P53	Homo sapiens	103-106
18823952-3	2008	Under the conditions that suppressed the dynamic instability, a sharp increase in the nuclear accumulation of p53 in MCF-7 cells was observed in the presence of benomyl.	Benomyl	161-168	P53	Homo sapiens	110-113
18823952-5	2008	Cisplatin caused an increase in the translocation of p53 into the nucleus in the presence of lower effective concentrations of benomyl while a decrease in the nuclear accumulation of p53 was observed in the presence of high concentrations of benomyl suggesting that the stabilized microtubules assist in the nuclear transportation of p53.	Benomyl	242-249	P53	Homo sapiens	183-186
18823952-4	2008	Up regulation of bax and the increased nuclear accumulation of p21 upon benomyl treatment confirmed the activation of p53.	Benomyl	72-79	P53	Homo sapiens	118-121
18823952-5	2008	Cisplatin caused an increase in the translocation of p53 into the nucleus in the presence of lower effective concentrations of benomyl while a decrease in the nuclear accumulation of p53 was observed in the presence of high concentrations of benomyl suggesting that the stabilized microtubules assist in the nuclear transportation of p53.	Benomyl	242-249	P53	Homo sapiens	183-186
18823952-5	2008	Cisplatin caused an increase in the translocation of p53 into the nucleus in the presence of lower effective concentrations of benomyl while a decrease in the nuclear accumulation of p53 was observed in the presence of high concentrations of benomyl suggesting that the stabilized microtubules assist in the nuclear transportation of p53.	Cisplatin	0-9	P53	Homo sapiens	53-56
18823952-7	2008	Together the data indicate that benomyl inhibits mitosis primarily by suppressing the dynamic instability of microtubules and support the hypothesis that the kinetic stabilization of microtubules enhances the microtubule-mediated transport of p53 into the nucleus.	Benomyl	32-39	P53	Homo sapiens	243-246
18823952-5	2008	Cisplatin caused an increase in the translocation of p53 into the nucleus in the presence of lower effective concentrations of benomyl while a decrease in the nuclear accumulation of p53 was observed in the presence of high concentrations of benomyl suggesting that the stabilized microtubules assist in the nuclear transportation of p53.	Benomyl	127-134	P53	Homo sapiens	53-56
18973751-0	2008	An epidermal growth factor inhibitor, Gefitinib, induces apoptosis through a p53-dependent upregulation of pro-apoptotic molecules and downregulation of anti-apoptotic molecules in human lung adenocarcinoma A549 cells.	Gefitinib	38-47	P53	Homo sapiens	77-80
19141477-9	2008	An shRNA-directed reduction in p53 protein by about 50% also results in extended cellular life span, reduced respiration and ROS, and increased glycolysis.	Reactive Oxygen Species	125-128	P53	Homo sapiens	31-34
18973751-5	2008	Thus, the current study was designed to examine the role of p53 in Gefitinib-induced apoptosis.	Gefitinib	67-76	P53	Homo sapiens	60-63
18973751-6	2008	Incubation of human lung adenocarcinoma A549 cells with 25 microM Gefitinib resulted in phosphorylation and activation of p53 such as enhanced DNA binding activity, which was accompanied by the upregulation of PUMA (p53 upregulated modulator of apoptosis) and Fas, and downregulation of survivin and XIAP (X-linked inhibitor of apoptosis protein).	Gefitinib	66-75	P53	Homo sapiens	122-125
18973751-6	2008	Incubation of human lung adenocarcinoma A549 cells with 25 microM Gefitinib resulted in phosphorylation and activation of p53 such as enhanced DNA binding activity, which was accompanied by the upregulation of PUMA (p53 upregulated modulator of apoptosis) and Fas, and downregulation of survivin and XIAP (X-linked inhibitor of apoptosis protein).	Gefitinib	66-75	P53	Homo sapiens	216-219
18973751-7	2008	The Gefitinib-mediated Fas, PUMA, survivin, XIAP regulation and subsequent apoptosis were significantly inhibited in stable p53-shRNA transfectants.	Gefitinib	4-13	P53	Homo sapiens	124-127
18973751-8	2008	Similarly, H1299/p53 cells were more sensitive to Gefitinib compared to H1299 cells in clonogenic survival assay.	Gefitinib	50-59	P53	Homo sapiens	17-20
18973751-10	2008	Collectively, the results support an important role of p53 in Gefitinib-induced apoptosis in human lung cancer cells.	Gefitinib	62-71	P53	Homo sapiens	55-58
18819919-0	2008	Post-transcriptional modulation of iron homeostasis during p53-dependent growth arrest.	Iron	35-39	P53	Homo sapiens	59-62
18929532-0	2008	Urocanic acid-modified chitosan-mediated p53 gene delivery inducing apoptosis of human hepatocellular carcinoma cell line HepG2 is involved in its antitumor effect in vitro and in vivo.	Urocanic Acid	0-13	P53	Homo sapiens	41-44
18929532-4	2008	In this study, the wild-type p53 (wt-p53) gene was transfected into human hepatocellular carcinoma cell line HepG(2) using the urocanic acid-modified chitosan (UAC) as a nonviral vector, and transfection efficiency was determined by FACS analysis.	Urocanic Acid	127-140	P53	Homo sapiens	29-32
18929532-4	2008	In this study, the wild-type p53 (wt-p53) gene was transfected into human hepatocellular carcinoma cell line HepG(2) using the urocanic acid-modified chitosan (UAC) as a nonviral vector, and transfection efficiency was determined by FACS analysis.	Urocanic Acid	127-140	P53	Homo sapiens	37-40
18723275-5	2008	Our results indicated that silibinin effectively inhibits the renal cancer carcinoma Caki-1 cell proliferation and induces apoptosis through inhibiting the activation of EGFR and ERK and the expression of survivin, up-regulating the expression of p53 and triggering the cascades of caspase pathways.	Silybin	27-36	P53	Homo sapiens	247-250
18794809-0	2008	Proline oxidase, a p53-induced gene, targets COX-2/PGE2 signaling to induce apoptosis and inhibit tumor growth in colorectal cancers.	Dinoprostone	51-55	P53	Homo sapiens	19-22
18840612-0	2008	Role for 53BP1 Tudor domain recognition of p53 dimethylated at lysine 382 in DNA damage signaling.	Lysine	63-69	P53	Homo sapiens	43-46
18840612-3	2008	Recently, lysine methylation has been shown also to play a role in regulating non-histone proteins, including the tumor suppressor protein p53 (Huang, J., and Berger, S. L. (2008) Curr.	Lysine	10-16	P53	Homo sapiens	139-142
18840612-8	2008	Here, we identify a novel p53 species that is dimethylated at lysine 382 (p53K382me2) and show that the tandem Tudor domain of the DNA damage response mediator 53BP1 acts as an "effector" for this mark.	Lysine	62-68	P53	Homo sapiens	26-29
20596387-6	2008	Oligonucleotide derived from human p53 gene with one-base substitution can be distinguished by a color change of the GNPs solution or a significant difference of the maximum absorption wavelength (lambda(max)), compared with wildtype sequences.	Oligonucleotides	0-15	P53	Homo sapiens	35-38
18819919-2	2008	In this report we investigate changes in proteins of iron metabolism during p53-mediated replicative arrest.	Iron	53-57	P53	Homo sapiens	76-79
18819919-9	2008	Collectively, these results suggest that p53 may induce cell cycle arrest not only by well described mechanisms involving the induction of cyclin-dependent kinase inhibitors but also by the recruitment of pathways that reduce the availability of intracellular iron.	Iron	260-264	P53	Homo sapiens	41-44
18841476-0	2008	Apoptosis signal-regulating kinase 1 (ASK1) and HIF-1alpha protein are essential factors for nitric oxide-dependent accumulation of p53 in THP-1 human myeloid macrophages.	Nitric Oxide	93-105	P53	Homo sapiens	132-135
18761330-7	2008	Moreover, ROSC induces in human MCF-7 cells phosphorylation of p53 protein at Ser-46 which in turn initiates caspase-independent apoptosis.	Serine	78-81	P53	Homo sapiens	63-66
18222060-2	2008	The inhibitory effects of esculetin on cell viability were found to be associated with a G1 arrest in cell cycle progression that was concomitant with an inhibition of cyclin E and an induction of cyclin-dependent kinase (Cdk) inhibitor p21/WAF1/CIP1 in a p53-independent manner.	esculetin	26-35	P53	Homo sapiens	256-259
18717684-0	2008	Deletions of BRCA1/2 and p53 R248W gain-of-function mutation suggest impaired homologous recombination repair in fragile histidine triad-negative sebaceous gland carcinomas.	Histidine	121-130	P53	Homo sapiens	25-28
18523732-5	2008	For example deregulation of Akt, ras and MYC as well as loss of p53 function have been reported to confer increased glucose metabolic rates in cancer cells.	Glucose	116-123	P53	Homo sapiens	64-67
19026164-7	2008	The downregulation of p53 in the cells overexpressing nm23-H1 resulted in a higher cellular ROS level and lower cell viability.	Reactive Oxygen Species	92-95	P53	Homo sapiens	22-25
18841476-7	2008	It has also been found that GSNO-mediated accumulation of p53 depends on activation of ASK1 since no GSNO-induced p53 stabilisation was observed in THP-1 cells transfected with dominant-negative form of this kinase.	S-Nitrosoglutathione	28-32	P53	Homo sapiens	58-61
18841476-6	2008	In addition, GSNO was found to induce accumulation of p53 in normal but not HIF-1alpha knockdown THP-1 cells, where expression of this protein was silenced by specific siRNA.	S-Nitrosoglutathione	13-17	P53	Homo sapiens	54-57
18487078-5	2008	Cell lines with p53 mutations were slightly more sensitive to cisplatin than those with wild-type p53.	Cisplatin	62-71	P53	Homo sapiens	16-19
19054132-7	2008	Accordingly, we demonstrated that reactive oxygen species (ROS) are highly produced in p53 yeast induced cell death as shown by dihydrorhodamine 123 staining.	Reactive Oxygen Species	34-57	P53	Homo sapiens	87-90
19054132-7	2008	Accordingly, we demonstrated that reactive oxygen species (ROS) are highly produced in p53 yeast induced cell death as shown by dihydrorhodamine 123 staining.	Reactive Oxygen Species	59-62	P53	Homo sapiens	87-90
19054132-8	2008	These results suggest that the generation of ROS is a key event in p53 yeast induced cell death.	Reactive Oxygen Species	45-48	P53	Homo sapiens	67-70
19127115-7	2008	Direct sequencing of TP53 gene exons 5, 6, 8, 9, and 11 revealed a ermline missense mutation, resulting in an amino acid change from an arginine to a histidine (g.13203G&gt;A, p.R175H).	Arginine	136-144	P53	Homo sapiens	21-25
19127115-7	2008	Direct sequencing of TP53 gene exons 5, 6, 8, 9, and 11 revealed a ermline missense mutation, resulting in an amino acid change from an arginine to a histidine (g.13203G&gt;A, p.R175H).	Histidine	150-159	P53	Homo sapiens	21-25
19011621-0	2008	Arginine methylation regulates the p53 response.	Arginine	0-8	P53	Homo sapiens	35-38
19011621-5	2008	Arginine methylation is regulated during the p53 response and affects the target gene specificity of p53.	Arginine	0-8	P53	Homo sapiens	45-48
19011621-5	2008	Arginine methylation is regulated during the p53 response and affects the target gene specificity of p53.	Arginine	0-8	P53	Homo sapiens	101-104
19011621-7	2008	Thus, methylation on arginine residues is an underlying mechanism of control during the p53 response.	Arginine	21-29	P53	Homo sapiens	88-91
19020741-5	2008	We also observed that curcumin induces p53 phosphorylation (Ser 15) and both compound C and SB203580 pretreatment inhibit p53 phosphorylation.	Curcumin	22-30	P53	Homo sapiens	39-42
19020741-5	2008	We also observed that curcumin induces p53 phosphorylation (Ser 15) and both compound C and SB203580 pretreatment inhibit p53 phosphorylation.	Serine	60-63	P53	Homo sapiens	39-42
18849542-9	2008	The Western blot analysis of cell lysates showed that HEGU suppressed DOX-induced increases in the levels of p53, phospho-p53 (Ser 15), and Bax.	Doxorubicin	70-73	P53	Homo sapiens	109-112
18849542-9	2008	The Western blot analysis of cell lysates showed that HEGU suppressed DOX-induced increases in the levels of p53, phospho-p53 (Ser 15), and Bax.	Doxorubicin	70-73	P53	Homo sapiens	122-125
23675098-3	2008	The TP53 codon 72 polymorphism is a single-nucleotide polymorphism (SNP) in exon 4, resulting in the expression of either arginine (CGC) or proline (CCC) residues.	Arginine	122-130	P53	Homo sapiens	4-8
23675098-3	2008	The TP53 codon 72 polymorphism is a single-nucleotide polymorphism (SNP) in exon 4, resulting in the expression of either arginine (CGC) or proline (CCC) residues.	Chlormequat	149-152	P53	Homo sapiens	4-8
18716605-4	2008	Genistein also decreased cisplatin-induced apoptosis by regulating p53 induction in kidney.	Cisplatin	25-34	P53	Homo sapiens	67-70
19043433-2	2008	Now, arginine methylation joins a panoply of other post-translational modifications that regulate p53.	Arginine	5-13	P53	Homo sapiens	98-101
19137883-9	2008	RESULTS: The genetic genotype of p53 gene codon 72 in keloids included Arg/Arg in 7 cases, Pro/Arg in 21 cases, Pro/ Pro in 7 cases.	Arginine	71-74	P53	Homo sapiens	33-36
19137883-9	2008	RESULTS: The genetic genotype of p53 gene codon 72 in keloids included Arg/Arg in 7 cases, Pro/Arg in 21 cases, Pro/ Pro in 7 cases.	Arginine	75-78	P53	Homo sapiens	33-36
19137883-9	2008	RESULTS: The genetic genotype of p53 gene codon 72 in keloids included Arg/Arg in 7 cases, Pro/Arg in 21 cases, Pro/ Pro in 7 cases.	Arginine	75-78	P53	Homo sapiens	33-36
19010910-1	2008	While the therapeutic activity of the deoxycytidine analogue decitabine is thought to reflect its ability to reactivate methylation-silenced genes, this agent is also known to trigger p53-dependent DNA damage responses.	Deoxycytidine	38-51	P53	Homo sapiens	184-187
19026785-5	2008	The activation of p53-POMC/MSH-MC1R signaling is required for the UV-induced melanogenic response because PAX3 functions in synergy with SOX10 in a cAMP-response element (CRE)-dependent manner to regulate the transcription of Mitf.	Cyclic AMP	148-152	P53	Homo sapiens	18-21
18606492-10	2008	These results suggest that the ROS-ASK1-p38/JNK-p53 and Bax pathway plays a critical role in HBI"s anti-cancer effects.	Reactive Oxygen Species	31-34	P53	Homo sapiens	48-51
19000447-10	2008	The strong expression of p53 was correlated with decreased inhibition rates of PTX and DDP on cancer cells (P&lt;0.05, P&lt;0.01).	Paclitaxel	79-82	P53	Homo sapiens	25-28
18952844-0	2008	Inhibition of Thr-55 phosphorylation restores p53 nuclear localization and sensitizes cancer cells to DNA damage.	Threonine	14-17	P53	Homo sapiens	46-49
18952844-4	2008	In this study, we report that Thr-55 phosphorylation induces the association of p53 with the nuclear export factor CRM1, leading to p53 nuclear export.	Threonine	30-33	P53	Homo sapiens	80-83
18952844-4	2008	In this study, we report that Thr-55 phosphorylation induces the association of p53 with the nuclear export factor CRM1, leading to p53 nuclear export.	Threonine	30-33	P53	Homo sapiens	132-135
18952844-6	2008	Interestingly, inhibition of Thr-55 phosphorylation by a dietary flavonoid, apigenin, specifically blocks the CRM1-p53 association, restores p53 nuclear localization, and sensitizes tumor cells with cytoplasm localized wild-type p53 to DNA damage.	Threonine	29-32	P53	Homo sapiens	115-118
18952844-6	2008	Interestingly, inhibition of Thr-55 phosphorylation by a dietary flavonoid, apigenin, specifically blocks the CRM1-p53 association, restores p53 nuclear localization, and sensitizes tumor cells with cytoplasm localized wild-type p53 to DNA damage.	Threonine	29-32	P53	Homo sapiens	141-144
18952844-6	2008	Interestingly, inhibition of Thr-55 phosphorylation by a dietary flavonoid, apigenin, specifically blocks the CRM1-p53 association, restores p53 nuclear localization, and sensitizes tumor cells with cytoplasm localized wild-type p53 to DNA damage.	Threonine	29-32	P53	Homo sapiens	141-144
19189638-6	2008	Conversely, RKO cells expressing wildtype p53, proteolytically activated caspase-8, -9, -7 and -3 and unmethylated caspase-8 were more responsive to 5-FU and selenous acid-induced apoptosis.	Fluorouracil	149-153	P53	Homo sapiens	42-45
18692035-4	2008	RESULTS: The -765GC+CC genotypes of COX2 and Pro/Pro+Pro/Arg genotypes of p53 were prevalent in patients with significant odds ratio, 2.05 and 2.30, respectively (p=0.001; p=0.009, respectively), as a consequence, the -765C and 72Pro alleles were prevalent (p&lt;or=0.001).	Arginine	57-60	P53	Homo sapiens	74-77
18058229-6	2008	However, combined analysis of the SNP"s showed that p53 (Arg/Arg and Arg/Pro) with TGFbeta1 (Pro/Pro and Leu/Pro) were associated with greater than 2 fold increased risk for breast cancer in Univariate (P=0.01) and Multivariate (P=0.003) analysis.	Arginine	57-60	P53	Homo sapiens	52-55
18058229-6	2008	However, combined analysis of the SNP"s showed that p53 (Arg/Arg and Arg/Pro) with TGFbeta1 (Pro/Pro and Leu/Pro) were associated with greater than 2 fold increased risk for breast cancer in Univariate (P=0.01) and Multivariate (P=0.003) analysis.	Arginine	61-64	P53	Homo sapiens	52-55
18058229-6	2008	However, combined analysis of the SNP"s showed that p53 (Arg/Arg and Arg/Pro) with TGFbeta1 (Pro/Pro and Leu/Pro) were associated with greater than 2 fold increased risk for breast cancer in Univariate (P=0.01) and Multivariate (P=0.003) analysis.	Arginine	61-64	P53	Homo sapiens	52-55
18971636-11	2008	This regulation is observed in a transgenic p53-inducible cell system as well as in cells with wild-type p53 treated with nutlin-3, doxorubicin or paclitaxel.	Doxorubicin	132-143	P53	Homo sapiens	44-47
18971636-11	2008	This regulation is observed in a transgenic p53-inducible cell system as well as in cells with wild-type p53 treated with nutlin-3, doxorubicin or paclitaxel.	Doxorubicin	132-143	P53	Homo sapiens	105-108
18971636-11	2008	This regulation is observed in a transgenic p53-inducible cell system as well as in cells with wild-type p53 treated with nutlin-3, doxorubicin or paclitaxel.	Paclitaxel	147-157	P53	Homo sapiens	44-47
19189664-0	2008	Berberine inhibits human neuroblastoma cell growth through induction of p53-dependent apoptosis.	Berberine	0-9	P53	Homo sapiens	72-75
19189664-3	2008	The p53-expressing cells, SK-N-SH (IC50=37 microM) were more susceptible to berberine than the p53-deficient cells, SK-N-MC (IC50 &gt; or =100 microM) without cytotoxic effect on the cortical neuronal cells.	Berberine	76-85	P53	Homo sapiens	4-7
19189664-7	2008	Therefore, these results showed that berberine causes p53-dependent apoptotic death of neuroblastoma cells, and suggested that berberine may be useful as an anticancer agent for neuroblastoma.	Berberine	37-46	P53	Homo sapiens	54-57
19189664-7	2008	Therefore, these results showed that berberine causes p53-dependent apoptotic death of neuroblastoma cells, and suggested that berberine may be useful as an anticancer agent for neuroblastoma.	Berberine	127-136	P53	Homo sapiens	54-57
18158619-8	2008	Taken together, we present a molecular mechanism where Id-1 regulates p53 and NF-kappaB pathways, which in turn regulates Bax and Bcl-2 genes, thus providing a survival advantage under exogenous stress such as serum-free or taxol treatment in MCF-7 breast cancer cells.	Paclitaxel	224-229	P53	Homo sapiens	70-73
18850315-0	2008	Progesterone inhibits human endothelial cell proliferation through a p53-dependent pathway.	Progesterone	0-12	P53	Homo sapiens	69-72
18850315-6	2008	Transfection of HUVEC with dominant negative p53 cDNA prevented the progesterone-induced increases in p21 and p27 promoter activity and protein level, decreases in thymidine incorporation, and capillary-like tube formation.	Progesterone	68-80	P53	Homo sapiens	45-48
18948736-3	2008	Indeed, we show that the disruption of the protein complex mutantp53/p73 and the consequent restoration of p73 transcriptional effects, through the activity of short interfering peptides, render mutant p53 cells more prone to the killing of adriamycin and cisplatin.	Doxorubicin	241-251	P53	Homo sapiens	65-68
18948736-3	2008	Indeed, we show that the disruption of the protein complex mutantp53/p73 and the consequent restoration of p73 transcriptional effects, through the activity of short interfering peptides, render mutant p53 cells more prone to the killing of adriamycin and cisplatin.	Cisplatin	256-265	P53	Homo sapiens	65-68
18949381-6	2008	The expression of p53, p21, bax and caspase-3 increased in Tan-I-treated cells.	tanshinone	59-64	P53	Homo sapiens	18-21
18697203-7	2008	For the repression, acetylation of the C-terminal lysines of p53 is important, and both acetyl-K373p53 and methyl-K370p53 became bound to the promoter.	Lysine	50-57	P53	Homo sapiens	61-64
18949386-10	2008	Therefore, it is suggested that vitamin C inhibits p53-induced senescence by preventing ROS generation, which in turn leads to the activation of p38 MAPKinase.	Reactive Oxygen Species	88-91	P53	Homo sapiens	51-54
18708163-5	2008	In contrast, the caspase inhibitors, p53-siRNA, and Noxa-siRNA suppressed H(2)O(2)-induced cell death.	Hydrogen Peroxide	74-82	P53	Homo sapiens	37-40
18949386-0	2008	Vitamin C inhibits p53-induced replicative senescence through suppression of ROS production and p38 MAPK activity.	Reactive Oxygen Species	77-80	P53	Homo sapiens	19-22
18949386-1	2008	We previously reported that tumor cells expressing p53 increase intracellular levels of reactive oxygen species (ROS).	Reactive Oxygen Species	88-111	P53	Homo sapiens	51-54
18949386-1	2008	We previously reported that tumor cells expressing p53 increase intracellular levels of reactive oxygen species (ROS).	Reactive Oxygen Species	113-116	P53	Homo sapiens	51-54
18949386-7	2008	We found that vitamin C inhibited this p53-induced ROS generation.	Reactive Oxygen Species	51-54	P53	Homo sapiens	39-42
19008647-4	2008	The results showed that 3,2",3",4"-tetrahydroxychalcone, a newly synthesized compound, inhibited the SIRT1-mediated deacetylation of a p53 acetylated peptide and recombinant protein in vitro.	3,2",3",4"-tetrahydroxychalcone	24-55	P53	Homo sapiens	135-138
18682572-0	2008	Regulation and pathological role of p53 in cisplatin nephrotoxicity.	Cisplatin	43-52	P53	Homo sapiens	36-39
18682572-3	2008	Recent studies, using both in vitro and in vivo experimental models, have suggested a critical role for p53 in cisplatin nephrotoxicity.	Cisplatin	111-120	P53	Homo sapiens	104-107
18682572-6	2008	Further research may integrate p53 signaling with other nephrotoxic signaling pathways, providing a comprehensive understanding of cisplatin nephrotoxicity and leading to the development of effective renoprotective strategies during cancer therapy.	Cisplatin	131-140	P53	Homo sapiens	31-34
18820009-6	2008	Pairwise analysis showed that combinations of the ERalpha G allele with the homozygous Trp genotype of CYP19A1 codon 39 (rs2236722), the methionine (Met) allele of COMT codon 158 (rs4680) or Pro allele of p53 codon 72 (rs1042522) were more frequent in ER-positive than ER-negative breast cancer, especially in patients less than 50-year old.	Tryptophan	87-90	P53	Homo sapiens	205-208
18788085-1	2008	Benzo[a]pyrene diol epoxide (B[a]PDE), the ultimate carcinogenic metabolite of benzo[a] pyrene, has been implicated in the mutagenesis of the p53 gene involved in smoking-associated lung cancer.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	0-27	P53	Homo sapiens	142-145
19010821-5	2008	In LNCaP and LNCaP-Res, these combination treatments elevated the levels of phospho-Ser(15) p53 with significant induction of p21(waf1/cip1), phospho-gammaH2AX, PUMA, and Bax levels and reduction of AR and bcl-2 expression.	Serine	84-87	P53	Homo sapiens	92-95
18779317-5	2008	Activation of p53 by 5-fluorouracil increased the TLR3 mRNA in epithelial cell lines with wild-type p53 but not in cell lines harboring mutant p53.	Fluorouracil	21-35	P53	Homo sapiens	14-17
18779317-5	2008	Activation of p53 by 5-fluorouracil increased the TLR3 mRNA in epithelial cell lines with wild-type p53 but not in cell lines harboring mutant p53.	Fluorouracil	21-35	P53	Homo sapiens	100-103
18779317-5	2008	Activation of p53 by 5-fluorouracil increased the TLR3 mRNA in epithelial cell lines with wild-type p53 but not in cell lines harboring mutant p53.	Fluorouracil	21-35	P53	Homo sapiens	100-103
21479491-3	2008	ASC was inducible under a 1% O2 hypoxic condition in pancreatic cancer cells, which was HIF1alpha-dependent but p53-independent.	Oxygen	29-31	P53	Homo sapiens	112-115
18676676-0	2008	Reactive oxygen species mediate p53 activation and apoptosis induced by sodium nitroprusside in SH-SY5Y cells.	Reactive Oxygen Species	0-23	P53	Homo sapiens	32-35
18676676-8	2008	The attenuation of p53 levels, obtained by oxy-radical scavengers, is consistent with the recovery of cell viability and ROS decrease, demonstrate that SNP-mediated p53 activation is an event triggered by ROS and/or ROS-mediated damages.	Reactive Oxygen Species	121-124	P53	Homo sapiens	19-22
18676676-8	2008	The attenuation of p53 levels, obtained by oxy-radical scavengers, is consistent with the recovery of cell viability and ROS decrease, demonstrate that SNP-mediated p53 activation is an event triggered by ROS and/or ROS-mediated damages.	Reactive Oxygen Species	121-124	P53	Homo sapiens	165-168
18676676-8	2008	The attenuation of p53 levels, obtained by oxy-radical scavengers, is consistent with the recovery of cell viability and ROS decrease, demonstrate that SNP-mediated p53 activation is an event triggered by ROS and/or ROS-mediated damages.	Reactive Oxygen Species	205-208	P53	Homo sapiens	19-22
18676676-8	2008	The attenuation of p53 levels, obtained by oxy-radical scavengers, is consistent with the recovery of cell viability and ROS decrease, demonstrate that SNP-mediated p53 activation is an event triggered by ROS and/or ROS-mediated damages.	Reactive Oxygen Species	205-208	P53	Homo sapiens	165-168
18676676-8	2008	The attenuation of p53 levels, obtained by oxy-radical scavengers, is consistent with the recovery of cell viability and ROS decrease, demonstrate that SNP-mediated p53 activation is an event triggered by ROS and/or ROS-mediated damages.	Reactive Oxygen Species	205-208	P53	Homo sapiens	19-22
18676676-8	2008	The attenuation of p53 levels, obtained by oxy-radical scavengers, is consistent with the recovery of cell viability and ROS decrease, demonstrate that SNP-mediated p53 activation is an event triggered by ROS and/or ROS-mediated damages.	Reactive Oxygen Species	205-208	P53	Homo sapiens	165-168
21479491-4	2008	Two representative chemotherapeutic agents for pancreatic cancer, 5-fluorouracil and gemcitabine, promoted cell death in a p53-dependent manner; however, 1% hypoxia caused chemoresistance to these drugs.	Fluorouracil	66-80	P53	Homo sapiens	123-126
18703674-9	2008	Over-expression of p53 reversed the effect of ghrelin on OT, caused it to be inhibitory to P(4) secretion, but did not modify its action on MAP3K5, PGF, or PGE.	Ghrelin	46-53	P53	Homo sapiens	19-22
18703674-0	2008	Transcription factor p53 can regulate proliferation, apoptosis and secretory activity of luteinizing porcine ovarian granulosa cell cultured with and without ghrelin and FSH.	Ghrelin	158-165	P53	Homo sapiens	21-24
18959823-6	2008	Inhibition of p53 blocked accumulation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential, suggesting that mitochondrial p53 acts as an upstream signal of ROS and activates the mitochondrial apoptosis pathway.	Reactive Oxygen Species	42-65	P53	Homo sapiens	14-17
18720420-8	2008	Finally, ascorbic acid could also protect SY5Y cells from DA-induced cellular apoptotic signal changes including PARP and P53.	Dopamine	58-60	P53	Homo sapiens	122-125
18959823-6	2008	Inhibition of p53 blocked accumulation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential, suggesting that mitochondrial p53 acts as an upstream signal of ROS and activates the mitochondrial apoptosis pathway.	Reactive Oxygen Species	42-65	P53	Homo sapiens	148-151
18959823-6	2008	Inhibition of p53 blocked accumulation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential, suggesting that mitochondrial p53 acts as an upstream signal of ROS and activates the mitochondrial apoptosis pathway.	Reactive Oxygen Species	67-70	P53	Homo sapiens	14-17
18959823-6	2008	Inhibition of p53 blocked accumulation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential, suggesting that mitochondrial p53 acts as an upstream signal of ROS and activates the mitochondrial apoptosis pathway.	Reactive Oxygen Species	67-70	P53	Homo sapiens	148-151
18959823-6	2008	Inhibition of p53 blocked accumulation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential, suggesting that mitochondrial p53 acts as an upstream signal of ROS and activates the mitochondrial apoptosis pathway.	Reactive Oxygen Species	182-185	P53	Homo sapiens	14-17
18959823-6	2008	Inhibition of p53 blocked accumulation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential, suggesting that mitochondrial p53 acts as an upstream signal of ROS and activates the mitochondrial apoptosis pathway.	Reactive Oxygen Species	182-185	P53	Homo sapiens	148-151
18778698-8	2008	Oligonucleotide arrays, coupled with use of a dominant-negative p53 construct in NT2 cells, identified 14 differentially regulated p53 target genes.	Oligonucleotides	0-15	P53	Homo sapiens	131-134
18783790-5	2008	This calcium-dependent conformational change opens up a hydrophobic binding pocket that is capable of binding to target proteins such as annexin A2, the tumor-suppressor protein p53 and myosin IIA.	Calcium	5-12	P53	Homo sapiens	178-181
18715874-5	2008	Using compound C, a specific inhibitor of AMPK and AMPK-specific small interfering RNA knockdown as well as AMPK activator, we found that AMPK serves as a positive regulator for p38 and p53 (Ser(15)) phosphorylation induced by UV radiation and H(2)O(2) treatment.	Serine	191-194	P53	Homo sapiens	186-189
18718914-6	2008	Pretreatment with SP600125 partially prevented the phosphorylation of p53 at serines 33 and 392 induced by 15d-PGJ(2).	Serine	77-84	P53	Homo sapiens	70-73
18718914-8	2008	Pretreatment with antioxidant N-acetylcysteine prevented the p53 accumulation, the phosphorylations of JNK and p38 MAPK, the inhibition of NF-kappaB activity, as well as the apoptosis induced by 15d-PGJ(2).	Acetylcysteine	30-46	P53	Homo sapiens	61-64
18818522-2	2008	Moreover, autophagy-inducing stimuli such as nutrient depletion, rapamycin or lithium cause the depletion of cytoplasmic p53, which in turn is required for the induction of autophagy.	Sirolimus	65-74	P53	Homo sapiens	121-124
18760266-4	2008	Celecoxib (80-100 microM for 24 h) significantly increased total p53 proteins and the phosphorylated p53 proteins at serine-15, -20, -46, and -392 in RKO cells.	Serine	117-123	P53	Homo sapiens	101-104
18760266-5	2008	However, the phospho-p53 (serine-15, -20, and -392) proteins were presented on the nuclei of cells but the phospho-p53 (serine-46) protein was located on the cytoplasma of apoptotic cells following treatment with celecoxib.	Serine	120-126	P53	Homo sapiens	115-118
18847491-9	2008	Triphala-induced apoptosis was linked with phosphorylation of p53 at Ser-15 and ERK at Thr-202/Tyr-204 in Capan-2 cells.	Serine	69-72	P53	Homo sapiens	62-65
18847491-12	2008	Moreover, NAC or U0126 pretreatment significantly attenuated Triphala-induced p53 transcriptional activity.	Acetylcysteine	10-13	P53	Homo sapiens	78-81
18193228-0	2008	7-Chloro-6-piperidin-1-yl-quinoline-5,8-dione (PT-262), a novel synthetic compound induces lung carcinoma cell death associated with inhibiting ERK and CDC2 phosphorylation via a p53-independent pathway.	Platinum	47-50	P53	Homo sapiens	179-182
18193228-13	2008	PT-262 elicited the cytotoxicity and accumulated the G2/M fractions in both the p53-wild type and p53-null lung cancer cells.	Platinum	0-2	P53	Homo sapiens	80-83
18193228-13	2008	PT-262 elicited the cytotoxicity and accumulated the G2/M fractions in both the p53-wild type and p53-null lung cancer cells.	Platinum	0-2	P53	Homo sapiens	98-101
18838865-4	2008	Chemical inducers of autophagy (including rapamycin, lithium, tunicamycin and ABT737) induced rapid depletion of the p53 protein.	Sirolimus	42-51	P53	Homo sapiens	117-120
18931711-7	2008	After being pulsed with p53 gene, dendritic cells expressed green fluorescence protein and immunofluorescence assay (Cy3 labeled anti-P53 antibody) showed that transfected dendritic cells emitted red fluorescence.	cy3	117-120	P53	Homo sapiens	24-27
18574470-6	2008	As the K320 p53 acetylation is the site predominantly affected in hypoxia, the PCAF histone acetyltransferase activity is the key regulator of the cellular fate modulated by p53 under these conditions.	5-Bromo-2-fluoropyridine	7-11	P53	Homo sapiens	12-15
18574470-6	2008	As the K320 p53 acetylation is the site predominantly affected in hypoxia, the PCAF histone acetyltransferase activity is the key regulator of the cellular fate modulated by p53 under these conditions.	5-Bromo-2-fluoropyridine	7-11	P53	Homo sapiens	174-177
18834353-8	2008	When cells were treated with 20 microM 5-fluorouracil and 200 microg/ml Bupleuri Radix simultaneously, Bax protein increased in HepG2 cells at 24 hr; however, p21 and p53 proteins were up-regulated in normal human lymphocytes.	Fluorouracil	39-53	P53	Homo sapiens	167-170
18813780-7	2008	Consistently, PTX increased p21WAF1, bax and MDM2 levels, suggesting that p53 is transcriptionally active.	Paclitaxel	14-17	P53	Homo sapiens	74-77
18573337-0	2008	PEGylated conjugated linoleic acid stimulation of apoptosis via a p53-mediated signaling pathway in MCF-7 breast cancer cells.	Linoleic Acid	21-34	P53	Homo sapiens	66-69
19145674-17	2008	CONCLUSION: Our results showed low incidence of p53 mutations and prevalence of Arg/Arg genotype polymorphic variant of codon 72 of p53 gene in early stages of cervical carcinoma.	Arginine	80-83	P53	Homo sapiens	132-135
18357466-0	2008	Prognostic role of p53 codon 72 polymorphism in gastric cancer patients treated with fluorouracil-based adjuvant chemotherapy.	Fluorouracil	85-97	P53	Homo sapiens	19-22
18357466-2	2008	Our aim was to investigate the association of p53 Arg72Pro polymorphism with the clinical outcome of gastric cancer patients treated with 5-FU-based adjuvant chemotherapy.	Fluorouracil	138-142	P53	Homo sapiens	46-49
18357466-3	2008	METHODS: The p53 codon 72 genotype was determined in blood samples from 110 Chinese patients with gastric cancer treated with 5-fluorouracil (5-FU)-based adjuvant chemotherapy, using polymerase chain reaction-ligation detection reaction (PCR-LDR) method.	Fluorouracil	126-140	P53	Homo sapiens	13-16
18357466-3	2008	METHODS: The p53 codon 72 genotype was determined in blood samples from 110 Chinese patients with gastric cancer treated with 5-fluorouracil (5-FU)-based adjuvant chemotherapy, using polymerase chain reaction-ligation detection reaction (PCR-LDR) method.	Fluorouracil	142-146	P53	Homo sapiens	13-16
18357466-6	2008	CONCLUSION: These results suggested that p53 codon 72 polymorphism appears to be an independent prognostic factor in gastric cancer patients treated with 5-FU-based adjuvant chemotherapy.	Fluorouracil	154-158	P53	Homo sapiens	41-44
19145674-17	2008	CONCLUSION: Our results showed low incidence of p53 mutations and prevalence of Arg/Arg genotype polymorphic variant of codon 72 of p53 gene in early stages of cervical carcinoma.	Arginine	84-87	P53	Homo sapiens	132-135
18712872-1	2008	Chlorofusin is a recently isolated, naturally occurring inhibitor of p53-MDM2 complex formation whose structure is composed of a densely functionalized azaphilone-derived chromophore linked through the terminal amine of ornithine to a nine residue cyclic peptide.	chlorofusin	0-11	P53	Homo sapiens	69-72
18639569-0	2008	Gene expression profiles modulated by the human carcinogen aristolochic acid I in human cancer cells and their dependence on TP53.	aristolochic acid I	59-78	P53	Homo sapiens	125-129
18639569-3	2008	We compared transcriptional and translational responses of two isogenic HCT116 cell lines, one expressing TP53 (p53-WT) and the other with this gene knocked out (p53-null), to treatment with aristolochic acid I (AAI) (50-100 microM) for 6-48 h. Modulation of 118 genes was observed in p53-WT cells and 123 genes in p53-null cells.	aristolochic acid I	191-208	P53	Homo sapiens	162-165
18639569-3	2008	We compared transcriptional and translational responses of two isogenic HCT116 cell lines, one expressing TP53 (p53-WT) and the other with this gene knocked out (p53-null), to treatment with aristolochic acid I (AAI) (50-100 microM) for 6-48 h. Modulation of 118 genes was observed in p53-WT cells and 123 genes in p53-null cells.	aristolochic acid I	191-208	P53	Homo sapiens	162-165
18639569-3	2008	We compared transcriptional and translational responses of two isogenic HCT116 cell lines, one expressing TP53 (p53-WT) and the other with this gene knocked out (p53-null), to treatment with aristolochic acid I (AAI) (50-100 microM) for 6-48 h. Modulation of 118 genes was observed in p53-WT cells and 123 genes in p53-null cells.	aristolochic acid I	191-208	P53	Homo sapiens	162-165
18331287-6	2008	RESULTS: p53 expression was significantly higher in users of tobacco and alcohol than in non-users.	Alcohols	73-80	P53	Homo sapiens	9-12
18812399-3	2008	The 14-3-3 family of proteins activates the DNA-binding affinity of p53 upon stress by binding to a site in its intrinsically disordered C-terminal domain containing a phosphorylated serine at 378.	Serine	183-189	P53	Homo sapiens	68-71
18806740-3	2008	RESULTS: Low dose of Taxol that cause apoptosis (25 nM) enhanced Rb protein phosphorylation, decreased the expression of cyclin-dependent kinase inhibitors p27(KIP1) and p21(WAF1) , and potentiated the accumulation of phosphorylated p53 and of the prolyl isomerase Pin1.	Paclitaxel	21-26	P53	Homo sapiens	233-236
18606816-9	2008	The p38MAPK pathway also activates ATR, leading to phosphorylation of p53 on Ser-18 and Ser-23, transcription of pro-apoptotic genes Bax, Fas, and Noxa, and apoptosis.	Serine	77-80	P53	Homo sapiens	70-73
18521083-7	2008	The target for CDK2 kinase in p53 molecule, Ser-315, also becomes dephosphorylated.	Serine	44-47	P53	Homo sapiens	30-33
18707164-2	2008	The result of the calculation, based on structures from nanosecond molecular dynamics simulation, revealed that (19)Phe, (22)Leu, and (23)Trp of p53 have the strongest binding interaction with MDM2 followed by (26)Leu and (27)Pro.	Tryptophan	138-141	P53	Homo sapiens	145-148
18707164-3	2008	The specific residues of MDM2 that have dominant binding interactions with p53 are specifically identified to be (51)Lys, (54)Leu, (62)Met, (67)Tyr, (72)Gln, (94)Lys, (96)His, and (100)Tyr.	Lysine	117-120	P53	Homo sapiens	75-78
18707164-3	2008	The specific residues of MDM2 that have dominant binding interactions with p53 are specifically identified to be (51)Lys, (54)Leu, (62)Met, (67)Tyr, (72)Gln, (94)Lys, (96)His, and (100)Tyr.	Tyrosine	144-147	P53	Homo sapiens	75-78
18707164-3	2008	The specific residues of MDM2 that have dominant binding interactions with p53 are specifically identified to be (51)Lys, (54)Leu, (62)Met, (67)Tyr, (72)Gln, (94)Lys, (96)His, and (100)Tyr.	Lysine	162-165	P53	Homo sapiens	75-78
18707164-3	2008	The specific residues of MDM2 that have dominant binding interactions with p53 are specifically identified to be (51)Lys, (54)Leu, (62)Met, (67)Tyr, (72)Gln, (94)Lys, (96)His, and (100)Tyr.	Histidine	171-174	P53	Homo sapiens	75-78
18707164-3	2008	The specific residues of MDM2 that have dominant binding interactions with p53 are specifically identified to be (51)Lys, (54)Leu, (62)Met, (67)Tyr, (72)Gln, (94)Lys, (96)His, and (100)Tyr.	Tyrosine	185-188	P53	Homo sapiens	75-78
18606222-5	2008	GC and epirubicin significantly reduced mRNA expression levels of human intestinal MDR1, MDR-associated protein (MRP)1, and MRP2; downregulated the MDR1 promoter region; suppressed the mRNA expression of Bcl-2; induced the mRNA expression of Bax; and significantly increased the Bax-to-Bcl-2 ratio and the mRNA levels of p53, caspase-9 and -3.	Epirubicin	7-17	P53	Homo sapiens	321-324
18765544-11	2008	CONCLUSIONS: ART and DHA have significant anticancer effects against human hepatoma cells, regardless of p53 status, with minimal effects on normal cells, indicating that they are promising therapeutics for human hepatoma used alone or in combination with other therapies.	dehydroacetic acid	21-24	P53	Homo sapiens	105-108
18794599-0	2008	High-efficiency transfer and expression of AdCMV-p53 in human hepatocellular carcinoma cells induced by low-dose carbon-ion radiation.	Carbon	113-119	P53	Homo sapiens	49-52
18768816-4	2008	It is shown that postmeiotic segregation 2 (PMS2), an MMR protein, is required for cisplatin-induced activation of p73, a member of the p53 family of transcription factors with proapoptotic activity.	Cisplatin	83-92	P53	Homo sapiens	136-139
18424439-6	2008	We identify ROS-independent modulations of ATM and p16(INK4a) and ROS-mediated activation of p53/p21(CIP1/WAF1/Sdi1) tumor suppressor pathways as major contributors to Foxo3-null hematopoietic stem cells defects.	Reactive Oxygen Species	12-15	P53	Homo sapiens	93-96
18424439-6	2008	We identify ROS-independent modulations of ATM and p16(INK4a) and ROS-mediated activation of p53/p21(CIP1/WAF1/Sdi1) tumor suppressor pathways as major contributors to Foxo3-null hematopoietic stem cells defects.	Reactive Oxygen Species	66-69	P53	Homo sapiens	93-96
18661100-4	2008	A375 cells exposed to SeC showed an increase in levels of total p53 and phosphorylated p53 (serine-15).	Serine	92-98	P53	Homo sapiens	87-90
18661100-6	2008	Moreover, generation of reactive oxygen species and subsequent induction of DNA strand breaks were found to be upstream mediators of p53 activation induced by SeC.	Reactive Oxygen Species	24-47	P53	Homo sapiens	133-136
18765533-6	2008	HDM-2 inhibition caused phosphorylation of p53 at multiple serine residues, including 15, 37, and 392, which coincided with low levels of DNA strand breaks.	Serine	59-65	P53	Homo sapiens	43-46
18619459-0	2008	Folate and vitamin B6 intake and risk of colon cancer in relation to p53 expression.	Folic Acid	0-6	P53	Homo sapiens	69-72
18619459-3	2008	METHODS: We immunohistochemically assayed p53 expression in paraffin-fixed colon cancer specimens in a large prospective cohort of women with 22 years of follow-up to examine the relationship of folate intake and intake of other one-carbon nutrients to risks by tumor p53 expression.	Paraffin	60-68	P53	Homo sapiens	42-45
18619459-5	2008	The effect of folate differed significantly according to p53 expression (P(heterogeneity) = .01).	Folic Acid	14-20	P53	Homo sapiens	57-60
18619459-9	2008	CONCLUSIONS: We found that low folate and vitamin B(6) intake was associated with an increased risk of p53-overexpressing colon cancers but not wild-type tumors.	Folic Acid	31-37	P53	Homo sapiens	103-106
18930000-6	2008	5-FU suppressed the expression of p27(kip1), p53, and cyclin E, whereas d-allose induced p53 and reduced cyclins D, A, and E. The expression of p27(kip1) remained unchanged by d-allose at transcriptional level, but increased at the protein level suggesting an increase in protein stability by TXNIP.	Fluorouracil	0-4	P53	Homo sapiens	45-48
18581285-6	2008	Indeed, histone lysine methyltransferases KMT5 (Set9), KMT3C (Smyd2), and KMT5A (Set8) methylate p53 at specific C-terminal lysines.	Lysine	124-131	P53	Homo sapiens	97-100
18581285-7	2008	Lysine methylation enhances or suppresses p53 transcriptional activity depending on the methylation site.	Lysine	0-6	P53	Homo sapiens	42-45
18511453-7	2008	Silencing of KLF4 expression by KLF4-specific small interfering RNA (siRNA) abrogated the inducing effects of ATRA on p53, SM22alpha and alpha-SMA expression and neutralized the inhibitory effects of ATRA on SMemb expression and VSMC proliferation and migration.	Tretinoin	110-114	P53	Homo sapiens	118-121
18930000-6	2008	5-FU suppressed the expression of p27(kip1), p53, and cyclin E, whereas d-allose induced p53 and reduced cyclins D, A, and E. The expression of p27(kip1) remained unchanged by d-allose at transcriptional level, but increased at the protein level suggesting an increase in protein stability by TXNIP.	allose	72-80	P53	Homo sapiens	89-92
18384098-4	2008	Curcumin can also activate apoptosis, down-regulate cell survival gene products, and up-regulate p53, p21, and p27.	Curcumin	0-8	P53	Homo sapiens	97-100
18758421-2	2008	A common polymorphism at codon 72 of exon 4 of the p53 gene encoding either an arginine or proline has been shown to confer susceptibility to the development of different human malignancies.	Arginine	79-87	P53	Homo sapiens	51-54
18460348-0	2008	Novel nitric oxide-donating compound (S,R)-3-phenyl-4,5-dihydro-5-isoxazole acetic acid-nitric oxide (GIT-27NO) induces p53 mediated apoptosis in human A375 melanoma cells.	Nitric Oxide	88-100	P53	Homo sapiens	120-123
18460348-0	2008	Novel nitric oxide-donating compound (S,R)-3-phenyl-4,5-dihydro-5-isoxazole acetic acid-nitric oxide (GIT-27NO) induces p53 mediated apoptosis in human A375 melanoma cells.	Nitric Oxide	6-18	P53	Homo sapiens	120-123
18697815-3	2008	Here, we show that wild-type p53 repressed repair of DNA double-strand breaks (DSBs) by HR in a manner partially requiring the ATM/ATR phosphorylation site, serine 15.	Serine	157-163	P53	Homo sapiens	29-32
18474260-2	2008	It has been shown that p53 is activated by nitric oxide, which can damage DNA at high concentrations.	Nitric Oxide	43-55	P53	Homo sapiens	23-26
18697815-5	2008	However, without targeted cleavage of the HR substrate, serine 315 phosphorylation was necessary for the activation of topoisomerase I-dependent HR by p53.	Serine	56-62	P53	Homo sapiens	151-154
18622903-6	2008	The expression of p53 and p21 and mitochondrial cytochrome c release were increased in tanshinone IIA-treated cells.	tanshinone	87-101	P53	Homo sapiens	18-21
18804536-0	2008	Simvastatin inhibits cell cycle progression in glucose-stimulated proliferation of aortic vascular smooth muscle cells by up-regulating cyclin dependent kinase inhibitors and p53.	Glucose	47-54	P53	Homo sapiens	175-178
19024321-4	2008	All of the cells were collected after treated with 10 micromol/L cisplatin for 24 h. The expressions of p53 mRNA and protein were detected by real-time RT-PCR and Western blot analysis.	Cisplatin	65-74	P53	Homo sapiens	104-107
18555006-4	2008	Furthermore, endogenous expression of p19(ras) and p73beta is significantly increased by Taxol treatment, and Taxol-enhanced endogenous p73beta transcriptional activities are further amplified by p19(ras), which markedly increased cellular apoptosis in p53-null SAOS2 cancer cell line.	Paclitaxel	110-115	P53	Homo sapiens	253-256
18656471-3	2008	We also demonstrate that both p53 and the MAP1B light chain (MAP1B-LC1) alter their localization from the cytoplasm to the nucleus when neuroblastoma cells, SH-SY5Y, are treated with doxorubicin.	Doxorubicin	183-194	P53	Homo sapiens	30-33
18656471-5	2008	Consequently, MAP1B-LC1 binds to p53 and this interaction leads to the inhibition of doxorubicin-induced apoptosis in SH-SY5Y cells.	Doxorubicin	85-96	P53	Homo sapiens	33-36
18725978-0	2008	CHEK2 mutations affecting kinase activity together with mutations in TP53 indicate a functional pathway associated with resistance to epirubicin in primary breast cancer.	Epirubicin	134-144	P53	Homo sapiens	69-73
20735960-11	2008	But the significant difference was not observed on MTT assay between CMAG2+ and its control, the reason might be due to the mutated p53, which had strong proliferation promoting effects, was also down-regulated by MAG-2"s over-expression in PLA801C, and the levels of cytoplasm calcium in CMAG2+ had 1.05 times more than that of vector control.	Calcium	278-285	P53	Homo sapiens	132-135
18446786-0	2008	Resveratrol causes COX-2- and p53-dependent apoptosis in head and neck squamous cell cancer cells.	Resveratrol	0-11	P53	Homo sapiens	30-33
18446786-6	2008	Resveratrol also caused p53 binding to the p21 promoter and increased abundance of COX-2 protein in UMSCC-22B cell nuclei.	Resveratrol	0-11	P53	Homo sapiens	24-27
18446786-10	2008	Resveratrol-inducible nuclear accumulation of COX-2 is essential for p53 activation and p53-dependent apoptosis in these cancer cells.	Resveratrol	0-11	P53	Homo sapiens	69-72
18446786-10	2008	Resveratrol-inducible nuclear accumulation of COX-2 is essential for p53 activation and p53-dependent apoptosis in these cancer cells.	Resveratrol	0-11	P53	Homo sapiens	88-91
18540044-11	2008	Inhibition of p53 protein expression using small interfering RNA abrogated DMNQ-induced Bax expression and significantly attenuated VSMC apoptosis.	2,3-dimethoxy-1,4-naphthoquinone	75-79	P53	Homo sapiens	14-17
18512237-2	2008	Here we show that p53 mutations in stromal fibroblasts, a genetic lesion that is detectable in primary breast, prostate and probably other cancers, while they accelerate tumorigenesis they also sensitize tumours against conventional chemotherapy by doxorubicin and cis-platinum.	Doxorubicin	249-260	P53	Homo sapiens	18-21
18512237-2	2008	Here we show that p53 mutations in stromal fibroblasts, a genetic lesion that is detectable in primary breast, prostate and probably other cancers, while they accelerate tumorigenesis they also sensitize tumours against conventional chemotherapy by doxorubicin and cis-platinum.	Cisplatin	265-277	P53	Homo sapiens	18-21
18540044-9	2008	PP1cgamma1 overexpression abrogated DMNQ-induced JNK1 activity, p53 Ser(15) phosphorylation, and Bax expression and protected VSMC against DMNQ-induced apoptosis.	2,3-dimethoxy-1,4-naphthoquinone	36-40	P53	Homo sapiens	64-67
18497562-0	2008	Resveratrol displays converse dose-related effects on 5-fluorouracil-evoked colon cancer cell apoptosis: the roles of caspase-6 and p53.	Resveratrol	0-11	P53	Homo sapiens	132-135
18604159-6	2008	Several distinct autophagy inducers (e.g., starvation, rapamycin, lithium, tunicamycin and thapsigargin) stimulate the rapid degradation of p53.	Sirolimus	55-64	P53	Homo sapiens	140-143
18604159-6	2008	Several distinct autophagy inducers (e.g., starvation, rapamycin, lithium, tunicamycin and thapsigargin) stimulate the rapid degradation of p53.	Thapsigargin	91-103	P53	Homo sapiens	140-143
17960385-0	2008	The effect of p53 gene expression on the inhibition of cell proliferation by paclitaxel.	Paclitaxel	77-87	P53	Homo sapiens	14-17
17960385-1	2008	BACKGROUND/AIMS: We evaluated the relationship between p53 status and paclitaxel (PTX)-induced inhibition of the growth of human stomach cancer cells.	Paclitaxel	70-80	P53	Homo sapiens	55-58
17960385-1	2008	BACKGROUND/AIMS: We evaluated the relationship between p53 status and paclitaxel (PTX)-induced inhibition of the growth of human stomach cancer cells.	Paclitaxel	82-85	P53	Homo sapiens	55-58
17960385-11	2008	CONCLUSION: Both p53 status and cyclin-B1 expression might be useful for predicting the therapeutic response of stomach cancer to PTX.	Paclitaxel	130-133	P53	Homo sapiens	17-20
18673568-8	2008	In a final example, the effect of reduced p53 levels on increased adriamycin sensitivity for colon carcinoma cells was demonstrated at the whole-well level using siRNA knockdown and in control and untreated cells at the single cell level.	Doxorubicin	66-76	P53	Homo sapiens	42-45
18497562-1	2008	We have reported that resveratrol (RSV) evoked apoptosis through caspase-6 activation in HCT116 human colon cancer cells wild-type (p53+/+) or knockout (p53-/-) for p53.	Resveratrol	35-38	P53	Homo sapiens	153-156
18497562-7	2008	Moreover, G(1)-arrest of the p53+/+ cells was elicited by lower doses of RSV and 5-FU in combination, but not with either agent alone.	Resveratrol	73-76	P53	Homo sapiens	29-32
18497562-7	2008	Moreover, G(1)-arrest of the p53+/+ cells was elicited by lower doses of RSV and 5-FU in combination, but not with either agent alone.	Fluorouracil	81-85	P53	Homo sapiens	29-32
18497562-9	2008	At lower doses (25 or 50 microM), it interacted with 5-FU in antagonistic (mean CI &gt; 1.1) and additive manners (0.9 &lt; mean CI &lt; 1.1) in p53+/+ and p53-/- cells respectively.	Fluorouracil	53-57	P53	Homo sapiens	145-148
18497562-1	2008	We have reported that resveratrol (RSV) evoked apoptosis through caspase-6 activation in HCT116 human colon cancer cells wild-type (p53+/+) or knockout (p53-/-) for p53.	Resveratrol	22-33	P53	Homo sapiens	132-135
18497562-9	2008	At lower doses (25 or 50 microM), it interacted with 5-FU in antagonistic (mean CI &gt; 1.1) and additive manners (0.9 &lt; mean CI &lt; 1.1) in p53+/+ and p53-/- cells respectively.	Fluorouracil	53-57	P53	Homo sapiens	156-159
18497562-13	2008	Conversely, it inhibits 5-FU-triggered apoptosis at lower concentrations in p53+/+ cells.	Fluorouracil	24-28	P53	Homo sapiens	76-79
18497562-1	2008	We have reported that resveratrol (RSV) evoked apoptosis through caspase-6 activation in HCT116 human colon cancer cells wild-type (p53+/+) or knockout (p53-/-) for p53.	Resveratrol	22-33	P53	Homo sapiens	153-156
18497571-4	2008	We found that DOX induced five phosphorylation sites of p53 (Ser15, 20, 37, 46 and 392); all of these sites were inhibited by si-AR.	Doxorubicin	14-17	P53	Homo sapiens	56-59
18497562-1	2008	We have reported that resveratrol (RSV) evoked apoptosis through caspase-6 activation in HCT116 human colon cancer cells wild-type (p53+/+) or knockout (p53-/-) for p53.	Resveratrol	22-33	P53	Homo sapiens	153-156
18497562-1	2008	We have reported that resveratrol (RSV) evoked apoptosis through caspase-6 activation in HCT116 human colon cancer cells wild-type (p53+/+) or knockout (p53-/-) for p53.	Resveratrol	35-38	P53	Homo sapiens	132-135
18497562-1	2008	We have reported that resveratrol (RSV) evoked apoptosis through caspase-6 activation in HCT116 human colon cancer cells wild-type (p53+/+) or knockout (p53-/-) for p53.	Resveratrol	35-38	P53	Homo sapiens	153-156
18690848-0	2008	NUPR1 interacts with p53, transcriptionally regulates p21 and rescues breast epithelial cells from doxorubicin-induced genotoxic stress.	Doxorubicin	99-110	P53	Homo sapiens	21-24
18589416-4	2008	We observed only a two fold increase in both phosphorylation of p53 at serine 15 and 53BP1 DNA damage foci and no detectable increase in p21(WAF).	Serine	71-77	P53	Homo sapiens	64-67
18330889-2	2008	We examined, for the first time, 196 paraffin-embedded CRC cases from Northern Iran for mutations in P53 exons 5-8 using PCR-direct sequencing.	Paraffin	37-45	P53	Homo sapiens	101-104
17931634-9	2008	An interaction between p53 and PTPN22 was observed: a protective action by the Arg/Arg genotype against endometriosis seems to be present only in carriers of the ( *)T allele of PTPN22.	Arginine	79-82	P53	Homo sapiens	23-26
17931634-9	2008	An interaction between p53 and PTPN22 was observed: a protective action by the Arg/Arg genotype against endometriosis seems to be present only in carriers of the ( *)T allele of PTPN22.	Arginine	83-86	P53	Homo sapiens	23-26
17931634-10	2008	CONCLUSION(S): The negative association between the Arg/Arg genotype of p53 codon 72 found in Chinese people has not been observed in Japanese and Italian populations.	Arginine	52-55	P53	Homo sapiens	72-75
17931634-10	2008	CONCLUSION(S): The negative association between the Arg/Arg genotype of p53 codon 72 found in Chinese people has not been observed in Japanese and Italian populations.	Arginine	56-59	P53	Homo sapiens	72-75
18498133-10	2008	A SNP in codon 72 of TP53 was revealed to be a key regulator of 5-FU metabolizing genes such as DHFR and MTHFR, constituting 50% of all significant associations observed after FUMI therapy.	Fluorouracil	64-68	P53	Homo sapiens	21-25
18060599-9	2008	The initial resistance to IR-induced apoptosis in these p53-deficient prostate cancer cell lines was overcome through an alternative proapoptotic pathway induced by 8-Cl-cAMP.	8-chloro-cyclic adenosine monophosphate	165-174	P53	Homo sapiens	56-59
18547707-9	2008	p53 and Bax mRNA are also upregulated by the metal.	Metals	45-50	P53	Homo sapiens	0-3
18719315-0	2008	Reactive oxygen species mediate oridonin-induced HepG2 apoptosis through p53, MAPK, and mitochondrial signaling pathways.	Reactive Oxygen Species	0-23	P53	Homo sapiens	73-76
18719315-2	2008	p53, a specific inhibitor of pifithrin alpha (PFT alpha), markedly inhibited ROS generation and apoptosis, showing that p53 was responsible for the cytotoxity of oridonin through mediation by ROS.	Reactive Oxygen Species	77-80	P53	Homo sapiens	0-3
18719315-2	2008	p53, a specific inhibitor of pifithrin alpha (PFT alpha), markedly inhibited ROS generation and apoptosis, showing that p53 was responsible for the cytotoxity of oridonin through mediation by ROS.	Reactive Oxygen Species	77-80	P53	Homo sapiens	120-123
18719315-2	2008	p53, a specific inhibitor of pifithrin alpha (PFT alpha), markedly inhibited ROS generation and apoptosis, showing that p53 was responsible for the cytotoxity of oridonin through mediation by ROS.	Reactive Oxygen Species	192-195	P53	Homo sapiens	0-3
18719315-2	2008	p53, a specific inhibitor of pifithrin alpha (PFT alpha), markedly inhibited ROS generation and apoptosis, showing that p53 was responsible for the cytotoxity of oridonin through mediation by ROS.	Reactive Oxygen Species	192-195	P53	Homo sapiens	120-123
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Reactive Oxygen Species	14-17	P53	Homo sapiens	85-88
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Reactive Oxygen Species	14-17	P53	Homo sapiens	260-263
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Reactive Oxygen Species	14-17	P53	Homo sapiens	260-263
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Reactive Oxygen Species	131-134	P53	Homo sapiens	85-88
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Reactive Oxygen Species	131-134	P53	Homo sapiens	260-263
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Reactive Oxygen Species	131-134	P53	Homo sapiens	260-263
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	145-162	P53	Homo sapiens	85-88
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	145-162	P53	Homo sapiens	260-263
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	145-162	P53	Homo sapiens	260-263
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	164-167	P53	Homo sapiens	85-88
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	164-167	P53	Homo sapiens	260-263
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	Acetylcysteine	164-167	P53	Homo sapiens	260-263
18723490-0	2008	Targeting tumor cells expressing p53 with a water-soluble inhibitor of Hdm2.	Water	44-49	P53	Homo sapiens	33-36
18723490-4	2008	We previously identified a family of small molecules (HLI98s, 7-nitro-10-aryl-5-deazaflavins) that inhibit the E3 activity of Hdm2, increase cellular p53, and selectively kill transformed cells expressing wild-type p53.	hli98s	54-60	P53	Homo sapiens	150-153
18723490-4	2008	We previously identified a family of small molecules (HLI98s, 7-nitro-10-aryl-5-deazaflavins) that inhibit the E3 activity of Hdm2, increase cellular p53, and selectively kill transformed cells expressing wild-type p53.	hli98s	54-60	P53	Homo sapiens	215-218
18391982-0	2008	Cancer-specific enhancement of cisplatin-induced cytotoxicity with triptolide through an interaction of inactivated glycogen synthase kinase-3beta with p53.	Cisplatin	31-40	P53	Homo sapiens	152-155
18391982-3	2008	Our results showed that a combined CDDP/triptolide therapy induced apoptosis in urothelial cancer cell lines with wild-type p53, but not in those with mutant-type p53 or normal human urothelium.	Cisplatin	35-39	P53	Homo sapiens	124-127
18391982-4	2008	As the mechanism, triptolide suppressed CDDP-induced p53 transcriptional activity, leading to p21 attenuation, which promoted apoptosis via the activation of c-Jun N-terminal kinase (JNK) and Bax.	Cisplatin	40-44	P53	Homo sapiens	53-56
18505818-1	2008	Histone Arg methylation has been correlated with transcriptional activation of p53 target genes.	Arginine	8-11	P53	Homo sapiens	79-82
18282165-9	2008	We conclude that carbon-ion irradiation induced cell death and senescence in a glioblastoma cell line with mutant TP53.	Carbon	17-23	P53	Homo sapiens	114-118
18586825-2	2008	APE1/Ref-1 has redox activity and AP endonuclease activity, and is able to enhance DNA-binding activity of several transcription factors, including NF-kappaB, AP-1 and p53, through reduction of their critical cysteine residues.	Cysteine	209-217	P53	Homo sapiens	168-171
19102934-6	2008	RESULTS: After treatment with DOX, the expression of p53 and p21 was increased, whereas that of survivin was reduced during 24 hours of the treatment.	Doxorubicin	30-33	P53	Homo sapiens	53-56
18502749-0	2008	Critical role of cysteine residue 81 of macrophage migration inhibitory factor (MIF) in MIF-induced inhibition of p53 activity.	Cysteine	17-25	P53	Homo sapiens	114-117
18456275-2	2008	The technique was further employed to detect low levels and measure DNA-binding activity of transcription factor p53 in leukemia cell lysates through its interaction with immobilized oligonucleotides and recognition by element-tagged antibodies.	Oligonucleotides	183-199	P53	Homo sapiens	113-116
18665269-7	2008	In vitro incubation of Mdm2 and FOXO results in ATP-dependent (multi)mono-ubiquitination of FOXO similar to p53.	Adenosine Triphosphate	48-51	P53	Homo sapiens	108-111
18469851-0	2008	Mechanism of G1-like arrest by low concentrations of paclitaxel: next cell cycle p53-dependent arrest with sub G1 DNA content mediated by prolonged mitosis.	Paclitaxel	53-63	P53	Homo sapiens	81-84
18469851-10	2008	We conclude that PTX directly affects cells only in mitosis and the duration of mitosis determines cell fate, including p53-dependent G1-like arrest.	Paclitaxel	17-20	P53	Homo sapiens	120-123
18477470-3	2008	Here, we show that ectopically expressed p53 induces acetylation and phosphorylation at Ser 536 of p65, an NF-kappaB component, and enhances DNA-binding activity of NF-kappaB.	Serine	88-91	P53	Homo sapiens	41-44
18502749-3	2008	This association was significantly reduced by a C81S mutation but not C57S or C60S mutations, suggesting that Cys(81) is essential for the in vivo association between MIF and p53.	Cysteine	110-113	P53	Homo sapiens	175-178
18502749-4	2008	This association also depended on Cys(242) (and, to some extent, on Cys(238)) within the central DNA binding domain of p53.	Cysteine	34-37	P53	Homo sapiens	119-122
18502749-4	2008	This association also depended on Cys(242) (and, to some extent, on Cys(238)) within the central DNA binding domain of p53.	Cysteine	68-71	P53	Homo sapiens	119-122
18635961-8	2008	It is well known that DNA-damaging agents such as doxorubicin enhance the expression of p53.	Doxorubicin	50-61	P53	Homo sapiens	88-91
18452174-7	2008	Both energy inhibitors strongly potentiated non-apoptotic concentrations of cisplatin in p53-wildtype as well as in p53-deficient, cisplatin-resistant HCT-116 colon carcinoma cells.	Cisplatin	76-85	P53	Homo sapiens	89-92
18452174-9	2008	We conclude that the long-term effects of cisplatin potentiation are important and either p53-independent or improved by a lack of p53.	Cisplatin	42-51	P53	Homo sapiens	90-93
18452174-9	2008	We conclude that the long-term effects of cisplatin potentiation are important and either p53-independent or improved by a lack of p53.	Cisplatin	42-51	P53	Homo sapiens	131-134
18635961-9	2008	Our results indicate that during doxorubicin treatment, PTB protein translocates from nucleus to the cytoplasm, probably to facilitate IRES mediated p53 translation.	Doxorubicin	33-44	P53	Homo sapiens	149-152
18325917-0	2008	p53 status and efficacy of primary anthracyclines/alkylating agent-based regimen according to breast cancer molecular classes.	Anthracyclines	35-49	P53	Homo sapiens	0-3
18490454-6	2008	Moreover, Cdk5 (cyclin-dependent kinase 5), a proline-directed Ser/Thr kinase, additionally increases p53 stability via post-translational modification of p53 in response to hydrogen peroxide.	Hydrogen Peroxide	174-191	P53	Homo sapiens	102-105
18490454-6	2008	Moreover, Cdk5 (cyclin-dependent kinase 5), a proline-directed Ser/Thr kinase, additionally increases p53 stability via post-translational modification of p53 in response to hydrogen peroxide.	Hydrogen Peroxide	174-191	P53	Homo sapiens	155-158
18490454-9	2008	Our results show that c-Abl and Cdk5 cooperatively regulate maximal activation of p53, resulting in neuronal death in response to oxidative stress by hydrogen peroxide.	Hydrogen Peroxide	150-167	P53	Homo sapiens	82-85
18193204-6	2008	Intrinsic tryptophan residues within the BRCA1 sequence detected p53 (311-393) with a detection limit of 0.559 nM (0.112 pmol).	Tryptophan	10-20	P53	Homo sapiens	65-68
18325917-1	2008	BACKGROUND: We hypothesized that, among molecular subclasses of breast cancer, p53 status may have a differential predictive value for the efficacy of anthracyclines/alkylating agents-based regimen.	Anthracyclines	151-165	P53	Homo sapiens	79-82
18325917-2	2008	We analysed the efficacy of a preoperative combination between 5-fluorouracil, anthracyclines and cyclophosphamide according to both p53 status and molecular classification.	Fluorouracil	63-77	P53	Homo sapiens	133-136
18325917-9	2008	CONCLUSION: p53 status may have a different predictive value for efficacy of anthracycline/alkylating agents-based regimen in each molecular subclass, a result which may explain the different results reported in literature.	Anthracyclines	77-90	P53	Homo sapiens	12-15
18421307-11	2008	In summary, HIF-1 targeted therapy to reverse hypoxia-related cisplatin resistance depends on normal p53 status.	Cisplatin	62-71	P53	Homo sapiens	101-104
18414057-11	2008	Our results show that sulfinosine and curcumin overcome MDR in non-small cell lung carcinoma cell line (NSCLC), especially in combination despite the presence of a mutated p53 gene.	Curcumin	38-46	P53	Homo sapiens	172-175
18780655-1	2008	AIM: To examine by means of immunohistochemistry the expression of the tumor suppressing gene p53 and gene p21 in cells of malignant melanoma of the uvea from formalin-paraffin material from patients, who were during the period 2000 - 2006 surgically treated due to malignant melanoma of the uvea at the Department of Ophthalmology in the University Hospital in Brno (Brunn), Czech Republic, E.U., and to correlate the results of the immunohistochemical detection with clinical signs of the tumor of each patient.	Paraffin	168-176	P53	Homo sapiens	94-97
18642443-3	2008	Depletion of p38 MAPK by transfection with a siRNA targeting the alpha isoform of p38 MAPK (p38alpha MAPK) abolishes the phosphorylation of p53 on serines 15 and 46 that is induced by Chk1 knockdown.	Serine	147-154	P53	Homo sapiens	140-143
18428185-0	2008	Isoquinolin-1-one inhibitors of the MDM2-p53 interaction.	isocarbostyril	0-17	P53	Homo sapiens	41-44
18428185-4	2008	The selected inhibitors were all able to induce apoptosis and the expression of p53-related genes, but only the isoquinolin-1-one-based inhibitors stabilised p53.	isocarbostyril	112-129	P53	Homo sapiens	158-161
18428185-5	2008	Our NMR experiments give a persuading explanation for these results, showing that isoquinolin-1-one derivates are able to dissociate the preformed MDM2-p53 complex in vitro, releasing a folded and soluble p53.	isocarbostyril	82-99	P53	Homo sapiens	152-155
18428185-5	2008	Our NMR experiments give a persuading explanation for these results, showing that isoquinolin-1-one derivates are able to dissociate the preformed MDM2-p53 complex in vitro, releasing a folded and soluble p53.	isocarbostyril	82-99	P53	Homo sapiens	205-208
21783897-1	2008	In A549 cells treated with zinc sulfate (ZnSO(4)), the levels of p53 phosphorylated at Ser15 and total p53 protein increased.	Zinc Sulfate	27-39	P53	Homo sapiens	65-68
21783897-1	2008	In A549 cells treated with zinc sulfate (ZnSO(4)), the levels of p53 phosphorylated at Ser15 and total p53 protein increased.	Zinc Sulfate	27-39	P53	Homo sapiens	103-106
18507431-3	2008	We show that resveratrol induces apoptosis in Jeko-1 cells and modulates several key molecules, including cyclin D1 (CCND1), p53 (TP53), p21 (CDKN1A), BCL2, BAX, Bcl XL (BCL2L1), caspase 9 (CASP9) and p27 (CDKN1B).	Resveratrol	13-24	P53	Homo sapiens	125-128
18549324-5	2008	RESULTS/CONCLUSION: The p53 gene is mutated in half of all human tumors and such cancers would be predicted to produce lower levels of CDAFs.	cdafs	135-140	P53	Homo sapiens	24-27
18549324-6	2008	We therefore believe that p53 function can be partially compensated by therapeutic use of CDAFs, which offers a promising new avenue for cancer treatment.	cdafs	90-95	P53	Homo sapiens	26-29
18593873-2	2008	A recent study in Genes &amp; Development by Xue and colleagues (1439-1444) now provides in vivo evidence that DLC1, a negative regulator of Rho, is a tumor suppressor gene deleted almost as frequently as p53 in common cancers such as breast, colon, and lung.	Adenosine Monophosphate	25-28	P53	Homo sapiens	205-208
18661375-5	2008	RESULTS: In radio-resistant subclones generated from wt p53-transfected SAOS-2 cells DNA deletions were remarkably reduced and the accumulation of "common" deletion at mtDNA (that may let the persistence of oxidative damage by precluding detoxification from reactive oxygen species [ROS]) completely abrogated.	Reactive Oxygen Species	258-281	P53	Homo sapiens	56-59
18661375-5	2008	RESULTS: In radio-resistant subclones generated from wt p53-transfected SAOS-2 cells DNA deletions were remarkably reduced and the accumulation of "common" deletion at mtDNA (that may let the persistence of oxidative damage by precluding detoxification from reactive oxygen species [ROS]) completely abrogated.	Reactive Oxygen Species	283-286	P53	Homo sapiens	56-59
18507431-3	2008	We show that resveratrol induces apoptosis in Jeko-1 cells and modulates several key molecules, including cyclin D1 (CCND1), p53 (TP53), p21 (CDKN1A), BCL2, BAX, Bcl XL (BCL2L1), caspase 9 (CASP9) and p27 (CDKN1B).	Resveratrol	13-24	P53	Homo sapiens	130-134
18645022-6	2008	Quinoline derivative triggered transient, p53-independent G(2)-M arrest in mutant p53 cells (SW620) and succeeding mitotic transition, whereby these cells underwent cell death probably due to aberrant mitosis (mitotic catastrophe).	quinoline	0-9	P53	Homo sapiens	42-45
18085531-6	2008	However, it led to a marked impairment of p53 induction in response to BPDE treatment.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	71-75	P53	Homo sapiens	42-45
18085531-9	2008	Further investigation revealed that MMA(III) dramatically inhibited p53 phosphorylation at serine 15, implying that MMA(III) destabilized p53 by inhibiting its phosphorylation.	Serine	91-97	P53	Homo sapiens	68-71
18085531-9	2008	Further investigation revealed that MMA(III) dramatically inhibited p53 phosphorylation at serine 15, implying that MMA(III) destabilized p53 by inhibiting its phosphorylation.	Serine	91-97	P53	Homo sapiens	138-141
18645022-6	2008	Quinoline derivative triggered transient, p53-independent G(2)-M arrest in mutant p53 cells (SW620) and succeeding mitotic transition, whereby these cells underwent cell death probably due to aberrant mitosis (mitotic catastrophe).	quinoline	0-9	P53	Homo sapiens	82-85
18645026-6	2008	Andro is capable of activating p53 via increased p53 phosphorylation and protein stabilization, a process mediated by enhanced reactive oxygen species production and subsequent c-Jun NH(2)-terminal kinase activation.	Reactive Oxygen Species	127-150	P53	Homo sapiens	31-34
18645026-7	2008	Pretreatment with an antioxidant (N-acetylcysteine) or a c-Jun NH(2)-terminal kinase inhibitor (SP600125) effectively prevented Andro-induced p53 activation and DR4 up-regulation and eventually blocked the Andro-induced sensitization on TRAIL-induced apoptosis.	Acetylcysteine	34-50	P53	Homo sapiens	142-145
18249029-0	2008	Arsenic-induced health effects and genetic damage in keratotic individuals: involvement of p53 arginine variant and chromosomal aberrations in arsenic susceptibility.	Arginine	95-103	P53	Homo sapiens	91-94
18249029-6	2008	Previously we have reported that the p53 codon 72 arginine (Arg) homozygous genotype is associated with the development of arsenic-induced keratosis.	Arginine	50-58	P53	Homo sapiens	37-40
18512960-13	2008	The average value of the experimental DeltaG(E)() for the six lysine methyl transfer reactions catalyzed by vSET, LSMT, and SET7/9 with p53 as a substrate is 22.1 +/- 1.0 kcal/mol, and the computed average (DeltaG(C)()) is 22.2 +/- 0.8 kcal/mol.	Lysine	62-68	P53	Homo sapiens	136-139
18249029-6	2008	Previously we have reported that the p53 codon 72 arginine (Arg) homozygous genotype is associated with the development of arsenic-induced keratosis.	Arginine	60-63	P53	Homo sapiens	37-40
18249029-13	2008	This study suggests that individuals with keratosis are more susceptible to arsenic-induced health effects and genetic damage and that the arginine variant of p53 can further influence the repair capacity of arsenic-exposed individuals, leading to increased accumulation of chromosomal aberrations.	Arginine	139-147	P53	Homo sapiens	159-162
18511948-4	2008	Consistently, response to epirubicin was impaired in NQO1(*)2-homozygous breast carcinoma cells in vitro, reflecting both p53-linked and p53-independent roles of NQO1.	Epirubicin	26-36	P53	Homo sapiens	122-125
18511948-4	2008	Consistently, response to epirubicin was impaired in NQO1(*)2-homozygous breast carcinoma cells in vitro, reflecting both p53-linked and p53-independent roles of NQO1.	Epirubicin	26-36	P53	Homo sapiens	137-140
18191923-3	2008	Suppression of S1 genome segment, which has three open reading frames, not only decreased the expression level of the structural protein sigmaC but also reduced cell fusion and the level of Ser(15)-phosphorylated p53 protein caused by the nonstructural proteins p10 and p17, respectively.	Serine	190-193	P53	Homo sapiens	213-216
18560558-6	2008	ATM was found indispensable for the activation of MAP kinase p38, which catalyzes the activating phosphorylation of p53 on serine 46, thereby causing p53 dependent apoptosis.	Serine	123-129	P53	Homo sapiens	116-119
18313840-0	2008	Ser-249 TP53 and CTNNB1 mutations in circulating free DNA of Egyptian patients with hepatocellular carcinoma versus chronic liver diseases.	Serine	0-3	P53	Homo sapiens	8-12
18313840-3	2008	Here we have examined the presence of mutations in TP53 at codon 249 (Ser-249, considered as a hallmark of mutagenesis by aflatoxin) and in CTNNB1 (gene encoding beta-catenin) in CFDNA of patients with HCC or chronic liver disease, from Alexandria, Egypt.	Serine	70-73	P53	Homo sapiens	51-55
18313840-5	2008	Ser-249 TP53 mutations were determined using PCR-restriction digestion (RFLP) in CFDNA of 255 subjects, and confirmed by sequencing.	Serine	0-3	P53	Homo sapiens	8-12
18560558-6	2008	ATM was found indispensable for the activation of MAP kinase p38, which catalyzes the activating phosphorylation of p53 on serine 46, thereby causing p53 dependent apoptosis.	Serine	123-129	P53	Homo sapiens	150-153
18523266-0	2008	Proteasome inhibitors enhance TRAIL-induced apoptosis through the intronic regulation of DR5: involvement of NF-kappa B and reactive oxygen species-mediated p53 activation.	Reactive Oxygen Species	124-147	P53	Homo sapiens	157-160
18468580-3	2008	Cisplatin (cDDP) yields intra- and inter-strand DNA cross-links and several proteins that recognise cDDP-induced DNA damage, such as p53, are also targets of poly(ADP-ribosyl)ation.	Cisplatin	0-9	P53	Homo sapiens	133-136
18468580-3	2008	Cisplatin (cDDP) yields intra- and inter-strand DNA cross-links and several proteins that recognise cDDP-induced DNA damage, such as p53, are also targets of poly(ADP-ribosyl)ation.	Cisplatin	11-15	P53	Homo sapiens	133-136
18468580-3	2008	Cisplatin (cDDP) yields intra- and inter-strand DNA cross-links and several proteins that recognise cDDP-induced DNA damage, such as p53, are also targets of poly(ADP-ribosyl)ation.	Cisplatin	100-104	P53	Homo sapiens	133-136
18468580-4	2008	We compared the effects of treatments with cDDP and the PARPs inhibitor PJ34 in p53 mutated carcinoma cell lines (HeLa, KB, HT29) that exhibited differential sensitivities to the drugs, in terms of cell growth inhibition and onset of apoptosis.	Cisplatin	43-47	P53	Homo sapiens	80-83
18559494-0	2008	Cisplatin induces p53-dependent FLICE-like inhibitory protein ubiquitination in ovarian cancer cells.	Cisplatin	0-9	P53	Homo sapiens	18-21
18559494-2	2008	Although p53 and FLICE-like inhibitory protein (FLIP) are determinants of CDDP sensitivity in ovarian cancer, the interaction between p53 and FLIP remains poorly understood.	Cisplatin	74-78	P53	Homo sapiens	9-12
18559494-3	2008	Here, using two chemosensitive ovarian cancer cell lines and various molecular and cellular approaches, we show that CDDP induces p53-dependent FLIP ubiquitination and degradation, and apoptosis in vitro.	Cisplatin	117-121	P53	Homo sapiens	130-133
18559494-4	2008	Moreover, we showed that Itch (an E3 ligase) forms a complex with FLIP and p53 upon CDDP treatment.	Cisplatin	84-88	P53	Homo sapiens	75-78
18559494-5	2008	These results suggest that p53 facilitates FLIP down-regulation by CDDP-induced FLIP ubiquitination and proteasomal degradation.	Cisplatin	67-71	P53	Homo sapiens	27-30
18523266-10	2008	Intracellular reactive oxygen species (ROS) generation after MG132 treatment contributed to p53, but not p65 nuclear translocation and DNA-binding activity.	Reactive Oxygen Species	14-37	P53	Homo sapiens	92-95
18523266-10	2008	Intracellular reactive oxygen species (ROS) generation after MG132 treatment contributed to p53, but not p65 nuclear translocation and DNA-binding activity.	Reactive Oxygen Species	39-42	P53	Homo sapiens	92-95
18523266-13	2008	These findings reveal that proteasome inhibitor-mediated NF-kappaB and ROS-dependent p53 activation are contributed to intronic regulation of DR5 transcription, and resulted in the subsequent enhancement of TRAIL-induced apoptosis in human lung cancer cells.	Reactive Oxygen Species	71-74	P53	Homo sapiens	85-88
18523266-7	2008	The protein stability, Ser(392) phosphorylation and Lys(373)/Lys(382) acetylation of p53 were enhanced by MG132.	Lysine	52-55	P53	Homo sapiens	85-88
18523266-7	2008	The protein stability, Ser(392) phosphorylation and Lys(373)/Lys(382) acetylation of p53 were enhanced by MG132.	Lysine	61-64	P53	Homo sapiens	85-88
18223681-3	2008	During cisplatin (CDDP)-mediated apoptosis in neuroblastoma SH-SY5Y cells, p53 was induced to accumulate in association with an increase in expression levels of NEDL1.	Cisplatin	7-16	P53	Homo sapiens	75-78
18402767-3	2008	During adriamycin (ADR)-mediated apoptosis, UNC5H4 was significantly induced in p53-proficient U2OS cells but not in p53-deficient H1299 cells.	Doxorubicin	7-17	P53	Homo sapiens	80-83
18223681-3	2008	During cisplatin (CDDP)-mediated apoptosis in neuroblastoma SH-SY5Y cells, p53 was induced to accumulate in association with an increase in expression levels of NEDL1.	Cisplatin	18-22	P53	Homo sapiens	75-78
18367875-4	2008	In the present study, we treated HT-29 (mutant p53) and LoVo (wild type p53) human colorectal cancer cells with different concentrations of GTP, which led to repression of cell proliferation and induction of apoptosis in both cell lines.	Guanosine Triphosphate	140-143	P53	Homo sapiens	47-50
18478141-1	2008	The newly synthesized water-soluble cyclodiphosphazane ligands and their gold(I) complexes inhibit HeLa cell proliferation by activating p53 protein and inducing apoptosis.	Water	22-27	P53	Homo sapiens	137-140
18397889-3	2008	Here, we use RNA interference to reduce p53 expression in CHRF cells and show that reduced p53 activity leads to a greater fraction of polyploid cells, higher mean and maximum ploidy, accelerated DNA synthesis, and delayed apoptosis and cell death upon phorbol 12-myristate 13-acetate-induced Mk differentiation.	Tetradecanoylphorbol Acetate	253-284	P53	Homo sapiens	91-94
18400748-4	2008	We found that after prolonged nocodazole exposure, the postmitotic checkpoint was facilitated by p53.	Nocodazole	30-40	P53	Homo sapiens	97-100
18506185-0	2008	Cisplatin alters nitric oxide synthase levels in human ovarian cancer cells: involvement in p53 regulation and cisplatin resistance.	Cisplatin	0-9	P53	Homo sapiens	92-95
18506185-5	2008	The NO donor S-nitroso-N-acetylpenicillamine (SNAP) increased p53 protein levels and induced apoptosis in both cell types, and enhanced cisplatin-induced apoptosis in C13(*) cells in a p53-dependent manner (i.e., enhancement blocked by p53 siRNA).	Cisplatin	136-145	P53	Homo sapiens	185-188
18506185-5	2008	The NO donor S-nitroso-N-acetylpenicillamine (SNAP) increased p53 protein levels and induced apoptosis in both cell types, and enhanced cisplatin-induced apoptosis in C13(*) cells in a p53-dependent manner (i.e., enhancement blocked by p53 siRNA).	Cisplatin	136-145	P53	Homo sapiens	185-188
18454317-7	2008	In melanoma cells, resveratrol inhibits STAT3 and NF-kappaB-dependent transcription, culminating in suppression of cFLIP and Bcl-xL expression, while activating the MAPK- and the ATM-Chk2-p53 pathways.	Resveratrol	19-30	P53	Homo sapiens	188-191
18367875-4	2008	In the present study, we treated HT-29 (mutant p53) and LoVo (wild type p53) human colorectal cancer cells with different concentrations of GTP, which led to repression of cell proliferation and induction of apoptosis in both cell lines.	Guanosine Triphosphate	140-143	P53	Homo sapiens	72-75
18367875-5	2008	Meanwhile, we also observed increased PUMA expression and decreased ERK (extracellular signal-regulated kinase) activity in both of GTP-treated tumor cell lines carrying different genotypes of p53.	Guanosine Triphosphate	132-135	P53	Homo sapiens	193-196
18367875-10	2008	Demonstration of the molecular mechanism involved in the anti-cancer effect of GTP may be useful in the therapeutic target selection for p53 deficient colorectal cancer.	Guanosine Triphosphate	79-82	P53	Homo sapiens	137-140
18954551-5	2008	Only three from the eight TP53 polymorphisms described in the analyzed region were polymorphic within our samples: the 11827 base from intron 2, the 16bp duplication in the intron3 and the codon 72 (Arg&gt;Pro) from exon 4.	Arginine	199-202	P53	Homo sapiens	26-30
18495657-4	2008	Mesalazine inhibited the growth of HCT-116 and HT-29 cells, two CRC cell lines that express either a wild-type or mutated p53.	Mesalamine	0-10	P53	Homo sapiens	122-125
18519674-9	2008	Third, PP-2A directly interacts with p53 and dephosphorylates p53 at Ser-15 in vitro and in vivo.	Serine	69-72	P53	Homo sapiens	62-65
18519674-11	2008	Inhibition of PP-2A activity enhances p53 phosphorylation at Ser-15 and up-regulates Bak expression to promote EGCG-induced apoptosis.	Serine	61-64	P53	Homo sapiens	38-41
18519674-13	2008	In summary, our results show that (a) PP-2A directly dephosphorylates p53 at Ser-15; (b) P53 directly controls Bak expression; and (c) EGCG negatively regulates PP-2A.	Serine	77-80	P53	Homo sapiens	70-73
18497992-1	2008	To understand one of the mechanisms of resistance to chemoradiation in colon cancer cells, we investigated whether 5-fluorouracil (5-FU) mediated the expression of epidermal growth factor receptor (EGFR) and modified repair of radiation-induced DNA damage, especially in a p53 independent pathway.	Fluorouracil	131-135	P53	Homo sapiens	273-276
18331776-6	2008	It was found that the treatment of OE33 cells with flavones and flavonols caused G2/M arrest through up-regulation of GADD45beta and 14-3-3sigma and down-regulation of cyclin B1 at the mRNA and protein levels, and induced p53-independent mitochondrial-mediated apoptosis through up-regulation of PIG3 and cleavage of caspase-9 and caspase-3.	Flavones	51-59	P53	Homo sapiens	222-225
18331776-6	2008	It was found that the treatment of OE33 cells with flavones and flavonols caused G2/M arrest through up-regulation of GADD45beta and 14-3-3sigma and down-regulation of cyclin B1 at the mRNA and protein levels, and induced p53-independent mitochondrial-mediated apoptosis through up-regulation of PIG3 and cleavage of caspase-9 and caspase-3.	Flavonols	64-73	P53	Homo sapiens	222-225
18272544-9	2008	Phosphorylation of p53 at site Ser15 and Chk1 at Ser317, as well as accumulation of p21(waf1/cip1), was observed within 8-24 h. Superoxide dismutase and catalase were unable to overcome this G2/M arrest, possibly indicating that neutrophil products other than superoxide or H(2)O(2) are involved in this cellular response.	Superoxides	260-270	P53	Homo sapiens	19-22
18395248-2	2008	HIPK2 regulates p53-apoptotic function via serine-46 (Ser46) phosphorylation and activation of p53 is a key determinant in ovarian cancer cell death.	Serine	43-49	P53	Homo sapiens	16-19
18395248-9	2008	Thus, 2008C13 cells were resistant to cisplatin but sensitive to adriamycin-induced apoptosis through activation of the HIPK2/p53Ser46 pathway.	Doxorubicin	65-75	P53	Homo sapiens	126-129
18410999-0	2008	Hdm2 and nitric oxide radicals contribute to the p53-dependent radioadaptive response.	Nitric Oxide	9-21	P53	Homo sapiens	49-52
18497992-9	2008	Interaction of EGFR and ERCC1 might correlate with radiation-induced DNA damage when p53 mutant colon cancer cell lines are exposed to 5-FU followed by radiation.	Fluorouracil	135-139	P53	Homo sapiens	85-88
18598164-0	2008	The ethanol extract from Artemisia princeps Pampanini induces p53-mediated G1 phase arrest in A172 human neuroblastoma cells.	Ethanol	4-11	P53	Homo sapiens	62-65
18566213-5	2008	Indeed, we found that CDDP treatment induced the up-regulation of p53 in both sensitive and resistant A2780 cell lines.	Cisplatin	22-26	P53	Homo sapiens	66-69
18443131-0	2008	Phosphorylation of Thr18 and Ser20 of p53 in Ad-p53-induced apoptosis.	UNII-PYZ33YLR8A	19-24	P53	Homo sapiens	48-51
18443131-5	2008	Here we use Ad-p53 constructs to test the hypothesis that simultaneous phosphorylation of p53 at threonine 18 (Thr18) and serine 20 (Ser20) is causally associated with p53-mediated apoptosis.	Threonine	97-106	P53	Homo sapiens	90-93
18454141-3	2008	Enhanced autophagy improved the survival of p53-deficient cancer cells under conditions of hypoxia and nutrient depletion, allowing them to maintain high ATP levels.	Adenosine Triphosphate	154-157	P53	Homo sapiens	44-47
18443131-5	2008	Here we use Ad-p53 constructs to test the hypothesis that simultaneous phosphorylation of p53 at threonine 18 (Thr18) and serine 20 (Ser20) is causally associated with p53-mediated apoptosis.	Threonine	97-106	P53	Homo sapiens	90-93
18443131-5	2008	Here we use Ad-p53 constructs to test the hypothesis that simultaneous phosphorylation of p53 at threonine 18 (Thr18) and serine 20 (Ser20) is causally associated with p53-mediated apoptosis.	UNII-PYZ33YLR8A	111-116	P53	Homo sapiens	90-93
18443131-5	2008	Here we use Ad-p53 constructs to test the hypothesis that simultaneous phosphorylation of p53 at threonine 18 (Thr18) and serine 20 (Ser20) is causally associated with p53-mediated apoptosis.	UNII-PYZ33YLR8A	111-116	P53	Homo sapiens	90-93
18443131-6	2008	Studies using phosphorylation-specific antibodies demonstrated that p53-induced apoptosis correlates with phosphorylation of p53 at Thr18 and Ser20 but not with carboxy-terminal phosphorylation (Ser392).	UNII-PYZ33YLR8A	132-137	P53	Homo sapiens	68-71
18443131-6	2008	Studies using phosphorylation-specific antibodies demonstrated that p53-induced apoptosis correlates with phosphorylation of p53 at Thr18 and Ser20 but not with carboxy-terminal phosphorylation (Ser392).	UNII-PYZ33YLR8A	132-137	P53	Homo sapiens	125-128
18516295-2	2008	We have previously shown that mutational inactivation of p53 results in sensitization to paclitaxel.	Paclitaxel	89-99	P53	Homo sapiens	57-60
18443131-11	2008	We thus conclude that phosphorylation of Thr18 and Ser20 is sufficient for inducing p53-mediated apoptosis in glioma cells.	UNII-PYZ33YLR8A	41-46	P53	Homo sapiens	84-87
18516295-7	2008	Sensitization to paclitaxel-induced apoptosis was also achieved by p53-siRNA transfection in wild type p53 H460 cells.	Paclitaxel	17-27	P53	Homo sapiens	67-70
18472002-0	2008	Arginine methylation of hnRNP K enhances p53 transcriptional activity.	Arginine	0-8	P53	Homo sapiens	41-44
18516295-7	2008	Sensitization to paclitaxel-induced apoptosis was also achieved by p53-siRNA transfection in wild type p53 H460 cells.	Paclitaxel	17-27	P53	Homo sapiens	103-106
18440733-0	2008	Benzo(a)pyrene increases phosphorylation of p53 at serine 392 in relation to p53 induction and cell death in MCF-7 cells.	Serine	51-57	P53	Homo sapiens	44-47
18440733-0	2008	Benzo(a)pyrene increases phosphorylation of p53 at serine 392 in relation to p53 induction and cell death in MCF-7 cells.	Serine	51-57	P53	Homo sapiens	77-80
18440733-7	2008	Phosphorylation of p53 protein at serines 15, 20, 46 and 392 increased in MCF-7 cells.	Serine	34-41	P53	Homo sapiens	19-22
18440733-10	2008	These results suggest that serine 392 phosphorylation is the first stabilizing event of p53 associated with BP exposure and subsequent cell death in MCF-7 cells.	Serine	27-33	P53	Homo sapiens	88-91
18600534-0	2008	Functional inactivity and mutations of p53 differentially affect sensitivity to 5-fluorouracil and antifolate inhibitors of thymidylate synthase (TS) by altering TS levels in colorectal cancer cells.	Fluorouracil	80-94	P53	Homo sapiens	39-42
18472002-1	2008	Previous studies have illustrated that hnRNP K, which could be methylated at arginine residues, plays a key role in coordinating transcriptional responses to DNA damage as a cofactor for p53.	Arginine	77-85	P53	Homo sapiens	187-190
18472002-3	2008	Furthermore, arginine methylation of hnRNP K enhanced its affinity with p53.	Arginine	13-21	P53	Homo sapiens	72-75
18472002-5	2008	These data suggested that arginine methylation of hnRNP K is a key element for p53 transcriptional activity.	Arginine	26-34	P53	Homo sapiens	79-82
18406507-7	2008	Activation of p53 was evidenced by its phosphorylation at serine 15 (Ser15) and acetylation at lysine 382 (Lys382).	Serine	58-64	P53	Homo sapiens	14-17
18406507-7	2008	Activation of p53 was evidenced by its phosphorylation at serine 15 (Ser15) and acetylation at lysine 382 (Lys382).	Lysine	95-101	P53	Homo sapiens	14-17
18406507-10	2008	SB203580 and PD98059, specific inhibitors of p38 MAPK and ERK, respectively, suppressed phosphorylation of p53 at Ser15, but the accumulation of p53 was only moderately reduced.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	13-20	P53	Homo sapiens	107-110
18406507-10	2008	SB203580 and PD98059, specific inhibitors of p38 MAPK and ERK, respectively, suppressed phosphorylation of p53 at Ser15, but the accumulation of p53 was only moderately reduced.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	13-20	P53	Homo sapiens	145-148
18261847-0	2008	Cooperation between p53 and p73 in cisplatin-induced apoptosis in ovarian carcinoma cells.	Cisplatin	35-44	P53	Homo sapiens	20-23
18406507-11	2008	Acetylation of p53 at Lys 382 was not affected by these inhibitors, suggesting that acetylation stabilizes p53 in response to DNA damage.	Lysine	22-25	P53	Homo sapiens	15-18
18342637-1	2008	Apigenin, a plant flavone, potentially activates wild-type p53 and induces apoptosis in cancer cells.	flavone	18-25	P53	Homo sapiens	59-62
18342637-3	2008	Exposure of human prostate cancer 22Rv1 cells, harboring wild-type p53, to growth-suppressive concentrations (10-80 microM) of apigenin resulted in the stabilization of p53 by phosphorylation on critical serine sites, p14ARF-mediated downregulation of MDM2 protein, inhibition of NF-kappaB/p65 transcriptional activity, and induction of p21/WAF-1 in a dose- and time-dependent manner.	Serine	204-210	P53	Homo sapiens	169-172
18342637-7	2008	Apigenin-mediated p53 activation and apoptosis were further attenuated by p53 antisense oligonucleotide treatment.	Oligonucleotides	88-103	P53	Homo sapiens	18-21
18342637-7	2008	Apigenin-mediated p53 activation and apoptosis were further attenuated by p53 antisense oligonucleotide treatment.	Oligonucleotides	88-103	P53	Homo sapiens	74-77
18261847-5	2008	Although p73 appears to be implicated mainly in response to high stress conditions, the available results support a cooperation between p53 and p73 in cisplatin-induced apoptosis in sensitive cells.	Cisplatin	151-160	P53	Homo sapiens	136-139
18269916-0	2008	Induction of p21 by p65 in p53 null cells treated with Doxorubicin.	Doxorubicin	55-66	P53	Homo sapiens	27-30
18395372-0	2008	Verminoside- and verbascoside-induced genotoxicity on human lymphocytes: involvement of PARP-1 and p53 proteins.	verminoside	0-11	P53	Homo sapiens	99-102
18269916-2	2008	Here we show that knockdown of p65 by IkappaBSR or p65 siRNA decreased the cytotoxic effect of DOX on HCT116 (p53+/+) cells, correlating with increased induction of p21.	Doxorubicin	95-98	P53	Homo sapiens	110-113
18269916-5	2008	In HCT116 (p53-/-) cells, downregulation of p65 expression enhanced the cytotoxic effect of DOX, due to decreased p21 expression levels.	Doxorubicin	92-95	P53	Homo sapiens	11-14
18269916-6	2008	We present evidence that in p53-null tumor cells treated with DOX, p65 was involved in induction of p21 expression by directly binding to the p21 promoter.	Doxorubicin	62-65	P53	Homo sapiens	28-31
18294283-2	2008	We have previously found that doxorubicin increased the p53 levels in cells containing p53-binding HBx protein and restored the p53-mediated transcriptional activity that was suppressed by HBx.	Doxorubicin	30-41	P53	Homo sapiens	56-59
18294283-2	2008	We have previously found that doxorubicin increased the p53 levels in cells containing p53-binding HBx protein and restored the p53-mediated transcriptional activity that was suppressed by HBx.	Doxorubicin	30-41	P53	Homo sapiens	87-90
18376141-1	2008	We showed that tumor cells with wild-type p53 and high levels of Bcl-x(L) are cisplatin resistant but are induced to undergo apoptosis by (-)-gossypol, making this a promising agent for overcoming cisplatin resistance.	Cisplatin	78-87	P53	Homo sapiens	42-45
18294283-2	2008	We have previously found that doxorubicin increased the p53 levels in cells containing p53-binding HBx protein and restored the p53-mediated transcriptional activity that was suppressed by HBx.	Doxorubicin	30-41	P53	Homo sapiens	87-90
18376141-1	2008	We showed that tumor cells with wild-type p53 and high levels of Bcl-x(L) are cisplatin resistant but are induced to undergo apoptosis by (-)-gossypol, making this a promising agent for overcoming cisplatin resistance.	Gossypol	138-150	P53	Homo sapiens	42-45
18376141-1	2008	We showed that tumor cells with wild-type p53 and high levels of Bcl-x(L) are cisplatin resistant but are induced to undergo apoptosis by (-)-gossypol, making this a promising agent for overcoming cisplatin resistance.	Cisplatin	197-206	P53	Homo sapiens	42-45
18294283-4	2008	We found that six phosphorylation sites of the Serine residues of p53 were efficiently phosphorylated in HBx-expressing ChangX-34 cells, suggesting that the binding of HBx to the p53 protein does not interfere with the phosphorylation of p53 by signaling kinases.	Serine	47-53	P53	Homo sapiens	66-69
18376141-3	2008	Conversely, tumor cells with low Bcl-x(L) expression and either wild type or mutant p53 are relatively cisplatin sensitive and do not exhibit such high levels of apoptosis.	Cisplatin	103-112	P53	Homo sapiens	84-87
18294283-4	2008	We found that six phosphorylation sites of the Serine residues of p53 were efficiently phosphorylated in HBx-expressing ChangX-34 cells, suggesting that the binding of HBx to the p53 protein does not interfere with the phosphorylation of p53 by signaling kinases.	Serine	47-53	P53	Homo sapiens	179-182
18294283-4	2008	We found that six phosphorylation sites of the Serine residues of p53 were efficiently phosphorylated in HBx-expressing ChangX-34 cells, suggesting that the binding of HBx to the p53 protein does not interfere with the phosphorylation of p53 by signaling kinases.	Serine	47-53	P53	Homo sapiens	179-182
18294283-6	2008	Intriguingly, reactivation of p53 was accompanied with a nuclear accumulation of p53 and the phosphorylated p53 at Serine15 was only detected in nuclear fraction, but not in cytosolic fraction of doxorubicin-treated ChangX-34 cells.	Doxorubicin	196-207	P53	Homo sapiens	30-33
18294283-6	2008	Intriguingly, reactivation of p53 was accompanied with a nuclear accumulation of p53 and the phosphorylated p53 at Serine15 was only detected in nuclear fraction, but not in cytosolic fraction of doxorubicin-treated ChangX-34 cells.	Doxorubicin	196-207	P53	Homo sapiens	81-84
18294283-6	2008	Intriguingly, reactivation of p53 was accompanied with a nuclear accumulation of p53 and the phosphorylated p53 at Serine15 was only detected in nuclear fraction, but not in cytosolic fraction of doxorubicin-treated ChangX-34 cells.	Doxorubicin	196-207	P53	Homo sapiens	81-84
18294283-7	2008	Functional restoration of the p53 protein in HBx-expressing cells occurs according to the dual effects of doxorubicin: a significant reduction of Hdm2 expression and a nuclear accumulation of the phosphorylated p53 protein.	Doxorubicin	106-117	P53	Homo sapiens	30-33
18294283-7	2008	Functional restoration of the p53 protein in HBx-expressing cells occurs according to the dual effects of doxorubicin: a significant reduction of Hdm2 expression and a nuclear accumulation of the phosphorylated p53 protein.	Doxorubicin	106-117	P53	Homo sapiens	211-214
18489080-7	2008	An RP-HPLC-ECD assay was used to detect the formation of 8-oxo-dGuo in p53 cDNA exposed to representative quinones, BP-7,8-dione, BA-3,4-dione, and DMBA-3,4-dione under redox cycling conditions.	dmba-3,4-dione	148-162	P53	Homo sapiens	71-74
18489080-10	2008	By contrast, micromolar concentrations of (+/-)- anti-BPDE generated (+)- trans- anti-BPDE-N (2)-dGuo adducts (detected by stable-isotope dilution LC/MS methodology) in p53 cDNA that correlated in a linear fashion with mutagenic frequency, but no 8-oxo-dGuo was detected.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	54-58	P53	Homo sapiens	169-172
17681772-8	2008	A significant increase in p53 exon 7-8 strand breaks was observed with decreasing folate in NCM460 cells.	Folic Acid	82-88	P53	Homo sapiens	26-29
18348286-2	2008	We have developed a high-throughput scanning assay with automatic calling to detect TP53 mutations in DNA from fresh frozen (FF) and formalin-fixed paraffin-embedded (FFPE) tissues.	Paraffin	148-156	P53	Homo sapiens	84-88
18630481-8	2008	In patients with GSTM1 null genotype and p53 Arg/Pro heterozygotes or Pro/Pro homozygotes the chance of survival is significantly lower than in the case of GSTM1+ and p53 Arg/Arg variants (p=0.009 and p=0.008, respectively).	Arginine	45-48	P53	Homo sapiens	41-44
18630481-8	2008	In patients with GSTM1 null genotype and p53 Arg/Pro heterozygotes or Pro/Pro homozygotes the chance of survival is significantly lower than in the case of GSTM1+ and p53 Arg/Arg variants (p=0.009 and p=0.008, respectively).	Arginine	171-174	P53	Homo sapiens	167-170
18630481-8	2008	In patients with GSTM1 null genotype and p53 Arg/Pro heterozygotes or Pro/Pro homozygotes the chance of survival is significantly lower than in the case of GSTM1+ and p53 Arg/Arg variants (p=0.009 and p=0.008, respectively).	Arginine	171-174	P53	Homo sapiens	167-170
18177348-10	2008	Finally, we propose a novel mechanism involving H2O2 in the regulation of tyrosinase via p53 through transcription of hepatocyte nuclear factor 1alpha which in turn can also affect the POMC response.	Hydrogen Peroxide	48-52	P53	Homo sapiens	89-92
18397472-6	2008	Immunoblotting revealed that the levels of p53 and p21(WAF1/CIP1) in TAM-treated cells increased in a time- and dose-dependent manner, whereas those of p27(KIP1) and p16 slightly increased or remained unchanged.	Tamoxifen	69-72	P53	Homo sapiens	43-46
18397472-8	2008	These results suggest that the tumorigenic effect of TAM on MCF-7 cells arises through antitumor effects that are due to the expression of cyclin-dependent kinase inhibitors, especially p21(WAF1/CIP1) and these are regulated by the decrease of wild-type p53.	Tamoxifen	53-56	P53	Homo sapiens	254-257
18425350-11	2008	Our results suggested that the PTL-induced apoptosis of A549 cells was due to the direct suppression of NF-kappaB activity in a p53- and hsp72-independent manner based on NF-kappaB signaling.	parthenolide	31-34	P53	Homo sapiens	128-131
18221322-6	2008	LOH in paraffin-embedded specimens was detected in 22.6% and 12.9% for FHIT and p53 respectively.	Paraffin	7-15	P53	Homo sapiens	80-83
18311036-6	2008	At 3 hours after UV irradiation, p53 was phosphorylated at Ser 15 and Ser 46, and accumulated in the cell nuclei, notably after exposure to 280-320 nm wavelengths.	Serine	59-62	P53	Homo sapiens	33-36
18311036-6	2008	At 3 hours after UV irradiation, p53 was phosphorylated at Ser 15 and Ser 46, and accumulated in the cell nuclei, notably after exposure to 280-320 nm wavelengths.	Serine	70-73	P53	Homo sapiens	33-36
18504201-0	2008	[P53 protein expression and chemosensitivity to cisplatin in patients with non-small cell lung cancer: a meta-analysis].	Cisplatin	48-57	P53	Homo sapiens	1-4
18355840-9	2008	In p53 codon72 Arg/Pro + Pro/Pro carriers the frequency of the AG + GG genotype of MSH3 exon23 was significantly increased in patients compared to controls (OR 2.1, 95% CI 1.05-4.34).	Arginine	15-18	P53	Homo sapiens	3-6
18296503-3	2008	The binding of hnRNPC1/C2 is strongly enhanced in response to the DNA-damaging drug cisplatin [cis-diamminedichloroplatinum(II)] and the cytostatic transcriptional inhibitor actinomycin D (dactinomycin), both known inducers of apoptosis and p53.	Cisplatin	84-93	P53	Homo sapiens	241-244
18296503-3	2008	The binding of hnRNPC1/C2 is strongly enhanced in response to the DNA-damaging drug cisplatin [cis-diamminedichloroplatinum(II)] and the cytostatic transcriptional inhibitor actinomycin D (dactinomycin), both known inducers of apoptosis and p53.	Cisplatin	95-123	P53	Homo sapiens	241-244
18505925-1	2008	p53R2 is a p53-inducible ribonucleotide reductase that contributes to DNA repair by supplying deoxynucleotide triphosphate pools in response to DNA damage.	deoxynucleotide triphosphate	94-122	P53	Homo sapiens	0-3
18505928-9	2008	p53 expression knockdown by small interfering RNA increased cisplatin sensitivity.	Cisplatin	60-69	P53	Homo sapiens	0-3
18455581-1	2008	OBJECTIVE: The objective of this study is to establish clinical evidence that the p53 genotype can serve as a predictive marker for response to cisplatin-based induction therapy.	Cisplatin	144-153	P53	Homo sapiens	82-85
18504201-1	2008	OBJECTIVE: To explore the relation between p53 protein expression and chemosensitivity to cisplatin in patients with non-small cell lung cancer (NSCLC).	Cisplatin	90-99	P53	Homo sapiens	43-46
18425390-0	2008	Alterations of the K-ras and p53 genes in Tamoxifen-associated endometrial carcinoma.	Tamoxifen	42-51	P53	Homo sapiens	29-32
18391940-0	2008	p53 regulates glucose metabolism through an IKK-NF-kappaB pathway and inhibits cell transformation.	Glucose	14-21	P53	Homo sapiens	0-3
18646516-9	2008	When AP-1 activities were inhibited by curcumin, overexpression of p53 induced by B(a)P was not markedly changed.	Curcumin	39-47	P53	Homo sapiens	67-70
18425390-3	2008	The median duration of TAM exposure was significantly longer in patients with p53 mutations than those without p53 mutations (62 vs. 30 months, p=0.028).	Tamoxifen	23-26	P53	Homo sapiens	78-81
18425390-3	2008	The median duration of TAM exposure was significantly longer in patients with p53 mutations than those without p53 mutations (62 vs. 30 months, p=0.028).	Tamoxifen	23-26	P53	Homo sapiens	111-114
18425390-4	2008	Our observation suggests that prolonged TAM exposure may directly inactivate the p53 gene by acting as a mutagen in a significant fraction of TAM-associated endometrial carcinomas.	Tamoxifen	40-43	P53	Homo sapiens	81-84
18425390-4	2008	Our observation suggests that prolonged TAM exposure may directly inactivate the p53 gene by acting as a mutagen in a significant fraction of TAM-associated endometrial carcinomas.	Tamoxifen	142-145	P53	Homo sapiens	81-84
18423915-4	2008	A G-to-C SNP at p53 codon 72 results in an Arg/Pro polymorphism, which is associated with apoptosis induction potential and p53 mutation status.	Arginine	43-46	P53	Homo sapiens	16-19
18423915-4	2008	A G-to-C SNP at p53 codon 72 results in an Arg/Pro polymorphism, which is associated with apoptosis induction potential and p53 mutation status.	Arginine	43-46	P53	Homo sapiens	124-127
18423915-7	2008	p53 codon 72 SNP Arg/Arg polymorphism was associated with the progression of OSCC, and the overall (OS) and disease-free survival (DFS) of irradiated patients.	Arginine	17-20	P53	Homo sapiens	0-3
18423915-7	2008	p53 codon 72 SNP Arg/Arg polymorphism was associated with the progression of OSCC, and the overall (OS) and disease-free survival (DFS) of irradiated patients.	Arginine	21-24	P53	Homo sapiens	0-3
18423915-9	2008	The combination of MDM2 SNP309 G/G and p53 codon 72 Arg/Arg polymorphism is associated with the worst OS and DFS.	Arginine	52-55	P53	Homo sapiens	39-42
18423915-9	2008	The combination of MDM2 SNP309 G/G and p53 codon 72 Arg/Arg polymorphism is associated with the worst OS and DFS.	Arginine	56-59	P53	Homo sapiens	39-42
18305112-2	2008	Here, we report that ARF associates with COMMD1 and promotes Lys(63)-mediated polyubiquitination of COMMD1 in a p53-independent manner.	Lysine	61-64	P53	Homo sapiens	112-115
18305112-8	2008	Together, these data suggest that the ability to promote Lys(63)-mediated polyubiquitination of COMMD1 is a novel property of ARF independent of p53.	Lysine	57-60	P53	Homo sapiens	145-148
20731894-16	2008	The IC50 of pEGFP-p53(RS)-801D cell line to 5-Fluorouracil(5FU) is 2.08+/-0.18 mug/mL, which is obviously lower than that of 801D(4.90+/-1.12 mug/mL,P &lt;0.05) and pEGFP-801D(3.41+/-0.86 mug/mL,P &lt;0.05).	Fluorouracil	59-62	P53	Homo sapiens	18-21
17998932-1	2008	Codon 72 of human p53 gene is polymorphic, encoding arginine or proline.	Arginine	52-60	P53	Homo sapiens	18-21
20731894-12	2008	The IC50 of pEGFP-p53(AS)-801D cell line(0.26+/-0.09 mug/mL) to Cisplatin(DDP) decreased markedly compared with 801D(0.55+/-0.19 mug/mL,P&lt;0.05)and pEGFP-801D(0.77+/-0.13mug/mL,P&lt;0.05).	Cisplatin	64-73	P53	Homo sapiens	18-21
20731894-14	2008	pEGFP-p53(RS)-801D cell line showed a notably smaller value of IC50(2.34+/-0.43 ng/mL) to Paclitaxel(TAX) than 801D(8.40+/-1.50 ng/mL, P &lt;0.05)did.	Paclitaxel	90-100	P53	Homo sapiens	6-9
18287100-6	2008	In LoVo and RKO cells, which respond to adriamycin with a p53-mediated induction of POX and generation of reactive oxygen species, we found that adriamycin also induced OH-POX gene expression and markedly increased OH-POX catalytic activity, and this increase in activity was not observed in the cell lines HT29 and HCT15, which do not have a functional p53.	Doxorubicin	40-50	P53	Homo sapiens	58-61
18287100-6	2008	In LoVo and RKO cells, which respond to adriamycin with a p53-mediated induction of POX and generation of reactive oxygen species, we found that adriamycin also induced OH-POX gene expression and markedly increased OH-POX catalytic activity, and this increase in activity was not observed in the cell lines HT29 and HCT15, which do not have a functional p53.	Reactive Oxygen Species	106-129	P53	Homo sapiens	58-61
18287100-6	2008	In LoVo and RKO cells, which respond to adriamycin with a p53-mediated induction of POX and generation of reactive oxygen species, we found that adriamycin also induced OH-POX gene expression and markedly increased OH-POX catalytic activity, and this increase in activity was not observed in the cell lines HT29 and HCT15, which do not have a functional p53.	Doxorubicin	145-155	P53	Homo sapiens	58-61
18287100-6	2008	In LoVo and RKO cells, which respond to adriamycin with a p53-mediated induction of POX and generation of reactive oxygen species, we found that adriamycin also induced OH-POX gene expression and markedly increased OH-POX catalytic activity, and this increase in activity was not observed in the cell lines HT29 and HCT15, which do not have a functional p53.	Doxorubicin	145-155	P53	Homo sapiens	354-357
17982488-6	2008	5-Fluorouracil treatment of colon carcinoma HCT116 cells expressing WT p53 results in a reduction of the cyclin B2 protein level suggesting that DNA damage may indeed cause repression of these genes.	Fluorouracil	0-14	P53	Homo sapiens	71-74
20731894-16	2008	The IC50 of pEGFP-p53(RS)-801D cell line to 5-Fluorouracil(5FU) is 2.08+/-0.18 mug/mL, which is obviously lower than that of 801D(4.90+/-1.12 mug/mL,P &lt;0.05) and pEGFP-801D(3.41+/-0.86 mug/mL,P &lt;0.05).	Fluorouracil	44-58	P53	Homo sapiens	18-21
20731894-17	2008	By the assay of flow cytometer, G2 phase arrest was observed when pEGFP-p53(AS)-801D was treated with DDP.	Cisplatin	102-105	P53	Homo sapiens	72-75
18413751-5	2008	TMPK knockdown significantly increased doxorubicin sensitivity dramatically in p53-proficient, p53-null HCT-116, and LoVo colon cancer cells.	Doxorubicin	39-50	P53	Homo sapiens	79-82
18275858-5	2008	Recent studies have revealed that each cellular concentration and distribution of p53 has a distinct cellular function and that ROS act as both an upstream signal that triggers p53 activation and a downstream factor that mediates apoptosis.	Reactive Oxygen Species	128-131	P53	Homo sapiens	82-85
18275858-5	2008	Recent studies have revealed that each cellular concentration and distribution of p53 has a distinct cellular function and that ROS act as both an upstream signal that triggers p53 activation and a downstream factor that mediates apoptosis.	Reactive Oxygen Species	128-131	P53	Homo sapiens	177-180
18275858-6	2008	Here, we examine the newly discovered role of p53 in regulating cellular ROS generation and how ROS modulate selective transactivation of p53 target genes.	Reactive Oxygen Species	73-76	P53	Homo sapiens	46-49
18275858-6	2008	Here, we examine the newly discovered role of p53 in regulating cellular ROS generation and how ROS modulate selective transactivation of p53 target genes.	Reactive Oxygen Species	96-99	P53	Homo sapiens	138-141
18358838-2	2008	Here we studied whether p53 mitochondrial translocation and subsequent apoptosis were affected by blocking mitochondrial permeability transition pore using cyclosporine A (CsA) and bongkrekic acid (BA) in skin epidermal JB6 cells and skin tissues.	Cyclosporine	156-170	P53	Homo sapiens	24-27
18358838-2	2008	Here we studied whether p53 mitochondrial translocation and subsequent apoptosis were affected by blocking mitochondrial permeability transition pore using cyclosporine A (CsA) and bongkrekic acid (BA) in skin epidermal JB6 cells and skin tissues.	Cyclosporine	172-175	P53	Homo sapiens	24-27
18358838-3	2008	Our results demonstrated that CsA and BA blocked TPA-induced p53 translocation, leading to protection against the loss of mitochondrial membrane potential and Complex I activity, and eventually suppression of apoptosis.	Cyclosporine	30-33	P53	Homo sapiens	61-64
18358838-3	2008	Our results demonstrated that CsA and BA blocked TPA-induced p53 translocation, leading to protection against the loss of mitochondrial membrane potential and Complex I activity, and eventually suppression of apoptosis.	Tetradecanoylphorbol Acetate	49-52	P53	Homo sapiens	61-64
18413751-5	2008	TMPK knockdown significantly increased doxorubicin sensitivity dramatically in p53-proficient, p53-null HCT-116, and LoVo colon cancer cells.	Doxorubicin	39-50	P53	Homo sapiens	95-98
18191509-4	2008	5-FU-loaded bola-niosomes were tested on SKMEL-28 (human melanoma) and HaCaT (non-melanoma skin cancer with a specific mutations in the p53 tumor suppressor gene) to assess the cytotoxic activity with respect to the free drug.	Fluorouracil	0-4	P53	Homo sapiens	136-139
17968319-4	2008	Resveratrol results in immortalization of mixed progenitor cells with mutant p53, but not human epithelial cells with wild type p53.	Resveratrol	0-11	P53	Homo sapiens	77-80
18454047-7	2008	The distinct p53 activation profile of LA-12 compared with cisplatin and doxorubicin provides a molecular explanation for the ability of this drug to treat cisplatin-resistant cells and indicates its potential usefulness as an alternative antitumour agent in first-line therapy or as a second-line therapy in patients with acquired cisplatin resistance.	Cisplatin	156-165	P53	Homo sapiens	13-16
18454047-7	2008	The distinct p53 activation profile of LA-12 compared with cisplatin and doxorubicin provides a molecular explanation for the ability of this drug to treat cisplatin-resistant cells and indicates its potential usefulness as an alternative antitumour agent in first-line therapy or as a second-line therapy in patients with acquired cisplatin resistance.	Cisplatin	156-165	P53	Homo sapiens	13-16
18381438-3	2008	With the combination therapy of SN-38 (the active metabolite of CPT-11) followed by flavopiridol, the induction of apoptosis was 5-fold greater in the p53+/+ cells compared with the p53-/- cells.	Irinotecan	64-70	P53	Homo sapiens	151-154
18296683-7	2008	We have applied this method to a mixed set of mutation spectra observed in exons 5, 7 and 8 of TP53 from cancers of brain, breast, skin, colon, oesophagus, liver, head and neck, stomach and lung (smokers and non-smokers) and spectra induced by benzo[a]pyrene diol epoxide, ultraviolet (UV) B, UVC, simulated sunlight and hydroxyl radicals in the cII, supF and yeast p53 model systems.	pyrene diol epoxide	252-271	P53	Homo sapiens	95-99
18381438-3	2008	With the combination therapy of SN-38 (the active metabolite of CPT-11) followed by flavopiridol, the induction of apoptosis was 5-fold greater in the p53+/+ cells compared with the p53-/- cells.	Irinotecan	32-37	P53	Homo sapiens	151-154
18381438-3	2008	With the combination therapy of SN-38 (the active metabolite of CPT-11) followed by flavopiridol, the induction of apoptosis was 5-fold greater in the p53+/+ cells compared with the p53-/- cells.	Irinotecan	64-70	P53	Homo sapiens	182-185
18381438-3	2008	With the combination therapy of SN-38 (the active metabolite of CPT-11) followed by flavopiridol, the induction of apoptosis was 5-fold greater in the p53+/+ cells compared with the p53-/- cells.	Irinotecan	32-37	P53	Homo sapiens	182-185
18381438-4	2008	This sequential treatment induced phosphorylation of p53 at Ser(15), which interacted with Rad51, a DNA repair protein involved in homologous recombination.	Serine	60-63	P53	Homo sapiens	53-56
18414047-8	2008	An association has been reported between women carrying the p53 codon 72 polymorphism (a proline to arginine change) with recurrent implantation failure, suggesting a similar function for p53 in humans.	Arginine	100-108	P53	Homo sapiens	60-63
18381438-5	2008	Rad51 bound to p53-Ser(15) within the first 5 hours of combination therapy, and then was transcriptionally suppressed at 24 hours by flavopiridol only in p53+/+ cells.	Serine	19-22	P53	Homo sapiens	15-18
18414047-8	2008	An association has been reported between women carrying the p53 codon 72 polymorphism (a proline to arginine change) with recurrent implantation failure, suggesting a similar function for p53 in humans.	Arginine	100-108	P53	Homo sapiens	188-191
18381438-7	2008	Depletion of Rad51 by small interfering RNA (siRNA) sensitized both p53+/+ and p53-/- cells to SN-38-induced apoptosis with increase of gamma H2AX, a marker of DNA damage.	Irinotecan	95-100	P53	Homo sapiens	79-82
18646327-4	2008	Mutagenicity of etidronic acid was detected by using denaturing high-pressure liquid chromatography analysis of cellular DNA amplified by PCR with primers for exons 5 through 8 of the human p53 gene.	Etidronic Acid	16-30	P53	Homo sapiens	190-193
18314014-6	2008	Both DNA repair proteins, containing Fe-S clusters, and the transcription factor, p53, which is regulated through thiol-disulfide switches, can be oxidized from a distance through DNA-mediated CT.	Iron	37-41	P53	Homo sapiens	82-85
18339539-3	2008	In particular, the tumor suppressor and transcription factor p53 has provided a model for lysine methylation on a non-histone protein.	Lysine	90-96	P53	Homo sapiens	61-64
18646327-7	2008	Mutations in the p53 gene were detected in MCF-7 cells treated with etidronic acid.	Etidronic Acid	68-82	P53	Homo sapiens	17-20
18646327-13	2008	Tumor cells that survive etidronic acid treatment may acquire drug resistance because of mutations in the p53 tumor-suppressor gene.	Etidronic Acid	25-39	P53	Homo sapiens	106-109
18211920-6	2008	In response to DNA damage agent adriamycin, the mRNA expression and promoter activity of beta1,4GalT II were significantly up-regulated and the binding of p53 to beta1,4GalT II promoter was obviously increased.	Doxorubicin	32-42	P53	Homo sapiens	155-158
18211920-7	2008	Furthermore, decreasing the expression of beta1,4GalT II using RNA interference inhibited p53-mediated HeLa cell apoptosis induced by adriamycin.	Doxorubicin	134-144	P53	Homo sapiens	90-93
18211920-8	2008	Collectively, these results suggested that beta1,4GalT II might serve as a target gene of p53 transcription factor during adriamycin-induced HeLa cell apoptosis, which elucidated a new mechanism of p53-mediated cell apoptosis.	Doxorubicin	122-132	P53	Homo sapiens	90-93
17901981-5	2008	The p53 effect of adriamycin-induced cell death by inhibitors of EGFR/IGF1R is investigated by cell growth curves.	Doxorubicin	18-28	P53	Homo sapiens	4-7
17879942-5	2008	However, other agents for example doxorubicin markedly induced p53 response in HeLaS(3) cells.	Doxorubicin	34-45	P53	Homo sapiens	63-66
18211920-8	2008	Collectively, these results suggested that beta1,4GalT II might serve as a target gene of p53 transcription factor during adriamycin-induced HeLa cell apoptosis, which elucidated a new mechanism of p53-mediated cell apoptosis.	Doxorubicin	122-132	P53	Homo sapiens	198-201
18419600-3	2008	Firstly, HCT116 p53(+)/(+) and p53(-)/(-) colorectal cancer cells were treated with H(2)O(2) for 6 hrs and 24 hrs (early/late response).	Hydrogen Peroxide	84-92	P53	Homo sapiens	31-34
17901981-10	2008	The facilitation of adriamycin-induced cell death by inhibitors of EGFR/IGF1R is p53-independent.	Doxorubicin	20-30	P53	Homo sapiens	81-84
17932951-4	2008	In this study, we have characterized the effect of the ultimate carcinogenic DEs, (+)-anti-BPDE and (-)-anti-DBPDE following short exposure times, on Mdm2 and p53 pathway in A549 human lung epithelial carcinoma cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	91-95	P53	Homo sapiens	159-162
18480997-9	2008	Western blotting showed that cisplatin decreased protein expression of E6 and increased protein expression of p53, p21 and Bax.	Cisplatin	29-38	P53	Homo sapiens	110-113
18480997-11	2008	It is concluded that cisplatin can induce apoptosis in HeLa cells by suppressing HPV E6 and thereby restoring the function of p53.	Cisplatin	21-30	P53	Homo sapiens	126-129
18272203-2	2008	In humans, we recently found that a TP53 codon 72 Arginine (Arg) to Proline (Pro) polymorphism affected both cancer incidence and longevity as well.	Arginine	50-58	P53	Homo sapiens	36-40
18272203-2	2008	In humans, we recently found that a TP53 codon 72 Arginine (Arg) to Proline (Pro) polymorphism affected both cancer incidence and longevity as well.	Arginine	50-53	P53	Homo sapiens	36-40
18216092-5	2008	F protein expression in epithelial cells caused phosphorylation of tumor suppressor p53 at serine 15, activation of p53 transcriptional activity, and conformational activation of proapoptotic Bax.	Serine	91-97	P53	Homo sapiens	84-87
17849424-1	2008	Nitric oxide (NO) has been implicated as a potential causative factor for endogenous p53 mutations in gastrointestinal malignancy.	Nitric Oxide	0-12	P53	Homo sapiens	85-88
17932951-6	2008	(+)-anti-BPDE-induced effects on Mdm2 were transient and correlated with transient p53 Ser15 phosphorylation.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	9-13	P53	Homo sapiens	83-86
18377724-6	2008	CAS overexpression enhanced p53 accumulation induced by doxorubicin, 5-fluorouracil, cisplatin, tamoxifen, and etoposide.	Doxorubicin	56-67	P53	Homo sapiens	28-31
17932951-0	2008	Anti-diol epoxide of benzo[a]pyrene induces transient Mdm2 and p53 Ser15 phosphorylation, while anti-diol epoxide of dibenzo[a,l]pyrene induces a nontransient p53 Ser15 phosphorylation.	diol epoxide	5-17	P53	Homo sapiens	63-66
17932951-0	2008	Anti-diol epoxide of benzo[a]pyrene induces transient Mdm2 and p53 Ser15 phosphorylation, while anti-diol epoxide of dibenzo[a,l]pyrene induces a nontransient p53 Ser15 phosphorylation.	diol epoxide	101-113	P53	Homo sapiens	159-162
18216278-8	2008	Furthermore, IGF-1R-dependent UVB-induced premature senescence required the phosphorylation of p53 serine 46.	Serine	99-105	P53	Homo sapiens	95-98
18497347-7	2008	Furthermore, abrogation of cyclin G1 enhanced p53 accumulation, phosphorylation of p53 at Ser-15 residue, and increased expression of cyclin-dependent kinase inhibitors p21 and p27.	Serine	90-93	P53	Homo sapiens	83-86
18377724-6	2008	CAS overexpression enhanced p53 accumulation induced by doxorubicin, 5-fluorouracil, cisplatin, tamoxifen, and etoposide.	Fluorouracil	69-83	P53	Homo sapiens	28-31
18377724-6	2008	CAS overexpression enhanced p53 accumulation induced by doxorubicin, 5-fluorouracil, cisplatin, tamoxifen, and etoposide.	Cisplatin	85-94	P53	Homo sapiens	28-31
18377724-6	2008	CAS overexpression enhanced p53 accumulation induced by doxorubicin, 5-fluorouracil, cisplatin, tamoxifen, and etoposide.	Tamoxifen	96-105	P53	Homo sapiens	28-31
18393238-3	2008	Immunohistochemical staining for P53 was performed on paraffin-embedded sections.	Paraffin	54-62	P53	Homo sapiens	33-36
18339864-3	2008	Under these conditions, phosphorylation of Rad17 was also suppressed, whereas phosphorylation of p53 at Ser(15) was not affected, indicating a specific defect in phosphorylation of a subset of the ATR kinase substrates.	Serine	104-107	P53	Homo sapiens	97-100
18174154-3	2008	During cisplatin-mediated apoptosis in COS7 cells in which the endogenous p53 is inactivated by SV40 large T antigen, p73 was induced to accumulate in association with a significant down-regulation of Plk1.	Cisplatin	7-16	P53	Homo sapiens	74-77
18242117-3	2008	As mutations in the tumour suppressor gene TP53 are the most common genetic alterations involved in human cancers, especially esophageal tumours, the aim of this work was to establish the mutational pattern induced by acetaldehyde in vitro on the TP53 gene, and to compare this pattern with that found in human alcohol-related tumours.	Alcohols	311-318	P53	Homo sapiens	43-47
18242117-3	2008	As mutations in the tumour suppressor gene TP53 are the most common genetic alterations involved in human cancers, especially esophageal tumours, the aim of this work was to establish the mutational pattern induced by acetaldehyde in vitro on the TP53 gene, and to compare this pattern with that found in human alcohol-related tumours.	Alcohols	311-318	P53	Homo sapiens	247-251
17906691-4	2008	Pharmacological activation of the R2 subunits by the cAMP analogue 8-Cl-cAMP inhibited proliferation and increased caspase-3 activity by 68.77+/-10.5 and 72+/-9% respectively, in all cell lines with the exception of the only p53-mutated one.	8-chloro-cyclic adenosine monophosphate	53-57	P53	Homo sapiens	225-228
17906691-4	2008	Pharmacological activation of the R2 subunits by the cAMP analogue 8-Cl-cAMP inhibited proliferation and increased caspase-3 activity by 68.77+/-10.5 and 72+/-9% respectively, in all cell lines with the exception of the only p53-mutated one.	8-chloro-cyclic adenosine monophosphate	67-76	P53	Homo sapiens	225-228
18310316-0	2008	Small molecular weight variants of p53 are expressed in human melanoma cells and are induced by the DNA-damaging agent cisplatin.	Cisplatin	119-128	P53	Homo sapiens	35-38
18310316-5	2008	We also characterized the relationship between the expression of p53, p53 isoforms, and p53 target genes following treatment with the DNA-damaging agent cisplatin.	Cisplatin	153-162	P53	Homo sapiens	65-68
18310316-5	2008	We also characterized the relationship between the expression of p53, p53 isoforms, and p53 target genes following treatment with the DNA-damaging agent cisplatin.	Cisplatin	153-162	P53	Homo sapiens	70-73
18310316-5	2008	We also characterized the relationship between the expression of p53, p53 isoforms, and p53 target genes following treatment with the DNA-damaging agent cisplatin.	Cisplatin	153-162	P53	Homo sapiens	70-73
18310316-9	2008	Treatment with cisplatin had differential effects on WTp53 and the small molecular weight form of p53 that were cell line dependent.	Cisplatin	15-24	P53	Homo sapiens	55-58
18281164-9	2008	Here we showed that cadmium induced p53-dependent apoptosis through cooperation between Bcl-xl down regulation without changing the Bcl-2 and Bax expression, the common target of p53.	Cadmium	20-27	P53	Homo sapiens	36-39
18281164-9	2008	Here we showed that cadmium induced p53-dependent apoptosis through cooperation between Bcl-xl down regulation without changing the Bcl-2 and Bax expression, the common target of p53.	Cadmium	20-27	P53	Homo sapiens	179-182
18281164-12	2008	All of these findings establish an important role of p53 and mitochondrial function in cadmium induced toxic environment in the host.	Cadmium	87-94	P53	Homo sapiens	53-56
18507046-6	2008	Platinum sensitivity was associated with heterozygosity at the TP53 locus (p = 0.006).	Platinum	0-8	P53	Homo sapiens	63-67
18260647-2	2008	After formation of the SET7/9.p53-Lys4-NH 3 (+).AdoMet complex, the following events occur: (i) the appearance of a water channel, (ii) a depronation of p53-Lys4-NH 3 (+) via this water channel into the aqueous solvent, and (iii) AdoMet methylation of p53-Lys4-NH 2 to form p53-Lys4-N(Me)H 2 (+).	Water	116-121	P53	Homo sapiens	30-33
18260647-2	2008	After formation of the SET7/9.p53-Lys4-NH 3 (+).AdoMet complex, the following events occur: (i) the appearance of a water channel, (ii) a depronation of p53-Lys4-NH 3 (+) via this water channel into the aqueous solvent, and (iii) AdoMet methylation of p53-Lys4-NH 2 to form p53-Lys4-N(Me)H 2 (+).	Water	116-121	P53	Homo sapiens	153-156
18260647-2	2008	After formation of the SET7/9.p53-Lys4-NH 3 (+).AdoMet complex, the following events occur: (i) the appearance of a water channel, (ii) a depronation of p53-Lys4-NH 3 (+) via this water channel into the aqueous solvent, and (iii) AdoMet methylation of p53-Lys4-NH 2 to form p53-Lys4-N(Me)H 2 (+).	Water	116-121	P53	Homo sapiens	153-156
18260647-2	2008	After formation of the SET7/9.p53-Lys4-NH 3 (+).AdoMet complex, the following events occur: (i) the appearance of a water channel, (ii) a depronation of p53-Lys4-NH 3 (+) via this water channel into the aqueous solvent, and (iii) AdoMet methylation of p53-Lys4-NH 2 to form p53-Lys4-N(Me)H 2 (+).	Water	116-121	P53	Homo sapiens	153-156
18260647-2	2008	After formation of the SET7/9.p53-Lys4-NH 3 (+).AdoMet complex, the following events occur: (i) the appearance of a water channel, (ii) a depronation of p53-Lys4-NH 3 (+) via this water channel into the aqueous solvent, and (iii) AdoMet methylation of p53-Lys4-NH 2 to form p53-Lys4-N(Me)H 2 (+).	Water	180-185	P53	Homo sapiens	30-33
18260647-2	2008	After formation of the SET7/9.p53-Lys4-NH 3 (+).AdoMet complex, the following events occur: (i) the appearance of a water channel, (ii) a depronation of p53-Lys4-NH 3 (+) via this water channel into the aqueous solvent, and (iii) AdoMet methylation of p53-Lys4-NH 2 to form p53-Lys4-N(Me)H 2 (+).	Water	180-185	P53	Homo sapiens	153-156
18260647-2	2008	After formation of the SET7/9.p53-Lys4-NH 3 (+).AdoMet complex, the following events occur: (i) the appearance of a water channel, (ii) a depronation of p53-Lys4-NH 3 (+) via this water channel into the aqueous solvent, and (iii) AdoMet methylation of p53-Lys4-NH 2 to form p53-Lys4-N(Me)H 2 (+).	Water	180-185	P53	Homo sapiens	153-156
18260647-2	2008	After formation of the SET7/9.p53-Lys4-NH 3 (+).AdoMet complex, the following events occur: (i) the appearance of a water channel, (ii) a depronation of p53-Lys4-NH 3 (+) via this water channel into the aqueous solvent, and (iii) AdoMet methylation of p53-Lys4-NH 2 to form p53-Lys4-N(Me)H 2 (+).	Water	180-185	P53	Homo sapiens	153-156
18260647-4	2008	Without a water channel, the substrate p53-Lys4-N(Me)H is not available because the proton dissociation p53-Lys4-N(Me)H 2 (+) --&gt; p53-Lys4-N(Me)H + H (+) does not occur.	Water	10-15	P53	Homo sapiens	39-42
18260647-4	2008	Without a water channel, the substrate p53-Lys4-N(Me)H is not available because the proton dissociation p53-Lys4-N(Me)H 2 (+) --&gt; p53-Lys4-N(Me)H + H (+) does not occur.	Water	10-15	P53	Homo sapiens	104-107
18260647-4	2008	Without a water channel, the substrate p53-Lys4-N(Me)H is not available because the proton dissociation p53-Lys4-N(Me)H 2 (+) --&gt; p53-Lys4-N(Me)H + H (+) does not occur.	Water	10-15	P53	Homo sapiens	104-107
18370854-4	2008	The potentially adverse sequelae of curcumin"s effects on proapoptotic genes, particularly p53, represent a cause for current debate.	Curcumin	36-44	P53	Homo sapiens	91-94
18260647-5	2008	The lack of formation of a water channel is due to the positioning of the methyl substituent of the SET7/9.p53-Lys4-N(Me)H 2 (+).AdoMet complex.	Water	27-32	P53	Homo sapiens	107-110
18506998-11	2008	Immunohistochemical staining showed increased expression of p65 after paclitaxel treatment, while paclitaxel in combination with AdIkappaBalpha intratumoral injection eliminated this expression accompanied by the slightly reduced expression of VEGF, with stable p53 status.	Paclitaxel	98-108	P53	Homo sapiens	262-265
18507060-5	2008	Immunohistochemical reactions were performed for p53 staining in paraffin embedded histological sections of oral leukoplakia lesions.	Paraffin	65-73	P53	Homo sapiens	49-52
18510179-11	2008	This study shows that the serum p53 Ab level is easily changed by taxane.	taxane	66-72	P53	Homo sapiens	32-35
18510179-8	2008	The expression of p53 Abs was significantly reduced by taxane (P = 0.006).	taxane	55-61	P53	Homo sapiens	18-21
18256546-1	2008	Florescence anisotropy measurements using FAM-labelled p53 peptides showed that the binding of the peptides to MDM2 was dependant upon the phosphorylation of p53 at Thr18 and that this binding was modulated by the electrostatic properties of MDM2.	UNII-PYZ33YLR8A	165-170	P53	Homo sapiens	55-58
18409049-2	2008	We previously reported that cAMP-dependent protein kinase (PKA)-mediated activator protein-2 (AP-2) activation was responsible for the expression of Her-2/ErbB2 in p53-inactivated mammary epithelial cells (Yang et al., 2006).	Cyclic AMP	28-32	P53	Homo sapiens	164-167
18174244-0	2008	Resveratrol modulates DNA double-strand break repair pathways in an ATM/ATR-p53- and -Nbs1-dependent manner.	Resveratrol	0-11	P53	Homo sapiens	76-79
18510179-13	2008	The p53 Ab-negative patients may predict a high clinical OR rate in anthracycline-based NAC.	Anthracyclines	68-81	P53	Homo sapiens	4-7
18064041-3	2008	Here, we have investigated the contribution of p53 and caspase-2 to apoptotic cell death and mitotic catastrophe in cisplatin-treated ovarian carcinoma cell lines.	Cisplatin	116-125	P53	Homo sapiens	47-50
18256546-1	2008	Florescence anisotropy measurements using FAM-labelled p53 peptides showed that the binding of the peptides to MDM2 was dependant upon the phosphorylation of p53 at Thr18 and that this binding was modulated by the electrostatic properties of MDM2.	UNII-PYZ33YLR8A	165-170	P53	Homo sapiens	158-161
18249159-4	2008	We show that the anti-cancer drug cisplatin or UV light activates both JNK and ERK in human glioblastoma cells lacking functional p53.	Cisplatin	34-43	P53	Homo sapiens	130-133
18316600-9	2008	Our results indicate that ERK and JNK MAPK/Elk-1/Egr-1 signal cascade is required for p53-independent transcriptional activation of p21(Waf1/Cip1) in response to curcumin in U-87MG human glioblastoma cells.	Curcumin	162-170	P53	Homo sapiens	86-89
18310282-4	2008	Reporter gene activity in p53(Delta)(5,6) MEC transfected with the aromatase promoter or the cAMP-responsive element (CRE) minimal promoter was higher than wild-type MEC.	Cyclic AMP	93-97	P53	Homo sapiens	26-29
18155176-1	2008	Overexpression of the tumor suppressor gene, wild-type p53 (wtp53), using adenoviral vectors (Adp53) has been suggested to kill cancer cells by hydroperoxide-mediated oxidative stress [1,2] and nutrient distress induced by the glucose analog, 2-deoxyglucose (2DG), has been suggested to enhance tumor cell killing by agents that induce oxidative stress via disrupting hydroperoxide metabolism [3,4].	Hydrogen Peroxide	144-157	P53	Homo sapiens	55-58
18155176-1	2008	Overexpression of the tumor suppressor gene, wild-type p53 (wtp53), using adenoviral vectors (Adp53) has been suggested to kill cancer cells by hydroperoxide-mediated oxidative stress [1,2] and nutrient distress induced by the glucose analog, 2-deoxyglucose (2DG), has been suggested to enhance tumor cell killing by agents that induce oxidative stress via disrupting hydroperoxide metabolism [3,4].	Glucose	227-234	P53	Homo sapiens	55-58
18438339-6	2008	p53 expression in T47D cells was higher than in MCF-7 cells where only doxorubicin induced strongly p53 expression.	Doxorubicin	71-82	P53	Homo sapiens	0-3
18155176-1	2008	Overexpression of the tumor suppressor gene, wild-type p53 (wtp53), using adenoviral vectors (Adp53) has been suggested to kill cancer cells by hydroperoxide-mediated oxidative stress [1,2] and nutrient distress induced by the glucose analog, 2-deoxyglucose (2DG), has been suggested to enhance tumor cell killing by agents that induce oxidative stress via disrupting hydroperoxide metabolism [3,4].	Hydrogen Peroxide	368-381	P53	Homo sapiens	55-58
18438339-6	2008	p53 expression in T47D cells was higher than in MCF-7 cells where only doxorubicin induced strongly p53 expression.	Doxorubicin	71-82	P53	Homo sapiens	100-103
18438339-9	2008	TGF-beta(1) production in carcinoma cells was associated with doxorubicine-mediated p53 expression in MCF-7 cells or high basal level of p53 in T47D cells.	Doxorubicin	62-74	P53	Homo sapiens	84-87
18380010-6	2008	Cisplatin treatment decreased the amount of 39 kDa C-terminal ASK1 fragments in mutant p53 cell lines suggesting a decrease in cleavage associated with apoptosis.	Cisplatin	0-9	P53	Homo sapiens	87-90
18191995-10	2008	While the level of p53 expression enhanced both the death-inducing and TRAIL-sensitizing effects of cisplatin, TRAIL-induced cell death was found to occur independent of p53.	Cisplatin	100-109	P53	Homo sapiens	19-22
18191995-12	2008	This result is due to both p53-dependent (cisplatin) and -independent (TRAIL) mechanisms.	Cisplatin	42-51	P53	Homo sapiens	27-30
17721990-8	2008	Pretreatment with nitric oxide (NO) scavengers could inhibit 5 microM MG/20 mM glucose-induced cytochrome c release, decrease activation of caspase-9 and caspase-3, and increase the gene expression and protein levels of p53 and p21, which are known to be involved in apoptotic signaling.	Nitric Oxide	18-30	P53	Homo sapiens	220-223
17879958-4	2008	We show that curcumin, an important inhibitor of CSN-associated kinases, can downregulate not only CSN5 but also MDM2, which results in p53 stabilization.	Curcumin	13-21	P53	Homo sapiens	136-139
17721990-8	2008	Pretreatment with nitric oxide (NO) scavengers could inhibit 5 microM MG/20 mM glucose-induced cytochrome c release, decrease activation of caspase-9 and caspase-3, and increase the gene expression and protein levels of p53 and p21, which are known to be involved in apoptotic signaling.	Glucose	79-86	P53	Homo sapiens	220-223
17721990-9	2008	Inhibition of p53 protein expression using small interfering RNA (siRNA) blocked the activation of p21 and the cell apoptosis induced by 5 microM MG/20 mM glucose.	Glucose	155-162	P53	Homo sapiens	14-17
18203319-4	2008	p53 activity to bind target DNA was evaluated by ELISA using a plate coated with oligonucleotide containing the consensus binding site for p53.	Oligonucleotides	81-96	P53	Homo sapiens	0-3
18205229-2	2008	The presence of Arg/Arg genotype at codon 72 of TP53 gene was characterized as a risk factor in development of cervical cancer.	Arginine	16-19	P53	Homo sapiens	48-52
18205229-2	2008	The presence of Arg/Arg genotype at codon 72 of TP53 gene was characterized as a risk factor in development of cervical cancer.	Arginine	20-23	P53	Homo sapiens	48-52
18203319-4	2008	p53 activity to bind target DNA was evaluated by ELISA using a plate coated with oligonucleotide containing the consensus binding site for p53.	Oligonucleotides	81-96	P53	Homo sapiens	139-142
18319335-6	2008	One of these ATFs, 3ZF-1-VP, promoted paclitaxel resistance in cell lines having mutated or inactivated p53, such as MDA-MB-435 and Kaposi"s sarcoma cell lines.	Paclitaxel	38-48	P53	Homo sapiens	104-107
18344606-3	2008	Phosphorylation of p53 protein at Ser-15 and Ser-20 residues was activated earlier than the obvious increase in p53 expression.	Serine	34-37	P53	Homo sapiens	19-22
18060474-3	2008	The objective of the present study was to elucidate the effect of hydrogen peroxide (H2O2) on apoptotic signal molecules in vitro in SiHa and CaSki cell lines expressing the human papilloma virus 16 E6 protein, which causes the ubiquitin-mediated degradation of p53 protein and is thus p53 deficient.	Hydrogen Peroxide	66-83	P53	Homo sapiens	262-265
18060474-3	2008	The objective of the present study was to elucidate the effect of hydrogen peroxide (H2O2) on apoptotic signal molecules in vitro in SiHa and CaSki cell lines expressing the human papilloma virus 16 E6 protein, which causes the ubiquitin-mediated degradation of p53 protein and is thus p53 deficient.	Hydrogen Peroxide	66-83	P53	Homo sapiens	286-289
18060474-3	2008	The objective of the present study was to elucidate the effect of hydrogen peroxide (H2O2) on apoptotic signal molecules in vitro in SiHa and CaSki cell lines expressing the human papilloma virus 16 E6 protein, which causes the ubiquitin-mediated degradation of p53 protein and is thus p53 deficient.	Hydrogen Peroxide	85-89	P53	Homo sapiens	262-265
18060474-3	2008	The objective of the present study was to elucidate the effect of hydrogen peroxide (H2O2) on apoptotic signal molecules in vitro in SiHa and CaSki cell lines expressing the human papilloma virus 16 E6 protein, which causes the ubiquitin-mediated degradation of p53 protein and is thus p53 deficient.	Hydrogen Peroxide	85-89	P53	Homo sapiens	286-289
18288414-2	2008	Several reports have focused on p53 polymorphisms as risk factors in lung cancer, in particular at codon 72 of exon 4, encoding either an arginine (Arg72R) or a proline (Pro72P) amino acid.	Arginine	138-146	P53	Homo sapiens	32-35
21479403-7	2008	The expression of Bax and cytochrome c, downstream targets of p53, was markedly increased by treatment with higher concentrations of equol.	Equol	133-138	P53	Homo sapiens	62-65
21479403-8	2008	Equol-induced cell cycle arrest and apoptosis apparently involves a p53-dependent pathway in different types of breast cancer cells.	Equol	0-5	P53	Homo sapiens	68-71
18082226-6	2008	Carbon- and neon-ion microbeam irradiation similarly caused almost twofold increments in the levels of serine 15-phosphorylated p53 proteins, irrespective of whether 0.00026, 0.0013 or 0.0066% of cells were targeted.	Carbon	0-6	P53	Homo sapiens	128-131
18082226-6	2008	Carbon- and neon-ion microbeam irradiation similarly caused almost twofold increments in the levels of serine 15-phosphorylated p53 proteins, irrespective of whether 0.00026, 0.0013 or 0.0066% of cells were targeted.	Serine	103-109	P53	Homo sapiens	128-131
18267949-0	2008	p53-dependent global nucleotide excision repair of cisplatin-induced intrastrand cross links in human cells.	Cisplatin	51-60	P53	Homo sapiens	0-3
18267949-5	2008	We have investigated whether the p53 tumour suppressor status affects global NER of cisplatin-induced intrastrand cross links in human cells.	Cisplatin	84-93	P53	Homo sapiens	33-36
18267949-7	2008	We demonstrate that the absence of functional p53 leads to persistence of both cisplatin-induced intrastrand cross links in the genome, suggesting that p53 regulates NER of these DNA lesions.	Cisplatin	79-88	P53	Homo sapiens	46-49
18267949-7	2008	We demonstrate that the absence of functional p53 leads to persistence of both cisplatin-induced intrastrand cross links in the genome, suggesting that p53 regulates NER of these DNA lesions.	Cisplatin	79-88	P53	Homo sapiens	152-155
18267949-9	2008	Given the frequency of p53 mutations in human tumours, these results may have implications for the use of cisplatin in cancer chemotherapy.	Cisplatin	106-115	P53	Homo sapiens	23-26
17983740-2	2008	In this paper, an on-chip oligonucleotide ligation approach that arrayed a series of functionalized beads in a single microfluidic channel was described for detection of low-abundant point mutations in p53 gene.	Oligonucleotides	26-41	P53	Homo sapiens	202-205
18315954-0	2008	Protective effect of p53 in vascular smooth muscle cells against nitric oxide-induced apoptosis is mediated by up-regulation of heme oxygenase-2.	Nitric Oxide	65-77	P53	Homo sapiens	21-24
18315954-2	2008	In this study, we investigated the role of p53 in nitric oxide (NO)-induced apoptosis in vascular smooth muscle cells (VSMCs).	Nitric Oxide	50-62	P53	Homo sapiens	43-46
18086244-2	2008	In this study, we have investigated the effects of naringenin (NG), a naturally occurring citrus flavonone, on the removal of UVB-induced cyclobutane pyrimidine dimers (CPD) from the genome and apoptosis in immortalized p53-mutant human keratinocyte HaCaT cells.	naringenin	51-61	P53	Homo sapiens	220-223
18086244-2	2008	In this study, we have investigated the effects of naringenin (NG), a naturally occurring citrus flavonone, on the removal of UVB-induced cyclobutane pyrimidine dimers (CPD) from the genome and apoptosis in immortalized p53-mutant human keratinocyte HaCaT cells.	naringenin	63-65	P53	Homo sapiens	220-223
18237807-11	2008	Furthermore, nuclear EGFR was found in complex with TP53, phosphorylated at S15, and with MDC1, following irradiation and BBI treatment.	Amiodarone	122-125	P53	Homo sapiens	52-56
18237807-16	2008	CONCLUSION: These data indicate that BBI stimulates complex formation between EGFR, TP53 and MDC1 protein in wt.	Amiodarone	37-40	P53	Homo sapiens	84-88
17846083-5	2008	Apoptosis was prevented by the p53 inhibitor pifithrin and by p53 antisense oligonucleotides, indicating dependency of force-induced apoptosis on p53.	Oligonucleotides	76-92	P53	Homo sapiens	62-65
17724473-4	2008	In this study, we found that P-TEFb inhibitors block the phosphorylation of p53 induced by doxorubicin.	Doxorubicin	91-102	P53	Homo sapiens	76-79
17724473-5	2008	Furthermore, treatment of cells with P-TEFb inhibitors together with doxorubicin inhibits doxorubicin-induced binding of p53 to DNA and p53 transcriptional activity.	Doxorubicin	69-80	P53	Homo sapiens	121-124
17724473-5	2008	Furthermore, treatment of cells with P-TEFb inhibitors together with doxorubicin inhibits doxorubicin-induced binding of p53 to DNA and p53 transcriptional activity.	Doxorubicin	69-80	P53	Homo sapiens	136-139
17724473-5	2008	Furthermore, treatment of cells with P-TEFb inhibitors together with doxorubicin inhibits doxorubicin-induced binding of p53 to DNA and p53 transcriptional activity.	Doxorubicin	90-101	P53	Homo sapiens	121-124
17724473-5	2008	Furthermore, treatment of cells with P-TEFb inhibitors together with doxorubicin inhibits doxorubicin-induced binding of p53 to DNA and p53 transcriptional activity.	Doxorubicin	90-101	P53	Homo sapiens	136-139
18284706-5	2008	Wild type full-length p53 protein was produced in fusion with biotin carboxyl carrier peptide (BCCP) or hexahistidine [(His)6] using pAK400 and pET15b(+) vectors, respectively.	biotin carboxyl carrier peptide	62-93	P53	Homo sapiens	22-25
18079115-0	2008	Inhibition of AMP-activated protein kinase sensitizes cancer cells to cisplatin-induced apoptosis via hyper-induction of p53.	Cisplatin	70-79	P53	Homo sapiens	121-124
18079115-6	2008	The inhibition of AMPK in those cells and in xenografts of HCT116 resulted in a remarkable increase in cisplatin-induced apoptosis, which was associated with hyper-induction of the tumor suppressor p53.	Cisplatin	103-112	P53	Homo sapiens	198-201
18079115-7	2008	We further showed that ERK, but not ATM (ataxia telangiectasia mutated) and ATR (ATM- and Rad3-related) kinases, was involved in the hyper-induction of p53 by the inhibition of cisplatin-induced AMPK.	Cisplatin	177-186	P53	Homo sapiens	152-155
18059187-0	2008	Application of doxorubicin-induced rAAV2-p53 gene delivery in combined chemotherapy and gene therapy for hepatocellular carcinoma.	Doxorubicin	15-26	P53	Homo sapiens	41-44
18059187-5	2008	Using reporter assays, we showed that the DOX-treated hepatomas became more susceptible to rAAV2 infection in comparison to untreated controls: the permissiveness increased &gt;350-fold and &gt;120-fold for HepG2 (p53 wild-type) and Hep3B (p53 null) hepatomas, respectively.	Doxorubicin	42-45	P53	Homo sapiens	214-217
18059187-5	2008	Using reporter assays, we showed that the DOX-treated hepatomas became more susceptible to rAAV2 infection in comparison to untreated controls: the permissiveness increased &gt;350-fold and &gt;120-fold for HepG2 (p53 wild-type) and Hep3B (p53 null) hepatomas, respectively.	Doxorubicin	42-45	P53	Homo sapiens	240-243
18059187-7	2008	Compared to rAAV2-p53 transduction alone, rAAV2-p53 transduction with DOX resulted in a &gt;16-fold induction of p53 expression.	Doxorubicin	70-73	P53	Homo sapiens	48-51
18059187-7	2008	Compared to rAAV2-p53 transduction alone, rAAV2-p53 transduction with DOX resulted in a &gt;16-fold induction of p53 expression.	Doxorubicin	70-73	P53	Homo sapiens	48-51
18059187-11	2008	The 50% reduction in DOX administration--from 1 microM to 0.5 microM--revealed the antitumor property of the rAAV2-p53 transduction as well as the joint cytotoxicity of DOX and rAAV2-p53 against the p53-null hepatomas.	Doxorubicin	21-24	P53	Homo sapiens	115-118
18059187-11	2008	The 50% reduction in DOX administration--from 1 microM to 0.5 microM--revealed the antitumor property of the rAAV2-p53 transduction as well as the joint cytotoxicity of DOX and rAAV2-p53 against the p53-null hepatomas.	Doxorubicin	21-24	P53	Homo sapiens	183-186
18059187-11	2008	The 50% reduction in DOX administration--from 1 microM to 0.5 microM--revealed the antitumor property of the rAAV2-p53 transduction as well as the joint cytotoxicity of DOX and rAAV2-p53 against the p53-null hepatomas.	Doxorubicin	21-24	P53	Homo sapiens	183-186
18059187-13	2008	Combined DOX and rAAV2-p53 administration may facilitate more efficient treatment for the HCC caused by p53 mutations.	Doxorubicin	9-12	P53	Homo sapiens	104-107
18056705-2	2008	In this study, we have found that glucose depletion promotes the phosphorylation of AMP-activated protein kinase catalytic subunit alpha (AMPKalpha) in association with a significant up-regulation of p53, thereby inducing p53-dependent apoptosis in vivo and in vitro.	Glucose	34-41	P53	Homo sapiens	200-203
18056705-2	2008	In this study, we have found that glucose depletion promotes the phosphorylation of AMP-activated protein kinase catalytic subunit alpha (AMPKalpha) in association with a significant up-regulation of p53, thereby inducing p53-dependent apoptosis in vivo and in vitro.	Glucose	34-41	P53	Homo sapiens	222-225
18056705-5	2008	Of note, glucose deprivation led to a significant accumulation of p53 phosphorylated at Ser-46, but not at Ser-15 and Ser-20, and a transcriptional induction of p53 as well as proapoptotic p53 AIP1.	Serine	88-91	P53	Homo sapiens	66-69
18056705-6	2008	Small interference RNA-mediated knockdown of p53 caused an inhibition of apoptosis following glucose depletion.	Glucose	93-100	P53	Homo sapiens	45-48
18056705-8	2008	Under our experimental conditions, down-regulation of AMPKalpha caused an attenuation of p53 accumulation and its phosphorylation at Ser-46.	Serine	133-136	P53	Homo sapiens	89-92
18056705-11	2008	Taken together, our present findings suggest that AMPK-dependent transcriptional induction and phosphorylation of p53 at Ser-46 play a crucial role in the induction of apoptosis under carbon source depletion.	Serine	121-124	P53	Homo sapiens	114-117
18056705-11	2008	Taken together, our present findings suggest that AMPK-dependent transcriptional induction and phosphorylation of p53 at Ser-46 play a crucial role in the induction of apoptosis under carbon source depletion.	Carbon	184-190	P53	Homo sapiens	114-117
18279610-1	2008	BACKGROUND &amp; OBJECTIVE: Peptide p53(N15)Ant from the amino-terminal of p53 fused with cell penetrating peptide antennapedia (Ant) can induce rapid cell death resembling necrosis in breast cancer and pancreatic cancer, whereas it is low cytotoxic to normal cells.	Adenosine Monophosphate	12-15	P53	Homo sapiens	36-39
18279610-1	2008	BACKGROUND &amp; OBJECTIVE: Peptide p53(N15)Ant from the amino-terminal of p53 fused with cell penetrating peptide antennapedia (Ant) can induce rapid cell death resembling necrosis in breast cancer and pancreatic cancer, whereas it is low cytotoxic to normal cells.	Adenosine Monophosphate	12-15	P53	Homo sapiens	75-78
18179182-5	2008	The cysteine residues on the exterior of the p53 molecule were derivatized for the attachment of gold nanoparticle/streptavidin conjugates capped with multiple ferrocene (Fc) groups.	Cysteine	4-12	P53	Homo sapiens	45-48
17959154-9	2008	Finally, we show that resveratrol induced ubiquitin-independent degradation of tumor suppressor gene protein p53 and inhibited p53-induced apoptosis in chondrocytes in a dose-dependent manner.	Resveratrol	22-33	P53	Homo sapiens	109-112
17959154-9	2008	Finally, we show that resveratrol induced ubiquitin-independent degradation of tumor suppressor gene protein p53 and inhibited p53-induced apoptosis in chondrocytes in a dose-dependent manner.	Resveratrol	22-33	P53	Homo sapiens	127-130
17959154-10	2008	Our results indicate that resveratrol seems to be an effective in vitro anti-inflammatory agent and has a chondroprotective capacity through suppression of (1) IL-1beta- (2) ROS- and (3) tumor suppressor protein p53-production.	Resveratrol	26-37	P53	Homo sapiens	212-215
18281754-4	2008	Glutathione S-transferase-pi and metallo- thionein have been related to the metabolism of platinum drugs, excision repair cross-complementing 1/2 to DNA repair systems, and p53 to apoptosis.	Platinum	90-98	P53	Homo sapiens	173-176
18297607-6	2008	The results also showed that the inhibition of p53 led to a resistance of the C6 cells to 20 microm Cd, decreased the apoptosis and increased the metallothioneins in these cells.	Cadmium	100-102	P53	Homo sapiens	47-50
18297607-7	2008	p53 restoration increased the sensitivity of HaCaT cells to Cd but did not affect the MT expression.	Cadmium	60-62	P53	Homo sapiens	0-3
17846083-5	2008	Apoptosis was prevented by the p53 inhibitor pifithrin and by p53 antisense oligonucleotides, indicating dependency of force-induced apoptosis on p53.	Oligonucleotides	76-92	P53	Homo sapiens	62-65
17846083-7	2008	Prevention of calpain activation by calpeptin or antisense oligonucleotides augmented strain-induced p53 expression and transcriptional activity, resulting in a further increase of apoptotic rate.	Oligonucleotides	59-75	P53	Homo sapiens	101-104
17628743-5	2008	We conclude that PARP inhibitor INO-1001 has high potential for enhancing the anti-tumor effects of chemotherapy agents such as Doxorubicin against p53 deficient breast cancer.	Doxorubicin	128-139	P53	Homo sapiens	148-151
17918180-0	2008	Akt promotes cisplatin resistance in human ovarian cancer cells through inhibition of p53 phosphorylation and nuclear function.	Cisplatin	13-22	P53	Homo sapiens	86-89
17918180-5	2008	Cisplatin induced apoptosis in chemosensitive, but not chemoresistant cells, and this was inhibited by downregulation of p53.	Cisplatin	0-9	P53	Homo sapiens	121-124
17918180-6	2008	Cisplatin upregulated PUMA in a p53-dependent manner, and the presence of PUMA was necessary, but not sufficient for cisplatin-induced apoptosis.	Cisplatin	0-9	P53	Homo sapiens	32-35
17918180-7	2008	p53 was phosphorylated on numerous N-terminal residues, including Ser15, Ser20, in response to cisplatin in chemosensitive, but not chemoresistant cells.	Cisplatin	95-104	P53	Homo sapiens	0-3
17918180-8	2008	Furthermore, activation of Akt inhibited the cisplatin-induced upregulation of PUMA, and suppressed cisplatin-induced p53 phosphorylation, while inhibition of Akt increased total and phospho-p53 contents and sensitized p53 wild-type, chemoresistant cells to cisplatin-induced apoptosis.	Cisplatin	45-54	P53	Homo sapiens	191-194
17918180-8	2008	Furthermore, activation of Akt inhibited the cisplatin-induced upregulation of PUMA, and suppressed cisplatin-induced p53 phosphorylation, while inhibition of Akt increased total and phospho-p53 contents and sensitized p53 wild-type, chemoresistant cells to cisplatin-induced apoptosis.	Cisplatin	45-54	P53	Homo sapiens	191-194
17918180-8	2008	Furthermore, activation of Akt inhibited the cisplatin-induced upregulation of PUMA, and suppressed cisplatin-induced p53 phosphorylation, while inhibition of Akt increased total and phospho-p53 contents and sensitized p53 wild-type, chemoresistant cells to cisplatin-induced apoptosis.	Cisplatin	100-109	P53	Homo sapiens	118-121
17918180-8	2008	Furthermore, activation of Akt inhibited the cisplatin-induced upregulation of PUMA, and suppressed cisplatin-induced p53 phosphorylation, while inhibition of Akt increased total and phospho-p53 contents and sensitized p53 wild-type, chemoresistant cells to cisplatin-induced apoptosis.	Cisplatin	100-109	P53	Homo sapiens	118-121
17918180-9	2008	Finally, mutation of Ser15 and/or Ser20, but not of Ser37, to alanine significantly attenuated the ability of p53 to facilitate CDDP-induced apoptosis, and this was independent of PUMA expression.	Cisplatin	128-132	P53	Homo sapiens	110-113
17918180-10	2008	These results support the hypothesis that p53 is a determinant of CDDP sensitivity, and suggest that Akt contributes to chemoresistance, in part, by attenuating p53-mediated PUMA upregulation and phosphorylation of p53, which are essential, but independent determinants of sensitivity to CDDP-induced apoptosis.	Cisplatin	66-70	P53	Homo sapiens	42-45
17918180-10	2008	These results support the hypothesis that p53 is a determinant of CDDP sensitivity, and suggest that Akt contributes to chemoresistance, in part, by attenuating p53-mediated PUMA upregulation and phosphorylation of p53, which are essential, but independent determinants of sensitivity to CDDP-induced apoptosis.	Cisplatin	66-70	P53	Homo sapiens	161-164
17977830-5	2008	Upon treatment with 5-aza-CdR, ATR activation is clearly associated with p53 phosphorylation at Ser(15), but not at Thr(18), Ser(20), or Ser(37).	Serine	96-99	P53	Homo sapiens	73-76
17918180-10	2008	These results support the hypothesis that p53 is a determinant of CDDP sensitivity, and suggest that Akt contributes to chemoresistance, in part, by attenuating p53-mediated PUMA upregulation and phosphorylation of p53, which are essential, but independent determinants of sensitivity to CDDP-induced apoptosis.	Cisplatin	66-70	P53	Homo sapiens	161-164
17918180-10	2008	These results support the hypothesis that p53 is a determinant of CDDP sensitivity, and suggest that Akt contributes to chemoresistance, in part, by attenuating p53-mediated PUMA upregulation and phosphorylation of p53, which are essential, but independent determinants of sensitivity to CDDP-induced apoptosis.	Cisplatin	288-292	P53	Homo sapiens	161-164
17918180-10	2008	These results support the hypothesis that p53 is a determinant of CDDP sensitivity, and suggest that Akt contributes to chemoresistance, in part, by attenuating p53-mediated PUMA upregulation and phosphorylation of p53, which are essential, but independent determinants of sensitivity to CDDP-induced apoptosis.	Cisplatin	288-292	P53	Homo sapiens	161-164
17977830-8	2008	It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells.	Lysine	83-86	P53	Homo sapiens	216-219
17977830-8	2008	It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells.	Lysine	83-86	P53	Homo sapiens	216-219
17977830-6	2008	This specific p53 phosphorylation at Ser(15) in turn results in acetylation of p53 at Lys(320) and Lys(373)/Lys(382) through transcriptional cofactors p300/CBP-associated factor and p300, respectively.	Serine	37-40	P53	Homo sapiens	14-17
17977830-6	2008	This specific p53 phosphorylation at Ser(15) in turn results in acetylation of p53 at Lys(320) and Lys(373)/Lys(382) through transcriptional cofactors p300/CBP-associated factor and p300, respectively.	Serine	37-40	P53	Homo sapiens	79-82
17977830-6	2008	This specific p53 phosphorylation at Ser(15) in turn results in acetylation of p53 at Lys(320) and Lys(373)/Lys(382) through transcriptional cofactors p300/CBP-associated factor and p300, respectively.	Lysine	86-89	P53	Homo sapiens	14-17
17977830-6	2008	This specific p53 phosphorylation at Ser(15) in turn results in acetylation of p53 at Lys(320) and Lys(373)/Lys(382) through transcriptional cofactors p300/CBP-associated factor and p300, respectively.	Lysine	86-89	P53	Homo sapiens	79-82
17977830-6	2008	This specific p53 phosphorylation at Ser(15) in turn results in acetylation of p53 at Lys(320) and Lys(373)/Lys(382) through transcriptional cofactors p300/CBP-associated factor and p300, respectively.	Lysine	99-102	P53	Homo sapiens	14-17
17977830-6	2008	This specific p53 phosphorylation at Ser(15) in turn results in acetylation of p53 at Lys(320) and Lys(373)/Lys(382) through transcriptional cofactors p300/CBP-associated factor and p300, respectively.	Lysine	99-102	P53	Homo sapiens	14-17
17977830-7	2008	These p53 posttranslational modifications are directly responsible for 5-aza-CdR induced p21(Waf1/Cip1) expression because the binding activity of acetylated p53 at Lys(320)/Lys(373)/Lys(382) to the p21(Waf1/Cip1) promoter, as well as p21(Waf1/Cip1) expression itself are significantly increased after 5-aza-CdR treatment.	Lysine	165-168	P53	Homo sapiens	6-9
17977830-7	2008	These p53 posttranslational modifications are directly responsible for 5-aza-CdR induced p21(Waf1/Cip1) expression because the binding activity of acetylated p53 at Lys(320)/Lys(373)/Lys(382) to the p21(Waf1/Cip1) promoter, as well as p21(Waf1/Cip1) expression itself are significantly increased after 5-aza-CdR treatment.	Lysine	165-168	P53	Homo sapiens	158-161
17977830-7	2008	These p53 posttranslational modifications are directly responsible for 5-aza-CdR induced p21(Waf1/Cip1) expression because the binding activity of acetylated p53 at Lys(320)/Lys(373)/Lys(382) to the p21(Waf1/Cip1) promoter, as well as p21(Waf1/Cip1) expression itself are significantly increased after 5-aza-CdR treatment.	Lysine	174-177	P53	Homo sapiens	6-9
17977830-7	2008	These p53 posttranslational modifications are directly responsible for 5-aza-CdR induced p21(Waf1/Cip1) expression because the binding activity of acetylated p53 at Lys(320)/Lys(373)/Lys(382) to the p21(Waf1/Cip1) promoter, as well as p21(Waf1/Cip1) expression itself are significantly increased after 5-aza-CdR treatment.	Lysine	174-177	P53	Homo sapiens	158-161
17977830-7	2008	These p53 posttranslational modifications are directly responsible for 5-aza-CdR induced p21(Waf1/Cip1) expression because the binding activity of acetylated p53 at Lys(320)/Lys(373)/Lys(382) to the p21(Waf1/Cip1) promoter, as well as p21(Waf1/Cip1) expression itself are significantly increased after 5-aza-CdR treatment.	Lysine	174-177	P53	Homo sapiens	6-9
17977830-7	2008	These p53 posttranslational modifications are directly responsible for 5-aza-CdR induced p21(Waf1/Cip1) expression because the binding activity of acetylated p53 at Lys(320)/Lys(373)/Lys(382) to the p21(Waf1/Cip1) promoter, as well as p21(Waf1/Cip1) expression itself are significantly increased after 5-aza-CdR treatment.	Lysine	174-177	P53	Homo sapiens	158-161
17977830-8	2008	It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells.	Serine	46-49	P53	Homo sapiens	23-26
17977830-8	2008	It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells.	Lysine	74-77	P53	Homo sapiens	23-26
17977830-8	2008	It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells.	Lysine	74-77	P53	Homo sapiens	216-219
17977830-8	2008	It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells.	Lysine	74-77	P53	Homo sapiens	216-219
17977830-8	2008	It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells.	Lysine	83-86	P53	Homo sapiens	23-26
17977830-8	2008	It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells.	Lysine	83-86	P53	Homo sapiens	216-219
17977830-8	2008	It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells.	Lysine	83-86	P53	Homo sapiens	216-219
17977830-8	2008	It is of interest that p53 phosphorylation at Ser(15) and acetylations at Lys(320)/Lys(373)/Lys(382) mutually interact in the 5-aza-CdR induced p21(Waf1/Cip1) expression shown by transfection of artificially mutated p53 expression vectors including S15A, K320R, and K373R/K382R into p53-null H1299 cells.	Lysine	83-86	P53	Homo sapiens	23-26
17918207-4	2008	p53 Arg/Arg genotype was significantly increased in ESCC cases compared with control subjects (85.7 vs. 49.6%, P &lt; 0.001), resulting in an elevated ESCC risk (OR = 6.48, 95% CI = 4.65-9.03).	Arginine	4-7	P53	Homo sapiens	0-3
18250140-4	2008	Odds ratio (OR) for patients with SLE and p53 Arg/Arg genotype was 1.875 [95% CI = 1.180-2.979], P = 0.0075 and OR of the Arg/Arg and Arg/Pro genotypes was 1.549 [95% CI = 0.752-3.195], P = 0.2328.	Arginine	46-49	P53	Homo sapiens	42-45
18250140-4	2008	Odds ratio (OR) for patients with SLE and p53 Arg/Arg genotype was 1.875 [95% CI = 1.180-2.979], P = 0.0075 and OR of the Arg/Arg and Arg/Pro genotypes was 1.549 [95% CI = 0.752-3.195], P = 0.2328.	Arginine	50-53	P53	Homo sapiens	42-45
18230104-11	2008	Thus, an up-regulation of p21 expression, via a p53-independent pathway, by cyclosporine A in gingival and oral epithelial cells was suggested.	Cyclosporine	76-90	P53	Homo sapiens	48-51
17918207-4	2008	p53 Arg/Arg genotype was significantly increased in ESCC cases compared with control subjects (85.7 vs. 49.6%, P &lt; 0.001), resulting in an elevated ESCC risk (OR = 6.48, 95% CI = 4.65-9.03).	Arginine	8-11	P53	Homo sapiens	0-3
18250140-4	2008	Odds ratio (OR) for patients with SLE and p53 Arg/Arg genotype was 1.875 [95% CI = 1.180-2.979], P = 0.0075 and OR of the Arg/Arg and Arg/Pro genotypes was 1.549 [95% CI = 0.752-3.195], P = 0.2328.	Arginine	50-53	P53	Homo sapiens	42-45
18250140-4	2008	Odds ratio (OR) for patients with SLE and p53 Arg/Arg genotype was 1.875 [95% CI = 1.180-2.979], P = 0.0075 and OR of the Arg/Arg and Arg/Pro genotypes was 1.549 [95% CI = 0.752-3.195], P = 0.2328.	Arginine	50-53	P53	Homo sapiens	42-45
18250140-4	2008	Odds ratio (OR) for patients with SLE and p53 Arg/Arg genotype was 1.875 [95% CI = 1.180-2.979], P = 0.0075 and OR of the Arg/Arg and Arg/Pro genotypes was 1.549 [95% CI = 0.752-3.195], P = 0.2328.	Arginine	50-53	P53	Homo sapiens	42-45
17918207-5	2008	In addition, among p53 Arg/Arg carriers, HPV infection, smoking, and drinking might further increase the risk of ESCC development.	Arginine	23-26	P53	Homo sapiens	19-22
17918207-5	2008	In addition, among p53 Arg/Arg carriers, HPV infection, smoking, and drinking might further increase the risk of ESCC development.	Arginine	27-30	P53	Homo sapiens	19-22
18155142-3	2008	These changes in apoptosis and p53 expression are purported to result from exposure to altered oxygen tension.	Oxygen	95-101	P53	Homo sapiens	31-34
18202783-3	2008	The data obtained show that normal human lymphocytes exposed in vitro to known DNA-damaging agents, e.g. H2O2, ionizing radiation and mitomycin C, exhibit an asynchronous replication of the genes TP53 and RB1.	Hydrogen Peroxide	105-109	P53	Homo sapiens	196-200
18155142-4	2008	Using a model of villous trophoblast turnover, we examined the effect of 20%, 6% and 1% ambient oxygen (O(2)) on apoptosis, necrosis, proliferation and expression of p53 and related regulators of cell turnover, compared to both fresh tissue.	Oxygen	104-108	P53	Homo sapiens	166-169
18155142-8	2008	The expression of p53, p21 and Mdm2 in both cytotrophoblast and stromal cells was increased following culture in 1% O(2).	Oxygen	116-120	P53	Homo sapiens	18-21
18155142-11	2008	The potential role of the p53-pathway in the control of cell turnover in villous trophoblast and the regulation of p53 by altered O(2) tension merits further investigation.	Oxygen	130-134	P53	Homo sapiens	115-118
17653088-2	2008	We obtained evidence that a type of p53-dependent stress, doxorubicin (Doxo) administration, causes accumulation of p53 in the nucleus of NB cells and phosphorylation of several serine residues in both Doxo-sensitive and -resistant cell lines.	Serine	178-184	P53	Homo sapiens	36-39
17637740-2	2008	We found that the cytotoxic drugs methotrexate (MTX) and 5-fluorouracil (5-FU) were both able to sensitize resistant tumor cells for induction of apoptosis by p53-mediated upregulation of caspase-8.	Fluorouracil	57-71	P53	Homo sapiens	159-162
17637740-2	2008	We found that the cytotoxic drugs methotrexate (MTX) and 5-fluorouracil (5-FU) were both able to sensitize resistant tumor cells for induction of apoptosis by p53-mediated upregulation of caspase-8.	Fluorouracil	73-77	P53	Homo sapiens	159-162
17653088-2	2008	We obtained evidence that a type of p53-dependent stress, doxorubicin (Doxo) administration, causes accumulation of p53 in the nucleus of NB cells and phosphorylation of several serine residues in both Doxo-sensitive and -resistant cell lines.	Doxorubicin	202-206	P53	Homo sapiens	36-39
17637740-3	2008	Increase in caspase-8 messenger RNA and protein expression disabled tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced proliferation and restored sensitivity toward TRAIL-induced apoptosis which was inhibited by transfection of p53 decoy oligonucleotides, p53 shRNA and caspase-8 shRNA.	Oligonucleotides	259-275	P53	Homo sapiens	249-252
17653088-3	2008	Upregulation of p53-downstream molecules in cells and upregulation of Noxa in the mitochondrial fraction were observed only in Doxo-sensitive NB cells.	Doxorubicin	127-131	P53	Homo sapiens	16-19
17653088-0	2008	Stress via p53 pathway causes apoptosis by mitochondrial Noxa upregulation in doxorubicin-treated neuroblastoma cells.	Doxorubicin	78-89	P53	Homo sapiens	11-14
17653088-6	2008	However, in the Doxo-resistant cells, the accumulation in the nucleus and phosphorylation of p53 did not induce p53-downstream p21(Cip1/Waf1) expression and the Noxa upregulation, resulting in the retention of the mitochondrial homeostasis.	Doxorubicin	16-20	P53	Homo sapiens	93-96
17653088-2	2008	We obtained evidence that a type of p53-dependent stress, doxorubicin (Doxo) administration, causes accumulation of p53 in the nucleus of NB cells and phosphorylation of several serine residues in both Doxo-sensitive and -resistant cell lines.	Doxorubicin	58-69	P53	Homo sapiens	36-39
17653088-2	2008	We obtained evidence that a type of p53-dependent stress, doxorubicin (Doxo) administration, causes accumulation of p53 in the nucleus of NB cells and phosphorylation of several serine residues in both Doxo-sensitive and -resistant cell lines.	Doxorubicin	58-69	P53	Homo sapiens	116-119
18230133-6	2008	RESULTS: The advantage of taxane-platinum therapy over platinum-based therapy was seen in the TP53(+), and not in the TP53(-) group.	Platinum	55-63	P53	Homo sapiens	94-98
17653088-2	2008	We obtained evidence that a type of p53-dependent stress, doxorubicin (Doxo) administration, causes accumulation of p53 in the nucleus of NB cells and phosphorylation of several serine residues in both Doxo-sensitive and -resistant cell lines.	Doxorubicin	71-75	P53	Homo sapiens	36-39
17653088-2	2008	We obtained evidence that a type of p53-dependent stress, doxorubicin (Doxo) administration, causes accumulation of p53 in the nucleus of NB cells and phosphorylation of several serine residues in both Doxo-sensitive and -resistant cell lines.	Doxorubicin	71-75	P53	Homo sapiens	116-119
18154926-12	2008	On the other hand, H(2)O(2) induces long-term p53 expression, late expression of PAK1 without activation of p21 promoter.	Hydrogen Peroxide	19-27	P53	Homo sapiens	46-49
18231594-5	2008	We find that expression of the human p53-Mdm2 module in yeast is sufficient to faithfully recapitulate key aspects of p53 regulation in higher eukaryotes, such as Mdm2-dependent targeting of p53 for degradation, sumoylation at lysine 386 and further regulation of this process by p14(ARF).	Lysine	227-233	P53	Homo sapiens	37-40
18231594-5	2008	We find that expression of the human p53-Mdm2 module in yeast is sufficient to faithfully recapitulate key aspects of p53 regulation in higher eukaryotes, such as Mdm2-dependent targeting of p53 for degradation, sumoylation at lysine 386 and further regulation of this process by p14(ARF).	Lysine	227-233	P53	Homo sapiens	118-121
18230133-7	2008	In the TP53(+) group taxane-platinum therapy enhanced the probability of complete remission (p = .018), platinum sensitivity (p = .014), platinum highly sensitive response (p = .038) and longer survival (OS, p = .008).	taxane	21-27	P53	Homo sapiens	7-11
18231594-5	2008	We find that expression of the human p53-Mdm2 module in yeast is sufficient to faithfully recapitulate key aspects of p53 regulation in higher eukaryotes, such as Mdm2-dependent targeting of p53 for degradation, sumoylation at lysine 386 and further regulation of this process by p14(ARF).	Lysine	227-233	P53	Homo sapiens	118-121
18230133-2	2008	TP53 protein plays a differential role in response to DNA-damaging agents and taxanes.	Taxoids	78-85	P53	Homo sapiens	0-4
18230133-6	2008	RESULTS: The advantage of taxane-platinum therapy over platinum-based therapy was seen in the TP53(+), and not in the TP53(-) group.	taxane	26-32	P53	Homo sapiens	94-98
18230133-7	2008	In the TP53(+) group taxane-platinum therapy enhanced the probability of complete remission (p = .018), platinum sensitivity (p = .014), platinum highly sensitive response (p = .038) and longer survival (OS, p = .008).	Platinum	28-36	P53	Homo sapiens	7-11
18230133-6	2008	RESULTS: The advantage of taxane-platinum therapy over platinum-based therapy was seen in the TP53(+), and not in the TP53(-) group.	Platinum	33-41	P53	Homo sapiens	94-98
18230133-7	2008	In the TP53(+) group taxane-platinum therapy enhanced the probability of complete remission (p = .018), platinum sensitivity (p = .014), platinum highly sensitive response (p = .038) and longer survival (OS, p = .008).	Platinum	104-112	P53	Homo sapiens	7-11
18230133-7	2008	In the TP53(+) group taxane-platinum therapy enhanced the probability of complete remission (p = .018), platinum sensitivity (p = .014), platinum highly sensitive response (p = .038) and longer survival (OS, p = .008).	Platinum	104-112	P53	Homo sapiens	7-11
18230133-8	2008	Poor tumor differentiation diminished the advantage from taxane-platinum therapy in the TP53(+) group.	taxane	57-63	P53	Homo sapiens	88-92
18230133-8	2008	Poor tumor differentiation diminished the advantage from taxane-platinum therapy in the TP53(+) group.	Platinum	64-72	P53	Homo sapiens	88-92
18230133-9	2008	In the TP53(-) group PC/PAC was at least equally efficient as taxane-platinum therapy and it enhanced the chance of platinum highly sensitive response (p = .010).	Platinum	116-124	P53	Homo sapiens	7-11
18230133-10	2008	However, in the TP53(-) group taxane-platinum therapy possibly diminished the risk of death in patients over 53 yrs (p = .077).	taxane	30-36	P53	Homo sapiens	16-20
18230133-10	2008	However, in the TP53(-) group taxane-platinum therapy possibly diminished the risk of death in patients over 53 yrs (p = .077).	Platinum	37-45	P53	Homo sapiens	16-20
18230133-12	2008	CONCLUSION: Our results suggest that taxane-platinum therapy is particularly justified in patients with TP53(+) tumors or older than 53 years.	taxane	37-43	P53	Homo sapiens	104-108
18230133-12	2008	CONCLUSION: Our results suggest that taxane-platinum therapy is particularly justified in patients with TP53(+) tumors or older than 53 years.	Platinum	44-52	P53	Homo sapiens	104-108
18036557-0	2008	p53 is important for the anti-proliferative effect of ibuprofen in colon carcinoma cells.	Ibuprofen	54-63	P53	Homo sapiens	0-3
18230133-13	2008	In the group of patients &lt; or =53 yrs and with TP53(-) tumors platinum-based therapy is possibly equally efficient.	Platinum	65-73	P53	Homo sapiens	50-54
18205918-8	2008	We further found stronger correlations of bFGF level and paclitaxel sensitivity in four tumor subgroups (high stage, positive p53 staining, negative aFGF staining, containing higher-than-median bFGF level), compared to all other groups.	Paclitaxel	57-67	P53	Homo sapiens	126-129
18036557-4	2008	Furthermore, results indicate that induction of apoptosis in HCT-116 p53(wt) cells after ibuprofen treatment is in part dependent on a signalling pathway including the neutrophin receptor p75(NTR), p53 and Bax.	Ibuprofen	89-98	P53	Homo sapiens	69-72
18036557-4	2008	Furthermore, results indicate that induction of apoptosis in HCT-116 p53(wt) cells after ibuprofen treatment is in part dependent on a signalling pathway including the neutrophin receptor p75(NTR), p53 and Bax.	Ibuprofen	89-98	P53	Homo sapiens	198-201
18042465-4	2008	In addition, the blockage of HO activity with the iron chelator DFO or with HO-1 siRNA inhibited the CoPP-induced expression of p53.	Iron	50-54	P53	Homo sapiens	128-131
18042465-7	2008	Based on these results, we conclude that HO activity is involved in the regulation of p53 expression in a ROS-independent mechanism, and also suggest that the expression of p53 in ARPE-19 cells is associated with heme metabolites such as biliverdin/bilirubin, carbon monoxide, and iron produced by the activity of HO.	Iron	281-285	P53	Homo sapiens	173-176
18206965-7	2008	Notably, FAK knockdown plus cisplatin triggered p53-dependent cell apoptosis, which was rescued by either full-length FAK or FAK FERM re-expression.	Cisplatin	28-37	P53	Homo sapiens	48-51
18193822-5	2008	ROS and RNS escape results in the activation of cytosolic stress pathways, DNA damage, and the upregulation of JNK, p38, and p53.	Reactive Oxygen Species	0-3	P53	Homo sapiens	125-128
18607961-5	2008	From these patients we chose 21 who had never smoked or drunk alcohol and performed immunohistochemical staining for p53 protein in paraffin-embedded archival blocks.	Paraffin	132-140	P53	Homo sapiens	117-120
18596987-10	2008	Reaction to gamma-radiation was different in PHA-stimulated lymphocytes: the p53 pathway was activated and p53 was phosphorylated on serines-15 and -392 4 h after irradiation by the dose of 4 Gy.	Serine	133-140	P53	Homo sapiens	107-110
18596987-11	2008	Phosphorylation of p53 at serine-15 increased in a dose-dependent manner in the studied dose range 0.2-7.5 Gy.	Serine	26-32	P53	Homo sapiens	19-22
18184456-1	2008	BACKGROUND &amp; OBJECTIVE: p53 gene plays an important role in regulating cell cycle, maintaining completeness of cellular genomes, inducing cell differentiation and apoptosis.	Adenosine Monophosphate	12-15	P53	Homo sapiens	28-31
18497060-5	2008	Here, we show that both tamoxifen (Tam) and three-dimensional prepared extracellular matrix culture (3-D rECM) induce apoptosis in HMEC cells with acute loss of p53 [*p53(-) HMECs] through induction of interferon regulatory factor-1 (IRF-1).	Tamoxifen	24-33	P53	Homo sapiens	167-170
18497060-5	2008	Here, we show that both tamoxifen (Tam) and three-dimensional prepared extracellular matrix culture (3-D rECM) induce apoptosis in HMEC cells with acute loss of p53 [*p53(-) HMECs] through induction of interferon regulatory factor-1 (IRF-1).	Tamoxifen	35-38	P53	Homo sapiens	161-164
18497060-5	2008	Here, we show that both tamoxifen (Tam) and three-dimensional prepared extracellular matrix culture (3-D rECM) induce apoptosis in HMEC cells with acute loss of p53 [*p53(-) HMECs] through induction of interferon regulatory factor-1 (IRF-1).	Tamoxifen	35-38	P53	Homo sapiens	167-170
18497060-5	2008	Here, we show that both tamoxifen (Tam) and three-dimensional prepared extracellular matrix culture (3-D rECM) induce apoptosis in HMEC cells with acute loss of p53 [*p53(-) HMECs] through induction of interferon regulatory factor-1 (IRF-1).	Tamoxifen	24-33	P53	Homo sapiens	161-164
18095870-6	2008	Cells expressing the p53 mutants were either more sensitive to cisplatin and melphalan or more resistant than the untransfected cells, depending on the mutation.	Cisplatin	63-72	P53	Homo sapiens	21-24
17984113-1	2008	The stilbene resveratrol (RV) initiates p53-dependent apoptosis via plasma membrane integrin alphaVbeta3 in human cancer cells.	Resveratrol	13-24	P53	Homo sapiens	40-43
18189286-6	2008	The p53 residues that are mainly involved in binding to Tat(47-57) are E343 and E349, which bind to the positively charged arginine-rich motif of Tat by a partly electrostatic mechanism.	Arginine	123-131	P53	Homo sapiens	4-7
17942461-9	2008	Taken together, these results give further insight into the role of p53 in the response of human cells to BaP and BPDE and suggest that loss of this tumour suppressor can influence the metabolic activation of BaP.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	114-118	P53	Homo sapiens	68-71
17938576-0	2008	The role of p53 in the trafficking of copper-64 to tumor cell nuclei.	Copper	38-44	P53	Homo sapiens	12-15
17984113-1	2008	The stilbene resveratrol (RV) initiates p53-dependent apoptosis via plasma membrane integrin alphaVbeta3 in human cancer cells.	Resveratrol	26-28	P53	Homo sapiens	40-43
17938576-7	2008	However, nuclear localization of (64)Cu-DOTA-cetuximab showed increased uptake in the nuclei of HCT 116 +/+ cells as early as 4 h. These data demonstrate that (64)Cu is delivered to tumor cell nuclei in a p53 positive cell line in significantly greater amounts than in p53 negative cells by both non-specific and receptor-mediated uptake mechanisms.	Copper	37-39	P53	Homo sapiens	205-208
17610031-13	2008	In addition, cadmium from 1 to 100 micromol/L induced the expression of p53 and phosphorylation of its Ser15 in IHH and NHH.	Cadmium	13-20	P53	Homo sapiens	72-75
17938576-7	2008	However, nuclear localization of (64)Cu-DOTA-cetuximab showed increased uptake in the nuclei of HCT 116 +/+ cells as early as 4 h. These data demonstrate that (64)Cu is delivered to tumor cell nuclei in a p53 positive cell line in significantly greater amounts than in p53 negative cells by both non-specific and receptor-mediated uptake mechanisms.	Copper	37-39	P53	Homo sapiens	269-272
17942461-2	2008	Exposure of cells to BPDE for up to 24 h resulted in gene expression profiles more distinguishable by duration of exposure than by p53 status, although a subset of genes were identified that had significantly different expression in p53 wild-type (WT) cells relative to p53-null cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	21-25	P53	Homo sapiens	131-134
17697133-5	2008	This suggests that WNVCp-mediated apoptosis requires p53.	wnvcp	19-24	P53	Homo sapiens	53-56
18006273-0	2008	Mechanisms underlying the pro-survival pathway of p53 in suppressing mitotic death induced by adriamycin.	Doxorubicin	94-104	P53	Homo sapiens	50-53
18006273-2	2008	Here we examined the pro-survival activity of p53 on the adriamycin-induced stress using H1299 cells stably expressing tsp53 V143A, a temperature-sensitive mutant activating only the subset of p53 target genes related to growth arrest and DNA repair, but not apoptosis.	Doxorubicin	57-67	P53	Homo sapiens	46-49
17610031-14	2008	In conclusion, we showed in this study that human hepatocytes were sensitive to cadmium and apoptosis induced at concentrations suggested in the literature to inhibit p53 DNA-binding and DNA repair.	Cadmium	80-87	P53	Homo sapiens	167-170
18519232-4	2008	Cisplatin added to the culture medium leads to the significant increase of P53 expression and decrease of BCL-2 expression.	Cisplatin	0-9	P53	Homo sapiens	75-78
18791269-6	2008	In DB-1 melanoma cells that overexpress tyrosinase (Tyr(+) cells), the threshold for phosphorylation of ATM and p53 at serine 15 was observed at a low dose of Qct (25 microM) when compared to the mock transfected pcDNA3 cells, which required a higher dose (75 microM).	Tyrosine	52-55	P53	Homo sapiens	112-115
18791269-6	2008	In DB-1 melanoma cells that overexpress tyrosinase (Tyr(+) cells), the threshold for phosphorylation of ATM and p53 at serine 15 was observed at a low dose of Qct (25 microM) when compared to the mock transfected pcDNA3 cells, which required a higher dose (75 microM).	Serine	119-125	P53	Homo sapiens	112-115
18791269-7	2008	Both pcDNA3 and Tyr(+) DB-1 cells demonstrated similar increases in phosphorylation of p53 at other serine sites, but in the Tyr(+) cells, DNApk expression was found to be reduced compared to control cells, indicating a shift towards an ATM-mediated response.	Tyrosine	16-19	P53	Homo sapiens	87-90
18791269-7	2008	Both pcDNA3 and Tyr(+) DB-1 cells demonstrated similar increases in phosphorylation of p53 at other serine sites, but in the Tyr(+) cells, DNApk expression was found to be reduced compared to control cells, indicating a shift towards an ATM-mediated response.	Serine	100-106	P53	Homo sapiens	87-90
18172257-10	2008	CONCLUSION: Our study provides evidence that both germ line and somatic alterations of the p53 pathway influence the incidence and survival of ovarian carcinoma, and it underscores the importance of assessing the functionality of p53 in order to predict the sensitivity of platinum-based chemotherapies and patient outcome.	Platinum	273-281	P53	Homo sapiens	91-94
21677822-6	2008	The multiple mechanisms by which hydrophobic bile acids contribute to genomic instability are discussed, and include oxidative DNA damage, p53 and other mutations, micronuclei formation and aneuploidy.	Bile Acids and Salts	45-55	P53	Homo sapiens	139-142
18172282-12	2008	CONCLUSION: These findings identified in vivo antitumor efficacy of silibinin against human bladder tumor cells involving down-regulation of survivin and an increase in p53 expression together with enhanced apoptosis.	Silybin	68-77	P53	Homo sapiens	169-172
18714570-11	2008	The frequency of p53 Arg/Arg was 57% and of the heterozygous allele Arg/Pro it was 39%.	Arginine	21-24	P53	Homo sapiens	17-20
18714570-11	2008	The frequency of p53 Arg/Arg was 57% and of the heterozygous allele Arg/Pro it was 39%.	Arginine	25-28	P53	Homo sapiens	17-20
18714570-11	2008	The frequency of p53 Arg/Arg was 57% and of the heterozygous allele Arg/Pro it was 39%.	Arginine	25-28	P53	Homo sapiens	17-20
19065769-3	2008	TP53 codon 72 polymorphism results in either the arginine or proline form of the p53 protein; several studies have investigated whether codon 72 polymorphisms are risk and prognostic factors for cancer.	Arginine	49-57	P53	Homo sapiens	0-4
18045546-0	2008	Neurotoxicity from glutathione depletion is mediated by Cu-dependent p53 activation.	Glutathione	19-30	P53	Homo sapiens	69-72
18045546-0	2008	Neurotoxicity from glutathione depletion is mediated by Cu-dependent p53 activation.	Copper	56-58	P53	Homo sapiens	69-72
18045546-8	2008	We found that both neurons and fibroblasts revealed increased expression and activation of p53 after depletion of GSH.	Glutathione	114-117	P53	Homo sapiens	91-94
18045546-9	2008	The increased p53 activity was induced by extracellular trace Cu.	Copper	62-64	P53	Homo sapiens	14-17
18045546-10	2008	Furthermore, we showed that in GSH-depleted cells, Cu induced an increase in oxidative stress resulting in DNA damage and activation of p53-dependent cell death.	Glutathione	31-34	P53	Homo sapiens	136-139
18403247-8	2008	We found that oncogenes c-myc, c-fos and tumor suppressor genes, P53, Rb were regulated by ginsenoside Rg1, cinnamic acid, and tanshinone IIA as well.	tanshinone	127-141	P53	Homo sapiens	65-68
18045546-10	2008	Furthermore, we showed that in GSH-depleted cells, Cu induced an increase in oxidative stress resulting in DNA damage and activation of p53-dependent cell death.	Copper	51-53	P53	Homo sapiens	136-139
18160328-12	2008	Furthermore, CQ inhibited H2O2-mediated up-regulation of p53 activity in the M17 cells and this was dependent on PI3K activation.	Hydrogen Peroxide	26-30	P53	Homo sapiens	57-60
17698398-8	2008	Furthermore, upon exposure to 5-Fluorouracil and UV irradiation, Cyr61 was rapidly induced in both p53(+/+) HepG2 and p53(-/-) Hep3B cells.	Fluorouracil	30-44	P53	Homo sapiens	99-102
17698398-8	2008	Furthermore, upon exposure to 5-Fluorouracil and UV irradiation, Cyr61 was rapidly induced in both p53(+/+) HepG2 and p53(-/-) Hep3B cells.	Fluorouracil	30-44	P53	Homo sapiens	118-121
17486587-4	2008	When treated with PKC alpha antisense oligonucleotides (ODN), both HA22T/VGH and SK-Hep-1 cells lines showed the reduction of PKC alpha expression, as well as a deceleration in the growth rate and in the level of cyclin D1, but the increase in the levels of p53 and p21(WAF1/CIP1).	Oligonucleotides	38-54	P53	Homo sapiens	258-261
18827421-0	2008	Transformation of p53-positive papillary thyroid carcinoma to anaplastic carcinoma of the liver following postoperative radioactive iodine-131 therapy.	radioactive iodine-131	120-142	P53	Homo sapiens	18-21
21423838-13	2008	The CAT-Tox data on the other hand indicate that copper overload induces proteotoxic effects (HMTIIA, HSP70, GRP78), inflammatory reactions/oxidative stress (c-fos), and growth arrest and DNA damage (p53, GADD153).	Copper	49-55	P53	Homo sapiens	200-203
17763999-0	2008	Down-regulation of the inhibitor of growth 1 (ING1) tumor suppressor sensitizes p53-deficient glioblastoma cells to cisplatin-induced cell death.	Cisplatin	116-125	P53	Homo sapiens	80-83
17763999-1	2008	Impaired tumor suppressor functions, such as deficient p53, are characteristic for glioblastoma multiforme (GBM) and can cause resistance to DNA-damaging agents like cisplatin.	Cisplatin	166-175	P53	Homo sapiens	55-58
17763999-4	2008	Using LN229 GBM cells, which express ING1 proteins and harbor mutant TP53, we are the first to show that DNA damage by cisplatin or ionizing radiation differentially induced the two major ING1 splicing isoforms.	Cisplatin	119-128	P53	Homo sapiens	69-73
17763999-9	2008	Also, ING1 down-regulation may sensitize GBM cells with deficient p53 to treatment with cisplatin.	Cisplatin	88-97	P53	Homo sapiens	66-69
19013355-11	2008	Copper induces apoptosis by p53 dependent and independent pathways.	Copper	0-6	P53	Homo sapiens	28-31
19013355-13	2008	Selenium induces apoptosis by producing superoxide that activates p53.	Superoxides	40-50	P53	Homo sapiens	66-69
20445773-3	2008	We found that among these 14 SNPs, R72P, intron 3 16-bp del/ins, and intron 6 G&gt;A in p53, -938C&gt;A in Bcl-2, and I522L in CASP10 were significant predictors of the BPDE-induced lymphocytic AC in single-locus analysis.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	169-173	P53	Homo sapiens	88-91
18803266-0	2008	p53 codon 72 proline/arginine polymorphism and autoimmune thyroid diseases.	Arginine	21-29	P53	Homo sapiens	0-3
18803266-7	2008	In conclusion, HT patients feature a greater ratio of arginine homozygosity at p53 codon 72 than in the case for normal subjects.	Arginine	54-62	P53	Homo sapiens	79-82
18803266-8	2008	The p53 codon 72 proline/arginine polymorphism may be a genetic marker to predict the increased susceptibility of development of HT.	Arginine	25-33	P53	Homo sapiens	4-7
17942552-6	2008	We showed that the ectopic expression of K-cyclin led to a sustained increase of p53 phosphorylation on Ser(33) in vivo, and the phosphorylation could be inhibited by a dominant negative Cdk9 mutant, dn-Cdk9.	Serine	104-107	P53	Homo sapiens	81-84
17967874-0	2008	Serine 15 phosphorylation of p53 directs its interaction with B56gamma and the tumor suppressor activity of B56gamma-specific protein phosphatase 2A.	Serine	0-6	P53	Homo sapiens	29-32
17912235-4	2008	This Dox-induced NF-kappaB activation and subsequent chemoresistance is dependent on expression of p53.	Doxorubicin	5-8	P53	Homo sapiens	99-102
18791921-11	2008	To validate the general notion that imbalance in copper and zinc levels may lead to higher prevalence of TP53 mutations, we compared the 3 variables, and no association was found between copper concentration and TP53 mutation status; but patients with TP53 mutant tumor had lower zinc levels than those with no mutation.	Copper	49-55	P53	Homo sapiens	105-109
18003626-8	2008	p53-proficient cells were more sensitive than p53-deficient cells to cisplatin, (+/-)-anti-benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide and UV-C; these differences in cellular sensitivity were more apparent in the 041 TR cells (up to 3.6-, 5.8- and 1.9-fold, respectively) than the WI38/VA13 cells (up to 2.3-, 1.4- and 1.4-fold, respectively).	Cisplatin	69-78	P53	Homo sapiens	0-3
18003626-8	2008	p53-proficient cells were more sensitive than p53-deficient cells to cisplatin, (+/-)-anti-benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide and UV-C; these differences in cellular sensitivity were more apparent in the 041 TR cells (up to 3.6-, 5.8- and 1.9-fold, respectively) than the WI38/VA13 cells (up to 2.3-, 1.4- and 1.4-fold, respectively).	Cisplatin	69-78	P53	Homo sapiens	46-49
18003626-8	2008	p53-proficient cells were more sensitive than p53-deficient cells to cisplatin, (+/-)-anti-benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide and UV-C; these differences in cellular sensitivity were more apparent in the 041 TR cells (up to 3.6-, 5.8- and 1.9-fold, respectively) than the WI38/VA13 cells (up to 2.3-, 1.4- and 1.4-fold, respectively).	pyrene-7,8-dihydrodiol-9,10-epoxide	99-134	P53	Homo sapiens	0-3
20016737-8	2008	In addition, the phosphorylation of p53 at the Ser-15 residue was observed with kaempferol.	Serine	47-50	P53	Homo sapiens	36-39
18060783-2	2007	Here, we report, on the basis of live-cell studies, that 75 nM anisomycin transiently (1 hr) activates p38 which, in turn, rapidly and completely blocks entry into mitosis for at least 4 hr in all primary, telomerase- or spontaneously immortalized (p53+ and pRB+) human cells.	Anisomycin	63-73	P53	Homo sapiens	249-252
19107196-7	2008	We also found that excess PPIX in ES cells led to elevated levels of reactive oxygen species which in turn triggered DNA damage signals as indicated by increased levels of gammaH2AX and phosphorylated p53.	protoporphyrin IX	26-30	P53	Homo sapiens	201-204
18612219-0	2008	Role of p53 codon 72 arginine allele in cell survival in vitro and in the clinical outcome of patients with advanced breast cancer.	Arginine	21-29	P53	Homo sapiens	8-11
18612219-1	2008	BACKGROUND: The p53 codon 72 polymorphism, which results in either an arginine or proline residue, plays a different role in vitro and in vivo in cell survival and drug resistance.	Arginine	70-78	P53	Homo sapiens	16-19
19112505-8	2008	The induction of p21 was mediated by increased level of phosphorylated p53 at ser-15.	Serine	78-81	P53	Homo sapiens	71-74
20020938-4	2008	Our studies showed that CAS over-expression increased p53 accumulation and apoptosis induced by 5-fluorouracil, doxorubicin, cisplatin, and tamoxifen in HT-29 cancer cells.	Fluorouracil	96-110	P53	Homo sapiens	54-57
20020938-4	2008	Our studies showed that CAS over-expression increased p53 accumulation and apoptosis induced by 5-fluorouracil, doxorubicin, cisplatin, and tamoxifen in HT-29 cancer cells.	Doxorubicin	112-123	P53	Homo sapiens	54-57
20020938-4	2008	Our studies showed that CAS over-expression increased p53 accumulation and apoptosis induced by 5-fluorouracil, doxorubicin, cisplatin, and tamoxifen in HT-29 cancer cells.	Cisplatin	125-134	P53	Homo sapiens	54-57
20020938-4	2008	Our studies showed that CAS over-expression increased p53 accumulation and apoptosis induced by 5-fluorouracil, doxorubicin, cisplatin, and tamoxifen in HT-29 cancer cells.	Tamoxifen	140-149	P53	Homo sapiens	54-57
17971768-2	2007	Here, we examined the role p53 plays in the antitumour effect of combination treatment with pegylated interferon (PEG-IFN)-alpha and 5-fluorouracil (5-FU), which has been shown to effectively treat advanced hepatocellular carcinoma (HCC).	Fluorouracil	133-147	P53	Homo sapiens	27-30
17854787-4	2007	The proteins of phosphorylation of p53 at serine-15, which located on the nuclei of cancer cells, were highly induced by radiation.	Serine	42-48	P53	Homo sapiens	35-38
18089808-3	2007	The protection was associated with suppression of the doxorubicin-induced senescence, where Hsp27 inhibited p53-mediated induction of p21, the major regulator of the senescence program.	Doxorubicin	54-65	P53	Homo sapiens	108-111
17976513-4	2007	THIF treatment also led to an inhibition of cdc2, which was accompanied by the phosphorylation of both p53 (Ser15) and Chk1 (Ser296) and the de-activation of cdc25C phosphatase.	orobol	0-4	P53	Homo sapiens	103-106
17976513-5	2007	We suggest the anti-proliferative actions of THIF may be mediated by initial oxidative DNA damage, activation of ATR and downstream regulation of the p53 and Chk1 pathways leading to cell cycle arrest in G2-M.	orobol	45-49	P53	Homo sapiens	150-153
17477370-3	2007	Results demonstrate that zinc and copper increased metal response elements (MREs) activity and MTF-1 expression in p53 positive MN1 and parental MCF7 cells.	Copper	34-40	P53	Homo sapiens	115-118
17477370-10	2007	The above results demonstrate that activation of p53 is an important factor in metal regulation of MT.	Metals	79-84	P53	Homo sapiens	49-52
18022393-0	2007	Novel homeodomain-interacting protein kinase family member, HIPK4, phosphorylates human p53 at serine 9.	Serine	95-101	P53	Homo sapiens	88-91
18022393-3	2007	We demonstrate that HIPK4 could phosphorylate human p53 protein at serine 9, both in vitro and in vivo.	Serine	67-73	P53	Homo sapiens	52-55
18022393-6	2007	These findings suggest that phosphorylation of p53 at serine 9 is important for p53 mediated transcriptional repression.	Serine	54-60	P53	Homo sapiens	47-50
18022393-6	2007	These findings suggest that phosphorylation of p53 at serine 9 is important for p53 mediated transcriptional repression.	Serine	54-60	P53	Homo sapiens	80-83
17971768-2	2007	Here, we examined the role p53 plays in the antitumour effect of combination treatment with pegylated interferon (PEG-IFN)-alpha and 5-fluorouracil (5-FU), which has been shown to effectively treat advanced hepatocellular carcinoma (HCC).	Fluorouracil	149-153	P53	Homo sapiens	27-30
17971768-7	2007	The antitumour effects of combination treatment is due in part to the elevation by PEG-IFN of p53 protein and mRNA expression and in part to the DNA damage that is generated by 5-FU, which induces p53 serine46 phosphorylation, which in turn upregulates p53AIP1 expression.	Polyethylene Glycols	83-86	P53	Homo sapiens	94-97
17971768-7	2007	The antitumour effects of combination treatment is due in part to the elevation by PEG-IFN of p53 protein and mRNA expression and in part to the DNA damage that is generated by 5-FU, which induces p53 serine46 phosphorylation, which in turn upregulates p53AIP1 expression.	Fluorouracil	177-181	P53	Homo sapiens	197-200
17982676-0	2007	Apoptosis, cell cycle progression and gene expression in TP53-depleted HCT116 colon cancer cells in response to short-term 5-fluorouracil treatment.	Fluorouracil	123-137	P53	Homo sapiens	57-61
18031612-10	2007	The expressions of p21 and p53 was upregulated with PAB treatment, and cyclin B1 was upregulated and transported from the cytoplasm to nuclei, and sustained stable levels.	pseudolaric acid B	52-55	P53	Homo sapiens	27-30
18254244-1	2007	We have reported that the protective effect of Magnolol on TBHP-induced injury in human nonsmall lung cancer H460 cells is partially via a p53 dependent mechanism.	magnolol	47-55	P53	Homo sapiens	139-142
18254244-1	2007	We have reported that the protective effect of Magnolol on TBHP-induced injury in human nonsmall lung cancer H460 cells is partially via a p53 dependent mechanism.	tert-Butylhydroperoxide	59-63	P53	Homo sapiens	139-142
17720501-8	2007	(b) Taxanes Microtubule-associated parameters (MTAP) such as the TAU protein, HER-2 gene amplification, and p-53 gene mutations, have been suggested as potential predictive markers for taxanes.	Taxoids	4-11	P53	Homo sapiens	108-112
17720501-8	2007	(b) Taxanes Microtubule-associated parameters (MTAP) such as the TAU protein, HER-2 gene amplification, and p-53 gene mutations, have been suggested as potential predictive markers for taxanes.	Taxoids	185-192	P53	Homo sapiens	108-112
18086774-0	2007	Adduction of human p53 gene by fecal water: an in vitro biomarker of mutagenesis in the human large bowel.	Water	37-42	P53	Homo sapiens	19-22
18086774-1	2007	A polymerase arrest assay was designed to determine sites of adduction in the human p53 gene induced by incubation with fecal water.	Water	126-131	P53	Homo sapiens	84-87
18086774-2	2007	Significant formation of adducts was observed on p53 DNA after a 2-h incubation in fecal water from 10 of 17 samples studied.	Water	89-94	P53	Homo sapiens	49-52
17982676-7	2007	Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells.	Fluorouracil	34-38	P53	Homo sapiens	47-51
17982676-7	2007	Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells.	Fluorouracil	34-38	P53	Homo sapiens	107-111
17982676-7	2007	Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells.	Fluorouracil	34-38	P53	Homo sapiens	107-111
17982676-1	2007	Loss of TP53 function may contribute to 5-fluorouracil (5-FU) resistance in colorectal cancer since TP53-deficient cells may be unable to undergo apoptosis in response to 5-FU-induced DNA damage.	Fluorouracil	40-54	P53	Homo sapiens	8-12
17982676-7	2007	Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells.	Fluorouracil	34-38	P53	Homo sapiens	107-111
17982676-7	2007	Alterations in gene expression in 5-FU-treated TP53-depleted HCT116 cultures confirmed previously-reported TP53 target genes and suggested potentially novel TP53 target genes (e.g. APOBEC3C, BIRC3, JMJD2B, LAMP3, MYO1E, PRRG1, SULF2, TACSTD2, TncRNA, ZFYVE20) that may play a role in mediating the 5-FU-induced DNA damage response in TP53-proficient cells.	Fluorouracil	298-302	P53	Homo sapiens	47-51
17982676-1	2007	Loss of TP53 function may contribute to 5-fluorouracil (5-FU) resistance in colorectal cancer since TP53-deficient cells may be unable to undergo apoptosis in response to 5-FU-induced DNA damage.	Fluorouracil	56-60	P53	Homo sapiens	8-12
17982676-8	2007	Abrogation of TP53 function in 5-FU-treated HCT116 cultures results in reduced apoptosis, TP53- and CDKN1A-independent G1/S phase arrests that may be protective against apoptosis, smaller intra-S phase arrests, and transcript level decreases of both reported TP53 target genes as well as potentially novel TP53 target genes.	Fluorouracil	31-35	P53	Homo sapiens	14-18
17982676-8	2007	Abrogation of TP53 function in 5-FU-treated HCT116 cultures results in reduced apoptosis, TP53- and CDKN1A-independent G1/S phase arrests that may be protective against apoptosis, smaller intra-S phase arrests, and transcript level decreases of both reported TP53 target genes as well as potentially novel TP53 target genes.	Fluorouracil	31-35	P53	Homo sapiens	90-94
17982676-1	2007	Loss of TP53 function may contribute to 5-fluorouracil (5-FU) resistance in colorectal cancer since TP53-deficient cells may be unable to undergo apoptosis in response to 5-FU-induced DNA damage.	Fluorouracil	56-60	P53	Homo sapiens	100-104
17982676-8	2007	Abrogation of TP53 function in 5-FU-treated HCT116 cultures results in reduced apoptosis, TP53- and CDKN1A-independent G1/S phase arrests that may be protective against apoptosis, smaller intra-S phase arrests, and transcript level decreases of both reported TP53 target genes as well as potentially novel TP53 target genes.	Fluorouracil	31-35	P53	Homo sapiens	90-94
17982676-8	2007	Abrogation of TP53 function in 5-FU-treated HCT116 cultures results in reduced apoptosis, TP53- and CDKN1A-independent G1/S phase arrests that may be protective against apoptosis, smaller intra-S phase arrests, and transcript level decreases of both reported TP53 target genes as well as potentially novel TP53 target genes.	Fluorouracil	31-35	P53	Homo sapiens	90-94
17982676-1	2007	Loss of TP53 function may contribute to 5-fluorouracil (5-FU) resistance in colorectal cancer since TP53-deficient cells may be unable to undergo apoptosis in response to 5-FU-induced DNA damage.	Fluorouracil	171-175	P53	Homo sapiens	8-12
17982676-2	2007	5-FU treatment of TP53-deficient cells would provide useful information on the apoptotic response to drug-induced DNA damage in the absence of TP53 and its transcriptional targets.	Fluorouracil	0-4	P53	Homo sapiens	18-22
17982676-6	2007	Compared to 5-FU-treated TP53-proficient HCT116 cultures, 5-FU-treated TP53-depleted HCT116 cultures showed lack of CDKN1A induction, decreased apoptotic levels, decreased FAS and TNFRSF10B transcript levels and cleaved PARP protein levels, G1/S transition arrests, decreased CCND1 protein levels, and smaller intra-S phase arrests.	Fluorouracil	12-16	P53	Homo sapiens	25-29
17982676-6	2007	Compared to 5-FU-treated TP53-proficient HCT116 cultures, 5-FU-treated TP53-depleted HCT116 cultures showed lack of CDKN1A induction, decreased apoptotic levels, decreased FAS and TNFRSF10B transcript levels and cleaved PARP protein levels, G1/S transition arrests, decreased CCND1 protein levels, and smaller intra-S phase arrests.	Fluorouracil	58-62	P53	Homo sapiens	71-75
18231749-1	2007	To explore the effects of Tanshinone II A on the proliferation, apoptosis and gene expression of p53 and bcl-2 in human gastric carcinoma MKN-45 cells.	tanshinone	26-41	P53	Homo sapiens	97-100
18032786-9	2007	We further demonstrate that the PCs with linoleic acid in their sn-2 position (18:2n6) induce phosphorylation of Ser15 in p53 in an ATR-dependent manner.	Linoleic Acid	41-54	P53	Homo sapiens	122-125
18231754-11	2007	Moreover, p38MAPK-mediated apoptosis in paclitaxel-resistant ovarian carcinoma cells depends on the activation of p53.	Paclitaxel	40-50	P53	Homo sapiens	114-117
18048815-4	2007	MATERIALS AND METHODS: The complete coding region of the p53 gene was queried using DNA from paraffin-embedded tissues and employing a p53 gene-sequencing chip.	Paraffin	93-101	P53	Homo sapiens	57-60
18231749-4	2007	Semi-quantitative RT-PCR was used to further verify the expression of p53 and bcl-2 gene after exposure to Tanshinone A in MKN-45 cells.	tanshinone	107-119	P53	Homo sapiens	70-73
18231749-7	2007	This resulted in apoptosis of MKN-45 cells and the apoptosis rate was as high as 43.91% after treatment with 2.0 microg/mL Tanshinone II A for 96 h. It was also found that Tanshinone II A up-regulated expression of p53 gene and down-regulated expression of bcl-2 gene.	tanshinone	123-138	P53	Homo sapiens	215-218
18231749-7	2007	This resulted in apoptosis of MKN-45 cells and the apoptosis rate was as high as 43.91% after treatment with 2.0 microg/mL Tanshinone II A for 96 h. It was also found that Tanshinone II A up-regulated expression of p53 gene and down-regulated expression of bcl-2 gene.	tanshinone	172-187	P53	Homo sapiens	215-218
17898049-5	2007	Treatment of E7-expressing cells with interferon ultimately resulted in cellular senescence through a process that is dependent upon acetylation of p53 by p300/CBP at lysine 382.	Lysine	167-173	P53	Homo sapiens	148-151
17594054-0	2007	Curcumin induces G2/M cell cycle arrest in a p53-dependent manner and upregulates ING4 expression in human glioma.	Curcumin	0-8	P53	Homo sapiens	45-48
17594054-12	2007	The results demonstrate that curcumin exerts inhibitory action on glioma cell growth and proliferation via induction of cell cycle arrest instead of induction of apoptosis in a p53-dependent manner, and ING4 possibly is in part involved in the signal pathways.	Curcumin	29-37	P53	Homo sapiens	177-180
17898049-8	2007	Finally, p53 acetylation at lysine 382 was found not to be an essential determinant of other types of senescence such as that induced by overexpression of Ras in human fibroblasts.	Lysine	28-34	P53	Homo sapiens	9-12
18088190-4	2007	Treatment with 5 microM parthenolide for 48 to 72 h inhibited constitutive NF-kappaB binding and cell growth, reduced plating efficiency, and induced apoptosis through stabilization of p53 (TP53), induction of the pro-apoptosis protein BAX, and phosphorylation of BID.	parthenolide	24-36	P53	Homo sapiens	185-188
18089710-3	2007	p53 status-dependent endoreduplication is observed upon treatment of cells with PHA-739358, and phosphorylation of histone H3 in Ser(10) is inhibited.	Serine	129-132	P53	Homo sapiens	0-3
17923702-7	2007	Mutation of lysine 3016 does not affect unstimulated ATM kinase activity but does abolish upregulation of ATM"s kinase activity by DNA damage, inhibits the conversion of inactive ATM dimers to active ATM monomers, and prevents the ATM-dependent phosphorylation of the p53 and chk2 proteins.	Lysine	12-18	P53	Homo sapiens	268-271
18084613-3	2007	Here we have used oligonucleotide microarrays to identify transcripts induced by variants of p53 with point mutations within subdomains 1, 2, or 1 and 2 (QS1, QS2, and QS1/QS2, respectively).	Oligonucleotides	18-33	P53	Homo sapiens	93-96
18088190-4	2007	Treatment with 5 microM parthenolide for 48 to 72 h inhibited constitutive NF-kappaB binding and cell growth, reduced plating efficiency, and induced apoptosis through stabilization of p53 (TP53), induction of the pro-apoptosis protein BAX, and phosphorylation of BID.	parthenolide	24-36	P53	Homo sapiens	190-194
17916563-4	2007	The use of NM23-H1 and STRAP mutants revealed that Cys(145) of NM23-H1 and Cys(152) (or Cys(270)) of STRAP were responsible for p53 binding.	Cysteine	51-54	P53	Homo sapiens	128-131
17916563-4	2007	The use of NM23-H1 and STRAP mutants revealed that Cys(145) of NM23-H1 and Cys(152) (or Cys(270)) of STRAP were responsible for p53 binding.	Cysteine	75-78	P53	Homo sapiens	128-131
17916563-4	2007	The use of NM23-H1 and STRAP mutants revealed that Cys(145) of NM23-H1 and Cys(152) (or Cys(270)) of STRAP were responsible for p53 binding.	Cysteine	75-78	P53	Homo sapiens	128-131
17916563-5	2007	Furthermore, Cys(176) and Cys(135) of p53 were required to bind NM23-H1 and STRAP, respectively.	Cysteine	13-16	P53	Homo sapiens	38-41
17916563-5	2007	Furthermore, Cys(176) and Cys(135) of p53 were required to bind NM23-H1 and STRAP, respectively.	Cysteine	26-29	P53	Homo sapiens	38-41
17929901-0	2007	Method for lipidomic analysis: p53 expression modulation of sulfatide, ganglioside, and phospholipid composition of U87 MG glioblastoma cells.	Phospholipids	88-100	P53	Homo sapiens	31-34
18025460-2	2007	Here we describe the oxidation of a cell-cycle regulatory protein, p53, from a distance through DNA-mediated CT. A consensus p53 binding site as well as three DNA promoters regulated by p53 were synthesized containing a tethered DNA photooxidant, anthraquinone.	Anthraquinones	247-260	P53	Homo sapiens	67-70
18025460-6	2007	Mass spectrometry results are consistent with disulfide bond formation in p53 upon DNA-mediated oxidation.	Disulfides	46-55	P53	Homo sapiens	74-77
18025460-7	2007	Furthermore, DNA-bound p53 oxidation is shown in vivo by up-regulation of p53 and subsequent irradiation in the presence of a rhodium photooxidant to give a new p53 adduct that can be reversed with thiol treatment.	Sulfhydryl Compounds	198-203	P53	Homo sapiens	23-26
18025460-7	2007	Furthermore, DNA-bound p53 oxidation is shown in vivo by up-regulation of p53 and subsequent irradiation in the presence of a rhodium photooxidant to give a new p53 adduct that can be reversed with thiol treatment.	Sulfhydryl Compounds	198-203	P53	Homo sapiens	74-77
18025460-7	2007	Furthermore, DNA-bound p53 oxidation is shown in vivo by up-regulation of p53 and subsequent irradiation in the presence of a rhodium photooxidant to give a new p53 adduct that can be reversed with thiol treatment.	Sulfhydryl Compounds	198-203	P53	Homo sapiens	74-77
18025460-8	2007	This DNA-mediated oxidation of p53 parallels that seen by treating cells with hydrogen peroxide.	Hydrogen Peroxide	78-95	P53	Homo sapiens	31-34
17900613-0	2007	A fluid salt-bridging cluster and the stabilization of p53.	fluid salt	2-12	P53	Homo sapiens	55-58
18006756-1	2007	PURPOSE: To determine the nature and potential pharmacologic reversibility of deficient TP53 expression and function in head and neck squamous cell carcinomas (HNSCC) with wild-type TP53, previously associated with decreased sensitivity to cisplatin therapy.	Cisplatin	240-249	P53	Homo sapiens	88-92
18006756-10	2007	CONCLUSIONS: Deficient TP53 mRNA and protein expression underlies decreased function in a subset of HNSCC with wild-type TP53 and can be restored together with cisplatin sensitization by quinacrine.	Cisplatin	160-169	P53	Homo sapiens	23-27
18006764-6	2007	RESULTS: The p53 codon 72 Arg/Arg genotype was associated with increased PSA recurrence risk compared with the Arg/Pro and Pro/Pro genotypes, although the difference did not reach significance (30.3% versus 20.4%, P = 0.247).	Arginine	26-29	P53	Homo sapiens	13-16
18006764-6	2007	RESULTS: The p53 codon 72 Arg/Arg genotype was associated with increased PSA recurrence risk compared with the Arg/Pro and Pro/Pro genotypes, although the difference did not reach significance (30.3% versus 20.4%, P = 0.247).	Arginine	30-33	P53	Homo sapiens	13-16
18006764-6	2007	RESULTS: The p53 codon 72 Arg/Arg genotype was associated with increased PSA recurrence risk compared with the Arg/Pro and Pro/Pro genotypes, although the difference did not reach significance (30.3% versus 20.4%, P = 0.247).	Arginine	30-33	P53	Homo sapiens	13-16
17563751-5	2007	Relative to the p53 consensus, the p63 consensus DNA-binding site (DBS) was more degenerate, particularly at positions 10 and 11, and was enriched for A/G at position 5 and C/T at position 16 of the consensus.	dbs	67-70	P53	Homo sapiens	16-19
17848574-3	2007	Given that MDM2 protein binds ATP, can interact with the Hsp90 chaperone, plays a role in the modulation of transcription factors and protection and activation of DNA polymerases, and is involved in ribosome assembly and nascent p53 protein biosynthesis, we have evaluated and found MDM2 protein to possess an intrinsic molecular chaperone activity.	Adenosine Triphosphate	30-33	P53	Homo sapiens	229-232
17848574-5	2007	This reaction is driven by recycling of MDM2 from the p53 complex, triggered by binding of ATP to MDM2.	Adenosine Triphosphate	91-94	P53	Homo sapiens	54-57
17848574-8	2007	MDM2 in which one of the Zn(2+) coordinating residues is mutated (C478S or C464A) blocks degradation but enhances folding of p53.	Zinc	25-27	P53	Homo sapiens	125-128
17848574-9	2007	This is the first demonstration that MDM2 possesses an intrinsic molecular chaperone activity, indicating that the ATP binding function of MDM2 can mediate its chaperone function toward the p53 tumor suppressor.	Adenosine Triphosphate	115-118	P53	Homo sapiens	190-193
17996705-3	2007	Here we show that the acetylation of two lysine residues in p53 promotes recruitment of the TFIID subunit TAF1 to the p21 promoter through its bromodomains.	Lysine	41-47	P53	Homo sapiens	60-63
17986867-1	2007	We have shown previously that wild-type p53 renders H460 human lung cancer cells more sensitive to apoptosis induction by environmental carcinogen benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE), but the mechanism of cell death is not fully understood.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	147-183	P53	Homo sapiens	40-43
17986867-1	2007	We have shown previously that wild-type p53 renders H460 human lung cancer cells more sensitive to apoptosis induction by environmental carcinogen benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE), but the mechanism of cell death is not fully understood.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	185-189	P53	Homo sapiens	40-43
17855337-8	2007	Our data show furthermore that when T1 cells were treated with streptolysin-O/granzyme B, specific phosphorylation of p53 at Ser-15 and Ser-37 residues was observed subsequent to the activation of the stress kinases ataxia telangiectasia mutated (ATM) and p38K.	Serine	125-128	P53	Homo sapiens	118-121
17996705-4	2007	UV irradiation of cells diacetylates p53 at lysines 373 and 382, which in turn recruits TAF1 to a distal p53-binding site on the p21 promoter prior to looping to the core promoter.	Lysine	44-51	P53	Homo sapiens	37-40
17900613-5	2007	Here we present molecular dynamics simulations of wild-type p53 and the R337His mutant at several different pH and salt conditions.	Salts	115-119	P53	Homo sapiens	60-63
18261311-1	2007	OBJECTIVE: To explore the effects of adenovirus-mediated wild-type p53 gene (Ad-p53) on the reversal of multidrug resistance (MDR) and multidrug resistance gene-1 (MDR1) in adriamycin (ADM) resistant human breast cancer cell.	Doxorubicin	173-183	P53	Homo sapiens	67-70
18261311-1	2007	OBJECTIVE: To explore the effects of adenovirus-mediated wild-type p53 gene (Ad-p53) on the reversal of multidrug resistance (MDR) and multidrug resistance gene-1 (MDR1) in adriamycin (ADM) resistant human breast cancer cell.	Doxorubicin	173-183	P53	Homo sapiens	80-83
17959036-8	2007	Moreover, the siRNA-mediated silencing of p53 significantly reduced the IFNalpha/doxorubicin combination-induced cytotoxicity and PARP cleavage.	Doxorubicin	81-92	P53	Homo sapiens	42-45
17959036-0	2007	Interferon-alpha enhances sensitivity of human osteosarcoma U2OS cells to doxorubicin by p53-dependent apoptosis.	Doxorubicin	74-85	P53	Homo sapiens	89-92
18261311-1	2007	OBJECTIVE: To explore the effects of adenovirus-mediated wild-type p53 gene (Ad-p53) on the reversal of multidrug resistance (MDR) and multidrug resistance gene-1 (MDR1) in adriamycin (ADM) resistant human breast cancer cell.	Doxorubicin	185-188	P53	Homo sapiens	67-70
17959036-6	2007	RESULTS: IFNalpha increased doxorubicin-induced cytotoxicity to a much greater degree through apoptosis in human osteosarcoma p53-wild U2OS cells, but not p53-mutant MG63 cells.	Doxorubicin	28-39	P53	Homo sapiens	126-129
17959036-9	2007	CONCLUSION: IFNalpha enhances the sensitivity of human osteosarcoma U2OS cells to doxorubicin by p53-dependent apoptosis.	Doxorubicin	82-93	P53	Homo sapiens	97-100
18261311-1	2007	OBJECTIVE: To explore the effects of adenovirus-mediated wild-type p53 gene (Ad-p53) on the reversal of multidrug resistance (MDR) and multidrug resistance gene-1 (MDR1) in adriamycin (ADM) resistant human breast cancer cell.	Doxorubicin	185-188	P53	Homo sapiens	80-83
17959036-7	2007	IFNalpha markedly upregulated p53, Bax, Mdm2, and p21, downregulated Bcl-2, and activated caspase-3 and PARP cleavage in response to doxorubicin in U2OS cells.	Doxorubicin	133-144	P53	Homo sapiens	30-33
17653713-3	2007	On the other hand, a common polymorphism of the tumour suppressor P53 gene results in either arginine (A) or proline (P) at amino-acid position 72.	Arginine	93-101	P53	Homo sapiens	66-69
17727682-7	2007	In addition, treatment with 30 microM genistein strongly induced phosphorylation of checkpoint kinase (CHK) 2 and p53 at serines 15, 20 and 37.	Serine	121-128	P53	Homo sapiens	114-117
17907783-17	2007	Mutagenesis of C8-AP-dG in a 12-mer containing the local DNA sequence around codon 273 of the p53 tumor suppressor gene, where the adduct was located at the second base of this codon, was also investigated.	c8-ap-dg	15-23	P53	Homo sapiens	94-97
17957141-3	2007	We analyzed the p53 transcriptional program upon activation by two DNA-damaging agents, UVC and doxorubicin, versus the non-genotoxic molecule Nutlin-3.	Doxorubicin	96-107	P53	Homo sapiens	16-19
17957142-0	2007	Modulation of the p53-MDM2 interaction by phosphorylation of Thr18: a computational study.	UNII-PYZ33YLR8A	61-66	P53	Homo sapiens	18-21
17957142-3	2007	The interaction with MDM2 is known to be abrogated by phosphorylation of Ser/Thr residues in the MDM2 N-terminal domain and in the p53 transactivation domain.	Serine	73-76	P53	Homo sapiens	131-134
17957142-3	2007	The interaction with MDM2 is known to be abrogated by phosphorylation of Ser/Thr residues in the MDM2 N-terminal domain and in the p53 transactivation domain.	Threonine	77-80	P53	Homo sapiens	131-134
17957142-6	2007	Molecular dynamics simulations of the p53 transactivation domain suggest that phosphorylation of either Thr18 or Ser20 does not disrupt its helical structure but does result in reduced affinities for MDM2.	UNII-PYZ33YLR8A	104-109	P53	Homo sapiens	38-41
17957142-9	2007	These suggest that repulsions will arise because the MDM2 surface will force the p53 to bind in a manner that will place the negatively charged phosphorylated Thr18 near this anionic region.	UNII-PYZ33YLR8A	159-164	P53	Homo sapiens	81-84
17974990-3	2007	The anticancer drug doxorubicin is known to increase p21 via p53-dependent and p53-independent mechanisms.	Doxorubicin	20-31	P53	Homo sapiens	61-64
17889823-0	2007	The calcium binding protein ALG-2 binds and stabilizes Scotin, a p53-inducible gene product localized at the endoplasmic reticulum membrane.	Calcium	4-11	P53	Homo sapiens	65-68
17893511-8	2007	p27 levels were slightly decreased, whereas p53 and p21 levels were significantly upregulated in doxorubicin-treated MCF-7 cells.	Doxorubicin	97-108	P53	Homo sapiens	44-47
17620057-8	2007	Deacetylated lysine residues within Rb formed a domain similar to the SIRT1-targeted domain of the p53 tumour suppressor protein.	Lysine	13-19	P53	Homo sapiens	99-102
17806102-1	2007	The NAD(+)-dependent protein deacetylase SIRT1 is linked to cellular survival pathways by virtue of keeping the tumor suppressor gene p53 and members of the forkhead transcription factor family deacetylated.	NAD	4-10	P53	Homo sapiens	134-137
17910628-6	2007	Bortezomib/PXD101 treatment markedly triggered reactive oxygen species (ROS) generation that was accompanied by p53, H2A.X and p38-mitogen-activated protein kinase phosphorylation.	Reactive Oxygen Species	72-75	P53	Homo sapiens	112-115
17850846-3	2007	Of the stress-related genes, the expressions of the aryl hydrocarbon receptor (AhR), cytochrome P450 (CYP) and p53 genes were most significantly induced by exposure to PCDDs/DFs.	Polychlorinated Dibenzodioxins	168-173	P53	Homo sapiens	111-114
17974990-0	2007	Involvement of sphingosine kinase 2 in p53-independent induction of p21 by the chemotherapeutic drug doxorubicin.	Doxorubicin	101-112	P53	Homo sapiens	39-42
17974990-3	2007	The anticancer drug doxorubicin is known to increase p21 via p53-dependent and p53-independent mechanisms.	Doxorubicin	20-31	P53	Homo sapiens	79-82
17974990-6	2007	Moreover, siSphK2 reduced doxorubicin-induced p21 expression in p53-inactivated MCF7 cells.	Doxorubicin	26-37	P53	Homo sapiens	64-67
17974990-7	2007	Likewise, in human wild-type p53- and p21-expressing HCT116 colon carcinoma cells, as well as in p53-null counterparts, down-regulation of SphK2 markedly reduced p21 induction by doxorubicin.	Doxorubicin	179-190	P53	Homo sapiens	97-100
17822515-6	2007	This article discusses three cellular regulators (p53, p21 and TRAIL) induced in synovial tissue that are important for iron metabolism.	Iron	120-124	P53	Homo sapiens	50-53
17974990-9	2007	Collectively, our results show that endogenous SphK2 is important for p53-independent induction of p21 expression by doxorubicin and suggest that SphK2 may influence the balance between cytostasis and apoptosis of human cancer cells.	Doxorubicin	117-128	P53	Homo sapiens	70-73
17912468-3	2007	In vitro studies have suggested that HPV-E6 interacts more efficiently with the arginine (Arg) p53 variant at position 72 as it appears to be more susceptible to degradation through the ubiquitin proteasome pathway.	Arginine	80-88	P53	Homo sapiens	95-98
17912468-3	2007	In vitro studies have suggested that HPV-E6 interacts more efficiently with the arginine (Arg) p53 variant at position 72 as it appears to be more susceptible to degradation through the ubiquitin proteasome pathway.	Arginine	90-93	P53	Homo sapiens	95-98
17942951-6	2007	A "signature" p53 mutation in the upper urothelial cancer associated with this disease provides evidence of long-term exposure to aristolochic acid.	aristolochic acid I	130-147	P53	Homo sapiens	14-17
17904593-3	2007	Our results suggest that the protective effects of esculin (10(-7), 10(-6) and 10(-5) M) on DA-induced cytotoxicity may be ascribed to its anti-oxidative properties by reducing ROS level, and its anti-apoptotic effect via protecting mitochondrion membrane potential (DeltaPsim), enhancing superoxide dismutaese (SOD) activity and reduced glutathione (GSH) levels, and regulating P53, Bax and Bcl-2 expression.	Dopamine	92-94	P53	Homo sapiens	379-382
17593335-5	2007	The level of phosphorylation on several serine residues within that region of p53 increases in response to disheveled activation, partially contributing to p53 activation.	Serine	40-46	P53	Homo sapiens	78-81
17593335-5	2007	The level of phosphorylation on several serine residues within that region of p53 increases in response to disheveled activation, partially contributing to p53 activation.	Serine	40-46	P53	Homo sapiens	156-159
17949986-2	2007	Since their discovery approximately ten years ago, significant progress has been made in understanding their subcellular targeting, their relationship to p53, their activation by bioactive phospholipids, and their key role in reading the histone code via PHD fingers, with subsequent effects on histone acetylation and transcriptional regulation.	Phospholipids	189-202	P53	Homo sapiens	154-157
17823933-0	2007	Paclitaxel enhanced radiation sensitization for the suppression of human prostate cancer tumor growth via a p53 independent pathway.	Paclitaxel	0-10	P53	Homo sapiens	108-111
17823933-1	2007	BACKGROUND: This study investigated the influence of p53 status on treatment using combined paclitaxel and irradiation for human prostate cancer (PC) in vitro and in vivo.	Paclitaxel	92-102	P53	Homo sapiens	53-56
17823933-2	2007	METHODS: Enhancement of the radiation response by paclitaxel was determined by MTT and clonogenic assays in four sublines of the human PC cell line, LNCaP, stably transfected to express different p53 mutations found in PC patients.	Paclitaxel	50-60	P53	Homo sapiens	196-199
17823933-5	2007	RESULTS: Paclitaxel (8-10 nM) suppressed cell proliferation by 50% by inducing G2M mitotic arrest in LNCaP cell lines transfected to overexpress wild-type or mutant p53.	Paclitaxel	9-19	P53	Homo sapiens	165-168
17823933-10	2007	CONCLUSIONS: Pre-treatment with paclitaxel enhances radiation efficacy on cell killing and suppression of growth of human PC cell lines in vitro and in vivo via p53 independent pathways.	Paclitaxel	32-42	P53	Homo sapiens	161-164
17823933-11	2007	Paclitaxel has potential for use as a radiosensitizer in the treatment of patients with PC with either wild-type or mutant p53 genetic status.	Paclitaxel	0-10	P53	Homo sapiens	123-126
17914575-6	2007	A comparison with the wild-type after 1 nano-second molecular dynamic simulation analysis revealed a significant structural change (over 4A displacement) in the contact loop Lys-Ser-Val which lies upstream and next to the mutated site in the TP53, that sterically prevents its DNA-binding activity.	Lysine	174-177	P53	Homo sapiens	242-246
17914575-6	2007	A comparison with the wild-type after 1 nano-second molecular dynamic simulation analysis revealed a significant structural change (over 4A displacement) in the contact loop Lys-Ser-Val which lies upstream and next to the mutated site in the TP53, that sterically prevents its DNA-binding activity.	Serine	178-181	P53	Homo sapiens	242-246
17914575-8	2007	To demonstrate the degree of loss of function, functional assays in yeast and bacteria with oligonucleotides for competitive electrophoretic mobility shift assays (EMSAs) were done proving that this mutation decreases TP53 ability to bind DNA of the TP53 response element from the human p21 gene.	Oligonucleotides	92-108	P53	Homo sapiens	218-222
17914575-8	2007	To demonstrate the degree of loss of function, functional assays in yeast and bacteria with oligonucleotides for competitive electrophoretic mobility shift assays (EMSAs) were done proving that this mutation decreases TP53 ability to bind DNA of the TP53 response element from the human p21 gene.	Oligonucleotides	92-108	P53	Homo sapiens	250-254
17940011-1	2007	A recently discovered phosphatidylinositol monophosphate, phosphatidylinositol 5-phosphate (PtdIns-5-P), plays an important role in nuclear signaling by influencing p53-dependent apoptosis.	phosphatidylinositol monophosphate	22-56	P53	Homo sapiens	165-168
17876337-1	2007	In advanced breast cancers, TP53 mutation is highly predictive of complete response to high-dose epirubicin/cyclophosphamide chemotherapy.	Epirubicin	97-107	P53	Homo sapiens	28-32
17954263-1	2007	A common polymorphism at codon 72 of TP53, the gene encoding the tumor suppressor protein p53, encodes either arginine or proline.	Arginine	110-118	P53	Homo sapiens	37-41
17912033-1	2007	We previously reported that the Polo-like Kinase 2 gene (Plk2/Snk) is a direct target for transcriptional regulation by p53 and that silencing Plk2 sensitizes cancer cells to Taxol-induced apoptosis.	Paclitaxel	175-180	P53	Homo sapiens	120-123
17954263-1	2007	A common polymorphism at codon 72 of TP53, the gene encoding the tumor suppressor protein p53, encodes either arginine or proline.	Arginine	110-118	P53	Homo sapiens	90-93
17927872-1	2007	BACKGROUND &amp; OBJECTIVE: 53BP1 is one of p53-binding proteins, which can enhance the transcriptional activation of p53 and plays a key role in tumor suppression.	Adenosine Monophosphate	12-15	P53	Homo sapiens	44-47
17582679-7	2007	Furthermore, LMP1-induced phosphorylation of p53 at Ser15 was directly by ERKs; at Ser20 and Thr81 by JNK, at Ser 15 and Ser392 by p38 kinase.	Serine	52-55	P53	Homo sapiens	45-48
17927872-1	2007	BACKGROUND &amp; OBJECTIVE: 53BP1 is one of p53-binding proteins, which can enhance the transcriptional activation of p53 and plays a key role in tumor suppression.	Adenosine Monophosphate	12-15	P53	Homo sapiens	118-121
17932466-6	2007	Our results demonstrate that the wild-type p53-expressing tumor xenografts exhibit high levels of glucose uptake, similar to those observed in p53-null tumor xenografts, by quantitative PET imaging indicative of the glycolytic switch.	Glucose	98-105	P53	Homo sapiens	43-46
17823286-4	2007	Here, we show that these organ-cultured HFs respond to a key cyclophosphamide metabolite, 4-hydroperoxycyclophosphamide (4-HC), in a manner that resembles chemotherapy-induced HF dystrophy as it occurs in vivo: namely, 4-HC induced melanin clumping and melanin incontinence, down-regulated keratinocyte proliferation, massively up-regulated apoptosis of hair matrix keratinocytes, prematurely induced catagen, and up-regulated p53.	perfosfamide	90-119	P53	Homo sapiens	427-430
17823286-4	2007	Here, we show that these organ-cultured HFs respond to a key cyclophosphamide metabolite, 4-hydroperoxycyclophosphamide (4-HC), in a manner that resembles chemotherapy-induced HF dystrophy as it occurs in vivo: namely, 4-HC induced melanin clumping and melanin incontinence, down-regulated keratinocyte proliferation, massively up-regulated apoptosis of hair matrix keratinocytes, prematurely induced catagen, and up-regulated p53.	perfosfamide	121-125	P53	Homo sapiens	427-430
17510082-7	2007	Moreover, aspirin induced cell death mainly in cells expressing p53.	Aspirin	10-17	P53	Homo sapiens	64-67
17510082-8	2007	Aspirin induced the phosphorylation of p53 at residue Ser15 within 8 h in a caffeine-dependent manner, and also caused the activation of checkpoint kinase 2 and the cleavage of caspase 7.	Aspirin	0-7	P53	Homo sapiens	39-42
17510082-9	2007	Our results suggest that aspirin induces a G1 arrest and apoptosis by activating p53 and p21Waf1/Cip1 in an ATM-dependent way.	Aspirin	25-32	P53	Homo sapiens	81-84
17979566-11	2007	CONCLUSIONS: Therefore, p53 seemed to have a significant role in cellular glucose metabolism and G2/M checkpoint, according to beta-irradiation, and could cause a different therapeutic response of (18)F-FDG uptake in cancer cells.	Glucose	74-81	P53	Homo sapiens	24-27
17644309-9	2007	These findings collectively support a novel mechanism in which the PKCdelta--&gt;IKKalpha signaling pathway contributes to ROS-induced activation of the p53 tumor suppressor.	Reactive Oxygen Species	123-126	P53	Homo sapiens	153-156
17612589-4	2007	We demonstrate that macaques progressing faster display greater expression of TGF-beta and Indoleamine 2,3 dioxygenase in particular in intestinal tissues associated with a phosphorylation of the p53 protein on serine 15 in CD8+ T cells from Mes lymph nodes.	Serine	211-217	P53	Homo sapiens	196-199
17938582-4	2007	The structure reveals that although the principle features of the Mdm2-p53 interaction are preserved in the Mdmx-p53 complex, the Mdmx hydrophobic cleft on which the p53 peptide binds is significantly altered: a part of the cleft is blocked by sidechains of Met and Tyr of the p53-binding pocket of Mdmx.	Tyrosine	266-269	P53	Homo sapiens	113-116
17938582-4	2007	The structure reveals that although the principle features of the Mdm2-p53 interaction are preserved in the Mdmx-p53 complex, the Mdmx hydrophobic cleft on which the p53 peptide binds is significantly altered: a part of the cleft is blocked by sidechains of Met and Tyr of the p53-binding pocket of Mdmx.	Tyrosine	266-269	P53	Homo sapiens	113-116
17938582-4	2007	The structure reveals that although the principle features of the Mdm2-p53 interaction are preserved in the Mdmx-p53 complex, the Mdmx hydrophobic cleft on which the p53 peptide binds is significantly altered: a part of the cleft is blocked by sidechains of Met and Tyr of the p53-binding pocket of Mdmx.	Tyrosine	266-269	P53	Homo sapiens	113-116
17275163-0	2007	Synergy of interferon-alpha and 5-fluorouracil in human renal cell carcinoma requires p53 activity.	Fluorouracil	32-46	P53	Homo sapiens	86-89
17275163-5	2007	RESULTS: We demonstrated synergy of IFN-alpha and 5-FU in five RCC cell lines with wild-type p53.	Fluorouracil	50-54	P53	Homo sapiens	93-96
17275163-8	2007	However, the synergistic inhibition by IFN-alpha and 5-FU was abolished when the cell lines were transfected with p53 dominant-negative vector.	Fluorouracil	53-57	P53	Homo sapiens	114-117
17275163-9	2007	CONCLUSIONS: The synergy of IFN-alpha and 5-FU requires p53 activity, suggesting that p53 status may serve as a predictive factor for response to the combination therapy.	Fluorouracil	42-46	P53	Homo sapiens	56-59
17275163-9	2007	CONCLUSIONS: The synergy of IFN-alpha and 5-FU requires p53 activity, suggesting that p53 status may serve as a predictive factor for response to the combination therapy.	Fluorouracil	42-46	P53	Homo sapiens	86-89
17275163-10	2007	Because metastatic RCC frequently has p53 mutations, therapy restoring p53 may markedly improve the response rate of immunochemical therapy combining IFN-alpha and 5-FU.	Fluorouracil	164-168	P53	Homo sapiens	38-41
17275163-10	2007	Because metastatic RCC frequently has p53 mutations, therapy restoring p53 may markedly improve the response rate of immunochemical therapy combining IFN-alpha and 5-FU.	Fluorouracil	164-168	P53	Homo sapiens	71-74
17786323-8	2007	Expression of Her2 or p53 was a significant prognostic indicator in the tamoxifen alone group.	Tamoxifen	72-81	P53	Homo sapiens	22-25
17646389-2	2007	Recently, we discovered that lysine methylation of p53 at K372 by Set7/9 (also known as SET7 and Set9) is important for transcriptional activation and stabilization of p53.	Lysine	29-35	P53	Homo sapiens	51-54
17499351-3	2007	Unlike the tumour suppressor gene encoding p53 that is notoriously prone to inactivating mutations but whose function is essential for induction of apoptosis by DNA-targeting agents (such as doxorubicin or 5-fluorouracil), mitochondria present targets that are not so compromised by genetic mutation and whose targeting overcomes problems with mutations of upstream targets such as p53.	Doxorubicin	191-202	P53	Homo sapiens	43-46
17499351-3	2007	Unlike the tumour suppressor gene encoding p53 that is notoriously prone to inactivating mutations but whose function is essential for induction of apoptosis by DNA-targeting agents (such as doxorubicin or 5-fluorouracil), mitochondria present targets that are not so compromised by genetic mutation and whose targeting overcomes problems with mutations of upstream targets such as p53.	Fluorouracil	206-220	P53	Homo sapiens	43-46
17646389-2	2007	Recently, we discovered that lysine methylation of p53 at K372 by Set7/9 (also known as SET7 and Set9) is important for transcriptional activation and stabilization of p53.	Lysine	29-35	P53	Homo sapiens	168-171
17646389-5	2007	Significantly, we show that lysine methylation of p53 is important for its subsequent acetylation, resulting in stabilization of the p53 protein.	Lysine	28-34	P53	Homo sapiens	50-53
17646389-5	2007	Significantly, we show that lysine methylation of p53 is important for its subsequent acetylation, resulting in stabilization of the p53 protein.	Lysine	28-34	P53	Homo sapiens	133-136
17951408-3	2007	The down-regulated expression of hOGG1 by its small interfering RNA prominently triggers the H(2)O(2)-induced apoptosis in human fibroblasts GM00637 and human lung carcinoma H1299 cells via the p53-mediated apoptotic pathway.	Hydrogen Peroxide	93-101	P53	Homo sapiens	194-197
17646389-8	2007	Collectively, these results suggest that the cross talk between lysine methylation and acetylation is critical for p53 activation in response to DNA damage and that Set7/9 may play an important role in tumor suppression.	Lysine	64-70	P53	Homo sapiens	115-118
17951408-5	2007	The p53-small interfering RNA transfection into the hOGG1-deficient GM00637 markedly inhibited the H(2)O(2)-induced activation of p53-downstream target proteins such as p21, Noxa, and caspase-3/7, which eventually resulted in the increased cell viability.	gm00637	68-75	P53	Homo sapiens	4-7
17951408-5	2007	The p53-small interfering RNA transfection into the hOGG1-deficient GM00637 markedly inhibited the H(2)O(2)-induced activation of p53-downstream target proteins such as p21, Noxa, and caspase-3/7, which eventually resulted in the increased cell viability.	gm00637	68-75	P53	Homo sapiens	130-133
17666403-3	2007	CHIP preferentially binds to the p53 mutant phenotype and restored the DNA binding activity of heat-denatured p53 in an ATP-independent manner.	Adenosine Triphosphate	120-123	P53	Homo sapiens	110-113
17951408-5	2007	The p53-small interfering RNA transfection into the hOGG1-deficient GM00637 markedly inhibited the H(2)O(2)-induced activation of p53-downstream target proteins such as p21, Noxa, and caspase-3/7, which eventually resulted in the increased cell viability.	Hydrogen Peroxide	99-107	P53	Homo sapiens	4-7
17951408-5	2007	The p53-small interfering RNA transfection into the hOGG1-deficient GM00637 markedly inhibited the H(2)O(2)-induced activation of p53-downstream target proteins such as p21, Noxa, and caspase-3/7, which eventually resulted in the increased cell viability.	Hydrogen Peroxide	99-107	P53	Homo sapiens	130-133
17951408-8	2007	Therefore, we suggest that although p53 is a major modulator of apoptosis, hOGG1 also plays a pivotal role in protecting cells against the H(2)O(2)-induced apoptosis at the upstream of the p53-dependent pathway to confer a survival advantage to human fibroblasts and human lung carcinomas through maintaining their genomic stability.	Hydrogen Peroxide	139-147	P53	Homo sapiens	189-192
17891139-3	2007	Here, we identify the major poly(ADP-ribosyl)ated sites of p53 by PARP-1 and find that PARP-1-mediated poly(ADP-ribosyl)ation blocks the interaction between p53 and the nuclear export receptor Crm1, resulting in nuclear accumulation of p53.	ribosyl)	37-45	P53	Homo sapiens	59-62
17891139-3	2007	Here, we identify the major poly(ADP-ribosyl)ated sites of p53 by PARP-1 and find that PARP-1-mediated poly(ADP-ribosyl)ation blocks the interaction between p53 and the nuclear export receptor Crm1, resulting in nuclear accumulation of p53.	ribosyl)	37-45	P53	Homo sapiens	157-160
17891139-3	2007	Here, we identify the major poly(ADP-ribosyl)ated sites of p53 by PARP-1 and find that PARP-1-mediated poly(ADP-ribosyl)ation blocks the interaction between p53 and the nuclear export receptor Crm1, resulting in nuclear accumulation of p53.	ribosyl)	37-45	P53	Homo sapiens	157-160
17651689-8	2007	In summary, we concluded that the nuclear Trx-1 is required to resist apoptosis of MCF-7 cells induced by cisplatin, probably through up-regulating the anti-apoptotic gene, p53.	Cisplatin	106-115	P53	Homo sapiens	173-176
17903248-10	2007	Endogenous axolotl p53 was activated following UV irradiation (100 j/m2) or treatment with an alkylating agent as measured using serine 15 phosphorylation and the expression of the endogenous p53 target Gadd45.	Serine	129-135	P53	Homo sapiens	19-22
17805299-1	2007	p53, the tumour suppressor and transcriptional activator, is regulated by numerous post-translational modifications, including lysine methylation.	Lysine	127-133	P53	Homo sapiens	0-3
17823410-8	2007	Furthermore, as expected from p53 binding to the mir-34b/c promoter, doxorubicin treatment of wild-type, but not p53-deficient, cells resulted in an increase of mir-34b/mir-34c expression.	Doxorubicin	69-80	P53	Homo sapiens	30-33
17636258-5	2007	Topotecan- and paclitaxel-resistant prostate cancer lines were as sensitive to p53p-Ant-induced targeted necrosis as parental lines.	Paclitaxel	15-25	P53	Homo sapiens	79-83
17805299-8	2007	These observations show that p53 is dynamically regulated by lysine methylation and demethylation and that the methylation status at a single lysine residue confers distinct regulatory output.	Lysine	61-67	P53	Homo sapiens	29-32
17805299-8	2007	These observations show that p53 is dynamically regulated by lysine methylation and demethylation and that the methylation status at a single lysine residue confers distinct regulatory output.	Lysine	142-148	P53	Homo sapiens	29-32
17626009-0	2007	Chronic treatment with resveratrol induces redox stress- and ataxia telangiectasia-mutated (ATM)-dependent senescence in p53-positive cancer cells.	Resveratrol	23-34	P53	Homo sapiens	121-124
17626009-7	2007	Molecular mediators on the way from increased ROS levels to the observed growth arrest include p38 MAPK, p53, and p21.	Reactive Oxygen Species	46-49	P53	Homo sapiens	105-108
17596534-6	2007	Furthermore, CsA exposure lead to a reduction of telomere length, increased p53 serine 15 phosphorylation, and caused an upregulation of the cell cycle inhibitor p21(Kip1) (CDKN1A) mRNA levels.	Cyclosporine	13-16	P53	Homo sapiens	76-79
17596534-6	2007	Furthermore, CsA exposure lead to a reduction of telomere length, increased p53 serine 15 phosphorylation, and caused an upregulation of the cell cycle inhibitor p21(Kip1) (CDKN1A) mRNA levels.	Serine	80-86	P53	Homo sapiens	76-79
17505786-0	2007	Apoptosis by cisplatin requires p53 mediated p38alpha MAPK activation through ROS generation.	Cisplatin	13-22	P53	Homo sapiens	32-35
17505786-8	2007	We conclude that the p53/ROS/p38alpha MAPK cascade is essential for cisplatin-induced cell death in HCT116 cells and the subsequent p38alpha/p53 positive feedback loop strongly enhances the initial p53 activation.	Reactive Oxygen Species	25-28	P53	Homo sapiens	141-144
17505786-0	2007	Apoptosis by cisplatin requires p53 mediated p38alpha MAPK activation through ROS generation.	Reactive Oxygen Species	78-81	P53	Homo sapiens	32-35
17698835-2	2007	Since the pro-apoptotic effect is associated with activation of p53, in this study we have investigated the efficacy of combination of ST1926 with cisplatin, a DNA-damaging agent that is known to induce p53-dependent apoptosis.	Cisplatin	147-156	P53	Homo sapiens	203-206
17505786-2	2007	The presence of wild type p53 has been suggested to be important for cisplatin cytotoxicity, hence we found that cisplatin induced apoptosis in cell lines with functional p53.	Cisplatin	69-78	P53	Homo sapiens	26-29
17505786-2	2007	The presence of wild type p53 has been suggested to be important for cisplatin cytotoxicity, hence we found that cisplatin induced apoptosis in cell lines with functional p53.	Cisplatin	113-122	P53	Homo sapiens	26-29
17505786-2	2007	The presence of wild type p53 has been suggested to be important for cisplatin cytotoxicity, hence we found that cisplatin induced apoptosis in cell lines with functional p53.	Cisplatin	113-122	P53	Homo sapiens	171-174
17505786-3	2007	Using the HCT116 colon carcinoma derived cell line we have established that the apoptotic activity of cisplatin requires the onset of a p53-mediated p38alpha MAPK pathway through generation of reactive oxygen species (ROS).	Cisplatin	102-111	P53	Homo sapiens	136-139
17970084-3	2007	Berberine enhanced the apoptosis of Ca Ski cells with the induction of a higher ratio of p53 and Bax/Bcl-2 proteins, increased levels of reactive oxygen species (ROS) and Ca2+, disruption of the mitochondrial membrane potential, and promotion of caspase-3 activity.	Berberine	0-9	P53	Homo sapiens	89-92
17505786-3	2007	Using the HCT116 colon carcinoma derived cell line we have established that the apoptotic activity of cisplatin requires the onset of a p53-mediated p38alpha MAPK pathway through generation of reactive oxygen species (ROS).	Reactive Oxygen Species	193-216	P53	Homo sapiens	136-139
17505786-3	2007	Using the HCT116 colon carcinoma derived cell line we have established that the apoptotic activity of cisplatin requires the onset of a p53-mediated p38alpha MAPK pathway through generation of reactive oxygen species (ROS).	Reactive Oxygen Species	218-221	P53	Homo sapiens	136-139
17505786-4	2007	HCT116 p53-deficient cells were much less sensitive to apoptosis by cisplatin than their p53wt counterparts, where apoptosis was strongly inhibited by antioxidants.	Cisplatin	68-77	P53	Homo sapiens	7-10
17505786-5	2007	Moreover, the presence of pifithrin-alpha, an inhibitor of p53 transcriptional activity, blocked cisplatin-induced apoptosis, reduced the generation of ROS produced upon cisplatin treatment.	Cisplatin	97-106	P53	Homo sapiens	59-62
17505786-5	2007	Moreover, the presence of pifithrin-alpha, an inhibitor of p53 transcriptional activity, blocked cisplatin-induced apoptosis, reduced the generation of ROS produced upon cisplatin treatment.	Cisplatin	170-179	P53	Homo sapiens	59-62
17505786-6	2007	In addition, we have identified p38alpha as the isoform necessary for cisplatin-induced apoptosis, upon activation by p53-mediated ROS production.	Cisplatin	70-79	P53	Homo sapiens	118-121
17505786-6	2007	In addition, we have identified p38alpha as the isoform necessary for cisplatin-induced apoptosis, upon activation by p53-mediated ROS production.	Reactive Oxygen Species	131-134	P53	Homo sapiens	118-121
17505786-8	2007	We conclude that the p53/ROS/p38alpha MAPK cascade is essential for cisplatin-induced cell death in HCT116 cells and the subsequent p38alpha/p53 positive feedback loop strongly enhances the initial p53 activation.	Reactive Oxygen Species	25-28	P53	Homo sapiens	21-24
17505786-8	2007	We conclude that the p53/ROS/p38alpha MAPK cascade is essential for cisplatin-induced cell death in HCT116 cells and the subsequent p38alpha/p53 positive feedback loop strongly enhances the initial p53 activation.	Reactive Oxygen Species	25-28	P53	Homo sapiens	141-144
17505786-8	2007	We conclude that the p53/ROS/p38alpha MAPK cascade is essential for cisplatin-induced cell death in HCT116 cells and the subsequent p38alpha/p53 positive feedback loop strongly enhances the initial p53 activation.	Cisplatin	68-77	P53	Homo sapiens	21-24
17505786-8	2007	We conclude that the p53/ROS/p38alpha MAPK cascade is essential for cisplatin-induced cell death in HCT116 cells and the subsequent p38alpha/p53 positive feedback loop strongly enhances the initial p53 activation.	Cisplatin	68-77	P53	Homo sapiens	141-144
17505786-8	2007	We conclude that the p53/ROS/p38alpha MAPK cascade is essential for cisplatin-induced cell death in HCT116 cells and the subsequent p38alpha/p53 positive feedback loop strongly enhances the initial p53 activation.	Cisplatin	68-77	P53	Homo sapiens	141-144
17700259-10	2007	The carbon ions had a stronger effect on p53 and p21 expression than the gamma-ray irradiation.	Carbon	4-10	P53	Homo sapiens	41-44
17640298-1	2007	Expression of excision repair cross-complementation group 1 (ERCC1), p53, or thioredoxin (TRX) is reported to be correlated with resistance to platinum-based drugs.	Platinum	143-151	P53	Homo sapiens	69-72
17079356-6	2007	Among the germline p53 codon 72 heterozygotes, the Pro allele was preferentially lost (p = 0.02) while the Arg allele was mutated in the majority of cases.	Arginine	107-110	P53	Homo sapiens	19-22
17707275-0	2007	Phenylbutyrate sensitizes human glioblastoma cells lacking wild-type p53 function to ionizing radiation.	Phenylbutyrates	0-14	P53	Homo sapiens	69-72
17707275-14	2007	There was no radiopotentiating effect in two cell lines with wild-type p53, but knockdown of wild-type p53 resulted in radiosensitization by PB.	Phenylbutyrates	141-143	P53	Homo sapiens	103-106
17707275-16	2007	This suggests the potential application of combined PB and radiotherapy in glioblastoma harboring mutant p53.	Phenylbutyrates	52-54	P53	Homo sapiens	105-108
17582597-9	2007	In the "inflammatory" scenario, p53, activated by DNA damage induced by oxygen and nitrogen species, recruits NF-kappaB to activate COX-2, resulting in antiapoptotic effects that contribute to cell expansion in inflammatory precursor lesions.	Oxygen	72-78	P53	Homo sapiens	32-35
17582597-9	2007	In the "inflammatory" scenario, p53, activated by DNA damage induced by oxygen and nitrogen species, recruits NF-kappaB to activate COX-2, resulting in antiapoptotic effects that contribute to cell expansion in inflammatory precursor lesions.	Nitrogen	83-91	P53	Homo sapiens	32-35
17671694-9	2007	It is suggested that the cisplatin-resistance of CP70 cells is mediated by stabilizing p53.	Cisplatin	25-34	P53	Homo sapiens	87-90
17671694-11	2007	Therefore, pGSK-3beta-ser-9 may confer the cisplatin resistance of ovarian carcinomas through the stabilization of p53 expression.	Serine	22-25	P53	Homo sapiens	115-118
17671694-11	2007	Therefore, pGSK-3beta-ser-9 may confer the cisplatin resistance of ovarian carcinomas through the stabilization of p53 expression.	Cisplatin	43-52	P53	Homo sapiens	115-118
17517898-2	2007	To develop a Chk1-specific cell-based assay, stable clones were established in which Chk1 kinase domain fused at its N-terminus with p53 through 4 tandem repeats of Gly-Gly-Gly-Gly-Ser was expressed in an inducible manner.	Serine	181-184	P53	Homo sapiens	133-136
17517898-4	2007	Only in the presence of an inducer molecule was phosphorylation of p53 at Ser-15 in the stable clones induced.	Serine	74-77	P53	Homo sapiens	67-70
17443686-3	2007	Manipulation of intracellular GSH content through pharmacological inhibition of glutamate-cysteine ligase (GCL) indicated that GSH depletion potentiated nitrosative stress, DNA damage, phosphorylation of the tumor suppressor p53 (Ser-18) and upregulation of p21(cip1/waf1) upon NO stimulation.	Glutathione	30-33	P53	Homo sapiens	225-228
17443686-3	2007	Manipulation of intracellular GSH content through pharmacological inhibition of glutamate-cysteine ligase (GCL) indicated that GSH depletion potentiated nitrosative stress, DNA damage, phosphorylation of the tumor suppressor p53 (Ser-18) and upregulation of p21(cip1/waf1) upon NO stimulation.	Glutathione	127-130	P53	Homo sapiens	225-228
17443686-5	2007	We found that the decrease in cyclin D1 levels induced by NO was GSH-sensitive implying that the redox regulation of NO-mediated cytostasis was a multifaceted process and that both p53/p21(cip1/waf1) and p53 independent cyclin D1 pathways were involved.	Glutathione	65-68	P53	Homo sapiens	181-184
17400331-9	2007	RFLP analysis of p53 codon 72 revealed 32 homozygotes for arg/arg allele (50.8%), 26 heterozygotes for arg/pro allele (41.3%), and 5 homozygotes for pro/pro allele (7.9%).	Arginine	58-61	P53	Homo sapiens	17-20
17443686-5	2007	We found that the decrease in cyclin D1 levels induced by NO was GSH-sensitive implying that the redox regulation of NO-mediated cytostasis was a multifaceted process and that both p53/p21(cip1/waf1) and p53 independent cyclin D1 pathways were involved.	Glutathione	65-68	P53	Homo sapiens	204-207
17400331-9	2007	RFLP analysis of p53 codon 72 revealed 32 homozygotes for arg/arg allele (50.8%), 26 heterozygotes for arg/pro allele (41.3%), and 5 homozygotes for pro/pro allele (7.9%).	Arginine	62-65	P53	Homo sapiens	17-20
17400331-9	2007	RFLP analysis of p53 codon 72 revealed 32 homozygotes for arg/arg allele (50.8%), 26 heterozygotes for arg/pro allele (41.3%), and 5 homozygotes for pro/pro allele (7.9%).	Arginine	62-65	P53	Homo sapiens	17-20
17718901-5	2007	Treatment of LNCaP cells with resveratrol resulted in generation of reactive oxygen species, translocation of Bax and p53 to mitochondria, subsequent drop in mitochondrial membrane potential, release of mitochondrial proteins (cytochrome c, AIF, Smac/DIABLO and Omi/HtrA2), activation of caspase-3 and caspase-9 and induction of apoptosis.	Resveratrol	30-41	P53	Homo sapiens	118-121
17898864-1	2007	gamma-Irradiation-mediated ataxia telangiectasia mutated (ATM)-dependent dephosphorylation of serine 376 (S376) at the carboxyl terminus of human p53 results in the exposure of the 14-3-3 consensus-binding site, which includes serine 378 (S378).	Serine	94-100	P53	Homo sapiens	146-149
17898864-1	2007	gamma-Irradiation-mediated ataxia telangiectasia mutated (ATM)-dependent dephosphorylation of serine 376 (S376) at the carboxyl terminus of human p53 results in the exposure of the 14-3-3 consensus-binding site, which includes serine 378 (S378).	Serine	227-233	P53	Homo sapiens	146-149
17531965-3	2007	RESULTS: The age-adjusted odds ratios (ORs) for the Ile/Val genotype of CYP1A1 Ile462Val polymorphism in women and the Arg/Pro genotype of TP53 Arg72Pro polymorphism in men were observed to be 2.70 (95% CI: 1.14-6.40) and 4.32 (95% CI: 1.08-17.2), respectively.	Arginine	119-122	P53	Homo sapiens	139-143
17711579-9	2007	We identified 37 p53-responsive genes that were altered after cisplatin exposure.	Cisplatin	62-71	P53	Homo sapiens	17-20
17707234-0	2007	Modulation of p53 function by SET8-mediated methylation at lysine 382.	Lysine	59-65	P53	Homo sapiens	14-17
17535811-2	2007	Here we found that NFBD1 protects cells from apoptotic cell death by inhibiting phosphorylation of p53 at Ser-15 under steady state as well as early phase of DNA damage, thereby blocking its transcriptional and pro-apoptotic activities.	Serine	106-109	P53	Homo sapiens	99-102
17535811-6	2007	Additionally, BRCT domains, which can interact with p53, reduced the adriamycin-induced phosphorylation levels of p53 at Ser-15 and also suppressed the transcriptional activity of p53.	Doxorubicin	69-79	P53	Homo sapiens	52-55
17535811-6	2007	Additionally, BRCT domains, which can interact with p53, reduced the adriamycin-induced phosphorylation levels of p53 at Ser-15 and also suppressed the transcriptional activity of p53.	Doxorubicin	69-79	P53	Homo sapiens	114-117
17535811-6	2007	Additionally, BRCT domains, which can interact with p53, reduced the adriamycin-induced phosphorylation levels of p53 at Ser-15 and also suppressed the transcriptional activity of p53.	Doxorubicin	69-79	P53	Homo sapiens	114-117
17535811-6	2007	Additionally, BRCT domains, which can interact with p53, reduced the adriamycin-induced phosphorylation levels of p53 at Ser-15 and also suppressed the transcriptional activity of p53.	Serine	121-124	P53	Homo sapiens	52-55
17535811-6	2007	Additionally, BRCT domains, which can interact with p53, reduced the adriamycin-induced phosphorylation levels of p53 at Ser-15 and also suppressed the transcriptional activity of p53.	Serine	121-124	P53	Homo sapiens	114-117
17535811-6	2007	Additionally, BRCT domains, which can interact with p53, reduced the adriamycin-induced phosphorylation levels of p53 at Ser-15 and also suppressed the transcriptional activity of p53.	Serine	121-124	P53	Homo sapiens	114-117
17707234-4	2007	We find that SET8 specifically monomethylates p53 at lysine 382 (p53K382me1).	Lysine	53-59	P53	Homo sapiens	46-49
17666793-0	2007	Irinotecan-induced apoptosis is inhibited by increased P-glycoprotein expression and decreased p53 in human hepatocellular carcinoma cells.	Irinotecan	0-10	P53	Homo sapiens	95-98
17666793-7	2007	SN-38 significantly induced apoptosis in Huh7 cells at 24 h. SN-38 also increased the expression of p53, Bax, and caspase-9 and decreased Bcl-xL expression in Huh7 cells.	Irinotecan	0-5	P53	Homo sapiens	100-103
17666793-7	2007	SN-38 significantly induced apoptosis in Huh7 cells at 24 h. SN-38 also increased the expression of p53, Bax, and caspase-9 and decreased Bcl-xL expression in Huh7 cells.	Irinotecan	61-66	P53	Homo sapiens	100-103
17666793-8	2007	SN-38 decreased p53 expression and increased P-gp expression after 120 h, resulting in inhibition of apoptosis.	Irinotecan	0-5	P53	Homo sapiens	16-19
17666793-10	2007	SN-38-induced P-gp expression was additionally enhanced by p53 decoy oligodeoxynucleotide.	Irinotecan	0-5	P53	Homo sapiens	59-62
17585903-4	2007	As a result, methyl 2,5-dihydromethylcinnimate (2,5-MeC), a tyrosine kinase inhibitor, enhanced expression and/or stability of PML proteins and induced PML-NB formation in p53 null H1299 cells established from non-small cell lung cancer (NSCLC) and wild-type p53-expressing U2OS cells derived from osteosarcoma.	methyl 2,5-dihydromethylcinnimate	13-46	P53	Homo sapiens	172-175
17585903-4	2007	As a result, methyl 2,5-dihydromethylcinnimate (2,5-MeC), a tyrosine kinase inhibitor, enhanced expression and/or stability of PML proteins and induced PML-NB formation in p53 null H1299 cells established from non-small cell lung cancer (NSCLC) and wild-type p53-expressing U2OS cells derived from osteosarcoma.	methyl 2,5-dihydromethylcinnimate	13-46	P53	Homo sapiens	259-262
17392828-6	2007	DeltaNp63alpha also induces apoptosis in HaCaT and SCC-13 cells, which encode inactive p53 genes, suggesting that the response is p53 independent in these cell lines.	deltanp63alpha	0-14	P53	Homo sapiens	87-90
17914225-4	2007	By computing the free energies of wild-type and mutant p53c binding to DNA and decomposing them into contributions from individual residues, the DNA-binding loss upon charge/noncharge -conserving mutation of Arg 273 was attributed not only to the loss of DNA phosphate contacts, but also to longer-range structural changes caused by the loss of the Asp 281 salt-bridge.	Arginine	208-211	P53	Homo sapiens	55-58
17914225-4	2007	By computing the free energies of wild-type and mutant p53c binding to DNA and decomposing them into contributions from individual residues, the DNA-binding loss upon charge/noncharge -conserving mutation of Arg 273 was attributed not only to the loss of DNA phosphate contacts, but also to longer-range structural changes caused by the loss of the Asp 281 salt-bridge.	Phosphates	259-268	P53	Homo sapiens	55-58
17914225-5	2007	The results herein and in previous works suggest that Asp 281 plays a critical role in the sequence-specific DNA-binding function of p53c by (i)orienting Arg 273 and Arg 280 in an optimal position to interact with the phosphate and base groups of the consensus DNA, respectively, and (ii) helping to maintain the proper DNA-binding protein conformation.	Arginine	154-157	P53	Homo sapiens	133-136
17914225-5	2007	The results herein and in previous works suggest that Asp 281 plays a critical role in the sequence-specific DNA-binding function of p53c by (i)orienting Arg 273 and Arg 280 in an optimal position to interact with the phosphate and base groups of the consensus DNA, respectively, and (ii) helping to maintain the proper DNA-binding protein conformation.	Arginine	166-169	P53	Homo sapiens	133-136
17914225-5	2007	The results herein and in previous works suggest that Asp 281 plays a critical role in the sequence-specific DNA-binding function of p53c by (i)orienting Arg 273 and Arg 280 in an optimal position to interact with the phosphate and base groups of the consensus DNA, respectively, and (ii) helping to maintain the proper DNA-binding protein conformation.	Phosphates	218-227	P53	Homo sapiens	133-136
17392828-6	2007	DeltaNp63alpha also induces apoptosis in HaCaT and SCC-13 cells, which encode inactive p53 genes, suggesting that the response is p53 independent in these cell lines.	deltanp63alpha	0-14	P53	Homo sapiens	130-133
17070097-6	2007	In addition, cotreatment with the AHR antagonist, 3"-methoxy-4"-nitroflavone (MNF) blocked the effects of TCDD and CSC on p53 and CYP1A1 expression.	Polychlorinated Dibenzodioxins	106-110	P53	Homo sapiens	122-125
17616157-4	2007	Using these modified SP microarrays, enhancement factors of 229 and 126 were obtained for prostate-specific antigen (PSA) and p53 oligonucleotide detection, respectively.	Oligonucleotides	130-145	P53	Homo sapiens	126-129
17070096-7	2007	Mutational analysis of p53 gene revealed an A--&gt;G transition at the second base of codon 220, resulting in amino acid substitution from tyrosine to cysteine in the protein.	Tyrosine	139-147	P53	Homo sapiens	23-26
17070096-7	2007	Mutational analysis of p53 gene revealed an A--&gt;G transition at the second base of codon 220, resulting in amino acid substitution from tyrosine to cysteine in the protein.	Cysteine	151-159	P53	Homo sapiens	23-26
17070097-5	2007	A role of the AHR in mediating these events is indicated by the observations that the TCDD and CSC-induced decreases in p15(INK4b), p16(INK4a) and p53 expression was accompanied by a corresponding increase in the expression levels of the AHR target gene, CYP1A1.	Polychlorinated Dibenzodioxins	86-90	P53	Homo sapiens	147-150
17668048-1	2007	Tumor suppressor SMAR1 interacts and stabilizes p53 through phosphorylation at its serine-15 residue.	Serine	83-89	P53	Homo sapiens	48-51
17668048-3	2007	Upon Doxorubicin induced DNA damage, acetylated p53 is recruited on SMAR1 promoter that allows activation of its transcription.	Doxorubicin	5-16	P53	Homo sapiens	48-51
17668048-4	2007	Once SMAR1 is induced, cell cycle arrest is observed that is correlated to increased phospho-ser-15-p53 and decreased p53 acetylation.	Serine	46-49	P53	Homo sapiens	100-103
17668048-4	2007	Once SMAR1 is induced, cell cycle arrest is observed that is correlated to increased phospho-ser-15-p53 and decreased p53 acetylation.	Serine	46-49	P53	Homo sapiens	118-121
17980096-10	2007	p53 Arg/Arg genotype may be a genetically susceptible factor to HPV-associated cervical carcinoma in Uigur.	Arginine	4-7	P53	Homo sapiens	0-3
17980096-10	2007	p53 Arg/Arg genotype may be a genetically susceptible factor to HPV-associated cervical carcinoma in Uigur.	Arginine	8-11	P53	Homo sapiens	0-3
21162257-3	2007	RESULTS: In the group of a 12 h long exposure to oxygen concentration of 0%, diazoxide (100 micromol/L), the K(ATP) channels agonist, reduced p53 expression and the hypoxia-induced apoptosis.	Oxygen	49-55	P53	Homo sapiens	142-145
17616578-2	2007	Here we show that transcription-blocking agents can induce phosphorylation of the Ser-15 site of p53 in a replication-independent manner.	Serine	82-85	P53	Homo sapiens	97-100
17616578-5	2007	First, accumulation of p53 is linked to diminished nuclear export of mRNA; and second, inhibition specifically of elongating RNA polymerase II complexes results in the phosphorylation of the Ser-15 site of p53 in a replication protein A (RPA)- and ATM and Rad3-related (ATR)-dependent manner.	Serine	191-194	P53	Homo sapiens	23-26
17616578-5	2007	First, accumulation of p53 is linked to diminished nuclear export of mRNA; and second, inhibition specifically of elongating RNA polymerase II complexes results in the phosphorylation of the Ser-15 site of p53 in a replication protein A (RPA)- and ATM and Rad3-related (ATR)-dependent manner.	Serine	191-194	P53	Homo sapiens	206-209
17512204-6	2007	The activation of DNA damage response as indicated by phosphorylation of H2AX histone, RPA-2 protein, and p53 at serine 15 by the most apoptotic compounds provides additional support to the hypothesis that the genotoxic stress is a critical event mediating apoptosis induction by compounds of this group.	Serine	113-119	P53	Homo sapiens	106-109
17297446-4	2007	Although p53 stabilization and phosphorylation at serine 15 increased with dose and time of exposure, Mdm2 and p21(CIP1/WAF1) protein levels displayed a biphasic response, as they accumulated at submicromolar doses and then decreased with increasing AF.	Serine	50-56	P53	Homo sapiens	9-12
17498666-7	2007	Cisplatin also inhibited the synthesis of HIF-1alpha protein for which p53 was dispensable.	Cisplatin	0-9	P53	Homo sapiens	71-74
17630506-1	2007	p53 ubiquitination at C-terminal lysines by MDM2 and other E3 ligases had been considered a straightforward negative regulation of p53 with only one function, that is marking the protein for proteasomal degradation.	Lysine	33-40	P53	Homo sapiens	0-3
17630506-1	2007	p53 ubiquitination at C-terminal lysines by MDM2 and other E3 ligases had been considered a straightforward negative regulation of p53 with only one function, that is marking the protein for proteasomal degradation.	Lysine	33-40	P53	Homo sapiens	131-134
17634554-10	2007	Levels of both the acetylated and phosphorylated forms of p53 were markedly increased upon doxorubicin exposure when compared with treatment with 5-FU, resulting in a significantly prolonged half-life of p53 (120 versus 20 min).	Doxorubicin	91-102	P53	Homo sapiens	58-61
17634554-10	2007	Levels of both the acetylated and phosphorylated forms of p53 were markedly increased upon doxorubicin exposure when compared with treatment with 5-FU, resulting in a significantly prolonged half-life of p53 (120 versus 20 min).	Doxorubicin	91-102	P53	Homo sapiens	204-207
17634554-0	2007	Regulation of p53 expression in response to 5-fluorouracil in human cancer RKO cells.	Fluorouracil	44-58	P53	Homo sapiens	14-17
17630511-0	2007	p53 regulates cellular responses to environmental carcinogen benzo[a]pyrene-7,8-diol-9,10-epoxide in human lung cancer cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	61-97	P53	Homo sapiens	0-3
17634554-1	2007	PURPOSE: The purpose of the study is to investigate the regulation of p53 expression in response to 5-fluorouracil (5-FU) in human colon cancer cells.	Fluorouracil	100-114	P53	Homo sapiens	70-73
17634554-10	2007	Levels of both the acetylated and phosphorylated forms of p53 were markedly increased upon doxorubicin exposure when compared with treatment with 5-FU, resulting in a significantly prolonged half-life of p53 (120 versus 20 min).	Fluorouracil	146-150	P53	Homo sapiens	204-207
17634554-1	2007	PURPOSE: The purpose of the study is to investigate the regulation of p53 expression in response to 5-fluorouracil (5-FU) in human colon cancer cells.	Fluorouracil	116-120	P53	Homo sapiens	70-73
17630511-1	2007	The p53 tumor suppressor is a mutational target of environmental carcinogen anti-benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE).	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	81-117	P53	Homo sapiens	4-7
17634554-3	2007	The levels of p53 expression and p53 protein stability in response to 5-FU and doxorubicin were investigated.	Fluorouracil	70-74	P53	Homo sapiens	14-17
17634554-13	2007	Studies are under way to define the specific mechanism(s) that control 5-FU-mediated translational regulation of p53.	Fluorouracil	71-75	P53	Homo sapiens	113-116
17630511-1	2007	The p53 tumor suppressor is a mutational target of environmental carcinogen anti-benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE).	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	119-123	P53	Homo sapiens	4-7
17634554-3	2007	The levels of p53 expression and p53 protein stability in response to 5-FU and doxorubicin were investigated.	Doxorubicin	79-90	P53	Homo sapiens	14-17
17634554-4	2007	In addition, the acetylation and phosphorylation status of p53 after 5-FU and doxorubicin treatment was analyzed by Western immunoblot analysis.	Fluorouracil	69-73	P53	Homo sapiens	59-62
17634554-4	2007	In addition, the acetylation and phosphorylation status of p53 after 5-FU and doxorubicin treatment was analyzed by Western immunoblot analysis.	Doxorubicin	78-89	P53	Homo sapiens	59-62
17634554-5	2007	RESULTS: Treatment of human colon cancer RKO cells with 10 micromol/L 5-FU resulted in significantly increased levels of p53 protein with maximal induction observed at 24 h. The level of acetylated p53 after 5-FU exposure remained unchanged, whereas the phosphorylated form of p53 was expressed only after 24 h drug treatment.	Fluorouracil	70-74	P53	Homo sapiens	121-124
17638885-0	2007	Systemic treatment with the antidiabetic drug metformin selectively impairs p53-deficient tumor cell growth.	Metformin	46-55	P53	Homo sapiens	76-79
17638885-2	2007	Treatment with metformin selectively suppressed the tumor growth of HCT116 p53(-/-) xenografts.	Metformin	15-24	P53	Homo sapiens	75-78
17630511-2	2007	We now demonstrate that p53 plays an important role in regulation of cellular responses to BPDE.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	91-95	P53	Homo sapiens	24-27
17638885-3	2007	Following treatment with metformin, we detected increased apoptosis in p53(-/-) tumor sections and an enhanced susceptibility of p53(-/-) cells to undergo apoptosis in vitro when subject to nutrient deprivation.	Metformin	25-34	P53	Homo sapiens	71-74
17638885-3	2007	Following treatment with metformin, we detected increased apoptosis in p53(-/-) tumor sections and an enhanced susceptibility of p53(-/-) cells to undergo apoptosis in vitro when subject to nutrient deprivation.	Metformin	25-34	P53	Homo sapiens	129-132
17634554-5	2007	RESULTS: Treatment of human colon cancer RKO cells with 10 micromol/L 5-FU resulted in significantly increased levels of p53 protein with maximal induction observed at 24 h. The level of acetylated p53 after 5-FU exposure remained unchanged, whereas the phosphorylated form of p53 was expressed only after 24 h drug treatment.	Fluorouracil	70-74	P53	Homo sapiens	198-201
17634554-5	2007	RESULTS: Treatment of human colon cancer RKO cells with 10 micromol/L 5-FU resulted in significantly increased levels of p53 protein with maximal induction observed at 24 h. The level of acetylated p53 after 5-FU exposure remained unchanged, whereas the phosphorylated form of p53 was expressed only after 24 h drug treatment.	Fluorouracil	70-74	P53	Homo sapiens	198-201
17638885-8	2007	Treatment with either metformin or AICAR also led to enhanced fatty acid beta-oxidation in p53(+/+) MEFs, but not in p53(-/-) MEFs.	Metformin	22-31	P53	Homo sapiens	91-94
17630511-6	2007	The H460 human lung cancer cell line (wild-type p53) was relatively more sensitive to BPDE-mediated growth inhibition and enrichment of sub-diploid apoptotic fraction compared with H1299 cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	86-90	P53	Homo sapiens	48-51
17638885-8	2007	Treatment with either metformin or AICAR also led to enhanced fatty acid beta-oxidation in p53(+/+) MEFs, but not in p53(-/-) MEFs.	Fatty Acids	62-72	P53	Homo sapiens	91-94
17634554-5	2007	RESULTS: Treatment of human colon cancer RKO cells with 10 micromol/L 5-FU resulted in significantly increased levels of p53 protein with maximal induction observed at 24 h. The level of acetylated p53 after 5-FU exposure remained unchanged, whereas the phosphorylated form of p53 was expressed only after 24 h drug treatment.	Fluorouracil	208-212	P53	Homo sapiens	198-201
17634554-5	2007	RESULTS: Treatment of human colon cancer RKO cells with 10 micromol/L 5-FU resulted in significantly increased levels of p53 protein with maximal induction observed at 24 h. The level of acetylated p53 after 5-FU exposure remained unchanged, whereas the phosphorylated form of p53 was expressed only after 24 h drug treatment.	Fluorouracil	208-212	P53	Homo sapiens	198-201
17638885-10	2007	Metformin-treated cells compensated for this suppression of oxidative phosphorylation by increasing their rate of glycolysis in a p53-dependent manner.	Metformin	0-9	P53	Homo sapiens	130-133
17630511-8	2007	Instead, the BPDE-treated H460 cells exhibited a nearly 8-fold increase in sub-diploid apoptotic cells that was accompanied by phosphorylation of p53 at multiple sites.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	13-17	P53	Homo sapiens	146-149
17638885-11	2007	Together, these data suggest that metformin treatment forces a metabolic conversion that p53(-/-) cells are unable to execute.	Metformin	34-43	P53	Homo sapiens	89-92
17638885-12	2007	Thus, metformin is selectively toxic to p53-deficient cells and provides a potential mechanism for the reduced incidence of tumors observed in patients being treated with metformin.	Metformin	6-15	P53	Homo sapiens	40-43
17630511-9	2007	Knockdown of p53 protein level in H460 cells attenuated BPDE-induced apoptosis but enforced activation of S and G(2) phase checkpoints.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	56-60	P53	Homo sapiens	13-16
17638885-12	2007	Thus, metformin is selectively toxic to p53-deficient cells and provides a potential mechanism for the reduced incidence of tumors observed in patients being treated with metformin.	Metformin	171-180	P53	Homo sapiens	40-43
17630511-10	2007	In conclusion, the present study points towards an important role of p53 in regulation of cellular responses to BPDE in human lung cancer cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	112-116	P53	Homo sapiens	69-72
17509529-2	2007	KCG165-induced phosphorylations of p53 at Ser(6), Ser(15), and Ser(20)(,) which are all key residues involved in the activation and stabilization of p53.	Serine	42-45	P53	Homo sapiens	35-38
17634554-7	2007	No differences were observed in the half-life of p53 protein in control and 5-FU-treated cells, suggesting that the increase in p53 was the direct result of newly synthesized protein.	Fluorouracil	76-80	P53	Homo sapiens	128-131
17634554-8	2007	In contrast, the maximal induction of p53, in response to doxorubicin, occurred at an earlier time point (4 h) when compared with cells treated with 5-FU (24 h).	Doxorubicin	58-69	P53	Homo sapiens	38-41
17509529-2	2007	KCG165-induced phosphorylations of p53 at Ser(6), Ser(15), and Ser(20)(,) which are all key residues involved in the activation and stabilization of p53.	Serine	50-53	P53	Homo sapiens	35-38
17509529-2	2007	KCG165-induced phosphorylations of p53 at Ser(6), Ser(15), and Ser(20)(,) which are all key residues involved in the activation and stabilization of p53.	Serine	50-53	P53	Homo sapiens	35-38
17555331-0	2007	Human p53 is inhibited by glutathionylation of cysteines present in the proximal DNA-binding domain during oxidative stress.	Cysteine	47-56	P53	Homo sapiens	6-9
17555331-3	2007	First, a rapid and direct incorporation of biotinylated GSH or GSSG into the purified recombinant p53 protein was observed.	Glutathione	56-59	P53	Homo sapiens	98-101
17555331-6	2007	GSH modification coexisted with the serine phophorylations in activated p53, and the thiol-conjugated protein was present in nuclei.	Glutathione	0-3	P53	Homo sapiens	72-75
17555331-6	2007	GSH modification coexisted with the serine phophorylations in activated p53, and the thiol-conjugated protein was present in nuclei.	Serine	36-42	P53	Homo sapiens	72-75
17555331-7	2007	When tumor cells treated with camptothecin or cisplatin were subsequently exposed to glutathione-enhancing agents, p53 underwent dethiolation accompanied by detectable increases in the level of p21waf1 expression, relative to the DNA-damaging drugs alone.	Cisplatin	46-55	P53	Homo sapiens	115-118
17555331-7	2007	When tumor cells treated with camptothecin or cisplatin were subsequently exposed to glutathione-enhancing agents, p53 underwent dethiolation accompanied by detectable increases in the level of p21waf1 expression, relative to the DNA-damaging drugs alone.	Glutathione	85-96	P53	Homo sapiens	115-118
17555331-8	2007	Mass spectrometry of GSH-modified p53 protein identified cysteines 124, 141, and 182, all present in the proximal DNA-binding domain, as the sites of glutathionylation.	Glutathione	21-24	P53	Homo sapiens	34-37
17555331-8	2007	Mass spectrometry of GSH-modified p53 protein identified cysteines 124, 141, and 182, all present in the proximal DNA-binding domain, as the sites of glutathionylation.	Cysteine	57-66	P53	Homo sapiens	34-37
17555331-9	2007	Biotinylated maleimide also reacted rapidly with Cys141, implying that this is the most reactive cysteine on the p53 surface.	Cysteine	97-105	P53	Homo sapiens	113-116
17555331-10	2007	The glutathionylatable cysteines were found to exist in a negatively charged microenvironment in cellular p53.	Cysteine	23-32	P53	Homo sapiens	106-109
17555331-12	2007	These results show for the first time that shielding of reactive cysteines contributes to a negative regulation for human p53 and imply that such an inactivation of the transcription factor may represent an acute defensive response with significant consequences for oncogenesis.	Cysteine	65-74	P53	Homo sapiens	122-125
17413032-7	2007	Increases in p53 phosphorylation on Ser-15 were observed in both SARS-CoV M and 3a transfected cells, suggesting that it might not correlate with the 3a-induced G0/G1 phase arrest.	Serine	36-39	P53	Homo sapiens	13-16
17442733-5	2007	Depletion of cellular polyamines by inhibiting ornithine decarboxylase (ODC) with alpha-difluoromethylornithine not only induced p53 but also increased NDRG1 transcription as indicated by induction of the NDRG1 promoter activity and increased levels of NDRG1 mRNA and protein, all of which were prevented by using specific p53 siRNA and in cells with a targeted deletion of p53.	Eflornithine	82-111	P53	Homo sapiens	129-132
17442733-5	2007	Depletion of cellular polyamines by inhibiting ornithine decarboxylase (ODC) with alpha-difluoromethylornithine not only induced p53 but also increased NDRG1 transcription as indicated by induction of the NDRG1 promoter activity and increased levels of NDRG1 mRNA and protein, all of which were prevented by using specific p53 siRNA and in cells with a targeted deletion of p53.	Eflornithine	82-111	P53	Homo sapiens	323-326
17442733-5	2007	Depletion of cellular polyamines by inhibiting ornithine decarboxylase (ODC) with alpha-difluoromethylornithine not only induced p53 but also increased NDRG1 transcription as indicated by induction of the NDRG1 promoter activity and increased levels of NDRG1 mRNA and protein, all of which were prevented by using specific p53 siRNA and in cells with a targeted deletion of p53.	Eflornithine	82-111	P53	Homo sapiens	323-326
17356895-6	2007	However, the RCMF-induced apoptosis was suppressed by transfecting the cells with antisense p53 oligonucleotides but not by treating them with a MAPK or caspase inhibitor.	Oligonucleotides	96-112	P53	Homo sapiens	92-95
17593032-0	2007	Hepcidin, a key regulator of iron metabolism, is transcriptionally activated by p53.	Iron	29-33	P53	Homo sapiens	80-83
17703737-0	2007	Protective effect of magnolol on TBHP-induced injury in H460 cells partially via a p53 dependent mechanism.	magnolol	21-29	P53	Homo sapiens	83-86
17703737-0	2007	Protective effect of magnolol on TBHP-induced injury in H460 cells partially via a p53 dependent mechanism.	tert-Butylhydroperoxide	33-37	P53	Homo sapiens	83-86
17703737-7	2007	Magnolol contributes to the cells survival through downregulated the p53 phosphorylation and PTEN expression, and upregulated Akt phosphorylation.	magnolol	0-8	P53	Homo sapiens	69-72
17703737-8	2007	Taken together, Magnolol was effective against DNA single strand breaks (SSB) formation, cytotoxicity and lipid peroxidation induced by TBHP, and its effects on p53 phosphorylation, PTEN and Akt phosphorylation were due to its antioxidative function, and partially via a p53 dependent mechanism in this protective effects.	magnolol	16-24	P53	Homo sapiens	161-164
17703737-8	2007	Taken together, Magnolol was effective against DNA single strand breaks (SSB) formation, cytotoxicity and lipid peroxidation induced by TBHP, and its effects on p53 phosphorylation, PTEN and Akt phosphorylation were due to its antioxidative function, and partially via a p53 dependent mechanism in this protective effects.	magnolol	16-24	P53	Homo sapiens	271-274
17593032-11	2007	We hypothesise that hepcidin upregulation by p53 is part of a defence mechanism against cancer, through iron deprivation.	Iron	104-108	P53	Homo sapiens	45-48
17389612-4	2007	In the studies examining changes in cell cycle and apoptosis regulators, isosilybin B and isosilybin A resulted in a decrease in the levels of both cyclins (D1, D3, E and A) and cyclin-dependent kinases (Cdk2, Cdk4 and cell division cycle 25A), but caused an increase in p21, p27 and p53 levels, except in 22Rv1 cells where isosilybin B caused a decrease in p21 protein level.	isosilybin A	90-102	P53	Homo sapiens	284-287
17301063-7	2007	Protein and Ser-15 phosphorylation levels of p53 did not show any association with the presence of Asc and there were no increases in p53-driven reporter activity in Cr-treated cells.	Serine	12-15	P53	Homo sapiens	45-48
17389612-4	2007	In the studies examining changes in cell cycle and apoptosis regulators, isosilybin B and isosilybin A resulted in a decrease in the levels of both cyclins (D1, D3, E and A) and cyclin-dependent kinases (Cdk2, Cdk4 and cell division cycle 25A), but caused an increase in p21, p27 and p53 levels, except in 22Rv1 cells where isosilybin B caused a decrease in p21 protein level.	isosilybin A	73-85	P53	Homo sapiens	284-287
17630850-3	2007	Western blotting and immunocytochemistry for p53 showed that p53 was increased in whole cell lysates by GSNO: 0.001 mM GSNO led to 1.3 +/- 0.5-fold increase compared to control, and significantly (p &lt; 0.05) increased to 1.6 +/- 0.2-fold after 0.01 mM GSNO.	S-Nitrosoglutathione	119-123	P53	Homo sapiens	45-48
17611411-0	2007	P14ARF sensitizes human osteosarcoma cells to cisplatin-induced apoptosis in a p53-independent manner.	Cisplatin	46-55	P53	Homo sapiens	79-82
17611411-4	2007	This sensitization of cisplatin-induced apoptosis was associated with upregulation of p53, Bax and p21 in U2OS cells.	Cisplatin	22-31	P53	Homo sapiens	86-89
17611411-7	2007	Together, we show here p14ARF sensitizes human osteosarcoma cells to cisplatin-induced apoptosis in a p53-independent manner.	Cisplatin	69-78	P53	Homo sapiens	102-105
17630850-3	2007	Western blotting and immunocytochemistry for p53 showed that p53 was increased in whole cell lysates by GSNO: 0.001 mM GSNO led to 1.3 +/- 0.5-fold increase compared to control, and significantly (p &lt; 0.05) increased to 1.6 +/- 0.2-fold after 0.01 mM GSNO.	S-Nitrosoglutathione	119-123	P53	Homo sapiens	61-64
17630850-0	2007	The role of p53 in nitric oxide-induced cardiomyocyte cell death.	Nitric Oxide	19-31	P53	Homo sapiens	12-15
17567683-6	2007	Under mild or severe H2O2-induced stress, p53-deficient SiHa cells exhibited much higher ROS levels than control SiHa cells.	Hydrogen Peroxide	21-25	P53	Homo sapiens	42-45
17630850-3	2007	Western blotting and immunocytochemistry for p53 showed that p53 was increased in whole cell lysates by GSNO: 0.001 mM GSNO led to 1.3 +/- 0.5-fold increase compared to control, and significantly (p &lt; 0.05) increased to 1.6 +/- 0.2-fold after 0.01 mM GSNO.	S-Nitrosoglutathione	104-108	P53	Homo sapiens	45-48
17630850-3	2007	Western blotting and immunocytochemistry for p53 showed that p53 was increased in whole cell lysates by GSNO: 0.001 mM GSNO led to 1.3 +/- 0.5-fold increase compared to control, and significantly (p &lt; 0.05) increased to 1.6 +/- 0.2-fold after 0.01 mM GSNO.	S-Nitrosoglutathione	104-108	P53	Homo sapiens	61-64
17630850-3	2007	Western blotting and immunocytochemistry for p53 showed that p53 was increased in whole cell lysates by GSNO: 0.001 mM GSNO led to 1.3 +/- 0.5-fold increase compared to control, and significantly (p &lt; 0.05) increased to 1.6 +/- 0.2-fold after 0.01 mM GSNO.	S-Nitrosoglutathione	119-123	P53	Homo sapiens	45-48
17630850-3	2007	Western blotting and immunocytochemistry for p53 showed that p53 was increased in whole cell lysates by GSNO: 0.001 mM GSNO led to 1.3 +/- 0.5-fold increase compared to control, and significantly (p &lt; 0.05) increased to 1.6 +/- 0.2-fold after 0.01 mM GSNO.	S-Nitrosoglutathione	119-123	P53	Homo sapiens	61-64
17490733-8	2007	CONCLUSION: The downregulation of p53 expression in type II Hec50co cells is linked to gefitinib resistance.	Gefitinib	87-96	P53	Homo sapiens	34-37
17584297-2	2007	Phosphorylation of Serine 46 (Ser(46)) of p53 is considered to be a primary determinant for the induction of apoptosis, by selectively inducing transactivation of p53 target genes that have proapoptotic function.	Serine	19-25	P53	Homo sapiens	42-45
17584297-2	2007	Phosphorylation of Serine 46 (Ser(46)) of p53 is considered to be a primary determinant for the induction of apoptosis, by selectively inducing transactivation of p53 target genes that have proapoptotic function.	Serine	19-25	P53	Homo sapiens	163-166
17584297-2	2007	Phosphorylation of Serine 46 (Ser(46)) of p53 is considered to be a primary determinant for the induction of apoptosis, by selectively inducing transactivation of p53 target genes that have proapoptotic function.	Serine	19-22	P53	Homo sapiens	42-45
17584297-2	2007	Phosphorylation of Serine 46 (Ser(46)) of p53 is considered to be a primary determinant for the induction of apoptosis, by selectively inducing transactivation of p53 target genes that have proapoptotic function.	Serine	19-22	P53	Homo sapiens	163-166
17584297-4	2007	We investigated the role of p53 phosphorylation in adriamycin (ADR)-induced apoptosis.	Doxorubicin	51-61	P53	Homo sapiens	28-31
17584297-7	2007	These results indicate that Ser(46) phosphorylation of p53 is not required for ADR-induced apoptosis.	Serine	28-31	P53	Homo sapiens	55-58
17567683-0	2007	Role of p53 in antioxidant defense of HPV-positive cervical carcinoma cells following H2O2 exposure.	Hydrogen Peroxide	86-90	P53	Homo sapiens	8-11
17567683-4	2007	Downregulation of p53 resulted in the inhibition of p53-regulated antioxidant enzymes and elevated intracellular ROS in SiHa cells.	ros	113-116	P53	Homo sapiens	18-21
17630850-7	2007	Pifithrin failed to block these morphologic changes, while it antagonized the similar cellular changes induced by adriamycin, which operates in part through p53.	Doxorubicin	114-124	P53	Homo sapiens	157-160
17630850-13	2007	Translocation of p53 from the cytosol to the nucleus occurred with a maximal increase of 2.9-fold in the nucleus following 1.0 mM GSNO for 24 h. These data indicate that in cardiomyocytes, NO induced marked DNA damage and translocation of p53 to the nucleus, suggesting that p53 is involved in the cellular response to NO, perhaps to modulate the genomic response to NO-induced cellular toxicity.	S-Nitrosoglutathione	130-134	P53	Homo sapiens	17-20
17630850-13	2007	Translocation of p53 from the cytosol to the nucleus occurred with a maximal increase of 2.9-fold in the nucleus following 1.0 mM GSNO for 24 h. These data indicate that in cardiomyocytes, NO induced marked DNA damage and translocation of p53 to the nucleus, suggesting that p53 is involved in the cellular response to NO, perhaps to modulate the genomic response to NO-induced cellular toxicity.	S-Nitrosoglutathione	130-134	P53	Homo sapiens	239-242
17630850-13	2007	Translocation of p53 from the cytosol to the nucleus occurred with a maximal increase of 2.9-fold in the nucleus following 1.0 mM GSNO for 24 h. These data indicate that in cardiomyocytes, NO induced marked DNA damage and translocation of p53 to the nucleus, suggesting that p53 is involved in the cellular response to NO, perhaps to modulate the genomic response to NO-induced cellular toxicity.	S-Nitrosoglutathione	130-134	P53	Homo sapiens	239-242
17490733-0	2007	Consequences of the loss of p53, RB1, and PTEN: relationship to gefitinib resistance in endometrial cancer.	Gefitinib	64-73	P53	Homo sapiens	28-31
17456577-10	2007	After irradiation, p53 phosphorylated on serine 15 was detected from 1-24 h in all cell types.	Serine	41-47	P53	Homo sapiens	19-22
17567683-6	2007	Under mild or severe H2O2-induced stress, p53-deficient SiHa cells exhibited much higher ROS levels than control SiHa cells.	ros	89-92	P53	Homo sapiens	42-45
17567683-7	2007	Furthermore, we analyzed cell viability and apoptosis after H2O2 treatment and found that p53 deficiency sensitized SiHa cells to H2O2 damage.	Hydrogen Peroxide	60-64	P53	Homo sapiens	90-93
17567683-7	2007	Furthermore, we analyzed cell viability and apoptosis after H2O2 treatment and found that p53 deficiency sensitized SiHa cells to H2O2 damage.	Hydrogen Peroxide	130-134	P53	Homo sapiens	90-93
17567683-8	2007	Inhibition of p53 resulted in excessive oxidation of DNA; control SiHa cells exhibited a more rapid removal of 8-oxo-7,8-dihydro-2"-deoxyguanosine from DNA compared with p53-deficient SiHa cells exposed to the same level of H2O2 challenge.	Hydrogen Peroxide	224-228	P53	Homo sapiens	14-17
17690521-6	2007	In the medium and high exposure groups, the incidence and/or quantity of mutant p53 protein in the stratum of PG II and/or III were significantly higher than that of PG I (p&lt;0.05).	pg ii	110-115	P53	Homo sapiens	80-83
17596214-6	2007	Curcumin reduced cell survival in a p53- and caspase-independent manner, an effect correlated with the inhibition of AP-1 and NFkappaB signaling pathways via prevention of constitutive JNK and Akt activation.	Curcumin	0-8	P53	Homo sapiens	36-39
17703463-4	2007	Using a combination of rigid-body protein docking, experimental mutagenesis information, and cluster analysis 10 main p53 DBD-AZ binding modes were generated.	dbd-az	122-128	P53	Homo sapiens	118-121
17395767-7	2007	In chromatin immunoprecipitation experiments, BeSO(4) caused p53 protein to associate with its DNA binding site in the promoter region of the p21 gene, indicating that p53 transcriptional activity is responsible for the large increase in p21 mRNA elicited by beryllium.	Beryllium	259-268	P53	Homo sapiens	61-64
17703463-6	2007	We found that the highest scored docking conformation for the p53 DBD-AZ complex also yielded the most favorable free energy value.	dbd-az	66-72	P53	Homo sapiens	62-65
17609585-6	2007	SN-38 binding motifs were detected in the proximal promoter of p53 (bases -433 to -317 and -814 to -711).	Irinotecan	0-5	P53	Homo sapiens	63-66
17609585-0	2007	Irinotecan activates p53 with its active metabolite, resulting in human hepatocellular carcinoma apoptosis.	Irinotecan	0-10	P53	Homo sapiens	21-24
17609585-7	2007	These results suggest that the p53-mediated apoptosis pathway is important in the anticancer effects of irinotecan in hepatocellular carcinoma.	Irinotecan	104-114	P53	Homo sapiens	31-34
17609585-4	2007	SN-38 significantly increased the expression of p53 protein and its phosphorylation at Ser(15) in the nucleus and apoptosis-inducing proteins Bax, caspase-9, and caspase-3, while it significantly decreased the antiapoptosis protein Bcl-xL of Huh7 cells.	Irinotecan	0-5	P53	Homo sapiens	48-51
17609585-4	2007	SN-38 significantly increased the expression of p53 protein and its phosphorylation at Ser(15) in the nucleus and apoptosis-inducing proteins Bax, caspase-9, and caspase-3, while it significantly decreased the antiapoptosis protein Bcl-xL of Huh7 cells.	Serine	87-90	P53	Homo sapiens	48-51
17467838-6	2007	In addition, alanine substitution at the residues Trp53, Glu55, and Arg56 in NS2B significantly reduced the cis- and trans-cleavage activities of the NS3 protease.	Alanine	13-20	P53	Homo sapiens	50-55
17609585-5	2007	SN-38-induced apoptosis was recovered after p53 antisense oligodeoxynucleotide (AS ODN) pretreatment, while Huh7 cells were precultured with p53 AS ODN, followed by the addition of SN-38 for 24 h. Furthermore, increases in p53 DNA-binding activity were observed in the nuclei of Huh7 cells after SN-38 treatment as shown by electrophoretic mobility shift analysis.	Irinotecan	0-5	P53	Homo sapiens	44-47
17609585-5	2007	SN-38-induced apoptosis was recovered after p53 antisense oligodeoxynucleotide (AS ODN) pretreatment, while Huh7 cells were precultured with p53 AS ODN, followed by the addition of SN-38 for 24 h. Furthermore, increases in p53 DNA-binding activity were observed in the nuclei of Huh7 cells after SN-38 treatment as shown by electrophoretic mobility shift analysis.	Irinotecan	0-5	P53	Homo sapiens	141-144
17609585-5	2007	SN-38-induced apoptosis was recovered after p53 antisense oligodeoxynucleotide (AS ODN) pretreatment, while Huh7 cells were precultured with p53 AS ODN, followed by the addition of SN-38 for 24 h. Furthermore, increases in p53 DNA-binding activity were observed in the nuclei of Huh7 cells after SN-38 treatment as shown by electrophoretic mobility shift analysis.	Irinotecan	0-5	P53	Homo sapiens	141-144
17393435-0	2007	A plant lignan, 3"-O-methyl-nordihydroguaiaretic acid, suppresses papillomavirus E6 protein function, stabilizes p53 protein, and induces apoptosis in cervical tumor cells.	Lignans	8-14	P53	Homo sapiens	113-116
17393435-12	2007	These results indicate that the loss of E6 protein in treated cells could be, in part, responsible for the stabilization of p53 within the lignan treated cells.	Lignans	139-145	P53	Homo sapiens	124-127
17334779-7	2007	Ser(15) phosphorylation of p53 was increased by anoxia in an NHE- and p38 MAPK-independent manner, while Akt activity was unaffected.	Serine	0-3	P53	Homo sapiens	27-30
17913962-8	2007	The effect of ET-1 on apoptosis in 20% oxygen is accompanied by reduced p53 expression and is correlated with enhanced expression of endothelin B receptor, compared to cultures in 8% or 1% oxygen.	Oxygen	39-45	P53	Homo sapiens	72-75
17466278-2	2007	Previous study in our laboratory considered p53 mutant cell lines A431 (parental) and A431/Pt (CDDP-resistant counterpart, resistance factor R.F.=2.6).	cddp	95-99	P53	Homo sapiens	44-47
17466278-12	2007	The presence of a wild-type p53 exalts either CDDP cytotoxicity (two-fold more active in U2-OS than in A431 cells) and CDDP resistance in comparison to a p53 mutant type.	cddp	46-50	P53	Homo sapiens	28-31
17466278-12	2007	The presence of a wild-type p53 exalts either CDDP cytotoxicity (two-fold more active in U2-OS than in A431 cells) and CDDP resistance in comparison to a p53 mutant type.	cddp	119-123	P53	Homo sapiens	28-31
17585201-3	2007	p21 knockdown by short hairpin RNA strongly increased p53 upregulation by a DNA-damaging drug doxorubicin in HT1080 fibrosarcoma cells.	Doxorubicin	94-105	P53	Homo sapiens	54-57
17530771-4	2007	After treatment with propolin H in H460 cells, the content of the CDK inhibitor p21Waf1/Cip1 protein increased in correlation with the elevation in p53 levels.	propolin H	21-31	P53	Homo sapiens	148-151
17530771-7	2007	Additionally, we found that propolin H enhanced the expression of p21Waf1/Cip1 in p53-mutant and p53-null lung carcinoma cell lines, following the induction of G1 arrest.	propolin H	28-38	P53	Homo sapiens	82-85
17530771-7	2007	Additionally, we found that propolin H enhanced the expression of p21Waf1/Cip1 in p53-mutant and p53-null lung carcinoma cell lines, following the induction of G1 arrest.	propolin H	28-38	P53	Homo sapiens	97-100
17530771-8	2007	Together, these findings suggest that the induction of p21Waf1/Cip1 expression occurred through p53-dependent and -independent pathways in propolin H-treated cells.	propolin H	139-149	P53	Homo sapiens	96-99
17452332-8	2007	Thus, our results strongly suggest that the nuclear IKK-alpha-mediated accumulation of p73alpha is one of the novel molecular mechanisms to induce apoptotic cell death in response to CDDP, which may be particularly important in killing tumor cells with p53 mutation.	Cisplatin	183-187	P53	Homo sapiens	253-256
17530733-2	2007	DMC was previously shown in our laboratory to exceed the cytotoxicity of MC in a human leukemia cell line that lacks a functional p53 pathway (K562).	10-decarbamoylmitomycin C	0-3	P53	Homo sapiens	130-133
17530733-5	2007	In cell lines lacking wild-type p53, DMC was reproducibly more cytotoxic than MC, but it generated barely detectable signal transduction markers associated with apoptotic death.	10-decarbamoylmitomycin C	37-40	P53	Homo sapiens	32-35
17530733-7	2007	Alkylating agents can induce increased PARP activity associated with programmed necrosis, and the biological activity of DMC in p53-null cell lines fits this paradigm.	10-decarbamoylmitomycin C	121-124	P53	Homo sapiens	128-131
17530733-8	2007	In cell lines with a functional p53 pathway, both MC and DMC induced apoptosis.	10-decarbamoylmitomycin C	57-60	P53	Homo sapiens	32-35
17530733-9	2007	In the presence of p53, both MC and DMC activate procaspases; however, the spectrum of procaspases involved differs for the two drugs, as does induction of p73.	10-decarbamoylmitomycin C	36-39	P53	Homo sapiens	19-22
17492690-2	2007	The TP53 polymorphism, in which an arginine (R) is changed to proline (P) at codon 72, is functionally significant and could therefore be a predisposing genetic defect.	Arginine	35-43	P53	Homo sapiens	4-8
17585201-4	2007	A protease inhibitor N-Ac-Leu-Leu-norleucinal (ALLN) drastically increased the amount of p53 in HCT116 colon carcinoma cells, but it had no effect on the already high p53 level in a p21(-/-) derivative of this cell line.	1-AMINO-1-CARBONYL PENTANE	34-45	P53	Homo sapiens	89-92
17535973-5	2007	The overall 12-yr survival was increased in p53 Arg/Pro heterozygotes with 3% (P = 0.003) and in Pro/Pro homozygotes with 6% (P = 0.002) versus Arg/Arg homozygotes, corresponding to an increase in median survival of 3 yr for Pro/Pro versus Arg/Arg homozygotes.	Arginine	48-51	P53	Homo sapiens	44-47
17512465-3	2007	However, the results from the present study suggest that busulfan (BU), an alkylating agent that causes DNA damage by cross-linking DNAs and DNA and proteins, induces senescence in normal human diploid WI38 fibroblasts through the extracellular signal-regulated kinase (Erk) and p38 mitogen-activated protein kinase (p38 MAPK) cascade independent of the p53-DNA damage pathway.	Busulfan	57-65	P53	Homo sapiens	354-357
17512465-3	2007	However, the results from the present study suggest that busulfan (BU), an alkylating agent that causes DNA damage by cross-linking DNAs and DNA and proteins, induces senescence in normal human diploid WI38 fibroblasts through the extracellular signal-regulated kinase (Erk) and p38 mitogen-activated protein kinase (p38 MAPK) cascade independent of the p53-DNA damage pathway.	Busulfan	67-69	P53	Homo sapiens	354-357
16973168-4	2007	The high-arsenic exposure group with GSTP1 variant genotypes of Ile/Val and Val/Val, and with the p53 variant genotypes of Arg/Pro and Pro/Pro had 6.0- and 3.1-fold higher risks of carotid atherosclerosis, respectively.	Arginine	123-126	P53	Homo sapiens	98-101
17113707-9	2007	Present findings indicate occurrence of sensitization to cisplatin by zoledronic acid in wild-type p53 osteosarcoma cells but not in p53-null cells nor in cells expressing a dominant-negative form of p53, supporting that wild-type p53 is required for synergistic interaction of cisplatin and zoledronic acid.	Cisplatin	57-66	P53	Homo sapiens	99-102
17369602-0	2007	p-53 gene mutations as a predictive marker in a population of advanced breast cancer patients randomly treated with doxorubicin or docetaxel in the context of a phase III clinical trial.	Doxorubicin	116-127	P53	Homo sapiens	0-4
17369602-1	2007	BACKGROUND: Preclinical data indicate that p-53 gene mutations predict resistance to doxorubicin (A) but not to docetaxel (Taxotere) (T).	Doxorubicin	85-96	P53	Homo sapiens	43-47
17369602-11	2007	Of the 16 patients carrying wild-type p-53- and topo II protein-positive tumors, seven (44%) responded to anthracyclines, while response rate to the same drug was 13% in the remaining cohorts [odds ratio 5.06 (95% confidence interval 1.19-21.41), P = 0.03].	Anthracyclines	106-120	P53	Homo sapiens	38-55
17395471-0	2007	Novel morpholin-3-one derivatives induced apoptosis and elevated the level of P53 and Fas in A549 lung cancer cells.	Morpholin-3-one	6-21	P53	Homo sapiens	78-81
17395471-4	2007	The results showed that the morpholin-3-one derivatives partly blocked the cells at G1 phase, induced apoptosis, and elevated the level of P53 and Fas proteins significantly.	Morpholin-3-one	28-43	P53	Homo sapiens	139-142
17307334-4	2007	In this study, we found that TAM treatment of MDA-MB-361 breast cancer cells activated p21Waf1/Cip1 gene transcription independently of p53.	Tamoxifen	29-32	P53	Homo sapiens	136-139
17514353-5	2007	Buffering of the calcium response attenuated mitochondrial impairment, recovered the cadmium-activated Akt, p53, JNK, ERK and p38, and subsequently blocked the apoptosis.	Calcium	17-24	P53	Homo sapiens	108-111
17321721-4	2007	CsA induced p21WAF1/Cip1 expression de novo in human glioblastoma cells with p53 deficiency.	Cyclosporine	0-3	P53	Homo sapiens	77-80
17321721-9	2007	It suggests that CsA activates p53-independent, transcriptional activation p21WAF1/Cip1 expression, mediated by ERK/c-Jun/AP-1 signaling pathway.	Cyclosporine	17-20	P53	Homo sapiens	31-34
17534149-6	2007	We and others have recently identified a novel modification on p53, acetylation of lysine 120 within the DNA binding domain.	Lysine	83-89	P53	Homo sapiens	63-66
17514353-0	2007	Calcium-mediated activation of PI3K and p53 leads to apoptosis in thyroid carcinoma cells.	Calcium	0-7	P53	Homo sapiens	40-43
17534149-8	2007	We demonstrate here that both the DNA damage response pathway and the p19ARF/oncogene stress pathway induce the acetylation of p53 at lysine 120.	Lysine	134-140	P53	Homo sapiens	127-130
17514353-3	2007	Cadmium caused the rapid elevation of intracellular calcium and induced phosphorylation of Akt, p53, JNK, ERK and p38.	Cadmium	0-7	P53	Homo sapiens	96-99
17545634-4	2007	Moreover, in MCF-7 human breast cancer cells, various p53-inducing agents (such as UV irradiation) or treatment with RITA (which inhibits the interaction of p53 with Mdm2) stabilized ERalpha and abolished its 17beta-estradiol-dependent turnover.	RITA	117-121	P53	Homo sapiens	157-160
17349663-11	2007	Fe-NTA enhanced the migration of TP53 signals into the comet tail of human leucocytes, indicating a high susceptibility of this tumour-relevant gene towards DNA damage induced by iron overload.	Iron	179-183	P53	Homo sapiens	33-37
17639046-7	2007	We selectively confirmed rosiglitazone-mediated effects on expression of key regulators of breast cancer proliferation and apoptosis, including p53, p21 and Bax.	Rosiglitazone	25-38	P53	Homo sapiens	144-147
17487378-7	2007	The ITAI was also correlated with CPT-11 response among cell lines derived from a variety of tissues that had inactivating p53 mutations or deletions, supporting its applicability for predicting response to camptothecins in other tissues regardless of p53 status.	Irinotecan	34-40	P53	Homo sapiens	123-126
17725105-0	2007	Schedule-dependent cytotoxicity of 5-fluorouracil and irinotecan in p53 mutant human colon cancer.	Fluorouracil	35-49	P53	Homo sapiens	68-71
17725105-0	2007	Schedule-dependent cytotoxicity of 5-fluorouracil and irinotecan in p53 mutant human colon cancer.	Irinotecan	54-64	P53	Homo sapiens	68-71
17725105-2	2007	We evaluated cytotoxic effects of a sequentially administered a combination of 5-FU with CPT-11 in human p53 mutant colon cancer.	Fluorouracil	79-83	P53	Homo sapiens	105-108
17725105-2	2007	We evaluated cytotoxic effects of a sequentially administered a combination of 5-FU with CPT-11 in human p53 mutant colon cancer.	Irinotecan	89-95	P53	Homo sapiens	105-108
17180249-9	2007	In all high-grade glioblastomas majority of the p53 protein existed as Ser 392 phosphorylated form as compared to low-grade gliomas.	Serine	71-74	P53	Homo sapiens	48-51
17180249-10	2007	In addition, the percentage of Ser 392 phosphorylated form of p53 protein was lower in meningiomas and other brain tumor types irrespective of tumor grade.	Serine	31-34	P53	Homo sapiens	62-65
17180249-11	2007	These results suggest involvement of Ser 392 phosphorylated form of p53 protein during the later stages of glioma development.	Serine	37-40	P53	Homo sapiens	68-71
17371838-5	2007	Levels of binding of p53 to the p21 promoter were comparable following treatment with doxorubicin or Mdm2 siRNA.	Doxorubicin	86-97	P53	Homo sapiens	21-24
17371838-3	2007	Treatment of cells with doxorubicin causes phosphorylation and acetylation of p53, transcriptional upregulation of p21 and other target genes, and growth arrest.	Doxorubicin	24-35	P53	Homo sapiens	78-81
17146434-4	2007	Here, we report that treatment of the p53-mutant malignant peripheral nerve sheath (MPNST) and p53-null HCT116 cells with cisplatin (Cis) and Nutlin-3a induced a degree of apoptosis that was significantly greater than either drug alone.	Cisplatin	122-131	P53	Homo sapiens	38-41
17403527-1	2007	A very common polymorphism of p53, that of codon 72, codes either for a proline (P72) or an arginine (R72).	Arginine	92-100	P53	Homo sapiens	30-33
17575104-6	2007	Furthermore, the antibody-mediated p53 response was dramatically increased when a peptide corresponding to the 4C6 epitope and bearing a COOH-terminal cysteine residue was added to the transduction mixture.	Carbonic Acid	137-141	P53	Homo sapiens	35-38
17575104-6	2007	Furthermore, the antibody-mediated p53 response was dramatically increased when a peptide corresponding to the 4C6 epitope and bearing a COOH-terminal cysteine residue was added to the transduction mixture.	Cysteine	151-159	P53	Homo sapiens	35-38
17481900-4	2007	Recent discoveries revealing new functions for p53 in the regulation of glucose metabolism and oxidative stress have brought together these two venerable fields of cancer biology.	Glucose	72-79	P53	Homo sapiens	47-50
17237827-4	2007	We, here, show that either endogenously expressed or exogenously added p53 protein localizes to the nucleolus in detergent-permeabilized cells in a concentration- and ATP hydrolysis-dependent manner.	Adenosine Triphosphate	167-170	P53	Homo sapiens	71-74
17146434-4	2007	Here, we report that treatment of the p53-mutant malignant peripheral nerve sheath (MPNST) and p53-null HCT116 cells with cisplatin (Cis) and Nutlin-3a induced a degree of apoptosis that was significantly greater than either drug alone.	Cisplatin	122-131	P53	Homo sapiens	95-98
17146434-5	2007	Nutlin-3a also increased the cytotoxicity of both carboplatin and doxorubicin in a series of p53-mutant human tumor cell lines.	Doxorubicin	66-77	P53	Homo sapiens	93-96
17130833-7	2007	Deletion analysis of CXCR4 promoter identified a seven-base pair p53-repressor element homologous to cyclic AMP/AP-1 response (CRE/AP-1) element.	Cyclic AMP	101-111	P53	Homo sapiens	65-68
17686239-12	2007	CONCLUSION: Residual tumor, p53, and Pgp expression are predictive factors for the response to platinum/paclitaxel first-line adjuvant chemotherapy in advanced ovarian cancer.	Platinum	95-103	P53	Homo sapiens	28-31
17510393-9	2007	The stability of Ras-induced increase in ROS was dependent on a p53 function: in the p53-positive cells displaying activation of p53 in response to Ras, only transient (4-7 days) elevation of ROS was observed, whereas in the p53-deficient cells the up-regulation was permanent.	Reactive Oxygen Species	41-44	P53	Homo sapiens	64-67
17510393-9	2007	The stability of Ras-induced increase in ROS was dependent on a p53 function: in the p53-positive cells displaying activation of p53 in response to Ras, only transient (4-7 days) elevation of ROS was observed, whereas in the p53-deficient cells the up-regulation was permanent.	Reactive Oxygen Species	41-44	P53	Homo sapiens	85-88
17510393-9	2007	The stability of Ras-induced increase in ROS was dependent on a p53 function: in the p53-positive cells displaying activation of p53 in response to Ras, only transient (4-7 days) elevation of ROS was observed, whereas in the p53-deficient cells the up-regulation was permanent.	Reactive Oxygen Species	41-44	P53	Homo sapiens	85-88
17510393-9	2007	The stability of Ras-induced increase in ROS was dependent on a p53 function: in the p53-positive cells displaying activation of p53 in response to Ras, only transient (4-7 days) elevation of ROS was observed, whereas in the p53-deficient cells the up-regulation was permanent.	Reactive Oxygen Species	41-44	P53	Homo sapiens	85-88
17510393-9	2007	The stability of Ras-induced increase in ROS was dependent on a p53 function: in the p53-positive cells displaying activation of p53 in response to Ras, only transient (4-7 days) elevation of ROS was observed, whereas in the p53-deficient cells the up-regulation was permanent.	Reactive Oxygen Species	192-195	P53	Homo sapiens	64-67
17510393-9	2007	The stability of Ras-induced increase in ROS was dependent on a p53 function: in the p53-positive cells displaying activation of p53 in response to Ras, only transient (4-7 days) elevation of ROS was observed, whereas in the p53-deficient cells the up-regulation was permanent.	Reactive Oxygen Species	192-195	P53	Homo sapiens	85-88
17510393-9	2007	The stability of Ras-induced increase in ROS was dependent on a p53 function: in the p53-positive cells displaying activation of p53 in response to Ras, only transient (4-7 days) elevation of ROS was observed, whereas in the p53-deficient cells the up-regulation was permanent.	Reactive Oxygen Species	192-195	P53	Homo sapiens	85-88
17510393-9	2007	The stability of Ras-induced increase in ROS was dependent on a p53 function: in the p53-positive cells displaying activation of p53 in response to Ras, only transient (4-7 days) elevation of ROS was observed, whereas in the p53-deficient cells the up-regulation was permanent.	Reactive Oxygen Species	192-195	P53	Homo sapiens	85-88
17510393-10	2007	The reversion to normal ROS levels in the Ras-expressing p53-positive cells correlated with up-regulation of p53-responsive genes, including reactivation of SESN1 gene.	Reactive Oxygen Species	24-27	P53	Homo sapiens	57-60
17510393-10	2007	The reversion to normal ROS levels in the Ras-expressing p53-positive cells correlated with up-regulation of p53-responsive genes, including reactivation of SESN1 gene.	Reactive Oxygen Species	24-27	P53	Homo sapiens	109-112
17371868-5	2007	Mutant p53 ubiquitination occurred at lysines in both the DNA-binding domain (DBD) and C terminus.	Lysine	38-45	P53	Homo sapiens	7-10
17371868-6	2007	Interestingly, Lys to Arg mutations that inhibited ubiquitination restored nuclear localization to mutant p53 but had no apparent effect on p53 conformation.	Lysine	15-18	P53	Homo sapiens	106-109
17371868-6	2007	Interestingly, Lys to Arg mutations that inhibited ubiquitination restored nuclear localization to mutant p53 but had no apparent effect on p53 conformation.	Arginine	22-25	P53	Homo sapiens	106-109
17353187-6	2007	HSCO specifically associates with histone deacetylase 1 (HDAC1) independently of Mdm2 and facilitates deacetylation of p53 at Lys-373/382 by HDAC1.	Lysine	126-129	P53	Homo sapiens	119-122
17523842-4	2007	Among the signaling molecules examined, levels of p53 phosphorylated at Ser-392 and p38 were higher in UVB-irradiated cells than in UVC-irradiated cells.	Serine	72-75	P53	Homo sapiens	50-53
17523842-6	2007	Furthermore, an inhibitor of p38 also blocked the phosphorylation of p53 at Ser-392.	Serine	76-79	P53	Homo sapiens	69-72
17510383-9	2007	Increased p53 and p73 responses following cisplatin treatment were also observed in HT1197 cells stably transfected with XPC cDNA.	Cisplatin	42-51	P53	Homo sapiens	10-13
17344208-11	2007	This is significant because superoxide production underlies the role of human PRODH in p53-mediated apoptosis, implying commonalities between eukaryotic and bacterial monofunctional PRODHs.	Superoxides	28-38	P53	Homo sapiens	87-90
17686239-12	2007	CONCLUSION: Residual tumor, p53, and Pgp expression are predictive factors for the response to platinum/paclitaxel first-line adjuvant chemotherapy in advanced ovarian cancer.	Paclitaxel	104-114	P53	Homo sapiens	28-31
17072341-5	2007	These experiments identify p53 as the main pathway producing a large-scale transcriptional response after cisplatin treatment in these cells containing wild-type p53.	Cisplatin	106-115	P53	Homo sapiens	27-30
17072341-5	2007	These experiments identify p53 as the main pathway producing a large-scale transcriptional response after cisplatin treatment in these cells containing wild-type p53.	Cisplatin	106-115	P53	Homo sapiens	162-165
17072341-6	2007	Consistent with a role for the p53 response in cisplatin sensitivity, knockdown of the p53 protein with small interfering RNA led to a twofold decrease in cell survival in the resistant cells.	Cisplatin	47-56	P53	Homo sapiens	31-34
17072341-6	2007	Consistent with a role for the p53 response in cisplatin sensitivity, knockdown of the p53 protein with small interfering RNA led to a twofold decrease in cell survival in the resistant cells.	Cisplatin	47-56	P53	Homo sapiens	87-90
17234160-7	2007	Copper decreased c-DDP-induced apoptosis, caspase-3/7 activation, p53 induction and PARP cleavage in cancer cell lines.	Copper	0-6	P53	Homo sapiens	66-69
17672938-1	2007	BACKGROUND &amp; OBJECTIVE: p53 gene is the main regulator of 14-3-3sigma.	Adenosine Monophosphate	12-15	P53	Homo sapiens	28-31
17595754-8	2007	There was a association between the absence of p53 and high serum progesterone (p = 0.046).	Progesterone	66-78	P53	Homo sapiens	47-50
17595776-6	2007	Those who had Arg/Arg at p53 codon 72 showed a 2.68-fold (95% confidence interval = 1.19-6.01) increased risk of oral cancer compared to those with Pro/Pro.	Arginine	14-17	P53	Homo sapiens	25-28
17595776-6	2007	Those who had Arg/Arg at p53 codon 72 showed a 2.68-fold (95% confidence interval = 1.19-6.01) increased risk of oral cancer compared to those with Pro/Pro.	Arginine	18-21	P53	Homo sapiens	25-28
17595776-9	2007	CONCLUSION: Our findings suggest that the homozygous Arg allele of the p53 codon 72 may be associated with the development of oral cancer and be a useful marker for primary prevention and anticancer intervention.	Arginine	53-56	P53	Homo sapiens	71-74
17380529-3	2007	METHODS: P53 expression was determined by immunohistochemistry in paraffin-embedded tissue specimens from 107 consecutive patients (107 primary squamous cell carcinomas of the supraglottic larynx and 46 matched lymph node metastases).	Paraffin	66-74	P53	Homo sapiens	9-12
17119966-10	2007	NF-kappaB transfected MCF-7 and p53 knockout HCT116 cells were resistant to 5-FU (4.4- and 2.4-fold, respectively) but not to TDX.	Fluorouracil	76-80	P53	Homo sapiens	32-35
17119966-13	2007	Loss of p53 function and NF-kappaB over-expression may be involved in TS-independent 5-FU chemoresistance in some cancer cell lines.	Fluorouracil	85-89	P53	Homo sapiens	8-11
17390010-8	2007	Interestingly, this mutant-p53 prevented Saos-2 cells from undergoing apoptosis after treatment with a DNA damaging agent, adriamycin.	Doxorubicin	123-133	P53	Homo sapiens	27-30
17631738-2	2007	The wild type p53 protein presents a common polymorphism at position 72 resulting in either a proline or an arginine residue at this position, leading to differences between the two variants in the induction of apoptosis.	Arginine	108-116	P53	Homo sapiens	14-17
17631738-7	2007	All of the RA patients and controls were genotyped by the polymerase chain reaction and allele-specific oligonucleotide techniques for p53 gene polymorphism Arg/Pro at codon 72.	Arginine	157-160	P53	Homo sapiens	135-138
17289842-8	2007	OxLDL activated p53 through production of mitochondria-derived reactive oxygen species.	Reactive Oxygen Species	63-86	P53	Homo sapiens	16-19
17289842-9	2007	In EDCs treated with a recombinant adenovirus expressing superoxide dismutase or N-acetyl-cysteine (but not catalase), the p53-Bax pathway activated by oxLDL was blocked, and apoptosis was prevented.	Acetylcysteine	81-98	P53	Homo sapiens	123-126
17289842-11	2007	These findings suggest that exposure of EDCs and endothelial cells to either experimentally prepared or naturally occurring modified LDL results in an increased transfer of mitochondria-derived superoxide anion to p53, which stimulates a conformational change in Bax favoring its translocation to the mitochondria with resultant apoptosis of these cells.	Superoxides	194-210	P53	Homo sapiens	214-217
17230520-8	2007	In LNCaP cells, we established superoxide as a primary mediator for selenite-induced DNA SSBs, p53 activation and caspase-mediated apoptosis.	Superoxides	31-41	P53	Homo sapiens	95-98
17230520-9	2007	Furthermore a p53-dominant negative mutant attenuated selenite-induced ROS, leading to a proportionate protection against apoptosis.	Reactive Oxygen Species	71-74	P53	Homo sapiens	14-17
17230520-10	2007	The results support the p53-mitochondria axis in a feedback loop for sustaining superoxide production to lead to efficient caspase-mediated apoptosis by selenite.	Superoxides	80-90	P53	Homo sapiens	24-27
17331670-7	2007	The p53 72 Arg allele showed a borderline association (p = 0.07).	Arginine	11-14	P53	Homo sapiens	4-7
17208332-1	2007	The TP53 gene has a polymorphism in exon 4 at codon 72 that presents the arginine or proline genotype.	Arginine	73-81	P53	Homo sapiens	4-8
17446929-2	2007	Here we demonstrated that the p53 family member p63 controls a pathway for p73-dependent cisplatin sensitivity specific to these "triple-negative" tumors.	Cisplatin	89-98	P53	Homo sapiens	30-33
17599946-1	2007	A TP53 gene polymorphism, resulting in an arginine (R) to proline (P) at codon 72 (TP53 R72P), has been associated with the susceptibility to various cancers.	Arginine	42-50	P53	Homo sapiens	2-6
17599946-1	2007	A TP53 gene polymorphism, resulting in an arginine (R) to proline (P) at codon 72 (TP53 R72P), has been associated with the susceptibility to various cancers.	Arginine	42-50	P53	Homo sapiens	83-87
17599946-6	2007	We conclude that the TP53 R72P polymorphism may contribute to the etiology of colorectal cancer in the Chinese population, particularly among alcohol consumers.	Alcohols	142-149	P53	Homo sapiens	21-25
17130844-5	2007	Consistently, such a protective effect can be at least partially due to the impairment of cisplatin-induced p53 activation, occurring early in committed, preapoptotic cells.	Cisplatin	90-99	P53	Homo sapiens	108-111
17339337-1	2007	Genetic and biochemical studies have shown that Ser(20) phosphorylation in the transactivation domain of p53 mediates p300-catalyzed DNA-dependent p53 acetylation and B-cell tumor suppression.	Serine	48-51	P53	Homo sapiens	105-108
17339337-1	2007	Genetic and biochemical studies have shown that Ser(20) phosphorylation in the transactivation domain of p53 mediates p300-catalyzed DNA-dependent p53 acetylation and B-cell tumor suppression.	Serine	48-51	P53	Homo sapiens	147-150
17339337-4	2007	Phosphorylation of a p53 transactivation domain fragment at Ser(20) by these enzymes in vitro can be mediated in trans by a docking site peptide derived from the BOX-V domain of p53, which also harbors the ubiquitin signal for MDM2.	Serine	60-63	P53	Homo sapiens	21-24
17339337-4	2007	Phosphorylation of a p53 transactivation domain fragment at Ser(20) by these enzymes in vitro can be mediated in trans by a docking site peptide derived from the BOX-V domain of p53, which also harbors the ubiquitin signal for MDM2.	Serine	60-63	P53	Homo sapiens	178-181
17513613-6	2007	Because we previously showed that reintroduction of wild-type p53 (wtp53) into STS cells harboring a p53 mutation led to increased doxorubicin chemosensitivity, we hypothesized that p53 participates in regulating Rad51 expression in STS.	Doxorubicin	131-142	P53	Homo sapiens	62-65
17513613-6	2007	Because we previously showed that reintroduction of wild-type p53 (wtp53) into STS cells harboring a p53 mutation led to increased doxorubicin chemosensitivity, we hypothesized that p53 participates in regulating Rad51 expression in STS.	Doxorubicin	131-142	P53	Homo sapiens	69-72
17513613-6	2007	Because we previously showed that reintroduction of wild-type p53 (wtp53) into STS cells harboring a p53 mutation led to increased doxorubicin chemosensitivity, we hypothesized that p53 participates in regulating Rad51 expression in STS.	Doxorubicin	131-142	P53	Homo sapiens	69-72
17474797-3	2007	The two non-synonymous single-nucleotide polymorphisms (SNPs) TP53 codon 72 Arg/Pro G&gt;C and CDKN1A codon 31 Ser/Arg C&gt;A were genotyped in 92 normal fibroblast cell strains of different radiosensitivity.	Arginine	76-79	P53	Homo sapiens	62-66
17371049-9	2007	After incorporating 6-19F-Trp, it is found that, in the triple mutant, Trp53 shows conformational heterogeneity at low temperature while Trp44, which is close to the P27A mutation, does not.	Tryptophan	26-29	P53	Homo sapiens	71-76
17387280-3	2007	This mixed experimental-simulation approach enabled us to decode the dynamics of the cytostatic and cytotoxic responses to cisplatin and doxorubicin treatments in a p53--proficient colon carcinoma cell line (HCT-116) and in its p53-deficient counterpart.	Cisplatin	123-132	P53	Homo sapiens	165-168
17387280-3	2007	This mixed experimental-simulation approach enabled us to decode the dynamics of the cytostatic and cytotoxic responses to cisplatin and doxorubicin treatments in a p53--proficient colon carcinoma cell line (HCT-116) and in its p53-deficient counterpart.	Cisplatin	123-132	P53	Homo sapiens	228-231
17387280-3	2007	This mixed experimental-simulation approach enabled us to decode the dynamics of the cytostatic and cytotoxic responses to cisplatin and doxorubicin treatments in a p53--proficient colon carcinoma cell line (HCT-116) and in its p53-deficient counterpart.	Doxorubicin	137-148	P53	Homo sapiens	165-168
17387280-3	2007	This mixed experimental-simulation approach enabled us to decode the dynamics of the cytostatic and cytotoxic responses to cisplatin and doxorubicin treatments in a p53--proficient colon carcinoma cell line (HCT-116) and in its p53-deficient counterpart.	Doxorubicin	137-148	P53	Homo sapiens	228-231
17307730-7	2007	Nampt overexpression also reduced the fraction of p53 that was acetylated on lysine 382, a target of SIRT1, suppressed an age-related increase in p53 expression, and increased the rate of p53 degradation.	Lysine	77-83	P53	Homo sapiens	50-53
17307730-7	2007	Nampt overexpression also reduced the fraction of p53 that was acetylated on lysine 382, a target of SIRT1, suppressed an age-related increase in p53 expression, and increased the rate of p53 degradation.	Lysine	77-83	P53	Homo sapiens	146-149
17307730-7	2007	Nampt overexpression also reduced the fraction of p53 that was acetylated on lysine 382, a target of SIRT1, suppressed an age-related increase in p53 expression, and increased the rate of p53 degradation.	Lysine	77-83	P53	Homo sapiens	146-149
17406354-1	2007	The preferential retention of the arginine allele at the p53 codon 72 locus is commonly observed in tumours from arginine/proline heterozygotes.	Arginine	34-42	P53	Homo sapiens	57-60
17406354-1	2007	The preferential retention of the arginine allele at the p53 codon 72 locus is commonly observed in tumours from arginine/proline heterozygotes.	Arginine	113-121	P53	Homo sapiens	57-60
17406354-3	2007	Here, we show that the transient transfection of the proline allele in p53 null cancer cells exposed to low oxygen tension or to the hypoxia-mimetic drug Desferoxamine induces a higher amount of cell death than the arginine allele.	Oxygen	108-114	P53	Homo sapiens	71-74
17406354-3	2007	Here, we show that the transient transfection of the proline allele in p53 null cancer cells exposed to low oxygen tension or to the hypoxia-mimetic drug Desferoxamine induces a higher amount of cell death than the arginine allele.	Arginine	215-223	P53	Homo sapiens	71-74
17406354-6	2007	These data indicate that the p53 codon 72 proline allele is less permissive for the growth of cancer cells in a hypoxic environment, and suggest that the preferential retention of the arginine allele in the tumour tissues of arginine/proline heterozygous patients may depend upon its lowered capacity to induce cell death in a hypoxic tumour environment.	Arginine	184-192	P53	Homo sapiens	29-32
17406354-6	2007	These data indicate that the p53 codon 72 proline allele is less permissive for the growth of cancer cells in a hypoxic environment, and suggest that the preferential retention of the arginine allele in the tumour tissues of arginine/proline heterozygous patients may depend upon its lowered capacity to induce cell death in a hypoxic tumour environment.	Arginine	225-233	P53	Homo sapiens	29-32
17195093-3	2007	Hypoxia-induced cell death was not associated with the activation of p53 while cisplatin-induced apoptosis is p53 dependent.	Cisplatin	79-88	P53	Homo sapiens	110-113
17397945-6	2007	p53 siRNA prevented cisplatin-mediated up-regulation of FLJ11259 in NT2/D1 cells.	Cisplatin	20-29	P53	Homo sapiens	0-3
17240359-6	2007	We found that curcumin enhanced the expression of tumor cyclin-dependent kinase (CDK) inhibitors p21 and p27 as well as tumor suppressor protein p53 but suppressed the expression of retinoblastoma protein.	Curcumin	14-22	P53	Homo sapiens	145-148
17397945-9	2007	In addition, chromatin immunoprecipitation assays indicate that p53 binds directly to this element in vivo and that binding is enhanced following cisplatin treatment.	Cisplatin	146-155	P53	Homo sapiens	64-67
17409429-3	2007	We found that PD98059, which itself has minimal apoptogenic activity, acts synergistically with Nutlin-3a to induce apoptosis in wild-type p53 AML cell lines OCI-AML-3 and MOLM-13.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	14-21	P53	Homo sapiens	139-142
17409429-4	2007	Interestingly, PD98059 enhanced nuclear proapototic function of p53 in these cells.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	15-22	P53	Homo sapiens	64-67
17409429-5	2007	In accordance with the activation of transcription-dependent apoptosis, PD98059 treatment promoted the translocation of p53 from the cytoplasm to the nucleus in OCI-AML-3 cells, in which p53 primarily initiates transcription-independent apoptosis when cells are treated with Nutlin-3a alone.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	72-79	P53	Homo sapiens	120-123
17409429-5	2007	In accordance with the activation of transcription-dependent apoptosis, PD98059 treatment promoted the translocation of p53 from the cytoplasm to the nucleus in OCI-AML-3 cells, in which p53 primarily initiates transcription-independent apoptosis when cells are treated with Nutlin-3a alone.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	72-79	P53	Homo sapiens	187-190
17409429-7	2007	PD98059 prevented p53-mediated induction of p21 at the transcriptional level.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	0-7	P53	Homo sapiens	18-21
17409429-8	2007	The repressed expression of antiapototic p21 also seemed to contribute to synergism between PD98059 and Nutlin-3a because (a) the synergistic apoptogenic effect was preserved in G(1) cells, (b) p53-mediated induction of p21 was preferentially seen in G(1) cells, (c) PD98059 strongly antagonized p21 induction by Nutlin-3a, and (d) cells with high p21 levels were resistant to apoptosis.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	92-99	P53	Homo sapiens	194-197
17454128-2	2007	We demonstrated that UVA-irradiated NADH induced damage to (32)P-labeled DNA fragments obtained from the p53 gene in the presence of Cu(II).	NAD	36-40	P53	Homo sapiens	105-108
17332930-11	2007	Overexpression of constitutively active AKT inhibited curcumin-induced p53 translocation to mitochondria, and Smac release to cytoplasm, whereas inhibition of AKT by dominant negative AKT enhanced curcumin-induced p53 translocation to mitochondria and Smac release.	Curcumin	54-62	P53	Homo sapiens	71-74
17332930-0	2007	Involvement of Bcl-2 family members, phosphatidylinositol 3"-kinase/AKT and mitochondrial p53 in curcumin (diferulolylmethane)-induced apoptosis in prostate cancer.	Curcumin	97-105	P53	Homo sapiens	90-93
17332930-11	2007	Overexpression of constitutively active AKT inhibited curcumin-induced p53 translocation to mitochondria, and Smac release to cytoplasm, whereas inhibition of AKT by dominant negative AKT enhanced curcumin-induced p53 translocation to mitochondria and Smac release.	Curcumin	54-62	P53	Homo sapiens	214-217
17332930-4	2007	Curcumin downregulated the expression of Bcl-2, and Bcl-XL and upregulated the expression of p53, Bax, Bak, PUMA, Noxa, and Bim.	Curcumin	0-8	P53	Homo sapiens	93-96
17575952-0	2007	Time and dose-dependent activation of p53 serine 15 phosphorylation among cell lines with different radiation sensitivity.	Serine	42-48	P53	Homo sapiens	38-41
17575952-2	2007	The serine 15 (Ser15) on p53 is crucial for p53 stabilization and a requirement for transient and permanent cell cycle arrest.	Serine	4-10	P53	Homo sapiens	25-28
17575952-2	2007	The serine 15 (Ser15) on p53 is crucial for p53 stabilization and a requirement for transient and permanent cell cycle arrest.	Serine	4-10	P53	Homo sapiens	44-47
17332930-5	2007	Curcumin upregulated the expression of p53 as well as its phosphorylation at serine 15, and acetylation in a concentration-dependent manner.	Curcumin	0-8	P53	Homo sapiens	39-42
17332930-12	2007	Our study establishes a role for AKT in modulating the direct action of p53 on the caspase-dependent mitochondrial death pathway and suggests that these important biological molecules interact at the level of the mitochondria to influence curcumin sensitivity.	Curcumin	239-247	P53	Homo sapiens	72-75
17332930-5	2007	Curcumin upregulated the expression of p53 as well as its phosphorylation at serine 15, and acetylation in a concentration-dependent manner.	Serine	77-83	P53	Homo sapiens	39-42
17332930-7	2007	Treatment of LNCaP cells with curcumin resulted in translocation of Bax and p53 to mitochondria, production of reactive oxygen species, drop in mitochondrial membrane potential, release of mitochondrial proteins (cytochrome c, Smac/DIABLO and Omi/HtrA2), activation of caspase-3 and induction of apoptosis.	Curcumin	30-38	P53	Homo sapiens	76-79
17575952-3	2007	Here, we sought to determine the relationship between p53 serine 15 phosphorylation (p53-p-Ser15) on cellular sensitivity and if this modification is associated with DNA double-strand break (DSB) repair.	Serine	58-64	P53	Homo sapiens	54-57
17575952-3	2007	Here, we sought to determine the relationship between p53 serine 15 phosphorylation (p53-p-Ser15) on cellular sensitivity and if this modification is associated with DNA double-strand break (DSB) repair.	Serine	58-64	P53	Homo sapiens	85-88
17332940-8	2007	Following silencing of p53 or p21 we observed extensive apoptosis concomitant with extensive depolarization of mitochondrial membrane and depletion of reduced glutathione.	Glutathione	159-170	P53	Homo sapiens	23-26
17406801-0	2007	Radiosensitization dependent on p53 function in bronchial carcinoma cells by the isoflavone genistein and estradiol in vitro.	Estradiol	106-115	P53	Homo sapiens	32-35
17063488-3	2007	We report that Carb or 5-FU upregulate Gadd45alpha and p53 in both these cells.	Fluorouracil	23-27	P53	Homo sapiens	55-58
17449938-7	2007	In addition, minoxidil plus ATRA elevated phosphorylated Erk, phosphorylated Akt and the ratio of Bcl-2/Bax, but decreased the expressions of P53 and P21 more effectively than by minoxidil alone.	Tretinoin	28-32	P53	Homo sapiens	142-145
17449938-8	2007	Our results suggest that minoxidil plus ATRA would additively enhance hair growth by mediating dual functions: 1) the prolongation of cell survival by activating the Erk and Akt signaling pathways, and 2) the prevention of apoptosis of DPCs and epithelial cells by increasing the ratio of Bcl-2/Bax and downregulating the expressions of P53 and P21.	Tretinoin	40-44	P53	Homo sapiens	337-340
17461764-9	2007	An extremely low concentration of cisplatin in addition to Ps-S-Oligos further up-regulated p53 activity, provoking massive apoptotic induction.	Cisplatin	34-43	P53	Homo sapiens	92-95
17515111-6	2007	We have found that apomorphine hydrochloride promotes degradation of intracellular AM and p53 attenuating oxidative stress-induced apoptosis.	Apomorphine	19-44	P53	Homo sapiens	90-93
17406801-10	2007	Incubation of nonfunctional TP53 cells with genistein or estradiol increased radiosensitivity in both tested concentrations.	Estradiol	57-66	P53	Homo sapiens	28-32
17406801-13	2007	CONCLUSION: NSCLC cells with nonfunctional TP53 might be sensitized against radiation by genistein or estradiol.	Estradiol	102-111	P53	Homo sapiens	43-47
17276397-4	2007	p53 accumulated in response to cisplatin (CDDP) and thereby promoting apoptosis in neuroblastoma SH-SY5Y cells bearing wild-type p53, whereas SK-N-AS cells did not undergo apoptosis.	Cisplatin	31-40	P53	Homo sapiens	0-3
17292432-0	2007	Phosphorylation of p53 at serine 15 in A549 pulmonary epithelial cells exposed to vanadate: involvement of ATM pathway.	Serine	26-32	P53	Homo sapiens	19-22
17292432-1	2007	When A549 cells were exposed to sodium metavanadate (NaVO(3)), the pentavalent species of vanadium (vanadate), phosphorylation of p53 protein at Ser15 was found in a time (8-48 h)- and dose (10-200 microM)-dependent manner.	Vanadium	90-98	P53	Homo sapiens	130-133
17292432-3	2007	Among serines in p53 protein immunoprecipitated from A549 cells treated with 100 microM NaVO(3) for 48 h, only Ser15 was markedly phosphorylated.	Serine	6-13	P53	Homo sapiens	17-20
17276397-4	2007	p53 accumulated in response to cisplatin (CDDP) and thereby promoting apoptosis in neuroblastoma SH-SY5Y cells bearing wild-type p53, whereas SK-N-AS cells did not undergo apoptosis.	Cisplatin	42-46	P53	Homo sapiens	0-3
17381838-10	2007	CONCLUSION: These observations support a role for p53-mediated transcriptional program in mammalian aging and suggest that mechanisms other than reactive oxygen species are involved in the age-related transcriptional activation of p53 targets.	Reactive Oxygen Species	145-168	P53	Homo sapiens	231-234
17242401-0	2007	5-fluorouracil activation of p53 involves an MDM2-ribosomal protein interaction.	Fluorouracil	0-14	P53	Homo sapiens	29-32
17242401-2	2007	The anti-tumor activity of 5-FU has been attributed in part to its ability to induce p53-dependent cell growth arrest and apoptosis.	Fluorouracil	27-31	P53	Homo sapiens	85-88
17242401-3	2007	However, the molecular mechanisms underlying p53 activation by 5-FU remain largely obscure.	Fluorouracil	63-67	P53	Homo sapiens	45-48
17242401-4	2007	Here we report that 5-FU treatment leads to p53 stabilization and activation by blocking MDM2 feedback inhibition through ribosomal proteins.	Fluorouracil	20-24	P53	Homo sapiens	44-47
17242401-5	2007	5-FU treatment increased the fraction of ribosome-free L5, L11, and L23 ribosomal proteins and their interaction with MDM2, leading to p53 activation and G1/S arrest.	Fluorouracil	0-4	P53	Homo sapiens	135-138
17242401-6	2007	Conversely, individual knockdown of these ribosomal proteins by small interfering RNA prevented the 5-FU-induced p53 activation and reversed the 5-FU-induced G1/S arrest.	Fluorouracil	100-104	P53	Homo sapiens	113-116
17242401-7	2007	These results demonstrate that 5-FU treatment triggers a ribosomal stress response so that ribosomal proteins L5, L11, and L23 are released from ribosome to activate p53 by ablating the MDM2-p53 feedback circuit.	Fluorouracil	31-35	P53	Homo sapiens	166-169
17242401-7	2007	These results demonstrate that 5-FU treatment triggers a ribosomal stress response so that ribosomal proteins L5, L11, and L23 are released from ribosome to activate p53 by ablating the MDM2-p53 feedback circuit.	Fluorouracil	31-35	P53	Homo sapiens	191-194
17293044-4	2007	Treatment of the cells with all trans retinoic acid (RA) generates a neuron-like, morphological change of differentiation, and results in the activation of ERK and Akt pathways, an inhibition of the nuclear translocation of p53 induced by GA, and induces higher resistance to the GA-induced apoptosis.	Tretinoin	38-51	P53	Homo sapiens	224-227
17297916-9	2007	We, therefore, generated an artificial p53, containing arginine residues N-terminal to the phospho-acceptor site, creating a better DAPK-1 peptide consensus and demonstrated that the Km for p531-66[ET--&gt;RR] and ATP is elevated.	Arginine	55-63	P53	Homo sapiens	39-42
17297916-9	2007	We, therefore, generated an artificial p53, containing arginine residues N-terminal to the phospho-acceptor site, creating a better DAPK-1 peptide consensus and demonstrated that the Km for p531-66[ET--&gt;RR] and ATP is elevated.	Adenosine Triphosphate	214-217	P53	Homo sapiens	39-42
17297920-0	2007	Zn(2+)-dependent misfolding of the p53 DNA binding domain.	Zinc	0-6	P53	Homo sapiens	35-38
17339891-4	2007	Lovo 175X2 cells (transfected with mt p53) were more resistant to 5-fluorouracil (5-FU; 2-fold), nolatrexed (3-fold), raltitrexed (3-fold) and pemetrexed (10-fold) in comparison with the wt p53 parental cells Lovo 92.	Fluorouracil	66-80	P53	Homo sapiens	38-41
17339891-4	2007	Lovo 175X2 cells (transfected with mt p53) were more resistant to 5-fluorouracil (5-FU; 2-fold), nolatrexed (3-fold), raltitrexed (3-fold) and pemetrexed (10-fold) in comparison with the wt p53 parental cells Lovo 92.	Fluorouracil	82-86	P53	Homo sapiens	38-41
17332358-1	2007	Phosphorylation of p53 at Ser(46) is important to activate the apoptotic program.	Serine	26-29	P53	Homo sapiens	19-22
17457979-3	2007	Cell proliferation was measured by CCK-8 assay, and the expression of two cell cycle regulators, p53 and p21, was determined by SDS-PAGE and Western blotting.	Sodium Dodecyl Sulfate	128-131	P53	Homo sapiens	97-100
17216584-5	2007	The ER stress-inducing agent thapsigargin also induced p53-independent Noxa expression.	Thapsigargin	29-41	P53	Homo sapiens	55-58
17216584-6	2007	Conversely, Noxa transcription in response to the chemotherapeutic agents cisplatin or temozolomide was inhibited by p53 knockdown.	Cisplatin	74-83	P53	Homo sapiens	117-120
17216584-7	2007	Apoptosis in response to cisplatin or temozolomide was also inhibited by abrogation of p53 expression yet apoptosis in response to fenretinide or thapsigargin was unaffected.	Cisplatin	25-34	P53	Homo sapiens	87-90
19690636-0	2007	BRCA1 Expression is an Important Biomarker for Chemosensitivity: Suppression of BRCA1 Increases the Apoptosis via Up-regulation of p53 and p21 During Cisplatin Treatment in Ovarian Cancer Cells.	Cisplatin	150-159	P53	Homo sapiens	131-134
19690636-5	2007	Reduced expression of BRCA1 by transfection of BRCA1-siRNA resulted in a 5.3-fold increase in sensitivity to cisplatin in p53-wild A2780 cells, but not in p53-mutated A2780/CDDP and p53-deleted SKOV3 cells.	Cisplatin	109-118	P53	Homo sapiens	122-125
19690636-9	2007	However, cisplatin treatment under suppression of BRCA1 showed a significantly increased apoptosis along with up-regulation of p53 and p21 in A2780 cells.	Cisplatin	9-18	P53	Homo sapiens	127-130
17332326-4	2007	In a human prostate cancer cell lines PC3 (p53(null)), curcumin reduced MDM2 protein and mRNA in a dose- and time-dependent manner, and enhanced the expression of the tumor suppressor p21(Waf1/CIP1).	Curcumin	55-63	P53	Homo sapiens	43-46
17332358-2	2007	The protein kinase that phosphorylates p53 Ser(46) in response to DNA double-strand breaks is currently unknown.	Serine	43-46	P53	Homo sapiens	39-42
17332358-5	2007	IR-induced HIPK2 up-regulation strictly correlates with p53 Ser(46) phosphorylation.	Serine	60-63	P53	Homo sapiens	56-59
17332358-6	2007	Down-regulation of HIPK2 by RNA interference specifically inhibits IR-induced phosphorylation of p53 at Ser(46).	Serine	104-107	P53	Homo sapiens	97-100
17332358-11	2007	Taken together, our findings indicate that HIPK2 is the IR-activated p53 Ser(46) kinase and is regulated by ATM.	Serine	73-76	P53	Homo sapiens	69-72
17050787-10	2007	However, modulator proteins p53, p21, and p27 were increased by resveratrol only in LNCaP cells.	Resveratrol	64-75	P53	Homo sapiens	28-31
17133364-4	2007	We now report that 22 oligonucleotides, 9-20 bases in length, with or without a 5" phosphate group and with varying homology (40-100%) to the 3" overhang, inhibit growth and induce apoptosis of human cell lines derived from breast cancers, pancreatic and ovarian carcinomas, and malignant melanoma, lines that lack p53 and/or p16 and harbor a variety of other abnormalities in key regulatory signaling pathways.	Oligonucleotides	22-38	P53	Homo sapiens	315-318
17121856-6	2007	Furthermore, the co-activator complexes initiate the recruitment of the components of the basal transcription apparatus to the basal promoter with markedly different outcomes because only Ac-Lys-373 p53 promotes the assembly of the basal transcriptional apparatus on the p21 promoter.	Lysine	191-194	P53	Homo sapiens	199-202
17203463-0	2007	Roscovitine-activated HIP2 kinase induces phosphorylation of wt p53 at Ser-46 in human MCF-7 breast cancer cells.	Serine	71-74	P53	Homo sapiens	64-67
17203463-4	2007	The p53 level increased despite upregulation of Hdm-2 protein and was attributable to the site-specific phosphorylation at Ser-46.	Serine	123-126	P53	Homo sapiens	4-7
17203463-5	2007	The p53 protein phosphorylated at serine 46 causes the up-regulation of the p53AIP1 protein, a component of mitochondria.	Serine	34-40	P53	Homo sapiens	4-7
17203463-8	2007	The overexpression of wild-type but not kinase inactive HIPK2 increased the basal and ROSC-induced level of p53 phosphorylation at Ser-46 and strongly enhanced the rate of apoptosis in cells exposed to ROSC.	Serine	131-134	P53	Homo sapiens	108-111
17203463-9	2007	We show that HIPK2 is activated by ROSC and mediates ROSC-induced P-Ser-46-p53, thereby stabilizing wt p53 and increasing the efficacy of drug-induced apoptosis in MCF-7 cells.	Serine	68-71	P53	Homo sapiens	75-78
17550137-0	2007	Synergic CSE1L/CAS, TNFR-1, and p53 apoptotic pathways in combined interferon-gamma/adriamycin-induced apoptosis of Hep G2 hepatoma cells.	Doxorubicin	84-94	P53	Homo sapiens	32-35
17550137-6	2007	Adriamycin increased p53 and Bax, but not TNFR- 1 and CAS levels.	Doxorubicin	0-10	P53	Homo sapiens	21-24
17550137-7	2007	Interferon-y did not increase p53 accumulation; nevertheless it enhanced adriamycin-induced p53 accumulation.	Doxorubicin	73-83	P53	Homo sapiens	92-95
17550137-8	2007	Overexpression of IRF-1 augmented the combined interferon-gamma/adriamycin-induced p53 accumulation.	Doxorubicin	64-74	P53	Homo sapiens	83-86
17550137-9	2007	Interferon-gamma co-treatment increased the stability of p53 protein induced by adriamycin.	Doxorubicin	80-90	P53	Homo sapiens	57-60
17218071-3	2007	DNA binding of benzo(a)pyrene-7,8-diol-9,10-epoxide (BPDE) was analyzed by synchronous fluorescence spectrophotometry and p53 protein by immunoblotting.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	15-51	P53	Homo sapiens	122-125
16924239-8	2007	This suggests that the presence of functional p53 protein may enhance death induction by rimcazole in part through greater induction of HIF-1alpha.	rimcazole	89-98	P53	Homo sapiens	46-49
16924240-4	2007	Expression of ubiquitin derivatives with all lysines mutated except K48 or K63 demonstrated that K48-linked p53-ubiquitin conjugates were specifically induced after DNA damage.	Lysine	45-52	P53	Homo sapiens	108-111
16870476-6	2007	RESULTS: Verapamil increased the tail moments induced by doxorubicin in all cell types over-expressing p53 mutant protein.	Doxorubicin	57-68	P53	Homo sapiens	103-106
17388661-0	2007	Exquisite sensitivity of TP53 mutant and basal breast cancers to a dose-dense epirubicin-cyclophosphamide regimen.	Epirubicin	78-88	P53	Homo sapiens	25-29
17388661-16	2007	CONCLUSIONS: This study demonstrates that, in noninflammatory breast cancers, TP53 status is a key predictive factor for response to this dose-dense epirubicin-cyclophosphamide regimen and further suggests that the basal subtype is exquisitely sensitive to this association.	Epirubicin	149-159	P53	Homo sapiens	78-82
17190831-8	2007	Furthermore, expression of p21, which correlates with taxane sensitivity, is regulated by CAV1 phosphorylation in a p53-dependent manner.	taxane	54-60	P53	Homo sapiens	116-119
17308111-7	2007	This activation, in combination with BaP-induced phosphorylated p53, promoted mitochondrial superoxide anion production, supporting the existence of a common target for NHE1 and p53.	Superoxides	92-108	P53	Homo sapiens	64-67
17147953-9	2007	Moreover, MNNG-induced increase in acetylation of p53, a representative target of sirtuin deacetylase activity, was suppressed by resveratrol.	Resveratrol	130-141	P53	Homo sapiens	50-53
17308111-7	2007	This activation, in combination with BaP-induced phosphorylated p53, promoted mitochondrial superoxide anion production, supporting the existence of a common target for NHE1 and p53.	Superoxides	92-108	P53	Homo sapiens	178-181
17285121-7	2007	MonoHER suppressed DOX-dependent activation of the mitochondrial apoptotic pathway in normal and A2780 cells as illustrated by p53 accumulation and activation of caspase-9 and -3 cleavage.	Doxorubicin	19-22	P53	Homo sapiens	127-130
17317843-0	2007	DNA mismatch repair initiates 6-thioguanine--induced autophagy through p53 activation in human tumor cells.	Thioguanine	30-43	P53	Homo sapiens	71-74
17317843-1	2007	PURPOSE: We investigate the roles of DNA mismatch repair (MMR) and p53 in mediating the induction of autophagy in human tumor cells after exposure to 6-thioguanine (6-TG), a chemotherapy drug recognized by MMR.	Thioguanine	150-163	P53	Homo sapiens	67-70
17317843-1	2007	PURPOSE: We investigate the roles of DNA mismatch repair (MMR) and p53 in mediating the induction of autophagy in human tumor cells after exposure to 6-thioguanine (6-TG), a chemotherapy drug recognized by MMR.	Thioguanine	165-169	P53	Homo sapiens	67-70
17236862-0	2007	Methionine inhibits cellular growth dependent on the p53 status of cells.	Methionine	0-10	P53	Homo sapiens	53-56
17236862-4	2007	However, the generalizability of this observation and the precise role of p53 in methionine-induced growth suppression needs to be determined.	Methionine	81-91	P53	Homo sapiens	74-77
17236862-8	2007	The effects of methionine on p53 expression were assessed by using reverse transcriptase-polymerase chain reaction (RT-PCR), immunohistochemistry, and Western blot analysis.	Methionine	15-25	P53	Homo sapiens	29-32
17236862-9	2007	The role of p53 in L-methionine-mediated growth suppression was evaluated using short-interference RNA for p53 (siRNA-p53), immunoprecipitation, and direct DNA sequencing.	Methionine	19-31	P53	Homo sapiens	12-15
17236862-9	2007	The role of p53 in L-methionine-mediated growth suppression was evaluated using short-interference RNA for p53 (siRNA-p53), immunoprecipitation, and direct DNA sequencing.	Methionine	19-31	P53	Homo sapiens	107-110
17236862-9	2007	The role of p53 in L-methionine-mediated growth suppression was evaluated using short-interference RNA for p53 (siRNA-p53), immunoprecipitation, and direct DNA sequencing.	Methionine	19-31	P53	Homo sapiens	107-110
17236862-11	2007	In association with the inhibition of growth, methionine also inhibited native p53 expression at the mRNA and protein levels, respectively.	Methionine	46-56	P53	Homo sapiens	79-82
17236862-12	2007	Furthermore, transfection with siRNA-p53, to knock down p53 expression, increased cell growth and proliferation of the LNCaP cells even when they were exposed to methionine.	Methionine	162-172	P53	Homo sapiens	37-40
17236862-15	2007	CONCLUSION: Our results extend a prior observation to other cell lines and demonstrate that high concentrations of methionine suppress the expression of native but not mutated p53.	Methionine	115-125	P53	Homo sapiens	176-179
17244262-5	2007	Paclitaxel treatment combined with apoptin expression significantly inhibited the survival of p53-positive human osteosarcoma U2OS and non-small lung carcinoma A549 cells, p53-negative human osteosarcoma Saos-2 cells and p53-mutant human prostate cancer Du145 cells, already at low doses of the chemotherapeutic agent.	Paclitaxel	0-10	P53	Homo sapiens	94-97
17244262-5	2007	Paclitaxel treatment combined with apoptin expression significantly inhibited the survival of p53-positive human osteosarcoma U2OS and non-small lung carcinoma A549 cells, p53-negative human osteosarcoma Saos-2 cells and p53-mutant human prostate cancer Du145 cells, already at low doses of the chemotherapeutic agent.	Paclitaxel	0-10	P53	Homo sapiens	172-175
17244262-5	2007	Paclitaxel treatment combined with apoptin expression significantly inhibited the survival of p53-positive human osteosarcoma U2OS and non-small lung carcinoma A549 cells, p53-negative human osteosarcoma Saos-2 cells and p53-mutant human prostate cancer Du145 cells, already at low doses of the chemotherapeutic agent.	Paclitaxel	0-10	P53	Homo sapiens	172-175
17223878-1	2007	BACKGROUND: p53 has a common polymorphism at amino acid 72, encoding either arginine or proline.	Arginine	76-84	P53	Homo sapiens	12-15
17283157-6	2007	Exposure to CDDP induced galectin-7 in cell lines with wild-type p53 but not in those with mutated p53.	Cisplatin	12-16	P53	Homo sapiens	65-68
16752155-3	2007	RA treatment resulted in an increase of p21, p27 and p53 protein levels and G1 arrest in UM cells, which correlated with significant down-modulation of surface Her2/neu proto-oncogene expression.	Tretinoin	0-2	P53	Homo sapiens	53-56
16926174-11	2007	These results are consistent with the hypothesis that nitrosation of glycine (or glycine derivatives) may contribute to characteristic human p53 mutation profiles.	Glycine	69-76	P53	Homo sapiens	141-144
16926174-11	2007	These results are consistent with the hypothesis that nitrosation of glycine (or glycine derivatives) may contribute to characteristic human p53 mutation profiles.	Glycine	81-88	P53	Homo sapiens	141-144
17283151-0	2007	p53 enhances gefitinib-induced growth inhibition and apoptosis by regulation of Fas in non-small cell lung cancer.	Gefitinib	13-22	P53	Homo sapiens	0-3
17283151-6	2007	NCI-H1299 cells, which had a p53-null genotype, were more resistant to gefitinib compared with A549 cells, which were wild-type p53 (IC(50), 40 micromol/L in NCI-H1299 and 5 micromol/L in A549).	Gefitinib	71-80	P53	Homo sapiens	29-32
17283157-7	2007	When the galectin-7 gene was transfected into cell lines with mutated p53, the sensitivity to CDDP increased compared with control transfectants.	Cisplatin	94-98	P53	Homo sapiens	70-73
17283151-7	2007	Treatment of A549 with gefitinib resulted in the translocation of p53 from cytosol to nucleus and the up-regulation of Fas, which was localized to the plasma membrane.	Gefitinib	23-32	P53	Homo sapiens	66-69
17218783-5	2007	Curcumin induced G(2)/M phase cell-cycle arrest in CR cells by enhancing the p53 phosphorylation and apoptosis through the activation of caspase-3 followed by PARP degradation.	Curcumin	0-8	P53	Homo sapiens	77-80
17283151-8	2007	In the stable H1299 cell line with tetracycline-inducible p53 expression, induced p53 enhanced growth inhibition and apoptosis by gefitinib through the up-regulation of Fas and restoration of caspase activation.	Gefitinib	130-139	P53	Homo sapiens	58-61
17211470-0	2007	Immunostaining of thymidylate synthase and p53 for predicting chemoresistance to S-1/cisplatin in gastric cancer.	Cisplatin	85-94	P53	Homo sapiens	43-46
17283151-8	2007	In the stable H1299 cell line with tetracycline-inducible p53 expression, induced p53 enhanced growth inhibition and apoptosis by gefitinib through the up-regulation of Fas and restoration of caspase activation.	Gefitinib	130-139	P53	Homo sapiens	82-85
17283151-10	2007	Conversely, inhibition of p53 using antisense oligonucleotide in A549 caused a significant decrease in apoptosis by gefitinib and down-regulation of Fas under the same conditions.	Oligonucleotides	46-61	P53	Homo sapiens	26-29
17283151-10	2007	Conversely, inhibition of p53 using antisense oligonucleotide in A549 caused a significant decrease in apoptosis by gefitinib and down-regulation of Fas under the same conditions.	Gefitinib	116-125	P53	Homo sapiens	26-29
17283151-11	2007	In conclusion, p53 may play a role in determining gefitinib sensitivity by regulating Fas expression in NSCLC.	Gefitinib	50-59	P53	Homo sapiens	15-18
17235397-5	2007	Systemic administration of tamoxifen led to p53 activation and tumor regression followed by tumor recurrence.	Tamoxifen	27-36	P53	Homo sapiens	44-47
17174366-6	2007	We first established that resveratrol (10 microM), a pro-apoptotic agent in other cancer cells, induced p53-dependent apoptosis and c-fos, c-jun and p21 gene expression in both papillary and follicular thyroid cancer cells.	Resveratrol	26-37	P53	Homo sapiens	104-107
17174366-7	2007	Induction of apoptosis by the stilbene required Ser-15 phosphorylation of p53.	Serine	48-51	P53	Homo sapiens	74-77
17085012-2	2007	By combining chromatin immunoprecipitation with oligonucleotide microarrays, we have mapped binding sites of p53 (p53-BS) in the genome of HCT116 human colon carcinoma cells, along with those of acetylated H3, acetylated H4, and methylated H3-K4.	Oligonucleotides	48-63	P53	Homo sapiens	109-112
17121789-5	2007	Two out of seven (29%) PEL cell lines harbored a mutant p53 allele (BCBL-1 and BCP-1) which led to doxorubicin resistance.	Doxorubicin	99-110	P53	Homo sapiens	56-59
17308072-0	2007	Sensitization of p53-mutated epithelial ovarian cancer to CD95-mediated apoptosis is synergistically induced by cisplatin pretreatment.	Cisplatin	112-121	P53	Homo sapiens	17-20
17308072-7	2007	In the present study, we examined both intrinsic and death receptor-dependent apoptotic signaling in p53mu OVCAR3 EOC cell line, showing that these cells are less susceptible to cisplatin treatment as compared with p53 wild-type EOC cells and also resist CD95-mediated apoptosis due to inefficient formation of the death-inducing signaling complex and weak mitochondrial signal amplification.	Cisplatin	178-187	P53	Homo sapiens	101-104
17308072-9	2007	The synergy of cisplatin pretreatment and CD95 triggering in inducing cell death was also shown in p53mu tumor cells derived from ascitic fluid of advanced-stage EOC patients.	Cisplatin	15-24	P53	Homo sapiens	99-102
17107963-12	2007	Ser-166 phosphorylation of Mdm2 has been shown to increase its ubiquitin ligase activity and increase p53 degradation, and our data indicated an attenuated p53 response to DNA damage in hepatocytes exhibiting high levels of pMdm2 Ser-166.	Serine	0-3	P53	Homo sapiens	102-105
17211470-9	2007	These results suggest that immunostaining for TS and p53 protein is useful for pretreatment selection of gastric cancer patients unresponsive to S-1/cisplatin chemotherapy.	Cisplatin	149-158	P53	Homo sapiens	53-56
17107963-12	2007	Ser-166 phosphorylation of Mdm2 has been shown to increase its ubiquitin ligase activity and increase p53 degradation, and our data indicated an attenuated p53 response to DNA damage in hepatocytes exhibiting high levels of pMdm2 Ser-166.	Serine	230-233	P53	Homo sapiens	156-159
17234770-5	2007	Expression array analyses revealed that RA induces the expression of several genes involved in cell cycle regulation, including the p53-controlled antiproliferative gene B-cell translocation gene, member 2 (Btg2) and the BTG family member Tob1.	Tretinoin	40-42	P53	Homo sapiens	132-135
17135250-7	2007	We have also observed induction of p53 target pro-apoptotic genes, e.g. puma (p53-up-regulated modulator of apoptosis), and bak in PpIX-treated cells.	protoporphyrin IX	131-135	P53	Homo sapiens	35-38
17135250-7	2007	We have also observed induction of p53 target pro-apoptotic genes, e.g. puma (p53-up-regulated modulator of apoptosis), and bak in PpIX-treated cells.	protoporphyrin IX	131-135	P53	Homo sapiens	78-81
17135250-8	2007	In addition, p53-independent growth suppression by PpIX was detected in p53-negative cells.	protoporphyrin IX	51-55	P53	Homo sapiens	13-16
17135250-8	2007	In addition, p53-independent growth suppression by PpIX was detected in p53-negative cells.	protoporphyrin IX	51-55	P53	Homo sapiens	72-75
17184774-0	2007	Diphenyleneiodonium induces ROS-independent p53 expression and apoptosis in human RPE cells.	ros	28-31	P53	Homo sapiens	44-47
17184774-5	2007	ROS have been implicated as a key factor in the activation of p53 by many chemotherapeutic drugs.	ros	0-3	P53	Homo sapiens	62-65
17184774-10	2007	We conclude that DPI induces the expression of p53 by ROS-independent mechanism in ARPE-19 cells, and renders cells sensitive to drug-induced apoptosis by induction of p53 expression.	ros	54-57	P53	Homo sapiens	47-50
17135248-8	2007	Importantly, we found that inhibition of Plk3 by wortmannin lead to a decrease in phosphorylation of p53 on serine 20 induced by DNA damage, demonstrating the effect of wortmannin on a downstream Plk3 target.	Serine	108-114	P53	Homo sapiens	101-104
17135250-0	2007	Protoporphyrin IX interacts with wild-type p53 protein in vitro and induces cell death of human colon cancer cells in a p53-dependent and -independent manner.	protoporphyrin IX	0-17	P53	Homo sapiens	43-46
17135250-0	2007	Protoporphyrin IX interacts with wild-type p53 protein in vitro and induces cell death of human colon cancer cells in a p53-dependent and -independent manner.	protoporphyrin IX	0-17	P53	Homo sapiens	120-123
17135250-5	2007	We have demonstrated here for the first time that the photosensitizer protoporphyrin IX (PpIX) binds to p53 and disrupts the interaction between p53 tumor suppressor protein and its negative regulator HDM2 in vitro and in cells.	protoporphyrin IX	70-87	P53	Homo sapiens	104-107
17135250-5	2007	We have demonstrated here for the first time that the photosensitizer protoporphyrin IX (PpIX) binds to p53 and disrupts the interaction between p53 tumor suppressor protein and its negative regulator HDM2 in vitro and in cells.	protoporphyrin IX	70-87	P53	Homo sapiens	145-148
17135250-5	2007	We have demonstrated here for the first time that the photosensitizer protoporphyrin IX (PpIX) binds to p53 and disrupts the interaction between p53 tumor suppressor protein and its negative regulator HDM2 in vitro and in cells.	protoporphyrin IX	89-93	P53	Homo sapiens	104-107
17135250-5	2007	We have demonstrated here for the first time that the photosensitizer protoporphyrin IX (PpIX) binds to p53 and disrupts the interaction between p53 tumor suppressor protein and its negative regulator HDM2 in vitro and in cells.	protoporphyrin IX	89-93	P53	Homo sapiens	145-148
17135250-6	2007	Moreover, HCT116 colon cancer cells exhibited a p53-dependent sensitivity to PpIX in a dose-dependent manner, as was demonstrated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and fluorescence-activated cell sorter (FACS) analysis of cell cycle profiles.	protoporphyrin IX	77-81	P53	Homo sapiens	48-51
17098746-6	2007	This is consistent with recent studies showing that a lysine to arginine mutation at Lys-320 significantly enhances p53 function, although Lys-320 was originally identified as an acetylation site involving PCAF-mediated activation of p53.	Lysine	54-60	P53	Homo sapiens	116-119
17098746-6	2007	This is consistent with recent studies showing that a lysine to arginine mutation at Lys-320 significantly enhances p53 function, although Lys-320 was originally identified as an acetylation site involving PCAF-mediated activation of p53.	Lysine	54-60	P53	Homo sapiens	234-237
17098746-6	2007	This is consistent with recent studies showing that a lysine to arginine mutation at Lys-320 significantly enhances p53 function, although Lys-320 was originally identified as an acetylation site involving PCAF-mediated activation of p53.	Lysine	85-88	P53	Homo sapiens	116-119
17098746-6	2007	This is consistent with recent studies showing that a lysine to arginine mutation at Lys-320 significantly enhances p53 function, although Lys-320 was originally identified as an acetylation site involving PCAF-mediated activation of p53.	Lysine	85-88	P53	Homo sapiens	234-237
17234782-5	2007	We found that coexpression of FUS1 and p53 by N-[1-(2,3-dioleoyloxyl)propyl]-NNN-trimethylammoniummethyl sulfate:cholesterol nanoparticle-mediated gene transfer significantly and synergistically inhibited NSCLC cell growth and induced apoptosis in vitro.	Cholesterol	113-124	P53	Homo sapiens	39-42
17327702-7	2007	Furthermore, MDMX overexpression promotes resistance to the chemotherapeutic agent 5-FU, which at low concentrations activates p53 by inhibiting RNA metabolism.	Fluorouracil	83-87	P53	Homo sapiens	127-130
17097637-9	2007	Since several p53-target genes and other apoptosis-related genes were up-regulated by Adox, we conclude that AdoHcy is involved in adenosine-induced apoptosis by altering gene expression.	Adenosine	131-140	P53	Homo sapiens	14-17
17255282-6	2007	CHIR-124 interacts synergistically with topoisomerase poisons (e.g., camptothecin or SN-38) in causing growth inhibition in several p53-mutant solid tumor cell lines as determined by isobologram or response surface analysis.	Irinotecan	85-90	P53	Homo sapiens	132-135
17098465-0	2007	Folate depletion in human lymphocytes up-regulates p53 expression despite marked induction of strand breaks in exons 5-8 of the gene.	Folic Acid	0-6	P53	Homo sapiens	51-54
17126811-4	2007	Western blotting analysis demonstrated that H/R-induced the accumulation of p53 and p63 proteins.	r	46-47	P53	Homo sapiens	76-79
17098465-9	2007	In primary human lymphocytes, folate depletion induces a marked increase in p53 exons 5-8 breaks, but does not reduce steady-state levels of p53 mRNA, protein, or impair downstream signaling.	Folic Acid	30-36	P53	Homo sapiens	76-79
17098465-10	2007	The induction of p53 strand breaks by folate depletion does not impair p53 expression or action within all human cell lines.	Folic Acid	38-44	P53	Homo sapiens	17-20
17174997-0	2007	p53-Dependent but ATM-independent inhibition of DNA synthesis and G2 arrest in cadmium-treated human fibroblasts.	Cadmium	79-86	P53	Homo sapiens	0-3
17174997-3	2007	Cells that were rendered p53-defective by expression of a dominant-negative p53 allele or knockdown of p53 mRNA were more resistant to cadmium-induced inactivation of colony formation than normal and ataxia telangiectasia (AT) cells.	Cadmium	135-142	P53	Homo sapiens	25-28
17174997-3	2007	Cells that were rendered p53-defective by expression of a dominant-negative p53 allele or knockdown of p53 mRNA were more resistant to cadmium-induced inactivation of colony formation than normal and ataxia telangiectasia (AT) cells.	Cadmium	135-142	P53	Homo sapiens	76-79
17174997-3	2007	Cells that were rendered p53-defective by expression of a dominant-negative p53 allele or knockdown of p53 mRNA were more resistant to cadmium-induced inactivation of colony formation than normal and ataxia telangiectasia (AT) cells.	Cadmium	135-142	P53	Homo sapiens	76-79
17174997-8	2007	Total p53 protein and ser15-phosphorylated p53 were induced by cadmium in normal and AT cells.	Cadmium	63-70	P53	Homo sapiens	6-9
17174997-8	2007	Total p53 protein and ser15-phosphorylated p53 were induced by cadmium in normal and AT cells.	Cadmium	63-70	P53	Homo sapiens	43-46
17174997-9	2007	The p53 transactivation target Gadd45alpha was induced in both p53-effective and p53-defective cells after 4 h cadmium treatment, and this was associated with an acute inhibition of mitosis.	Cadmium	111-118	P53	Homo sapiens	4-7
17174997-10	2007	Cadmium produced a very unusual pattern of toxicity in human fibroblasts, inhibiting DNA replication and inducing p53-dependent growth arrest but without induction of p21(Cip1/Waf1) or activation of Chk1.	Cadmium	0-7	P53	Homo sapiens	114-117
17184779-6	2007	Furthermore, several differential proteins including HSP27, HSP70, GRP75 and GRP78 were verified as p53 interacting proteins in NPC by immunoprecipitation and Western blot analysis, and the suppression of HSP27 expression by HSP27 antisense oligonucleotides could decrease the p53 protein level.	Oligonucleotides	241-257	P53	Homo sapiens	100-103
17098465-5	2007	Cells grown in 15 nM folate developed significant levels of p53 strand breaks, reflected by reductions in amplifiable DNA from p53 exons 5-8 (approximately 40% loss, P&lt;0.0001) and exons 7-8 (approximately 26% loss, P&lt;0.0001) compared to 30 and 120 nM.	Folic Acid	21-27	P53	Homo sapiens	60-63
17098465-5	2007	Cells grown in 15 nM folate developed significant levels of p53 strand breaks, reflected by reductions in amplifiable DNA from p53 exons 5-8 (approximately 40% loss, P&lt;0.0001) and exons 7-8 (approximately 26% loss, P&lt;0.0001) compared to 30 and 120 nM.	Folic Acid	21-27	P53	Homo sapiens	127-130
17098465-7	2007	p53 protein abundance increased with decreasing media folate, as did p21 transcript.	Folic Acid	54-60	P53	Homo sapiens	0-3
16935849-6	2007	ATRA induced apoptosis and increased the expression of p53 protein in a dose-dependent fashion.	Tretinoin	0-4	P53	Homo sapiens	55-58
17138942-4	2007	Although nutlin-3 and doxorubicin induced a comparable p53 accumulation in endothelial cells, nutlin-3 was significantly more efficient than doxorubicin in upregulating the p53 target genes CDKN1A/p21, MDM2, and GDF-15, as well as in inhibiting cell cycle progression.	Doxorubicin	22-33	P53	Homo sapiens	55-58
17138942-4	2007	Although nutlin-3 and doxorubicin induced a comparable p53 accumulation in endothelial cells, nutlin-3 was significantly more efficient than doxorubicin in upregulating the p53 target genes CDKN1A/p21, MDM2, and GDF-15, as well as in inhibiting cell cycle progression.	Doxorubicin	141-152	P53	Homo sapiens	173-176
17113036-7	2007	This effect was paralleled by an increase in total p53 level in the nucleus and the induction of its phosphorylation at Ser-15 site.	Serine	120-123	P53	Homo sapiens	51-54
17565390-8	2007	The amount of p53 protein and its form phosphorylated on Ser-392 increased 1 h after irradiation (1-10 Gy).	Serine	57-60	P53	Homo sapiens	14-17
17565390-10	2007	At the time of phosphorylation of p53, we found simultaneous phosphorylation of the oncoprotein Mdm2 on Ser-166.	Serine	104-107	P53	Homo sapiens	34-37
17569210-4	2007	Curcumin decreased the expression of antiapoptotic members of the Bcl-2 family and elevated the expression of p53, Bax, procaspases 3, 8, and 9.	Curcumin	0-8	P53	Homo sapiens	110-113
17595514-0	2007	H2O2 accelerates cellular senescence by accumulation of acetylated p53 via decrease in the function of SIRT1 by NAD+ depletion.	Hydrogen Peroxide	0-4	P53	Homo sapiens	67-70
17404016-0	2007	Effect of distinct anticancer drugs on the phosphorylation of p53 protein at serine 46 in human MCF-7 breast cancer cells.	Serine	77-83	P53	Homo sapiens	62-65
17404016-5	2007	ROSC induced phosphorylation of p53 protein at serine 46.	Serine	47-53	P53	Homo sapiens	32-35
17404016-6	2007	Therefore, we decided to examine whether other anticancer drugs are also able to induce phosphorylation of wt p53 protein at serine 46.	Serine	125-131	P53	Homo sapiens	110-113
17404016-7	2007	Exposure of MCF-7 cells to doxorubicin (DOX) at doses inducing a strong G2 arrest resulted in a weak upregulation of p53.	Doxorubicin	27-38	P53	Homo sapiens	117-120
17404016-7	2007	Exposure of MCF-7 cells to doxorubicin (DOX) at doses inducing a strong G2 arrest resulted in a weak upregulation of p53.	Doxorubicin	40-43	P53	Homo sapiens	117-120
17404024-0	2007	The epidermal growth factor receptor tyrosine kinase inhibitor ZD1839 (Iressa) suppresses proliferation and invasion of human oral squamous carcinoma cells via p53 independent and MMP, uPAR dependent mechanism.	Gefitinib	63-69	P53	Homo sapiens	160-163
17404024-0	2007	The epidermal growth factor receptor tyrosine kinase inhibitor ZD1839 (Iressa) suppresses proliferation and invasion of human oral squamous carcinoma cells via p53 independent and MMP, uPAR dependent mechanism.	Gefitinib	71-77	P53	Homo sapiens	160-163
16905748-2	2007	We show here that the secondary bile acid, deoxycholic acid (DCA), is the only one of the commonly refluxed bile acids tested here, to show genotoxicity, in terms of chromosome damage and mutation induction in the human p53 gene.	Bile Acids and Salts	32-41	P53	Homo sapiens	220-223
17136320-6	2007	Most importantly, sulindac-derived ROS activated p38 mitogen-activated protein kinase and p53.	Reactive Oxygen Species	35-38	P53	Homo sapiens	90-93
17056233-0	2007	Inhibition of Fas expression by RNAi modulates 5-fluorouracil-induced apoptosis in HCT116 cells expressing wild-type p53.	Fluorouracil	47-61	P53	Homo sapiens	117-120
17056233-2	2007	In addition, the clinical value of p53 as a predictive marker for 5-FU-based chemotherapy remains a matter of debate.	Fluorouracil	66-70	P53	Homo sapiens	35-38
17056233-13	2007	In conclusion, 5-FU exerts its cytotoxic effects, in part, through a p53/Fas-dependent apoptotic pathway that involves Bax translocation and mitochondrial permeabilization.	Fluorouracil	15-19	P53	Homo sapiens	69-72
17945002-0	2007	Implication of BRCA2 -26G&gt;A 5" untranslated region polymorphism in susceptibility to sporadic breast cancer and its modulation by p53 codon 72 Arg&gt;Pro polymorphism.	Arginine	146-149	P53	Homo sapiens	133-136
17945002-9	2007	The p53 codon 72 Arg homozygous genotype was found to be over-represented in patients (P = 0.0005, OR = 2.3, 95% CI = 1.4 to 3.6).	Arginine	17-20	P53	Homo sapiens	4-7
17595514-1	2007	It has been reported that p53 acetylation, which promotes cellular senescence, can be regulated by the NAD(+)-dependent deacetylase SIRT1, the human homolog of yeast Sir2, a protein that modulates lifespan.	NAD	103-109	P53	Homo sapiens	26-29
17636407-5	2007	The induction of wt p53 function by use of Adriamycin resulted in the inhibition of the invasion/migration capacity in association with the up-regulation of p53 target genes to a far greater degree in 213Q and wt cells than in 273H cells.	Doxorubicin	43-53	P53	Homo sapiens	20-23
17636407-5	2007	The induction of wt p53 function by use of Adriamycin resulted in the inhibition of the invasion/migration capacity in association with the up-regulation of p53 target genes to a far greater degree in 213Q and wt cells than in 273H cells.	Doxorubicin	43-53	P53	Homo sapiens	157-160
17508933-6	2007	Several clusters of the Trp/Met/Phe residues are involved in the p53 protein-protein interactions.	Tryptophan	24-27	P53	Homo sapiens	65-68
17319790-11	2007	In the younger women group, the p53 BstUI polymorphism genotype frequencies were 6.2% for BstUIPro/Pro, 31.0% for BstUIArg/Pro and 62.8% for BstUIArg/Arg in controls and 11.11 %, 40.74% and 48.15% in cases respectively.	Arginine	119-122	P53	Homo sapiens	32-35
17116745-6	2007	NaHS treatment also resulted in stabilization of p53 coupled with induction of downstream proteins such as p21, Bax, and cytochrome c, as well as translocation of Bax from the cytosol to the mitochondria and release of cytochrome c from mitochondria.	sodium bisulfide	0-4	P53	Homo sapiens	49-52
17848273-5	2007	RESULTS: HNSCC cell lines selected for cisplatin resistance had wild-type p53 and high levels of Bcl-xL.	Cisplatin	39-48	P53	Homo sapiens	74-77
17848273-6	2007	Expression of wild-type p53 in cell lines with low Bcl-xL enhanced cisplatin sensitivity.	Cisplatin	67-76	P53	Homo sapiens	24-27
17848273-7	2007	Expression of both Bcl-xL and wild-type p53 caused tumor cells to become cisplatin resistant.	Cisplatin	73-82	P53	Homo sapiens	40-43
17848273-9	2007	Novel agents that inhibit Bcl-xL or activate p53 function may target cisplatin-resistant HNSCC.	Cisplatin	69-78	P53	Homo sapiens	45-48
17848273-10	2007	CONCLUSION: Cisplatin resistance in HNSCC is mediated, at least in part, by high Bcl-xL and functional p53.	Cisplatin	12-21	P53	Homo sapiens	103-106
17237273-7	2007	Western blot analyses showed that SSAT protein expression was dramatically enhanced when DENSpm was combined with oxaliplatin or 5-FU in HCT116 p53(+/+) cells.	Fluorouracil	129-133	P53	Homo sapiens	144-147
18161532-0	2007	Antiproliferative activity of cisplatin detected by CFSE in p53-proficient and p53-deficient cells.	Cisplatin	30-39	P53	Homo sapiens	60-63
18161532-0	2007	Antiproliferative activity of cisplatin detected by CFSE in p53-proficient and p53-deficient cells.	Cisplatin	30-39	P53	Homo sapiens	79-82
18161532-2	2007	The method was applied here to analyze the role of p53 in the effect of the anticancer drug cisplatin, distinguishing events occurring in the first generation of cells from those in the second and subsequent generations.	Cisplatin	92-101	P53	Homo sapiens	51-54
18415980-10	2007	Recently the G245C substitution has been assumed to result in formation of a novel Zn(2+)-binding site in the p53 protein.	Zinc	83-89	P53	Homo sapiens	110-113
17991682-5	2007	Long ADP-ribose chains (55-mer) promoted the formation of three specific complexes with p53.	Adenosine Diphosphate	5-8	P53	Homo sapiens	88-91
17213797-3	2006	BaP 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of BaP, attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 mutations.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	27-31	P53	Homo sapiens	129-132
17534123-0	2007	Resveratrol-induced apoptosis is associated with activation of p53 and inhibition of protein translation in T47D human breast cancer cells.	Resveratrol	0-11	P53	Homo sapiens	63-66
17534123-7	2007	RSVL-induced apoptosis is associated with the activation of the p53 in a dose- and a time-dependent manner.	Resveratrol	0-4	P53	Homo sapiens	64-67
17534123-8	2007	Phosphatidylinositol 3-kinase (PI3K) inhibitors, wortmannin and LY294002 abolished the effect of RSVL on p53 activation.	Resveratrol	97-101	P53	Homo sapiens	105-108
17534123-10	2007	CONCLUSIONS AND IMPLICATIONS: These findings demonstrate that RSVL affects multiple intracellular signaling transduction pathways such as p53 activation/protein translation inhibition/apoptosis, and strongly support a contemplated use of this natural compound as a preventive and/or an adjuvant therapeutic drug for breast cancer.	Resveratrol	62-66	P53	Homo sapiens	138-141
17077087-8	2006	Considering that p53-induced apoptosis requires an accumulation of reactive oxygen species, this negative control on the Nrf2 transactivation appears to be aimed to prevent the generation of a strong anti-oxidant intracellular environment that could hinder the induction of apoptosis.	Reactive Oxygen Species	67-90	P53	Homo sapiens	17-20
17189187-4	2006	Mutation of K120 to arginine, as occurs in human cancer, debilitates K120 acetylation and diminishes p53-mediated apoptosis without affecting cell-cycle arrest.	Arginine	20-28	P53	Homo sapiens	101-104
17663174-1	2007	The study was concerned with identification of predictive value of p53 expression on sensitivity to tamoxifen in breast cancer management.	Tamoxifen	100-109	P53	Homo sapiens	67-70
17663174-2	2007	Estrogen receptor-positive cell line MCF-7 was used to establish p53 expression influence on the rate of cell proliferation after tamoxifen.	Tamoxifen	130-139	P53	Homo sapiens	65-68
17213797-0	2006	An association between BPDE-like DNA adduct levels and P53 gene mutation in pterygium.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	23-27	P53	Homo sapiens	55-58
17213797-3	2006	BaP 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of BaP, attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 mutations.	Deoxyguanosine	73-87	P53	Homo sapiens	129-132
17213797-4	2006	The relationship between BPDE-like DNA adduct levels and abnormal p53 has not been clear in pterygium.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	25-29	P53	Homo sapiens	66-69
17160924-4	2006	This nitrogenous urea compound has a high mutation inducibility affecting the expression of oncogenes such as p53, neu/erbB-2 and Ras.	Urea	17-21	P53	Homo sapiens	110-113
16970927-5	2006	Oligonucleotide precipitation showed that I3C increased the level of activated p53 nuclear protein that is competent to bind its DNA target site on the p21 promoter.	Oligonucleotides	0-15	P53	Homo sapiens	79-82
17054906-4	2006	p53 was induced to be accumulated and associated with APP in response to cisplatin.	Cisplatin	73-82	P53	Homo sapiens	0-3
17178853-3	2006	We report here that exposure of human mesothelioma or lung carcinoma cells to nitric oxide (NO) in the presence of crocidolite asbestos resulted in a marked decrease in intracellular nitrosation and diminished NO-induced posttranslational modifications of tumor-associated proteins (hypoxia-inducible factor-1alpha and p53).	Nitric Oxide	78-90	P53	Homo sapiens	319-322
17055453-7	2006	Except for ZNF415-1, overexpression of the other ZNF415 isoforms in COS-7 cells inhibits the transcriptional activities of AP-1 and p53, suggesting that the ZNF415 protein may be involved in AP-1- and p53-mediated transcriptional activity.	carbonyl sulfide	68-71	P53	Homo sapiens	132-135
17055453-7	2006	Except for ZNF415-1, overexpression of the other ZNF415 isoforms in COS-7 cells inhibits the transcriptional activities of AP-1 and p53, suggesting that the ZNF415 protein may be involved in AP-1- and p53-mediated transcriptional activity.	carbonyl sulfide	68-71	P53	Homo sapiens	201-204
16849690-2	2006	Using cell culture models, recent work has suggested the involvement of p53 in renal cell apoptosis during cisplatin treatment.	Cisplatin	107-116	P53	Homo sapiens	72-75
17166391-4	2006	For example, paclitaxel is regarded as a relatively sensitive drug and may be chosen for the tumors with high expression of p53, while it is predicted as relatively resistant drug and should be avoided for the tumors with high expression of P-glycoprotein (P-gp).	Paclitaxel	13-23	P53	Homo sapiens	124-127
16849690-10	2006	During cisplatin incubation, VAD protected ATM and enhanced p53 phosphorylation.	Cisplatin	7-16	P53	Homo sapiens	60-63
16849690-11	2006	In vitro assay of protein kinase activity further showed that ATM immunoprecipitated from cisplatin-treated cells had significantly lower kinase activity toward p53 than that from control cells.	Cisplatin	90-99	P53	Homo sapiens	161-164
17051326-8	2006	Over-expression of sigmaC resulted in the upregulation of p53, p53 serine-46 phosphorylation, p53-driven reporter activity and accumulation of bax.	Serine	67-73	P53	Homo sapiens	63-66
16946128-8	2006	A549-rho degrees cells that are incapable of mitochondrial reactive oxygen species production were protected against PM-induced DeltaPsi m, p53 expression, and apoptosis.	Reactive Oxygen Species	59-82	P53	Homo sapiens	140-143
17341630-6	2006	During first hours after the beginning of cultivation with VA in both studied concentrations (2 and 4 mM) an increase of p53 and its phosphorylation on serine 392 is detected, as well as a phosphorylation of Mdm2 on serine 166.	Serine	152-158	P53	Homo sapiens	121-124
17051326-8	2006	Over-expression of sigmaC resulted in the upregulation of p53, p53 serine-46 phosphorylation, p53-driven reporter activity and accumulation of bax.	Serine	67-73	P53	Homo sapiens	63-66
17049505-6	2006	l-Lysine up-regulated p53, p21, and Bax protein levels and a down-regulation of Bcl-2alpha in all the cell lines tested.	Lysine	0-8	P53	Homo sapiens	22-25
17088865-7	2006	Lovastatin attenuated the doxorubicin-induced increase in p53 as well as activation of checkpoint kinase (Chk-1) and stress-activated protein kinase/c-Jun-N-terminal kinase (SAPK/JNK).	Doxorubicin	26-37	P53	Homo sapiens	58-61
16895524-5	2006	This decrease was also observed when HepG2 cells were exposed to UV irradiation or doxorubicin, both of which increased endogenous p53 protein levels.	Doxorubicin	83-94	P53	Homo sapiens	131-134
16895524-7	2006	Chromatin immunoprecipitation also showed that endogenous p53 bound the HNF4alpha P1 promoter in vivo after doxorubicin treatment.	Doxorubicin	108-119	P53	Homo sapiens	58-61
16528528-1	2006	PURPOSE: Ferredoxin reductase (FDXR) is a putative contributor to p53-mediated apoptosis from 5-fluorouracil (5-FU) through the generation of oxidative stress in the mitochondria.	Fluorouracil	94-108	P53	Homo sapiens	66-69
16528528-1	2006	PURPOSE: Ferredoxin reductase (FDXR) is a putative contributor to p53-mediated apoptosis from 5-fluorouracil (5-FU) through the generation of oxidative stress in the mitochondria.	Fluorouracil	110-114	P53	Homo sapiens	66-69
16528528-10	2006	FDXR gene expression, which is regulated at least in part by p53, is associated with both response and survival when metastatic colorectal cancer is treated with 5-FU plus LV.	Fluorouracil	162-166	P53	Homo sapiens	61-64
16528528-11	2006	In addition, analysis of p53 mutation combined with FDXR gene expression might be useful in estimating the outcome in 5-FU-treated patients.	Fluorouracil	118-122	P53	Homo sapiens	25-28
17257079-2	2006	Growth modification caused by FSC iron involves a diminished expression of Bcl-2 and an overexpression of p53 proto-oncogene, accompanied by an increased incidence of apoptosis.	Iron	34-38	P53	Homo sapiens	106-109
17145881-11	2006	Our results suggest that this MAPK-dependent ROS/p53 feedback loop is a point of vulnerability of melanoma cells that can be exploited for rational drug design.	Reactive Oxygen Species	45-48	P53	Homo sapiens	49-52
16971506-10	2006	p53 phosphorylation was induced by serum withdrawal and other chemotherapeutic reagents such as actinomycin D, doxorubicin, and etoposide.	Doxorubicin	111-122	P53	Homo sapiens	0-3
17088997-4	2006	Resveratrol decreased the expression of BCL6 protein, concomitant with the increased expression of several BCL6 regulated gene products, including p27, p53 and CD69.	Resveratrol	0-11	P53	Homo sapiens	152-155
17168673-6	2006	In human breast and prostate cancer cells with different tumor suppressor p53 status, synthetic bile acid-induced growth inhibition and apoptosis were associated with up-regulation of Bax and p21(WAF1/CIP1) via a p53-independent pathway.	Bile Acids and Salts	96-105	P53	Homo sapiens	74-77
17168673-6	2006	In human breast and prostate cancer cells with different tumor suppressor p53 status, synthetic bile acid-induced growth inhibition and apoptosis were associated with up-regulation of Bax and p21(WAF1/CIP1) via a p53-independent pathway.	Bile Acids and Salts	96-105	P53	Homo sapiens	213-216
16971507-6	2006	Conversely, p53 phosphorylation on Ser-15 did not play any role in apoptosis.	Serine	35-38	P53	Homo sapiens	12-15
16767497-10	2006	Folate contribution of intestinal bacteria was found to influence p53 protein levels.	Folic Acid	0-6	P53	Homo sapiens	66-69
16751801-5	2006	Expression of green fluorescent protein (GFP)-P1 in different mammalian cell lines activates p53 phosphorylation on serine 15, induces an upregulation of p21 and the release of the Cyt-C and apoptosis-inducing factor proapoptotic proteins triggering caspase-dependent and caspase-independent apoptosis.	Serine	116-122	P53	Homo sapiens	93-96
17172431-9	2006	Reexpression of wild-type p53 in PC3 cells resulted in increases in superoxide production, apoptosis, and caspase-9 activity and a decrease in mitochondrial membrane potential following cotreatment with SeMet and METase.	Superoxides	68-78	P53	Homo sapiens	26-29
17089054-6	2006	High-dose zeranol induced the formation of a sub-G1 fraction and the up-regulation of the apoptosis stimulator p53, suggesting the induction of apoptosis.	Zeranol	10-17	P53	Homo sapiens	111-114
16931776-10	2006	In vitro exposure of hMSCs to cisplatin, vincristine, and etoposide resulted in an increased p53 expression, independent of apoptosis induction.	Cisplatin	30-39	P53	Homo sapiens	93-96
16872707-2	2006	It plays a crucial role in p53-dependent cellular response to DNA damage and oxidative stress by providing deoxyribonucleotides (dNTPs) to the DNA repair machinery and by scavenging reactive oxygen species (ROS).	Reactive Oxygen Species	182-205	P53	Homo sapiens	27-30
16872707-2	2006	It plays a crucial role in p53-dependent cellular response to DNA damage and oxidative stress by providing deoxyribonucleotides (dNTPs) to the DNA repair machinery and by scavenging reactive oxygen species (ROS).	Reactive Oxygen Species	207-210	P53	Homo sapiens	27-30
17110336-3	2006	E4F1 stimulates oligo-ubiquitylation in the hinge region of p53 on lysine residues distinct from those targeted by Hdm2 and previously described to be acetylated by the acetyltransferase PCAF.	Lysine	67-73	P53	Homo sapiens	60-63
17108971-2	2006	The tumour suppressor p53 (refs 4-7) is one of only a few non-histone proteins known to be regulated by lysine methylation.	Lysine	104-110	P53	Homo sapiens	22-25
17108971-3	2006	Here we report a lysine methyltransferase, Smyd2, that methylates a previously unidentified site, Lys 370, in p53.	Lysine	98-101	P53	Homo sapiens	110-113
17108971-4	2006	This methylation site, in contrast to the known site Lys 372, is repressing to p53-mediated transcriptional regulation.	Lysine	53-56	P53	Homo sapiens	79-82
17108971-8	2006	In addition, we show that the inhibitory effect of Lys 372 methylation on Lys 370 methylation is caused, in part, by blocking the interaction between p53 and Smyd2.	Lysine	51-54	P53	Homo sapiens	150-153
17108971-8	2006	In addition, we show that the inhibitory effect of Lys 372 methylation on Lys 370 methylation is caused, in part, by blocking the interaction between p53 and Smyd2.	Lysine	74-77	P53	Homo sapiens	150-153
17108971-9	2006	Thus, similar to histones, p53 is subject to both activating and repressing lysine methylation.	Lysine	76-82	P53	Homo sapiens	27-30
17123452-6	2006	When evaluated by several pathway and biological process analysis programs, these proteins are demonstrated to be involved with a high degree of confidence (p values &lt; 2.0 E-05) in glycolysis, propanoate metabolism, pyruvate metabolism, urea cycle and arginine/proline metabolism, as well as in the non-metabolic p53 and FAS pathways.	Urea	240-244	P53	Homo sapiens	316-319
17123452-6	2006	When evaluated by several pathway and biological process analysis programs, these proteins are demonstrated to be involved with a high degree of confidence (p values &lt; 2.0 E-05) in glycolysis, propanoate metabolism, pyruvate metabolism, urea cycle and arginine/proline metabolism, as well as in the non-metabolic p53 and FAS pathways.	Arginine	255-263	P53	Homo sapiens	316-319
16984892-4	2006	In this study, we found that c-Jun NH2-terminal kinase 1 activation triggered CtBP phosphorylation on Ser-422 and subsequent degradation, inducing p53-independent apoptosis in human lung cancer cells.	Serine	102-105	P53	Homo sapiens	147-150
17012228-9	2006	Site-directed mutagenesis studies showed that Lys-386 of p53, the SUMO-1 modification site, is also the modification site for SUMO-2/3.	Lysine	46-49	P53	Homo sapiens	57-60
17012228-10	2006	In addition, H2O2 treatment of untransfected cells caused an increase in p53 sumoylation by SUMO-2/3, whereas that by SUMO-1 remained unchanged.	Hydrogen Peroxide	13-17	P53	Homo sapiens	73-76
17049121-0	2006	Antisense oligonucleotide targeting p53 increased apoptosis of MCF-7 cells induced by ionizing radiation.	Oligonucleotides	10-25	P53	Homo sapiens	36-39
17108111-0	2006	Mutant p53 protects cells from 12-O-tetradecanoylphorbol-13-acetate-induced death by attenuating activating transcription factor 3 induction.	Tetradecanoylphorbol Acetate	31-67	P53	Homo sapiens	7-10
17108111-3	2006	In this study, we explore how the status of p53 affects the immediate response gene activating transcription factor 3 (ATF3) in the 12-O-tetradecanoylphorbol-13-acetate (TPA)-protein kinase C (PKC) pathway.	Tetradecanoylphorbol Acetate	132-168	P53	Homo sapiens	44-47
17108111-3	2006	In this study, we explore how the status of p53 affects the immediate response gene activating transcription factor 3 (ATF3) in the 12-O-tetradecanoylphorbol-13-acetate (TPA)-protein kinase C (PKC) pathway.	Tetradecanoylphorbol Acetate	170-173	P53	Homo sapiens	44-47
17108111-4	2006	We show that high doses of TPA induce ATF3 in a WT p53-independent manner correlating with PKCs depletion and cell death.	Tetradecanoylphorbol Acetate	27-30	P53	Homo sapiens	51-54
17108111-5	2006	We show that cells harboring mutant p53 have attenuated ATF3 induction and are less sensitive to TPA-induced death compared with their p53-null counterparts.	Tetradecanoylphorbol Acetate	97-100	P53	Homo sapiens	36-39
16894566-8	2006	Reintroduction of p53 decreases Akt1 and Akt2 activation and restores CDDP sensitivity in p53-null but not p53-null-Aurora-A cells.	Cisplatin	70-74	P53	Homo sapiens	18-21
16894566-8	2006	Reintroduction of p53 decreases Akt1 and Akt2 activation and restores CDDP sensitivity in p53-null but not p53-null-Aurora-A cells.	Cisplatin	70-74	P53	Homo sapiens	90-93
16894566-8	2006	Reintroduction of p53 decreases Akt1 and Akt2 activation and restores CDDP sensitivity in p53-null but not p53-null-Aurora-A cells.	Cisplatin	70-74	P53	Homo sapiens	90-93
16963839-3	2006	We examined whether p53 activated by the DNA-damaging drug 5-fluorouracil (5-FU) also induces CES-2 expression.	Fluorouracil	59-73	P53	Homo sapiens	20-23
17201158-6	2006	Curcumin also promoted the expression of Bax, cytochrome C, p53 and p21 but inhibited the expression of Bcl-2.	Curcumin	0-8	P53	Homo sapiens	60-63
17010455-12	2006	For the S100B-p53 interaction, it was found that phosphorylation of specific serine and/or threonine residues reduces the affinity of the S100B-p53 interaction by as much as an order of magnitude, and is important for protecting p53 from S100B-dependent down-regulation, a scenario that is similar to what is found for the Hdm2-p53 complex.	Serine	77-83	P53	Homo sapiens	144-147
17010455-12	2006	For the S100B-p53 interaction, it was found that phosphorylation of specific serine and/or threonine residues reduces the affinity of the S100B-p53 interaction by as much as an order of magnitude, and is important for protecting p53 from S100B-dependent down-regulation, a scenario that is similar to what is found for the Hdm2-p53 complex.	Threonine	91-100	P53	Homo sapiens	14-17
17010455-12	2006	For the S100B-p53 interaction, it was found that phosphorylation of specific serine and/or threonine residues reduces the affinity of the S100B-p53 interaction by as much as an order of magnitude, and is important for protecting p53 from S100B-dependent down-regulation, a scenario that is similar to what is found for the Hdm2-p53 complex.	Threonine	91-100	P53	Homo sapiens	144-147
17010455-12	2006	For the S100B-p53 interaction, it was found that phosphorylation of specific serine and/or threonine residues reduces the affinity of the S100B-p53 interaction by as much as an order of magnitude, and is important for protecting p53 from S100B-dependent down-regulation, a scenario that is similar to what is found for the Hdm2-p53 complex.	Threonine	91-100	P53	Homo sapiens	144-147
17010455-12	2006	For the S100B-p53 interaction, it was found that phosphorylation of specific serine and/or threonine residues reduces the affinity of the S100B-p53 interaction by as much as an order of magnitude, and is important for protecting p53 from S100B-dependent down-regulation, a scenario that is similar to what is found for the Hdm2-p53 complex.	Threonine	91-100	P53	Homo sapiens	144-147
16777994-5	2006	Pifithrin-alpha, a p53 inhibitor, reversed silibinin-induced caspase activation including caspase 2; however, caspase 2 inhibitor also reversed p53 phosphorylation suggesting a bidirectional regulation between them.	Silybin	43-52	P53	Homo sapiens	19-22
16777994-6	2006	Further, silibinin caused a rapid translocation of p53 and Bid into mitochondria leading to increased permeabilization of mitochondrial membrane and cytochrome c release into the cytosol.	Silybin	9-18	P53	Homo sapiens	51-54
16777994-9	2006	Together, these results suggested the novel mechanisms for apoptosis induction by silibinin involving p53-caspase 2 activation and caspase-mediated cleavage of Cip1/p21.	Silybin	82-91	P53	Homo sapiens	102-105
17010455-12	2006	For the S100B-p53 interaction, it was found that phosphorylation of specific serine and/or threonine residues reduces the affinity of the S100B-p53 interaction by as much as an order of magnitude, and is important for protecting p53 from S100B-dependent down-regulation, a scenario that is similar to what is found for the Hdm2-p53 complex.	Serine	77-83	P53	Homo sapiens	14-17
17010455-12	2006	For the S100B-p53 interaction, it was found that phosphorylation of specific serine and/or threonine residues reduces the affinity of the S100B-p53 interaction by as much as an order of magnitude, and is important for protecting p53 from S100B-dependent down-regulation, a scenario that is similar to what is found for the Hdm2-p53 complex.	Serine	77-83	P53	Homo sapiens	144-147
17010455-12	2006	For the S100B-p53 interaction, it was found that phosphorylation of specific serine and/or threonine residues reduces the affinity of the S100B-p53 interaction by as much as an order of magnitude, and is important for protecting p53 from S100B-dependent down-regulation, a scenario that is similar to what is found for the Hdm2-p53 complex.	Serine	77-83	P53	Homo sapiens	144-147
16774943-9	2006	In addition, we found that BPDE increased p53 activity and apoptosis in MCF-10A; however, transient transfection of constitutively active Akt attenuated both BPDE-dependent apoptosis and p53 activity.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	27-31	P53	Homo sapiens	42-45
16777994-0	2006	Silibinin activates p53-caspase 2 pathway and causes caspase-mediated cleavage of Cip1/p21 in apoptosis induction in bladder transitional-cell papilloma RT4 cells: evidence for a regulatory loop between p53 and caspase 2.	Silybin	0-9	P53	Homo sapiens	20-23
16777994-0	2006	Silibinin activates p53-caspase 2 pathway and causes caspase-mediated cleavage of Cip1/p21 in apoptosis induction in bladder transitional-cell papilloma RT4 cells: evidence for a regulatory loop between p53 and caspase 2.	Silybin	0-9	P53	Homo sapiens	203-206
16777994-2	2006	Here, we studied the mechanisms involved in silibinin-induced apoptosis of RT4 cells having intact p53.	Silybin	44-53	P53	Homo sapiens	99-102
16777994-3	2006	Silibinin increased p53 protein level together with its increased phosphorylation at serine 15, activated caspase cascade and caused Bid cleavage for apoptosis.	Silybin	0-9	P53	Homo sapiens	20-23
16777994-4	2006	Silibinin-caused p53 activation was mediated via ATM-Chk2 pathway, which in turn induced caspase 2-mediated apoptosis.	Silybin	0-9	P53	Homo sapiens	17-20
17079468-5	2006	When U87MG (wild-type p53) and MCF-7 cells (wild-type p53) were exposed to adverse growth conditions of serum starvation or treated with the chemotherapeutic agent cisplatin, cells underwent apoptosis and cell cycle arrest accompanied by increase in p53 and HIC-1 transcript levels.	Cisplatin	164-173	P53	Homo sapiens	22-25
17079468-5	2006	When U87MG (wild-type p53) and MCF-7 cells (wild-type p53) were exposed to adverse growth conditions of serum starvation or treated with the chemotherapeutic agent cisplatin, cells underwent apoptosis and cell cycle arrest accompanied by increase in p53 and HIC-1 transcript levels.	Cisplatin	164-173	P53	Homo sapiens	54-57
17079468-5	2006	When U87MG (wild-type p53) and MCF-7 cells (wild-type p53) were exposed to adverse growth conditions of serum starvation or treated with the chemotherapeutic agent cisplatin, cells underwent apoptosis and cell cycle arrest accompanied by increase in p53 and HIC-1 transcript levels.	Cisplatin	164-173	P53	Homo sapiens	54-57
16990991-6	2006	Finally, we showed that treatment of the cells with 17beta-estradiol (10(-9) M) resulted in a marked increase in p53 level both in the resistant cells undergoing apoptosis and in the parent MCF-7 cells insensitive to apoptotic estrogen action.	Estradiol	52-68	P53	Homo sapiens	113-116
16963839-3	2006	We examined whether p53 activated by the DNA-damaging drug 5-fluorouracil (5-FU) also induces CES-2 expression.	Fluorouracil	75-79	P53	Homo sapiens	20-23
16963839-4	2006	Our experiments showed that 5-FU induced CES-2 expression in two colon carcinoma cell lines that express wild-type p53 (HCT116 p53(+/+) and RKO) but not in five lines that are p53-null (HCT116 p53(-/- )) or express mutated p53 (HT29, KM12C, KM12SM, and KM12L4A).	Fluorouracil	28-32	P53	Homo sapiens	115-118
16963839-4	2006	Our experiments showed that 5-FU induced CES-2 expression in two colon carcinoma cell lines that express wild-type p53 (HCT116 p53(+/+) and RKO) but not in five lines that are p53-null (HCT116 p53(-/- )) or express mutated p53 (HT29, KM12C, KM12SM, and KM12L4A).	Fluorouracil	28-32	P53	Homo sapiens	127-130
17207318-0	2006	5-fluorouracil mediates apoptosis and G1/S arrest in laryngeal squamous cell carcinoma via a p53-independent pathway.	Fluorouracil	0-14	P53	Homo sapiens	93-96
16963839-4	2006	Our experiments showed that 5-FU induced CES-2 expression in two colon carcinoma cell lines that express wild-type p53 (HCT116 p53(+/+) and RKO) but not in five lines that are p53-null (HCT116 p53(-/- )) or express mutated p53 (HT29, KM12C, KM12SM, and KM12L4A).	Fluorouracil	28-32	P53	Homo sapiens	127-130
17207318-2	2006	5-FU can induce cell cycle arrest or apoptosis in various cancers via either a p53-dependent or a p53-independent pathway; however, its pathway of action in laryngeal carcinoma is unknown.	Fluorouracil	0-4	P53	Homo sapiens	79-82
17207318-2	2006	5-FU can induce cell cycle arrest or apoptosis in various cancers via either a p53-dependent or a p53-independent pathway; however, its pathway of action in laryngeal carcinoma is unknown.	Fluorouracil	0-4	P53	Homo sapiens	98-101
16963839-4	2006	Our experiments showed that 5-FU induced CES-2 expression in two colon carcinoma cell lines that express wild-type p53 (HCT116 p53(+/+) and RKO) but not in five lines that are p53-null (HCT116 p53(-/- )) or express mutated p53 (HT29, KM12C, KM12SM, and KM12L4A).	Fluorouracil	28-32	P53	Homo sapiens	127-130
17207318-3	2006	In this study, we aim to investigate the role that p53 plays in the cytotoxic effect of 5-FU on laryngeal squamous carcinoma cells.	Fluorouracil	88-92	P53	Homo sapiens	51-54
16963839-4	2006	Our experiments showed that 5-FU induced CES-2 expression in two colon carcinoma cell lines that express wild-type p53 (HCT116 p53(+/+) and RKO) but not in five lines that are p53-null (HCT116 p53(-/- )) or express mutated p53 (HT29, KM12C, KM12SM, and KM12L4A).	Fluorouracil	28-32	P53	Homo sapiens	127-130
17207318-8	2006	RESULTS: 5-FU induces apoptosis in both UMSCC12 and UMSCC11A cells in a dose- and time-dependent manner, suggesting that the pathway was p53-independent.	Fluorouracil	9-13	P53	Homo sapiens	137-140
17207318-12	2006	In order to gain an insight into the role p53 plays in response to 5-FU treatment in laryngeal carcinoma, we further transfected either a wildtype p53 plasmid or an empty pcDNA3.1 vector into UMSCC12 cells.	Fluorouracil	67-71	P53	Homo sapiens	42-45
16963839-6	2006	A reporter gene assay showed that the luciferase construct with the p53-binding element responded to 5-FU treatment, whereas the reporter construct without the binding element did not.	Fluorouracil	101-105	P53	Homo sapiens	68-71
17207318-13	2006	We found that 5-FU increased pRb and p21WAF1/CIP1 expression in both p53-transfected and vector-transfected cells without the significant accumulation of p53.	Fluorouracil	14-18	P53	Homo sapiens	69-72
17207318-14	2006	DISCUSSION: Our results suggest that 5-FU mediates apoptosis and G1/S cell cycle phase arrest in laryngeal carcinoma via a p53-independent but p21WAF1/CIP1-dependent or p21WAF1/CIP1-Rb-dependent pathway.	Fluorouracil	37-41	P53	Homo sapiens	123-126
16963839-7	2006	Chromatin immunoprecipitation assay confirmed that p53 bound the CES-2 fragment containing the p53-binding element after 5-FU treatment, whereas p21 binding to p53 was present with or without chemotherapy.	Fluorouracil	121-125	P53	Homo sapiens	51-54
16963839-7	2006	Chromatin immunoprecipitation assay confirmed that p53 bound the CES-2 fragment containing the p53-binding element after 5-FU treatment, whereas p21 binding to p53 was present with or without chemotherapy.	Fluorouracil	121-125	P53	Homo sapiens	95-98
16963839-7	2006	Chromatin immunoprecipitation assay confirmed that p53 bound the CES-2 fragment containing the p53-binding element after 5-FU treatment, whereas p21 binding to p53 was present with or without chemotherapy.	Fluorouracil	121-125	P53	Homo sapiens	95-98
17177838-8	2006	In conclusion, based on the findings of this study, it is suggested that p53 Arg homozygosity could act as a potential risk factor for the tumorigenesis of the cervix.	Arginine	77-80	P53	Homo sapiens	73-76
17085670-0	2006	Schedule-dependent synergy between the heat shock protein 90 inhibitor 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin and doxorubicin restores apoptosis to p53-mutant lymphoma cell lines.	Doxorubicin	129-140	P53	Homo sapiens	163-166
17053786-3	2006	Using ATP-stabilised p53, we have employed cryoelectron microscopy and single particle analysis to solve the first three-dimensional structure of the full-length p53 tetramer (resolution 13.7 A).	Adenosine Triphosphate	6-9	P53	Homo sapiens	21-24
17053786-3	2006	Using ATP-stabilised p53, we have employed cryoelectron microscopy and single particle analysis to solve the first three-dimensional structure of the full-length p53 tetramer (resolution 13.7 A).	Adenosine Triphosphate	6-9	P53	Homo sapiens	162-165
16690105-7	2006	In the gemcitabine plus cisplatin treatment arm compared to either alone, there was also downregulation of MSH2, p53, and ERCC1 expression.	Cisplatin	24-33	P53	Homo sapiens	113-116
17177838-10	2006	p53 Arg homozygosity and HR-HPV E6 positive simultaneously can predict the fate of cervical lesions.	Arginine	4-7	P53	Homo sapiens	0-3
16882877-0	2006	Busulfan selectively induces cellular senescence but not apoptosis in WI38 fibroblasts via a p53-independent but extracellular signal-regulated kinase-p38 mitogen-activated protein kinase-dependent mechanism.	Busulfan	0-8	P53	Homo sapiens	93-96
17056795-0	2006	Global DNA and p53 region-specific hypomethylation in human colonic cells is induced by folate depletion and reversed by folate supplementation.	Folic Acid	88-94	P53	Homo sapiens	15-18
17056795-0	2006	Global DNA and p53 region-specific hypomethylation in human colonic cells is induced by folate depletion and reversed by folate supplementation.	Folic Acid	121-127	P53	Homo sapiens	15-18
17056795-8	2006	These results confirm that decreased folate levels are capable of inducing DNA hypomethylation in colon cells and particularly in the region of the p53 gene, suggesting that a more optimal folate status in vivo may normalize any DNA hypomethylation, offering potential protective effects against carcinogenesis.	Folic Acid	37-43	P53	Homo sapiens	148-151
17056795-8	2006	These results confirm that decreased folate levels are capable of inducing DNA hypomethylation in colon cells and particularly in the region of the p53 gene, suggesting that a more optimal folate status in vivo may normalize any DNA hypomethylation, offering potential protective effects against carcinogenesis.	Folic Acid	189-195	P53	Homo sapiens	148-151
17121917-8	2006	We also show that in a p53-deficient cell line (H1299), pretreatment with atorvastatin sensitized cells to etoposide, doxorubicin, and 5-fluorouracil and increased the level of apoptosis.	Atorvastatin	74-86	P53	Homo sapiens	23-26
16940182-5	2006	Compared to the wild-type form, Chk2 with alanine substitutions at S19, S33, and S35 (Chk2(S3A)) showed impaired dimerization, defective auto- and trans-phosphorylation activities, and reduced ability to promote degradation of Hdmx, a phosphorylation target of Chk2 and regulator of p53 activity.	Alanine	42-49	P53	Homo sapiens	283-286
17014693-8	2006	The results demonstrate the anti-proliferative and apoptosis-inducing effects of melatonin; these changes were associated with cell cycle arrest, upregulation of P53 and Bax and downregulation of Bcl-2.	Melatonin	81-90	P53	Homo sapiens	162-165
17014693-10	2006	P53 and Bax/Bcl-2 expression changes may be involved in these actions of melatonin.	Melatonin	73-82	P53	Homo sapiens	0-3
16957011-10	2006	Expression of p53 and p21WAF/CIP1 increased in cells incubated with Fe-S, but not with Fe-D. Bcl-2 expression was significantly down-regulated in cells incubated with Fe-S in comparison with Fe-D, while Bax expression was not modified by the iron compounds.	Iron	167-171	P53	Homo sapiens	14-17
16957011-10	2006	Expression of p53 and p21WAF/CIP1 increased in cells incubated with Fe-S, but not with Fe-D. Bcl-2 expression was significantly down-regulated in cells incubated with Fe-S in comparison with Fe-D, while Bax expression was not modified by the iron compounds.	Iron	68-72	P53	Homo sapiens	14-17
16957011-10	2006	Expression of p53 and p21WAF/CIP1 increased in cells incubated with Fe-S, but not with Fe-D. Bcl-2 expression was significantly down-regulated in cells incubated with Fe-S in comparison with Fe-D, while Bax expression was not modified by the iron compounds.	Iron	242-246	P53	Homo sapiens	14-17
17029827-3	2006	The p53 protein activation appeared to have been a downstream response to the benzo[a]pyrene-induced DNA damage, suggesting p53 plays important roles in the defense against benzo[a]pyrene-induced genotoxicity.	pyrene	86-92	P53	Homo sapiens	4-7
17236590-4	2006	RESULTS: Under the condition of normal concentration oxygen, P53 was highly expressed in the placenta of pregnant women with ICP (P &lt; 0.01), however the HIF-1alpha expression was not up to higher than in normal control.	Oxygen	53-59	P53	Homo sapiens	61-64
17236590-5	2006	Under the condition of lower concentration oxygen (2% O2), the HIF-1alpha and P53 expressions were detected from the placental villous tissues cultured for 4 h of normal control and patient with ICP, and with HIF-1alpha and P53 proteins increased in the placenta of pregnant women with ICP (P &lt; 0.05 and P &lt; 0.001 respectively).	Oxygen	43-49	P53	Homo sapiens	78-81
17236590-5	2006	Under the condition of lower concentration oxygen (2% O2), the HIF-1alpha and P53 expressions were detected from the placental villous tissues cultured for 4 h of normal control and patient with ICP, and with HIF-1alpha and P53 proteins increased in the placenta of pregnant women with ICP (P &lt; 0.05 and P &lt; 0.001 respectively).	Oxygen	54-56	P53	Homo sapiens	78-81
17029827-3	2006	The p53 protein activation appeared to have been a downstream response to the benzo[a]pyrene-induced DNA damage, suggesting p53 plays important roles in the defense against benzo[a]pyrene-induced genotoxicity.	pyrene	86-92	P53	Homo sapiens	124-127
17029827-3	2006	The p53 protein activation appeared to have been a downstream response to the benzo[a]pyrene-induced DNA damage, suggesting p53 plays important roles in the defense against benzo[a]pyrene-induced genotoxicity.	pyrene	181-187	P53	Homo sapiens	4-7
17029827-3	2006	The p53 protein activation appeared to have been a downstream response to the benzo[a]pyrene-induced DNA damage, suggesting p53 plays important roles in the defense against benzo[a]pyrene-induced genotoxicity.	pyrene	181-187	P53	Homo sapiens	124-127
17047080-1	2006	Induction of mRNA for BIK proapoptotic protein by doxorubicin or gamma-irradiation requires the DNA-binding transcription factor activity of p53.	Doxorubicin	50-61	P53	Homo sapiens	141-144
16721787-3	2006	Among 856 colorectal adenoma cases and 1,184 controls, we observed a modest association with p53 Arg72Pro genotype (multivariate odds ratio (OR) = 1.25, 95% confidence interval (CI) = 1.04-1.50 for Arg/Pro and Pro/Pro vs. Arg/Arg).	Arginine	97-100	P53	Homo sapiens	93-96
16721787-3	2006	Among 856 colorectal adenoma cases and 1,184 controls, we observed a modest association with p53 Arg72Pro genotype (multivariate odds ratio (OR) = 1.25, 95% confidence interval (CI) = 1.04-1.50 for Arg/Pro and Pro/Pro vs. Arg/Arg).	Arginine	198-201	P53	Homo sapiens	93-96
16721787-3	2006	Among 856 colorectal adenoma cases and 1,184 controls, we observed a modest association with p53 Arg72Pro genotype (multivariate odds ratio (OR) = 1.25, 95% confidence interval (CI) = 1.04-1.50 for Arg/Pro and Pro/Pro vs. Arg/Arg).	Arginine	198-201	P53	Homo sapiens	93-96
17047080-6	2006	Whereas both fulvestrant and doxorubicin induced BIK mRNA, only doxorubicin enhanced the DNA-binding activity of p53 and induced PUMA mRNA.	Doxorubicin	64-75	P53	Homo sapiens	113-116
16930632-5	2006	This prompted us to study the association of three p53 polymorphisms with arsenic induced keratosis in a population exposed to arsenic through drinking water.	Water	152-157	P53	Homo sapiens	51-54
16997395-2	2006	Phosphorylation of ATM at serine 1981 (ATMpSer1981) by DNA damage activates ATM, which subsequently phosphorylates H2AX Ser139 (gammaH2AX), Chk2 Thr68 (Chk2pThr68), and p53 Ser15 (p53pSer15).	Serine	26-32	P53	Homo sapiens	169-172
16652144-2	2006	Moreover, p53 activation itself contributes to ROS accumulation.	Reactive Oxygen Species	47-50	P53	Homo sapiens	10-13
16652144-3	2006	Here we show that treatment of p53-null cancer cells with sublethal concentrations of ROS triggered an arrest with some morphological similarities to cellular senescence.	Reactive Oxygen Species	86-89	P53	Homo sapiens	31-34
16826413-9	2006	In addition, to study whether wild type p53 was expressed, induction of p53 by cis-platinum was assessed by Western blot.	Cisplatin	79-91	P53	Homo sapiens	72-75
16826413-16	2006	In POSE and NPOSE, p53 was induced by cis-platinum to a similar extent.	Cisplatin	38-50	P53	Homo sapiens	19-22
16942782-6	2006	Capsaicin induced G0-G1 phase arrest underwent the promotion of p53 and p21, which is an inhibitor of Cdk2 and cyclin E complex before leading to the inhibitions of both compounds.	Capsaicin	0-9	P53	Homo sapiens	64-67
17002294-0	2006	Determinants of specificity of MDM2 for the activation domains of p53 and p65: proline27 disrupts the MDM2-binding motif of p53.	proline27	79-88	P53	Homo sapiens	66-69
17002294-0	2006	Determinants of specificity of MDM2 for the activation domains of p53 and p65: proline27 disrupts the MDM2-binding motif of p53.	proline27	79-88	P53	Homo sapiens	124-127
17002294-8	2006	Replacement of the highly conserved residue Pro27 of p53 with Ser from p65 resulted in a 2.3 kcal mol(-1) improvement in binding to MDM2, generating a ligand (p53-P27S) (Kd = 4.7 nM) that exhibits the highest MDM2 affinity observed for a genetically encodable ligand.	Serine	62-65	P53	Homo sapiens	53-56
17002294-8	2006	Replacement of the highly conserved residue Pro27 of p53 with Ser from p65 resulted in a 2.3 kcal mol(-1) improvement in binding to MDM2, generating a ligand (p53-P27S) (Kd = 4.7 nM) that exhibits the highest MDM2 affinity observed for a genetically encodable ligand.	Serine	62-65	P53	Homo sapiens	159-162
17018618-0	2006	Distinct effects of annexin A7 and p53 on arachidonate lipoxygenation in prostate cancer cells involve 5-lipoxygenase transcription.	Arachidonic Acid	42-54	P53	Homo sapiens	35-38
16840547-11	2006	PD98059 inhibited this delayed activation of ERK and effects of S179D PRL on all measures except p53 levels or activity of the Bax promoter.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	0-7	P53	Homo sapiens	97-100
17015431-5	2006	Nocodazole, a microtubule poison that provokes centrosome/mitotic apparatus dysfunction, induces Lats2 translocation from centrosomes to the nucleus and p53 accumulation.	Nocodazole	0-10	P53	Homo sapiens	153-156
16981908-0	2006	DNA modification with cisplatin affects sequence-specific DNA binding of p53 and p73 proteins in a target site-dependent manner.	Cisplatin	22-31	P53	Homo sapiens	73-76
17015431-7	2006	Abrogation of Lats2 promotes accumulation of polyploid cells upon exposure to nocodazole, which can be prevented by direct activation of p53.	Nocodazole	78-88	P53	Homo sapiens	137-140
16981908-3	2006	It has been demonstrated previously that DNA modification with the antitumor drug cisplatin inhibits p53 binding to a synthetic p53 DNA-binding site.	Cisplatin	82-91	P53	Homo sapiens	101-104
16835015-0	2006	Further studies with a cell immortalization assay to investigate the mutation signature of aristolochic acid in human p53 sequences.	aristolochic acid I	91-108	P53	Homo sapiens	118-121
16981908-3	2006	It has been demonstrated previously that DNA modification with the antitumor drug cisplatin inhibits p53 binding to a synthetic p53 DNA-binding site.	Cisplatin	82-91	P53	Homo sapiens	128-131
16981908-4	2006	Here we demonstrate that the effects of global DNA modification with cisplatin on binding of the p53 or p73 proteins to various p53 DNA-binding sites differed significantly, depending on the nucleotide sequence of the given target site.	Cisplatin	69-78	P53	Homo sapiens	97-100
16981908-4	2006	Here we demonstrate that the effects of global DNA modification with cisplatin on binding of the p53 or p73 proteins to various p53 DNA-binding sites differed significantly, depending on the nucleotide sequence of the given target site.	Cisplatin	69-78	P53	Homo sapiens	128-131
16981908-7	2006	Distinct effects of cisplatin DNA modification on the recognition of different response elements by the p53 family proteins may have impacts on regulation pathways in cisplatin-treated cells.	Cisplatin	20-29	P53	Homo sapiens	104-107
16981908-7	2006	Distinct effects of cisplatin DNA modification on the recognition of different response elements by the p53 family proteins may have impacts on regulation pathways in cisplatin-treated cells.	Cisplatin	167-176	P53	Homo sapiens	104-107
17062352-2	2006	It was found that the p53 gene condon 282 mutation (Arg/Leu) may destabilize the H2 helix and DNA binding in the major groove by compromising the contacts of p53 protein with the beta-hairpin of DNA binding surface.	Arginine	52-55	P53	Homo sapiens	22-25
17062352-2	2006	It was found that the p53 gene condon 282 mutation (Arg/Leu) may destabilize the H2 helix and DNA binding in the major groove by compromising the contacts of p53 protein with the beta-hairpin of DNA binding surface.	Arginine	52-55	P53	Homo sapiens	158-161
17007666-5	2006	DNA was extracted from the buccal swabs obtained from 70 women experiencing implantation failure and polymerase chain reaction amplification of p53 arginine (Arg) 72 and proline (Pro) 72 variants were performed.	Arginine	148-156	P53	Homo sapiens	144-147
16797627-5	2006	In this study, we show that AZT, cisplatin (CDDP) and docetaxel (DTX) all induce unique molecular responses in OVCAR-3 ovarian carcinoma cells carrying a mutated p53, while in A2780, ovarian carcinoma and MCF-7 breast carcinoma cells with wild type p53, all of these drugs cause similar p53 responses.	Cisplatin	33-42	P53	Homo sapiens	162-165
16797627-5	2006	In this study, we show that AZT, cisplatin (CDDP) and docetaxel (DTX) all induce unique molecular responses in OVCAR-3 ovarian carcinoma cells carrying a mutated p53, while in A2780, ovarian carcinoma and MCF-7 breast carcinoma cells with wild type p53, all of these drugs cause similar p53 responses.	Cisplatin	33-42	P53	Homo sapiens	249-252
16797627-5	2006	In this study, we show that AZT, cisplatin (CDDP) and docetaxel (DTX) all induce unique molecular responses in OVCAR-3 ovarian carcinoma cells carrying a mutated p53, while in A2780, ovarian carcinoma and MCF-7 breast carcinoma cells with wild type p53, all of these drugs cause similar p53 responses.	Cisplatin	33-42	P53	Homo sapiens	249-252
16797627-5	2006	In this study, we show that AZT, cisplatin (CDDP) and docetaxel (DTX) all induce unique molecular responses in OVCAR-3 ovarian carcinoma cells carrying a mutated p53, while in A2780, ovarian carcinoma and MCF-7 breast carcinoma cells with wild type p53, all of these drugs cause similar p53 responses.	Cisplatin	44-48	P53	Homo sapiens	162-165
16797627-5	2006	In this study, we show that AZT, cisplatin (CDDP) and docetaxel (DTX) all induce unique molecular responses in OVCAR-3 ovarian carcinoma cells carrying a mutated p53, while in A2780, ovarian carcinoma and MCF-7 breast carcinoma cells with wild type p53, all of these drugs cause similar p53 responses.	Cisplatin	44-48	P53	Homo sapiens	249-252
16797627-5	2006	In this study, we show that AZT, cisplatin (CDDP) and docetaxel (DTX) all induce unique molecular responses in OVCAR-3 ovarian carcinoma cells carrying a mutated p53, while in A2780, ovarian carcinoma and MCF-7 breast carcinoma cells with wild type p53, all of these drugs cause similar p53 responses.	Cisplatin	44-48	P53	Homo sapiens	249-252
16826403-9	2006	Treatment with AN-7 or doxorubicin increased p53 acetylation that was further potentiated by their combination.	Doxorubicin	23-34	P53	Homo sapiens	45-48
16826403-10	2006	CONCLUSION: The AN-7 combined with doxorubicin overcame drug resistance; at least in part by the intracellularly releasable formaldehyde that augmented formation of doxorubicin-DNA adducts and butyric acid that induced histone and p53 acetylation.	Doxorubicin	35-46	P53	Homo sapiens	231-234
16964247-2	2006	Here, we show that Ser 149 of p53 is O-GlcNAcylated and that this modification is associated with decreased phosphorylation of p53 at Thr 155, which is a site that is targeted by the COP9 signalosome, resulting in decreased p53 ubiquitination.	Serine	19-22	P53	Homo sapiens	30-33
16964247-2	2006	Here, we show that Ser 149 of p53 is O-GlcNAcylated and that this modification is associated with decreased phosphorylation of p53 at Thr 155, which is a site that is targeted by the COP9 signalosome, resulting in decreased p53 ubiquitination.	Serine	19-22	P53	Homo sapiens	127-130
16964247-2	2006	Here, we show that Ser 149 of p53 is O-GlcNAcylated and that this modification is associated with decreased phosphorylation of p53 at Thr 155, which is a site that is targeted by the COP9 signalosome, resulting in decreased p53 ubiquitination.	Serine	19-22	P53	Homo sapiens	127-130
16964247-2	2006	Here, we show that Ser 149 of p53 is O-GlcNAcylated and that this modification is associated with decreased phosphorylation of p53 at Thr 155, which is a site that is targeted by the COP9 signalosome, resulting in decreased p53 ubiquitination.	Threonine	134-137	P53	Homo sapiens	30-33
16964247-2	2006	Here, we show that Ser 149 of p53 is O-GlcNAcylated and that this modification is associated with decreased phosphorylation of p53 at Thr 155, which is a site that is targeted by the COP9 signalosome, resulting in decreased p53 ubiquitination.	Threonine	134-137	P53	Homo sapiens	127-130
16964247-2	2006	Here, we show that Ser 149 of p53 is O-GlcNAcylated and that this modification is associated with decreased phosphorylation of p53 at Thr 155, which is a site that is targeted by the COP9 signalosome, resulting in decreased p53 ubiquitination.	Threonine	134-137	P53	Homo sapiens	127-130
16964247-3	2006	Accordingly, O-GlcNAcylation at Ser 149 stabilizes p53 by blocking ubiquitin-dependent proteolysis.	Serine	32-35	P53	Homo sapiens	51-54
16964247-4	2006	Our results indicate that the dynamic interplay between O-GlcNAc and O-phosphate modifications coordinately regulate p53 stability and activity.	Phosphates	69-80	P53	Homo sapiens	117-120
16459017-0	2006	Prognostic significance of p53 mutation in suboptimally resected advanced ovarian carcinoma treated with the combination chemotherapy of paclitaxel and carboplatin.	Paclitaxel	137-147	P53	Homo sapiens	27-30
16835015-3	2006	Here we examine p53 mutations induced by aristolochic acid I (AAI)), the carcinogen probably responsible for Chinese herbal nephropathy.	aristolochic acid I	41-60	P53	Homo sapiens	16-19
16835015-6	2006	One of the mutations was identical in position (codon 139) and base change (A to T on the non-transcribed strand) to the single p53 mutation that has thus far been characterized in a urothelial tumor of a nephropathy patient with documented AAI exposure.	aristolochic acid I	241-244	P53	Homo sapiens	128-131
17007014-5	2006	Resveratrol up-regulated p53 protein in SNU-1 and AGS cells but there was a difference in response of intracellular apoptotic signals between these cell lines.	Resveratrol	0-11	P53	Homo sapiens	25-28
16829532-5	2006	Introduction of intracellular- or extracellular-generated O2- during NO generation resulted in a concomitant increase in oxidative intermediates with a decrease in steady-state NO concentrations and a proportional reduction in the levels of sGC, ERK, HIF-1alpha, and p53 regulation.	Superoxides	58-60	P53	Homo sapiens	267-270
16652156-11	2006	As suppression of caspase-2 expression in 5-FU-treated cells also affects the level of the p53 protein, possibilities of a reciprocal interaction between these proteins are discussed.	Fluorouracil	42-46	P53	Homo sapiens	91-94
20641411-8	2004	Several research studies have reported that resveratrol has the ability to induce p53-dependent apoptosis in several cancer cell lines, and that the signal transduction pathways implicated in resveratrol action includes those of extracellular-regulated kinases 1 and 2 (ERK1/2), p38 kinase, and Jun N-terminal kinase (JNK) (6, 7).	Resveratrol	44-55	P53	Homo sapiens	82-85
20641411-8	2004	Several research studies have reported that resveratrol has the ability to induce p53-dependent apoptosis in several cancer cell lines, and that the signal transduction pathways implicated in resveratrol action includes those of extracellular-regulated kinases 1 and 2 (ERK1/2), p38 kinase, and Jun N-terminal kinase (JNK) (6, 7).	Resveratrol	192-203	P53	Homo sapiens	82-85
20641411-10	2004	showed that the binding of resveratrol to integrin alphaVss3, principally to the ss3 monomer, was essential for transduction of the stilbene signal into p53-dependent apoptosis of breast cancer cells.	Resveratrol	27-38	P53	Homo sapiens	153-156
16636671-3	2006	We report here that enforced Bcl-2 expression in MCF7 cells stabilizes p53, induces phosphorylation of p53 serine 15 (p53pSer15) and inhibits MCF7 cell growth.	Serine	107-113	P53	Homo sapiens	103-106
16636671-3	2006	We report here that enforced Bcl-2 expression in MCF7 cells stabilizes p53, induces phosphorylation of p53 serine 15 (p53pSer15) and inhibits MCF7 cell growth.	Serine	107-113	P53	Homo sapiens	118-127
16829532-8	2006	H2O2 in bolus or generated from the dismutation of O2- by SOD, was cytotoxic at high concentrations and activated p53 independent of NO.	Hydrogen Peroxide	0-4	P53	Homo sapiens	114-117
16829532-8	2006	H2O2 in bolus or generated from the dismutation of O2- by SOD, was cytotoxic at high concentrations and activated p53 independent of NO.	Superoxides	2-4	P53	Homo sapiens	114-117
16798066-6	2006	o-PD and Cl-PD caused piperidine-labile and formamidopyrimidine-DNA glycosylase-sensitive lesions at cytosine and guanine residues respectively in the 5"-ACG-3" sequence, complementary to codon 273, a well-known hotspot of the human p53 tumor suppressor gene.	1,2-diaminobenzene	0-4	P53	Homo sapiens	233-236
17094395-0	2006	The p53 codon 72 arg/arg homozygous women in central Italy are at increased risk for HPV infections.	Arginine	17-20	P53	Homo sapiens	4-7
17094395-0	2006	The p53 codon 72 arg/arg homozygous women in central Italy are at increased risk for HPV infections.	Arginine	21-24	P53	Homo sapiens	4-7
17094395-1	2006	BACKGROUND: The oncoprotein E6 binds to and degrades the p53 tumor suppressor protein, with different efficacy depending on the p53 codon 72 (arg/pro) polymorphism.	Arginine	142-145	P53	Homo sapiens	57-60
16325375-3	2006	Here, we report that overexpression of CKIP-1 in SK-BR-3 breast cancer cells prevents p53 degradation induced by cycloheximide treatment through increase of p53 N-terminal Ser-15 phosphorylation level.	Serine	172-175	P53	Homo sapiens	157-160
16989090-6	2006	The specificity of this p53 DNA binding SPA was confirmed using competition by oligonucleotides either from the same gene or from mutated versions of this sequence.	Oligonucleotides	79-95	P53	Homo sapiens	24-27
16966622-7	2006	Phosphorylation of p53-serine-15, a marker for activation of p53 via genotoxic mechanisms, was absent.	Serine	23-29	P53	Homo sapiens	19-22
16951143-6	2006	In this study, we used chromatin immunoprecipitation to determine that p53 preferentially occupied the promoters of growth arrest genes p21 and GADD45 in senescent normal human diploid fibroblasts but not the promoters of other target genes that recruited p53 following doxorubicin-induced DNA damage, such as apoptosis regulators TNFRSF10b, TNFRSF6, and PUMA.	Doxorubicin	270-281	P53	Homo sapiens	71-74
16534616-5	2006	RESULTS: The apoptotic index, the extent of DNA damage and the representation of p53 were much lower in the OSCORT cell cultures if the cells were exposed to ECM after treatment with doxorubicin.	Doxorubicin	183-194	P53	Homo sapiens	81-84
16931914-4	2006	In this study we have uncovered a novel positive feedback that involves the transcriptional activation of the anti-apoptotic molecule deltaNp63 by the anti-apoptotic molecules deltaNp73 and mutant p53, and that is put into motion upon treatment with a subset of DNA damaging agents such as Doxorubicin and 5-FU.	Doxorubicin	290-301	P53	Homo sapiens	197-200
16931914-4	2006	In this study we have uncovered a novel positive feedback that involves the transcriptional activation of the anti-apoptotic molecule deltaNp63 by the anti-apoptotic molecules deltaNp73 and mutant p53, and that is put into motion upon treatment with a subset of DNA damaging agents such as Doxorubicin and 5-FU.	Fluorouracil	306-310	P53	Homo sapiens	197-200
16931914-5	2006	DeltaNp73 and mutant p53 associate with the deltaNp63 promoter inducing its transcription and this is enhanced by doxorubicin treatment.	Doxorubicin	114-125	P53	Homo sapiens	21-24
16951143-7	2006	This differential recruitment of p53 in senescent versus doxorubicin-treated fibroblasts was accompanied by differences in post-translational modification of p53.	Doxorubicin	57-68	P53	Homo sapiens	33-36
16951143-7	2006	This differential recruitment of p53 in senescent versus doxorubicin-treated fibroblasts was accompanied by differences in post-translational modification of p53.	Doxorubicin	57-68	P53	Homo sapiens	158-161
16741990-0	2006	Prostate derived factor in human prostate cancer cells: gene induction by vitamin D via a p53-dependent mechanism and inhibition of prostate cancer cell growth.	Vitamin D	74-83	P53	Homo sapiens	90-93
16557594-0	2006	Transcriptional profiling of MCF7 breast cancer cells in response to 5-Fluorouracil: relationship with cell cycle changes and apoptosis, and identification of novel targets of p53.	Fluorouracil	69-83	P53	Homo sapiens	176-179
16741955-0	2006	Cdk9 phosphorylates p53 on serine 392 independently of CKII.	Serine	27-33	P53	Homo sapiens	20-23
16741955-5	2006	We demonstrate that cdk9 phosphorylates p53 on serine 392 through their direct physical interaction.	Serine	47-53	P53	Homo sapiens	40-43
16741955-8	2006	Interestingly, cdk9 phosphorylates serine 392 of p53, which could be also phosphorylated by casein kinase II.	Serine	35-41	P53	Homo sapiens	49-52
16865258-7	2006	Interestingly, the doxorubicin- and radiation-induced S-/G2-phase arrests were suppressed by p53 in wt conformation.	Doxorubicin	19-30	P53	Homo sapiens	93-96
16954562-11	2006	CONCLUSION: These data suggest that abrogation of p53 in breast cancer is associated with specific changes in glucose metabolism detected by PET.	Glucose	110-117	P53	Homo sapiens	50-53
16797759-3	2006	By Western blot, the expression of 14-3-3sigma, p53 and p21 was coordinately upregulated in astrocytes following exposure to hydrogen peroxide, 4-hydroxy-2-nonenal (4-HNE) or etoposide, a topoisomerase II inhibitor.	Hydrogen Peroxide	125-142	P53	Homo sapiens	48-51
16918599-10	2006	Similar to the primary tumour, the cell line showed p53 overexpression and had p53 mutation at codon 132: AAG (lys)--&gt;AAT (asp).	Lysine	111-114	P53	Homo sapiens	79-82
16953122-0	2006	Involvement of JNK-initiated p53 accumulation and phosphorylation of p53 in pseudolaric acid B induced cell death.	pseudolaric acid B	76-94	P53	Homo sapiens	29-32
16953122-0	2006	Involvement of JNK-initiated p53 accumulation and phosphorylation of p53 in pseudolaric acid B induced cell death.	pseudolaric acid B	76-94	P53	Homo sapiens	69-72
16953122-3	2006	These results indicate that p53 is partially regulated by JNK in pseudolaric acid B-induced HeLa cell death and that PKC participates in pseudolaric acid B-induced HeLa cell death.	pseudolaric acid B	65-83	P53	Homo sapiens	28-31
16807237-7	2006	Chromatin immunoprecipitation of doxorubicin treated wild-type HCT116 cells showed the presence of DNMT1, p53, H3K9me2, and the transcriptional repressor HDAC1 on the Cdc25C and Cdc2 promoters, suggesting their involvement as repressive complexes in Cdc25C and Cdc2 gene silencing.	Doxorubicin	33-44	P53	Homo sapiens	106-109
16925398-1	2006	The most potent inhibitor of the p53-MDM2 interaction reported to date is an 8-mer p53 peptide analogue (Novartis peptide), which contains 6-chlorotryptophane (Cl-Trp) and phosphonomethylphenylalanine (Pmp) as key residues for the enhanced activity.	phosphonomethylphenylalanine	172-200	P53	Homo sapiens	33-36
16925398-1	2006	The most potent inhibitor of the p53-MDM2 interaction reported to date is an 8-mer p53 peptide analogue (Novartis peptide), which contains 6-chlorotryptophane (Cl-Trp) and phosphonomethylphenylalanine (Pmp) as key residues for the enhanced activity.	phosphonomethylphenylalanine	172-200	P53	Homo sapiens	83-86
16814250-3	2006	In the present study, we have found that p53 family member p73 as well as 14-3-3sigma is down-regulated in response to adriamycin (ADR) in ADR-resistant human breast cancer-derived MBA-MD-436 cells which carry p53 mutation.	Doxorubicin	119-129	P53	Homo sapiens	41-44
16568081-5	2006	ATRA-mediated apoptosis in CHP134 and NB-39-nu cells was associated with a significant activation of caspase-9 and caspase-3 as well as cytoplasmic release of cytochrome c from mitochondria in a p53-independent manner.	Tretinoin	0-4	P53	Homo sapiens	195-198
16931761-4	2006	Ionizing radiation triggered an ATM-dependent movement of COP1 from the nucleus to the cytoplasm, and ATM-dependent phosphorylation of COP1 on Ser(387) was both necessary and sufficient to disrupt the COP1-p53 complex and subsequently to abrogate the ubiquitination and degradation of p53.	Serine	143-146	P53	Homo sapiens	206-209
16931761-4	2006	Ionizing radiation triggered an ATM-dependent movement of COP1 from the nucleus to the cytoplasm, and ATM-dependent phosphorylation of COP1 on Ser(387) was both necessary and sufficient to disrupt the COP1-p53 complex and subsequently to abrogate the ubiquitination and degradation of p53.	Serine	143-146	P53	Homo sapiens	285-288
16931761-5	2006	Furthermore, phosphorylation of COP1 on Ser(387) was required to permit p53 to become stabilized and to exert its tumor suppressor properties in response to DNA damage.	Serine	40-43	P53	Homo sapiens	72-75
16815295-0	2006	p73 and MDM2 confer the resistance of epidermoid carcinoma to cisplatin by blocking p53.	Cisplatin	62-71	P53	Homo sapiens	84-87
16814250-3	2006	In the present study, we have found that p53 family member p73 as well as 14-3-3sigma is down-regulated in response to adriamycin (ADR) in ADR-resistant human breast cancer-derived MBA-MD-436 cells which carry p53 mutation.	Doxorubicin	119-129	P53	Homo sapiens	210-213
16815295-4	2006	p73 and MDM2 were kept at low levels in the cisplatin-sensitive KB-3-1 cells, whereas p53 was induced to be phosphorylated at Ser-15 in response to cisplatin.	Serine	126-129	P53	Homo sapiens	86-89
16815295-4	2006	p73 and MDM2 were kept at low levels in the cisplatin-sensitive KB-3-1 cells, whereas p53 was induced to be phosphorylated at Ser-15 in response to cisplatin.	Cisplatin	148-157	P53	Homo sapiens	86-89
16935784-3	2006	Unquestionable biological data must be taken into account to raise relevant questions, such as the role of topoisomerase II in the response to anthracyclines or the role of p53 in the response to taxanes.	Taxoids	196-203	P53	Homo sapiens	173-176
16815295-5	2006	In contrast, p73 and MDM2 were expressed at higher levels, and cisplatin-mediated p53 phosphorylation was undetectable in the cisplatin-resistant KCP-4 cells.	Cisplatin	63-72	P53	Homo sapiens	82-85
16815295-7	2006	Collectively, our results suggest that a loss of the cisplatin sensitivity is at least in part due to a lack of cisplatin-induced p53 phosphorylation, and p73 might cooperate with MDM2 to be involved in this process.	Cisplatin	112-121	P53	Homo sapiens	130-133
16740634-10	2006	Using ChIP assays and immunoprecipitation, we further demonstrated that p53 interacts with Sp1 to suppress both the constitutive and 12-O-tetradecanoylphorbol-13-acetate-stimulated expression of the MnSOD gene.	Tetradecanoylphorbol Acetate	133-169	P53	Homo sapiens	72-75
16965670-1	2006	BACKGROUND &amp; OBJECTIVE: It is important to overcome gene therapy resistance caused by wt-p53 in non-small cell lung cancer (NSCLC) .	Adenosine Monophosphate	12-15	P53	Homo sapiens	93-96
16945015-3	2006	Thus, nocodazole-treated cells were fluorescently labeled for different cell cycle-associated properties, including DNA content, retinoblastoma (Rb) and histone H3 phosphorylation, p53 and p21(WAF1) expression, nuclear and cell sizes, and cell morphology, and automatically imaged, analyzed, and correlated using HCA.	Nocodazole	6-16	P53	Homo sapiens	181-184
16880619-0	2006	The course of uncarinic acid E-induced apoptosis of HepG2 cells from damage to DNA and p53 activation to mitochondrial release of cytochrome c.	uncarinic acid-E	14-30	P53	Homo sapiens	87-90
16880619-6	2006	Uncarinic acid E significantly increased the expression of p53 proteins indicates that p53 plays a pivotal role in the initiation phase of uncarinic acid E-induced HepG2 cell apoptosis.	uncarinic acid-E	0-16	P53	Homo sapiens	59-62
16880619-6	2006	Uncarinic acid E significantly increased the expression of p53 proteins indicates that p53 plays a pivotal role in the initiation phase of uncarinic acid E-induced HepG2 cell apoptosis.	uncarinic acid-E	0-16	P53	Homo sapiens	87-90
16880619-6	2006	Uncarinic acid E significantly increased the expression of p53 proteins indicates that p53 plays a pivotal role in the initiation phase of uncarinic acid E-induced HepG2 cell apoptosis.	uncarinic acid-E	139-155	P53	Homo sapiens	59-62
16880619-6	2006	Uncarinic acid E significantly increased the expression of p53 proteins indicates that p53 plays a pivotal role in the initiation phase of uncarinic acid E-induced HepG2 cell apoptosis.	uncarinic acid-E	139-155	P53	Homo sapiens	87-90
16880619-7	2006	The phoshatidylinositol 3-kinase (PI3-K) family inhibitor wortmanin and the MEK inhibitor (PD98059) rescued the viability loss induced by uncarinic acid E through the expression of p53.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	91-98	P53	Homo sapiens	181-184
16880619-7	2006	The phoshatidylinositol 3-kinase (PI3-K) family inhibitor wortmanin and the MEK inhibitor (PD98059) rescued the viability loss induced by uncarinic acid E through the expression of p53.	uncarinic acid-E	138-154	P53	Homo sapiens	181-184
16880619-8	2006	Taken together, uncarinic acid E induces apoptosis in HepG2 cells via accumulation of p53, alters the Bax/Bcl-2 ratio, and activates caspases, resulting in cytochrome c release from the mitochondria.	uncarinic acid-E	16-32	P53	Homo sapiens	86-89
16872361-4	2006	The results here demonstrate evidence for approximately 25% apoptosis after treatment with calcium salicylate, which up-regulatd the expression of p53, p21 and Bax, and down-regulated Bcl-2 in HT-1080 cells.	calcium salicylate	91-109	P53	Homo sapiens	147-150
16872365-0	2006	Extent of constitutive histone H2AX phosphorylation on Ser-139 varies in cells with different TP53 status.	Serine	55-58	P53	Homo sapiens	94-98
16872365-5	2006	Because the tumour suppressor p53 (tumour protein p53) is known to induce transcription of genes associated with cell response to oxidative stress, we have compared the intensity of constitutive H2AX phosphorylation, and the effect of N-acetyl-L-cysteine on it, in cells with different tumour protein p53 status.	Acetylcysteine	235-254	P53	Homo sapiens	30-33
16790523-3	2006	This receptor is linked to induction by resveratrol of extracellular-regulated kinases 1 and 2 (ERK1/2)- and serine-15-p53-dependent phosphorylation leading to apoptosis.	Serine	109-115	P53	Homo sapiens	119-122
16835507-3	2006	We evaluated the linkage of the polymorphic variants (Arg/Pro) on TP53 codon 72 with nasopharyngeal cancer development in a case-control study with 392 individuals from a northern Portuguese population, including 107 patients with nasopharyngeal carcinoma and 285 healthy controls.	Arginine	54-57	P53	Homo sapiens	66-70
16790523-3	2006	This receptor is linked to induction by resveratrol of extracellular-regulated kinases 1 and 2 (ERK1/2)- and serine-15-p53-dependent phosphorylation leading to apoptosis.	Resveratrol	40-51	P53	Homo sapiens	119-122
16790523-4	2006	The integrin receptor is near the Arg-Gly-Asp (RGD) recognition site on the integrin; an integrin-binding RGD peptide inhibits induction by resveratrol of ERK1/2- and p53-dependent apoptosis.	Arginine	34-37	P53	Homo sapiens	167-170
16790523-4	2006	The integrin receptor is near the Arg-Gly-Asp (RGD) recognition site on the integrin; an integrin-binding RGD peptide inhibits induction by resveratrol of ERK1/2- and p53-dependent apoptosis.	Resveratrol	140-151	P53	Homo sapiens	167-170
16790523-9	2006	In conclusion, binding of resveratrol to integrin alphaVbeta3, principally to the beta3 monomer, is essential for transduction of the stilbene signal into p53-dependent apoptosis of breast cancer cells.	Resveratrol	26-37	P53	Homo sapiens	155-158
16928824-6	2006	The interaction of COX-2, p53, and p300, as well as resveratrol-induced apoptosis, was inhibited by a MAPK activation inhibitor, PD98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	129-136	P53	Homo sapiens	26-29
17133770-3	2006	Environmentally induced alterations in p53 protein have been reported to contribute to pathogenesis of leukemia in soft-shell clam Mya arenaria inhabiting polluted water, suggesting that p53 proteins can also be used as pollution markers.	Water	164-169	P53	Homo sapiens	39-42
16788846-6	2006	CONCLUSIONS: We were unable to demonstrate any association between the GST genotypes studied and the risk of ovarian cancer but the inheritance of a heterozygous Arg/Pro genotype of p53 increased the risk of ovarian cancer more than 2.5 times (OR = 2.571; 95% CI = 1.453-4.550).	Arginine	162-165	P53	Homo sapiens	182-185
16908595-1	2006	Methionine deprivation stress (MDS) eliminates mitotic activity in melanoma cells regardless of stage, grade, or TP53 status, whereas it has a negligible effect on normal skin fibroblasts.	Methionine	0-10	P53	Homo sapiens	113-117
16545436-0	2006	Over-expression of PTEN sensitizes human ovarian cancer cells to cisplatin-induced apoptosis in a p53-dependent manner.	Cisplatin	65-74	P53	Homo sapiens	98-101
16545436-3	2006	Activation of p53 is a key determinant of sensitivity to cisplatin-induced apoptosis.	Cisplatin	57-66	P53	Homo sapiens	14-17
16820892-7	2006	Gemcitabine and paclitaxel are highly efficient in the induction of apoptosis in ovarian cancer cells, which express a particular subset of the growth suppressor protein p53.	Paclitaxel	16-26	P53	Homo sapiens	170-173
16632641-8	2006	Activation of JNK by plumbagin phosphorylated p53 at serine 15, resulting in increased stability of p53 by decreasing p53 and MDM2 interaction.	Serine	53-59	P53	Homo sapiens	46-49
16928824-0	2006	Resveratrol-induced cyclooxygenase-2 facilitates p53-dependent apoptosis in human breast cancer cells.	Resveratrol	0-11	P53	Homo sapiens	49-52
16928824-5	2006	Nuclear COX-2 in resveratrol-treated cells colocalizes with Ser(15)-phosphorylated p53 and with p300, a coactivator for p53-dependent gene expression.	Resveratrol	17-28	P53	Homo sapiens	83-86
16928824-5	2006	Nuclear COX-2 in resveratrol-treated cells colocalizes with Ser(15)-phosphorylated p53 and with p300, a coactivator for p53-dependent gene expression.	Resveratrol	17-28	P53	Homo sapiens	120-123
16928824-5	2006	Nuclear COX-2 in resveratrol-treated cells colocalizes with Ser(15)-phosphorylated p53 and with p300, a coactivator for p53-dependent gene expression.	Serine	60-63	P53	Homo sapiens	83-86
16928824-7	2006	A specific inhibitor of COX-2, NS398, and small interfering RNA knockdown of COX-2 were associated with reduced p53 phosphorylation and consequent decrease in p53-dependent apoptosis in resveratrol-treated cells.	Resveratrol	186-197	P53	Homo sapiens	112-115
16928824-7	2006	A specific inhibitor of COX-2, NS398, and small interfering RNA knockdown of COX-2 were associated with reduced p53 phosphorylation and consequent decrease in p53-dependent apoptosis in resveratrol-treated cells.	Resveratrol	186-197	P53	Homo sapiens	159-162
16928824-8	2006	We conclude that nuclear accumulation of COX-2 can be induced by resveratrol and that the COX has a novel intranuclear colocalization with Ser(15)-phosphorylated p53 and p300, which facilitates apoptosis in resveratrol-treated breast cancer cells.	Serine	139-142	P53	Homo sapiens	162-165
16928824-8	2006	We conclude that nuclear accumulation of COX-2 can be induced by resveratrol and that the COX has a novel intranuclear colocalization with Ser(15)-phosphorylated p53 and p300, which facilitates apoptosis in resveratrol-treated breast cancer cells.	Resveratrol	207-218	P53	Homo sapiens	162-165
16837854-6	2006	The expression of bax and bim, proapoptotic genes known to be regulated by p53 and Forkhead, respectively, was enhanced in cortical neurons deprived of serum, a condition known to cause K+ loss, whereas the expression of c-fos, a cAMP-responsive element-binding protein target gene, was inhibited.	Cyclic AMP	230-234	P53	Homo sapiens	75-78
16714289-0	2006	Prostaglandin E2 stimulates p53 transactivational activity through specific serine 15 phosphorylation in human synovial fibroblasts.	Dinoprostone	0-16	P53	Homo sapiens	28-31
16714289-7	2006	PGE(2)-stimulated [phospho-Ser(15)]p53 transactivated a p53 response element (GADD45)-luciferase reporter in transiently transfected HSF (SN7); the effect was compromised by overexpression of a dominant-negative mutant (dnm) of p53 or excess p53S15A expression plasmid but mimicked by a constitutively active p53S15E expression construct.	Serine	27-30	P53	Homo sapiens	56-59
16714289-12	2006	PGE(2)-stimulated [phospho-Ser(15)]p53 abrogated the DNA binding of c/EBPbeta dimers and c/EBPbeta/NF-kappaB p65 heterodimers.	Dinoprostone	0-6	P53	Homo sapiens	35-38
16714289-12	2006	PGE(2)-stimulated [phospho-Ser(15)]p53 abrogated the DNA binding of c/EBPbeta dimers and c/EBPbeta/NF-kappaB p65 heterodimers.	Serine	27-30	P53	Homo sapiens	35-38
16714289-13	2006	Our data suggest that COX-2 prostaglandins may be implicated in p53 function and p53 target gene expression.	Prostaglandins	28-42	P53	Homo sapiens	64-67
16714289-13	2006	Our data suggest that COX-2 prostaglandins may be implicated in p53 function and p53 target gene expression.	Prostaglandins	28-42	P53	Homo sapiens	81-84
16759640-4	2006	Suppression of HASMC proliferation by resveratrol was accompanied by a dose-dependent increase in the expression of tumor suppressor gene p53 and heat shock protein HSP27.	Resveratrol	38-49	P53	Homo sapiens	138-141
16714289-0	2006	Prostaglandin E2 stimulates p53 transactivational activity through specific serine 15 phosphorylation in human synovial fibroblasts.	Serine	76-82	P53	Homo sapiens	28-31
16714289-3	2006	We examined the regulation of the tumor suppressor gene p53 and p53 target genes by prostaglandin E(2) (PGE(2)) in human synovial fibroblasts (HSF).	Dinoprostone	84-102	P53	Homo sapiens	56-59
16714289-3	2006	We examined the regulation of the tumor suppressor gene p53 and p53 target genes by prostaglandin E(2) (PGE(2)) in human synovial fibroblasts (HSF).	Dinoprostone	84-102	P53	Homo sapiens	64-67
16714289-3	2006	We examined the regulation of the tumor suppressor gene p53 and p53 target genes by prostaglandin E(2) (PGE(2)) in human synovial fibroblasts (HSF).	Dinoprostone	104-110	P53	Homo sapiens	56-59
16714289-3	2006	We examined the regulation of the tumor suppressor gene p53 and p53 target genes by prostaglandin E(2) (PGE(2)) in human synovial fibroblasts (HSF).	Dinoprostone	104-110	P53	Homo sapiens	64-67
16714289-4	2006	PGE(2) induced a time-dependent increase in p53 Ser(15) phosphorylation, with no discernible change in overall p53 levels.	Serine	48-51	P53	Homo sapiens	44-47
16714289-6	2006	Overexpression of a MKK3 construct, but not MKK1, stimulated SB202190-sensitive p53 Ser(15) phosphorylation.	Serine	84-87	P53	Homo sapiens	80-83
16714289-7	2006	PGE(2)-stimulated [phospho-Ser(15)]p53 transactivated a p53 response element (GADD45)-luciferase reporter in transiently transfected HSF (SN7); the effect was compromised by overexpression of a dominant-negative mutant (dnm) of p53 or excess p53S15A expression plasmid but mimicked by a constitutively active p53S15E expression construct.	Dinoprostone	0-6	P53	Homo sapiens	35-38
16714289-7	2006	PGE(2)-stimulated [phospho-Ser(15)]p53 transactivated a p53 response element (GADD45)-luciferase reporter in transiently transfected HSF (SN7); the effect was compromised by overexpression of a dominant-negative mutant (dnm) of p53 or excess p53S15A expression plasmid but mimicked by a constitutively active p53S15E expression construct.	Dinoprostone	0-6	P53	Homo sapiens	56-59
16714289-7	2006	PGE(2)-stimulated [phospho-Ser(15)]p53 transactivated a p53 response element (GADD45)-luciferase reporter in transiently transfected HSF (SN7); the effect was compromised by overexpression of a dominant-negative mutant (dnm) of p53 or excess p53S15A expression plasmid but mimicked by a constitutively active p53S15E expression construct.	Dinoprostone	0-6	P53	Homo sapiens	56-59
16714289-7	2006	PGE(2)-stimulated [phospho-Ser(15)]p53 transactivated a p53 response element (GADD45)-luciferase reporter in transiently transfected HSF (SN7); the effect was compromised by overexpression of a dominant-negative mutant (dnm) of p53 or excess p53S15A expression plasmid but mimicked by a constitutively active p53S15E expression construct.	Serine	27-30	P53	Homo sapiens	35-38
16714289-7	2006	PGE(2)-stimulated [phospho-Ser(15)]p53 transactivated a p53 response element (GADD45)-luciferase reporter in transiently transfected HSF (SN7); the effect was compromised by overexpression of a dominant-negative mutant (dnm) of p53 or excess p53S15A expression plasmid but mimicked by a constitutively active p53S15E expression construct.	Serine	27-30	P53	Homo sapiens	56-59
16584912-0	2006	Relationship between p53 status and 5-fluorouracil sensitivity in 3 cell lines.	Fluorouracil	36-50	P53	Homo sapiens	21-24
16857806-14	2006	Doxorubicin-induced growth suppression was associated with elevation of p53 and p21(Cip1/Waf1).	Doxorubicin	0-11	P53	Homo sapiens	72-75
16579792-6	2006	The p53(F270A:6KR) chimaeric mutant (where 6KR refers to the simultaneous mutation of lysine residues at positions 370, 372, 373, 381, 382 and 386 to arginine) maintains the high-molecular-mass covalent adducts and is modified in an MDM2-dependent manner.	Lysine	86-92	P53	Homo sapiens	4-7
16579792-6	2006	The p53(F270A:6KR) chimaeric mutant (where 6KR refers to the simultaneous mutation of lysine residues at positions 370, 372, 373, 381, 382 and 386 to arginine) maintains the high-molecular-mass covalent adducts and is modified in an MDM2-dependent manner.	Arginine	150-158	P53	Homo sapiens	4-7
16814113-0	2006	Potent antiproliferative effects of resveratrol on human osteosarcoma SJSA1 cells: Novel cellular mechanisms involving the ERKs/p53 cascade.	Resveratrol	36-47	P53	Homo sapiens	128-131
16814113-3	2006	In this study, we investigated the involvement of the mitogen activated protein kinase (MAPK)/p53 signal transduction mechanism in RSVL-induced growth inhibition using a human osteosarcoma cell line.	Resveratrol	131-135	P53	Homo sapiens	94-97
16814113-8	2006	Likewise, RSVL increased the phosphorylation of p53 tumor suppressor protein (at Ser15).	Resveratrol	10-14	P53	Homo sapiens	48-51
16814113-9	2006	The effects of RSVL on ERKs and on p53 phosphorylation were abrogated by either the MAPK inhibitor PD98059 or the p53 inhibitor pifithrine-alpha.	Resveratrol	15-19	P53	Homo sapiens	35-38
16814113-9	2006	The effects of RSVL on ERKs and on p53 phosphorylation were abrogated by either the MAPK inhibitor PD98059 or the p53 inhibitor pifithrine-alpha.	Resveratrol	15-19	P53	Homo sapiens	114-117
16814113-9	2006	The effects of RSVL on ERKs and on p53 phosphorylation were abrogated by either the MAPK inhibitor PD98059 or the p53 inhibitor pifithrine-alpha.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	99-106	P53	Homo sapiens	35-38
16814113-10	2006	The present study indicates that RSVL antiproliferative effects on osteosarcoma cells are mediated by the activation of the ERKs/p53 signaling pathway and therefore identifies new targets for strategies to treat and/or prevent osteosarcoma.	Resveratrol	33-37	P53	Homo sapiens	129-132
16839880-6	2006	The decrease of intracellular ROS levels in response to TIGAR may also play a role in the ability of p53 to protect from the accumulation of genomic damage.	Reactive Oxygen Species	30-33	P53	Homo sapiens	101-104
16810754-8	2006	CONCLUSION: Our study suggests that somatic chromosomal mutations, especially in exon 6 of Tp53 gene, among esophageal cancer patients of an ethnically homogenous population of Kashmir valley are closely related to continued exposure to various common dietary risk factors, especially hot salty tea, meat, baked bread and "Hakh", that are rich in nitrosoamines and familial cancer history.	nitrosoamines	347-360	P53	Homo sapiens	91-95
16827804-3	2006	In vitro, adenovirus-mediated transduction of the p53-46F gene induced apoptosis more efficiently than wild-type p53 in a number of cancer cell lines, whereas Ser-15 phosphorylation of p53-46F was enhanced in all cancer cell lines examined.	Serine	159-162	P53	Homo sapiens	50-53
16763167-3	2006	We report that in a model of insulin-dependent diabetes mellitus, the generation of reactive oxygen species (ROS) leads to telomeric shortening, expression of the senescent associated proteins p53 and p16INK4a, and apoptosis of CPCs, impairing the growth reserve of the heart.	Reactive Oxygen Species	84-107	P53	Homo sapiens	193-196
16763167-3	2006	We report that in a model of insulin-dependent diabetes mellitus, the generation of reactive oxygen species (ROS) leads to telomeric shortening, expression of the senescent associated proteins p53 and p16INK4a, and apoptosis of CPCs, impairing the growth reserve of the heart.	Reactive Oxygen Species	109-112	P53	Homo sapiens	193-196
16835330-6	2006	p53 protein accumulation was assessed immunohistochemically using sections of paraffin-embedded benign breast tissue from 104 cases and 385 controls; for 82 of these cases and 327 of the controls, DNA was successfully extracted from the breast tissue for p53 gene analysis using PCR-single-strand conformation polymorphism/direct sequencing.	Paraffin	78-86	P53	Homo sapiens	0-3
16843260-0	2006	Differential utilization of two ATP-generating pathways is regulated by p53.	Adenosine Triphosphate	32-35	P53	Homo sapiens	72-75
16814724-2	2006	Loss of p53 results in decreased oxygen consumption and aerobic respiration and promotes a switch to glycolysis, thereby reducing endurance during physical exercise.	Oxygen	33-39	P53	Homo sapiens	8-11
16773194-1	2006	The present study aims to investigate the role of p73 in response to cisplatin treatment in p53 wild-type neuroblastoma SH-SY5Y cells.	Cisplatin	69-78	P53	Homo sapiens	92-95
16824197-6	2006	Interestingly, 15d-PGJ(2)-induced ATM activation leads to p53 activation and apoptosis, but not to Chk2 or H2AX phosphorylation.	15-deoxyprostaglandin J2	15-25	P53	Homo sapiens	58-61
16766179-0	2006	Tumour response to preoperative anthracycline-based chemotherapy in operable breast cancer: the predictive role of p53 expression.	Anthracyclines	32-45	P53	Homo sapiens	115-118
16766179-9	2006	In conclusion, our data suggest p53 expression is of predictive significance in anthracycline-containing chemotherapeutic regimens.	Anthracyclines	80-93	P53	Homo sapiens	32-35
16761963-2	2006	We investigated the mechanism of the antiproliferative effect of resveratrol in A431-transformed keratinocytes harbouring mutant p53, and show that it is accompanied by G1 cell cycle arrest, which coincides with a marked inhibition of G1 cell cycle regulatory proteins, including cyclins A and D1 and cyclin-dependent kinase (CDK)6 and p53-independent induction of p21WAF1.	Resveratrol	65-76	P53	Homo sapiens	129-132
16761963-2	2006	We investigated the mechanism of the antiproliferative effect of resveratrol in A431-transformed keratinocytes harbouring mutant p53, and show that it is accompanied by G1 cell cycle arrest, which coincides with a marked inhibition of G1 cell cycle regulatory proteins, including cyclins A and D1 and cyclin-dependent kinase (CDK)6 and p53-independent induction of p21WAF1.	Resveratrol	65-76	P53	Homo sapiens	336-339
16773194-2	2006	Results showed that cisplatin induced a dose-dependent up-regulation of p53, p73, and a number of p53-responsive genes.	Cisplatin	20-29	P53	Homo sapiens	72-75
16773194-2	2006	Results showed that cisplatin induced a dose-dependent up-regulation of p53, p73, and a number of p53-responsive genes.	Cisplatin	20-29	P53	Homo sapiens	98-101
16773194-7	2006	Collectively, our results suggest that wt-p53 SH-SY5Y cells respond to cisplatin by inducing p73 isoform regulation and sustaining p53-dependent apoptosis that is independent of TAp73alpha.	Cisplatin	71-80	P53	Homo sapiens	42-45
16773194-7	2006	Collectively, our results suggest that wt-p53 SH-SY5Y cells respond to cisplatin by inducing p73 isoform regulation and sustaining p53-dependent apoptosis that is independent of TAp73alpha.	Cisplatin	71-80	P53	Homo sapiens	131-134
16538517-0	2006	Lack of prognostic impact of p53 gene mutation and p53 phosphorylation at serine 15 in multimodally treated adenocarcinomas of the gastroesophageal junction.	Serine	74-80	P53	Homo sapiens	51-54
16538517-2	2006	As p53 protein phosphorylation at serine 15 indicates stabilization and protection against mdm-2 the presence of this phosphorylation state was subsequently evaluated.	Serine	34-40	P53	Homo sapiens	3-6
16538517-4	2006	The presence of p53 protein phosphorylation at serine 15 was evaluated by immunohistochemistry.	Serine	47-53	P53	Homo sapiens	16-19
16538517-6	2006	Phosphorylation at serine 15 of p53 was detected in 14 samples, being neither associated with p53 mutation nor with patient"s survival.	Serine	19-25	P53	Homo sapiens	32-35
16891474-6	2006	Selenite induced a rapid generation of superoxide and p53 Ser(15) phosphorylation and increased Bax abundance and translocation into the mitochondria.	Serine	58-61	P53	Homo sapiens	54-57
16786124-1	2006	The TP53 polymorphism occurs at codon 72 of exon 4 with two alleles encoding either arginine or proline.	Arginine	84-92	P53	Homo sapiens	4-8
16768444-0	2006	Effect of Zn2+ on DNA recognition and stability of the p53 DNA-binding domain.	Zinc	10-14	P53	Homo sapiens	55-58
16768444-3	2006	We have carried out molecular dynamics simulations to investigate the influence of Zn2+ on the p53 DNA recognition and the stability of the DBD.	Zinc	83-87	P53	Homo sapiens	95-98
16768444-8	2006	Our results suggest that L2 may be a frustrated and highly flexible element and play an important role in aggregation of Zn-free p53.	Zinc	121-123	P53	Homo sapiens	129-132
16759106-0	2006	Imino-tetrahydro-benzothiazole derivatives as p53 inhibitors: discovery of a highly potent in vivo inhibitor and its action mechanism.	imino-tetrahydro-benzothiazole	0-30	P53	Homo sapiens	46-49
16785031-7	2006	Although SIRT1 did not affect H(2)O(2)-mediated phosphorylation of mitogen-activated protein (MAP) kinase, it interacted with p53 and inhibited H(2)O(2)-mediated p53 acetylation but not phosphorylation in MMCs.	Hydrogen Peroxide	144-152	P53	Homo sapiens	162-165
16600594-1	2006	Guided by structure-based drug design, modification of the 1,4-benzodiazepin-2,5-dione lead compound 1 resulted in the discovery of 19, a potent and orally bioavailable antagonist of the HDM2-p53 protein-protein interaction (FP IC50 = 0.7 microM, F approximately 100%).	1,4-benzodiazepin-2,5-dione	59-86	P53	Homo sapiens	192-195
16728583-0	2006	Folic acid and its metabolites modulate IGF-I receptor gene expression in colon cancer cells in a p53-dependent manner.	Folic Acid	0-10	P53	Homo sapiens	98-101
16331344-10	2006	Furthermore, in TP53 72Pro carriers with p21 Ser/Ser genotype, the occurrence of acute toxicity was reduced in normal weight but not overweight patients.	Serine	45-48	P53	Homo sapiens	16-20
16331344-10	2006	Furthermore, in TP53 72Pro carriers with p21 Ser/Ser genotype, the occurrence of acute toxicity was reduced in normal weight but not overweight patients.	Serine	49-52	P53	Homo sapiens	16-20
16762630-1	2006	BACKGROUND &amp; AIMS: Human cervical cancer oncogene (HCCR-1) has appeared to act as a negative regulator of p53 and contributes to tumorigenesis of various organs including the colon.	Adenosine Monophosphate	12-15	P53	Homo sapiens	110-113
16704422-5	2006	Both VRK2 isoforms have an identical catalytic N-terminal domain and phosphorylate p53 in vitro uniquely in Thr18.	UNII-PYZ33YLR8A	108-113	P53	Homo sapiens	83-86
16704422-8	2006	Only overexpression of the nuclear VRK2B isoform induces p53 stabilization by post-translational modification, largely due to Thr18 phosphorylation.	UNII-PYZ33YLR8A	126-131	P53	Homo sapiens	57-60
16704422-11	2006	Endogenous p53 is also phosphorylated in Thr18 by VRK2B, promoting its stabilization and transcriptional activation in A549 cells.	UNII-PYZ33YLR8A	41-46	P53	Homo sapiens	11-14
16673384-3	2006	Recent studies have implicated cysteine thiols present in various transcription factors, such as NF-kappaB, AP-1, and p53 as redox sensors in transcriptional regulation of many genes essential for maintaining cellular homeostasis.	cysteine thiols	31-46	P53	Homo sapiens	118-121
16510697-1	2006	In this study, a cationic water-soluble ceramide analog L-threo-C6-pyridinium-ceramide-bromide (L-t-C6-Pyr-Cer), which exhibits high solubility and bioavailability, inhibited the growth of various human head and neck squamous cell carcinoma (HNSCC) cell lines at low IC50 concentrations, independent of their p53 status.	Water	26-31	P53	Homo sapiens	309-312
16705155-3	2006	Either GAS41 small interfering RNA-mediated knockdown of GAS41 expression or specific interruptions of the carboxy-terminal coiled-coil motif of the GAS41 protein activate the p53 tumor suppressor pathway, as evidenced by p53 up-regulation, p53 serine-15 phosphorylation, and p21 transcriptional activation.	Serine	245-251	P53	Homo sapiens	176-179
15990222-0	2006	Induction of p53 and drug resistance following treatment with cisplatin or paclitaxel in ovarian cancer cell lines.	Cisplatin	62-71	P53	Homo sapiens	13-16
16818520-5	2006	Prolonged exposure was also associated with a reduced phosphorylation of p53 on serines 15 and 20, a limited and delayed phosphorylation on serine 392, and a less prominent increase in p21 levels.	Serine	80-87	P53	Homo sapiens	73-76
16818520-5	2006	Prolonged exposure was also associated with a reduced phosphorylation of p53 on serines 15 and 20, a limited and delayed phosphorylation on serine 392, and a less prominent increase in p21 levels.	Serine	80-86	P53	Homo sapiens	73-76
16600182-1	2006	PRPK phosphorylates serine-15 residue of p53 and enhances transcriptional activity.	Serine	20-26	P53	Homo sapiens	41-44
16600182-6	2006	Both Ray wild type and GTP-restrictively binding mutant Ray-Q67L, but not guanine nucleotide unstable binding mutant Ray-N120I, partially distributed the over-expressed PRPK to the cytosol and also suppressed the PRPK-induced p53-transcriptional activity profoundly.	Guanosine Triphosphate	23-26	P53	Homo sapiens	226-229
16501611-0	2006	Protein serine/threonine phosphatase-1 dephosphorylates p53 at Ser-15 and Ser-37 to modulate its transcriptional and apoptotic activities.	Serine	63-66	P53	Homo sapiens	56-59
16501611-6	2006	In the present study, we demonstrate that PP-1 can dephosphorylate p53 at Ser-15 and Ser-37 through co-immunoprecipitation, in vitro and in vivo dephosphorylation assays, overexpression and silence of the gene encoding the catalytic subunit for PP-1.	Serine	74-77	P53	Homo sapiens	67-70
16818496-6	2006	Indeed, the inactivation of p53 may explain the relative resistance to 5-fluorouracil, whereas Bcl-2 overexpression is associated with reduced sensitivity to gemcitabine.	Fluorouracil	71-85	P53	Homo sapiens	28-31
16732889-3	2006	RESULTS: We constructed an adenoviral vector coding a chimeric p53 protein by fusing p53 sequence with the 21 COOH term amino acids sequence of H-Ras.	Carbonic Acid	110-114	P53	Homo sapiens	63-66
16700548-8	2006	On the basis of the comparison of the NQO1 structure in complex with different NQO1 inhibitors and our previous analysis of NQO1 mutants, we propose that the specific conformation of Tyr 128 and Phe 232 is important for NQO1 interaction with p53 and other client proteins.	Tyrosine	183-186	P53	Homo sapiens	242-245
15990222-0	2006	Induction of p53 and drug resistance following treatment with cisplatin or paclitaxel in ovarian cancer cell lines.	Paclitaxel	75-85	P53	Homo sapiens	13-16
16681385-6	2006	Treatment of p53-null Saos-2 cells with reversibly cationized p53 revealed that all events examined as indications of the activation of p53 in cells, such as reduction of disulfide bonds followed by tetramer formation, localization into the nucleus, induction of p53 target genes, and induction of apoptosis of cells, occurred.	Disulfides	171-180	P53	Homo sapiens	13-16
15990222-3	2006	Cells (UL-3A, UL-3B) that recovered from cisplatin (Cis) and paclitaxel (Tax) treatments showed higher levels of p53, mdr-1 and chemoresistance than untreated controls.	Cisplatin	41-50	P53	Homo sapiens	113-116
16681385-6	2006	Treatment of p53-null Saos-2 cells with reversibly cationized p53 revealed that all events examined as indications of the activation of p53 in cells, such as reduction of disulfide bonds followed by tetramer formation, localization into the nucleus, induction of p53 target genes, and induction of apoptosis of cells, occurred.	Disulfides	171-180	P53	Homo sapiens	62-65
15990222-3	2006	Cells (UL-3A, UL-3B) that recovered from cisplatin (Cis) and paclitaxel (Tax) treatments showed higher levels of p53, mdr-1 and chemoresistance than untreated controls.	Paclitaxel	61-71	P53	Homo sapiens	113-116
16681385-6	2006	Treatment of p53-null Saos-2 cells with reversibly cationized p53 revealed that all events examined as indications of the activation of p53 in cells, such as reduction of disulfide bonds followed by tetramer formation, localization into the nucleus, induction of p53 target genes, and induction of apoptosis of cells, occurred.	Disulfides	171-180	P53	Homo sapiens	62-65
16681385-6	2006	Treatment of p53-null Saos-2 cells with reversibly cationized p53 revealed that all events examined as indications of the activation of p53 in cells, such as reduction of disulfide bonds followed by tetramer formation, localization into the nucleus, induction of p53 target genes, and induction of apoptosis of cells, occurred.	Disulfides	171-180	P53	Homo sapiens	62-65
16709241-5	2006	RESULTS: 5-FU treatment for 24 hours resulted in S phase arrests, p53 accumulation, up-regulation of p53-target genes on DNA damage response (ATF3, GADD34, GADD45A, PCNA), cell cycle-regulatory (CDKN1A), and apoptosis-regulatory pathways (FAS), and apoptosis induction in the parental and resistant cell lines.	Fluorouracil	9-13	P53	Homo sapiens	66-69
16709241-5	2006	RESULTS: 5-FU treatment for 24 hours resulted in S phase arrests, p53 accumulation, up-regulation of p53-target genes on DNA damage response (ATF3, GADD34, GADD45A, PCNA), cell cycle-regulatory (CDKN1A), and apoptosis-regulatory pathways (FAS), and apoptosis induction in the parental and resistant cell lines.	Fluorouracil	9-13	P53	Homo sapiens	101-104
16631755-1	2006	Doxorubicin, cis-diamminedichloroplatinum (II) and 5-fluorouracil used in chemotherapy induce apoptosis in Hep3B cells in the absence of p53, p73, and functional Fas.	Fluorouracil	51-65	P53	Homo sapiens	137-140
16827107-5	2006	MATERIALS AND METHODS: Immunohistochemistry was employed to analyze the protein expression of p53, deltaNp73 and deltaNp63 in paraffin-embedded tumor samples from 132 well-characterized lung cancer patients.	Paraffin	126-134	P53	Homo sapiens	94-97
16686938-2	2006	Here, we address the individual role of p53 and its transcriptional targets, p21CIP/WAF-1 and Bax, on apoptosis induced by individual components of multimodal anticancer therapy, i.e. 5-fluorouracil (5-FU), ionising gamma-radiation (IR) and heat shock/hyperthermia.	Fluorouracil	184-198	P53	Homo sapiens	40-43
16686938-2	2006	Here, we address the individual role of p53 and its transcriptional targets, p21CIP/WAF-1 and Bax, on apoptosis induced by individual components of multimodal anticancer therapy, i.e. 5-fluorouracil (5-FU), ionising gamma-radiation (IR) and heat shock/hyperthermia.	Fluorouracil	200-204	P53	Homo sapiens	40-43
16686938-10	2006	In contrast, loss of p21CIP/WAF-1 or, to a lesser extent, p53 sensitized predominantly for 5-FU and IR.	Fluorouracil	91-95	P53	Homo sapiens	58-61
16601678-1	2006	The serine/threonine kinase HIPK2 phosphorylates the p53 protein at Ser 46, thus promoting p53-dependent gene expression and subsequent apoptosis.	Serine	68-71	P53	Homo sapiens	53-56
16601678-1	2006	The serine/threonine kinase HIPK2 phosphorylates the p53 protein at Ser 46, thus promoting p53-dependent gene expression and subsequent apoptosis.	Serine	68-71	P53	Homo sapiens	91-94
16544101-3	2006	Apoptosis induced in HeLa cells at 24 h of cisplatin treatment was confirmed by nuclear fragmentation, increase in subdiploid population and the enhanced activation of ERK and upregulation of p53.	Cisplatin	43-52	P53	Homo sapiens	192-195
16611376-0	2006	In vitro folate deficiency induces apoptosis by a p53, Fas (Apo-1, CD95) independent, bcl-2 related mechanism in phytohaemagglutinin-stimulated human peripheral blood lymphocytes.	Folic Acid	9-15	P53	Homo sapiens	50-53
16687915-4	2006	If a cell stays in mitosis too long, (e.g. mitotic arrest caused by Taxol or nocodazole), then p53 accumulates.	Paclitaxel	68-73	P53	Homo sapiens	95-98
16611376-4	2006	The results indicate that p53 expression was downregulated in folate-deficient lymphocytes when compared with the control lymphocytes during the relevant period of S phase accumulation and apoptosis.	Folic Acid	62-68	P53	Homo sapiens	26-29
16611376-9	2006	These results suggest that IL-2 depletion by folate deficiency in lymphocytes reduces the bcl-2 level, thereby triggering deoxynucleoside triphosphate pool imbalance and p53-independent apoptosis.	Folic Acid	45-51	P53	Homo sapiens	170-173
16651424-4	2006	NIC-1 inhibited p53 by inhibiting its activating phosphorylations at Ser(15), Ser(20), and Ser(392) as well as nuclear localization.	Serine	69-72	P53	Homo sapiens	16-19
16651424-4	2006	NIC-1 inhibited p53 by inhibiting its activating phosphorylations at Ser(15), Ser(20), and Ser(392) as well as nuclear localization.	Serine	78-81	P53	Homo sapiens	16-19
16651424-4	2006	NIC-1 inhibited p53 by inhibiting its activating phosphorylations at Ser(15), Ser(20), and Ser(392) as well as nuclear localization.	Serine	78-81	P53	Homo sapiens	16-19
16651424-5	2006	In addition, we found that inhibition of p53 by NIC-1 mainly occurs through mammalian target of rapamycin (mTOR) using phosphatidylinositol 3-kinase (PI3K)-Akt/protein kinase B (PKB) pathway as the mTOR inhibitor, rapamycin treatment abrogated NIC-1 inhibition of p53 and reversed the chemoresistance.	Sirolimus	96-105	P53	Homo sapiens	41-44
16651424-5	2006	In addition, we found that inhibition of p53 by NIC-1 mainly occurs through mammalian target of rapamycin (mTOR) using phosphatidylinositol 3-kinase (PI3K)-Akt/protein kinase B (PKB) pathway as the mTOR inhibitor, rapamycin treatment abrogated NIC-1 inhibition of p53 and reversed the chemoresistance.	Sirolimus	96-105	P53	Homo sapiens	264-267
16630142-4	2006	Furthermore, MCS-C2 induced cell cycle arrest in the G1 phase through the upregulated phosphorylation of the p53 protein at Ser-15 and activation of its downstream target gene p21WAF1/CIP1.	Serine	124-127	P53	Homo sapiens	109-112
16721047-9	2006	The effect of p53 activation was checked by RT-PCR and transfections in HCT116 wt, E6 and p53-/- cells: most promoters were actively repressed upon Adriamycin treatment or following p53 transfection in p53-/- cells.	Doxorubicin	148-158	P53	Homo sapiens	14-17
16721047-9	2006	The effect of p53 activation was checked by RT-PCR and transfections in HCT116 wt, E6 and p53-/- cells: most promoters were actively repressed upon Adriamycin treatment or following p53 transfection in p53-/- cells.	Doxorubicin	148-158	P53	Homo sapiens	90-93
16687915-4	2006	If a cell stays in mitosis too long, (e.g. mitotic arrest caused by Taxol or nocodazole), then p53 accumulates.	Nocodazole	77-87	P53	Homo sapiens	95-98
16721047-9	2006	The effect of p53 activation was checked by RT-PCR and transfections in HCT116 wt, E6 and p53-/- cells: most promoters were actively repressed upon Adriamycin treatment or following p53 transfection in p53-/- cells.	Doxorubicin	148-158	P53	Homo sapiens	90-93
16687923-4	2006	A recent study using RNA interference in human SCC-derived cell lines shows that DeltaNp63alpha mediates an essential survival function in human SCC cells by virtue of its ability to suppress the pro-apoptotic function of the related p53 family member p73.	deltanp63alpha	81-95	P53	Homo sapiens	234-237
16721047-9	2006	The effect of p53 activation was checked by RT-PCR and transfections in HCT116 wt, E6 and p53-/- cells: most promoters were actively repressed upon Adriamycin treatment or following p53 transfection in p53-/- cells.	Doxorubicin	148-158	P53	Homo sapiens	90-93
16697770-9	2006	Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033].	Arginine	66-69	P53	Homo sapiens	47-50
16527552-10	2006	Both Wortmannin and PD98059 elevated the level of p53 expression strikingly, however, only PD98059 suppressed the up-regulation trend of c-Myc expression induced by etoposide.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	20-27	P53	Homo sapiens	50-53
16700663-5	2006	An immunohistochemical method was used to investigate the expression of COX-2 and p53 proteins on formalin-fixed, paraffin-embedded tissue specimens of squamous cell carcinomas (SCC), basal cell carcinomas (BCC), Bowen"s disease (BD), actinic keratosis (AK) and porokeratosis.	Paraffin	114-122	P53	Homo sapiens	82-85
16697770-9	2006	Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033].	Arginine	88-91	P53	Homo sapiens	47-50
16697770-9	2006	Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033].	Arginine	88-91	P53	Homo sapiens	47-50
16697770-9	2006	Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033].	Arginine	88-91	P53	Homo sapiens	47-50
16697770-9	2006	Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033].	Arginine	88-91	P53	Homo sapiens	47-50
16697770-9	2006	Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033].	Arginine	88-91	P53	Homo sapiens	47-50
16697770-9	2006	Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033].	Serine	170-173	P53	Homo sapiens	47-50
16529824-8	2006	Our study thus demonstrates that morphine induces Jurkat cell apoptosis through FADD/p53, anti-apoptotic PI3K/Akt and NF-kappaB pathways.	Morphine	33-41	P53	Homo sapiens	85-88
16529824-0	2006	Morphine promotes Jurkat cell apoptosis through pro-apoptotic FADD/P53 and anti-apoptotic PI3K/Akt/NF-kappaB pathways.	Morphine	0-8	P53	Homo sapiens	67-70
16697770-9	2006	Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033].	Serine	192-195	P53	Homo sapiens	47-50
16529824-5	2006	Furthermore, suppression of endogenous p53 expression by RNA interference technology considerably attenuated the morphine-induced apoptosis.	Morphine	113-121	P53	Homo sapiens	39-42
16697770-9	2006	Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033].	Serine	192-195	P53	Homo sapiens	47-50
16731756-9	2006	We conclude that separate from effects on sensitivity to the acute cytotoxic effect of cisplatin, loss of MMR, especially when combined with loss of p53, results in rapid evolution of cisplatin resistance during sequential rounds of drug exposure that is likely mediated by enhanced mutagenic translesion synthesis.	Cisplatin	184-193	P53	Homo sapiens	149-152
16731756-10	2006	The DNA damage response activated by cisplatin is accompanied by a p53- and MMR-dependent increase in homologous recombination even between adduct-free sequences.	Cisplatin	37-46	P53	Homo sapiens	67-70
16731756-0	2006	DNA mismatch repair and p53 function are major determinants of the rate of development of cisplatin resistance.	Cisplatin	90-99	P53	Homo sapiens	24-27
16731759-7	2006	Additional studies revealed that GSE causes DNA damage-induced activation of ataxia telangiectasia mutated kinase and Chk2, as well as p53 Ser(15) phosphorylation and its translocation to mitochondria, suggesting this to be an additional mechanism for apoptosis induction.	Serine	139-142	P53	Homo sapiens	135-138
16731756-4	2006	Loss of either MMR or p53 alone increased the rate of development of resistance to cisplatin by 1.8- and 2.4-fold, respectively; however, loss of both MMR and p53 increased the rate by 4.8-fold.	Cisplatin	83-92	P53	Homo sapiens	22-25
16731756-4	2006	Loss of either MMR or p53 alone increased the rate of development of resistance to cisplatin by 1.8- and 2.4-fold, respectively; however, loss of both MMR and p53 increased the rate by 4.8-fold.	Cisplatin	83-92	P53	Homo sapiens	159-162
16518417-4	2006	On the other hand, pretreatment with dicoumarol enhanced cytotoxicity of CDDP in three cell lines with wild type of p53 (RT112, 253J and LNCap), but not in three other cell lines with mutant p53 or in RT112 stable transfectants with a dominant-negative mutant of p53.	Cisplatin	73-77	P53	Homo sapiens	116-119
16731756-8	2006	In the p53- and MMR-proficient cells, cisplatin induced a 17-fold increase in homologous recombination even when the recombining sequences that did not contain cisplatin adducts; the magnitude of induction was even greater in cells that had lost either one or both functions.	Cisplatin	38-47	P53	Homo sapiens	7-10
16609366-9	2006	CONCLUSION: The present report indicates that the codon 72 polymorphism in the p53 gene may be a predictor of tamoxifen response, suggesting that breast cancer patients lacking the Pro72 allele might be candidates for other therapies.	Tamoxifen	110-119	P53	Homo sapiens	79-82
16761419-4	2006	RESULTS: The frequencies of p53 Arg homozygosity in cervical squamous cancer, cervical adenocarcinoma and CIN (II - III) were 58.020%, 55.55% and 59.09% respectively, greater than those of p53 Arg/Pro heterozygosity (30.86%, 27.78%, 21.59%) and those of p53 Pro homozygosity (11.12%, 16.67%, 19.32%).	Arginine	32-35	P53	Homo sapiens	28-31
16761419-4	2006	RESULTS: The frequencies of p53 Arg homozygosity in cervical squamous cancer, cervical adenocarcinoma and CIN (II - III) were 58.020%, 55.55% and 59.09% respectively, greater than those of p53 Arg/Pro heterozygosity (30.86%, 27.78%, 21.59%) and those of p53 Pro homozygosity (11.12%, 16.67%, 19.32%).	Arginine	193-196	P53	Homo sapiens	28-31
16761419-5	2006	The normal cervical samples also showed less frequency of p53 Arg homozygosity (23.33%) than cervical squamous cancer.	Arginine	62-65	P53	Homo sapiens	58-61
16518417-0	2006	Dicoumarol potentiates cisplatin-induced apoptosis mediated by c-Jun N-terminal kinase in p53 wild-type urogenital cancer cell lines.	Cisplatin	23-32	P53	Homo sapiens	90-93
16596182-2	2006	While the role of p53 in CDDP-induced cell death has been stressed, evidence exists that CDDP can also kill p53-mutated cells.	Cisplatin	89-93	P53	Homo sapiens	108-111
16596182-8	2006	Therefore, the JNK pathway appears to be an ideal target for the modulation of the lethal action of CDDP in multiple types of p53-mutated cells.	Cisplatin	100-104	P53	Homo sapiens	126-129
16761419-9	2006	The frequency of p53 Arg homozygosity in HRHPV E6-positive cervical squamous cancers (64.06%) was greater than in HRHPV E6-negative cervical squamous cancers (35.29%) and in HRHPV E6-positive normal samples (33.33%).	Arginine	21-24	P53	Homo sapiens	17-20
16518417-4	2006	On the other hand, pretreatment with dicoumarol enhanced cytotoxicity of CDDP in three cell lines with wild type of p53 (RT112, 253J and LNCap), but not in three other cell lines with mutant p53 or in RT112 stable transfectants with a dominant-negative mutant of p53.	Cisplatin	73-77	P53	Homo sapiens	191-194
21144291-9	2006	(4)The expression levels of P53, P21, Fas, FasL and Bax were remarkably up-regulated after treatment with MSA.	methylselenic acid	106-109	P53	Homo sapiens	28-31
16518417-4	2006	On the other hand, pretreatment with dicoumarol enhanced cytotoxicity of CDDP in three cell lines with wild type of p53 (RT112, 253J and LNCap), but not in three other cell lines with mutant p53 or in RT112 stable transfectants with a dominant-negative mutant of p53.	Cisplatin	73-77	P53	Homo sapiens	191-194
21144296-12	2006	Meanwhile the apoptotic rate of A549 cells was 28.99%+-1.07% in Ad-p53+DDP group, which was significantly higher than that in Ad-p53 group (15.35%+-1.31%, P &lt; 0.001) and DDP group (1.74%+-0.77%, P &lt; 0.001).	Cisplatin	71-74	P53	Homo sapiens	67-70
21144296-13	2006	The apoptotic rate of GLC-82 cells was 62.98%+-2.43% in Ad-p53+DDP group, which was significantly higher than that in Ad-p53 group (20.88%+-0.71%, P &lt; 0.001) and DDP group (6.91%+-1.52%, P &lt; 0.001).	Cisplatin	63-66	P53	Homo sapiens	59-62
16518417-5	2006	In RT112 and LNCap, CDDP induced p53 and p21 expression, while pretreatment of dicoumarol suppressed induction of p53/p21 and resulted in sequential activation of c-Jun N-terminal kinase (JNK) in a time-dependent manner.	Cisplatin	20-24	P53	Homo sapiens	33-36
16518417-7	2006	These results suggested that dicoumarol could enhance cytotoxicity of CDDP in urogenital cancer cells with wild-type p53 through the p53/p21/JNK pathways.	Cisplatin	70-74	P53	Homo sapiens	117-120
16518417-7	2006	These results suggested that dicoumarol could enhance cytotoxicity of CDDP in urogenital cancer cells with wild-type p53 through the p53/p21/JNK pathways.	Cisplatin	70-74	P53	Homo sapiens	133-136
16518418-3	2006	In FaDu xenografts, a poorly differentiated tumor-expressing mutant p53, the cure rate was increased from 30% with irinotecan alone to 100% with the combination of irinotecan and MSC.	Irinotecan	115-125	P53	Homo sapiens	68-71
16518418-3	2006	In FaDu xenografts, a poorly differentiated tumor-expressing mutant p53, the cure rate was increased from 30% with irinotecan alone to 100% with the combination of irinotecan and MSC.	Irinotecan	164-174	P53	Homo sapiens	68-71
16585172-13	2006	p53+/+ mitochondrial extracts had higher DNA polymerase-gamma activity measured by (32)P-dCTP incorporation into a single-nucleotide gap oligonucleotide, and recombinant p53 complemented p53-/- mitochondrial extract DNA polymerase-gamma activity.	Oligonucleotides	137-152	P53	Homo sapiens	170-173
16618762-1	2006	SIRT1 and other NAD-dependent deacetylases have been implicated in control of cellular responses to stress and in tumorigenesis through deacetylation of important regulatory proteins, including p53 and the BCL6 oncoprotein.	NAD	16-19	P53	Homo sapiens	194-197
16287077-9	2006	Cells treated with E2 or 4-OHE2 at doses of 0.007 nM and 70 nM and 2-OHE2 only at a higher dose (3.6 microM) exhibited a 5 bp deletion in p53 exon 4.	Estradiol	19-21	P53	Homo sapiens	138-141
16625088-12	2006	Expression of p53 was present in 92% of the FS areas and in only 3% of adjacent DFSP areas.	phenylalanylserine	44-46	P53	Homo sapiens	14-17
16585172-9	2006	Mitochondrial extracts from p53+/+ cells more efficiently stimulated (32)P-dCTP incorporation into a uracil-oligonucleotide.	(32)p-dctp	69-79	P53	Homo sapiens	28-31
16585172-10	2006	Recombinant p53 complemented p53-/- mitochondrial extract repair of uracil or 8-oxo-G-containing oligonucleotides.	Oligonucleotides	97-113	P53	Homo sapiens	12-15
16585172-10	2006	Recombinant p53 complemented p53-/- mitochondrial extract repair of uracil or 8-oxo-G-containing oligonucleotides.	Oligonucleotides	97-113	P53	Homo sapiens	29-32
16585172-11	2006	As a measure of DNA glycosylase activity, p53+/+ mitochondrial extracts more efficiently incised uracil or 8-oxo-G oligonucleotides, although recombinant p53 could not stimulate oligonucleotide incision.	Oligonucleotides	115-130	P53	Homo sapiens	42-45
16585172-13	2006	p53+/+ mitochondrial extracts had higher DNA polymerase-gamma activity measured by (32)P-dCTP incorporation into a single-nucleotide gap oligonucleotide, and recombinant p53 complemented p53-/- mitochondrial extract DNA polymerase-gamma activity.	2'-deoxycytidine 5'-triphosphate	89-93	P53	Homo sapiens	0-3
16585172-13	2006	p53+/+ mitochondrial extracts had higher DNA polymerase-gamma activity measured by (32)P-dCTP incorporation into a single-nucleotide gap oligonucleotide, and recombinant p53 complemented p53-/- mitochondrial extract DNA polymerase-gamma activity.	2'-deoxycytidine 5'-triphosphate	89-93	P53	Homo sapiens	170-173
16585172-13	2006	p53+/+ mitochondrial extracts had higher DNA polymerase-gamma activity measured by (32)P-dCTP incorporation into a single-nucleotide gap oligonucleotide, and recombinant p53 complemented p53-/- mitochondrial extract DNA polymerase-gamma activity.	2'-deoxycytidine 5'-triphosphate	89-93	P53	Homo sapiens	170-173
16616141-0	2006	Evidence that low doses of Taxol enhance the functional transactivatory properties of p53 on p21 waf promoter in MCF-7 breast cancer cells.	Paclitaxel	27-32	P53	Homo sapiens	86-89
16616141-1	2006	In the present study, we evidence how in breast cancer cells low doses of Taxol for 18 h determined the upregulation of p53 and p21 waf expression concomitantly with a decrease of the anti-apoptotic Bcl-2.	Paclitaxel	74-79	P53	Homo sapiens	120-123
16616141-3	2006	Indeed, the most important finding of this study consists with the evidence that Taxol at lower concentrations is able to produce the activation of p21 promoter via p53.	Paclitaxel	81-86	P53	Homo sapiens	165-168
16414312-4	2006	Our results show that, following introduction of the oligonucleotide, the DNA-damage response pathway is activated, evidenced by the presence of phosphorylated p53, Chk1 and Chk2, respectively.	Oligonucleotides	53-68	P53	Homo sapiens	160-163
16288207-0	2006	Regulation of p53 and suppression of apoptosis by the soluble guanylyl cyclase/cGMP pathway in human ovarian cancer cells.	Cyclic GMP	79-83	P53	Homo sapiens	14-17
16288207-11	2006	Thus, the current study establishes that basal sGC/cGMP activity regulates p53 protein stability, content, and function, possibly by altering p53 phosphorylation and stabilization, and promotes cell survival in part through regulation of caspase-3 and p53.	Cyclic GMP	51-55	P53	Homo sapiens	75-78
16288207-11	2006	Thus, the current study establishes that basal sGC/cGMP activity regulates p53 protein stability, content, and function, possibly by altering p53 phosphorylation and stabilization, and promotes cell survival in part through regulation of caspase-3 and p53.	Cyclic GMP	51-55	P53	Homo sapiens	142-145
16288207-11	2006	Thus, the current study establishes that basal sGC/cGMP activity regulates p53 protein stability, content, and function, possibly by altering p53 phosphorylation and stabilization, and promotes cell survival in part through regulation of caspase-3 and p53.	Cyclic GMP	51-55	P53	Homo sapiens	142-145
16211088-0	2006	Adenovirus-mediated p53 gene therapy in osteosarcoma cell lines: sensitization to cisplatin and doxorubicin.	Cisplatin	82-91	P53	Homo sapiens	20-23
16211088-0	2006	Adenovirus-mediated p53 gene therapy in osteosarcoma cell lines: sensitization to cisplatin and doxorubicin.	Doxorubicin	96-107	P53	Homo sapiens	20-23
16314399-6	2006	Furthermore, we found a significant gene-gene interaction between P53BP1 Gln1136Lys and p53 Arg72Pro variants in relation to breast cancer, and the OR of interaction for the presence of both P53BP1 1136Gln/Lys+Lys/Lys and p53 72Arg/Pro+Pro/Pro genotypes was 1.93 (95% CI 1.06-3.52) (P=0.031 for interaction).	Lysine	80-83	P53	Homo sapiens	222-225
16314399-6	2006	Furthermore, we found a significant gene-gene interaction between P53BP1 Gln1136Lys and p53 Arg72Pro variants in relation to breast cancer, and the OR of interaction for the presence of both P53BP1 1136Gln/Lys+Lys/Lys and p53 72Arg/Pro+Pro/Pro genotypes was 1.93 (95% CI 1.06-3.52) (P=0.031 for interaction).	Lysine	206-209	P53	Homo sapiens	88-91
16314399-6	2006	Furthermore, we found a significant gene-gene interaction between P53BP1 Gln1136Lys and p53 Arg72Pro variants in relation to breast cancer, and the OR of interaction for the presence of both P53BP1 1136Gln/Lys+Lys/Lys and p53 72Arg/Pro+Pro/Pro genotypes was 1.93 (95% CI 1.06-3.52) (P=0.031 for interaction).	Lysine	206-209	P53	Homo sapiens	222-225
16314399-6	2006	Furthermore, we found a significant gene-gene interaction between P53BP1 Gln1136Lys and p53 Arg72Pro variants in relation to breast cancer, and the OR of interaction for the presence of both P53BP1 1136Gln/Lys+Lys/Lys and p53 72Arg/Pro+Pro/Pro genotypes was 1.93 (95% CI 1.06-3.52) (P=0.031 for interaction).	Lysine	206-209	P53	Homo sapiens	88-91
16314399-6	2006	Furthermore, we found a significant gene-gene interaction between P53BP1 Gln1136Lys and p53 Arg72Pro variants in relation to breast cancer, and the OR of interaction for the presence of both P53BP1 1136Gln/Lys+Lys/Lys and p53 72Arg/Pro+Pro/Pro genotypes was 1.93 (95% CI 1.06-3.52) (P=0.031 for interaction).	Lysine	206-209	P53	Homo sapiens	222-225
16585172-13	2006	p53+/+ mitochondrial extracts had higher DNA polymerase-gamma activity measured by (32)P-dCTP incorporation into a single-nucleotide gap oligonucleotide, and recombinant p53 complemented p53-/- mitochondrial extract DNA polymerase-gamma activity.	Oligonucleotides	137-152	P53	Homo sapiens	0-3
16585172-13	2006	p53+/+ mitochondrial extracts had higher DNA polymerase-gamma activity measured by (32)P-dCTP incorporation into a single-nucleotide gap oligonucleotide, and recombinant p53 complemented p53-/- mitochondrial extract DNA polymerase-gamma activity.	Oligonucleotides	137-152	P53	Homo sapiens	170-173
16605112-3	2006	AAG to AGT transversion at codon 249 of the P53 gene arg-ser (249ser) has been identified as a hotspot, reflecting DNA damage caused by aflatoxin B1 metabolites in HCC.	Arginine	53-56	P53	Homo sapiens	44-47
16605112-3	2006	AAG to AGT transversion at codon 249 of the P53 gene arg-ser (249ser) has been identified as a hotspot, reflecting DNA damage caused by aflatoxin B1 metabolites in HCC.	Serine	57-60	P53	Homo sapiens	44-47
18603889-0	2006	Evaluation of endometrial changes and p53 expression in tamoxifen treated women: comparison of various methods.	Tamoxifen	56-65	P53	Homo sapiens	38-41
16518869-2	2006	RSV induced apoptosis in all the cells in a dose-dependent manner; however, Bax+/- and p53+/+ cells were more susceptible than their knockout counterparts (Bax-/- and p53-/-, respectively).	Resveratrol	0-3	P53	Homo sapiens	87-90
16499995-11	2006	Somatic TP53 mutations were found in 62 out of 240 NSCLC patients (26%), more frequently in Pro carriers (31%) than in Arg homozygotes (20%, p = 0.06).	Arginine	119-122	P53	Homo sapiens	8-12
16537920-0	2006	Acetylation of p53 at lysine 373/382 by the histone deacetylase inhibitor depsipeptide induces expression of p21(Waf1/Cip1).	Lysine	22-28	P53	Homo sapiens	15-18
16537920-4	2006	That p53 was acetylated after depsipeptide treatment was tested by sequential immunoprecipitation/Western immunoblot analysis with anti-acetylated lysines and anti-p53 antibodies.	Lysine	147-154	P53	Homo sapiens	5-8
16436515-4	2006	First, it induced the acetylation of p53 at lysine 320 and its dephosphorylation at serine 392 but not p53 activity.	Lysine	44-50	P53	Homo sapiens	37-40
16436515-5	2006	Later on, it triggered a DNA signaling pathway, the phosphorylation of p53 at serine 15 and its transcriptional activity.	Serine	78-84	P53	Homo sapiens	71-74
16436515-8	2006	More important, RNA interference against ATM inhibited p53 phosphorylation at serine 15, p53 activity and senescence in response to beta-interferon.	Serine	78-84	P53	Homo sapiens	55-58
16518869-2	2006	RSV induced apoptosis in all the cells in a dose-dependent manner; however, Bax+/- and p53+/+ cells were more susceptible than their knockout counterparts (Bax-/- and p53-/-, respectively).	Resveratrol	0-3	P53	Homo sapiens	167-170
16540663-9	2006	Inhibition of Akt facilitated Smac release and sensitized chemoresistant cells to CDDP in a p53-dependent manner.	Cisplatin	82-86	P53	Homo sapiens	92-95
16457841-0	2006	Kinetic computational alanine scanning: application to p53 oligomerization.	Alanine	22-29	P53	Homo sapiens	55-58
16352595-1	2006	Although protein phosphatase magnesium-dependent 1 delta (PPM1D) was initially characterized as a p53-regulated phosphatase responsible for inactivation of p38 MAPK and consequent inactivation of p53, its overexpression and amplification in human breast cancers led us to assess its role in steroid hormone action.	Steroids	291-306	P53	Homo sapiens	98-101
16540646-6	2006	Moreover, inhibition of HMGA1 expression in thyroid cancer cells resulted in increased p53 oligomerization in response to the DNA-damaging agent doxorubicin.	Doxorubicin	145-156	P53	Homo sapiens	87-90
16540663-0	2006	Akt-mediated cisplatin resistance in ovarian cancer: modulation of p53 action on caspase-dependent mitochondrial death pathway.	Cisplatin	13-22	P53	Homo sapiens	67-70
16540663-1	2006	Akt is a determinant of cisplatin [cis-diammine-dichloroplatinum (CDDP)] resistance in ovarian cancer cells, and this may be related to the regulation of p53.	Cisplatin	24-33	P53	Homo sapiens	154-157
16446370-1	2006	DNA damage induced by the topoisomerase I inhibitor irinotecan (CPT-11) triggers in p53(WT) colorectal carcinoma cells a long term cell cycle arrest and in p53MUT cells a transient arrest followed by apoptosis (Magrini, R., Bhonde, M. R., Hanski, M. L., Notter, M., Scherubl, H., Boland, C. R., Zeitz, M., and Hanski, C. (2002) Int.	Irinotecan	52-62	P53	Homo sapiens	84-87
16446370-1	2006	DNA damage induced by the topoisomerase I inhibitor irinotecan (CPT-11) triggers in p53(WT) colorectal carcinoma cells a long term cell cycle arrest and in p53MUT cells a transient arrest followed by apoptosis (Magrini, R., Bhonde, M. R., Hanski, M. L., Notter, M., Scherubl, H., Boland, C. R., Zeitz, M., and Hanski, C. (2002) Int.	Irinotecan	52-62	P53	Homo sapiens	156-159
16446370-1	2006	DNA damage induced by the topoisomerase I inhibitor irinotecan (CPT-11) triggers in p53(WT) colorectal carcinoma cells a long term cell cycle arrest and in p53MUT cells a transient arrest followed by apoptosis (Magrini, R., Bhonde, M. R., Hanski, M. L., Notter, M., Scherubl, H., Boland, C. R., Zeitz, M., and Hanski, C. (2002) Int.	Irinotecan	64-70	P53	Homo sapiens	84-87
16446370-1	2006	DNA damage induced by the topoisomerase I inhibitor irinotecan (CPT-11) triggers in p53(WT) colorectal carcinoma cells a long term cell cycle arrest and in p53MUT cells a transient arrest followed by apoptosis (Magrini, R., Bhonde, M. R., Hanski, M. L., Notter, M., Scherubl, H., Boland, C. R., Zeitz, M., and Hanski, C. (2002) Int.	Irinotecan	64-70	P53	Homo sapiens	156-159
16446370-5	2006	Here we used five p53WT and five p53MUT established colon carcinoma cell lines to identify gene expression alterations associated with apoptosis in p53MUT cells after treatment with SN-38, the irinotecan metabolite.	Irinotecan	182-187	P53	Homo sapiens	18-21
16446370-5	2006	Here we used five p53WT and five p53MUT established colon carcinoma cell lines to identify gene expression alterations associated with apoptosis in p53MUT cells after treatment with SN-38, the irinotecan metabolite.	Irinotecan	182-187	P53	Homo sapiens	33-36
16446370-10	2006	Together, these data indicate that the high expression of mitotic genes in p53MUT cells after SN-38 treatment contributes to DNA damage-induced apoptosis, whereas their suppression in p53WT cells acts as a safeguard mechanism preventing mitosis initiation and the subsequent apoptosis.	Irinotecan	94-99	P53	Homo sapiens	75-78
16533058-4	2006	Like ionizing radiation (IR) and other radiomimetics, breaks induced by C-1027 efficiently activate ATM by phosphorylation at Ser1981, yet unlike other radiomimetics and IR, DNA breaks induced by C-1027 result in normal phosphorylation of p53 and the cell cycle checkpoint kinases (Chk1 and Chk2) in the absence of ATM.	Carbon	72-73	P53	Homo sapiens	239-242
16492706-0	2006	Disruption of G1-phase phospholipid turnover by inhibition of Ca2+-independent phospholipase A2 induces a p53-dependent cell-cycle arrest in G1 phase.	Phospholipids	23-35	P53	Homo sapiens	106-109
16492706-9	2006	Thus, our study reveals hitherto unrecognized cooperation between p53 and iPLA2 to monitor membrane-phospholipid turnover in G1 phase.	Phospholipids	100-112	P53	Homo sapiens	66-69
16492706-10	2006	Disrupting the G1-phase phospholipid turnover by inhibition of iPLA2 activates the p53-p21cip1 checkpoint mechanism, thereby blocking the entry of G1-phase cells into S phase.	Phospholipids	24-36	P53	Homo sapiens	83-86
16540663-1	2006	Akt is a determinant of cisplatin [cis-diammine-dichloroplatinum (CDDP)] resistance in ovarian cancer cells, and this may be related to the regulation of p53.	Cisplatin	35-64	P53	Homo sapiens	154-157
16540663-1	2006	Akt is a determinant of cisplatin [cis-diammine-dichloroplatinum (CDDP)] resistance in ovarian cancer cells, and this may be related to the regulation of p53.	Cisplatin	66-70	P53	Homo sapiens	154-157
16540663-5	2006	Here we show that CDDP induces mitochondrial p53 accumulation, the mitochondrial release of Smac, cytochrome c, and HTR/Omi, and apoptosis in chemosensitive but not in resistant ovarian cancer cells.	Cisplatin	18-22	P53	Homo sapiens	45-48
16540674-0	2006	Capsaicin, a component of red peppers, inhibits the growth of androgen-independent, p53 mutant prostate cancer cells.	Capsaicin	0-9	P53	Homo sapiens	84-87
16552814-8	2006	CONCLUSION: The findings of the present study indicate that p53 codon 72 arginine homozygous genotype may represent a genetic predisposing factor for colon cancer development.	Arginine	73-81	P53	Homo sapiens	60-63
16319070-7	2006	Furthermore, troglitazone induced Ser-392 phosphorylation of p53 via a PPARgamma-dependent pathway and up-regulation of Bax in a p53 wild-type glioma.	Serine	34-37	P53	Homo sapiens	61-64
16180010-6	2006	In contrast, a specific inhibitor of ERK kinase (U0126 or PD98059) could abolish the accumulation as well as the phosphorylation of p53 at Ser15.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	58-65	P53	Homo sapiens	132-135
16377624-3	2006	Recent studies revealed that phosphorylation of p53 on Ser(46) was associated with induction of p53AIP1 expression, resulting in the commitment of the cell fate into apoptotic cell death.	Serine	55-58	P53	Homo sapiens	48-51
16377624-4	2006	Moreover, upon exposure to genotoxic stress, p53DINP1 was expressed and recruited a kinase(s) to p53 that specifically phosphorylated Ser(46).	Serine	134-137	P53	Homo sapiens	45-48
16377624-5	2006	Here, we show that the pro-apoptotic kinase, protein kinase C delta (PKCdelta), is involved in phosphorylation of p53 on Ser(46).	Serine	121-124	P53	Homo sapiens	114-117
16377624-8	2006	Consistent with these results, PKCdelta potentiates p53-dependent apoptosis by Ser(46) phosphorylation in response to genotoxic stress.	Serine	79-82	P53	Homo sapiens	52-55
16619520-0	2006	Antisense p53 oligonucleotides inhibit proliferation and induce chemosensitivity in follicular thyroid cancer cells.	Oligonucleotides	14-30	P53	Homo sapiens	10-13
16508959-11	2006	Caveolin 1 induction and stresses with both IL-1beta and H2O2 up-regulated p53 and p21 and down-regulated phosphorylated retinoblastoma (Rb), suggesting that the p53/p21/Rb phosphorylation pathway, as well as prolonged p38 MAPK activation, may mediate the features of chondrocyte senescence induced by stress.	Hydrogen Peroxide	57-61	P53	Homo sapiens	75-78
16508959-11	2006	Caveolin 1 induction and stresses with both IL-1beta and H2O2 up-regulated p53 and p21 and down-regulated phosphorylated retinoblastoma (Rb), suggesting that the p53/p21/Rb phosphorylation pathway, as well as prolonged p38 MAPK activation, may mediate the features of chondrocyte senescence induced by stress.	Hydrogen Peroxide	57-61	P53	Homo sapiens	162-165
16549753-0	2006	Cisplatin-induced growth arrest of head and neck cancer cells correlates with increased expression of p16 and p53.	Cisplatin	0-9	P53	Homo sapiens	110-113
16549753-8	2006	RESULTS: There was increased expression of p16, p21, p53, BCLxL, and BCLxS genes with cisplatin treatment in the CCL23 and CCL23AS cells.	Cisplatin	86-95	P53	Homo sapiens	53-56
16251206-7	2006	We have found that the sequence specificities of Cr(III)-DNA and Cr(III)-histidine-DNA adducts in the p53 gene sequence are identical and that both types of adducts are preferentially formed at -NGG- sequences, including codons 245, 248 and 249, the mutational hotspots in human lung cancer.	Histidine	73-82	P53	Homo sapiens	102-105
16549753-15	2006	CONCLUSIONS: These results, in combination with increased expression of the p53 downstream effecter p21, indicate that the cisplatin-induced cell cycle arrest operates through the p16/p53-dependent pathway, and a caspase-independent pathway may be involved.	Cisplatin	123-132	P53	Homo sapiens	76-79
16549753-15	2006	CONCLUSIONS: These results, in combination with increased expression of the p53 downstream effecter p21, indicate that the cisplatin-induced cell cycle arrest operates through the p16/p53-dependent pathway, and a caspase-independent pathway may be involved.	Cisplatin	123-132	P53	Homo sapiens	184-187
16376585-5	2006	A decrease in expression of Bcl-2, Bcl-X(L) and pro-caspase-3 was observed after exposure to 40 microM curcumin, while the levels of p53 and Bax were increased in the curcumin-treated cells.	Curcumin	103-111	P53	Homo sapiens	133-136
17073159-4	2006	Estradiol stimulated p53 expression and decreased DNA-binding activity of NF-kappaB.	Estradiol	0-9	P53	Homo sapiens	21-24
16376585-5	2006	A decrease in expression of Bcl-2, Bcl-X(L) and pro-caspase-3 was observed after exposure to 40 microM curcumin, while the levels of p53 and Bax were increased in the curcumin-treated cells.	Curcumin	167-175	P53	Homo sapiens	133-136
16481746-4	2006	Third, the molecular features of p53 residues 47-58 imitate those of single stranded DNA in their interaction with the oligonucleotide oliogsaccharide-binding (OB) fold of the N-terminal domain of RPA70.	Oligonucleotides	119-134	P53	Homo sapiens	33-36
16152620-3	2006	This report shows that U0126 inhibits early response (ERK) kinase activation and cyclin A expression in wt p53 C8161 melanoma exposed to either UV radiation or betulinic acid.	betulinic acid	160-174	P53	Homo sapiens	107-110
16569192-5	2006	Induction of p53 and p21(Waf1/Cip1) by DOX were delayed in LNCaP cells stably overexpressing PCGEM1 (LNCaP-PCGEM1 cells) compared to control LNCaP cells.	Doxorubicin	39-42	P53	Homo sapiens	13-16
16393695-0	2006	Insulin-like growth factor-1 prevents Abeta[25-35]/(H2O2)- induced apoptosis in lymphocytes by reciprocal NF-kappaB activation and p53 inhibition via PI3K-dependent pathway.	Hydrogen Peroxide	52-56	P53	Homo sapiens	131-134
16544944-0	2006	Threshold effects of nitric oxide-induced toxicity and cellular responses in wild-type and p53-null human lymphoblastoid cells.	Nitric Oxide	21-33	P53	Homo sapiens	91-94
16552184-0	2006	CDK9 phosphorylates p53 on serine residues 33, 315 and 392.	Serine	27-33	P53	Homo sapiens	20-23
16397624-5	2006	DeltaNp73 downregulation by an antisense oligonucleotide leads to transcriptional re-activation of p53-regulated genes and apoptosis.	Oligonucleotides	41-56	P53	Homo sapiens	99-102
16569330-6	2006	DNA was extracted from the buccal swabs and PCR amplification of p53 arginine(Arg)72 and proline(Pro)72 variants was performed.	Arginine	69-77	P53	Homo sapiens	65-68
16474133-6	2006	As a consequence, vIRF1 expression greatly reduced the level of serine 15 phosphorylation of p53, resulting in an increase of p53 ubiquitination and thereby a decrease of its protein stability.	Serine	64-70	P53	Homo sapiens	93-96
16787365-5	2006	In addition to inducing p300 degradation curcumin inhibited the acetyltransferase activity of purified p300 as assessed using either histone H3 or p53 as substrate.	Curcumin	41-49	P53	Homo sapiens	147-150
16546733-6	2006	Clonogenic survival assays up to 12 Gy demonstrated that p53-defective Hep3b cells (SER of 2.68+/-0.24) were sensitized by PTX (2 mmol/L).	Serine	84-87	P53	Homo sapiens	57-60
16646561-2	2006	The codon 72 polymorphism on exon 4 in the p53 gene produces variant proteins with either arginine (Arg) or proline (Pro), and is associated with an increased susceptibility of cancers of the lung, esophagus, breast, cervix and nasopharynx on a genetic basis.	Arginine	90-98	P53	Homo sapiens	43-46
16646561-2	2006	The codon 72 polymorphism on exon 4 in the p53 gene produces variant proteins with either arginine (Arg) or proline (Pro), and is associated with an increased susceptibility of cancers of the lung, esophagus, breast, cervix and nasopharynx on a genetic basis.	Arginine	100-103	P53	Homo sapiens	43-46
16646561-8	2006	As the frequency of p53 Arg allele increased, the cancer was of a more poorly differentiated type.	Arginine	24-27	P53	Homo sapiens	20-23
16646561-10	2006	Increased frequency of p53 Arg allele is associated with more poorly differentiated cancers.	Arginine	27-30	P53	Homo sapiens	23-26
16385586-2	2006	Since genomic instability and phenotypic change are observed in presenescent cells without specific exposure to mutagens, we hypothesized that reactive oxygen species (ROS) produced during normal cell metabolism coupled with deficient p53 dependent DNA damage repair pathways make a significant contribution to immortalization related parameters.	Reactive Oxygen Species	143-166	P53	Homo sapiens	235-238
16385586-2	2006	Since genomic instability and phenotypic change are observed in presenescent cells without specific exposure to mutagens, we hypothesized that reactive oxygen species (ROS) produced during normal cell metabolism coupled with deficient p53 dependent DNA damage repair pathways make a significant contribution to immortalization related parameters.	Reactive Oxygen Species	168-171	P53	Homo sapiens	235-238
16247456-0	2006	Defect in serine 46 phosphorylation of p53 contributes to acquisition of p53 resistance in oral squamous cell carcinoma cells.	Serine	10-16	P53	Homo sapiens	39-42
16736613-8	2006	Associated with p53, HIF-1alpha may induce apoptosis, which decreases oxygen consumption and lightens hypoxia in the scar maturation.	Oxygen	70-76	P53	Homo sapiens	16-19
16338954-10	2006	Arsenite raised the levels of phospho-p53 (serine-15) and p53 (DO-1) proteins in both the securin-wild-type and -null cells.	Serine	43-49	P53	Homo sapiens	38-41
16318864-6	2006	After adjustment for other possible confounders, the incidence of p53 overexpression was significantly decreased in patients with Pro/Pro genotype with an odds ratio (OR) of 0.21 (95% CI: 0.067-0.64) (p = 0.0065) compared with incidence in patients with Arg/Arg genotype.	Arginine	254-257	P53	Homo sapiens	66-69
16318864-6	2006	After adjustment for other possible confounders, the incidence of p53 overexpression was significantly decreased in patients with Pro/Pro genotype with an odds ratio (OR) of 0.21 (95% CI: 0.067-0.64) (p = 0.0065) compared with incidence in patients with Arg/Arg genotype.	Arginine	258-261	P53	Homo sapiens	66-69
16318864-7	2006	The incidence of p53 overexpression was additively increased with environmental exposure to cigarette smoke, alcohol, and areca quid.	Alcohols	109-116	P53	Homo sapiens	17-20
16318864-11	2006	There was also a higher incidence of, but without reaching a statistical significance, p53 mutation in patients with p53 overexpression (OR[95% CI]: 2.18 [0.52-9.6]) and codon 72 Arg/Arg genotype (OR [95% CI] of 0.8 [0.13-4.2], comparing genotypes of Pro/Pro and Arg/Pro with Arg/Arg).	Arginine	179-182	P53	Homo sapiens	87-90
16318864-11	2006	There was also a higher incidence of, but without reaching a statistical significance, p53 mutation in patients with p53 overexpression (OR[95% CI]: 2.18 [0.52-9.6]) and codon 72 Arg/Arg genotype (OR [95% CI] of 0.8 [0.13-4.2], comparing genotypes of Pro/Pro and Arg/Pro with Arg/Arg).	Arginine	183-186	P53	Homo sapiens	87-90
16318864-11	2006	There was also a higher incidence of, but without reaching a statistical significance, p53 mutation in patients with p53 overexpression (OR[95% CI]: 2.18 [0.52-9.6]) and codon 72 Arg/Arg genotype (OR [95% CI] of 0.8 [0.13-4.2], comparing genotypes of Pro/Pro and Arg/Pro with Arg/Arg).	Arginine	183-186	P53	Homo sapiens	87-90
16318864-11	2006	There was also a higher incidence of, but without reaching a statistical significance, p53 mutation in patients with p53 overexpression (OR[95% CI]: 2.18 [0.52-9.6]) and codon 72 Arg/Arg genotype (OR [95% CI] of 0.8 [0.13-4.2], comparing genotypes of Pro/Pro and Arg/Pro with Arg/Arg).	Arginine	183-186	P53	Homo sapiens	87-90
16318864-11	2006	There was also a higher incidence of, but without reaching a statistical significance, p53 mutation in patients with p53 overexpression (OR[95% CI]: 2.18 [0.52-9.6]) and codon 72 Arg/Arg genotype (OR [95% CI] of 0.8 [0.13-4.2], comparing genotypes of Pro/Pro and Arg/Pro with Arg/Arg).	Arginine	183-186	P53	Homo sapiens	87-90
16247456-0	2006	Defect in serine 46 phosphorylation of p53 contributes to acquisition of p53 resistance in oral squamous cell carcinoma cells.	Serine	10-16	P53	Homo sapiens	73-76
16247456-4	2006	We found that phosphorylation of exogenous p53 on serine 46 (Ser46) was severely impaired in HSC-3 but not HSC-4 cells.	Serine	50-56	P53	Homo sapiens	43-46
16108013-0	2006	Small interfering RNA targeting survivin sensitizes lung cancer cell with mutant p53 to adriamycin.	Doxorubicin	88-98	P53	Homo sapiens	81-84
16461914-4	2006	The NMR spectrum (15N,1H transverse relaxation optimized spectroscopy) of full-length p53 was close to that expected from the sum of the spectra of isolated individual domains.	Hydrogen	22-24	P53	Homo sapiens	86-89
16489034-0	2006	Expression of p53 enhances selenite-induced superoxide production and apoptosis in human prostate cancer cells.	Superoxides	44-54	P53	Homo sapiens	14-17
16489034-4	2006	In addition, we also showed that superoxide production by selenite was p53 dependent.	Superoxides	33-43	P53	Homo sapiens	71-74
16489034-10	2006	On the other hand, restoration of wild-type p53 expression in PC3 cells increased cellular sensitivity to selenite and resulted in increased superoxide production, caspase-9 activation, and apoptosis following selenite treatment.	Superoxides	141-151	P53	Homo sapiens	44-47
16489034-11	2006	These results suggest that selenite induces apoptosis by producing superoxide to activate p53 and to induce p53 mitochondrial translocation.	Superoxides	67-77	P53	Homo sapiens	90-93
16489034-12	2006	Activation of p53 in turn synergistically enhances superoxide production and apoptosis induced by selenite.	Superoxides	51-61	P53	Homo sapiens	14-17
16427050-2	2006	We found that LXR-mediated trans-activation was inhibited by 3-methylchoranthrene (MC) and doxorubicin (Dox) in HepG2 cells carrying wild-type p53, but not in Hep3B cells possessing mutant p53.	Doxorubicin	104-107	P53	Homo sapiens	143-146
16521213-10	2006	When only the data from the 11 patients treated with anthraquinone drug, mitoxantrone, were analyzed, however, the number of patients who showed poor response to treatment was significantly higher among the p53-positive patients (P=0.012), irrespective of the survival outcome.	Anthraquinones	53-66	P53	Homo sapiens	207-210
16521213-12	2006	Similarly, immunostaining to evaluate p53 protein may be useful to predict the response in patients treated with an anthraquinone drug.	Anthraquinones	116-129	P53	Homo sapiens	38-41
16378598-0	2006	Inhibition of the PI3 kinase/Akt pathway enhances doxorubicin-induced apoptotic cell death in tumor cells in a p53-dependent manner.	Doxorubicin	50-61	P53	Homo sapiens	111-114
16378598-3	2006	Although a PI3 kinase inhibitor, LY294002, by itself does not induce apoptotic cell death, LY294002 selectively and markedly enhances the apoptosis-inducing efficacy of doxorubicin: such an enhanced cell death is only detected in tumor cells in which the PI3 kinase/Akt pathway is constitutively activated, and it is totally dependent on the functional p53 pathway.	Doxorubicin	169-180	P53	Homo sapiens	353-356
16378598-4	2006	These results suggest that the combination of a PI3 kinase/Akt pathway inhibitor and doxorubicin provides an efficient chemotherapeutic strategy for the treatment of tumor cells in which the PI3 kinase/Akt pathway is constitutively activated and the p53 pathway is functional.	Doxorubicin	85-96	P53	Homo sapiens	250-253
16360120-4	2006	Large foci containing phosphorylated ATM and gamma-H2AX co-localized and foci with p53 phosphorylated at serine 15 also showed the same distribution.	Serine	105-111	P53	Homo sapiens	83-86
16442104-5	2006	Treatment of IMR-90 cells with CKII inhibitors 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole and apigenin led cells to acquire a senescent phenotype as judged by the senescence-associated beta-galactosidase marker and overexpression of p53 and p21(Waf-1).	Dichlororibofuranosylbenzimidazole	47-95	P53	Homo sapiens	239-242
16364249-0	2006	TP53 and P21 polymorphisms: response to cisplatinum/paclitaxel-based chemotherapy in ovarian cancer.	Cisplatin	40-51	P53	Homo sapiens	0-4
16483679-7	2006	In previous work, we demonstrated that TNF-alpha promotes DOX-induced cell death and anti-cancer effect through downregulation of p21 in p53-deficient tumor cells.	Doxorubicin	58-61	P53	Homo sapiens	137-140
16364249-0	2006	TP53 and P21 polymorphisms: response to cisplatinum/paclitaxel-based chemotherapy in ovarian cancer.	Paclitaxel	52-62	P53	Homo sapiens	0-4
16428935-5	2006	In contrast, LDM induced only G2/M arrest in p53-mutant MCF-7/DOX cells.	Doxorubicin	62-65	P53	Homo sapiens	45-48
16357521-0	2006	ENU administration causes genomic instability along with single nucleotide polymorphisms in p53 during gliomagenesis: T11TS administration demonstrated in vivo apoptosis of these genetically altered tumor cells.	t11ts	118-123	P53	Homo sapiens	92-95
16477330-2	2006	This study investigated the genotype distribution of p53 codon 72 polymorphism in hypopharyngeal cancer patients and non-cancer controls matched for age, gender, alcohol consumption and smoking habit.	Alcohols	162-169	P53	Homo sapiens	53-56
16433685-6	2006	Normal human dermal fibroblasts exposed in vitro to IR accumulated p53 protein, involving p53 stabilization and phosphorylation of serine 15 (Ser15) and Ser20.	Serine	131-137	P53	Homo sapiens	67-70
16293626-0	2006	DNA damage promotes histone deacetylase 4 nuclear localization and repression of G2/M promoters, via p53 C-terminal lysines.	Lysine	116-123	P53	Homo sapiens	101-104
16280384-7	2006	The AFB1-mediated decrease in p53 continued for at least 12 h after 30-min exposures to 1.5 muM AFB(1).	afb	4-7	P53	Homo sapiens	30-33
16432214-10	2006	In response to doxorubicin-induced DNA damage, there was clear allele discrimination based on p53 binding at the FLT1-T but not FLT1-C promoters as well as p53-dependent induction of flt-1 mRNA, which required the presence of FLT1-T. Our results establish that p53 can differentially stimulate transcription at a polymorphic variant of the flt-1 promoter and directly places the VEGF system in the p53 stress-response network via flt-1 in a significant fraction of the human population.	Doxorubicin	15-26	P53	Homo sapiens	94-97
16432214-10	2006	In response to doxorubicin-induced DNA damage, there was clear allele discrimination based on p53 binding at the FLT1-T but not FLT1-C promoters as well as p53-dependent induction of flt-1 mRNA, which required the presence of FLT1-T. Our results establish that p53 can differentially stimulate transcription at a polymorphic variant of the flt-1 promoter and directly places the VEGF system in the p53 stress-response network via flt-1 in a significant fraction of the human population.	Doxorubicin	15-26	P53	Homo sapiens	156-159
16432214-10	2006	In response to doxorubicin-induced DNA damage, there was clear allele discrimination based on p53 binding at the FLT1-T but not FLT1-C promoters as well as p53-dependent induction of flt-1 mRNA, which required the presence of FLT1-T. Our results establish that p53 can differentially stimulate transcription at a polymorphic variant of the flt-1 promoter and directly places the VEGF system in the p53 stress-response network via flt-1 in a significant fraction of the human population.	Doxorubicin	15-26	P53	Homo sapiens	156-159
16432214-10	2006	In response to doxorubicin-induced DNA damage, there was clear allele discrimination based on p53 binding at the FLT1-T but not FLT1-C promoters as well as p53-dependent induction of flt-1 mRNA, which required the presence of FLT1-T. Our results establish that p53 can differentially stimulate transcription at a polymorphic variant of the flt-1 promoter and directly places the VEGF system in the p53 stress-response network via flt-1 in a significant fraction of the human population.	Doxorubicin	15-26	P53	Homo sapiens	156-159
16513842-11	2006	The synergistic effect of simultaneous treatment with trichostatin A and doxorubicin is mediated via inhibition of AR expression, induction of protease activity, increased expression of p53, and proteolysis of p21.	Doxorubicin	73-84	P53	Homo sapiens	186-189
16391851-13	2006	These findings suggest that the possible mechanism of cell death in Doxorubicin and Docetaxel/Doxorubicin treatment groups is related to apoptosis through the p53 pathway.	Doxorubicin	68-79	P53	Homo sapiens	159-162
16391851-13	2006	These findings suggest that the possible mechanism of cell death in Doxorubicin and Docetaxel/Doxorubicin treatment groups is related to apoptosis through the p53 pathway.	Doxorubicin	94-105	P53	Homo sapiens	159-162
16750013-0	2006	[Association of the responsiveness of advanced non-small cell lung cancer to platinum-based chemotherapy with p53 and p73 polymorphisms].	Platinum	77-85	P53	Homo sapiens	110-113
16750013-2	2006	This study examined the relationship between p53 and p73 genetic polymorphisms and the response to platinum-based chemotherapy in patients with advanced non-small cell lung cancer (NSCLC).	Platinum	99-107	P53	Homo sapiens	45-48
16750013-10	2006	CONCLUSION: Those results suggest that p53 and p73 polymorphisms may be associated with clinical responsiveness to platinum-based chemotherapy in advanced NSCLC.	Platinum	115-123	P53	Homo sapiens	39-42
16303758-2	2006	We and others have shown that POX is a p53-induced gene that can mediate apoptosis through generation of reactive oxygen species (ROS).	Reactive Oxygen Species	105-128	P53	Homo sapiens	39-42
16293626-5	2006	The C-terminal lysines of p53, which are acetylated and methylated, are required for HDAC4 recruitment and transcriptional repression.	Lysine	15-22	P53	Homo sapiens	26-29
16303758-2	2006	We and others have shown that POX is a p53-induced gene that can mediate apoptosis through generation of reactive oxygen species (ROS).	Reactive Oxygen Species	130-133	P53	Homo sapiens	39-42
16291740-0	2006	Charge modification at multiple C-terminal lysine residues regulates p53 oligomerization and its nucleus-cytoplasm trafficking.	Lysine	43-49	P53	Homo sapiens	69-72
16434701-6	2006	Reporter gene assays confirmed the expected responsiveness of the respective promoter regions to the p53 inducer 5-fluorouracil and 1alpha,25(OH)2D3.	Fluorouracil	113-127	P53	Homo sapiens	101-104
16291740-1	2006	The basal level of the tumor suppressor p53 is regulated by MDM2-mediated ubiquitination at specific lysines, which leads to p53 nuclear export and degradation.	Lysine	101-108	P53	Homo sapiens	40-43
16291740-4	2006	This activity is independent of MDM2 but requires a p53 nuclear export signal and acetylation of multiple lysines by p300.	Lysine	106-113	P53	Homo sapiens	52-55
16291740-1	2006	The basal level of the tumor suppressor p53 is regulated by MDM2-mediated ubiquitination at specific lysines, which leads to p53 nuclear export and degradation.	Lysine	101-108	P53	Homo sapiens	125-128
16291740-5	2006	Mechanistically, we showed that conversion of a minimal four of these lysines to alanines but not arginines mimics p300-mediated p53 nuclear export, and these lysine-neutralizing mutations effectively prevent p53 tetramerization, thus exposing the oligomerization-regulated nuclear export signal.	Lysine	70-77	P53	Homo sapiens	129-132
16291740-5	2006	Mechanistically, we showed that conversion of a minimal four of these lysines to alanines but not arginines mimics p300-mediated p53 nuclear export, and these lysine-neutralizing mutations effectively prevent p53 tetramerization, thus exposing the oligomerization-regulated nuclear export signal.	Lysine	70-77	P53	Homo sapiens	209-212
16291740-2	2006	Upon p53 activation, however, these lysines become acetylated by p300/CREB-binding protein.	Lysine	36-43	P53	Homo sapiens	5-8
16291740-5	2006	Mechanistically, we showed that conversion of a minimal four of these lysines to alanines but not arginines mimics p300-mediated p53 nuclear export, and these lysine-neutralizing mutations effectively prevent p53 tetramerization, thus exposing the oligomerization-regulated nuclear export signal.	Alanine	81-89	P53	Homo sapiens	129-132
16291740-5	2006	Mechanistically, we showed that conversion of a minimal four of these lysines to alanines but not arginines mimics p300-mediated p53 nuclear export, and these lysine-neutralizing mutations effectively prevent p53 tetramerization, thus exposing the oligomerization-regulated nuclear export signal.	Alanine	81-89	P53	Homo sapiens	209-212
16300733-0	2006	Recognition of cisplatin-damaged DNA by p53 protein: critical role of the p53 C-terminal domain.	Cisplatin	15-24	P53	Homo sapiens	40-43
16291740-5	2006	Mechanistically, we showed that conversion of a minimal four of these lysines to alanines but not arginines mimics p300-mediated p53 nuclear export, and these lysine-neutralizing mutations effectively prevent p53 tetramerization, thus exposing the oligomerization-regulated nuclear export signal.	Lysine	70-76	P53	Homo sapiens	129-132
16291740-5	2006	Mechanistically, we showed that conversion of a minimal four of these lysines to alanines but not arginines mimics p300-mediated p53 nuclear export, and these lysine-neutralizing mutations effectively prevent p53 tetramerization, thus exposing the oligomerization-regulated nuclear export signal.	Lysine	70-76	P53	Homo sapiens	209-212
16291740-6	2006	Our study suggested a threshold mechanism whereby the degree of acetylation regulates p53 nucleus-cytoplasm trafficking by neutralizing a lysine-dependent charge patch, which in turn, controls oligomerization-dependent p53 nuclear export.	Lysine	138-144	P53	Homo sapiens	86-89
16291740-6	2006	Our study suggested a threshold mechanism whereby the degree of acetylation regulates p53 nucleus-cytoplasm trafficking by neutralizing a lysine-dependent charge patch, which in turn, controls oligomerization-dependent p53 nuclear export.	Lysine	138-144	P53	Homo sapiens	219-222
16313886-4	2006	Phosphospecific antibodies indicated that TG2 phosphorylated p53 at Ser(15) and Ser(20), residues that are critically important in the interaction of p53 with Mdm2.	Serine	68-71	P53	Homo sapiens	61-64
16313886-4	2006	Phosphospecific antibodies indicated that TG2 phosphorylated p53 at Ser(15) and Ser(20), residues that are critically important in the interaction of p53 with Mdm2.	Serine	80-83	P53	Homo sapiens	150-153
16300733-0	2006	Recognition of cisplatin-damaged DNA by p53 protein: critical role of the p53 C-terminal domain.	Cisplatin	15-24	P53	Homo sapiens	74-77
16300733-1	2006	It was shown previously that the p53 protein can recognize DNA modified with antitumor agent cisplatin (cisPt-DNA).	Cisplatin	93-102	P53	Homo sapiens	33-36
16300733-5	2006	Oxidation of cysteine residues within the CD of posttranslationally unmodified full length p53 did not affect its ability to recognize cisPt-DNA.	Cysteine	13-21	P53	Homo sapiens	91-94
16300733-5	2006	Oxidation of cysteine residues within the CD of posttranslationally unmodified full length p53 did not affect its ability to recognize cisPt-DNA.	Cadmium	42-44	P53	Homo sapiens	91-94
16356831-7	2006	Lower doses of 2-ME and paclitaxel resulted in G1 (but not G2/M) cell cycle arrest in the p53 wild type LNCaP cell line, but with minimal induction of apoptosis.	Paclitaxel	24-34	P53	Homo sapiens	90-93
16440412-6	2006	In SNU-5 cells treated with 25-200 micromol/L berberine, G2/M cell cycle arrest was observed which was associated with a marked increment of the expression of p53, Wee1 and CDk1 proteins and decreased cyclin B.	Berberine	46-55	P53	Homo sapiens	159-162
16440412-10	2006	CONCLUSION: Berberine induces p53 expression and leads to the decrease of the mitochondrial membrane potential, Cytochrome C release and activation of caspase-3 for the induction of apoptosis.	Berberine	12-21	P53	Homo sapiens	30-33
16649377-4	2006	Proper quality paraffin blocks were chosen for immunohistochemical staining for P53 through the immunoperoxidase method.	Paraffin	15-23	P53	Homo sapiens	80-83
16644573-0	2006	p53 mutation and cyclin D1 amplification correlate with cisplatin sensitivity in xenografted human squamous cell carcinomas from head and neck.	Cisplatin	56-65	P53	Homo sapiens	0-3
16739339-0	2006	P53 gene status in patients with advanced serous epithelial ovarian cancer in relation to response to paclitaxel- plus platinum-based chemotherapy and long-term clinical outcome.	Paclitaxel	102-112	P53	Homo sapiens	0-3
16739339-0	2006	P53 gene status in patients with advanced serous epithelial ovarian cancer in relation to response to paclitaxel- plus platinum-based chemotherapy and long-term clinical outcome.	Platinum	119-127	P53	Homo sapiens	0-3
16739339-1	2006	BACKGROUND: The aim of this retrospective study was to assess whether p53 gene status has any predictive or prognostic relevance in patients with advanced, poorly-differentiated serous epithelial ovarian cancer treated with paclitaxel- plus platinum-based chemotherapy.	Paclitaxel	224-234	P53	Homo sapiens	70-73
16644573-8	2006	Xenografts with p53 mutation showed significantly higher resistance to cisplatin (p &lt; 0.001) and also tumours with cyclin D1 amplification showed significantly higher resistance (p &lt; 0.001).	Cisplatin	71-80	P53	Homo sapiens	16-19
16699611-4	2006	AIM: To investigate the possible association between p53 arginine/72 proline polymorphism and susceptibility to colorectal cancer.	Arginine	57-65	P53	Homo sapiens	53-56
16426974-1	2006	Lysine acetylation of human tumor suppressor p53 in response to cellular stress signals is required for its function as a transcription factor that regulates cell cycle arrest, senescence, or apoptosis.	Lysine	0-6	P53	Homo sapiens	45-48
16319535-5	2006	When mitotic spindle is disrupted by nocodazole, ATM is displaced from centrosomes and colocalizes with phospho-Ser15-p53 under the form of spots dispersed in the mitotic cytoplasm.	Nocodazole	37-47	P53	Homo sapiens	118-121
16319535-6	2006	After release from nocodazole-block, as soon as cells exit mitosis, p53 is redirected to the nucleus and its Ser15 phosphorylation is substituted by phosphorylation at Ser46.	Nocodazole	19-29	P53	Homo sapiens	68-71
17113725-1	2006	BACKGROUND: A common Arg/Pro polymorphism at codon 72 of the TP53 gene has been investigated as a risk factor for cancer in different populations.	Arginine	21-24	P53	Homo sapiens	61-65
16951535-11	2006	These results indicated that some p53-null non-small cell lung cancers could be successfully treated when X-ray radiotherapy was administered with subsequent or concurrent cisplatin chemotherapy.	Cisplatin	172-181	P53	Homo sapiens	34-37
16426974-2	2006	Here, we report small molecules that block lysine 382-acetylated p53 association with the bromodomain of the coactivator CBP, an interaction essential for p53-induced transcription of the cell cycle inhibitor p21 in response to DNA damage.	Lysine	43-49	P53	Homo sapiens	65-68
16426974-2	2006	Here, we report small molecules that block lysine 382-acetylated p53 association with the bromodomain of the coactivator CBP, an interaction essential for p53-induced transcription of the cell cycle inhibitor p21 in response to DNA damage.	Lysine	43-49	P53	Homo sapiens	155-158
17168719-10	2006	Furthermore apoptosis mechanisms are under the control of the cholinergic system (nicotine antiapoptotic via induction of NF-kappaB complexes and phosphorylation of Bad at S112, curare proapoptotic via G0-G1 arrest p21waf-1-dependent, but p53-independent) [16].	Nicotine	82-90	P53	Homo sapiens	239-242
16310931-11	2006	The transduction of 11R-p53 enhanced CDDP-dependent induction of apoptosis.	cddp	37-41	P53	Homo sapiens	24-27
16819112-1	2006	Three groups of four oligonucleotides with special single nucleotide polymorphisms (SNP) sites in exon 4 of the p53 gene were analyzed with ion-pair reversed-phase high-performance liquid chromatography electrospray ionization mass spectrometry tandem mass spectrometry.	Oligonucleotides	21-37	P53	Homo sapiens	112-115
16168468-3	2006	RESULTS: When p53 codon 72 genotype was classified into two subgroups of Arg/Arg and Arg/Pro + Pro/Pro, the Arg/Arg genotype was associated with an increased risk for the development of endometrial cancer (OR = 1.86, 95% CI = 1.06 to 3.26) compared with the Arg/Pro + Pro/Pro genotype (P = 0.0301).	Arginine	73-76	P53	Homo sapiens	14-17
16168468-3	2006	RESULTS: When p53 codon 72 genotype was classified into two subgroups of Arg/Arg and Arg/Pro + Pro/Pro, the Arg/Arg genotype was associated with an increased risk for the development of endometrial cancer (OR = 1.86, 95% CI = 1.06 to 3.26) compared with the Arg/Pro + Pro/Pro genotype (P = 0.0301).	Arginine	77-80	P53	Homo sapiens	14-17
16168468-3	2006	RESULTS: When p53 codon 72 genotype was classified into two subgroups of Arg/Arg and Arg/Pro + Pro/Pro, the Arg/Arg genotype was associated with an increased risk for the development of endometrial cancer (OR = 1.86, 95% CI = 1.06 to 3.26) compared with the Arg/Pro + Pro/Pro genotype (P = 0.0301).	Arginine	77-80	P53	Homo sapiens	14-17
16168468-3	2006	RESULTS: When p53 codon 72 genotype was classified into two subgroups of Arg/Arg and Arg/Pro + Pro/Pro, the Arg/Arg genotype was associated with an increased risk for the development of endometrial cancer (OR = 1.86, 95% CI = 1.06 to 3.26) compared with the Arg/Pro + Pro/Pro genotype (P = 0.0301).	Arginine	77-80	P53	Homo sapiens	14-17
16168468-3	2006	RESULTS: When p53 codon 72 genotype was classified into two subgroups of Arg/Arg and Arg/Pro + Pro/Pro, the Arg/Arg genotype was associated with an increased risk for the development of endometrial cancer (OR = 1.86, 95% CI = 1.06 to 3.26) compared with the Arg/Pro + Pro/Pro genotype (P = 0.0301).	Arginine	77-80	P53	Homo sapiens	14-17
16168468-3	2006	RESULTS: When p53 codon 72 genotype was classified into two subgroups of Arg/Arg and Arg/Pro + Pro/Pro, the Arg/Arg genotype was associated with an increased risk for the development of endometrial cancer (OR = 1.86, 95% CI = 1.06 to 3.26) compared with the Arg/Pro + Pro/Pro genotype (P = 0.0301).	Arginine	77-80	P53	Homo sapiens	14-17
16168468-6	2006	CONCLUSION: Homozygous Arg at codon 72 of the p53 gene may be a risk factor for developing endometrial cancer in a Japanese population.	Arginine	23-26	P53	Homo sapiens	46-49
16569359-1	2006	Our study is aimed at evaluating the presence of p53 and Ki67 expression by immunohistochemistry in a series of 11 paraffin-embedded penile carcinomas.	Paraffin	115-123	P53	Homo sapiens	49-52
16003746-6	2006	Furthermore, BA-induced caspase activation was seen to a minor extent in only 1 of the 10 BL cell lines tested (Ramos, a p53-deficient cell line), but was readily detected in Jurkat cells.	betulinic acid	13-15	P53	Homo sapiens	121-124
16327987-0	2006	Induction of p53-mediated apoptosis and recovery of chemosensitivity through p53 transduction in human glioblastoma cells by cisplatin.	Cisplatin	125-134	P53	Homo sapiens	13-16
16327987-0	2006	Induction of p53-mediated apoptosis and recovery of chemosensitivity through p53 transduction in human glioblastoma cells by cisplatin.	Cisplatin	125-134	P53	Homo sapiens	77-80
16327987-1	2006	Cisplatin is a DNA-damaging chemotherapeutic drug that may have a role in the adjuvant chemotherapy of several solid tumors, such as malignant glioblastoma, and the status of p53 tumor suppressor protein is a critical determinant of cisplatin chemosensitivity.	Cisplatin	0-9	P53	Homo sapiens	175-178
16327987-1	2006	Cisplatin is a DNA-damaging chemotherapeutic drug that may have a role in the adjuvant chemotherapy of several solid tumors, such as malignant glioblastoma, and the status of p53 tumor suppressor protein is a critical determinant of cisplatin chemosensitivity.	Cisplatin	233-242	P53	Homo sapiens	175-178
16327987-2	2006	In the present study, we showed the relationship of p53 status and chemosensitivity of cisplatin between two human malignant glioblastoma cell lines, A172 and T98G, harboring wild-type and mutant-type p53, respectively.	Cisplatin	87-96	P53	Homo sapiens	52-55
16327987-2	2006	In the present study, we showed the relationship of p53 status and chemosensitivity of cisplatin between two human malignant glioblastoma cell lines, A172 and T98G, harboring wild-type and mutant-type p53, respectively.	Cisplatin	87-96	P53	Homo sapiens	201-204
16327987-5	2006	Cisplatin induced the accumulation of p53 and p21 proteins in A172 cells, but not in T98G cells.	Cisplatin	0-9	P53	Homo sapiens	38-41
16896365-4	2006	P53 gene polymorphisms include codon11 Glu/Gln or Lys (GAG-&gt;CAG or AAG), codon 72 Arg/Pro (CGC-&gt;CCC), and codon 248 Arg/Thr (CGG-&gt;TCG).	Glutamic Acid	39-42	P53	Homo sapiens	0-3
16896365-4	2006	P53 gene polymorphisms include codon11 Glu/Gln or Lys (GAG-&gt;CAG or AAG), codon 72 Arg/Pro (CGC-&gt;CCC), and codon 248 Arg/Thr (CGG-&gt;TCG).	GUANOSINE 5'-TRIPHOSPHATE P3-[1-(2-NITROPHENYL)ETHYL ESTER]	63-66	P53	Homo sapiens	0-3
16896365-4	2006	P53 gene polymorphisms include codon11 Glu/Gln or Lys (GAG-&gt;CAG or AAG), codon 72 Arg/Pro (CGC-&gt;CCC), and codon 248 Arg/Thr (CGG-&gt;TCG).	Arginine	85-88	P53	Homo sapiens	0-3
16327987-7	2006	These data strongly suggest that the expression of p53 is essential for the cytotoxic effect of cisplatin in human malignant glioblastoma cells, A172 and T98G, and the introduction of apoptotic signal molecules, such as p53, will be beneficial to achieve chemosensitivity in malignant glioma.	Cisplatin	96-105	P53	Homo sapiens	51-54
17120736-0	2006	P53 regulation of leukemia cells with the blockage of MDM2 by antisense oligonucleotides.	Oligonucleotides	72-88	P53	Homo sapiens	0-3
17120736-1	2006	The changes of expression and function of MDM2 and P53 by MDM2 specific antisense oligonucleotides were investigated in HL60 cells.	Oligonucleotides	82-98	P53	Homo sapiens	51-54
17120736-4	2006	Our results showed that the transfection of MDM2 specific antisense oligonucleotides obviously inhibited MDM2 expression (P &lt; 0.01) and increased the expression of P53 (P &lt; 0.05).	Oligonucleotides	68-84	P53	Homo sapiens	167-170
16720917-13	2006	CONCLUSION: We found that tumors with large volumes, N2 node status, low cellular proliferation rate, positive immunoreactivity to p53, and low differentiation grade have a lower response to neoadjuvant chemotherapy with anthracycline.	Anthracyclines	221-234	P53	Homo sapiens	131-134
16299809-6	2006	There was a negative significant correlation of patients" age and percentage of Ser 392 phosphorylated p53 protein.	Serine	80-83	P53	Homo sapiens	103-106
16580789-0	2006	p53 protein or BID protein select the route to either apoptosis (programmed cell death) or to cell cycle arrest opposing carcinogenesis after DNA damage by ROS.	Reactive Oxygen Species	156-159	P53	Homo sapiens	0-3
16580789-3	2006	Moreover, oxidative stress by reactive oxygen species (ROS) such as the hydroxyl radical (*OH) produced by ionizing radiation (carcinogenic) triggers p53 activation in response to the damage of DNA (followed by initiation of DNA-repair mechanisms).	Reactive Oxygen Species	30-53	P53	Homo sapiens	150-153
16580789-3	2006	Moreover, oxidative stress by reactive oxygen species (ROS) such as the hydroxyl radical (*OH) produced by ionizing radiation (carcinogenic) triggers p53 activation in response to the damage of DNA (followed by initiation of DNA-repair mechanisms).	Reactive Oxygen Species	55-58	P53	Homo sapiens	150-153
16267831-6	2006	TPA-induced activation of ERK1/2 was sustained in wild-type p53 cells, while only a transient activation was seen in mutant p53 cells.	Tetradecanoylphorbol Acetate	0-3	P53	Homo sapiens	124-127
16299809-7	2006	The tumor samples obtained from younger patients of 35 yr and below showed higher percentage of Ser 392 phosphorylated p53 protein compared to the tumors of older patients.	Serine	96-99	P53	Homo sapiens	119-122
16267831-7	2006	Inhibition of MAPK kinase (MEK), an upstream kinase, by U0126, blocked TPA-induced activation of ERK1/2 in wild-type p53 cells and in mutant p53 cells.	Tetradecanoylphorbol Acetate	71-74	P53	Homo sapiens	117-120
16267831-6	2006	TPA-induced activation of ERK1/2 was sustained in wild-type p53 cells, while only a transient activation was seen in mutant p53 cells.	Tetradecanoylphorbol Acetate	0-3	P53	Homo sapiens	60-63
16267831-7	2006	Inhibition of MAPK kinase (MEK), an upstream kinase, by U0126, blocked TPA-induced activation of ERK1/2 in wild-type p53 cells and in mutant p53 cells.	Tetradecanoylphorbol Acetate	71-74	P53	Homo sapiens	141-144
16299809-8	2006	The increased percentage of Ser 392 phosphorylated p53 protein indicates that it could be involved in the acceleration of tumor growth in the younger patients.	Serine	28-31	P53	Homo sapiens	51-54
16267831-8	2006	Treatment of wild-type p53 (SK-Mel 186) cells with small interfering RNA (siRNA) of p53 displayed a transient induction of activation of ERK1/2 following TPA treatment, indicating that p53 has a role in the regulation of the activation of ERK1/2.	Tetradecanoylphorbol Acetate	154-157	P53	Homo sapiens	23-26
16369916-2	2006	Both processes may be modulated at the level of gene expression, viz., p53 and c-Ha-ras, by dietary bioactive components such as resveratrol.	Resveratrol	129-140	P53	Homo sapiens	71-74
16267831-8	2006	Treatment of wild-type p53 (SK-Mel 186) cells with small interfering RNA (siRNA) of p53 displayed a transient induction of activation of ERK1/2 following TPA treatment, indicating that p53 has a role in the regulation of the activation of ERK1/2.	Tetradecanoylphorbol Acetate	154-157	P53	Homo sapiens	84-87
16267831-8	2006	Treatment of wild-type p53 (SK-Mel 186) cells with small interfering RNA (siRNA) of p53 displayed a transient induction of activation of ERK1/2 following TPA treatment, indicating that p53 has a role in the regulation of the activation of ERK1/2.	Tetradecanoylphorbol Acetate	154-157	P53	Homo sapiens	84-87
16267831-10	2006	The expression of either wild-type or mutant p53 had a similar effect on TPA-induced Jun N-terminal kinase (JNK) activation, indicating specificity for the ERK pathway.	Tetradecanoylphorbol Acetate	73-76	P53	Homo sapiens	45-48
16432175-0	2006	Benzodiazepinedione inhibitors of the Hdm2:p53 complex suppress human tumor cell proliferation in vitro and sensitize tumors to doxorubicin in vivo.	Doxorubicin	128-139	P53	Homo sapiens	43-46
16446403-3	2006	Lysine residues at the COOH-terminal region of p53 are implicated as sites for ubiquitination and other post-translational modifications.	Lysine	0-6	P53	Homo sapiens	47-50
16446403-8	2006	In contrast, several conserved lysine residues in the DNA-binding domain are critical for p53 ubiquitination.	Lysine	31-37	P53	Homo sapiens	90-93
16354677-3	2006	Treatment with EX-527 dramatically increased acetylation at lysine 382 of p53 after different types of DNA damage in primary human mammary epithelial cells and several cell lines.	6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide	15-21	P53	Homo sapiens	74-77
16354677-3	2006	Treatment with EX-527 dramatically increased acetylation at lysine 382 of p53 after different types of DNA damage in primary human mammary epithelial cells and several cell lines.	Lysine	60-66	P53	Homo sapiens	74-77
16354677-6	2006	EX-527 and TSA acted synergistically to increase acetyl-p53 levels, confirming that p53 acetylation is regulated by both SIRT1 and HDACs.	6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide	0-6	P53	Homo sapiens	56-59
16354677-6	2006	EX-527 and TSA acted synergistically to increase acetyl-p53 levels, confirming that p53 acetylation is regulated by both SIRT1 and HDACs.	6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide	0-6	P53	Homo sapiens	84-87
16533421-6	2006	Moreover, it appeared that wildtype p53 was required for sensitization to cisplatin because the effect was marginal in A549 and Calu-1 cells, where the p53 pathway is altered and simultaneous restoration of p53 and Fhit in Calu-1 cells increased cisplatin sensitivity.	Cisplatin	74-83	P53	Homo sapiens	36-39
16533421-6	2006	Moreover, it appeared that wildtype p53 was required for sensitization to cisplatin because the effect was marginal in A549 and Calu-1 cells, where the p53 pathway is altered and simultaneous restoration of p53 and Fhit in Calu-1 cells increased cisplatin sensitivity.	Cisplatin	74-83	P53	Homo sapiens	152-155
16533421-6	2006	Moreover, it appeared that wildtype p53 was required for sensitization to cisplatin because the effect was marginal in A549 and Calu-1 cells, where the p53 pathway is altered and simultaneous restoration of p53 and Fhit in Calu-1 cells increased cisplatin sensitivity.	Cisplatin	74-83	P53	Homo sapiens	152-155
16533421-6	2006	Moreover, it appeared that wildtype p53 was required for sensitization to cisplatin because the effect was marginal in A549 and Calu-1 cells, where the p53 pathway is altered and simultaneous restoration of p53 and Fhit in Calu-1 cells increased cisplatin sensitivity.	Cisplatin	246-255	P53	Homo sapiens	36-39
16369916-8	2006	In summary, resveratrol at &lt;8 h induced p53-mediated effects, including apoptosis and cell-cycle arrest (G2/M).	Resveratrol	12-23	P53	Homo sapiens	43-46
17065086-1	2006	Previously, we have found that activation of deoxycytidine kinase elicited by various DNA-damaging chemical agents could be prevented by BAPTA-AM, a cell-permeable calcium chelator or by pifithrin-alpha, a pharmacological inhibitor of p53.	Calcium	164-171	P53	Homo sapiens	235-238
17065050-6	2006	Catalytically inactive p53 seems to increase the sensitivity to troxacitabine.	troxacitabine	64-77	P53	Homo sapiens	23-26
17135787-0	2006	Additional gene therapy with rAAV-wt-p53 enhanced the efficacy of cisplatin in human bladder cancer cells.	Cisplatin	66-75	P53	Homo sapiens	37-40
16554913-9	2006	Our results suggest that Arg allele at codon 72 of p53 gene might affect the risk of ultraviolet-induced basal cell carcinoma.	Arginine	25-28	P53	Homo sapiens	51-54
16470928-5	2006	SGC-7901 cells with mutant p53 showed higher chemotherapeutic sensitivity to 5-Fu than that with mp53+sv40Tag and control (P&lt;0.05), but no difference between those with mp53+sv40Tag and control (P&gt;0.05).	Fluorouracil	77-81	P53	Homo sapiens	27-30
18528466-5	2006	These two p53-regulated proteins control microtubule dynamics, regulate the sensitivity to taxanes and vinca alkaloids by changing the polymerization dynamics of tubulin and affecting the binding of drugs to microtubules.	Taxoids	91-98	P53	Homo sapiens	10-13
18528466-10	2006	We also discovered that p53 could regulate the expression of multidrug resistance protein-1 (MRP1), a member of the ABC family of transporters that mediates the sensitivity to vinca alkaloids and anthracyclines.	Anthracyclines	196-210	P53	Homo sapiens	24-27
18528466-12	2006	We went on to show that p53 regulated the expression of MRP1 and that this produced resistance to doxorubicin and vinblastine.	Doxorubicin	98-109	P53	Homo sapiens	24-27
16626549-9	2006	CONCLUSIONS: The p53 pathway in VSMC was activated post emodin exposure in a concentration-dependent manner and which might be responsible for the observed antiproliferative effects of emodin in vascular smooth muscle cells.	vsmc	32-36	P53	Homo sapiens	17-20
16230356-0	2005	tumor suppressor p53 binds with high affinity to CTG.CAG trinucleotide repeats and induces topological alterations in mismatched duplexes.	trinucleotide	57-70	P53	Homo sapiens	17-20
16230356-5	2005	We demonstrate for the first time that conformationally flexible CTG.CAG trinucleotide repeats comprise a novel class of p53-binding sites targeted by p53 in a DNA structure-dependent mode in vitro and in vivo.	trinucleotide	73-86	P53	Homo sapiens	121-124
16230356-5	2005	We demonstrate for the first time that conformationally flexible CTG.CAG trinucleotide repeats comprise a novel class of p53-binding sites targeted by p53 in a DNA structure-dependent mode in vitro and in vivo.	trinucleotide	73-86	P53	Homo sapiens	151-154
16219768-0	2005	WOX1 is essential for tumor necrosis factor-, UV light-, staurosporine-, and p53-mediated cell death, and its tyrosine 33-phosphorylated form binds and stabilizes serine 46-phosphorylated p53.	Tyrosine	110-118	P53	Homo sapiens	188-191
16219768-0	2005	WOX1 is essential for tumor necrosis factor-, UV light-, staurosporine-, and p53-mediated cell death, and its tyrosine 33-phosphorylated form binds and stabilizes serine 46-phosphorylated p53.	Serine	163-169	P53	Homo sapiens	188-191
16219768-4	2005	Here, we determined that UV light, anisomycin, etoposide, and hypoxic stress rapidly induced phosphorylation of p53 at Ser46 and WOX1 at Tyr33 (phospho-WOX1) and their binding interactions in several tested cancer cells.	Anisomycin	35-45	P53	Homo sapiens	112-115
16275167-4	2005	Cilostazol decreases the activity of phosphodiesterase type 3, leading to the accumulation of cyclic adenosine monophosphate, which initiates a cascade of events including upregulation of anti-oncogenes p53 and p21 and upregulation of hepatocyte growth factor (HGF).	Cyclic AMP	94-124	P53	Homo sapiens	203-206
16236544-2	2005	For the purpose of constructing an easy-operating genotoxicity test system using human cell lines, we developed a p53R2-dependent luciferase reporter gene assay, and demonstrated dose-dependent luminescence caused by adriamycin in two human cell lines that express wild-type p53, MCF-7 and HepG2.	Doxorubicin	217-227	P53	Homo sapiens	114-117
16326430-7	2005	Ethanol-mediated changes in proteins regulated apoptosis (p53 and bcl-2), antioxidant (vitamin E and catalase) activities, generation of reactive oxygen species (ROS), and oxidative DNA damage shown as 8-hydroxy-2"-deoxyguanosine (8-OHdG) were measured in embryonic midbrain cells.	Ethanol	0-7	P53	Homo sapiens	58-61
16326430-9	2005	The levels of p53, bcl-2, and 8-OHdG were concomitantly changed by alcohol and acetaldehyde treatment in midbrain cells.	Alcohols	67-74	P53	Homo sapiens	14-17
15908180-6	2005	Furthermore, the synergistic effect of TNF-alpha/IFN-gamma on apoptosis and ROS production was further potentiated by the overexpression of wild-type p53, but not with mutant p53.	ros	76-79	P53	Homo sapiens	150-153
16333030-12	2005	Blockade of Bax, Bim, and p53 mRNA expression by siRNA reduced estradiol-induced apoptosis relative to control by 76% [95% confidence interval (CI) = 73% to 79%, P &lt; .001], 85% [95% CI = 90% to 80%, P &lt; .001], and 40% [95% CI = 45% to 35%, P &lt; .001], respectively, whereas blockade of FasL by siRNA had no effect.	Estradiol	63-72	P53	Homo sapiens	26-29
16159878-6	2005	Additionally Trx increased p53-DNA binding and expression in response to anthracyclines.	Anthracyclines	73-87	P53	Homo sapiens	27-30
16059916-2	2005	Human cancer cells HeLa (cervix cancer, p53(+/+)), Saos-2 and Saos-2-His-273 (osteosarcoma, p53(-/-) and p53 His-273 mutant, respectively), H1299tTA and H1299tTA-His175 (lung carcinoma, p53(-/-) and p53 His-175 mutant), and normal human fibroblasts VH-10 (p53(+/+)) were used.	Histidine	69-72	P53	Homo sapiens	92-95
16059916-2	2005	Human cancer cells HeLa (cervix cancer, p53(+/+)), Saos-2 and Saos-2-His-273 (osteosarcoma, p53(-/-) and p53 His-273 mutant, respectively), H1299tTA and H1299tTA-His175 (lung carcinoma, p53(-/-) and p53 His-175 mutant), and normal human fibroblasts VH-10 (p53(+/+)) were used.	Histidine	69-72	P53	Homo sapiens	92-95
16059916-2	2005	Human cancer cells HeLa (cervix cancer, p53(+/+)), Saos-2 and Saos-2-His-273 (osteosarcoma, p53(-/-) and p53 His-273 mutant, respectively), H1299tTA and H1299tTA-His175 (lung carcinoma, p53(-/-) and p53 His-175 mutant), and normal human fibroblasts VH-10 (p53(+/+)) were used.	Histidine	69-72	P53	Homo sapiens	92-95
16059916-2	2005	Human cancer cells HeLa (cervix cancer, p53(+/+)), Saos-2 and Saos-2-His-273 (osteosarcoma, p53(-/-) and p53 His-273 mutant, respectively), H1299tTA and H1299tTA-His175 (lung carcinoma, p53(-/-) and p53 His-175 mutant), and normal human fibroblasts VH-10 (p53(+/+)) were used.	Histidine	69-72	P53	Homo sapiens	92-95
16059916-2	2005	Human cancer cells HeLa (cervix cancer, p53(+/+)), Saos-2 and Saos-2-His-273 (osteosarcoma, p53(-/-) and p53 His-273 mutant, respectively), H1299tTA and H1299tTA-His175 (lung carcinoma, p53(-/-) and p53 His-175 mutant), and normal human fibroblasts VH-10 (p53(+/+)) were used.	Histidine	69-72	P53	Homo sapiens	92-95
16302093-0	2005	Curcumin induces human HT-29 colon adenocarcinoma cell apoptosis by activating p53 and regulating apoptosis-related protein expression.	Curcumin	0-8	P53	Homo sapiens	79-82
16302093-5	2005	The colon adenocarcinoma cells were treated with curcumin (0-75 microM) for 0-24 h. We observed that p53 was highly expressed in HT-29 cells and curcumin could up-regulate the serine phosphorylation of p53 in a time- and concentration-dependent manner.	Curcumin	49-57	P53	Homo sapiens	101-104
16302093-5	2005	The colon adenocarcinoma cells were treated with curcumin (0-75 microM) for 0-24 h. We observed that p53 was highly expressed in HT-29 cells and curcumin could up-regulate the serine phosphorylation of p53 in a time- and concentration-dependent manner.	Curcumin	49-57	P53	Homo sapiens	202-205
16302093-5	2005	The colon adenocarcinoma cells were treated with curcumin (0-75 microM) for 0-24 h. We observed that p53 was highly expressed in HT-29 cells and curcumin could up-regulate the serine phosphorylation of p53 in a time- and concentration-dependent manner.	Curcumin	145-153	P53	Homo sapiens	101-104
16302093-5	2005	The colon adenocarcinoma cells were treated with curcumin (0-75 microM) for 0-24 h. We observed that p53 was highly expressed in HT-29 cells and curcumin could up-regulate the serine phosphorylation of p53 in a time- and concentration-dependent manner.	Curcumin	145-153	P53	Homo sapiens	202-205
16302093-5	2005	The colon adenocarcinoma cells were treated with curcumin (0-75 microM) for 0-24 h. We observed that p53 was highly expressed in HT-29 cells and curcumin could up-regulate the serine phosphorylation of p53 in a time- and concentration-dependent manner.	Serine	176-182	P53	Homo sapiens	101-104
16302093-8	2005	These data suggest a possible underlying molecular mechanism whereby curcumin could induce the apoptosis signaling pathway in human HT-29 colon adenocarcinoma cells by p53 activation and by the regulation of apoptosis-related proteins.	Curcumin	69-77	P53	Homo sapiens	168-171
16365016-1	2005	A mutation in codon 249 of the TP53 gene (249(Ser)), related to aflatoxin B(1) exposure, has previously been associated with hepatocellular carcinoma risk.	Serine	46-49	P53	Homo sapiens	31-35
16322229-10	2005	HCV core expression abrogated both p53 serine 15 phosphorylation and lysine 382 acetylation, two p53-activating posttranslational modifications which were previously linked to an increased PML-NB formation.	Serine	39-45	P53	Homo sapiens	35-38
16322252-4	2005	We found that DFMO caused a p53-independent increase in p21 and its association with cyclin-dependent kinase (cdk)-2 and decreased cdk-2 protein as well as its phosphorylation on Thr160.	Eflornithine	14-18	P53	Homo sapiens	28-31
16354872-7	2005	CONCLUSIONS: HPV detected in a small proportion of lung cancer patients in India demonstrated an exclusive prevalence of HPV type 18, and there was a significantly higher frequency of p53 Arg/Arg genotype when compared to that of control subjects.	Arginine	188-191	P53	Homo sapiens	184-187
16322298-1	2005	PURPOSE: We aimed to determine the clinical role of the p53 family members p53 and p73 in the responsiveness to platinum-based chemotherapy and survival in ovarian cancer, considering their cross-talk and the p53 polymorphism at codon 72.	Platinum	112-120	P53	Homo sapiens	56-59
16322298-1	2005	PURPOSE: We aimed to determine the clinical role of the p53 family members p53 and p73 in the responsiveness to platinum-based chemotherapy and survival in ovarian cancer, considering their cross-talk and the p53 polymorphism at codon 72.	Platinum	112-120	P53	Homo sapiens	75-78
16322298-1	2005	PURPOSE: We aimed to determine the clinical role of the p53 family members p53 and p73 in the responsiveness to platinum-based chemotherapy and survival in ovarian cancer, considering their cross-talk and the p53 polymorphism at codon 72.	Platinum	112-120	P53	Homo sapiens	75-78
16322298-10	2005	p53 mutational status was an important determinant of responsiveness to platinum-based chemotherapy in all patients with a residual tumor of &lt;2 cm in diameter after initial surgery (wild-type versus mutant, P = 0.029).	Platinum	72-80	P53	Homo sapiens	0-3
16362795-2	2005	TP53 codon 72, which produces variant proteins with an arginine (Arg) or proline (Pro), has been reported to be associated with cancers of the lung, oesophagus, stomach and cervix.	Arginine	55-63	P53	Homo sapiens	0-4
16354872-7	2005	CONCLUSIONS: HPV detected in a small proportion of lung cancer patients in India demonstrated an exclusive prevalence of HPV type 18, and there was a significantly higher frequency of p53 Arg/Arg genotype when compared to that of control subjects.	Arginine	192-195	P53	Homo sapiens	184-187
16362795-2	2005	TP53 codon 72, which produces variant proteins with an arginine (Arg) or proline (Pro), has been reported to be associated with cancers of the lung, oesophagus, stomach and cervix.	Arginine	65-68	P53	Homo sapiens	0-4
16362795-9	2005	The allele frequencies of the TP53 polymorphism were: Arg=0.74 and Pro=0.26.	Arginine	54-57	P53	Homo sapiens	30-34
16354872-8	2005	Observation of a shorter duration of symptoms (&lt; or = 4 months) in as many as 78% (seven of nine stage IV patients) with Arg/Pro genotype may be an indication that lung cancer patients with the heterozygous p53 genotype are more susceptible to early progression.	Arginine	124-127	P53	Homo sapiens	210-213
16228292-2	2005	We characterized the effects of bcl-2 antisense and cisplatin combination therapy in two human isogenic breast carcinoma cells p53(+)MCF-7 and p53(-)MCF-7/E6.	Cisplatin	52-61	P53	Homo sapiens	143-146
16311126-6	2005	A p53 protein immunohistochemical analysis was performed on paraffin-embedded tissues.	Paraffin	60-68	P53	Homo sapiens	2-5
16311126-11	2005	Of 10 serous papillary carcinomas, 8 (80%) for which paraffin blocks were available overexpressed the p53 protein.	Paraffin	53-61	P53	Homo sapiens	102-105
16099193-7	2005	After cisplatin-induced DNA damage, the increasing levels of p53 lead to the trans-activation of a number of genes but not of p21(Waf1/Cip1), preferentially directing TGCT cells into apoptosis or programmed cell death, both via the mitochondrial and the death receptor apoptosis pathways.	Cisplatin	6-15	P53	Homo sapiens	61-64
16375215-4	2005	Immunostaining for p53 protein was performed on formalin-fixed, paraffin-embedded tissue sections, using the alkaline phosphatase antialkaline phosphatase (APAAP) method.	Paraffin	64-72	P53	Homo sapiens	19-22
16169939-4	2005	We further analyzed the signaling pathways underlying these effects, and we showed that both RDCs and cisplatin induced p53 and p73 protein levels but with different intensities and kinetics.	Cisplatin	102-111	P53	Homo sapiens	120-123
16272802-6	2005	As for the association with environmental factors, p53 mutations occurred with higher frequency in patients with a daily intake of spicy foods and in those who used unboiled well water in the low-incidence area.	Water	179-184	P53	Homo sapiens	51-54
16272802-8	2005	Thus, higher frequency of spicy food intake and use of unboiled well water may be risk factors of esophageal cancer via p53 mutations in China.	Water	69-74	P53	Homo sapiens	120-123
16226226-10	2005	In contrast, p53 mutated Huh-7 hepatocellular cancer cells proved to be less sensitive towards cetuximab, but when combined with TKIs or fluvastatin or doxorubicin a pronounced reduction of cell growth was observed.	Doxorubicin	152-163	P53	Homo sapiens	13-16
16307686-2	2005	Furthermore, the polymorphism at codon 72 (encoding either arginine or proline) of the p53 tumor-suppressor gene is discussed as a possible determinant for cancer risk.	Arginine	59-67	P53	Homo sapiens	87-90
16225614-0	2005	Differential effects of 5-aminolaevulinic acid photodynamic therapy and psoralen + ultraviolet A therapy on p53 phosphorylation in normal human skin in vivo.	Ficusin	72-80	P53	Homo sapiens	108-111
16552971-1	2005	BACKGROUND &amp; OBJECTIVE: P53 pathway plays a critical role in carcinogenesis of pancreatic carcinoma.	Adenosine Monophosphate	12-15	P53	Homo sapiens	28-31
16288013-2	2005	Here, we describe the gene expression profiles associated with four microenvironmental components of the inflammatory response (NO*, H2O2, DNA replication arrest, and hypoxia) that result in p53 stabilization and activation.	Hydrogen Peroxide	133-137	P53	Homo sapiens	191-194
16014005-7	2005	We have also shown that FDH elevation results in p53 phosphorylation at Ser-6 and Ser-20 in the p53 transactivation domain, and Ser-392 in the C-terminal domain, but only Ser-6 is strictly required to mediate FDH effects.	Serine	72-75	P53	Homo sapiens	49-52
16225614-6	2005	Importantly, PUVA treatment resulted in p53 kinase activation, as defined by p53 modification at AT (serine-15) and CK2/FACT (serine-392) sites within the proliferative compartment.	Serine	101-107	P53	Homo sapiens	40-43
16312222-5	2005	All nucleotides in the TP53 gene from exon 2-9 are included on the chip by synthesis and application of sequence-specific oligonucleotides.	Oligonucleotides	122-138	P53	Homo sapiens	23-27
16225614-6	2005	Importantly, PUVA treatment resulted in p53 kinase activation, as defined by p53 modification at AT (serine-15) and CK2/FACT (serine-392) sites within the proliferative compartment.	Serine	101-107	P53	Homo sapiens	77-80
16120770-9	2005	We also observed a decrease in E7 expression with a concurrent increase in p53 protein levels upon cotreatment with shRNA and cisplatin over that seen with individual treatment alone.	Cisplatin	126-135	P53	Homo sapiens	75-78
16271069-12	2005	Noticeably, alcohol consumption could enhance this peculiar spectrum of p53 mutation in ESCC.	Alcohols	12-19	P53	Homo sapiens	72-75
16246896-0	2005	Copper alters the conformation and transcriptional activity of the tumor suppressor protein p53 in human Hep G2 cells.	Copper	0-6	P53	Homo sapiens	92-95
16246896-2	2005	To test the effect of copper on the transcriptional activity of p53, Hep G2 cells were transiently transfected with a luciferase reporter gene downstream from multiple p53 response elements.	Copper	22-28	P53	Homo sapiens	64-67
16246896-5	2005	Oligonucleotide arrays representing 145 known p53-associated genes were hybridized with biotinylated cDNAs from mRNA extracted from control and copper-treated Hep G2 cells.	Oligonucleotides	0-15	P53	Homo sapiens	46-49
16246896-7	2005	Although control Hep G2 cells synthesize wild-type p53, immunocytochemistry identified not only wild type, but also mutant p53 in the presence of copper and other agents that induce oxidative damage.	Copper	146-152	P53	Homo sapiens	123-126
16246896-8	2005	Thus, this report not only identifies genes that may play a role in copper-mediated apoptosis, but also suggests that copper-induced oxidative processes result in the synthesis of mutant p53 with altered transcriptional properties.	Copper	68-74	P53	Homo sapiens	187-190
16246896-8	2005	Thus, this report not only identifies genes that may play a role in copper-mediated apoptosis, but also suggests that copper-induced oxidative processes result in the synthesis of mutant p53 with altered transcriptional properties.	Copper	118-124	P53	Homo sapiens	187-190
16096850-7	2005	In OMS, apoptosis increased, cell proliferation decreased, and p53/p21 expression increased more pronounced following CDDP+RT.	Cisplatin	118-122	P53	Homo sapiens	63-66
16227609-0	2005	DNA damage-induced phosphorylation of MdmX at serine 367 activates p53 by targeting MdmX for Mdm2-dependent degradation.	Serine	46-52	P53	Homo sapiens	67-70
16081268-7	2005	Resveratrol consistently increased by &gt; or =6-fold Mdm2 expression and other downstream p53 effectors, but not p53 itself at 24 h. Subsequent cell cycle analysis indicated a significant accumulation of cells in G2/M, and a decrease in G1/G0 suggesting a G2/M blockade.	Resveratrol	0-11	P53	Homo sapiens	91-94
16120770-10	2005	Our results provide strong evidence that loss of E6 and E7 results in increased sensitivity to cisplatin, probably because of increased p53 levels.	Cisplatin	95-104	P53	Homo sapiens	136-139
16188274-7	2005	Refolding was commenced from unfolded protein in 8M urea, and both the Trp53 to C25-TNB distance and the Trp53 to C62-TNB distance were found to contract upon dilution of urea.	Urea	171-175	P53	Homo sapiens	71-76
16087277-5	2005	CsA induced a senescence-associated growth arrest, in U87-MG glioma cells with functional p53, while in U373 and T98G glioma cells with mutated p53, CsA treatment triggered cell death associated with alterations of cell morphology, cytoplasm vacuolation, and condensation of chromatin.	Cyclosporine	0-3	P53	Homo sapiens	90-93
16087277-5	2005	CsA induced a senescence-associated growth arrest, in U87-MG glioma cells with functional p53, while in U373 and T98G glioma cells with mutated p53, CsA treatment triggered cell death associated with alterations of cell morphology, cytoplasm vacuolation, and condensation of chromatin.	Cyclosporine	149-152	P53	Homo sapiens	144-147
16188274-7	2005	Refolding was commenced from unfolded protein in 8M urea, and both the Trp53 to C25-TNB distance and the Trp53 to C62-TNB distance were found to contract upon dilution of urea.	Urea	171-175	P53	Homo sapiens	105-110
16230611-4	2005	Dizocilpine reduces the phosphorylation of cAMP-responsive element binding protein, suppresses the expression of cyclin D1, up-regulates the cell cycle regulators and tumor suppressor proteins p21 and p53, and increases the number of lung adenocarcinoma cells in the G(2) and S phases of the cell cycle.	Dizocilpine Maleate	0-11	P53	Homo sapiens	201-204
16123044-6	2005	In this regard, it has been recently observed that the prolyl isomerase Pin1 can interact with proteins phosphorylated on serine or threonine residues that precede prolines (pS/T-P), such as the transcription factors p53 and c-Jun, thereby controlling their activity by promoting the cis-trans isomerization of these pS/T-P bonds.	Serine	122-128	P53	Homo sapiens	217-220
16123044-6	2005	In this regard, it has been recently observed that the prolyl isomerase Pin1 can interact with proteins phosphorylated on serine or threonine residues that precede prolines (pS/T-P), such as the transcription factors p53 and c-Jun, thereby controlling their activity by promoting the cis-trans isomerization of these pS/T-P bonds.	Threonine	132-141	P53	Homo sapiens	217-220
16234232-5	2005	The H2 helix of p53 structurally mimics the binding of ssDNA to the oligonucleotide/oligosaccharide-binding fold.	Oligonucleotides	68-83	P53	Homo sapiens	16-19
16273653-6	2005	RESULTS: The group transfected with pCMVp53 alone exhibited higher luciferase activity and higher apoptosis rate, otherwise, the p53 expression and reporter activity of PG13-CAT or P21-luc as well as cell apoptosis rate were obviously higher in the group cotransfected of pCMVp53 with pCMVHBVa, but not in the other cotransfected group.	pcmvhbva	285-293	P53	Homo sapiens	40-43
16007154-3	2005	In proliferating keratinocytes, the activity of p53 is blunted by its inhibitor DeltaNp63alpha.	deltanp63alpha	80-94	P53	Homo sapiens	48-51
15849742-0	2005	P73 functionally replaces p53 in Adriamycin-treated, p53-deficient breast cancer cells.	Doxorubicin	33-43	P53	Homo sapiens	26-29
16109433-11	2005	Activation of genes associated with cell cycle arrest, the p53 and TNF-related pathways, and chemokines and chemokine receptors, were particularly evident for the reactive oxygen compounds.	reactive oxygen compounds	163-188	P53	Homo sapiens	59-62
16103882-7	2005	Suppression of p53 activation by bFGF was frequently but not always accompanied by upregulation of the p53-inhibitory protein MDM2 and/or phosphorylation of MDM2 at serine 166, and was associated with impaired transcriptional activation of the p53 target gene p21.	Serine	165-171	P53	Homo sapiens	15-18
16230424-5	2005	We observed an increased risk of ESCC associated with the P53 Pro/Pro (OR, 1.83; 95% CI, 1.43-2.35; P &lt; 0.001) or MDM2 GG (OR, 1.49; 95% CI, 1.16-1.91; P = 0.002) genotype, compared with the P53 Arg/Arg or MDM2 TT genotype, respectively.	Arginine	198-201	P53	Homo sapiens	58-61
16230424-5	2005	We observed an increased risk of ESCC associated with the P53 Pro/Pro (OR, 1.83; 95% CI, 1.43-2.35; P &lt; 0.001) or MDM2 GG (OR, 1.49; 95% CI, 1.16-1.91; P = 0.002) genotype, compared with the P53 Arg/Arg or MDM2 TT genotype, respectively.	Arginine	202-205	P53	Homo sapiens	58-61
16243804-9	2005	CONCLUSION: Our study indicates that breast cancer patients with the Pro/Pro variant may be less sensitive to anthracycline-based treatment than those with the Pro/Arg or Arg/Arg variant and suggests that analysis of p53 codon 72 polymorphism may provide a simple predictive marker for selecting the right breast cancer patients to anthracycline-based neoadjuvant chemotherapy in clinical setting.	Anthracyclines	110-123	P53	Homo sapiens	217-220
15849742-0	2005	P73 functionally replaces p53 in Adriamycin-treated, p53-deficient breast cancer cells.	Doxorubicin	33-43	P53	Homo sapiens	53-56
16204068-2	2005	We found that 5-fluorouracil (5-FU) and oxaliplatin only sensitized p53 wild-type (WT) colorectal cancer cell lines to Fas-mediated apoptosis.	Fluorouracil	14-28	P53	Homo sapiens	68-71
16163384-3	2005	Here, we report that the tumor suppressor molecule p53 has a novel role in maintaining mitochondrial genetic stability through its ability to translocate to mitochondria and interact with mtDNA polymerase gamma (pol gamma) in response to mtDNA damage induced by exogenous and endogenous insults including ROS.	Reactive Oxygen Species	305-308	P53	Homo sapiens	51-54
16163384-6	2005	This study provides a mechanistic explanation for the accelerating genetic instability and increased ROS stress in cancer cells associated with loss of p53.	Reactive Oxygen Species	101-104	P53	Homo sapiens	152-155
16204068-2	2005	We found that 5-fluorouracil (5-FU) and oxaliplatin only sensitized p53 wild-type (WT) colorectal cancer cell lines to Fas-mediated apoptosis.	Fluorouracil	30-34	P53	Homo sapiens	68-71
16204068-3	2005	In contrast, irinotecan (CPT-11) and tomudex sensitized p53 WT, mutant, and null cells to Fas-mediated cell death.	Irinotecan	13-23	P53	Homo sapiens	56-59
16204068-3	2005	In contrast, irinotecan (CPT-11) and tomudex sensitized p53 WT, mutant, and null cells to Fas-mediated cell death.	Irinotecan	25-31	P53	Homo sapiens	56-59
16204068-4	2005	Furthermore, CPT-11 and tomudex, but not 5-FU or oxaliplatin, up-regulated Fas cell surface expression in a p53-independent manner.	Irinotecan	13-19	P53	Homo sapiens	108-111
15905205-2	2005	The codon 72 polymorphism has been proposed to alter the phenotype of TP53 mutations, and TP53 mutations have been reported to occur preferentially on the arginine allele.	Arginine	155-163	P53	Homo sapiens	90-94
16204068-5	2005	In addition, increased Fas cell surface expression in p53 mutant and null cell lines in response to CPT-11 and tomudex was accompanied by only a slight increase in total Fas mRNA and protein expression, suggesting that these agents trigger p53-independent trafficking of Fas to the plasma membrane.	Irinotecan	100-106	P53	Homo sapiens	54-57
16204068-6	2005	Treatment with CPT-11 or tomudex induced STAT1 phosphorylation (Ser727) in the p53-null HCT116 cell line but not the p53 WT cell line.	Irinotecan	15-21	P53	Homo sapiens	79-82
16204068-10	2005	We conclude that CPT-11 and tomudex may be more effective than 5-FU and oxaliplatin in the treatment of p53 mutant colorectal cancer tumors by sensitizing them to Fas-mediated apoptosis in a STAT1-dependent manner.	Irinotecan	17-23	P53	Homo sapiens	104-107
16054204-8	2005	The p21 arginine allele was significantly associated with CaCx in the p53 proline non-homozygous group of subjects (OR(age-adjusted) = 2.68; 95% CI: 1.21-5.91; P = 0.01), and specifically in the p53 heterozygous group (OR(age-adjusted) = 2.91; 95% CI = 1.12-7.56; P = 0.03).	Arginine	8-16	P53	Homo sapiens	70-73
16232203-0	2005	Cisplatin-controlled p53 gene therapy for human non-small cell lung cancer xenografts in athymic nude mice via the CArG elements.	Cisplatin	0-9	P53	Homo sapiens	21-24
16232203-5	2005	Wt-p53 production in cultured tumor cells and xenografts treated with the combination of AdEgr-p53 and cisplatin were detected by enzyme-linked immunosorbent assays.	Cisplatin	103-112	P53	Homo sapiens	3-6
16232203-7	2005	We found that p53 was produced in tumor cells and xenografts treated with a combination of AdEgr-p53 and cisplatin.	Cisplatin	105-114	P53	Homo sapiens	14-17
16232203-10	2005	Cisplatin-inducible p53 gene therapy may provide a means to control transgene expression while enhancing the effectiveness of commonly used chemotherapeutic agents.	Cisplatin	0-9	P53	Homo sapiens	20-23
16203772-1	2005	PURPOSE: The Arg/Pro polymorphism in codon 72 of p53 was recently associated with age of onset of colorectal cancer in Lynch syndrome.	Arginine	13-16	P53	Homo sapiens	49-52
16203773-0	2005	Reduced cisplatin sensitivity of head and neck squamous cell carcinoma cell lines correlates with mutations affecting the COOH-terminal nuclear localization signal of p53.	Cisplatin	8-17	P53	Homo sapiens	167-170
16203773-11	2005	Cisplatin sensitivity was highly reduced in the group with loss of nuclear p53 signal compared with those with detectable nuclear signal.	Cisplatin	0-9	P53	Homo sapiens	75-78
16203773-13	2005	CONCLUSION: Taken together, these data suggest that "loss of nuclear p53 signal" correlates with cisplatin resistance in HNSCC.	Cisplatin	97-106	P53	Homo sapiens	69-72
16018998-8	2005	Furthermore, the survival rate of p53(-/-)/Mdm2(-/-) cells exposed to thapsigargin was increased when cultured at 32 degrees C compared with 37 degrees C. In conclusion, mild hypothermia protects cells from a variety of stress by p53-dependent and p53-independent mechanisms.	Thapsigargin	70-82	P53	Homo sapiens	34-37
16018998-8	2005	Furthermore, the survival rate of p53(-/-)/Mdm2(-/-) cells exposed to thapsigargin was increased when cultured at 32 degrees C compared with 37 degrees C. In conclusion, mild hypothermia protects cells from a variety of stress by p53-dependent and p53-independent mechanisms.	Thapsigargin	70-82	P53	Homo sapiens	230-233
16018998-8	2005	Furthermore, the survival rate of p53(-/-)/Mdm2(-/-) cells exposed to thapsigargin was increased when cultured at 32 degrees C compared with 37 degrees C. In conclusion, mild hypothermia protects cells from a variety of stress by p53-dependent and p53-independent mechanisms.	Thapsigargin	70-82	P53	Homo sapiens	230-233
16054204-8	2005	The p21 arginine allele was significantly associated with CaCx in the p53 proline non-homozygous group of subjects (OR(age-adjusted) = 2.68; 95% CI: 1.21-5.91; P = 0.01), and specifically in the p53 heterozygous group (OR(age-adjusted) = 2.91; 95% CI = 1.12-7.56; P = 0.03).	Arginine	8-16	P53	Homo sapiens	195-198
20818013-5	2005	Specifically, we present an improved immobilization method that covalently anchors one end (5" end) of a dual labelled (5"-thiol, 3"-biotin) p53 DNA molecule onto a gold substrate via gold-thiol chemistry, whilst the biotinylated 3" end is available for "pick-up" using a streptavidin modified AFM tip.	Sulfhydryl Compounds	123-128	P53	Homo sapiens	141-144
16142332-0	2005	2-Chloroethyl-3-sarcosinamide-1-nitrosourea (SarCNU) exhibits p53-dependent and -independent antiproliferative activity in human nasopharyngeal carcinoma cells in vitro and in vivo.	2-((((2-chloroethyl)nitrosoamino)carbonyl)amino)propanamide	0-43	P53	Homo sapiens	62-65
16142332-0	2005	2-Chloroethyl-3-sarcosinamide-1-nitrosourea (SarCNU) exhibits p53-dependent and -independent antiproliferative activity in human nasopharyngeal carcinoma cells in vitro and in vivo.	2-((((2-chloroethyl)nitrosoamino)carbonyl)amino)propanamide	45-51	P53	Homo sapiens	62-65
16142332-4	2005	In vitro study showed that wild-type p53 HK-1 cells were 3-fold more sensitive to SarCNU than p53 mutant CNE-2 cells.	2-((((2-chloroethyl)nitrosoamino)carbonyl)amino)propanamide	82-88	P53	Homo sapiens	37-40
16142332-6	2005	Upregulation of p53, phosphorylated p53 at Ser15 and biochemical markers for apoptosis, such as cleaved caspase-3, cleaved caspase-7 and cleaved PARP, were observed in SarCNU-treated HK-1 but not CNE-2 cells.	2-((((2-chloroethyl)nitrosoamino)carbonyl)amino)propanamide	168-174	P53	Homo sapiens	16-19
16142332-6	2005	Upregulation of p53, phosphorylated p53 at Ser15 and biochemical markers for apoptosis, such as cleaved caspase-3, cleaved caspase-7 and cleaved PARP, were observed in SarCNU-treated HK-1 but not CNE-2 cells.	2-((((2-chloroethyl)nitrosoamino)carbonyl)amino)propanamide	168-174	P53	Homo sapiens	36-39
16142332-9	2005	Introduction of mutant p53 into HK-1 cells resulted in growth enhancement in vivo and increased resistance to SarCNU-induced apoptosis in vitro.	2-((((2-chloroethyl)nitrosoamino)carbonyl)amino)propanamide	110-116	P53	Homo sapiens	23-26
16142332-10	2005	Furthermore, CNE-2 cells transfected with wild-type p53 became susceptible to SarCNU-induced apoptosis in vitro but not their growth rate in vivo.	2-((((2-chloroethyl)nitrosoamino)carbonyl)amino)propanamide	78-84	P53	Homo sapiens	52-55
16199549-1	2005	The polymorphic variants at codon 72 of the p53 gene were shown to be functionally distinct in vitro, whereby the arginine (arg) variant induces apoptosis more efficiently than the proline (pro) variant.	Arginine	114-122	P53	Homo sapiens	44-47
16199549-1	2005	The polymorphic variants at codon 72 of the p53 gene were shown to be functionally distinct in vitro, whereby the arginine (arg) variant induces apoptosis more efficiently than the proline (pro) variant.	Arginine	114-117	P53	Homo sapiens	44-47
16043423-6	2005	However, following the onset of calcium-induced differentiation, basal levels of p53 were nearly undetectable by 12 days of differentiation when global repair activity was unaffected.	Calcium	32-39	P53	Homo sapiens	81-84
16087156-0	2005	Knockdown of p53 by RNAi in ES cells facilitates RA-induced differentiation into muscle cells.	Tretinoin	49-51	P53	Homo sapiens	13-16
16087156-5	2005	With RA treatment, silencing of p53 by RNAi in ES cells leads to dominant muscle cell production but lack of neuronal cell, indicating that p53 indeed plays a role during muscle and neuronal fate commitment.	Tretinoin	5-7	P53	Homo sapiens	32-35
16087156-5	2005	With RA treatment, silencing of p53 by RNAi in ES cells leads to dominant muscle cell production but lack of neuronal cell, indicating that p53 indeed plays a role during muscle and neuronal fate commitment.	Tretinoin	5-7	P53	Homo sapiens	140-143
16043423-7	2005	Following ultraviolet radiation, induction of p53 following ultraviolet radiation was abrogated by 6 days of calcium-induced differentiation.	Calcium	109-116	P53	Homo sapiens	46-49
16202244-3	2005	Here we showed that etoposide can induce the similar degree of cell death in p53-deficient HCT 116 cells, whereas 5"-FU-mediated cell death is strongly dependent on the existence of functional p53 in HCT 116 cells.	Fluorouracil	114-119	P53	Homo sapiens	193-196
16007197-0	2005	Quantitation of p53 nuclear relocation in response to stress using a yeast functional assay: effects of irradiation and modulation by heavy metal ions.	Metals	140-145	P53	Homo sapiens	16-19
16007197-7	2005	Cd2+ and Hg2+, two metal ions inducing DNA damage as well as conformational changes in p53, have opposite effects on p53 relocation in response to DNA damage.	Metals	19-24	P53	Homo sapiens	117-120
16166444-11	2005	CONCLUSIONS: p21 expression in colorectal cancer, especially in combination with p53 mutation, is a predictor of resistance to the combination chemotherapy with gefitinib.	Gefitinib	161-170	P53	Homo sapiens	81-84
16121349-1	2005	BACKGROUND AND OBJECTIVES: To ascertain the prevalence of deregulating mutations of beta-catenin gene, and to correlate this with the occurrence of 249(serine) p53 gene mutation and hepatitis B virus infection in southern African Blacks with hepatocellular carcinoma.	Serine	152-158	P53	Homo sapiens	160-163
15940259-8	2005	Interestingly, in p53 knockdown cells nearly the entire set of identified cisplatin targets fail to respond or have a diminished response to cisplatin, suggesting that many are new direct or indirect targets of p53 including GPR87, STK17A, INPP5D, FLJ11259, and EPS8L2.	Cisplatin	74-83	P53	Homo sapiens	18-21
16141331-2	2005	Recently, we have shown distinct thresholds for NO to regulate p53-Ser-15P, phosphorylated extracellular signal-regulated kinase (pERK), and hypoxia inducible factor 1alpha in tumor cells.	Serine	67-70	P53	Homo sapiens	63-66
15940259-0	2005	A p53-dominant transcriptional response to cisplatin in testicular germ cell tumor-derived human embryonal carcinoma.	Cisplatin	43-52	P53	Homo sapiens	2-5
15940259-7	2005	Specific siRNA to p53 prevents cisplatin-mediated activation of p53 and p53 pathway genes and renders embryonal carcinoma cells relatively resistant to cisplatin cytotoxicity.	Cisplatin	31-40	P53	Homo sapiens	18-21
15940259-7	2005	Specific siRNA to p53 prevents cisplatin-mediated activation of p53 and p53 pathway genes and renders embryonal carcinoma cells relatively resistant to cisplatin cytotoxicity.	Cisplatin	31-40	P53	Homo sapiens	64-67
15940259-7	2005	Specific siRNA to p53 prevents cisplatin-mediated activation of p53 and p53 pathway genes and renders embryonal carcinoma cells relatively resistant to cisplatin cytotoxicity.	Cisplatin	31-40	P53	Homo sapiens	64-67
15940259-8	2005	Interestingly, in p53 knockdown cells nearly the entire set of identified cisplatin targets fail to respond or have a diminished response to cisplatin, suggesting that many are new direct or indirect targets of p53 including GPR87, STK17A, INPP5D, FLJ11259, and EPS8L2.	Cisplatin	74-83	P53	Homo sapiens	211-214
15940259-7	2005	Specific siRNA to p53 prevents cisplatin-mediated activation of p53 and p53 pathway genes and renders embryonal carcinoma cells relatively resistant to cisplatin cytotoxicity.	Cisplatin	152-161	P53	Homo sapiens	18-21
15940259-8	2005	Interestingly, in p53 knockdown cells nearly the entire set of identified cisplatin targets fail to respond or have a diminished response to cisplatin, suggesting that many are new direct or indirect targets of p53 including GPR87, STK17A, INPP5D, FLJ11259, and EPS8L2.	Cisplatin	141-150	P53	Homo sapiens	18-21
15985438-3	2005	Expression of the ErbB-4 ICD fragment leads to its constitutive association with Mdm2 and tyrosine phosphorylation of Mdm2, a protein that is predominantly localized in the nucleus and that regulates p53 levels.	Tyrosine	90-98	P53	Homo sapiens	200-203
15983031-1	2005	We demonstrate the role of p53-mediated caspase-2 activation in the mitochondrial release of apoptosis-inducing factor (AIF) in cisplatin-treated renal tubular epithelial cells.	Cisplatin	128-137	P53	Homo sapiens	27-30
16082224-1	2005	A common polymorphism at codon 72 in p53 gene leads to an arginine to proline aminoacidic substitution which affects in an age-dependent manner the susceptibility of cells to undergo apoptosis after oxidative stress.	Arginine	58-66	P53	Homo sapiens	37-40
15983031-8	2005	Caspase-2 activation was a critical response from p53, which was markedly induced and phosphorylated in cisplatin-treated cells.	Cisplatin	104-113	P53	Homo sapiens	50-53
15983031-10	2005	The p53 inhibitor pifithrin-alpha or p53 siRNA prevented both cisplatin-induced caspase-2 activation and mitochondrial release of AIF.	Cisplatin	62-71	P53	Homo sapiens	4-7
15983031-10	2005	The p53 inhibitor pifithrin-alpha or p53 siRNA prevented both cisplatin-induced caspase-2 activation and mitochondrial release of AIF.	Cisplatin	62-71	P53	Homo sapiens	37-40
15983031-11	2005	Caspase-2 activation was dependent on the p53-responsive gene, PIDD, a death domain-containing protein that was induced by cisplatin in a p53-dependent manner.	Cisplatin	123-132	P53	Homo sapiens	42-45
15983031-11	2005	Caspase-2 activation was dependent on the p53-responsive gene, PIDD, a death domain-containing protein that was induced by cisplatin in a p53-dependent manner.	Cisplatin	123-132	P53	Homo sapiens	138-141
15983031-12	2005	These results suggest that caspase-2 activation mediated by p53 is an important pathway involved in the mitochondrial release of AIF in response to cisplatin injury.	Cisplatin	148-157	P53	Homo sapiens	60-63
16082226-0	2005	Blockage of NF-kappaB induces serine 15 phosphorylation of mutant p53 by JNK kinase in prostate cancer cells.	Serine	30-36	P53	Homo sapiens	66-69
16082226-4	2005	Here we report that inhibition of NF-kappaB in DU145 prostate cancer cells results in p53 mutant phosphorylation at serine 15 (Ser15), leading to an increase of p53 stability, DNA binding and gain of function.	Serine	116-122	P53	Homo sapiens	86-89
16007417-11	2005	CONCLUSION: The Arg/Arg genotype of the Arg72Pro polymorphism in p53 is associated with increased likelihood of a bad outcome at discharge from the SICU.	Arginine	16-19	P53	Homo sapiens	65-68
16084079-8	2005	Further, silibinin modulates mitogenic and survival signalling, p53, Cip1/p21 and other cell cycle regulatory molecules to prevent UVB-induced skin carcinogenesis.	Silybin	9-18	P53	Homo sapiens	64-67
16172238-1	2005	Polymorphism at codon 72 of p53 results in either the arginine or proline form of p53, whose functional significance in carcinogenesis is controversial.	Arginine	54-62	P53	Homo sapiens	28-31
16172238-2	2005	We have investigated if the expression of these p53 polymorphs is selectively regulated, using mRNA from peripheral blood of healthy Asian (Chinese) and the Caucasian (Polish) arginine/proline (arg/pro) heterozygote subjects.	Arginine	176-184	P53	Homo sapiens	48-51
16172238-2	2005	We have investigated if the expression of these p53 polymorphs is selectively regulated, using mRNA from peripheral blood of healthy Asian (Chinese) and the Caucasian (Polish) arginine/proline (arg/pro) heterozygote subjects.	Arginine	176-179	P53	Homo sapiens	48-51
16172238-6	2005	Together, the data suggest that the expression of the different p53 polymorphs is selectively regulated in different ethnic populations, and that the arg allele is activated during cancer development in Asians.	Arginine	150-153	P53	Homo sapiens	64-67
16007417-11	2005	CONCLUSION: The Arg/Arg genotype of the Arg72Pro polymorphism in p53 is associated with increased likelihood of a bad outcome at discharge from the SICU.	Arginine	20-23	P53	Homo sapiens	65-68
15795939-9	2005	In addition to a reduced MMP and increased reactive oxygen species, phosphorylation of p38 and p53 (serine 15) and impaired DNA binding of p53 were observed.	Serine	100-106	P53	Homo sapiens	95-98
16170025-5	2005	Although methionine stress-induced toxicity is not solely dependent on p53, the gain in p21 and loss in CDK1 transcription are more enhanced in wild-type p53 tumors.	Methionine	9-19	P53	Homo sapiens	154-157
16193384-6	2005	In contrast, p53 inactivation rendered D54 and U87MG cells significantly more resistant to cis-dichlorodiamminoplatinum (CDDP), another chemotherapeutic to which high-grade astrocytomas sometimes respond.	cddp	121-125	P53	Homo sapiens	13-16
16140998-8	2005	CONCLUSIONS: The p53 codon 72 Arg/Pro polymorphism is not associated with age of onset or severity of glaucoma.	Arginine	30-33	P53	Homo sapiens	17-20
16170037-6	2005	The increase in p53 protein and its nuclear accumulation suggests a possible involvement of p53 in CDDP protection.	cddp	99-103	P53	Homo sapiens	16-19
16170037-6	2005	The increase in p53 protein and its nuclear accumulation suggests a possible involvement of p53 in CDDP protection.	cddp	99-103	P53	Homo sapiens	92-95
15993843-0	2005	Inhibition of melanoma cell proliferation by resveratrol is correlated with upregulation of quinone reductase 2 and p53.	Resveratrol	45-56	P53	Homo sapiens	116-119
15979383-0	2005	Nitric oxide induces oral squamous cell carcinoma cells apoptosis with p53 accumulation.	Nitric Oxide	0-12	P53	Homo sapiens	71-74
15979383-13	2005	Exogenous nitric oxide had an inhibitory effect on Tca8113 cells proliferation in a dose and time-dependent manners and possibly via p53 dependent apoptosis pathway.	Nitric Oxide	10-22	P53	Homo sapiens	133-136
16054425-0	2005	Nitric oxide induces oral squamous cell carcinoma cell apoptosis with p53 accumulation [Oral Oncology 41 (8) (2005) 785-790].	Nitric Oxide	0-12	P53	Homo sapiens	70-73
16077963-0	2005	The evaluation of gastric cancer sensitivity to 5-FU/CDDP in terms of induction of apoptosis: time- and p53 expression-dependency of anti-cancer drugs.	Fluorouracil	48-52	P53	Homo sapiens	104-107
16077963-0	2005	The evaluation of gastric cancer sensitivity to 5-FU/CDDP in terms of induction of apoptosis: time- and p53 expression-dependency of anti-cancer drugs.	Cisplatin	53-57	P53	Homo sapiens	104-107
16468334-0	2005	[Effects of curcumin on the acetylation of histone H3, P53 and the proliferation of NB4 cells].	Curcumin	12-20	P53	Homo sapiens	55-58
16468334-1	2005	OBJECTIVE: To investigate the effects of curcumin on the acetylation of histone H3, P53 and the proliferation of NB4 cells.	Curcumin	41-49	P53	Homo sapiens	84-87
16468334-7	2005	CONCLUSION: Curcumin functions as a deacetylase inhibitor,which could increase the level of acetylated histone H3, enhance the expression and activity of tumor suppressor P53, and inhibit the proliferation of NB4 cells.	Curcumin	12-20	P53	Homo sapiens	171-174
16077963-9	2005	These results indicated that the type of p53 expression in cancer cells could be a promising factor in predicting response to FP therapy and the administration of CDDP prior to 5-FU may be more effective in inducing apoptosis of gastric cancer cells with wild-type p53 expression.	Cisplatin	163-167	P53	Homo sapiens	265-268
15914462-1	2005	Proline oxidase is a p53-induced redox gene that can generate reactive oxygen species (ROS) and mediate apoptosis in tumor cells.	Reactive Oxygen Species	62-85	P53	Homo sapiens	21-24
15897882-2	2005	We previously demonstrated the specific involvement of homeodomain interacting protein-kinase 2 (HIPK2), a nuclear serine/threonine kinase, in inducing p53-dependent apoptosis through selective p53 phosphorylation at serine 46 after severe genotoxic damage.	Serine	115-121	P53	Homo sapiens	152-155
16109171-1	2005	BACKGROUND: A common sequence polymorphism at codon 72 of the p53 gene encoding either arginine or proline was recently shown to be functionally relevant for apoptosis induction in vitro.	Arginine	87-95	P53	Homo sapiens	62-65
15880691-13	2005	However, metal-induced activation of p53 and mitochondrial depolarization appears to be independent of ERK.	Metals	9-14	P53	Homo sapiens	37-40
19565011-0	2005	Progesterone inhibition of MDM2 p90 protein in MCF-7 human breast cancer cell line is dependent on p53 levels.	Progesterone	0-12	P53	Homo sapiens	99-102
19565011-3	2005	We have recently shown that growth inhibition of MCF-7 human breast cancer cells by progesterone is associated with P53 down-regulation.	Progesterone	84-96	P53	Homo sapiens	116-119
19565011-7	2005	The inhibition of MDM2 p90 protein by progesterone was abrogated in MCF-7 cells transfected with a P53 expressing vector.	Progesterone	38-50	P53	Homo sapiens	99-102
19565011-10	2005	The data indicate that expression of MDM2 p90 is regulated through a P53-dependent pathway in response to progesterone.	Progesterone	106-118	P53	Homo sapiens	69-72
16085052-2	2005	The mechanism underlying this tyrosine phosphorylation is thought to involve the sequential action of two protein tyrosine kinases, Syk (p72syk) and Lyn (p53/56lyn).	Tyrosine	30-38	P53	Homo sapiens	154-157
15880691-3	2005	We demonstrated that expression of wild-type p53 induced by copper or zinc significantly reduced phosphorylation of extracellular signal regulated kinase (ERK) in epithelial breast cancer MCF7 cells.	Copper	60-66	P53	Homo sapiens	45-48
15880691-6	2005	Furthermore, inhibition of ERK through addition of PD98059 stimulated p53 activation in MCF7 cells and also led to upregulation of p53 downstream targets, p21 and Bax, which is a proapototic member of Bcl-2 family triggering mitochondrial pore opening.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	51-58	P53	Homo sapiens	70-73
15880691-6	2005	Furthermore, inhibition of ERK through addition of PD98059 stimulated p53 activation in MCF7 cells and also led to upregulation of p53 downstream targets, p21 and Bax, which is a proapototic member of Bcl-2 family triggering mitochondrial pore opening.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	51-58	P53	Homo sapiens	131-134
15880691-8	2005	Disruption of p53 expression attenuated the depolarization of the mitochondrial membrane and ROS generation.	ros	93-96	P53	Homo sapiens	14-17
15914462-1	2005	Proline oxidase is a p53-induced redox gene that can generate reactive oxygen species (ROS) and mediate apoptosis in tumor cells.	Reactive Oxygen Species	87-90	P53	Homo sapiens	21-24
15914462-4	2005	Both proline oxidase- and p53-induced activation of NFAT were sensitive to the calcineurin inhibitors cyclosporin A and FK-506, to scavengers of ROS, and to inhibitors of calcium mobilization.	Cyclosporine	102-115	P53	Homo sapiens	26-29
15914462-4	2005	Both proline oxidase- and p53-induced activation of NFAT were sensitive to the calcineurin inhibitors cyclosporin A and FK-506, to scavengers of ROS, and to inhibitors of calcium mobilization.	Reactive Oxygen Species	145-148	P53	Homo sapiens	26-29
15914462-4	2005	Both proline oxidase- and p53-induced activation of NFAT were sensitive to the calcineurin inhibitors cyclosporin A and FK-506, to scavengers of ROS, and to inhibitors of calcium mobilization.	Calcium	171-178	P53	Homo sapiens	26-29
15914462-7	2005	Inhibitors of calcineurin and calcium mobilization abolished proline oxidase-mediated apoptosis and reduced p53-induced apoptosis.	Calcium	30-37	P53	Homo sapiens	108-111
16012788-0	2005	Enhanced P53 and BAX gene expression and apoptosis in A549 cells by cis-Pt(II) complex of 3-aminoflavone in comparison with cis-DDP.	Cisplatin	68-78	P53	Homo sapiens	9-12
16177561-0	2005	Acridine derivatives activate p53 and induce tumor cell death through Bax.	Acridines	0-8	P53	Homo sapiens	30-33
16177561-4	2005	We also found that several randomly chosen acridine derivatives, including 9-aminoacridine, amsacrine, quinacrine and acridine orange, induced p53 transcriptional activity.	Acridines	43-51	P53	Homo sapiens	143-146
16177561-5	2005	All these acridine derivatives stabilized p53 protein by blocking its ubiquitination, without phosphorylation of ser15 or ser20 on p53.	Acridines	10-18	P53	Homo sapiens	42-45
16177561-6	2005	Furthermore, acridine derivatives induced p53-dependent cell death.	Acridines	13-21	P53	Homo sapiens	42-45
16177561-7	2005	Knockout of Bax, a p53 target and a key cell death inducer in both intrinsic and extrinsic apoptotic pathways, blocked acridine derivatives from inducing cell death.	Acridines	119-127	P53	Homo sapiens	19-22
16177561-9	2005	Our results reveal that DNA-intercalating acridine derivatives can induce p53 stabilization by a manner similar to CP-31398.	Acridines	42-50	P53	Homo sapiens	74-77
16083495-1	2005	BACKGROUND: Inhibition of the COP9 signalosome (CSN) associated kinases CK2 and PKD by curcumin causes stabilization of the tumor suppressor p53.	Curcumin	87-95	P53	Homo sapiens	141-144
16082197-4	2005	Recent findings suggest that p53 also undergoes ubiquitin-independent degradation by the 20S proteasomes and that this process is regulated by NAD(P)H quinone oxidoreductase 1 (NQO1) together with NADH.	NAD	197-201	P53	Homo sapiens	29-32
19956517-0	2005	Thymidylate synthase, thymidine phosphorylase, VEGF and p53 protein expression in primary colorectal cancer for predicting response to 5-fluorouracil-based chemotherapy.	Fluorouracil	135-149	P53	Homo sapiens	56-59
19956517-3	2005	The expression levels of thymidylate synthase (TS), thymidine phosphorylase (TP) and p53 have been known to be associated with the clinical response to 5-FU-based therapy as well as the prognosis, and that of vascular endothelial growth factor (VEGF) is associated with poor survival.	Fluorouracil	152-156	P53	Homo sapiens	85-88
16024799-3	2005	ING2 protein expression increased in late-passage human primary cells, and it colocalizes with serine 15-phosphorylated p53.	Serine	95-101	P53	Homo sapiens	120-123
15908516-6	2005	When treatment with E6 siRNA was coupled with chemotherapy, the p53 activity after treatment with carboplatin and paclitaxel was additively increased, whereas the p53 activation induced by the rest of the drugs was synergistically increased.	Paclitaxel	114-124	P53	Homo sapiens	64-67
16048565-0	2005	249ser p53 mutation in the serum of black southern African patients with hepatocellular carcinoma.	249ser	0-6	P53	Homo sapiens	7-10
16048565-1	2005	BACKGROUND AND AIMS: A specific mutation at codon 249 of the p53 tumor suppressor gene (guanine to thymine; arginine to serine [249(serine)p53]) is present in the cell-free plasma of 30-47% of patients with hepatocellular carcinoma (HCC) in regions with uniformly high levels of dietary exposure to the fungal toxin, aflatoxin B(1).	Arginine	108-116	P53	Homo sapiens	61-64
16048565-1	2005	BACKGROUND AND AIMS: A specific mutation at codon 249 of the p53 tumor suppressor gene (guanine to thymine; arginine to serine [249(serine)p53]) is present in the cell-free plasma of 30-47% of patients with hepatocellular carcinoma (HCC) in regions with uniformly high levels of dietary exposure to the fungal toxin, aflatoxin B(1).	Arginine	108-116	P53	Homo sapiens	139-142
16048565-1	2005	BACKGROUND AND AIMS: A specific mutation at codon 249 of the p53 tumor suppressor gene (guanine to thymine; arginine to serine [249(serine)p53]) is present in the cell-free plasma of 30-47% of patients with hepatocellular carcinoma (HCC) in regions with uniformly high levels of dietary exposure to the fungal toxin, aflatoxin B(1).	Serine	120-126	P53	Homo sapiens	61-64
16048565-1	2005	BACKGROUND AND AIMS: A specific mutation at codon 249 of the p53 tumor suppressor gene (guanine to thymine; arginine to serine [249(serine)p53]) is present in the cell-free plasma of 30-47% of patients with hepatocellular carcinoma (HCC) in regions with uniformly high levels of dietary exposure to the fungal toxin, aflatoxin B(1).	Serine	120-126	P53	Homo sapiens	139-142
16048565-1	2005	BACKGROUND AND AIMS: A specific mutation at codon 249 of the p53 tumor suppressor gene (guanine to thymine; arginine to serine [249(serine)p53]) is present in the cell-free plasma of 30-47% of patients with hepatocellular carcinoma (HCC) in regions with uniformly high levels of dietary exposure to the fungal toxin, aflatoxin B(1).	Serine	132-138	P53	Homo sapiens	61-64
16048565-1	2005	BACKGROUND AND AIMS: A specific mutation at codon 249 of the p53 tumor suppressor gene (guanine to thymine; arginine to serine [249(serine)p53]) is present in the cell-free plasma of 30-47% of patients with hepatocellular carcinoma (HCC) in regions with uniformly high levels of dietary exposure to the fungal toxin, aflatoxin B(1).	Serine	132-138	P53	Homo sapiens	139-142
16048565-9	2005	CONCLUSIONS: The 249(serine)p53 mutation is found less often in the serum of patients with HCC in a region with variable levels of exposure to aflatoxin B(1) than in those with uniformly high levels of exposure, but the mutation does occur in black Africans with presumed lower levels of exposure to the fungal toxin.	Serine	21-27	P53	Homo sapiens	28-31
16080576-3	2005	The IHC method of streptavidin biotin peroxidase on paraffin tissue sections was used to detect bcl2 and p53 oncoproteins and PAR4 pro-apoptotic protein expression in surgical specimens.	Paraffin	52-60	P53	Homo sapiens	105-108
16011614-6	2005	Nicotine treatment increased p21 expression in immortalized cells (HaCaT, IHOK) and oral cancer cells (HN4, HN12), but decreased pRb and p53 expression in oral cancer cells.	Nicotine	0-8	P53	Homo sapiens	137-140
15843377-0	2005	Phosphorylation of human p53 at serine 46 determines promoter selection and whether apoptosis is attenuated or amplified.	Serine	32-38	P53	Homo sapiens	25-28
15843377-3	2005	High dose chemotherapy induced the phosphorylation of p53 on serine 46, whereas low dose chemotherapy did not.	Serine	61-67	P53	Homo sapiens	54-57
15843377-6	2005	These observations show that phosphorylation of serine 46 in p53 is sufficient for it to induce the PTEN (phosphatase and tensin homolog deleted on chromosome ten) tumor suppressor protein in preference to MDM2.	Serine	48-54	P53	Homo sapiens	61-64
16093429-4	2005	Transient transfection of H460 lung cancer cells and human umbilical vascular endothelial cells (HUVEC) with antisense oligonucleotides (ASODN) against MDM2 resulted in a reduced level of MDM2 and increased levels of p21 and p53.	Oligonucleotides	119-135	P53	Homo sapiens	225-228
15996866-3	2005	A recent article provides in vitro biophysical evidence supporting a direct interaction between p53 and the oxygen-dependent degradation domain of the HIF-1alpha subunit.	Oxygen	108-114	P53	Homo sapiens	96-99
16024610-0	2005	Nitric oxide-induced apoptosis in lymphoblastoid and fibroblast cells dependent on the phosphorylation and activation of p53.	Nitric Oxide	0-12	P53	Homo sapiens	121-124
15855171-5	2005	Inhibition of p53 with small interfering p53 RNA resulted in a decreased complex of FAK and p53 proteins in 293 cells, and induction of p53 with doxorubicin in normal human fibroblasts caused an increase of FAK and p53 interaction.	Doxorubicin	145-156	P53	Homo sapiens	14-17
16009172-6	2005	MAIN OUTCOME MEASURE(S): Genotyping was performed by polymerase chain reaction-based amplification of the Arg and Pro variants at codon 72 of the p53 gene and by restriction fragment length polymorphism analysis of the G/G and G/A alleles in exon 4 of the ANGPT2 gene.	Arginine	106-109	P53	Homo sapiens	146-149
15833387-0	2005	Liriodenine inhibits the proliferation of human hepatoma cell lines by blocking cell cycle progression and nitric oxide-mediated activation of p53 expression.	Nitric Oxide	107-119	P53	Homo sapiens	143-146
16020667-7	2005	Thus, cisplatin selected for wild-type p53 and high Bcl-x(L) expression in these cells.	Cisplatin	6-15	P53	Homo sapiens	39-42
15964795-5	2005	Proline 82 of p53 was identified to be essential for its interaction with the checkpoint kinase 2 (Chk2) and consequent phosphorylation of p53 on serine 20, following DNA damage.	Serine	146-152	P53	Homo sapiens	14-17
15964795-5	2005	Proline 82 of p53 was identified to be essential for its interaction with the checkpoint kinase 2 (Chk2) and consequent phosphorylation of p53 on serine 20, following DNA damage.	Serine	146-152	P53	Homo sapiens	139-142
16020667-2	2005	We observed that larynx preservation and response to chemotherapy is significantly associated with p53 overexpression, and that most HNSCC cell lines with mutant p53 are more sensitive to cisplatin than those with wild-type p53.	Cisplatin	188-197	P53	Homo sapiens	162-165
16020667-10	2005	Thus, cisplatin-resistant cells seem to depend on wild-type p53 and Bcl-x(L) for survival and BH3 mimetic agents, such as (-)-gossypol, may be useful adjuncts to overcome cisplatin resistance in HNSCC.	Cisplatin	6-15	P53	Homo sapiens	60-63
16020667-2	2005	We observed that larynx preservation and response to chemotherapy is significantly associated with p53 overexpression, and that most HNSCC cell lines with mutant p53 are more sensitive to cisplatin than those with wild-type p53.	Cisplatin	188-197	P53	Homo sapiens	162-165
16020671-5	2005	At both normoxia and hypoxia, 2 and 4 mumol/L As(2)O(3) induced evident cell death in the drug-sensitive SH-SY5Y and IMR-32 cells as well as in the multidrug-resistant SK-N-BE(2)c (with a mutated p53) and SK-N-FI cells after 72 hours of exposure.	hippuric acid	48-52	P53	Homo sapiens	196-199
15705792-0	2005	Stress-induced activation of the p53 tumor suppressor in leukemia cells and normal lymphocytes requires mitochondrial activity and reactive oxygen species.	Reactive Oxygen Species	131-154	P53	Homo sapiens	33-36
16277093-0	2005	Expression of p53 protein and DNA flow cytometry in gastric adenocarcinoma: implications in patients treated with adjuvant etoposide, adriamycin and cisplatin.	Doxorubicin	134-144	P53	Homo sapiens	14-17
16277093-0	2005	Expression of p53 protein and DNA flow cytometry in gastric adenocarcinoma: implications in patients treated with adjuvant etoposide, adriamycin and cisplatin.	Cisplatin	149-158	P53	Homo sapiens	14-17
16277102-4	2005	RESULTS: P53 alteration occurred in 20 of 45 tumors (44%) and was more common among younger patients (58% versus 36% for younger versus older patients, respectively) and those lacking tobacco/alcohol exposure (53% versus 40% for "no-risk" and "risk" groups, respectively), but the differences were not statistically significant.	Alcohols	192-199	P53	Homo sapiens	9-12
16188130-1	2005	OBJECTIVE: To evaluate the efficacy and safety of recombinant adenovirus-p53 gene (Gendicine) therapy combined with radiotherapy for head and neck squamous-cell carcinoma (HNSCC).	gendicine	83-92	P53	Homo sapiens	73-76
16188130-10	2005	The apparent improved results of combined therapy with Gendicine and radiation suggest that p53 gene therapy has promising therapeutic potential in cancer treatment.	gendicine	55-64	P53	Homo sapiens	92-95
15806145-0	2005	Differences in the association of p53 phosphorylated on serine 15 and key enzymes of homologous recombination.	Serine	56-62	P53	Homo sapiens	34-37
15806145-1	2005	Phosphorylation of p53 on serine 15 by ATM or ATR is a frequent modification and initiates a cascade of post-translational modifications.	Serine	26-32	P53	Homo sapiens	19-22
15806145-2	2005	To identify possible mechanisms that modulate p53 functions in recombination surveillance, we compared the nuclear localization of p53 phosphorylated on serine 15 (p53pSer15) and the key enzymes of homologous recombination (HR) after replication fork stalling.	Serine	153-159	P53	Homo sapiens	131-134
15806145-2	2005	To identify possible mechanisms that modulate p53 functions in recombination surveillance, we compared the nuclear localization of p53 phosphorylated on serine 15 (p53pSer15) and the key enzymes of homologous recombination (HR) after replication fork stalling.	Serine	153-159	P53	Homo sapiens	164-173
15705792-6	2005	Reactive oxygen species (ROS) localized to mitochondria decreased in the presence of oligomycin, and stress-induced p53 activation showed strong ROS sensitivity both in leukemic and normal cells.	Reactive Oxygen Species	145-148	P53	Homo sapiens	116-119
15938631-0	2005	Investigating DNA adduct-targeted mutagenicity of tamoxifen: preferential formation of tamoxifen-DNA adducts in the human p53 gene in SV40 immortalized hepatocytes but not endometrial carcinoma cells.	Tamoxifen	50-59	P53	Homo sapiens	122-125
15938631-0	2005	Investigating DNA adduct-targeted mutagenicity of tamoxifen: preferential formation of tamoxifen-DNA adducts in the human p53 gene in SV40 immortalized hepatocytes but not endometrial carcinoma cells.	Tamoxifen	87-96	P53	Homo sapiens	122-125
15806165-12	2005	This study also showed that cAMP elevation and PI3K inhibition increases U6-driven siRNA activity directed towards an endogenous gene, p53.	Cyclic AMP	28-32	P53	Homo sapiens	135-138
15928081-6	2005	In addition, glucose starvation not only signals to shut down mTOR, but also results in the transient phosphorylation of the p53 protein.	Glucose	13-20	P53	Homo sapiens	125-128
15850808-0	2005	Increased BNip3 and decreased mutant p53 in cisplatin-sensitive PDT-resistant HT29 cells.	Cisplatin	44-53	P53	Homo sapiens	37-40
15850808-4	2005	In addition, the cisplatin sensitivity of the PDT-resistant HT29 variants and several other clonal variants of HT29 cells correlated with increased BNip3 and decreased mutant p53 protein levels, but not Hsp27 protein levels.	Cisplatin	17-26	P53	Homo sapiens	175-178
15899386-2	2005	TP53 has two common polymorphic forms encoding either proline or arginine, at position 72, and the presence of homozygous arginine has been reported as a risk factor for cervical cancer in many populations.	Arginine	65-73	P53	Homo sapiens	0-4
15750621-0	2005	Aminothiol WR1065 induces differential gene expression in the presence of wild-type p53.	Aminothiol	0-10	P53	Homo sapiens	84-87
15939931-0	2005	DNA microarrays on a dendron-modified surface improve significantly the detection of single nucleotide variations in the p53 gene.	dendron	21-28	P53	Homo sapiens	121-124
15939931-4	2005	DNA microarrays on the dendron-modified surface were subjected to the detection of single nucleotide variations in the exons 5-8 of the p53 gene in genomic DNAs from cancer cell lines.	dendron	23-30	P53	Homo sapiens	136-139
15856030-6	2005	Using isogenic colon cancer cell lines that differ only by the presence of the mutant Ras allele, HCT116 and Hke-3 cells, we demonstrated that signaling by oncogenic Ras promotes both accumulation of p53 and its phosphorylation on serine15 in response to 5-FU, a situation that favors apoptosis over growth arrest.	Fluorouracil	255-259	P53	Homo sapiens	200-203
15899386-2	2005	TP53 has two common polymorphic forms encoding either proline or arginine, at position 72, and the presence of homozygous arginine has been reported as a risk factor for cervical cancer in many populations.	Arginine	122-130	P53	Homo sapiens	0-4
15870870-0	2005	Apoptosis induced by 5-fluorouracil, cisplatin and paclitaxel are associated with p53 gene status in gastric cancer cell lines.	Fluorouracil	21-35	P53	Homo sapiens	82-85
15870870-0	2005	Apoptosis induced by 5-fluorouracil, cisplatin and paclitaxel are associated with p53 gene status in gastric cancer cell lines.	Cisplatin	37-46	P53	Homo sapiens	82-85
15870870-0	2005	Apoptosis induced by 5-fluorouracil, cisplatin and paclitaxel are associated with p53 gene status in gastric cancer cell lines.	Paclitaxel	51-61	P53	Homo sapiens	82-85
15870870-5	2005	From these results, our previous study suggests that cells with mutant-type p53 may be less responsive to FP treatment and the present study indicates that another anti-cancer drug like paclitaxel, which might be mediated by a p53-independent pathway, should be selected.	Paclitaxel	186-196	P53	Homo sapiens	76-79
15870870-5	2005	From these results, our previous study suggests that cells with mutant-type p53 may be less responsive to FP treatment and the present study indicates that another anti-cancer drug like paclitaxel, which might be mediated by a p53-independent pathway, should be selected.	Paclitaxel	186-196	P53	Homo sapiens	227-230
15870947-8	2005	Our findings also indicate that anti-apoptotic Bcl-xL and pro-apoptotic p53 are necessary but not sufficient for resistance to cisplatin-induced apoptosis in NSCLC cells.	Cisplatin	127-136	P53	Homo sapiens	72-75
16158823-10	2005	We found overexpression of the p53 protein in lymphoid cells and a point missense mutation in codon 280 at exon 8 that changed AGA (Arg) to AGT (Ser).	Arginine	132-135	P53	Homo sapiens	31-34
16158823-10	2005	We found overexpression of the p53 protein in lymphoid cells and a point missense mutation in codon 280 at exon 8 that changed AGA (Arg) to AGT (Ser).	Serine	145-148	P53	Homo sapiens	31-34
16158823-11	2005	This case may indicate the existence of a more aggressive subset of SMZL, suggesting a reconsideration of the roles of splenectomy and p53 overexpression in the diagnostic and therapeutic approaches to patients with SMZL.	smzl	68-72	P53	Homo sapiens	135-138
15956257-8	2005	Treatment of melanoma cells with cisplatin induces DNA damage and cytotoxicity, which is thought to be via p53-dependent and -independent mechanisms.	Cisplatin	33-42	P53	Homo sapiens	107-110
15755852-7	2005	We also show that estradiol increases p53 levels, which may contribute to p21 induction.	Estradiol	18-27	P53	Homo sapiens	38-41
16204849-0	2005	The contribution of the Trp/Met/Phe residues to physical interactions of p53 with cellular proteins.	Tryptophan	24-27	P53	Homo sapiens	73-76
15892716-7	2005	Inhibiting p53 function by a dominant negative p53 (p53(175His)) confirmed that the HDAC inhibitor induced apoptosis was independent of wild-type p53, even though TSA slightly activated p53 in a reporter assay.	175his	56-62	P53	Homo sapiens	11-14
15892716-7	2005	Inhibiting p53 function by a dominant negative p53 (p53(175His)) confirmed that the HDAC inhibitor induced apoptosis was independent of wild-type p53, even though TSA slightly activated p53 in a reporter assay.	175his	56-62	P53	Homo sapiens	47-50
15892716-7	2005	Inhibiting p53 function by a dominant negative p53 (p53(175His)) confirmed that the HDAC inhibitor induced apoptosis was independent of wild-type p53, even though TSA slightly activated p53 in a reporter assay.	175his	56-62	P53	Homo sapiens	47-50
15892716-7	2005	Inhibiting p53 function by a dominant negative p53 (p53(175His)) confirmed that the HDAC inhibitor induced apoptosis was independent of wild-type p53, even though TSA slightly activated p53 in a reporter assay.	175his	56-62	P53	Homo sapiens	47-50
15892716-7	2005	Inhibiting p53 function by a dominant negative p53 (p53(175His)) confirmed that the HDAC inhibitor induced apoptosis was independent of wild-type p53, even though TSA slightly activated p53 in a reporter assay.	175his	56-62	P53	Homo sapiens	47-50
16204849-8	2005	Several clusters of the Trp/Met/Phe residues are involved in the p53 protein-protein interactions.	Tryptophan	24-27	P53	Homo sapiens	65-68
15888975-8	2005	This mutation causes an amino-acid replacement (Tyr to Cys), which was previously proven to attenuate p53 function.	Tyrosine	48-51	P53	Homo sapiens	102-105
15888975-8	2005	This mutation causes an amino-acid replacement (Tyr to Cys), which was previously proven to attenuate p53 function.	Cysteine	55-58	P53	Homo sapiens	102-105
15863265-1	2005	In this study, we analyzed the role of the p53 status for paclitaxel/Taxol sensitivity in renal cell carcinomas (RCCs) of the clear cell type.	Paclitaxel	58-68	P53	Homo sapiens	43-46
15863265-1	2005	In this study, we analyzed the role of the p53 status for paclitaxel/Taxol sensitivity in renal cell carcinomas (RCCs) of the clear cell type.	Paclitaxel	69-74	P53	Homo sapiens	43-46
15920103-8	2005	Transcriptional activation of p21(WAF1/CIP1) and Bax by p53 on exposure to cisplatin was completely blocked by introducing the p53 decoy oligonucleotide.	Oligonucleotides	137-152	P53	Homo sapiens	56-59
15782130-5	2005	We demonstrate that BARD1 binds to unphosphorylated and serine-15 phosphorylated forms of p53 in several cell types and that the region required for binding comprises the region sufficient for apoptosis induction.	Serine	56-62	P53	Homo sapiens	90-93
15920103-0	2005	Targeted disruption of transcriptional regulatory function of p53 by a novel efficient method for introducing a decoy oligonucleotide into nuclei.	Oligonucleotides	118-133	P53	Homo sapiens	62-65
15920103-8	2005	Transcriptional activation of p21(WAF1/CIP1) and Bax by p53 on exposure to cisplatin was completely blocked by introducing the p53 decoy oligonucleotide.	Cisplatin	75-84	P53	Homo sapiens	56-59
15920103-8	2005	Transcriptional activation of p21(WAF1/CIP1) and Bax by p53 on exposure to cisplatin was completely blocked by introducing the p53 decoy oligonucleotide.	Oligonucleotides	137-152	P53	Homo sapiens	127-130
15920103-8	2005	Transcriptional activation of p21(WAF1/CIP1) and Bax by p53 on exposure to cisplatin was completely blocked by introducing the p53 decoy oligonucleotide.	Cisplatin	75-84	P53	Homo sapiens	127-130
15657900-6	2005	Co-exposure to C75 and Taxol induced a remarkable nuclear accumulation of activated p38 mitogen-activated protein kinase (p38 MAPK), which was accompanied by a synergistic nuclear accumulation of the p53 tumor-suppressor protein that was phosphorylated at Ser46, a p38 MAPK-regulated pro-apoptotic modification of p53.	Paclitaxel	23-28	P53	Homo sapiens	200-203
15657900-6	2005	Co-exposure to C75 and Taxol induced a remarkable nuclear accumulation of activated p38 mitogen-activated protein kinase (p38 MAPK), which was accompanied by a synergistic nuclear accumulation of the p53 tumor-suppressor protein that was phosphorylated at Ser46, a p38 MAPK-regulated pro-apoptotic modification of p53.	Paclitaxel	23-28	P53	Homo sapiens	314-317
15823547-0	2005	TNF-alpha promotes Doxorubicin-induced cell apoptosis and anti-cancer effect through downregulation of p21 in p53-deficient tumor cells.	Doxorubicin	19-30	P53	Homo sapiens	110-113
15823547-2	2005	Here we show that effective Doxorubicin (DOX)-induced apoptosis is p53-dependent.	Doxorubicin	28-39	P53	Homo sapiens	67-70
15823547-2	2005	Here we show that effective Doxorubicin (DOX)-induced apoptosis is p53-dependent.	Doxorubicin	41-44	P53	Homo sapiens	67-70
15823547-3	2005	However, an alternative treatment of DOX/TNF-alpha/DOX restored sensitivity of p53-deficient cells to DOX-induced apoptosis.	Doxorubicin	37-40	P53	Homo sapiens	79-82
15823547-3	2005	However, an alternative treatment of DOX/TNF-alpha/DOX restored sensitivity of p53-deficient cells to DOX-induced apoptosis.	Doxorubicin	51-54	P53	Homo sapiens	79-82
15823547-3	2005	However, an alternative treatment of DOX/TNF-alpha/DOX restored sensitivity of p53-deficient cells to DOX-induced apoptosis.	Doxorubicin	51-54	P53	Homo sapiens	79-82
15850555-4	2005	In the presence of 50 microM H(2)O(2), arrest was observed in the G2-phase of the cell cycle, along with p53-independent apoptosis.	Water	29-34	P53	Homo sapiens	105-108
15738001-0	2005	Curcumin selectively induces apoptosis in deregulated cyclin D1-expressed cells at G2 phase of cell cycle in a p53-dependent manner.	Curcumin	0-8	P53	Homo sapiens	111-114
15738001-3	2005	In our search toward delineating the molecular mechanisms behind such differential activities of curcumin, we found that it selectively increases p53 expression at G(2) phase of carcinoma cells and releases cytochrome c from mitochondria, which is an essential requirement for apoptosis.	Curcumin	97-105	P53	Homo sapiens	146-149
15738001-4	2005	Further experiments using p53-null as well as dominant-negative and wild-type p53-transfected cells have established that curcumin induces apoptosis in carcinoma cells via a p53-dependent pathway.	Curcumin	122-130	P53	Homo sapiens	26-29
15738001-4	2005	Further experiments using p53-null as well as dominant-negative and wild-type p53-transfected cells have established that curcumin induces apoptosis in carcinoma cells via a p53-dependent pathway.	Curcumin	122-130	P53	Homo sapiens	78-81
15738001-4	2005	Further experiments using p53-null as well as dominant-negative and wild-type p53-transfected cells have established that curcumin induces apoptosis in carcinoma cells via a p53-dependent pathway.	Curcumin	122-130	P53	Homo sapiens	78-81
15870257-4	2005	PPM1D also dephosphorylates p53 at phospho-Ser 15.	Serine	43-46	P53	Homo sapiens	28-31
15800853-8	2005	Evidence in support of this model, in which excess glucose metabolism inhibits expression of Pax3, thereby derepressing p53-dependent apoptosis of neuroepithelium and leading to NTD will be discussed.	Glucose	51-58	P53	Homo sapiens	120-123
15770664-5	2005	Unlike K562 cells, JURL-MK1 cells possess a probably functional p53 protein inducible by TPA (tetradecanoyl phorbol acetate) or UV-B irradiation.	Tetradecanoylphorbol Acetate	89-92	P53	Homo sapiens	64-67
15770664-5	2005	Unlike K562 cells, JURL-MK1 cells possess a probably functional p53 protein inducible by TPA (tetradecanoyl phorbol acetate) or UV-B irradiation.	Tetradecanoylphorbol Acetate	94-123	P53	Homo sapiens	64-67
16158936-5	2005	Immunohistochemical staining for p53 was performed on paraffin-embedded tissue sections using the avidin-biotin-peroxidase method.	Paraffin	54-62	P53	Homo sapiens	33-36
15899818-5	2005	To address the putative mechanisms that underlie resistance to PKC/p53-induced cell death, we generated a phorbol 12-myristate 13-acetate/p53-resistant SW480 subline and compared the gene expression profile of resistant and parental cells by DNA microarray analysis.	Tetradecanoylphorbol Acetate	106-137	P53	Homo sapiens	67-70
15966238-0	2005	Arginine and proline alleles of the p53 gene are associated with different locations of gastric cancer.	Arginine	0-8	P53	Homo sapiens	36-39
15886465-5	2005	The expression of p53 protein was increased after treatment with cisplatin and 5-FU, but not radiation.	Cisplatin	65-74	P53	Homo sapiens	18-21
15886465-5	2005	The expression of p53 protein was increased after treatment with cisplatin and 5-FU, but not radiation.	Fluorouracil	79-83	P53	Homo sapiens	18-21
15886465-10	2005	Cisplatin induced p53-dependent apoptosis and p21(WAF1/CIP1)-independent S-phase cell cycle arrest and 5-FU induced p53 and p21(WAF1/CIP1)-dependent G1-phase cell cycle arrest, not apoptosis.	Cisplatin	0-9	P53	Homo sapiens	18-21
15886465-10	2005	Cisplatin induced p53-dependent apoptosis and p21(WAF1/CIP1)-independent S-phase cell cycle arrest and 5-FU induced p53 and p21(WAF1/CIP1)-dependent G1-phase cell cycle arrest, not apoptosis.	Fluorouracil	103-107	P53	Homo sapiens	116-119
15886465-11	2005	Cisplatin and 5-FU induced p53-dependent pathways, but radiation p53-independent pathway.	Cisplatin	0-9	P53	Homo sapiens	27-30
15886465-11	2005	Cisplatin and 5-FU induced p53-dependent pathways, but radiation p53-independent pathway.	Cisplatin	0-9	P53	Homo sapiens	65-68
15886465-11	2005	Cisplatin and 5-FU induced p53-dependent pathways, but radiation p53-independent pathway.	Fluorouracil	14-18	P53	Homo sapiens	27-30
15886465-11	2005	Cisplatin and 5-FU induced p53-dependent pathways, but radiation p53-independent pathway.	Fluorouracil	14-18	P53	Homo sapiens	65-68
15867370-1	2005	The tumor suppressor gene p53 is activated by reactive oxygen species-generating agents.	Reactive Oxygen Species	46-69	P53	Homo sapiens	26-29
15867370-3	2005	Herein, we show that p53 translocation to mitochondria precedes its translocation to nucleus in JB6 skin epidermal cells treated with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA).	Tetradecanoylphorbol Acetate	153-189	P53	Homo sapiens	21-24
15867370-3	2005	Herein, we show that p53 translocation to mitochondria precedes its translocation to nucleus in JB6 skin epidermal cells treated with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA).	Tetradecanoylphorbol Acetate	191-194	P53	Homo sapiens	21-24
15867370-4	2005	Translocation of p53 to mitochondria occurs within 10 minutes after TPA application.	Tetradecanoylphorbol Acetate	68-71	P53	Homo sapiens	17-20
15867370-5	2005	In the mitochondria, p53 interacts with the primary antioxidant enzyme, manganese superoxide dismutase (MnSOD), consistent with the reduction of its superoxide scavenging activity, and a subsequent decrease of mitochondrial membrane potential.	Superoxides	82-92	P53	Homo sapiens	21-24
15867370-6	2005	In contrast to the immediate action on mitochondria, p53 transcriptional activity in the nucleus increases at 1 hour following TPA application, accompanied by an increase in the levels of its target gene bax at 15 hours following TPA treatment.	Tetradecanoylphorbol Acetate	127-130	P53	Homo sapiens	53-56
15867370-6	2005	In contrast to the immediate action on mitochondria, p53 transcriptional activity in the nucleus increases at 1 hour following TPA application, accompanied by an increase in the levels of its target gene bax at 15 hours following TPA treatment.	Tetradecanoylphorbol Acetate	230-233	P53	Homo sapiens	53-56
15940066-0	2005	Relationship between hormonal receptors, HER-2, p53 protein, Bcl-2, and MIB-1 status and the antitumor effects of neoadjuvant anthracycline-based chemotherapy in invasive breast cancer patients.	Anthracyclines	126-139	P53	Homo sapiens	48-51
15942101-4	2005	Direct sequencing revealed that they all had missense mutation in codon 175 (G to A) of arginine switched to histidine, suggesting a germline mutation of TP53.	Arginine	88-96	P53	Homo sapiens	154-158
15942101-4	2005	Direct sequencing revealed that they all had missense mutation in codon 175 (G to A) of arginine switched to histidine, suggesting a germline mutation of TP53.	Histidine	109-118	P53	Homo sapiens	154-158
15809720-2	2005	With this system we quantitatively analyzed adriamycin (ADR)-induced cell death using manganese superoxide dismutase (MnSOD)- and wild-type p53-gene transfectants on SaOS(2), a p53-deficient human osteosarcoma cell line.	Doxorubicin	44-54	P53	Homo sapiens	177-180
15809720-13	2005	These findings indicate that hydrogen peroxide overload on p53-independent pathway due to MnSOD overexpression plus BSO might increase the apoptosis frequency without acceleration of apoptotic process of each cell, resulting in negating ADR-tolerance of MnSOD-overexpressing cell lines.	Hydrogen Peroxide	29-46	P53	Homo sapiens	59-62
15728246-2	2005	In our study, we characterized the signaling pathway linking oxidative stress induced by sublethal concentrations of H2O2 to p53 in primary human endothelial cells through the interferon (IFN)-inducible gene IFI16.	Hydrogen Peroxide	117-121	P53	Homo sapiens	125-128
16075975-2	2005	METHOD: p53 protein overexpression was detected in 76 squamous cell carcinoma and the tissue beside the LSCC with SP method of Immuno-histochemical staining [IHC].	TFF2 protein, human	114-116	P53	Homo sapiens	8-11
15781256-2	2005	Herein we investigated whether the chemosensitizing action of PDMP impinged on any unspecific effect of this compound on doxorubicin-induced expression of p53 and/or p21(Cip1/Waf1), namely two proteins reported to modulate the apoptotic response to DNA-damaging agents, in a positive or negative fashion, respectively.	Doxorubicin	121-132	P53	Homo sapiens	155-158
15749705-1	2005	The NAD+-dependent protein deacetylase family, Sir2 (or sirtuins), is important for many cellular processes including gene silencing, regulation of p53, fatty acid metabolism, cell cycle regulation, and life span extension.	Fatty Acids	153-163	P53	Homo sapiens	148-151
15749705-6	2005	To examine the requirements for resveratrol activation of SIRT1, we synthesized three p53 acetylpeptide substrates either lacking a fluorophore or containing a 7-amino-4-methylcoumarin (p53-AMC) or rhodamine 110 (p53-R110).	7-amino-4-methylcoumarin	190-193	P53	Homo sapiens	186-189
15749705-6	2005	To examine the requirements for resveratrol activation of SIRT1, we synthesized three p53 acetylpeptide substrates either lacking a fluorophore or containing a 7-amino-4-methylcoumarin (p53-AMC) or rhodamine 110 (p53-R110).	7-amino-4-methylcoumarin	190-193	P53	Homo sapiens	186-189
15749705-10	2005	Without resveratrol, the coumarin of p53-AMC peptide is solvent-exposed and makes no significant contacts with SIRT1.	7-amino-4-methylcoumarin	41-44	P53	Homo sapiens	37-40
15671037-3	2005	We previously showed that RelA-NF-kappaB functioned as a proapoptotic factor by activating the p53-signaling pathway in response to doxycycline-induced superoxide.	Superoxides	152-162	P53	Homo sapiens	95-98
15671037-6	2005	Plk3 formed a complex with p53 and was involved in the phosphorylation of p53 on Ser-20 in response to superoxide.	Serine	81-84	P53	Homo sapiens	27-30
15671037-6	2005	Plk3 formed a complex with p53 and was involved in the phosphorylation of p53 on Ser-20 in response to superoxide.	Serine	81-84	P53	Homo sapiens	74-77
15671037-6	2005	Plk3 formed a complex with p53 and was involved in the phosphorylation of p53 on Ser-20 in response to superoxide.	Superoxides	103-113	P53	Homo sapiens	27-30
15671037-6	2005	Plk3 formed a complex with p53 and was involved in the phosphorylation of p53 on Ser-20 in response to superoxide.	Superoxides	103-113	P53	Homo sapiens	74-77
15807522-1	2005	Wip1, the wild-type p53-induced phosphatase, selectively dephosphorylates a threonine residue on p38 MAPK and mediates a negative feedback loop of the p38 MAPK-p53 signaling pathway.	Threonine	76-85	P53	Homo sapiens	20-23
15866171-5	2005	AMPK activation induces phosphorylation of p53 on serine 15, and this phosphorylation is required to initiate AMPK-dependent cell-cycle arrest.	Serine	50-56	P53	Homo sapiens	43-46
15866171-6	2005	AMPK-induced p53 activation promotes cellular survival in response to glucose deprivation, and cells that have undergone a p53-dependent metabolic arrest can rapidly reenter the cell cycle upon glucose restoration.	Glucose	70-77	P53	Homo sapiens	13-16
15879716-7	2005	The alanine-replaced BAF53 mutants also stimulated p53-dependent transcription, in which the SWI/SNF and TRRAP complexes are involved.	Alanine	4-11	P53	Homo sapiens	51-54
15752772-6	2005	The SD.IFN-beta also induced p53 and phosphorylation of p53 at Ser(15).	Serine	63-66	P53	Homo sapiens	56-59
15809436-0	2005	Inhibition of NAD(P)H:quinone oxidoreductase 1 activity and induction of p53 degradation by the natural phenolic compound curcumin.	Curcumin	122-130	P53	Homo sapiens	73-76
15899123-9	2005	Phosphorylation of ERK resulted in up-regulation of p53 expression, which was blocked by mitogen-activated protein kinase (MEK), inhibitor PD 98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	139-147	P53	Homo sapiens	52-55
15833870-0	2005	Phenoxodiol, a novel isoflavone, induces G1 arrest by specific loss in cyclin-dependent kinase 2 activity by p53-independent induction of p21WAF1/CIP1.	Isoflavones	21-31	P53	Homo sapiens	109-112
15809436-2	2005	NQO1 binds and stabilizes WT p53, whereas NQO1 inhibitors including dicoumarol and various other coumarins and flavones induce ubiquitin-independent proteasomal p53 degradation and thus inhibit p53-induced apoptosis.	Flavones	111-119	P53	Homo sapiens	161-164
15809436-2	2005	NQO1 binds and stabilizes WT p53, whereas NQO1 inhibitors including dicoumarol and various other coumarins and flavones induce ubiquitin-independent proteasomal p53 degradation and thus inhibit p53-induced apoptosis.	Flavones	111-119	P53	Homo sapiens	161-164
15809436-3	2005	Here, we show that curcumin, a natural phenolic compound found in the spice turmeric, induced ubiquitin-independent degradation of WT p53 and inhibited p53-induced apoptosis in normal thymocytes and myeloid leukemic cells.	Curcumin	19-27	P53	Homo sapiens	134-137
15809436-3	2005	Here, we show that curcumin, a natural phenolic compound found in the spice turmeric, induced ubiquitin-independent degradation of WT p53 and inhibited p53-induced apoptosis in normal thymocytes and myeloid leukemic cells.	Curcumin	19-27	P53	Homo sapiens	152-155
15809436-4	2005	Like dicoumarol, curcumin inhibited the activity of recombinant NQO1 in vitro, inhibited the activity of endogenous cellular NQO1 in vivo, and dissociated NQO1-WT p53 complexes.	Curcumin	17-25	P53	Homo sapiens	163-166
15809436-7	2005	The results indicate that curcumin induces p53 degradation and inhibits p53-induced apoptosis by an NQO1-dependent pathway.	Curcumin	26-34	P53	Homo sapiens	43-46
15807522-1	2005	Wip1, the wild-type p53-induced phosphatase, selectively dephosphorylates a threonine residue on p38 MAPK and mediates a negative feedback loop of the p38 MAPK-p53 signaling pathway.	Threonine	76-85	P53	Homo sapiens	160-163
15809436-7	2005	The results indicate that curcumin induces p53 degradation and inhibits p53-induced apoptosis by an NQO1-dependent pathway.	Curcumin	26-34	P53	Homo sapiens	72-75
15551330-9	2005	p53 mutations were significantly (p = 0.04) less common in NSCLC from patients with codon 326 Ser/Cys or Cys/Cys genotypes (21 of 51; 41%) than in NSCLC from Ser/Ser homozygotes (53 of 90; 59%).	Serine	94-97	P53	Homo sapiens	0-3
15551330-9	2005	p53 mutations were significantly (p = 0.04) less common in NSCLC from patients with codon 326 Ser/Cys or Cys/Cys genotypes (21 of 51; 41%) than in NSCLC from Ser/Ser homozygotes (53 of 90; 59%).	Cysteine	98-101	P53	Homo sapiens	0-3
15551330-9	2005	p53 mutations were significantly (p = 0.04) less common in NSCLC from patients with codon 326 Ser/Cys or Cys/Cys genotypes (21 of 51; 41%) than in NSCLC from Ser/Ser homozygotes (53 of 90; 59%).	Cysteine	105-108	P53	Homo sapiens	0-3
15551330-9	2005	p53 mutations were significantly (p = 0.04) less common in NSCLC from patients with codon 326 Ser/Cys or Cys/Cys genotypes (21 of 51; 41%) than in NSCLC from Ser/Ser homozygotes (53 of 90; 59%).	Cysteine	105-108	P53	Homo sapiens	0-3
15551330-9	2005	p53 mutations were significantly (p = 0.04) less common in NSCLC from patients with codon 326 Ser/Cys or Cys/Cys genotypes (21 of 51; 41%) than in NSCLC from Ser/Ser homozygotes (53 of 90; 59%).	Serine	158-161	P53	Homo sapiens	0-3
15551330-9	2005	p53 mutations were significantly (p = 0.04) less common in NSCLC from patients with codon 326 Ser/Cys or Cys/Cys genotypes (21 of 51; 41%) than in NSCLC from Ser/Ser homozygotes (53 of 90; 59%).	Serine	158-161	P53	Homo sapiens	0-3
15551330-10	2005	The decrease in p53 mutation frequency among carriers of the Cys allele was more evident in lung squamous cell cancer [7 of 17 (41%) for Cys/Cys and Ser/Cys vs. 27 of 38 (71%) for Ser/Ser; p = 0.04] than in nonbronchoalveolar adenocarcinoma [11 of 26 (42%) for Cys/Cys and Ser/Cys vs. 20 of 35 (57%) for Ser/Ser; p = 0.25].	Cysteine	61-64	P53	Homo sapiens	16-19
15551330-10	2005	The decrease in p53 mutation frequency among carriers of the Cys allele was more evident in lung squamous cell cancer [7 of 17 (41%) for Cys/Cys and Ser/Cys vs. 27 of 38 (71%) for Ser/Ser; p = 0.04] than in nonbronchoalveolar adenocarcinoma [11 of 26 (42%) for Cys/Cys and Ser/Cys vs. 20 of 35 (57%) for Ser/Ser; p = 0.25].	Cysteine	137-140	P53	Homo sapiens	16-19
15551330-10	2005	The decrease in p53 mutation frequency among carriers of the Cys allele was more evident in lung squamous cell cancer [7 of 17 (41%) for Cys/Cys and Ser/Cys vs. 27 of 38 (71%) for Ser/Ser; p = 0.04] than in nonbronchoalveolar adenocarcinoma [11 of 26 (42%) for Cys/Cys and Ser/Cys vs. 20 of 35 (57%) for Ser/Ser; p = 0.25].	Cysteine	137-140	P53	Homo sapiens	16-19
15551330-10	2005	The decrease in p53 mutation frequency among carriers of the Cys allele was more evident in lung squamous cell cancer [7 of 17 (41%) for Cys/Cys and Ser/Cys vs. 27 of 38 (71%) for Ser/Ser; p = 0.04] than in nonbronchoalveolar adenocarcinoma [11 of 26 (42%) for Cys/Cys and Ser/Cys vs. 20 of 35 (57%) for Ser/Ser; p = 0.25].	Serine	149-152	P53	Homo sapiens	16-19
15551330-10	2005	The decrease in p53 mutation frequency among carriers of the Cys allele was more evident in lung squamous cell cancer [7 of 17 (41%) for Cys/Cys and Ser/Cys vs. 27 of 38 (71%) for Ser/Ser; p = 0.04] than in nonbronchoalveolar adenocarcinoma [11 of 26 (42%) for Cys/Cys and Ser/Cys vs. 20 of 35 (57%) for Ser/Ser; p = 0.25].	Cysteine	137-140	P53	Homo sapiens	16-19
15551330-10	2005	The decrease in p53 mutation frequency among carriers of the Cys allele was more evident in lung squamous cell cancer [7 of 17 (41%) for Cys/Cys and Ser/Cys vs. 27 of 38 (71%) for Ser/Ser; p = 0.04] than in nonbronchoalveolar adenocarcinoma [11 of 26 (42%) for Cys/Cys and Ser/Cys vs. 20 of 35 (57%) for Ser/Ser; p = 0.25].	Serine	180-183	P53	Homo sapiens	16-19
15551330-10	2005	The decrease in p53 mutation frequency among carriers of the Cys allele was more evident in lung squamous cell cancer [7 of 17 (41%) for Cys/Cys and Ser/Cys vs. 27 of 38 (71%) for Ser/Ser; p = 0.04] than in nonbronchoalveolar adenocarcinoma [11 of 26 (42%) for Cys/Cys and Ser/Cys vs. 20 of 35 (57%) for Ser/Ser; p = 0.25].	Serine	180-183	P53	Homo sapiens	16-19
15551330-10	2005	The decrease in p53 mutation frequency among carriers of the Cys allele was more evident in lung squamous cell cancer [7 of 17 (41%) for Cys/Cys and Ser/Cys vs. 27 of 38 (71%) for Ser/Ser; p = 0.04] than in nonbronchoalveolar adenocarcinoma [11 of 26 (42%) for Cys/Cys and Ser/Cys vs. 20 of 35 (57%) for Ser/Ser; p = 0.25].	Cysteine	137-140	P53	Homo sapiens	16-19
15551330-10	2005	The decrease in p53 mutation frequency among carriers of the Cys allele was more evident in lung squamous cell cancer [7 of 17 (41%) for Cys/Cys and Ser/Cys vs. 27 of 38 (71%) for Ser/Ser; p = 0.04] than in nonbronchoalveolar adenocarcinoma [11 of 26 (42%) for Cys/Cys and Ser/Cys vs. 20 of 35 (57%) for Ser/Ser; p = 0.25].	Cysteine	137-140	P53	Homo sapiens	16-19
15551330-10	2005	The decrease in p53 mutation frequency among carriers of the Cys allele was more evident in lung squamous cell cancer [7 of 17 (41%) for Cys/Cys and Ser/Cys vs. 27 of 38 (71%) for Ser/Ser; p = 0.04] than in nonbronchoalveolar adenocarcinoma [11 of 26 (42%) for Cys/Cys and Ser/Cys vs. 20 of 35 (57%) for Ser/Ser; p = 0.25].	Serine	180-183	P53	Homo sapiens	16-19
15551330-10	2005	The decrease in p53 mutation frequency among carriers of the Cys allele was more evident in lung squamous cell cancer [7 of 17 (41%) for Cys/Cys and Ser/Cys vs. 27 of 38 (71%) for Ser/Ser; p = 0.04] than in nonbronchoalveolar adenocarcinoma [11 of 26 (42%) for Cys/Cys and Ser/Cys vs. 20 of 35 (57%) for Ser/Ser; p = 0.25].	Cysteine	137-140	P53	Homo sapiens	16-19
15551330-10	2005	The decrease in p53 mutation frequency among carriers of the Cys allele was more evident in lung squamous cell cancer [7 of 17 (41%) for Cys/Cys and Ser/Cys vs. 27 of 38 (71%) for Ser/Ser; p = 0.04] than in nonbronchoalveolar adenocarcinoma [11 of 26 (42%) for Cys/Cys and Ser/Cys vs. 20 of 35 (57%) for Ser/Ser; p = 0.25].	Serine	180-183	P53	Homo sapiens	16-19
15551330-10	2005	The decrease in p53 mutation frequency among carriers of the Cys allele was more evident in lung squamous cell cancer [7 of 17 (41%) for Cys/Cys and Ser/Cys vs. 27 of 38 (71%) for Ser/Ser; p = 0.04] than in nonbronchoalveolar adenocarcinoma [11 of 26 (42%) for Cys/Cys and Ser/Cys vs. 20 of 35 (57%) for Ser/Ser; p = 0.25].	Serine	180-183	P53	Homo sapiens	16-19
15551330-12	2005	In summary, the hOGG1 codon 326 Cys allele was associated with a decrease in p53 mutations and no effect on G:C-to-T:A transversions in NSCLC.	Cysteine	32-35	P53	Homo sapiens	77-80
15578696-0	2005	p53-R175H mutant gains new function in regulation of doxorubicin-induced apoptosis.	Doxorubicin	53-64	P53	Homo sapiens	0-3
15578696-2	2005	Transfection of mutant p53 (R175H) to p53-null osteosarcoma Saos-2 cells suppressed apoptosis induced by doxorubicin (DOX), cisplatin and gamma radiation.	Doxorubicin	105-116	P53	Homo sapiens	23-26
15578696-2	2005	Transfection of mutant p53 (R175H) to p53-null osteosarcoma Saos-2 cells suppressed apoptosis induced by doxorubicin (DOX), cisplatin and gamma radiation.	Doxorubicin	105-116	P53	Homo sapiens	38-41
15578696-2	2005	Transfection of mutant p53 (R175H) to p53-null osteosarcoma Saos-2 cells suppressed apoptosis induced by doxorubicin (DOX), cisplatin and gamma radiation.	Doxorubicin	118-121	P53	Homo sapiens	23-26
15578696-2	2005	Transfection of mutant p53 (R175H) to p53-null osteosarcoma Saos-2 cells suppressed apoptosis induced by doxorubicin (DOX), cisplatin and gamma radiation.	Doxorubicin	118-121	P53	Homo sapiens	38-41
15578696-2	2005	Transfection of mutant p53 (R175H) to p53-null osteosarcoma Saos-2 cells suppressed apoptosis induced by doxorubicin (DOX), cisplatin and gamma radiation.	Cisplatin	124-133	P53	Homo sapiens	23-26
15578696-2	2005	Transfection of mutant p53 (R175H) to p53-null osteosarcoma Saos-2 cells suppressed apoptosis induced by doxorubicin (DOX), cisplatin and gamma radiation.	Cisplatin	124-133	P53	Homo sapiens	38-41
15578696-4	2005	After 48 hr of DOX treatment, the rate of procasapse-3 activation into 17 kDa active form was about 3-fold higher in the control cells than that in the p53-R175H counterpart.	Doxorubicin	15-18	P53	Homo sapiens	152-155
15578696-5	2005	Gene silencing of p53-R175H expression by p53 siRNA upregulate the procaspase-3 protein level and restored DOX-induced apoptosis in p53-R175H cells.	Doxorubicin	107-110	P53	Homo sapiens	18-21
15578696-5	2005	Gene silencing of p53-R175H expression by p53 siRNA upregulate the procaspase-3 protein level and restored DOX-induced apoptosis in p53-R175H cells.	Doxorubicin	107-110	P53	Homo sapiens	42-45
16054986-4	2005	One cellular consequence of sustained oxidative stress and redox imbalance resulting from the combined actions of alcohol and iron is lipid peroxidation, resulting in the production of aldehydic products such as 4-hydroxy-2-nonenal, which has been linked to site-specific mutations of the p53 gene.	Alcohols	114-121	P53	Homo sapiens	289-292
16054986-4	2005	One cellular consequence of sustained oxidative stress and redox imbalance resulting from the combined actions of alcohol and iron is lipid peroxidation, resulting in the production of aldehydic products such as 4-hydroxy-2-nonenal, which has been linked to site-specific mutations of the p53 gene.	Iron	126-130	P53	Homo sapiens	289-292
15578696-5	2005	Gene silencing of p53-R175H expression by p53 siRNA upregulate the procaspase-3 protein level and restored DOX-induced apoptosis in p53-R175H cells.	Doxorubicin	107-110	P53	Homo sapiens	42-45
15578696-6	2005	Our results suggest that p53-R175H mutation may gain new function in decreasing DOX-induced apoptotic response through suppression of caspase-3 level and its activation.	Doxorubicin	80-83	P53	Homo sapiens	25-28
15846087-4	2005	We found that when comparing p53 to the transcriptional activator, GAL4-VP16, both of which are classified as acidic activators, that stimulation of transcription by p53 is dependent upon low Mg2+ concentrations and limiting amounts of extract.	magnesium ion	192-196	P53	Homo sapiens	29-32
15618970-0	2005	Adenovirus-mediated p53 gene therapy in pediatric soft-tissue sarcoma cell lines: sensitization to cisplatin and doxorubicin.	Cisplatin	99-108	P53	Homo sapiens	20-23
15618970-0	2005	Adenovirus-mediated p53 gene therapy in pediatric soft-tissue sarcoma cell lines: sensitization to cisplatin and doxorubicin.	Doxorubicin	113-124	P53	Homo sapiens	20-23
15805289-9	2005	However, IMR90 and LNCaP cells became more sensitive to doxorubicin or doxorubicin plus UCN-01 when both p53 and ATM functions were suppressed.	Doxorubicin	56-67	P53	Homo sapiens	105-108
15805289-9	2005	However, IMR90 and LNCaP cells became more sensitive to doxorubicin or doxorubicin plus UCN-01 when both p53 and ATM functions were suppressed.	Doxorubicin	71-82	P53	Homo sapiens	105-108
15774934-13	2005	p53 as an antiproliferative drug has the potential to replace mitomycin C and 5-fluorouracil in glaucoma surgery.	Fluorouracil	78-92	P53	Homo sapiens	0-3
15805253-0	2005	p53 mutations in benzo(a)pyrene-exposed human p53 knock-in murine fibroblasts correlate with p53 mutations in human lung tumors.	pyrene	25-31	P53	Homo sapiens	0-3
15805253-0	2005	p53 mutations in benzo(a)pyrene-exposed human p53 knock-in murine fibroblasts correlate with p53 mutations in human lung tumors.	pyrene	25-31	P53	Homo sapiens	46-49
15846102-1	2005	We have previously shown that the HDAC inhibitors (HDACI) activate the p53 molecule through acetylation of 320 and 373 lysine residues, upregulate PIG3 and NOXA and induce apoptosis in cancer cells expressing wild and pseudo-wild type p53 genes (Terui T, et al.	Lysine	119-125	P53	Homo sapiens	71-74
15846087-4	2005	We found that when comparing p53 to the transcriptional activator, GAL4-VP16, both of which are classified as acidic activators, that stimulation of transcription by p53 is dependent upon low Mg2+ concentrations and limiting amounts of extract.	magnesium ion	192-196	P53	Homo sapiens	166-169
15814660-9	2005	Significant DeltaPsim loss and glutathione (GSH) depletion in response to TPZ was observed in p53-functional cell lines (SMS-SAN, SMS-SAN EV, and CHLA-15) but not in p53-nonfunctional cell lines (SMS-SAN E6 and CHLA-90).	Glutathione	44-47	P53	Homo sapiens	94-97
16027880-0	2005	Olivomycin induces tumor cell apoptosis and suppresses p53-induced transcription.	Olivomycins	0-10	P53	Homo sapiens	55-58
16027880-1	2005	Olivomycin (DNA-binding antibiotic) in nanomolar concentrations induces apoptosis of human tumor cells and inhibits p53-dependent transcription of the reporter gene (basal and induced by antitumor drugs).	Olivomycins	0-10	P53	Homo sapiens	116-119
15814660-12	2005	Thus, TPZ cytotoxicity for neuroblastoma cell lines in hypoxia occurred via a p53-dependent mitochondrial pathway that caused induction of p53 and p21, DeltaPsim decrease, GSH depletion, and apoptosis.	Glutathione	172-175	P53	Homo sapiens	78-81
15814626-2	2005	An Arg/Pro polymorphism at codon 72 of the p53 gene alters the ability of the p53 protein to induce apoptosis, influences the behavior of mutant p53, decreases DNA repair capacity, and may be linked with an increased risk of lung cancer.	Arginine	3-6	P53	Homo sapiens	43-46
15814626-2	2005	An Arg/Pro polymorphism at codon 72 of the p53 gene alters the ability of the p53 protein to induce apoptosis, influences the behavior of mutant p53, decreases DNA repair capacity, and may be linked with an increased risk of lung cancer.	Arginine	3-6	P53	Homo sapiens	78-81
15608028-3	2005	In addition, recent data provide evidence that p53 plays a critical role in mediating pregnancy by regulating steroid hormone activation.	Steroids	110-117	P53	Homo sapiens	47-50
15814626-2	2005	An Arg/Pro polymorphism at codon 72 of the p53 gene alters the ability of the p53 protein to induce apoptosis, influences the behavior of mutant p53, decreases DNA repair capacity, and may be linked with an increased risk of lung cancer.	Arginine	3-6	P53	Homo sapiens	78-81
15814626-7	2005	p53 mutations were significantly (P = 0.01) associated with the number of codon 72 Pro alleles: Pro/Pro homozygotes, 17 of 26 (65%); Arg/Pro heterozygotes, 45 of 79 (57%); and Arg/Arg homozygotes, 31 of 77 (40%).	Arginine	133-136	P53	Homo sapiens	0-3
15814626-7	2005	p53 mutations were significantly (P = 0.01) associated with the number of codon 72 Pro alleles: Pro/Pro homozygotes, 17 of 26 (65%); Arg/Pro heterozygotes, 45 of 79 (57%); and Arg/Arg homozygotes, 31 of 77 (40%).	Arginine	176-179	P53	Homo sapiens	0-3
15814626-7	2005	p53 mutations were significantly (P = 0.01) associated with the number of codon 72 Pro alleles: Pro/Pro homozygotes, 17 of 26 (65%); Arg/Pro heterozygotes, 45 of 79 (57%); and Arg/Arg homozygotes, 31 of 77 (40%).	Arginine	176-179	P53	Homo sapiens	0-3
15790450-4	2005	The objective of this study was to determine if p53 is involved in the mechanism of RA radiosensitization.	Tretinoin	84-86	P53	Homo sapiens	48-51
15842252-7	2005	p53-independent apoptosis was seen with cisplatin treatment, a novel finding.	Cisplatin	40-49	P53	Homo sapiens	0-3
15842252-9	2005	Cisplatin may induce p53-independent apoptosis.	Cisplatin	0-9	P53	Homo sapiens	21-24
15790450-6	2005	RESULTS: RA (5 microM 9-cis-RA) radiosensitized the SiHa and CC-1 cell lines that contain HPV-degraded p53, but did not radiosensitize the SW962 cell line, which is HPV negative and contains wild-type p53, nor the C33a cell line, which contains mutant p53 (R273C).	Tretinoin	9-11	P53	Homo sapiens	103-106
15608028-6	2005	METHODS: Genotyping was performed by PCR-based amplification of the p53 Arg and Pro variants at codon 72 in 175 cases of IRM and 143 controls.	Arginine	72-75	P53	Homo sapiens	68-71
15790450-6	2005	RESULTS: RA (5 microM 9-cis-RA) radiosensitized the SiHa and CC-1 cell lines that contain HPV-degraded p53, but did not radiosensitize the SW962 cell line, which is HPV negative and contains wild-type p53, nor the C33a cell line, which contains mutant p53 (R273C).	Tretinoin	9-11	P53	Homo sapiens	201-204
15790450-6	2005	RESULTS: RA (5 microM 9-cis-RA) radiosensitized the SiHa and CC-1 cell lines that contain HPV-degraded p53, but did not radiosensitize the SW962 cell line, which is HPV negative and contains wild-type p53, nor the C33a cell line, which contains mutant p53 (R273C).	Tretinoin	9-11	P53	Homo sapiens	201-204
15849679-3	2005	One of the mechanisms of tumoural progression consists in the protein inactivation resulting from the NO nitration of tyrosine from proteins coded for by tumour-suppressing genes, such as p53.	Tyrosine	118-126	P53	Homo sapiens	188-191
15795422-7	2005	In contrast, cells treated with apigenin remained DCF and phospho-p53 staining positive in response to H2O2.	Hydrogen Peroxide	103-107	P53	Homo sapiens	66-69
15837074-8	2005	Although BaP had no effect on total cellular p53 levels, phosphorylation of p53 at serine 15 (p53 ser-15phos) was markedly increased.	Serine	83-89	P53	Homo sapiens	76-79
15837074-8	2005	Although BaP had no effect on total cellular p53 levels, phosphorylation of p53 at serine 15 (p53 ser-15phos) was markedly increased.	Serine	83-89	P53	Homo sapiens	76-79
15837074-8	2005	Although BaP had no effect on total cellular p53 levels, phosphorylation of p53 at serine 15 (p53 ser-15phos) was markedly increased.	Serine	83-86	P53	Homo sapiens	76-79
15837074-8	2005	Although BaP had no effect on total cellular p53 levels, phosphorylation of p53 at serine 15 (p53 ser-15phos) was markedly increased.	Serine	83-86	P53	Homo sapiens	76-79
15837074-9	2005	The presence of Wortmannin, an inhibitor of PI-3 kinases, decreased BaP-induced p53 ser-15phos, as did the presence of the antioxidant vitamin E.	Serine	84-87	P53	Homo sapiens	80-83
15756275-6	2005	We conclude that arginine homozygosity at codon 72 of the p53 gene is associated with a significant increased breast cancer risk in Jewish high-risk population.	Arginine	17-25	P53	Homo sapiens	58-61
15770215-0	2005	Aspirin-induced nuclear translocation of NFkappaB and apoptosis in colorectal cancer is independent of p53 status and DNA mismatch repair proficiency.	Aspirin	0-7	P53	Homo sapiens	103-106
15770215-8	2005	Here, we set out to determine the p53 and hMLH1 dependency of the effects of aspirin on NFkappaB signalling and apoptosis in CRC.	Aspirin	77-84	P53	Homo sapiens	34-37
15711598-7	2005	Paclitaxel impairs microtubule function, causes G2/M cell cycle blockade, mitochondria damage, and p53-independent apoptosis.	Paclitaxel	0-10	P53	Homo sapiens	99-102
15797377-2	2005	Here we show that RAD001 (everolimus), a rapamycin derivative, dramatically enhances cisplatin-induced apoptosis in wild-type p53, but not mutant p53 tumor cells.	Cisplatin	85-94	P53	Homo sapiens	126-129
15797377-4	2005	We further show that RAD001 sensitizes cells to cisplatin by inhibiting p53-induced p21 expression.	Cisplatin	48-57	P53	Homo sapiens	72-75
15611068-0	2005	A novel NF-kappaB pathway involving IKKbeta and p65/RelA Ser-536 phosphorylation results in p53 Inhibition in the absence of NF-kappaB transcriptional activity.	Serine	57-60	P53	Homo sapiens	92-95
15611068-4	2005	We now present evidence that suggests that the upstream kinase IKKbeta plays an important role in Tax-induced p53 inhibition through phosphorylation of p65/RelA at Ser-536.	Serine	164-167	P53	Homo sapiens	110-113
15611068-8	2005	Fourth, we show that phosphorylation of p65/RelA at Ser-536 is important for Tax inhibition of p53 using MEF p65/RelA-/-cells transfected with p65/RelA WT or mutant plasmids.	Serine	52-55	P53	Homo sapiens	95-98
15591050-2	2005	Prolonged molecular dynamics simulation of ACh-binding protein showed that binding of ACh establishes close register of Trps from adjacent subunits, Trp(143) and Trp(53), and draws the peripheral C-loop inward to occlude the entrance to the binding cavity.	Acetylcholine	43-46	P53	Homo sapiens	162-168
15591050-2	2005	Prolonged molecular dynamics simulation of ACh-binding protein showed that binding of ACh establishes close register of Trps from adjacent subunits, Trp(143) and Trp(53), and draws the peripheral C-loop inward to occlude the entrance to the binding cavity.	Acetylcholine	86-89	P53	Homo sapiens	162-168
15591050-2	2005	Prolonged molecular dynamics simulation of ACh-binding protein showed that binding of ACh establishes close register of Trps from adjacent subunits, Trp(143) and Trp(53), and draws the peripheral C-loop inward to occlude the entrance to the binding cavity.	Tryptophan	120-124	P53	Homo sapiens	162-168
15591050-2	2005	Prolonged molecular dynamics simulation of ACh-binding protein showed that binding of ACh establishes close register of Trps from adjacent subunits, Trp(143) and Trp(53), and draws the peripheral C-loop inward to occlude the entrance to the binding cavity.	Tryptophan	120-123	P53	Homo sapiens	162-168
15591050-3	2005	Close register of Trp(143) and Trp(53) was demonstrated by ACh-mediated quenching of intrinsic Trp fluorescence, elimination of quenching by mutation of one or both Trps to Phe, and decreased lifetime of Trp fluorescence by bound ACh.	Acetylcholine	59-62	P53	Homo sapiens	31-37
15591050-3	2005	Close register of Trp(143) and Trp(53) was demonstrated by ACh-mediated quenching of intrinsic Trp fluorescence, elimination of quenching by mutation of one or both Trps to Phe, and decreased lifetime of Trp fluorescence by bound ACh.	Tryptophan	165-169	P53	Homo sapiens	31-37
15591050-3	2005	Close register of Trp(143) and Trp(53) was demonstrated by ACh-mediated quenching of intrinsic Trp fluorescence, elimination of quenching by mutation of one or both Trps to Phe, and decreased lifetime of Trp fluorescence by bound ACh.	Acetylcholine	230-233	P53	Homo sapiens	31-37
15786529-0	2005	Effects of folic acid on epithelial apoptosis and expression of Bcl-2 and p53 in premalignant gastric lesions.	Folic Acid	11-21	P53	Homo sapiens	74-77
15786529-7	2005	Both the epithelial apoptosis rate and the tumor suppressor p53 expression in gastric mucosa significantly increased after folic acid treatment.	Folic Acid	123-133	P53	Homo sapiens	60-63
15780856-11	2005	Plasma TRP is significantly lower in low-weight patients than in healthy control subjects (TRP = 53.73 [SD = 8.21]), but there was no significant difference between control subjects and normal-weight patients.	Tryptophan	7-10	P53	Homo sapiens	91-99
15710360-5	2005	Here, we show that treatment of the human colon carcinoma cell line HCT116 with different concentrations of R-flurbiprofen leads to an accumulation of p53 protein which is accompanied by an increase in phosphorylated p53 at serine 15.	Serine	224-230	P53	Homo sapiens	151-154
15710360-5	2005	Here, we show that treatment of the human colon carcinoma cell line HCT116 with different concentrations of R-flurbiprofen leads to an accumulation of p53 protein which is accompanied by an increase in phosphorylated p53 at serine 15.	Serine	224-230	P53	Homo sapiens	217-220
15710360-9	2005	In conclusion, we were able to show that induction of apoptosis in HCT116 cells after R-flurbiprofen treatment is at least partly dependent on the tumor suppressor gene p53 and that mutation of p53 at serine 15 impairs the apoptotic potency of R-flurbiprofen.	Serine	201-207	P53	Homo sapiens	194-197
15592835-10	2005	The phosphorylation degree of serine 15 of p53, which is thought to be an active form of p53 in response to cellular DNA damage, remained in a steady state.	Serine	30-36	P53	Homo sapiens	43-46
15592835-10	2005	The phosphorylation degree of serine 15 of p53, which is thought to be an active form of p53 in response to cellular DNA damage, remained in a steady state.	Serine	30-36	P53	Homo sapiens	89-92
15854413-0	2005	[Roles of mutant p53 gene in malignant phenotypes and resistance to drugs in anti-7,8-dihydrodiol-9,10-epoxide benzo(a)pyrene-induced lung cancer cells].	7,8-dihydrodiol-9,10-epoxide	82-110	P53	Homo sapiens	17-20
15625077-8	2005	Thus, in HepG2 cells pravastatin and simvastatin pretreatment attenuated the p53 response to DNA damage induced by 5-fluorouracil and benzo(a)pyrene.	Fluorouracil	115-129	P53	Homo sapiens	77-80
15854413-1	2005	OBJECTIVE: To study the role of mutant p53 gene induced by anti-7,8-dihydrodiol-9,10-epoxide benzo(a)pyrene (BPDE) in the development of lung cancer and the effects of wild-type p53 substitution on malignant phenotype and resistance to drugs.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	109-113	P53	Homo sapiens	178-181
15854413-2	2005	METHODS: BPDE-induced human lung cancer cells (16HBE, a human bronchial epithelial cell line, treated by BPDE) with mutant p53 gene were transfected with pShuttle-cmv-wild p53, followed by soft-agar colony formation assay and cell growth assay.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	9-13	P53	Homo sapiens	123-126
15810875-7	2005	Furthermore, we demonstrated that the removal of endogenous nitric oxide in melanoma cell lines led to increased sensitivity to cisplatin-induced apoptosis in a p53-dependent manner.	Nitric Oxide	60-72	P53	Homo sapiens	161-164
15810875-7	2005	Furthermore, we demonstrated that the removal of endogenous nitric oxide in melanoma cell lines led to increased sensitivity to cisplatin-induced apoptosis in a p53-dependent manner.	Cisplatin	128-137	P53	Homo sapiens	161-164
15744586-3	2005	Here we demonstrate that treatment of gastric adenocarcinoma SNU-1 cells with resveratrol results in time and concentration dependent accumulation of tumor suppressors p21(cip1/WAF-1) and p53 and is preceded by loss of membrane-associated PKC delta protein and a concomitant increase in cytosolic PKC alpha.	Resveratrol	78-89	P53	Homo sapiens	188-191
15797684-8	2005	The mechanism of cell death induced by these fatty acids seemed to involve mitochondrial depolarization, lipid accumulation, and overexpression of C-MYC and P53.	Fatty Acids	45-56	P53	Homo sapiens	157-160
16335246-3	2005	An increase in p53 protein expression was found in A549 and MCF7 (WT) cells treated with cisplatin, methotrexate, and doxorubicin, whereas the level of p53 was not statistically significantly changed in the MCF7 DOX/R cells.	Cisplatin	89-98	P53	Homo sapiens	15-18
16335246-3	2005	An increase in p53 protein expression was found in A549 and MCF7 (WT) cells treated with cisplatin, methotrexate, and doxorubicin, whereas the level of p53 was not statistically significantly changed in the MCF7 DOX/R cells.	Doxorubicin	118-129	P53	Homo sapiens	15-18
16335246-3	2005	An increase in p53 protein expression was found in A549 and MCF7 (WT) cells treated with cisplatin, methotrexate, and doxorubicin, whereas the level of p53 was not statistically significantly changed in the MCF7 DOX/R cells.	Doxorubicin	212-215	P53	Homo sapiens	15-18
16335246-4	2005	In the untreated MCF7 DOX/R cells the level of p53 protein was markedly higher than in the untreated WT MCF7 cells.	Doxorubicin	22-25	P53	Homo sapiens	47-50
16335246-5	2005	A potential role of p53 protein in the development of doxorubicin-resistance in carcinoma cells is discussed.	Doxorubicin	54-65	P53	Homo sapiens	20-23
15854413-2	2005	METHODS: BPDE-induced human lung cancer cells (16HBE, a human bronchial epithelial cell line, treated by BPDE) with mutant p53 gene were transfected with pShuttle-cmv-wild p53, followed by soft-agar colony formation assay and cell growth assay.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	9-13	P53	Homo sapiens	172-175
15854413-6	2005	In addition, the lung cancer cells transfected with wild-type p53 gene showed enhanced sensitivity to adriamycin (ADM) to which the cells before transfection was resistant.	Doxorubicin	102-112	P53	Homo sapiens	62-65
15854413-6	2005	In addition, the lung cancer cells transfected with wild-type p53 gene showed enhanced sensitivity to adriamycin (ADM) to which the cells before transfection was resistant.	Doxorubicin	114-117	P53	Homo sapiens	62-65
15854413-0	2005	[Roles of mutant p53 gene in malignant phenotypes and resistance to drugs in anti-7,8-dihydrodiol-9,10-epoxide benzo(a)pyrene-induced lung cancer cells].	pyrene	119-125	P53	Homo sapiens	17-20
15854413-1	2005	OBJECTIVE: To study the role of mutant p53 gene induced by anti-7,8-dihydrodiol-9,10-epoxide benzo(a)pyrene (BPDE) in the development of lung cancer and the effects of wild-type p53 substitution on malignant phenotype and resistance to drugs.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	109-113	P53	Homo sapiens	39-42
15608686-5	2005	Similarly, constitutive hTERT expression inhibited wild-type p53-dependent apoptosis in response to mitomycin C or 5-fluorouracil in HCT116 colon carcinoma cells carrying endogenous p53.	Fluorouracil	115-129	P53	Homo sapiens	61-64
15674351-2	2005	We have previously shown that p53 repression in TGCT-derived human embryonal carcinoma (EC) is relieved upon treatment with all-trans retinoic acid (RA), resulting in enhanced p53 transactivation activity.	Tretinoin	134-147	P53	Homo sapiens	30-33
15674351-2	2005	We have previously shown that p53 repression in TGCT-derived human embryonal carcinoma (EC) is relieved upon treatment with all-trans retinoic acid (RA), resulting in enhanced p53 transactivation activity.	Tretinoin	134-147	P53	Homo sapiens	176-179
15674351-2	2005	We have previously shown that p53 repression in TGCT-derived human embryonal carcinoma (EC) is relieved upon treatment with all-trans retinoic acid (RA), resulting in enhanced p53 transactivation activity.	Tretinoin	149-151	P53	Homo sapiens	30-33
15674351-2	2005	We have previously shown that p53 repression in TGCT-derived human embryonal carcinoma (EC) is relieved upon treatment with all-trans retinoic acid (RA), resulting in enhanced p53 transactivation activity.	Tretinoin	149-151	P53	Homo sapiens	176-179
15674351-11	2005	While RA alone had no effect on p53-NRD activity, cotreatment with RA and the histone deacetylase inhibitor trichostatin-A (TSA) completely relieved p53-NRD-mediated repression.	Tretinoin	67-69	P53	Homo sapiens	149-152
15561702-0	2005	Nitric oxide inhibition of homocysteine-induced human endothelial cell apoptosis by down-regulation of p53-dependent Noxa expression through the formation of S-nitrosohomocysteine.	Nitric Oxide	0-12	P53	Homo sapiens	103-106
15709766-5	2005	Gel retardation assays showed that dephosphorylation of serine 392 in the C-terminal domain of p53 greatly reduces Holliday junction and lesion recognition.	Serine	56-62	P53	Homo sapiens	95-98
15592498-5	2005	In contrast, activation of p53 and p21(WAF1/Cip1) induced by doxorubicin in MCF-7/Cav1 cells remains largely unaffected.	Doxorubicin	61-72	P53	Homo sapiens	27-30
15608685-2	2005	Moreover, p53 regulates the expression of various proteins participating in autoregulatory feedback loops, including proteins that negatively control p53 stability (Mdm2 and Pirh2) or modulate stress-induced phosphorylation of p53 on Ser-46 (p53DINP1 or Wip1), a key event for p53-induced apoptosis.	Serine	234-237	P53	Homo sapiens	10-13
15608685-2	2005	Moreover, p53 regulates the expression of various proteins participating in autoregulatory feedback loops, including proteins that negatively control p53 stability (Mdm2 and Pirh2) or modulate stress-induced phosphorylation of p53 on Ser-46 (p53DINP1 or Wip1), a key event for p53-induced apoptosis.	Serine	234-237	P53	Homo sapiens	150-153
15608685-2	2005	Moreover, p53 regulates the expression of various proteins participating in autoregulatory feedback loops, including proteins that negatively control p53 stability (Mdm2 and Pirh2) or modulate stress-induced phosphorylation of p53 on Ser-46 (p53DINP1 or Wip1), a key event for p53-induced apoptosis.	Serine	234-237	P53	Homo sapiens	150-153
15608685-2	2005	Moreover, p53 regulates the expression of various proteins participating in autoregulatory feedback loops, including proteins that negatively control p53 stability (Mdm2 and Pirh2) or modulate stress-induced phosphorylation of p53 on Ser-46 (p53DINP1 or Wip1), a key event for p53-induced apoptosis.	Serine	234-237	P53	Homo sapiens	150-153
15608685-3	2005	Here, we describe a new systematic analysis of p53 targets using oligonucleotide chips, and report the identification of dapk1 as a novel p53 target.	Oligonucleotides	65-80	P53	Homo sapiens	47-50
15456408-0	2005	PARP inhibition sensitizes p53-deficient breast cancer cells to doxorubicin-induced apoptosis.	Doxorubicin	64-75	P53	Homo sapiens	27-30
15746064-4	2005	Here we have investigated the effect of combined treatment with ionizing radiation and patupilone or paclitaxel in the P-glycoprotein-overexpressing, p53-mutated human colon adenocarcinoma cell line SW480 and in murine, genetically defined E1A/ras-transformed paclitaxel-sensitive embryo fibroblasts.	Paclitaxel	101-111	P53	Homo sapiens	150-153
15456408-1	2005	p53 deficiency confers resistance to doxo (doxorubicin), a clinically active and widely used antitumour anthracycline antibiotic.	Doxorubicin	43-54	P53	Homo sapiens	0-3
15456408-1	2005	p53 deficiency confers resistance to doxo (doxorubicin), a clinically active and widely used antitumour anthracycline antibiotic.	Anthracyclines	104-117	P53	Homo sapiens	0-3
15691646-1	2005	We measured the expression of the p53 nuclear protein and epidermal growth factor receptor (EGFR) in 46 biopsy samples from patients with advanced head and neck cancer treated with induction combination chemotherapy of 5-fluorouracil, cisplatin, and paclitaxel.	Cisplatin	235-244	P53	Homo sapiens	34-37
15550400-13	2005	Finally, forced expression of COX-2 suppressed both basal and hypoxia-induced p53 transcriptional activity, and this effect was mimicked by the addition of PGE2 to wild-type cells.	Dinoprostone	156-160	P53	Homo sapiens	78-81
15720190-10	2005	Small molecules that have been reported to disrupt the p53-MDM2 binding, thereby enhancing p53 activity to elicit anticancer effects include the following: synthetic chalcones, norbornane derivatives, cis-imidazoline derivatives (Nutlins), a pyrazolidinedione sulfonamide and 1,4-benzodiazepine-2,5-diones, as well as tryptophan derivatives.	Tryptophan	318-328	P53	Homo sapiens	55-58
15720190-10	2005	Small molecules that have been reported to disrupt the p53-MDM2 binding, thereby enhancing p53 activity to elicit anticancer effects include the following: synthetic chalcones, norbornane derivatives, cis-imidazoline derivatives (Nutlins), a pyrazolidinedione sulfonamide and 1,4-benzodiazepine-2,5-diones, as well as tryptophan derivatives.	Tryptophan	318-328	P53	Homo sapiens	91-94
15546879-3	2005	We therefore examined whether combinations of 5-FU with drugs that specifically target polyamine metabolism, i.e. N1,N11-diethylnorspermine (DENSPM) or alpha-difluoromethylornithine (DFMO), have synergistic effects in killing HCT116 colon carcinoma cells with wild-type or absent p53.	Fluorouracil	46-50	P53	Homo sapiens	280-283
15546879-4	2005	Our results showed that simultaneous 5-FU and DENSPM, a spermine analogue, synergistically increased transcript levels of the polyamine catabolism enzyme spermidine/spermine N1-acetyltransferase, depleted spermine and spermidine, increased acetylated spermidine, and produced synergistic tumor cell apoptosis in both p53 wild-type and p53-null variants.	Fluorouracil	37-41	P53	Homo sapiens	317-320
15546879-4	2005	Our results showed that simultaneous 5-FU and DENSPM, a spermine analogue, synergistically increased transcript levels of the polyamine catabolism enzyme spermidine/spermine N1-acetyltransferase, depleted spermine and spermidine, increased acetylated spermidine, and produced synergistic tumor cell apoptosis in both p53 wild-type and p53-null variants.	Fluorouracil	37-41	P53	Homo sapiens	335-338
15546879-6	2005	Some pre-treatment and post-treatment regimens of DENSPM and DFMO were antagonistic to 5-FU depending on cellular p53 status.	Eflornithine	61-65	P53	Homo sapiens	114-117
15546879-6	2005	Some pre-treatment and post-treatment regimens of DENSPM and DFMO were antagonistic to 5-FU depending on cellular p53 status.	Fluorouracil	87-91	P53	Homo sapiens	114-117
15652229-9	2005	Western blot analysis indicated a concentration-dependent p53 level increase in both lines (higher after cisplatin treatment).	Cisplatin	105-114	P53	Homo sapiens	58-61
15691646-1	2005	We measured the expression of the p53 nuclear protein and epidermal growth factor receptor (EGFR) in 46 biopsy samples from patients with advanced head and neck cancer treated with induction combination chemotherapy of 5-fluorouracil, cisplatin, and paclitaxel.	Fluorouracil	219-233	P53	Homo sapiens	34-37
15691646-1	2005	We measured the expression of the p53 nuclear protein and epidermal growth factor receptor (EGFR) in 46 biopsy samples from patients with advanced head and neck cancer treated with induction combination chemotherapy of 5-fluorouracil, cisplatin, and paclitaxel.	Paclitaxel	250-260	P53	Homo sapiens	34-37
15474986-4	2005	Based on our western blot analysis, the phosphorylation of serine at the 15th residue (Ser15) of p53 was activated by 4-NQO, whereas the level of p53 in the cells did not change much.	Serine	59-65	P53	Homo sapiens	97-100
15832264-9	2005	We also showed that a parallel determination of ER, PgR and p53 expression may carry high predictive value as to response to tamoxifen treatment.	Tamoxifen	125-134	P53	Homo sapiens	60-63
15685549-9	2005	Infliximab induced accumulation of reactive oxygen species and up-regulation of Bax, Bak, and p21(WAF1/CIP1) proteins, suggesting the involvement of p53 activation.	Reactive Oxygen Species	35-58	P53	Homo sapiens	149-152
15875665-4	2005	The protein expression of p53 was measured using Western blotting in the sensitive cells and resistant cells to explore the effect of brassinolide.	brassinolide	134-146	P53	Homo sapiens	26-29
15496615-6	2005	Expression of tumor suppressor p53 and the cell cycle regulatory protein p21 was stimulated within 5 to 10 min by cisplatin in p53-positive LX-1 small cell lung carcinoma cells, and this effect was blocked by NAC.	Cisplatin	114-123	P53	Homo sapiens	31-34
15496615-6	2005	Expression of tumor suppressor p53 and the cell cycle regulatory protein p21 was stimulated within 5 to 10 min by cisplatin in p53-positive LX-1 small cell lung carcinoma cells, and this effect was blocked by NAC.	Cisplatin	114-123	P53	Homo sapiens	127-130
15496615-6	2005	Expression of tumor suppressor p53 and the cell cycle regulatory protein p21 was stimulated within 5 to 10 min by cisplatin in p53-positive LX-1 small cell lung carcinoma cells, and this effect was blocked by NAC.	Acetylcysteine	209-212	P53	Homo sapiens	31-34
15496615-6	2005	Expression of tumor suppressor p53 and the cell cycle regulatory protein p21 was stimulated within 5 to 10 min by cisplatin in p53-positive LX-1 small cell lung carcinoma cells, and this effect was blocked by NAC.	Acetylcysteine	209-212	P53	Homo sapiens	127-130
15496615-7	2005	In p53-negative SKOV3 cells, cisplatin toxicity and NAC chemoprotection remained effective, suggesting that chemoprotection may be mediated through both p53-dependent and -independent pathways.	Cisplatin	29-38	P53	Homo sapiens	3-6
15496615-7	2005	In p53-negative SKOV3 cells, cisplatin toxicity and NAC chemoprotection remained effective, suggesting that chemoprotection may be mediated through both p53-dependent and -independent pathways.	Acetylcysteine	52-55	P53	Homo sapiens	3-6
27407732-7	2005	RESULTS: On correlating histological grades with p53 immunoscore it was found that 90.76% of cases graded as negative for dysplasia on H &amp; E, got an immunoscore of 0 and other 9.24% cases which were graded as negative for dysplasia got a score 1+.	Adenosine Monophosphate	138-141	P53	Homo sapiens	49-52
15713892-3	2005	Here, we report that treatment of JB6 C141 cells (preneoplastic epidermal keratinocytes) and p53+/+ fibroblasts with silymarin and silibinin (a major constituent of silymarin) resulted in a dose-dependent inhibition of cell viability and induction of apoptosis in an identical manner.	Silybin	131-140	P53	Homo sapiens	93-96
15875732-0	2005	p53 alterations in sequential biopsies of Asian follicular lymphoma: a study of immunohistochemical staining pattern and gene mutations by PCR-SSCP in paraffin-embedded tissues.	Paraffin	151-159	P53	Homo sapiens	0-3
15875732-3	2005	We aimed to investigate the frequency of p53 gene alterations in paraffin-embedded tissue using commercially available PCR-SSCP, and to correlate the results with P53 protein expression by immunohistochemistry.	Paraffin	65-73	P53	Homo sapiens	41-44
15664249-14	2005	CONCLUSIONS: Our results indicate that, in liver cancer, the cytotoxic somatostatin analogue AN-238 is a powerful agent that can induce apoptosis, through sst(s) and independently of p53.	Ethanol	93-96	P53	Homo sapiens	183-186
15875665-11	2005	After brassinolide treatment, the expression of p53 in CCRF-VCR cells restored to the level of sensitive cells.	brassinolide	6-18	P53	Homo sapiens	48-51
15875665-13	2005	To down regulate the abnormal expression of p53 maybe one of the mechanisms of reversing MDR for brassinolide.	brassinolide	97-109	P53	Homo sapiens	44-47
15854392-0	2005	[Relationship between the acquired multi-drug resistance of human large cell lung cancer cell line NCI-H460 by cisplatin selection and p53 mutation].	Cisplatin	111-120	P53	Homo sapiens	135-138
15842803-2	2005	METHODS: Four different p53-GST (glutathione S-transferase) fusion proteins and GST were expressed in E. coli and purified through glutathione sepharose 4B beads.	Glutathione	33-44	P53	Homo sapiens	24-27
15854392-8	2005	It was found that P53 protein translocated from nuclear to cytoplasm and could not phosphorate after the stimulation of cisplatin.	Cisplatin	120-129	P53	Homo sapiens	18-21
15946545-2	2005	METHODS: Plasmid containing mutant p53-GFP was constructed by site-directed mutagenesis by which 5 amino scid residues in the nuclear localization signal (NLS) were replaced by alanine to produce mutant p53KRKKK-GFP.	Alanine	177-184	P53	Homo sapiens	35-38
15854392-12	2005	CONCLUSIONS: p53 mutation induced by cisplatin/carboplatin might play an important role in the development of acquired multi-drug resistance of lung cancer chemotherapy.	Cisplatin	37-46	P53	Homo sapiens	13-16
15583690-7	2005	Thus, the present study revealed that (a) the Arg allele is associated with p53 mutations, (b) the Pro allele is preferentially lost in OSCCs associated with cigarette smoking and AQ chewing, while the frequency of Arg allele loss is increased with alcohol drinking, and (c) haploinsufficiency of p53 is in itself likely to contribute to tumour progression in Taiwanese OSCCs.	Arginine	46-49	P53	Homo sapiens	76-79
15580302-4	2005	Treatment of p53-positive cell lines U2OS and MCF-7 with the DNA damaging drug, doxorubicin, which increases p53 protein level, induced expression of Ipaf mRNA but similar treatment of MCF-7-mp53 (a clone of MCF-7 cells expressing mutant p53) and p53-negative K562 cells showed much less induction of Ipaf gene expression.	Doxorubicin	80-91	P53	Homo sapiens	13-16
15580302-4	2005	Treatment of p53-positive cell lines U2OS and MCF-7 with the DNA damaging drug, doxorubicin, which increases p53 protein level, induced expression of Ipaf mRNA but similar treatment of MCF-7-mp53 (a clone of MCF-7 cells expressing mutant p53) and p53-negative K562 cells showed much less induction of Ipaf gene expression.	Doxorubicin	80-91	P53	Homo sapiens	109-112
15580302-4	2005	Treatment of p53-positive cell lines U2OS and MCF-7 with the DNA damaging drug, doxorubicin, which increases p53 protein level, induced expression of Ipaf mRNA but similar treatment of MCF-7-mp53 (a clone of MCF-7 cells expressing mutant p53) and p53-negative K562 cells showed much less induction of Ipaf gene expression.	Doxorubicin	80-91	P53	Homo sapiens	109-112
15580302-4	2005	Treatment of p53-positive cell lines U2OS and MCF-7 with the DNA damaging drug, doxorubicin, which increases p53 protein level, induced expression of Ipaf mRNA but similar treatment of MCF-7-mp53 (a clone of MCF-7 cells expressing mutant p53) and p53-negative K562 cells showed much less induction of Ipaf gene expression.	Doxorubicin	80-91	P53	Homo sapiens	109-112
15592521-10	2005	Strikingly, CYR61 overexpression impaired the accumulation of wild-type p53 following Taxol exposure, while inhibition of alphavbeta3 or ERK1/ERK2 MAPK signalings completely restored Taxol-induced upregulation of p53.	Paclitaxel	86-91	P53	Homo sapiens	72-75
15592521-10	2005	Strikingly, CYR61 overexpression impaired the accumulation of wild-type p53 following Taxol exposure, while inhibition of alphavbeta3 or ERK1/ERK2 MAPK signalings completely restored Taxol-induced upregulation of p53.	Paclitaxel	183-188	P53	Homo sapiens	213-216
15580302-5	2005	Expression analysis for Ipaf mRNA in doxorubicin-treated human tumor cell lines suggests that p53-dependent as well as p53-independent mechanisms are involved in the regulation of Ipaf gene expression in a cell-type-specific manner.	Doxorubicin	37-48	P53	Homo sapiens	94-97
15580302-5	2005	Expression analysis for Ipaf mRNA in doxorubicin-treated human tumor cell lines suggests that p53-dependent as well as p53-independent mechanisms are involved in the regulation of Ipaf gene expression in a cell-type-specific manner.	Doxorubicin	37-48	P53	Homo sapiens	119-122
15580310-4	2005	Here, we determined that 17beta-estradiol (E(2)) activated WOX1, p53 and ERK in COS7 fibroblasts, primary lung epithelial cells, and androgen receptor (AR)-negative prostate DU145 cells, but not in estrogen receptor (ER)-positive breast MCF7 cells.	Estradiol	25-41	P53	Homo sapiens	65-68
15642743-1	2005	The proapoptotic activity of the transcription factor p53 critically depends on the phosphorylation of serine 46 (p53S46P).	Serine	103-109	P53	Homo sapiens	54-57
15642743-3	2005	In this latter model, cell death was the result of a sequential process involving cell fusion, nuclear fusion (karyogamy), phosphorylation of serine 15 (p53S15P), later on serine 46 (p53S46P), and transcription of p53 target genes.	Serine	142-148	P53	Homo sapiens	153-156
15583690-7	2005	Thus, the present study revealed that (a) the Arg allele is associated with p53 mutations, (b) the Pro allele is preferentially lost in OSCCs associated with cigarette smoking and AQ chewing, while the frequency of Arg allele loss is increased with alcohol drinking, and (c) haploinsufficiency of p53 is in itself likely to contribute to tumour progression in Taiwanese OSCCs.	Arginine	215-218	P53	Homo sapiens	297-300
15642743-6	2005	Recombinant p38 phosphorylated recombinant p53 on serine 46 in vitro.	Serine	50-56	P53	Homo sapiens	43-46
15574463-8	2005	After exposure to ionizing radiation, a dose-dependent defect in ataxia telangiectasia mutated (ATM)-serine 1981, p53-serine 15 and Chk2 phosphorylation, and p53 stabilization were noted, together with a failure to form Mre11 foci and enhanced radiation sensitivity.	Serine	118-124	P53	Homo sapiens	114-117
15607904-4	2005	SK-N-BE human neuroblastoma cells express the three p53 family proteins and can be used for the study of their induction.	Beryllium	5-7	P53	Homo sapiens	52-55
15533933-4	2005	Phosphorylation on Chk1(Ser-345), Chk2(Thr-68), and p53(Ser-15) following oxidative damage by IR involved both ATM and ATR.	Serine	56-59	P53	Homo sapiens	52-55
15616590-0	2005	5-Lipoxygenase regulates senescence-like growth arrest by promoting ROS-dependent p53 activation.	Reactive Oxygen Species	68-71	P53	Homo sapiens	82-85
15543231-8	2005	At the opposite, upon treatment with topoisomerase II inhibitors (doxorubicin or etoposide), the expression of TAp63 isoforms was clearly induced, independently of the TP53 status of cells.	Doxorubicin	66-77	P53	Homo sapiens	168-172
15571721-5	2005	Electrophoretic mobility shift assay and intrinsic tryptophan fluorescence experiments also demonstrate that, although intrinsically disordered, polypeptides from the central region are able to mediate interactions with DNA and p53 with affinities in the low micromolar range.	Tryptophan	51-61	P53	Homo sapiens	228-231
15711927-0	2005	Role of p53 and reactive oxygen species in apoptotic response to copper and zinc in epithelial breast cancer cells.	Copper	65-71	P53	Homo sapiens	8-11
15603752-11	2005	Nevertheless, other regular participants in the DNA damage response, such as Gadd45a, Gadd153, p53, Hsp70, and ATM are still upregulated by high NaCl.	Sodium Chloride	145-149	P53	Homo sapiens	95-98
16400524-8	2005	NAC treatment also restored cell cycle progression inhibited by rk-2 and down-regulated p53 and nuclear p21(Waf1/Cip1) expression induced by rk-2.These data suggest that rk-2 induces the BCE cell cycle arrest at G(0)-G(1) phase through inhibition of the cyclin D1/CDK4 complex caused by increase of ROS generation and nuclear cyclin-dependent kinase inhibitors.	Acetylcysteine	0-3	P53	Homo sapiens	88-91
15711927-9	2005	Copper treatment did not result in accumulation of ROS in these cell lines with an inactive p53 even after exposure to 50 microM of copper for 6 h, indicating a key role for p53 in the ROS generation.	Reactive Oxygen Species	185-188	P53	Homo sapiens	174-177
16082409-12	2005	Using specific phospho-serine antibodies, we identified phosphorylation of baculovirally expressed p53 protein at five distinct sites.	Serine	23-29	P53	Homo sapiens	99-102
15608418-0	2005	p53, p63 and p73 expression in squamous cell carcinomas of the head and neck and their response to cisplatin exposure.	Cisplatin	99-108	P53	Homo sapiens	0-3
15608418-2	2005	Unlike the p53 gene, both encode for several isoforms which vary in their NH2 and COOH termini with variable and, in part, opposed biological functions.	Carbonic Acid	82-86	P53	Homo sapiens	11-14
15608418-3	2005	The objective of the present study was to analyse the expression profiles of p53 family members in squamous cell carcinomas of the head and neck (HNSCC) and their alterations caused by exposure to the clinically active drug cisplatin.	Cisplatin	224-233	P53	Homo sapiens	77-80
15711927-1	2005	Previous studies revealed that cells may differ in their response to metal stress depending on their p53 status; however, the sequence of events leading to copper-induced apoptosis is still unclear.	Metals	69-74	P53	Homo sapiens	101-104
15816541-9	2005	In our analysis, the constitutive dephosphorylation at Ser 376 correlated with the nuclear accumulation of p53, but not with the transcriptional activity of the protein.	Serine	55-58	P53	Homo sapiens	107-110
15711927-10	2005	Pretreatment of MCF7 cells with p53 inhibitor, pifithrin-alpha, resulted in decrease of copper and zinc induced ROS production to the control level, suppression of both Bax expression and AIF release.	Copper	88-94	P53	Homo sapiens	32-35
15711927-2	2005	Exposure of copper (10 and 25 microM) and zinc (10 and 25 microM) caused activation of p53 in ER+/p53+ human epithelial breast cancer MCF7 cells and resulted in up-regulation of p21.	Copper	12-18	P53	Homo sapiens	87-90
15711927-10	2005	Pretreatment of MCF7 cells with p53 inhibitor, pifithrin-alpha, resulted in decrease of copper and zinc induced ROS production to the control level, suppression of both Bax expression and AIF release.	Reactive Oxygen Species	112-115	P53	Homo sapiens	32-35
15711927-2	2005	Exposure of copper (10 and 25 microM) and zinc (10 and 25 microM) caused activation of p53 in ER+/p53+ human epithelial breast cancer MCF7 cells and resulted in up-regulation of p21.	Copper	12-18	P53	Homo sapiens	98-101
15711927-3	2005	Transactivation of p53 in MCF7 cells also led to increase in expression of Bax, proapototic Bcl-2 family member, triggering mitochondrial pore opening, and PIG3 (p53-induced gene 3 product), and also generation of intracellular reactive oxygen species (ROS).	Reactive Oxygen Species	228-251	P53	Homo sapiens	19-22
15711927-11	2005	Therefore, the activation of p53 seems to play a crucial role in copper and zinc induced generation of ROS in epithelial breast cancer cells, and expression of downstream targets of p53, such as PIG3 and Bax, responsible for increased generation of the intracellular ROS, as well as disruption of mitochondrial integrity.	Copper	65-71	P53	Homo sapiens	29-32
15711927-11	2005	Therefore, the activation of p53 seems to play a crucial role in copper and zinc induced generation of ROS in epithelial breast cancer cells, and expression of downstream targets of p53, such as PIG3 and Bax, responsible for increased generation of the intracellular ROS, as well as disruption of mitochondrial integrity.	Reactive Oxygen Species	103-106	P53	Homo sapiens	29-32
15711927-11	2005	Therefore, the activation of p53 seems to play a crucial role in copper and zinc induced generation of ROS in epithelial breast cancer cells, and expression of downstream targets of p53, such as PIG3 and Bax, responsible for increased generation of the intracellular ROS, as well as disruption of mitochondrial integrity.	Reactive Oxygen Species	267-270	P53	Homo sapiens	29-32
15711927-11	2005	Therefore, the activation of p53 seems to play a crucial role in copper and zinc induced generation of ROS in epithelial breast cancer cells, and expression of downstream targets of p53, such as PIG3 and Bax, responsible for increased generation of the intracellular ROS, as well as disruption of mitochondrial integrity.	Reactive Oxygen Species	267-270	P53	Homo sapiens	182-185
15711927-3	2005	Transactivation of p53 in MCF7 cells also led to increase in expression of Bax, proapototic Bcl-2 family member, triggering mitochondrial pore opening, and PIG3 (p53-induced gene 3 product), and also generation of intracellular reactive oxygen species (ROS).	Reactive Oxygen Species	253-256	P53	Homo sapiens	19-22
15711927-4	2005	The treatment of MCF7 cells with either copper or zinc for 4 h also caused decrease in mitochondrial membrane potential (Delta psi(m)), accompanied by an elevation in the ROS production and redistribution of p53 into mitochondria.	Copper	40-46	P53	Homo sapiens	208-211
15365767-3	2005	In the work reported here we investigated the ability of docosahexaenoic acid (DHA) to potentiate the antineoplastic activity of 5-fluorouracil (5-FU) in p53-wildtype (LS-174 and Colo 320) and p53-mutant (HT-29 and Colo 205) human colon cancer cells.	Fluorouracil	129-143	P53	Homo sapiens	154-157
16168113-9	2005	The sequence Dox--&gt;Pacl--&gt;48-h washout--&gt;5-FU produced a synergistic and highly schedule-dependent interaction (combination index &lt; 1), resulting in an induction of apoptosis in both experimental models regardless of hormonal, p53, bcl-2 or bax status.	Doxorubicin	13-16	P53	Homo sapiens	239-242
16168113-9	2005	The sequence Dox--&gt;Pacl--&gt;48-h washout--&gt;5-FU produced a synergistic and highly schedule-dependent interaction (combination index &lt; 1), resulting in an induction of apoptosis in both experimental models regardless of hormonal, p53, bcl-2 or bax status.	Fluorouracil	50-54	P53	Homo sapiens	239-242
15742811-0	2005	Pseudolaric acid B induces apoptosis through p53 and Bax/Bcl-2 pathways in human melanoma A375-S2 cells.	pseudolaric acid B	0-18	P53	Homo sapiens	45-48
15339849-3	2005	p53 deletions were associated with higher serum calcium (P = .0062) and creatinine (P = .013) levels, but there were no association with patient age, gender, beta2-microglobulin, C-reactive protein, hemoglobin, albumin or bone lytic lesions, or immunoglobulin isotype.	Calcium	48-55	P53	Homo sapiens	0-3
15339849-3	2005	p53 deletions were associated with higher serum calcium (P = .0062) and creatinine (P = .013) levels, but there were no association with patient age, gender, beta2-microglobulin, C-reactive protein, hemoglobin, albumin or bone lytic lesions, or immunoglobulin isotype.	Creatinine	72-82	P53	Homo sapiens	0-3
15365767-3	2005	In the work reported here we investigated the ability of docosahexaenoic acid (DHA) to potentiate the antineoplastic activity of 5-fluorouracil (5-FU) in p53-wildtype (LS-174 and Colo 320) and p53-mutant (HT-29 and Colo 205) human colon cancer cells.	Fluorouracil	145-149	P53	Homo sapiens	154-157
15662138-0	2005	The tumor suppressor p33ING1b enhances taxol-induced apoptosis by p53-dependent pathway in human osteosarcoma U2OS cells.	Paclitaxel	39-44	P53	Homo sapiens	66-69
16289503-5	2005	The TP53 Arg/Arg codon 72 genotype was detected in 21.9% of ICSCC and in 18.2% of CIN3 but only in 6% of CIN1-2 and in 5.2% of controls (P&lt;0.05).	Arginine	9-12	P53	Homo sapiens	4-8
15662138-4	2005	The results showed that p33ING1b markedly increased taxol-induced growth inhibition and apoptosis in p53+/+ U2OS cells, but not in p53-mutant MG63 cells.	Paclitaxel	52-57	P53	Homo sapiens	101-104
15662138-6	2005	Taken together, our data demonstrate that p33ING1b enhances taxol-induced apoptosis through p53-dependent pathway in human osteosarcoma cells.	Paclitaxel	60-65	P53	Homo sapiens	92-95
16122882-1	2005	BACKGROUND: The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene has been implicated in increasing susceptibility of the cervix to human papillomavirus (HPV) infection and thus altering cancer risk.	Arginine	16-19	P53	Homo sapiens	78-81
16122882-1	2005	BACKGROUND: The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene has been implicated in increasing susceptibility of the cervix to human papillomavirus (HPV) infection and thus altering cancer risk.	Arginine	20-23	P53	Homo sapiens	78-81
16122882-1	2005	BACKGROUND: The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene has been implicated in increasing susceptibility of the cervix to human papillomavirus (HPV) infection and thus altering cancer risk.	Arginine	20-23	P53	Homo sapiens	78-81
16289503-5	2005	The TP53 Arg/Arg codon 72 genotype was detected in 21.9% of ICSCC and in 18.2% of CIN3 but only in 6% of CIN1-2 and in 5.2% of controls (P&lt;0.05).	Arginine	13-16	P53	Homo sapiens	4-8
16289503-8	2005	We conclude that TP53 Arg/Arg codon 72 genotype is a relevant risk factor for invasive squamous cell carcinoma of the conjunctiva and for CIN3 in the Ugandan population.	Arginine	22-25	P53	Homo sapiens	17-21
16289503-8	2005	We conclude that TP53 Arg/Arg codon 72 genotype is a relevant risk factor for invasive squamous cell carcinoma of the conjunctiva and for CIN3 in the Ugandan population.	Arginine	26-29	P53	Homo sapiens	17-21
15671536-6	2005	After treatment of Adriamycin with serial dose for 24 hours, we measured the uptake of 125I and did Western blot analysis to evaluate expression of p53 protein.	Doxorubicin	19-29	P53	Homo sapiens	148-151
15619007-2	2005	Isogenic and isophenotypic human thyroid papillary carcinoma cell line variants for p53 differently expressed cycle genes after cisplatin treatment.	Cisplatin	128-137	P53	Homo sapiens	84-87
15619007-4	2005	While cisplatin treatment increased their expression in p53 wild-type cells it decreased it in cells with inactivated p53 and had no or less effect on cells with mutated p53.	Cisplatin	6-15	P53	Homo sapiens	56-59
15619007-4	2005	While cisplatin treatment increased their expression in p53 wild-type cells it decreased it in cells with inactivated p53 and had no or less effect on cells with mutated p53.	Cisplatin	6-15	P53	Homo sapiens	118-121
15619007-4	2005	While cisplatin treatment increased their expression in p53 wild-type cells it decreased it in cells with inactivated p53 and had no or less effect on cells with mutated p53.	Cisplatin	6-15	P53	Homo sapiens	118-121
15619007-5	2005	These results show that in a well-defined system, different alterations of p53 can lead to a different regulation of genes and hence to either resistance or sensitivity to cisplatin.	Cisplatin	172-181	P53	Homo sapiens	75-78
15671536-11	2005	As Adriamycin dose increased, radioiodide uptake was significantly correlated with activated p53 as well as total p53 protein level.	Doxorubicin	3-13	P53	Homo sapiens	93-96
15671536-11	2005	As Adriamycin dose increased, radioiodide uptake was significantly correlated with activated p53 as well as total p53 protein level.	Doxorubicin	3-13	P53	Homo sapiens	114-117
15720258-5	2005	It is known that the tumor-suppressor proteins p53 and p73, and the oncoprotein c-Myc, which function as transcription factors, influence cellular sensitivity to cisplatin.	Cisplatin	162-171	P53	Homo sapiens	47-50
16248785-1	2005	S100B interacts with the p53 protein in a calcium-dependent manner and down-regulates its function as a tumor suppressor.	Calcium	42-49	P53	Homo sapiens	25-28
15827887-6	2005	Hippocampal cultures pretreated with ZnCl2 before anoxia showed decreased immunoreactivity for p53 and BAX, connected with BCL-2 overexpression, whereas the cultures exposed to zinc chelating agent - TPEN or TPEN connected with anoxia showed significant increase of immunorectivity for p53 and BAX.	zinc chloride	37-42	P53	Homo sapiens	95-98
16122187-1	2005	PURPOSE: In this study the relationship between therapy with paclitaxel, cisplatin, vinorelbine and titanocene dichloride and of the expression of proliferation markers (ki67 and S-phase fraction) and tumour suppressor gene p53 was analyzed using a human ovarian cancer xenograft model.	Paclitaxel	61-71	P53	Homo sapiens	224-227
16122187-1	2005	PURPOSE: In this study the relationship between therapy with paclitaxel, cisplatin, vinorelbine and titanocene dichloride and of the expression of proliferation markers (ki67 and S-phase fraction) and tumour suppressor gene p53 was analyzed using a human ovarian cancer xenograft model.	Cisplatin	73-82	P53	Homo sapiens	224-227
15732191-9	2005	Replacement of arginine (Arg) by proline (Pro) at position 72 of human p53 decreases its apoptotic potential [Dumont et al., 2003.	Arginine	15-23	P53	Homo sapiens	71-74
15732191-9	2005	Replacement of arginine (Arg) by proline (Pro) at position 72 of human p53 decreases its apoptotic potential [Dumont et al., 2003.	Arginine	25-28	P53	Homo sapiens	71-74
15732191-14	2005	Using a formal meta-analysis of the published literature we show that carriers of the TP53 codon 72 Pro/Pro genotype have an increased cancer risk compared to Arg/Arg carriers (p&lt;0.05).	Arginine	159-162	P53	Homo sapiens	86-90
15732191-14	2005	Using a formal meta-analysis of the published literature we show that carriers of the TP53 codon 72 Pro/Pro genotype have an increased cancer risk compared to Arg/Arg carriers (p&lt;0.05).	Arginine	163-166	P53	Homo sapiens	86-90
15827887-6	2005	Hippocampal cultures pretreated with ZnCl2 before anoxia showed decreased immunoreactivity for p53 and BAX, connected with BCL-2 overexpression, whereas the cultures exposed to zinc chelating agent - TPEN or TPEN connected with anoxia showed significant increase of immunorectivity for p53 and BAX.	zinc chloride	37-42	P53	Homo sapiens	286-289
15827887-7	2005	This strong immunoreactivity of proapototic proteins (p53 and BAX) in hippocampal cultures exposed to anoxia or/and TPEN correlated with previous ultrastructural evidences of anoxia- and TPEN-induced apoptosis, while the overexpression of anti-apoptotic protein (BCL-2 and BCL-X) in zinc-pretreated cultures evidenced the protective ability of this metal against apoptosis in model of anoxia in vitro.	Metals	349-354	P53	Homo sapiens	54-57
15583825-15	2005	These findings strongly suggest that: a) TP53 is a novel molecular sensor of energy imbalance after the perturbation of endogenous fatty acid metabolism in breast cancer cells; b) TP53 function closely influences the decision between apoptosis and growth arrest following FAS blockade; and c) pharmacological inhibitors of FAS activity may be clinically useful against breast carcinomas exhibiting mutation or aberrant expression of TP53.	Fatty Acids	131-141	P53	Homo sapiens	180-184
15583825-0	2005	RNA interference-mediated silencing of the p53 tumor-suppressor protein drastically increases apoptosis after inhibition of endogenous fatty acid metabolism in breast cancer cells.	Fatty Acids	135-145	P53	Homo sapiens	43-46
15615778-3	2005	The p53-independent pathway involves a phosphorylation cascade that activates the Chk1 effector kinase and induces G2 arrest through inhibitory tyrosine phosphorylation of Cdc2.	Tyrosine	144-152	P53	Homo sapiens	4-7
15583825-15	2005	These findings strongly suggest that: a) TP53 is a novel molecular sensor of energy imbalance after the perturbation of endogenous fatty acid metabolism in breast cancer cells; b) TP53 function closely influences the decision between apoptosis and growth arrest following FAS blockade; and c) pharmacological inhibitors of FAS activity may be clinically useful against breast carcinomas exhibiting mutation or aberrant expression of TP53.	Fatty Acids	131-141	P53	Homo sapiens	41-45
15583825-15	2005	These findings strongly suggest that: a) TP53 is a novel molecular sensor of energy imbalance after the perturbation of endogenous fatty acid metabolism in breast cancer cells; b) TP53 function closely influences the decision between apoptosis and growth arrest following FAS blockade; and c) pharmacological inhibitors of FAS activity may be clinically useful against breast carcinomas exhibiting mutation or aberrant expression of TP53.	Fatty Acids	131-141	P53	Homo sapiens	180-184
16302680-7	2005	In conclusion, our finding suggests the functional p53 codon 72 polymorphism may be associated with SLE susceptibility, suggesting individuals who carry the Pro allele may have a higher risk to SLE susceptibility than those with the Arg allele.	Arginine	233-236	P53	Homo sapiens	51-54
15623478-1	2005	BACKGROUND: The predictive value of codon 72 arginine homozygosity at the p53 gene for human papilloma virus associated cervical cancer risk remains inconclusive.	Arginine	45-53	P53	Homo sapiens	74-77
15623478-7	2005	The p53 codon 72 arginine homozygous genotype was significantly over represented in patients compared with controls.	Arginine	17-25	P53	Homo sapiens	4-7
15623478-10	2005	CONCLUSION: p53 codon 72 arginine homozygotes appear to be at greater risk of developing squamous cell carcinoma of the uterine cervix.	Arginine	25-33	P53	Homo sapiens	12-15
15657356-5	2005	Induction of apoptosis by EGCG could be corroborated to the increased expression of tumor suppressor protein p53 and its phosphorylation at Ser 15 residue.	Serine	140-143	P53	Homo sapiens	109-112
15860933-0	2005	Overexpression of protein kinase Cdelta enhances cisplatin-induced cytotoxicity correlated with p53 in gastric cancer cell line.	Cisplatin	49-58	P53	Homo sapiens	96-99
16127286-7	2005	This outcome is consistent with the clinical observation that the efficacy of topotecan in the treatment of relapsed ovarian carcinoma patients is dependent on platinum sensitivity, because platinum-sensitive tumors are expected to carry wild-type p53.	Platinum	160-168	P53	Homo sapiens	248-251
16127286-7	2005	This outcome is consistent with the clinical observation that the efficacy of topotecan in the treatment of relapsed ovarian carcinoma patients is dependent on platinum sensitivity, because platinum-sensitive tumors are expected to carry wild-type p53.	Platinum	190-198	P53	Homo sapiens	248-251
16127286-8	2005	Although untreated mutant p53 tumors may be responsive to first-line paclitaxel-containing therapy, it is likely that loss of p53 leads to genomic instability resulting in rapid progression to drug resistance.	Paclitaxel	69-79	P53	Homo sapiens	26-29
16391388-0	2005	Expression profiling of p53-target genes in copper-mediated neuronal apoptosis.	Copper	44-50	P53	Homo sapiens	24-27
16391388-2	2005	Our previous work in cultured human NTERA-2-N neurons showed that copper-induced neuronal apoptosis is dependent on the induction and nuclear translocation of the tumor suppressor protein, p53.	Copper	66-72	P53	Homo sapiens	189-192
16391388-3	2005	Because p53 acts as a DNA-binding transcription factor, this work used an oligonucleotide array to identify p53 target genes that are differentially regulated in copper-loaded neurons.	Copper	162-168	P53	Homo sapiens	8-11
16391388-3	2005	Because p53 acts as a DNA-binding transcription factor, this work used an oligonucleotide array to identify p53 target genes that are differentially regulated in copper-loaded neurons.	Copper	162-168	P53	Homo sapiens	108-111
16391388-4	2005	Arrays representing 145 human genes expressed downstream of p53 were hybridized with labeled mRNA from control and copper-treated neurons.	Copper	115-121	P53	Homo sapiens	60-63
15860933-8	2005	Moreover, overexpression of both wild-type p53 and exogenous PKCdelta in MKN28 increased cisplatin-induced cell death in MKN28.	Cisplatin	89-98	P53	Homo sapiens	43-46
15860933-9	2005	CONCLUSION: These results suggest that PKCdelta, in cooperation with p53, possibly regulates cisplatin-induced caspase-3-mediated cell death in gastric cancer.	Cisplatin	93-102	P53	Homo sapiens	69-72
15860933-2	2005	Cisplatin is one of the DNA-damaging agents and several factors including p53 are related to the sensitivity to cisplatin in cancer.	Cisplatin	0-9	P53	Homo sapiens	74-77
15860933-2	2005	Cisplatin is one of the DNA-damaging agents and several factors including p53 are related to the sensitivity to cisplatin in cancer.	Cisplatin	112-121	P53	Homo sapiens	74-77
15860933-4	2005	In our present study, we examined whether overexpression of PKCdelta and p53 increases the sensitivity of the human gastric cancer cell line, MKN28, which has a mutation of p53 gene, to cisplatin.	Cisplatin	186-195	P53	Homo sapiens	73-76
15844595-1	2005	OBJECTIVE: To investigate the codon-72 polymorphism of the tumor suppressor gene p53, codon-72 encodes arginine (Arg) or proline (Pro) for a genetic predisposition,to keloid or hypertrophic scar.	Arginine	103-111	P53	Homo sapiens	81-84
15389812-3	2005	RESULTS: CDDP and DACH-Ac-Pt were equiactive against mutant p53 and androgen-independent DU-145 or PC-3 tumor cells.	cddp	9-13	P53	Homo sapiens	60-63
15389812-4	2005	In wild-type p53 cells, CDDP was threefold more potent against androgen-dependent LNCaP than isogenic androgen-independent LNCaP-LN3 cells.	cddp	24-28	P53	Homo sapiens	13-16
15389812-6	2005	The greater potency of DACH-Ac-Pt than CDDP in wild-type p53 cells was not due to increased cellular drug uptake or increased adduct levels, but correlated with a lower tolerance to DNA damage.	cddp	39-43	P53	Homo sapiens	57-60
15456759-9	2004	Small interfering RNA was used to show that hPTIP is required for ATM-mediated phosphorylation of p53 at Ser(15) and for IR-induced up-regulation of the cyclin-dependent kinase inhibitor p21.	Serine	105-108	P53	Homo sapiens	98-101
15844595-1	2005	OBJECTIVE: To investigate the codon-72 polymorphism of the tumor suppressor gene p53, codon-72 encodes arginine (Arg) or proline (Pro) for a genetic predisposition,to keloid or hypertrophic scar.	Arginine	113-116	P53	Homo sapiens	81-84
15665582-3	2004	UV-damage and the damage caused by certain chemotherapeutics including cisplatin and nitrogen mustards are known to be repaired by the nucleotide excision repair (NER) pathway which is reportedly regulated by p53 and its downstream genes.	Cisplatin	71-80	P53	Homo sapiens	209-212
15665582-3	2004	UV-damage and the damage caused by certain chemotherapeutics including cisplatin and nitrogen mustards are known to be repaired by the nucleotide excision repair (NER) pathway which is reportedly regulated by p53 and its downstream genes.	Nitrogen	85-93	P53	Homo sapiens	209-212
15531296-9	2004	Western blotting showed that the synthesis of intracellular p53 and bax protein was gradually up-regulated in the virus-loading period of 72 h. Naloxone had an apparent additive rather than antagonistic effect on the morphine-associated enhancement of bax expression.	Morphine	217-225	P53	Homo sapiens	60-63
15471885-7	2004	We conclude that p53 phosphorylation on six major serine sites is not required for activation of p53 target genes or biological responses in vivo.	Serine	50-56	P53	Homo sapiens	17-20
15595848-9	2004	Thus, the mutational "hot spot" at codon 273 in P53 may reflect either sequence-specific reactivity of BPDE and/or inefficient repair of BPDE-DNA adducts positioned at this site.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	137-141	P53	Homo sapiens	48-51
15595848-0	2004	Mutagenic potential of benzo[a]pyrene-derived DNA adducts positioned in codon 273 of the human P53 gene.	pyrene	31-37	P53	Homo sapiens	95-98
15595848-2	2004	We incorporated a single (+)- or (-)-trans-anti-benzo[a]pyrene diol epoxide (BPDE) DNA adduct at the second position of codon 273 of the human P53 gene and explored the mutagenic potential of this lesion in mammalian cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	77-81	P53	Homo sapiens	143-146
15595848-9	2004	Thus, the mutational "hot spot" at codon 273 in P53 may reflect either sequence-specific reactivity of BPDE and/or inefficient repair of BPDE-DNA adducts positioned at this site.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	103-107	P53	Homo sapiens	48-51
15489221-4	2004	Using several ATM-proficient and ATM-deficient cell lines, we have observed ATM-dependent nuclear accumulation of p53 and ATM-dependent phosphorylation of p53 on seven serine residues.	Serine	168-174	P53	Homo sapiens	155-158
15471885-0	2004	Phosphorylation of p53 on key serines is dispensable for transcriptional activation and apoptosis.	Serine	30-37	P53	Homo sapiens	19-22
15471885-4	2004	We therefore investigated the role of p53 phosphorylation on six key serine residues (Ser(6), Ser(15), Ser(20), Ser(37), Ser(46), and Ser(392)) for p53 activation using nutlin-3, a recently developed small molecule MDM2 antagonist.	Serine	69-75	P53	Homo sapiens	38-41
15529313-0	2004	2-Chloroethyl-3-sarcosinamide-1-nitrosourea (SarCNU) inhibits prostate carcinoma cell growth via p53-dependent and p53-independent pathways.	2-((((2-chloroethyl)nitrosoamino)carbonyl)amino)propanamide	0-43	P53	Homo sapiens	97-100
15471885-4	2004	We therefore investigated the role of p53 phosphorylation on six key serine residues (Ser(6), Ser(15), Ser(20), Ser(37), Ser(46), and Ser(392)) for p53 activation using nutlin-3, a recently developed small molecule MDM2 antagonist.	Serine	69-75	P53	Homo sapiens	148-151
15471885-4	2004	We therefore investigated the role of p53 phosphorylation on six key serine residues (Ser(6), Ser(15), Ser(20), Ser(37), Ser(46), and Ser(392)) for p53 activation using nutlin-3, a recently developed small molecule MDM2 antagonist.	Serine	86-89	P53	Homo sapiens	38-41
15471885-4	2004	We therefore investigated the role of p53 phosphorylation on six key serine residues (Ser(6), Ser(15), Ser(20), Ser(37), Ser(46), and Ser(392)) for p53 activation using nutlin-3, a recently developed small molecule MDM2 antagonist.	Serine	86-89	P53	Homo sapiens	148-151
15471885-6	2004	Comparison of the activity of unphosphorylated and phosphorylated p53 induced by the genotoxic drugs doxorubicin and etoposide in HCT116 and RKO cells revealed no difference in their sequence-specific DNA binding and ability to transactivate p53 target genes and to induce p53-dependent apoptosis.	Doxorubicin	101-112	P53	Homo sapiens	66-69
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Acetylcysteine	73-89	P53	Homo sapiens	177-180
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Acetylcysteine	73-89	P53	Homo sapiens	182-185
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Doxorubicin	120-131	P53	Homo sapiens	177-180
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Doxorubicin	120-131	P53	Homo sapiens	182-185
15529313-0	2004	2-Chloroethyl-3-sarcosinamide-1-nitrosourea (SarCNU) inhibits prostate carcinoma cell growth via p53-dependent and p53-independent pathways.	2-((((2-chloroethyl)nitrosoamino)carbonyl)amino)propanamide	0-43	P53	Homo sapiens	115-118
15529313-0	2004	2-Chloroethyl-3-sarcosinamide-1-nitrosourea (SarCNU) inhibits prostate carcinoma cell growth via p53-dependent and p53-independent pathways.	2-((((2-chloroethyl)nitrosoamino)carbonyl)amino)propanamide	45-51	P53	Homo sapiens	97-100
15601469-0	2004	Role of the p53/p21 system in the response of human colon carcinoma cells to Doxorubicin.	Doxorubicin	77-88	P53	Homo sapiens	12-15
15529313-0	2004	2-Chloroethyl-3-sarcosinamide-1-nitrosourea (SarCNU) inhibits prostate carcinoma cell growth via p53-dependent and p53-independent pathways.	2-((((2-chloroethyl)nitrosoamino)carbonyl)amino)propanamide	45-51	P53	Homo sapiens	115-118
15601469-4	2004	The present study investigates the role of the p53/p21 system in the response of human colon carcinoma cells to treatment with the cytotoxic agent doxorubicin (DOX) and the possibility to modify the therapeutic index of DOX by modulation of p53 and/or p21 protein levels.	Doxorubicin	147-158	P53	Homo sapiens	47-50
15601469-4	2004	The present study investigates the role of the p53/p21 system in the response of human colon carcinoma cells to treatment with the cytotoxic agent doxorubicin (DOX) and the possibility to modify the therapeutic index of DOX by modulation of p53 and/or p21 protein levels.	Doxorubicin	147-158	P53	Homo sapiens	241-244
15601469-12	2004	CONCLUSIONS: p21 induction may significantly contribute to the response of colon adenocarcinomas cells to DOX treatment; and small molecules that can exploit p53-independent pathways for p21 induction, such as TPL, may find a place in chemotherapeutic protocols for the clinical management of colorectal cancer, where p53 function is often lost, due to genetic or epigenetic defects or to post-transcriptional inactivating mechanisms.	Doxorubicin	106-109	P53	Homo sapiens	158-161
15601469-12	2004	CONCLUSIONS: p21 induction may significantly contribute to the response of colon adenocarcinomas cells to DOX treatment; and small molecules that can exploit p53-independent pathways for p21 induction, such as TPL, may find a place in chemotherapeutic protocols for the clinical management of colorectal cancer, where p53 function is often lost, due to genetic or epigenetic defects or to post-transcriptional inactivating mechanisms.	Doxorubicin	106-109	P53	Homo sapiens	318-321
15601469-4	2004	The present study investigates the role of the p53/p21 system in the response of human colon carcinoma cells to treatment with the cytotoxic agent doxorubicin (DOX) and the possibility to modify the therapeutic index of DOX by modulation of p53 and/or p21 protein levels.	Doxorubicin	160-163	P53	Homo sapiens	47-50
15529313-13	2004	CONCLUSIONS: SarCNU induced G2/M arrest in prostate carcinoma cells via p53-dependent up-regulation of p21Cip1/Waf1 and p53-independent phosphorylation of Cdc-2 at Tyr15.	2-((((2-chloroethyl)nitrosoamino)carbonyl)amino)propanamide	13-19	P53	Homo sapiens	72-75
15601469-4	2004	The present study investigates the role of the p53/p21 system in the response of human colon carcinoma cells to treatment with the cytotoxic agent doxorubicin (DOX) and the possibility to modify the therapeutic index of DOX by modulation of p53 and/or p21 protein levels.	Doxorubicin	220-223	P53	Homo sapiens	47-50
15601469-4	2004	The present study investigates the role of the p53/p21 system in the response of human colon carcinoma cells to treatment with the cytotoxic agent doxorubicin (DOX) and the possibility to modify the therapeutic index of DOX by modulation of p53 and/or p21 protein levels.	Doxorubicin	220-223	P53	Homo sapiens	241-244
15529313-13	2004	CONCLUSIONS: SarCNU induced G2/M arrest in prostate carcinoma cells via p53-dependent up-regulation of p21Cip1/Waf1 and p53-independent phosphorylation of Cdc-2 at Tyr15.	2-((((2-chloroethyl)nitrosoamino)carbonyl)amino)propanamide	13-19	P53	Homo sapiens	120-123
15601469-5	2004	METHODS: The relationship between p53 and p21 protein levels and the cytotoxic effect of DOX was investigated, by MTT assay and western blot analysis, in HCT116 (p53-positive) and HT29 (p53-negative) colon cancer cells.	Doxorubicin	89-92	P53	Homo sapiens	34-37
15601469-5	2004	METHODS: The relationship between p53 and p21 protein levels and the cytotoxic effect of DOX was investigated, by MTT assay and western blot analysis, in HCT116 (p53-positive) and HT29 (p53-negative) colon cancer cells.	Doxorubicin	89-92	P53	Homo sapiens	162-165
15534883-3	2004	p53 is a tumor suppressor gene, and X-ray cross-complementing group 1 (XRCC1) is involved in the base-excision repair of ROS-induced DNA damage.	Reactive Oxygen Species	121-124	P53	Homo sapiens	0-3
15601469-5	2004	METHODS: The relationship between p53 and p21 protein levels and the cytotoxic effect of DOX was investigated, by MTT assay and western blot analysis, in HCT116 (p53-positive) and HT29 (p53-negative) colon cancer cells.	Doxorubicin	89-92	P53	Homo sapiens	162-165
15469940-8	2004	Downstream target genes of p53, such as p21Cip/WAF1 and PTEN, were inhibited by Aurora-A in a Ser-215 phosphorylation-dependent manner (i.e. phosphomimic p53-S215D lost and non-phosphorylatable p53-S215A retained normal p53 function).	Serine	94-97	P53	Homo sapiens	27-30
15604280-3	2004	Whereas irinotecan-induced up-regulation of the proapoptotic proteins PUMA and Noxa requires p53, we find that irinotecan inhibits Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 and 5 (STAT3/5) signaling in both p53-proficient and p53-deficient tumor cells.	Irinotecan	111-121	P53	Homo sapiens	238-241
15604280-4	2004	We show that irinotecan inhibits JAK2-STAT3/5-dependent expression of survival proteins (Bcl-x(L) and XIAP) and cooperates with Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (Apo2L/TRAIL) to facilitate p53-independent apoptosis of colon cancer cells.	Irinotecan	13-23	P53	Homo sapiens	224-227
15604280-5	2004	Whereas xenografts of p53-deficient colon cancer cells are relatively resistant to irinotecan compared with their p53-proficient counterparts, combined treatment with irinotecan and Apo2L/TRAIL eliminates hepatic metastases of both p53-proficient and p53-deficient cancer cells in vivo and significantly improves the survival of animals relative to treatment with either agent alone.	Irinotecan	83-93	P53	Homo sapiens	22-25
15604280-5	2004	Whereas xenografts of p53-deficient colon cancer cells are relatively resistant to irinotecan compared with their p53-proficient counterparts, combined treatment with irinotecan and Apo2L/TRAIL eliminates hepatic metastases of both p53-proficient and p53-deficient cancer cells in vivo and significantly improves the survival of animals relative to treatment with either agent alone.	Irinotecan	167-177	P53	Homo sapiens	114-117
15604280-6	2004	Although the synergy between chemotherapy and Apo2L/TRAIL has been ascribed to p53, our data demonstrate that irinotecan enhances Apo2L/TRAIL-induced apoptosis of tumor cells via a distinct p53-independent mechanism involving inhibition of JAK2-STAT3/5 signaling.	Irinotecan	110-120	P53	Homo sapiens	190-193
15604280-7	2004	These findings identify a novel p53-independent channel of cross-talk between topoisomerase I inhibitors and Apo2L/TRAIL and suggest that the addition of Apo2L/TRAIL can improve the therapeutic index of irinotecan against both p53-proficient and p53-deficient colorectal cancers, including those that have metastasized to the liver.	Irinotecan	203-213	P53	Homo sapiens	32-35
15604280-7	2004	These findings identify a novel p53-independent channel of cross-talk between topoisomerase I inhibitors and Apo2L/TRAIL and suggest that the addition of Apo2L/TRAIL can improve the therapeutic index of irinotecan against both p53-proficient and p53-deficient colorectal cancers, including those that have metastasized to the liver.	Irinotecan	203-213	P53	Homo sapiens	227-230
15604280-7	2004	These findings identify a novel p53-independent channel of cross-talk between topoisomerase I inhibitors and Apo2L/TRAIL and suggest that the addition of Apo2L/TRAIL can improve the therapeutic index of irinotecan against both p53-proficient and p53-deficient colorectal cancers, including those that have metastasized to the liver.	Irinotecan	203-213	P53	Homo sapiens	227-230
15386387-0	2004	Aberrant p53 alters DNA damage checkpoints in response to cisplatin: downregulation of CDK expression and activity.	Cisplatin	58-67	P53	Homo sapiens	9-12
15386387-3	2004	In our study, we examined the effect of expressing a human p53 cDNA, encoding a histidine to leucine amino acid substitution at codon 179 (H179L), on the ability of wild-type p53-containing NIH3T3 cells to respond to treatment with the chemotherapeutic cisplatin.	Cisplatin	253-262	P53	Homo sapiens	59-62
15386387-3	2004	In our study, we examined the effect of expressing a human p53 cDNA, encoding a histidine to leucine amino acid substitution at codon 179 (H179L), on the ability of wild-type p53-containing NIH3T3 cells to respond to treatment with the chemotherapeutic cisplatin.	Cisplatin	253-262	P53	Homo sapiens	175-178
15386387-6	2004	In contrast, cells stably expressing H179L-p53 arrested in S-phase following cisplatin treatment, which correlated with a marked decrease in the expression of cdc2, cyclin B1 and cyclin A, and a decrease in CDK2 and cyclin A-associated kinase activity.	Cisplatin	77-86	P53	Homo sapiens	43-46
15386387-7	2004	Interestingly, H179L p53 expressing cells underwent apoptosis earlier than control cells, indicating that this aberrant p53 may enhance cisplatin chemosensitivity.	Cisplatin	136-145	P53	Homo sapiens	21-24
15386387-7	2004	Interestingly, H179L p53 expressing cells underwent apoptosis earlier than control cells, indicating that this aberrant p53 may enhance cisplatin chemosensitivity.	Cisplatin	136-145	P53	Homo sapiens	120-123
15386387-8	2004	These data suggest that dominant-negative p53 can influence the expression and activity of CDK complexes, thereby modifying cell behavior following cisplatin-induced genotoxicity.	Cisplatin	148-157	P53	Homo sapiens	42-45
15530855-3	2004	We recently reported that exposure to oligonucleotides homologous to the telomere 3" overhang (T-oligos) activates both the p53 and pRb pathways and leads to senescence in primary human fibroblasts.	Oligonucleotides	38-54	P53	Homo sapiens	124-127
15604280-0	2004	Elimination of hepatic metastases of colon cancer cells via p53-independent cross-talk between irinotecan and Apo2 ligand/TRAIL.	Irinotecan	95-105	P53	Homo sapiens	60-63
15604280-2	2004	Using isogenic human colon cancer cells that differ only in their p53 status, we demonstrate that loss of p53 renders tumor cells relatively resistant to the topoisomerase I inhibitor, irinotecan.	Irinotecan	185-195	P53	Homo sapiens	106-109
15604280-3	2004	Whereas irinotecan-induced up-regulation of the proapoptotic proteins PUMA and Noxa requires p53, we find that irinotecan inhibits Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 and 5 (STAT3/5) signaling in both p53-proficient and p53-deficient tumor cells.	Irinotecan	8-18	P53	Homo sapiens	93-96
15604280-3	2004	Whereas irinotecan-induced up-regulation of the proapoptotic proteins PUMA and Noxa requires p53, we find that irinotecan inhibits Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 and 5 (STAT3/5) signaling in both p53-proficient and p53-deficient tumor cells.	Irinotecan	8-18	P53	Homo sapiens	238-241
15604280-3	2004	Whereas irinotecan-induced up-regulation of the proapoptotic proteins PUMA and Noxa requires p53, we find that irinotecan inhibits Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 and 5 (STAT3/5) signaling in both p53-proficient and p53-deficient tumor cells.	Irinotecan	8-18	P53	Homo sapiens	238-241
15604280-3	2004	Whereas irinotecan-induced up-regulation of the proapoptotic proteins PUMA and Noxa requires p53, we find that irinotecan inhibits Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 and 5 (STAT3/5) signaling in both p53-proficient and p53-deficient tumor cells.	Irinotecan	111-121	P53	Homo sapiens	238-241
15611505-0	2004	Prediction of TP53 status for primary cisplatin, fluorouracil, and leucovorin chemotherapy in ethmoid sinus intestinal-type adenocarcinoma.	Cisplatin	38-47	P53	Homo sapiens	14-18
15611505-0	2004	Prediction of TP53 status for primary cisplatin, fluorouracil, and leucovorin chemotherapy in ethmoid sinus intestinal-type adenocarcinoma.	Fluorouracil	49-61	P53	Homo sapiens	14-18
15469940-0	2004	Aurora-A abrogation of p53 DNA binding and transactivation activity by phosphorylation of serine 215.	Serine	90-96	P53	Homo sapiens	23-26
15469940-3	2004	Here we show that p53 is phosphorylated by the mitotic kinase Aurora-A at serine 215.	Serine	74-80	P53	Homo sapiens	18-21
15469940-7	2004	15, 164-171), the phosphorylation of p53 by Aurora-A at Ser-215 abrogates p53 DNA binding and transactivation activity.	Serine	56-59	P53	Homo sapiens	37-40
15469940-7	2004	15, 164-171), the phosphorylation of p53 by Aurora-A at Ser-215 abrogates p53 DNA binding and transactivation activity.	Serine	56-59	P53	Homo sapiens	74-77
15489892-2	2004	The time course of p53 activation by mithramycin A was similar to the known chemotherapeutic compound 5-fluorouracil (5-FU).	Fluorouracil	118-122	P53	Homo sapiens	19-22
15469940-8	2004	Downstream target genes of p53, such as p21Cip/WAF1 and PTEN, were inhibited by Aurora-A in a Ser-215 phosphorylation-dependent manner (i.e. phosphomimic p53-S215D lost and non-phosphorylatable p53-S215A retained normal p53 function).	Serine	94-97	P53	Homo sapiens	154-157
15489892-3	2004	Both 5-FU and mithramycin A induced site-specific phosphorylation of p53 at serine 15.	Fluorouracil	5-9	P53	Homo sapiens	69-72
15489892-3	2004	Both 5-FU and mithramycin A induced site-specific phosphorylation of p53 at serine 15.	Serine	76-82	P53	Homo sapiens	69-72
15469940-8	2004	Downstream target genes of p53, such as p21Cip/WAF1 and PTEN, were inhibited by Aurora-A in a Ser-215 phosphorylation-dependent manner (i.e. phosphomimic p53-S215D lost and non-phosphorylatable p53-S215A retained normal p53 function).	Serine	94-97	P53	Homo sapiens	154-157
15489892-4	2004	However, in contrast to 5-FU, mithramycin A failed to activate p53 target genes including the cell cycle inhibitor p21Cip1 gene as well as the proapoptotic genes PUMA (p53-upregulated mediator of apotosis) and BAK (bcl2-homologous antagonist/killer) and blocked the induction of the above genes by 5-FU.	Fluorouracil	298-302	P53	Homo sapiens	168-171
15469940-8	2004	Downstream target genes of p53, such as p21Cip/WAF1 and PTEN, were inhibited by Aurora-A in a Ser-215 phosphorylation-dependent manner (i.e. phosphomimic p53-S215D lost and non-phosphorylatable p53-S215A retained normal p53 function).	Serine	94-97	P53	Homo sapiens	154-157
15489892-6	2004	Using chromatin immunoprecipitation assays and a novel protein-protein interaction assay based on biotinylation in vivo, we established that 5-FU enhanced the formation of p53-Sp1 complexes in solution and the subsequent recruitment of both factors to the p21Cip1 promoter.	Fluorouracil	141-145	P53	Homo sapiens	172-175
15469940-14	2004	Our data indicate that phosphorylation of p53 at Ser-215 by Aurora-A is a major mechanism to inactivate p53 and can provide a molecular insight for Aurora-A function.	Serine	49-52	P53	Homo sapiens	42-45
15469940-14	2004	Our data indicate that phosphorylation of p53 at Ser-215 by Aurora-A is a major mechanism to inactivate p53 and can provide a molecular insight for Aurora-A function.	Serine	49-52	P53	Homo sapiens	104-107
15383533-5	2004	Furthermore, curcumin could also inhibit the p300-mediated acetylation of p53 in vivo.	Curcumin	13-21	P53	Homo sapiens	74-77
15592306-6	2004	The apoptotic index was reduced by &gt;/=30% ( P &lt;.001), and the expression of p53 was 2-fold lower ( P &lt;.02) in troglitazone-exposed cells under hypoxia for &lt;/=16 hours but not different after &gt;24 hours of low oxygen.	Oxygen	223-229	P53	Homo sapiens	82-85
15679113-6	2004	hTERT-transduced limbal and conjunctival keratinocytes are capable to respond to both growth inhibitory and differentiation stimuli, since they undergo growth arrest in response to phorbol esters, and activate p53 upon DNA damage.	htert	0-5	P53	Homo sapiens	210-213
15681814-9	2004	The intracellular protein and transcription factor, p53, is activated by the Alzheimer"s disease toxic peptide, Abeta, as well as by excess glutamate and hypoxia to trigger neural cell death.	Glutamic Acid	140-149	P53	Homo sapiens	52-55
15459092-0	2004	Additional data for oligonucleotide arrays of the p53 gene in DNA from formalin-fixed, paraffin-embedded tissue.	Oligonucleotides	20-35	P53	Homo sapiens	50-53
15459092-0	2004	Additional data for oligonucleotide arrays of the p53 gene in DNA from formalin-fixed, paraffin-embedded tissue.	Paraffin	87-95	P53	Homo sapiens	50-53
15331571-11	2004	These data indicate that p53 plays a key role in luteinization of the primate ovarian follicle though the regulation of steroidogenic enzymes leading to progesterone synthesis.	Progesterone	153-165	P53	Homo sapiens	25-28
15258697-4	2004	At the lowest doses, the TGFbeta-RII-mutated and KRAS2-mutated cell line, TOV-21G, and the BRCA2-mutated cell line, TOV-81D, demonstrated a significantly higher sensitivity to cisplatin and gamma-irradiation than the TP53-mutated cell lines, TOV-112D and OV-90.	Cisplatin	176-185	P53	Homo sapiens	217-221
15258697-5	2004	At higher doses, differences between the TP53-mutated lines were observed with TOV-112D being less sensitive to cisplatin than OV-90 that also harbors a CDNK2A mutation.	Cisplatin	112-121	P53	Homo sapiens	41-45
15547693-8	2004	DNA sequencing in FaDu cells showed a G/T point mutation at codon 248 in exon 7 of p53 gene, resulting in an arginine-to-leucine substitution.	Arginine	109-117	P53	Homo sapiens	83-86
15547708-6	2004	The anti-proliferative effects of NaBu were accompanied by diminished expression of p53.	sethoxydim	34-38	P53	Homo sapiens	84-87
15547708-7	2004	Similarly, mRNA encoding c-Myc, a well-known regulator of p53, was decreased in NaBu-treated cells, while p21(Waf1/Cip1) mRNA was increased.	sethoxydim	80-84	P53	Homo sapiens	58-61
15364927-2	2004	Here we show that via its acidic domain, Daxx binds to the COOH-terminal domain of p53, whose positive charges are critical for this interaction, as Lys to Arg mutations preserved, but Lys to Ala or Ser to Glu mutations abolished Daxx-p53 interaction.	Glutamic Acid	206-209	P53	Homo sapiens	235-238
15515126-13	2004	CONCLUSIONS: Our study has shown that p53 status is important for CD::UPRT/5-FC treatment.	Cadmium	66-68	P53	Homo sapiens	38-41
15542844-8	2004	VRK1 phosphorylates human p53 in Thr18 and disrupts p53-Mdm2 interaction in vitro, although a significant decrease in p53 ubiquitination by Mdm2 in vivo was not detected.	UNII-PYZ33YLR8A	33-38	P53	Homo sapiens	26-29
15475174-10	2004	PBDE-99, but not Aroclor 1254, caused apoptotic cell death in astrocytoma cells, assessed by the TUNEL method and by Hoechst 33258 staining, via a p53 dependent mechanism.	2,2',4,4',5-brominated diphenyl ether	0-7	P53	Homo sapiens	147-150
15365822-2	2004	A recent report suggests that a polymorphism of the p53 tumor suppressor gene that results in the substitution of a proline residue with an arginine residue at position 72 of the p53 protein might act as a risk factor in the malignant transformation of colorectal adenoma to cancer.	Arginine	140-148	P53	Homo sapiens	52-55
15365822-2	2004	A recent report suggests that a polymorphism of the p53 tumor suppressor gene that results in the substitution of a proline residue with an arginine residue at position 72 of the p53 protein might act as a risk factor in the malignant transformation of colorectal adenoma to cancer.	Arginine	140-148	P53	Homo sapiens	179-182
15577317-2	2004	METHODS: The expression of p53 and Bcl-2 protein was assessed by immunohistochemistry from paraffin blocks.	Paraffin	91-99	P53	Homo sapiens	27-30
15648263-8	2004	Induction of p53-phosphorylation at serine 15 was suppressed in JNKI and JNK2 knockout cells.	Serine	36-42	P53	Homo sapiens	13-16
15364927-2	2004	Here we show that via its acidic domain, Daxx binds to the COOH-terminal domain of p53, whose positive charges are critical for this interaction, as Lys to Arg mutations preserved, but Lys to Ala or Ser to Glu mutations abolished Daxx-p53 interaction.	Lysine	149-152	P53	Homo sapiens	83-86
15364927-2	2004	Here we show that via its acidic domain, Daxx binds to the COOH-terminal domain of p53, whose positive charges are critical for this interaction, as Lys to Arg mutations preserved, but Lys to Ala or Ser to Glu mutations abolished Daxx-p53 interaction.	Lysine	149-152	P53	Homo sapiens	235-238
15364927-9	2004	As p53 is required for 5-fluorouracil-induced cell death, our data show that Daxx can suppress cell death induced by p53 overexpression and p53-dependent stress response.	Fluorouracil	23-37	P53	Homo sapiens	3-6
15364927-2	2004	Here we show that via its acidic domain, Daxx binds to the COOH-terminal domain of p53, whose positive charges are critical for this interaction, as Lys to Arg mutations preserved, but Lys to Ala or Ser to Glu mutations abolished Daxx-p53 interaction.	Arginine	156-159	P53	Homo sapiens	83-86
15364927-2	2004	Here we show that via its acidic domain, Daxx binds to the COOH-terminal domain of p53, whose positive charges are critical for this interaction, as Lys to Arg mutations preserved, but Lys to Ala or Ser to Glu mutations abolished Daxx-p53 interaction.	Arginine	156-159	P53	Homo sapiens	235-238
15364927-9	2004	As p53 is required for 5-fluorouracil-induced cell death, our data show that Daxx can suppress cell death induced by p53 overexpression and p53-dependent stress response.	Fluorouracil	23-37	P53	Homo sapiens	117-120
15364927-2	2004	Here we show that via its acidic domain, Daxx binds to the COOH-terminal domain of p53, whose positive charges are critical for this interaction, as Lys to Arg mutations preserved, but Lys to Ala or Ser to Glu mutations abolished Daxx-p53 interaction.	Lysine	185-188	P53	Homo sapiens	83-86
15364927-2	2004	Here we show that via its acidic domain, Daxx binds to the COOH-terminal domain of p53, whose positive charges are critical for this interaction, as Lys to Arg mutations preserved, but Lys to Ala or Ser to Glu mutations abolished Daxx-p53 interaction.	Lysine	185-188	P53	Homo sapiens	235-238
15364927-9	2004	As p53 is required for 5-fluorouracil-induced cell death, our data show that Daxx can suppress cell death induced by p53 overexpression and p53-dependent stress response.	Fluorouracil	23-37	P53	Homo sapiens	117-120
15364927-2	2004	Here we show that via its acidic domain, Daxx binds to the COOH-terminal domain of p53, whose positive charges are critical for this interaction, as Lys to Arg mutations preserved, but Lys to Ala or Ser to Glu mutations abolished Daxx-p53 interaction.	Alanine	192-195	P53	Homo sapiens	83-86
15358769-10	2004	Interestingly, Hsp90 in an ATP-dependent manner can positively modulate p53 DNA binding after incubation at physiological temperature of 37 degrees C. Other recombinant human chaperones from Hsp70 and Hsp40 families were not able to efficiently substitute Hsp90 in this reaction.	Adenosine Triphosphate	27-30	P53	Homo sapiens	72-75
15364927-2	2004	Here we show that via its acidic domain, Daxx binds to the COOH-terminal domain of p53, whose positive charges are critical for this interaction, as Lys to Arg mutations preserved, but Lys to Ala or Ser to Glu mutations abolished Daxx-p53 interaction.	Alanine	192-195	P53	Homo sapiens	235-238
15364927-2	2004	Here we show that via its acidic domain, Daxx binds to the COOH-terminal domain of p53, whose positive charges are critical for this interaction, as Lys to Arg mutations preserved, but Lys to Ala or Ser to Glu mutations abolished Daxx-p53 interaction.	Serine	199-202	P53	Homo sapiens	83-86
15364927-2	2004	Here we show that via its acidic domain, Daxx binds to the COOH-terminal domain of p53, whose positive charges are critical for this interaction, as Lys to Arg mutations preserved, but Lys to Ala or Ser to Glu mutations abolished Daxx-p53 interaction.	Glutamic Acid	206-209	P53	Homo sapiens	83-86
15526030-2	2004	We show that Axin interacts with homeodomain-interacting protein kinase-2 (HIPK2), which is linked to UV-induced p53-dependent apoptosis by interacting with, and phosphorylating Ser 46 of, p53.	Serine	178-181	P53	Homo sapiens	113-116
15526030-2	2004	We show that Axin interacts with homeodomain-interacting protein kinase-2 (HIPK2), which is linked to UV-induced p53-dependent apoptosis by interacting with, and phosphorylating Ser 46 of, p53.	Serine	178-181	P53	Homo sapiens	189-192
15337767-1	2004	Two high affinity Ser-20-phospho-LXXLL p53-binding domains of p300 map to the C-terminal interferon-binding domain (IBiD) and N-terminal IBiD homology domain (IHD) regions.	Serine	18-21	P53	Homo sapiens	39-42
15337767-2	2004	Purified fractions of a recombinant IHD miniprotein are active in a set of in vitro assays highlighting its affinity to the N-terminal LXXLL domain of p53 including (i) dose-dependent binding to Ser-20-phosphorylated p53 tetramers; (ii) DNA-stimulated binding to p53 tetramers; and (iii) inhibition of MDM2-mediated p53 ubiquitination.	Serine	195-198	P53	Homo sapiens	151-154
15525938-0	2004	Regulation of p53 activity through lysine methylation.	Lysine	35-41	P53	Homo sapiens	14-17
15525938-3	2004	Here we report a novel mechanism of p53 regulation through lysine methylation by Set9 methyltransferase.	Lysine	59-65	P53	Homo sapiens	36-39
15450950-9	2004	Cd induced the upregulation of Bcl-2 and the degradation of p53 protein.	Cadmium	0-2	P53	Homo sapiens	60-63
15382061-8	2004	In studies with multicellular spheroids, which frequently are more resistant to cytotoxic anticancer drugs than monolayers, those from wt p53 C8161 melanoma underwent PARP fragmentation in response to RuCl2(KTZ)2.	ruthenium dichloride	201-206	P53	Homo sapiens	138-141
15382061-11	2004	In contrast to the antitumor action of cisplatin, which is known to be hampered by p53 dysfunction, we show that RuCl2(KTZ)2 is active irrespective of p53 functional status against several adherent tumor cells and synergizes with anti-EGF receptor C225 MAb to kill tumor spheroids resistant to either agent.	Cisplatin	39-48	P53	Homo sapiens	83-86
15566643-1	2004	BACKGROUND &amp; OBJECTIVE: The p53 codon 72 polymorphism affects human papillomavirus (HPV) E6-mediated degradation of p53.	Adenosine Monophosphate	12-15	P53	Homo sapiens	32-35
15566643-1	2004	BACKGROUND &amp; OBJECTIVE: The p53 codon 72 polymorphism affects human papillomavirus (HPV) E6-mediated degradation of p53.	Adenosine Monophosphate	12-15	P53	Homo sapiens	120-123
15382061-4	2004	PARP cleavage and a decrease in S+G2 cells were evident after RuCl2(KTZ)2 treatment in genetically matched C8161 melanoma monolayers with unequal p53 functional status.	ruthenium dichloride	62-67	P53	Homo sapiens	146-149
15505427-0	2004	Sensitization by glycerol for CDDP-therapy against human cultured cancer cells and tumors bearing mutated p53 gene.	cddp	30-34	P53	Homo sapiens	106-109
15505427-2	2004	Human tongue cell carcinoma (SAS) cells transfected with mutated p53 gene (SAS/m p53) showed CDDP-resistance compared with the cells with neo control gene (SAS/ neo).	cddp	93-97	P53	Homo sapiens	65-68
15505427-2	2004	Human tongue cell carcinoma (SAS) cells transfected with mutated p53 gene (SAS/m p53) showed CDDP-resistance compared with the cells with neo control gene (SAS/ neo).	cddp	93-97	P53	Homo sapiens	81-84
15505427-3	2004	When those cultured cells were pre-treated with glycerol, CDDP-induced apoptosis was enhanced by glycerol in SAS/m p53 cells but not in SAS/ neo cells.	cddp	58-62	P53	Homo sapiens	115-118
15505427-7	2004	These results showed that the CDDP-induced growth inhibition of the tumors is p53 -dependent and that the enhanced growth delay by glycerol may be due to the increased apoptosis.	cddp	30-34	P53	Homo sapiens	78-81
15337531-2	2004	We show here that a decrease in Ras in SW480 cells induced either by the Ras inhibitor farnesylthiosalicylic acid (FTS) or by K-Ras antisense oligonucleotides, resulted in a similar increase in p53 protein.	Oligonucleotides	142-158	P53	Homo sapiens	194-197
15533911-1	2004	A polymorphism at codon 72 of the human tumor suppressor p53 determines translation into either arginine or proline.	Arginine	96-104	P53	Homo sapiens	57-60
15520210-0	2004	Nitric oxide and ionizing radiation synergistically promote apoptosis and growth inhibition of cancer by activating p53.	Nitric Oxide	0-12	P53	Homo sapiens	116-119
15510008-12	2004	Together, the combination of docetaxel and Ad-p53 altered expression of key regulators in the cell cycle, apoptosis and signal transduction pathways with an increase in the expression of p53, bax, cleaved PARP, cleaved caspase-3 and phosphorylation of c-Jun at position at Ser.	Serine	273-276	P53	Homo sapiens	46-49
15579018-8	2004	Furthermore apoptosis mechanisms in mesothelioma cells are under the control of the cholinergic system (nicotine antiapoptotic via induction of NF-kappaB complexes and phosphorilation of Bad at Serine(112), curare proapoptotic via G(0)-G(1) arrest p21(waf-1)-dependent, but p53-independent).	Nicotine	104-112	P53	Homo sapiens	274-277
15585135-8	2004	In addition, we could observe reduction of HPV-18 E6/E7 gene expression and activation of p53, pRb, and p21waf1 proteins by 5-FU treatment in HeLa cervical carcinoma cells.	Fluorouracil	124-128	P53	Homo sapiens	90-93
15501776-0	2004	Role of protein tyrosine kinase p53/56lyn in diminished lipopolysaccharide priming of formylmethionylleucyl- phenylalanine-induced superoxide production in human newborn neutrophils.	Superoxides	131-141	P53	Homo sapiens	32-35
15603096-3	2004	p53 Protein was detected in paraffin sections using the monoclonal p53 antibody.	Paraffin	28-36	P53	Homo sapiens	0-3
15540784-3	2004	MATERIALS AND METHODS: LNCaP cells were used to determine the effect of doxorubicin on p53 and PSA expression.	Doxorubicin	72-83	P53	Homo sapiens	87-90
15540784-6	2004	RESULTS: Enzyme-linked immunosorbent and immunoblot assays indicated that doxorubicin treatment increased p53 expression but inhibited PSA levels in LNCaP cells.	Doxorubicin	74-85	P53	Homo sapiens	106-109
15540784-8	2004	Mutation of the p53 response element GGGCATGTCT to GGGAGGATCT abolished the blocking effects of doxorubicin on PSA gene promoter activity.	Doxorubicin	96-107	P53	Homo sapiens	16-19
15566678-1	2004	BACKGROUND &amp; OBJECTIVE: P53 and proliferating cell nuclear antigen(PCNA) relate with tumorigenesis, development, and prognosis of malignant tumors.	Adenosine Monophosphate	12-15	P53	Homo sapiens	28-31
15479836-7	2004	Analysis of c-Myc- and E2F1-mediated inhibition of a panel of Zta mutants shows parallel genetics and inhibition maps to a small bipartite sequence located between amino acids 29 and 53 of Zta, containing homology to the proline-rich domain of the tumor suppressor protein p53.	zta	62-65	P53	Homo sapiens	273-276
15479836-7	2004	Analysis of c-Myc- and E2F1-mediated inhibition of a panel of Zta mutants shows parallel genetics and inhibition maps to a small bipartite sequence located between amino acids 29 and 53 of Zta, containing homology to the proline-rich domain of the tumor suppressor protein p53.	zta	189-192	P53	Homo sapiens	273-276
15308759-1	2004	We tested the hypothesis that bifunctional DNA adducts formed by a nitrogen mustard-based anticancer drug were more efficient than monofunctional adducts at causing elevation of p53, consistent with the difference in cytotoxicity.	Nitrogen	67-75	P53	Homo sapiens	178-181
15542774-10	2004	Resveratrol also induced p53 phosphorylation in LNCaP prostate cancer cells, an effect also inhibited by EGF.	Resveratrol	0-11	P53	Homo sapiens	25-28
15509798-0	2004	NAD+ modulates p53 DNA binding specificity and function.	NAD	0-4	P53	Homo sapiens	15-18
15542774-1	2004	Resveratrol, a naturally occurring stilbene with antitumor properties, caused mitogen-activated protein kinase [MAPK, extracellular signal-regulated kinase 1/2 (ERK1/2)] activation, nuclear translocation of Ser15-phosphorylated p53, and p53-dependent apoptosis in hormone-insensitive DU145 prostate cancer cells.	Resveratrol	0-11	P53	Homo sapiens	228-231
15542774-1	2004	Resveratrol, a naturally occurring stilbene with antitumor properties, caused mitogen-activated protein kinase [MAPK, extracellular signal-regulated kinase 1/2 (ERK1/2)] activation, nuclear translocation of Ser15-phosphorylated p53, and p53-dependent apoptosis in hormone-insensitive DU145 prostate cancer cells.	Resveratrol	0-11	P53	Homo sapiens	237-240
15509798-7	2004	Small-molecule manipulation of p53 DNA binding activity has been an elusive goal, but here we show that NAD(+) binds to p53 tetramers, induces a conformational change, and modulates p53 DNA binding specificity in vitro.	NAD	104-110	P53	Homo sapiens	31-34
15509798-7	2004	Small-molecule manipulation of p53 DNA binding activity has been an elusive goal, but here we show that NAD(+) binds to p53 tetramers, induces a conformational change, and modulates p53 DNA binding specificity in vitro.	NAD	104-110	P53	Homo sapiens	120-123
15542774-4	2004	An inhibitor of protein kinase C (PKC)-alpha, -beta, and -gamma (CGP41251) enhanced Ser15 phosphorylation of p53 by resveratrol in the absence of EGF and blocked EGF inhibition of the resveratrol effect.	Resveratrol	116-127	P53	Homo sapiens	109-112
15573749-5	2004	Both TK6 and WTK1 cells showed effective post-damage repair capacity in incubation time of 0.5 h to 1 h. The background level of P53 protein in WTK1 was higher than that in TK6, but the level of P53 protein in H2O2-treated TK6 increased significantly higher than that in H2O2-treated WTK1.	Hydrogen Peroxide	210-214	P53	Homo sapiens	129-132
15542774-4	2004	An inhibitor of protein kinase C (PKC)-alpha, -beta, and -gamma (CGP41251) enhanced Ser15 phosphorylation of p53 by resveratrol in the absence of EGF and blocked EGF inhibition of the resveratrol effect.	Resveratrol	184-195	P53	Homo sapiens	109-112
15542774-7	2004	DU145 cells transfected with a dominant-negative PKC-alpha construct showed resveratrol-induced ERK1/2 phosphorylation and Ser15 phosphorylation of p53 but were unresponsive to EGF.	Resveratrol	76-87	P53	Homo sapiens	148-151
15492778-8	2004	In addition, it is generally accepted that cytotoxicity of cisplatin is mediated through induction of apoptosis and arrest of cell cycle resulting from its interaction with DNA, such as the formation of cisplatin-DNA adducts, which activates multiple signaling pathways, including those involving p53, Bcl-2 family, caspases, cyclins, CDKs, pRb, PKC, MAPK and PI3K/Akt.	Cisplatin	59-68	P53	Homo sapiens	297-300
15492778-8	2004	In addition, it is generally accepted that cytotoxicity of cisplatin is mediated through induction of apoptosis and arrest of cell cycle resulting from its interaction with DNA, such as the formation of cisplatin-DNA adducts, which activates multiple signaling pathways, including those involving p53, Bcl-2 family, caspases, cyclins, CDKs, pRb, PKC, MAPK and PI3K/Akt.	Cisplatin	203-212	P53	Homo sapiens	297-300
15573749-5	2004	Both TK6 and WTK1 cells showed effective post-damage repair capacity in incubation time of 0.5 h to 1 h. The background level of P53 protein in WTK1 was higher than that in TK6, but the level of P53 protein in H2O2-treated TK6 increased significantly higher than that in H2O2-treated WTK1.	Hydrogen Peroxide	271-275	P53	Homo sapiens	129-132
15509798-7	2004	Small-molecule manipulation of p53 DNA binding activity has been an elusive goal, but here we show that NAD(+) binds to p53 tetramers, induces a conformational change, and modulates p53 DNA binding specificity in vitro.	NAD	104-110	P53	Homo sapiens	120-123
15509798-9	2004	These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity.	NAD	51-57	P53	Homo sapiens	61-64
15509798-9	2004	These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity.	NAD	51-57	P53	Homo sapiens	139-142
15509798-9	2004	These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity.	NAD	51-57	P53	Homo sapiens	139-142
15509798-9	2004	These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity.	NAD	112-118	P53	Homo sapiens	61-64
15509798-9	2004	These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity.	NAD	112-118	P53	Homo sapiens	139-142
15509798-9	2004	These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity.	NAD	112-118	P53	Homo sapiens	139-142
15217838-9	2004	Oligonucleotide pull-down experiments showed a physical STAT1/p53 interaction.	Oligonucleotides	0-15	P53	Homo sapiens	62-65
15302882-9	2004	Results from glutathione S-transferase pull-down assay showed the association of Vpr with p53 in extracts containing Sp1.	Glutathione	13-24	P53	Homo sapiens	90-93
15381086-0	2004	Stabilization of alanine substituted p53 protein at Ser15, Thr18, and Ser20 in response to ionizing radiation.	Alanine	17-24	P53	Homo sapiens	37-40
15381086-0	2004	Stabilization of alanine substituted p53 protein at Ser15, Thr18, and Ser20 in response to ionizing radiation.	UNII-PYZ33YLR8A	59-64	P53	Homo sapiens	37-40
15381086-1	2004	Phosphorylation of p53 at Ser15, Thr18, and Ser20 has been thought to be important for p53 stabilization in response to ionizing radiation.	UNII-PYZ33YLR8A	33-38	P53	Homo sapiens	19-22
15381086-1	2004	Phosphorylation of p53 at Ser15, Thr18, and Ser20 has been thought to be important for p53 stabilization in response to ionizing radiation.	UNII-PYZ33YLR8A	33-38	P53	Homo sapiens	87-90
15381086-2	2004	In the present study, we examined the X-ray-induced stabilization of Ala-substituted p53 protein at Ser15, Thr18, and Ser20, whose gene expression was controlled under an ecdyson-inducible promoter.	Alanine	69-72	P53	Homo sapiens	85-88
15381086-2	2004	In the present study, we examined the X-ray-induced stabilization of Ala-substituted p53 protein at Ser15, Thr18, and Ser20, whose gene expression was controlled under an ecdyson-inducible promoter.	UNII-PYZ33YLR8A	107-112	P53	Homo sapiens	85-88
15381086-3	2004	We found that all single-, double-, or triple-Ala-substituted p53 at Ser15, Yhr18, and Ser20 were accumulated in the nucleus similarly to wild-type p53 after X-irradiation.	Alanine	46-49	P53	Homo sapiens	62-65
15381086-4	2004	These results indicate that the phosphorylation of p53 at Ser15, Thr18, and Ser20 is not necessarily needed for p53 stabilization in response to ionizing radiation.	UNII-PYZ33YLR8A	65-70	P53	Homo sapiens	51-54
15464845-4	2004	B1R is able to hyperphosphorylate p53 in several residues in the N-terminal transactivation domain, including Ser15 and Thr18.	UNII-PYZ33YLR8A	120-125	P53	Homo sapiens	34-37
15464845-7	2004	The over-expressed B1R protein induces the degradation of p53 in a concentration-dependent manner and is lost when Ser15 and Th18 are changed to alanine or when the B1R kinase is inactivated by introducing the K149Q substitution.	Alanine	145-152	P53	Homo sapiens	58-61
15361831-5	2004	In BaF3 cells and transiently transfected MCF7 breast cancer cells, elevation of total and phospho-Ser15-p53 in response to Adriamycin is blocked by Survivin and enhanced by Survivin disruption.	Doxorubicin	124-134	P53	Homo sapiens	105-108
15361831-6	2004	Furthermore, in Adriamycin-treated MCF7 cells, ectopic Survivin decreased p53 mRNA and increased mRNA and protein of the p53 homologues DeltaNp63 and TAp73 and mRNA for DeltaNp73, suggesting that Survivin may differentially regulate p53 family transcription.	Doxorubicin	16-26	P53	Homo sapiens	74-77
15361831-6	2004	Furthermore, in Adriamycin-treated MCF7 cells, ectopic Survivin decreased p53 mRNA and increased mRNA and protein of the p53 homologues DeltaNp63 and TAp73 and mRNA for DeltaNp73, suggesting that Survivin may differentially regulate p53 family transcription.	Doxorubicin	16-26	P53	Homo sapiens	121-124
15361831-6	2004	Furthermore, in Adriamycin-treated MCF7 cells, ectopic Survivin decreased p53 mRNA and increased mRNA and protein of the p53 homologues DeltaNp63 and TAp73 and mRNA for DeltaNp73, suggesting that Survivin may differentially regulate p53 family transcription.	Doxorubicin	16-26	P53	Homo sapiens	121-124
15452549-8	2004	Microarray analysis revealed the induction of p53-regulated genes and regulators of checkpoint control and apoptosis in pxn100 tumours following cisplatin-treatment.	Cisplatin	145-154	P53	Homo sapiens	46-49
15452549-11	2004	Our observations show that a marked in vivo response to cisplatin can occur via p53-dependent apoptosis or independently of p53 status in human ovarian xenografts.	Cisplatin	56-65	P53	Homo sapiens	80-83
15452549-11	2004	Our observations show that a marked in vivo response to cisplatin can occur via p53-dependent apoptosis or independently of p53 status in human ovarian xenografts.	Cisplatin	56-65	P53	Homo sapiens	124-127
15486204-0	2004	Differential recognition by the tumor suppressor protein p53 of DNA modified by the novel antitumor trinuclear platinum drug BBR3464 and cisplatin.	Platinum	111-119	P53	Homo sapiens	57-60
15486204-0	2004	Differential recognition by the tumor suppressor protein p53 of DNA modified by the novel antitumor trinuclear platinum drug BBR3464 and cisplatin.	Cisplatin	137-146	P53	Homo sapiens	57-60
15486204-3	2004	In contrast, on average, cells with mutant p53 are more resistant to the effect of cisplatin.	Cisplatin	83-92	P53	Homo sapiens	43-46
15486204-4	2004	It has been hypothesized that the sensitivity or resistance of tumor cells to cisplatin might be also associated with cell cycle control and repair processes that involve p53.	Cisplatin	78-87	P53	Homo sapiens	171-174
15486204-5	2004	DNA is a major pharmacological target of platinum compounds and DNA binding activity of the p53 protein is crucial for its tumor suppressor function.	Platinum	41-49	P53	Homo sapiens	92-95
15486204-6	2004	This study, using gel-mobility-shift assays, was undertaken to examine the interactions of active and latent p53 protein with DNA fragments and oligodeoxyribonucleotide duplexes modified by BBR3464 in a cell free medium and to compare these results with those describing the interactions of these proteins with DNA modified by cisplatin.	Cisplatin	327-336	P53	Homo sapiens	109-112
15486204-7	2004	The results indicate that structurally different DNA adducts of BBR3464 and cisplatin exhibit a different efficiency to affect the binding affinity of the modified DNA to p53 protein.	Cisplatin	76-85	P53	Homo sapiens	171-174
15486204-8	2004	It has been suggested that different structural perturbations induced in DNA by the adducts of BBR3464 and cisplatin produce a differential response to p53 protein activation and recognition and that a "molecular approach" to control of downstream effects such as protein recognition and pathways of apoptosis induction may consist in design of structurally unique DNA adducts as cell signals.	Cisplatin	107-116	P53	Homo sapiens	152-155
15280358-6	2004	We mapped the TBP-interacting region in the C terminus of ZNF76 to a glutamic acid-rich domain, which acts in a dominant negative manner to enhance p53-mediated transactivation in reporter assays.	Glutamic Acid	69-82	P53	Homo sapiens	148-151
15456252-0	2004	Identification and characterization of small molecule inhibitors of the calcium-dependent S100B-p53 tumor suppressor interaction.	Calcium	72-79	P53	Homo sapiens	96-99
15467449-6	2004	Together, these findings suggest that p21(Cip1/WAF1) partially protects p53-null human leukemia cells from paclitaxel-mediated lethality, and raise the possibility that p21(Cip1/WAF1)-associated perturbations in signal transduction pathways as well as Bcl-2 phosphorylation status may play a role in this phenomenon.	Paclitaxel	107-117	P53	Homo sapiens	72-75
15361841-1	2004	A mutant version of p53 (p53-121F), in which phenylalanine replaces the 121st serine residue, can induce apoptosis more effectively than wild-type p53 (wt-p53).	Serine	78-84	P53	Homo sapiens	20-23
15361841-1	2004	A mutant version of p53 (p53-121F), in which phenylalanine replaces the 121st serine residue, can induce apoptosis more effectively than wild-type p53 (wt-p53).	Serine	78-84	P53	Homo sapiens	25-28
15361841-1	2004	A mutant version of p53 (p53-121F), in which phenylalanine replaces the 121st serine residue, can induce apoptosis more effectively than wild-type p53 (wt-p53).	Serine	78-84	P53	Homo sapiens	25-28
15361841-1	2004	A mutant version of p53 (p53-121F), in which phenylalanine replaces the 121st serine residue, can induce apoptosis more effectively than wild-type p53 (wt-p53).	Serine	78-84	P53	Homo sapiens	25-28
15473923-1	2004	BACKGROUND &amp; OBJECTIVE: P53 gene is a tumor suppressor gene,and its mutation in human tumor cells is frequently observed.	Adenosine Monophosphate	12-15	P53	Homo sapiens	28-31
15492278-8	2004	Western blot analysis confirmed that methionine stress caused the following: (a) a marked increase of GADD45alpha and gamma in the wt-p53 cell lines SWB61 and 40; (b) an increase in GADD34 and p21 protein in all of the methionine-dependent lines; and (c) the induction of MDA7 and phospho-p38 in DAOY and SWB39, consistent with marked transcriptional activation of the former under methionine stress.	Methionine	37-47	P53	Homo sapiens	134-137
15373832-4	2004	In the absence of antibody, reduced p53 preferentially bound scDNA lacking p53CON in the presence of 3 kb linear plasmid DNAs or 20 mer oligonucleotides, both containing and lacking the p53CON.	Oligonucleotides	136-152	P53	Homo sapiens	36-39
15390206-0	2004	Mutation of p53 in head and neck squamous cell carcinoma correlates with Bcl-2 expression and increased susceptibility to cisplatin-induced apoptosis.	Cisplatin	122-131	P53	Homo sapiens	12-15
15390206-11	2004	Further investigation showed that SCCHN cells expressing predominantly mutant p53 and decreased Bcl-2 were more susceptible to cisplatin-induced apoptosis than vector-transfected controls (p &lt; .0001).	Cisplatin	127-136	P53	Homo sapiens	78-81
15472230-0	2004	Wild-type p53 protein is up-regulated upon cyclic adenosine monophosphate-induced differentiation of human endometrial stromal cells.	Cyclic AMP	43-73	P53	Homo sapiens	10-13
15310764-6	2004	Moreover, NPM inhibits hypoxia-induced p53 phosphorylation at Ser-15 and interacts with p53 in hypoxic cells.	Serine	62-65	P53	Homo sapiens	39-42
15472230-3	2004	We now report a massive and sustained up-regulation of p53 tumor suppressor protein during cAMP-induced decidualization of cultured endometrial stromal cells.	Cyclic AMP	91-95	P53	Homo sapiens	55-58
15475475-6	2004	Paclitaxel activated p53 protein at low concentrations but exhibited G2/M cell cycle blocking activity at higher concentrations where microtubules were stabilized.	Paclitaxel	0-10	P53	Homo sapiens	21-24
15472230-7	2004	In cAMP-treated decidualized cells, p53 accumulation was associated with decreased nuclear Mdm2 and cytoplasmic PKB/Akt levels.	Cyclic AMP	3-7	P53	Homo sapiens	36-39
15258567-3	2004	We report here that forced expression of p14ARF enhances phosphorylation of p53 serine 15 (p53S15) in NIH3T3, IMR90 and MCF7 cells.	Serine	80-86	P53	Homo sapiens	76-79
15364135-2	2004	p53 Overexpression has been associated with resistance to cisplatin-based chemotherapy in patients (pts) with NSCLC.	Cisplatin	58-67	P53	Homo sapiens	0-3
15258255-11	2004	Taken together, our results show that exposure to C-1305 is accompanied by the formation of low levels of potent cleavable complexes that are selectively toxic toward tumor cells with defective p53 function.	Carbon	50-51	P53	Homo sapiens	194-197
15486197-7	2004	In addition, paclitaxel, at cytostatic concentrations, early initiates an apoptotic signaling pathway associated with increases in the mitochondrial reducing potential, mitochondrial membrane potential, p53 expression, and Bax/Bcl-2 ratio.	Paclitaxel	13-23	P53	Homo sapiens	203-206
15375518-0	2004	Radiosensitization of a human soft tissue sarcoma cell line US8-93 (mt-p53) with the oxidizer sodium peroxodisulfate.	sodium persulfate	94-116	P53	Homo sapiens	71-74
15371598-5	2004	Assays with phage-displayed Nef from HIV(NL4-3) were used to identify a series of guanidine alkaloid-based inhibitors of Nef interactions with p53, actin, and p56(lck).	guanidine alkaloid	82-100	P53	Homo sapiens	143-146
15802048-5	2004	Here we have used (1)H MRS to characterize the choline phospholipid metabolite levels of p53(+/ +) and p53(-/-) cells, and demonstrated that loss of p53 function results in increased phosphocholine and total choline.	Phospholipids	55-67	P53	Homo sapiens	89-92
15802048-5	2004	Here we have used (1)H MRS to characterize the choline phospholipid metabolite levels of p53(+/ +) and p53(-/-) cells, and demonstrated that loss of p53 function results in increased phosphocholine and total choline.	Phospholipids	55-67	P53	Homo sapiens	103-106
15802048-5	2004	Here we have used (1)H MRS to characterize the choline phospholipid metabolite levels of p53(+/ +) and p53(-/-) cells, and demonstrated that loss of p53 function results in increased phosphocholine and total choline.	Phospholipids	55-67	P53	Homo sapiens	103-106
15802048-6	2004	These data suggest that the increased malignancy of cancer cells resulting from loss of p53 may be mediated, in part, through the choline phospholipid pathway.	Phospholipids	138-150	P53	Homo sapiens	88-91
15334064-4	2004	Doxorubicin treatment activated p53, downregulated survivin and survivin-DeltaEx3 but upregulated survivin-2B in EU-3, an acute lymphocytic leukemia (ALL) cell line with wild-type (wt)-p53 phenotype.	Doxorubicin	0-11	P53	Homo sapiens	32-35
15334064-4	2004	Doxorubicin treatment activated p53, downregulated survivin and survivin-DeltaEx3 but upregulated survivin-2B in EU-3, an acute lymphocytic leukemia (ALL) cell line with wild-type (wt)-p53 phenotype.	Doxorubicin	0-11	P53	Homo sapiens	185-188
15269203-10	2004	In addition, it was shown that NBS1, SMC1, and p53 were phosphorylated in an ATM-dependent manner, and p53 phosphorylation on serine 20 is dependent on CHK2 after irofulven treatment.	Serine	126-132	P53	Homo sapiens	47-50
15269203-10	2004	In addition, it was shown that NBS1, SMC1, and p53 were phosphorylated in an ATM-dependent manner, and p53 phosphorylation on serine 20 is dependent on CHK2 after irofulven treatment.	Serine	126-132	P53	Homo sapiens	103-106
15374966-0	2004	Retinoic acid increases the expression of p53 and proapoptotic caspases and sensitizes keratinocytes to apoptosis: a possible explanation for tumor preventive action of retinoids.	Tretinoin	0-13	P53	Homo sapiens	42-45
15374966-8	2004	Inhibition of p53 and caspases with alpha-pifithrin and z-Val-Ala-Asp-fluoromethyl ketone, respectively, blocked UVB- and doxorubicin-induced apoptosis in ATRA-treated KCs.	Tretinoin	155-159	P53	Homo sapiens	14-17
15374966-9	2004	Analogous to the observed ATRA effects in monolayer cultures, in vitro-generated organotypic skin cultures reacted with up-regulation of p53 and proapoptotic caspases and displayed increased sensitivity to UVB-induced apoptosis.	Tretinoin	26-30	P53	Homo sapiens	137-140
15374966-6	2004	Analysis by real-time PCR and Western blot revealed that ATRA treatment strongly increased the mRNA and protein expression of p53 and caspase-3, -6, -7, and -9, which are key regulators of apoptosis.	Tretinoin	57-61	P53	Homo sapiens	126-129
15374966-7	2004	UVB irradiation of ATRA-treated cells but not of control cells led to the accumulation of p53 protein and of its target gene Noxa.	Tretinoin	19-23	P53	Homo sapiens	90-93
15374978-8	2004	Conversely, concurrent treatment with SN-38 and UCN-01 resulted in S-phase checkpoint override, an amplified DNA damage response including increased phosphorylation of the DNA double-strand breakage marker H2AX and augmentation of clonogenic inhibition, which was independent of p53.	Irinotecan	38-43	P53	Homo sapiens	279-282
15374966-8	2004	Inhibition of p53 and caspases with alpha-pifithrin and z-Val-Ala-Asp-fluoromethyl ketone, respectively, blocked UVB- and doxorubicin-induced apoptosis in ATRA-treated KCs.	Doxorubicin	122-133	P53	Homo sapiens	14-17
15155458-7	2004	Phosphorylation of p53 at serines 15 and 392 is critical for complex formation.	Serine	26-33	P53	Homo sapiens	19-22
15312749-5	2004	We observed two peaks of p53 activity during continuous treatment of 17-[beta]-estradiol (E2) for 72h.	Estradiol	69-88	P53	Homo sapiens	25-28
15363194-1	2004	BACKGROUND &amp; OBJECTIVE: Tumor suppressor gene p53 and oncogene C-erbB-2 are confirmed to have close relation with endometrioid adenocarcinoma (EC), few documents have been reported about their correlation.	Adenosine Monophosphate	12-15	P53	Homo sapiens	50-53
15517885-3	2004	The growth-inhibitory effects of resveratrol are mediated through cell-cycle arrest; upregulation of p21Cip1/WAF1, p53 and Bax; down-regulation of survivin, cyclin D1, cyclin E, Bcl-2, Bcl-xL and clAPs; and activation of caspases.	Resveratrol	33-44	P53	Homo sapiens	115-118
15131588-1	2004	A common arginine to proline polymorphism is harboured at codon 72 of the human p53 gene.	Arginine	9-17	P53	Homo sapiens	80-83
15131591-3	2004	Restoration of functional p53 sensitized glioma cells expressing mutant p53 to TNF-alpha by accumulation of O2-*.	Superoxides	108-110	P53	Homo sapiens	26-29
15326376-4	2004	We here show that inhibition of Chk1 but not of Chk2 in p21(-/-) and p53(-/-) cells caused a greater abrogation of G(2) block induced by ionizing radiation and cis-diamine-dichloroplatinum treatments and a greater sensitization to the same treatments than in the parental cell line with p53 and p21 wild type proteins.	cis-diamine	160-171	P53	Homo sapiens	69-72
15131591-3	2004	Restoration of functional p53 sensitized glioma cells expressing mutant p53 to TNF-alpha by accumulation of O2-*.	Superoxides	108-110	P53	Homo sapiens	72-75
15131591-6	2004	Two separate signaling cascades, p53-mediated ROS-dependent and -independent pathways, both of which are initiated by caspase-8 activation, thus contribute to ceramide formation in TNF-alpha-induced apoptosis of human glioma cells.	Reactive Oxygen Species	46-49	P53	Homo sapiens	33-36
15254427-0	2004	p53-Dependent activation of a molecular beacon in tumor cells following exposure to doxorubicin chemotherapy.	Doxorubicin	84-95	P53	Homo sapiens	0-3
15254427-3	2004	Strong nuclear signal was observed following treatment of wild-type p53-expressing human H460 lung cancer cells for 8 hours with the chemotherapeutic agent doxorubicin (adriamycin).	Doxorubicin	156-167	P53	Homo sapiens	68-71
15254427-3	2004	Strong nuclear signal was observed following treatment of wild-type p53-expressing human H460 lung cancer cells for 8 hours with the chemotherapeutic agent doxorubicin (adriamycin).	Doxorubicin	169-179	P53	Homo sapiens	68-71
15254427-6	2004	Increased signal from the phosphorothioate-modified p21-beacon in doxorubicin-treated cells likely resulted from sequence-specific hybridization as well as sequence-independent cleavage that may occur due to p53-dependent activation of endonucleases during apoptosis.	Doxorubicin	66-77	P53	Homo sapiens	208-211
15342409-7	2004	HCT116 p53+/+ cells exhibit a more rapid removal of 8-oxoG from DNA than p53-/- cells exposed to the same levels of reactive oxygen species (ROS) stress.	Reactive Oxygen Species	116-139	P53	Homo sapiens	7-10
15342409-0	2004	Role of p53 in sensing oxidative DNA damage in response to reactive oxygen species-generating agents.	Reactive Oxygen Species	59-82	P53	Homo sapiens	8-11
15342409-7	2004	HCT116 p53+/+ cells exhibit a more rapid removal of 8-oxoG from DNA than p53-/- cells exposed to the same levels of reactive oxygen species (ROS) stress.	Reactive Oxygen Species	141-144	P53	Homo sapiens	7-10
15342409-8	2004	Together, these results suggest that p53 participates in sensing oxidative DNA damage and modulates BER function in response to persistent ROS stress.	Reactive Oxygen Species	139-142	P53	Homo sapiens	37-40
15342418-1	2004	We have demonstrated previously that interferon (IFN)-gamma sensitizes human colon carcinoma cell lines to the cytotoxic effects of 5-fluorouracil combined with leucovorin and to the thymidylate synthase inhibitor, ZD9331, dependent on thymineless stress-induced DNA damage, independent of p53.	Fluorouracil	132-146	P53	Homo sapiens	290-293
15355354-0	2004	Structured DNA promotes phosphorylation of p53 by DNA-dependent protein kinase at serine 9 and threonine 18.	Serine	82-88	P53	Homo sapiens	43-46
15467443-6	2004	This may be explained by the status of p53 serine 20 phosphorylation.	Serine	43-49	P53	Homo sapiens	39-42
15467443-7	2004	In non-stressed CML cells, serine 20 of p53 is constitutively phosphorylated by Chk1, and is inhibited by STI571.	Serine	27-33	P53	Homo sapiens	40-43
15763944-7	2004	Moreover, Ang-1 inhibits DOX-induced up-regulation of p53 through PI3K/Akt.	Doxorubicin	25-28	P53	Homo sapiens	54-57
15763945-10	2004	Doxil minimally affected the expression levels of p53, whereas other anthracyclines induced p53 protein levels to a significant level, resulting in endothelial cell apoptosis.	Anthracyclines	69-83	P53	Homo sapiens	92-95
15355354-0	2004	Structured DNA promotes phosphorylation of p53 by DNA-dependent protein kinase at serine 9 and threonine 18.	Threonine	95-104	P53	Homo sapiens	43-46
15355354-6	2004	We report here the identification of p53 phosphorylation at two novel sites for DNA-PK, Thr18 and Ser9.	UNII-PYZ33YLR8A	88-93	P53	Homo sapiens	37-40
15489061-8	2004	Both cell lines displayed a higher DNA-binding activity of p53 and HIF-1 72 h after H2O2 exposure.	Hydrogen Peroxide	84-88	P53	Homo sapiens	59-62
15090465-0	2004	Curcumin impairs tumor suppressor p53 function in colon cancer cells.	Curcumin	0-8	P53	Homo sapiens	34-37
15090465-5	2004	In compounds other than curcumin this same electrophilic moiety is associated with inactivation of the tumor suppressor, p53.	Curcumin	24-32	P53	Homo sapiens	121-124
15090465-7	2004	It disrupts the conformation of the p53 protein required for its serine phosphorylation, its binding to DNA, its transactivation of p53-responsive genes and p53-mediated cell cycle arrest.	Serine	65-71	P53	Homo sapiens	36-39
15090465-7	2004	It disrupts the conformation of the p53 protein required for its serine phosphorylation, its binding to DNA, its transactivation of p53-responsive genes and p53-mediated cell cycle arrest.	Serine	65-71	P53	Homo sapiens	132-135
15090465-7	2004	It disrupts the conformation of the p53 protein required for its serine phosphorylation, its binding to DNA, its transactivation of p53-responsive genes and p53-mediated cell cycle arrest.	Serine	65-71	P53	Homo sapiens	132-135
15489061-9	2004	Our results indicate that similar mechanisms involving p21(WAF-1) and probably p53 are at work in BJ and hTERT-BJ1 HDFs under H2O2-induced SIPS, suggesting that generalized DNA damage rather than telomere length/telomerase plays a crucial role in H2O2induced SIPS.	Hydrogen Peroxide	126-130	P53	Homo sapiens	79-82
15289875-4	2004	CDDP treatment caused steady induction of p53 protein in both cancer cell types, although it was more dramatic in CDDP-resistant HEp-2 cells, which was correlated well with p53 Ser15 phosphorylation, but not with the expression level of HPV type 18 E6 oncoprotein in these cells.	Cisplatin	0-4	P53	Homo sapiens	42-45
15289867-10	2004	Additionally, flavone induced apoptosis in primary colon carcinoma cells COLO205-X with appearance of DNA ladders, caspase 3 protein procession, PARP protein cleavage, and an increase in p21 (not p53) protein.	flavone	14-21	P53	Homo sapiens	196-199
15523893-6	2004	In this study, p53 protein immunoreactivity was investigated in paraffin sections of primary nasopharyngeal tumors and metastatic cervical lymph nodes and association with clinical and histopathological characteristics was evaluated.	Paraffin	64-72	P53	Homo sapiens	15-18
15289875-4	2004	CDDP treatment caused steady induction of p53 protein in both cancer cell types, although it was more dramatic in CDDP-resistant HEp-2 cells, which was correlated well with p53 Ser15 phosphorylation, but not with the expression level of HPV type 18 E6 oncoprotein in these cells.	Cisplatin	0-4	P53	Homo sapiens	173-176
15289875-4	2004	CDDP treatment caused steady induction of p53 protein in both cancer cell types, although it was more dramatic in CDDP-resistant HEp-2 cells, which was correlated well with p53 Ser15 phosphorylation, but not with the expression level of HPV type 18 E6 oncoprotein in these cells.	Cisplatin	114-118	P53	Homo sapiens	173-176
21241554-1	2004	BACKGROUND: To assess the effects of exogenous p73 gene on chemosensitivity of wild-type p53 human lung adenocarcinoma cell A549 to cisplatin (DDP) and adriamycin (ADM).	Cisplatin	132-141	P53	Homo sapiens	89-92
15548361-1	2004	According to recent reports, some cancer types exhibit nonrandom allele loss at codon 72 in exon 4 of the p53 gene [coding for proline (72Pro) or arginine (72Arg)].	Arginine	146-154	P53	Homo sapiens	106-109
15548364-2	2004	Besides, p73 was shown to be activated by only a subset of signals that activate p53, such as gamma-irradiation and cisplatin, but not by other common genotoxic stress-inducing agents such as ultraviolet (UV) irradiation, although many of these signals are also capable of inducing p53-independent cell death.	Cisplatin	116-125	P53	Homo sapiens	81-84
15613785-0	2004	Hypergravity induces phosphorylation of p53 at serine 15, but not an expression of p53-downstream genes.	Serine	47-53	P53	Homo sapiens	40-43
15613785-2	2004	Hypergravity (20 x g) induced the accumulation of p53 and the phosphorylation of p53 at Ser-15.	Serine	88-91	P53	Homo sapiens	81-84
15322241-5	2004	Reporter gene assays revealed the presence of several Ah receptor response-element motifs in the promoter and first intron of the p21(WAF1/CIP1) gene that respond to TCDD-mediated Ah receptor activation independently of p53.	Polychlorinated Dibenzodioxins	166-170	P53	Homo sapiens	220-223
15603542-6	2004	Functional assays confirming cell dysfunction and increased apoptosis revealed the rat kidney to be more sensitive to the effects of cisplatin than human kidney as demonstrated by significant decreases in slice ATP and GSH levels, significant increases in caspase 9 and 3 activity, p53 protein levels, and increased DNA laddering.	Cisplatin	133-142	P53	Homo sapiens	282-285
15218033-1	2004	Under serum-free conditions, rapamycin, an inhibitor of mammalian target of rapamycin (mTOR), induces a cellular stress response characterized by rapid and sustained activation of the apoptosis signal-regulating kinase 1 (ASK1) signaling pathway and selective apoptosis of cells lacking functional p53.	Sirolimus	29-38	P53	Homo sapiens	298-301
15246568-0	2004	Analysis of p53 mutations in cells taken from paraffin-embedded tissue sections of ductal carcinoma in situ and atypical ductal hyperplasia of the breast.	Paraffin	46-54	P53	Homo sapiens	12-15
15358195-5	2004	Expression of wt p53, but not that of p53-175 mutant, diminished JAK2 tyrosine phosphorylation in MDAH2774 and Caov-3 cell lines.	Tyrosine	70-78	P53	Homo sapiens	17-20
15358195-9	2004	These findings present a possible p53-dependent cellular process of modulating JAK2 tyrosine phosphorylation in ovarian cancer cell lines.	Tyrosine	84-92	P53	Homo sapiens	34-37
15247902-5	2004	Here, we document that human HCT116 colorectal carcinoma cells treated with adriamycin or 5-fluorouracil (5FU) can accumulate total p53 to equally high levels, and mitochondrial p53 to proportionate levels, although only 5FU treatment provoked p53-dependent apoptosis.	Doxorubicin	76-86	P53	Homo sapiens	132-135
15247902-5	2004	Here, we document that human HCT116 colorectal carcinoma cells treated with adriamycin or 5-fluorouracil (5FU) can accumulate total p53 to equally high levels, and mitochondrial p53 to proportionate levels, although only 5FU treatment provoked p53-dependent apoptosis.	Doxorubicin	76-86	P53	Homo sapiens	178-181
15247902-5	2004	Here, we document that human HCT116 colorectal carcinoma cells treated with adriamycin or 5-fluorouracil (5FU) can accumulate total p53 to equally high levels, and mitochondrial p53 to proportionate levels, although only 5FU treatment provoked p53-dependent apoptosis.	Doxorubicin	76-86	P53	Homo sapiens	178-181
15247902-5	2004	Here, we document that human HCT116 colorectal carcinoma cells treated with adriamycin or 5-fluorouracil (5FU) can accumulate total p53 to equally high levels, and mitochondrial p53 to proportionate levels, although only 5FU treatment provoked p53-dependent apoptosis.	Fluorouracil	90-104	P53	Homo sapiens	132-135
15247902-5	2004	Here, we document that human HCT116 colorectal carcinoma cells treated with adriamycin or 5-fluorouracil (5FU) can accumulate total p53 to equally high levels, and mitochondrial p53 to proportionate levels, although only 5FU treatment provoked p53-dependent apoptosis.	Fluorouracil	90-104	P53	Homo sapiens	178-181
15247902-5	2004	Here, we document that human HCT116 colorectal carcinoma cells treated with adriamycin or 5-fluorouracil (5FU) can accumulate total p53 to equally high levels, and mitochondrial p53 to proportionate levels, although only 5FU treatment provoked p53-dependent apoptosis.	Fluorouracil	90-104	P53	Homo sapiens	178-181
15247902-5	2004	Here, we document that human HCT116 colorectal carcinoma cells treated with adriamycin or 5-fluorouracil (5FU) can accumulate total p53 to equally high levels, and mitochondrial p53 to proportionate levels, although only 5FU treatment provoked p53-dependent apoptosis.	Fluorouracil	106-109	P53	Homo sapiens	132-135
15247902-5	2004	Here, we document that human HCT116 colorectal carcinoma cells treated with adriamycin or 5-fluorouracil (5FU) can accumulate total p53 to equally high levels, and mitochondrial p53 to proportionate levels, although only 5FU treatment provoked p53-dependent apoptosis.	Fluorouracil	106-109	P53	Homo sapiens	178-181
15247902-5	2004	Here, we document that human HCT116 colorectal carcinoma cells treated with adriamycin or 5-fluorouracil (5FU) can accumulate total p53 to equally high levels, and mitochondrial p53 to proportionate levels, although only 5FU treatment provoked p53-dependent apoptosis.	Fluorouracil	106-109	P53	Homo sapiens	178-181
15197326-2	2004	The p53-family members, p63 and p73, are highly similar to p53, yet are differentially activated by IR, UV and cis-platinum via ATM and c-abl/ATR signaling pathways.	Cisplatin	111-123	P53	Homo sapiens	4-7
15288541-4	2004	The FACIM assay was used to evaluate the mutagenesis of the flounder TP53 exposed in vitro to benzo[a]pyrene diol epoxide (BPDE).	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	94-121	P53	Homo sapiens	69-73
15288541-4	2004	The FACIM assay was used to evaluate the mutagenesis of the flounder TP53 exposed in vitro to benzo[a]pyrene diol epoxide (BPDE).	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	123-127	P53	Homo sapiens	69-73
15154850-1	2004	The transcriptional co-activator CBP [CREB (cAMP-response-element-binding protein)-binding protein] and its paralogue p300 play a key role in the regulation of both activity and stability of the tumour suppressor p53.	Cyclic AMP	44-48	P53	Homo sapiens	213-216
15154850-3	2004	Direct protein-protein interaction between a central domain of MDM2 and the TAZ1 (transcriptional adaptor zinc-binding domain) [C/H1 (cysteine/histidine-rich region 1)] domain of p300 and subsequent formation of a ternary complex including p53 have been reported previously.	Cysteine	134-142	P53	Homo sapiens	240-243
15167899-0	2004	Sensitizing glioma cells to cisplatin by abrogating the p53 response with antisense oligonucleotides.	Cisplatin	28-37	P53	Homo sapiens	56-59
15167899-0	2004	Sensitizing glioma cells to cisplatin by abrogating the p53 response with antisense oligonucleotides.	Oligonucleotides	84-100	P53	Homo sapiens	56-59
15167899-2	2004	However, as there is also some evidence to the contrary, we studied the relationship of the p53 status to the cellular response of glioma cells that were exposed to cisplatin.	Cisplatin	165-174	P53	Homo sapiens	92-95
15167899-5	2004	In U87MG cells, blocking the p53 response by antisense oligonucleotides also sensitized the cells to 2.5 microg/ml cisplatin, and shifted the cellular response from arrest to caspase 3-mediated apoptosis.	Oligonucleotides	55-71	P53	Homo sapiens	29-32
15167899-5	2004	In U87MG cells, blocking the p53 response by antisense oligonucleotides also sensitized the cells to 2.5 microg/ml cisplatin, and shifted the cellular response from arrest to caspase 3-mediated apoptosis.	Cisplatin	115-124	P53	Homo sapiens	29-32
15302922-6	2004	Multiple p53 sequence alignments with 41 additional species confirmed that Arg-174 is highly conserved.	Arginine	75-78	P53	Homo sapiens	9-12
15302922-10	2004	A DNA-free p53 structure model predicts that Arg-174 is important for dimerization, whereas Spalax Lys-174 prevents such interactions.	Arginine	45-48	P53	Homo sapiens	11-14
15302922-10	2004	A DNA-free p53 structure model predicts that Arg-174 is important for dimerization, whereas Spalax Lys-174 prevents such interactions.	Lysine	99-102	P53	Homo sapiens	11-14
15358233-5	2004	Furthermore, His-p53 and FLAG-XPG, but not PCNA, stimulated the Tg DNA glycosylase/AP lyase activity of GST-NTH1 or NTH1.	Histidine	13-16	P53	Homo sapiens	17-20
15266324-4	2004	In vitro experiments on neoplastic germ cell lines showed that their exquisite sensitivity to CDDP could be attributed to p53-dependent and -independent pathways.	Cisplatin	94-98	P53	Homo sapiens	122-125
15266324-5	2004	Applying cDNA macroarray, semiquantitative RT-PCR and Western blot analyses, blocking experiments, caspase activity assays, and morphological methods, we sought here to define the p53-independent pathway(s) involved in the CDDP-induced apoptosis.	Cisplatin	223-227	P53	Homo sapiens	180-183
15266324-6	2004	For this purpose, we used the human TGCT cell line NCCIT, the mutated p53 of which is known to remain inactive during the course of CDDP-induced apoptosis.	Cisplatin	132-136	P53	Homo sapiens	70-73
15266324-10	2004	Thus, our data suggest that CDDP mediates its p53-independent apoptosis-inducing effect on the malignant human testicular germ cells--at least partially--through activation of the MEK-ERK signalling pathway.	Cisplatin	28-32	P53	Homo sapiens	46-49
15197326-2	2004	The p53-family members, p63 and p73, are highly similar to p53, yet are differentially activated by IR, UV and cis-platinum via ATM and c-abl/ATR signaling pathways.	Cisplatin	111-123	P53	Homo sapiens	59-62
15181149-0	2004	p53 localization at centrosomes during mitosis and postmitotic checkpoint are ATM-dependent and require serine 15 phosphorylation.	Serine	104-110	P53	Homo sapiens	0-3
15297111-7	2004	The mechanism of cell death induced by these fatty acids seem to involve with mitochondrial depolarization, lipid accumulation and the levels of C-MYC and P53 mRNA expression.	Fatty Acids	45-56	P53	Homo sapiens	155-158
15554555-8	2004	Our results suggest that homozygous arginine at codon 72 of p53 may represent a risk factor for developing ovarian malignancies and may affect the differentiation of endometrial cancer.	Arginine	36-44	P53	Homo sapiens	60-63
15254726-5	2004	Expression of p53, p21 and bax was increased, and bcl-2 was decreased in melanoma cells after exposure to atRA at different concentrations for various periods of time.	Tretinoin	106-110	P53	Homo sapiens	14-17
15254726-8	2004	These data indicate that p53, p21, bax and bcl-2 proteins were involved in atRA-induced apoptosis in melanoma cells.	Tretinoin	75-79	P53	Homo sapiens	25-28
15253698-6	2004	We also showed that p53 is the mediator of apoptosis in the setting of GTP depletion and ischemic injury.	Guanosine Triphosphate	71-74	P53	Homo sapiens	20-23
15253698-7	2004	Indeed, salvage of GTP with guanosine prevented the ischemia-induced increase in p53 protein.	Guanosine Triphosphate	19-22	P53	Homo sapiens	81-84
15353127-12	2004	The XPC defect reduces the cisplatin treatment-mediated p53 response.	Cisplatin	27-36	P53	Homo sapiens	56-59
15254726-0	2004	Expression profiles of p53, p21, bax and bcl-2 proteins in all-trans-retinoic acid treated primary and metastatic melanoma cells.	Tretinoin	69-82	P53	Homo sapiens	23-26
15254726-3	2004	In this study, we used a similar cell culture model system of matched primary and metastatic melanoma cells from the same patient to investigate whether p53 and bcl-2 family proteins were involved in atRA-induced apoptosis.	Tretinoin	200-204	P53	Homo sapiens	153-156
15254702-6	2004	In this study, we examined induced apoptosis in colon cancer cell lines and the status of p53 expression in response to treatment of HCT116, COLO320, SW480 and DLD1 with 5-FU alone, CDDP alone and FP treatment under flow cytometric analysis.	Fluorouracil	170-174	P53	Homo sapiens	90-93
15260130-3	2004	H2O2 increased both the ratio of bax/bcl-2 and the p53 mRNA expression.	Hydrogen Peroxide	0-4	P53	Homo sapiens	51-54
15159397-6	2004	Moreover, prior ATM/ATR-dependent phosphorylation of BRCA1 at Ser-1423 or Ser-1524 regulates the ability of ATM/ATR to phosphorylate p53(Ser-15) efficiently.	Serine	62-65	P53	Homo sapiens	133-136
15259070-3	2004	Lipofectin mediated p53 or HCV NS5A expression vectors were used to transfect hepatoma cell lines to observe whether HCV NS5A could abrogate the binding ability of p53 to its specific DNA sequence and p53 transactivation on p21 promoter.	1,2-dielaidoylphosphatidylethanolamine	0-10	P53	Homo sapiens	20-23
15363320-0	2004	[Application of immunohistochemistry-laser microdissection-PCR technique in detecting p53 gene mutation in paraffin sections of gastric cancer].	Paraffin	107-115	P53	Homo sapiens	86-89
15363320-2	2004	METHODS: The expression of p53 protein in 41 paraffin-embedded advanced gastric cancer samples was assessed by immunohistochemistry.	Paraffin	45-53	P53	Homo sapiens	27-30
15363320-12	2004	CONCLUSIONS: IHC-LMD-PCR technique can be successfully applied in paraffin sections of gastric cancers for the detection of p53 gene mutations.	Paraffin	66-74	P53	Homo sapiens	124-127
15159397-6	2004	Moreover, prior ATM/ATR-dependent phosphorylation of BRCA1 at Ser-1423 or Ser-1524 regulates the ability of ATM/ATR to phosphorylate p53(Ser-15) efficiently.	Serine	74-77	P53	Homo sapiens	133-136
15159397-6	2004	Moreover, prior ATM/ATR-dependent phosphorylation of BRCA1 at Ser-1423 or Ser-1524 regulates the ability of ATM/ATR to phosphorylate p53(Ser-15) efficiently.	Serine	74-77	P53	Homo sapiens	133-136
15159397-7	2004	Phosphorylation of p53(Ser-15) is necessary for an IR-induced G(1)/S arrest via transcriptional induction of the cyclin-dependent kinase inhibitor p21.	Serine	23-26	P53	Homo sapiens	19-22
15159397-8	2004	Consistent with these data, repressing p53(Ser-15) phosphorylation by BRCA1-BARD1 depletion compromises p21 induction and the G(1)/S checkpoint arrest in response to IR but not UV radia-tion.	Serine	43-46	P53	Homo sapiens	39-42
15251465-0	2004	Thymidylate synthase inhibition triggers glucose-dependent apoptosis in p53-negative leukemic cells.	Glucose	41-48	P53	Homo sapiens	72-75
15183530-1	2004	A common germline polymorphism of p53 gene produces an Arginine to Proline change at aminoacid position 72.	Arginine	55-63	P53	Homo sapiens	34-37
15183535-12	2004	The higher frequency of p53 somatic mutation in p5372Arg/Arg homozygotes than p5372Pro/Pro homozygotes is consistent with the thesis that the function of p5372Pro/Pro is impaired so that a further alteration of p53 gene is less required in p5372Pro/Pro homozygotes than p5372Arg/Arg homozygotes.	Arginine	53-56	P53	Homo sapiens	24-27
15183535-12	2004	The higher frequency of p53 somatic mutation in p5372Arg/Arg homozygotes than p5372Pro/Pro homozygotes is consistent with the thesis that the function of p5372Pro/Pro is impaired so that a further alteration of p53 gene is less required in p5372Pro/Pro homozygotes than p5372Arg/Arg homozygotes.	Arginine	53-56	P53	Homo sapiens	48-51
15183535-12	2004	The higher frequency of p53 somatic mutation in p5372Arg/Arg homozygotes than p5372Pro/Pro homozygotes is consistent with the thesis that the function of p5372Pro/Pro is impaired so that a further alteration of p53 gene is less required in p5372Pro/Pro homozygotes than p5372Arg/Arg homozygotes.	Arginine	57-60	P53	Homo sapiens	24-27
15183535-12	2004	The higher frequency of p53 somatic mutation in p5372Arg/Arg homozygotes than p5372Pro/Pro homozygotes is consistent with the thesis that the function of p5372Pro/Pro is impaired so that a further alteration of p53 gene is less required in p5372Pro/Pro homozygotes than p5372Arg/Arg homozygotes.	Arginine	57-60	P53	Homo sapiens	48-51
15256442-8	2004	Ser(392) nonphosphorylated p53 was present in human breast tumors expressing mutant p53 including p53H175.	Serine	0-3	P53	Homo sapiens	27-30
15212949-3	2004	Decreasing phospho-ERK with the pharmacological inhibitors, PD98059 and U0126, markedly suppresses hyperoxia-stimulated phospho-p53(Ser15), p53, and p21(CIP1), and also restores the hyperoxia-reduced kinase activities of cyclin D1/E1-Cdks.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	60-67	P53	Homo sapiens	128-131
15212949-3	2004	Decreasing phospho-ERK with the pharmacological inhibitors, PD98059 and U0126, markedly suppresses hyperoxia-stimulated phospho-p53(Ser15), p53, and p21(CIP1), and also restores the hyperoxia-reduced kinase activities of cyclin D1/E1-Cdks.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	60-67	P53	Homo sapiens	140-143
15094782-3	2004	We have previously found that the kinase and mRNA synthesis inhibitor DRB (5,6-dichloro-1-b-D-ribofuranosylbenzimidazole) induces the nuclear accumulation of p53 without concomitant phosphorylation of the ser15 site of p53, which is thought to be a modification important for the attenuation of p53-MDM2 interaction.	Dichlororibofuranosylbenzimidazole	70-73	P53	Homo sapiens	158-161
15094782-3	2004	We have previously found that the kinase and mRNA synthesis inhibitor DRB (5,6-dichloro-1-b-D-ribofuranosylbenzimidazole) induces the nuclear accumulation of p53 without concomitant phosphorylation of the ser15 site of p53, which is thought to be a modification important for the attenuation of p53-MDM2 interaction.	Dichlororibofuranosylbenzimidazole	70-73	P53	Homo sapiens	219-222
15256442-8	2004	Ser(392) nonphosphorylated p53 was present in human breast tumors expressing mutant p53 including p53H175.	Serine	0-3	P53	Homo sapiens	84-87
15094782-3	2004	We have previously found that the kinase and mRNA synthesis inhibitor DRB (5,6-dichloro-1-b-D-ribofuranosylbenzimidazole) induces the nuclear accumulation of p53 without concomitant phosphorylation of the ser15 site of p53, which is thought to be a modification important for the attenuation of p53-MDM2 interaction.	Dichlororibofuranosylbenzimidazole	70-73	P53	Homo sapiens	219-222
15256442-9	2004	Together, these results demonstrated a novel function of Ser(392) phosphorylation in regulating the oncogenic function of mutant p53.	Serine	57-60	P53	Homo sapiens	129-132
15077171-4	2004	Abrogation of cyclin G enhances p53 accumulation and phosphorylation of p53 at the Ser-15 residue, resulting in cell cycle arrest.	Serine	83-86	P53	Homo sapiens	72-75
15172127-0	2004	p53 is an independent pre-treatment markers for long-term survival in stage II and III colorectal cancers: an analysis of interaction between genetic markers and fluorouracil-based adjuvant therapy.	Fluorouracil	162-174	P53	Homo sapiens	0-3
15237427-14	2004	CONCLUSION: Tanshinone II-A could inhibit the growth and proliferation of HCC cell effectively in vitro by apoptosis induction, which was associated with up-regulation of fas, p53, bax, expression and down-regulation of bcl-2 and c-myc.	tanshinone	12-27	P53	Homo sapiens	176-179
15077171-5	2004	Ectopically expressed cyclin G significantly reduces the steady-state levels of p53 as well as that of phosphorylated p53 at Ser-15 after DNA damage in normal human dermal fibroblasts containing normal ATM.	Serine	125-128	P53	Homo sapiens	118-121
15177184-5	2004	Purified ATM was phosphorylated on serine 1981 and was active towards a variety of known ATM substrates, including p53 and the Bloom Syndrome helicase, BLM.	Serine	35-41	P53	Homo sapiens	115-118
15248926-2	2004	The purpose of this study was to evaluate the relationship of the cisplatin sensitivity/prognosis with the expression of excision repair cross complement-1 (ERCC-1), metallothionein (MT), and p53 in the paraffin-embedded tissue of advanced non-small cell lung cancer (NSCLC).	Cisplatin	66-75	P53	Homo sapiens	192-195
15248906-1	2004	BACKGROUND &amp; OBJECTIVE: It was reported that the hepatitis B virus X could inhibit the function of p53 and have contrary effects on p21(WAF1), a downstream gene of p53, but the mechanism is not clear up to now.	Adenosine Monophosphate	12-15	P53	Homo sapiens	103-106
15248906-1	2004	BACKGROUND &amp; OBJECTIVE: It was reported that the hepatitis B virus X could inhibit the function of p53 and have contrary effects on p21(WAF1), a downstream gene of p53, but the mechanism is not clear up to now.	Adenosine Monophosphate	12-15	P53	Homo sapiens	168-171
15188005-0	2004	Oestrogen inhibits resveratrol-induced post-translational modification of p53 and apoptosis in breast cancer cells.	Resveratrol	19-30	P53	Homo sapiens	74-77
15188005-4	2004	E(2) inhibited resveratrol-stimulated phosphorylation of serines 15, 20 and 392 of p53 and acetylation of p53 in a concentration- and time-dependent manner.	Resveratrol	15-26	P53	Homo sapiens	83-86
15188005-4	2004	E(2) inhibited resveratrol-stimulated phosphorylation of serines 15, 20 and 392 of p53 and acetylation of p53 in a concentration- and time-dependent manner.	Resveratrol	15-26	P53	Homo sapiens	106-109
15188005-4	2004	E(2) inhibited resveratrol-stimulated phosphorylation of serines 15, 20 and 392 of p53 and acetylation of p53 in a concentration- and time-dependent manner.	Serine	57-64	P53	Homo sapiens	83-86
15188005-7	2004	Electrophoretic mobility studies of p53 binding to DNA and of p21 expression indicated that E(2) inhibited resveratrol-induced, p53-directed transcriptional activity.	Resveratrol	107-118	P53	Homo sapiens	36-39
15188005-7	2004	Electrophoretic mobility studies of p53 binding to DNA and of p21 expression indicated that E(2) inhibited resveratrol-induced, p53-directed transcriptional activity.	Resveratrol	107-118	P53	Homo sapiens	128-131
15248926-2	2004	The purpose of this study was to evaluate the relationship of the cisplatin sensitivity/prognosis with the expression of excision repair cross complement-1 (ERCC-1), metallothionein (MT), and p53 in the paraffin-embedded tissue of advanced non-small cell lung cancer (NSCLC).	Paraffin	203-211	P53	Homo sapiens	192-195
15230885-0	2004	Association of p53 arginine polymorphism with skin cancer.	Arginine	19-27	P53	Homo sapiens	15-18
14729588-6	2004	We applied LwPy53 to exons 5, 7 and 8 of p53 using benzo[a]pyrene diol epoxide (BPDE)-induced mutation data for supF to obtain a predicted BPDE G--&gt;T transversion spectrum after hypothetical treatment with BPDE.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	51-78	P53	Homo sapiens	41-44
14729588-6	2004	We applied LwPy53 to exons 5, 7 and 8 of p53 using benzo[a]pyrene diol epoxide (BPDE)-induced mutation data for supF to obtain a predicted BPDE G--&gt;T transversion spectrum after hypothetical treatment with BPDE.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	80-84	P53	Homo sapiens	41-44
14729588-6	2004	We applied LwPy53 to exons 5, 7 and 8 of p53 using benzo[a]pyrene diol epoxide (BPDE)-induced mutation data for supF to obtain a predicted BPDE G--&gt;T transversion spectrum after hypothetical treatment with BPDE.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	139-143	P53	Homo sapiens	41-44
15257943-1	2004	A single nucleotide polymorphism at TP53 codon 72 means that two alleles exist: A1 (proline residue, Pro72) and A2 (arginine residue, Arg72).	Arginine	116-124	P53	Homo sapiens	36-40
15221786-4	2004	The type of TP53 sequence variant (transition A:T&gt;G:C vs. G:C&gt;A:T at CpG dinucleotides, and transversion G:C&gt;T:A) had significant correlation with patients" age (P=0.04) with more A:T&gt;G:C in patients over 60 years old.	cytidylyl-3'-5'-guanosine	75-92	P53	Homo sapiens	12-16
15202011-7	2004	In addition, the synthetic bile acid derivatives markedly induced the level of Cdk inhibitor, p21WAF1/CIP1, in a p53-independent manner.	Bile Acids and Salts	27-36	P53	Homo sapiens	113-116
15230885-1	2004	BACKGROUND: The presence of arginine at codon 72 in p53 protein is proposed to be a genetic risk factor in human papillomavirus (HPV)-related carcinogenesis.	Arginine	28-36	P53	Homo sapiens	52-55
15230885-4	2004	RESULTS: All EV patients with the malignant form of EV were homozygous for arginine (Arg/Arg) at codon 72 of the p53 gene, in contrast to none with the benign form (P &lt; 0.0001).	Arginine	75-83	P53	Homo sapiens	113-116
15230885-4	2004	RESULTS: All EV patients with the malignant form of EV were homozygous for arginine (Arg/Arg) at codon 72 of the p53 gene, in contrast to none with the benign form (P &lt; 0.0001).	Arginine	85-88	P53	Homo sapiens	113-116
15230885-4	2004	RESULTS: All EV patients with the malignant form of EV were homozygous for arginine (Arg/Arg) at codon 72 of the p53 gene, in contrast to none with the benign form (P &lt; 0.0001).	Arginine	89-92	P53	Homo sapiens	113-116
15230885-5	2004	CONCLUSIONS: p53 arginine polymorphism is likely to be associated with the development of skin malignancies in EV patients from Brazil.	Arginine	17-25	P53	Homo sapiens	13-16
15213307-2	2004	We found that methioninase-activated MSC potentiates 7-ethyl-10-hydroxycamptothecin (SN-38)-induced cell lethality in vitro in the p53-defective human head and neck carcinoma A253 cells.	Irinotecan	53-83	P53	Homo sapiens	131-134
15213307-2	2004	We found that methioninase-activated MSC potentiates 7-ethyl-10-hydroxycamptothecin (SN-38)-induced cell lethality in vitro in the p53-defective human head and neck carcinoma A253 cells.	Irinotecan	85-90	P53	Homo sapiens	131-134
15102862-7	2004	Our results demonstrate that NF-kappaB plays an essential role in activation of wild-type p53 tumor suppressor to initiate proapoptotic signaling in response to overgeneration of superoxide.	Superoxides	179-189	P53	Homo sapiens	90-93
15252149-0	2004	Selenite-induced p53 Ser-15 phosphorylation and caspase-mediated apoptosis in LNCaP human prostate cancer cells.	Serine	21-24	P53	Homo sapiens	17-20
15252149-6	2004	Selenite treatment led to a significant increase in p53 phosphorylation on Ser-15 (Ser15P).	Serine	75-78	P53	Homo sapiens	52-55
15222051-1	2004	AIM: To observe the reversal effects of wide-type p53 gene on multi-drug resistance to 5-FU (LOVO/5-FU).	Fluorouracil	87-91	P53	Homo sapiens	50-53
15222051-1	2004	AIM: To observe the reversal effects of wide-type p53 gene on multi-drug resistance to 5-FU (LOVO/5-FU).	Fluorouracil	98-102	P53	Homo sapiens	50-53
15222051-2	2004	METHODS: After treatment with Ad-p53, LOVO/5-FU sensitivity to 5-Fu was investigated using tetrazolium dye assay.	Fluorouracil	63-67	P53	Homo sapiens	33-36
15096505-3	2004	We have demonstrated that DNA damage by doxorubicin and cisplatin caused a steady elevation of the R2 protein in p53(-/-) HCT-116 human colon carcinoma cells but induced degradation of the protein in p53(+/+) cells.	Doxorubicin	40-51	P53	Homo sapiens	113-116
15096505-3	2004	We have demonstrated that DNA damage by doxorubicin and cisplatin caused a steady elevation of the R2 protein in p53(-/-) HCT-116 human colon carcinoma cells but induced degradation of the protein in p53(+/+) cells.	Doxorubicin	40-51	P53	Homo sapiens	200-203
15096505-3	2004	We have demonstrated that DNA damage by doxorubicin and cisplatin caused a steady elevation of the R2 protein in p53(-/-) HCT-116 human colon carcinoma cells but induced degradation of the protein in p53(+/+) cells.	Cisplatin	56-65	P53	Homo sapiens	113-116
15096505-3	2004	We have demonstrated that DNA damage by doxorubicin and cisplatin caused a steady elevation of the R2 protein in p53(-/-) HCT-116 human colon carcinoma cells but induced degradation of the protein in p53(+/+) cells.	Cisplatin	56-65	P53	Homo sapiens	200-203
15226429-3	2004	CDK2 inhibition triggers a p53-p21 response via ATM- and ATR-dependent p53 phosphorylation at serine 15.	Serine	94-100	P53	Homo sapiens	27-30
15226429-3	2004	CDK2 inhibition triggers a p53-p21 response via ATM- and ATR-dependent p53 phosphorylation at serine 15.	Serine	94-100	P53	Homo sapiens	71-74
15226436-5	2004	However, IR-activated, ATM-mediated phosphorylation of p53 at serine 15 (human) or 18 (mouse) [Ser15(h)/18(m)], and apoptosis occurred in myoblasts but was impaired in myotubes.	Serine	62-68	P53	Homo sapiens	55-58
15242600-4	2004	However, three loops, involved in DNA and Zn binding in human p53, contain small alpha helices in Cep-1.	Zinc	42-44	P53	Homo sapiens	62-65
15242600-5	2004	The alpha helix in loop L3 of Cep-1 orients the side chains of two conserved arginines toward DNA; in human p53, both arginines are mutation hotspots, but only one contacts DNA.	Arginine	118-127	P53	Homo sapiens	108-111
15102862-3	2004	In this report, we show that doxycycline increased superoxide generation and subsequently activated NF-kappaB, which in turn up-regulated p53 expression and increased the stability and DNA binding activity of p53.	Superoxides	51-61	P53	Homo sapiens	138-141
15102862-3	2004	In this report, we show that doxycycline increased superoxide generation and subsequently activated NF-kappaB, which in turn up-regulated p53 expression and increased the stability and DNA binding activity of p53.	Superoxides	51-61	P53	Homo sapiens	209-212
15140517-1	2004	OBJECTIVE: To test the hypothesis that p53 homozygous Arg/Arg genotype at codon 72 is a significant risk factor for the development of HPV induced cervical cancer.	Arginine	54-57	P53	Homo sapiens	39-42
15159015-4	2004	Furthermore, combined administrations of insulin and paclitaxel affected MAPK pathway, Raf-1 activation and p53 expression levels.	Paclitaxel	53-63	P53	Homo sapiens	108-111
15095302-0	2004	Ser-249TP53 mutation in tumour and plasma DNA of hepatocellular carcinoma patients from a high incidence area in the Gambia, West Africa.	Serine	0-3	P53	Homo sapiens	7-11
15095302-2	2004	A selective mutation in TP53 (AGG--&gt;AGT at codon 249, Arg--&gt;Ser) has been identified as a hotspot in HCCs from such areas, reflecting DNA damage caused by aflatoxin metabolites.	Arginine	57-60	P53	Homo sapiens	24-28
15095302-2	2004	A selective mutation in TP53 (AGG--&gt;AGT at codon 249, Arg--&gt;Ser) has been identified as a hotspot in HCCs from such areas, reflecting DNA damage caused by aflatoxin metabolites.	Serine	66-69	P53	Homo sapiens	24-28
15140517-1	2004	OBJECTIVE: To test the hypothesis that p53 homozygous Arg/Arg genotype at codon 72 is a significant risk factor for the development of HPV induced cervical cancer.	Arginine	58-61	P53	Homo sapiens	39-42
15178317-0	2004	Protein phosphatase 1, but not protein phosphatase 2A, dephosphorylates DNA-damaging stress-induced phospho-serine 15 of p53.	Serine	108-114	P53	Homo sapiens	121-124
15178764-0	2004	Hypoxic inducible factor 1alpha, extracellular signal-regulated kinase, and p53 are regulated by distinct threshold concentrations of nitric oxide.	Nitric Oxide	134-146	P53	Homo sapiens	76-79
15178764-5	2004	Hypoxic inducible factor 1alpha (HIF-1alpha) accumulation was associated with an intermediate amount of NO (&gt;100 nM), whereas p53 serine 15 phosphorylation occurred at considerably higher levels (&gt;300 nM).	Serine	133-139	P53	Homo sapiens	129-132
15178764-7	2004	HIF-1alpha stabilization paralleled the presence of NO, whereas p53 serine 15 phosphorylation was detected during, and persisted after, NO exposure.	Serine	68-74	P53	Homo sapiens	64-67
15054096-3	2004	DOX-mediated cardiomyopathy is linked to its ability to induce apoptosis in endothelial cells and cardiomyocytes by activation of p53 protein and reactive oxygen species.	Doxorubicin	0-3	P53	Homo sapiens	130-133
15054096-4	2004	We evaluated the potential roles of H(2)O(2) and p53 in DOX-induced apoptosis in normal bovine aortic endothelial cells and adult rat cardiomyocytes and in tumor cell lines PA-1 (human ovarian teratocarcinoma) and MCF-7 (human breast adenocarcinoma).	Doxorubicin	56-59	P53	Homo sapiens	49-52
15054096-6	2004	In contrast, DOX caused early activation of p53 in tumor cells that was followed by caspase-3 activation and DNA fragmentation.	Doxorubicin	13-16	P53	Homo sapiens	44-47
15054096-7	2004	These findings suggest that the transcriptional activation of p53 in DOX-induced apoptosis in endothelial cells may not be as crucial as it is in tumor cells.	Doxorubicin	69-72	P53	Homo sapiens	62-65
15054096-9	2004	Pifithrin-alpha completely suppressed DOX-induced activation of p53 in both normal and tumor cell lines and prevented apoptosis in tumor cell lines but not in endothelial cells and cardiomyocytes.	Doxorubicin	38-41	P53	Homo sapiens	64-67
15175154-3	2004	Both ATM and hSMG-1 phosphorylate Ser/Thr-Gln-containing target sequences in the checkpoint protein p53 and the nonsense-mediated mRNA decay (NMD) protein hUpf1.	Serine	34-37	P53	Homo sapiens	100-103
15175154-3	2004	Both ATM and hSMG-1 phosphorylate Ser/Thr-Gln-containing target sequences in the checkpoint protein p53 and the nonsense-mediated mRNA decay (NMD) protein hUpf1.	Threonine	38-41	P53	Homo sapiens	100-103
15150572-6	2004	In particular, we found that CA-Akt-expressing cells displayed increased expression of the antiapoptotic Bcl-2 family member protein Bcl-x(l), and a delayed onset of the p53 pathway after treatment with cisplatin or Mitoxantrone.	Cisplatin	203-212	P53	Homo sapiens	170-173
15024021-4	2004	During the cisplatin-induced apoptosis in human neuroblastoma SH-SY5Y cells, the expression level of Plk1 was significantly decreased both at mRNA and protein levels, whereas cisplatin treatment caused a remarkable stabilization of p53.	Cisplatin	11-20	P53	Homo sapiens	232-235
15024021-4	2004	During the cisplatin-induced apoptosis in human neuroblastoma SH-SY5Y cells, the expression level of Plk1 was significantly decreased both at mRNA and protein levels, whereas cisplatin treatment caused a remarkable stabilization of p53.	Cisplatin	175-184	P53	Homo sapiens	232-235
15145520-1	2004	We have previously shown that oligonucleotides designed to bind in triplex fashion to a specific p53 binding site homology inhibit the proliferation of colon cancer cells in vitro.	Oligonucleotides	30-46	P53	Homo sapiens	97-100
15135642-0	2004	Mutational biases associated with potential iron-binding DNA motifs in rodent lacI and human p53 mutational databases.	Iron	44-48	P53	Homo sapiens	93-96
15178317-2	2004	We investigated whether the inhibition of PP1 by OA promotes the phosphorylation of the serine 15 of p53.	Serine	88-94	P53	Homo sapiens	101-104
15178317-5	2004	This report provides the first evidence that PP1, but not PP2A, dephosphorylates phospho-serine 15 of p53.	Serine	89-95	P53	Homo sapiens	102-105
14742318-8	2004	Our data were consistent with increased likelihood of tumors with p53 mutations for premenopausal breast cancer with increased alcohol intake 10 or 20 years previous; for intake of 16 or more drinks per month in the period 20 years before the interview compared with non-drinkers, the OR was 5.25, 95% CI 1.48-18.58.	Alcohols	127-134	P53	Homo sapiens	66-69
14742318-0	2004	Diet and alcohol consumption in relation to p53 mutations in breast tumors.	Alcohols	9-16	P53	Homo sapiens	44-47
15191663-1	2004	BACKGROUND &amp; OBJECTIVE: Recent studies have shown that wild-type p53 gene can enhance the chemosensitivity of the majority of non-small cell lung cancers.	Adenosine Monophosphate	12-15	P53	Homo sapiens	69-72
14742318-9	2004	For postmenopausal women, there was increased likelihood of tumors with p53 mutations among women with higher folate.	Folic Acid	110-116	P53	Homo sapiens	72-75
14742318-12	2004	For premenopausal women, alcohol consumption in the past was associated with p53 mutations.	Alcohols	25-32	P53	Homo sapiens	77-80
15179184-4	2004	Curcumin induced melanoma cell apoptosis and cell cycle arrest, which is associated with the downregulation of NFkappaB activation, iNOS and DNA-dependent protein kinase catalytic subunit expression, and upregulation of p53, p21(Cip1), p27(Kip1) and checkpoint kinase 2.	Curcumin	0-8	P53	Homo sapiens	220-223
15145278-1	2004	OBJECTIVES: Although some studies have reported that the arginine isoform on codon 72 of p53 increases the susceptibility to invasive cervical cancer, such data remain controversial.	Arginine	57-65	P53	Homo sapiens	89-92
15179185-4	2004	The effect on p53 was not a direct result of inhibition of extracellular signal-regulated kinase-1/2 (ERK1/2) activation by TSA, as treatment of the cells with the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase-1 (MEK1) inhibitor PD98059 did not result in decreased p53 protein level.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	261-268	P53	Homo sapiens	14-17
15138567-13	2004	In this pilot study with a limited number of patients to evaluate the predictive value of p53 mutations for an anthracycline/taxane combination therapy in the neoadjuvant setting, stable disease was observed more often in patients with wild-type p53 but statistical significance was not quite reached for this clear trend.	Anthracyclines	111-124	P53	Homo sapiens	90-93
15269478-6	2004	MATERIALS AND METHODS: p53 protein expression was evaluated on formalin-fixed paraffin-embedded sections using streptavidin biotin immunoperoxidase technique after high temperature antigen retrieval.	Paraffin	78-86	P53	Homo sapiens	23-26
14967811-9	2004	However, cells overexpressing anterior gradient-2 attenuate p53 phosphorylation at both Ser(15) and Ser(392) and silence p53 transactivation function in ultraviolet (UV)-damaged cells.	Serine	88-91	P53	Homo sapiens	60-63
14967811-9	2004	However, cells overexpressing anterior gradient-2 attenuate p53 phosphorylation at both Ser(15) and Ser(392) and silence p53 transactivation function in ultraviolet (UV)-damaged cells.	Serine	100-103	P53	Homo sapiens	60-63
15138567-13	2004	In this pilot study with a limited number of patients to evaluate the predictive value of p53 mutations for an anthracycline/taxane combination therapy in the neoadjuvant setting, stable disease was observed more often in patients with wild-type p53 but statistical significance was not quite reached for this clear trend.	taxane	125-131	P53	Homo sapiens	90-93
15064747-6	2004	By using cDNA arrays to examine global p53-dependent gene expression in response to adriamycin or p14ARF, we found that most genes were regulated similarly by the two treatments.	Doxorubicin	84-94	P53	Homo sapiens	39-42
15161352-1	2004	The accumulation of the cell cycle regulators TP53 and CDKN1A (p21/CIP1/WAF1) was investigated after exposure to X rays and carbon ions (170 keV microm(-1)) and xenon, bismuth and uranium ions (8900-15,000 keV microm(-1)) in normal human fibroblasts.	Carbon	124-130	P53	Homo sapiens	46-50
15161352-1	2004	The accumulation of the cell cycle regulators TP53 and CDKN1A (p21/CIP1/WAF1) was investigated after exposure to X rays and carbon ions (170 keV microm(-1)) and xenon, bismuth and uranium ions (8900-15,000 keV microm(-1)) in normal human fibroblasts.	Uranium	180-187	P53	Homo sapiens	46-50
15142674-8	2004	A decrease in expression of p53, bcl-2, and bcl-X(L) was observed after 12 h exposure of 40 microM curcumin.	Curcumin	99-107	P53	Homo sapiens	28-31
15064747-7	2004	However, a subset of p53-regulated genes whose products have proliferative roles or regulate VEGF activity, newly described here, are repressed by p14ARF much more than by adriamycin.	Doxorubicin	172-182	P53	Homo sapiens	21-24
15064747-2	2004	In human U2OS cells, treatment with adriamycin causes p53 to be phosphorylated on all six serine residues tested, leading to the dissociation of p53 from MDM2 and transcription of the p21 and mdm2 genes.	Doxorubicin	36-46	P53	Homo sapiens	54-57
15064747-2	2004	In human U2OS cells, treatment with adriamycin causes p53 to be phosphorylated on all six serine residues tested, leading to the dissociation of p53 from MDM2 and transcription of the p21 and mdm2 genes.	Doxorubicin	36-46	P53	Homo sapiens	145-148
15064747-8	2004	We conclude that the phosphorylation of p53 on N-terminal serine residues is not required for increased transcription of the great majority of p53-responsive genes and that the induction of p53 by p14ARF, with little phosphorylation, leads to substantial repression of genes whose products have roles in proliferation.	Serine	58-64	P53	Homo sapiens	40-43
15064747-2	2004	In human U2OS cells, treatment with adriamycin causes p53 to be phosphorylated on all six serine residues tested, leading to the dissociation of p53 from MDM2 and transcription of the p21 and mdm2 genes.	Serine	90-96	P53	Homo sapiens	54-57
15138488-9	2004	TPA (10(-12)-10(-8) mol l(-1)) treatment of LNCaP cells caused their growth inhibition, cell cycle arrest, upregulation of p53 and p21waf1, and induction of apoptosis.	Tetradecanoylphorbol Acetate	0-3	P53	Homo sapiens	123-126
15161716-8	2004	Inactivation of p53 in MCF-7 and HCT116 cell lines blocked 5-FU- and antifolate-mediated up-regulation of Fas.	Fluorouracil	59-63	P53	Homo sapiens	16-19
15161716-10	2004	Lack of Fas up-regulation in the p53-null and -mutant lines abolished the synergistic interaction between 5-FU and CH-11.	Fluorouracil	106-110	P53	Homo sapiens	33-36
15140256-14	2004	In addition, curcumin affected expression of metallothionein genes, tubulin genes, p53 and other genes involved in colon carcinogenesis.	Curcumin	13-21	P53	Homo sapiens	83-86
15161705-0	2004	Rapid and sensitive p53 alteration analysis in biopsies from lung cancer patients using a functional assay and a universal oligonucleotide array: a prospective study.	Oligonucleotides	123-138	P53	Homo sapiens	20-23
15105048-3	2004	The p53 gene displays a common genetic Arg/Pro polymorphism at codon 72 with functional significance, that has been investigated as risk factor in several cancer models.	Arginine	39-42	P53	Homo sapiens	4-7
15016801-2	2004	To this end, we assessed the transcriptional response of HCT116 colorectal cancer cells during apoptosis induced by the anticancer drug 5-fluorouracil as the function of p53 status, and we identified 230 potential targets that are regulated by p53.	Fluorouracil	136-150	P53	Homo sapiens	170-173
15016801-2	2004	To this end, we assessed the transcriptional response of HCT116 colorectal cancer cells during apoptosis induced by the anticancer drug 5-fluorouracil as the function of p53 status, and we identified 230 potential targets that are regulated by p53.	Fluorouracil	136-150	P53	Homo sapiens	244-247
15016801-4	2004	Strikingly, we found that p53 regulates gene expression primarily through transcriptional repression (n = 189) rather than activation (n = 41), and selective blockade of p53-dependent gene repression resulted in the reduction in 5-fluorouracil-induced apoptosis.	Fluorouracil	229-243	P53	Homo sapiens	26-29
15016801-4	2004	Strikingly, we found that p53 regulates gene expression primarily through transcriptional repression (n = 189) rather than activation (n = 41), and selective blockade of p53-dependent gene repression resulted in the reduction in 5-fluorouracil-induced apoptosis.	Fluorouracil	229-243	P53	Homo sapiens	170-173
15081425-6	2004	Overexpression of RFT caused G1-S arrest and upregulated both the phosphorylation of p53 at Ser-15 and the expression level of p21(Waf1).	Serine	92-95	P53	Homo sapiens	85-88
15142443-1	2004	BACKGROUND &amp; OBJECTIVE: A p53 response element like binding sequence, 5"-TGCC(G)T-TGCCT-3" was found at upstream of hepatitis B virus (HBV) enhancer I from 1047 to 1059 nucleotides after analyzing the HBV genome by a computer program in our previous work.	Adenosine Monophosphate	12-15	P53	Homo sapiens	30-33
18969416-1	2004	In combination with abasic site (AP site)-containing oligodeoxynucleotides (ODNs), we demonstrate potential use of a hydrogen bond forming ligand, 2-amino-7-methyl-1,8-naphthyridine (AMND), for the fluorescence detection of the cytosine (C)/guanine (G) mutation sequence of the cancer repression gene p53.	Hydrogen	117-125	P53	Homo sapiens	301-304
15274301-3	2004	The main dietary form is selenomethionine, which we showed modulated p53 activity by causing redox regulation of key p53 cysteine residues.	Cysteine	121-129	P53	Homo sapiens	69-72
15163458-11	2004	CONCLUSIONS: This study provides evidence that redox-active (Fe2+), (Mn2+), (Cu2+), and (Zn2+) ion-induced apoptosis in PBL by (H2O2)/(.OH) generation, resulting in mitochondria depolarization, caspase-3 activation, and nuclear fragmentation independent of NF-kappaB and p53 transcription factors activation.	Zinc	89-93	P53	Homo sapiens	271-274
15163458-11	2004	CONCLUSIONS: This study provides evidence that redox-active (Fe2+), (Mn2+), (Cu2+), and (Zn2+) ion-induced apoptosis in PBL by (H2O2)/(.OH) generation, resulting in mitochondria depolarization, caspase-3 activation, and nuclear fragmentation independent of NF-kappaB and p53 transcription factors activation.	Hydrogen Peroxide	128-132	P53	Homo sapiens	271-274
15258465-6	2004	In addition, inhibition of the mitochondrial permeability transition pores by cyclosporine A significantly reduced the Delta Psi m loss and the sub-G1 DNA content in p53 positive cells.	Cyclosporine	78-92	P53	Homo sapiens	166-169
15274301-3	2004	The main dietary form is selenomethionine, which we showed modulated p53 activity by causing redox regulation of key p53 cysteine residues.	Cysteine	121-129	P53	Homo sapiens	117-120
15274301-8	2004	Methyl-seleninic acid caused phosphorylation of one or more p53 threonine residues, but did not affect any known serine phosphorylation sites.	methylselenic acid	0-21	P53	Homo sapiens	60-63
15274301-8	2004	Methyl-seleninic acid caused phosphorylation of one or more p53 threonine residues, but did not affect any known serine phosphorylation sites.	Threonine	64-73	P53	Homo sapiens	60-63
15274301-9	2004	By contrast sodium selenite caused phosphorylation of p53 serines 20, 37 and 46 known to mediate apoptosis.	Serine	58-65	P53	Homo sapiens	54-57
15081873-4	2004	Similarly, the cell-permeable SN50 peptide, which is known to block NF-kappaB nuclear translocation, prevented both H(2)O(2)-induced p53 expression and apoptosis.	Hydrogen Peroxide	116-124	P53	Homo sapiens	133-136
15124184-6	2004	We found high expression of p53 during activation-induced cell death of TJK cells mediated by anti-CD8 antibody and apoptosis of TJK and T3JK induced by 5-FU, implicating p53 involvement in apoptosis of leukemia cells induced by anti-CD8 antibody and 5-FU.	Fluorouracil	153-157	P53	Homo sapiens	171-174
15126337-0	2004	Apoptotic signaling pathways induced by nitric oxide in human lymphoblastoid cells expressing wild-type or mutant p53.	Nitric Oxide	40-52	P53	Homo sapiens	114-117
15107622-5	2004	This process requires the phosphorylation of p53 at serine 315 and serine 376, which is mediated by the activation of glycogen synthase kinase-3beta (GSK-3beta).	Serine	52-58	P53	Homo sapiens	45-48
15124184-6	2004	We found high expression of p53 during activation-induced cell death of TJK cells mediated by anti-CD8 antibody and apoptosis of TJK and T3JK induced by 5-FU, implicating p53 involvement in apoptosis of leukemia cells induced by anti-CD8 antibody and 5-FU.	Fluorouracil	251-255	P53	Homo sapiens	28-31
15124184-6	2004	We found high expression of p53 during activation-induced cell death of TJK cells mediated by anti-CD8 antibody and apoptosis of TJK and T3JK induced by 5-FU, implicating p53 involvement in apoptosis of leukemia cells induced by anti-CD8 antibody and 5-FU.	Fluorouracil	251-255	P53	Homo sapiens	171-174
15124184-8	2004	Our results showed that combined treatment with 5-FU and anti-CD8 antibody could enhance the rate of apoptosis induced by 5-FU or anti-CD8 antibody through increased expression of p53 and by promoting activation of caspase-3 and Bid.	Fluorouracil	48-52	P53	Homo sapiens	180-183
15124184-8	2004	Our results showed that combined treatment with 5-FU and anti-CD8 antibody could enhance the rate of apoptosis induced by 5-FU or anti-CD8 antibody through increased expression of p53 and by promoting activation of caspase-3 and Bid.	Fluorouracil	122-126	P53	Homo sapiens	180-183
15143945-6	2004	MKN45 that has wild-type p53 showed severe inhibition by irinotecan compared with MKN28, which has mutated p53.	Irinotecan	57-67	P53	Homo sapiens	25-28
15099948-3	2004	Demonstration of p53 polymorphism was performed in DNA extracted from paraffin-embedded sections using the polymerase chain reaction (PCR).	Paraffin	70-78	P53	Homo sapiens	17-20
15099969-2	2004	In this regard, genetic polymorphism at codon 72 (CCC/proline to CGC/arginine [Pro(72)Arg]) of the p53 gene is one of the most frequently studied subjects.	Chlormequat	50-53	P53	Homo sapiens	99-102
15099969-2	2004	In this regard, genetic polymorphism at codon 72 (CCC/proline to CGC/arginine [Pro(72)Arg]) of the p53 gene is one of the most frequently studied subjects.	Arginine	69-77	P53	Homo sapiens	99-102
15099969-3	2004	An association between endometrial cancer and the polymorphism at codon 31 (AGC/serine to AGA/arginine [Ser(31)Arg]) of the p21 gene, which is known to be a downstream mediator of p53, has also been reported.	Serine	80-86	P53	Homo sapiens	180-183
15099969-3	2004	An association between endometrial cancer and the polymorphism at codon 31 (AGC/serine to AGA/arginine [Ser(31)Arg]) of the p21 gene, which is known to be a downstream mediator of p53, has also been reported.	Arginine	94-102	P53	Homo sapiens	180-183
15216398-9	2004	The frequency of pro/pro, pro/arg, and arg/arg in p53 codon 72 in cases was 15% (15/99), 58% (57/99), and 27% (27/99) and in controls was 17% (34/193), 48% (92/193), and 35% (67/193), respectively, which was not significantly different.	Arginine	30-33	P53	Homo sapiens	50-53
15140868-5	2004	17beta-Estradiol up-regulates epidermal growth factor (EGF) receptor, but down-regulates p53 protein in leiomyoma cells, whereas progesterone augments EGF and Bcl-2 protein, but inhibits insulin-like growth factor (IGF-I) and tumour necrosis factor (TNFalpha).	Estradiol	0-16	P53	Homo sapiens	89-92
15216398-9	2004	The frequency of pro/pro, pro/arg, and arg/arg in p53 codon 72 in cases was 15% (15/99), 58% (57/99), and 27% (27/99) and in controls was 17% (34/193), 48% (92/193), and 35% (67/193), respectively, which was not significantly different.	Arginine	39-42	P53	Homo sapiens	50-53
15216398-9	2004	The frequency of pro/pro, pro/arg, and arg/arg in p53 codon 72 in cases was 15% (15/99), 58% (57/99), and 27% (27/99) and in controls was 17% (34/193), 48% (92/193), and 35% (67/193), respectively, which was not significantly different.	Arginine	39-42	P53	Homo sapiens	50-53
15069555-2	2004	The p53 codon 72 Arg right curved arrow Pro polymorphism has been suggested to be associated with risk for different kind of cancers, but the data on gastric cancer (GC) is very limited.	Arginine	17-20	P53	Homo sapiens	4-7
15141020-4	2004	Adriamycin promotes the G(1) checkpoint through activation of the p53-p21(CIP1/WAF1) pathway and decrease of pRb phosphorylation.	Doxorubicin	0-10	P53	Homo sapiens	66-69
15141020-5	2004	Phosphorylation of p53(Ser20) after Adriamycin treatment is ATM dependent, but is not required for the full activation of p53.	Doxorubicin	36-46	P53	Homo sapiens	19-22
15153330-7	2004	PCAF induction by p53 activity was further demonstrated in wild-type p53 MCF10A cells when PCAF expression was induced following activation of endogenous wild-type p53 with doxorubicin in a dose- and time-dependent manner.	Doxorubicin	173-184	P53	Homo sapiens	18-21
15153330-7	2004	PCAF induction by p53 activity was further demonstrated in wild-type p53 MCF10A cells when PCAF expression was induced following activation of endogenous wild-type p53 with doxorubicin in a dose- and time-dependent manner.	Doxorubicin	173-184	P53	Homo sapiens	69-72
15153330-7	2004	PCAF induction by p53 activity was further demonstrated in wild-type p53 MCF10A cells when PCAF expression was induced following activation of endogenous wild-type p53 with doxorubicin in a dose- and time-dependent manner.	Doxorubicin	173-184	P53	Homo sapiens	69-72
15153330-8	2004	Furthermore, the doxorubicin-induced increase in PCAF expression was blocked by pretreatment of the MCF10A cells with siRNA (small interfering RNA) targeted against p53 mRNA.	Doxorubicin	17-28	P53	Homo sapiens	165-168
15069555-7	2004	While the results suggest that the p53 codon 72 polymorphism may contribute to gastric cancer susceptibility, further larger studies are needed to substantiate our findings and to explore a possible interaction between p53 codon 72 polymorphism and alcohol in the etiology of gastric cancer.	Alcohols	249-256	P53	Homo sapiens	35-38
15069555-5	2004	The frequency of the p53 Arg allele was 57.4% in the cases and 54.9% in the controls, and the genotype frequencies of p53 Arg/Arg, Arg/Pro, and Pro/Pro were 29.6%, 55.6%, and 14.8%, respectively, in the cases, and 29.6%, 50.5%, and 19.9%, respectively, in the controls (p=0.207).	Arginine	25-28	P53	Homo sapiens	21-24
15069555-5	2004	The frequency of the p53 Arg allele was 57.4% in the cases and 54.9% in the controls, and the genotype frequencies of p53 Arg/Arg, Arg/Pro, and Pro/Pro were 29.6%, 55.6%, and 14.8%, respectively, in the cases, and 29.6%, 50.5%, and 19.9%, respectively, in the controls (p=0.207).	Arginine	122-125	P53	Homo sapiens	118-121
15069555-5	2004	The frequency of the p53 Arg allele was 57.4% in the cases and 54.9% in the controls, and the genotype frequencies of p53 Arg/Arg, Arg/Pro, and Pro/Pro were 29.6%, 55.6%, and 14.8%, respectively, in the cases, and 29.6%, 50.5%, and 19.9%, respectively, in the controls (p=0.207).	Arginine	122-125	P53	Homo sapiens	118-121
15069555-5	2004	The frequency of the p53 Arg allele was 57.4% in the cases and 54.9% in the controls, and the genotype frequencies of p53 Arg/Arg, Arg/Pro, and Pro/Pro were 29.6%, 55.6%, and 14.8%, respectively, in the cases, and 29.6%, 50.5%, and 19.9%, respectively, in the controls (p=0.207).	Arginine	122-125	P53	Homo sapiens	118-121
15116093-1	2004	We recently reported that exposure of human cervical carcinoma cells to doxorubicin results in extracellular signal-regulated kinase (ERK)2 activation, which in turn phosphorylates p53 on a previously uncharacterized site, Thr55.	Doxorubicin	72-83	P53	Homo sapiens	181-184
15072824-8	2004	The high formation of BPDE-N(2)-dG adducts in bronchial epithelial cells and investigations showing that the profile of mutations induced by BPDE in these cells is similar to that seen in the p53 gene isolated from human lung tumors implicates benzo[a]pyrene as important carcinogen in tobacco-induced lung cancer in human beings.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	22-26	P53	Homo sapiens	192-195
15116093-0	2004	Phosphorylation of p53 on Thr55 by ERK2 is necessary for doxorubicin-induced p53 activation and cell death.	Doxorubicin	57-68	P53	Homo sapiens	19-22
15116093-3	2004	In breast carcinoma MCF7 cells, doxorubicin (300 nM) activated ERK2 and induced phosphorylation of p53 on Thr55 residues.	Doxorubicin	32-43	P53	Homo sapiens	99-102
15116093-0	2004	Phosphorylation of p53 on Thr55 by ERK2 is necessary for doxorubicin-induced p53 activation and cell death.	Doxorubicin	57-68	P53	Homo sapiens	77-80
15116093-4	2004	Pretreatment of MCF7 cells with an ERK2 chemical inhibitor, PD98059 or U0126, blocked doxorubicin-induced p53 activation and suppressed phosphorylation of p53Thr55.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	60-67	P53	Homo sapiens	106-109
15116093-4	2004	Pretreatment of MCF7 cells with an ERK2 chemical inhibitor, PD98059 or U0126, blocked doxorubicin-induced p53 activation and suppressed phosphorylation of p53Thr55.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	60-67	P53	Homo sapiens	155-158
15116093-4	2004	Pretreatment of MCF7 cells with an ERK2 chemical inhibitor, PD98059 or U0126, blocked doxorubicin-induced p53 activation and suppressed phosphorylation of p53Thr55.	Doxorubicin	86-97	P53	Homo sapiens	106-109
15116093-5	2004	MCF55a cells were established by transfection of full-length p53 carrying Thr55 mutation (Thr to Ala) into MCF7 cells.	Threonine	74-77	P53	Homo sapiens	61-64
15116093-5	2004	MCF55a cells were established by transfection of full-length p53 carrying Thr55 mutation (Thr to Ala) into MCF7 cells.	Alanine	97-100	P53	Homo sapiens	61-64
15116093-9	2004	In summary, our results suggest that phosphorylation of p53Thr55 by ERK2 is important for doxorubicin-induced p53 activation and cell death.	Doxorubicin	90-101	P53	Homo sapiens	56-59
15116093-9	2004	In summary, our results suggest that phosphorylation of p53Thr55 by ERK2 is important for doxorubicin-induced p53 activation and cell death.	Doxorubicin	90-101	P53	Homo sapiens	110-113
14764594-11	2004	Therefore, Bcl-x(L) and E1B-19K inhibit p53-induced senescence by preventing ROS generation, which in turn leads to the activation of p38 kinase.	Reactive Oxygen Species	77-80	P53	Homo sapiens	40-43
14764594-0	2004	Bcl-xL and E1B-19K proteins inhibit p53-induced irreversible growth arrest and senescence by preventing reactive oxygen species-dependent p38 activation.	Reactive Oxygen Species	104-127	P53	Homo sapiens	36-39
14764594-4	2004	First, we found that that ROS are increased during p53-induced senescence.	Reactive Oxygen Species	26-29	P53	Homo sapiens	51-54
14764594-5	2004	Moreover, Bcl-x(L) and E1B-19K inhibit this p53-induced ROS generation.	Reactive Oxygen Species	56-59	P53	Homo sapiens	44-47
15087501-4	2004	Using colon carcinoma cells that express a temperature-sensitive variant of p53 and undergo p53-dependent apoptosis after UV irradiation, we found that the number of p53-induced genes identified by oligonucleotide microarray analysis decreased in a UV dose-dependent manner.	Oligonucleotides	198-213	P53	Homo sapiens	76-79
14764594-6	2004	Second, antioxidants prevent the induction of senescence and ROS by p53, but not the persistence of the senescence phenotype.	Reactive Oxygen Species	61-64	P53	Homo sapiens	68-71
15087501-4	2004	Using colon carcinoma cells that express a temperature-sensitive variant of p53 and undergo p53-dependent apoptosis after UV irradiation, we found that the number of p53-induced genes identified by oligonucleotide microarray analysis decreased in a UV dose-dependent manner.	Oligonucleotides	198-213	P53	Homo sapiens	92-95
15087501-4	2004	Using colon carcinoma cells that express a temperature-sensitive variant of p53 and undergo p53-dependent apoptosis after UV irradiation, we found that the number of p53-induced genes identified by oligonucleotide microarray analysis decreased in a UV dose-dependent manner.	Oligonucleotides	198-213	P53	Homo sapiens	92-95
15093669-6	2004	While vanadium deficiency accounts for several physiological malfunctionings including thyroid, glucose and lipid metabolism, etc., several genes are regulated by this element or by its compounds, which include genes for tumor necrosis factor-alpha (TNF-alpha), Interleukin-8 (IL-8), activator protein-1 (AP-1), ras, c-raf-1, mitogen activated protein kinase (MAPK), p53, nuclear factors-kappaB, etc.	Vanadium	6-14	P53	Homo sapiens	367-370
15105503-2	2004	We show that sestrins, a family of proteins whose expression is modulated by p53, are required for regeneration of Prxs containing Cys-SO(2)H, thus reestablishing the antioxidant firewall.	Cysteine	131-134	P53	Homo sapiens	77-80
15077186-1	2004	A single-nucleotide polymorphism (SNP) in exon 4 results in expression of either arginine (72R) or proline (72P) at codon 72 of p53.	Arginine	81-89	P53	Homo sapiens	128-131
15107491-6	2004	Western blot hybridization results revealed that the XPC defect reduced the p53 responses to the cisplatin treatment.	Cisplatin	97-106	P53	Homo sapiens	76-79
15107491-8	2004	These results suggest that the XPC protein plays a critical role in initiating the cisplatin DNA damaging treatment-mediated signal transduction process, resulting in activation of the p53 pathway and cell cycle arrest that allow DNA repair and apoptosis to take place.	Cisplatin	83-92	P53	Homo sapiens	185-188
15042566-0	2004	DNA adducts and p53 mutations in a patient with aristolochic acid-associated nephropathy.	aristolochic acid I	48-65	P53	Homo sapiens	16-19
15102660-10	2004	A multivariate analysis, including tumor stage, gender, TP53 mutations, and MMP3 polymorphism, showed that the 6A/6A genotype was an independent factor of response to 5-fluorouracil-cisplatin chemotherapy in head and neck cancer patients with an odds ratio of 6.7 as compared with the 5A/5A genotype.	Fluorouracil	167-181	P53	Homo sapiens	56-60
15102660-10	2004	A multivariate analysis, including tumor stage, gender, TP53 mutations, and MMP3 polymorphism, showed that the 6A/6A genotype was an independent factor of response to 5-fluorouracil-cisplatin chemotherapy in head and neck cancer patients with an odds ratio of 6.7 as compared with the 5A/5A genotype.	Cisplatin	182-191	P53	Homo sapiens	56-60
14981545-7	2004	However, treatment with ADR or cisplatin is accompanied by a significant increase and redistribution of RAD6 to DNA, and RAD6, RAD18, PCNA, phosphohistone H3, as well as p53 proteins are all found in the DNA fractions.	Cisplatin	31-40	P53	Homo sapiens	170-173
15135086-12	2004	Our results suggest also that aside from the BCR/ABL other factors such as p53 level, signal transduction pathways and DNA repair processes can be responsible for the increased sensitivity of K562 cells to cisplatin compared with normal lymphocytes.	Cisplatin	206-215	P53	Homo sapiens	75-78
15087041-1	2004	BACKGROUND &amp; OBJECTIVE: Studies have revealed that overexpression of p53 protein has close relation to induction of drug resistance in cancer patients and it can be used as a predictor for chemosensitivity of tumor.	Adenosine Monophosphate	12-15	P53	Homo sapiens	73-76
15087041-6	2004	METHOD: Serum analysis of p53 antibodies was performed by enzyme-linked immunosorbent assay (ELISA) in 38 patients with esophageal cancer preoperatively, then surgically resected specimens were analyzed for their chemosensitivity to cisdichlorodiammineplatinum (DDP),5-fluorouracil (5-FU), and Adriamycin (ADM) by in vitro drug response assay MTT colorimetry.	Fluorouracil	267-281	P53	Homo sapiens	26-29
15042566-5	2004	In DNA from the breast and liver tumors the authors showed the same missense mutation in codon 245 (GGC--&gt;GAC; Gly--&gt;Asp) of exon 7 of p53.	Glycine	114-117	P53	Homo sapiens	141-144
15087041-6	2004	METHOD: Serum analysis of p53 antibodies was performed by enzyme-linked immunosorbent assay (ELISA) in 38 patients with esophageal cancer preoperatively, then surgically resected specimens were analyzed for their chemosensitivity to cisdichlorodiammineplatinum (DDP),5-fluorouracil (5-FU), and Adriamycin (ADM) by in vitro drug response assay MTT colorimetry.	Fluorouracil	283-287	P53	Homo sapiens	26-29
15087041-6	2004	METHOD: Serum analysis of p53 antibodies was performed by enzyme-linked immunosorbent assay (ELISA) in 38 patients with esophageal cancer preoperatively, then surgically resected specimens were analyzed for their chemosensitivity to cisdichlorodiammineplatinum (DDP),5-fluorouracil (5-FU), and Adriamycin (ADM) by in vitro drug response assay MTT colorimetry.	Doxorubicin	294-304	P53	Homo sapiens	26-29
15059920-10	2004	Mutations within the DNA-binding domain of p53, which are usually associated with malignancy, were found to impair the repressive effect of p53 on transcriptional activity of the GLUT1 and GLUT4 gene promoters, thereby resulting in increased glucose metabolism and cell energy supply.	Glucose	242-249	P53	Homo sapiens	43-46
15087041-6	2004	METHOD: Serum analysis of p53 antibodies was performed by enzyme-linked immunosorbent assay (ELISA) in 38 patients with esophageal cancer preoperatively, then surgically resected specimens were analyzed for their chemosensitivity to cisdichlorodiammineplatinum (DDP),5-fluorouracil (5-FU), and Adriamycin (ADM) by in vitro drug response assay MTT colorimetry.	Doxorubicin	306-309	P53	Homo sapiens	26-29
15087041-12	2004	The chemosensitivity to DDP, 5-FU, and ADM (11.1%,16.1%,and 16.1%, respectively) of the patients with positive serum p53-Ab was significantly lower than that of the patients with negative p53-Ab (60%, 45%, and 35%; P&lt; 0.01,P&lt; 0.05, and P&lt; 0.05, respectively).	Fluorouracil	29-33	P53	Homo sapiens	117-120
15087041-12	2004	The chemosensitivity to DDP, 5-FU, and ADM (11.1%,16.1%,and 16.1%, respectively) of the patients with positive serum p53-Ab was significantly lower than that of the patients with negative p53-Ab (60%, 45%, and 35%; P&lt; 0.01,P&lt; 0.05, and P&lt; 0.05, respectively).	Doxorubicin	39-42	P53	Homo sapiens	117-120
14527925-0	2004	p53 N-terminal Ser-15 approximately P and Ser-20 approximately P levels in squamous cell lung cancer after radio/chemotherapy.	Serine	15-18	P53	Homo sapiens	0-3
14527925-1	2004	Functional regulation of p53 protein, a critical regulator of cell cycle and apoptosis, was investigated in fiberoptic bronchoscopy biopsy samples taken from 23 patients suffering from recurrent squamous cell lung cancer by analyzing the expression and phosphorylation status of the p53 at Ser15 and Ser20 before and after treatment with radiotherapy/cisplatin/vinorelbine.	Cisplatin	351-360	P53	Homo sapiens	25-28
15039212-0	2004	Retention of the arginine allele in codon 72 of the p53 gene correlates with poor apoptosis in head and neck cancer.	Arginine	17-25	P53	Homo sapiens	52-55
15039212-1	2004	The allele constitution at codon 72 of the p53 gene (CGC-arginine or CCC-proline) plays a major role in inducing apoptosis in p53 mutant cells.	cgc-arginine	53-65	P53	Homo sapiens	43-46
15039212-1	2004	The allele constitution at codon 72 of the p53 gene (CGC-arginine or CCC-proline) plays a major role in inducing apoptosis in p53 mutant cells.	cgc-arginine	53-65	P53	Homo sapiens	126-129
15039212-9	2004	p53 mutations were detected in 29.6% of SCCHN and preferentially occurred at the arginine allele (P = 0.01).	Arginine	81-89	P53	Homo sapiens	0-3
15041222-4	2004	The TP53 gene has a single polymorphism at codon 72 of exon 4 that encodes either arginine (Arg) or proline (Pro).	Arginine	82-90	P53	Homo sapiens	4-8
15041222-4	2004	The TP53 gene has a single polymorphism at codon 72 of exon 4 that encodes either arginine (Arg) or proline (Pro).	Arginine	92-95	P53	Homo sapiens	4-8
15059920-10	2004	Mutations within the DNA-binding domain of p53, which are usually associated with malignancy, were found to impair the repressive effect of p53 on transcriptional activity of the GLUT1 and GLUT4 gene promoters, thereby resulting in increased glucose metabolism and cell energy supply.	Glucose	242-249	P53	Homo sapiens	140-143
14977881-5	2004	VSMC exposed to serum-free medium conditioned by apoptotic EC showed increased ERK 1/2 phosphorylation, enhanced Bcl-xl expression, and inhibition of p53 expression.	vsmc	0-4	P53	Homo sapiens	150-153
15037523-0	2004	Role of p53 and p38 MAP kinase in nitric oxide-induced G2/M arrest and apoptosis in the human lung carcinoma cells.	Nitric Oxide	34-46	P53	Homo sapiens	8-11
15059885-1	2004	p53-mediated apoptosis may involve the induction of redox-controlling genes, resulting in the production of reactive oxygen species.	Reactive Oxygen Species	108-131	P53	Homo sapiens	0-3
15059885-10	2004	We observed both the release of cytochrome C and Ca(2+) from the mitochondria into the cytoplasm and an increased frequency of apoptotic cells after p53 induction in the TR9-7 cells that coincided with an increased expression of MnSOD and GPx, and the level of reactive oxygen species.	Reactive Oxygen Species	261-284	P53	Homo sapiens	149-152
15041112-4	2004	p53 immunostaining was performed on paraffin-embedded tissues using monoclonal antibody DO7 and an automated immunostainer.	Paraffin	36-44	P53	Homo sapiens	0-3
15034933-3	2004	Prior reports have demonstrated that BRCA1 can exist in cells in a complex with the BRG1-based SWI/SNF ATP-dependent chromatin remodeling enzymes and that SWI/SNF components contribute to p53-mediated gene activation.	Adenosine Triphosphate	103-106	P53	Homo sapiens	188-191
15057642-5	2004	Published data suggest that betulinic acid induces apoptosis in sensitive cells in a p53- and CD95-independent fashion.	betulinic acid	28-42	P53	Homo sapiens	85-88
15010816-0	2004	Expression of p53 protein as a predictor of the response to 5-fluorouracil and cisplatin chemotherapy in human gastrointestinal cancer cell lines evaluated with apoptosis by use of thin layer collagen gel.	Fluorouracil	60-74	P53	Homo sapiens	14-17
15010816-0	2004	Expression of p53 protein as a predictor of the response to 5-fluorouracil and cisplatin chemotherapy in human gastrointestinal cancer cell lines evaluated with apoptosis by use of thin layer collagen gel.	Cisplatin	79-88	P53	Homo sapiens	14-17
15165403-0	2004	Identification of a p53-dependent pathway in the induction of apoptosis of human breast cancer cells by the natural product, resveratrol.	Resveratrol	125-136	P53	Homo sapiens	20-23
15165403-5	2004	RESULTS: Apoptosis induced by resveratrol was found to occur only in breast cancer cells expressing wild-type p53 but not in mutant p53-expressing cells.	Resveratrol	30-41	P53	Homo sapiens	110-113
15165403-6	2004	CONCLUSIONS: We therefore conclude that the natural product, resveratrol, induces apoptosis in breast cancer cells via p53-dependent pathways.	Resveratrol	61-72	P53	Homo sapiens	119-122
14968111-5	2004	In both cases, however, HCV core protein increased the p53 DNA-binding affinity in gel retardation analyses, likely due to the hyperacetylation of p53 Lys(373) and Lys(382) residues.	Lysine	151-154	P53	Homo sapiens	55-58
14968111-5	2004	In both cases, however, HCV core protein increased the p53 DNA-binding affinity in gel retardation analyses, likely due to the hyperacetylation of p53 Lys(373) and Lys(382) residues.	Lysine	151-154	P53	Homo sapiens	147-150
14968111-5	2004	In both cases, however, HCV core protein increased the p53 DNA-binding affinity in gel retardation analyses, likely due to the hyperacetylation of p53 Lys(373) and Lys(382) residues.	Lysine	164-167	P53	Homo sapiens	55-58
14968111-6	2004	Additionally, HCV core protein, depending on its expression level, had differential effects on the Ser(15) phosphorylation of p53.	Serine	99-102	P53	Homo sapiens	126-129
15010881-7	2004	In addition, the extent to which harringtonine altered the expression of select DNA damage response genes (p53, P16, ERCC1 and XPB) was determined using RT-PCR and Southern hybridization in A2780 and A2780/CP70 cells.	harringtonin	33-46	P53	Homo sapiens	107-110
15010881-9	2004	However, harringtonine altered expression of p53 and P16 RNAs in both cell lines, although the down-regulation of p53 and P16 RNAs by harringtonine were more pronounced in A2780 cells.	harringtonin	9-22	P53	Homo sapiens	45-48
15010881-9	2004	However, harringtonine altered expression of p53 and P16 RNAs in both cell lines, although the down-regulation of p53 and P16 RNAs by harringtonine were more pronounced in A2780 cells.	harringtonin	134-147	P53	Homo sapiens	114-117
15010889-4	2004	To further investigate the molecular mechanisms underlying bladder carcinogenesis with this specific etiology, mutation analysis of p53 gene (exon 5-8) was performed for 11 and 18 paraffin-embedded bladder cancers in Ukrainians, respectively collected before and after the Chernobyl disaster.	Paraffin	180-188	P53	Homo sapiens	132-135
15026814-10	2004	Gene transfer of p53 14/19 in combination with the administration of doxorubicin or cisplatin is a potential therapeutic approach for cancers expressing high levels of Mdm2.	Doxorubicin	69-80	P53	Homo sapiens	17-20
15053879-0	2004	Phosphorylation on Thr-55 by TAF1 mediates degradation of p53: a role for TAF1 in cell G1 progression.	Threonine	19-22	P53	Homo sapiens	58-61
15053879-4	2004	TAF1 interacts with and phosphorylates p53 at Thr-55 in vivo.	Threonine	46-49	P53	Homo sapiens	39-42
15084981-11	2004	These results strongly suggest that AxdAdB-3 possesses a wider therapeutic potential than previously believed, given that most pancreatic cancers have abnormalities in both the TP53 and RB pathways.	axdadb-3	36-44	P53	Homo sapiens	177-181
15053879-8	2004	Significantly, the Thr-55 phosphorylation was reduced following DNA damage, suggesting that this phosphorylation contributes to the stabilization of p53 in response to DNA damage.	Threonine	19-22	P53	Homo sapiens	149-152
15026814-0	2004	A modified p53 enhances apoptosis in sarcoma cell lines mediated by doxorubicin.	Doxorubicin	68-79	P53	Homo sapiens	11-14
15026814-6	2004	We demonstrate that doxorubicin induces phosphorylation of both wt p53 and p53 14/19 protein at multiple sites.	Doxorubicin	20-31	P53	Homo sapiens	67-70
15026814-6	2004	We demonstrate that doxorubicin induces phosphorylation of both wt p53 and p53 14/19 protein at multiple sites.	Doxorubicin	20-31	P53	Homo sapiens	75-78
15026814-10	2004	Gene transfer of p53 14/19 in combination with the administration of doxorubicin or cisplatin is a potential therapeutic approach for cancers expressing high levels of Mdm2.	Cisplatin	84-93	P53	Homo sapiens	17-20
14755247-5	2004	The p53 protein remains short-lived in confluent cultures regardless of the extent of DNA damage, even though it undergoes efficient phosphorylation on the mouse equivalent of human p53 serine 15.	Serine	186-192	P53	Homo sapiens	182-185
15041737-9	2004	Using semiquantitative reverse transcription-PCR, we have demonstrated down-regulation of thymidine phosphorylase mRNA in both p53(+/+) and p53(-/-) 5-FU-resistant cells, suggesting that decreased production of 5-FU active metabolites may be an important resistance mechanism in these lines.	Fluorouracil	149-153	P53	Homo sapiens	140-143
15041737-0	2004	Characterization of p53 wild-type and null isogenic colorectal cancer cell lines resistant to 5-fluorouracil, oxaliplatin, and irinotecan.	Fluorouracil	94-108	P53	Homo sapiens	20-23
15041737-0	2004	Characterization of p53 wild-type and null isogenic colorectal cancer cell lines resistant to 5-fluorouracil, oxaliplatin, and irinotecan.	Irinotecan	127-137	P53	Homo sapiens	20-23
15041737-5	2004	In addition, we found that resistance to 5-FU and oxaliplatin was higher in parental p53(-/-) cells compared with parental p53(+/+) cells, with an approximately 5-fold increase in IC(50 (72 h)) for each drug.	Fluorouracil	41-45	P53	Homo sapiens	85-88
15001399-0	2004	Differential regulation of signal transduction pathways in wild type and mutated p53 breast cancer epithelial cells by copper and zinc.	Copper	119-125	P53	Homo sapiens	81-84
15001399-2	2004	This study was undertaken to investigate the role of PI3K/Akt signaling pathway in metal resistance in human breast cancer epithelial cells with different p53 and estrogen receptor status.	Metals	83-88	P53	Homo sapiens	155-158
15001399-3	2004	Exposure to copper and zinc increased Akt phosphorylation with its nuclear localization only in MDA-MB-231 cells with no estrogen receptor and mutated p53.	Copper	12-18	P53	Homo sapiens	151-154
15001399-6	2004	In contrast, in MCF-7 cells with wild type p53 and estrogen receptor, there was no change in Akt activation, while suppression of p53 activity by pifithrin-alpha increased phosphorylation of Akt after the treatment with copper.	Copper	220-226	P53	Homo sapiens	130-133
15001399-7	2004	In MCF-7 cells, the metal treatment increased the phosphorylation of p53 at serine 15, up-regulated p21 expression, and resulted in cell-cycle arrest in G1 phase with apoptosis.	Metals	20-25	P53	Homo sapiens	69-72
15001399-7	2004	In MCF-7 cells, the metal treatment increased the phosphorylation of p53 at serine 15, up-regulated p21 expression, and resulted in cell-cycle arrest in G1 phase with apoptosis.	Serine	76-82	P53	Homo sapiens	69-72
15001399-8	2004	These results demonstrate that copper-induced apoptosis in MCF-7 cells is p53 dependent, whereas the metal resistance in MDA-MB-231 cells may be due to activation of Akt in the absence of a functional p53.	Copper	31-37	P53	Homo sapiens	74-77
15041737-8	2004	These data suggest that p53 may be an important determinant of sensitivity to 5-FU and oxaliplatin but not CPT-11.	Fluorouracil	78-82	P53	Homo sapiens	24-27
15041737-5	2004	In addition, we found that resistance to 5-FU and oxaliplatin was higher in parental p53(-/-) cells compared with parental p53(+/+) cells, with an approximately 5-fold increase in IC(50 (72 h)) for each drug.	Fluorouracil	41-45	P53	Homo sapiens	123-126
15041737-7	2004	Furthermore, apoptosis after treatment with 5-FU and oxaliplatin, but not CPT-11, was significantly reduced in parental p53(-/-) cells compared with parental p53(+/+) cells.	Fluorouracil	44-48	P53	Homo sapiens	120-123
15041737-7	2004	Furthermore, apoptosis after treatment with 5-FU and oxaliplatin, but not CPT-11, was significantly reduced in parental p53(-/-) cells compared with parental p53(+/+) cells.	Fluorouracil	44-48	P53	Homo sapiens	158-161
15041737-9	2004	Using semiquantitative reverse transcription-PCR, we have demonstrated down-regulation of thymidine phosphorylase mRNA in both p53(+/+) and p53(-/-) 5-FU-resistant cells, suggesting that decreased production of 5-FU active metabolites may be an important resistance mechanism in these lines.	Fluorouracil	211-215	P53	Homo sapiens	127-130
14701864-1	2004	C-terminal truncation of ADAMTS-4 from the p68 form to the p53 form is required for activation of its capacity to cleave the Glu(373)-Ala(374) interglobular domain bond of aggrecan.	Glutamic Acid	125-128	P53	Homo sapiens	59-62
14699137-3	2004	We report here that the tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate prevents DNA damage-induced up-regulation of p53 by down-regulating PKC delta.	Tetradecanoylphorbol Acetate	54-90	P53	Homo sapiens	136-139
14701864-1	2004	C-terminal truncation of ADAMTS-4 from the p68 form to the p53 form is required for activation of its capacity to cleave the Glu(373)-Ala(374) interglobular domain bond of aggrecan.	Alanine	134-137	P53	Homo sapiens	59-62
14701864-5	2004	Specific glycosaminoglycan lyase digestions, followed by product analyses using fluorescence-assisted carbohydrate electrophoresis and immunoprecipitation experiments, showed that the p53 form is associated with syndecan-1 through both chondroitin sulfate and heparan sulfate.	Carbohydrates	102-114	P53	Homo sapiens	184-187
15177039-3	2004	We previously showed that genistein, a naturally occurring isoflavonoid, induced increased ATM protein kinase activity, ATM-dependent phosphorylation of p53 on serine 15 and activation of the DNA-binding properties of p53.	Serine	160-166	P53	Homo sapiens	153-156
15177039-4	2004	Here, we show that genistein also induces phosphorylation of p53 at serines 6, 9, 20, 46, and 392, and that genistein-induced accumulation and phosphorylation of p53 is reduced in two ATM-deficient human cell lines.	Serine	68-75	P53	Homo sapiens	61-64
15001986-6	2004	Activated wt-p53 increased apoptosis and enhanced sensitivity to CPT-11.	Irinotecan	65-71	P53	Homo sapiens	13-16
15001986-0	2004	Enhanced sensitivity to irinotecan by Cdk1 inhibition in the p53-deficient HT29 human colon cancer cell line.	Irinotecan	24-34	P53	Homo sapiens	61-64
15023836-0	2004	Association between p53 gene mutations and tobacco and alcohol exposure in laryngeal squamous cell carcinoma.	Alcohols	55-62	P53	Homo sapiens	20-23
15001986-3	2004	Since the DNA-damage checkpoint depends on p53 activation, the status of p53 might critically influence the response to CPT-11.	Irinotecan	120-126	P53	Homo sapiens	43-46
15001986-3	2004	Since the DNA-damage checkpoint depends on p53 activation, the status of p53 might critically influence the response to CPT-11.	Irinotecan	120-126	P53	Homo sapiens	73-76
15001986-10	2004	We demonstrate a gain of sensitivity to CPT-11 in a p53-mutated colon cancer model either by restoring wild-type p53 function or by sequential treatment with cdk-Is.	Irinotecan	40-46	P53	Homo sapiens	52-55
15001986-10	2004	We demonstrate a gain of sensitivity to CPT-11 in a p53-mutated colon cancer model either by restoring wild-type p53 function or by sequential treatment with cdk-Is.	Irinotecan	40-46	P53	Homo sapiens	113-116
15023836-1	2004	OBJECTIVES: To analyze the relationship between p53 gene mutations, tobacco smoke, and alcohol consumption in patients with laryngeal squamous cell carcinoma.	Alcohols	87-94	P53	Homo sapiens	48-51
15161054-7	2004	CONCLUSION: Observations suggest that the cytotoxicity, cell cycle arrest and apoptosis induced by curcumin and resveratrol in NB cells may be mediated via functionally activated p53 and merit further study.	Curcumin	99-107	P53	Homo sapiens	179-182
15161054-0	2004	Curcumin and resveratrol induce apoptosis and nuclear translocation and activation of p53 in human neuroblastoma.	Curcumin	0-8	P53	Homo sapiens	86-89
15161054-0	2004	Curcumin and resveratrol induce apoptosis and nuclear translocation and activation of p53 in human neuroblastoma.	Resveratrol	13-24	P53	Homo sapiens	86-89
15161054-7	2004	CONCLUSION: Observations suggest that the cytotoxicity, cell cycle arrest and apoptosis induced by curcumin and resveratrol in NB cells may be mediated via functionally activated p53 and merit further study.	Resveratrol	112-123	P53	Homo sapiens	179-182
15152939-6	2004	Inactivation of wild-type p53 abrogated the 5-FU-mediated induction of SSAT and annexin II.	Fluorouracil	44-48	P53	Homo sapiens	26-29
14757188-1	2004	It has been recently shown that ionizing radiation (IR) and the mRNA synthesis inhibitor 5,6-dichloro-1-b-D-ribofuranosylbenzimidazole (DRB) act in synergy to induce p53-mediated transactivation of reporter plasmids in human cells [Oncogene 19 (2000) 3829].	Dichlororibofuranosylbenzimidazole	136-139	P53	Homo sapiens	166-169
15025498-3	2004	Our studies of the effects of noncytotoxic concentrations of Cd2+ on the levels of p53 and p21 in (+/-)-anti-benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE)-treated human fibroblasts showed that Cd2+ decreased BPDE-induced p21 levels in a dose-dependent manner whereas p53 accumulation is attenuated only at higher noncytotoxic concentrations of cadmium.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	147-151	P53	Homo sapiens	83-86
15025498-3	2004	Our studies of the effects of noncytotoxic concentrations of Cd2+ on the levels of p53 and p21 in (+/-)-anti-benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE)-treated human fibroblasts showed that Cd2+ decreased BPDE-induced p21 levels in a dose-dependent manner whereas p53 accumulation is attenuated only at higher noncytotoxic concentrations of cadmium.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	206-210	P53	Homo sapiens	83-86
15025498-3	2004	Our studies of the effects of noncytotoxic concentrations of Cd2+ on the levels of p53 and p21 in (+/-)-anti-benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE)-treated human fibroblasts showed that Cd2+ decreased BPDE-induced p21 levels in a dose-dependent manner whereas p53 accumulation is attenuated only at higher noncytotoxic concentrations of cadmium.	Cadmium	342-349	P53	Homo sapiens	83-86
15025498-4	2004	These findings suggest that both the activity and the accumulation of p53 in response of BPDE treatment are inhibited by Cd2+ although the possibility of p53-independent p21 transactivation cannot be ruled out.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	89-93	P53	Homo sapiens	70-73
15025498-8	2004	Our findings indicate that cadmium not only inhibits NER pathway-dependent repair of BPDE-damaged DNA but also impairs p53 and p21 responses and overrides BPDE-induced G1-S cell cycle arrest.	Cadmium	27-34	P53	Homo sapiens	119-122
14991767-0	2004	Cisplatin restores p53 function and enhances the radiosensitivity in HPV16 E6 containing SiHa cells.	Cisplatin	0-9	P53	Homo sapiens	19-22
14991767-2	2004	Treatment with 0-20 microM cisplatin for 24 h in HPV16 E6 containing SiHa cells suppressed E6 mRNA, reduced E6 protein, and restored p53 expression in dose-dependent manners.	Cisplatin	27-36	P53	Homo sapiens	133-136
14991767-4	2004	After 0-10 microM cisplatin treatment, slightly more apoptotic cells appeared from SiHa cells than those from dominant negative p53-transfected SiHa cells.	Cisplatin	18-27	P53	Homo sapiens	128-131
14991767-7	2004	These accompanied with prolonged p53 restoration in irradiated-SiHa cells after 24 h cisplatin treatment and thereafter.	Cisplatin	85-94	P53	Homo sapiens	33-36
14991767-10	2004	Therefore, cisplatin restored p53 expression and prolonged IR-induced p53 restoration would be possible candidates to response more sub-G(1) apoptosis in irradiated SiHa cells.	Cisplatin	11-20	P53	Homo sapiens	30-33
15012603-5	2004	Evidence is presented that the effects of taxol on ER alpha gene transcription may be mediated through the induction of p53.	Paclitaxel	42-47	P53	Homo sapiens	120-123
14665630-4	2004	Compared with cells expressing exogenous wild type p53, the apoptotic response to 5-fluorouracil (5FU) was &gt;50% reduced in cells expressing S15A or S20A mutant p53, and even more reduced by combined mutation of serines 6, 9, 15, 20, 33, and 37 (N6A).	Fluorouracil	82-96	P53	Homo sapiens	51-54
14665630-4	2004	Compared with cells expressing exogenous wild type p53, the apoptotic response to 5-fluorouracil (5FU) was &gt;50% reduced in cells expressing S15A or S20A mutant p53, and even more reduced by combined mutation of serines 6, 9, 15, 20, 33, and 37 (N6A).	Fluorouracil	82-96	P53	Homo sapiens	163-166
14665630-4	2004	Compared with cells expressing exogenous wild type p53, the apoptotic response to 5-fluorouracil (5FU) was &gt;50% reduced in cells expressing S15A or S20A mutant p53, and even more reduced by combined mutation of serines 6, 9, 15, 20, 33, and 37 (N6A).	Fluorouracil	98-101	P53	Homo sapiens	51-54
14665630-4	2004	Compared with cells expressing exogenous wild type p53, the apoptotic response to 5-fluorouracil (5FU) was &gt;50% reduced in cells expressing S15A or S20A mutant p53, and even more reduced by combined mutation of serines 6, 9, 15, 20, 33, and 37 (N6A).	Fluorouracil	98-101	P53	Homo sapiens	163-166
14726466-0	2004	Evaluation of oligonucleotide arrays for sequencing of the p53 gene in DNA from formalin-fixed, paraffin-embedded breast cancer specimens.	Oligonucleotides	14-29	P53	Homo sapiens	59-62
14726466-0	2004	Evaluation of oligonucleotide arrays for sequencing of the p53 gene in DNA from formalin-fixed, paraffin-embedded breast cancer specimens.	Paraffin	96-104	P53	Homo sapiens	59-62
14726466-2	2004	The purpose of this study was to determine whether a p53 microarray could be used to sequence the p53 gene in DNA extracted from formalin-fixed, paraffin-embedded (FFPE) tissues.	Paraffin	145-153	P53	Homo sapiens	98-101
14993250-3	2004	The nuclear factor kappaB (NF-kappaB) super repressor had an antimitotic and antiapoptotic effect and prevented the Env-elicited phosphorylation of p53 on serine 15 and 46, as well as the activation of AP1.	Serine	155-161	P53	Homo sapiens	148-151
15009673-5	2004	Testosterone treatment induced all gene targets of p53, and amplified the induction of these genes induced by kainate.	Testosterone	0-12	P53	Homo sapiens	51-54
14623946-12	2004	Fas-mediated apoptosis was significantly suppressed by anti-sense p53 oligonucleotides and by p53DN.	Oligonucleotides	70-86	P53	Homo sapiens	66-69
14660625-9	2004	rho(0) cells were resistant to p53, and intracellular ROS contents after p53 expression were lower compared with parental cells.	ros	54-57	P53	Homo sapiens	73-76
14757188-5	2004	Furthermore, the nuclear export inhibitor leptomycin B showed a similar synergy with IR as did DRB regarding ser15 phosphorylation of p53 and p21 induction.	Dichlororibofuranosylbenzimidazole	95-98	P53	Homo sapiens	134-137
14729469-0	2004	Homeodomain-interacting protein kinase-2 activity and p53 phosphorylation are critical events for cisplatin-mediated apoptosis.	Cisplatin	98-107	P53	Homo sapiens	54-57
14982997-4	2004	Here, we show that unacetylated p53 is able to bind weakly to its consensus site within the context of large DNA fragments, although it completely fails to bind the same site within short oligonucleotide probes.	Oligonucleotides	188-203	P53	Homo sapiens	32-35
14729469-5	2004	HIPK2 gene silencing efficiently reduces the p53-mediated transcriptional activation of apoptotic gene promoters as well as apoptotic cell death after treatment with cisplatin.	Cisplatin	166-175	P53	Homo sapiens	45-48
14729469-6	2004	These findings, along with the involvement of p53 phosphorylation at serine 46 (Ser46) in the transcriptional activation of apoptotic gene promoters, suggest a critical role for HIPK2 in triggering p53-dependent apoptosis in response to the antineoplastic drug cisplatin.	Serine	69-75	P53	Homo sapiens	46-49
14729469-6	2004	These findings, along with the involvement of p53 phosphorylation at serine 46 (Ser46) in the transcriptional activation of apoptotic gene promoters, suggest a critical role for HIPK2 in triggering p53-dependent apoptosis in response to the antineoplastic drug cisplatin.	Serine	69-75	P53	Homo sapiens	198-201
14729469-6	2004	These findings, along with the involvement of p53 phosphorylation at serine 46 (Ser46) in the transcriptional activation of apoptotic gene promoters, suggest a critical role for HIPK2 in triggering p53-dependent apoptosis in response to the antineoplastic drug cisplatin.	Cisplatin	261-270	P53	Homo sapiens	198-201
15093128-4	2004	This type of calcium signal promotes activation of the transcription factor CREB (cAMP response element binding protein) leading to cell cycle arrest in G1 phase via transactivation of p53/p21 signaling pathways.	Calcium	13-20	P53	Homo sapiens	185-188
14961077-4	2004	Using 19 glioblastoma cell lines, including 15 low-passage ex vivo cell lines derived from patients, as well as isogenic glioblastoma cells varying in p53 status, we show that clinically relevant levels of SN-38 potently induce cell cycle arrest and temporary senescence in glioblastoma cells with wild-type p53 while causing massive apoptosis in p53-deficient cells (P&lt;0.0002).	Irinotecan	206-211	P53	Homo sapiens	151-154
14961077-4	2004	Using 19 glioblastoma cell lines, including 15 low-passage ex vivo cell lines derived from patients, as well as isogenic glioblastoma cells varying in p53 status, we show that clinically relevant levels of SN-38 potently induce cell cycle arrest and temporary senescence in glioblastoma cells with wild-type p53 while causing massive apoptosis in p53-deficient cells (P&lt;0.0002).	Irinotecan	206-211	P53	Homo sapiens	308-311
14961077-4	2004	Using 19 glioblastoma cell lines, including 15 low-passage ex vivo cell lines derived from patients, as well as isogenic glioblastoma cells varying in p53 status, we show that clinically relevant levels of SN-38 potently induce cell cycle arrest and temporary senescence in glioblastoma cells with wild-type p53 while causing massive apoptosis in p53-deficient cells (P&lt;0.0002).	Irinotecan	206-211	P53	Homo sapiens	308-311
14965371-0	2004	p53-independent anti-tumor effects of the nitrogen-containing bisphosphonate zoledronic acid.	Nitrogen	42-50	P53	Homo sapiens	0-3
14712090-0	2004	Tocotrienol-rich fraction of palm oil activates p53, modulates Bax/Bcl2 ratio and induces apoptosis independent of cell cycle association.	Palm Oil	29-37	P53	Homo sapiens	48-51
14871840-0	2004	Induction of apoptosis in leukemic cells by homovanillic acid derivative, capsaicin, through oxidative stress: implication of phosphorylation of p53 at Ser-15 residue by reactive oxygen species.	Homovanillic Acid	44-61	P53	Homo sapiens	145-148
14871840-0	2004	Induction of apoptosis in leukemic cells by homovanillic acid derivative, capsaicin, through oxidative stress: implication of phosphorylation of p53 at Ser-15 residue by reactive oxygen species.	Capsaicin	74-83	P53	Homo sapiens	145-148
14871840-0	2004	Induction of apoptosis in leukemic cells by homovanillic acid derivative, capsaicin, through oxidative stress: implication of phosphorylation of p53 at Ser-15 residue by reactive oxygen species.	Serine	152-155	P53	Homo sapiens	145-148
14871840-0	2004	Induction of apoptosis in leukemic cells by homovanillic acid derivative, capsaicin, through oxidative stress: implication of phosphorylation of p53 at Ser-15 residue by reactive oxygen species.	Reactive Oxygen Species	170-193	P53	Homo sapiens	145-148
14871840-7	2004	Interestingly, capsaicin-sensitive leukemic cells were possessed of wild-type p53, resulting in the phosphorylation of p53 at the Ser-15 residue by the treatment of capsaicin.	Capsaicin	15-24	P53	Homo sapiens	78-81
14871840-7	2004	Interestingly, capsaicin-sensitive leukemic cells were possessed of wild-type p53, resulting in the phosphorylation of p53 at the Ser-15 residue by the treatment of capsaicin.	Capsaicin	15-24	P53	Homo sapiens	119-122
14871840-7	2004	Interestingly, capsaicin-sensitive leukemic cells were possessed of wild-type p53, resulting in the phosphorylation of p53 at the Ser-15 residue by the treatment of capsaicin.	Serine	130-133	P53	Homo sapiens	78-81
14719081-4	2004	The anti-proliferative effects of resveratrol were associated with a marked inhibition of cyclin D and cyclin-dependent kinase (Cdk) 4 proteins, and induction of p53 and Cdk inhibitor p21WAF1/CIP.	Resveratrol	34-45	P53	Homo sapiens	162-165
14871840-7	2004	Interestingly, capsaicin-sensitive leukemic cells were possessed of wild-type p53, resulting in the phosphorylation of p53 at the Ser-15 residue by the treatment of capsaicin.	Serine	130-133	P53	Homo sapiens	119-122
14871840-7	2004	Interestingly, capsaicin-sensitive leukemic cells were possessed of wild-type p53, resulting in the phosphorylation of p53 at the Ser-15 residue by the treatment of capsaicin.	Capsaicin	165-174	P53	Homo sapiens	78-81
14871840-7	2004	Interestingly, capsaicin-sensitive leukemic cells were possessed of wild-type p53, resulting in the phosphorylation of p53 at the Ser-15 residue by the treatment of capsaicin.	Capsaicin	165-174	P53	Homo sapiens	119-122
14871840-8	2004	Abrogation of p53 expression by the antisense oligonucleotides significantly attenuated capsaicin-induced cell cycle arrest and apoptosis.	Oligonucleotides	46-62	P53	Homo sapiens	14-17
14871840-8	2004	Abrogation of p53 expression by the antisense oligonucleotides significantly attenuated capsaicin-induced cell cycle arrest and apoptosis.	Capsaicin	88-97	P53	Homo sapiens	14-17
14871840-9	2004	Pretreatment with the antioxidant N-acetyl-L-cystein and catalase, but not superoxide dismutase, completely inhibited capsaicin-induced apoptosis by inhibiting phosphorylation of Ser-15 residue of p53.	Capsaicin	118-127	P53	Homo sapiens	197-200
14729946-2	2004	Recently, it has been proposed that phosphorylation of serine 15 in human p53 by ATM (mutated in ataxia telangiectasia) kinase induces p53 activity by interfering with the Mdm2-p53 complex formation and inhibiting Mdm2-mediated destabilization of p53.	Serine	55-61	P53	Homo sapiens	74-77
14729946-2	2004	Recently, it has been proposed that phosphorylation of serine 15 in human p53 by ATM (mutated in ataxia telangiectasia) kinase induces p53 activity by interfering with the Mdm2-p53 complex formation and inhibiting Mdm2-mediated destabilization of p53.	Serine	55-61	P53	Homo sapiens	135-138
14729946-2	2004	Recently, it has been proposed that phosphorylation of serine 15 in human p53 by ATM (mutated in ataxia telangiectasia) kinase induces p53 activity by interfering with the Mdm2-p53 complex formation and inhibiting Mdm2-mediated destabilization of p53.	Serine	55-61	P53	Homo sapiens	135-138
14729946-2	2004	Recently, it has been proposed that phosphorylation of serine 15 in human p53 by ATM (mutated in ataxia telangiectasia) kinase induces p53 activity by interfering with the Mdm2-p53 complex formation and inhibiting Mdm2-mediated destabilization of p53.	Serine	55-61	P53	Homo sapiens	135-138
14744935-3	2004	The mechanism of inhibition involves the increased cytoplasmic localization of p53 due to phosphorylation at serine 315 and serine 376, which is mediated by glycogen synthase kinase-3 beta (GSK-3beta).	Serine	109-115	P53	Homo sapiens	79-82
14744935-3	2004	The mechanism of inhibition involves the increased cytoplasmic localization of p53 due to phosphorylation at serine 315 and serine 376, which is mediated by glycogen synthase kinase-3 beta (GSK-3beta).	Serine	124-130	P53	Homo sapiens	79-82
14706517-11	2004	A transient up-regulation of p53 occurred 1h post-IR in BGC823 cells but not in MGC803 cells.	Hydrogen	42-44	P53	Homo sapiens	29-32
14759370-1	2004	Lysine acetylation of the tumor suppressor protein p53 in response to a wide variety of cellular stress signals is required for its activation as a transcription factor that regulates cell cycle arrest, senescence, or apoptosis.	Lysine	0-6	P53	Homo sapiens	51-54
14759370-2	2004	Here, we report that the conserved bromo-domain of the transcriptional coactivator CBP (CREB binding protein) binds specifically to p53 at the C-terminal acetylated lysine 382.	Lysine	165-171	P53	Homo sapiens	132-135
14759370-4	2004	We further present the three-dimensional nuclear magnetic resonance structure of the CBP bromodomain in complex with a lysine 382-acetylated p53 peptide.	Lysine	119-125	P53	Homo sapiens	141-144
14713953-6	2004	FOXO3a influences p53 activity by regulating the level of reactive oxygen species.	Reactive Oxygen Species	58-81	P53	Homo sapiens	18-21
15844633-1	2004	The arginine variant of the p53 codon 72 polymorphism as well as anogenital and epidermodysplasia verruciformis (EV) types of human papilloma virus (HPV) are suggested to confer increased risk for developing cutaneous squamous cell carcinoma (SCC).	Arginine	4-12	P53	Homo sapiens	28-31
14712210-0	2004	Phosphorylation of p53 at serine 37 is important for transcriptional activity and regulation in response to DNA damage.	Serine	26-32	P53	Homo sapiens	19-22
14576150-0	2004	Depletion of endogenous nitric oxide enhances cisplatin-induced apoptosis in a p53-dependent manner in melanoma cell lines.	Nitric Oxide	24-36	P53	Homo sapiens	79-82
14576150-0	2004	Depletion of endogenous nitric oxide enhances cisplatin-induced apoptosis in a p53-dependent manner in melanoma cell lines.	Cisplatin	46-55	P53	Homo sapiens	79-82
14576150-7	2004	Strikingly, we observed that the depletion of nitric oxide inhibits cisplatin-induced wild type p53 accumulation and p21(Waf1/Cip1/Sdi1) expression in melanoma cells.	Nitric Oxide	46-58	P53	Homo sapiens	96-99
14576150-7	2004	Strikingly, we observed that the depletion of nitric oxide inhibits cisplatin-induced wild type p53 accumulation and p21(Waf1/Cip1/Sdi1) expression in melanoma cells.	Cisplatin	68-77	P53	Homo sapiens	96-99
14576150-8	2004	When cisplatin-induced p53 binding to the p21(Waf1/Cip1/Sdi1) promoter was examined, it was found that nitric oxide depletion significantly reduced the presence of p53-DNA complexes after cisplatin treatment.	Cisplatin	5-14	P53	Homo sapiens	23-26
14576150-8	2004	When cisplatin-induced p53 binding to the p21(Waf1/Cip1/Sdi1) promoter was examined, it was found that nitric oxide depletion significantly reduced the presence of p53-DNA complexes after cisplatin treatment.	Cisplatin	5-14	P53	Homo sapiens	164-167
14576150-8	2004	When cisplatin-induced p53 binding to the p21(Waf1/Cip1/Sdi1) promoter was examined, it was found that nitric oxide depletion significantly reduced the presence of p53-DNA complexes after cisplatin treatment.	Nitric Oxide	103-115	P53	Homo sapiens	23-26
14576150-8	2004	When cisplatin-induced p53 binding to the p21(Waf1/Cip1/Sdi1) promoter was examined, it was found that nitric oxide depletion significantly reduced the presence of p53-DNA complexes after cisplatin treatment.	Nitric Oxide	103-115	P53	Homo sapiens	164-167
14704126-1	2004	AIM: To study the effect of wild type (wt) p53 gene transfection on drug resistant human hepatocellular carcinoma (HCC) cells induced by 5-Fluorouracil (5-FU).	Fluorouracil	137-151	P53	Homo sapiens	43-46
14704126-1	2004	AIM: To study the effect of wild type (wt) p53 gene transfection on drug resistant human hepatocellular carcinoma (HCC) cells induced by 5-Fluorouracil (5-FU).	Fluorouracil	153-157	P53	Homo sapiens	43-46
14704126-10	2004	CONCLUSION: These results indicated that the wt p53 gene transfection not only induced suppression of cell growth, but also increased the sensitivity of Bel7402/5-FU cells to 5-FU, vincristine, and doxorubicin.	Fluorouracil	161-165	P53	Homo sapiens	48-51
12959929-2	2004	Although H2O2 and other peroxides have been shown to induce ataxia telangiectasia-mutated (ATM)-dependent p53 phosphorylation in response to DNA damage, the signal transduction mechanisms in response to hyperoxia are currently unknown.	Hydrogen Peroxide	9-13	P53	Homo sapiens	106-109
12959929-12	2004	Together, our data suggest that hyperoxia activates the ATR-Chk1 pathway and phosphorylates p53 at multiple sites in an ATM-independent manner, which is different from other forms of oxidative stress such as H2O2 or UV light.	Hydrogen Peroxide	208-212	P53	Homo sapiens	92-95
14729628-5	2004	The phosphorylated p53 (Thr 55) was increased in the cytoplasm and nucleus of MCF+FIR but not in the sham-FIR control cells.	Threonine	24-27	P53	Homo sapiens	19-22
14729643-3	2004	Here, we discovered a novel function of the chemopreventive agent resveratrol: resveratrol is a potent sensitizer of tumor cells for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis through p53-independent induction of p21 and p21-mediated cell cycle arrest associated with survivin depletion.	Resveratrol	66-77	P53	Homo sapiens	223-226
14744727-1	2004	The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene has been implicated as a risk marker in cervical neoplasia.	Arginine	4-7	P53	Homo sapiens	66-69
14744727-1	2004	The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene has been implicated as a risk marker in cervical neoplasia.	Arginine	8-11	P53	Homo sapiens	66-69
14744727-1	2004	The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene has been implicated as a risk marker in cervical neoplasia.	Arginine	8-11	P53	Homo sapiens	66-69
14576150-8	2004	When cisplatin-induced p53 binding to the p21(Waf1/Cip1/Sdi1) promoter was examined, it was found that nitric oxide depletion significantly reduced the presence of p53-DNA complexes after cisplatin treatment.	Cisplatin	188-197	P53	Homo sapiens	164-167
14576150-9	2004	Furthermore, dominant negative inhibition of p53 activity enhanced cisplatin-induced apoptosis.	Cisplatin	67-76	P53	Homo sapiens	45-48
14576150-10	2004	Together, these data strongly suggest that endogenously produced nitric oxide is required for cisplatin-induced p53 activation and p21(Waf1/Cip1/Sdi1) expression, which can regulate melanoma sensitivity to cisplatin.	Nitric Oxide	65-77	P53	Homo sapiens	112-115
14576150-10	2004	Together, these data strongly suggest that endogenously produced nitric oxide is required for cisplatin-induced p53 activation and p21(Waf1/Cip1/Sdi1) expression, which can regulate melanoma sensitivity to cisplatin.	Cisplatin	94-103	P53	Homo sapiens	112-115
14704126-10	2004	CONCLUSION: These results indicated that the wt p53 gene transfection not only induced suppression of cell growth, but also increased the sensitivity of Bel7402/5-FU cells to 5-FU, vincristine, and doxorubicin.	Fluorouracil	175-179	P53	Homo sapiens	48-51
14704126-10	2004	CONCLUSION: These results indicated that the wt p53 gene transfection not only induced suppression of cell growth, but also increased the sensitivity of Bel7402/5-FU cells to 5-FU, vincristine, and doxorubicin.	Doxorubicin	198-209	P53	Homo sapiens	48-51
15015586-9	2004	Moreover, DOX at 0.01 and 0.1 microM induced p53 and p21(WAF-1/CIP-1) to the same extent in both MCF-7 and MCF-7/Adr-20 cells.	Doxorubicin	10-13	P53	Homo sapiens	45-48
15015586-10	2004	Therefore, while DOX triggers growth arrest and induces p53 and p21(WAF-1/CIP-1) in these cells, defects in activation of the initiator and executioner caspases play a major role in resistance to apoptosis triggered by DOX.	Doxorubicin	17-20	P53	Homo sapiens	56-59
15015604-6	2004	RESULTS: The statistical analysis of results showed that the cases of tetraploid and/or multiploid RMS, overexpressing p53 (W&amp;M and mutated) and MDR-1, were characterized by an overall worse prognosis.	Adenosine Monophosphate	126-129	P53	Homo sapiens	119-122
14555612-7	2004	Doxorubicin and hydrogen peroxide (H2O2) treatment, although inducing p53 stabilization, did not cause the activation of glycosylase.	Doxorubicin	0-11	P53	Homo sapiens	70-73
14555612-7	2004	Doxorubicin and hydrogen peroxide (H2O2) treatment, although inducing p53 stabilization, did not cause the activation of glycosylase.	Hydrogen Peroxide	16-33	P53	Homo sapiens	70-73
14555612-7	2004	Doxorubicin and hydrogen peroxide (H2O2) treatment, although inducing p53 stabilization, did not cause the activation of glycosylase.	Hydrogen Peroxide	35-39	P53	Homo sapiens	70-73
14729643-3	2004	Here, we discovered a novel function of the chemopreventive agent resveratrol: resveratrol is a potent sensitizer of tumor cells for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis through p53-independent induction of p21 and p21-mediated cell cycle arrest associated with survivin depletion.	Resveratrol	79-90	P53	Homo sapiens	223-226
14729645-6	2004	For example, the functionality of the p53-activated pathway appeared positively correlated with the cytotoxicity of all platinum compounds.	Platinum	120-128	P53	Homo sapiens	38-41
15582268-3	2004	In our earlier studies with prostate cancer cells using cDNA microarray analysis, we indicated the importance of p53-mediated molecular targets of resveratrol.	Resveratrol	147-158	P53	Homo sapiens	113-116
12970678-0	2004	p53-independent induction of p21(waf1/cip1) contributes to the activation of caspases in GTP-depletion-induced apoptosis of insulin-secreting cells.	Guanosine Triphosphate	89-92	P53	Homo sapiens	0-3
15603511-1	2004	The p53 protein is an inducible transcription factor with multiple anti-proliferative roles in response to genotoxic damage; unprogrammed proliferative stimuli; and deprivation of oxygen, nutrients, or ribonucleotides.	Oxygen	180-186	P53	Homo sapiens	4-7
14734460-8	2004	TP53 codon 72 Arg/Pro or Pro/Pro variants were associated with negative axillary lymph node status (OR, 0.7; 95% confidence interval, 0.49-0.94).	Arginine	14-17	P53	Homo sapiens	0-4
14734461-5	2004	However, the age-related increase in the percentage of codon 72 arginine p53 was not correlated to the prognosis for gastric cancer patients.	Arginine	64-72	P53	Homo sapiens	73-76
14734461-8	2004	CONCLUSIONS: These findings indicate that codon 72 arginine p53 may not be associated with a prolonged survival in patients with advanced gastric adenocarcinoma, but further study is needed to assess whether this polymorphism is associated with a late onset or slow progress of early gastric adenocarcinoma.	Arginine	51-59	P53	Homo sapiens	60-63
14965474-0	2004	TIAF1 and p53 functionally interact in mediating apoptosis and silencing of TIAF1 abolishes nuclear translocation of serine 15-phosphorylated p53.	Serine	117-123	P53	Homo sapiens	10-13
15581406-5	2004	In primary cultures of mesencephalon, this form of injury is mediated through release of calcium from intracellular stores (CICR), leading to loss of calcium homeostasis, oxidative stress, and activation of the transcription factor NFkappaB and the cell death protein p53.	Calcium	89-96	P53	Homo sapiens	268-271
15581406-5	2004	In primary cultures of mesencephalon, this form of injury is mediated through release of calcium from intracellular stores (CICR), leading to loss of calcium homeostasis, oxidative stress, and activation of the transcription factor NFkappaB and the cell death protein p53.	cicr	124-128	P53	Homo sapiens	268-271
14965474-0	2004	TIAF1 and p53 functionally interact in mediating apoptosis and silencing of TIAF1 abolishes nuclear translocation of serine 15-phosphorylated p53.	Serine	117-123	P53	Homo sapiens	142-145
14584049-5	2004	Exposure of proliferating KCs to UV-light induces post-translational modifications of p53 including acetylation of lysine-382 residues.	Lysine	115-121	P53	Homo sapiens	86-89
14764039-6	2004	The women who had p53 (Arg/Arg), IRF-1 (T/T), and &lt;6 years of education showed a 14.7-fold increased risk of cervix cancer compared to the women who had p53 ( approximately Pro), IRF-1 ( approximately C), and &gt;15 years of education.	Arginine	23-26	P53	Homo sapiens	18-21
14764039-6	2004	The women who had p53 (Arg/Arg), IRF-1 (T/T), and &lt;6 years of education showed a 14.7-fold increased risk of cervix cancer compared to the women who had p53 ( approximately Pro), IRF-1 ( approximately C), and &gt;15 years of education.	Arginine	27-30	P53	Homo sapiens	18-21
14764039-7	2004	The women who had p53 (Arg/Arg), p21 (Ser/Ser), and &gt;3 children showed a 6.4-fold increased risk of cervix cancer compared to the women who had p53 ( approximately Pro), p21 ( approximately Arg), and no children.	Arginine	23-26	P53	Homo sapiens	18-21
14764039-7	2004	The women who had p53 (Arg/Arg), p21 (Ser/Ser), and &gt;3 children showed a 6.4-fold increased risk of cervix cancer compared to the women who had p53 ( approximately Pro), p21 ( approximately Arg), and no children.	Arginine	27-30	P53	Homo sapiens	18-21
14764039-7	2004	The women who had p53 (Arg/Arg), p21 (Ser/Ser), and &gt;3 children showed a 6.4-fold increased risk of cervix cancer compared to the women who had p53 ( approximately Pro), p21 ( approximately Arg), and no children.	Arginine	27-30	P53	Homo sapiens	18-21
14764039-8	2004	The women who had p53 (Arg/Arg), IRF-1 (T/T), and first sexual intercourse before 22 years old showed a 5.5-fold increased risk of cervix cancer compared to the women who had p53 ( approximately Pro), IRF-1 ( approximately C), and first sexual intercourse after 26 years old.	Arginine	23-26	P53	Homo sapiens	18-21
15199542-7	2004	induced p53 accumulation and phosphorylation, particularly at ser-15, via ATM and ATR kinases, which then led to cell cycle arrest at G(2)/M.	Serine	62-65	P53	Homo sapiens	8-11
15053067-4	2004	RESULTS: We observed 14 cases (46.6%) of bcl-2 and four cases (13.3%) of p53 positivity; p53 expression showed an opposite correlation to bcl-2 staining, estrogen and progesterone.	Progesterone	167-179	P53	Homo sapiens	89-92
12827409-8	2004	CONCLUSION: Considering also our own findings, this review presents the latest developments in the scientific discussion of the tumor suppressor/oncogenes p53, k-ras, and DCC, biochemical determinants of the 5-fluorouracil metabolism, and defects of the DNA repair system.	Fluorouracil	208-222	P53	Homo sapiens	155-158
14584049-7	2004	Exposure of KCs to IFN-gamma plus TPA reduced total cellular p53 levels and reduced the transcriptional activity of p53.	Tetradecanoylphorbol Acetate	34-37	P53	Homo sapiens	61-64
14584049-7	2004	Exposure of KCs to IFN-gamma plus TPA reduced total cellular p53 levels and reduced the transcriptional activity of p53.	Tetradecanoylphorbol Acetate	34-37	P53	Homo sapiens	116-119
14584049-9	2004	Pre-treatment of epidermal equivalents with IFN-gamma plus TPA also blocked UV-light induced increase in p53 levels, and reduced apoptosis.	Tetradecanoylphorbol Acetate	59-62	P53	Homo sapiens	105-108
14986171-3	2004	Expression of ALDH4 mRNA was induced in HCT116 cells in response to DNA damage caused by adriamycin treatment, in a p53-dependent manner.	Doxorubicin	89-99	P53	Homo sapiens	116-119
14986171-6	2004	Inhibition of ALDH4 expression by antisense oligonucleotides was able to enhance cell death induced by infection with Ad-p53.	Oligonucleotides	44-60	P53	Homo sapiens	121-124
14986171-9	2004	These results suggest that p53 might play a protective role against cell damage induced by generation of intracellular ROS, through transcriptional activation of ALDH4.	Reactive Oxygen Species	119-122	P53	Homo sapiens	27-30
15539919-0	2004	Prognostic significance of serine 392 phosphorylation in overexpressed p53 protein in human esophageal squamous cell carcinoma.	Serine	27-33	P53	Homo sapiens	71-74
15064503-0	2004	Identification of TP53 mutations in human cancers using oligonucleotide microarrays.	Oligonucleotides	56-71	P53	Homo sapiens	18-22
14525955-5	2004	By using conformation-specific antibodies and immunocytochemistry we found that in bromocriptine-resistant cells p53 adopts a mutant conformation that precludes its nuclear translocation and transcriptional activity.	Bromocriptine	83-96	P53	Homo sapiens	113-116
15520875-10	2004	In addition to the increase of apoptosis rate, the expression of p53 protein, caused by 5-FU was further potentiated by UdR.	Fluorouracil	88-92	P53	Homo sapiens	65-68
15520875-11	2004	CONCLUSION: This study demonstrated a potential novel approach to increase the efficacy of 5-FU by EUdR, which incorporated two complementary molecular actions, the selective modulation of TS inhibition and potentiation of the p53 protein expression, consequently leading to an increase in the apoptotic rate.	Fluorouracil	91-95	P53	Homo sapiens	227-230
14749479-10	2004	We also found that Ad-p53 infection induced phosphorylation of p53 at Ser(46) in p53-sensitive H1299 cells in vitro but not in p53-resistant H226Br cells, suggesting that phosphorylation of Ser(46) is involved in p53-dependent apoptosis.	Serine	70-73	P53	Homo sapiens	22-25
14749479-10	2004	We also found that Ad-p53 infection induced phosphorylation of p53 at Ser(46) in p53-sensitive H1299 cells in vitro but not in p53-resistant H226Br cells, suggesting that phosphorylation of Ser(46) is involved in p53-dependent apoptosis.	Serine	70-73	P53	Homo sapiens	63-66
14749479-10	2004	We also found that Ad-p53 infection induced phosphorylation of p53 at Ser(46) in p53-sensitive H1299 cells in vitro but not in p53-resistant H226Br cells, suggesting that phosphorylation of Ser(46) is involved in p53-dependent apoptosis.	Serine	70-73	P53	Homo sapiens	63-66
14749479-10	2004	We also found that Ad-p53 infection induced phosphorylation of p53 at Ser(46) in p53-sensitive H1299 cells in vitro but not in p53-resistant H226Br cells, suggesting that phosphorylation of Ser(46) is involved in p53-dependent apoptosis.	Serine	70-73	P53	Homo sapiens	63-66
14749479-10	2004	We also found that Ad-p53 infection induced phosphorylation of p53 at Ser(46) in p53-sensitive H1299 cells in vitro but not in p53-resistant H226Br cells, suggesting that phosphorylation of Ser(46) is involved in p53-dependent apoptosis.	Serine	70-73	P53	Homo sapiens	63-66
14749479-10	2004	We also found that Ad-p53 infection induced phosphorylation of p53 at Ser(46) in p53-sensitive H1299 cells in vitro but not in p53-resistant H226Br cells, suggesting that phosphorylation of Ser(46) is involved in p53-dependent apoptosis.	Serine	190-193	P53	Homo sapiens	22-25
14749479-10	2004	We also found that Ad-p53 infection induced phosphorylation of p53 at Ser(46) in p53-sensitive H1299 cells in vitro but not in p53-resistant H226Br cells, suggesting that phosphorylation of Ser(46) is involved in p53-dependent apoptosis.	Serine	190-193	P53	Homo sapiens	63-66
14749479-10	2004	We also found that Ad-p53 infection induced phosphorylation of p53 at Ser(46) in p53-sensitive H1299 cells in vitro but not in p53-resistant H226Br cells, suggesting that phosphorylation of Ser(46) is involved in p53-dependent apoptosis.	Serine	190-193	P53	Homo sapiens	63-66
14749479-10	2004	We also found that Ad-p53 infection induced phosphorylation of p53 at Ser(46) in p53-sensitive H1299 cells in vitro but not in p53-resistant H226Br cells, suggesting that phosphorylation of Ser(46) is involved in p53-dependent apoptosis.	Serine	190-193	P53	Homo sapiens	63-66
14749479-10	2004	We also found that Ad-p53 infection induced phosphorylation of p53 at Ser(46) in p53-sensitive H1299 cells in vitro but not in p53-resistant H226Br cells, suggesting that phosphorylation of Ser(46) is involved in p53-dependent apoptosis.	Serine	190-193	P53	Homo sapiens	63-66
15031599-12	2004	CONCLUSIONS: p53-independent mitochondrial pathways and stress-reaction-induced pathways play critical roles in PTX-induced apoptosis in ovarian cancer cells.	Paclitaxel	112-115	P53	Homo sapiens	13-16
14707723-7	2004	At this time, Cy3-labeled p53-PT-ODN was found in solid tumor formations.	cy3	14-17	P53	Homo sapiens	26-29
14682762-0	2003	Solid-phase synthesis of the cyclic peptide portion of chlorofusin, an inhibitor of p53-MDM2 interactions.	chlorofusin	55-66	P53	Homo sapiens	84-87
15263792-7	2004	The proline form of p53 gene codon 72 was significantly higher than the arginine form, with an odds ratio of 2.606 (95% CI = 1.052-6.455).	Arginine	72-80	P53	Homo sapiens	20-23
15263792-11	2004	The proline form of p53 gene codon 72 might be a more significant risk factor for the development of metastasis than the arginine form.	Arginine	121-129	P53	Homo sapiens	20-23
14660794-5	2003	Mutation was detected by sequence analysis of the p53 gene at codon 155: ACC [Thr] --&gt; CCC [Pro].	Threonine	78-81	P53	Homo sapiens	50-53
17564309-4	2004	Moreover, the detection of p53 in immune complexes is complicated by the presence of comigrating immunoglobulin chains in SDS-polyacrylamide gels.	Sodium Dodecyl Sulfate	122-125	P53	Homo sapiens	27-30
15651660-2	2004	The functional oligonucleotide polymorphism of the p53 gene causes the substitution of arginine (Arg) for praline (Pro) in the codon 72.	Oligonucleotides	15-30	P53	Homo sapiens	51-54
15651660-2	2004	The functional oligonucleotide polymorphism of the p53 gene causes the substitution of arginine (Arg) for praline (Pro) in the codon 72.	Arginine	87-95	P53	Homo sapiens	51-54
15651660-2	2004	The functional oligonucleotide polymorphism of the p53 gene causes the substitution of arginine (Arg) for praline (Pro) in the codon 72.	Arginine	97-100	P53	Homo sapiens	51-54
14695155-2	2003	Importantly, the cytotoxic effects of thymidine deprivation induced by 5-fluorouracil (FUra) combined with leucovorin (LV) was enhanced by IFN-gamma, and the synergism was shown to be dependent on Fas, FUra-induced DNA damage, and independent of p53.	Fluorouracil	71-85	P53	Homo sapiens	246-249
21310133-4	2003	Cisplatin could obviously down-regulate telomerase activity, decrease S phase cells, increase G0/G1 phase cells, decline the expressions of bcl-2 and PCNA proteins and induce the expression of p53 protein of SLC-89 cells in a concentration-dependent fashion.	Cisplatin	0-9	P53	Homo sapiens	193-196
21310133-5	2003	CONCLUSIONS: Cisplatin can obviously inhibit the proliferation of SLC-89, change the distribution of cell cycle, decline telomerase activity and expressions of bcl-2 and PCNA proteins, and induce expression of p53 protein, which may be the important mechanisms of cisplatin"s anticancer action.	Cisplatin	13-22	P53	Homo sapiens	210-213
14661947-3	2003	Interestingly, the Gcn5/PCAF HAT family has a remarkable ability to acetylate lysine residues within diverse cognate sites such as those found around lysines 14, 8, and 320 of histones H3, H4, and p53, respectively.	Lysine	78-84	P53	Homo sapiens	197-200
14661947-3	2003	Interestingly, the Gcn5/PCAF HAT family has a remarkable ability to acetylate lysine residues within diverse cognate sites such as those found around lysines 14, 8, and 320 of histones H3, H4, and p53, respectively.	Lysine	150-157	P53	Homo sapiens	197-200
12967322-0	2003	Ceramide and glutathione define two independently regulated pathways of cell death initiated by p53 in Molt-4 leukaemia cells.	Glutathione	13-24	P53	Homo sapiens	96-99
12967322-4	2003	In a model of irradiation-induced cell death of Molt-4 leukaemia cells, it was found that ceramide accumulation and glutathione depletion were dependent on p53 up-regulation.	Glutathione	116-127	P53	Homo sapiens	156-159
14695155-2	2003	Importantly, the cytotoxic effects of thymidine deprivation induced by 5-fluorouracil (FUra) combined with leucovorin (LV) was enhanced by IFN-gamma, and the synergism was shown to be dependent on Fas, FUra-induced DNA damage, and independent of p53.	Fluorouracil	87-91	P53	Homo sapiens	246-249
14637145-0	2003	Hydrogen peroxide increases a 55-kDa tyrosinase concomitantly with induction of p53-dependent p21 waf1 expression and a greater Bax/Bcl-2 ratio in pigmented melanoma.	Hydrogen Peroxide	0-17	P53	Homo sapiens	80-83
14637145-5	2003	Together, these data suggest that response to hydrogen peroxide involves p53-mediated growth-restrictive signaling and unequal induction of specific DOPA oxidases in melanocytic cells with unequal basal pigmentation.	Hydrogen Peroxide	46-63	P53	Homo sapiens	73-76
14634213-4	2003	We now show that, like dicoumarol, several other coumarin and flavone inhibitors of NQO1 activity, which compete with NAD(P)H for binding to NQO1, induced ubiquitin-independent p53 degradation and inhibited wild-type p53-mediated apoptosis.	flavone	62-69	P53	Homo sapiens	177-180
14634213-7	2003	Further mutational analysis showed that arginines at positions 175 and 248 were essential for dicoumarol-induced p53 degradation.	Arginine	40-49	P53	Homo sapiens	113-116
14634213-4	2003	We now show that, like dicoumarol, several other coumarin and flavone inhibitors of NQO1 activity, which compete with NAD(P)H for binding to NQO1, induced ubiquitin-independent p53 degradation and inhibited wild-type p53-mediated apoptosis.	flavone	62-69	P53	Homo sapiens	217-220
14645705-4	2003	Here, we imaged p53 transcriptional activity in Bax-/- carcinomas by using bioluminescence, in vivo, and find that p53 is required for sensitization to TRAIL by CPT-11.	Irinotecan	161-167	P53	Homo sapiens	115-118
14551737-2	2003	We have used high dose methylprednisolone (HDMP) to treat 25 patients with advanced refractory CLL of whom 45% had p53 abnormalities shown by one or more methods: flow cytometry, fluorescent in situ hybridisation and direct DNA sequencing.	hdmp	43-47	P53	Homo sapiens	115-118
14517211-2	2003	We now report that the p53-dependent G1 checkpoint is blocked in human carcinoma cell lines after inhibition of de novo purine synthesis by folate analogs inhibitory to glycinamide ribonucleotide formyltransferase (GART).	Folic Acid	140-146	P53	Homo sapiens	23-26
14517211-5	2003	The p53 accumulating in these cells was nuclear but was not phosphorylated at serines 6, 15, and 20, nor was it acetylated at lysines 373 or 382.	Lysine	126-133	P53	Homo sapiens	4-7
14695212-0	2003	Induction of PIG3 and NOXA through acetylation of p53 at 320 and 373 lysine residues as a mechanism for apoptotic cell death by histone deacetylase inhibitors.	Lysine	69-75	P53	Homo sapiens	50-53
14695212-3	2003	By Western blotting, using specific antibodies, we then demonstrated that residues 320, 373, and 382 lysines of p53 were acetylated in KATO-III cells transfected with wild-type p53 (KATO-III/p53) treated with a HDAC inhibitor.	Lysine	101-108	P53	Homo sapiens	112-115
14695212-3	2003	By Western blotting, using specific antibodies, we then demonstrated that residues 320, 373, and 382 lysines of p53 were acetylated in KATO-III cells transfected with wild-type p53 (KATO-III/p53) treated with a HDAC inhibitor.	Lysine	101-108	P53	Homo sapiens	177-180
14695212-3	2003	By Western blotting, using specific antibodies, we then demonstrated that residues 320, 373, and 382 lysines of p53 were acetylated in KATO-III cells transfected with wild-type p53 (KATO-III/p53) treated with a HDAC inhibitor.	Lysine	101-108	P53	Homo sapiens	177-180
14551737-15	2003	This study demonstrates that HDMP alone or in combination with other agents is a useful treatment strategy in refractory CLL including patients with p53 abnormalities.	hdmp	29-33	P53	Homo sapiens	149-152
26680985-2	2003	We undertook this study to determine whether the introduction of the wild type p53 gene into GBCE (human gallbladder cancer cell line with a heterozygous p53 mutation) by an adenoviral vector could increase the sensitivity of the cell to 5-FU, a commonly used drug in the treatment of gallbladder cancer.	Fluorouracil	238-242	P53	Homo sapiens	79-82
15033732-9	2003	We observed an increase of cellular p53 after cisplatin (CP) treatment.	Cisplatin	46-55	P53	Homo sapiens	36-39
14662026-0	2003	Leptomycin B enhances CDDP-sensitivity via nuclear accumulation of p53 protein in HPV-positive cells.	Cisplatin	22-26	P53	Homo sapiens	67-70
14662026-2	2003	Because the oncoprotein E6, derived from HPV, inhibits the function of p53 protein, the inhibition of apoptosis via the p53 pathway by HPV may be related to cisplatin (CDDP)-sensitivity in cervical cancer.	Cisplatin	157-166	P53	Homo sapiens	71-74
14662026-2	2003	Because the oncoprotein E6, derived from HPV, inhibits the function of p53 protein, the inhibition of apoptosis via the p53 pathway by HPV may be related to cisplatin (CDDP)-sensitivity in cervical cancer.	Cisplatin	157-166	P53	Homo sapiens	120-123
14662026-2	2003	Because the oncoprotein E6, derived from HPV, inhibits the function of p53 protein, the inhibition of apoptosis via the p53 pathway by HPV may be related to cisplatin (CDDP)-sensitivity in cervical cancer.	Cisplatin	168-172	P53	Homo sapiens	71-74
14662026-2	2003	Because the oncoprotein E6, derived from HPV, inhibits the function of p53 protein, the inhibition of apoptosis via the p53 pathway by HPV may be related to cisplatin (CDDP)-sensitivity in cervical cancer.	Cisplatin	168-172	P53	Homo sapiens	120-123
14751837-6	2003	The antisense oligonucleotides also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel.	Oligonucleotides	14-30	P53	Homo sapiens	63-66
14751837-6	2003	The antisense oligonucleotides also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel.	Doxorubicin	147-157	P53	Homo sapiens	63-66
14751837-6	2003	The antisense oligonucleotides also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel.	Fluorouracil	159-173	P53	Homo sapiens	63-66
14751837-6	2003	The antisense oligonucleotides also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel.	Paclitaxel	179-189	P53	Homo sapiens	63-66
14712316-7	2003	Adding cisplatin to rAAV-p53-infected cells led to a significant growth inhibition between 81 and 91% indicating a synergistic effect between cisplatin and rAAV-p53.	Cisplatin	7-16	P53	Homo sapiens	25-28
14712316-7	2003	Adding cisplatin to rAAV-p53-infected cells led to a significant growth inhibition between 81 and 91% indicating a synergistic effect between cisplatin and rAAV-p53.	Cisplatin	7-16	P53	Homo sapiens	161-164
14712316-7	2003	Adding cisplatin to rAAV-p53-infected cells led to a significant growth inhibition between 81 and 91% indicating a synergistic effect between cisplatin and rAAV-p53.	Cisplatin	142-151	P53	Homo sapiens	25-28
26680985-9	2003	Tumor colony formation was more inhibited with p53 gene transfection than with mock transfection in the presence of 5-FU.	Fluorouracil	116-120	P53	Homo sapiens	47-50
14662026-7	2003	After exposure to LMB or CDDP alone, we observed weak p53 staining in HeLa, SiHa and Yumoto cells.	Cisplatin	25-29	P53	Homo sapiens	54-57
15147044-12	2003	Combined study on the distribution of GSTM1, GSTT1 and p53 genotypes revealed that null GSTM1 genotype was associated with the Arg allele of p53 codon 72 in 58 lung carcinoma cells and null GSTT1 genotype was associated with the Pro/Pro homozygote in 104 tumor cell lines examined.	Arginine	127-130	P53	Homo sapiens	55-58
14662026-8	2003	Nuclear p53 staining was significantly increased by combined treatment with CDDP and LMB in HeLa and SiHa cells, but not in Yumoto cells.	Cisplatin	76-80	P53	Homo sapiens	8-11
14662026-9	2003	The expression of p53 and Bax protein increased with exposure to CDDP and was enhanced by LMB in HeLa and SiHa cells.	Cisplatin	65-69	P53	Homo sapiens	18-21
14662026-10	2003	The present study demonstrated that LMB enhanced CDDP-sensitivity via nuclear accumulation of p53 protein in HPV-positive cells.	Cisplatin	49-53	P53	Homo sapiens	94-97
12962703-1	2003	We had earlier shown that higher concentration of hydrogen peroxide (H(2)O(2)) induced p53-dependent apoptosis in glioma cell line with wild type p53 but had minimal effect on cells with mutated p53.	Hydrogen Peroxide	50-67	P53	Homo sapiens	87-90
12962703-1	2003	We had earlier shown that higher concentration of hydrogen peroxide (H(2)O(2)) induced p53-dependent apoptosis in glioma cell line with wild type p53 but had minimal effect on cells with mutated p53.	Hydrogen Peroxide	50-67	P53	Homo sapiens	146-149
12962703-1	2003	We had earlier shown that higher concentration of hydrogen peroxide (H(2)O(2)) induced p53-dependent apoptosis in glioma cell line with wild type p53 but had minimal effect on cells with mutated p53.	Hydrogen Peroxide	50-67	P53	Homo sapiens	146-149
12962703-1	2003	We had earlier shown that higher concentration of hydrogen peroxide (H(2)O(2)) induced p53-dependent apoptosis in glioma cell line with wild type p53 but had minimal effect on cells with mutated p53.	Hydrogen Peroxide	69-77	P53	Homo sapiens	87-90
12962703-1	2003	We had earlier shown that higher concentration of hydrogen peroxide (H(2)O(2)) induced p53-dependent apoptosis in glioma cell line with wild type p53 but had minimal effect on cells with mutated p53.	Hydrogen Peroxide	69-77	P53	Homo sapiens	146-149
12962703-1	2003	We had earlier shown that higher concentration of hydrogen peroxide (H(2)O(2)) induced p53-dependent apoptosis in glioma cell line with wild type p53 but had minimal effect on cells with mutated p53.	Hydrogen Peroxide	69-77	P53	Homo sapiens	146-149
12962703-3	2003	HA sensitized both p53 wild type and mutated glioma cells to 0.25 mM H(2)O(2).	Water	69-74	P53	Homo sapiens	19-22
12962703-8	2003	The results suggest that higher levels of intracellular ROS, generated by HA+H(2)O(2) act as a molecular switch in activating a rapidly acting p53-independent mitochondrial apoptotic pathway.	Reactive Oxygen Species	56-59	P53	Homo sapiens	143-146
15147044-12	2003	Combined study on the distribution of GSTM1, GSTT1 and p53 genotypes revealed that null GSTM1 genotype was associated with the Arg allele of p53 codon 72 in 58 lung carcinoma cells and null GSTT1 genotype was associated with the Pro/Pro homozygote in 104 tumor cell lines examined.	Arginine	127-130	P53	Homo sapiens	141-144
14513366-10	2003	CONCLUSION: These studies demonstrate that cisplatin and DACH-Ac-Pt differentially phosphorylate p53 through independent DNA damage-induced pathways, and that the kinase-mediated phosphorylation of p53 at Ser-15 or Ser-392 is unaltered in resistance.	Cisplatin	43-52	P53	Homo sapiens	97-100
14513366-0	2003	Status of p53 phosphorylation and function in sensitive and resistant human cancer models exposed to platinum-based DNA damaging agents.	Platinum	101-109	P53	Homo sapiens	10-13
14513366-1	2003	PURPOSE: Resistance to chemotherapeutic drugs is a hallmark of many human cancers, which can occur independent of p53 gene status; however, the presence of wild-type p53 in chemorefractory tumors confers greater resistance to cisplatin, but such tumors do not display complete cross-resistance to the platinum analog (1R,2R-diaminocyclohexane)(trans-diacetato)(dichloro)platinumIV (DACH-Ac-Pt).	Cisplatin	226-235	P53	Homo sapiens	166-169
14513366-10	2003	CONCLUSION: These studies demonstrate that cisplatin and DACH-Ac-Pt differentially phosphorylate p53 through independent DNA damage-induced pathways, and that the kinase-mediated phosphorylation of p53 at Ser-15 or Ser-392 is unaltered in resistance.	Cisplatin	43-52	P53	Homo sapiens	198-201
14513366-1	2003	PURPOSE: Resistance to chemotherapeutic drugs is a hallmark of many human cancers, which can occur independent of p53 gene status; however, the presence of wild-type p53 in chemorefractory tumors confers greater resistance to cisplatin, but such tumors do not display complete cross-resistance to the platinum analog (1R,2R-diaminocyclohexane)(trans-diacetato)(dichloro)platinumIV (DACH-Ac-Pt).	Platinum	301-309	P53	Homo sapiens	166-169
14513366-10	2003	CONCLUSION: These studies demonstrate that cisplatin and DACH-Ac-Pt differentially phosphorylate p53 through independent DNA damage-induced pathways, and that the kinase-mediated phosphorylation of p53 at Ser-15 or Ser-392 is unaltered in resistance.	Serine	205-208	P53	Homo sapiens	198-201
14513366-2	2003	In this article we examine DNA damage-induced phosphorylation of p53 and downstream p53-dependent transactivation events in cisplatin-sensitive and cisplatin-resistant human cancer cell lines possessing wild-type p53.	Cisplatin	124-133	P53	Homo sapiens	65-68
14513366-2	2003	In this article we examine DNA damage-induced phosphorylation of p53 and downstream p53-dependent transactivation events in cisplatin-sensitive and cisplatin-resistant human cancer cell lines possessing wild-type p53.	Cisplatin	124-133	P53	Homo sapiens	84-87
14513366-10	2003	CONCLUSION: These studies demonstrate that cisplatin and DACH-Ac-Pt differentially phosphorylate p53 through independent DNA damage-induced pathways, and that the kinase-mediated phosphorylation of p53 at Ser-15 or Ser-392 is unaltered in resistance.	Serine	215-218	P53	Homo sapiens	198-201
14513366-2	2003	In this article we examine DNA damage-induced phosphorylation of p53 and downstream p53-dependent transactivation events in cisplatin-sensitive and cisplatin-resistant human cancer cell lines possessing wild-type p53.	Cisplatin	124-133	P53	Homo sapiens	84-87
14513366-2	2003	In this article we examine DNA damage-induced phosphorylation of p53 and downstream p53-dependent transactivation events in cisplatin-sensitive and cisplatin-resistant human cancer cell lines possessing wild-type p53.	Cisplatin	148-157	P53	Homo sapiens	65-68
14675203-0	2003	p53 codon 72 Arg homozygotes are associated with an increased risk of cutaneous melanoma.	Arginine	13-16	P53	Homo sapiens	0-3
14513366-2	2003	In this article we examine DNA damage-induced phosphorylation of p53 and downstream p53-dependent transactivation events in cisplatin-sensitive and cisplatin-resistant human cancer cell lines possessing wild-type p53.	Cisplatin	148-157	P53	Homo sapiens	84-87
14513366-2	2003	In this article we examine DNA damage-induced phosphorylation of p53 and downstream p53-dependent transactivation events in cisplatin-sensitive and cisplatin-resistant human cancer cell lines possessing wild-type p53.	Cisplatin	148-157	P53	Homo sapiens	84-87
14513366-3	2003	METHODS: Western-blot analysis was utilized to study the effect of cisplatin and the analog on p53 phosphorylation and p53-dependent target genes.	Cisplatin	67-76	P53	Homo sapiens	95-98
14513366-3	2003	METHODS: Western-blot analysis was utilized to study the effect of cisplatin and the analog on p53 phosphorylation and p53-dependent target genes.	Cisplatin	67-76	P53	Homo sapiens	119-122
14513366-4	2003	RESULTS: In response to CDDP and DACH-Ac-Pt, both CDDP-sensitive and CDDP-resistant models demonstrated time- and dose-dependent inductions of total p53 protein and an increase in Ser-15 phosphorylation, which was more pronounced with CDDP.	cddp	24-28	P53	Homo sapiens	149-152
14513366-4	2003	RESULTS: In response to CDDP and DACH-Ac-Pt, both CDDP-sensitive and CDDP-resistant models demonstrated time- and dose-dependent inductions of total p53 protein and an increase in Ser-15 phosphorylation, which was more pronounced with CDDP.	cddp	50-54	P53	Homo sapiens	149-152
14513366-4	2003	RESULTS: In response to CDDP and DACH-Ac-Pt, both CDDP-sensitive and CDDP-resistant models demonstrated time- and dose-dependent inductions of total p53 protein and an increase in Ser-15 phosphorylation, which was more pronounced with CDDP.	cddp	50-54	P53	Homo sapiens	149-152
14513366-4	2003	RESULTS: In response to CDDP and DACH-Ac-Pt, both CDDP-sensitive and CDDP-resistant models demonstrated time- and dose-dependent inductions of total p53 protein and an increase in Ser-15 phosphorylation, which was more pronounced with CDDP.	cddp	50-54	P53	Homo sapiens	149-152
14513366-5	2003	Although phosphorylation of p53 at Ser-392 was also observed in CDDP-treated sensitive and resistant cells, it was weak or absent in response to DACH-Ac-Pt.	Serine	35-38	P53	Homo sapiens	28-31
14513366-5	2003	Although phosphorylation of p53 at Ser-392 was also observed in CDDP-treated sensitive and resistant cells, it was weak or absent in response to DACH-Ac-Pt.	cddp	64-68	P53	Homo sapiens	28-31
14675203-6	2003	The frequency of the p53 Arg allele was 78.2% in cases and 73.2% in controls (p=0.045), and the genotype frequencies of p53 Arg/Arg, Arg/Pro, and Pro/Pro were 62.6%, 31.1%, and 6.3%, respectively, in the cases, and 53.9%, 38.6%, and 7.5%, respectively, in the controls (p=0.096).	Arginine	25-28	P53	Homo sapiens	21-24
14675203-7	2003	Logistic regression analysis revealed that the p53 Arg/Arg genotype was associated with a significantly increased risk of melanoma (adjusted odds ratio (OR)=1.43; 95% confidence interval (CI)=1.02-2.02) compared with other genotypes, and this association was more evident in subgroups of older subjects (OR=2.32; 95% CI=1.39-388), and subjects with Fitzpatrick"s skin type III or IV (OR=1.69; 95% CI=1.11-2.59).	Arginine	51-54	P53	Homo sapiens	47-50
14675203-7	2003	Logistic regression analysis revealed that the p53 Arg/Arg genotype was associated with a significantly increased risk of melanoma (adjusted odds ratio (OR)=1.43; 95% confidence interval (CI)=1.02-2.02) compared with other genotypes, and this association was more evident in subgroups of older subjects (OR=2.32; 95% CI=1.39-388), and subjects with Fitzpatrick"s skin type III or IV (OR=1.69; 95% CI=1.11-2.59).	Arginine	55-58	P53	Homo sapiens	47-50
14675203-8	2003	In conclusion, this study found some evidence that in subjects over 50, p53 Arg/Arg genotype is associated with increased risk of CM as compared to genotypes Arg/Pro or Pro/Pro.	Arginine	76-79	P53	Homo sapiens	72-75
14675203-8	2003	In conclusion, this study found some evidence that in subjects over 50, p53 Arg/Arg genotype is associated with increased risk of CM as compared to genotypes Arg/Pro or Pro/Pro.	Arginine	80-83	P53	Homo sapiens	72-75
14675203-8	2003	In conclusion, this study found some evidence that in subjects over 50, p53 Arg/Arg genotype is associated with increased risk of CM as compared to genotypes Arg/Pro or Pro/Pro.	Arginine	80-83	P53	Homo sapiens	72-75
14986813-6	2003	Hepatocyte necrosis and regeneration and the generation of oxygen and nitrogen reactive species resulting from chronic HBV infection increase the likelihood of the AFB1-induced p53 249ser and other mutations and the subsequent clonal expansion of cells containing these mutations.	Oxygen	59-65	P53	Homo sapiens	177-180
14617104-5	2003	The effect of AGI-1140 and UVB on phosphorylation of p53 serine 15 in human keratinocytes was examined by Western blotting, while the release of tumor necrosis factor-alpha (TNF-alpha) and prostaglandin E2 (PGE2) was determined by enzyme-linked immunosorbent assay.	Dinoprostone	207-211	P53	Homo sapiens	53-56
14674700-4	2003	In both cell types, treatment of hypoxic cells with a reversible selective iNOs inhibitor, Now-nitro-L-arginine (LNNA), blocked iNOs, Bcl-2, and HSP-70 mRNA, but increased p53.	now-nitro-l-arginine	91-111	P53	Homo sapiens	172-175
14617104-5	2003	The effect of AGI-1140 and UVB on phosphorylation of p53 serine 15 in human keratinocytes was examined by Western blotting, while the release of tumor necrosis factor-alpha (TNF-alpha) and prostaglandin E2 (PGE2) was determined by enzyme-linked immunosorbent assay.	Serine	57-63	P53	Homo sapiens	53-56
14617104-9	2003	However, whereas UVB induced G2 cell cycle arrest with phosphorylation of p53 at serine 15, AGI-1140 induced G1 cell cycle arrest without this phosphorylation.	Serine	81-87	P53	Homo sapiens	74-77
14506283-5	2003	Tryptophan fluorescence assays showed that an EBNA1 peptide mapping to residues 395-450 was sufficient to bind the USP7 N-terminal domain and did so with a dissociation constant of 0.9-2 microM, whereas p53 peptides spanning the USP7-binding region gave dissociation constants of 9-17 microM in the same assay.	Tryptophan	0-10	P53	Homo sapiens	203-206
14703431-1	2003	OBJECTIVE: To investigate the relationship between apoptosis induced by CD3epsilon and 5-fluorouracil (5-FU), and study the P53 expression in the apoptosis process provide a novel insight and useful information of the apoptosis signaling pathway induced by CD3epsilon and/or 5-FU, and an important implication for the treatment of T-lymphocyte leukemia.	Fluorouracil	275-279	P53	Homo sapiens	124-127
14703431-5	2003	RESULTS: CD3epsilon or 5-FU induced apoptosis of TJK with increase of P53 expression.	Fluorouracil	23-27	P53	Homo sapiens	70-73
14703431-6	2003	Co-treatment with CD3epsilon specific antibody and 5-FU elevated the apoptotic rates and P53 expression in TJK cells remarkably.	Fluorouracil	51-55	P53	Homo sapiens	89-92
14703431-7	2003	The cells transfected with wild-type p53 exhibited more sensitivity to 5-FU than that transfected with mutant p53.	Fluorouracil	71-75	P53	Homo sapiens	37-40
14703431-8	2003	CONCLUSION: Co-treatment of CD3epsilon and 5-FU increases the apoptosis and p53 expression, suggesting that there is a synergetic role of CD3epsilon and 5-FU on T lymphocytes.	Fluorouracil	43-47	P53	Homo sapiens	76-79
14703431-8	2003	CONCLUSION: Co-treatment of CD3epsilon and 5-FU increases the apoptosis and p53 expression, suggesting that there is a synergetic role of CD3epsilon and 5-FU on T lymphocytes.	Fluorouracil	153-157	P53	Homo sapiens	76-79
14654539-0	2003	TP53 gene mutations predict the response to neoadjuvant treatment with 5-fluorouracil and mitomycin in locally advanced breast cancer.	Fluorouracil	71-85	P53	Homo sapiens	0-4
14633737-9	2003	Treatment with Let, Tam, or E2W resulted in a dose- and time-dependent increase in active caspase-7 and up-regulation of p53 and p21 protein.	Tamoxifen	20-23	P53	Homo sapiens	121-124
14654539-1	2003	PURPOSE: Recent studies have found an association between certain TP53 mutations and resistance to anthracycline-based primary medical therapy in breast cancer.	Anthracyclines	99-112	P53	Homo sapiens	66-70
14654539-2	2003	The purpose of this study was to investigate whether TP53 mutational status also might influence the response to a non-anthracycline-containing regimen in primary breast cancer.	Anthracyclines	119-132	P53	Homo sapiens	53-57
14654539-6	2003	CONCLUSION: This study revealed a significant association between lack of response to 5-fluorouracil and mitomycin and mutations affecting the L2/L3 domains of the p53 protein.	Fluorouracil	86-100	P53	Homo sapiens	164-167
14654539-7	2003	Together with our previous finding that such mutations predict resistance to weekly doxorubicin, our data suggest that mutations affecting this particular domain of the p53 protein may cause resistance to several different cytotoxic compounds applied in breast cancer treatment.	Doxorubicin	84-95	P53	Homo sapiens	169-172
14595027-4	2003	Fl-CDB3 was taken up into the cytoplasm and nucleus and induced a substantial up-regulation of wild-type p53 protein and representative mutants.	fl-cdb3	0-7	P53	Homo sapiens	105-108
14592451-0	2003	Profound negative regulatory effects by resveratrol on vascular smooth muscle cells: a role of p53-p21(WAF1/CIP1) pathway.	Resveratrol	40-51	P53	Homo sapiens	95-98
14592451-5	2003	Resveratrol caused a dose-dependent increase in intracellular p53 and p21(WAF1/CIP1) levels.	Resveratrol	0-11	P53	Homo sapiens	62-65
14595027-5	2003	The mutants, His-273 and His-175 p53, adopted the active conformation, with a dramatic decrease in the fraction of denatured protein.	Histidine	25-28	P53	Homo sapiens	33-36
14595027-7	2003	Fl-CDB3 sensitized cancer cells that carried wild-type p53 to p53-dependent gamma-radiation-induced apoptosis.	fl-cdb3	0-7	P53	Homo sapiens	55-58
14595027-7	2003	Fl-CDB3 sensitized cancer cells that carried wild-type p53 to p53-dependent gamma-radiation-induced apoptosis.	fl-cdb3	0-7	P53	Homo sapiens	62-65
14595027-8	2003	Although Fl-CDB3 did not elicit a full biological response, it did bind to and rescue p53 in cells and so can serve as a lead for the development of novel drugs for anticancer therapy.	fl-cdb3	9-16	P53	Homo sapiens	86-89
14598320-7	2003	Conversely, DNA damage-induced reactive oxygen species generation was inhibited significantly by gene disruption of p53, Apaf-1, or caspase-9, and combined deficiency of Bax and Bak, but not by caspase-3 or caspase-6 deficiency.	Reactive Oxygen Species	31-54	P53	Homo sapiens	116-119
14603254-4	2003	To further evaluate the link between IkBm and sensitivity to Dox and VCR, we demonstrated that both endogenous IkBalpha and ectopic IkBm bind to p53.	Doxorubicin	61-64	P53	Homo sapiens	145-148
14603254-5	2003	In response to Dox, the cytosolic p53.IkBalpha complex rapidly dissociated due to downregulation of IkBalpha.	Doxorubicin	15-18	P53	Homo sapiens	34-37
14603254-7	2003	Although treatment of EU-1/IkBm cells with Dox increased the expression of p53, the nondissociating p53.IkBm complex resulted in decreased p53 function, as demonstrated by absence of cell-cycle arrest and induction of p53 target genes.	Doxorubicin	43-46	P53	Homo sapiens	75-78
14603254-7	2003	Although treatment of EU-1/IkBm cells with Dox increased the expression of p53, the nondissociating p53.IkBm complex resulted in decreased p53 function, as demonstrated by absence of cell-cycle arrest and induction of p53 target genes.	Doxorubicin	43-46	P53	Homo sapiens	100-103
14603254-7	2003	Although treatment of EU-1/IkBm cells with Dox increased the expression of p53, the nondissociating p53.IkBm complex resulted in decreased p53 function, as demonstrated by absence of cell-cycle arrest and induction of p53 target genes.	Doxorubicin	43-46	P53	Homo sapiens	100-103
14603254-7	2003	Although treatment of EU-1/IkBm cells with Dox increased the expression of p53, the nondissociating p53.IkBm complex resulted in decreased p53 function, as demonstrated by absence of cell-cycle arrest and induction of p53 target genes.	Doxorubicin	43-46	P53	Homo sapiens	100-103
14981901-6	2003	Only one tumour, which previously had shown expression and mutation in the p53, had a point mutation at codon 117 of exon 2 of the p21 gene with a resulting Cys--&gt;Tyr amino acid substitution.	Cysteine	157-160	P53	Homo sapiens	75-78
14612499-1	2003	We established previously that X-linked inhibitor of apoptosis protein (Xiap) is a determinant of cisplatin (CDDP) resistance in human ovarian cancer cells and that down-regulation of Xiap sensitizes cells to CDDP in the presence of wild-type p53.	Cisplatin	98-107	P53	Homo sapiens	243-246
14612499-1	2003	We established previously that X-linked inhibitor of apoptosis protein (Xiap) is a determinant of cisplatin (CDDP) resistance in human ovarian cancer cells and that down-regulation of Xiap sensitizes cells to CDDP in the presence of wild-type p53.	Cisplatin	109-113	P53	Homo sapiens	243-246
14612499-1	2003	We established previously that X-linked inhibitor of apoptosis protein (Xiap) is a determinant of cisplatin (CDDP) resistance in human ovarian cancer cells and that down-regulation of Xiap sensitizes cells to CDDP in the presence of wild-type p53.	Cisplatin	209-213	P53	Homo sapiens	243-246
14612499-5	2003	Furthermore, dominant-negative Akt sensitizes ovarian cancer cells to CDDP (10 micro M), an effect that is absent in cells expressing mutant p53 or treated with the p53 inhibitor pifithrin-alpha-hydrobromide (30 micro M) but restored by exogenous wild-type p53.	Cisplatin	70-74	P53	Homo sapiens	165-168
14612499-5	2003	Furthermore, dominant-negative Akt sensitizes ovarian cancer cells to CDDP (10 micro M), an effect that is absent in cells expressing mutant p53 or treated with the p53 inhibitor pifithrin-alpha-hydrobromide (30 micro M) but restored by exogenous wild-type p53.	Cisplatin	70-74	P53	Homo sapiens	165-168
14612499-5	2003	Furthermore, dominant-negative Akt sensitizes ovarian cancer cells to CDDP (10 micro M), an effect that is absent in cells expressing mutant p53 or treated with the p53 inhibitor pifithrin-alpha-hydrobromide (30 micro M) but restored by exogenous wild-type p53.	pifithrin-alpha-hydrobromide	179-207	P53	Homo sapiens	165-168
14612499-5	2003	Furthermore, dominant-negative Akt sensitizes ovarian cancer cells to CDDP (10 micro M), an effect that is absent in cells expressing mutant p53 or treated with the p53 inhibitor pifithrin-alpha-hydrobromide (30 micro M) but restored by exogenous wild-type p53.	pifithrin-alpha-hydrobromide	179-207	P53	Homo sapiens	165-168
14612499-6	2003	CDDP increased p53, decreased Xiap content, and induced apoptosis in OV2008 cells but not in the resistant counterpart (C13*).	Cisplatin	0-4	P53	Homo sapiens	15-18
14612499-10	2003	These results suggest that whereas Xiap, Akt2, and p53 are important mediators of chemoresistance in ovarian cancer cells, Akt2 may be an important regulator of both Xiap and p53 contents after CDDP challenge.	Cisplatin	194-198	P53	Homo sapiens	175-178
14675321-2	2003	Studies have suggested that steroid hormones may enhance the expression of these genes leading to loss of p53 gene-mediated cell apoptosis.	Steroids	28-44	P53	Homo sapiens	106-109
14608092-0	2003	Conjugated linoleic acid inhibits cell proliferation through a p53-dependent mechanism: effects on the expression of G1-restriction points in breast and colon cancer cells.	Linoleic Acid	11-24	P53	Homo sapiens	63-66
12925958-12	2003	These results suggest that HCV NS5A as a Bcl-2 homologue interacts with Bax to protect p53-negative HCC cells from NaPB-induced apoptosis.	4-phenylbutylamine	115-119	P53	Homo sapiens	87-90
14534679-8	2003	Mechanisms explaining cisplatin resistance include the reduction in cisplatin accumulation inside cancer cells because of barriers across the cell membrane, the faster repair of cisplatin adducts, the modulation of apoptotic pathways in various cells, the upregulation in transcription factors, the loss of p53 and other protein functions and a higher concentration of glutathione and metallothioneins in some type of tumors.	Cisplatin	22-31	P53	Homo sapiens	307-310
14534679-9	2003	A number of experimental strategies to overcome cisplatin resistance are at the preclinical or clinical level such as introduction of the bax gene, inhibition of the JNK pathway, introduction of a functional p53 gene, treatment of tumors with aldose reductase inhibitors and others.	Cisplatin	48-57	P53	Homo sapiens	208-211
14693272-7	2003	To determine whether cisplatin increases sensitivity of J82 cells to Ad5CMV-p53, we performed median effect analysis for cisplatin combined with Ad5CMV-p53 or DL312.	Cisplatin	21-30	P53	Homo sapiens	76-79
14572637-8	2003	In adriamycin-treated cells, p53 was stabilized and induced the expression of p21(CIP1/WAF1), but the expression of ING1b was not affected.	Doxorubicin	3-13	P53	Homo sapiens	29-32
14693272-0	2003	Adenoviral p53 gene transfer in human bladder cancer cell lines: cytotoxicity and synergy with cisplatin.	Cisplatin	95-104	P53	Homo sapiens	11-14
14555213-1	2003	Glucocorticoids (GC) such as hydrocortisone and dexamethasone (DEX) protect steroidogenic granulosa cells against apoptosis induced by serum deprivation, cAMP, tumor necrosis factor alpha stimulation or p53 activation.	Hydrocortisone	29-43	P53	Homo sapiens	203-206
14562046-4	2003	In cells responding to cisplatin, although p53 is stabilized and activated, EBV latent gene expression appears to inhibit the accumulation of newly synthesized p21(WAF1/CIP1) and the downregulation of cyclin D2 that occur in the normal cells.	Cisplatin	23-32	P53	Homo sapiens	43-46
14555213-1	2003	Glucocorticoids (GC) such as hydrocortisone and dexamethasone (DEX) protect steroidogenic granulosa cells against apoptosis induced by serum deprivation, cAMP, tumor necrosis factor alpha stimulation or p53 activation.	Dexamethasone	48-61	P53	Homo sapiens	203-206
14555213-1	2003	Glucocorticoids (GC) such as hydrocortisone and dexamethasone (DEX) protect steroidogenic granulosa cells against apoptosis induced by serum deprivation, cAMP, tumor necrosis factor alpha stimulation or p53 activation.	Dexamethasone	63-66	P53	Homo sapiens	203-206
14583461-9	2003	Conversely, phosphorylation of serine 10 (S10P) is elevated in p53-/- cells and reduced after UV plus TSA treatment.	Serine	31-37	P53	Homo sapiens	63-66
14581358-0	2003	Retention of the p53 codon 72 arginine allele is associated with a reduction of disease-free and overall survival in arginine/proline heterozygous breast cancer patients.	Arginine	30-38	P53	Homo sapiens	17-20
14581358-0	2003	Retention of the p53 codon 72 arginine allele is associated with a reduction of disease-free and overall survival in arginine/proline heterozygous breast cancer patients.	Arginine	117-125	P53	Homo sapiens	17-20
14581358-5	2003	RESULTS: We found that the retention of the p53 codon 72 arginine allele in the tumor tissue of proline/arginine heterozygous breast cancer patients is associated with statistically significant reduced disease-free and overall survivals.	Arginine	57-65	P53	Homo sapiens	44-47
14581358-5	2003	RESULTS: We found that the retention of the p53 codon 72 arginine allele in the tumor tissue of proline/arginine heterozygous breast cancer patients is associated with statistically significant reduced disease-free and overall survivals.	Arginine	104-112	P53	Homo sapiens	44-47
14581358-6	2003	CONCLUSIONS: Our findings suggest that the genotyping for p53 codon 72 locus in both the tumor tissue and in the lymph node of breast cancer patients could contribute to identify a subset of arginine/proline heterozygous patients who have a reduced survival that is associated with the specific retention of the arginine allele in the tumor tissue.	Arginine	191-199	P53	Homo sapiens	58-61
14581358-6	2003	CONCLUSIONS: Our findings suggest that the genotyping for p53 codon 72 locus in both the tumor tissue and in the lymph node of breast cancer patients could contribute to identify a subset of arginine/proline heterozygous patients who have a reduced survival that is associated with the specific retention of the arginine allele in the tumor tissue.	Arginine	312-320	P53	Homo sapiens	58-61
14583461-11	2003	Abnormal S10P in p53-/- cells was also observed under completely different experimental conditions where cells were treated with nocodazole to induce G(2)-M arrest and elevation of S10P (which is linked with G(2)-M of the cell cycle).	Nocodazole	129-139	P53	Homo sapiens	17-20
14583461-0	2003	Loss of p53 has site-specific effects on histone H3 modification, including serine 10 phosphorylation important for maintenance of ploidy.	Serine	76-82	P53	Homo sapiens	8-11
14583461-12	2003	On removal of nocodazole, the p53+/+ cells exhibited rapid reduction in S10P levels and cell cycle recovery.	Nocodazole	14-24	P53	Homo sapiens	30-33
14583461-7	2003	We provide evidence that p53 influences histone H3 acetylation at lysine 9 (K9) and K14, whereas acetylation of K18 appears to be p53 independent.	Lysine	66-72	P53	Homo sapiens	25-28
12890678-6	2003	Similarly, p53 activation by H2O2 was inhibited by kinase-inactive forms of the PDGF beta receptor or ATM.	Hydrogen Peroxide	29-33	P53	Homo sapiens	11-14
12890678-9	2003	Thus, these data link PDGF beta receptor transactivation to H2O2-induced p53 phosphorylation and suggest a functional role for growth factor receptors in modulation of p53 function.	Hydrogen Peroxide	60-64	P53	Homo sapiens	73-76
12890678-3	2003	In response to H2O2, we observed phosphorylation of p53 specifically at serine 15, but not serine 9, 20, or 392.	Hydrogen Peroxide	15-19	P53	Homo sapiens	52-55
12844488-8	2003	However, the p53 mutation frequency increased with the increased number of the combined genotypes among XPD 312WT (Asp/Asp), XPD 751VT (Lys/Gln or Gln/Gln) or XRCC1 399VT (Arg/Gln or Gln/Gln) (P = 0.01, trend test).	Lysine	136-139	P53	Homo sapiens	13-16
12890678-3	2003	In response to H2O2, we observed phosphorylation of p53 specifically at serine 15, but not serine 9, 20, or 392.	Serine	72-78	P53	Homo sapiens	52-55
12890678-4	2003	Phosphorylation of Ser-15 was correlated with enhanced induction and functional activation of p53 manifest as transcription of the p53 target p21CIP/WAF.	Serine	19-22	P53	Homo sapiens	94-97
12890678-4	2003	Phosphorylation of Ser-15 was correlated with enhanced induction and functional activation of p53 manifest as transcription of the p53 target p21CIP/WAF.	Serine	19-22	P53	Homo sapiens	131-134
12890678-5	2003	We found that H2O2 induced phosphorylation of the PDGF beta receptor and increased ATM kinase activity, two events integral to p53 activation as either AG1433 (a PDGF beta receptor inhibitor) or caffeine (an ATM kinase inhibitor) inhibited Ser-15 phosphorylation.	Hydrogen Peroxide	14-18	P53	Homo sapiens	127-130
12869419-0	2003	The effect of potent iron chelators on the regulation of p53: examination of the expression, localization and DNA-binding activity of p53 and the transactivation of WAF1.	Iron	21-25	P53	Homo sapiens	57-60
14580323-0	2003	Formation of disulfide bond in p53 correlates with inhibition of DNA binding and tetramerization.	Disulfides	13-22	P53	Homo sapiens	31-34
14580323-2	2003	The goal of the current research was to determine the nature of the cysteine residue thiol oxidation that prevents p53 from binding its DNA target and its effect on p53 structure.	Cysteine	68-76	P53	Homo sapiens	115-118
14580323-2	2003	The goal of the current research was to determine the nature of the cysteine residue thiol oxidation that prevents p53 from binding its DNA target and its effect on p53 structure.	Cysteine	68-76	P53	Homo sapiens	165-168
14580323-2	2003	The goal of the current research was to determine the nature of the cysteine residue thiol oxidation that prevents p53 from binding its DNA target and its effect on p53 structure.	Sulfhydryl Compounds	85-90	P53	Homo sapiens	115-118
14580323-2	2003	The goal of the current research was to determine the nature of the cysteine residue thiol oxidation that prevents p53 from binding its DNA target and its effect on p53 structure.	Sulfhydryl Compounds	85-90	P53	Homo sapiens	165-168
14580323-3	2003	Recombinant p53, purified in the presence of the reducing agent dithiothreitol (DTT), contains five free thiol groups on the surface of the protein.	Sulfhydryl Compounds	105-110	P53	Homo sapiens	12-15
14580323-4	2003	In the absence of DTT, p53 contains only four thiol groups, indicating that an average of one surface thiol group is readily susceptible to oxidation.	Sulfhydryl Compounds	46-51	P53	Homo sapiens	23-26
14580323-4	2003	In the absence of DTT, p53 contains only four thiol groups, indicating that an average of one surface thiol group is readily susceptible to oxidation.	Sulfhydryl Compounds	102-107	P53	Homo sapiens	23-26
14580323-5	2003	Sulfite-mediated disulfide bond cleavage followed by reaction with 2-nitro-5-thiosulfobenzoate showed that oxidized p53 contains a single disulfide bond per monomer.	Sulfites	0-7	P53	Homo sapiens	116-119
14580323-5	2003	Sulfite-mediated disulfide bond cleavage followed by reaction with 2-nitro-5-thiosulfobenzoate showed that oxidized p53 contains a single disulfide bond per monomer.	Disulfides	17-26	P53	Homo sapiens	116-119
14580323-5	2003	Sulfite-mediated disulfide bond cleavage followed by reaction with 2-nitro-5-thiosulfobenzoate showed that oxidized p53 contains a single disulfide bond per monomer.	Disulfides	138-147	P53	Homo sapiens	116-119
14580323-10	2003	The possibility that oxidized p53 contained significant amounts of sulfenic (-SOH), sulfinic (-SO2H), or sulfonic acid (-SO3H) was ruled out.	sulfinic	84-92	P53	Homo sapiens	30-33
12869419-0	2003	The effect of potent iron chelators on the regulation of p53: examination of the expression, localization and DNA-binding activity of p53 and the transactivation of WAF1.	Iron	21-25	P53	Homo sapiens	134-137
12869419-10	2003	Our experiments demonstrated: (i) that the elevated WAF1 mRNA expression after Fe chelation was due to increased transcription and also to a post-transcriptional mechanism that was sensitive to cycloheximide; and (ii) that Fe-chelation increased WAF1 expression through a p53-independent pathway.	Iron	79-81	P53	Homo sapiens	272-275
12844488-8	2003	However, the p53 mutation frequency increased with the increased number of the combined genotypes among XPD 312WT (Asp/Asp), XPD 751VT (Lys/Gln or Gln/Gln) or XRCC1 399VT (Arg/Gln or Gln/Gln) (P = 0.01, trend test).	Arginine	172-175	P53	Homo sapiens	13-16
14619538-2	2003	HCT116 had wild-type p53 expression and 5-fluorouracil (5-FU) in combination with cisplatinum (CDDP) increased both Sub G1 DNA content and the proportion of apoptotic cells.	Cisplatin	95-99	P53	Homo sapiens	21-24
14559799-1	2003	Ferredoxin reductase (FDXR) is a putative contributor to TP53-mediated apoptosis from 5-fluorouracil chemotherapy through the generation of oxidative stress.	Fluorouracil	86-100	P53	Homo sapiens	57-61
14559802-10	2003	Progressive telomere shortening leading to growth inhibition and cell death in MM.1S cells was associated with up-regulation of p21 and phosphorylation of p53 (Ser-15).	Serine	160-163	P53	Homo sapiens	155-158
14511359-0	2003	Activation of p53 signalling in acetylsalicylic acid-induced apoptosis in OC2 human oral cancer cells.	Aspirin	32-52	P53	Homo sapiens	14-17
14511359-2	2003	The aim of this study was to investigate the possible existence of a putative p53-dependent pathway underlying the ASA-induced apoptosis in OC2 cells, a human oral cancer cell line.	Aspirin	115-118	P53	Homo sapiens	78-81
14511359-10	2003	In the meanwhile, phosphorylation of p53 at serine 15, accumulation of p53 and increased the expression of its downstream target genes, p21 and Bax induced by ASA.	Serine	44-50	P53	Homo sapiens	37-40
14511359-10	2003	In the meanwhile, phosphorylation of p53 at serine 15, accumulation of p53 and increased the expression of its downstream target genes, p21 and Bax induced by ASA.	Aspirin	159-162	P53	Homo sapiens	37-40
14511359-10	2003	In the meanwhile, phosphorylation of p53 at serine 15, accumulation of p53 and increased the expression of its downstream target genes, p21 and Bax induced by ASA.	Aspirin	159-162	P53	Homo sapiens	71-74
14511359-13	2003	Inhibited the activation of p42/p44 mitogen-activated protein kinase (MAPK) by PD98059, a specific inhibitor of extracellular regulatory kinase (ERK), significantly decreased cell viability and enhanced the expression of p53 induced by ASA.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	79-86	P53	Homo sapiens	221-224
14511359-13	2003	Inhibited the activation of p42/p44 mitogen-activated protein kinase (MAPK) by PD98059, a specific inhibitor of extracellular regulatory kinase (ERK), significantly decreased cell viability and enhanced the expression of p53 induced by ASA.	Aspirin	236-239	P53	Homo sapiens	221-224
14511359-16	2003	Our study presents evidences that activation of p53 signalling involved in apoptosis induced by ASA.	Aspirin	96-99	P53	Homo sapiens	48-51
14619538-5	2003	These results indicate that the type of p53 expression might play an important role in the determination of response to low-dose CDDP + 5-FU therapy in colon cancer patients.	Cisplatin	129-133	P53	Homo sapiens	40-43
14619538-5	2003	These results indicate that the type of p53 expression might play an important role in the determination of response to low-dose CDDP + 5-FU therapy in colon cancer patients.	Fluorouracil	136-140	P53	Homo sapiens	40-43
14577584-0	2003	Polymorphism of the p53 codon 72 Arg/Pro and the risk of HPV type 16/18-associated cervical and oral cancer in India.	Arginine	33-36	P53	Homo sapiens	20-23
14507860-0	2003	Vitamin D analogues increase p53, p21, and apoptosis in a xenograft model of human retinoblastoma.	Vitamin D	0-9	P53	Homo sapiens	29-32
14507860-12	2003	There was an increase in staining for p53 and p21 in areas associated with cell death in specimens treated with vitamin D analogues.	Vitamin D	112-121	P53	Homo sapiens	38-41
14529565-0	2003	Overexpression of wild-type p53 gene renders MCF-7 breast cancer cells more sensitive to the antiproliferative effect of progesterone.	Progesterone	121-133	P53	Homo sapiens	28-31
14529565-2	2003	Because the tumor suppressor protein p53 plays a central role in normal cell growth and in tumor suppression, we have examined the effect of progesterone on the levels of this protein in MCF-7 cells.	Progesterone	141-153	P53	Homo sapiens	37-40
14529565-7	2003	We show here that progesterone significantly enhances growth inhibition and apoptosis in MCF-7 cells overexpressing p53, but not in cells transfected with the control vector.	Progesterone	18-30	P53	Homo sapiens	116-119
14529565-8	2003	These data suggest that re-establishing p53 function in MCF-7 breast cancer cells renders them more sensitive to the growth inhibitory effect of progesterone.	Progesterone	145-157	P53	Homo sapiens	40-43
14517281-7	2003	We found that 14-3-3 sigma interacted with p53 in response to the DNA-damaging agent adriamycin.	Doxorubicin	85-95	P53	Homo sapiens	43-46
12963997-4	2003	This anti-proliferative effect of resveratrol was associated with a marked inhibition of the phosphorylation of the retinoblastoma protein (pRB) and concomitant induction of cyclin-dependent kinase (Cdk) inhibitor p21WAF1/CIP, which appears to be transcriptionally upregulated and is p53- dependent.	Resveratrol	34-45	P53	Homo sapiens	284-287
14502645-2	2003	Accordingly, HDAC inhibitors such as trichostatin A (TSA) have potential utility in pancreatic cancer, as most of these tumors possess mutations in p53, which in fact is the main cause of chemoresistance to 5-fluorouracil.	Fluorouracil	207-221	P53	Homo sapiens	148-151
14577584-3	2003	This degradation is controlled by a common polymorphism of the p53 gene encoding either a proline or an arginine at its codon 72 in exon 4.	Arginine	104-112	P53	Homo sapiens	63-66
14578467-4	2003	Using doxorubicin treatment in the HCT116 colon cancer cell line, we have shown that MIC-1 secretion into culture media is correlated with p53 pathway activation as measured by the up-regulation of its downstream transcriptional target p21.	Doxorubicin	6-17	P53	Homo sapiens	139-142
14578467-6	2003	Treatment of these animals with a single dose of doxorubicin led to activation of the p53 pathway and a nearly 4-fold elevation of the plasma MIC-1 level, which was paralleled by p21 induction in the tumor xenografts.	Doxorubicin	49-60	P53	Homo sapiens	86-89
14577584-4	2003	Recently, it has been demonstrated that the presence of homozygous arginine at codon 72 renders p53 about seven times more susceptible to E6-mediated proteolytic degradation as well as to cervical cancer than those with proline homozygotes or proline/arginine heterozygotes.	Arginine	67-75	P53	Homo sapiens	96-99
14577584-4	2003	Recently, it has been demonstrated that the presence of homozygous arginine at codon 72 renders p53 about seven times more susceptible to E6-mediated proteolytic degradation as well as to cervical cancer than those with proline homozygotes or proline/arginine heterozygotes.	Arginine	251-259	P53	Homo sapiens	96-99
14577584-12	2003	Thus the interaction between HPV oncoproteins and the p53 gene polymorphism specifically, homozygous arginine at codon 72 appears to play no role in the development of either cervical or oral cancer and also it can not serve as a biomarker for early identification of cervical, oral or breast cancer.	Arginine	101-109	P53	Homo sapiens	54-57
12857758-4	2003	Presently, we show that p53 is phosphorylated on Ser-15 following DNA damage and this occurs independently of the CDK pathway.	Serine	49-52	P53	Homo sapiens	24-27
12860987-1	2003	Modification-specific antibodies were used to characterize the phosphorylation and acetylation of human p53 in response to genotoxic (UV, IR, and adriamycin) and non-genotoxic (PALA, taxol, nocodazole) stress in cultured human cells at 14 known modification sites.	Doxorubicin	146-156	P53	Homo sapiens	104-107
12860987-1	2003	Modification-specific antibodies were used to characterize the phosphorylation and acetylation of human p53 in response to genotoxic (UV, IR, and adriamycin) and non-genotoxic (PALA, taxol, nocodazole) stress in cultured human cells at 14 known modification sites.	Paclitaxel	183-188	P53	Homo sapiens	104-107
12860987-1	2003	Modification-specific antibodies were used to characterize the phosphorylation and acetylation of human p53 in response to genotoxic (UV, IR, and adriamycin) and non-genotoxic (PALA, taxol, nocodazole) stress in cultured human cells at 14 known modification sites.	Nocodazole	190-200	P53	Homo sapiens	104-107
12860987-3	2003	IR-induced phosphorylation reached a maximum 2 h after treatment and returned to near pretreatment levels by 72 h; UV light and adriamycin induced a less rapid but more robust and prolonged p53 phosphorylation, which reached a maximum between 8 and 24 h, but persisted (UV) even 96 h after treatment.	Doxorubicin	128-138	P53	Homo sapiens	190-193
12860987-5	2003	The non-genotoxic agents PALA, taxol and nocodazole induced p53 accumulation and phosphorylation at Ser6, Ser33, Ser46, and Ser392.	Paclitaxel	31-36	P53	Homo sapiens	60-63
12860987-5	2003	The non-genotoxic agents PALA, taxol and nocodazole induced p53 accumulation and phosphorylation at Ser6, Ser33, Ser46, and Ser392.	Nocodazole	41-51	P53	Homo sapiens	60-63
12860987-8	2003	Analysis of single site mutant p53s indicated clear interdependences between N-terminal phosphorylation sites, which could be classified in four clusters: Ser6 and Ser9; Ser9, Ser15, Thr18 and Ser20; Ser33 and Ser37; and Ser46.	UNII-PYZ33YLR8A	183-188	P53	Homo sapiens	31-34
12969788-6	2003	Furthermore, the synthetic bile acids increased the levels of Cdk inhibitor, p21WAF1/CIP1, expression and activated the reporter construct of p21WAF1/CIP1 promoter in p53-independent manner, and p21WAF1/CIP1 proteins induced by the synthetic bile acid derivatives were associated with Cdk2 and proliferating cell nuclear antigen.	Bile Acids and Salts	27-37	P53	Homo sapiens	167-170
13130078-10	2003	MDM2 inhibitors such as second-generation antisense oligonucleotides have a broad spectrum of antitumor activities in human cancers regardless of p53 status, providing novel approaches to therapy of human prostate cancer.	Oligonucleotides	52-68	P53	Homo sapiens	146-149
12969788-6	2003	Furthermore, the synthetic bile acids increased the levels of Cdk inhibitor, p21WAF1/CIP1, expression and activated the reporter construct of p21WAF1/CIP1 promoter in p53-independent manner, and p21WAF1/CIP1 proteins induced by the synthetic bile acid derivatives were associated with Cdk2 and proliferating cell nuclear antigen.	Bile Acids and Salts	27-36	P53	Homo sapiens	167-170
14522900-11	2003	In addition, we found that p33(ING1b) physically interacts with hSIR2, reverses its ability to induce the AFP promoter, and induces acetylation of p53 residues at Lys(373) and/or Lys(382).	Lysine	163-166	P53	Homo sapiens	147-150
12866025-1	2003	In cells lacking a functional p53 tumor suppressor protein, the endogenous free radical nitric oxide (NO) appears to inhibit apoptosis, and thereby promotes growth of cancer cells.	Nitric Oxide	88-100	P53	Homo sapiens	30-33
12866025-8	2003	In conclusion, NO effectively inhibits apoptosis by scavenging superoxide anions generated in the mitochondria of p53 mutant cells and thereby prevents the downregulation of the antiapoptotic factor bcl-X(L), which controls the mitochondrial apoptosis pathway.	Superoxides	63-80	P53	Homo sapiens	114-117
12968928-5	2003	X-ray-induced phosphorylation of Ser 15 of p53/TP53, accumulation of both p53/TP53 and p21/WAF1/CDKN1A, and phosphorylation of XRCC4 were all suppressed.	Serine	33-36	P53	Homo sapiens	43-46
12968928-5	2003	X-ray-induced phosphorylation of Ser 15 of p53/TP53, accumulation of both p53/TP53 and p21/WAF1/CDKN1A, and phosphorylation of XRCC4 were all suppressed.	Serine	33-36	P53	Homo sapiens	47-51
12927789-0	2003	Morphine suppresses lymphocyte apoptosis by blocking p53-mediated death signaling.	Morphine	0-8	P53	Homo sapiens	53-56
12919725-1	2003	The p53 gene has a polymorphism at codon 72 that presents the arginine or proline genotype, although this polymorphism has been associated with genetically determined susceptibility to lung cancers, the literature has not been consistent with this association.	Arginine	62-70	P53	Homo sapiens	4-7
12939617-6	2003	We show that the potent activator resveratrol, a polyphenol found in red wine, lowers the Michaelis constant of SIRT1 for both the acetylated substrate and NAD(+), and increases cell survival by stimulating SIRT1-dependent deacetylation of p53.	Resveratrol	34-45	P53	Homo sapiens	240-243
12927789-5	2003	Pretreatment of the cells with 10nM morphine caused a transient, naloxone-reversible suppression of the appearance of activated p53 and the generation of DNA laddering.	Morphine	36-44	P53	Homo sapiens	128-131
12899928-0	2003	Reactive oxygen species mediate doxorubicin induced p53-independent apoptosis.	Reactive Oxygen Species	0-23	P53	Homo sapiens	52-55
14500353-3	2003	Electrophilic prostaglandins (PGs) are known to sequester and inactivate p53 in the cytoplasm, an effect that is likely to occur when cyclooxygenase (COX)-2 levels become elevated during colon carcinogenesis.	Prostaglandins	14-28	P53	Homo sapiens	73-76
12899928-0	2003	Reactive oxygen species mediate doxorubicin induced p53-independent apoptosis.	Doxorubicin	32-43	P53	Homo sapiens	52-55
12927814-0	2003	Nitric oxide prevents UV-induced phosphorylation of the p53 tumor-suppressor protein at serine 46: a possible role in inhibition of apoptosis.	Nitric Oxide	0-12	P53	Homo sapiens	56-59
12927814-0	2003	Nitric oxide prevents UV-induced phosphorylation of the p53 tumor-suppressor protein at serine 46: a possible role in inhibition of apoptosis.	Serine	88-94	P53	Homo sapiens	56-59
12927814-1	2003	Ser-46 of p53 is phosphorylated in response to DNA-damage in vivo, and it plays a pivotal role for apoptotic signaling by p53 through regulating the transcriptional activation of genes involved in apoptosis.	Serine	0-3	P53	Homo sapiens	10-13
12927814-1	2003	Ser-46 of p53 is phosphorylated in response to DNA-damage in vivo, and it plays a pivotal role for apoptotic signaling by p53 through regulating the transcriptional activation of genes involved in apoptosis.	Serine	0-3	P53	Homo sapiens	122-125
12927814-5	2003	Our results suggest that NO-mediated protection of apoptosis is p53-dependent, occurring at least partly through NO-inhibition of phosphorylation of p53 on Ser-46.	Serine	156-159	P53	Homo sapiens	64-67
12927814-5	2003	Our results suggest that NO-mediated protection of apoptosis is p53-dependent, occurring at least partly through NO-inhibition of phosphorylation of p53 on Ser-46.	Serine	156-159	P53	Homo sapiens	149-152
14500353-14	2003	Inhibition of COX-2 by celecoxib appears to alleviate this effect on p53 by reducing electrophilic PG synthesis.	Prostaglandins	99-101	P53	Homo sapiens	69-72
14500353-15	2003	Thus, COX-2 inhibition of electrophilic PG formation appears to protect p53 tumor suppressor function.	Prostaglandins	40-42	P53	Homo sapiens	72-75
14500353-3	2003	Electrophilic prostaglandins (PGs) are known to sequester and inactivate p53 in the cytoplasm, an effect that is likely to occur when cyclooxygenase (COX)-2 levels become elevated during colon carcinogenesis.	Prostaglandins	30-33	P53	Homo sapiens	73-76
12871082-11	2003	Taken together, BBI is recommended as a radioprotector for normal tissue expressing wild type TP53 during treatment of tumors characterized by a mutant TP53.	Amiodarone	16-19	P53	Homo sapiens	152-156
14562283-6	2003	An immunohistochemical study of p53 expression was performed on paraffin-embedded tissue.	Paraffin	64-72	P53	Homo sapiens	32-35
12871082-8	2003	Since a high amount of tumors have lost TP53 function during tumor development, the clinical application of BBI to protect normal tissue from radiation damage would effectively improve the therapeutic outcome of radiation therapy.	Amiodarone	108-111	P53	Homo sapiens	40-44
12871082-11	2003	Taken together, BBI is recommended as a radioprotector for normal tissue expressing wild type TP53 during treatment of tumors characterized by a mutant TP53.	Amiodarone	16-19	P53	Homo sapiens	94-98
14693485-0	2003	Effect of topical tretinoin, chemical peeling and dermabrasion on p53 expression in facial skin.	Tretinoin	18-27	P53	Homo sapiens	66-69
14693485-6	2003	Topical tretinoin therapy was found to induce a significant decrease in the expression of p53 up to 6 months of therapy followed by a significant increase after 10 months of therapy.	Tretinoin	8-17	P53	Homo sapiens	90-93
12935767-8	2003	The induction and nuclear translocation of p53 by H2O2 was blocked by pyruvate and appeared to be somewhat enhanced by L-lactate or aminooxyacetate in association with oxidant generation.	Hydrogen Peroxide	50-54	P53	Homo sapiens	43-46
12891704-4	2003	Ninety-seven kiloDaltons eEF2 was found to coimmunoprecipitate in a salt-stable complex with p53.	Salts	68-72	P53	Homo sapiens	93-96
12935767-8	2003	The induction and nuclear translocation of p53 by H2O2 was blocked by pyruvate and appeared to be somewhat enhanced by L-lactate or aminooxyacetate in association with oxidant generation.	L-lactate	119-128	P53	Homo sapiens	43-46
14555710-3	2003	Total glutathione (GSH) was significantly up-regulated (1.8- to 2.8-fold) after eGFP (but not CD80) transduction in cell lines with, but not in those lacking, functional p53.	Glutathione	6-17	P53	Homo sapiens	170-173
12935767-10	2003	The pyruvate-related redox manipulation inhibited the H2O2-induced p53 activation, restored the downregulated bcl-2 and the upregulated bax, and hence enhanced the bcl-2/bax expression ratio.	Hydrogen Peroxide	54-58	P53	Homo sapiens	67-70
12944468-4	2003	Here we show that the two basic amino acid groups in the p53 bipartite NLS function collaboratively to import p53.	Amino Acids, Basic	26-42	P53	Homo sapiens	57-60
12944468-4	2003	Here we show that the two basic amino acid groups in the p53 bipartite NLS function collaboratively to import p53.	Amino Acids, Basic	26-42	P53	Homo sapiens	110-113
14555710-3	2003	Total glutathione (GSH) was significantly up-regulated (1.8- to 2.8-fold) after eGFP (but not CD80) transduction in cell lines with, but not in those lacking, functional p53.	Glutathione	19-22	P53	Homo sapiens	170-173
14555710-5	2003	Thus, oxidative stress produced by GFP selects for cells with up-regulated GSH in a p53-dependent manner, and also enhanced the cytotoxicity of anticancer drugs in neuroblastoma cell lines.	Glutathione	75-78	P53	Homo sapiens	84-87
12898523-10	2003	Using specific phospho-serine antibodies, we identified phosphorylation of baculovirally expressed p53 protein at five distinct sites.	Serine	23-29	P53	Homo sapiens	99-102
12944903-3	2003	Tritium labeling also led to nuclear accumulation of p53 and induction of the p53-regulated gene p21(WAF1) and its encoded protein (p21).	Tritium	0-7	P53	Homo sapiens	53-56
12944903-3	2003	Tritium labeling also led to nuclear accumulation of p53 and induction of the p53-regulated gene p21(WAF1) and its encoded protein (p21).	Tritium	0-7	P53	Homo sapiens	78-81
12805649-12	2003	These results demonstrate that, in this cell lineage, sensitivity to oxidative DNA damage by H2O2 decreases with tumorigenicity (i.e., MCF-10A vs. MCF-10ATG3B), and show that DNA repair, altered Ras, and p53 expression, or compensatory mechanisms involving elevated antioxidant enzymes are involved in mediating these effects.	Hydrogen Peroxide	93-97	P53	Homo sapiens	204-207
12810724-8	2003	PML neutralizes the inhibitory effects of Mdm2 by prolonging the stress-induced phosphorylation of p53 on serine 20, a site of the checkpoint kinase 2 (Chk2).	Serine	106-112	P53	Homo sapiens	99-102
12788915-5	2003	Analysis of the transcriptional activity of the two most common p53 mutants found in human breast tumors that are associated with resistance to doxorubicin reveals that these mutations completely eliminate the ability of p53 protein to transactivate CD95 gene expression.	Doxorubicin	144-155	P53	Homo sapiens	64-67
12788915-5	2003	Analysis of the transcriptional activity of the two most common p53 mutants found in human breast tumors that are associated with resistance to doxorubicin reveals that these mutations completely eliminate the ability of p53 protein to transactivate CD95 gene expression.	Doxorubicin	144-155	P53	Homo sapiens	221-224
12871714-1	2003	We examined ultraviolet (UV) irradiation and cisplatin treatment damage formation and repair efficiency in the p53 tumor suppressor gene of various cultured cell lines and lymphocytes using a nonradioactive multiplex long quantitative polymerase chain reaction (QPCR) assay, which amplified a 7-kb fragment of the target gene and a 500-bp fragment of the template control to successfully increase the sensitivity and reliability of the assay.	Cisplatin	45-54	P53	Homo sapiens	111-114
12871714-5	2003	The data indicated that the lesion frequency in the p53 gene was 1.27-1.75 times higher in the H23 cisplatin-sensitive cell than in the H1435 cisplatin-resistant cell at the IC(70) dose.	Cisplatin	99-108	P53	Homo sapiens	52-55
12871714-5	2003	The data indicated that the lesion frequency in the p53 gene was 1.27-1.75 times higher in the H23 cisplatin-sensitive cell than in the H1435 cisplatin-resistant cell at the IC(70) dose.	Cisplatin	142-151	P53	Homo sapiens	52-55
12917633-0	2003	Role of protein kinase C and the Sp1-p53 complex in activation of p21(WAF-1) expression by 12-O-tetradecanoylphorbol-13-acetate in human T cells.	Tetradecanoylphorbol Acetate	91-127	P53	Homo sapiens	37-40
12756247-4	2003	Chk1 stimulates the kinase activity of DNA-PK (protein kinase) complexes, which leads to increased phosphorylation of p53 on Ser-15 and Ser-37.	Serine	125-128	P53	Homo sapiens	118-121
12907245-0	2003	The JNK, ERK and p53 pathways play distinct roles in apoptosis mediated by the antitumor agents vinblastine, doxorubicin, and etoposide.	Doxorubicin	109-120	P53	Homo sapiens	17-20
12875991-4	2003	Analogously, higher PgE2 levels were documented in p53-mutated HNSCCs when compared with wild-type p53 tumors (P = 0.015) and COX-2 protein expression was higher in p53-mutated HNSCCs (P = 0.007).	Dinoprostone	20-24	P53	Homo sapiens	51-54
12875991-5	2003	A431 cancer cells expressing a p53 temperature-sensitive mutant showed an approximately 1.9- and 2.6-fold decrease in spontaneous NO(2-)/NO(3-) and PgE2 synthesis at permissive temperature, respectively, when compared with the same cells at nonpermissive temperature (P &lt;or= 0.001).	Dinoprostone	148-152	P53	Homo sapiens	31-34
12902982-3	2003	Both Myc and E2F1 activation rapidly induced p53 phosphorylation at Ser-15, p53 protein accumulation, and upregulation of the p53 target genes MDM2 and p21.	Serine	68-71	P53	Homo sapiens	45-48
12875991-3	2003	We also found that p53-mutated HNSCCs (25 cases, 58.1%) showed higher levels of iNOS activity and cGMP in comparison with wild-type p53 tumors (18 cases, 41.9%) (P = 0.0005 and P = 0.01), as well as higher iNOS immunohistochemical expression (P = 0.03).	Cyclic GMP	98-102	P53	Homo sapiens	19-22
12907245-10	2003	In contrast, doxorubicin and VP-16 induced p53, and inhibition of p53 decreased drug-induced cell death, suggesting a pro-apoptotic role for p53.	Doxorubicin	13-24	P53	Homo sapiens	43-46
12907638-7	2003	The 5-FU-induced activation of MAT-8, thymosin-beta-10, and chaperonin-10 was abrogated by inactivation of p53 in MCF-7 cells, whereas induction of SSAT and annexin II was significantly reduced in the absence of p53.	Fluorouracil	4-8	P53	Homo sapiens	107-110
12907596-7	2003	Whereas the architecture of HIPK domains is PML independent, HIPK2-mediated enhancement of p53-dependent transcription, p53 serine 46 phosphorylation and the antiproliferative function of HIPK2 strictly rely on the presence of PML.	Serine	124-130	P53	Homo sapiens	120-123
12807757-8	2003	Depleting glutathione with buthionine sulfoximine in B[a]P-treated cells to levels similar to those obtained with acrolein decreased p53 DNA binding substantially less than with acrolein.	Glutathione	10-21	P53	Homo sapiens	133-136
12907638-7	2003	The 5-FU-induced activation of MAT-8, thymosin-beta-10, and chaperonin-10 was abrogated by inactivation of p53 in MCF-7 cells, whereas induction of SSAT and annexin II was significantly reduced in the absence of p53.	Fluorouracil	4-8	P53	Homo sapiens	212-215
12907638-8	2003	Moreover, each of these genes contained more than one potential p53-binding site, suggesting that p53 may play an important regulatory role in 5-FU-induced expression of these genes.	Fluorouracil	143-147	P53	Homo sapiens	64-67
12907638-8	2003	Moreover, each of these genes contained more than one potential p53-binding site, suggesting that p53 may play an important regulatory role in 5-FU-induced expression of these genes.	Fluorouracil	143-147	P53	Homo sapiens	98-101
12884349-0	2003	P53 mutation correlates with cisplatin sensitivity in head and neck squamous cell carcinoma lines.	Cisplatin	29-38	P53	Homo sapiens	0-3
12912974-8	2003	p53 serine 15 phosphorylation and protein accumulation were detected 2 h after treatment.	Serine	4-10	P53	Homo sapiens	0-3
12897801-3	2003	Two peptides derived from the DNA-binding domain of p53 bind to CHK2 and stimulate phosphorylation of full-length p53 at Thr 18 and Ser 20, thus identifying CHK2-docking sites.	Threonine	121-124	P53	Homo sapiens	52-55
12897801-3	2003	Two peptides derived from the DNA-binding domain of p53 bind to CHK2 and stimulate phosphorylation of full-length p53 at Thr 18 and Ser 20, thus identifying CHK2-docking sites.	Threonine	121-124	P53	Homo sapiens	114-117
12897801-3	2003	Two peptides derived from the DNA-binding domain of p53 bind to CHK2 and stimulate phosphorylation of full-length p53 at Thr 18 and Ser 20, thus identifying CHK2-docking sites.	Serine	132-135	P53	Homo sapiens	52-55
12897801-3	2003	Two peptides derived from the DNA-binding domain of p53 bind to CHK2 and stimulate phosphorylation of full-length p53 at Thr 18 and Ser 20, thus identifying CHK2-docking sites.	Serine	132-135	P53	Homo sapiens	114-117
12897801-4	2003	CHK2 can be fully activated in trans by the two p53 DNA-binding-domain peptides, and can phosphorylate BOX-I transactivation-domain fragments of p53 at Thr 18 and Ser 20.	Threonine	152-155	P53	Homo sapiens	145-148
12897801-4	2003	CHK2 can be fully activated in trans by the two p53 DNA-binding-domain peptides, and can phosphorylate BOX-I transactivation-domain fragments of p53 at Thr 18 and Ser 20.	Serine	163-166	P53	Homo sapiens	48-51
12897801-8	2003	A database search identified a p53 BOX-I-homology motif in p21(WAF1) and although CHK2 is inactive towards this protein, the p53 DNA-binding-domain peptides induce phosphorylation of p21(WAF1) at Ser 146.	Serine	196-199	P53	Homo sapiens	31-34
12897801-8	2003	A database search identified a p53 BOX-I-homology motif in p21(WAF1) and although CHK2 is inactive towards this protein, the p53 DNA-binding-domain peptides induce phosphorylation of p21(WAF1) at Ser 146.	Serine	196-199	P53	Homo sapiens	125-128
12893182-6	2003	Repair of cisplatin-induced DNA damage was reduced in A2780 cells overexpressing MDM2, compared to A2780 cells in which wild-type p53 function was intact.	Cisplatin	10-19	P53	Homo sapiens	130-133
12884349-3	2003	METHODS: To determine the relationship of p53 mutations to sensitivity to cisplatin in vitro, 23 head and neck squamous cell carcinoma (HNSCC) cell lines were analyzed for cisplatin sensitivity, p53 expression, and p53 mutation status.	Cisplatin	74-83	P53	Homo sapiens	42-45
12884349-7	2003	CONCLUSIONS: These in vitro data support a role for mutation of the p53 tumor suppressor gene as a marker for response to cisplatin in HNSCC.	Cisplatin	122-131	P53	Homo sapiens	68-71
12893186-7	2003	The cellular growth inhibition and apoptosis of DDC-mediated p53 transfection were assessed by trypan blue exclusion assay and annexin-V staining, respectively.	Zalcitabine	48-51	P53	Homo sapiens	61-64
12939400-4	2003	It was found that while alkylating agents induced both apoptosis and phosphorylation of the Ser-15 site of p53 in a MLH1-dependent manner, induction of apoptosis, but not p53 phosphorylation, was MLH1 dependent following treatment with H2O2.	Serine	92-95	P53	Homo sapiens	107-110
12811820-1	2003	Methylxantine derivative, caffeine, is known to prevent the p53-dependent apoptosis pathway via inhibition of ATM (ataxia telangiectasia mutated) kinase, which activates p53 by phosphorylation of the Ser-15 residue.	Serine	200-203	P53	Homo sapiens	60-63
12811820-1	2003	Methylxantine derivative, caffeine, is known to prevent the p53-dependent apoptosis pathway via inhibition of ATM (ataxia telangiectasia mutated) kinase, which activates p53 by phosphorylation of the Ser-15 residue.	Serine	200-203	P53	Homo sapiens	170-173
12811820-6	2003	Caffeine induced G(2)/M phase cell cycle arrest in NB4 cells in association with the induction of phosphorylation at the Ser-15 residue of p53 and induction of tyrosine phosphorylation of cdc2.	Serine	121-124	P53	Homo sapiens	139-142
12811820-8	2003	Interestingly, the antisense oligonucleotides for p53 significantly reduced p53 expression and caffeine-induced G(2)/M phase cell cycle arrest in NB4 cells.	Oligonucleotides	29-45	P53	Homo sapiens	50-53
12811820-8	2003	Interestingly, the antisense oligonucleotides for p53 significantly reduced p53 expression and caffeine-induced G(2)/M phase cell cycle arrest in NB4 cells.	Oligonucleotides	29-45	P53	Homo sapiens	76-79
12811820-9	2003	These results suggest that caffeine induces cell cycle arrest and apoptosis in association with activation of p53 by a novel pathway to phosphorylate the Ser-15 residue and induction of phosphorylation of cdc 2 in leukemic cells with normal p53.	Serine	154-157	P53	Homo sapiens	110-113
12897130-0	2003	Silencing of the novel p53 target gene Snk/Plk2 leads to mitotic catastrophe in paclitaxel (taxol)-exposed cells.	Paclitaxel	80-90	P53	Homo sapiens	23-26
12897130-0	2003	Silencing of the novel p53 target gene Snk/Plk2 leads to mitotic catastrophe in paclitaxel (taxol)-exposed cells.	Paclitaxel	92-97	P53	Homo sapiens	23-26
12869633-8	2003	K2-5F induced by exogenous p53 dramatically reduced the expression of HSV-TK in human embryonic kidney 293 cells, and it subsequently increased cell survival in response to GCV.	k2-5f	0-5	P53	Homo sapiens	27-30
12939400-4	2003	It was found that while alkylating agents induced both apoptosis and phosphorylation of the Ser-15 site of p53 in a MLH1-dependent manner, induction of apoptosis, but not p53 phosphorylation, was MLH1 dependent following treatment with H2O2.	Hydrogen Peroxide	236-240	P53	Homo sapiens	107-110
12897130-6	2003	Since siRNA directed against Snk/Plk2 promoted death of paclitaxel-treated cells in mitosis, we envision a mitotic checkpoint wherein p53-dependent activation of Snk/Plk2 prevents mitotic catastrophe following spindle damage.	Paclitaxel	56-66	P53	Homo sapiens	134-137
12893432-2	2003	To address on the genetic risk factor for NPC, we investigated association between the p53 codon 72 polymorphism (Pro/Arg) and NPC susceptibility in the Thai.	Arginine	118-121	P53	Homo sapiens	87-90
12859235-7	2003	Four hours after irradiation (8 Gy), the expression of TP53 and phospho-p53 ((15)Ser) was induced in the parental cells but not in M054-S8, M054-Y2 or M054-SY4 cells.	Serine	81-84	P53	Homo sapiens	55-59
12859235-7	2003	Four hours after irradiation (8 Gy), the expression of TP53 and phospho-p53 ((15)Ser) was induced in the parental cells but not in M054-S8, M054-Y2 or M054-SY4 cells.	Serine	81-84	P53	Homo sapiens	72-75
12918120-8	2003	NADH could not only eliminate the apoptosis induced by X-ray irradiation, but also up-regulate expression of bcl-2 protein and down-regulate expression of p53, bax, fas and fasL proteins (P&lt;0.05).	NAD	0-4	P53	Homo sapiens	155-158
12918120-10	2003	CONCLUSION: NADH has marked anti-radiation effect, its mechanism may be associated with up-regulation of bcl-2 expression and down-regulation of p53, bax fas and fasL expression, as well as decline of intracellular ROS.	NAD	12-16	P53	Homo sapiens	145-148
12867035-6	2003	This interaction, and consequent repression of p53-dependent transcription, is relieved under hypoxia or hypoxia-mimicking conditions that are known to increase levels of intracellular NADH.	NAD	185-189	P53	Homo sapiens	47-50
12724314-0	2003	Identification and characterization of a novel p300-mediated p53 acetylation site, lysine 305.	Lysine	83-89	P53	Homo sapiens	61-64
12690107-6	2003	When Ad-Bid and cisplatin were used together, chemosensitivity was restored in p53-null H358 cells, increasing death from 35% following treatment with cisplatin and Ad-LacZ to &gt;90% death with Ad-Bid and cisplatin (Ad-Bid alone induced 50% cell death under these conditions).	Cisplatin	16-25	P53	Homo sapiens	79-82
12690107-6	2003	When Ad-Bid and cisplatin were used together, chemosensitivity was restored in p53-null H358 cells, increasing death from 35% following treatment with cisplatin and Ad-LacZ to &gt;90% death with Ad-Bid and cisplatin (Ad-Bid alone induced 50% cell death under these conditions).	Cisplatin	151-160	P53	Homo sapiens	79-82
12724314-9	2003	Thus, p300 may further regulate the transcriptional activity of p53 through a novel acetylation site, Lys-305.	Lysine	102-105	P53	Homo sapiens	64-67
12690107-6	2003	When Ad-Bid and cisplatin were used together, chemosensitivity was restored in p53-null H358 cells, increasing death from 35% following treatment with cisplatin and Ad-LacZ to &gt;90% death with Ad-Bid and cisplatin (Ad-Bid alone induced 50% cell death under these conditions).	Cisplatin	151-160	P53	Homo sapiens	79-82
12821135-4	2003	TPCK promoted dephosphorylation of p53 on serine residues at 6, 9, 46, 376, and 378 in parallel with the activation of p53 transcriptional activity.	Serine	42-48	P53	Homo sapiens	35-38
12821135-5	2003	HCT116 p53-/- cells expressing p53 mutant, in which serine residues at 6, 9, 46, 376, and 378 were replaced by aspartic acids, were resistant to TPCK-induced apoptosis suggesting the requirement of dephosphorylation of p53 on serine residues during TPCK-induced apoptosis.	Serine	52-58	P53	Homo sapiens	7-10
12821135-5	2003	HCT116 p53-/- cells expressing p53 mutant, in which serine residues at 6, 9, 46, 376, and 378 were replaced by aspartic acids, were resistant to TPCK-induced apoptosis suggesting the requirement of dephosphorylation of p53 on serine residues during TPCK-induced apoptosis.	Serine	52-58	P53	Homo sapiens	31-34
12821135-5	2003	HCT116 p53-/- cells expressing p53 mutant, in which serine residues at 6, 9, 46, 376, and 378 were replaced by aspartic acids, were resistant to TPCK-induced apoptosis suggesting the requirement of dephosphorylation of p53 on serine residues during TPCK-induced apoptosis.	Serine	52-58	P53	Homo sapiens	31-34
12821135-5	2003	HCT116 p53-/- cells expressing p53 mutant, in which serine residues at 6, 9, 46, 376, and 378 were replaced by aspartic acids, were resistant to TPCK-induced apoptosis suggesting the requirement of dephosphorylation of p53 on serine residues during TPCK-induced apoptosis.	Serine	226-232	P53	Homo sapiens	31-34
12821135-5	2003	HCT116 p53-/- cells expressing p53 mutant, in which serine residues at 6, 9, 46, 376, and 378 were replaced by aspartic acids, were resistant to TPCK-induced apoptosis suggesting the requirement of dephosphorylation of p53 on serine residues during TPCK-induced apoptosis.	Serine	226-232	P53	Homo sapiens	31-34
12837832-5	2003	Association of clinical and pathologic variables (e.g., alcohol consumption, sex, age, pathologic stage) with mutation of the p53 gene was determined by logistic regression.	Alcohols	56-63	P53	Homo sapiens	126-129
12834351-1	2003	The evolution of the nanosecond dynamics of the core tryptophan, Trp53, of barstar has been monitored during the induction of collapse and structure formation in the denatured D form at pH 12, by addition of increasing concentrations of the stabilizing salt Na(2)SO(4).	Tryptophan	53-63	P53	Homo sapiens	65-70
12834351-1	2003	The evolution of the nanosecond dynamics of the core tryptophan, Trp53, of barstar has been monitored during the induction of collapse and structure formation in the denatured D form at pH 12, by addition of increasing concentrations of the stabilizing salt Na(2)SO(4).	Salts	253-257	P53	Homo sapiens	65-70
12834351-2	2003	Time-resolved fluorescence methods have been used to monitor the dynamics of Trp53 in the intermediates that are populated during the salt-induced transition of the D form to the molten globule B form.	Salts	134-138	P53	Homo sapiens	77-82
12716906-3	2003	The application of a laminar flow (12 dyn/cm2) increased the deacetylation at Lys-320 and Lys-373 of p53 and the acetylation at Lys-382 in human umbilical vein endothelial cells.	Lysine	78-81	P53	Homo sapiens	101-104
12716906-3	2003	The application of a laminar flow (12 dyn/cm2) increased the deacetylation at Lys-320 and Lys-373 of p53 and the acetylation at Lys-382 in human umbilical vein endothelial cells.	Lysine	90-93	P53	Homo sapiens	101-104
12716906-3	2003	The application of a laminar flow (12 dyn/cm2) increased the deacetylation at Lys-320 and Lys-373 of p53 and the acetylation at Lys-382 in human umbilical vein endothelial cells.	Lysine	90-93	P53	Homo sapiens	101-104
12716906-5	2003	Treating human umbilical vein endothelial cells with trichostatin A (TSA), an HDAC inhibitor, abolished the flow-induced p53 deacetylation at Lys-320 and Lys-373.	Lysine	142-145	P53	Homo sapiens	121-124
12726776-5	2003	Another is its intrinsic and associated enzymatic activity, which transfers an acetyl-base to the epsilon ( epsilon ) portion of lysine-residues in histones and certain nuclear proteins (factor acetyltransferases; FATs), such as p53, lymphoid enhancer-binding factor (LEF), and transcription factor IIE (TFIIE), which often results in increased transcriptional activity.	Lysine	129-135	P53	Homo sapiens	229-232
12926093-0	2003	P53 mutation predicts intravesical adriamycin instillation failure in superficial transitional cell carcinoma of bladder.	Doxorubicin	35-45	P53	Homo sapiens	0-3
12853365-0	2003	p53 expression and disease outcome of breast cancer patients undergoing primary chemotherapy with anthracycline-containing regimens.	Anthracyclines	98-111	P53	Homo sapiens	0-3
12824702-6	2003	When a comparison of the distribution of the p53 codon 72 polymorphism was made between patients with a first-degree family history and all control subjects, the adjusted odds ratios (ORs) for prostate cancer associated with the Arg/Arg, Arg/Pro and Pro/Pro genotypes were 1.00, 0.99 [95% confidence interval (CI) 0.53-1.88] and 2.80 (95% CI 1.04-7.53), respectively.	Arginine	229-232	P53	Homo sapiens	45-48
12807744-6	2003	Furthermore, caffeine also inhibited the accumulation of p53 by a variety of stress-inducing agents in vivo, such as 5-fluorouracil, doxorubicin, mitomycin C, camptothecin and roscovitine.	Fluorouracil	117-131	P53	Homo sapiens	57-60
12807744-6	2003	Furthermore, caffeine also inhibited the accumulation of p53 by a variety of stress-inducing agents in vivo, such as 5-fluorouracil, doxorubicin, mitomycin C, camptothecin and roscovitine.	Doxorubicin	133-144	P53	Homo sapiens	57-60
12792779-1	2003	5-Fluorouracil (5FU) exposure can lead to both G1/S arrest and apoptosis induction which are dependent of P53 induction.	Fluorouracil	0-14	P53	Homo sapiens	106-109
12792779-1	2003	5-Fluorouracil (5FU) exposure can lead to both G1/S arrest and apoptosis induction which are dependent of P53 induction.	Fluorouracil	16-19	P53	Homo sapiens	106-109
12792782-6	2003	During UA treatment, we also demonstrated that p53 was phosphorylated at serine 392 and translocated to the nucleus.	Serine	73-79	P53	Homo sapiens	47-50
12792793-13	2003	If white patients were stratified according to the type and location of TP53 mutations, patients with mutations affecting amino acids directly involved in DNA or Zn binding displayed a poor prognosis.	Zinc	162-164	P53	Homo sapiens	72-76
12839966-7	2003	Binding of mtTFA to cisplatin-modified DNA was significantly enhanced by p53, whereas binding to oxidized DNA was inhibited.	Cisplatin	20-29	P53	Homo sapiens	73-76
12769774-9	2003	The down-regulation of Bcl-2 and/or the upregulation of p53 and p21/WAF-1 are certainly one of the important modes of apoptosis induction by taxanes.	Taxoids	141-148	P53	Homo sapiens	56-59
12818446-1	2003	OBJECTIVE: [corrected] An experimental study has indicated that individuals homozygous for the Arg-encoding allele of p53 gene may have an increased susceptibility to HPV-related cervical cancer but many epidemiological studies have failed to repeat this result.	Arginine	95-98	P53	Homo sapiens	118-121
12818446-3	2003	The aim of the present work was to investigate whether the p53 arginine allele confers a risk factor for cervical carcinogenesis.	Arginine	63-71	P53	Homo sapiens	59-62
12821336-1	2003	INTRODUCTION: We aimed to verify not only whether homozygous Arg at codon 72 of the p53 apoptotic domain is a possible risk factor for cervical human papillomavirus (HPV)-related cancer, but whether degraded p53 may have an effect on a G2 checkpoint of the cell cycle.	Arginine	61-64	P53	Homo sapiens	84-87
12821336-1	2003	INTRODUCTION: We aimed to verify not only whether homozygous Arg at codon 72 of the p53 apoptotic domain is a possible risk factor for cervical human papillomavirus (HPV)-related cancer, but whether degraded p53 may have an effect on a G2 checkpoint of the cell cycle.	Arginine	61-64	P53	Homo sapiens	208-211
12824702-6	2003	When a comparison of the distribution of the p53 codon 72 polymorphism was made between patients with a first-degree family history and all control subjects, the adjusted odds ratios (ORs) for prostate cancer associated with the Arg/Arg, Arg/Pro and Pro/Pro genotypes were 1.00, 0.99 [95% confidence interval (CI) 0.53-1.88] and 2.80 (95% CI 1.04-7.53), respectively.	Arginine	233-236	P53	Homo sapiens	45-48
12824702-6	2003	When a comparison of the distribution of the p53 codon 72 polymorphism was made between patients with a first-degree family history and all control subjects, the adjusted odds ratios (ORs) for prostate cancer associated with the Arg/Arg, Arg/Pro and Pro/Pro genotypes were 1.00, 0.99 [95% confidence interval (CI) 0.53-1.88] and 2.80 (95% CI 1.04-7.53), respectively.	Arginine	233-236	P53	Homo sapiens	45-48
12884365-3	2003	Instead, p53-dependent activation and apoptosis were not only induced by PFTalpha itself but were also enhanced by a combination of PFTalpha with UVB or Dox.	Doxorubicin	153-156	P53	Homo sapiens	9-12
12823592-9	2003	The p53 positive group had a daily ethanol intake significantly higher in respect to that of the p53 negative group (P &lt; 0.05).	Ethanol	35-42	P53	Homo sapiens	4-7
12823592-10	2003	Alimentary history documented that patients with a p53 over-expression had a lower intake of total calories, monounsaturated fatty acids, vitamin C and riboflavin.	Riboflavin	152-162	P53	Homo sapiens	51-54
14511408-6	2003	Our observations also indicate that although functional p53 is absent, the p53 kin, p73, is inducible by doxorubicin in AsPC-1 cells.	Doxorubicin	105-116	P53	Homo sapiens	75-78
12921557-4	2003	The expression of bcl-2 protein decreased and p53 protein increased in BGC-823 cells treated with D-limonene, compared with the control cells.	Limonene	98-108	P53	Homo sapiens	46-49
12910706-2	2003	METHODS: An immunohistochemical technique (SP method) was applied to study the changes of P53 expression in normal oral mucosa and oral leukoplakia(OLK) in different age groups.	TFF2 protein, human	43-45	P53	Homo sapiens	90-93
21266112-0	2003	[Effect of exogenous wild type p53 expression on sensitization of lung cancer cell line to cisplatin and cloning of the corresponding genes].	Cisplatin	91-100	P53	Homo sapiens	31-34
12682067-5	2003	At one subunit interface of AChBP, the side chain of Tyr-89 closely approaches a positively charged nitrogen in d-TC but is farther away from the equivalent nitrogen in metocurine, whereas, at the opposing interface, side chains of Trp-53 and Gln-55 closely approach the metocurine scaffold but not that of d-TC.	Tyrosine	53-56	P53	Homo sapiens	232-238
21266112-1	2003	BACKGROUND: To isolate and clone the cisplatin genes in 801-D cell line, a kind of lung cancer cell line, with the emphasis of the objective genes regulated by wild type p53 (wtp53).	Cisplatin	37-46	P53	Homo sapiens	170-173
21266112-10	2003	It is possible for p53 to regulate the sensitization of lung cancer cells to cisplatin through its downstream target genes.	Cisplatin	77-86	P53	Homo sapiens	19-22
12802279-5	2003	Here, we show that 2-AP suppresses p53 phosphorylation in response to gamma radiation, adriamycin, or ultraviolet treatment.	Doxorubicin	87-97	P53	Homo sapiens	35-38
12810654-11	2003	The ansamycins inhibited DDP-induced activation of caspases 8 and 3 in HT29 and HCTp5.2 but not in HCT116 cells, which we postulate to be the basis for higher survival of p53-deficient cells when treated with combinations of the two drugs.	Lactams, Macrocyclic	4-14	P53	Homo sapiens	171-174
12810654-11	2003	The ansamycins inhibited DDP-induced activation of caspases 8 and 3 in HT29 and HCTp5.2 but not in HCT116 cells, which we postulate to be the basis for higher survival of p53-deficient cells when treated with combinations of the two drugs.	Cisplatin	25-28	P53	Homo sapiens	171-174
12802279-8	2003	Biologically, the 2-AP-mediated inhibition of p53 stabilization enables wild-type p53-containing cells to bypass adriamycin-induced G(2)/M arrest.	Doxorubicin	113-123	P53	Homo sapiens	46-49
12802279-8	2003	Biologically, the 2-AP-mediated inhibition of p53 stabilization enables wild-type p53-containing cells to bypass adriamycin-induced G(2)/M arrest.	Doxorubicin	113-123	P53	Homo sapiens	82-85
12771997-2	2003	Mut-p53 cells were significantly resistant to the cytotoxicity of the microtubule-targeted drugs (vinca alkaloids and taxanes), as compared with wt-p53 cells.	Taxoids	118-125	P53	Homo sapiens	4-7
12654917-5	2003	Phosphorylation of p53 at serine 20, accumulation of p53 protein, transcriptional activation of p53 target genes, and cell cycle arrest and apoptotic death phenotypes were completely intact regardless of CHK2 status.	Serine	26-32	P53	Homo sapiens	19-22
12782576-4	2003	In these cells, only ectopically expressed p73 activates the proapoptotic p53 target P53AIP1, whereas phosphorylation of p53 at Ser-46, shown to regulate transcriptional activation of P53AIP1, is missing.	Serine	128-131	P53	Homo sapiens	121-124
12734658-4	2003	In the present study, we screened paraffin-embedded brain tissue from different areas of 18 cases (8 autopsy cases and 10 biopsies) for alterations in the TP53 and PTEN genes.	Paraffin	34-42	P53	Homo sapiens	155-159
12734658-8	2003	In the second case, in tumor samples from one hemisphere, nuclear accumulation of p53 was caused by a G--&gt;A transition in codon 244 (Gly--&gt;Asp).	Glycine	136-139	P53	Homo sapiens	82-85
12796380-0	2003	Age-associated increase of codon 72 Arginine p53 frequency in gastric cardia and non-cardia adenocarcinoma.	Arginine	36-44	P53	Homo sapiens	45-48
12796380-6	2003	A significant stepwise increased frequency of codon 72 Arg p53 with age was observed in patients with gastric cancer, but not in noncancer patients (P = 0.01).	Arginine	55-58	P53	Homo sapiens	59-62
12796380-8	2003	After adjustment for age and gender, a logistic regression analysis suggested that the risk for a p53 Arg homozygous patient to develop cardia cancer is 3.1 95% confidence interval, 1.4-7.3) times greater than for p53 Pro homozygous and p53 Arg/Pro heterozygous patients.	Arginine	102-105	P53	Homo sapiens	98-101
12796380-8	2003	After adjustment for age and gender, a logistic regression analysis suggested that the risk for a p53 Arg homozygous patient to develop cardia cancer is 3.1 95% confidence interval, 1.4-7.3) times greater than for p53 Pro homozygous and p53 Arg/Pro heterozygous patients.	Arginine	102-105	P53	Homo sapiens	214-217
12796380-8	2003	After adjustment for age and gender, a logistic regression analysis suggested that the risk for a p53 Arg homozygous patient to develop cardia cancer is 3.1 95% confidence interval, 1.4-7.3) times greater than for p53 Pro homozygous and p53 Arg/Pro heterozygous patients.	Arginine	102-105	P53	Homo sapiens	214-217
12796380-8	2003	After adjustment for age and gender, a logistic regression analysis suggested that the risk for a p53 Arg homozygous patient to develop cardia cancer is 3.1 95% confidence interval, 1.4-7.3) times greater than for p53 Pro homozygous and p53 Arg/Pro heterozygous patients.	Arginine	241-244	P53	Homo sapiens	98-101
12796380-10	2003	CONCLUSIONS: These findings indicate that codon 72 Arg p53 may be associated with a prolonged survival for patients who have had gastric adenocarcinoma, especially non-cardia adenocarcinoma.	Arginine	51-54	P53	Homo sapiens	55-58
12796400-0	2003	Chromosomal instability rather than p53 mutation is associated with response to neoadjuvant cisplatin-based chemotherapy in gastric carcinoma.	Cisplatin	92-101	P53	Homo sapiens	36-39
12743373-1	2003	Using DNA microarray and clustering of expressed genes we have analyzed the mechanism of inhibition of wild-type p53-induced apoptosis by the cytokine interleukin 6 (IL-6) and the calcium mobilizer thapsigargin (TG).	Thapsigargin	198-210	P53	Homo sapiens	113-116
13678348-5	2003	Western blot analysis revealed that the time required to reach the highest level of wild-type p53 protein in B3 was longer than the time in MOLT-4 and that the p53 may be stabilized by the phosphorylation at Ser-15.	Serine	208-211	P53	Homo sapiens	94-97
13678348-5	2003	Western blot analysis revealed that the time required to reach the highest level of wild-type p53 protein in B3 was longer than the time in MOLT-4 and that the p53 may be stabilized by the phosphorylation at Ser-15.	Serine	208-211	P53	Homo sapiens	160-163
12776195-3	2003	By contrast, isogenic p53-null cells exposed to hypoxic conditions exhibited a 6-10-fold higher level of apoptosis, suggesting that p53 acts as a survival factor under limiting oxygen concentrations.	Oxygen	177-183	P53	Homo sapiens	22-25
12776195-3	2003	By contrast, isogenic p53-null cells exposed to hypoxic conditions exhibited a 6-10-fold higher level of apoptosis, suggesting that p53 acts as a survival factor under limiting oxygen concentrations.	Oxygen	177-183	P53	Homo sapiens	132-135
12776195-4	2003	Surprisingly, hypoxia-dependent growth arrest in p53(+/+) cells did not result in either p21(WAF1) or HIF-1 protein stabilization, but rather promoted a significant decrease in Ser(392)-site phosphorylation at the CK2/FACT site.	Serine	177-180	P53	Homo sapiens	49-52
12776195-6	2003	In contrast to hypoxia, 5-flourouracil (5-FU)-induced p53-dependent cell death correlated with enhanced Ser(392) phosphorylation of p53 and elevated p21(WAF1) protein levels.	Fluorouracil	40-44	P53	Homo sapiens	54-57
12776195-6	2003	In contrast to hypoxia, 5-flourouracil (5-FU)-induced p53-dependent cell death correlated with enhanced Ser(392) phosphorylation of p53 and elevated p21(WAF1) protein levels.	Fluorouracil	40-44	P53	Homo sapiens	132-135
12776195-6	2003	In contrast to hypoxia, 5-flourouracil (5-FU)-induced p53-dependent cell death correlated with enhanced Ser(392) phosphorylation of p53 and elevated p21(WAF1) protein levels.	Serine	104-107	P53	Homo sapiens	54-57
12776195-6	2003	In contrast to hypoxia, 5-flourouracil (5-FU)-induced p53-dependent cell death correlated with enhanced Ser(392) phosphorylation of p53 and elevated p21(WAF1) protein levels.	Serine	104-107	P53	Homo sapiens	132-135
12776195-7	2003	Hypoxia inhibited 5-FU-induced p53-dependent cell death and attenuated p53 phosphorylation at the ATM and CK2/FACT phosphorylation sites.	Fluorouracil	18-22	P53	Homo sapiens	31-34
12820963-1	2003	Under serum-free conditions, rapamycin, an inhibitor of mammalian target of rapamycin (mTOR), induces apoptosis of cells lacking functional p53.	Sirolimus	29-38	P53	Homo sapiens	140-143
12743373-1	2003	Using DNA microarray and clustering of expressed genes we have analyzed the mechanism of inhibition of wild-type p53-induced apoptosis by the cytokine interleukin 6 (IL-6) and the calcium mobilizer thapsigargin (TG).	Thapsigargin	212-214	P53	Homo sapiens	113-116
12753897-0	2003	Identification of two serine residues important for p53 DNA binding and protein stability.	Serine	22-28	P53	Homo sapiens	52-55
12753897-3	2003	However, the substitution of the serine residues with the aspartic acid (S116/127D) abolished p53 DNA binding and led to protein stabilization.	Serine	33-39	P53	Homo sapiens	94-97
12637545-8	2003	We also show that physiological targets of ATM, p53 Ser-15 and Chk2 Thr-68, were phosphorylated by Cr(VI) exposure in an ATM-dependent fashion.	Serine	52-55	P53	Homo sapiens	48-51
12761496-3	2003	We demonstrated here that low doses of PTX that are unable to activate the spindle assembly checkpoint, upregulate p21 by a p53-dependent pathway and induce its translocation to the cytoplasm.	Paclitaxel	39-42	P53	Homo sapiens	124-127
12771935-3	2003	Following 8 h of exposure to taxol, the cell line DoHH2 (p53 wild type) exhibited mitotic arrest and engagement of apoptosis, whereas the cell line SU-DHL-4 (p53 mutant) breached cell-cycle arrest with progression to an abnormal cycle and a 24 h delay in the engagement of apoptosis.	Paclitaxel	29-34	P53	Homo sapiens	57-60
12771935-3	2003	Following 8 h of exposure to taxol, the cell line DoHH2 (p53 wild type) exhibited mitotic arrest and engagement of apoptosis, whereas the cell line SU-DHL-4 (p53 mutant) breached cell-cycle arrest with progression to an abnormal cycle and a 24 h delay in the engagement of apoptosis.	Paclitaxel	29-34	P53	Homo sapiens	158-161
12853327-0	2003	The role of caspase III inhibition in methamphetamine-induced alterations in p53 and bcl-2 expression: correlation with dopaminergic neurotoxicity.	Methamphetamine	38-53	P53	Homo sapiens	77-80
12926120-4	2003	The objective response rate by cisplatin (CDDP)-based chemotherapy was significantly lower in patients with p53-positive tumors compared to those with p53-negative tumors (22% versus 59%, p = 0.0143).	Cisplatin	31-40	P53	Homo sapiens	108-111
12750254-5	2003	p29ING4 and p28ING5 enhance p53 acetylation at Lys-382 residues, and physically interact with p300, a member of histone acetyl transferase complexes, and p53 in vivo.	Lysine	47-50	P53	Homo sapiens	28-31
12750254-5	2003	p29ING4 and p28ING5 enhance p53 acetylation at Lys-382 residues, and physically interact with p300, a member of histone acetyl transferase complexes, and p53 in vivo.	Lysine	47-50	P53	Homo sapiens	154-157
12894503-3	2003	Caffeine, a nonspecific inhibitor of ATR, enhanced the cytotoxic effect of cisplatin, modestly decreased the p53 and p21WAF-1 response to cisplatin, and affected the cdc2-p34/cyclin B1 complex by decreasing both cyclin B1 protein accumulation and cdc2-p34 tyrosine 15 phosphorylation.	Cisplatin	138-147	P53	Homo sapiens	109-112
12926120-4	2003	The objective response rate by cisplatin (CDDP)-based chemotherapy was significantly lower in patients with p53-positive tumors compared to those with p53-negative tumors (22% versus 59%, p = 0.0143).	Cisplatin	31-40	P53	Homo sapiens	151-154
12926120-4	2003	The objective response rate by cisplatin (CDDP)-based chemotherapy was significantly lower in patients with p53-positive tumors compared to those with p53-negative tumors (22% versus 59%, p = 0.0143).	Cisplatin	42-46	P53	Homo sapiens	108-111
12926120-4	2003	The objective response rate by cisplatin (CDDP)-based chemotherapy was significantly lower in patients with p53-positive tumors compared to those with p53-negative tumors (22% versus 59%, p = 0.0143).	Cisplatin	42-46	P53	Homo sapiens	151-154
12534344-6	2003	In cultured cortical neurons, we found that A beta increased p53 protein expression and phosphorylation of p53 at Ser(15).	Serine	114-117	P53	Homo sapiens	107-110
12750239-10	2003	After adjustment for age, cigarette smoking, areca quid chewing, and alcohol drinking, the Gln/Gln genotype still showed an independent association with the frequency of p53 mutation (odd ratio, 4.50; 95% confidence interval, 1.52-13.36).	Alcohols	69-76	P53	Homo sapiens	170-173
12944180-1	2003	Aberrant p53 protein accumulation was measured immunohistologically in 342 colorectal paraffin-embedded tissue sections from 115 patients (24 with adenocarcinoma, 59 with adenoma and 32 "hospital controls").	Paraffin	86-94	P53	Homo sapiens	9-12
12706118-5	2003	We have found up-regulated levels of the cyclin-dependent kinase 2 (cdk2) protein in HDF expressing 143(ala) mutant p53 as compared to senescent controls, together with an increase in p21-free cdk2 which, in conjunction with cyclin E, is able to form an active kinase which can phosphorylate the retinoblastoma protein.	Alanine	104-107	P53	Homo sapiens	116-119
12772781-5	2003	The incidence of p53 mutation in hepatocellular cancer patients with chronic liver disease due to hepatitis B virus infection was significantly higher than in those with chronic liver disease due to alcohol, indicating that not alcohol but hepatitis B virus, in fact induces the mutations in p53 gene.	Alcohols	228-235	P53	Homo sapiens	17-20
12684687-4	2003	We report that Brca1-deficiency in p53-null cells was associated with increased sensitivity to the topoisomerase I poisons camptothecin and topotecan, the topoisomerase II poisons doxorubicin, mitoxantrone and etoposide, and to the platinum compounds carboplatin and oxaliplatin, but not to the antimetabolites 5-fluorouracil and gemcitabine and the taxanes docetaxel and paclitaxel.	Doxorubicin	180-191	P53	Homo sapiens	35-38
12684687-4	2003	We report that Brca1-deficiency in p53-null cells was associated with increased sensitivity to the topoisomerase I poisons camptothecin and topotecan, the topoisomerase II poisons doxorubicin, mitoxantrone and etoposide, and to the platinum compounds carboplatin and oxaliplatin, but not to the antimetabolites 5-fluorouracil and gemcitabine and the taxanes docetaxel and paclitaxel.	Platinum	232-240	P53	Homo sapiens	35-38
12684687-4	2003	We report that Brca1-deficiency in p53-null cells was associated with increased sensitivity to the topoisomerase I poisons camptothecin and topotecan, the topoisomerase II poisons doxorubicin, mitoxantrone and etoposide, and to the platinum compounds carboplatin and oxaliplatin, but not to the antimetabolites 5-fluorouracil and gemcitabine and the taxanes docetaxel and paclitaxel.	Fluorouracil	311-325	P53	Homo sapiens	35-38
12684687-4	2003	We report that Brca1-deficiency in p53-null cells was associated with increased sensitivity to the topoisomerase I poisons camptothecin and topotecan, the topoisomerase II poisons doxorubicin, mitoxantrone and etoposide, and to the platinum compounds carboplatin and oxaliplatin, but not to the antimetabolites 5-fluorouracil and gemcitabine and the taxanes docetaxel and paclitaxel.	Taxoids	350-357	P53	Homo sapiens	35-38
12684687-4	2003	We report that Brca1-deficiency in p53-null cells was associated with increased sensitivity to the topoisomerase I poisons camptothecin and topotecan, the topoisomerase II poisons doxorubicin, mitoxantrone and etoposide, and to the platinum compounds carboplatin and oxaliplatin, but not to the antimetabolites 5-fluorouracil and gemcitabine and the taxanes docetaxel and paclitaxel.	Paclitaxel	372-382	P53	Homo sapiens	35-38
12692899-6	2003	It was found that expression of p53 was induced by oxidative stress, particularly when glucose had been omitted from the culture medium.	Glucose	87-94	P53	Homo sapiens	32-35
12715164-0	2003	p53 expression and resistance against paclitaxel in patients with metastatic breast cancer.	Paclitaxel	38-48	P53	Homo sapiens	0-3
12715164-13	2003	CONCLUSION: The immunohistochemical detection of p53 characterizes patients with metastatic breast cancer unlikely to respond to paclitaxel.	Paclitaxel	129-139	P53	Homo sapiens	49-52
12694871-0	2003	Recognition of DNA modified by antitumor cisplatin by "latent" and "active" protein p53.	Cisplatin	41-50	P53	Homo sapiens	84-87
12802925-2	2003	The cell line, designated TMBL-1, carried a His-175 mutant p53.	Histidine	44-47	P53	Homo sapiens	59-62
12802925-9	2003	Moreover, TMBL-1 cells are sensitive to paclitaxel, which could induce p53-independent apoptosis.	Paclitaxel	40-50	P53	Homo sapiens	71-74
12698197-0	2003	Doxorubicin and vinorelbine act independently via p53 expression and p38 activation respectively in breast cancer cell lines.	Doxorubicin	0-11	P53	Homo sapiens	50-53
12698197-4	2003	The aim of this study was to establish the effects of doxorubicin and vinorelbine, as single agents, in combination, and as sequential treatments, on signal transduction and p53 in the breast cancer cell lines MCF-7 and MDA-MB-468.	Doxorubicin	54-65	P53	Homo sapiens	174-177
12698197-7	2003	Doxorubicin treatment resulted in increased p53 expression, without changes in MAPK or p38 activity.	Doxorubicin	0-11	P53	Homo sapiens	44-47
12698197-9	2003	This additivism, where doxorubicin acts via p53 expression and vinorelbine through p38 activation, may contribute to the high clinical response rate when the two drugs are used together in the treatment of breast cancer.	Doxorubicin	23-34	P53	Homo sapiens	44-47
12694301-5	2003	Radical (i.e., superoxide) (O2-) formation in response to oxLDL is associated with p53, as well as HIF-1 alpha accumulation in human macrophages, a process that is antagonized by NO.	Superoxides	15-25	P53	Homo sapiens	83-86
12694301-5	2003	Radical (i.e., superoxide) (O2-) formation in response to oxLDL is associated with p53, as well as HIF-1 alpha accumulation in human macrophages, a process that is antagonized by NO.	Superoxides	28-30	P53	Homo sapiens	83-86
12684648-2	2003	A sequence polymorphism at codon 72 of the p53 gene results in either a proline or an arginine and may induce different functional activities.	Arginine	86-94	P53	Homo sapiens	43-46
12684648-4	2003	It has been reported that the p53 Arg homozygous genotype could be a potential genetic risk factor for cancer.	Arginine	34-37	P53	Homo sapiens	30-33
12684648-8	2003	A significantly higher prevalence of homozygosity for the p53 Arg allele was observed in the patients as compared to the controls.	Arginine	62-65	P53	Homo sapiens	58-61
12534345-9	2003	These results provide novel information on the functional interplay between CTF2 and p53/p73 as important determinants of their function in cell proliferation, apoptosis, DNA repair and cisplatin resistance.	Cisplatin	186-195	P53	Homo sapiens	85-88
12702563-7	2003	Both microPET imaging and biodistribution studies showed time- and dose-dependent increases in accumulation of the reporter substrate 9-(4-[(18)F]-fluoro-3-hydroxymethylbutyl)guanine only in p53-TAg tumors.	9-(4-fluoro-3-hydroxymethylbutyl)guanine	134-182	P53	Homo sapiens	191-194
12702572-8	2003	Instead, morphine caused an NH(2)-terminal phosphorylation of p53 at Ser(9) and/or Ser(15) and a stabilization of p53 in MCF-7 cells that express wild-type p53.	Morphine	9-17	P53	Homo sapiens	62-65
12702572-8	2003	Instead, morphine caused an NH(2)-terminal phosphorylation of p53 at Ser(9) and/or Ser(15) and a stabilization of p53 in MCF-7 cells that express wild-type p53.	Morphine	9-17	P53	Homo sapiens	114-117
12702572-8	2003	Instead, morphine caused an NH(2)-terminal phosphorylation of p53 at Ser(9) and/or Ser(15) and a stabilization of p53 in MCF-7 cells that express wild-type p53.	Morphine	9-17	P53	Homo sapiens	114-117
12702572-8	2003	Instead, morphine caused an NH(2)-terminal phosphorylation of p53 at Ser(9) and/or Ser(15) and a stabilization of p53 in MCF-7 cells that express wild-type p53.	Serine	69-72	P53	Homo sapiens	62-65
12702572-14	2003	Our results suggest that morphine, alone or in combination with Nx, may reduce the growth of certain tumors, apparently in part through activation of p53.	Morphine	25-33	P53	Homo sapiens	150-153
12694871-4	2003	Binding of active, latent, and in vitro-activated p53 protein to DNA fragments modified by antitumor cisplatin was studied using electrophoretic mobility shift assay in agarose gels and immunoblotting analysis.	Cisplatin	101-110	P53	Homo sapiens	50-53
12694871-5	2003	We found that both latent and active p53 forms bound to random sequences of DNA globally modified by cisplatin with a higher affinity than to unmodified DNA.	Cisplatin	101-110	P53	Homo sapiens	37-40
12694871-8	2003	Competition experiments involving a 20-bp consensus sequence of p53 suggested that the p53 core domain was a primary binding site of the active p53 when it bound to DNA fragments lacking consensus sequence, but modified by cisplatin.	Cisplatin	223-232	P53	Homo sapiens	64-67
12694871-8	2003	Competition experiments involving a 20-bp consensus sequence of p53 suggested that the p53 core domain was a primary binding site of the active p53 when it bound to DNA fragments lacking consensus sequence, but modified by cisplatin.	Cisplatin	223-232	P53	Homo sapiens	87-90
12694871-8	2003	Competition experiments involving a 20-bp consensus sequence of p53 suggested that the p53 core domain was a primary binding site of the active p53 when it bound to DNA fragments lacking consensus sequence, but modified by cisplatin.	Cisplatin	223-232	P53	Homo sapiens	87-90
12659830-1	2003	PRPK (p53-related protein kinase) has been reported as a novel protein kinase which binds to the tumor suppressor protein p53 and induces phosphorylation of p53 at Ser 15.	Serine	164-167	P53	Homo sapiens	6-9
12687016-2	2003	Our previous study showed that the antitumor activity of resveratrol occurs through mitogen-activated protein kinases-mediated p53 activation and induction of apoptosis.	Resveratrol	57-68	P53	Homo sapiens	127-130
12499368-2	2003	Phosphorylation at the CHK2 site (Ser(20)) in the N-terminal activation domain of p53 stabilized p300 binding.	Serine	34-37	P53	Homo sapiens	82-85
12499368-8	2003	The phosphopeptide binding activity of p300 is critical for DNA-dependent acetylation, as p53 acetylation was inhibited by phospho-Ser(20) peptides.	Serine	131-134	P53	Homo sapiens	90-93
12659830-1	2003	PRPK (p53-related protein kinase) has been reported as a novel protein kinase which binds to the tumor suppressor protein p53 and induces phosphorylation of p53 at Ser 15.	Serine	164-167	P53	Homo sapiens	122-125
12628744-3	2003	Here we show that, in neuronal cells, divergent cellular insults, i.e. the exposure to glutamate, beta-amyloid (Abeta) or H(2)O(2), may converge to a common pathway that initiate with elevation of p53 protein levels.	Glutamic Acid	87-96	P53	Homo sapiens	197-200
12501250-3	2003	Because Tat has been shown to interact with histone acetyltransferase domains of p300/cAMP-responsive element-binding protein (CREB)-binding protein and p300/CREB-binding protein-associated factor, we have investigated whether Tat might alter p53 acetylation and tumor suppressor-responsive transcription.	Cyclic AMP	86-90	P53	Homo sapiens	243-246
12501250-5	2003	Further, p53 trans-activation of the 14-3-3varsigma promoter was markedly repressed by Tat-histone acetyltransferase interactions, and p53 acetylation by p300/CREB-binding protein-associated factor on residue Lys(320) was diminished as a result of Tat-histone acetyltransferase binding in vivo and in vitro.	Lysine	209-212	P53	Homo sapiens	9-12
12501250-7	2003	Finally, HIV-1-infected Molt-4 cells displayed reduced p53 acetylation on lysines 320 and 373 in response to UV irradiation.	Lysine	74-81	P53	Homo sapiens	55-58
12531896-0	2003	The cytoprotective aminothiol WR1065 activates p53 through a non-genotoxic signaling pathway involving c-Jun N-terminal kinase.	Aminothiol	19-29	P53	Homo sapiens	47-50
12531896-5	2003	Furthermore, WR1065 activates the JNK (c-Jun N-terminal kinase), decreases complex formation between p53 and inactive JNK, and phosphorylates p53 at Thr-81, a known site of phosphorylation by JNK.	Threonine	149-152	P53	Homo sapiens	142-145
12606123-3	2003	Furthermore, p53 phosphorylation at serine 15 is delayed or diminished in Msh2-deficient cells, suggesting that Msh2 may act upstream of p53 in a post-UVB apoptosis or growth arrest response pathway.	Serine	36-42	P53	Homo sapiens	13-16
12606123-3	2003	Furthermore, p53 phosphorylation at serine 15 is delayed or diminished in Msh2-deficient cells, suggesting that Msh2 may act upstream of p53 in a post-UVB apoptosis or growth arrest response pathway.	Serine	36-42	P53	Homo sapiens	137-140
12628747-0	2003	Nitric oxide evoked p53-accumulation and apoptosis.	Nitric Oxide	0-12	P53	Homo sapiens	20-23
12670900-0	2003	Fas-mediated apoptosis is dependent on wild-type p53 status in human cancer cells expressing a temperature-sensitive p53 mutant alanine-143.	Alanine	128-135	P53	Homo sapiens	117-120
12646262-3	2003	A549 lung adenocarcinoma cells, in which p53 was eliminated with the HPV16 E6 gene, exhibited efficient arrest in the G2 phase when treated with adriamycin.	Doxorubicin	145-155	P53	Homo sapiens	41-44
12663048-0	2003	Activation of p53 by the cytoprotective aminothiol WR1065: DNA-damage-independent pathway and redox-dependent modulation of p53 DNA-binding activity.	Aminothiol	40-50	P53	Homo sapiens	14-17
12663048-4	2003	Here, we demonstrated that p53 accumulation by WR1065 in MCF-7 cells did not result from the formation of DNA-damage as measured by DNA fragmentation and Comet assay, nor from oxidative stress as detected by measurement of glutathione levels, lipid peroxidation and reactive oxygen species production.	Glutathione	223-234	P53	Homo sapiens	27-30
12663048-4	2003	Here, we demonstrated that p53 accumulation by WR1065 in MCF-7 cells did not result from the formation of DNA-damage as measured by DNA fragmentation and Comet assay, nor from oxidative stress as detected by measurement of glutathione levels, lipid peroxidation and reactive oxygen species production.	Reactive Oxygen Species	266-289	P53	Homo sapiens	27-30
12663048-7	2003	Direct reduction by WR1065 of key cysteines in p53 may play an important role in this alternative pathway, as shown by the fact that WR1065 activated the redox-dependent, DNA-binding activity of p53 in vitro.	Cysteine	34-43	P53	Homo sapiens	47-50
12663048-7	2003	Direct reduction by WR1065 of key cysteines in p53 may play an important role in this alternative pathway, as shown by the fact that WR1065 activated the redox-dependent, DNA-binding activity of p53 in vitro.	Cysteine	34-43	P53	Homo sapiens	195-198
12719724-0	2003	Nitric oxide promotes p53 nuclear retention and sensitizes neuroblastoma cells to apoptosis by ionizing radiation.	Nitric Oxide	0-12	P53	Homo sapiens	22-25
12719724-1	2003	Nitric oxide (NO) is a potent activator of the p53 tumor suppressor protein.	Nitric Oxide	0-12	P53	Homo sapiens	47-50
12719724-5	2003	NO induces phosphorylation of p53 on serine 15, which does not require ATM but rather appears to depend on the ATM-related ATR kinase.	Serine	37-43	P53	Homo sapiens	30-33
12719724-6	2003	An ATR-kinase dead mutant or caffeine, which blocks the kinase activity of ATR, effectively abolishes the ability of NO to cause p53 nuclear retention, concomitant with its inhibition of p53 serine 15 phosphorylation.	Serine	191-197	P53	Homo sapiens	187-190
12648751-2	2003	We performed a case-control association study between sporadic AD and the common proline/arginine polymorphism at codon 72 in the pro-apoptotic gene p53, in 109 sporadic AD patients and in 111 controls.	Arginine	89-97	P53	Homo sapiens	149-152
12675680-4	2003	p53 interacts with mitochondria either directly or through activation of the genes for pro-apoptotic proteins such as Bax or NOXA or genes that encode redox enzymes responsible for the production of reactive oxygen species (ROS).	Reactive Oxygen Species	199-222	P53	Homo sapiens	0-3
12675680-4	2003	p53 interacts with mitochondria either directly or through activation of the genes for pro-apoptotic proteins such as Bax or NOXA or genes that encode redox enzymes responsible for the production of reactive oxygen species (ROS).	Reactive Oxygen Species	224-227	P53	Homo sapiens	0-3
12726864-3	2003	A polymorphism encoding either arginine (72R) or proline (72P) at codon 72 of p53 influences inhibition of p73 by a range of p53 mutants identified in squamous cancers.	Arginine	31-39	P53	Homo sapiens	78-81
12726864-3	2003	A polymorphism encoding either arginine (72R) or proline (72P) at codon 72 of p53 influences inhibition of p73 by a range of p53 mutants identified in squamous cancers.	Arginine	31-39	P53	Homo sapiens	125-128
26680929-12	2003	CONCLUSION: From these results, it was concluded that p53-defected SaOS2 cells are much more sensitive to Taxol-induced apoptosis than p53-expressed U2OS cells.	Paclitaxel	106-111	P53	Homo sapiens	54-57
26680929-2	2003	In this study, to further demonstrate the differential effect of the tumor suppressor gene, p53, on the Taxol-induced apoptosis in osteogenic sarcoma cell lines, we used p53-defected SaOS2 cells and wild type p53-expressed U2OS cells.	Paclitaxel	104-109	P53	Homo sapiens	92-95
26680929-4	2003	To examine whether the differential expressions of p53, in U2OS and SaOS2 cells, were associated with Taxol-induced apoptosis, DNA fragmentation assays were performed on both cytosolic and genomic DNA.	Paclitaxel	102-107	P53	Homo sapiens	51-54
12676607-5	2003	Among serines in p53 protein immunoprecipitated from A549 cells treated with chrysotile, only Ser15 was markedly phosphorylated.	Serine	6-13	P53	Homo sapiens	17-20
26680929-6	2003	RESULTS: The cell viability of the p53-defected SaOS2 cells was markedly decreased with Taxol treatment.	Paclitaxel	88-93	P53	Homo sapiens	35-38
26680929-10	2003	The Taxol-induced apoptosis in p53 defected-osteogenic sarcoma cells was associated with the PARP cleavage as a result of the increased activity of caspase 3, and the high expressions of cyclin B1 and PLK.	Paclitaxel	4-9	P53	Homo sapiens	31-34
12684432-0	2003	Low-dose fractionated radiation potentiates the effects of Paclitaxel in wild-type and mutant p53 head and neck tumor cell lines.	Paclitaxel	59-69	P53	Homo sapiens	94-97
12684432-7	2003	The cell cycle regulator p53 and its target genes p21(waf1/cip1) and BAX were induced in SCC-61 cells treated with 2 Gy, Paclitaxel, or in combination, but not in SQ-20B cells.	Paclitaxel	121-131	P53	Homo sapiens	25-28
12684392-0	2003	Combined vascular endothelial growth factor and TP53 status predicts poor response to tamoxifen therapy in estrogen receptor-positive advanced breast cancer.	Tamoxifen	86-95	P53	Homo sapiens	48-52
12684392-5	2003	RESULTS: In univariate analysis, both TP53 gene mutation (28% of the tumors) and a VEGF level above the median value were significantly associated with a short progression-free survival, post-relapse overall survival, and a poor rate of response to tamoxifen.	Tamoxifen	249-258	P53	Homo sapiens	38-42
12684392-6	2003	In Cox multivariate regression analysis including the traditional predictive factors, the addition of TP53 gene mutation and VEGF status, alone or in combination, significantly predicted a poor efficacy of tamoxifen treatment.	Tamoxifen	206-215	P53	Homo sapiens	102-106
12684392-9	2003	CONCLUSIONS: Combined TP53 gene mutation status and high VEGF levels of ER-positive primary breast tumors independently predict a poor course of the disease of patients with advanced breast cancer treated with tamoxifen.	Tamoxifen	210-219	P53	Homo sapiens	22-26
12841678-7	2003	p53 protein accumulation was determined by immunohistochemistry on paraffin-embedded tumor specimens from 58/71 samples available for this study.	Paraffin	67-75	P53	Homo sapiens	0-3
12640128-8	2003	We found that centrosomal p53 is poly(ADP-ribosyl)ated in vivo and centrosomal PARP-1 directly catalyzes poly(ADP-ribosyl)ation of p53 in vitro.	Adenosine Diphosphate	37-41	P53	Homo sapiens	26-29
12686631-9	2003	Ehp53 also contains seven of the eight DNA-binding residues and two of the four Zn(2+)-binding sites described for p53.	Zinc	80-86	P53	Homo sapiens	2-5
12644594-0	2003	Resveratrol increases serine15-phosphorylated but transcriptionally impaired p53 and induces a reversible DNA replication block in serum-activated vascular smooth muscle cells.	Resveratrol	0-11	P53	Homo sapiens	77-80
12905708-2	2003	METHODS: The p21WAF1 and p53 gene were transfected respectively into a human lung adenocarcinoma cell line, GLC-82.	Glucose	108-111	P53	Homo sapiens	25-28
12644594-5	2003	This is of particular interest because phosphorylated p53 protein (serine(15)) is strongly enhanced by this substance.	Serine	67-73	P53	Homo sapiens	54-57
12668287-0	2003	Prognostic value of overexpression of p53 in human ovarian carcinoma patients receiving cisplatin.	Cisplatin	88-97	P53	Homo sapiens	38-41
12668287-3	2003	The aim of this study was to investigate the independent prognostic significance of p53 overexpression in patients with ovarian carcinoma who are treated with cisplatin.	Cisplatin	159-168	P53	Homo sapiens	84-87
12668287-12	2003	These findings suggest that overexpression of p53 in ovarian carcinoma is associated with unfavorable clinical outcome in patients treated with cisplatin-based chemotherapy.	Cisplatin	144-153	P53	Homo sapiens	46-49
12668287-13	2003	Therefore, detection of p53 overexpression using the DO7 antibody may be considered as a predictive marker of chemoresistance for cisplatin in patients with ovarian carcinoma.	Cisplatin	130-139	P53	Homo sapiens	24-27
12671666-4	2003	In particular, we highlight the interaction between nitric oxide and p53 as a crucial pathway in inflammatory-mediated carcinogenesis.	Nitric Oxide	52-64	P53	Homo sapiens	69-72
12692263-5	2003	E2FBP1/DRIL1was induced by p53 and up-regulated following DNA damage caused by UV radiation or doxorubicin treatment in a manner dependent on endogenous p53.	Doxorubicin	95-106	P53	Homo sapiens	153-156
12679912-1	2003	AIM: One of the characteristics of hepatocellular carcinoma (HCC) in Qidong area is the selective mutation resulting in a serine substitution at codon 249 of the p53 gene (1, 20), and it has been identified as a "hotspot" mutation in heptocellular carcinomas occurring in populations exposed to aflatoxin and with high prevalence of hepatitis B virus carriers (2,3,9, 10,16,24).	Serine	122-128	P53	Homo sapiens	162-165
12679912-6	2003	RESULTS: We found in exon 7 of p53 gene G-T transversion at the third base of codon 249 resulting 249(Arg) - 249(Ser) mutation in 10/25 (40 %) hepatocellular carcinoma cases, 4/20 (20 %) cirrhotics, and 2/30 (7 %) healthy controls.	Arginine	102-105	P53	Homo sapiens	31-34
12679912-6	2003	RESULTS: We found in exon 7 of p53 gene G-T transversion at the third base of codon 249 resulting 249(Arg) - 249(Ser) mutation in 10/25 (40 %) hepatocellular carcinoma cases, 4/20 (20 %) cirrhotics, and 2/30 (7 %) healthy controls.	Serine	113-116	P53	Homo sapiens	31-34
12679912-8	2003	CONCLUSION: These data show that the 249(Ser) p53 mutation in plasma is strongly associated with hepatocellular carcinoma in Qidong patients.	Serine	41-44	P53	Homo sapiens	46-49
12634062-2	2003	Circular dichroism, Fourier transform infrared spectroscopy and staining with Congo red and thioflavin T showed that p53tet-wt and p53tet-R337H adopt an alternative beta-sheet conformation (p53tet-wt-beta and p53tet-R337H-beta, respectively), characteristic of amyloid-like fibrils, when incubated at pH 4.0 and elevated temperatures.	Congo Red	78-87	P53	Homo sapiens	117-120
12648880-0	2003	P53 expression in spontaneous and estradiol-induced endometrial hyperplasia during menopause.	Estradiol	34-43	P53	Homo sapiens	0-3
12634062-2	2003	Circular dichroism, Fourier transform infrared spectroscopy and staining with Congo red and thioflavin T showed that p53tet-wt and p53tet-R337H adopt an alternative beta-sheet conformation (p53tet-wt-beta and p53tet-R337H-beta, respectively), characteristic of amyloid-like fibrils, when incubated at pH 4.0 and elevated temperatures.	Congo Red	78-87	P53	Homo sapiens	131-134
12648880-1	2003	OBJECTIVE: To determine the percentage of endometrial hyperplasia positive for p53 expression in both spontaneously occurring cases or following the use of unopposed estradiol.	Estradiol	166-175	P53	Homo sapiens	79-82
12648880-4	2003	P53 expression was detected in paraffin-embedded endometrial specimens by immunohistochemical methods.	Paraffin	31-39	P53	Homo sapiens	0-3
12569576-0	2003	Differential expression of genes induced by resveratrol in LNCaP cells: P53-mediated molecular targets.	Resveratrol	44-55	P53	Homo sapiens	72-75
12648880-5	2003	RESULTS: The percentage of endometrial hyperplasia positive for p53 expression was significantly greater in spontaneously occurring hyperplasia than in cases induced by the unopposed use of estradiol.	Estradiol	190-199	P53	Homo sapiens	64-67
12618886-2	2003	Amifostine induced a G1 arrest and protected against paclitaxel toxicity in p53-proficient but not in p53-deficient cells.	Paclitaxel	53-63	P53	Homo sapiens	76-79
12519780-0	2003	Identification of a functional link for the p53 tumor suppressor protein in dexamethasone-induced growth suppression.	Dexamethasone	76-89	P53	Homo sapiens	44-47
12519780-3	2003	To characterize the relationship of PP5, glucocorticoid receptor activation and p53, here we describe the development of chimeric antisense oligonucleotides that potently inhibit human p53 expression.	Oligonucleotides	140-156	P53	Homo sapiens	80-83
12519780-3	2003	To characterize the relationship of PP5, glucocorticoid receptor activation and p53, here we describe the development of chimeric antisense oligonucleotides that potently inhibit human p53 expression.	Oligonucleotides	140-156	P53	Homo sapiens	185-188
12519780-6	2003	Suppression of p53 also blocks dexamethasone-induced p21(WAF1/Cip1) expression and G(1)-growth arrest.	Dexamethasone	31-44	P53	Homo sapiens	15-18
12519780-9	2003	However, dexamethasone treatment is associated with an increase in p53 phosphorylation at Ser-15.	Dexamethasone	9-22	P53	Homo sapiens	67-70
12519780-9	2003	However, dexamethasone treatment is associated with an increase in p53 phosphorylation at Ser-15.	Serine	90-93	P53	Homo sapiens	67-70
12519780-10	2003	Suppression of PP5 expression with ISIS 15534 also results in the hyperphosphorylation of p53 at Ser-15.	Serine	97-100	P53	Homo sapiens	90-93
12519780-11	2003	Together, these findings indicate that the basal expression of p53 plays a functional role in a glucocorticoid receptor-mediated response regulating the expression of p21(Waf1/Cip1) via a mechanism that is suppressed by PP5 and associated with the phosphorylation of p53 at Ser-15.	Serine	274-277	P53	Homo sapiens	63-66
12532420-5	2003	The mutation status of exons 5-8 of p53 was analyzed by denaturing high pressure liquid chromatography (DHPLC) in formalin-fixed, paraffin-embedded tumor sections, followed by direct sequencing of cases with aberrant chromatographic patterns.	Paraffin	130-138	P53	Homo sapiens	36-39
12601175-0	2003	Interaction of mismatch repair protein PMS2 and the p53-related transcription factor p73 in apoptosis response to cisplatin.	Cisplatin	114-123	P53	Homo sapiens	52-55
12600206-11	2003	Through a combination of induced p53 aggregation and diminished site-specific DNA binding activity, Zn(2+) loss may represent a significant inactivation pathway for p53 in the cell.	Zinc	100-106	P53	Homo sapiens	33-36
12695658-0	2003	There"s NO business like p53 business: nitric oxide regulates phosphorylation of p53 in chronic inflammatory disease.	Nitric Oxide	39-51	P53	Homo sapiens	25-28
12600206-11	2003	Through a combination of induced p53 aggregation and diminished site-specific DNA binding activity, Zn(2+) loss may represent a significant inactivation pathway for p53 in the cell.	Zinc	100-106	P53	Homo sapiens	165-168
12598349-0	2003	Correlation of p53 status with outcome of neoadjuvant chemotherapy using paclitaxel and doxorubicin in stage IIIB breast cancer.	Paclitaxel	73-83	P53	Homo sapiens	15-18
12598349-0	2003	Correlation of p53 status with outcome of neoadjuvant chemotherapy using paclitaxel and doxorubicin in stage IIIB breast cancer.	Doxorubicin	88-99	P53	Homo sapiens	15-18
12615724-5	2003	However, in contrast to p53 wild-type epithelium, estrogen and progesterone, singly or in combination, strongly enhance tumorigenesis in p53-null mammary epithelium.	Progesterone	63-75	P53	Homo sapiens	137-140
12695658-0	2003	There"s NO business like p53 business: nitric oxide regulates phosphorylation of p53 in chronic inflammatory disease.	Nitric Oxide	39-51	P53	Homo sapiens	81-84
12751373-1	2003	We previously reported that defects in apoptotic pathways (mutations in the TP53 gene) predicted resistance to doxorubicin monotherapy.	Doxorubicin	111-122	P53	Homo sapiens	76-80
12824923-0	2003	Enhanced sensitivity to cis-diamminedichloroplatinum(II) of a human carcinoma cell line with mutated p53 gene by cyclin-dependent kinase inhibitor p21(WAF1) expression.	Cisplatin	24-52	P53	Homo sapiens	101-104
12628849-2	2003	A common polymorphism at codon 72 of exon 4 encoding either arginine (Arg) or proline (Pro) has been shown to affect HPV-mediated degradation of p53 in vitro, and may represent a risk factor for HPV-induced carcinogenesis.	Arginine	60-68	P53	Homo sapiens	145-148
12628849-2	2003	A common polymorphism at codon 72 of exon 4 encoding either arginine (Arg) or proline (Pro) has been shown to affect HPV-mediated degradation of p53 in vitro, and may represent a risk factor for HPV-induced carcinogenesis.	Arginine	70-73	P53	Homo sapiens	145-148
12628849-7	2003	Among the TP53 amplified samples, the rate of Arg homozygosity in penile SCC was 61% compared with 68% in BL (non-significant (NS)).	Arginine	46-49	P53	Homo sapiens	10-14
12751374-0	2003	A mutant TP53 gene status is associated with a poor prognosis and anthracycline-resistance in breast cancer patients.	Anthracyclines	66-79	P53	Homo sapiens	9-13
12751374-9	2003	The response rate to anthracycline-based chemotherapy in metastatic disease was low in the p53-positive cases.	Anthracyclines	21-34	P53	Homo sapiens	91-94
12514115-6	2003	We found that CsA-induced cell death is independent of caspase activation, p53 induction, and calcineurin inhibition.	Cyclosporine	14-17	P53	Homo sapiens	75-78
12751374-10	2003	Our results help to clarify the independent prognostic role of a mutated p53 status in breast cancer patients, indicating that this gene might be predictive of anthracycline resistance.	Anthracyclines	160-173	P53	Homo sapiens	73-76
14505437-7	2003	Northern analysis revealed that expression of p53 in methionine-treated MCF-7 cells was approximately 70% lower than that of control cells.	Methionine	53-63	P53	Homo sapiens	46-49
12619112-4	2003	Several in vitro, animal and clinical studies have shown that normal p53 is required for the response of colorectal cancers to 5-fluorouracil-based chemotherapy.	Fluorouracil	127-141	P53	Homo sapiens	69-72
14505437-10	2003	This study shows that excess methionine (5 g/L) inhibited proliferation of MCF-7 breast cancer cells, and down regulation of p53 is correlated with this inhibition.	Methionine	29-39	P53	Homo sapiens	125-128
12570841-2	2003	Recent studies have focused on the mechanism of inhibition of phosphorylation of the mutant type of p53 protein, structural characterisation of the drug-DNA complex, the synthesis of carbohydrate derivatives and calculations of physical parameters, including dipole moments, as potential screens to allow identification of new active derivatives.	Carbohydrates	183-195	P53	Homo sapiens	100-103
12623637-0	2003	p53-dependent hyperthermic enhancement of tumour growth inhibition by X-ray or carbon-ion beam irradiation.	Carbon	79-85	P53	Homo sapiens	0-3
12628584-6	2003	Further, we found that nitric oxide synthase inhibitor N(G)-nitro-L-arginine prevented deltamethrin-induced neuronal apoptosis and altered expression of p53, Bax, and Bcl-2.	Nitric Oxide	23-35	P53	Homo sapiens	153-156
12612087-6	2003	Moreover, unlike the DNA-damaging agent adriamycin, which induces strong phosphorylation of p53 on serines 15 and 20, CP-31398 exposure leads to no measurable phosphorylation on these sites.	Doxorubicin	40-50	P53	Homo sapiens	92-95
12612087-6	2003	Moreover, unlike the DNA-damaging agent adriamycin, which induces strong phosphorylation of p53 on serines 15 and 20, CP-31398 exposure leads to no measurable phosphorylation on these sites.	Serine	99-106	P53	Homo sapiens	92-95
12592393-1	2003	It has been shown that methylation of CpG dinucleotides located in the promoter region of TP53 is associated with low expression levels of this gene.	cytidylyl-3'-5'-guanosine	38-55	P53	Homo sapiens	90-94
12567188-1	2003	The gene TP53, encoding p53, has a common sequence polymorphism that results in either proline or arginine at amino-acid position 72.	Arginine	98-106	P53	Homo sapiens	9-13
12567188-1	2003	The gene TP53, encoding p53, has a common sequence polymorphism that results in either proline or arginine at amino-acid position 72.	Arginine	98-106	P53	Homo sapiens	24-27
12609712-7	2003	Oxoguanine modifications persisted in cells affected by ovulation in which synthesis of p53 was negated in culture by an antisense oligonucleotide.	Oligonucleotides	131-146	P53	Homo sapiens	88-91
12578368-4	2003	The unfolding kinetics of the four mutant forms of barstar were monitored by measurement of the changes in the fluorescence intensity of Trp53 in the unlabeled and TNB-labeled proteins.	Trinitrobenzenesulfonic Acid	164-167	P53	Homo sapiens	137-142
12578368-5	2003	The rate of change of fluorescence of the single-tryptophan residue, Trp53, in the unlabeled protein, where no FRET occurs, yields the rate of solvation of the core.	Tryptophan	49-59	P53	Homo sapiens	69-74
12578368-7	2003	The rate of the increase in the fluorescence of Trp53 in the labeled protein, where FRET from the tryptophan to the TNB label occurs, yields the rate of decrease in FRET efficiency during unfolding.	Tryptophan	98-108	P53	Homo sapiens	48-53
12578368-7	2003	The rate of the increase in the fluorescence of Trp53 in the labeled protein, where FRET from the tryptophan to the TNB label occurs, yields the rate of decrease in FRET efficiency during unfolding.	Trinitrobenzenesulfonic Acid	116-119	P53	Homo sapiens	48-53
12518324-7	2003	The antisense oligonucleotide also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel.	Oligonucleotides	14-29	P53	Homo sapiens	62-65
12518324-7	2003	The antisense oligonucleotide also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel.	Doxorubicin	146-156	P53	Homo sapiens	62-65
12518324-7	2003	The antisense oligonucleotide also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel.	Fluorouracil	158-172	P53	Homo sapiens	62-65
12518324-7	2003	The antisense oligonucleotide also potentiated the effects of p53 activation and p21 induction by chemotherapeutic agents 10-hydroxycamptothecin, adriamycin, 5-fluorouracil, and paclitaxel.	Paclitaxel	178-188	P53	Homo sapiens	62-65
12586367-5	2003	Accordingly, we confirm that the effect of E6 and p53 is independent of the six C-terminal lysine residues in p53, which have previously been described to play an important role for effective ubiquitination and degradation of 53 mediated by Mdm2.	Lysine	91-97	P53	Homo sapiens	110-113
12468545-1	2003	Oxidants such as H(2)O(2) play a role in the toxicity of certain DNA-damaging agents, a process that often involves the tumor suppressor p53.	Hydrogen Peroxide	17-25	P53	Homo sapiens	137-140
12700649-6	2003	The p53-binding region in the first intron of the Fas gene was partially methylated in Caco(2), and 5-azadC potentiated Ad-wtp53-induced upregulation of Fas expression.	caco(2)	87-94	P53	Homo sapiens	4-7
12613590-1	2003	The mode of action of the secondary metabolite chlorofusin, which antagonises the interaction between p53 and MDM2, involves direct binding to the N-terminal domain of MDM2.	chlorofusin	47-58	P53	Homo sapiens	102-105
12647018-6	2003	Transfection with antisense MRP1 oligonucleotides demonstrated a DOX sensitization effect (about 2-fold) in p53-R175H transfectants but not in control cells.	Oligonucleotides	33-49	P53	Homo sapiens	108-111
12647018-6	2003	Transfection with antisense MRP1 oligonucleotides demonstrated a DOX sensitization effect (about 2-fold) in p53-R175H transfectants but not in control cells.	Doxorubicin	65-68	P53	Homo sapiens	108-111
12647018-5	2003	Furthermore, the p53-R175H cells were 2.5-fold more resistant to doxorubicin (DOX) and had a 4-fold greater DOX efflux rate than the control cells 1 h after DOX treatment.	Doxorubicin	65-76	P53	Homo sapiens	17-20
12524418-1	2003	During a search for causative genes in patients with concurrent multiple primary colon tumours, we found a novel case with a germline mutation of the p53 gene, from GCC (Ala) to GTC (Val) at codon 189.	Alanine	170-173	P53	Homo sapiens	150-153
12647018-5	2003	Furthermore, the p53-R175H cells were 2.5-fold more resistant to doxorubicin (DOX) and had a 4-fold greater DOX efflux rate than the control cells 1 h after DOX treatment.	Doxorubicin	78-81	P53	Homo sapiens	17-20
12647018-5	2003	Furthermore, the p53-R175H cells were 2.5-fold more resistant to doxorubicin (DOX) and had a 4-fold greater DOX efflux rate than the control cells 1 h after DOX treatment.	Doxorubicin	108-111	P53	Homo sapiens	17-20
12647018-5	2003	Furthermore, the p53-R175H cells were 2.5-fold more resistant to doxorubicin (DOX) and had a 4-fold greater DOX efflux rate than the control cells 1 h after DOX treatment.	Doxorubicin	108-111	P53	Homo sapiens	17-20
12647018-7	2003	In addition, transfection with antisense p53 oligonucleotides greatly suppressed MRP1 expression and reversed DOX resistance in p53-R175H cells but had no effect in control cells.	Oligonucleotides	45-61	P53	Homo sapiens	41-44
12647018-7	2003	In addition, transfection with antisense p53 oligonucleotides greatly suppressed MRP1 expression and reversed DOX resistance in p53-R175H cells but had no effect in control cells.	Oligonucleotides	45-61	P53	Homo sapiens	128-131
12647018-7	2003	In addition, transfection with antisense p53 oligonucleotides greatly suppressed MRP1 expression and reversed DOX resistance in p53-R175H cells but had no effect in control cells.	Doxorubicin	110-113	P53	Homo sapiens	41-44
12647018-7	2003	In addition, transfection with antisense p53 oligonucleotides greatly suppressed MRP1 expression and reversed DOX resistance in p53-R175H cells but had no effect in control cells.	Doxorubicin	110-113	P53	Homo sapiens	128-131
12647018-8	2003	The results suggested that p53-R175H might induce MRP1 expression and DOX resistance in cells.	Doxorubicin	70-73	P53	Homo sapiens	27-30
12570658-0	2003	Mechanisms controlling sensitivity to platinum complexes: role of p53 and DNA mismatch repair.	Platinum	38-46	P53	Homo sapiens	66-69
12570658-5	2003	Among the main pathways affecting cell sensitivity of these drugs a role for p53 has been proposed at least for cisplatin and BBR 3464.	Cisplatin	112-121	P53	Homo sapiens	77-80
12570658-9	2003	Thus, platinum compounds are endowed with differential capability to activate pathways of p53-dependent or independent apoptosis, and differential recognition by specific cellular systems is likely to be the critical determinant of the cell fate (death/survival) after drug exposure.	Platinum	6-14	P53	Homo sapiens	90-93
12559346-4	2003	METHODS: p16 and p53 expression were detected by immunohistochemical analysis of 90 paraffin specimens of resected NSCLC, including 35 squamous cell carcinoma, 47 adenocarcinoma, and eight large cell carcinoma, between stages I and IV.	Paraffin	84-92	P53	Homo sapiens	17-20
12538824-0	2003	p53-mediated regulation of expression of a rabbit liver carboxylesterase confers sensitivity to 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (CPT-11).	Irinotecan	96-161	P53	Homo sapiens	0-3
12538824-0	2003	p53-mediated regulation of expression of a rabbit liver carboxylesterase confers sensitivity to 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (CPT-11).	Irinotecan	163-169	P53	Homo sapiens	0-3
12538824-3	2003	Upon transfection of these plasmids into cells expressing either wt or mutant p53, differential expression of the CE has been observed, resulting in sensitization of the cells expressing the latter protein to the anticancer prodrug irinotecan, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carb- onyloxycamptothecin (CPT-11).	Irinotecan	232-242	P53	Homo sapiens	78-81
12538824-3	2003	Upon transfection of these plasmids into cells expressing either wt or mutant p53, differential expression of the CE has been observed, resulting in sensitization of the cells expressing the latter protein to the anticancer prodrug irinotecan, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carb- onyloxycamptothecin (CPT-11).	Irinotecan	244-312	P53	Homo sapiens	78-81
12538824-3	2003	Upon transfection of these plasmids into cells expressing either wt or mutant p53, differential expression of the CE has been observed, resulting in sensitization of the cells expressing the latter protein to the anticancer prodrug irinotecan, 7-ethyl-10-[4-(1-piperidino)-1-piperidino] carb- onyloxycamptothecin (CPT-11).	Irinotecan	314-320	P53	Homo sapiens	78-81
12538824-5	2003	These studies indicate that the inactivation of wtp53 by mutant p53 in human tumor cells may be sufficient enough to generate a therapeutic window for enhanced cytotoxicity with CPT-11.	Irinotecan	178-184	P53	Homo sapiens	50-53
12535653-0	2003	Aspirin inhibits human coronary artery endothelial cell proliferation by upregulation of p53.	Aspirin	0-7	P53	Homo sapiens	89-92
12628512-6	2003	We also found that resveratrol-induced activation of p53 and resveratrol-induced apoptosis occurred through a p53-dependent pathway.	Resveratrol	19-30	P53	Homo sapiens	53-56
12628512-6	2003	We also found that resveratrol-induced activation of p53 and resveratrol-induced apoptosis occurred through a p53-dependent pathway.	Resveratrol	19-30	P53	Homo sapiens	110-113
12628512-6	2003	We also found that resveratrol-induced activation of p53 and resveratrol-induced apoptosis occurred through a p53-dependent pathway.	Resveratrol	61-72	P53	Homo sapiens	110-113
12628512-7	2003	The MAP kinases, ERKs, JNKs, or p38 kinases, are involved in resveratrol-induced activation of p53 and apoptosis.	Resveratrol	61-72	P53	Homo sapiens	95-98
12535653-9	2003	Western blot analysis revealed that the expression of p53 protein was increased after treatment of the cells with ASA.	Aspirin	114-117	P53	Homo sapiens	54-57
12535653-10	2003	These observations indicate that ASA decreases endothelial cell proliferation through cell cycle arrest mediated by enhanced p53 expression.	Aspirin	33-36	P53	Homo sapiens	125-128
12543789-1	2003	The mTOR inhibitor rapamycin induces G1 cell cycle accumulation and p53-independent apoptosis of the human rhabdomyosarcoma cell line Rh1.	Sirolimus	19-28	P53	Homo sapiens	68-71
12427754-4	2003	Heat shock induced phosphorylation of p53 at serine 15 in an ATM kinase-dependent fashion, which may contribute partially to heat-induced p53 accumulation.	Serine	45-51	P53	Homo sapiens	38-41
12427754-4	2003	Heat shock induced phosphorylation of p53 at serine 15 in an ATM kinase-dependent fashion, which may contribute partially to heat-induced p53 accumulation.	Serine	45-51	P53	Homo sapiens	138-141
12527914-0	2003	Thiol alkylation inhibits the mitogenic effects of platelet-derived growth factor and renders it proapoptotic via activation of STATs and p53 and induction of expression of caspase1 and p21(waf1/cip1).	Sulfhydryl Compounds	0-5	P53	Homo sapiens	138-141
12424231-5	2003	This mechanism accounts fully for the unusual p53 phenotype in cells exposed to electrophilic prostaglandins.	Prostaglandins	94-108	P53	Homo sapiens	46-49
12527914-6	2003	Thiol alkylation via inducing the expression of p21(waf1/cip1) in a STAT1- and p53-dependent manner antagonized the downregulation of this cell cycle inhibitory molecule by PDGF-BB.	Sulfhydryl Compounds	0-5	P53	Homo sapiens	79-82
12424231-0	2003	Electrophilic prostaglandins and lipid aldehydes repress redox-sensitive transcription factors p53 and hypoxia-inducible factor by impairing the selenoprotein thioredoxin reductase.	Prostaglandins	14-28	P53	Homo sapiens	95-98
12518062-5	2003	In noncancerous colon tissues from patients with ulcerative colitis (a cancer-prone chronic inflammatory disease), inducible NO synthase protein levels were positively correlated with p53 serine 15 phosphorylation levels.	Serine	188-194	P53	Homo sapiens	184-187
12495814-5	2003	Moreover, DA induced apoptotic cell death, which was observed by nuclear and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining and measurement of caspase-3 activity; this compound up-regulated apoptotic factor p53 while down-regulating anti-apoptotic factor Bcl-2.	Dopamine	10-12	P53	Homo sapiens	247-250
12561442-1	2003	BACKGROUND &amp; OBJECTIVE: p53 expression was a marker to predict the poor prognosis of laryngeal cancer.	Adenosine Monophosphate	12-15	P53	Homo sapiens	28-31
12509267-0	2003	Resistance of p53 knockout cells to doxorubicin is related to reduced formation of DNA strand breaks rather than impaired apoptotic signaling.	Doxorubicin	36-47	P53	Homo sapiens	14-17
12509267-2	2003	A variety of mechanisms has been proposed to be involved in doxorubicin-induced cytotoxicity such as DNA intercalation, oxidative stress, DNA strand breakage by inhibition of topoisomerase II, activation of death receptors, and altered p53 expression.	Doxorubicin	60-71	P53	Homo sapiens	236-239
12509267-6	2003	Resistance of p53(-/-) cells to doxorubicin is related to reduced induction of apoptosis.	Doxorubicin	32-43	P53	Homo sapiens	14-17
12509267-8	2003	However, we observed a clearly lower level of doxorubicin-induced DNA strand breaks in p53(-/-) cells compared to the wt.	Doxorubicin	46-57	P53	Homo sapiens	87-90
12673364-5	2003	HCC from high-incidence regions showing also a high prevalence of a specific Ser-249 TP53 mutation is one of the most striking examples of a mutagen fingerprint.	Serine	77-80	P53	Homo sapiens	85-89
15314976-0	2003	Expression of p53 gene in stage IIIA non-small cell lung cancer in patients after neoadjuvant chemotherapy with Vepesid and Cisplatin.	Cisplatin	124-133	P53	Homo sapiens	14-17
12497212-0	2003	Sensitivity to cisplatin treatment of human K1 thyroid carcinoma cell lines with altered p53 function.	Cisplatin	15-24	P53	Homo sapiens	89-92
12473386-7	2003	Addition of the specific PARP-1 inhibitor 3-AB to 2-CdA-treated cells rendered p53+/+ cells resistant to this drug.	3-aminobenzamide	42-46	P53	Homo sapiens	79-82
14513722-2	2003	(1998) implicated the proline/argine polymorphism of the codon 72 of the tumor-suppressor gene p53 in the development of cervical cancer (CC) with the observation that the p53 protein is more efficiently inactivated by the E6 oncoprotein of human papillomavirus in p53 arginine as compared with its proline isoform.	Arginine	269-277	P53	Homo sapiens	95-98
14513722-2	2003	(1998) implicated the proline/argine polymorphism of the codon 72 of the tumor-suppressor gene p53 in the development of cervical cancer (CC) with the observation that the p53 protein is more efficiently inactivated by the E6 oncoprotein of human papillomavirus in p53 arginine as compared with its proline isoform.	Arginine	269-277	P53	Homo sapiens	172-175
14513722-2	2003	(1998) implicated the proline/argine polymorphism of the codon 72 of the tumor-suppressor gene p53 in the development of cervical cancer (CC) with the observation that the p53 protein is more efficiently inactivated by the E6 oncoprotein of human papillomavirus in p53 arginine as compared with its proline isoform.	Arginine	269-277	P53	Homo sapiens	172-175
12893078-3	2003	The primary objective of the current investigation was to determine whether folic acid would prevent LOH of the three tumor suppressor genes, deleted in colorectal cancer (DCC), adenomatous polyposis coli (APC) and p53 in macroscopically normal appearing rectal mucosa of patients with adenomatous polyps.	Folic Acid	76-86	P53	Homo sapiens	215-218
12538356-0	2003	Simulated sunlight and benzo[a]pyrene diol epoxide induced mutagenesis in the human p53 gene evaluated by the yeast functional assay: lack of correspondence to tumor mutation spectra.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	23-50	P53	Homo sapiens	84-87
12951835-6	2003	CHS 828 induced phosphorylation of p53 protein at Ser-15 in normal cells.	Serine	50-53	P53	Homo sapiens	35-38
14995078-2	2003	This was a retrospective study in which MT and p53 immunopositive staining in 32 laryngeal SCC paraffin-embedded sections, were correlated with clinical recurrence.	Paraffin	95-103	P53	Homo sapiens	47-50
12407735-6	2003	Tobacco-specific carcinogens, in particular BPDE, cause a unique spectrum of p53 mutations, quite distinct from those found in cancers that are not associated with smoking.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	44-48	P53	Homo sapiens	77-80
12708345-1	2003	In codon 72 of the p53 antioncogene there are two alleles, arginine and proline; the arg/arg genotype has recently been identified as a risk factor for developing of cervicouterine cancer (CuCa) associated to human papillomavirus (HVP) infection.	Arginine	59-67	P53	Homo sapiens	19-22
12708345-1	2003	In codon 72 of the p53 antioncogene there are two alleles, arginine and proline; the arg/arg genotype has recently been identified as a risk factor for developing of cervicouterine cancer (CuCa) associated to human papillomavirus (HVP) infection.	Arginine	59-62	P53	Homo sapiens	19-22
12708345-1	2003	In codon 72 of the p53 antioncogene there are two alleles, arginine and proline; the arg/arg genotype has recently been identified as a risk factor for developing of cervicouterine cancer (CuCa) associated to human papillomavirus (HVP) infection.	Arginine	85-88	P53	Homo sapiens	19-22
12708345-5	2003	From 102 analyzed samples, p53-arginine allele corresponded to 67.64% and p53-proline allele corresponded to 32.36%; 47 women (46.10%) were arg/arg homocygotes, 11 women (10.77%) were pro/pro homocygotes, 44 women (43.13%) were arg/pro heterocigotes; the genotype distribution was within the Hardy-Weinberg equilibrium.	Arginine	31-39	P53	Homo sapiens	27-30
12708345-5	2003	From 102 analyzed samples, p53-arginine allele corresponded to 67.64% and p53-proline allele corresponded to 32.36%; 47 women (46.10%) were arg/arg homocygotes, 11 women (10.77%) were pro/pro homocygotes, 44 women (43.13%) were arg/pro heterocigotes; the genotype distribution was within the Hardy-Weinberg equilibrium.	Arginine	31-34	P53	Homo sapiens	27-30
14977434-4	2003	The antiproliferative effect of resveratrol was associated with the inhibition of D-type cyclins and cyclin-dependent kinase (Cdk) 4 expression, and the induction of tumor suppressor p53 and Cdk inhibitor p21.	Resveratrol	32-43	P53	Homo sapiens	183-186
12499093-0	2003	Relevance of p53, bcl-2 and Rb expression on resistance to cisplatin-based chemotherapy in advanced non-small cell lung cancer.	Cisplatin	59-68	P53	Homo sapiens	13-16
12499093-1	2003	PURPOSE: Tumors with p53 overexpression have been associated with enhanced resistance to cisplatin-based chemotherapy in a few and small studies involving non-small cell lung cancer.	Cisplatin	89-98	P53	Homo sapiens	21-24
12499093-8	2003	In multivariate analyses p53 positive immunostaining was identified as an independent predictive factor for resistance to cisplatin-based chemotherapy (P=0.006).	Cisplatin	122-131	P53	Homo sapiens	25-28
12499093-9	2003	CONCLUSIONS: Our study confirmed an association of p53 immunostaining and response rate of patients treated with cisplatin-based chemotherapy.	Cisplatin	113-122	P53	Homo sapiens	51-54
14680293-0	2003	Gamma irradiation results in phosphorylation of p53 at serine-392 in human T-lymphocyte leukaemia cell line MOLT-4.	Serine	55-61	P53	Homo sapiens	48-51
14680293-4	2003	In this study, we proved that the transcriptionally active p53 variant occurs in the MOLT-4 cells and its abundance alteration is triggered in the gamma-irradiated cell population concomitantly with phosphorylation at both the serine-392 and serine-15 residues.	Serine	227-233	P53	Homo sapiens	59-62
14680293-4	2003	In this study, we proved that the transcriptionally active p53 variant occurs in the MOLT-4 cells and its abundance alteration is triggered in the gamma-irradiated cell population concomitantly with phosphorylation at both the serine-392 and serine-15 residues.	Serine	242-248	P53	Homo sapiens	59-62
12493030-0	2003	p53 expression in normal paraffin-embedded tissue using different antibodies and antigen retrieval buffer systems.	Paraffin	25-33	P53	Homo sapiens	0-3
12493030-1	2003	AIMS: The study was undertaken to demonstrate wild-type p53 in normal paraffin-embedded tissues using two widely used antibodies, DO7 and 1801 and two different antigen retrieval buffer systems.	Paraffin	70-78	P53	Homo sapiens	56-59
12493030-10	2003	CONCLUSIONS: Our study demonstrates the presence of p53 in normal paraffin-embedded tissue with nuclear and/or cytoplasmic localization in some instances.	Paraffin	66-74	P53	Homo sapiens	52-55
12767266-5	2003	RESULTS: G--&gt;T transversion at the third base of 249 codon resulting in 249(Arg)--&gt;249(Ser) mutation in exon 7 of p53 gene were found in 11/25(44%) hepatocellular carcinoma cases, 4/20 (20%) cirrhotics, and 2/30 (7%) healthy controls (p&lt;0.01).	Arginine	79-82	P53	Homo sapiens	120-123
12767266-5	2003	RESULTS: G--&gt;T transversion at the third base of 249 codon resulting in 249(Arg)--&gt;249(Ser) mutation in exon 7 of p53 gene were found in 11/25(44%) hepatocellular carcinoma cases, 4/20 (20%) cirrhotics, and 2/30 (7%) healthy controls (p&lt;0.01).	Serine	93-96	P53	Homo sapiens	120-123
12767266-6	2003	CONCLUSIONS: These data show that the 249(Ser) p53 mutation in plasma is strongly associated with hepatocellular carcinoma patients in Qidong area and the mutation should be screened as a new early diagnostic marker for HCC.	Serine	42-45	P53	Homo sapiens	47-50
12635827-4	2003	The genotype of p53 codon 72 (Arg/Arg, Arg/Pro, or Pro/Pro) was determined for all subjects by polymerase chain reaction-restricted fragment length polymorphism (PCR-RFLP).	Arginine	30-33	P53	Homo sapiens	16-19
12635827-4	2003	The genotype of p53 codon 72 (Arg/Arg, Arg/Pro, or Pro/Pro) was determined for all subjects by polymerase chain reaction-restricted fragment length polymorphism (PCR-RFLP).	Arginine	34-37	P53	Homo sapiens	16-19
12635827-4	2003	The genotype of p53 codon 72 (Arg/Arg, Arg/Pro, or Pro/Pro) was determined for all subjects by polymerase chain reaction-restricted fragment length polymorphism (PCR-RFLP).	Arginine	34-37	P53	Homo sapiens	16-19
12768477-8	2003	These results suggest that induction of p53 by ALLN may be potentially important for triggering H(2)O(2)-induced apoptosis processes in RA synovial cells.	Hydrogen Peroxide	96-104	P53	Homo sapiens	40-43
12824531-6	2003	p53 DBS affinity chromatography compares the stability of p53 from different cellular extracts with different DBS.	dbs	4-7	P53	Homo sapiens	0-3
12824531-6	2003	p53 DBS affinity chromatography compares the stability of p53 from different cellular extracts with different DBS.	dbs	4-7	P53	Homo sapiens	58-61
12824531-6	2003	p53 DBS affinity chromatography compares the stability of p53 from different cellular extracts with different DBS.	dbs	110-113	P53	Homo sapiens	0-3
12824531-6	2003	p53 DBS affinity chromatography compares the stability of p53 from different cellular extracts with different DBS.	dbs	110-113	P53	Homo sapiens	58-61
12824531-10	2003	Methods for comparing p53 from three different cellular sources with different DBS are presented here.	dbs	79-82	P53	Homo sapiens	22-25
12824535-1	2003	This chapter describes the techniques necessary to identify p53 genomic mutations in either frozen or paraffin-embedded tumor samples.	Paraffin	102-110	P53	Homo sapiens	60-63
12824536-4	2003	The most important is immunocytochemical p53 staining of sections from paraffin embedded tissues.	Paraffin	71-79	P53	Homo sapiens	41-44
12937839-5	2003	p53 phosphorylated on Ser-392 was also increased by approximately 70% in patients treated with radiotherapy and with chemotherapy and correlated with elevated poly-ADP-ribose levels.	Serine	22-25	P53	Homo sapiens	0-3
12937839-5	2003	p53 phosphorylated on Ser-392 was also increased by approximately 70% in patients treated with radiotherapy and with chemotherapy and correlated with elevated poly-ADP-ribose levels.	Adenosine Diphosphate	164-167	P53	Homo sapiens	0-3
12457032-0	2003	Clinical application of oligonucleotide probe array for full-length gene sequencing of TP53 in colon cancer.	Oligonucleotides	24-39	P53	Homo sapiens	87-91
12759537-2	2003	The expression of the markers examined - Bcl-2, c-erbB-2, p53 - was detected in paraffin sections of the tumors by the streptavidin-biotin peroxidase method following heat-induced antigen retrieval, and the apoptosis rate was determined by the TUNEL method.	Paraffin	80-88	P53	Homo sapiens	58-61
14622914-3	2003	We also analyzed the involvement of Ca2+, mitochondria and reactive oxygen species in p53 activation.	Reactive Oxygen Species	59-82	P53	Homo sapiens	86-89
14622914-8	2003	Treatments of neuronal cultures with the permeability transitory pore blockers cyclosporin A and bongkrekic acid prevented veratridine-induced p53 immunoreactivity and neuronal death, placing mitochondria upstream of veratridine-induced p53 immunoreactivity.	Cyclosporine	79-92	P53	Homo sapiens	143-146
14622914-8	2003	Treatments of neuronal cultures with the permeability transitory pore blockers cyclosporin A and bongkrekic acid prevented veratridine-induced p53 immunoreactivity and neuronal death, placing mitochondria upstream of veratridine-induced p53 immunoreactivity.	Cyclosporine	79-92	P53	Homo sapiens	237-240
14622914-9	2003	Reactive oxygen species also participated in veratridine-induced neurotoxicity and p53 activation.	Reactive Oxygen Species	0-23	P53	Homo sapiens	83-86
12457032-2	2003	We studied whether the recently developed oligonucleotide microarray technique, GeneChip p53 assay, can be applied to sensitive detection of TP53 gene mutations in surgical specimens from colon cancer patients.	Oligonucleotides	42-57	P53	Homo sapiens	141-145
12505283-5	2002	For example, oxyradical overload diseases such as Wilson disease and hemochromatosis result in the generation of oxygen/nitrogen species that can cause mutations in the p53 tumor suppressor gene.	Oxygen	113-119	P53	Homo sapiens	169-172
14512646-14	2003	Although some basic studies provide some important supports, studies including larger patient cohorts would still be required to prove the hypothesis that p53 and HER-2/neu-coexpressing tumors have a worse prognosis and are more resistant to a cisplatin-based multidrug regimen.	Cisplatin	244-253	P53	Homo sapiens	155-158
12566814-4	2003	Immunohistochemical analysis for p53 was done on paraffin-fixed tissues with DO-7 antibodies.	Paraffin	49-57	P53	Homo sapiens	33-36
12903851-13	2003	For example, a phase II randomized trial of topical DFMO reduced AK number, suppressed polyamines, and reduced p53 protein.	Eflornithine	52-56	P53	Homo sapiens	111-114
12660452-5	2003	An immunohistochemical technique with monoclonal antibodies (DO-7) was used to detect the p53 phenotype in paraffin-fixed material.	Paraffin	107-115	P53	Homo sapiens	90-93
12421820-2	2002	Interestingly, both acetylation and ubiquitination can modify the same lysine residues at the C terminus of p53, implicating a role of acetylation in the regulation of p53 stability.	Lysine	71-77	P53	Homo sapiens	108-111
12421820-2	2002	Interestingly, both acetylation and ubiquitination can modify the same lysine residues at the C terminus of p53, implicating a role of acetylation in the regulation of p53 stability.	Lysine	71-77	P53	Homo sapiens	168-171
12505283-5	2002	For example, oxyradical overload diseases such as Wilson disease and hemochromatosis result in the generation of oxygen/nitrogen species that can cause mutations in the p53 tumor suppressor gene.	Nitrogen	120-128	P53	Homo sapiens	169-172
12393879-0	2002	p53 serine 392 phosphorylation increases after UV through induction of the assembly of the CK2.hSPT16.SSRP1 complex.	Serine	4-10	P53	Homo sapiens	0-3
12393879-3	2002	Also, UV irradiation apparently induces the association of the complex, thereby increasing the specificity of CK2 for p53 at the expense of other cellular CK2 substrates and leading to an overall increase in p53 serine 392 phosphorylation.	Serine	212-218	P53	Homo sapiens	118-121
12393879-3	2002	Also, UV irradiation apparently induces the association of the complex, thereby increasing the specificity of CK2 for p53 at the expense of other cellular CK2 substrates and leading to an overall increase in p53 serine 392 phosphorylation.	Serine	212-218	P53	Homo sapiens	208-211
12499281-0	2002	Chemoradiation of cervical cancer cells: targeting human papillomavirus E6 and p53 leads to either augmented or attenuated apoptosis depending on the platinum carrier ligand.	Platinum	150-158	P53	Homo sapiens	79-82
12406560-4	2002	Unsaturated fatty acids also showed cytotoxicity against a SNU16 human stomach cancer cell line and conjugated linoleic acid suppressed mRNA expression of several myc-target genes; ornithine decarboxylase, p53, cdc25a in the SNU16 cells.	Linoleic Acid	111-124	P53	Homo sapiens	206-209
12499281-9	2002	In contrast, dominant negative p53 or ectopic HPV 16 E6 sensitized the cells to cisplatin.	Cisplatin	80-89	P53	Homo sapiens	31-34
12499281-11	2002	Taken together, p53 has a significant role in the cellular response to chemoradiation treatment in cervical cancer cell lines, but p53 activity may have a dramatically different effect on cell survival depending on the platinum carrier ligand.	Platinum	219-227	P53	Homo sapiens	131-134
12459171-2	2002	In this report, we addressed the question whether the natural variability at p53 locus (the proline-arginine substitution at codon 72) affects the capacity of peripheral-blood mononuclear cells from healthy subjects to undergo in vitro apoptosis in response to the cytotoxic drug cytosine arabinoside.	Arginine	100-108	P53	Homo sapiens	77-80
12388558-2	2002	The increase in p53 stability depends critically on its phosphorylation on serine/threonine residues, including those preceding a proline (Ser(P)/Thr-Pro).	Serine	75-81	P53	Homo sapiens	16-19
12388558-2	2002	The increase in p53 stability depends critically on its phosphorylation on serine/threonine residues, including those preceding a proline (Ser(P)/Thr-Pro).	Threonine	82-91	P53	Homo sapiens	16-19
12183079-5	2002	Treatment with A23187, a Ca(2+) ionophore, or thapsigargin, a Ca(2+)-ATPase inhibitor, alone enhanced p53 nuclear accumulation, indicating that p53 accumulation is dependent on intracellular Ca(2+) increase.	Thapsigargin	46-58	P53	Homo sapiens	102-105
12388558-2	2002	The increase in p53 stability depends critically on its phosphorylation on serine/threonine residues, including those preceding a proline (Ser(P)/Thr-Pro).	Serine	139-142	P53	Homo sapiens	16-19
12388558-2	2002	The increase in p53 stability depends critically on its phosphorylation on serine/threonine residues, including those preceding a proline (Ser(P)/Thr-Pro).	Threonine	146-149	P53	Homo sapiens	16-19
12388558-6	2002	Here we found that DNA damage enhanced the interaction between Pin1 and p53, which depended on the WW domain in Pin1 and Ser(33/46)-Pro motifs in p53.	Serine	121-124	P53	Homo sapiens	72-75
12388558-6	2002	Here we found that DNA damage enhanced the interaction between Pin1 and p53, which depended on the WW domain in Pin1 and Ser(33/46)-Pro motifs in p53.	Serine	121-124	P53	Homo sapiens	146-149
12324477-7	2002	BCR ligation resulted in p53 activation including its phosphorylation at Ser(15), nuclear translocation, and target gene p53AIP1 induction.	Serine	73-76	P53	Homo sapiens	25-28
12393587-7	2002	We demonstrate that p53-dependent apoptosis results in mitochondrial damage as shown by loss of mitochondrial membrane potential, increase in intracellular calcium, and release of mitochondrial cytochrome c into the cytosol.	Calcium	156-163	P53	Homo sapiens	20-23
12478472-0	2002	Apoptosis and growth arrest induced by platinum compounds in U2-OS cells reflect a specific DNA damage recognition associated with a different p53-mediated response.	Platinum	39-47	P53	Homo sapiens	143-146
12478472-1	2002	Mononuclear and multinuclear platinum complexes are known to induce distinct types of DNA lesions and exhibit different profiles of antitumor activity, in relation to p53 mutational status.	Platinum	29-37	P53	Homo sapiens	167-170
12478472-6	2002	The regulation of p21(WAF1) after cisplatin or BBR 3464 exposure required a p53 signal, as documented using stable transfectants expressing a dominant-negative form of p53 (175(his)).	Cisplatin	34-43	P53	Homo sapiens	76-79
12432549-1	2002	The new disaccharide anthracycline MEN 10755 induces activation of both NF-kappaB and p53 transcription factors in A2780 cells.	Anthracyclines	21-34	P53	Homo sapiens	86-89
12213282-5	2002	The ability of glycolic acid to inhibit the UVB-induced cytotoxicity, apoptosis and expression of apoptosis-regulatory genes (p53 and p21) was examined.	glycolic acid	15-28	P53	Homo sapiens	126-129
12213282-8	2002	Glycolic acid also inhibited the UVB-induced expression of c-fos and the activation of transcription factor AP-1, and inhibited mRNA levels of apoptosis-regulatory gene (p53 and p21).	glycolic acid	0-13	P53	Homo sapiens	170-173
12213282-9	2002	These results suggest that glycolic acid may exert the inhibitory effect on the UVB-induced skin tumor development by blocking the UVB-induced of apoptosis and cytotoxicity through inhibition of c-fos expression and activation of AP-1 in addition to the inhibition of p53-p2l response pathway.	glycolic acid	27-40	P53	Homo sapiens	268-271
12466962-4	2002	Results showed that curcumin treatment causes p53- and p21-independent G(2)/M phase arrest and apoptosis in HCT-116(p53(+/+)), HCT-116(p53(-/-)) and HCT-116(p21(-/-)) cell lines.	Curcumin	20-28	P53	Homo sapiens	46-49
12466962-4	2002	Results showed that curcumin treatment causes p53- and p21-independent G(2)/M phase arrest and apoptosis in HCT-116(p53(+/+)), HCT-116(p53(-/-)) and HCT-116(p21(-/-)) cell lines.	Curcumin	20-28	P53	Homo sapiens	116-119
12466962-4	2002	Results showed that curcumin treatment causes p53- and p21-independent G(2)/M phase arrest and apoptosis in HCT-116(p53(+/+)), HCT-116(p53(-/-)) and HCT-116(p21(-/-)) cell lines.	Curcumin	20-28	P53	Homo sapiens	116-119
12183079-4	2002	In addition, AA profoundly increased protein level of p53, which was also inhibited by BAPTA/AM, an intracellular Ca(2+) chelator, TMB-8 and dantrolene.	8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate	131-136	P53	Homo sapiens	54-57
12478472-6	2002	The regulation of p21(WAF1) after cisplatin or BBR 3464 exposure required a p53 signal, as documented using stable transfectants expressing a dominant-negative form of p53 (175(his)).	Cisplatin	34-43	P53	Homo sapiens	168-171
12478472-8	2002	Multinuclear platinum complexes could be regarded as useful tools for investigating the p53-mediated process of cell cycle arrest in response to DNA damage.	Platinum	13-21	P53	Homo sapiens	88-91
12183079-5	2002	Treatment with A23187, a Ca(2+) ionophore, or thapsigargin, a Ca(2+)-ATPase inhibitor, alone enhanced p53 nuclear accumulation, indicating that p53 accumulation is dependent on intracellular Ca(2+) increase.	Thapsigargin	46-58	P53	Homo sapiens	144-147
12447382-5	2002	Interestingly, in cancer cell lines expressing mutant p53, 53BP1 was localized to distinct nuclear foci and ATM-dependent phosphorylation of Chk2 at Thr 68 was detected, even in the absence of irradiation.	Threonine	149-152	P53	Homo sapiens	54-57
12507920-1	2002	Benzo[a]pyrene diol epoxide (BPDE)-DNA adducts are involved in the induction of p53 mutations and probably in the causation of human lung cancer associated with cigarette smoking.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	0-27	P53	Homo sapiens	80-83
12507920-1	2002	Benzo[a]pyrene diol epoxide (BPDE)-DNA adducts are involved in the induction of p53 mutations and probably in the causation of human lung cancer associated with cigarette smoking.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	29-33	P53	Homo sapiens	80-83
12464630-6	2002	Mutation analysis indicates that excessive nucleostemin, particularly mutants that lack the GTP-regulatory domain, prevents cells from entering mitosis and causes apoptosis in a p53-dependent manner.	Guanosine Triphosphate	92-95	P53	Homo sapiens	178-181
12427123-3	2002	We hypothesized that estradiol would reverse TGF-beta1-induced mesangial cell apoptosis by antagonizing the stimulatory effects of TGF-beta1 on casein kinase 2 activity, thereby preventing p53 activation.	Estradiol	21-30	P53	Homo sapiens	189-192
12427123-7	2002	TGF-beta1-induced p53 activation and all the intermediary steps leading to mesangial cell apoptosis were reversed by estradiol (10-9 mol/L) and by DRB, potent inhibitors of CK2 activity, but not by inhibitors of the p38 MAPK, ERK or JNK signaling cascades.	Estradiol	117-126	P53	Homo sapiens	18-21
12427123-7	2002	TGF-beta1-induced p53 activation and all the intermediary steps leading to mesangial cell apoptosis were reversed by estradiol (10-9 mol/L) and by DRB, potent inhibitors of CK2 activity, but not by inhibitors of the p38 MAPK, ERK or JNK signaling cascades.	Dichlororibofuranosylbenzimidazole	147-150	P53	Homo sapiens	18-21
12496062-1	2002	An Arg/Pro polymorphism in codon 72 of the TP53 gene was analyzed in blood samples from 390 breast and 162 colorectal cancer patients previously investigated for TP53 mutations in their tumors.	Arginine	3-6	P53	Homo sapiens	43-47
12507133-8	2002	A p53 missense mutation was detected at codon 161 (GCC--&gt;ACC, Ala--&gt;Thr) in only one oligoastrocytoma without allelic loss.	Threonine	74-77	P53	Homo sapiens	2-5
12435813-7	2002	We demonstrate that PKCzeta inhibited p53/p56 Lyn phosphorylation and stimulation in drug- or H(2)O(2)-treated cells, suggesting that p53/p56 Lyn redox regulation is altered in PKCzeta-overexpressing cells.	Hydrogen Peroxide	94-102	P53	Homo sapiens	134-137
12221076-4	2002	With the loss of the p53 gene, the levels of phosphorylation of Ser-63 of c-Jun and Thr-183/Tyr-185 of JNK1/2 in p53-/- cells did not increase as markedly as in p53+/+ cells in response to a 1-h treatment with nocodazole or other microtubule-disrupting drugs such as vinblastine and colchicine.	Nocodazole	210-220	P53	Homo sapiens	21-24
12427017-0	2002	Nitric oxide-mediated inhibition of Hdm2-p53 binding.	Nitric Oxide	0-12	P53	Homo sapiens	41-44
12427017-2	2002	We tested in vitro whether nitric oxide may indirectly control p53 by S-nitrosylation and inactivation of the p53 negative regulator, Hdm2.	Nitric Oxide	27-39	P53	Homo sapiens	63-66
12427017-3	2002	Treatment of Hdm2 with a nitric oxide donor inhibits Hdm2-p53 binding, a critical step in Hdm2 regulation of p53.	Nitric Oxide	25-37	P53	Homo sapiens	58-61
12427017-3	2002	Treatment of Hdm2 with a nitric oxide donor inhibits Hdm2-p53 binding, a critical step in Hdm2 regulation of p53.	Nitric Oxide	25-37	P53	Homo sapiens	109-112
12427017-5	2002	Moreover, nitric oxide inhibition of Hdm2-p53 binding was found to be reversible.	Nitric Oxide	10-22	P53	Homo sapiens	42-45
12427017-7	2002	Finally, we have identified a critical cysteine residue that nitric oxide modifies to disrupt Hdm2-p53 binding.	Cysteine	39-47	P53	Homo sapiens	99-102
12427017-7	2002	Finally, we have identified a critical cysteine residue that nitric oxide modifies to disrupt Hdm2-p53 binding.	Nitric Oxide	61-73	P53	Homo sapiens	99-102
12409142-0	2002	Resveratrol- induced apoptosis is mediated by p53-dependent pathway in Hep G2 cells.	Resveratrol	0-11	P53	Homo sapiens	46-49
12409142-3	2002	Our results showed that resveratrol inhibited cell growth in p53-positive Hep G2 cells only.	Resveratrol	24-35	P53	Homo sapiens	61-64
12409142-4	2002	This anticancer effect was a result of cellular apoptotic death induced by resveratrol via the p53-dependent pathway.	Resveratrol	75-86	P53	Homo sapiens	95-98
12409142-7	2002	In contrast, the p53-negative Hep 3B cells treated with resveratrol did not show the antiproliferation effect neither did they show significant changes in p21 nor Fas/APO-1 levels.	Resveratrol	56-67	P53	Homo sapiens	17-20
12409142-9	2002	Furthermore, these results implied that resveratrol might also be a new potent chemopreventive drug candidate for liver cancer as it played an important role to trigger p53-mediated molecules involved in the mechanism of p53-dependent apoptotic signal pathway.	Resveratrol	40-51	P53	Homo sapiens	169-172
12409142-9	2002	Furthermore, these results implied that resveratrol might also be a new potent chemopreventive drug candidate for liver cancer as it played an important role to trigger p53-mediated molecules involved in the mechanism of p53-dependent apoptotic signal pathway.	Resveratrol	40-51	P53	Homo sapiens	221-224
12221076-0	2002	Nocodazole-induced p53-dependent c-Jun N-terminal kinase activation reduces apoptosis in human colon carcinoma HCT116 cells.	Nocodazole	0-10	P53	Homo sapiens	19-22
12221076-4	2002	With the loss of the p53 gene, the levels of phosphorylation of Ser-63 of c-Jun and Thr-183/Tyr-185 of JNK1/2 in p53-/- cells did not increase as markedly as in p53+/+ cells in response to a 1-h treatment with nocodazole or other microtubule-disrupting drugs such as vinblastine and colchicine.	Serine	64-67	P53	Homo sapiens	21-24
12221076-4	2002	With the loss of the p53 gene, the levels of phosphorylation of Ser-63 of c-Jun and Thr-183/Tyr-185 of JNK1/2 in p53-/- cells did not increase as markedly as in p53+/+ cells in response to a 1-h treatment with nocodazole or other microtubule-disrupting drugs such as vinblastine and colchicine.	Nocodazole	210-220	P53	Homo sapiens	113-116
12221076-4	2002	With the loss of the p53 gene, the levels of phosphorylation of Ser-63 of c-Jun and Thr-183/Tyr-185 of JNK1/2 in p53-/- cells did not increase as markedly as in p53+/+ cells in response to a 1-h treatment with nocodazole or other microtubule-disrupting drugs such as vinblastine and colchicine.	Nocodazole	210-220	P53	Homo sapiens	113-116
12221076-7	2002	Inhibition of p53 expression by its antisense oligonucleotide also attenuated nocodazole-induced JNK activation in p53+/+ cells.	Oligonucleotides	46-61	P53	Homo sapiens	14-17
12221076-7	2002	Inhibition of p53 expression by its antisense oligonucleotide also attenuated nocodazole-induced JNK activation in p53+/+ cells.	Oligonucleotides	46-61	P53	Homo sapiens	115-118
12221076-7	2002	Inhibition of p53 expression by its antisense oligonucleotide also attenuated nocodazole-induced JNK activation in p53+/+ cells.	Nocodazole	78-88	P53	Homo sapiens	14-17
12221076-7	2002	Inhibition of p53 expression by its antisense oligonucleotide also attenuated nocodazole-induced JNK activation in p53+/+ cells.	Nocodazole	78-88	P53	Homo sapiens	115-118
12426395-4	2002	The HDAC1 complex binds MDM2 in a p53-independent manner and deacetylates p53 at all known acetylated lysines in vivo.	Lysine	102-109	P53	Homo sapiens	74-77
12221076-8	2002	Surprisingly, cotransfection of p53+/+ cells with dominant negative mutants of JNK isoforms and treatment of p53+/+ cells with the JNK inhibitor SP600125 actually further enhanced apoptosis in p53+/+ cells by up to 2-fold in response to nocodazole.	Nocodazole	237-247	P53	Homo sapiens	32-35
12426395-8	2002	As the acetylated p53 lysine residues overlap with those that are ubiquitylated, our results suggest that one major function of p53 acetylation is to promote p53 stability by preventing MDM2-dependent ubiquitylation, while recruitment of HDAC1 by MDM2 promotes p53 degradation by removing these acetyl groups.	Lysine	22-28	P53	Homo sapiens	18-21
12426395-8	2002	As the acetylated p53 lysine residues overlap with those that are ubiquitylated, our results suggest that one major function of p53 acetylation is to promote p53 stability by preventing MDM2-dependent ubiquitylation, while recruitment of HDAC1 by MDM2 promotes p53 degradation by removing these acetyl groups.	Lysine	22-28	P53	Homo sapiens	128-131
12221076-8	2002	Surprisingly, cotransfection of p53+/+ cells with dominant negative mutants of JNK isoforms and treatment of p53+/+ cells with the JNK inhibitor SP600125 actually further enhanced apoptosis in p53+/+ cells by up to 2-fold in response to nocodazole.	Nocodazole	237-247	P53	Homo sapiens	109-112
12426395-8	2002	As the acetylated p53 lysine residues overlap with those that are ubiquitylated, our results suggest that one major function of p53 acetylation is to promote p53 stability by preventing MDM2-dependent ubiquitylation, while recruitment of HDAC1 by MDM2 promotes p53 degradation by removing these acetyl groups.	Lysine	22-28	P53	Homo sapiens	128-131
12426395-8	2002	As the acetylated p53 lysine residues overlap with those that are ubiquitylated, our results suggest that one major function of p53 acetylation is to promote p53 stability by preventing MDM2-dependent ubiquitylation, while recruitment of HDAC1 by MDM2 promotes p53 degradation by removing these acetyl groups.	Lysine	22-28	P53	Homo sapiens	128-131
12221076-8	2002	Surprisingly, cotransfection of p53+/+ cells with dominant negative mutants of JNK isoforms and treatment of p53+/+ cells with the JNK inhibitor SP600125 actually further enhanced apoptosis in p53+/+ cells by up to 2-fold in response to nocodazole.	Nocodazole	237-247	P53	Homo sapiens	109-112
12526226-1	2002	BACKGROUND &amp; OBJECTIVE: p53 and proliferating cell nuclear antigen (PCNA) play an important role in the development of malignant tumor.	Adenosine Monophosphate	12-15	P53	Homo sapiens	28-31
12420228-7	2002	Thus, a major regulation of p53 activity occurs at the level of p53 DBS themselves by posing additional requirements for the successful utilization of apoptosis-related DBS.	dbs	68-71	P53	Homo sapiens	28-31
12420228-7	2002	Thus, a major regulation of p53 activity occurs at the level of p53 DBS themselves by posing additional requirements for the successful utilization of apoptosis-related DBS.	dbs	68-71	P53	Homo sapiens	64-67
12420228-7	2002	Thus, a major regulation of p53 activity occurs at the level of p53 DBS themselves by posing additional requirements for the successful utilization of apoptosis-related DBS.	dbs	169-172	P53	Homo sapiens	28-31
12420228-7	2002	Thus, a major regulation of p53 activity occurs at the level of p53 DBS themselves by posing additional requirements for the successful utilization of apoptosis-related DBS.	dbs	169-172	P53	Homo sapiens	64-67
12213802-2	2002	H2O2 produced early activation of Akt/PKB and also DNA damage that was followed by stabilization of p53 levels, formation of reactive oxygen species (ROS), and generation of ceramide through activation of a glutathione-sensitive neutral sphingomyelinase.	Hydrogen Peroxide	0-4	P53	Homo sapiens	100-103
12417331-5	2002	Transient transfection assays of luciferase reporter plasmids demonstrate that human TRAIL-R3 promoter can be induced in doxorubicin-treated MCF-7 cells in a p53-independent manner.	Doxorubicin	121-132	P53	Homo sapiens	158-161
12552965-5	2002	Immunohistochemical analysis was performed to determine BRCA1 and the apoptosis-related proteins bcl-2, Bax and p53 in paraffin-embedded tissues of 156 sporadic invasive ductal carcinomas.	Paraffin	119-127	P53	Homo sapiens	112-115
12397013-0	2002	Hydrogen peroxide induces upregulation of Fas in human airway epithelial cells via the activation of PARP-p53 pathway.	Hydrogen Peroxide	0-17	P53	Homo sapiens	106-109
12397013-9	2002	Inhibitors of poly(ADP-ribose) polymerase abrogated the H(2)O(2)-induced Fas translocation to the plasma membrane and p53 activation.	Hydrogen Peroxide	56-64	P53	Homo sapiens	118-121
12397013-11	2002	These results indicate that H(2)O(2) induces Fas upregulation by promoting cytoplasmic transport of Fas to the cell surface in human airway epithelial cells, and that the activation of the poly(ADP-ribose) polymerase-p53 pathway may be involved in this mechanism.	Hydrogen Peroxide	28-36	P53	Homo sapiens	217-220
12530065-0	2002	Reduced expression of p53 and p21WAF1/CIP1 sensitizes human breast cancer cells to paclitaxel and its combination with 5-fluorouracil.	Paclitaxel	83-93	P53	Homo sapiens	22-25
12530074-4	2002	RESULTS: p53 wild-type fibroblasts, in contrast to p53-deficient cells, survive much higher doses of 5-fluorouracil when incubated at 28 degrees C than at 37 degrees C. Among tumor cells, the loss of the p53 function coincides with the inability to arrest cell cycle progression at low temperature and with increased sensitivity to prolonged hypothermia as a single modality.	Fluorouracil	101-115	P53	Homo sapiens	9-12
12530065-0	2002	Reduced expression of p53 and p21WAF1/CIP1 sensitizes human breast cancer cells to paclitaxel and its combination with 5-fluorouracil.	Fluorouracil	119-133	P53	Homo sapiens	22-25
12404284-11	2002	This raises the possibility that p53 mutation, which frequently is present in HNSCC, may result in increased angiogenesis and invasiveness related to increased nitric oxide and MMP production by tumor cells, ultimately contributing to tumor progression.	Nitric Oxide	160-172	P53	Homo sapiens	33-36
12530065-6	2002	RESULTS: Tumor cells transfected with antisense p53 or p21WAF1/CIP1 exhibited a significant increase in their sensitivity to paclitaxel.	Paclitaxel	125-135	P53	Homo sapiens	48-51
12530065-7	2002	The reduced protein levels of p53 and p21WAF1/CIP1 were also found to abrogate the inhibitory effects of 5-FU on paclitaxel-induced mitotic arrest and apoptosis.	Fluorouracil	105-109	P53	Homo sapiens	30-33
12530065-7	2002	The reduced protein levels of p53 and p21WAF1/CIP1 were also found to abrogate the inhibitory effects of 5-FU on paclitaxel-induced mitotic arrest and apoptosis.	Paclitaxel	113-123	P53	Homo sapiens	30-33
12530065-8	2002	CONCLUSION: These findings suggest that the status of p53 and p21WAF1/CIP1 might play an important role in tumor cell susceptibility to paclitaxel and its combination with other drugs such as 5-FU.	Paclitaxel	136-146	P53	Homo sapiens	54-57
12530065-8	2002	CONCLUSION: These findings suggest that the status of p53 and p21WAF1/CIP1 might play an important role in tumor cell susceptibility to paclitaxel and its combination with other drugs such as 5-FU.	Fluorouracil	192-196	P53	Homo sapiens	54-57
12392819-4	2002	In MDA-MB-231, resveratrol (up to 200 microM) lowered the expression and kinase activities of positive G1/S and G2/M cell cycle regulators and inhibited ribonucleotide reductase activity in a concentration dependent manner, without a significant effect on the low expression of tumor suppressors p21, p27, and p53.	Resveratrol	15-26	P53	Homo sapiens	310-313
12530090-2	2002	The human tumor suppressor gene TP53 contains single nucleotide polymorphism that encodes either arginin (Arg) or proline (Pro) at amino acid codon 72 of the p53 protein.	Arginine	97-104	P53	Homo sapiens	32-36
12530090-2	2002	The human tumor suppressor gene TP53 contains single nucleotide polymorphism that encodes either arginin (Arg) or proline (Pro) at amino acid codon 72 of the p53 protein.	Arginine	97-104	P53	Homo sapiens	158-161
12530090-2	2002	The human tumor suppressor gene TP53 contains single nucleotide polymorphism that encodes either arginin (Arg) or proline (Pro) at amino acid codon 72 of the p53 protein.	Arginine	106-109	P53	Homo sapiens	32-36
12530090-2	2002	The human tumor suppressor gene TP53 contains single nucleotide polymorphism that encodes either arginin (Arg) or proline (Pro) at amino acid codon 72 of the p53 protein.	Arginine	106-109	P53	Homo sapiens	158-161
12548019-2	2002	Plk3 physically interacts with p53 and phosphorylates this tumor suppressor protein on serine-20, suggesting that the role of Plk3 in cell cycle progression is mediated, at least in part, through direct regulation of p53.	Serine	87-93	P53	Homo sapiens	31-34
12439598-3	2002	Activation of ERK is required for accumulation and phosphorylation of p53 following cisplatin treatment.	Cisplatin	84-93	P53	Homo sapiens	70-73
12439598-8	2002	Treatment of cells with PD98059 or UO126 after cisplatin incubation or inhibition of signaling through ERK by tetracycline-regulated expression of dominant-inhibitory ERK enhanced resistance to cisplatin in p53-negative osteosarcoma cells and reduced cisplatin-induced apoptosis.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	24-31	P53	Homo sapiens	207-210
12439598-8	2002	Treatment of cells with PD98059 or UO126 after cisplatin incubation or inhibition of signaling through ERK by tetracycline-regulated expression of dominant-inhibitory ERK enhanced resistance to cisplatin in p53-negative osteosarcoma cells and reduced cisplatin-induced apoptosis.	Cisplatin	194-203	P53	Homo sapiens	207-210
12439598-8	2002	Treatment of cells with PD98059 or UO126 after cisplatin incubation or inhibition of signaling through ERK by tetracycline-regulated expression of dominant-inhibitory ERK enhanced resistance to cisplatin in p53-negative osteosarcoma cells and reduced cisplatin-induced apoptosis.	Cisplatin	194-203	P53	Homo sapiens	207-210
12439598-9	2002	P53 was stabilized and phosphorylated in a MEK1-dependent manner after cisplatin incubation in Kelly neuroblastoma cells.	Cisplatin	71-80	P53	Homo sapiens	0-3
12395332-4	2002	The 249ser-p53 mutation was found in 54% (97/181) of HCC cases and in all 7 cases with tissue for analysis from the hepatitis cohort but in none of 42 matched cases from Beijing.	249ser	4-10	P53	Homo sapiens	11-14
12395332-7	2002	A similar relative risk was found using 249ser-p53 mutation as a marker for aflatoxin exposure.	249ser	40-46	P53	Homo sapiens	47-50
12395332-9	2002	The 249ser-p53 mutation appears to result from coexposure to aflatoxin and HBV infection.	249ser	4-10	P53	Homo sapiens	11-14
12401821-7	2002	p53 immunoexpression in more than 25% of the neoplastic cells was significantly associated with smoking but not with alcohol consumption.	Alcohols	117-124	P53	Homo sapiens	0-3
12642691-3	2002	The p53 induced by FR901228 was functional as evidenced by mdm-2 and p21 transactivation, and its further accumulation following DNA damage by doxorubicin.	Doxorubicin	143-154	P53	Homo sapiens	4-7
12445252-1	2002	Recently it has been found that the presence of homozygous arginine polymorphism at codon 72 of p53, represents a significant risk factor in the development of HPV-associated cervical cancer.	Arginine	59-67	P53	Homo sapiens	96-99
12445252-4	2002	The aim of the present study was to assess the frequency distribution of the p53 homozygous arginine polymorphism in cervical cancer patients and in a population sample of healthy Israeli Jewish women in order to determine whether the incidence pattern among them is genetically based.	Arginine	92-100	P53	Homo sapiens	77-80
12445252-12	2002	It may be assumed that the low incidence of cervical cancer in Israeli Jewish women and the differences between the ethnic groups may be related to the frequency pattern of the homozygous arginine p53 polymorphism	Arginine	188-196	P53	Homo sapiens	197-200
12458344-2	2002	Previous studies have reported that a common polymorphism of the wild type p53 gene at codon 72 of exon 4 (Arg/Arg) is associated with a sevenfold increased risk of HPV-associated cancer compared to Arg/Pro and Pro/Pro polymorphisms.	Arginine	107-110	P53	Homo sapiens	75-78
12458344-2	2002	Previous studies have reported that a common polymorphism of the wild type p53 gene at codon 72 of exon 4 (Arg/Arg) is associated with a sevenfold increased risk of HPV-associated cancer compared to Arg/Pro and Pro/Pro polymorphisms.	Arginine	111-114	P53	Homo sapiens	75-78
12458344-2	2002	Previous studies have reported that a common polymorphism of the wild type p53 gene at codon 72 of exon 4 (Arg/Arg) is associated with a sevenfold increased risk of HPV-associated cancer compared to Arg/Pro and Pro/Pro polymorphisms.	Arginine	111-114	P53	Homo sapiens	75-78
12548019-2	2002	Plk3 physically interacts with p53 and phosphorylates this tumor suppressor protein on serine-20, suggesting that the role of Plk3 in cell cycle progression is mediated, at least in part, through direct regulation of p53.	Serine	87-93	P53	Homo sapiens	217-220
12487430-3	2002	Unlabelled multiply phosphorylated peptides corresponding to this amino-terminal transactivation domain proved to be powerful tools in analysing the phosphate specificity of existing anti-p53 monoclonal and polyclonal antibodies using direct ELISA.	Phosphates	149-158	P53	Homo sapiens	188-191
12500542-3	2002	Inverse PCR with degenerate oligonucleotides specific for the p53 binding site was subsequently performed on immunoprecipitated DNA and fragments containing putative p53 target genes were subcloned and sequenced.	Oligonucleotides	28-44	P53	Homo sapiens	62-65
12391296-1	2002	Histone acetyltransferases (HATs) use acetyl CoA to acetylate target lysine residues within histones and other transcription factors, such as the p53 tumor suppressor, to promote gene activation.	Lysine	69-75	P53	Homo sapiens	146-149
12397361-3	2002	Here we report that DNA damage specifically induces p53 phosphorylation on Ser/Thr-Pro motifs, which facilitates its interaction with Pin1, a member of peptidyl-prolyl isomerase.	Serine	75-78	P53	Homo sapiens	52-55
12397361-3	2002	Here we report that DNA damage specifically induces p53 phosphorylation on Ser/Thr-Pro motifs, which facilitates its interaction with Pin1, a member of peptidyl-prolyl isomerase.	Threonine	79-82	P53	Homo sapiens	52-55
12397361-6	2002	The Pin1-mediated p53 activation requires the WW domain, a phosphorylated Ser/Thr-Pro motif interaction module, and the isomerase activity of Pin1.	Serine	74-77	P53	Homo sapiens	18-21
12397361-6	2002	The Pin1-mediated p53 activation requires the WW domain, a phosphorylated Ser/Thr-Pro motif interaction module, and the isomerase activity of Pin1.	Threonine	78-81	P53	Homo sapiens	18-21
12397362-4	2002	The interaction is strictly dependent on p53 phosphorylation, and requires Ser 33, Thr 81 and Ser 315.	Serine	75-78	P53	Homo sapiens	41-44
12397362-4	2002	The interaction is strictly dependent on p53 phosphorylation, and requires Ser 33, Thr 81 and Ser 315.	Threonine	83-86	P53	Homo sapiens	41-44
12397362-4	2002	The interaction is strictly dependent on p53 phosphorylation, and requires Ser 33, Thr 81 and Ser 315.	Serine	94-97	P53	Homo sapiens	41-44
12434294-0	2002	Association of p53 codon 72 polymorphism with advanced lung cancer: the Arg allele is preferentially retained in tumours arising in Arg/Pro germline heterozygotes.	Arginine	72-75	P53	Homo sapiens	15-18
12434294-0	2002	Association of p53 codon 72 polymorphism with advanced lung cancer: the Arg allele is preferentially retained in tumours arising in Arg/Pro germline heterozygotes.	Arginine	132-135	P53	Homo sapiens	15-18
12434294-5	2002	p53 Arg/Arg genotype was significantly increased in lung cancer patients compared to normal controls (50% vs 24.2%, P&lt;0.002).	Arginine	4-7	P53	Homo sapiens	0-3
12163498-4	2002	Expression of TauT was decreased after activation of p53 by doxorubicin, a DNA-damaging drug, in 293 and NRK-52E renal cells.	Doxorubicin	60-71	P53	Homo sapiens	53-56
12434294-5	2002	p53 Arg/Arg genotype was significantly increased in lung cancer patients compared to normal controls (50% vs 24.2%, P&lt;0.002).	Arginine	8-11	P53	Homo sapiens	0-3
12434294-7	2002	Loss of heterozygosity at the TP53 locus was found in 14 out of 27 Arg/Pro patients (51.85%).	Arginine	67-70	P53	Homo sapiens	30-34
12434294-9	2002	Our results suggest that p53 codon 72 Arg homozygosity is associated with advanced lung cancer, and that the Arg allele is preferentially retained in patients heterozygous for this polymorphism.	Arginine	38-41	P53	Homo sapiens	25-28
12370832-0	2002	Mdm-2 binding and TAF(II)31 recruitment is regulated by hydrogen bond disruption between the p53 residues Thr18 and Asp21.	Hydrogen	56-64	P53	Homo sapiens	93-96
12384533-3	2002	Here we show that UCN-01 prevented IR-induced p53 up-regulation and p53 phosphorylation on serine 20, a site previously identified for Chk2 (or/and Chk1) kinase.	Serine	91-97	P53	Homo sapiens	68-71
12370832-0	2002	Mdm-2 binding and TAF(II)31 recruitment is regulated by hydrogen bond disruption between the p53 residues Thr18 and Asp21.	UNII-PYZ33YLR8A	106-111	P53	Homo sapiens	93-96
12370809-10	2002	Our data support a model of feed-forward loop for p53 activity, that is, various cellular stresses, including reactive oxygen species (ROS), activate p53, which induces the expression of FDXR; and the FDXR gene product, FR, in turn sensitizes cells to ROS-mediated apoptosis.	Reactive Oxygen Species	110-133	P53	Homo sapiens	50-53
12370809-10	2002	Our data support a model of feed-forward loop for p53 activity, that is, various cellular stresses, including reactive oxygen species (ROS), activate p53, which induces the expression of FDXR; and the FDXR gene product, FR, in turn sensitizes cells to ROS-mediated apoptosis.	Reactive Oxygen Species	110-133	P53	Homo sapiens	150-153
12370809-10	2002	Our data support a model of feed-forward loop for p53 activity, that is, various cellular stresses, including reactive oxygen species (ROS), activate p53, which induces the expression of FDXR; and the FDXR gene product, FR, in turn sensitizes cells to ROS-mediated apoptosis.	Reactive Oxygen Species	135-138	P53	Homo sapiens	50-53
12370809-10	2002	Our data support a model of feed-forward loop for p53 activity, that is, various cellular stresses, including reactive oxygen species (ROS), activate p53, which induces the expression of FDXR; and the FDXR gene product, FR, in turn sensitizes cells to ROS-mediated apoptosis.	Reactive Oxygen Species	135-138	P53	Homo sapiens	150-153
12370809-10	2002	Our data support a model of feed-forward loop for p53 activity, that is, various cellular stresses, including reactive oxygen species (ROS), activate p53, which induces the expression of FDXR; and the FDXR gene product, FR, in turn sensitizes cells to ROS-mediated apoptosis.	Reactive Oxygen Species	252-255	P53	Homo sapiens	50-53
12370809-10	2002	Our data support a model of feed-forward loop for p53 activity, that is, various cellular stresses, including reactive oxygen species (ROS), activate p53, which induces the expression of FDXR; and the FDXR gene product, FR, in turn sensitizes cells to ROS-mediated apoptosis.	Reactive Oxygen Species	252-255	P53	Homo sapiens	150-153
12151394-7	2002	However, unlike ATM-deficient cells, these MMR-deficient cells displayed rapid phosphorylation of the p53 residue serine 15 after MNNG.	Serine	114-120	P53	Homo sapiens	102-105
12370832-1	2002	Analyses of five wild-type p53 containing cell lines revealed lineage specific differences in phosphorylation of Thr18 after treatment with ionizing (IR) or ultraviolet (UV) radiation.	UNII-PYZ33YLR8A	113-118	P53	Homo sapiens	27-30
12370832-2	2002	Importantly, Thr18 phosphorylation correlated with induction of the p53 downstream targets p21(Waf1/Cip1) (p21) and Mdm-2, suggesting a transactivation enhancing role.	UNII-PYZ33YLR8A	13-18	P53	Homo sapiens	68-71
12370832-4	2002	Mutagenesis-derived hydrogen bond disruption attenuated the interaction of p53 with the transactivation repressor Mdm-2 but had no direct effect on the interaction of p53 with the basal transcription factor TAF(II)31.	Hydrogen	20-28	P53	Homo sapiens	75-78
12370832-6	2002	Consistently, p53-null cells transfected with hydrogen bond disrupting p53 mutants demonstrated enhanced endogenous p21 expression, whereas p53/Mdm-2-double null cells exhibited no discernible differences in p21 expression.	Hydrogen	46-54	P53	Homo sapiens	14-17
12370832-6	2002	Consistently, p53-null cells transfected with hydrogen bond disrupting p53 mutants demonstrated enhanced endogenous p21 expression, whereas p53/Mdm-2-double null cells exhibited no discernible differences in p21 expression.	Hydrogen	46-54	P53	Homo sapiens	71-74
12370832-6	2002	Consistently, p53-null cells transfected with hydrogen bond disrupting p53 mutants demonstrated enhanced endogenous p21 expression, whereas p53/Mdm-2-double null cells exhibited no discernible differences in p21 expression.	Hydrogen	46-54	P53	Homo sapiens	71-74
12370832-7	2002	We conclude disruption of intramolecular hydrogen bonding between Thr18 and Asp21 enhances p53 transactivation by modulating Mdm-2 binding, facilitating TAF(II)31 recruitment.	Hydrogen	41-49	P53	Homo sapiens	91-94
12370832-7	2002	We conclude disruption of intramolecular hydrogen bonding between Thr18 and Asp21 enhances p53 transactivation by modulating Mdm-2 binding, facilitating TAF(II)31 recruitment.	UNII-PYZ33YLR8A	66-71	P53	Homo sapiens	91-94
12376468-0	2002	Reporter gene transactivation by human p53 is inhibited in thioredoxin reductase null yeast by a mechanism associated with thioredoxin oxidation and independent of changes in the redox state of glutathione.	Glutathione	194-205	P53	Homo sapiens	39-42
12508651-7	2002	RESULTS: Antisense alpha 1, 4Gal-T oligonucleotide signifantly inhibited cell growth (P &lt; 0.01), induced the apoptosis (P &lt; 0.05), downregulated expression of bcl-2 protein (P &lt; 0.01) and upregulated expressions of fas and bax protein (P &lt; 0.01), but did not influence p53 expression in glioma cell line SWO-38.	alpha 1, 4gal-t oligonucleotide	19-50	P53	Homo sapiens	281-284
12359750-4	2002	Reactive oxygen species apparently derived from a flavin-containing oxidase enzyme [presumably an NAD(P)H-oxidase] appeared to be major contributors to the bystander-induced up-regulation of p53 and p21(Waf1) as well as micronucleus formation, as evidenced by the inhibition of these effects with diphenyliodonium.	Reactive Oxygen Species	0-23	P53	Homo sapiens	191-194
12376463-5	2002	Tamoxifen induced growth suppression was independent of p53 status but resulted in up-regulation of cyclin dependent kinase inhibitors (CDKIs) p21/Waf-1, p27/Kip1 and p15/INK4a.	Tamoxifen	0-9	P53	Homo sapiens	56-59
12376463-7	2002	Cisplatin induced p53 independent apoptosis in both head and neck cancer cell lines.	Cisplatin	0-9	P53	Homo sapiens	18-21
12376468-2	2002	The basis for p53 inhibition was investigated by measuring the redox state of thioredoxin and glutathione in wild-type and Deltatrr1 yeast.	Glutathione	94-105	P53	Homo sapiens	14-17
12468337-1	2002	OBJECTIVE: The objective of this study was to verify the correlation between p53 immunostaining at initial diagnosis and at positive reassessment after completing platinum-based chemotherapy and to assess prognostic differences between patients whose tumors display positive immunostaining versus those that have negative immunostaining at such reassessment.	Platinum	163-171	P53	Homo sapiens	77-80
26680888-6	2002	The women who had p53 (Arg/Arg), IRF-1 (T/T) and an education of less than 6 years showed a 14.7 fold increased risk of cervical cancer than those women who had p53 (~Pro), IRF-1 (~C) and an education of more than 15 years.	Arginine	23-26	P53	Homo sapiens	18-21
26680888-6	2002	The women who had p53 (Arg/Arg), IRF-1 (T/T) and an education of less than 6 years showed a 14.7 fold increased risk of cervical cancer than those women who had p53 (~Pro), IRF-1 (~C) and an education of more than 15 years.	Arginine	27-30	P53	Homo sapiens	18-21
26680888-7	2002	The women who had p53 (Arg/Arg), p21 (Ser/Ser) and more than 3 children showed a 6.4 fold increased risk of cervical cancer than those women who had p53 (~Pro), p21 (~Arg) and had borne no child.	Arginine	23-26	P53	Homo sapiens	18-21
26680888-7	2002	The women who had p53 (Arg/Arg), p21 (Ser/Ser) and more than 3 children showed a 6.4 fold increased risk of cervical cancer than those women who had p53 (~Pro), p21 (~Arg) and had borne no child.	Arginine	27-30	P53	Homo sapiens	18-21
26680888-7	2002	The women who had p53 (Arg/Arg), p21 (Ser/Ser) and more than 3 children showed a 6.4 fold increased risk of cervical cancer than those women who had p53 (~Pro), p21 (~Arg) and had borne no child.	Arginine	27-30	P53	Homo sapiens	18-21
26680888-8	2002	The women who had p53 (Arg/Arg), IRF-1 (T/T) and had experience of first sexual intercourse before the age of 22-years showed a 5.5 fold increased risk of cervical cancer than those women who had p53 (~Pro), IRF-1 (~C) and had experience of first sexual intercourse after the age of 26-years.	Arginine	23-26	P53	Homo sapiens	18-21
12435289-6	2002	The p53 gene mutations seem to be the most promising predictive markers because preclinical data suggest that taxane-induced apoptosis is p53 independent.	taxane	110-116	P53	Homo sapiens	4-7
12435289-6	2002	The p53 gene mutations seem to be the most promising predictive markers because preclinical data suggest that taxane-induced apoptosis is p53 independent.	taxane	110-116	P53	Homo sapiens	138-141
26680888-8	2002	The women who had p53 (Arg/Arg), IRF-1 (T/T) and had experience of first sexual intercourse before the age of 22-years showed a 5.5 fold increased risk of cervical cancer than those women who had p53 (~Pro), IRF-1 (~C) and had experience of first sexual intercourse after the age of 26-years.	Arginine	27-30	P53	Homo sapiens	18-21
12235242-2	2002	Here we report that the chemotherapeutic drug doxorubicin, a DNA-damaging agent, activates a p53-survivin signaling pathway inducing cell cycle arrest and apoptosis in childhood acute lymphoblastic leukemia (ALL).	Doxorubicin	46-57	P53	Homo sapiens	93-96
12416732-14	2002	Hepatic DNA of iron-loaded patients shows evidence of damage, including mutations of the tumor suppressor gene p53.	Iron	15-19	P53	Homo sapiens	111-114
12235242-6	2002	With a p53-null cell line (EU-4), although doxorubicin treatment arrested cells in G(2)/M, survivin expression was unchanged, and cells underwent only limited apoptosis.	Doxorubicin	43-54	P53	Homo sapiens	7-10
12235242-3	2002	Treatment of wild-type (wt) p53 ALL cells (EU-3 cell line) with doxorubicin caused accumulation of p53, resulting in dramatic down-regulation of survivin, depletion of cells in G(2)/M, and apoptosis (increased sub-G(1) compartment).	Doxorubicin	64-75	P53	Homo sapiens	28-31
12235242-7	2002	However, re-expression of wt-p53 in EU-4 cells could restore the doxorubicin-p53-survivin pathway, resulting in significantly decreased survivin expression and increased apoptosis in these cells after doxorubicin treatment.	Doxorubicin	65-76	P53	Homo sapiens	29-32
12235242-7	2002	However, re-expression of wt-p53 in EU-4 cells could restore the doxorubicin-p53-survivin pathway, resulting in significantly decreased survivin expression and increased apoptosis in these cells after doxorubicin treatment.	Doxorubicin	65-76	P53	Homo sapiens	77-80
12235242-3	2002	Treatment of wild-type (wt) p53 ALL cells (EU-3 cell line) with doxorubicin caused accumulation of p53, resulting in dramatic down-regulation of survivin, depletion of cells in G(2)/M, and apoptosis (increased sub-G(1) compartment).	Doxorubicin	64-75	P53	Homo sapiens	99-102
12235242-7	2002	However, re-expression of wt-p53 in EU-4 cells could restore the doxorubicin-p53-survivin pathway, resulting in significantly decreased survivin expression and increased apoptosis in these cells after doxorubicin treatment.	Doxorubicin	201-212	P53	Homo sapiens	29-32
12235242-4	2002	In contrast, doxorubicin treatment of mutant (mut) p53 cells (EU-6/ALL line) up-regulated survivin and induced G(2)/M arrest without inducing apoptosis.	Doxorubicin	13-24	P53	Homo sapiens	51-54
12481430-1	2002	DNA damaging agents such as cisplatin arrest cell cycle progression at either G1, S, or G2 phase, although the G1 arrest is only seen in cells expressing the wild-type p53 tumor suppressor protein.	Cisplatin	28-37	P53	Homo sapiens	168-171
12481430-8	2002	This analogue abrogated S and G2 phase arrest and enhanced cytotoxicity induced by cisplatin only in p53 defective cells.	Cisplatin	83-92	P53	Homo sapiens	101-104
12481427-8	2002	Moreover, 11R-p53 enhanced the cisplatin-dependent induction of apoptosis of the cells.	Cisplatin	31-40	P53	Homo sapiens	14-17
12232053-8	2002	In vitro studies indicate that dicoumarol-induced p53 degradation was ubiquitin-independent and ATP-dependent.	Adenosine Triphosphate	96-99	P53	Homo sapiens	50-53
12065086-3	2002	The p53 codon 72 Arg/Pro polymorphism has been suggested to be associated with susceptibility to tobacco-related cancers, but this association remains controversial.	Arginine	17-20	P53	Homo sapiens	4-7
12214265-1	2002	By inducing p53-dependent G2 arrest, the pretreatment with low concentrations of DNA damaging drugs (e.g., doxorubicin, DOX) can prevent cell death caused by microtubule-active drugs (e.g., paclitaxel, PTX), thus potentially permitting selective killing of p53-deficient cancer cells.	Doxorubicin	120-123	P53	Homo sapiens	12-15
12165443-4	2002	In this p53/DNA-ELISA, we use streptavidin-coated microplates to capture biotinylated oligonucleotides containing p53 consensus sequences (p53CON).	Oligonucleotides	86-102	P53	Homo sapiens	8-11
12165443-4	2002	In this p53/DNA-ELISA, we use streptavidin-coated microplates to capture biotinylated oligonucleotides containing p53 consensus sequences (p53CON).	Oligonucleotides	86-102	P53	Homo sapiens	114-117
12214265-1	2002	By inducing p53-dependent G2 arrest, the pretreatment with low concentrations of DNA damaging drugs (e.g., doxorubicin, DOX) can prevent cell death caused by microtubule-active drugs (e.g., paclitaxel, PTX), thus potentially permitting selective killing of p53-deficient cancer cells.	Paclitaxel	190-200	P53	Homo sapiens	12-15
12214265-2	2002	However, DOX still protects a subset of tumor cell lines lacking wt p53 (HL60 and Jurkat leukemia cells), thus limiting the utility of protection of cells with wt p53 (e.g., normal cells).	Doxorubicin	9-12	P53	Homo sapiens	68-71
12101184-0	2002	Adriamycin-induced senescence in breast tumor cells involves functional p53 and telomere dysfunction.	Doxorubicin	0-10	P53	Homo sapiens	72-75
12101184-3	2002	Cells acutely exposed to adriamycin exhibited an increase in p53 activity, a decline in telomerase activity, and a dramatic increase in beta-galactosidase, a marker of senescence.	Doxorubicin	25-35	P53	Homo sapiens	61-64
12101184-4	2002	Inactivation of wild-type p53 resulted in a transition of the cellular response to adriamycin treatment from replicative senescence to delayed apoptosis, demonstrating that p53 plays an integral role in the fate of breast tumor cells treated with DNA-damaging agents.	Doxorubicin	83-93	P53	Homo sapiens	26-29
12101184-4	2002	Inactivation of wild-type p53 resulted in a transition of the cellular response to adriamycin treatment from replicative senescence to delayed apoptosis, demonstrating that p53 plays an integral role in the fate of breast tumor cells treated with DNA-damaging agents.	Doxorubicin	83-93	P53	Homo sapiens	173-176
12101184-8	2002	To our knowledge, these data are the first to demonstrate that the mechanism of adriamycin-induced senescence is dependent on both functional p53 and telomere dysfunction rather than overall shortening.	Doxorubicin	80-90	P53	Homo sapiens	142-145
12234998-0	2002	p53 controls global nucleotide excision repair of low levels of structurally diverse benzo(g)chrysene-DNA adducts in human fibroblasts.	chrysene	93-101	P53	Homo sapiens	0-3
12209989-0	2002	Escape of p53 protein from E6-mediated degradation in HeLa cells after cisplatin therapy.	Cisplatin	71-80	P53	Homo sapiens	10-13
12214265-1	2002	By inducing p53-dependent G2 arrest, the pretreatment with low concentrations of DNA damaging drugs (e.g., doxorubicin, DOX) can prevent cell death caused by microtubule-active drugs (e.g., paclitaxel, PTX), thus potentially permitting selective killing of p53-deficient cancer cells.	Doxorubicin	107-118	P53	Homo sapiens	12-15
12214265-3	2002	The present work overcomes this obstacle by adding an abrogator of p53-independent checkpoint (e.g., UCN-01) to the DOX-PTX sequence.	Doxorubicin	116-119	P53	Homo sapiens	67-70
12214265-4	2002	By inhibiting a p53-independent pathway, UCN-01 overrode DOX-induced G2 arrest and instead induced G1 arrest in HL60 and Jurkat, thus propelling these p53-deficient cells from G2 to G1.	Doxorubicin	57-60	P53	Homo sapiens	16-19
12091386-0	2002	p38 kinase regulates nitric oxide-induced apoptosis of articular chondrocytes by accumulating p53 via NFkappa B-dependent transcription and stabilization by serine 15 phosphorylation.	Nitric Oxide	21-33	P53	Homo sapiens	94-97
12091386-1	2002	Nitric oxide (NO) during primary culture of articular chondrocytes causes apoptosis via p38 mitogen-activated protein kinase in association with elevation of p53 protein level, caspase-3 activation, and differentiation status.	Nitric Oxide	0-12	P53	Homo sapiens	158-161
12091386-4	2002	Activated p38 kinase also physically associates and phosphorylates the serine 15 residue of p53, which results in accumulation of p53 protein during NO-induced apoptosis.	Serine	71-77	P53	Homo sapiens	92-95
12091386-4	2002	Activated p38 kinase also physically associates and phosphorylates the serine 15 residue of p53, which results in accumulation of p53 protein during NO-induced apoptosis.	Serine	71-77	P53	Homo sapiens	130-133
12508548-1	2002	BACKGROUND &amp; OBJECTIVE: Experimental study proved that the coexpression of p53 and vascular endothelial growth factor (VEGF) play an important role in angiogenesis of tumor.	Adenosine Monophosphate	12-15	P53	Homo sapiens	79-82
12203114-4	2002	Whereas induction of Hi95 by prolonged hypoxia or by oxidative stress is most likely p53-independent, its induction in response to DNA damaging treatments (gamma- or UV-irradiation, or doxorubicin) occurs in a p53-dependent manner.	Doxorubicin	185-196	P53	Homo sapiens	210-213
12500660-3	2002	DNA breaks in p53 gene produced by restriction endonuclease AfaI were detected by using this new method followed by Southern hybridization with DIG-labeled probe.	digitoxose	144-147	P53	Homo sapiens	14-17
12175696-1	2002	The correlation between inactivation of the TP53 gene through mutation or the presence of high-risk human papillomavirus (HPV) DNA and intrinsic paclitaxel sensitivity was studied in 27 gynaecological cancer cell lines.	Paclitaxel	145-155	P53	Homo sapiens	44-48
12209584-0	2002	Cellular effects of CPT-11 on colon carcinoma cells: dependence on p53 and hMLH1 status.	Irinotecan	20-26	P53	Homo sapiens	67-70
12530022-2	2002	Our previous work suggested tamoxifen-associated endometrial cancers might be associated with p53 mutations.	Tamoxifen	28-37	P53	Homo sapiens	94-97
12459315-0	2002	Differential p53 protein expression level in human cancer-derived cell lines after estradiol treatment.	Estradiol	83-92	P53	Homo sapiens	13-16
12459315-3	2002	The aim of this study was to evaluate the effect of low and high doses of estradiol in p53 gene expression in epithelial cancer-derived cell lines from the reproductive tract.	Estradiol	74-83	P53	Homo sapiens	87-90
12459315-4	2002	METHODS: p53 gene expression was assessed by Northern and Western blot methods in three human epithelial cancer-derived cell lines after estradiol treatment.	Estradiol	137-146	P53	Homo sapiens	9-12
12459315-6	2002	p53 protein content was nearly constant in HeLa and C-33 cell lines at administration of 10 nM of estradiol.	Estradiol	98-107	P53	Homo sapiens	0-3
12459315-7	2002	However, when estradiol was administered at a higher dose (1 micro M), an increase in p53 protein was observed over time in HeLa and CaLo cell lines.	Estradiol	14-23	P53	Homo sapiens	86-89
12459315-9	2002	CONCLUSIONS: Overall results indicate that estradiol induces variations of p53 protein levels in epithelial cancer-derived cell lines from the reproductive tract in vitro and that this effect may be related with status p53 and/or presence of E6/E7 from human papillomavirus.	Estradiol	43-52	P53	Homo sapiens	75-78
12459315-9	2002	CONCLUSIONS: Overall results indicate that estradiol induces variations of p53 protein levels in epithelial cancer-derived cell lines from the reproductive tract in vitro and that this effect may be related with status p53 and/or presence of E6/E7 from human papillomavirus.	Estradiol	43-52	P53	Homo sapiens	219-222
12168112-2	2002	p53 wild- and mutant-type gastric and colon cancer cell lines were treated by 5FU alone, TRAIL alone, and a combination of 5FU and TRAIL, and cell viability after each treatment was determined by MTT assay.	Fluorouracil	78-81	P53	Homo sapiens	0-3
12168112-2	2002	p53 wild- and mutant-type gastric and colon cancer cell lines were treated by 5FU alone, TRAIL alone, and a combination of 5FU and TRAIL, and cell viability after each treatment was determined by MTT assay.	Fluorouracil	123-126	P53	Homo sapiens	0-3
12127561-9	2002	Sequencing of the TP53 gene revealed a mutation (codon 147(valine--&gt;glycine)) in exon 5.	Glycine	71-78	P53	Homo sapiens	18-22
12167711-4	2002	Mutants with serine-to-alanine substitutions between residues 244 and 260 abolished or at least reduced the capacity of Mdm2 to promote p53 degradation.	Serine	13-19	P53	Homo sapiens	136-139
12167711-4	2002	Mutants with serine-to-alanine substitutions between residues 244 and 260 abolished or at least reduced the capacity of Mdm2 to promote p53 degradation.	Alanine	23-30	P53	Homo sapiens	136-139
12160929-3	2002	Human lung adenocarcinoma cells NCI-H460 (p53-wild-type) have constitutively lower levels of GSH than NCI-H1299 (p53-null) cells.	Glutathione	93-96	P53	Homo sapiens	42-45
21329584-6	2002	The expression of p53, Fas and Bax genes in Tanshinone group was up-regulated markedly, but Bcl-2 was obviously down-regulated.	tanshinone	44-54	P53	Homo sapiens	18-21
12160929-10	2002	These data suggest that, in human lung cancer cells, GSH plays a vital role in the protection of TCE- and PERC-induced oxidative stress and apoptosis, which may be mediated through a p53-dependent pathway.	Glutathione	53-56	P53	Homo sapiens	183-186
12387362-0	2002	Abeta[25-35] peptide and iron promote apoptosis in lymphocytes by an oxidative stress mechanism: involvement of H2O2, caspase-3, NF-kappaB, p53 and c-Jun.	Iron	25-29	P53	Homo sapiens	140-143
12080066-5	2002	Moreover, full-length p53 and a C-terminal polypeptide (residues 373-383) inhibit the BLM and WRN helicase activities, but phosphorylation at Ser(376) or Ser(378) completely abolishes this inhibition.	Serine	142-145	P53	Homo sapiens	22-25
12080066-6	2002	Following blockage of DNA replication, Ser(15) phospho-p53, BLM, and RAD51 colocalize in nuclear foci at sites likely to contain DNA replication intermediates in cells.	Serine	39-42	P53	Homo sapiens	55-58
12175902-3	2002	The results show that the removal of anti-BPDE DNA adducts from the genome overall and NTS by GGR was significantly reduced in HPV-16E6 protein expressing cells as compared to that in normal and HPV-16E7 protein expressing cells, indicating the role of p53 and not pRb in nucleotide excision repair (NER).	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	42-46	P53	Homo sapiens	253-256
12160929-4	2002	The results showed that exposure to vapor TCE and PERC produced a dose-dependent and more pronounced accumulation of H(2)O(2) in p53-WT H460 than p53-null H1299 cells.	Hydrogen Peroxide	117-125	P53	Homo sapiens	129-132
12160929-5	2002	The accumulation of H(2)O(2) was accompanied by severe cellular damage, as indicated by the significant increase of lipid peroxidation and apoptosis in p53-WT H460 cells, but not p53-null H1299 cells.	Hydrogen Peroxide	20-28	P53	Homo sapiens	152-155
12160929-7	2002	In contrast, depletion of GSH in p53-null H1299 cells enhanced TCE- or PERC-induced lipid peroxidation.	Glutathione	26-29	P53	Homo sapiens	33-36
12177781-4	2002	In addition, we examined whether the Fragile histidine triad and mismatch repair protein expression correlated with p53 expression and clinicopathological findings.	Histidine	45-54	P53	Homo sapiens	116-119
12136132-0	2002	Nitric oxide-induced genotoxicity, mitochondrial damage, and apoptosis in human lymphoblastoid cells expressing wild-type and mutant p53.	Nitric Oxide	0-12	P53	Homo sapiens	133-136
11925449-5	2002	Mutation of conserved amino acids in the linker at Ser(261) and Leu(264), which bridges the S9-S10 beta-sheets, stimulated p53 activity from reporter templates and increased MDM2-dependent ubiquitination of p53.	Serine	51-54	P53	Homo sapiens	123-126
11925449-5	2002	Mutation of conserved amino acids in the linker at Ser(261) and Leu(264), which bridges the S9-S10 beta-sheets, stimulated p53 activity from reporter templates and increased MDM2-dependent ubiquitination of p53.	Serine	51-54	P53	Homo sapiens	207-210
11925449-7	2002	Introducing an Ala(19) mutation into the p53(F270A) protein abolished both RNA.MDM2 complex binding and hyper-ubiquitination in vivo, thus indicating that p53(F270A) protein hyper-ubiquitination depends upon MDM2 binding to its primary site in the BOX-I domain.	Alanine	15-18	P53	Homo sapiens	41-46
11925449-7	2002	Introducing an Ala(19) mutation into the p53(F270A) protein abolished both RNA.MDM2 complex binding and hyper-ubiquitination in vivo, thus indicating that p53(F270A) protein hyper-ubiquitination depends upon MDM2 binding to its primary site in the BOX-I domain.	Alanine	15-18	P53	Homo sapiens	155-160
12107071-6	2002	Reducing [Zn(2+)](i), using N,N,N",N"-tetrakis(2-pyridylmethyl)ethylenediamine, caused rapid apoptosis in both p53(wt) and p53(mut) cells, although cotreatment with VP-16 exacerbated apoptosis only in p53(wt) cells.	Zinc	10-16	P53	Homo sapiens	111-114
12107071-6	2002	Reducing [Zn(2+)](i), using N,N,N",N"-tetrakis(2-pyridylmethyl)ethylenediamine, caused rapid apoptosis in both p53(wt) and p53(mut) cells, although cotreatment with VP-16 exacerbated apoptosis only in p53(wt) cells.	Zinc	10-16	P53	Homo sapiens	123-126
12107071-6	2002	Reducing [Zn(2+)](i), using N,N,N",N"-tetrakis(2-pyridylmethyl)ethylenediamine, caused rapid apoptosis in both p53(wt) and p53(mut) cells, although cotreatment with VP-16 exacerbated apoptosis only in p53(wt) cells.	Zinc	10-16	P53	Homo sapiens	123-126
12107071-8	2002	We conclude that the DNA damage-induced transient is p53-independent up to a damage threshold, beyond which competent cells reduce [Zn(2+)](i) before apoptosis.	Zinc	132-138	P53	Homo sapiens	53-56
12107071-9	2002	Early stress responses in p53(wt) cells take place in an environment of enhanced Zn(2+) availability.	Zinc	81-87	P53	Homo sapiens	26-29
12101396-0	2002	Transfection of mutant p53 gene depresses X-ray- or CDDP-induced apoptosis in a human squamous cell carcinoma of the head and neck.	cddp	52-56	P53	Homo sapiens	23-26
12101396-6	2002	SAS/Trp248 cells showed X-ray- and CDDP-resistance due to the dominant negative nature of mutant p53, compared with SAS/neo cells.	cddp	35-39	P53	Homo sapiens	97-100
12101396-9	2002	The present results strongly suggest that the X-ray- and CDDP-sensitivities of human squamous cell carcinomas are p53-dependent, and that the sensitivities are tightly correlated with the induction of apoptosis through caspase-3 activation.	cddp	57-61	P53	Homo sapiens	114-117
12101396-10	2002	The p53-dependent X-ray- or CDDP-sensitivity was supported by results from p53-null human lung cancer H1299 cells which were transfected with wild-type or mutant p53 gene.	cddp	28-32	P53	Homo sapiens	4-7
12101396-10	2002	The p53-dependent X-ray- or CDDP-sensitivity was supported by results from p53-null human lung cancer H1299 cells which were transfected with wild-type or mutant p53 gene.	cddp	28-32	P53	Homo sapiens	75-78
12192480-2	2002	MATERIAL AND METHODS: Immunohistochemical techniques were used to evaluate p53 expression in paraffin-embedded tissue specimens of 50 EOC cases.	Paraffin	93-101	P53	Homo sapiens	75-78
12101396-10	2002	The p53-dependent X-ray- or CDDP-sensitivity was supported by results from p53-null human lung cancer H1299 cells which were transfected with wild-type or mutant p53 gene.	cddp	28-32	P53	Homo sapiens	75-78
12176837-2	2002	The trained neural network uses as input the fluorescence intensities of DNA hybridized to oligonucleotides on the surface of the chip and makes between zero and four errors in the predicted 1300 bp sequence when tested on wild-type TP53 sequence.	Oligonucleotides	91-107	P53	Homo sapiens	233-237
11964141-0	2002	Copper uptake is required for pyrrolidine dithiocarbamate-mediated oxidation and protein level increase of p53 in cells.	Copper	0-6	P53	Homo sapiens	107-110
11964141-8	2002	Our results show that a low level of copper accumulation in the range of 25-40 microg/g of cellular protein increases the steady-state levels of p53.	Copper	37-43	P53	Homo sapiens	145-148
11964141-9	2002	At copper accumulation levels higher than 60 microg/g of cellular protein, p53 is oxidized.	Copper	3-9	P53	Homo sapiens	75-78
11964141-10	2002	These results suggest that p53 is vulnerable to free radical-mediated oxidation at cysteine residues.	Cysteine	83-91	P53	Homo sapiens	27-30
12067581-9	2002	Similarly, the disruption of correct p53 folding and DNA binding by Cd(II), Ni(II) and Co(II) has been shown by other authors.	Nickel(2+)	76-82	P53	Homo sapiens	37-40
12139723-0	2002	Superior effect of 9-cis retinoic acid (RA) compared with all-trans RA and 13-cis RA on the inhibition of clonogenic cell growth and the induction of apoptosis in OCI/AML-2 subclones: is the p53 pathway involved?	Tretinoin	40-42	P53	Homo sapiens	191-194
12139723-1	2002	In the present study, the effects of 9-cis retinoic acid (RA) and 13-cis RA on acute myeloblastic leukaemia (AML) cell growth and the induction of apoptosis as well as its relationship with bcl-2 and p53 were compared with those of all-trans RA (ATRA).	Tretinoin	58-60	P53	Homo sapiens	200-203
12139723-4	2002	In addition, Western blotting revealed the most obvious translocation of p53 from cytosol to nucleus in the case of 9-cis RA, which was the only retinoid able to change the conformation of p53 from mutational to wild type, as demonstrated by flow cytometry.	Tretinoin	122-124	P53	Homo sapiens	73-76
12139723-4	2002	In addition, Western blotting revealed the most obvious translocation of p53 from cytosol to nucleus in the case of 9-cis RA, which was the only retinoid able to change the conformation of p53 from mutational to wild type, as demonstrated by flow cytometry.	Tretinoin	122-124	P53	Homo sapiens	189-192
12142377-7	2002	The p53 codon 72 arginine allele showed a suggestive negative association with cervical cancer (HET, OR = 0.49; 95% CI, 0.14-1.63; homozygotes, OR = 0.35; 95% CI, 0.11-1.17).	Arginine	17-25	P53	Homo sapiens	4-7
12151346-2	2002	Doxorubicin (Dx), an anthracycline used commonly as a chemotherapeutic agent in relapsed prostate cancer, is a strong inducer of p53 expression and p21(CIP1/WAF1) (p21) transactivation.	Doxorubicin	0-11	P53	Homo sapiens	129-132
12151346-2	2002	Doxorubicin (Dx), an anthracycline used commonly as a chemotherapeutic agent in relapsed prostate cancer, is a strong inducer of p53 expression and p21(CIP1/WAF1) (p21) transactivation.	Anthracyclines	21-34	P53	Homo sapiens	129-132
12171874-1	2002	Potentiation of 5-fluorouracil/leucovorin (FUra/LV) cytotoxicity by IFN-gamma in colon carcinoma cells is dependent on FUra-induced DNA damage, the Fas death receptor, and independent of p53 and RNA-mediated FUra toxicity, which occurs in normal gastrointestinal tissues.	Fluorouracil	16-30	P53	Homo sapiens	187-190
12142057-4	2002	Notably, the simultaneous exposure to ZD0473 and paclitaxel for 96 h resulted in synergy (as defined by a median effect analysis) in all four cell lines (i.e. independent of cisplatin resistance and p53 status).	amminedichloro(2-methylpyridine)platinum(II)	38-44	P53	Homo sapiens	199-202
12142057-4	2002	Notably, the simultaneous exposure to ZD0473 and paclitaxel for 96 h resulted in synergy (as defined by a median effect analysis) in all four cell lines (i.e. independent of cisplatin resistance and p53 status).	Paclitaxel	49-59	P53	Homo sapiens	199-202
12144822-7	2002	The frequency of distribution of the three genotypes of p53 codon 72 in a subgroup of the HPV16/18-positive cervical cancer patients was Pro/Pro 0.18 and Arg/Arg 0.26, with the heterozygous Pro/Arg 0.56, differing significantly from the genotype frequency in the normal healthy women (chi(2) = 6.928, df = 2, P &lt; 0.05).	Arginine	158-161	P53	Homo sapiens	56-59
12144822-2	2002	A common polymorphism of p53 in exon 4 codon 72, resulting in either proline (Pro) or arginine (Arg), affects HPV16/18 E6-mediated degradation of p53 protein in vivo.	Arginine	86-94	P53	Homo sapiens	25-28
12144822-10	2002	The p53 genotype distribution indicated that women homozygous for Arg genotype were at a 2.4-fold higher risk for developing HPV16/18-associated cervical carcinomas, compared to those showing heterozygous Pro/Arg genotype (odds ratio 2.4, 95% confidence interval 1.89 to 3.04).	Arginine	66-69	P53	Homo sapiens	4-7
12144822-2	2002	A common polymorphism of p53 in exon 4 codon 72, resulting in either proline (Pro) or arginine (Arg), affects HPV16/18 E6-mediated degradation of p53 protein in vivo.	Arginine	86-94	P53	Homo sapiens	146-149
12144822-2	2002	A common polymorphism of p53 in exon 4 codon 72, resulting in either proline (Pro) or arginine (Arg), affects HPV16/18 E6-mediated degradation of p53 protein in vivo.	Arginine	96-99	P53	Homo sapiens	25-28
12144822-2	2002	A common polymorphism of p53 in exon 4 codon 72, resulting in either proline (Pro) or arginine (Arg), affects HPV16/18 E6-mediated degradation of p53 protein in vivo.	Arginine	96-99	P53	Homo sapiens	146-149
12144822-7	2002	The frequency of distribution of the three genotypes of p53 codon 72 in a subgroup of the HPV16/18-positive cervical cancer patients was Pro/Pro 0.18 and Arg/Arg 0.26, with the heterozygous Pro/Arg 0.56, differing significantly from the genotype frequency in the normal healthy women (chi(2) = 6.928, df = 2, P &lt; 0.05).	Arginine	154-157	P53	Homo sapiens	56-59
12144822-7	2002	The frequency of distribution of the three genotypes of p53 codon 72 in a subgroup of the HPV16/18-positive cervical cancer patients was Pro/Pro 0.18 and Arg/Arg 0.26, with the heterozygous Pro/Arg 0.56, differing significantly from the genotype frequency in the normal healthy women (chi(2) = 6.928, df = 2, P &lt; 0.05).	Arginine	158-161	P53	Homo sapiens	56-59
12115529-5	2002	Immunoreactivity for maspin and p53 antibodies with paraffin-embedded carcinoma tissue was investigated using labeled streptavidin-biotin methods.	Paraffin	52-60	P53	Homo sapiens	32-35
12194756-5	2002	RESULTS: Clonogenic survival assays up to 8 Gy demonstrated that p53-defective HT-29 cells (sensitizer enhancement ratio [SER]=1.54) were sensitized by PTX (2 mM) to a significantly higher degree than p53 wild-type MCF-7 (SER=1.14) cells.	Serine	122-125	P53	Homo sapiens	65-68
12118335-0	2002	Curcumin inhibits cell cycle progression of immortalized human umbilical vein endothelial (ECV304) cells by up-regulating cyclin-dependent kinase inhibitor, p21WAF1/CIP1, p27KIP1 and p53.	Curcumin	0-8	P53	Homo sapiens	183-186
12118335-3	2002	Curcumin was found to induce G0/G1 and/or G2/M phase cell cycle arrest, up-regulate CDKIs, p21WAF1/CIP1, p27KIP1, and p53, and slightly down-regulate cyclin B1 and cdc2 in ECV304 cells.	Curcumin	0-8	P53	Homo sapiens	118-121
12194756-5	2002	RESULTS: Clonogenic survival assays up to 8 Gy demonstrated that p53-defective HT-29 cells (sensitizer enhancement ratio [SER]=1.54) were sensitized by PTX (2 mM) to a significantly higher degree than p53 wild-type MCF-7 (SER=1.14) cells.	Serine	222-225	P53	Homo sapiens	65-68
12716463-0	2002	Estradiol stabilizes p53 protein in breast cancer cell line, MCF-7.	Estradiol	0-9	P53	Homo sapiens	21-24
12200603-8	2002	RESULTS: A G:C to A:T mutation at codon 175 of p53 resulting in an arginine --&gt; histidine substitution was detected, confirming the clinical diagnosis of LFS.	Arginine	67-75	P53	Homo sapiens	47-50
12200603-8	2002	RESULTS: A G:C to A:T mutation at codon 175 of p53 resulting in an arginine --&gt; histidine substitution was detected, confirming the clinical diagnosis of LFS.	Histidine	83-92	P53	Homo sapiens	47-50
12131363-0	2002	Resveratrol induced serine phosphorylation of p53 causes apoptosis in a mutant p53 prostate cancer cell line.	Resveratrol	0-11	P53	Homo sapiens	46-49
12131363-0	2002	Resveratrol induced serine phosphorylation of p53 causes apoptosis in a mutant p53 prostate cancer cell line.	Resveratrol	0-11	P53	Homo sapiens	79-82
12131363-0	2002	Resveratrol induced serine phosphorylation of p53 causes apoptosis in a mutant p53 prostate cancer cell line.	Serine	20-26	P53	Homo sapiens	46-49
12131363-8	2002	The stilbene activated MAPK and caused increased abundance of p53 and serine-15 phosphorylated p53.	Serine	70-76	P53	Homo sapiens	95-98
12161533-0	2002	p53 Tumor suppressor protein content in human uterine leiomyomas and its down-regulation by 17 beta-estradiol.	Estradiol	92-109	P53	Homo sapiens	0-3
12161533-3	2002	The present study was conducted to elucidate the p53 protein content in human leiomyomas and its regulation by sex steroid hormones.	Steroids	115-131	P53	Homo sapiens	49-52
12131363-9	2002	Resveratrol induced serine-15 phosphorylation of p53 was blocked by PD 98059 (Calbiochem), a MAPK kinase inhibitor, implicating MAPK activation in the phosphorylation of p53.	Resveratrol	0-11	P53	Homo sapiens	49-52
12716463-2	2002	In MCF-7 breast cancer cell line possessing wild-type p53, ERalpha, and overexpressing MDM2, p53 accumulation was stimulated by 17beta-estradiol (E2) in a concentration-dependent manner.	Estradiol	128-144	P53	Homo sapiens	54-57
12131363-9	2002	Resveratrol induced serine-15 phosphorylation of p53 was blocked by PD 98059 (Calbiochem), a MAPK kinase inhibitor, implicating MAPK activation in the phosphorylation of p53.	Resveratrol	0-11	P53	Homo sapiens	170-173
12131363-9	2002	Resveratrol induced serine-15 phosphorylation of p53 was blocked by PD 98059 (Calbiochem), a MAPK kinase inhibitor, implicating MAPK activation in the phosphorylation of p53.	Serine	20-26	P53	Homo sapiens	49-52
12131363-9	2002	Resveratrol induced serine-15 phosphorylation of p53 was blocked by PD 98059 (Calbiochem), a MAPK kinase inhibitor, implicating MAPK activation in the phosphorylation of p53.	Serine	20-26	P53	Homo sapiens	170-173
12716463-2	2002	In MCF-7 breast cancer cell line possessing wild-type p53, ERalpha, and overexpressing MDM2, p53 accumulation was stimulated by 17beta-estradiol (E2) in a concentration-dependent manner.	Estradiol	128-144	P53	Homo sapiens	93-96
12131363-11	2002	These results suggest that apoptosis induction by resveratrol in DU 145 cells requires serine-15 phosphorylation of p53 by MAPK.	Resveratrol	50-61	P53	Homo sapiens	116-119
12131363-11	2002	These results suggest that apoptosis induction by resveratrol in DU 145 cells requires serine-15 phosphorylation of p53 by MAPK.	Serine	87-93	P53	Homo sapiens	116-119
12130688-4	2002	Our recent investigations with electrophilic prostaglandins enabled us to devise a pharmacophore and mechanism of action hypothesis relevant to this problem: a cross-conjugated alpha,beta-unsaturated dienone with two sterically accessible electrophilic beta-carbons is a molecular determinant that confers activity among this class of ubiquitin isopeptidases inhibitors, and that inhibitors of ubiquitin isopeptidases cause cell death in vitro independently of p53.	Prostaglandins	45-59	P53	Homo sapiens	461-464
12131363-12	2002	Inhibition of MAPK dependent serine-15 phosphorylation resulted in reduced p53 binding to a p53 specific oligonucleotide on electrophoretic mobility shift assay.	Serine	29-35	P53	Homo sapiens	75-78
12131363-12	2002	Inhibition of MAPK dependent serine-15 phosphorylation resulted in reduced p53 binding to a p53 specific oligonucleotide on electrophoretic mobility shift assay.	Serine	29-35	P53	Homo sapiens	92-95
12131363-12	2002	Inhibition of MAPK dependent serine-15 phosphorylation resulted in reduced p53 binding to a p53 specific oligonucleotide on electrophoretic mobility shift assay.	Oligonucleotides	105-120	P53	Homo sapiens	75-78
12131363-12	2002	Inhibition of MAPK dependent serine-15 phosphorylation resulted in reduced p53 binding to a p53 specific oligonucleotide on electrophoretic mobility shift assay.	Oligonucleotides	105-120	P53	Homo sapiens	92-95
12131363-13	2002	Pifithrin-alpha (Calbiochem), a p53 inhibitor, blocked resveratrol induced serine-15 phosphorylation of p53 and p53 binding to DNA.	Resveratrol	55-66	P53	Homo sapiens	32-35
12131363-13	2002	Pifithrin-alpha (Calbiochem), a p53 inhibitor, blocked resveratrol induced serine-15 phosphorylation of p53 and p53 binding to DNA.	Resveratrol	55-66	P53	Homo sapiens	104-107
12131363-13	2002	Pifithrin-alpha (Calbiochem), a p53 inhibitor, blocked resveratrol induced serine-15 phosphorylation of p53 and p53 binding to DNA.	Resveratrol	55-66	P53	Homo sapiens	104-107
12131363-13	2002	Pifithrin-alpha (Calbiochem), a p53 inhibitor, blocked resveratrol induced serine-15 phosphorylation of p53 and p53 binding to DNA.	Serine	75-81	P53	Homo sapiens	32-35
12131363-13	2002	Pifithrin-alpha (Calbiochem), a p53 inhibitor, blocked resveratrol induced serine-15 phosphorylation of p53 and p53 binding to DNA.	Serine	75-81	P53	Homo sapiens	104-107
12131363-13	2002	Pifithrin-alpha (Calbiochem), a p53 inhibitor, blocked resveratrol induced serine-15 phosphorylation of p53 and p53 binding to DNA.	Serine	75-81	P53	Homo sapiens	104-107
12131363-14	2002	Resveratrol caused a p53 stimulated increase in p21 messenger RNA.	Resveratrol	0-11	P53	Homo sapiens	21-24
12131363-15	2002	Transfection of additional wild-type p53 into DU 145 cells induced apoptosis, which was further enhanced by resveratrol treatment.	Resveratrol	108-119	P53	Homo sapiens	37-40
12131363-17	2002	This action depends on the activation of MAPK, increase in cellular p53 content, serine-15 phosphorylation of p53 and increased p53 binding to DNA.	Serine	81-87	P53	Homo sapiens	110-113
12131363-17	2002	This action depends on the activation of MAPK, increase in cellular p53 content, serine-15 phosphorylation of p53 and increased p53 binding to DNA.	Serine	81-87	P53	Homo sapiens	110-113
12492119-0	2002	Regulation of p53 stabilization by DNA damage and protein kinase C. We have demonstrated previously that the protein kinase C (PKC) signal transduction pathway acts upstream of caspases to regulate caspase activation and apoptosis induced by the DNA-damaging agent cisplatin (CP).	Cisplatin	265-274	P53	Homo sapiens	14-17
12145335-2	2002	17beta-Estradiol (E2) induced a 2-fold increase in p53 mRNA levels and a 2- to 3-fold increase in p53 protein.	Estradiol	0-16	P53	Homo sapiens	51-54
12145335-2	2002	17beta-Estradiol (E2) induced a 2-fold increase in p53 mRNA levels and a 2- to 3-fold increase in p53 protein.	Estradiol	0-16	P53	Homo sapiens	98-101
12145335-5	2002	Hormonal activation of constructs containing p53 promoter inserts (-106 to -40) and the GAL4-p65 fusion proteins was inhibited by the intracellular Ca2+ ion chelator EGTA-AM and Ca2+/calmodulin-dependent protein kinase (CaMK) inhibitor KN-93.	Egtazic Acid	166-170	P53	Homo sapiens	45-48
12130688-4	2002	Our recent investigations with electrophilic prostaglandins enabled us to devise a pharmacophore and mechanism of action hypothesis relevant to this problem: a cross-conjugated alpha,beta-unsaturated dienone with two sterically accessible electrophilic beta-carbons is a molecular determinant that confers activity among this class of ubiquitin isopeptidases inhibitors, and that inhibitors of ubiquitin isopeptidases cause cell death in vitro independently of p53.	Carbon	258-265	P53	Homo sapiens	461-464
12145335-5	2002	Hormonal activation of constructs containing p53 promoter inserts (-106 to -40) and the GAL4-p65 fusion proteins was inhibited by the intracellular Ca2+ ion chelator EGTA-AM and Ca2+/calmodulin-dependent protein kinase (CaMK) inhibitor KN-93.	KN 93	236-241	P53	Homo sapiens	45-48
12130688-6	2002	Shikoccin (a diterpene), dibenzylideneacetone, and curcumin fit the pharmacophore hypothesis, inhibit cellular isopeptidases, and cause cell death independently of p53 in isogenic pairs of RKO and HCT 116 cells with differential p53 status.	Curcumin	51-59	P53	Homo sapiens	164-167
12130688-6	2002	Shikoccin (a diterpene), dibenzylideneacetone, and curcumin fit the pharmacophore hypothesis, inhibit cellular isopeptidases, and cause cell death independently of p53 in isogenic pairs of RKO and HCT 116 cells with differential p53 status.	Curcumin	51-59	P53	Homo sapiens	229-232
12105992-8	2002	ROS levels in cells with abrogated TP53 function were decreased in magnitude and duration.	Reactive Oxygen Species	0-3	P53	Homo sapiens	35-39
12115545-1	2002	p53 codon 72, which produces variant proteins with an arginine (Arg) or proline (Pro), has been reported to be associated with cancers of the lung, esophagus and cervix.	Arginine	54-62	P53	Homo sapiens	0-3
12115540-2	2002	We found that there was a slight tendency (not statistically significant) for the p53 inactivated cells to be less sensitive to 5-FU after 6 days continuous treatment.	Fluorouracil	128-132	P53	Homo sapiens	82-85
12115545-1	2002	p53 codon 72, which produces variant proteins with an arginine (Arg) or proline (Pro), has been reported to be associated with cancers of the lung, esophagus and cervix.	Arginine	64-67	P53	Homo sapiens	0-3
12115540-3	2002	Simultaneous administration of RPR-115135 and 5-FU, at subtoxic concentrations, resulted in a synergistic enhancement of 5-FU cytotoxicity in the p53 wildtype cells (HCT-116, RKO, DLD-1, Colo-320, LoVo).	Fluorouracil	46-50	P53	Homo sapiens	146-149
12115540-3	2002	Simultaneous administration of RPR-115135 and 5-FU, at subtoxic concentrations, resulted in a synergistic enhancement of 5-FU cytotoxicity in the p53 wildtype cells (HCT-116, RKO, DLD-1, Colo-320, LoVo).	Fluorouracil	121-125	P53	Homo sapiens	146-149
12110584-0	2002	Tyrosine phosphorylation of Mdm2 by c-Abl: implications for p53 regulation.	Tyrosine	0-8	P53	Homo sapiens	60-63
12115540-9	2002	Although RPR-115135 can potentiate the effect of 5-FU in cells in which p53 function is disrupted, these data suggest strongly that RPR-115135 significantly enhances the efficacy of 5-FU only when p53 is functioning.	Fluorouracil	49-53	P53	Homo sapiens	72-75
12115540-9	2002	Although RPR-115135 can potentiate the effect of 5-FU in cells in which p53 function is disrupted, these data suggest strongly that RPR-115135 significantly enhances the efficacy of 5-FU only when p53 is functioning.	Fluorouracil	182-186	P53	Homo sapiens	197-200
12084458-7	2002	Studies thus far involving colorectal tumors obtained from patients have focused predominantly on the predictive value of levels of TS expression and p53 mutations in determining response to 5-FU.	Fluorouracil	191-195	P53	Homo sapiens	150-153
12071847-8	2002	In these cells, UVB triggered a p38-dependent phosphorylation of p53 on Ser-15.	Serine	72-75	P53	Homo sapiens	65-68
12096336-0	2002	Novel gain of function activity of p53 mutants: activation of the dUTPase gene expression leading to resistance to 5-fluorouracil.	Fluorouracil	115-129	P53	Homo sapiens	35-38
12096336-6	2002	Using tetracycline-regulated retroviral vectors for conditional expression of p53 mutants, we found that transcription of the dUTPase gene is increased within 24 h after tetracycline withdrawal, and the cells acquire higher resistance to 5-FU.	Fluorouracil	238-242	P53	Homo sapiens	78-81
12089322-4	2002	A p53-dependent increase in procaspase-6 protein level allows for an increase in caspase-6 activity and caspase-6-specific Lamin A cleavage in response to Adriamycin exposure.	Doxorubicin	155-165	P53	Homo sapiens	2-5
12071847-12	2002	However, UVB induced an SB203580-insensitive phosphorylation on Ser-15 of mutated p53.	Serine	64-67	P53	Homo sapiens	82-85
12150453-3	2002	Taxol treatment resulted in elevated expression of p53 and of p21, which was more pronounced and persistent in cyclin D1 overexpressing cells.	Paclitaxel	0-5	P53	Homo sapiens	51-54
12182321-0	2002	Radiation could induce p53-independent and cell cycle--unrelated apoptosis in 5-fluorouracil radiosensitized head and neck carcinoma cells.	Fluorouracil	78-92	P53	Homo sapiens	23-26
12182322-6	2002	Results indicate that p53 is involved in the response of TK6 cells to fast neutrons and carbon ions, as measured by cell proliferation and occurrence of apoptosis.	Carbon	88-94	P53	Homo sapiens	22-25
12221910-1	2002	A polymorphism at codon 72 in the p53 gen has been reported as a potential risk factor to cervical cancer (CC) because human papillomavirus (HPV) is more effective at degrading p53 Arg-72 than p53 Pro-72, making individuals homozygous for p53 Arg-72 seven times more likely to develop HPV-associated CC.	Arginine	181-184	P53	Homo sapiens	34-37
12432259-2	2002	By causing p53-mediated arrest, pretreatment with low concentrations of doxorubicin (DOX) protected HCT116 cells from the cytotoxicity caused by PTX.	Doxorubicin	72-83	P53	Homo sapiens	11-14
12432259-2	2002	By causing p53-mediated arrest, pretreatment with low concentrations of doxorubicin (DOX) protected HCT116 cells from the cytotoxicity caused by PTX.	Doxorubicin	85-88	P53	Homo sapiens	11-14
12432259-2	2002	By causing p53-mediated arrest, pretreatment with low concentrations of doxorubicin (DOX) protected HCT116 cells from the cytotoxicity caused by PTX.	Paclitaxel	145-148	P53	Homo sapiens	11-14
12105864-1	2002	BACKGROUND &amp; AIMS: The functional abrogation of several tumor suppressor genes, including p16, DPC4, and p53, is a major mechanism underlying pancreatic ductal carcinogenesis.	Adenosine Monophosphate	12-15	P53	Homo sapiens	109-112
12221910-1	2002	A polymorphism at codon 72 in the p53 gen has been reported as a potential risk factor to cervical cancer (CC) because human papillomavirus (HPV) is more effective at degrading p53 Arg-72 than p53 Pro-72, making individuals homozygous for p53 Arg-72 seven times more likely to develop HPV-associated CC.	Arginine	181-184	P53	Homo sapiens	177-180
12221910-1	2002	A polymorphism at codon 72 in the p53 gen has been reported as a potential risk factor to cervical cancer (CC) because human papillomavirus (HPV) is more effective at degrading p53 Arg-72 than p53 Pro-72, making individuals homozygous for p53 Arg-72 seven times more likely to develop HPV-associated CC.	Arginine	181-184	P53	Homo sapiens	177-180
12221910-1	2002	A polymorphism at codon 72 in the p53 gen has been reported as a potential risk factor to cervical cancer (CC) because human papillomavirus (HPV) is more effective at degrading p53 Arg-72 than p53 Pro-72, making individuals homozygous for p53 Arg-72 seven times more likely to develop HPV-associated CC.	Arginine	181-184	P53	Homo sapiens	177-180
12221910-1	2002	A polymorphism at codon 72 in the p53 gen has been reported as a potential risk factor to cervical cancer (CC) because human papillomavirus (HPV) is more effective at degrading p53 Arg-72 than p53 Pro-72, making individuals homozygous for p53 Arg-72 seven times more likely to develop HPV-associated CC.	Arginine	243-246	P53	Homo sapiens	34-37
12221910-1	2002	A polymorphism at codon 72 in the p53 gen has been reported as a potential risk factor to cervical cancer (CC) because human papillomavirus (HPV) is more effective at degrading p53 Arg-72 than p53 Pro-72, making individuals homozygous for p53 Arg-72 seven times more likely to develop HPV-associated CC.	Arginine	243-246	P53	Homo sapiens	177-180
12221910-1	2002	A polymorphism at codon 72 in the p53 gen has been reported as a potential risk factor to cervical cancer (CC) because human papillomavirus (HPV) is more effective at degrading p53 Arg-72 than p53 Pro-72, making individuals homozygous for p53 Arg-72 seven times more likely to develop HPV-associated CC.	Arginine	243-246	P53	Homo sapiens	177-180
12221910-1	2002	A polymorphism at codon 72 in the p53 gen has been reported as a potential risk factor to cervical cancer (CC) because human papillomavirus (HPV) is more effective at degrading p53 Arg-72 than p53 Pro-72, making individuals homozygous for p53 Arg-72 seven times more likely to develop HPV-associated CC.	Arginine	243-246	P53	Homo sapiens	177-180
12221910-6	2002	Among cases with CC the proportions of the p53 genotypes at codon 72 were 0.05 to proline homozygous, 0.5 to heterozygous, and 0.45 to arginine-homozygous.	Arginine	135-143	P53	Homo sapiens	43-46
12221910-9	2002	We conclude than In our population, as other worldwide countries, the homozygous for arginine at codon 72 of the p53 gene is not a risk factor to cervical cancer.	Arginine	85-93	P53	Homo sapiens	113-116
12144687-1	2002	The usefulness of the arginine (Arg) residue at codon 72 of the p53 tumor suppressor gene as a marker for the risk of cervical cancer remains unclear.	Arginine	22-30	P53	Homo sapiens	64-67
12062599-5	2002	The status of p53 was immunohistochemically assessed in paraffin-embedded pretreatment biopsy specimens, along with appropriate controls.	Paraffin	56-64	P53	Homo sapiens	14-17
12144687-1	2002	The usefulness of the arginine (Arg) residue at codon 72 of the p53 tumor suppressor gene as a marker for the risk of cervical cancer remains unclear.	Arginine	32-35	P53	Homo sapiens	64-67
12144687-9	2002	It would appear that, in the absence of HPV 16/18 infections, the Arg allele at codon 72 of the p53 tumor suppressor gene may constitute a risk factor for carcinogenesis of the cervix.	Arginine	66-69	P53	Homo sapiens	96-99
12408761-3	2002	The effect of curcumin on the expression of c-myc, bcl-2, mutant-type p53 and Fas protein and mRNA was studied by flow cytometry (FCM) and reverse transcription-polymerase chain reaction (RT-PCR).	Curcumin	14-22	P53	Homo sapiens	70-73
12065694-2	2002	The goal of these studies was to examine the role of p53, caspase 3, 8, and 9, and mitochondria in the signaling of cisplatin-induced apoptosis.	Cisplatin	116-125	P53	Homo sapiens	53-56
12065694-6	2002	Cisplatin increased nuclear p53 expression 4 h after treatment, preceding both caspase 3 activation and chromatin condensation.	Cisplatin	0-9	P53	Homo sapiens	28-31
12065694-7	2002	Treatment with the p53 inhibitor alpha-2-(2-imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone (PFT) before cisplatin exposure inhibited p53 nuclear expression at 4, 8, and 12 h and inhibited phosphatidylserine externalization and caspase 3 activation at 12 h. Neither DEVD-fmk nor ZVAD-fmk inhibited cisplatin-induced p53 nuclear expression.	Cisplatin	118-127	P53	Homo sapiens	19-22
12065694-7	2002	Treatment with the p53 inhibitor alpha-2-(2-imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone (PFT) before cisplatin exposure inhibited p53 nuclear expression at 4, 8, and 12 h and inhibited phosphatidylserine externalization and caspase 3 activation at 12 h. Neither DEVD-fmk nor ZVAD-fmk inhibited cisplatin-induced p53 nuclear expression.	Cisplatin	311-320	P53	Homo sapiens	19-22
12065694-8	2002	Both DEVD-fmk and ZVAD-fmk completely inhibited caspase 3 activity but, like PFT, partially inhibited cisplatin-induced chromatin condensation, annexin V labeling, and DNA hypoploidy after 24 h. These data demonstrate that at least 50% of cisplatin-induced apoptosis in RPTC is mediated by p53 and that p53 activates caspase 3 independently of either caspase 9 or 8 or mitochondrial dysfunction.	Cisplatin	102-111	P53	Homo sapiens	290-293
12065694-8	2002	Both DEVD-fmk and ZVAD-fmk completely inhibited caspase 3 activity but, like PFT, partially inhibited cisplatin-induced chromatin condensation, annexin V labeling, and DNA hypoploidy after 24 h. These data demonstrate that at least 50% of cisplatin-induced apoptosis in RPTC is mediated by p53 and that p53 activates caspase 3 independently of either caspase 9 or 8 or mitochondrial dysfunction.	Cisplatin	102-111	P53	Homo sapiens	303-306
12385241-0	2002	[Detection of P53 and K-ras gene mutations in lung cancer with oligonucleotide chip].	Oligonucleotides	63-78	P53	Homo sapiens	14-17
12164929-1	2002	Upregulation of p53 protein induces either growth arrest or apoptosis in response to cellular injury This is signaled from a highly conserved p53 domain between codons 64 and 92, where a functional polymorphism results in either a proline (p53-72P) or an arginine (p53-72R) at codon 72.	Arginine	255-263	P53	Homo sapiens	16-19
12164929-1	2002	Upregulation of p53 protein induces either growth arrest or apoptosis in response to cellular injury This is signaled from a highly conserved p53 domain between codons 64 and 92, where a functional polymorphism results in either a proline (p53-72P) or an arginine (p53-72R) at codon 72.	Arginine	255-263	P53	Homo sapiens	142-145
12164929-1	2002	Upregulation of p53 protein induces either growth arrest or apoptosis in response to cellular injury This is signaled from a highly conserved p53 domain between codons 64 and 92, where a functional polymorphism results in either a proline (p53-72P) or an arginine (p53-72R) at codon 72.	Arginine	255-263	P53	Homo sapiens	142-145
12164929-1	2002	Upregulation of p53 protein induces either growth arrest or apoptosis in response to cellular injury This is signaled from a highly conserved p53 domain between codons 64 and 92, where a functional polymorphism results in either a proline (p53-72P) or an arginine (p53-72R) at codon 72.	Arginine	255-263	P53	Homo sapiens	142-145
12065694-9	2002	Furthermore, 50% of cisplatin-induced RPTC apoptosis is independent of p53 and caspases 3, 8, and 9.	Cisplatin	20-29	P53	Homo sapiens	71-74
12167105-7	2002	Paraffin immunohistochemical analysis was carried out using anti-p53 and anti-Ki-67 antibodies on the initial tumor tissues.	Paraffin	0-8	P53	Homo sapiens	65-68
12408761-8	2002	The expression of c-myc, bcl-2, mutant-type p53 protein and mRNA was decreased sharply in CA46 cells treated with curcumin, while Fas protein and mRNA was increased.	Curcumin	114-122	P53	Homo sapiens	44-47
12408761-9	2002	CONCLUSION: Curcumin is able to inhibit the proliferation of CA46 cells and induce the cell apoptosis by down-regulating the expression of c-myc, bcl-2, mutant-type p53 and up-regulating the expression of Fas.	Curcumin	12-20	P53	Homo sapiens	165-168
12067251-0	2002	Reactive oxygen species generated by PAH o-quinones cause change-in-function mutations in p53.	Reactive Oxygen Species	0-23	P53	Homo sapiens	90-93
12049655-0	2002	Doxorubicin and octreotide induce a 40 kDa breakdown product of p53 in human hepatoma and tumoral colon cell lines.	Doxorubicin	0-11	P53	Homo sapiens	64-67
12049655-1	2002	The chemotherapeutic drug doxorubicin and the anti-proliferative long-acting somatostatin analogue octreotide, both used in cancer treatment, have been shown to increase the expression of the p53 tumour suppressor protein.	Doxorubicin	26-37	P53	Homo sapiens	192-195
12049655-10	2002	These results also suggest that octreotide, a molecule with different signalling pathways, was able as doxorubicin to generate a p53 breakdown product.	Doxorubicin	103-114	P53	Homo sapiens	129-132
11927575-4	2002	Moreover, phosphorylation of p53 Ser-15 induced by C-1027 was independent of ATM, ATR, or DNA-PK function.	Serine	33-36	P53	Homo sapiens	29-32
11927575-4	2002	Moreover, phosphorylation of p53 Ser-15 induced by C-1027 was independent of ATM, ATR, or DNA-PK function.	Carbon	51-52	P53	Homo sapiens	29-32
12093475-0	2002	JM216-, JM118-, and cisplatin-induced cytotoxicity in relation to platinum-DNA adduct formation, glutathione levels and p53 status in human tumour cell lines with different sensitivities to cisplatin.	Cisplatin	20-29	P53	Homo sapiens	120-123
12093475-1	2002	The aim of this study is to establish anti-tumour potency of the new oral platinum drug JM216 and its metabolite JM118 in relation to the platinum (Pt)-DNA adduct formation, glutathione (GSH)-levels, and p53 status in human cancer cell lines with different sensitivities to cisplatin (CDDP).	Platinum	74-82	P53	Homo sapiens	204-207
12082016-8	2002	Tp53 was also strongly induced by an N-oxide of quinoline and by dabequine, an experimental antimalarial evaluated in humans; dabequine was reported to be negative in other screens of mutagenicity and clastogenicity but carcinogenic in animal studies.	quinoline	48-57	P53	Homo sapiens	0-4
12036943-4	2002	To test this hypothesis, the effect of exogenous mutant p53 protein expression on genomic instability in human p53-/- Saos-2 cells was measured by the frequency of formation of N-(phosphoacetyl)-L-aspartate (PALA)-resistant (PALA(R)) colonies, mediated by gene amplification.	Nitrogen	177-178	P53	Homo sapiens	56-59
12067251-5	2002	We employed a yeast reporter system to determine whether PAH o-quinones or the ROS they generate cause change-in-function mutations in p53.	Reactive Oxygen Species	79-82	P53	Homo sapiens	135-138
12067251-8	2002	Treatment of p53 cDNA with micromolar concentrations of (+/-)-anti-7,8-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydro-benzo[a]pyrene, (anti-BPDE, an ultimate carcinogen) or sub-micromolar concentrations of BP-7,8-dione in the presence of redox-cycling conditions (NADPH and CuCl(2)) also caused p53 mutations in a dose-dependent manner.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	144-148	P53	Homo sapiens	13-16
12067251-10	2002	p53 mutagenesis by BP-7,8-dione was attenuated by ROS scavengers and completely abrogated by a combination of superoxide dismutase and catalase, indicating that both superoxide anion and hydroxyl radicals were the responsible mutagens.	Reactive Oxygen Species	50-53	P53	Homo sapiens	0-3
12082025-2	2002	Here we show that the treatment of cells with low doses of gamma-irradiation or cisplatin resulted in an immediate enhancement of p53-dependent DNA repair, measured by base excision repair (BER) activity.	Cisplatin	80-89	P53	Homo sapiens	130-133
12067251-10	2002	p53 mutagenesis by BP-7,8-dione was attenuated by ROS scavengers and completely abrogated by a combination of superoxide dismutase and catalase, indicating that both superoxide anion and hydroxyl radicals were the responsible mutagens.	Superoxides	166-182	P53	Homo sapiens	0-3
12067251-14	2002	Together these data suggest that PAH o-quinones generate an endogenous mutagen (ROS) which leads to p53 inactivation.	Reactive Oxygen Species	80-83	P53	Homo sapiens	100-103
12124178-5	2002	Compared to WT fibroblasts, IKK1/2(-/-) fibroblasts showed increased cell death and p53 induction in response to the chemotherapeutic agent, doxorubicin.	Doxorubicin	141-152	P53	Homo sapiens	84-87
12124178-6	2002	Reconstitution of IKK2, but not IKK1, increased Mdm2 levels and decreased doxorubicin-induced p53 stabilization and cell death.	Doxorubicin	74-85	P53	Homo sapiens	94-97
12011992-10	2002	The KOSCC-11 cell line contained a frameshift mutation and the other cell lines harbored an identical p53 mutation at codon 175 from CGC (Arg) to CTC (Leu).	Arginine	138-141	P53	Homo sapiens	102-105
12045262-9	2002	CD2-activated LPTs displayed a striking upregulation of p53, whose blockade by antisense oligonucleotides accelerated their S phase transit time to that of CD3-activated PBTs.	Oligonucleotides	89-105	P53	Homo sapiens	56-59
12024039-7	2002	BRCA1 also conferred diminished cell death in a p53-dependent manner in response to adriamycin compared to that conferred by controls.	Doxorubicin	84-94	P53	Homo sapiens	48-51
12060398-10	2002	Our results suggest that TP53 arginine/arginine genotype could represent a potential risk factor for the development of squamous cell carcinoma in renal transplant recipients compared to immunocompetent patients.	Arginine	30-38	P53	Homo sapiens	25-29
12060398-10	2002	Our results suggest that TP53 arginine/arginine genotype could represent a potential risk factor for the development of squamous cell carcinoma in renal transplant recipients compared to immunocompetent patients.	Arginine	39-47	P53	Homo sapiens	25-29
12065679-8	2002	Furthermore, treatment with PD98059 significantly decreased the level of p21 protein, a p53-dependent gene product.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	28-35	P53	Homo sapiens	88-91
12088801-6	2002	Our data also indicate that p53 is required for the folate depletion-induced apoptosis.	Folic Acid	52-58	P53	Homo sapiens	28-31
12065679-7	2002	In these studies using mitogen-activated protein kinase inhibitors, infection-induced increases in the p53 level were partially blocked by PD98059, a synthetic inhibitor of MEK1 that is the immediate upstream kinase of extracellular signal-regulated kinases 1/2 (ERK1/2), but not by SB202190, a potent p38 kinase inhibitor.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	139-146	P53	Homo sapiens	103-106
12065773-3	2002	Overexpression of p53 protein has been detected in eight CCSKs in one study, and in two in another, yet no molecular correlation with p53 gene mutations has been carried out.	ccsks	57-62	P53	Homo sapiens	18-21
12034820-0	2002	Redox state of tumor suppressor p53 regulates its sequence-specific DNA binding in DNA-damaged cells by cysteine 277.	Cysteine	104-112	P53	Homo sapiens	32-35
12048682-0	2002	[Effects of wild-type p53 gene on the chemotherapy sensitivity of ovarian cancer SKOV-3 cells to cisplatin].	Cisplatin	97-106	P53	Homo sapiens	22-25
12076704-3	2002	Mutational screening of the coding region of TP53 revealed an A>T transversion in codon 144 of exon 5 (CAG>CTG, Gln>Leu) in the germline of one of the three affected members, with loss of heterozygosity (LOH) in the tumour tissue.	GUANOSINE 5'-TRIPHOSPHATE P3-[1-(2-NITROPHENYL)ETHYL ESTER]	103-106	P53	Homo sapiens	45-49
12048682-1	2002	OBJECTIVE: To assess the effect of wild-type p53 gene on the chemotherapy sensitivity of ovarian cancer SKOV-3 cells to cisplatin.	Cisplatin	120-129	P53	Homo sapiens	45-48
12048682-9	2002	CONCLUSION: The exogenous introduction of wild-type p53 cDNA into ovarian cancer SKOV-3 cells increased the chemotherapy sensitivity to cisplatin.	Cisplatin	136-145	P53	Homo sapiens	52-55
12032289-4	2002	An oligonucleotide microarray analysis demonstrated that, in addition to the heat shock-responsive and redox-responsive genes, the p53-responsive genes, such as gadd45, cyclin G1, and cathepsin D, were significantly up-regulated in the cells treated with 15d-PGJ(2).	Oligonucleotides	3-18	P53	Homo sapiens	131-134
11888672-1	2002	p53 codon 72 Arg homozygosity has been associated with increased risk of developing cervical cancer.	Arginine	13-16	P53	Homo sapiens	0-3
11888672-6	2002	The distribution of p53 alleles in bladder cancer patients and in controls was statistically significant (P&lt;0.002; odds ratio, 2.67; 95% confidence interval, 1.38-5.20), and homozygosity for arginine at residue 72 was associated with an increased risk for bladder cancer (P&lt;0.00002; odds ratio, 4.69; 95% confidence interval, 2.13-10.41).	Arginine	194-202	P53	Homo sapiens	20-23
11888672-9	2002	Our results provide evidence that this p53 polymorphism is implicated in bladder carcinogenesis and that individuals harboring the Arg/Arg genotype have an increased risk of developing bladder cancer.	Arginine	131-134	P53	Homo sapiens	39-42
11888672-9	2002	Our results provide evidence that this p53 polymorphism is implicated in bladder carcinogenesis and that individuals harboring the Arg/Arg genotype have an increased risk of developing bladder cancer.	Arginine	135-138	P53	Homo sapiens	39-42
12032289-5	2002	Indeed, the 15d-PGJ(2) induced accumulation and phosphorylation of p53, which was accompanied by a preferential redistribution of the p53 protein in the nuclei of the cells and by a time-dependent increase in p53 DNA binding activity, suggesting that p53 accumulated in response to the treatment with 15d-PGJ(2) was functional.	15-deoxyprostaglandin J2	12-22	P53	Homo sapiens	67-70
12032289-5	2002	Indeed, the 15d-PGJ(2) induced accumulation and phosphorylation of p53, which was accompanied by a preferential redistribution of the p53 protein in the nuclei of the cells and by a time-dependent increase in p53 DNA binding activity, suggesting that p53 accumulated in response to the treatment with 15d-PGJ(2) was functional.	15-deoxyprostaglandin J2	12-22	P53	Homo sapiens	134-137
12032289-5	2002	Indeed, the 15d-PGJ(2) induced accumulation and phosphorylation of p53, which was accompanied by a preferential redistribution of the p53 protein in the nuclei of the cells and by a time-dependent increase in p53 DNA binding activity, suggesting that p53 accumulated in response to the treatment with 15d-PGJ(2) was functional.	15-deoxyprostaglandin J2	12-22	P53	Homo sapiens	134-137
12032289-5	2002	Indeed, the 15d-PGJ(2) induced accumulation and phosphorylation of p53, which was accompanied by a preferential redistribution of the p53 protein in the nuclei of the cells and by a time-dependent increase in p53 DNA binding activity, suggesting that p53 accumulated in response to the treatment with 15d-PGJ(2) was functional.	15-deoxyprostaglandin J2	12-22	P53	Homo sapiens	134-137
12032289-5	2002	Indeed, the 15d-PGJ(2) induced accumulation and phosphorylation of p53, which was accompanied by a preferential redistribution of the p53 protein in the nuclei of the cells and by a time-dependent increase in p53 DNA binding activity, suggesting that p53 accumulated in response to the treatment with 15d-PGJ(2) was functional.	15-deoxyprostaglandin J2	301-311	P53	Homo sapiens	67-70
12032289-6	2002	The 15d-PGJ(2)-induced accumulation of p53 resulted in the activation of a death-inducing caspase cascade mediated by Fas and the Fas ligand.	15-deoxyprostaglandin J2	4-14	P53	Homo sapiens	39-42
11877452-7	2002	KChAP increases p53 levels and stimulates phosphorylation of p53 residue serine 15.	Serine	73-79	P53	Homo sapiens	61-64
12032848-4	2002	Here we show that, in response to a non apoptotic DNA damage induced by low doses of doxorubicin, p53 binds in vivo, as detected by a p53-specific chromatin immunoprecipitation assay, and activates the P2-p73 promoter.	Doxorubicin	85-96	P53	Homo sapiens	98-101
12032848-4	2002	Here we show that, in response to a non apoptotic DNA damage induced by low doses of doxorubicin, p53 binds in vivo, as detected by a p53-specific chromatin immunoprecipitation assay, and activates the P2-p73 promoter.	Doxorubicin	85-96	P53	Homo sapiens	134-137
12019159-8	2002	Indicator variables were created to evaluate the risk for individuals with the following DVs: GSTP1 GG + GSTM1-null and GSTP1 GG + p53 Arg/Pro or Pro/Pro.	Arginine	135-138	P53	Homo sapiens	131-134
12019170-10	2002	Modeling of p53 interaction with DNA suggests that R283H mutation may weaken the sequence-specific interaction of p53 lysine 120 with the BAX gene but not the CDKN1A p53-responsive elements.	Lysine	118-124	P53	Homo sapiens	12-15
12019170-10	2002	Modeling of p53 interaction with DNA suggests that R283H mutation may weaken the sequence-specific interaction of p53 lysine 120 with the BAX gene but not the CDKN1A p53-responsive elements.	Lysine	118-124	P53	Homo sapiens	114-117
12082529-5	2002	Steady state levels of p53 increased in irradiated cells, and the increase was accompanied by phosphorylation of serine 9 and serine 15, but not serine 6 residues.	Serine	113-119	P53	Homo sapiens	23-26
12019170-10	2002	Modeling of p53 interaction with DNA suggests that R283H mutation may weaken the sequence-specific interaction of p53 lysine 120 with the BAX gene but not the CDKN1A p53-responsive elements.	Lysine	118-124	P53	Homo sapiens	114-117
12011430-1	2002	A G to T mutation has been observed at the third position of codon 249 of the p53 tumor-suppressor gene in over 50% of the hepatocellular carcinoma cases associated with high exposure to aflatoxin B(1) (AFB(1)).	afb	203-206	P53	Homo sapiens	78-81
12082540-3	2002	Our results demonstrate that expression of wt p53 but not mutant p53 significantly reduced tyrosine phosphorylation of Stat3 and inhibited Stat3 DNA binding activity in both DU145 and Tsu prostate cancer cell lines that express constitutively active Stat3.	Tyrosine	91-99	P53	Homo sapiens	46-49
12082529-5	2002	Steady state levels of p53 increased in irradiated cells, and the increase was accompanied by phosphorylation of serine 9 and serine 15, but not serine 6 residues.	Serine	126-132	P53	Homo sapiens	23-26
12082529-5	2002	Steady state levels of p53 increased in irradiated cells, and the increase was accompanied by phosphorylation of serine 9 and serine 15, but not serine 6 residues.	Serine	126-132	P53	Homo sapiens	23-26
12006509-2	2002	The purpose of this study was to examine p53 mutations in leukemias after ovarian cancer, for which treatment with platinum analogues was widely used.	Platinum	115-123	P53	Homo sapiens	41-44
11947902-0	2002	Nitric oxide prevents oxidised LDL-induced p53 accumulation, cytochrome c translocation, and apoptosis in macrophages via guanylate cyclase stimulation.	Nitric Oxide	0-12	P53	Homo sapiens	43-46
11947902-10	2002	Stabilisation of p53 was prevented by preincubation with the NO-donor GSNO or 8-br-cGMP, thus implying a downmodulatory effect of cGMP on pathways that upregulate the tumor suppressor p53.	S-Nitrosoglutathione	70-74	P53	Homo sapiens	17-20
11947902-10	2002	Stabilisation of p53 was prevented by preincubation with the NO-donor GSNO or 8-br-cGMP, thus implying a downmodulatory effect of cGMP on pathways that upregulate the tumor suppressor p53.	S-Nitrosoglutathione	70-74	P53	Homo sapiens	184-187
11947902-10	2002	Stabilisation of p53 was prevented by preincubation with the NO-donor GSNO or 8-br-cGMP, thus implying a downmodulatory effect of cGMP on pathways that upregulate the tumor suppressor p53.	Cyclic GMP	83-87	P53	Homo sapiens	17-20
11973611-6	2002	This assumption was further supported by the following observations: (i) the p53 DNA-binding activity to its consensus sequence was not stimulated following TNF alpha treatment, (ii) phosphorylation at Ser-15, -20 or -392 was not detected in response to TNF alpha, (iii) the transcription rate of Ddb2, another p53 target gene, was not stimulated by TNF alpha.	Serine	202-205	P53	Homo sapiens	77-80
12006519-0	2002	A Phase I/pilot study of sequential doxorubicin/vinorelbine: effects on p53 and microtubule-associated protein 4.	Doxorubicin	36-47	P53	Homo sapiens	72-75
12006519-7	2002	RESULTS: After doxorubicin treatment, p53 increased in 12 of 14 PBMNC and 4 of 10 tumor samples.	Doxorubicin	15-26	P53	Homo sapiens	38-41
12168882-5	2002	The amino acid residue at this position is either arginine (p53-Arg) or proline (p53-Pro).	Arginine	50-58	P53	Homo sapiens	60-63
12168882-5	2002	The amino acid residue at this position is either arginine (p53-Arg) or proline (p53-Pro).	Arginine	64-67	P53	Homo sapiens	60-63
11980662-0	2002	The role of thymidylate synthase induction in modulating p53-regulated gene expression in response to 5-fluorouracil and antifolates.	Fluorouracil	102-116	P53	Homo sapiens	57-60
11980662-6	2002	Inactivation of p53 significantly increased resistance to 5-FU and the antifolates with IC-50(72 h) doses for 5-FU and TDX of &gt;100 and &gt;10 microM, respectively, in the M7TS90-E6 cell line.	Fluorouracil	58-62	P53	Homo sapiens	16-19
11980662-6	2002	Inactivation of p53 significantly increased resistance to 5-FU and the antifolates with IC-50(72 h) doses for 5-FU and TDX of &gt;100 and &gt;10 microM, respectively, in the M7TS90-E6 cell line.	Fluorouracil	110-114	P53	Homo sapiens	16-19
11980662-7	2002	Furthermore, p53 inactivation completely abrogated the cell cycle arrest and apoptosis induced by 5-FU.	Fluorouracil	98-102	P53	Homo sapiens	13-16
12006537-1	2002	PURPOSE: It is known that a common p53 polymorphism, encodingeither proline (Pro) or arginine (Arg) at residue 72, produces marked change in the structure of p53.	Arginine	85-93	P53	Homo sapiens	35-38
12006537-1	2002	PURPOSE: It is known that a common p53 polymorphism, encodingeither proline (Pro) or arginine (Arg) at residue 72, produces marked change in the structure of p53.	Arginine	85-93	P53	Homo sapiens	158-161
12006537-1	2002	PURPOSE: It is known that a common p53 polymorphism, encodingeither proline (Pro) or arginine (Arg) at residue 72, produces marked change in the structure of p53.	Arginine	95-98	P53	Homo sapiens	35-38
12006537-1	2002	PURPOSE: It is known that a common p53 polymorphism, encodingeither proline (Pro) or arginine (Arg) at residue 72, produces marked change in the structure of p53.	Arginine	95-98	P53	Homo sapiens	158-161
12006537-7	2002	RESULTS: There was a bias to mutate and express the Arg allele in the p53 -mutated TCCs arising in individuals with heterozygosity (Pro/Arg).	Arginine	52-55	P53	Homo sapiens	70-73
12006537-7	2002	RESULTS: There was a bias to mutate and express the Arg allele in the p53 -mutated TCCs arising in individuals with heterozygosity (Pro/Arg).	Arginine	136-139	P53	Homo sapiens	70-73
12081208-0	2002	Frequent phosphorylation at serine 392 in overexpressed p53 protein due to missense mutation in carcinoma of the urinary tract.	Serine	28-34	P53	Homo sapiens	56-59
11980715-3	2002	Here we show that p21 increased intracellular levels of ROS both in normal fibroblasts and in p53-negative cancer cells.	Reactive Oxygen Species	56-59	P53	Homo sapiens	94-97
11956312-7	2002	We conclude that expression of anti-chromodomain intracellular antibodies is sufficient to trigger a p53-independent apoptotic pathway that is only partly dependent on the known Z-VAD-inhibitable caspases, suggesting that CD function is essential for cell survival.	Cadmium	222-224	P53	Homo sapiens	101-104
11981003-3	2002	Other proposed determinants of clinical taxane sensitivity/resistance include p53, members of the epidermal growth factor receptor (EGFR) superfamily (e.g., HER2, EGFR), and estrogen receptors and progesterone receptors.	taxane	40-46	P53	Homo sapiens	78-81
11943391-5	2002	In contrast to free doxorubicin, which is a strong inducer of p53 expression, increased p53 expression was never observed after the treatment with the polymeric drug.	Doxorubicin	20-31	P53	Homo sapiens	62-65
12133503-13	2002	Apoptosis is not a consequence of the proceeding mitosis arrest and is induced p53-dependently by HMBA.	hmba	98-102	P53	Homo sapiens	79-82
12007018-10	2002	Cisplatin-induced p21 transactivation assays and G(1) cell cycle arrest analyses showed that p21 transactivation and G(1) arrest occurred in both CCSK and CMN cultures, demonstrating integrity of the p53 signal transduction pathway.	Cisplatin	0-9	P53	Homo sapiens	200-203
12062426-2	2002	In the present study, we investigated the activity of P53(gly(281)) in P53-null PC3 human prostate cancer cells and found that the P53(gly(281)) induced apoptosis as efficiently as the wild-type P53 (wtP53).	Glycine	58-61	P53	Homo sapiens	71-74
12062426-1	2002	A common mutation in P53 protein occurs at amino acid residue 281 in the DNA binding domain (P53(gly(281))), which results in loss of transcriptional regulation of P53 target genes and has been reported to gain pro-oncogenic functions.	Glycine	97-100	P53	Homo sapiens	21-24
12062426-1	2002	A common mutation in P53 protein occurs at amino acid residue 281 in the DNA binding domain (P53(gly(281))), which results in loss of transcriptional regulation of P53 target genes and has been reported to gain pro-oncogenic functions.	Glycine	97-100	P53	Homo sapiens	93-96
12062426-2	2002	In the present study, we investigated the activity of P53(gly(281)) in P53-null PC3 human prostate cancer cells and found that the P53(gly(281)) induced apoptosis as efficiently as the wild-type P53 (wtP53).	Glycine	135-138	P53	Homo sapiens	54-57
12062426-1	2002	A common mutation in P53 protein occurs at amino acid residue 281 in the DNA binding domain (P53(gly(281))), which results in loss of transcriptional regulation of P53 target genes and has been reported to gain pro-oncogenic functions.	Glycine	97-100	P53	Homo sapiens	93-96
12062426-2	2002	In the present study, we investigated the activity of P53(gly(281)) in P53-null PC3 human prostate cancer cells and found that the P53(gly(281)) induced apoptosis as efficiently as the wild-type P53 (wtP53).	Glycine	58-61	P53	Homo sapiens	54-57
12062426-2	2002	In the present study, we investigated the activity of P53(gly(281)) in P53-null PC3 human prostate cancer cells and found that the P53(gly(281)) induced apoptosis as efficiently as the wild-type P53 (wtP53).	Glycine	135-138	P53	Homo sapiens	71-74
12062426-2	2002	In the present study, we investigated the activity of P53(gly(281)) in P53-null PC3 human prostate cancer cells and found that the P53(gly(281)) induced apoptosis as efficiently as the wild-type P53 (wtP53).	Glycine	58-61	P53	Homo sapiens	71-74
12062426-2	2002	In the present study, we investigated the activity of P53(gly(281)) in P53-null PC3 human prostate cancer cells and found that the P53(gly(281)) induced apoptosis as efficiently as the wild-type P53 (wtP53).	Glycine	58-61	P53	Homo sapiens	71-74
12062426-2	2002	In the present study, we investigated the activity of P53(gly(281)) in P53-null PC3 human prostate cancer cells and found that the P53(gly(281)) induced apoptosis as efficiently as the wild-type P53 (wtP53).	Glycine	135-138	P53	Homo sapiens	71-74
12062426-2	2002	In the present study, we investigated the activity of P53(gly(281)) in P53-null PC3 human prostate cancer cells and found that the P53(gly(281)) induced apoptosis as efficiently as the wild-type P53 (wtP53).	Glycine	135-138	P53	Homo sapiens	71-74
21320405-6	2002	Expression of p53, p21 was up-regulated obviously but CDKN2 was down-regulated markedly by Tanshinone IIA.	tanshinone	91-105	P53	Homo sapiens	14-17
21320405-7	2002	CONCLUSIONS: Tanshinone IIA can inhibit cell growth and clone formation in human lung cancer cell line (SPC-A-1) and its possible molecular mechanism may be inhibiting DNA synthesis by up-regulating p53, p21 and down-regulating CDKN2.	tanshinone	13-27	P53	Homo sapiens	199-202
11971195-0	2002	Multiple lysine mutations in the C-terminus of p53 make it resistant to degradation mediated by MDM2 but not by human papillomavirus E6 and induce growth inhibition in MDM2-overexpressing cells.	Lysine	9-15	P53	Homo sapiens	47-50
11875057-2	2002	In response to ionizing radiation (IR), ATM, the gene product mutated in ataxia telangiectasia, stabilizes and activates p53 through phosphorylation of Ser(15) and (indirectly) Ser(20).	Serine	152-155	P53	Homo sapiens	121-124
11875057-2	2002	In response to ionizing radiation (IR), ATM, the gene product mutated in ataxia telangiectasia, stabilizes and activates p53 through phosphorylation of Ser(15) and (indirectly) Ser(20).	Serine	177-180	P53	Homo sapiens	121-124
11875057-3	2002	Here we show that phosphorylation of p53 on Ser(46), a residue important for p53 apoptotic activity, as well as on Ser(9), in response to IR also is dependent on the ATM protein kinase.	Serine	44-47	P53	Homo sapiens	37-40
11875057-3	2002	Here we show that phosphorylation of p53 on Ser(46), a residue important for p53 apoptotic activity, as well as on Ser(9), in response to IR also is dependent on the ATM protein kinase.	Serine	44-47	P53	Homo sapiens	77-80
11875057-3	2002	Here we show that phosphorylation of p53 on Ser(46), a residue important for p53 apoptotic activity, as well as on Ser(9), in response to IR also is dependent on the ATM protein kinase.	Serine	115-118	P53	Homo sapiens	37-40
11875057-5	2002	p53 C-terminal acetylation at Lys(320) and Lys(382), which may stabilize p53 and activate sequence-specific DNA binding, required Ser(15) phosphorylation by ATM and was enhanced by phosphorylation at nearby residues including Ser(6), Ser(9), and Thr(18).	Lysine	30-33	P53	Homo sapiens	0-3
11875057-5	2002	p53 C-terminal acetylation at Lys(320) and Lys(382), which may stabilize p53 and activate sequence-specific DNA binding, required Ser(15) phosphorylation by ATM and was enhanced by phosphorylation at nearby residues including Ser(6), Ser(9), and Thr(18).	Lysine	30-33	P53	Homo sapiens	73-76
11971195-2	2002	In the present study, we showed that when lysine residues 372, 373, 381, and 382 of p53 were substituted with alanine, the resulting A4 protein was resistant to MDM2-mediated proteosomal degradation but was highly sensitive to human papillomavirus E6-mediated proteolysis.	Alanine	110-117	P53	Homo sapiens	84-87
11937560-4	2002	Anti-TGF-beta Ab also attenuated morphine-induced p53 as well as inducible NO synthase expression; in contrast, N(G)-nitro-L-arginine methyl ester, an inhibitor of NO synthase, inhibited morphine-induced P38 MAPK phosphorylation and Bax expression.	Morphine	33-41	P53	Homo sapiens	50-53
11937560-7	2002	In addition, macrophages either deficient in FasL or lacking p53 showed resistance to the effect of morphine.	Morphine	100-108	P53	Homo sapiens	61-64
11937560-11	2002	Both TGF-beta and inducible NO synthase play an important role in morphine-induced downstream signaling, which seems to activate proteins involved in both extrinsic (Fas and FasL) and intrinsic (p53 and Bax) cell death pathways.	Morphine	66-74	P53	Homo sapiens	195-198
11875057-5	2002	p53 C-terminal acetylation at Lys(320) and Lys(382), which may stabilize p53 and activate sequence-specific DNA binding, required Ser(15) phosphorylation by ATM and was enhanced by phosphorylation at nearby residues including Ser(6), Ser(9), and Thr(18).	Lysine	43-46	P53	Homo sapiens	0-3
11875057-5	2002	p53 C-terminal acetylation at Lys(320) and Lys(382), which may stabilize p53 and activate sequence-specific DNA binding, required Ser(15) phosphorylation by ATM and was enhanced by phosphorylation at nearby residues including Ser(6), Ser(9), and Thr(18).	Lysine	43-46	P53	Homo sapiens	73-76
11875057-5	2002	p53 C-terminal acetylation at Lys(320) and Lys(382), which may stabilize p53 and activate sequence-specific DNA binding, required Ser(15) phosphorylation by ATM and was enhanced by phosphorylation at nearby residues including Ser(6), Ser(9), and Thr(18).	Serine	130-133	P53	Homo sapiens	0-3
11875057-5	2002	p53 C-terminal acetylation at Lys(320) and Lys(382), which may stabilize p53 and activate sequence-specific DNA binding, required Ser(15) phosphorylation by ATM and was enhanced by phosphorylation at nearby residues including Ser(6), Ser(9), and Thr(18).	Serine	130-133	P53	Homo sapiens	73-76
11875057-5	2002	p53 C-terminal acetylation at Lys(320) and Lys(382), which may stabilize p53 and activate sequence-specific DNA binding, required Ser(15) phosphorylation by ATM and was enhanced by phosphorylation at nearby residues including Ser(6), Ser(9), and Thr(18).	Serine	226-229	P53	Homo sapiens	0-3
11875057-5	2002	p53 C-terminal acetylation at Lys(320) and Lys(382), which may stabilize p53 and activate sequence-specific DNA binding, required Ser(15) phosphorylation by ATM and was enhanced by phosphorylation at nearby residues including Ser(6), Ser(9), and Thr(18).	Serine	226-229	P53	Homo sapiens	73-76
11875057-5	2002	p53 C-terminal acetylation at Lys(320) and Lys(382), which may stabilize p53 and activate sequence-specific DNA binding, required Ser(15) phosphorylation by ATM and was enhanced by phosphorylation at nearby residues including Ser(6), Ser(9), and Thr(18).	Serine	226-229	P53	Homo sapiens	0-3
11875057-5	2002	p53 C-terminal acetylation at Lys(320) and Lys(382), which may stabilize p53 and activate sequence-specific DNA binding, required Ser(15) phosphorylation by ATM and was enhanced by phosphorylation at nearby residues including Ser(6), Ser(9), and Thr(18).	Serine	226-229	P53	Homo sapiens	73-76
11875057-5	2002	p53 C-terminal acetylation at Lys(320) and Lys(382), which may stabilize p53 and activate sequence-specific DNA binding, required Ser(15) phosphorylation by ATM and was enhanced by phosphorylation at nearby residues including Ser(6), Ser(9), and Thr(18).	Threonine	246-249	P53	Homo sapiens	0-3
11875057-5	2002	p53 C-terminal acetylation at Lys(320) and Lys(382), which may stabilize p53 and activate sequence-specific DNA binding, required Ser(15) phosphorylation by ATM and was enhanced by phosphorylation at nearby residues including Ser(6), Ser(9), and Thr(18).	Threonine	246-249	P53	Homo sapiens	73-76
11875057-6	2002	These observations, together with the proposed role of Ser(46) phosphorylation in mediating apoptosis, suggest that ATM is involved in the initiation of p53-dependent apoptosis after IR in human lymphoblastoid cells.	Serine	55-58	P53	Homo sapiens	153-156
11971195-1	2002	We have recently shown that lysine mutations in p53"s putative C-terminal acetylation sites result in increased stability and cytoplasmic distribution of the p53 protein in a human lung cancer cell line.	Lysine	28-34	P53	Homo sapiens	48-51
11971195-1	2002	We have recently shown that lysine mutations in p53"s putative C-terminal acetylation sites result in increased stability and cytoplasmic distribution of the p53 protein in a human lung cancer cell line.	Lysine	28-34	P53	Homo sapiens	158-161
11971195-2	2002	In the present study, we showed that when lysine residues 372, 373, 381, and 382 of p53 were substituted with alanine, the resulting A4 protein was resistant to MDM2-mediated proteosomal degradation but was highly sensitive to human papillomavirus E6-mediated proteolysis.	Lysine	42-48	P53	Homo sapiens	84-87
11914633-10	2002	Examination of the microdissected paraffin-embedded tissues revealed p53 mutations in the malignant epithelioid areas in AML but not in the renal parenchyma or typical AML areas.	Paraffin	34-42	P53	Homo sapiens	69-72
12058967-5	2002	Ultraviolet light, cisplatin, and nitrogen mustards produce damage that is repaired by a p53-regulated pathway.	Cisplatin	19-28	P53	Homo sapiens	89-92
12058967-5	2002	Ultraviolet light, cisplatin, and nitrogen mustards produce damage that is repaired by a p53-regulated pathway.	Nitrogen	34-42	P53	Homo sapiens	89-92
12575207-1	2002	OBJECTIVE: A polymorphism at codon 72 of the human tumor-suppressor gene, p53, results in translation to either arginine or proline.	Arginine	112-120	P53	Homo sapiens	74-77
12575207-8	2002	CONCLUSION: In this population, individuals homozygous for the arginine variant of codon 72 of the p53 gene were at increased risk of cervical cancer.	Arginine	63-71	P53	Homo sapiens	99-102
12149568-0	2002	Anti-tumor efficacy of a novel antisense anti-MDM2 mixed-backbone oligonucleotide in human colon cancer models: p53-dependent and p53-independent mechanisms.	Oligonucleotides	66-81	P53	Homo sapiens	112-115
11894120-5	2002	In LS174T cells, the antisense oligonucleotide, but not the mismatch oligonucleotide, specifically inhibited MDM2 expression, resulting in a significant increase in irinotecan-associated p53 activation and p21 induction.	Oligonucleotides	31-46	P53	Homo sapiens	187-190
11894120-5	2002	In LS174T cells, the antisense oligonucleotide, but not the mismatch oligonucleotide, specifically inhibited MDM2 expression, resulting in a significant increase in irinotecan-associated p53 activation and p21 induction.	Irinotecan	165-175	P53	Homo sapiens	187-190
11894120-6	2002	In DLD-1 cells, the antisense oligonucleotide specifically inhibited MDM2 expression, resulting in a significant increase in irinotecan-associated p21 induction although mutant p53 levels remained unchanged.	Oligonucleotides	30-45	P53	Homo sapiens	177-180
11920608-0	2002	Resistance of colon cancer cells to long-term 5-fluorouracil exposure is correlated to the relative level of Bcl-2 and Bcl-X(L) in addition to Bax and p53 status.	Fluorouracil	46-60	P53	Homo sapiens	151-154
11920608-5	2002	In p53(+/+) cell lines but not in p53(-/0) cell lines, a low level of the pro-apoptotic Bax protein was correlated with a greater resistance of cells to 5-FU.	Fluorouracil	153-157	P53	Homo sapiens	3-6
11920608-6	2002	In addition, we found that high levels of anti-apoptotic Bcl-2 and Bcl-x(L) proteins combined with a low level of Bax were correlated to high 5-FU resistance of wild-type p53 cell lines.	Fluorouracil	142-146	P53	Homo sapiens	171-174
12149568-0	2002	Anti-tumor efficacy of a novel antisense anti-MDM2 mixed-backbone oligonucleotide in human colon cancer models: p53-dependent and p53-independent mechanisms.	Oligonucleotides	66-81	P53	Homo sapiens	130-133
11917017-8	2002	The predicted DNA binding affinity and specificity of both mutant p53-CDs were also in accord with experimental data.	Cadmium	70-73	P53	Homo sapiens	66-69
12149568-4	2002	MATERIALS AND METHODS: The selected antisense mixed-backbone oligonucleotide was evaluated for its in vitro and in vivo antitumor activity in human colon cancer models: LS174T cell line containing wild-type p53 and DLD-1 cell line containing mutant p53.	Oligonucleotides	61-76	P53	Homo sapiens	207-210
11917017-9	2002	The non-detectable DNA binding of the 273H p53-CD is due mainly to the disruption of a hydrogen-bonding network involving R273, D281 and R280, leading to a loss of major groove binding by R280 and K120.	Hydrogen	87-95	P53	Homo sapiens	43-46
12149568-4	2002	MATERIALS AND METHODS: The selected antisense mixed-backbone oligonucleotide was evaluated for its in vitro and in vivo antitumor activity in human colon cancer models: LS174T cell line containing wild-type p53 and DLD-1 cell line containing mutant p53.	Oligonucleotides	61-76	P53	Homo sapiens	249-252
11779855-0	2002	Doxorubicin induces apoptosis and CD95 gene expression in human primary endothelial cells through a p53-dependent mechanism.	Doxorubicin	0-11	P53	Homo sapiens	100-103
11927338-3	2002	METHODS: The expression of p53, mdm2, and bcl-2 protein was studied by immunohistochemical methods in paraffin-embedded nephrectomy specimens from 112 patients whose clinicopathologic data confirmed renal cell carcinoma.	Paraffin	102-110	P53	Homo sapiens	27-30
11779855-2	2002	Here we show that doxorubicin (Dox), a drug used in antitumor therapy, triggered a marked accumulation of p53 and induced CD95 gene expression and apoptosis in proliferating human umbilical vein endothelial cells (HUVECs).	Doxorubicin	31-34	P53	Homo sapiens	106-109
11779855-2	2002	Here we show that doxorubicin (Dox), a drug used in antitumor therapy, triggered a marked accumulation of p53 and induced CD95 gene expression and apoptosis in proliferating human umbilical vein endothelial cells (HUVECs).	Doxorubicin	18-29	P53	Homo sapiens	106-109
11779855-3	2002	Transfection and site-directed mutagenesis experiments using the CD95 promoter fused to an intronic enhancer indicated the requirement for a p53 site for Dox-induced promoter activation.	Doxorubicin	154-157	P53	Homo sapiens	141-144
11779855-4	2002	Furthermore, the p53 inhibitor pifithrin-alpha (PFT-alpha) blocked both promoter inducibility and protein up-regulation of CD95 in response to Dox.	Doxorubicin	143-146	P53	Homo sapiens	17-20
11960374-5	2002	Inhibition of p53 expression with p53 antisense oligonucleotides inhibits apoptosis and prevents the increase in Bax and decrease in Bcl-2.	Oligonucleotides	48-64	P53	Homo sapiens	14-17
11779855-7	2002	The analysis of apoptosis in the presence of PFT-alpha and benzyloxycarbonyl-Val-Ala-dl-Asp-fluoromethylketone revealed that both p53 and caspase activation are required for Dox-mediated apoptosis of HUVECs.	benzyloxycarbonyl-Val-Ala-DL-Asp-fluoromethylketone	59-110	P53	Homo sapiens	130-133
11779855-7	2002	The analysis of apoptosis in the presence of PFT-alpha and benzyloxycarbonyl-Val-Ala-dl-Asp-fluoromethylketone revealed that both p53 and caspase activation are required for Dox-mediated apoptosis of HUVECs.	Doxorubicin	174-177	P53	Homo sapiens	130-133
11779855-9	2002	These results highlight the role of p53 in the response of primary endothelial cells to genotoxic drugs and may reveal a novel mechanism underlying the antitumoral properties of Dox, related to its ability to induce apoptosis in proliferating endothelial cells.	Doxorubicin	178-181	P53	Homo sapiens	36-39
11948395-6	2002	CP-31398 also decreased sequence-specific DNA binding of wild-type p53 and His-273 mutant p53.	Histidine	75-78	P53	Homo sapiens	90-93
11960383-1	2002	Mutation of four lysine residues in the p53 C-terminal domain inhibits MDM2-dependent ubiquitination of p53 and alters its subcellular distribution.	Lysine	17-23	P53	Homo sapiens	40-43
11960383-1	2002	Mutation of four lysine residues in the p53 C-terminal domain inhibits MDM2-dependent ubiquitination of p53 and alters its subcellular distribution.	Lysine	17-23	P53	Homo sapiens	104-107
11960383-3	2002	In this study, we demonstrated that p53 with lysine residues 372, 373, 381, and 382 mutated to alanine (the A4 mutant) retained the transactivation activity of wild-type p53, although the transactivation activity of p21 promoter by the A4 mutant was slightly reduced.	Lysine	45-51	P53	Homo sapiens	36-39
11960383-3	2002	In this study, we demonstrated that p53 with lysine residues 372, 373, 381, and 382 mutated to alanine (the A4 mutant) retained the transactivation activity of wild-type p53, although the transactivation activity of p21 promoter by the A4 mutant was slightly reduced.	Lysine	45-51	P53	Homo sapiens	170-173
11960383-3	2002	In this study, we demonstrated that p53 with lysine residues 372, 373, 381, and 382 mutated to alanine (the A4 mutant) retained the transactivation activity of wild-type p53, although the transactivation activity of p21 promoter by the A4 mutant was slightly reduced.	Alanine	95-102	P53	Homo sapiens	36-39
11960383-3	2002	In this study, we demonstrated that p53 with lysine residues 372, 373, 381, and 382 mutated to alanine (the A4 mutant) retained the transactivation activity of wild-type p53, although the transactivation activity of p21 promoter by the A4 mutant was slightly reduced.	Alanine	95-102	P53	Homo sapiens	170-173
11960374-5	2002	Inhibition of p53 expression with p53 antisense oligonucleotides inhibits apoptosis and prevents the increase in Bax and decrease in Bcl-2.	Oligonucleotides	48-64	P53	Homo sapiens	34-37
11960374-6	2002	Furthermore, pretreatment with p53 antisense oligonucleotides markedly inhibits the induction of caspase activity.	Oligonucleotides	45-61	P53	Homo sapiens	31-34
11890931-1	2002	p53 is an important player in the cellular response to genotoxic stress whose functions are regulated by phosphorylation of a number of serine and threonine residues.	Serine	136-142	P53	Homo sapiens	0-3
11890931-1	2002	p53 is an important player in the cellular response to genotoxic stress whose functions are regulated by phosphorylation of a number of serine and threonine residues.	Threonine	147-156	P53	Homo sapiens	0-3
11867759-8	2002	Heterozygous mutant thymocytes had a severe defect in p53-dependent apoptotic pathways after treatment with gamma irradiation or doxorubicin, whereas p53-independent apoptotic pathways were intact.	Doxorubicin	129-140	P53	Homo sapiens	54-57
11879190-3	2002	Incubation of control and Hsp70-transfected macrophages with S-nitrosoglutathione induced accumulation of the tumour suppressor p53, expression of p21(WAF1/CIP1) (where WAF1 corresponds to wild-type p53-activated fragment 1 and CIP1 corresponds to cyclin-dependent kinase-interacting protein 1) and G(1) cell-cycle arrest.	S-Nitrosoglutathione	61-81	P53	Homo sapiens	128-131
11879190-3	2002	Incubation of control and Hsp70-transfected macrophages with S-nitrosoglutathione induced accumulation of the tumour suppressor p53, expression of p21(WAF1/CIP1) (where WAF1 corresponds to wild-type p53-activated fragment 1 and CIP1 corresponds to cyclin-dependent kinase-interacting protein 1) and G(1) cell-cycle arrest.	S-Nitrosoglutathione	61-81	P53	Homo sapiens	199-202
11912124-1	2002	The cornerstone of the systemic treatment of advanced colorectal cancer is 5-fluorouracil.However, 5-fluorouracil-induced apoptosis is dependent on p53, a tumor suppressor gene that is lost or inactivated in at least 85% of human colorectal cancers.	Fluorouracil	99-113	P53	Homo sapiens	148-151
12014658-2	2002	This study was undertaken to evaluate the impact of wild-type or mutant p53 status on the synergistic effects of 5-Fluorouracil (5-FU) and radiation (XRT) in pancreatic tumors.	Fluorouracil	113-127	P53	Homo sapiens	72-75
12168940-0	2002	Correlation of clinical outcome with p53 and p21 status in patients with advanced transitional-cell carcinoma treated with paclitaxel and carboplatin.	Paclitaxel	123-133	P53	Homo sapiens	37-40
12451999-2	2002	METHODS: Seventy-nine patients with cervical cancer and 23 with cases of normal cervical epithelium in geriatric people were investigated immunohistochemically for expression of p53 and c-erbB2 in paraffin sections.	Paraffin	197-205	P53	Homo sapiens	178-181
12168940-1	2002	BACKGROUND: The purpose of the present study was to correlate the nuclear expression of p53 and p21 with response to paclitaxel and carboplatin, progression-free survival (PFS) as well as overall survival (OS), in patients with urothelial metastatic transitional-cell carcinoma (TCC).	Paclitaxel	117-127	P53	Homo sapiens	88-91
12014658-10	2002	Clonogenic assays showed enhanced radiosensitizing effect when 5-Fluorouracil was added to cell lines lacking functional p53.	Fluorouracil	63-77	P53	Homo sapiens	121-124
11895857-0	2002	Resveratrol enhances the expression of non-steroidal anti-inflammatory drug-activated gene (NAG-1) by increasing the expression of p53.	Resveratrol	0-11	P53	Homo sapiens	131-134
11911839-0	2002	p53-Independent induction of Fas and apoptosis in leukemic cells by an adenosine derivative, Cl-IB-MECA.	Adenosine	71-80	P53	Homo sapiens	0-3
11888884-5	2002	Inhibition of CABC1 expression by transfection with antisense oligonucleotide significantly reduced the apoptotic response induced by wild-type p53.	Oligonucleotides	62-77	P53	Homo sapiens	144-147
11883897-1	2002	The vaccinia-related kinase 1 (VRK1) protein is a nuclear Ser-Thr kinase that phosphorylates p53 in Thr18.	UNII-PYZ33YLR8A	100-105	P53	Homo sapiens	93-96
11895857-5	2002	Resveratrol increases the expression of p53, tumor suppressor protein, prior to NAG-1 induction, indicating that NAG-1 expression by resveratrol is mediated by p53 expression.	Resveratrol	0-11	P53	Homo sapiens	40-43
11895857-5	2002	Resveratrol increases the expression of p53, tumor suppressor protein, prior to NAG-1 induction, indicating that NAG-1 expression by resveratrol is mediated by p53 expression.	Resveratrol	133-144	P53	Homo sapiens	160-163
11895857-6	2002	We also show that the p53 binding sites within the promoter region of NAG-1 play a pivotal role to control NAG-1 expression by resveratrol.	Resveratrol	127-138	P53	Homo sapiens	22-25
11895857-7	2002	Derivatives of resveratrol were examined for NAG-1 induction, and the data suggest that resveratrol-induced NAG-1 and p53 induction is not dependent on its anti-oxidant activity.	Resveratrol	88-99	P53	Homo sapiens	118-121
11854596-7	2002	In addition, a new p53 mutation not previously reported in ET/pPNET involving exon 5 codon 138: GCC to GAC (Ala/Asp) was detected.	Alanine	108-111	P53	Homo sapiens	19-22
12170778-2	2002	We find that the Xeroderma Pigmentosum Complementation group E (XPE) mutated Damaged-DNA binding protein p48 (DDB2) is upregulated by BRCA1 in a p53-dependent manner following UVC, Adriamycin, or Cisplatin exposure.	Doxorubicin	181-191	P53	Homo sapiens	145-148
12170778-2	2002	We find that the Xeroderma Pigmentosum Complementation group E (XPE) mutated Damaged-DNA binding protein p48 (DDB2) is upregulated by BRCA1 in a p53-dependent manner following UVC, Adriamycin, or Cisplatin exposure.	Cisplatin	196-205	P53	Homo sapiens	145-148
11889192-0	2002	Resveratrol induces apoptosis in thyroid cancer cell lines via a MAPK- and p53-dependent mechanism.	Resveratrol	0-11	P53	Homo sapiens	75-78
12390773-4	2002	RESULT: NADH not only inhibited the apoptosis induced by UVB irradiation, but also up-regulated the expression of Bcl-2 protein and down-regulated expressions of p53 and Bax proteins (P&lt;0.01).	NAD	8-12	P53	Homo sapiens	162-165
12390773-6	2002	CONCLUSION: NADH significantly inhibits apoptosis induced by UVB irradiation possibly by the mechanism of up-regulating Bcl-2 expression and down-regulating p53 and Bax expressions.	NAD	12-16	P53	Homo sapiens	157-160
11914922-2	2002	This study describes the induction of ELCS in p53 mutated Burkitt"s lymphoma cell lines after treatment with irradiation or the microtubule inhibitor, SK&amp;F 96365.	Adenosine Monophosphate	154-157	P53	Homo sapiens	46-49
11856771-3	2002	During a survey of risk factors for renal and cardiovascular disease in one such community, an association between a common polymorphism at codon 72 (Arg/Pro) of the p53 gene and markers of renal disease was sought.	Arginine	150-153	P53	Homo sapiens	166-169
11857392-7	2002	TP53 mutations, mainly transversions, were more frequently found in heavy smokers (p = 0.03), with the same tendency after chronic alcohol consumption.	Alcohols	131-138	P53	Homo sapiens	0-4
11857452-13	2002	Heat shock causes phosphorylation of p53 at Serine-15, but there is no correlation between phosphorylation at this site and activation of the protein.	Serine	44-50	P53	Homo sapiens	37-40
11935300-6	2002	RESULTS: Ex vivo chemosensitivity testing showed that tumors with p53 mutations were significantly more resistant to the cyclophosphamide/etoposide/epirubicin regimen than with normal p53 gene ( P = 0.012).	Epirubicin	148-158	P53	Homo sapiens	66-69
11889192-4	2002	Addition of pifithrin-alpha, a specific inhibitor of p53, or transfection of p53 antisense oligonucleotides caused decreased RV-induced p53 and p21 expression in PTC and FTC cells.	Oligonucleotides	91-107	P53	Homo sapiens	77-80
11889192-4	2002	Addition of pifithrin-alpha, a specific inhibitor of p53, or transfection of p53 antisense oligonucleotides caused decreased RV-induced p53 and p21 expression in PTC and FTC cells.	Oligonucleotides	91-107	P53	Homo sapiens	77-80
11865061-1	2002	Previous studies have demonstrated that phosphorylation of human p53 on serine 15 contributes to protein stabilization after DNA damage and that this is mediated by the ATM family of kinases.	Serine	72-78	P53	Homo sapiens	65-68
12071473-7	2002	The expression of p53 and p21WAF1 proteins significantly increased after 24 or 48 hr of incubation with either melatonin or D3.	Melatonin	111-120	P53	Homo sapiens	18-21
12071473-9	2002	These data support the hypothesis that melatonin reduces MCF-7 cell proliferation by modulating cell-cycle length through the control of the p53-p21 pathway, but without clearly inducing apoptosis.	Melatonin	39-48	P53	Homo sapiens	141-144
11870884-0	2002	Restoration of wild-type conformation and activity of a temperature-sensitive mutant of p53 (p53(V272M)) by the cytoprotective aminothiol WR1065 in the esophageal cancer cell line TE-1.	Aminothiol	127-137	P53	Homo sapiens	88-91
11865061-2	2002	However, cellular exposure to hypoxia does not induce any detectable level of DNA lesions compared to ionizing radiation, and the oxygen dependency of p53 protein accumulation differs from that of HIF-1, the hypoxia-inducible transcription factor.	Oxygen	130-136	P53	Homo sapiens	151-154
11870884-0	2002	Restoration of wild-type conformation and activity of a temperature-sensitive mutant of p53 (p53(V272M)) by the cytoprotective aminothiol WR1065 in the esophageal cancer cell line TE-1.	Aminothiol	127-137	P53	Homo sapiens	93-96
11865061-4	2002	Inhibition of ATR kinase activity substantially reduces hypoxia-induced phosphorylation of p53 protein on serine 15 as well as p53 protein accumulation.	Serine	106-112	P53	Homo sapiens	91-94
11870884-4	2002	This cell line contains a mutation in codon 272 of p53 (p53(V272M), with methionine instead of a valine), conferring temperature-sensitive properties to the p53 protein.	Methionine	73-83	P53	Homo sapiens	51-54
11870884-4	2002	This cell line contains a mutation in codon 272 of p53 (p53(V272M), with methionine instead of a valine), conferring temperature-sensitive properties to the p53 protein.	Methionine	73-83	P53	Homo sapiens	56-59
21315017-0	2002	[Effects of p53 antisense RNA on malignant phenotype and sensitivity to cisplatin of human lung cancer cell line].	Cisplatin	72-81	P53	Homo sapiens	12-15
11870884-4	2002	This cell line contains a mutation in codon 272 of p53 (p53(V272M), with methionine instead of a valine), conferring temperature-sensitive properties to the p53 protein.	Methionine	73-83	P53	Homo sapiens	56-59
11896587-0	2002	Role of MAP kinases in UVB-induced phosphorylation of p53 at serine 20.	Serine	61-67	P53	Homo sapiens	54-57
11896587-2	2002	Serine 20 phosphorylation of p53 has been shown to be required for the activation of p53 following UV radiation, but the signaling pathway mediating UV-induced phosphorylation is unknown.	Serine	0-6	P53	Homo sapiens	29-32
11896587-2	2002	Serine 20 phosphorylation of p53 has been shown to be required for the activation of p53 following UV radiation, but the signaling pathway mediating UV-induced phosphorylation is unknown.	Serine	0-6	P53	Homo sapiens	85-88
11896587-3	2002	Here, we determined the role of MAP kinases in UVB-induced phosphorylation and found that JNKs are directly involved in the phosphorylation of p53 at serine 20.	Serine	150-156	P53	Homo sapiens	143-146
11896587-4	2002	In a mouse JB6 epidermal cell line, dominant negative JNK1 abrogated UVB-induced phosphorylation of p53 at serine 20, whereas dominant negative p38 kinase or its inhibitor, SB202190, partially attenuated the phosphorylation.	Serine	107-113	P53	Homo sapiens	100-103
11880544-3	2002	Moreover, p53 also participates in base excision repair of hydrogen peroxide-induced damage, still at an early stage of investigation.	Hydrogen Peroxide	59-76	P53	Homo sapiens	10-13
11896587-6	2002	Importantly, UVB-activated or active recombinant JNK1/2, or the p38 kinase downstream target, MAPKAPK-2, but not ERKs or p38 kinase, phosphorylated p53 at serine 20 in vitro.	Serine	155-161	P53	Homo sapiens	148-151
11896587-7	2002	Furthermore, phosphorylation of p53 at serine 20 by UVB-activated JNKs and UVB-induced p53-dependent transcriptional activity were suppressed in Jnk1 or Jnk2 knockout (Jnk1(-/-) or Jnk2(-/-)) cells.	Serine	39-45	P53	Homo sapiens	32-35
11896587-9	2002	These findings strongly suggest that JNKs are the major direct signaling mediators of UVB-induced p53 phosphorylation at serine 20.	Serine	121-127	P53	Homo sapiens	98-101
11991255-3	2002	In Hep3B cells, apoptosis induced by cisplatin was p53-independent, and was associated with up-regulation of cell cycle regulators, pro-apoptotic genes, growth receptors, and genes involved in signal transduction.	Cisplatin	37-46	P53	Homo sapiens	51-54
21315017-1	2002	BACKGROUND: To study the effects of extraneous p53 antisense RNA on malignant growth and sensitivity to cisplatin of human lung cancer cell line.	Cisplatin	104-113	P53	Homo sapiens	47-50
21315017-13	2002	The sensitivity of PEGFP-p53(AS)-801D cells to cisplatin was increased.	Cisplatin	47-56	P53	Homo sapiens	25-28
21315017-15	2002	CONCLUSIONS: p53 mutation at 248 code plays an important role on malignant growth and resistance to cisplatin of human lung cancer cell line 801D.	Cisplatin	100-109	P53	Homo sapiens	13-16
21315017-16	2002	Malignant growth of cells with p53 deletion and mutation at 248 codon can be inhibited by extraneous p53 antisense RNA, and simultaneously the sensitivity to cisplatin is also increased.	Cisplatin	158-167	P53	Homo sapiens	31-34
11850850-5	2002	On the other hand upon serum stimulation, when Akt becomes active and enhances cell survival, phosphorylation occurs at an Akt consensus site (serine 166) within the Mdm2 protein, a key regulator of p53 function.	Serine	143-149	P53	Homo sapiens	199-202
11822871-5	2002	Moreover, expression of functional p53 protein using a temperature-sensitive human p53val(138) induced ceramide generation by activation of neutral SMase but not acid SMase through ROS formation.	Reactive Oxygen Species	181-184	P53	Homo sapiens	35-38
11861384-13	2002	These results suggest that phosphorylation of p53 at serine 15 and serine 20 is critical for apoptosis induction in p53 gene therapy for gliomas.	Serine	53-59	P53	Homo sapiens	46-49
11861384-13	2002	These results suggest that phosphorylation of p53 at serine 15 and serine 20 is critical for apoptosis induction in p53 gene therapy for gliomas.	Serine	53-59	P53	Homo sapiens	116-119
11861384-13	2002	These results suggest that phosphorylation of p53 at serine 15 and serine 20 is critical for apoptosis induction in p53 gene therapy for gliomas.	Serine	67-73	P53	Homo sapiens	116-119
11861384-5	2002	Because phosphorylation of p53 at serines 15, 20, and 392 may play a role in regulating p53-mediated apoptotic activity, we determined the phosphorylation status of exogenous p53 in mutant and wild-type gliomas after Ad-p53 transfer.	Serine	34-41	P53	Homo sapiens	27-30
11861384-10	2002	When wild-type p53 glioma cells were exposed to radiation after Ad-p53 infection, phospho-Ser15-p53 and phospho-Ser20-p53 were detected at high levels, and the cells subsequently underwent apoptosis; no change in serine 392 was detected.	Serine	213-219	P53	Homo sapiens	15-18
11861384-11	2002	The induction of apoptosis and the expression of phospho-Ser15 and phospho-Ser20 in these cells were also enhanced by the combination of Ad-p53 and other DNA-damaging agents such as cisplatin and bichloroethyl nitrosourea.	Cisplatin	182-191	P53	Homo sapiens	140-143
11852106-0	2002	Curcumin induces apoptosis in human breast cancer cells through p53-dependent Bax induction.	Curcumin	0-8	P53	Homo sapiens	64-67
11852106-2	2002	From quantitative image analysis data showing an increase in the percentage of cells with a sub-G0/G1 DNA content, we demonstrated curcumin-induced apoptosis in the breast cancer cell line MCF-7, in which expression of wild-type p53 could be induced.	Curcumin	131-139	P53	Homo sapiens	229-232
11852106-4	2002	Further experiments using p53-null MDAH041 cell as well as low and high p53-expressing TR9-7 cell, in which p53 expression is under tight control of tetracycline, established that curcumin induced apoptosis in tumor cells via a p53-dependent pathway in which Bax is the downstream effector of p53.	Curcumin	180-188	P53	Homo sapiens	26-29
11852106-4	2002	Further experiments using p53-null MDAH041 cell as well as low and high p53-expressing TR9-7 cell, in which p53 expression is under tight control of tetracycline, established that curcumin induced apoptosis in tumor cells via a p53-dependent pathway in which Bax is the downstream effector of p53.	Curcumin	180-188	P53	Homo sapiens	72-75
11852106-4	2002	Further experiments using p53-null MDAH041 cell as well as low and high p53-expressing TR9-7 cell, in which p53 expression is under tight control of tetracycline, established that curcumin induced apoptosis in tumor cells via a p53-dependent pathway in which Bax is the downstream effector of p53.	Curcumin	180-188	P53	Homo sapiens	72-75
11852106-4	2002	Further experiments using p53-null MDAH041 cell as well as low and high p53-expressing TR9-7 cell, in which p53 expression is under tight control of tetracycline, established that curcumin induced apoptosis in tumor cells via a p53-dependent pathway in which Bax is the downstream effector of p53.	Curcumin	180-188	P53	Homo sapiens	72-75
11852106-4	2002	Further experiments using p53-null MDAH041 cell as well as low and high p53-expressing TR9-7 cell, in which p53 expression is under tight control of tetracycline, established that curcumin induced apoptosis in tumor cells via a p53-dependent pathway in which Bax is the downstream effector of p53.	Curcumin	180-188	P53	Homo sapiens	72-75
11805282-0	2002	Functional p53 chimeras containing the Epstein-Barr virus Gly-Ala repeat are protected from Mdm2- and HPV-E6-induced proteolysis.	Glycine	58-61	P53	Homo sapiens	11-14
11711532-3	2002	ATR has been shown to phosphorylate p53 at Ser(15), and this damage-induced phosphorylation is diminished by expression of a catalytically inactive (ATR-kd) mutant.	Serine	43-46	P53	Homo sapiens	36-39
11711532-6	2002	Indeed, ATR-kd expression sensitized these cells to DNA damage and caused a transient decrease in damage-induced serine 15 phosphorylation of p53.	Serine	113-119	P53	Homo sapiens	142-145
11807792-3	2002	A common polymorphism of p53, encoding either proline (Pro) or arginine (Arg) at position 72, affects the susceptibility of p53 to E6 mediated degradation in vivo.	Arginine	63-71	P53	Homo sapiens	25-28
11807792-3	2002	A common polymorphism of p53, encoding either proline (Pro) or arginine (Arg) at position 72, affects the susceptibility of p53 to E6 mediated degradation in vivo.	Arginine	63-71	P53	Homo sapiens	124-127
11807792-3	2002	A common polymorphism of p53, encoding either proline (Pro) or arginine (Arg) at position 72, affects the susceptibility of p53 to E6 mediated degradation in vivo.	Arginine	73-76	P53	Homo sapiens	25-28
11807792-3	2002	A common polymorphism of p53, encoding either proline (Pro) or arginine (Arg) at position 72, affects the susceptibility of p53 to E6 mediated degradation in vivo.	Arginine	73-76	P53	Homo sapiens	124-127
11807792-8	2002	Our results also indicate that the p53 codon 72 genotype frequencies in Indian Oral Cancer patients are 0.55 (Arg) and 0.45 (Pro) as per Hardy-Weinberg equilibrium.	Arginine	110-113	P53	Homo sapiens	35-38
11805282-0	2002	Functional p53 chimeras containing the Epstein-Barr virus Gly-Ala repeat are protected from Mdm2- and HPV-E6-induced proteolysis.	Alanine	62-65	P53	Homo sapiens	11-14
11885700-3	2002	We showed that VCA induced apoptosis in both SK-Hep-1 (p53-positive) and Hep 3B (p53-negative) cells through p53- and p21-independent pathways.	cis-vaccenic acid	15-18	P53	Homo sapiens	55-58
11866879-11	2002	CONCLUSION: Heparin and ADM appear to interact in a synergistic manner, which may be related to the over-expression of p53 and p21 mRNA and the elevated ratio of Bax/Bcl-2 mRNA.	Heparin	12-19	P53	Homo sapiens	119-122
11866879-11	2002	CONCLUSION: Heparin and ADM appear to interact in a synergistic manner, which may be related to the over-expression of p53 and p21 mRNA and the elevated ratio of Bax/Bcl-2 mRNA.	Doxorubicin	24-27	P53	Homo sapiens	119-122
11885700-3	2002	We showed that VCA induced apoptosis in both SK-Hep-1 (p53-positive) and Hep 3B (p53-negative) cells through p53- and p21-independent pathways.	cis-vaccenic acid	15-18	P53	Homo sapiens	81-84
11885700-3	2002	We showed that VCA induced apoptosis in both SK-Hep-1 (p53-positive) and Hep 3B (p53-negative) cells through p53- and p21-independent pathways.	cis-vaccenic acid	15-18	P53	Homo sapiens	81-84
11841447-7	2002	We found that the expression of the cell cycle checkpoint protein Chk1 was reduced in the etoposide-treated p53-transfected cells by 24 h, and this correlated with a reduction in the extent of etoposide-induced phosphorylation of CDK1 at tyrosine 15 (Y15).	Tyrosine	238-246	P53	Homo sapiens	108-111
11841447-5	2002	p53-transfected and control cells were treated with etoposide and trapped at mitosis with nocodazole.	Nocodazole	90-100	P53	Homo sapiens	0-3
11862428-5	2002	Functionality of the p53 pathway was evaluated by incubating cells with carboplatin or doxorubicin and monitoring the effects on the levels of the p53, p21(WAF1/CIP1), and MDM 2 proteins by Western blot analyses.	Doxorubicin	87-98	P53	Homo sapiens	21-24
11830533-6	2002	Equitoxic doses of AN-238, AN-201, or DOX affected p53, p21, and PCNA differently.	Doxorubicin	38-41	P53	Homo sapiens	51-54
11830533-7	2002	Analysis of the p21:p53 ratios revealed that DOX increased p53 levels, but most of p53 was mutated and inactive, whereas AN-238 produced smaller changes in p53 concentrations but enhanced its activity.	Doxorubicin	45-48	P53	Homo sapiens	59-62
11830533-7	2002	Analysis of the p21:p53 ratios revealed that DOX increased p53 levels, but most of p53 was mutated and inactive, whereas AN-238 produced smaller changes in p53 concentrations but enhanced its activity.	Doxorubicin	45-48	P53	Homo sapiens	59-62
11830533-7	2002	Analysis of the p21:p53 ratios revealed that DOX increased p53 levels, but most of p53 was mutated and inactive, whereas AN-238 produced smaller changes in p53 concentrations but enhanced its activity.	Doxorubicin	45-48	P53	Homo sapiens	59-62
12002339-2	2002	p53 immunohistochemical expression was determined in archival paraffin embedded tissue blocks of 30 breast sarcoma patients, (19 fibrosarcomas, nine malignant fibrohistiocytomas and two liposarcomas) treated at the Hospital do Cancer AC Camargo, Sao Paulo, Brazil from 1955 to 1990.	Paraffin	62-70	P53	Homo sapiens	0-3
11864911-1	2002	We have investigated the mechanism of S-phase arrest elicited by the carcinogen benzo(a)pyrene dihydrodiol epoxide (BPDE) in p53-deficient cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	116-120	P53	Homo sapiens	125-128
11802206-0	2002	P53 overexpression predicts poor chemosensitivity to high-dose 5-fluorouracil plus leucovorin chemotherapy for stage IV colorectal cancers after palliative bowel resection.	Fluorouracil	63-77	P53	Homo sapiens	0-3
11812076-10	2002	The present in vitro study showed that wild-type p53 gene transduction significantly enhanced sensitivity to CDDP and the apoptotic index in HRA cells.	Cisplatin	109-113	P53	Homo sapiens	49-52
11809417-0	2002	p53 dependent apoptosis in glioma cell lines in response to hydrogen peroxide induced oxidative stress.	Hydrogen Peroxide	60-77	P53	Homo sapiens	0-3
11809417-3	2002	The role of p53 in ROS induced cell death has not been consistent and has been shown to be cell type dependent.	Reactive Oxygen Species	19-22	P53	Homo sapiens	12-15
11809417-8	2002	H(2)O(2) induced cell death was significantly reduced by antisense p53 oligonucleotide.	Oligonucleotides	71-86	P53	Homo sapiens	67-70
11809417-10	2002	The U373MG cell line, having mutated p53, was comparatively resistant to H(2)O(2) induced cell death.	Hydrogen Peroxide	73-81	P53	Homo sapiens	37-40
11836677-4	2002	Subjects homozygous for the p53 Pro allele had a more than 2-fold increased risk of developing ESCC (OR=2.18; 95%CI=1.10-4.35, adjusted for age, sex, and smoking), whereas the Arg/Pro genotype was not associated with elevated risk of the cancer (adjusted OR=0.84; 95%CI=0.42-1.68).	Arginine	176-179	P53	Homo sapiens	28-31
11850804-2	2002	We have previously shown that estradiol (E(2)) treatment of T47D cells causes an increase in the level of p53 and a concomitant phosphorylation of retinoblastoma protein (pRb).	Estradiol	30-39	P53	Homo sapiens	106-109
11798189-0	2002	p53 inhibits adriamycin-induced down-regulation of cyclin D1 expression in human cancer cells.	Doxorubicin	13-23	P53	Homo sapiens	0-3
11798189-4	2002	Here we show that infection with an adenovirus vector expressing the wild-type p53 gene (Ad-p53) caused an increase in cyclin D1 protein levels in human colorectal cancer cell lines DLD-1 and SW620; treatment with the anti-cancer drug adriamycin, however, down-regulated their cyclin D1 protein expression in a dose-dependent manner.	Doxorubicin	235-245	P53	Homo sapiens	79-82
11798189-4	2002	Here we show that infection with an adenovirus vector expressing the wild-type p53 gene (Ad-p53) caused an increase in cyclin D1 protein levels in human colorectal cancer cell lines DLD-1 and SW620; treatment with the anti-cancer drug adriamycin, however, down-regulated their cyclin D1 protein expression in a dose-dependent manner.	Doxorubicin	235-245	P53	Homo sapiens	92-95
11798189-5	2002	The suppression of cyclin D1 expression following adriamycin treatment could be blocked by simultaneous Ad-p53 infection.	Doxorubicin	50-60	P53	Homo sapiens	107-110
11706017-6	2002	MC also activated p38 mitogen-activated protein kinase (MAPK) at 16-24 h. Accumulation of p53 and p53 phosphorylated at serine 15 was not changed by SB203580, a specific inhibitor of p38 MAPK or overexpression of a dominant negative mutant of p38 MAPK at 8 h after MC treatment, whereas the accumulation was suppressed at 24 h. These results suggest that MC induces accumulation and phosphorylation of p53 via a p38 MAPK-independent (early) and p38 MAPK-dependent (late) pathway.	Serine	120-126	P53	Homo sapiens	98-101
11707453-2	2002	Following DNA damage or cellular stress, p53 is phosphorylated within the Mdm2 binding domain on threonine 18 and serine 20.	Threonine	97-106	P53	Homo sapiens	41-44
11706017-6	2002	MC also activated p38 mitogen-activated protein kinase (MAPK) at 16-24 h. Accumulation of p53 and p53 phosphorylated at serine 15 was not changed by SB203580, a specific inhibitor of p38 MAPK or overexpression of a dominant negative mutant of p38 MAPK at 8 h after MC treatment, whereas the accumulation was suppressed at 24 h. These results suggest that MC induces accumulation and phosphorylation of p53 via a p38 MAPK-independent (early) and p38 MAPK-dependent (late) pathway.	Serine	120-126	P53	Homo sapiens	98-101
11707453-2	2002	Following DNA damage or cellular stress, p53 is phosphorylated within the Mdm2 binding domain on threonine 18 and serine 20.	Serine	114-120	P53	Homo sapiens	41-44
11799059-4	2002	A product of ATM kinase activity, Ser 18-phosphorylated p53, was detected similarly at these breaks, arguing that ATM phosphorylates target proteins in situ.	Serine	34-37	P53	Homo sapiens	56-59
11707453-6	2002	Analysis of p53-dependent transcription following UV revealed that the phosphorylation of threonine 18 is required for transactivation of the p21, Hdm2 (the human ortholog of Mdm2), and GADD45 genes.	Threonine	90-99	P53	Homo sapiens	12-15
12197224-4	2002	We hypothesized that tumors staining for p53 would be resistant to cisplatin.	Cisplatin	67-76	P53	Homo sapiens	41-44
11734332-4	2002	Antiproliferative activity of betulinic acid was related to a cytotoxic effect on two p53 wild-type and on one p53 mutant cell lines and to a cytostatic effect on one p53 mutant melanoma clone.	betulinic acid	30-44	P53	Homo sapiens	86-89
11734332-4	2002	Antiproliferative activity of betulinic acid was related to a cytotoxic effect on two p53 wild-type and on one p53 mutant cell lines and to a cytostatic effect on one p53 mutant melanoma clone.	betulinic acid	30-44	P53	Homo sapiens	111-114
11734332-4	2002	Antiproliferative activity of betulinic acid was related to a cytotoxic effect on two p53 wild-type and on one p53 mutant cell lines and to a cytostatic effect on one p53 mutant melanoma clone.	betulinic acid	30-44	P53	Homo sapiens	111-114
11734333-5	2002	Low-dose cisplatin induced a transient G(1) arrest, S phase block and upregulation of p53 and p21(WAF1/CIP1) expression in HepG2, but not in Hep3B cells.	Cisplatin	9-18	P53	Homo sapiens	86-89
11734333-7	2002	In HepG2, upregulation of p53 and p21(WAF1/CIP1) was observed before apoptosis occurred, suggesting that cisplatin-induced apoptosis in HepG2 might be p53-dependent.	Cisplatin	105-114	P53	Homo sapiens	26-29
11734333-7	2002	In HepG2, upregulation of p53 and p21(WAF1/CIP1) was observed before apoptosis occurred, suggesting that cisplatin-induced apoptosis in HepG2 might be p53-dependent.	Cisplatin	105-114	P53	Homo sapiens	151-154
11734333-10	2002	In conclusion, cisplatin induced apoptosis in hepatoma cells via both p53-dependent and -independent pathways.	Cisplatin	15-24	P53	Homo sapiens	70-73
11791171-5	2002	In PA1-neo cells with wild-type p53, the activation of caspases including caspases 9, 8, 7 and 3 and cleavage of PARP were detected following adriamycin or etoposide treatment, whereas no such changes were observed in PA1-E6 cells whose p53 is degraded, suggesting that loss of p53 impairs caspase activation.	Doxorubicin	142-152	P53	Homo sapiens	32-35
11791171-5	2002	In PA1-neo cells with wild-type p53, the activation of caspases including caspases 9, 8, 7 and 3 and cleavage of PARP were detected following adriamycin or etoposide treatment, whereas no such changes were observed in PA1-E6 cells whose p53 is degraded, suggesting that loss of p53 impairs caspase activation.	Doxorubicin	142-152	P53	Homo sapiens	237-240
11791171-5	2002	In PA1-neo cells with wild-type p53, the activation of caspases including caspases 9, 8, 7 and 3 and cleavage of PARP were detected following adriamycin or etoposide treatment, whereas no such changes were observed in PA1-E6 cells whose p53 is degraded, suggesting that loss of p53 impairs caspase activation.	Doxorubicin	142-152	P53	Homo sapiens	237-240
11791172-6	2002	Our results with 5-FU thus show that genetically separable functions of p53 are involved in its ability to respond to DNA-damaging agents to induce apoptosis.	Fluorouracil	17-21	P53	Homo sapiens	72-75
12017271-4	2002	Synergistic effects on p53 and p21 levels between the oligonucleotide and chemotherapeutic agents were also observed in vitro.	Oligonucleotides	54-69	P53	Homo sapiens	23-26
11782367-6	2002	Conversely, treatment with the B[a]P metabolite 7r,8t-dihydroxy-9t,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE) repressed BRCA-1 promoter activity and protein, while increasing p53 and p21 protein levels.	7r,8t-dihydroxy-9t,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene	48-109	P53	Homo sapiens	182-185
11782367-7	2002	Transient expression of dominant-negative p53 ((175)Arg--&gt;His) counteracted the detrimental effects of BPDE on BRCA-1 promoter activity and protein levels.	Arginine	52-55	P53	Homo sapiens	42-45
11782367-7	2002	Transient expression of dominant-negative p53 ((175)Arg--&gt;His) counteracted the detrimental effects of BPDE on BRCA-1 promoter activity and protein levels.	Histidine	61-64	P53	Homo sapiens	42-45
11782367-7	2002	Transient expression of dominant-negative p53 ((175)Arg--&gt;His) counteracted the detrimental effects of BPDE on BRCA-1 promoter activity and protein levels.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	106-110	P53	Homo sapiens	42-45
11782367-9	2002	We conclude that activation of the aromatic hydrocarbon receptor is not sufficient for down-regulation of BRCA-1 transcription, which is, however, inhibited by the B[a]P metabolite BPDE through a p53-dependent pathway.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	181-185	P53	Homo sapiens	196-199
11774260-0	2002	Apoptosis induced by low-dose paclitaxel is associated with p53 upregulation in nasopharyngeal carcinoma cells.	Paclitaxel	30-40	P53	Homo sapiens	60-63
11774260-6	2002	We showed that paclitaxel inhibited growth and induced apoptosis in both cell lines but that the p53 mutant line (CNE-2) was less sensitive to treatment with low-dose paclitaxel.	Paclitaxel	167-177	P53	Homo sapiens	97-100
11774260-8	2002	We observed a striking increase of p53 protein levels in NPC cells exposed to 1 and 10 nM paclitaxel but a marked inhibition at 100 nM paclitaxel treatment.	Paclitaxel	90-100	P53	Homo sapiens	35-38
11774260-8	2002	We observed a striking increase of p53 protein levels in NPC cells exposed to 1 and 10 nM paclitaxel but a marked inhibition at 100 nM paclitaxel treatment.	Paclitaxel	135-145	P53	Homo sapiens	35-38
11774260-10	2002	In summary, low-dose paclitaxel inhibited cell growth in NPC cells and induced apoptosis possibly by upregulation of p53.	Paclitaxel	21-31	P53	Homo sapiens	117-120
11855756-9	2002	In Huh-7 cells (mutated p53), which were most sensitive to DOX, there was neither G1 nor G2 arrest, and the level of p53 mutated protein was downregulated after DOX treatment.	Doxorubicin	59-62	P53	Homo sapiens	24-27
11855756-9	2002	In Huh-7 cells (mutated p53), which were most sensitive to DOX, there was neither G1 nor G2 arrest, and the level of p53 mutated protein was downregulated after DOX treatment.	Doxorubicin	161-164	P53	Homo sapiens	24-27
11855756-9	2002	In Huh-7 cells (mutated p53), which were most sensitive to DOX, there was neither G1 nor G2 arrest, and the level of p53 mutated protein was downregulated after DOX treatment.	Doxorubicin	161-164	P53	Homo sapiens	117-120
11855756-11	2002	p21 was upregulated following p53 activation at low doses of DOX in HepG2 cells, but at higher doses, p21 was downregulated in Huh-7 and HepG2 cells.	Doxorubicin	61-64	P53	Homo sapiens	30-33
11855756-12	2002	CONCLUSION: DOX confers different chemosensitivity on different hepatoma cell lines with different p53 status.	Doxorubicin	12-15	P53	Homo sapiens	99-102
11855756-13	2002	The contrasting relationships between chemosensitivity and p53 status and expression suggest that DOX-induced apoptosis and cell death involve pathways that are independent of p53.	Doxorubicin	98-101	P53	Homo sapiens	59-62
11991084-0	2002	Cadmium-induced apoptosis of primary epithelial lung cells: involvement of Bax and p53, but not of oxidative stress.	Cadmium	0-7	P53	Homo sapiens	83-86
11991084-4	2002	On exposure to 10 micromol/L CdAc, the levels of the apoptosis-modulating proteins p53 and Bax were increased at 2 h and 5-12 h, respectively.	cadmium acetate	29-33	P53	Homo sapiens	83-86
11750847-14	2002	Treatment of Caki-1 cells with 5-FU enhanced the expression of p53 and bax, but had no effect on the expression of bcl-2.	Fluorouracil	31-35	P53	Homo sapiens	63-66
11801552-10	2002	In skin biopsies from the same study, we demonstrate that topical DFMO significantly reduces the percentage of p53-positive cells (22%; P = 0.04); however, there were no significant changes in proliferating cell nuclear antigen or apoptotic indices, or in the frequency of p53 mutations (25% at baseline, 21% after placebo, and 26% after DFMO).	Eflornithine	66-70	P53	Homo sapiens	111-114
11801552-10	2002	In skin biopsies from the same study, we demonstrate that topical DFMO significantly reduces the percentage of p53-positive cells (22%; P = 0.04); however, there were no significant changes in proliferating cell nuclear antigen or apoptotic indices, or in the frequency of p53 mutations (25% at baseline, 21% after placebo, and 26% after DFMO).	Eflornithine	66-70	P53	Homo sapiens	273-276
11801552-11	2002	We conclude that inhibition of the premalignant AK lesions as well as a reduction in the expression of p53 and in spermidine concentrations may serve as surrogate endpoint biomarkers of DFMO and possibly other topically administered skin cancer chemopreventive agents.	Eflornithine	186-190	P53	Homo sapiens	103-106
11801555-8	2002	The p53 oligonucleotide array detected 65 point mutations and four splice site mutations in different exons but missed all five frameshift mutations.	Oligonucleotides	8-23	P53	Homo sapiens	4-7
12599424-0	2002	[Effects of wild-type p53 gene transfection on the growth and cisplatin sensitivity of cervical cancer cell line HeLa].	Cisplatin	62-71	P53	Homo sapiens	22-25
11779589-6	2002	MAIN OUTCOME MEASURE(S): Polymerase chain reaction was used to detect p53 codon 72 polymorphisms (arginine homozygosity, heterozygosity, and proline homozygosity).	Arginine	98-106	P53	Homo sapiens	70-73
11779589-11	2002	p53 arginine homozygotes have lower risk for endometriosis.	Arginine	4-12	P53	Homo sapiens	0-3
12056646-5	2002	A series of 129 oral squamous cell cancers was investgated retrospectively for expression of P53 protein by immunohistochemistry of paraffin-embedded tissue sections.	Paraffin	132-140	P53	Homo sapiens	93-96
12599424-7	2002	Wild-type p53-positive HeLa was more sensitive to cisplatin, compared with the control cell lines.	Cisplatin	50-59	P53	Homo sapiens	10-13
12658781-6	2002	When combined treatment of wild-type p53 gene transfection and cisplatin was used, that was significantly increased [IR (91.64 +/- 1.00)%, (94.98 +/- 1.67)%, (95.32 +/- 2.01)%, (95.65 +/- 1.00)%].	Cisplatin	63-72	P53	Homo sapiens	37-40
12440809-5	2002	In ovarian cancer p53 status is a strong predictor of response to platinum-based chemotherapy.	Platinum	66-74	P53	Homo sapiens	18-21
12440809-6	2002	Patients whose tumors have p53 mutations experience a lower chance of achieving a complete response following platinum-based regimens when compared to patients without p53 mutations.	Platinum	110-118	P53	Homo sapiens	27-30
12440809-7	2002	Conversely, experimental and clinical data seem to show that paclitaxel enhances apoptosis through a p53-independent pathway, that probably involves the Bax gene.	Paclitaxel	61-71	P53	Homo sapiens	101-104
12440809-8	2002	Whereas patients with wild-type p53 tumors have a good chance to respond to platinum, patients with mutant p53 tumors may have a clinical benefit from the addition of paclitaxel to platinum-based chemotherapy.	Platinum	76-84	P53	Homo sapiens	32-35
12440809-8	2002	Whereas patients with wild-type p53 tumors have a good chance to respond to platinum, patients with mutant p53 tumors may have a clinical benefit from the addition of paclitaxel to platinum-based chemotherapy.	Paclitaxel	167-177	P53	Homo sapiens	107-110
12440809-8	2002	Whereas patients with wild-type p53 tumors have a good chance to respond to platinum, patients with mutant p53 tumors may have a clinical benefit from the addition of paclitaxel to platinum-based chemotherapy.	Platinum	181-189	P53	Homo sapiens	107-110
12088100-0	2002	Changes in apoptosis, mitosis, Her-2, p53 and Bcl2 expression in breast carcinomas after short-term tamoxifen treatment.	Tamoxifen	100-109	P53	Homo sapiens	38-41
11995810-9	2002	They inhibited CEP-induced apoptosis in U251MG cells (a p53-mutant cell line), but not in U87MG cells (a p53 wild-type cell line), suggesting that in CEP-induced apoptosis two possible cascades are in play.	cepharanthine	15-18	P53	Homo sapiens	56-59
11995810-9	2002	They inhibited CEP-induced apoptosis in U251MG cells (a p53-mutant cell line), but not in U87MG cells (a p53 wild-type cell line), suggesting that in CEP-induced apoptosis two possible cascades are in play.	cepharanthine	150-153	P53	Homo sapiens	56-59
11862326-0	2002	Proliferation-dependent induction of apoptosis by the retinoid CD437 in p53-mutated keratinocytes.	CD 437	63-68	P53	Homo sapiens	72-75
11862326-3	2002	We demonstrate that CD437 is also capable of inducing apoptosis in the non-tumorigenic keratinocyte cell line HaCaT that carries UV-type mutations on both alleles of the p53 gene.	CD 437	20-25	P53	Homo sapiens	170-173
11862326-7	2002	The potent, selective, and p53-independent apoptosis-inducing efficacy of CD437 is of utmost importance for the prophylaxis and treatment of skin cancer caused by mutational inactivation of the p53 gene.	CD 437	74-79	P53	Homo sapiens	27-30
11862326-7	2002	The potent, selective, and p53-independent apoptosis-inducing efficacy of CD437 is of utmost importance for the prophylaxis and treatment of skin cancer caused by mutational inactivation of the p53 gene.	CD 437	74-79	P53	Homo sapiens	194-197
11752120-3	2002	We found that, relative to control transfectants, there was a slight tendency for the p53 inactivated cells to be less sensitive to 5-FU after 6 days of continuous treatment.	Fluorouracil	132-136	P53	Homo sapiens	86-89
11780126-2	2002	Here we demonstrate that homeodomain-interacting protein kinase-2 (HIPK2), a member of a novel family of nuclear serine/threonine kinases, binds to and activates p53 by directly phosphorylating it at Ser 46.	Serine	200-203	P53	Homo sapiens	162-165
11740489-3	2002	HIPK2 is activated by ultraviolet (UV) radiation and selectively phosphorylates p53 at Ser 46, thus facilitating the CBP-mediated acetylation of p53 at Lys 382, and promoting p53-dependent gene expression.	Serine	87-90	P53	Homo sapiens	80-83
11740489-3	2002	HIPK2 is activated by ultraviolet (UV) radiation and selectively phosphorylates p53 at Ser 46, thus facilitating the CBP-mediated acetylation of p53 at Lys 382, and promoting p53-dependent gene expression.	Lysine	152-155	P53	Homo sapiens	80-83
12095159-3	2002	Thus, this work explored the ability of Zn to protect human neurons in culture (NT2-N) from Cu-mediated death and tested the hypotheses that the tumor-suppressor protein p53 plays a role in Cu-induced neuronal death and is part of the mechanism of Zn protection.	Copper	190-192	P53	Homo sapiens	170-173
11740489-3	2002	HIPK2 is activated by ultraviolet (UV) radiation and selectively phosphorylates p53 at Ser 46, thus facilitating the CBP-mediated acetylation of p53 at Lys 382, and promoting p53-dependent gene expression.	Lysine	152-155	P53	Homo sapiens	145-148
11740489-3	2002	HIPK2 is activated by ultraviolet (UV) radiation and selectively phosphorylates p53 at Ser 46, thus facilitating the CBP-mediated acetylation of p53 at Lys 382, and promoting p53-dependent gene expression.	Lysine	152-155	P53	Homo sapiens	145-148
11780126-0	2002	Homeodomain-interacting protein kinase-2 phosphorylates p53 at Ser 46 and mediates apoptosis.	Serine	63-66	P53	Homo sapiens	56-59
11780126-1	2002	Phosphorylation of p53 at Ser 46 was shown to regulate p53 apoptotic activity.	Serine	26-29	P53	Homo sapiens	19-22
11780126-1	2002	Phosphorylation of p53 at Ser 46 was shown to regulate p53 apoptotic activity.	Serine	26-29	P53	Homo sapiens	55-58
12088100-2	2002	Following tamoxifen treatment expression of HER-2 and p53 decreased but Bcl2 remained unchanged.	Tamoxifen	10-19	P53	Homo sapiens	54-57
12095159-3	2002	Thus, this work explored the ability of Zn to protect human neurons in culture (NT2-N) from Cu-mediated death and tested the hypotheses that the tumor-suppressor protein p53 plays a role in Cu-induced neuronal death and is part of the mechanism of Zn protection.	Zinc	248-250	P53	Homo sapiens	170-173
12095159-5	2002	However, the addition of 700 microM Zn to Cu-treated cells resulted in neuronal viability that was not different from untreated controls through 24 h. p53 mRNA abundance, while increased by the addition of Cu and 100 microM Zn, was decreased to 50% of control with the addition of 500 microM Zn in Cu-treated cells, and to 10% of control with 700 microM Zn.	Zinc	36-38	P53	Homo sapiens	151-154
12095159-5	2002	However, the addition of 700 microM Zn to Cu-treated cells resulted in neuronal viability that was not different from untreated controls through 24 h. p53 mRNA abundance, while increased by the addition of Cu and 100 microM Zn, was decreased to 50% of control with the addition of 500 microM Zn in Cu-treated cells, and to 10% of control with 700 microM Zn.	Copper	42-44	P53	Homo sapiens	151-154
12095159-5	2002	However, the addition of 700 microM Zn to Cu-treated cells resulted in neuronal viability that was not different from untreated controls through 24 h. p53 mRNA abundance, while increased by the addition of Cu and 100 microM Zn, was decreased to 50% of control with the addition of 500 microM Zn in Cu-treated cells, and to 10% of control with 700 microM Zn.	Copper	206-208	P53	Homo sapiens	151-154
12095159-5	2002	However, the addition of 700 microM Zn to Cu-treated cells resulted in neuronal viability that was not different from untreated controls through 24 h. p53 mRNA abundance, while increased by the addition of Cu and 100 microM Zn, was decreased to 50% of control with the addition of 500 microM Zn in Cu-treated cells, and to 10% of control with 700 microM Zn.	Zinc	224-226	P53	Homo sapiens	151-154
12095159-5	2002	However, the addition of 700 microM Zn to Cu-treated cells resulted in neuronal viability that was not different from untreated controls through 24 h. p53 mRNA abundance, while increased by the addition of Cu and 100 microM Zn, was decreased to 50% of control with the addition of 500 microM Zn in Cu-treated cells, and to 10% of control with 700 microM Zn.	Zinc	224-226	P53	Homo sapiens	151-154
12095159-5	2002	However, the addition of 700 microM Zn to Cu-treated cells resulted in neuronal viability that was not different from untreated controls through 24 h. p53 mRNA abundance, while increased by the addition of Cu and 100 microM Zn, was decreased to 50% of control with the addition of 500 microM Zn in Cu-treated cells, and to 10% of control with 700 microM Zn.	Copper	206-208	P53	Homo sapiens	151-154
12095159-5	2002	However, the addition of 700 microM Zn to Cu-treated cells resulted in neuronal viability that was not different from untreated controls through 24 h. p53 mRNA abundance, while increased by the addition of Cu and 100 microM Zn, was decreased to 50% of control with the addition of 500 microM Zn in Cu-treated cells, and to 10% of control with 700 microM Zn.	Zinc	224-226	P53	Homo sapiens	151-154
12095159-6	2002	Consistent with its role as a transcription factor, both Western analysis and immunocytochemistry showed significant increases in nuclear p53 protein levels in Cu toxicity.	Copper	160-162	P53	Homo sapiens	138-141
12095159-7	2002	The role of p53 in Cu-mediated apoptosis was further confirmed by elimination of apoptosis in Cu-treated cells that had been transfected with a dominant-negative p53 construct to prevent p53 expression.	Copper	19-21	P53	Homo sapiens	12-15
12095159-7	2002	The role of p53 in Cu-mediated apoptosis was further confirmed by elimination of apoptosis in Cu-treated cells that had been transfected with a dominant-negative p53 construct to prevent p53 expression.	Copper	19-21	P53	Homo sapiens	162-165
12095159-7	2002	The role of p53 in Cu-mediated apoptosis was further confirmed by elimination of apoptosis in Cu-treated cells that had been transfected with a dominant-negative p53 construct to prevent p53 expression.	Copper	19-21	P53	Homo sapiens	162-165
12095159-7	2002	The role of p53 in Cu-mediated apoptosis was further confirmed by elimination of apoptosis in Cu-treated cells that had been transfected with a dominant-negative p53 construct to prevent p53 expression.	Copper	94-96	P53	Homo sapiens	12-15
12095159-7	2002	The role of p53 in Cu-mediated apoptosis was further confirmed by elimination of apoptosis in Cu-treated cells that had been transfected with a dominant-negative p53 construct to prevent p53 expression.	Copper	94-96	P53	Homo sapiens	162-165
12095159-7	2002	The role of p53 in Cu-mediated apoptosis was further confirmed by elimination of apoptosis in Cu-treated cells that had been transfected with a dominant-negative p53 construct to prevent p53 expression.	Copper	94-96	P53	Homo sapiens	162-165
12095159-8	2002	Furthermore, the addition of 500-700 microM Zn prevented the movement of p53 into the nucleus suggesting that Zn not only protects neurons from Cu toxicity by regulating p53 mRNA abundance but also by preventing the translocation of p53 to the nucleus.	Zinc	44-46	P53	Homo sapiens	73-76
12095159-8	2002	Furthermore, the addition of 500-700 microM Zn prevented the movement of p53 into the nucleus suggesting that Zn not only protects neurons from Cu toxicity by regulating p53 mRNA abundance but also by preventing the translocation of p53 to the nucleus.	Zinc	44-46	P53	Homo sapiens	170-173
12095159-8	2002	Furthermore, the addition of 500-700 microM Zn prevented the movement of p53 into the nucleus suggesting that Zn not only protects neurons from Cu toxicity by regulating p53 mRNA abundance but also by preventing the translocation of p53 to the nucleus.	Zinc	44-46	P53	Homo sapiens	170-173
11914604-5	2002	Thus, use of both alcohol and cigarettes is clearly associated with a high frequency of p53 protein accumulation in multiple oesophageal squamous cell carcinoma present at the same time.	Alcohols	18-25	P53	Homo sapiens	88-91
12095159-8	2002	Furthermore, the addition of 500-700 microM Zn prevented the movement of p53 into the nucleus suggesting that Zn not only protects neurons from Cu toxicity by regulating p53 mRNA abundance but also by preventing the translocation of p53 to the nucleus.	Zinc	110-112	P53	Homo sapiens	73-76
12065876-2	2002	METHODS: The expression of p53 and mdm2 was analyzed by an immunohistochemical assay in 80 formalin-fixed paraffin embedded primary tumour samples and related to the clinical response to 5-fluorouracil therapy and to the prognosis of the patients.	Paraffin	106-114	P53	Homo sapiens	27-30
12095159-8	2002	Furthermore, the addition of 500-700 microM Zn prevented the movement of p53 into the nucleus suggesting that Zn not only protects neurons from Cu toxicity by regulating p53 mRNA abundance but also by preventing the translocation of p53 to the nucleus.	Zinc	110-112	P53	Homo sapiens	170-173
12065876-2	2002	METHODS: The expression of p53 and mdm2 was analyzed by an immunohistochemical assay in 80 formalin-fixed paraffin embedded primary tumour samples and related to the clinical response to 5-fluorouracil therapy and to the prognosis of the patients.	Fluorouracil	187-201	P53	Homo sapiens	27-30
12095159-8	2002	Furthermore, the addition of 500-700 microM Zn prevented the movement of p53 into the nucleus suggesting that Zn not only protects neurons from Cu toxicity by regulating p53 mRNA abundance but also by preventing the translocation of p53 to the nucleus.	Zinc	110-112	P53	Homo sapiens	170-173
12095159-8	2002	Furthermore, the addition of 500-700 microM Zn prevented the movement of p53 into the nucleus suggesting that Zn not only protects neurons from Cu toxicity by regulating p53 mRNA abundance but also by preventing the translocation of p53 to the nucleus.	Copper	144-146	P53	Homo sapiens	73-76
12199376-4	2002	The levels of a cell cycle regulatory protein, P53, in response to the treatment of isoflavones, were also determined.	Isoflavones	84-95	P53	Homo sapiens	47-50
11983027-10	2001	The supposedly anti-apoptotic homozygous Arg 72-p53 genotype may increase susceptibility of some cancers.	Arginine	41-44	P53	Homo sapiens	48-51
11741290-7	2001	The p53 induced by both drugs was able to bind to DNA; however, only the p53 induced by camptothecin was phosphorylated at serine-392.	Serine	123-129	P53	Homo sapiens	4-7
11741290-7	2001	The p53 induced by both drugs was able to bind to DNA; however, only the p53 induced by camptothecin was phosphorylated at serine-392.	Serine	123-129	P53	Homo sapiens	73-76
11716543-2	2001	We found that curcumin caused cell death in eight melanoma cell lines, four with wild-type and four with mutant p53.	Curcumin	14-22	P53	Homo sapiens	112-115
11716543-10	2001	Since melanoma cells with mutant p53 are strongly resistant to conventional chemotherapy, curcumin may overcome the chemoresistance of these cells and provide potential new avenues for treatment.	Curcumin	90-98	P53	Homo sapiens	33-36
11744405-13	2001	However, permanent H(2)O(2) levels induce the tumour suppressor p53 which in turn downregulates cytosolic TR.	Hydrogen Peroxide	19-27	P53	Homo sapiens	64-67
12030785-6	2001	In addition, the status of ATM, p53, PTEN/Akt and 14-3-3 are also associated with rapamycin sensitivity.	Sirolimus	82-91	P53	Homo sapiens	32-35
11753676-4	2001	However, RA sensitive CA-OV3 cells expressed higher levels of p53, p27, p21, and p16 compared to RA resistant SK-OV3 cells.	Tretinoin	9-11	P53	Homo sapiens	62-65
11813984-10	2001	MAL-PEG conjugation coupled to western analysis detected a minimum of 0.23 pmol of oxidized p53.	Polyethylene Glycols	4-7	P53	Homo sapiens	92-95
11728383-6	2001	We also observed that a paclitaxel-resistant cell line expressed Bax at a much lower level than the sensitive parental line [A2780(1A9)], consistent with its mutant p53 status.	Paclitaxel	24-34	P53	Homo sapiens	165-168
11745454-3	2001	Using the human wild-type p53-expressing HCT116 colon carcinoma cell line and HCT116 cells with both p53 alleles inactivated by homologous recombination, we show in the current study that resveratrol at concentrations comparable to those found in some foods can induce apoptosis independently of p53.	Resveratrol	188-199	P53	Homo sapiens	26-29
11745454-3	2001	Using the human wild-type p53-expressing HCT116 colon carcinoma cell line and HCT116 cells with both p53 alleles inactivated by homologous recombination, we show in the current study that resveratrol at concentrations comparable to those found in some foods can induce apoptosis independently of p53.	Resveratrol	188-199	P53	Homo sapiens	101-104
11745454-3	2001	Using the human wild-type p53-expressing HCT116 colon carcinoma cell line and HCT116 cells with both p53 alleles inactivated by homologous recombination, we show in the current study that resveratrol at concentrations comparable to those found in some foods can induce apoptosis independently of p53.	Resveratrol	188-199	P53	Homo sapiens	101-104
11745454-6	2001	When compared with 5-FU, resveratrol stimulated p53 accumulation and activity only weakly and with delayed kinetics and neither the increased levels nor the activity affected apoptosis detectably.	Resveratrol	25-36	P53	Homo sapiens	48-51
11745454-9	2001	Thus, resveratrol triggers a p53-independent apoptotic pathway in HCT116 cells that may be linked to differentiation.	Resveratrol	6-17	P53	Homo sapiens	29-32
11720736-7	2001	Although several different exogenous carcinogens have been shown to selectively target p53, evidence supporting the endogenous insult of p53 from oxyradical and nitrogen-oxyradicals is accumulating.	Nitrogen	161-169	P53	Homo sapiens	137-140
11713288-6	2001	The extreme C terminus of p53 harbors several lysine residues whose ubiquitination by MDM2 appears to be the initial event in p53 nuclear export, as evidenced by the impaired nucleocytoplasmic shuttling of p53 mutants bearing simultaneous substitutions of lysines 370, 372, 373, 381, 382, and 386 to arginines (6KR) or alanines (6KA).	Lysine	46-52	P53	Homo sapiens	26-29
11713288-6	2001	The extreme C terminus of p53 harbors several lysine residues whose ubiquitination by MDM2 appears to be the initial event in p53 nuclear export, as evidenced by the impaired nucleocytoplasmic shuttling of p53 mutants bearing simultaneous substitutions of lysines 370, 372, 373, 381, 382, and 386 to arginines (6KR) or alanines (6KA).	Lysine	46-52	P53	Homo sapiens	126-129
11713288-6	2001	The extreme C terminus of p53 harbors several lysine residues whose ubiquitination by MDM2 appears to be the initial event in p53 nuclear export, as evidenced by the impaired nucleocytoplasmic shuttling of p53 mutants bearing simultaneous substitutions of lysines 370, 372, 373, 381, 382, and 386 to arginines (6KR) or alanines (6KA).	Lysine	46-52	P53	Homo sapiens	126-129
11713288-6	2001	The extreme C terminus of p53 harbors several lysine residues whose ubiquitination by MDM2 appears to be the initial event in p53 nuclear export, as evidenced by the impaired nucleocytoplasmic shuttling of p53 mutants bearing simultaneous substitutions of lysines 370, 372, 373, 381, 382, and 386 to arginines (6KR) or alanines (6KA).	Lysine	256-263	P53	Homo sapiens	26-29
11713288-6	2001	The extreme C terminus of p53 harbors several lysine residues whose ubiquitination by MDM2 appears to be the initial event in p53 nuclear export, as evidenced by the impaired nucleocytoplasmic shuttling of p53 mutants bearing simultaneous substitutions of lysines 370, 372, 373, 381, 382, and 386 to arginines (6KR) or alanines (6KA).	Lysine	256-263	P53	Homo sapiens	126-129
11713288-6	2001	The extreme C terminus of p53 harbors several lysine residues whose ubiquitination by MDM2 appears to be the initial event in p53 nuclear export, as evidenced by the impaired nucleocytoplasmic shuttling of p53 mutants bearing simultaneous substitutions of lysines 370, 372, 373, 381, 382, and 386 to arginines (6KR) or alanines (6KA).	Lysine	256-263	P53	Homo sapiens	126-129
11713288-6	2001	The extreme C terminus of p53 harbors several lysine residues whose ubiquitination by MDM2 appears to be the initial event in p53 nuclear export, as evidenced by the impaired nucleocytoplasmic shuttling of p53 mutants bearing simultaneous substitutions of lysines 370, 372, 373, 381, 382, and 386 to arginines (6KR) or alanines (6KA).	Arginine	300-309	P53	Homo sapiens	26-29
11713288-6	2001	The extreme C terminus of p53 harbors several lysine residues whose ubiquitination by MDM2 appears to be the initial event in p53 nuclear export, as evidenced by the impaired nucleocytoplasmic shuttling of p53 mutants bearing simultaneous substitutions of lysines 370, 372, 373, 381, 382, and 386 to arginines (6KR) or alanines (6KA).	Arginine	300-309	P53	Homo sapiens	126-129
11713288-6	2001	The extreme C terminus of p53 harbors several lysine residues whose ubiquitination by MDM2 appears to be the initial event in p53 nuclear export, as evidenced by the impaired nucleocytoplasmic shuttling of p53 mutants bearing simultaneous substitutions of lysines 370, 372, 373, 381, 382, and 386 to arginines (6KR) or alanines (6KA).	Arginine	300-309	P53	Homo sapiens	126-129
11713288-6	2001	The extreme C terminus of p53 harbors several lysine residues whose ubiquitination by MDM2 appears to be the initial event in p53 nuclear export, as evidenced by the impaired nucleocytoplasmic shuttling of p53 mutants bearing simultaneous substitutions of lysines 370, 372, 373, 381, 382, and 386 to arginines (6KR) or alanines (6KA).	Alanine	319-327	P53	Homo sapiens	26-29
11713288-6	2001	The extreme C terminus of p53 harbors several lysine residues whose ubiquitination by MDM2 appears to be the initial event in p53 nuclear export, as evidenced by the impaired nucleocytoplasmic shuttling of p53 mutants bearing simultaneous substitutions of lysines 370, 372, 373, 381, 382, and 386 to arginines (6KR) or alanines (6KA).	Alanine	319-327	P53	Homo sapiens	126-129
11713288-6	2001	The extreme C terminus of p53 harbors several lysine residues whose ubiquitination by MDM2 appears to be the initial event in p53 nuclear export, as evidenced by the impaired nucleocytoplasmic shuttling of p53 mutants bearing simultaneous substitutions of lysines 370, 372, 373, 381, 382, and 386 to arginines (6KR) or alanines (6KA).	Alanine	319-327	P53	Homo sapiens	126-129
11713288-7	2001	Finally, the region between the DBD and the oligomerization domain of p53, specifically lysine 305, also plays a critical role in fully revealing p53NES.	Lysine	88-94	P53	Homo sapiens	70-73
11753684-7	2001	To examine the role of p53 in these functions, we showed that suppression of p53 level with antisense oligonucleotide abrogated triptolide-induced apoptosis and over-expression of dominant negative p53 abolished the inhibitory effect on NF-kappaB activation.	Oligonucleotides	102-117	P53	Homo sapiens	77-80
11753684-7	2001	To examine the role of p53 in these functions, we showed that suppression of p53 level with antisense oligonucleotide abrogated triptolide-induced apoptosis and over-expression of dominant negative p53 abolished the inhibitory effect on NF-kappaB activation.	Oligonucleotides	102-117	P53	Homo sapiens	77-80
11551930-10	2001	In vitro kinase assays followed by immunoblotting showed that serine 20 of p53 was a target of Plk3.	Serine	62-68	P53	Homo sapiens	75-78
11551930-11	2001	Furthermore, expression of a kinase-defective Plk3 mutant (Plk3(K52R)) resulted in significant reduction of p53 phosphorylation on serine 20, which was correlated with a decrease in the expression of p21 and with a concomitant increase in cell proliferation.	Serine	131-137	P53	Homo sapiens	108-111
11719428-2	2001	In a kindred with LFS without an inherited TP53 mutation, we have previously reported a truncating mutation (1100delC) in CHK2, encoding a kinase that phosphorylates p53 on Ser(20).	Serine	173-176	P53	Homo sapiens	166-169
11709716-8	2001	Moreover, upregulation of p53 through serine 20 phosphorylation, does not occur in G2.	Serine	38-44	P53	Homo sapiens	26-29
11709055-7	2001	These observations suggest a model in which the NF-kappaB switch from an anti-apoptotic to a pro-apoptotic role within the cell results from modulation of its ability to stimulate gene expression, possibly as a result of the ability of p53 to sequester transcriptional co-activator proteins such as p300/CREB (cAMP-response-element-binding protein)-binding protein.	Cyclic AMP	310-314	P53	Homo sapiens	236-239
11698570-0	2001	Oxidative stress and p53 mutations in the carcinogenesis of iron overload-associated hepatocellular carcinoma.	Iron	60-64	P53	Homo sapiens	21-24
11720475-4	2001	Using molecular and immunohistochemical analyses we examined TP53 and its downstream genes p21, BAX and BCL-2 in ovarian tumour tissues and have evaluated the results in relation to clinico-pathological parameters, clinical outcome and response to platinum-based chemotherapy.	Platinum	248-256	P53	Homo sapiens	61-65
11911261-2	2001	In vitro study using a breast cancer cell line, T47D, demonstrated an increase in p53 gene expression and induction of apoptosis by the administration of progesterone.	Progesterone	154-166	P53	Homo sapiens	82-85
11673079-0	2001	The detection of mutations induced in vitro in the human p53 gene by hydrogen peroxide with the restriction site mutation (RSM) assay.	Hydrogen Peroxide	69-86	P53	Homo sapiens	57-60
11673079-1	2001	We have analysed five mutation hotspots within the p53 gene (codons 175, 213, 248, 249, and 282) for mutations induced by hydrogen peroxide (H(2)O(2)), employing the restriction site mutation (RSM) assay.	Hydrogen Peroxide	122-139	P53	Homo sapiens	51-54
11761456-0	2001	Regulation of p53 target gene expression by cisplatin-induced extracellular signal-regulated kinase.	Cisplatin	44-53	P53	Homo sapiens	14-17
11761456-7	2001	These results provide evidence that ERK activity during the cisplatin DNA damage response, regulates in part, these cell cycle control (p21WAF1, Gadd45), DNA repair (Gadd45) and p53-regulatory (Mdm2) proteins.	Cisplatin	60-69	P53	Homo sapiens	178-181
11761456-3	2001	Furthermore, we have demonstrated that cisplatin-induced ERK activation is required for optimal p53 protein accumulation following cisplatin-induced DNA damage.	Cisplatin	39-48	P53	Homo sapiens	96-99
11761456-3	2001	Furthermore, we have demonstrated that cisplatin-induced ERK activation is required for optimal p53 protein accumulation following cisplatin-induced DNA damage.	Cisplatin	131-140	P53	Homo sapiens	96-99
11761456-4	2001	In the present study, we expanded our investigations to examine the effect of cisplatin-induced ERK activation on the expression of p53-targeted genes that have been shown to be important in the cellular response to DNA damage including Bax, Bcl-2, Bcl-x1, Cyclin G, Gadd45, p21WAF1, and Mdm2.	Cisplatin	78-87	P53	Homo sapiens	132-135
11710828-10	2001	The results indicate that women homozygotic for arg/arg in codon 72 of the p53 gene are at an increased risk for the development of cervical adenocarcinomas.	Arginine	48-51	P53	Homo sapiens	75-78
11677114-0	2001	Steroid-mediated inhibition of radiation-induced apoptosis in C4-1 cervical carcinoma cells is p53-dependent.	Steroids	0-7	P53	Homo sapiens	95-98
11677114-1	2001	In human papillomavirus (HPV) infected cervical epithelial cells the synthetic steroid dexamethasone inhibits radiation-induced apoptosis and increases the transcription of HPV E6/E7, enhancing p53 degradation.	Steroids	79-86	P53	Homo sapiens	194-197
11677114-1	2001	In human papillomavirus (HPV) infected cervical epithelial cells the synthetic steroid dexamethasone inhibits radiation-induced apoptosis and increases the transcription of HPV E6/E7, enhancing p53 degradation.	Dexamethasone	87-100	P53	Homo sapiens	194-197
11677114-7	2001	Steroid-dependent inhibition of radiation-induced apoptosis in carcinoma of the cervix involves E6 modulation of p53 expression and may adversely affect treatment.	Steroids	0-7	P53	Homo sapiens	113-116
11694645-0	2001	Short-chain fatty acids inhibit invasive human colon cancer by modulating uPA, TIMP-1, TIMP-2, mutant p53, Bcl-2, Bax, p21 and PCNA protein expression in an in vitro cell culture model.	Fatty Acids, Volatile	0-23	P53	Homo sapiens	102-105
11673474-9	2001	Our results indicate that suppression of p53 expression in HMECs by HPV-16 E6 and ODNs may sensitize cells to rECM-induced apoptosis and suggest a role for the alpha3/beta1-heterodimer in mediating apoptosis in HMECs grown in contact with rECM.	recm	110-114	P53	Homo sapiens	41-44
11673474-9	2001	Our results indicate that suppression of p53 expression in HMECs by HPV-16 E6 and ODNs may sensitize cells to rECM-induced apoptosis and suggest a role for the alpha3/beta1-heterodimer in mediating apoptosis in HMECs grown in contact with rECM.	recm	239-243	P53	Homo sapiens	41-44
11672522-3	2001	Nicotinamide (Vitamin B3) inhibits an NAD-dependent p53 deacetylation induced by Sir2alpha, and also enhances the p53 acetylation levels in vivo.	NAD	38-41	P53	Homo sapiens	52-55
11672523-0	2001	hSIR2(SIRT1) functions as an NAD-dependent p53 deacetylase.	NAD	29-32	P53	Homo sapiens	43-46
11594760-0	2001	p53 unfolding detected by CD but not by tryptophan fluorescence.	Cadmium	26-28	P53	Homo sapiens	0-3
11594760-1	2001	Full-length human p53 protein was examined using tryptophan fluorescence and circular dichroism spectroscopy (CD) to monitor unfolding.	Tryptophan	49-59	P53	Homo sapiens	18-21
11594760-9	2001	Examination of X-ray structures containing two of the four tryptophan residues of a p53 monomer suggested local environments consistent with quenched fluorophores.	Tryptophan	59-69	P53	Homo sapiens	84-87
11489880-3	2001	Restoration of p53 triggered a G(2)/M cell cycle arrest and enhanced BAX protein expression, without inducing apoptosis or potentiating the cytotoxic effect of etoposide, vincristine, and cis-platinum.	Cisplatin	188-200	P53	Homo sapiens	15-18
11495913-3	2001	Among the postulated phosphorylation sites involved in p53 stabilization or activation (Ser(15), Ser(20), Ser(33), and Ser(46)), only Ser(33) was phosphorylated.	Serine	88-91	P53	Homo sapiens	55-58
11710828-10	2001	The results indicate that women homozygotic for arg/arg in codon 72 of the p53 gene are at an increased risk for the development of cervical adenocarcinomas.	Arginine	52-55	P53	Homo sapiens	75-78
11495913-4	2001	Furthermore, interaction of p53 with the transcriptional coactivator p300 was induced, and Lys(382) of p53 was acetylated.	Lysine	91-94	P53	Homo sapiens	28-31
11495913-4	2001	Furthermore, interaction of p53 with the transcriptional coactivator p300 was induced, and Lys(382) of p53 was acetylated.	Lysine	91-94	P53	Homo sapiens	103-106
11518699-4	2001	Phosphorylation of p300 at serine 89 by AMP-kinase dramatically reduced its interaction, in vitro and in vivo, with the nuclear receptors peroxisome proliferator-activated receptor gamma, thyroid receptor, retinoic acid receptor, and retinoid X receptor, but did not affect its interaction with the non-nuclear receptor transcription factors E1a, p53, or GATA4.	Serine	27-33	P53	Homo sapiens	347-350
11495913-7	2001	Activated p38(MAPK) phosphorylated endogenous p53 at Ser(33) in living cells.	Serine	53-56	P53	Homo sapiens	46-49
11495913-9	2001	These results suggest that phosphorylation at Ser(33) by p38(MAPK) is critical for activation of p53 following osmotic shock.	Serine	46-49	P53	Homo sapiens	97-100
11594730-4	2001	Experiments in vitro demonstrate that peroxynitrite treatment of recombinant wild-type p53 at physiological concentrations results in formation of higher molecular weight aggregates, tyrosine nitration, and loss of specific DNA binding.	Tyrosine	183-191	P53	Homo sapiens	87-90
11687964-0	2001	Difference in the centrosome duplication regulatory activity among p53 "hot spot" mutants: potential role of Ser 315 phosphorylation-dependent centrosome binding of p53.	Serine	109-112	P53	Homo sapiens	165-168
11687964-9	2001	Since cyclin-dependent kinase 2 (CDK2) triggers initiation of centrosome duplication, and p53 is phosphorylated on Ser 315 by CDK2, we examined the p53 mutants with a replacement of Ser 315 to Ala (A) and Asp (D), both of which retain the transactivation function.	Serine	115-118	P53	Homo sapiens	90-93
11687964-12	2001	Thus, p53 controls the centrosome duplication cycle both in transactivation-dependent and transactivation-independent manners, and the ability to bind to unduplicated centrosomes, which is controlled by phosphorylation on Ser 315, may be important for the overall p53-mediated regulation of centrosome duplication.	Serine	222-225	P53	Homo sapiens	6-9
11687964-12	2001	Thus, p53 controls the centrosome duplication cycle both in transactivation-dependent and transactivation-independent manners, and the ability to bind to unduplicated centrosomes, which is controlled by phosphorylation on Ser 315, may be important for the overall p53-mediated regulation of centrosome duplication.	Serine	222-225	P53	Homo sapiens	264-267
11583595-3	2001	Previous studies have suggested that DNA-damage-induced phosphorylation of p53 at key N-terminal sites has a pivotal role in regulating the interaction with Mdm2 but the precise role of phosphorylation of serines 15 and 20 is still unclear.	Serine	205-212	P53	Homo sapiens	75-78
11583595-5	2001	In contrast, replacement of serine 20 makes p53 highly sensitive to Mdm2-mediated turnover.	Serine	28-34	P53	Homo sapiens	44-47
11602639-2	2001	In syncytial apoptosis, phosphorylation of p53 on serine 15 (p53S15) precedes Bax upregulation, the apoptosis-linked conformational change of Bax, the insertion of Bax in mitochondrial membranes, subsequent release of cytochrome c, caspase activation, and apoptosis.	Serine	50-56	P53	Homo sapiens	43-46
11594730-5	2001	Peroxynitrite treatment of human glioma cell lysates similarly resulted in selective tyrosine nitration of p53 and was also associated with loss of p53 DNA binding ability.	Tyrosine	85-93	P53	Homo sapiens	107-110
11709715-0	2001	P53 plays a protective role against UV- and cisplatin-induced apoptosis in transcription-coupled repair proficient fibroblasts.	Cisplatin	44-53	P53	Homo sapiens	0-3
11576999-0	2001	p53-independent apoptosis mediated by tachpyridine, an anti-cancer iron chelator.	Iron	67-71	P53	Homo sapiens	0-3
11477076-5	2001	However, glutathione S-transferase-fused and thus dimerized p63 and p53 core domains had similar affinity and specificity for the p53 consensus sites p21, gadd45, cyclin G, and bax.	Glutathione	9-20	P53	Homo sapiens	68-71
11477076-5	2001	However, glutathione S-transferase-fused and thus dimerized p63 and p53 core domains had similar affinity and specificity for the p53 consensus sites p21, gadd45, cyclin G, and bax.	Glutathione	9-20	P53	Homo sapiens	130-133
11686576-3	2001	Previously, we demonstrated that the demise of human hepatoma Hep G2 cells mediated by folate deficiency proceeded via a p53-independent apoptosis, and the perturbation of intracellular calcium homeostasis was also shown to be involved.	Folic Acid	87-93	P53	Homo sapiens	121-124
11709715-5	2001	We found that TCR-deficient (XP-A, XP-B and CS-B) fibroblasts were more sensitive than TCR-proficient cells (XP-C and normal) to both UV light and cisplatin treatment and this increase in sensitivity was not p53 dependent.	Cisplatin	147-156	P53	Homo sapiens	208-211
11709715-8	2001	Therefore, we propose that p53 protects against UV- and cisplatin-induced apoptosis in a TCR-dependent manner and that p53 does not contribute strongly to the induction of apoptosis in TCR-deficient fibroblasts.	Cisplatin	56-65	P53	Homo sapiens	27-30
11576999-13	2001	Since over 50% of human tumors contain a functionally defective p53 that reduces sensitivity to commonly used chemotherapeutic agents, such as etoposide and cisplatin, the ability of tachpyridine to induce apoptosis independently of p53 may offer an advantage in anti-tumor therapy.	Cisplatin	157-166	P53	Homo sapiens	64-67
11585742-0	2001	Methylated CpG dinucleotides are the preferential targets for G-to-T transversion mutations induced by benzo[a]pyrene diol epoxide in mammalian cells: similarities with the p53 mutation spectrum in smoking-associated lung cancers.	cytidylyl-3'-5'-guanosine	11-28	P53	Homo sapiens	173-176
11585742-0	2001	Methylated CpG dinucleotides are the preferential targets for G-to-T transversion mutations induced by benzo[a]pyrene diol epoxide in mammalian cells: similarities with the p53 mutation spectrum in smoking-associated lung cancers.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	103-130	P53	Homo sapiens	173-176
11585742-3	2001	p53 codons containing methylated CpG sequences are preferential targets for formation of adducts by (+/-) anti-7beta,8alpha-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE).	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	190-194	P53	Homo sapiens	0-3
11585729-3	2001	One of these modifications is dephosphorylation of Ser(376), which leads to association of p53 with 14-3-3 proteins.	Serine	51-54	P53	Homo sapiens	91-94
11574421-2	2001	At a high glucose concentration, O-glycosylation of p53 occurred between 10 and 20 min, reached its peak at 1 h, and then decreased with time.	Glucose	10-17	P53	Homo sapiens	52-55
11595686-0	2001	Correlation of p53 mutations with resistance to platinum-based chemotherapy and shortened survival in ovarian cancer.	Platinum	48-56	P53	Homo sapiens	15-18
11595686-8	2001	Resistance to adjuvant cisplatin or carboplatin chemotherapy was significantly more frequent in patients with p53 overexpression (P = 0.001) or p53 missense mutations (P = 0.008) than patients with normal p53.	Cisplatin	23-32	P53	Homo sapiens	110-113
11595686-8	2001	Resistance to adjuvant cisplatin or carboplatin chemotherapy was significantly more frequent in patients with p53 overexpression (P = 0.001) or p53 missense mutations (P = 0.008) than patients with normal p53.	Cisplatin	23-32	P53	Homo sapiens	144-147
11595686-8	2001	Resistance to adjuvant cisplatin or carboplatin chemotherapy was significantly more frequent in patients with p53 overexpression (P = 0.001) or p53 missense mutations (P = 0.008) than patients with normal p53.	Cisplatin	23-32	P53	Homo sapiens	144-147
11595686-9	2001	CONCLUSIONS: p53 alterations correlate significantly with resistance to platinum-based chemotherapy, early relapse, and shortened overall survival in ovarian cancer patients in univariate analysis.	Platinum	72-80	P53	Homo sapiens	13-16
11574421-3	2001	Angiotensin II synthesis increased at 45 min and 1 h, resulting in p38 mitogen-activated protein (MAP) kinase-driven p53 phosphorylation at Ser 390.	Serine	140-143	P53	Homo sapiens	117-120
11574421-5	2001	Phosphorylated p53 at Ser 18 and activated c-Jun NH(2)-terminal kinases were identified with hyperglycemia, whereas extracellular signal-regulated kinase was not phosphorylated.	Serine	22-25	P53	Homo sapiens	15-18
11682009-1	2001	PURPOSE: To investigate the dependence on p53 gene status of the thermal enhancement of cellular sensitivity against different levels of linear energy transfer (LET) from X-rays or carbon-ion (C-) beams.	Carbon	181-187	P53	Homo sapiens	42-45
11740051-3	2001	Immunohistochemical staining method was used for detecting p53 and bcl-2 expression on paraffin blocks of three pure insular, five follicular or papillary thyroid carcinomas with a major insular component (more than 50%) and six with a minor insular component (20-50%).	Paraffin	87-95	P53	Homo sapiens	59-62
11564578-1	2001	The p53 codon 72 polymorphism, resulting in either an arginine or a proline residue has been proposed to affect the susceptibility of p53 protein to human papilloma virus (HPV) E6-mediated degradation in vitro.	Arginine	54-62	P53	Homo sapiens	4-7
11590433-0	2001	Ferredoxin reductase affects p53-dependent, 5-fluorouracil-induced apoptosis in colorectal cancer cells.	Fluorouracil	44-58	P53	Homo sapiens	29-32
11590433-1	2001	Loss of p53 gene function, which occurs in most colon cancer cells, has been shown to abolish the apoptotic response to 5-fluorouracil (5-FU).	Fluorouracil	120-134	P53	Homo sapiens	8-11
11590433-1	2001	Loss of p53 gene function, which occurs in most colon cancer cells, has been shown to abolish the apoptotic response to 5-fluorouracil (5-FU).	Fluorouracil	136-140	P53	Homo sapiens	8-11
11590433-2	2001	To identify genes downstream of p53 that might mediate these effects, we assessed global patterns of gene expression following 5-FU treatment of isogenic cells differing only in their p53 status.	Fluorouracil	127-131	P53	Homo sapiens	32-35
11590433-3	2001	The gene encoding mitochondrial ferredoxin reductase (protein, FR; gene, FDXR) was one of the few genes significantly induced by p53 after 5-FU treatment.	Fluorouracil	139-143	P53	Homo sapiens	129-132
11590433-6	2001	These data, coupled with the effects of pharmacologic inhibitors of reactive oxygen species, indicate that FR contributes to p53-mediated apoptosis through the generation of oxidative stress in mitochondria.	Reactive Oxygen Species	68-91	P53	Homo sapiens	125-128
11564575-1	2001	Tobacco smoking and alcohol drinking are the principal factors associated with p53 expression in oral squamous cell carcinomas (OSCC) in the west, whereas betel quid chewing and smokeless tobacco are important factors in the east.	Alcohols	20-27	P53	Homo sapiens	79-82
11564575-5	2001	Multivariate modelling showed that lifetime exposure to alcohol drinking was significantly positively associated with p53 expression (likelihood ratio P value 0.01).	Alcohols	56-63	P53	Homo sapiens	118-121
11564578-1	2001	The p53 codon 72 polymorphism, resulting in either an arginine or a proline residue has been proposed to affect the susceptibility of p53 protein to human papilloma virus (HPV) E6-mediated degradation in vitro.	Arginine	54-62	P53	Homo sapiens	134-137
11447225-0	2001	Reactive oxygen species-induced phosphorylation of p53 on serine 20 is mediated in part by polo-like kinase-3.	Reactive Oxygen Species	0-23	P53	Homo sapiens	51-54
11447225-8	2001	Furthermore, although H(2)O(2) strongly induced serine 15 phosphorylation of p53, it failed to induce serine 20 phosphorylation in Plk3-dificient Daudi cells.	Water	22-27	P53	Homo sapiens	77-80
11568365-0	2001	p53-dependent induction of p21(Cip1/WAF1/Sdi1) protects against oxygen-induced toxicity.	Oxygen	64-70	P53	Homo sapiens	0-3
11568365-2	2001	Cells respond to oxygen-induced damage by expressing the tumor suppressor p53 and the cyclin-dependent kinase inhibitor p21(Cip1/WAF1/Sdi1) (p21), which limits proliferation by blocking entry into S phase.	Oxygen	17-23	P53	Homo sapiens	74-77
11568365-5	2001	Hyperoxia (95% O2, 5% CO2) increased p53 abundance, phosphorylation of p53 on serine 15, and p21 mRNA and protein in parental HCT116 cells that ceased proliferation.	Oxygen	15-17	P53	Homo sapiens	37-40
11568365-5	2001	Hyperoxia (95% O2, 5% CO2) increased p53 abundance, phosphorylation of p53 on serine 15, and p21 mRNA and protein in parental HCT116 cells that ceased proliferation.	Oxygen	15-17	P53	Homo sapiens	71-74
11568365-5	2001	Hyperoxia (95% O2, 5% CO2) increased p53 abundance, phosphorylation of p53 on serine 15, and p21 mRNA and protein in parental HCT116 cells that ceased proliferation.	Serine	78-84	P53	Homo sapiens	71-74
11568365-8	2001	The observation that p53-dependent induction of p21 prevents exit from G1 and promotes survival during hyperoxia is consistent with the importance of limiting DNA replication during genotoxic stress caused by oxygen exposure.	Oxygen	209-215	P53	Homo sapiens	21-24
11447225-8	2001	Furthermore, although H(2)O(2) strongly induced serine 15 phosphorylation of p53, it failed to induce serine 20 phosphorylation in Plk3-dificient Daudi cells.	Serine	48-54	P53	Homo sapiens	77-80
11447225-0	2001	Reactive oxygen species-induced phosphorylation of p53 on serine 20 is mediated in part by polo-like kinase-3.	Serine	58-64	P53	Homo sapiens	51-54
11470783-0	2001	p53 Phosphorylation at serine 15 is required for transcriptional induction of the plasminogen activator inhibitor-1 (PAI-1) gene by the alkylating agent N-methyl-N"-nitro-N-nitrosoguanidine.	Serine	23-29	P53	Homo sapiens	0-3
11447225-1	2001	Upon exposure of cells to hydrogen peroxide (H(2)O(2)) phosphorylation of p53 was rapidly induced in human fibroblast GM00637, and this phosphorylation occurred on serine 9, serine 15, serine 20, but not on serine 392.	Hydrogen Peroxide	26-43	P53	Homo sapiens	74-77
11470783-5	2001	MNNG induced p53 phosphorylation at serine 15, resulting in stabilization of the p53 protein, and this phosphorylation event was central for p53-dependent PAI-1 transcription.	Serine	36-42	P53	Homo sapiens	13-16
11447225-1	2001	Upon exposure of cells to hydrogen peroxide (H(2)O(2)) phosphorylation of p53 was rapidly induced in human fibroblast GM00637, and this phosphorylation occurred on serine 9, serine 15, serine 20, but not on serine 392.	Serine	164-170	P53	Homo sapiens	74-77
11470783-5	2001	MNNG induced p53 phosphorylation at serine 15, resulting in stabilization of the p53 protein, and this phosphorylation event was central for p53-dependent PAI-1 transcription.	Serine	36-42	P53	Homo sapiens	81-84
11470783-5	2001	MNNG induced p53 phosphorylation at serine 15, resulting in stabilization of the p53 protein, and this phosphorylation event was central for p53-dependent PAI-1 transcription.	Serine	36-42	P53	Homo sapiens	81-84
11447225-1	2001	Upon exposure of cells to hydrogen peroxide (H(2)O(2)) phosphorylation of p53 was rapidly induced in human fibroblast GM00637, and this phosphorylation occurred on serine 9, serine 15, serine 20, but not on serine 392.	Serine	174-180	P53	Homo sapiens	74-77
11447225-1	2001	Upon exposure of cells to hydrogen peroxide (H(2)O(2)) phosphorylation of p53 was rapidly induced in human fibroblast GM00637, and this phosphorylation occurred on serine 9, serine 15, serine 20, but not on serine 392.	Serine	174-180	P53	Homo sapiens	74-77
11447225-1	2001	Upon exposure of cells to hydrogen peroxide (H(2)O(2)) phosphorylation of p53 was rapidly induced in human fibroblast GM00637, and this phosphorylation occurred on serine 9, serine 15, serine 20, but not on serine 392.	Serine	174-180	P53	Homo sapiens	74-77
11447225-2	2001	In addition, H(2)O(2)-induced phosphorylation of p53 was followed by induction of p21, suggesting functional activation of p53.	Hydrogen Peroxide	13-21	P53	Homo sapiens	49-52
11447225-2	2001	In addition, H(2)O(2)-induced phosphorylation of p53 was followed by induction of p21, suggesting functional activation of p53.	Hydrogen Peroxide	13-21	P53	Homo sapiens	123-126
11447225-3	2001	Induction of phosphorylation of p53 on multiple serine residues by H(2)O(2) was caffeine-sensitive and blocked in ATM(-/-) cells.	Serine	48-54	P53	Homo sapiens	32-35
11447225-5	2001	Recombinant His(6)-Plk3 phosphorylated glutathione S-transferase (GST)-p53 fusion protein but not GST alone.	Histidine	12-15	P53	Homo sapiens	71-74
11447225-6	2001	When phoshorylated in vitro by His(6)-Plk3, but not by the kinase-defective mutant His6-Plk3(K52R), GST-p53 was recognized by an antibody specifically to serine 20-phosphorylated p53, indicating that serine 20 is an in vitro target of Plk3.	Histidine	31-34	P53	Homo sapiens	104-107
11447225-6	2001	When phoshorylated in vitro by His(6)-Plk3, but not by the kinase-defective mutant His6-Plk3(K52R), GST-p53 was recognized by an antibody specifically to serine 20-phosphorylated p53, indicating that serine 20 is an in vitro target of Plk3.	Serine	154-160	P53	Homo sapiens	104-107
11447225-6	2001	When phoshorylated in vitro by His(6)-Plk3, but not by the kinase-defective mutant His6-Plk3(K52R), GST-p53 was recognized by an antibody specifically to serine 20-phosphorylated p53, indicating that serine 20 is an in vitro target of Plk3.	Serine	200-206	P53	Homo sapiens	104-107
11447225-7	2001	Also serine 20-phosphorylated p53 was coimmunoprecipitated with Plk3 in cells treated with H(2)O(2).	Serine	5-11	P53	Homo sapiens	30-33
11447225-7	2001	Also serine 20-phosphorylated p53 was coimmunoprecipitated with Plk3 in cells treated with H(2)O(2).	Water	91-96	P53	Homo sapiens	30-33
11562347-4	2001	Dex inhibits the functions of p53 (apoptosis, Bax, and p21(WAF1/CIP1) expression) and GR (PEPCK and G-6-Pase expression).	Dexamethasone	0-3	P53	Homo sapiens	30-33
11559530-1	2001	The expression of genes involved in p53-mediated apoptosis was studied using cDNA microarray after treating isogenic cell lines with either ionizing radiation or doxorubicin.	Doxorubicin	162-173	P53	Homo sapiens	36-39
11562347-3	2001	Dexamethasone (Dex) stimulates the degradation of endogenous GR and p53 by the proteasome pathway in HUVEC under hypoxia and mitomycin C treatments, and also in hepatoma cells (HepG2) under normoxia.	Dexamethasone	0-13	P53	Homo sapiens	68-71
11562347-3	2001	Dexamethasone (Dex) stimulates the degradation of endogenous GR and p53 by the proteasome pathway in HUVEC under hypoxia and mitomycin C treatments, and also in hepatoma cells (HepG2) under normoxia.	Dexamethasone	0-3	P53	Homo sapiens	68-71
11562347-6	2001	Disruption of the p53-HDM2 interaction prevents Dex-induced ubiquitylation of GR and p53.	Dexamethasone	48-51	P53	Homo sapiens	18-21
11562347-6	2001	Disruption of the p53-HDM2 interaction prevents Dex-induced ubiquitylation of GR and p53.	Dexamethasone	48-51	P53	Homo sapiens	85-88
11554164-4	2001	Positivity for p53 was associated with shorter survival in 5-fluorouracil-treated and untreated patients.	Fluorouracil	59-73	P53	Homo sapiens	15-18
11745235-12	2001	Furthermore, higher intracellular accumulations of Dox were found in wt p53 transfectants than that in SKLMS-1 cells.	Doxorubicin	51-54	P53	Homo sapiens	72-75
11745235-13	2001	CONCLUSIONS: Reintroduction of wt p53 into STS cells harboring p53 mutations can enhance their chemosensitivity to Dox through the inhibition of MDR-1 P-gp expression.	Doxorubicin	115-118	P53	Homo sapiens	34-37
11745235-13	2001	CONCLUSIONS: Reintroduction of wt p53 into STS cells harboring p53 mutations can enhance their chemosensitivity to Dox through the inhibition of MDR-1 P-gp expression.	Doxorubicin	115-118	P53	Homo sapiens	63-66
11527429-6	2001	S100A4 had a greater affinity for wild-type or mutant arg-175-his p53 than for non-muscle myosin.	Arginine	54-57	P53	Homo sapiens	66-69
11527429-6	2001	S100A4 had a greater affinity for wild-type or mutant arg-175-his p53 than for non-muscle myosin.	Histidine	62-65	P53	Homo sapiens	66-69
11745235-0	2001	Wild type p53 sensitizes soft tissue sarcoma cells to doxorubicin by down-regulating multidrug resistance-1 expression.	Doxorubicin	54-65	P53	Homo sapiens	10-13
11745235-2	2001	Doxorubicin (Dox) is one of the most active single agents in STS but is less effective in STS with p53 mutations.	Doxorubicin	0-11	P53	Homo sapiens	99-102
11745235-2	2001	Doxorubicin (Dox) is one of the most active single agents in STS but is less effective in STS with p53 mutations.	Doxorubicin	0-3	P53	Homo sapiens	99-102
11745235-3	2001	The effect of reintroducing wild type (wt) p53 into STS cells harboring p53 mutations on the cytotoxicity of DOX in vitro and in vivo was studied.	Doxorubicin	109-112	P53	Homo sapiens	72-75
11745235-8	2001	RESULTS: The 50% inhibitory concentration (IC(50)) of Dox for the SKLMS-1 wt p53 transfectants decreased 16-fold compared with SKLMS-1 parental cells expressing mutant p53.	Doxorubicin	54-57	P53	Homo sapiens	77-80
11745235-8	2001	RESULTS: The 50% inhibitory concentration (IC(50)) of Dox for the SKLMS-1 wt p53 transfectants decreased 16-fold compared with SKLMS-1 parental cells expressing mutant p53.	Doxorubicin	54-57	P53	Homo sapiens	168-171
11745235-9	2001	Colony formation of SKLMS-1 cells after Dox treatment also was inhibited by wt p53 reintroduction.	Doxorubicin	40-43	P53	Homo sapiens	79-82
11522624-0	2001	Mutability of p53 hotspot codons to benzo(a)pyrene diol epoxide (BPDE) and the frequency of p53 mutations in nontumorous human lung.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	36-63	P53	Homo sapiens	14-17
11522624-0	2001	Mutability of p53 hotspot codons to benzo(a)pyrene diol epoxide (BPDE) and the frequency of p53 mutations in nontumorous human lung.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	65-69	P53	Homo sapiens	14-17
11522624-3	2001	In the present study, we have used a highly sensitive mutation assay to determine the p53 mutation load in nontumorous human lung and to study the mutability of p53 codons 157, 248, 249, and 250 to benzo(a)pyrene-diol-epoxide (BPDE), an active metabolite of BP in human bronchial epithelial BEAS-2B cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	227-231	P53	Homo sapiens	161-164
11532872-2	2001	In this study, we used PCR-single strand conformation polymorphism and DNA sequencing to analyze the conserved regions of the p53 gene (exons 5-9) in OSCC tumor specimens from 187 patients with varied histories of betel quid, tobacco and alcohol use.	Alcohols	238-245	P53	Homo sapiens	126-129
11532872-5	2001	However, alcohol drinkers exhibited a significantly higher incidence (57/101, 56.44%) of p53 mutations than non-users (39.53%, 34/86) (P = 0.02).	Alcohols	9-16	P53	Homo sapiens	89-92
11780391-6	2001	ATRA might induce p21WAF1/CIP1 expression in ATRA-sensitive cell lines through p53-dependent and p53-independent pathways.	Tretinoin	0-4	P53	Homo sapiens	79-82
11532872-6	2001	The effect of alcohol on the incidence of p53 mutations was still statistically significant (RR = 2.24; 95% CI, 1.21-4.15) after adjustment for cigarette smoking and betel quid (BQ) chewing.	Alcohols	14-21	P53	Homo sapiens	42-45
11780391-6	2001	ATRA might induce p21WAF1/CIP1 expression in ATRA-sensitive cell lines through p53-dependent and p53-independent pathways.	Tretinoin	0-4	P53	Homo sapiens	97-100
11559355-0	2001	Hydrogen exchange of the tetramerization domain of the human tumour suppressor p53 probed by denaturants and temperature.	Hydrogen	0-8	P53	Homo sapiens	79-82
11559355-1	2001	We have analysed the hydrogen/deuterium exchange of the tetramerization domain of human tumour suppressor p53 under mild chemical denaturation conditions, and at different temperatures.	Hydrogen	21-29	P53	Homo sapiens	106-109
11494044-4	2001	Results show that p53 protein becomes phosphorylated at serine 15 (Ser15) and Ser392 residues after treatment with MMS in a time-dependent manner.	Serine	56-62	P53	Homo sapiens	18-21
11774736-6	2001	p53 gene transduction markedly enhanced the sensitivity to cisplatin (CDDP) and CDDP-induced apoptosis, but did not affect the sensitivity to paclitaxel (PTX) nor PTX-induced apoptosis in ovarian cancer cells without p53 gene.	Cisplatin	59-68	P53	Homo sapiens	0-3
11774736-6	2001	p53 gene transduction markedly enhanced the sensitivity to cisplatin (CDDP) and CDDP-induced apoptosis, but did not affect the sensitivity to paclitaxel (PTX) nor PTX-induced apoptosis in ovarian cancer cells without p53 gene.	Cisplatin	70-74	P53	Homo sapiens	0-3
11774736-6	2001	p53 gene transduction markedly enhanced the sensitivity to cisplatin (CDDP) and CDDP-induced apoptosis, but did not affect the sensitivity to paclitaxel (PTX) nor PTX-induced apoptosis in ovarian cancer cells without p53 gene.	Cisplatin	80-84	P53	Homo sapiens	0-3
11774736-7	2001	The combination treatment with a recombinant adenovirus carrying a wild-type p53 gene (AxCAp53) and CDDP significantly suppressed tumor growth of ovarian cancer cells with and without p53 gene, compared with a single treatment of either AxCAp53 or CDDP in ovarian cancer xenograft.	Cisplatin	248-252	P53	Homo sapiens	77-80
11774736-7	2001	The combination treatment with a recombinant adenovirus carrying a wild-type p53 gene (AxCAp53) and CDDP significantly suppressed tumor growth of ovarian cancer cells with and without p53 gene, compared with a single treatment of either AxCAp53 or CDDP in ovarian cancer xenograft.	Cisplatin	248-252	P53	Homo sapiens	91-94
11774736-10	2001	In conclusion, p53 gene status contributes the sensitivity to CDDP in ovarian cancer.	Cisplatin	62-66	P53	Homo sapiens	15-18
11774736-11	2001	Additionally, combination treatment of p53 gene transduction and CDDP may be an effective therapeutic modality for ovarian cancer without wild-type p53 gene.	Cisplatin	65-69	P53	Homo sapiens	148-151
11522376-0	2001	Induction of apoptotic cell death by a p53-independent pathway in neuronal SK-N-MC cells after treatment with 2,2",5,5"-tetrachlorobiphenyl.	sk-n-mc	75-82	P53	Homo sapiens	39-42
11406618-0	2001	Neurons are protected from excitotoxic death by p53 antisense oligonucleotides delivered in anionic liposomes.	Oligonucleotides	62-78	P53	Homo sapiens	48-51
12536724-2	2001	METHODS: SP immunohistochemical technique was used to detect the expressions of of p-MAPK, cyclin D1 and p53 protein among the 58 osteosarcomas and 14 osteoid osteomas samples.	TFF2 protein, human	9-11	P53	Homo sapiens	105-108
11406618-5	2001	Exposure of hippocampal neurons to glutamate increased p53 protein expression 4-fold and decreased neuronal survival to approximately 35%.	Glutamic Acid	35-44	P53	Homo sapiens	55-58
11406618-6	2001	Treatment with 1 microm p53 antisense oligonucleotides in anionic liposomes prevented glutamate-induced up-regulation of p53 and increased neuronal survival to approximately 75%.	Oligonucleotides	38-54	P53	Homo sapiens	24-27
11406618-6	2001	Treatment with 1 microm p53 antisense oligonucleotides in anionic liposomes prevented glutamate-induced up-regulation of p53 and increased neuronal survival to approximately 75%.	Oligonucleotides	38-54	P53	Homo sapiens	121-124
11406618-6	2001	Treatment with 1 microm p53 antisense oligonucleotides in anionic liposomes prevented glutamate-induced up-regulation of p53 and increased neuronal survival to approximately 75%.	Glutamic Acid	86-95	P53	Homo sapiens	24-27
11406618-6	2001	Treatment with 1 microm p53 antisense oligonucleotides in anionic liposomes prevented glutamate-induced up-regulation of p53 and increased neuronal survival to approximately 75%.	Glutamic Acid	86-95	P53	Homo sapiens	121-124
11406618-7	2001	Encapsulated phosphorothioate p53 antisense oligonucleotides were neuroprotective at 5-10-fold lower concentrations than when unencapsulated.	Oligonucleotides	44-60	P53	Homo sapiens	30-33
11406618-9	2001	p53 antisense oligonucleotides complexed with cationic liposomes were ineffective.	Oligonucleotides	14-30	P53	Homo sapiens	0-3
11526498-0	2001	Activation of p53 transcriptional activity requires ATM"s kinase domain and multiple N-terminal serine residues of p53.	Serine	96-102	P53	Homo sapiens	14-17
11406618-10	2001	Neuroprotection by p53 antisense oligonucleotides in anionic liposomes was comparable with that by glutamate receptor antagonists and a chemical inhibitor of p53.	Oligonucleotides	33-49	P53	Homo sapiens	19-22
11526498-0	2001	Activation of p53 transcriptional activity requires ATM"s kinase domain and multiple N-terminal serine residues of p53.	Serine	96-102	P53	Homo sapiens	115-118
11493433-4	2001	These pathways are themselves influenced by a number of lipid products (diacylglycerol, sphingosine-1 phosphate, and glucosyl ceramide), reactive oxygen species, oncogenes (such as the tumor suppressor gene p53), protein kinases (protein kinase C and phosphoinositide-3 kinase), and external stimuli (hematopoietic growth factors and the extracellular matrix).	Glucosylceramides	117-134	P53	Homo sapiens	207-210
11526498-8	2001	However, double mutations of either serines 15 and 20 or serines 33 and 37 blocked the ability of ATM to activate p53.	Serine	36-43	P53	Homo sapiens	114-117
11526498-8	2001	However, double mutations of either serines 15 and 20 or serines 33 and 37 blocked the ability of ATM to activate p53.	Serine	57-64	P53	Homo sapiens	114-117
11526498-10	2001	In addition, activation of p53 by ATM requires multiple serine residues in p53"s transactivation domain.	Serine	56-62	P53	Homo sapiens	27-30
11526498-10	2001	In addition, activation of p53 by ATM requires multiple serine residues in p53"s transactivation domain.	Serine	56-62	P53	Homo sapiens	75-78
11493433-4	2001	These pathways are themselves influenced by a number of lipid products (diacylglycerol, sphingosine-1 phosphate, and glucosyl ceramide), reactive oxygen species, oncogenes (such as the tumor suppressor gene p53), protein kinases (protein kinase C and phosphoinositide-3 kinase), and external stimuli (hematopoietic growth factors and the extracellular matrix).	Reactive Oxygen Species	137-160	P53	Homo sapiens	207-210
11481424-7	2001	Furthermore, p33ING2 expression increases the acetylation of p53 at Lys-382.	Lysine	68-71	P53	Homo sapiens	61-64
11390388-1	2001	Electrophilic eicosanoids of the J series, with their distinctive cross-conjugated alpha,beta-unsaturated ketone, inactivate genetically wild type tumor suppressor p53 in a manner analogous to prostaglandins of the A series.	Eicosanoids	14-25	P53	Homo sapiens	164-167
11390388-1	2001	Electrophilic eicosanoids of the J series, with their distinctive cross-conjugated alpha,beta-unsaturated ketone, inactivate genetically wild type tumor suppressor p53 in a manner analogous to prostaglandins of the A series.	Prostaglandins	193-207	P53	Homo sapiens	164-167
11498783-7	2001	Although the basal mRNA levels of these genes did not depend on the presence of p53, we observed a p53-dependent induction of all these targets in response to gamma-irradiation and a p53-independent regulation for p21 and KILLER/DR5 in response to dexamethasone.	Dexamethasone	248-261	P53	Homo sapiens	99-102
11390388-2	2001	Like the prostaglandins of the A series, prostaglandins of the J series have a structural determinant (endocyclic cyclopentenone) that confers the ability to impair the conformation, the phosphorylation, and the transcriptional activity of the p53 tumor suppressor with equivalent potency and efficacy.	Prostaglandins	41-55	P53	Homo sapiens	244-247
11390388-4	2001	In seeking to understand how J series prostaglandins cause apoptosis despite their inactivation of p53, we discovered that they inhibit the ubiquitin isopeptidase activity of the proteasome pathway.	Prostaglandins	38-52	P53	Homo sapiens	99-102
11521201-4	2001	We observed that an unmodified C-terminus was required for the suppression of apoptosis by the p53 135(Ala to Val) oncogenic p53 mutant.	Alanine	103-106	P53	Homo sapiens	95-98
11521201-4	2001	We observed that an unmodified C-terminus was required for the suppression of apoptosis by the p53 135(Ala to Val) oncogenic p53 mutant.	Alanine	103-106	P53	Homo sapiens	125-128
11498783-7	2001	Although the basal mRNA levels of these genes did not depend on the presence of p53, we observed a p53-dependent induction of all these targets in response to gamma-irradiation and a p53-independent regulation for p21 and KILLER/DR5 in response to dexamethasone.	Dexamethasone	248-261	P53	Homo sapiens	99-102
11771346-6	2001	Moreover, there was also an interesting correlation between the degree of positivity to p53 and exposure to smoke, and to a lesser extent to alcohol, in the oncological patients.	Alcohols	141-148	P53	Homo sapiens	88-91
11505395-2	2001	This combination also enhanced sensitivity to paclitaxel in a bcl-2 and mutant p53 expressing renal carcinoma cell line.	Paclitaxel	46-56	P53	Homo sapiens	79-82
11470744-6	2001	An increase in p53 phosphorylated on serine 15 accompanied the rise in p21 (cip-1).	Serine	37-43	P53	Homo sapiens	15-18
11554448-3	2001	p53 is a zinc-binding protein containing several reactive cysteines, and its key biochemical property, sequence-specific DNA binding, is dependent upon metal and redox regulation in vitro.	Cysteine	58-67	P53	Homo sapiens	0-3
11554448-3	2001	p53 is a zinc-binding protein containing several reactive cysteines, and its key biochemical property, sequence-specific DNA binding, is dependent upon metal and redox regulation in vitro.	Metals	152-157	P53	Homo sapiens	0-3
11554448-4	2001	In this review, we describe the main features of p53 as a metalloprotein and we discuss how metal binding and oxidation-reduction may affect p53 activity in vivo.	Metals	58-63	P53	Homo sapiens	49-52
11554448-8	2001	In this network, p53 can control the timely production of reactive oxygen intermediates (e.g., to initiate apoptosis), but this activity is itself under the control of changes in metal levels and in cellular redox status.	Metals	179-184	P53	Homo sapiens	17-20
11483405-0	2001	Transcription factors p53 and HIF-1alpha as targets of nitric oxide.	Nitric Oxide	55-67	P53	Homo sapiens	22-25
11561778-0	2001	Reversal of cytosine arabinoside (ara-C) resistance by the synergistic combination of 6-thioguanine plus ara-C plus PEG-asparaginase (TGAP) in human leukemia lines lacking or expressing p53 protein.	Thioguanine	86-99	P53	Homo sapiens	186-189
11445851-3	2001	To characterize the involvement of the p53 gene abnormality in this disease, we analyzed expression and sequence alteration of p53 by immunohistochemical analysis of the protein expression and quantitative DNA/PCR and PCR-SSCP assays of the gene in 28 paraffin-embedded tissue specimens.	Paraffin	252-260	P53	Homo sapiens	127-130
11483519-2	2001	A core domain mutant p53 (143 Val to Ala), in which two N-terminal residues (22 and 23) essential for transactivation were also mutated (Leu to Glu and Trp to Ser, respectively), was examined.	Serine	159-162	P53	Homo sapiens	21-24
11445854-2	2001	Apoptotic inductions in MKN-45 and MKN-74 were stronger than those in MKN-28 and KATO-III, suggesting that wild-type p53 may contribute to the induction of apoptosis.	MKN	24-27	P53	Homo sapiens	117-120
11445854-9	2001	In conclusion, our observations suggested that p53 mutation may be associated with apoptotic induction by 5-FU; however, p53 status may not strongly affect TS induction by 5-FU.	Fluorouracil	106-110	P53	Homo sapiens	47-50
11551417-6	2001	Cisplatin treatment dramatically increased p53 expression in parental cells but not in H460/CIS cells which expressed basal levels of p53.	Cisplatin	0-9	P53	Homo sapiens	43-46
11458051-0	2001	Functional p53 mutation as a molecular determinant of paclitaxel and gemcitabine susceptibility in human bladder cancer.	Paclitaxel	54-64	P53	Homo sapiens	11-14
11458051-4	2001	Susceptibility of these inducible p53 TCC cells to paclitaxel and gemcitabine induced cytotoxicity was evaluated and kill significance determined between sub-lethal and lethal doses.	Paclitaxel	51-61	P53	Homo sapiens	34-37
11458051-5	2001	RESULTS: Significant paclitaxel dose dependent cytotoxicity was observed in J82 TCC cells lacking normal p53 and tsp53 transfected cells at 37C, which was the mutant p53 temperature in transfectants between maximal and minimal kill concentrations for either (p &lt;0.001).	Paclitaxel	21-31	P53	Homo sapiens	105-108
11458051-5	2001	RESULTS: Significant paclitaxel dose dependent cytotoxicity was observed in J82 TCC cells lacking normal p53 and tsp53 transfected cells at 37C, which was the mutant p53 temperature in transfectants between maximal and minimal kill concentrations for either (p &lt;0.001).	Paclitaxel	21-31	P53	Homo sapiens	115-118
11458051-8	2001	CONCLUSIONS: Paclitaxel requires functionally mutated p53 to induce cell death in human bladder cells, indicating that it may be more effective against TCC with p53 mutations than against TCC, which lacks p53 abnormalities, while gemcitabine is effective regardless of p53 function.	Paclitaxel	13-23	P53	Homo sapiens	54-57
11458051-8	2001	CONCLUSIONS: Paclitaxel requires functionally mutated p53 to induce cell death in human bladder cells, indicating that it may be more effective against TCC with p53 mutations than against TCC, which lacks p53 abnormalities, while gemcitabine is effective regardless of p53 function.	Paclitaxel	13-23	P53	Homo sapiens	161-164
11458051-8	2001	CONCLUSIONS: Paclitaxel requires functionally mutated p53 to induce cell death in human bladder cells, indicating that it may be more effective against TCC with p53 mutations than against TCC, which lacks p53 abnormalities, while gemcitabine is effective regardless of p53 function.	Paclitaxel	13-23	P53	Homo sapiens	161-164
11458051-8	2001	CONCLUSIONS: Paclitaxel requires functionally mutated p53 to induce cell death in human bladder cells, indicating that it may be more effective against TCC with p53 mutations than against TCC, which lacks p53 abnormalities, while gemcitabine is effective regardless of p53 function.	Paclitaxel	13-23	P53	Homo sapiens	161-164
11551417-6	2001	Cisplatin treatment dramatically increased p53 expression in parental cells but not in H460/CIS cells which expressed basal levels of p53.	Cisplatin	0-9	P53	Homo sapiens	134-137
11568584-0	2001	All-trans-retinoic acid enhances the effect of adenovirus-mediated wild-type p53 gene transfer in head and neck squamous cell carcinoma.	Tretinoin	0-23	P53	Homo sapiens	77-80
11448240-6	2001	WTK1 cells (mutant TP53) were more resistant to the cytotoxic effects of both gamma rays and (56)Fe particles, but showed greater cytogenetic and mutagenic damage than TK6 cells (TP53(+)).	Iron	97-99	P53	Homo sapiens	19-23
11505223-4	2001	In cultured lymphocytes treated with 2.5 microM BPDE for 18 h, increased levels of p53 were found, which were positively related to BPDE-DNA adduct levels assessed by ICC (rs = 0.66, P &lt; 0.001) and 32P-postlabelling (rs = 0.56, P &lt; 0.001) and appeared to be higher in GSTM1(-/-) than in GSTM1(+) subjects (P = 0.003).	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	48-52	P53	Homo sapiens	83-86
11505223-4	2001	In cultured lymphocytes treated with 2.5 microM BPDE for 18 h, increased levels of p53 were found, which were positively related to BPDE-DNA adduct levels assessed by ICC (rs = 0.66, P &lt; 0.001) and 32P-postlabelling (rs = 0.56, P &lt; 0.001) and appeared to be higher in GSTM1(-/-) than in GSTM1(+) subjects (P = 0.003).	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	132-136	P53	Homo sapiens	83-86
11602059-7	2001	Cytotoxicity assays revealed that the wt-p53 transfectants were more sensitive to doxorubicin and mitomycin compared with the pNeo transformants.	Doxorubicin	82-93	P53	Homo sapiens	41-44
11602059-8	2001	Flow cytometry showed that the accumulation of doxorubicin in wt-p53 transfectants was as 13 times as that of the pNeo transformants.	Doxorubicin	47-58	P53	Homo sapiens	65-68
11454885-2	2001	HER2, epidermal growth factor receptor (EGFR), and p53 have all been suggested as possible markers of tamoxifen resistance.	Tamoxifen	102-111	P53	Homo sapiens	51-54
11331294-4	2001	Here we show that the expression of PP5, an evolutionarily conserved Ser/Thr phosphatase that functions as an inhibitor of glucocorticoid- and p53-induced signaling cascades leading to growth suppression, is responsive to 17beta-estradiol (E(2)) in ER-positive human breast carcinoma cells (MCF-7).	Estradiol	222-238	P53	Homo sapiens	143-146
11454885-3	2001	The aim of this study was to investigate interactions between adjuvant treatment with tamoxifen and the content of EGFR, HER2, and p53 in steroid receptor-positive patients.	Tamoxifen	86-95	P53	Homo sapiens	131-134
11454885-9	2001	Patients with steroid receptor-positive tumors and positive immunohistochemical staining for HER2, EGFR or p53 benefited from treatment with tamoxifen for 1 year, although the latter variable contained independent prognostic information by itself.	Tamoxifen	141-150	P53	Homo sapiens	107-110
11449307-2	2001	The purpose of the present study was to analyze the expression of the oncogenes c-erbB-2 and c-myc and of the suppressor gene p53 by immunohistochemical techniques in archival paraffin-embedded tissue blocks of 48 male breast cancer patients, treated at the A.C. Camargo Cancer Hospital, Sao Paulo, SP, Brazil.	Paraffin	176-184	P53	Homo sapiens	126-129
11429426-2	2001	A recent report suggests that a polymorphism of the p53 tumour suppressor gene that results in the substitution of a proline residue with an arginine residue at position 72 of the p53 protein might act as a risk factor in HPV associated malignancies.	Arginine	141-149	P53	Homo sapiens	52-55
11522280-5	2001	p53 content of MCF-7 breast cancer cells (wild-type) was increased by caffeic acid, decreased by resveratrol, and showed a twofold increase with catechin, that reached borderline statistical significance; however, none of these effects were dose-responsive.	Resveratrol	97-108	P53	Homo sapiens	0-3
11522280-5	2001	p53 content of MCF-7 breast cancer cells (wild-type) was increased by caffeic acid, decreased by resveratrol, and showed a twofold increase with catechin, that reached borderline statistical significance; however, none of these effects were dose-responsive.	Catechin	145-153	P53	Homo sapiens	0-3
11522280-6	2001	Colo 320 HSR (+) cells (with a mutant p53 gene) had lower p53 content upon stimulation, reaching borderline statistical significance, but without being dose-responsive, in the presence of caffeic acid and resveratrol.	Resveratrol	205-216	P53	Homo sapiens	38-41
11431734-6	2001	Ectopic expression of transcriptionally active p53 alone was not sufficient for the activation of apoptosis in p53-null Hep3B cells, but apoptosis was induced when endogenous Bcl-xL was simultaneously inhibited by antisense oligonucleotide in these cells.	Oligonucleotides	224-239	P53	Homo sapiens	47-50
11395250-0	2001	High linear energy transfer carbon radiation effectively kills cultured glioma cells with either mutant or wild-type p53.	Carbon	28-34	P53	Homo sapiens	117-120
11395250-8	2001	The effects of the carbon beams were not dependent on the p53 gene status but were reduced by G(1) arrest, which was independent of p21 expression.	Carbon	19-25	P53	Homo sapiens	58-61
11471984-1	2001	The objective was to test the hypothesis that wild-type p53-function is required for the enhancement of the cytotoxicity of cis-diammine-dichloroplatinum(II) (cDDP) cytotoxicity by hyperthermia (HT).	Cisplatin	124-157	P53	Homo sapiens	56-59
11471984-1	2001	The objective was to test the hypothesis that wild-type p53-function is required for the enhancement of the cytotoxicity of cis-diammine-dichloroplatinum(II) (cDDP) cytotoxicity by hyperthermia (HT).	Cisplatin	159-163	P53	Homo sapiens	56-59
11429426-2	2001	A recent report suggests that a polymorphism of the p53 tumour suppressor gene that results in the substitution of a proline residue with an arginine residue at position 72 of the p53 protein might act as a risk factor in HPV associated malignancies.	Arginine	141-149	P53	Homo sapiens	180-183
11429426-7	2001	RESULTS: The proportions of p53 codon 72 genotypes found were 78% arginine homozygous, 2% proline homozygous, and 20% heterozygous among patients with skin cancer and 79% arginine homozygous, 3.5% proline homozygous, and 17.5% heterozygous among the control population.	Arginine	66-74	P53	Homo sapiens	28-31
11390204-10	2001	However, in the presence of melatonin, this apoptotic population decreased up to 4.5% at 10(-5) M. The p53 and p21 protein levels of skin fibroblasts increased 4 h after 8 Gy irradiation, but melatonin pretreatment did not change those levels.	Melatonin	28-37	P53	Homo sapiens	103-106
11429426-7	2001	RESULTS: The proportions of p53 codon 72 genotypes found were 78% arginine homozygous, 2% proline homozygous, and 20% heterozygous among patients with skin cancer and 79% arginine homozygous, 3.5% proline homozygous, and 17.5% heterozygous among the control population.	Arginine	171-179	P53	Homo sapiens	28-31
11390204-10	2001	However, in the presence of melatonin, this apoptotic population decreased up to 4.5% at 10(-5) M. The p53 and p21 protein levels of skin fibroblasts increased 4 h after 8 Gy irradiation, but melatonin pretreatment did not change those levels.	Melatonin	192-201	P53	Homo sapiens	103-106
11699407-3	2001	Fluorescent OL(1) p53, was used to demonstrate oligonucleotide uptake and retention by the WMN cells.	Oligonucleotides	47-62	P53	Homo sapiens	18-21
11435891-0	2001	Various forms of mutant p53 confer sensitivity to cisplatin and doxorubicin in bladder cancer cells.	Cisplatin	50-59	P53	Homo sapiens	24-27
11435891-0	2001	Various forms of mutant p53 confer sensitivity to cisplatin and doxorubicin in bladder cancer cells.	Doxorubicin	64-75	P53	Homo sapiens	24-27
11435891-7	2001	RESULTS: The expression of all forms of mutant p53 protein except p53His273 enhanced sensitivity to cisplatin and doxorubicin.	Cisplatin	100-109	P53	Homo sapiens	47-50
11435891-7	2001	RESULTS: The expression of all forms of mutant p53 protein except p53His273 enhanced sensitivity to cisplatin and doxorubicin.	Cisplatin	100-109	P53	Homo sapiens	66-69
11435891-7	2001	RESULTS: The expression of all forms of mutant p53 protein except p53His273 enhanced sensitivity to cisplatin and doxorubicin.	Doxorubicin	114-125	P53	Homo sapiens	47-50
11435891-7	2001	RESULTS: The expression of all forms of mutant p53 protein except p53His273 enhanced sensitivity to cisplatin and doxorubicin.	Doxorubicin	114-125	P53	Homo sapiens	66-69
11518751-3	2001	PCR/direct sequencing analysis revealed the presence of a nucleotide substitution, AGC (Ser) to AGG (Arg), at codon 106 of the p53 gene in DNA from non-cancerous breast tissue.	Serine	88-91	P53	Homo sapiens	127-130
11518751-3	2001	PCR/direct sequencing analysis revealed the presence of a nucleotide substitution, AGC (Ser) to AGG (Arg), at codon 106 of the p53 gene in DNA from non-cancerous breast tissue.	Arginine	101-104	P53	Homo sapiens	127-130
11699407-9	2001	Therefore, synergistic cytotoxicity of Idarubicin for lymphoma cells treated with an oligonucleotide targeting p53 message was demonstrated at oligonucleotide and Idarubicin concentrations which were minimally toxic to hematopoietic progenitor cells.	Oligonucleotides	85-100	P53	Homo sapiens	111-114
11699407-9	2001	Therefore, synergistic cytotoxicity of Idarubicin for lymphoma cells treated with an oligonucleotide targeting p53 message was demonstrated at oligonucleotide and Idarubicin concentrations which were minimally toxic to hematopoietic progenitor cells.	Oligonucleotides	143-158	P53	Homo sapiens	111-114
11511362-2	2001	Cell death induced by DNA double-strand breaks (DSBs), as well as Ser46 phosphorylation of p53 and induction of p53AIP1, were blocked when we inhibited expression of p53DINP1 by means of an antisense oligonucleotide.	Oligonucleotides	200-215	P53	Homo sapiens	91-94
11439344-0	2001	Low concentrations of paclitaxel induce cell type-dependent p53, p21 and G1/G2 arrest instead of mitotic arrest: molecular determinants of paclitaxel-induced cytotoxicity.	Paclitaxel	22-32	P53	Homo sapiens	60-63
11409876-0	2001	Nuclear extracellular signal-regulated kinase 2 phosphorylates p53 at Thr55 in response to doxorubicin.	Doxorubicin	91-102	P53	Homo sapiens	63-66
11409876-1	2001	In this study, we showed that nuclear ERK2 phosphorylates p53 at Thr55 in response to doxorubicin.	Doxorubicin	86-97	P53	Homo sapiens	58-61
11410793-5	2001	Furthermore, p53 overexpression by tumors was almost twice as common in the RSCM group as in the RSCB group.	rscb	97-101	P53	Homo sapiens	13-16
11439344-5	2001	Furthermore, we observed that the levels of p53 and p21 induced by adriamycin and by low concentrations of PTX in A549 cells were comparable.	Doxorubicin	67-77	P53	Homo sapiens	44-47
11439344-3	2001	At these low concentrations that are insufficient to inhibit mitotic progression, PTX induced both p53 and p21 causing G1 and G2 arrest in A549.	Paclitaxel	82-85	P53	Homo sapiens	99-102
11439344-5	2001	Furthermore, we observed that the levels of p53 and p21 induced by adriamycin and by low concentrations of PTX in A549 cells were comparable.	Paclitaxel	107-110	P53	Homo sapiens	44-47
11439344-6	2001	This observation led us to conclude that low concentrations of PTX can induce p53 and p21 sufficiently to cause G1 and G2.	Paclitaxel	63-66	P53	Homo sapiens	78-81
11406570-0	2001	c-myc/p53 interaction determines sensitivity of human colon carcinoma cells to 5-fluorouracil in vitro and in vivo.	Fluorouracil	79-93	P53	Homo sapiens	6-9
11406570-6	2001	Finally, the in vitro data predicted that only patients with both amplified c-myc and wild-type p53 in their primary tumors would be responsive to 5FU-based therapy, which was borne out by analysis of tumors from 135 patients entered into a Phase III clinical trial of 5FU-based adjuvant therapy.	Fluorouracil	147-150	P53	Homo sapiens	96-99
11375905-3	2001	In this study we have investigated the effect of bile acids on the tumor suppressor p53 using the human colon tumor cell line HCT116, which retains the wild-type p53 gene and functional p53 signaling in response to DNA damage.	Bile Acids and Salts	49-59	P53	Homo sapiens	84-87
11323100-1	2001	In esophageal squamous cell carcinoma (SCC), we used immunohistochemical analysis to further elucidate the correlation of p53 protein expression with clinicopathological factors, as well as with risk factors, such as tobacco smoking, alcohol consumption and a family history of cancer, using odds ratios (ORs).	Alcohols	234-241	P53	Homo sapiens	122-125
11323100-6	2001	The esophageal SCC in either smokers or alcohol users was 4.67-5.83 times more likely to express p53 protein, while the likelihood of p53 expression in patients who use both tobacco and alcohol was more than 14.0 times.	Alcohols	40-47	P53	Homo sapiens	97-100
11323100-6	2001	The esophageal SCC in either smokers or alcohol users was 4.67-5.83 times more likely to express p53 protein, while the likelihood of p53 expression in patients who use both tobacco and alcohol was more than 14.0 times.	Alcohols	186-193	P53	Homo sapiens	134-137
11323100-9	2001	In contrast, tobacco smoking and alcohol consumption were shown to be strongly associated with p53 mutations in esophageal carcinogenesis.	Alcohols	33-40	P53	Homo sapiens	95-98
11409938-8	2001	Experiments with 32P-labeled DNA fragments obtained from the human p53 tumor suppressor gene and the c-Ha-ras-1 protooncogene suggested that KBrO3 induced 8-oxodG formation at 5"-site guanine of GG and GGG sequences of double-stranded DNA in the presence of GSH and that treatment of formamidopyrimidine-DNA glycosylase led to chain cleavages at the guanine residues.	kbro3	141-146	P53	Homo sapiens	67-70
11397945-3	2001	We identified a previously unknown nuclear export signal (NES) in the amino terminus of p53, spanning residues 11 to 27 and containing two serine residues phosphorylated after DNA damage, which was required for p53 nuclear export in colloboration with the carboxyl-terminal NES.	Serine	139-145	P53	Homo sapiens	88-91
11397945-3	2001	We identified a previously unknown nuclear export signal (NES) in the amino terminus of p53, spanning residues 11 to 27 and containing two serine residues phosphorylated after DNA damage, which was required for p53 nuclear export in colloboration with the carboxyl-terminal NES.	Serine	139-145	P53	Homo sapiens	211-214
11397945-4	2001	Serine-15-phosphorylated p53 induced by ultraviolet irradiation was not exported.	Serine	0-6	P53	Homo sapiens	25-28
11423996-3	2001	To study genes activated in the p53 induced apoptotic process, we used a mouse myeloid leukemic cell line (LTR6) expressing the temperature-sensitive p53 (val135) that undergoes apoptosis upon shifting the temperature to 32 degrees C. We analysed the gene expression profile at different time points after p53 activation using oligonucleotide microarray capable of detecting approximately 11,000 mRNA species.	Oligonucleotides	327-342	P53	Homo sapiens	150-153
11484952-6	2001	RESULTS: Expression of both p53 and Rb correlated with survival benefit after 5-FU treatment.	Fluorouracil	78-82	P53	Homo sapiens	28-31
11384107-4	2001	IC(50)to cisplatin (CDDP) was 12.9 microM for SK-OV-3 cells and 9.2 microM for p53 gene-transducted SK-OV-3 cells.	Cisplatin	9-18	P53	Homo sapiens	79-82
11384107-4	2001	IC(50)to cisplatin (CDDP) was 12.9 microM for SK-OV-3 cells and 9.2 microM for p53 gene-transducted SK-OV-3 cells.	Cisplatin	20-24	P53	Homo sapiens	79-82
11384107-6	2001	Additionally, p53 gene transduction significantly enhanced CDDP-induced apoptosis.	Cisplatin	59-63	P53	Homo sapiens	14-17
11384107-8	2001	In SK-OV-3 cells with transduction of the p53 gene, the expression of p53 and Bax proteins increased after exposure to CDDP.	Cisplatin	119-123	P53	Homo sapiens	42-45
11384107-8	2001	In SK-OV-3 cells with transduction of the p53 gene, the expression of p53 and Bax proteins increased after exposure to CDDP.	Cisplatin	119-123	P53	Homo sapiens	70-73
11401911-3	2001	A G to T transversion at codon 249 of the p53 gene (249(ser)) is commonly found in HCCs from patients in regions with dietary aflatoxin exposure.	Serine	56-59	P53	Homo sapiens	42-45
11401911-4	2001	Because HBV infection is often endemic in high aflatoxin exposure areas, it is still unclear whether HBV acts as a confounder or as a synergistic partner in the development of the 249(ser) p53 mutation.	Serine	184-187	P53	Homo sapiens	189-192
11697035-1	2001	The mechanism of metal-mediated DNA damage by carcinogenic danthron (1,8-dihydroxyanthraquinone) and anthraquinone was investigated by the DNA sequencing technique using 32P-labeled human DNA fragments obtained from the human c-Ha-ras-1 protooncogene and the p53 tumor suppressor gene.	Metals	17-22	P53	Homo sapiens	259-262
26680792-9	2001	CONCLUSION: These findings suggest that Arg/Arg homozygocity of the p53 codon 72 would be a protective factor against the development of cervical adenocarcinoma.	Arginine	40-43	P53	Homo sapiens	68-71
26680792-9	2001	CONCLUSION: These findings suggest that Arg/Arg homozygocity of the p53 codon 72 would be a protective factor against the development of cervical adenocarcinoma.	Arginine	44-47	P53	Homo sapiens	68-71
11484935-2	2001	We found that four anticancer agents: etoposide, doxorubicin, bleomycin and paclitaxel induced apoptosis in human umbilical vein endothelial cells (HUVECs) (as judged by DNA fragmentation) with a time- and concentration-dependent decrease in bcl-2 protein but without the involvement of p53.	Doxorubicin	49-60	P53	Homo sapiens	287-290
11484935-2	2001	We found that four anticancer agents: etoposide, doxorubicin, bleomycin and paclitaxel induced apoptosis in human umbilical vein endothelial cells (HUVECs) (as judged by DNA fragmentation) with a time- and concentration-dependent decrease in bcl-2 protein but without the involvement of p53.	Paclitaxel	76-86	P53	Homo sapiens	287-290
11465510-3	2001	In order to determine if the genotype of the p53 donor or the genotype of the sp donor determined the binding efficiency, p53 expression was induced by retinoic acid and sp synthesis by bleomycin.	Tretinoin	152-165	P53	Homo sapiens	122-125
11358908-10	2001	All tumour regions showed a point mutation in p53 gene at exon 7 (GGC (glycine)--&gt;GTC (valine) at codon 245).	Glycine	71-78	P53	Homo sapiens	46-49
11376010-2	2001	Here we report that a transient inhibition of spindle assembly induced by nocodazole, a tubulin-depolymerizing drug, triggers a stable activation of p53, which can transduce a cell cycle inhibitory signal even when the spindle-damaging agent is removed and the spindle is allowed to reassemble.	Nocodazole	74-84	P53	Homo sapiens	149-152
11358908-11	2001	The distal portion of the duodenal tumour showed an additional point mutation in p53 gene at exon 5 (GCC (alanine)--&gt;GTC (valine) at codon 129).	Alanine	106-113	P53	Homo sapiens	81-84
11340581-12	2001	However, in other p53-deficient cells (osteosarcoma SAOS), taxane treatment was associated with hyperploid progression and the introduction of wild-type p53 resulted in a reduced sensivity.	taxane	59-65	P53	Homo sapiens	18-21
11340581-13	2001	Although our approach does not allow definitive conclusions, these results suggest that loss of p53-dependent post-mitotic checkpoint results in a different time-course of taxane-induced cell death following DNA reduplication.	taxane	172-178	P53	Homo sapiens	96-99
11340581-0	2001	A role for loss of p53 function in sensitivity of ovarian carcinoma cells to taxanes.	Taxoids	77-84	P53	Homo sapiens	19-22
11340581-1	2001	Loss of p53 function has been linked to increased responsiveness to taxane treatment of ovarian carcinoma in clinical studies.	taxane	68-74	P53	Homo sapiens	8-11
11340581-2	2001	We recently reported that the acquisition of cisplatin resistance in an ovarian carcinoma cell line (IGROV-1) was associated with mutation of p53 and collateral sensitivity to paclitaxel.	Cisplatin	45-54	P53	Homo sapiens	142-145
11376010-3	2001	Cells transiently exposed to nocodazole continue to express high levels of p53 and p21 in the cell cycle that follows the transient exposure to nocodazole and become arrested in G(1), regardless of whether they carry a diploid or polyploid genome after mitotic exit.	Nocodazole	29-39	P53	Homo sapiens	75-78
11376010-3	2001	Cells transiently exposed to nocodazole continue to express high levels of p53 and p21 in the cell cycle that follows the transient exposure to nocodazole and become arrested in G(1), regardless of whether they carry a diploid or polyploid genome after mitotic exit.	Nocodazole	144-154	P53	Homo sapiens	75-78
11356930-5	2001	In nontransformed cells, WR-1065 protected cells from the cytotoxic effects of paclitaxel in a p53-dependent manner.	Paclitaxel	79-89	P53	Homo sapiens	95-98
11484788-3	2001	In transformed TP53-mutated cell lines, however, the BBI-mediated radioprotection was absent.	Amiodarone	53-56	P53	Homo sapiens	15-19
11484788-4	2001	At the molecular level, the radioprotective effect of BBI can be correlated with BBI-mediated stabilisation of TP53 protein prior to irradiation.	Amiodarone	54-57	P53	Homo sapiens	111-115
11484788-4	2001	At the molecular level, the radioprotective effect of BBI can be correlated with BBI-mediated stabilisation of TP53 protein prior to irradiation.	Amiodarone	81-84	P53	Homo sapiens	111-115
11484788-6	2001	Thus, the cell and molecular biological data presented suggest that BBI is able to protect cells with functional TP53 from UVB-induced DNA damage.	Amiodarone	68-71	P53	Homo sapiens	113-117
11423970-3	2001	We found that treatment with roscovitine and olomoucin, which were originally developed as cyclin-dependent kinase (CDK) inhibitors, can efficiently stabilize and activate nuclear p53 in tumor cells with MDM2 amplification or cytoplasmic p53.	butyrolactone I	45-54	P53	Homo sapiens	180-183
11482451-8	2001	In the TP53 mutant cell lines, DU145 and BM1604, dose enhancement factors (EFs) were found to be in the region of 4.20 for cisplatin, 3.70 for vinblastine, and 3.20 for etoposide.	Cisplatin	123-132	P53	Homo sapiens	7-11
11482451-9	2001	In the TP53 wild-type cell line, LNCaP, the enhancement factors were low and in the region of 1.20 for cisplatin, vinblastine and etoposide.	Cisplatin	103-112	P53	Homo sapiens	7-11
11423970-3	2001	We found that treatment with roscovitine and olomoucin, which were originally developed as cyclin-dependent kinase (CDK) inhibitors, can efficiently stabilize and activate nuclear p53 in tumor cells with MDM2 amplification or cytoplasmic p53.	butyrolactone I	45-54	P53	Homo sapiens	238-241
11279110-5	2001	Second, we examined the relationship between p53 and HDM2 in the adriamycin-mediated stabilization of p53 in NB.	Doxorubicin	65-75	P53	Homo sapiens	45-48
11311495-4	2001	5-fluorouracil (5FU) treatment resulted in a substantial increase in the p53-positive signet-ring cell population (from 17% to 45%) and in an increased Mdm2 immunoreactivity.	Fluorouracil	0-14	P53	Homo sapiens	73-76
11311495-4	2001	5-fluorouracil (5FU) treatment resulted in a substantial increase in the p53-positive signet-ring cell population (from 17% to 45%) and in an increased Mdm2 immunoreactivity.	Fluorouracil	16-19	P53	Homo sapiens	73-76
11279192-5	2001	Results of electrophoretic mobility shift assay showed specific interactions of p53 protein with p53-binding site oligonucleotides.	Oligonucleotides	114-130	P53	Homo sapiens	80-83
11279110-5	2001	Second, we examined the relationship between p53 and HDM2 in the adriamycin-mediated stabilization of p53 in NB.	Doxorubicin	65-75	P53	Homo sapiens	102-105
11279192-5	2001	Results of electrophoretic mobility shift assay showed specific interactions of p53 protein with p53-binding site oligonucleotides.	Oligonucleotides	114-130	P53	Homo sapiens	97-100
11279192-6	2001	The DNA-protein complex formed in electrophoretic mobility shift assay was competed with unlabeled excess of p53-binding site oligonucleotide, unaffected with p53-binding site mutant or Sp1-binding site oligonucleotides, and supershifted with anti-p53 antibodies.	Oligonucleotides	126-141	P53	Homo sapiens	109-112
11279110-7	2001	In support of this notion, p53 stabilization following adriamycin resulted in an inhibition of both p53 ubiquitination and HDM2 ligase activity.	Doxorubicin	55-65	P53	Homo sapiens	27-30
11279192-9	2001	However, the treatment of cells with DNA alkylating agents methylmethane sulfonate and N-methyl-N"-nitro-N-nitrosoguanidine, which cause phosphorylation of p53 at Ser(15) and Ser(392), induced pAPCP promoter activity in HCT-116(p53(+/+)) cells.	Serine	163-166	P53	Homo sapiens	156-159
11279110-7	2001	In support of this notion, p53 stabilization following adriamycin resulted in an inhibition of both p53 ubiquitination and HDM2 ligase activity.	Doxorubicin	55-65	P53	Homo sapiens	100-103
11279192-9	2001	However, the treatment of cells with DNA alkylating agents methylmethane sulfonate and N-methyl-N"-nitro-N-nitrosoguanidine, which cause phosphorylation of p53 at Ser(15) and Ser(392), induced pAPCP promoter activity in HCT-116(p53(+/+)) cells.	Serine	163-166	P53	Homo sapiens	228-231
11279192-9	2001	However, the treatment of cells with DNA alkylating agents methylmethane sulfonate and N-methyl-N"-nitro-N-nitrosoguanidine, which cause phosphorylation of p53 at Ser(15) and Ser(392), induced pAPCP promoter activity in HCT-116(p53(+/+)) cells.	Serine	175-178	P53	Homo sapiens	156-159
11279186-7	2001	In addition, only major 1,2-GG intrastrand cross-links of cisplatin are responsible for this enhanced binding affinity of p53.	Cisplatin	58-67	P53	Homo sapiens	122-125
11279192-9	2001	However, the treatment of cells with DNA alkylating agents methylmethane sulfonate and N-methyl-N"-nitro-N-nitrosoguanidine, which cause phosphorylation of p53 at Ser(15) and Ser(392), induced pAPCP promoter activity in HCT-116(p53(+/+)) cells.	Serine	175-178	P53	Homo sapiens	228-231
11350044-3	2001	In this study we compared the cisplatin-induced response of p53 protein and its downstream targets p21WAF-1 and Mdm2 in the cisplatin-sensitive ovarian carcinoma cell line A2780 and its cisplatin-resistant derivative CP70.	Cisplatin	30-39	P53	Homo sapiens	60-63
11350044-3	2001	In this study we compared the cisplatin-induced response of p53 protein and its downstream targets p21WAF-1 and Mdm2 in the cisplatin-sensitive ovarian carcinoma cell line A2780 and its cisplatin-resistant derivative CP70.	Cisplatin	124-133	P53	Homo sapiens	60-63
11350044-3	2001	In this study we compared the cisplatin-induced response of p53 protein and its downstream targets p21WAF-1 and Mdm2 in the cisplatin-sensitive ovarian carcinoma cell line A2780 and its cisplatin-resistant derivative CP70.	Cisplatin	124-133	P53	Homo sapiens	60-63
11350044-4	2001	A higher dose of cisplatin and a longer exposure time was required to achieve the same level of p53, p21WAF-1, and Mdm2 protein accumulation in the cisplatin-resistant CP70 cells versus cisplatin-sensitive A2780 cells.	Cisplatin	17-26	P53	Homo sapiens	96-99
11350044-5	2001	A significant difference between the two cell lines was observed in cisplatin-induced stabilization of p53 protein.	Cisplatin	68-77	P53	Homo sapiens	103-106
11350044-8	2001	These results demonstrate that in A2780 and CP70 cells resistance to cisplatin correlates with prolonged p53 protein stabilization and accumulation.	Cisplatin	69-78	P53	Homo sapiens	105-108
11358811-3	2001	We identified mutations in exons 5-8 of p53 using DNA extracted from formalin-fixed paraffin-embedded tissue blocks from 146 whites and 26 non-whites with astrocytic glioma by PCR-single-strand conformation polymorphism and direct sequencing.	Paraffin	84-92	P53	Homo sapiens	40-43
11279079-9	2001	Latent full-length p53 dissociated DNA aggregates via its core and CTD, and this effect was potentiated by GTP.	Guanosine Triphosphate	107-110	P53	Homo sapiens	19-22
11279186-0	2001	Different recognition of DNA modified by aatitumor cisplatin and its clinically ineffective trans isomer by tumor suppressor protein p53.	Cisplatin	51-60	P53	Homo sapiens	133-136
11279186-1	2001	The p53 gene encodes a nuclear phosphoprotein that is biologically activated in response to genotoxic stresses including treatment with anticancer platinum drugs.	Platinum	147-155	P53	Homo sapiens	4-7
11279186-3	2001	DNA interactions of active wild-type human p53 protein with DNA fragments and oligodeoxyribonucleotide duplexes modified by antitumor cisplatin and its clinically ineffective trans isomer (transplatin) were investigated by using a gel mobility shift assay.	Cisplatin	134-143	P53	Homo sapiens	43-46
11279186-4	2001	It was found that DNA adducts of cisplatin reduced binding affinity of the consensus DNA sequence to p53, whereas transplatin adducts did not.	Cisplatin	33-42	P53	Homo sapiens	101-104
11279186-5	2001	This result was interpreted to mean that the precise steric fit required for the formation and stability of the tetrameric complex of p53 with the consensus sequence cannot be attained, as a consequence of severe conformational perturbations induced in DNA by cisplatin adducts.	Cisplatin	260-269	P53	Homo sapiens	134-137
11279186-6	2001	The results also demonstrate an increase of the binding affinity of p53 to DNA lacking the consensus sequence and modified by cisplatin but not by transplatin.	Cisplatin	126-135	P53	Homo sapiens	68-71
11279186-8	2001	The data base on structures of various DNA adducts of cisplatin and transplatin reveals distinctive structural features of 1,2-intrastrand cross-links of cisplatin, suggesting a unique role for this adduct in the binding of p53 to DNA lacking the consensus sequence.	Cisplatin	54-63	P53	Homo sapiens	224-227
11279186-8	2001	The data base on structures of various DNA adducts of cisplatin and transplatin reveals distinctive structural features of 1,2-intrastrand cross-links of cisplatin, suggesting a unique role for this adduct in the binding of p53 to DNA lacking the consensus sequence.	Cisplatin	154-163	P53	Homo sapiens	224-227
11279186-9	2001	The results support the hypothesis that the mechanism of antitumor activity of cisplatin may also be associated with its efficiency to affect the binding affinity of platinated DNA to active p53 protein.	Cisplatin	79-88	P53	Homo sapiens	191-194
11497278-2	2001	We studied the mechanism of the growth-inhibitory effect of cisplatin (CDDP) on human pancreatic cancer cells in connection with the status of the p53 gene and expression of the bcl-2 family.	Cisplatin	60-69	P53	Homo sapiens	147-150
11497278-2	2001	We studied the mechanism of the growth-inhibitory effect of cisplatin (CDDP) on human pancreatic cancer cells in connection with the status of the p53 gene and expression of the bcl-2 family.	Cisplatin	71-75	P53	Homo sapiens	147-150
11497278-7	2001	Increased expression of bax and reduced expression of bcl-2 are involved in the growth-inhibitory effect of CDDP on pancreatic cancer cells with wild-type p53 gene.	Cisplatin	108-112	P53	Homo sapiens	155-158
11350911-7	2001	The negative regulation of MGMT expression by wt p53 was confirmed in two other human isogenic cell lines, namely, the GM47.23 glioblastoma, which contains a dexamethasone-inducible wt p53, and the H460 lung cancer cell line, in which wt p53 had been inactivated by the human papillomavirus E6 protein.	Dexamethasone	158-171	P53	Homo sapiens	49-52
11350904-12	2001	CONCLUSIONS: Our findings suggest that p53 alteration and MSI could be clinically useful molecular predictive markers for the identification of CRC patients who might benefit from 5-fluorouracil-based chemotherapy.	Fluorouracil	180-194	P53	Homo sapiens	39-42
11477455-6	2001	The combination of Ad5CMV-p53 and cisplatin resulted in approximately 25% greater cytotoxicity compared to that observed with cisplatin alone in either cell line.	Cisplatin	126-135	P53	Homo sapiens	26-29
11350911-7	2001	The negative regulation of MGMT expression by wt p53 was confirmed in two other human isogenic cell lines, namely, the GM47.23 glioblastoma, which contains a dexamethasone-inducible wt p53, and the H460 lung cancer cell line, in which wt p53 had been inactivated by the human papillomavirus E6 protein.	Dexamethasone	158-171	P53	Homo sapiens	185-188
11350916-4	2001	Loss of cell viability, bcl-2 down-regulation, and poly(ADP-ribose) polymerase cleavage, indicative of apoptosis, also occurred in wt p53 C8161 cells on treatment with oligonucleotide 4625.	Oligonucleotides	168-183	P53	Homo sapiens	134-137
11350911-7	2001	The negative regulation of MGMT expression by wt p53 was confirmed in two other human isogenic cell lines, namely, the GM47.23 glioblastoma, which contains a dexamethasone-inducible wt p53, and the H460 lung cancer cell line, in which wt p53 had been inactivated by the human papillomavirus E6 protein.	Dexamethasone	158-171	P53	Homo sapiens	185-188
11350916-6	2001	In contrast to many other anticancer agents to which the apoptotic response is decreased because of p53 mutations, our data suggest that the bcl-2/bcl-xL bispecific antisense oligonucleotide 4625 effectively induces p53-independent apoptosis in human C8161 melanoma cells.	Oligonucleotides	175-190	P53	Homo sapiens	216-219
11350916-0	2001	p53-Independent induction of apoptosis in human melanoma cells by a bcl-2/bcl-xL bispecific antisense oligonucleotide.	Oligonucleotides	102-117	P53	Homo sapiens	0-3
11350916-3	2001	Upon treatment with oligonucleotide 4625, p53-mut C8161 cells showed earlier DNA damage, which occurred concomitantly with the reduction of bcl-2 and bcl-xL expression and the increase in the expression of proapoptotic bax.	Oligonucleotides	20-35	P53	Homo sapiens	42-45
11295047-2	2001	A block of cell cycle checkpoint by dexamethasone and genistein correlates with a selective induction of cyclin-dependent kinase (Cdk) inhibitor p21WAF1/CIP1 in a tumor suppressor p53-independent manner and abolishment of Cdk2 phosphorylation.	Dexamethasone	36-49	P53	Homo sapiens	180-183
11331603-0	2001	ATM-dependent phosphorylation of Mdm2 on serine 395: role in p53 activation by DNA damage.	Serine	41-47	P53	Homo sapiens	61-64
11313183-7	2001	In astrocytoma cells, cisplatin treatment resulted in the upregulation of p53, p21 and bax, while only p21 induction was observed after BBR3464 treatment.	Cisplatin	22-31	P53	Homo sapiens	74-77
11313183-8	2001	In cisplatin-resistant cells, the reduced sensitivity to cisplatin paralleled a resistance to the induction of p53/p21 pathway by cisplatin, while the same doses of BBR3464 induced p21 to a similar extent in the resistant cells as in the parental cells.	Cisplatin	3-12	P53	Homo sapiens	111-114
11313183-8	2001	In cisplatin-resistant cells, the reduced sensitivity to cisplatin paralleled a resistance to the induction of p53/p21 pathway by cisplatin, while the same doses of BBR3464 induced p21 to a similar extent in the resistant cells as in the parental cells.	Cisplatin	57-66	P53	Homo sapiens	111-114
11313183-8	2001	In cisplatin-resistant cells, the reduced sensitivity to cisplatin paralleled a resistance to the induction of p53/p21 pathway by cisplatin, while the same doses of BBR3464 induced p21 to a similar extent in the resistant cells as in the parental cells.	Cisplatin	57-66	P53	Homo sapiens	111-114
11316543-4	2001	METHODS AND MATERIALS: The nuclear expression of HAP1 and p53 proteins was studied by immunohistochemistry in paraffin-embedded material from 95 patients with locally advanced squamous cell head-and-neck cancer (HNC) treated with radical radiotherapy (38 cases with induction platinum-based chemotherapy and 57 with concurrent platinum chemoradiotherapy).	Paraffin	110-118	P53	Homo sapiens	58-61
11783085-5	2001	Induction of p53 expression could be blocked by phosphorothiate analogs of antisense oligonucleotides to NF-kappa B p65 and LMP1, but not by NF-kappa B p50.	Oligonucleotides	85-101	P53	Homo sapiens	13-16
11340094-0	2001	Tumor suppressor protein p53 mRNA and subcellular localization are altered by changes in cellular copper in human Hep G2 cells.	Copper	98-104	P53	Homo sapiens	25-28
11340094-4	2001	Using Northern analysis, Western analysis, immunocytochemistry and the human hepatoma cell line Hep G2, this work showed that elevations in hepatocyte copper consistent with Wilson"s disease (5.7-fold increase) induced p53 mRNA and confirmed that copper toxicity is correlated with apoptotic cell death.	Copper	151-157	P53	Homo sapiens	219-222
11340094-4	2001	Using Northern analysis, Western analysis, immunocytochemistry and the human hepatoma cell line Hep G2, this work showed that elevations in hepatocyte copper consistent with Wilson"s disease (5.7-fold increase) induced p53 mRNA and confirmed that copper toxicity is correlated with apoptotic cell death.	Copper	247-253	P53	Homo sapiens	219-222
11340094-5	2001	However, Western analysis and immunocytochemistry showed that post-transcriptional mechanisms are a significant part of the process, with p53 translocation from the cytosol into the nucleus of copper-treated cells.	Copper	193-199	P53	Homo sapiens	138-141
11340094-6	2001	Treatment of Hep G2 cells with increasing concentrations of the copper chelator tetraethylenepentamine (TEPA, 0-50 micromol/L, 48 h) reduced cellular copper and increased mean p53 mRNA abundance by over fourfold with nuclear translocation of the wild-type protein.	Copper	64-70	P53	Homo sapiens	176-179
11295094-6	2001	Pre-treatment with cis-diamminedichloroplatinum (II) (CDDP) at 0.1 microg/ml significantly suppressed tumor cell viability in NY and HuO-3N1 (mutated), but not in the other three lines including HT-1080 carrying the wild-type p53 gene, implying the existence of different mechanisms for the tumor suppressive effect of p53 gene transfection and CDDP.	Cisplatin	19-52	P53	Homo sapiens	226-229
11295094-6	2001	Pre-treatment with cis-diamminedichloroplatinum (II) (CDDP) at 0.1 microg/ml significantly suppressed tumor cell viability in NY and HuO-3N1 (mutated), but not in the other three lines including HT-1080 carrying the wild-type p53 gene, implying the existence of different mechanisms for the tumor suppressive effect of p53 gene transfection and CDDP.	Cisplatin	19-52	P53	Homo sapiens	319-322
11295094-6	2001	Pre-treatment with cis-diamminedichloroplatinum (II) (CDDP) at 0.1 microg/ml significantly suppressed tumor cell viability in NY and HuO-3N1 (mutated), but not in the other three lines including HT-1080 carrying the wild-type p53 gene, implying the existence of different mechanisms for the tumor suppressive effect of p53 gene transfection and CDDP.	Cisplatin	54-58	P53	Homo sapiens	226-229
11295094-6	2001	Pre-treatment with cis-diamminedichloroplatinum (II) (CDDP) at 0.1 microg/ml significantly suppressed tumor cell viability in NY and HuO-3N1 (mutated), but not in the other three lines including HT-1080 carrying the wild-type p53 gene, implying the existence of different mechanisms for the tumor suppressive effect of p53 gene transfection and CDDP.	Cisplatin	54-58	P53	Homo sapiens	319-322
11295094-7	2001	These results indicate that wild-type p53 gene transfection with CDDP is a promising therapy for some, but not all, non-resectable bone-and soft tissue sarcomas, regardless of intrinsic p53 gene status.	Cisplatin	65-69	P53	Homo sapiens	38-41
11295099-0	2001	Regulation of BRCA1 and BRCA2 transcript in response to cisplatin, adriamycin, taxol and ionising radiation is correlated to p53 functional status in ovarian cancer cell lines.	Cisplatin	56-65	P53	Homo sapiens	125-128
11295099-0	2001	Regulation of BRCA1 and BRCA2 transcript in response to cisplatin, adriamycin, taxol and ionising radiation is correlated to p53 functional status in ovarian cancer cell lines.	Doxorubicin	67-77	P53	Homo sapiens	125-128
11295099-0	2001	Regulation of BRCA1 and BRCA2 transcript in response to cisplatin, adriamycin, taxol and ionising radiation is correlated to p53 functional status in ovarian cancer cell lines.	Paclitaxel	79-84	P53	Homo sapiens	125-128
11278961-6	2001	The (99m)technetium-tricarbonyl-labeled tetrameric 4D5-p53 miniantibody localized with the highest dose at the tumor and remained stably bound for at least 72 h. The highest total dose was 4.3% injected dose/g after 24 h, whereas the highest tumor-to-blood ratio was found to be 13.5:1 after 48 h, with a total dose of 3.2% injected dose/g.	technetium-tricarbonyl	9-31	P53	Homo sapiens	55-58
11302731-6	2001	The present results showed that cadmium induces phosphorylation of p53 at Ser 15 in MCF-7 cells depending on phosphatidylinositol 3-kinase related kinases, but not on mitogen-activated protein kinases.	Cadmium	32-39	P53	Homo sapiens	67-70
11402317-1	2001	The transcriptional program regulated by the tumor suppressor p53 was analysed using oligonucleotide microarrays.	Oligonucleotides	85-100	P53	Homo sapiens	62-65
11302731-0	2001	Cadmium induces phosphorylation of p53 at serine 15 in MCF-7 cells.	Cadmium	0-7	P53	Homo sapiens	35-38
11302731-6	2001	The present results showed that cadmium induces phosphorylation of p53 at Ser 15 in MCF-7 cells depending on phosphatidylinositol 3-kinase related kinases, but not on mitogen-activated protein kinases.	Serine	74-77	P53	Homo sapiens	67-70
11302731-0	2001	Cadmium induces phosphorylation of p53 at serine 15 in MCF-7 cells.	Serine	42-48	P53	Homo sapiens	35-38
11302731-1	2001	When MCF-7 cells were incubated with 10 or 20 microM CdCl(2), p53 protein level increased after 18 h. Among serines in p53 protein immunoprecipitated from cells treated with CdCl(2), only Ser 15 was phosphorylated.	cdcl	53-57	P53	Homo sapiens	62-65
21044462-9	2001	The different biological effect between 172Leu and 172His shows that some p53 variants such as 172 Arg-&gt;Leu may act as wild-type p53.	Arginine	99-102	P53	Homo sapiens	74-77
11302731-1	2001	When MCF-7 cells were incubated with 10 or 20 microM CdCl(2), p53 protein level increased after 18 h. Among serines in p53 protein immunoprecipitated from cells treated with CdCl(2), only Ser 15 was phosphorylated.	cdcl	53-57	P53	Homo sapiens	119-122
11302731-1	2001	When MCF-7 cells were incubated with 10 or 20 microM CdCl(2), p53 protein level increased after 18 h. Among serines in p53 protein immunoprecipitated from cells treated with CdCl(2), only Ser 15 was phosphorylated.	Serine	108-115	P53	Homo sapiens	62-65
11302731-1	2001	When MCF-7 cells were incubated with 10 or 20 microM CdCl(2), p53 protein level increased after 18 h. Among serines in p53 protein immunoprecipitated from cells treated with CdCl(2), only Ser 15 was phosphorylated.	Serine	108-115	P53	Homo sapiens	119-122
11302731-1	2001	When MCF-7 cells were incubated with 10 or 20 microM CdCl(2), p53 protein level increased after 18 h. Among serines in p53 protein immunoprecipitated from cells treated with CdCl(2), only Ser 15 was phosphorylated.	cdcl	174-178	P53	Homo sapiens	62-65
11302731-1	2001	When MCF-7 cells were incubated with 10 or 20 microM CdCl(2), p53 protein level increased after 18 h. Among serines in p53 protein immunoprecipitated from cells treated with CdCl(2), only Ser 15 was phosphorylated.	cdcl	174-178	P53	Homo sapiens	119-122
11302731-1	2001	When MCF-7 cells were incubated with 10 or 20 microM CdCl(2), p53 protein level increased after 18 h. Among serines in p53 protein immunoprecipitated from cells treated with CdCl(2), only Ser 15 was phosphorylated.	Serine	188-191	P53	Homo sapiens	62-65
11302731-1	2001	When MCF-7 cells were incubated with 10 or 20 microM CdCl(2), p53 protein level increased after 18 h. Among serines in p53 protein immunoprecipitated from cells treated with CdCl(2), only Ser 15 was phosphorylated.	Serine	188-191	P53	Homo sapiens	119-122
11302731-3	2001	Accumulation of p53 protein phosphorylated at Ser 15 was also found after 18 h exposure.	Serine	46-49	P53	Homo sapiens	16-19
21044462-9	2001	The different biological effect between 172Leu and 172His shows that some p53 variants such as 172 Arg-&gt;Leu may act as wild-type p53.	Arginine	99-102	P53	Homo sapiens	132-135
11309295-0	2001	p53/p21(CIP1) cooperate in enforcing rapamycin-induced G(1) arrest and determine the cellular response to rapamycin.	Sirolimus	37-46	P53	Homo sapiens	0-3
11296226-0	2001	p53 induction of heparin-binding EGF-like growth factor counteracts p53 growth suppression through activation of MAPK and PI3K/Akt signaling cascades.	Heparin	17-24	P53	Homo sapiens	0-3
11296226-0	2001	p53 induction of heparin-binding EGF-like growth factor counteracts p53 growth suppression through activation of MAPK and PI3K/Akt signaling cascades.	Heparin	17-24	P53	Homo sapiens	68-71
11309295-6	2001	Infection of Rh30 cells with either Ad-p53 or Ad-p21, but not control virus (Ad-beta-gal), induced G(1) accumulation, up-regulation of p21(CIP1), and complete protection of cells from rapamycin-induced apoptosis.	Sirolimus	184-193	P53	Homo sapiens	39-42
11287297-11	2001	In conclusion, our current study strongly suggests that CuQ induces gene mutation, global DNA damage, and P53 expression through a ROS-dependent mechanism.	Reactive Oxygen Species	131-134	P53	Homo sapiens	106-109
11309295-13	2001	In contrast, rapamycin significantly induced apoptosis in cells deficient in p53 ( approximately 2.4-fold) or p21(CIP1) ( approximately 5.5-fold).	Sirolimus	13-22	P53	Homo sapiens	77-80
11309295-20	2001	Taken together, the data suggest that p53 cooperates in enforcing G(1) cell cycle arrest, leading to a cytostatic response to rapamycin.	Sirolimus	126-135	P53	Homo sapiens	38-41
11285227-7	2001	Curcumin, a CSN kinase inhibitor, blocks E6-dependent p53 degradation in reticulocyte lysates.	Curcumin	0-8	P53	Homo sapiens	54-57
11275363-0	2001	Taxol-induced cell cycle arrest and apoptosis: dose-response relationship in lung cancer cells of different wild-type p53 status and under isogenic condition.	Paclitaxel	0-5	P53	Homo sapiens	118-121
11275363-3	2001	DNA content analyses in A 549 (p53, +/+) and H 1299 (p53, -/-) cells, showed that taxol progressively induced G2/M arrest in both cell lines in a concentration-dependent manner, which was accompanied by a parallel decrease in the G1 population.	Paclitaxel	82-87	P53	Homo sapiens	31-34
11275363-3	2001	DNA content analyses in A 549 (p53, +/+) and H 1299 (p53, -/-) cells, showed that taxol progressively induced G2/M arrest in both cell lines in a concentration-dependent manner, which was accompanied by a parallel decrease in the G1 population.	Paclitaxel	82-87	P53	Homo sapiens	53-56
11278253-8	2001	Treatment of p53-positive MCF-7 cells with the DNA-damaging drug, doxorubicin, which increases p53 levels, enhanced caspase-1 promoter activity 4-5-fold, but similar treatment of MCF-7-mp53 (a clone of MCF-7 cells expressing mutant p53) and p53-negative HeLa cells with doxorubicin did not increase caspase-1 promoter activity.	Doxorubicin	66-77	P53	Homo sapiens	13-16
11278253-8	2001	Treatment of p53-positive MCF-7 cells with the DNA-damaging drug, doxorubicin, which increases p53 levels, enhanced caspase-1 promoter activity 4-5-fold, but similar treatment of MCF-7-mp53 (a clone of MCF-7 cells expressing mutant p53) and p53-negative HeLa cells with doxorubicin did not increase caspase-1 promoter activity.	Doxorubicin	66-77	P53	Homo sapiens	95-98
11278253-8	2001	Treatment of p53-positive MCF-7 cells with the DNA-damaging drug, doxorubicin, which increases p53 levels, enhanced caspase-1 promoter activity 4-5-fold, but similar treatment of MCF-7-mp53 (a clone of MCF-7 cells expressing mutant p53) and p53-negative HeLa cells with doxorubicin did not increase caspase-1 promoter activity.	Doxorubicin	66-77	P53	Homo sapiens	95-98
11278253-8	2001	Treatment of p53-positive MCF-7 cells with the DNA-damaging drug, doxorubicin, which increases p53 levels, enhanced caspase-1 promoter activity 4-5-fold, but similar treatment of MCF-7-mp53 (a clone of MCF-7 cells expressing mutant p53) and p53-negative HeLa cells with doxorubicin did not increase caspase-1 promoter activity.	Doxorubicin	66-77	P53	Homo sapiens	95-98
11278253-8	2001	Treatment of p53-positive MCF-7 cells with the DNA-damaging drug, doxorubicin, which increases p53 levels, enhanced caspase-1 promoter activity 4-5-fold, but similar treatment of MCF-7-mp53 (a clone of MCF-7 cells expressing mutant p53) and p53-negative HeLa cells with doxorubicin did not increase caspase-1 promoter activity.	Doxorubicin	270-281	P53	Homo sapiens	13-16
11300786-8	2001	In summary, MS analysis uniquely revealed increased, site-specific phosphorylations on p53 after phosphatase inhibition, particularly at Ser(315), which may be critical molecular events in defining p53 activity.	Serine	137-140	P53	Homo sapiens	87-90
11300786-8	2001	In summary, MS analysis uniquely revealed increased, site-specific phosphorylations on p53 after phosphatase inhibition, particularly at Ser(315), which may be critical molecular events in defining p53 activity.	Serine	137-140	P53	Homo sapiens	198-201
11706756-2	2001	The aim of this study was to determine the predictive value of p53 mutation or the expression of GML, a target of p53, for sensitivity to 5-FU and MMC.	Fluorouracil	138-142	P53	Homo sapiens	63-66
11309351-8	2001	Cell lines with faster doubling times and wild-type p53 were significantly more sensitive to 5-FU and FDURD: CONCLUSIONS: The lack of correlation may in part be attributable to the influence of downstream factors such as p53, the observation that the more sensitive cell lines with faster doubling times also had higher TS levels, and the standard procedure of the screen that uses a relatively short (48-h) drug exposure.	Fluorouracil	93-97	P53	Homo sapiens	52-55
11331958-0	2001	Transcriptional activation of p21 by vitamin D(3) or vitamin K(2) leads to differentiation of p53-deficient MG-63 osteosarcoma cells.	Vitamin D	37-46	P53	Homo sapiens	94-97
11331958-6	2001	The transcriptional activation of p21 by vitamin D(3) or vitamin K(2) in p53-deficient osteosarcoma cells demonstrated the p53-independent role of p21 in human osseous differentiation.	Vitamin D	41-50	P53	Homo sapiens	73-76
11706756-2	2001	The aim of this study was to determine the predictive value of p53 mutation or the expression of GML, a target of p53, for sensitivity to 5-FU and MMC.	Fluorouracil	138-142	P53	Homo sapiens	114-117
11283254-0	2001	Jun NH2-terminal kinase phosphorylation of p53 on Thr-81 is important for p53 stabilization and transcriptional activities in response to stress.	Threonine	50-53	P53	Homo sapiens	43-46
11368358-9	2001	Therefore, wt p53 leukemic cells respond to HHT-specific cellular stress by induction of ROS-independent apoptotic pathway characterized by translocation of Bax, mitochondrial cytochrome c release and activation of caspases.	Reactive Oxygen Species	89-92	P53	Homo sapiens	14-17
11283254-0	2001	Jun NH2-terminal kinase phosphorylation of p53 on Thr-81 is important for p53 stabilization and transcriptional activities in response to stress.	Threonine	50-53	P53	Homo sapiens	74-77
11401473-6	2001	Accumulation of P53 and its target gene bax then sensitized HeLa cells to cell-cycle arrest, cell death/apoptosis induced by cisplatin, and etoposide.	Cisplatin	125-134	P53	Homo sapiens	16-19
11291926-0	2001	Caspase-3 activation downstream from reactive oxygen species in heat-induced apoptosis of pancreatic carcinoma cells carrying a mutant p53 gene.	Reactive Oxygen Species	37-60	P53	Homo sapiens	135-138
11291926-7	2001	These results suggest a possible pathway by which reactive oxygen species lead to caspase-3 activation to cause heat-induced death of pancreatic carcinoma cells carrying mutant p53.	Reactive Oxygen Species	50-73	P53	Homo sapiens	177-180
11802967-7	2001	SP immunohistological staining method was performed to detect the changes of expressions of p53, Bcl-2 and Bax gene.	TFF2 protein, human	0-2	P53	Homo sapiens	92-95
11106643-1	2001	The relationship between loss of functional p53 and human reduced folate carrier (hRFC) levels and function was examined in REH lymphoblastic leukemia cells, which express wild type p53, and in p53-null K562 cells (K562(pTet-on/p53)) engineered to express wild type p53 under control of a tetracycline-inducible promoter.	Folic Acid	66-72	P53	Homo sapiens	44-47
11274414-4	2001	Allele-discriminating oligonucleotide probes in conjunction with RCA also were used to discriminate wild-type and mutant alleles in the cystic fibrosis transmembrane conductance regulator, p53, BRCA-1, and Gorlin syndrome genes in the nuclei of cultured cells or in DNA fibers.	Oligonucleotides	22-37	P53	Homo sapiens	189-192
11313880-8	2001	Moreover, expression of functional p53 protein in glioma cells expressing mutant p53 using a temperature-sensitive human p53(Val138) induced ceramide accumulation by the activation of neutral sphingomyelinase which was dependent on the generation of O2-*.	Superoxides	250-254	P53	Homo sapiens	35-38
11289122-0	2001	Influence of TP53 gene alterations and c-erbB-2 expression on the response to treatment with doxorubicin in locally advanced breast cancer.	Doxorubicin	93-104	P53	Homo sapiens	13-17
11289122-8	2001	Our data are consistent with the hypothesis that certain TP53 mutations predict for resistance to doxorubicin in breast cancer patients.	Doxorubicin	98-109	P53	Homo sapiens	57-61
11289122-10	2001	Our findings are consistent with the hypothesis that other defects may act in concert with loss of p53 function, causing resistance to doxorubicin in breast cancers.	Doxorubicin	135-146	P53	Homo sapiens	99-102
11313875-6	2001	Constitutive nuclear accumulation was observed in an SK-N-SH variant, AW-1, which has a point mutation in p53 at Cys176&gt;Ser, disturbing the same motif.	Serine	123-126	P53	Homo sapiens	106-109
11259085-2	2001	A p53 Pro/Arg polymorphism at exon 4 codon 72, has been suggested to be involved in susceptibility to cancers as well.	Arginine	10-13	P53	Homo sapiens	2-5
11313880-8	2001	Moreover, expression of functional p53 protein in glioma cells expressing mutant p53 using a temperature-sensitive human p53(Val138) induced ceramide accumulation by the activation of neutral sphingomyelinase which was dependent on the generation of O2-*.	Superoxides	250-254	P53	Homo sapiens	81-84
11313880-0	2001	p53 regulates ceramide formation by neutral sphingomyelinase through reactive oxygen species in human glioma cells.	Reactive Oxygen Species	69-92	P53	Homo sapiens	0-3
11313880-8	2001	Moreover, expression of functional p53 protein in glioma cells expressing mutant p53 using a temperature-sensitive human p53(Val138) induced ceramide accumulation by the activation of neutral sphingomyelinase which was dependent on the generation of O2-*.	Superoxides	250-254	P53	Homo sapiens	81-84
11313880-3	2001	p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2",7"-dichlorofluorescin (DCFH) into 2",7"-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase.	Reactive Oxygen Species	48-71	P53	Homo sapiens	0-3
11313880-3	2001	p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2",7"-dichlorofluorescin (DCFH) into 2",7"-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase.	Reactive Oxygen Species	73-76	P53	Homo sapiens	0-3
11313880-9	2001	Taken together, these results suggest that p53 may modulate ceramide generation by activation of neutral sphingomyelinase through the formation of O2-*, but not its downstream compounds H2O2 or * OH.	Superoxides	147-149	P53	Homo sapiens	43-46
11313880-3	2001	p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2",7"-dichlorofluorescin (DCFH) into 2",7"-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase.	Superoxides	79-95	P53	Homo sapiens	0-3
11313880-3	2001	p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2",7"-dichlorofluorescin (DCFH) into 2",7"-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase.	Superoxides	97-99	P53	Homo sapiens	0-3
11258898-0	2001	Thyroid hormone promotes serine phosphorylation of p53 by mitogen-activated protein kinase.	Serine	25-31	P53	Homo sapiens	51-54
11313880-3	2001	p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2",7"-dichlorofluorescin (DCFH) into 2",7"-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase.	Hydrogen Peroxide	157-174	P53	Homo sapiens	0-3
11313880-3	2001	p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2",7"-dichlorofluorescin (DCFH) into 2",7"-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase.	Hydrogen Peroxide	176-180	P53	Homo sapiens	0-3
11106654-0	2001	Interaction with p53 enhances binding of cisplatin-modified DNA by high mobility group 1 protein.	Cisplatin	41-50	P53	Homo sapiens	17-20
11106654-6	2001	Cisplatin-modified DNA binding by HMG1 was significantly enhanced by p53.	Cisplatin	0-9	P53	Homo sapiens	69-72
11258898-2	2001	The oncogene suppressor protein, p53, is serine phosphorylated by several kinases and is known to interact with TRbeta1.	Serine	41-47	P53	Homo sapiens	33-36
11258898-3	2001	We studied whether association of p53 and TR is modulated by T(4) and involves serine phosphorylation of p53 by MAPK.	Serine	79-85	P53	Homo sapiens	34-37
11258898-3	2001	We studied whether association of p53 and TR is modulated by T(4) and involves serine phosphorylation of p53 by MAPK.	Serine	79-85	P53	Homo sapiens	105-108
11258898-7	2001	T(4)-induced nuclear complexing of p53 and MAPK was inhibited by PD 98059 (PD) and U0126, two MAPK kinase (MEK) inhibitors, and was absent in cells treated with MEK antisense oligonucleotide and in dominant negative Ras cells.	Oligonucleotides	175-190	P53	Homo sapiens	35-38
11280728-9	2001	We hypothesize that proline oxidation supports the generation of ROS by donating reducing potential to an electron transport chain altered either by p53-dependent mechanisms or by overexpression of POX.	Reactive Oxygen Species	65-68	P53	Homo sapiens	149-152
11243864-1	2001	We have previously demonstrated that the activation of p53 signaling may contribute to tumor growth inhibition by the CRE-decoy oligonucleotide containing CRE sequence (5"-TGACGTCA-3") (Lee et al., Biochemistry 39, 4863-4868, 2000).	Oligonucleotides	128-143	P53	Homo sapiens	55-58
11260082-9	2001	As gene amplification is frequently associated with protein overexpression, the observed accumulation of p53 in the nuclei of H &amp; RS cells could be as a result of elevated MDM2 protein levels resulting in stabilization of p53 protein.	Adenosine Monophosphate	8-11	P53	Homo sapiens	105-108
11280728-0	2001	Proline oxidase, encoded by p53-induced gene-6, catalyzes the generation of proline-dependent reactive oxygen species.	Reactive Oxygen Species	94-117	P53	Homo sapiens	28-31
11280728-3	2001	Using Adriamycin to initiate p53-dependent apoptosis, we showed that the expression of POX is up-regulated in a time- and dose-dependent manner in a human colon cancer cell line (LoVo).	Doxorubicin	6-16	P53	Homo sapiens	29-32
11237724-0	2001	Nitric oxide prevents gamma-radiation-induced cell cycle arrest by impairing p53 function in MCF-7 cells.	Nitric Oxide	0-12	P53	Homo sapiens	77-80
11237724-1	2001	We previously reported that nitric oxide (NO) released from S-nitrosoglutathione induces conformational change of the p53 tumor-suppressor protein that impairs its DNA-binding activity in vitro.	Nitric Oxide	28-40	P53	Homo sapiens	118-121
11237724-1	2001	We previously reported that nitric oxide (NO) released from S-nitrosoglutathione induces conformational change of the p53 tumor-suppressor protein that impairs its DNA-binding activity in vitro.	S-Nitrosoglutathione	60-80	P53	Homo sapiens	118-121
11267864-5	2001	Cisplatin-resistant A2780/cDDP had a p53 mutation and exhibited attenuated Bax induction after cisplatin treatment, which may explain why supplementation of Bax was effective in this chemoresistant ovarian cancer.	Cisplatin	0-9	P53	Homo sapiens	37-40
11289281-4	2001	METHODS: Mutation screening of the hot spots of the K-ras gene and of the evolutionarily conserved regions of the TP53 gene was performed by denaturing gradient gel electrophoresis technique in formalin-fixed paraffin-embedded specimens of 55 consecutive patients with Dukes C colon cancer treated with adjuvant 5-fluorouracil-based chemotherapy.	Paraffin	209-217	P53	Homo sapiens	114-118
11289281-4	2001	METHODS: Mutation screening of the hot spots of the K-ras gene and of the evolutionarily conserved regions of the TP53 gene was performed by denaturing gradient gel electrophoresis technique in formalin-fixed paraffin-embedded specimens of 55 consecutive patients with Dukes C colon cancer treated with adjuvant 5-fluorouracil-based chemotherapy.	Fluorouracil	312-326	P53	Homo sapiens	114-118
11314044-0	2001	Phosphorylation of serines 15 and 37 is necessary for efficient accumulation of p53 following irradiation with UV.	Serine	19-26	P53	Homo sapiens	80-83
11428453-6	2001	Tumor growth was inhibited more by p53 gene transfection relative to mock transfection in the presence of Adriamycin.	Doxorubicin	106-116	P53	Homo sapiens	35-38
11160753-5	2001	DNA-PKcs that was bound to EBNA-LP phosphorylated p53 or EBNA-LP in vitro, and the phosphorylation of EBNA-LP was inhibited by Wortmannin, a specific in vitro inhibitor of DNA-PKcs.	N-tert-Butyl-N-ethylnitrosamine	27-31	P53	Homo sapiens	50-53
11273776-3	2001	In this report, we describe an improved extruded DOTAP:cholesterol (DOTAP:Chol) cationic liposome that efficiently delivers therapeutic tumor suppressor genes p53 and FHIT, which are frequently altered in lung cancer, to localized human primary lung cancers and to experimental disseminated metastases.	Cholesterol	55-66	P53	Homo sapiens	159-162
11314044-4	2001	Mutation of serine 15, serine 37 or both impaired the accumulation of the protein after exposing the cells to ultraviolet radiation (50-100% increase for the mutant proteins, 500% increase for wild-type p53) but not after treatment with adriamycin.	Serine	12-18	P53	Homo sapiens	203-206
11314044-4	2001	Mutation of serine 15, serine 37 or both impaired the accumulation of the protein after exposing the cells to ultraviolet radiation (50-100% increase for the mutant proteins, 500% increase for wild-type p53) but not after treatment with adriamycin.	Serine	23-29	P53	Homo sapiens	203-206
11314044-6	2001	Analysis of p53-dependent transcription revealed that phosphorylation of serine 15 is required to maintain basal levels of p21 mRNA.	Serine	73-79	P53	Homo sapiens	12-15
11314044-7	2001	These results provide new evidence for an important function of serine 37 phosphorylation, clearly distinguish the pathways of p53 activation in response to ultraviolet radiation or DNA damage inflicted by adriamycin, and reveal that serine 15 is crucial to support the p53-mediated basal expression of p21.	Doxorubicin	206-216	P53	Homo sapiens	127-130
11314044-7	2001	These results provide new evidence for an important function of serine 37 phosphorylation, clearly distinguish the pathways of p53 activation in response to ultraviolet radiation or DNA damage inflicted by adriamycin, and reveal that serine 15 is crucial to support the p53-mediated basal expression of p21.	Serine	234-240	P53	Homo sapiens	127-130
11314044-7	2001	These results provide new evidence for an important function of serine 37 phosphorylation, clearly distinguish the pathways of p53 activation in response to ultraviolet radiation or DNA damage inflicted by adriamycin, and reveal that serine 15 is crucial to support the p53-mediated basal expression of p21.	Serine	234-240	P53	Homo sapiens	270-273
11094056-0	2001	Tamoxifen but not 4-hydroxytamoxifen initiates apoptosis in p53(-) normal human mammary epithelial cells by inducing mitochondrial depolarization.	Tamoxifen	0-9	P53	Homo sapiens	60-63
11182788-4	2001	Likewise, accumulation of these proteins was observed in the wild-type TP53 cells after exposure to conditioned medium from irradiated mutant TP53 cells, and the accumulation was abolished by the addition of a specific nitric oxide scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide, to the medium.	Nitric Oxide	219-231	P53	Homo sapiens	71-75
11182788-4	2001	Likewise, accumulation of these proteins was observed in the wild-type TP53 cells after exposure to conditioned medium from irradiated mutant TP53 cells, and the accumulation was abolished by the addition of a specific nitric oxide scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide, to the medium.	Nitric Oxide	219-231	P53	Homo sapiens	142-146
11125280-0	2001	Expression and mutation of p53 in tumor effusion cells of patients with ovarian carcinoma: response to cisplatin-based chemotherapy.	Cisplatin	103-112	P53	Homo sapiens	27-30
11125280-1	2001	p53 alterations are considered as one of the most important factors responsible for drug resistance in ovarian carcinomas, although the relationship between p53 gene status and response to cisplatin-based chemotherapy in ovarian cancer patients remains unclear.	Cisplatin	189-198	P53	Homo sapiens	157-160
11096075-6	2001	Furthermore, a dominant-negative p53 protein, impairing doxorubicin-induced G2 arrest, prevents transcriptional down-regulation of the mitotic cyclins, cdk1, and cdc25C genes.	Doxorubicin	56-67	P53	Homo sapiens	33-36
11314025-5	2001	Inhibition of focal contacts development by plating of cells onto poly-L-lysine abrogated both Erk1/2 and p53 activations in colcemid-treated cells, while plating of cells onto fibronectin caused transient up-regulation of p53 even in the absence of colcemid.	Lysine	66-79	P53	Homo sapiens	106-109
11314025-6	2001	Pre-treatment of cells with the specific MEK1 inhibitor PD098059 also attenuated colcemid-induced p53 activation and G1 cell cycle arrest.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	56-64	P53	Homo sapiens	98-101
11125280-2	2001	The aim of the study was to evaluate the relationship between p53 protein accumulation, p53 gene mutation and response to cisplatin-based chemotherapy in patients with ovarian carcinoma considering conventional clinicopathological parameters.	Cisplatin	122-131	P53	Homo sapiens	62-65
11125280-2	2001	The aim of the study was to evaluate the relationship between p53 protein accumulation, p53 gene mutation and response to cisplatin-based chemotherapy in patients with ovarian carcinoma considering conventional clinicopathological parameters.	Cisplatin	122-131	P53	Homo sapiens	88-91
11125280-7	2001	A significant correlation between p53 accumulation and p53 gene alteration and poor response to cisplatin-based chemotherapy was shown.	Cisplatin	96-105	P53	Homo sapiens	34-37
11125280-7	2001	A significant correlation between p53 accumulation and p53 gene alteration and poor response to cisplatin-based chemotherapy was shown.	Cisplatin	96-105	P53	Homo sapiens	55-58
11125280-9	2001	A strong p53 expression especially accompanied by p53 changes detectable by PCR-SSCP analysis appears to be a good indicator of the resistance to cisplatin-based chemotherapy.	Cisplatin	146-155	P53	Homo sapiens	9-12
11125280-9	2001	A strong p53 expression especially accompanied by p53 changes detectable by PCR-SSCP analysis appears to be a good indicator of the resistance to cisplatin-based chemotherapy.	Cisplatin	146-155	P53	Homo sapiens	50-53
11222091-0	2001	Sp1-p53 heterocomplex mediates activation of HTLV-I long terminal repeat by 12-O-tetradecanoylphorbol-13-acetate that is antagonized by protein kinase C. We have previously demonstrated that 12-O-tetradecanoylphorbol-13-acetate (TPA) activates human T-cell leukemia virus type-I long terminal repeat (LTR) in Jurkat cells by a protein kinase C (PKC)-independent mechanism involving a posttranslational activation of Sp1 binding to an Sp1 site located within the Ets responsive region-1 (ERR-1).	Tetradecanoylphorbol Acetate	76-112	P53	Homo sapiens	4-7
11222091-0	2001	Sp1-p53 heterocomplex mediates activation of HTLV-I long terminal repeat by 12-O-tetradecanoylphorbol-13-acetate that is antagonized by protein kinase C. We have previously demonstrated that 12-O-tetradecanoylphorbol-13-acetate (TPA) activates human T-cell leukemia virus type-I long terminal repeat (LTR) in Jurkat cells by a protein kinase C (PKC)-independent mechanism involving a posttranslational activation of Sp1 binding to an Sp1 site located within the Ets responsive region-1 (ERR-1).	Tetradecanoylphorbol Acetate	191-227	P53	Homo sapiens	4-7
11222091-0	2001	Sp1-p53 heterocomplex mediates activation of HTLV-I long terminal repeat by 12-O-tetradecanoylphorbol-13-acetate that is antagonized by protein kinase C. We have previously demonstrated that 12-O-tetradecanoylphorbol-13-acetate (TPA) activates human T-cell leukemia virus type-I long terminal repeat (LTR) in Jurkat cells by a protein kinase C (PKC)-independent mechanism involving a posttranslational activation of Sp1 binding to an Sp1 site located within the Ets responsive region-1 (ERR-1).	Tetradecanoylphorbol Acetate	229-232	P53	Homo sapiens	4-7
11222091-8	2001	Therefore, we speculate that there might be several other PKC-independent biological effects of TPA which result from interaction of such Sp1-p53 complexes with Sp1 recognition sites residing in the promoters of a wide variety of cellular and viral genes.	Tetradecanoylphorbol Acetate	96-99	P53	Homo sapiens	142-145
11078726-2	2001	A phospho-specific monoclonal antibody to the C-terminal Ser(315) phospho-epitope was used to determine whether phosphorylation of endogenous p53 at Ser(315) can be detected in vivo, whether steady-state Ser(315) phosphorylation increases or decreases in an irradiated cell, and whether this phosphorylation event activates or inhibits p53 in vivo.	Serine	149-152	P53	Homo sapiens	142-145
11078726-2	2001	A phospho-specific monoclonal antibody to the C-terminal Ser(315) phospho-epitope was used to determine whether phosphorylation of endogenous p53 at Ser(315) can be detected in vivo, whether steady-state Ser(315) phosphorylation increases or decreases in an irradiated cell, and whether this phosphorylation event activates or inhibits p53 in vivo.	Serine	149-152	P53	Homo sapiens	142-145
11078726-3	2001	A native phospho-specific IgG binding assay was developed for quantitating the extent of p53 phosphorylation at Ser(315) where one, two, three, or four phosphates/tetramer could be defined after in vitro phosphorylation by cyclin-dependent protein kinases.	Serine	112-115	P53	Homo sapiens	89-92
11078726-3	2001	A native phospho-specific IgG binding assay was developed for quantitating the extent of p53 phosphorylation at Ser(315) where one, two, three, or four phosphates/tetramer could be defined after in vitro phosphorylation by cyclin-dependent protein kinases.	Phosphates	152-162	P53	Homo sapiens	89-92
11078726-4	2001	Using this assay, near-stoichiometric Ser(315) phosphorylation of endogenous p53 protein was detected in vivo after UV irradiation of MCF7 and A375 cells, coinciding with elevated p53-dependent transcription.	Serine	38-41	P53	Homo sapiens	77-80
11078726-4	2001	Using this assay, near-stoichiometric Ser(315) phosphorylation of endogenous p53 protein was detected in vivo after UV irradiation of MCF7 and A375 cells, coinciding with elevated p53-dependent transcription.	Serine	38-41	P53	Homo sapiens	180-183
11078726-5	2001	Transfection of the p53 gene with an alanine mutation at the Ser(315) site into Saos-2 cells gave rise to a form of p53 protein with a substantially reduced specific activity as a transcription factor.	Alanine	37-44	P53	Homo sapiens	20-23
11078726-5	2001	Transfection of the p53 gene with an alanine mutation at the Ser(315) site into Saos-2 cells gave rise to a form of p53 protein with a substantially reduced specific activity as a transcription factor.	Alanine	37-44	P53	Homo sapiens	116-119
11078726-5	2001	Transfection of the p53 gene with an alanine mutation at the Ser(315) site into Saos-2 cells gave rise to a form of p53 protein with a substantially reduced specific activity as a transcription factor.	Serine	61-64	P53	Homo sapiens	20-23
11078726-5	2001	Transfection of the p53 gene with an alanine mutation at the Ser(315) site into Saos-2 cells gave rise to a form of p53 protein with a substantially reduced specific activity as a transcription factor.	Serine	61-64	P53	Homo sapiens	116-119
11078726-7	2001	These results indicate that the majority of p53 protein has been phosphorylated at Ser(315) after irradiation damage and identify a cyclin-dependent kinase pathway that plays a role in stimulating p53 function.	Serine	83-86	P53	Homo sapiens	44-47
11078726-7	2001	These results indicate that the majority of p53 protein has been phosphorylated at Ser(315) after irradiation damage and identify a cyclin-dependent kinase pathway that plays a role in stimulating p53 function.	Serine	83-86	P53	Homo sapiens	197-200
11094056-3	2001	We developed an in vitro model of early breast cancer prevention to investigate how tamoxifen and 4-hydroxytamoxifen may act in normal human mammary epithelial cells (HMECs) that have acutely lost p53 function.	Tamoxifen	84-93	P53	Homo sapiens	197-200
11342217-0	2001	p53 binds to cisplatin-damaged DNA.	Cisplatin	13-22	P53	Homo sapiens	0-3
11094056-5	2001	Tamoxifen, but not 4-hydroxytamoxifen, rapidly induced apoptosis in p53(-) HMEC-E6 cells as evidenced by characteristic morphologic changes, annexin V binding, and DNA fragmentation.	Tamoxifen	0-9	P53	Homo sapiens	68-71
11342217-1	2001	We have previously shown that bacterially expressed p53 protein or p53 protein isolated from cis-diamminedichloroplatinum II (cisplatin)-damaged cells is capable of binding to double-stranded platinated DNA molecules lacking any p53 DNA binding sites.	Cisplatin	93-124	P53	Homo sapiens	52-55
11342217-1	2001	We have previously shown that bacterially expressed p53 protein or p53 protein isolated from cis-diamminedichloroplatinum II (cisplatin)-damaged cells is capable of binding to double-stranded platinated DNA molecules lacking any p53 DNA binding sites.	Cisplatin	93-124	P53	Homo sapiens	67-70
11094056-6	2001	We observed that a decrease in mitochondrial membrane potential, mitochondrial condensation, and caspase activation preceded the morphologic appearance of apoptosis in tamoxifen-treated early passage p53(-) HMEC-E6 cells.	Tamoxifen	168-177	P53	Homo sapiens	200-203
11342217-1	2001	We have previously shown that bacterially expressed p53 protein or p53 protein isolated from cis-diamminedichloroplatinum II (cisplatin)-damaged cells is capable of binding to double-stranded platinated DNA molecules lacking any p53 DNA binding sites.	Cisplatin	93-124	P53	Homo sapiens	67-70
11342217-1	2001	We have previously shown that bacterially expressed p53 protein or p53 protein isolated from cis-diamminedichloroplatinum II (cisplatin)-damaged cells is capable of binding to double-stranded platinated DNA molecules lacking any p53 DNA binding sites.	Cisplatin	126-135	P53	Homo sapiens	52-55
11342217-1	2001	We have previously shown that bacterially expressed p53 protein or p53 protein isolated from cis-diamminedichloroplatinum II (cisplatin)-damaged cells is capable of binding to double-stranded platinated DNA molecules lacking any p53 DNA binding sites.	Cisplatin	126-135	P53	Homo sapiens	67-70
11342217-1	2001	We have previously shown that bacterially expressed p53 protein or p53 protein isolated from cis-diamminedichloroplatinum II (cisplatin)-damaged cells is capable of binding to double-stranded platinated DNA molecules lacking any p53 DNA binding sites.	Cisplatin	126-135	P53	Homo sapiens	67-70
11342217-7	2001	Taken together, these results suggest that in addition to binding to p53 DNA binding sites, p53 also interacts with cisplatin-damaged DNA molecules.	Cisplatin	116-125	P53	Homo sapiens	69-72
11342217-7	2001	Taken together, these results suggest that in addition to binding to p53 DNA binding sites, p53 also interacts with cisplatin-damaged DNA molecules.	Cisplatin	116-125	P53	Homo sapiens	92-95
11094056-7	2001	p53(-) HMEC-E6 cells rapidly developed resistance to tamoxifen-mediated apoptosis within 10 passages in vitro.	Tamoxifen	53-62	P53	Homo sapiens	0-3
11094056-8	2001	Resistance to tamoxifen in late passage p53(-) HMEC-E6 cells correlated with an increase in mitochondrial mass and a lack of mitochondrial depolarization and caspase activation following tamoxifen treatment.	Tamoxifen	14-23	P53	Homo sapiens	40-43
11096068-5	2001	Here we show that genistein induces the up-regulation of p53 protein, phosphorylation of p53 at serine 15, activation of the sequence-specific DNA binding properties of p53, and phosphorylation of the hCds1/Chk2 protein kinase at threonine 68.	Serine	96-102	P53	Homo sapiens	89-92
11096068-5	2001	Here we show that genistein induces the up-regulation of p53 protein, phosphorylation of p53 at serine 15, activation of the sequence-specific DNA binding properties of p53, and phosphorylation of the hCds1/Chk2 protein kinase at threonine 68.	Serine	96-102	P53	Homo sapiens	89-92
11245458-1	2001	This study examined how the DNA mismatch repair (MMR) system and p53 interact to maintain genomic integrity in the presence of the mutagenic stress induced by cisplatin (DDP).	Cisplatin	159-168	P53	Homo sapiens	65-68
11245458-0	2001	P53 modulates the effect of loss of DNA mismatch repair on the sensitivity of human colon cancer cells to the cytotoxic and mutagenic effects of cisplatin.	Cisplatin	145-154	P53	Homo sapiens	0-3
11321044-0	2001	The p53 tumor suppressor: critical regulator of life &amp; death in cancer.	Adenosine Monophosphate	54-57	P53	Homo sapiens	4-7
11163111-0	2001	Novel bile acid derivatives induce apoptosis via a p53-independent pathway in human breast carcinoma cells.	Bile Acids and Salts	6-15	P53	Homo sapiens	51-54
11163111-5	2001	These findings suggest that these cytotoxic effects of novel bile acid derivatives on human breast carcinoma cells were mediated via apoptosis through a p53-independent pathway.	Bile Acids and Salts	61-70	P53	Homo sapiens	153-156
11245471-8	2001	Expression of p73 resulted in a reduction of the ectopically expressed p53 in transient transfections or of the endogenous p53 induced by Adriamycin- or UV-mediated damage.	Doxorubicin	138-148	P53	Homo sapiens	123-126
11245472-0	2001	Resveratrol-induced activation of p53 and apoptosis is mediated by extracellular-signal-regulated protein kinases and p38 kinase.	Resveratrol	0-11	P53	Homo sapiens	34-37
11245472-2	2001	Our previous study showed that the antitumor activity of resveratrol occurs through p53-mediated apoptosis.	Resveratrol	57-68	P53	Homo sapiens	84-87
11245472-3	2001	In this study, we have elucidated the potential signaling components underlying resveratrol-induced p53 activation and induction of apoptosis.	Resveratrol	80-91	P53	Homo sapiens	100-103
11245472-4	2001	We found that in a mouse JB6 epidermal cell line, resveratrol activated extracellular-signal-regulated protein kinases (ERKs), c-Jun NH2-terminal kinases (JNKs), and p38 kinase and induced serine 15 phosphorylation of p53.	Resveratrol	50-61	P53	Homo sapiens	218-221
11245472-5	2001	Stable expression of a dominant negative mutant of ERK2 or p38 kinase or their respective inhibitor, PD98059 or SB202190, repressed the phosphorylation of p53 at serine 15.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	101-108	P53	Homo sapiens	155-158
11245472-5	2001	Stable expression of a dominant negative mutant of ERK2 or p38 kinase or their respective inhibitor, PD98059 or SB202190, repressed the phosphorylation of p53 at serine 15.	Serine	162-168	P53	Homo sapiens	155-158
11245472-7	2001	Most importantly, ERKs and p38 kinase formed a complex with p53 after treatment with resveratrol.	Resveratrol	85-96	P53	Homo sapiens	60-63
11245472-8	2001	Strikingly, resveratrol-activated ERKs and p38 kinase, but not JNKs, phosphorylated p53 at serine 15 in vitro.	Resveratrol	12-23	P53	Homo sapiens	84-87
11245472-8	2001	Strikingly, resveratrol-activated ERKs and p38 kinase, but not JNKs, phosphorylated p53 at serine 15 in vitro.	Serine	91-97	P53	Homo sapiens	84-87
11245472-9	2001	Furthermore, pretreatment of the cells with PD98059 or SB202190 or stable expression of a dominant negative mutant of ERK2 or p38 kinase impaired resveratrol-induced p53-dependent transcriptional activity and apoptosis, whereas constitutively active MEK1 increased the transcriptional activity of p53.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	44-51	P53	Homo sapiens	166-169
11245472-9	2001	Furthermore, pretreatment of the cells with PD98059 or SB202190 or stable expression of a dominant negative mutant of ERK2 or p38 kinase impaired resveratrol-induced p53-dependent transcriptional activity and apoptosis, whereas constitutively active MEK1 increased the transcriptional activity of p53.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	44-51	P53	Homo sapiens	297-300
11245472-9	2001	Furthermore, pretreatment of the cells with PD98059 or SB202190 or stable expression of a dominant negative mutant of ERK2 or p38 kinase impaired resveratrol-induced p53-dependent transcriptional activity and apoptosis, whereas constitutively active MEK1 increased the transcriptional activity of p53.	Resveratrol	146-157	P53	Homo sapiens	166-169
11245472-9	2001	Furthermore, pretreatment of the cells with PD98059 or SB202190 or stable expression of a dominant negative mutant of ERK2 or p38 kinase impaired resveratrol-induced p53-dependent transcriptional activity and apoptosis, whereas constitutively active MEK1 increased the transcriptional activity of p53.	Resveratrol	146-157	P53	Homo sapiens	297-300
11245472-10	2001	These data strongly suggest that both ERKs and p38 kinase mediate resveratrol-induced activation of p53 and apoptosis through phosphorylation of p53 at serine 15.	Resveratrol	66-77	P53	Homo sapiens	100-103
11245472-10	2001	These data strongly suggest that both ERKs and p38 kinase mediate resveratrol-induced activation of p53 and apoptosis through phosphorylation of p53 at serine 15.	Resveratrol	66-77	P53	Homo sapiens	145-148
11245472-10	2001	These data strongly suggest that both ERKs and p38 kinase mediate resveratrol-induced activation of p53 and apoptosis through phosphorylation of p53 at serine 15.	Serine	152-158	P53	Homo sapiens	100-103
11245472-10	2001	These data strongly suggest that both ERKs and p38 kinase mediate resveratrol-induced activation of p53 and apoptosis through phosphorylation of p53 at serine 15.	Serine	152-158	P53	Homo sapiens	145-148
11258706-1	2001	The N-terminal BOX-I domain of p53 containing a docking site for the negative regulator MDM2 and the positive effector p300, harbours two recently identified phosphorylation sites at Thr18 or Ser20O whose affect on p300 is undefined.	UNII-PYZ33YLR8A	183-188	P53	Homo sapiens	31-34
11159853-6	2001	Dex reduced apoptosis (to 33% of control) in cultures after activation of p53 by shifting the temperature from 37 to 32 C. Moreover, Dex suppressed apoptosis induced by serum deprivation (to 40% of control) or forskolin stimulation (to 28% and 40% at 37 and at 32 C, respectively).	Dexamethasone	133-136	P53	Homo sapiens	74-77
11159853-7	2001	The protective effect of Dex on cAMP-, p53-, and serum deprivation-induced apoptosis was confirmed by both 4",6-diamido-2-phenylindole hydrochloride DNA staining and terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling with an ED(50) of 7 nM Dex.	Dexamethasone	25-28	P53	Homo sapiens	39-42
11181455-0	2001	Resveratrol analog, 3,4,5,4"-tetrahydroxystilbene, differentially induces pro-apoptotic p53/Bax gene expression and inhibits the growth of transformed cells but not their normal counterparts.	Resveratrol	0-11	P53	Homo sapiens	88-91
11159853-13	2001	However, it augmented by 1.2-fold the p53-induced apoptosis in cells shifted from 37 to 32 C. Dex further enhanced apoptosis by 1.9-fold in p53-activated cultures (32 C).	Dexamethasone	94-97	P53	Homo sapiens	38-41
11258706-5	2001	These results suggest that phosphorylation of p53 at Thr18 or Ser20 can activate p53 by stabilizing the p300-p53 complex and also identify a class of small molecular weight ligands capable of selective discrimination between MDM2- and p300-dependent activities.	UNII-PYZ33YLR8A	53-58	P53	Homo sapiens	46-49
11159853-13	2001	However, it augmented by 1.2-fold the p53-induced apoptosis in cells shifted from 37 to 32 C. Dex further enhanced apoptosis by 1.9-fold in p53-activated cultures (32 C).	Dexamethasone	94-97	P53	Homo sapiens	140-143
11258706-5	2001	These results suggest that phosphorylation of p53 at Thr18 or Ser20 can activate p53 by stabilizing the p300-p53 complex and also identify a class of small molecular weight ligands capable of selective discrimination between MDM2- and p300-dependent activities.	UNII-PYZ33YLR8A	53-58	P53	Homo sapiens	81-84
11258706-5	2001	These results suggest that phosphorylation of p53 at Thr18 or Ser20 can activate p53 by stabilizing the p300-p53 complex and also identify a class of small molecular weight ligands capable of selective discrimination between MDM2- and p300-dependent activities.	UNII-PYZ33YLR8A	53-58	P53	Homo sapiens	81-84
11563689-4	2001	In order to determine whether these conformational changes are consistent for other p53 mutants, we have now used molecular dynamics to determine the structure of the DNA-binding core domain of seven other environmentally induced, cancer-related p53 mutants, namely His 175, Asp 245, Asn 245, Trp 248, Met 249, Ser 278, and Lys 286.	Histidine	266-269	P53	Homo sapiens	246-249
11428715-0	2001	cAMP-induced apoptosis in granulosa cells is associated with up-regulation of P53 and bax and down-regulation of clusterin.	Cyclic AMP	0-4	P53	Homo sapiens	78-81
11428715-5	2001	The apoptotic effect of cAMP was accompanied by an increase in the expression of P53 and bax proteins as evaluated by Western blot and immunocytochemistry.	Cyclic AMP	24-28	P53	Homo sapiens	81-84
11428715-7	2001	These data suggest that cAMP may activate apoptosis in granulosa cells by shifting the ratio of the death promoter to death repressor genes via alteration of P53 and bax expression.	Cyclic AMP	24-28	P53	Homo sapiens	158-161
11172619-0	2001	Enhancement of the antiproliferative function of p53 by phosphorylation at serine 20: an inference from site-directed mutagenesis studies.	Serine	75-81	P53	Homo sapiens	49-52
11273008-3	2001	The first tumor contained 2 p53 mutations, in codon 213 (CGA--&gt;TGA, Arg--&gt;stop) and codon 306 (CGA--&gt;TGA, Arg--&gt;stop), further, 1 missense PTEN mutation (codon 257, TTC--&gt;TTA, Phe--&gt;Leu) and a silent PTEN mutation (codon 154, TTC--&gt;TTT, Phe--&gt;Phe).	Arginine	71-74	P53	Homo sapiens	28-31
11273008-4	2001	The second glioblastoma also contained multiple, but different mutations: p53 mutations in codons 158 (CGC--&gt;CAC, Arg--&gt;His) and 273 (CGT--&gt;TGT, Arg--&gt;Cys), and a PTEN mutation in codon 233 (CGA--&gt;TGA, Arg--&gt;Stop).	Arginine	117-120	P53	Homo sapiens	74-77
11273008-4	2001	The second glioblastoma also contained multiple, but different mutations: p53 mutations in codons 158 (CGC--&gt;CAC, Arg--&gt;His) and 273 (CGT--&gt;TGT, Arg--&gt;Cys), and a PTEN mutation in codon 233 (CGA--&gt;TGA, Arg--&gt;Stop).	Histidine	126-129	P53	Homo sapiens	74-77
11273008-4	2001	The second glioblastoma also contained multiple, but different mutations: p53 mutations in codons 158 (CGC--&gt;CAC, Arg--&gt;His) and 273 (CGT--&gt;TGT, Arg--&gt;Cys), and a PTEN mutation in codon 233 (CGA--&gt;TGA, Arg--&gt;Stop).	Arginine	154-157	P53	Homo sapiens	74-77
11273008-4	2001	The second glioblastoma also contained multiple, but different mutations: p53 mutations in codons 158 (CGC--&gt;CAC, Arg--&gt;His) and 273 (CGT--&gt;TGT, Arg--&gt;Cys), and a PTEN mutation in codon 233 (CGA--&gt;TGA, Arg--&gt;Stop).	Cysteine	163-166	P53	Homo sapiens	74-77
11273008-4	2001	The second glioblastoma also contained multiple, but different mutations: p53 mutations in codons 158 (CGC--&gt;CAC, Arg--&gt;His) and 273 (CGT--&gt;TGT, Arg--&gt;Cys), and a PTEN mutation in codon 233 (CGA--&gt;TGA, Arg--&gt;Stop).	Arginine	154-157	P53	Homo sapiens	74-77
11162600-0	2001	p53 independent G(1) arrest induced by DL-alpha-difluoromethylornithine.	Eflornithine	39-71	P53	Homo sapiens	0-3
11284622-5	2001	Because p53 status influences the expression of microtubule-associated proteins and hence the sensitivity of a tumor to taxanes, it is possible that molecular markers could be used to customize chemotherapy to individual patients.	Taxoids	120-127	P53	Homo sapiens	8-11
11239457-1	2001	Phosphorylation of the human p53 protein at Ser-392 has been shown to be responsive to UV but not gamma irradiation.	Serine	44-47	P53	Homo sapiens	29-32
11239457-2	2001	Here we describe identification and purification of a mammalian UV-activated protein kinase complex that phosphorylates Ser-392 of p53 in vitro.	Serine	120-123	P53	Homo sapiens	131-134
28140079-5	2001	Because p53 status influences the expression of microtubule-associated proteins and hence the sensitivity of a tumor to taxanes, it is possible that molecular markers could be used to customize chemotherapy to individual patients.	Taxoids	120-127	P53	Homo sapiens	8-11
11162600-5	2001	DFMO induced MKN45 cell G(1) phase arrest after 48 h, and the percentage of G(1) arrest cells continued to increase until 72 h. Expression of p21 and phosphorylation of Stat1 were significantly induced by DFMO at 24 h. Luciferase assay and gel shift assay showed specific binding of Stat1 to the p21 promoter, and promoter activity was activated at 24 h. In dominant negative p53 expressing cells, DFMO significantly induced p21 expression, arrested cells at G(1) phase, and suppressed cell growth effectively.	Eflornithine	0-4	P53	Homo sapiens	376-379
11162600-5	2001	DFMO induced MKN45 cell G(1) phase arrest after 48 h, and the percentage of G(1) arrest cells continued to increase until 72 h. Expression of p21 and phosphorylation of Stat1 were significantly induced by DFMO at 24 h. Luciferase assay and gel shift assay showed specific binding of Stat1 to the p21 promoter, and promoter activity was activated at 24 h. In dominant negative p53 expressing cells, DFMO significantly induced p21 expression, arrested cells at G(1) phase, and suppressed cell growth effectively.	Eflornithine	205-209	P53	Homo sapiens	376-379
11228099-7	2001	In the TP53 mutant cell lines, azadirachtin reduced the proportion of dividing cells and induced formation of micronuclei.	azadirachtin	31-43	P53	Homo sapiens	7-11
11162600-5	2001	DFMO induced MKN45 cell G(1) phase arrest after 48 h, and the percentage of G(1) arrest cells continued to increase until 72 h. Expression of p21 and phosphorylation of Stat1 were significantly induced by DFMO at 24 h. Luciferase assay and gel shift assay showed specific binding of Stat1 to the p21 promoter, and promoter activity was activated at 24 h. In dominant negative p53 expressing cells, DFMO significantly induced p21 expression, arrested cells at G(1) phase, and suppressed cell growth effectively.	Eflornithine	205-209	P53	Homo sapiens	376-379
11162600-6	2001	These results suggest that DFMO induced MKN45 cell arrest at G(1) phase in a p53 independent manner, and Stat1 is, at least in part, involved in G(1) arrest.	Eflornithine	27-31	P53	Homo sapiens	77-80
11162602-6	2001	However, cisplatin neither reduced cyclin B1 expression nor induced G2 phase arrest, while it induced a comparable amount of p53 protein.	Cisplatin	9-18	P53	Homo sapiens	125-128
11313973-4	2001	By prolonged nocodazole treatment, U251MG human glioma cell, which has a p53 mutation, underwent transient arrest at mitosis, and subsequently exited from mitotic arrest (termed "mitotic slippage") followed by DNA replication without cytokinesis, resulting in hyperploid formation.	Nocodazole	13-23	P53	Homo sapiens	73-76
11139340-5	2001	In contrast, betulinic acid, a novel chemotherapeutic compound, induced apoptosis and KILLER/DR5 mRNA in melanoma and glioblastoma cells through a p53-independent mechanism.	betulinic acid	13-27	P53	Homo sapiens	147-150
11313973-6	2001	By employing LN382 glioma cell that has a temperature-sensitive p53 mutation, we found that the activation of p53 prevents hyperploid formation after the prolonged nocodazole treatment.	Nocodazole	164-174	P53	Homo sapiens	64-67
11313973-6	2001	By employing LN382 glioma cell that has a temperature-sensitive p53 mutation, we found that the activation of p53 prevents hyperploid formation after the prolonged nocodazole treatment.	Nocodazole	164-174	P53	Homo sapiens	110-113
11139340-6	2001	The synthetic glucocorticoid dexamethasone elevated KILLER/DR5 mRNA in glioblastoma, ovarian cancer, and colon cancer cell lines with mutant p53 undergoing apoptosis, and this induction was inhibited by the transcriptional inhibitor actinomycin D.	Dexamethasone	29-42	P53	Homo sapiens	141-144
11313957-3	2001	Basal levels of p53 and p21(WAF1/CIP1), phosphorylation on serine 15 of p53, and the Tyr15-phosphorylated form of cdc2 are chronically elevated in these cells.	Serine	59-65	P53	Homo sapiens	72-75
11076933-1	2001	We previously reported that p73, like p53, utilizes p300 or cAMP-response element-binding protein-binding protein as its coactivator.	Cyclic AMP	60-64	P53	Homo sapiens	38-41
11146441-10	2001	Co-incubation with p53 anti-sense oligo-nucleotide suppressed As(2)O(3)-induced intracellular p53 over-expression and apoptosis.	Oligonucleotides	34-50	P53	Homo sapiens	19-22
11146441-10	2001	Co-incubation with p53 anti-sense oligo-nucleotide suppressed As(2)O(3)-induced intracellular p53 over-expression and apoptosis.	Oligonucleotides	34-50	P53	Homo sapiens	94-97
11149936-6	2001	These changes in p21(Waf1) expression correlated with both the induction of DNA damage (as measured by micronucleus formation) as well as increased Ser-15 phosphorylation of p53.	Serine	148-151	P53	Homo sapiens	174-177
11212257-2	2001	It was suggested that HPV 16 E6 variants and the p53 codon 72 arginine polymorphism could be progression markers.	Arginine	62-70	P53	Homo sapiens	49-52
11212257-3	2001	Indeed, it has been demonstrated that specific E6 variants and p53 arginine were both enriched in cancer.	Arginine	67-75	P53	Homo sapiens	63-66
11212257-5	2001	Our aim was thus to investigate whether p53 arginine is important for cervical carcinogenesis by scaling up samples of the two European cohorts, the initial results of which were reported previously.	Arginine	44-52	P53	Homo sapiens	40-43
11212257-7	2001	We found p53 arginine to be increased in cancer of both cohorts, consistent with our previous concept.	Arginine	13-21	P53	Homo sapiens	9-12
11212257-8	2001	Although specific E6 genotypes increased gradually with the severity of the lesion, p53 arginine was enriched in cancer only.	Arginine	88-96	P53	Homo sapiens	84-87
11212257-10	2001	It is concluded that p53 arginine is a risk factor for cervical cancer but probably acts independently of E6 variants.	Arginine	25-33	P53	Homo sapiens	21-24
11212259-0	2001	Human papillomavirus type 16 E6 inactivation of p53 in normal human mammary epithelial cells promotes tamoxifen-mediated apoptosis.	Tamoxifen	102-111	P53	Homo sapiens	48-51
11212259-4	2001	Early passage p53(-) HMEC-E6-transduced cells treated with 1.0 microM tamoxifen rapidly underwent apoptosis.	Tamoxifen	70-79	P53	Homo sapiens	14-17
11212259-5	2001	In contrast, early passage p53(+) HMEC-LXSN vector controls treated with 1.0 microM tamoxifen underwent G1-G0-phase arrest but did not undergo apoptosis.	Tamoxifen	84-93	P53	Homo sapiens	27-30
11212259-6	2001	p53(-) HMEC-E6 cells rapidly acquired resistance to tamoxifen-mediated apoptosis after 10 passages in culture (in the absence of tamoxifen).	Tamoxifen	52-61	P53	Homo sapiens	0-3
11212259-8	2001	Tamoxifen-mediated apoptosis in p53(-) HMEC-E6 cells was not blocked by inhibitors of transcription and protein synthesis.	Tamoxifen	0-9	P53	Homo sapiens	32-35
11212259-9	2001	These data suggest that the acute loss of p53 function in HMECs by expression of HPV-16 E6 results in marked sensitivity to tamoxifen-mediated apoptosis but that resistance to apoptosis rapidly develops within 10 passages in vitro.	Tamoxifen	124-133	P53	Homo sapiens	42-45
11212244-8	2001	p53 expression was significantly elevated in the cells treated with CV787 and taxane.	taxane	78-84	P53	Homo sapiens	0-3
11313944-0	2001	Taxol-induced apoptosis depends on MAP kinase pathways (ERK and p38) and is independent of p53.	Paclitaxel	0-5	P53	Homo sapiens	91-94
11313944-4	2001	We found that Taxol treatment strongly activated ERK, p38 MAP kinase and p53 in MAP kinase MCF7 cells prior to apoptosis.	Paclitaxel	14-19	P53	Homo sapiens	73-76
11313944-8	2001	However, cells with inactivated p53, unlike cells harboring wild type p53, failed to arrest in G2/M after treatment with Taxol and continued to divide or go into apoptosis.	Paclitaxel	121-126	P53	Homo sapiens	32-35
11313944-9	2001	Our data show that both ERK and p38 MAP kinase cascades are essential for apoptotic response to Taxol-induced cellular killing and are independent of p53 activity.	Paclitaxel	96-101	P53	Homo sapiens	150-153
11313944-10	2001	However, p53 may serve as a survival factor in breast carcinoma cells treated with Taxol by blocking cells in G2/M phase of the cell cycle.	Paclitaxel	83-88	P53	Homo sapiens	9-12
11036071-3	2001	Recently we reported that Tax inhibits p53 function in Jurkat cells and mouse embryo fibroblasts through a mechanism involving the nuclear factor kappa B pathway and correlates with phosphorylation on serines 15 and 392 of p53.	Serine	201-208	P53	Homo sapiens	39-42
11244509-6	2001	p53 phosphorylation also varied in a MTI-dependent manner, as Taxol and Vincristine induced more p53 phospho-forms than nocodazole.	Paclitaxel	62-67	P53	Homo sapiens	0-3
11244509-6	2001	p53 phosphorylation also varied in a MTI-dependent manner, as Taxol and Vincristine induced more p53 phospho-forms than nocodazole.	Nocodazole	120-130	P53	Homo sapiens	0-3
11244509-7	2001	Further, MTI treatment increased phosphorylation of p53 on serine-15 in epithelial tumor cells.	Serine	59-65	P53	Homo sapiens	52-55
11244509-8	2001	In contrast, serine-15 phosphorylation of p53 did not increase in MTI-treated primary cultures of human fibroblasts.	Serine	13-19	P53	Homo sapiens	42-45
11244509-9	2001	Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53.	Paclitaxel	67-72	P53	Homo sapiens	127-130
11244509-9	2001	Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53.	Paclitaxel	67-72	P53	Homo sapiens	127-130
11244509-9	2001	Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53.	Nocodazole	78-88	P53	Homo sapiens	34-37
11669337-10	2001	A common polymorphism in p53 at codon 72 (arginine/proline) was found in 6/8 of the patients.	Arginine	42-50	P53	Homo sapiens	25-28
11244509-9	2001	Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53.	Nocodazole	78-88	P53	Homo sapiens	127-130
11244509-9	2001	Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53.	Nocodazole	78-88	P53	Homo sapiens	127-130
11244509-9	2001	Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53.	Serine	166-172	P53	Homo sapiens	34-37
11244509-9	2001	Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53.	Serine	166-172	P53	Homo sapiens	127-130
11244509-9	2001	Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53.	Serine	166-172	P53	Homo sapiens	127-130
11244509-9	2001	Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53.	Threonine	180-189	P53	Homo sapiens	127-130
11244509-9	2001	Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53.	Threonine	180-189	P53	Homo sapiens	127-130
11244509-9	2001	Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53.	Paclitaxel	212-217	P53	Homo sapiens	127-130
11244509-9	2001	Analysis of ectopically expressed p53 phospho-mutant proteins from Taxol- and nocodazole-treated cells indicated that multiple p53 amino terminal residues, including serine-15 and threonine-18, were required for Taxol-mediated phosphorylation of p53.	Paclitaxel	212-217	P53	Homo sapiens	127-130
11642302-3	2001	Adaptive response by 5~20 cGy of such C- or Fe-ion irradiation to both lethal and mutagenic effects of the challenging X-ray exposure (1~3 Gy) was difficult to be seen in this TK6 cells, but surprisingly, a relatively high level of p53 and its related proteins induction was observed after low-dose irradiations of heavy-ions.	Iron	44-46	P53	Homo sapiens	232-235
11197251-2	2001	This study investigated the effect of folate supplementation on genomic DNA methylation and DNA strand breaks in exons 5-8 of the p53 gene of the colonic mucosa, two provisional biomarkers of colon cancer.	Folic Acid	38-44	P53	Homo sapiens	130-133
11174479-1	2001	OBJECTIVE: It has recently been suggested that white women who are homozygous for the allele of the gene for wild-type p53 protein (TP53) that encodes arginine at position 72 are more susceptible to human papillomavirus-associated cervical carcinoma than are women who are heterozygous for this polymorphism and women who are homozygous for the allele that encodes proline at that position.	Arginine	151-159	P53	Homo sapiens	119-122
11174479-1	2001	OBJECTIVE: It has recently been suggested that white women who are homozygous for the allele of the gene for wild-type p53 protein (TP53) that encodes arginine at position 72 are more susceptible to human papillomavirus-associated cervical carcinoma than are women who are heterozygous for this polymorphism and women who are homozygous for the allele that encodes proline at that position.	Arginine	151-159	P53	Homo sapiens	132-136
11197251-7	2001	Similarly, folate supplementation decreased the extent of p53 strand breaks in exons 5-8 at 6 months and 1 yr (p &lt; 0.02), whereas placebo administration was associated with a decrease in the extent of p53 strand breaks only at 1 yr.	Folic Acid	11-17	P53	Homo sapiens	58-61
11197251-7	2001	Similarly, folate supplementation decreased the extent of p53 strand breaks in exons 5-8 at 6 months and 1 yr (p &lt; 0.02), whereas placebo administration was associated with a decrease in the extent of p53 strand breaks only at 1 yr.	Folic Acid	11-17	P53	Homo sapiens	204-207
11483158-0	2001	Glycogen synthase kinase3 beta phosphorylates serine 33 of p53 and activates p53"s transcriptional activity.	Serine	46-52	P53	Homo sapiens	59-62
11133492-8	2001	This radiation-induced increase in MMP-2 expression was mediated via p53 because the p53 antisense oligonucleotide abolished the increase in MMP-2 activity as well as the accumulation of p53 after irradiation in A549 cells.	Oligonucleotides	99-114	P53	Homo sapiens	69-72
11133492-8	2001	This radiation-induced increase in MMP-2 expression was mediated via p53 because the p53 antisense oligonucleotide abolished the increase in MMP-2 activity as well as the accumulation of p53 after irradiation in A549 cells.	Oligonucleotides	99-114	P53	Homo sapiens	85-88
11133492-8	2001	This radiation-induced increase in MMP-2 expression was mediated via p53 because the p53 antisense oligonucleotide abolished the increase in MMP-2 activity as well as the accumulation of p53 after irradiation in A549 cells.	Oligonucleotides	99-114	P53	Homo sapiens	85-88
11299739-6	2001	We therefore concluded that immunohistochemical studies for p53 and p21 were useful for predicting the chemosensitivities of colon and gastric cancer to MMC and 5-FU.	Fluorouracil	161-165	P53	Homo sapiens	60-63
11299740-5	2001	RESULTS: We found that adriamycin induced a p53 and p21 response as well as a G1 arrest in 184B5 cells, but not in its E6 transformed cells.	Doxorubicin	23-33	P53	Homo sapiens	44-47
11299740-7	2001	In addition, staurosporine or UCNO1 specifically sensitized p53 incompetent cells to adriamycin.	Doxorubicin	85-95	P53	Homo sapiens	60-63
11483158-6	2001	Our results demonstrate that phosphorylation of serine 37 of p53 by DNA-PK creates a site for GSK3beta phosphorylation at serine 33 in vitro.	Serine	48-54	P53	Homo sapiens	61-64
11483158-6	2001	Our results demonstrate that phosphorylation of serine 37 of p53 by DNA-PK creates a site for GSK3beta phosphorylation at serine 33 in vitro.	Serine	122-128	P53	Homo sapiens	61-64
11483158-9	2001	Mutation of either serine 33 or serine 37 of p53 to alanine blocked the ability of GSK3beta to regulate p53 transcriptional activity.	Serine	19-25	P53	Homo sapiens	104-107
11483158-9	2001	Mutation of either serine 33 or serine 37 of p53 to alanine blocked the ability of GSK3beta to regulate p53 transcriptional activity.	Serine	32-38	P53	Homo sapiens	45-48
11483158-9	2001	Mutation of either serine 33 or serine 37 of p53 to alanine blocked the ability of GSK3beta to regulate p53 transcriptional activity.	Serine	32-38	P53	Homo sapiens	104-107
11483158-9	2001	Mutation of either serine 33 or serine 37 of p53 to alanine blocked the ability of GSK3beta to regulate p53 transcriptional activity.	Alanine	52-59	P53	Homo sapiens	45-48
11483158-9	2001	Mutation of either serine 33 or serine 37 of p53 to alanine blocked the ability of GSK3beta to regulate p53 transcriptional activity.	Alanine	52-59	P53	Homo sapiens	104-107
11483158-13	2001	CONCLUSIONS: GSK3beta can regulate p53"s transcriptional activity by phosphorylating serine 33.	Serine	85-91	P53	Homo sapiens	35-38
11196199-0	2001	Human homologue of yeast Rad23 protein A interacts with p300/cyclic AMP-responsive element binding (CREB)-binding protein to down-regulate transcriptional activity of p53.	Cyclic AMP	61-71	P53	Homo sapiens	167-170
11146880-2	2001	Under low levels of oxygen (hypoxia), cells expressing wild-type p53 undergo programmed cell death (apoptosis), whereas cells expressing mutations in the p53 gene may survive and express angiogenic growth factors that stimulate tumour vascularization.	Oxygen	20-26	P53	Homo sapiens	65-68
11146880-4	2001	In this paper a mathematical model is presented to investigate the effects of alternating periods of hypoxia and normoxia (normal oxygen levels) on a population of wild-type and mutant p53 tumour cells.	Oxygen	130-136	P53	Homo sapiens	185-188
11159751-0	2001	Sequence-specific detection of aristolochic acid-DNA adducts in the human p53 gene by terminal transferase-dependent PCR.	aristolochic acid I	31-48	P53	Homo sapiens	74-77
11269743-0	2001	P53-independent downregulation of p73 in human cancer cells treated with Adriamycin.	Doxorubicin	73-83	P53	Homo sapiens	0-3
11196204-5	2001	However, both the dephosphorylation of serine 376 of p53 (contained in the PAb-421 epitope) and the specific DNA binding activity, as well as apoptosis, were enhanced toward the G2-M populations.	Serine	39-45	P53	Homo sapiens	53-56
11120603-3	2001	We established a p53-deficient derivative of these cells, in which G2 arrest also occurred after treatment with Adriamycin, suggesting that the arrest we observed in these cells is independent of the p53 pathway.	Doxorubicin	112-122	P53	Homo sapiens	17-20
11482901-8	2001	However, only wild-type p53 transcripts were amplified by RT-PCR of MOLT-4 cells exposed to phytohaemagglutinin, linoleic acid or linolelaidic acid.	Linoleic Acid	113-126	P53	Homo sapiens	24-27
11482901-8	2001	However, only wild-type p53 transcripts were amplified by RT-PCR of MOLT-4 cells exposed to phytohaemagglutinin, linoleic acid or linolelaidic acid.	Linoleic Acid	130-147	P53	Homo sapiens	24-27
11405176-0	2001	Mitomycin C and cisplatin enhanced the antitumor activity of p53-expressing adenovirus in cervical cancer cells.	Cisplatin	16-25	P53	Homo sapiens	61-64
11544635-15	2001	Furthermore, the inhibition of PARP-1 activity in G1 arrested cells by 3-aminobenzamide abolished its stabilizing effect on the wild-type p53 protein.	3-aminobenzamide	71-87	P53	Homo sapiens	138-141
11872944-0	2001	Dopamine induces phenotypic differentiation or apoptosis in a dose-dependent fashion: involvement of the dopamine transporter and p53.	Dopamine	0-8	P53	Homo sapiens	130-133
11872944-6	2001	High concentrations of dopamine, which induced apoptosis, also increased p53 levels, detected by RT-PCR analysis and immunoblotting, whereas lower dopamine concentrations, which induced a differentiated phenotype, did not increase p53 immunoblotting.	Dopamine	23-31	P53	Homo sapiens	73-76
11120603-4	2001	Low doses of Adriamycin (100-200 ng/ml) induced G2 arrest, while late S-phase arrest was observed at high doses (500-1000 ng/ml) in both FL and p53-deficient FL cells.	Doxorubicin	13-23	P53	Homo sapiens	144-147
11500921-9	2001	The level of the p53 mRNA reached its maximum at 12 h and decreased after 24 h of incubation with progesterone.	Progesterone	98-110	P53	Homo sapiens	17-20
11423998-6	2001	Tyrosine-phosphorylation of p53/p46Shc isoforms were found in CD34+ but not in the majority of CD34- cases.	Tyrosine	0-8	P53	Homo sapiens	28-31
11508859-0	2001	New monoclonal antibodies recognizing p53 protein phosphorylated by casein kinase II at serine 392.	Serine	88-94	P53	Homo sapiens	38-41
11208917-3	2001	We have also shown that reactive iron (Fe3+) and cGMP staining spatially resemble that of HO-1; which, in turn, colocalizes in motor neurons with transcription factors: Fas-associated protein containing death domain (FADD), tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and p53.	Iron	33-37	P53	Homo sapiens	298-301
11208917-3	2001	We have also shown that reactive iron (Fe3+) and cGMP staining spatially resemble that of HO-1; which, in turn, colocalizes in motor neurons with transcription factors: Fas-associated protein containing death domain (FADD), tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and p53.	Cyclic GMP	49-53	P53	Homo sapiens	298-301
11384868-4	2001	Supplementation of culture medium containing stripped serum with 0.1-1 nM estradiol (E(2)) restored p53 to its level seen in the control within 6-24 h. Under above conditions, treatment of cells with R5020 or RU486 reduced (15-30%) the level of p53.	Estradiol	74-83	P53	Homo sapiens	100-103
11384868-4	2001	Supplementation of culture medium containing stripped serum with 0.1-1 nM estradiol (E(2)) restored p53 to its level seen in the control within 6-24 h. Under above conditions, treatment of cells with R5020 or RU486 reduced (15-30%) the level of p53.	Estradiol	74-83	P53	Homo sapiens	245-248
11464863-0	2001	Retinoic acid-induced apoptosis of the CHP134 neuroblastoma cell line is associated with nuclear accumulation of p53 and is rescued by the GDNF/Ret signal.	Tretinoin	0-13	P53	Homo sapiens	113-116
11464863-11	2001	The present results suggest that the RA-induced apoptosis of NBL cells is associated with activation of both the caspase cascade and the p53-mediated pathway with its nuclear translocation.	Tretinoin	37-39	P53	Homo sapiens	137-140
11125034-7	2001	Notably, when MDM2 expression is inhibited in S-type cells, with a phosphorothioated antisense oligonucleotide (AS5), then p53 accumulates in the nucleus and the SH-EP1 cells undergo apoptosis.	Oligonucleotides	95-110	P53	Homo sapiens	123-126
11462854-0	2001	Gene therapy approaches to sensitization of human prostate carcinoma to cisplatin by adenoviral expression of p53 and by antisense jun kinase oligonucleotide methods.	Cisplatin	72-81	P53	Homo sapiens	110-113
11255264-4	2001	We set out a case-control study to determine the risk of squamous cell carcinoma of the skin in individuals with the p53 codon 72 arginine genotype in order to establish the possible need for screening.	Arginine	130-138	P53	Homo sapiens	117-120
21340840-7	2001	We have identified a missense mutation in the p53 gene in the 2774 ovarian cancer cell line that converts an arginine residue in the DNA binding region of the protein to a histidine residue (6).	Arginine	109-117	P53	Homo sapiens	46-49
21340840-7	2001	We have identified a missense mutation in the p53 gene in the 2774 ovarian cancer cell line that converts an arginine residue in the DNA binding region of the protein to a histidine residue (6).	Histidine	172-181	P53	Homo sapiens	46-49
11121242-3	2001	X irradiation caused persistent phosphorylation of TP53 at Ser 15 and accumulation of the TP53 protein, followed by the induction of CDKN1A (also known as p21(Waf1/Cip1)) and CDKN2A (also known as p16), preceded the expression of SA-beta-gal.	Serine	59-62	P53	Homo sapiens	51-55
11148457-1	2001	Expression of p53 protein and MDM2 was evaluated in paraffin-embedded tissue from 78 patients with papillary carcinomas of the thyroid (PCT), in order to elucidate the relationship between them and their correlations with some clinicopathologic features implicated in tumor progression.	Paraffin	52-60	P53	Homo sapiens	14-17
11326311-0	2001	Cisplatinum and taxol induce different patterns of p53 phosphorylation.	Cisplatin	0-11	P53	Homo sapiens	51-54
11326311-0	2001	Cisplatinum and taxol induce different patterns of p53 phosphorylation.	Paclitaxel	16-21	P53	Homo sapiens	51-54
11326311-1	2001	Posttranslational modifications of p53 induced by two widely used anticancer agents, cisplatinum (DDP) and taxol were investigated in two human cancer cell lines.	Cisplatin	85-96	P53	Homo sapiens	35-38
11326311-1	2001	Posttranslational modifications of p53 induced by two widely used anticancer agents, cisplatinum (DDP) and taxol were investigated in two human cancer cell lines.	Cisplatin	98-101	P53	Homo sapiens	35-38
11326311-1	2001	Posttranslational modifications of p53 induced by two widely used anticancer agents, cisplatinum (DDP) and taxol were investigated in two human cancer cell lines.	Paclitaxel	107-112	P53	Homo sapiens	35-38
11326311-2	2001	Although both drugs were able to induce phosphorylation at serine 20 (Ser20), only DDP treatment induced p53 phosphorylation at serine 15 (Ser15).	Serine	128-134	P53	Homo sapiens	105-108
11692147-2	2001	Immunohistochemical analysis of MDM2 and p53 proteins on paraffin embedded sections from 64 surgically resected ESCCs and matched histologically normal tissues showed overexpression of MDM2 protein in 23/64 (36%) ESCCs, while the histopathologically normal esophageal tissues did not show detectable level of MDM2 immunoreactivity.	Paraffin	57-65	P53	Homo sapiens	41-44
11785103-0	2001	[Role of the antioxidant system and redox-dependent regulation of transcription factors bcl-2 and p53 in forming resistance of human K562 erythroleukemia cells to doxorubicin].	Doxorubicin	163-174	P53	Homo sapiens	98-101
11495153-11	2001	The presence of serum p53-Abs was associated with decreased in vitro chemosensitivity to CDDP and 5-FU.	Cisplatin	89-93	P53	Homo sapiens	22-25
11495153-11	2001	The presence of serum p53-Abs was associated with decreased in vitro chemosensitivity to CDDP and 5-FU.	Fluorouracil	98-102	P53	Homo sapiens	22-25
11695560-4	2001	Two hormones that are human tumorigens, diethylstilbestrol and 17beta-estradiol, gave positive and equivocal results, respectively, in the pituitary with p53-deficient mice showing a greater incidence of proliferative lesions than wild type.	Estradiol	63-79	P53	Homo sapiens	154-157
11156383-0	2000	Preferential retention of codon 72 arginine p53 in squamous cell carcinomas of the vulva occurs in cancers positive and negative for human papillomavirus.	Arginine	35-43	P53	Homo sapiens	44-47
11016934-6	2000	Using a combination of alanine scanning, polymer blot analysis, and photoaffinity labeling, we have identified poly(ADP-ribose)-binding sites in the following proteins: p53, p21(CIP1/WAF1), xeroderma pigmentosum group A complementing protein, MSH6, DNA ligase III, XRCC1, DNA polymerase epsilon, DNA-PK(CS), Ku70, NF-kappaB, inducible nitric-oxide synthase, caspase-activated DNase, and telomerase.	Alanine	23-30	P53	Homo sapiens	169-172
11097743-5	2000	Co-transfection of the p53 His(273)expression construct with a luciferase gene controlled by the p21(WAF1)promoter showed that the p53 His(273)was inactive, although TNF-alpha increased the transcriptional rate of p21(WAF1)in these cells.	Histidine	27-30	P53	Homo sapiens	23-26
11175334-0	2000	DNA damage-induced phosphorylation of p53 at serine 20 correlates with p21 and Mdm-2 induction in vivo.	Serine	45-51	P53	Homo sapiens	38-41
11175336-4	2000	We found the formation of previously unreported nuclear complexes between the tumor suppressor protein p53 and the pro-apoptotic protein Bax, in human melanoma cell lines induced into apoptosis following cisplatin exposure.	Cisplatin	204-213	P53	Homo sapiens	103-106
11175336-6	2000	Three channel fluorescence laser scanning confocal image microscopy revealed that the nuclear Bax/p53 complexes remained in the nucleus and localized proximal to DNA fragmentation sites as assayed by TUNEL after cisplatin exposure.	Cisplatin	212-221	P53	Homo sapiens	98-101
11175336-7	2000	Two human melanoma cell lines, expressing wt p53, were induced into apoptosis after cisplatin exposure, however they differed in the timing of this induction.	Cisplatin	84-93	P53	Homo sapiens	45-48
11175336-9	2000	The degree of apoptosis induced by different concentrations of cisplatin correlated with the amount of nuclear Bax/p53 complexes.	Cisplatin	63-72	P53	Homo sapiens	115-118
11175336-11	2000	Additionally, the human prostate cancer cell line, LNCaP, also formed nuclear Bax/p53 complexes only after apoptosis was induced by paclitaxel.	Paclitaxel	132-142	P53	Homo sapiens	82-85
11090076-8	2000	These findings indicate that treatment with etoposide, Ara-C, or doxorubicin up-regulates DR5 levels in a p53-independent manner and sensitizes human acute leukemia cells to Apo-2L-induced apoptosis.	Doxorubicin	65-76	P53	Homo sapiens	106-109
11156235-8	2000	These data suggest that LOH at chromosome 17p13 is associated with a good clinical response to cisplatin-based chemotherapy, suggesting that altered p53 function might render cells more sensitive to therapy.	Cisplatin	95-104	P53	Homo sapiens	149-152
11097743-5	2000	Co-transfection of the p53 His(273)expression construct with a luciferase gene controlled by the p21(WAF1)promoter showed that the p53 His(273)was inactive, although TNF-alpha increased the transcriptional rate of p21(WAF1)in these cells.	Histidine	135-138	P53	Homo sapiens	23-26
11097743-5	2000	Co-transfection of the p53 His(273)expression construct with a luciferase gene controlled by the p21(WAF1)promoter showed that the p53 His(273)was inactive, although TNF-alpha increased the transcriptional rate of p21(WAF1)in these cells.	Histidine	135-138	P53	Homo sapiens	131-134
11133809-1	2000	In human fibroblasts, N:-phosphoacetyl-L-aspartate (PALA) and gamma-radiation induce reversible and irreversible p53-mediated G(1) cell cycle arrest, respectively.	Nitrogen	22-23	P53	Homo sapiens	113-116
11097743-5	2000	Co-transfection of the p53 His(273)expression construct with a luciferase gene controlled by the p21(WAF1)promoter showed that the p53 His(273)was inactive, although TNF-alpha increased the transcriptional rate of p21(WAF1)in these cells.	Histidine	27-30	P53	Homo sapiens	131-134
11153146-6	2000	CONCLUSIONS: This data indicates that in high-risk breast cancer patients the immunohistochemical evaluation of p53 and bcl-2 may be of clinical value in distinguishing different responses to adjuvant anthracycline-based chemotherapy.	Anthracyclines	201-214	P53	Homo sapiens	112-115
11072252-4	2000	In this study, we have used a novel oligonucleotide anti-sense MDM2, with mixed-backbone structure and demonstrate that it causes inhibition of MDM2 expression, induction of both p53 and p21/WAF1 expression and a dose-dependent, growth-inhibitory effect in human GEO colon-cancer cells.	Oligonucleotides	36-51	P53	Homo sapiens	179-182
11099323-1	2000	PURPOSE: The p53 gene plays a critical role in cellular response to DNA damage and has been implicated in the response to platinum compounds in ovarian carcinoma patients.	Platinum	122-130	P53	Homo sapiens	13-16
11099323-2	2000	Because taxanes could induce p53-independent apoptosis, we assessed the relevance of p53 gene status to response in ovarian carcinoma patients receiving paclitaxel and platinum-containing chemotherapy.	Taxoids	8-15	P53	Homo sapiens	29-32
11099323-2	2000	Because taxanes could induce p53-independent apoptosis, we assessed the relevance of p53 gene status to response in ovarian carcinoma patients receiving paclitaxel and platinum-containing chemotherapy.	Paclitaxel	153-163	P53	Homo sapiens	85-88
11099323-2	2000	Because taxanes could induce p53-independent apoptosis, we assessed the relevance of p53 gene status to response in ovarian carcinoma patients receiving paclitaxel and platinum-containing chemotherapy.	Platinum	168-176	P53	Homo sapiens	85-88
11099323-14	2000	CONCLUSION: In contrast to the limited efficacy of treatment with paclitaxel in combination with standard platinum doses against wild-type p53 ovarian tumors, patients with mutant p53 ovarian tumors were more responsive to paclitaxel-based chemotherapy.	Paclitaxel	66-76	P53	Homo sapiens	139-142
11099323-14	2000	CONCLUSION: In contrast to the limited efficacy of treatment with paclitaxel in combination with standard platinum doses against wild-type p53 ovarian tumors, patients with mutant p53 ovarian tumors were more responsive to paclitaxel-based chemotherapy.	Paclitaxel	223-233	P53	Homo sapiens	180-183
11163861-7	2000	Next, we examined the expression of TRX and p53 in breast cancer cell line MCF-7 cells after CDDP treatment or irradiation.	cddp	93-97	P53	Homo sapiens	44-47
11163861-8	2000	CDDP treatment or irradiation augmented expression of TRX and p53 in MCF-7 cells by western blotting.	cddp	0-4	P53	Homo sapiens	62-65
11133047-4	2000	The accumulation of hsp72 and p53 was observed in A-172 cells after exposure to the conditioned medium of the T98G cells irradiated with accelerated carbon-ion beams, and the accumulation was abolished by the addition of an inhibitor for inducible nitric oxide synthase to the medium.	Carbon	149-155	P53	Homo sapiens	30-33
11153146-0	2000	Role of P53 and BCL-2 in high-risk breast cancer patients treated with adjuvant anthracycline-based chemotherapy.	Anthracyclines	80-93	P53	Homo sapiens	8-11
11071927-4	2000	We show that upon treatment of HepG2 cells with 5-fluorouracil or methotrexate, p53 levels increase while concentrations of cyclin B2 mRNA, measured by RT-PCR with the LightCycler system, are reduced.	Fluorouracil	48-62	P53	Homo sapiens	80-83
11096420-0	2000	Abrogation of G(2)/M-phase block enhances the cytotoxicity of daunorubicin, melphalan and cisplatin in TP53 mutant human tumor cells.	Cisplatin	90-99	P53	Homo sapiens	103-107
11096420-3	2000	In the TP53-mutated cell lines MeWo and 4451, the survival ratio at 7 Gy measured by colony formation was 2.3-2.8, 8.6-85 and 52-74 for daunorubicin, melphalan and cisplatin, respectively.	Cisplatin	164-173	P53	Homo sapiens	7-11
11099651-10	2000	Many of the "fingerprint genes" identified in these studies were consistent with previous observations reported in the literature (e. g., the well-characterized induction by cisplatin of p53-regulated transcripts such as p21(waf1/cip1) and PCNA [proliferating cell nuclear antigen]).	Cisplatin	174-183	P53	Homo sapiens	187-190
11277327-0	2000	Adriamycin induced G2/M cell cycle arrest in transitional cell cancer cells with wt p53 and p21(WAF1/CIP1) genes.	Doxorubicin	0-10	P53	Homo sapiens	84-87
11129661-0	2000	Modulation of nitric oxide-evoked apoptosis by the p53-downstream target p21(WAF1/CIP1).	Nitric Oxide	14-26	P53	Homo sapiens	51-54
11129661-1	2000	When produced in excess, the inflammatory mediator nitric oxide (NO) attenuates cell-cycle progression at the G1 phase in tight correlation with p21(WAF1/CIP1) expression, provokes accumulation of the tumor suppressor p53, and initiates apoptosis/necrosis as judged on cell accumulation in the sub-G1 phase.	Nitric Oxide	51-63	P53	Homo sapiens	218-221
11094089-0	2000	Multiple lysine mutations in the C-terminal domain of p53 interfere with MDM2-dependent protein degradation and ubiquitination.	Lysine	9-15	P53	Homo sapiens	54-57
11080152-2	2000	We found that dexamethasone-activated endogenous and exogenous GR inhibit p53-dependent functions, including transactivation, up- (Bax and p21(WAF1/CIP1)) and down- (Bcl2) regulation of endogenous genes, cell cycle arrest and apoptosis.	Dexamethasone	14-27	P53	Homo sapiens	74-77
11103796-9	2000	p53 phosphorylation on serine 15 was also confirmed by immunoblotting technique in arsenite- and X-ray-treated HFW cells but was not observed in UV- or N-acetyl-Leu-Leu-norleucinal-treated HFW cells.	Serine	23-29	P53	Homo sapiens	0-3
11103825-2	2000	Recently, we demonstrated that CD437 induces apoptosis in human non-small cell lung cancer (NSCLC) cells expressing wild-type p53 by increasing the level of the death domain-containing cell surface receptor Killer/DR5.	CD 437	31-36	P53	Homo sapiens	126-129
11080808-5	2000	Tax does not accomplish this by directly binding to p53, but rather by a unique mechanism that includes constitutive phosphorylation of p53 at Ser-15 and Ser-392.	Serine	143-146	P53	Homo sapiens	136-139
11050162-7	2000	These results are consistent with the hypothesis that the generation of oxygen/nitrogen species and unsaturated aldehydes from iron and copper overload in hemochromatosis and WD causes mutations in the p53 tumor suppressor gene.	Oxygen	72-78	P53	Homo sapiens	202-205
11050162-7	2000	These results are consistent with the hypothesis that the generation of oxygen/nitrogen species and unsaturated aldehydes from iron and copper overload in hemochromatosis and WD causes mutations in the p53 tumor suppressor gene.	Nitrogen	79-87	P53	Homo sapiens	202-205
11050162-7	2000	These results are consistent with the hypothesis that the generation of oxygen/nitrogen species and unsaturated aldehydes from iron and copper overload in hemochromatosis and WD causes mutations in the p53 tumor suppressor gene.	Iron	127-131	P53	Homo sapiens	202-205
11050162-7	2000	These results are consistent with the hypothesis that the generation of oxygen/nitrogen species and unsaturated aldehydes from iron and copper overload in hemochromatosis and WD causes mutations in the p53 tumor suppressor gene.	Copper	136-142	P53	Homo sapiens	202-205
11077439-0	2000	Metalloregulation of the tumor suppressor protein p53: zinc mediates the renaturation of p53 after exposure to metal chelators in vitro and in intact cells.	Metals	111-116	P53	Homo sapiens	50-53
11077439-0	2000	Metalloregulation of the tumor suppressor protein p53: zinc mediates the renaturation of p53 after exposure to metal chelators in vitro and in intact cells.	Metals	111-116	P53	Homo sapiens	89-92
11080808-11	2000	Importantly, using phosphospecific antibodies, we demonstrate that phosphorylation of p53 at Ser-15 and Ser-392 correlates with Tax-mediated inhibition.	Serine	93-96	P53	Homo sapiens	86-89
11080808-12	2000	In addition, mutation of p53 at Ser-15 and Ser-392 to alanines renders p53 resistant to Tax inhibition.	Serine	32-35	P53	Homo sapiens	25-28
11080808-12	2000	In addition, mutation of p53 at Ser-15 and Ser-392 to alanines renders p53 resistant to Tax inhibition.	Serine	32-35	P53	Homo sapiens	71-74
11080808-12	2000	In addition, mutation of p53 at Ser-15 and Ser-392 to alanines renders p53 resistant to Tax inhibition.	Serine	43-46	P53	Homo sapiens	71-74
11080808-12	2000	In addition, mutation of p53 at Ser-15 and Ser-392 to alanines renders p53 resistant to Tax inhibition.	Alanine	54-62	P53	Homo sapiens	25-28
11080808-12	2000	In addition, mutation of p53 at Ser-15 and Ser-392 to alanines renders p53 resistant to Tax inhibition.	Alanine	54-62	P53	Homo sapiens	71-74
11064345-0	2000	Low dose fractionated radiation enhances the radiosensitization effect of paclitaxel in colorectal tumor cells with mutant p53.	Paclitaxel	74-84	P53	Homo sapiens	123-126
11205220-1	2000	BACKGROUND: The aim of this study was to assess the relationship between p53 status and the clinical outcome of patients with advanced ovarian cancer treated with a paclitaxel-based regimen.	Paclitaxel	165-175	P53	Homo sapiens	73-76
11205220-9	2000	These results are consistent with experimental data showing that paclitaxel cytotoxicity in ovarian cancer is likely to be mediated by a p53-independent pathway.	Paclitaxel	65-75	P53	Homo sapiens	137-140
11008128-8	2000	Additionally, the combination of ALLnL and cisplatin potently increased p53 levels in cell lysates and stimulated the binding of p53 to chromatin.	Cisplatin	43-52	P53	Homo sapiens	72-75
11008128-8	2000	Additionally, the combination of ALLnL and cisplatin potently increased p53 levels in cell lysates and stimulated the binding of p53 to chromatin.	Cisplatin	43-52	P53	Homo sapiens	129-132
11044365-2	2000	Nevertheless cell cycle arrest and apoptosis induction can be observed in p53-defective cells after exposure to DNA-damaging agents such as 5-fluorouracil (5-FU) suggesting the importance of alternative pathways via p53-independent mechanisms.	Fluorouracil	140-154	P53	Homo sapiens	74-77
11044365-2	2000	Nevertheless cell cycle arrest and apoptosis induction can be observed in p53-defective cells after exposure to DNA-damaging agents such as 5-fluorouracil (5-FU) suggesting the importance of alternative pathways via p53-independent mechanisms.	Fluorouracil	140-154	P53	Homo sapiens	216-219
11044365-2	2000	Nevertheless cell cycle arrest and apoptosis induction can be observed in p53-defective cells after exposure to DNA-damaging agents such as 5-fluorouracil (5-FU) suggesting the importance of alternative pathways via p53-independent mechanisms.	Fluorouracil	156-160	P53	Homo sapiens	74-77
11044365-2	2000	Nevertheless cell cycle arrest and apoptosis induction can be observed in p53-defective cells after exposure to DNA-damaging agents such as 5-fluorouracil (5-FU) suggesting the importance of alternative pathways via p53-independent mechanisms.	Fluorouracil	156-160	P53	Homo sapiens	216-219
11044365-5	2000	5-FU induced a rise in p53 mRNA expression in mt p53 cell lines and in human papilloma virus positive wt p53 cell line, whereas significant decrease in p53 mRNA expression was found in wt p53 cell line.	Fluorouracil	0-4	P53	Homo sapiens	23-26
11044365-5	2000	5-FU induced a rise in p53 mRNA expression in mt p53 cell lines and in human papilloma virus positive wt p53 cell line, whereas significant decrease in p53 mRNA expression was found in wt p53 cell line.	Fluorouracil	0-4	P53	Homo sapiens	49-52
11044365-5	2000	5-FU induced a rise in p53 mRNA expression in mt p53 cell lines and in human papilloma virus positive wt p53 cell line, whereas significant decrease in p53 mRNA expression was found in wt p53 cell line.	Fluorouracil	0-4	P53	Homo sapiens	49-52
11044365-5	2000	5-FU induced a rise in p53 mRNA expression in mt p53 cell lines and in human papilloma virus positive wt p53 cell line, whereas significant decrease in p53 mRNA expression was found in wt p53 cell line.	Fluorouracil	0-4	P53	Homo sapiens	49-52
11044365-5	2000	5-FU induced a rise in p53 mRNA expression in mt p53 cell lines and in human papilloma virus positive wt p53 cell line, whereas significant decrease in p53 mRNA expression was found in wt p53 cell line.	Fluorouracil	0-4	P53	Homo sapiens	49-52
11044365-7	2000	In relation with p53 functionality, but independently of p53 mutational status, after exposure to 5-FU equitoxic concentration, all cell lines were able to arrest in G1.	Fluorouracil	98-102	P53	Homo sapiens	17-20
11129289-4	2000	Paclitaxel was chosen for combination therapy in the preclinical study reported here due to its extensive use as a first-line therapy in ovarian cancer, its synergy with SCH58500 in preclinical cancer models, and its activation of p53-independent apoptosis, which might result in a "lowered threshold" for tumor cell death.	Paclitaxel	0-10	P53	Homo sapiens	231-234
11205289-0	2000	Restoration of wild-type p53 activity enhances the sensitivity of pleural metastasis to cisplatin through an apoptotic mechanism.	Cisplatin	88-97	P53	Homo sapiens	25-28
11205289-9	2000	In conclusion our results suggested that DOTAP is an efficient vector for mediating gene transfer in pleural metastatic cells offering advantages compared to viral vectors, while tumor suppressor genes such as p53 may be good candidates in combination with conventional therapy with CDDP that could be further developed for their use in local cancer gene therapy.	Cisplatin	283-287	P53	Homo sapiens	210-213
11050000-5	2000	Expression of wt p53 also leads to cell cycle arrest and protection from doxorubicin (Dox)- and melphalan (Mel)-induced apoptosis.	Doxorubicin	73-84	P53	Homo sapiens	17-20
11050000-5	2000	Expression of wt p53 also leads to cell cycle arrest and protection from doxorubicin (Dox)- and melphalan (Mel)-induced apoptosis.	Doxorubicin	86-89	P53	Homo sapiens	17-20
11044365-9	2000	Moreover, after 5-FU exposure, Bax and Bcl-2 proteins regulation was under p53 protein control and a statistically significant relationship (r = 0.880, P = 0.0097) was observed between Bcl-2/Bax ratio and 5-FU sensitivity.	Fluorouracil	16-20	P53	Homo sapiens	75-78
11064345-1	2000	BACKGROUND: The current study was undertaken to investigate the influence of wild-type or mutant p53 status on the radiosensitizing effect of paclitaxel in colorectal tumor cell lines.	Paclitaxel	142-152	P53	Homo sapiens	97-100
11053243-0	2000	Progesterone facilitates chromosome instability (aneuploidy) in p53 null normal mammary epithelial cells.	Progesterone	0-12	P53	Homo sapiens	64-67
11106264-1	2000	We examined the patterns of induction of apoptosis, Fas expression, and the influence of the status of the p53 tumor suppressor gene, in response to treatment of human colon carcinoma cell lines to 5-fluorouracil (FUra) combined with leucovorin (LV) under conditions of both DNA-directed (HT29, VRC5/c1, and RKO) and RNA-directed (HCT8 and HCT116) cytotoxicity.	Fluorouracil	198-212	P53	Homo sapiens	107-110
11106264-1	2000	We examined the patterns of induction of apoptosis, Fas expression, and the influence of the status of the p53 tumor suppressor gene, in response to treatment of human colon carcinoma cell lines to 5-fluorouracil (FUra) combined with leucovorin (LV) under conditions of both DNA-directed (HT29, VRC5/c1, and RKO) and RNA-directed (HCT8 and HCT116) cytotoxicity.	Fluorouracil	214-218	P53	Homo sapiens	107-110
11106256-15	2000	In conclusion, we have shown that tamoxifen-stimulated T47D p53 mutant tumors can be developed rapidly with high-dose therapy (1.5 mg daily).	Tamoxifen	34-43	P53	Homo sapiens	60-63
11106256-16	2000	The results from this model provide new opportunities to investigate the rapid development of drug resistance to adjuvant tamoxifen in patients with mutant p53 breast tumors.	Tamoxifen	122-131	P53	Homo sapiens	156-159
12214088-5	2000	H2O2-treatment resulted in dose-dependent increases in cell death due to genomic and mitochondrial DNA damage associated with increased levels of 8-OHdG and the p53 and CD95 pro-apoptosis genes, reduced levels of the Bcl-2 survival gene, activation of JNK and p38 stress kinases, and inhibition of PI3 kinase survival signaling.	Hydrogen Peroxide	0-4	P53	Homo sapiens	161-164
10922372-0	2000	Vanadate induces p53 transactivation through hydrogen peroxide and causes apoptosis.	Hydrogen Peroxide	45-62	P53	Homo sapiens	17-20
11095436-7	2000	Furthermore, wt-p53 expression renders two out of four carcinoma cell lines (FRO and NPA) more sensitive to doxorubicin and one (FRO) to 5-fluorouracil, independent of treatment schedule.	Doxorubicin	108-119	P53	Homo sapiens	16-19
11095436-7	2000	Furthermore, wt-p53 expression renders two out of four carcinoma cell lines (FRO and NPA) more sensitive to doxorubicin and one (FRO) to 5-fluorouracil, independent of treatment schedule.	Fluorouracil	137-151	P53	Homo sapiens	16-19
11032919-0	2000	Increased expression levels of p53 correlate with good response to cisplatin-based chemotherapy in non-small cell lung cancer.	Cisplatin	67-76	P53	Homo sapiens	31-34
11032919-8	2000	It is suggested that high p53 expression levels in tumors correlate with both good response to cisplatin-based chemotherapy and good survival of patients with advanced NSCLC.	Cisplatin	95-104	P53	Homo sapiens	26-29
11119931-0	2000	Existence of serum p53 antibodies in cyclosporine A-treated transplant patients: possible detection of p53 protein over-expression.	Cyclosporine	37-51	P53	Homo sapiens	19-22
11119931-0	2000	Existence of serum p53 antibodies in cyclosporine A-treated transplant patients: possible detection of p53 protein over-expression.	Cyclosporine	37-51	P53	Homo sapiens	103-106
11035798-1	2000	Ser-15 of human p53 (corresponding to Ser-18 of mouse p53) is phosphorylated by ataxia-telangiectasia mutated (ATM) family kinases in response to ionizing radiation (IR) and UV light.	Serine	0-3	P53	Homo sapiens	16-19
11035798-1	2000	Ser-15 of human p53 (corresponding to Ser-18 of mouse p53) is phosphorylated by ataxia-telangiectasia mutated (ATM) family kinases in response to ionizing radiation (IR) and UV light.	Serine	38-41	P53	Homo sapiens	16-19
10922372-9	2000	These results demonstrate that vanadate induces p53 activation mainly through H(2)O(2) generation, and this activation is required for vanadate-induced apoptosis.	Hydrogen Peroxide	78-86	P53	Homo sapiens	48-51
11046142-0	2000	Multiple C-terminal lysine residues target p53 for ubiquitin-proteasome-mediated degradation.	Lysine	20-26	P53	Homo sapiens	43-46
11046142-6	2000	Simultaneous mutation of lysine residues 370, 372, 373, 381, 382, and 386 to arginine residues (6KR p53 mutant) generates a p53 molecule with potent transcriptional activity that is resistant to Mdm2-induced degradation and is refractory to Mdm2-mediated ubiquitination.	Lysine	25-31	P53	Homo sapiens	100-103
11046142-6	2000	Simultaneous mutation of lysine residues 370, 372, 373, 381, 382, and 386 to arginine residues (6KR p53 mutant) generates a p53 molecule with potent transcriptional activity that is resistant to Mdm2-induced degradation and is refractory to Mdm2-mediated ubiquitination.	Lysine	25-31	P53	Homo sapiens	124-127
11046142-6	2000	Simultaneous mutation of lysine residues 370, 372, 373, 381, 382, and 386 to arginine residues (6KR p53 mutant) generates a p53 molecule with potent transcriptional activity that is resistant to Mdm2-induced degradation and is refractory to Mdm2-mediated ubiquitination.	Arginine	77-85	P53	Homo sapiens	100-103
11046142-6	2000	Simultaneous mutation of lysine residues 370, 372, 373, 381, 382, and 386 to arginine residues (6KR p53 mutant) generates a p53 molecule with potent transcriptional activity that is resistant to Mdm2-induced degradation and is refractory to Mdm2-mediated ubiquitination.	Arginine	77-85	P53	Homo sapiens	124-127
11046142-8	2000	Those differences are also manifest in HeLa cells which express the human papillomavirus E6 protein, suggesting that p53 C-terminal lysine residues are also implicated in E6-AP-mediated ubiquitination.	Lysine	132-138	P53	Homo sapiens	117-120
11046142-9	2000	These data suggest that p53 C-terminal lysine residues are the main sites of ubiquitin ligation, which target p53 for proteasome-mediated degradation.	Lysine	39-45	P53	Homo sapiens	24-27
11046142-9	2000	These data suggest that p53 C-terminal lysine residues are the main sites of ubiquitin ligation, which target p53 for proteasome-mediated degradation.	Lysine	39-45	P53	Homo sapiens	110-113
11064453-0	2000	Chemotherapeutic drug, adriamycin, restores the function of p53 protein in hepatitis B virus X (HBx) protein-expressing liver cells.	Doxorubicin	23-33	P53	Homo sapiens	60-63
11064453-5	2000	Surprisingly, anticancer drug, adriamycin induces the nuclear translocation of p53 protein sequestered in the cytoplasm.	Doxorubicin	31-41	P53	Homo sapiens	79-82
11033015-4	2000	For each of these mAbs we localized the epitope recognized on human p53 by the Spot method of multiple peptide synthesis, defined critical residues on p53 involved in the interaction by alanine scanning replacement experiments and determined kinetic parameters using real-time interaction analysis.	Alanine	186-193	P53	Homo sapiens	68-71
11033015-4	2000	For each of these mAbs we localized the epitope recognized on human p53 by the Spot method of multiple peptide synthesis, defined critical residues on p53 involved in the interaction by alanine scanning replacement experiments and determined kinetic parameters using real-time interaction analysis.	Alanine	186-193	P53	Homo sapiens	151-154
10884389-2	2000	In this study, we show that BRCA1 is initially up-regulated, followed by a reduction to below basal levels in response to treatment with the DNA-damaging agents adriamycin and mitomycin C, and that the reduction of BRCA1 expression is dependent on the presence of wild-type p53.	Doxorubicin	161-171	P53	Homo sapiens	274-277
11042698-0	2000	A serine 37 mutation associated with two missense mutations at highly conserved regions of p53 affect pro-apoptotic genes expression in a T-lymphoblastoid drug resistant cell line.	Serine	2-8	P53	Homo sapiens	91-94
11042698-3	2000	The serines 15 and 37 present in the amino terminal region of p53 are phosphorylated by the DNA-dependent protein kinase (DNA-PK) in response to DNA damage.	Serine	4-11	P53	Homo sapiens	62-65
11034077-2	2000	A2780 human ovarian carcinoma cells, which are sensitive to cisplatin and paclitaxel, express wild-type p53 and exhibit a p53-mediated increase in p21 in response to the chemotherapeutic agents.	Cisplatin	60-69	P53	Homo sapiens	122-125
11051374-4	2000	Mutation detection of the KRAS and TP53 genes was performed on paraffin-embedded tumor material, using denaturating gradient gel electrophoresis.	Paraffin	63-71	P53	Homo sapiens	35-39
10998350-2	2000	Methoxy-polyethylene glycol-maleimide MW 2000 (MAL-PEG) was used to covalently tag p53 protein that was oxidized at cysteine residues in cultured cells.	Polyethylene Glycols	51-54	P53	Homo sapiens	83-86
10998350-2	2000	Methoxy-polyethylene glycol-maleimide MW 2000 (MAL-PEG) was used to covalently tag p53 protein that was oxidized at cysteine residues in cultured cells.	Cysteine	116-124	P53	Homo sapiens	83-86
10998350-3	2000	Treatment of MCF7 breast cancer cells with pyrrolidine dithiocarbamate (PDTC), a metal chelator, resulted in a minimum of 25% oxidation of p53.	Metals	81-86	P53	Homo sapiens	139-142
10998350-4	2000	The oxidized p53 had an average of one cysteine residue oxidized per p53 protein molecule.	Cysteine	39-47	P53	Homo sapiens	13-16
10998350-4	2000	The oxidized p53 had an average of one cysteine residue oxidized per p53 protein molecule.	Cysteine	39-47	P53	Homo sapiens	69-72
10998350-9	2000	The data indicate that an average of one cysteine residue per p53 protein molecule is highly sensitive to oxidation and that p53 can be efficiently oxidized by PDTC in cultured cells.	Cysteine	41-49	P53	Homo sapiens	62-65
11024181-2	2000	In order to understand which structural features in DNA the C-teminal domain recognises we have studied the interaction of p53 protein with different types of DNA oligonucleotides imitating damaged DNA.	Oligonucleotides	163-179	P53	Homo sapiens	123-126
11042688-2	2000	Although all cell lines contain the same p53 mutations at codons 175 (Arg--&gt;His) and 248 (Arg--&gt;Gln), the constitutive levels of p53 were progressively increased with the resistance of the cells to teniposide.	Histidine	79-82	P53	Homo sapiens	135-138
11042688-2	2000	Although all cell lines contain the same p53 mutations at codons 175 (Arg--&gt;His) and 248 (Arg--&gt;Gln), the constitutive levels of p53 were progressively increased with the resistance of the cells to teniposide.	Arginine	93-96	P53	Homo sapiens	135-138
11042688-8	2000	Specifically, while the mutant p53 was phosphorylated at serine-15 in response to ionizing radiation in all these cell lines, mutant p53 induction in response to teniposide or ionizing radiation and induction of the p53-target genes, p21 and GADD45 only occurred in the drug-sensitive CEM cells.	Serine	57-63	P53	Homo sapiens	31-34
11129738-3	2000	It showed that HCPT at a dose of 0.1 microg/ml increased the expression of P53, c-Myc and Bax protein, and decreased the expression of Bcl-2 and AFP.	10-hydroxycamptothecin	15-19	P53	Homo sapiens	75-78
11129738-4	2000	The increase of P53, which was remarkable after only 3 h incubation with HCPT, occurred much earlier than the changes of other proteins, suggesting that the increase of P53 expression may be the upstream event in the apoptosis of Hep G2 cells induced by HCPT.	10-hydroxycamptothecin	73-77	P53	Homo sapiens	16-19
11129738-4	2000	The increase of P53, which was remarkable after only 3 h incubation with HCPT, occurred much earlier than the changes of other proteins, suggesting that the increase of P53 expression may be the upstream event in the apoptosis of Hep G2 cells induced by HCPT.	10-hydroxycamptothecin	254-258	P53	Homo sapiens	16-19
11129738-4	2000	The increase of P53, which was remarkable after only 3 h incubation with HCPT, occurred much earlier than the changes of other proteins, suggesting that the increase of P53 expression may be the upstream event in the apoptosis of Hep G2 cells induced by HCPT.	10-hydroxycamptothecin	254-258	P53	Homo sapiens	169-172
11045785-13	2000	In conclusion, the codon 72 germ-line polymorphism (Arg/Pro) of the common tumor suppressor gene p53 contributes to heritable susceptibility for smoke-induced lung adenocarcinoma.	Arginine	52-55	P53	Homo sapiens	97-100
11034077-2	2000	A2780 human ovarian carcinoma cells, which are sensitive to cisplatin and paclitaxel, express wild-type p53 and exhibit a p53-mediated increase in p21 in response to the chemotherapeutic agents.	Paclitaxel	74-84	P53	Homo sapiens	122-125
11034077-6	2000	Experiments with additional ovarian carcinoma cell lines revealed that PI3K is involved in the expression of p21 induced by cisplatin or paclitaxel in OVCAR-10 cells, which have wild-type p53, but not in OVCAR-5 cells, which lack functional p53.	Cisplatin	124-133	P53	Homo sapiens	188-191
11034077-6	2000	Experiments with additional ovarian carcinoma cell lines revealed that PI3K is involved in the expression of p21 induced by cisplatin or paclitaxel in OVCAR-10 cells, which have wild-type p53, but not in OVCAR-5 cells, which lack functional p53.	Cisplatin	124-133	P53	Homo sapiens	241-244
11899648-1	2000	This study assesses the potential value of the tumor markers p53, HER2, and Bcl-2 in predicting the clinical response to doxorubicin and paclitaxel as single agents in the treatment of metastatic breast cancer.	Doxorubicin	121-132	P53	Homo sapiens	61-64
11899648-1	2000	This study assesses the potential value of the tumor markers p53, HER2, and Bcl-2 in predicting the clinical response to doxorubicin and paclitaxel as single agents in the treatment of metastatic breast cancer.	Paclitaxel	137-147	P53	Homo sapiens	61-64
11020329-6	2000	Preparative gel electrophoresis of the PGK1 and p53 genes from 300 microg of restriction endonuclease-digested genomic DNA showed a 25-fold enrichment for the genes and, after endonuclease digestion followed by LMPCR, gave sufficient signal to map the frequency of oxidized bases from human cells treated with 50 microM H2O2.	Hydrogen Peroxide	320-324	P53	Homo sapiens	48-51
11101222-0	2000	Assignment of 1H(N), 15N, 13C(alpha), 13CO and 13C(beta) resonances in a 67 kDa p53 dimer using 4D-TROSY NMR spectroscopy.	Hydrogen	14-16	P53	Homo sapiens	80-83
11000583-7	2000	These findings suggest that multiple factors, including p53 and DNA mismatch repair, participate in diverse cell growth modulations in cells treated with 5-FU.	Fluorouracil	154-158	P53	Homo sapiens	56-59
11023973-4	2000	This mode of regulation may serve as a paradigm for redox-sensing by eukaryotic transcription factors as most-including NF-kappaB, AP-1, and p53-contain reactive thiols in their DNA binding regions, the modification of which alters binding in vitro.	Sulfhydryl Compounds	162-168	P53	Homo sapiens	141-144
11072671-2	2000	In invasive cervical cancer, the arginine form of the p53 gene is estimated to be more susceptible to degradation mediated by tumour-associated human papilloma viruses (HPV) than the proline form.	Arginine	33-41	P53	Homo sapiens	54-57
11025661-2	2000	Treatment with vincristine or paclitaxel before DNA-damage or before leptomycin B treatment reduces nuclear accumulation of p53 and expression of mdm2 and p21.	Paclitaxel	30-40	P53	Homo sapiens	124-127
10995814-0	2000	Uncertain identity of doxorubicin-resistant MCF-7 cell lines expressing mutated p53.	Doxorubicin	22-33	P53	Homo sapiens	80-83
11030628-0	2000	p53AIP1, a potential mediator of p53-dependent apoptosis, and its regulation by Ser-46-phosphorylated p53.	Serine	80-83	P53	Homo sapiens	0-3
11008209-4	2000	The codon 72 p53 Pro allele was more frequently found in ESCC patients [odds ratio (OR) 1.86, 95% confidence interval (CI) 1.04-3.35 for Arg/Pro genotype and OR 2.56, 95% CI 1.29-5.08 for Pro/Pro genotype].	Arginine	137-140	P53	Homo sapiens	13-16
11016658-3	2000	However, a similar response was obtained by treatment of BL-41tsp53-2 cells expressing mutant ts p53 with a p53 antisense oligonucleotide.	Oligonucleotides	122-137	P53	Homo sapiens	64-67
11016658-3	2000	However, a similar response was obtained by treatment of BL-41tsp53-2 cells expressing mutant ts p53 with a p53 antisense oligonucleotide.	Oligonucleotides	122-137	P53	Homo sapiens	97-100
11030628-0	2000	p53AIP1, a potential mediator of p53-dependent apoptosis, and its regulation by Ser-46-phosphorylated p53.	Serine	80-83	P53	Homo sapiens	33-36
11032416-5	2000	Fluorescence anisotropy was employed to measure directly the binding of hdm2(1-126) to a p53 N-terminal peptide labeled with Oregon Green (an analogue of fluorescein).	2-(2,7-difluoro-6-hydroxy-3-oxo-3H-xanthen-9-yl)benzoic acid	125-137	P53	Homo sapiens	89-92
11032416-8	2000	This suggests that phosphorylation of Thr18 could be a regulatory mechanism that disrupts the hdm2-p53 complex, thus activating p53 in response to DNA damage.	UNII-PYZ33YLR8A	38-43	P53	Homo sapiens	99-102
11030628-2	2000	Ectopically expressed p53AIP1, which is localized within mitochondria, leads to apoptotic cell death through dissipation of mitochondrial A(psi)m. We have found that upon severe DNA damage, Ser-46 on p53 is phosphorylated and apoptosis is induced.	Serine	190-193	P53	Homo sapiens	22-25
11032416-8	2000	This suggests that phosphorylation of Thr18 could be a regulatory mechanism that disrupts the hdm2-p53 complex, thus activating p53 in response to DNA damage.	UNII-PYZ33YLR8A	38-43	P53	Homo sapiens	128-131
11030628-3	2000	In addition, substitution of Ser-46 inhibits the ability of p53 to induce apoptosis and selectively blocks expression of p53AIP1.	Serine	29-32	P53	Homo sapiens	60-63
11030628-4	2000	Our results suggest that p53AIP1 is likely to play an important role in mediating p53-dependent apoptosis, and phosphorylation of Ser-46 regulates the transcriptional activation of this apoptosis-inducing gene.	Serine	130-133	P53	Homo sapiens	25-28
10994962-3	2000	PCR products of the proline [5"-x(G17)-x(C38)x-3"] and arginine variants [(5"-x(Gl7)-x(G38)x-3"] of the p53 gene are distinguished by an SNP (cytosine or guanine) and were discriminated using both quadrupole and quadrupole ion trap MS analysis.	Arginine	55-63	P53	Homo sapiens	104-107
10942736-1	2000	The present study investigates whether reactive oxygen species (ROS) are involved in p53 activation, and if they are, which species is responsible for the activation.	Reactive Oxygen Species	64-67	P53	Homo sapiens	85-88
10942736-11	2000	Sodium formate and aspirin,.OH radical scavengers, also suppressed p53 activation.	Aspirin	19-26	P53	Homo sapiens	67-70
10942736-12	2000	Deferoxamine, a metal chelator, inhibited p53 activation by chelating Cr(V) to make it incapable of generating radicals from H(2)O(2).	Metals	16-21	P53	Homo sapiens	42-45
10942736-12	2000	Deferoxamine, a metal chelator, inhibited p53 activation by chelating Cr(V) to make it incapable of generating radicals from H(2)O(2).	Water	125-130	P53	Homo sapiens	42-45
11007451-5	2000	We have described a chk2/hcds1-independent DNA damage signaling pathway that targets Ser-376 within the COOH terminus of p53 for dephosphorylation and leads to increased p53 functional activity.	Serine	85-88	P53	Homo sapiens	121-124
11268475-3	2000	PATIENTS AND METHODS: Nuclear immunohistochemical expression of p53 protein was determined in formalin-fixed paraffin-embedded archival tumor tissue samples from 190 primary colorectal adenocarcinomas.	Paraffin	109-117	P53	Homo sapiens	64-67
11042678-1	2000	Resveratrol (3,5,4"-trihydroxy-trans-stilbene), in the concentration range of 20 microM and above, induced arrest in the S-phase and apoptosis in the T cell-derived T-ALL lymphocytic leukemia cell line CEM-C7H2 which is deficient in functional p53 and p16.	Resveratrol	0-11	P53	Homo sapiens	244-247
11079153-2	2000	Clonogenic survival studies indicate that EB 1089 shifts the dose-response curve for sensitivity to adriamycin by approximately six-fold in p53 wild-type MCF-7 cells; comparative studies in MCF-7 cells with a temperature-sensitive dominant negative p53 mutation show less than a two-fold shift in adriamycin sensitivity in the presence of EB 1089.	Doxorubicin	100-110	P53	Homo sapiens	140-143
11079153-3	2000	The combination of EB 1089 with adriamycin also promotes apoptotic cell death in the p53 wild-type MCF-7 cells but not in the MCF-7 cells expressing mutant p53.	Doxorubicin	32-42	P53	Homo sapiens	85-88
11079169-17	2000	The concomitant use of cisplatin, an inducer of apoptosis that is dependent on the normal function of p53, makes the interpretation of these results difficult.	Cisplatin	23-32	P53	Homo sapiens	102-105
11007451-5	2000	We have described a chk2/hcds1-independent DNA damage signaling pathway that targets Ser-376 within the COOH terminus of p53 for dephosphorylation and leads to increased p53 functional activity.	Serine	85-88	P53	Homo sapiens	170-173
11007451-6	2000	We now report that in several human melanoma cell lines that express wild-type p53, the phosphorylation state of Ser-376 was not regulated by DNA damage.	Serine	113-116	P53	Homo sapiens	79-82
10953132-2	2000	MATERIALS AND METHODS: Immunohistochemical staining for p53 was semiquantitatively scored in archival formalin fixed, paraffin embedded tumor tissue obtained at diagnosis in 221 patients with prostate cancer.	Paraffin	118-126	P53	Homo sapiens	56-59
10938392-0	2000	CDDP induces p53-dependent apoptosis in tongue cancer cells.	cddp	0-4	P53	Homo sapiens	13-16
10938392-3	2000	On the other hand, overexpression of p53 in HSC-4 was observed without CDDP treatment and no elevation of Bax could be detected.	cddp	71-75	P53	Homo sapiens	37-40
10938392-6	2000	It is suggested that p53 status may have predictive potential with regard to response to CDDP therapy.	cddp	89-93	P53	Homo sapiens	21-24
10974634-6	2000	(c) Treatment of tumour cells by either gamma radiation or by cisplatin resulted in the induction of p53 independent of the origin of the tumour.	Cisplatin	62-71	P53	Homo sapiens	101-104
10974634-7	2000	(d) Susceptibility of two cell lines, one with and one without constitutive expression of p53 showed that the expressing cells were more sensitive to gamma radiation (the percentage inhibition at 250 cGy was 57% versus -15%, P&lt;0.01), and also cisplatin (the percentage inhibition at 1 microgram/ml was 71.0+/-6.0 versus 2.6+/-7.0, P&lt;0.001).	Cisplatin	246-255	P53	Homo sapiens	90-93
10974634-13	2000	Alternatively, if TP53 is wild-type, then the increased levels of p53 expression would enable the cells to become more susceptible to DNA damaging treatments such as cisplatin or gamma radiation.	Cisplatin	166-175	P53	Homo sapiens	18-22
10974634-13	2000	Alternatively, if TP53 is wild-type, then the increased levels of p53 expression would enable the cells to become more susceptible to DNA damaging treatments such as cisplatin or gamma radiation.	Cisplatin	166-175	P53	Homo sapiens	66-69
10974635-1	2000	We conducted this study to determine whether the sensitivity of ovarian cancer cells to paclitaxel (PTX) relates to cells undergoing p53-dependent apoptosis.	Paclitaxel	88-98	P53	Homo sapiens	133-136
10974635-1	2000	We conducted this study to determine whether the sensitivity of ovarian cancer cells to paclitaxel (PTX) relates to cells undergoing p53-dependent apoptosis.	Paclitaxel	100-103	P53	Homo sapiens	133-136
10974635-3	2000	In SK-OV-3 and KP cells, which have a homozygous deletion of the TP53 gene, wild-type TP53 gene-transduction markedly enhanced the sensitivity to cisplatin (CDDP), but did not enhance the sensitivity to PTX.	Cisplatin	146-155	P53	Homo sapiens	65-69
10974635-3	2000	In SK-OV-3 and KP cells, which have a homozygous deletion of the TP53 gene, wild-type TP53 gene-transduction markedly enhanced the sensitivity to cisplatin (CDDP), but did not enhance the sensitivity to PTX.	Cisplatin	146-155	P53	Homo sapiens	86-90
10974635-3	2000	In SK-OV-3 and KP cells, which have a homozygous deletion of the TP53 gene, wild-type TP53 gene-transduction markedly enhanced the sensitivity to cisplatin (CDDP), but did not enhance the sensitivity to PTX.	Cisplatin	157-161	P53	Homo sapiens	65-69
10974635-3	2000	In SK-OV-3 and KP cells, which have a homozygous deletion of the TP53 gene, wild-type TP53 gene-transduction markedly enhanced the sensitivity to cisplatin (CDDP), but did not enhance the sensitivity to PTX.	Cisplatin	157-161	P53	Homo sapiens	86-90
10974635-3	2000	In SK-OV-3 and KP cells, which have a homozygous deletion of the TP53 gene, wild-type TP53 gene-transduction markedly enhanced the sensitivity to cisplatin (CDDP), but did not enhance the sensitivity to PTX.	Paclitaxel	203-206	P53	Homo sapiens	65-69
10974635-3	2000	In SK-OV-3 and KP cells, which have a homozygous deletion of the TP53 gene, wild-type TP53 gene-transduction markedly enhanced the sensitivity to cisplatin (CDDP), but did not enhance the sensitivity to PTX.	Paclitaxel	203-206	P53	Homo sapiens	86-90
10974635-5	2000	After exposure to CDDP, p53 and Bax protein expression increased and Bcl-xL expression decreased in the KF cells and TP53 gene-transducted SK-OV-3 cells.	Cisplatin	18-22	P53	Homo sapiens	24-27
10974635-5	2000	After exposure to CDDP, p53 and Bax protein expression increased and Bcl-xL expression decreased in the KF cells and TP53 gene-transducted SK-OV-3 cells.	Cisplatin	18-22	P53	Homo sapiens	117-121
10974635-7	2000	Therefore, the role of p53 in CDDP-induced apoptosis depends upon the cell type.	Cisplatin	30-34	P53	Homo sapiens	23-26
10974636-1	2000	To clarify the effect of a combination treatment consisting of a recombinant adenovirus carrying a wild-type TP53 gene (AxCATP53) and cisplatin (CDDP), we examined p53-dependent apoptosis in ovarian cancer xenografts with and without the wild-type TP53 gene.	Cisplatin	145-149	P53	Homo sapiens	164-167
11070791-4	2000	Restoration of p53 protein function in LN382 cells at 34 degrees C reduced the cytotoxicity of etoposide and paclitaxel, whereas that of cisplatin and ACNU was not affected.	Paclitaxel	109-119	P53	Homo sapiens	15-18
11070791-8	2000	These results indicate that cell cycle arrest induced by wild-type p53 function may abrogate the cytotoxic effects of etoposide and paclitaxel, which are dependent on G2M-associated apoptosis.	Paclitaxel	132-142	P53	Homo sapiens	67-70
11240705-1	2000	Recent analysis of the codon-72 polymorphism of the p53 gene, the allele encoding proline or arginine, suggested that the homozygous Arg/Arg genotype is a significant risk factor for cervical cancer associated with human papillomavirus (HPV).	Arginine	93-101	P53	Homo sapiens	52-55
11240705-1	2000	Recent analysis of the codon-72 polymorphism of the p53 gene, the allele encoding proline or arginine, suggested that the homozygous Arg/Arg genotype is a significant risk factor for cervical cancer associated with human papillomavirus (HPV).	Arginine	133-136	P53	Homo sapiens	52-55
11240705-1	2000	Recent analysis of the codon-72 polymorphism of the p53 gene, the allele encoding proline or arginine, suggested that the homozygous Arg/Arg genotype is a significant risk factor for cervical cancer associated with human papillomavirus (HPV).	Arginine	137-140	P53	Homo sapiens	52-55
10948336-3	2000	To characterize the involvement of the p53 gene abnormality in this disease, we analyzed expression and sequence alteration of p53 by immunohistochemical analysis of the protein expression and quantitative DNA/PCR and PCR-SSCP assays of the gene in 33 paraffin-embedded tissue specimens.	Paraffin	252-260	P53	Homo sapiens	127-130
11191113-7	2000	These findings suggest that the AhR mediated the inverse expression patterns of BRCA-1 and p53 upon exposure to B[a]P. The treatment with BPDE induced S-phase arrest and reduced BRCA-1 mRNA levels.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	138-142	P53	Homo sapiens	91-94
10948341-5	2000	Immunostaining for p53 protein with 4 different antibodies was performed on paraffin-embedded specimens from 69 patients with adenocarcinoma and squamous cell carcinoma of the oesophagus.	Paraffin	76-84	P53	Homo sapiens	19-22
11798837-2	2000	METHODS: Human lung adenocarcinoma cell line GLC-82 was transfected with adenovirus-mediated p53 gene (Ad-p53) combining with administration of either kind of chemotherapeutic agents-cisplatin (CDDP) and arsenic trioxide (As(2)O(3)).	Cisplatin	183-192	P53	Homo sapiens	106-109
11126384-4	2000	Aflatoxin B1 exposure leads to mutations in the p53 tumor suppressor gene, most commonly a transversion in codon 249 that leads to a substitution of serine for arginine in the p53 protein.	Serine	149-155	P53	Homo sapiens	48-51
11126384-4	2000	Aflatoxin B1 exposure leads to mutations in the p53 tumor suppressor gene, most commonly a transversion in codon 249 that leads to a substitution of serine for arginine in the p53 protein.	Serine	149-155	P53	Homo sapiens	176-179
11126384-4	2000	Aflatoxin B1 exposure leads to mutations in the p53 tumor suppressor gene, most commonly a transversion in codon 249 that leads to a substitution of serine for arginine in the p53 protein.	Arginine	160-168	P53	Homo sapiens	48-51
11126384-4	2000	Aflatoxin B1 exposure leads to mutations in the p53 tumor suppressor gene, most commonly a transversion in codon 249 that leads to a substitution of serine for arginine in the p53 protein.	Arginine	160-168	P53	Homo sapiens	176-179
10944184-2	2000	A series of hydrophilic mutations at Met-340 and Leu-344 of human p53 were designed to disrupt the hydrophobic dimer-dimer interface of the tetrameric oligomerization domain of p53 (residues 325-355).	Methionine	37-40	P53	Homo sapiens	177-180
11798837-2	2000	METHODS: Human lung adenocarcinoma cell line GLC-82 was transfected with adenovirus-mediated p53 gene (Ad-p53) combining with administration of either kind of chemotherapeutic agents-cisplatin (CDDP) and arsenic trioxide (As(2)O(3)).	Cisplatin	183-192	P53	Homo sapiens	93-96
11798837-2	2000	METHODS: Human lung adenocarcinoma cell line GLC-82 was transfected with adenovirus-mediated p53 gene (Ad-p53) combining with administration of either kind of chemotherapeutic agents-cisplatin (CDDP) and arsenic trioxide (As(2)O(3)).	Cisplatin	194-198	P53	Homo sapiens	93-96
10944184-2	2000	A series of hydrophilic mutations at Met-340 and Leu-344 of human p53 were designed to disrupt the hydrophobic dimer-dimer interface of the tetrameric oligomerization domain of p53 (residues 325-355).	Methionine	37-40	P53	Homo sapiens	66-69
11798837-9	2000	CONCLUSION: After introduced into GLC-82 cells, Ad-p53 shows enhanced therapeutic efficiency for GLC-82 cells when combined with CDDP or As(2)O(3).	Cisplatin	129-133	P53	Homo sapiens	51-54
10993958-5	2000	Additional cell loss occurred in 40-16 and HCT116 p53-/- cells following administration of Taxol before IR and 5-FU.	Paclitaxel	91-96	P53	Homo sapiens	50-53
10962580-3	2000	We identified genomic DNA fragments to which mut p53 (Gly245--&gt;Ser) could be cross-linked in vivo.	Serine	66-69	P53	Homo sapiens	49-52
10962580-4	2000	Purified recombinant mut p53 (Gly245--&gt;Ser) was able to bind specifically to such elements in PCR-EMSA in vitro, supporting the idea that this mut p53 protein interacts with genomic DNA in vivo.	Serine	42-45	P53	Homo sapiens	25-28
10962580-4	2000	Purified recombinant mut p53 (Gly245--&gt;Ser) was able to bind specifically to such elements in PCR-EMSA in vitro, supporting the idea that this mut p53 protein interacts with genomic DNA in vivo.	Serine	42-45	P53	Homo sapiens	150-153
10962580-6	2000	Therefore we propose that structural determinants within these DNA elements are important for their interaction with mut p53 (Gly245--&gt;Ser) in vivo.	Serine	138-141	P53	Homo sapiens	121-124
10962580-0	2000	Identification of genomic DNA sequences bound by mutant p53 protein (Gly245--&gt;Ser) in vivo.	Serine	81-84	P53	Homo sapiens	56-59
10962580-2	2000	Therefore we analysed the binding of mutant (mut) p53 (Gly245--&gt;Ser) in Onda 11 glioma cells to cellular DNA in vivo, using p53-specific chromatin immunoprecipitation (CHIP) after in vivo cross-linking of mut p53 to genomic DNA with cisplatin.	Serine	67-70	P53	Homo sapiens	50-53
20955676-2	2000	METHODS: Expression of p53 protein , ER and PR in 147 NSCLC specimen was detected by SP immunohistochemistry method.	TFF2 protein, human	85-87	P53	Homo sapiens	23-26
10993958-6	2000	Radiation sensitivity was unaffected by combined treatments, except for Taxol, irradiation, and 5-FU sequence in the HCT116 p53-/- and 40-16 cell lines, where radiation sensitivity determined by clonogenic survival curve slopes was doubled or quadrupled, respectively.	Fluorouracil	96-100	P53	Homo sapiens	124-127
10951339-9	2000	The 1-year survival rates for patients with and without p53 mutation after treatment with weekly paclitaxel were 63% (95% confidence interval [CI], 31-100%) and 53% (95% CI, 33-86%), respectively.	Paclitaxel	97-107	P53	Homo sapiens	56-59
10962554-9	2000	The p53-dependent expression of GIPs was confirmed by dependence of expression upon induction of wt p53 expression in the EB-1 cellular model and by up-regulation following activation of an endogenous wt p53 by treatment with adriamycin.	Doxorubicin	226-236	P53	Homo sapiens	4-7
10933801-0	2000	Phosphorylation of human p53 on Thr-55.	Threonine	32-35	P53	Homo sapiens	25-28
10933801-4	2000	Phosphoamino acid analysis and manual Edman degradation of the isolated phosphopeptides enabled us to unequivocally identify Thr-55 as the major phosphorylation site on p53.	Threonine	125-128	P53	Homo sapiens	169-172
10933801-7	2000	These data define Thr-55 as a novel phosphorylation site and for the first time show threonine phosphorylation of human p53.	Threonine	18-21	P53	Homo sapiens	120-123
10933801-7	2000	These data define Thr-55 as a novel phosphorylation site and for the first time show threonine phosphorylation of human p53.	Threonine	85-94	P53	Homo sapiens	120-123
10951339-11	2000	These results provide clinical support for in vitro observations that paclitaxel can bypass mutant p53 and lead to tumor cell death by alternate pathway(s).	Paclitaxel	70-80	P53	Homo sapiens	99-102
10951339-12	2000	Paclitaxel should be considered as a component of treatment for patients with metastatic NSCLC with tumors that have p53 mutations.	Paclitaxel	0-10	P53	Homo sapiens	117-120
10918193-12	2000	Homozygous codon-72 p53-Arg apparently confers a higher susceptibility to HPV-associated cervical tumorigenesis.	Arginine	24-27	P53	Homo sapiens	20-23
10969820-3	2000	Reactive oxygen species are known to be powerful inducers of p53 activity; moreover, they play a role in the execution of p53-dependent apoptosis.	Reactive Oxygen Species	0-23	P53	Homo sapiens	61-64
10969820-3	2000	Reactive oxygen species are known to be powerful inducers of p53 activity; moreover, they play a role in the execution of p53-dependent apoptosis.	Reactive Oxygen Species	0-23	P53	Homo sapiens	122-125
10951577-4	2000	The present study tested the hypothesis that reactive oxygen species (ROS) released from mitochondria regulate the cytosolic redox state and are required for the stabilization of p53 protein levels in response to hypoxia.	Reactive Oxygen Species	45-68	P53	Homo sapiens	179-182
10951577-4	2000	The present study tested the hypothesis that reactive oxygen species (ROS) released from mitochondria regulate the cytosolic redox state and are required for the stabilization of p53 protein levels in response to hypoxia.	Reactive Oxygen Species	70-73	P53	Homo sapiens	179-182
10951577-5	2000	Our results indicate that hypoxia (1.5% O2) increases mitochondrial ROS generation and increases p53 protein levels in human breast carcinoma MCF-7 cells and in normal human diploid fibroblast IMR-90 cells.	Oxygen	40-42	P53	Homo sapiens	97-100
10951577-7	2000	The antioxidant N-acetylcysteine and the Cu/Zn superoxide dismutase inhibitor diethyldithiocarbamic acid abolished the hypoxia-induced increases in ROS and p53 levels.	Acetylcysteine	16-32	P53	Homo sapiens	156-159
10951577-8	2000	Rotenone, an inhibitor of mitochondrial complex I, and 4,4"-diisothiocyanato-stilbene-2,2"-disulfonate, a mitochondrial anion channel inhibitor, also abolished the increase in ROS signal and p53 levels during hypoxia.	4,4"-diisothiocyanato-stilbene-2,2"-disulfonate	55-102	P53	Homo sapiens	191-194
10951577-8	2000	Rotenone, an inhibitor of mitochondrial complex I, and 4,4"-diisothiocyanato-stilbene-2,2"-disulfonate, a mitochondrial anion channel inhibitor, also abolished the increase in ROS signal and p53 levels during hypoxia.	Reactive Oxygen Species	176-179	P53	Homo sapiens	191-194
10951577-12	2000	These results indicate that mitochondria regulate p53 protein levels during hypoxia through a redox-dependent mechanism involving ROS.	Reactive Oxygen Species	130-133	P53	Homo sapiens	50-53
10945628-4	2000	Because poly(ADP-ribose) polymerase (PARP)-mediated NAD+/ATP depletion has been implicated in the nucleoside-induced killing of normal resting lymphocytes, we postulated that this mechanism might account for the p53-independent component of nucleoside cytotoxicity in CLL.	NAD	52-56	P53	Homo sapiens	212-215
11038045-1	2000	BACKGROUND: We assessed the hypothesis that a compromised p53 function could account for the non response of colon cancer patients with low thymidylate synthase (TS) expression receiving a bolus 5-fluorouracil (5-FU) leucovorin (LV) combination.	Fluorouracil	195-209	P53	Homo sapiens	58-61
11038045-1	2000	BACKGROUND: We assessed the hypothesis that a compromised p53 function could account for the non response of colon cancer patients with low thymidylate synthase (TS) expression receiving a bolus 5-fluorouracil (5-FU) leucovorin (LV) combination.	Fluorouracil	211-215	P53	Homo sapiens	58-61
10945628-4	2000	Because poly(ADP-ribose) polymerase (PARP)-mediated NAD+/ATP depletion has been implicated in the nucleoside-induced killing of normal resting lymphocytes, we postulated that this mechanism might account for the p53-independent component of nucleoside cytotoxicity in CLL.	Adenosine Triphosphate	57-60	P53	Homo sapiens	212-215
10945617-9	2000	Analysis of the p53 cDNA from several focus-derived strains lacking p53 activity revealed that each contained the same mutation, an A to G transition at codon 215, resulting in a change from serine to glycine.	Serine	191-197	P53	Homo sapiens	16-19
10945617-9	2000	Analysis of the p53 cDNA from several focus-derived strains lacking p53 activity revealed that each contained the same mutation, an A to G transition at codon 215, resulting in a change from serine to glycine.	Serine	191-197	P53	Homo sapiens	68-71
10945617-9	2000	Analysis of the p53 cDNA from several focus-derived strains lacking p53 activity revealed that each contained the same mutation, an A to G transition at codon 215, resulting in a change from serine to glycine.	Glycine	201-208	P53	Homo sapiens	16-19
10945617-9	2000	Analysis of the p53 cDNA from several focus-derived strains lacking p53 activity revealed that each contained the same mutation, an A to G transition at codon 215, resulting in a change from serine to glycine.	Glycine	201-208	P53	Homo sapiens	68-71
10897038-7	2000	In A2780 cells, glutathione exposure was followed by p21 and Bax induction and p53 up-regulation, as expected for genotoxic stress.	Glutathione	16-27	P53	Homo sapiens	79-82
10955812-0	2000	Evidence for a dose-response effect between p53 (but not p21WAF1/Cip1) protein concentrations, survival, and responsiveness in patients with epithelial ovarian cancer treated with platinum-based chemotherapy.	Platinum	180-188	P53	Homo sapiens	44-47
10897038-9	2000	Taken together, these results indicate that the cytotoxic effect of extracellular glutathione, related to membrane metabolism, is mediated by production of H(2)O(2) leading to DNA damage and a cellular response involving p53.	Glutathione	82-93	P53	Homo sapiens	221-224
10891529-0	2000	Theophylline and cisplatin synergize in down regulation of BCL-2 induction of apoptosis in human granulosa cells transformed by a mutated p53 (p53 val135) and Ha-ras oncogene.	Cisplatin	17-26	P53	Homo sapiens	138-141
10891529-0	2000	Theophylline and cisplatin synergize in down regulation of BCL-2 induction of apoptosis in human granulosa cells transformed by a mutated p53 (p53 val135) and Ha-ras oncogene.	Cisplatin	17-26	P53	Homo sapiens	143-146
10893182-3	2000	As hydrogen peroxide and other oxidants can affect signal transduction pathways at several levels, the present study was aimed to verify: (i) the occurrence of GGT-dependent production of hydrogen peroxide in melanoma cells; (ii) the effects of GGT-dependent prooxidant reactions on known redox-sensitive cellular targets, i.e. protein thiols, the nuclear transcription factor NF-kappa B and p53.	Hydrogen Peroxide	188-205	P53	Homo sapiens	392-395
10908664-0	2000	Inactivation of wild-type p53 tumor suppressor by electrophilic prostaglandins.	Prostaglandins	64-78	P53	Homo sapiens	26-29
10942242-7	2000	Treatment with Me-Lex and 3-aminobenzamide results in augmented expression of p53 protein and of the X-ray repair cross-complementing 1 transcript (a component of base excision repair).	3-aminobenzamide	26-42	P53	Homo sapiens	78-81
11055588-9	2000	p53 antisense oligonucleotides not only reduced the level of p53 proteins but correspondingly also blocked the expression of p21(waf1/cip1) in FTS-treated colon cancer cells.	Oligonucleotides	14-30	P53	Homo sapiens	0-3
11055588-9	2000	p53 antisense oligonucleotides not only reduced the level of p53 proteins but correspondingly also blocked the expression of p21(waf1/cip1) in FTS-treated colon cancer cells.	Oligonucleotides	14-30	P53	Homo sapiens	61-64
10899928-5	2000	Untreated cells from both lines expressed negligible p53 levels; on the other hand, whereas p53 and p21(Cip1/Waf1) were rapidly up-regulated in doxorubicin-treated SH-SY5Y cells, such a response was not observed in CHP-100 cells.	Doxorubicin	144-155	P53	Homo sapiens	53-56
10899928-5	2000	Untreated cells from both lines expressed negligible p53 levels; on the other hand, whereas p53 and p21(Cip1/Waf1) were rapidly up-regulated in doxorubicin-treated SH-SY5Y cells, such a response was not observed in CHP-100 cells.	Doxorubicin	144-155	P53	Homo sapiens	92-95
10891493-6	2000	PCAF binds to the E1B 55-kDa protein and to a region near the C terminus of p53 encompassing Lys-320, the specific PCAF acetylation site.	Lysine	93-96	P53	Homo sapiens	76-79
10908664-1	2000	The electrophilic eicosanoids prostaglandins A(1) or A(2) impaired p53-dependent transcription of endogenous genes and exogenous p53-luciferase reporter plasmids in RKO and HCT 116 colon cancer cells.	Eicosanoids	18-29	P53	Homo sapiens	67-70
10908664-1	2000	The electrophilic eicosanoids prostaglandins A(1) or A(2) impaired p53-dependent transcription of endogenous genes and exogenous p53-luciferase reporter plasmids in RKO and HCT 116 colon cancer cells.	Eicosanoids	18-29	P53	Homo sapiens	129-132
10908664-1	2000	The electrophilic eicosanoids prostaglandins A(1) or A(2) impaired p53-dependent transcription of endogenous genes and exogenous p53-luciferase reporter plasmids in RKO and HCT 116 colon cancer cells.	Prostaglandins A	30-46	P53	Homo sapiens	67-70
10908664-1	2000	The electrophilic eicosanoids prostaglandins A(1) or A(2) impaired p53-dependent transcription of endogenous genes and exogenous p53-luciferase reporter plasmids in RKO and HCT 116 colon cancer cells.	Prostaglandins A	30-46	P53	Homo sapiens	129-132
10908664-2	2000	Cellular accumulation of genetically wild-type, but transcriptionally silent p53 varied as a function of exposure time and concentration of prostaglandins A(1) and A(2).	Prostaglandins A	140-156	P53	Homo sapiens	77-80
10908664-3	2000	Prostaglandins A(1) and A(2) induced a conformational change in wild-type p53 that corresponded with its inactivation and its aberrant redistribution from the cytosol to the nucleus.	Prostaglandins A	0-16	P53	Homo sapiens	74-77
10908664-5	2000	We conclude that electrophilic eicosanoids impair the role of wild-type p53 as a guardian of genomic integrity by a process distinct from somatic mutation or viral oncoprotein binding.	Eicosanoids	31-42	P53	Homo sapiens	72-75
10951572-0	2000	The human vaccinia-related kinase 1 (VRK1) phosphorylates threonine-18 within the mdm-2 binding site of the p53 tumour suppressor protein.	Threonine	58-67	P53	Homo sapiens	108-111
10925118-4	2000	RESULTS: Ad5CMV-p53 substantially enhanced cisplatin chemosensitivity in a dose-dependent manner, reducing the median IC(50) by more than 50%.	Cisplatin	43-52	P53	Homo sapiens	16-19
10930428-0	2000	Human p53 is phosphorylated on serines 6 and 9 in response to DNA damage-inducing agents.	Serine	31-38	P53	Homo sapiens	6-9
10930428-2	2000	Several attempts to generate an antibody to p53 phosphorylated at Ser(6) using a phosphoserine-containing peptide as an immunogen were unsuccessful; however, phosphorylation-specific antibodies were produced by using the phosphoserine mimetic, l-2-amino-4-phosphono-4, 4-difluorobutanoic acid (F(2)Pab), in place of phosphoserine.	Serine	66-69	P53	Homo sapiens	44-47
10930428-4	2000	Affinity-purified antibodies elicited by immunizing rabbits with an F(2)Pab peptide coupled to keyhole limpet hemocyanin recognized a p53(1-39) peptide phosphorylated only at Ser(6) but not the unphosphorylated peptide or the same peptide phosphorylated at Ser(9), Ser(15), Ser(20), Ser(33), or Ser(37).	Serine	257-260	P53	Homo sapiens	134-137
10930428-4	2000	Affinity-purified antibodies elicited by immunizing rabbits with an F(2)Pab peptide coupled to keyhole limpet hemocyanin recognized a p53(1-39) peptide phosphorylated only at Ser(6) but not the unphosphorylated peptide or the same peptide phosphorylated at Ser(9), Ser(15), Ser(20), Ser(33), or Ser(37).	Serine	257-260	P53	Homo sapiens	134-137
10930428-4	2000	Affinity-purified antibodies elicited by immunizing rabbits with an F(2)Pab peptide coupled to keyhole limpet hemocyanin recognized a p53(1-39) peptide phosphorylated only at Ser(6) but not the unphosphorylated peptide or the same peptide phosphorylated at Ser(9), Ser(15), Ser(20), Ser(33), or Ser(37).	Serine	257-260	P53	Homo sapiens	134-137
10930428-4	2000	Affinity-purified antibodies elicited by immunizing rabbits with an F(2)Pab peptide coupled to keyhole limpet hemocyanin recognized a p53(1-39) peptide phosphorylated only at Ser(6) but not the unphosphorylated peptide or the same peptide phosphorylated at Ser(9), Ser(15), Ser(20), Ser(33), or Ser(37).	Serine	257-260	P53	Homo sapiens	134-137
10930428-4	2000	Affinity-purified antibodies elicited by immunizing rabbits with an F(2)Pab peptide coupled to keyhole limpet hemocyanin recognized a p53(1-39) peptide phosphorylated only at Ser(6) but not the unphosphorylated peptide or the same peptide phosphorylated at Ser(9), Ser(15), Ser(20), Ser(33), or Ser(37).	Serine	257-260	P53	Homo sapiens	134-137
10951572-10	2000	This threonine is within the p53 hydrophobic loop (residues 13-23) required for the interaction of p53 with the cleft of its inhibitor mdm-2.	Threonine	5-14	P53	Homo sapiens	29-32
10951572-10	2000	This threonine is within the p53 hydrophobic loop (residues 13-23) required for the interaction of p53 with the cleft of its inhibitor mdm-2.	Threonine	5-14	P53	Homo sapiens	99-102
10817929-3	2000	Pretreatment of the cultures with aspirin, which inhibits NF-kappaB activation, or with specific p53 antisense oligonucleotide, which inhibits p53 transcription, resulted in a complete prevention of glutamate-induced p53 induction and apoptosis.	Glutamic Acid	199-208	P53	Homo sapiens	143-146
10896848-11	2000	Compared with adriamycin, a known inducer of p53, MCTP-treated HPAEC expressed p53 only at high concentrations and p53 expression was not coordinated with G2 arrest or polyploidy.	Doxorubicin	14-24	P53	Homo sapiens	45-48
10884347-5	2000	An alanine mutation at any one of four key positions abrogates the efficacy of a synthetic peptide containing this motif as an inhibitor of cyclin A-cdk2 phosphorylation of p53 protein.	Alanine	3-10	P53	Homo sapiens	173-176
10914720-8	2000	p53 was a significant predictor for poor cCR in the subset submitted to epirubicin (3.6 versus 25.5%; P &lt; 0.02; in patients with p53+ and p53- BC, respectively); by contrast, only a trend toward lower cCR has been observed in patients with p53+ tumors receiving CMF +/- tamoxifen with respect to p53- ones.	Epirubicin	72-82	P53	Homo sapiens	0-3
10914720-8	2000	p53 was a significant predictor for poor cCR in the subset submitted to epirubicin (3.6 versus 25.5%; P &lt; 0.02; in patients with p53+ and p53- BC, respectively); by contrast, only a trend toward lower cCR has been observed in patients with p53+ tumors receiving CMF +/- tamoxifen with respect to p53- ones.	Epirubicin	72-82	P53	Homo sapiens	132-135
10914720-8	2000	p53 was a significant predictor for poor cCR in the subset submitted to epirubicin (3.6 versus 25.5%; P &lt; 0.02; in patients with p53+ and p53- BC, respectively); by contrast, only a trend toward lower cCR has been observed in patients with p53+ tumors receiving CMF +/- tamoxifen with respect to p53- ones.	Epirubicin	72-82	P53	Homo sapiens	132-135
10914720-8	2000	p53 was a significant predictor for poor cCR in the subset submitted to epirubicin (3.6 versus 25.5%; P &lt; 0.02; in patients with p53+ and p53- BC, respectively); by contrast, only a trend toward lower cCR has been observed in patients with p53+ tumors receiving CMF +/- tamoxifen with respect to p53- ones.	Epirubicin	72-82	P53	Homo sapiens	132-135
10914720-8	2000	p53 was a significant predictor for poor cCR in the subset submitted to epirubicin (3.6 versus 25.5%; P &lt; 0.02; in patients with p53+ and p53- BC, respectively); by contrast, only a trend toward lower cCR has been observed in patients with p53+ tumors receiving CMF +/- tamoxifen with respect to p53- ones.	Epirubicin	72-82	P53	Homo sapiens	132-135
10914720-8	2000	p53 was a significant predictor for poor cCR in the subset submitted to epirubicin (3.6 versus 25.5%; P &lt; 0.02; in patients with p53+ and p53- BC, respectively); by contrast, only a trend toward lower cCR has been observed in patients with p53+ tumors receiving CMF +/- tamoxifen with respect to p53- ones.	Tamoxifen	273-282	P53	Homo sapiens	0-3
10914720-13	2000	The role of mutated p53 in preventing response is more evident in patients submitted to epirubicin, and this may be caused by the up-regulation of multidrug resistance gene expression by p53 inactivation.	Epirubicin	88-98	P53	Homo sapiens	20-23
10914720-13	2000	The role of mutated p53 in preventing response is more evident in patients submitted to epirubicin, and this may be caused by the up-regulation of multidrug resistance gene expression by p53 inactivation.	Epirubicin	88-98	P53	Homo sapiens	187-190
10817929-0	2000	Contribution of NF-kappaB and p53 in the glutamate-induced apoptosis.	Glutamic Acid	41-50	P53	Homo sapiens	30-33
10817929-2	2000	Among the intracellular events triggered by glutamate, we identified two transcriptional factors: the p50 member of the NF-kappaB family and the tumor suppressor phosphoprotein p53.	Glutamic Acid	44-53	P53	Homo sapiens	177-180
10817929-3	2000	Pretreatment of the cultures with aspirin, which inhibits NF-kappaB activation, or with specific p53 antisense oligonucleotide, which inhibits p53 transcription, resulted in a complete prevention of glutamate-induced p53 induction and apoptosis.	Oligonucleotides	111-126	P53	Homo sapiens	97-100
10817929-3	2000	Pretreatment of the cultures with aspirin, which inhibits NF-kappaB activation, or with specific p53 antisense oligonucleotide, which inhibits p53 transcription, resulted in a complete prevention of glutamate-induced p53 induction and apoptosis.	Oligonucleotides	111-126	P53	Homo sapiens	143-146
10817929-3	2000	Pretreatment of the cultures with aspirin, which inhibits NF-kappaB activation, or with specific p53 antisense oligonucleotide, which inhibits p53 transcription, resulted in a complete prevention of glutamate-induced p53 induction and apoptosis.	Oligonucleotides	111-126	P53	Homo sapiens	143-146
10817929-3	2000	Pretreatment of the cultures with aspirin, which inhibits NF-kappaB activation, or with specific p53 antisense oligonucleotide, which inhibits p53 transcription, resulted in a complete prevention of glutamate-induced p53 induction and apoptosis.	Glutamic Acid	199-208	P53	Homo sapiens	97-100
10825467-1	2000	The dietary isothiocyanates and cancer chemopreventive agents phenethyl isothiocyanate and allyl isothiocyanate and their cysteine conjugates inhibited the growth and induced apoptosis of human leukaemia HL60 (p53-) and human myeloblastic leukaemia-1 cells (p53+) in vitro.	Cysteine	122-130	P53	Homo sapiens	210-213
10825467-1	2000	The dietary isothiocyanates and cancer chemopreventive agents phenethyl isothiocyanate and allyl isothiocyanate and their cysteine conjugates inhibited the growth and induced apoptosis of human leukaemia HL60 (p53-) and human myeloblastic leukaemia-1 cells (p53+) in vitro.	Cysteine	122-130	P53	Homo sapiens	258-261
10825467-10	2000	This suggests that caspase-8 has a critical role, and caspase-3 a supporting role, in isothiocyanate-induced apoptosis in which p53 is not an obligatory participant.	isothiocyanic acid	86-100	P53	Homo sapiens	128-131
10910364-6	2000	p53 is acetylated at lysine 382 upon Ras expression, an event that is essential for its biological function.	Lysine	21-27	P53	Homo sapiens	0-3
10893263-5	2000	A mutant defective in GTP binding does not trigger apoptosis, indicating that increased levels of dyn2.GTP, rather than protein levels per se, are required to transduce signals that activate p53.	Guanosine Triphosphate	22-25	P53	Homo sapiens	191-194
10817929-3	2000	Pretreatment of the cultures with aspirin, which inhibits NF-kappaB activation, or with specific p53 antisense oligonucleotide, which inhibits p53 transcription, resulted in a complete prevention of glutamate-induced p53 induction and apoptosis.	Glutamic Acid	199-208	P53	Homo sapiens	143-146
10817929-5	2000	Then, we studied the expression of two p53 downstream genes that could participate in the glutamate-induced pro-apoptotic pathway: p21, which codes for an inhibitor of different cyclin dependent kinases, and MSH2, which codes for a protein involved in the recognition and repair of DNA mismatches.	Glutamic Acid	90-99	P53	Homo sapiens	39-42
10817929-7	2000	However, very soon after a brief exposure of the cells to glutamate, the expression of both proteins was dramatically enhanced.On these bases, we propose NF-kappaB, p53, p21 and MSH2 as relevant contributors of the glutamate-induced pro-apoptotic pathway.	Glutamic Acid	58-67	P53	Homo sapiens	165-168
10817929-7	2000	However, very soon after a brief exposure of the cells to glutamate, the expression of both proteins was dramatically enhanced.On these bases, we propose NF-kappaB, p53, p21 and MSH2 as relevant contributors of the glutamate-induced pro-apoptotic pathway.	Glutamic Acid	215-224	P53	Homo sapiens	165-168
11100817-7	2000	Upon treatment with retinoic acid (RA) and dibutyryl cyclic AMP (dbcAMP), overall GSP staining were increased concomitant with suppression of nuclear m-p53.	Tretinoin	20-33	P53	Homo sapiens	152-155
11100817-7	2000	Upon treatment with retinoic acid (RA) and dibutyryl cyclic AMP (dbcAMP), overall GSP staining were increased concomitant with suppression of nuclear m-p53.	Tretinoin	35-37	P53	Homo sapiens	152-155
10749849-9	2000	The physiological relevance of GKLF in mediating p53-dependent induction of p21(WAF1/Cip1) is demonstrated by the ability of antisense Gklf oligonucleotides to block the production of p21(WAF1/Cip1) in response to p53 activation.	Oligonucleotides	140-156	P53	Homo sapiens	49-52
10848610-7	2000	Consistent with our biochemical observations, we show that stimulation of the intracellular cyclic AMP (cAMP) pathway, which leads to CREB phosphorylation, strongly enhances both the transcriptional activation and apoptotic properties of p53.	Cyclic AMP	92-102	P53	Homo sapiens	238-241
10848610-7	2000	Consistent with our biochemical observations, we show that stimulation of the intracellular cyclic AMP (cAMP) pathway, which leads to CREB phosphorylation, strongly enhances both the transcriptional activation and apoptotic properties of p53.	Cyclic AMP	104-108	P53	Homo sapiens	238-241
10854551-0	2000	Raf-1 kinase activity predicts for paclitaxel resistance in TP53mut, but not TP53wt human ovarian cancer cells.	Paclitaxel	35-45	P53	Homo sapiens	60-67
10854551-0	2000	Raf-1 kinase activity predicts for paclitaxel resistance in TP53mut, but not TP53wt human ovarian cancer cells.	Paclitaxel	35-45	P53	Homo sapiens	60-64
10854551-7	2000	However, in the ovarian cancer cell lines (CA-OV3, SK-OV3, 2780/CP and OAW42/CP) that have a mutant TP53 (TP53mut), the cytotoxicity induced by 60 nM paclitaxel exhibited the same relationship to Raf-1 kinase activity as previously observed in cervical tumor cell lines.	Paclitaxel	150-160	P53	Homo sapiens	100-104
10854551-7	2000	However, in the ovarian cancer cell lines (CA-OV3, SK-OV3, 2780/CP and OAW42/CP) that have a mutant TP53 (TP53mut), the cytotoxicity induced by 60 nM paclitaxel exhibited the same relationship to Raf-1 kinase activity as previously observed in cervical tumor cell lines.	Paclitaxel	150-160	P53	Homo sapiens	106-113
10854551-8	2000	These data suggest that the therapeutic efficacy of paclitaxel in ovarian cancer patient whose tumors have TP53mut might be increased if it is administered in combination with Raf-1 kinase inhibitors, e.g., ISIS 5132.	Paclitaxel	52-62	P53	Homo sapiens	107-111
10876230-0	2000	Where cancer meets calcium--p53 crosstalk with EF-hands.	Calcium	19-26	P53	Homo sapiens	28-31
10918568-0	2000	Spontaneous development of drug resistance: mismatch repair and p53 defects in resistance to cisplatin in human tumor cells.	Cisplatin	93-102	P53	Homo sapiens	64-67
10918568-1	2000	The contributions of defective mismatch repair and mutated p53 to cisplatin resistance of human tumor cells were analysed.	Cisplatin	66-75	P53	Homo sapiens	59-62
10918568-7	2000	Firstly, separate introduction of a p53 defect into A2780 cells significantly increased their cisplatin resistance; defective hMLH1 provided less extensive protection.	Cisplatin	94-103	P53	Homo sapiens	36-39
10918568-9	2000	Both approaches indicate that defective p53 status is a major determinant of cisplatin resistance and defective mismatch repair is a minor, and independent, contributor.	Cisplatin	77-86	P53	Homo sapiens	40-43
10871860-0	2000	Paclitaxel selects for mutant or pseudo-null p53 in drug resistance associated with tubulin mutations in human cancer.	Paclitaxel	0-10	P53	Homo sapiens	45-48
10871860-2	2000	While the role of p53 in the intrinsic sensitivity of human cancer cells to paclitaxel (PTX) remains controversial, its role in acquired paclitaxel resistance has never been addressed.	Paclitaxel	76-86	P53	Homo sapiens	18-21
10871860-3	2000	In this study we examined the p53 status of three paclitaxel selected human ovarian carcinoma sublines, resistant to paclitaxel due to acquired beta-tubulin mutations which impair paclitaxel"s interaction with tubulin.	Paclitaxel	50-60	P53	Homo sapiens	30-33
10871860-4	2000	In contrast to parental cells which have wt p53, in all PTX-resistant sublines p53 was functionally inactive.	Paclitaxel	56-59	P53	Homo sapiens	44-47
10871860-4	2000	In contrast to parental cells which have wt p53, in all PTX-resistant sublines p53 was functionally inactive.	Paclitaxel	56-59	P53	Homo sapiens	79-82
10871860-8	2000	While PTX resistance is primarily conferred by the tubulin mutations, the loss of functional p53 observed in all clones, suggests that this loss may facilitate the development of resistance potentially by providing a clonal advantage which promotes the isolation of paclitaxel resistant cells.	Paclitaxel	266-276	P53	Homo sapiens	93-96
10764786-0	2000	The p53 tumor suppressor stimulates the catalytic activity of human topoisomerase IIalpha by enhancing the rate of ATP hydrolysis.	Adenosine Triphosphate	115-118	P53	Homo sapiens	4-7
10764786-7	2000	ATP hydrolysis assays revealed that the ATPase activity of topoisomerase IIalpha was specifically enhanced by p53.	Adenosine Triphosphate	0-3	P53	Homo sapiens	110-113
10749849-9	2000	The physiological relevance of GKLF in mediating p53-dependent induction of p21(WAF1/Cip1) is demonstrated by the ability of antisense Gklf oligonucleotides to block the production of p21(WAF1/Cip1) in response to p53 activation.	Oligonucleotides	140-156	P53	Homo sapiens	214-217
10747897-4	2000	Furthermore, we demonstrate that anisomycin- and tumor necrosis factor-alpha-induced phosphorylation of p53 at Ser-392, which is important for the transcriptional activity of this growth suppressor protein, requires p38 MAP kinase and CK2 activities.	Anisomycin	33-43	P53	Homo sapiens	104-107
10866304-0	2000	Alcohol consumption and cigarette smoking increase the frequency of p53 mutations in non-small cell lung cancer.	Alcohols	0-7	P53	Homo sapiens	68-71
10866304-6	2000	p53 mutations were more common in patients who used alcohol than in patients who consumed less than one drink per day (72 versus 39%; P = 0.003), and were detected more often smokers than nonsmokers (58% versus 10%, P = 0.02).	Alcohols	52-59	P53	Homo sapiens	0-3
10866304-7	2000	Mutations in the p53 gene were present more often (P = 0.01) in alcohol drinkers who smoked cigarettes [76% (31 of 41)], than in nondrinkers (&lt;1 drink per day) who smoked cigarettes [42% (20 of 48)] or in nondrinkers who did not smoke [14% (1 of 7)].	Alcohols	64-71	P53	Homo sapiens	17-20
10866304-8	2000	In conclusion, alcohol consumption and tobacco use are both associated with p53 mutations in non-small cell lung cancer.	Alcohols	15-22	P53	Homo sapiens	76-79
10866304-9	2000	The link between exposure to both alcohol and tobacco and p53 mutations raises the possibility that alcohol may enhance the mutagenic effects of cigarette smoke in the lung.	Alcohols	34-41	P53	Homo sapiens	58-61
10866304-9	2000	The link between exposure to both alcohol and tobacco and p53 mutations raises the possibility that alcohol may enhance the mutagenic effects of cigarette smoke in the lung.	Alcohols	100-107	P53	Homo sapiens	58-61
10828488-9	2000	However, high concentrations of exogenous ROS can also stimulate smooth muscle cell apoptosis as shown for other cell types probably via activation of p53.	Reactive Oxygen Species	42-45	P53	Homo sapiens	151-154
10747897-4	2000	Furthermore, we demonstrate that anisomycin- and tumor necrosis factor-alpha-induced phosphorylation of p53 at Ser-392, which is important for the transcriptional activity of this growth suppressor protein, requires p38 MAP kinase and CK2 activities.	Serine	111-114	P53	Homo sapiens	104-107
10911952-9	2000	By inducing premature senescence with a pulse treatment of H2O2, we can study the role of the cell cycle checkpoint proteins p53, p21, p16 and Rb in gaining each feature of senescence.	Hydrogen Peroxide	59-63	P53	Homo sapiens	125-128
10837373-3	2000	In the present study, the induction of p53 target gene expression after the treatment with either benzo(a)pyrene (B[a]P) or 1-nitropyrene (1-NP) was investigated.	1-nitropyrene	124-137	P53	Homo sapiens	39-42
10864201-2	2000	We characterized the ATM protein expression in immortalized cells from AT and AT-variant patients, and heterozygotes and correlated it with two ATM-dependent radiation responses, G1 checkpoint arrest and p53-Ser 15 phosphorylation.	Serine	208-211	P53	Homo sapiens	204-207
10839309-0	2000	Alcohol consumption and cigarette smoking in relation to high frequency of p53 protein accumulation in oesophageal squamous cell carcinoma in the Japanese.	Alcohols	0-7	P53	Homo sapiens	75-78
10864201-0	2000	ATM protein and p53-serine 15 phosphorylation in ataxia-telangiectasia (AT) patients and at heterozygotes.	Serine	20-26	P53	Homo sapiens	16-19
10839309-2	2000	A significantly larger proportion of heavy alcohol drinkers and cigarette smokers was evident in the p53-positive group.	Alcohols	43-50	P53	Homo sapiens	101-104
10864201-6	2000	The radiation-induced phosphorylation of p53 protein at serine 15, largely mediated by ATM kinase, was defective in AT, A(-T) and in 2/4 heterozygous carriers, while the G1 cell cycle checkpoint was disrupted in all AT and A(-T) cases, and in 3/10 AT heterozygotes.	Serine	56-62	P53	Homo sapiens	41-44
10941537-0	2000	Effect of cisplatin-based chemotherapy on emergence of cisplatin resistance, and its correlation with intracellular glutathione levels and accumulation of p53 protein in human ovarian cancer.	Cisplatin	10-19	P53	Homo sapiens	155-158
10850407-2	2000	The arginine allele at codon 72 of p53 was found to be more susceptible to degradation by HPV E6 protein than is the proline allele in vivo, thus resulting in a high frequency of cervical SCC in individuals homozygous for arginine at the codon.	Arginine	4-12	P53	Homo sapiens	35-38
10850407-2	2000	The arginine allele at codon 72 of p53 was found to be more susceptible to degradation by HPV E6 protein than is the proline allele in vivo, thus resulting in a high frequency of cervical SCC in individuals homozygous for arginine at the codon.	Arginine	222-230	P53	Homo sapiens	35-38
10941537-8	2000	Pre-exposure to cisPt based chemotherapy appears to result in the emergence of cisPt resistance, elevated intracellular GSH levels as well as p53 positivity.	Cisplatin	16-21	P53	Homo sapiens	142-145
10897215-7	2000	Furthermore, significant statistical differences in chemosensitivity to 5-FU and CDDP were revealed depending on the presence of serum p53 antibodies.	Fluorouracil	72-76	P53	Homo sapiens	135-138
10850547-2	2000	A novel polymerase chain reaction (PCR) approach for the analysis of the entire p53 coding and splice site regions from microdissected, formalin-fixed, paraffin-embedded tumor tissues has been developed which allows multiple genetic analyses to be performed from one primary amplification reaction.	Paraffin	152-160	P53	Homo sapiens	80-83
10897215-7	2000	Furthermore, significant statistical differences in chemosensitivity to 5-FU and CDDP were revealed depending on the presence of serum p53 antibodies.	cddp	81-85	P53	Homo sapiens	135-138
10842159-10	2000	CONCLUSION: Nitric oxide inhibits VSMC proliferation in association with the upregulation of p21; both occur independent of p53 and cGMP while being partially mediated through the p42/44 MAPK signaling cascade.	Nitric Oxide	12-24	P53	Homo sapiens	124-127
10838140-4	2000	A disproportionally high number of mutations in p53 (and other genes) are found at methylated CpG dinucleotides.	cytidylyl-3'-5'-guanosine	94-111	P53	Homo sapiens	48-51
10874665-6	2000	Mdm2 and p53 were demonstrated by immunohistology on formalin-fixed and paraffin-embedded tumor tissue.	Paraffin	72-80	P53	Homo sapiens	9-12
10897337-3	2000	This is a highly selective approach, whereby immunostained sections of formalin fixed, paraffin wax embedded tissue are exposed to ultraviolet irradiation to damage the DNA in p53 negative cells.	Paraffin	87-99	P53	Homo sapiens	176-179
10825186-2	2000	Using three cell model systems, each isogenic, we showed that either ectopic or endogenous p53 sustained a G(2) arrest activated by ionizing radiation or adriamycin.	Doxorubicin	154-164	P53	Homo sapiens	91-94
11032762-3	2000	The purpose of this study was to examine whether p53 Arg at the polymorphic position 72 could represent a risk factor for women with breast lesions.	Arginine	53-56	P53	Homo sapiens	49-52
11032762-7	2000	The allele frequency of p53 Arg/Arg was much higher than that of the normal samples (61% versus 20%).	Arginine	28-31	P53	Homo sapiens	24-27
11032762-7	2000	The allele frequency of p53 Arg/Arg was much higher than that of the normal samples (61% versus 20%).	Arginine	32-35	P53	Homo sapiens	24-27
11032762-8	2000	Based on the findings of this study, it is suggested that p53 Arg homozygosity could represent a risk factor for the tumorigenesis of the breast.	Arginine	62-65	P53	Homo sapiens	58-61
10929428-14	2000	Mutant p53 expression was more decreased in the EJ cells treated with RA or Ni(RA)2.3H2O than in the control.	Tretinoin	70-72	P53	Homo sapiens	7-10
11127510-0	2000	Mutation analysis of the p53 tumor suppressor gene using paraffin-embedded specimens of human transitional cell carcinomas by the direct sequencing method.	Paraffin	57-65	P53	Homo sapiens	25-28
10825146-11	2000	Although further refinement would be helpful to improve the detection of certain types of TPS3 alterations, oligonucleotide microarrays were shown to be a powerful and effective tool for TP53 mutation detection.	Oligonucleotides	108-123	P53	Homo sapiens	187-191
10747932-6	2000	These analyses identified a subset of cysteine and histidine residues required for stimulation of late gene expression, physical interaction with E1b 55k, and p53 destabilization.	Cysteine	38-46	P53	Homo sapiens	159-162
10747932-6	2000	These analyses identified a subset of cysteine and histidine residues required for stimulation of late gene expression, physical interaction with E1b 55k, and p53 destabilization.	Histidine	51-60	P53	Homo sapiens	159-162
10825127-0	2000	Estradiol induces functional inactivation of p53 by intracellular redistribution.	Estradiol	0-9	P53	Homo sapiens	45-48
10825127-7	2000	In addition, the estradiol-induced inactivation of p53 could be involved in the tumorigenesis of estrogen-dependent neoplasm.	Estradiol	17-26	P53	Homo sapiens	51-54
10845425-2	2000	A calpain inhibitor, n-acetyl-leu-leu-norleucinal (calpain inhibitor 1), was assessed for ability to enhance p53-dependent apoptosis in human tumor cell lines with endogenous wild-type p53 and in altered p53 cell lines with the replacement of wild-type p53 by a recombinant adenovirus (rAd-p53).	1-AMINO-1-CARBONYL PENTANE	38-49	P53	Homo sapiens	109-112
10832914-5	2000	RESULTS: Ethanol-treated PNET2 neuronal cells exhibited increased apoptosis mediated by increased levels of p53 and phospho-amino-terminal c-jun kinase (phospho-JNK), and reduced levels of Bcl-2, phosphoinositol 3-kinase (PI3 K), and intact (approximately 116 kD) poly (ADP ribose) polymerase (PARP), a deoxyribonucleic acid repair enzyme and important substrate for caspase 3.	Ethanol	9-16	P53	Homo sapiens	108-111
10928171-6	2000	There was a trend towards an association between disease recurrence and the presence of the p53 codon 72 arginine homozygous genotype (OR = 3.41, p = 0.23).	Arginine	105-113	P53	Homo sapiens	92-95
10811125-6	2000	In contrast, we observed that p38 associates physically with p53, and we provide evidence that this MAPK phosphorylates the NH2-terminal transactivation domain of p53 in serine 33, thereby stimulating its functional activity.	Serine	170-176	P53	Homo sapiens	61-64
10811125-6	2000	In contrast, we observed that p38 associates physically with p53, and we provide evidence that this MAPK phosphorylates the NH2-terminal transactivation domain of p53 in serine 33, thereby stimulating its functional activity.	Serine	170-176	P53	Homo sapiens	163-166
10788439-9	2000	The SUMO-1 attachment site in p53 (Lys-386) resides within a region known to regulate the DNA binding activity of the protein.	Lysine	35-38	P53	Homo sapiens	30-33
10775450-4	2000	Recently, we showed that sublethal doses of hypochlorous acid increased levels of the transcription factor protein 53 (p53) and the wild-type activating fragment-1/cyclin-dependent kinase inhibitory protein-1 (WAF1/CIP1) in cultured human skin fibroblasts.	Hypochlorous Acid	44-61	P53	Homo sapiens	119-122
10775450-8	2000	Growth arrest was dependent on p53 because it was blocked when cells were transfected with a p53-binding oligonucleotide.	Oligonucleotides	105-120	P53	Homo sapiens	31-34
10775450-8	2000	Growth arrest was dependent on p53 because it was blocked when cells were transfected with a p53-binding oligonucleotide.	Oligonucleotides	105-120	P53	Homo sapiens	93-96
10817508-4	2000	Irradiated C4-1 cells showed increased p53 expression, while dexamethasone treatment prior to irradiation decreased p53 protein expression.	Dexamethasone	61-74	P53	Homo sapiens	116-119
10817508-5	2000	In addition, p21 mRNA was regulated by irradiation and dexamethasone in accordance with the observed changes in p53.	Dexamethasone	55-68	P53	Homo sapiens	112-115
10813720-3	2000	RESULTS: Among these polymorphisms, the individuals carrying arginine/proline genotypes of p53 showed a 9.5-fold increase of cervical carcinoma risk (95% confidence interval [CI], 4.9-18.6) compared with those individuals carrying arginine/arginine genotypes.	Arginine	61-69	P53	Homo sapiens	91-94
10813720-3	2000	RESULTS: Among these polymorphisms, the individuals carrying arginine/proline genotypes of p53 showed a 9.5-fold increase of cervical carcinoma risk (95% confidence interval [CI], 4.9-18.6) compared with those individuals carrying arginine/arginine genotypes.	Arginine	231-239	P53	Homo sapiens	91-94
10813720-3	2000	RESULTS: Among these polymorphisms, the individuals carrying arginine/proline genotypes of p53 showed a 9.5-fold increase of cervical carcinoma risk (95% confidence interval [CI], 4.9-18.6) compared with those individuals carrying arginine/arginine genotypes.	Arginine	231-239	P53	Homo sapiens	91-94
10813720-6	2000	The individuals carrying both the arginine/proline genotype of p53 and the null genotype of GSTT1 showed a 3.5-fold increase of cervical carcinoma risk (95% CI, 1.8-7.1) compared with those individuals carrying both the arginine/arginine genotype of p53 and the GSTT1 positive genotype.	Arginine	34-42	P53	Homo sapiens	63-66
10813720-6	2000	The individuals carrying both the arginine/proline genotype of p53 and the null genotype of GSTT1 showed a 3.5-fold increase of cervical carcinoma risk (95% CI, 1.8-7.1) compared with those individuals carrying both the arginine/arginine genotype of p53 and the GSTT1 positive genotype.	Arginine	34-42	P53	Homo sapiens	250-253
10813720-6	2000	The individuals carrying both the arginine/proline genotype of p53 and the null genotype of GSTT1 showed a 3.5-fold increase of cervical carcinoma risk (95% CI, 1.8-7.1) compared with those individuals carrying both the arginine/arginine genotype of p53 and the GSTT1 positive genotype.	Arginine	220-228	P53	Homo sapiens	63-66
10813720-6	2000	The individuals carrying both the arginine/proline genotype of p53 and the null genotype of GSTT1 showed a 3.5-fold increase of cervical carcinoma risk (95% CI, 1.8-7.1) compared with those individuals carrying both the arginine/arginine genotype of p53 and the GSTT1 positive genotype.	Arginine	220-228	P53	Homo sapiens	63-66
10813720-9	2000	CONCLUSIONS: The results of the current study suggested that the arginine/proline genotype of p53, independently or in conjunction with the GSTT1 null genotype, could affect the genetic susceptibility for cervical carcinoma, and HPV positive women carrying both null genotypes of GSTT1 and GSTM1 have an increased risk of cervical carcinoma developing before age 40 years.	Arginine	65-73	P53	Homo sapiens	94-97
10930093-6	2000	Treatment of the p53-mutant T-47D breast cancer cell line with adriamycin also results in up-regulation of both isoforms, suggesting that adriamycin up-regulates TRAIL-R2/Killer/DR5 expression independent of functional p53.	Doxorubicin	63-73	P53	Homo sapiens	17-20
10930093-6	2000	Treatment of the p53-mutant T-47D breast cancer cell line with adriamycin also results in up-regulation of both isoforms, suggesting that adriamycin up-regulates TRAIL-R2/Killer/DR5 expression independent of functional p53.	Doxorubicin	63-73	P53	Homo sapiens	219-222
10815906-4	2000	The overexpression of mdm2 and p53 proteins was investigated on paraffin-embedded material by using monoclonal antibodies.	Paraffin	64-72	P53	Homo sapiens	31-34
10930093-6	2000	Treatment of the p53-mutant T-47D breast cancer cell line with adriamycin also results in up-regulation of both isoforms, suggesting that adriamycin up-regulates TRAIL-R2/Killer/DR5 expression independent of functional p53.	Doxorubicin	138-148	P53	Homo sapiens	17-20
10885605-5	2000	p53 staining was performed by immunohistochemistry, using the monoclonal antibody DO7 on paraffin-embedded tissue.	Paraffin	89-97	P53	Homo sapiens	0-3
10885602-0	2000	Histological response of cisplatin predicts patients" survival in oesophageal cancer and p53 protein accumulation in pretreatment biopsy is associated with cisplatin sensitivity.	Cisplatin	156-165	P53	Homo sapiens	89-92
10885602-4	2000	Furthermore, to evaluate the relationship between the effect of preoperative cisplatin treatment and p53 and cyclin D1 expression, we investigated p53 and cyclin D1 expression in pretreatment biopsy samples using an immunohistochemical analysis and compared the results with the histological effect to cisplatin in the resected oesophagus.	Cisplatin	77-86	P53	Homo sapiens	101-104
10785598-0	2000	Molecular downstream events and induction of thymidylate synthase in mutant and wild-type p53 colon cancer cell lines after treatment with 5-fluorouracil and the thymidylate synthase inhibitor raltitrexed.	Fluorouracil	139-153	P53	Homo sapiens	90-93
10785598-4	2000	Exposure to 5-FU (50 and 100 microM) and ZD1694 (50 and 100 nM) for 24 and 48 h induced p53 and p21 expression in wt p53 cells, but not in mt p53 cells.	Fluorouracil	12-16	P53	Homo sapiens	88-91
10785598-4	2000	Exposure to 5-FU (50 and 100 microM) and ZD1694 (50 and 100 nM) for 24 and 48 h induced p53 and p21 expression in wt p53 cells, but not in mt p53 cells.	Fluorouracil	12-16	P53	Homo sapiens	117-120
10785598-4	2000	Exposure to 5-FU (50 and 100 microM) and ZD1694 (50 and 100 nM) for 24 and 48 h induced p53 and p21 expression in wt p53 cells, but not in mt p53 cells.	Fluorouracil	12-16	P53	Homo sapiens	117-120
10885602-5	2000	The cases that showed immunohistochemical p53 staining in the pretreatment biopsy samples were resistant to cisplatin (P = 0.032).	Cisplatin	108-117	P53	Homo sapiens	42-45
10866285-1	2000	PURPOSE: This study tests the hypothesis that p53 status, i.e. wild type versus mutant form, is a determinant in radiation protection of human glioma cells by WR-1065, the active thiol form of amifostine (WR-2721).	Sulfhydryl Compounds	179-184	P53	Homo sapiens	46-49
10842327-7	2000	P53 induction occurred in HPV-16 E6 and HPV-16 E6/E7 expressing cells after exposure to cisplatin or MMC, though never to levels found in normal untreated HKCs.	Cisplatin	88-97	P53	Homo sapiens	0-3
10815759-0	2000	Cell-cycle arrest and p53-independent induction of apoptosis in vitro by the new anticancer drugs 5-FdUrd-P-FdCydOct and dCydPam-P-FdUrd in DU-145 human prostate cancer cells.	dcydpam-p	121-130	P53	Homo sapiens	22-25
10810237-10	2000	DADLE acted against this effect of METH at least in part by attenuating the mRNA expressions of a tumor necrosis factor p53 and an immediate early gene c-fos.	Methamphetamine	35-39	P53	Homo sapiens	120-123
10802655-3	2000	The binding of such mutants is influenced by whether TP53 (encoding p53) codon 72, by virtue of a common polymorphism in the human population, encodes Arg or Pro.	Arginine	151-154	P53	Homo sapiens	53-57
10909873-0	2000	Sequence-specific 1H, 15N, and 13C assignment of the N-terminal domain of the human oncoprotein MDM2 that binds to p53.	Hydrogen	18-20	P53	Homo sapiens	115-118
10779327-10	2000	Finally, we present evidence that phosphorylation of serines 15 and 392 correlates with inactivation of p53 by Tax in T cells.	Serine	53-60	P53	Homo sapiens	104-107
10802655-3	2000	The binding of such mutants is influenced by whether TP53 (encoding p53) codon 72, by virtue of a common polymorphism in the human population, encodes Arg or Pro.	Arginine	151-154	P53	Homo sapiens	68-71
10802655-4	2000	The ability of mutant p53 to bind p73, neutralize p73-induced apoptosis and transform cells in cooperation with EJ-Ras was enhanced when codon 72 encoded Arg.	Arginine	154-157	P53	Homo sapiens	22-25
10935506-0	2000	Driving p53 response to Bax activation greatly enhances sensitivity to taxol by inducing massive apoptosis.	Paclitaxel	71-76	P53	Homo sapiens	8-11
10935506-4	2000	The clones expressing bax under the control of p53 obtained from the wild-type (wt) p53-expressing cell line A2780 were much more sensitive (500- to 1000-fold) to the anticancer agent taxol than the parent cell line, with a higher percentage of cells undergoing apoptosis after drug treatment that was clearly p53-dependent and bax-mediated.	Paclitaxel	184-189	P53	Homo sapiens	47-50
10935506-4	2000	The clones expressing bax under the control of p53 obtained from the wild-type (wt) p53-expressing cell line A2780 were much more sensitive (500- to 1000-fold) to the anticancer agent taxol than the parent cell line, with a higher percentage of cells undergoing apoptosis after drug treatment that was clearly p53-dependent and bax-mediated.	Paclitaxel	184-189	P53	Homo sapiens	84-87
10935506-4	2000	The clones expressing bax under the control of p53 obtained from the wild-type (wt) p53-expressing cell line A2780 were much more sensitive (500- to 1000-fold) to the anticancer agent taxol than the parent cell line, with a higher percentage of cells undergoing apoptosis after drug treatment that was clearly p53-dependent and bax-mediated.	Paclitaxel	184-189	P53	Homo sapiens	84-87
10935506-7	2000	In conclusion, driving the p53 response (after taxol treatment) by activating the bax gene rather than the p21 gene results in induction of massive apoptosis, in vitro and in vivo, and greatly enhances sensitivity to the drug.	Paclitaxel	47-52	P53	Homo sapiens	27-30
10754463-0	2000	Homozygous arginine at codon 72 of p53 has no prognostic significance in cervical cancer.	Arginine	11-19	P53	Homo sapiens	35-38
10799339-0	2000	Cadmium induces c-myc, p53, and c-jun expression in normal human prostate epithelial cells as a prelude to apoptosis.	Cadmium	0-7	P53	Homo sapiens	23-26
10799339-4	2000	Treatment with 10 microM cadmium resulted in transient increases in c-myc and p53 mRNA levels that peaked at 2-fold and 1.4-fold, respectively, compared to control after 2 h. In contrast, c-jun mRNA levels were increased &gt;3-fold after 2, 4, and 6 h and 20-fold after 24 h. DNA synthesis decreased after 24 h of cadmium exposure.	Cadmium	25-32	P53	Homo sapiens	78-81
10754463-2	2000	The findings of increased susceptibility to degradation of p53 by E6 protein of HPV16/18 in cervical cancer with homozygous arginine at codon 72 (HA72) of p53 led to this study on whether cervical cancers with HA72 were more aggressive with the increase in the rate of loss of p53 function.	Arginine	124-132	P53	Homo sapiens	59-62
10754463-2	2000	The findings of increased susceptibility to degradation of p53 by E6 protein of HPV16/18 in cervical cancer with homozygous arginine at codon 72 (HA72) of p53 led to this study on whether cervical cancers with HA72 were more aggressive with the increase in the rate of loss of p53 function.	Arginine	124-132	P53	Homo sapiens	155-158
10754463-2	2000	The findings of increased susceptibility to degradation of p53 by E6 protein of HPV16/18 in cervical cancer with homozygous arginine at codon 72 (HA72) of p53 led to this study on whether cervical cancers with HA72 were more aggressive with the increase in the rate of loss of p53 function.	Arginine	124-132	P53	Homo sapiens	155-158
10769144-0	2000	CRE-transcription factor decoy oligonucleotide inhibition of MCF-7 breast cancer cells: cross-talk with p53 signaling pathway.	Oligonucleotides	31-46	P53	Homo sapiens	104-107
10777712-6	2000	The GSH analogue, gamma-glutamylcysteinyl-ethyl ester, down-regulated Bax/p53 abundance but restored that of Bcl-2, thereby increasing Bcl-2/Bax.	Glutathione	4-7	P53	Homo sapiens	74-77
10777712-7	2000	The antioxidant and GSH precursor N-acetyl-l-cysteine favored Bcl-2 at the expense of Bax/p53, whereas pyrrolidine dithiocarbamate induced Bax against Bcl-2, with mild effect on p53.	Acetylcysteine	34-53	P53	Homo sapiens	90-93
11832064-7	2000	Intralesional injection of steroid could increase c-myc and p53 gene expression of hypertrophic scars in vivo, which induced apoptosis of cells.	Steroids	27-34	P53	Homo sapiens	60-63
10769144-8	2000	Herein, we report that CRE-decoy oligonucleotide treatment results in an increase in the p53 protein level in MCF-7 human breast cancer cells that express wild-type p53.	Oligonucleotides	33-48	P53	Homo sapiens	89-92
10769144-7	2000	To elucidate the molecular mechanism(s) of the growth inhibition by the CRE-decoy oligonucleotide, we investigated the p53 signaling pathway.	Oligonucleotides	82-97	P53	Homo sapiens	119-122
10769144-8	2000	Herein, we report that CRE-decoy oligonucleotide treatment results in an increase in the p53 protein level in MCF-7 human breast cancer cells that express wild-type p53.	Oligonucleotides	33-48	P53	Homo sapiens	165-168
10769144-11	2000	The decoy oligonucleotide treatment also enhanced the p53 promotor-directed transcription in vivo along with the increase in p53-CBP (CREB-binding protein) complex formation.	Oligonucleotides	10-25	P53	Homo sapiens	54-57
10801407-2	2000	This is known to depend on the kinase ATM; recent results suggest ATM acts via the downstream kinase Chk2/hCds1, which stabilises p53 at least in part by direct phosphorylation of residue serine 20.	Serine	188-194	P53	Homo sapiens	130-133
10769144-11	2000	The decoy oligonucleotide treatment also enhanced the p53 promotor-directed transcription in vivo along with the increase in p53-CBP (CREB-binding protein) complex formation.	Oligonucleotides	10-25	P53	Homo sapiens	125-128
10769144-12	2000	Thus, the stabilization and activation of p53 may have contributed to the growth inhibition induced by CRE-transcription factor decoy oligonucleotide in MCF-7 breast cancer cells.	Oligonucleotides	134-149	P53	Homo sapiens	42-45
10815802-3	2000	ATRA treatment of cells that express wild-type p53 (A549 and H460), or null p53 (H1299), or mutant p53 (H596) increased the number of TNF receptors, as determined by the specific binding of 125I-labeled TNF to these cells, in a dose- and time-dependent manner.	Tretinoin	0-4	P53	Homo sapiens	47-50
10815802-3	2000	ATRA treatment of cells that express wild-type p53 (A549 and H460), or null p53 (H1299), or mutant p53 (H596) increased the number of TNF receptors, as determined by the specific binding of 125I-labeled TNF to these cells, in a dose- and time-dependent manner.	Tretinoin	0-4	P53	Homo sapiens	76-79
10815802-3	2000	ATRA treatment of cells that express wild-type p53 (A549 and H460), or null p53 (H1299), or mutant p53 (H596) increased the number of TNF receptors, as determined by the specific binding of 125I-labeled TNF to these cells, in a dose- and time-dependent manner.	Tretinoin	0-4	P53	Homo sapiens	76-79
10786679-5	2000	TP53 mutation was significantly associated with a poor response to tamoxifen [31% versus 66%; odds ratio (OR), 0.22; 95% confidence interval (CI), 0.12-0.42; P &lt; 0.0001].	Tamoxifen	67-76	P53	Homo sapiens	0-4
10749685-0	2000	Apoptosis or senescence-like growth arrest: influence of cell-cycle position, p53, p21 and bax in H2O2 response of normal human fibroblasts.	Hydrogen Peroxide	98-102	P53	Homo sapiens	78-81
10786695-4	2000	In this study, we have investigated the role of p53 protein in modulating nucleotide excision repair of anti-benzo-(a)pyrene-diol-epoxide (BPDE)-DNA adducts and related effects using human fibroblasts with normal (p53-WT) and altered p53 protein (p53Mut and p53-Null).	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	139-143	P53	Homo sapiens	48-51
10786679-6	2000	Patients with TP53 gene mutations in codons that directly contact DNA or with mutations in the zinc-binding domain loop L3 showed the lowest response to tamoxifen (18% and 15% response rates, respectively).	Tamoxifen	153-162	P53	Homo sapiens	14-18
10786695-9	2000	Furthermore, p53-Mut and p53-Null cells were more sensitive than p53-WT cells and displayed increased levels of anti-BPDE-induced apoptosis.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	117-121	P53	Homo sapiens	13-16
10786695-9	2000	Furthermore, p53-Mut and p53-Null cells were more sensitive than p53-WT cells and displayed increased levels of anti-BPDE-induced apoptosis.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	117-121	P53	Homo sapiens	25-28
10786679-8	2000	In multivariate analysis for response including the classical parameters age and menopausal status, disease-free interval, dominant site of relapse, and levels of estrogen receptor and progesterone receptor, TP53 mutation was a significant predictor of poor response in the tamoxifen-treated group (OR, 0.29; 95% CI, 0.13-0.63; P = 0.0014).	Tamoxifen	274-283	P53	Homo sapiens	208-212
10786695-9	2000	Furthermore, p53-Mut and p53-Null cells were more sensitive than p53-WT cells and displayed increased levels of anti-BPDE-induced apoptosis.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	117-121	P53	Homo sapiens	25-28
10786679-10	2000	Interestingly, the response of patients with TP53 mutations to chemotherapy after tamoxifen was not worse than that of patients without these mutations (50% versus 42%; OR, 1.35, nonsignificant).	Tamoxifen	82-91	P53	Homo sapiens	45-49
10786695-10	2000	Thus, wild-type p53 is required for the efficient global genomic repair of anti-BPDE-induced DNA adducts from the overall genome, but not for transcription-coupled repair of actively transcribed genes.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	80-84	P53	Homo sapiens	16-19
10786679-11	2000	The median progression-free survival after systemic treatment was shorter for patients with a TP53 mutation than for patients with wild-type TP53 (6.6 and 0.6 months less for tamoxifen and up-front chemotherapy, respectively).	Tamoxifen	175-184	P53	Homo sapiens	94-98
10786679-12	2000	In conclusion, TP53 gene mutation of the primary tumor is helpful in predicting the response of patients with metastatic breast disease to tamoxifen therapy.	Tamoxifen	139-148	P53	Homo sapiens	15-19
10753954-7	2000	Rapamycin blocked p70(S6k) phosphorylation induced by NO and also inhibited p53 phosphorylation and p21 expression whereas PD98059 only prevented the NO-induced increase in p21 protein without influencing either p53 activation or p21 mRNA expression.	Sirolimus	0-9	P53	Homo sapiens	76-79
10753954-7	2000	Rapamycin blocked p70(S6k) phosphorylation induced by NO and also inhibited p53 phosphorylation and p21 expression whereas PD98059 only prevented the NO-induced increase in p21 protein without influencing either p53 activation or p21 mRNA expression.	Sirolimus	0-9	P53	Homo sapiens	212-215
10751633-3	2000	We hypothesize that point mutations at serine 17 could block its phosphorylation and thereby increase the p53-Mdm2 interaction.	Serine	39-45	P53	Homo sapiens	106-109
10738214-2	2000	The most frequent mutation of the p53 gene in HCC is an AGG(Arg) to AGT(Ser) missense mutation at codon 249 of exon 7.	Arginine	60-63	P53	Homo sapiens	34-37
11324469-6	2000	When Hep G2 cells grew in a medium containing HCPT 5 micrograms.L-1 for 6 d, the p53 expression level markedly increased in comparison with the control cells.	10-hydroxycamptothecin	46-50	P53	Homo sapiens	81-84
10847455-8	2000	TS inhibition by either 5-FU or antifolates can also result in a depression of TS protein mediated inhibition of TS mRNA translation leading to induction of more TS protein synthesis, and p53 protein may further deregulate this process.	Fluorouracil	24-28	P53	Homo sapiens	188-191
10898536-8	2000	Furthermore, considerable evidence indicates that mutated p53 plays a significant role in the development of cisplatin resistance since several genes implicated in drug resistance and apoptosis (e.g. mismatch repair, bcl-2, high mobility group proteins, DNA polymerases alpha and beta, PCNA, and insulin-like growth factor) are known to be regulated by the p53 oncoprotein.	Cisplatin	109-118	P53	Homo sapiens	58-61
10898536-8	2000	Furthermore, considerable evidence indicates that mutated p53 plays a significant role in the development of cisplatin resistance since several genes implicated in drug resistance and apoptosis (e.g. mismatch repair, bcl-2, high mobility group proteins, DNA polymerases alpha and beta, PCNA, and insulin-like growth factor) are known to be regulated by the p53 oncoprotein.	Cisplatin	109-118	P53	Homo sapiens	357-360
10738214-2	2000	The most frequent mutation of the p53 gene in HCC is an AGG(Arg) to AGT(Ser) missense mutation at codon 249 of exon 7.	Serine	72-75	P53	Homo sapiens	34-37
10766163-2	2000	In this report, using the glutathione S-transferase pull-down methodology, we show the ligand-independent interaction of ERalpha with the NH2-terminal region of p53, a region known to bind the p300 and human double minute-2 (hdm2) regulatory factors.	Glutathione	26-37	P53	Homo sapiens	161-164
10811471-1	2000	The infection of recombinant adenovirus expressing wild-type p53 (Ad-p53) to lung cancer cells that harbor mutant p53 genes improves their response to cis-diamminedichloroplatinum(II).	Cisplatin	151-179	P53	Homo sapiens	61-64
10811471-1	2000	The infection of recombinant adenovirus expressing wild-type p53 (Ad-p53) to lung cancer cells that harbor mutant p53 genes improves their response to cis-diamminedichloroplatinum(II).	Cisplatin	151-179	P53	Homo sapiens	69-72
10811471-1	2000	The infection of recombinant adenovirus expressing wild-type p53 (Ad-p53) to lung cancer cells that harbor mutant p53 genes improves their response to cis-diamminedichloroplatinum(II).	Cisplatin	151-179	P53	Homo sapiens	69-72
10811471-4	2000	Ad-p53 and DNA-damaging agents (cis-diamminedichloroplatinum(II), etoposide, and 7-ethyl-10-hydrocycamptothecin) showed synergistic effects in six of seven cell lines but additive effects against a p53-mutated cell line.	Cisplatin	32-60	P53	Homo sapiens	3-6
10811471-4	2000	Ad-p53 and DNA-damaging agents (cis-diamminedichloroplatinum(II), etoposide, and 7-ethyl-10-hydrocycamptothecin) showed synergistic effects in six of seven cell lines but additive effects against a p53-mutated cell line.	Cisplatin	32-60	P53	Homo sapiens	198-201
10811471-5	2000	In contrast, Ad-p53 showed additive effects with the antitubulin agents (paclitaxel and docetaxel) in all four of the cell lines tested.	Paclitaxel	73-83	P53	Homo sapiens	16-19
10794489-1	2000	A case-control study was performed to investigate the risk of cervical cancer associated with p53 polymorphism at codon 72, encoding either arginine or proline.	Arginine	140-148	P53	Homo sapiens	94-97
10717242-0	2000	The effect of p53-function on the sensitivity to paclitaxel with or without hyperthermia in human colorectal carcinoma cells.	Paclitaxel	49-59	P53	Homo sapiens	14-17
10809364-4	2000	28 gastric dysplasia, 45 Early GC and 98 Advanced Gastric Cancers were evaluated for expression of the oncogenes p53, c-ErbB2, c-myc and the EGFr in paraffin-embedded material utilizing Avidin-Biotin immunohistochemistry techniques.	Paraffin	149-157	P53	Homo sapiens	113-116
10830578-1	2000	In 1998, Storey and co-workers suggested that individuals homozygous for arginine (Arg) at codon 72 of the p53 gene are about seven times more susceptible to human papillomavirus (HPV)-related carcinogenesis than heterozygotes.	Arginine	73-81	P53	Homo sapiens	107-110
10830578-1	2000	In 1998, Storey and co-workers suggested that individuals homozygous for arginine (Arg) at codon 72 of the p53 gene are about seven times more susceptible to human papillomavirus (HPV)-related carcinogenesis than heterozygotes.	Arginine	83-86	P53	Homo sapiens	107-110
10830578-8	2000	p53 Arg homozygosity (Arg/Arg) alone was associated with four-, six- or eight-fold increased risks for LGCIN, HGCIN or invasive cancer, respectively.	Arginine	4-7	P53	Homo sapiens	0-3
10830578-8	2000	p53 Arg homozygosity (Arg/Arg) alone was associated with four-, six- or eight-fold increased risks for LGCIN, HGCIN or invasive cancer, respectively.	Arginine	22-25	P53	Homo sapiens	0-3
10830578-8	2000	p53 Arg homozygosity (Arg/Arg) alone was associated with four-, six- or eight-fold increased risks for LGCIN, HGCIN or invasive cancer, respectively.	Arginine	22-25	P53	Homo sapiens	0-3
10830578-18	2000	Our present small study results, which suggest a biologically relevant association, provide strong evidence that homozygous arginine at codon 72 of p53 may confer a higher susceptibility to HPV-associated intra-epithelial and invasive cervical neoplasia.	Arginine	124-132	P53	Homo sapiens	148-151
10719058-9	2000	There was a difference in the distribution of p53 genotypes between high risk HPV-skin lesions and the controls, and the allele frequency of p53 Arg/Arg was much higher than the controls (65.5% versus 20%).	Arginine	149-152	P53	Homo sapiens	141-144
10717242-1	2000	The importance of p53-function for the sensitivity to paclitaxel with and without hyperthermia (HT) was studied in an isogenic cell line system.	Paclitaxel	54-64	P53	Homo sapiens	18-21
10719058-10	2000	Therefore, it is suggested that p53 Arg homozygosity could represent a potential risk factor for tumorigenesis of the skin.	Arginine	36-39	P53	Homo sapiens	32-35
10719058-4	2000	It was revealed that the arginine form of p53 is more susceptible to degradation by the HPV E6 protein than the proline form and that patients with the arginine form have a higher risk of developing cancer than those with the proline form.	Arginine	25-33	P53	Homo sapiens	42-45
10717242-2	2000	The inactivation of p53 decreased sensitivity to paclitaxel (1.1-2.5-fold), which correlated with a lower induction of apoptosis.	Paclitaxel	49-59	P53	Homo sapiens	20-23
10719058-4	2000	It was revealed that the arginine form of p53 is more susceptible to degradation by the HPV E6 protein than the proline form and that patients with the arginine form have a higher risk of developing cancer than those with the proline form.	Arginine	152-160	P53	Homo sapiens	42-45
10717242-5	2000	In conclusion, cellular sensitivity to paclitaxel depends on p53-function by its ability to induce apoptosis.	Paclitaxel	39-49	P53	Homo sapiens	61-64
10728603-6	2000	P(GFLG)-DOX effectively killed both types of tumors inducing apoptosis and necrosis through the activation of p53, Apaf-1, caspase 9, c-fos, or c-jun pathways, and the downregulation of the bcl-2 gene.	Doxorubicin	8-11	P53	Homo sapiens	110-113
10719058-5	2000	The purpose of this study was to examine whether p53 Arg at the polymorphic position 72 could represent a risk factor for patients with high risk HPV-associated malignant skin lesions.	Arginine	53-56	P53	Homo sapiens	49-52
10780666-3	2000	Expression and mutations of the p53 gene were examined in the paraffin-embedded specimens of the nasal lesions from 42 Chinese (Beijing and Chengdu) and Japanese (Okinawa and Osaka) patients with nasal NK/T-cell lymphoma by the immunohistochemistry and single strand conformation polymorphism (SSCP) analysis of polymerase chain reaction (PCR) amplified products followed by direct sequencing.	Paraffin	62-70	P53	Homo sapiens	32-35
10719058-9	2000	There was a difference in the distribution of p53 genotypes between high risk HPV-skin lesions and the controls, and the allele frequency of p53 Arg/Arg was much higher than the controls (65.5% versus 20%).	Arginine	145-148	P53	Homo sapiens	141-144
10760090-12	2000	Positive staining for both iNOS and p53 proteins was observed in all cell lines incubated with CsA that were inhibited by CHX; L-NAME inhibited only p53 staining.	Cyclosporine	95-98	P53	Homo sapiens	36-39
10760090-13	2000	CONCLUSIONS: CsA induces apoptosis in various renal cell lines, and this effect is mediated by the induction of iNOS via p53.	Cyclosporine	13-16	P53	Homo sapiens	121-124
10858956-6	2000	Seven serines and one threonine in the first 46 residues of the transactivation domain and four to five serines in the carboxyl-terminal domain are now known to be phosphorylated, and Lys320 and Lys382 in the carboxyl-terminal domain (human p53) can be acetylated.	Serine	6-13	P53	Homo sapiens	241-244
10748527-3	2000	Using this method, we fabricated DNA microarrays that carried 64 groups of 18-mer oligonucleotides encoding all possible three-base mutations in the mutational "hot spot" of the p53 tumor-suppressor gene.	Oligonucleotides	82-98	P53	Homo sapiens	178-181
10733583-3	2000	Using a series of antibodies with phosphorylation-sensitive epitopes, we now show that senescence is associated with major changes at putative regulatory sites in the N and C termini of p53 consistent with increased phosphorylation at serine-15, threonine-18, and serine-376 and decreased phosphorylation at serine-392.	Serine	235-241	P53	Homo sapiens	186-189
10733583-3	2000	Using a series of antibodies with phosphorylation-sensitive epitopes, we now show that senescence is associated with major changes at putative regulatory sites in the N and C termini of p53 consistent with increased phosphorylation at serine-15, threonine-18, and serine-376 and decreased phosphorylation at serine-392.	Threonine	246-255	P53	Homo sapiens	186-189
10733583-3	2000	Using a series of antibodies with phosphorylation-sensitive epitopes, we now show that senescence is associated with major changes at putative regulatory sites in the N and C termini of p53 consistent with increased phosphorylation at serine-15, threonine-18, and serine-376 and decreased phosphorylation at serine-392.	Serine	264-270	P53	Homo sapiens	186-189
10733583-3	2000	Using a series of antibodies with phosphorylation-sensitive epitopes, we now show that senescence is associated with major changes at putative regulatory sites in the N and C termini of p53 consistent with increased phosphorylation at serine-15, threonine-18, and serine-376 and decreased phosphorylation at serine-392.	Serine	264-270	P53	Homo sapiens	186-189
10736495-13	2000	The high response rate to this regimen despite frequent p53 mutation is consistent with the p53-independent mechanism of paclitaxel.	Paclitaxel	121-131	P53	Homo sapiens	92-95
10812392-6	2000	Ouabain prolongs the irradiation-induced G2 delay in TP53 mutant tumor cell lines by a factor greater than 2, but not in the normal lung fibroblast L132, where the cell recovery is not altered in the presence of ouabain.	Ouabain	0-7	P53	Homo sapiens	53-57
10777207-9	2000	In p53-wild-type but not -mutant or -null cell lines, doxorubicin treatment stabilized p53 protein, and increased specific binding to BS2 as revealed by EMSA, and upregulated the KILLER/DR5 promoter-luciferase reporter gene.	Doxorubicin	54-65	P53	Homo sapiens	3-6
10751531-3	2000	Silver staining PCR-SSCP method was used to detect mutations in exons 5, 6, 7, 8 of p53 gene and MSI at 4 loci on chromosomes 2, 5, 17 in the 73 paraffin-embedded biopsy specimens, and the relationship between them was studied further.	Paraffin	145-153	P53	Homo sapiens	84-87
10762058-1	2000	Cytotoxic effect of either cisplatin or p53 gene transfection of lung cancer cells may be different depending on the p53 status of cells.	Cisplatin	27-36	P53	Homo sapiens	117-120
10762058-7	2000	These results suggest that cisplatin induced p53 protein phosphorylation and may activate the downstream of p53 gene expression such as p21 and Bax.	Cisplatin	27-36	P53	Homo sapiens	45-48
10762058-7	2000	These results suggest that cisplatin induced p53 protein phosphorylation and may activate the downstream of p53 gene expression such as p21 and Bax.	Cisplatin	27-36	P53	Homo sapiens	108-111
10734067-0	2000	Damage-mediated phosphorylation of human p53 threonine 18 through a cascade mediated by a casein 1-like kinase.	Threonine	45-54	P53	Homo sapiens	41-44
10734067-4	2000	Here we show that the direct association between a p53 N-terminal peptide and Mdm2 is disrupted by phosphorylation of the peptide on Thr(18) but not by phosphorylation at other N-terminal sites, including Ser(15) and Ser(37).	Threonine	133-136	P53	Homo sapiens	51-54
10734067-4	2000	Here we show that the direct association between a p53 N-terminal peptide and Mdm2 is disrupted by phosphorylation of the peptide on Thr(18) but not by phosphorylation at other N-terminal sites, including Ser(15) and Ser(37).	Serine	205-208	P53	Homo sapiens	51-54
10734067-4	2000	Here we show that the direct association between a p53 N-terminal peptide and Mdm2 is disrupted by phosphorylation of the peptide on Thr(18) but not by phosphorylation at other N-terminal sites, including Ser(15) and Ser(37).	Serine	217-220	P53	Homo sapiens	51-54
10734067-7	2000	Our results suggest that stabilization of p53 after ionizing radiation may result, in part, from an inhibition of Mdm2 binding through a phosphorylation-phosphorylation cascade involving DNA damage-activated phosphorylation of p53 Ser(15) followed by phosphorylation of Thr(18).	Serine	231-234	P53	Homo sapiens	42-45
10734067-7	2000	Our results suggest that stabilization of p53 after ionizing radiation may result, in part, from an inhibition of Mdm2 binding through a phosphorylation-phosphorylation cascade involving DNA damage-activated phosphorylation of p53 Ser(15) followed by phosphorylation of Thr(18).	Serine	231-234	P53	Homo sapiens	227-230
10734067-7	2000	Our results suggest that stabilization of p53 after ionizing radiation may result, in part, from an inhibition of Mdm2 binding through a phosphorylation-phosphorylation cascade involving DNA damage-activated phosphorylation of p53 Ser(15) followed by phosphorylation of Thr(18).	Threonine	270-273	P53	Homo sapiens	42-45
10734067-7	2000	Our results suggest that stabilization of p53 after ionizing radiation may result, in part, from an inhibition of Mdm2 binding through a phosphorylation-phosphorylation cascade involving DNA damage-activated phosphorylation of p53 Ser(15) followed by phosphorylation of Thr(18).	Threonine	270-273	P53	Homo sapiens	227-230
10777207-9	2000	In p53-wild-type but not -mutant or -null cell lines, doxorubicin treatment stabilized p53 protein, and increased specific binding to BS2 as revealed by EMSA, and upregulated the KILLER/DR5 promoter-luciferase reporter gene.	Doxorubicin	54-65	P53	Homo sapiens	87-90
10713094-4	2000	Serine 15 of p53 is phosphorylated in vivo in response to ionizing radiation, and antibodies to ATM immunoprecipitate a protein kinase activity that, in the presence of manganese, phosphorylates p53 at serine 15.	Serine	0-6	P53	Homo sapiens	13-16
10734236-1	2000	The modification of intracellular redox conditions with diethylmaleate (DEM), a glutathione-depleting agent, induces a p53-independent growth arrest mediated by the accumulation of p21(waf1) mRNA and protein.	Glutathione	80-91	P53	Homo sapiens	119-122
10754498-8	2000	Interestingly, heavy drinking had a significant positive correlation with the p53 mutation, but heavy smoking did not, suggesting that prolonged exposure to alcohol is more related to p53 mutation in oropharyngeal SCC than to tobacco consumption.	Alcohols	157-164	P53	Homo sapiens	78-81
10754498-8	2000	Interestingly, heavy drinking had a significant positive correlation with the p53 mutation, but heavy smoking did not, suggesting that prolonged exposure to alcohol is more related to p53 mutation in oropharyngeal SCC than to tobacco consumption.	Alcohols	157-164	P53	Homo sapiens	184-187
10713094-4	2000	Serine 15 of p53 is phosphorylated in vivo in response to ionizing radiation, and antibodies to ATM immunoprecipitate a protein kinase activity that, in the presence of manganese, phosphorylates p53 at serine 15.	Serine	202-208	P53	Homo sapiens	195-198
10713094-7	2000	Highly purified ATM phosphorylated PHAS-I, the 32-kDa subunit of RPA, serine 15 of p53, and Chk2 in vitro.	Serine	70-76	P53	Homo sapiens	83-86
10708576-5	2000	The increase in multiubiquitinated proteins as well as the stabilization of p53 following CsA addition argues in favor of this hypothesis.	Cyclosporine	90-93	P53	Homo sapiens	76-79
10713094-4	2000	Serine 15 of p53 is phosphorylated in vivo in response to ionizing radiation, and antibodies to ATM immunoprecipitate a protein kinase activity that, in the presence of manganese, phosphorylates p53 at serine 15.	Serine	0-6	P53	Homo sapiens	195-198
10713094-4	2000	Serine 15 of p53 is phosphorylated in vivo in response to ionizing radiation, and antibodies to ATM immunoprecipitate a protein kinase activity that, in the presence of manganese, phosphorylates p53 at serine 15.	Serine	202-208	P53	Homo sapiens	13-16
10723139-7	2000	When we mutated the seven cysteine residues of RING finger domain of MDM2 in the carboxyl terminus, the disruption of each residue in the RING finger completely diminished the ubiquitin ligase activity of MDM2 toward MDM2 itself and toward tumor suppressor p53.	Cysteine	26-34	P53	Homo sapiens	257-260
10734308-4	2000	(1998a, b) we found that the phosphorylation of p53 on Ser 15 is not a major cause of the Tax-mediated inactivation of p53.	Serine	55-58	P53	Homo sapiens	48-51
10749144-4	2000	Phosphorylation of p53 at serine 15 and acetylation at lysine 382 were detected after drug treatment.	Serine	26-32	P53	Homo sapiens	19-22
10723129-3	2000	Though downstream targets of the ATM kinase are still being elucidated, it has been demonstrated that ATM acts upstream of p53 in a signal transduction pathway initiated by IR and can phosphorylate p53 at serine 15.	Serine	205-211	P53	Homo sapiens	123-126
10716435-4	2000	Expression of p53R2, but not R2, was induced by ultraviolet and gamma-irradiation and adriamycin treatment in a wild-type p53-dependent manner.	Doxorubicin	86-96	P53	Homo sapiens	14-17
10723129-3	2000	Though downstream targets of the ATM kinase are still being elucidated, it has been demonstrated that ATM acts upstream of p53 in a signal transduction pathway initiated by IR and can phosphorylate p53 at serine 15.	Serine	205-211	P53	Homo sapiens	198-201
10716435-5	2000	Induction of p53R2 in p53-deficient cells caused G2/M arrest and prevented cells from death in response to adriamycin.	Doxorubicin	107-117	P53	Homo sapiens	13-16
10810342-6	2000	The sensitivity of wt p53-transfected cells (H358/p53) to paclitaxel was approximately 3-fold lower than that of H358 cells.	Paclitaxel	58-68	P53	Homo sapiens	22-25
10810342-6	2000	The sensitivity of wt p53-transfected cells (H358/p53) to paclitaxel was approximately 3-fold lower than that of H358 cells.	Paclitaxel	58-68	P53	Homo sapiens	50-53
10728689-6	2000	Like the increased intracellular ROS bystander effect, this "decreased TP53/CDKN1A response" can be mimicked in otherwise untreated cells by the addition of low concentrations of TGF-beta1.	Reactive Oxygen Species	33-36	P53	Homo sapiens	71-75
10717525-9	2000	Clinically a good response to CDDP-based chemo(thermo)therapy for NSCLC patients with tumour residue or recurrence, was observed only in those with p53-negative accumulation and GML gene expression, in agreement with in vitro results.	Cisplatin	30-34	P53	Homo sapiens	148-151
10718209-7	2000	In the present study the authors optimized a polymerase chain reaction-based mutation screening method, fluorescence-single strand conformation polymorphism (F-SSCP), that allows p53 status to be assessed accurately and reproducibly in routinely handled, formalin-fixed and paraffin-embedded tumor specimens.	Paraffin	274-282	P53	Homo sapiens	179-182
10741907-10	2000	Meanwhile, Ad-p53 gene transfer combined with taxol, cisplatin, doxorubicin or mitomycin C was shown to be even more effective in suppressing growth in the two cell lines.	Paclitaxel	46-51	P53	Homo sapiens	14-17
10927863-3	2000	Paraffin sections were stained by using monoclonal antibody D07 for p53 protein and PC-10 for PCNA.	Paraffin	0-8	P53	Homo sapiens	68-71
12501603-3	2000	This exonuclease activity is intrinsic to wildtype P53 protein, dependent on Mg2+, and it can be inhibited by addition of 5 mmol/L nucleoside monophosphates.	magnesium ion	77-81	P53	Homo sapiens	51-54
11240661-0	2000	Emergence of cisplatin-resistant cells from the OVCAR-3 ovarian carcinoma cell line with p53 mutations, altered tumorigenicity, and increased apoptotic sensitivity to p53 gene replacement.	Cisplatin	13-22	P53	Homo sapiens	89-92
11240661-0	2000	Emergence of cisplatin-resistant cells from the OVCAR-3 ovarian carcinoma cell line with p53 mutations, altered tumorigenicity, and increased apoptotic sensitivity to p53 gene replacement.	Cisplatin	13-22	P53	Homo sapiens	167-170
11240661-8	2000	Together, the results suggest that alterations in tumor growth and gene mutations characterize cDDP-resistance in OVCAR-3 cells, and viral replacement of one of these defective genes (p53) may provide an effective treatment for elimination of drug-resistant cells.	Cisplatin	95-99	P53	Homo sapiens	184-187
10741907-10	2000	Meanwhile, Ad-p53 gene transfer combined with taxol, cisplatin, doxorubicin or mitomycin C was shown to be even more effective in suppressing growth in the two cell lines.	Cisplatin	53-62	P53	Homo sapiens	14-17
10741907-10	2000	Meanwhile, Ad-p53 gene transfer combined with taxol, cisplatin, doxorubicin or mitomycin C was shown to be even more effective in suppressing growth in the two cell lines.	Doxorubicin	64-75	P53	Homo sapiens	14-17
10939520-3	2000	Analysis of flow cytometry indicated that H2O2 can decrease the level of CD95(APO-1/Fas), and it is confirmed that H2O2 can also activate the differential expression of some specific gene such as p53 by means of RT-PCR technique.	Hydrogen Peroxide	42-46	P53	Homo sapiens	196-199
10939520-0	2000	Hydrogen peroxide-induced apoptosis in human hepatoma cells is mediated by CD95(APO-1/Fas) receptor/ligand system and may involve activation of wild-type p53.	Hydrogen Peroxide	0-17	P53	Homo sapiens	154-157
10939520-3	2000	Analysis of flow cytometry indicated that H2O2 can decrease the level of CD95(APO-1/Fas), and it is confirmed that H2O2 can also activate the differential expression of some specific gene such as p53 by means of RT-PCR technique.	Hydrogen Peroxide	115-119	P53	Homo sapiens	196-199
10939520-4	2000	The results indicated that CD95 signal transduction system may be involved in the H2O2-induced apoptosis, and can regulate some specific genes associated with apoptosis in transcription and translation levels such as p53.	Hydrogen Peroxide	82-86	P53	Homo sapiens	217-220
10684646-0	2000	p53 regulates caveolin gene transcription, cell cholesterol, and growth by a novel mechanism.	Cholesterol	48-59	P53	Homo sapiens	0-3
10719037-0	2000	p53 mutations experimentally induced by 8-methoxypsoralen plus UVA (PUVA) differ from those found in human skin cancers in PUVA-treated patients.	Methoxsalen	40-57	P53	Homo sapiens	0-3
10671669-0	2000	Comparison of effects of doxorubicin and radiation on p53-dependent apoptosis in vivo.	Doxorubicin	25-36	P53	Homo sapiens	54-57
10671669-5	2000	In NNE with wild-type p53, doxorubicin induced growth delay of tumors (tumor volume doubling time; 13.7+/-3.3 days in control group vs 30.4+/-1.5 days in doxorubicin group), but no growth delay of tumors in KYG and GLS with mutant type p53.	Doxorubicin	27-38	P53	Homo sapiens	22-25
10671669-5	2000	In NNE with wild-type p53, doxorubicin induced growth delay of tumors (tumor volume doubling time; 13.7+/-3.3 days in control group vs 30.4+/-1.5 days in doxorubicin group), but no growth delay of tumors in KYG and GLS with mutant type p53.	Doxorubicin	27-38	P53	Homo sapiens	236-239
10671669-8	2000	Doxorubicin-induced apoptosis may be correlated with p53 phenotype because apoptosis was induced only in tumor with wild-type p53, but it appeared less frequently and later than radiation-induced apoptosis.	Doxorubicin	0-11	P53	Homo sapiens	53-56
10671669-8	2000	Doxorubicin-induced apoptosis may be correlated with p53 phenotype because apoptosis was induced only in tumor with wild-type p53, but it appeared less frequently and later than radiation-induced apoptosis.	Doxorubicin	0-11	P53	Homo sapiens	126-129
11023067-7	2000	Mutations of p53 were present in 3 of 38 HPV-positive samples: one with an ATG--&gt;TTG transversion (Met--&gt;Leu) in codon 237 of exon 7; and the others with a TGC--&gt;TGG transversion (Cys--&gt;Trp) in codon 242 of exon 7, and a CGT--&gt;CCT transversion (Arg--&gt;Pro) in codon 273 of exon 8, respectively.	Cysteine	189-192	P53	Homo sapiens	13-16
11023067-7	2000	Mutations of p53 were present in 3 of 38 HPV-positive samples: one with an ATG--&gt;TTG transversion (Met--&gt;Leu) in codon 237 of exon 7; and the others with a TGC--&gt;TGG transversion (Cys--&gt;Trp) in codon 242 of exon 7, and a CGT--&gt;CCT transversion (Arg--&gt;Pro) in codon 273 of exon 8, respectively.	Tryptophan	198-201	P53	Homo sapiens	13-16
11023067-7	2000	Mutations of p53 were present in 3 of 38 HPV-positive samples: one with an ATG--&gt;TTG transversion (Met--&gt;Leu) in codon 237 of exon 7; and the others with a TGC--&gt;TGG transversion (Cys--&gt;Trp) in codon 242 of exon 7, and a CGT--&gt;CCT transversion (Arg--&gt;Pro) in codon 273 of exon 8, respectively.	Arginine	260-263	P53	Homo sapiens	13-16
10692490-0	2000	Effect of p53 status on sensitivity to platinum complexes in a human ovarian cancer cell line.	Platinum	39-47	P53	Homo sapiens	10-13
10692490-1	2000	Wild-type p53 is frequently mutated in late-stage ovarian cancer and has been proposed as a determinant of cisplatin chemosensitivity.	Cisplatin	107-116	P53	Homo sapiens	10-13
10692490-10	2000	Our results suggest that the loss of functional p53 can increase cisplatin cytotoxicity in A2780, with loss of G(1)/S checkpoint control and decreased cisplatin-DNA adduct repair, but these effects can be circumvented by the use of JM335, which forms different DNA-platinum adducts.	Cisplatin	65-74	P53	Homo sapiens	48-51
10692490-10	2000	Our results suggest that the loss of functional p53 can increase cisplatin cytotoxicity in A2780, with loss of G(1)/S checkpoint control and decreased cisplatin-DNA adduct repair, but these effects can be circumvented by the use of JM335, which forms different DNA-platinum adducts.	Cisplatin	151-160	P53	Homo sapiens	48-51
10692490-10	2000	Our results suggest that the loss of functional p53 can increase cisplatin cytotoxicity in A2780, with loss of G(1)/S checkpoint control and decreased cisplatin-DNA adduct repair, but these effects can be circumvented by the use of JM335, which forms different DNA-platinum adducts.	Platinum	265-273	P53	Homo sapiens	48-51
10788533-6	2000	Of the p53 functional mutations, a substitution of Gly at amino acid residue 245 to Asp (G245D) was identified in two patients in three subclones.	Glycine	51-54	P53	Homo sapiens	7-10
10774750-4	2000	The alkylation sites observed in exon 9 of the p53 gene revealed that the most high reactivity sites for altromycin B were found to be N7 of guanine in a 5"-AG* sequence.	altromycin B	105-117	P53	Homo sapiens	47-50
10679306-6	2000	We show that overexpression of Prx-V prevented the p53-dependent generation of reactive oxygen species.	Reactive Oxygen Species	79-102	P53	Homo sapiens	51-54
10660538-4	2000	Contrary to bax, another known pro-apoptotic p53-target gene, both mouse and human FAS p53REs are still activated by the discriminatory p53 mutants Pro-175 and Ala-143, a class of mutants unable to induce apoptosis.	Alanine	160-163	P53	Homo sapiens	87-90
10671549-2	2000	Tumor suppressor protein p53 and cell cycle inhibitor p21 accumulate as an early sign of S-nitrosoglutathione-mediated toxicity.	S-Nitrosoglutathione	89-109	P53	Homo sapiens	25-28
10706125-12	2000	Functional analysis of two immortalized lymphoblastoid cell lines derived from patients with the p53 13964GC mutation demonstrated prolonged in vitro survival in response to cisplatinum treatment and showed decreased chemotherapy-induced apoptosis.	Cisplatin	174-185	P53	Homo sapiens	97-100
10713709-0	2000	The cytoprotective aminothiol WR1065 activates p21waf-1 and down regulates cell cycle progression through a p53-dependent pathway.	Aminothiol	19-29	P53	Homo sapiens	108-111
10713709-8	2000	These data indicate that WR1065, a polyamine analog with thiol anti-oxidant properties, activates a cell cycle check-point involving p53.	Sulfhydryl Compounds	57-62	P53	Homo sapiens	133-136
10706117-10	2000	In addition, standard chemotherapeutic agents (paclitaxol and cisplatin) showed a synergistic effect when combined with ONYX-015, and this effect was p53 mutant dependent.	Paclitaxel	47-57	P53	Homo sapiens	150-153
10706117-10	2000	In addition, standard chemotherapeutic agents (paclitaxol and cisplatin) showed a synergistic effect when combined with ONYX-015, and this effect was p53 mutant dependent.	Cisplatin	62-71	P53	Homo sapiens	150-153
10660538-4	2000	Contrary to bax, another known pro-apoptotic p53-target gene, both mouse and human FAS p53REs are still activated by the discriminatory p53 mutants Pro-175 and Ala-143, a class of mutants unable to induce apoptosis.	Alanine	160-163	P53	Homo sapiens	87-90
10682666-3	2000	Immunohistochemical p53 (pAb 1801 mAb) and TS (TS106 mAb) expression on formalin-fixed paraffin-embedded primary tumour specimens was related to probability of clinical response to chemotherapy, time to progression and overall survival.	Paraffin	87-95	P53	Homo sapiens	20-23
10698490-0	2000	Overexpression of the wild-type p53 gene inhibits NF-kappaB activity and synergizes with aspirin to induce apoptosis in human colon cancer cells.	Aspirin	89-96	P53	Homo sapiens	32-35
10698490-8	2000	We also found that the wt-p53 gene transfer was synergistic with aspirin (acetylsalicylic acid) in inhibiting NF-kappaB constitutive activity, resulting in enhanced apoptotic cell death.	Aspirin	65-72	P53	Homo sapiens	26-29
10698490-8	2000	We also found that the wt-p53 gene transfer was synergistic with aspirin (acetylsalicylic acid) in inhibiting NF-kappaB constitutive activity, resulting in enhanced apoptotic cell death.	Aspirin	74-94	P53	Homo sapiens	26-29
10696460-2	2000	STUDY DESIGN: We analyzed the differential expression of different apoptosis modulators, Bcl-2, Bax, p53 and Fas, for their potential role in PB-induced apoptosis using relative quantitative flow cytometry (FCM).	Phenylbutyrates	142-144	P53	Homo sapiens	101-104
10696460-8	2000	In a p53-positive cell line (DU145), p53 was repressed by 70% and Fas elevated sixfold with 10 mM PB.	Phenylbutyrates	98-100	P53	Homo sapiens	5-8
10696460-8	2000	In a p53-positive cell line (DU145), p53 was repressed by 70% and Fas elevated sixfold with 10 mM PB.	Phenylbutyrates	98-100	P53	Homo sapiens	37-40
10696460-9	2000	CONCLUSION: Our data show that PB-induced PCa apoptosis is associated with the relative repression of Bcl-2 and with up-regulation of Bax and Fas proteins and that this PB-induced apoptosis is independent of p53 and androgen-dependency status of PCa cell lines.	Phenylbutyrates	31-33	P53	Homo sapiens	208-211
10680816-2	2000	Sequencing of the p53 gene, exon 4, showed heterozygosity (Arg-Pro) at codon 72 in five of six PML patients.	Arginine	59-62	P53	Homo sapiens	18-21
10682666-1	2000	The purpose of this work was to analyse the ability of p53 and thymidilate synthase (TS) primary tumour expression to retrospectively predict clinical response to chemotherapy and long-term prognosis in patients with advanced colorectal cancers homogeneously treated by methotrexate (MTX)-modulated-5-fluorouracil (5-FU-FA).	Fluorouracil	299-313	P53	Homo sapiens	55-58
10676627-0	2000	p53-dependent global genomic repair of benzo[a]pyrene-7,8-diol-9,10-epoxide adducts in human cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	39-75	P53	Homo sapiens	0-3
10732742-3	2000	DNA sequencing confirmed the presence of a G to T base substitution within the Haelll site spanning codons 249 and 250 of the p53 gene that results in replacement of arginine (wild-type) by methionine at residue 249.	Arginine	166-174	P53	Homo sapiens	126-129
10732742-3	2000	DNA sequencing confirmed the presence of a G to T base substitution within the Haelll site spanning codons 249 and 250 of the p53 gene that results in replacement of arginine (wild-type) by methionine at residue 249.	Methionine	190-200	P53	Homo sapiens	126-129
10732766-0	2000	Sensitivity to CPT-11 of xenografted human colorectal cancers as a function of microsatellite instability and p53 status.	Irinotecan	15-21	P53	Homo sapiens	110-113
10732766-16	2000	Taken together, these observations indicate that MSI and p53 alterations could be associated with different CPT-11 sensitivities; MSI phenotype moderately influences the CPT-11 sensitivity, MSI+ being more sensitive than MSI(-)CRC freshly obtained from patients, mutp53 status being associated with a poor response to CPT-11.	Irinotecan	108-114	P53	Homo sapiens	57-60
10732740-1	2000	An initial report suggested that patients homozygous for the arginine allele at codon 72 of P53 were at increased risk for human papillomavirus (HPV)-related cervical cancer, but other groups have not confirmed this finding.	Arginine	61-69	P53	Homo sapiens	92-95
10657969-0	2000	Transition mutation in codon 248 of the p53 tumor suppressor gene induced by reactive oxygen species and a nitric oxide-releasing compound.	Reactive Oxygen Species	77-100	P53	Homo sapiens	40-43
10657969-0	2000	Transition mutation in codon 248 of the p53 tumor suppressor gene induced by reactive oxygen species and a nitric oxide-releasing compound.	Nitric Oxide	107-119	P53	Homo sapiens	40-43
10676627-2	2000	At low BPDE adduct levels (10-50 adducts/10(8) nucleotides), repair was rapid and essentially complete within 24 h in p53+ cells, whereas no repair was detected within 72 h in similarly treated p53- cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	7-11	P53	Homo sapiens	118-121
10676627-2	2000	At low BPDE adduct levels (10-50 adducts/10(8) nucleotides), repair was rapid and essentially complete within 24 h in p53+ cells, whereas no repair was detected within 72 h in similarly treated p53- cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	7-11	P53	Homo sapiens	194-197
10676627-3	2000	At 10-fold higher BPDE adduct levels, repair under both conditions was rapid up to 8 h, after which a low level of adducts persisted only in p53- cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	18-22	P53	Homo sapiens	141-144
10698487-3	2000	), 393: 229-234, 1998)] reported a 7-fold increased risk of cervical cancer associated with having an Arg/Arg polymorphism at codon 72 of p53 compared with the Pro/Arg heterozygotes (odds ratio, 7.4; 95% confidence interval, 2.1-29.4).	Arginine	102-105	P53	Homo sapiens	138-141
10676627-4	2000	These results demonstrate a dependence on p53 for the efficient repair of BPDE adducts at levels that are relevant to human environmental exposure and, thus, have significant implications for human carcinogenesis.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	74-78	P53	Homo sapiens	42-45
10698487-3	2000	), 393: 229-234, 1998)] reported a 7-fold increased risk of cervical cancer associated with having an Arg/Arg polymorphism at codon 72 of p53 compared with the Pro/Arg heterozygotes (odds ratio, 7.4; 95% confidence interval, 2.1-29.4).	Arginine	106-109	P53	Homo sapiens	138-141
10698487-3	2000	), 393: 229-234, 1998)] reported a 7-fold increased risk of cervical cancer associated with having an Arg/Arg polymorphism at codon 72 of p53 compared with the Pro/Arg heterozygotes (odds ratio, 7.4; 95% confidence interval, 2.1-29.4).	Arginine	106-109	P53	Homo sapiens	138-141
10693987-10	2000	Four of the five mutations in the p53 antibody-positive patients affected a Tyr residue, whereas none of the gene abnormalities in the seronegative patients had such an effect.	Tyrosine	76-79	P53	Homo sapiens	34-37
10770640-11	2000	These findings suggest that CPT-11 and 5-FU may thus be useful as possible anticancer agents for use in a combination therapy regimen using wt p53 gene transfer.	Irinotecan	28-34	P53	Homo sapiens	143-146
10770640-11	2000	These findings suggest that CPT-11 and 5-FU may thus be useful as possible anticancer agents for use in a combination therapy regimen using wt p53 gene transfer.	Fluorouracil	39-43	P53	Homo sapiens	143-146
10693987-12	2000	Further, p53 antibody-positive patients do not have higher frequency of p53 gene mutations than p53 antibody-negative patients, but the former patient group is associated with a Tyr substitution in the protein product.	Tyrosine	178-181	P53	Homo sapiens	9-12
10673500-6	2000	In vitro, Chk2/hCds1 phosphorylated p53 on Ser-20 and dissociated preformed complexes of p53 with Mdm2, a protein that targets p53 for degradation.	Serine	43-46	P53	Homo sapiens	36-39
10673500-7	2000	In vivo, ectopic expression of wild-type Chk2/hCds1 led to increased p53 stabilization after DNA damage, whereas expression of a dominant-negative Chk2/hCds1 mutant abrogated both phosphorylation of p53 on Ser-20 and p53 stabilization.	Serine	206-209	P53	Homo sapiens	199-202
10673500-7	2000	In vivo, ectopic expression of wild-type Chk2/hCds1 led to increased p53 stabilization after DNA damage, whereas expression of a dominant-negative Chk2/hCds1 mutant abrogated both phosphorylation of p53 on Ser-20 and p53 stabilization.	Serine	206-209	P53	Homo sapiens	199-202
10673501-1	2000	Upon DNA damage, the amino terminus of p53 is phosphorylated at a number of serine residues including S20, a site that is particularly important in regulating stability and function of the protein.	Serine	76-82	P53	Homo sapiens	39-42
10653876-0	2000	Adenovirus-mediated p53 gene transfer in sequence with cisplatin to tumors of patients with non-small-cell lung cancer.	Cisplatin	55-64	P53	Homo sapiens	20-23
10716643-1	2000	PURPOSE: The radioprotective effect of the Bowman-Birk protease inhibitor (BBI) was previously shown to result from a TP53 dependent mechanism.	Amiodarone	75-78	P53	Homo sapiens	118-122
10653876-1	2000	PURPOSE: To determine the safety and tolerability of adenovirus-mediated p53 (Adp53) gene transfer in sequence with cisplatin when given by intratumor injection in patients with non-small-cell lung cancer (NSCLC).	Cisplatin	116-125	P53	Homo sapiens	73-76
10683383-3	2000	Low doses of the DNA-damaging drug doxorubicin cause predominantly G(2) arrest without killing HCT116 cells that harbor wt p53.	Doxorubicin	35-46	P53	Homo sapiens	123-126
10683383-8	2000	Therefore, (a) p53-dependent p21 induction caused by doxorubicin protects from microtubule drug-induced cytotoxicity, and (b) pretreatment with cytostatic doses of DNA-damaging drugs before treatment with microtubule drugs results in selective cytotoxicity to cancer cells with defective p53/p21-dependent checkpoint.	Doxorubicin	53-64	P53	Homo sapiens	15-18
10639517-0	2000	Ser-249 p53 mutations in plasma DNA of patients with hepatocellular carcinoma from The Gambia.	Serine	0-3	P53	Homo sapiens	8-11
10644829-6	2000	However, HPV-16 350T variants were significantly over-represented in p53 Arg homozygous women with cervical cancer.	Arginine	73-76	P53	Homo sapiens	69-72
10644829-7	2000	This suggests that, in p53 Arg/Arg women, infection with HPV-16 350T variants confers a higher risk of cervical cancer.	Arginine	27-30	P53	Homo sapiens	23-26
10644829-7	2000	This suggests that, in p53 Arg/Arg women, infection with HPV-16 350T variants confers a higher risk of cervical cancer.	Arginine	31-34	P53	Homo sapiens	23-26
10761703-0	2000	p53-independent induction of p21 (WAF1/CIP1), reduction of cyclin B1 and G2/M arrest by the isoflavone genistein in human prostate carcinoma cells.	Isoflavones	92-102	P53	Homo sapiens	0-3
10775508-4	2000	The purpose of this study was to examine whether p53 Arg at the polymorphic position 72 could represent a risk factor for women with high-risk HPV-associated premalignant and malignant cervical lesions.	Arginine	53-56	P53	Homo sapiens	49-52
10775508-9	2000	The allele frequency of p53 Arg/Arg was much higher than the normal samples (46.5% versus 20.5% in HPV-negative normal smears and 20% in blood samples).	Arginine	28-31	P53	Homo sapiens	24-27
10775508-9	2000	The allele frequency of p53 Arg/Arg was much higher than the normal samples (46.5% versus 20.5% in HPV-negative normal smears and 20% in blood samples).	Arginine	32-35	P53	Homo sapiens	24-27
10656682-3	2000	Recent reports have shown that p53 is phosphorylated at both serines 15 and 392 in response to UV radiation.	Serine	61-68	P53	Homo sapiens	31-34
10656682-4	2000	Phosphorylation at serine 15 prevents the binding of HDM2, a negative regulator of p53.	Serine	19-25	P53	Homo sapiens	83-86
10719811-1	2000	A common polymorphism of the wild type p53 is known at codon 72 of exon 4, with 2 alleles encoding either arginine (CGC, p53Arg) or proline (CCC, p53Pro).	Arginine	106-114	P53	Homo sapiens	39-42
10654447-5	2000	Dexamethasone inhibited the increase of mutated p53 expression but had little effect on p2Wafl/Cip1 expression.	Dexamethasone	0-13	P53	Homo sapiens	48-51
10775508-10	2000	Based on the findings of this study, it is suggested that p53 Arg homozygosity could possibly represent a potential risk factor for the tumorigenesis of the cervix.	Arginine	62-65	P53	Homo sapiens	58-61
10775510-0	2000	P53-independent down-regulation of Mdm2 in human cancer cells treated with adriamycin.	Doxorubicin	75-85	P53	Homo sapiens	0-3
10644693-5	2000	Furthermore, the hCdc14 phosphatases were found to dephosphorylate p53 specifically at the p34(Cdc2)/clb phosphorylation site (p53-phosphor-Ser(315)).	Serine	140-143	P53	Homo sapiens	67-70
10644693-5	2000	Furthermore, the hCdc14 phosphatases were found to dephosphorylate p53 specifically at the p34(Cdc2)/clb phosphorylation site (p53-phosphor-Ser(315)).	Serine	140-143	P53	Homo sapiens	127-130
10631110-0	2000	Nitric oxide nitrates tyrosine residues of tumor-suppressor p53 protein in MCF-7 cells.	Nitric Oxide	0-12	P53	Homo sapiens	60-63
10631110-0	2000	Nitric oxide nitrates tyrosine residues of tumor-suppressor p53 protein in MCF-7 cells.	Tyrosine	22-30	P53	Homo sapiens	60-63
10631110-1	2000	It has been reported that mammalian cells incubated with excess nitric oxide (NO) accumulate p53 protein but concomitantly this p53 loses its capacity for binding to its DNA consensus sequence.	Nitric Oxide	64-76	P53	Homo sapiens	93-96
10631110-1	2000	It has been reported that mammalian cells incubated with excess nitric oxide (NO) accumulate p53 protein but concomitantly this p53 loses its capacity for binding to its DNA consensus sequence.	Nitric Oxide	64-76	P53	Homo sapiens	128-131
10631110-2	2000	As nitration of tyrosine residues in various proteins has been shown to inhibit their functions, we examined whether NO nitrates tyrosine residues in p53 protein.	Tyrosine	129-137	P53	Homo sapiens	150-153
10631110-5	2000	Incubation with 2 mM S-nitrosoglutathione induced a significant increase in the nitrotyrosine level in p53 protein compared to nontreated cells.	S-Nitrosoglutathione	21-41	P53	Homo sapiens	103-106
10656682-5	2000	Phosphorylation at serine 392 induces the DNA-binding function of p53.	Serine	19-25	P53	Homo sapiens	66-69
10656682-6	2000	We examined the requirement for phosphorylation at both serines and show that both these modifications occur on the same molecule of p53.	Serine	56-63	P53	Homo sapiens	133-136
10656682-9	2000	Phosphorylation at serine 392, on the other hand, stimulates the DNA-binding ability of p53 but does not make it immune to binding and inhibition by HDM2.	Serine	19-25	P53	Homo sapiens	88-91
10639517-7	2000	The Ser-249 p53 mutation was detected by restriction endonuclease digestion of polymerase chain reaction products from exon 7 and was confirmed by direct sequencing of the amplified DNA.	Serine	4-7	P53	Homo sapiens	12-15
10639517-8	2000	RESULTS: The Ser-249 p53 mutation was detected in plasma DNA from 19 (36%) of the 53 patients with HCC, two (15%) of the 13 patients with cirrhosis, and three (6%) of the 53 control subjects.	Serine	13-16	P53	Homo sapiens	21-24
10639517-11	2000	CONCLUSION: The Ser-249 p53 mutation in plasma DNA is strongly associated with HCC in Gambian patients.	Serine	16-19	P53	Homo sapiens	24-27
10639517-13	2000	Use of the Ser-249 p53 mutation should facilitate further molecular epidemiologic studies on the development of HCC.	Serine	11-14	P53	Homo sapiens	19-22
10940651-0	2000	p53 pathway in apoptosis induced by all-trans-retinoic acid in acute myeloblastic leukaemia cells.	Tretinoin	36-59	P53	Homo sapiens	0-3
11996107-1	2000	A polymorphism at codon 72 of gene p53 results in the presence of either arginine or proline at this position.	Arginine	73-81	P53	Homo sapiens	35-38
10645001-4	2000	Inhibition of MDM2 expression using antisense oligonucleotide, inhibition of MDM2 function by the tumor suppressor ARF or a MDM2 deletion mutant result in the accumulation of nuclear p53.	Oligonucleotides	46-61	P53	Homo sapiens	183-186
10940651-1	2000	The role of the p53 pathway in apoptosis induced by all-trans-retinoic acid (ATRA) was studied in 5 human acute myeloid leukaemia (AML) cell lines, OU-AML-3, -4, -5, -7 and -8, previously established and characterized by the authors.	Tretinoin	52-75	P53	Homo sapiens	16-19
10940651-1	2000	The role of the p53 pathway in apoptosis induced by all-trans-retinoic acid (ATRA) was studied in 5 human acute myeloid leukaemia (AML) cell lines, OU-AML-3, -4, -5, -7 and -8, previously established and characterized by the authors.	Tretinoin	77-81	P53	Homo sapiens	16-19
10863531-2	2000	In vivo and in vitro DNA base modification patterns inflicted by reactive oxygen species (ROS) in the human P53 and PGK1 gene were nearly identical in vitro and in vivo.	Reactive Oxygen Species	65-88	P53	Homo sapiens	108-111
10632483-9	2000	The p53 gene product was rarely overexpressed in non-anaplastic CCSKs, but strikingly overexpressed in two of three anaplastic CCSKs.	ccsks	64-69	P53	Homo sapiens	4-7
10632483-9	2000	The p53 gene product was rarely overexpressed in non-anaplastic CCSKs, but strikingly overexpressed in two of three anaplastic CCSKs.	ccsks	127-132	P53	Homo sapiens	4-7
11026496-0	2000	Induction of p53 in the glutamate-induced cell death program.	Glutamic Acid	24-33	P53	Homo sapiens	13-16
11026496-2	2000	Among the intracellular events triggered by glutamate, we identified two transcriptional factors, i.e. the p50 member of the NF-kappaB family and the tumor suppressor phosphoprotein p53, that are apparently linked by a sequential trascriptional program.	Glutamic Acid	44-53	P53	Homo sapiens	182-185
11026496-3	2000	We found that pretreatment of the cultures with aspirin (ASA), which inhibits NF-kappaB activation, resulted in a complete prevention of glutamate-induced p53 immunoreactivity.	Aspirin	48-55	P53	Homo sapiens	155-158
11026496-3	2000	We found that pretreatment of the cultures with aspirin (ASA), which inhibits NF-kappaB activation, resulted in a complete prevention of glutamate-induced p53 immunoreactivity.	Aspirin	57-60	P53	Homo sapiens	155-158
11026496-3	2000	We found that pretreatment of the cultures with aspirin (ASA), which inhibits NF-kappaB activation, resulted in a complete prevention of glutamate-induced p53 immunoreactivity.	Glutamic Acid	137-146	P53	Homo sapiens	155-158
11026496-4	2000	The same results were obtained pretreating the cells with a specific p53 antisense oligonucleotide.	Oligonucleotides	83-98	P53	Homo sapiens	69-72
11026496-5	2000	Both ASA and p53 antisense abolished glutamate-induced apoptosis.	Glutamic Acid	37-46	P53	Homo sapiens	13-16
11026496-6	2000	We also found that two other proteins, the cyclin dependent kinase inhibitor p21 and DNA mismatches repair MSH2, whose encoding genes are well known target of p53, were upregulated by glutamate.	Glutamic Acid	184-193	P53	Homo sapiens	159-162
11026496-7	2000	On these bases, we propose NF-kappaB, p53, p21 and MSH2 as relevant contributors of the glutamate-induced pro-apoptotic pathway.	Glutamic Acid	88-97	P53	Homo sapiens	38-41
10863531-2	2000	In vivo and in vitro DNA base modification patterns inflicted by reactive oxygen species (ROS) in the human P53 and PGK1 gene were nearly identical in vitro and in vivo.	Reactive Oxygen Species	90-93	P53	Homo sapiens	108-111
11708215-0	2000	Measurements of hydrogen peroxide induced premature senescence: senescence-associated beta-galactosidase and DNA synthesis index in human diploid fibroblasts with down-regulated p53 or Rb.	Hydrogen Peroxide	16-33	P53	Homo sapiens	178-181
10769661-0	2000	Sensitization and caffeine potentiation of cisplatin cytotoxicity resulting from introduction of wild-type p53 gene in human osteosarcoma.	Cisplatin	43-52	P53	Homo sapiens	107-110
10769661-1	2000	The present study was performed to investigate whether the introduction of a wild-type p53 gene into human osteosarcoma cells could alter the growth rate and enhance the cytocidal effect of cisplatin (CDDP) and the synergistic antitumor effect of caffeine.	Cisplatin	190-199	P53	Homo sapiens	87-90
10769661-1	2000	The present study was performed to investigate whether the introduction of a wild-type p53 gene into human osteosarcoma cells could alter the growth rate and enhance the cytocidal effect of cisplatin (CDDP) and the synergistic antitumor effect of caffeine.	Cisplatin	201-205	P53	Homo sapiens	87-90
10769661-4	2000	The colorimetric WST-1 assay demonstrated that Saos2/p53 cells were twice as sensitive to CDDP alone at a 50% inhibition concentration than the parental Saos2 cells.	Cisplatin	90-94	P53	Homo sapiens	53-56
10769661-5	2000	Caffeine significantly potentiated the cytocidal effect of CDDP in the Saos2/p53 cells.	Cisplatin	59-63	P53	Homo sapiens	77-80
10769661-6	2000	Furthermore, the TUNEL assay revealed that following treatment both with CDDP alone and with CDDP combined with caffeine, a higher percentage of the Saos2/p53 cells underwent apoptosis than did the parental Saos2 cells.	Cisplatin	73-77	P53	Homo sapiens	155-158
10769661-6	2000	Furthermore, the TUNEL assay revealed that following treatment both with CDDP alone and with CDDP combined with caffeine, a higher percentage of the Saos2/p53 cells underwent apoptosis than did the parental Saos2 cells.	Cisplatin	93-97	P53	Homo sapiens	155-158
10769661-7	2000	Therefore the cytocidal effect of CDDP and the synergistic antitumor effect of caffeine are enhanced by the introduction of a wild-type p53 gene into a human osteosarcoma cell line null for p53.	Cisplatin	34-38	P53	Homo sapiens	136-139
10769676-0	2000	Exogenous mutant p53 DNA enhanced cisplatin-induced apoptosis in TSGH-8301 human bladder cancer cells.	Cisplatin	34-43	P53	Homo sapiens	17-20
10769676-2	2000	In this study, the requirement for p53 in the cisplatin-induced apoptosis of human bladder cancer cells TSGH-8301 was investigated.	Cisplatin	46-55	P53	Homo sapiens	35-38
10769676-6	2000	RESULTS: Cells containing an exogenous mutant p53 sequence had increased sensitivity to cisplatin by undergoing apoptosis compared with parental TSGH8301 cells.	Cisplatin	88-97	P53	Homo sapiens	46-49
10769676-9	2000	CONCLUSION: The transfectants had lost the expression of mutant p53 during selection; however, they could still enhance the expression of wild-type p53, which conferred sensitivity to cisplatin.	Cisplatin	184-193	P53	Homo sapiens	148-151
10605931-4	2000	Second, they regulate the DNA-binding activity of p53 by modulating the redox status of a critical set of cysteines in the DNA-binding domain, which are also involved in the coordination of zinc.	Cysteine	106-115	P53	Homo sapiens	50-53
10754986-9	2000	By comparison, median survival for patients with p53 mutation or p53 overexpression was both 158 days after BB2516 treatment.	marimastat	108-114	P53	Homo sapiens	49-52
10618603-4	2000	Immunohistochemical expression of nuclear p53 protein was assessed in formalin fixed, paraffin embedded archival tumor tissue.	Paraffin	86-94	P53	Homo sapiens	42-45
10754986-9	2000	By comparison, median survival for patients with p53 mutation or p53 overexpression was both 158 days after BB2516 treatment.	marimastat	108-114	P53	Homo sapiens	65-68
10656431-12	2000	The efficiency of paclitaxel during mitosis might be supported by lack of G1 arrest due to p53 deficiency.	Paclitaxel	18-28	P53	Homo sapiens	91-94
11052631-0	2000	Multiple factors other than p53 influence colon cancer sensitivity to paclitaxel.	Paclitaxel	70-80	P53	Homo sapiens	28-31
10656431-13	2000	Therefore, patients with p53-deficient tumors may benefit from paclitaxel.	Paclitaxel	63-73	P53	Homo sapiens	25-28
10656431-9	2000	Combination of sequencing and IHC results revealed a significant association between abnormal p53 and response to paclitaxel (P = 0.011).	Paclitaxel	114-124	P53	Homo sapiens	94-97
10656431-11	2000	Whereas clinical response to FEC was found to be dependent on normal p53, the cytotoxicity of paclitaxel was related to defective p53.	Paclitaxel	94-104	P53	Homo sapiens	130-133
10656450-6	2000	cDDP stimulated a 2-fold increase in p53 levels in both drug-sensitive and drug-resistant cells but caused a delayed reduction in p21WAF1 levels, suggesting p53-independent regulation of p21WAF1 in ME-180 cells.	cddp	0-4	P53	Homo sapiens	37-40
10656450-6	2000	cDDP stimulated a 2-fold increase in p53 levels in both drug-sensitive and drug-resistant cells but caused a delayed reduction in p21WAF1 levels, suggesting p53-independent regulation of p21WAF1 in ME-180 cells.	cddp	0-4	P53	Homo sapiens	157-160
22607421-0	2000	Effects of Oxidation Agents and Metal Ions on Binding of p53 to Supercoiled DNA.	Metals	32-37	P53	Homo sapiens	57-60
10640274-3	2000	We find that p53 promotes Mdm2-mediated ubiquitination and proteasomal degradation of the HIF-1alpha subunit of hypoxia-inducible factor 1 (HIF-1), a heterodimeric transcription factor that regulates cellular energy metabolism and angiogenesis in response to oxygen deprivation.	Oxygen	259-265	P53	Homo sapiens	13-16
10895031-3	2000	The homozygous p53 arginine allele (Arg/Arg) was detected in 22 (31%), the homozygous p53 proline allele (Pro/Pro) in 14 (19%) and the heterozygous allele (Arg/Pro) in 36 (50%) cases, respectively.	Arginine	19-27	P53	Homo sapiens	15-18
10642304-0	2000	Cyclic AMP inhibited proliferation of human aortic vascular smooth muscle cells, accompanied by induction of p53 and p21.	Cyclic AMP	0-10	P53	Homo sapiens	109-112
10642304-6	2000	Upregulation of p53 protein by cAMP was further confirmed by the observation that the decrease in p21, a p53-inducible protein, by PDGF was significantly attenuated by cilostazol in a dose-dependent manner (P&lt;0.01).	Cyclic AMP	31-35	P53	Homo sapiens	16-19
10642304-6	2000	Upregulation of p53 protein by cAMP was further confirmed by the observation that the decrease in p21, a p53-inducible protein, by PDGF was significantly attenuated by cilostazol in a dose-dependent manner (P&lt;0.01).	Cyclic AMP	31-35	P53	Homo sapiens	105-108
10642304-7	2000	These results revealed that accumulation of cAMP inhibited VSMC proliferation, which was at least in part due to an increase in p53-p21 expression.	Cyclic AMP	44-48	P53	Homo sapiens	128-131
10642304-7	2000	These results revealed that accumulation of cAMP inhibited VSMC proliferation, which was at least in part due to an increase in p53-p21 expression.	vsmc	59-63	P53	Homo sapiens	128-131
10642304-11	2000	Overall, these results demonstrated that cAMP inhibited the proliferation of human aortic VSMCs, accompanied by p53-p21-mediated apoptosis.	Cyclic AMP	41-45	P53	Homo sapiens	112-115
10585590-4	2000	Moreover, expression of wt-p53 in MCF7/Adr cells induced the production of reactive oxygen intermediates (ROIs) and caused glutathione (GSH) depletion, indicating disturbances in the cellular redox state.	Glutathione	123-134	P53	Homo sapiens	27-30
10585590-4	2000	Moreover, expression of wt-p53 in MCF7/Adr cells induced the production of reactive oxygen intermediates (ROIs) and caused glutathione (GSH) depletion, indicating disturbances in the cellular redox state.	Glutathione	136-139	P53	Homo sapiens	27-30
10585590-5	2000	Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity.	Glutathione	56-67	P53	Homo sapiens	133-136
10585590-5	2000	Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity.	Glutathione	56-67	P53	Homo sapiens	273-276
10585590-5	2000	Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity.	Glutathione	69-72	P53	Homo sapiens	133-136
10585590-5	2000	Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity.	Glutathione	69-72	P53	Homo sapiens	273-276
10585590-5	2000	Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity.	Acetylcysteine	84-100	P53	Homo sapiens	133-136
10585590-5	2000	Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity.	Acetylcysteine	84-100	P53	Homo sapiens	273-276
10585590-5	2000	Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity.	Acetylcysteine	102-105	P53	Homo sapiens	133-136
10585590-5	2000	Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity.	Acetylcysteine	102-105	P53	Homo sapiens	273-276
10585590-5	2000	Additional treatment of cells with the anti-oxidant and glutathione (GSH) precursor N-acetylcysteine (NAC) resulted in inhibition of p53-induced ROIs production and in partial restoration of intracellular GSH levels, which was associated with the ability of NAC to inhibit p53-modulated TNF-induced cytotoxicity.	Acetylcysteine	258-261	P53	Homo sapiens	133-136
10644891-7	2000	The representative cell line NCI-H1437 cells transfected with wild-type p53 gene (H1437/wtp53) showed a dramatic increase in susceptibility to three anticancer agents (7-fold to cisplatin, 21-fold to etoposide, and 20-fold to camptothecin) compared to untransfected or neotransfected H1437 cells.	Cisplatin	178-187	P53	Homo sapiens	72-75
10637254-1	2000	PURPOSE: To determine whether p53 gene status predicts tumor responses to platinum- and fluorouracil-based induction chemotherapy in locoregionally advanced squamous cell carcinomas of the head and neck.	Platinum	74-82	P53	Homo sapiens	30-33
10637254-1	2000	PURPOSE: To determine whether p53 gene status predicts tumor responses to platinum- and fluorouracil-based induction chemotherapy in locoregionally advanced squamous cell carcinomas of the head and neck.	Fluorouracil	88-100	P53	Homo sapiens	30-33
22607421-7	2000	Compared to the intrinsic zinc strongly bound to Cys 176, Cys 238, Cys 242 and His 179 in the p53 core domain, binding of additional Zn(2+) to p53 was much weaker as shown by an easy removal of the latter ions by low concentrations of EDTA.	Zinc	133-135	P53	Homo sapiens	143-146
22607421-14	2000	We suggested that the irreversibility of p53 oxidation was due, at least in part, to the removal of intrinsic zinc from its position in the DNA binding domain (after oxidation of the three cysteines to which the zinc ion is coordinated in the reduced protein) accompanied by a change in the p53 conformation.	Cysteine	189-198	P53	Homo sapiens	41-44
10636514-5	2000	Immunohistochemical staining was performed to assess p53 expression in paraffin-embedded ovarian cancers.	Paraffin	71-79	P53	Homo sapiens	53-56
10930054-6	2000	Analysis of patient urine following administration of OL(1)p53 reveals a 7.5-fold increase in iron excretion at low doses (0.05 mg/kg/h).	Iron	94-98	P53	Homo sapiens	59-62
10772725-4	2000	p53 protein removes beta-D-nucleoside analogs more efficiently compared to that of beta-L-nucleoside analogs.	beta-d-nucleoside	20-37	P53	Homo sapiens	0-3
11389540-7	2000	In support to this assumption, human mutant p53 (Gly(245)--&gt;Ser) was shown to bind to repetitive DNA elements in vivo that might be part of MAR elements.	Glycine	49-52	P53	Homo sapiens	44-47
11389540-7	2000	In support to this assumption, human mutant p53 (Gly(245)--&gt;Ser) was shown to bind to repetitive DNA elements in vivo that might be part of MAR elements.	Serine	63-66	P53	Homo sapiens	44-47
10601254-1	1999	The Sp1 transcription factor plays an important role in mediating the p53-independent activation of the p21(WAF1) (WAF1) promoter by phorbol 12-myristate13-acetate (PMA) in hematopoietic cells.	Tetradecanoylphorbol Acetate	133-163	P53	Homo sapiens	70-73
10601598-10	2000	Namely, untreated ovarian dysfunction such as PCOS with unopposed estrogenic action in the endometrium may be associated with development and growth of EC in younger women, yet abnormality of p53 gene may be more concerned with the development of the post-menopausal EC, independently of sex steroid influence.	Steroids	292-299	P53	Homo sapiens	192-195
10729920-0	2000	Colonic mucin-carbohydrate components in colorectal tumors and their possible relationship to MUC2, p53 and DCC immunoreactivities.	Carbohydrates	14-26	P53	Homo sapiens	100-103
10974929-1	2000	The purpose of the study was to assess the expression of p53 in non-small cell lung cancer (NSCLC) before and after treatment with cisplatin and vepeside (PE) and to define a relationship between p53 expression and responsiveness to chemotherapy prior to surgery.	Cisplatin	131-140	P53	Homo sapiens	57-60
10974929-1	2000	The purpose of the study was to assess the expression of p53 in non-small cell lung cancer (NSCLC) before and after treatment with cisplatin and vepeside (PE) and to define a relationship between p53 expression and responsiveness to chemotherapy prior to surgery.	etoposide phosphate	145-153	P53	Homo sapiens	57-60
10974929-4	2000	p53 protein accumulation was detected by immunohistochemistry using antibodies against p53: NCL-p53 (clone BP-53-12) (Novocastra) on paraffin embedded specimens.	Paraffin	133-141	P53	Homo sapiens	0-3
11417748-7	2000	Western blotting showed that p53 induction was not detectable in mutant (mt) p53 WiDr and increased much earlier in wild-type (wt) Lovo cells after 5-FU and MTA (24 h) than after AG337 exposure (72 h).	Fluorouracil	148-152	P53	Homo sapiens	29-32
10601254-1	1999	The Sp1 transcription factor plays an important role in mediating the p53-independent activation of the p21(WAF1) (WAF1) promoter by phorbol 12-myristate13-acetate (PMA) in hematopoietic cells.	Tetradecanoylphorbol Acetate	165-168	P53	Homo sapiens	70-73
10618705-3	1999	DNA damage is perhaps the best-studied stress which activates p53, and recent data implicate phosphorylation at N-terminal serine residues as critical in this process.	Serine	123-129	P53	Homo sapiens	62-65
10600518-1	1999	Recent studies have implicated acetylation of several nuclear proteins such as histones and p53 on their epsilon-portion of lysine residues in eukaryotic transcription.	Lysine	124-130	P53	Homo sapiens	92-95
10585464-9	1999	cis-Diamminedichloroplatinum (II) (CDDP) induced p53 activation and p21 transactivation.	Cisplatin	0-33	P53	Homo sapiens	49-52
10585464-9	1999	cis-Diamminedichloroplatinum (II) (CDDP) induced p53 activation and p21 transactivation.	Cisplatin	35-39	P53	Homo sapiens	49-52
10585464-10	1999	The p53-dependent p21 transactivation induced by CDDP was inhibited by mTRX overexpression, suggesting that TRX-dependent redox regulation is physiologically involved in p53 regulation.	Cisplatin	49-53	P53	Homo sapiens	4-7
10585464-10	1999	The p53-dependent p21 transactivation induced by CDDP was inhibited by mTRX overexpression, suggesting that TRX-dependent redox regulation is physiologically involved in p53 regulation.	Cisplatin	49-53	P53	Homo sapiens	170-173
10716237-2	1999	Recently, Messmer and Brune suggested that nitric oxide-induced apoptosis is intimately related with p53-dependent signaling pathway, and de la Monte et al.	Nitric Oxide	43-55	P53	Homo sapiens	101-104
10588903-4	1999	The interaction of p53 and the p53CD with p53CON induced a noticeable salt-dependent bending of the DNA axis.	Salts	70-74	P53	Homo sapiens	19-22
10588903-4	1999	The interaction of p53 and the p53CD with p53CON induced a noticeable salt-dependent bending of the DNA axis.	Salts	70-74	P53	Homo sapiens	31-34
10588903-5	1999	According to quantitative analysis with folded Gaussian distributions, the bending induced by p53 varied from approximately 40 degrees to 48 degrees upon decreasing of the KCl concentration from 50 mM to approximately 1 mM in the mounting buffer used for adsorption of the complexes to the carbon film surface.	Carbon	290-296	P53	Homo sapiens	94-97
10588903-7	1999	The bending angle of the p53/DNA complex under low salt conditions showed a somewhat broader distribution (sigma approximately 39 degrees ) than at high salt concentration (sigma approximately 31 degrees ) or for p53CD (sigma approximately 24-27 degrees ).	Salts	51-55	P53	Homo sapiens	25-28
10588903-7	1999	The bending angle of the p53/DNA complex under low salt conditions showed a somewhat broader distribution (sigma approximately 39 degrees ) than at high salt concentration (sigma approximately 31 degrees ) or for p53CD (sigma approximately 24-27 degrees ).	Salts	153-157	P53	Homo sapiens	25-28
10574974-6	1999	p53 is activated by Cr(VI), mostly by ROS-mediated free radical reactions.	Reactive Oxygen Species	38-41	P53	Homo sapiens	0-3
10606817-6	1999	Sequence analysis of exons 5 through 8 of p53 was performed on cloned PCR-amplified DNA of formalin-fixed, paraffin-embedded tumors.	Paraffin	107-115	P53	Homo sapiens	42-45
10668097-5	1999	In order to study the contribution of p53 to the cyclin B1 accumulation in response to UV exposure, we inhibited p53 induction using p53 antisense oligonucleotides.	Oligonucleotides	147-163	P53	Homo sapiens	113-116
10604724-0	1999	Schedule-dependent cytotoxicity of SN-38 in p53 wild-type and mutant colon adenocarcinoma cell lines.	Irinotecan	35-40	P53	Homo sapiens	44-47
10604724-10	1999	Dose-dependent p53-associated G1 arrest, in the absence of DNA synthesis indicates an additional cytotoxic mechanism for SN-38, which requires higher concentrations than the S phase mechanism, and detection of which seems to involve p53.	Irinotecan	121-126	P53	Homo sapiens	15-18
10604724-12	1999	Although expression of wild-type p53 leads to a more rapid induction of apoptosis, SN-38 cytotoxicity was generally greater in cells with mutant p53, as wild-type cells escaped apoptosis by p53 associated prolonged cell cycle arrest.	Irinotecan	83-88	P53	Homo sapiens	145-148
10604724-12	1999	Although expression of wild-type p53 leads to a more rapid induction of apoptosis, SN-38 cytotoxicity was generally greater in cells with mutant p53, as wild-type cells escaped apoptosis by p53 associated prolonged cell cycle arrest.	Irinotecan	83-88	P53	Homo sapiens	145-148
10571245-1	1999	DNA-damaging agents such as cisplatin arrest cell cycle progression at either the G1, S, or G2 phase, although the G1 arrest is seen only in cells expressing the wild-type p53 tumor suppressor protein.	Cisplatin	28-37	P53	Homo sapiens	172-175
10571245-4	1999	We show here that UCN-01 at non-cytotoxic concentrations abrogated S and G2 arrest induced by cisplatin in two p53-defective human breast cancer cell lines.	Cisplatin	94-103	P53	Homo sapiens	111-114
10668097-5	1999	In order to study the contribution of p53 to the cyclin B1 accumulation in response to UV exposure, we inhibited p53 induction using p53 antisense oligonucleotides.	Oligonucleotides	147-163	P53	Homo sapiens	113-116
10632346-0	1999	Prognostic value of p53, glutathione S-transferase pi, and thymidylate synthase for neoadjuvant cisplatin-based chemotherapy in head and neck cancer.	Cisplatin	96-105	P53	Homo sapiens	20-23
10632350-1	1999	To evaluate both the clinicopathological and prognostic significance of p53 protein, the expression of p53 protein was immunohistochemically examined by use of CM1, PAb1801, DO7, and DO1 antibodies on paraffin-embedded colorectal adenocarcinomas from 293 patients.	Paraffin	201-209	P53	Homo sapiens	103-106
10647890-2	1999	A common p53 polymorphism at codon-72 of exon 4 results in translation to either arginine or proline.	Arginine	81-89	P53	Homo sapiens	9-12
10629550-1	1999	In breast cancer, mutations located in the zinc-binding functional domains of the p53 gene have been reported to predict a worse prognosis and a worse response to treatment with doxorubicin, compared with mutations in other parts within exons 5-8 of the gene.	Doxorubicin	178-189	P53	Homo sapiens	82-85
10567656-12	1999	There was no difference in the distribution of p53 proline and arginine alleles between HPV-16-positive cervical carcinoma patients and local controls, and no influence on clinical outcome; however, there was a trend for an increased frequency of p53 arginine homozygotes among the 350T carcinoma patients.	Arginine	251-259	P53	Homo sapiens	247-250
10568814-0	1999	Cisplatin-induced p53-independent growth arrest and cell death in cancer cells.	Cisplatin	0-9	P53	Homo sapiens	18-21
10568814-5	1999	These findings provide further evidence that cells carrying mutations resulting in loss of function in the p53 gene can be killed by cisplatin via a p53-independent route with some similarities to replicative senescence, but not apoptosis.	Cisplatin	133-142	P53	Homo sapiens	107-110
10568814-5	1999	These findings provide further evidence that cells carrying mutations resulting in loss of function in the p53 gene can be killed by cisplatin via a p53-independent route with some similarities to replicative senescence, but not apoptosis.	Cisplatin	133-142	P53	Homo sapiens	149-152
10569615-0	1999	Synergistic enhancement of resistance to cisplatin in human bladder cancer cells by overexpression of mutant-type p53 and Bcl-2.	Cisplatin	41-50	P53	Homo sapiens	114-117
10569615-1	1999	PURPOSE: The objective of this study was to characterize the effect of mutant-type p53 and Bcl-2 expression on the sensitivity to cisplatin in a human bladder cancer cell line both in vitro and in vivo.	Cisplatin	130-139	P53	Homo sapiens	83-86
10569615-3	1999	The effects of the overexpression of mutant-type p53, Bcl-2, or both on the sensitivity to cisplatin and the apoptotic features in vitro were evaluated by the MTT assay, staining with Hoechst 33258 and a DNA fragmentation assay.	Cisplatin	91-100	P53	Homo sapiens	49-52
10569615-5	1999	RESULTS: The introduction of mutant-type p53 or Bcl-2 conferred resistance to cisplatin on KoTCC-1 cells through the inhibition of apoptosis.	Cisplatin	78-87	P53	Homo sapiens	41-44
10569615-7	1999	Furthermore, the KoTCC-1 cells transfected with both mutant-type p53 and Bcl-2 exhibited significantly higher resistance to cisplatin treatment than cells transfected with mutant-type p53 or Bcl-2 alone in experimental models in vivo.	Cisplatin	124-133	P53	Homo sapiens	65-68
10569615-7	1999	Furthermore, the KoTCC-1 cells transfected with both mutant-type p53 and Bcl-2 exhibited significantly higher resistance to cisplatin treatment than cells transfected with mutant-type p53 or Bcl-2 alone in experimental models in vivo.	Cisplatin	124-133	P53	Homo sapiens	184-187
10665656-0	1999	Cisplatin-resistant HeLa cells are resistant to apoptosis via p53-dependent and -independent pathways.	Cisplatin	0-9	P53	Homo sapiens	62-65
10569615-8	1999	CONCLUSIONS: These findings suggest that the overexpression of both mutant-type p53 and Bcl-2 in bladder cancer cells synergistically interferes with the therapeutic effect of cisplatin through the inhibition of the apoptotic pathway.	Cisplatin	176-185	P53	Homo sapiens	80-83
10665656-7	1999	Transfection of wild-type p53 gene enhanced the cytotoxicity of cisplatin and cisplatin-induced apoptosis in HeLa cells but not in HeLa/CDDP cells, although it caused p53 overexpression in both cell lines.	Cisplatin	64-73	P53	Homo sapiens	26-29
10544021-3	1999	In the present study, we showed that the topoisomerase II inhibitor of widely used anticancer drugs etoposide and doxorubicin activated wt p53 in BL2, a Burkitt"s lymphoma cell line which overexpressed MDM2.	Doxorubicin	114-125	P53	Homo sapiens	139-142
10665656-7	1999	Transfection of wild-type p53 gene enhanced the cytotoxicity of cisplatin and cisplatin-induced apoptosis in HeLa cells but not in HeLa/CDDP cells, although it caused p53 overexpression in both cell lines.	Cisplatin	78-87	P53	Homo sapiens	26-29
10665656-10	1999	p53 gene transfection did not affect the extent of DNA fragmentation in either cell line, suggesting that paclitaxel may induce p53-independent apoptosis.	Paclitaxel	106-116	P53	Homo sapiens	128-131
10628802-1	1999	TP53 and MDM2 genes and their protein expression were evaluated in frozen and paraffin-embedded tissue from 27 patients with malignant fibrous histiocytoma to elucidate the relationship between them, their implication in tumor progression mechanisms and their possible diagnostic-prognostic value in malignant fibrous histiocytoma.	Paraffin	78-86	P53	Homo sapiens	0-4
10551826-4	1999	To characterize further the function of these two domains, we demonstrate in this report that the previously described major nuclear localization signal works together with Lys(305)-Arg(306) to form a bipartite and functional nuclear localization sequence (NLS) for p53 nuclear import.	Lysine	173-176	P53	Homo sapiens	266-269
10551826-4	1999	To characterize further the function of these two domains, we demonstrate in this report that the previously described major nuclear localization signal works together with Lys(305)-Arg(306) to form a bipartite and functional nuclear localization sequence (NLS) for p53 nuclear import.	Arginine	182-185	P53	Homo sapiens	266-269
10661763-4	1999	In this model, TAM resistance resulted in an increase in the detectable basal levels of cyclin E, GADD 153, p16, BAX, Bcl-XL, and wild-type and mutant p53, an increase in TAM induction of p16, and a decrease in the detectable basal levels of cyclin D1, p21 and p27.	Tamoxifen	15-18	P53	Homo sapiens	151-154
10935502-0	1999	p53-independent inhibition of proliferation and p21(WAF1/Cip1)-modulated induction of cell death by the antioxidants N-acetylcysteine and vitamin E.	Acetylcysteine	117-133	P53	Homo sapiens	0-3
10935502-5	1999	The antioxidants, N-acetylcysteine (NAC) and vitamin E either inhibited proliferation in a p53-independent manner without affecting cell viability or induced cell death.	Acetylcysteine	18-34	P53	Homo sapiens	91-94
10935502-5	1999	The antioxidants, N-acetylcysteine (NAC) and vitamin E either inhibited proliferation in a p53-independent manner without affecting cell viability or induced cell death.	Acetylcysteine	36-39	P53	Homo sapiens	91-94
10570149-0	1999	Phosphorylation of Ser-20 mediates stabilization of human p53 in response to DNA damage.	Serine	19-22	P53	Homo sapiens	58-61
10570149-3	1999	The ATM and ATR kinases, whose activation in response to ionizing radiation (IR) and UV light, respectively, is required for p53 stabilization, directly phosphorylate p53 on Ser-15.	Serine	174-177	P53	Homo sapiens	125-128
10570149-3	1999	The ATM and ATR kinases, whose activation in response to ionizing radiation (IR) and UV light, respectively, is required for p53 stabilization, directly phosphorylate p53 on Ser-15.	Serine	174-177	P53	Homo sapiens	167-170
10570149-4	1999	However, phosphorylation of Ser-15 is critical for the apoptotic activity of p53 and not for p53 stabilization.	Serine	28-31	P53	Homo sapiens	77-80
10570149-6	1999	We analyzed the IR- and UV light-induced stabilization of p53 proteins with substitutions of Ser known to be posttranslationally modified after DNA damage.	Serine	93-96	P53	Homo sapiens	58-61
10570149-8	1999	Furthermore, both IR and UV light induced phosphorylation of p53 on Ser-20, which involved the majority of nuclear p53 protein and weakened the interaction of p53 with Mdm2 in vitro.	Serine	68-71	P53	Homo sapiens	61-64
10570149-8	1999	Furthermore, both IR and UV light induced phosphorylation of p53 on Ser-20, which involved the majority of nuclear p53 protein and weakened the interaction of p53 with Mdm2 in vitro.	Serine	68-71	P53	Homo sapiens	115-118
10570149-8	1999	Furthermore, both IR and UV light induced phosphorylation of p53 on Ser-20, which involved the majority of nuclear p53 protein and weakened the interaction of p53 with Mdm2 in vitro.	Serine	68-71	P53	Homo sapiens	115-118
10570149-10	1999	We therefore propose that ATM and ATR activate an, as yet unidentified, kinase that stabilizes p53 by phosphorylating it on Ser-20.	Serine	124-127	P53	Homo sapiens	95-98
10597277-8	1999	We show directly that, like ATM and DNA-PK, ATR phosphorylates the genome surveillance protein p53 on serine 15, a site which is up-regulated in response to DNA damage.	Serine	102-108	P53	Homo sapiens	95-98
10562558-3	1999	A lysine residue at amino acid position 386 of p53 is required for this previously undescribed modification, strongly suggesting that this lysine residue serves as the major attachment site for SUMO-1.	Lysine	2-8	P53	Homo sapiens	47-50
10562558-3	1999	A lysine residue at amino acid position 386 of p53 is required for this previously undescribed modification, strongly suggesting that this lysine residue serves as the major attachment site for SUMO-1.	Lysine	139-145	P53	Homo sapiens	47-50
10597241-0	1999	p53 accumulation in apoptotic macrophages is an energy demanding process that precedes cytochrome c release in response to nitric oxide.	Nitric Oxide	123-135	P53	Homo sapiens	0-3
10597241-4	1999	S-nitrosoglutathione and spermine-NO caused a fast p53 accumulation, followed by Bcl-xL downregulation, Cyt c release, and caspase activation.	S-Nitrosoglutathione	0-20	P53	Homo sapiens	51-54
10597241-4	1999	S-nitrosoglutathione and spermine-NO caused a fast p53 accumulation, followed by Bcl-xL downregulation, Cyt c release, and caspase activation.	spermine-no	25-36	P53	Homo sapiens	51-54
10597241-11	1999	Moreover, pulse-chase-experiments in combination with the ATP-depletion protocol identified p53 accumulation and stabilization as an energy requiring process.	Adenosine Triphosphate	58-61	P53	Homo sapiens	92-95
10597241-12	1999	This allowed to dissect two ATP-dependent steps, one is in association with Apaf-1 formation, while the other resides in p53 accumulation.	Adenosine Triphosphate	28-31	P53	Homo sapiens	121-124
10597242-3	1999	Thus GM glioblastoma cells carrying an inducible MMTV-driven p53 gene undergo cell cycle arrest and upregulate p21 but not KILLER/DR5 expression upon dexamethasone exposure.	Dexamethasone	150-163	P53	Homo sapiens	61-64
10619896-6	1999	A correlation was found between alcohol intake and p53 expression.	Alcohols	32-39	P53	Homo sapiens	51-54
10544021-5	1999	Activation of p53 was accompanied by phosphorylation of p53 at Ser-15 and elevated p21 and MDM2, both of which were at least partly blocked by wortmannin, a kinase inhibitor against proteins with a PI3 kinase domain.	Serine	63-66	P53	Homo sapiens	14-17
10544021-5	1999	Activation of p53 was accompanied by phosphorylation of p53 at Ser-15 and elevated p21 and MDM2, both of which were at least partly blocked by wortmannin, a kinase inhibitor against proteins with a PI3 kinase domain.	Serine	63-66	P53	Homo sapiens	56-59
10544021-8	1999	This p53 was co-immunoprecipitated with MDM2, but p53 activated by etoposide or doxorubicin barely complexed with MDM2.	Doxorubicin	80-91	P53	Homo sapiens	50-53
10697561-5	1999	The identification of DNA-fragmentation and p53 and Ki-67 genes expression suggest that the mechanism of NADH action is different from disregulation of genes considered as check-points in cell cycle.	NAD	105-109	P53	Homo sapiens	44-47
10697517-0	1999	Effect of paclitaxel pretreatment on radiation-induced p53-dependent apoptosis.	Paclitaxel	10-20	P53	Homo sapiens	55-58
10697517-1	1999	The aim of this study was to investigate the effect of paclitaxel on radiation-induced p53-dependent apoptosis.	Paclitaxel	55-65	P53	Homo sapiens	87-90
10527691-0	1999	Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, c-myc, bcl-XL, NF-kappa B, and p53.	Curcumin	0-8	P53	Homo sapiens	126-129
10697517-9	1999	The present study indicates that p53-dependent apoptosis was frequently induced in the human tumor in vivo by irradiation, but not by paclitaxel alone.	Paclitaxel	134-144	P53	Homo sapiens	33-36
10697522-0	1999	De novo deletions of p53 gene and wild-type p53 correlate with acquired cisplatin-resistance in human osteosarcoma OST cell line.	Cisplatin	72-81	P53	Homo sapiens	21-24
10697522-0	1999	De novo deletions of p53 gene and wild-type p53 correlate with acquired cisplatin-resistance in human osteosarcoma OST cell line.	Cisplatin	72-81	P53	Homo sapiens	44-47
10697522-2	1999	We investigated the relationship between p53 status and the development of resistance to cisplatin in osteosarcoma cell lines.	Cisplatin	89-98	P53	Homo sapiens	41-44
10697522-9	1999	Furthermore, p53 induction was lost in OST/R cells after cisplatin exposure.	Cisplatin	57-66	P53	Homo sapiens	13-16
10697522-10	1999	CONCLUSIONS: De novo deletions of the p53 gene and wild-type p53 were associated with the acquisition of cisplatin-resistance in osteosarcoma.	Cisplatin	105-114	P53	Homo sapiens	38-41
10697522-10	1999	CONCLUSIONS: De novo deletions of the p53 gene and wild-type p53 were associated with the acquisition of cisplatin-resistance in osteosarcoma.	Cisplatin	105-114	P53	Homo sapiens	61-64
10674873-3	1999	Repair of cisplatin-induced DNA damage was reduced in MCF7 cells overexpressing Mdm2, compared to MCF7 cells in which wild-type p53 function was intact.	Cisplatin	10-19	P53	Homo sapiens	128-131
10674873-6	1999	MCF7 cells with intact wild-type p53, on the other hand, arrested primarily in G2/M phase after cisplatin treatment.	Cisplatin	96-105	P53	Homo sapiens	33-36
10674873-7	1999	These findings indicate that Mdm2 overexpression can recapitulate the effect of p53 mutations on DNA repair of cisplatin lesions.	Cisplatin	111-120	P53	Homo sapiens	80-83
10527691-5	1999	Furthermore, curcumin downregulated the expression of survival genes egr-1, c-myc, and bcl-X(L) as well as the tumor suppressor gene p53 in B cells.	Curcumin	13-21	P53	Homo sapiens	133-136
10545114-0	1999	p53 regulates mitochondrial membrane potential through reactive oxygen species and induces cytochrome c-independent apoptosis blocked by Bcl-2.	Reactive Oxygen Species	55-78	P53	Homo sapiens	0-3
10589764-0	1999	TP53 accumulation predicts improved survival in patients resistant to systemic cisplatin-based chemotherapy for muscle-invasive bladder cancer.	Cisplatin	79-88	P53	Homo sapiens	0-4
10545114-8	1999	p53 induced ROS generation, which then caused a transient increase of Deltapsi followed by a decrease.	Reactive Oxygen Species	12-15	P53	Homo sapiens	0-3
10545114-12	1999	Thus, the ROS-mediated disruption of Deltapsi constitutes a pivotal step in the apoptotic pathway of p53, and this pathway does not involve cytochrome c release.	Reactive Oxygen Species	10-13	P53	Homo sapiens	101-104
10626170-4	1999	METHODOLOGY: In a retrospective case-series p53 expression was assessed using standard immunohistochemical methods in the paraffin-embedded specimens of 45 liver resections for colorectal metastases, performed in 43 patients in a single institution between "86 and "96.	Paraffin	122-130	P53	Homo sapiens	44-47
10527623-2	1999	We examined the in vitro effects of CD437 and found that CD437 induces S phase arrest within 24 to 48 h, followed by cell death, in the p53-negative Hep3B and the p53-positive HepG2 human hepatoma cell lines.	CD 437	57-62	P53	Homo sapiens	136-139
10527623-2	1999	We examined the in vitro effects of CD437 and found that CD437 induces S phase arrest within 24 to 48 h, followed by cell death, in the p53-negative Hep3B and the p53-positive HepG2 human hepatoma cell lines.	CD 437	57-62	P53	Homo sapiens	163-166
10518116-8	1999	The expression of the proteins of the protooncogene Bcl-2 and the tumor suppressor gene p53 following staurosporine or retinoic acid treatment was assessed by Western blot and immunocytochemistry.	Tretinoin	119-132	P53	Homo sapiens	88-91
10534572-11	1999	Moreover, up-regulation of p53 and down-regulation of Bcl-2 was observed only in HPAC cells treated with Taxol.	Paclitaxel	105-110	P53	Homo sapiens	27-30
10502297-2	1999	The stable expression of wild-type p53 resulted in a significant increase in sensitivity to the topoisomerase II poisons etoposide and doxorubicin, but not to the topoisomerase II inhibitors razoxane and ADR-529.	Doxorubicin	135-146	P53	Homo sapiens	35-38
10518116-10	1999	The opposite alteration of Bcl-2 (anti-apoptotic) and p53 (apoptotic) contents in SH-SY5Y cells with retinoic acid and staurosporine are attributed to the changes in cell vulnerability.	Tretinoin	101-114	P53	Homo sapiens	54-57
10518116-9	1999	Retinoic acid increased Bcl-2 and decreased p53 levels, whereas staurosporine decreased Bcl-2 and increased p53 levels.	Tretinoin	0-13	P53	Homo sapiens	44-47
10523638-0	1999	An ATP/ADP-dependent molecular switch regulates the stability of p53-DNA complexes.	Adenosine Triphosphate	3-6	P53	Homo sapiens	65-68
10516009-3	1999	Previous studies showed that the EBV-encoded immediate-early transcription factor, Zta, can induce expression of the cyclin-dependent kinase inhibitors, p21 and p27, the tumor suppressor, p53, and cell growth arrest.	zta	83-86	P53	Homo sapiens	188-191
10516009-5	1999	Here we show that substitution of Zta"s basic DNA binding domain with the analogous region of the Zta homologue, c-Fos, abrogates Zta"s ability to induce growth arrest and to induce p21, p27, or p53 expression, suggesting that protein-protein interactions between this region of Zta and key cell cycle control proteins are involved in signaling cell cycle arrest.	zta	34-37	P53	Homo sapiens	195-198
10516009-5	1999	Here we show that substitution of Zta"s basic DNA binding domain with the analogous region of the Zta homologue, c-Fos, abrogates Zta"s ability to induce growth arrest and to induce p21, p27, or p53 expression, suggesting that protein-protein interactions between this region of Zta and key cell cycle control proteins are involved in signaling cell cycle arrest.	zta	98-101	P53	Homo sapiens	195-198
10516009-5	1999	Here we show that substitution of Zta"s basic DNA binding domain with the analogous region of the Zta homologue, c-Fos, abrogates Zta"s ability to induce growth arrest and to induce p21, p27, or p53 expression, suggesting that protein-protein interactions between this region of Zta and key cell cycle control proteins are involved in signaling cell cycle arrest.	zta	98-101	P53	Homo sapiens	195-198
10516009-5	1999	Here we show that substitution of Zta"s basic DNA binding domain with the analogous region of the Zta homologue, c-Fos, abrogates Zta"s ability to induce growth arrest and to induce p21, p27, or p53 expression, suggesting that protein-protein interactions between this region of Zta and key cell cycle control proteins are involved in signaling cell cycle arrest.	zta	98-101	P53	Homo sapiens	195-198
10516009-7	1999	Last, we provide evidence that Zta-mediated inductions of p21, p27, and p53 occur, at least in part, through distinct pathways.	zta	31-34	P53	Homo sapiens	72-75
10523638-0	1999	An ATP/ADP-dependent molecular switch regulates the stability of p53-DNA complexes.	Adenosine Diphosphate	7-10	P53	Homo sapiens	65-68
10531402-0	1999	Modulation of cisplatinum cytotoxicity by p53: effect of p53-mediated apoptosis and DNA repair.	Cisplatin	14-25	P53	Homo sapiens	42-45
10531402-0	1999	Modulation of cisplatinum cytotoxicity by p53: effect of p53-mediated apoptosis and DNA repair.	Cisplatin	14-25	P53	Homo sapiens	57-60
10523638-2	1999	We now show, for the first time, that the interaction of p53 with DNA can be stabilized by small molecules, such as ADP and dADP.	Adenosine Diphosphate	116-119	P53	Homo sapiens	57-60
10523638-3	1999	Our results also indicate an ATP/ADP molecular switch mechanism which determines the off-on states for p53-DNA binding.	Adenosine Triphosphate	29-32	P53	Homo sapiens	103-106
10523638-3	1999	Our results also indicate an ATP/ADP molecular switch mechanism which determines the off-on states for p53-DNA binding.	Adenosine Diphosphate	33-36	P53	Homo sapiens	103-106
10523638-4	1999	This ATP/ADP molecular switch requires dimer-dimer interaction of the p53 tetramer.	Adenosine Triphosphate	5-8	P53	Homo sapiens	70-73
10523638-4	1999	This ATP/ADP molecular switch requires dimer-dimer interaction of the p53 tetramer.	Adenosine Diphosphate	9-12	P53	Homo sapiens	70-73
10523638-5	1999	Dissociation of p53-DNA complexes by ATP is independent of ATP hydrolysis.	Adenosine Triphosphate	37-40	P53	Homo sapiens	16-19
10523638-6	1999	Low-level ATPase activity is nonetheless associated with ATP-p53 interaction and may serve to regenerate ADP-p53, thus recycling the high-affinity DNA binding form of p53.	Adenosine Diphosphate	105-108	P53	Homo sapiens	61-64
10523638-6	1999	Low-level ATPase activity is nonetheless associated with ATP-p53 interaction and may serve to regenerate ADP-p53, thus recycling the high-affinity DNA binding form of p53.	Adenosine Diphosphate	105-108	P53	Homo sapiens	109-112
10523638-6	1999	Low-level ATPase activity is nonetheless associated with ATP-p53 interaction and may serve to regenerate ADP-p53, thus recycling the high-affinity DNA binding form of p53.	Adenosine Diphosphate	105-108	P53	Homo sapiens	109-112
10523638-7	1999	The ATP/ADP regulatory mechanism applies to two distinct types of p53 interaction with DNA, namely, sequence-specific DNA binding (via the core domain of the p53 protein) and binding to sites of DNA damage (via the C-terminal domain).	Adenosine Triphosphate	4-7	P53	Homo sapiens	66-69
10523638-7	1999	The ATP/ADP regulatory mechanism applies to two distinct types of p53 interaction with DNA, namely, sequence-specific DNA binding (via the core domain of the p53 protein) and binding to sites of DNA damage (via the C-terminal domain).	Adenosine Triphosphate	4-7	P53	Homo sapiens	158-161
10523638-7	1999	The ATP/ADP regulatory mechanism applies to two distinct types of p53 interaction with DNA, namely, sequence-specific DNA binding (via the core domain of the p53 protein) and binding to sites of DNA damage (via the C-terminal domain).	Adenosine Diphosphate	8-11	P53	Homo sapiens	66-69
10523638-7	1999	The ATP/ADP regulatory mechanism applies to two distinct types of p53 interaction with DNA, namely, sequence-specific DNA binding (via the core domain of the p53 protein) and binding to sites of DNA damage (via the C-terminal domain).	Adenosine Diphosphate	8-11	P53	Homo sapiens	158-161
10523638-8	1999	Further studies indicate that ADP not only stabilizes p53-DNA complexes but also renders the complexes susceptible to dissociation by specific p53 binding proteins.	Adenosine Diphosphate	30-33	P53	Homo sapiens	54-57
10523638-8	1999	Further studies indicate that ADP not only stabilizes p53-DNA complexes but also renders the complexes susceptible to dissociation by specific p53 binding proteins.	Adenosine Diphosphate	30-33	P53	Homo sapiens	143-146
10523638-9	1999	We propose a model in which the DNA binding functions of p53 are regulated by an ATP/ADP molecular switch, and we suggest that this mechanism may function during the cellular response to DNA damage.	Adenosine Triphosphate	81-84	P53	Homo sapiens	57-60
10523638-9	1999	We propose a model in which the DNA binding functions of p53 are regulated by an ATP/ADP molecular switch, and we suggest that this mechanism may function during the cellular response to DNA damage.	Adenosine Diphosphate	85-88	P53	Homo sapiens	57-60
10531375-4	1999	Cadmium at 10-30 microM impairs the p53 induction in response to DNA-damaging agents such as actinomycin D, methylmethane sulfonate, and hydrogen peroxide.	Hydrogen Peroxide	137-154	P53	Homo sapiens	36-39
10531375-5	1999	Exposure to cadmium at 20 microM also suppresses the p53-dependent cell cycle arrest in G(1) and G(2)/M phases induced by gamma-irradiation.	Cadmium	12-19	P53	Homo sapiens	53-56
10531375-0	1999	Cadmium induces conformational modifications of wild-type p53 and suppresses p53 response to DNA damage in cultured cells.	Cadmium	0-7	P53	Homo sapiens	58-61
10531375-0	1999	Cadmium induces conformational modifications of wild-type p53 and suppresses p53 response to DNA damage in cultured cells.	Cadmium	0-7	P53	Homo sapiens	77-80
10531375-1	1999	The p53 tumor suppressor protein is a transcription factor that binds DNA in a sequence-specific manner through a protein domain stabilized by the coordination of zinc within a tetrahedral cluster of three cysteine residues and one histidine residue.	Cysteine	206-214	P53	Homo sapiens	4-7
10531375-1	1999	The p53 tumor suppressor protein is a transcription factor that binds DNA in a sequence-specific manner through a protein domain stabilized by the coordination of zinc within a tetrahedral cluster of three cysteine residues and one histidine residue.	Histidine	232-241	P53	Homo sapiens	4-7
10531375-3	1999	In human breast cancer MCF7 cells (expressing wild-type p53), exposure to cadmium (5-40 microM) disrupts native (wild-type) p53 conformation, inhibits DNA binding, and down-regulates transcriptional activation of a reporter gene.	Cadmium	74-81	P53	Homo sapiens	56-59
10531375-3	1999	In human breast cancer MCF7 cells (expressing wild-type p53), exposure to cadmium (5-40 microM) disrupts native (wild-type) p53 conformation, inhibits DNA binding, and down-regulates transcriptional activation of a reporter gene.	Cadmium	74-81	P53	Homo sapiens	124-127
10531375-4	1999	Cadmium at 10-30 microM impairs the p53 induction in response to DNA-damaging agents such as actinomycin D, methylmethane sulfonate, and hydrogen peroxide.	Cadmium	0-7	P53	Homo sapiens	36-39
10531375-6	1999	These observations indicate that cadmium at subtoxic levels impairs p53 function by inducing conformational changes in the wild-type protein.	Cadmium	33-40	P53	Homo sapiens	68-71
10529369-1	1999	Overexpression of the tumor suppressor p53 in HeLa cells leads to loss of the estradiol- and genistein-induced human estrogen receptor (ERalpha) transactivity.	Estradiol	78-87	P53	Homo sapiens	39-42
10529369-6	1999	These results may explain how p53 down-regulates the expression of some estrogen-responsive genes such as c-fos, c-jun, TPA, and bcl-2.	Tetradecanoylphorbol Acetate	120-123	P53	Homo sapiens	30-33
10535931-3	1999	Furthermore, treatment of human cells with the S(N)1 DNA methylators N-methyl-N-nitrosourea or N-methyl-N"-nitro-N-nitrosoguanidine results in p53 phosphorylation on serine residues 15 and 392, and these phosphorylation events depend on the presence of functional hMutSalpha and hMutLalpha.	Serine	166-172	P53	Homo sapiens	143-146
10547071-9	1999	The effect of OM on p53 expression seems to be mediated through the extracellular signal-regulated kinase (ERK) pathway, inasmuch as the inhibition of ERK activation with a specific inhibitor (PD98059) to the ERK upstream kinase mitogen/extracellular-regulated protein kinase kinase abrogated the OM inhibitory activity on p53 expression in a dose-dependent manner.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	193-200	P53	Homo sapiens	20-23
10471519-1	1999	Recent studies on paclitaxel (Taxol), a microtubule-stabilizing agent and effective anti-cancer drug, have identified numerous cellular and molecular effects, such as induction of cytokines and tumor-suppressor genes, indirect cytotoxicity due to secretion of tumor necrosis factor, vast activation of signal-transduction pathways and selective activity against cells lacking functional p53.	Paclitaxel	18-28	P53	Homo sapiens	387-390
10471519-1	1999	Recent studies on paclitaxel (Taxol), a microtubule-stabilizing agent and effective anti-cancer drug, have identified numerous cellular and molecular effects, such as induction of cytokines and tumor-suppressor genes, indirect cytotoxicity due to secretion of tumor necrosis factor, vast activation of signal-transduction pathways and selective activity against cells lacking functional p53.	Paclitaxel	30-35	P53	Homo sapiens	387-390
10541367-9	1999	Taxanes are particularly attractive as synergistic agents for RIT because they induce cell cycle arrest in the radiosensitive G2-M phase and p53-independent apoptosis.	Taxoids	0-7	P53	Homo sapiens	141-144
10523857-0	1999	RNA synthesis block by 5, 6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) triggers p53-dependent apoptosis in human colon carcinoma cells.	Dichlororibofuranosylbenzimidazole	23-72	P53	Homo sapiens	88-91
10523857-0	1999	RNA synthesis block by 5, 6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) triggers p53-dependent apoptosis in human colon carcinoma cells.	Dichlororibofuranosylbenzimidazole	74-77	P53	Homo sapiens	88-91
10523857-3	1999	Here we report that 5, 6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), an inhibitor of CDK7 TFIIH-associated kinase, CKI and CKII kinases, blocking RNA polymerase II in the early elongation stage, triggers p53-dependent apoptosis in human colon adenocarcinoma cells in a transcription independent manner.	Dichlororibofuranosylbenzimidazole	20-69	P53	Homo sapiens	212-215
10523857-3	1999	Here we report that 5, 6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), an inhibitor of CDK7 TFIIH-associated kinase, CKI and CKII kinases, blocking RNA polymerase II in the early elongation stage, triggers p53-dependent apoptosis in human colon adenocarcinoma cells in a transcription independent manner.	Dichlororibofuranosylbenzimidazole	71-74	P53	Homo sapiens	212-215
10519395-8	1999	Taken together, these data indicate that vitamin D compounds induce apoptosis via a novel caspase- and p53-independent pathway that can be inhibited by Bcl-2.	Vitamin D	41-50	P53	Homo sapiens	103-106
10547071-9	1999	The effect of OM on p53 expression seems to be mediated through the extracellular signal-regulated kinase (ERK) pathway, inasmuch as the inhibition of ERK activation with a specific inhibitor (PD98059) to the ERK upstream kinase mitogen/extracellular-regulated protein kinase kinase abrogated the OM inhibitory activity on p53 expression in a dose-dependent manner.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	193-200	P53	Homo sapiens	323-326
10547071-10	1999	In addition to OM, we showed that the p53 protein expression in MCF-7 cells was also decreased by phorbol 12-myristate 13-acetate treatment (PMA).	Tetradecanoylphorbol Acetate	98-129	P53	Homo sapiens	38-41
10549596-9	1999	ATM binds to p53 in a complex fashion and activates the molecule in response to breaks in DNA by phosphorylating it at serine 15 close to the N-terminus and by controlling other phosphorylation and dephosphorylation changes on the molecule.	Serine	119-125	P53	Homo sapiens	13-16
10626356-0	1999	Role of p53 in the ability of 1,2-diaminocyclohexane-diacetato-dichloro-Pt(IV) to circumvent cisplatin resistance.	Cisplatin	93-102	P53	Homo sapiens	8-11
10626356-8	1999	The data indicate that cisplatin resistance due to an increase in DNA damage tolerance can arise through a loss of p53 function, and that functional activation of latent wild-type p53 by the analog facilitates cell death and circumvents this resistance mechanism.	Cisplatin	23-32	P53	Homo sapiens	115-118
10550840-6	1999	High levels of p53 expression and DNA-damaging agents like cisplatin (Platinol) and ionizing radiation work synergistically to induce apoptosis in cancer cells.	Cisplatin	59-68	P53	Homo sapiens	15-18
10518106-5	1999	METHODS: p53 expression in formalin-fixed, paraffin-embedded samples of 239 patients with primary esophageal squamous cell carcinoma (TNM stage I:79 cases, stage II: 82 cases, stage III: 78 cases), who underwent esophageal resection without additional treatment, were analyzed by immunohistochemical staining using a polyclonal antibody, RSP53.	Paraffin	43-51	P53	Homo sapiens	9-12
10573131-0	1999	p53 gene status and chemosensitivity of childhood acute lymphoblastic leukemia cells to adriamycin.	Doxorubicin	88-98	P53	Homo sapiens	0-3
10602776-10	1999	Decoy oligonucleotides, but not an unrelated control oligonucleotide, weakened cAMP-evoked protection and re-established a p53 response following NO addition.	Oligonucleotides	6-22	P53	Homo sapiens	123-126
10602776-10	1999	Decoy oligonucleotides, but not an unrelated control oligonucleotide, weakened cAMP-evoked protection and re-established a p53 response following NO addition.	Oligonucleotides	6-21	P53	Homo sapiens	123-126
10550840-6	1999	High levels of p53 expression and DNA-damaging agents like cisplatin (Platinol) and ionizing radiation work synergistically to induce apoptosis in cancer cells.	Cisplatin	70-78	P53	Homo sapiens	15-18
10486243-3	1999	These two bases make contact with cysteine-277 of the human p53.	Cysteine	34-42	P53	Homo sapiens	60-63
10500142-7	1999	Furthermore, purified ATM contains a kinase activity that phosphorylates serine-15 of p53 in a DNA-stimulated manner.	Serine	73-79	P53	Homo sapiens	86-89
10556577-1	1999	Exposure of p53 mutated estrogen-receptor-negative MDA-MB231 human breast tumor cells to a pharmacological concentration of estradiol enhances liposome-mediated uptake and expression of SV-40 luciferase.	Estradiol	124-133	P53	Homo sapiens	12-15
10556577-4	1999	In order to demonstrate that the influence of estradiol on gene uptake and expression is translated into a functional response, the effects of estradiol on the function of an exogenous gene, in this case the apoptotic function of p53, were assessed in the p53 mutated MDA-MB231 breast tumor cell.	Estradiol	46-55	P53	Homo sapiens	230-233
10556577-4	1999	In order to demonstrate that the influence of estradiol on gene uptake and expression is translated into a functional response, the effects of estradiol on the function of an exogenous gene, in this case the apoptotic function of p53, were assessed in the p53 mutated MDA-MB231 breast tumor cell.	Estradiol	143-152	P53	Homo sapiens	230-233
10556577-4	1999	In order to demonstrate that the influence of estradiol on gene uptake and expression is translated into a functional response, the effects of estradiol on the function of an exogenous gene, in this case the apoptotic function of p53, were assessed in the p53 mutated MDA-MB231 breast tumor cell.	Estradiol	143-152	P53	Homo sapiens	256-259
10556577-7	1999	The capacity of estradiol to promote apoptosis in MDA-MB231 cells by a p53-liposome complex is likely to be related to the preferential redistribution of the gene from the cytoplasm to the nucleus which could occur during both the uptake and post-uptake phases.	Estradiol	16-25	P53	Homo sapiens	71-74
10554637-11	1999	Human lymphoblasts with mutated p53 (WTK1, LD50 = 75 microM) were more resistant to paclitaxel than wild type p53 cells (TK6, LD50 = 25 microM).	Paclitaxel	84-94	P53	Homo sapiens	32-35
10449610-0	1999	p53 codon 72 ARG/PRO polymorphism is not related to HPV type or lesion grade in low- and high-grade squamous intra-epithelial lesions and invasive squamous carcinoma of the cervix.	Arginine	13-16	P53	Homo sapiens	0-3
10449610-1	1999	A polymorphism at codon 72 of the p53 gene, resulting in either an arginine or a proline residue in the protein, has been reported to affect the susceptibility of p53 to human papillomavirus (HPV) E6-mediated degradation in cultured cells.	Arginine	67-75	P53	Homo sapiens	34-37
10449610-1	1999	A polymorphism at codon 72 of the p53 gene, resulting in either an arginine or a proline residue in the protein, has been reported to affect the susceptibility of p53 to human papillomavirus (HPV) E6-mediated degradation in cultured cells.	Arginine	67-75	P53	Homo sapiens	163-166
10460757-0	1999	Oxygen induces S-phase growth arrest and increases p53 and p21(WAF1/CIP1) expression in human bronchial smooth-muscle cells.	Oxygen	0-6	P53	Homo sapiens	51-54
10464313-8	1999	We conclude that the irreversibility of p53 oxidation is due, at least in part, to the removal of intrinsic zinc from its position in the DNA binding domain accompanied by a conformational change of the p53 molecule after oxidation of the three cysteines to which the zinc ion is coordinated in the reduced protein.	Cysteine	245-254	P53	Homo sapiens	40-43
10464313-8	1999	We conclude that the irreversibility of p53 oxidation is due, at least in part, to the removal of intrinsic zinc from its position in the DNA binding domain accompanied by a conformational change of the p53 molecule after oxidation of the three cysteines to which the zinc ion is coordinated in the reduced protein.	Cysteine	245-254	P53	Homo sapiens	203-206
10460757-2	1999	Recent studies indicate that oxygen augments the expression of p53 and p21(WAF1/CIP1), and increases apoptotic labeling of airway epithelial cells.	Oxygen	29-35	P53	Homo sapiens	63-66
10460757-4	1999	The present study was conducted to determine whether oxygen alters the expression of p53 and p21(WAF1/CIP1) in human bronchial smooth-muscle cells (BSMC).	Oxygen	53-59	P53	Homo sapiens	85-88
10460757-12	1999	Furthermore, high oxygen levels induce S-phase arrest and increased expression of p53 and p21(WAF1/CIP1).	Oxygen	18-24	P53	Homo sapiens	82-85
10628393-5	1999	In contrast to previous studies showing p53-dependent GML expression, of the 3 cell lines expressing GML mRNA, one had a p53 gene mutation (codon 245: Gly to Cys).	Glycine	151-154	P53	Homo sapiens	121-124
10628393-5	1999	In contrast to previous studies showing p53-dependent GML expression, of the 3 cell lines expressing GML mRNA, one had a p53 gene mutation (codon 245: Gly to Cys).	Cysteine	158-161	P53	Homo sapiens	121-124
10484981-7	1999	In the analyses of tumor tissues from the propositus and his daughter, a P16INK4A codon 94 missense point mutation (GCG-->GAG; Ala-->Glu) was observed with the hereditary TP53 mutation.	Alanine	127-130	P53	Homo sapiens	171-175
10469618-5	1999	It has recently been reported that the extent of p53 dysfunction caused by HPVs depends on the status of a polymorphism at codon 72 of p53, Pro or Arg.	Arginine	147-150	P53	Homo sapiens	49-52
10484981-7	1999	In the analyses of tumor tissues from the propositus and his daughter, a P16INK4A codon 94 missense point mutation (GCG-->GAG; Ala-->Glu) was observed with the hereditary TP53 mutation.	Glutamic Acid	133-136	P53	Homo sapiens	171-175
10485466-5	1999	The mechanism of induction appears to be an increased rate of protein translation because immunoprecipitation analyses demonstrated increased levels of 35S-labeled p53 protein, even after a short 15-min labeling time.	Sulfur-35	152-155	P53	Homo sapiens	164-167
11717960-0	1999	Interaction between gene p53 and oncogene mdm2 in human glandular lung cancer cell line GLC-82.	Glucose	88-91	P53	Homo sapiens	25-28
10487550-1	1999	PURPOSE: To assess the prognostic significance of p53 protein expression in patients with primary epidermoid carcinoma of the anal canal managed by radiation therapy (XRT), 5-fluorouracil (5-FU), and mitomycin C (MMC).	Fluorouracil	173-187	P53	Homo sapiens	50-53
12212278-4	1999	The positive rate of P53 protein were 0%, 33.33% and 75.00% in mild, moderate and severe AHE, respectively.	S-formylglutathione	89-92	P53	Homo sapiens	21-24
10425273-2	1999	A polymorphism at codon 72 of p53 results in translation to either arginine (p53Arg) or proline (p53Pro), and recent study showed that Caucasian women with arginine form of p53 are more susceptible to HPV-associated carcinoma of the cervix.	Arginine	67-75	P53	Homo sapiens	30-33
10425273-2	1999	A polymorphism at codon 72 of p53 results in translation to either arginine (p53Arg) or proline (p53Pro), and recent study showed that Caucasian women with arginine form of p53 are more susceptible to HPV-associated carcinoma of the cervix.	Arginine	67-75	P53	Homo sapiens	77-80
10425273-2	1999	A polymorphism at codon 72 of p53 results in translation to either arginine (p53Arg) or proline (p53Pro), and recent study showed that Caucasian women with arginine form of p53 are more susceptible to HPV-associated carcinoma of the cervix.	Arginine	156-164	P53	Homo sapiens	30-33
10425273-2	1999	A polymorphism at codon 72 of p53 results in translation to either arginine (p53Arg) or proline (p53Pro), and recent study showed that Caucasian women with arginine form of p53 are more susceptible to HPV-associated carcinoma of the cervix.	Arginine	156-164	P53	Homo sapiens	77-80
10427139-5	1999	Sequence analysis of exons 5 through 8 of p53 was performed on subcloned PCR-amplified DNA, extracted from formalin-fixed, paraffin-embedded tumors.	Paraffin	123-131	P53	Homo sapiens	42-45
10487550-1	1999	PURPOSE: To assess the prognostic significance of p53 protein expression in patients with primary epidermoid carcinoma of the anal canal managed by radiation therapy (XRT), 5-fluorouracil (5-FU), and mitomycin C (MMC).	Fluorouracil	189-193	P53	Homo sapiens	50-53
10487550-20	1999	For patients managed with combined XRT, 5-FU, and MMC, percent p53 protein expression is of prognostic value for DFS independent of other clinical factors such as T category, gender, and histology.	Fluorouracil	40-44	P53	Homo sapiens	63-66
12541388-2	1999	METHOD: The SP immunohistochemical method was used to detect the expression of p16, p21 and p53 protein in 116 cases of NPC and 15 cases of non-tumour nasopharyngeal tissue.	TFF2 protein, human	12-14	P53	Homo sapiens	92-95
10469339-4	1999	Nitric oxide treated skin showed significant increases in cells expressing CD3, CD4, CD8, CD68, neutrophil elastase, ICAM-1, VCAM-1, nitrosotyrosine, p53, and apoptotic cells compared with skin treated with ascorbic acid alone.	Nitric Oxide	0-12	P53	Homo sapiens	150-153
10469339-9	1999	Apoptosis, cytotoxicity, and p53 staining were relatively greater after 48 h exposure than after 24 h. These results suggest that nitric oxide is pro-inflammatory and is toxic to DNA, leading to the accumulation of p53 and subsequent apoptosis.	Nitric Oxide	130-142	P53	Homo sapiens	29-32
10469339-9	1999	Apoptosis, cytotoxicity, and p53 staining were relatively greater after 48 h exposure than after 24 h. These results suggest that nitric oxide is pro-inflammatory and is toxic to DNA, leading to the accumulation of p53 and subsequent apoptosis.	Nitric Oxide	130-142	P53	Homo sapiens	215-218
10454534-2	1999	Comparison between normal human foreskin fibroblasts (HFFs) and HFFs in which p53 was eliminated by transduction with human papillomavirus type 16 E6 showed that treatment with adriamycin initiated arrest in G(2) with active cyclin B/CDC2 kinase, regardless of p53 status.	Doxorubicin	177-187	P53	Homo sapiens	78-81
10454534-2	1999	Comparison between normal human foreskin fibroblasts (HFFs) and HFFs in which p53 was eliminated by transduction with human papillomavirus type 16 E6 showed that treatment with adriamycin initiated arrest in G(2) with active cyclin B/CDC2 kinase, regardless of p53 status.	Doxorubicin	177-187	P53	Homo sapiens	261-264
10490814-3	1999	Doxorubicin treatment induced the senescence-like phenotype (SLP) and its associated terminal growth arrest in wild-type HCT116 colon carcinoma cells; this response was strongly decreased but not abolished in HCT116 lines with homozygous knockout of p53 or p21.	Doxorubicin	0-11	P53	Homo sapiens	250-253
10487521-3	1999	To further elucidate the mechanism of growth suppression caused by p53-273L, we used squamous cell carcinoma cell line HSC3 to isolate subclones containing Zn2+-inducible wild-type (wt) p53, p53-175H, and p53-273L.	Zinc	156-160	P53	Homo sapiens	186-189
10487521-3	1999	To further elucidate the mechanism of growth suppression caused by p53-273L, we used squamous cell carcinoma cell line HSC3 to isolate subclones containing Zn2+-inducible wild-type (wt) p53, p53-175H, and p53-273L.	Zinc	156-160	P53	Homo sapiens	186-189
10487521-3	1999	To further elucidate the mechanism of growth suppression caused by p53-273L, we used squamous cell carcinoma cell line HSC3 to isolate subclones containing Zn2+-inducible wild-type (wt) p53, p53-175H, and p53-273L.	Zinc	156-160	P53	Homo sapiens	186-189
10487521-0	1999	Induction of apoptosis by the p53-273L (Arg --&gt; Leu) mutant in HSC3 cells without transactivation of p21Waf1/Cip1/Sdi1 and bax.	Arginine	40-43	P53	Homo sapiens	30-33
10487521-2	1999	We have previously reported that a mutation at codon 273, p53-273L (Arg --&gt; Leu), suppresses cell growth despite its having no p53-specific transactivation activity.	Arginine	68-71	P53	Homo sapiens	58-61
10521575-4	1999	The temporal profile of p53, c-Myc, Bcl-2, Bax expression and caspases activation after glutamate treatment suggest that Bcl-2, c-Myc and caspase-3 play important roles in the excitotoxic neuronal cell death.	Glutamic Acid	88-97	P53	Homo sapiens	24-27
10467415-5	1999	Apoptosis induced by doxorubicin was suppressed in LCLs retrovirally transduced with the Human Papillomavirus 16 E6 oncoprotein, consistent with the hypothesis that this is a p53-dependent process.	Doxorubicin	21-32	P53	Homo sapiens	175-178
10446162-2	1999	It has recently been shown that BPDE preferentially modifies the guanine in methylated 5"-CpG-3" sequences in the human p53 gene, providing one explanation for why these sites are mutational hot spots.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	32-36	P53	Homo sapiens	120-123
10467415-7	1999	Similar changes in the expression of apoptosis-effector genes, p53, and p53-responsive genes p21Cip1/WAF-1/Sid1 (p21), gadd45, bcl-2 and bax were observed in normal and XPD LCLs after treatment with doxorubicin, indicating that delayed apoptosis was not a consequence of defective transcription of these genes.	Doxorubicin	199-210	P53	Homo sapiens	72-75
10424768-6	1999	FUra exposure resulted in transient induction of p53 and p21, which returned to basal levels 24 hr after drug removal.	Fluorouracil	0-4	P53	Homo sapiens	49-52
10432310-0	1999	Novel phosphorylation sites of human tumour suppressor protein p53 at Ser20 and Thr18 that disrupt the binding of mdm2 (mouse double minute 2) protein are modified in human cancers.	UNII-PYZ33YLR8A	80-85	P53	Homo sapiens	63-66
10432310-1	1999	The ability to separate the isoforms of human tumour suppressor protein p53 expressed in insect cells using heparin-Sepharose correlates with differences in the isoelectric point of p53, demonstrating that p53 can be heterogeneously modified and providing support for the use of insect cells as a model system for identifying novel signalling pathways that target p53.	Heparin	108-115	P53	Homo sapiens	72-75
10432310-1	1999	The ability to separate the isoforms of human tumour suppressor protein p53 expressed in insect cells using heparin-Sepharose correlates with differences in the isoelectric point of p53, demonstrating that p53 can be heterogeneously modified and providing support for the use of insect cells as a model system for identifying novel signalling pathways that target p53.	Heparin	108-115	P53	Homo sapiens	182-185
10432310-1	1999	The ability to separate the isoforms of human tumour suppressor protein p53 expressed in insect cells using heparin-Sepharose correlates with differences in the isoelectric point of p53, demonstrating that p53 can be heterogeneously modified and providing support for the use of insect cells as a model system for identifying novel signalling pathways that target p53.	Heparin	108-115	P53	Homo sapiens	182-185
10432310-1	1999	The ability to separate the isoforms of human tumour suppressor protein p53 expressed in insect cells using heparin-Sepharose correlates with differences in the isoelectric point of p53, demonstrating that p53 can be heterogeneously modified and providing support for the use of insect cells as a model system for identifying novel signalling pathways that target p53.	Heparin	108-115	P53	Homo sapiens	182-185
10432310-3	1999	A synthetic peptide from the N-terminal domain of p53 containing phosphate at Ser(20) inhibited DO-1 binding, thus identifying the phosphorylation site responsible for DO-1 epitope masking.	Phosphates	65-74	P53	Homo sapiens	50-53
10432310-3	1999	A synthetic peptide from the N-terminal domain of p53 containing phosphate at Ser(20) inhibited DO-1 binding, thus identifying the phosphorylation site responsible for DO-1 epitope masking.	Serine	78-81	P53	Homo sapiens	50-53
10432310-5	1999	A monoclonal antibody highly specific for phospho-Ser(20) detected significant phosphorylation of human p53 expressed in insect cells, whereas the relative proportion of p53 modified at Thr(18) was substantially lower.	Serine	50-53	P53	Homo sapiens	104-107
10432310-5	1999	A monoclonal antibody highly specific for phospho-Ser(20) detected significant phosphorylation of human p53 expressed in insect cells, whereas the relative proportion of p53 modified at Thr(18) was substantially lower.	Threonine	186-189	P53	Homo sapiens	170-173
10432310-6	1999	The relevance of these two novel phosphorylation sites to p53 regulation in human cells was made evident by the extensive phosphorylation of human p53 at Thr(18) and Ser(20) in a panel of human breast cancers with a wild-type p53 status.	Threonine	154-157	P53	Homo sapiens	58-61
10432310-6	1999	The relevance of these two novel phosphorylation sites to p53 regulation in human cells was made evident by the extensive phosphorylation of human p53 at Thr(18) and Ser(20) in a panel of human breast cancers with a wild-type p53 status.	Threonine	154-157	P53	Homo sapiens	147-150
10432310-6	1999	The relevance of these two novel phosphorylation sites to p53 regulation in human cells was made evident by the extensive phosphorylation of human p53 at Thr(18) and Ser(20) in a panel of human breast cancers with a wild-type p53 status.	Threonine	154-157	P53	Homo sapiens	147-150
10432310-6	1999	The relevance of these two novel phosphorylation sites to p53 regulation in human cells was made evident by the extensive phosphorylation of human p53 at Thr(18) and Ser(20) in a panel of human breast cancers with a wild-type p53 status.	Serine	166-169	P53	Homo sapiens	58-61
10432310-8	1999	These results provide evidence in vivo for two novel phosphorylation sites within p53 at Ser(20) and Thr(18) that can affect p53 protein-protein interactions and indicate that some human cancers might have amplified one or more Ser(20) and Thr(18) kinase signalling cascades to modulate p53 activity.	Serine	89-92	P53	Homo sapiens	82-85
10432310-8	1999	These results provide evidence in vivo for two novel phosphorylation sites within p53 at Ser(20) and Thr(18) that can affect p53 protein-protein interactions and indicate that some human cancers might have amplified one or more Ser(20) and Thr(18) kinase signalling cascades to modulate p53 activity.	Serine	89-92	P53	Homo sapiens	125-128
10432310-8	1999	These results provide evidence in vivo for two novel phosphorylation sites within p53 at Ser(20) and Thr(18) that can affect p53 protein-protein interactions and indicate that some human cancers might have amplified one or more Ser(20) and Thr(18) kinase signalling cascades to modulate p53 activity.	Serine	89-92	P53	Homo sapiens	125-128
10432310-8	1999	These results provide evidence in vivo for two novel phosphorylation sites within p53 at Ser(20) and Thr(18) that can affect p53 protein-protein interactions and indicate that some human cancers might have amplified one or more Ser(20) and Thr(18) kinase signalling cascades to modulate p53 activity.	Threonine	101-104	P53	Homo sapiens	125-128
10432310-8	1999	These results provide evidence in vivo for two novel phosphorylation sites within p53 at Ser(20) and Thr(18) that can affect p53 protein-protein interactions and indicate that some human cancers might have amplified one or more Ser(20) and Thr(18) kinase signalling cascades to modulate p53 activity.	Threonine	101-104	P53	Homo sapiens	125-128
10432310-8	1999	These results provide evidence in vivo for two novel phosphorylation sites within p53 at Ser(20) and Thr(18) that can affect p53 protein-protein interactions and indicate that some human cancers might have amplified one or more Ser(20) and Thr(18) kinase signalling cascades to modulate p53 activity.	Serine	228-231	P53	Homo sapiens	82-85
10432310-8	1999	These results provide evidence in vivo for two novel phosphorylation sites within p53 at Ser(20) and Thr(18) that can affect p53 protein-protein interactions and indicate that some human cancers might have amplified one or more Ser(20) and Thr(18) kinase signalling cascades to modulate p53 activity.	Serine	228-231	P53	Homo sapiens	125-128
10432310-8	1999	These results provide evidence in vivo for two novel phosphorylation sites within p53 at Ser(20) and Thr(18) that can affect p53 protein-protein interactions and indicate that some human cancers might have amplified one or more Ser(20) and Thr(18) kinase signalling cascades to modulate p53 activity.	Serine	228-231	P53	Homo sapiens	125-128
10432310-8	1999	These results provide evidence in vivo for two novel phosphorylation sites within p53 at Ser(20) and Thr(18) that can affect p53 protein-protein interactions and indicate that some human cancers might have amplified one or more Ser(20) and Thr(18) kinase signalling cascades to modulate p53 activity.	Threonine	240-243	P53	Homo sapiens	82-85
10432310-8	1999	These results provide evidence in vivo for two novel phosphorylation sites within p53 at Ser(20) and Thr(18) that can affect p53 protein-protein interactions and indicate that some human cancers might have amplified one or more Ser(20) and Thr(18) kinase signalling cascades to modulate p53 activity.	Threonine	240-243	P53	Homo sapiens	125-128
10432310-8	1999	These results provide evidence in vivo for two novel phosphorylation sites within p53 at Ser(20) and Thr(18) that can affect p53 protein-protein interactions and indicate that some human cancers might have amplified one or more Ser(20) and Thr(18) kinase signalling cascades to modulate p53 activity.	Threonine	240-243	P53	Homo sapiens	125-128
10425175-0	1999	Inhibition of mutant p53 phosphorylation at serine 15 or serine 315 partially restores the function of wild-type p53.	Serine	44-50	P53	Homo sapiens	21-24
10425175-0	1999	Inhibition of mutant p53 phosphorylation at serine 15 or serine 315 partially restores the function of wild-type p53.	Serine	44-50	P53	Homo sapiens	113-116
10425175-0	1999	Inhibition of mutant p53 phosphorylation at serine 15 or serine 315 partially restores the function of wild-type p53.	Serine	57-63	P53	Homo sapiens	113-116
10468305-1	1999	Homozygous arginine at codon 72 (HA72) of p53 was found in 22% of normal cervices and 30.0% of cervical cancers and no significant difference was detected between normal and cervical cancer with or without HPV 16/18.	Arginine	11-19	P53	Homo sapiens	42-45
10471039-0	1999	A novel charged trinuclear platinum complex effective against cisplatin-resistant tumours: hypersensitivity of p53-mutant human tumour xenografts.	Platinum	27-35	P53	Homo sapiens	111-114
10471039-0	1999	A novel charged trinuclear platinum complex effective against cisplatin-resistant tumours: hypersensitivity of p53-mutant human tumour xenografts.	Cisplatin	62-71	P53	Homo sapiens	111-114
10471039-8	1999	The results showed that the transfer of functional p53 resulted in a marked (tenfold) reduction of cellular chemosensitivity to the multinuclear platinum complex but in a moderate sensitization to cisplatin.	Platinum	145-153	P53	Homo sapiens	51-54
10471039-8	1999	The results showed that the transfer of functional p53 resulted in a marked (tenfold) reduction of cellular chemosensitivity to the multinuclear platinum complex but in a moderate sensitization to cisplatin.	Cisplatin	197-206	P53	Homo sapiens	51-54
10441517-6	1999	Our results suggest a possible connection between p53-dependent apoptosis and the production of reactive oxygen species.	Reactive Oxygen Species	96-119	P53	Homo sapiens	50-53
10459542-6	1999	P53 mutations were analyzed on DNA extracted from paraffin-embedded specimens with use of single strand conformation polymorphism, followed by direct sequencing.	Paraffin	50-58	P53	Homo sapiens	0-3
10430944-13	1999	We provide evidence that Zta up-regulation of p53 leads to p53-mediated interference with JAK/STAT activation of Qp.	zta	25-28	P53	Homo sapiens	46-49
10430944-13	1999	We provide evidence that Zta up-regulation of p53 leads to p53-mediated interference with JAK/STAT activation of Qp.	zta	25-28	P53	Homo sapiens	59-62
10446979-0	1999	DNA damage increases sensitivity to vinca alkaloids and decreases sensitivity to taxanes through p53-dependent repression of microtubule-associated protein 4.	Taxoids	81-88	P53	Homo sapiens	97-100
10446957-8	1999	As a result, we detected enhanced phosphorylation of p53 Ser-18, which corresponds to Ser-15 of human p53, and significant expression of p21 and mdm2 following ionizing radiation.	Serine	57-60	P53	Homo sapiens	53-56
10446957-8	1999	As a result, we detected enhanced phosphorylation of p53 Ser-18, which corresponds to Ser-15 of human p53, and significant expression of p21 and mdm2 following ionizing radiation.	Serine	57-60	P53	Homo sapiens	102-105
10446979-6	1999	Increased expression of MAP4, which occurs when p53 is transcriptionally inactive, increases microtubule polymerization, paclitaxel binding, and sensitivity to paclitaxel, a drug that stabilizes polymerized microtubules.	Paclitaxel	160-170	P53	Homo sapiens	48-51
10446957-8	1999	As a result, we detected enhanced phosphorylation of p53 Ser-18, which corresponds to Ser-15 of human p53, and significant expression of p21 and mdm2 following ionizing radiation.	Serine	86-89	P53	Homo sapiens	53-56
10424768-7	1999	p53 and p21 protein content also increased markedly during paclitaxel exposure, accompanied by phosphorylation of Bcl-2.	Paclitaxel	59-69	P53	Homo sapiens	0-3
10446957-8	1999	As a result, we detected enhanced phosphorylation of p53 Ser-18, which corresponds to Ser-15 of human p53, and significant expression of p21 and mdm2 following ionizing radiation.	Serine	86-89	P53	Homo sapiens	102-105
10446979-9	1999	UV irradiation, bleomycin, and doxorubicin increased wild-type p53 expression and decreased MAP4 expression.	Doxorubicin	31-42	P53	Homo sapiens	63-66
10615232-1	1999	This retrospective study of ovarian cancer aimed to elucidate whether expression of apoptosis-related proteins, bcl-2, p53 or MDM-2, is associated with resistance to chemotherapy, especially cisplatin (CDDP) based chemotherapy.	Cisplatin	191-200	P53	Homo sapiens	119-122
10446993-2	1999	Moderate doses of doxorubicin induced this senescence-like phenotype (SLP) in 11 of 14 tested cell lines derived from different types of human solid tumors, including all of the lines with wild-type p53 and half of p53-mutated cell lines.	Doxorubicin	18-29	P53	Homo sapiens	199-202
10446993-2	1999	Moderate doses of doxorubicin induced this senescence-like phenotype (SLP) in 11 of 14 tested cell lines derived from different types of human solid tumors, including all of the lines with wild-type p53 and half of p53-mutated cell lines.	Doxorubicin	18-29	P53	Homo sapiens	215-218
10430607-4	1999	In contrast, p53 disruption rendered cells strikingly resistant to the effects of the antimetabolite 5-fluorouracil (5-FU), the mainstay of adjuvant therapy for colorectal cancer.	Fluorouracil	101-115	P53	Homo sapiens	13-16
10454440-13	1999	Overall, these data first demonstrated that the antioncogenes p53 and Rb negatively regulated the cell cycle in VSMC, suggesting that the modulation of their activity may mediate VSMC growth such as that in restenosis and atherosclerosis.	vsmc	112-116	P53	Homo sapiens	62-65
10543370-5	1999	Activation of protein kinase C by phorbol 12-myristate 13-acetate produced an almost complete inhibition of p53-independent apoptosis following irradiation, whereas no significant effect was observed on the rate of p53-induced apoptosis.	Tetradecanoylphorbol Acetate	34-65	P53	Homo sapiens	108-111
10543370-6	1999	Although phorbol 12-myristate 13-acetate strongly induced p21 and stabilised p53 in the resting transfected Jurkat cells, neither apoptosis nor cell arrest was observed.	Tetradecanoylphorbol Acetate	9-40	P53	Homo sapiens	77-80
10500967-6	1999	Urothelial cancers harboring p53 aberration may be resistant to cisplatin-based chemotherapy because of impairment of apoptosis induction.	Cisplatin	64-73	P53	Homo sapiens	29-32
10430607-4	1999	In contrast, p53 disruption rendered cells strikingly resistant to the effects of the antimetabolite 5-fluorouracil (5-FU), the mainstay of adjuvant therapy for colorectal cancer.	Fluorouracil	117-121	P53	Homo sapiens	13-16
10604188-0	1999	Metal ions as regulators of the conformation and function of the tumour suppressor protein p53: implications for carcinogenesis.	Metals	0-5	P53	Homo sapiens	91-94
10465111-5	1999	Furthermore, three missense mutations (V92M) and two silent mutations (CGA (Arg) to CGG (Arg), codon 213, exon 6) were found in the MC1R and p53 genes, respectively.	Arginine	76-79	P53	Homo sapiens	141-144
10465111-5	1999	Furthermore, three missense mutations (V92M) and two silent mutations (CGA (Arg) to CGG (Arg), codon 213, exon 6) were found in the MC1R and p53 genes, respectively.	Arginine	89-92	P53	Homo sapiens	141-144
10604188-3	1999	The p53 protein is a metal-binding transcription factor that is inactivated by metal chelation and by oxidation in vitro.	Metals	21-26	P53	Homo sapiens	4-7
10604188-3	1999	The p53 protein is a metal-binding transcription factor that is inactivated by metal chelation and by oxidation in vitro.	Metals	79-84	P53	Homo sapiens	4-7
10604188-4	1999	In intact cells, p53 protein activity is crucially dependent on the availability of Zn ions and is impaired by exposure to Cd, a metal which readily substitutes for Zn in a number of transcription factors.	Zinc	84-86	P53	Homo sapiens	17-20
10604188-4	1999	In intact cells, p53 protein activity is crucially dependent on the availability of Zn ions and is impaired by exposure to Cd, a metal which readily substitutes for Zn in a number of transcription factors.	Cadmium	123-125	P53	Homo sapiens	17-20
10604188-4	1999	In intact cells, p53 protein activity is crucially dependent on the availability of Zn ions and is impaired by exposure to Cd, a metal which readily substitutes for Zn in a number of transcription factors.	Metals	129-134	P53	Homo sapiens	17-20
10604188-4	1999	In intact cells, p53 protein activity is crucially dependent on the availability of Zn ions and is impaired by exposure to Cd, a metal which readily substitutes for Zn in a number of transcription factors.	Zinc	165-167	P53	Homo sapiens	17-20
10604188-5	1999	Inactivation by Cd suppresses the p53-dependent responses to DNA damage.	Cadmium	16-18	P53	Homo sapiens	34-37
10604188-6	1999	Overall, these findings indicate that regulation by metals plays an important role in the control of p53, and that perturbation of this control may explain the carcinogenic potential of several metal compounds.	Metals	52-57	P53	Homo sapiens	101-104
10421546-0	1999	Paclitaxel sensitivity correlates with p53 status and DNA fragmentation, but not G2/M accumulation.	Paclitaxel	0-10	P53	Homo sapiens	39-42
10421546-3	1999	Although initial studies demonstrated that various DNA-damaging agents can induce p53, more recent studies have also shown p53 induction following nonDNA-damaging agents, including paclitaxel.	Paclitaxel	181-191	P53	Homo sapiens	123-126
10421546-10	1999	RESULTS: A 4-fold increase in paclitaxel sensitivity was observed among RKO cells deficient in p53 function compared with wild-type RKO cells (IC 50: 4 nM, 1 nM, 1nM for RKO, RKO.p53.13, RC 10.3, respectively).	Paclitaxel	30-40	P53	Homo sapiens	95-98
10421546-10	1999	RESULTS: A 4-fold increase in paclitaxel sensitivity was observed among RKO cells deficient in p53 function compared with wild-type RKO cells (IC 50: 4 nM, 1 nM, 1nM for RKO, RKO.p53.13, RC 10.3, respectively).	Paclitaxel	30-40	P53	Homo sapiens	179-182
10517975-8	1999	For example, exposure to ultraviolet light is correlated with transition mutations at dipyrimidine sites; aflatoxin B(1) exposure is correlated with a G:C to T:A transversion that leads to a serine substitution at residue 249 of p53 in hepatocellular carcinoma; and exposure to cigarette smoke is correlated with G:C to T:A transversions in lung carcinoma.	Serine	191-197	P53	Homo sapiens	229-232
10421546-11	1999	The increased cytotoxic effect in RKO cells with inactive p53 correlated with an increased propensity towards micronucleation and DNA fragmentation following paclitaxel treatment.	Paclitaxel	158-168	P53	Homo sapiens	58-61
10421546-13	1999	CONCLUSIONS: RKO cells lacking functional p53 demonstrate significantly enhanced sensitivity to paclitaxel compared with that of wild-type RKO cells.	Paclitaxel	96-106	P53	Homo sapiens	42-45
10413457-4	1999	PP5 has no apparent effect on the binding of hormone to the GR, and dexamethasone-mediated growth arrest correlates with an increase in p53 phosphorylation.	Dexamethasone	68-81	P53	Homo sapiens	136-139
10421546-15	1999	Although previous published reports of enhanced paclitaxel sensitivity in p53-deficient cells correlated this finding with increased G2/M arrest, we did not observe any significant correlation between paclitaxel-induced cell kill and the degree of mitotic arrest.	Paclitaxel	48-58	P53	Homo sapiens	74-77
10393722-14	1999	IMPLICATIONS: 4-HPR may form the basis for a novel, p53-independent chemotherapy that operates through increased intracellular levels of ceramide and that retains cytotoxicity under reduced oxygen conditions.	Oxygen	190-196	P53	Homo sapiens	52-55
10391892-2	1999	Accumulation of p53 and induction of apoptosis in RAW 264.7 macrophages in response to nitric oxide are well established.	Nitric Oxide	87-99	P53	Homo sapiens	16-19
10391892-3	1999	However, the molecular mechanisms involved in nitric oxide-induced p53 accumulation are unknown.	Nitric Oxide	46-58	P53	Homo sapiens	67-70
10391892-6	1999	Moreover, chemically diverse nitric oxide donors interfere with proteasome-mediated degradation of polyubiquitinated p53 in vitro.	Nitric Oxide	29-41	P53	Homo sapiens	117-120
10391892-7	1999	These data imply that nitric oxide-induced apoptosis and accumulation of p53 are, at least in part, mediated by inhibition of the proteasome.	Nitric Oxide	22-34	P53	Homo sapiens	73-76
10629648-5	1999	Mutant p53 protein IHC overexpression was examined from paraffin embedded tissues using monoclonal DO-7 Ab.	Paraffin	56-64	P53	Homo sapiens	7-10
10435622-2	1999	DNA damage-induced phosphorylation of p53 occurs at serine-15 in vivo.	Serine	52-58	P53	Homo sapiens	38-41
10435622-3	1999	Phosphorylation of p53 at serine-15 leads to a stabilization of the polypeptide by inhibiting its interaction with Mdm2, a protein that targets p53 for ubiquitin-dependent degradation.	Serine	26-32	P53	Homo sapiens	19-22
10435622-3	1999	Phosphorylation of p53 at serine-15 leads to a stabilization of the polypeptide by inhibiting its interaction with Mdm2, a protein that targets p53 for ubiquitin-dependent degradation.	Serine	26-32	P53	Homo sapiens	144-147
10435622-5	1999	Here, we report the identification of a novel DNA-activated protein kinase that phosphorylates p53 on serine-15.	Serine	102-108	P53	Homo sapiens	95-98
10435622-7	1999	Immunoprecipitation studies of recombinant ATR reveal that catalytic activity of this polypeptide is required for DNA-stimulated phosphorylation of p53 on serine-15.	Serine	155-161	P53	Homo sapiens	148-151
10397271-0	1999	Nitric oxide is an initiator of intercellular signal transduction for stress response after hyperthermia in mutant p53 cells of human glioblastoma.	Nitric Oxide	0-12	P53	Homo sapiens	115-118
10397271-2	1999	Recently, it was suggested that nitric oxide is involved in p53-dependent response to many kinds of stress, such as heat shock and changes in cellular metabolism.	Nitric Oxide	32-44	P53	Homo sapiens	60-63
10437915-0	1999	Emergence of p53 mutant cisplatin-resistant ovarian carcinoma cells following drug exposure: spontaneously mutant selection.	Cisplatin	24-33	P53	Homo sapiens	13-16
10397271-7	1999	In addition, the accumulation of hsp72 and p53 in the wtp53 cells was induced by the administration of an nitric oxide-generating agent, S-nitroso-N-acetylpenicillamine, to the medium.	Nitric Oxide	106-118	P53	Homo sapiens	43-46
10437915-1	1999	We have previously shown that p53 mutations are associated with cisplatin resistance in ovarian carcinoma IGROV-1/Pt 1 cells.	Cisplatin	64-73	P53	Homo sapiens	30-33
10397271-9	1999	Our finding of the accumulation of hsp72 and p53 in nitric oxide-recipient cells cocultivated with heated nitric oxide-donor cells provides the first evidence for an intercellular signal transduction pathway via nitric oxide as intermediate without cell-to-cell interactions such as gap junctions.	Nitric Oxide	52-64	P53	Homo sapiens	45-48
10437915-10	1999	This is the first observation that indicates that a subpopulation of p53 mutant cells can occasionally be selected by cisplatin treatment.	Cisplatin	118-127	P53	Homo sapiens	69-72
10483067-2	1999	MATERIALS AND METHODS: The expression of p53 and MDM2 proteins was determined immunohistochemically in 51 formalin-fixed, paraffin embedded specimens of odontogenic cysts and tumours.	Paraffin	122-130	P53	Homo sapiens	41-44
17883223-4	1999	A new model incorporating cell-specific parameters is proposed here to quantify the survival advantage of mutant or null p53 cells over their wild-type counterparts at any level of oxygen deprivation.	Oxygen	181-187	P53	Homo sapiens	121-124
10381403-11	1999	The results explain the enhanced reaction of BPDE at m5CpG in DNA and the origin of G-T mutational hotspots in the p53 gene in cancer.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	45-49	P53	Homo sapiens	115-118
10389868-7	1999	Furthermore, significant statistical differences in chemosensitivity to 5-fluorouracil and CDDP were revealed depending on the presence of serum p53 antibodies.	Fluorouracil	72-86	P53	Homo sapiens	145-148
10377423-3	1999	p53 mutations were either detected by using both techniques or, if only detected by one technique, were confirmed by using mutation-specific oligonucleotide hybridization.	Oligonucleotides	141-156	P53	Homo sapiens	0-3
10383145-7	1999	Mitogen activation further suppressed cisplatin-induced p53 expression, and the inhibition was mainly dependent on the Ca2+ pathway.	Cisplatin	38-47	P53	Homo sapiens	56-59
10383157-5	1999	In addition, Hsp90 family chaperone-associated proteins, such as p185erbB2, Raf-1, cyclin-dependent kinase 4, and mutant p53, were depleted by KF25706 at a dose comparable to that required for antiproliferative activity.	KF 25706	143-150	P53	Homo sapiens	121-124
10358069-1	1999	Phosphorylation at serine 15 of the human p53 tumor suppressor protein is induced by DNA damage and correlates with accumulation of p53 and its activation as a transcription factor.	Serine	19-25	P53	Homo sapiens	42-45
10358069-1	1999	Phosphorylation at serine 15 of the human p53 tumor suppressor protein is induced by DNA damage and correlates with accumulation of p53 and its activation as a transcription factor.	Serine	19-25	P53	Homo sapiens	132-135
10358069-2	1999	The DNA-dependent protein kinase (DNA-PK) can phosphorylate serine 15 of human p53 and the homologous serine 18 of murine p53 in vitro.	Serine	60-66	P53	Homo sapiens	79-82
10420846-6	1999	Treatment of HepG2 cells with p53-specific antisense oligonucleotide could effectively block the antiapoptotic effect of thermal stress on UVC-induced apoptosis and increase of intracellular wild-type p53 protein by transfecting wtp53 expression plasmid into Hep3B cells yielded more resistance to UVC irradiation after prior thermal stress exposure.	Oligonucleotides	53-68	P53	Homo sapiens	30-33
10420846-6	1999	Treatment of HepG2 cells with p53-specific antisense oligonucleotide could effectively block the antiapoptotic effect of thermal stress on UVC-induced apoptosis and increase of intracellular wild-type p53 protein by transfecting wtp53 expression plasmid into Hep3B cells yielded more resistance to UVC irradiation after prior thermal stress exposure.	Oligonucleotides	53-68	P53	Homo sapiens	201-204
10405166-5	1999	Apoptosis induced by PTP-S2 in MCF7 cells was inhibited by cotransfection with mutant p53 (Arg-273 --&gt; His) but not by wild type p53.	Arginine	91-94	P53	Homo sapiens	86-89
10364268-0	1999	Retinoic acid confers resistance to p53-dependent apoptosis in SH-SY5Y neuroblastoma cells by modulating nuclear import of p53.	Tretinoin	0-13	P53	Homo sapiens	36-39
10364268-0	1999	Retinoic acid confers resistance to p53-dependent apoptosis in SH-SY5Y neuroblastoma cells by modulating nuclear import of p53.	Tretinoin	0-13	P53	Homo sapiens	123-126
10364268-3	1999	We examine here the possible contribution of the p53 pathway to the chemoresistance response associated with the RA treatment in NB cells.	Tretinoin	113-115	P53	Homo sapiens	49-52
10364268-4	1999	Upon treatment with RA (1-10 microM) for 4 days, the human NB cells, SH-SY5Y, developed resistance selectively to p53-dependent apoptotic stimuli including gamma-irradiation, etoposide, and 1-(5-isoquinolinyl sulfonyl)-2-methylpiperazine (H-7).	Tretinoin	20-22	P53	Homo sapiens	114-117
10364268-5	1999	Interestingly, RA affected the ability of H-7 to induce nuclear accumulation of the p53 protein without altering its effect on elevating the steady-state level of p53, suggesting that drug-induced up-regulation and nuclear accumulation of the wild-type p53 protein are separable processes.	Tretinoin	15-17	P53	Homo sapiens	84-87
10364268-6	1999	The modulation of nuclear import of p53 protein by RA may thus represent a potential mechanism by which certain tumor cells with the wild-type p53 gene develop resistance to chemotherapeutic agents.	Tretinoin	51-53	P53	Homo sapiens	36-39
10364268-6	1999	The modulation of nuclear import of p53 protein by RA may thus represent a potential mechanism by which certain tumor cells with the wild-type p53 gene develop resistance to chemotherapeutic agents.	Tretinoin	51-53	P53	Homo sapiens	143-146
10359739-5	1999	Both H2O2- and O2--induced apoptosis of cardiomyocytes were associated with an increase in p53 protein content, whereas protein levels of Bax and Bcl-2 were unaltered.	Hydrogen Peroxide	5-9	P53	Homo sapiens	91-94
10359739-5	1999	Both H2O2- and O2--induced apoptosis of cardiomyocytes were associated with an increase in p53 protein content, whereas protein levels of Bax and Bcl-2 were unaltered.	Superoxides	7-9	P53	Homo sapiens	91-94
10357792-0	1999	Use of UvrABC nuclease to quantify benzo[a]pyrene diol epoxide-DNA adduct formation at methylated versus unmethylated CpG sites in the p53 gene.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	35-62	P53	Homo sapiens	135-138
10339661-4	1999	However, the sensitivity to radiation was significantly improved by the transduction and T.Tn/p53 cells became markedly susceptible to cisplatin and etoposide compared with parental cells.	Cisplatin	135-144	P53	Homo sapiens	94-97
10336521-3	1999	BA-induced apoptosis requires new protein, but not RNA, synthesis, is independent of p53, and results in p21 protein accumulation in the absence of a cell cycle arrest.	betulinic acid	0-2	P53	Homo sapiens	85-88
10389868-7	1999	Furthermore, significant statistical differences in chemosensitivity to 5-fluorouracil and CDDP were revealed depending on the presence of serum p53 antibodies.	Cisplatin	91-95	P53	Homo sapiens	145-148
10469393-8	1999	The number of p21-positive H &amp; RS cells was significantly related with that of the p53-positive cells.	Adenosine Monophosphate	30-33	P53	Homo sapiens	87-90
10347252-7	1999	Overexpression of p21(waf1) in SaOs-2 cells lacking both p53 and functional retinoblastoma protein may decrease the G2-M arrest induced by paclitaxel due to suppression of the S-G2 checkpoint, resulting in a decreased apoptotic response of cells to paclitaxel.	Paclitaxel	139-149	P53	Homo sapiens	57-60
10359526-0	1999	Mutations in serines 15 and 20 of human p53 impair its apoptotic activity.	Serine	13-20	P53	Homo sapiens	40-43
10403664-0	1999	Methyl methanesulfonate and hydrogen peroxide differentially regulate p53 accumulation in hepatoblastoma cells.	Hydrogen Peroxide	28-45	P53	Homo sapiens	70-73
10403664-5	1999	At non-lethal doses, both H2O2 and MMS induced high level of p53 protein accumulation.	Hydrogen Peroxide	26-30	P53	Homo sapiens	61-64
10403664-6	1999	Nevertheless, while the amount of p53 protein increased with the dose of MMS and the occurrence of apoptotic cell death events, H2O2 doses that induce cell apoptosis attenuated the p53 protein accumulation level.	Hydrogen Peroxide	128-132	P53	Homo sapiens	181-184
12548778-4	1999	In RA-sensitive cell lines, ATRA-induced G0/G1 arrest is associated with down regulaton of c-myc and hyperphosphorylated Rb expression, and up regulation of p21WAF1/CIP1 and p53 expression.	Tretinoin	28-32	P53	Homo sapiens	174-177
10359526-4	1999	This mutational analysis comprised serine residues located at positions 6, 9, 15, 20, 33 and 37 of human p53.	Serine	35-41	P53	Homo sapiens	105-108
10359526-6	1999	However, the ability of p53 to induce apoptosis was impaired by specific serine substitutions.	Serine	73-79	P53	Homo sapiens	24-27
10359526-7	1999	Mutations in all six N-terminal serines together reduced the apoptotic activity of p53 in H1299 cells by 50%.	Serine	32-39	P53	Homo sapiens	83-86
10359526-9	1999	Our results suggest that these serines play a role in the regulation of p53-mediated apoptosis.	Serine	31-38	P53	Homo sapiens	72-75
10334203-5	1999	Using 32P-5"-end-labeled DNA fragments obtained from human p53 tumor suppressor gene and c-Ha-ras-1 protooncogene, we showed that PBQ plus NADH, and also PHQ, induced DNA damage frequently at thymine residues, in the presence of Cu(II).	NAD	139-143	P53	Homo sapiens	59-62
10334492-7	1999	A p53 mutation in codon 273 (CGT--&gt;TGT, Arg--&gt;Cys) was identified in the first biopsy and persisted throughout the course of the disease.	Arginine	43-46	P53	Homo sapiens	2-5
10334492-7	1999	A p53 mutation in codon 273 (CGT--&gt;TGT, Arg--&gt;Cys) was identified in the first biopsy and persisted throughout the course of the disease.	Cysteine	52-55	P53	Homo sapiens	2-5
10326590-6	1999	We examined TP53 protein expression from paraffin-embedded colon tissue of the patient with an immunohistochemical method.	Paraffin	41-49	P53	Homo sapiens	12-16
10225454-3	1999	Mutant (mt) p53-expressing NCCIT and S2 (no p53 protein) were both readily triggered into apoptosis by cisplatin and doxorubicin, while wild-type(wt)-p53-transactivation-competent 2102 EP cells failed to undergo drug-induced apoptosis.	Cisplatin	103-112	P53	Homo sapiens	12-15
10225454-3	1999	Mutant (mt) p53-expressing NCCIT and S2 (no p53 protein) were both readily triggered into apoptosis by cisplatin and doxorubicin, while wild-type(wt)-p53-transactivation-competent 2102 EP cells failed to undergo drug-induced apoptosis.	Doxorubicin	117-128	P53	Homo sapiens	12-15
10422567-0	1999	[Roles of p53 in adriamycin-induced cell death and in acquisition of adriamycin resistance in adult T-cell leukemia (ATL) cells].	Doxorubicin	17-27	P53	Homo sapiens	10-13
10220573-9	1999	When grown in CultiSphers, cells with abrogated p53 function (A549/16E6 and NCI-H1299) were less sensitive to cisplatin than the corresponding monolayer cells, indicating that the decrease in sensitivity is p53 independent.	Cisplatin	110-119	P53	Homo sapiens	48-51
10422567-7	1999	(6) In the cell cycle analysis, ADM-treatment induced G1- and G2-arrest and then apoptosis in the cell lines with wild-type p53, whereas it induced only G2-arrest and then apoptosis in the cell line with mutated-type p53 at the same time course as in those with wild-type p53.	Doxorubicin	32-35	P53	Homo sapiens	124-127
10422567-7	1999	(6) In the cell cycle analysis, ADM-treatment induced G1- and G2-arrest and then apoptosis in the cell lines with wild-type p53, whereas it induced only G2-arrest and then apoptosis in the cell line with mutated-type p53 at the same time course as in those with wild-type p53.	Doxorubicin	32-35	P53	Homo sapiens	217-220
10422567-7	1999	(6) In the cell cycle analysis, ADM-treatment induced G1- and G2-arrest and then apoptosis in the cell lines with wild-type p53, whereas it induced only G2-arrest and then apoptosis in the cell line with mutated-type p53 at the same time course as in those with wild-type p53.	Doxorubicin	32-35	P53	Homo sapiens	217-220
10223459-11	1999	CONCLUSIONS: The present study indicates that clotrimazole inhibits cell proliferation accompanied by morphological changes toward differentiation of glioblastoma cells and that this drug synergistically enhances the antitumor effect of cisplatin by inducing wild-type p53-mediated apoptosis.	Cisplatin	237-246	P53	Homo sapiens	269-272
10226945-4	1999	The other tumor (case 33) had a point mutation at codon 266, changing GGA to AGA and causing a substitution of glycine to arginine in the p53 protein.	Glycine	111-118	P53	Homo sapiens	138-141
10226945-4	1999	The other tumor (case 33) had a point mutation at codon 266, changing GGA to AGA and causing a substitution of glycine to arginine in the p53 protein.	Arginine	122-130	P53	Homo sapiens	138-141
10207063-6	1999	Lys residues within the peptide were critical for both p53 activation and core domain binding.	Lysine	0-3	P53	Homo sapiens	55-58
10349985-4	1999	bcl-2 and p53 protein expression were demonstrated by immunohistochemical methods, using formalin-fixed, paraffin-embedded biopsy tissues.	Paraffin	105-113	P53	Homo sapiens	10-13
10621843-3	1999	p53 protein expression was evaluated by immunohistochemical analysis on paraffin-embedded sections of 62 representative oral cancer biopsies and 22 leukoplakias, using p53-specific monoclonal antibody DO-7.	Paraffin	72-80	P53	Homo sapiens	0-3
10212189-0	1999	p38 kinase mediates UV-induced phosphorylation of p53 protein at serine 389.	Serine	65-71	P53	Homo sapiens	50-53
10417679-11	1999	Overexpression of p53 protein was recognized in 12% of VA, in 24% of mucosal components of CIVA and in 18% of invasive components of CIVA.	civa	91-95	P53	Homo sapiens	18-21
10417679-11	1999	Overexpression of p53 protein was recognized in 12% of VA, in 24% of mucosal components of CIVA and in 18% of invasive components of CIVA.	civa	133-137	P53	Homo sapiens	18-21
10212189-8	1999	Incubation of active p38 kinase with p53 protein caused the phosphorylation of p53 protein at serine 389 in vitro, while no phosphorylation of p53 at serine 389 was observed when p53 was incubated with activated JNK2 or ERK2.	Serine	94-100	P53	Homo sapiens	37-40
10212189-8	1999	Incubation of active p38 kinase with p53 protein caused the phosphorylation of p53 protein at serine 389 in vitro, while no phosphorylation of p53 at serine 389 was observed when p53 was incubated with activated JNK2 or ERK2.	Serine	94-100	P53	Homo sapiens	79-82
10212189-8	1999	Incubation of active p38 kinase with p53 protein caused the phosphorylation of p53 protein at serine 389 in vitro, while no phosphorylation of p53 at serine 389 was observed when p53 was incubated with activated JNK2 or ERK2.	Serine	94-100	P53	Homo sapiens	79-82
10212189-3	1999	Very recently it has been reported that UV induced a functional activation of p53 via phosphorylation at serine 389.	Serine	105-111	P53	Homo sapiens	78-81
10212189-8	1999	Incubation of active p38 kinase with p53 protein caused the phosphorylation of p53 protein at serine 389 in vitro, while no phosphorylation of p53 at serine 389 was observed when p53 was incubated with activated JNK2 or ERK2.	Serine	94-100	P53	Homo sapiens	79-82
10212189-4	1999	Here, we report that the UV-induced phosphorylation of p53 at serine 389 is mediated by p38 kinase.	Serine	62-68	P53	Homo sapiens	55-58
10212189-10	1999	These results strongly suggest that the p38 kinase is at least one of the most important mediators of p53 phosphorylation at serine 389 induced by UVC radiation.	Serine	125-131	P53	Homo sapiens	102-105
10212189-5	1999	UVC-induced phosphorylation of p53 at serine 389 was markedly impaired by either pretreatment of cells with p38 kinase inhibitor, SB202190, or stable expression of a dominant negative mutant of p38 kinase.	Serine	38-44	P53	Homo sapiens	31-34
10202144-5	1999	In response to DNA damage, p53 is phosphorylated at several N-terminal serines.	Serine	71-78	P53	Homo sapiens	27-30
10348343-0	1999	The double-stranded RNA activated protein kinase PKR physically associates with the tumor suppressor p53 protein and phosphorylates human p53 on serine 392 in vitro.	Serine	145-151	P53	Homo sapiens	101-104
10348343-0	1999	The double-stranded RNA activated protein kinase PKR physically associates with the tumor suppressor p53 protein and phosphorylates human p53 on serine 392 in vitro.	Serine	145-151	P53	Homo sapiens	138-141
10348347-6	1999	The cooperative nature of transcriptional activation by these factors was documented by repression of c-fos or NF-kappaB1 translation: Pretreatment of the cells with a c-fos or p50(NF-kappaB1) antisense oligonucleotide suppresses transcription from the human p53 promoter completely.	Oligonucleotides	203-218	P53	Homo sapiens	259-262
10348347-7	1999	In addition, we show that (a) the level of endogenous p53 mRNA and (b) transcription from the strictly p53-dependent human mdm2 promoter are reduced in the presence of c-fos, c-jun, p50(NF-kappaB1), p65RelA or c-myc antisense oligonucleotides, underscoring the importance of these transcription factors for the expression of functional p53.	Oligonucleotides	226-242	P53	Homo sapiens	54-57
10348347-7	1999	In addition, we show that (a) the level of endogenous p53 mRNA and (b) transcription from the strictly p53-dependent human mdm2 promoter are reduced in the presence of c-fos, c-jun, p50(NF-kappaB1), p65RelA or c-myc antisense oligonucleotides, underscoring the importance of these transcription factors for the expression of functional p53.	Oligonucleotides	226-242	P53	Homo sapiens	103-106
10348347-7	1999	In addition, we show that (a) the level of endogenous p53 mRNA and (b) transcription from the strictly p53-dependent human mdm2 promoter are reduced in the presence of c-fos, c-jun, p50(NF-kappaB1), p65RelA or c-myc antisense oligonucleotides, underscoring the importance of these transcription factors for the expression of functional p53.	Oligonucleotides	226-242	P53	Homo sapiens	103-106
10094816-3	1999	This RA-induced apoptosis was accompanied by p53-independent up-regulation of endogenous p21(CIPI/Waf1) and Bax proteins, as well as activation of p34(cdc2) kinase, and increase of Rb2 protein level and phosphorylation pattern.	Tretinoin	5-7	P53	Homo sapiens	45-48
10187847-4	1999	We have confirmed a calcium-dependent interaction of the S100B with a synthetic peptide corresponding to the C-terminal region of p53 (residues 319-393 in human p53) using plasmon resonance experiments on a BIAcore system.	Calcium	20-27	P53	Homo sapiens	130-133
10187847-4	1999	We have confirmed a calcium-dependent interaction of the S100B with a synthetic peptide corresponding to the C-terminal region of p53 (residues 319-393 in human p53) using plasmon resonance experiments on a BIAcore system.	Calcium	20-27	P53	Homo sapiens	161-164
10327055-0	1999	Wild-type p53 protein shows calcium-dependent binding to F-actin.	Calcium	28-35	P53	Homo sapiens	10-13
10327055-8	1999	Here we show that, in the presence of free calcium ions, p53 binds directly to F-actin with a dissocation constant of about 10 microM.	Calcium	43-50	P53	Homo sapiens	57-60
10327055-9	1999	Thus, part of the regulatory machinery in normal cell cycling may involve p53-actin interactions regulated by calcium fluxes and the dynamic turnover of F-actin.	Calcium	110-117	P53	Homo sapiens	74-77
10327056-3	1999	In the present study, we analysed the mechanisms by which CD437 induces apoptosis in two human NSCLC cell lines: H460 with wild-type p53 and H1792 with mutant p53.	CD 437	58-63	P53	Homo sapiens	133-136
10327056-3	1999	In the present study, we analysed the mechanisms by which CD437 induces apoptosis in two human NSCLC cell lines: H460 with wild-type p53 and H1792 with mutant p53.	CD 437	58-63	P53	Homo sapiens	159-162
10327056-8	1999	These results suggest that CD437-induced apoptosis is more extensive in NSCLC cells that express wild-type p53, possibly due to the involvement of the p53 regulated genes Killer/DR5, and Bax although CD437 can also induce apoptosis by means of a p53-independent mechanism.	CD 437	27-32	P53	Homo sapiens	107-110
10327056-8	1999	These results suggest that CD437-induced apoptosis is more extensive in NSCLC cells that express wild-type p53, possibly due to the involvement of the p53 regulated genes Killer/DR5, and Bax although CD437 can also induce apoptosis by means of a p53-independent mechanism.	CD 437	27-32	P53	Homo sapiens	151-154
10327056-8	1999	These results suggest that CD437-induced apoptosis is more extensive in NSCLC cells that express wild-type p53, possibly due to the involvement of the p53 regulated genes Killer/DR5, and Bax although CD437 can also induce apoptosis by means of a p53-independent mechanism.	CD 437	27-32	P53	Homo sapiens	151-154
10445426-6	1999	Curcumin treatment caused a reduction in the expression of Ki67, PCNA, and p53 mRNAs in breast cancer cells.	Curcumin	0-8	P53	Homo sapiens	75-78
10208433-3	1999	Using stable and transient transfections for the analysis of p53 mutant proteins, we have ruled out a role in stabilization by UV, gamma irradiation or actinomycin C for the following putative phosphorylation sites in the p53 protein: serines 6, 9, 15, 33, 315 and 392, and threonine 18.	Serine	235-242	P53	Homo sapiens	222-225
10213272-0	1999	Src-family kinase-p53/ Lyn p56 plays an important role in TNF-alpha-stimulated production of O2- by human neutrophils adherent to fibrinogen.	Superoxides	93-95	P53	Homo sapiens	18-21
10082548-0	1999	Requirement of ATM in phosphorylation of the human p53 protein at serine 15 following DNA double-strand breaks.	Serine	66-72	P53	Homo sapiens	51-54
10082548-3	1999	HaeIII-induced p53 protein in normal fibroblasts is phosphorylated at serine 15, as determined by immunostaining with an antibody specific for phosphorylated serine 15 of p53.	Serine	70-76	P53	Homo sapiens	15-18
10082548-3	1999	HaeIII-induced p53 protein in normal fibroblasts is phosphorylated at serine 15, as determined by immunostaining with an antibody specific for phosphorylated serine 15 of p53.	Serine	70-76	P53	Homo sapiens	171-174
10082548-3	1999	HaeIII-induced p53 protein in normal fibroblasts is phosphorylated at serine 15, as determined by immunostaining with an antibody specific for phosphorylated serine 15 of p53.	Serine	158-164	P53	Homo sapiens	15-18
10082548-3	1999	HaeIII-induced p53 protein in normal fibroblasts is phosphorylated at serine 15, as determined by immunostaining with an antibody specific for phosphorylated serine 15 of p53.	Serine	158-164	P53	Homo sapiens	171-174
10082548-6	1999	Following microinjection of HaeIII into lactacystin-treated normal fibroblasts, lactacystin-induced p53 protein is phosphorylated at serine 15 and stabilized even in the presence of cycloheximide.	Serine	133-139	P53	Homo sapiens	100-103
10082548-8	1999	These results indicate the significance of serine 15 phosphorylation for p53 stabilization after DNA double-strand breaks and an absolute requirement for ATM in this phosphorylation process.	Serine	43-49	P53	Homo sapiens	73-76
10210535-0	1999	Role of p53 and p16 gene alterations in determining response to concurrent paclitaxel and radiation in solid tumor.	Paclitaxel	75-85	P53	Homo sapiens	8-11
10210535-8	1999	Recent evidence suggests that paclitaxel is unique in its ability to activate apoptosis in tumor cells with p53 mutations in vitro and in vivo.	Paclitaxel	30-40	P53	Homo sapiens	108-111
10210536-12	1999	On a molecular level, taxanes activate a number of genes, but it appears that their effects are mainly p53-independent and primarily involve phosphorylation of the Bcl-2 gene.	Taxoids	22-29	P53	Homo sapiens	103-106
10210540-5	1999	This finding suggested that paclitaxel/RT was a rational treatment approach for other malignancies that frequently harbor p53 mutations, such as upper gastrointestinal malignancies.	Paclitaxel	28-38	P53	Homo sapiens	122-125
10037682-5	1999	Exposure of cerebellar granule cells to glutamate induces a rapid increase in p53 and Bax mRNA and protein levels with no apparent effect on Bcl-2 expression.	Glutamic Acid	40-49	P53	Homo sapiens	78-81
10037682-6	1999	Pretreatment with LiCl for 7 days prevents glutamate-induced increase in p53 and Bax expression and maintains Bcl-2 in an elevated state.	Glutamic Acid	43-52	P53	Homo sapiens	73-76
12953991-0	1999	P53 gene of chang-liver cells (Atcc-Ccl13) exposed to aflatoxin B1 (Afb): the effect of lysine on mutation at codon 249 of exon 7.	Lysine	88-94	P53	Homo sapiens	0-3
12953991-1	1999	The effect of different regimes of lysine-pre treatment on mutation at the 3rd nucleotide base of codon 249 which is located at the 7th exon of p53 gene of Chang-liver cells (CCIL13) exposed to aflatoxin B1 (AFB1) has been investigated.	Lysine	35-41	P53	Homo sapiens	144-147
10096970-0	1999	The TP53 genotype but not immunohistochemical result is predictive of response to cisplatin-based neoadjuvant therapy in stage III non-small cell lung cancer.	Cisplatin	82-91	P53	Homo sapiens	4-8
10096970-1	1999	BACKGROUND: The cytotoxic effects of cisplatin and anthracyclins have been attributed to apoptosis induction, which has been recognized as a major function of the TP53 gene.	Cisplatin	37-46	P53	Homo sapiens	163-167
10096970-10	1999	CONCLUSIONS: In a small cohort of patients with advanced non-small cell lung cancer we found a direct link between normal TP53 genotype and response to cisplatin-based induction treatment and also between mutant genotype and resistance to treatment, whereas p53 immunohistochemical result was predictive of neither.	Cisplatin	152-161	P53	Homo sapiens	122-126
10096970-10	1999	CONCLUSIONS: In a small cohort of patients with advanced non-small cell lung cancer we found a direct link between normal TP53 genotype and response to cisplatin-based induction treatment and also between mutant genotype and resistance to treatment, whereas p53 immunohistochemical result was predictive of neither.	Cisplatin	152-161	P53	Homo sapiens	258-261
10321742-1	1999	It has been reported that Lysine-305 is needed for the nuclear import of the p53 protein (Liang et al., 1998).	Lysine	26-32	P53	Homo sapiens	77-80
10321742-2	1999	In the present study, further mutagenesis analyses were carried out between Lys-305 and the major nuclear localization signal (NLS I) of p53.	Lysine	76-79	P53	Homo sapiens	137-140
10321742-3	1999	It was found that a single mutation of Arg-306 resulted in the defect of p53 nuclear import.	Arginine	39-42	P53	Homo sapiens	73-76
10079089-4	1999	Ribozyme derivatives that combine a mutation which indirectly slows down the rate of the chemical cleavage step by weakening guanosine binding with additional mutations that weaken substrate binding have greatly enhanced specificity with short oligonucleotide substrates and an mRNA fragment derived from the p53 gene.	Oligonucleotides	244-259	P53	Homo sapiens	309-312
10189126-10	1999	Among those patients whose tumors overexpressed p53, there was a trend toward improved outcome in the arm that received 5-FU and mitomycin-C compared with the arm that received 5-FU only.	Fluorouracil	120-124	P53	Homo sapiens	48-51
10189126-10	1999	Among those patients whose tumors overexpressed p53, there was a trend toward improved outcome in the arm that received 5-FU and mitomycin-C compared with the arm that received 5-FU only.	Fluorouracil	177-181	P53	Homo sapiens	48-51
10037739-3	1999	Similarly, in MCF7 cells stably expressing either Bcl-2 or Bcl-2(DeltaTM), nuclear levels of p53 protein were up-regulated upon treatment with the DNA-damaging agents doxorubicin and UV radiation, whereas p53-responsive promoter activity and expression of p21(CIP1/WAF1) were strongly reduced in MCF7-Bcl-2 cells but not in MCF7-Bcl-2(DeltaTM) or control MCF7 cells.	Doxorubicin	167-178	P53	Homo sapiens	93-96
10087941-9	1999	Homozygous deletion in p16INK4A/p15INK4B genes and a codon 259 missense point mutation (GAC--&gt;TAC; Asp--&gt;Tyr) in the TP53 gene were observed in one human papilloma positive scrotal carcinoma case.	Tyrosine	111-114	P53	Homo sapiens	123-127
10100719-0	1999	Expression of p53 in cisplatin-resistant ovarian cancer cell lines: modulation with the novel platinum analogue (1R, 2R-diaminocyclohexane)(trans-diacetato)(dichloro)-platinum(IV).	Cisplatin	21-30	P53	Homo sapiens	14-17
10100719-13	1999	In particular, the greater activity of DACH-acetato-Pt in cisplatin-resistant wild-type p53 ovarian tumor models can be ascribed to its ability to more efficiently induce p53 protein and activate p53 functions.	Cisplatin	58-67	P53	Homo sapiens	88-91
10100719-0	1999	Expression of p53 in cisplatin-resistant ovarian cancer cell lines: modulation with the novel platinum analogue (1R, 2R-diaminocyclohexane)(trans-diacetato)(dichloro)-platinum(IV).	Platinum	94-102	P53	Homo sapiens	14-17
10100719-13	1999	In particular, the greater activity of DACH-acetato-Pt in cisplatin-resistant wild-type p53 ovarian tumor models can be ascribed to its ability to more efficiently induce p53 protein and activate p53 functions.	Cisplatin	58-67	P53	Homo sapiens	171-174
10100719-13	1999	In particular, the greater activity of DACH-acetato-Pt in cisplatin-resistant wild-type p53 ovarian tumor models can be ascribed to its ability to more efficiently induce p53 protein and activate p53 functions.	Cisplatin	58-67	P53	Homo sapiens	171-174
10100719-3	1999	Cisplatin was relatively more effective against mutant or null p53 cell lines (continuous drug exposure IC50, 1.2-3.3 microM) than it was against those harboring wild-type p53 (IC50, 2.8-9.9 microM).	Cisplatin	0-9	P53	Homo sapiens	63-66
10100719-3	1999	Cisplatin was relatively more effective against mutant or null p53 cell lines (continuous drug exposure IC50, 1.2-3.3 microM) than it was against those harboring wild-type p53 (IC50, 2.8-9.9 microM).	Cisplatin	0-9	P53	Homo sapiens	172-175
10100719-6	1999	Differences between the two platinum agents were also evident in cell cycle studies: cisplatin arrested both wild-type and mutant p53 cells in G2-M, whereas DACH-acetato-Pt arrested wild-type p53 cells in G1 and mutant p53 cells in G2-M.	Platinum	28-36	P53	Homo sapiens	130-133
10100719-6	1999	Differences between the two platinum agents were also evident in cell cycle studies: cisplatin arrested both wild-type and mutant p53 cells in G2-M, whereas DACH-acetato-Pt arrested wild-type p53 cells in G1 and mutant p53 cells in G2-M.	Platinum	28-36	P53	Homo sapiens	192-195
10100719-6	1999	Differences between the two platinum agents were also evident in cell cycle studies: cisplatin arrested both wild-type and mutant p53 cells in G2-M, whereas DACH-acetato-Pt arrested wild-type p53 cells in G1 and mutant p53 cells in G2-M.	Platinum	28-36	P53	Homo sapiens	192-195
10390076-5	1999	In oncohematology, a number of trials have been initiated with antisense oligonucleotides directed against molecular targets, including the bcl-2, c-myc, bcr-abl, c-myb or p53 oncogenes and tumor suppressor genes.	Oligonucleotides	73-89	P53	Homo sapiens	172-175
10100719-6	1999	Differences between the two platinum agents were also evident in cell cycle studies: cisplatin arrested both wild-type and mutant p53 cells in G2-M, whereas DACH-acetato-Pt arrested wild-type p53 cells in G1 and mutant p53 cells in G2-M.	Cisplatin	85-94	P53	Homo sapiens	130-133
10051470-10	1999	Significantly increased risk associated with the p53 genotype was observed only among smokers who were glutathione S-transferase-null (Pro/Pro vs. Arg/Arg: odds ratio = 6.46; 95% CI = 1.55-26.94).	Arginine	147-150	P53	Homo sapiens	49-52
10408787-0	1999	Comprehensive TP53-denaturing gradient gel electrophoresis mutation detection assay also applicable to archival paraffin-embedded tissue.	Paraffin	112-120	P53	Homo sapiens	14-18
10408787-4	1999	When testing the assay on DNA from cultured lung cancer cell lines and from paraffin-embedded Dukes C colorectal carcinomas, significant TP53 mutations were observed at high frequencies in 15 of 16 lung cancer cell lines (94%) and in 21 of 30 paraffin-embedded tissue samples of Dukes C colorectal carcinomas (70%).	Paraffin	76-84	P53	Homo sapiens	137-141
10408787-4	1999	When testing the assay on DNA from cultured lung cancer cell lines and from paraffin-embedded Dukes C colorectal carcinomas, significant TP53 mutations were observed at high frequencies in 15 of 16 lung cancer cell lines (94%) and in 21 of 30 paraffin-embedded tissue samples of Dukes C colorectal carcinomas (70%).	Paraffin	243-251	P53	Homo sapiens	137-141
10051470-10	1999	Significantly increased risk associated with the p53 genotype was observed only among smokers who were glutathione S-transferase-null (Pro/Pro vs. Arg/Arg: odds ratio = 6.46; 95% CI = 1.55-26.94).	Arginine	151-154	P53	Homo sapiens	49-52
10398108-7	1999	Abuse of alcohol, an additional factor in these HNSCC patients, together with the abuse of tobacco, might play a role in the development of the p53-positive clusters.	Alcohols	9-16	P53	Homo sapiens	144-147
11812373-2	1999	METHODS: The p16, p21 and p53 genes mediated by Stearylamine/DOPE (SA liposome) were introduced alone and jointly into the non-small cell lung cancer (NSCLC) cell line A549 and small cell lung cancer (SCLC) SH77.	stearylamine	48-60	P53	Homo sapiens	26-29
10331640-2	1999	We show that nicotinamide and the resulting cellular NAD concentration modulate expression of the tumor suppressor protein, p53, in human breast, skin, and lung cells.	NAD	53-56	P53	Homo sapiens	124-127
10331640-5	1999	Since NAD is important in modulating ADP-ribose polymer metabolism, cyclic ADP-ribose synthesis, and stress response proteins, such as p53, following DNA damage, understanding how NAD metabolism is regulated in the human has important implications in developing both prevention and treatment strategies in carcinogenesis.	NAD	6-9	P53	Homo sapiens	135-138
10331640-5	1999	Since NAD is important in modulating ADP-ribose polymer metabolism, cyclic ADP-ribose synthesis, and stress response proteins, such as p53, following DNA damage, understanding how NAD metabolism is regulated in the human has important implications in developing both prevention and treatment strategies in carcinogenesis.	NAD	180-183	P53	Homo sapiens	135-138
10022902-10	1999	Addition of Mg2+ ions to the binding assay indeed started the p53 exonuclease and promoted rapid degradation of the bound, but not of the unbound, substrate, indicating that specifically recognized targets can be subjected to exonucleolytic degradation by p53 under defined conditions.	magnesium ion	12-16	P53	Homo sapiens	62-65
10022902-10	1999	Addition of Mg2+ ions to the binding assay indeed started the p53 exonuclease and promoted rapid degradation of the bound, but not of the unbound, substrate, indicating that specifically recognized targets can be subjected to exonucleolytic degradation by p53 under defined conditions.	magnesium ion	12-16	P53	Homo sapiens	256-259
10222219-0	1999	Apoptosis induced by nitric oxide is associated with nuclear p53 protein expression in cultured osteoarthritic synoviocytes.	Nitric Oxide	21-33	P53	Homo sapiens	61-64
10029520-1	1999	The inflammatory mediator nitric oxide (NO*) promotes apoptotic cell death based on morphological evidence, accumulation of the tumor suppressor p53, caspase-3 activation, and DNA fragmentation in RAW 264.7 macrophages.	Nitric Oxide	26-38	P53	Homo sapiens	145-148
10094469-1	1999	S100A2, a calcium binding protein of the EF-hand family, was recently identified to be inducible by etoposide, a p53 activator.	Calcium	10-17	P53	Homo sapiens	113-116
10029080-0	1999	Rapamycin causes poorly reversible inhibition of mTOR and induces p53-independent apoptosis in human rhabdomyosarcoma cells.	Sirolimus	0-9	P53	Homo sapiens	66-69
9931317-6	1999	After stimulation by CRP or collagen, the Src-family kinases p59fyn and p53/56lyn became associated with several tyrosine-phosphorylated proteins including the FcR gamma chain.	Tyrosine	113-121	P53	Homo sapiens	72-75
10029520-7	1999	Decreased apoptosis by JNK1/2 depletion prevented p53 accumulation after the addition of GSNO, which positions JNK1/2 upstream of the p53 response at low agonist concentrations.	S-Nitrosoglutathione	89-93	P53	Homo sapiens	50-53
10029520-7	1999	Decreased apoptosis by JNK1/2 depletion prevented p53 accumulation after the addition of GSNO, which positions JNK1/2 upstream of the p53 response at low agonist concentrations.	S-Nitrosoglutathione	89-93	P53	Homo sapiens	134-137
10029520-9	1999	However, with higher GSNO concentrations apoptotic transducing pathways, including p53 accumulation, were JNK1/2 unrelated.	S-Nitrosoglutathione	21-25	P53	Homo sapiens	83-86
10189892-7	1999	Moreover, mdm2 antisense oligonucleotides prevented E2-induced accumulation of p53.	Oligonucleotides	25-41	P53	Homo sapiens	79-82
10050883-4	1999	In an effort to identify potential signaling cascades through which Tpo illicits these effects on p53, we report here that treating M07e cells with MAPK kinase inhibitor PD98059 dramatically suppressed Tpo-induced conformational change in p53 as well as Tpo-enhanced viability in M07e cells in a p53-dependent manner.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	170-177	P53	Homo sapiens	98-101
10050883-4	1999	In an effort to identify potential signaling cascades through which Tpo illicits these effects on p53, we report here that treating M07e cells with MAPK kinase inhibitor PD98059 dramatically suppressed Tpo-induced conformational change in p53 as well as Tpo-enhanced viability in M07e cells in a p53-dependent manner.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	170-177	P53	Homo sapiens	239-242
10050883-4	1999	In an effort to identify potential signaling cascades through which Tpo illicits these effects on p53, we report here that treating M07e cells with MAPK kinase inhibitor PD98059 dramatically suppressed Tpo-induced conformational change in p53 as well as Tpo-enhanced viability in M07e cells in a p53-dependent manner.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	170-177	P53	Homo sapiens	239-242
9973219-0	1999	N-(2-chloroethyl)-N-nitrosourea tethered to lexitropsin induces minor groove lesions at the p53 cDNA that are more cytotoxic than mutagenic.	1-(2-Chloroethyl)-1-nitrosourea	0-31	P53	Homo sapiens	92-95
10069459-0	1999	Resveratrol suppresses cell transformation and induces apoptosis through a p53-dependent pathway.	Resveratrol	0-11	P53	Homo sapiens	75-78
10069459-4	1999	Resveratrol suppresses tumor promoter-induced cell transformation and markedly induces apoptosis, transactivation of p53 activity and expression of p53 protein in the same cell line and at the same dosage.	Resveratrol	0-11	P53	Homo sapiens	117-120
10069459-4	1999	Resveratrol suppresses tumor promoter-induced cell transformation and markedly induces apoptosis, transactivation of p53 activity and expression of p53 protein in the same cell line and at the same dosage.	Resveratrol	0-11	P53	Homo sapiens	148-151
10069459-5	1999	Also, resveratrol-induced apoptosis occurs only in cells expressing wild-type p53 (p53+/+), but not in p53-deficient (p53-/-) cells, while there is no difference in apoptosis induction between normal lymphoblasts and sphingomyelinase-deficient cell lines.	Resveratrol	6-17	P53	Homo sapiens	78-81
10069459-5	1999	Also, resveratrol-induced apoptosis occurs only in cells expressing wild-type p53 (p53+/+), but not in p53-deficient (p53-/-) cells, while there is no difference in apoptosis induction between normal lymphoblasts and sphingomyelinase-deficient cell lines.	Resveratrol	6-17	P53	Homo sapiens	83-86
10069459-5	1999	Also, resveratrol-induced apoptosis occurs only in cells expressing wild-type p53 (p53+/+), but not in p53-deficient (p53-/-) cells, while there is no difference in apoptosis induction between normal lymphoblasts and sphingomyelinase-deficient cell lines.	Resveratrol	6-17	P53	Homo sapiens	83-86
10069459-5	1999	Also, resveratrol-induced apoptosis occurs only in cells expressing wild-type p53 (p53+/+), but not in p53-deficient (p53-/-) cells, while there is no difference in apoptosis induction between normal lymphoblasts and sphingomyelinase-deficient cell lines.	Resveratrol	6-17	P53	Homo sapiens	83-86
10069459-6	1999	These results demonstrate for the first time that resveratrol induces apoptosis through activation of p53 activity, suggesting that its anti-tumor activity may occur through the induction of apoptosis.	Resveratrol	50-61	P53	Homo sapiens	102-105
9882333-6	1999	The p53 gene of the parental PGE cells was found to be overexpressed, perhaps thereby conferring the basal potential for long-term survival in vitro.	phenylglycidyl ether	29-32	P53	Homo sapiens	4-7
10022646-7	1999	Folic acid supplementation had a small, significant protective effect for p53 mutations (RR 0.97, CI 0.94-1.00).	Folic Acid	0-10	P53	Homo sapiens	74-77
10022646-8	1999	CONCLUSION: p53 Mutations 1) are associated with, and likely precede, dysplasia and cancer, 2) are associated with cancer-related mortality, and 3) may possibly be prevented by folic acid supplementation.	Folic Acid	177-187	P53	Homo sapiens	12-15
10023783-2	1999	Most recently, p53 protein containing an arginine residue in codon 72 was shown to be more effectively degraded by the E6 oncoprotein of human papillomavirus (HPV) than the corresponding proline isoform in cervical carcinoma cells.	Arginine	41-49	P53	Homo sapiens	15-18
9989808-3	1999	Here we report on the correlation between inhibition of mRNA synthesis and the induction of p53, p21WAF1 and apoptosis in diploid human fibroblasts treated with either UV light, cisplatin or the RNA synthesis inhibitors actinomycin D, DRB, H7 and alpha-amanitin.	Cisplatin	178-187	P53	Homo sapiens	92-95
9891044-1	1999	The wild-type p53 protein exhibits a common polymorphism at amino acid 72, resulting in either a proline residue (p53Pro) or an arginine residue (p53Arg) at this position.	Arginine	128-136	P53	Homo sapiens	14-17
9927633-0	1999	Induction of p53-dependent, insulin-like growth factor-binding protein-3-mediated apoptosis in glioblastoma multiforme cells by a protein kinase Calpha antisense oligonucleotide.	Oligonucleotides	162-177	P53	Homo sapiens	13-16
9927633-3	1999	PKCalpha antisense oligonucleotide treatment was accompanied by reduction in PKCalpha levels and the induction of wild-type p53 and insulin-like growth factor-binding protein-3 (IGFBP3) 24-72 h after treatment, a period that coincided with the appearance of apoptotic cell death as detected by DNA fragmentation.	Oligonucleotides	19-34	P53	Homo sapiens	124-127
9931282-5	1999	Cisplatin caused an 11-fold increase of recombination frequency in yeast and induced transcriptional activation of the DNA damage-associated promoters such as the minimum promoter containing p53 response elements and the GADD45 promoter in addition to activating the promoters for c-fos, heat shock protein 70, metallothionine IIa, and the minimum promoter containing nuclear factor kappa(kappa)B response elements.	Cisplatin	0-9	P53	Homo sapiens	191-194
10190571-10	1999	Moreover, the p53 protein accumulates early in glioma cells as a result of Pt(IV)-bis (monoglutarate) treatment.	bis (monoglutarate)	82-101	P53	Homo sapiens	14-17
10190571-11	1999	These data indicate that the Pt(IV)-bis (monoglutarate) complex induces apoptosis in glioma cells through a p53-dependent pathway.	bis (monoglutarate)	36-55	P53	Homo sapiens	108-111
9989825-9	1999	This detrimental effect of NF-kappaB mediating hydrogen peroxide-induced cell death presumably relies on the induced expression of death effector genes such as p53, which was NF-kappaB-dependently upregulated in the presence of H2O2.	Hydrogen Peroxide	47-64	P53	Homo sapiens	160-163
9989825-9	1999	This detrimental effect of NF-kappaB mediating hydrogen peroxide-induced cell death presumably relies on the induced expression of death effector genes such as p53, which was NF-kappaB-dependently upregulated in the presence of H2O2.	Hydrogen Peroxide	228-232	P53	Homo sapiens	160-163
9891054-5	1999	In this study, we demonstrate that PCAF also acetylates p53 in vitro at a lysine residue distinct from that acetylated by p300 and thereby increases p53"s ability to bind to its cognate DNA site.	Lysine	74-80	P53	Homo sapiens	56-59
9891054-5	1999	In this study, we demonstrate that PCAF also acetylates p53 in vitro at a lysine residue distinct from that acetylated by p300 and thereby increases p53"s ability to bind to its cognate DNA site.	Lysine	74-80	P53	Homo sapiens	149-152
9891054-6	1999	We have generated antibodies to acetylated p53 peptides at either of the two lysine residues that are targeted by PCAF or p300 and have demonstrated that these antibodies are highly specific for both acetylation and the particular site.	Lysine	77-83	P53	Homo sapiens	43-46
9989808-6	1999	Furthermore, cisplatin-induced accumulation of active p53 in repair-deficient XP-A cells occurred despite the lack of DNA strand break induction.	Cisplatin	13-22	P53	Homo sapiens	54-57
9925639-1	1999	Phosphorylation at Ser-15 may be a critical event in the up-regulation and functional activation of p53 during cellular stress.	Serine	19-22	P53	Homo sapiens	100-103
9890630-0	1999	Hydrogen peroxide-induced apoptosis mediated by p53 protein in glial cells.	Hydrogen Peroxide	0-17	P53	Homo sapiens	48-51
9890630-5	1999	After treatment with H2O2, p53 protein was highly expressed and protein levels of Bak, p21WAF1/CIP1 and GADD45 were also enhanced.	Hydrogen Peroxide	21-25	P53	Homo sapiens	27-30
9890630-8	1999	In addition, p53-deficient astrocytes were more resistant to H2O2-induced apoptosis than wild-type and heterozygous astrocytes.	Hydrogen Peroxide	61-65	P53	Homo sapiens	13-16
9925639-5	1999	ATR phosphorylated p53 at Ser-15 and Ser-37 in vitro, suggesting that p53 is a target for phosphorylation by ATR in DNA-damaged cells.	Serine	26-29	P53	Homo sapiens	19-22
9925639-5	1999	ATR phosphorylated p53 at Ser-15 and Ser-37 in vitro, suggesting that p53 is a target for phosphorylation by ATR in DNA-damaged cells.	Serine	26-29	P53	Homo sapiens	70-73
9925639-5	1999	ATR phosphorylated p53 at Ser-15 and Ser-37 in vitro, suggesting that p53 is a target for phosphorylation by ATR in DNA-damaged cells.	Serine	37-40	P53	Homo sapiens	70-73
10453723-5	1999	Ectopic expression of mutant and wild-type p53val135 attenuated taxol cytotoxicity in both T98G cells, which are mutant for p53, and LN-229 cells, which exhibit functional wild-type p53 activity.	Paclitaxel	64-69	P53	Homo sapiens	43-46
9920742-1	1999	The reactivity of guanines in an oligonucleotide containing mutational hot spots within the p53 gene (codons 248 and 249), 5"-CCG1G2AG3G4CCCA-3", toward dimethyl sulfate (DMS) and aflatoxin B1-8,9-epoxide (AFB1-8,9-epoxide) was investigated by a modified Maxam-Gilbert technique.	Oligonucleotides	33-48	P53	Homo sapiens	92-95
10071687-3	1999	Immunostaining for p53 protein was performed on paraffin and frozen sections from 61 patients with different grades of meningiomas using monoclonal antibodies (mAbs) DO-1 and pAb240.	Paraffin	48-56	P53	Homo sapiens	19-22
10226585-4	1999	Furthermore, 3H-thymidine incorporation in KOSC-3 cells, which display the p53 gene mutation, was inhibited by protons much more than by gamma-rays.	Tritium	13-15	P53	Homo sapiens	75-78
10226587-7	1999	We also propose that apoptosis induced by G-Rs3 is related to the elevations of p53 and p21WAF1 in the cells.	g-rs3	42-47	P53	Homo sapiens	80-83
9927204-7	1999	In contrast, p53His175 and p53His273 exerted very similar effects on the cellular response to cisplatin; both conferred increased resistance to low concentrations of the drug (2.5 microg/ml), but did not protect at all against high concentrations (10 microg/ml).	Cisplatin	94-103	P53	Homo sapiens	13-16
9926927-7	1999	Our results suggest that the PA26 gene is a novel p53 target gene with properties common to the GADD family of growth arrest and DNA damage-inducible stress-response genes, and, thus, a potential novel regulator of cellular growth.	gadd	96-100	P53	Homo sapiens	50-53
10025726-9	1999	In addition, growth in normal calcium medium lowered the UVB-induced stimulation of the p53 protein and altered the normal subcellular localization pattern of p53.	Calcium	30-37	P53	Homo sapiens	88-91
10025726-9	1999	In addition, growth in normal calcium medium lowered the UVB-induced stimulation of the p53 protein and altered the normal subcellular localization pattern of p53.	Calcium	30-37	P53	Homo sapiens	159-162
10412949-9	1999	RESULTS: p53 Ad combined with cisplatin, doxorubicin, 5-fluorouracil, methotrexate, or etoposide inhibited cell proliferation more effectively than chemotherapy alone in SCC-9 head and neck, SCC-15 head and neck, SCC-25 head and neck, SK-OV-3 ovarian, DU-145 prostate, MDA-MB-468 breast, and MDA-MB-231 breast tumor cells.	Doxorubicin	41-52	P53	Homo sapiens	9-12
10412949-9	1999	RESULTS: p53 Ad combined with cisplatin, doxorubicin, 5-fluorouracil, methotrexate, or etoposide inhibited cell proliferation more effectively than chemotherapy alone in SCC-9 head and neck, SCC-15 head and neck, SCC-25 head and neck, SK-OV-3 ovarian, DU-145 prostate, MDA-MB-468 breast, and MDA-MB-231 breast tumor cells.	Fluorouracil	54-68	P53	Homo sapiens	9-12
10453723-6	1999	Interestingly, wild-type p53val135 abrogated the taxol-imposed G2/M arrest in both cell lines.	Paclitaxel	49-54	P53	Homo sapiens	25-28
9950218-6	1999	Increased expression of p53 protein is observed in ATRA-treated HMECs at 72 h; however, initiation of G1-S-phase arrest starts at 24 h, suggesting that this observed induction of p53 is a secondary event.	Tretinoin	51-55	P53	Homo sapiens	24-27
10690631-3	1999	The positive clones selected by ELISA were found to exhibit strong staining of nuclear p53 in both fresh and archival paraffin embedded breast tumour tissue sections.	Paraffin	118-126	P53	Homo sapiens	87-90
9950218-6	1999	Increased expression of p53 protein is observed in ATRA-treated HMECs at 72 h; however, initiation of G1-S-phase arrest starts at 24 h, suggesting that this observed induction of p53 is a secondary event.	Tretinoin	51-55	P53	Homo sapiens	179-182
9950218-13	1999	Our results emphasize the chemotherapeutic potential of ATRA and antiestrogens, particularly for suppressing the growth of tumors lacking functional p53.	Tretinoin	56-60	P53	Homo sapiens	149-152
10425040-0	1999	Highly sensitive mutation screening by REF with low concentrations of urea: A blinded analysis of a 2-kb region of the p53 gene reveals two common haplotypes.	Urea	70-74	P53	Homo sapiens	119-122
10200544-0	1999	Possible role of NF-kappaB and p53 in the glutamate-induced pro-apoptotic neuronal pathway.	Glutamic Acid	42-51	P53	Homo sapiens	31-34
10063313-0	1999	The relationship between cisplatin-induced apoptosis and p53, bcl-2 and bax expression in human lung cancer cells.	Cisplatin	25-34	P53	Homo sapiens	57-60
12938516-1	1999	To understand the relationship between expression of P53 protein and HPV16/18 infection in laryngeal papillomas, PCR and immunohistochemical techniques were used to examine the paraffin-embedded tissue samples of laryngeal papillomas from 35 subjects.	Paraffin	177-185	P53	Homo sapiens	53-56
10359137-2	1999	One study has reported a special "hotspot" mutation at codon 249 of p53 in lung cancers of former uranium miners.	Uranium	98-105	P53	Homo sapiens	68-71
10363568-2	1999	The aim of this work was to investigate the role of p53 in the apoptosis of colorectal cancer cells in vitro, induced by 5-fluorouracil (5-FU) and hydroxy-camptothecin (HCPT).	Fluorouracil	121-135	P53	Homo sapiens	52-55
10363568-2	1999	The aim of this work was to investigate the role of p53 in the apoptosis of colorectal cancer cells in vitro, induced by 5-fluorouracil (5-FU) and hydroxy-camptothecin (HCPT).	Fluorouracil	137-141	P53	Homo sapiens	52-55
10063313-8	1999	Cancer cells with the natural expression of bcl-2 and p53 mutation may be more resistant to cisplatin and less susceptible to apoptosis.	Cisplatin	92-101	P53	Homo sapiens	54-57
9879988-2	1998	To understand the functional interaction between these two proteins, the effects of a PARP inhibitor, 3-aminobenzamide (3AB), on the p53 pathway were investigated in human glioblastoma cells with different p53 status.	3-aminobenzamide	102-118	P53	Homo sapiens	133-136
10527075-0	1999	In vivo studies of adenovirus-mediated p53 gene therapy for cis-platinum-resistant human ovarian tumor xenografts.	Cisplatin	60-72	P53	Homo sapiens	39-42
10527075-1	1999	We have recently reported that mutations of the tumor suppressor p53 gene are associated with the development of resistance to cis-platinum in human ovarian cancer cells, and that adenovirus-mediated reintroduction of the wild-type p53 (wtp53) gene in ovarian tumor cells resulted in the sensitization of tumor cells to cis-diamminedichloroplatinum (II) (CDDP).	Cisplatin	127-139	P53	Homo sapiens	65-68
10527075-1	1999	We have recently reported that mutations of the tumor suppressor p53 gene are associated with the development of resistance to cis-platinum in human ovarian cancer cells, and that adenovirus-mediated reintroduction of the wild-type p53 (wtp53) gene in ovarian tumor cells resulted in the sensitization of tumor cells to cis-diamminedichloroplatinum (II) (CDDP).	Cisplatin	320-353	P53	Homo sapiens	65-68
10527075-1	1999	We have recently reported that mutations of the tumor suppressor p53 gene are associated with the development of resistance to cis-platinum in human ovarian cancer cells, and that adenovirus-mediated reintroduction of the wild-type p53 (wtp53) gene in ovarian tumor cells resulted in the sensitization of tumor cells to cis-diamminedichloroplatinum (II) (CDDP).	Cisplatin	320-353	P53	Homo sapiens	232-235
10527075-1	1999	We have recently reported that mutations of the tumor suppressor p53 gene are associated with the development of resistance to cis-platinum in human ovarian cancer cells, and that adenovirus-mediated reintroduction of the wild-type p53 (wtp53) gene in ovarian tumor cells resulted in the sensitization of tumor cells to cis-diamminedichloroplatinum (II) (CDDP).	Cisplatin	355-359	P53	Homo sapiens	65-68
10527075-1	1999	We have recently reported that mutations of the tumor suppressor p53 gene are associated with the development of resistance to cis-platinum in human ovarian cancer cells, and that adenovirus-mediated reintroduction of the wild-type p53 (wtp53) gene in ovarian tumor cells resulted in the sensitization of tumor cells to cis-diamminedichloroplatinum (II) (CDDP).	Cisplatin	355-359	P53	Homo sapiens	232-235
10527075-3	1999	treatment of CDDP-resistant tumor cells expressing mutant p53 (mutp53) with a recombinant adenovirus expressing wtp53 (Adwtp53) would result in the sensitization of resistant cells to CDDP.	Cisplatin	13-17	P53	Homo sapiens	58-61
10527075-3	1999	treatment of CDDP-resistant tumor cells expressing mutant p53 (mutp53) with a recombinant adenovirus expressing wtp53 (Adwtp53) would result in the sensitization of resistant cells to CDDP.	Cisplatin	184-188	P53	Homo sapiens	58-61
9918821-1	1998	The observation that 3-aminobenzamide, which inhibits a variety of ADP-ribose transferases, prolongs the gamma-irradiation-induced increase in intracellular p53 concentration suggested that one or more of such enzymes may determine the duration of the p53 response during G1 arrest.	3-aminobenzamide	21-37	P53	Homo sapiens	157-160
9918821-1	1998	The observation that 3-aminobenzamide, which inhibits a variety of ADP-ribose transferases, prolongs the gamma-irradiation-induced increase in intracellular p53 concentration suggested that one or more of such enzymes may determine the duration of the p53 response during G1 arrest.	3-aminobenzamide	21-37	P53	Homo sapiens	252-255
9865721-1	1998	Oxygen-deprived regions of a solid tumor can induce tumor suppressor p53 expression and hence select for p53-mutant tumor cells with diminished apoptotic potential.	Oxygen	0-6	P53	Homo sapiens	69-72
9865721-1	1998	Oxygen-deprived regions of a solid tumor can induce tumor suppressor p53 expression and hence select for p53-mutant tumor cells with diminished apoptotic potential.	Oxygen	0-6	P53	Homo sapiens	105-108
9865721-4	1998	The iron chelator deferoxamine induced both HIF-1alpha and p53, but p53 up-regulation could still be detected in HIF-1alpha-deficient cells, suggesting that mechanisms other than HIF-1alpha activation contribute to oxygen-regulated p53 induction.	Iron	4-8	P53	Homo sapiens	59-62
9830059-0	1998	Phosphorylation of p53 serine 15 increases interaction with CBP.	Serine	23-29	P53	Homo sapiens	19-22
10421427-0	1999	Melatonin increases p53 and p21WAF1 expression in MCF-7 human breast cancer cells in vitro.	Melatonin	0-9	P53	Homo sapiens	20-23
10421427-5	1999	These results demonstrate that melatonin inhibits MCF-7 cell proliferation by inducing an arrest of cell cycle dependent on an increased expression of p21WAF1 protein, which is mediated by the p53 pathway.	Melatonin	31-40	P53	Homo sapiens	193-196
11601009-4	1999	The latter p53 gene encoding protein contained an Arg--&gt;His substitution at the same position, and pBLuscript plasmid was used as control.	Arginine	50-53	P53	Homo sapiens	11-14
11601009-10	1999	CONCLUSION: Codon 172 mutant (Arg--&gt;Leu) p53 genomic DNA exhibited a strong suppressive transfecting effects on carcinoma cell, so it is a possible candidate to be used in cancer gene therapy.	Arginine	30-33	P53	Homo sapiens	44-47
9865749-0	1998	Correspondence re: S. Fulda et al., Betulinic acid triggers CD95 (Apo1/Fas)- and p53-independent apoptosis via activation of caspases in neuroectodermal tumors.	betulinic acid	36-50	P53	Homo sapiens	81-84
9879997-8	1998	TPA-induced apoptosis appears to be mediated through a p53-independent pathway, and the up-regulation of p21WAF1 and Bax may be the molecular mechanisms by which TPA induces apoptosis.	Tetradecanoylphorbol Acetate	0-3	P53	Homo sapiens	55-58
9879988-2	1998	To understand the functional interaction between these two proteins, the effects of a PARP inhibitor, 3-aminobenzamide (3AB), on the p53 pathway were investigated in human glioblastoma cells with different p53 status.	3-aminobenzamide	120-123	P53	Homo sapiens	133-136
9879997-4	1998	We found up-regulation of p21WAF1 and Bax expressions, however, the expressions of p53 and Bcl-2 genes remained unchanged in TPA-treated cells.	Tetradecanoylphorbol Acetate	125-128	P53	Homo sapiens	83-86
9865905-9	1998	The second finding that drug-induced apoptosis was equal or higher in tumors that expressed Pgp, p53, and Bcl-2 compared to tumors that did not express these proteins supports the use of paclitaxel in treating Pgp-, p53- and Bcl-2-positive tumors.	Paclitaxel	187-197	P53	Homo sapiens	97-100
14646475-1	1998	The natural metabolic byproduct of estradiol, 2-methoxyestradiol (2-MeOE2), induces apoptosis in human lung cancer cells by a p53-dependent mechanism.	Estradiol	35-44	P53	Homo sapiens	126-129
9886570-3	1998	Exons 5-8 of the p53 gene were examined for mutations by the polymerase chain reaction-single strand conformation polymorphism technique and DNA sequencing, using DNA from formalin-fixed paraffin-embedded tissues.	Paraffin	187-195	P53	Homo sapiens	17-20
9865905-9	1998	The second finding that drug-induced apoptosis was equal or higher in tumors that expressed Pgp, p53, and Bcl-2 compared to tumors that did not express these proteins supports the use of paclitaxel in treating Pgp-, p53- and Bcl-2-positive tumors.	Paclitaxel	187-197	P53	Homo sapiens	216-219
9865921-1	1998	Paclitaxel induces a cell cycle block at G2-M phase by preventing the depolymerization of microtubules and induces p53-independent apoptosis in many cancer cells.	Paclitaxel	0-10	P53	Homo sapiens	115-118
9951689-4	1998	Chemosensitivity data, according to a short-term assay (FMCA), indicated that tumours with p53 mutation were more resistant to cisplatin and cyclophosphamide.	Cisplatin	127-136	P53	Homo sapiens	91-94
9927805-8	1998	The p53 gene encodes a transcription factor that contributes to several different cellular activities, including apoptosis, the cellular response to radiation, and the activation of proteins such as GADD, Bcl-2 (represses to apoptosis) and Bax.	gadd	199-203	P53	Homo sapiens	4-7
10098455-2	1998	By developing an oxidative-induced DNA damage mapping version of the Ligation-mediated polymerase chain reaction (LMPCR) technique, we investigated the il vivo and in vitro frequencies of DNA base modifications caused by ROS in the human p53 and PGK1 gene.	Reactive Oxygen Species	221-224	P53	Homo sapiens	238-241
10098455-13	1998	CEE provided a 24-fold increase in the signal strength attributable to strand breaks plus modified bases created by ROS in the human p53 and PGK1 genes, detected by LMPCR.	Reactive Oxygen Species	116-119	P53	Homo sapiens	133-136
10081494-0	1998	EAT/mcl-1, a member of the bcl-2 related genes, confers resistance to apoptosis induced by cis-diammine dichloroplatinum (II) via a p53-independent pathway.	Cisplatin	91-120	P53	Homo sapiens	132-135
10081494-8	1998	Since CDDP and carboplatin damage DNA and then activate c-abl and the JNK/SAPK pathway, EAT/mcl-1 may inhibit p53-independent apoptosis through a c-abl/JNK (SAPK)-dependent mechanism.	Cisplatin	6-10	P53	Homo sapiens	110-113
9840184-6	1998	Based on experiments using TP53 antisense oligonucleotides, the radioprotective effect of BBI could be correlated with the function of wild-type TP53.	Amiodarone	90-93	P53	Homo sapiens	145-149
9846573-4	1998	Our data indicate that tumor-associated nitric oxide production may promote cancer progression by providing a selective growth advantage to tumor cells with mutant p53, and that inhibitors of inducible nitric oxide synthase may have therapeutic activity in these tumors.	Nitric Oxide	40-52	P53	Homo sapiens	164-167
9843217-7	1998	Recombinant ATM protein phosphorylates p53 on serine 15 near the N terminus.	Serine	46-52	P53	Homo sapiens	39-42
9843217-9	1998	These results demonstrate that ATM can bind p53 directly and is responsible for its serine 15 phosphorylation, thereby contributing to the activation and stabilization of p53 during the IR-induced DNA damage response.	Serine	84-90	P53	Homo sapiens	44-47
9843217-9	1998	These results demonstrate that ATM can bind p53 directly and is responsible for its serine 15 phosphorylation, thereby contributing to the activation and stabilization of p53 during the IR-induced DNA damage response.	Serine	84-90	P53	Homo sapiens	171-174
9840184-2	1998	It was shown that BBI reduced the radiation-induced protein stabilization and DNA-binding activity of TP53 (formerly known as p53) in normal fibroblasts.	Amiodarone	18-21	P53	Homo sapiens	102-106
9811860-4	1998	Addition of GC-clamps to the respective MAR-oligonucleotides or introducing mutations into the unwinding motif strongly reduced DNA strand separation, but supported the formation of tight complexes between mutant p53 and such oligonucleotides.	Oligonucleotides	44-60	P53	Homo sapiens	213-216
9840184-2	1998	It was shown that BBI reduced the radiation-induced protein stabilization and DNA-binding activity of TP53 (formerly known as p53) in normal fibroblasts.	Amiodarone	18-21	P53	Homo sapiens	126-129
9840184-6	1998	Based on experiments using TP53 antisense oligonucleotides, the radioprotective effect of BBI could be correlated with the function of wild-type TP53.	Amiodarone	90-93	P53	Homo sapiens	27-31
9848359-0	1998	Homozygous arginine-72 in wild type p53 and risk of cervical cancer.	Arginine	11-19	P53	Homo sapiens	36-39
9837785-3	1998	Cell cycle arrest and apoptosis were evaluated in LCL expressing varying p53 levels achieved by treating the cells with increasing concentrations of cisplatin, and we supplemented this approach with experiments in EBV-infected Burkitt"s lymphoma (BL) cells transfected with a temperature-sensitive (ts) mutant human p53 and studies in LCL infected with recombinant adenoviruses expressing wt and ts mutant p53.	Cisplatin	149-158	P53	Homo sapiens	73-76
9840938-4	1998	To learn if transcriptional activation of downstream genes by p53 plays a role in this putative checkpoint, three cell lines were exposed to nocodazole.	Nocodazole	141-151	P53	Homo sapiens	62-65
9840938-7	1998	Incubation with nocodazole of cells containing wild-type p53 results in accumulation of both 2N and 4N populations of cells.	Nocodazole	16-26	P53	Homo sapiens	57-60
9865315-0	1998	In vitro transcription and translation of the tumour suppressor protein P53: qualitative and quantitative effects of FK506 and rapamycin.	Sirolimus	127-136	P53	Homo sapiens	72-75
9823314-8	1998	Although p53 was not endogenously poly (ADP-ribosyl)ated in situ, incubation of cell extracts with full-length PARP from calf thymus and [32P]beta NAD+ resulted in its time-dependent poly(ADP-ribosyl)ation.	NAD	147-151	P53	Homo sapiens	9-12
9769393-6	1998	On the other hand, an A to G substitution at codon 170 in exon 5 of p53 gene resulting in glutamic acid (ACG) to glycine (GCG) was detected in the DNA of her tongue cancer.	Glutamic Acid	90-103	P53	Homo sapiens	68-71
9811465-0	1998	Human lymphoblastoid cell lines expressing mutant p53 exhibit decreased sensitivity to cisplatin-induced cytotoxicity.	Cisplatin	87-96	P53	Homo sapiens	50-53
9811465-3	1998	We found that compared to the parental cell line, cells overexpressing mutant p53 (either 246val or 135ser) exhibited decreased apoptosis in response to gamma-radiation or cisplatin as measured by: propidium iodide (PI) staining of the cellular DNA (cell cycle analysis) and decrease in PARP (poly ADP-ribose polymerase) cleavage as detected by Western blotting.	Cisplatin	172-181	P53	Homo sapiens	78-81
9811465-4	1998	Interestingly the cells expressing mutant p53(135ser) protein were less resistant to cisplatin-induced apoptosis than the p53(246val)-bearing cell line.	Cisplatin	85-94	P53	Homo sapiens	42-45
9811465-5	1998	A significant decrease in the G1/S arrest assayed by bromodeoxyuridine and PI staining (cell cycle/proliferation assay) was also observed in response to irradiation and cisplatin in cell lines expressing either of the mutant p53 constructs.	Cisplatin	169-178	P53	Homo sapiens	225-228
9811465-6	1998	A lower basal level and reduced magnitude of protein induction of the cell cycle inhibitor p21/Waf1 was seen both after cisplatin and gamma-radiation treatment in the mutant p53 expressing lymphoblastoid variant when compared to the wild type p53 parental cell line but induction of the p53 regulator MDM2 was comparable in both.	Cisplatin	120-129	P53	Homo sapiens	174-177
9811465-8	1998	Unexpectedly, following cisplatin treatment we observed an increase in mutant and wild type p53 RNA steady state levels in addition to increased levels of p53 protein.	Cisplatin	24-33	P53	Homo sapiens	92-95
9811465-8	1998	Unexpectedly, following cisplatin treatment we observed an increase in mutant and wild type p53 RNA steady state levels in addition to increased levels of p53 protein.	Cisplatin	24-33	P53	Homo sapiens	155-158
9811465-9	1998	These results suggest that irradiation or cisplatin treatment may not only stabilize wild type p53 protein but also may increase the steady state p53 RNA levels.	Cisplatin	42-51	P53	Homo sapiens	95-98
9811465-9	1998	These results suggest that irradiation or cisplatin treatment may not only stabilize wild type p53 protein but also may increase the steady state p53 RNA levels.	Cisplatin	42-51	P53	Homo sapiens	146-149
9811465-10	1998	Finally these results indicate that both irradiation and cisplatin should be used with caution in the treatment of lymphoid tumors bearing mutations of p53.	Cisplatin	57-66	P53	Homo sapiens	152-155
9846203-0	1998	Progesterone inhibits growth and induces apoptosis in breast cancer cells: inverse effects on Bcl-2 and p53.	Progesterone	0-12	P53	Homo sapiens	104-107
9792903-5	1998	This suggested that paclitaxel/RT was a rationale treatment approach for other malignancies which frequently harbor p53 mutations such as upper gastrointestinal malignancies.	Paclitaxel	20-30	P53	Homo sapiens	116-119
9772293-7	1998	The accumulated p53 was biochemically active, as measured in a transient transfection assay upon treatment with gemcitabine, cisplatin, etoposide, and Taxol.	Cisplatin	125-134	P53	Homo sapiens	16-19
9772293-7	1998	The accumulated p53 was biochemically active, as measured in a transient transfection assay upon treatment with gemcitabine, cisplatin, etoposide, and Taxol.	Paclitaxel	151-156	P53	Homo sapiens	16-19
9772293-8	1998	Activity was dependent on the drug dose applied and proportional to the level of accumulated p53, except for Taxol-induced p53 accumulation which correlated inversely with p53 biochemical activity.	Paclitaxel	109-114	P53	Homo sapiens	123-126
9772293-8	1998	Activity was dependent on the drug dose applied and proportional to the level of accumulated p53, except for Taxol-induced p53 accumulation which correlated inversely with p53 biochemical activity.	Paclitaxel	109-114	P53	Homo sapiens	123-126
9825943-3	1998	This report presents clinical, neuropathological and molecular genetic data from 2 families in France with an identical p53 germline mutation in codon 248 (CGG-&gt;TGG; Arg-&gt;Trp) and a clustering of CNS tumors.	Arginine	169-172	P53	Homo sapiens	120-123
9825943-3	1998	This report presents clinical, neuropathological and molecular genetic data from 2 families in France with an identical p53 germline mutation in codon 248 (CGG-&gt;TGG; Arg-&gt;Trp) and a clustering of CNS tumors.	Tryptophan	177-180	P53	Homo sapiens	120-123
9891537-6	1998	P53 was overexpressed in 73% of tamoxifen users compared to 53% of non-users.	Tamoxifen	32-41	P53	Homo sapiens	0-3
9891537-10	1998	CONCLUSIONS: In this small study, tamoxifen associated tumors expressed p53 more frequently than non-users, while the opposite was observed with p21WAF1/CIP1.	Tamoxifen	34-43	P53	Homo sapiens	72-75
9891537-11	1998	This suggests that p53 mutations might play a role in development of tamoxifen associated tumors.	Tamoxifen	69-78	P53	Homo sapiens	19-22
9891541-0	1998	p53 and bcl-2 expression in locally advanced squamous cell head-neck cancer treated with platinum based chemotherapy and radiotherapy.	Platinum	89-97	P53	Homo sapiens	0-3
9891551-2	1998	The aim of this study was to establish the status of p53 gene and p53-regulated proteins (Bax, Bcl-2 and Waf-1) expression in head and neck simultaneous preneoplastic and invasive lesions from patients with chronic alcohol and tobacco exposure.	Alcohols	215-222	P53	Homo sapiens	53-56
9891551-2	1998	The aim of this study was to establish the status of p53 gene and p53-regulated proteins (Bax, Bcl-2 and Waf-1) expression in head and neck simultaneous preneoplastic and invasive lesions from patients with chronic alcohol and tobacco exposure.	Alcohols	215-222	P53	Homo sapiens	66-69
9794481-6	1998	Basic fibroblast growth factor (bFGF) effectively blocks the p53/cAMP-induced apoptosis, but suppresses steroidogenesis.	Cyclic AMP	65-69	P53	Homo sapiens	61-64
9794481-8	1998	While cAMP markedly suppresses the p53-induced Mdm2 expression, bFGF and ECM elevate Mdm2 expression 3-5-fold.	Cyclic AMP	6-10	P53	Homo sapiens	35-38
9930367-0	1998	p53- and p21-independent apoptosis of squamous cell carcinoma cells induced by 5-fluorouracil and radiation.	Fluorouracil	79-93	P53	Homo sapiens	0-3
9930367-12	1998	These findings indicate that 5-FU and gamma-rays induce apoptosis of squamous cell carcinoma cells in p53- and p21-independent manners, in the S and G2/M phases, respectively.	Fluorouracil	29-33	P53	Homo sapiens	102-105
9769393-6	1998	On the other hand, an A to G substitution at codon 170 in exon 5 of p53 gene resulting in glutamic acid (ACG) to glycine (GCG) was detected in the DNA of her tongue cancer.	Glycine	113-120	P53	Homo sapiens	68-71
9806590-2	1998	The extent of modulation of TP53 and CDKN1A is significantly reduced in the presence of the gap junction inhibitor lindane and in irradiated low-density cell populations.	Hexachlorocyclohexane	115-122	P53	Homo sapiens	28-32
11825490-6	1998	Both p53 mutation protein and p53 gene mutations were prevalent in steroid and progesterone receptors negative tumors (P &lt; 0.05).	Steroids	67-74	P53	Homo sapiens	5-8
11825490-6	1998	Both p53 mutation protein and p53 gene mutations were prevalent in steroid and progesterone receptors negative tumors (P &lt; 0.05).	Steroids	67-74	P53	Homo sapiens	30-33
9804172-8	1998	These results suggest that the G1 phase arrest by flavone is due to p53-independent transcriptional induction of the p21/WAF1 gene and the subsequent dephosphorylation of RB protein.	flavone	50-57	P53	Homo sapiens	68-71
9774464-5	1998	In this way, profound effects of protein kinase A were identified and corroborated in vivo by the protection conferred by cAMP against diverse triggers of p53-dependent apoptosis.	Cyclic AMP	122-126	P53	Homo sapiens	155-158
9788435-4	1998	Whereas p21waf1 overexpression conferred increased resistance to killing by either drug, p53 overexpression enhanced the cytotoxic effect of cisplatin but protected against etoposide cytotoxicity.	Cisplatin	141-150	P53	Homo sapiens	89-92
9788606-2	1998	A common polymorphism of p53, encoding either proline or arginine at position 72, affects the susceptibility of p53 to E6-mediated degradation in vivo; Caucasian women homozygous for arginine 72 reportedly are about seven times more susceptible to HPV-associated carcinoma of the cervix than heterozygotes.	Arginine	57-65	P53	Homo sapiens	25-28
9788606-2	1998	A common polymorphism of p53, encoding either proline or arginine at position 72, affects the susceptibility of p53 to E6-mediated degradation in vivo; Caucasian women homozygous for arginine 72 reportedly are about seven times more susceptible to HPV-associated carcinoma of the cervix than heterozygotes.	Arginine	57-65	P53	Homo sapiens	112-115
9788606-2	1998	A common polymorphism of p53, encoding either proline or arginine at position 72, affects the susceptibility of p53 to E6-mediated degradation in vivo; Caucasian women homozygous for arginine 72 reportedly are about seven times more susceptible to HPV-associated carcinoma of the cervix than heterozygotes.	Arginine	183-191	P53	Homo sapiens	25-28
9801791-4	1998	The replacement of Trp53 by alanine resulted in a complete loss of the haemagglutinating activity, suggesting that the tryptophan residue in the heptapeptide sequence is essential for carbohydrate binding.	Carbohydrates	184-196	P53	Homo sapiens	19-24
9788606-2	1998	A common polymorphism of p53, encoding either proline or arginine at position 72, affects the susceptibility of p53 to E6-mediated degradation in vivo; Caucasian women homozygous for arginine 72 reportedly are about seven times more susceptible to HPV-associated carcinoma of the cervix than heterozygotes.	Arginine	183-191	P53	Homo sapiens	112-115
9792140-3	1998	We sought to determine the roles played by the p53 and Bcl-2 family of proteins in 5-fluorouracil (5-FU)-induced apoptosis of human colon cancer cell lines.	Fluorouracil	83-97	P53	Homo sapiens	47-50
9792140-3	1998	We sought to determine the roles played by the p53 and Bcl-2 family of proteins in 5-fluorouracil (5-FU)-induced apoptosis of human colon cancer cell lines.	Fluorouracil	99-103	P53	Homo sapiens	47-50
9792140-6	1998	Using five human colon cancer cell lines, we found that equitoxic (IC50) doses of 5-FU induced apoptosis in both wild-type p53 and mutant p53 cells.	Fluorouracil	82-86	P53	Homo sapiens	123-126
9792140-6	1998	Using five human colon cancer cell lines, we found that equitoxic (IC50) doses of 5-FU induced apoptosis in both wild-type p53 and mutant p53 cells.	Fluorouracil	82-86	P53	Homo sapiens	138-141
9792140-11	1998	In cells containing wild-type p53 (e.g. LoVo), 5-FU-induced apoptosis was accompanied by increased expression of Bax and Bak without consistent modulation of other bcl-2 family proteins.	Fluorouracil	47-51	P53	Homo sapiens	30-33
10895614-7	1998	p53 tumour suppressor gene mutations are the most frequently found genetic errors in oral cancer and the p53 gene is a likely target for tobacco and alcohol.	Alcohols	149-156	P53	Homo sapiens	0-3
10895614-7	1998	p53 tumour suppressor gene mutations are the most frequently found genetic errors in oral cancer and the p53 gene is a likely target for tobacco and alcohol.	Alcohols	149-156	P53	Homo sapiens	105-108
9801791-4	1998	The replacement of Trp53 by alanine resulted in a complete loss of the haemagglutinating activity, suggesting that the tryptophan residue in the heptapeptide sequence is essential for carbohydrate binding.	Tryptophan	119-129	P53	Homo sapiens	19-24
9766444-6	1998	The differentiation response to transfected p53 with or without INF-gamma was inhibited by cyclic adenosine monophosphate (cAMP)-inducing agents (dibutyryl cyclic adenosine 3":5"-monophosphate, forskolin, and 3-isobutyl-1-methylxanthine) in a dose-dependent manner.	Cyclic AMP	91-121	P53	Homo sapiens	44-47
9796984-4	1998	The inhibition of cell growth in FUdR-treated cells by PB was more sustained in U4 than U9 cells and was associated with an increased and sustained expression of p21waf1 protein, secretion of transforming growth factor beta1, mediators of p53-dependent or -independent G1 cell cycle arrest, and an increase in the alkaline phosphatase activity as well, considered a marker of differentiation in colon carcinoma cells.	Phenylbutyrates	55-57	P53	Homo sapiens	239-242
9893672-0	1998	A newly developed adenovirus-mediated transfer of a wild-type p53 gene increases sensitivity to cis-diamminedichloroplatinum (II) in p53-deleted ovarian cancer cells.	Cisplatin	96-124	P53	Homo sapiens	62-65
9893672-0	1998	A newly developed adenovirus-mediated transfer of a wild-type p53 gene increases sensitivity to cis-diamminedichloroplatinum (II) in p53-deleted ovarian cancer cells.	Cisplatin	96-124	P53	Homo sapiens	133-136
9893672-3	1998	It was found that the sensitivity of the cells to CDDP correlated with the amount of infectious units of virus per cell of AxCAp53 which correlated with p53 protein expression.	Cisplatin	50-54	P53	Homo sapiens	127-130
9766444-6	1998	The differentiation response to transfected p53 with or without INF-gamma was inhibited by cyclic adenosine monophosphate (cAMP)-inducing agents (dibutyryl cyclic adenosine 3":5"-monophosphate, forskolin, and 3-isobutyl-1-methylxanthine) in a dose-dependent manner.	Cyclic AMP	123-127	P53	Homo sapiens	44-47
9766444-6	1998	The differentiation response to transfected p53 with or without INF-gamma was inhibited by cyclic adenosine monophosphate (cAMP)-inducing agents (dibutyryl cyclic adenosine 3":5"-monophosphate, forskolin, and 3-isobutyl-1-methylxanthine) in a dose-dependent manner.	5"-monophosphate	176-192	P53	Homo sapiens	44-47
9766444-7	1998	In contrast, the differentiation response of p53-negative U-937 cells to 1,25-dihydroxychole-calciferol or all-trans retinoic acid was enhanced by cAMP-inducing agents at optimal concentrations and inhibited at higher concentrations.	Tretinoin	107-130	P53	Homo sapiens	45-48
9766444-7	1998	In contrast, the differentiation response of p53-negative U-937 cells to 1,25-dihydroxychole-calciferol or all-trans retinoic acid was enhanced by cAMP-inducing agents at optimal concentrations and inhibited at higher concentrations.	Cyclic AMP	147-151	P53	Homo sapiens	45-48
9790097-7	1998	p53 staining following microwave enhancement of alcohol-fixed tissue showed a significant incidence of conversion of negative results to positive and of positive staining in unexpected tissue components.	Alcohols	48-55	P53	Homo sapiens	0-3
9784320-3	1998	p53 expression was studied in archival paraffin-embedded tissue by immunohistochemistry.	Paraffin	39-47	P53	Homo sapiens	0-3
9796924-6	1998	Triggering of sIg induced, within seconds, identical tyrosine phosphorylation of p53/56lyn protein tyrosine kinase (PTK) and p55blk PTK in both of the cell lines; however, a prominent tyrosine phosphorylation and activation of p72syk PTK only in HF-1.3.4 cells.	Tyrosine	53-61	P53	Homo sapiens	81-84
9796924-6	1998	Triggering of sIg induced, within seconds, identical tyrosine phosphorylation of p53/56lyn protein tyrosine kinase (PTK) and p55blk PTK in both of the cell lines; however, a prominent tyrosine phosphorylation and activation of p72syk PTK only in HF-1.3.4 cells.	Tyrosine	99-107	P53	Homo sapiens	81-84
9764849-0	1998	Curcumin induces a p53-dependent apoptosis in human basal cell carcinoma cells.	Curcumin	0-8	P53	Homo sapiens	19-22
9764849-3	1998	In our study, consistent with the occurrence of DNA fragmentation, nuclear p53 protein initially increased at 12 h and peaked at 48 h after curcumin treatment.	Curcumin	140-148	P53	Homo sapiens	75-78
9764849-4	1998	Prior treatment of cells with cycloheximide or actinomycin D abolished the p53 increase and apoptosis induced by curcumin, suggesting that either de novo p53 protein synthesis or some proteins synthesis for stabilization of p53 is required for apoptosis.	Curcumin	113-121	P53	Homo sapiens	75-78
9764849-4	1998	Prior treatment of cells with cycloheximide or actinomycin D abolished the p53 increase and apoptosis induced by curcumin, suggesting that either de novo p53 protein synthesis or some proteins synthesis for stabilization of p53 is required for apoptosis.	Curcumin	113-121	P53	Homo sapiens	154-157
9764849-4	1998	Prior treatment of cells with cycloheximide or actinomycin D abolished the p53 increase and apoptosis induced by curcumin, suggesting that either de novo p53 protein synthesis or some proteins synthesis for stabilization of p53 is required for apoptosis.	Curcumin	113-121	P53	Homo sapiens	154-157
9764849-5	1998	In electrophoretic mobility gel-shift assays, nuclear extracts of cells treated with curcumin displayed distinct patterns of binding between p53 and its consensus binding site.	Curcumin	85-93	P53	Homo sapiens	141-144
9764849-6	1998	Supportive of these findings, p53 downstream targets, including p21(CIP1/WAF1) and Gadd45, could be induced to localize on the nucleus by curcumin with similar p53 kinetics.	Curcumin	138-146	P53	Homo sapiens	30-33
9764849-6	1998	Supportive of these findings, p53 downstream targets, including p21(CIP1/WAF1) and Gadd45, could be induced to localize on the nucleus by curcumin with similar p53 kinetics.	Curcumin	138-146	P53	Homo sapiens	160-163
9764849-10	1998	Finally, treatment of cells with p53 antisense oligonucleotide could effectively prevent curcumin-induced intracellular p53 protein increase and apoptosis, but sense p53 oligonucleotide could not.	Oligonucleotides	47-62	P53	Homo sapiens	33-36
9764849-10	1998	Finally, treatment of cells with p53 antisense oligonucleotide could effectively prevent curcumin-induced intracellular p53 protein increase and apoptosis, but sense p53 oligonucleotide could not.	Oligonucleotides	47-62	P53	Homo sapiens	120-123
9764849-10	1998	Finally, treatment of cells with p53 antisense oligonucleotide could effectively prevent curcumin-induced intracellular p53 protein increase and apoptosis, but sense p53 oligonucleotide could not.	Oligonucleotides	47-62	P53	Homo sapiens	120-123
9764849-10	1998	Finally, treatment of cells with p53 antisense oligonucleotide could effectively prevent curcumin-induced intracellular p53 protein increase and apoptosis, but sense p53 oligonucleotide could not.	Curcumin	89-97	P53	Homo sapiens	33-36
9764849-10	1998	Finally, treatment of cells with p53 antisense oligonucleotide could effectively prevent curcumin-induced intracellular p53 protein increase and apoptosis, but sense p53 oligonucleotide could not.	Curcumin	89-97	P53	Homo sapiens	120-123
9764849-10	1998	Finally, treatment of cells with p53 antisense oligonucleotide could effectively prevent curcumin-induced intracellular p53 protein increase and apoptosis, but sense p53 oligonucleotide could not.	Curcumin	89-97	P53	Homo sapiens	120-123
9764849-10	1998	Finally, treatment of cells with p53 antisense oligonucleotide could effectively prevent curcumin-induced intracellular p53 protein increase and apoptosis, but sense p53 oligonucleotide could not.	Oligonucleotides	170-185	P53	Homo sapiens	33-36
9764849-11	1998	Thus, our data suggest that the p53-associated signaling pathway is critically involved in curcumin-mediated apoptotic cell death.	Curcumin	91-99	P53	Homo sapiens	32-35
9714063-11	1998	Our results suggest an overall association between wild type P53 and radiation and platinum drug sensitivity in these ovarian cancer cell lines.	Platinum	83-91	P53	Homo sapiens	61-64
11245004-1	1998	OBJECTIVE: To establish a tetracycline-regulated expression model and to determine and verify whether a specific point mutant type p53 minigene, containing an Arg--&gt;Leu substitution at amino acid 172, possesses a suppressing effect on human lung cancer.	Arginine	159-162	P53	Homo sapiens	131-134
9794234-1	1998	Dexamethasone (DEX)-mediated inhibition of drug-induced, but not CD95 ligand-induced, apoptosis in malignant glioma cells correlates with wild-type p53 status.	Dexamethasone	0-13	P53	Homo sapiens	148-151
9794234-1	1998	Dexamethasone (DEX)-mediated inhibition of drug-induced, but not CD95 ligand-induced, apoptosis in malignant glioma cells correlates with wild-type p53 status.	Dexamethasone	15-18	P53	Homo sapiens	148-151
9794234-5	1998	p53val135-transfected cells retained responsiveness to DEX at restrictive temperature, suggesting that p53 activity is not required for cytoprotection.	Dexamethasone	55-58	P53	Homo sapiens	0-3
9794234-6	1998	Forced expression of wild-type p53val135 abrogated the protective effect of DEX, suggesting redundant cytoprotective effects of DEX and p53.	Dexamethasone	76-79	P53	Homo sapiens	31-34
9794234-6	1998	Forced expression of wild-type p53val135 abrogated the protective effect of DEX, suggesting redundant cytoprotective effects of DEX and p53.	Dexamethasone	76-79	P53	Homo sapiens	136-139
9794234-6	1998	Forced expression of wild-type p53val135 abrogated the protective effect of DEX, suggesting redundant cytoprotective effects of DEX and p53.	Dexamethasone	128-131	P53	Homo sapiens	31-34
9794234-7	1998	Indeed, DEX induced moderate accumulation of p21WAF1/CIP1 in U87MG, LN-229 and p53 mutant LN-18 cells, but not in p53 mutant LN-308 or T98G cells.	Dexamethasone	8-11	P53	Homo sapiens	79-82
9794234-8	1998	LN-18 is also the p53 mutant cell line with the best cytoprotective response to DEX.	Dexamethasone	80-83	P53	Homo sapiens	18-21
9794234-10	1998	Wild-type p53 was not required for this DEX effect since DEX induced p21WAF1/CIP1 accumulation in p53val135-transfected LN-229 cells, too.	Dexamethasone	57-60	P53	Homo sapiens	98-101
9794234-14	1998	The present study links DEX-mediated protection from cancer chemotherapy to a p53-independent pathway of regulating p21WAF1/CIP1 expression in glioma cells but this effect appears to cell type-specific.	Dexamethasone	24-27	P53	Homo sapiens	78-81
9744860-4	1998	p300 acetylates Lys-382 in the carboxy-terminal region of p53, whereas PCAF acetylates Lys-320 in the nuclear localization signal.	Lysine	16-19	P53	Homo sapiens	58-61
9744860-6	1998	Using a polyclonal antisera specific for p53 that is phosphorylated or acetylated at specific residues, we show that Lys-382 of human p53 becomes acetylated and Ser-33 and Ser-37 become phosphorylated in vivo after exposing cells to UV light or ionizing radiation.	Lysine	117-120	P53	Homo sapiens	41-44
9744860-6	1998	Using a polyclonal antisera specific for p53 that is phosphorylated or acetylated at specific residues, we show that Lys-382 of human p53 becomes acetylated and Ser-33 and Ser-37 become phosphorylated in vivo after exposing cells to UV light or ionizing radiation.	Lysine	117-120	P53	Homo sapiens	134-137
9744860-6	1998	Using a polyclonal antisera specific for p53 that is phosphorylated or acetylated at specific residues, we show that Lys-382 of human p53 becomes acetylated and Ser-33 and Ser-37 become phosphorylated in vivo after exposing cells to UV light or ionizing radiation.	Serine	161-164	P53	Homo sapiens	41-44
9744860-6	1998	Using a polyclonal antisera specific for p53 that is phosphorylated or acetylated at specific residues, we show that Lys-382 of human p53 becomes acetylated and Ser-33 and Ser-37 become phosphorylated in vivo after exposing cells to UV light or ionizing radiation.	Serine	161-164	P53	Homo sapiens	134-137
9744860-6	1998	Using a polyclonal antisera specific for p53 that is phosphorylated or acetylated at specific residues, we show that Lys-382 of human p53 becomes acetylated and Ser-33 and Ser-37 become phosphorylated in vivo after exposing cells to UV light or ionizing radiation.	Serine	172-175	P53	Homo sapiens	41-44
9744860-6	1998	Using a polyclonal antisera specific for p53 that is phosphorylated or acetylated at specific residues, we show that Lys-382 of human p53 becomes acetylated and Ser-33 and Ser-37 become phosphorylated in vivo after exposing cells to UV light or ionizing radiation.	Serine	172-175	P53	Homo sapiens	134-137
9744860-7	1998	In vitro, amino-terminal p53 peptides phosphorylated at Ser-33 and/or at Ser-37 differentially inhibited p53 acetylation by each HAT.	Serine	56-59	P53	Homo sapiens	25-28
9744860-7	1998	In vitro, amino-terminal p53 peptides phosphorylated at Ser-33 and/or at Ser-37 differentially inhibited p53 acetylation by each HAT.	Serine	56-59	P53	Homo sapiens	105-108
9744860-7	1998	In vitro, amino-terminal p53 peptides phosphorylated at Ser-33 and/or at Ser-37 differentially inhibited p53 acetylation by each HAT.	Serine	73-76	P53	Homo sapiens	25-28
9744860-7	1998	In vitro, amino-terminal p53 peptides phosphorylated at Ser-33 and/or at Ser-37 differentially inhibited p53 acetylation by each HAT.	Serine	73-76	P53	Homo sapiens	105-108
9742979-1	1998	BACKGROUND: A polymorphism at codon 72 of the human tumour-suppressor gene, p53, results in translation to either arginine or proline.	Arginine	114-122	P53	Homo sapiens	76-79
9733514-5	1998	ATM phosphorylated p53 in vitro on a single residue, serine-15, which is phosphorylated in vivo in response to DNA damage.	Serine	53-59	P53	Homo sapiens	19-22
9733515-1	1998	The p53 tumor suppressor protein is activated and phosphorylated on serine-15 in response to various DNA damaging agents.	Serine	68-74	P53	Homo sapiens	4-7
9733515-3	1998	Immunoprecipitated ATM had intrinsic protein kinase activity and phosphorylated p53 on serine-15 in a manganese-dependent manner.	Serine	87-93	P53	Homo sapiens	80-83
9733515-5	1998	These observations, along with the fact that phosphorylation of p53 on serine-15 in response to ionizing radiation is reduced in ataxia telangiectasia cells, suggest that ATM is a protein kinase that phosphorylates p53 in vivo.	Serine	71-77	P53	Homo sapiens	64-67
9742979-8	1998	INTERPRETATION: In the population studied, individuals homozygous for the arginine variant of codon 72 of the p53 gene were not at increased risk of cervical cancer.	Arginine	74-82	P53	Homo sapiens	110-113
9731490-7	1998	Given the role of p53 in the response of cells to irradiation, we evaluated whether p53 function affects the observed radiation-induced resistance to cisplatin.	Cisplatin	150-159	P53	Homo sapiens	84-87
14646487-6	1998	One model indicates that p53 induces redox-related genes that generate reactive oxygen species and promote the oxidative degradation of mitochondrial components.	Reactive Oxygen Species	71-94	P53	Homo sapiens	25-28
9743293-8	1998	Thus, although p53-dependent apoptosis is induced by camptothecin, topotecan and SN-38 in this human ovarian carcinoma cell line, these drugs induce p53-independent death, as measured by clonogenic assay.	Irinotecan	81-86	P53	Homo sapiens	15-18
9731490-8	1998	By examining isogenic cell lines differing only in p53 function, we demonstrated that radiation conferred resistance to cisplatin independently of p53.	Cisplatin	120-129	P53	Homo sapiens	51-54
10921032-2	1998	METHODS: The expression of p53 protein and PCNA was examined by means of SP immunohistochemical technique in 32 cases of peripheral lung cancer proved by pathology; the relationship between the results and preoperative CT features was analyzed retrospectively.	TFF2 protein, human	73-75	P53	Homo sapiens	27-30
9713990-6	1998	Under conditions of cellular stress (ultraviolet irradiation or exposure to bleomycin or cisplatin), expression of TP53TG1 was induced in a wild-type TP53-dependent manner, indicating that this gene is likely to play an important role in the signaling pathway of TP53 and may function in response to cellular damage.	Cisplatin	89-98	P53	Homo sapiens	115-119
9713990-6	1998	Under conditions of cellular stress (ultraviolet irradiation or exposure to bleomycin or cisplatin), expression of TP53TG1 was induced in a wild-type TP53-dependent manner, indicating that this gene is likely to play an important role in the signaling pathway of TP53 and may function in response to cellular damage.	Cisplatin	89-98	P53	Homo sapiens	150-154
9712657-5	1998	The activation of alpha-Bgt-AChRs by nicotine results in the induction of the tumor suppressor protein p53 and the cdk inhibitor p21.	Nicotine	37-45	P53	Homo sapiens	103-106
9796399-8	1998	Analysis of the p53 gene by the polymerase chain reaction-single strand conformation polymorphism method showed one base transposition, from TAT to TGT (Tyr to Cys), at codon 220 of exon 6.	Tyrosine	153-156	P53	Homo sapiens	16-19
9796399-8	1998	Analysis of the p53 gene by the polymerase chain reaction-single strand conformation polymorphism method showed one base transposition, from TAT to TGT (Tyr to Cys), at codon 220 of exon 6.	Cysteine	160-163	P53	Homo sapiens	16-19
9771923-12	1998	However, the basal level of p53 was higher in resistant clones and addition of 2- or 4-hydroxyestrone increased p53 to levels equivalent to those observed following UVB irradiation.	2- or 4-hydroxyestrone	79-101	P53	Homo sapiens	112-115
9790785-8	1998	Exons 2 through 11 of the p53 gene were analyzed by direct DNA sequencing, revealing a homozygous mutation at codon 281 in exon 8, GAC to CAC (Asp--&gt;His).	Histidine	152-155	P53	Homo sapiens	26-29
9729267-8	1998	Linear regression analysis detected a significant increase in the number of 6-TG-resistant clones in both AHH-1 tk+/- (p53+/-) and L3 (p53+/+).	Thioguanine	76-80	P53	Homo sapiens	119-122
9729267-8	1998	Linear regression analysis detected a significant increase in the number of 6-TG-resistant clones in both AHH-1 tk+/- (p53+/-) and L3 (p53+/+).	Thioguanine	76-80	P53	Homo sapiens	135-138
9751262-0	1998	p53-independent dephosphorylation and cleavage of retinoblastoma protein during tamoxifen-induced apoptosis in human breast carcinoma cells.	Tamoxifen	80-89	P53	Homo sapiens	0-3
9747884-4	1998	Using antibodies that can detect serine 392-phosphorylation of p53, we demonstrate that UV radiation can trigger extensive phosphorylation at the CK2 site.	Serine	33-39	P53	Homo sapiens	63-66
9747884-6	1998	However, a striking increase in UV-induced serine 392 phosphorylation and p53 transactivation function at higher levels of DRB suggests that a DRB-resistant/stress-activated pathway may target serine 392 in vivo.	Dichlororibofuranosylbenzimidazole	123-126	P53	Homo sapiens	74-77
9747884-6	1998	However, a striking increase in UV-induced serine 392 phosphorylation and p53 transactivation function at higher levels of DRB suggests that a DRB-resistant/stress-activated pathway may target serine 392 in vivo.	Serine	193-199	P53	Homo sapiens	74-77
9747884-7	1998	These data demonstrate that radiation-induced phosphorylation of p53 can occur in vivo at serine 392 and implicate a CK2-independent signal cascade that can function to modulate serine 392 phosphorylation in cells.	Serine	90-96	P53	Homo sapiens	65-68
9747884-7	1998	These data demonstrate that radiation-induced phosphorylation of p53 can occur in vivo at serine 392 and implicate a CK2-independent signal cascade that can function to modulate serine 392 phosphorylation in cells.	Serine	178-184	P53	Homo sapiens	65-68
9751262-2	1998	We show that the treatment of either MCF-7 (containing wild-type p53) or MDA-MB-231 cells (containing mutant p53) with tamoxifen resulted in apoptotic nuclear changes and an increase in the pre-G1 apoptotic population.	Tamoxifen	119-128	P53	Homo sapiens	65-68
9685342-2	1998	E1A expression caused accumulation of wild type p53 more than 10-fold within 24 h after dexamethasone treatment.	Dexamethasone	88-101	P53	Homo sapiens	48-51
9751262-2	1998	We show that the treatment of either MCF-7 (containing wild-type p53) or MDA-MB-231 cells (containing mutant p53) with tamoxifen resulted in apoptotic nuclear changes and an increase in the pre-G1 apoptotic population.	Tamoxifen	119-128	P53	Homo sapiens	109-112
9685342-4	1998	p53 accumulated was degraded efficiently in vitro in the S10-0 extract (S10-0) prepared from MA1 cells in an ATP and ubiquitin-dependent manner, but not in S10-24 prepared after treatment with dexamethasone for 24 h. The p53 polyubiquitination activity in S100-0 was calcium-dependent and reduced greatly in S100-24.	Adenosine Triphosphate	109-112	P53	Homo sapiens	0-3
9685342-4	1998	p53 accumulated was degraded efficiently in vitro in the S10-0 extract (S10-0) prepared from MA1 cells in an ATP and ubiquitin-dependent manner, but not in S10-24 prepared after treatment with dexamethasone for 24 h. The p53 polyubiquitination activity in S100-0 was calcium-dependent and reduced greatly in S100-24.	Dexamethasone	193-206	P53	Homo sapiens	0-3
9773808-0	1998	Mitoguazone induces apoptosis via a p53-independent mechanism.	Mitoguazone	0-11	P53	Homo sapiens	36-39
9685342-4	1998	p53 accumulated was degraded efficiently in vitro in the S10-0 extract (S10-0) prepared from MA1 cells in an ATP and ubiquitin-dependent manner, but not in S10-24 prepared after treatment with dexamethasone for 24 h. The p53 polyubiquitination activity in S100-0 was calcium-dependent and reduced greatly in S100-24.	Calcium	267-274	P53	Homo sapiens	0-3
9773808-8	1998	The present study demonstrated that mitoguazone induces apoptosis in all the different human cancer cell lines tested in a concentration- and time-dependent way, and triggers a p53-independent programmed cell death in the human breast cancer MCF7 cell line.	Mitoguazone	36-47	P53	Homo sapiens	177-180
9703286-0	1998	Therapy effect of either paclitaxel or cyclophosphamide combination treatment in patients with epithelial ovarian cancer and relation to TP53 gene status.	Paclitaxel	25-35	P53	Homo sapiens	137-141
9703286-3	1998	The TP53 status has been analysed at the DNA level in tumours from 45 ovarian cancer patients randomized to treatment with paclitaxel and cisplatin or cyclophosphamide and cisplatin.	Cisplatin	138-147	P53	Homo sapiens	4-8
9703286-3	1998	The TP53 status has been analysed at the DNA level in tumours from 45 ovarian cancer patients randomized to treatment with paclitaxel and cisplatin or cyclophosphamide and cisplatin.	Cisplatin	172-181	P53	Homo sapiens	4-8
9703286-8	1998	When relapse-free survival was estimated for all patients with TP53 alterations in their tumours, a significant better outcome for the paclitaxel/cisplatin group was found compared with the patient group receiving cyclophosphamide and cisplatin therapy (P = 0.002).	Paclitaxel	135-145	P53	Homo sapiens	63-67
9694807-2	1998	The ability of E1A to induce p53 and its transcriptional targets is severely compromised in ARF-null cells, which remain resistant to apoptosis following serum depletion or adriamycin treatment.	Doxorubicin	173-183	P53	Homo sapiens	29-32
9664116-6	1998	Butyrolactone I inhibited proliferation of all colon carcinoma cell lines at 100 microM and it induced apoptosis in LoVo cell line with induction of p53.	butyrolactone I	0-15	P53	Homo sapiens	149-152
9664115-3	1998	Treatment with cisplatin and carboplatin also provoked an increase in the level of p53 and p21, and a lowering in Bcl-2.	Cisplatin	15-24	P53	Homo sapiens	83-86
9677415-0	1998	Cooperation of a single lysine mutation and a C-terminal domain in the cytoplasmic sequestration of the p53 protein.	Lysine	24-30	P53	Homo sapiens	104-107
9712551-2	1998	MATERIAL AND METHODS: The effect of BBI pre-treatment on p53 protein level and on mRNA levels of downstream genes (ERCC3, Gadd45 and p53) was investigated.	Amiodarone	36-39	P53	Homo sapiens	57-60
9712551-4	1998	In non-irradiated cells, pre-incubation with BBI resulted in an increased level of p53 protein.	Amiodarone	45-48	P53	Homo sapiens	83-86
9664139-11	1998	Major differences between DEX and MEL were also observed with respect to their effects on the levels of bcl-2 and p53.	Dexamethasone	26-29	P53	Homo sapiens	114-117
9677415-6	1998	Mutagenesis analysis demonstrated that a single amino acid mutation of Lys-305 (mt p53) caused cytoplasmic sequestration of the p53 protein in the MCF-7 and RKO cells, whereas the fusion protein was distributed in both the cytoplasm and the nucleus of SAOS-2 cells.	Lysine	71-74	P53	Homo sapiens	83-86
9697772-4	1998	We find that hypoxia/hypoglycaemia-regulated genes involved in controlling the cell cycle are either HIF-1alpha-dependent (those encoding the proteins p53, p21, Bcl-2) or HIF-1alpha-independent (p27, GADD153), suggesting that there are at least two different adaptive responses to being deprived of oxygen and nutrients.	Oxygen	299-305	P53	Homo sapiens	151-154
9677415-6	1998	Mutagenesis analysis demonstrated that a single amino acid mutation of Lys-305 (mt p53) caused cytoplasmic sequestration of the p53 protein in the MCF-7 and RKO cells, whereas the fusion protein was distributed in both the cytoplasm and the nucleus of SAOS-2 cells.	Lysine	71-74	P53	Homo sapiens	128-131
9677415-10	1998	Lys-305 is needed for nuclear import of p53 protein, and amino acid residues 326-355 can sequester mt p53 in the cytoplasm.	Lysine	0-3	P53	Homo sapiens	40-43
9677415-10	1998	Lys-305 is needed for nuclear import of p53 protein, and amino acid residues 326-355 can sequester mt p53 in the cytoplasm.	Lysine	0-3	P53	Homo sapiens	102-105
9692554-3	1998	Using mimosine, a p21Waf1/Cip1 inducer that bypasses the requirement for transcriptional transactivation by p53, we demonstrated that a G1 cell cycle arrest can prevent apoptosis following UV-irradiation or treatment with an RNA polymerase 11 inhibitor.	Mimosine	6-14	P53	Homo sapiens	108-111
9710241-1	1998	We examined the mechanism of DNA damage induced by a mutagenic tyrosine metabolite, homogentisic acid (HGA), using 32P-5"-end-labeled DNA fragments obtained from the human p53 tumor suppressor gene.	Homogentisic Acid	84-101	P53	Homo sapiens	172-175
9690520-3	1998	Here we report that exposure of macrophages to lipopolysaccharide/interferon-gamma or lipophilic cAMP analogs such as dibutyryl-cAMP or 8-bromo-cAMP for 15 h attenuated DNA fragmentation and accumulation of the tumor suppressor p53 in response to the chemotherapeutic agents cisplatin and etoposide, compared to cells that received chemotherapeutic agents only.	Cyclic AMP	97-101	P53	Homo sapiens	228-231
9690520-8	1998	Incubating macrophages with decoy, but not with control oligonucleotides, reduced cAMP evoked protection and simultaneously restored p53 accumulation in response to chemotherapeutic agents.	Cyclic AMP	82-86	P53	Homo sapiens	133-136
9690520-9	1998	Our studies demonstrate that cAMP-initiated gene activation regulates the sensitivity towards DNA damaging agents via inhibition of a p53 dependent pathway.	Cyclic AMP	29-33	P53	Homo sapiens	134-137
9651310-6	1998	The cyclic AMP-response element in the PCNA core promoter, besides being crucial for basal transcription, synergizes with p53 to activate transcription.	Cyclic AMP	4-14	P53	Homo sapiens	122-125
9668066-0	1998	Pyrrolidine dithiocarbamate prevents p53 activation and promotes p53 cysteine residue oxidation.	Cysteine	69-77	P53	Homo sapiens	65-68
9668066-9	1998	We found that PDTC increased p53 cysteine residue oxidation in vivo.	Cysteine	33-41	P53	Homo sapiens	29-32
9665463-2	1998	In this study we investigated by immunohistochemistry and Western blotting whether calcium and the phorbol ester 12-O-tetradecanoylphorbol-13-acetate, well characterized differentiation signals, induce p21WAF1 in cultured normal human keratinocytes and whether induction of p21WAF1 in this system depends on protein kinase C activation or functional p53.	Calcium	83-90	P53	Homo sapiens	350-353
9713515-5	1998	RESULTS: The introduction of wild-type p53 gene into HT1376 markedly enhanced the sensitivity to cisplatin in vitro.	Cisplatin	97-106	P53	Homo sapiens	39-42
9688948-4	1998	We found that three mesothelioma cell lines (1 with wild-type p53) were highly resistant to apoptosis induced by oxidant stimuli (asbestos, H2O2) or nonoxidant stimuli (calcium ionophore) compared with primary cultured mesothelial cells.	Hydrogen Peroxide	140-144	P53	Homo sapiens	62-65
9655287-4	1998	Histopathologic/genetic analysis of p53 was performed on formalin fixed, paraffin embedded tissues.	Paraffin	73-81	P53	Homo sapiens	36-39
9703910-0	1998	An exogenous cdk inhibitor, butyrolactone-I, induces apoptosis with increased Bax/Bcl-2 ratio in p53-mutated pancreatic cancer cells.	butyrolactone I	28-43	P53	Homo sapiens	97-100
9703910-5	1998	In butyrolactone-I-treated PANC-1 cells, expression of p53 protein was unchanged, but Bax expression was slightly upregulated and Bcl-2 expression was predominantly down-regulated.	butyrolactone I	3-18	P53	Homo sapiens	55-58
9661907-5	1998	cAMP intracellular levels were higher in thyroid cells transfected with the p53 gene mutated at the 392 site than in the untransfected thyroid cells, but lower in the cells transfected with the other mutated p53 genes.	Cyclic AMP	0-4	P53	Homo sapiens	76-79
9649454-1	1998	BACKGROUND &amp; AIMS: We previously discovered anti-p53 antibodies predating a cancer diagnosis in subjects at increased risk for liver, lung, breast, and prostate cancer.	Adenosine Monophosphate	12-15	P53	Homo sapiens	53-56
9661907-5	1998	cAMP intracellular levels were higher in thyroid cells transfected with the p53 gene mutated at the 392 site than in the untransfected thyroid cells, but lower in the cells transfected with the other mutated p53 genes.	Cyclic AMP	0-4	P53	Homo sapiens	208-211
9661907-7	1998	The results of this study suggest that p53 exerts effects on cAMP transduction pathway in thyroid cells, which are exquisitely sensitive to cAMP.	Cyclic AMP	61-65	P53	Homo sapiens	39-42
9661907-7	1998	The results of this study suggest that p53 exerts effects on cAMP transduction pathway in thyroid cells, which are exquisitely sensitive to cAMP.	Cyclic AMP	140-144	P53	Homo sapiens	39-42
9703382-7	1998	Serum ionized calcium tended to be higher in p53-positive glands in all histopathological groups; however, the difference was only significant in nodular hyperplasias (P = 0.018).	Calcium	14-21	P53	Homo sapiens	45-48
9698467-0	1998	Lisofylline sensitizes p53 mutant human ovarian carcinoma cells to the cytotoxic effects of cis-diamminedichloroplatinum (II).	Cisplatin	92-120	P53	Homo sapiens	23-26
9698467-5	1998	Restoration of wild-type p53 phenotype by transfection of SKOV3 cells with a p53 cDNA expression vector showed reversal of sensitization by Lisofylline to CDDP cytotoxicity.	Cisplatin	155-159	P53	Homo sapiens	25-28
9698467-5	1998	Restoration of wild-type p53 phenotype by transfection of SKOV3 cells with a p53 cDNA expression vector showed reversal of sensitization by Lisofylline to CDDP cytotoxicity.	Cisplatin	155-159	P53	Homo sapiens	77-80
9698467-8	1998	Our results show that the combination of CDDP and Lisofylline preferentially sensitizes p53-defective cancer cells to the cytotoxic effect of CDDP by a yet undetermined mechanism.	Cisplatin	41-45	P53	Homo sapiens	88-91
9698467-8	1998	Our results show that the combination of CDDP and Lisofylline preferentially sensitizes p53-defective cancer cells to the cytotoxic effect of CDDP by a yet undetermined mechanism.	Cisplatin	142-146	P53	Homo sapiens	88-91
9687977-0	1998	Cytotoxic effect of accelerated carbon beams on glioblastoma cell lines with p53 mutation: clonogenic survival and cell-cycle analysis.	Carbon	32-38	P53	Homo sapiens	77-80
9698472-2	1998	Immunostaining for p53 protein was performed on formalin-fixed, paraffin-embedded sections from 158 patients with verified uterine sarcomas using monoclonal p53 antibody (DO-1).	Paraffin	64-72	P53	Homo sapiens	19-22
9652857-7	1998	CONCLUSION: Suppression of heat-induced hsp72 accumulation by CDDP contributes to an interactive hyperthermic enhancement of CDDP cytotoxicity in the cells bearing the wild-type p53 gene.	cddp	125-129	P53	Homo sapiens	178-181
9652857-1	1998	PURPOSE: The kinetics of the accumulation of inducible 72-kD heat shock protein (hsp72) and the activation of heat shock transcriptional factor (HSF) after hyperthermia and/or CDDP treatment in two human glioblastoma cell lines, A-172 having the wild-type p53 gene and T98G having the mutated p53 gene were evaluated.	cddp	176-180	P53	Homo sapiens	256-259
9652857-1	1998	PURPOSE: The kinetics of the accumulation of inducible 72-kD heat shock protein (hsp72) and the activation of heat shock transcriptional factor (HSF) after hyperthermia and/or CDDP treatment in two human glioblastoma cell lines, A-172 having the wild-type p53 gene and T98G having the mutated p53 gene were evaluated.	cddp	176-180	P53	Homo sapiens	293-296
9652857-4	1998	This was due to the p53-dependent inhibition of heat-induced HSF activation by CDDP.	cddp	79-83	P53	Homo sapiens	20-23
9652857-7	1998	CONCLUSION: Suppression of heat-induced hsp72 accumulation by CDDP contributes to an interactive hyperthermic enhancement of CDDP cytotoxicity in the cells bearing the wild-type p53 gene.	cddp	62-66	P53	Homo sapiens	178-181
9687977-1	1998	PURPOSE: The cytotoxic effect of high-LET carbon beams was analysed on p53 mutant and wild-type glioblastoma cell lines.	Carbon	42-48	P53	Homo sapiens	71-74
9687977-7	1998	Although p53 mutants were more resistant than wild-types for all radiation qualities, carbon beams yielded a higher RBE in p53 mutants than in wild-types.	Carbon	86-92	P53	Homo sapiens	123-126
9687977-9	1998	A G1 block was noticed after irradiation with gamma-rays and carbon beams of 20 and 40keV/microm in p53 wild-types.	Carbon	61-67	P53	Homo sapiens	100-103
9687977-11	1998	CONCLUSION: Accelerated carbon beams can yield higher RBE in gamma-resistant glioblastoma cell lines with p53 mutations.	Carbon	24-30	P53	Homo sapiens	106-109
9661637-11	1998	All three cell lines became more sensitive to adriamycin after wt p53 expression, with a 10-fold decrease in IC50 values.	Doxorubicin	46-56	P53	Homo sapiens	66-69
9636999-1	1998	We tested the hypothesis that the instability of the trinucleotide CTG at the myotonic dystrophy (DM) locus could be an intrinsic DNA damage recognisable by the p53 cell-cycle checkpoint system.	trinucleotide	53-66	P53	Homo sapiens	161-164
9666152-8	1998	Antisense oligonucleotides for p53 significantly increased the number of surviving neurons during hypoxic exposure.	Oligonucleotides	10-26	P53	Homo sapiens	31-34
9681825-5	1998	Apoptosis caused by DNA damage induced with gamma-irradiation, doxorubicin or cisplatin, was enhanced in cells expressing wild type p53 as compared to that seen in parental p53 non-producer cells; mutant p53 expressing clones were found to be more resistant to apoptosis induced by these factors.	Doxorubicin	63-74	P53	Homo sapiens	132-135
9681825-5	1998	Apoptosis caused by DNA damage induced with gamma-irradiation, doxorubicin or cisplatin, was enhanced in cells expressing wild type p53 as compared to that seen in parental p53 non-producer cells; mutant p53 expressing clones were found to be more resistant to apoptosis induced by these factors.	Cisplatin	78-87	P53	Homo sapiens	132-135
9652798-1	1998	The prognostic value of the mutation of the p53 tumor suppressor gene in non-small cell lung carcinomas (NSCLC) is controversial and a polymorphism of the p53 gene at codon 72 consisting of two alleles, arginine (Arg) and proline (Pro), has been reported to be associated with the incidence of smoking-related NSCLC.	Arginine	203-211	P53	Homo sapiens	155-158
9652798-1	1998	The prognostic value of the mutation of the p53 tumor suppressor gene in non-small cell lung carcinomas (NSCLC) is controversial and a polymorphism of the p53 gene at codon 72 consisting of two alleles, arginine (Arg) and proline (Pro), has been reported to be associated with the incidence of smoking-related NSCLC.	Arginine	213-216	P53	Homo sapiens	155-158
9667752-4	1998	N-Methyl-N"-nitro-nitrosoguanidine and N-ethyl-N-nitrosourea, two direct-acting genotoxic (DNA-reactive) carcinogens, caused p53 induction as early as 2 h following treatment, with peak increases within 4-12 h. Aflatoxin B1 and 2-acetylaminofluorene, indirect-acting genotoxic carcinogens, caused a later induction of p53, with the peak increase appearing between 16 and 24 h following treatment.	2-Acetylaminofluorene	228-249	P53	Homo sapiens	125-128
9636999-6	1998	The escape of trinucleotide expansion from the p53-mediated DNA repair system could explain some of the biological characteristics of genome instability.	trinucleotide	14-27	P53	Homo sapiens	47-50
9661042-0	1998	Evidence of p53-induced apoptosis in cancer cells exposed to taxol.	Paclitaxel	61-66	P53	Homo sapiens	12-15
9581865-5	1998	Not only murine but also human mutant p53 proteins carrying the mutational hot spot amino acid exchanges 175Arg--&gt;His, 273Arg--&gt;Pro, or 273Arg--&gt;His bound to the Xbal-IgE-MAR-DNA fragment.	Histidine	117-120	P53	Homo sapiens	38-41
9581865-5	1998	Not only murine but also human mutant p53 proteins carrying the mutational hot spot amino acid exchanges 175Arg--&gt;His, 273Arg--&gt;Pro, or 273Arg--&gt;His bound to the Xbal-IgE-MAR-DNA fragment.	Histidine	154-157	P53	Homo sapiens	38-41
9645763-3	1998	In the present study, p53 gene mutations were analyzed on paraffin-embedded specimens from 24 patients with PRS (4 men and 20 women) by polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) followed by direct sequencing.	Paraffin	58-66	P53	Homo sapiens	22-25
9656718-0	1998	[A case of Cronkhite-Canada syndrome with multiple adenomas and a carcinoma of rectum detected after improvement of polyposis due to steroid treatment--an analysis of expression of p53 protein in polyps].	Steroids	133-140	P53	Homo sapiens	181-184
9620776-7	1998	In nonirradiated cells, serines 376 and 378 of p53 were phosphorylated.	Serine	24-31	P53	Homo sapiens	47-50
9584191-7	1998	By comparison, the DNA-damaging drugs methotrexate and doxorubicin had no effect on Bcl2 hyperphosphorylation but induced p53 expression.	Doxorubicin	55-66	P53	Homo sapiens	122-125
9600977-5	1998	These results demonstrate an ultraviolet responsive and specific phosphorylation site at serine-389 of the mouse or serine-392 of the human p53 protein.	Serine	89-95	P53	Homo sapiens	140-143
9600977-5	1998	These results demonstrate an ultraviolet responsive and specific phosphorylation site at serine-389 of the mouse or serine-392 of the human p53 protein.	Serine	116-122	P53	Homo sapiens	140-143
9671115-1	1998	Nitric oxide (NO) promotes apoptotic cell death in the mouse macrophage cell line RAW 264.7 and in the human promyelocytic leukaemia cell line U937, which exemplifies p53-dependent and p53-independent executive death pathways.	Nitric Oxide	0-12	P53	Homo sapiens	167-170
9633517-0	1998	Inactivation of p53 in a human ovarian cancer cell line increases the sensitivity to paclitaxel by inducing G2/M arrest and apoptosis.	Paclitaxel	85-95	P53	Homo sapiens	16-19
9633517-1	1998	Paclitaxel-induced cytotoxicity, cell cycle perturbation, and apoptosis were determined in a human ovarian cancer cell line expressing wt p53 (A2780) and in a subclone (A2780/E6) obtained upon transfection with the product of the E6 gene of the human papilloma virus HPV16.	Paclitaxel	0-10	P53	Homo sapiens	138-141
9633517-2	1998	The inactivation of wt p53 in A2780/E6 was verified by measuring the inability of the clone to induce p53 and p21 expression after paclitaxel treatment.	Paclitaxel	131-141	P53	Homo sapiens	23-26
9633517-3	1998	The p53-negative clone (A2780/E6) was approximately 50-fold more sensitive to paclitaxel than wt p53-expressing A2780 cells.	Paclitaxel	78-88	P53	Homo sapiens	4-7
9633517-5	1998	This different cell cycle arrest was accompanied by increased frequency of paclitaxel-induced p53-independent apoptosis.	Paclitaxel	75-85	P53	Homo sapiens	94-97
9607760-2	1998	A common polymorphism that occurs in the p53 amino-acid sequence results in the presence of either a proline or an arginine at position 72.	Arginine	115-123	P53	Homo sapiens	41-44
9607760-3	1998	The effect of this polymorphism on the susceptibility of p53 to E6-mediated degradation has been investigated and the arginine form of p53 was found to be significantly more susceptible than the proline form.	Arginine	118-126	P53	Homo sapiens	57-60
9607760-3	1998	The effect of this polymorphism on the susceptibility of p53 to E6-mediated degradation has been investigated and the arginine form of p53 was found to be significantly more susceptible than the proline form.	Arginine	118-126	P53	Homo sapiens	135-138
9607760-4	1998	Moreover, allelic analysis of patients with HPV-associated tumours revealed a striking overrepresentation of homozygous arginine-72 p53 compared with the normal population, which indicated that individuals homozygous for arginine 72 are about seven times more susceptible to HPV-associated tumorigenesis than heterozygotes.	Arginine	120-128	P53	Homo sapiens	132-135
9607760-4	1998	Moreover, allelic analysis of patients with HPV-associated tumours revealed a striking overrepresentation of homozygous arginine-72 p53 compared with the normal population, which indicated that individuals homozygous for arginine 72 are about seven times more susceptible to HPV-associated tumorigenesis than heterozygotes.	Arginine	221-229	P53	Homo sapiens	132-135
9671115-1	1998	Nitric oxide (NO) promotes apoptotic cell death in the mouse macrophage cell line RAW 264.7 and in the human promyelocytic leukaemia cell line U937, which exemplifies p53-dependent and p53-independent executive death pathways.	Nitric Oxide	0-12	P53	Homo sapiens	185-188
9576849-0	1998	Molecular analysis of H2O2-induced senescent-like growth arrest in normal human fibroblasts: p53 and Rb control G1 arrest but not cell replication.	Hydrogen Peroxide	22-26	P53	Homo sapiens	93-96
9575138-8	1998	Finally, depletion of doxorubicin-induced endogenous p53 by E6 protein attenuates doxorubicin-stimulated inhibition of HIF, suggesting that a p53 level sufficient for HIF inhibition can be achieved in vivo.	Doxorubicin	22-33	P53	Homo sapiens	53-56
9575138-8	1998	Finally, depletion of doxorubicin-induced endogenous p53 by E6 protein attenuates doxorubicin-stimulated inhibition of HIF, suggesting that a p53 level sufficient for HIF inhibition can be achieved in vivo.	Doxorubicin	22-33	P53	Homo sapiens	142-145
9575138-8	1998	Finally, depletion of doxorubicin-induced endogenous p53 by E6 protein attenuates doxorubicin-stimulated inhibition of HIF, suggesting that a p53 level sufficient for HIF inhibition can be achieved in vivo.	Doxorubicin	82-93	P53	Homo sapiens	53-56
9576849-3	1998	To understand the molecular basis for the H2O2-induced growth arrest, we determined the cell cycle distribution, levels of p53 tumour suppressor and p21 cyclin-dependent kinase inhibitor proteins, and the status of Rb phosphorylation in H2O2-treated cells.	Hydrogen Peroxide	42-46	P53	Homo sapiens	123-126
9575138-8	1998	Finally, depletion of doxorubicin-induced endogenous p53 by E6 protein attenuates doxorubicin-stimulated inhibition of HIF, suggesting that a p53 level sufficient for HIF inhibition can be achieved in vivo.	Doxorubicin	82-93	P53	Homo sapiens	142-145
9576849-6	1998	The level of p53 protein increased 2- to 3-fold within 1.5 h after H2O2 exposure but returned to the control level by 48 h. The induction of p53 protein was dose dependent, beginning at 50-75 microM and reaching a maximum at 100-250 microM.	Hydrogen Peroxide	67-71	P53	Homo sapiens	13-16
9582268-1	1998	The contribution of almost each amino acid side chain to the thermodynamic stability of the tetramerization domain (residues 326-353) of human p53 has been quantitated using 25 mutants with single-residue truncations to alanine (or glycine).	Alanine	220-227	P53	Homo sapiens	143-146
9576849-6	1998	The level of p53 protein increased 2- to 3-fold within 1.5 h after H2O2 exposure but returned to the control level by 48 h. The induction of p53 protein was dose dependent, beginning at 50-75 microM and reaching a maximum at 100-250 microM.	Hydrogen Peroxide	67-71	P53	Homo sapiens	141-144
9576849-10	1998	The induction of p53 by H2O2 was abolished by the iron chelator deferoxamine and the protein synthesis inhibitor cycloheximide.	Hydrogen Peroxide	24-28	P53	Homo sapiens	17-20
9576849-10	1998	The induction of p53 by H2O2 was abolished by the iron chelator deferoxamine and the protein synthesis inhibitor cycloheximide.	Iron	50-54	P53	Homo sapiens	17-20
9576849-14	1998	Thus H2O2-treated cells show a transient elevation of p53, high level of p21, lack of Rb phosphorylation, G1 arrest and inability to replicate when G1 arrest is inactivated.	Hydrogen Peroxide	5-9	P53	Homo sapiens	54-57
9627114-3	1998	Gel shift assays demonstrated that p53 specifically binds to an oligonucleotide derived from the p53 binding site of the p22/PRG1 promoter.	Oligonucleotides	64-79	P53	Homo sapiens	35-38
9605744-3	1998	Using a UvrABC incision method, we have found that cytosine methylation greatly enhances guanine alkylation at all CpG sites in the p53 gene by a variety of carcinogens, including benzo(a)pyrene diol epoxide, benzo(g)chrysene diol epoxide, aflatoxin B1 8,9-epoxide, and N-acetoxy-2-acetylaminofluorene.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	180-207	P53	Homo sapiens	132-135
9605749-3	1998	A carboxyl-terminal fragment containing the last 92 amino acids of p53 (GST-299-390) was sufficient for binding to topoisomerase I. Nanomolar concentrations of either GST-p53 or GST-299-390 enhanced the catalytic activity of purified human topoisomerase I. Purified wild-type human p53 and point mutants Ser-239, Ser-245, and His-273 were equivalent in their enhancement of human topoisomerase I activity.	Serine	304-307	P53	Homo sapiens	67-70
9605749-3	1998	A carboxyl-terminal fragment containing the last 92 amino acids of p53 (GST-299-390) was sufficient for binding to topoisomerase I. Nanomolar concentrations of either GST-p53 or GST-299-390 enhanced the catalytic activity of purified human topoisomerase I. Purified wild-type human p53 and point mutants Ser-239, Ser-245, and His-273 were equivalent in their enhancement of human topoisomerase I activity.	Serine	304-307	P53	Homo sapiens	171-174
9605749-3	1998	A carboxyl-terminal fragment containing the last 92 amino acids of p53 (GST-299-390) was sufficient for binding to topoisomerase I. Nanomolar concentrations of either GST-p53 or GST-299-390 enhanced the catalytic activity of purified human topoisomerase I. Purified wild-type human p53 and point mutants Ser-239, Ser-245, and His-273 were equivalent in their enhancement of human topoisomerase I activity.	Serine	304-307	P53	Homo sapiens	171-174
9605749-3	1998	A carboxyl-terminal fragment containing the last 92 amino acids of p53 (GST-299-390) was sufficient for binding to topoisomerase I. Nanomolar concentrations of either GST-p53 or GST-299-390 enhanced the catalytic activity of purified human topoisomerase I. Purified wild-type human p53 and point mutants Ser-239, Ser-245, and His-273 were equivalent in their enhancement of human topoisomerase I activity.	Serine	313-316	P53	Homo sapiens	67-70
9605749-3	1998	A carboxyl-terminal fragment containing the last 92 amino acids of p53 (GST-299-390) was sufficient for binding to topoisomerase I. Nanomolar concentrations of either GST-p53 or GST-299-390 enhanced the catalytic activity of purified human topoisomerase I. Purified wild-type human p53 and point mutants Ser-239, Ser-245, and His-273 were equivalent in their enhancement of human topoisomerase I activity.	Serine	313-316	P53	Homo sapiens	171-174
9605749-3	1998	A carboxyl-terminal fragment containing the last 92 amino acids of p53 (GST-299-390) was sufficient for binding to topoisomerase I. Nanomolar concentrations of either GST-p53 or GST-299-390 enhanced the catalytic activity of purified human topoisomerase I. Purified wild-type human p53 and point mutants Ser-239, Ser-245, and His-273 were equivalent in their enhancement of human topoisomerase I activity.	Serine	313-316	P53	Homo sapiens	171-174
9605749-3	1998	A carboxyl-terminal fragment containing the last 92 amino acids of p53 (GST-299-390) was sufficient for binding to topoisomerase I. Nanomolar concentrations of either GST-p53 or GST-299-390 enhanced the catalytic activity of purified human topoisomerase I. Purified wild-type human p53 and point mutants Ser-239, Ser-245, and His-273 were equivalent in their enhancement of human topoisomerase I activity.	Histidine	326-329	P53	Homo sapiens	67-70
9605749-3	1998	A carboxyl-terminal fragment containing the last 92 amino acids of p53 (GST-299-390) was sufficient for binding to topoisomerase I. Nanomolar concentrations of either GST-p53 or GST-299-390 enhanced the catalytic activity of purified human topoisomerase I. Purified wild-type human p53 and point mutants Ser-239, Ser-245, and His-273 were equivalent in their enhancement of human topoisomerase I activity.	Histidine	326-329	P53	Homo sapiens	171-174
9605749-3	1998	A carboxyl-terminal fragment containing the last 92 amino acids of p53 (GST-299-390) was sufficient for binding to topoisomerase I. Nanomolar concentrations of either GST-p53 or GST-299-390 enhanced the catalytic activity of purified human topoisomerase I. Purified wild-type human p53 and point mutants Ser-239, Ser-245, and His-273 were equivalent in their enhancement of human topoisomerase I activity.	Histidine	326-329	P53	Homo sapiens	171-174
9627114-3	1998	Gel shift assays demonstrated that p53 specifically binds to an oligonucleotide derived from the p53 binding site of the p22/PRG1 promoter.	Oligonucleotides	64-79	P53	Homo sapiens	97-100
9627114-8	1998	Gamma-irradiation of rat splenocytes or doxorubicin-treatment of Hela cells increased p53 levels followed by transcriptional activation of p22/PRG1 and p21/Waf1 in parallel.	Doxorubicin	40-51	P53	Homo sapiens	86-89
9620551-0	1998	Human male germ cell tumor resistance to cisplatin is linked to TP53 gene mutation.	Cisplatin	41-50	P53	Homo sapiens	64-68
9607583-9	1998	In this study, we also present data linking specific p53 point mutations to TS expression levels and resistance to 5-FU.	Fluorouracil	115-119	P53	Homo sapiens	53-56
9620551-8	1998	The simplest explanation for the resistance of this subset of GCTs that are resistant to cisplatin-based chemotherapy, is the inability of the cells to mount an apoptotic response following exposure due to a functionally inactivating mutation in the TP53 gene.	Cisplatin	89-98	P53	Homo sapiens	250-254
9620557-4	1998	Moreover, a HeLa clone stably transfected with a temperature sensitive (ts) 143 Ala p53 mutant exhibited temperature-dependent regulation of H19 expression.	Alanine	80-83	P53	Homo sapiens	84-87
9635829-0	1998	Expression of p53, Bcl-2 and Bax in cisplatin-induced apoptosis in testicular germ cell tumour cell lines.	Cisplatin	36-45	P53	Homo sapiens	14-17
9635829-5	1998	We next analysed the relationship between p53 status and cisplatin-induced up-regulation of p53, and the susceptibility to cisplatin-induced apoptosis.	Cisplatin	57-66	P53	Homo sapiens	42-45
9635829-5	1998	We next analysed the relationship between p53 status and cisplatin-induced up-regulation of p53, and the susceptibility to cisplatin-induced apoptosis.	Cisplatin	57-66	P53	Homo sapiens	92-95
9635829-11	1998	The present study suggests that, at least in our panel of TGCT cell lines, hypersensitivity for cisplatin-induced apoptosis might not be necessarily correlated with the presence of wild-type p53 and is probably not associated with Bcl-2 and Bax expression.	Cisplatin	96-105	P53	Homo sapiens	191-194
9595036-8	1998	Strong positive nuclear staining of the p53 protein was detected in both normal and tumor paraffin-embedded tissues.	Paraffin	90-98	P53	Homo sapiens	40-43
9652752-5	1998	In fact, in A2780 cells, TX (with or without CDDP) treatment markedly increased p53 as well as p21waf1 protein expression.	Cisplatin	45-49	P53	Homo sapiens	80-83
9602097-9	1998	Given that both p53 and Myc have been implicated in gene signalling pathways which mediate programmed cell death, our findings which demonstrate that 4-VO produces persistent elevations of p53- and Myc-like immunoreactivities in vulnerable neurons suggest that these proteins may also contribute to delayed neuronal death following an episode of transient forebrain ischemia.	4-vo	150-154	P53	Homo sapiens	16-19
9602097-9	1998	Given that both p53 and Myc have been implicated in gene signalling pathways which mediate programmed cell death, our findings which demonstrate that 4-VO produces persistent elevations of p53- and Myc-like immunoreactivities in vulnerable neurons suggest that these proteins may also contribute to delayed neuronal death following an episode of transient forebrain ischemia.	4-vo	150-154	P53	Homo sapiens	189-192
9607592-3	1998	The sensitization ratio due to the transfected wt p53 varied from about 2-fold for cisplatin to over 50-fold for thymidine.	Cisplatin	83-92	P53	Homo sapiens	50-53
9797696-10	1998	There was a statistically significant dose-response effect of platinum-based chemotherapy in patients with p53 negative tumours, which could not be seen in patients with p53 positive tumours (P = 0.01 versus P = 0.553).	Platinum	62-70	P53	Homo sapiens	107-110
9628583-0	1998	Induction of p53 without increase in p21WAF1 in betulinic acid-mediated cell death is preferential for human metastatic melanoma.	betulinic acid	48-62	P53	Homo sapiens	13-16
9628583-4	1998	Our data suggest that betulinic acid exerts its inhibitory effect partly by increasing p53 without a comparable effect on p21WAF1.	betulinic acid	22-36	P53	Homo sapiens	87-90
9797697-4	1998	Immunohistochemical expression of p53 protein was evaluated in formalin-fixed paraffin-embedded sections of CRC liver metastases using the monoclonal antibodies (MAbs) D01 and Pab 1801.	Paraffin	78-86	P53	Homo sapiens	34-37
9620358-4	1998	After stimulation with anti-CD3 monoclonal antibody (mAb) OKT3 and phorbol myristate acetate (PMA), T cells from young humans exhibited severalfold increases in p53 protein expression compared with resting T cells.	Tetradecanoylphorbol Acetate	67-92	P53	Homo sapiens	161-164
9579543-3	1998	p53 protein immunohistochemistry was performed on 37 paraffin embedded biopsies from 27 patients with CTCL; LCT was present in 15 biopsies.	Paraffin	53-61	P53	Homo sapiens	0-3
9620358-4	1998	After stimulation with anti-CD3 monoclonal antibody (mAb) OKT3 and phorbol myristate acetate (PMA), T cells from young humans exhibited severalfold increases in p53 protein expression compared with resting T cells.	Tetradecanoylphorbol Acetate	94-97	P53	Homo sapiens	161-164
9610658-7	1998	CONCLUSIONS: Immunohistochemically detected p53 protein status in NSCLC patients may be a promising indicator in determining in vitro chemosensitivity to some anticancer drugs, especially 5-Fu and ADM.	Fluorouracil	188-192	P53	Homo sapiens	44-47
9584207-8	1998	These data suggest that apoptosis in A2780 and A2780/cp70 is associated with an increased level of Bak and 21 kDa Bax after drug-induced damage and that functional p53 may be required for this effect after cisplatin but not after paclitaxel.	Cisplatin	206-215	P53	Homo sapiens	164-167
9584207-8	1998	These data suggest that apoptosis in A2780 and A2780/cp70 is associated with an increased level of Bak and 21 kDa Bax after drug-induced damage and that functional p53 may be required for this effect after cisplatin but not after paclitaxel.	Paclitaxel	230-240	P53	Homo sapiens	164-167
9584207-0	1998	Cisplatin- and paclitaxel-induced apoptosis of ovarian carcinoma cells and the relationship between bax and bak up-regulation and the functional status of p53.	Cisplatin	0-9	P53	Homo sapiens	155-158
9584207-0	1998	Cisplatin- and paclitaxel-induced apoptosis of ovarian carcinoma cells and the relationship between bax and bak up-regulation and the functional status of p53.	Paclitaxel	15-25	P53	Homo sapiens	155-158
9588214-6	1998	As expected, PD98059 inhibited induction of p53 mRNA and p21WAF1/CIP1 promoter by IGF I.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	13-20	P53	Homo sapiens	44-47
9584207-1	1998	We investigated the roles of p53 and Bcl-2 homologues in the induction of apoptosis by cisplatin and paclitaxel in wild-type p53-expressing human ovarian carcinoma cells and cisplatin-resistant derivatives that have lost p53 function.	Cisplatin	87-96	P53	Homo sapiens	29-32
9584207-1	1998	We investigated the roles of p53 and Bcl-2 homologues in the induction of apoptosis by cisplatin and paclitaxel in wild-type p53-expressing human ovarian carcinoma cells and cisplatin-resistant derivatives that have lost p53 function.	Paclitaxel	101-111	P53	Homo sapiens	125-128
9584207-1	1998	We investigated the roles of p53 and Bcl-2 homologues in the induction of apoptosis by cisplatin and paclitaxel in wild-type p53-expressing human ovarian carcinoma cells and cisplatin-resistant derivatives that have lost p53 function.	Paclitaxel	101-111	P53	Homo sapiens	125-128
9531612-2	1998	We examined the role of the p53 tumor suppressor gene in hematopoietic recovery in vivo after treatment with the cytotoxic drug 5-fluorouracil (5-FU).	Fluorouracil	128-142	P53	Homo sapiens	28-31
9619832-11	1998	However, the adriamycin-induced reduction in BRCA1 and BRCA2 mRNA levels was correlated with p53 functional status.	Doxorubicin	13-23	P53	Homo sapiens	93-96
9619832-12	1998	MCF-7 cells transfected with a dominant negative mutant p53 (143 val--&gt;ala) required at least tenfold higher doses of adriamycin to down-regulate BRCA1 and BRCA2 mRNAs than did parental MCF-7 cells or control-transfected MCF-7 clones.	Doxorubicin	121-131	P53	Homo sapiens	56-59
9619834-8	1998	The p53 gene was found to be wild-type in all cases where mdm2-P2 levels were induced by cisplatin.	Cisplatin	89-98	P53	Homo sapiens	4-7
9531612-2	1998	We examined the role of the p53 tumor suppressor gene in hematopoietic recovery in vivo after treatment with the cytotoxic drug 5-fluorouracil (5-FU).	Fluorouracil	144-148	P53	Homo sapiens	28-31
9531612-4	1998	Analysis of the repopulation ability and clonogenic activity of hematopoietic stem cells (HSCs) and their lineage-committed descendants showed a greater number of HSCs responsible for reconstitution of lethally irradiated recipients in p53-/- bone marrow cells (BMCs) recovering after 5-FU treatment than in the corresponding p53+/+ BMCs.	Fluorouracil	285-289	P53	Homo sapiens	236-239
9531612-7	1998	The pool of HSCs from 5-FU-treated p53-/- BMCs was exhausted more slowly than that from the p53+/+ population as shown in vivo using pre-spleen colony-forming unit (CFU-S) assay and in vitro using long-term culture-initiating cells (LTC-ICs) and methylcellulose replating assays.	Fluorouracil	22-26	P53	Homo sapiens	35-38
9531612-9	1998	Despite all these changes and the dramatic difference in sensitivity of p53-/- and p53+/+ BMCs to 5-FU-induced apoptosis, lineage commitment and differentiation of hematopoietic progenitors appeared to be independent of p53 status.	Fluorouracil	98-102	P53	Homo sapiens	72-75
9531612-9	1998	Despite all these changes and the dramatic difference in sensitivity of p53-/- and p53+/+ BMCs to 5-FU-induced apoptosis, lineage commitment and differentiation of hematopoietic progenitors appeared to be independent of p53 status.	Fluorouracil	98-102	P53	Homo sapiens	83-86
9563466-1	1998	The death receptor (DR) KILLER/DR5 gene has recently been identified as a doxorubicin-regulated transcript that was also induced by exogenous wild-type p53 in p53-negative cells.	Doxorubicin	74-85	P53	Homo sapiens	152-155
9531612-9	1998	Despite all these changes and the dramatic difference in sensitivity of p53-/- and p53+/+ BMCs to 5-FU-induced apoptosis, lineage commitment and differentiation of hematopoietic progenitors appeared to be independent of p53 status.	Fluorouracil	98-102	P53	Homo sapiens	83-86
9563466-1	1998	The death receptor (DR) KILLER/DR5 gene has recently been identified as a doxorubicin-regulated transcript that was also induced by exogenous wild-type p53 in p53-negative cells.	Doxorubicin	74-85	P53	Homo sapiens	159-162
9563490-7	1998	N-Acetylcysteine elevated p53 expression posttranscriptionally by increasing the rate of p53 mRNA translation rather than by altering the protein stability.	Acetylcysteine	0-16	P53	Homo sapiens	26-29
9563490-7	1998	N-Acetylcysteine elevated p53 expression posttranscriptionally by increasing the rate of p53 mRNA translation rather than by altering the protein stability.	Acetylcysteine	0-16	P53	Homo sapiens	89-92
9607618-9	1998	p53 mutant status was assessed immunohistochemically from sections of the formalin-fixed, paraffin-embedded pretreatment biopsy and the resected specimen.	Paraffin	90-98	P53	Homo sapiens	0-3
9636834-1	1998	BACKGROUND: Alteration in apoptosis pathways (in particular mutations of p53 gene) may result in resistance of ovarian carcinoma to cisplatin.	Cisplatin	132-141	P53	Homo sapiens	73-76
9636834-18	1998	Finally, the finding that Taxol was very effective in inducing apoptosis in resistant sublines with p53 mutation supports the expression of an intact p53-independent pathway of apoptosis and suggests the pharmacological interest of Taxol in the treatment of p53-mutated tumors.	Paclitaxel	26-31	P53	Homo sapiens	100-103
9548807-9	1998	Inhibition of ROS production by the antioxidant enzyme catalase reduced AZQ- and DZQ-mediated p53 induction by about 45%.	Reactive Oxygen Species	14-17	P53	Homo sapiens	94-97
9636834-18	1998	Finally, the finding that Taxol was very effective in inducing apoptosis in resistant sublines with p53 mutation supports the expression of an intact p53-independent pathway of apoptosis and suggests the pharmacological interest of Taxol in the treatment of p53-mutated tumors.	Paclitaxel	26-31	P53	Homo sapiens	150-153
9636834-18	1998	Finally, the finding that Taxol was very effective in inducing apoptosis in resistant sublines with p53 mutation supports the expression of an intact p53-independent pathway of apoptosis and suggests the pharmacological interest of Taxol in the treatment of p53-mutated tumors.	Paclitaxel	26-31	P53	Homo sapiens	150-153
9636834-18	1998	Finally, the finding that Taxol was very effective in inducing apoptosis in resistant sublines with p53 mutation supports the expression of an intact p53-independent pathway of apoptosis and suggests the pharmacological interest of Taxol in the treatment of p53-mutated tumors.	Paclitaxel	232-237	P53	Homo sapiens	100-103
9636834-18	1998	Finally, the finding that Taxol was very effective in inducing apoptosis in resistant sublines with p53 mutation supports the expression of an intact p53-independent pathway of apoptosis and suggests the pharmacological interest of Taxol in the treatment of p53-mutated tumors.	Paclitaxel	232-237	P53	Homo sapiens	150-153
9636834-18	1998	Finally, the finding that Taxol was very effective in inducing apoptosis in resistant sublines with p53 mutation supports the expression of an intact p53-independent pathway of apoptosis and suggests the pharmacological interest of Taxol in the treatment of p53-mutated tumors.	Paclitaxel	232-237	P53	Homo sapiens	150-153
9548807-5	1998	In this study, we investigated the ability of diaziridinylbenzoquinones to increase p53 levels in the human breast cancer cell line MCF-7.	diaziridinylbenzoquinones	46-71	P53	Homo sapiens	84-87
9546285-10	1998	Only one PCNSL showed a mutation of the TP53 gene, i.e., a missense mutation at codon 248 (CGG to TGG:Arg to Trp).	Arginine	102-105	P53	Homo sapiens	40-44
9546285-10	1998	Only one PCNSL showed a mutation of the TP53 gene, i.e., a missense mutation at codon 248 (CGG to TGG:Arg to Trp).	Tryptophan	109-112	P53	Homo sapiens	40-44
9529014-5	1998	Immunohistochemical staining of the paraffin sections was performed using monoclonal antibodies to cyclin E and p53.	Paraffin	36-44	P53	Homo sapiens	112-115
9548807-11	1998	The nonalkylator oxygen-radical-generating agent menadione (MD) caused p53 induction only when MCF-7 cells were allowed to recover in drug-free media.	Reactive Oxygen Species	17-31	P53	Homo sapiens	71-74
9553810-0	1998	Random nuclear p53 overexpression pattern in tamoxifen-mediated endometrial carcinoma.	Tamoxifen	45-54	P53	Homo sapiens	15-18
9609668-0	1998	Simultaneous detection of p53 nuclear protein and chromosome aberrations on sections from formalin-fixed, paraffin-embedded breast cancer tissue.	Paraffin	106-114	P53	Homo sapiens	26-29
9499438-0	1998	Upregulation of p21WAF1/CIP1 in human breast cancer cell lines MCF-7 and MDA-MB-468 undergoing apoptosis induced by natural product anticancer drugs 10-hydroxycamptothecin and camptothecin through p53-dependent and independent pathways.	10-hydroxycamptothecin	149-171	P53	Homo sapiens	197-200
9499438-6	1998	The levels of p53 and p21WAF1/CIP1 protein increased in MCF-7 cells treated with HCPT or CPT in a dose- and time-dependent manner.	10-hydroxycamptothecin	81-85	P53	Homo sapiens	14-17
9563876-15	1998	In the p53null SK-OV-3 xenograft model of ovarian cancer, a dosing schedule of p53 Ad that, by itself, had a relatively minimal effect on tumor burden (16%) caused a much greater decrease in tumor burden (55%) when combined with paclitaxel.	Paclitaxel	229-239	P53	Homo sapiens	7-10
9563876-15	1998	In the p53null SK-OV-3 xenograft model of ovarian cancer, a dosing schedule of p53 Ad that, by itself, had a relatively minimal effect on tumor burden (16%) caused a much greater decrease in tumor burden (55%) when combined with paclitaxel.	Paclitaxel	229-239	P53	Homo sapiens	79-82
9563876-17	1998	In summary, p53 Ad for cancer shows enhanced efficacy when combined with paclitaxel.	Paclitaxel	73-83	P53	Homo sapiens	12-15
9563901-1	1998	In the present study, we report our findings on the impact of p53 disruption on the sensitivity of human cell lines to the antimitotic agents Taxol and vincristine.	Paclitaxel	142-147	P53	Homo sapiens	62-65
9563901-5	1998	We also found that contrary to gamma-irradiation, Taxol and vincristine could induce apoptosis in lymphoma cell lines harboring p53 mutations.	Paclitaxel	50-55	P53	Homo sapiens	128-131
9563901-9	1998	The effect of p53 disruption on Taxol sensitivity was explored further in the breast carcinoma MCF-7 and colon carcinoma HCT-116 cell lines that had been stably transfected with either the human papillomavirus type-16 E6 gene or a dominant-negative mutant p53 gene.	Paclitaxel	32-37	P53	Homo sapiens	14-17
9535218-2	1998	We found that induction of apoptosis in Mphi by oxLDL, C2-ceramide, tumor necrosis factor alpha (TNF-alpha), and hydrogen peroxide (H2O2) was associated with enhanced expression of manganese superoxide dismutase (MnSOD) and p53.	Hydrogen Peroxide	132-136	P53	Homo sapiens	224-227
9535218-3	1998	Treatment of cells with p53 or MnSOD antisense oligonucleotides prior to stimulation with oxLDL, C2-ceramide, TNF-alpha, or H2O2 caused an inhibition of the expression of the respective protein together with a marked reduction of apoptosis.	Hydrogen Peroxide	124-128	P53	Homo sapiens	24-27
9535218-4	1998	Exposure to N-acetylcysteine before treatment with oxLDL, C2-ceramide, TNF-alpha, or H2O2 reversed a decrease in cellular glutathione concentrations as well as the enhanced production of p53 and MnSOD mRNA and protein.	Acetylcysteine	12-28	P53	Homo sapiens	187-190
9535218-4	1998	Exposure to N-acetylcysteine before treatment with oxLDL, C2-ceramide, TNF-alpha, or H2O2 reversed a decrease in cellular glutathione concentrations as well as the enhanced production of p53 and MnSOD mRNA and protein.	Hydrogen Peroxide	85-89	P53	Homo sapiens	187-190
9499438-11	1998	These results suggest that treatment with HCPT and CPT results in increased levels of p21WAF1/CIP1 protein and mRNA, and that they induce apoptosis in human breast cancer cells through both p53-dependent and -independent pathways.	10-hydroxycamptothecin	42-46	P53	Homo sapiens	190-193
9553810-6	1998	Diffuse and intense nuclear reactivity for p53 protein was present in only one TAM-related case.	Tamoxifen	79-82	P53	Homo sapiens	43-46
10923485-2	1998	METHODS: The expression of HCV NS3 and P53 protein was detected by immuno-histochemical technique (SP method) in specimens of HCC and their surrounding liver tissues from 47 patients with negative HBV.	TFF2 protein, human	99-101	P53	Homo sapiens	39-42
9515788-3	1998	We analyzed p53 mutations on paraffin-embedded specimens from 21 patients with PAL by PCR-single-strand conformational polymorphism followed by direct sequencing.	Paraffin	29-37	P53	Homo sapiens	12-15
9506540-3	1998	When p53 was expressed at sublethal levels, it sensitized cells to the DNA-damaging drugs Adriamycin, mitomycin C, actinomycin D, etoposide (VP16), cisplatin and CPT11.	Doxorubicin	90-100	P53	Homo sapiens	5-8
9506540-3	1998	When p53 was expressed at sublethal levels, it sensitized cells to the DNA-damaging drugs Adriamycin, mitomycin C, actinomycin D, etoposide (VP16), cisplatin and CPT11.	Cisplatin	148-157	P53	Homo sapiens	5-8
9506540-3	1998	When p53 was expressed at sublethal levels, it sensitized cells to the DNA-damaging drugs Adriamycin, mitomycin C, actinomycin D, etoposide (VP16), cisplatin and CPT11.	Irinotecan	162-167	P53	Homo sapiens	5-8
9515799-12	1998	In stage III, adjuvant therapy with 5FU plus levamisole improved 7-year survival in patients with wild-type Ki-ras (76 versus 44%; HR, 0.4; 95% CI, 0.2-0.8) and in those without p53 overexpression (64 versus 26%; HR, 0.3; 95% CI, 0.1-0.7).	Fluorouracil	36-39	P53	Homo sapiens	178-181
9546425-1	1998	Using UvrABC incision in combination with ligation-mediated PCR (LMPCR) we have previously shown that benzo(a)pyrene diol epoxide (BPDE) adduct formation along the nontranscribed strand of the human p53 gene is highly selective; the preferential binding sites coincide with the major mutation hotspots found in human lung cancers.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	102-129	P53	Homo sapiens	199-202
9546425-1	1998	Using UvrABC incision in combination with ligation-mediated PCR (LMPCR) we have previously shown that benzo(a)pyrene diol epoxide (BPDE) adduct formation along the nontranscribed strand of the human p53 gene is highly selective; the preferential binding sites coincide with the major mutation hotspots found in human lung cancers.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	131-135	P53	Homo sapiens	199-202
9519827-6	1998	However, p53 is only degraded early in the infectious cycle due to a lack of ATP at later times.	Adenosine Triphosphate	77-80	P53	Homo sapiens	9-12
9528861-2	1998	In the HCT116 colon carcinoma cell line, which retains a wild-type inducible p53 gene, we show that the anthracycline daunomycin is a potent inducer of p53 and NF-kappaB transcription factors.	Anthracyclines	104-117	P53	Homo sapiens	77-80
9528861-2	1998	In the HCT116 colon carcinoma cell line, which retains a wild-type inducible p53 gene, we show that the anthracycline daunomycin is a potent inducer of p53 and NF-kappaB transcription factors.	Anthracyclines	104-117	P53	Homo sapiens	152-155
9492043-5	1998	Similarly, wild-type p53 decreased IGF-I-induced tyrosine phosphorylation of IRS-1.	Tyrosine	49-57	P53	Homo sapiens	21-24
9492043-10	1998	In conclusion, p53 regulates IGF-IR expression, as reflected by a reduction in IGF-IR protein and a parallel reduction in IGF-I-induced tyrosine phosphorylation of the IGF-IR and IRS-1 in an osteosarcoma cell line.	Tyrosine	136-144	P53	Homo sapiens	15-18
9488661-7	1998	The results suggest that p53 can form disulfides and that these disulfides must be reduced in order for the protein to function as a transcription factor.	Disulfides	38-48	P53	Homo sapiens	25-28
9488661-7	1998	The results suggest that p53 can form disulfides and that these disulfides must be reduced in order for the protein to function as a transcription factor.	Disulfides	64-74	P53	Homo sapiens	25-28
9578140-6	1998	Upon treatment with epidermal growth factor (EGF) and dibutyrylcyclic AMP, overall cytoplasmic GFAP and GS levels were increased while nuclear p53 was suppressed but a mutually exclusive expression pattern between these proteins was maintained.	Adenosine Monophosphate	70-73	P53	Homo sapiens	143-146
9492043-0	1998	p53 regulates insulin-like growth factor-I (IGF-I) receptor expression and IGF-I-induced tyrosine phosphorylation in an osteosarcoma cell line: interaction between p53 and Sp1.	Tyrosine	89-97	P53	Homo sapiens	0-3
9472095-1	1998	The polymorphism of p53 gene at codon 72 consisting of either arginine (Arg)- or proline (Pro)-encoded allele is suggested to be associated with the susceptibility of tobacco-related lung cancer.	Arginine	62-70	P53	Homo sapiens	20-23
9472095-1	1998	The polymorphism of p53 gene at codon 72 consisting of either arginine (Arg)- or proline (Pro)-encoded allele is suggested to be associated with the susceptibility of tobacco-related lung cancer.	Arginine	72-75	P53	Homo sapiens	20-23
9472102-9	1998	In a cell clone derived from line VMCub1 by stable transfection with wild-type p53 under the control of a metallothionein promotor, p21 was induced along with p53 upon activation of the promoter with zinc chloride.	zinc chloride	200-213	P53	Homo sapiens	79-82
9472102-9	1998	In a cell clone derived from line VMCub1 by stable transfection with wild-type p53 under the control of a metallothionein promotor, p21 was induced along with p53 upon activation of the promoter with zinc chloride.	zinc chloride	200-213	P53	Homo sapiens	159-162
9488455-5	1998	Unexpectedly, UVC treatment was also found to block the induction of p21Waf1 by various stress-inducing agents such as mimosine in the p53-deficient cells.	Mimosine	119-127	P53	Homo sapiens	135-138
9740272-3	1998	One case harbored a p53 gene mutation in codon 282 in exon 8, CGG (arginine) to TGG (tryptophan), but the mutation was not found in other patient"s tissues with similar histological features.	Arginine	67-75	P53	Homo sapiens	20-23
9682769-6	1998	p53 protein expression was evaluated by immunohistochemistry (IHC) on paraffin-embedded sections.	Paraffin	70-78	P53	Homo sapiens	0-3
9499782-15	1998	This mutation, characteristic of bulky carcinogens, substituted phenylalanine for cysteine 277, a residue that participates in hydrogen bonding to the p53 DNA binding consensus sequence.	Hydrogen	127-135	P53	Homo sapiens	151-154
9740272-3	1998	One case harbored a p53 gene mutation in codon 282 in exon 8, CGG (arginine) to TGG (tryptophan), but the mutation was not found in other patient"s tissues with similar histological features.	Tryptophan	85-95	P53	Homo sapiens	20-23
9485322-8	1998	In this paper, we report that S100B(beta beta) binds to the p53 peptide (CaK3 &lt; or = 23.5 +/- 6.6 microM) in a Ca(2+)-dependent manner, and that the presence of the p53 peptide was found to increase the binding affinity of Ca2+ to S100B(beta beta) by 3-fold using EPR and PRR methods, whereas the peptide had no effect on Zn2+ binding to S100B(beta beta).	Zinc	325-329	P53	Homo sapiens	60-63
10920952-3	1998	RESULTS: p53 gene mutation was detected in 60.1% of cancer, 31.3% of Dys and 11.8% of IM.	dys	69-72	P53	Homo sapiens	9-12
9479003-4	1998	Moreover, we established that 3-methyladenine, a relatively minor DNA lesion produced by most methylating agents (which form mainly 7-methylguanine), can specifically induce sister chromatid exchange, chromatid and chromosome gaps and breaks, S phase arrest, the accumulation of p53, and apoptosis.	3-methyladenine	30-45	P53	Homo sapiens	279-282
9454845-9	1998	The glutamate-induced increase in Bax protein was dependent on the presence of the p53 gene.	Glutamic Acid	4-13	P53	Homo sapiens	83-86
9485023-0	1998	Independent pathways of p53 induction by cisplatin and X-rays in a cisplatin-resistant ovarian tumor cell line.	Cisplatin	41-50	P53	Homo sapiens	24-27
9485023-0	1998	Independent pathways of p53 induction by cisplatin and X-rays in a cisplatin-resistant ovarian tumor cell line.	Cisplatin	67-76	P53	Homo sapiens	24-27
9485023-2	1998	Our studies were initiated by asking whether the translational product of the p53 gene is associated with cisplatin resistance in the 2780CP human ovarian tumor model.	Cisplatin	106-115	P53	Homo sapiens	78-81
9485023-3	1998	We have demonstrated by single-strand conformation polymorphism analysis and sequencing that p53 in parental cisplatin-sensitive A2780 cells was wild type.	Cisplatin	109-118	P53	Homo sapiens	93-96
9485023-9	1998	In parallel investigations using the Western technique, exposure of A2780 cells to clinically relevant concentrations of cisplatin (1-20 microM) resulted in time- and dose-dependent increases in p53, together with coordinate increases in p21Waf1/Cip1.	Cisplatin	121-130	P53	Homo sapiens	195-198
9485023-11	1998	The results indicate that a defect exists in the signal transduction pathway for p53 induction following cisplatin-induced DNA damage in 2780CP cells, and this may represent a significant mechanism of cisplatin resistance.	Cisplatin	105-114	P53	Homo sapiens	81-84
9485023-11	1998	The results indicate that a defect exists in the signal transduction pathway for p53 induction following cisplatin-induced DNA damage in 2780CP cells, and this may represent a significant mechanism of cisplatin resistance.	Cisplatin	201-210	P53	Homo sapiens	81-84
9472015-5	1998	We demonstrate that recombinant His-tagged HMG-1 enhances p53 DNA binding in vitro and also that HMG-1 and p53 can interact directly in vitro.	Histidine	32-35	P53	Homo sapiens	58-61
9472015-5	1998	We demonstrate that recombinant His-tagged HMG-1 enhances p53 DNA binding in vitro and also that HMG-1 and p53 can interact directly in vitro.	Histidine	32-35	P53	Homo sapiens	107-110
9469450-11	1998	Morphine promoted the synthesis of Bax and p53 proteins by Mphi.	Morphine	0-8	P53	Homo sapiens	43-46
9453486-1	1998	BACKGROUND &amp; AIMS: The p53 and BAX genes have been linked to apoptosis.	Adenosine Monophosphate	12-15	P53	Homo sapiens	27-30
9469450-13	1998	These studies suggest that morphine activates the induction phase of the apoptotic pathway through accumulation of p53.	Morphine	27-35	P53	Homo sapiens	115-118
9490416-4	1998	Using a chimaeric p53 fusion protein with the oestrogen receptor (p53ER) to supply p53 (p53 is induced upon binding of p53ER to oestradiol) in a p53-deficient cell line, we found that p85 is upregulated by p53 and that its involvement in p53-mediated apoptosis is independent of PI(3)K. We propose that p85 acts as a signal transducer in the cellular response to oxidative stress, mediating cell death regulated by p53.	Estradiol	128-138	P53	Homo sapiens	18-21
9490416-4	1998	Using a chimaeric p53 fusion protein with the oestrogen receptor (p53ER) to supply p53 (p53 is induced upon binding of p53ER to oestradiol) in a p53-deficient cell line, we found that p85 is upregulated by p53 and that its involvement in p53-mediated apoptosis is independent of PI(3)K. We propose that p85 acts as a signal transducer in the cellular response to oxidative stress, mediating cell death regulated by p53.	Estradiol	128-138	P53	Homo sapiens	66-69
9490416-4	1998	Using a chimaeric p53 fusion protein with the oestrogen receptor (p53ER) to supply p53 (p53 is induced upon binding of p53ER to oestradiol) in a p53-deficient cell line, we found that p85 is upregulated by p53 and that its involvement in p53-mediated apoptosis is independent of PI(3)K. We propose that p85 acts as a signal transducer in the cellular response to oxidative stress, mediating cell death regulated by p53.	Estradiol	128-138	P53	Homo sapiens	66-69
9490416-4	1998	Using a chimaeric p53 fusion protein with the oestrogen receptor (p53ER) to supply p53 (p53 is induced upon binding of p53ER to oestradiol) in a p53-deficient cell line, we found that p85 is upregulated by p53 and that its involvement in p53-mediated apoptosis is independent of PI(3)K. We propose that p85 acts as a signal transducer in the cellular response to oxidative stress, mediating cell death regulated by p53.	Estradiol	128-138	P53	Homo sapiens	66-69
9490416-4	1998	Using a chimaeric p53 fusion protein with the oestrogen receptor (p53ER) to supply p53 (p53 is induced upon binding of p53ER to oestradiol) in a p53-deficient cell line, we found that p85 is upregulated by p53 and that its involvement in p53-mediated apoptosis is independent of PI(3)K. We propose that p85 acts as a signal transducer in the cellular response to oxidative stress, mediating cell death regulated by p53.	Estradiol	128-138	P53	Homo sapiens	66-69
9490416-4	1998	Using a chimaeric p53 fusion protein with the oestrogen receptor (p53ER) to supply p53 (p53 is induced upon binding of p53ER to oestradiol) in a p53-deficient cell line, we found that p85 is upregulated by p53 and that its involvement in p53-mediated apoptosis is independent of PI(3)K. We propose that p85 acts as a signal transducer in the cellular response to oxidative stress, mediating cell death regulated by p53.	Estradiol	128-138	P53	Homo sapiens	66-69
9490416-4	1998	Using a chimaeric p53 fusion protein with the oestrogen receptor (p53ER) to supply p53 (p53 is induced upon binding of p53ER to oestradiol) in a p53-deficient cell line, we found that p85 is upregulated by p53 and that its involvement in p53-mediated apoptosis is independent of PI(3)K. We propose that p85 acts as a signal transducer in the cellular response to oxidative stress, mediating cell death regulated by p53.	Estradiol	128-138	P53	Homo sapiens	66-69
9490416-4	1998	Using a chimaeric p53 fusion protein with the oestrogen receptor (p53ER) to supply p53 (p53 is induced upon binding of p53ER to oestradiol) in a p53-deficient cell line, we found that p85 is upregulated by p53 and that its involvement in p53-mediated apoptosis is independent of PI(3)K. We propose that p85 acts as a signal transducer in the cellular response to oxidative stress, mediating cell death regulated by p53.	Estradiol	128-138	P53	Homo sapiens	66-69
9461094-7	1998	Morphine at concentrations of 10(-8) to 10(-4) M promoted apoptosis of kidney fibroblasts and also enhanced the synthesis of p53 by kidney fibroblasts.	Morphine	0-8	P53	Homo sapiens	125-128
9461094-8	1998	We speculate that morphine-induced kidney fibroblast proliferation may be mediated through the activation of early growth related genes, whereas morphine induced kidney fibroblast apoptosis may be mediated through the generation of p53.	Morphine	145-153	P53	Homo sapiens	232-235
9468185-8	1998	Cell death of p53-transduced VSMCs was induced only by additional treatment with an apoptosis-stimulating reagent, doxorubicin.	Doxorubicin	115-126	P53	Homo sapiens	14-17
9530523-8	1998	The results of these experiments demonstrate that: (1) there were mutations in p53 exon 5 and 8 in 35% (14 out of 40 samples) of human renal cancer tissues as revealed by PCR-SSCP analysis; (2) DNA sequencing of samples showing frame-shift have hot spot of p53 mutation on exon 8 at codon 244 (GGC--&gt;TGC) and exon 5 at codon 132 [AAG (Lys)--&gt;AGG (Arg)].	Lysine	338-341	P53	Homo sapiens	79-82
9530523-8	1998	The results of these experiments demonstrate that: (1) there were mutations in p53 exon 5 and 8 in 35% (14 out of 40 samples) of human renal cancer tissues as revealed by PCR-SSCP analysis; (2) DNA sequencing of samples showing frame-shift have hot spot of p53 mutation on exon 8 at codon 244 (GGC--&gt;TGC) and exon 5 at codon 132 [AAG (Lys)--&gt;AGG (Arg)].	Arginine	353-356	P53	Homo sapiens	79-82
9458352-0	1998	Role of p53 and apoptosis in sensitization of cis-diamminedichloroplatinum antitumor activity by interleukin-1 in ovarian carcinoma cells.	Cisplatin	46-74	P53	Homo sapiens	8-11
9458352-4	1998	IL-1 and CDDP treatment induced p53 protein in NIH:OVCAR-3 tumor cells.	Cisplatin	9-13	P53	Homo sapiens	32-35
9458352-7	1998	The synergistic interactions of IL-1 with CDDP may involve the enhancement of p53-dependent apoptosis.	Cisplatin	42-46	P53	Homo sapiens	78-81
9548450-1	1998	It has been controversial whether cancer cells harboring loss or inactivation of the tumor suppressor p53 are resistant or sensitive to DNA-damaging agents including cisplatin and doxorubicin.	Cisplatin	166-175	P53	Homo sapiens	102-105
9548450-1	1998	It has been controversial whether cancer cells harboring loss or inactivation of the tumor suppressor p53 are resistant or sensitive to DNA-damaging agents including cisplatin and doxorubicin.	Doxorubicin	180-191	P53	Homo sapiens	102-105
9548451-3	1998	Immunocytochemical analysis demonstrated that MDM2-positive tumors, even with p53-negative phenotype, were significantly more resistant to doxorubicin treatment compared to MDM2-negative tumors.	Doxorubicin	139-150	P53	Homo sapiens	78-81
9508372-3	1998	Cisplatin, at 10 microM, virtually killed all the cells in the wild-type p53 cell lines, while 57-95% of the cells in the mutant p53 cell lines survived (P = 0.005).	Cisplatin	0-9	P53	Homo sapiens	73-76
9508372-8	1998	Cisplatin, camptothecin and vincristine all induced apoptosis in wild-type p53 melanoma cells, but not in mutant p53 cells.	Cisplatin	0-9	P53	Homo sapiens	75-78
9510045-3	1998	MATERIALS AND METHODS: Immunostaining for p53 protein was performed on paraffin-embedded specimens from 69 patients with adeno- and squamous cell carcinoma of the oesophagus.	Paraffin	71-79	P53	Homo sapiens	42-45
9455805-3	1998	Here, using normal human fibroblasts (NHFs), we show that cisplatin and UV radiation induce G2/M arrest which is temporally linked to p53-protein induction.	Cisplatin	58-67	P53	Homo sapiens	134-137
9455805-4	1998	To study the contribution of p53 to this G2/M arrest, we inhibited p53 induction in NHFs using p53 anti-sense oligonucleotides.	Oligonucleotides	110-126	P53	Homo sapiens	67-70
9464250-2	1998	We used doxorubicin (DOX) and sodium butyrate (NaB) to accumulate p53 protein.	Doxorubicin	8-19	P53	Homo sapiens	66-69
9464250-2	1998	We used doxorubicin (DOX) and sodium butyrate (NaB) to accumulate p53 protein.	Doxorubicin	21-24	P53	Homo sapiens	66-69
9464250-4	1998	P53 protein induction in response to DOX accompanied up-regulation of p21/waf-1 and cyclinG expression.	Doxorubicin	37-40	P53	Homo sapiens	0-3
9455805-4	1998	To study the contribution of p53 to this G2/M arrest, we inhibited p53 induction in NHFs using p53 anti-sense oligonucleotides.	Oligonucleotides	110-126	P53	Homo sapiens	67-70
9445187-12	1998	CONCLUSIONS: In this study, p53p overexpression was infrequent in paraffin embedded melanoma specimens and independent of the primary melanoma"s anatomic site.	Paraffin	66-74	P53	Homo sapiens	28-32
9467949-4	1998	The p34cdc2 binding site on human p53 maps to one distinct C-terminal site LQIRGRERFE (aa 330-339) close to the corresponding phosphorylation site at serine 315.	Serine	150-156	P53	Homo sapiens	34-37
10069444-5	1998	In one case, p53 codon 282 mutation (CGG--&gt;TGG; arg--&gt;trp) were observed in initial diagnosis.	Arginine	51-54	P53	Homo sapiens	13-16
9580543-4	1998	Expression of mutant p53 was evaluated in 655 human breast carcinomas (349 node-positive and 306 node-negative patients) with long-term clinical follow-up by immunohistochemistry in sections from paraffin embedded tumors.	Paraffin	196-204	P53	Homo sapiens	21-24
9472635-6	1998	Similarly, high concentrations of taxol were required to induce p53 activity in the p53 wild-type cell line LN-229.	Paclitaxel	34-39	P53	Homo sapiens	64-67
9472635-6	1998	Similarly, high concentrations of taxol were required to induce p53 activity in the p53 wild-type cell line LN-229.	Paclitaxel	34-39	P53	Homo sapiens	84-87
9516963-3	1998	A wtp53 cDNA was subcloned into the pGRE5-2/EBV vector with dexamethasone-inducible overexpression and transfected into Rh30 ARMS cells that express Pax3/FKHR and a mutant p53 phenotype.	Dexamethasone	60-73	P53	Homo sapiens	4-7
9516963-6	1998	Data demonstrated p53-dependent sensitization (&gt; or = 4-fold) to bleomycin, actinomycin D, and 5-fluorouracil and considerably less p53-dependence (&lt; or = 2-fold) for doxorubicin, topotecan, etoposide, and cisplatin in Cl.#27 compared to an equivalent clone containing the pGRE5-EBV vector alone (VC#3).	Fluorouracil	98-112	P53	Homo sapiens	18-21
9773296-1	1998	Immunohistochemical detection of p53 in paraffin-embedded biopsy specimens has important diagnostic, prognostic and therapeutic applications.	Paraffin	40-48	P53	Homo sapiens	33-36
9773296-8	1998	The most suitable fixatives for immunohistochemical detection of p53 are 70% ethanol and Carnoy solution.	Ethanol	77-84	P53	Homo sapiens	65-68
9618042-3	1998	We set out to determine whether p53 overexpression of the colorectum was associated with a patient"s history of aspirin use.	Aspirin	112-119	P53	Homo sapiens	32-35
9618042-9	1998	An inverse association of regular aspirin use (two times per week or more) was found both for cases with p53 overexpression (OR: 0.79; 95% CI: 0.39-1.59), and for cases without p53 overexpression (OR: 0.56; 95% CI: 0.25-1.22).	Aspirin	34-41	P53	Homo sapiens	105-108
9618042-9	1998	An inverse association of regular aspirin use (two times per week or more) was found both for cases with p53 overexpression (OR: 0.79; 95% CI: 0.39-1.59), and for cases without p53 overexpression (OR: 0.56; 95% CI: 0.25-1.22).	Aspirin	34-41	P53	Homo sapiens	177-180
9464331-10	1998	Accordingly, consolidation chemotherapy is necessary for patients with stage I a who are positive p53 and highly PA. Platinum-based chemotherapy for patients who had minimal residual tumor was effective, but 5 patients who had &gt; or = 2 cm tumor burden were not effective at all.	Platinum	117-125	P53	Homo sapiens	98-101
9464331-11	1998	The response rate for platinum-based chemotherapy was 20% (1/5) among p53 positive, in contrast to 66.7% (4/6) among p53 negative patients.	Platinum	22-30	P53	Homo sapiens	70-73
9474928-5	1998	Restoration of wild-type p53 function markedly enhanced the antitumor effect of a common chemotherapeutic agent, cisplatin, in human non-small cell lung cancer cells as well as human colon cancer cells.	Cisplatin	113-122	P53	Homo sapiens	25-28
10069444-5	1998	In one case, p53 codon 282 mutation (CGG--&gt;TGG; arg--&gt;trp) were observed in initial diagnosis.	Tryptophan	60-63	P53	Homo sapiens	13-16
9719502-4	1998	In addition, p53 protein overexpression was assessed by immunohistochemistry using the monoclonal antibody DO-7 on paraffin-embedded tissue sections.	Paraffin	115-123	P53	Homo sapiens	13-16
9498829-7	1998	Interestingly, apoptosis occurred in mt-p53 tumors although only at high doses of cisplatin and not at the magnitude detected in wt-p53 tumors.	Cisplatin	82-91	P53	Homo sapiens	40-43
9718082-8	1998	An increase in the level of immunophenotypic expression of wild type p53 was also noted after treatment with all trans retinoic acid and 9-cis retinoic acid.	Tretinoin	119-132	P53	Homo sapiens	69-72
9440732-0	1998	p53 protein accumulation predicts poor response to tamoxifen therapy of patients with recurrent breast cancer.	Tamoxifen	51-60	P53	Homo sapiens	0-3
9440732-3	1998	We studied whether p53 protein accumulation is a predictive factor for response to tamoxifen treatment in patients with recurrent breast cancer.	Tamoxifen	83-92	P53	Homo sapiens	19-22
9440732-8	1998	In a test for trend, we observed an association of p53 protein levels with response to tamoxifen therapy.	Tamoxifen	87-96	P53	Homo sapiens	51-54
9440732-11	1998	Also in multivariate analysis, reduced survival after the start of tamoxifen therapy was observed in the p53-high group (relative hazards rate [RHR], 1.56, 95% CI, 1.17 to 2.10; P = .002).	Tamoxifen	67-76	P53	Homo sapiens	105-108
9440732-12	1998	A statistically significant association between p53 levels and decreased tamoxifen response was seen only in the subset of patients whose tumors expressed low levels of ER or PgR (&lt;75 fmol/mg protein).	Tamoxifen	73-82	P53	Homo sapiens	48-51
9440732-13	1998	CONCLUSION: Measurement of primary tumor p53 levels may be effective in predicting response to tamoxifen therapy in recurrent breast disease.	Tamoxifen	95-104	P53	Homo sapiens	41-44
9436988-6	1998	Because of the role of IMPD in the production and balance of GTP and ATP, essential nucleotides for signal transduction, these results suggest that p53 controls cell division signals by regulating purine ribonucleotide metabolism.	Guanosine Triphosphate	61-64	P53	Homo sapiens	148-151
9436988-6	1998	Because of the role of IMPD in the production and balance of GTP and ATP, essential nucleotides for signal transduction, these results suggest that p53 controls cell division signals by regulating purine ribonucleotide metabolism.	Adenosine Triphosphate	69-72	P53	Homo sapiens	148-151
9482165-11	1998	These results coupled with the observation that various fatty acids can alter the activity of cell membrane bound enzymes such as sodium-potassium-ATPase and 5"-nucleotidase, levels of various anti-oxidants, p53 expression and the concentrations of protein kinase C suggest that essential fatty acids and their metabolites can reverse tumour cell drug-resistance at least in vitro.	Fatty Acids	56-67	P53	Homo sapiens	208-211
9460707-0	1998	Nitric oxide donor-induced p53-sensitive cell death is enhanced by Bcl-2 reduction in human neuroblastoma cells.	Nitric Oxide	0-12	P53	Homo sapiens	27-30
9700726-0	1998	DNA binding activities of p53 protein following cisplatin damage of ovarian cells.	Cisplatin	48-57	P53	Homo sapiens	26-29
9700726-1	1998	In this study the transactivation potential and DNA binding activities of p53 protein were examined following exposure of A2780 cells, a human ovarian carcinoma cell line, to the DNA damaging agent, cis-diamminedichloroplatinum II (cisplatin).	Cisplatin	199-230	P53	Homo sapiens	74-77
9700726-1	1998	In this study the transactivation potential and DNA binding activities of p53 protein were examined following exposure of A2780 cells, a human ovarian carcinoma cell line, to the DNA damaging agent, cis-diamminedichloroplatinum II (cisplatin).	Cisplatin	232-241	P53	Homo sapiens	74-77
9700726-7	1998	At low doses of cisplatin, these latent pools of p53 increased in parallel with mdm-2 gene activation and were detectable as early as 4 h following cisplatin treatment.	Cisplatin	16-25	P53	Homo sapiens	49-52
9700726-7	1998	At low doses of cisplatin, these latent pools of p53 increased in parallel with mdm-2 gene activation and were detectable as early as 4 h following cisplatin treatment.	Cisplatin	148-157	P53	Homo sapiens	49-52
9700726-9	1998	Even though cisplatin-induced p53 lacked sequence-specific DNA binding activity, it does possess an increased affinity for cisplatin-damaged duplex DNA molecules.	Cisplatin	12-21	P53	Homo sapiens	30-33
9700726-9	1998	Even though cisplatin-induced p53 lacked sequence-specific DNA binding activity, it does possess an increased affinity for cisplatin-damaged duplex DNA molecules.	Cisplatin	123-132	P53	Homo sapiens	30-33
9700726-10	1998	This represents the first identification where cisplatin treatment induces a p53 protein, lacking sequence-specific DNA binding but with an increased affinity for platinated DNA molecules.	Cisplatin	47-56	P53	Homo sapiens	77-80
9405613-6	1997	One Zn2+ ion remains tightly bound in the holo-form of p53 throughout the denaturation curve.	Zinc	4-8	P53	Homo sapiens	55-58
15678851-4	1998	In this study we analyzed the expression of p53 protein in a variety of salivary gland malignant tumors fixed in formalin and included in paraffin, using the method of immunohistochemical coloring with the anti-p53 DO-7 antibody.	Paraffin	138-146	P53	Homo sapiens	44-47
9405685-6	1997	Like p53, p53CP also binds both double- and single-stranded DNA oligonucleotides.	Oligonucleotides	64-80	P53	Homo sapiens	5-8
15678854-6	1998	Immunohistochemical determination of p53 protein was performed on tissular samples formalin fixed and paraffin embedded, using mouse monoclonal antibody DAKO--p53 DO 7 p53 human antiprotein.	Paraffin	102-110	P53	Homo sapiens	37-40
9776848-10	1998	Neither neonatal nor normal adult skin fibroblasts expressed either antigen but could be induced to express p53 by exposure to adriamycin.	Doxorubicin	127-137	P53	Homo sapiens	108-111
9461043-16	1997	Our results suggest that CAP induces apoptotic cell death in human gastric cancer cells (SNU-1) in vitro which may be possibly mediated by the overexpression of p53 and/or c-myc genes.	Capsaicin	25-28	P53	Homo sapiens	161-164
9459175-0	1997	Relationship between nitrogen mustard drug resistance in B-cell chronic lymphocytic leukemia (B-CLL) and protein expression of Bcl-2, Bax, Bcl-X and p53.	Nitrogen	21-29	P53	Homo sapiens	149-152
9407038-3	1997	This peptide represents the first 24 amino acids of p53 and contains three phosphorylated serine residues.	Serine	90-96	P53	Homo sapiens	52-55
9407038-4	1997	A specific p53 phosphopeptide antibody identified serine-15 as one of the two serines in p53 that becomes phosphorylated following DNA damage induced by either ionizing irradiation (IR) or ultraviolet (UV) irradiation in multiple cell types.	Serine	50-56	P53	Homo sapiens	11-14
9407038-4	1997	A specific p53 phosphopeptide antibody identified serine-15 as one of the two serines in p53 that becomes phosphorylated following DNA damage induced by either ionizing irradiation (IR) or ultraviolet (UV) irradiation in multiple cell types.	Serine	50-56	P53	Homo sapiens	89-92
9407038-4	1997	A specific p53 phosphopeptide antibody identified serine-15 as one of the two serines in p53 that becomes phosphorylated following DNA damage induced by either ionizing irradiation (IR) or ultraviolet (UV) irradiation in multiple cell types.	Serine	78-85	P53	Homo sapiens	11-14
9407038-4	1997	A specific p53 phosphopeptide antibody identified serine-15 as one of the two serines in p53 that becomes phosphorylated following DNA damage induced by either ionizing irradiation (IR) or ultraviolet (UV) irradiation in multiple cell types.	Serine	78-85	P53	Homo sapiens	89-92
9407038-8	1997	In contrast, phosphorylation of p53 on serine-15 is similar in normal and AT cells after UV irradiation.	Serine	39-45	P53	Homo sapiens	32-35
9407038-9	1997	Our results indicate that p53 is phosphorylated in response to DNA damage, that this de novo phosphorylation may be involved in the subsequent induction and activation of p53, and that although ATM affects the kinetics of p53 phosphorylation after IR, it is not absolutely required for phosphorylation of p53 on serine-15.	Serine	312-318	P53	Homo sapiens	26-29
9407038-9	1997	Our results indicate that p53 is phosphorylated in response to DNA damage, that this de novo phosphorylation may be involved in the subsequent induction and activation of p53, and that although ATM affects the kinetics of p53 phosphorylation after IR, it is not absolutely required for phosphorylation of p53 on serine-15.	Serine	312-318	P53	Homo sapiens	171-174
9407038-9	1997	Our results indicate that p53 is phosphorylated in response to DNA damage, that this de novo phosphorylation may be involved in the subsequent induction and activation of p53, and that although ATM affects the kinetics of p53 phosphorylation after IR, it is not absolutely required for phosphorylation of p53 on serine-15.	Serine	312-318	P53	Homo sapiens	171-174
9407038-9	1997	Our results indicate that p53 is phosphorylated in response to DNA damage, that this de novo phosphorylation may be involved in the subsequent induction and activation of p53, and that although ATM affects the kinetics of p53 phosphorylation after IR, it is not absolutely required for phosphorylation of p53 on serine-15.	Serine	312-318	P53	Homo sapiens	171-174
9416838-4	1997	In this study we addressed the possible prognostic value of the molecular alterations identified in exons 5-8 of the TP53 gene in DNAs from 151 paraffin-embedded NSCLC sections corresponding to 59 Spanish and 92 Polish stage I-IIIA resected patients.	Paraffin	144-152	P53	Homo sapiens	117-121
9415415-5	1997	MCF-7 cells showed a block in the G1 phase after treatment with 50 nM epirubicin for 24 hours, in agreement with the actions of p53 at the G1 checkpoint.	Epirubicin	70-80	P53	Homo sapiens	128-131
9373250-10	1997	p53-specific antisense oligonucleotide treatment recapitulated the effects of Tpo treatment on the levels of Bax, Mdm-2, and Bcl-2.	Oligonucleotides	23-38	P53	Homo sapiens	0-3
9409811-7	1997	Moreover, addition of glutathione monoethylester to the culture restored the level of reduced glutathione in VSM cells, and prevented the NO-induced increase in p53 expression and programmed cell death.	S-ethyl glutathione	22-48	P53	Homo sapiens	161-164
9372954-7	1997	We have mapped a major site of phosphorylation by CAK to Ser-33 of p53 and have demonstrated as well that p53 is phosphorylated at this site in vivo.	Serine	57-60	P53	Homo sapiens	67-70
9372954-7	1997	We have mapped a major site of phosphorylation by CAK to Ser-33 of p53 and have demonstrated as well that p53 is phosphorylated at this site in vivo.	Serine	57-60	P53	Homo sapiens	106-109
9392545-0	1997	Original p53 status predicts for pathological response in locally advanced breast cancer patients treated preoperatively with continuous infusion 5-fluorouracil and radiation therapy.	Fluorouracil	146-160	P53	Homo sapiens	9-12
10374328-2	1997	METHODS: The expression of p53 protein was determined in the paraffin embedded tissues of 171 cases of cervical carcinoma, 68 cases of SIL and 29 cases of chronic cervicitis, using ABC immunohistochemical method.	Paraffin	61-69	P53	Homo sapiens	27-30
9409811-7	1997	Moreover, addition of glutathione monoethylester to the culture restored the level of reduced glutathione in VSM cells, and prevented the NO-induced increase in p53 expression and programmed cell death.	Glutathione	22-33	P53	Homo sapiens	161-164
9403032-7	1997	Since HeLa cells lost most of their p53 protein due to a specific E6-dependent degradation, cisplatin could be inhibiting this degradation, since the p53 total levels were not increased during the exposure to the drug.	Cisplatin	92-101	P53	Homo sapiens	150-153
9389577-6	1997	We further demonstrated that the p53-independent differential cisplatin sensitivity among the testicular germ cell tumour (TGCT) cell lines was not due to differences in cellular cisplatin accumulation or DNA platination.	Cisplatin	62-71	P53	Homo sapiens	33-36
9389577-9	1997	We conclude that the cisplatin-induced apoptotic pathway in TGCT cell lines might be p53-independent and is probably not associated with differences in the Bcl-2/Bax rheostat.	Cisplatin	21-30	P53	Homo sapiens	85-88
9570369-4	1997	In wt-p53 transfected cells, the expression of MDRI gene was significantly increased, accumulation of adriamycin (ADM) was decreased, and the sensitivity to vincristine (VCR), ADM and 5-fluorouracil (5-FU) was increased compared with the parent KBv200 cells.	Doxorubicin	102-112	P53	Homo sapiens	6-9
9395239-8	1997	Introduction of functional p53 into CEM cells enhanced their sensitivity to the DNA-damaging agent doxorubicin, but not to the tubulin-active compound vincristine.	Doxorubicin	99-110	P53	Homo sapiens	27-30
9570369-4	1997	In wt-p53 transfected cells, the expression of MDRI gene was significantly increased, accumulation of adriamycin (ADM) was decreased, and the sensitivity to vincristine (VCR), ADM and 5-fluorouracil (5-FU) was increased compared with the parent KBv200 cells.	Fluorouracil	184-198	P53	Homo sapiens	6-9
9570369-4	1997	In wt-p53 transfected cells, the expression of MDRI gene was significantly increased, accumulation of adriamycin (ADM) was decreased, and the sensitivity to vincristine (VCR), ADM and 5-fluorouracil (5-FU) was increased compared with the parent KBv200 cells.	Fluorouracil	200-204	P53	Homo sapiens	6-9
9467850-3	1997	The first of these TPA states is senescence, and several recent studies have shown that abrogation of p53 function permits temporary escape from senescence that ends in a poorly characterized form of arrest (referred to as p53-minus TPA) in which the pRB and p16INK4 genes appear to be involved.	Tetradecanoylphorbol Acetate	19-22	P53	Homo sapiens	102-105
9359484-4	1997	Treatment with the chemotherapeutic drug cisplatin following infection with a replication-deficient, recombinant adenoviral vector expressing wt-p53 (termed AdCMVp53) significantly suppressed the growth of WiDr cells compared to single treatments alone.	Cisplatin	41-50	P53	Homo sapiens	145-148
9366703-12	1997	A significant correlation existed with both p53 gene mutation status and HPV status with respect to alcohol and tobacco use.	Alcohols	100-107	P53	Homo sapiens	44-47
9366703-13	1997	The presence of the p53 gene mutation positively correlated with increased tobacco and alcohol use, whereas infection with HPV predicted a significantly lower rate of alcohol and tobacco consumption.	Alcohols	87-94	P53	Homo sapiens	20-23
9366703-15	1997	Conversely, there is a strong association between heavy alcohol and tobacco use and mutation of the p53 gene.	Alcohols	56-63	P53	Homo sapiens	100-103
9494587-2	1997	We investigated the localization of p53 protein in association with HPV in paraffin sections of 10 dysplastic and 12 malignant laryngeal squamous epithelium specimens by using immunohistochemical and in situ hybridization techniques.	Paraffin	75-83	P53	Homo sapiens	36-39
9467850-3	1997	The first of these TPA states is senescence, and several recent studies have shown that abrogation of p53 function permits temporary escape from senescence that ends in a poorly characterized form of arrest (referred to as p53-minus TPA) in which the pRB and p16INK4 genes appear to be involved.	Tetradecanoylphorbol Acetate	233-236	P53	Homo sapiens	102-105
9815592-6	1997	The SKOV3ip1 cells do not express p53 protein; hence, the induction of apoptosis by paclitaxel is through a p53-independent pathway.	Paclitaxel	84-94	P53	Homo sapiens	108-111
9354463-0	1997	Betulinic acid triggers CD95 (APO-1/Fas)- and p53-independent apoptosis via activation of caspases in neuroectodermal tumors.	betulinic acid	0-14	P53	Homo sapiens	46-49
9449526-8	1997	EMSA of an oligonucleotide sequence derived from the HIV-LTR sequence demonstrated a slight decrease in Sp1 DNA binding activity with nuclear extract derived from the cell line expressing a high level of wild-type p53.	Oligonucleotides	11-26	P53	Homo sapiens	214-217
9354463-3	1997	BA-induced apoptosis was independent of CD95-ligand/receptor interaction and accumulation of wild-type p53 protein, but it critically depended on activation of caspases (interleukin 1beta-converting enzyme/Ced-3-like proteases).	betulinic acid	0-2	P53	Homo sapiens	103-106
9536982-3	1997	In this study, we have analysed the relationships between p53 protein induction, cell cycle arrest and cell survival following exposure of normal human fibroblasts (NHFs) to various genotoxic agents such as cisplatin, UV radiation and gamma radiation.	Cisplatin	207-216	P53	Homo sapiens	58-61
9536982-5	1997	However, following inhibition of p53 induction by an antisense oligonucleotide, this G2/M arrest is even more important and correlates with an enhanced sensitivity of NHFs to UV radiation.	Oligonucleotides	63-78	P53	Homo sapiens	33-36
9815601-11	1997	p53 wild-type cells seem to be more sensitive to the cytotoxic effects of the combination of UCN-01 + CDDP than the p53 mutant cells.	Cisplatin	102-106	P53	Homo sapiens	0-3
9815601-12	1997	This was confirmed in cells in which p53 wild-type function was restored by transfection of p53 cDNA, but these cells are also significantly more sensitive to CDDP alone.	Cisplatin	159-163	P53	Homo sapiens	37-40
9815601-10	1997	The degree of sensitization to CDDP conferred by UCN-01, however, was found to correlate with p53 gene status.	Cisplatin	31-35	P53	Homo sapiens	94-97
9397628-4	1997	Paraffin-embedded tissue blocks of surgical margins from 24 patients with oral cavity and oropharyngeal squamous cell carcinoma were immunostained for p53 protein.	Paraffin	0-8	P53	Homo sapiens	151-154
9470815-0	1997	Short- and long-term oestradiol treatment inhibits growth and alters expression of p21WAF1/Cip1 in an endometrial adenocarcinoma cell line lacking functional p53.	Estradiol	21-31	P53	Homo sapiens	158-161
9470815-2	1997	To examine this, a mutant p53-expressing human endometrial adenocarcinoma cell line of the oestradiol-inhibited growth phenotype was treated with oestradiol for 2 weeks (short-term) and 6 months (long-term).	Estradiol	91-101	P53	Homo sapiens	26-29
9470815-2	1997	To examine this, a mutant p53-expressing human endometrial adenocarcinoma cell line of the oestradiol-inhibited growth phenotype was treated with oestradiol for 2 weeks (short-term) and 6 months (long-term).	Estradiol	146-156	P53	Homo sapiens	26-29
9470815-10	1997	Our results suggest the existence of a p53-independent pathway of oestradiol regulation of growth and proliferation in this human endometrial adenocarcinoma, resulting in accumulation of cells in G0/G1 through p21WAF1/Cip1 induction and, after prolonged treatment, downregulation of bcl-2 protein.	Estradiol	66-76	P53	Homo sapiens	39-42
21528311-0	1997	Rapamycin-induced apoptosis is p53-independent in human prostate carcinoma PC-3 cells.	Sirolimus	0-9	P53	Homo sapiens	31-34
9368590-1	1997	We investigated the expression of p53 in 82 formalin-fixed, paraffin-embedded archival tissue specimens of lip and intraoral squamous cell carcinomas (SCCs) from the period 1930-1995, by immunohistochemistry using three monoclonal antibodies (MAbs DO-7, DO-1 and 1801).	Paraffin	60-68	P53	Homo sapiens	34-37
9363941-2	1997	Here we show that phosphorylation of human p53 at serine 15 occurs after DNA damage and that this leads to reduced interaction of p53 with its negative regulator, the oncoprotein MDM2, in vivo and in vitro.	Serine	50-56	P53	Homo sapiens	43-46
9363941-2	1997	Here we show that phosphorylation of human p53 at serine 15 occurs after DNA damage and that this leads to reduced interaction of p53 with its negative regulator, the oncoprotein MDM2, in vivo and in vitro.	Serine	50-56	P53	Homo sapiens	130-133
9363941-3	1997	Furthermore, using purified DNA-dependent protein kinase (DNA-PK), we demonstrate that phosphorylation of p53 at serines 15 and 37 impairs the ability of MDM2 to inhibit p53-dependent transactivation.	Serine	113-120	P53	Homo sapiens	106-109
9363941-3	1997	Furthermore, using purified DNA-dependent protein kinase (DNA-PK), we demonstrate that phosphorylation of p53 at serines 15 and 37 impairs the ability of MDM2 to inhibit p53-dependent transactivation.	Serine	113-120	P53	Homo sapiens	170-173
9332764-2	1997	We used a case-case analysis, comparing tumors with and without overexpression of the p53 gene product to evaluate the association of putative p53 mutations with tamoxifen use and other risk factors for endometrial cancer.	Tamoxifen	162-171	P53	Homo sapiens	143-146
9332764-5	1997	There was a small association between p53 overexpression and treatment with tamoxifen for breast cancer (OR = 2.6; 95% CI, 0.69-9.8).	Tamoxifen	76-85	P53	Homo sapiens	38-41
9332764-8	1997	The results suggest that use of tamoxifen may be associated with an increase in tumors that overexpress p53, although the results could be due to chance.	Tamoxifen	32-41	P53	Homo sapiens	104-107
9312058-7	1997	In vivo generation of a C-terminal cleavage product of endogenous p53 similar in size to p50(DeltaC) correlated with up-regulation of p21 expression in ML-1 cells exposed to either adriamycin or cisplatin.	Doxorubicin	181-191	P53	Homo sapiens	66-69
9312058-7	1997	In vivo generation of a C-terminal cleavage product of endogenous p53 similar in size to p50(DeltaC) correlated with up-regulation of p21 expression in ML-1 cells exposed to either adriamycin or cisplatin.	Cisplatin	195-204	P53	Homo sapiens	66-69
9315628-10	1997	The data reported here indicate that intracellular levels and redox activity of copper are critical for p53 protein conformation and DNA-binding activity and suggest that copper ions may participate in the physiological control of p53 function.	Copper	80-86	P53	Homo sapiens	104-107
9315628-10	1997	The data reported here indicate that intracellular levels and redox activity of copper are critical for p53 protein conformation and DNA-binding activity and suggest that copper ions may participate in the physiological control of p53 function.	Copper	80-86	P53	Homo sapiens	231-234
9315628-0	1997	Regulation of p53 by metal ions and by antioxidants: dithiocarbamate down-regulates p53 DNA-binding activity by increasing the intracellular level of copper.	Metals	21-26	P53	Homo sapiens	14-17
9315628-0	1997	Regulation of p53 by metal ions and by antioxidants: dithiocarbamate down-regulates p53 DNA-binding activity by increasing the intracellular level of copper.	Copper	150-156	P53	Homo sapiens	14-17
9315628-10	1997	The data reported here indicate that intracellular levels and redox activity of copper are critical for p53 protein conformation and DNA-binding activity and suggest that copper ions may participate in the physiological control of p53 function.	Copper	171-177	P53	Homo sapiens	104-107
9315628-10	1997	The data reported here indicate that intracellular levels and redox activity of copper are critical for p53 protein conformation and DNA-binding activity and suggest that copper ions may participate in the physiological control of p53 function.	Copper	171-177	P53	Homo sapiens	231-234
9290950-4	1997	The expression of p53 was determined by immunohistochemistry in 19 pheochromocytomas and in 17 MTCs using two antibodies (D01 and D07) on frozen and paraffin-embedded tissues.	Paraffin	149-157	P53	Homo sapiens	18-21
9275165-7	1997	Using this approach it has been possible to simplify the production of site-specifically modified oligonucleotides containing AFB1 adducts in the sequence context of a p53 mutational hotspot.	Oligonucleotides	98-114	P53	Homo sapiens	168-171
9421067-13	1997	The single strong and diffuse p53 immunopositive tumor was negative for WAF-1 and was shown to contain a missense p53 point mutation (exon 7-codon 248 tryptophan).	Tryptophan	151-161	P53	Homo sapiens	30-33
9421067-13	1997	The single strong and diffuse p53 immunopositive tumor was negative for WAF-1 and was shown to contain a missense p53 point mutation (exon 7-codon 248 tryptophan).	Tryptophan	151-161	P53	Homo sapiens	114-117
9305847-7	1997	These observations stimulated additional biochemical and pharmacological experiments suggesting that p53 results in apoptosis through a three-step process: (1) the transcriptional induction of redox-related genes; (2) the formation of reactive oxygen species; and (3) the oxidative degradation of mitochondrial components, culminating in cell death.	Reactive Oxygen Species	235-258	P53	Homo sapiens	101-104
9294607-0	1997	Ethanol upregulates the expression of p21 WAF1/CIP1 and prolongs G1 transition via a p53-independent pathway in human epithelial cells.	Ethanol	0-7	P53	Homo sapiens	85-88
9294607-6	1997	The results also indicate that, at these non-cytotoxic concentrations, ethanol exhibits its effects through a p53-independent mechanism.	Ethanol	71-78	P53	Homo sapiens	110-113
9413185-6	1997	The results suggested that in Panc-1 cells cisplatin and VP-16 induced apoptotic cell death which was mediated through the interaction of Bax expression in the presence of mutated p53.	Cisplatin	43-52	P53	Homo sapiens	180-183
9436034-6	1997	ATRA also arrested the cell cycle in G1 and reduced the percentage of the S phase cell in terms of wild type p53, leading to apoptosis in part.	Tretinoin	0-4	P53	Homo sapiens	109-112
10325638-1	1997	To explore the carcinogenic effect of asbestos at molecular level, we directly analyzed the mutations of exon 5, 7 and 8 of anti-oncogene p53 in paraffin-embedded human lung tissue affected by asbestos for the first time.	Paraffin	145-153	P53	Homo sapiens	138-141
9446323-5	1997	The p53 Arg/Pro polymorphism study revealed the elevated frequency of Arg allele in lung and stomach cancer groups.	Arginine	8-11	P53	Homo sapiens	4-7
10920912-2	1997	METHODS: Levels of c-erbB-2 and p53 protein were detected by immunohistochemistry in 184 paraffin-embeded blocks.	Paraffin	89-97	P53	Homo sapiens	32-35
9446323-5	1997	The p53 Arg/Pro polymorphism study revealed the elevated frequency of Arg allele in lung and stomach cancer groups.	Arginine	70-73	P53	Homo sapiens	4-7
9266962-6	1997	Because MG-132 and lactacycstin are highly specific inhibitors of the proteasome protease, our results suggest that the proteasome influences post-translational processes involved in proper folding and cytoplasmic clearing of E2F-1 and p53.	lactacycstin	19-31	P53	Homo sapiens	236-239
9291435-6	1997	Our results suggest that mdm-2, which is known to disrupt p53 function, sensitizes ovarian-cancer cells to cisplatin/cyclophosphamide, possibly by inhibition of p53-mediated G1 cell-cycle arrest and p53-stimulated nucleotide-excision repair.	Cisplatin	107-116	P53	Homo sapiens	58-61
9291435-6	1997	Our results suggest that mdm-2, which is known to disrupt p53 function, sensitizes ovarian-cancer cells to cisplatin/cyclophosphamide, possibly by inhibition of p53-mediated G1 cell-cycle arrest and p53-stimulated nucleotide-excision repair.	Cisplatin	107-116	P53	Homo sapiens	161-164
9291435-6	1997	Our results suggest that mdm-2, which is known to disrupt p53 function, sensitizes ovarian-cancer cells to cisplatin/cyclophosphamide, possibly by inhibition of p53-mediated G1 cell-cycle arrest and p53-stimulated nucleotide-excision repair.	Cisplatin	107-116	P53	Homo sapiens	161-164
9269997-0	1997	Nitric oxide induces conformational and functional modifications of wild-type p53 tumor suppressor protein.	Nitric Oxide	0-12	P53	Homo sapiens	78-81
9254608-0	1997	Phosphorylation of serine 392 stabilizes the tetramer formation of tumor suppressor protein p53.	Serine	19-25	P53	Homo sapiens	92-95
9285694-5	1997	Comparatively, a treatment of the cells with 100 nM 4OH-tamoxifen (OHT) decreased cell number to 40% of the control without a concomitant decrease in the p53 levels suggesting a differential ability of these antiestrogens to regulate p53 levels in cells cultured in whole serum.	Tamoxifen	67-70	P53	Homo sapiens	154-157
9285694-5	1997	Comparatively, a treatment of the cells with 100 nM 4OH-tamoxifen (OHT) decreased cell number to 40% of the control without a concomitant decrease in the p53 levels suggesting a differential ability of these antiestrogens to regulate p53 levels in cells cultured in whole serum.	Tamoxifen	67-70	P53	Homo sapiens	234-237
9285694-6	1997	When cells were cultured in medium containing serum depleted of endogenous steroids (charcoal stripped serum), cell number and p53 levels declined.	Steroids	75-83	P53	Homo sapiens	127-130
9293894-9	1997	TMC revealed the highest incidence of intense p53 positivity, and the highest mean MIB-1 index, and absence of the apoptosis-inhibitor protein bcl-2.	tmc	0-3	P53	Homo sapiens	46-49
9299183-4	1997	In the colon, the "toxicology" of 5 fluorouracil (5FU) is entirely dependent on p53, since p53 knockouts lose the pathology of 5FU damage.	Fluorouracil	36-48	P53	Homo sapiens	80-83
9299183-4	1997	In the colon, the "toxicology" of 5 fluorouracil (5FU) is entirely dependent on p53, since p53 knockouts lose the pathology of 5FU damage.	Fluorouracil	36-48	P53	Homo sapiens	91-94
9242502-6	1997	Down-regulation of p53 with an anti-sense oligonucleotide did not affect apoptosis in glass-plated keratinocytes but effectively suppressed apoptosis in keratinocytes adhering via beta1 integrin.	Oligonucleotides	42-57	P53	Homo sapiens	19-22
9263993-0	1997	Nitric oxide and superoxide induced p53 and Bax accumulation during mesangial cell apoptosis.	Nitric Oxide	0-12	P53	Homo sapiens	36-39
9263993-0	1997	Nitric oxide and superoxide induced p53 and Bax accumulation during mesangial cell apoptosis.	Superoxides	17-27	P53	Homo sapiens	36-39
9257692-0	1997	Active oxygen species mediate the solar ultraviolet radiation-dependent increase in the tumour suppressor protein p53 in human skin fibroblasts.	Oxygen	7-13	P53	Homo sapiens	114-117
11596302-1	1997	Recent studies indicate that wild-type p53 can trigger cell apoptosis induced by many chemotherapeutic agents which induce DNA damage or cause disruptions of DNA metabolism, such as ADM, 5-FU, VP-16 and radiation.	Fluorouracil	187-191	P53	Homo sapiens	39-42
9257692-4	1997	Here I show that p53 in cultured human skin fibroblasts is elevated after treatment with hydrogen peroxide, an oxidant produced in cells during exposure to solar UV radiation.	Hydrogen Peroxide	89-106	P53	Homo sapiens	17-20
9257692-5	1997	Simulated solar UV radiation increased p53, and agents that scavenge active oxygen species, N-acetylcysteine, ascorbate and alpha-tocopherol, inhibited the increase.	Oxygen	76-82	P53	Homo sapiens	39-42
9214306-3	1997	Fluorescence energy transfer between the tryptophans as well as quenching by their local structural environments complicates the analysis of the contributions of the individual tryptophans to the fluorescence of the wt protein, but it is demonstrated that Trp53, which is completely buried within the hydrophobic core, makes the dominant contribution to the fluorescence, while the fluorescence of Trp38 is largely quenched in the fully folded protein.	Tryptophan	41-52	P53	Homo sapiens	256-261
9257692-5	1997	Simulated solar UV radiation increased p53, and agents that scavenge active oxygen species, N-acetylcysteine, ascorbate and alpha-tocopherol, inhibited the increase.	Acetylcysteine	92-108	P53	Homo sapiens	39-42
9233778-3	1997	Stable Hep 3B cell lines were generated in which inducible p53 was introduced using either a temperature-sensitive mutant (p53val135) or a tamoxifen-regulated p53-estrogen receptor chimera (p53-mERtm-pBabepuro).	Tamoxifen	139-148	P53	Homo sapiens	59-62
9212237-7	1997	At the same time, we found strong induction of p53, waf-1 and bax protein levels after CDDP treatment in the A2780, but not in the A2780-DX3, cell line.	Cisplatin	87-91	P53	Homo sapiens	47-50
9212237-10	1997	A significant proportion of p53 in A2780-DX3 cells was found in the cytoplasmic compartment, and CDDP treatment induced a functional p53 protein in the nucleus of A2780 much more strongly than in A2780-DX3, which coincides with an increase of transcriptional activity of p53 in treated A2780 cells.	Cisplatin	97-101	P53	Homo sapiens	133-136
9212237-10	1997	A significant proportion of p53 in A2780-DX3 cells was found in the cytoplasmic compartment, and CDDP treatment induced a functional p53 protein in the nucleus of A2780 much more strongly than in A2780-DX3, which coincides with an increase of transcriptional activity of p53 in treated A2780 cells.	Cisplatin	97-101	P53	Homo sapiens	133-136
9212237-11	1997	We propose that the cross-resistance to CDDP in the A2780-DX3 cell line may be due to inactivation of a CDDP-dependent p53-accumulation pathway.	Cisplatin	40-44	P53	Homo sapiens	119-122
9214672-7	1997	Mutation of the p53 gene was indicated by overexpression of p53 protein (i.e., cellular accumulation of mutant p53 protein) in paraffin-embedded ovarian cancer tissue blocks; the mutant protein was detected by means of standard immunohistochemical techniques.	Paraffin	127-135	P53	Homo sapiens	16-19
9214672-7	1997	Mutation of the p53 gene was indicated by overexpression of p53 protein (i.e., cellular accumulation of mutant p53 protein) in paraffin-embedded ovarian cancer tissue blocks; the mutant protein was detected by means of standard immunohistochemical techniques.	Paraffin	127-135	P53	Homo sapiens	60-63
9214672-7	1997	Mutation of the p53 gene was indicated by overexpression of p53 protein (i.e., cellular accumulation of mutant p53 protein) in paraffin-embedded ovarian cancer tissue blocks; the mutant protein was detected by means of standard immunohistochemical techniques.	Paraffin	127-135	P53	Homo sapiens	60-63
9212237-11	1997	We propose that the cross-resistance to CDDP in the A2780-DX3 cell line may be due to inactivation of a CDDP-dependent p53-accumulation pathway.	Cisplatin	104-108	P53	Homo sapiens	119-122
9301456-1	1997	This short report describes the detection of mutations of the TP53 tumour suppressor gene in sporadic ovarian carcinomas using archival paraffin-embedded tissues and automated fluorescent DNA sequencing.	Paraffin	136-144	P53	Homo sapiens	62-66
9253509-2	1997	Codon 72 of the p53 gene is highly polymorphic with a reported arginine/proline allelotype frequency of 0.65/0.35 for Caucasians and a reversal of this ratio in African-Americans.	Arginine	63-71	P53	Homo sapiens	16-19
9236923-7	1997	METHODS: Expression of p53 and PCNA were detected by immunocytochemistry in paraffin-embedded sections of infiltrating duct carcinoma and control breast tissue (normal tissue and adenoma).	Paraffin	76-84	P53	Homo sapiens	23-26
9226370-5	1997	The Mdmx protein, which, based on SDS-PAGE, has a MW of 80 kDa, can bind p53 in vitro.	Sodium Dodecyl Sulfate	34-37	P53	Homo sapiens	73-76
9234928-3	1997	We examined the growth effects of oligonucleotides designed to interfere with p53 expression and/or activity in p53-mutant/overexpressing endometrial cancer cell lines.	Oligonucleotides	34-50	P53	Homo sapiens	78-81
9234928-3	1997	We examined the growth effects of oligonucleotides designed to interfere with p53 expression and/or activity in p53-mutant/overexpressing endometrial cancer cell lines.	Oligonucleotides	34-50	P53	Homo sapiens	112-115
9215525-6	1997	Despite Dox ability to activate the DNA-damage dependent p53/p21 pathway, when induced in the absence of MyoD or other MRFs, p21 fails to maintain the postmitotic state in Dox-treated myocytes induced to differentiate.	Doxorubicin	8-11	P53	Homo sapiens	57-60
9246643-3	1997	This region is phosphorylated at several evolutionarily conserved serines, suggesting that phosphorylation may be an important regulator of p53 function.	Serine	66-73	P53	Homo sapiens	140-143
9246643-4	1997	In order to determine the effect of phosphorylation on tetramer formation, we synthesized phosphopeptides corresponding to p53(Ser303-Asp393) with phosphate incorporated at Ser315, Ser378, or Ser392, and at both Ser315 and Ser392.	Phosphates	147-156	P53	Homo sapiens	123-126
9256014-4	1997	The primers used were oligonucleotides corresponding to the sequence of exon 5 on p53.	Oligonucleotides	22-38	P53	Homo sapiens	82-85
21590120-2	1997	Pentoxifylline has recently been shown to sensitize breast cancer cells in which the wild-type p53 function was abrogated to cisplatin-induced apoptosis.	Cisplatin	125-134	P53	Homo sapiens	95-98
9216855-4	1997	To assess the relationship between the LOH status of the p53 gene in the liver cirrhosis stage and that in HCC, we analyzed the samples microdissected from paraffin-embedded tissues using the polymerase-chain-reaction-based assay.	Paraffin	156-164	P53	Homo sapiens	57-60
9192825-11	1997	Treatment of cells with 5-FU increased p53 protein levels, whereas sulindac metabolites did not induce expression.	Fluorouracil	24-28	P53	Homo sapiens	39-42
9772449-2	1997	METHODS: p53 gene mutations were detected by a-32P-dCTP labelled radiative PCR-SSCP and the biochemical analyses of lipids in serum and AS tissues.	2'-deoxycytidine 5'-triphosphate	51-55	P53	Homo sapiens	9-12
9812577-0	1997	[Detection of p53 gene mutation in paraffin-embedded asbestos-related lung cancer tissue].	Paraffin	35-43	P53	Homo sapiens	14-17
9812585-1	1997	Expression of P53 protein was determined in the process and the end of induction of malignant transformation in human fetal lung cells, with organic extract from tap water in a river of City G, to study its molecular mechanism.	Water	166-171	P53	Homo sapiens	14-17
9191518-5	1997	METHODS: The authors analyzed the numeric aberrations of chromosome 17 and p53 gene deletions in 11 paraffin embedded pleomorphic adenomas (PA) and 9 carcinomas in pleomorphic adenoma (CIPA), using FISH techniques.	Paraffin	100-108	P53	Homo sapiens	75-78
9248088-4	1997	More recently, the prognostic role of biological parameters such as p53 gene or enzymes implicated in 5-fluorouracil metabolisms has been identified.	Fluorouracil	102-116	P53	Homo sapiens	68-71
9178766-4	1997	Full length p53, but also a peptide representing a C-terminal fragment of the tumor suppressor gene product p53 (amino acids 264-393 which also harbors the CK2beta interaction site at amino acids 287-340) mimicked the polylysine effect in all respects, ie.	Polylysine	218-228	P53	Homo sapiens	12-15
9185695-3	1997	We analyzed p53 mutations on paraffin-embedded specimens from 33 patients with AS by polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) followed by direct sequencing.	Paraffin	29-37	P53	Homo sapiens	12-15
9178766-4	1997	Full length p53, but also a peptide representing a C-terminal fragment of the tumor suppressor gene product p53 (amino acids 264-393 which also harbors the CK2beta interaction site at amino acids 287-340) mimicked the polylysine effect in all respects, ie.	Polylysine	218-228	P53	Homo sapiens	108-111
9178766-0	1997	The carboxy terminus of p53 mimics the polylysine effect of protein kinase CK2-catalyzed MDM2 phosphorylation.	Polylysine	39-49	P53	Homo sapiens	24-27
9215611-9	1997	Curcumin-induced cell death was neither due to apoptosis nor to any significant change in the expression of apoptosis-related genes, including Bcl-2, p53, cyclin B and transglutaminase.	Curcumin	0-8	P53	Homo sapiens	150-153
9189093-4	1997	METHODS: Expression of p53 protein was assayed in ten benign melanocytic naevi (BMN) and 50 surgically excised ethanol-fixed melanomas.	Ethanol	111-118	P53	Homo sapiens	23-26
9179065-7	1997	p53 immunostaining was performed on paraffin embedded tissue.	Paraffin	36-44	P53	Homo sapiens	0-3
9815771-4	1997	In IGROV-1/Pt1 cells, cisplatin resistance has been ascribed to a reduced susceptibility to apoptosis as a consequence of p53 mutation and inactivation of its function.	Cisplatin	22-31	P53	Homo sapiens	122-125
9815771-5	1997	In the A2780 cisplatin-resistant subline, which retained the wild-type p53 gene status, the development of resistance has been possibly related to increased cell ability to repair drug-induced DNA damage.	Cisplatin	13-22	P53	Homo sapiens	71-74
9205870-0	1997	Detectability of retinoblastoma (Rb) gene product and p53 antigen expression decreases in stored paraffin sections.	Paraffin	97-105	P53	Homo sapiens	54-57
9264325-5	1997	Transcription from a p53 binding response element was inhibited in MM96L by a 24 hr ABHA treatment but enhanced in HeLa.	azelaic bishydroxamic acid	84-88	P53	Homo sapiens	21-24
9186003-3	1997	Cisplatin-treated cells arrest in the G1 phase of the cell cycle, most likely due to a signal generated by the stabilization of p53 and the subsequent induction of p21WAF-1/Cip1.	Cisplatin	0-9	P53	Homo sapiens	128-131
9187098-5	1997	Among p53 mutations at various sites, mutation at codon 242 (C TGC --&gt; C CGC; Cys --&gt; Arg) was specifically observed in both skin cancers and actinic keratoses.	Cysteine	81-84	P53	Homo sapiens	6-9
9187098-5	1997	Among p53 mutations at various sites, mutation at codon 242 (C TGC --&gt; C CGC; Cys --&gt; Arg) was specifically observed in both skin cancers and actinic keratoses.	Arginine	92-95	P53	Homo sapiens	6-9
11324502-0	1997	p53 independent G1 arrest and apoptosis induced by adriamycin.	Doxorubicin	51-61	P53	Homo sapiens	0-3
11324502-2	1997	In MCF-7 cells that harbor wild-type p53, adriamycin-induced G1 arrest and apoptosis was accompanied by p53-independent regulation of WAF1/CIP1 as well as bax mRNA levels.	Doxorubicin	42-52	P53	Homo sapiens	37-40
11324502-2	1997	In MCF-7 cells that harbor wild-type p53, adriamycin-induced G1 arrest and apoptosis was accompanied by p53-independent regulation of WAF1/CIP1 as well as bax mRNA levels.	Doxorubicin	42-52	P53	Homo sapiens	104-107
11324502-3	1997	In MDA-MB-231 cells which possess a mutant p53, adriamycin-induced G1 arrest and apoptosis was also associated with a concomitant up-regulation of WAF1/CIP1 mRNA while these cells did not express bax or bcl-2 messages.	Doxorubicin	48-58	P53	Homo sapiens	43-46
11324502-4	1997	Thus, adriamycin induces G1 arrest and apoptosis via a unique pathway which appears to involve activation of downstream effectors of p53-independent manner.	Doxorubicin	6-16	P53	Homo sapiens	133-136
9191791-4	1997	However, the cytoprotective effects of DEX appeared to be more prominent in cell lines with wild-type p53 status (n = 2) than in p53 mutant cell lines (n = 3).	Dexamethasone	39-42	P53	Homo sapiens	102-105
9213246-1	1997	The human hepatocellular carcinoma (HCC) cell line, HLF, expresses only mutant-type p53 (mt-p53), which has an amino acid substitution at the 244th residue from glycine to alanine.	Glycine	161-168	P53	Homo sapiens	84-87
9213246-1	1997	The human hepatocellular carcinoma (HCC) cell line, HLF, expresses only mutant-type p53 (mt-p53), which has an amino acid substitution at the 244th residue from glycine to alanine.	Glycine	161-168	P53	Homo sapiens	92-95
9213246-1	1997	The human hepatocellular carcinoma (HCC) cell line, HLF, expresses only mutant-type p53 (mt-p53), which has an amino acid substitution at the 244th residue from glycine to alanine.	Alanine	172-179	P53	Homo sapiens	84-87
9213246-1	1997	The human hepatocellular carcinoma (HCC) cell line, HLF, expresses only mutant-type p53 (mt-p53), which has an amino acid substitution at the 244th residue from glycine to alanine.	Alanine	172-179	P53	Homo sapiens	92-95
9154813-4	1997	Treatment of cytoplasmic extracts with RNase or puromycin in the presence of high salt, both of which are known to disrupt ribosomal function, dissociated p53 polypeptide from the ribosomes.	Salts	82-86	P53	Homo sapiens	155-158
9154814-6	1997	We have directly tested for cooperativity between neu and mutant p53 in mammary tumorigenesis by creating bitransgenic mice carrying MMTV-neu and 172Arg-to-His p53 mutant (p53-172H).	Histidine	156-159	P53	Homo sapiens	160-163
9154814-6	1997	We have directly tested for cooperativity between neu and mutant p53 in mammary tumorigenesis by creating bitransgenic mice carrying MMTV-neu and 172Arg-to-His p53 mutant (p53-172H).	Histidine	156-159	P53	Homo sapiens	160-163
9174048-1	1997	We have previously shown that p53 disruption sensitizes certain cancer cell types to cisplatin (CDDP) (Fan et al., 1995).	Cisplatin	85-94	P53	Homo sapiens	30-33
9149021-0	1997	Progesterone induces apoptosis and up-regulation of p53 expression in human ovarian carcinoma cell lines.	Progesterone	0-12	P53	Homo sapiens	52-55
9174048-1	1997	We have previously shown that p53 disruption sensitizes certain cancer cell types to cisplatin (CDDP) (Fan et al., 1995).	Cisplatin	96-100	P53	Homo sapiens	30-33
9174048-9	1997	Investigations into a possible cause of this enhanced sensitivity revealed that HCT-116 cells lacking p53 or p21 function exhibited a reduced ability to repair cisplatin-damaged CAT-reporter plasmids transfected into the cells.	Cisplatin	160-169	P53	Homo sapiens	102-105
9158397-18	1997	Paucity of p53 mutations may be explained by the absence of exposure to tobacco smoke or alcohol.	Alcohols	89-96	P53	Homo sapiens	11-14
9111352-8	1997	Conversely, activation of calpains by calcium ionophore led to a reduction of p53 in mammalian cells, and the effect was blocked by cell-permeant calpain inhibitors.	Calcium	38-45	P53	Homo sapiens	78-81
9158397-17	1997	CONCLUSIONS: Our results suggest that p53 gene mutations are less frequent in squamous carcinomas occurring in nonsmoking young patients who do not drink alcohol than in young smokers or in the general population.	Alcohols	154-161	P53	Homo sapiens	38-41
9206986-9	1997	This suggested that paclitaxel/RT would be a rational treatment approach for other malignancies with a high frequency of p53 mutations, such as gastric and pancreatic cancers.	Paclitaxel	20-30	P53	Homo sapiens	121-124
9164202-1	1997	PURPOSE: To test the hypothesis that high bcl-2 expression and accumulation of p53 protein, both of which should inhibit apoptosis, are associated with a poorer tamoxifen response and a more aggressive clinical course in estrogen receptor (ER)-positive metastatic breast cancer.	Tamoxifen	161-170	P53	Homo sapiens	79-82
9225073-0	1997	Modulation of p53, WAF1/p21 and BCL-2 expression during retinoic acid-induced differentiation of NB4 promyelocytic cells.	Tretinoin	56-69	P53	Homo sapiens	14-17
21590081-0	1997	Induction of p53 protein by carbon-ion and proton beam irradiation in two close human lymphoblastoid cell lines with different p53 status.	Carbon	28-34	P53	Homo sapiens	13-16
21590081-1	1997	In this study, we compared the kinetics of the postirradiation p53 protein expression for carbon ion beam (290 MeV/n, LET 75 keV/mu m) and proton beam (65 MeV) with that of (13)7Cs-gamma ray.	Carbon	90-96	P53	Homo sapiens	63-66
9129144-5	1997	Positive staining of p53 protein was observed in three of the paraffin embedded tissues that were available: brain tumor, rhabdomyosarcoma, and lymphocytes from a normal lymph node from the rhabdomyosarcoma patient.	Paraffin	62-70	P53	Homo sapiens	21-24
9108094-3	1997	Taxol (paclitaxel) is more effective in the presence of mutant p53.	Paclitaxel	0-5	P53	Homo sapiens	63-66
9108094-3	1997	Taxol (paclitaxel) is more effective in the presence of mutant p53.	Paclitaxel	7-17	P53	Homo sapiens	63-66
9108094-13	1997	The synergistic therapeutic effect of Taxol with (90)Y-ChL6 may relate to the p53 mutant status and BCL2 expression in HBT 3477 cells, observations that increase the likelihood that the results of this study are relevant to therapy for breast cancer in patients.	Paclitaxel	38-43	P53	Homo sapiens	78-81
9083038-6	1997	We show that cross-linking of ICAM-1 on the B lymphoma line A20 induces an increase in tyrosine phosphorylation of several cellular proteins, including the Src family kinase p53/p56(lyn).	Tyrosine	87-95	P53	Homo sapiens	174-177
9108075-1	1997	In the P53 tumor suppressor gene, a remarkably large number of somatic mutations are found at methylated CpG dinucleotides.	cytidylyl-3'-5'-guanosine	105-122	P53	Homo sapiens	7-27
9108075-5	1997	To investigate other possible mechanisms underlying the selectivity of BPDE binding, we have mapped the adducts in plasmid DNA containing genomic P53 sequences.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	71-75	P53	Homo sapiens	146-149
9074626-0	1997	The induction of apoptosis in proliferating human fibroblasts by oxygen radicals is associated with a p53- and p21WAF1CIP1 induction.	Reactive Oxygen Species	65-80	P53	Homo sapiens	102-105
9149846-0	1997	Antisense oligonucleotides to p53 tumor suppressor suppress the induction of apoptosis by epidermal growth factor in NCI-H 596 human lung cancer cells.	Oligonucleotides	10-26	P53	Homo sapiens	30-33
9149846-5	1997	Results showed that EGF plus p53 sense oligonucleotides induced EGF-dependent and p53-dependent apoptosis in NCI-H 596 cells within 8 hours.	Oligonucleotides	39-55	P53	Homo sapiens	29-32
9149846-5	1997	Results showed that EGF plus p53 sense oligonucleotides induced EGF-dependent and p53-dependent apoptosis in NCI-H 596 cells within 8 hours.	Oligonucleotides	39-55	P53	Homo sapiens	82-85
9149846-6	1997	On the other hand, antisense gene therapy using antisense oligonucleotides to p53 tumor suppressor suppressed the induction of EGF-dependent and p53-dependent apoptosis.	Oligonucleotides	58-74	P53	Homo sapiens	78-81
9149846-6	1997	On the other hand, antisense gene therapy using antisense oligonucleotides to p53 tumor suppressor suppressed the induction of EGF-dependent and p53-dependent apoptosis.	Oligonucleotides	58-74	P53	Homo sapiens	145-148
9149846-7	1997	Mutated p53 antisense-containing mutated CG dinucleotides had the same effect as that of p53 antisense on suppression of apoptosis in NCI-H 596 cells.	cytidylyl-3'-5'-guanosine	41-57	P53	Homo sapiens	8-11
9149846-8	1997	We found that a new nucleic acid drug, another mutated p53 antisense-containing mutation at three bases immediately 5" and 3" from the CG dinucleotides, potentiated the induction of apoptosis and failed to suppress the induction of EGF-dependent apoptosis.	cytidylyl-3'-5'-guanosine	135-151	P53	Homo sapiens	55-58
9149846-9	1997	These results suggest that gene therapy using antisense oligonucleotides to the p53 tumor suppressor is effective on EGF-dependent apoptosis of NCI-H 596 human non-small cell lung cancer.	Oligonucleotides	56-72	P53	Homo sapiens	80-83
12114668-5	1997	Immunohistochemical staining for p53 was performed on paraffin sections of formalin-fixed tumor tissue.	Paraffin	54-62	P53	Homo sapiens	33-36
9136508-1	1997	Immunohistochemical analysis of the p53 protein was performed on paraffin sections of tumor tissue from 210 breast cancer patients.	Paraffin	65-73	P53	Homo sapiens	36-39
9070661-4	1997	In these cells, wild type for the p53 gene, we have overexpressed the mutant p53(175(Arg&gt;His)) protein leading to a p53 mutant phenotype, as verified by the absence of a G1 arrest after gamma-irradiation.	Arginine	85-88	P53	Homo sapiens	34-37
9070661-4	1997	In these cells, wild type for the p53 gene, we have overexpressed the mutant p53(175(Arg&gt;His)) protein leading to a p53 mutant phenotype, as verified by the absence of a G1 arrest after gamma-irradiation.	Arginine	85-88	P53	Homo sapiens	77-80
9070661-4	1997	In these cells, wild type for the p53 gene, we have overexpressed the mutant p53(175(Arg&gt;His)) protein leading to a p53 mutant phenotype, as verified by the absence of a G1 arrest after gamma-irradiation.	Arginine	85-88	P53	Homo sapiens	77-80
9215149-1	1997	AIM: To document the frequency and extent of p53 gene product expression in paraffin sections of resected non-small cell carcinoma of the lung and in cytological preparations of the same tumours; to determine the effect of microwave antigen retrieval on antigen detection.	Paraffin	76-84	P53	Homo sapiens	45-48
10743138-2	1997	The results indicated that after treated with ST and RA, the cells became well-differentiated, the cell growth was suppressed, contact suppress was partially recovered, colony forming was decreased, protooncogenes (C-myc bcl-2) protein was decreased, tumor suppressor gene (p53) protein was increased.	Tretinoin	53-55	P53	Homo sapiens	274-277
9092641-8	1997	Hydrogen peroxide treatment of cells cotransfected with p53 results in a marked decrease in CAT activity, suggesting that oxidation of p53 decreases the ability of the protein to bind to consensus DNA and transactivate target genes in vivo.	Hydrogen Peroxide	0-17	P53	Homo sapiens	56-59
9092641-8	1997	Hydrogen peroxide treatment of cells cotransfected with p53 results in a marked decrease in CAT activity, suggesting that oxidation of p53 decreases the ability of the protein to bind to consensus DNA and transactivate target genes in vivo.	Hydrogen Peroxide	0-17	P53	Homo sapiens	135-138
9071734-0	1997	A rapid and nonisotopic method for the screening and sequencing of p53 gene mutations in formalin-fixed, paraffin-embedded tumors.	Paraffin	105-113	P53	Homo sapiens	67-70
9076236-3	1997	DESIGN: We screened for p53 protein expression in a variety of benign epithelial lesions of upper respiratory tract using monoclonal antibody DO-1 on paraffin-embedded material.	Paraffin	150-158	P53	Homo sapiens	24-27
9041188-4	1997	By using for each cell line the paclitaxel IC50, we found that these concentrations were sufficient to induce an increase in p53 levels in all of the four wt p53-expressing cells, whereas in the mutated p53-expressing cells, the levels were unaffected.	Paclitaxel	32-42	P53	Homo sapiens	125-128
9041188-4	1997	By using for each cell line the paclitaxel IC50, we found that these concentrations were sufficient to induce an increase in p53 levels in all of the four wt p53-expressing cells, whereas in the mutated p53-expressing cells, the levels were unaffected.	Paclitaxel	32-42	P53	Homo sapiens	158-161
9041188-4	1997	By using for each cell line the paclitaxel IC50, we found that these concentrations were sufficient to induce an increase in p53 levels in all of the four wt p53-expressing cells, whereas in the mutated p53-expressing cells, the levels were unaffected.	Paclitaxel	32-42	P53	Homo sapiens	158-161
9041254-6	1997	Furthermore, a CGC--&gt;CAC transition in the p53 gene of the adenoma resulted in an Arg--&gt;His missense mutation in codon 175.	Arginine	85-88	P53	Homo sapiens	46-49
9071730-2	1997	A recent study reported diminished p53 immunoreactivity in slides that had been sectioned from parafinn-embedded tissue blocks and stored at room temperature.	parafinn	95-103	P53	Homo sapiens	35-38
9071734-2	1997	In this study, we describe a sensitive, rapid, nonisotopic and inexpensive procedure for the polymerase chain reaction (PCR)-single-stranded conformational polymorphism (SSCP) detection and subsequent sequencing of p53 mutations in formalin-fixed and paraffin-embedded tumor (PET) samples.	Paraffin	251-259	P53	Homo sapiens	215-218
9042396-9	1997	The mutation in codon 170 is adjacent to a mutation hotspot of the human p53 gene (codon 175) and eliminates a critical zinc-coordinating cysteine residue such that the mutant protein is likely to be denatured and have a dominant negative effect on normal p53 function.	Cysteine	138-146	P53	Homo sapiens	73-76
9047387-8	1997	On the contrary, inhibition of protein kinase C (PKC) by calphostin-C led to an abrogation of (+/-)-anti-BPDE mediated p53 induction.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	105-109	P53	Homo sapiens	119-122
9055811-3	1997	It features many characteristics found in all p53 proteins: (i) the five domains highly conserved during evolution, (ii) an acidic N terminus, (iii) a hydrophilic C terminus and (iv) a penultimate serine residue.	Serine	197-203	P53	Homo sapiens	46-49
9058378-5	1997	Strikingly, cotransfection of either the murine or human wild type p53, but not a mutant p53, repressed the dexamethasone-stimulated transactivation of reporter plasmids containing either the sgkGRE or a consensus GRE.	Dexamethasone	108-121	P53	Homo sapiens	67-70
9058378-7	1997	The p53-mediated repression of dexamethasone-induced sgkGRE activity required both the DNA binding and transactivation functions of the p53 protein.	Dexamethasone	31-44	P53	Homo sapiens	4-7
9058378-7	1997	The p53-mediated repression of dexamethasone-induced sgkGRE activity required both the DNA binding and transactivation functions of the p53 protein.	Dexamethasone	31-44	P53	Homo sapiens	136-139
9075790-1	1997	The relationship between p53 overexpression and clinicopathologic variables in gastric cancer was evaluated using 304 paraffin-embedded gastric tumor tissues.	Paraffin	118-126	P53	Homo sapiens	25-28
9047387-0	1997	Modulation of (+/-)-anti-BPDE mediated p53 accumulation by inhibitors of protein kinase C and poly(ADP-ribose) polymerase.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	25-29	P53	Homo sapiens	39-42
9047387-5	1997	The poly(ADP-ribose) polymerase inhibitor, 3-aminobenzamide (3-AB), diminished the p53 induction response by concomitantly decreasing the extent of (+/-)-anti-BPDE induced DNA damage in cells pretreated with the inhibitor.	3-aminobenzamide	43-59	P53	Homo sapiens	83-86
9047387-5	1997	The poly(ADP-ribose) polymerase inhibitor, 3-aminobenzamide (3-AB), diminished the p53 induction response by concomitantly decreasing the extent of (+/-)-anti-BPDE induced DNA damage in cells pretreated with the inhibitor.	3-aminobenzamide	61-65	P53	Homo sapiens	83-86
9047387-5	1997	The poly(ADP-ribose) polymerase inhibitor, 3-aminobenzamide (3-AB), diminished the p53 induction response by concomitantly decreasing the extent of (+/-)-anti-BPDE induced DNA damage in cells pretreated with the inhibitor.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	159-163	P53	Homo sapiens	83-86
9020141-0	1997	1-(5-Isoquinolinesulfonyl)-2-methylpiperazine induces apoptosis in human neuroblastoma cells, SH-SY5Y, through a p53-dependent pathway.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	0-45	P53	Homo sapiens	113-116
9020141-8	1997	Only cell lines harboring the wild-type p53 gene were responsive to the stimulatory effect of H-7 on nuclear accumulation of p53.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	94-97	P53	Homo sapiens	40-43
9020141-8	1997	Only cell lines harboring the wild-type p53 gene were responsive to the stimulatory effect of H-7 on nuclear accumulation of p53.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	94-97	P53	Homo sapiens	125-128
9020141-9	1997	Furthermore, cell lines carrying a mutated p53 gene were resistant to the cytotoxic effect of H-7.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	94-97	P53	Homo sapiens	43-46
9020141-11	1997	Taken together, these data strongly suggest that a p53-dependent mechanism contributes to the cytotoxicity of H-7 in human neuroblastoma cells.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	110-113	P53	Homo sapiens	51-54
9042396-9	1997	The mutation in codon 170 is adjacent to a mutation hotspot of the human p53 gene (codon 175) and eliminates a critical zinc-coordinating cysteine residue such that the mutant protein is likely to be denatured and have a dominant negative effect on normal p53 function.	Cysteine	138-146	P53	Homo sapiens	256-259
18726304-2	1997	It was confirmed that the mt-p53 cDNA contained the complete coding sequence of p53 gene but mutated at codon 245 (G--&gt;T) and resulted in glycine to cysteine by sequencing analysis.	Glycine	141-148	P53	Homo sapiens	29-32
9058631-4	1997	METHODS: The p53 expression in tumour tissue was studied by immunohistochemistry using CM1 polyclonal rabbit antibody and formalin-fixed, paraffin-embedded material.	Paraffin	138-146	P53	Homo sapiens	13-16
18726304-2	1997	It was confirmed that the mt-p53 cDNA contained the complete coding sequence of p53 gene but mutated at codon 245 (G--&gt;T) and resulted in glycine to cysteine by sequencing analysis.	Cysteine	152-160	P53	Homo sapiens	29-32
9000576-1	1997	Growth arrest and differentiation of leukemic cells by phorbol 12-myristate 13-acetate (PMA) is accompanied by p53-independent activation of p21WAF1/CIP1 and c-myc down-regulation.	Tetradecanoylphorbol Acetate	55-86	P53	Homo sapiens	111-114
9018111-0	1997	Inhibition of the growth of WI-38 fibroblasts by benzyloxycarbonyl-Leu-Leu-Tyr diazomethyl ketone: evidence that cleavage of p53 by a calpain-like protease is necessary for G1 to S-phase transition.	benzyloxycarbonyl-leu-leu-tyr diazomethyl ketone	49-97	P53	Homo sapiens	125-128
9018111-6	1997	Chelation of extracellular Ca2+ by addition of EGTA inhibited the p53 degradation.	Egtazic Acid	47-51	P53	Homo sapiens	66-69
9053847-6	1997	Moreover, detection of ThaI polymorphism of codon 72 showed that MCF-7 cells predominantly express wild-type p53 with proline, while mutated p53 in MCF-7/Adr cells contains an arginine residue at codon 72.	Arginine	176-184	P53	Homo sapiens	141-144
9000576-1	1997	Growth arrest and differentiation of leukemic cells by phorbol 12-myristate 13-acetate (PMA) is accompanied by p53-independent activation of p21WAF1/CIP1 and c-myc down-regulation.	Tetradecanoylphorbol Acetate	88-91	P53	Homo sapiens	111-114
9010220-0	1997	Identification of p53 genetic suppressor elements which confer resistance to cisplatin.	Cisplatin	77-86	P53	Homo sapiens	18-21
9010231-4	1997	As a preliminary study, we demonstrated in breast adenocarcinoma cell lines that the nuclear accumulation of the inhibitor of cyclin dependent kinase p21(WAFl/CIP1), in response to adriamycin treatment, specifically reflected the activity of a functional wild-type p53 protein.	Doxorubicin	181-191	P53	Homo sapiens	265-268
9010220-1	1997	Loss of p53 function is associated with the acquisition of cisplatin resistance in the human ovarian adenocarcinoma A2780 cell line.	Cisplatin	59-68	P53	Homo sapiens	8-11
9010220-7	1997	A synthetic peptide, representing the predicted amino acid sequence of this GSE, conferred resistance to cisplatin when introduced into A2780 cells and inhibited the sequence specific DNA binding activity of p53 protein in vitro.	Cisplatin	105-114	P53	Homo sapiens	208-211
9010220-8	1997	Overall, these results directly indicate that inactivation of p53 function confers cisplatin resistance in these human ovarian tumour cells.	Cisplatin	83-92	P53	Homo sapiens	62-65
9013707-0	1997	The p53-regulated cyclin G gene promotes cell growth: p53 downstream effectors cyclin G and Gadd45 exert different effects on cisplatin chemosensitivity.	Cisplatin	126-135	P53	Homo sapiens	4-7
8985102-3	1997	The mutant p53 gene (mp53: codon273Arg-His) was introduced into normal human fibroblasts (OUMS-24 line) and a G418-resistant clone, OUMS-24/P6 line, was obtained.	codon273arg	27-38	P53	Homo sapiens	11-14
8985102-3	1997	The mutant p53 gene (mp53: codon273Arg-His) was introduced into normal human fibroblasts (OUMS-24 line) and a G418-resistant clone, OUMS-24/P6 line, was obtained.	Histidine	39-42	P53	Homo sapiens	11-14
9013707-0	1997	The p53-regulated cyclin G gene promotes cell growth: p53 downstream effectors cyclin G and Gadd45 exert different effects on cisplatin chemosensitivity.	Cisplatin	126-135	P53	Homo sapiens	54-57
9013707-8	1997	Overexpression of another p53-regulated gene, GADD45, by contrast, protected cells from cisplatin killing.	Cisplatin	88-97	P53	Homo sapiens	26-29
9013707-9	1997	These findings suggest that different downstream effectors of the p53 pathway may exert different effects on cellular survival after treatment with cancer chemotherapy drugs such as cisplatin.	Cisplatin	182-191	P53	Homo sapiens	66-69
8980360-3	1997	Genomic p53 was amplified with the polymerase chain reaction (PCR) from formalin-fixed, paraffin-embedded tissues.	Paraffin	88-96	P53	Homo sapiens	8-11
8988912-6	1997	Folate insufficiency has been implicated in the development of several human and experimental cancers, and aberrations within these regions of the p53 gene that were examined in this study are thought to play an integral role in carcinogenesis.	Folic Acid	0-6	P53	Homo sapiens	147-150
9030234-9	1997	On the other hand, p53-depleted cells were reported to be more sensitive to taxanes than p53-proficient cells.	Taxoids	76-83	P53	Homo sapiens	19-22
9313826-2	1997	The p53 immunohistochemistry was performed on paraffin sections from 88 tumour samples.	Paraffin	46-54	P53	Homo sapiens	4-7
9323493-0	1997	Changes in levels of expression of p53 and the product of the bcl-2 in lines of gastric cancer cells during cisplatin-induced apoptosis.	Cisplatin	108-117	P53	Homo sapiens	35-38
9323493-2	1997	After incubation with cisplatin, apoptotic cells were detected more frequently among MKN-45 and MKN-74 cells with a wild-type gene for p53 and without expression of the bcl-2 protein than among HSC-39, MKN-28, and KATO-III cells with a mutation or complete deletion of the gene for p53 and with overexpression of the bcl-2 protein.	Cisplatin	22-31	P53	Homo sapiens	135-138
9323493-2	1997	After incubation with cisplatin, apoptotic cells were detected more frequently among MKN-45 and MKN-74 cells with a wild-type gene for p53 and without expression of the bcl-2 protein than among HSC-39, MKN-28, and KATO-III cells with a mutation or complete deletion of the gene for p53 and with overexpression of the bcl-2 protein.	Cisplatin	22-31	P53	Homo sapiens	282-285
9323493-3	1997	The levels of p53 protein increased after treatment with cisplatin in MKN-74 cells.	Cisplatin	57-66	P53	Homo sapiens	14-17
8995554-6	1997	We conclude that PCR-TGGE is an appropriate method for detection of p53 point mutations in paraffin-embedded material.	Paraffin	91-99	P53	Homo sapiens	68-71
14646556-3	1997	Here we studied Adriamycin (ADM)-induced apoptosis in four human bladder cancer cell lines in respect of p53, p21WAF1/CIP1 and Bcl-2 family proteins.	Doxorubicin	16-26	P53	Homo sapiens	105-108
14646556-3	1997	Here we studied Adriamycin (ADM)-induced apoptosis in four human bladder cancer cell lines in respect of p53, p21WAF1/CIP1 and Bcl-2 family proteins.	Doxorubicin	28-31	P53	Homo sapiens	105-108
14646558-0	1997	5-Fluorouracil (5-FU) induced apoptosis in gastric cancer cell lines: role of the p53 gene.	Fluorouracil	0-14	P53	Homo sapiens	82-85
14646558-0	1997	5-Fluorouracil (5-FU) induced apoptosis in gastric cancer cell lines: role of the p53 gene.	Fluorouracil	16-20	P53	Homo sapiens	82-85
14646558-1	1997	We examined chemosensitivity to 5-fluorouracil (5-FU) in four human gastric cancer cell lines, by analyzing the expression of p53 and its related genes.	Fluorouracil	32-46	P53	Homo sapiens	126-129
14646558-1	1997	We examined chemosensitivity to 5-fluorouracil (5-FU) in four human gastric cancer cell lines, by analyzing the expression of p53 and its related genes.	Fluorouracil	48-52	P53	Homo sapiens	126-129
14646558-4	1997	On the other hand, 50 microM 5-FU had little effect on the induction of apoptosis in MKN-74 cells, the value being approximately 2% after 72 h. Induction of P53 expression was noted 3 h after initiating the treatment, followed by the induction of P21/Waf1 after 6 h in both MKN-74 and MKN-45 cells.	Fluorouracil	29-33	P53	Homo sapiens	157-160
14646558-8	1997	These results might indicate that (1) 1mM 5-FU induces apoptosis in cultured gastric cancer cells carrying the wild-type p53 gene, but not those carrying the mutated type or a gene deletion, and (2) the elevated Bax/Bcl-2 expression ratio plays a more crucial role than the higher expression of P21/Waf1 in the induction of p53- gene dependent apoptosis.	Fluorouracil	42-46	P53	Homo sapiens	121-124
14646558-8	1997	These results might indicate that (1) 1mM 5-FU induces apoptosis in cultured gastric cancer cells carrying the wild-type p53 gene, but not those carrying the mutated type or a gene deletion, and (2) the elevated Bax/Bcl-2 expression ratio plays a more crucial role than the higher expression of P21/Waf1 in the induction of p53- gene dependent apoptosis.	Fluorouracil	42-46	P53	Homo sapiens	324-327
9374378-4	1997	Drug resistance was associated with considerably enhanced expression of the p53 suppressor protein in HeLa-C3 cells after cisplatin exposure but seemed not to be regulated by the bcl-2-dependent pathway.	Cisplatin	122-131	P53	Homo sapiens	76-79
9032539-2	1997	MATERIALS AND METHODS: The p53 protein in the paraffin-embedded materials taken from 72 patients with RCCs was evaluated immunohistochemically and was compared with the histological findings, expression of proliferating cell nuclear antigen (PCNA), genetic instability as assessed by 2c deviation index (2cDI) and 5c exceeding rate (5cER) as well as clinical outcome.	Paraffin	46-54	P53	Homo sapiens	27-30
9393591-3	1997	p53 nuclear accumulation was detected in 48% of the primary tumours using the PAb1801 antibody in archival paraffin-embedded tissue sections.	Paraffin	107-115	P53	Homo sapiens	0-3
9868092-1	1997	Using polymerase chain reaction single strand conformational polymorphism (PCR-SSCP) and EB staining technique, paraffin-embeded sections of 20 hydatidiform mole and 4 choriocarcinoma were detected in the exons 5 and 8 of p53 gene.	Paraffin	112-120	P53	Homo sapiens	222-225
10073037-0	1997	[Study of detecting p53 gene of laryngeal carcinoma on paraffin-embedded tissue sections by in situ polymerase chain reaction].	Paraffin	55-63	P53	Homo sapiens	20-23
10073037-1	1997	In order to investigate alterations of p53 gene in laryngeal carcinoma, five cases of paraffin-embedded tissue were detected by in situ polymerase chain reaction (PCR).	Paraffin	86-94	P53	Homo sapiens	39-42
9177500-4	1997	METHODS: We analysed p53 expression in a group of transplanted, cyclosporin A-treated, KS patients by immunohistochemistry, utilizing the DO-7 (with and without the antigen retrieval pretreatment), and the PAb 240 monoclonal anti-p53 antibodies, the latter of which is able to detect a mutated epitope, and evaluating staining intensity and localization, whether cytoplasmic or nuclear.	Cyclosporine	64-77	P53	Homo sapiens	21-24
9521509-1	1997	The immunohistological expression of p53 and MDM2 oncoproteins was examined in paraffin embedded tissue from 106 patients with transitional cell carcinoma of the urinary bladder and was related to various clinicopathological features, the expression of proliferation associated markers (proliferating cell nuclear antigen - PCNA - and Ki-67), c-erb B-2 oncoprotein and epidermal growth factor receptor (EGFR), as well as to survival.	Paraffin	79-87	P53	Homo sapiens	37-40
9020384-5	1997	A novel germline p53 mutation was identified at codon 133 (ATG-->AGG) in exon 5, resulting in the substitution of arginine for methionine, in all four cancer-affected individuals and in three apparently healthy individuals.	Arginine	114-122	P53	Homo sapiens	17-20
9020384-5	1997	A novel germline p53 mutation was identified at codon 133 (ATG-->AGG) in exon 5, resulting in the substitution of arginine for methionine, in all four cancer-affected individuals and in three apparently healthy individuals.	Methionine	127-137	P53	Homo sapiens	17-20
9342752-6	1997	Our results indicate that IHC could be applied for studies of p53 protein accumulation in archival formalin fixed, paraffin-embedded bladder tumours.	Paraffin	115-123	P53	Homo sapiens	62-65
9260591-4	1997	The expression of the proteins p53 and mdm2 was determined immunohistochemically using formalin-fixed, paraffin-embedded material.	Paraffin	103-111	P53	Homo sapiens	31-34
8996169-0	1997	Antisense oligonucleotides targeting p53.	Oligonucleotides	10-26	P53	Homo sapiens	37-40
9563008-0	1997	Sensitization of cis-platinum by a recombinant adenovirus vector expressing wild-type p53 gene in human ovarian carcinomas.	Cisplatin	17-29	P53	Homo sapiens	86-89
9563008-2	1997	We have examined the role of wild-type p53 in resistance to cis-diamminedichloroplatinum (II) (CDDP) in human ovarian cancer cells using a recombinant adenovirus containing human wild-type p53 cDNA (Adwtp53).	Cisplatin	60-93	P53	Homo sapiens	39-42
9563008-3	1997	In this study we used the human ovarian A2780 tumor cells (wtp53), which are sensitive to CDDP and A2780/CP tumor cells (nonfunctional/mutant p53) and are resistant to CDDP.	Cisplatin	90-94	P53	Homo sapiens	61-64
9816160-8	1996	Conversely, the hazard increased with the increase of p53-positive cells only for tumors with a [3H]dT LI lower than 7.5%.	Tritium	97-99	P53	Homo sapiens	54-57
8980242-4	1996	The probability of clinical response to biochemically modulated 5-FU was independent of p53 and PCNA expression.	Fluorouracil	64-68	P53	Homo sapiens	88-91
8954910-0	1996	Cytokine and low-level nitric oxide prestimulation block p53 accumulation and apoptosis of RAW 264.7 macrophages.	Nitric Oxide	23-35	P53	Homo sapiens	57-60
8954910-2	1996	The cellular response to the NO donor S-nitrosoglutathione (GSNO) comprises an apoptotic morphology and DNA fragmentation, which largely depends on the accumulation of the tumor suppressor gene product p53.	S-Nitrosoglutathione	38-58	P53	Homo sapiens	202-205
8954910-2	1996	The cellular response to the NO donor S-nitrosoglutathione (GSNO) comprises an apoptotic morphology and DNA fragmentation, which largely depends on the accumulation of the tumor suppressor gene product p53.	S-Nitrosoglutathione	60-64	P53	Homo sapiens	202-205
8954910-6	1996	Upregulation of protective mechanisms in response to non-lethal NO concentrations or by LPS, cytokine pre-stimulation may redirect the ability of nitric oxide to upregulate p53 and to initiate macrophage apoptosis, thereby modulating cellular susceptibility towards NO-intoxication.	Nitric Oxide	146-158	P53	Homo sapiens	173-176
8985154-2	1996	The two alternative forms of Lyn (p53 and p56) were found to be tyrosine-phosphorylated within 30 s after the stimulation with acetyl LDL.	Tyrosine	64-72	P53	Homo sapiens	34-37
8986612-7	1996	After removal of Dex, SV40T-p53 dots gradually disappear, while the PML structures remain.	Dexamethasone	17-20	P53	Homo sapiens	28-31
8957074-4	1996	Moreover, p53 was immunologically detected in protein complexes formed on oligonucleotides from both the TATA-containing and TATA-less promoters.	Oligonucleotides	74-90	P53	Homo sapiens	10-13
8968086-2	1996	Recently published data have suggested a possible role of p53 in nucleotide excision repair: an association of p53 and xeroderma pigmentosum group B protein and a greater sensitivity to cisplatin of RKO cells transfected with the E6 protein of human papilloma virus (inactivating p53).	Cisplatin	186-195	P53	Homo sapiens	58-61
8942496-3	1996	STUDY DESIGN: Immunohistochemical evaluation was used to examine p53 expression in paraffin blocks from 179 endometrial adenocarcinomas.	Paraffin	83-91	P53	Homo sapiens	65-68
9038605-4	1996	In 4 cases, the mutations lead to distinct changes in the primary or secondary structure of the protein (cysteine--&gt;tyrosine, proline--&gt;leucine) and were associated with marked accumulation of p53 protein.	Cysteine	105-113	P53	Homo sapiens	199-202
9038605-4	1996	In 4 cases, the mutations lead to distinct changes in the primary or secondary structure of the protein (cysteine--&gt;tyrosine, proline--&gt;leucine) and were associated with marked accumulation of p53 protein.	Tyrosine	119-127	P53	Homo sapiens	199-202
8918047-6	1996	seropositive IHAT (1/64) and low LTT (20 &amp; 40%) gave positive P53 antibody and moderate (1) and marked (1) degrees Cathepsin D.	Adenosine Monophosphate	42-45	P53	Homo sapiens	66-69
8989916-0	1996	Induction of HSP70 gene expression by modulation of Ca(+2) ion and cellular p53 protein by curcumin in colorectal carcinoma cells.	Curcumin	91-99	P53	Homo sapiens	76-79
8989916-5	1996	The reduction of p53 gene expression was accompanied by the induction of HSP70 gene expression in the curcumin-treated cells.	Curcumin	102-110	P53	Homo sapiens	17-20
8989916-6	1996	These findings suggest that curcumin may induce the expression of the HSP70 gene through the initial depletion of intracellular Ca(+2), followed by the suppression of p53 gene function in the target cells.	Curcumin	28-36	P53	Homo sapiens	167-170
9182295-5	1996	Single strand conformation polymorphism analysis (SSCP-PCR) from DNA obtained by microdissection demonstrated the presence of a mutation (TAT--&gt;TGT; Tyr--&gt;Cys) in codon 220, exon six of the p53 gene in the anaplastic component, that was absent in the well-differentiated follicular areas.	Tyrosine	152-155	P53	Homo sapiens	196-199
9182295-5	1996	Single strand conformation polymorphism analysis (SSCP-PCR) from DNA obtained by microdissection demonstrated the presence of a mutation (TAT--&gt;TGT; Tyr--&gt;Cys) in codon 220, exon six of the p53 gene in the anaplastic component, that was absent in the well-differentiated follicular areas.	Cysteine	161-164	P53	Homo sapiens	196-199
8943066-0	1996	BAX enhances paclitaxel-induced apoptosis through a p53-independent pathway.	Paclitaxel	13-23	P53	Homo sapiens	52-55
8955620-0	1996	Detection of p53 gene abnormality by sequence analysis of archival paraffin tissue.	Paraffin	67-75	P53	Homo sapiens	13-16
21541641-4	1996	Increased p53 protein levels have previously been shown to correlate with disease progression in a series of colorectal carcinoma patients treated with 5-FU/folinic acid biomodulated chemotherapy.	Fluorouracil	152-156	P53	Homo sapiens	10-13
8967975-1	1996	With the use of clonogenic survival assays, we show that wild-type p53-expressing A2780 human ovarian cell lines transfected with a dominant negative mutant p53 gene (codon 143, valine to alanine) acquired cross-resistance to ionizing radiation, cisplatin, doxorubicin, and 1-beta-D-arabinofuranosylcytosine.	Alanine	188-195	P53	Homo sapiens	67-70
8967975-1	1996	With the use of clonogenic survival assays, we show that wild-type p53-expressing A2780 human ovarian cell lines transfected with a dominant negative mutant p53 gene (codon 143, valine to alanine) acquired cross-resistance to ionizing radiation, cisplatin, doxorubicin, and 1-beta-D-arabinofuranosylcytosine.	Alanine	188-195	P53	Homo sapiens	157-160
8967975-1	1996	With the use of clonogenic survival assays, we show that wild-type p53-expressing A2780 human ovarian cell lines transfected with a dominant negative mutant p53 gene (codon 143, valine to alanine) acquired cross-resistance to ionizing radiation, cisplatin, doxorubicin, and 1-beta-D-arabinofuranosylcytosine.	Cisplatin	246-255	P53	Homo sapiens	67-70
8967975-1	1996	With the use of clonogenic survival assays, we show that wild-type p53-expressing A2780 human ovarian cell lines transfected with a dominant negative mutant p53 gene (codon 143, valine to alanine) acquired cross-resistance to ionizing radiation, cisplatin, doxorubicin, and 1-beta-D-arabinofuranosylcytosine.	Cisplatin	246-255	P53	Homo sapiens	157-160
8967975-1	1996	With the use of clonogenic survival assays, we show that wild-type p53-expressing A2780 human ovarian cell lines transfected with a dominant negative mutant p53 gene (codon 143, valine to alanine) acquired cross-resistance to ionizing radiation, cisplatin, doxorubicin, and 1-beta-D-arabinofuranosylcytosine.	Doxorubicin	257-268	P53	Homo sapiens	67-70
8967975-1	1996	With the use of clonogenic survival assays, we show that wild-type p53-expressing A2780 human ovarian cell lines transfected with a dominant negative mutant p53 gene (codon 143, valine to alanine) acquired cross-resistance to ionizing radiation, cisplatin, doxorubicin, and 1-beta-D-arabinofuranosylcytosine.	Doxorubicin	257-268	P53	Homo sapiens	157-160
8945622-4	1996	When exposed to DNA-damaging agents, cisplatin or mitomycin C, apoptosis was induced in RT4 with the wild-type (wt) p53/wt p21, whereas T24 with the p53 non-sense mutation/wt p21 was resistant.	Cisplatin	37-46	P53	Homo sapiens	116-119
8945622-4	1996	When exposed to DNA-damaging agents, cisplatin or mitomycin C, apoptosis was induced in RT4 with the wild-type (wt) p53/wt p21, whereas T24 with the p53 non-sense mutation/wt p21 was resistant.	Cisplatin	37-46	P53	Homo sapiens	149-152
8950204-4	1996	Northern blot analyses showed that p53 and p21Waf1/Cip1 mRNA were detectable in all untreated cells, and increasing amounts of these transcripts were identified in all cell lines treated with cisplatin.	Cisplatin	192-201	P53	Homo sapiens	35-38
8950204-7	1996	Our results show that there were differences in sensitivity to cisplatin among four types of high risk HPV-positive cells, possibly due to different levels of p21Waf1/Cip1 up-regulation by functional p53.	Cisplatin	63-72	P53	Homo sapiens	200-203
8942499-3	1996	Overexpression of p53 protein was determined with the use of immunohistochemistry on fixed and paraffin-embedded tissue.	Paraffin	95-103	P53	Homo sapiens	18-21
9042268-3	1996	The cytotoxic effects of DNA-crosslinking chemotherapeutica such as cisplatin could be enhanced by mutated p53 which is no longer able to repair drug-induced DNA damage.	Cisplatin	68-77	P53	Homo sapiens	107-110
9042268-4	1996	In contrast, DNA synthesis blockers such as fluorouracil can induce apoptosis through p53-dependent mechanisms.	Fluorouracil	44-56	P53	Homo sapiens	86-89
9042215-4	1996	Among the 21 patients with stage III-IV disease, a complete clinical response to front-line platinum-based chemotherapy was obtained by 46.2% of the 13 patients without anti-p53 antibodies and 25.0% of the 8 patients with anti-p53 antibodies.	Platinum	92-100	P53	Homo sapiens	174-177
8895764-3	1996	In this report, we describe the mechanism by which the retinoid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid (CD437) induces p21WAF1/CIP1 in breast carcinoma cells possessing either a wild-type (MCF-7 cells) or mutated (MDA-MB-468 cells) p53.	CD 437	64-129	P53	Homo sapiens	259-262
9042215-4	1996	Among the 21 patients with stage III-IV disease, a complete clinical response to front-line platinum-based chemotherapy was obtained by 46.2% of the 13 patients without anti-p53 antibodies and 25.0% of the 8 patients with anti-p53 antibodies.	Platinum	92-100	P53	Homo sapiens	227-230
9042218-3	1996	The regulatory and controlling influence of Tamoxifen on numerous genes involved in apoptosis (p53, Bcl 2, c-myc, erb-B2 and others) will be discussed in this review.	Tamoxifen	44-53	P53	Homo sapiens	95-98
8895764-10	1996	Thus, CD437 is a novel retinoid which enhances p21WAF1/CIP1 mRNA levels through stabilization of the message regardless of the p53 status of the cell.	CD 437	6-11	P53	Homo sapiens	127-130
8895764-3	1996	In this report, we describe the mechanism by which the retinoid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid (CD437) induces p21WAF1/CIP1 in breast carcinoma cells possessing either a wild-type (MCF-7 cells) or mutated (MDA-MB-468 cells) p53.	CD 437	131-136	P53	Homo sapiens	259-262
8903408-5	1996	Introduction of WT-p53 into AFP-positive HCC cells by retroviral infection markedly inhibited their clonal growth in monolayer and soft agar cultures, and increased the sensitivity of these cells to the chemotherapeutic drug, cisplatin.	Cisplatin	226-235	P53	Homo sapiens	19-22
8960021-8	1996	The association we found between alcohol intake and mutant p53 expression may deserve further investigation.	Alcohols	33-40	P53	Homo sapiens	59-62
8875976-4	1996	Three peaks of p53NK activity were observed following fractionation of HeLa cell lysates; these activities were each able to catalyse phosphorylation of up to three residues (serines 4, 6 and 9 in murine p53) within the N-terminus of the p53 protein.	Serine	175-182	P53	Homo sapiens	15-18
8956076-4	1996	The C-terminal segment p53(361-393) (3) and its derivative phosphorylated at serine 392 (3P392) were synthesized as partially protected peptides in the solid phase using Fmoc chemistry.	Serine	77-83	P53	Homo sapiens	23-26
8956076-5	1996	Phosphoamino acid was incorporated into the N-terminal segment (1P315) at the residue corresponding to p53 serine 315 as Boc-Ser(PO3(Bzl)2)-OH during synthesis.	Serine	107-113	P53	Homo sapiens	103-106
8956076-7	1996	A derivative phosphorylated at serine 378 was synthesized in a one-step condensation of the unphosphorylated N-terminal segment (1) and the phosphorylated long C-terminal segment p53(335-393) (2-3P378).	Serine	31-37	P53	Homo sapiens	179-182
8911337-1	1996	A more effective gene therapy strategy for lung cancer using sequential cisplatin administration and adenovirus-mediated p53 gene transfer was developed on the basis of our previous observation of enhanced expression of a reporter gene in malignant cells exposed to cisplatin before gene transfer.	Cisplatin	266-275	P53	Homo sapiens	121-124
8911337-2	1996	Transfer of the normal (wildtype) p53 gene into cisplatin-treated H1299 cells, in which p53 is homozygously deleted, resulted in up to a 60% further inhibition of cell proliferation in vitro than p53 transfer into untreated H1299 cells.	Cisplatin	48-57	P53	Homo sapiens	34-37
8911337-2	1996	Transfer of the normal (wildtype) p53 gene into cisplatin-treated H1299 cells, in which p53 is homozygously deleted, resulted in up to a 60% further inhibition of cell proliferation in vitro than p53 transfer into untreated H1299 cells.	Cisplatin	48-57	P53	Homo sapiens	88-91
8911337-2	1996	Transfer of the normal (wildtype) p53 gene into cisplatin-treated H1299 cells, in which p53 is homozygously deleted, resulted in up to a 60% further inhibition of cell proliferation in vitro than p53 transfer into untreated H1299 cells.	Cisplatin	48-57	P53	Homo sapiens	88-91
8911337-3	1996	The cisplatin plus p53 gene transfer strategy yielded significantly greater apoptosis and tumor growth suppression in an animal model of subcutaneous H1299 tumor nodules than wildtype p53 gene transfer alone.	Cisplatin	4-13	P53	Homo sapiens	184-187
8911337-4	1996	The timing of cisplatin administration and p53 gene transfer was shown to be critical: cisplatin administration simultaneous with or subsequent to p53 gene transfer was less effective than cisplatin-first sequential treatment.	Cisplatin	14-23	P53	Homo sapiens	147-150
8911337-4	1996	The timing of cisplatin administration and p53 gene transfer was shown to be critical: cisplatin administration simultaneous with or subsequent to p53 gene transfer was less effective than cisplatin-first sequential treatment.	Cisplatin	87-96	P53	Homo sapiens	43-46
8911337-4	1996	The timing of cisplatin administration and p53 gene transfer was shown to be critical: cisplatin administration simultaneous with or subsequent to p53 gene transfer was less effective than cisplatin-first sequential treatment.	Cisplatin	87-96	P53	Homo sapiens	43-46
8876226-0	1996	Reactive oxygen species are downstream mediators of p53-dependent apoptosis.	Reactive Oxygen Species	0-23	P53	Homo sapiens	52-55
8876226-3	1996	We sought to determine whether a central modulator of apoptosis, p53, regulates the levels of intracellular ROS and whether a rise in ROS levels is required for the induction of p53-dependent apoptosis.	Reactive Oxygen Species	108-111	P53	Homo sapiens	65-68
8876226-3	1996	We sought to determine whether a central modulator of apoptosis, p53, regulates the levels of intracellular ROS and whether a rise in ROS levels is required for the induction of p53-dependent apoptosis.	Reactive Oxygen Species	134-137	P53	Homo sapiens	178-181
8876226-5	1996	Cells sensitive to p53-mediated apoptosis produced ROS concomitantly with p53 overexpression, whereas cells resistant to p53 failed to produce ROS.	Reactive Oxygen Species	51-54	P53	Homo sapiens	19-22
8876226-7	1996	These results suggest that p53 acts to regulate the intracellular redox state and induces apoptosis by a pathway that is dependent on ROS production.	Reactive Oxygen Species	134-137	P53	Homo sapiens	27-30
8832894-2	1996	The distribution of benzo[a]pyrene diol epoxide (BPDE) adducts along exons of the P53 gene in BPDE-treated HeLa cells and bronchial epithelial cells was mapped at nucleotide resolution.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	20-47	P53	Homo sapiens	82-85
8832894-2	1996	The distribution of benzo[a]pyrene diol epoxide (BPDE) adducts along exons of the P53 gene in BPDE-treated HeLa cells and bronchial epithelial cells was mapped at nucleotide resolution.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	49-53	P53	Homo sapiens	82-85
8832894-2	1996	The distribution of benzo[a]pyrene diol epoxide (BPDE) adducts along exons of the P53 gene in BPDE-treated HeLa cells and bronchial epithelial cells was mapped at nucleotide resolution.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	94-98	P53	Homo sapiens	82-85
8810317-1	1996	We have examined in detail the DNA binding properties of several immunopurified tumor-derived mutant p53 proteins (Val-143 --&gt; Ala, Arg-175 --&gt; His, Arg-248 --&gt; Trp, Arg-249 --&gt; Ser, and Arg-273 --&gt; His).	Alanine	130-133	P53	Homo sapiens	101-104
8810317-1	1996	We have examined in detail the DNA binding properties of several immunopurified tumor-derived mutant p53 proteins (Val-143 --&gt; Ala, Arg-175 --&gt; His, Arg-248 --&gt; Trp, Arg-249 --&gt; Ser, and Arg-273 --&gt; His).	Arginine	135-138	P53	Homo sapiens	101-104
8810317-1	1996	We have examined in detail the DNA binding properties of several immunopurified tumor-derived mutant p53 proteins (Val-143 --&gt; Ala, Arg-175 --&gt; His, Arg-248 --&gt; Trp, Arg-249 --&gt; Ser, and Arg-273 --&gt; His).	Histidine	150-153	P53	Homo sapiens	101-104
8810317-1	1996	We have examined in detail the DNA binding properties of several immunopurified tumor-derived mutant p53 proteins (Val-143 --&gt; Ala, Arg-175 --&gt; His, Arg-248 --&gt; Trp, Arg-249 --&gt; Ser, and Arg-273 --&gt; His).	Arginine	155-158	P53	Homo sapiens	101-104
8810317-1	1996	We have examined in detail the DNA binding properties of several immunopurified tumor-derived mutant p53 proteins (Val-143 --&gt; Ala, Arg-175 --&gt; His, Arg-248 --&gt; Trp, Arg-249 --&gt; Ser, and Arg-273 --&gt; His).	Tryptophan	170-173	P53	Homo sapiens	101-104
8810317-1	1996	We have examined in detail the DNA binding properties of several immunopurified tumor-derived mutant p53 proteins (Val-143 --&gt; Ala, Arg-175 --&gt; His, Arg-248 --&gt; Trp, Arg-249 --&gt; Ser, and Arg-273 --&gt; His).	Arginine	155-158	P53	Homo sapiens	101-104
8810317-1	1996	We have examined in detail the DNA binding properties of several immunopurified tumor-derived mutant p53 proteins (Val-143 --&gt; Ala, Arg-175 --&gt; His, Arg-248 --&gt; Trp, Arg-249 --&gt; Ser, and Arg-273 --&gt; His).	Serine	190-193	P53	Homo sapiens	101-104
8810317-1	1996	We have examined in detail the DNA binding properties of several immunopurified tumor-derived mutant p53 proteins (Val-143 --&gt; Ala, Arg-175 --&gt; His, Arg-248 --&gt; Trp, Arg-249 --&gt; Ser, and Arg-273 --&gt; His).	Arginine	155-158	P53	Homo sapiens	101-104
8810317-1	1996	We have examined in detail the DNA binding properties of several immunopurified tumor-derived mutant p53 proteins (Val-143 --&gt; Ala, Arg-175 --&gt; His, Arg-248 --&gt; Trp, Arg-249 --&gt; Ser, and Arg-273 --&gt; His).	Histidine	214-217	P53	Homo sapiens	101-104
8892753-3	1996	In contrast, the gadd gene stress response to base-damaging agents, such as methylmethane sulfonate (MMS) or UV radiation, or medium depletion (starvation) occurs in all mammalian cells examined to date regardless of p53 status for both GADD45 and also GADD153, which is not IR-responsive in many lines with functional p53.	gadd	17-21	P53	Homo sapiens	319-322
8870682-0	1996	Nitric oxide-induced apoptosis: p53-dependent and p53-independent signalling pathways.	Nitric Oxide	0-12	P53	Homo sapiens	32-35
8870682-0	1996	Nitric oxide-induced apoptosis: p53-dependent and p53-independent signalling pathways.	Nitric Oxide	0-12	P53	Homo sapiens	50-53
8870682-4	1996	With the use of S-nitroglutathione (GSNO) we correlated a dose-dependent p53 up-regulation to DNA fragmentation measured after 4 h and 8 h, respectively.	S-Nitrosoglutathione	36-40	P53	Homo sapiens	73-76
8870682-7	1996	Clones with down-regulated p53 levels in response to GSNO exhibited a marked reduction in DNA fragmentation.	S-Nitrosoglutathione	53-57	P53	Homo sapiens	27-30
17180111-0	1996	Bile acid activation of the gadd153 promoter and of p53-independent apoptosis: relevance to colon cancer.	Bile Acids and Salts	0-9	P53	Homo sapiens	52-55
17180111-5	1996	We also show that bile acid induction of apoptosis is p53-independent.	Bile Acids and Salts	18-27	P53	Homo sapiens	54-57
9816112-6	1996	However, we find that the induction of wild-type p53 powerfully potentiates the cytotoxicity of both irradiation and 5-fluorouracil, two agents that are used clinically in the treatment of colorectal cancer.	Fluorouracil	117-131	P53	Homo sapiens	49-52
8910043-6	1996	In invasive ductal adenocarcinoma of the pancrease (7 cases), ras, c-erbB-2, p53 and Rb gene products were expressed in 3/7 (43%), 6/7 (86%), 2/7 (29%) and 3/&amp; (43%) cases respectively.	Adenosine Monophosphate	159-162	P53	Homo sapiens	77-80
8931502-2	1996	METHOD: A dexamethazone-inducible wt-p53 cDNA was introduced into two cervical carcinoma cell lines (TMCC-1 and ME180) and morphological changes were examined under a phase contrast microscope and following Papanicolaou staining.	Dexamethasone	10-23	P53	Homo sapiens	37-40
8931502-3	1996	RESULTS: TMCC-1 clones obtained by transfection with wt-p53 gene had an altered morphology especially after induction of p53 expression by treatment with dexamethazone.	Dexamethasone	154-167	P53	Homo sapiens	56-59
8931502-3	1996	RESULTS: TMCC-1 clones obtained by transfection with wt-p53 gene had an altered morphology especially after induction of p53 expression by treatment with dexamethazone.	Dexamethasone	154-167	P53	Homo sapiens	121-124
21541584-12	1996	The mean TPA percentage was significantly higher in the p53-positive tumors or tumor components (EC and YST) when compared with the mean TPA percentage in those neoplasms that were focally positive or negative for p53 protein (Ki-67, P=0.003; PCNA, P=0.046).	Tetradecanoylphorbol Acetate	9-12	P53	Homo sapiens	56-59
21541584-13	1996	p53 expression was also associated with histologically aggressive tumors (ECs and YSTs) that also exhibit high TPA.	Tetradecanoylphorbol Acetate	111-114	P53	Homo sapiens	0-3
8808919-3	1996	MATERIALS AND METHODS: The expression of p53 and bcl-2 was evaluated in archival paraffin-embedded RP specimens from 175 patients followed from 1 to 9 years (mean = 4.6 years) and correlated with stage, grade, race and serologic (PSA) recurrence following surgery.	Paraffin	81-89	P53	Homo sapiens	41-44
8910896-0	1996	A nonsense mutation (Arg-196-Term) in exon 6 of the human TP53 gene identified in small cell lung carcinoma.	Arginine	21-24	P53	Homo sapiens	58-62
8837616-5	1996	To determine whether tumor-derived p53 mutants are irreversibly inactivated, we introduced basic residues in their DNA binding domains, aiming to establish novel contacts between p53 and the DNA phosphate backbone.	Phosphates	195-204	P53	Homo sapiens	35-38
8837616-5	1996	To determine whether tumor-derived p53 mutants are irreversibly inactivated, we introduced basic residues in their DNA binding domains, aiming to establish novel contacts between p53 and the DNA phosphate backbone.	Phosphates	195-204	P53	Homo sapiens	179-182
8921985-12	1996	Recent studies have provided additional evidence that reactive oxygen species (ROS) and oxidative DNA damage may be involved in AFB1-induced p53 and ras mutations.	Reactive Oxygen Species	54-77	P53	Homo sapiens	141-144
8808702-6	1996	In this study, we show that WAF1/CIP1 was induced in p53-dependent apoptosis of U87-MG glioma cells by cis-diamminedichloroplatinum (cisplatin), and overexpression of WAF1/CIP1 induced apoptosis in U87-MG cells without cisplatin treatment.	Cisplatin	133-142	P53	Homo sapiens	53-56
8921985-12	1996	Recent studies have provided additional evidence that reactive oxygen species (ROS) and oxidative DNA damage may be involved in AFB1-induced p53 and ras mutations.	Reactive Oxygen Species	79-82	P53	Homo sapiens	141-144
8895543-0	1996	Cisplatin-induced apoptosis and p53 gene status in a cisplatin-resistant human ovarian carcinoma cell line.	Cisplatin	53-62	P53	Homo sapiens	32-35
8895543-16	1996	Therefore, the presence of non-functional p53 in resistant cells might be involved in the relative failure of cisplatin-induced apoptosis in these cells.	Cisplatin	110-119	P53	Homo sapiens	42-45
8798554-9	1996	Exogenously added H2O2 increased p58(c-fgr) and p53/56(lyn) activities in nonadherent neutrophils.	Hydrogen Peroxide	18-22	P53	Homo sapiens	48-51
8798554-11	1996	Tyrosine phosphorylation of proteins in adherent, CGD neutrophils was only partially inhibited, suggesting that the full activation of p58(c-fgr) and p53/56(lyn), which depends on endogenously produced ROI, does not represent an absolute requirement for protein tyrosine phosphorylation.	Tyrosine	0-8	P53	Homo sapiens	150-153
8927716-8	1996	Phorbol 12-myristate 13-acetate (PMA) induced phosphorylation of p53 and pRb1O5 in MCF-7 cells, but EMF exposure had no effect.	Tetradecanoylphorbol Acetate	0-31	P53	Homo sapiens	65-68
8927716-8	1996	Phorbol 12-myristate 13-acetate (PMA) induced phosphorylation of p53 and pRb1O5 in MCF-7 cells, but EMF exposure had no effect.	Tetradecanoylphorbol Acetate	33-36	P53	Homo sapiens	65-68
8808702-0	1996	WAF1/CIP1 increases the susceptibility of p53 non-functional malignant glioma cells to cisplatin-induced apoptosis.	Cisplatin	87-96	P53	Homo sapiens	42-45
8808702-6	1996	In this study, we show that WAF1/CIP1 was induced in p53-dependent apoptosis of U87-MG glioma cells by cis-diamminedichloroplatinum (cisplatin), and overexpression of WAF1/CIP1 induced apoptosis in U87-MG cells without cisplatin treatment.	Cisplatin	103-131	P53	Homo sapiens	53-56
8808702-6	1996	In this study, we show that WAF1/CIP1 was induced in p53-dependent apoptosis of U87-MG glioma cells by cis-diamminedichloroplatinum (cisplatin), and overexpression of WAF1/CIP1 induced apoptosis in U87-MG cells without cisplatin treatment.	Cisplatin	219-228	P53	Homo sapiens	53-56
8808702-7	1996	In contrast, the p53-independent apoptosis of GB-1 glioma cells by cisplatin did not express WAF1/CIP1.	Cisplatin	67-76	P53	Homo sapiens	17-20
8836183-3	1996	We previously demonstrated that ssDNA oligonucleotides interact with the C-terminal domain of p53 and stimulate binding to internal segments of long ssDNA by the p53 core domain.	Oligonucleotides	38-54	P53	Homo sapiens	94-97
8826941-3	1996	In vitro data and animal studies suggest that paclitaxel may have a unique ability to activate tumor cell apoptosis in the absence of wild-type p53 function.	Paclitaxel	46-56	P53	Homo sapiens	144-147
8826941-4	1996	The authors sought to determine whether p53 mutations affect response to paclitaxel/RT in patients with locally advanced NSCLC.	Paclitaxel	73-83	P53	Homo sapiens	40-43
8826941-13	1996	These results suggest that paclitaxel/RT may be an active regimen for patients with other locally advanced neoplasms with high rates of p53 gene mutations.	Paclitaxel	27-37	P53	Homo sapiens	136-139
8836183-3	1996	We previously demonstrated that ssDNA oligonucleotides interact with the C-terminal domain of p53 and stimulate binding to internal segments of long ssDNA by the p53 core domain.	Oligonucleotides	38-54	P53	Homo sapiens	162-165
8806692-6	1996	To address these questions, we analysed p53 functions in SW 756 cervical cancer cells in which the expression of endogenous HPV 18 E6-E7 genes can be downregulated by dexamethasone.	Dexamethasone	167-180	P53	Homo sapiens	40-43
9816318-0	1996	Alteration of p53 damage response by tamoxifen treatment.	Tamoxifen	37-46	P53	Homo sapiens	14-17
8920796-0	1996	Expression of p53 and apoptosis of tumor cells in locally advanced cervical carcinoma after cisplatin based neoadjuvant chemotherapy.	Cisplatin	92-101	P53	Homo sapiens	14-17
8920796-10	1996	Our study seems to define the relationship between p53 expression and sensitivity to cisplatin based chemotherapy in locally advanced cervical carcinoma, supporting the notion that the cytotoxic action of cisplatin can activate p53 mediated apoptosis.	Cisplatin	85-94	P53	Homo sapiens	51-54
8920796-10	1996	Our study seems to define the relationship between p53 expression and sensitivity to cisplatin based chemotherapy in locally advanced cervical carcinoma, supporting the notion that the cytotoxic action of cisplatin can activate p53 mediated apoptosis.	Cisplatin	85-94	P53	Homo sapiens	228-231
8920796-10	1996	Our study seems to define the relationship between p53 expression and sensitivity to cisplatin based chemotherapy in locally advanced cervical carcinoma, supporting the notion that the cytotoxic action of cisplatin can activate p53 mediated apoptosis.	Cisplatin	205-214	P53	Homo sapiens	51-54
8920796-10	1996	Our study seems to define the relationship between p53 expression and sensitivity to cisplatin based chemotherapy in locally advanced cervical carcinoma, supporting the notion that the cytotoxic action of cisplatin can activate p53 mediated apoptosis.	Cisplatin	205-214	P53	Homo sapiens	228-231
8896794-7	1996	The dehydrating (coagulant) fixatives (e.g., ethanol and methanol) preserved immunorecognition of p53 and broad spectrum keratins best while the slow cross-linking fixatives (e.g., unbuffered zinc formalin) were best for demonstrating TGF alpha and p185erbB-2.	Ethanol	45-52	P53	Homo sapiens	98-101
8824527-12	1996	At this passage, mutation of the p53 gene was detected at codon 273 of exon 8, with G to T conversion (Arg to Leu).	Arginine	103-106	P53	Homo sapiens	33-36
8841466-7	1996	Further separation of the patient-derived fats indicated that the amplification of p53 gene expression in HT-29 cells could be achieved primarily by addition of the diacylglycerides fraction.	diacylglycerides	165-181	P53	Homo sapiens	83-86
8841466-8	1996	Addition of the purified fatty acids, comprising the diglyceride fraction, indicated that the fatty acids, 16:1, 18:0, and 18:1, induced the most significant increases in p53 expression by HT-29 cells.	Fatty Acids	25-36	P53	Homo sapiens	171-174
8841466-8	1996	Addition of the purified fatty acids, comprising the diglyceride fraction, indicated that the fatty acids, 16:1, 18:0, and 18:1, induced the most significant increases in p53 expression by HT-29 cells.	Fatty Acids	94-105	P53	Homo sapiens	171-174
8756655-1	1996	Human wild-type (wt) p53 can induce apoptosis in transiently transfected H1299 cells maintained at 37 degrees C, whereas tumor-derived mutant forms of p53 (with the mutation Ala-143, His-175, or Trp-248) fail to do so.	Alanine	174-177	P53	Homo sapiens	151-154
8756655-1	1996	Human wild-type (wt) p53 can induce apoptosis in transiently transfected H1299 cells maintained at 37 degrees C, whereas tumor-derived mutant forms of p53 (with the mutation Ala-143, His-175, or Trp-248) fail to do so.	Histidine	183-186	P53	Homo sapiens	151-154
8756655-2	1996	At 37 degrees C, p53 with a mutation to Ala at amino acid 143 (p53Ala143) was transcriptionally inactive.	Alanine	40-43	P53	Homo sapiens	17-20
8683636-1	1996	BACKGROUND: We previously observed decreased p53 immunostaining over time in paraffin-embedded sections of ductal carcinoma in situ of the breast of women; these sections had been stored on slides at room temperature.	Paraffin	77-85	P53	Homo sapiens	45-48
9387269-1	1996	Paraffin-embedded hepatocellular carcinoma (HCC) samples were used to study point mutation of p53 gene at 249 codon in the exon 7 by polymerase chain reaction and gel electrophoresis under Hae III enzyme digestion.	Paraffin	0-8	P53	Homo sapiens	94-97
8879300-2	1996	The accumulation of p53 protein was studied immunohistochemically using monoclonal antibody BP53-12 on formalin-fixed paraffin-embedded sections of 36 KS lesions, of which 14 were classified histologically as early type and 22 as spindle-cell or mixed type.	Paraffin	118-126	P53	Homo sapiens	20-23
21541525-3	1996	We have recently studied the steady-state levels of mRNA transcripts for bcl-2, bar and P53 in 8 MM cell lines and found inverse correlation between the levels of bcl-2 mRNA transcripts and sensitivity to dexamethasone (DEX) induced apoptosis.	Dexamethasone	205-218	P53	Homo sapiens	88-91
8878954-0	1996	Antisense oligonucleotide-mediated inhibition of mutant p53 expression.	Oligonucleotides	10-25	P53	Homo sapiens	56-59
8761369-0	1996	TP53 mutation analyses on breast carcinomas: a study of paraffin-embedded archival material.	Paraffin	56-64	P53	Homo sapiens	0-4
8761369-1	1996	The aim of this investigation was to examine the possibility of analysing TP53 mutations in archival paraffin-embedded material with the constant denaturant gel electrophoresis (CDGE) method.	Paraffin	101-109	P53	Homo sapiens	74-78
21541525-5	1996	In this study, we determined the steady-state levels of bcl-2, P53 and bar proteins in 4 myeloma cell lines, and the levels were correlated with sensitivity to DEX induced apoptosis.	Dexamethasone	160-163	P53	Homo sapiens	63-66
21541525-10	1996	Induction of apoptosis in the DEX sensitive cells resulted in an early down-regulation of bcl-2 and P53 protein, whereas the levels of bar protein were only slightly decreased.	Dexamethasone	30-33	P53	Homo sapiens	100-103
21541525-11	1996	In contrast to the DEX sensitive cell lines, the levels of bcl-2, bar and P53 proteins in the DEX resistant cell lines were unchanged during 72 h of treatment with DEX.	Dexamethasone	94-97	P53	Homo sapiens	74-77
21541525-11	1996	In contrast to the DEX sensitive cell lines, the levels of bcl-2, bar and P53 proteins in the DEX resistant cell lines were unchanged during 72 h of treatment with DEX.	Dexamethasone	94-97	P53	Homo sapiens	74-77
8881915-2	1996	METHODS: Expression of p53 was evaluated immunocytochemically in a retrospective study of formalin fixed, paraffin wax embedded tissue.	Paraffin	106-118	P53	Homo sapiens	23-26
8797205-1	1996	Evaluation of the p53 gene protein expression and proliferative potential with MIB-1 monoclonal antibody (MBL Co.), a new marker of cellular proliferation that binds Ki67 in paraffin sections, by immunohistochemical studies were made in 10 cases of the non-recurrent meningiomas and the 8 cases (17 samples) of the recurrent meningiomas.	Paraffin	174-182	P53	Homo sapiens	18-21
8760308-4	1996	We show here that A-T cells are more sensitive than normal lymphoblastoid cells to cisplatin treatment but the rate of induction of p53 by cisplatin is similar in both cell types.	Cisplatin	139-148	P53	Homo sapiens	132-135
8707413-5	1996	Ad-p53, but not Ad-LacZ, infection of cancer cells was followed by nuclear accumulation of the CDK inhibitor p21WAFI/CIPI, cell cycle arrest and loss of viability.	cipi	117-121	P53	Homo sapiens	3-6
8760308-6	1996	The use of a reporter assay to determine the functional status of p53 confirmed the results obtained in the induction experiments with cisplatin.	Cisplatin	135-144	P53	Homo sapiens	66-69
8912347-3	1996	In this study we examined both benign and borderline malignant/malignant mucinous neoplasms for p53 protein accumulation by the means of an anti-human p53 protein monoclonal antibody on paraffin sections.	Paraffin	186-194	P53	Homo sapiens	96-99
8707413-8	1996	Ad-p53-infected SKBr3 breast cancer cells were more sensitive to cytotoxicity of the DNA damaging drugs mitomycin C or Adriamycin, but not the M-phase specific drug vincristine.	Doxorubicin	119-129	P53	Homo sapiens	3-6
8707413-9	1996	Our results suggest that Ad-p53 is capable of infecting and killing cancer cells of diverse tissue origins (including multi-drug resistant cancer cells), that p21WAFI/CIPI may be a useful marker of p53 infectivity and that there may be synergy between Ad-p53 and either mitomycin C or Adriamycin induced cell death in tumors with p53 mutations.	Doxorubicin	285-295	P53	Homo sapiens	28-31
8667426-15	1996	UCN-01 markedly enhanced the cell-killing activity of cisplatin in MCF-7 cells defective for p53 function.	Cisplatin	54-63	P53	Homo sapiens	93-96
8663952-2	1996	OBJECTIVE: To demonstrate how the detection of p53 protein in formaldehyde-fixed, paraffin-embedded oropharyngeal carcinoma may be used as a factor in estimating prognosis.	Paraffin	82-90	P53	Homo sapiens	47-50
8665492-3	1996	Only 1/45 samples showed the incidence of a homozygous mutation at codon 179 (exon 5) of the p53 gene that replaces histidine with tyrosine.	Histidine	116-125	P53	Homo sapiens	93-96
8665492-3	1996	Only 1/45 samples showed the incidence of a homozygous mutation at codon 179 (exon 5) of the p53 gene that replaces histidine with tyrosine.	Tyrosine	131-139	P53	Homo sapiens	93-96
8809407-0	1996	p21WAF1/CIP1/SDI1 is elevated through a p53-independent pathway by mimosine.	Mimosine	67-75	P53	Homo sapiens	40-43
8816839-4	1996	Protein p53 expression was evaluated by immunohistochemistry using Pab 1801, Pab 240, DO7 and CM1 antibodies on paraffin-embedded sections.	Paraffin	112-120	P53	Homo sapiens	8-11
8763853-0	1996	The interaction of taxol and vinblastine with radiation induction of p53 and p21 WAF1/CIP1.	Paclitaxel	19-24	P53	Homo sapiens	69-72
8763853-4	1996	We examined the induction of p53 and its downstream target, p21WAF1/CIP1, by the microtubule active agents taxol and vinblastine with radiation.	Paclitaxel	107-112	P53	Homo sapiens	29-32
8763853-5	1996	An increase in induction of both p53 and p21 WAF1/CIP1 was demonstrated when radiation was added to either taxol or vinblastine treatment.	Paclitaxel	107-112	P53	Homo sapiens	33-36
8706243-4	1996	Methotrexate-resistant MCF-7 cells were unusual heterozygotes that expressed a wild-type and dominant, in-frame p53 deletion mutant and the doxorubicin-resistant cells expressed only mutant p53.	Doxorubicin	140-151	P53	Homo sapiens	190-193
8809407-4	1996	In this study, we showed that mimosine can increase both p21 mRNA and protein levels, indirectly inhibit cyclin E-associated kinase activity without affecting the cyclin E protein level, block human breast cancer cells (21PT) in the late G1 phase of the cell cycle, and induce a p53-independent p21 pathway in these cells.	Mimosine	30-38	P53	Homo sapiens	279-282
12114639-0	1996	Possible Relation of p53 and mdm-2 Oncoprotein Expression in Thyroid Carcinoma: A Molecular-Pathological and Immunohistochemical Study on Paraffin-Embedded Tissue.	Paraffin	138-146	P53	Homo sapiens	21-24
8683246-3	1996	bcl2 and p53 protein expression was studied on paraffin-embedded tumor tissue by immunohistochemistry in relation to clinical factors.	Paraffin	47-55	P53	Homo sapiens	9-12
8818693-2	1996	To investigate whether overexpressed bcl-2 and abnormally stabilized p53 are associated with reduced apoptosis in paraffin sections of non-small cell lung carcinoma, apoptotic, mitotic, and Ki-67 labelling indices were determined and correlated with bcl-2 and p53 immunoreactivity in 54 squamous cell carcinomas and 22 adenocarcinomas.	Paraffin	114-122	P53	Homo sapiens	69-72
8687228-0	1996	[Therapeutic effect of adenovirus-mediated transfer of the wild-type p53 gene with cisplatin].	Cisplatin	83-92	P53	Homo sapiens	69-72
8698624-0	1996	p53 antisense oligonucleotide inhibits growth of human colon tumor and normal cell lines.	Oligonucleotides	14-29	P53	Homo sapiens	0-3
8903423-7	1996	The effects of the vitamin D compounds on the expression of two oncoproteins which may regulate apoptosis, bcl-2 and p53 were examined by Western analysis.	Vitamin D	19-28	P53	Homo sapiens	117-120
8903423-9	1996	In addition, the p21 protein, whose gene WAF-1 is induced by wild type p53, was also increased by both vitamin D compounds.	Vitamin D	103-112	P53	Homo sapiens	71-74
8698624-1	1996	We examined the relationship between the expression of mutant p53 proteins and tumor cell growth using a p53 antisense oligonucleotide (5"-CCCTGCTCCCCCCTGGCTCC-3").	Oligonucleotides	119-134	P53	Homo sapiens	105-108
8698624-2	1996	The oligonucleotide inhibited the growth of three human colon tumor cell lines (DLD-a, SW620 and WiDr), which produce only mutant p53 proteins with different mutation sites.	Oligonucleotides	4-19	P53	Homo sapiens	130-133
8698624-3	1996	Treatment of DLD-1 cells with the p53 antisense oligonucleotide caused a decrease in the level of p53 mutant protein.	Oligonucleotides	48-63	P53	Homo sapiens	34-37
8698624-3	1996	Treatment of DLD-1 cells with the p53 antisense oligonucleotide caused a decrease in the level of p53 mutant protein.	Oligonucleotides	48-63	P53	Homo sapiens	98-101
8674115-3	1996	This exonuclease activity is intrinsic to the wild-type p53 protein: it copurified with p53 during p53 preparation; only purified wild-type p53, but not identically purified mutant p53 proteins displayed exonuclease activity; the exonuclease activity could be reconstituted from SDS gel-purified and urea-renatured p53 protein and mapped to the core domain of the p53 molecule; and finally, purified p53 protein could be UV-cross-linked to GMP.	Sodium Dodecyl Sulfate	279-282	P53	Homo sapiens	56-59
8673928-3	1996	Differentiation of these teratocarcinoma cells with retinoic acid results in a marked decrease in p53 protein levels but is accompanied by a marked increase in p53-mediated transcriptional activity.	Tretinoin	52-65	P53	Homo sapiens	98-101
8673928-3	1996	Differentiation of these teratocarcinoma cells with retinoic acid results in a marked decrease in p53 protein levels but is accompanied by a marked increase in p53-mediated transcriptional activity.	Tretinoin	52-65	P53	Homo sapiens	160-163
8673929-0	1996	Specific P53 mutations are associated with de novo resistance to doxorubicin in breast cancer patients.	Doxorubicin	65-76	P53	Homo sapiens	9-12
8673929-4	1996	In vitro investigations have shown intact p53 to play a critical role executing cell death in response to treatment with cytotoxic drugs like 5-fluorouracil, etoposide and doxorubicin.	Fluorouracil	142-156	P53	Homo sapiens	42-45
8673929-4	1996	In vitro investigations have shown intact p53 to play a critical role executing cell death in response to treatment with cytotoxic drugs like 5-fluorouracil, etoposide and doxorubicin.	Doxorubicin	172-183	P53	Homo sapiens	42-45
8673929-7	1996	In this study we present data linking specific mutations in the P53 gene to primary resistance to doxorubicin therapy and early relapse in breast cancer patients.	Doxorubicin	98-109	P53	Homo sapiens	64-67
8674115-3	1996	This exonuclease activity is intrinsic to the wild-type p53 protein: it copurified with p53 during p53 preparation; only purified wild-type p53, but not identically purified mutant p53 proteins displayed exonuclease activity; the exonuclease activity could be reconstituted from SDS gel-purified and urea-renatured p53 protein and mapped to the core domain of the p53 molecule; and finally, purified p53 protein could be UV-cross-linked to GMP.	Urea	300-304	P53	Homo sapiens	56-59
8674115-3	1996	This exonuclease activity is intrinsic to the wild-type p53 protein: it copurified with p53 during p53 preparation; only purified wild-type p53, but not identically purified mutant p53 proteins displayed exonuclease activity; the exonuclease activity could be reconstituted from SDS gel-purified and urea-renatured p53 protein and mapped to the core domain of the p53 molecule; and finally, purified p53 protein could be UV-cross-linked to GMP.	guanosine 5'-monophosphorothioate	440-443	P53	Homo sapiens	56-59
8649776-2	1996	By using recombination PCR in vitro mutagenesis, we introduced point mutations into the codon 273 of wild-type (wt) p53 (pC53-SN3) from Arg to His (pC53-273H [273H]), Asp (273D), Pro (273P), Lys (273K), Leu (273L) or Thr (273T), and compared their biological and biochemical activities with wt p53 and cancer-derived 175H, 248W and 273H/309S.	Arginine	136-139	P53	Homo sapiens	116-119
8654372-2	1996	Expression of Zta results in induction of the tumor suppressor protein, p53, and the cyclin-dependent kinase inhibitors, p21 and p27, as well as accumulation of hypophosphorylated pRb.	zta	14-17	P53	Homo sapiens	72-75
8649776-2	1996	By using recombination PCR in vitro mutagenesis, we introduced point mutations into the codon 273 of wild-type (wt) p53 (pC53-SN3) from Arg to His (pC53-273H [273H]), Asp (273D), Pro (273P), Lys (273K), Leu (273L) or Thr (273T), and compared their biological and biochemical activities with wt p53 and cancer-derived 175H, 248W and 273H/309S.	Histidine	143-146	P53	Homo sapiens	116-119
8649776-2	1996	By using recombination PCR in vitro mutagenesis, we introduced point mutations into the codon 273 of wild-type (wt) p53 (pC53-SN3) from Arg to His (pC53-273H [273H]), Asp (273D), Pro (273P), Lys (273K), Leu (273L) or Thr (273T), and compared their biological and biochemical activities with wt p53 and cancer-derived 175H, 248W and 273H/309S.	Lysine	191-194	P53	Homo sapiens	116-119
8649776-2	1996	By using recombination PCR in vitro mutagenesis, we introduced point mutations into the codon 273 of wild-type (wt) p53 (pC53-SN3) from Arg to His (pC53-273H [273H]), Asp (273D), Pro (273P), Lys (273K), Leu (273L) or Thr (273T), and compared their biological and biochemical activities with wt p53 and cancer-derived 175H, 248W and 273H/309S.	Threonine	217-220	P53	Homo sapiens	116-119
8651706-4	1996	Seventy-seven percent of immunoprecipitated, [35S]-methionine-labeled, recombinant p53 protein resided in the cytoplasm of Sf9 cells, while 15% localized to the nucleus and 8% was released extracellularly.	Sulfur-35	46-49	P53	Homo sapiens	83-86
8651706-4	1996	Seventy-seven percent of immunoprecipitated, [35S]-methionine-labeled, recombinant p53 protein resided in the cytoplasm of Sf9 cells, while 15% localized to the nucleus and 8% was released extracellularly.	Methionine	51-61	P53	Homo sapiens	83-86
8653690-0	1996	Modulation of p53 expression by human recombinant interferon-alpha2a correlates with abrogation of cisplatin resistance in a human melanoma cell line.	Cisplatin	99-108	P53	Homo sapiens	14-17
8645592-2	1996	Alcohol use as well as medication with hydralazine-containing antihypertensive drugs, but not heredity were associated with p53 staining.	Alcohols	0-7	P53	Homo sapiens	124-127
8818255-2	1996	This is a longitudinal study of p53 expression in fixed, paraffin-embedded tissue from 3 patients with multiple, recurrent, squamous cell carcinomas of floor of mouth (n = 4, 4, 3).	Paraffin	57-65	P53	Homo sapiens	32-35
8653690-1	1996	G3361/CP cells, a cisplatin (CDDP)-resistant subclone of the human melanoma cell line G3361, overexpress wild-type p53 protein and demonstrate an increase in the percentage of cells in G0--G1 arrest compared to parental cells.	Cisplatin	29-33	P53	Homo sapiens	115-118
8653690-3	1996	These findings suggest that recombinant IFN-alpha2a disrupts p53-mediated cell cycle regulation to restore CDDP sensitivity in G3361/CP cells.	Cisplatin	107-111	P53	Homo sapiens	61-64
8647200-2	1996	Engagement of CD22 with a monoclonal antibody (HB22.23) that blocks the binding of CD22 to its ligands results in rapid CD22 tyrosine phosphorylation and in increased association of CD22 with p53/56lyn kinase, p85 phosphatidyl inositol-3 kinase, and p72syk kinase.	Tyrosine	125-133	P53	Homo sapiens	192-195
16696068-0	1996	Nested PCR-SSCP assay for the detection of p53 mutations in paraffin wax embedded bone tumours: improvement of sensitivity and fidelity.	Paraffin	60-72	P53	Homo sapiens	43-46
10330207-3	1996	Mutational analysis of p53 was performed retrospectively by means of topographic genotyping (TG), using formalin-fixed, paraffin-embedded tissue of the primary and recurrent tumor.	Paraffin	120-128	P53	Homo sapiens	23-26
8666362-4	1996	Paraffin-embedded tissue sections were immunostained with monoclonal antibody to p53 and MDM2 proteins.	Paraffin	0-8	P53	Homo sapiens	81-84
8782209-10	1996	We used the DO-7 monoclonal antibody reactive for the N-terminal of the p53 protein on formalin-fixed paraffin-embedded tissue.	Paraffin	102-110	P53	Homo sapiens	72-75
9162298-3	1996	A germline polymorphism of p53 with a single-base change at codon 72 that causes an amino acid replacement of arginine (Arg; CGC) by proline (PRO; CCC) has also been reported to be associated with cancer susceptibility in a Japanese population.	Arginine	110-118	P53	Homo sapiens	27-30
8702238-1	1996	We studied the pharmacomodulating effects of a marine substance, bistramide D, which is capable of inducing terminal differentiation on the expression of the c-erb-B1, ras, src, myc and p53 genes in the NSCLC-N6 cell line established from a non-small cell lung carcinoma.	bistramide D	65-77	P53	Homo sapiens	186-189
8640663-3	1996	METHODS: The expression of p53 was studied immunohistochemically in 200 gastric carcinomas using paraffin embedded surgical specimens and endoscopic biopsies.	Paraffin	97-105	P53	Homo sapiens	27-30
8767868-3	1996	Expression of p53 protein was examined by immunohistochemistry in paraffin-embedded sections.	Paraffin	66-74	P53	Homo sapiens	14-17
8634048-6	1996	A significant correlation between p53 immunoreactivity and preparathyroidectomy calcium levels of &gt; 1.5 mmol/L was detected (P &lt; 0.005) although no correlation was noted between p53 immunoreactivity and higher levels of preparathyroidectomy intact parathyroid hormone (PTH) levels.	Calcium	80-87	P53	Homo sapiens	34-37
8634048-7	1996	CONCLUSION: A relationship is postulated between abnormal serum calcium regulation and p53 mutation in hypercalcaemic states associated with hyperparathyroidism.	Calcium	64-71	P53	Homo sapiens	87-90
8616869-2	1996	We have found that Bcl-2 and p53, two proteins implicated in the control of apoptosis, are differently expressed in the ovarian cell line A2780 and its cisplatin-resistant variant 2780CP, with the resistant line overexpressing both proteins.	Cisplatin	152-161	P53	Homo sapiens	29-32
8616869-3	1996	Transfection of the A2780 cells with a Bcl-2- or p53-expressing plasmid increases resistance to various drugs, including cisplatin, suggesting that Bcl-2 and p53 expression may influence the sensitivity of ovarian cancer cell lines to chemotherapy.	Cisplatin	121-130	P53	Homo sapiens	49-52
8616869-3	1996	Transfection of the A2780 cells with a Bcl-2- or p53-expressing plasmid increases resistance to various drugs, including cisplatin, suggesting that Bcl-2 and p53 expression may influence the sensitivity of ovarian cancer cell lines to chemotherapy.	Cisplatin	121-130	P53	Homo sapiens	158-161
9162298-3	1996	A germline polymorphism of p53 with a single-base change at codon 72 that causes an amino acid replacement of arginine (Arg; CGC) by proline (PRO; CCC) has also been reported to be associated with cancer susceptibility in a Japanese population.	Arginine	120-123	P53	Homo sapiens	27-30
9162298-8	1996	The study of the p53 polymorphism in the healthy population showed allele frequencies of 0.79 (Arg) and 0.21 (Pro).	Arginine	95-98	P53	Homo sapiens	17-20
8781385-11	1996	In human lung cancer, p53 mutations (both the mutation pattern and frequency) have been linked with tobacco smoking; the type of mutation most frequently observed is G:C to T:A transversion, a mutation preferentially induced by benzo[a]pyrene diol epoxide.	pyrene diol epoxide	236-255	P53	Homo sapiens	22-25
8835823-1	1996	The expression of p53 protein was studied in odontogenic keratocysts (OKC, 11 solitary, 5 recurrent and 6 NBCCS cysts), radicular (RC, n = 5) and dentigerous (DC, n = 5) cysts, using a panel of antibodies to p53 (clone BP53-12, clone 1801 and polyclonal CM1) and a sensitive biotin-streptavidin method on paraffin embedded sections.	Paraffin	305-313	P53	Homo sapiens	18-21
8622078-9	1996	CONCLUSION: p53 expression appears to be indicative of clinical outcome in postmenopausal patients treated with tamoxifen.	Tamoxifen	112-121	P53	Homo sapiens	12-15
8743957-6	1996	Pretreatment of cells with N-acetylcysteine, an agent known to counteract oxidative stress, attenuates the cellular p53 response to ultraviolet light by reducing the number of cells with high p53 levels but does not affect the response to ionizing radiation.	Acetylcysteine	27-43	P53	Homo sapiens	116-119
8743957-6	1996	Pretreatment of cells with N-acetylcysteine, an agent known to counteract oxidative stress, attenuates the cellular p53 response to ultraviolet light by reducing the number of cells with high p53 levels but does not affect the response to ionizing radiation.	Acetylcysteine	27-43	P53	Homo sapiens	192-195
8819013-3	1996	These mutations result in an Arg--&gt;Trp amino acid substitution at residue 249 and an Ile--&gt;Phe amino acid substitution at residue 255 in a highly conserved region in the DNA-binding core domain of the p53 protein.	Arginine	29-32	P53	Homo sapiens	207-210
8819013-3	1996	These mutations result in an Arg--&gt;Trp amino acid substitution at residue 249 and an Ile--&gt;Phe amino acid substitution at residue 255 in a highly conserved region in the DNA-binding core domain of the p53 protein.	Tryptophan	38-41	P53	Homo sapiens	207-210
8819013-4	1996	To determine the effects of these substitutions on the three-dimensional structure of the p53 protein, we have performed molecular dynamics calculations on this core domain of the wild-type and the Trp-249 and Phe-255 mutants to compute the average structures of each of the three forms.	Tryptophan	198-201	P53	Homo sapiens	90-93
8634092-0	1996	Preferential DNA damage in the p53 gene by benzo[a]pyrene metabolites in cytochrome P4501A1-expressing xeroderma pigmentosum group A cells.	pyrene	51-57	P53	Homo sapiens	31-34
8634092-7	1996	The lesion frequencies in the p53 and beta-globin genes in purified DNA treated with BPDE in vitro were the same, indicating that there was no sequence-specific basis for preferential lesion formation in the p53 gene in treated cells.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	85-89	P53	Homo sapiens	30-33
8634091-0	1996	Induction of p53 and p21/WAF1/CIP1 expression by nitric oxide and their association with apoptosis in human cancer cells.	Nitric Oxide	49-61	P53	Homo sapiens	13-16
8634092-8	1996	DNA damage in both the p53 and beta-globin genes showed a dose response to [3H](-)-BPD.	Tritium	76-78	P53	Homo sapiens	23-26
8603385-0	1996	Effects of sodium saccharin and linoleic acid on mRNA levels of Her2/neu and p53 in a human breast epithelial cell line.	Linoleic Acid	32-45	P53	Homo sapiens	77-80
8603385-1	1996	The effects of two food-related chemicals (sodium saccharin and linoleic acid) on the levels of Her2/neu and p53 mRNA in a non-cancerous human breast epithelial cell line (HBL-100) were tested in comparison with the effects of the known tumor promoter phorbol 12-myristate 13-acetate (TPA).	Linoleic Acid	64-77	P53	Homo sapiens	109-112
8612815-2	1996	With the use of NO donors such as S-nitrosoglutathione or spermine-NO we established that PARP digestion occurs in parallel with DNA fragmentation, and is preceded by accumulation of the tumor suppressor gene product p53.	S-Nitrosoglutathione	34-54	P53	Homo sapiens	217-220
8606380-5	1996	METHODS: Immunohistochemical analysis with a monoclonal antibody (DO7) specific for p53 protein was used to detect expression of the protein in formalin-fixed, paraffin-embedded tumor samples from 69 head and neck cancer patients treated with definitive local therapy (surgery and/or radiotherapy) between January 1980 and October 1983 at The University of Texas M. D. Anderson Cancer Center.	Paraffin	160-168	P53	Homo sapiens	84-87
8626117-5	1996	Immunohistochemical staining for the p53 protein with monoclonal antibody PAb 1801 was performed in the paraffin-embedded tissue of each case to screen for p53 overexpression.	Paraffin	104-112	P53	Homo sapiens	37-40
8622872-2	1996	Cell type specific differences in p53-independent p21 expression and cell cycle arrest were found following treatment of human tumour cell lines with serum, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), or okadaic acid (OA).	Tetradecanoylphorbol Acetate	157-194	P53	Homo sapiens	34-37
8622872-2	1996	Cell type specific differences in p53-independent p21 expression and cell cycle arrest were found following treatment of human tumour cell lines with serum, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), or okadaic acid (OA).	Tetradecanoylphorbol Acetate	196-199	P53	Homo sapiens	34-37
8611406-2	1996	Expression of P53 protein was detected by an immunohistochemical approach using the monoclonal antibody PAb1801 on paraffin-embedded sections of tumours obtained surgically from 102 stage II - IIIa patients with non-small-cell lung cancer (52 squamous cell carcinomas, 50 adenocarcinomas).	Paraffin	115-123	P53	Homo sapiens	14-17
8608838-0	1996	p53 protein overexpression and response to biomodulated 5-fluorouracil chemotherapy in patients with advanced colorectal cancer.	Fluorouracil	56-70	P53	Homo sapiens	0-3
8608838-9	1996	p53 protein overexpression was determined immunohistochemically from paraffin sections of the original primary tumour and resected metastases.	Paraffin	69-77	P53	Homo sapiens	0-3
8619835-0	1996	DNA-dependent protein kinase inhibitor (OK-1035) suppresses p21 expression in HCT116 cells containing wild-type p53 induced by adriamycin.	Doxorubicin	127-137	P53	Homo sapiens	112-115
8619835-4	1996	Treatment of HCT116, a human colon carcinoma cell line, with adriamycin induced the expression of wt-p53 and p21.	Doxorubicin	61-71	P53	Homo sapiens	101-104
8605209-1	1996	Oxidative DNA damage by NAD(P)H in the presence of metal ions has been characterized by using 32P 5" end-labeled DNA fragments obtained from human p53 tumor suppressor gene and c-Ha-ras-1 protooncogene.	Metals	51-56	P53	Homo sapiens	147-150
8695259-1	1996	The expression of mutated p53 protein was studied in paraffin-embedded, formalin-fixed tumour specimens from 183 women with endometrial carcinoma.	Paraffin	53-61	P53	Homo sapiens	26-29
21544419-0	1996	The role of p53, bcl-2 and bax network in dexamethasone induced apoptosis in multiple myeloma cell lines.	Dexamethasone	42-55	P53	Homo sapiens	12-15
21544419-3	1996	We, therefore, decided to conduct a detailed study of the role of the bcl-2/bax/p53 network in dexamethasone (DEX) induced apoptosis in MM cells.	Dexamethasone	95-108	P53	Homo sapiens	80-83
21544419-3	1996	We, therefore, decided to conduct a detailed study of the role of the bcl-2/bax/p53 network in dexamethasone (DEX) induced apoptosis in MM cells.	Dexamethasone	110-113	P53	Homo sapiens	80-83
21544419-9	1996	Induction of apoptosis in 8226 and ARP-1 cells (DEX sensitive) resulted, within 24 h, in a transient but marked down-regulation of mRNA transcripts for bcl-2 and p53, whereas the level of expression of bax mRNA transcripts were unchanged, except for ARP-1 cells (lacking p53), where slight down-regulation of mRNA transcripts for bax, was observed.	Dexamethasone	48-51	P53	Homo sapiens	162-165
21544419-9	1996	Induction of apoptosis in 8226 and ARP-1 cells (DEX sensitive) resulted, within 24 h, in a transient but marked down-regulation of mRNA transcripts for bcl-2 and p53, whereas the level of expression of bax mRNA transcripts were unchanged, except for ARP-1 cells (lacking p53), where slight down-regulation of mRNA transcripts for bax, was observed.	Dexamethasone	48-51	P53	Homo sapiens	271-274
21544419-10	1996	In contrast to the DEX sensitive cell lines, the level of expression of bcl-2, bax and p53 mRNA transcripts in the DEX resistant cell lines, were unchanged during 72 h of treatment with DEX (up to 10 mu M).	Dexamethasone	115-118	P53	Homo sapiens	87-90
8648390-0	1996	Phase I trial of an antisense oligonucleotide OL(1)p53 in hematologic malignancies.	Oligonucleotides	30-45	P53	Homo sapiens	51-54
21544419-10	1996	In contrast to the DEX sensitive cell lines, the level of expression of bcl-2, bax and p53 mRNA transcripts in the DEX resistant cell lines, were unchanged during 72 h of treatment with DEX (up to 10 mu M).	Dexamethasone	115-118	P53	Homo sapiens	87-90
8648390-2	1996	In vitro incubation of acute myelogenous leukemia with OL(1)p53, a 20-mer phosphorothioate oligonucleotide complementary to p53 mRNA, results in leukemic cell death.	Oligonucleotides	91-106	P53	Homo sapiens	60-63
21544419-11	1996	We, therefore, conclude that bcl-2 and perhaps p53 are involved in resistance to DEX in myeloma cell lines.	Dexamethasone	81-84	P53	Homo sapiens	47-50
8599213-5	1996	Mutation of lysine residues within the C-terminus of p53 resulted in resistance to E6-mediated degradation in vitro, although the ability of the two proteins to form a complex was not affected.	Lysine	12-18	P53	Homo sapiens	53-56
8733010-6	1996	Apoptosis can also be induced in immortalized steroidogenic granulosa cells, transformed by SV40 DNA and Ha-ras oncogene, by overexpression of the wild-type p53 tumor suppressor gene in cAMP-stimulated cells.	Cyclic AMP	186-190	P53	Homo sapiens	157-160
8733010-7	1996	Omitting the cAMP stimulus prevents the p53-induced apoptosis in these cells, suggesting cross-talk between p53 and c-AMP-generated signals in the induction of apoptosis.	Cyclic AMP	13-17	P53	Homo sapiens	40-43
8733010-7	1996	Omitting the cAMP stimulus prevents the p53-induced apoptosis in these cells, suggesting cross-talk between p53 and c-AMP-generated signals in the induction of apoptosis.	Cyclic AMP	13-17	P53	Homo sapiens	108-111
8925599-3	1996	We used a set of 6 different antibodies against p53, suitable for paraffin section (PAb1801, PAb240, DO-1, DO-7, BP53-12, CM-1).	Paraffin	66-74	P53	Homo sapiens	48-51
8600043-4	1996	Ki67 (MIB-1) and p53 monoclonal antibodies (active on paraffin embedded tissues) provide insight into nuclear proliferation and control, respectively.	Paraffin	54-62	P53	Homo sapiens	17-20
8617769-0	1996	Modification of an N-terminal regulatory domain of T antigen restores p53-T antigen complex formation in the absence of an essential metal ion cofactor.	Metals	133-138	P53	Homo sapiens	70-73
8691320-1	1996	To examine the expression of p53 protein and gene alterations in oral epithelial lesions including epithelial dysplasias and primary squamous cell carcinomas, immunohistochemical and temperature gradient gel electrophoresis (TGGE) methods were applied to formalin-fixed and paraffin-embedded tissues.	Paraffin	274-282	P53	Homo sapiens	29-32
8711933-3	1996	In this study, we investigated the immunohistochemical expression of p53 in formalin fixed paraffin embedded archival specimens of 36 extrahepatic bile duct cancers in which p53 expression was found in eighteen (50%) cases.	Paraffin	91-99	P53	Homo sapiens	69-72
8637893-0	1996	Nitric oxide-induced p53 accumulation and regulation of inducible nitric oxide synthase expression by wild-type p53.	Nitric Oxide	0-12	P53	Homo sapiens	21-24
8637893-0	1996	Nitric oxide-induced p53 accumulation and regulation of inducible nitric oxide synthase expression by wild-type p53.	Nitric Oxide	0-12	P53	Homo sapiens	112-115
8637893-2	1996	Therefore, we hypothesized that p53 performs a similar role in response to putative endogenous mutagens, such as nitric oxide (NO).	Nitric Oxide	113-125	P53	Homo sapiens	32-35
8649799-3	1996	Here we address this question in an intact cell system using normal human diploid fibroblasts in which p53 function is manipulated by expression of a dominant-negative mutant (ala(143)) introduced by a retroviral vector.	Alanine	176-179	P53	Homo sapiens	103-106
8615678-8	1996	The level of the tumor suppressor p53 increases in response to NO donors like GSNO and effectively senses NO intoxication in macrophages.	S-Nitrosoglutathione	78-82	P53	Homo sapiens	34-37
8615678-9	1996	GSNO removal concomitantly allows p53 to decline with only a small percentage of cells showing DNA fragmentation.	S-Nitrosoglutathione	0-4	P53	Homo sapiens	34-37
8774641-10	1996	The growth of the Ad5CMV-p53-infected cells was greatly suppressed as detected by both cell count and [3H]thymidine incorporation assay.	Tritium	103-105	P53	Homo sapiens	25-28
8778328-2	1996	This immunohistochemical study on formalin-fixed, paraffin-embedded material found p53 expression in 43 per cent (n = 51) of carcinomas using a monoclonal antibody (DO-1), whereas no immunoreactivity for p53 was present in tumour-associated non-neoplastic gastric mucosa or tumour stroma.	Paraffin	50-58	P53	Homo sapiens	83-86
8631030-8	1996	The delay in S phase progression was coincident with the induction of p53 protein levels in LXSN-containing HFFs, suggesting a role for p53 in DNA repair of cisplatin-induced damage.	Cisplatin	157-166	P53	Homo sapiens	70-73
8631030-8	1996	The delay in S phase progression was coincident with the induction of p53 protein levels in LXSN-containing HFFs, suggesting a role for p53 in DNA repair of cisplatin-induced damage.	Cisplatin	157-166	P53	Homo sapiens	136-139
8603737-3	1996	We found that phorbol myristate acetate (PMA) activates the src family tyrosine kinases p58c-fgr and p53/56lyn in suspended PMNs.	Tetradecanoylphorbol Acetate	14-39	P53	Homo sapiens	101-104
8630996-2	1996	Since the p53 gene becomes inactivated in over one-half of advanced ovarian carcinoma, in this study we have examined the relationships between p53 gene alterations, p53 immunoreactivity, and response to cisplatin-based chemotherapy in ovarian cancer patients.	Cisplatin	204-213	P53	Homo sapiens	144-147
8630996-2	1996	Since the p53 gene becomes inactivated in over one-half of advanced ovarian carcinoma, in this study we have examined the relationships between p53 gene alterations, p53 immunoreactivity, and response to cisplatin-based chemotherapy in ovarian cancer patients.	Cisplatin	204-213	P53	Homo sapiens	10-13
8630996-2	1996	Since the p53 gene becomes inactivated in over one-half of advanced ovarian carcinoma, in this study we have examined the relationships between p53 gene alterations, p53 immunoreactivity, and response to cisplatin-based chemotherapy in ovarian cancer patients.	Cisplatin	204-213	P53	Homo sapiens	144-147
8630996-11	1996	A significant correlation has been found between p53 accumulation, type of mutation (i.e., missense mutations), and pathological response to cisplatin-based therapy.	Cisplatin	141-150	P53	Homo sapiens	49-52
8603737-3	1996	We found that phorbol myristate acetate (PMA) activates the src family tyrosine kinases p58c-fgr and p53/56lyn in suspended PMNs.	Tetradecanoylphorbol Acetate	41-44	P53	Homo sapiens	101-104
8603737-4	1996	Moreover, we found that up to about 20% of p58c-fgr and p53/56lyn redistribute to a Triton X-100-insoluble fraction after PMA stimulation, and it is this fraction of the two kinases which diplays an increased activity.	Tetradecanoylphorbol Acetate	122-125	P53	Homo sapiens	56-59
8603737-5	1996	These changes of p58c-fgr and p53/56lyn distribution and activity correlate with tyrosine phosphorylation of endogenous substrates.	Tyrosine	81-89	P53	Homo sapiens	30-33
8615376-0	1996	Suppression of cellular proliferation using p53 DNA recognition site-related oligonucleotides.	Oligonucleotides	77-93	P53	Homo sapiens	44-47
8615376-1	1996	A number of oligonucleotides were designed to bind through Hoogsteen triple helix or Watson-Crick hydrogen bonds to the p53 consensus sequence homology localized within the human nontranscribed rRNA spacer region.	Oligonucleotides	12-28	P53	Homo sapiens	120-123
8615376-1	1996	A number of oligonucleotides were designed to bind through Hoogsteen triple helix or Watson-Crick hydrogen bonds to the p53 consensus sequence homology localized within the human nontranscribed rRNA spacer region.	Hydrogen	98-106	P53	Homo sapiens	120-123
8625447-1	1996	The p53 tumor suppressor gene is often mutated in various human cancers and a common polymorphism is known at codon 72 of exon 4, with two alleles encoding either arginine (CGC) or proline (CCC).	Arginine	163-171	P53	Homo sapiens	4-7
8625447-1	1996	The p53 tumor suppressor gene is often mutated in various human cancers and a common polymorphism is known at codon 72 of exon 4, with two alleles encoding either arginine (CGC) or proline (CCC).	Chlormequat	190-193	P53	Homo sapiens	4-7
8564971-0	1996	Association between cisplatin resistance and mutation of p53 gene and reduced bax expression in ovarian carcinoma cell systems.	Cisplatin	20-29	P53	Homo sapiens	57-60
8564971-8	1996	Following exposure to ionizing radiation or cisplatin, accumulation of the p53 protein was markedly enhanced only in the sensitive cells.	Cisplatin	44-53	P53	Homo sapiens	75-78
8801209-5	1996	The expression of p53 protein was detected immunohistochemically in paraffin wax embedded liver specimens, after microwave pretreatment.	Paraffin	68-80	P53	Homo sapiens	18-21
8564971-13	1996	Taken together, these observations support a role for mutations of the p53 gene in the development of cisplatin resistance in ovarian cancer as a consequence of loss of the ability of p53 to transactivate bax, an apoptosis-inducing gene.	Cisplatin	102-111	P53	Homo sapiens	71-74
8564971-13	1996	Taken together, these observations support a role for mutations of the p53 gene in the development of cisplatin resistance in ovarian cancer as a consequence of loss of the ability of p53 to transactivate bax, an apoptosis-inducing gene.	Cisplatin	102-111	P53	Homo sapiens	184-187
9816181-8	1996	Prostate cancer cell lines overexpressing P-glycoprotein or possessing heterogeneous molecular alterations, including p53 mutations, are also sensitive to the effects of PB.	Phenylbutyrates	170-172	P53	Homo sapiens	118-121
21544361-2	1996	We observed that platinum-resistant tumors showed higher mRNA levels of p53, ERCC1, and XPA than platinum-sensitive tumors; mRNA expression patterns in responders differed substantially from nonresponders; and p53 expression showed a strong correlation with the expression of ERCC1, and of XPA in platinum-sensitive tumor tissues, but not with platinum-resistant tumors.	Platinum	97-105	P53	Homo sapiens	210-213
8552392-4	1996	Using the conformational domain of p53 fused with protein A, we have shown that the p53 conformational domain possesses Zn+2-dependent, sequence-specific DNA-binding activity.	Zinc	120-124	P53	Homo sapiens	35-38
8762431-1	1996	An immunohistochemical method utilizing microwave oven treated avidin-biotin complex (ABC) technique was used in this study to detect P53 protein expression in 87 parafin-embedded fibrous neoplasm tissues.	parafin	163-170	P53	Homo sapiens	134-137
21544361-0	1996	Platinum-sensitive and platinum-resistant ovarian cancer tissues show differences in the relationships between mRNA levels of p53, ERCC1 and XPA.	Platinum	0-8	P53	Homo sapiens	126-129
21544361-0	1996	Platinum-sensitive and platinum-resistant ovarian cancer tissues show differences in the relationships between mRNA levels of p53, ERCC1 and XPA.	Platinum	23-31	P53	Homo sapiens	126-129
21544361-2	1996	We observed that platinum-resistant tumors showed higher mRNA levels of p53, ERCC1, and XPA than platinum-sensitive tumors; mRNA expression patterns in responders differed substantially from nonresponders; and p53 expression showed a strong correlation with the expression of ERCC1, and of XPA in platinum-sensitive tumor tissues, but not with platinum-resistant tumors.	Platinum	17-25	P53	Homo sapiens	72-75
21544361-2	1996	We observed that platinum-resistant tumors showed higher mRNA levels of p53, ERCC1, and XPA than platinum-sensitive tumors; mRNA expression patterns in responders differed substantially from nonresponders; and p53 expression showed a strong correlation with the expression of ERCC1, and of XPA in platinum-sensitive tumor tissues, but not with platinum-resistant tumors.	Platinum	17-25	P53	Homo sapiens	210-213
21544361-2	1996	We observed that platinum-resistant tumors showed higher mRNA levels of p53, ERCC1, and XPA than platinum-sensitive tumors; mRNA expression patterns in responders differed substantially from nonresponders; and p53 expression showed a strong correlation with the expression of ERCC1, and of XPA in platinum-sensitive tumor tissues, but not with platinum-resistant tumors.	Platinum	97-105	P53	Homo sapiens	210-213
21544361-2	1996	We observed that platinum-resistant tumors showed higher mRNA levels of p53, ERCC1, and XPA than platinum-sensitive tumors; mRNA expression patterns in responders differed substantially from nonresponders; and p53 expression showed a strong correlation with the expression of ERCC1, and of XPA in platinum-sensitive tumor tissues, but not with platinum-resistant tumors.	Platinum	97-105	P53	Homo sapiens	210-213
8920221-0	1996	Immunohistochemical detection of P53 overexpression in paraffin wax-embedded squamous cell carcinomas of cattle, horses, cats and dogs.	Paraffin	55-67	P53	Homo sapiens	33-36
8632215-7	1996	Furthermore, Bax mRNA, an apoptosis-inducer gene, was increased with addition of AMP, suggesting that the induction of apoptosis may be channeled through the p53 pathway.	Adenosine Monophosphate	81-84	P53	Homo sapiens	158-161
8552618-0	1996	Induction of the WAF1/CIP1 protein and apoptosis in human T-cell leukemia virus type I-transformed lymphocytes after treatment with adriamycin by using a p53-independent pathway.	Doxorubicin	132-142	P53	Homo sapiens	154-157
8552392-4	1996	Using the conformational domain of p53 fused with protein A, we have shown that the p53 conformational domain possesses Zn+2-dependent, sequence-specific DNA-binding activity.	Zinc	120-124	P53	Homo sapiens	84-87
8552392-8	1996	Selective elution of the p53-binding proteins from the p53 hybrid protein by using a sequential step-wise NaCl gradient implicated one protein of 35K M(r) as contributing to a greater than four-fold activation of p53 DNA-binding activity.	Sodium Chloride	106-110	P53	Homo sapiens	25-28
8552392-8	1996	Selective elution of the p53-binding proteins from the p53 hybrid protein by using a sequential step-wise NaCl gradient implicated one protein of 35K M(r) as contributing to a greater than four-fold activation of p53 DNA-binding activity.	Sodium Chloride	106-110	P53	Homo sapiens	55-58
8552392-8	1996	Selective elution of the p53-binding proteins from the p53 hybrid protein by using a sequential step-wise NaCl gradient implicated one protein of 35K M(r) as contributing to a greater than four-fold activation of p53 DNA-binding activity.	Sodium Chloride	106-110	P53	Homo sapiens	55-58
9431695-0	1996	Immunoreactivity of new antibodies anti-p53 and anti-MDM-2 in paraffin embedded tissue samples.	Paraffin	62-70	P53	Homo sapiens	40-43
9431695-1	1996	Detection of various epitopes of the p53 and MDM-2 proteins, using new antibodies was performed on formalin-fixed and paraffin-embedded tissue samples from breast cancer and compared with results obtained using well-characterized antibodies.	Paraffin	118-126	P53	Homo sapiens	37-40
9081399-20	1996	Several genes are involved in control of this process; these include the p53 gene, mutations of which have been linked to cisplatin resistance in our laboratory studies, as well as in clinical trials with carboplatin.	Cisplatin	122-131	P53	Homo sapiens	73-76
8954175-1	1996	The polymerase chain reaction and HaeIII enzymatic digestion were used to study the seventh exon of the p53 gene in 29 primary and recurrent hepatomas in paraffin-embedded samples from 11 patients.	Paraffin	154-162	P53	Homo sapiens	104-107
8832944-4	1996	OBJECTIVE AND METHODS: The aim of the present study is to examine the frequency of immunohistochemically detectable p53 protein by using two monoclonal antibodies (D07 and BP53-12) in 8 cases of formalin-fixed and paraffin-embedded specimens of verrucous skin carcinoma.	Paraffin	214-222	P53	Homo sapiens	116-119
8726808-0	1996	Estradiol influences p53 expression in a human endometrial adenocarcinoma heterotransplanted into nude mice.	Estradiol	0-9	P53	Homo sapiens	21-24
8726808-1	1996	The influence of different estradiol concentrations on the expression of the p53 suppressor gene and on cell kinetics was examined by semiquantitative analysis of protein and bromodeoxyuridine labelling in a human endometrial adenocarcinoma grown in nude mice.	Estradiol	27-36	P53	Homo sapiens	77-80
8564846-0	1996	Loss of normal p53 function confers sensitization to Taxol by increasing G2/M arrest and apoptosis.	Paclitaxel	53-58	P53	Homo sapiens	15-18
8564846-2	1996	Normal human fibroblasts depleted of functional p53 by SV40 T antigen or HPV-16 E6, and primary embryo fibroblasts from p53 null mice showed seven- to ninefold increased cytotoxicity by paclitaxel.	Paclitaxel	186-196	P53	Homo sapiens	120-123
8564846-3	1996	Reduced levels of p53 correlated with increased G2/M phase arrest, micronucleation, and p53-independent paclitaxel-induced apoptosis.	Paclitaxel	104-114	P53	Homo sapiens	18-21
8564846-3	1996	Reduced levels of p53 correlated with increased G2/M phase arrest, micronucleation, and p53-independent paclitaxel-induced apoptosis.	Paclitaxel	104-114	P53	Homo sapiens	88-91
8979269-6	1996	A253-p53 cells could be distinguished from native A253 cells by prolonged doubling times (2-5 fold) and by a marked reduction of [3H]-thymidine uptake.	Tritium	130-132	P53	Homo sapiens	5-8
8549741-3	1995	The p53BP2-PP1 complex was stable to NaCl at concentrations which dissociate the p53-p53BP2 complex, and the binding of PP1 and p53 to p53BP2 was mutually exclusive.	Sodium Chloride	37-41	P53	Homo sapiens	4-7
8533007-2	1996	The latter are exemplified by protein thiol modification followed by subsequent NAD(+)-dependent automodification of the glycolytic enzyme GAPDH, or by mechanisms inducing accumulation of the tumor suppressor gene p53 and causing apoptotic cell death.	Sulfhydryl Compounds	38-43	P53	Homo sapiens	214-217
8732103-0	1996	[Detection of point mutation of p53 gene by silver staining PCR-SSCP in paraffin-embedded malignant fibrous histiocytoma].	Paraffin	72-80	P53	Homo sapiens	32-35
8732103-1	1996	Silver staining PCR-SSCP method was used to detect point mutation of p53 gene in paraffin-embedded malignant fibrous histiocytoma (MFH) tissues.	Paraffin	81-89	P53	Homo sapiens	69-72
8549741-3	1995	The p53BP2-PP1 complex was stable to NaCl at concentrations which dissociate the p53-p53BP2 complex, and the binding of PP1 and p53 to p53BP2 was mutually exclusive.	Sodium Chloride	37-41	P53	Homo sapiens	81-84
8521385-0	1995	Microtubule-active drugs taxol, vinblastine, and nocodazole increase the levels of transcriptionally active p53.	Nocodazole	49-59	P53	Homo sapiens	108-111
8521385-2	1995	We examined the ability of three microtubule-active agents, taxol, vinblastine, and nocodazole, to increase p53 levels and activate p53-dependent processes.	Paclitaxel	60-65	P53	Homo sapiens	108-111
8521385-0	1995	Microtubule-active drugs taxol, vinblastine, and nocodazole increase the levels of transcriptionally active p53.	Paclitaxel	25-30	P53	Homo sapiens	108-111
8521385-2	1995	We examined the ability of three microtubule-active agents, taxol, vinblastine, and nocodazole, to increase p53 levels and activate p53-dependent processes.	Paclitaxel	60-65	P53	Homo sapiens	132-135
8521385-2	1995	We examined the ability of three microtubule-active agents, taxol, vinblastine, and nocodazole, to increase p53 levels and activate p53-dependent processes.	Nocodazole	84-94	P53	Homo sapiens	108-111
8521385-2	1995	We examined the ability of three microtubule-active agents, taxol, vinblastine, and nocodazole, to increase p53 levels and activate p53-dependent processes.	Nocodazole	84-94	P53	Homo sapiens	132-135
8521409-4	1995	We show here that cis-diamminedichloroplatinum (cisplatin) induces the expression of interleukin-1 beta-converting enzyme (ICE), a mammalian homologue of the Caenorhabditis elegans cell death gene ced-3, in murine and human malignant glioma cells during apoptosis regardless of their p53 status.	Cisplatin	18-46	P53	Homo sapiens	284-287
8521409-4	1995	We show here that cis-diamminedichloroplatinum (cisplatin) induces the expression of interleukin-1 beta-converting enzyme (ICE), a mammalian homologue of the Caenorhabditis elegans cell death gene ced-3, in murine and human malignant glioma cells during apoptosis regardless of their p53 status.	Cisplatin	48-57	P53	Homo sapiens	284-287
8924223-9	1995	These findings indicate altered expression of p53 protein occurs in H&amp;N lymphomas, especially in late event lymphoma progression and appears to play a role in the development of EBER positive T cell lymphomas.	Adenosine Monophosphate	70-73	P53	Homo sapiens	46-49
8599466-1	1995	The accumulation of p53 protein was studied immunohistochemically on paraffin-embedded sections of 26 Spitz nevi (SNs), 26 primary invasive cutaneous malignant melanomas (MMs), 20 metastases of MM, and 17 ordinary compound nevi (CNs), using monoclonal antibody BP53-12.	Paraffin	69-77	P53	Homo sapiens	20-23
8599466-4	1995	We believe that the immunohistochemical detection of p53 protein with the use of monoclonal antibodies such as BP53-12 on paraffin sections, especially when strong nuclear reactivity is demonstrated, may prove to be an adjunctive tool in the histopathologic differentiation of MM from SN.	Paraffin	122-130	P53	Homo sapiens	53-56
8634783-0	1995	A universal method for the mutational analysis of K-ras and p53 gene in non-small-cell lung cancer using formalin-fixed paraffin-embedded tissue.	Paraffin	120-128	P53	Homo sapiens	60-63
7499360-5	1995	Supplementation of culture medium containing charcoal-treated calf serum with 0.1-1 nM 17 beta-estradiol restored p53 to its normal levels.	Estradiol	90-104	P53	Homo sapiens	114-117
7499360-9	1995	Since estradiol is known to promote cell proliferation, the induction of p53 observed in this study leads us to propose that estradiol stimulates p53 to regulate proliferation of T47D cells in culture.	Estradiol	6-15	P53	Homo sapiens	73-76
7499360-9	1995	Since estradiol is known to promote cell proliferation, the induction of p53 observed in this study leads us to propose that estradiol stimulates p53 to regulate proliferation of T47D cells in culture.	Estradiol	6-15	P53	Homo sapiens	146-149
7499360-9	1995	Since estradiol is known to promote cell proliferation, the induction of p53 observed in this study leads us to propose that estradiol stimulates p53 to regulate proliferation of T47D cells in culture.	Estradiol	125-134	P53	Homo sapiens	73-76
7499360-9	1995	Since estradiol is known to promote cell proliferation, the induction of p53 observed in this study leads us to propose that estradiol stimulates p53 to regulate proliferation of T47D cells in culture.	Estradiol	125-134	P53	Homo sapiens	146-149
8519417-5	1995	Transient wild-type p53 expression after high-efficiency gene transfer by a p53 adenovirus also sensitized the cells to cisplatin and correlated with the induction of apoptosis.	Cisplatin	120-129	P53	Homo sapiens	20-23
8640471-0	1995	Immunohistochemical detection of p53 overexpression in formalin-fixed, paraffin-embedded sections of endometrial carcinoma.	Paraffin	71-79	P53	Homo sapiens	33-36
8640471-2	1995	However using CM1 and an enhanced method based on microwave heating and protease digestion enabled the immunohistochemical detection of p53 overexpression in formalin-fixed, paraffin-embedded sections of endometrial carcinoma, although very few positive stainings were obtained without such an enhanced treatment.	Paraffin	174-182	P53	Homo sapiens	136-139
8640471-7	1995	CONCLUSION: Enhanced immunodetection of p53 in paraffin-embedded tissues will provide a useful alternative to the usual fresh-tissue assay.	Paraffin	47-55	P53	Homo sapiens	40-43
8519417-4	1995	Stable transfectants that co-expressed mutant and wild-type p53 had enhanced sensitivity to cisplatin and gamma radiation, compared with parental cells, control vector-transduced cells, and transduced cells that had lost expression of wild-type p53.	Cisplatin	92-101	P53	Homo sapiens	60-63
8519417-5	1995	Transient wild-type p53 expression after high-efficiency gene transfer by a p53 adenovirus also sensitized the cells to cisplatin and correlated with the induction of apoptosis.	Cisplatin	120-129	P53	Homo sapiens	76-79
7477163-0	1995	More on p53 antigen loss in stored paraffin slides.	Paraffin	35-43	P53	Homo sapiens	8-11
8751332-4	1995	To explore the differences in the expression of p53 protein in these two tumor types, we performed immunohistochemistry on 10 conventional pulmonary adenocarcinomas and 12 bronchioalveolar carcinomas on formalin-fixed and paraffin-embedded material, using the commercially available monoclonal antibody against the mutant p53 protein.	Paraffin	222-230	P53	Homo sapiens	48-51
7578083-5	1995	In many cancers, the most frequent class of mutations is C to T changes within CG dinucleotides of the tumor suppressor gene p53.	cytidylyl-3'-5'-guanosine	79-95	P53	Homo sapiens	125-128
7478539-0	1995	UREB1, a tyrosine phosphorylated nuclear protein, inhibits p53 transactivation.	Tyrosine	9-17	P53	Homo sapiens	59-62
7478539-7	1995	These data suggest that optimal suppression of p53 transactivation requires tyrosine phosphorylated UREB1 and that tyrosine phosphorylation and dephosphorylation processes may be involved in the regulation of p53 transactivation.	Tyrosine	76-84	P53	Homo sapiens	47-50
7478539-7	1995	These data suggest that optimal suppression of p53 transactivation requires tyrosine phosphorylated UREB1 and that tyrosine phosphorylation and dephosphorylation processes may be involved in the regulation of p53 transactivation.	Tyrosine	115-123	P53	Homo sapiens	209-212
7585548-0	1995	Aberrant p53 expression predicts clinical resistance to cisplatin-based chemotherapy in locally advanced non-small cell lung cancer.	Cisplatin	56-65	P53	Homo sapiens	9-12
7479838-3	1995	We show that alanine substitution mutations in a single loop of TBP can disrupt its association in vitro with the activation domains of the herpes simplex virus activator VP16 and of the human tumor suppressor protein p53; these mutations do not, however, disrupt the transcriptional response of TBP to either activation domain in vivo.	Alanine	13-20	P53	Homo sapiens	218-221
7585548-2	1995	In vitro studies indicate that p53 can modulate cisplatin-induced cytotoxicity, but the molecular genetic features determining response or resistance to cisplatin in vivo must be defined.	Cisplatin	48-57	P53	Homo sapiens	31-34
7585548-8	1995	Only 7 of 52 cases examined before and after chemotherapy treatment exhibited a change in the level of p53 expression after cisplatin-based chemotherapy.	Cisplatin	124-133	P53	Homo sapiens	103-106
7585548-9	1995	These results indicate that cisplatin alters p53 expression infrequently and suggest a direct link between aberrant p53 expression and resistance to cisplatin-based chemotherapy in NSCLC.	Cisplatin	28-37	P53	Homo sapiens	45-48
7585548-9	1995	These results indicate that cisplatin alters p53 expression infrequently and suggest a direct link between aberrant p53 expression and resistance to cisplatin-based chemotherapy in NSCLC.	Cisplatin	149-158	P53	Homo sapiens	116-119
8697990-7	1995	Immunohistochemistry (ABC method) on section of paraffin embedded tissue is a reliable method for detecting c-myc and p53 gene expression in HCC.	Paraffin	48-56	P53	Homo sapiens	118-121
7586197-6	1995	Treatment of PBLs with 2.5 microM of (+/-)-anti-BPDE and 1 mM of 3-aminobenzamide, an inhibitor of the DNA strand break-dependent enzyme poly(ADP-ribose) polymerase, resulted in increased p53 levels, in comparison to cells treated with (+/-)-anti-BPDE alone.	3-aminobenzamide	65-81	P53	Homo sapiens	188-191
7586197-8	1995	These findings suggest that (+/-)-anti-BPDE-induced DNA strand break formation is responsible for the observed p53 accumulation.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	39-43	P53	Homo sapiens	111-114
7586197-3	1995	Both immunocytochemical and immunoblot analysis indicated that treatment of PBLs with (+/-)-anti-BPDE results in p53 accumulation.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	97-101	P53	Homo sapiens	113-116
7586197-5	1995	Further, (+/-)-anti-BPDE-induced p53 accumulation in PBLs was found to be time-dependent with accumulation up to 24 h after the onset of treatment.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	20-24	P53	Homo sapiens	33-36
7586197-6	1995	Treatment of PBLs with 2.5 microM of (+/-)-anti-BPDE and 1 mM of 3-aminobenzamide, an inhibitor of the DNA strand break-dependent enzyme poly(ADP-ribose) polymerase, resulted in increased p53 levels, in comparison to cells treated with (+/-)-anti-BPDE alone.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	48-52	P53	Homo sapiens	188-191
9815924-1	1995	Immunohistochemical (IHC) staining for p53 protein nuclear expression was evaluated in archival paraffin-embedded radical prostatectomy specimens from 139 patients with clinically localized prostate cancer followed up from 1 to 8 (mean, 4) years.	Paraffin	96-104	P53	Homo sapiens	39-42
8822113-1	1995	The expression of p53 and bcl-2 was immunohistochemically investigated in 61 formalin-fixed, paraffin-embedded invasive breast carcinomas.	Paraffin	93-101	P53	Homo sapiens	18-21
8745486-2	1995	METHODS: Expression of p53 was studied by immunohistochemistry in paraffin sections from 23 normal endometrium, 44 endometrial hyperplasia and 103 endometrial carcinoma.	Paraffin	66-74	P53	Homo sapiens	23-26
7553639-0	1995	Taxol induction of p21WAF1 and p53 requires c-raf-1.	Paclitaxel	0-5	P53	Homo sapiens	31-34
7559631-6	1995	An in vitro glutathione S-transferase pull-down assay establishes a linear correlation between p53 TAD-mediated transactivation in vivo and the binding activity of p53 TAD to TATA-binding protein (TBP) in vitro.	Glutathione	12-23	P53	Homo sapiens	95-98
7559631-6	1995	An in vitro glutathione S-transferase pull-down assay establishes a linear correlation between p53 TAD-mediated transactivation in vivo and the binding activity of p53 TAD to TATA-binding protein (TBP) in vitro.	Glutathione	12-23	P53	Homo sapiens	164-167
7579380-6	1995	The results of immunohistochemistry analysis using a monoclonal anti-p53 antibody on paraffin-embedded specimens were compared with the SSCP data, the tumor karyotypes, and clinical course of each patient.	Paraffin	85-93	P53	Homo sapiens	69-72
7588628-1	1995	Cisplatin treatment of Epstein-Barr virus-immortalized human B lymphoblastoid cell lines (LCLs) results in p53-mediated apoptosis which occurs largely in a population of cells at the G1/S boundary of the cell cycle.	Cisplatin	0-9	P53	Homo sapiens	107-110
7553639-8	1995	Previous depletion of c-raf-1 inhibited both the p21WAF1- and p53-inducing properties of taxol, as well as the activation of MAP kinase.	Paclitaxel	89-94	P53	Homo sapiens	62-65
7553639-10	1995	Furthermore, the ability of taxol to both induce wild-type p53 in MCF7 cells and activate MAP kinase is also dependent on c-raf-1 expression.	Paclitaxel	28-33	P53	Homo sapiens	59-62
7553639-3	1995	Herein, we show that taxol induced dose- and time-dependent accumulation of the cyclin inhibitor p21WAF1 in both p53 wild-type and p53-null cells, although the degree of induction was greater in cells expressing wild-type p53.	Paclitaxel	21-26	P53	Homo sapiens	113-116
7553639-3	1995	Herein, we show that taxol induced dose- and time-dependent accumulation of the cyclin inhibitor p21WAF1 in both p53 wild-type and p53-null cells, although the degree of induction was greater in cells expressing wild-type p53.	Paclitaxel	21-26	P53	Homo sapiens	131-134
7553639-3	1995	Herein, we show that taxol induced dose- and time-dependent accumulation of the cyclin inhibitor p21WAF1 in both p53 wild-type and p53-null cells, although the degree of induction was greater in cells expressing wild-type p53.	Paclitaxel	21-26	P53	Homo sapiens	131-134
7553639-4	1995	In MCF7 cells, wild-type p53 protein was also induced after taxol treatment, and this induction was mediated primarily by increased protein stability.	Paclitaxel	60-65	P53	Homo sapiens	25-28
7553639-5	1995	Taxol induced both p21WAF1 and wild-type p53 optimally in MCF7 cells after 20-24-h exposure with an EC50(3) of 5 nM.	Paclitaxel	0-5	P53	Homo sapiens	41-44
7553639-6	1995	In p53-null PC3M cells, p21WAF1 was similarly induced after 24-h exposure to taxol.	Paclitaxel	77-82	P53	Homo sapiens	3-6
8590632-0	1995	Iron deprivation results in an increase in p53 expression.	Iron	0-4	P53	Homo sapiens	43-46
7478541-4	1995	Examination of Bcl-2 and p53 protein levels in pairs of cis-platin sensitive and resistant ovarian cell lines demonstrated that the resistant variants over-express Bcl-2 and/or p53, apparently due to progressive expansion of Bcl-2 and/or p53 positive subpopulations during the in vitro development of resistance.	Cisplatin	56-66	P53	Homo sapiens	25-28
7488003-0	1995	Phorbol esters attenuate the expression of p53 in cells treated with doxorubicin and protect TS-P53/K562 from apoptosis.	Doxorubicin	69-80	P53	Homo sapiens	43-46
7488003-1	1995	The induction of p53 by doxorubicin in normal human fibroblasts was completely reverted by TPA, a phorbol ester.	Doxorubicin	24-35	P53	Homo sapiens	17-20
8590632-1	1995	Deferoxamine (DFO)-induced iron deprivation caused an increase in p53 expression in ML-1 and Raji cells.	Iron	27-31	P53	Homo sapiens	66-69
8590632-5	1995	Although increases in wild type p53 protein in ML-1 cells resulted in increases in a p53 target gene, p21cipl/wafl/sdil, this effect was not observed in Raji cells which express a mutant p53 protein.	sdil	115-119	P53	Homo sapiens	32-35
8590632-5	1995	Although increases in wild type p53 protein in ML-1 cells resulted in increases in a p53 target gene, p21cipl/wafl/sdil, this effect was not observed in Raji cells which express a mutant p53 protein.	sdil	115-119	P53	Homo sapiens	85-88
8590632-5	1995	Although increases in wild type p53 protein in ML-1 cells resulted in increases in a p53 target gene, p21cipl/wafl/sdil, this effect was not observed in Raji cells which express a mutant p53 protein.	sdil	115-119	P53	Homo sapiens	85-88
9815913-3	1995	To test the hypothesis that a p53 mutation could result in tamoxifen resistance and estrogen-independent growth, the MCF-7 cell line was transfected with p53 cDNA which was mutated at codon 179 (histidine to glutamine).	Tamoxifen	59-68	P53	Homo sapiens	30-33
8630898-2	1995	METHODS: p53 protein expression was studied by immunohistochemistry from paraffin embedded tissue in a series of 136 patients with malignant ovarian epithelial tumors.	Paraffin	73-81	P53	Homo sapiens	9-12
9815913-4	1995	MCF-7 is an estrogen receptor-positive, estrogen-dependent, tamoxifen-sensitive cell line with only wild-type p53.	Tamoxifen	60-69	P53	Homo sapiens	110-113
7560079-6	1995	While p53 was detected in MCF-7 cells, evidence for TPA-induced stimulation of p53 transcriptional activity was not evident.	Tetradecanoylphorbol Acetate	52-55	P53	Homo sapiens	79-82
8575459-2	1995	Differences in the p53 content in extracts from the p53 antisense transfected HeLa clones compared to the parental HeLa cells were demonstrated by protein binding to the p53 consensus oligonucleotide and in transactivation assays.	Oligonucleotides	184-199	P53	Homo sapiens	19-22
8575459-2	1995	Differences in the p53 content in extracts from the p53 antisense transfected HeLa clones compared to the parental HeLa cells were demonstrated by protein binding to the p53 consensus oligonucleotide and in transactivation assays.	Oligonucleotides	184-199	P53	Homo sapiens	52-55
8575459-2	1995	Differences in the p53 content in extracts from the p53 antisense transfected HeLa clones compared to the parental HeLa cells were demonstrated by protein binding to the p53 consensus oligonucleotide and in transactivation assays.	Oligonucleotides	184-199	P53	Homo sapiens	52-55
8575459-6	1995	Reconstitution experiments with HeLa cells treated with a short p53 antisense oligonucleotide gave similar results: growth inhibition and giant cells.	Oligonucleotides	78-93	P53	Homo sapiens	64-67
7554069-8	1995	Positive nuclear immunostaining for the p53 tumor suppressor protein, a hallmark of human pancreatic cancer and a transient response to DNA damage, was observed in only a small percentage of BOP-induced pancreatic lesions and was not influenced Oltipraz administration.	nitrosobis(2-oxopropyl)amine	191-194	P53	Homo sapiens	40-43
7560890-0	1995	Detection of P53 expression and S-phase cell fraction in paraffin-embedded tissue by a double-labeling technique.	Paraffin	57-65	P53	Homo sapiens	13-16
7560890-3	1995	In breast cancer, we observed a poor correlation (rs = 0.17) between P53 expression and proliferative activity evaluated as [3H]-thymidine ([3H]-dT) labeling index and an independent prognostic relevance of the two variables.	Tritium	125-127	P53	Homo sapiens	69-72
7560890-3	1995	In breast cancer, we observed a poor correlation (rs = 0.17) between P53 expression and proliferative activity evaluated as [3H]-thymidine ([3H]-dT) labeling index and an independent prognostic relevance of the two variables.	Tritium	125-128	P53	Homo sapiens	69-72
7560890-7	1995	A weak direct relation between P53 positivity and [3H]-dT incorporation (rs = 0.4) was observed on the overall series of P53+ tumors and was maintained in subgroups defined by several biological and pathological features, except for estrogen receptor-negative tumors.	Tritium	51-53	P53	Homo sapiens	31-34
7560890-7	1995	A weak direct relation between P53 positivity and [3H]-dT incorporation (rs = 0.4) was observed on the overall series of P53+ tumors and was maintained in subgroups defined by several biological and pathological features, except for estrogen receptor-negative tumors.	Tritium	51-53	P53	Homo sapiens	121-124
7490678-0	1995	Detection of loss of heterozygosity of p53 gene in paraffin-embedded breast cancers by non-isotopic PCR-SSCP.	Paraffin	51-59	P53	Homo sapiens	39-42
7490678-1	1995	A rapid non-isotopic PCR-SSCP (polymerase chain reaction-single-stranded conformation polymorphism) method was developed in this study to detect polymorphism and loss of heterozygosity (LOH) of p53 in formalin-fixed and paraffin-embedded samples of normal breast tissue and of breast cancer.	Paraffin	220-228	P53	Homo sapiens	194-197
8771158-3	1995	Tumor p53 protein expression was detected by means of immunohistochemistry using the monoclonal antibody D07 on formalin fixed paraffin-embedded tissue sections.	Paraffin	127-135	P53	Homo sapiens	6-9
8771158-7	1995	Our study suggested that the immunohistochemical assay was a simple method of detection of mutant p53 proteins in routinely processed paraffin-embedded tissues of primary mammary carcinoma.	Paraffin	134-142	P53	Homo sapiens	98-101
7554056-0	1995	Nitric oxide and ethylnitrosourea: relative mutagenicity in the p53 tumor suppressor and hypoxanthine-phosphoribosyltransferase genes.	Nitric Oxide	0-12	P53	Homo sapiens	64-67
8519683-1	1995	We have earlier shown that wild-type (wt) p53 expressed from a temperature-sensitive construct (ts p53) triggers apoptosis in the v-myc retrovirus-induced, p53-negative T-cell lymphoma line J3D (Y. Wang et al., Cell Growth &amp; Differ., 4: 467-473, 1993).	Adenosine Monophosphate	224-227	P53	Homo sapiens	42-45
7667317-4	1995	Cells released from a mimosine block early in S phase stopped predominantly in G2/M in the presence of p53, confirming that p53 can mediate arrest at this stage, as well as in G1.	Mimosine	22-30	P53	Homo sapiens	103-106
8575232-2	1995	Quantitative analysis of P53 protein expression was performed on paraffin-embedded tissues from 55 smooth muscle tumors of the gastrointestinal tract, using immunofluorescence and flow cytometry.	Paraffin	65-73	P53	Homo sapiens	25-28
7594817-2	1995	A-7 was found to contain a mutant p53 gene in which the arginine codon at position 175 was substituted by a histidine codon.	Arginine	56-64	P53	Homo sapiens	34-37
7594817-2	1995	A-7 was found to contain a mutant p53 gene in which the arginine codon at position 175 was substituted by a histidine codon.	Histidine	108-117	P53	Homo sapiens	34-37
7472782-3	1995	p53 expression was evaluated by immunohistochemistry in formalin-fixed, paraffin-embedded tissue from 23 leiomyosarcomas, 10 tumours of uncertain malignant potential (TUMPs), and 18 leiomyomas.	Paraffin	72-80	P53	Homo sapiens	0-3
8697968-3	1995	The expression of p53 protein was also immunohistochemically studied in formalin-fixed paraffin embedded specimens of 76 colorectal adenocarcinomas and 112 colorectal polyps.	Paraffin	87-95	P53	Homo sapiens	18-21
7667317-4	1995	Cells released from a mimosine block early in S phase stopped predominantly in G2/M in the presence of p53, confirming that p53 can mediate arrest at this stage, as well as in G1.	Mimosine	22-30	P53	Homo sapiens	124-127
7563172-0	1995	Accumulation of p53 protein as a possible predictor of response to adjuvant combination chemotherapy with cyclophosphamide, methotrexate, fluorouracil, and prednisone for breast cancer.	Fluorouracil	138-150	P53	Homo sapiens	16-19
7657383-0	1995	Detection of TP53 gene mutation in human meningiomas: a study using immunohistochemistry, polymerase chain reaction/single-strand conformation polymorphism and DNA sequencing techniques on paraffin-embedded samples.	Paraffin	189-197	P53	Homo sapiens	13-17
7657383-7	1995	In this case, we identified a mutation in the TP53 gene at codon 161 changing GCC to ACC and resulting in an alteration of alanine to threonine in this position.	Alanine	123-130	P53	Homo sapiens	46-50
7657383-7	1995	In this case, we identified a mutation in the TP53 gene at codon 161 changing GCC to ACC and resulting in an alteration of alanine to threonine in this position.	Threonine	134-143	P53	Homo sapiens	46-50
7627952-4	1995	Here we show that mAb PAb421 when microinjected into human SW480 colorectal carcinoma cells restores the transcription activation function to the resident mutant p53 (arg to his 273, pro to ser 309).	Arginine	167-170	P53	Homo sapiens	162-165
7627952-4	1995	Here we show that mAb PAb421 when microinjected into human SW480 colorectal carcinoma cells restores the transcription activation function to the resident mutant p53 (arg to his 273, pro to ser 309).	Histidine	174-177	P53	Homo sapiens	162-165
7627952-4	1995	Here we show that mAb PAb421 when microinjected into human SW480 colorectal carcinoma cells restores the transcription activation function to the resident mutant p53 (arg to his 273, pro to ser 309).	Serine	190-193	P53	Homo sapiens	162-165
7614454-6	1995	This is the first report where germline transmission of replication-damaged p53 trinucleotide repeats is associated with the Li-Fraumeni syndrome.	trinucleotide	80-93	P53	Homo sapiens	76-79
7559095-2	1995	The wild-type p53 gene has a polymorphism at codon 72 that presents the arginine (CGC) or proline (CCC) genotype, which recently has been reported to be associated with genetically determined susceptibility to smoking-related lung cancers.	Arginine	72-80	P53	Homo sapiens	14-17
9816057-0	1995	Induction of apoptosis and cell cycle-specific change in expression of p53 in normal lymphocytes and MOLT-4 leukemic cells by nitrogen mustard.	Nitrogen	126-134	P53	Homo sapiens	71-74
9816057-5	1995	Exposure of normal lymphocytes to 5 microM nitrogen mustard caused their arrest in G1, an increase in p53 expression which was maximal in such cells, and significant apoptosis in cells located beyond the arrest point (S and G2 + M cells).	Nitrogen	43-51	P53	Homo sapiens	102-105
9816057-7	1995	Expression of p53 was highest for S and G2 + M MOLT-4 cells in response to the nitrogen mustard.	Nitrogen	79-87	P53	Homo sapiens	14-17
9816057-9	1995	These data suggest that DNA damage caused by nitrogen mustard provides a signal that results in stabilization of wild-type p53, preferentially in G1 cells, causes cell arrest in G1, and induces apoptosis of the cells that either were in the S-phase at the time of drug administration and/or escaped G1 arrest.	Nitrogen	45-53	P53	Homo sapiens	123-126
16696005-1	1995	Aim-To investigate the expression of p53 protein in invasive squamous cell carcinoma (SCC) of the larynx and dysplasia in relation to histological grade and tobacco smoking.Method-Paraffin wax embedded tissue sections from 41 cases of invasive SCC of the larynx, 28 cases of dysplasia and 14 control laryngeal biopsy specimens were studied immunohistochemically using two anti-p53 monoclonal antibodies (DO7 and 1801).	Paraffin	180-192	P53	Homo sapiens	37-40
7559095-2	1995	The wild-type p53 gene has a polymorphism at codon 72 that presents the arginine (CGC) or proline (CCC) genotype, which recently has been reported to be associated with genetically determined susceptibility to smoking-related lung cancers.	Chlormequat	99-102	P53	Homo sapiens	14-17
7623839-2	1995	We show that exposure of cells to various genotoxic agents, including anticancer drugs such as mitomycin and 5-fluorouracil, results in an increase in p53 mRNA levels and in p53 promoter activation, indicating that the p53 genotoxic stress response is partly regulated at the transcriptional level.	Fluorouracil	109-123	P53	Homo sapiens	151-154
7623839-2	1995	We show that exposure of cells to various genotoxic agents, including anticancer drugs such as mitomycin and 5-fluorouracil, results in an increase in p53 mRNA levels and in p53 promoter activation, indicating that the p53 genotoxic stress response is partly regulated at the transcriptional level.	Fluorouracil	109-123	P53	Homo sapiens	174-177
7623839-2	1995	We show that exposure of cells to various genotoxic agents, including anticancer drugs such as mitomycin and 5-fluorouracil, results in an increase in p53 mRNA levels and in p53 promoter activation, indicating that the p53 genotoxic stress response is partly regulated at the transcriptional level.	Fluorouracil	109-123	P53	Homo sapiens	174-177
8625105-5	1995	Immunohistochemical staining for p53 was performed on paraffin embedded tissue of each case.	Paraffin	54-62	P53	Homo sapiens	33-36
7624152-9	1995	In the present study, the wild type p53 protein in human fibrosarcoma HT1080 cells were targeted with HPV-18 E6 and the viability of these cells in response to treatment with adriamycin, u.v.-irradiation and gamma-irradiation was examined.	Doxorubicin	175-185	P53	Homo sapiens	36-39
7624116-1	1995	A human p53 mutant, p53Val-138 (amino acid 138, Alanine--&gt;Valine), generated by in vitro mutagenesis was introduced into Saos-2 human osteosarcoma and Jurkat acute T-lymphoblastic leukemia cell lines, both lacking p53 protein expression.	Alanine	48-55	P53	Homo sapiens	8-11
7624116-1	1995	A human p53 mutant, p53Val-138 (amino acid 138, Alanine--&gt;Valine), generated by in vitro mutagenesis was introduced into Saos-2 human osteosarcoma and Jurkat acute T-lymphoblastic leukemia cell lines, both lacking p53 protein expression.	Alanine	48-55	P53	Homo sapiens	20-23
7624134-0	1995	Cdk2 kinase phosphorylates serine 315 of human p53 in vitro.	Serine	27-33	P53	Homo sapiens	47-50
7624134-8	1995	Mutation of serine 315 of p53 to alanine (p53-S315A) abolished phosphorylation by cdk2 kinase.	Serine	12-18	P53	Homo sapiens	26-29
7624134-8	1995	Mutation of serine 315 of p53 to alanine (p53-S315A) abolished phosphorylation by cdk2 kinase.	Serine	12-18	P53	Homo sapiens	42-45
7624134-8	1995	Mutation of serine 315 of p53 to alanine (p53-S315A) abolished phosphorylation by cdk2 kinase.	Alanine	33-40	P53	Homo sapiens	26-29
7624134-8	1995	Mutation of serine 315 of p53 to alanine (p53-S315A) abolished phosphorylation by cdk2 kinase.	Alanine	33-40	P53	Homo sapiens	42-45
7624134-10	1995	The results demonstrate that ser 315 of p53 is phosphorylated by cdk2 in vitro.	Serine	29-32	P53	Homo sapiens	40-43
7624134-11	1995	However, ser 315 of wtp53 is not required for transcriptional activity in vivo, suggesting that cdk2 phosphorylation of p53 may be involved in regulating other cellular functions of wtp53.	Serine	9-12	P53	Homo sapiens	22-25
7784087-2	1995	It has recently been shown (Lin et al., 1994b) that the transcriptional activator domain of the p53 protein contains two amino acids, leu-22 and trp-23, which are required by the wild-type p53 protein for transcriptional activity.	Tryptophan	145-148	P53	Homo sapiens	96-99
21597798-6	1995	Western immunoblotting with commercial monoclonal antibodies and SDS-PAGE identified the isolated antigens as the p53 protein.	Sodium Dodecyl Sulfate	65-68	P53	Homo sapiens	114-117
7784087-2	1995	It has recently been shown (Lin et al., 1994b) that the transcriptional activator domain of the p53 protein contains two amino acids, leu-22 and trp-23, which are required by the wild-type p53 protein for transcriptional activity.	Tryptophan	145-148	P53	Homo sapiens	189-192
7611786-3	1995	All the cell lines expressing very low or undetectable level of sdil mRNA contains p53 gene abnormalities, while the cell lines expressing high level of sdil shares wild type p53 gene.	sdil	64-68	P53	Homo sapiens	83-86
7546049-2	1995	Quantitation of DNA ploidy was determined on Feulgen-stained touch imprints with an image analyzer, whereas localization of the immunohistochemical reaction of Erb-B2 and p53 protein was evaluated in paraffin-embedded tumor specimens with microscopy.	Paraffin	200-208	P53	Homo sapiens	171-174
7605578-3	1995	This p53 mutation resulted in the same change, an Arg--&gt;Ser substitution, as in the human p53 gene at position 249.	Arginine	50-53	P53	Homo sapiens	93-96
7539102-5	1995	Similarly, K562, cells stably transfected with a plasmid vector containing the temperature-sensitive human p53 mutant Ala-143 demonstrated a four- to sixfold upregulation of Fas/APO-1 by flow-cytometric analysis at the permissive temperature of 32.5 degrees C. Temperature-sensitive upregulation of Fas/APO-1 in K562 Ala-143 cells was verified by immunoprecipitation and demonstrated to result from enhanced mRNA production by nuclear run-on and Northern (RNA) analyses.	Alanine	118-121	P53	Homo sapiens	107-110
7539102-6	1995	Stably transfected K562 cells expressing temperature-insensitive, transcriptionally inactive p53 mutants (His-175, Trp-248, His-273, or Gly-281) failed to upregulate Fas/APO-1 at either 32.5 degrees or 37.5 degrees C. The temperature-sensitive transcription of Fas/APO-1 occurred in the presence of cycloheximide, indicating that de novo protein synthesis was not required and suggested a direct involvement of p53.	Tryptophan	115-118	P53	Homo sapiens	93-96
7761574-5	1995	We discovered p53 loss of heterozygosity and a point mutation in the remaining allele of the p53 gene in adriamycin-resistant cells.	Doxorubicin	105-115	P53	Homo sapiens	14-17
7739705-0	1995	p53 antigen loss in stored paraffin slides.	Paraffin	27-35	P53	Homo sapiens	0-3
7605578-1	1995	A mutation in the tumor suppressor p53 gene resulting in an Arg--&gt;Ser substitution in position 249 is found frequently in human hepatocellular carcinomas associated with hepatitis B infection and with aflatoxin exposure.	Arginine	60-63	P53	Homo sapiens	35-38
7605578-1	1995	A mutation in the tumor suppressor p53 gene resulting in an Arg--&gt;Ser substitution in position 249 is found frequently in human hepatocellular carcinomas associated with hepatitis B infection and with aflatoxin exposure.	Serine	69-72	P53	Homo sapiens	35-38
7605578-3	1995	This p53 mutation resulted in the same change, an Arg--&gt;Ser substitution, as in the human p53 gene at position 249.	Arginine	50-53	P53	Homo sapiens	5-8
7605578-3	1995	This p53 mutation resulted in the same change, an Arg--&gt;Ser substitution, as in the human p53 gene at position 249.	Serine	59-62	P53	Homo sapiens	5-8
7605578-3	1995	This p53 mutation resulted in the same change, an Arg--&gt;Ser substitution, as in the human p53 gene at position 249.	Serine	59-62	P53	Homo sapiens	93-96
7761574-5	1995	We discovered p53 loss of heterozygosity and a point mutation in the remaining allele of the p53 gene in adriamycin-resistant cells.	Doxorubicin	105-115	P53	Homo sapiens	93-96
7761100-4	1995	In this study, we show that the expression of both wild-type p53 and MDM2 (murine double minute 2) proteins was induced when cis-diamminedichloroplatinum (cisplatin) caused apoptosis in human glioblastoma U87-MG cells, which expressed neither wild-type p53 nor MDM2 protein prior to treatment.	Cisplatin	125-153	P53	Homo sapiens	253-256
7761100-4	1995	In this study, we show that the expression of both wild-type p53 and MDM2 (murine double minute 2) proteins was induced when cis-diamminedichloroplatinum (cisplatin) caused apoptosis in human glioblastoma U87-MG cells, which expressed neither wild-type p53 nor MDM2 protein prior to treatment.	Cisplatin	155-164	P53	Homo sapiens	253-256
7743505-8	1995	This increase in the WAF1/Cip1 mRNA level was observed 30 min after irradiation and continued for at least 48 h. A mobility shift assay performed using the sequence of the putative p53 DNA binding site on the WAF1/Cip1 and GADD45 genes as a probe showed that nuclear protein extracted from primary thyroid cells, anti-p53 antibody, and probe oligonucleotide-bound complex was clearly shifted.	Oligonucleotides	342-357	P53	Homo sapiens	181-184
7750085-4	1995	In contrast, thapsigargin antagonized only drug-induced nuclear accumulation of p53 protein.	Thapsigargin	13-25	P53	Homo sapiens	80-83
7729953-0	1995	Decreased cytotoxic effects of doxorubicin in a human ovarian cancer-cell line expressing wild-type p53 and WAF1/CIP1 genes.	Doxorubicin	31-42	P53	Homo sapiens	100-103
7729953-2	1995	In contrast, Doxorubicin was less cytotoxic in cells expressing wild-type p53 than in cells expressing no p53 or mutated p53.	Doxorubicin	13-24	P53	Homo sapiens	74-77
7729953-2	1995	In contrast, Doxorubicin was less cytotoxic in cells expressing wild-type p53 than in cells expressing no p53 or mutated p53.	Doxorubicin	13-24	P53	Homo sapiens	106-109
7729953-2	1995	In contrast, Doxorubicin was less cytotoxic in cells expressing wild-type p53 than in cells expressing no p53 or mutated p53.	Doxorubicin	13-24	P53	Homo sapiens	106-109
7729953-5	1995	A clear induction of WAF1/CIP1 and GADD45 genes in cells expressing wild-type p53 after Doxorubicin treatment was found.	Doxorubicin	88-99	P53	Homo sapiens	78-81
7734291-8	1995	Our data suggest that subjects with increased susceptibility to carcingogens after exposure to tobacco or alcohol are at higher risk for multiple cancers in which one of the most common genetic events is aberrant p53 expression.	Alcohols	106-113	P53	Homo sapiens	213-216
7729953-7	1995	Doxorubicin was also able to induce the transcription of WAF1/CIP1 gene in SKN cells (not expressing p53) or in SK23a cells at 37 degrees C (expressing mutated p53), indicating that the expression of this gene also, in some tumor-cell lines, is not necessarily or uniquely induced by wild-type p53.	Doxorubicin	0-11	P53	Homo sapiens	101-104
7729953-7	1995	Doxorubicin was also able to induce the transcription of WAF1/CIP1 gene in SKN cells (not expressing p53) or in SK23a cells at 37 degrees C (expressing mutated p53), indicating that the expression of this gene also, in some tumor-cell lines, is not necessarily or uniquely induced by wild-type p53.	Doxorubicin	0-11	P53	Homo sapiens	160-163
7729953-7	1995	Doxorubicin was also able to induce the transcription of WAF1/CIP1 gene in SKN cells (not expressing p53) or in SK23a cells at 37 degrees C (expressing mutated p53), indicating that the expression of this gene also, in some tumor-cell lines, is not necessarily or uniquely induced by wild-type p53.	Doxorubicin	0-11	P53	Homo sapiens	160-163
7727777-7	1995	We show here that TGF-beta treatment of phorbol myristate acetate (PMA) or anti-Ig-activated RL cells results in growth inhibition through a dual effect on Rb and mutant p53.	Tetradecanoylphorbol Acetate	40-65	P53	Homo sapiens	170-173
7727777-7	1995	We show here that TGF-beta treatment of phorbol myristate acetate (PMA) or anti-Ig-activated RL cells results in growth inhibition through a dual effect on Rb and mutant p53.	Tetradecanoylphorbol Acetate	67-70	P53	Homo sapiens	170-173
7737366-0	1995	Involvement of p53 expression in cAMP-mediated apoptosis in immortalized granulosa cells.	Cyclic AMP	33-37	P53	Homo sapiens	15-18
7737366-2	1995	In the present work, we examined the effect of overexpression of either wild-type or mutant p53 on cAMP-mediated apoptosis in steroidogenic granulosa cell lines transfected with SV40 DNA together with the Ha-ras oncogene and a temperature-sensitive variant of p53, p53val135.	Cyclic AMP	99-103	P53	Homo sapiens	92-95
7737366-5	1995	Progesterone production in such cells treated with cAMP was significantly higher at 32 degrees C than at 37.5 degrees C, suggesting that wild-type p53 can also enhance granulosa cell differentiation.	Progesterone	0-12	P53	Homo sapiens	147-150
7737366-5	1995	Progesterone production in such cells treated with cAMP was significantly higher at 32 degrees C than at 37.5 degrees C, suggesting that wild-type p53 can also enhance granulosa cell differentiation.	Cyclic AMP	51-55	P53	Homo sapiens	147-150
8542510-9	1995	SSCP analysis and sequencing of the p53 gene in both tumors revealed in the dedifferentiated chondrosarcoma a mutation in exon-8 with the transversion from G to T in codon 294 resulting in a substitution of a stop codon for GLU.	Glutamic Acid	224-227	P53	Homo sapiens	36-39
7622024-1	1995	The effect of the expression of the exogenous human mutant p53 (Arg--&gt;His in codon 273) on the amplification rate of the gene dhfr in permissive Rat-1 and LIM1215 cells was studied.	Arginine	64-67	P53	Homo sapiens	59-62
7607381-2	1995	It is possible to demonstrate the presence of mutant p 53 protein types in tumour cell nuclei by applying immunohistochemical procedures to paraffin sections (Clon DO 1, Dianova).	Paraffin	140-148	P53	Homo sapiens	53-57
7663341-1	1995	The backbone dynamics of the tetrameric p53 oligomerization domain (residues 319-360) have been investigated by two-dimensional inverse detected heteronuclear 1H-15N NMR spectroscopy at 500 and 600 MHz.	Hydrogen	159-161	P53	Homo sapiens	40-43
7616356-8	1995	Tumours with p53 gene mutations at exon 5 had a higher median [3H]thymidine labelling index (17 per cent) than those with mutations at exons 6, 7, and 8 (11.8 per cent).	Tritium	63-65	P53	Homo sapiens	13-16
7790313-3	1995	Immunostaining revealed nuclear accumulation of p53 within 6 h after various stresses [heat shock, osmotic shock, heavy metal (Cd), blockers of the cellular respiratory system (NaN3), amino acid analogues (azetidine and canavanine), an inhibitor of protein synthesis (puromycin), and oxygen free radicals (H2O2)].	Metals	120-125	P53	Homo sapiens	48-51
7790313-3	1995	Immunostaining revealed nuclear accumulation of p53 within 6 h after various stresses [heat shock, osmotic shock, heavy metal (Cd), blockers of the cellular respiratory system (NaN3), amino acid analogues (azetidine and canavanine), an inhibitor of protein synthesis (puromycin), and oxygen free radicals (H2O2)].	Cadmium	127-129	P53	Homo sapiens	48-51
7790313-3	1995	Immunostaining revealed nuclear accumulation of p53 within 6 h after various stresses [heat shock, osmotic shock, heavy metal (Cd), blockers of the cellular respiratory system (NaN3), amino acid analogues (azetidine and canavanine), an inhibitor of protein synthesis (puromycin), and oxygen free radicals (H2O2)].	azetidine	206-215	P53	Homo sapiens	48-51
7790313-3	1995	Immunostaining revealed nuclear accumulation of p53 within 6 h after various stresses [heat shock, osmotic shock, heavy metal (Cd), blockers of the cellular respiratory system (NaN3), amino acid analogues (azetidine and canavanine), an inhibitor of protein synthesis (puromycin), and oxygen free radicals (H2O2)].	Hydrogen Peroxide	306-310	P53	Homo sapiens	48-51
8521300-8	1995	RESULTS: Within seconds of stimulation, LPS and Taxol induce in Lps(n) macrophages a depression of autophosphorylation, followed within minutes by autophosphorylation of both p53 and p56 lyn species.	Paclitaxel	48-53	P53	Homo sapiens	175-178
7766306-0	1995	Benzo[a]pyrene-induced mutagenesis of p53 hot-spot codons 248 and 249 in human hepatocytes.	pyrene	8-14	P53	Homo sapiens	38-41
7766306-1	1995	Human tobacco-related cancers show a high frequency of G-to-T transversions in several mutation hot-spot regions of the p53 tumor suppressor gene, probably the result of specific mutagens in tobacco smoke, most notably benzo[a]pyrene.	pyrene	227-233	P53	Homo sapiens	120-123
7766306-2	1995	To gain insight into the mechanism of formation of these G-to-T transversions in tobacco-associated carcinogenesis, we studied the mutagenesis of p53 codons 247-250 by benzo[a]pyrene in human hepatocellular carcinoma cells by restriction fragment length polymorphism-polymerase chain reaction genotypic analysis.	pyrene	176-182	P53	Homo sapiens	146-149
7727392-9	1995	The stability of p53tet is dependent on pH and salt concentration.	Salts	47-51	P53	Homo sapiens	17-20
7783370-3	1995	The results of several fixation methods demonstrated that formalin and methanol, formalin and ethanol (1:9) and buffered formalin acetone gave good results for detecting p53 protein.	Ethanol	72-79	P53	Homo sapiens	170-173
7615358-2	1995	Mutations in exons 5 through 8 of the p53 gene were identified by a denaturing gradient gel electrophoresis (DGGE) assay and cycle sequencing, whereas p53 protein accumulation was detected in paraffin-embedded tissue by immunostaining using 2 different murine monoclonal antibodies (MAbs) (BP53-12 and DO7).	Paraffin	192-200	P53	Homo sapiens	151-154
7729416-8	1995	When the physiologically activated primary B cells were exposed to cisplatin, although p53 accumulated as in LCLs, the outcome was growth-arrest rather than gross cell death.	Cisplatin	67-76	P53	Homo sapiens	87-90
7712469-0	1995	Disruption of p53 function sensitizes breast cancer MCF-7 cells to cisplatin and pentoxifylline.	Cisplatin	67-76	P53	Homo sapiens	14-17
7712469-5	1995	Survival assays showed that p53 disruption sensitized MCF-7 cells to cisplatin (CDDP) but not to several other DNA-damaging agents.	Cisplatin	69-78	P53	Homo sapiens	28-31
7712469-5	1995	Survival assays showed that p53 disruption sensitized MCF-7 cells to cisplatin (CDDP) but not to several other DNA-damaging agents.	Cisplatin	80-84	P53	Homo sapiens	28-31
7712469-6	1995	CDDP sensitization was not limited to MCF-7 cells since p53 disruption in human colon carcinoma RKO cells also enhanced sensitivity to CDDP.	Cisplatin	0-4	P53	Homo sapiens	56-59
7712469-6	1995	CDDP sensitization was not limited to MCF-7 cells since p53 disruption in human colon carcinoma RKO cells also enhanced sensitivity to CDDP.	Cisplatin	135-139	P53	Homo sapiens	56-59
7712469-7	1995	Contrary to the other DNA-damaging agents tested, CDDP-induced DNA lesions are repaired extensively by nucleotide excision, and in agreement with a defect in this process, MCF-7/E6 and MCF-7/mu-p53 cells exhibited a reduced ability to repair a CDDP-damaged chloramphenicol acetyltransferase-reporter plasmid transfected into the cells.	Cisplatin	50-54	P53	Homo sapiens	194-197
7712469-8	1995	Therefore, we attributed the increased CDDP sensitivity of MCF-7 cells with disrupted p53 to defects in G1 checkpoint control, nucleotide excision repair, or both.	Cisplatin	39-43	P53	Homo sapiens	86-89
7712469-12	1995	Our results show that a combination of CDDP and pentoxifylline is capable of synergistic and preferential killing of p53-defective tumor cells that do not readily undergo apoptosis.	Cisplatin	39-43	P53	Homo sapiens	117-120
7627557-2	1995	We have examined potential p53-mediated effects of metabolically labeling cultured mammalian cells with [35S]methionine and [3H]thymidine, methods that are commonly used to study the biochemical properties, synthesis, processing and degradation of proteins and the replication of DNA in proliferating cells.	Sulfur-35	105-108	P53	Homo sapiens	27-30
7726729-0	1995	A microwave method that enhances detection of aberrant p53 expression in formalin-fixed, paraffin-embedded tissues.	Paraffin	89-97	P53	Homo sapiens	55-58
7726729-10	1995	CONCLUSIONS: Microwave pretreatment in conjunction with the use of either PAb1801 or DO7 is highly efficacious in the immunohistochemical detection of aberrant p53 expression in formalin-fixed, paraffin-embedded tissues.	Paraffin	194-202	P53	Homo sapiens	160-163
7627557-2	1995	We have examined potential p53-mediated effects of metabolically labeling cultured mammalian cells with [35S]methionine and [3H]thymidine, methods that are commonly used to study the biochemical properties, synthesis, processing and degradation of proteins and the replication of DNA in proliferating cells.	Methionine	109-119	P53	Homo sapiens	27-30
7627557-2	1995	We have examined potential p53-mediated effects of metabolically labeling cultured mammalian cells with [35S]methionine and [3H]thymidine, methods that are commonly used to study the biochemical properties, synthesis, processing and degradation of proteins and the replication of DNA in proliferating cells.	Tritium	125-127	P53	Homo sapiens	27-30
7576299-1	1995	The expression of the p53 protein (p53) was compared with those of several oncogenes including c-fos (Fos), c-jun (Jun), and epidermal growth factor receptor (EGFR1) using immunohistochemistry in frozen and paraffin-embedded sections of 25 basal cell carcinomas (BCCs) to find out any correlation between p53 and oncogenes in the pathogenesis of human BCC.	Paraffin	207-215	P53	Homo sapiens	22-25
7854378-2	1995	We performed a molecular analysis to determine the pattern of mutations in the p53 gene in neoplasms from patients with squamous-cell carcinoma of the head and neck and a history of tobacco or alcohol use.	Alcohols	193-200	P53	Homo sapiens	79-82
7620345-11	1995	We demonstrate that antigen retrieval techniques increase p53 immunoreactivity in paraffin embedded melanocytic tissues.	Paraffin	82-90	P53	Homo sapiens	58-61
7897229-10	1995	Third, p53-56lyn was probably activated after cell stimulation with zymosan, because the phosphorylation levels of a synthetic copolymer of glutamine-tyrosine were increased in Triton X-100-insoluble fraction.	Tyrosine	150-158	P53	Homo sapiens	7-10
7705936-1	1995	We introduced the mutant p53 gene (codon 273Arg-His) into human fibroblasts (SUSM-I cells) previously immortalized with 4-nitroquinoline I-oxide (4NQO) and obtained 2 clonal cell lines (SUSM-i/p53-1 and SUSM-1/p53-6) expressing the mutant p53.	Histidine	48-51	P53	Homo sapiens	25-28
7854378-9	1995	CONCLUSIONS: In our study, a history of tobacco and alcohol use was associated with a high frequency of p53 mutations in patients with squamous-cell carcinoma of the head and neck.	Alcohols	52-59	P53	Homo sapiens	104-107
7896460-0	1995	Analysis of the p53 gene in relation to tobacco and alcohol in cancers of the upper aero-digestive tract.	Alcohols	52-59	P53	Homo sapiens	16-19
7898180-3	1995	P53 antibodies were detected in 42 cases (12%) and were negatively related to oestradiol and progesterone receptors.	Estradiol	78-88	P53	Homo sapiens	0-3
7534296-4	1995	In this report we provide evidence that phosphorylation of serine 378 within the carboxyl-terminal negative regulatory domain of the human p53 protein by protein kinase C correlates with loss of PAb421 reactivity and a concomitant activation of sequence-specific DNA binding.	Serine	59-65	P53	Homo sapiens	139-142
7898929-6	1995	Oligonucleotide competition analyses with various p53 target sequences and methylation interference experiments establish that wild-type and mutant p53 differ significantly in their sequence-specific interactions.	Oligonucleotides	0-15	P53	Homo sapiens	50-53
7898929-6	1995	Oligonucleotide competition analyses with various p53 target sequences and methylation interference experiments establish that wild-type and mutant p53 differ significantly in their sequence-specific interactions.	Oligonucleotides	0-15	P53	Homo sapiens	148-151
7880719-0	1995	Antisense oligonucleotides directed against p53 have antiproliferative effects unrelated to effects on p53 expression.	Oligonucleotides	10-26	P53	Homo sapiens	44-47
7880719-1	1995	Antisense oligonucleotides targeting p53 have been hailed as a potentially new technique for treating patients with cancer, and there have been encouraging reports of good patient tolerance in vivo and of antiproliferative effects in vitro.	Oligonucleotides	10-26	P53	Homo sapiens	37-40
7880719-2	1995	However, evidence is lacking that these oligonucleotides are acting via an antisense interaction to modulate p53 expression.	Oligonucleotides	40-56	P53	Homo sapiens	109-112
7727133-2	1995	A nuclear phosphoprotein, p53, was isolated by immunoprecipitation after biosynthetic labeling with 35S, 32P or 33P in cultured human cells.	Sulfur-35	100-103	P53	Homo sapiens	26-29
7853526-4	1995	Instead, HBx enhanced p53"s oligomerization state on a DNA oligonucleotide containing a p53 response element.	Oligonucleotides	59-74	P53	Homo sapiens	22-25
7853526-4	1995	Instead, HBx enhanced p53"s oligomerization state on a DNA oligonucleotide containing a p53 response element.	Oligonucleotides	59-74	P53	Homo sapiens	88-91
21556589-4	1995	Sequencing of p53 cDNA revealed a mutation CGC(Arg)--&gt;CAC(His) at codon 175 of the gene encoding for an abundant nuclear protein.	Arginine	47-50	P53	Homo sapiens	14-17
7727133-7	1995	The relative phosphorylation of each p53 isoform was estimated by normalizing 33P or 32P isoform volumes with the corresponding 35S volume and showed progressive phosphorylation of acidic isoforms.	Sulfur-35	128-131	P53	Homo sapiens	37-40
7852482-5	1995	Putative p53 mutations were detected by immunohistochemistry on paraffin-embedded sections using polyclonal CM-1 and monoclonal DO-7 and PAb1801 antibodies.	Paraffin	64-72	P53	Homo sapiens	9-12
7796648-2	1995	Detection of overexpression of p53 protein was carried out by immunohistochemical staining (IHS) using the monoclonal antibody DO-1 on paraffin sections.	Paraffin	135-143	P53	Homo sapiens	31-34
7556591-6	1995	Nuclear p53 immunoreactivity was assessed using a monoclonal antibody, DO-1, on Formalin-fixed paraffin-embedded specimens.	Paraffin	95-103	P53	Homo sapiens	8-11
7734516-12	1995	Immunohistochemical analysis of the same paraffin-embedded sections showed that infectivity and level of expression of p53 in lung tissue were dose-dependent.	Paraffin	41-49	P53	Homo sapiens	119-122
7841034-3	1995	In vitro, the conformation and DNA-binding activity of wild-type p53 are subject to redox modulation and are abrogated by exposure to metal chelators.	Metals	134-139	P53	Homo sapiens	65-68
7841034-6	1995	Destabilisation of p53 tertiary structure induced protein aggregation through hydrophobic interactions, consistent with the notion that wild-type p53 contains a hydrophobic core which may become exposed by metal chelation.	Metals	206-211	P53	Homo sapiens	19-22
7841034-6	1995	Destabilisation of p53 tertiary structure induced protein aggregation through hydrophobic interactions, consistent with the notion that wild-type p53 contains a hydrophobic core which may become exposed by metal chelation.	Metals	206-211	P53	Homo sapiens	146-149
7834638-4	1995	We show that p53-independent induction of WAF1/CIP1 occurs in human leukemia cells treated with 12-O-tetradecanoylphorbol-13-acetate, okadaic acid, or IFN-gamma but not with retinoic acid, vitamin D3, or DMSO.	Tetradecanoylphorbol Acetate	96-132	P53	Homo sapiens	13-16
7860045-1	1995	Several studies of benign breast lesions using methacran-fixed, paraffin-embedded tissues and cytological preparations have suggested that p53 accumulation in these lesions as detected by immunohistochemical (IHC) staining is rare to absent.	Paraffin	64-72	P53	Homo sapiens	139-142
7860046-5	1995	Image analysis showed that the surfaces positive with anti-p53 and the staining intensity were decreased (P &lt; .01) on paraffin sections.	Paraffin	121-129	P53	Homo sapiens	59-62
7745116-2	1995	METHODS: The expression of p53, Rb and bcl-2 proteins in paraffin wax embedded tonsil tissue sections was detected by immunohistochemistry using an (APAAP) technique following microwave irradiation.	Paraffin	57-69	P53	Homo sapiens	27-30
7819040-5	1995	The immunohistochemical detection of mutations of the p53 gene has been demonstrated to be a reliable, easily performed and thereby widely available technique for the investigation of fresh-frozen or paraffin-embedded tumour specimens.	Paraffin	200-208	P53	Homo sapiens	54-57
7730147-3	1995	We investigated the relationship between p53-dependent apoptosis and differentiation induction using human promyelocytic leukemia HL-60 cells transfected with pMAMneo expression vectors containing dexamethasone-inducible wild-type p53 (wt-p53) cDNA inserts.	Dexamethasone	197-210	P53	Homo sapiens	231-234
7730147-3	1995	We investigated the relationship between p53-dependent apoptosis and differentiation induction using human promyelocytic leukemia HL-60 cells transfected with pMAMneo expression vectors containing dexamethasone-inducible wild-type p53 (wt-p53) cDNA inserts.	Dexamethasone	197-210	P53	Homo sapiens	231-234
7730147-4	1995	Continuous exposure of the pMAMneo/wt-p53 transfectants to 1 microM dexamethasone for more than 24 h caused overexpression of wt-p53 followed by cell death with morphological changes typical of apoptosis.	Dexamethasone	68-81	P53	Homo sapiens	38-41
7730147-4	1995	Continuous exposure of the pMAMneo/wt-p53 transfectants to 1 microM dexamethasone for more than 24 h caused overexpression of wt-p53 followed by cell death with morphological changes typical of apoptosis.	Dexamethasone	68-81	P53	Homo sapiens	129-132
7730147-6	1995	All-trans retinoic acid (all-trans RA) at 1 nM or granulocyte macrophage colony-stimulating factor (GM-CSF) at 35 pM inhibited the wt-p53-induced apoptosis over a 42-h treatment.	Tretinoin	10-23	P53	Homo sapiens	134-137
7829527-7	1995	Wild type p53 stimulation of MDRCAT expression also occurred in parental and doxorubicin-resistant SW620 colon and parental 2780 ovarian cancer cell lines, indicating that wild type p53-mediated simulation of the MDR1 promoter is not restricted to a single cell line.	Doxorubicin	77-88	P53	Homo sapiens	10-13
8720438-4	1995	The role of p53 in the modulation of different aspects of cytotoxic activity of these cells was analyzed by studying the effects of p53 abrogation by antisense oligonucleotide (p53 AS) treatment in comparison with p53 sense or scrambled (missense) oligonucleotide (p53 S or p53 MS) treatment.	Oligonucleotides	160-175	P53	Homo sapiens	132-135
8720438-4	1995	The role of p53 in the modulation of different aspects of cytotoxic activity of these cells was analyzed by studying the effects of p53 abrogation by antisense oligonucleotide (p53 AS) treatment in comparison with p53 sense or scrambled (missense) oligonucleotide (p53 S or p53 MS) treatment.	Oligonucleotides	160-175	P53	Homo sapiens	132-135
8720438-4	1995	The role of p53 in the modulation of different aspects of cytotoxic activity of these cells was analyzed by studying the effects of p53 abrogation by antisense oligonucleotide (p53 AS) treatment in comparison with p53 sense or scrambled (missense) oligonucleotide (p53 S or p53 MS) treatment.	Oligonucleotides	160-175	P53	Homo sapiens	132-135
8720438-4	1995	The role of p53 in the modulation of different aspects of cytotoxic activity of these cells was analyzed by studying the effects of p53 abrogation by antisense oligonucleotide (p53 AS) treatment in comparison with p53 sense or scrambled (missense) oligonucleotide (p53 S or p53 MS) treatment.	Oligonucleotides	160-175	P53	Homo sapiens	132-135
8720438-4	1995	The role of p53 in the modulation of different aspects of cytotoxic activity of these cells was analyzed by studying the effects of p53 abrogation by antisense oligonucleotide (p53 AS) treatment in comparison with p53 sense or scrambled (missense) oligonucleotide (p53 S or p53 MS) treatment.	Oligonucleotides	160-175	P53	Homo sapiens	132-135
7720108-0	1994	[Detection of point mutation of p53 gene by non-isotopic PCR-SSCP in paraffin-embedded breast cancer tissue].	Paraffin	69-77	P53	Homo sapiens	32-35
8867673-8	1995	In fact, only in the presence of Mg2+, but not in the absence of divalent cations or in the presence of Ca2+ alone, TNF increased p58c-fgr and p53/56lyn kinase activities; and this was prevented by anti-CD18 antibodies.	magnesium ion	33-37	P53	Homo sapiens	143-146
8867673-11	1995	Detergent extraction of proteins showed that the Mg(2+)-dependent, TNF-stimulated adhesion redistributed p58c-fgr and p53/56lyn to a Triton-insoluble fraction.	magnesium ion	49-55	P53	Homo sapiens	118-121
7811703-0	1994	Divalent metal ions induce conformational change in pure, human wild-type p53 tumor suppressor protein.	Metals	9-14	P53	Homo sapiens	74-77
7811703-3	1994	Our results show that the presence of Zn2+ ions at physiological concentrations, directly reduced or blocked accessibility of epitopes on pure wild-type p53, an effect which was reversed by chelating agents.	Zinc	38-42	P53	Homo sapiens	153-156
7811703-5	1994	Analytical sucrose density gradient ultracentrifugation studies also confirmed that Zn(2+)-induced conformational changes partially affected the pattern of p53 oligomerisation.	Zinc	84-90	P53	Homo sapiens	156-159
7527509-5	1994	In the second part of the study, accumulation of p53 protein was determined in 42 archival paraffin-embedded specimens from oral leukoplakia and correlated with the degree of epithelial dysplasia.	Paraffin	91-99	P53	Homo sapiens	49-52
9117440-3	1995	The [3H]LPS-binding fragments had low bouyant densities and were enriched, when compared to high-density membrane fragments, in CD14 (a receptor for LPS and other microbial molecules), p53/56lyn, GTP-binding proteins, ouabain-inhibitable Na+/K+ ATPase, sphingomyelin, and GM1 ganglioside.	Tritium	5-7	P53	Homo sapiens	185-188
7704245-1	1995	The expression of p53 protein was studied in formalin-fixed paraffin-embedded specimens of 41 well-differentiated adenocarcinomas of the gall-bladder, six cases of acute cholecystitis and 23 cases of chronic cholecystitis, using a monoclonal p53 (PAb 1801) antibody and streptavidin-biotin.	Paraffin	60-68	P53	Homo sapiens	18-21
7597296-5	1995	Analysis of p53 gene showed mutation only in one case of mycosis fungoides in tumoral stage, at codon 163 of p53 gene (TAC--&gt;CAC; Tyr--&gt; Asp).	Tyrosine	133-136	P53	Homo sapiens	12-15
7597296-5	1995	Analysis of p53 gene showed mutation only in one case of mycosis fungoides in tumoral stage, at codon 163 of p53 gene (TAC--&gt;CAC; Tyr--&gt; Asp).	Tyrosine	133-136	P53	Homo sapiens	109-112
7530754-6	1994	While the p53 response was defective after radiation, agents that interfered with cell cycle progression such as mimosine, aphidicolin and deprivation of serum led to a normal p53 response in A-T cells.	Mimosine	113-121	P53	Homo sapiens	176-179
7876377-2	1994	METHODS: Immunocytochemistry for p53 was performed in 65 specimens of formalin fixed, paraffin wax embedded cervical tissue using a polyclonal antibody against recombinant p53.	Paraffin	86-98	P53	Homo sapiens	33-36
7969121-3	1994	Recent findings indicate that c-Myc/Max heterodimers can bind to an essential CA(C/T)GTG-containing site in the p53 promoter and elevate its expression.	Guanosine Triphosphate	85-88	P53	Homo sapiens	112-115
7720108-1	1994	Non-isotopic PCR-SSCP method was used to detect point mutation of p53 gene in paraffin-embedded breast cancers.	Paraffin	78-86	P53	Homo sapiens	66-69
7720110-3	1994	The result showed that mutation of both cell lines occurred on the 154th codon in exon5 of p53 gene, where GGC was displaced by GTC resulting a substitution of Val for Gly, nevertheless, N-ras oncogene and the exon7 of p53 gene are normal.	Glycine	168-171	P53	Homo sapiens	91-94
7720110-3	1994	The result showed that mutation of both cell lines occurred on the 154th codon in exon5 of p53 gene, where GGC was displaced by GTC resulting a substitution of Val for Gly, nevertheless, N-ras oncogene and the exon7 of p53 gene are normal.	Glycine	168-171	P53	Homo sapiens	219-222
7954409-1	1994	The present study assessed the role of the p53 tumor suppressor gene in cell cycle arrest and apoptosis following treatment of Burkitt"s lymphoma and lymphoblastoid cell lines with gamma-rays, etoposide, nitrogen mustard, and cisplatin.	Cisplatin	226-235	P53	Homo sapiens	43-46
7525358-0	1994	p53 expression in nitric oxide-induced apoptosis.	Nitric Oxide	18-30	P53	Homo sapiens	0-3
7525358-5	1994	NO-synthase inhibitors such as NG-monomethyl-L-arginine prevent the inducible NO generation as well as p53 expression and apoptosis.	omega-N-Methylarginine	31-55	P53	Homo sapiens	103-106
7954409-8	1994	We also observed an inverse sensitivity relationship between nitrogen mustard/cisplatin and etoposide in the mutant p53 lines and this was found to correlate with topoisomerase II mRNA levels in the cells.	Nitrogen	61-69	P53	Homo sapiens	116-119
7954409-8	1994	We also observed an inverse sensitivity relationship between nitrogen mustard/cisplatin and etoposide in the mutant p53 lines and this was found to correlate with topoisomerase II mRNA levels in the cells.	Cisplatin	78-87	P53	Homo sapiens	116-119
7942634-1	1994	Immunohistochemical staining for the p53 protein was performed in microwave-fixed, paraffin-embedded sections of normal, premalignant and malignant tissues of the female genital tract using a monoclonal antibody, PAb 1801.	Paraffin	83-91	P53	Homo sapiens	37-40
11578436-3	1994	We also examined the expression of p53 in paraffin tissues by immunohistochemical staining and determined the incidence of human papillomavirus (HPV) sequences in the same tissues by multitype PCR analysis to correlate them to the allelic loss on chromosome 17p13 and p53 mutation.	Paraffin	42-50	P53	Homo sapiens	35-38
7957681-3	1994	A recombinant human wild type p53 fused with glutathione S-transferase was immobilized on glutathione-agarose as a ligand for affinity column.	Glutathione	45-56	P53	Homo sapiens	30-33
7957681-7	1994	The glutathione fraction that contained the p53 glutathione S-transferase fused protein also showed the same activity.	Glutathione	4-15	P53	Homo sapiens	44-47
7959668-1	1994	Immunohistochemical expression of the cellular phosphoprotein p53 was investigated in archival, formalin-fixed, and paraffin-embedded surgical breast tissue specimens from 543 patients using the polyclonal antibody CM-1.	Paraffin	116-124	P53	Homo sapiens	62-65
7852968-6	1994	However, when expression of the p53 protein in normal HEF cells was suppressed by the antisense oligonucleotide of the p53 gene, growth stimulation was not observed.	Oligonucleotides	96-111	P53	Homo sapiens	32-35
7962351-5	1994	Putative p53 mutations were detected by immunohistochemistry on paraffin-embedded sections using polyclonal CM-1 and monoclonal DO-7 and PAb1801 antibodies.	Paraffin	64-72	P53	Homo sapiens	9-12
7852968-6	1994	However, when expression of the p53 protein in normal HEF cells was suppressed by the antisense oligonucleotide of the p53 gene, growth stimulation was not observed.	Oligonucleotides	96-111	P53	Homo sapiens	119-122
7580888-2	1994	Sequences of the p53 gene have been obtained from DNA extracted from frozen and formalin-fixed paraffin-embedded cancer tissues.	Paraffin	95-103	P53	Homo sapiens	17-20
7936649-0	1994	The carboxy-terminal serine 392 phosphorylation site of human p53 is not required for wild-type activities.	Serine	21-27	P53	Homo sapiens	62-65
7936649-3	1994	Serine 386 of murine p53 and the homologous residue of human p53, serine 392, are phosphorylated in vivo and can be phosphorylated in vitro by casein kinase II (CKII).	Serine	0-6	P53	Homo sapiens	61-64
7936649-3	1994	Serine 386 of murine p53 and the homologous residue of human p53, serine 392, are phosphorylated in vivo and can be phosphorylated in vitro by casein kinase II (CKII).	Serine	66-72	P53	Homo sapiens	61-64
7936649-4	1994	We constructed mutants that changed serine 392 of human p53 to alanine (p53-S392A) or aspartic acid (p53-S392D); cotransfection of both these mutants with a reporter gene carrying a p53-responsive element into the p53-null Saos-2 cell line activated transcription as well as did wild-type p53.	Serine	36-42	P53	Homo sapiens	56-59
7922972-6	1994	METHODS: p53 expression in formalin fixed, paraffin embedded samples of 204 patients with primary squamous cell carcinoma of the esophagus, who underwent esophageal resection, were analyzed immunohistochemically with DO-1, a monoclonal antibody that detects wild-type and mutant forms of p53.	Paraffin	43-51	P53	Homo sapiens	9-12
8084608-0	1994	A single nucleotide substitution at codon 31 (Ser/Arg) defines a polymorphism in a highly conserved region of the p53-inducible gene WAF1/CIP1.	Serine	46-49	P53	Homo sapiens	114-117
8084608-0	1994	A single nucleotide substitution at codon 31 (Ser/Arg) defines a polymorphism in a highly conserved region of the p53-inducible gene WAF1/CIP1.	Arginine	50-53	P53	Homo sapiens	114-117
7823248-2	1994	Genomic p53 was amplified by the polymerase chain reaction (PCR) from paraffin-embedded sections of tumour and non-tumour tissue.	Paraffin	70-78	P53	Homo sapiens	8-11
7936649-6	1994	A stable derivative of the T98G human glioblastoma cell line was established that expressed p53-S392A in response to dexamethasone.	Dexamethasone	117-130	P53	Homo sapiens	92-95
7848689-1	1994	BACKGROUND AND METHODS: p53 protein expression was studied immunohistochemically in 73 colorectal adenocarcinomas, using monoclonal antibody D07 in alcohol fixed, paraffin embedded tissue.	Alcohols	148-155	P53	Homo sapiens	24-27
7848689-1	1994	BACKGROUND AND METHODS: p53 protein expression was studied immunohistochemically in 73 colorectal adenocarcinomas, using monoclonal antibody D07 in alcohol fixed, paraffin embedded tissue.	Paraffin	163-171	P53	Homo sapiens	24-27
7530851-0	1994	p53 immunolabeling in archival paraffin-embedded tissues: optimal protocol based on microwave heating for eight antibodies on lung carcinomas.	Paraffin	31-39	P53	Homo sapiens	0-3
7708439-9	1994	P53 was investigated by immunohistochemistry, using a monoclonal anti-p53 antibody (DO-7), on formalin fixed, paraffin embedded tissue.	Paraffin	110-118	P53	Homo sapiens	0-3
7847818-5	1994	Wild-type p53 as well as one mutant p53 [(mutation of arginine to histidine at codon 273 (His 273)], had strong transactivating activity, but all other mutant p53s were inactive in transcriptional activation, including the double mutant Tyr141/His273 suggesting that the Tyr141 mutation was dominant over the His273 mutation in the same protein.	Histidine	90-93	P53	Homo sapiens	10-13
7847818-5	1994	Wild-type p53 as well as one mutant p53 [(mutation of arginine to histidine at codon 273 (His 273)], had strong transactivating activity, but all other mutant p53s were inactive in transcriptional activation, including the double mutant Tyr141/His273 suggesting that the Tyr141 mutation was dominant over the His273 mutation in the same protein.	Histidine	90-93	P53	Homo sapiens	36-39
7847818-5	1994	Wild-type p53 as well as one mutant p53 [(mutation of arginine to histidine at codon 273 (His 273)], had strong transactivating activity, but all other mutant p53s were inactive in transcriptional activation, including the double mutant Tyr141/His273 suggesting that the Tyr141 mutation was dominant over the His273 mutation in the same protein.	Histidine	90-93	P53	Homo sapiens	36-39
8082749-0	1994	Transient stabilization of p53 in non-small cell lung carcinoma cultures arrested for growth by retinoic acid.	Tretinoin	96-109	P53	Homo sapiens	27-30
8082749-3	1994	Levels of p53 transcripts remained unchanged during the time of increases in protein expression in retinoic acid-treated H460a cells, suggesting that a post-translational mechanism was involved in the increased expression of the protein.	Tretinoin	99-112	P53	Homo sapiens	10-13
8082749-4	1994	Pulse-chase analysis demonstrated that wild-type p53 was significantly more stabile in H460a cells treated with retinoic acid, exhibiting a half-life greater than 6 h, in contrast to 3 h for the protein in untreated control cells.	Tretinoin	112-125	P53	Homo sapiens	49-52
8082749-5	1994	The retinoic acid-mediated effect was specific for wild-type p53, since expression of mutant p53 in the H596b and H322j cell lines remained relatively unchanged even after 72 h exposure to retinoic acid.	Tretinoin	4-17	P53	Homo sapiens	61-64
8082749-5	1994	The retinoic acid-mediated effect was specific for wild-type p53, since expression of mutant p53 in the H596b and H322j cell lines remained relatively unchanged even after 72 h exposure to retinoic acid.	Tretinoin	4-17	P53	Homo sapiens	93-96
8082749-5	1994	The retinoic acid-mediated effect was specific for wild-type p53, since expression of mutant p53 in the H596b and H322j cell lines remained relatively unchanged even after 72 h exposure to retinoic acid.	Tretinoin	189-202	P53	Homo sapiens	61-64
8082749-5	1994	The retinoic acid-mediated effect was specific for wild-type p53, since expression of mutant p53 in the H596b and H322j cell lines remained relatively unchanged even after 72 h exposure to retinoic acid.	Tretinoin	189-202	P53	Homo sapiens	93-96
8082749-6	1994	We conclude that retinoic acid induces stabilization of wild-type p53 in NSCLC cells by a post-translational mechanism.	Tretinoin	17-30	P53	Homo sapiens	66-69
8082749-7	1994	Furthermore, increases in expression of p53 were not responsible for the retinoic acid-induced transient inhibition of growth of NSCLC cells, since the growth of H358 p53-null cells also was inhibited by retinoic acid.	Tretinoin	204-217	P53	Homo sapiens	167-170
8036011-3	1994	We have studied the capacity of hydrogen peroxide plus ferric chloride (FeCl3) to induce base pair changes in the hotspot codons 248 and 249 of the p53 tumor suppressor gene in human fibroblasts.	Hydrogen Peroxide	32-49	P53	Homo sapiens	148-151
8036011-7	1994	It is evident that H2O2/FeCl3 possesses essentially the same mutagenic specificity for codons 249 and 250 of p53 as bulky carcinogens such as aflatoxin B1, benzo(a)pyrene or heterocyclic amines.	Hydrogen Peroxide	19-23	P53	Homo sapiens	109-112
7882774-1	1994	Quantitative analysis of p53 protein expression was performed on paraffin-embedded tissues from 55 smooth muscle tumors of the gastrointestinal tract by using immunofluorescence and flow cytometry.	Paraffin	65-73	P53	Homo sapiens	25-28
8037710-6	1994	Nevertheless nuclear p53 accumulation is at much higher extent, whereas 32P-orthophosphate labelling, followed by immunoprecipitation, demonstrates a decrease of phosphorylation of both cytoplasmic and nuclear p53.	Phosphates	76-90	P53	Homo sapiens	210-213
8034027-11	1994	In this study, we demonstrate that conjugates of p53 generated in the presence of purified, E1, E2, E6-AP, E6, ubiquitin and ATP, are specifically recognized by the 26S protease complex and degraded.	Adenosine Triphosphate	125-128	P53	Homo sapiens	49-52
7937752-3	1994	Using conformational energy analysis based on ECEPP (Empirical Conformational Energy for Peptides Program), we have determined the low-energy three-dimensional structures for this dodecapeptide sequence for the human wild-type p53 protein and three environmentally induced, cancer-related mutant p53 proteins with His-151, Ser-152, and Val-154, respectively.	Histidine	314-317	P53	Homo sapiens	227-230
7937752-3	1994	Using conformational energy analysis based on ECEPP (Empirical Conformational Energy for Peptides Program), we have determined the low-energy three-dimensional structures for this dodecapeptide sequence for the human wild-type p53 protein and three environmentally induced, cancer-related mutant p53 proteins with His-151, Ser-152, and Val-154, respectively.	Serine	323-326	P53	Homo sapiens	227-230
7833367-5	1994	[3H]Thymidine incorporation assays showed that the recombinant adenoviruses were capable of inhibiting DNA synthesis in a p53-specific, dose-dependent fashion.	Tritium	1-3	P53	Homo sapiens	122-125
21559604-2	1994	Positive staining for p53 protein was detected in 44 of 71 (62%) of these tumors on paraffin-embedded tissue, even in dysplastic areas.	Paraffin	84-92	P53	Homo sapiens	22-25
8065358-4	1994	Here we show that hypoxia and heat, agents that induce cellular stress primarily by inhibiting oxygen-dependent metabolism and denaturing proteins, respectively, also cause an increase in p53 protein levels.	Oxygen	95-101	P53	Homo sapiens	188-191
8062826-1	1994	In an effort to correlate the biological activity of the p53 protein with its conformation, we analysed 14 p53 mutants representative of the most frequently observed protein alterations in human cancers, at codons 175, 248 and 273 (22% of all mutations thus far reported), all three of which contained a CpG dinucleotide.	cytidylyl-3'-5'-guanosine	304-320	P53	Homo sapiens	57-60
8062826-7	1994	All these results suggest that the occurrence of a mutation is dependent on two criteria: (i) the mutability of a given codon, such as those containing a CpG dinucleotide; (ii) the resulting amino acids, eventually leading to synthesis of a p53 conferring a growth advantage on the cell.	cytidylyl-3'-5'-guanosine	154-170	P53	Homo sapiens	241-244
7928628-0	1994	Nuclear accumulation of p53 protein correlates with mutations in the p53 gene on archival paraffin-embedded tissues of human breast cancer.	Paraffin	90-98	P53	Homo sapiens	24-27
7928628-0	1994	Nuclear accumulation of p53 protein correlates with mutations in the p53 gene on archival paraffin-embedded tissues of human breast cancer.	Paraffin	90-98	P53	Homo sapiens	69-72
7928628-8	1994	We conclude that the immunohistochemical detection of nuclear p53 protein accumulation is highly associated with p53 gene mutations in archival paraffin-embedded tissues, and that this method is useful for rapid screening of p53 abnormalities.	Paraffin	144-152	P53	Homo sapiens	62-65
8033090-6	1994	Expression of a dominant-negative mutant of p53 (codon 143, Val to Ala) in transfectants of the radiosensitive human ovarian cell line A2780 abrogates the radiation-induced G1 arrest.	Alanine	67-70	P53	Homo sapiens	44-47
8055938-1	1994	Dimerization of p53 is required for high-affinity DNA binding and cysteine oxidation inhibits p53 DNA binding.	Cysteine	66-74	P53	Homo sapiens	94-97
8055938-8	1994	Further characterization of the purified p53 revealed that the protein possesses highly reactive cysteine residues.	Cysteine	97-105	P53	Homo sapiens	41-44
8055938-9	1994	We show that intrachain disulfide bonds form within the purified p53 molecules during storage in the absence of reducing agent.	Disulfides	24-33	P53	Homo sapiens	65-68
8055938-10	1994	Zn2+ binding to p53 protect sulfhydryl groups from oxidation.	Zinc	0-4	P53	Homo sapiens	16-19
8055938-12	1994	The oxidation of the p53 cysteine residues was also observed for nuclear p53 in baculovirus-infected insect cells.	Cysteine	25-33	P53	Homo sapiens	21-24
8055938-12	1994	The oxidation of the p53 cysteine residues was also observed for nuclear p53 in baculovirus-infected insect cells.	Cysteine	25-33	P53	Homo sapiens	73-76
8055938-13	1994	The redox status of the nuclear p53 regulates its DNA-binding activity in vitro confirming the essential role of the reduced state of cysteine residues in p53 for detectable DNA-binding activity.	Cysteine	134-142	P53	Homo sapiens	32-35
8055938-13	1994	The redox status of the nuclear p53 regulates its DNA-binding activity in vitro confirming the essential role of the reduced state of cysteine residues in p53 for detectable DNA-binding activity.	Cysteine	134-142	P53	Homo sapiens	155-158
8207805-9	1994	In the ACH-2 cell line, which is now demonstrated to contain an endogenous mutant form of p53 (amino acid 248, Arg to Gln), additional mutant p53 proteins did not alter HIV-1 replication.	Arginine	111-114	P53	Homo sapiens	90-93
7913577-10	1994	Both p53 protein and p185 antibodies work well on routine, formalin-fixed, paraffin-embedded tissue and are easily used in routine diagnostic procedures.	Paraffin	75-83	P53	Homo sapiens	5-8
8021299-10	1994	We show that a portion of both hsp70 and p53 indeed are present within the centrosome in Hela, COS, and 3T3 cells.	carbonyl sulfide	95-98	P53	Homo sapiens	41-44
7931842-4	1994	We examined 62 endoscopic oesophageal biopsies and 36 oesophageal resections for p53 overexpression using the monoclonal antibody DO-7 on paraffin-embedded tissue.	Paraffin	138-146	P53	Homo sapiens	81-84
7805554-1	1994	The monoclonal antibody to p53 and a rapid immunohistochemical method were used in this study to detect p53 expression in 50 paraffin-embedded breast cancers and 7 benign hyperplastic diseases of breast.	Paraffin	125-133	P53	Homo sapiens	104-107
8208536-13	1994	In contrast, the p53 in cell lines with either homozygous 175His or 248His p53 mutations, were unable either to transactivate or bind to the p53 response element.	175his	58-64	P53	Homo sapiens	17-20
8012775-2	1994	PATIENTS AND METHODS: The immunohistochemical status of the p53 protein in 28 pT1 primary bladder cancers was determined on frozen tissue and archival paraffin block sections using three primary antibodies (CM-1, PAB1801 and D07).	Paraffin	151-159	P53	Homo sapiens	60-63
8200229-3	1994	METHODS: IgG1 monoclonal antibody to human p53 protein (PAb 1801) was used to detect p53 in formalin-fixed, paraffin-embedded archival tumors resected from 84 patients with tumor limited to the bowel wall.	Paraffin	108-116	P53	Homo sapiens	85-88
8183576-4	1994	Here we report the novel observation that human p53 protein can bind ATP and exhibits an intrinsic ATP stimulated DNA strand reassociation activity.	Adenosine Triphosphate	69-72	P53	Homo sapiens	48-51
8183576-4	1994	Here we report the novel observation that human p53 protein can bind ATP and exhibits an intrinsic ATP stimulated DNA strand reassociation activity.	Adenosine Triphosphate	99-102	P53	Homo sapiens	48-51
7926727-5	1994	Rather, the hydrophobic amino acid residues Leu-22 and Trp-23 of human p53 are both required for trans-activation activity, binding to the adenovirus E1B 55-kD protein and the human mdm-2-p53 protein in vitro.	Tryptophan	55-58	P53	Homo sapiens	71-74
7926727-5	1994	Rather, the hydrophobic amino acid residues Leu-22 and Trp-23 of human p53 are both required for trans-activation activity, binding to the adenovirus E1B 55-kD protein and the human mdm-2-p53 protein in vitro.	Tryptophan	55-58	P53	Homo sapiens	188-191
8187062-0	1994	Up-regulation of a mutant form of p53 by doxorubicin in human squamous carcinoma cells.	Doxorubicin	41-52	P53	Homo sapiens	34-37
8187062-2	1994	The cells carry only a mutated form of the p53 gene, the G--&gt;A mutation at codon 273 which results in an arginine to histidine substitution (mp53).	Arginine	108-116	P53	Homo sapiens	43-46
8187062-2	1994	The cells carry only a mutated form of the p53 gene, the G--&gt;A mutation at codon 273 which results in an arginine to histidine substitution (mp53).	Histidine	120-129	P53	Homo sapiens	43-46
8196660-2	1994	We investigated the methylation status of the CpG dinucleotide at codon 248 in exon 7 of the p53 gene because this codon is a hot spot for inactivating mutations in the germ line and in most human somatic tissues examined.	cytidylyl-3'-5'-guanosine	46-62	P53	Homo sapiens	93-96
7808790-3	1994	At present, our aim was, firstly, to see which were the best technical conditions for detection of p53 in the available paraffin-embedded tumor specimens, using several antibodies, specific for various epitopes; secondly, to investigate if some relation might exist between this expression and the histological features of these tumors.	Paraffin	120-128	P53	Homo sapiens	99-102
8012776-4	1994	p53 expression was determined by immuno-histochemistry on paraffin embedded sections and flow cytometry was performed on cell suspensions derived from the same blocks.	Paraffin	58-66	P53	Homo sapiens	0-3
8151752-9	1994	Consistent with this hypothesis, we detected a significant increase in p53 levels upon dexamethasone-induced repression of papillomavirus E6-E7 oncogene expression.	Dexamethasone	87-100	P53	Homo sapiens	71-74
8133533-4	1994	METHODS: The expression of Bcl-2 and p53 was detected by immunohistochemistry on paraffin-embedded sections from 283 node-negative resectable breast cancers treated with local-regional therapy alone until relapse.	Paraffin	81-89	P53	Homo sapiens	37-40
8174105-4	1994	We report here that p53-deficient hepatoma cells (Hep3B) transfected with mutant p53-249ser (codon 249 Arg--&gt;Ser) acquire a new phenotype with an increased in vitro survival and mitotic activity.	Arginine	103-106	P53	Homo sapiens	20-23
8152811-4	1994	We therefore introduced the pC53-SCX3 143 (Val-Ala) p53 mutation into a non tumorigenic adenoma derived cell line, AA/C1, which contained a truncating APC mutation, activating K-ras mutation but was wild-type for the p53 protein.	Alanine	47-50	P53	Homo sapiens	52-55
8174105-4	1994	We report here that p53-deficient hepatoma cells (Hep3B) transfected with mutant p53-249ser (codon 249 Arg--&gt;Ser) acquire a new phenotype with an increased in vitro survival and mitotic activity.	Arginine	103-106	P53	Homo sapiens	81-84
8174105-4	1994	We report here that p53-deficient hepatoma cells (Hep3B) transfected with mutant p53-249ser (codon 249 Arg--&gt;Ser) acquire a new phenotype with an increased in vitro survival and mitotic activity.	Serine	112-115	P53	Homo sapiens	20-23
8174105-4	1994	We report here that p53-deficient hepatoma cells (Hep3B) transfected with mutant p53-249ser (codon 249 Arg--&gt;Ser) acquire a new phenotype with an increased in vitro survival and mitotic activity.	Serine	112-115	P53	Homo sapiens	81-84
7909221-5	1994	Positive staining for both p53 and HER-2/neu in paraffin-embedded tissues indicates an underlying genetic abnormality: point mutations in the p53 gene and amplification of the HER-2/neu gene.	Paraffin	48-56	P53	Homo sapiens	27-30
8043159-9	1994	Since p53 (PAb 1801) expression can withstand formalin fixation and pepsin treatment of paraffin-embedded tissues, flow cytometric analysis of archival specimens is feasible, and clinical correlations such as these may be carried out in retrospective studies of other tumors.	Paraffin	88-96	P53	Homo sapiens	6-9
8178805-5	1994	In addition, single-strand conformation polymorphism analysis and PCR-direct sequencing of BC cells revealed a point mutation at codon 203 of the p53 gene, GTG to GAG (Val to Glu), and loss of the normal allele.	Glutamic Acid	175-178	P53	Homo sapiens	146-149
7909221-5	1994	Positive staining for both p53 and HER-2/neu in paraffin-embedded tissues indicates an underlying genetic abnormality: point mutations in the p53 gene and amplification of the HER-2/neu gene.	Paraffin	48-56	P53	Homo sapiens	142-145
8027368-8	1994	Fragments of the p53 gene were successfully amplified up to 408 base pairs in water boiled extracts, up to 647 in Chelex boiled preparates, and up to 984 in proteinase K digested and proteinase K digested-Chelex boiled samples, although with decreased sensitivity in the last case.	Water	78-83	P53	Homo sapiens	17-20
8168507-7	1994	Using metal affinity chromatography, we have established that pure p53 binds the immobilised divalent ions Zn2+, Ni2+ and Co2+ with high affinity.	Metals	6-11	P53	Homo sapiens	67-70
8168507-7	1994	Using metal affinity chromatography, we have established that pure p53 binds the immobilised divalent ions Zn2+, Ni2+ and Co2+ with high affinity.	Zinc	107-111	P53	Homo sapiens	67-70
8168507-7	1994	Using metal affinity chromatography, we have established that pure p53 binds the immobilised divalent ions Zn2+, Ni2+ and Co2+ with high affinity.	Nickel(2+)	113-117	P53	Homo sapiens	67-70
7908608-10	1994	The p53 arginine allele was found to be more common in Caucasians (0.71) than African-Americans (0.50).	Arginine	8-16	P53	Homo sapiens	4-7
8027368-8	1994	Fragments of the p53 gene were successfully amplified up to 408 base pairs in water boiled extracts, up to 647 in Chelex boiled preparates, and up to 984 in proteinase K digested and proteinase K digested-Chelex boiled samples, although with decreased sensitivity in the last case.	chelex	114-120	P53	Homo sapiens	17-20
8141761-0	1994	Increased salt concentration reversibly destabilizes p53 quaternary structure and sequence-specific DNA binding.	Salts	10-14	P53	Homo sapiens	53-56
8051396-6	1994	Sequencing of polymerase chain reaction products showed that all mutations in exon 5 were clustered at codon 166 and were T/A transversions resulting in an amino acid change from serine to threonine, identifying a new hot-spot for point mutations in the p53 gene.	Serine	179-185	P53	Homo sapiens	254-257
8051396-6	1994	Sequencing of polymerase chain reaction products showed that all mutations in exon 5 were clustered at codon 166 and were T/A transversions resulting in an amino acid change from serine to threonine, identifying a new hot-spot for point mutations in the p53 gene.	Threonine	189-198	P53	Homo sapiens	254-257
8141761-4	1994	We conclude that high salt can reversibly destabilize the quaternary structure of p53 that is most efficient for sequence-specific DNA binding.	Salts	22-26	P53	Homo sapiens	82-85
8119988-6	1994	Moreover, an oligonucleotide containing Rb promoter sequences between -63 and -88 was sufficient to confer stimulation by p53 when inserted upstream from a minimal heterologous promoter.	Oligonucleotides	13-28	P53	Homo sapiens	122-125
8119773-5	1994	The growth kinetics of wt-p53 transfectants were suppressed compared with those of parental cells, vector transfectants, or mut-p53 transfectants, as assayed by growth-curve measurements and 3H-thymidine incorporation; however, RNA dot blot and Western blot analyses demonstrated that wt-p53 and mut-p53 transfectants expressed higher amounts of TGF-beta 1 and TGF-beta 2 mRNA and intracellular TGF-beta isoform proteins, respectively, than parental cells.	Tritium	191-193	P53	Homo sapiens	26-29
8156496-3	1994	METHODS: The status of the p53 gene was studied by immunohistochemistry of formalin-fixed paraffin-embedded biopsy samples from 72 patients with atypical endometrial hyperplasia or endometrioid carcinoma who underwent hysterectomy immediately after biopsy and from 5 patients with benign endometria.	Paraffin	90-98	P53	Homo sapiens	27-30
8119988-7	1994	Gel mobility shift analysis was used to demonstrate that p53 can bind to a sequence within the -63 to -88 oligonucleotide with homology to a p53 binding site.	Oligonucleotides	106-121	P53	Homo sapiens	57-60
8119988-7	1994	Gel mobility shift analysis was used to demonstrate that p53 can bind to a sequence within the -63 to -88 oligonucleotide with homology to a p53 binding site.	Oligonucleotides	106-121	P53	Homo sapiens	141-144
21607363-0	1994	Immunohistochemical expression of p53 paraffin sections from colon-cancer specimens - comparison between 2 new monoclonal-antibodies.	Paraffin	38-46	P53	Homo sapiens	34-37
8123475-7	1994	Antisense oligonucleotides to p53 were used to suppress p53 protein expression in blasts with non-autocrine growth and also the factor-dependent human erythroleukaemia cell line TF-1.	Oligonucleotides	10-26	P53	Homo sapiens	30-33
8123475-7	1994	Antisense oligonucleotides to p53 were used to suppress p53 protein expression in blasts with non-autocrine growth and also the factor-dependent human erythroleukaemia cell line TF-1.	Oligonucleotides	10-26	P53	Homo sapiens	56-59
8018565-1	1994	Activation of the protein kinase C signaling pathway by tumor-promoting phorbol esters, such as 4 beta-phorbol 12-myristate 13-acetate (PMA), induced a decrease in the level of p53 mRNA in several serum-starved human cell lines.	Tetradecanoylphorbol Acetate	96-134	P53	Homo sapiens	177-180
8018565-1	1994	Activation of the protein kinase C signaling pathway by tumor-promoting phorbol esters, such as 4 beta-phorbol 12-myristate 13-acetate (PMA), induced a decrease in the level of p53 mRNA in several serum-starved human cell lines.	Tetradecanoylphorbol Acetate	136-139	P53	Homo sapiens	177-180
8018565-7	1994	PMA induced a similar transient decrease in the level of p53 protein in the A549 cell line.	Tetradecanoylphorbol Acetate	0-3	P53	Homo sapiens	57-60
8162251-3	1994	We have developed a method utilizing polymerase chain reaction (PCR) for the direct analysis of p53 mutation by single-strand conformation polymorphism (SSCP) and by direct DNA sequencing of the p53 gene using a single 10-microns paraffin-embedded tissue section.	Paraffin	230-238	P53	Homo sapiens	195-198
8162251-4	1994	We applied this method to screen for p53 gene mutations in exons 5-8 in human gliomas utilizing paraffin-embedded tissues.	Paraffin	96-104	P53	Homo sapiens	37-40
8108142-5	1994	Mutant p53 specifically increases TPA induction of VEGF without affecting the expression of other TPA inducible genes.	Tetradecanoylphorbol Acetate	34-37	P53	Homo sapiens	7-10
8108142-6	1994	TPA dependent VEGF expression is also enhanced by human p53 mutated at amino acid 175.	Tetradecanoylphorbol Acetate	0-3	P53	Homo sapiens	56-59
21607363-2	1994	We examined the immunohistochemical expression of p53 in 40 paraffin-embedded samples obtained from colon carcinomas using the two new MAbs DO-1 and DO-7.	Paraffin	60-68	P53	Homo sapiens	50-53
8305445-0	1994	DNA recognition by alternate strand triple helix formation: affinities of oligonucleotides for a site in the human p53 gene.	Oligonucleotides	74-90	P53	Homo sapiens	115-118
8116572-1	1994	The authors had previously reported that the accumulation of p53 is clearly demonstrable in microwave-fixed, paraffin-embedded sections of colorectal carcinomas.	Paraffin	109-117	P53	Homo sapiens	61-64
8311654-4	1994	Positive nuclear p53 immunoreactivity was detected in 37% of paraffin-embedded primary tumors (21.8% in the Japanese group, 52.6% in the American group) and in 50% of xenotransplanted carcinoma cell lines.	Paraffin	61-69	P53	Homo sapiens	17-20
8311654-8	1994	The fact that more than half of the ethanol-fixed fine-needle aspirates were positive for p53 suggests that this type of immunostain may be of potential diagnostic significance.	Ethanol	36-43	P53	Homo sapiens	90-93
8008749-1	1994	p53 expression in formalin-fixed, paraffin-embedded archival specimens of intrahepatic cholangiocarcinoma: retrieval of p53 antigenicity by microwave oven heating of tissue sections.	Paraffin	34-42	P53	Homo sapiens	0-3
8106638-13	1994	As p53 protein is a regulator of guanine nucleotide synthesis, the loss of normal inhibitory regulation by the p53 mutation would serve to increase the availability of GTP for the transduction of signals essential for increased cell growth and hormone expression in the adrenal tumors.	Guanosine Triphosphate	168-171	P53	Homo sapiens	3-6
8106638-13	1994	As p53 protein is a regulator of guanine nucleotide synthesis, the loss of normal inhibitory regulation by the p53 mutation would serve to increase the availability of GTP for the transduction of signals essential for increased cell growth and hormone expression in the adrenal tumors.	Guanosine Triphosphate	168-171	P53	Homo sapiens	111-114
8008749-4	1994	We investigated expression of p53 in formalin-fixed, paraffin-embedded archival specimens of 40 CCs (22 autopsy cases and 18 surgical cases) by immunohistochemistry using four antibodies (PAb1801, DO-7, BP53-12, CM1).	Paraffin	53-61	P53	Homo sapiens	30-33
8008749-10	1994	These results shows that a pretreatment of tissue sections by microwave oven heating is a very good method for demonstrating p53 protein in formalin-fixed, paraffin-embedded archival materials and that DO-7, BP53-12, and CM1 are useful antibodies for detection of p53 in formalin-fixed, paraffin-embedded archival materials.	Paraffin	156-164	P53	Homo sapiens	125-128
8275497-1	1994	We investigated the expression of p53 in paraformaldehyde-lysine-periodate fixed normal and chronic myelogenous leukemia (CML) hemopoietic cells with flow cytometry and two monoclonal antibodies, PAb1801 and the mutant-conformation-associated PAb240.	Lysine	58-64	P53	Homo sapiens	34-37
8032216-5	1994	We found point mutations in 25% (9 of 36) of cultured melanomas and 0% in 34 fresh melanoma biopsies; however, increased p53 expression was found in 42% of paraffin-embedded melanoma specimens and 7% of benign lesions.	Paraffin	156-164	P53	Homo sapiens	121-124
8290256-5	1994	Two mutations were identified in the p53 cDNA from HC11 cells: a missense mutation at codon 138, substituting Trp for Cys, and a microdeletion, codon 123 to 130, of exon 5.	Tryptophan	110-113	P53	Homo sapiens	37-40
8290256-5	1994	Two mutations were identified in the p53 cDNA from HC11 cells: a missense mutation at codon 138, substituting Trp for Cys, and a microdeletion, codon 123 to 130, of exon 5.	Cysteine	118-121	P53	Homo sapiens	37-40
8290256-8	1994	Wt p53 was introduced into HC11 cells by means of a retroviral vector, under the control of a Cd(++)-inducible promoter.	Cadmium	94-100	P53	Homo sapiens	3-6
8290606-6	1994	Mozambican-type of hepatocellular carcinomas are characterized by a high incidence of p53 mutations related to aflatoxins.	mozambican	0-10	P53	Homo sapiens	86-89
8293408-5	1994	Immunostaining for mutant p53 proteins was performed on tissues fixed in formaldehyde solution and embedded in paraffin; the tissues were from these 44 astrocytomas and another 103 astrocytomas obtained from archival material.	Paraffin	111-119	P53	Homo sapiens	26-29
8275497-4	1994	Treatment of chronic-phase CML cells with p53 antisense oligonucleotides resulted in significantly increased numbers of granulocyte-macrophage colony-forming unit colonies in 12 of 17 cases studied.	Oligonucleotides	56-72	P53	Homo sapiens	42-45
8278402-4	1994	Mutant p53 fusion proteins carrying amino acid substitutions Glu-213, Ile-237, or Tyr-238, derived from mutant p53 genes of Burkitt lymphomas, failed to catalyze these reactions.	Glutamic Acid	61-64	P53	Homo sapiens	7-10
8136126-5	1994	Affinities of oligonucleotide probes toward radiolabeled wild-type and mutant p53 DNA duplexes were quantitated by electrophoretic mobility shift assays.	Oligonucleotides	14-29	P53	Homo sapiens	78-81
8110876-4	1994	p53 mutations were restricted to one case of myeloid blast crisis, showing a CGC--&gt;TGC (Arg--&gt;Cys) mutation at codon 283; two additional cases displayed LOH at 17p13 in the absence of p53 mutations.	Arginine	91-94	P53	Homo sapiens	0-3
8110876-4	1994	p53 mutations were restricted to one case of myeloid blast crisis, showing a CGC--&gt;TGC (Arg--&gt;Cys) mutation at codon 283; two additional cases displayed LOH at 17p13 in the absence of p53 mutations.	Cysteine	100-103	P53	Homo sapiens	0-3
8278402-4	1994	Mutant p53 fusion proteins carrying amino acid substitutions Glu-213, Ile-237, or Tyr-238, derived from mutant p53 genes of Burkitt lymphomas, failed to catalyze these reactions.	Tyrosine	82-85	P53	Homo sapiens	7-10
8136126-6	1994	Recombinant plasmids carrying wild-type or microdeleted forms of the p53 homopurine sites of interest were created.	homopurine	73-83	P53	Homo sapiens	69-72
8076381-10	1994	Immunodetection of p53 in 11 biopsies from the same tumors alternatively fixed in 70% ethanol or formalin gave comparable results for adenocarcinomas but was not consistent for adenomas.	Ethanol	86-93	P53	Homo sapiens	19-22
7506924-1	1994	The availability of antibodies which recognise p53 protein in paraffin-embedded tissue has created the opportunity to use immunohistochemistry to study the expression of p53 in a wide variety of clinical material.	Paraffin	62-70	P53	Homo sapiens	47-50
8076382-0	1994	p53 expression and mutations in squamous cell carcinoma of the head and neck: expression correlates with the patients" use of tobacco and alcohol.	Alcohols	138-145	P53	Homo sapiens	0-3
8261459-4	1994	Three samples showed mutations in the p53 gene, two in exon 5 (both GC to AT transition at a CpG dinucleotide) and one in exon 7 (AT to GC transition).	cytidylyl-3'-5'-guanosine	93-109	P53	Homo sapiens	38-41
7735330-6	1994	We have expressed the p53 mini-protein in mammalian cells and shown by phosphopeptide mapping that it is phosphorylated at a single physiological phosphorylation site, serine 386.	Serine	168-174	P53	Homo sapiens	22-25
7931822-1	1994	Immunocytochemical detection of p53 protein products in paraffin sections is possible with a number of antisera, monoclonal and polyclonal.	Paraffin	56-64	P53	Homo sapiens	32-35
7719291-0	1994	p53 mutant gene expression in paraffin embedded and fresh frozen tissue of different urogenital tumors.	Paraffin	30-38	P53	Homo sapiens	0-3
7909153-9	1994	This study demonstrates the use of paraffin sections in the analysis of p53 alterations in neoplasia.	Paraffin	35-43	P53	Homo sapiens	72-75
7894617-5	1994	The mutation in another case was a nonsense G:C-A:T transition at codon 52 (TGG-TGA; Trp-stop codon) leading to a truncated p53 peptide.	Tryptophan	85-88	P53	Homo sapiens	124-127
8247533-6	1993	Agents that produced double-strand breaks in DNA and/or inhibition of transcription caused an induction of p53 in the absence of radiation in control cells but not in ataxia-telangiectasia, but inhibitors of cell cycle progression such as mimosine and aphidicolin led to an increase in p53 in both cell types in the absence of radiation.	Mimosine	239-247	P53	Homo sapiens	107-110
7787250-9	1994	The T24 cell line was found to contain a novel p53 mutant having an in-frame deletion of tyrosine 126.	Tyrosine	89-97	P53	Homo sapiens	47-50
8302593-10	1994	The second detected 35S-labelled p53 bound to biotinylated target DNA in the absence of PAb421.	Sulfur-35	20-23	P53	Homo sapiens	33-36
8186888-0	1994	Polymerase chain reaction-single strand conformation polymorphism analysis of the p53 gene in paraffin-embedded surgical material from human renal cell carcinomas.	Paraffin	94-102	P53	Homo sapiens	82-85
8238731-3	1993	The goal of this study was to determine the frequency and relationship of p53 gene alterations and hepatitis B in formalin-fixed, paraffin-embedded HCCs resected in the United States.	Paraffin	130-138	P53	Homo sapiens	74-77
8165016-0	1994	Paraffin section p53 protein immunohistochemistry in neuroectodermal tumors.	Paraffin	0-8	P53	Homo sapiens	17-20
8252480-5	1993	METHODS: Tumor tissues of 156 patients with primary invasive breast cancer were analyzed immunohistochemically for the presence of p53 protein in paraffin-embedded material.	Paraffin	146-154	P53	Homo sapiens	131-134
8117626-1	1993	In order to clarify the role of the p53 tumor suppressor gene in controlling growth and differentiation of human epithelial cells, we transfected a wild-type p53 complementary DNA, driven by a dexamethasone-inducible mouse mammary tumor virus promoter, into SqCC/Y1 human head-and-neck squamous carcinoma cells.	Dexamethasone	193-206	P53	Homo sapiens	36-39
8117626-2	1993	When treated with dexamethasone, 2 of 8 independent clones that contained integrated vector sequences expressed wild-type p53-specific mRNA as well as nuclear p53 protein.	Dexamethasone	18-31	P53	Homo sapiens	122-125
8117626-2	1993	When treated with dexamethasone, 2 of 8 independent clones that contained integrated vector sequences expressed wild-type p53-specific mRNA as well as nuclear p53 protein.	Dexamethasone	18-31	P53	Homo sapiens	159-162
8276239-5	1993	Because the fragment does not contain the cdc2 phosphorylation site at Ser-315, we conclude that the the site-specific DNA-binding domain of p53 spans the central region of the protein.	Serine	71-74	P53	Homo sapiens	141-144
8158458-1	1993	The expression of the nuclear protein p53 in oligodendrogliomas was investigated by immunohistochemistry, using a monoclonal anti-p53 antibody (DO-7) on formalin-fixed, paraffin-embedded material in 84 histologically verified cases, and compared with the histopathological grade and survival.	Paraffin	169-177	P53	Homo sapiens	38-41
7907850-3	1993	In this study we investigated whether tamoxifen administration affects the histopathological characteristics of cervical cancer and the expression of ER, PgR, HER-2/neu and p53 protein.	Tamoxifen	38-47	P53	Homo sapiens	173-176
7901994-13	1993	We conclude that the immunohistochemical detection of p53 nuclear accumulation in formalin-fixed, paraffin-embedded tissue is highly associated with mutations in the p53 gene; this association has now been demonstrated in a large number of tumors.	Paraffin	98-106	P53	Homo sapiens	54-57
7901994-13	1993	We conclude that the immunohistochemical detection of p53 nuclear accumulation in formalin-fixed, paraffin-embedded tissue is highly associated with mutations in the p53 gene; this association has now been demonstrated in a large number of tumors.	Paraffin	98-106	P53	Homo sapiens	166-169
7692889-0	1993	Retrieval of p53 protein in paraffin-embedded head and neck tumor tissues.	Paraffin	28-36	P53	Homo sapiens	13-16
8221671-5	1993	The DNA-binding activity of wild-type p53 hybrid protein was inhibited by the metal chelator 1,10-phenanthroline.	Metals	78-83	P53	Homo sapiens	38-41
8221671-7	1993	Furthermore, metal ions may regulate binding of p53 to DNA by modulating its conformation.	Metals	13-18	P53	Homo sapiens	48-51
8221663-2	1993	Mutations of the p53 gene were found in six of seven ES cell lines: a missense mutation of TGC (Cys)--&gt;TAC (Try) at codon 141 in one, a missense mutation of CGT (Arg)--&gt;TGT (Cys) at codon 273 in one, a missense mutation of TGC (Cys)--&gt;TTC (Phe) at codon 176 in three, and one base deletion of CGC--&gt;CG at codon 283 in one.	Cysteine	96-99	P53	Homo sapiens	17-20
8221663-3	1993	Further analysis of 14 ES and related primary tumors showed mutations of the p53 gene in only two: one base insertion of CCG--&gt;CCCG at codon 152 in one and a missense mutation of GGC (Gly)--&gt;GTC (Val) at codon 154 in the other.	Glycine	187-190	P53	Homo sapiens	77-80
7692889-1	1993	OBJECTIVES: To improve the detection of p53 protein in formalin-fixed, paraffin-embedded head and neck tumor tissues.	Paraffin	71-79	P53	Homo sapiens	40-43
7692889-8	1993	RESULTS: An antigen retrieval method facilitated the unmasking of previously inaccessible p53 antigenic determinants in formalin-fixed, paraffin-embedded tissues.	Paraffin	136-144	P53	Homo sapiens	90-93
7692889-11	1993	CONCLUSIONS: Antigen retrieval method in formalin-fixed, paraffin-embedded tissue demonstrated a significant increase in p53 immunostaining.	Paraffin	57-65	P53	Homo sapiens	121-124
8221663-2	1993	Mutations of the p53 gene were found in six of seven ES cell lines: a missense mutation of TGC (Cys)--&gt;TAC (Try) at codon 141 in one, a missense mutation of CGT (Arg)--&gt;TGT (Cys) at codon 273 in one, a missense mutation of TGC (Cys)--&gt;TTC (Phe) at codon 176 in three, and one base deletion of CGC--&gt;CG at codon 283 in one.	Arginine	165-168	P53	Homo sapiens	17-20
8221663-2	1993	Mutations of the p53 gene were found in six of seven ES cell lines: a missense mutation of TGC (Cys)--&gt;TAC (Try) at codon 141 in one, a missense mutation of CGT (Arg)--&gt;TGT (Cys) at codon 273 in one, a missense mutation of TGC (Cys)--&gt;TTC (Phe) at codon 176 in three, and one base deletion of CGC--&gt;CG at codon 283 in one.	Cysteine	180-183	P53	Homo sapiens	17-20
8221663-2	1993	Mutations of the p53 gene were found in six of seven ES cell lines: a missense mutation of TGC (Cys)--&gt;TAC (Try) at codon 141 in one, a missense mutation of CGT (Arg)--&gt;TGT (Cys) at codon 273 in one, a missense mutation of TGC (Cys)--&gt;TTC (Phe) at codon 176 in three, and one base deletion of CGC--&gt;CG at codon 283 in one.	Cysteine	180-183	P53	Homo sapiens	17-20
8414520-4	1993	We show that p53 binds to a target oligonucleotide as a protein homodimer and that p53 dimerisation is required for detectable DNA binding.	Oligonucleotides	35-50	P53	Homo sapiens	13-16
21573436-4	1993	Expression of p53 protein and P-170 glycoprotein was detected by immunohistochemistry using the PAb1801 and C219 monoclonal antibody respectively, on sections from paraffin-embedded tumor biopsies.	Paraffin	164-172	P53	Homo sapiens	14-17
21573446-8	1993	The point mutation of p53 gene was found at codon 181 contained C to T transversions (Amino acid switch: Arg --&gt; Cys) in ES-4 esophageal cancer.	Arginine	105-108	P53	Homo sapiens	22-25
21573446-8	1993	The point mutation of p53 gene was found at codon 181 contained C to T transversions (Amino acid switch: Arg --&gt; Cys) in ES-4 esophageal cancer.	Cysteine	116-119	P53	Homo sapiens	22-25
21573446-9	1993	The accumulations of p53 proteins were also associated with the down regulated intra-cellular-cAMP induced by high concentrations of EGF.	Cyclic AMP	94-98	P53	Homo sapiens	21-24
8244324-3	1993	We describe the localization of p53 protein in association with HPV in paraffin sections of a spectrum of benign, dysplastic, and malignant anogenital squamous epithelia using immunohistochemical and in situ hybridization techniques.	Paraffin	71-79	P53	Homo sapiens	32-35
8231251-5	1993	We found that the introduction of p53 antisense oligonucleotides can specifically inhibit the translation of the p53 mRNA.	Oligonucleotides	48-64	P53	Homo sapiens	34-37
8231251-5	1993	We found that the introduction of p53 antisense oligonucleotides can specifically inhibit the translation of the p53 mRNA.	Oligonucleotides	48-64	P53	Homo sapiens	113-116
8402615-2	1993	Here we show that both conformation and sequence-specific DNA binding of p53 translated in vitro can be modulated by metal chelators and oxidizing agents.	Metals	117-122	P53	Homo sapiens	73-76
8223615-1	1993	Expression of a human tumour-derived p53 His 273 cDNA induced growth arrest in fission yeast Schizosaccharomyces pombe.	Histidine	41-44	P53	Homo sapiens	37-40
8415687-1	1993	We report that p53her, a chimeric protein consisting of the complete human wild-type p53 and the human estrogen receptor hormone-binding domain, strongly suppresses proliferation and induces characteristic morphological changes in Saos-2 human osteosarcoma cells when induced by 17 beta-estradiol.	Estradiol	282-296	P53	Homo sapiens	15-18
8415687-3	1993	However, coexpression of p53her and oncoprotein MDM-2, which associates with and presumably inactivates p53, results in suppression of p53her-mediated transactivation in the absence, but not the presence, of estradiol.	Estradiol	208-217	P53	Homo sapiens	25-28
8415687-4	1993	Similarly, p53her induces expression of an endogenous MDM-2 transcript only in the presence of estradiol.	Estradiol	95-104	P53	Homo sapiens	11-14
8406999-0	1993	Increased accumulation of p53 protein in cisplatin-resistant ovarian cell lines.	Cisplatin	41-50	P53	Homo sapiens	26-29
8406999-1	1993	We have examined p53 protein levels in cell lines selected for resistance to the chemotherapeutic drug cis-diamminedichloroplatinum (II), cisplatin.	Cisplatin	103-131	P53	Homo sapiens	17-20
8406999-1	1993	We have examined p53 protein levels in cell lines selected for resistance to the chemotherapeutic drug cis-diamminedichloroplatinum (II), cisplatin.	Cisplatin	138-147	P53	Homo sapiens	17-20
8406999-2	1993	The majority of the independent cisplatin-resistant clones isolated by a single selection with cisplatin from the ovarian tumour cell line A2780 showed increased levels of p53 protein compared to the parental cell line.	Cisplatin	32-41	P53	Homo sapiens	172-175
8406999-2	1993	The majority of the independent cisplatin-resistant clones isolated by a single selection with cisplatin from the ovarian tumour cell line A2780 showed increased levels of p53 protein compared to the parental cell line.	Cisplatin	95-104	P53	Homo sapiens	172-175
8406999-3	1993	Elevated p53 protein levels were also observed in cisplatin-resistant ovarian human tumour lines isolated after multiple exposures to cisplatin (A2780/cp70 and OVIP/DDP).	Cisplatin	50-59	P53	Homo sapiens	9-12
8406999-3	1993	Elevated p53 protein levels were also observed in cisplatin-resistant ovarian human tumour lines isolated after multiple exposures to cisplatin (A2780/cp70 and OVIP/DDP).	Cisplatin	134-143	P53	Homo sapiens	9-12
8406999-8	1993	Transfection of a mutant p53 gene construct (containing a mutation at codon 143, val to ala) into the A2780/cp70 resistant cells conferred a significantly increased sensitivity to cisplatin, suggesting that p53 is a direct determinant of cisplatin resistance in these cells.	Alanine	88-91	P53	Homo sapiens	25-28
8406999-8	1993	Transfection of a mutant p53 gene construct (containing a mutation at codon 143, val to ala) into the A2780/cp70 resistant cells conferred a significantly increased sensitivity to cisplatin, suggesting that p53 is a direct determinant of cisplatin resistance in these cells.	Alanine	88-91	P53	Homo sapiens	207-210
8406999-8	1993	Transfection of a mutant p53 gene construct (containing a mutation at codon 143, val to ala) into the A2780/cp70 resistant cells conferred a significantly increased sensitivity to cisplatin, suggesting that p53 is a direct determinant of cisplatin resistance in these cells.	Cisplatin	180-189	P53	Homo sapiens	25-28
8406999-8	1993	Transfection of a mutant p53 gene construct (containing a mutation at codon 143, val to ala) into the A2780/cp70 resistant cells conferred a significantly increased sensitivity to cisplatin, suggesting that p53 is a direct determinant of cisplatin resistance in these cells.	Cisplatin	180-189	P53	Homo sapiens	207-210
8406999-8	1993	Transfection of a mutant p53 gene construct (containing a mutation at codon 143, val to ala) into the A2780/cp70 resistant cells conferred a significantly increased sensitivity to cisplatin, suggesting that p53 is a direct determinant of cisplatin resistance in these cells.	Cisplatin	238-247	P53	Homo sapiens	25-28
8406999-8	1993	Transfection of a mutant p53 gene construct (containing a mutation at codon 143, val to ala) into the A2780/cp70 resistant cells conferred a significantly increased sensitivity to cisplatin, suggesting that p53 is a direct determinant of cisplatin resistance in these cells.	Cisplatin	238-247	P53	Homo sapiens	207-210
15335855-6	1993	Furthermore, crosslinking of the chimeras resulted in tyrosine phosphorylation of the Ig-alpha and Tg-beta tails and their association with the tyrosine kinases PTK72, p53/56(lyn) and p59(fyn).	Tyrosine	54-62	P53	Homo sapiens	168-171
7508232-3	1993	Using streptavidin-biotin complex method, p53 was identified in 33% of dysplastic squamous lesions, 50% of squamous cell carcinomas (SCCs) and 36% of basal cell carcinomas (BCCs) on frozen section, whereas 25% of dysplastic squamous lesions, 40% of SCCs, and 32% of BCCs showed p53 positivity on paraffin-embedded sections.	Paraffin	296-304	P53	Homo sapiens	42-45
11706422-0	1993	Relationship of tobacco/alcohol use to p53 expression in patients with lingual squamous cell carcinomas.	Alcohols	24-31	P53	Homo sapiens	39-42
11706422-1	1993	This study examined p53 expression immunocytochemically in 40 lingual squamous cell carcinomas from Dutch patients with known histories of smoking and/or drinking alcohol.	Alcohols	163-170	P53	Homo sapiens	20-23
11706422-4	1993	25% (3/12) of p53-positive neoplasms and 71.4% (20/28) of p53-negative neoplasms were found in patients who had been exposed to both alcohol and tobacco.	Alcohols	133-140	P53	Homo sapiens	14-17
11706422-4	1993	25% (3/12) of p53-positive neoplasms and 71.4% (20/28) of p53-negative neoplasms were found in patients who had been exposed to both alcohol and tobacco.	Alcohols	133-140	P53	Homo sapiens	58-61
11706422-5	1993	A similar negative association with p53 reactivity was also found when either tobacco or alcohol were used in isolation.	Alcohols	89-96	P53	Homo sapiens	36-39
11706422-6	1993	The results contrast with previous observations in head/neck and oral carcinomas and indicate that the association of alcohol/tobacco and p53 expression remains open to question.	Alcohols	118-125	P53	Homo sapiens	138-141
8375929-4	1993	The IGF-I-induced DNA synthesis coincided with an elevated level of phosphorylation of p53 on tyrosine and an alteration in the subcellular distribution of the protein from the nucleus to the cytoplasm.	Tyrosine	94-102	P53	Homo sapiens	87-90
8221631-4	1993	The p53-hsc73 protein complexes dissociate with the addition of ATP, indicating that the dissociation is dependent upon the ATP-hydrolysis.	Adenosine Triphosphate	64-67	P53	Homo sapiens	4-7
8221631-4	1993	The p53-hsc73 protein complexes dissociate with the addition of ATP, indicating that the dissociation is dependent upon the ATP-hydrolysis.	Adenosine Triphosphate	124-127	P53	Homo sapiens	4-7
8283348-6	1993	Overexpression of the p53 protein was found by immunostaining of sections from formalin-fixed, paraffin-embedded material in 55 per cent (51/92) of the tumours.	Paraffin	95-103	P53	Homo sapiens	22-25
8283352-0	1993	Immunocytochemical p53 detection by microwave oven heating of routinely formalin-fixed paraffin sections.	Paraffin	87-95	P53	Homo sapiens	19-22
8352280-1	1993	A rare germ-line polymorphism in codon 47 of the p53 gene replaces the wild-type proline (CCG) with a serine (TCG).	Serine	102-108	P53	Homo sapiens	49-52
8397412-6	1993	Since the latter mutations are not observed in HCC it follows that both mutability on the DNA level and altered function of the mutant serine 249 p53 protein are responsible for the observed mutational hot spot in p53 in HCC from AFB1-contaminated areas.	Serine	135-141	P53	Homo sapiens	146-149
8397412-6	1993	Since the latter mutations are not observed in HCC it follows that both mutability on the DNA level and altered function of the mutant serine 249 p53 protein are responsible for the observed mutational hot spot in p53 in HCC from AFB1-contaminated areas.	Serine	135-141	P53	Homo sapiens	214-217
8352280-8	1993	These findings indicate that the p53 variant with a serine at codon 47 should be considered as a rare germ-line polymorphism that does not alter the growth-suppression activity of p53.	Serine	52-58	P53	Homo sapiens	33-36
8361764-4	1993	A third mutant 175 (Arg--&gt;His) bound to the p53CON but did not activate transcription.	Arginine	20-23	P53	Homo sapiens	47-50
8248107-1	1993	p53 overexpression was studied immunohistochemically in paraffin-embedded bone marrow biopsies using a recently described technique for antigen retrieval based on microwave oven heating of paraffin sections.	Paraffin	56-64	P53	Homo sapiens	0-3
8248107-1	1993	p53 overexpression was studied immunohistochemically in paraffin-embedded bone marrow biopsies using a recently described technique for antigen retrieval based on microwave oven heating of paraffin sections.	Paraffin	189-197	P53	Homo sapiens	0-3
21573382-5	1993	Three patients responded to cisplatinum chemotherapy treatment, two of whom had p53 positive staining.	Cisplatin	28-39	P53	Homo sapiens	80-83
8361764-4	1993	A third mutant 175 (Arg--&gt;His) bound to the p53CON but did not activate transcription.	Histidine	29-32	P53	Homo sapiens	47-50
8112175-1	1993	Expression of P53 protein was detected immunohistochemically in formalin-fixed, paraffin-embedded tissues from 67 patients with bladder carcinoma and 6 normal bladder controls.	Paraffin	80-88	P53	Homo sapiens	14-17
8347496-1	1993	The expression of p53 protein was immunohistochemically studied in formalin-fixed paraffin-embedded biopsy specimens of 203 colorectal carcinomas by use of a monoclonal antibody specific for the p53 protein.	Paraffin	82-90	P53	Homo sapiens	18-21
8415589-1	1993	The p53 gene was examined in a series of formalin-fixed paraffin-embedded astrocytic neoplasms of various types by polymerase chain reaction (PCR), single-strand conformation polymorphism analysis (SSCP), and direct sequencing of amplified DNA.	Paraffin	56-64	P53	Homo sapiens	4-7
8363836-0	1993	A method for PCR sequencing of the p53 gene from a single 10-microns frozen or paraffin-embedded tissue section.	Paraffin	79-87	P53	Homo sapiens	35-38
8327466-4	1993	Here we show that Ser-15 and Ser-9 in the N-terminal transactivation domain of wild-type human p53 are phosphorylated in vivo in cells derived from the human glioblastoma line T98G.	Serine	18-21	P53	Homo sapiens	95-98
8327466-0	1993	Phosphorylation at Ser-15 and Ser-392 in mutant p53 molecules from human tumors is altered compared to wild-type p53.	Serine	19-22	P53	Homo sapiens	48-51
8327466-4	1993	Here we show that Ser-15 and Ser-9 in the N-terminal transactivation domain of wild-type human p53 are phosphorylated in vivo in cells derived from the human glioblastoma line T98G.	Serine	29-32	P53	Homo sapiens	95-98
8327466-0	1993	Phosphorylation at Ser-15 and Ser-392 in mutant p53 molecules from human tumors is altered compared to wild-type p53.	Serine	19-22	P53	Homo sapiens	113-116
8327466-0	1993	Phosphorylation at Ser-15 and Ser-392 in mutant p53 molecules from human tumors is altered compared to wild-type p53.	Serine	30-33	P53	Homo sapiens	48-51
8390283-8	1993	The 12th mutation GTG--&gt;GGG (valine--&gt;glycine) at codon 216 was expressed in line SCC-12 clone B along with an apparently normal p53 allele and is to our knowledge a novel mutation.	Glycine	44-51	P53	Homo sapiens	135-138
8327466-0	1993	Phosphorylation at Ser-15 and Ser-392 in mutant p53 molecules from human tumors is altered compared to wild-type p53.	Serine	30-33	P53	Homo sapiens	113-116
8496982-5	1993	METHODS: Expression of mutant p53 protein was detected by an immunohistochemical technique using a 1:50 dilution of PAb1801 monoclonal antibody on paraffin-embedded tumor specimens obtained from 256 axillary lymph node-negative breast cancer patients, with long-term follow-up (median, 72 months).	Paraffin	147-155	P53	Homo sapiens	30-33
8496982-13	1993	Based on these findings, p53 overexpression should be used with other established prognostic factors, such as [3H]thymidine labeling index and estrogen receptor status, to further refine the prognostic assessment of node-negative breast cancer.	Tritium	111-113	P53	Homo sapiens	25-28
8392521-3	1993	METHODS: The presence and localisation of the p53 protein in formalin fixed, paraffin wax embedded specimens of anal squamous epithelium (normal and neoplastic) was examined using immunohistochemical staining with a panel of two monoclonal antibodies (DO-1, DO-7) and one polyclonal antibody (CM-1).	Paraffin	77-89	P53	Homo sapiens	46-49
32370448-2	1993	In the present study, p53 immunoreactivity was investigated in formalin-fixed, paraffin-embedded tissues from human and animal pituitary tumors, using the avidin-biotin-peroxidase complex technique.	Paraffin	79-87	P53	Homo sapiens	22-25
8389669-2	1993	The wild-type of p53 protein exists as at least two forms of variants among human populations, ascribed to amino acid replacement at codon 72 of Arg by Pro.	Arginine	145-148	P53	Homo sapiens	17-20
8389669-3	1993	In this study, we show that this germ line Arg-Pro polymorphism at codon 72 of the p53 gene is associated with genetically determined susceptibility to smoking-induced lung cancer; a susceptible genotype Pro/Pro has a 1.7-fold higher risk of this cancer compared with other genotypes.	Arginine	43-46	P53	Homo sapiens	83-86
8502477-0	1993	Mutation of the serine 15 phosphorylation site of human p53 reduces the ability of p53 to inhibit cell cycle progression.	Serine	16-22	P53	Homo sapiens	56-59
8502477-0	1993	Mutation of the serine 15 phosphorylation site of human p53 reduces the ability of p53 to inhibit cell cycle progression.	Serine	16-22	P53	Homo sapiens	83-86
8502477-3	1993	DNA-PK was recently shown to phosphorylate serines 15 and 37 of human p53 (Lees-Miller et al., 1992.	Serine	43-50	P53	Homo sapiens	70-73
8502477-8	1993	Expression of p53-Ala-37 in stably transformed T98G cells blocked progression of the cells into S phase as well as did the expression of wild-type p53.	Alanine	18-21	P53	Homo sapiens	14-17
8502477-8	1993	Expression of p53-Ala-37 in stably transformed T98G cells blocked progression of the cells into S phase as well as did the expression of wild-type p53.	Alanine	18-21	P53	Homo sapiens	147-150
8502477-10	1993	Several cell clones transformed with the mutant p53-Ala-15 gene expressed normal levels of p53 mRNA but accumulated little or no detectable p53 protein.	Alanine	52-55	P53	Homo sapiens	48-51
8502477-10	1993	Several cell clones transformed with the mutant p53-Ala-15 gene expressed normal levels of p53 mRNA but accumulated little or no detectable p53 protein.	Alanine	52-55	P53	Homo sapiens	91-94
8502477-10	1993	Several cell clones transformed with the mutant p53-Ala-15 gene expressed normal levels of p53 mRNA but accumulated little or no detectable p53 protein.	Alanine	52-55	P53	Homo sapiens	91-94
8502477-12	1993	These results suggest that phosphorylation of Ser-15 may affect p53 function.	Serine	46-49	P53	Homo sapiens	64-67
8476634-0	1993	Retinoic acid and calcium regulation of p53, transforming growth factor-beta 1, and transforming growth factor-alpha gene expression and growth in adenovirus 12-SV40-transformed human tracheal gland epithelial cells.	Tretinoin	0-13	P53	Homo sapiens	40-43
8485705-2	1993	Activation of p53-DNA binding was seen for treatment with radiation, hydrogen peroxide, actinomycin D, Adriamycin, etoposide, camptothecin, 5-fluorouracil, mitomycin C, and cisplatin.	Hydrogen Peroxide	69-86	P53	Homo sapiens	14-17
8485705-2	1993	Activation of p53-DNA binding was seen for treatment with radiation, hydrogen peroxide, actinomycin D, Adriamycin, etoposide, camptothecin, 5-fluorouracil, mitomycin C, and cisplatin.	Doxorubicin	103-113	P53	Homo sapiens	14-17
8485705-2	1993	Activation of p53-DNA binding was seen for treatment with radiation, hydrogen peroxide, actinomycin D, Adriamycin, etoposide, camptothecin, 5-fluorouracil, mitomycin C, and cisplatin.	Fluorouracil	140-154	P53	Homo sapiens	14-17
8485705-2	1993	Activation of p53-DNA binding was seen for treatment with radiation, hydrogen peroxide, actinomycin D, Adriamycin, etoposide, camptothecin, 5-fluorouracil, mitomycin C, and cisplatin.	Cisplatin	173-182	P53	Homo sapiens	14-17
7688167-1	1993	Expression of p53 protein was examined in 67 cases of primary transitional cell carcinoma of the bladder and 6 normal controls using an immunohistochemical method on paraffin sections.	Paraffin	166-174	P53	Homo sapiens	14-17
8476634-12	1993	These results demonstrate that RA regulates growth of HTGE cells mainly by upregulating the p53 gene; Ca2+, which enhances TGF-beta 1 expression, had no effect on growth.	Tretinoin	31-33	P53	Homo sapiens	92-95
7684193-2	1993	Immunohistochemical staining with a monoclonal antibody (DO-7) and a polyclonal antibody (CM-1) to p53 protein (both wild type and mutant) on formalin-fixed paraffin sections showed a strong correlation with malignancy grade.	Paraffin	157-165	P53	Homo sapiens	99-102
8389256-6	1993	The p53 point mutations in the three HCC cell lines from Japan resulted in the amino acid changes of cysteine for tyrosine in cell line HuH 7 at codon 220 (A:T--&gt;G:C), alanine for glycine in cell line HLF at codon 244 (G:C--&gt;C:G), and serine for arginine in cell line HLE at codon 249 (G:C--&gt;C:G).	Cysteine	101-109	P53	Homo sapiens	4-7
8389256-6	1993	The p53 point mutations in the three HCC cell lines from Japan resulted in the amino acid changes of cysteine for tyrosine in cell line HuH 7 at codon 220 (A:T--&gt;G:C), alanine for glycine in cell line HLF at codon 244 (G:C--&gt;C:G), and serine for arginine in cell line HLE at codon 249 (G:C--&gt;C:G).	Tyrosine	114-122	P53	Homo sapiens	4-7
8389256-6	1993	The p53 point mutations in the three HCC cell lines from Japan resulted in the amino acid changes of cysteine for tyrosine in cell line HuH 7 at codon 220 (A:T--&gt;G:C), alanine for glycine in cell line HLF at codon 244 (G:C--&gt;C:G), and serine for arginine in cell line HLE at codon 249 (G:C--&gt;C:G).	Alanine	171-178	P53	Homo sapiens	4-7
8389256-6	1993	The p53 point mutations in the three HCC cell lines from Japan resulted in the amino acid changes of cysteine for tyrosine in cell line HuH 7 at codon 220 (A:T--&gt;G:C), alanine for glycine in cell line HLF at codon 244 (G:C--&gt;C:G), and serine for arginine in cell line HLE at codon 249 (G:C--&gt;C:G).	Glycine	183-190	P53	Homo sapiens	4-7
8389256-6	1993	The p53 point mutations in the three HCC cell lines from Japan resulted in the amino acid changes of cysteine for tyrosine in cell line HuH 7 at codon 220 (A:T--&gt;G:C), alanine for glycine in cell line HLF at codon 244 (G:C--&gt;C:G), and serine for arginine in cell line HLE at codon 249 (G:C--&gt;C:G).	Serine	241-247	P53	Homo sapiens	4-7
8389256-6	1993	The p53 point mutations in the three HCC cell lines from Japan resulted in the amino acid changes of cysteine for tyrosine in cell line HuH 7 at codon 220 (A:T--&gt;G:C), alanine for glycine in cell line HLF at codon 244 (G:C--&gt;C:G), and serine for arginine in cell line HLE at codon 249 (G:C--&gt;C:G).	Arginine	252-260	P53	Homo sapiens	4-7
8389256-8	1993	The cell line PLC/PRF/5 that showed p53 mutation at codon 249 (G:C--&gt;T:A) with substitution of serine for arginine was derived from a South African patient.	Serine	98-104	P53	Homo sapiens	36-39
8467489-0	1993	A structural role for metal ions in the "wild-type" conformation of the tumor suppressor protein p53.	Metals	22-27	P53	Homo sapiens	97-100
8467489-2	1993	Here we show that exposure to the metal chelator 1,10-phenanthroline induces wild-type p53 to adopt the mutant conformation and that this process is reversible.	Metals	34-39	P53	Homo sapiens	87-90
8467489-4	1993	We propose that binding of metal ions, most probably zinc, to conserved cysteinyl residues stabilizes the tertiary structure of wild-type p53.	Metals	27-32	P53	Homo sapiens	138-141
8467489-4	1993	We propose that binding of metal ions, most probably zinc, to conserved cysteinyl residues stabilizes the tertiary structure of wild-type p53.	lysyl-cysteinyl-cysteinyl-arginyl-cysteinyl-lysine	72-81	P53	Homo sapiens	138-141
8476634-0	1993	Retinoic acid and calcium regulation of p53, transforming growth factor-beta 1, and transforming growth factor-alpha gene expression and growth in adenovirus 12-SV40-transformed human tracheal gland epithelial cells.	Calcium	18-25	P53	Homo sapiens	40-43
8476634-10	1993	RA inhibited both cell proliferation and AIG growth, which was accompanied by enhanced expression of p53.	Tretinoin	0-2	P53	Homo sapiens	101-104
8384406-1	1993	Striking differences were found between different histological types of breast cancer when 263 invasive breast carcinomas were tested for nuclear p53 accumulation in formaldehyde-fixed paraffin sections.	Paraffin	185-193	P53	Homo sapiens	146-149
8384408-1	1993	The spectrum of p53 gene mutations was determined in formalin-fixed, paraffin-embedded samples of small-cell lung cancer derived from 28 patients.	Paraffin	69-77	P53	Homo sapiens	16-19
8458321-4	1993	A serine 135 p53 mutant has an intermediate transforming potential, while the histidine codon 273 allele transforms weakly, if at all.	Serine	2-8	P53	Homo sapiens	13-16
8483890-0	1993	p53 protein immunostaining in routinely processed paraffin-embedded sections.	Paraffin	50-58	P53	Homo sapiens	0-3
8483890-3	1993	We report a technique for immunostaining of the altered p53 protein in routinely processed paraffin-embedded tissue sections, comparing this method with a frozen-section immunostain method for concordance.	Paraffin	91-99	P53	Homo sapiens	56-59
8483890-9	1993	We propose that this new paraffin-embedded section immunostaining method will be of value as a screening technique for the investigation of p53 mutations in archived human tumors.	Paraffin	25-33	P53	Homo sapiens	140-143
8382111-3	1993	All of the nine mutations in the p53 gene detected in HCC from Qi-Dong were clustered at the third base of codon 249, i.e. G:C to T:A, leading to an arginine to serine change.	Arginine	149-157	P53	Homo sapiens	33-36
8434637-0	1993	Detection of p53 overexpression in routinely paraffin-embedded tissue of human carcinomas using a novel target unmasking fluid.	Paraffin	45-53	P53	Homo sapiens	13-16
8434637-1	1993	With the aid of a newly developed target unmasking fluid (TUF), p53 overexpression was visualized by immunohistochemistry on recent and archival paraffin-embedded tissue samples of colon, stomach, and pancreas neoplasms.	Paraffin	145-153	P53	Homo sapiens	64-67
8382111-3	1993	All of the nine mutations in the p53 gene detected in HCC from Qi-Dong were clustered at the third base of codon 249, i.e. G:C to T:A, leading to an arginine to serine change.	Serine	161-167	P53	Homo sapiens	33-36
8430068-1	1993	Human tobacco-related cancers exhibit a high frequency of G to T transversions in the mutation hot spot region of the p53 tumor suppressor gene, possibly the result of specific mutagens in tobacco smoke, most notably benzo[a]pyrene (B[a]P).	pyrene	225-231	P53	Homo sapiens	118-121
8101139-3	1993	We used newly-developed PCR-RFLP technique to detect the point mutation of the 7th exon of p53 gene in fresh and paraffin embedded tissues of hepatocellular carcinoma in studying 40 cases.	Paraffin	113-121	P53	Homo sapiens	91-94
8318988-4	1993	Here we describe a simple technique for DNA isolation that permits mutational analysis of p53 from minimal amounts of paraffin-embedded archival tissue samples.	Paraffin	118-126	P53	Homo sapiens	90-93
8382897-6	1993	In this study, we stained paraffin sections from eight samples of gliosarcomas from seven patients with an antibody to p53.	Paraffin	26-34	P53	Homo sapiens	119-122
8416202-3	1993	When the cells were arrested in mitotic metaphase by the use of nocodazole, p34cdc2 kinase activity was induced and p53 was apparently phosphorylated.	Nocodazole	64-74	P53	Homo sapiens	116-119
8380785-5	1993	Sequencing analysis revealed a single-base mutation at codon 273 from CGT to CAT(Arg--&gt;His) and immunocytochemical studies provided evidence that the p53 protein was overexpressed in this cell line.	Arginine	81-84	P53	Homo sapiens	153-156
8352891-9	1993	Both p53-hybridizing transcripts were downregulated by prolonged 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment (24 h) regardless of the stage of progression.	Tetradecanoylphorbol Acetate	103-106	P53	Homo sapiens	5-8
8433213-0	1993	Immunohistochemical analysis of the p53 oncoprotein on paraffin sections using a series of novel monoclonal antibodies.	Paraffin	55-63	P53	Homo sapiens	36-39
8352891-9	1993	Both p53-hybridizing transcripts were downregulated by prolonged 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment (24 h) regardless of the stage of progression.	Tetradecanoylphorbol Acetate	65-101	P53	Homo sapiens	5-8
8518412-2	1993	Using sodium dodecyl sulfate electrophoresis followed by immunoblotting on nitrocellulose membrane, the p53 protein was identified in 36 nuclear fractions obtained from 60 primary breast cancers; semiquantitation of p53 was performed by densitometric scanning.	Sodium Dodecyl Sulfate	6-28	P53	Homo sapiens	104-107
8352891-10	1993	We conclude from this study that in JB6 variants (1) mutational activation of Ha-ras and inactivation of p53 are unlikely to be involved in preneoplastic progression; (2) increased amounts of p53 protein may be involved in a subset of transformed cells, possibly reflecting a longer half-life, as demonstrated in other systems; and (3) late downregulation of p53 mRNA but not protein expression may be a secondary response in the TPA-mediated signal transduction pathway.	Tetradecanoylphorbol Acetate	430-433	P53	Homo sapiens	192-195
8352891-10	1993	We conclude from this study that in JB6 variants (1) mutational activation of Ha-ras and inactivation of p53 are unlikely to be involved in preneoplastic progression; (2) increased amounts of p53 protein may be involved in a subset of transformed cells, possibly reflecting a longer half-life, as demonstrated in other systems; and (3) late downregulation of p53 mRNA but not protein expression may be a secondary response in the TPA-mediated signal transduction pathway.	Tetradecanoylphorbol Acetate	430-433	P53	Homo sapiens	192-195
8506620-2	1993	Using a microwave oven heating method, we have detected over-expression of p53 in buffered-formalin fixed, paraffin-embedded sections of oesophageal carcinomas immunohistochemically and examined the relationship between the p53 over-expression and postoperative survival.	Paraffin	107-115	P53	Homo sapiens	75-78
8476653-1	1993	p53 gene which is known as a tumor suppressor gene locates in chromosome 17p and has a polymorphism at codon 72 (Arginine CGC--&gt;Proline CCC).	Arginine	113-121	P53	Homo sapiens	0-3
1484319-0	1992	p53 immunostaining in the distinction between benign and malignant mesothelial proliferations using formalin-fixed paraffin sections.	Paraffin	115-123	P53	Homo sapiens	0-3
1459195-4	1992	When cells were transfected with a dexamethasone-inducible wild-type p53 cDNA expression plasmid, induction of p53 expression resulted in a decreased growth rate and a decreased proportion of S-phase cells.	Dexamethasone	35-48	P53	Homo sapiens	69-72
1459195-4	1992	When cells were transfected with a dexamethasone-inducible wild-type p53 cDNA expression plasmid, induction of p53 expression resulted in a decreased growth rate and a decreased proportion of S-phase cells.	Dexamethasone	35-48	P53	Homo sapiens	111-114
1459195-5	1992	Continuous treatment with dexamethasone resulted in continued p53 expression for 16 days, but beyond that time expression ceased and could not be reinduced.	Dexamethasone	26-39	P53	Homo sapiens	62-65
1484319-2	1992	The object of this study was to examine the frequency of immunohistochemically detectable p53 overexpression in routinely processed, paraffin-embedded tissue from pleural mesotheliomas and from pleura showing reactive mesothelial hyperplasia, using a polyclonal antibody to formalin-resistant p53 epitopes, and to consider the diagnostic utility of this antibody in the distinction between mesothelioma and reactive mesothelium in pleural biopsy specimens.	Paraffin	133-141	P53	Homo sapiens	90-93
1484319-6	1992	In conclusion, this study suggests that p53 immunostaining can help to distinguish epithelial or biphasic mesothelioma from reactive mesothelial hyperplasia in formalin-fixed, paraffin-embedded pleural biopsy specimens.	Paraffin	176-184	P53	Homo sapiens	40-43
1358781-3	1992	Immunoreactive p53 was observed in the nuclei of tumor cells in 4% paraformaldehyde-fixed, frozen sections (12 of 15) and paraffin-embedded sections (11 of 15), but not in routinely processed (10% formalin-fixed) specimens.	Paraffin	122-130	P53	Homo sapiens	15-18
1454521-4	1992	These data suggest that the anti-proliferative activity of p53 is activated by phosphorylation at serine 386, and establish a direct link between the covalent modification of a growth suppressor protein and regulation of its activity in mammalian cells.	Serine	98-104	P53	Homo sapiens	59-62
1486864-9	1992	The p53 gene is a tumor-suppressor gene that can encode either a proline or an arginine in the 72nd residue.	Arginine	79-87	P53	Homo sapiens	4-7
1295480-7	1992	Mutant p53-protein, as detected by immunohistochemistry in paraffin embedded tumor tissue, does not appear to influence metastasis-free survival in patients with breast cancer.	Paraffin	59-67	P53	Homo sapiens	7-10
1406679-4	1992	Other serines in these p53 peptides, and serines in other p53 peptides, including peptides containing the serine 315 p34cdc2 site and the serine 392 casein kinase II site, were not recognized by DNA-PK or were phosphorylated less efficiently.	Serine	6-12	P53	Homo sapiens	23-26
1406679-0	1992	Human DNA-activated protein kinase phosphorylates serines 15 and 37 in the amino-terminal transactivation domain of human p53.	Serine	50-57	P53	Homo sapiens	122-125
1406679-5	1992	Phosphorylation of the conserved serine 15 in human p53 peptides depended on the presence of an adjacent glutamine, and phosphorylation was inhibited by the presence of a nearby lysine.	Serine	33-39	P53	Homo sapiens	52-55
1406679-3	1992	Serines 15 and 37 in the amino-terminal transactivation domain of human p53, and serines 7 and 18 of mouse p53, were phosphorylated by DNA-PK in the context of synthetic peptides.	Serine	0-7	P53	Homo sapiens	72-75
1406679-5	1992	Phosphorylation of the conserved serine 15 in human p53 peptides depended on the presence of an adjacent glutamine, and phosphorylation was inhibited by the presence of a nearby lysine.	Lysine	178-184	P53	Homo sapiens	52-55
1406679-4	1992	Other serines in these p53 peptides, and serines in other p53 peptides, including peptides containing the serine 315 p34cdc2 site and the serine 392 casein kinase II site, were not recognized by DNA-PK or were phosphorylated less efficiently.	Serine	6-13	P53	Homo sapiens	23-26
1406679-4	1992	Other serines in these p53 peptides, and serines in other p53 peptides, including peptides containing the serine 315 p34cdc2 site and the serine 392 casein kinase II site, were not recognized by DNA-PK or were phosphorylated less efficiently.	Serine	41-48	P53	Homo sapiens	58-61
1406679-7	1992	Our study suggests that DNA-PK may have a role in regulating cell growth and indicates how phosphorylation of serine 15 in DNA-bound p53 could alter p53 function.	Serine	110-116	P53	Homo sapiens	133-136
1406679-7	1992	Our study suggests that DNA-PK may have a role in regulating cell growth and indicates how phosphorylation of serine 15 in DNA-bound p53 could alter p53 function.	Serine	110-116	P53	Homo sapiens	149-152
1406686-2	1992	After treatment with proteinase K, the sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) band of p53 yields a single, discrete 157-nucleotide RNA, which was cloned, sequenced, and identified as 5.8S rRNA.	Sodium Dodecyl Sulfate	39-61	P53	Homo sapiens	116-119
1406686-2	1992	After treatment with proteinase K, the sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) band of p53 yields a single, discrete 157-nucleotide RNA, which was cloned, sequenced, and identified as 5.8S rRNA.	Sodium Dodecyl Sulfate	98-101	P53	Homo sapiens	116-119
1406686-3	1992	5.8S rRNA was obtained only after proteolysis of the p53 SDS-PAGE band.	Sodium Dodecyl Sulfate	57-60	P53	Homo sapiens	53-56
1406686-7	1992	The covalence of the p53-5.8S rRNA linkage was demonstrated by the following findings: (i) p53 and the linked 5.8S rRNA comigrated in SDS-PAGE; (ii) only after treatment of the p53-RNA complex with proteinase K did the 5.8S rRNA migrate differently from p53-linked 5.8S rRNA; and (iii) this isolated RNA was found linked to phosphoserine, presumably at the 5" end.	Sodium Dodecyl Sulfate	134-137	P53	Homo sapiens	21-24
1406686-7	1992	The covalence of the p53-5.8S rRNA linkage was demonstrated by the following findings: (i) p53 and the linked 5.8S rRNA comigrated in SDS-PAGE; (ii) only after treatment of the p53-RNA complex with proteinase K did the 5.8S rRNA migrate differently from p53-linked 5.8S rRNA; and (iii) this isolated RNA was found linked to phosphoserine, presumably at the 5" end.	Sodium Dodecyl Sulfate	134-137	P53	Homo sapiens	91-94
1406686-7	1992	The covalence of the p53-5.8S rRNA linkage was demonstrated by the following findings: (i) p53 and the linked 5.8S rRNA comigrated in SDS-PAGE; (ii) only after treatment of the p53-RNA complex with proteinase K did the 5.8S rRNA migrate differently from p53-linked 5.8S rRNA; and (iii) this isolated RNA was found linked to phosphoserine, presumably at the 5" end.	Sodium Dodecyl Sulfate	134-137	P53	Homo sapiens	91-94
1406686-7	1992	The covalence of the p53-5.8S rRNA linkage was demonstrated by the following findings: (i) p53 and the linked 5.8S rRNA comigrated in SDS-PAGE; (ii) only after treatment of the p53-RNA complex with proteinase K did the 5.8S rRNA migrate differently from p53-linked 5.8S rRNA; and (iii) this isolated RNA was found linked to phosphoserine, presumably at the 5" end.	Sodium Dodecyl Sulfate	134-137	P53	Homo sapiens	91-94
1444195-0	1992	Improved immunohistochemical detection of p53 protein in paraffin--embedded tissues reveals elevated levels in most head and neck and lung carcinomas: correlation with clinicopathological parameters.	Paraffin	57-65	P53	Homo sapiens	42-45
1408139-6	1992	Five of the six cases showed involvement of the p53 gene as assessed by LOH at the AccII site within the gene, and by immunoreactivity to CM-1, an antibody which recognizes the mutated form of the p53 protein in paraffin-embedded material.	Paraffin	212-220	P53	Homo sapiens	48-51
1408139-6	1992	Five of the six cases showed involvement of the p53 gene as assessed by LOH at the AccII site within the gene, and by immunoreactivity to CM-1, an antibody which recognizes the mutated form of the p53 protein in paraffin-embedded material.	Paraffin	212-220	P53	Homo sapiens	197-200
1466808-3	1992	Using conformational energy analysis based on ECEPP (Empirical Conformational Energies for Polypeptides Program), we have determined the preferred three dimensional structures for this tridecapeptide sequence for the human wild-type p53 protein and four cancer-related mutant p53 proteins (Ala 245, Ile 246, Trp 248, Ser 249).	Alanine	290-293	P53	Homo sapiens	233-236
1466808-3	1992	Using conformational energy analysis based on ECEPP (Empirical Conformational Energies for Polypeptides Program), we have determined the preferred three dimensional structures for this tridecapeptide sequence for the human wild-type p53 protein and four cancer-related mutant p53 proteins (Ala 245, Ile 246, Trp 248, Ser 249).	Alanine	290-293	P53	Homo sapiens	276-279
1466808-3	1992	Using conformational energy analysis based on ECEPP (Empirical Conformational Energies for Polypeptides Program), we have determined the preferred three dimensional structures for this tridecapeptide sequence for the human wild-type p53 protein and four cancer-related mutant p53 proteins (Ala 245, Ile 246, Trp 248, Ser 249).	Tryptophan	308-311	P53	Homo sapiens	233-236
1466808-3	1992	Using conformational energy analysis based on ECEPP (Empirical Conformational Energies for Polypeptides Program), we have determined the preferred three dimensional structures for this tridecapeptide sequence for the human wild-type p53 protein and four cancer-related mutant p53 proteins (Ala 245, Ile 246, Trp 248, Ser 249).	Tryptophan	308-311	P53	Homo sapiens	276-279
1466808-3	1992	Using conformational energy analysis based on ECEPP (Empirical Conformational Energies for Polypeptides Program), we have determined the preferred three dimensional structures for this tridecapeptide sequence for the human wild-type p53 protein and four cancer-related mutant p53 proteins (Ala 245, Ile 246, Trp 248, Ser 249).	Serine	317-320	P53	Homo sapiens	233-236
1466808-3	1992	Using conformational energy analysis based on ECEPP (Empirical Conformational Energies for Polypeptides Program), we have determined the preferred three dimensional structures for this tridecapeptide sequence for the human wild-type p53 protein and four cancer-related mutant p53 proteins (Ala 245, Ile 246, Trp 248, Ser 249).	Serine	317-320	P53	Homo sapiens	276-279
1519662-4	1992	We used 35S-labeled anti-sense single-stranded synthetic oligonucleotide probe ON102, which hybridized with DNA sequence near the 5" end of p53, for in situ hybridization.	Sulfur-35	8-11	P53	Homo sapiens	140-143
1519662-4	1992	We used 35S-labeled anti-sense single-stranded synthetic oligonucleotide probe ON102, which hybridized with DNA sequence near the 5" end of p53, for in situ hybridization.	Oligonucleotides	57-72	P53	Homo sapiens	140-143
1444195-3	1992	However, the antibody is effective in AMeX-fixed specimens, thereby permitting the improved morphologic localization of p53 phosphoprotein in paraffin embedded tissue.	Paraffin	142-150	P53	Homo sapiens	120-123
1444195-1	1992	We have analyzed the expression of the p53 tumor suppressor gene in paraffin-embedded sections of normal and malignant head and neck and lung tumors by immunohistochemistry using the PAb 1801 monoclonal antibody (MAb).	Paraffin	68-76	P53	Homo sapiens	39-42
1501881-1	1992	The cellular p53 protein is so called because of its molecular weight as determined by SDS-polyacrylamide gel electrophoresis.	Sodium Dodecyl Sulfate	87-90	P53	Homo sapiens	13-16
1520594-1	1992	p53 expression was examined in 55 gastric and 107 colorectal carcinomas with an immunoperoxidase technique, using the polyclonal antibody CM1 on routinely fixed, paraffin embedded tissue.	Paraffin	162-170	P53	Homo sapiens	0-3
1280773-4	1992	Sodium dodecyl sulfate-polyacrylamide gel electrophoretic analysis demonstrated unequivocal heterogeneity of migration rate in p53 bands.	Sodium Dodecyl Sulfate	0-22	P53	Homo sapiens	127-130
1644930-6	1992	The other nonhereditary p53 mutation was a transition at codon 248 (CGG to CAG, arginine to glutamine) found in the lymphoblasts of a patient with a preleukemic syndrome and acute lymphoblastic leukemia (ALL) whose brother is a long-term survivor of ALL.	Arginine	80-88	P53	Homo sapiens	24-27
1450522-2	1992	The sequence -Thr-Pro-Ala-Pro-Lys-, as found in p53 protein, was also phosphorylated by this enzyme, but less efficiently than in the sequence described above.	Threonine	14-17	P53	Homo sapiens	48-51
1450522-2	1992	The sequence -Thr-Pro-Ala-Pro-Lys-, as found in p53 protein, was also phosphorylated by this enzyme, but less efficiently than in the sequence described above.	Alanine	22-25	P53	Homo sapiens	48-51
1450522-2	1992	The sequence -Thr-Pro-Ala-Pro-Lys-, as found in p53 protein, was also phosphorylated by this enzyme, but less efficiently than in the sequence described above.	Lysine	30-33	P53	Homo sapiens	48-51
1322785-6	1992	The glutathione S-transferase-wild type p53 fusion protein bound to simian virus 40 large T antigen in COS-1 cell lysate.	carbonyl sulfide	103-106	P53	Homo sapiens	40-43
1639275-1	1992	A common polymorphism at codon 72 of the p53 gene in patients with acute myelogenous leukemia (AML) was analyzed by single-strand conformation polymorphism assay and sodium dodecyl sulfate polyacrylamide-gel electrophoresis of immunoprecipitated 35S-labeled P53 protein.	Sodium Dodecyl Sulfate	166-188	P53	Homo sapiens	41-44
1639275-1	1992	A common polymorphism at codon 72 of the p53 gene in patients with acute myelogenous leukemia (AML) was analyzed by single-strand conformation polymorphism assay and sodium dodecyl sulfate polyacrylamide-gel electrophoresis of immunoprecipitated 35S-labeled P53 protein.	Sulfur-35	246-249	P53	Homo sapiens	41-44
1352359-8	1992	Overexpression of the p53 and c-erbB-2 proteins was studied immunohistochemically in archival paraffin-embedded tumor samples, using the CM-1 polyclonal and the TAb 250 monoclonal antibodies, respectively.	Paraffin	94-102	P53	Homo sapiens	22-25
1279244-2	1992	We therefore investigated the immunohistochemical reactivity of the anti-p53 antibody, PAb1801, in specimens taken from 149 cases of primary gastric cancer and processed by acetone fixation, in order to elucidate the incidence and clinicopathological significance of p53 alterations in gastric cancer.	Acetone	173-180	P53	Homo sapiens	73-76
1319835-9	1992	Also, carcinoma cells with p53 mutations existing within adenoma tissues are detectable by immunostaining, even in formalin-fixed, paraffin-embedded specimens.	Paraffin	131-139	P53	Homo sapiens	27-30
1619684-9	1992	Protein expression of TP53 was seen by immunostaining of sections from paraffin-embedded material using a mouse monoclonal antibody.	Paraffin	71-79	P53	Homo sapiens	22-26
1584781-2	1992	Repeated inductions of the metallothionein wild-type p53 gene with zinc chloride results in progressive detachment of wild-type p53 cells grown on culture dishes.	zinc chloride	67-80	P53	Homo sapiens	53-56
1607637-0	1992	p53 overexpression in formalin-fixed, paraffin-embedded tissue detected by immunohistochemistry.	Paraffin	38-46	P53	Homo sapiens	0-3
1607637-3	1992	We examined p53 expression in paraffin-embedded tissues from 50 epithelial ovarian cancers and 25 primary breast cancers with a modified immunohistochemical (IHC) technique developed in this laboratory, using monoclonal antibody (MAb) PAb1801.	Paraffin	30-38	P53	Homo sapiens	12-15
1607637-6	1992	Immunodetection of p53 in paraffin-embedded tissue blocks will be a useful alternative to the standard fresh-tissue assay and can accurately reflect the level of p53 expression in human tumors.	Paraffin	26-34	P53	Homo sapiens	19-22
1535157-3	1992	Here, we identified the p53-responsive element within the Tax-responsive element [21-base-pair (bp) enhancer] of human T-cell leukemia virus type I. Mutation analysis of the 21-bp enhancer indicated that the 16-bp sequence containing the cAMP-responsive element and its surrounding sequence was responsible for p53-induced transactivation.	Cyclic AMP	238-242	P53	Homo sapiens	24-27
21584507-1	1992	The nuclear phosphoprotein p53, named according to its apparent molecular weight on SDS-polyacrylamide gels is expressed, albeit at low levels, in a variety of cell types.	Sodium Dodecyl Sulfate	84-87	P53	Homo sapiens	27-30
1584757-2	1992	The p34cdc2 kinase, which is involved in regulation of the cell cycle, phosphorylates serine-315 of human p53 in vitro.	Serine	86-92	P53	Homo sapiens	106-109
1317462-3	1992	METHODS: IgG1 monoclonal antibody to human p53 protein (PAb 1801) and immunohistochemical methods were used to detect p53 protein accumulation in archival formalin-fixed, paraffin-embedded, randomly selected carcinomas.	Paraffin	171-179	P53	Homo sapiens	118-121
1510215-1	1992	A total of 26 specimens of histologically determined, cutaneous Bowen"s disease from 23 patients were investigated for the incidence of mutant p53 protein expression by an indirect immunoperoxidase technique using the monoclonal antiserum CM1 on paraffin-embedded formalin-fixed tissue sections.	Paraffin	246-254	P53	Homo sapiens	143-146
1584781-2	1992	Repeated inductions of the metallothionein wild-type p53 gene with zinc chloride results in progressive detachment of wild-type p53 cells grown on culture dishes.	zinc chloride	67-80	P53	Homo sapiens	128-131
1322917-4	1992	Immunoprecipitation of 35S-labelled cellular proteins with anti-p53 and anti-T antibodies revealed that the level of the cellular protein, p53, declined markedly in the presence of sodium butyrate.	Sulfur-35	23-26	P53	Homo sapiens	64-67
1322917-4	1992	Immunoprecipitation of 35S-labelled cellular proteins with anti-p53 and anti-T antibodies revealed that the level of the cellular protein, p53, declined markedly in the presence of sodium butyrate.	Sulfur-35	23-26	P53	Homo sapiens	139-142
1737400-4	1992	In the present study, mutations in the p53 gene were investigated by direct sequencing analysis after polymerase chain reaction amplification of exons 5 to 8, using paraffin-embedded primary tumors and cultured cells.	Paraffin	165-173	P53	Homo sapiens	39-42
1559227-6	1992	The p53 mutations in cell lines included a codon 248 C to T transition (arginine to tryptophan) in RD and a codon 280 A to T transversion (arginine to serine) in RH30.	Arginine	72-80	P53	Homo sapiens	4-7
1559227-6	1992	The p53 mutations in cell lines included a codon 248 C to T transition (arginine to tryptophan) in RD and a codon 280 A to T transversion (arginine to serine) in RH30.	Tryptophan	84-94	P53	Homo sapiens	4-7
1559227-6	1992	The p53 mutations in cell lines included a codon 248 C to T transition (arginine to tryptophan) in RD and a codon 280 A to T transversion (arginine to serine) in RH30.	Arginine	139-147	P53	Homo sapiens	4-7
1559227-6	1992	The p53 mutations in cell lines included a codon 248 C to T transition (arginine to tryptophan) in RD and a codon 280 A to T transversion (arginine to serine) in RH30.	Serine	151-157	P53	Homo sapiens	4-7
1549103-4	1992	A new dominant mutation of p53, resulting in the change of a cysteine to an arginine at amino acid residue 141, was identified.	Cysteine	61-69	P53	Homo sapiens	27-30
1549103-4	1992	A new dominant mutation of p53, resulting in the change of a cysteine to an arginine at amino acid residue 141, was identified.	Arginine	76-84	P53	Homo sapiens	27-30
1567424-4	1992	In addition, the Pro-17-Gly peptide competitively inhibited association between hsp70 and p53, an activity which was determined by immunoprecipitation with anti-p53 monoclonal antibody PAb240.	Glycine	24-27	P53	Homo sapiens	90-93
1567424-4	1992	In addition, the Pro-17-Gly peptide competitively inhibited association between hsp70 and p53, an activity which was determined by immunoprecipitation with anti-p53 monoclonal antibody PAb240.	Glycine	24-27	P53	Homo sapiens	161-164
1506270-3	1992	Immunoprecipitation analysis revealed that mutant p53 was phosphorylated at tyrosine in the anchorage-provided cells.	Tyrosine	76-84	P53	Homo sapiens	50-53
1506270-6	1992	These results demonstrated that the growth inhibition by anchorage-deficiency or by herbimycin A is associated with an elevated p53 level and reduced p53 phosphorylation at tyrosine.	Tyrosine	173-181	P53	Homo sapiens	150-153
1347094-3	1992	Mutations were not found in Ki-ras, but 9 p53 mutations, including 2 deletions, were found in 7 patients by direct DNA sequencing after polymerase chain reaction amplification of DNA from formalin-fixed, paraffin-embedded tissue.	Paraffin	204-212	P53	Homo sapiens	42-45
1918170-4	1991	We previously identified a case of human acute myelogenous leukemia (AML) in which both alleles of the p53 gene had undergone independent missense mutations (at codons 135 cys to ser and 246 met to val).	Cysteine	172-175	P53	Homo sapiens	103-106
1545817-1	1992	Human wild-type and mutant p53 genes were expressed under the control of a galactose-inducible promoter in Saccharomyces cerevisiae.	Galactose	75-84	P53	Homo sapiens	27-30
1737852-7	1992	The other two nonhereditary p53 mutations included a T to G transversion at codon 270 (phenylalanine to cysteine) and a G to C transversion at codon 248 (arginine to proline).	Cysteine	104-112	P53	Homo sapiens	28-31
1737852-7	1992	The other two nonhereditary p53 mutations included a T to G transversion at codon 270 (phenylalanine to cysteine) and a G to C transversion at codon 248 (arginine to proline).	Arginine	154-162	P53	Homo sapiens	28-31
1727381-4	1992	These data are consistent with the hypothesis that Ni(II)-induced mutation in the p53 gene can be involved in the escape from senescence of kidney epithelial cells.	Nickel(2+)	51-57	P53	Homo sapiens	82-85
1569122-5	1992	Most importantly, they also permit the detection of p53 in archival tumour material that has been conventionally fixed in formalin and embedded in paraffin wax.	Paraffin	147-159	P53	Homo sapiens	52-55
1546693-0	1992	Immunohistochemical study of p53 expression in microwave-fixed, paraffin-embedded sections of colorectal carcinoma and adenoma.	Paraffin	64-72	P53	Homo sapiens	29-32
1546693-1	1992	Expression of p53, a tumor-suppressor gene product, was studied immunohistochemically in microwave-fixed, paraffin-embedded sections of 84 colorectal carcinomas and 44 adenomas.	Paraffin	106-114	P53	Homo sapiens	14-17
1546693-9	1992	The immunohistochemical detection of p53 in microwave-fixed, paraffin-embedded sections of colorectal carcinoma and adenoma can provide valuable information about the mechanism of carcinogenesis in colorectal epithelium.	Paraffin	61-69	P53	Homo sapiens	37-40
1731521-8	1992	This is the first demonstration of widespread p53 overexpression in alcohol-fixed, embedded tissue and confirms the major role played by p53 in human malignancies.	Alcohols	68-75	P53	Homo sapiens	46-49
1741160-6	1992	Upon retinoic acid-induced differentiation of the LA-N-5 neuroblastoma cell line, the level of p53 protein declined, as did the level of p53 mRNA, but the half-life of the protein remained unchanged.	Tretinoin	5-18	P53	Homo sapiens	95-98
1741160-6	1992	Upon retinoic acid-induced differentiation of the LA-N-5 neuroblastoma cell line, the level of p53 protein declined, as did the level of p53 mRNA, but the half-life of the protein remained unchanged.	Tretinoin	5-18	P53	Homo sapiens	137-140
1413493-1	1992	The expression of the p53 gene product was investigated immunocytochemically in a retrospective series of 164 formalin-fixed paraffin-embedded invasive breast carcinomas with pathologically proven negative lymph nodes.	Paraffin	125-133	P53	Homo sapiens	22-25
1764370-4	1991	One of the antibodies, CM1, recognises p53 in formalin-fixed, paraffin-embedded archival material and using this reagent we found immunodetectable p53 in 28 of 124 (23%) pancreatic cancers.	Paraffin	62-70	P53	Homo sapiens	39-42
1918170-4	1991	We previously identified a case of human acute myelogenous leukemia (AML) in which both alleles of the p53 gene had undergone independent missense mutations (at codons 135 cys to ser and 246 met to val).	Serine	179-182	P53	Homo sapiens	103-106
2259385-8	1990	This mutation leads to substitution of aspartic acid for glycine in one of the regions identified as a frequent target of point mutations in p53.	Glycine	57-64	P53	Homo sapiens	141-144
1906503-4	1991	The production of p53 became detectable 3 to 6 h after addition of phorbol, 12,13,-dibutyrate and ionomycin, and peaked at 30 to 42 h. To further delineate the relationship of the synthesis and metabolism of the proteins to cell cycle progression, we used three agents to arrest progression of activated T cells at various points in the cell cycle.	Ionomycin	98-107	P53	Homo sapiens	18-21
1999338-1	1991	We describe a simple method for characterizing a frequent polymorphism (that substitutes an arginine for a proline) in the coding sequence of the Tp53 gene in patients with colonic cancer and in a control population.	Arginine	92-100	P53	Homo sapiens	146-150
1924172-5	1991	The original paraffin-embedded specimen from which this mutant cell line was established was obtained, and sequence analysis detected the identical mutation in the p53 gene as that seen in the derived cell line.	Paraffin	13-21	P53	Homo sapiens	164-167
1935458-0	1991	Flow cytometric measurement of p53 protein expression and DNA content in paraffin-embedded tissue from bronchial carcinomas.	Paraffin	73-81	P53	Homo sapiens	31-34
1935458-3	1991	After immunostaining, the nuclei prepared from paraffin-embedded tissue were stained with propidium iodide for simultaneous measurement of DNA content; 17 of 24 lung cancers were p53 positive.	Paraffin	47-55	P53	Homo sapiens	179-182
1935458-9	1991	In conclusion, using the monoclonal antibody PAb 1801, p53 is detectable in cell nuclei prepared from paraffin-embedded bronchial carcinoma biopsies.	Paraffin	102-110	P53	Homo sapiens	55-58
1923535-2	1991	Immunohistochemical staining with new polyclonal (CM-1) and monoclonal antibodies (BP 53-12 and BP53-24) to p53 on methacarn-fixed paraffin sections showed positive staining in 161 (76%).	Paraffin	131-139	P53	Homo sapiens	108-111
1868448-6	1991	Similarly, p53 levels increased and DNA synthesis decreased during 12-O-tetradecanoylphorbol-13-acetate-induced differentiation of ML-1 myeloblastic leukemia cells.	Tetradecanoylphorbol Acetate	67-103	P53	Homo sapiens	11-14
2052362-5	1991	Heparin efficiently inhibited the p53 associated protein kinase whereas the polyamine spermidine stimulated enzymatic activity.	Heparin	0-7	P53	Homo sapiens	34-37
2052362-6	1991	A synthetic peptide which was shown to be specifically phosphorylated by casein kinase II blocked the in vitro phosphorylation of p53, whereas a synthetic peptide with a potential phosphorylation site on human p53 at ser 315 was ineffective in blocking the phosphorylation of p53.	Serine	217-220	P53	Homo sapiens	210-213
2052362-6	1991	A synthetic peptide which was shown to be specifically phosphorylated by casein kinase II blocked the in vitro phosphorylation of p53, whereas a synthetic peptide with a potential phosphorylation site on human p53 at ser 315 was ineffective in blocking the phosphorylation of p53.	Serine	217-220	P53	Homo sapiens	210-213
2052362-10	1991	A mutant p53 with a ser 389 to ala exchange was not phosphorylated in vitro by the p53 associated protein kinase.	Serine	20-23	P53	Homo sapiens	9-12
2052362-10	1991	A mutant p53 with a ser 389 to ala exchange was not phosphorylated in vitro by the p53 associated protein kinase.	Alanine	31-34	P53	Homo sapiens	9-12
1680118-3	1991	In this study immunohistochemical staining for p53-protein was performed on frozen- and paraffin-embedded samples from patients with Hodgkin"s (HD) and non-Hodgkin"s lymphomas (NHL).	Paraffin	88-96	P53	Homo sapiens	47-50
2141685-6	1990	Phosphoamino acid analysis of in vitro phosphorylated p53 revealed a phosphorylation predominantly on serine residues similar to p53 phosphorylated in vivo.	Serine	102-108	P53	Homo sapiens	54-57
2254323-7	1990	N alpha-Acetyl[D-Phe45, Arg47] hirudin45-65 (P53) emerged as a pure competitive inhibitor with a Ki = 2.8 +/- 0.9 nM and IC50 = 4.0 +/- 0.8 nM (human alpha-thrombin) and is designated as a "bifunctional" inhibitor.	Cysteine	7-14	P53	Homo sapiens	45-48
2399261-4	1990	Two-dimensional gel electrophoresis experiments of [35S]methionine-labeled intracellular polypeptides revealed that FKIF cells express two proteins, p53/6.1 and p48/7.5, that are not present in normal kidney and skin fibroblasts.	Methionine	56-66	P53	Homo sapiens	149-156
2155427-5	1990	Immunoprecipitation after [35S]methionine labeling of HCC cells demonstrated that p53 protein was absent in Hep 3B and FOCUS and reduced in concentration in PLC/PRF/5 cells.	Sulfur-35	27-30	P53	Homo sapiens	82-85
2156209-2	1990	Mutation of basic amino acid residues in this region of p53 (residues 312 to 323; SSSPQPKKKP) compromises transport of p53 protein to the nucleus.	Amino Acids, Basic	12-28	P53	Homo sapiens	56-59
2156209-2	1990	Mutation of basic amino acid residues in this region of p53 (residues 312 to 323; SSSPQPKKKP) compromises transport of p53 protein to the nucleus.	Amino Acids, Basic	12-28	P53	Homo sapiens	119-122
2156209-4	1990	Serine 315 within this p53 structural motif is phosphorylated in vitro by the cell cycle kinase p34cdc2.	Serine	0-6	P53	Homo sapiens	23-26
2155427-5	1990	Immunoprecipitation after [35S]methionine labeling of HCC cells demonstrated that p53 protein was absent in Hep 3B and FOCUS and reduced in concentration in PLC/PRF/5 cells.	Methionine	31-41	P53	Homo sapiens	82-85
2155427-6	1990	p53 synthesized by Mahlavu cells showed a slower migration on SDS/polyacrylamide gels suggesting it was an abnormal protein.	Sodium Dodecyl Sulfate	62-65	P53	Homo sapiens	0-3
33794285-4	2021	In the presented work, we have aimed to investigate the effect of pharmacodynamical interaction between two anti-cancer drugs, nutlin-3a and aspirin in the activation of p53 protein.	Aspirin	141-148	P53	Homo sapiens	170-173
2157184-6	1990	The p53 molecules from HOS cells and any of the HOS derivatives were underphosphorylated and showed unusual methionine- and phosphate-containing peptide fingerprints when compared with "normal" human p53, which can associate with SV40 large-T.	Methionine	108-118	P53	Homo sapiens	4-7
2157184-6	1990	The p53 molecules from HOS cells and any of the HOS derivatives were underphosphorylated and showed unusual methionine- and phosphate-containing peptide fingerprints when compared with "normal" human p53, which can associate with SV40 large-T.	Phosphates	124-133	P53	Homo sapiens	4-7
33794285-0	2021	Effect of pharmacodynamical interaction between nutlin-3a and aspirin in the activation of p53.	Aspirin	62-69	P53	Homo sapiens	91-94
33794285-10	2021	When a high dose of aspirin is administered it acts as input disturbance and leads to undesirable over-expression of p53 protein.	Aspirin	20-27	P53	Homo sapiens	117-120
33939887-10	2021	Breast tissue-occurring metabolites" antiproliferation was mainly exerted in p53-wild-type MCF-7 cells by curcuminoids through cell cycle arrest, senescence, and apoptosis induction via p53/p21 induction, while isoflavone-derived metabolites exerted estrogenic-like activity.	Isoflavones	211-221	P53	Homo sapiens	77-80
33798680-7	2021	As the p53-specific adaptor of the nuclear import, KPNA4 upregulated with the same pattern of p53 in hydrogen peroxide-induced apoptosis in human lens epithelia cells.	Hydrogen Peroxide	101-118	P53	Homo sapiens	7-10
33798680-7	2021	As the p53-specific adaptor of the nuclear import, KPNA4 upregulated with the same pattern of p53 in hydrogen peroxide-induced apoptosis in human lens epithelia cells.	Hydrogen Peroxide	101-118	P53	Homo sapiens	94-97
33591455-9	2021	Important findings of this study suggest that doxorubicin is more cytotoxic to primary renal cancer 786-0 cells with mutant VHL and p53 than the metastatic Caki-1 cells with wild-type VHL and p53, and this differential response was independent of p53 expression level.	Doxorubicin	46-57	P53	Homo sapiens	132-135
33591455-10	2021	This study suggests that combination of doxorubicin with epigenetic therapeutics could potentially be beneficial in clinical treatment of renal cancer patients with wild-type VHL and p53 but not in patients with mutant VHL and p53.	Doxorubicin	40-51	P53	Homo sapiens	183-186
33941774-8	2021	By activating the P53/P21 pathway, APG-115 exhibited potent antiproliferative and apoptogenic activities, and induced cell cycle arrest, in TP53 wild-type AML lines.	AA-115	35-42	P53	Homo sapiens	18-21
33941774-8	2021	By activating the P53/P21 pathway, APG-115 exhibited potent antiproliferative and apoptogenic activities, and induced cell cycle arrest, in TP53 wild-type AML lines.	AA-115	35-42	P53	Homo sapiens	140-144
33771522-5	2021	PTX increased miR-221-3p expression and regulated MDM2/P53 expression in the PTX-sensitive NSCLC strain (A549).	Paclitaxel	0-3	P53	Homo sapiens	55-58
33771522-5	2021	PTX increased miR-221-3p expression and regulated MDM2/P53 expression in the PTX-sensitive NSCLC strain (A549).	Paclitaxel	77-80	P53	Homo sapiens	55-58
33771522-13	2021	In conclusion, miR-221-3p overexpression could regulate MDM2/p53 signaling pathway to reverse the PTX resistance of NSCLC and induce apoptosis in vitro and vivo.	Paclitaxel	98-101	P53	Homo sapiens	61-64
33939887-10	2021	Breast tissue-occurring metabolites" antiproliferation was mainly exerted in p53-wild-type MCF-7 cells by curcuminoids through cell cycle arrest, senescence, and apoptosis induction via p53/p21 induction, while isoflavone-derived metabolites exerted estrogenic-like activity.	Isoflavones	211-221	P53	Homo sapiens	186-189
33773191-11	2021	DS-1 treatment in combination with cisplatin could enhance activated p-p53 (Ser15) and p53 downstream signaling (Bax, Bcl-2, and Akt), leading to a higher level of apoptosis.	Cisplatin	35-44	P53	Homo sapiens	71-74
33773191-11	2021	DS-1 treatment in combination with cisplatin could enhance activated p-p53 (Ser15) and p53 downstream signaling (Bax, Bcl-2, and Akt), leading to a higher level of apoptosis.	Cisplatin	35-44	P53	Homo sapiens	87-90
33773191-13	2021	Molecular docking simulation further evidenced that DS-1 interacts with MDM2 within the p53-binding domain by carbon-hydrogen bond interaction at Lys27, pi-alkyl interactions at Ile37 and Leu30, and van der Waals interactions at Ile75, Val51, Val69, Phe67, Met38, Tyr43, Gly34, and Phe31.	Carbon	110-116	P53	Homo sapiens	88-91
33773191-13	2021	Molecular docking simulation further evidenced that DS-1 interacts with MDM2 within the p53-binding domain by carbon-hydrogen bond interaction at Lys27, pi-alkyl interactions at Ile37 and Leu30, and van der Waals interactions at Ile75, Val51, Val69, Phe67, Met38, Tyr43, Gly34, and Phe31.	Hydrogen	117-125	P53	Homo sapiens	88-91
33764853-4	2021	To understand pre-binding factors contributing to the temporal gene regulation by p53, we performed time-course RNA sequencing experiments in human colon cancer cell line HCT116 treated with fluorouracil to identify early and late genes.	Fluorouracil	191-203	P53	Homo sapiens	82-85
33821368-11	2021	Ozone induced G2/M phase cell cycle arrest, which could be elucidated by the change of protein levels of p53, p21, Cyclin D1, cyclin B1, cdc2, and CDK4.	Ozone	0-5	P53	Homo sapiens	105-108
33798968-4	2021	We showed that Pos3Aa-mediated delivery of tumor suppressor p53 protein, a promising therapeutic candidate found to be inactivated in nearly half of human cancers, resulted in the restoration of p53 function in p53-deficient cancer cells, and thereby sensitized them to 5-fluorouracil chemotherapy as demonstrated in in vitro and in vivo models.	Fluorouracil	270-284	P53	Homo sapiens	60-63
33798968-4	2021	We showed that Pos3Aa-mediated delivery of tumor suppressor p53 protein, a promising therapeutic candidate found to be inactivated in nearly half of human cancers, resulted in the restoration of p53 function in p53-deficient cancer cells, and thereby sensitized them to 5-fluorouracil chemotherapy as demonstrated in in vitro and in vivo models.	Fluorouracil	270-284	P53	Homo sapiens	195-198
33798968-4	2021	We showed that Pos3Aa-mediated delivery of tumor suppressor p53 protein, a promising therapeutic candidate found to be inactivated in nearly half of human cancers, resulted in the restoration of p53 function in p53-deficient cancer cells, and thereby sensitized them to 5-fluorouracil chemotherapy as demonstrated in in vitro and in vivo models.	Fluorouracil	270-284	P53	Homo sapiens	195-198
33821487-8	2021	It summarises the excess-iron-induced alterations in MSC components, processes and discusses signalling pathways involving ROS, PI3K/AKT, MAPK, p53, AMPK/MFF/DRP1 and Wnt.	Iron	25-29	P53	Homo sapiens	144-147
33803748-9	2021	c-Jun N-terminal kinase 1 (JNK1) and p53 as downstream mediators of oxidative stress contributed to the synergistic toxicity by co-exposure of patulin and cadmium, while p53/JNK1 activation promoted the second-round ROS production through a positive feedback loop.	Cadmium	155-162	P53	Homo sapiens	37-40
33782397-6	2021	TP53I3 is transcriptionally activated by p53 and believed to play a role in DNA damage response and reactive oxygen species-induced apoptosis.	Reactive Oxygen Species	100-123	P53	Homo sapiens	41-44
33761734-9	2021	Our GSEA analysis found that signaling pathways including glycolysis, p53 pathway, notch signaling, estrogen response late, cholesterol homeostasis, estrogen response early, mitotic spindle, and transforming growth factor beta signaling were enriched in the group with higher MMP28 expression.High expression of MMP28 could be identified in PC, which also served as an independent risk element for PC.	gsea	4-8	P53	Homo sapiens	70-73
33809462-8	2021	This review discusses curcumin"s anticancer mechanism through modulation of Rb, p53, MAPK, P13K/Akt, JAK/STAT, Shh, and NF-kappaB pathways, which are commonly involved and dysregulated in preclinical and clinical GBM models.	Curcumin	22-30	P53	Homo sapiens	80-83
33767588-0	2021	miR-26b enhances the sensitivity of hepatocellular carcinoma to Doxorubicin via USP9X-dependent degradation of p53 and regulation of autophagy.	Doxorubicin	64-75	P53	Homo sapiens	111-114
33777934-7	2021	The regular dephosphorylation of NPM"s tyrosines by DUSP3 balances the p53 functioning and favors the repair of UV-promoted DNA lesions needed for the maintenance of genomic stability.	Tyrosine	39-48	P53	Homo sapiens	71-74
33767588-6	2021	Delivery of the proteasome inhibitor, MG132, reversed the inhibitory effect of miR-26b on the level of p53 following doxorubicin treatment.	Doxorubicin	117-128	P53	Homo sapiens	103-106
33767588-11	2021	Our current data indicate that miR-26b enhances HCC cell sensitivity to doxorubicin through diminishing USP9X-mediated p53 de-ubiquitination caused by DNA damaging drugs and autophagy regulation.	Doxorubicin	72-83	P53	Homo sapiens	119-122
33034274-7	2020	P53-upregulated modulator of apoptosis, which is essential in the modulation of cisplatin sensitivity in a variety of cancers, acts as a downstream effector of Nipped-B-like protein.	Cisplatin	80-89	P53	Homo sapiens	0-3
33236130-4	2021	In the present study, it was confirmed that resveratrol inhibited the HPV E6 mRNA, HPV E6 protein and phosphorylated retinoblastoma protein (p-pRb1) levels, and increased the p53 protein levels in HeLa and Ca Ski cells, as well as in subcutaneous tumor tissue grown from HeLa cells.	Resveratrol	44-55	P53	Homo sapiens	175-178
33236135-0	2021	Metformin induces apoptosis and inhibits migration by activating the AMPK/p53 axis and suppressing PI3K/AKT signaling in human cervical cancer cells.	Metformin	0-9	P53	Homo sapiens	74-77
33236135-5	2021	Following metformin treatment, the protein expression levels of p-AMP-activated protein kinase (p-AMPK), which promotes cell death, and the tumor suppressor protein p-p53 were remarkably upregulated in CaSki and C33A cells compared with the control group.	Metformin	10-19	P53	Homo sapiens	167-170
32796711-0	2020	Cellular Responses to Platinum-Based Anticancer Drugs and UVC: Role of p53 and Implications for Cancer Therapy.	Platinum	22-30	P53	Homo sapiens	71-74
33034274-9	2020	Conversely, the silencing of P53-upregulated modulator of apoptosis in Nipped-B-like protein-depleted esophageal squamous cell carcinoma rendered cells resistant to cisplatin.	Cisplatin	165-174	P53	Homo sapiens	29-32
33034274-11	2020	In summary, our study addresses the involvement of Nipped-B-like protein in the development of esophageal squamous cell carcinoma, and the modulation of cisplatin sensitivity via regulation of P53-upregulated modulator of apoptosis.	Cisplatin	153-162	P53	Homo sapiens	193-196
26560363-0	2015	Regulation of iron homeostasis by the p53-ISCU pathway.	Iron	14-18	P53	Homo sapiens	38-41
30428555-7	2018	We also found a significant decrease of caspase-3 and p53 expression after 48 h, accompanied by a down-regulation of NF-kappaB in cells exposed to MWCNT-COOH-CDDP system which promotes apoptosis escape and thus failing to overcome the triple negative breast cancer (TNBC) cells resistance.	Carbonic Acid	153-157	P53	Homo sapiens	54-57
30428555-7	2018	We also found a significant decrease of caspase-3 and p53 expression after 48 h, accompanied by a down-regulation of NF-kappaB in cells exposed to MWCNT-COOH-CDDP system which promotes apoptosis escape and thus failing to overcome the triple negative breast cancer (TNBC) cells resistance.	cddp	158-162	P53	Homo sapiens	54-57
27452519-3	2017	Among different covalent modifications found on p53 the most controversial one is lysine methylation.	Lysine	82-88	P53	Homo sapiens	48-51
30578154-9	2019	The up-regulated miRNAs were mainly enriched in pathways as GO:0000122-negative regulation of transcription from RNA polymerase II promoter, phosphatidylinositol phosphorylation, MAPK signaling pathway, and Ras signaling pathway, etc., while the down-regulated miRNAs were enriched in pathways as, response to reactive oxygen species, p53 signaling pathway, calcium signaling pathway, etc.	Reactive Oxygen Species	310-333	P53	Homo sapiens	335-338
30578154-9	2019	The up-regulated miRNAs were mainly enriched in pathways as GO:0000122-negative regulation of transcription from RNA polymerase II promoter, phosphatidylinositol phosphorylation, MAPK signaling pathway, and Ras signaling pathway, etc., while the down-regulated miRNAs were enriched in pathways as, response to reactive oxygen species, p53 signaling pathway, calcium signaling pathway, etc.	Calcium	358-365	P53	Homo sapiens	335-338
26560363-2	2015	Here, we report that p53 regulates iron metabolism through the transcriptional regulation of ISCU (iron-sulfur cluster assembly enzyme), which encodes a scaffold protein that plays a critical role in Fe-S cluster biogenesis.	Iron	35-39	P53	Homo sapiens	21-24
26560363-2	2015	Here, we report that p53 regulates iron metabolism through the transcriptional regulation of ISCU (iron-sulfur cluster assembly enzyme), which encodes a scaffold protein that plays a critical role in Fe-S cluster biogenesis.	Iron	99-103	P53	Homo sapiens	21-24
26560363-2	2015	Here, we report that p53 regulates iron metabolism through the transcriptional regulation of ISCU (iron-sulfur cluster assembly enzyme), which encodes a scaffold protein that plays a critical role in Fe-S cluster biogenesis.	Iron	200-202	P53	Homo sapiens	21-24
26560363-5	2015	In addition, in response to DNA damage, p53 induced FTH1 and suppressed transferrin receptor, which regulates iron entry into cells.	Iron	110-114	P53	Homo sapiens	40-43
26560363-6	2015	HCT116 p53(+/+) cells were resistant to iron accumulation, but HCT116 p53(-/-) cells accumulated intracellular iron after DNA damage.	Iron	111-115	P53	Homo sapiens	70-73
26560363-9	2015	Our finding revealed a novel role of the p53-ISCU pathway in the maintenance of iron homeostasis in hepatocellular carcinogenesis.	Iron	80-84	P53	Homo sapiens	41-44
34919898-4	2022	The immunosensor was fabricated by immobilizing anti-p53 antibodies onto the pencil graphite electrode (PGE).	phenylglycidyl ether	104-107	P53	Homo sapiens	53-56
24909504-5	2014	RESULTS: Patients in the doxorubicin trial with TP53-mutated tumours experienced a shorter recurrence-free (RFS; 14 vs. 83 months, p &lt; 0.001) and overall survival (OS; 35 vs. 90 months, p &lt; 0.001) than patients with TP53 wt tumours.	Doxorubicin	25-36	P53	Homo sapiens	48-52
24909504-5	2014	RESULTS: Patients in the doxorubicin trial with TP53-mutated tumours experienced a shorter recurrence-free (RFS; 14 vs. 83 months, p &lt; 0.001) and overall survival (OS; 35 vs. 90 months, p &lt; 0.001) than patients with TP53 wt tumours.	Doxorubicin	25-36	P53	Homo sapiens	222-226
22233820-2	2011	5-FU blocks thymidylate synthase (TS) which cross-links p53 mRNA, inhibiting its synthesis.	Fluorouracil	0-4	P53	Homo sapiens	56-59
22233820-4	2011	Enough p53 mutations can confer resistance to chemotherapy using anthracyclines and 5-FU, while are associated with improved responses to TXT.	Anthracyclines	65-79	P53	Homo sapiens	7-10
22233820-4	2011	Enough p53 mutations can confer resistance to chemotherapy using anthracyclines and 5-FU, while are associated with improved responses to TXT.	Fluorouracil	84-88	P53	Homo sapiens	7-10
23266121-0	2013	Lead optimization of novel p53-MDM2 interaction inhibitors possessing dihydroimidazothiazole scaffold.	dihydroimidazothiazole	70-92	P53	Homo sapiens	27-30
23266121-1	2013	With the aim of discovering potent inhibitors of the p53-MDM2 interaction and thus obtaining a potent anticancer drug, we have pursued synthesis and optimization of dihydroimidazothiazole derivatives, which have been discovered via scaffold hopping by mimicing the mode of interaction between MDM2 and Nutlins.	dihydroimidazothiazole	165-187	P53	Homo sapiens	53-56
9799559-0	1998	Hypochlorous acid activates the tumor suppressor protein p53 in cultured human skin fibroblasts.	Hypochlorous Acid	0-17	P53	Homo sapiens	57-60
9799559-4	1998	The increase in p53 required the myeloperoxidase-dependent generation of hypochlorous acid and could be mimicked by exposing cells to a flux of hypochlorous acid produced by purified myeloperoxidase and a hydrogen peroxide-generating system.	Hypochlorous Acid	73-90	P53	Homo sapiens	16-19
9799559-4	1998	The increase in p53 required the myeloperoxidase-dependent generation of hypochlorous acid and could be mimicked by exposing cells to a flux of hypochlorous acid produced by purified myeloperoxidase and a hydrogen peroxide-generating system.	Hypochlorous Acid	144-161	P53	Homo sapiens	16-19
9799559-4	1998	The increase in p53 required the myeloperoxidase-dependent generation of hypochlorous acid and could be mimicked by exposing cells to a flux of hypochlorous acid produced by purified myeloperoxidase and a hydrogen peroxide-generating system.	Hydrogen Peroxide	205-222	P53	Homo sapiens	16-19
9799559-5	1998	Levels of p53 were very sensitive to hypochlorous acid, with fluxes as low as 0.2 microM per min being effective.	Hypochlorous Acid	37-54	P53	Homo sapiens	10-13
9799559-6	1998	Levels of the p53-dependent protein WAF1/CIP1 were also elevated when fibroblasts were treated with hypochlorous acid.	Hypochlorous Acid	100-117	P53	Homo sapiens	14-17
9799559-7	1998	This result indicates that the p53 in the cells treated with hypochlorous acid was transcriptionally active.	Hypochlorous Acid	61-78	P53	Homo sapiens	31-34
9799559-8	1998	Hydrogen peroxide alone also elevated p53 and WAF1/CIP1, but the fluxes required were nearly 10-fold higher than those that were effective for hypochlorous acid.	Hydrogen Peroxide	0-17	P53	Homo sapiens	38-41
34821461-4	2022	Moreover, the generation of tamoxifen resistance involved in apoptosis escape via a reactive oxygen species-regulated p53 signaling pathway.	Tamoxifen	28-37	P53	Homo sapiens	118-121
34821461-4	2022	Moreover, the generation of tamoxifen resistance involved in apoptosis escape via a reactive oxygen species-regulated p53 signaling pathway.	Reactive Oxygen Species	84-107	P53	Homo sapiens	118-121
34636125-8	2022	RESULTS: Under high glucose conditions, the viability of ARPE-19 was decreased and the apoptosis rate increased, the protein expressions of Bax, Caspase-3, LC3-II/LC3-I, and p-p53 were all increased and the expressions of Bcl-2, p62, and p-mTOR decreased, and autophagic flux was increased compared with that of the controls.	Glucose	20-27	P53	Homo sapiens	176-179
34384758-2	2022	Recent studies have emphasized on major drivers and regulators such as Myc, mutant p53, SREBP2, LXRs and oncogenic signaling pathways that play crucial roles in tumor cholesterol metabolic reprogramming.	Cholesterol	167-178	P53	Homo sapiens	83-86
34636125-11	2022	CONCLUSIONS: Our findings indicate that through the p53/mTOR autophagy pathway, PC may protect RPE cells from high glucose-induced injury.	Glucose	115-122	P53	Homo sapiens	52-55
34871862-10	2022	We also observed a marked upregulation of p53, known to be negatively correlated with KIAA0101 in Dox and miR-197-5p combination treatment compared to Dox alone.	Doxorubicin	98-101	P53	Homo sapiens	42-45
34856073-12	2022	This study constructed a TF-miRNA regulatory network with TP53 and E2F as the main central genes to elucidate the molecular mechanism of resveratrol in the treatment of breast cancer.	Resveratrol	137-148	P53	Homo sapiens	58-62
34597653-0	2022	Combination of Compound Kushen Injection and cisplatin shows synergistic antitumor activity in p53-R273H/P309S mutant colorectal cancer cells through inducing apoptosis.	Cisplatin	45-54	P53	Homo sapiens	95-98
34728188-9	2022	DOX exerted its effects through DNA damage and oxidative stress that led to p53 upregulation, and p53 inhibited cell cycle progression.	Doxorubicin	0-3	P53	Homo sapiens	76-79
34728188-9	2022	DOX exerted its effects through DNA damage and oxidative stress that led to p53 upregulation, and p53 inhibited cell cycle progression.	Doxorubicin	0-3	P53	Homo sapiens	98-101
34817806-5	2022	Next to TP53 and PTEN, FBXW7 was reported with the highest percentage of arginine substitution among mutations related to cancer.	Arginine	73-81	P53	Homo sapiens	8-12
34772529-5	2022	Mechanistically, MIR002 and GEM144 induced acetylation of p53, activation of p21, G1/S cell cycle arrest, and apoptosis.	gem144	28-34	P53	Homo sapiens	58-61
34667024-12	2022	These include irinotecan, which induces apoptosis of DDLS cells in a C/EBPalpha-dependent, p53-independent manner and should be clinically evaluated in patients with advanced DDLS.	Irinotecan	14-24	P53	Homo sapiens	91-94
34871862-10	2022	We also observed a marked upregulation of p53, known to be negatively correlated with KIAA0101 in Dox and miR-197-5p combination treatment compared to Dox alone.	Doxorubicin	151-154	P53	Homo sapiens	42-45
34928233-4	2022	AIMS: To explore whether homebox D3 binding to lysine (K)-specific demethylase 5C promoted malignant progression of diffuse large B-cell lymphoma by decreasing p53 expression.	Lysine	47-53	P53	Homo sapiens	160-163
34783124-8	2022	Moreover, ginsenoside Rg1 treatment before doxorubicin activates the DNA damage response elements (ATM, H2AX, RAD51, and XRCC1) and subsequent apoptosis-related gene expression (p21, TP53.	Doxorubicin	43-54	P53	Homo sapiens	183-187
34826438-9	2022	Moreover, veratramine was sufficient to affect the phosphatidylinositol-3-kinase/serine-threonine kinase/mechanistic target of rapamycin signaling pathway and its downstream Mdm2/p53/p21 pathway in human glioblastoma cell lines.	veratramine	10-21	P53	Homo sapiens	179-182
34826438-10	2022	SIGNIFICANCE: Antitumor effects of veratramine in suppression of glioma progression was mediated by the regulation of PI3K/Akt/mTOR and Mdm2/p53/p21 signaling pathway.	veratramine	35-46	P53	Homo sapiens	141-144
34896432-9	2022	Furthermore, curcumin was found that it could not only reduce the mRNA and protein levels of mitophagy (PINK1, Parkin, LC3, p62) and pro-apoptotic genes (p53, Bax, Caspase-3, Cytc), but also increased the levels of anti-apoptotic genes (Bcl-2).	Curcumin	13-21	P53	Homo sapiens	154-157
34634383-10	2021	Furthermore, the functional p53/IGFBP7-AS1/IGFBP7 axis facilitates apoptosis by suppressing the production and secretion of the NPPB signal peptide and further regulating the cGMP-PKG signalling pathway.	Cyclic GMP	175-179	P53	Homo sapiens	28-31
34785775-7	2022	Interestingly, ODN-induced p53 and Bax upregulation were modulated by the production of mitochondrial reactive oxygen species (ROS).	Reactive Oxygen Species	102-125	P53	Homo sapiens	27-30
34785775-7	2022	Interestingly, ODN-induced p53 and Bax upregulation were modulated by the production of mitochondrial reactive oxygen species (ROS).	Reactive Oxygen Species	127-130	P53	Homo sapiens	27-30
34785775-8	2022	Mitochondrial ROS scavengers prevented OTUB1-mediated p53 stabilization and Bax upregulation by ODN.	Reactive Oxygen Species	14-17	P53	Homo sapiens	54-57
34963005-10	2022	This observation was due to a statistically significantly increased number of platinum-based chemotherapy lines in gBRCA1/2 mutation carriers vs noncarriers (PPM1D: mean (SD) = 2.04 (1.27) vs 1.04 (0.99), P < .001; TP53: mean (SD) =2.83 (1.33) vs 1.07 (1.01), P < .001).	Platinum	78-86	P53	Homo sapiens	215-219
34958576-4	2022	Hoping to create a novel class of membrane-permeable PPI inhibitors, the phenylalanine, tryptophan, and leucine residues that play a critical role in inhibiting the p53-HDM2 interaction were grafted into the framework of CADY2 a cell-penetrating peptide (CPP) having a helical propensity.	Tryptophan	88-98	P53	Homo sapiens	165-168
34928233-16	2022	CONCLUSION: Homebox D3 up-regulating lysine (K)-specific demethylase 5C promotes malignant progression of diffuse large B-cell lymphoma by decreasing p53 expression.	Lysine	37-43	P53	Homo sapiens	150-153
34919052-5	2021	Mechanistic analysis suggests that NMNAT interferes with DNA damage-p53-caspase-3 apoptosis signaling pathway by enhancing NAD+-dependent posttranslational modifications (PTMs) poly(ADP-ribosyl)ation (PARylation) and deacetylation of p53.	NAD	123-127	P53	Homo sapiens	68-71
34731023-4	2021	Recent Advances: Cisplatin ototoxicity results from several mechanisms, including: redox imbalance caused by reactive oxygen species (ROS) production and lipid peroxidation, activation of inflammation, p53 and its downstream pathways that culminate in apoptosis.	Cisplatin	17-26	P53	Homo sapiens	202-205
34919052-7	2021	Our findings reveal a novel tumorigenic mechanism involving protein complex formation of p53 with NAD+ synthetic enzyme NMNAT and NAD+-dependent PTM enzymes that regulates glioma growth.	NAD	98-102	P53	Homo sapiens	89-92
34919052-7	2021	Our findings reveal a novel tumorigenic mechanism involving protein complex formation of p53 with NAD+ synthetic enzyme NMNAT and NAD+-dependent PTM enzymes that regulates glioma growth.	NAD	130-134	P53	Homo sapiens	89-92
34948101-7	2021	Moreover, a higher level of p53 protein in the presence of rapamycin or doxorubicin and the combination of both antibiotics was noticed in PCBP2-overexpressed cells compared to control cells.	Sirolimus	59-68	P53	Homo sapiens	28-31
34919323-6	2022	And then it was attested that cells had a lower level of p53 but SIRT1 expression was upregulated on RSV-AA-P(CL-DLLA), which might be related with resveratrol release from RSV-AA-P(CL-DLLA).	Resveratrol	148-159	P53	Homo sapiens	57-60
34919323-7	2022	It also suggested cell senescence on RSV-AA-P(CL-DLLA) was regulated by p53 and SIRT1 signaling pathway.	rsv-aa	37-43	P53	Homo sapiens	72-75
34970530-8	2021	Mechanistically, 2b induced apoptosis-dependent anticancer effect (43%) higher than that of 5-fluorouracil (34.95%) in three studied cancer cell lines, activated p53 (47%), downregulated the Bcl2 gene (1.25-fold), and upregulated p21 (2-fold) in the treated cancer cells.	Fluorouracil	92-106	P53	Homo sapiens	162-165
34903608-5	2022	In the p53-null KG-1 and THP-1 AML cell lines, EZH2 inhibitor and doxorubicin co-treatment induced transcriptional reprogramming that was, in part, dependent on de-repression of H3K27me3-marked gene promoters and led to increased expression of cell death-promoting and growth-inhibitory genes.	Doxorubicin	66-77	P53	Homo sapiens	7-10
34687773-7	2021	Taken together, CYN may induce ROS overproduction, leading to increased p53 expression and ultimately promoting VSMC apoptosis.	Reactive Oxygen Species	31-34	P53	Homo sapiens	72-75
34948101-7	2021	Moreover, a higher level of p53 protein in the presence of rapamycin or doxorubicin and the combination of both antibiotics was noticed in PCBP2-overexpressed cells compared to control cells.	Doxorubicin	72-83	P53	Homo sapiens	28-31
34878954-0	2021	Autophagy inhibition mediated by MCOLN1/TRPML1 suppresses cancer metastasis via regulating a ROS-driven TP53/p53 pathway.	ros	93-96	P53	Homo sapiens	104-108
34886886-11	2021	CONCLUSION: Evidence indicated that the endogenous p53 status affected the sensitivity of ATC cells to EVO-induced apoptosis and G2/M arrest, revealing the potential role of p53 related to increased ROS production and disrupted MMP in the anticancer actions of EVO, and alkylation at position 14 of EVO is a critical substitution for apoptosis of ATC cells.	Reactive Oxygen Species	199-202	P53	Homo sapiens	51-54
34886886-11	2021	CONCLUSION: Evidence indicated that the endogenous p53 status affected the sensitivity of ATC cells to EVO-induced apoptosis and G2/M arrest, revealing the potential role of p53 related to increased ROS production and disrupted MMP in the anticancer actions of EVO, and alkylation at position 14 of EVO is a critical substitution for apoptosis of ATC cells.	Reactive Oxygen Species	199-202	P53	Homo sapiens	174-177
34878954-0	2021	Autophagy inhibition mediated by MCOLN1/TRPML1 suppresses cancer metastasis via regulating a ROS-driven TP53/p53 pathway.	ros	93-96	P53	Homo sapiens	109-112
34880421-6	2021	Once freed from PEPD, p53 mutants undergo multiple posttranslational modifications, especially lysine 373 acetylation, which cause them to refold and regain tumor suppressor activities that are typically displayed by p53.	Lysine	95-101	P53	Homo sapiens	22-25
34878954-2	2021	This study demonstrates that autophagy inhibition induced by MCOLN1/TRPML1 suppresses cancer metastasis by evoking the ROS-mediated TP53/p53 pathway.	ros	119-122	P53	Homo sapiens	132-136
34880421-6	2021	Once freed from PEPD, p53 mutants undergo multiple posttranslational modifications, especially lysine 373 acetylation, which cause them to refold and regain tumor suppressor activities that are typically displayed by p53.	Lysine	95-101	P53	Homo sapiens	217-220
34878954-2	2021	This study demonstrates that autophagy inhibition induced by MCOLN1/TRPML1 suppresses cancer metastasis by evoking the ROS-mediated TP53/p53 pathway.	ros	119-122	P53	Homo sapiens	137-140
34878954-5	2021	Third, we demonstrate that the elevated ROS resulting from autophagy inhibition subsequently triggers TP53 activity, which in turn modulates expression of its downstream targets which are involved in a broad spectrum of the metastatic cascade to suppress metastasis including MMP members and TWIST.	ros	40-43	P53	Homo sapiens	102-106
34878954-6	2021	In summary, our findings have established a mechanism by which autophagy inhibition suppresses metastasis via the ROS-TP53 signaling pathway.	ros	114-117	P53	Homo sapiens	118-122
34876239-5	2021	However, the expression levels of other tumor-related factors, including Ki67, p27, p53, Bcl-2-associated X protein (Bax), B-cell lymphoma 2 (Bcl-2), caspase-3 (Cas-3), matrix metallopeptidase 2 (MMP2) and vascular endothelial growth factor (VEGF) proteins, were constantly maintained in the tumors of all three substrains after cisplatin treatment.	Cisplatin	329-338	P53	Homo sapiens	84-87
34880123-2	2022	We have previously shown that cAMP-activating factors present in the bone marrow render ALL cells less sensitive to DNA damage-induced apoptosis, by enhancing autophagy and suppressing p53.	Cyclic AMP	30-34	P53	Homo sapiens	185-188
34947995-3	2021	In this study, we investigated the posttranslationally modified p53, including p53 acetylated at lysine 382 (K382), p53 phosphorylated at serine 46 (S46), and the p53 cofactor TTC5/STRAP (Tetratricopeptide repeat domain 5/ Stress-responsive activator of p300-TTC5) proteins in lung cancer.	Lysine	97-103	P53	Homo sapiens	79-82
34944790-6	2021	Accordingly, genetic knockdown of p53 increases SLC7A11 transcript levels; conversely, over-expressing p53 in p53-null GBM cells downregulates xCT expression and glutamate release.	Glutamic Acid	162-171	P53	Homo sapiens	103-106
34877784-8	2022	GSEA identified an association of high DKK1 expression with TP53, MTOR, and VEGF expression.	gsea	0-4	P53	Homo sapiens	60-64
34947995-3	2021	In this study, we investigated the posttranslationally modified p53, including p53 acetylated at lysine 382 (K382), p53 phosphorylated at serine 46 (S46), and the p53 cofactor TTC5/STRAP (Tetratricopeptide repeat domain 5/ Stress-responsive activator of p300-TTC5) proteins in lung cancer.	Serine	138-144	P53	Homo sapiens	116-119
34708319-0	2021	High-dose copper activates p53-independent apoptosis through the induction of nucleolar stress in human cell lines.	Copper	10-16	P53	Homo sapiens	27-30
34855924-0	2021	Retraction: miR-24-3p Suppresses Malignant Behavior of Lacrimal Adenoid Cystic Carcinoma by Targeting PRKCH to Regulate p53/p21 Pathway.	mir-24-3p	12-21	P53	Homo sapiens	120-123
34862374-0	2021	Structural basis of reactivation of oncogenic p53 mutants by a small molecule: methylene quinuclidinone (MQ).	memoquin	105-107	P53	Homo sapiens	46-49
34862374-3	2021	PRIMA-1 and eprenetapopt (APR-246/PRIMA-1MET) are small molecules that are converted into the biologically active compound, methylene quinuclidinone (MQ), shown to reactivate mutant p53 by binding covalently to cysteine residues.	memoquin	150-152	P53	Homo sapiens	182-185
34862374-3	2021	PRIMA-1 and eprenetapopt (APR-246/PRIMA-1MET) are small molecules that are converted into the biologically active compound, methylene quinuclidinone (MQ), shown to reactivate mutant p53 by binding covalently to cysteine residues.	Cysteine	211-219	P53	Homo sapiens	182-185
34085157-9	2021	The mechanism for down-regulation of p53 expression in MCF-7iPOX cells was found at the level of p53-PEPD complex formation that was counteracted by hydrogen peroxide treatment.	Hydrogen Peroxide	149-166	P53	Homo sapiens	37-40
34085157-9	2021	The mechanism for down-regulation of p53 expression in MCF-7iPOX cells was found at the level of p53-PEPD complex formation that was counteracted by hydrogen peroxide treatment.	Hydrogen Peroxide	149-166	P53	Homo sapiens	97-100
34708319-9	2021	Blockage in ribosome synthesis under copper-treatment induced nucleolar stress and triggered p53-independent apoptosis pathways.	Copper	37-43	P53	Homo sapiens	93-96
34461288-5	2021	Using a microarray assay to detect the dysregulated genes in IDD patients with obesity, we identified 33 differentially expressed genes and verified only two proapoptotic genes, including Puma (p53 upregulated modulator of apoptosis) and BAX (BCL2 associated X) responded to glucose.	Glucose	275-282	P53	Homo sapiens	194-197
34794098-7	2021	The most balanced potent and safe derivatives; 5i and 5q were more active than 5-fluorouracil, exhibited low mumrange MDM2 binding (KD=1.32and 1.72 mum, respectively), induced apoptosis-dependent anticancer activities up to 50%, activated p53 by 47-63%, downregulated the BCL2 gene to 59.8%, and reduced its protein level (13.75%) in the treated cancer cells.	Fluorouracil	79-93	P53	Homo sapiens	239-242
34967559-0	2021	Effect of XPD and TP53 Gene Polymorphisms on the Risk of Platinum-Based Chemotherapy Induced Toxicity in Bangladeshi Lung Cancer Patients.	Platinum	57-65	P53	Homo sapiens	18-22
34967559-4	2021	Therefore, this study aimed to investigate XPD Lys751Gln and TP53 Arg72Pro polymorphisms on the risk of platinum-based chemotherapy-induced toxicity in lung cancer patients in the Bangladeshi population.	Platinum	104-112	P53	Homo sapiens	61-65
34346836-6	2021	Genome-wide analysis showed that aberrant amplification of TP53 and MYC in gastric cancer was associated with abnormal cholesterol anabolic metabolism.	Cholesterol	119-130	P53	Homo sapiens	59-63
34794242-0	2021	The endocytic pathway of Pt nanoclusters and their induced apoptosis of A549 and A549/Cis cells through c-Myc/p53 and Bcl-2/caspase-3 signaling pathways.	Platinum	25-27	P53	Homo sapiens	110-113
34647981-13	2021	TP53 CHIP was associated with longer prior exposure to platinum (mean 14.0 months of 15 TP53 CHIP cases vs 11.1 months of 49 non-TP53 CHIP cases; P = .02).	Platinum	55-63	P53	Homo sapiens	0-4
34855076-1	2021	Incubation of primary culture of pulmonary fibroblasts with non-opiate analogue of leuenkephalin (NALE; Phe-D-Ala-Gly-Phe-Leu-Arg, 0.1 muM) reduced generation of superoxide anion-radical (by 20.7%) and decreased the number of p53+ cells (by 40.2%) induced by exposure to H2O2 (60 muM).	Hydrogen Peroxide	271-275	P53	Homo sapiens	226-229
34855076-3	2021	Incubation of pulmonary fibroblasts culture with peptide G (Phe-D-Ala-Gly-Phe-Leu-Gly, 0.1 muM) also significantly reduced the damaging effect of H2O2: the number of p53+ cells decreased by 73.5%, the area of cell nuclei returned to normal, and generation of superoxide anion-radical decreased by 18.4%.	Hydrogen Peroxide	146-150	P53	Homo sapiens	166-169
34779146-7	2021	Impaired EPR in TP53-mutated breast cancer cases was independent from the Oncotype DX Recurrence Score group and was seen both with tamoxifen- and aromatase inhibitor-based pET (p = 0.0005 each).	Tamoxifen	132-141	P53	Homo sapiens	16-20
34719737-5	2021	VAP-1 generated hydrogen peroxide acts via the p53 signaling pathway to regulate HSC proliferation.	Hydrogen Peroxide	16-33	P53	Homo sapiens	47-50
34647981-13	2021	TP53 CHIP was associated with longer prior exposure to platinum (mean 14.0 months of 15 TP53 CHIP cases vs 11.1 months of 49 non-TP53 CHIP cases; P = .02).	Platinum	55-63	P53	Homo sapiens	88-92
34258881-0	2021	Mechanistic insights into p53-regulated cytotoxicity of combined entinostat and irinotecan against colorectal cancer cells.	Irinotecan	80-90	P53	Homo sapiens	26-29
34928029-6	2021	The CPD regulates the expression levels of Caspase-3, p53, and Bcl-2 genes by increasing intracellular reactive oxygen species (ROS) levels and reducing mitochondrial membrane potential, which indicates that mitochondrial-mediated pathways are involved in apoptosis.	Reactive Oxygen Species	103-126	P53	Homo sapiens	54-57
34901834-9	2021	Factors other than DPYD polymorphisms (e.g., miR-27a, TYMS, ENOSF1, p53) also affect 5-FU toxicity.	Fluorouracil	85-89	P53	Homo sapiens	68-71
34637097-7	2021	The combination of 5-FU and Quer compared to 5-FU alone improved apoptosis by increasing the gene expression of Bax and p53 and caspase-9 activity and decreasing the Bcl2 gene expression.	Fluorouracil	19-23	P53	Homo sapiens	120-123
34637097-7	2021	The combination of 5-FU and Quer compared to 5-FU alone improved apoptosis by increasing the gene expression of Bax and p53 and caspase-9 activity and decreasing the Bcl2 gene expression.	Fluorouracil	45-49	P53	Homo sapiens	120-123
34928029-6	2021	The CPD regulates the expression levels of Caspase-3, p53, and Bcl-2 genes by increasing intracellular reactive oxygen species (ROS) levels and reducing mitochondrial membrane potential, which indicates that mitochondrial-mediated pathways are involved in apoptosis.	Reactive Oxygen Species	128-131	P53	Homo sapiens	54-57
34885154-3	2021	PPM1D encodes a serine/threonine phosphatase, WIP1, that is a negative regulator of p53 activity as well as key proteins involved in cell cycle control, DNA repair and apoptosis.	Serine	16-22	P53	Homo sapiens	84-87
34837558-9	2021	In vitro experiments showed that OST and lobaplatin could significantly induce apoptosis in the MDA-MB-231 cells (P < 0.05), as indicated by elevation in the translation level of p53/Bax/caspase-3 p17 and downregulation of the Bcl-2 protein.	lobaplatin	41-51	P53	Homo sapiens	179-182
34917611-12	2021	KEGG and GSEA enrichment results suggested that the IL-17 signaling pathway and antigen processing and presentation pathways were significantly enriched in the TP53-mutant group.	gsea	9-13	P53	Homo sapiens	160-164
34579932-0	2021	Expression of concern: "Tyrosine phosphatase inhibitors combined with retinoic acid can enhance differentiation of neuroblastoma cells and trigger ERK- and AKT-dependent, p53-independent senescence" Cancer Letters, Volume 328, Issue 1, 1 January 2013, Pages 44-54.	Tretinoin	70-83	P53	Homo sapiens	171-174
34837558-10	2021	Finally, combined treatment with OST and lobaplatin had an enhanced anti-tumor effect (P < 0.05) on proliferation and apoptosis, as well as more obvious effects on the related proteins (p53, Bax, Bcl-2, and caspase-3 p17).	lobaplatin	41-51	P53	Homo sapiens	186-189
34900672-15	2021	GSEA was used to identify typical pathways and biological processes related to 9-mRNA, cell cycle, hypoxia, p53 pathway, and PI3K/AKT/mTOR pathway, as well as biological processes related to the model.	gsea	0-4	P53	Homo sapiens	108-111
34822033-0	2021	USP39 attenuates the antitumor activity of cisplatin on colon cancer cells dependent on p53.	Cisplatin	43-52	P53	Homo sapiens	88-91
34822033-9	2021	Further studies show that USP39 regulates cisplatin-induced apoptosis dependent on p53.	Cisplatin	42-51	P53	Homo sapiens	83-86
34822033-11	2021	Collectively, our findings reveal that USP39 might be a negative factor of the p53 mediated cisplatin sensitivity of colon cancer, and suggest USP39 as a potential molecular target for cisplatin chemotherapy of colon cancer.	Cisplatin	92-101	P53	Homo sapiens	79-82
34822033-11	2021	Collectively, our findings reveal that USP39 might be a negative factor of the p53 mediated cisplatin sensitivity of colon cancer, and suggest USP39 as a potential molecular target for cisplatin chemotherapy of colon cancer.	Cisplatin	185-194	P53	Homo sapiens	79-82
34834551-0	2021	Bioinformatics Analysis Identifies Precision Treatment with Paclitaxel for Hepatocellular Carcinoma Patients Harboring Mutant TP53 or Wild-Type CTNNB1 Gene.	Paclitaxel	60-70	P53	Homo sapiens	126-130
34840111-5	2022	Recently, emerging roles for p53 in mediating lipid metabolism have come to light with intriguing metabolic roles in regulating cholesterol homeostasis and lipid droplet formation.	Cholesterol	128-139	P53	Homo sapiens	29-32
34888245-0	2021	High-LET Carbon and Iron Ions Elicit a Prolonged and Amplified p53 Signaling and Inflammatory Response Compared to low-LET X-Rays in Human Peripheral Blood Mononuclear Cells.	Carbon	9-15	P53	Homo sapiens	63-66
34888245-0	2021	High-LET Carbon and Iron Ions Elicit a Prolonged and Amplified p53 Signaling and Inflammatory Response Compared to low-LET X-Rays in Human Peripheral Blood Mononuclear Cells.	Iron	20-24	P53	Homo sapiens	63-66
34832966-4	2021	Secondly, we chose SK-N-FI (mutated at TP53) and SK-N-Be(2) (wild-type TP53) cell lines, treated them with chemotherapeutic agents (doxorubicin, etoposide, cisplatin, and melphalan) and with two isomers of retinoic acid (RA): (9-cis and all-trans).	sk-n-fi	19-26	P53	Homo sapiens	39-43
34832966-9	2021	Treatment of SK-N-FI and SK-N-Be(2) cells with doxorubicin, etoposide, cisplatin, and melphalan increased apoptosis and blocked the cycle in G2/M, while retinoic acid isomers induced apoptosis and decreased the percentage of cells in S phase in TP53 mutated SK-N-FI cells, but not in TP53 wild-type SK-N-Be(2) cells.	sk-n-fi	13-20	P53	Homo sapiens	245-249
34787057-6	2021	Of the many, Thr18 at transactivational domain (TAD) of p53 is reported to amplify p53 activity upon phosphorylation.	UNII-PYZ33YLR8A	13-18	P53	Homo sapiens	56-59
34787057-6	2021	Of the many, Thr18 at transactivational domain (TAD) of p53 is reported to amplify p53 activity upon phosphorylation.	UNII-PYZ33YLR8A	13-18	P53	Homo sapiens	83-86
34787057-10	2021	The results of this computational study further explain the importance of the Thr18 as a PTM site in atomistic detail, hence shedding further light to the understanding of how PTMs are imperative for p53 activity to protect the cellular world.Communicated by Ramaswamy H. Sarma.	UNII-PYZ33YLR8A	78-83	P53	Homo sapiens	200-203
34783301-6	2021	The development of AIC was significantly related to Arg/Arg of p53 protein gene (OR = 2.972; p = 0.001), T/T of NOS3 gene (OR = 3.059, p = 0.018), T/T of NADPH oxidase gene (OR = 2.753, p = 0.008), and C/C of GPX1 (OR = 2.345; p = 0.007).	Arginine	52-55	P53	Homo sapiens	63-66
34867391-7	2021	Overexpression of p53 or miR-628-3p can inhibit the growth and promote apoptosis of A549 and PC-9 cells, while silencing p53 or miR-628-3p has the opposite effect.	mir-628-3p	128-138	P53	Homo sapiens	18-21
34653407-6	2021	We found that AZD2461 reduced cell proliferation in wtp53 and p53-/- cancer cells by increasing ROS and DNA damage, while R273H mutant (mut) p53 counteracted these effects.	ros	96-99	P53	Homo sapiens	62-65
34447990-5	2021	On the other hand, treatment with the antioxidant N-acetylcysteine (NAC) increased glutathione concentration, decreased basal H2O2 production, p53 levels and sensitivity to AA treatment in the XPC-null back to the levels found in XPC-wt cells.	Acetylcysteine	50-66	P53	Homo sapiens	143-146
34447990-5	2021	On the other hand, treatment with the antioxidant N-acetylcysteine (NAC) increased glutathione concentration, decreased basal H2O2 production, p53 levels and sensitivity to AA treatment in the XPC-null back to the levels found in XPC-wt cells.	Acetylcysteine	68-71	P53	Homo sapiens	143-146
34447990-6	2021	Thus, the results suggest a critical role for mitochondrially-generated H2O2 in the regulation of p53 expression, which in turn modulates XP-C sensitivity to agents that cause mitochondrial stress.	Hydrogen Peroxide	72-76	P53	Homo sapiens	98-101
34747967-4	2021	The triphosphates were substrates for DNA polymerase in the enzymatic synthesis of modified DNA probes that showed only very weak fluorescence in aqueous buffer but a significant light-up and blue shift were observed when they interacted with proteins (histone H3.1 or p53 for double-stranded DNA probes or single-strand binding protein for single-stranded oligonucleotide probes).	triphosphoric acid	4-17	P53	Homo sapiens	269-272
34887234-5	2021	The prediction was that treated water would result in increased cell proliferation, that more cells would enter the cell cycle growth phase, and that there would be increased expression of genes (NANOG, OCT4 and SOX2) associated with improved cell growth and decreased expression of genes (p16, p21, and p53) associated with a decline in cell growth.	Water	32-37	P53	Homo sapiens	304-307
34823034-14	2022	RESULTS: At 2-4 h after PDT treatment, ROS was dramatically elevated in lewis cells, DNA double-strand breaks (DDSB) occurred, as well as up-regulation of DDR proteins gamma-H2A.X, p-ATM, and p53.	Reactive Oxygen Species	39-42	P53	Homo sapiens	192-195
34832966-9	2021	Treatment of SK-N-FI and SK-N-Be(2) cells with doxorubicin, etoposide, cisplatin, and melphalan increased apoptosis and blocked the cycle in G2/M, while retinoic acid isomers induced apoptosis and decreased the percentage of cells in S phase in TP53 mutated SK-N-FI cells, but not in TP53 wild-type SK-N-Be(2) cells.	Tretinoin	153-166	P53	Homo sapiens	245-249
34832966-9	2021	Treatment of SK-N-FI and SK-N-Be(2) cells with doxorubicin, etoposide, cisplatin, and melphalan increased apoptosis and blocked the cycle in G2/M, while retinoic acid isomers induced apoptosis and decreased the percentage of cells in S phase in TP53 mutated SK-N-FI cells, but not in TP53 wild-type SK-N-Be(2) cells.	sk-n-fi	258-265	P53	Homo sapiens	245-249
34832966-10	2021	Treatment with cisplatin, melphalan, or 9-cis RA decreased p53 expression levels in SK-N-FI cells but not in SK-N-Be (2).	Cisplatin	15-24	P53	Homo sapiens	59-62
34832966-10	2021	Treatment with cisplatin, melphalan, or 9-cis RA decreased p53 expression levels in SK-N-FI cells but not in SK-N-Be (2).	Tretinoin	46-48	P53	Homo sapiens	59-62
34832966-14	2021	In conclusion, TP53 mutated SK-N-FI cells respond better to the retinoic isomers than TP53 wild-type SK-N-Be(2) cells.	sk-n-fi	28-35	P53	Homo sapiens	15-19
34783301-6	2021	The development of AIC was significantly related to Arg/Arg of p53 protein gene (OR = 2.972; p = 0.001), T/T of NOS3 gene (OR = 3.059, p = 0.018), T/T of NADPH oxidase gene (OR = 2.753, p = 0.008), and C/C of GPX1 (OR = 2.345; p = 0.007).	Arginine	56-59	P53	Homo sapiens	63-66
34834551-7	2021	Accordingly, HCC cell lines harboring mutant TP53 or wild-type CTNNB1 genes are more sensitive to paclitaxel treatment.	Paclitaxel	98-108	P53	Homo sapiens	45-49
34831372-0	2021	Redox Sensitive Cysteine Residues as Crucial Regulators of Wild-Type and Mutant p53 Isoforms.	Cysteine	16-24	P53	Homo sapiens	80-83
34834551-8	2021	Therefore, our results imply that HCC patients with mutant TP53 or wild-type CTNNB1 genes may benefit from the paclitaxel therapy.	Paclitaxel	111-121	P53	Homo sapiens	59-63
34831372-7	2021	We will also discuss therapeutic opportunities using small molecules targeting cysteines capable of modifying the structure and function of the p53 mutant isoforms in view of possible anticancer therapies for patients possessing the mutation in the TP53 gene.	Cysteine	79-88	P53	Homo sapiens	144-147
34868940-0	2021	Elevated Sodium Pump alpha3 Subunit Expression Promotes Colorectal Liver Metastasis via the p53-PTEN/IGFBP3-AKT-mTOR Axis.	Sodium	9-15	P53	Homo sapiens	92-95
34337761-7	2021	Docking studies revealed the high binding affinity of Nuatigenin at significant sites with apoptotic proteins Bcl-2, Bax, caspase-3, caspase-8, p53 and apoptosis inducing factor along with cell surface receptors estrogen receptor, projesterone receptor, epidermal growth factor receptor, and human epidermal growth factor receptor-2.	nuatigenin	54-64	P53	Homo sapiens	144-147
34610339-5	2021	Interestingly, we found that the mRNA and protein level of TP53 and PPP1R13L fluctuated as a wave in BPDE-induced malignant transformation under wild-type TP53 genetic background.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	101-105	P53	Homo sapiens	59-63
34610339-5	2021	Interestingly, we found that the mRNA and protein level of TP53 and PPP1R13L fluctuated as a wave in BPDE-induced malignant transformation under wild-type TP53 genetic background.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	101-105	P53	Homo sapiens	155-159
34599296-2	2021	APR-246 induces apoptosis by restoring transcriptional ability of mutant p53, and may be a promising therapeutic agent to overcome chemo-resistance in ESCC.	eprenetapopt	0-7	P53	Homo sapiens	73-76
34584548-9	2021	Molecular analysis based on microarray data demonstrated that podofilox altered the expression levels of genes involved in the cell cycle, c-Myc and p53 signaling.	Podophyllotoxin	62-71	P53	Homo sapiens	149-152
34425189-0	2021	3,3"-diselenodipropionic acid (DSePA) induces reductive stress in A549 cells triggering p53-independent apoptosis: A novel mechanism for diselenides.	diselenides	137-148	P53	Homo sapiens	88-91
34370268-10	2021	STAT3 inhibitor further down-regulated the expression of MMP2, MMP9, ROR1, ABCB1 and BCl2, while up-regulated the expression of p53, bax and cleaved caspase3 in HCC827 Ge-r cells treated with gefitinib, which was partially reversed by ROR1 overexpression.	Gefitinib	192-201	P53	Homo sapiens	128-131
34370268-12	2021	In conclusion, STAT3 inhibitor enhanced the antitumor effect of gefitinib on EGFR-mutated NSCLC cells through regulating ROR1/ABCB1/P53 pathway.	Gefitinib	64-73	P53	Homo sapiens	132-135
34583309-1	2021	TP53 (tumor protein 53)-induced glycolysis and apoptosis regulator (TIGAR) belongs to the phosphatases family of proteins that modulates the level of reactive oxygen species in tumor cells.	Oxygen	159-165	P53	Homo sapiens	0-4
34583309-1	2021	TP53 (tumor protein 53)-induced glycolysis and apoptosis regulator (TIGAR) belongs to the phosphatases family of proteins that modulates the level of reactive oxygen species in tumor cells.	Oxygen	159-165	P53	Homo sapiens	6-22
34715860-9	2021	The reviewed research data implies that these co-therapies exhibited a synergistic effect on various cancer cells, where apigenin sensitized the chemo drug through different pathways including a significant reduction in overexpressed genes, AKT phosphorylation, NFkappaB, inhibition of Nrf2, overexpression of caspases, up-regulation of p53 and MAPK, compared to the monotherapies.	Apigenin	121-129	P53	Homo sapiens	337-340
34799910-0	2021	P1-39: Paclitaxel induces growth inhibition in gefitinib-resistant PC9-MET cells by downregulating MDM2 and activating p53.	Paclitaxel	7-17	P53	Homo sapiens	119-122
34799910-0	2021	P1-39: Paclitaxel induces growth inhibition in gefitinib-resistant PC9-MET cells by downregulating MDM2 and activating p53.	Gefitinib	47-56	P53	Homo sapiens	119-122
34562873-10	2021	Therefore, apigenin may improve the therapeutic efficacy of 5-FU against CRC by suppressing TS, but apoptosis induction is mainly dependent on functional P53.	Apigenin	11-19	P53	Homo sapiens	154-157
34562873-10	2021	Therefore, apigenin may improve the therapeutic efficacy of 5-FU against CRC by suppressing TS, but apoptosis induction is mainly dependent on functional P53.	Fluorouracil	60-64	P53	Homo sapiens	154-157
34912912-12	2021	Moreover, kombucha increased the expression levels of p21, p53, and B-cell leukemia/lymphoma 2 (Bcl-2)-associated X protein genes (2, 2.5, and 1.5 fold, respectively) while it decreased Bcl-2 gene expression level (5-8 fold) compared with doxorubicin alone.	Doxorubicin	239-250	P53	Homo sapiens	59-62
34343634-9	2021	Moreover, RRP15 depletion in p53-mutant PLC5 and p53-deleted Hep3B cells induced metabolic shift from the glycolytic pentose-phosphate to mitochondrial oxidative phosphorylation via regulating a series of key genes such as HK2 and TIGAR, and thus, promoted the generation of ROS and apoptosis.	ros	275-278	P53	Homo sapiens	29-32
34769213-0	2021	The Role of TP53 in Cisplatin Resistance in Mediastinal and Testicular Germ Cell Tumors.	Cisplatin	20-29	P53	Homo sapiens	12-16
34769213-6	2021	The full knock-out of TP53 in 2102Ep and resistant NCCIT resulted in an increase in cisplatin resistance, suggesting a contributing role for P53, even in NCCIT, in which P53 had been reported to be non-functional.	Cisplatin	84-93	P53	Homo sapiens	22-26
34769213-6	2021	The full knock-out of TP53 in 2102Ep and resistant NCCIT resulted in an increase in cisplatin resistance, suggesting a contributing role for P53, even in NCCIT, in which P53 had been reported to be non-functional.	Cisplatin	84-93	P53	Homo sapiens	141-144
34769213-6	2021	The full knock-out of TP53 in 2102Ep and resistant NCCIT resulted in an increase in cisplatin resistance, suggesting a contributing role for P53, even in NCCIT, in which P53 had been reported to be non-functional.	Cisplatin	84-93	P53	Homo sapiens	170-173
34769213-7	2021	In conclusion, these results suggest that TP53 mutations contribute to the cisplatin-resistant phenotype of mediastinal GCTs and, therefore, are a potential candidate for targeted treatment.	Cisplatin	75-84	P53	Homo sapiens	42-46
34343634-9	2021	Moreover, RRP15 depletion in p53-mutant PLC5 and p53-deleted Hep3B cells induced metabolic shift from the glycolytic pentose-phosphate to mitochondrial oxidative phosphorylation via regulating a series of key genes such as HK2 and TIGAR, and thus, promoted the generation of ROS and apoptosis.	ros	275-278	P53	Homo sapiens	49-52
34681897-12	2021	Cotreatment with tamoxifen, an estrogen receptor inhibitor, increased the sensitivity to doxorubicin, which decreased the colony formation of P53(+) U2OS cells.	Tamoxifen	17-26	P53	Homo sapiens	142-145
34831070-8	2021	Suppressing iron metabolism by MSM also regulated p38/p53/ERK signaling and microRNA expressions, such as upregulating miR-130a and downregulating miR-221 and miR-222, which resulted in TRAIL induction and thereby extrinsic pathway of apoptosis.	Iron	12-16	P53	Homo sapiens	54-57
34786438-2	2021	This interplay is particularly evident in zinc-binding transcription factors such as the p53 tumor suppressor, whose DNA-binding activity can critically depend on levels of intracellular zinc as well as point mutations that alter either metal binding or folding stability.	Metals	237-242	P53	Homo sapiens	89-92
34768862-0	2021	p53 Transactivation Domain Mediates Binding and Phase Separation with Poly-PR/GR.	poly-pr	70-77	P53	Homo sapiens	0-3
34768862-2	2021	Recently, it was shown that poly-PR/GR alters chromatin accessibility, which results in the stabilization and enhancement of transcriptional activity of the tumor suppressor p53 in several neurodegenerative disease models.	poly-pr	28-35	P53	Homo sapiens	174-177
34768862-3	2021	A reduction in p53 protein levels protects against poly-PR and partially against poly-GR neurotoxicity in cells.	poly-pr	51-58	P53	Homo sapiens	15-18
34768862-4	2021	Moreover, in model organisms, a reduction of p53 protein levels protects against neurotoxicity of poly-PR.	poly-pr	98-105	P53	Homo sapiens	45-48
34768862-5	2021	Here, we aimed to study the detailed molecular mechanisms of how p53 contributes to poly-PR/GR-mediated neurodegeneration.	poly-pr	84-91	P53	Homo sapiens	65-68
34768862-6	2021	Using a combination of biophysical techniques such as nuclear magnetic resonance (NMR) spectroscopy, fluorescence polarization, turbidity assays, and differential interference contrast (DIC) microscopy, we found that p53 physically interacts with poly-PR/GR and triggers liquid-liquid phase separation of p53.	poly-pr	247-254	P53	Homo sapiens	217-220
34768862-8	2021	Our findings might help to understand the mechanistic role of p53 in poly-PR/GR-associated neurodegeneration.	poly-pr	69-76	P53	Homo sapiens	62-65
34478701-11	2021	Furthermore, we found shifting populations of hydrogen bonds and salt bridges reduce pair-wise electrostatic energies within p53DBD in its DNA-bound state.	Hydrogen	46-54	P53	Homo sapiens	125-128
34681897-12	2021	Cotreatment with tamoxifen, an estrogen receptor inhibitor, increased the sensitivity to doxorubicin, which decreased the colony formation of P53(+) U2OS cells.	Doxorubicin	89-100	P53	Homo sapiens	142-145
34681897-13	2021	Cell cycle arrest in the S phase was observed in P53(+) U2OS cells cotreated with low doses of doxorubicin and tamoxifen, while increased levels of apoptosis factors indicated cell death.	Doxorubicin	95-106	P53	Homo sapiens	49-52
34681897-13	2021	Cell cycle arrest in the S phase was observed in P53(+) U2OS cells cotreated with low doses of doxorubicin and tamoxifen, while increased levels of apoptosis factors indicated cell death.	Tamoxifen	111-120	P53	Homo sapiens	49-52
34628485-5	2022	Here, we show that p53 functions to support repair and recovery from CCl4-mediated liver damage, control reactive oxygen species (ROS) and limit the development of hepatocellular carcinoma (HCC), in part through the activation of a detoxification cytochrome P450, CYP2A5 (CYP2A6 in humans).	Reactive Oxygen Species	105-128	P53	Homo sapiens	19-22
34679762-0	2021	Anti-Oxidative, Anti-Inflammatory and Anti-Apoptotic Effects of Flavonols: Targeting Nrf2, NF-kappaB and p53 Pathways in Neurodegeneration.	Flavonols	64-73	P53	Homo sapiens	105-108
34679762-7	2021	Herein, we review the current understanding of the therapeutic potential and limitations of flavonols in neuroprotection, with emphasis on their anti-oxidative, anti-inflammatory and anti-apoptotic effects along the Nrf2, NF-kappaB and p53 pathways.	Flavonols	92-101	P53	Homo sapiens	236-239
34681647-9	2021	Compound 6c-induced DNA damage was characterized by comet assay, p53 phosphorylation, and gammaH2A.X, which was diminished by pretreatment with NAC.	Carbon	9-11	P53	Homo sapiens	65-68
34681647-9	2021	Compound 6c-induced DNA damage was characterized by comet assay, p53 phosphorylation, and gammaH2A.X, which was diminished by pretreatment with NAC.	Acetylcysteine	144-147	P53	Homo sapiens	65-68
34628485-5	2022	Here, we show that p53 functions to support repair and recovery from CCl4-mediated liver damage, control reactive oxygen species (ROS) and limit the development of hepatocellular carcinoma (HCC), in part through the activation of a detoxification cytochrome P450, CYP2A5 (CYP2A6 in humans).	Reactive Oxygen Species	130-133	P53	Homo sapiens	19-22
34660779-4	2021	Treatment with PAC and ATRA induced cell cycle arrest at the G2/M phase and apoptosis by upregulating p53 and caspase-8 expression and increased the intracellular calcium (Ca2+) level possibly by enhancing Ca2+ uptake via plasma membrane channels.	Paclitaxel	15-18	P53	Homo sapiens	102-105
34729253-5	2021	Likewise, CRISPR-Cas9 targeted insertion of poly(A) tracks into the coding sequence of the endogenous human genes AUF1 and TP53 results in a programmable reduction of targeted protein and mRNA levels.	Poly A	44-51	P53	Homo sapiens	123-127
34729253-8	2021	Finally, decreases in TP53 protein affect the same cellular pathways in poly(A) track-engineered cells as in cancer cells, indicating these variants" biological relevance.	Poly A	72-79	P53	Homo sapiens	22-26
34660779-4	2021	Treatment with PAC and ATRA induced cell cycle arrest at the G2/M phase and apoptosis by upregulating p53 and caspase-8 expression and increased the intracellular calcium (Ca2+) level possibly by enhancing Ca2+ uptake via plasma membrane channels.	Tretinoin	23-27	P53	Homo sapiens	102-105
34679713-0	2021	p53 Forms Redox-Dependent Protein-Protein Interactions through Cysteine 277.	Cysteine	63-71	P53	Homo sapiens	0-3
34859139-1	2021	The calcium-independent phospholipase iPLA2beta has been identified as a transcriptional target of the tumor suppressor TP53 (or p53).	Calcium	4-11	P53	Homo sapiens	120-124
34679713-4	2021	In the past few decades, p53 has been shown to be a redox-sensitive protein, and undergoes reversible cysteine oxidation both in vitro and in vivo.	Cysteine	102-110	P53	Homo sapiens	25-28
34679713-5	2021	It is not clear, however, whether p53 also forms intermolecular disulfides with interacting proteins and whether these redox-dependent interactions contribute to the regulation of p53.	Disulfides	64-74	P53	Homo sapiens	34-37
34679713-6	2021	In the present study, by combining (co-)immunoprecipitation, quantitative mass spectrometry and Western blot we found that p53 forms disulfide-dependent interactions with several proteins under oxidizing conditions.	Disulfides	133-142	P53	Homo sapiens	123-126
34679713-7	2021	Cysteine 277 is required for most of the disulfide-dependent interactions of p53, including those with 14-3-3theta and 53BP1.	Cysteine	0-8	P53	Homo sapiens	77-80
34679713-7	2021	Cysteine 277 is required for most of the disulfide-dependent interactions of p53, including those with 14-3-3theta and 53BP1.	Disulfides	41-50	P53	Homo sapiens	77-80
34692517-8	2021	High glucose instigated suppression in the intracellular accumulation of anticancer drug doxorubicin and drug-induced chromatin compactness along with declined expression of drug efflux pump MDR-1 and transcription factors and signal transducers governing the survival, aggressiveness, and apoptotic cell death (p53, HIF-1alpha, mTOR, MYC, STAT3).	Glucose	5-12	P53	Homo sapiens	312-315
34859139-1	2021	The calcium-independent phospholipase iPLA2beta has been identified as a transcriptional target of the tumor suppressor TP53 (or p53).	Calcium	4-11	P53	Homo sapiens	129-132
34607550-0	2022	Antitumor activity of zinc nanoparticles synthesized with berberine on human epithelial colorectal adenocarcinoma (Caco-2) cells through acting on Cox-2/NF-kB and p53 pathways.	Berberine	58-67	P53	Homo sapiens	163-166
34270989-6	2021	Consistent with the in vivo findings, high glucose induced endothelial senescence, impaired endothelial function and elevated DDR1 expression, accompanied by the elevation of senescence-related genes p53 and p21 expression, and these effects were reversed by DDR1 siRNA.	Glucose	43-50	P53	Homo sapiens	200-203
34270989-9	2021	In conclusion, our data demonstrated that miR-199a-3p/DDR1/p53/p21 signaling pathway was involved in endothelial senescence under diabetic conditions, and therapeutic targeting DDR1 would be exploited to inhibit endothelial senescence owing to high glucose exposure.	Glucose	249-256	P53	Homo sapiens	59-62
34608124-3	2021	In contrast, bortezomib and paclitaxel could drive U2OS or MG63 toward apoptosis effectively, suggesting that apoptosis induced by bortezomib or paclitaxel is p53-independent.	Paclitaxel	145-155	P53	Homo sapiens	159-162
34303663-6	2021	Pimozide induced G1 cell cycle arrest concomitant with the upregulation of p21/p27/p53, and suppression of cyclin D2/E, cyclin-dependent kinase 2/4/6 and c-Myc expression, and pRb phosphorylation.	Pimozide	0-8	P53	Homo sapiens	83-86
34676202-11	2021	In metformin-treated samples, the CEBPA, TP53 and USF1 transcription factors appeared to be involved in the regulation of several factors (SOD1, SOD2, CAT, GLRX, GSTP1) blocking ROS.	Metformin	3-12	P53	Homo sapiens	41-45
34676202-11	2021	In metformin-treated samples, the CEBPA, TP53 and USF1 transcription factors appeared to be involved in the regulation of several factors (SOD1, SOD2, CAT, GLRX, GSTP1) blocking ROS.	Reactive Oxygen Species	178-181	P53	Homo sapiens	41-45
34273903-6	2021	We propose this model as a reliable approach to TP53 germline variant classification and emphasize its use in contributing to optimise TP53-specific ACMG/AMP guidelines.	Adenosine Monophosphate	154-157	P53	Homo sapiens	48-52
34426149-7	2021	Thus, the novel unsaturated pyrrolidone p53-MDM2 inhibitors could be developed as novel antitumor agents.	unsaturated pyrrolidone	16-39	P53	Homo sapiens	40-43
34506766-4	2021	We also found that the accumulation of reactive oxygen species (ROS) mediated A-24 induced apoptosis is p53-independent.	Reactive Oxygen Species	39-62	P53	Homo sapiens	104-107
34506766-4	2021	We also found that the accumulation of reactive oxygen species (ROS) mediated A-24 induced apoptosis is p53-independent.	Reactive Oxygen Species	64-67	P53	Homo sapiens	104-107
34504568-12	2021	Furthermore, C5aRA prevented DOX-induced cellular senescence and decreased the levels of positive SA-beta-gal staining in H9c2 and AC16 cardiomyocytes, in addition to downregulating the expression levels of p53, p16, p21 and IGFBP3.	Doxorubicin	29-32	P53	Homo sapiens	207-210
34273903-6	2021	We propose this model as a reliable approach to TP53 germline variant classification and emphasize its use in contributing to optimise TP53-specific ACMG/AMP guidelines.	Adenosine Monophosphate	154-157	P53	Homo sapiens	135-139
34562089-5	2022	KEY FINDINGS: Oxidative stress and p53 play an important role in DOX-associated cardiotoxicity.	Doxorubicin	65-68	P53	Homo sapiens	35-38
34117917-5	2021	RESULTS: Our results demonstrated that co-administration of HPRP-A1 with iRGD increased the apoptosis, while these two peptides in combination with 5FU increased the intracellular level of p53 that upregulate the pro-apoptotic gene BAX and downregulate the anti-apoptotic gene BCL2.	Fluorouracil	148-151	P53	Homo sapiens	189-192
33875094-6	2021	The most significantly altered genes and pathways by Cu NPs exposure were NRF2 (nuclear factor erythroid 2 related factor 2)-mediated oxidative stress response, protein ubiquitination, Tumor protein p53 (p53), phase I and II metabolizing enzymes, antioxidant proteins and phase III detoxifying gene pathways.Messenger RNA-microRNA interaction from MicroRNA Target Filter Analyses revealed more signaling pathways altered in Cu NPs treated samples than transcriptomics alone, including cell proliferation, DNA methylation, endoplasmic reticulum (ER) stress, apoptosis, autophagy, reactive oxygen species, inflammation, tumorigenesis, extracellular matrix/angiogenesis and protein synthesis.	Copper	53-55	P53	Homo sapiens	199-202
33875094-6	2021	The most significantly altered genes and pathways by Cu NPs exposure were NRF2 (nuclear factor erythroid 2 related factor 2)-mediated oxidative stress response, protein ubiquitination, Tumor protein p53 (p53), phase I and II metabolizing enzymes, antioxidant proteins and phase III detoxifying gene pathways.Messenger RNA-microRNA interaction from MicroRNA Target Filter Analyses revealed more signaling pathways altered in Cu NPs treated samples than transcriptomics alone, including cell proliferation, DNA methylation, endoplasmic reticulum (ER) stress, apoptosis, autophagy, reactive oxygen species, inflammation, tumorigenesis, extracellular matrix/angiogenesis and protein synthesis.	Copper	53-55	P53	Homo sapiens	204-207
34683888-8	2021	The docking results confirmed the ability of both NPs to bind to the p53 gene with relevant potency in binding to other tested gens and participation of cysteine SH-functional group in such interaction.	Cysteine	153-161	P53	Homo sapiens	69-72
34638899-9	2021	The present results indicate a shift towards synergism in cells with mutant or null p53, treated with olaparib combined with metformin, providing a new approach to the treatment of gynecologic cancers.	Metformin	125-134	P53	Homo sapiens	84-87
34570775-13	2021	GSEA showed that the p53, WNT signaling, TGF-beta signaling pathways, etc.	gsea	0-4	P53	Homo sapiens	21-24
34562089-6	2022	DOX activates nicotinamide adenine dinucleotide phosphate NADPH oxidase (NOX) in the heart, resulting in excessive reactive oxygen species that can induce cardiomyocyte apoptosis through phosphorylation of p53, DNA damage and/or mitogen-activated protein kinases-mediated cardiomyocyte apoptosis.	Doxorubicin	0-3	P53	Homo sapiens	206-209
34562089-6	2022	DOX activates nicotinamide adenine dinucleotide phosphate NADPH oxidase (NOX) in the heart, resulting in excessive reactive oxygen species that can induce cardiomyocyte apoptosis through phosphorylation of p53, DNA damage and/or mitogen-activated protein kinases-mediated cardiomyocyte apoptosis.	NAD	14-47	P53	Homo sapiens	206-209
34562089-6	2022	DOX activates nicotinamide adenine dinucleotide phosphate NADPH oxidase (NOX) in the heart, resulting in excessive reactive oxygen species that can induce cardiomyocyte apoptosis through phosphorylation of p53, DNA damage and/or mitogen-activated protein kinases-mediated cardiomyocyte apoptosis.	Oxygen	124-130	P53	Homo sapiens	206-209
34638542-7	2021	One such pathway depends on the activation of NFkappaB by the p53/RSK1 complex through its phosphorylation at Serine 536 (pNFkappaB Ser536).	Serine	110-116	P53	Homo sapiens	62-65
34479596-8	2021	RESULTS: CAP treatment resulted in a significant downregulation of p53 and apoptotic protease activating factor (APAF)-1, caspase (CASP)9, CASP3, BCL2 Antagonist/Killer (BAK)1, and B-Cell Lymphoma (BCL)2 mRNA expression at 1 d. An inhibitory effect of CAP on apoptotic genes was also shown under inflammatory and apoptotic conditions.	cap	9-12	P53	Homo sapiens	67-70
34572923-5	2021	Additionally, we have illustrated how commonly deregulated signaling pathways in PC (PI3K/AKT/MTOR, MAPK, AR and p53) are linked with cholesterol homeostasis regulation.	Cholesterol	134-145	P53	Homo sapiens	113-116
34528900-0	2021	Metformin-induced chemosensitization to cisplatin depends on P53 status and is inhibited by Jarid1b overexpression in non-small cell lung cancer cells.	Metformin	0-9	P53	Homo sapiens	61-64
34528900-0	2021	Metformin-induced chemosensitization to cisplatin depends on P53 status and is inhibited by Jarid1b overexpression in non-small cell lung cancer cells.	Cisplatin	40-49	P53	Homo sapiens	61-64
34528900-3	2021	Here we test if the presence of P53 could predict the activity of metformin as an adjuvant for cisplatin-based therapy in non-small cell lung cancer (NSCLC).	Metformin	66-75	P53	Homo sapiens	32-35
34528900-3	2021	Here we test if the presence of P53 could predict the activity of metformin as an adjuvant for cisplatin-based therapy in non-small cell lung cancer (NSCLC).	Cisplatin	95-104	P53	Homo sapiens	32-35
34528900-7	2021	Metformin sensitized A549 and HCC 827 cells (but not H1299 and H358 cells) to cisplatin in a P53-dependent manner, changing its subcellular localization to the mitochondria.	Metformin	0-9	P53	Homo sapiens	93-96
34217708-5	2021	Phosphorylation of p53 at serines 15 and 20 may be one of the pivotal factors for cell cycle arrest and apoptosis after treatment of iso-suillin in A549 cells.	Serine	26-33	P53	Homo sapiens	19-22
34502536-4	2021	Long-term exposure to TiO2 nanoparticles co-doped with 1% of iron and nitrogen led to the alteration of p53 protein activity and the gene expression controlled by this suppressor (NF-kB and mdm2), DNA damage, cell cycle disruptions at the G2/M and S phases, and lysosomal membrane permeabilization and the subsequent release of cathepsin B, triggering the intrinsic pathway of apoptosis in a Bax- and p53-independent manner.	Iron	61-65	P53	Homo sapiens	104-107
34502536-4	2021	Long-term exposure to TiO2 nanoparticles co-doped with 1% of iron and nitrogen led to the alteration of p53 protein activity and the gene expression controlled by this suppressor (NF-kB and mdm2), DNA damage, cell cycle disruptions at the G2/M and S phases, and lysosomal membrane permeabilization and the subsequent release of cathepsin B, triggering the intrinsic pathway of apoptosis in a Bax- and p53-independent manner.	Iron	61-65	P53	Homo sapiens	401-404
34502536-4	2021	Long-term exposure to TiO2 nanoparticles co-doped with 1% of iron and nitrogen led to the alteration of p53 protein activity and the gene expression controlled by this suppressor (NF-kB and mdm2), DNA damage, cell cycle disruptions at the G2/M and S phases, and lysosomal membrane permeabilization and the subsequent release of cathepsin B, triggering the intrinsic pathway of apoptosis in a Bax- and p53-independent manner.	Nitrogen	70-78	P53	Homo sapiens	104-107
34502536-4	2021	Long-term exposure to TiO2 nanoparticles co-doped with 1% of iron and nitrogen led to the alteration of p53 protein activity and the gene expression controlled by this suppressor (NF-kB and mdm2), DNA damage, cell cycle disruptions at the G2/M and S phases, and lysosomal membrane permeabilization and the subsequent release of cathepsin B, triggering the intrinsic pathway of apoptosis in a Bax- and p53-independent manner.	Nitrogen	70-78	P53	Homo sapiens	401-404
34500819-4	2021	Then, they discovered that these organo-ruthenium/osmium complexes could act independently of DNA damage and bypass the requirement for the tumor suppressor gene TP53 to induce the endoplasmic reticulum (ER) stress pathway, which is an original cell death pathway.	organo-ruthenium	33-49	P53	Homo sapiens	162-166
34500819-4	2021	Then, they discovered that these organo-ruthenium/osmium complexes could act independently of DNA damage and bypass the requirement for the tumor suppressor gene TP53 to induce the endoplasmic reticulum (ER) stress pathway, which is an original cell death pathway.	Osmium	50-56	P53	Homo sapiens	162-166
34528900-7	2021	Metformin sensitized A549 and HCC 827 cells (but not H1299 and H358 cells) to cisplatin in a P53-dependent manner, changing its subcellular localization to the mitochondria.	Cisplatin	78-87	P53	Homo sapiens	93-96
34528900-8	2021	Treatment with a sub-lethal dose of cisplatin increased Jarid1b expression, yet downregulated P53 levels, protecting A549Res cells from metformin-induced chemosensitization to cisplatin and favored a glycolytic phenotype.	Cisplatin	36-45	P53	Homo sapiens	94-97
34528900-8	2021	Treatment with a sub-lethal dose of cisplatin increased Jarid1b expression, yet downregulated P53 levels, protecting A549Res cells from metformin-induced chemosensitization to cisplatin and favored a glycolytic phenotype.	Metformin	136-145	P53	Homo sapiens	94-97
34528900-8	2021	Treatment with a sub-lethal dose of cisplatin increased Jarid1b expression, yet downregulated P53 levels, protecting A549Res cells from metformin-induced chemosensitization to cisplatin and favored a glycolytic phenotype.	Cisplatin	176-185	P53	Homo sapiens	94-97
34528900-10	2021	In conclusion, metformin could potentially be used as an adjuvant for cisplatin-based therapy in NSCLC cells if wild type P53 is present.	Metformin	15-24	P53	Homo sapiens	122-125
34216644-0	2021	Cytoskeleton-associated protein 2 (CKAP2) is regulated by vascular endothelial growth factor and p53 in retinal capillary endothelial cells under high-glucose conditions.	Glucose	151-158	P53	Homo sapiens	97-100
34539974-11	2021	Progesterone replacement therapy induced a significant increase in MnSOD, P53, sestrin 2 (SENS2), and TERF2 mRNA expression when compared to basal conditions.	Progesterone	0-12	P53	Homo sapiens	74-77
34503286-1	2021	APR-246 (Eprenetapopt/PRIMA-1Met) is a very potent anti-cancer drug in clinical trials and was initially developed as a p53 refolding agent.	eprenetapopt	0-7	P53	Homo sapiens	120-123
34500758-0	2021	Chemo-Preventive Action of Resveratrol: Suppression of p53-A Molecular Targeting Approach.	Resveratrol	27-38	P53	Homo sapiens	55-58
34500758-6	2021	This review aims to collect and present the latest published studies on resveratrol and its impact on cancer prevention, molecular signals (especially p53 protein participation), and its therapeutic prospects.	Resveratrol	72-83	P53	Homo sapiens	151-154
34166715-1	2021	In our previous study, it showed that P-3F, a podophyllotoxin derivative, causes the increased level of p53 expression by enhancing p53 stability, resulting from blockage of the Mdm2-p53 feedback loop via nucleolus-to-nucleoplasm translocation of Rps27a in human cervical cancer HeLa cell line.	Podophyllotoxin	46-61	P53	Homo sapiens	104-107
34166715-4	2021	Also remarkably, reduction of serine phosphorylation of STMN1 at position 16 induced by P-3F was required in the downregulation of PICT1, in which p53 activity was likely to be directly involved.	Serine	30-36	P53	Homo sapiens	147-150
34166715-1	2021	In our previous study, it showed that P-3F, a podophyllotoxin derivative, causes the increased level of p53 expression by enhancing p53 stability, resulting from blockage of the Mdm2-p53 feedback loop via nucleolus-to-nucleoplasm translocation of Rps27a in human cervical cancer HeLa cell line.	Podophyllotoxin	46-61	P53	Homo sapiens	132-135
34212455-5	2021	MK-1775 synergized with CDDP to block proliferation, inducing apoptosis and mitotic catastrophe in TP53-mutant UC cells but not in TP53-wild-type cells.	Cisplatin	24-28	P53	Homo sapiens	99-103
34080040-7	2021	All patients with CCNE1 amplification (n = 7), TP53 R175H substitution (n = 6), and RB1 mutation (n = 4) had poor response to paclitaxel plus carboplatin.	Paclitaxel	126-136	P53	Homo sapiens	47-51
34212455-6	2021	Knocking down TP53 in TP53-wild-type cells induced synergism of MK-1775 and CDDP.	Cisplatin	76-80	P53	Homo sapiens	14-18
34212455-6	2021	Knocking down TP53 in TP53-wild-type cells induced synergism of MK-1775 and CDDP.	Cisplatin	76-80	P53	Homo sapiens	22-26
34697746-8	2021	The viability, migration, and mitochondrial transmembrane potential of GC cells increased in association with decreased levels of ROS and mitochondrial apoptosis in the P53-silenced group.	Reactive Oxygen Species	130-133	P53	Homo sapiens	169-172
34212455-7	2021	In UMUC3 cell xenografts and two patient-derived xenograft lines with MDM2 overexpression, in which the p53/cell cycle pathway was inactivated, AZD-1775 combined with CDDP suppressed tumor growth inducing both M-phase entry and apoptosis, whereas AZD-1775 alone was as effective as the combination in RT4 cell xenografts.	Cisplatin	167-171	P53	Homo sapiens	104-107
34212455-11	2021	Differential anti-tumor efficacy of WEE1 blockade alone or combined with CDDP may exist according to p53/cell cycle pathway activity, which may be predictable using an ex vivo 3D primary culture system.	Cisplatin	73-77	P53	Homo sapiens	101-104
34383983-8	2021	After exposure to BPDE or in RM tissues, p53 was upregulated, which might promote p53-mediated lnc-HZ04 transcription.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	18-22	P53	Homo sapiens	41-44
34369624-5	2021	Among these, the p53-responsive carbohydrate metabolic genes Tp53-induced glycolysis and apoptosis regulator (TIGAR) and Cytochrome C Oxidase assembly protein 2 (SCO2), which are the key regulators of glycolysis and oxidative phosphorylation respectively, are under direct regulation of TCF19.	Carbohydrates	32-44	P53	Homo sapiens	17-20
34369624-6	2021	Remarkably, TCF19 can form different transcription activation/repression complexes which show substantial overlap with that of p53, depending on glucose-mediated variant stress situations as obtained from IP/MS studies.	Glucose	145-152	P53	Homo sapiens	127-130
34369624-7	2021	Interestingly, we observed that TCF19/p53 complexes either have CBP or HDAC1 to epigenetically program the expression of TIGAR and SCO2 genes depending on short-term high glucose or prolonged high glucose conditions.	Glucose	171-178	P53	Homo sapiens	38-41
34369624-7	2021	Interestingly, we observed that TCF19/p53 complexes either have CBP or HDAC1 to epigenetically program the expression of TIGAR and SCO2 genes depending on short-term high glucose or prolonged high glucose conditions.	Glucose	197-204	P53	Homo sapiens	38-41
34369624-8	2021	TCF19 or p53 knockdown significantly altered the cellular lactate production and led to increased extracellular acidification rate.	Lactic Acid	58-65	P53	Homo sapiens	9-12
34369624-9	2021	Similarly, OCR and cellular ATP production were reduced and mitochondrial membrane potential was compromised upon depletion of TCF19 or p53.	Adenosine Triphosphate	28-31	P53	Homo sapiens	136-139
34383983-8	2021	After exposure to BPDE or in RM tissues, p53 was upregulated, which might promote p53-mediated lnc-HZ04 transcription.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	18-22	P53	Homo sapiens	82-85
34314818-4	2021	EAA pretreatment increased the HaCaT cell viability but suppressed ROS-mediated p53/POMC/alpha-MSH pathways in UVA-irradiated cells.	ros	67-70	P53	Homo sapiens	80-83
34298093-7	2021	Heme-iron induced lipid peroxidation and DNA oxidation by interacting with Nox4-independent mechanisms, promoting p53/p21 activity and cellular senescence.	Iron	5-9	P53	Homo sapiens	114-117
34502426-8	2021	The effect of resveratrol and IR enhanced the expression of apoptotic genes, such as Bax, p53, and caspase 8, leading to apoptosis.	Resveratrol	14-25	P53	Homo sapiens	90-93
34314818-4	2021	EAA pretreatment increased the HaCaT cell viability but suppressed ROS-mediated p53/POMC/alpha-MSH pathways in UVA-irradiated cells.	3-O-ethylascorbic acid	0-3	P53	Homo sapiens	80-83
34647281-7	2021	Furthermore, D-galactose increased the mRNA expression of p16, p21, and p53.	Galactose	13-24	P53	Homo sapiens	72-75
34082063-4	2021	TP53-induced glycolysis and apoptotic regulators (TIGAR) may facilitate the production of nicotinamide adenine dinucleotide phosphoric acid (NADPH) via the pentose phosphate pathway (PPP) to inhibit oxidative stress and neuroinflammation.	nicotinamide adenine dinucleotide phosphoric acid	90-139	P53	Homo sapiens	0-4
34331475-0	2021	Curcumin induced G2/M cycle arrest in SK-N-SH neuroblastoma cells through the ROS-mediated p53 signaling pathway.	Curcumin	0-8	P53	Homo sapiens	91-94
34331475-0	2021	Curcumin induced G2/M cycle arrest in SK-N-SH neuroblastoma cells through the ROS-mediated p53 signaling pathway.	ros	78-81	P53	Homo sapiens	91-94
34331475-6	2021	Furthermore, curcumin promoted the overproduction of intracellular ROS and apoptosis induced by activating p53 and Bcl-2 signal pathways.	Curcumin	13-21	P53	Homo sapiens	107-110
34331475-6	2021	Furthermore, curcumin promoted the overproduction of intracellular ROS and apoptosis induced by activating p53 and Bcl-2 signal pathways.	ros	67-70	P53	Homo sapiens	107-110
34144191-1	2021	Stabilization and activation of the p53 tumor suppressor are triggered in response to various cellular stresses, including DNA damaging agents and elevated Reactive Oxygen Species (ROS) like H2O2.	Reactive Oxygen Species	156-179	P53	Homo sapiens	36-39
34192651-0	2021	TP53 mutations in circulating tumor DNA in advanced epidermal growth factor receptor-mutant lung adenocarcinoma patients treated with gefitinib.	Gefitinib	134-143	P53	Homo sapiens	0-4
34192651-11	2021	Patients with TP53 mutations, especially in exons 6 and 7, had a lower response rate and shorter PFS and OS when treated with gefitinib.	Gefitinib	126-135	P53	Homo sapiens	14-18
34126112-0	2021	A coordinated ruthenium-rifampicin complex reprogramming the colon carcinoma micro-environment mediated by modulation of p53/AkT/mTOR/VEGF pathway.	ruthenium-rifampicin	14-34	P53	Homo sapiens	121-124
34126112-7	2021	Along with that, p53 could be modulated by the ruthenium-rifampicin complex to interfere with apoptosis in colon carcinoma, initiated by the intrinsic apoptotic trail facilitated through Bcl2 and Bax, thus controlling the Akt/mTOR/VEGF pathway coupled through the WNT/beta-catenin trail.	ruthenium-rifampicin	47-67	P53	Homo sapiens	17-20
34577580-6	2021	Our network and pathway analyses implicated the four targets of AKT1, RELA, MAPK1, and TP53 that could be involved in the inhibitory effects of curcumin on influenza.	Curcumin	144-152	P53	Homo sapiens	87-91
34144191-1	2021	Stabilization and activation of the p53 tumor suppressor are triggered in response to various cellular stresses, including DNA damaging agents and elevated Reactive Oxygen Species (ROS) like H2O2.	Reactive Oxygen Species	181-184	P53	Homo sapiens	36-39
34144191-1	2021	Stabilization and activation of the p53 tumor suppressor are triggered in response to various cellular stresses, including DNA damaging agents and elevated Reactive Oxygen Species (ROS) like H2O2.	Hydrogen Peroxide	191-195	P53	Homo sapiens	36-39
34144191-4	2021	However, H2O2 also induces signaling through stress-activated kinases (SAPK, e.g., JNK and p38MAPK) that can activate p53.	Hydrogen Peroxide	9-13	P53	Homo sapiens	118-121
34445588-5	2021	It describes a protein-protein interaction network that indicates highly dysregulated TP53, MDM2, and CDKN1A genes as they encode the top networking proteins that may be involved in cisplatin tolerance, these all being upregulated in cisplatin-resistant cells.	Cisplatin	182-191	P53	Homo sapiens	86-90
34417460-2	2021	Deficiency or excess of nutrients causes cellular metabolic stress, and we hypothesized that p53 could be linked to glucose maintenance.	Glucose	116-123	P53	Homo sapiens	93-96
34417460-8	2021	Finally, protein levels of p53, as well as genes responsible of O-GlcNAcylation are elevated in the liver of type 2 diabetic patients and positively correlate with glucose and HOMA-IR.	Glucose	164-171	P53	Homo sapiens	27-30
34410893-0	2021	Calcium-oxidative stress signaling axis and casein kinase 1alpha mediate eryptosis and hemolysis elicited by novel p53 agonist inauhzin.	inauzhin	127-135	P53	Homo sapiens	115-118
34410893-1	2021	Inauhzin (INZ) is a novel p53 agonist with antitumor activity.	inauzhin	0-8	P53	Homo sapiens	26-29
34410893-1	2021	Inauhzin (INZ) is a novel p53 agonist with antitumor activity.	inauzhin	10-13	P53	Homo sapiens	26-29
34445588-5	2021	It describes a protein-protein interaction network that indicates highly dysregulated TP53, MDM2, and CDKN1A genes as they encode the top networking proteins that may be involved in cisplatin tolerance, these all being upregulated in cisplatin-resistant cells.	Cisplatin	234-243	P53	Homo sapiens	86-90
34365455-6	2021	Our results clearly show that acute low-dose doxorubicin treatment-induced senescence, as evidenced by morphological and molecular markers, including enlarged and flattened nuclei, DNA damage response foci, and increased expression of cell cycle inhibitor p16INK4a, p53, and ROS.	Doxorubicin	45-56	P53	Homo sapiens	266-269
34445495-3	2021	Previously, we have demonstrated that the combined inhibition of EGFR and MDM2-p53 pathways, by gefitinib and JNJ-26854165, exerts a strong synergistic lethal effect on HGSOC cells.	Gefitinib	96-105	P53	Homo sapiens	79-82
34445495-5	2021	The targeted inhibition responses of gefitinib and JNJ-26854165, in p53R248Q-overexpressing cells, were extensively evaluated.	Gefitinib	37-46	P53	Homo sapiens	68-71
34445495-9	2021	Next, we analyzed the gefitinib and JNJ-26854165 responses and found differential sensitivity to the single- or combined-drug inhibitions in p53R248Q-overexpressing cells.	Gefitinib	22-31	P53	Homo sapiens	141-144
34452218-3	2021	This innovative approach explored the great capacity of both polyamidoamine (PAMAM)-paclitaxel (PTX) conjugate and polyethylenimine (PEI) polymers to complex a p53-encoding plasmid DNA (pDNA), highlighting the utility of considering two compacting agents.	Paclitaxel	84-94	P53	Homo sapiens	160-163
34393505-5	2021	Results: The distribution of TP53 Pro72Arg differed in T2DM patients from the controls, with a moderately increased proportion of TP53 Arg72 variant carriers (Pro/Arg and Arg/Arg genotypes) (88.3% vs 81.2%, p=0.022; OR=1.089, 95% CI=1.018-1.164).	Arginine	163-166	P53	Homo sapiens	29-33
34393505-5	2021	Results: The distribution of TP53 Pro72Arg differed in T2DM patients from the controls, with a moderately increased proportion of TP53 Arg72 variant carriers (Pro/Arg and Arg/Arg genotypes) (88.3% vs 81.2%, p=0.022; OR=1.089, 95% CI=1.018-1.164).	Arginine	163-166	P53	Homo sapiens	130-134
34393505-5	2021	Results: The distribution of TP53 Pro72Arg differed in T2DM patients from the controls, with a moderately increased proportion of TP53 Arg72 variant carriers (Pro/Arg and Arg/Arg genotypes) (88.3% vs 81.2%, p=0.022; OR=1.089, 95% CI=1.018-1.164).	Arginine	171-174	P53	Homo sapiens	29-33
34393505-5	2021	Results: The distribution of TP53 Pro72Arg differed in T2DM patients from the controls, with a moderately increased proportion of TP53 Arg72 variant carriers (Pro/Arg and Arg/Arg genotypes) (88.3% vs 81.2%, p=0.022; OR=1.089, 95% CI=1.018-1.164).	Arginine	171-174	P53	Homo sapiens	130-134
34393505-5	2021	Results: The distribution of TP53 Pro72Arg differed in T2DM patients from the controls, with a moderately increased proportion of TP53 Arg72 variant carriers (Pro/Arg and Arg/Arg genotypes) (88.3% vs 81.2%, p=0.022; OR=1.089, 95% CI=1.018-1.164).	Arginine	175-178	P53	Homo sapiens	29-33
34393505-5	2021	Results: The distribution of TP53 Pro72Arg differed in T2DM patients from the controls, with a moderately increased proportion of TP53 Arg72 variant carriers (Pro/Arg and Arg/Arg genotypes) (88.3% vs 81.2%, p=0.022; OR=1.089, 95% CI=1.018-1.164).	Arginine	175-178	P53	Homo sapiens	130-134
34393505-8	2021	Conclusion: There was a significant association of the TP53 Pro72Arg polymorphism with susceptibility to T2DM, and the homozygous Arg/Arg genotype of this gene locus might be a protective factor for diabetic complications.	Arginine	130-133	P53	Homo sapiens	55-59
34393505-8	2021	Conclusion: There was a significant association of the TP53 Pro72Arg polymorphism with susceptibility to T2DM, and the homozygous Arg/Arg genotype of this gene locus might be a protective factor for diabetic complications.	Arginine	134-137	P53	Homo sapiens	55-59
34340691-14	2021	La3+, Ce3+, and F- are probably the main toxic substances in WSPM, and may be regulate the A549 cell cycle by affecting the expression of genes, such as MDM2, RB1, ATM, TP53, E2F1, CDK2 and CDK4.	lanthanum(3+)	0-4	P53	Homo sapiens	169-173
34151400-7	2021	Based on analysis of the differentially expressed genes, the most prominent molecular pathways affected by 5-FU included cell cycle, p53 signalling, mitochondrial ATP synthesis and apoptosis.	Fluorouracil	107-111	P53	Homo sapiens	133-136
34130091-0	2021	Restoring NAD+ by NAMPT is essential for the SIRT1/p53-mediated survival of UVA- and UVB-irradiated epidermal keratinocytes.	NAD	10-14	P53	Homo sapiens	51-54
34216619-0	2021	STING-mediated degradation of IFI16 negatively regulates apoptosis by inhibiting p53 phosphorylation at serine-392.	Serine	104-110	P53	Homo sapiens	81-84
34216619-5	2021	Protein kinase R (PKR)-triggered phosphorylation of p53 at serine-392 (Ser392) is critical for the IFI16-p53-dependent apoptosis.	Serine	59-65	P53	Homo sapiens	52-55
34216619-5	2021	Protein kinase R (PKR)-triggered phosphorylation of p53 at serine-392 (Ser392) is critical for the IFI16-p53-dependent apoptosis.	Serine	59-65	P53	Homo sapiens	105-108
34130091-9	2021	Moreover, the NAMPT inhibitor abrogated the sirtuin-1 (SIRT1)-mediated deacetylation of p53 and significantly inhibited the proliferation of UVA/B-irradiated cells, suggesting that the NAMPT-NAD+-SIRT1 axis regulates p53 functions upon UVA/B stress.	NAD	191-195	P53	Homo sapiens	88-91
34130091-9	2021	Moreover, the NAMPT inhibitor abrogated the sirtuin-1 (SIRT1)-mediated deacetylation of p53 and significantly inhibited the proliferation of UVA/B-irradiated cells, suggesting that the NAMPT-NAD+-SIRT1 axis regulates p53 functions upon UVA/B stress.	NAD	191-195	P53	Homo sapiens	217-220
34261004-5	2021	From a list of differential expressed genes, cisplatin downregulated the cyclin-dependent kinase inhibitor 1 (CDKN1A), tumor necrosis factor (FAS), and sestrin-1 (SESN1) genes responsible for modifying signaling pathways, including the p53, JAK-STAT, FOXO, MAPK, mTOR, P13-AKT, Toll-like receptor (TLR), adipocytokine, and insulin signaling pathways.	Cisplatin	45-54	P53	Homo sapiens	236-239
34165168-0	2021	MicroRNA-10b modulates cisplatin tolerance by targeting p53 directly in lung cancer cells.	Cisplatin	23-32	P53	Homo sapiens	56-59
34149899-6	2021	Compared with the PBS control group, the A549, A549/DDP and A549/Taxol cells treated with NaI131, GA or a combination of the drugs exhibited G2/M arrest and increased percentages of total apoptotic cells, as well as significantly decreased protein levels of CDK1, cyclin B, mtp53, HSP90, Bcl-2 and P-gp, increased protein levels of Bax and decreased mRNA levels of p53 and HSP90.	nai131	90-96	P53	Homo sapiens	365-368
34165168-6	2021	In functional assays, upregulation of the p53 signaling pathway following cisplatin treatment was associated with decreased levels of miR-10b and upregulation of the luciferase activity of wild-type, but not 1,584, 2,032-dual-mutant, p53 3"-UTR.	Cisplatin	74-83	P53	Homo sapiens	42-45
34165168-7	2021	The ectopic expression of miR-10b-agomir attenuated the stability of p53 3"-UTR and the expression of p53 and its downstream effectors induced by cisplatin.	Cisplatin	146-155	P53	Homo sapiens	69-72
34165168-7	2021	The ectopic expression of miR-10b-agomir attenuated the stability of p53 3"-UTR and the expression of p53 and its downstream effectors induced by cisplatin.	Cisplatin	146-155	P53	Homo sapiens	102-105
34244606-8	2021	Overall, this study proposes a novel strategy of VM suppression through Chk2 induction, which prevents PKM2-mediated glucose flux in p53-mutated TNBC.	Glucose	117-124	P53	Homo sapiens	133-136
34165168-8	2021	By contrast, the knockdown of miR-10b induced the stability of p53 3"-UTR and increased levels of p53 and the sensitivity of A549 cells to cisplatin treatment.	Cisplatin	139-148	P53	Homo sapiens	63-66
34165168-8	2021	By contrast, the knockdown of miR-10b induced the stability of p53 3"-UTR and increased levels of p53 and the sensitivity of A549 cells to cisplatin treatment.	Cisplatin	139-148	P53	Homo sapiens	98-101
34165168-12	2021	These findings indicate a novel pathway in which cisplatin induces the levels of p53 by increasing mRNA stability via miR-10b, indicating a novel oncogenic role of miR-10b in promoting the malignant characteristics of non-small cell lung carcinoma.	Cisplatin	49-58	P53	Homo sapiens	81-84
34309458-9	2022	The increase in p53, Bax, p38 MAPK, and PTEN gene expression levels compared to the control group was 1.71, 1.42, 3.26, and 3.29-fold with 5-FU + L treatment, respectively, while this increase was 8.43, 1.65, 3.55, and 3.54-fold with 5-FU + Q treatment, respectively.	Fluorouracil	139-143	P53	Homo sapiens	16-19
34452150-6	2021	Simultaneously, 5-FU determined the increase of p53 and caspase-1 expressions, both at gene and protein levels.	Fluorouracil	16-20	P53	Homo sapiens	48-51
34395436-7	2021	The 6,542 decreased chromatin-accessible regions were identified for the declined doxorubicin-associated biological processes, for instance, endocrine and insulin resistance, central carbon metabolism, signaling pathways of TGF-beta and P53.	Doxorubicin	82-93	P53	Homo sapiens	237-240
34395447-0	2021	The p53 Family: A Role in Lipid and Iron Metabolism.	Iron	36-40	P53	Homo sapiens	4-7
34395447-3	2021	In this review, we strive to cover the relevant studies that demonstrate the roles of p53, p63, and p73 in lipid and iron metabolism.	Iron	117-121	P53	Homo sapiens	86-89
34315513-14	2021	Instead, sublethal Dox induces expression of multiple SFK-including Fyn, Yes, and Src-partly in a p53 and ATR-dependent manner.	Doxorubicin	19-22	P53	Homo sapiens	98-101
34309458-9	2022	The increase in p53, Bax, p38 MAPK, and PTEN gene expression levels compared to the control group was 1.71, 1.42, 3.26, and 3.29-fold with 5-FU + L treatment, respectively, while this increase was 8.43, 1.65, 3.55, and 3.54-fold with 5-FU + Q treatment, respectively.	Fluorouracil	234-238	P53	Homo sapiens	16-19
34255515-3	2021	The bromodomains of CREBBP and EP300 enable the binding of acetylated lysine residues from histones and a number of other important proteins, including p53, p73, E2F, and GATA1.	Lysine	70-76	P53	Homo sapiens	152-155
34405016-5	2021	Interestingly, massive accumulation of ROS inhibits tumor growth in two ways: (1) by blocking cancer cell proliferation by suppressing the proliferation signaling pathway, cell cycle, and the biosynthesis of nucleotides and ATP and (2) by inducing cancer cell death via activating endoplasmic reticulum stress-, mitochondrial-, and P53- apoptotic pathways and the ferroptosis pathway.	Reactive Oxygen Species	39-42	P53	Homo sapiens	332-335
34301789-7	2021	Our studies reveal an unexpected role for mitochondria downstream of NPM1c and implicate a mitochondrial/ROS/PML/TP53 senescence pathway as an effector of ActD-based therapies.	ros	105-108	P53	Homo sapiens	113-117
34301750-0	2021	Phase 1 Trial of ALRN-6924, a Dual Inhibitor of MDMX and MDM2, in Patients with Solid Tumors and Lymphomas Bearing Wild-Type TP53.	alrn-6924	17-26	P53	Homo sapiens	125-129
34301750-1	2021	PURPOSE: We describe the first-in-human dose-escalation trial for ALRN-6924, a stabilized, cell-permeating peptide that disrupts p53 inhibition by MDM2 and MDMX to induce cell cycle arrest or apoptosis in TP53 wild-type tumors.	alrn-6924	66-75	P53	Homo sapiens	129-132
34301750-1	2021	PURPOSE: We describe the first-in-human dose-escalation trial for ALRN-6924, a stabilized, cell-permeating peptide that disrupts p53 inhibition by MDM2 and MDMX to induce cell cycle arrest or apoptosis in TP53 wild-type tumors.	alrn-6924	66-75	P53	Homo sapiens	205-209
34301750-4	2021	ALRN-6924 showed dose-dependent pharmacokinetics and increased serum levels of MIC-1, a biomarker of p53 activation.	alrn-6924	0-9	P53	Homo sapiens	101-104
34270461-7	2021	Mechanically, upon interaction with p53, BMI1 was recruited on the promoter of miR-3682-3p gene concomitant with an increase in the mono-ubiquitination of histone H2A lysine 119, leading to transcription repression of miR-3682-3p gene followed by derepression of ABCB1 (ATP binding cassette subfamily B member 1) gene.	Lysine	167-173	P53	Homo sapiens	36-39
34335745-13	2021	GSEA revealed that gene sets correlated with biological processes including cell cycle, DNA replication, base excision repair, and P53 signaling pathway were highly enriched in high-risk group.	gsea	0-4	P53	Homo sapiens	131-134
34285189-4	2021	Therefore, we aimed to investigate the involvement of radiosensitivity, cell death modalities and p53 status in response to carbon-ion radiation (CIR) here.	Carbon	124-130	P53	Homo sapiens	98-101
34244426-2	2021	Here, we show that the mitochondrial methylenetetrahydrofolate dehydrogenase (MTHFD2) is transcriptionally suppressed by p53, and its up-regulation by p53 inactivation leads to increased folate metabolism, de novo purine synthesis, and tumor growth in vivo and in vitro.	Folic Acid	187-193	P53	Homo sapiens	151-154
34335587-12	2021	In the mechanistic study, we found that the induction of p53 deacetylation, due to either the resveratrol/quercetin -induced activation of the deacetylase Sirtuin 1 (Sirt1) or the mutation of the acetylated lysine site in p53, promoted RTEC autophagy and alleviated SAKI.	Resveratrol	94-105	P53	Homo sapiens	57-60
34335587-12	2021	In the mechanistic study, we found that the induction of p53 deacetylation, due to either the resveratrol/quercetin -induced activation of the deacetylase Sirtuin 1 (Sirt1) or the mutation of the acetylated lysine site in p53, promoted RTEC autophagy and alleviated SAKI.	Lysine	207-213	P53	Homo sapiens	57-60
34335587-12	2021	In the mechanistic study, we found that the induction of p53 deacetylation, due to either the resveratrol/quercetin -induced activation of the deacetylase Sirtuin 1 (Sirt1) or the mutation of the acetylated lysine site in p53, promoted RTEC autophagy and alleviated SAKI.	Lysine	207-213	P53	Homo sapiens	222-225
34298945-6	2021	D-Gal treatment significantly increased the expression levels of senescence markers, such as p53 and p21, in the heart and hippocampal tissues, while this effect was reversed in the Lico D-treated animals.	Galactose	0-5	P53	Homo sapiens	93-96
34298639-6	2021	The current review has highlighted the anticancer activity of curcumin in hormone-independent breast cancer via focusing on its impact on key signaling pathways including the PI3K/Akt/mTOR pathway, JAK/STAT pathway, MAPK pathway, NF-kB pathway, p53 pathway, and Wnt/beta-catenin, as well as apoptotic and cell cycle pathways.	Curcumin	62-70	P53	Homo sapiens	245-248
34298618-9	2021	Collectively, our findings implicate nuclear HKII-P-p53(Ser15) interaction in chemosensitivity and could provide an effective clinical strategy as a promising biomarker during platinum-based therapy.	Platinum	176-184	P53	Homo sapiens	52-55
34281219-2	2021	The exquisite cisplatin sensitivity has been mainly explained by the over-expression in GCTs of wild-type TP53 protein and the lack of TP53 somatic mutations; however, several other mechanisms seem to be involved, many of which remain still elusive.	Cisplatin	14-23	P53	Homo sapiens	106-110
34306024-11	2021	GSEA enrichment analysis revealed significant differences in high- and low-risk groups in pathways like pentose phosphate pathway, ubiquitin mediated proteolysis, and P53 signaling pathway.	gsea	0-4	P53	Homo sapiens	167-170
34282771-14	2021	(4) Conclusions: TP53 mutations are associated with shorter DFS and increased response to anthracyclines.	Anthracyclines	90-104	P53	Homo sapiens	17-21
34224393-11	2021	Furthermore, GSEA demonstrated that this signature was involved in many cancer-related pathways, including TGF-beta, p53, mTOR and WNT signaling pathway.	gsea	13-17	P53	Homo sapiens	117-120
34281219-2	2021	The exquisite cisplatin sensitivity has been mainly explained by the over-expression in GCTs of wild-type TP53 protein and the lack of TP53 somatic mutations; however, several other mechanisms seem to be involved, many of which remain still elusive.	Cisplatin	14-23	P53	Homo sapiens	135-139
34281219-4	2021	In the following report we explore the complex role of TP53 in GCTs cisplatin-sensitivity and resistance mechanisms, passing through several recent genomic studies, as well as its role in GCT patients with SCs, going through our experience of Center of reference for both GCTs and cancer predisposing syndromes.	Cisplatin	68-77	P53	Homo sapiens	55-59
34302638-3	2021	G-Rg2 significantly inhibited protein and mRNA expression of cell cycle G1-S phase regulators, including p-Rb, cyclin D1, CDK4, and CDK6, whereas it enhanced the protein and mRNA expression of cell cycle arrest and apoptotic molecules including cleaved PARP, p21, p27, p53 and Bak through ROS production.	ginsenoside Rg2	0-5	P53	Homo sapiens	269-272
34279763-6	2021	Our western blot experiment results showed that while Suramin decreased SIRT5 and RSV decreased FOXO3a protein expressions significantly in HCT-116 p53 -/- cells, 5-FU decreased significantly SIRT5 and FOXO3a protein expressions in a p53 independent manner.	Fluorouracil	163-167	P53	Homo sapiens	234-237
34564972-3	2021	We evaluated the antitumoral effect of iRNA-PFK-1 and the combined therapy iRNA-PFK-1 + metformin in RKO p53-positive cells.	Metformin	88-97	P53	Homo sapiens	105-108
34187948-0	2021	Luteolin inhibits H2O2-induced cellular senescence via modulation of SIRT1 and p53.	Hydrogen Peroxide	18-22	P53	Homo sapiens	79-82
34279763-0	2021	The role of SIRT5 and p53 proteins in the sensitivity of colon cancer cells to chemotherapeutic agent 5-Fluorouracil.	Fluorouracil	102-116	P53	Homo sapiens	22-25
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	P53	Homo sapiens	74-77
34188177-0	2022	Novel CDK9 inhibitor oroxylin A promotes wild-type P53 stability and prevents hepatocellular carcinoma progression by disrupting both MDM2 and SIRT1 signaling.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	21-31	P53	Homo sapiens	51-54
34181793-6	2021	Cell cycle arrest at G2 /M phase caused by surfactin was demonstrated through p53 and p21 accumulation combined p34cdc2 , phosphorylated p34cdc2 and cyclin B1 inhibition, which was regulated by NADPH oxidase-derived ROS.	surfactin peptide	43-52	P53	Homo sapiens	78-81
34209006-7	2021	Moreover, S-Equol activates the PI3K/Akt pathway, which is an upstream regulation of p53 and NO production and is associated with apoptosis and matrix degradation.	Equol	10-17	P53	Homo sapiens	85-88
34306252-10	2021	The main compounds of XYS include Quercetin, Naringenin, Isorhamnetin, and Stigmasterol, which mainly regulate the targets such as TP53, Akt1, and MYC and PI3K/Akt, p53, and cell cycle signal pathways.	naringenin	45-55	P53	Homo sapiens	131-135
34306252-10	2021	The main compounds of XYS include Quercetin, Naringenin, Isorhamnetin, and Stigmasterol, which mainly regulate the targets such as TP53, Akt1, and MYC and PI3K/Akt, p53, and cell cycle signal pathways.	naringenin	45-55	P53	Homo sapiens	165-168
34181793-6	2021	Cell cycle arrest at G2 /M phase caused by surfactin was demonstrated through p53 and p21 accumulation combined p34cdc2 , phosphorylated p34cdc2 and cyclin B1 inhibition, which was regulated by NADPH oxidase-derived ROS.	Reactive Oxygen Species	216-219	P53	Homo sapiens	78-81
34257824-7	2021	Other polyphenols such as resveratrol upregulate p53 expression in several cancer cell lines by promoting p53 stability, which in colon cancer cells results in the activation of p53-mediated apoptosis.	Resveratrol	26-37	P53	Homo sapiens	49-52
34257824-7	2021	Other polyphenols such as resveratrol upregulate p53 expression in several cancer cell lines by promoting p53 stability, which in colon cancer cells results in the activation of p53-mediated apoptosis.	Resveratrol	26-37	P53	Homo sapiens	106-109
34257824-7	2021	Other polyphenols such as resveratrol upregulate p53 expression in several cancer cell lines by promoting p53 stability, which in colon cancer cells results in the activation of p53-mediated apoptosis.	Resveratrol	26-37	P53	Homo sapiens	178-181
34257824-8	2021	Finally, among vitamins, folic acid seems to play an important role in the chemoprevention of gastric carcinogenesis by enhancing gastric epithelial apoptosis in patients with premalignant lesions by significantly increased expression of p53.	Folic Acid	25-35	P53	Homo sapiens	238-241
34168122-7	2021	Conversely, induction of p53 expression with small molecule inhibitors of the p53-MDM2 binding (MI-773, APG-115) was sufficient to inhibit VEGF-induced vasculogenic differentiation.	AA-115	104-111	P53	Homo sapiens	25-28
34168122-7	2021	Conversely, induction of p53 expression with small molecule inhibitors of the p53-MDM2 binding (MI-773, APG-115) was sufficient to inhibit VEGF-induced vasculogenic differentiation.	AA-115	104-111	P53	Homo sapiens	78-81
34168274-8	2021	The hub targets for aspirin in preventing preeclampsia were tumor protein p53 (TP53), C-X-C motif chemokine ligand 8 (CXCL8), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 14 (MAPK14), epidermal growth factor receptor (EGFR), estrogen receptor (ESR1), and prostaglandin-endoperoxide synthase 2 (PTGS2).	Aspirin	20-27	P53	Homo sapiens	79-83
34144984-4	2021	p53 loss up-regulates the expression of a Golgi scaffolding protein, progestin and adipoQ receptor 11 (PAQR11), which recruits an adenosine diphosphate ribosylation factor 1-containing protein complex that loads cargos into secretory vesicles.	Adenosine	130-139	P53	Homo sapiens	0-3
34239689-0	2021	UNC5B Promotes Vascular Endothelial Cell Senescence via the ROS-Mediated P53 Pathway.	Reactive Oxygen Species	60-63	P53	Homo sapiens	73-76
34239689-11	2021	These findings suggest that UNC5B promotes endothelial cell senescence, potentially by activating the ROS-P53 pathway.	Reactive Oxygen Species	102-105	P53	Homo sapiens	106-109
34131139-1	2021	Here, we identify iPLA2beta as a critical regulator for p53-driven ferroptosis upon reactive oxygen species (ROS)-induced stress.	Reactive Oxygen Species	109-112	P53	Homo sapiens	56-59
34208645-6	2021	Moreover, melatonin modulates critical players in cancer development, such as HIF-1 and p53.	Melatonin	10-19	P53	Homo sapiens	88-91
34195018-16	2021	The expression of apoptosis regulatory genes assessed by PCR revealed an upregulation of p53 by ME, accompanied by downregulation of Bcl-2 and high expression of Bax after treatment with curcumin.	Curcumin	187-195	P53	Homo sapiens	89-92
34131139-3	2021	We found that iPLA2beta-mediated detoxification of peroxidized lipids is sufficient to suppress p53-driven ferroptosis upon ROS-induced stress, even in GPX4-null cells.	Reactive Oxygen Species	124-127	P53	Homo sapiens	96-99
34204834-5	2021	While CisPt + RSV treatment induced apoptosis in PE/CA-PJ49 cells by inhibition of BCL-2 associated with high levels of MDM-2 and subsequently led to inhibition of TP53 gene expression.	Cisplatin	6-11	P53	Homo sapiens	164-168
34204834-4	2021	In FaDu cells, combined CisPt + RSV treatment induced an increase in apoptosis, which was associated with an increase in c-MYC and TP53 and a decrease in BCL-2 expression.	Cisplatin	24-29	P53	Homo sapiens	131-135
34204834-4	2021	In FaDu cells, combined CisPt + RSV treatment induced an increase in apoptosis, which was associated with an increase in c-MYC and TP53 and a decrease in BCL-2 expression.	Resveratrol	32-35	P53	Homo sapiens	131-135
34204834-5	2021	While CisPt + RSV treatment induced apoptosis in PE/CA-PJ49 cells by inhibition of BCL-2 associated with high levels of MDM-2 and subsequently led to inhibition of TP53 gene expression.	Resveratrol	14-17	P53	Homo sapiens	164-168
34126912-14	2022	The results revealed an increase of 12.40-19.10 in p53 level compared to the test cells and that p53 protein level of 7a, 7c, and 11 was significantly inductive (636, 861 and 987 pg/mL, respectively) in relation to doxorubicin (1263 pg/mL).	Doxorubicin	215-226	P53	Homo sapiens	51-54
34135572-0	2021	Metformin Decreases Insulin Resistance in Type 1 Diabetes Through Regulating P53 and RAP2A in vitro and in vivo (Retraction).	Metformin	0-9	P53	Homo sapiens	77-80
34103468-0	2021	A carbazole compound, 9-ethyl-9H-carbazole-3-carbaldehyde, plays an antitumor function through reactivation of the p53 pathway in human melanoma cells.	carbazole	2-11	P53	Homo sapiens	115-118
34103468-10	2021	In summary, our study demonstrates that the carbazole derivative, ECCA, induces melanoma cell apoptosis and senescence through the activation of p53 to significantly and selectively suppress the growth of melanoma cells without affecting normal human melanocytes, suggesting its potential to develop a new drug for melanoma therapy.	carbazole	44-53	P53	Homo sapiens	145-148
34149863-13	2021	SCDP key active ingredients are mainly quercetin, wogonin, baicalein, acacetin, oroxylin A, and beta-sitosterol, which function mainly by regulating targets, such as PTGS2, CASP3, TP53, IL-6, TNF, and AKT1, and are associated with multiple signaling pathways as pathways in cancer, PI3K-Akt signaling pathway, apoptosis, IL-17 signaling pathways.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	80-90	P53	Homo sapiens	180-184
34099041-5	2021	Further, we found that SPD significantly reduced basal or hydrogen peroxide (H2O2)-induced up-regulated protein expression of the aging markers, cyclin dependent kinase inhibitor 2A (p16/CDKN2A) and tumor protein 53 (p53).	Hydrogen Peroxide	58-75	P53	Homo sapiens	199-215
34099041-5	2021	Further, we found that SPD significantly reduced basal or hydrogen peroxide (H2O2)-induced up-regulated protein expression of the aging markers, cyclin dependent kinase inhibitor 2A (p16/CDKN2A) and tumor protein 53 (p53).	Hydrogen Peroxide	58-75	P53	Homo sapiens	217-220
34099041-5	2021	Further, we found that SPD significantly reduced basal or hydrogen peroxide (H2O2)-induced up-regulated protein expression of the aging markers, cyclin dependent kinase inhibitor 2A (p16/CDKN2A) and tumor protein 53 (p53).	Hydrogen Peroxide	77-81	P53	Homo sapiens	199-215
34099041-5	2021	Further, we found that SPD significantly reduced basal or hydrogen peroxide (H2O2)-induced up-regulated protein expression of the aging markers, cyclin dependent kinase inhibitor 2A (p16/CDKN2A) and tumor protein 53 (p53).	Hydrogen Peroxide	77-81	P53	Homo sapiens	217-220
34141624-9	2021	Variant clonality and co-occuring TP53 variants affect the predictive value of HRR pathogenic variants for platinum agents in patients with EOC.	Platinum	107-115	P53	Homo sapiens	34-38
34075143-5	2021	Glucose 20 mmol/L accelerates senescence of HREC: population doubling time (+ 58%, p < 0.001) beta-galactosidase activity (+ 60%, p < 0.002) intracellular oxidative stress (+ 65%, p < 0.01), expression of p53 gene (+ 118%, p < 0.001).	Glucose	0-7	P53	Homo sapiens	205-208
34155600-12	2021	Moreover, the H2O2 treatment group showed significantly downregulated expression of SIRT1 (P < 0.01) but significantly upregulated expressions of p53 and Caspase3 (P < 0.01) compared to the control group.	Hydrogen Peroxide	14-18	P53	Homo sapiens	146-149
34155600-14	2021	This study suggests that SPPA inhibits H2O2-induced human KGN cell apoptosis through antioxidation, and the SIRT1/p53 signal pathway mediates the antioxidation.	Hydrogen Peroxide	39-43	P53	Homo sapiens	114-117
34221338-5	2021	We synthesized a set of chemically homogeneous full-length p53 carrying one (Ser20ph and Ser15ph) or two (Ser15,20ph) naturally occurring, damage-associated phosphoryl marks.	ser15ph	89-96	P53	Homo sapiens	59-62
34127929-13	2021	GSEA showed that the high expression phenotype of miR-3614-5p differentially enriches the P53 pathway.	gsea	0-4	P53	Homo sapiens	90-93
34073371-0	2021	TNFalpha Enhances Tamoxifen Sensitivity through Dissociation of ERalpha-p53-NCOR1 Complexes in ERalpha-Positive Breast Cancer.	Tamoxifen	18-27	P53	Homo sapiens	72-75
34069902-15	2021	Negative correlation of tumor p53 protein with free cholesterol indicates a role of p53 in cholesterol metabolism.	Cholesterol	52-63	P53	Homo sapiens	84-87
34069902-15	2021	Negative correlation of tumor p53 protein with free cholesterol indicates a role of p53 in cholesterol metabolism.	Cholesterol	91-102	P53	Homo sapiens	30-33
34069902-15	2021	Negative correlation of tumor p53 protein with free cholesterol indicates a role of p53 in cholesterol metabolism.	Cholesterol	91-102	P53	Homo sapiens	84-87
34066331-3	2021	miR-125b-5p is a controversial microRNA with a dual role in cancer that has been reported to target specifically TP53 in colon adenocarcinomas.	mir-125b-5p	0-11	P53	Homo sapiens	113-117
34122059-8	2021	Mechanistically, p53-driven apoptosis induction and cell cycle arrest played essential role in DOX-PMs-NPMBP-induced anti-leukemia effects.	Doxorubicin	95-98	P53	Homo sapiens	17-20
34122059-8	2021	Mechanistically, p53-driven apoptosis induction and cell cycle arrest played essential role in DOX-PMs-NPMBP-induced anti-leukemia effects.	npmbp	103-108	P53	Homo sapiens	17-20
34113336-5	2021	We herein report the first case of triple-hit RR DLBCL with TP53 mutation who was treated with piggyBac-generated CAR19-T cells and accompanied by grade 2 cytokine release syndrome.	piggybac	95-103	P53	Homo sapiens	60-64
34063628-5	2021	Interestingly, pretreatment with jorunnamycin A at 0.5 muM for 24 h considerably sensitized lung CSCs to cisplatin-induced apoptosis, as evidenced by upregulated p53 and decreased Bcl-2 in jorunnamycin A-pretreated CSC-enriched spheroids.	Cisplatin	105-114	P53	Homo sapiens	162-165
34183962-10	2021	Piperine (20 muM) and cisplatin (5 muM) for 24 h induce apoptosis strongly through reduction of Bcl-2 and increase of caspase 3, p53, caspase 9, and Bax.	Cisplatin	22-31	P53	Homo sapiens	129-132
34183962-11	2021	Conclusion: Piperine in combination with cisplatin could trigger p53-mediated apoptosis more effective than cisplatin alone in MCF-7 breast cancer cells, reducing the toxic dose of cisplatin used in cancer chemotherapy.	Cisplatin	41-50	P53	Homo sapiens	65-68
34183962-11	2021	Conclusion: Piperine in combination with cisplatin could trigger p53-mediated apoptosis more effective than cisplatin alone in MCF-7 breast cancer cells, reducing the toxic dose of cisplatin used in cancer chemotherapy.	Cisplatin	181-190	P53	Homo sapiens	65-68
34257551-10	2021	GSEA showed that the cell cycle, DNA replication, p53 signaling pathway and mismatch repair were differentially enriched in the high Rac3 expression phenotype.	gsea	0-4	P53	Homo sapiens	50-53
34163823-4	2021	p53C phase separated in the presence of the crowding agent polyethylene glycol (PEG).	Polyethylene Glycols	59-78	P53	Homo sapiens	0-3
34163823-4	2021	p53C phase separated in the presence of the crowding agent polyethylene glycol (PEG).	Polyethylene Glycols	80-83	P53	Homo sapiens	0-3
34915755-7	2021	Moreover, Cisplatin-induced activation of mammalian target of rapamycin mTOR and inactivation of AMPK/PI3K/Akt signal pathway, and was coupled with induction of p53 activity and the executioner caspase3 to induce apoptotic renal cell death.	Cisplatin	10-19	P53	Homo sapiens	161-164
34749615-4	2021	RSV is thought to have an impressive outcome in colorectal cancer (CRC) treatment through the vital molecules and cancer signaling pathways, including SIRT1, P53, P21, AMPK, ROS, BMP7, COX-2, NO, Caspases, Wnt, TNFs, NF-kappaB, EMT, and pentose phosphate pathway.	Resveratrol	0-3	P53	Homo sapiens	158-161
34163734-1	2021	Dye-loaded UiO-66 metal-organic framework nanoparticles (NMOFs) modified with catalytic hemin/G-quadruplex DNAzyme labels act as functional hybrid modules for the chemiluminescence resonance energy transfer (CRET) analysis of miRNAs (miRNA-155 or miRNA-21) or genes (p53 or BRCA1).	Metals	18-23	P53	Homo sapiens	267-270
35487360-6	2022	Some metal ions could bind to p53 core domain, impair its function and induce the development of cancer risk, but its mechanisms were still unclear.	Metals	5-10	P53	Homo sapiens	30-33
34485982-0	2021	Activation of P53 Via Nutlin-3a Reveals Role for P53 In ROS Signaling During Cardiac Differentiation of hiPSCs.	ros	56-59	P53	Homo sapiens	49-52
34976246-11	2021	Conclusions: Colicin E7 decreased the expression of bcl2 and increased P53.	colicin e7	13-23	P53	Homo sapiens	71-74
35635928-5	2022	The experimental results suggest that a direct relationship exists between the inhibitory effect of these STK160830 derivatives on the expression level of p53 and their radioprotective activity and that the suppression of p53 by STK160830 derivatives contribute to protecting MOLT-4 cells from apoptosis that is induced by exposure to radiation.	4-{(Z)-[4-(methoxycarbonyl)-1-(3-methoxyphenyl)-5-methyl-2-oxo-1,2-dihydro-3H-pyrrol-3-ylidene]methyl}benzoic acid	106-115	P53	Homo sapiens	155-158
35635928-5	2022	The experimental results suggest that a direct relationship exists between the inhibitory effect of these STK160830 derivatives on the expression level of p53 and their radioprotective activity and that the suppression of p53 by STK160830 derivatives contribute to protecting MOLT-4 cells from apoptosis that is induced by exposure to radiation.	4-{(Z)-[4-(methoxycarbonyl)-1-(3-methoxyphenyl)-5-methyl-2-oxo-1,2-dihydro-3H-pyrrol-3-ylidene]methyl}benzoic acid	106-115	P53	Homo sapiens	222-225
35635928-5	2022	The experimental results suggest that a direct relationship exists between the inhibitory effect of these STK160830 derivatives on the expression level of p53 and their radioprotective activity and that the suppression of p53 by STK160830 derivatives contribute to protecting MOLT-4 cells from apoptosis that is induced by exposure to radiation.	4-{(Z)-[4-(methoxycarbonyl)-1-(3-methoxyphenyl)-5-methyl-2-oxo-1,2-dihydro-3H-pyrrol-3-ylidene]methyl}benzoic acid	229-238	P53	Homo sapiens	222-225
34386946-6	2021	Conjugation of the p53 short-chain peptide of 25 amino acids occurs through a combination of electrostatic interactions and covalent bonds between cysteine residues at the N-terminal of the peptide and the surface of the AuNPs.	Cysteine	147-155	P53	Homo sapiens	19-22
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	Zinc	213-217	P53	Homo sapiens	160-163
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	Zinc	213-217	P53	Homo sapiens	165-168
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	Nickel(2+)	225-229	P53	Homo sapiens	160-163
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	Nickel(2+)	225-229	P53	Homo sapiens	165-168
35487360-11	2022	The metal ions with weak hydrolysis constants and strong polarization forces could readily interact with N-containing histidine and S-containing cysteine of p53 DBD, which resulted in high Ka values.	Metals	4-9	P53	Homo sapiens	157-160
35487360-11	2022	The metal ions with weak hydrolysis constants and strong polarization forces could readily interact with N-containing histidine and S-containing cysteine of p53 DBD, which resulted in high Ka values.	Nitrogen	105-106	P53	Homo sapiens	157-160
35487360-11	2022	The metal ions with weak hydrolysis constants and strong polarization forces could readily interact with N-containing histidine and S-containing cysteine of p53 DBD, which resulted in high Ka values.	Histidine	118-127	P53	Homo sapiens	157-160
35487360-11	2022	The metal ions with weak hydrolysis constants and strong polarization forces could readily interact with N-containing histidine and S-containing cysteine of p53 DBD, which resulted in high Ka values.	Cysteine	145-153	P53	Homo sapiens	157-160
35487360-12	2022	This study identified p53 as potential target for metal ions, revealed the key characteristics affecting the actions and provide a basic understanding of metal ions-p53 DBD interaction.	Metals	50-55	P53	Homo sapiens	22-25
35487360-12	2022	This study identified p53 as potential target for metal ions, revealed the key characteristics affecting the actions and provide a basic understanding of metal ions-p53 DBD interaction.	Metals	154-159	P53	Homo sapiens	22-25
35487360-12	2022	This study identified p53 as potential target for metal ions, revealed the key characteristics affecting the actions and provide a basic understanding of metal ions-p53 DBD interaction.	Metals	154-159	P53	Homo sapiens	165-168
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	Metals	183-188	P53	Homo sapiens	160-163
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	Metals	183-188	P53	Homo sapiens	165-168
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	magnesium ion	195-199	P53	Homo sapiens	160-163
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	magnesium ion	195-199	P53	Homo sapiens	165-168
35551917-6	2022	In human umbilical vein endothelial cells (HUVEC) cultures, Doxo (10-100 nM) increased the number of SA-beta-gal positive cells and the levels of gammaH2AX, p21 and p53, used as markers of senescence.	Doxorubicin	60-64	P53	Homo sapiens	165-168
35460908-6	2022	The liberated Met blocks the glycolysis process via suppressing the activity of HK2 and impairing ATP production, which activates the AMP-activated protein kinase (AMPK) pathway and p53 pathway and damages the Warburg effect, eventually leading to cells apoptosis.	Adenosine Triphosphate	98-101	P53	Homo sapiens	182-185
35395477-0	2022	Ultrasound-triggered reactive oxygen species effector nanoamplifier for enhanced combination therapy of mutant p53 tumors.	Reactive Oxygen Species	21-44	P53	Homo sapiens	111-114
35395477-2	2022	In this study, we built an ultrasound-triggered ROS damage nanoamplifier using a synergistic strategy consisting of ROS damage and decreased tumor self-protection capability to enhance the treatment efficacy of mutant p53 tumors.	Reactive Oxygen Species	48-51	P53	Homo sapiens	218-221
35395477-2	2022	In this study, we built an ultrasound-triggered ROS damage nanoamplifier using a synergistic strategy consisting of ROS damage and decreased tumor self-protection capability to enhance the treatment efficacy of mutant p53 tumors.	Reactive Oxygen Species	116-119	P53	Homo sapiens	218-221
35395477-5	2022	In addition, TH287 allies with ROS to eliminate the mutated p53 protein in tumor cells, thus reducing the self-protective capacity of tumor cells.	Reactive Oxygen Species	31-34	P53	Homo sapiens	60-63
35395477-7	2022	The construction of a ROS nanoamplifier not only provides an effective strategy for the treatment of mutant p53 tumors but also supplies an integrated platform for tumor diagnosis and therapy.	Reactive Oxygen Species	22-25	P53	Homo sapiens	108-111
35447365-3	2022	The ferroptosis is mainly regulated by the metabolism of iron, lipids and amino acids through System Xc-, voltage-dependent anion channels, p53, p62-Keap1-Nrf2, mevalonate and other pathways.	Iron	57-61	P53	Homo sapiens	140-143
35421634-3	2022	Doxorubicin and etoposide were used to induce cell senescence as determined by the cessation of cell proliferation, augmented senescence-associated beta-galactosidase (SA-beta-Gal) staining, and increased p53 expression levels.	Doxorubicin	0-11	P53	Homo sapiens	205-208
35584694-7	2022	We show that beta-hydroxybutyrate functions as an HDAC inhibitor within MuSCs, leading to acetylation and activation of an HDAC1 target protein p53.	3-Hydroxybutyric Acid	13-33	P53	Homo sapiens	144-147
35460908-11	2022	The liberated Met blocks the glycolysis process via suppressing the activity of HK2 and impairing ATP production, which activates the AMP-activated protein kinase (AMPK) pathway and p53 pathway and damages the Warburg effect, eventually leading to cells apoptosis.	Adenosine Triphosphate	98-101	P53	Homo sapiens	182-185
35311459-10	2022	However, the amounts of p53 in the total count and in the nucleus were much lower with the combination than with doxorubicin alone, suggesting that p53 played no role in either the compound stress, doxorubicin-only or bortezomib-induced apoptosis.	Doxorubicin	113-124	P53	Homo sapiens	24-27
35324521-7	2022	Interestingly, DHMBA increased the levels of cancer suppressor p53, p21, Rb, and regucalcin.	3,5-dihydroxy-4-methoxybenzyl alcohol	15-20	P53	Homo sapiens	63-66
35311459-1	2022	We examined the apoptotic response of two glioblastoma cells, p53 wild type U87 and p53 mutated T98G, to doxorubicin, bortezomib, and vorinostat, which respectively target DNA, 26S proteasome and histone deacetylase, to clarify p53"s function in apoptosis.	Doxorubicin	105-116	P53	Homo sapiens	62-65
35311459-1	2022	We examined the apoptotic response of two glioblastoma cells, p53 wild type U87 and p53 mutated T98G, to doxorubicin, bortezomib, and vorinostat, which respectively target DNA, 26S proteasome and histone deacetylase, to clarify p53"s function in apoptosis.	Doxorubicin	105-116	P53	Homo sapiens	84-87
35346500-14	2022	The potential pathways relative to cisplatin resistance were obtained, such as p53 signaling pathway and Oxidative phosphorylation.	Cisplatin	35-44	P53	Homo sapiens	79-82
35436464-6	2022	Furthermore, mutated LCL displayed lower levels of phospho-Chk1 and phospho-Chk2 following hydrogen peroxide-induced oxidative stress, indicating a poorly effective DNA damage checkpoint, as well as reduced basal levels of p53.	Hydrogen Peroxide	91-108	P53	Homo sapiens	223-226
35546176-5	2022	The levels of cellular senescence-associated p53 and p21 significantly increased in H2O2-induced senescent House Ear Institute-Organ of Corti 1 (HEI-OC1) cells and cochlear explants.	Hydrogen Peroxide	84-88	P53	Homo sapiens	45-48
35500522-11	2022	One sentence summary: TRPM4 is repressed in the p53 pathway leading to reduced currents and increased calcium signaling.	Calcium	102-109	P53	Homo sapiens	48-51
35483139-0	2022	Environmental BPDE induced human trophoblast cell apoptosis by up-regulating lnc-HZ01/p53 positive feedback loop.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	14-18	P53	Homo sapiens	86-89
35483139-10	2022	Upon BPDE exposure, BPDE up-regulated the expression levels of lnc-HZ01 and p53, triggered this positive feedback loop, activated the p53/caspase-3 apoptosis pathway, and then induced miscarriage.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	5-9	P53	Homo sapiens	76-79
35483139-10	2022	Upon BPDE exposure, BPDE up-regulated the expression levels of lnc-HZ01 and p53, triggered this positive feedback loop, activated the p53/caspase-3 apoptosis pathway, and then induced miscarriage.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	5-9	P53	Homo sapiens	134-137
35483139-10	2022	Upon BPDE exposure, BPDE up-regulated the expression levels of lnc-HZ01 and p53, triggered this positive feedback loop, activated the p53/caspase-3 apoptosis pathway, and then induced miscarriage.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	20-24	P53	Homo sapiens	76-79
35483139-10	2022	Upon BPDE exposure, BPDE up-regulated the expression levels of lnc-HZ01 and p53, triggered this positive feedback loop, activated the p53/caspase-3 apoptosis pathway, and then induced miscarriage.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	20-24	P53	Homo sapiens	134-137
35487028-9	2022	We observed that both p53 (p = 0.0006) and Delta40p53 (p = 0.0014) induced apoptosis in cisplatin-treated SiHa cells; however in cisplatin-treated HeLa cells, only p53 induced apoptosis (p = 0.0029).	Cisplatin	88-97	P53	Homo sapiens	22-25
35487028-9	2022	We observed that both p53 (p = 0.0006) and Delta40p53 (p = 0.0014) induced apoptosis in cisplatin-treated SiHa cells; however in cisplatin-treated HeLa cells, only p53 induced apoptosis (p = 0.0029).	Cisplatin	88-97	P53	Homo sapiens	164-167
35487028-11	2022	Our findings suggest a possible therapeutic application for the combining of p53 or Delta40p53 with cisplatin to induce an increased apoptosis of cancer cells expressing E6 isoforms from HPV-16.	Cisplatin	100-109	P53	Homo sapiens	77-80
35636434-5	2022	In addition, qRT-PCR results showed that the expressions of miR-181 and P53, CYLD, CBX7 and BCL2 genes change in MG63 cells after treatment with the combination of cisplatin and melatonin, so that the expression of P53, CYLD and CBX7 increased and the expression of BCL2 and miR-181b decreases significantly.	Cisplatin	164-173	P53	Homo sapiens	72-75
35636434-5	2022	In addition, qRT-PCR results showed that the expressions of miR-181 and P53, CYLD, CBX7 and BCL2 genes change in MG63 cells after treatment with the combination of cisplatin and melatonin, so that the expression of P53, CYLD and CBX7 increased and the expression of BCL2 and miR-181b decreases significantly.	Cisplatin	164-173	P53	Homo sapiens	215-218
35636434-5	2022	In addition, qRT-PCR results showed that the expressions of miR-181 and P53, CYLD, CBX7 and BCL2 genes change in MG63 cells after treatment with the combination of cisplatin and melatonin, so that the expression of P53, CYLD and CBX7 increased and the expression of BCL2 and miR-181b decreases significantly.	Melatonin	178-187	P53	Homo sapiens	72-75
35636434-5	2022	In addition, qRT-PCR results showed that the expressions of miR-181 and P53, CYLD, CBX7 and BCL2 genes change in MG63 cells after treatment with the combination of cisplatin and melatonin, so that the expression of P53, CYLD and CBX7 increased and the expression of BCL2 and miR-181b decreases significantly.	Melatonin	178-187	P53	Homo sapiens	215-218
35589683-3	2022	p53 inhibits the mammalian target of rapamycin complex 1 (mTORC1) signaling to attenuate the protein level of mitochondrial fission process 1 (MTFP1), which fosters the pro-fission dynamin-related protein 1 (Drp1) phosphorylation.	Sirolimus	37-46	P53	Homo sapiens	0-3
35589688-5	2022	E2 increased DNA methyltransferase 1 (DNMT1) expression to enhance methylation in the TP53 promoter, which led to the downregulation of p53.	Estradiol	0-2	P53	Homo sapiens	86-90
35589688-5	2022	E2 increased DNA methyltransferase 1 (DNMT1) expression to enhance methylation in the TP53 promoter, which led to the downregulation of p53.	Estradiol	0-2	P53	Homo sapiens	136-139
35274753-2	2022	This study aimed to assess the utility of p53 immunohistochemistry (p53-IHC) in assessing BE-IND specimens.	be-ind	90-96	P53	Homo sapiens	42-45
35274753-2	2022	This study aimed to assess the utility of p53 immunohistochemistry (p53-IHC) in assessing BE-IND specimens.	be-ind	90-96	P53	Homo sapiens	68-71
35274753-10	2022	Use of p53-IHC led to a >40% reduction in BE-IND diagnoses (P<.001), and increased IOA for all BE grades (kappa=0.46 (NDBE), 0.26 (BE-IND), 0.49 (LGD), 0.35 (HGD/IMC)).	be-ind	42-48	P53	Homo sapiens	7-10
35274753-10	2022	Use of p53-IHC led to a >40% reduction in BE-IND diagnoses (P<.001), and increased IOA for all BE grades (kappa=0.46 (NDBE), 0.26 (BE-IND), 0.49 (LGD), 0.35 (HGD/IMC)).	be-ind	131-137	P53	Homo sapiens	7-10
35274753-11	2022	An aberrant p53-IHC pattern significantly increased the likelihood of reclassifying BE-IND to definite dysplasia (odds ratio 44.3, 95%CI:18.8-113.0).	be-ind	84-90	P53	Homo sapiens	12-15
35274753-12	2022	INTERPRETATION: P53-IHC reduces the rate of BE-IND diagnoses and improves the IOA among pathologists when reporting BE with equivocal epithelial changes.	be-ind	44-50	P53	Homo sapiens	16-19
35274753-12	2022	INTERPRETATION: P53-IHC reduces the rate of BE-IND diagnoses and improves the IOA among pathologists when reporting BE with equivocal epithelial changes.	Beryllium	116-118	P53	Homo sapiens	16-19
35487055-9	2022	Generally, both cell lines treated with the combination of Curcumin and As2O3 displayed decreased angiogenesis genes (VEGFA and VEGFC), apoptosis genes (BAX and Bcl2), and prostate cancer marker (KLK2), the zinc-finger protein (SNAIL); and an increase in expression (P < 0.05) of cell-cell adhesion molecule (E-cadherin) and tumor suppressor gene (P53) genes.	Curcumin	59-67	P53	Homo sapiens	348-351
35608342-5	2022	In addition, p53 levels increase in HPV16+ head and neck cancer cell lines following treatment with cisplatin.	Cisplatin	100-109	P53	Homo sapiens	13-16
35608342-11	2022	The results demonstrate that p53 expression is critical during the HPV16 life cycle, and that this may be due to a functional interaction between E2 and p53.	Estradiol	146-148	P53	Homo sapiens	29-32
35608342-11	2022	The results demonstrate that p53 expression is critical during the HPV16 life cycle, and that this may be due to a functional interaction between E2 and p53.	Estradiol	146-148	P53	Homo sapiens	153-156
35609756-10	2022	Furthermore, after stimulated by EX527 (a SIRT1 inhibitor), the SIRT1-dependent neuroprotective effects of ARF were determined by measuring SRIT1 and p53 expression in SH-SY5Y aging cells induced by D-gal.	6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide	33-38	P53	Homo sapiens	150-153
35609756-10	2022	Furthermore, after stimulated by EX527 (a SIRT1 inhibitor), the SIRT1-dependent neuroprotective effects of ARF were determined by measuring SRIT1 and p53 expression in SH-SY5Y aging cells induced by D-gal.	Galactose	199-204	P53	Homo sapiens	150-153
35609756-14	2022	In D-gal-induced SH-SY5Y cells, the effects of ARF on SIRT1 and p53, and the ability of scavenging ROS were mostly abolished after incubation with the EX527.	Galactose	3-8	P53	Homo sapiens	64-67
35598358-7	2022	TP53 mutations and brain metastases were associated with shorter PFS under platinum doublets and EGFR inhibitors (HR 3.3-6.1, p < 0.01), and shorter OS for patients receiving both treatments (p < 0.05).	Platinum	75-83	P53	Homo sapiens	0-4
35574675-4	2022	Phosphorylation levels of p53 was assessed using immunoblotting at sites known to be phosphorylated (Serine 15 and 37) in response to DNA damage or reduced oxygen signaling.	Serine	101-107	P53	Homo sapiens	26-29
35574675-4	2022	Phosphorylation levels of p53 was assessed using immunoblotting at sites known to be phosphorylated (Serine 15 and 37) in response to DNA damage or reduced oxygen signaling.	Oxygen	156-162	P53	Homo sapiens	26-29
35574675-9	2022	Cytoplasmic accumulation of Ser-15 p-p53 was observed during anoxia when proteins from cytoplasmic and nuclear fractions were measured.	Serine	28-31	P53	Homo sapiens	37-40
35574675-11	2022	The results suggest that p53 might play a protective role in crayfish defense against low oxygen stress.	Oxygen	90-96	P53	Homo sapiens	25-28
35381263-0	2022	Kurarinone induced p53-Independent G0/G1 cell cycle arrest by degradation of K-RAS via WDR76 in human colorectal cancer cells.	kurarinone	0-10	P53	Homo sapiens	19-22
35594815-5	2022	TP53 interacts with the majority of lung disease-related genes and regulates important and commonly occurring biological functions and pathways, including gland development, aging, reactive oxygen species metabolic process, the response to oxygen levels, and fluid shear stress, among others.	Oxygen	240-246	P53	Homo sapiens	0-4
35601652-3	2022	p53 activation in response to neurodegenerative stress is closely associated with the degeneration of dopaminergic neurons accompanied by mitochondrial dysfunction, reactive oxygen species (ROS) production, abnormal protein aggregation, and impairment of autophagy, and these pathogenic events have been implicated in the pathogenesis of PD.	Reactive Oxygen Species	165-188	P53	Homo sapiens	0-3
35601652-3	2022	p53 activation in response to neurodegenerative stress is closely associated with the degeneration of dopaminergic neurons accompanied by mitochondrial dysfunction, reactive oxygen species (ROS) production, abnormal protein aggregation, and impairment of autophagy, and these pathogenic events have been implicated in the pathogenesis of PD.	Reactive Oxygen Species	190-193	P53	Homo sapiens	0-3
35505371-1	2022	BACKGROUND: Ferroptosis is an iron dependent cell death closely associated with p53 signaling pathway and is aberrantly regulated in glioblastoma (GBM), yet the underlying mechanism needs more exploration.	Iron	30-34	P53	Homo sapiens	80-83
35532255-7	2022	By constructing the disease-common target-compound network, five ingredients (quercetin, arachidonate, beta-sitosterol, beta-carotene, and cholesterol) were selected out as the key ingredients of YJD, which can interact with the 10 hub genes (VEGFA, AKT1, TP53, ALB, TNF, PIK3CA, IGF1, INS, IL1B, PTEN) against PCOS.	Cholesterol	139-150	P53	Homo sapiens	256-260
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	Metals	38-43	P53	Homo sapiens	65-68
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	Metals	38-43	P53	Homo sapiens	101-104
35511749-7	2022	One of the combinations, MK-1775 with Doxorubicin, significantly reduced tumor growth in a sporadic PDOX model (MPNST-SP-01) (sevenfold) and in an NF1-PDOX model (MPNST-NF1-09) (fourfold) and presented greater effects in TP53 mutated MPNST cell lines.	Doxorubicin	38-49	P53	Homo sapiens	221-225
35532255-7	2022	By constructing the disease-common target-compound network, five ingredients (quercetin, arachidonate, beta-sitosterol, beta-carotene, and cholesterol) were selected out as the key ingredients of YJD, which can interact with the 10 hub genes (VEGFA, AKT1, TP53, ALB, TNF, PIK3CA, IGF1, INS, IL1B, PTEN) against PCOS.	Arachidonic Acid	89-101	P53	Homo sapiens	256-260
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	Tannins	240-251	P53	Homo sapiens	65-68
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	Tannins	240-251	P53	Homo sapiens	101-104
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	Tannins	253-255	P53	Homo sapiens	65-68
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	Tannins	253-255	P53	Homo sapiens	101-104
35513212-4	2022	The highly cytotoxic ROS was continuously produced via Fe2+-mediated and TA-assisted enhanced Fenton reaction as well as Ce6-induced photosensitive reaction, and meanwhile, the intratumoral upregulated p53 expression inactivated glutathione peroxidase 4 (GPX4) to suppress lipid peroxidation (LPO) resistance, thus resulting in amplified oxidative stress and intensified ferroptosis-apoptosis therapy.	Reactive Oxygen Species	21-24	P53	Homo sapiens	202-205
35513212-4	2022	The highly cytotoxic ROS was continuously produced via Fe2+-mediated and TA-assisted enhanced Fenton reaction as well as Ce6-induced photosensitive reaction, and meanwhile, the intratumoral upregulated p53 expression inactivated glutathione peroxidase 4 (GPX4) to suppress lipid peroxidation (LPO) resistance, thus resulting in amplified oxidative stress and intensified ferroptosis-apoptosis therapy.	Tannins	73-75	P53	Homo sapiens	202-205
35501580-4	2022	We further demonstrate that RIP140 reduces the transcription of the glucose transporter GLUT3 gene, by inhibiting the transcriptional activity of hypoxia inducible factor HIF-2alpha in cooperation with p53.	Glucose	68-75	P53	Homo sapiens	202-205
35488931-5	2022	In this review, we will discuss the role of Zn in the proper function of the p53 protein in cancer.	Zinc	44-46	P53	Homo sapiens	77-80
35087226-3	2022	Unlike apoptotic cell death, activation of p53 alone is not sufficient to induce ferroptosis directly; instead, through its metabolic targets, p53 is able to modulate the ferroptosis response in the presence of ferroptosis inducers such as GPX4 inhibitors or high levels of ROS.	ros	274-277	P53	Homo sapiens	143-146
35522909-0	2022	Exosome-transmitted miR-769-5p confers cisplatin resistance and progression in gastric cancer by targeting CASP9 and promoting the ubiquitination degradation of p53.	Cisplatin	39-48	P53	Homo sapiens	161-164
35522909-11	2022	CONCLUSIONS: These findings indicate that exosome-transmitted miR-769-5p confers cisplatin resistance and progression in gastric cancer by targeting CASP9 and promoting the ubiquitination degradation of p53.	Cisplatin	81-90	P53	Homo sapiens	203-206
35167826-1	2022	Cisplatin is a member of a widely utilized class of chemotherapeutic agent that initiates DNA damage response, cell cycle arrest, and p53-dependent apoptotic cell death in concert with DNA-platinum adduct formation.	Cisplatin	0-9	P53	Homo sapiens	134-137
35398141-0	2022	Graphene oxide leads to mitochondrial-dependent apoptosis by activating ROS-p53-mPTP pathway in intestinal cells.	Reactive Oxygen Species	72-75	P53	Homo sapiens	76-79
35221291-13	2022	Our study confirms the protective role of RES as an anti-ROS agent and its ability to alleviate DNA damage through a pathway involving p53/p21 signaling.	Resveratrol	42-45	P53	Homo sapiens	135-138
35398238-8	2022	In addition, ATA treatment increased the levels of p53 and p21 proteins, which blocked cell cycle progression in the G1/S phase.	acetyltanshinone IIA	13-16	P53	Homo sapiens	51-54
35488931-9	2022	This includes understanding the relative populations of the Zn-bound and Zn-free p53 in wild-type and mutant forms, and the development of metallochaperones to re-populate the Zn binding site to restore mutant p53 activity.	Zinc	176-178	P53	Homo sapiens	210-213
35488931-9	2022	This includes understanding the relative populations of the Zn-bound and Zn-free p53 in wild-type and mutant forms, and the development of metallochaperones to re-populate the Zn binding site to restore mutant p53 activity.	Zinc	60-62	P53	Homo sapiens	81-84
35510223-13	2022	The molecular docking results showed that there was a certain affinity between the main compounds (kaempferol, quercetin, beta-sitosterol, naringenin) and core target genes (PTGS2, CASP3, MAPK1, MAPK3, TP53).	naringenin	139-149	P53	Homo sapiens	202-206
35574389-6	2022	We found that peptide cyclization enhances Pep8 affinity for eIF4E, induction of p53 and tumor cell growth suppression.	pep8	43-47	P53	Homo sapiens	81-84
35468881-0	2022	JMJD2C mediates the MDM2/p53/IL5RA axis to promote CDDP resistance in uveal melanoma.	Cisplatin	51-55	P53	Homo sapiens	25-28
35517499-6	2022	The elevated cAMP not only inhibited DNA damage-induced apoptosis through abrogating p53 accumulation, but also suppressed the proliferation of cytotoxic T lymphocytes by enhancing the expression of immunosuppressive factors DKK1.	Cyclic AMP	13-17	P53	Homo sapiens	85-88
35566044-9	2022	In contrast, 5 nM Paclitaxel induces TP53 transcription in excess of BCL-2 and Bax.	Paclitaxel	18-28	P53	Homo sapiens	37-41
35517847-1	2022	Background: Resveratrol, a well-known natural compound and nutrient, activates the deacetylation ability of SIRT1, demonstrating p53-dependent apoptosis functions in many diseases.	Resveratrol	12-23	P53	Homo sapiens	129-132
35517847-10	2022	Knockdown of SIRT1 and Hsp60 provides evidence that resveratrol downregulated Hsp60 through SIRT1 and that Hsp60 decreased p53 through the Akt pathway.	Resveratrol	52-63	P53	Homo sapiens	123-126
35517847-11	2022	Conclusions: This study revealed dynamic changes in the nascent proteome and transcriptome in response to resveratrol in HEK 293T cells and demonstrated that resveratrol downregulates Hsp60 by activating SIRT1, which may be a possible mechanism by which resveratrol prevents p53-dependent apoptosis by regulating Hsp60.	Resveratrol	158-169	P53	Homo sapiens	275-278
35410287-4	2022	RESULTS: By combining single-cell imaging and mathematical modeling of dose-dependent p53 dynamics induced by three chemotherapeutics of distinct mechanism-of-actions, including Etoposide, Nutlin-3a and 5-fluorouracil, and in five cancer cell types, we uncovered novel and highly variable p53 dynamic responses, in particular p53 transitional dynamics induced at intermediate drug concentrations, and identified the functional roles of distinct positive and negative feedback motifs of the p53 pathway in modulating the central p53-Mdm2 negative feedback to generate stimulus- and cell type-specific signaling responses.	Fluorouracil	203-217	P53	Homo sapiens	86-89
35418568-8	2022	Furthermore, downregulation of REST by H2O2 treatment induced apoptosis in the House Ear Institute Organ of Corti 1 cell, through the upregulation of p53.	Hydrogen Peroxide	39-43	P53	Homo sapiens	150-153
35312310-10	2022	Dithiothreitol-reduced protein was more efficiently cross-linked indicating that p53 cysteine residues play a key role in protein modification.	Cysteine	85-93	P53	Homo sapiens	81-84
35312310-12	2022	The formation of intermolecular complexes was a consequence of HN2 cross-linked cysteine residues between two molecules of p53.	Cysteine	80-88	P53	Homo sapiens	123-126
35541904-5	2022	Significantly, SKI-V also provoked programmed necrosis cascade in cervical cancer cells, as it induced mitochondrial p53-cyclophilin-D-adenine nucleotide translocator-1 (ANT1) complexation, mitochondrial membrane potential collapse, reactive oxygen species production and the release of lactate dehydrogenase into the medium.	Reactive Oxygen Species	233-256	P53	Homo sapiens	117-120
35456022-0	2022	Apoptotic and DNA Damage Effect of 1,2,3,4,6-Penta-O-galloyl-beta-D-glucose in Cisplatin-Resistant Non-Small Lung Cancer Cells via Phosphorylation of H2AX, CHK2 and p53.	Glucose	68-75	P53	Homo sapiens	165-168
35456022-0	2022	Apoptotic and DNA Damage Effect of 1,2,3,4,6-Penta-O-galloyl-beta-D-glucose in Cisplatin-Resistant Non-Small Lung Cancer Cells via Phosphorylation of H2AX, CHK2 and p53.	Cisplatin	79-88	P53	Homo sapiens	165-168
35359247-4	2022	The presence of a tryptophan-rich sequence in the central acidic domain of MDMX has also been implicated in regulating the interaction between MDMX and p53, directly interacting with the p53 DNA-binding domain.	Tryptophan	18-28	P53	Homo sapiens	152-155
35478958-0	2022	Hesperidin Ameliorates Dexamethasone-Induced Osteoporosis by Inhibiting p53.	Dexamethasone	23-36	P53	Homo sapiens	72-75
35478958-7	2022	Our in vitro results showed that hesperidin partially reversed dexamethasone-induced inhibition of osteogenic differentiation by suppressing the activation of p53, and suggest that hesperidin may be a promising candidate for the treatment against dexamethasone-induced osteoporosis.	Dexamethasone	63-76	P53	Homo sapiens	159-162
35398929-7	2022	CONCLUSIONS: Collectively, our findings demonstrate that SOAT1 participates in hepatocarcinogenesis by increasing cholesterol esterification, thus indicating that SOAT1 is a potential biomarker and therapeutic target in P53-deficient HCC.	Cholesterol	114-125	P53	Homo sapiens	220-223
35388101-7	2022	RNAseq and functional analysis reveal that DNA damage induces a shift in cell response to EGFR triggering that potentiates DDR-induced p53 pathway and cell cycle arrest.	ddr	123-126	P53	Homo sapiens	135-138
35202675-4	2022	At 5% O2, the drugs decreased HIF-1alpha expression and increased p53 levels.	Oxygen	6-8	P53	Homo sapiens	66-69
35202675-7	2022	These results show that the maintenance of HIF-1alpha expression blocked doxorubicin-dependent increases in p53 expression.	Doxorubicin	73-84	P53	Homo sapiens	108-111
35409939-8	2022	Immunochemistry, in particular HER-2 expression, could be of some help in predicting the response to such drugs, and high levels of mutated p53 appear after exposure to anthracyclines and impair their antitumor effect.	Anthracyclines	169-183	P53	Homo sapiens	140-143
35359247-4	2022	The presence of a tryptophan-rich sequence in the central acidic domain of MDMX has also been implicated in regulating the interaction between MDMX and p53, directly interacting with the p53 DNA-binding domain.	Tryptophan	18-28	P53	Homo sapiens	187-190
35149588-4	2022	We found that CDK4/6 bind and phosphorylate the p53 family member p73 at threonine 86, which sequesters p73 in the cytoplasm.	Threonine	73-82	P53	Homo sapiens	48-51
35107378-5	2022	Moreover, the expressions of HUWE1 and TRAF6 were significantly down-regulated during WSSV (White spot syndrome virus) infection, and therefore the ubiquitination of p53 was interrupted, leading to the activation of apoptosis and ROS (Reactive oxygen species) signals through p53 accumulation, which eventually suppressed viral invasion in mud crab.	Reactive Oxygen Species	230-233	P53	Homo sapiens	166-169
35065161-6	2022	Increased ROS production by IMPAs also promotes p53 mediated cell cycle arrest through the inactivation of p38MAPK.	ros	10-13	P53	Homo sapiens	48-51
35065218-6	2022	Pre-treatment with NAC was efficient to prevent cell damage at lower Cl2 concentrations in part by averting the formation of apoptotic-like bodies and increasing the expression of the anti-apoptotic proteins clusterin and phosphorylated tumour protein p53(S46).	Acetylcysteine	19-22	P53	Homo sapiens	252-255
35107378-5	2022	Moreover, the expressions of HUWE1 and TRAF6 were significantly down-regulated during WSSV (White spot syndrome virus) infection, and therefore the ubiquitination of p53 was interrupted, leading to the activation of apoptosis and ROS (Reactive oxygen species) signals through p53 accumulation, which eventually suppressed viral invasion in mud crab.	Reactive Oxygen Species	235-258	P53	Homo sapiens	166-169
35107378-5	2022	Moreover, the expressions of HUWE1 and TRAF6 were significantly down-regulated during WSSV (White spot syndrome virus) infection, and therefore the ubiquitination of p53 was interrupted, leading to the activation of apoptosis and ROS (Reactive oxygen species) signals through p53 accumulation, which eventually suppressed viral invasion in mud crab.	Reactive Oxygen Species	235-258	P53	Homo sapiens	276-279
35152538-11	2022	Finally, ethanol induced hepatocellular steatosis, SREBP1 transcription, and modulated the expression of SREBP1c, ACAC, ACLY, FASN, IL-1beta, IL-6, TNF-alpha, GPC3, FLNB and p53.	Ethanol	9-16	P53	Homo sapiens	174-177
35557569-11	2022	GSEA results showed that ITGB1-DT may be involved in STAD progression through the insulin, p53, mechanistic target of rapamycin kinase (MTOR), and other signaling pathways.	gsea	0-4	P53	Homo sapiens	91-94
34992144-0	2022	Small-molecule NSC59984 induces mutant p53 degradation through a ROS-ERK2-MDM2 axis in cancer cells.	Reactive Oxygen Species	65-68	P53	Homo sapiens	39-42
34992144-4	2022	We used a small-molecule NSC59984 to explore elimination of mutant p53 in cancer cells, and identified an inducible ROS-ERK2-MDM2 axis as a vulnerability for induction of mutant p53 degradation in cancer cells.	Reactive Oxygen Species	116-119	P53	Homo sapiens	67-70
34992144-4	2022	We used a small-molecule NSC59984 to explore elimination of mutant p53 in cancer cells, and identified an inducible ROS-ERK2-MDM2 axis as a vulnerability for induction of mutant p53 degradation in cancer cells.	Reactive Oxygen Species	116-119	P53	Homo sapiens	178-181
34992144-8	2022	High cellular ROS increases the efficacy of NSC59984 targeting mutant p53 degradation and anti-tumor effects.	Reactive Oxygen Species	14-17	P53	Homo sapiens	70-73
34992144-9	2022	Our data suggest that mutant p53 stabilization has a vulnerability under high ROS cellular conditions, which can be exploited by compounds to target mutant p53 protein degradation through the activation of a ROS-ERK2-MDM2 axis in cancer cells.	Reactive Oxygen Species	78-81	P53	Homo sapiens	29-32
34992144-9	2022	Our data suggest that mutant p53 stabilization has a vulnerability under high ROS cellular conditions, which can be exploited by compounds to target mutant p53 protein degradation through the activation of a ROS-ERK2-MDM2 axis in cancer cells.	Reactive Oxygen Species	78-81	P53	Homo sapiens	156-159
34992144-9	2022	Our data suggest that mutant p53 stabilization has a vulnerability under high ROS cellular conditions, which can be exploited by compounds to target mutant p53 protein degradation through the activation of a ROS-ERK2-MDM2 axis in cancer cells.	Reactive Oxygen Species	208-211	P53	Homo sapiens	29-32
34992144-9	2022	Our data suggest that mutant p53 stabilization has a vulnerability under high ROS cellular conditions, which can be exploited by compounds to target mutant p53 protein degradation through the activation of a ROS-ERK2-MDM2 axis in cancer cells.	Reactive Oxygen Species	208-211	P53	Homo sapiens	156-159
34992144-10	2022	Implications: An inducible ROS-ERK2-MDM2 axis exposes a vulnerability in mutant p53 stabilization and can be exploited by small molecule compounds to induce mutant p53 degradation for cancer therapy.	Reactive Oxygen Species	27-30	P53	Homo sapiens	80-83
34992144-10	2022	Implications: An inducible ROS-ERK2-MDM2 axis exposes a vulnerability in mutant p53 stabilization and can be exploited by small molecule compounds to induce mutant p53 degradation for cancer therapy.	Reactive Oxygen Species	27-30	P53	Homo sapiens	164-167
35191521-8	2022	The present results suggested that AZD6738 enhanced the effect of 5-FU in p53-mutated colorectal cancer.	Fluorouracil	66-70	P53	Homo sapiens	74-77
35419287-8	2022	The ferroptosis-related p53-SLC7A11-GPX4 pathway was also altered under different treatment propofol, doxorubicin, or paclitaxel regimens.	Doxorubicin	102-113	P53	Homo sapiens	24-27
35419287-8	2022	The ferroptosis-related p53-SLC7A11-GPX4 pathway was also altered under different treatment propofol, doxorubicin, or paclitaxel regimens.	Paclitaxel	118-128	P53	Homo sapiens	24-27
35107378-11	2022	Our findings revealed that p53 ubiquitination could affect ROS and apoptosis signals to cope with WSSV infection in mud crab, which firstly clarified the immunologic functions and mechanisms of p53 ubiquitination in invertebrates.	Reactive Oxygen Species	59-62	P53	Homo sapiens	27-30
35107378-11	2022	Our findings revealed that p53 ubiquitination could affect ROS and apoptosis signals to cope with WSSV infection in mud crab, which firstly clarified the immunologic functions and mechanisms of p53 ubiquitination in invertebrates.	Reactive Oxygen Species	59-62	P53	Homo sapiens	194-197
35107378-5	2022	Moreover, the expressions of HUWE1 and TRAF6 were significantly down-regulated during WSSV (White spot syndrome virus) infection, and therefore the ubiquitination of p53 was interrupted, leading to the activation of apoptosis and ROS (Reactive oxygen species) signals through p53 accumulation, which eventually suppressed viral invasion in mud crab.	Reactive Oxygen Species	230-233	P53	Homo sapiens	276-279
35328718-0	2022	p62 Promotes the Mitochondrial Localization of p53 through Its UBA Domain and Participates in Regulating the Sensitivity of Ovarian Cancer Cells to Cisplatin.	Cisplatin	148-157	P53	Homo sapiens	47-50
35391801-8	2022	One of the key role players in cancer development and suppression, Tumour Protein 53 (TP53), is crucial in regulating the biogenesis of cholesterol and is targeted by several phytochemicals.	Cholesterol	136-147	P53	Homo sapiens	67-84
35391801-8	2022	One of the key role players in cancer development and suppression, Tumour Protein 53 (TP53), is crucial in regulating the biogenesis of cholesterol and is targeted by several phytochemicals.	Cholesterol	136-147	P53	Homo sapiens	86-90
35406150-9	2022	Zn-BTC@CS stimulated the apoptotic process through up-regulating P53 expression and down-regulating Bcl-2 expression.	zn-btc	0-6	P53	Homo sapiens	65-68
35025136-4	2022	Similarly, since p53 can be ubiquitylated at different lysine residues, it remains unclear if the eventual effect depends on the position of the lysine modified.	Lysine	55-61	P53	Homo sapiens	17-20
35328718-5	2022	We found that the combined use of the proteasome inhibitor epoxomicin and cisplatin led to the accumulation of p53 and sequestosome1(p62) in the mitochondria, downregulated mitochondrial DNA (mtDNA) transcription, inhibited mitochondrial functions, and ultimately promoted apoptosis by enhancing cisplatin sensitivity in ovarian cancer cells.	Cisplatin	74-83	P53	Homo sapiens	111-114
35328718-5	2022	We found that the combined use of the proteasome inhibitor epoxomicin and cisplatin led to the accumulation of p53 and sequestosome1(p62) in the mitochondria, downregulated mitochondrial DNA (mtDNA) transcription, inhibited mitochondrial functions, and ultimately promoted apoptosis by enhancing cisplatin sensitivity in ovarian cancer cells.	Cisplatin	296-305	P53	Homo sapiens	111-114
35371279-10	2022	HDAC3 is indirectly involved in the cGMP-PKG signaling pathway, thereby indirectly regulating the expression levels of p53 and p21 genes in patients with LAML.	Cyclic GMP	36-40	P53	Homo sapiens	119-122
35327653-6	2022	Finally, we found that ZnCl2 supplementation rescued the cisplatin cytotoxic effects, as it impaired NRF2 activation, restoring p53 activity.	zinc chloride	23-28	P53	Homo sapiens	128-131
35074406-0	2022	HIWI2 induces G2/M cell cycle arrest and apoptosis in human fibrosarcoma via the ROS/DNA damage/p53 axis.	ros	81-84	P53	Homo sapiens	96-99
35074406-11	2022	SIGNIFICANCE: These results are the first to show that HIWI2 acts as a tumor suppressor in fibrosarcoma by modulating the ROS/DNA damage/p53 pathway.	ros	122-125	P53	Homo sapiens	137-140
35264873-12	2022	GSEA analysis found that they positively correlated with N glycan biosynthesis and p53 signaling pathways.	gsea	0-4	P53	Homo sapiens	83-86
35266593-2	2022	Heat shock protein 90 (Hsp90) inhibitors are anti-inflammatory agents and P53 inducers, which reduce the production of reactive oxygen species (ROS) in a diverse variety of human tissues.	Reactive Oxygen Species	119-142	P53	Homo sapiens	74-77
35266593-2	2022	Heat shock protein 90 (Hsp90) inhibitors are anti-inflammatory agents and P53 inducers, which reduce the production of reactive oxygen species (ROS) in a diverse variety of human tissues.	Reactive Oxygen Species	144-147	P53	Homo sapiens	74-77
35356282-14	2022	Pre-treatment with rapamycin or PFT-alpha significantly down-regulated the levels of SA beta-Gal, SAHF, p-p53, p21, autophagy related protein p62, the percentage of cells in the G0/G1 phase, and significantly up-regulated DeltaPsim, autophagy related protein BECN1, autophagosomes and autolysosomes compared with cells only treated with AOPPs.	Sirolimus	19-28	P53	Homo sapiens	106-109
35350243-15	2022	The GSEA showed that primary pathways were the P53 signaling pathway and tumor necrosis factor-mediated signaling pathway.	gsea	4-8	P53	Homo sapiens	47-50
35269477-7	2022	Moreover, we found that the MDM2/4 inhibitor ALRN-6924 impairs growth of DNMT3AWT/R882X primary cells in vitro by inducing cell cycle arrest through upregulation of p53 target genes.	alrn-6924	45-54	P53	Homo sapiens	165-168
35085581-0	2022	Piperlongumine induces ROS mediated apoptosis by transcriptional regulation of SMAD4/P21/P53 genes and synergizes with doxorubicin in osteosarcoma cells.	Reactive Oxygen Species	23-26	P53	Homo sapiens	89-92
35286235-8	2022	Mechanistically, GSEA identified that LEMD1 promoted PC aggressiveness, as well as affecting cell cycle dysregulation and apoptosis resistance, by p53 suppression and the activation of the mTORC1 signal pathway.	gsea	17-21	P53	Homo sapiens	147-150
35088369-1	2022	Cadmium exhibits both toxic and carcinogenic effects, and its cytotoxicity is linked to various cellular pathways, such as oxidative stress, ubiquitin-proteasome, and p53-mediated response pathways.	Cadmium	0-7	P53	Homo sapiens	167-170
35066375-2	2022	For this effect, ATRA downregulated both protein and enzyme activity levels of DNA methyltransferase 1 and 3b and activated E6AP expression via promoter hypomethylation in HepG2 cells but not in Hep3B cells, in which p53 was absent.	Tretinoin	17-21	P53	Homo sapiens	217-220
35066375-3	2022	Ectopic p53 expression but not E6AP overexpression restored the ability of ATRA to downregulate HCV Core levels in Hep3B cells, suggesting a direct role of p53 in the E6AP-mediated ubiquitination of HCV Core.	Tretinoin	75-79	P53	Homo sapiens	8-11
35066375-3	2022	Ectopic p53 expression but not E6AP overexpression restored the ability of ATRA to downregulate HCV Core levels in Hep3B cells, suggesting a direct role of p53 in the E6AP-mediated ubiquitination of HCV Core.	Tretinoin	75-79	P53	Homo sapiens	156-159
34995485-5	2022	When CAPE was combined with cisplatin in nine cell lines representative of various histotypes a synergistic effect was observed in TOV112D cells and in the cisplatin-resistant IGROV-1/Pt1 variant, both of endometrioid type and carrying mutant TP53.	Cisplatin	28-37	P53	Homo sapiens	243-247
35192728-4	2022	Together with extended tumor exposure to therapeutically effective drug levels via reversible conjugation to Pluronic F-108 (PF108), these features translated into rapid tumor regression and long-term survival in models of both ABCG2-overexpressing and p53-mutant high-risk neuroblastomas, in contrast to a marginal effect of the clinically used camptothecin derivative, irinotecan.	Irinotecan	371-381	P53	Homo sapiens	253-256
35197630-7	2022	Our results show that irinotecan and CHEK1 inhibition have synergistic effects in microsatellite-stable or KRAS-TP53 double-mutant colon cancer cells, leading to apoptosis and suppression of tumour xenograft growth.	Irinotecan	22-32	P53	Homo sapiens	112-116
35227162-0	2022	The role of p53 and p21 on 8-chloro-adenosine-induced cellular response.	Adenosine	36-45	P53	Homo sapiens	12-15
35196199-11	2022	Our study shows that treatments targeting pathways to enhance autophagy have the potential for treating early AMD and provide support for the use of metformin, which has been found to reduce the risk of AMD development in human patients.Abbreviations:AMD: age-related macular degeneration; AMPK: 5" adenosine monophosphate-activated protein kinase APOE: apolipoprotein E; ATM: ataxia telangiectasia mutated; BCL2L1/Bcl-xL: BCL2-like 1; DAPI: 4"-6-diamidino-2-phenylindole; ERG: electroretinogram; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GCL: ganglion cell layer; INL: inner nuclear layer; IPL: inner plexiform layer; IS/OS: inner and outer photoreceptor segments; LAMP1: lysosomal-associated membrane protein 1; MAP1LC3B/LC3: microtubule-associated protein 1 light chain 3 beta; MTOR: mechanistic target of rapamycin kinase; OCT: optical coherence tomography; ONL: outer nuclear layer; OPs: oscillatory potentials; p-EIF4EBP1: phosphorylated eukaryotic translation initiation factor 4E binding protein 1; p-MAPK14/p38: phosphorylated mitogen-activated protein kinase 14; RPE: retinal pigment epithelium; RPS6KB/p70 S6 kinase: ribosomal protein S6 kinase; SQSTM1/p62: sequestosome 1; TP53/TRP53/p53: tumor related protein 53; TSC2: TSC complex subunit 2; WT: wild type.	Metformin	149-158	P53	Homo sapiens	1192-1196
35592280-10	2022	Moreover, CUR/CDP treatment at 20 and 40 mug/ml inhibited H2O2-induced increase in phosphorylated-p53 and caspase-3 expression, indicating that CUR/CDP suppressed cell apoptosis to alleviate liver injury.	Hydrogen Peroxide	58-62	P53	Homo sapiens	98-101
35269416-0	2022	Effects of the Mutant TP53 Reactivator APR-246 on Therapeutic Sensitivity of Pancreatic Cancer Cells in the Presence and Absence of WT-TP53.	eprenetapopt	39-46	P53	Homo sapiens	22-26
35269416-4	2022	APR-246 is one such molecule, and it is referred to as a mutant TP53 reactivator.	eprenetapopt	0-7	P53	Homo sapiens	64-68
35196199-11	2022	Our study shows that treatments targeting pathways to enhance autophagy have the potential for treating early AMD and provide support for the use of metformin, which has been found to reduce the risk of AMD development in human patients.Abbreviations:AMD: age-related macular degeneration; AMPK: 5" adenosine monophosphate-activated protein kinase APOE: apolipoprotein E; ATM: ataxia telangiectasia mutated; BCL2L1/Bcl-xL: BCL2-like 1; DAPI: 4"-6-diamidino-2-phenylindole; ERG: electroretinogram; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GCL: ganglion cell layer; INL: inner nuclear layer; IPL: inner plexiform layer; IS/OS: inner and outer photoreceptor segments; LAMP1: lysosomal-associated membrane protein 1; MAP1LC3B/LC3: microtubule-associated protein 1 light chain 3 beta; MTOR: mechanistic target of rapamycin kinase; OCT: optical coherence tomography; ONL: outer nuclear layer; OPs: oscillatory potentials; p-EIF4EBP1: phosphorylated eukaryotic translation initiation factor 4E binding protein 1; p-MAPK14/p38: phosphorylated mitogen-activated protein kinase 14; RPE: retinal pigment epithelium; RPS6KB/p70 S6 kinase: ribosomal protein S6 kinase; SQSTM1/p62: sequestosome 1; TP53/TRP53/p53: tumor related protein 53; TSC2: TSC complex subunit 2; WT: wild type.	Metformin	149-158	P53	Homo sapiens	1197-1202
35196199-11	2022	Our study shows that treatments targeting pathways to enhance autophagy have the potential for treating early AMD and provide support for the use of metformin, which has been found to reduce the risk of AMD development in human patients.Abbreviations:AMD: age-related macular degeneration; AMPK: 5" adenosine monophosphate-activated protein kinase APOE: apolipoprotein E; ATM: ataxia telangiectasia mutated; BCL2L1/Bcl-xL: BCL2-like 1; DAPI: 4"-6-diamidino-2-phenylindole; ERG: electroretinogram; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; GCL: ganglion cell layer; INL: inner nuclear layer; IPL: inner plexiform layer; IS/OS: inner and outer photoreceptor segments; LAMP1: lysosomal-associated membrane protein 1; MAP1LC3B/LC3: microtubule-associated protein 1 light chain 3 beta; MTOR: mechanistic target of rapamycin kinase; OCT: optical coherence tomography; ONL: outer nuclear layer; OPs: oscillatory potentials; p-EIF4EBP1: phosphorylated eukaryotic translation initiation factor 4E binding protein 1; p-MAPK14/p38: phosphorylated mitogen-activated protein kinase 14; RPE: retinal pigment epithelium; RPS6KB/p70 S6 kinase: ribosomal protein S6 kinase; SQSTM1/p62: sequestosome 1; TP53/TRP53/p53: tumor related protein 53; TSC2: TSC complex subunit 2; WT: wild type.	Metformin	149-158	P53	Homo sapiens	1203-1206
35220706-16	2022	At 48 h after seeding, the expression levels of senescence-related proteins p16 and p53 both were significantly higher in HDFs of high glucose group than those in low glucose group (with t values of 11.85 and 3.02, respectively, P<0.05 or P<0.01).	Glucose	167-174	P53	Homo sapiens	84-87
35273907-10	2021	Lastly, patients with EGFR and TP53 co-alterations showed similar responses to Gefitinib and Icotinib, and the co-occurring TP53 mutation was most likely to be a poor prognostic factor for patients receiving Gefitinib, indicating that the distributions and types of TP53 mutations may contribute to the efficacy and prognosis of molecular targeted therapy.	Gefitinib	208-217	P53	Homo sapiens	124-128
35204316-10	2022	Furthermore, 300 microM H2O2 affected genes related to the p53 pathway and cell cycle.	Hydrogen Peroxide	24-28	P53	Homo sapiens	59-62
35204825-8	2022	The p53 complexes with SIRT2, MUL1, USP7, TXN, PIN1 and PPIF control regulation of p53 function through post-translational modifications, such as lysine acetylation or ubiquitination, cysteine/cystine redox transformation and peptidyl-prolyl cis-trans isomerization.	Lysine	146-152	P53	Homo sapiens	4-7
35204825-9	2022	Redox sensitivity of p53 functions is supported by (i) thioredoxin-dependent reduction of p53 disulfides, (ii) inhibition of the thioredoxin-dependent deoxyribonucleotide synthesis by p53 binding to RRM2B and (iii) changed intracellular distribution of p53 through its oxidation by CHCHD4 in the mitochondrial intermembrane space.	Disulfides	94-104	P53	Homo sapiens	90-93
35204825-8	2022	The p53 complexes with SIRT2, MUL1, USP7, TXN, PIN1 and PPIF control regulation of p53 function through post-translational modifications, such as lysine acetylation or ubiquitination, cysteine/cystine redox transformation and peptidyl-prolyl cis-trans isomerization.	Lysine	146-152	P53	Homo sapiens	83-86
35204825-8	2022	The p53 complexes with SIRT2, MUL1, USP7, TXN, PIN1 and PPIF control regulation of p53 function through post-translational modifications, such as lysine acetylation or ubiquitination, cysteine/cystine redox transformation and peptidyl-prolyl cis-trans isomerization.	Cysteine	184-192	P53	Homo sapiens	4-7
35204825-8	2022	The p53 complexes with SIRT2, MUL1, USP7, TXN, PIN1 and PPIF control regulation of p53 function through post-translational modifications, such as lysine acetylation or ubiquitination, cysteine/cystine redox transformation and peptidyl-prolyl cis-trans isomerization.	Cysteine	184-192	P53	Homo sapiens	83-86
35204825-9	2022	Redox sensitivity of p53 functions is supported by (i) thioredoxin-dependent reduction of p53 disulfides, (ii) inhibition of the thioredoxin-dependent deoxyribonucleotide synthesis by p53 binding to RRM2B and (iii) changed intracellular distribution of p53 through its oxidation by CHCHD4 in the mitochondrial intermembrane space.	Disulfides	94-104	P53	Homo sapiens	21-24
35215995-9	2022	The ROS scavenger N-acetyl-l-cysteine (NAC) and the p53 specific inhibitor Pifithrin-alpha (PFT-alpha) suppressed PEDV-induced apoptosis and impeded viral replication, suggesting that ROS and p53 play an important role in PEDV-induced apoptosis and viral replication.	ros	4-7	P53	Homo sapiens	192-195
35216325-9	2022	Differential gene expression analysis showed that gefitinib perturbed signal transduction pathways, apoptosis, cell cycle, FOXO-mediated transcription, p53 signalling pathway, and metabolic pathways.	Gefitinib	50-59	P53	Homo sapiens	152-155
35215995-9	2022	The ROS scavenger N-acetyl-l-cysteine (NAC) and the p53 specific inhibitor Pifithrin-alpha (PFT-alpha) suppressed PEDV-induced apoptosis and impeded viral replication, suggesting that ROS and p53 play an important role in PEDV-induced apoptosis and viral replication.	Acetylcysteine	39-42	P53	Homo sapiens	192-195
35215995-9	2022	The ROS scavenger N-acetyl-l-cysteine (NAC) and the p53 specific inhibitor Pifithrin-alpha (PFT-alpha) suppressed PEDV-induced apoptosis and impeded viral replication, suggesting that ROS and p53 play an important role in PEDV-induced apoptosis and viral replication.	ros	184-187	P53	Homo sapiens	52-55
35143532-6	2022	When the cells were treated with concentrations of SN38 ranging from 0-30 ng/ml, all four cell lines accumulated p53 which was phosphorylated on serines 15 and 20.	Serine	145-152	P53	Homo sapiens	113-116
35205642-7	2022	Cisplatin-induced and EP300-dependent transcriptional activation of ABCC10 was only possible in the presence of p53.	Cisplatin	0-9	P53	Homo sapiens	112-115
35222383-8	2022	Furthermore, GSEA and GSVA revealed significant enrichment of p53 pathway and mismatch repair pathways in high risk-score subgroups.	gsea	13-17	P53	Homo sapiens	62-65
35223843-0	2022	Harpagoside Protects Against Doxorubicin-Induced Cardiotoxicity via P53-Parkin-Mediated Mitophagy.	Doxorubicin	29-40	P53	Homo sapiens	68-71
35069864-8	2022	Preliminary results indicated that PCA suppressed ROS-induced senescence in NP cells via both the p16 and p53 pathways.	ros	50-53	P53	Homo sapiens	106-109
35204775-0	2022	APR-246-The Mutant TP53 Reactivator-Increases the Effectiveness of Berberine and Modified Berberines to Inhibit the Proliferation of Pancreatic Cancer Cells.	Berberine	67-76	P53	Homo sapiens	19-23
35204775-0	2022	APR-246-The Mutant TP53 Reactivator-Increases the Effectiveness of Berberine and Modified Berberines to Inhibit the Proliferation of Pancreatic Cancer Cells.	Berberine	90-100	P53	Homo sapiens	19-23
35204775-5	2022	We examined the ability of the TP53 reactivator APR-246 to interact with eleven modified berberine compounds (NAX compounds) in the presence and absence of WT-TP53 in two PDAC cell lines: the MIA-PaCa-2, which has gain of function (GOF) TP53 mutations on both alleles, and PANC-28, which lacks expression of the WT TP53 protein.	Berberine	89-98	P53	Homo sapiens	31-35
35204775-6	2022	Our results indicate the TP53 reactivator-induced increase in therapeutic potential of many modified berberines.	Berberine	101-111	P53	Homo sapiens	25-29
35225471-9	2022	Quantitative real-time PCR analysis demonstrated that BA increased p53, Bax and caspase-3 expression whilst it decreased Bcl-2 expression in the HuCCA cells in a dose dependent manner.	betulinic acid	54-56	P53	Homo sapiens	67-70
35204748-6	2022	Moreover, phosphorylation of the apoptotic p53 protein was reduced while the activity of the AKT/mTOR signaling pathway was increased, which was further enhanced by oxidative stress (H2O2) in granulocytes and erythroleukemic K562 cells.	Hydrogen Peroxide	183-187	P53	Homo sapiens	43-46
35237000-1	2022	We analyzed the treatment effects of chidamide and decitabine in combination with a HAG (homoharringtonine, cytarabine, G-CSF) priming regimen (CDHAG) in acute myeloid leukemia (AML) patients with TP53 mutation.	cdhag	144-149	P53	Homo sapiens	197-201
35237000-2	2022	Seven TP53 mutated AML patients were treated with CDHAG.	cdhag	50-55	P53	Homo sapiens	6-10
35237000-10	2022	The CDHAG regimen clearly improved the ORR (71.4%) of TP53-mutated AML patients, with no severe side effects.	cdhag	4-9	P53	Homo sapiens	54-58
35069864-13	2022	Furthermore, PCA suppressed H2O2-induced changes in the protein expression of p16, p53 and collagen-2.	Hydrogen Peroxide	28-32	P53	Homo sapiens	83-86
35069864-11	2022	PCA also reduced the gene expression of Cox-2, iNOS, p53 and p16 induced by H2O2.	Hydrogen Peroxide	76-80	P53	Homo sapiens	53-56
35042627-0	2022	The involvement of ERK1/2 and p38 MAPK in the premature senescence of melanocytes induced by H2O2 through a p53-independent p21 pathway.	Hydrogen Peroxide	93-97	P53	Homo sapiens	108-111
35042627-9	2022	H2O2 treatment tended to induce premature senescence in melanocytes through a p53-independent p21 pathway.	Hydrogen Peroxide	0-4	P53	Homo sapiens	78-81
35042627-15	2022	CONCLUSION: H2O2 increases ROS levels, which activates the ERK1/2 and p38 MAPK pathways to induce the premature senescence of melanocytes through p21 via a p53-independent pathway and consequently disrupts melanosome transfer.	Hydrogen Peroxide	12-16	P53	Homo sapiens	156-159
35042627-15	2022	CONCLUSION: H2O2 increases ROS levels, which activates the ERK1/2 and p38 MAPK pathways to induce the premature senescence of melanocytes through p21 via a p53-independent pathway and consequently disrupts melanosome transfer.	ros	27-30	P53	Homo sapiens	156-159
35140788-12	2022	GSEA determined several crucial pathways related with HNSCC, which are the p53 pathway, TNF-alpha signaling via NFKB, and hypoxia.	gsea	0-4	P53	Homo sapiens	75-78
35141433-9	2022	Melatonin suppressed cell proliferation in the G2/M phase of the cell cycle (34.97 +- 0.92%) and induced apoptosis (12.43 +- 0.73%) through up-regulating p21 and p53 that was confirmed by the reduction of PCNA and Ki-67 expressions.	Melatonin	0-9	P53	Homo sapiens	162-165
35127290-6	2022	Results: SA-beta-gal staining, PCR, and western blot revealed that aspirin could alleviate the cellular expression of senescence-related indicators of BM-MSCs, including a decrease of SA-beta-gal-positive cells and staining intensity, and downregulation of p16, p21, and p53 expression after aspirin treatment.	Aspirin	67-74	P53	Homo sapiens	271-274
35073843-6	2022	Using this approach, we predicted that: (1) cisplatin promotes the anti-tumor activity of TP53 family members but suppresses the cancer-inducing function of MYCs; (2) inhibition of RELA and E2F1 is pivotal for leflunomide to exhibit antiproliferative activity; and (3) CHD8 mediates valproic acid-induced autism.	Cisplatin	44-53	P53	Homo sapiens	90-94
35088678-0	2022	Platycodon D-induced A549 cell apoptosis through RRM1-regulated p53/VEGF/MMP2 pathway.	platycodon d	0-12	P53	Homo sapiens	64-67
35078992-0	2022	Correction: Intrinsic adriamycin resistance in p53-mutated breast cancer is related to the miR-30c/FANCF/REV1-mediated DNA damage response.	Doxorubicin	22-32	P53	Homo sapiens	47-50
35074928-5	2022	Mechanistically, stabilization of wild-type p53 and induction of the p53 target gene CDKN1A (p21) leads to decreased expression of the ribonucleotide reductase (RNR) subunits RRM1 and RRM2 RNR is the rate-limiting enzyme of de novo nucleotide synthesis that reduces ribonucleotides to deoxyribonucleotides in a glutathione-dependent manner.	Glutathione	311-322	P53	Homo sapiens	69-72
35053130-2	2022	In this study, we used Zinc chloride alone or in combination with 2 Gy radiation to treat Primary Effusion Lymphoma (PEL) cells, an aggressive B-cell lymphoma associated with KSHV that harbors wt or partially functioning p53.	zinc chloride	23-36	P53	Homo sapiens	221-224
35163037-2	2022	In this work, we show that the two structurally-related sesquiterpene lactones, a 2-bromobenzyloxy derivative of dehydrosantonin (BdS) and alantolactone (ATL) sensitise p53 wildtype, homologous recombination-proficient cancer cells to low-dose treatment with the PARP inhibitor, olaparib.	Dibenzyl disulfide	130-133	P53	Homo sapiens	169-172
35058503-6	2022	Knockdown of p53, RBL2, or the DREAM component LIN37 increased AURKA/B pathway gene expression and reduced paclitaxel and radiation toxicity in NSCLC cells.	Paclitaxel	107-117	P53	Homo sapiens	13-16
35045962-0	2022	Correction: Phase I Trial of ALRN-6924, a Dual Inhibitor of MDMX and MDM2, in Patients with Solid Tumors and Lymphomas Bearing Wild-type TP53.	alrn-6924	29-38	P53	Homo sapiens	137-141
35074928-5	2022	Mechanistically, stabilization of wild-type p53 and induction of the p53 target gene CDKN1A (p21) leads to decreased expression of the ribonucleotide reductase (RNR) subunits RRM1 and RRM2 RNR is the rate-limiting enzyme of de novo nucleotide synthesis that reduces ribonucleotides to deoxyribonucleotides in a glutathione-dependent manner.	Glutathione	311-322	P53	Homo sapiens	44-47
35053325-6	2022	Conversely, Dox induced p53 expression, reduced mTOR-dependent translation, and inhibited global protein synthesis.	Doxorubicin	12-15	P53	Homo sapiens	24-27
35118064-5	2021	In this review, we focus on recent advances in our understanding of the interplay between p53 and metabolism of glucose, fatty acid as well as amino acid, and discuss how the deregulation of p53 in these processes could lead to cancer.	Glucose	112-119	P53	Homo sapiens	90-93
35118064-5	2021	In this review, we focus on recent advances in our understanding of the interplay between p53 and metabolism of glucose, fatty acid as well as amino acid, and discuss how the deregulation of p53 in these processes could lead to cancer.	Glucose	112-119	P53	Homo sapiens	191-194
35096810-6	2021	Moreover, combination of HAUS6 knockdown and 5-FU treatment further enhanced the suppression of cell proliferation of CRC cells by increasing activation of the p53/p21 pathway.	Fluorouracil	45-49	P53	Homo sapiens	160-163
35090313-8	2022	MP treatment alleviated the H2O2-induced increases in ROS levels, inhibited apoptosis, relieved cell cycle arrest, and downregulated cleaved caspase 3 and P53 protein expression.	Hydrogen Peroxide	28-32	P53	Homo sapiens	155-158
34994335-10	2022	These compounds combined with cisplatin caused upregulation in the pro-apoptotic Bax, Bid, caspase-3, caspase-8, caspase-9, Fas, and p53 gene expressions while downregulating anti-apoptotic DFFA, NFkB1, and Bcl2 gene expressions.	Cisplatin	30-39	P53	Homo sapiens	133-136
35072516-6	2022	The role of a gene variant in Tp53 that modifies proline to arginine was examined using nasal brushings from study participants in the Lovelace Smokers Cohort, primary human AECs, and mice with a modified Tp53 gene.	Arginine	60-68	P53	Homo sapiens	30-34
35154466-6	2022	Meanwhile, CP-25 and 5-Fu activated the intrinsic mitochondrial apoptosis pathway induced by P53, inhibited anti-apoptotic B-cell lymphoma (Bcl-2), induced the pro-apoptotic Bcl-2-associated X protein (Bax), Cytochrome-C and caspases.	Fluorouracil	21-25	P53	Homo sapiens	93-96
35053211-5	2022	Our studies evidenced that both DOX and GCD@DOX induced p53 and p21 signalling resulting in G0/G1 cell cycle arrest.	Doxorubicin	32-35	P53	Homo sapiens	56-59
35070983-13	2021	The KEGG pathway analysis revealed that quercetin and cisplatin may affect cervical cancer through platinum drug resistance and the p53 and HIF-1 pathways.	Cisplatin	54-63	P53	Homo sapiens	132-135
35071232-0	2021	Deficient or R273H and R248W Mutations of p53 Promote Chemoresistance to 5-FU via TCF21/CD44 Axis-Mediated Enhanced Stemness in Colorectal Carcinoma.	Fluorouracil	73-77	P53	Homo sapiens	42-45
35071232-11	2021	GSEA analysis showed that oncogenic signatures were enriched in the mutant p53 group.	gsea	0-4	P53	Homo sapiens	75-78
35071232-14	2021	Xenografts also confirmed that HCT116 cells harboring deficient or mutant p53 promoted cancer growth and 5-FU tolerance.	Fluorouracil	105-109	P53	Homo sapiens	74-77
35072516-8	2022	Study participants who were homozygous for p53 arginine compared with the proline variant showed higher mucin 5AC (MUC5AC) mRNA levels in nasal brushings if they reported WS exposure.	Arginine	47-55	P53	Homo sapiens	43-46
6323746-8	1984	In contrast, all of the detectable p53 carries the PAb1104-reactive determinant.	pab1104	51-58	P53	Homo sapiens	35-38
33938965-2	2021	AA-I forms the 7-(2"-deoxyadenosin-N6-yl)aristolactam I (dA-AL-I) adduct, which induces multiple A:T-to-T:A transversion mutations in TP53 of AA-I exposed UTUC patients.	7-(2'-Deoxyadenosin-N6-yl)aristolactam I	57-64	P53	Homo sapiens	134-138
34055057-9	2021	In summary, the present study suggested that hirsutanol A inhibited Jurkat cell viability through induction of cell cycle arrest and p53-dependent initiation of apoptosis, thus hirsutanol may serve as a promising compound for the treatment of T-ALL.	hirsutanol A	45-57	P53	Homo sapiens	133-136
33990641-0	2021	trans-Fatty acids promote p53-dependent apoptosis triggered by cisplatin-induced DNA interstrand crosslinks via the Nox-RIP1-ASK1-MAPK pathway.	Trans Fatty Acids	0-17	P53	Homo sapiens	26-29
33990641-7	2021	These results demonstrate that in response to CDDP ICLs, TFAs promote p53-dependent apoptosis through the enhancement of the Nox-RIP1-ASK1-MAPK pathway activation, providing insight into the diverse pathogenetic mechanisms of TFAs according to the types of DNA damage.	Trans Fatty Acids	57-61	P53	Homo sapiens	70-73
33990641-7	2021	These results demonstrate that in response to CDDP ICLs, TFAs promote p53-dependent apoptosis through the enhancement of the Nox-RIP1-ASK1-MAPK pathway activation, providing insight into the diverse pathogenetic mechanisms of TFAs according to the types of DNA damage.	Trans Fatty Acids	226-230	P53	Homo sapiens	70-73
33551183-4	2021	now establish that poly(PR) remodels the neuronal epigenome to promote proapoptotic p53 activity involving PUMA, which drives neurodegeneration in several models.	poly(pr)	19-27	P53	Homo sapiens	84-87
34055057-0	2021	Hirsutanol A inhibits T-acute lymphocytic leukemia Jurkat cell viability through cell cycle arrest and p53-dependent induction of apoptosis.	hirsutanol A	0-12	P53	Homo sapiens	103-106
34055057-8	2021	Of note, hirsutanol A induced the expression of the tumor suppressor p53, whereas simultaneous treatment with pifithrin-alpha, an inhibitor of p53, significantly reduced Jurkat cell apoptosis induced by hirsutanol A.	hirsutanol A	9-21	P53	Homo sapiens	69-72
33879103-7	2021	RESULTS: Samples with co-altered RB1&TP53: a) were enriched in immunity effectors (CD8 cytotoxic lymphocytes, NK cells) and display higher scores of a T cell inflamed signature; b) have a higher TMB, higher number of SNV predicted neoantigens and higher TILs fractions; c) have a higher number of DDR mutated and deep deleted DDR genes; d) have DNA somatic signatures 2 and 13 related to APOBEC mutagenesis.	1,2,4,5-tetramethoxybenzene	195-198	P53	Homo sapiens	33-41
33529725-8	2021	For instance, kynurenine pathway interacts with phospoinosisitide-3 kinase (PI3K), extracellular signal-regulated kinase (ERK), Wnt/beta-catenin, P53, bridging integrator 1 (BIN-1), cyclooxygenase 2 (COX-2), cyclin-dependent kinase (CDK) and collagen type XII alpha1 chain (COL12A1).	Kynurenine	14-24	P53	Homo sapiens	146-149
33879103-8	2021	Using the IMVigor 210 dataset, RB1&TP53 samples had the highest response rate to atezolizumab and a strong correlation with TMB and TMM.	1,2,4,5-tetramethoxybenzene	124-127	P53	Homo sapiens	31-39
33918637-5	2021	Based on their structural similarity, these compounds resemble tyrosine kinase inhibitors and the p53 reactivator CP-31398.	CP 31398	114-122	P53	Homo sapiens	98-101
33652124-6	2021	Our results have shown that glibenclamide and glimepiride decrease 1.2B4 cells viability with accompanied increase in intracellular Ca2+ concentration and increased expression of apoptosis-related CASP-3 and TP53.	Glyburide	28-41	P53	Homo sapiens	208-212
33906321-0	2021	Epigallocatechin Gallate Enhances Inhibition Effect of DDP on the Proliferation of Gastric Cancer BGC-823 Cells by Regulating p19Arf-p53-p21Cip1 Signaling Pathway.	epigallocatechin gallate	0-24	P53	Homo sapiens	133-136
34026634-10	2021	The most frequently mutated genes in afatinib-resistant patients were TP53 (44%) and EGFR (33%).	Afatinib	37-45	P53	Homo sapiens	70-74
33918387-0	2021	Distinct Classes of Flavonoids and Epigallocatechin Gallate, Polyphenol Affects an Oncogenic Mutant p53 Protein, Cell Growth and Invasion in a TNBC Breast Cancer Cell Line.	epigallocatechin gallate	35-59	P53	Homo sapiens	100-103
33906321-10	2021	EGCG combined with DDP treatment caused cell cycle arrest in G1 phase in BGC-823 cells, increase of apoptosis (21.3%) vs EGCG (7.25%) and DDP (3.86%) single-use group (p <0.01), up-regulated gene and protein expressions of p19Arf, p53, p21Cip1 (p <0.01).	epigallocatechin gallate	0-4	P53	Homo sapiens	231-234
33653952-4	2021	We report that the p53 mutant R248Q (R, arginine; Q, glutamine) forms, both in cancer cells and in solutions, a condensate with unique properties, mesoscopic protein-rich clusters.	Glutamine	53-62	P53	Homo sapiens	19-22
33454519-9	2021	The median TMB was higher in TP53-mutant tumors than in wild-type tumors (10.1 versus 7.2 mutations/Mb, p = 0.019).	1,2,4,5-tetramethoxybenzene	11-14	P53	Homo sapiens	29-33
33953402-8	2021	Hydroxyurea-induced replication stress6,7 triggered ATR-CHK1- and p53-dependent cell extrusion from a mammalian epithelial monolayer.	Hydroxyurea	0-11	P53	Homo sapiens	66-69
33996530-9	2020	TP53 mutations also influence TMB distribution (P < 0.001).	1,2,4,5-tetramethoxybenzene	30-33	P53	Homo sapiens	0-4
33906321-11	2021	CONCLUSION: EGCG can enhance the effect of DDP on inhibiting BGC-823 cell proliferation and inducing apoptosis via activating the p19Arf-p53-p21Cip1 signaling pathway.	epigallocatechin gallate	12-16	P53	Homo sapiens	137-140
33987249-13	2021	Moreover, many top gene set enrichment analysis (GSEA) results, including amino sugar and nucleotide sugar metabolism, nucleotide excision repair, or p53 signaling pathway, were enriched significantly with TMB level as phenotype.	1,2,4,5-tetramethoxybenzene	206-209	P53	Homo sapiens	150-153
33567038-8	2021	The apoptotic rates (p=0.002) of mitomycin C treated basal cell carcinoma were higher than those of the other treated cells, and their TP53 was significantly upregulated (p=0.0001).	Mitomycin	33-44	P53	Homo sapiens	135-139
33745946-6	2021	Administration of KPT-8602, an XPO1 inhibitor, followed by AZD-6738, an ATR inhibitor, resulted in dramatic antitumor effects and prolonged survival in TP53-mutant models of CRC.	Eltanexor	18-26	P53	Homo sapiens	152-156
33603772-0	2021	Prevalence of the Brazilian TP53 Founder c.1010G>A (p.Arg337His) in Lung Adenocarcinoma: Is Genotyping Warranted in All Brazilian Patients?	arg337his	54-63	P53	Homo sapiens	28-32
33603772-1	2021	In Southern and Southeastern Brazil, there is a germline pathogenic variant with incomplete penetrance located in the oligomerization domain of TP53, c.1010G>A (p.Arg337His).	arg337his	163-172	P53	Homo sapiens	144-148
33534927-10	2021	The top 3 enriched reactome pathway ID are RAB GEFs exchange GTP for GDP on RABs, Regulation of TP53 Degradation and Regulation of TP53 Expression and Degradation.	Guanosine Diphosphate	69-72	P53	Homo sapiens	96-100
33534927-10	2021	The top 3 enriched reactome pathway ID are RAB GEFs exchange GTP for GDP on RABs, Regulation of TP53 Degradation and Regulation of TP53 Expression and Degradation.	Guanosine Diphosphate	69-72	P53	Homo sapiens	131-135
33710818-11	2021	PD166866 and RG7112, an MDM2/p53 inhibitor, cooperatively inhibited the colony formation and distal seeding of LSCC cells (P < 0.01), and upregulated the expression of p53 and p21.	RG7112	13-19	P53	Homo sapiens	29-32
33844607-11	2021	PBM restored proliferation by regulating Rb and p53 in ionizing radiated thyroid follicular tissues.	pbm	0-3	P53	Homo sapiens	48-51
33399091-9	2021	Genetically, NRAS mutations, TP53 mutations, and NF2 deletions were significantly associated with resistance to CPIs (P < 0.05).	cpis	112-116	P53	Homo sapiens	29-33
33710818-11	2021	PD166866 and RG7112, an MDM2/p53 inhibitor, cooperatively inhibited the colony formation and distal seeding of LSCC cells (P < 0.01), and upregulated the expression of p53 and p21.	RG7112	13-19	P53	Homo sapiens	168-171
33538587-1	2021	We identified a set of thiosemicarbazone (TSC) metal ion chelators that reactivate specific zinc-deficient p53 mutants using a mechanism called zinc metallochaperones (ZMCs) that restore zinc binding by shuttling zinc into cells.	Thiosemicarbazones	23-40	P53	Homo sapiens	107-110
33629325-0	2021	Zinc oxide nanoparticles promotes liver cancer cell apoptosis through inducing autophagy and promoting p53.	Zinc Oxide	0-10	P53	Homo sapiens	103-106
33570057-6	2021	Mechanistically, rhamnetin increased expression of miR-148a (which is tumor-suppressive) in a P53-dependent manner, leading to inhibition of PXR expression and decrease in expression of its downstream genes.	rhamnetin	17-26	P53	Homo sapiens	94-97
33570057-7	2021	Rhamnetin enhanced miRNA-148a transcription by repressing Sirt1 activation to enhance acetylation at residue-373 of P53.	rhamnetin	0-9	P53	Homo sapiens	116-119
33884928-0	2021	Chelidonine Induces Apoptosis via GADD45a-p53 Regulation in Human Pancreatic Cancer Cells.	chelidonine	0-11	P53	Homo sapiens	42-45
33538587-1	2021	We identified a set of thiosemicarbazone (TSC) metal ion chelators that reactivate specific zinc-deficient p53 mutants using a mechanism called zinc metallochaperones (ZMCs) that restore zinc binding by shuttling zinc into cells.	Thiosemicarbazones	42-45	P53	Homo sapiens	107-110
33884928-7	2021	These results suggest that chelidonine induces pancreatic cancer apoptosis through the p53 and GADD45A pathways.	chelidonine	27-38	P53	Homo sapiens	87-90
33713860-4	2021	NC loaded with omega 3 polyunsaturated fatty acid (NC-EPA:DHA 6:1) were more effective than native EPA:DHA 6:1 to prevent Ang II-induced VCAM-1 and p53 upregulation, and SA-beta- galactosidase activity in coronary artery segments.	omega 3 polyunsaturated fatty acid	15-49	P53	Homo sapiens	148-151
33546743-2	2021	We aimed to explore the interaction of the silica-induced epithelial-mesenchymal transition (EMT)-related transcripts with the cellular metabolism regulated by p53.	Silicon Dioxide	43-49	P53	Homo sapiens	160-163
33627632-8	2021	The interaction between RCP and P-gp was verified endogenously and loss of RCP or mutant p53 rendered cells more sensitive to cisplatin and etoposide.	Etoposide	140-149	P53	Homo sapiens	89-92
32933334-7	2021	Furthermore, Western blot analysis showed that capsanthin application increased p53 and Bax protein expressions and caused a decrease in Bcl-2 protein level.	capsanthin	47-57	P53	Homo sapiens	80-83
32933334-9	2021	These results show that the capsanthin causes oxidative stress and DNA damage, and increases mitochondrial apoptotic mechanism-mediated cell death after p53 and Bax protein activations.	capsanthin	28-38	P53	Homo sapiens	153-156
33546743-5	2021	RESULTS: Fifty-two mRNAs showed significantly altered expression in the HBE p53-KO cells post-silica exposure.	Silicon Dioxide	94-100	P53	Homo sapiens	76-79
33546743-6	2021	A total of 42 metabolites were putatively involved in p53-dependent silica-mediated HBE cell dysfunction.	Silicon Dioxide	68-74	P53	Homo sapiens	54-57
33546743-7	2021	Through integrated data analysis, we obtained five significant p53-dependent metabolic pathways including phenylalanine, glyoxylate, dicarboxylate, and linoleic acid metabolism, and the citrate cycle.	glyoxylic acid	121-131	P53	Homo sapiens	63-66
33579943-0	2021	EGCG binds intrinsically disordered N-terminal domain of p53 and disrupts p53-MDM2 interaction.	epigallocatechin gallate	0-4	P53	Homo sapiens	57-60
33376857-10	2020	Furthermore, we found that GW9508 ameliorated ox-LDL-induced endothelial cell cycle arrest at the G0/G1 phase and the expression of key senescence proteins, including p53 and plasminogen activator inhibitor-1(PAI-1).	GW9508	27-33	P53	Homo sapiens	167-170
33546743-8	2021	Through metabolite screening, we further identified that benzeneacetic acid, a key regulation metabolite in the phenylalanine metabolic pathway, attenuated the silica-induced EMT in HBE cells in a p53-dependent manner.	Silicon Dioxide	160-166	P53	Homo sapiens	197-200
33579943-0	2021	EGCG binds intrinsically disordered N-terminal domain of p53 and disrupts p53-MDM2 interaction.	epigallocatechin gallate	0-4	P53	Homo sapiens	74-77
33546743-10	2021	CONCLUSIONS: Our study offers new insights into the molecular mechanisms by which epithelial cells respond to silica exposure and provide fresh perspective and direction for future clinical biomarker research and potential clinically sustainable and translatable role of p53.	Silicon Dioxide	110-116	P53	Homo sapiens	271-274
33579943-2	2021	Using SPR and NMR, here we report a direct, muM interaction between EGCG and the tumor suppressor p53 (KD = 1.6 +- 1.4 muM), with the disordered N-terminal domain (NTD) identified as the major binding site (KD = 4 +- 2 muM).	epigallocatechin gallate	68-72	P53	Homo sapiens	98-101
33579943-4	2021	The EGCG-p53 interaction disrupts p53 interaction with its regulatory E3 ligase MDM2 and inhibits ubiquitination of p53 by MDM2 in an in vitro ubiquitination assay, likely stabilizing p53 for anti-tumor activity.	epigallocatechin gallate	4-8	P53	Homo sapiens	9-12
33579943-4	2021	The EGCG-p53 interaction disrupts p53 interaction with its regulatory E3 ligase MDM2 and inhibits ubiquitination of p53 by MDM2 in an in vitro ubiquitination assay, likely stabilizing p53 for anti-tumor activity.	epigallocatechin gallate	4-8	P53	Homo sapiens	34-37
33579943-4	2021	The EGCG-p53 interaction disrupts p53 interaction with its regulatory E3 ligase MDM2 and inhibits ubiquitination of p53 by MDM2 in an in vitro ubiquitination assay, likely stabilizing p53 for anti-tumor activity.	epigallocatechin gallate	4-8	P53	Homo sapiens	34-37
33579943-4	2021	The EGCG-p53 interaction disrupts p53 interaction with its regulatory E3 ligase MDM2 and inhibits ubiquitination of p53 by MDM2 in an in vitro ubiquitination assay, likely stabilizing p53 for anti-tumor activity.	epigallocatechin gallate	4-8	P53	Homo sapiens	34-37
33579943-5	2021	Our work provides insights into the mechanisms for EGCG"s anticancer activity and identifies p53 NTD as a target for cancer drug discovery through dynamic interactions with small molecules.	epigallocatechin gallate	51-55	P53	Homo sapiens	93-96
33488754-12	2020	DDI-CPI identified the top 25 proteins related with PI3K/AKT, apoptosis, and the p53 pathways.	ddi-cpi	0-7	P53	Homo sapiens	81-84
33530952-9	2021	INI-43 pre-treatment resulted in moderately stabilized p53 and induced p53 reporter activity, which translated to increased p21 and decreased Mcl-1 upon cisplatin combination treatment.	INI-43	0-6	P53	Homo sapiens	55-58
32755565-5	2020	The PUFA overload increased mitochondrial reactive oxygen species, impaired mitochondrial respiratory functions, and triggered mitochondrial stress-activated p53-independent apoptosis in CYP4V2 mutant RPE cells.	Fatty Acids, Unsaturated	4-8	P53	Homo sapiens	158-161
33546743-0	2021	Transcriptomic and metabolomic profiling reveal the p53-dependent benzeneacetic acid attenuation of silica-induced epithelial-mesenchymal transition in human bronchial epithelial cells.	Silicon Dioxide	100-106	P53	Homo sapiens	52-55
33530952-9	2021	INI-43 pre-treatment resulted in moderately stabilized p53 and induced p53 reporter activity, which translated to increased p21 and decreased Mcl-1 upon cisplatin combination treatment.	INI-43	0-6	P53	Homo sapiens	71-74
33360044-0	2021	Synergy between vinorelbine and afatinib in the inhibition of non-small cell lung cancer progression by EGFR and p53 signaling pathways.	Afatinib	32-40	P53	Homo sapiens	113-116
32432260-6	2020	Protein expression profile sets [Au(dmap)(Et3P)]+ further apart from auranofin, with proteolytic degradation of caspase-3 and poly(ADP-ribose)-polymerase (PARP), DNA strand-break induced phosphorylation of Chk2 Thr68 and increased p53 ser15 phosphorylation.	Auranofin	69-78	P53	Homo sapiens	231-234
33360044-10	2021	The low doses of vinorelbine plus afatinib blocked the phosphorylation of AKT, ERK, JNK, and p38, but restored the expression of p53.	Afatinib	34-42	P53	Homo sapiens	129-132
33530952-12	2021	CONCLUSIONS: Taken together, this study shows that INI-43 pre-treatment significantly enhances cisplatin sensitivity in cervical cancer cells, mediated through stabilization of p53 and decreased nuclear import of NFkappaB.	INI-43	51-57	P53	Homo sapiens	177-180
33524216-11	2021	Nutlin-3 increased Notch signaling (NICD, Hes1) and DAPT inhibition of Notch activation prevented Nutlin-3 (p53)-induced asymmetric SC self-renewal divisions in aged keratinocytes.	nutlin 3	98-106	P53	Homo sapiens	108-111
33360419-10	2021	In addition, HES treatment reduced the mRNA level of p21 but increased the mRNA level of cyclin D1 and p53 in the mammosphere.	Hesperidin	13-16	P53	Homo sapiens	103-106
33360419-12	2021	More importantly, this study highlighted p53 as a key protein in inhibition of BCSCs by HES.	Hesperidin	88-91	P53	Homo sapiens	41-44
33368049-9	2020	The PI3K/Akt/ERK phosphorylation was inhibited, while p21 and p53, death receptor, expression was promoted by DPMPP treatment.	dpmpp	110-115	P53	Homo sapiens	62-81
33303573-1	2021	In this study, we explored whether Nutlin-3a, a well-known nontoxic small-molecule compound antagonizing the inhibitory interaction of MDM2 with the tumor suppressor p53, may restore ligands for natural killer (NK) cell-activating receptors (NK-ARs) on neuroblastoma (NB) cells to enhance the NK cell-mediated killing.	nutlin 3	35-44	P53	Homo sapiens	166-169
32786121-7	2021	We further show that SENP1 depletion synergizes with DNA damage-inducing agent etoposide to induce p53 activation and the expression of p21, leading to synergistic growth inhibition of cancer cells.	Etoposide	79-88	P53	Homo sapiens	99-102
33275947-0	2021	Up-regulation of miRNA-151-3p enhanced the neuroprotective effect of dexmedetomidine against beta-amyloid by targeting DAPK-1 and TP53.	Dexmedetomidine	69-84	P53	Homo sapiens	130-134
33183422-4	2021	Western blot was used to detect the expression of p53 protein in A549 cells after nanoplatin treatment.	demplatin pegraglumer	82-92	P53	Homo sapiens	50-53
32633026-14	2020	Collectively, CP-31398-regulated Slug downregulation represses the p53-mutated EC via the p53/Wnt/Puma pathway.	CP 31398	14-22	P53	Homo sapiens	67-70
32633026-14	2020	Collectively, CP-31398-regulated Slug downregulation represses the p53-mutated EC via the p53/Wnt/Puma pathway.	CP 31398	14-22	P53	Homo sapiens	90-93
33275947-7	2021	As indicated by western blot, Dex stimulates both pro-apoptosis (activating death-associated protein kinase 1 [DAPK-1] and p53) and anti-apoptotic (up-regulating bcl-2 and bcl-xL) signals in Abeta-treated neuronal cells.	Dexmedetomidine	30-33	P53	Homo sapiens	123-126
33275947-9	2021	To eliminate the pro-apoptotic effect of Dex while retaining its anti-apoptosis action, we screened miRNA-151-3p to target DAPK-1 and p53.	Dexmedetomidine	41-44	P53	Homo sapiens	134-137
33075425-2	2021	However, 2"-fluoro-4"-seleno-ara-C (F-Se-Ara-C), a new generation of cytarabine (Ara-C) analogs, exhibited potent antitumor activity against the p53-deficient prostate cancer cell line PC-3.	2'-Fluoro-4'-seleno-ara-C	9-34	P53	Homo sapiens	145-148
33275947-10	2021	Transfection with miRNA-151-3p mimics suppressed DAPK-1 and TP53 expression induced by Dex and increased Nrf-2 and SOD expression.	Dexmedetomidine	87-90	P53	Homo sapiens	60-64
32743759-14	2020	OS in the high TMB cohort was significantly better than that in the low TMB in patients with TP53 MUT(43.2 m vs 32.4 m; P = 0.007, HR = 0.52, 95% CI: 0.34-0.81), as well as in the combination of TP53 MUT and EGFR WT group (44.4 m vs 31.2 m; P = 0.021, HR = 0.55, 95% CI 0.34 - 0.89).	1,2,4,5-tetramethoxybenzene	15-18	P53	Homo sapiens	195-199
32743759-14	2020	OS in the high TMB cohort was significantly better than that in the low TMB in patients with TP53 MUT(43.2 m vs 32.4 m; P = 0.007, HR = 0.52, 95% CI: 0.34-0.81), as well as in the combination of TP53 MUT and EGFR WT group (44.4 m vs 31.2 m; P = 0.021, HR = 0.55, 95% CI 0.34 - 0.89).	1,2,4,5-tetramethoxybenzene	72-75	P53	Homo sapiens	93-97
33275947-13	2021	miRNA-151-3p enhanced the neuroprotective effect of Dex against Abeta by targeting DAPK-1 and TP53.	Dexmedetomidine	52-55	P53	Homo sapiens	94-98
33137455-0	2021	p53-dependent glutamine usage determines susceptibility to oxidative stress in radioresistant head and neck cancer cells.	Glutamine	14-23	P53	Homo sapiens	0-3
33178836-14	2020	The TMB and mutations of KRAS, EGFR, STK11, and TP53 were correlated with GNPNAT1.	1,2,4,5-tetramethoxybenzene	4-7	P53	Homo sapiens	48-52
33575281-0	2021	Case Report: Long-Term Chemotherapy With Hydroxyurea and Prednisolone in a Cat With a Meningioma: Correlation of FDG Uptake and Tumor Grade Assessed by Histopathology and Expression of Ki-67 and p53.	Hydroxyurea	41-52	P53	Homo sapiens	195-198
33137455-1	2021	The manner in which p53 maintains redox homeostasis and the means by which two key metabolic elements, glucose and glutamine, contribute to p53-dependent redox stability remain unclear.	Glutamine	115-124	P53	Homo sapiens	140-143
33137455-5	2021	However, in glucose-deprived and ROS-prone conditions, HN3R-B, the subclone with the original p53 increased the utilization of glutamine by GLS2, thereby maintaining redox homeostasis and ATP.	Glutamine	127-136	P53	Homo sapiens	94-97
33137455-6	2021	Conversely, HN3R-A, the p53-deficient radioresistant subclone displayed an impairment in glutamine usage and high susceptibility to metabolic stresses as well as ROS-inducing agents despite the increased ROS scavenging system.	Glutamine	89-98	P53	Homo sapiens	24-27
33039867-0	2021	ROS-mediated genotoxic stress is involved in NaAsO2-induced cell cycle arrest, stemness enhancement and chemoresistance of prostate cancer cells in a p53-independent manner.	sodium arsenite	45-51	P53	Homo sapiens	150-153
33108147-0	2020	Resveratrol enhances apoptosis induced by the heterocyclic aromatic amines in p53-wt LoVo cells, but not in p53-deficient HaCaT cells.	heterocyclic	46-58	P53	Homo sapiens	78-81
33137455-7	2021	Collectively, our findings suggest that p53 governs the alternative utilization of metabolic ingredients, such as glucose and glutamine, in ROS-prone conditions.	Glutamine	126-135	P53	Homo sapiens	40-43
33039867-10	2021	Phosphor-p53, a downstream molecule of ATM signaling, and p21, a direct target of p53, were upregulated in NaAsO2-exposed DU145 cells.	sodium arsenite	107-113	P53	Homo sapiens	9-12
33039867-10	2021	Phosphor-p53, a downstream molecule of ATM signaling, and p21, a direct target of p53, were upregulated in NaAsO2-exposed DU145 cells.	sodium arsenite	107-113	P53	Homo sapiens	82-85
33391418-9	2021	And TP53 mutations were also associated with higher TMB in the TCGA and Chinese cohort (P = 0.0005 and 0.0010, respectively).	1,2,4,5-tetramethoxybenzene	52-55	P53	Homo sapiens	4-8
33039867-11	2021	Unexpectedly, p21 was also elevated in NaAsO2-exposed p53-null PC-3 cells.	sodium arsenite	39-45	P53	Homo sapiens	54-57
33039867-13	2021	These results suggest that ROS-mediated genotoxic stress is involved in NaAsO2-induced cell cycle arrest, stemness enhancement and chemoresistance of prostate cancer cells in a p53-independent manner.	sodium arsenite	72-78	P53	Homo sapiens	177-180
32578917-6	2020	Results of ethidium bromide/acridine orange (EtBr/AO), 4,6-diamidino-2-phenylindole, comet, and lactate dehydrogenase assays revealed that 4-FPAC caused cytotoxicity via reactive oxygen species-induced p53-mediated mechanism, which involves both extrinsic and intrinsic pathways of apoptosis.	4-fpac	139-145	P53	Homo sapiens	202-205
33391418-12	2021	Conclusions: The results suggest that LRP1B or TP53 mutations are associated with higher TMB and a poor prognostic factor in HCC.	1,2,4,5-tetramethoxybenzene	89-92	P53	Homo sapiens	47-51
33318190-0	2020	Sulfated glycosaminoglycans mediate prion-like behavior of p53 aggregates.	A73025	0-27	P53	Homo sapiens	59-62
33072585-5	2020	Results: KRAS mutation with concurrent TP53 or STK11 mutations had higher TMB and CNA compared to KRAS mutation alone.	1,2,4,5-tetramethoxybenzene	74-77	P53	Homo sapiens	39-43
33072585-6	2020	The KRAS G12C and G > T mutation subgroups, with TP53 or STK11 co-mutation, also had higher TMB and CNA.	1,2,4,5-tetramethoxybenzene	92-95	P53	Homo sapiens	49-53
33096451-0	2021	Trans-chalcone induces death by autophagy mediated by p53 up-regulation and beta-catenin down-regulation on human hepatocellular carcinoma HuH7.5 cell line.	Chalcone	0-14	P53	Homo sapiens	54-57
33425912-12	2020	EGCG enhanced the anti-tumor effect of DOX in bladder cancer via NF-kappaB/MDM2/p53 pathway, suggesting the potential clinical application against bladder cancer patients.	epigallocatechin gallate	0-4	P53	Homo sapiens	80-83
33425912-0	2020	EGCG Enhanced the Anti-tumor Effect of Doxorubicine in Bladder Cancer via NF-kappaB/MDM2/p53 Pathway.	epigallocatechin gallate	0-4	P53	Homo sapiens	89-92
33425912-8	2020	Further mechanistic studies determined that the combination of DOX and EGCG inhibited phosphorylated NF-kappaB and MDM2 expression, and up-regulated p53 expression in tumor, as assessed by western blot and immunohistochemistry.	epigallocatechin gallate	71-75	P53	Homo sapiens	149-152
33381272-0	2020	Olaquindox-Induced Liver Damage Involved the Crosstalk of Oxidative Stress and p53 In Vivo and In Vitro.	olaquindox	0-10	P53	Homo sapiens	79-82
32687844-10	2020	DpdtC treatment resulted in upregulation of p53, but, the addition of p53 inhibitor, PFT-alpha could significantly neutralize the action of DpdtC on ferritinophagy induction and EMT inhibition.	di-n-propyldithiocarbamate	140-145	P53	Homo sapiens	70-73
32687844-12	2020	In addition to upregulation of p53, its down-stream targets, AKT/mTor were also downregulated, supporting that DpdtC induced EMT inhibition was achieved through ferritinophagy-ROS vicious cycle mediated p53/AKT/mTor pathway.	di-n-propyldithiocarbamate	111-116	P53	Homo sapiens	31-34
33425912-9	2020	Western blot in SW780 cells also confirmed that the combined use of EGCG and DOX caused significant increase in p53, p21, and cleaved-PARP expression, and induced significant inhibition in phosphorylated NF-kappaB and MDM2.	epigallocatechin gallate	68-72	P53	Homo sapiens	112-115
32687844-12	2020	In addition to upregulation of p53, its down-stream targets, AKT/mTor were also downregulated, supporting that DpdtC induced EMT inhibition was achieved through ferritinophagy-ROS vicious cycle mediated p53/AKT/mTor pathway.	di-n-propyldithiocarbamate	111-116	P53	Homo sapiens	203-206
33381272-3	2020	The present study was aimed at investigating the roles of oxidative stress and p53 in OLA-caused liver damage.	olaquindox	86-89	P53	Homo sapiens	79-82
33381272-8	2020	Moreover, loss of p53 decreased OLA-induced mitochondrial dysfunction and caspase activations, with the evidence of inhibited activation of phosphorylation- (p-) p38 and p-JNK and upregulated cell autophagy via activation of the LC3 and Beclin1 pathway in HCT116 and L02 cells.	olaquindox	32-35	P53	Homo sapiens	18-21
33381272-9	2020	Taken together, our findings provided a support that p53 primarily played a proapoptotic role in OLA-induced liver damage against oxidative stress and mitochondrial dysfunction, which were largely dependent on suppression of the JNK/p38 pathway and upregulation of the autophagy pathway via activation of LC3 and Beclin1.	olaquindox	97-100	P53	Homo sapiens	53-56
33409152-9	2020	Treatment with DSF/Cu induced oxidative stress and DNA damage response by elevating the reactive oxygen species levels; increasing the expression of P53, P21, and gamma-H2AX proteins; and inhibiting Wnt/beta-catenin signaling in vitro and in vivo.	Disulfiram	15-18	P53	Homo sapiens	149-152
33363171-11	2020	Although TP53-MT was associated with a high TMB, the expression of most immune checkpoint molecules and immune-related genes was lower in TP53-MT patients than TP53-WT patients, which may reflect low immunogenicity.	1,2,4,5-tetramethoxybenzene	44-47	P53	Homo sapiens	9-13
32613269-4	2020	Therefore, we performed a meta-analysis to investigate the predictive value of TP53 mutations to outcomes of HMA therapy in patients with MDS and related neoplasms.	5-(N,N-hexamethylene)amiloride	109-112	P53	Homo sapiens	79-83
32613269-9	2020	The results showed that the presence of TP53 mutation predicted an increased overall response rate with HMA treatment in the subsets that restricted patients in de novo disease, MDS by WHO (World Health Organization) criteria, or NGS (next-generation sequence) group (P = 0.005, P = 0.003, P = 0.0005, respectively).	5-(N,N-hexamethylene)amiloride	104-107	P53	Homo sapiens	40-44
32722075-8	2020	In addition, LY and TAM combination induced the apoptotic genes Caspase-3, Caspase-7, and p53, as well as p21 as cell cycle promotor, and significantly downregulated the anti-apoptotic genes Bcl-2 and survivin.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	13-15	P53	Homo sapiens	90-93
33381593-5	2020	Further research found ellagic acid and corilagin induced G2 phase cell cycle arrest by upregulating levels of P53, Bcl-2, caspase 3, and caspase 9, while the Bax was reduced.	Ellagic Acid	23-35	P53	Homo sapiens	111-114
31988438-10	2020	Here we further show that Romidepsin can reactivate p53 targeted genes which are dysregulated in TP53mut cells and preferentially targets TP53mut subpopulation.	romidepsin	26-36	P53	Homo sapiens	52-55
31988438-10	2020	Here we further show that Romidepsin can reactivate p53 targeted genes which are dysregulated in TP53mut cells and preferentially targets TP53mut subpopulation.	romidepsin	26-36	P53	Homo sapiens	97-101
33225610-0	2020	PIDDosome-induced p53-dependent ploidy restriction facilitates hepatocarcinogenesis.	piddosome	0-9	P53	Homo sapiens	18-21
33363036-8	2020	We found cases with TP53 alterations had less EGFR alterations in KSCC (P = 0.013, OR = 0.158).	kscc	66-70	P53	Homo sapiens	20-24
32611259-8	2020	In addition, the C18-CAMEL/p53 plasmid complexes and the MDM2 inhibitor nutlin-3a showed significantly synergistic anticancer activity against MCF-7 cells expressing wild-type p53.	nutlin 3	72-81	P53	Homo sapiens	176-179
31988438-10	2020	Here we further show that Romidepsin can reactivate p53 targeted genes which are dysregulated in TP53mut cells and preferentially targets TP53mut subpopulation.	romidepsin	26-36	P53	Homo sapiens	138-142
33457005-0	2020	Genome-wide association study of the TP53 R249S mutation in hepatocellular carcinoma with aflatoxin B1 exposure and infection with hepatitis B virus.	Aflatoxin B1	90-102	P53	Homo sapiens	37-41
32565942-10	2020	In conclusion, to the best of our knowledge, this is the first study to report that dasatinib can induce pyroptosis in tumor cells and increase the protein levels of GSDMD and GSDME in a p53-independent manner.	Dasatinib	84-93	P53	Homo sapiens	187-190
33457005-1	2020	Background: Exposure to dietary aflatoxin B1 (AFB1) induces DNA damage and mutation in the TP53 gene at codon 249, known as the TP53 R249S mutation, and is a major risk factor for hepatocellular carcinoma (HCC).	Aflatoxin B1	32-44	P53	Homo sapiens	91-95
32985761-10	2020	Treatment with both TCDD and PUFAs collaboratively enhanced the levels of AHR, CYP1A1, p53, p21, Rb and regucalcin.	Fatty Acids, Unsaturated	29-34	P53	Homo sapiens	87-90
32617130-5	2020	UA pretreatment of HDFs also attenuated the UVB-induced expression of inflammatory (TNF-alpha and NF-kappaB) and apoptotic (p53, Bax, and caspase-3) and MMPs (MMP-2 and MMP-9) and enhanced the Bcl-2 protein levels in 20 muM UA treatment, when compared to concentrations.	ursolic acid	0-2	P53	Homo sapiens	124-127
33457005-1	2020	Background: Exposure to dietary aflatoxin B1 (AFB1) induces DNA damage and mutation in the TP53 gene at codon 249, known as the TP53 R249S mutation, and is a major risk factor for hepatocellular carcinoma (HCC).	Aflatoxin B1	32-44	P53	Homo sapiens	128-132
33457005-1	2020	Background: Exposure to dietary aflatoxin B1 (AFB1) induces DNA damage and mutation in the TP53 gene at codon 249, known as the TP53 R249S mutation, and is a major risk factor for hepatocellular carcinoma (HCC).	Aflatoxin B1	46-50	P53	Homo sapiens	91-95
33457005-1	2020	Background: Exposure to dietary aflatoxin B1 (AFB1) induces DNA damage and mutation in the TP53 gene at codon 249, known as the TP53 R249S mutation, and is a major risk factor for hepatocellular carcinoma (HCC).	Aflatoxin B1	46-50	P53	Homo sapiens	128-132
33211826-5	2020	The impact of TP53mut VAF on clinical outcomes was driven by patients treated with a cytarabine-based regimen (median OS, 4.7 vs 7.3 months for VAF >40% vs <=40%; P = .006), whereas VAF did not significantly affect OS in patients treated with HMA.	5-(N,N-hexamethylene)amiloride	243-246	P53	Homo sapiens	14-21
32272174-6	2020	Conversely, levels of senescence-associated genes TP53, SERPINE1, IGFBP3 were slightly but significantly reduced in patients compared to uninfected matched individuals and this effect is related to NNRTI-containing treatments.	nnrti	198-203	P53	Homo sapiens	50-54
33160274-3	2020	More intriguingly, the disruption of p53 in hESCs leads to dramatic upregulation of phosphatidylcholine and decrease of total choline in both pluripotent and differentiated state of hESCs, suggesting abnormal choline metabolism in the absence of p53.	Phosphatidylcholines	84-103	P53	Homo sapiens	37-40
33177551-9	2020	Pathway enrichment analyses of these metabolites and corresponding transcriptional data correlated N-acetylneuraminate with immunoregulatory interactions between lymphoid and non-lymphoid cells, and correlated pyridoxate with p53-regulated metabolic genes and mitochondrial translation.	pyridoxate	210-220	P53	Homo sapiens	226-229
32615160-10	2020	Bergenin-mediated SIRT1 activation was further confirmed by results indicating decreased acetylation levels of NF-kappaB-p65 and p53.	bergenin	0-8	P53	Homo sapiens	129-132
33219256-9	2020	TMB-associated mutations included CDKN2A, LRP1B, LRP2, TP53, and EGFR.	1,2,4,5-tetramethoxybenzene	0-3	P53	Homo sapiens	55-59
32382022-8	2020	Lenvatinib and Cabozantinib were particularly effective in moderately to poorly differentiated cells with mutated or lacking p53 that have lower basal oxygen consumption rate (OCR), ATP, and maximal respiration capacity than observed in differentiated HCC cells.	lenvatinib	0-10	P53	Homo sapiens	125-128
32633026-0	2020	A Slug-dependent mechanism is responsible for tumor suppression of p53-stabilizing compound CP-31398 in p53-mutated endometrial carcinoma.	CP 31398	92-100	P53	Homo sapiens	67-70
32633026-0	2020	A Slug-dependent mechanism is responsible for tumor suppression of p53-stabilizing compound CP-31398 in p53-mutated endometrial carcinoma.	CP 31398	92-100	P53	Homo sapiens	104-107
32633026-2	2020	Recently, CP-31398, a p53-stabilizing compound, has been indicated to possess the ability to alter the expression of non-p53 target genes in addition to p53 downstream genes in tumor cells.	CP 31398	10-18	P53	Homo sapiens	22-25
32633026-2	2020	Recently, CP-31398, a p53-stabilizing compound, has been indicated to possess the ability to alter the expression of non-p53 target genes in addition to p53 downstream genes in tumor cells.	CP 31398	10-18	P53	Homo sapiens	121-124
32633026-2	2020	Recently, CP-31398, a p53-stabilizing compound, has been indicated to possess the ability to alter the expression of non-p53 target genes in addition to p53 downstream genes in tumor cells.	CP 31398	10-18	P53	Homo sapiens	121-124
32633026-3	2020	Herein, we explore the alternative mechanisms underlying the restoration of EC tumor suppressor function in mutant p53 by CP-31398.	CP 31398	122-130	P53	Homo sapiens	115-118
32276266-0	2020	Inhibition of esophageal-carcinoma cell proliferation by genistein via suppression of JAK1/2-STAT3 and AKT/MDM2/p53 signaling pathways.	Genistein	57-66	P53	Homo sapiens	112-115
32633026-4	2020	A p53-mutated EC cell was constructed in AN3CA cells with restored or partial loss of Slug using lentiviral vectors, followed by treatment with 25 muM CP-31398.	CP 31398	151-159	P53	Homo sapiens	2-5
32860803-7	2020	The p38-p53 axis was also further activated by the combination of AOAA or PAG with DIM.	3,3'-diindolylmethane	83-86	P53	Homo sapiens	8-11
32931795-12	2020	However, a significant upregulation of p53 only following PA treatment was found.	protoapigenone	58-60	P53	Homo sapiens	39-42
32273511-0	2020	p53-mediated control of aspartate-asparagine homeostasis dictates LKB1 activity and modulates cell survival.	Asparagine	34-44	P53	Homo sapiens	0-3
32273511-3	2020	Here, we report that p53 suppresses asparagine synthesis through the transcriptional downregulation of ASNS expression and disrupts asparagine-aspartate homeostasis, leading to lymphoma and colon tumour growth inhibition in vivo and in vitro.	Asparagine	36-46	P53	Homo sapiens	21-24
32273511-3	2020	Here, we report that p53 suppresses asparagine synthesis through the transcriptional downregulation of ASNS expression and disrupts asparagine-aspartate homeostasis, leading to lymphoma and colon tumour growth inhibition in vivo and in vitro.	Asparagine	132-142	P53	Homo sapiens	21-24
32273511-4	2020	Moreover, the removal of asparagine from culture medium or the inhibition of ASNS impairs cell proliferation and induces p53/p21-dependent senescence and cell cycle arrest.	Asparagine	25-35	P53	Homo sapiens	121-124
32273511-5	2020	Mechanistically, asparagine and aspartate regulate AMPK-mediated p53 activation by physically binding to LKB1 and oppositely modulating LKB1 activity.	Asparagine	17-27	P53	Homo sapiens	65-68
33137997-4	2020	Moreover, we showed that the hydroxytyrosol treatment of melanoma cells leads to a significant increase of p53 and gammaH2AX expression, a significant decrease of AKT expression and the inhibition of cell colony formation ability.	3,4-dihydroxyphenylethanol	29-43	P53	Homo sapiens	107-110
33113830-5	2020	Also, analysis of mRNA level variations of the focal adhesion kinase (FAK), P53 and SLC11A2/DMT1 human genes showed that the DM/n-HA-treated cells retain tracts of physiological responsiveness compared to the DM-treated cells.	n-ha	128-132	P53	Homo sapiens	76-79
33113830-5	2020	Also, analysis of mRNA level variations of the focal adhesion kinase (FAK), P53 and SLC11A2/DMT1 human genes showed that the DM/n-HA-treated cells retain tracts of physiological responsiveness compared to the DM-treated cells.	dm	125-127	P53	Homo sapiens	76-79
31587305-3	2020	Other studies have shown that knockdown of RB1 and TP53 increases the expression of neuroendocrine markers, decreases the sensitivity to enzalutamide, and increases the expression of SOX2.	enzalutamide	137-149	P53	Homo sapiens	51-55
33089100-6	2020	Moreover, we show that salinomycin, an anti-CSC agent, disrupts nucleolus by inducing nucleoplasm translocation of p53 and sensitizing CSC to chemotherapy drugs.	salinomycin	23-34	P53	Homo sapiens	115-118
31587305-4	2020	Importantly, knockdown of SOX2 in the context of RB1 and TP53 depletion restored sensitivity to enzalutamide and reduced the expression of neuroendocrine markers.	enzalutamide	96-108	P53	Homo sapiens	57-61
31596511-7	2020	Pathway analysis suggested that differential TMB-related signature correlated with multiple cancer-related crosstalk, including cell cycle, DNA replication, cellular senescence, and p53 signaling pathway.	1,2,4,5-tetramethoxybenzene	45-48	P53	Homo sapiens	182-185
32749686-9	2020	Whole-exome sequencing demonstrated that the ESCC genomes of patients who demonstrated a response to afatinib were enriched with genomic alterations of TP53 and epidermal growth factor receptor (EGFR).	Afatinib	101-109	P53	Homo sapiens	152-156
32749686-10	2020	As a predictive marker, a score derived from TP53 disruptive mutations and EGFR amplifications and/or missense mutations demonstrated a significant association with the response to afatinib.	Afatinib	181-189	P53	Homo sapiens	45-49
32934219-7	2020	CDK9 inhibitor atuveciclib downregulated MDM4 and enhanced p53 activity induced by nutlin-3a, an inhibitor of p53-MDM2 interaction, and synergized with nutlin-3a in killing A375 melanoma cells.	nutlin 3	83-92	P53	Homo sapiens	59-62
32749686-11	2020	The score based on the mutational status of EGFR and TP53 achieved a performance of an area under the curve of 0.86 in predicting the sensitivity of afatinib.	Afatinib	149-157	P53	Homo sapiens	53-57
32749686-13	2020	Identification of TP53 alterations and EGFR amplifications may serve as predictive markers with which to identify patients with R/M-ESCC who may benefit from afatinib.	Afatinib	158-166	P53	Homo sapiens	18-22
32749686-16	2020	Whole-exome sequencing analysis of 41 cases of ESCC further revealed that the patients harboring epidermal growth factor receptor (EGFR) amplifications and disruptive TP53 mutations are more likely to benefit from treatment with afatinib.	Afatinib	229-237	P53	Homo sapiens	167-171
32749686-17	2020	The results of the current study have highlighted the clinical value of EGFR and TP53 as predictive biomarkers of platinum-resistant recurrent and/or metastatic ESCC for afatinib sensitivity.	Afatinib	170-178	P53	Homo sapiens	81-85
32060420-10	2020	Using TP53-mutated AML cell line THP1 and patient-derived AML cells, we tested a new echinomycin formulation with longer half-life and significantly improved therapeutic effect.	Echinomycin	85-96	P53	Homo sapiens	6-10
32934219-7	2020	CDK9 inhibitor atuveciclib downregulated MDM4 and enhanced p53 activity induced by nutlin-3a, an inhibitor of p53-MDM2 interaction, and synergized with nutlin-3a in killing A375 melanoma cells.	nutlin 3	83-92	P53	Homo sapiens	110-113
32899699-7	2020	Nevertheless, a lower effect was observed in DLD-1 cells, which has a single Ser241Phe mutation in the P53 DNA binding domain.	ser241phe	77-86	P53	Homo sapiens	103-106
32218859-6	2020	In the present study, CP-31398, a p53-restoring agent, was used to improve the therapeutic efficacy of sorafenib in SW579 cells, an ATC cell line harboring p53 mutations.	CP 31398	22-30	P53	Homo sapiens	34-37
32800832-9	2020	Overexpression of MDM2 ameliorated the inhibitory effect of FBXO31 on SiHa cells, while the MDM2/p53 axis-specific inhibitor Nutlin-3a facilitated this inhibitory effect.	nutlin 3	125-134	P53	Homo sapiens	97-100
31967380-10	2020	Alkannin counteracted the growth of PANC-1 cells through inhibiting proliferation, migration, and invasion and facilitating apoptosis, which was evidenced by the modulation on PCNA, CyclinD1, p53, and cleavage of caspases.	alkannin	0-8	P53	Homo sapiens	192-195
32927274-8	2020	On the other-side, both TP53 missense and nonsense mutations are associated with elevated TMB and neoantigen levels and contribute equally to DNA damage repair deficiency.	1,2,4,5-tetramethoxybenzene	90-93	P53	Homo sapiens	24-28
32687844-10	2020	DpdtC treatment resulted in upregulation of p53, but, the addition of p53 inhibitor, PFT-alpha could significantly neutralize the action of DpdtC on ferritinophagy induction and EMT inhibition.	di-n-propyldithiocarbamate	0-5	P53	Homo sapiens	44-47
32151917-8	2020	EEMC caused G2/M cell cycle arrest, mitochondrial damage, and caspase activation of USCs, accompanied by p53 accumulation.	eemc	0-4	P53	Homo sapiens	105-108
32943925-3	2020	In this study, the effect of hydroxytyrosol on the expression of genes effective in apoptosis - BAX, BCL2, CASP3, P53, PPAR G, and NFE2L2 - and antioxidant-enzyme activity in LS180 cells of human colorectal cancer was investigated.	3,4-dihydroxyphenylethanol	29-43	P53	Homo sapiens	114-117
32151917-9	2020	In p53KO human iPSCs, EEMC had no cytotoxicity, reinforcing that EEMC-mediated apoptosis of USCs is p53-dependent.	eemc	65-69	P53	Homo sapiens	3-6
32151917-9	2020	In p53KO human iPSCs, EEMC had no cytotoxicity, reinforcing that EEMC-mediated apoptosis of USCs is p53-dependent.	eemc	65-69	P53	Homo sapiens	100-103
32881622-0	2020	Essential amino acid supplementation alters the p53 transcriptional response and cytokine gene expression following TKA.	Amino Acids, Essential	0-20	P53	Homo sapiens	48-51
32990229-0	2020	[Epigallocatechin gallate induces CHD5 gene demethylation to promote acute myeloid leukemia cell apoptosis in vitro by regulating p19Arf-p53-p21Cip1 signaling pathway].	epigallocatechin gallate	1-25	P53	Homo sapiens	137-140
32256964-0	2020	DpdtC-Induced EMT Inhibition in MGC-803 Cells Was Partly through Ferritinophagy-Mediated ROS/p53 Pathway.	di-n-propyldithiocarbamate	0-5	P53	Homo sapiens	93-96
32533954-9	2020	Collectively, our findings suggest that GNA induces ferroptosis in TGF-beta1-stimulated melanoma cells via the p53/SLC7A11/GPX4 signaling pathway.	neo-gambogic acid	40-43	P53	Homo sapiens	111-114
32156073-4	2020	TP53 missense mutations were observed in 17 tissue specimens and in baseline cfDNA for 4/8 patients by AmpliSeq, 6/9 patients by Oncomine, and 4/6 patients by dPCR.	ampliseq	103-111	P53	Homo sapiens	0-4
32156073-4	2020	TP53 missense mutations were observed in 17 tissue specimens and in baseline cfDNA for 4/8 patients by AmpliSeq, 6/9 patients by Oncomine, and 4/6 patients by dPCR.	oncomine	129-137	P53	Homo sapiens	0-4
32990229-6	2020	EGCG treatment caused obvious cell cycle arrest in G1 phase, significantly increased cell apoptosis, downregulated the expression of DNMT1 and upregulated the expressions of CHD5, p19Arf, p53 and p21Cip1 in KG-1 and THP-1 cells (P < 0.05).	epigallocatechin gallate	0-4	P53	Homo sapiens	188-191
32990229-7	2020	CONCLUSIONS: EGCG reduces hypermethylation of CHD5 gene in KG-1 and THP-1 cells by downregulating DNMT1 to restore its expression, which results in upregulated expressions of p19Arf, p53 and p21Cip1 and induces cell apoptosis.	epigallocatechin gallate	13-17	P53	Homo sapiens	183-186
32742376-5	2020	In HCT116 cells expressing wild-type (wt) TP53, SIRT inhibitors were found to act antagonistically with multiple chemotherapeutic agents (cisplatin, 5-fluorouracil, oxaliplatin, gefitinib, LY294002 and metformin), and decreased the anti-tumor effects of these agents.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	189-197	P53	Homo sapiens	42-46
32908121-9	2020	Ultimately, miR-210-3p facilitated aerobic glycolysis through modulating the downstream glycolytic genes of HIF-1alpha and p53.	mir-210-3p	12-22	P53	Homo sapiens	123-126
31868281-5	2020	The interactions of rhytidenone F with PA28gamma would lead to the accumulation of p53 which is an essential tumor suppressor in humans.	Fluorine	20-33	P53	Homo sapiens	83-86
32097779-5	2020	PURPOSE: To explore the anticancer mechanism of action of the triterpenoid alkaloid KBA01 compound by targeting mutant p53 degradation.	Triterpenes	62-74	P53	Homo sapiens	119-122
32705888-8	2021	Genistein increased the expression levels of p53 and p21 with decreased phosphorylated p21, but did not affect the levels of major cyclin-CDK complexes.	Genistein	0-9	P53	Homo sapiens	45-48
32238876-9	2020	There was scattered weak to moderate p53 staining (conventional wild type) in 1/25 (4%) SCC and 2/20 (10%) EDAC.	Ethyldimethylaminopropyl Carbodiimide	107-111	P53	Homo sapiens	37-40
32238876-11	2020	One EDAC had a TP53 missense mutation and exhibited "markedly reduced (null-like)" staining.	Ethyldimethylaminopropyl Carbodiimide	4-8	P53	Homo sapiens	15-19
32754299-6	2020	We observed a correlation between FLT3-ITD mutations and midostaurin sensitivity as expected and observed KRAS and TP53 mutations correlating with midostaurin resistance in FLT3-ITD negative samples.	midostaurin	147-158	P53	Homo sapiens	115-119
32874188-9	2020	Isogenic HCT116 p53-wt/null cancer cells demonstrated that CD276 is induced on the cell surface by Nutlin-3 in a p53-dependent manner.	nutlin 3	99-107	P53	Homo sapiens	16-19
32874188-9	2020	Isogenic HCT116 p53-wt/null cancer cells demonstrated that CD276 is induced on the cell surface by Nutlin-3 in a p53-dependent manner.	nutlin 3	99-107	P53	Homo sapiens	113-116
32041553-9	2020	In contrast, p53 mostly existed in inactive quaternary conformations containing >=2 Delta40 or Delta133p53 in relapse BCP-ALL.	bcp	118-121	P53	Homo sapiens	13-16
31761381-1	2020	Forty-eight analogues of CP-31398, an antitumor agent modulated the mutant p53 gene were synthesized and their cytotoxicities against four cancer cell lines with different p-53 status including bladder cell T24 (w-p53), gastric cell MGC-803 (m-p53), prostate cell DU145 (m-p53), prostate cell PC-3 (null-p53), lung cell A549 (w-p53) and normal liver cell line HL-7702 (w-p53) were examined.	CP 31398	25-33	P53	Homo sapiens	214-217
31761381-1	2020	Forty-eight analogues of CP-31398, an antitumor agent modulated the mutant p53 gene were synthesized and their cytotoxicities against four cancer cell lines with different p-53 status including bladder cell T24 (w-p53), gastric cell MGC-803 (m-p53), prostate cell DU145 (m-p53), prostate cell PC-3 (null-p53), lung cell A549 (w-p53) and normal liver cell line HL-7702 (w-p53) were examined.	CP 31398	25-33	P53	Homo sapiens	214-217
31761381-1	2020	Forty-eight analogues of CP-31398, an antitumor agent modulated the mutant p53 gene were synthesized and their cytotoxicities against four cancer cell lines with different p-53 status including bladder cell T24 (w-p53), gastric cell MGC-803 (m-p53), prostate cell DU145 (m-p53), prostate cell PC-3 (null-p53), lung cell A549 (w-p53) and normal liver cell line HL-7702 (w-p53) were examined.	CP 31398	25-33	P53	Homo sapiens	214-217
32504186-12	2020	Future research needs to further dissect the impact of the various TP53 aberrations in HMA-based combination therapies.	5-(N,N-hexamethylene)amiloride	87-90	P53	Homo sapiens	67-71
32907364-0	2020	Targeted Modulation of FAK/PI3K/PDK1/AKT and FAK/p53 Pathways by Cucurbitacin B for the Antiproliferation Effect Against Human Cholangiocarcinoma Cells.	cucurbitacin B	65-79	P53	Homo sapiens	49-52
32641480-17	2020	Fortunately, p53 phosphorylation can also be provided by drugs such as Nutlin-3, leading to synergistic reactivation of EBV.	nutlin 3	71-79	P53	Homo sapiens	13-16
32449282-5	2020	As results, the bioinformatic findings showed the core anti-NPC targets played by calycosin included tumor protein p53 (TP53), mitogen-activated protein kinase 14 (MAPK14), caspase 8 (CASP8), mitogen-activated protein kinase 3 (MAPK3), caspase 3 (CASP3), receptor interacting protein kinase 1 (RIPK1), proto-oncogene c (JUN), and estrogen receptor 1 (ESR1).	7,3'-dihydroxy-4'-methoxyisoflavone	82-91	P53	Homo sapiens	115-118
32468177-0	2020	Combination of a p53-activating CP-31398 and an MDM2 or a FAK inhibitor produces growth suppressive effects in mesothelioma with wild-type p53 genotype.	CP 31398	32-40	P53	Homo sapiens	17-20
32468177-0	2020	Combination of a p53-activating CP-31398 and an MDM2 or a FAK inhibitor produces growth suppressive effects in mesothelioma with wild-type p53 genotype.	CP 31398	32-40	P53	Homo sapiens	139-142
32468177-2	2020	We examined a growth suppressive activity of CP-31398 which was developed to restore the p53 functions irrespective of the genotype in mesothelioma with wild-type or mutated p53.	CP 31398	45-53	P53	Homo sapiens	89-92
32468177-2	2020	We examined a growth suppressive activity of CP-31398 which was developed to restore the p53 functions irrespective of the genotype in mesothelioma with wild-type or mutated p53.	CP 31398	45-53	P53	Homo sapiens	174-177
32468177-3	2020	CP-31398 up-regulated p53 levels in cells with wild-type p53 genotype but induced cell growth suppression in a p53-independent manner.	CP 31398	0-8	P53	Homo sapiens	22-25
32468177-3	2020	CP-31398 up-regulated p53 levels in cells with wild-type p53 genotype but induced cell growth suppression in a p53-independent manner.	CP 31398	0-8	P53	Homo sapiens	57-60
31767563-7	2020	Ex vivo Nutlin-3 (MDM2 inhibitor) treatment of blood and BM increased p53 and p21 expression in CTCs and DTCs compared with DMSO controls.	nutlin 3	8-16	P53	Homo sapiens	70-73
31797597-6	2020	Interestingly, both EGCG binding and N29K/N30D could also induce long-range structural reorganizations and lead to more compact structures that could shield key binding sites of p53-TAD regulators.	epigallocatechin gallate	20-24	P53	Homo sapiens	178-181
31871844-8	2019	Three drugs, mitomycin-C, doxorubicin and gemcitabine, were especially more sensitive to bladder cancer with the TP53 mutation.	Mitomycin	13-24	P53	Homo sapiens	113-117
32468177-3	2020	CP-31398 up-regulated p53 levels in cells with wild-type p53 genotype but induced cell growth suppression in a p53-independent manner.	CP 31398	0-8	P53	Homo sapiens	57-60
32468177-5	2020	We investigated a combinatory effect of CP-31398 and nutlin-2a and found the combination produced synergistic growth inhibition in mesothelioma with the wild-type p53 but not with mutated p53.	CP 31398	40-48	P53	Homo sapiens	163-166
32468177-7	2020	Combination of CP-31398 and defactinib, a FAK inhibitor, also achieved synergistic inhibitory effects and increased p53 with FAK dephosphorylation levels greater than the single treatment.	CP 31398	15-23	P53	Homo sapiens	116-119
32468177-7	2020	Combination of CP-31398 and defactinib, a FAK inhibitor, also achieved synergistic inhibitory effects and increased p53 with FAK dephosphorylation levels greater than the single treatment.	defactinib	28-38	P53	Homo sapiens	116-119
32468177-8	2020	These data indicated that a p53-activating CP-31398 achieved growth inhibitory effects in combination with a MDM2 or a FAK inhibitor and suggested a possible reciprocal pathway between p53 elevation and FAK inactivation.	CP 31398	43-51	P53	Homo sapiens	28-31
32468177-8	2020	These data indicated that a p53-activating CP-31398 achieved growth inhibitory effects in combination with a MDM2 or a FAK inhibitor and suggested a possible reciprocal pathway between p53 elevation and FAK inactivation.	CP 31398	43-51	P53	Homo sapiens	185-188
32449282-5	2020	As results, the bioinformatic findings showed the core anti-NPC targets played by calycosin included tumor protein p53 (TP53), mitogen-activated protein kinase 14 (MAPK14), caspase 8 (CASP8), mitogen-activated protein kinase 3 (MAPK3), caspase 3 (CASP3), receptor interacting protein kinase 1 (RIPK1), proto-oncogene c (JUN), and estrogen receptor 1 (ESR1).	7,3'-dihydroxy-4'-methoxyisoflavone	82-91	P53	Homo sapiens	120-124
32179199-10	2020	As showed in immunostaining, calycosin-treated OS cells exhibited intracellular up-regulation of TP53, CASP3 expressions, and decreased XIAP expressions.	7,3'-dihydroxy-4'-methoxyisoflavone	29-38	P53	Homo sapiens	97-101
32664789-3	2020	Data from The Genomics of Drug Sensitivity in Cancer database showed that three drugs: (5Z)-7-oxozeaenol, dabrafenib and nutlin-3a (-), have shown more resistance in patients with TP53 mutation.	nutlin 3	121-130	P53	Homo sapiens	180-184
31678282-8	2019	Unpredictably, bevacizumab-treated tumors exhibited the highest cell proliferation coupled with PDE4A, HIF1alpha and AKT upregulation and p53 downregulation and reversed by co-treatment with rolipram.	Rolipram	191-199	P53	Homo sapiens	138-141
32456284-9	2020	The neuroprotective effects of miR-23a-3p administration may not only involve the direct inhibition of pro-apoptotic Bcl-2 molecules downstream of p53 but also include the attenuation of secondary DNA damage upstream of p53.	mir-23a-3p	31-41	P53	Homo sapiens	147-150
31220953-4	2019	NRF2 was examined as a mediating mechanism of salicin"s impact on cellular senescence and was found to account for salicin"s impact on SA-beta-Gal, p21, PAI-1 and p53.	salicin	46-53	P53	Homo sapiens	163-166
31220953-4	2019	NRF2 was examined as a mediating mechanism of salicin"s impact on cellular senescence and was found to account for salicin"s impact on SA-beta-Gal, p21, PAI-1 and p53.	salicin	115-122	P53	Homo sapiens	163-166
32739866-9	2020	Finally, TP53 mutations are associated with higher TMB score in metastatic but not primary tumors, and poorer response to immune checkpoint inhibitors for the latter.	1,2,4,5-tetramethoxybenzene	51-54	P53	Homo sapiens	9-13
32632752-6	2020	Interestingly, BTX306 did show some reduced activity in lenalidomide-resistant cell line models but nonetheless retained its nanomolar potency in vitro, overcame bortezomib resistance, and was equipotent against otherwise isogenic cell line models with either wild-type or knockout TP53.	btx306	15-21	P53	Homo sapiens	282-286
31560893-18	2019	The MLL-complex antagonists MI-2-2 (inhibitor of protein interaction) and OICR-9492 (inhibitor of activity) specifically inhibited proliferation of HCC cells that express TP53R249S at nanomolar concentrations.	5-hydroxy-6-methoxyindole	28-34	P53	Homo sapiens	171-175
32456284-9	2020	The neuroprotective effects of miR-23a-3p administration may not only involve the direct inhibition of pro-apoptotic Bcl-2 molecules downstream of p53 but also include the attenuation of secondary DNA damage upstream of p53.	mir-23a-3p	31-41	P53	Homo sapiens	220-223
32494130-7	2020	We demonstrated that CuONPs uptake induced DNA damage in HUVECs as evidenced by gammaH2AX foci formation and increased phosphorylation levels of ATR, ATM, p53 and H2AX.	cuonps	21-27	P53	Homo sapiens	155-158
31668020-16	2019	TP53, EGFR and KRAS mutations are associated with expression of glucose and glutamine metabolism-related markers in NSCLC.	Glutamine	76-85	P53	Homo sapiens	0-4
32694238-7	2020	These findings demonstrate that truncating TP53 mutations correlate with poor immunotherapy outcomes in NSCLC patients with low TMB.	1,2,4,5-tetramethoxybenzene	128-131	P53	Homo sapiens	43-47
32382022-11	2020	By contrast, Lenvatinib and Cabozantinib appeared more effective in moderately to poorly differentiated cells with mutated p53 and low mitochondrial respiration.	lenvatinib	13-23	P53	Homo sapiens	123-126
32685741-9	2020	Conclusion: These data suggested that TES may play a critical role for promoting reverse-translational studies, including investigations of the biology of TP53 mutations in different stages of SCLC.	TES	38-41	P53	Homo sapiens	155-159
32332775-4	2020	This interaction was enhanced by treatment with the antineoplastic drug etoposide, which suggests a role for the IL-1alpha p53 interaction in genotoxic stress.	Etoposide	72-81	P53	Homo sapiens	123-126
32904132-6	2020	Aflatoxin B1 (AFB1)-specific codon 249 TP53 mutation was determined by NGS in circulating cell-free plasma DNA.	Aflatoxin B1	0-12	P53	Homo sapiens	39-43
32904132-6	2020	Aflatoxin B1 (AFB1)-specific codon 249 TP53 mutation was determined by NGS in circulating cell-free plasma DNA.	Aflatoxin B1	14-18	P53	Homo sapiens	39-43
30521787-1	2019	Cabazitaxel as microtubule inhibitor and thymoquinone as HDAC inhibitor affects the important genes like p53, STAT3, Bax, BCL-2, p21 and down regulation of NF-kappaB are reported for potential activity against breast tumors.	cabazitaxel	0-11	P53	Homo sapiens	105-108
32276266-7	2020	Additionally, genistein dramatically decreased epidermal growth factor receptor (EGFR) expression and attenuated its down-stream signaling molecules STAT3, MDM2, Akt and JAK1/2 phosphorylation, resulting in inhibited nuclear translocation of STAT3 and MDM2, thereby inhibiting the JAK1/2-STAT3 and AKT/MDM2/p53 signaling pathways.	Genistein	14-23	P53	Homo sapiens	307-310
31664085-3	2019	Here we evaluate the use of IBSAFE, an ultra-sensitive droplet digital PCR (ddPCR) method, for detecting TP53 mutations in liquid-based Pap samples collected from fifteen women at the time of diagnosis (diagnostic samples) and/or up to seven years prior to diagnosis (archival samples).	ibsafe	28-34	P53	Homo sapiens	105-109
32276266-10	2020	Taken together, genistein suppressed the JAK1/2-STAT3 and AKT/MDM2/p53 signaling pathways by decreasing EGFR expression, leading to cell apoptosis, cell cycle arrest, and proliferation inhibition in EsC cells.	Genistein	16-25	P53	Homo sapiens	67-70
32695207-0	2020	Ginsenoside Rh1 Alleviates HK-2 Apoptosis by Inhibiting ROS and the JNK/p53 Pathways.	ginsenoside Rh1	0-15	P53	Homo sapiens	72-75
32695207-9	2020	Ginsenoside Rh1 was found to inhibit the expression of JNK, p53, caspase-3, Bax, and NGAL in a cisplatin-induced injury model.	ginsenoside Rh1	0-15	P53	Homo sapiens	60-63
32695207-10	2020	Conclusion: Ginsenoside Rh1 alleviated HK-2 apoptosis in a cisplatin-induced injury model by inhibiting ROS production and the JNK/p53 pathway.	ginsenoside Rh1	12-27	P53	Homo sapiens	131-134
32273511-6	2020	Thus, we found that p53 regulates asparagine metabolism and dictates cell survival by generating an auto-amplification loop via asparagine-aspartate-mediated LKB1-AMPK signalling.	Asparagine	34-44	P53	Homo sapiens	20-23
31502598-7	2019	The feasibility of the method for the screening of the DNA-PK inhibitor and the inhibitor of p53-MDM2 interaction has been demonstrated and the half-maximal inhibitory concentration (IC50) values of wortmannin and Nutlin-3 (21 nM and 83 nM, respectively) were highly comparable with those obtained by other methods.	nutlin 3	214-222	P53	Homo sapiens	93-96
32273511-6	2020	Thus, we found that p53 regulates asparagine metabolism and dictates cell survival by generating an auto-amplification loop via asparagine-aspartate-mediated LKB1-AMPK signalling.	Asparagine	128-138	P53	Homo sapiens	20-23
31822380-8	2020	However, TP53 GOF mutations had a positive association with prior abiraterone/enzalutamide therapy (P = .047).	enzalutamide	78-90	P53	Homo sapiens	9-13
31434476-10	2019	Codelivery of functional gene (pCEP4-p53) and drug (doxorubicin) was accomplished in vitro and in vivo with the chitosan-pyridine imine vector, (py)CS(CH2COOH), and the newly synthesized doxorubicin oxime ether, CS(Dox).	Cesium	148-150	P53	Homo sapiens	37-40
32605139-6	2020	Our results show that treatment of HCT-116 colon cancer cells with the deoxyhypusine (DHS) inhibitor N1-guanyl-1,7-diamineheptane (GC7) caused both inhibition of eIF5A hypusination and a significant reduction of p53 expression in UV-treated cells, and that eIF5A controls p53 expression at the level of protein synthesis.	n1-guanyl-1,7-diamineheptane	101-129	P53	Homo sapiens	212-215
32605139-6	2020	Our results show that treatment of HCT-116 colon cancer cells with the deoxyhypusine (DHS) inhibitor N1-guanyl-1,7-diamineheptane (GC7) caused both inhibition of eIF5A hypusination and a significant reduction of p53 expression in UV-treated cells, and that eIF5A controls p53 expression at the level of protein synthesis.	n1-guanyl-1,7-diamineheptane	101-129	P53	Homo sapiens	272-275
32605139-6	2020	Our results show that treatment of HCT-116 colon cancer cells with the deoxyhypusine (DHS) inhibitor N1-guanyl-1,7-diamineheptane (GC7) caused both inhibition of eIF5A hypusination and a significant reduction of p53 expression in UV-treated cells, and that eIF5A controls p53 expression at the level of protein synthesis.	2-(7-aminoheptyl)guanidine	131-134	P53	Homo sapiens	212-215
32605139-6	2020	Our results show that treatment of HCT-116 colon cancer cells with the deoxyhypusine (DHS) inhibitor N1-guanyl-1,7-diamineheptane (GC7) caused both inhibition of eIF5A hypusination and a significant reduction of p53 expression in UV-treated cells, and that eIF5A controls p53 expression at the level of protein synthesis.	2-(7-aminoheptyl)guanidine	131-134	P53	Homo sapiens	272-275
32218826-6	2020	Further analysis using The Cancer Genome Atlas Liver Hepatocellular Carcinoma database showed that TP53, CTNNB1 and MLL mutations were positively correlated with TMB-H.	1,2,4,5-tetramethoxybenzene	162-165	P53	Homo sapiens	99-103
32559584-2	2020	PURPOSE: We evaluated the cytotoxic potential of a naturally occurring N-acetylglycoside of oleanolic acid, aridanin, on 18 cancer cell lines, including sensitive and drug-resistant phenotypes mediated by P-glycoprotein, BCRP, p53 knockout, deletion-mutated EGFR, or BRAF mutations.	aridanin	108-116	P53	Homo sapiens	227-230
31383362-1	2019	In several cancer cells, luteolin (3",4",5,7-tetrahydroxyflavone) exerts anticancer effects by upregulation of oxidative stress and endoplasmic reticulum (ER) stress, which are shown to activate p53-dependent cell death.	luteolin (3",4",5,7-tetrahydroxyflavone	25-64	P53	Homo sapiens	195-198
32218859-0	2020	Potential synergistic effects of sorafenib and CP-31398 for treating anaplastic thyroid cancer with p53 mutations.	CP 31398	47-55	P53	Homo sapiens	100-103
32468080-8	2020	This correlated with differential upregulation of p53/p21 pathway, with S and G2/M arrests by cisplatin and satraplatin in contrast to G1 arrest by oxaliplatin and DAP.	satraplatin	108-119	P53	Homo sapiens	50-53
32212969-6	2020	DNA fragmentation and up-regulated of caspase-3 and p53 had illustrated the apoptotic effect of MCF-7 treated with GEM-ANPS/CS.	Cesium	124-126	P53	Homo sapiens	52-55
32124130-8	2020	Dual-luciferase assay was employed to identify interaction between p53 and miR-29b in HTFs.	htfs	86-90	P53	Homo sapiens	67-70
31397557-10	2019	These results contribute to the evidence that the TGx-DDI biomarker is useful for identifying chemicals that cause DDI and activate p53.	Didanosine	54-57	P53	Homo sapiens	132-135
31783043-6	2020	Five PGAs with high-grade dysplasia/adenocarcinoma exhibited mutations in several genes including APC, CTNNB1, KRAS, GNAS, TP53, CDKN2A, PIK3CA, and EPHA5 genes but did not exhibit mutations in the triad of APC, KRAS, and GNAS genes.	pgas	5-9	P53	Homo sapiens	123-127
31158746-11	2019	Moreover, it was shown that an interaction of 1,4-quinone fragment with the hydrophobic matrix of the active site near Tyr128, Phe178, Trp105 and FAD cofactor could explain the observed increase of TP53 gene expression.	Flavin-Adenine Dinucleotide	146-149	P53	Homo sapiens	198-202
32321249-3	2020	Lead inhibitor 13a shows picomolar or low nanomolar IC50 against HDAC1 and HDAC3 and exhibits differential toxicity profiles toward multiple cancer cells with different FLT3 and p53 status.	13a	15-18	P53	Homo sapiens	178-181
32321249-4	2020	13a indirectly inhibits the FLT3 signaling pathway and down-regulates the master anti-apoptotic proteins, resulting in the activation of pro-caspase3 in in wt-p53 FLT3-ITD MV4-11 cells.	13a	0-3	P53	Homo sapiens	159-162
31426331-0	2019	Silica Nanoparticles Provoke Cell Death Independent of p53 and BAX in Human Colon Cancer Cells.	Silicon Dioxide	0-6	P53	Homo sapiens	55-58
32124101-7	2020	Quantitative real-time PCR data showed that the mRNA levels of apoptotic marker genes such as p53, bax, and caspase-3 were upregulated, whereas bcl-2, an anti-apoptotic gene, was downregulated; therefore, apoptosis was mediated through the p53, bax, caspase-3, and bcl-2 pathways, suggesting a possible mechanism by which QDs and NPs of ZnO mediate their toxicity.Graphic abstract.	Zinc Oxide	337-340	P53	Homo sapiens	94-97
31426331-13	2019	As loss of p53 in colon cancer cells contributes to resistance against anticancer drugs, and thus to reoccurrence of colon cancer, targeted delivery of silica NPs could be envisioned to also deplete p53 deficient tumor cells.	Silicon Dioxide	152-158	P53	Homo sapiens	11-14
31426331-13	2019	As loss of p53 in colon cancer cells contributes to resistance against anticancer drugs, and thus to reoccurrence of colon cancer, targeted delivery of silica NPs could be envisioned to also deplete p53 deficient tumor cells.	Silicon Dioxide	152-158	P53	Homo sapiens	199-202
32321249-6	2020	The MDM2 antagonist and the proteasome inhibitor promote 13a-triggered apoptosis by preventing p53 degradation.	13a	57-60	P53	Homo sapiens	95-98
32101536-6	2020	We experimentally validated that afatinib has the strongest cytotoxic activity on BT474 (IC50 = 55.5 nM, BRCA2 and TP53 co-mutant) compared to MCF7 (IC50 = 7.7 muM, both BRCA2 and TP53 wild type) and MDA-MB-231 (IC50 = 7.9 muM, BRCA2 wild type but TP53 mutant).	Afatinib	33-41	P53	Homo sapiens	115-119
32367104-5	2020	A key feature of this 1,3-dipolar cycloaddition is the wide substrate applicability, even with alkyl aldehyde-derived azomethine ylide; thus it has streamlined a highly enantioselective access to a new class of antiproliferative agents, MDM2-p53.	azomethine ylide	118-134	P53	Homo sapiens	242-245
32428506-18	2020	The MLL-complex antagonists MI-2-2 (inhibitor of protein interaction) and OICR-9492 (inhibitor of activity) specifically inhibited proliferation of HCC cells that express TP53R249S at nanomolar concentrations.	5-hydroxy-6-methoxyindole	28-34	P53	Homo sapiens	171-175
31029907-0	2019	Epigallocatechin gallate prevents mitochondrial impairment and cell apoptosis by regulating miR-30a/p53 axis.	epigallocatechin gallate	0-24	P53	Homo sapiens	100-103
31029907-1	2019	PURPOSE: This study was designed to investigate whether EGCG prevents cardiac I/R mitochondrial impairment and cell apoptosis by regulating miR-30a/p53 axis.	epigallocatechin gallate	56-60	P53	Homo sapiens	148-151
31029907-11	2019	The beneficial effect of EGCG was associated with restored levels of miR-30a expression in the I/R injury that correspond to p53 mRNA downregulation.	epigallocatechin gallate	25-29	P53	Homo sapiens	125-128
31029907-13	2019	More importantly, EGCG pretreatment inhibited the expression of mitochondrial apoptotic related proteins downstream of the miR-30a/p53 pathway.	epigallocatechin gallate	18-22	P53	Homo sapiens	131-134
31029907-14	2019	CONCLUSION: This study demonstrated that EGCG pretreatment may attenuate mitochondrial impairment and myocardial apoptosis by regulation of miR-30a/p53 axis.	epigallocatechin gallate	41-45	P53	Homo sapiens	148-151
32353067-6	2020	We find that not only the epitope residues (F19, W23 and L26), but also the hydrocarbon linker of the stapled p53 impart significant contributions.	Hydrocarbons	76-87	P53	Homo sapiens	110-113
32101536-6	2020	We experimentally validated that afatinib has the strongest cytotoxic activity on BT474 (IC50 = 55.5 nM, BRCA2 and TP53 co-mutant) compared to MCF7 (IC50 = 7.7 muM, both BRCA2 and TP53 wild type) and MDA-MB-231 (IC50 = 7.9 muM, BRCA2 wild type but TP53 mutant).	Afatinib	33-41	P53	Homo sapiens	180-184
32101536-6	2020	We experimentally validated that afatinib has the strongest cytotoxic activity on BT474 (IC50 = 55.5 nM, BRCA2 and TP53 co-mutant) compared to MCF7 (IC50 = 7.7 muM, both BRCA2 and TP53 wild type) and MDA-MB-231 (IC50 = 7.9 muM, BRCA2 wild type but TP53 mutant).	Afatinib	33-41	P53	Homo sapiens	180-184
31251988-2	2019	The experimental results showed that 20-25 muM of MH for 24 h of treatment was very potent to reduce the cell proliferation through apoptosis with arresting the cells in G0/G1 in both ER+/p53WT MCF-7 and triple negative/p53Mut MDA-MB-231 cells.	mahanine	50-52	P53	Homo sapiens	188-191
31251988-2	2019	The experimental results showed that 20-25 muM of MH for 24 h of treatment was very potent to reduce the cell proliferation through apoptosis with arresting the cells in G0/G1 in both ER+/p53WT MCF-7 and triple negative/p53Mut MDA-MB-231 cells.	mahanine	50-52	P53	Homo sapiens	220-223
32103135-5	2020	We found bryostatin can target multiple types of protein other than only protein kinase C. Functional network analysis of the target profile and differential expressed genes suggested that bryostatin may activate a few novel pathways such as pyrimidine metabolism, purine metabolism and p53 signaling pathway, besides commonly known pathways DNA replication, cell cycle and so on.	Bryostatins	9-19	P53	Homo sapiens	287-290
32139108-0	2020	CpG Oligodeoxynucleotides Induces Apoptosis of Human Bladder Cancer Cells via Caspase-3-Bax/Bcl-2-p53 Axis.	Oligodeoxyribonucleotides	4-25	P53	Homo sapiens	98-101
31587475-7	2020	In addition, SA provoked the apoptosis by expanding the p53 and Bax levels, terminal deoxynucleotidyl transferase dUTP nick end labeling, and expression of caspase-3.	sodium arsenite	13-15	P53	Homo sapiens	56-59
31046065-0	2019	Androgen Receptor Burden and Poor Response to Abiraterone or Enzalutamide in TP53 Wild-Type Metastatic Castration-Resistant Prostate Cancer.	enzalutamide	61-73	P53	Homo sapiens	77-81
32103135-5	2020	We found bryostatin can target multiple types of protein other than only protein kinase C. Functional network analysis of the target profile and differential expressed genes suggested that bryostatin may activate a few novel pathways such as pyrimidine metabolism, purine metabolism and p53 signaling pathway, besides commonly known pathways DNA replication, cell cycle and so on.	Bryostatins	189-199	P53	Homo sapiens	287-290
32103135-6	2020	The results suggest that bryostatin may reactivate the HIV-latent cells through up-regulation of pyrimidine and purine metabolism or through starting the cell-cycle arrest and apoptosis induced by up-regulation of p53 signaling pathway.	Bryostatins	25-35	P53	Homo sapiens	214-217
31691131-7	2020	In addition, nutlin-3 effectively abrogated the intracellular survival of mycobacteria in both TB patients and healthy controls after H37Ra infection for 24 h, indicating that the enhancement of p53 production effectively suppressed the intracellular survival of Mtb in hosts.	nutlin 3	13-21	P53	Homo sapiens	195-198
31164161-7	2019	High tumor mutation burden (TMB) gathered in TP53 wild-type tumors (p = 0.045).	1,2,4,5-tetramethoxybenzene	28-31	P53	Homo sapiens	45-49
31400201-0	2020	Role of Asparagine Endopeptidase in Mediating Wild-Type p53 Inactivation of Glioblastoma.	Asparagine	8-18	P53	Homo sapiens	56-59
31464976-8	2020	Inhibition of ROS generation by NAC or p38 MAPK signaling by SB203580 attenuated the p53-mediated cell cycle arrest and apoptosis induced by LY.	lycorine	141-143	P53	Homo sapiens	85-88
32063580-7	2020	Our results demonstrate that Nutlin-3 but not RITA (reactivation of p53 and induction of tumor cell apoptosis) effectively disrupted the p53-MDM2-MDM4 complex to activate p53, which increased robustly with cisplatin/Nutlin-3 combination and enhanced antitumor effects more than either agent alone.	nutlin 3	29-37	P53	Homo sapiens	137-140
32063580-7	2020	Our results demonstrate that Nutlin-3 but not RITA (reactivation of p53 and induction of tumor cell apoptosis) effectively disrupted the p53-MDM2-MDM4 complex to activate p53, which increased robustly with cisplatin/Nutlin-3 combination and enhanced antitumor effects more than either agent alone.	nutlin 3	29-37	P53	Homo sapiens	137-140
32060420-0	2020	Therapeutic targeting of TP53-mutated acute myeloid leukemia by inhibiting HIF-1alpha with echinomycin.	Echinomycin	91-102	P53	Homo sapiens	25-29
32060420-4	2020	To determine the role of this activation, we tested efficacy of HIF-1alpha inhibitor echinomycin in TP53-mutated AML samples in vitro and in vivo.	Echinomycin	85-96	P53	Homo sapiens	100-104
32218859-6	2020	In the present study, CP-31398, a p53-restoring agent, was used to improve the therapeutic efficacy of sorafenib in SW579 cells, an ATC cell line harboring p53 mutations.	CP 31398	22-30	P53	Homo sapiens	156-159
32218859-9	2020	These results indicate a potential clinical application of CP-31398 for patients with ATC harboring p53 abnormalities, since these individuals generally respond poorly to sorafenib alone.	CP 31398	59-67	P53	Homo sapiens	100-103
31316744-1	2019	All-hydrocarbon, i, i+7 stapled peptide inhibitors of the p53-Mdm2 interaction have emerged as promising new leads for cancer therapy.	Hydrocarbons	4-15	P53	Homo sapiens	58-61
31018506-11	2019	Activation of the key regulators p53 and p21 inhibited the cyclin-dependent kinases Cdk2 and Cdk4, suggesting that p53 and p21 activation in GO-PtNP-treated cells caused genotoxic stress and apoptosis.	(4-toluoyl-3-nitro)piperazine	144-148	P53	Homo sapiens	33-36
31018506-11	2019	Activation of the key regulators p53 and p21 inhibited the cyclin-dependent kinases Cdk2 and Cdk4, suggesting that p53 and p21 activation in GO-PtNP-treated cells caused genotoxic stress and apoptosis.	(4-toluoyl-3-nitro)piperazine	144-148	P53	Homo sapiens	115-118
30943920-13	2019	As a consequence, p53 activation by etoposide was reduced, and cell survival enhanced.	Etoposide	36-45	P53	Homo sapiens	18-21
32256964-8	2020	As expected, an upregulation of p53 was observed after DpdtC insulting; however, the addition of a p53 inhibitor, PFT-alpha, could significantly attenuate the action of DpdtC on ferritinophagy induction and EMT inhibition.	di-n-propyldithiocarbamate	55-60	P53	Homo sapiens	32-35
32256964-8	2020	As expected, an upregulation of p53 was observed after DpdtC insulting; however, the addition of a p53 inhibitor, PFT-alpha, could significantly attenuate the action of DpdtC on ferritinophagy induction and EMT inhibition.	di-n-propyldithiocarbamate	169-174	P53	Homo sapiens	32-35
32256964-8	2020	As expected, an upregulation of p53 was observed after DpdtC insulting; however, the addition of a p53 inhibitor, PFT-alpha, could significantly attenuate the action of DpdtC on ferritinophagy induction and EMT inhibition.	di-n-propyldithiocarbamate	169-174	P53	Homo sapiens	99-102
32256964-9	2020	In addition, autophagy inhibitors or NAC could counteract the effect of DpdtC and restore the level of p53 to the control group, indicating that the upregulation of p53 was caused by ferritinophagy-mediated ROS production.	di-n-propyldithiocarbamate	72-77	P53	Homo sapiens	165-168
32256964-10	2020	In conclusion, our data demonstrated that the inhibition of EMT induced by DpdtC was realized through ferritinophagy-mediated ROS/p53 pathway, which supported that the activation of ferritinophagic flux was the main driving force in EMT inhibition in gastric cancer cells, and further strengthening the concept that NCOA4 participates in EMT process.	di-n-propyldithiocarbamate	75-80	P53	Homo sapiens	130-133
32027268-6	2020	Western blot analysis showed that sorafenib combined with decitabine significantly up-regulated the levels of Bax/Bcl-2, P53, C-Caspase3 and C-PARP and activated apoptosis by inhibiting PI3K-AKT pathway.	sorafenib	34-43	P53	Homo sapiens	121-124
32001831-8	2020	Furthermore, prolonged nicotine exposure interferes with p53 function triggered by sodium arsenite.	sodium arsenite	83-98	P53	Homo sapiens	57-60
30246261-0	2019	Potentiating apoptosis and modulation of p53, Bcl2, and Bax by a novel chrysin ruthenium complex for effective chemotherapeutic efficacy against breast cancer.	chrysin ruthenium complex	71-96	P53	Homo sapiens	41-44
30865893-0	2019	p53 Promotes Cancer Cell Adaptation to Glutamine Deprivation by Upregulating Slc7a3 to Increase Arginine Uptake.	Glutamine	39-48	P53	Homo sapiens	0-3
32027268-7	2020	CONCLUSION: Sorafenib combined with decitabine induces the apoptosis of diffuse large B-cell lymphoma cell line OCI-LY1 by inhibiting PI3K-AKT pathway and activating P53.	sorafenib	12-21	P53	Homo sapiens	166-169
30865893-4	2019	To better understand the molecular mechanisms by which p53 activation promotes cancer cell adaptation to glutamine deprivation, we identified p53-dependent genes that are induced upon glutamine deprivation by using RNA-seq analysis.	Glutamine	105-114	P53	Homo sapiens	55-58
30865893-4	2019	To better understand the molecular mechanisms by which p53 activation promotes cancer cell adaptation to glutamine deprivation, we identified p53-dependent genes that are induced upon glutamine deprivation by using RNA-seq analysis.	Glutamine	105-114	P53	Homo sapiens	142-145
31995555-9	2020	These findings indicate that the combination of CGA, TC-HT, and LIPEF may be a promising modality for cancer treatment, as it can induce p53-dependent cell cycle arrest and apoptosis through accumulation of ROS in PANC-1 cells.	lipef	64-69	P53	Homo sapiens	137-140
30865893-4	2019	To better understand the molecular mechanisms by which p53 activation promotes cancer cell adaptation to glutamine deprivation, we identified p53-dependent genes that are induced upon glutamine deprivation by using RNA-seq analysis.	Glutamine	184-193	P53	Homo sapiens	55-58
30865893-4	2019	To better understand the molecular mechanisms by which p53 activation promotes cancer cell adaptation to glutamine deprivation, we identified p53-dependent genes that are induced upon glutamine deprivation by using RNA-seq analysis.	Glutamine	184-193	P53	Homo sapiens	142-145
30865893-6	2019	We also show that increased intracellular arginine levels following glutamine deprivation are dependent on p53.	Glutamine	68-77	P53	Homo sapiens	107-110
31866490-7	2020	CDK9 inhibitors further showed synergistic effects in killing p53+/+ HCT116 cells when combined with the MDM2 inhibitor Nutlin-3.	nutlin 3	120-128	P53	Homo sapiens	62-65
31949255-13	2020	We are the first to identify the involvement of a cysteine metabolism/reactive oxygen species/p53/Bax/caspase 9/caspase 3 pathway in celastrol-triggered mitochondrial apoptosis in HL-60 and NB-4 cells, providing a novel underlying mechanism through which celastrol could be used to treat acute myeloid leukaemia, especially acute promyelocytic leukaemia.	celastrol	133-142	P53	Homo sapiens	94-97
31774938-7	2020	The most potent library member (Ki = 0.095 mum) identified is almost as active as Nutlin-3, a potent inhibitor of the p53-MDM2 PPI.	nutlin 3	82-90	P53	Homo sapiens	118-121
30895171-0	2019	Targeting Oxidative Stress With Auranofin or Prima-1Met to Circumvent p53 or Bax/Bak Deficiency in Myeloma Cells.	Auranofin	32-41	P53	Homo sapiens	70-73
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	Polymers	29-36	P53	Homo sapiens	80-83
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	Polymers	29-36	P53	Homo sapiens	99-102
32010620-0	2019	Involvement of Glutathione Depletion in Selective Cytotoxicity of Oridonin to p53-Mutant Esophageal Squamous Carcinoma Cells.	oridonin	66-74	P53	Homo sapiens	78-81
30792807-0	2019	Anticancer response to disulfiram may be enhanced by co-treatment with MEK inhibitor or oxaliplatin: modulation by tetrathiomolybdate, KRAS/BRAF mutations and c-MYC/p53 status.	Disulfiram	23-33	P53	Homo sapiens	165-168
32069905-2	2020	Recently, two photo-switchable diastereomeric benzodiazopyrrole derivatives 1RR and 1RS have been reported as microtubules targeting agents (MTAs) on human colorectal carcinoma p53 null cell line (HCT 116 p53-/-).	benzodiazopyrrole	46-63	P53	Homo sapiens	177-180
32069905-2	2020	Recently, two photo-switchable diastereomeric benzodiazopyrrole derivatives 1RR and 1RS have been reported as microtubules targeting agents (MTAs) on human colorectal carcinoma p53 null cell line (HCT 116 p53-/-).	benzodiazopyrrole	46-63	P53	Homo sapiens	205-208
32010620-7	2019	At the same time, we also found that oridonin showed selective cytotoxicity to esophageal squamous carcinoma cell with p53 mutation since mut-p53 cells had lower SLC7A11 expression, a component of the cystine/glutamate antiporter.	oridonin	37-45	P53	Homo sapiens	119-122
31918545-2	2020	All the probes showed potent inhibitory and acceptable cell toxicity compared with commercially available p53-MDM2 inhibitor Nutlin-3, and can increase the protein expression level of p53 and MDM2 in A549 cell line, in particular, probe 10 and 11 can increase the protein expression level of p53 than nutlin-3.	nutlin 3	125-133	P53	Homo sapiens	106-109
31918545-2	2020	All the probes showed potent inhibitory and acceptable cell toxicity compared with commercially available p53-MDM2 inhibitor Nutlin-3, and can increase the protein expression level of p53 and MDM2 in A549 cell line, in particular, probe 10 and 11 can increase the protein expression level of p53 than nutlin-3.	nutlin 3	125-133	P53	Homo sapiens	184-187
31918545-2	2020	All the probes showed potent inhibitory and acceptable cell toxicity compared with commercially available p53-MDM2 inhibitor Nutlin-3, and can increase the protein expression level of p53 and MDM2 in A549 cell line, in particular, probe 10 and 11 can increase the protein expression level of p53 than nutlin-3.	nutlin 3	125-133	P53	Homo sapiens	184-187
31524143-11	2019	Functional enrichment study suggested that the 9 lncRNAs may be mainly involved in metabolism-related pathways, phosphatidylinositol signaling system, p53 signaling pathway, and notch signaling pathway.	Phosphatidylinositols	112-132	P53	Homo sapiens	151-154
32010620-7	2019	At the same time, we also found that oridonin showed selective cytotoxicity to esophageal squamous carcinoma cell with p53 mutation since mut-p53 cells had lower SLC7A11 expression, a component of the cystine/glutamate antiporter.	oridonin	37-45	P53	Homo sapiens	142-145
32010620-10	2019	Esophageal squamous carcinoma cells with p53-mutation showed hypersensitivity to oridonin because of the suppression of SLC7A11 expression by p53 mutation.	oridonin	81-89	P53	Homo sapiens	41-44
30393117-7	2019	p53 stability was enhanced by miR-944s targeting E3 ligases COP1 and MDM2.	mir-944s	30-38	P53	Homo sapiens	0-3
32010620-10	2019	Esophageal squamous carcinoma cells with p53-mutation showed hypersensitivity to oridonin because of the suppression of SLC7A11 expression by p53 mutation.	oridonin	81-89	P53	Homo sapiens	142-145
31809756-11	2020	When Akt and p53 were suppressed by LY294002 and PFTalpha, respectively, sesamin exerted no additional effects.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	36-44	P53	Homo sapiens	13-16
30501707-13	2018	CONCLUSION: IPSS staging, complex karyotype, Plt count doubling after 1 course treatment and hENT1 mRNA expression, TP53 gene mutation can be used to predict the tharapeutic efficacy of dectitabine for treatment of MDS.	dectitabine	186-197	P53	Homo sapiens	116-120
31855686-0	2020	Histone H2A-peptide-hybrided upconversion mesoporous silica nanoparticles for bortezomib/p53 delivery and apoptosis induction.	Silicon Dioxide	53-59	P53	Homo sapiens	89-92
31676337-5	2020	Furthermore, BAX, TP53 and ATM were found to be upregulated in DU145 and MCF7 treated with RuPro and RuThr, in which, a higher ASCT2 gene expression was also observed.	peptide T amide	101-106	P53	Homo sapiens	18-22
31940492-3	2020	In this study, we report that FBXW7, a substrate recognition component of the SKP1-CUL1-F-box (SCF) E3 ligase, interacts with and targets p53 for polyubiquitination and proteasomal degradation after exposure to ionizing radiation or etoposide.	Etoposide	233-242	P53	Homo sapiens	138-141
31963392-2	2020	Herein, we unveiled that p53 activation by (S)-tryptophanol-derived oxazoloisoindolinone (SLMP53-1) mediated the reprograming of glucose metabolism in cancer cells and xenograft human tumor tissue, interfering with angiogenesis and migration.	oxazoloisoindolinone	68-88	P53	Homo sapiens	25-28
30462771-0	2018	Oridonin induces growth inhibition and apoptosis in human gastric carcinoma cells by enhancement of p53 expression and function.	oridonin	0-8	P53	Homo sapiens	100-103
30462771-11	2018	Moreover, the mRNA and protein expression of p53 was significantly up-regulated in oridonin-treated cells, while Mdm2 expression was down-regulated.	oridonin	83-91	P53	Homo sapiens	45-48
30462771-12	2018	Furthermore, oridonin enhanced p53 function and induced DNA damage.	oridonin	13-21	P53	Homo sapiens	31-34
30103170-0	2018	Metronomic oral doxorubicin in combination of Chk1 inhibitor MK-8776 for p53-deficient breast cancer treatment.	MK-8776	61-68	P53	Homo sapiens	73-76
30103170-3	2018	In this light, within the limits of p53-deficient breast cancer, we demonstrate the enhanced anticancer effect of metronomic chemotherapy using doxorubicin when combined with Chk1 inhibitor MK-8776 by specifically augmenting the direct cytotoxic effect on cancer cells.	MK-8776	190-197	P53	Homo sapiens	36-39
30103170-5	2018	MK-8776 selectively enhanced the cytotoxic effect of low-concentration doxorubicin in p53-deficient breast cancer cells by abrogating the Chk1-dependent cell cycle arrest in vitro.	MK-8776	0-7	P53	Homo sapiens	86-89
30103170-6	2018	Consistently, combining MK-8776 significantly improved the anticancer effect of the daily administered oral doxorubicin in p53-deficient breast cancer xenografts especially in a lower dose of doxorubicin without evident systemic toxicities.	MK-8776	24-31	P53	Homo sapiens	123-126
30103170-7	2018	Combination therapy of MK-8776 and metronomic oral doxorubicin would be thus promising in the treatment of p53-deficient breast cancer benefited from the augmented direct cytotoxic effect and low risk of toxicities.	MK-8776	23-30	P53	Homo sapiens	107-110
31761381-0	2020	2-Styryl-4-aminoquinazoline derivatives as potent DNA-cleavage, p53-activation and in vivo effective anticancer agents.	4-aminoquinazoline	0-27	P53	Homo sapiens	64-67
31761381-1	2020	Forty-eight analogues of CP-31398, an antitumor agent modulated the mutant p53 gene were synthesized and their cytotoxicities against four cancer cell lines with different p-53 status including bladder cell T24 (w-p53), gastric cell MGC-803 (m-p53), prostate cell DU145 (m-p53), prostate cell PC-3 (null-p53), lung cell A549 (w-p53) and normal liver cell line HL-7702 (w-p53) were examined.	CP 31398	25-33	P53	Homo sapiens	75-78
31761381-1	2020	Forty-eight analogues of CP-31398, an antitumor agent modulated the mutant p53 gene were synthesized and their cytotoxicities against four cancer cell lines with different p-53 status including bladder cell T24 (w-p53), gastric cell MGC-803 (m-p53), prostate cell DU145 (m-p53), prostate cell PC-3 (null-p53), lung cell A549 (w-p53) and normal liver cell line HL-7702 (w-p53) were examined.	CP 31398	25-33	P53	Homo sapiens	214-217
31940492-6	2020	Biologically, FBXW7 inactivation sensitizes cancer cells to radiation or etoposide by stabilizing p53 to induce cell-cycle arrest and apoptosis.	Etoposide	73-82	P53	Homo sapiens	98-101
31761381-1	2020	Forty-eight analogues of CP-31398, an antitumor agent modulated the mutant p53 gene were synthesized and their cytotoxicities against four cancer cell lines with different p-53 status including bladder cell T24 (w-p53), gastric cell MGC-803 (m-p53), prostate cell DU145 (m-p53), prostate cell PC-3 (null-p53), lung cell A549 (w-p53) and normal liver cell line HL-7702 (w-p53) were examined.	CP 31398	25-33	P53	Homo sapiens	214-217
31761381-1	2020	Forty-eight analogues of CP-31398, an antitumor agent modulated the mutant p53 gene were synthesized and their cytotoxicities against four cancer cell lines with different p-53 status including bladder cell T24 (w-p53), gastric cell MGC-803 (m-p53), prostate cell DU145 (m-p53), prostate cell PC-3 (null-p53), lung cell A549 (w-p53) and normal liver cell line HL-7702 (w-p53) were examined.	CP 31398	25-33	P53	Homo sapiens	214-217
32907364-7	2020	Additional molecular studies demonstrated that cucurbitacin B suppressed the activation of focal adhesion kinase (FAK) which consequently resulted in inhibition of its kinase-dependent and kinase-independent downstream targets contributing to the regulation of cell proliferation including PI3K/PDK1/AKT and p53 proteins.	cucurbitacin B	47-61	P53	Homo sapiens	308-311
29976747-8	2018	Moreover, the combined use of MDM2- and FLT3-inhibitors was superior to single agent treatment, and the combination of midostaurin and NVP-HDM201 was as specific and effective against FLT3-ITD positive TP53 wild type cells as the combination of midostaurin with conventional induction therapy.	midostaurin	119-130	P53	Homo sapiens	202-206
29976747-9	2018	In summary, the combined use of the MDM2 inhibitor NVP-HDM201 and the FLT3 inhibitor midostaurin was a most effective and specific treatment to target TP53 and NPM1 wild type acute myeloid leukemia cells with high allelic FLT3-ITD ratio.	midostaurin	85-96	P53	Homo sapiens	151-155
31668372-7	2020	What is more, circ_0001546 inhibits the chemoresistance of HGC-27 cells to L-OPH (Oxaliplatin) may through the activation of the ATM/checkpoint kinase 2 (Chk2)/p53-dependent signaling pathway.	methylphosphite	75-80	P53	Homo sapiens	160-163
32067620-12	2020	CONCLUSION: The results suggested that podophyllum derivatives containing fluorine atom in the 3-position of 2-aminopyridine could inhibit the growth of HCC harboring p53-R249S by restoring the activity of p53 with decreasing the level of c-Myc.	Fluorine	74-82	P53	Homo sapiens	167-170
31605433-4	2020	Spalax fibroblasts undergo replicative senescence (RS) and etoposide-induced senescence (EIS), evidenced by an increased activity of senescence-associated beta-galactosidase (SA-beta-Gal), growth arrest, and overexpression of p21, p16, and p53 mRNAs.	Etoposide	59-68	P53	Homo sapiens	240-243
31734849-7	2020	Arsenic trioxide (As2O3; 1-5 muM) significantly induced senescence in human articular chondrocytes by increasing senescence-associated beta-galactosidase (SA-beta-Gal) activity and protein expression of p16, p53, and p21.	ato	0-16	P53	Homo sapiens	208-211
30362332-0	2018	Synergistic Action of 1,2-Epoxy-3 (3- (3,4-dimethoxyphenyl)- 4H-1-benzopiyran-4-on) Propane with Doxorubicin and Cisplatin through Increasing of p53, TIMP-3, and MicroRNA-34a in Cervical Cancer Cell Line (HeLa) Objective: Cervical cancer is the second most common cancer among women worldwide, with a high mortality rateespecially in developing countries.	1,2-epoxy-3 (3- (3,4-dimethoxyphenyl)- 4h-1-benzopiyran-4-on) propane	22-91	P53	Homo sapiens	145-148
30215795-0	2018	The impact of p53 function on the metabolic activation of the carcinogenic air pollutant 3-nitrobenzanthrone and its metabolites 3-aminobenzanthrone and N-hydroxy-3-aminobenzanthrone in human cells.	3-nitrobenzanthrone	89-108	P53	Homo sapiens	14-17
32067620-12	2020	CONCLUSION: The results suggested that podophyllum derivatives containing fluorine atom in the 3-position of 2-aminopyridine could inhibit the growth of HCC harboring p53-R249S by restoring the activity of p53 with decreasing the level of c-Myc.	Fluorine	74-82	P53	Homo sapiens	206-209
29990856-4	2018	In addition, we also observed that tumor suppressor p53 was increased under genistein treatment.	Genistein	76-85	P53	Homo sapiens	52-55
29990856-6	2018	Therefore, our findings suggest that genistein can suppress laryngeal cancer cell survival through p53 -miR-1469-Mcl1pathway.	Genistein	37-46	P53	Homo sapiens	99-102
31538264-3	2020	COTI-2 is a third-generation thiosemicarbazone engineered for high efficacy and low toxicity which acts by reactivating mutant p53 to a WT form.	Thiosemicarbazones	29-46	P53	Homo sapiens	127-130
31536751-3	2020	Recently, we have reported the (S)-tryptophanol-derived oxazoloisoindolinone SLMP53-1 as a new reactivator of wt and mutp53 R280K with in vitro and in vivo p53-dependent antitumor activity.	oxazoloisoindolinone	56-76	P53	Homo sapiens	120-123
31969092-12	2020	Lupeol also modulates the molecules involved in cell cycle regulation such as Cyclins, CDKs, P53, P21, and PCNA in different cancer types.	lupeol	0-6	P53	Homo sapiens	93-96
29803744-9	2018	Co-immunoprecipitation assay showed that SIRT1 could bind to p53, reduce its acetylation level, and treatment with nutlin-3A reversed the effect of SIRT1 on the level of p53 in ADSCs.	nutlin 3	115-124	P53	Homo sapiens	61-64
31747859-1	2020	p53-R249S (p53-RS) is frequently detected in human hepatocellular carcinoma (HCC) that is highly associated with hepatitis B infection and aflatoxin B1 exposure.	Aflatoxin B1	139-151	P53	Homo sapiens	0-3
29803744-9	2018	Co-immunoprecipitation assay showed that SIRT1 could bind to p53, reduce its acetylation level, and treatment with nutlin-3A reversed the effect of SIRT1 on the level of p53 in ADSCs.	nutlin 3	115-124	P53	Homo sapiens	170-173
30513211-15	2018	On the other hand, O-EGCG induced HCT116 cells apoptosis mainly by increasing the expression of p53 and cleaved caspase-3, which might be the underlying reason why O-EGCG had stronger inhibitory effect on HCT116 cells line than EGCG.	epigallocatechin gallate	21-25	P53	Homo sapiens	96-99
31765699-6	2020	After ligustilide treatment, the proportion of CAFs in the G2-M phase of the cell cycle increased, and the expression of apoptosis-related proteins (p-P53, Bcl-2, Caspase9 and Cytochrome C) changed.	ligustilide	6-17	P53	Homo sapiens	151-154
31747859-1	2020	p53-R249S (p53-RS) is frequently detected in human hepatocellular carcinoma (HCC) that is highly associated with hepatitis B infection and aflatoxin B1 exposure.	Aflatoxin B1	139-151	P53	Homo sapiens	11-14
31747859-4	2020	Indeed, co-treatment of p53-RS-containing, but not wild-type p53 or p53-null, HCC cells with PD-0332991 (PD), a CDK4/6 inhibitor, and CP-31398 (CP), a compound that can restore the intrinsic conformation and transcriptional activity of mutant p53, drastically repressed the c-Myc activation function of p53-RS.	CP 31398	134-142	P53	Homo sapiens	24-27
30739221-0	2019	The sodium pump alpha1 subunit regulates bufalin sensitivity of human glioblastoma cells through the p53 signaling pathway.	bufalin	41-48	P53	Homo sapiens	101-104
31807880-9	2020	TMB was significantly higher in men, current or former smokers, and in patients with squamous cell carcinoma, tumor size >= 2.8 cm, wild-type EGFR, TP53 gene mutation-positive status, and cyclin-dependent kinase-inhibitor gene 2A mutation-positive status.	1,2,4,5-tetramethoxybenzene	0-3	P53	Homo sapiens	148-152
30739221-9	2019	Mechanistic studies confirmed the important roles of Src and p53 signaling in mediating bufalin-induced apoptosis.	bufalin	88-95	P53	Homo sapiens	61-64
30739221-11	2019	In conclusion, our study indicated that therapies targeting the ATP1A1 and p53 signaling-mediated mitochondrial apoptotic pathways regulated by bufalin might be potential treatments for human glioma, and these findings will provide molecular bases for developing bufalin into a drug candidate for the treatment of malignant glioma.	bufalin	144-151	P53	Homo sapiens	75-78
30739221-11	2019	In conclusion, our study indicated that therapies targeting the ATP1A1 and p53 signaling-mediated mitochondrial apoptotic pathways regulated by bufalin might be potential treatments for human glioma, and these findings will provide molecular bases for developing bufalin into a drug candidate for the treatment of malignant glioma.	bufalin	263-270	P53	Homo sapiens	75-78
29997047-5	2018	Moreover, these steroidal benzylidenes regulate ERalpha signaling and reveal p53-independent mechanism of pro-apoptotic action in MCF-7 cells.	benzylidenes	26-38	P53	Homo sapiens	77-80
31807880-10	2020	According to multivariate analysis, TMB was significantly associated with EGFR gene mutation-negative status (p = 0.0111) and TP53 gene mutation-positive status (p = 0.0425).	1,2,4,5-tetramethoxybenzene	36-39	P53	Homo sapiens	126-130
32098913-0	2020	beta-Actin facilitates etoposide-induced p53 nuclear import.	Etoposide	23-32	P53	Homo sapiens	41-44
30355102-7	2018	The interaction of MDM2 with p53 was disrupted by neuronal treatment with nutlin-3a.	nutlin 3	74-83	P53	Homo sapiens	29-32
31780660-0	2019	Repurposing auranofin to treat TP53-mutated or PTEN-deleted refractory B-cell lymphoma.	Auranofin	12-21	P53	Homo sapiens	31-35
31597953-4	2020	Using the microarray assay, we noted that miR-149-3p was involved in the chemoresistance of CRC, which was modulated by wild-type p53 after DCA treatment.	mir-149-3p	42-52	P53	Homo sapiens	130-133
32280825-14	2020	Presence and activation of p53 are required for exertion of the radiosensitizing effect by nutlin-3, but this is not the sole determinant of the effect.	nutlin 3	91-99	P53	Homo sapiens	27-30
31781509-9	2019	Interestingly, the combination of PJ-1 or PJ-9 with SOR exhibited restoring cell viability of normal cells via controlling Raf-1 and P53 genes expression.	sorafenib	52-55	P53	Homo sapiens	133-136
29205062-0	2018	MicroRNA-150 protects against cigarette smoke-induced lung inflammation and airway epithelial cell apoptosis through repressing p53: MicroRNA-150 in CS-induced lung inflammation.	Cesium	149-151	P53	Homo sapiens	128-131
29205062-12	2018	Collectively, miR-150 suppresses CS-induced lung inflammation and airway epithelial cell apoptosis, which is causally linked to repression of p53 expression and NF-kappaB activity.	Cesium	33-35	P53	Homo sapiens	142-145
31568878-0	2019	Co-delivery of p53 and MDM2 inhibitor RG7388 using a hydroxyl terminal PAMAM dendrimer derivative for synergistic cancer therapy.	Hydroxyl Radical	53-61	P53	Homo sapiens	15-18
29800662-6	2018	The critical groups and significant binding sites for the interaction between alisol monomers and p53DNA include C19-OH and C22-OH of the alisols; N2 and H21 of the guanine deoxynucleotide (DG8), N2-H21 of the DG7, O4" of the DG9 in the f-chain of p53DNA; and C2-O2 of the cytosine deoxynucleotide (DC16) in the e-chain of p53DNA.	alisol	78-84	P53	Homo sapiens	98-101
29800662-6	2018	The critical groups and significant binding sites for the interaction between alisol monomers and p53DNA include C19-OH and C22-OH of the alisols; N2 and H21 of the guanine deoxynucleotide (DG8), N2-H21 of the DG7, O4" of the DG9 in the f-chain of p53DNA; and C2-O2 of the cytosine deoxynucleotide (DC16) in the e-chain of p53DNA.	alisol	78-84	P53	Homo sapiens	248-251
29800662-6	2018	The critical groups and significant binding sites for the interaction between alisol monomers and p53DNA include C19-OH and C22-OH of the alisols; N2 and H21 of the guanine deoxynucleotide (DG8), N2-H21 of the DG7, O4" of the DG9 in the f-chain of p53DNA; and C2-O2 of the cytosine deoxynucleotide (DC16) in the e-chain of p53DNA.	alisol	78-84	P53	Homo sapiens	248-251
29800662-6	2018	The critical groups and significant binding sites for the interaction between alisol monomers and p53DNA include C19-OH and C22-OH of the alisols; N2 and H21 of the guanine deoxynucleotide (DG8), N2-H21 of the DG7, O4" of the DG9 in the f-chain of p53DNA; and C2-O2 of the cytosine deoxynucleotide (DC16) in the e-chain of p53DNA.	guanine deoxynucleotide	165-188	P53	Homo sapiens	98-101
31243806-8	2019	Moreover, miR-488-3p activated the p53 pathway through suppressing ZBTB2.	mir-488-3p	10-20	P53	Homo sapiens	35-38
31243806-11	2019	In sum, this study revealed that miR-488-3p inhibited proliferation and induced apoptosis by targeting ZBTB2 and activating p53 pathway in esophageal squamous cell carcinoma, providing a novel biological target for ESCC.	mir-488-3p	33-43	P53	Homo sapiens	124-127
31568878-0	2019	Co-delivery of p53 and MDM2 inhibitor RG7388 using a hydroxyl terminal PAMAM dendrimer derivative for synergistic cancer therapy.	PEG-PAMAM	71-76	P53	Homo sapiens	15-18
31568878-2	2019	In the present study we utilized a PAMAM-OH derivative (PAMSPF) to co-deliver p53 plasmid and MDM2 inhibitor (RG7388) to the tumor site and evaluated the synergistic anti-tumor effect of p53 plasmid and RG7388.	PEG-PAMAM	35-43	P53	Homo sapiens	78-81
31652556-5	2019	In this study, biotinylated PAMAM G3 dendrimers substituted with the recognized anticancer agents cyclooxygenase-2 (COX-2) inhibitor celecoxib and peroxisome proliferator-activated receptor gamma (PPARgamma) agonist Fmoc-L-Leucine (G3-BCL) were tested in vitro on human cell lines with different p53 status: glioblastoma (U-118 MG), normal fibroblasts (BJ) and immortalized keratinocytes (HaCaT).	PEG-PAMAM	28-33	P53	Homo sapiens	296-299
31779626-4	2019	BBN-induced tumors in mice recapitulate the histology of human BC and were characterized with an overexpression of markers typical for basal-like cancer subtype in addition to a high mutational burden with frequent mutations in Trp53, similar to human muscle invasive BC.	Butylhydroxybutylnitrosamine	0-3	P53	Homo sapiens	228-233
30118500-0	2018	Trans-chalcone increases p53 activity via DNAJB1/HSP40 induction and CRM1 inhibition.	Chalcone	0-14	P53	Homo sapiens	25-28
30118500-2	2018	Compared to other chalcones, trans-chalcone exhibits superior inhibitory activity in cancer cell growth as shown via in vitro assays, and exerts anti-cancerous effects via the activation of the p53 tumor suppressor protein.	Chalcone	29-43	P53	Homo sapiens	194-197
30118500-3	2018	Thus, characterization of the specific mechanisms, by which trans-chalcone activates p53, can aid development of new chemotherapeutic drugs that can be used individually or synergistically with other drugs.	Chalcone	60-74	P53	Homo sapiens	85-88
30118500-4	2018	In this report, we found that trans-chalcone modulates many p53 target genes, HSP40 being the most induced gene in the RNA-Seq data using trans-chalcone-treated cells.	Chalcone	30-44	P53	Homo sapiens	60-63
30118500-4	2018	In this report, we found that trans-chalcone modulates many p53 target genes, HSP40 being the most induced gene in the RNA-Seq data using trans-chalcone-treated cells.	Chalcone	138-152	P53	Homo sapiens	60-63
29980405-8	2018	Furthermore, in some cases, cells with WT-TP53 were more sensitive to the combination of drugs and suboptimal doses of the MDM2 inhibitor nutlin-3a.	nutlin 3	138-147	P53	Homo sapiens	42-46
31297844-12	2019	Our data, therefore, suggest that enzalutamide"s high efficacy is at least partially independent of AR and p53 protein expression, which are frequently lost in advanced PC.	enzalutamide	34-46	P53	Homo sapiens	107-110
31720601-0	2019	The hydrophobically-tagged MDM2-p53 interaction inhibitor Nutlin-3a-HT is more potent against tumor cells than Nutlin-3a.	nutlin 3	58-70	P53	Homo sapiens	32-35
29740674-5	2018	Deacetylmycoepoxydiene (DA-MED), a cytotoxic natural polyketide, functions as a Rac1 agonist in p53-null NSCLC H1299 cells.	deacetyl-mycoepoxydiene	0-22	P53	Homo sapiens	96-99
29740674-5	2018	Deacetylmycoepoxydiene (DA-MED), a cytotoxic natural polyketide, functions as a Rac1 agonist in p53-null NSCLC H1299 cells.	deacetyl-mycoepoxydiene	24-30	P53	Homo sapiens	96-99
31574980-3	2019	Atorvastatin increased cytotoxicity, sub G1 population, the number of apoptotic bodies, cleaved poly (ADP-ribose) polymerase (PARP) and caspase 3 and activated p53 in H1299, H596, and H460 cells.	atorvastatin	0-12	P53	Homo sapiens	160-163
31720601-2	2019	Nutlin-3a-HT, created by fusing the hydrophobic tag HyT13 to the MDM2-p53 interaction inhibitor Nutlin-3a, prevented cellular accumulation of MDM2 upon p53 reactivation, and had a stronger effect on cell viability and the induction of apoptosis than Nutlin-3a.	nutlin 3	0-12	P53	Homo sapiens	70-73
31720601-2	2019	Nutlin-3a-HT, created by fusing the hydrophobic tag HyT13 to the MDM2-p53 interaction inhibitor Nutlin-3a, prevented cellular accumulation of MDM2 upon p53 reactivation, and had a stronger effect on cell viability and the induction of apoptosis than Nutlin-3a.	nutlin 3	0-12	P53	Homo sapiens	152-155
31446323-0	2019	Loading of some quinoxaline derivatives in poly (l-lactic) acid/Pluronic  F-127 nanofibers enhances their anticancer efficiency and induces a p53 and p21 apoptotic-signaling pathway.	Poloxamer	64-79	P53	Homo sapiens	142-145
31541080-3	2019	Here, we show that the pharmalogical reactivation of a wt-like p53 function in p53-mutated breast cancer cells using the small molecule CP-31398 increases their sensitivity to NK-mediated lysis.	CP 31398	136-144	P53	Homo sapiens	63-66
31541080-3	2019	Here, we show that the pharmalogical reactivation of a wt-like p53 function in p53-mutated breast cancer cells using the small molecule CP-31398 increases their sensitivity to NK-mediated lysis.	CP 31398	136-144	P53	Homo sapiens	79-82
30049386-0	2018	A Nucleolar Stress-Specific p53-miR-101 Molecular Circuit Functions as an Intrinsic Tumor-Suppressor Network.	mir-101	32-39	P53	Homo sapiens	28-31
30049386-5	2018	FINDINGS: We discovered a functional link between p53 and miR-101, which form a molecular circuit in response to nucleolar stress.	mir-101	58-65	P53	Homo sapiens	50-53
30049386-6	2018	Inhibition of RNA polymerase I (Pol I) transcription resulted in the post-transcriptional activation of miR-101 in a p53-dependent manner.	mir-101	104-111	P53	Homo sapiens	117-120
30049386-7	2018	miR-101 induced G2 phase-specific feedback regulation of p53 through direct repression of its target, EG5, resulting in elevated phosphorylation of ATM.	mir-101	0-7	P53	Homo sapiens	57-60
30049386-8	2018	In lung cancer patients, low expression of miR-101 was associated with significantly poorer prognosis exclusively in p53 WT cases.	mir-101	43-50	P53	Homo sapiens	117-120
29754265-0	2018	Resveratrol analogue, (E)-N-(2-(4-methoxystyryl) phenyl) furan-2-carboxamide induces G2/M cell cycle arrest through the activation of p53-p21CIP1/WAF1 in human colorectal HCT116 cells.	(e)-n-(2-(4-methoxystyryl) phenyl) furan-2-carboxamide	22-76	P53	Homo sapiens	134-137
31212046-0	2019	Chitosan capped ZnO nanoparticles with cell specific apoptosis induction through P53 activation and G2/M arrest in breast cancer cells - In vitro approaches.	Zinc Oxide	16-19	P53	Homo sapiens	81-84
31674840-4	2021	Further mechanism of action study indicated that melognine demonstrated the ability to induce apoptosis by activation of caspase-3 and p53, and downregulation of Bcl-2 in BT549 cells.	melognine	49-58	P53	Homo sapiens	135-138
31229654-5	2019	PipeIT is able to identify pathogenic variants in BRAF, KRAS, PIK3CA, CTNNB1, TP53, and other cancer genes that the clinical-grade Oncomine workflow identified.	oncomine	131-139	P53	Homo sapiens	78-82
29302046-0	2018	p53 status in the primary tumor predicts efficacy of subsequent abiraterone and enzalutamide in castration-resistant prostate cancer.	enzalutamide	80-92	P53	Homo sapiens	0-3
31632084-6	2019	Interaction between miR-942 and ribonucleotide reductase regulatory TP53 inducible subunit M2B (RRM2B) was determined by RT-PCR, Western blot and luciferase assay.	Ribonucleotides	32-46	P53	Homo sapiens	68-72
29756671-0	2018	Wasabi 6-(methylsulfinyl)hexyl isothiocyanate induces apoptosis in human colorectal cancer cells through p53-independent mitochondrial dysfunction pathway.	wasabi 6-(methylsulfinyl)hexyl isothiocyanate	0-45	P53	Homo sapiens	105-108
31299263-7	2019	Furthermore, systemic delivery of CCL660 increased miRNA levels in tumors and significantly reduced tumor growth in two different P53 wild-type PDXs without off-target effects.	ccl660	34-40	P53	Homo sapiens	130-133
31299263-9	2019	Interestingly, anti-tumoral effects of CCL660 also in P53 mutant PDXs but with a functional p21 pathway were observed.	ccl660	39-45	P53	Homo sapiens	54-57
31482012-2	2019	In addition to doxorubicin, our results here indicated that camptothecin and bortezomib, which are a topoisomerase 1 poison and a 26 S proteasome inhibitor, respectively, could also induce apoptosis in a p53-dependent manner in prostate cancer.	Camptothecin	60-72	P53	Homo sapiens	204-207
31482012-4	2019	By using dominant negative p53 to compete with wild-type p53 in transcription activity, we demonstrated that p53-mediated apoptosis in response to doxorubicin- or camptothecin-induced genotoxic stress is transcription-independent.	Camptothecin	163-175	P53	Homo sapiens	27-30
31482012-4	2019	By using dominant negative p53 to compete with wild-type p53 in transcription activity, we demonstrated that p53-mediated apoptosis in response to doxorubicin- or camptothecin-induced genotoxic stress is transcription-independent.	Camptothecin	163-175	P53	Homo sapiens	57-60
29854627-4	2018	Thalidomide and carboplatin induced up-regulation of the expression of p53, tumor necrosis factor-alpha and interleukin-6 in brain and kidney.	Thalidomide	0-11	P53	Homo sapiens	71-74
32042215-0	2019	Zinc Oxide nanoparticles induce oxidative and proteotoxic stress in ovarian cancer cells and trigger apoptosis Independent of p53-mutation status.	Zinc Oxide	0-10	P53	Homo sapiens	126-129
29713280-4	2018	In the present study, we evaluated the cytotoxicity of oridonin toward a panel of drug-resistant cancer cells overexpressing ABCB1, ABCG2, or DeltaEGFR or with a knockout deletion of TP53.	oridonin	55-63	P53	Homo sapiens	183-187
31482012-4	2019	By using dominant negative p53 to compete with wild-type p53 in transcription activity, we demonstrated that p53-mediated apoptosis in response to doxorubicin- or camptothecin-induced genotoxic stress is transcription-independent.	Camptothecin	163-175	P53	Homo sapiens	57-60
31482012-6	2019	Interestingly, we also found that doxorubicin-induced p21 expression is activated by p53 in transcription-dependent manner, while camptothecin-induced p21 expression is p53-independent.	Camptothecin	130-142	P53	Homo sapiens	169-172
31482012-7	2019	We then investigated the p53 ratio of nucleus to cytosol corresponding to low and high dose doxorubicin, camptothecin, or bortezomib treatment.	Camptothecin	105-117	P53	Homo sapiens	25-28
31339234-0	2019	Oridonin induces Mdm2-p60 to promote p53-mediated apoptosis and cell cycle arrest in neuroblastoma.	oridonin	0-8	P53	Homo sapiens	37-40
30940656-0	2019	Auranofin Protects Intestine against Radiation Injury by Modulating p53/p21 Pathway and Radiosensitizes Human Colon Tumor.	Auranofin	0-9	P53	Homo sapiens	68-71
30940656-9	2019	RESULTS: Both in the mouse model of intestinal injury and in the human nonmalignant colon organoid culture, auranofin pretreatment prevented radiation toxicity and improved survival with the activation of p53/p21-mediated reversible cell-cycle arrest.	Auranofin	108-117	P53	Homo sapiens	205-208
29595201-5	2018	Moreover, acetylation of p53 K164 is reported to be deacetylated by SIRT2 for the first time.	5,6-dihydrothymine	29-33	P53	Homo sapiens	25-28
31339234-2	2019	Here, oridonin was confirmed to cause the reactivation of p53 (cellular tumor antigen p53) to promote the expression of a series of apoptosis- and cell cycle arrest-related proteins for the biological effects.	oridonin	6-14	P53	Homo sapiens	58-61
31339234-2	2019	Here, oridonin was confirmed to cause the reactivation of p53 (cellular tumor antigen p53) to promote the expression of a series of apoptosis- and cell cycle arrest-related proteins for the biological effects.	oridonin	6-14	P53	Homo sapiens	63-89
31339234-3	2019	During the process, oridonin relied on the caspase activation to cleave p53-induced Mdm2 (E3 ubiquitin-protein ligase Mdm2) to generate Mdm2-p60.	oridonin	20-28	P53	Homo sapiens	72-75
31339234-5	2019	In our research, it was also found that the reactivation of p53 induced by oridonin was closely related with the generation of ROS (reactive oxygen species).	oridonin	75-83	P53	Homo sapiens	60-63
31339234-6	2019	Taken together, these findings explain that oridonin exerts its anticancer activity partially by targeting the Mdm2-p53 axis in NB cells, which lay an experimental base for future research of exploring the effects and molecular mechanisms of oridonin.	oridonin	44-52	P53	Homo sapiens	116-119
29397400-10	2018	We suggest that the damage to mitochondria is a major contributing factor involved in ETP-induced cardiotoxicity and the activation of the p53-mediated ferroptosis pathway by ETP is likely the critical pathway in ETP-induced cardiotoxicity.	Etoposide	175-178	P53	Homo sapiens	139-142
29397400-10	2018	We suggest that the damage to mitochondria is a major contributing factor involved in ETP-induced cardiotoxicity and the activation of the p53-mediated ferroptosis pathway by ETP is likely the critical pathway in ETP-induced cardiotoxicity.	Etoposide	175-178	P53	Homo sapiens	139-142
31329636-4	2019	Using TP53 point mutations as a marker for tumor-derived cells, we earlier reported that MVP was partially converted from tumor cells via mesenchymal transition.	mvp	89-92	P53	Homo sapiens	6-10
31538075-7	2019	In the CaSki cells, the p-ERK1/2 level decreased by 37%, the p53 expression level increased by 304%, and the cleaved caspase 3 level increased by 115% in the cisplatin+genistein group compared to that in the cisplatin group.	Genistein	168-177	P53	Homo sapiens	61-64
31173964-7	2019	TMB was correlated with TP53 genotype, human papilloma virus (HPV) status, immune expression signatures and survival parameters.	1,2,4,5-tetramethoxybenzene	0-3	P53	Homo sapiens	24-28
31173964-10	2019	High TMB was significantly associated with an increased prevalence of TP53 mutations and immune gene expression patterns unrelated to T cell-inflamed gene expression profiles.	1,2,4,5-tetramethoxybenzene	5-8	P53	Homo sapiens	70-74
29309885-6	2018	Upregulation of p53 and p21 upon etoposide treatment is attenuated in HBXIP knock-down cells.	Etoposide	33-42	P53	Homo sapiens	16-19
31528096-12	2019	Apoptosis induced by GAS2 was dependent on p53, which was increased by etoposide addition.	Etoposide	71-80	P53	Homo sapiens	43-46
29193903-3	2018	In this study, seven polymorphisms in genes related to development (FGF8, FGF10, BMP4, SHH, TP53, TP63, and TP73) were analyzed in people with thalidomide embryopathy (TE) and compared to people without malformations.	Thalidomide	143-154	P53	Homo sapiens	92-96
30951608-11	2019	CONCLUSION: In general, in the current study, the antitumor effects of ZnO-NPs were confirmed by the enhancement of P53 and Bax genes expression profile, which are indicated the apoptotic induction in HUH7 cell line.	Zinc Oxide	71-74	P53	Homo sapiens	116-119
31396480-5	2019	EI24 (etoposide-induced gene 2.4 kb; PIG8, p53-induced gene 8) acts as a tumor suppressor, inhibiting cell growth and inducing apoptosis in breast, cervical, and prostate cancer cells.	Etoposide	6-15	P53	Homo sapiens	43-46
30921731-3	2019	Here, we describe the design, via assembly of a p53-activating peptide termed PMI, functionalized PEG and fluorescent lanthanide oxyfluoride nanocrystals, of a novel nanotheranostic shaped in flexible rods.	fluorine monoxide	129-140	P53	Homo sapiens	48-51
29545424-4	2018	On the basis of these findings, the patient was diagnosed with chronic myelogenous leukaemia (CML) in chronic phase with a p53 mutation and treated with hydroxyurea, dasatinib and nilotinib.	Hydroxyurea	153-164	P53	Homo sapiens	123-126
31097220-1	2019	Etoposide-induced 2.4 kb transcript (EI24, also known as PIG8) is a p53 target gene involved in cell growth suppression and apoptosis and known to be frequently altered in human cancers.	Etoposide	0-9	P53	Homo sapiens	68-71
29202419-8	2018	Moreover, the higher accumulation of DNA damage response proteins (gammaH2AX, pATM, p-p53), suggested that exposure to ultrafine PM induces DNA damage and triggers phosphatidylinositol 3 kinase mediated response pathway.	ultrafine pm	119-131	P53	Homo sapiens	86-89
30958996-0	2019	Quercetin enhances the antitumor activity of trichostatin A through up-regulation of p300 protein expression in p53 null cancer cells.	trichostatin A	45-59	P53	Homo sapiens	112-115
31134974-0	2019	Dual-channel surface plasmon resonance monitoring of intracellular levels of the p53-MDM2 complex and caspase-3 induced by MDM2 antagonist Nutlin-3.	nutlin 3	139-147	P53	Homo sapiens	81-84
30614034-0	2019	Signaling Crosstalk of FHIT, p53, and p38 in etoposide-induced apoptosis in MCF-7 cells.	Etoposide	45-54	P53	Homo sapiens	29-32
30614034-4	2019	The time course study showed that the expression of FHIT, p53, and p38MAPK started after 1 hour following etoposide treatment.	Etoposide	106-115	P53	Homo sapiens	58-61
30614034-8	2019	Thus, activation of p38 upon etoposide treatment leads to increase in FHIT and p53 expression.	Etoposide	29-38	P53	Homo sapiens	79-82
28776671-13	2018	All the data suggested that beta-asarone could reduce the cell proliferation and promote autophagy possible via the P53 pathway in U251 cells.	asarone	28-40	P53	Homo sapiens	116-119
30614034-9	2019	In p53 knockdown MCF-7, the FHIT induction was hampered but p38 activation was induced in lower doses of etoposide.	Etoposide	105-114	P53	Homo sapiens	3-6
30478995-0	2019	CtIP promotes G2/M arrest in etoposide-treated HCT116 cells in a p53-independent manner.	Etoposide	29-38	P53	Homo sapiens	65-68
30614034-11	2019	Our data demonstrated that the exposure of MCF-7 cells to etoposide increases apoptosis through a mechanism involving the activation of the p38-FHIT-p53 pathway.	Etoposide	58-67	P53	Homo sapiens	149-152
29707344-7	2018	In the P53 (+) group, the rate of patients with PD-L1 (+) in TCs was significantly higher than in the P53 (-) group (85.3% vs. 45.5%, P=0.001).	9-ethyl-N-(3,4,5-trimethoxyphenyl)carbazole-3-sulfonamide	61-64	P53	Homo sapiens	7-10
31082419-0	2019	JNK activation-mediated nuclear SIRT1 protein suppression contributes to silica nanoparticle-induced pulmonary damage via p53 acetylation and cytoplasmic localisation.	Silicon Dioxide	73-79	P53	Homo sapiens	122-125
28804127-4	2018	Intriguingly, all T-PLL samples were sensitive to the cyclin-dependent kinase inhibitor SNS-032, which overcame stromal-cell-mediated protection and elicited robust p53-activation and apoptosis.	N-(5-(((5-(1,1-dimethylethyl)-2-oxazolyl)methyl)thio)-2-thiazolyl)-4-piperidinecarboxamide	88-95	P53	Homo sapiens	165-168
30520099-7	2019	The effects of miR-590-3p upregulation on the acetylation of p53 as well as cell viability and apoptosis were assessed by Western blot analysis, WST-1 assay, and flow cytometry, respectively.	mir-590-3p	15-25	P53	Homo sapiens	61-64
30900772-8	2019	Blood or bone marrow samples from typical CK/MK AML patients showed defective p53 signaling upon induction by etoposide.	Etoposide	110-119	P53	Homo sapiens	78-81
30548678-6	2019	SIRT1 inhibitor (nicotinamide) decreased SIRT1, reduced the effects of miRNA-141 on nerve cell apoptosis in vitro model of epilepsy through SIRT1/p53.	mirna-141	71-80	P53	Homo sapiens	146-149
30802707-0	2019	Design and synthesis of new substituted spirooxindoles as potential inhibitors of the MDM2-p53 interaction.	spirooxindoles	40-54	P53	Homo sapiens	91-94
29463243-0	2018	Anacardic acid inhibits pancreatic cancer cell growth, and potentiates chemotherapeutic effect by Chmp1A - ATM - p53 signaling pathway.	anacardic acid	0-14	P53	Homo sapiens	113-116
29463243-12	2018	Mechanistically, Anacardic acid exerted its anticancer activity via the activation of Chmp1A, ATM, and p53.	anacardic acid	17-31	P53	Homo sapiens	103-106
30946933-4	2019	TP53 mutations and ERBB2 amplification were more frequent in SDCXPA than in SDCDN (P = .0007 and P = .01, respectively).	sdcxpa	61-67	P53	Homo sapiens	0-4
29483845-12	2018	A rescue in the expression of both MLL genes was observed in KCL22S, a CML cell line sensitive to IM, after treatment with dasatinib or nilotinib which was associated with a higher rate of apoptosis, an enhanced expression of p21 (CDKN1A) and a concomitant decrease in the expression of CDK2, CDK4 and Cyclin B1 (CCNB1) in comparison to untreated KCL22S control or IM resistant KCL22R cell line, which suggests involvement of p53 regulated pathway.	Dasatinib	123-132	P53	Homo sapiens	426-429
30802707-5	2019	Molecular modeling revealed that the compound 4d binds through hydrophobic-hydrophobic interactions with the essential amino acids (LEU: 57, GLY: 58, ILE: 61, and HIS: 96) in the p53-binding cleft, as a standard p53-MDM2 inhibitor (6SJ).	Amino Acids, Essential	109-130	P53	Homo sapiens	179-182
30802707-5	2019	Molecular modeling revealed that the compound 4d binds through hydrophobic-hydrophobic interactions with the essential amino acids (LEU: 57, GLY: 58, ILE: 61, and HIS: 96) in the p53-binding cleft, as a standard p53-MDM2 inhibitor (6SJ).	Amino Acids, Essential	109-130	P53	Homo sapiens	212-215
30831390-0	2019	Anticancer activity and mechanism of bis-pyrimidine based dimetallic Ru(II)(eta6-p-cymene) complex in human non-small cell lung cancer via p53-dependent pathway.	bis-pyrimidine	37-51	P53	Homo sapiens	139-142
30946933-4	2019	TP53 mutations and ERBB2 amplification were more frequent in SDCXPA than in SDCDN (P = .0007 and P = .01, respectively).	sdcdn	76-81	P53	Homo sapiens	0-4
29135079-3	2018	Western blot assay revealed that the protein expressions of p53, Bax, and CCAAT-enhancer-binding protein homologous protein (CHOP) increased, while the levels of Bcl-2 were reduced following CS extract treatment.	Cesium	191-193	P53	Homo sapiens	60-63
31097096-2	2019	We hypothesized that TP53 mutations could reflect TMB and be associated with ICI benefit.	1,2,4,5-tetramethoxybenzene	50-53	P53	Homo sapiens	21-25
30784913-0	2019	Integrated analysis of the prognostic value of TP53 dependent etoposide-induced gene 24 in non-small cell lung cancer.	Etoposide	62-71	P53	Homo sapiens	47-51
30784913-1	2019	BACKGROUND: Etoposide-induced gene 24 (EI24) is an induction target of TP53-mediated apoptosis in human cancer cells.	Etoposide	12-21	P53	Homo sapiens	71-75
30737644-0	2019	ERbeta modulates genistein"s cisplatin-enhancing activities in breast cancer MDA-MB-231 cells via P53-independent pathway.	Genistein	17-26	P53	Homo sapiens	98-101
30966857-4	2019	Activation of p53 by treatment with either etoposide or the small-molecule MDM2 inhibitor nutlin 3A yields strikingly similar genome-wide binding of p53 and concomitant changes to local chromatin modifications and structure.	Etoposide	43-52	P53	Homo sapiens	14-17
29113888-2	2018	In this work, p53-antibody was immobilized onto a green and biocompatible nanocomposite containing poly l-cysteine (P-Cys) as conductive matrix and graphene quantum dots (GQDs)/gold nanoparticles (GNPs) as dual amplification elements.	p-cys	116-121	P53	Homo sapiens	14-17
29113888-3	2018	Therefore, a novel multilayer film based on P-Cys, GQDs, and GNPs was exploited to develop a highly sensitive immunosensor for detection of p53.	p-cys	44-49	P53	Homo sapiens	140-143
29113888-5	2018	Under optimized condition the calibration curve for p53 concentration was linear up to 0.000197-0.016 pM (by SWV technique) and 0.195-50 pM (by DPV technique) with lower limit of quantification of 0.065 fM.	diperoxovanadate	144-147	P53	Homo sapiens	52-55
30966857-4	2019	Activation of p53 by treatment with either etoposide or the small-molecule MDM2 inhibitor nutlin 3A yields strikingly similar genome-wide binding of p53 and concomitant changes to local chromatin modifications and structure.	Etoposide	43-52	P53	Homo sapiens	149-152
30966857-4	2019	Activation of p53 by treatment with either etoposide or the small-molecule MDM2 inhibitor nutlin 3A yields strikingly similar genome-wide binding of p53 and concomitant changes to local chromatin modifications and structure.	nutlin 3	90-99	P53	Homo sapiens	14-17
31120902-0	2019	The antimalarial drug mefloquine enhances TP53 premature termination codon readthrough by aminoglycoside G418.	Mefloquine	22-32	P53	Homo sapiens	42-46
30966857-4	2019	Activation of p53 by treatment with either etoposide or the small-molecule MDM2 inhibitor nutlin 3A yields strikingly similar genome-wide binding of p53 and concomitant changes to local chromatin modifications and structure.	nutlin 3	90-99	P53	Homo sapiens	149-152
30886346-8	2019	Our results point to a previously unrecognized role of nuclear phosphoinositide signalling in regulating p53 stability and implicate this pathway as a promising therapeutic target in cancer.	Phosphatidylinositols	63-79	P53	Homo sapiens	105-108
29207130-10	2018	Furthermore, treatment or co-treatment with LY294002 (phosphoinositide-3-kinase/Akt inhibitor) or Pifithrin-alpha (p53 inhibitor) with CME resulted in CME-induced G1 arrest which occurred through the p53-independent signaling pathway in hepatocellular carcinoma cells.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	44-52	P53	Homo sapiens	200-203
31120902-7	2019	The two enantiomers composing pharmaceutical mefloquine potentiated readthrough to similar levels in HDQ-P1 cells and also in SW900, NCI-H1688 and HCC1937 cancer cells with different TP53 nonsense mutations.	Mefloquine	45-55	P53	Homo sapiens	183-187
31120902-8	2019	Exposure to G418 and mefloquine increased p53 phosphorylation at Ser15 and P21 transcript levels following DNA damage, indicating p53 produced via readthrough was functional.	Mefloquine	21-31	P53	Homo sapiens	42-45
31120902-8	2019	Exposure to G418 and mefloquine increased p53 phosphorylation at Ser15 and P21 transcript levels following DNA damage, indicating p53 produced via readthrough was functional.	Mefloquine	21-31	P53	Homo sapiens	130-133
31210846-7	2019	In addition, overexpression of BOP1 in human aortic smooth muscle cells (HASMCs) inhibited apoptosis and accumulation of p53 under hypoxic conditions, while knockdown of BOP1 decreased the protein synthesis rate and motility of HASMCs.	hasmcs	73-79	P53	Homo sapiens	121-124
29124793-7	2018	It was demonstrated that oligomerization and stabilization of p53 wild-type conformation results in differential exposure of conformational epitopes PAb1620, PAb240, and DO12 that indicates a reduction in the "unfolded" conformation and increases in the folded conformation coincide with increases in its oligomerization state.	pab240	158-164	P53	Homo sapiens	62-65
31367336-0	2019	Physical binding of the tobacco smoke carcinogen NNK diazonium ion to the human tumor suppressor gene TP53 Exon 5.	diazynium	53-62	P53	Homo sapiens	102-106
31367336-7	2019	We present the first study of the physical interaction of NNK diazonium ion with TP53 (exon 5), a frequently mutated human tumor suppressor gene.	diazynium	62-71	P53	Homo sapiens	81-85
29233643-0	2018	Trichostatin A inhibits deacetylation of histone H3 and p53 by SIRT6.	trichostatin A	0-14	P53	Homo sapiens	56-59
30456590-7	2019	Presence of EGCG (50 and 100 muM) showed significant downregulation of PI3K/Akt/mTOR and AMPK signaling along with the suppression of ROS, iNOS, Cox-2, NF-kappaB, SASP and p53 mediated cell cycle inhibition in preadipocytes.	epigallocatechin gallate	12-16	P53	Homo sapiens	172-175
30608603-3	2019	p53-R249S is the sole hotspot mutation in hepatocellular carcinoma (HCC) that is highly associated with chronic hepatitis B virus (HBV) infection and dietary exposure to aflatoxin B1 (AFB1).	Aflatoxin B1	170-182	P53	Homo sapiens	0-3
30637701-14	2018	Interestingly, nano-formulated tunicamycin is three times more potent in inhibiting the cell cycle progression than the native tunicamycin and is supported by downregulation of the ratio of phospho-p53 to total-p53 as well as phospho-Rb to total Rb.	Tunicamycin	31-42	P53	Homo sapiens	198-201
30637701-14	2018	Interestingly, nano-formulated tunicamycin is three times more potent in inhibiting the cell cycle progression than the native tunicamycin and is supported by downregulation of the ratio of phospho-p53 to total-p53 as well as phospho-Rb to total Rb.	Tunicamycin	31-42	P53	Homo sapiens	211-214
30608603-3	2019	p53-R249S is the sole hotspot mutation in hepatocellular carcinoma (HCC) that is highly associated with chronic hepatitis B virus (HBV) infection and dietary exposure to aflatoxin B1 (AFB1).	Aflatoxin B1	184-188	P53	Homo sapiens	0-3
30684461-0	2019	p53 mediates hydroxyurea resistance in aneuploid cells of colon cancer.	Hydroxyurea	13-24	P53	Homo sapiens	0-3
29030066-0	2018	Etoposide induced NMI promotes cell apoptosis by activating the ARF-p53 signaling pathway in lung carcinoma.	Etoposide	0-9	P53	Homo sapiens	68-71
29030066-4	2018	Furthermore, etoposide treatment up-regulates the expression of NMI and ARF, enhances the interaction of NMI and ARF and promotes the p53 transcriptional activities.	Etoposide	13-22	P53	Homo sapiens	134-137
30628640-10	2019	The EC cells treated with CP-31398 or siRNA against MDM2 exhibited an increased apoptosis and a suppressed migration and invasion, corresponding to an increased expression of p53, p21, Bad, Bax, Cyt-c and caspase-3, as well as to a decreased expression of Bcl-2, Cox-2, MMP-2 and MMP-9.	CP 31398	26-34	P53	Homo sapiens	175-178
29030066-6	2018	These investigations demonstrated etoposide-induced NMI can suppress tumor proliferation and promote cell apoptosis by activating the ARF-p53 signaling pathway in lung carcinoma.	Etoposide	34-43	P53	Homo sapiens	138-141
30198376-8	2018	In addition, our results revealed that the apoptosis in response to DNA replication stress induced by CFS-1686, a catalytic inhibitor of topoisomerase, is p53-independent.	CFS-1686	102-110	P53	Homo sapiens	155-158
30550954-5	2019	Early results from our group indicated that 4-nerolidylcatechol (4-NC), a catechol compound extracted from Pothomorphe umbellata, induces DNA damage, ROS production, increased p53 expression culminating in apoptosis in melanoma but with no data regarding the 4-NC effects in cells resistant to BRAFi or MEKi.	4-nerolidylcatechol	44-63	P53	Homo sapiens	176-179
32982042-3	2018	As a proof of concept, conjugation PSP to a D-peptide activator of tumor suppressor p53 termed DPMI (1492.5 Da) generated hollow spheres ~80 nm in diameter named PSP-DPMI that disintegrated only in the acidic microenvironment of tumor tissues, followed by integrin-mediated cellular uptake of PSP-DPMI monomers.	psp-dpmi	162-170	P53	Homo sapiens	84-87
30778058-4	2019	Mechanistically, miR-135 accumulates specifically in response to glutamine deprivation and requires ROS-dependent activation of mutant p53, which directly promotes miR-135 expression.	Glutamine	65-74	P53	Homo sapiens	135-138
30636605-2	2018	In our previous studies, we demonstrated that p53 directly regulates Bak in mouse JB6 cells and that p53-Bak signaling axis plays an important role in mediating EGCG-induced apoptosis.	epigallocatechin gallate	161-165	P53	Homo sapiens	101-104
30408460-0	2019	A synthetic chalcone derivative, 2-hydroxy-3",5,5"-trimethoxychalcone (DK-139), triggers reactive oxygen species-induced apoptosis independently of p53 in A549 lung cancer cells.	2-hydroxy-3',5,5'-trimethoxychalcone	33-69	P53	Homo sapiens	148-151
29094329-0	2018	Allopurinol protects human glomerular endothelial cells from high glucose-induced reactive oxygen species generation, p53 overexpression and endothelial dysfunction.	Allopurinol	0-11	P53	Homo sapiens	118-121
29094329-8	2018	Allopurinol reduced p53 and p-p53 levels induced by high glucose suggesting an axis of xanthine oxidase-derived ROS, DNA damage, p53 stabilization and endothelial dysfunction that may contribute to the pathogenesis of diabetic nephropathy.	Allopurinol	0-11	P53	Homo sapiens	20-23
29094329-8	2018	Allopurinol reduced p53 and p-p53 levels induced by high glucose suggesting an axis of xanthine oxidase-derived ROS, DNA damage, p53 stabilization and endothelial dysfunction that may contribute to the pathogenesis of diabetic nephropathy.	Allopurinol	0-11	P53	Homo sapiens	30-33
30755813-2	2019	We examined effects of CP-31398 which potentially increased expression of wild-type p53 or converted mutated p53 to the wild-type.	CP 31398	23-31	P53	Homo sapiens	84-87
29094329-8	2018	Allopurinol reduced p53 and p-p53 levels induced by high glucose suggesting an axis of xanthine oxidase-derived ROS, DNA damage, p53 stabilization and endothelial dysfunction that may contribute to the pathogenesis of diabetic nephropathy.	Allopurinol	0-11	P53	Homo sapiens	30-33
29094329-9	2018	CONCLUSIONS: Allopurinol protects GEnC from high glucose-induced ROS generation, p53 overexpression and endothelial dysfunction.	Allopurinol	13-24	P53	Homo sapiens	81-84
30755813-2	2019	We examined effects of CP-31398 which potentially increased expression of wild-type p53 or converted mutated p53 to the wild-type.	CP 31398	23-31	P53	Homo sapiens	109-112
30755813-6	2019	CP-31398 influenced expression of p53 and the downstream molecules in a cell-dependent manner, but constantly increased p21 expression at the transcriptional level with decreased YY1 expression.	CP 31398	0-8	P53	Homo sapiens	34-37
29295500-5	2017	Q-RT-PCR assays showed that TP73 was expressed in 57% of TP53wt HMCLs (4 out of 7) and 11% of TP53 abnormal (TP53abn) HMCLs (2 out of 18) (p = 0.0463).	hmcls	118-123	P53	Homo sapiens	94-98
29295500-5	2017	Q-RT-PCR assays showed that TP73 was expressed in 57% of TP53wt HMCLs (4 out of 7) and 11% of TP53 abnormal (TP53abn) HMCLs (2 out of 18) (p = 0.0463).	hmcls	118-123	P53	Homo sapiens	94-98
30289575-7	2018	TP53 mutations were frequently identified in plasma and tumor samples, with most such mutations also having been detected before afatinib treatment.	Afatinib	129-137	P53	Homo sapiens	0-4
29225033-2	2017	Here we report a unique mechanism underlying the GOF of p53-R249S (p53-RS), a p53 mutant frequently detected in human hepatocellular carcinoma (HCC) that is highly related to hepatitis B infection and aflatoxin B1.	Aflatoxin B1	201-213	P53	Homo sapiens	56-59
29225033-2	2017	Here we report a unique mechanism underlying the GOF of p53-R249S (p53-RS), a p53 mutant frequently detected in human hepatocellular carcinoma (HCC) that is highly related to hepatitis B infection and aflatoxin B1.	Aflatoxin B1	201-213	P53	Homo sapiens	67-70
29225033-2	2017	Here we report a unique mechanism underlying the GOF of p53-R249S (p53-RS), a p53 mutant frequently detected in human hepatocellular carcinoma (HCC) that is highly related to hepatitis B infection and aflatoxin B1.	Aflatoxin B1	201-213	P53	Homo sapiens	67-70
30091208-8	2018	This implied that the deactivated Akt caused by MC/DMC was p53-dependent.	Mitomycin	48-50	P53	Homo sapiens	59-62
30091208-13	2018	In summary, MC/DMC regulate Akt activation in a p53-dependent manner.	Mitomycin	12-14	P53	Homo sapiens	48-51
30809370-4	2019	Here we report a novel peptide stapling strategy based on the dithiocarbamate chemistry linking the side chains of residues Lys(i) and Cys(i + 4) of unprotected peptides and apply it to a series of dodecameric peptide antagonists of the p53-inhibitory oncogenic proteins MDM2 and MDMX.	Dithiocarbamate	62-77	P53	Homo sapiens	237-240
28886428-0	2017	Tris (2-chloroethyl) phosphate induces senescence-like phenotype of hepatocytes via the p21Waf1/Cip1-Rb pathway in a p53-independent manner.	tris(chloroethyl)phosphate	0-30	P53	Homo sapiens	117-120
28886428-7	2017	The findings demonstrated that TCEP induced senescence-like growth arrest via the p21Waf1/Cip1-Rb pathway in a p53-independent manner, without activation of the IL-6/IL6R, p38MAPK-NF-kappaB pathways in hepatocytes.	tris(chloroethyl)phosphate	31-35	P53	Homo sapiens	111-114
28774804-2	2017	In this work, biotin conjugated p53-antibody (anti-p53) was immobilized onto a green and biocompatible nanocomposite containing poly l-cysteine (P-Cys) as conductive matrix and 3D gold nanoparticles (GNPs) as signal amplification element.	p-cys	145-150	P53	Homo sapiens	32-35
28774804-2	2017	In this work, biotin conjugated p53-antibody (anti-p53) was immobilized onto a green and biocompatible nanocomposite containing poly l-cysteine (P-Cys) as conductive matrix and 3D gold nanoparticles (GNPs) as signal amplification element.	p-cys	145-150	P53	Homo sapiens	51-54
30122553-0	2018	A Role for p53 in the Adaptation to Glutamine Starvation through the Expression of SLC1A3.	Glutamine	36-45	P53	Homo sapiens	11-14
28774804-3	2017	Therefore, a novel nanocomposite film based on P-Cys and GNPs was exploited to develop a highly sensitive immunosensor for detection of p53 protein.	p-cys	47-52	P53	Homo sapiens	136-139
28774804-8	2017	Under optimized condition the calibration curve for p53 concentration by SWV and DPV was linear in 0.0369-50pM and 0.018-2.5pM with lower limit of quantification of 48fM and 18fM, respectively.	diperoxovanadate	81-84	P53	Homo sapiens	52-55
30122553-3	2018	We show here that p53 promotes the expression of SLC1A3, an aspartate/glutamate transporter that allows the utilization of aspartate to support cells in the absence of extracellular glutamine.	Glutamine	182-191	P53	Homo sapiens	18-21
31966544-9	2017	UDCA also increased the expression of LC3B and p53 in vitro (Student"s t-test, P&lt;0.05).	2-methyl-3-(2-((4-nitrooxybutyloxy)carbonyl)vinyl)phenyl ursodeoxycholic acid ester	0-4	P53	Homo sapiens	47-50
28935563-4	2017	Further study indicated that oridonin induced G2/M phase arrest in OSCC cells, which was associated with the downregulation of proteins related to G2/M transition including cdc25C, cdc2 and cyclin B1, as well as the upregulation of p53 and phosphorylated-cdc2.	oridonin	29-37	P53	Homo sapiens	232-235
30132514-0	2018	Anticancer effects of oridonin on colon cancer are mediated via BMP7/p38 MAPK/p53 signaling.	oridonin	22-30	P53	Homo sapiens	78-81
30166403-0	2018	Role of P53-Senescence Induction in Suppression of LNCaP Prostate Cancer Growth by Cardiotonic Compound Bufalin.	bufalin	104-111	P53	Homo sapiens	8-11
28790111-9	2017	On the other hand, we did not find a significant systemic toxicity in mice treated with amiloride.Conclusions: Overall, our results demonstrate the antimyeloma activity of amiloride and provide a mechanistic rationale for its use as an alternative treatment option for relapsed multiple myeloma patients, especially those with 17p deletion or TP53 mutations that are resistant to current therapies.	Amiloride	172-181	P53	Homo sapiens	343-347
30166403-3	2018	In prostate cancer cell models, P53-dependent and independent caspase-mediated apoptosis and androgen receptor (AR) antagonism have been described for bufalin at micromolar concentrations.	bufalin	151-158	P53	Homo sapiens	32-35
30166403-5	2018	Bufalin exposure induced protein abundance of P53 (not mRNA) and P21CIP1 (CDKN1A), G2 arrest, and increased senescence-like phenotype (SA-galactosidase).	bufalin	0-7	P53	Homo sapiens	46-49
30166403-6	2018	Small RNAi knocking down of P53 attenuated bufalin-induced senescence, whereas knocking down of P21CIP1 exacerbated bufalin-induced caspase-mediated apoptosis.	bufalin	43-50	P53	Homo sapiens	28-31
30166403-9	2018	Our data suggest potential applications of bufalin in therapy of prostate cancer in patients or chemo-interception of prostate precancerous lesions, engaging a selective activation of P53 senescence.	bufalin	43-50	P53	Homo sapiens	184-187
30057298-4	2018	However, the Az-triphenylphosphonium conjugate, Az-TPP-O3, localizes mainly to mitochondria of cancer cells where it inhibits the mortalin-p53 interaction and induces mitochondrial outer membrane permeabilization, consequently leading to mitochondria-mediated apoptosis.	az-tpp-o3	48-57	P53	Homo sapiens	139-142
29132471-9	2017	Compared with the control group, Jurkat cells treated with 5 mumol/L oridonin had reduced expression of Brg1 and C-myc but elevated expression of P53.	oridonin	69-77	P53	Homo sapiens	146-149
30235848-0	2018	Chalcone Derivatives 4"-Amino-1-Naphthyl-Chalcone (D14) and 4"-Amino-4-Methyl-1-Naphthyl-Chalcone (D15) Suppress Migration and Invasion of Osteosarcoma Cells Mediated by p53 Regulating EMT-Related Genes.	Chalcone	0-8	P53	Homo sapiens	170-173
28754818-8	2017	Nutlin-3a-targeted p53 signaling induced cytotoxicity preclinically, along with new compounds such as ibrutinib, PrimaMet, or CP31398 that bypass p53 pathway in WM, paving the path for future treatment-tailored options.Conclusions: Our results highlight the clinical significance of detection of TP53 alteration in WM to determine the prognosis of WM and guide the treatment choice.	CP 31398	126-133	P53	Homo sapiens	146-149
30209161-0	2019	TP53 Outperforms Other Androgen Receptor Biomarkers to Predict Abiraterone or Enzalutamide Outcome in Metastatic Castration-Resistant Prostate Cancer.	enzalutamide	78-90	P53	Homo sapiens	0-4
29852310-0	2018	Pyran-2-one derivatives from Croton crassifolius as potent apoptosis inducers in HepG2 cells via p53-mediated Ras/Raf/ERK pathway.	Pyrones	0-11	P53	Homo sapiens	97-100
30602570-2	2019	p53 reactivation with induction of massive apoptosis-1 (PRIMA-1) and its primary active metabolite, 2-methylene-3-quinuclidinone (MQ), can restore unfolded p53 mutants to a native conformation that induces apoptosis and activates several p53 target genes.	2-methylenequinuclidin-3-one	100-128	P53	Homo sapiens	0-3
30602570-2	2019	p53 reactivation with induction of massive apoptosis-1 (PRIMA-1) and its primary active metabolite, 2-methylene-3-quinuclidinone (MQ), can restore unfolded p53 mutants to a native conformation that induces apoptosis and activates several p53 target genes.	2-methylenequinuclidin-3-one	100-128	P53	Homo sapiens	156-159
30602570-2	2019	p53 reactivation with induction of massive apoptosis-1 (PRIMA-1) and its primary active metabolite, 2-methylene-3-quinuclidinone (MQ), can restore unfolded p53 mutants to a native conformation that induces apoptosis and activates several p53 target genes.	2-methylenequinuclidin-3-one	100-128	P53	Homo sapiens	156-159
27861885-7	2017	TP53-depeleted LNCaP and NCI-H460 cells using shRNA targeting human TP53 were more sensitive to cell death by treatment of genistein.	Genistein	123-132	P53	Homo sapiens	0-4
27861885-7	2017	TP53-depeleted LNCaP and NCI-H460 cells using shRNA targeting human TP53 were more sensitive to cell death by treatment of genistein.	Genistein	123-132	P53	Homo sapiens	68-72
27861885-9	2017	These data suggest that genistein may be a promising anticancer drug candidate due to its inhibitory activity against Plk1 as well as EGFR and effectiveness toward cancer cells, especially those with p53-mutation.	Genistein	24-33	P53	Homo sapiens	200-203
30118500-5	2018	CRM1 is also inhibited by trans-chalcone, resulting in the accumulation of p53 and other tumor suppressor proteins in the nucleus.	Chalcone	26-40	P53	Homo sapiens	75-78
28888100-5	2017	In contrast to their wt counterparts, the p53- or p21-deficient cells treated with SCH900776 and cisplatin or LA-12 enter mitosis and become polyploid, and the senescence phenotype is strongly suppressed.	MK-8776	83-92	P53	Homo sapiens	42-45
29842899-4	2018	To stimulate p53 in synergistic fashion, we exposed A549 lung cancer cells to actinomycin D and nutlin-3a (A + N).	nutlin 3	96-105	P53	Homo sapiens	13-16
28710679-8	2017	Thus, the Carboxy-terminal p53 region was shown to be the target of the isolated phage as well as by its derived Fluorescein isothiocyanate-peptide.	fluorescein isothiocyanate-peptide	113-147	P53	Homo sapiens	27-30
30837643-5	2019	Moreover, CHK1 knockdown or addition of a CHK1 inhibitor such as MK-8776, rabusertib or prexasertib enhances CPX-351-induced apoptosis in multiple TP53-null and TP53-wildtype AML cell lines.	MK-8776	65-72	P53	Homo sapiens	147-151
30837643-5	2019	Moreover, CHK1 knockdown or addition of a CHK1 inhibitor such as MK-8776, rabusertib or prexasertib enhances CPX-351-induced apoptosis in multiple TP53-null and TP53-wildtype AML cell lines.	MK-8776	65-72	P53	Homo sapiens	161-165
29940201-4	2018	EGCG markedly decreased the levels of inflammatory and oxidative stress factors including nuclear factor kappaB (NF-kappaB), tumor necrosis factor-alpha, interleukin-6, reactive oxygen species, malondialdehyde and p53 protein, and markedly increased superoxide dismutases (SOD), glutathione peroxidase and SOD2 protein.	epigallocatechin gallate	0-4	P53	Homo sapiens	214-217
30660931-5	2019	A diazonium modified screen-printed carbon electrode immobilized with a DNA sequence related to the p53 tumour suppressor gene, the most commonly affected gene in human UV-induced skin cancer, was applied as an electrochemical DNA sensor.	diazynium	2-11	P53	Homo sapiens	100-103
29039564-7	2017	Knockdown of TGF-beta1 by LY364947 (10 nM) reduced cell proliferation and migration, induced apoptosis, expression of Bax, caspase-3 and p53 protein and suppressed TGF-beta1 and p-SMAD2 protein expression of NSCLC cells transfected with miR-124 mimics.	Ly-364947	26-34	P53	Homo sapiens	137-140
28928376-5	2017	Subsequent administration of Oligo-Fucoidan to etoposide-treated cells promotes p53 accumulation, p21 expression and significant decreases in ataxia-telangiectasia-mutated (ATM), checkpoint kinase 1 (Chk1) and gamma-H2AX phosphorylation in p53+/+ cells compared with p53-/- cells.	Etoposide	47-56	P53	Homo sapiens	80-83
28928376-5	2017	Subsequent administration of Oligo-Fucoidan to etoposide-treated cells promotes p53 accumulation, p21 expression and significant decreases in ataxia-telangiectasia-mutated (ATM), checkpoint kinase 1 (Chk1) and gamma-H2AX phosphorylation in p53+/+ cells compared with p53-/- cells.	Etoposide	47-56	P53	Homo sapiens	240-243
28928376-5	2017	Subsequent administration of Oligo-Fucoidan to etoposide-treated cells promotes p53 accumulation, p21 expression and significant decreases in ataxia-telangiectasia-mutated (ATM), checkpoint kinase 1 (Chk1) and gamma-H2AX phosphorylation in p53+/+ cells compared with p53-/- cells.	Etoposide	47-56	P53	Homo sapiens	240-243
28928376-6	2017	Similarly, co-administration of Oligo-Fucoidan with etoposide inhibits ATM, Chk1 and gamma-H2AX phosphorylation, particularly in the presence of p53.	Etoposide	52-61	P53	Homo sapiens	145-148
30144069-3	2019	STK31 overexpression significantly activated PDCD5 stabilization and p53-mediated apoptosis in response to etoposide (ET).	Etoposide	107-116	P53	Homo sapiens	69-72
30144069-3	2019	STK31 overexpression significantly activated PDCD5 stabilization and p53-mediated apoptosis in response to etoposide (ET).	Etoposide	118-120	P53	Homo sapiens	69-72
29750510-3	2018	Bioactivated aflatoxin B1 was reacted with a 32 bp exon 7 fragment of the p53 gene using eight microsomal cytochrome (cyt) P450 enzymes from different organs coated on magnetic beads.	Aflatoxin B1	13-25	P53	Homo sapiens	74-77
28919752-7	2017	ZnO NP-treated cells showed upregulation of p53 and LC3, indicating that ZnO NPs are able to upregulate apoptosis and autophagy.	Zinc Oxide	0-3	P53	Homo sapiens	44-47
29750510-5	2018	This is the first demonstration in a cell-free medium that the aflatoxin B1 metabolite selectively causes abasic site formation and strand breaks at codon 249 of the p53 probe, corresponding to the chemical pathway and mutations of p53 in human liver cells and tumors.	Aflatoxin B1	63-75	P53	Homo sapiens	166-169
30229997-5	2019	Further mechanism studies revealed that oridonin led cell cycle arrest in esophageal cancer cells via downregulating cell cycle-related proteins, such as cyclin B1 and CDK2, while upregulating p53 and p21.	oridonin	40-48	P53	Homo sapiens	193-196
29750510-5	2018	This is the first demonstration in a cell-free medium that the aflatoxin B1 metabolite selectively causes abasic site formation and strand breaks at codon 249 of the p53 probe, corresponding to the chemical pathway and mutations of p53 in human liver cells and tumors.	Aflatoxin B1	63-75	P53	Homo sapiens	232-235
28442502-7	2017	Clofarabine, a purine nucleoside analogue that inhibits RRM1, induced growth arrest and apoptosis in p53 wild-type cell lines.	Clofarabine	0-11	P53	Homo sapiens	101-104
29656126-5	2018	Quantitative reverse transcription polymerase chain reaction revealed the positive influence of EGCG on several innate immune-related genes, including IMD, proPO, QM, myosin, Rho, Rab7, p53, TNF-alpha, MAPK, and NOS, and we observed positive influences on three immune parameters, including total hemocyte count and phenoloxidase and superoxide dismutase activities, by EGCG treatment.	epigallocatechin gallate	96-100	P53	Homo sapiens	186-189
28982757-3	2017	1738-1753) identify the p53 family member and p73 isoform TAp73 as a crucial factor causing glutamine addiction in aggressive medulloblastomas.	Glutamine	92-101	P53	Homo sapiens	24-27
29156743-1	2017	All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells.	Vitamin A	75-84	P53	Homo sapiens	174-177
29156743-1	2017	All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to induce p14 expression via promoter hypomethylation to activate the p14-MDM2-p53 pathway, which leads to activation of the p53-dependent apoptotic pathway and subsequent induction of apoptosis in human hepatoma cells.	Vitamin A	75-84	P53	Homo sapiens	220-223
30808373-5	2019	METHODS: We used bioinformatics and molecular docking tools to investigate the structural changes between the wild type and mutant p53 proteins (p53V143A, p53R249S, p53R273H and p53Y220C) and explored the therapeutic potential of Withaferin A and Withanone for restoration of wild type p53 function in cancer cells.	withanone	247-256	P53	Homo sapiens	131-134
30808373-12	2019	Using human cell lines containing specific p53 mutant proteins, we demonstrated that Withaferin A, Withanone and the extract rich in these withanolides caused restoration of wild type p53 function in mutant p53Y220C cells.	withanone	99-108	P53	Homo sapiens	43-46
29658571-8	2018	According to GO and KEGG analyses, the co-expressed genes may be involved in "dGTP metabolic processes", "network-forming collagen trimers", "centromeric DNA binding" and "the p53 signaling pathway".	deoxyguanosine triphosphate	78-82	P53	Homo sapiens	176-179
30808373-12	2019	Using human cell lines containing specific p53 mutant proteins, we demonstrated that Withaferin A, Withanone and the extract rich in these withanolides caused restoration of wild type p53 function in mutant p53Y220C cells.	withanone	99-108	P53	Homo sapiens	184-187
28798402-3	2017	In this study, we show that treatment of various p53-defective bortezomib-resistant solid tumor cells with bortezomib plus nutlin-3 induces paraptosis, which is a cell death mode accompanied by dilation of the endoplasmic reticulum (ER) and mitochondria.	nutlin 3	123-131	P53	Homo sapiens	49-52
29860266-9	2018	The apoptosis-related protein expression levels of p-p53, Bad, cleaved caspase-3, cleaved PARP and p-JNK were increased in quinalizarin-treated cells, while protein expression levels Bcl-2, p-Akt, p-ERK, and p-STAT3 were decreased.	1,2,5,8-tetrahydroxy anthraquinone	123-135	P53	Homo sapiens	53-56
29029480-7	2017	In this study, we demonstrate that the p53-activating small molecule CP-31398 (CP) effectively inhibits the growth of MM cell lines and primary MM isolates from patients.	CP 31398	69-77	P53	Homo sapiens	39-42
30863051-0	2019	A chemoenzymatically synthesized cholesterol-g-poly(amine-co-ester)-mediated p53 gene delivery for achieving antitumor efficacy in prostate cancer.	poly(amine-co-ester)	47-67	P53	Homo sapiens	77-80
29508061-4	2018	In the presence of elevated levels of H2S and thiosulfate, the sulfhydryl groups of p53 protein as well as Bcl-2 protein could be modified via HBITC-induced S-sulfuration or by oxidative stress.	Thiosulfates	46-57	P53	Homo sapiens	84-87
30325501-5	2019	RESULTS: The dose response with mifepristone treatment suggested an optimal effect with 10 mum mifepristone, exhibiting >90% viability and significantly reducing growth signaling markers (TP53 and MAPK3).	Mifepristone	32-44	P53	Homo sapiens	188-192
30325501-5	2019	RESULTS: The dose response with mifepristone treatment suggested an optimal effect with 10 mum mifepristone, exhibiting >90% viability and significantly reducing growth signaling markers (TP53 and MAPK3).	Mifepristone	95-107	P53	Homo sapiens	188-192
28720827-9	2017	In the SH-SY5Y human cells, tunicamycin (TM), a PERK activator, promoted transcription of hsp27; and necrosis induced by glutamate could be rescued by TM, associated with reduced p53 accumulation.	Tunicamycin	28-39	P53	Homo sapiens	179-182
28247504-8	2017	Therefore, EGCG was found to promote greater cytotoxicity to BEAS-2B co-treated with BaP and BEAS-2BBaP upon gefitinib co-treatment through regulating metabolism enzymes and signaling pathways involving EGFR and p53.	epigallocatechin gallate	11-15	P53	Homo sapiens	212-215
30325501-6	2019	Furthermore, combined treatment with progesterone plus mifepristone (PG+MIFE) gave an enhanced anti-proliferative effect in comparison with hydrocortisone plus mifepristone (HC+MIFE) by significantly reducing markers of proliferation (BrdU+ and Ki67 expression) and tumor suppressors (PTEN, TP53), and increasing the percentage of pro-apoptotic cells.	Mifepristone	55-67	P53	Homo sapiens	291-295
29030986-3	2018	Using a cell-based screening method with a p53-responsive luciferase-reporter assay system involving benzoxazole derivatives, we found that AU14022 administration significantly increased p53 transcriptional activity in a concentration-dependent manner.	au14022	140-147	P53	Homo sapiens	43-46
28245170-10	2017	CFEZO treatments induced upregulation of p53 and p21 expression and downregulation of cyclin D1 and cyclin-dependent kinase-4 expression, which were accompanied by G2/M phase arrest.	cfezo	0-5	P53	Homo sapiens	41-44
29030986-3	2018	Using a cell-based screening method with a p53-responsive luciferase-reporter assay system involving benzoxazole derivatives, we found that AU14022 administration significantly increased p53 transcriptional activity in a concentration-dependent manner.	au14022	140-147	P53	Homo sapiens	187-190
29653431-0	2018	Inhibition of NAMPT sensitizes MOLT4 leukemia cells for etoposide treatment through the SIRT2-p53 pathway.	Etoposide	56-65	P53	Homo sapiens	94-97
28903398-3	2017	In this study, we have identified a panel of cobalt complexes that were able to specifically induce collateral sensitivity in taxol-resistant and p53-deficient cancer cells.	Cobalt	45-51	P53	Homo sapiens	146-149
28318508-6	2017	TBMEHP induced a marked G0/G1 cell cycle arrest and robust cell apoptosis at 1mug/mL by inducing expression of p53, GADD45alpha and cyclin dependent kinase (CDK) inhibitors (p21and p27) while suppressing the expression of cyclin D1, CDK2, CDK6, and Bcl-2.	tbmehp	0-6	P53	Homo sapiens	111-114
30562697-0	2019	The p53 stabilizing agent CP-31398 and multi-kinase inhibitors.	CP 31398	26-34	P53	Homo sapiens	4-7
30562697-3	2019	In the current study, the p53 protein reactivator CP-31398 was tested against a panel of kinases on the assumption that it was structurally similar to other active inhibitors.	CP 31398	50-58	P53	Homo sapiens	26-29
29653431-7	2018	After combining etoposide and FK866 treatment SIRTUIN2 was further decreased and accumulation and acetylation of the downstream target p53 was further enhanced in MOLT4 cells.	Etoposide	16-25	P53	Homo sapiens	135-138
28318508-8	2017	TBMEHP decreased mitochondrial membrane potential and increased caspase-3 activity at 1mug/mL, suggesting that activation of p53 and mitochondrial pathway were involved in the cell apoptosis.	tbmehp	0-6	P53	Homo sapiens	125-128
29684847-6	2018	In p53+ group, the expression of Ser20 significantly increased after camptothecin and paclitaxel (p &lt; 0.05).	Camptothecin	69-81	P53	Homo sapiens	3-6
29911263-0	2019	Novel Competitive Chemiluminescence DNA Assay Based on Fe3O4@SiO2@Au-Functionalized Magnetic Nanoparticles for Sensitive Detection of p53 Tumor Suppressor Gene.	Silicon Dioxide	61-65	P53	Homo sapiens	134-137
29875999-0	2018	Transcriptional activation of p21Waf1 contributes to suppression of HR by p53 in response to replication arrest induced by camptothecin.	Camptothecin	123-135	P53	Homo sapiens	74-77
29911263-1	2019	A simple, rapid response time and ultrahigh sensitive chemiluminescence (CL) DNA assay based on Fe3O4@SiO2@Au-functionalized magnetic nanoparticles (Au-MNPs) was developed for detection of p53 tumor suppressor gene.	Silicon Dioxide	102-106	P53	Homo sapiens	189-192
28588714-8	2017	Oxymatrine also induced apoptosis and cell cycle arrest in the cells, in association with the upregulation of caspase-3 and Bax, and the downregulation of survivin, Bcl-2 and p53 expression.	oxymatrine	0-10	P53	Homo sapiens	175-178
28588714-9	2017	Overall, oxymatrine inhibits the proliferation of human bladder cancer cells by inducing apoptosis and cell cycle arrest via mechanisms that involve p53-Bax signaling and the downregulation of survivin expression.	oxymatrine	9-19	P53	Homo sapiens	149-152
29756671-8	2018	Taken together, Wasabi 6-MSITC induced apoptosis of human colorectal cancer cells in p53-independent mitochondrial dysfunction pathway.	wasabi 6-msitc	16-30	P53	Homo sapiens	85-88
28464864-2	2017	We then examined anti-tumor effects of metformin, an agent for type 2 diabetes, and combinatory effects of metformin and nutlin-3a, an inhibitor for ubiquitin-mediated p53 degradation, on human mesothelioma.	nutlin 3	121-130	P53	Homo sapiens	168-171
30442421-1	2019	Methyltrioxorhenium mediated oxidative addition/elimination nucleophilic substitution yielded alkylamino and arylamino cambinol derivatives characterized by anti-proliferative activity against wild-type and p53 mutated MGH-U1 and RT112 bladder cancer cell lines.	methyltrioxorhenium VII	0-19	P53	Homo sapiens	207-210
29735783-8	2018	CONCLUSION: We were able to demonstrate Wnt/ beta-catenin pathway modulation through E-cadherin up-regulation induced by 5aza-dC and TSA treatments, under an activation-pathway background, like CTNNB1 and TP53 mutations.	trichostatin A	133-136	P53	Homo sapiens	205-209
30318011-10	2019	CONCLUSION: The combination treatment of p53-null HL-60 cells with DNA-damaging agent CLB and HDACIs NaBu and TSA triggered additive to synergistic effects on apoptosis and upregulated BCL6 and p21 expression.	trichostatin A	110-113	P53	Homo sapiens	41-44
27982581-6	2017	Etoposide caused rapid accumulation of 53bp1-GFP in DNA damage foci, which was later followed by the concentration dependent nuclear accumulation of p53-GFP and subsequent induction of p21-GFP.	Etoposide	0-9	P53	Homo sapiens	149-152
29700097-7	2018	In addition, PGE2/sulprostone was able to stimulate the expression of Gi1, phosphorylated-extracellular signal-regulated kinases 1/2 (p-ERK1/2) and p53.	sulprostone	18-29	P53	Homo sapiens	148-151
30389549-7	2019	Using primary samples from acute leukemia patients, we show that the combination of Nutlin-3 plus Tanshinone IIA synergistically induces cytotoxicity by activating p53 and inhibiting the AKT/mTOR pathway.	nutlin 3	84-92	P53	Homo sapiens	164-167
29488603-8	2018	Flow cytometry assays indicated that miR-124 transfection attenuated apoptosis resistance of osteosarcoma to tunicamycin, potentially via the downregulation of P53 and Bcl-2 apoptosis regulator expression.	Tunicamycin	109-120	P53	Homo sapiens	160-163
30655814-0	2019	Trichostatin A induces p53-dependent endoplasmic reticulum stress in human colon cancer cells.	trichostatin A	0-14	P53	Homo sapiens	23-26
30655814-8	2019	Furthermore, cell viability and apoptosis were revealed to depend on p53 during TSA treatment.	trichostatin A	80-83	P53	Homo sapiens	69-72
30655814-10	2019	In conclusion, the current study revealed that TSA may induce ER stress via a p53-dependent mechanism in colon cancer cells.	trichostatin A	47-50	P53	Homo sapiens	78-81
30655816-3	2019	In addition, treatment with rhamnetin was able to significantly promote the expression of p53 protein and microRNA (miR-)34a compared with untreated cells.	rhamnetin	28-37	P53	Homo sapiens	90-93
29854627-8	2018	GSPE co-treatment with thalidomide and carboplatin reduced their brain and renal damage, oxidative stress, diminished cytokines, p53, neurotransmitters and biochemical parameters, and inhibited brain and renal cell apoptosis.	Thalidomide	23-34	P53	Homo sapiens	129-132
29508534-5	2018	Biological evaluation showed that the sulfamate is essential for biological activity, and modification of the acyl group on the bicycloketal can improve the inhibitory activity against the p53-Hdm2 interaction.	sulfamic acid	38-47	P53	Homo sapiens	189-192
30319075-11	2019	Moreover, this temperature-induced p53 induction was inhibited on exposure to 40 C in the presence of NF-kappaB pathway inhibitor, pyrrolidinedithiocarbamate (PDTC) or endonuclease-prepared small interfering RNA (esiRNA) targeting p65.	pyrrolidine dithiocarbamic acid	131-157	P53	Homo sapiens	35-38
30319075-11	2019	Moreover, this temperature-induced p53 induction was inhibited on exposure to 40 C in the presence of NF-kappaB pathway inhibitor, pyrrolidinedithiocarbamate (PDTC) or endonuclease-prepared small interfering RNA (esiRNA) targeting p65.	pyrrolidine dithiocarbamic acid	159-163	P53	Homo sapiens	35-38
29619114-0	2018	Omega-3 fatty acid DHA modulates p53, survivin, and microRNA-16-1 expression in KRAS-mutant colorectal cancer stem-like cells.	Fatty Acids, Omega-3	0-18	P53	Homo sapiens	33-36
28004224-10	2017	Moreover, TBBE and TBWE treated MCF-7, HeLa and U87 cells showed upregulation of p53 and p21 proteins.	tbbe	10-14	P53	Homo sapiens	81-84
29367767-4	2018	BBN tumors showed overexpression of markers of basal cancer subtype, and had a high mutation burden with frequent Trp53 (80%), Kmt2d (70%), and Kmt2c (90%) mutations by exome sequencing, similar to human MIBC.	Butylhydroxybutylnitrosamine	0-3	P53	Homo sapiens	114-119
27995497-6	2017	Mechanically, salinomycin-induced cell growth inhibition against human glioma was mainly achieved by induction of G1-phase arrest via triggering reactive oxide species (ROS)-mediated DNA damage, as convinced by the activation of histone, p53, p21 and p27.	salinomycin	14-25	P53	Homo sapiens	238-241
30587121-0	2018	Post-treatment de-phosphorylation of p53 correlates with dasatinib responsiveness in malignant melanoma.	Dasatinib	57-66	P53	Homo sapiens	37-40
30587121-9	2018	We found that treatment-induced de-phosphorylation of p53 correlates with dasatinib responsiveness in malignant melanoma.	Dasatinib	74-83	P53	Homo sapiens	54-57
30587121-10	2018	CONCLUSIONS: Loss of p53 phosphorylation might be an interesting candidate for a kinetic marker of dasatinib responsiveness in melanoma, pending more comprehensive validation in future studies.	Dasatinib	99-108	P53	Homo sapiens	21-24
29228353-8	2018	The increase in cleaved caspase-3 and cleaved mammalian sterile-20-like-1 kinase levels induced by hydroxyurea was also P53-dependent; in contrast, the increase in phosphorylated H2AX, a marker of DNA double-strand breaks, in response to hydroxyurea treatment was only partially P53-dependent.	Hydroxyurea	99-110	P53	Homo sapiens	120-123
30103008-0	2018	Activation of p53 by costunolide blocks glutaminolysis and inhibits proliferation in human colorectal cancer cells.	costunolide	21-32	P53	Homo sapiens	14-17
30103008-10	2018	Finally, costunolide increased phosphorylation and nuclear translocation of p53 in HCT116 cells.	costunolide	9-20	P53	Homo sapiens	76-79
28195382-3	2017	This study evaluated chemical specificity of the p53 pathway response by manipulating p53 or its upstream kinases and assessing the effect on DNA damage and cellular responses to prototype chemicals: etoposide (ETP, topoisomerase II inhibitor) and methyl methane sulfonate (MMS, alkylating agent).	Etoposide	211-214	P53	Homo sapiens	49-52
29228353-8	2018	The increase in cleaved caspase-3 and cleaved mammalian sterile-20-like-1 kinase levels induced by hydroxyurea was also P53-dependent; in contrast, the increase in phosphorylated H2AX, a marker of DNA double-strand breaks, in response to hydroxyurea treatment was only partially P53-dependent.	Hydroxyurea	99-110	P53	Homo sapiens	279-282
29228353-8	2018	The increase in cleaved caspase-3 and cleaved mammalian sterile-20-like-1 kinase levels induced by hydroxyurea was also P53-dependent; in contrast, the increase in phosphorylated H2AX, a marker of DNA double-strand breaks, in response to hydroxyurea treatment was only partially P53-dependent.	Hydroxyurea	238-249	P53	Homo sapiens	120-123
28196907-7	2017	However, upon genotoxic stress through exposure to etoposide, the deacetylase sirtuin 1 (SIRT1) deacetylated MDM2 at Lys182 and Lys185, thereby promoting self-ubiquitination and less ubiquitination and subsequent degradation of p53, thus increasing p53-dependent apoptosis.	Etoposide	51-60	P53	Homo sapiens	228-231
30103008-11	2018	Both p53 inhibitor pifithrin-alpha and p53 siRNA significantly rescued costunolide suppression of GLS1 promoter activity and expression in HCT116 cells.	costunolide	71-82	P53	Homo sapiens	5-8
29471073-7	2018	Our results indicate that the underlying mechanisms whereby etoposide and ellipticine regulate CYP1A1 expression must be different and may not be linked to p53 activation alone.	Etoposide	60-69	P53	Homo sapiens	156-159
30103008-11	2018	Both p53 inhibitor pifithrin-alpha and p53 siRNA significantly rescued costunolide suppression of GLS1 promoter activity and expression in HCT116 cells.	costunolide	71-82	P53	Homo sapiens	39-42
30103008-12	2018	These data in aggregate suggested that activation of p53 was required for costunolide inhibition of GLS1 resulting in blockade of glutaminolysis and inhibition of proliferation in colorectal cancer cells, which was a novel mechanism underlying the antitumor activity of costunolide against colorectal cancer.	costunolide	74-85	P53	Homo sapiens	53-56
30103008-12	2018	These data in aggregate suggested that activation of p53 was required for costunolide inhibition of GLS1 resulting in blockade of glutaminolysis and inhibition of proliferation in colorectal cancer cells, which was a novel mechanism underlying the antitumor activity of costunolide against colorectal cancer.	costunolide	270-281	P53	Homo sapiens	53-56
28196907-7	2017	However, upon genotoxic stress through exposure to etoposide, the deacetylase sirtuin 1 (SIRT1) deacetylated MDM2 at Lys182 and Lys185, thereby promoting self-ubiquitination and less ubiquitination and subsequent degradation of p53, thus increasing p53-dependent apoptosis.	Etoposide	51-60	P53	Homo sapiens	249-252
28098804-5	2017	The results showed that olaquindox could induce reactive oxygen species (ROS)-mediated DNA damage and S-phase arrest, where increases of GADD45a, cyclin A, Cdk 2, p21 and p53 protein expression, decrease of cyclin D1 and the activation of phosphorylation-c-Jun N-terminal kinases (p-JNK), phosphorylation-p38 (p-p38) and phosphorylation-extracellular signal-regulated kinases (p-ERK) were involved.	olaquindox	24-34	P53	Homo sapiens	171-174
29367107-6	2018	Further, selected active SAL analogs induced characteristics of apoptotic cell death and increased expression of p53.	salinomycin	25-28	P53	Homo sapiens	113-116
28081228-12	2017	In contrast to cisplatin, functional p53-knock-down increased the resistance of MSC to etoposide.	Etoposide	87-96	P53	Homo sapiens	37-40
30520728-3	2018	RNA-Seq analysis of TFEB/TFE3 double-knockout cells exposed to etoposide reveals a profound dysregulation of the DNA damage response, including upstream regulators and downstream p53 targets.	Etoposide	63-72	P53	Homo sapiens	179-182
30091208-2	2018	MC analog, 10-decarbamoyl mitomycin C (DMC), unlike MC, has stronger effects on cancer with p53 mutation.	Mitomycin	0-2	P53	Homo sapiens	92-95
30091208-2	2018	MC analog, 10-decarbamoyl mitomycin C (DMC), unlike MC, has stronger effects on cancer with p53 mutation.	Mitomycin	40-42	P53	Homo sapiens	92-95
27890807-0	2017	Diosmin-induced senescence, apoptosis and autophagy in breast cancer cells of different p53 status and ERK activity.	Diosmin	0-7	P53	Homo sapiens	88-91
30091208-3	2018	We previously demonstrated that MC/DMC could activate p21WAF 1/ CIP 1 in MCF-7 (p53-proficient) and K562 (p53-deficient) cells in a p53-independent mode.	Mitomycin	32-34	P53	Homo sapiens	80-83
29745082-13	2018	Cho/NAA and Cho/Cr in the tumor were positively correlated with p53 in the tumor, but negatively correlated with PTEN in the tumor.	Creatine	16-18	P53	Homo sapiens	64-67
30091208-3	2018	We previously demonstrated that MC/DMC could activate p21WAF 1/ CIP 1 in MCF-7 (p53-proficient) and K562 (p53-deficient) cells in a p53-independent mode.	Mitomycin	32-34	P53	Homo sapiens	106-109
30091208-3	2018	We previously demonstrated that MC/DMC could activate p21WAF 1/ CIP 1 in MCF-7 (p53-proficient) and K562 (p53-deficient) cells in a p53-independent mode.	Mitomycin	32-34	P53	Homo sapiens	106-109
30478303-0	2018	IKKbeta activates p53 to promote cancer cell adaptation to glutamine deprivation.	Glutamine	59-68	P53	Homo sapiens	18-21
30478303-5	2018	Here, we report that IkappaB-kinase beta (IKKbeta) is needed to promote survival and its activation is accompanied by phosphorylation of the metabolic sensor, p53, in response to glutamine deprivation.	Glutamine	179-188	P53	Homo sapiens	159-162
27890807-4	2017	Diosmin caused G2/M cell cycle arrest, elevation in p53, p21 and p27 levels and stress-induced premature senescence when used at lower concentrations (5 and 10muM).	Diosmin	0-7	P53	Homo sapiens	52-55
29164963-0	2017	Amorphous silica nanoparticles induce malignant transformation and tumorigenesis of human lung epithelial cells via P53 signaling.	Silicon Dioxide	10-16	P53	Homo sapiens	116-119
29213352-8	2017	The results revealed that pretreatment of echinacoside ameliorated the skin injury; attenuated oxidative stress, DNA damage, and apoptosis caused by UVB exposure; and normalized the protein levels of ATR, p53, PIAS3, hnRNP K, PARP, and XPA.	echinacoside	42-54	P53	Homo sapiens	205-208
30478303-6	2018	Knockdown of IKKbeta decreases the level of wild-type and mutant p53 phosphorylation and its transcriptional activity, indicating a novel relationship between IKKbeta and p53 in mediating cancer cell survival in response to glutamine withdrawal.	Glutamine	224-233	P53	Homo sapiens	65-68
30478303-6	2018	Knockdown of IKKbeta decreases the level of wild-type and mutant p53 phosphorylation and its transcriptional activity, indicating a novel relationship between IKKbeta and p53 in mediating cancer cell survival in response to glutamine withdrawal.	Glutamine	224-233	P53	Homo sapiens	171-174
29328462-6	2018	We also identified the expression level of SGK1 and the p53 pathway including downstream apoptotic proteins under the stimulation of gamma-radiation and SGK1 inhibitor GSK650394, which presented a series of dynamic fluctuations.	2-cyclopentyl-4-(5-phenyl-1H-pyrrolo(2,3-b)pyridin-3-yl)-benzoic acid	168-177	P53	Homo sapiens	56-59
30478303-7	2018	Phosphopeptide mass spectrometry analysis further reveals that IKKbeta phosphorylates p53 on Ser392 to facilitate its activation upon glutamine deprivation, independent of the NF-kappaB pathway.	Glutamine	134-143	P53	Homo sapiens	86-89
30478303-8	2018	The results of this study offer an insight into the metabolic reprogramming in cancer cells that is dependent on a previously unidentified IKKbeta-p53 signaling axis in response to glutamine depletion.	Glutamine	181-190	P53	Homo sapiens	147-150
30774867-6	2019	A peptide corresponding to the iASPP 764-780 sequence stabilized the NAF-1 cluster, inhibited NAF-1 interaction with iASPP, and inhibited staurosporine-induced apoptosis activation in human breast cancer, as well as in PC-3 prostate cancer cells in which p53 is inactive.	Staurosporine	138-151	P53	Homo sapiens	255-258
27822577-0	2016	Combined bortezomib-based chemotherapy and p53 gene therapy using hollow mesoporous silica nanospheres for p53 mutant non-small cell lung cancer treatment.	Silicon Dioxide	84-90	P53	Homo sapiens	43-46
27822577-0	2016	Combined bortezomib-based chemotherapy and p53 gene therapy using hollow mesoporous silica nanospheres for p53 mutant non-small cell lung cancer treatment.	Silicon Dioxide	84-90	P53	Homo sapiens	107-110
28744014-0	2018	Low-burden TP53 mutations in chronic phase of myeloproliferative neoplasms: association with age, hydroxyurea administration, disease type and JAK2 mutational status.	Hydroxyurea	98-109	P53	Homo sapiens	11-15
27709883-0	2016	A Unique Mdm2-Binding Mode of the 3-Pyrrolin-2-one- and 2-Furanone-Based Antagonists of the p53-Mdm2 Interaction.	butenolide	56-66	P53	Homo sapiens	92-95
27709883-3	2016	Here, we present the syntheses, activities, and crystal structures of two novel classes of Mdm2-p53 inhibitors that are based on the 3-pyrrolin-2-one and 2-furanone scaffolds.	butenolide	154-164	P53	Homo sapiens	96-99
30462771-13	2018	Knockdown of p53 or employing the caspase inhibitor, Boc-D-FMK, reversed the effect of oridonin on cell viability and apoptosis-related protein expression.	oridonin	87-95	P53	Homo sapiens	13-16
30462771-14	2018	The present study demonstrated that oridonin exhibited an anti-tumor effect on GC SNU-216 cells through regulating p53 expression and function.	oridonin	36-44	P53	Homo sapiens	115-118
29207064-0	2018	Quinalizarin exerts an anti-tumour effect on lung cancer A549 cells by modulating the Akt, MAPK, STAT3 and p53 signalling pathways.	1,2,5,8-tetrahydroxy anthraquinone	0-12	P53	Homo sapiens	107-110
30212393-12	2018	The immunolabeling of invasive PDAC and COD for p53 and Smad4 supports the high prevalence of COD observed on hematoxylin and eosin and highlights the utility of p53 and Smad4 immunolabeling in differentiating COD and HG-PanIN.	Eosine Yellowish-(YS)	126-131	P53	Homo sapiens	48-51
27748805-12	2016	Taken together, our data indicate that YH-304 may represent a novel therapeutic option for the treatment of cancer in a p53-independent manner.	yh-304	39-45	P53	Homo sapiens	120-123
29207064-9	2018	Furthermore, quinalizarin activated mitogen-activated protein kinase (MAPK) and p53, and inhibited the protein kinase B and signal transducer and activator of transcription-3 (STAT3) signalling pathways.	1,2,5,8-tetrahydroxy anthraquinone	13-25	P53	Homo sapiens	80-83
28749203-8	2018	R175H p53 expression was rescued by addition of proteasome inhibitor MG132 to CB002, suggesting a role for ubiquitin-mediated degradation of the mutant protein.	CB002	78-83	P53	Homo sapiens	6-9
29282909-6	2016	The expressions of PSA, Cyclin D1, and PCNA were gradually down-regulated while that of P53 up-regulated with the increased concentration of GEN (P&lt;0.05).	Genistein	141-144	P53	Homo sapiens	88-91
29941676-5	2018	In human somatic cells, loss of TP53 thus triggers activation of DHEAS transport proteins and steroid sulfatase, which converts circulating DHEAS into intracellular DHEA, and hexokinase which increases glucose-6-phosphate substrate concentration.	Glucose-6-Phosphate	202-221	P53	Homo sapiens	32-36
28884479-6	2018	Treatment with trichostatin A (TSA), a HDAC1 inhibitor, disrupted the interaction of p53-HDAC1-mSin3a complex with the nucleotides -365~-345 region, and enhanced the Aurora-A promoter activity and gene expression.	trichostatin A	15-29	P53	Homo sapiens	85-88
30405797-6	2018	Combined treatment of Lenvatinib and rAd-p53 markedly inhibited NSCLC cell growth, migration and invasion, and promoted apoptosis compared to either lenvatinib or rAd-p53 alone.	lenvatinib	22-32	P53	Homo sapiens	167-170
30405797-6	2018	Combined treatment of Lenvatinib and rAd-p53 markedly inhibited NSCLC cell growth, migration and invasion, and promoted apoptosis compared to either lenvatinib or rAd-p53 alone.	lenvatinib	149-159	P53	Homo sapiens	41-44
27514406-8	2016	IMPLICATIONS: This study provides a solid rationale for the stratification of lung adenocarcinoma patients according to the functional ERCC1- and mutational TP53 status, where functionally ERCC1-incompetent patients could benefit from sequential cisplatin and etoposide chemotherapy.	Etoposide	260-269	P53	Homo sapiens	157-161
30405797-8	2018	Outcomes indicated that combined treatment of lenvatinib and rAd-p53 markedly inhibited tumor growth compared to lenvatinib and rAd-p53 alone for NSCLC patients.	lenvatinib	113-123	P53	Homo sapiens	65-68
28884479-6	2018	Treatment with trichostatin A (TSA), a HDAC1 inhibitor, disrupted the interaction of p53-HDAC1-mSin3a complex with the nucleotides -365~-345 region, and enhanced the Aurora-A promoter activity and gene expression.	trichostatin A	31-34	P53	Homo sapiens	85-88
27690219-0	2016	MK-8776, a novel chk1 kinase inhibitor, radiosensitizes p53-defective human tumor cells.	MK-8776	0-7	P53	Homo sapiens	56-59
29539615-9	2018	In addition, AG1478 reduced the levels of phosphorylated AKT (p-AKT), ERK, p-ERK, cyclin D1, and brain-derived neurotrophic factor (BDNF), while enhancing p53 levels.	RTKI cpd	13-19	P53	Homo sapiens	155-158
27626308-10	2016	GSK2830371 and the MDM2 inhibitor Nutlin-3a acted synergistically in p53 wild-type cells.	nutlin 3	34-43	P53	Homo sapiens	69-72
30307971-10	2018	Tumor sections showed that 3,5-DMAP down-regulated c-Myc expression but up-regulated p53 and cytochrome c, all of which might result in tumor growth arrest.	3,5-dimethylaminophenol	27-35	P53	Homo sapiens	85-88
30096294-0	2018	PIM2 survival kinase is upregulated in a p53-dependent manner in cells treated with camptothecin or co-treated with actinomycin D and nutlin-3a.	Camptothecin	84-96	P53	Homo sapiens	41-44
30096294-0	2018	PIM2 survival kinase is upregulated in a p53-dependent manner in cells treated with camptothecin or co-treated with actinomycin D and nutlin-3a.	nutlin 3	134-143	P53	Homo sapiens	41-44
27780269-0	2016	Comparative Assessment of Vitamin-B12, Folic Acid and Homocysteine Levels in Relation to p53 Expression in Megaloblastic Anemia.	Vitamin B 12	26-37	P53	Homo sapiens	89-92
29416773-0	2018	Reactivating TP53 signaling by the novel MDM2 inhibitor DS-3032b as a therapeutic option for high-risk neuroblastoma.	DS-3032B	56-64	P53	Homo sapiens	13-17
27782836-6	2016	CONCLUSIONS: Our results elucidated a link between SiO2-induced fibrosis and MCPIP1/p53 signaling-mediated autophagy.	Silicon Dioxide	51-55	P53	Homo sapiens	84-87
30124901-0	2018	Zinc oxide nanoparticles affect the expression of p53, Ras p21 and JNKs: an ex vivo/in vitro exposure study in respiratory disease patients.	Zinc Oxide	0-10	P53	Homo sapiens	50-53
29141234-5	2017	We demonstrated that direct inactivation of p53 by SV40 large T antigen, a short hairpin RNA against Trp53, or genetic ablation of Trp53 in Dgcr8-/- PSCs enables neural differentiation, while activation of p53 by the MDM2 inhibitor nutlin-3a in wild-type ESCs inhibits neural differentiation.	nutlin 3	232-241	P53	Homo sapiens	44-47
29729264-9	2018	Similar to the effects of rapamycin, pretreatment with Dex also decreased the number of senescent tubular cells and weakened the protein expression of senescence-associated markers such as p53, p21, and p16.	Dexmedetomidine	55-58	P53	Homo sapiens	189-192
27582538-8	2016	Applying metabolic inhibitors in the presence and absence of D-glucose and L-glutamine in cell culture experiments resulted in higher glycolytic and mitochondrial activity in TP53 mutant breast cancer cell lines.	Glutamine	75-86	P53	Homo sapiens	175-179
29068287-1	2017	All-trans retinoic acid (ATRA), the most biologically active metabolite of vitamin A, is known to activate p14 expression via promoter hypermethylation to induce p53-dependent apoptosis in human hepatocytes.	Vitamin A	75-84	P53	Homo sapiens	162-165
27498709-6	2016	The H2O2-exposed hMSCs showed cellular senescence with significantly increased protein levels of acetyl-p53 and p21 in comparison with the untreated hMSCs, and these effects were prevented by pre-treatment with EGCG.	epigallocatechin gallate	211-215	P53	Homo sapiens	104-107
27498709-7	2016	By contrast, in Nrf2-knockdown hMSCs, EGCG lost its antioxidant effect, exhibiting high levels of acetyl-p53 and p21 following EGCG pre-treatment and H2O2 exposure.	epigallocatechin gallate	38-42	P53	Homo sapiens	105-108
29842910-0	2018	Activation of the p53 pathway with digiferrol isolated from Rubia philippinensis induces cell cycle arrest, apoptosis, and autophagy in colon cancer cells.	1,4-dihydroxy-2-(hydroxymethyl)anthracene-9,10-dione	35-45	P53	Homo sapiens	18-21
27498709-8	2016	This indicates that Nrf2 and p53/p21 may be involved in the anti-senescent effect of EGCG in hMSCs.	epigallocatechin gallate	85-89	P53	Homo sapiens	29-32
28849080-0	2017	Histone deacetylase inhibitor quisinostat activates caspase signaling and upregulates p53 acetylation to inhibit the proliferation of HepG2 cells.	quisinostat	30-41	P53	Homo sapiens	86-89
29044182-8	2017	In vitro, BBG was required to induce VEGF, p53 and Parkin expression in human umbelical vascular endothelial cells.	bbg	10-13	P53	Homo sapiens	43-46
26294168-0	2016	Anti-cancer activity of trans-chalcone in osteosarcoma: Involvement of Sp1 and p53.	Chalcone	24-38	P53	Homo sapiens	79-82
26294168-5	2016	Building on this knowledge, we evaluated the ability of trans-chalcone to reduce viability, to induce apoptosis, and to alter gene expression of p53 and Sp1 in human osteosarcoma cell lines.	Chalcone	56-70	P53	Homo sapiens	145-148
26294168-7	2016	Further experiments suggest that trans-chalcone affected Sp1 down-regulation at the transcriptional level, whereas trans-chalcone up-regulated p53 expression at the post-translational level.	Chalcone	115-129	P53	Homo sapiens	143-146
29473162-2	2018	Immuno-proteomic screening has identified several tumor-associated autoantibodies (AAb) that may have diagnostic capacity for invasive epithelial ovarian cancer, with AAbs to P53 proteins and cancer-testis antigens (CTAGs) as prominent examples.	p-Aminoazobenzene	167-171	P53	Homo sapiens	175-178
28892622-6	2017	As Au-NPFe2O3NC possess high peroxidase-like activity for the oxidation of TMB in the presence of H2O2 [TMB is a common chromogenic substrate for HRP in enzyme-linked immunosorbent assays (ELISAs)], we envisage that our assay could find a wide range of application in developing ELISA-based sensing approaches in the fields of medicine (i.e., detection of other biomarkers the same as p53 autoantibody), biotechnology, and environmental sciences.	1,2,4,5-tetramethoxybenzene	75-78	P53	Homo sapiens	385-388
29331023-4	2018	We found that PMX 465 could reduce MGMT expression by increasing the binding of wild-type p53 to the MGMT promoter and reducing the binding of Sp1 to the MGMT promoter.	(+)-xylariamide A	14-17	P53	Homo sapiens	90-93
27716272-12	2016	Furthermore, siRNA assays were performed to analyse the role of p21 and p53 on TSA-mediated anti-lymphangiogenic effects.	trichostatin A	79-82	P53	Homo sapiens	72-75
28892622-6	2017	As Au-NPFe2O3NC possess high peroxidase-like activity for the oxidation of TMB in the presence of H2O2 [TMB is a common chromogenic substrate for HRP in enzyme-linked immunosorbent assays (ELISAs)], we envisage that our assay could find a wide range of application in developing ELISA-based sensing approaches in the fields of medicine (i.e., detection of other biomarkers the same as p53 autoantibody), biotechnology, and environmental sciences.	1,2,4,5-tetramethoxybenzene	104-107	P53	Homo sapiens	385-388
29665227-6	2018	Cytotoxicity of SEL24-B489 was similar in TP53-mutant and TP53 wild-type cells.	UNII-9M7X64VTLI	16-26	P53	Homo sapiens	42-46
28757460-4	2017	As a result, olaquindox promoted production of ROS, suppressed the protein expression p21 in p53-independent way and phosphorylated p21.	olaquindox	13-23	P53	Homo sapiens	93-96
29665227-6	2018	Cytotoxicity of SEL24-B489 was similar in TP53-mutant and TP53 wild-type cells.	UNII-9M7X64VTLI	16-26	P53	Homo sapiens	58-62
29665367-2	2018	We report here that the bichalcone analog TSWU-CD4 induces S phase arrest of human cancer cells by inhibiting the formation of cyclin A-phospho (p)-cyclin-dependent kinase 2 (CDK2, threonine [Thr] 39) complexes, independent of mutant p53 expression.	rhuschalcone-1	24-34	P53	Homo sapiens	234-237
27569455-4	2016	Theanine and DTBrC completely suppressed HGF- and EGF+HGF-induced migration with a reduction of p53 tumor suppressor level and enhanced the p53 protein expression in HHC cells.	theanine	0-8	P53	Homo sapiens	96-99
27569455-4	2016	Theanine and DTBrC completely suppressed HGF- and EGF+HGF-induced migration with a reduction of p53 tumor suppressor level and enhanced the p53 protein expression in HHC cells.	theanine	0-8	P53	Homo sapiens	140-143
27267810-0	2016	Harnessing Fluorine-Sulfur Contacts and Multipolar Interactions for the Design of p53 Mutant Y220C Rescue Drugs.	Fluorine	11-19	P53	Homo sapiens	82-85
29394130-3	2018	Wild-type p53 expressing HCT116 colon cancer cells were resistant to apoptosis in response to the MDM2 antagonist Nutlin-3a.	nutlin 3	114-123	P53	Homo sapiens	10-13
28927457-3	2017	Tetracyclines and macrolides via inhibiting p450 enzymes attenuate ATRA degradation, thereby increase p53.	Macrolides	18-28	P53	Homo sapiens	102-105
29754265-7	2018	CS caused cytotoxicity in HCT116 cells through several apoptotic events including activation of the Fas death receptor, FADD, caspase 8, caspase 3, caspase 9, and cleaved PARP, which occurred alongside cell cycle arrest from the up-regulation of p53 and p21.	Cesium	0-2	P53	Homo sapiens	246-249
29754265-8	2018	The results show that CS causes apoptosis via the activation of an extrinsic pathway leading to caspase activation and cell cycle arrest from activated p53.	Cesium	22-24	P53	Homo sapiens	152-155
27467582-10	2016	CP-31398, a p53 rescue compound, suppressed levels of Aha1, Hsp90 ATPase activity, levels of PKM2 and HIF-1alpha, and aromatase expression in LFS stromal cells.	CP 31398	0-8	P53	Homo sapiens	12-15
28927457-4	2017	Benzoyl peroxide and hydrogen peroxide elicit oxidative stress, which upregulates p53.	Benzoyl Peroxide	0-16	P53	Homo sapiens	82-85
28979810-5	2017	It was found that chemotherapy drugs, such as epirubicin (EPB) and mitomycin C (MMC), effectively blocked expression of PcG in p53-wild-type HepG2 cells but not in PLC/PRF5 and Hep3B cells with p53 mutation or deletion.	Mitomycin	67-78	P53	Homo sapiens	127-130
27374097-4	2016	Firstly, multiple assays indicated that celastrol could induce apoptosis of APL cells via p53-activated mitochondrial pathway.	celastrol	40-49	P53	Homo sapiens	90-93
29488156-6	2018	The up-regulation of p53, a tumor-suppressor protein, was elucidated in human lung cancer cells treated with 10-50 microM of TDB.	TDB	125-128	P53	Homo sapiens	21-24
29488156-7	2018	Alteration to down-stream signaling of p53 including activation of pro-apoptosis protein (Bcl-2-associated X protein; Bax), reduction of anti-apoptosis (B cell lymphoma 2; Bcl-2 and myeloid cell leukemia 1; Mcl-1) and suppression on protein kinase B (Akt) survival pathway were notified in TDB-treated lung cancer cells.	TDB	290-293	P53	Homo sapiens	39-42
29684847-5	2018	RESULTS: Cell lines and tumor cells p53+, p53- revealed a significant decrease in cell survival after camptothecin, paclitaxel, cisplatin treatment, compared to the control group (p &lt; 0.01).	Camptothecin	102-114	P53	Homo sapiens	36-39
29684847-5	2018	RESULTS: Cell lines and tumor cells p53+, p53- revealed a significant decrease in cell survival after camptothecin, paclitaxel, cisplatin treatment, compared to the control group (p &lt; 0.01).	Camptothecin	102-114	P53	Homo sapiens	42-45
28979810-5	2017	It was found that chemotherapy drugs, such as epirubicin (EPB) and mitomycin C (MMC), effectively blocked expression of PcG in p53-wild-type HepG2 cells but not in PLC/PRF5 and Hep3B cells with p53 mutation or deletion.	Mitomycin	67-78	P53	Homo sapiens	194-197
29471073-4	2018	We found that etoposide and ellipticine induced CYP1A1 in TP53(+/+) cells but not in TP53(-/-) cells, demonstrating that the mechanism of CYP1A1 induction is p53-dependent; cisplatin had no such effect.	Etoposide	14-23	P53	Homo sapiens	58-62
26844908-4	2016	SiO2@Au nanocomposites served as nanocarriers for co-immobilization of both d-Ab and signal reporters (ATCP/SiO2@Au/p53(15)d-Ab, ATLP/SiO2@Au/p53(392)d-Ab), which greatly amplified the detection signal.	Silicon Dioxide	0-4	P53	Homo sapiens	116-119
29471073-4	2018	We found that etoposide and ellipticine induced CYP1A1 in TP53(+/+) cells but not in TP53(-/-) cells, demonstrating that the mechanism of CYP1A1 induction is p53-dependent; cisplatin had no such effect.	Etoposide	14-23	P53	Homo sapiens	158-161
26844908-4	2016	SiO2@Au nanocomposites served as nanocarriers for co-immobilization of both d-Ab and signal reporters (ATCP/SiO2@Au/p53(15)d-Ab, ATLP/SiO2@Au/p53(392)d-Ab), which greatly amplified the detection signal.	Silicon Dioxide	0-4	P53	Homo sapiens	142-145
28979810-5	2017	It was found that chemotherapy drugs, such as epirubicin (EPB) and mitomycin C (MMC), effectively blocked expression of PcG in p53-wild-type HepG2 cells but not in PLC/PRF5 and Hep3B cells with p53 mutation or deletion.	Mitomycin	80-83	P53	Homo sapiens	127-130
29471073-5	2018	Co-incubation experiments with the drugs and 2.5 muM BaP showed that: (i) etoposide increased CYP1A1 expression in TP53(+/+) cells, and to a lesser extent in TP53(-/-) cells, compared to cells treated with BaP alone; (ii) ellipticine decreased CYP1A1 expression in TP53(+/+) cells in BaP co-incubations; and (iii) cisplatin did not affect BaP-mediated CYP1A1 expression.	Etoposide	74-83	P53	Homo sapiens	115-119
28979810-5	2017	It was found that chemotherapy drugs, such as epirubicin (EPB) and mitomycin C (MMC), effectively blocked expression of PcG in p53-wild-type HepG2 cells but not in PLC/PRF5 and Hep3B cells with p53 mutation or deletion.	Mitomycin	80-83	P53	Homo sapiens	194-197
29024968-9	2017	Quantitative analysis of immunohistochemical staining revealed that human ovarian tissue sections with positive Prussian blue staining had lower levels of proliferating cell nuclear antigen expression, but higher levels of p21, p53, and CDC25C expression than those with negative Prussian blue staining.	prussian	112-120	P53	Homo sapiens	228-231
29595211-0	2018	Correction: A smart pH-responsive nano-carrier as a drug delivery system for the targeted delivery of ursolic acid: suppresses cancer growth and metastasis by modulating P53/MMP-9/PTEN/CD44 mediated multiple signaling pathways.	ursolic acid	102-114	P53	Homo sapiens	170-173
29595211-1	2018	Correction for "A smart pH-responsive nano-carrier as a drug delivery system for the targeted delivery of ursolic acid: suppresses cancer growth and metastasis by modulating P53/MMP-9/PTEN/CD44 mediated multiple signaling pathways" by Kai Jiang et al., Nanoscale, 2017, 9, 9428-9439.	ursolic acid	106-118	P53	Homo sapiens	174-177
27246693-7	2016	Here, we provide evidence that cristacarpin promotes senescence in a p53-independent manner.	cristacarpin	31-43	P53	Homo sapiens	69-72
28879097-2	2017	In the Metabric dataset (n = 2059, cBioPortal), SHARPIN GCN-Increase occurs preferentially or mutual exclusively with mutations in TP53, PIK3CA, and CDH1.	gcn	56-59	P53	Homo sapiens	131-135
27064014-0	2016	Isololiolide, a carotenoid metabolite isolated from the brown alga Cystoseira tamariscifolia, is cytotoxic and able to induce apoptosis in hepatocarcinoma cells through caspase-3 activation, decreased Bcl-2 levels, increased p53 expression and PARP cleavage.	isololiolide	0-12	P53	Homo sapiens	225-228
27064014-11	2016	Moreover, western blot analysis showed that isololiolide altered the expression of proteins that are important in the apoptotic cascade, increasing PARP cleavage and p53 expression while decreasing procaspase-3 and Bcl-2 levels.	isololiolide	44-56	P53	Homo sapiens	166-169
29515122-0	2018	Pan-class I  PI3-kinase inhibitor BKM120 induces MEK1/2-dependent mitotic catastrophe in non-Hodgkin lymphoma leading to apoptosis or polyploidy determined by Bax/Bak and p53.	NVP-BKM120	34-40	P53	Homo sapiens	171-174
29515122-8	2018	Upon re-expression of wt p53 in these p53 mutated cells, BKM120-induced polyploidy is strongly reduced demonstrating that the genetic status of the cells determines the outcome of a BKM120-mediated pathway inhibition.	NVP-BKM120	57-63	P53	Homo sapiens	25-28
29515122-8	2018	Upon re-expression of wt p53 in these p53 mutated cells, BKM120-induced polyploidy is strongly reduced demonstrating that the genetic status of the cells determines the outcome of a BKM120-mediated pathway inhibition.	NVP-BKM120	57-63	P53	Homo sapiens	38-41
29515122-8	2018	Upon re-expression of wt p53 in these p53 mutated cells, BKM120-induced polyploidy is strongly reduced demonstrating that the genetic status of the cells determines the outcome of a BKM120-mediated pathway inhibition.	NVP-BKM120	182-188	P53	Homo sapiens	25-28
29515122-8	2018	Upon re-expression of wt p53 in these p53 mutated cells, BKM120-induced polyploidy is strongly reduced demonstrating that the genetic status of the cells determines the outcome of a BKM120-mediated pathway inhibition.	NVP-BKM120	182-188	P53	Homo sapiens	38-41
27148686-3	2016	Costunolide induced an ROS-dependent increase in p53 abrogated telomerase activity.	costunolide	0-11	P53	Homo sapiens	49-52
28655792-3	2017	In this study, we discovered that C646, a reversible p300 inhibitor, downregulates p53 transcription and selectively protects noncancerous cells from p53-dependent apoptosis.	C646	34-38	P53	Homo sapiens	83-86
29448173-6	2018	We have determined that the CLUV treatment activates p53 and we found an increase of DDB2 and XPC gene expression.	cluv	28-32	P53	Homo sapiens	53-56
28776671-0	2018	beta-asarone inhibited cell growth and promoted autophagy via P53/Bcl-2/Bclin-1 and P53/AMPK/mTOR pathways in Human Glioma U251 cells.	asarone	0-12	P53	Homo sapiens	62-65
28776671-0	2018	beta-asarone inhibited cell growth and promoted autophagy via P53/Bcl-2/Bclin-1 and P53/AMPK/mTOR pathways in Human Glioma U251 cells.	asarone	0-12	P53	Homo sapiens	84-87
26876786-3	2016	Further, SAHA and NaB decrease the phosphorylation, protein and mRNA levels of mutant p53 (mtp53) in TNBC cells.	nab	18-21	P53	Homo sapiens	86-89
26876786-7	2016	The luciferase assay and ChIP analysis reveal that both SAHA and NaB can reduce the binding of transcription factor Yin Yang 1 (YY1) with the -102 to -96 position of human p53 promoter.	nab	65-68	P53	Homo sapiens	172-175
28655792-3	2017	In this study, we discovered that C646, a reversible p300 inhibitor, downregulates p53 transcription and selectively protects noncancerous cells from p53-dependent apoptosis.	C646	34-38	P53	Homo sapiens	150-153
26876786-9	2016	Further, SAHA and NaB can inhibit the association of HDAC8 and YY1, increase acetylation of residues 170-200 of YY1, then decrease its transcription activities, and finally suppress YY1 induced p53 transcription.	nab	18-21	P53	Homo sapiens	194-197
28776671-12	2018	We got the results that beta-asarone changed the cellular morphology, inhibited cell proliferation, and enhanced the expression of P53, LC3-II/I, Beclin-1, AMPK, and pAMPK while inhibiting the expression of P62, Bcl-2, mTOR, and pmTOR.	asarone	24-36	P53	Homo sapiens	131-134
28655792-4	2017	C646 treatment blocked acetylation of specific lysine residues that regulate p53 activity.	C646	0-4	P53	Homo sapiens	77-80
28655792-5	2017	Exploitation of differential p53 genetic backgrounds between human hematopoietic and colorectal cancer cells improved the therapeutic index of doxorubicin with C646 cotreatment.	C646	160-164	P53	Homo sapiens	29-32
28771563-10	2017	In a multivariate analysis hazard ratio of p53 mutation was about 5 and 3.8 for OS and DFS respectively.	aspartyl-phenylalanine	87-90	P53	Homo sapiens	43-46
29541168-0	2018	Etoposide radiosensitizes p53-defective cholangiocarcinoma cell lines independent of their G2 checkpoint efficacies.	Etoposide	0-9	P53	Homo sapiens	26-29
29541168-5	2018	The present study evaluated the radiosensitization potential of etoposide in p53-defective CCA KKU-M055 and KKU-M214 cell lines.	Etoposide	64-73	P53	Homo sapiens	77-80
29541168-6	2018	Treatment with etoposide enhanced the responsiveness of two p53-defective CCA cell lines to radiation independent of G2 checkpoint function.	Etoposide	15-24	P53	Homo sapiens	60-63
29541168-8	2018	These findings indicate that etoposide could be used as a radiation sensitizer for p53-defective tumors, independent of the function of G2 checkpoint.	Etoposide	29-38	P53	Homo sapiens	83-86
26985734-6	2016	The mRNA expression of apoptotic gene p53 and caspase 3 was up-regulated following ZnO nanoparticle exposure, which confirms the occurrence of apoptosis at the transcriptional level.	Zinc Oxide	83-86	P53	Homo sapiens	38-41
27104558-10	2016	Chemical inhibition of p53 by pifithrin-alpha robustly prevented palmitate-induced cell death.	Palmitates	65-74	P53	Homo sapiens	23-26
28609685-8	2017	Moreover, knockdown of TLR4 significantly blocked palmitate-induced ROS generation and VSMC apoptosis accompanied by inhibition of caspase 3, caspase 9, p53 expression and restoration of BCL-2 expression.	Palmitates	50-59	P53	Homo sapiens	153-156
26967735-9	2016	Strikingly the reduced biliary injury towards the oxidative stress inducer DCC was accompanied by enhanced hepatocellular injury and formation of HCCs in Rb and p53 deficient livers.	Dicyclohexylcarbodiimide	75-78	P53	Homo sapiens	161-164
29467390-14	2018	Indeed, p53 accumulates at mitochondria upon etoposide treatment and inhibition of p53 mitochondrial localization using pifithrin-micro inhibits apoptosis of COV434 cells.	Etoposide	45-54	P53	Homo sapiens	8-11
29467390-15	2018	FGF1 also decreases mitochondrial accumulation of p53 induced by etoposide.	Etoposide	65-74	P53	Homo sapiens	50-53
28609685-9	2017	CONCLUSIONS: Our results suggest that palmitate-induced apoptosis depends on the activation of the TLR4/ROS/p53 signaling pathway, and that TLR4 may be a potential therapeutic target for the prevention and treatment of atherosclerosis.	Palmitates	38-47	P53	Homo sapiens	108-111
28571773-6	2017	In addition, DATS enhances TRAIL-induced apoptosis through the downregulation of anti-apoptotic protein (Mcl-1) and the upregulation of DR5 receptors through actions on the ROS- induced-p53.	diallyl trisulfide	13-17	P53	Homo sapiens	186-189
29432478-0	2018	Correction: Apoptosis by [Pt(O,O"-acac)(gamma-acac)(DMS)] requires PKC-delta mediated p53 activation in malignant pleural mesothelioma.	pt(o,o"-acac)	26-39	P53	Homo sapiens	86-89
26988436-10	2016	Further, increases in p53 expression, Bax expression, cytochrome c release, along with reduction of Bcl-2 level and caspase-3 activation were observed after Psorinum 6x treatment, which eventually drove A549 cells towards the mitochondria-mediated caspase-3-dependent pathway.	psorinum 6x	157-168	P53	Homo sapiens	22-25
26988436-12	2016	CONCLUSION: Psorinum 6x triggered apoptosis in A549 cells via both up- and down-regulations of relevant signal proteins, including p53, caspase-3, Bax and Bcl-2.	psorinum 6x	12-23	P53	Homo sapiens	131-134
28159923-4	2017	In this context our investigation documents that Vandetanib in combination with the clinically available PI3K inhibitor GDC-0941 leads to enhanced cytotoxicity against MYC-amplified and SHH-TP53-mutated medulloblastoma.	2-(1H-indazol-4-yl)-6-(4-methanesulfonylpiperazin-1-ylmethyl)-4-morpholin-4-ylthieno(3,2-d)pyrimidine	120-128	P53	Homo sapiens	190-194
26768552-0	2016	The enhancing effect of genistein on apoptosis induced by trichostatin A in lung cancer cells with wild type p53 genes is associated with upregulation of histone acetyltransferase.	Genistein	24-33	P53	Homo sapiens	109-112
26768552-0	2016	The enhancing effect of genistein on apoptosis induced by trichostatin A in lung cancer cells with wild type p53 genes is associated with upregulation of histone acetyltransferase.	trichostatin A	58-72	P53	Homo sapiens	109-112
26768552-5	2016	We found that the enhancing effect of genistein on cell-growth-arrest in ABC-1 cells (p53 mutant) was less than in A549 and H460 cells.	Genistein	38-47	P53	Homo sapiens	86-89
26768552-7	2016	After silencing p53 expression in A549 and H460 cells, the enhancing effect of genistein was diminished.	Genistein	79-88	P53	Homo sapiens	16-19
26768552-10	2016	The inhibitor of acetyltransferase, anacardic acid, diminished the enhancing effect of genistein on all TSA-induced histone/p53 acetylation and apoptosis.	anacardic acid	36-50	P53	Homo sapiens	124-127
26768552-10	2016	The inhibitor of acetyltransferase, anacardic acid, diminished the enhancing effect of genistein on all TSA-induced histone/p53 acetylation and apoptosis.	Genistein	87-96	P53	Homo sapiens	124-127
26768552-10	2016	The inhibitor of acetyltransferase, anacardic acid, diminished the enhancing effect of genistein on all TSA-induced histone/p53 acetylation and apoptosis.	trichostatin A	104-107	P53	Homo sapiens	124-127
26768552-13	2016	Taken together, these results suggest that the enhancing effects of genistein on TSA-induced apoptosis in lung cancer cells were p53-dependent and were associated with histone/non-histone protein acetylation.	Genistein	68-77	P53	Homo sapiens	129-132
26768552-13	2016	Taken together, these results suggest that the enhancing effects of genistein on TSA-induced apoptosis in lung cancer cells were p53-dependent and were associated with histone/non-histone protein acetylation.	trichostatin A	81-84	P53	Homo sapiens	129-132
29096294-0	2018	The size-dependent effects of silica nanoparticles on endothelial cell apoptosis through activating the p53-caspase pathway.	Silicon Dioxide	30-36	P53	Homo sapiens	104-107
29193609-8	2018	Our data collectively suggest that 2-ME treatment inhibits hypoxia/anoxia-induced angiogenesis dependently on ID-1 down-regulation and p53 up-regulation, providing a potential alternative medical treatment for un-ruptured AVM patients.	2-Methoxyestradiol	35-39	P53	Homo sapiens	135-138
29258820-7	2018	But activation of p53 with nutlin-3alpha prevented PA-induced reduction of glucose consumption and suppression of insulin signaling pathways.	Palmitates	51-53	P53	Homo sapiens	18-21
28159923-7	2017	Of note, the combination of Vandetanib, GDC-0941 and Etoposide results in MYC-amplified and SHH-TP53-mutated cell lines in complete loss of cell viability.	2-(1H-indazol-4-yl)-6-(4-methanesulfonylpiperazin-1-ylmethyl)-4-morpholin-4-ylthieno(3,2-d)pyrimidine	40-48	P53	Homo sapiens	96-100
28159923-7	2017	Of note, the combination of Vandetanib, GDC-0941 and Etoposide results in MYC-amplified and SHH-TP53-mutated cell lines in complete loss of cell viability.	Etoposide	53-62	P53	Homo sapiens	96-100
26973857-2	2016	The tumor suppressor, p53 is central for apoptotic response to multiple DNA damaging agents used to treat aggressive B-cell lymphomas, including etoposide.	Etoposide	145-154	P53	Homo sapiens	22-25
28660943-0	2017	A smart pH-responsive nano-carrier as a drug delivery system for the targeted delivery of ursolic acid: suppresses cancer growth and metastasis by modulating P53/MMP-9/PTEN/CD44 mediated multiple signaling pathways.	ursolic acid	90-102	P53	Homo sapiens	158-161
26973857-5	2016	Using B-cell lymphoma cell lines resistant to etoposide induced cell death; we show that p53 is dramatically down regulated and MDMX, a negative regulator of p53, is significantly up regulated.	Etoposide	46-55	P53	Homo sapiens	89-92
29372665-2	2018	Chemoresistant ESC-like embryonal carcinoma PA1 cells treated with etoposide (ETO) were previously found to undergo prolonged G2 arrest with transient p53-dependent upregulation of opposing fate regulators, p21CIP1 (senescence) and OCT4A (self-renewal).	Etoposide	67-76	P53	Homo sapiens	151-154
29372665-2	2018	Chemoresistant ESC-like embryonal carcinoma PA1 cells treated with etoposide (ETO) were previously found to undergo prolonged G2 arrest with transient p53-dependent upregulation of opposing fate regulators, p21CIP1 (senescence) and OCT4A (self-renewal).	Etoposide	78-81	P53	Homo sapiens	151-154
30109812-5	2018	In this study we characterize the biological effects of a novel class of non-genotoxic isatin Schiff and Mannich base derivatives (ISMBDs) that stabilize p53 on the protein level.	isatin schiff	87-100	P53	Homo sapiens	154-157
28660943-7	2017	Mechanistically, UA@M-CS-FA induced cancer cell apoptosis and inhibited migration via cell cycle arrest in the G0/G1 stage, regulating the PARP/Bcl-2/MMP-9/CD44/PTEN/P53.	ursolic acid	17-19	P53	Homo sapiens	166-169
26735173-0	2016	Reactivation of wild-type and mutant p53 by tryptophanolderived oxazoloisoindolinone SLMP53-1, a novel anticancer small-molecule.	oxazoloisoindolinone	64-84	P53	Homo sapiens	37-40
26735173-2	2016	Herein, we report the identification of the enantiopure tryptophanol-derived oxazoloisoindolinone SLMP53-1 as a novel reactivator of wild-type (wt) and mut p53, using a yeast-based screening strategy.	oxazoloisoindolinone	77-97	P53	Homo sapiens	156-159
28704484-0	2017	Apoptosis by [Pt(O,O"-acac)(gamma-acac)(DMS)] requires PKC-delta mediated p53 activation in malignant pleural mesothelioma.	pt(o,o"-acac)	14-27	P53	Homo sapiens	74-77
26735173-8	2016	Collectively, besides the potential use of SLMP53-1 as anticancer drug, the tryptophanol-derived oxazoloisoindolinone scaffold represents a promissing starting point for the development of effective p53-reactivating drugs.	oxazoloisoindolinone	97-117	P53	Homo sapiens	199-202
26625199-4	2016	In HCT116 p53+/+ cells treated with the DNA-damaging agent, etoposide, HBZ reduced p53-mediated activation of p21/CDKN1A and GADD45A expression, which was associated with a delay in G2 phase-arrest.	Etoposide	60-69	P53	Homo sapiens	10-13
29953997-7	2018	The suppression of STAT3 activation by CDDO-me in W4P-LHB-NIH3T3 cells was further confirmed by decreased cyclin D1 protein levels and increased p21 and p53 mRNA synthesis.	bardoxolone methyl	39-46	P53	Homo sapiens	153-156
29039462-3	2017	In the present study, a dithiocarbamate derivative, di-2-pyridylhydrazone dithiocarbamate s-acetic acid (DpdtaA) was prepared to address the issue whether the molecular mechanism behind biological behavior showed by dithiocarbamate was p53 mediated.	Dithiocarbamate	24-39	P53	Homo sapiens	236-239
28247504-3	2017	Co-treatment with 5 microM BaP and 20 microM EGCG in BEAS-2B promoted a significant reduction in cell viability and greater G2/M cell cycle arrest, induction of ROS, and reductions in BaP-induced CYP1A1/CYP1B1/COMT, EGFR, p-Akt (Ser473), p-p53 (Thr55), and survivin mRNA/protein expression, as well as an increase in p-p53 (Ser15).	epigallocatechin gallate	45-49	P53	Homo sapiens	240-243
26625199-4	2016	In HCT116 p53+/+ cells treated with the DNA-damaging agent, etoposide, HBZ reduced p53-mediated activation of p21/CDKN1A and GADD45A expression, which was associated with a delay in G2 phase-arrest.	Etoposide	60-69	P53	Homo sapiens	83-86
28247504-3	2017	Co-treatment with 5 microM BaP and 20 microM EGCG in BEAS-2B promoted a significant reduction in cell viability and greater G2/M cell cycle arrest, induction of ROS, and reductions in BaP-induced CYP1A1/CYP1B1/COMT, EGFR, p-Akt (Ser473), p-p53 (Thr55), and survivin mRNA/protein expression, as well as an increase in p-p53 (Ser15).	epigallocatechin gallate	45-49	P53	Homo sapiens	319-322
28918747-0	2017	Omega-3 Polyunsaturated Fatty Acids Eicosapentaenoic Acid and Docosahexaenoic Acid Enhance Dexamethasone Sensitivity in Multiple Myeloma Cells by the p53/miR-34a/Bcl-2 Axis.	omega-3 polyunsaturated fatty acids	0-35	P53	Homo sapiens	150-153
27039825-7	2016	EpoA and SITA induced higher p53 levels than MET.	Sitagliptin Phosphate	9-13	P53	Homo sapiens	29-32
29152662-5	2017	Oxymatrine treatment also induced apoptosis, induced the activities of caspase-3 and caspase-9, promoted p53 and Bax protein expression, and suppressed cyclin D protein expression in these cells.	oxymatrine	0-10	P53	Homo sapiens	105-108
27530507-11	2017	Teneligliptin improves proliferation rates in human umbilical vein endothelial cells exposed to high glucose, regulating the expression of cell-cycle inhibitors markers (P53, P21 and P27), and reducing proapoptotic genes (BAX and CASP3), while promotes BCL2 expression.	3-(4-(4-(3-methyl-1-phenyl-1H-pyrazol-5-yl)piperazin-1-yl)pyrrolidin-2-ylcarbonyl)thiazolidine	0-13	P53	Homo sapiens	170-173
28526934-8	2017	In both Gln-free medium and Gln-supplemented medium, Pro induced expression of p53 and HIF-1alpha.	Glutamine	8-11	P53	Homo sapiens	79-82
28526934-8	2017	In both Gln-free medium and Gln-supplemented medium, Pro induced expression of p53 and HIF-1alpha.	Glutamine	28-31	P53	Homo sapiens	79-82
29042482-4	2017	The concomitant activation of p53 was coupled to the expression of gene products that regulate cell metabolism, leading to a metabolic reprogramming that was characterized by decreased glycolysis, increased glutamine consumption, and a shift to oxidative phosphorylation.	Glutamine	207-216	P53	Homo sapiens	30-33
26521020-0	2016	Violacein induces apoptosis in human breast cancer cells through up regulation of BAX, p53 and down regulation of MDM2.	violacein	0-9	P53	Homo sapiens	87-90
27859531-7	2017	Rolipram (10 muM) and DC-TA-46 (0.5 muM) produced a decrease of cyclin expression, in particular of cyclin A, as well as an increase in p21, p27 and p53, as evaluated by Western blot analysis.	Rolipram	0-8	P53	Homo sapiens	149-152
26556313-7	2016	Supportively, molecular docking studies revealed considerable homology in the docking mode of G613 and the known Mdm2 inhibitor Nutlin-3, to p53 binding pocket of Mdm2.	nutlin 3	128-136	P53	Homo sapiens	141-144
26555243-0	2015	Novel beta-Carboline/Hydroxamic Acid Hybrids Targeting Both Histone Deacetylase and DNA Display High Anticancer Activity via Regulation of the p53 Signaling Pathway.	norharman	6-20	P53	Homo sapiens	143-146
28627468-0	2017	A novel chalcone derivative, LQFM064, induces breast cancer cells death via p53, p21, KIT and PDGFRA.	Chalcone	8-16	P53	Homo sapiens	76-79
28743509-0	2017	Synthesis and evaluation of modified chalcone based p53 stabilizing agents.	Chalcone	37-45	P53	Homo sapiens	52-55
28743509-7	2017	Further analysis of these compounds revealed that (E)-3-(4-chlorophenyl)-1-phenylprop-2-en-1-one (SSE14105) and (E)-3-(4-methoxyphenyl)-1-phenylprop-2-en-1-one (SSE14106) caused rapid (4 and 8-h post-treatment) accumulation of p53 in HCT116 cells similar to its induction by positive control, Nutlin-3.	4'-methoxychalcone	112-159	P53	Homo sapiens	227-230
27859531-7	2017	Rolipram (10 muM) and DC-TA-46 (0.5 muM) produced a decrease of cyclin expression, in particular of cyclin A, as well as an increase in p21, p27 and p53, as evaluated by Western blot analysis.	7-benzylamino-6-chloro-2-piperazino-4-pyrrolidinopteridine	22-30	P53	Homo sapiens	149-152
28296148-4	2017	Here, we describe the synthesis of the new tryptophanol-derived oxazoloisoindolinone DIMP53-1 and identify its activity as a dual inhibitor of the p53-MDM2/X interactions using a yeast-based assay.	oxazoloisoindolinone	64-84	P53	Homo sapiens	147-150
28927122-10	2017	The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group.	epigallocatechin gallate	29-33	P53	Homo sapiens	18-21
28927122-10	2017	The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group.	epigallocatechin gallate	29-33	P53	Homo sapiens	46-49
28927122-10	2017	The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group.	epigallocatechin gallate	29-33	P53	Homo sapiens	46-49
28927122-10	2017	The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group.	epigallocatechin gallate	117-121	P53	Homo sapiens	18-21
26592508-7	2015	Furthermore, treatment of HCT116 cells with ACBPs (35 mug/mL) for 6-12 h significantly enhanced UV-induced apoptosis, increased the expression of PARP and p53, and decreased the expression of Mcl-1.	acbps	44-49	P53	Homo sapiens	155-158
28320780-0	2017	Thiosemicarbazones Functioning as Zinc Metallochaperones to Reactivate Mutant p53.	Thiosemicarbazones	0-18	P53	Homo sapiens	78-81
26592508-9	2015	CONCLUSION: Administration of ACBPs inhibits human colorectal tumor cell growth and induces apoptosis in vitro and in vivo through modulating the PARP-p53-Mcl-1 signaling pathway.	acbps	30-35	P53	Homo sapiens	151-154
28927122-11	2017	The Bcl-2 expression level in the EGCG-combined si-P53 group was lower than that of the si-P53 group and higher than that of the EGCG group.	epigallocatechin gallate	34-38	P53	Homo sapiens	51-54
28927122-11	2017	The Bcl-2 expression level in the EGCG-combined si-P53 group was lower than that of the si-P53 group and higher than that of the EGCG group.	epigallocatechin gallate	34-38	P53	Homo sapiens	91-94
27915270-2	2017	The objective of the study was to test the potential ovarian cancer chemopreventive effect of the p53 stabilizing compound CP-31398 on hens that spontaneously present the ovarian cancer phenotype.	CP 31398	123-131	P53	Homo sapiens	98-101
28882572-6	2017	In addition to the top candidate p53, we identified several other interesting TFs that modulated gamma-H2AX after BaP and AFB1 treatment.	Aflatoxin B1	122-126	P53	Homo sapiens	33-36
26576741-4	2015	Here, to elucidate the role of p53 in fibrosis induced by silica, both the upstream molecular mechanisms and the functional effects on cell proliferation and migration were investigated.	Silicon Dioxide	58-64	P53	Homo sapiens	31-34
26576741-5	2015	Experiments using primary cultured adult human pulmonary fibroblasts led to the following results: 1) SiO2 treatment resulted in a rapid and sustained increase in p53 and PUMA protein levels; 2) the MAPK and PI3K pathways were involved in the SiO2-induced alteration of p53 and PUMA expression; and 3) RNA interference targeting p53 and PUMA prevented the SiO2-induced increases in fibroblast activation and migration.	Silicon Dioxide	102-106	P53	Homo sapiens	163-166
26576741-5	2015	Experiments using primary cultured adult human pulmonary fibroblasts led to the following results: 1) SiO2 treatment resulted in a rapid and sustained increase in p53 and PUMA protein levels; 2) the MAPK and PI3K pathways were involved in the SiO2-induced alteration of p53 and PUMA expression; and 3) RNA interference targeting p53 and PUMA prevented the SiO2-induced increases in fibroblast activation and migration.	Silicon Dioxide	102-106	P53	Homo sapiens	270-273
26576741-5	2015	Experiments using primary cultured adult human pulmonary fibroblasts led to the following results: 1) SiO2 treatment resulted in a rapid and sustained increase in p53 and PUMA protein levels; 2) the MAPK and PI3K pathways were involved in the SiO2-induced alteration of p53 and PUMA expression; and 3) RNA interference targeting p53 and PUMA prevented the SiO2-induced increases in fibroblast activation and migration.	Silicon Dioxide	102-106	P53	Homo sapiens	270-273
26576741-6	2015	Our study elucidated a link between SiO2-induced p53/PUMA expression in fibroblasts and cell migration, thereby providing novel insight into the potential use of p53/PUMA in the development of novel therapeutic strategies for silicosis treatment.	Silicon Dioxide	36-40	P53	Homo sapiens	49-52
28160167-6	2017	As underlying molecular events, we found that ERK1/2 was de-phosphorylated and that the c-Myc and mutant p53 protein levels were reduced after VPA and, to a lesser extent, after TSA treatment.	trichostatin A	178-181	P53	Homo sapiens	105-108
26576741-6	2015	Our study elucidated a link between SiO2-induced p53/PUMA expression in fibroblasts and cell migration, thereby providing novel insight into the potential use of p53/PUMA in the development of novel therapeutic strategies for silicosis treatment.	Silicon Dioxide	36-40	P53	Homo sapiens	162-165
29048426-6	2017	In both cell lines, the genotoxic drug etoposide induced a classical mitochondrial p53-dependent apoptosis.	Etoposide	39-48	P53	Homo sapiens	83-86
28854261-14	2017	Upregulation of uPA abolished CP-31398-mediated restoration of mutant p53 transcriptional activity in panc-1 CSCs.	CP 31398	30-38	P53	Homo sapiens	70-73
26437226-4	2015	V158411 potentiated the cytotoxicity of gemcitabine, cisplatin, SN38 and camptothecin in a variety of p53 deficient human tumor cell lines in vitro, p53 proficient cells were unaffected.	Camptothecin	73-85	P53	Homo sapiens	102-105
28854272-7	2017	Somatic mutations in TP53, ADAMTS2, CNN2 and multiple genes in the Wnt and PI3K-AKT pathway were observed in post-afatinib tumors of six afatinib-responding and in one non-responding patient.	Afatinib	114-122	P53	Homo sapiens	21-25
28259944-10	2017	Data indicated that ursolic acid nanoparticles, indeed, significantly suppress cervial cancer cell proliferation, invasion and migration compared to the control group, and apoptosis was induced by ursolic acid nanoparticles in cervical cancer cells through activating caspases, p53 and suppressing anti-apoptosis-related signals.	ursolic acid	20-32	P53	Homo sapiens	278-281
28854272-7	2017	Somatic mutations in TP53, ADAMTS2, CNN2 and multiple genes in the Wnt and PI3K-AKT pathway were observed in post-afatinib tumors of six afatinib-responding and in one non-responding patient.	Afatinib	137-145	P53	Homo sapiens	21-25
28819586-0	2017	The cardiac glycoside convallatoxin inhibits the growth of colorectal cancer cells in a p53-independent manner.	convallatoxin	22-35	P53	Homo sapiens	88-91
26819918-2	2015	Clofarabine-induced defect in DNA replication, induces p53 and subsequently P53R2 genes as subunit of RR.	Clofarabine	0-11	P53	Homo sapiens	55-58
26115576-1	2015	Previous studies on the natural product chlorofusin have shown that the full peptide and azaphilone structure are required for inhibition of the interaction between MDM2 and p53.	azaphilone	89-99	P53	Homo sapiens	174-177
26115576-3	2015	From this small library the first ever non-azaphilone containing chlorofusin analog with MDM2/p53 activity was identified.	azaphilone	43-53	P53	Homo sapiens	94-97
26115576-4	2015	Further studies then suggested that the simple structure of the Fmoc-norvaline amino acid that had undergone a click reaction was also able to inhibit MDM2/p53 interaction.	fmoc-norvaline amino acid	64-89	P53	Homo sapiens	156-159
28819586-3	2017	Our data suggest that convallatoxin may be useful in the treatment of cancers that harbor inactivating mutations in the p53 signaling pathway.	convallatoxin	22-35	P53	Homo sapiens	120-123
28259944-10	2017	Data indicated that ursolic acid nanoparticles, indeed, significantly suppress cervial cancer cell proliferation, invasion and migration compared to the control group, and apoptosis was induced by ursolic acid nanoparticles in cervical cancer cells through activating caspases, p53 and suppressing anti-apoptosis-related signals.	ursolic acid	197-209	P53	Homo sapiens	278-281
28113103-7	2017	Analyses of caspase 3 activity, p53 acetylation and SIRT1 protein levels revealed the apoptotic nature of etoposide-evoked cell death and that fisetin and luteolin augmented the etoposide-induced acetylation of p53 and decreased SIRT1 levels.	Etoposide	178-187	P53	Homo sapiens	211-214
28777796-0	2017	Isoalantolactone induces intrinsic apoptosis through p53 signaling pathway in human lung squamous carcinoma cells.	isoalantolactone	0-16	P53	Homo sapiens	53-56
28777796-9	2017	Our results reveal that Isoalantolactone induces intrinsic apoptosis in SK-MES-1 cells through p53 signaling pathway, which suggests that Isoalantolactone could be a potential leading compound for future development of anti-lung cancer drugs.	isoalantolactone	24-40	P53	Homo sapiens	95-98
28777796-9	2017	Our results reveal that Isoalantolactone induces intrinsic apoptosis in SK-MES-1 cells through p53 signaling pathway, which suggests that Isoalantolactone could be a potential leading compound for future development of anti-lung cancer drugs.	isoalantolactone	138-154	P53	Homo sapiens	95-98
26490659-4	2015	This study aimed to evaluate the predictive significance of the serum p53 antibody status in metastatic colorectal cancer (mCRC) patients treated with fluoropyrimidine, oxaliplatin, plus bevacizumab as first-line chemotherapy.	2-fluoropyrimidine	151-167	P53	Homo sapiens	70-73
28361991-5	2017	The anti-cancer agent camptothecin specifically suppressed p53beta induction.	Camptothecin	22-34	P53	Homo sapiens	59-62
26469967-5	2015	to show that genistein, a major component of isoflavone that is known to have anti-tumor activities in a variety of models, induces Bax/p53-independent cell death in HCT116 Bax knockout (KO), HCT116 p53 KO, DU145 Bax KO, or DU145 p53 KO cells that express wild-type (WT) Bak.	Genistein	13-22	P53	Homo sapiens	136-139
26469967-5	2015	to show that genistein, a major component of isoflavone that is known to have anti-tumor activities in a variety of models, induces Bax/p53-independent cell death in HCT116 Bax knockout (KO), HCT116 p53 KO, DU145 Bax KO, or DU145 p53 KO cells that express wild-type (WT) Bak.	Genistein	13-22	P53	Homo sapiens	199-202
26469967-5	2015	to show that genistein, a major component of isoflavone that is known to have anti-tumor activities in a variety of models, induces Bax/p53-independent cell death in HCT116 Bax knockout (KO), HCT116 p53 KO, DU145 Bax KO, or DU145 p53 KO cells that express wild-type (WT) Bak.	Genistein	13-22	P53	Homo sapiens	199-202
28609685-0	2017	Palmitate induces VSMC apoptosis via toll like receptor (TLR)4/ROS/p53 pathway.	Palmitates	0-9	P53	Homo sapiens	67-70
28609685-7	2017	RESULTS: Palmitate significantly promotes VSMC apoptosis, ROS generation, and expression of caspase 3, caspase 9 and p53; while NADPH oxidase inhibitor pretreatment markedly attenuated these effects.	Palmitates	9-18	P53	Homo sapiens	117-120
28349922-0	2017	Coumarin-chalcone hybrid instigates DNA damage by minor groove binding and stabilizes p53 through post translational modifications.	Chalcone	9-17	P53	Homo sapiens	86-89
28781641-0	2017	Anticancer effects of liriodenine on the cell growth and apoptosis of human breast cancer MCF-7 cells through the upregulation of p53 expression.	liriodenine	22-33	P53	Homo sapiens	130-133
28781641-8	2017	Therefore, the present results indicated that the anticancer effects of liriodenine suppress cell growth and induce the apoptosis of human breast cancer MCF-7 cells through inhibition of Bcl-2, cyclin D1 and VEGF expression, and upregulation of p53 expression.	liriodenine	72-83	P53	Homo sapiens	245-248
26004085-10	2015	Our findings strongly indicate that concomitant inactivation of the p53- and pRB- pathways predict resistance towards anthracyclines and mitomycin in breast cancer in vivo.	Mitomycin	137-146	P53	Homo sapiens	68-71
28291250-4	2017	NQO1 is a FAD-dependent, two-domain multifunctional stress protein acting as a Phase II enzyme, activating cancer pro-drugs and stabilizing p53 and p73alpha oncosuppressors.	Flavin-Adenine Dinucleotide	10-13	P53	Homo sapiens	140-143
26211519-3	2015	This in combination with the glucose oxidation at the carbon nanotube/Meldola"s blue/glucose dehydrogenase bioanode can result in a current/or power decrease of BFC in the presence of wild-type p53.	bioanode	107-115	P53	Homo sapiens	194-197
28765552-4	2017	In addition, gammaCdcPLI induced modulation of important mediators of apoptosis pathways such as p53, MAPK-ERK, BIRC5 and MDM2.	gammacdcpli	13-24	P53	Homo sapiens	97-100
28228262-4	2017	Combination treatment with the AR signaling inhibitor enzalutamide (ENZ) and the Chk1/2 inhibitor AZD7762 demonstrates synergy with regard to inhibition of AR-CDC6-ATR-Chk1 signaling, ATM phosphorylation induction, and apoptosis in VCaP (mutant p53) and LNCaP-C4-2b (wild-type p53) cells.	enzalutamide	54-66	P53	Homo sapiens	245-248
28366708-7	2017	Moreover, the simultaneous treatment of leukemia cells with ABT-737 and resveratrol resulted in a reduction in mitochondrial membrane potential, an increase of p53 protein level and up-regulation of the Bax/Bcl-2 ratio.	ABT-737	60-67	P53	Homo sapiens	160-163
28498805-7	2017	Recent studies showed that MIBCs can be subclassified in breast cancer-like subtypes: basal, luminal and p53-like.	mibcs	27-32	P53	Homo sapiens	105-108
26628835-0	2015	Fluorine-18 Fluorodeoxyglucose Uptake in Hepatocellular Carcinoma: Correlation with Glucose Transporters and p53 Expression.	Fluorine	0-8	P53	Homo sapiens	109-112
26070487-3	2015	Through an unbiased genome-wide ChIP-seq analysis, we have found that 5-lipoxygenase (ALOX5, 5-LO) which is a key enzyme of leukotriene (LT) biosynthesis, is a direct target gene of p53 and its expression is induced by genotoxic stress via actinomycin D (Act.D) or etoposide (Eto) treatment.	Etoposide	265-274	P53	Homo sapiens	182-185
26070487-3	2015	Through an unbiased genome-wide ChIP-seq analysis, we have found that 5-lipoxygenase (ALOX5, 5-LO) which is a key enzyme of leukotriene (LT) biosynthesis, is a direct target gene of p53 and its expression is induced by genotoxic stress via actinomycin D (Act.D) or etoposide (Eto) treatment.	Etoposide	276-279	P53	Homo sapiens	182-185
29137250-4	2017	This chaperone-mediated mutated p53-TAp73alpha complex induced chemoresistance to DNA damaging reagents, like Cisplatin, Doxorubicin, Etoposide or Camptothecin.	Etoposide	134-143	P53	Homo sapiens	32-35
28228262-4	2017	Combination treatment with the AR signaling inhibitor enzalutamide (ENZ) and the Chk1/2 inhibitor AZD7762 demonstrates synergy with regard to inhibition of AR-CDC6-ATR-Chk1 signaling, ATM phosphorylation induction, and apoptosis in VCaP (mutant p53) and LNCaP-C4-2b (wild-type p53) cells.	enzalutamide	54-66	P53	Homo sapiens	277-280
29137250-4	2017	This chaperone-mediated mutated p53-TAp73alpha complex induced chemoresistance to DNA damaging reagents, like Cisplatin, Doxorubicin, Etoposide or Camptothecin.	Camptothecin	147-159	P53	Homo sapiens	32-35
25995247-13	2015	Oncomine data analysis of a large number of samples has revealed that overexpression of FBP1 in most HCC tumors with chronic hepatitis C is significantly linked with the decreased expression level of p53.	oncomine	0-8	P53	Homo sapiens	200-203
27939982-9	2017	Taxane-platinum therapy showed advantage over the platinum-cyclophosphamide one in the entire group of patients and in the TP53+ subgroup.	taxane-platinum	0-15	P53	Homo sapiens	123-127
25959860-10	2015	Sitagliptin did not affect the action of WP 631 in HepG2 cancer cells, however, it increased the p53 level.	Sitagliptin Phosphate	0-11	P53	Homo sapiens	97-100
28416637-9	2017	To better probe the p53 response, SJSA cells (shCDK19 versus shCTRL) were treated with the p53 activator nutlin-3.	nutlin 3	105-113	P53	Homo sapiens	91-94
28400230-5	2017	Achiral oxoapomorphine, which was converted from chiral apomorphines under aerobic conditions, served as the reactive species to form a covalent bond at Cys77 of MDM2, leading to the inhibitory effect against the binding to p53.	oxoapomorphine	8-22	P53	Homo sapiens	224-227
27838375-9	2017	Using specific HDACi, we find that the class I subgroup of HDACs, but not the class IIb deacetylase HDAC6, are required for the hydroxyurea-induced crosstalk between p53 and NF-kappaB.	Hydroxyurea	128-139	P53	Homo sapiens	166-169
28618955-4	2017	We found that Oridonin at sub-toxic concentrations synergistically enhanced Nutlin-3-mediated cell viability inhibition in wild-type p53 U2OS and SJSA-1, but not in p53-mutant MNNG/HOS and in null-p53 Saos-2 osteosarcoma cell lines.	oridonin	14-22	P53	Homo sapiens	133-136
26790307-8	2015	The results showed that lycorine significantly inhibited the proliferation of A549 cells (P &lt; 0.05), induced the apoptosis on A549 cells (P &lt; 0.05), increased the activities of Bax and p53, reduced Bcl-2 activity and mitochondrial membrane potential, and notably changed the gene expressions of Bcl-2, Bax, p53 and Survivin (P &lt; 0.05).	lycorine	24-32	P53	Homo sapiens	191-194
26790307-8	2015	The results showed that lycorine significantly inhibited the proliferation of A549 cells (P &lt; 0.05), induced the apoptosis on A549 cells (P &lt; 0.05), increased the activities of Bax and p53, reduced Bcl-2 activity and mitochondrial membrane potential, and notably changed the gene expressions of Bcl-2, Bax, p53 and Survivin (P &lt; 0.05).	lycorine	24-32	P53	Homo sapiens	313-316
28957796-0	2017	Wild-Type P53 Induces Sodium/Iodide Symporter Expression Allowing Radioiodide Therapy in Anaplastic Thyroid Cancer.	radioiodide	66-77	P53	Homo sapiens	10-13
26145175-2	2015	Here we show that the microRNA-101 (miR-101) targets the proteasome maturation protein POMP, leading to impaired proteasome assembly and activity, and resulting in accumulation of p53 and cyclin-dependent kinase inhibitors, cell cycle arrest, and apoptosis.	mir-101	36-43	P53	Homo sapiens	180-183
28487147-4	2017	We used polymer statistics to estimate a global KD value for p53 binding to MdmX in the presence of the flexible linker and the intramolecular binding motif by assuming the flexible linker behaves as a wormlike chain.	Polymers	8-15	P53	Homo sapiens	61-64
28957796-7	2017	Radioiodide uptake assay and flow cytometry analysis were used to detect the role of wild-type p53 on radioiodide uptake.and cell apoptosis in ATC cell line.	radioiodide	102-113	P53	Homo sapiens	95-98
29955703-10	2017	GEN and EGCG reduced BRCA1 CpG methylation and cell proliferation associated with increased p53.	epigallocatechin gallate	8-12	P53	Homo sapiens	92-95
26158294-9	2015	Treatment with nutlin-3a or etoposide induced CST5 in a p53-dependent manner.	nutlin 3	15-24	P53	Homo sapiens	56-59
29130967-6	2017	The mutant p53 cell lines were treated with tunicamycin to induce ERS and rapamycin in order to inhibit mTOR.	Tunicamycin	44-55	P53	Homo sapiens	11-14
26158294-9	2015	Treatment with nutlin-3a or etoposide induced CST5 in a p53-dependent manner.	Etoposide	28-37	P53	Homo sapiens	56-59
27721412-0	2017	Tumor-associated mutant p53 promotes cancer cell survival upon glutamine deprivation through p21 induction.	Glutamine	63-72	P53	Homo sapiens	24-27
26047480-9	2015	EADs is postulated to induce cell cycle arrest that is p53- and p21-dependent based on the upregulated expression of p53 and p21 (P&lt;0.05).	eads	0-4	P53	Homo sapiens	55-58
28240161-6	2017	Meanwhile, we confirmed that DHM showed antitumor activity by regulating the activation of the p53-dependent pathways (MDM2, P-MDM2, BAX and Bcl-2).	Dihydromorphine	29-32	P53	Homo sapiens	95-98
26047480-9	2015	EADs is postulated to induce cell cycle arrest that is p53- and p21-dependent based on the upregulated expression of p53 and p21 (P&lt;0.05).	eads	0-4	P53	Homo sapiens	117-120
25088203-7	2015	Furthermore, the phosphorylation of ATM targets, including gammaH2AX, threonine 68 (T68) on CHK2 (CHK2 pT68) and serine 15 (S15) on p53 were decreased in overexpression and increased in knockdown BMI1 cells in response to ETOP.	Etoposide	222-226	P53	Homo sapiens	132-135
27721412-2	2017	We have previously reported that p53 protein, although a well-known tumor suppressor, can contribute to cancer cell survival and adaptation to low-glutamine conditions.	Glutamine	147-156	P53	Homo sapiens	33-36
27721412-5	2017	Interestingly, cancer cells expressing mutp53 proteins are more resistant to glutamine deprivation than cells with wild-type p53.	Glutamine	77-86	P53	Homo sapiens	42-45
27721412-6	2017	Depletion of endogenous mutp53 protein in human lymphoma cells leads to cell sensitivity to glutamine withdrawal, whereas expression of mutp53 in p53 null cells results in resistance to glutamine deprivation.	Glutamine	92-101	P53	Homo sapiens	27-30
27721412-7	2017	Furthermore, we found that mutp53 proteins hyper-transactivate p53-target gene CDKN1A upon glutamine deprivation, thus triggering cell cycle arrest and promoting cell survival.	Glutamine	91-100	P53	Homo sapiens	30-33
28384067-0	2017	miR-101 Enhances Cisplatin-Induced DNA Damage Through Decreasing Nicotinamide Adenine Dinucleotide Phosphate Levels by Directly Repressing Tp53-Induced Glycolysis and Apoptosis Regulator Expression in Prostate Cancer Cells.	mir-101	0-7	P53	Homo sapiens	139-143
25829495-7	2015	Expression of acetylated p53 and the conformationally active form of Bax were found to be significantly higher in both sirtinol- and EX-527-treated platelets, implicating the p53-Bax axis in apoptosis induced by sirtuin inhibitors.	sirtinol	119-127	P53	Homo sapiens	25-28
28240161-7	2017	These findings defined and supported a novel mechanism that DHM could induce cell apoptosis by reducing TGF-beta via p53 signal pathway in HepG2 cells.	Dihydromorphine	60-63	P53	Homo sapiens	117-120
25829495-7	2015	Expression of acetylated p53 and the conformationally active form of Bax were found to be significantly higher in both sirtinol- and EX-527-treated platelets, implicating the p53-Bax axis in apoptosis induced by sirtuin inhibitors.	sirtinol	119-127	P53	Homo sapiens	175-178
28259931-8	2017	In addition, knockdown of CD164 was demonstrated to upregulate the Bax/Bcl2 ratio and phosphatase and tensin homolog (PTEN) expression, reduce protein kinase B (AKT) phosphorylation and promote the expression of p53 in U87 cells.	cd164	26-31	P53	Homo sapiens	212-215
27934110-6	2016	Next we evaluated the performance of the biosensor in HepG2 cells by treatment with ginkgolic acid, a drug that reduces p53 sumoylation, as well as trichostatin A, a potential inducer of p53 sumoylation by enhancement of its nuclear export.	trichostatin A	148-162	P53	Homo sapiens	187-190
26109778-0	2015	Anti-lung cancer potential of pure esteric-glycoside condurangogenin A against nonsmall-cell lung cancer cells in vitro via p21/p53 mediated cell cycle modulation and DNA damage-induced apoptosis.	esteric-glycoside	35-52	P53	Homo sapiens	128-131
27423454-8	2016	Bioinformatics analysis indicated that effects of quisinostat on NSCLC cells were associated with activated p53 signaling pathway.	quisinostat	50-61	P53	Homo sapiens	108-111
25437011-5	2015	Activation of the Wnt pathway by treatment with Wnt3a-conditioned medium or glycogen synthase kinase 3beta inhibitors, such as SB-216763 and 6-bromoindirubin-3"-oxime, delays the progression of cellular senescence as shown by the decrease in the senescence effectors p53 and pRb, lowered senescence-associated beta-galactosidase activity, and increased telomerase activity.	SB 216763	127-136	P53	Homo sapiens	267-270
28454475-5	2017	Detailed signaling pathway analysis by western blotting demonstrated that the expression levels of p53 and p21 were upregulated, whereas the expression of cyclin-dependent kinase 1 was downregulated following oridonin treatment, which led to cell cycle arrest in the G2/M phase.	oridonin	209-217	P53	Homo sapiens	99-102
28454475-10	2017	In conclusion, the results of the present study suggested that oridonin is able to inactivate the PI3K/Akt pathway and activate p53 pathways in prostate cancer cells, resulting in the suppression of proliferation and the induction of caspase-mediated apoptosis.	oridonin	63-71	P53	Homo sapiens	128-131
27423454-9	2016	We found that quisinostat increased p53 acetylation at K382/K373 sites, upregulated the expression of p21(Waf1/Cip1), and resulted in G1 phase arrest.	quisinostat	14-25	P53	Homo sapiens	36-39
28147244-11	2017	Protein microarray analyses showed that treatment with TMZ+GDC-0941+IR induced higher levels of p53 and glycogen synthase kinase 3-beta (GSK3-beta) expression in SHG44GBM cells than those induced by other treatments.	2-(1H-indazol-4-yl)-6-(4-methanesulfonylpiperazin-1-ylmethyl)-4-morpholin-4-ylthieno(3,2-d)pyrimidine	59-67	P53	Homo sapiens	96-99
25672479-4	2015	Among six distinct human breast cancer cell lines, hirsutine showed strong cytotoxicity against HER2-positive/p53-mutated MDA-MB-453 and BT474 cell lines.	hirsutine	51-60	P53	Homo sapiens	110-113
27748805-6	2016	The p53-dependency and therapeutic spectrum of YH-304 was assessed by western blot analysis, real-time PCR, and cell viability assays in cells expressing endogenous wild or mutant p53.	yh-304	47-53	P53	Homo sapiens	4-7
25672479-5	2015	Conversely, HER2-negative/p53 wild-type MCF-7 and ZR-75-1 cell lines showed resistance against hirsutine-induced cytotoxicity.	hirsutine	95-104	P53	Homo sapiens	26-29
27748805-6	2016	The p53-dependency and therapeutic spectrum of YH-304 was assessed by western blot analysis, real-time PCR, and cell viability assays in cells expressing endogenous wild or mutant p53.	yh-304	47-53	P53	Homo sapiens	180-183
25829764-8	2015	MG treatment also induced the expression of p53 and B-cell lymphoma-2-associated X and cleavage of BH3 interacting-domain with a concomitant decrease in B-cell lymphoma-2 expression.	methyl gallate	0-2	P53	Homo sapiens	44-47
26676339-1	2016	Wild-type TP53 exons 5-8 contain CpG dinucleotides that are prone to methylation-dependent mutation during carcinogenesis, but the regulatory effects of methylation affecting these CpG sites are unclear.	Dinucleoside Phosphates	37-50	P53	Homo sapiens	10-14
25651847-6	2015	Detailed signaling pathway analysis by western blot analysis revealed that low-dose oridonin treatment inhibited BxPC-3 cell proliferation by up-regulating p53 and down-regulating cyclin-dependent kinase 1 (CDK1), which led to cell cycle arrest in the G2/M phase.	oridonin	84-92	P53	Homo sapiens	156-159
27993669-6	2017	Suppression of etoposide-induced cell death correlated with a downregulation of p53 expression, which, among other functions, regulates the expression of death receptor 5, one of the activators of caspase-8.	Etoposide	15-24	P53	Homo sapiens	80-83
28195382-0	2017	Contribution of ATM and ATR kinase pathways to p53-mediated response in etoposide and methyl methanesulfonate induced DNA damage.	Etoposide	72-81	P53	Homo sapiens	47-50
27824003-12	2016	Moreover, IKKbeta inhibitor SC-514 totally reversed the upregulation of IKKbeta and downregulation of p53 and p21 by LPS in SiHa cells.	SC 514	28-34	P53	Homo sapiens	102-105
28230866-0	2017	Oridonin induces autophagy via inhibition of glucose metabolism in p53-mutated colorectal cancer cells.	oridonin	0-8	P53	Homo sapiens	67-70
25639717-0	2015	CR389, a benzoimidazolyl pyridinone analog, induces cell cycle arrest and apoptosis via p53 activation in human ovarian cancer PA-1 cells.	benzoimidazolyl pyridinone	9-35	P53	Homo sapiens	88-91
27665868-9	2016	UA increases the expression level of p53 in a concentration-dependent manner, and inhibition of p53 reduces the anticancer effect of UA in 143B cells.	ursolic acid	0-2	P53	Homo sapiens	37-40
25733816-8	2015	Western blot analysis also indicated that the DHAQC (2) increased BAX, p53, and cytochrome c levels in MCF-7 cells, which subsequently activated apoptosis as observed in annexin V/propidium iodide and cell cycle analyses.	1,3-dihydroxy-9,10-anthraquinone-2-carboxylic acid	46-51	P53	Homo sapiens	71-74
27813088-4	2017	In order to improve the selectivity of the HIMA for HUFs harbouring TP53 mutations, we explored the use of Nutlin-3a, an MDM2 inhibitor that leads to stabilisation and activation of wild-type (WT) p53.	nutlin 3	107-116	P53	Homo sapiens	197-200
27665868-9	2016	UA increases the expression level of p53 in a concentration-dependent manner, and inhibition of p53 reduces the anticancer effect of UA in 143B cells.	ursolic acid	133-135	P53	Homo sapiens	96-99
27177180-7	2017	Pharmacodynamic studies demonstrated that inhibition of cell growth following exposure to TMZ/nutlin3a correlated with: 1) activation of the p53 pathway, 2) downregulation of DNA repair proteins, 3) persistence of DNA damage, and 4) decreased invasion.	nutlin 3	94-102	P53	Homo sapiens	141-144
27665868-10	2016	Moreover, inhibition of p53 partly reverses the UA-induced downregulation of beta-catenin, as do the targets of Wnt/beta-catenin signaling, such as c-Myc and cyclin D1.	ursolic acid	48-50	P53	Homo sapiens	24-27
25567764-1	2015	We report in this work that the Abeta peptide directly interacts with tubulin close to the vinblastine and GTP/GDP binding site, inhibits the tubulin polymerization rate, induces tubulin aggregation, causes cell shrinking, enhances Mad2, BubR1, p53, and p21 activation in MCF7 cells and induces the apoptotic death of A549, HeLa and MCF7 cells.	Guanosine Diphosphate	111-114	P53	Homo sapiens	245-248
25444898-8	2015	However, DNAJB1 knockdown in A549 cells increased the etoposide-induced activation of the p53-mediated apoptosis pathway and repressed cancer cell growth.	Etoposide	54-63	P53	Homo sapiens	90-93
28103869-6	2017	In addition, our results suggested that sinularin triggered DNA damage and subsequently induced cell cycle G2/M arrest associated with up-regulation of p-ATM (Ser(1981)), p-Chk2 (Tyr(68)), p-cdc2 (Tyr(15)), and p53 coupled with increased expression of downstream proteins p21 and down-regulation of p-cdc25 (Ser(216)).	sinularin	40-49	P53	Homo sapiens	211-214
28337243-2	2016	The quantitative interaction profile of the intrinsically disordered transactivation domain of p53 and its mutants with anionic silica nanoparticles is reported at atomic resolution using nuclear magnetic spin relaxation experiments.	Silicon Dioxide	128-134	P53	Homo sapiens	95-98
28051100-3	2017	Overexpression of wild-type PPEF-1, but not inactive PPEF-1D172N, efficiently suppressed CK2alpha-mediated stabilization of PDCD5 and p53-mediated apoptosis in response to etoposide (ET).	Etoposide	172-181	P53	Homo sapiens	134-137
30123836-7	2017	This review article mainly summarizes extrinsic factors that induce liver cancer and potentially have etiological association with p53, including aflatoxin B1, vinyl chloride, non-alcoholic fatty liver disease, iron overload, and infection of hepatitis viruses.	Aflatoxin B1	146-158	P53	Homo sapiens	131-134
25434486-8	2015	Diosgenin inhibited Akt phosphorylation and upregulated p21 and p27 expression, but did not alter the expression of p53, suggesting diosgenin-induced upregulation of p21 and p57 is p53-independent in HCC cells.	Diosgenin	0-9	P53	Homo sapiens	181-184
25434486-8	2015	Diosgenin inhibited Akt phosphorylation and upregulated p21 and p27 expression, but did not alter the expression of p53, suggesting diosgenin-induced upregulation of p21 and p57 is p53-independent in HCC cells.	Diosgenin	132-141	P53	Homo sapiens	181-184
25446071-3	2015	Here we report for the first time that cadmium, nickel and cobalt, which have already been shown to disturb various DNA repair mechanisms, can also influence p63 and p73 sequence-specific DNA binding activity and transactivation of p53 family target genes.	Cobalt	59-65	P53	Homo sapiens	232-235
25446071-9	2015	Nickel and cobalt abolished DNA-p53 interaction at sub-millimolar concentrations while inhibition of p63 and p73 DNA binding was observed at millimolar concentrations.	Cobalt	11-17	P53	Homo sapiens	32-35
27877082-0	2016	Histone Deacetylase Inhibitor Trichostatin a Promotes the Apoptosis of Osteosarcoma Cells through p53 Signaling Pathway Activation.	trichostatin A	30-44	P53	Homo sapiens	98-101
25515622-8	2015	Investigation of Forkhead box O1 (FOXO1), superoxide dismutase 2 (SOD2), and p53 levels to determine intracellular signaling by TSA in oxidative stress-induced MSCs demonstrated that expression of phosphorylated-FOXO1 and phosphorylated-SOD2 decreased in H2 O2 -treated MSCs while levels of p53 increased.	trichostatin A	128-131	P53	Homo sapiens	291-294
29362667-0	2017	Xylopine Induces Oxidative Stress and Causes G2/M Phase Arrest, Triggering Caspase-Mediated Apoptosis by p53-Independent Pathway in HCT116 Cells.	xylopine	0-8	P53	Homo sapiens	105-108
29362667-5	2017	Moreover, pretreatment with a caspase-3 inhibitor (Z-DEVD-FMK), but not with a p53 inhibitor (cyclic pifithrin-alpha), reduced xylopine-induced apoptosis, indicating induction of caspase-mediated apoptosis by the p53-independent pathway.	xylopine	127-135	P53	Homo sapiens	213-216
29362667-8	2017	In conclusion, xylopine has potent cytotoxicity to different cancer cell lines and is able to induce oxidative stress and G2/M phase arrest, triggering caspase-mediated apoptosis by the p53-independent pathway in HCT116 cells.	xylopine	15-23	P53	Homo sapiens	186-189
28240161-5	2017	It is very interesting that we found DHM could regulate TGF-beta signal pathway and which has a crosstalk with P53, Smad3 and P-Smad2/3 proteins.	Dihydromorphine	37-40	P53	Homo sapiens	111-114
27877082-6	2016	TSA significantly inhibited the growth of MG63 cells and promoted apoptosis in a dose-dependent manner through p53 signaling pathway activation.	trichostatin A	0-3	P53	Homo sapiens	111-114
27599915-7	2016	In conclusion, we suggest NVP-BKM120 induces apoptosis through p53-dependent and -independent mechanisms, indicating the potential application of the inhibitor in both wild-type and deficient p53-expressing leukemic cells.	NVP-BKM120	30-36	P53	Homo sapiens	63-66
25866679-4	2015	As expected, etoposide-treated wild-type p53-containing cell lines, LFS 2852 and control Jurkat, showed a greater rate of caspase- and annexin V-induced apoptotic cell death compared to the p53-mutant LFS 2673 cell line although mitochondrial and nuclear assays could not detect apoptosis in these organelles.	Etoposide	13-22	P53	Homo sapiens	41-44
25866679-4	2015	As expected, etoposide-treated wild-type p53-containing cell lines, LFS 2852 and control Jurkat, showed a greater rate of caspase- and annexin V-induced apoptotic cell death compared to the p53-mutant LFS 2673 cell line although mitochondrial and nuclear assays could not detect apoptosis in these organelles.	Etoposide	13-22	P53	Homo sapiens	190-193
27676608-5	2016	Specifically, (-)-bassianolide induced G0/G1 arrest associated with a decrease of cyclin A, D1 and an increase of p53, MDM2, and p21 expression in MDA-MB 231 cells.	bassianolide	14-30	P53	Homo sapiens	114-117
27599915-7	2016	In conclusion, we suggest NVP-BKM120 induces apoptosis through p53-dependent and -independent mechanisms, indicating the potential application of the inhibitor in both wild-type and deficient p53-expressing leukemic cells.	NVP-BKM120	30-36	P53	Homo sapiens	192-195
27298278-5	2016	Three naphthoquinones had moderate cytotoxic effects with IC50 values ranging from 1.51 to 9.56 muM, through up-regulation of p53 transcriptional activity.	Naphthoquinones	6-21	P53	Homo sapiens	126-129
27835895-0	2016	Enhancement of 5-FU sensitivity by the proapoptotic rpL3 gene in p53 null colon cancer cells through combined polymer nanoparticles.	Polymers	110-117	P53	Homo sapiens	65-68
25624096-0	2015	A silica-polymer composite nano system for tumor-targeted imaging and p53 gene therapy of lung cancer.	Silicon Dioxide	2-8	P53	Homo sapiens	70-73
25624096-0	2015	A silica-polymer composite nano system for tumor-targeted imaging and p53 gene therapy of lung cancer.	Polymers	9-16	P53	Homo sapiens	70-73
27556362-6	2016	Among the p53-positive ependymomas, the vast majority exhibited a RELA fusion leading to the hypothesis that p53 inactivation might be linked to RELA positivity.In order to assess the potential of p53 reactivation through MDM2 inhibition in ependymoma, we evaluated the effects of Actinomycin-D and Nutlin-3 treatment in two preclinical ependymoma models representing the high-risk subtypes PF-EPN-A and ST-EPN-RELA.	nutlin 3	299-307	P53	Homo sapiens	109-112
25179905-8	2014	These results show that among 2-MeO-E2-induced apoptotic events, including prometaphase arrest, up-regulation of Bax level, down-regulation of Bcl-2 level, activation of both Bak and Bax, and mitochondria-dependent caspase activation, the modulation of Bax and Bcl-2 levels is the target of the pro-apoptotic action of p53.	2-Methoxyestradiol	30-38	P53	Homo sapiens	319-322
25296356-9	2014	Fe2O3 MFH can induce high Hsp70 expression at an early stage, enhance the expression of Bax, and decrease the expression of mutant p53, which promotes the apoptosis of tumor cells.	fe2o3 mfh	0-9	P53	Homo sapiens	131-134
27765354-9	2016	EGCG decreased mRNA and transcriptional activity of beta-catenin in p53 wild-type KB cells.	epigallocatechin gallate	0-4	P53	Homo sapiens	68-71
27665868-11	2016	Our findings indicated that UA can inhibit the proliferation of 143B OS cells through inactivation of Wnt/beta-catenin signaling, which may be mediated partly by upregulating the expression of p53.	ursolic acid	28-30	P53	Homo sapiens	193-196
27666201-0	2016	Mitomycin C and decarbamoyl mitomycin C induce p53-independent p21WAF1/CIP1 activation.	Mitomycin	0-11	P53	Homo sapiens	47-50
27666201-13	2016	Knocking down p53 in MCF-7 did not attenuate MC and DMC induced p21WAF1/CIP1 activation.	Mitomycin	21-23	P53	Homo sapiens	14-17
27556362-6	2016	Among the p53-positive ependymomas, the vast majority exhibited a RELA fusion leading to the hypothesis that p53 inactivation might be linked to RELA positivity.In order to assess the potential of p53 reactivation through MDM2 inhibition in ependymoma, we evaluated the effects of Actinomycin-D and Nutlin-3 treatment in two preclinical ependymoma models representing the high-risk subtypes PF-EPN-A and ST-EPN-RELA.	nutlin 3	299-307	P53	Homo sapiens	109-112
27542305-3	2016	As part of our effort to identify new classes of p53-MDM2 inhibitors that could lead to additional clinical candidates, we report here the design of highly potent inhibitors having a pyrazolopyrrolidinone core structure.	pyrazolopyrrolidinone	183-204	P53	Homo sapiens	49-52
27517620-7	2016	Inhibition of glucosylceramide synthase with d-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) sensitized p53-R273H cancer cells and tumor xenografts to doxorubicin treatments.	RV 538	45-101	P53	Homo sapiens	120-123
27556692-4	2016	In p53-proficient NALM-6 cells, SCH900776 added to NAs enhanced signaling towards Chk1 (pSer317/pSer345), effectively blocked Chk1 activation (Ser296 autophosphorylation), increased replication stress (p53 and gamma-H2AX accumulation) and temporarily potentiated apoptosis.	MK-8776	32-41	P53	Homo sapiens	3-6
27556692-4	2016	In p53-proficient NALM-6 cells, SCH900776 added to NAs enhanced signaling towards Chk1 (pSer317/pSer345), effectively blocked Chk1 activation (Ser296 autophosphorylation), increased replication stress (p53 and gamma-H2AX accumulation) and temporarily potentiated apoptosis.	MK-8776	32-41	P53	Homo sapiens	202-205
23554011-7	2014	Western blotting assay showed that ellagic acid promoted p21, p53 and decreased CDC2 and WEE1 for leading to G0/G1 phase arrest and promoting BAD expression, AIF and Endo G, cytochrome c, caspase-9 and -3 for leading to apoptosis in TSGH8301 cells.	Ellagic Acid	35-47	P53	Homo sapiens	62-65
23661569-4	2014	Zeb also induced A549 cell death, which was accompanied by the loss of mitochondrial membrane potential (MMP; DeltaPsim ), Bcl-2 decrease, Bax increase, p53 increase and activation of caspase-3 and -8.	pyrimidin-2-one beta-ribofuranoside	0-3	P53	Homo sapiens	153-156
27672670-8	2016	San Biagio, 2012) [2] "Effect of zinc oxide nanomaterials induced oxidative stress on the p53 pathway" (M.I.	Zinc Oxide	33-43	P53	Homo sapiens	90-93
27517620-7	2016	Inhibition of glucosylceramide synthase with d-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) sensitized p53-R273H cancer cells and tumor xenografts to doxorubicin treatments.	RV 538	103-107	P53	Homo sapiens	120-123
27187187-0	2016	Amphipathic silica nanoparticles induce cytotoxicity through oxidative stress mediated and p53 dependent apoptosis pathway in human liver cell line HL-7702 and rat liver cell line BRL-3A.	Silicon Dioxide	12-18	P53	Homo sapiens	91-94
27402830-7	2016	Treatment with the OGA inhibitor Thiamet-G (TMG), silencing of OGA, or overexpression of OGA and OGT led to p53 stabilization, increased nuclear localization, and increased protein and mRNA levels of p53 target genes.	thiamet G	33-42	P53	Homo sapiens	108-111
27402830-7	2016	Treatment with the OGA inhibitor Thiamet-G (TMG), silencing of OGA, or overexpression of OGA and OGT led to p53 stabilization, increased nuclear localization, and increased protein and mRNA levels of p53 target genes.	thiamet G	33-42	P53	Homo sapiens	200-203
27402830-7	2016	Treatment with the OGA inhibitor Thiamet-G (TMG), silencing of OGA, or overexpression of OGA and OGT led to p53 stabilization, increased nuclear localization, and increased protein and mRNA levels of p53 target genes.	thiamet G	44-47	P53	Homo sapiens	108-111
27402830-7	2016	Treatment with the OGA inhibitor Thiamet-G (TMG), silencing of OGA, or overexpression of OGA and OGT led to p53 stabilization, increased nuclear localization, and increased protein and mRNA levels of p53 target genes.	thiamet G	44-47	P53	Homo sapiens	200-203
25268459-3	2014	Therefore, it is a goal to develop S100B inhibitors (SBiXs) that inhibit the S100B-p53 complex and restore active p53 in this deadly cancer.	sbixs	53-58	P53	Homo sapiens	83-86
25268459-3	2014	Therefore, it is a goal to develop S100B inhibitors (SBiXs) that inhibit the S100B-p53 complex and restore active p53 in this deadly cancer.	sbixs	53-58	P53	Homo sapiens	114-117
24998890-3	2014	The focus of this study was on the development of new superparamagnetic polymer microspheres for the specific isolation of the tumor suppressor protein p53.	Polymers	72-79	P53	Homo sapiens	152-155
27545311-7	2016	Among these genes, 2 genes (PRODH and DAO) were found to be directly regulated by p53, and ectopic expression of 4 genes (PRODH, DAO, EPN3, and GPR172B) affected senescence phenotypes induced by etoposide treatment.	Etoposide	195-204	P53	Homo sapiens	82-85
26378498-8	2016	We suggest that both of the most important proapoptotic and anticancer proteins, p53 and TSPO, are damaged by CS, paving the way for lung cancer initiation and progression.	Cesium	110-112	P53	Homo sapiens	81-84
27323408-5	2016	LACE1 physically interacts with p53 and is necessary for mitomycin c-induced translocation of p53 into mitochondria.	Mitomycin	57-68	P53	Homo sapiens	32-35
27500741-5	2016	Quantitative PCR analysis demonstrated that CIMO decreases the relative mRNA expression of genes that are involved in cell cycle progression (CCND1) and cell survival (BCL2, BCL-xL, BAD, CASP 3/7/9, and TP53).	cimo	44-48	P53	Homo sapiens	203-207
24308434-4	2014	Both drugs induced expression of p53 targets, p21, Puma and DR5, only in TP53(wt) HMCLs.	hmcls	82-87	P53	Homo sapiens	33-36
25135721-6	2014	Both PDOX and DOX caused an up-regulation of the P53/P21-related signal pathway, and PDOX significantly increased expression of P53 and caspase 3, and arrested the cell cycle at the G1/G2 phase.	acetyl-phenylalanyl-lysyl-para-aminobenzyloxycarbonyl-adriamycin	5-9	P53	Homo sapiens	49-52
27323408-5	2016	LACE1 physically interacts with p53 and is necessary for mitomycin c-induced translocation of p53 into mitochondria.	Mitomycin	57-68	P53	Homo sapiens	94-97
27261574-0	2016	Curcumin and Ellagic acid synergistically induce ROS generation, DNA damage, p53 accumulation and apoptosis in HeLa cervical carcinoma cells.	Ellagic Acid	13-25	P53	Homo sapiens	77-80
24926563-9	2014	p53 mutations characteristic of smoking were frequently observed in the CS&gt;0 groups contrary to non-specific mutations in the CS=0, AB&gt;0 groups.	Cesium	72-74	P53	Homo sapiens	0-3
24743655-5	2014	Transcriptome profiling, using RNAseq, in response to the DNA-damaging agent etoposide revealed a large number of Tp53-regulated transcripts, but also a subset of transcripts that were TP53Pro72Arg allele specific.	Etoposide	77-86	P53	Homo sapiens	114-118
24743655-5	2014	Transcriptome profiling, using RNAseq, in response to the DNA-damaging agent etoposide revealed a large number of Tp53-regulated transcripts, but also a subset of transcripts that were TP53Pro72Arg allele specific.	Etoposide	77-86	P53	Homo sapiens	185-189
27078502-0	2016	Costunolide Induces Apoptosis through Generation of ROS and Activation of P53 in Human Esophageal Cancer Eca-109 Cells.	costunolide	0-11	P53	Homo sapiens	74-77
27078502-5	2016	Costunolide induced apoptosis of Eca-109 cells as well as cell cycle arrest in G1/S phase by upregulation of P53 and P21.	costunolide	0-11	P53	Homo sapiens	109-112
27545131-13	2016	(7) The expression of P53 was significantly higher in GSNO group than in the blank control group (P&lt; 0.05), which could be significantly down regulated by pretreatment with high, medium and low concentration ICA in a concentration-dependent manner, above effects could be blocked by LY294002(all P&lt;0.05).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	286-294	P53	Homo sapiens	22-25
27570453-8	2016	These findings suggest that the ZnO NPs induced cell cycle arrest at G2/M, which was associated with epigenetic changes and accompanied by p53-Bax mitochondrial pathway-mediated apoptosis.	Zinc Oxide	32-35	P53	Homo sapiens	139-142
27261574-5	2016	Besides this, Curcumin and Ellagic acid also restore p53, induce ROS formation and DNA damage.	Ellagic Acid	27-39	P53	Homo sapiens	53-56
24675086-0	2014	Chromosome breakage induced by the genotoxic agents mitomycin C and cytosine arabinoside is concentration and p53 dependent.	Mitomycin	52-63	P53	Homo sapiens	110-113
24675086-7	2014	Low levels of micronucleus and p53 induction were observed in TK6 cells treated with MMC.	Mitomycin	85-88	P53	Homo sapiens	31-34
27176636-0	2016	Emulsified isoflurane treatment inhibits the cell cycle and respiration of human bronchial epithelial 16HBE cells in a p53-independent manner.	Isoflurane	11-21	P53	Homo sapiens	119-122
24956278-5	2014	The quinic acid derivative KZ-41 lessened leukocyte adhesion and paxillin-dependent proliferation via inhibition of p38MAPK-p53-ICAM-1 signaling.	Quinic Acid	4-15	P53	Homo sapiens	124-127
27496965-0	2016	Ursolic acid, a pentacyclin triterpene, potentiates TRAIL-induced apoptosis through p53-independent up-regulation of death receptors.	ursolic acid	0-12	P53	Homo sapiens	84-87
27080185-0	2016	Structure-activity relationship study of 4-substituted piperidines at Leu26 moiety of novel p53-hDM2 inhibitors.	4-substituted piperidines	41-66	P53	Homo sapiens	92-95
27470351-0	2016	Histone deacetylase inhibitor, Romidepsin (FK228) inhibits endometrial cancer cell growth through augmentation of p53-p21 pathway.	romidepsin	43-48	P53	Homo sapiens	114-117
27470351-9	2016	Moreover, FK228 treatment significantly increased the mRNA and protein expressions of p53, p21, cleaved caspases such as 3, 7 and 8 and PARP.	romidepsin	10-15	P53	Homo sapiens	86-89
27470351-11	2016	CONCLUSION: In conclusion, FK228 inhibits EC tumor cell proliferation and induces apoptosis by activation caspase/PARP via the induction of p53/p21 signaling cascades, suggesting that FK228 is a potential therapeutic agent for EC.	romidepsin	27-32	P53	Homo sapiens	140-143
27470351-11	2016	CONCLUSION: In conclusion, FK228 inhibits EC tumor cell proliferation and induces apoptosis by activation caspase/PARP via the induction of p53/p21 signaling cascades, suggesting that FK228 is a potential therapeutic agent for EC.	romidepsin	184-189	P53	Homo sapiens	140-143
27483224-1	2016	We previously reported that prenylated chalcone 2 (PC2), the O-prenyl derivative (2) of 2"-hydroxy-3,4,4",5,6"-pentamethoxychalcone (1), induced cytotoxicity of tumor cells via disruption of p53-MDM2 interaction.	o-prenyl	61-69	P53	Homo sapiens	191-194
24813735-0	2014	Discovery of 1-arylpyrrolidone derivatives as potent p53-MDM2 inhibitors based on molecule fusing strategy.	1-arylpyrrolidone	13-30	P53	Homo sapiens	53-56
24114315-9	2014	Regarding the TP53 Arg72Pro, we showed statistical significance for ProPro + ProArg comparing to ArgArg (OR 2.34, 95 %, CI 1.17-4.70) in hereditary compared to sporadic group.	propro + proarg	68-83	P53	Homo sapiens	14-18
27082635-0	2016	Theaflavin-3, 3"-digallate induces apoptosis and G2 cell cycle arrest through the Akt/MDM2/p53 pathway in cisplatin-resistant ovarian cancer A2780/CP70 cells.	theaflavin-3,3'-digallate	0-26	P53	Homo sapiens	91-94
24632713-3	2014	The present results demonstrate that GO-203 and BTZ synergistically downregulate expression of the p53-inducible regulator of glycolysis and apoptosis (TIGAR), which promotes shunting of glucose-6-phosphate into the pentose phosphate pathway to generate reduced glutathione (GSH).	Glucose-6-Phosphate	187-206	P53	Homo sapiens	99-102
27302173-8	2016	The ability of BE3 to induce programmed cell death was examined in human colon cancer cell lines LS180 and HT-29 by measuring caspase activation, DNA fragmentation and expression of BAX, BCL2, TP53 and CDKN1A genes.	be3	15-18	P53	Homo sapiens	193-197
27133761-0	2016	Retraction notice to "ss-elemene against human lung cancer via up-regulation of P53 protein expression to promote the release of exosome": LUNG 86/2 (2014) 144-150.	ss-elemene	22-32	P53	Homo sapiens	80-83
27420968-7	2016	We also observed a significant increase in ERCC1 expression, and decrease in p53 and EGFR expression, in EC-9706 cells treated with SNX-2112 (P &lt; 0.05), indicating the regulation of EC by SNX-2112.	2-[(2-methoxyethyl)amino]-4-(4-oxo-1,2,3,4-tetrahydro-9H-carbazol-9-yl)benzamide	132-135	P53	Homo sapiens	77-80
27094403-9	2016	The pretreatments with monohydroxy-DMC and monohydroxy-BDMC reduced c-jun and c-fos mRNA expression and p53 tumor suppressor protein expression and increased HO-1 protein expression and glutathione peroxidase (GPx) activity, respectively, compared to cells with direct hydrogen peroxide treatments.	monohydroxy-dmc	23-38	P53	Homo sapiens	104-107
27228201-9	2016	Finally, we have shown that the inclusion complex of alpha-CD and curcumin (CCC) preferentially enters into the human lung cancer cell (A549) as compared to the normal lung fibroblast cell (WI38), causes apoptotic death, activates tumor suppressor protein (p53) and cyclin-dependent kinase inhibitor 1 (p21), and inhibits 3D spheroid growth of cancer cell.	alpha-cyclodextrin	53-61	P53	Homo sapiens	257-260
24375173-7	2014	Mechanistically, the nuclear transportation of p65 and p53 was reduced by UA administration prior to UVR exposure while the levels of p65 and p53 nuclear transportation in SM cells were sustained at a substantially higher level.	ursolic acid	74-76	P53	Homo sapiens	55-58
24375173-9	2014	These results were consistent with reduced proliferation observed in the clonogenic assay, indicating that UA treatment enhanced the phototoxicity of UVR, by modulating the activation of p53 and NF-kappaB and initiating a mitogenic response to optical radiation that triggered mitochondria-dependent apoptosis, particularly in skin melanoma cells.	ursolic acid	107-109	P53	Homo sapiens	187-190
27210019-5	2016	On the other hand, by changing these lysines to glutamine (2KQ-p53), thereby neutralizing their positive charge and potentially mimicking acetylation, p53 is impaired in the induction of cell cycle arrest and yet can still effectively induce cell death.	Glutamine	48-57	P53	Homo sapiens	63-66
26648479-1	2016	In this in vitro study, a series of novel pyrazole derivatives were designed, synthesized, and evaluated against five human cancer cell lines (PC3, A549, HL60, HCT116, and SW620) for their antiproliferative and p53-MDM2 binding inhibitory activities.	pyrazole	42-50	P53	Homo sapiens	211-214
27210019-5	2016	On the other hand, by changing these lysines to glutamine (2KQ-p53), thereby neutralizing their positive charge and potentially mimicking acetylation, p53 is impaired in the induction of cell cycle arrest and yet can still effectively induce cell death.	Glutamine	48-57	P53	Homo sapiens	151-154
26669750-7	2016	Aotaphenazine (1) enhanced the levels of apoptosis inducing proteins DR4, DR5, p53 and also decreased the levels of cell survival protein Bcl-2 in TRAIL-resistant human gastric adenocarcinoma (AGS) cells in a dose-dependent manner.	Aotaphenazine	0-13	P53	Homo sapiens	79-82
24658405-0	2014	Induction of nuclear translocation of mutant cytoplasmic p53 by geranylgeranoic acid in a human hepatoma cell line.	geranylgeranic acid	64-84	P53	Homo sapiens	57-60
24618722-6	2014	Thiacremonone (0-50 mug/ml) inhibited lung cancer cell growth in a concentration dependent manner through induction of apoptotic cell death accompanied by induction of cleaved caspase-3, -8, -9, Bax, p21 and p53, but decrease of xIAP, cIAP and Bcl2 expression.	thiacremonone	0-13	P53	Homo sapiens	208-211
26980707-0	2016	Oridonin, a novel lysine acetyltransferases inhibitor, inhibits proliferation and induces apoptosis in gastric cancer cells through p53- and caspase-3-mediated mechanisms.	oridonin	0-8	P53	Homo sapiens	132-135
24618722-9	2014	In an allograft in vivo model, thiacremonone (30 mg/kg) also inhibited tumor growth accompanied with the reduction of PRDX6 expression and glutathione peroxidase activity, but increased expression of cleaved caspase-3, -8, -9, Bax, p21 and p53.	thiacremonone	31-44	P53	Homo sapiens	240-243
26921178-0	2016	Combinatorial treatment with anacardic acid followed by TRAIL augments induction of apoptosis in TRAIL resistant cancer cells by the regulation of p53, MAPK and NFkappabeta pathways.	anacardic acid	29-43	P53	Homo sapiens	147-150
26980707-3	2016	In gastric cancer cells, oridonin treatment inhibited cell proliferation in a concentration-dependent manner and down-regulated the expression of p53 downstream genes, whereas p53 inhibition by PFT-alpha reversed the antiproliferative effects of oridonin.	oridonin	25-33	P53	Homo sapiens	146-149
26986476-8	2016	The results showed that knockdown of PTEN strongly antagonized ATM activation in response to etoposide treatment, and thereby reduced the phosphorylation level of ATM substrates, including H2AX, P53 and Chk2.	Etoposide	93-102	P53	Homo sapiens	195-198
26980707-3	2016	In gastric cancer cells, oridonin treatment inhibited cell proliferation in a concentration-dependent manner and down-regulated the expression of p53 downstream genes, whereas p53 inhibition by PFT-alpha reversed the antiproliferative effects of oridonin.	oridonin	246-254	P53	Homo sapiens	176-179
26980707-6	2016	In conclusion, our study identified oridonin as a novel KATi and demonstrated its tumor suppressive effects in gastric cancer cells at least partially through p53-and caspase-3-mediated mechanisms.	oridonin	36-44	P53	Homo sapiens	159-162
24411335-5	2014	The results of an inverted fluorescence microscopy, flow cytometry (FCM) and western blotting methods demonstrated that PC-3 prostate cancer cells treated with EGFP-p53/PEI/PAH-Cit/AuNP-CS expressed higher levels of GFP than cells treated with EGFP-p53/PEI.	p-Aminohippuric Acid	173-176	P53	Homo sapiens	249-252
26942461-4	2016	Here, we show that hydralazine induced caspase-dependent apoptotic cell death in human p53-mutant leukemic T cells.	Hydralazine	19-30	P53	Homo sapiens	87-90
27547448-7	2016	Consistent with the inhibitory effect of PXR on p53, elevated PXR levels decreased doxorubicin- or nutlin-3a-mediated toxicity and promoted malignant transformation in colon cancer cells.	nutlin 3	99-108	P53	Homo sapiens	48-51
24411335-5	2014	The results of an inverted fluorescence microscopy, flow cytometry (FCM) and western blotting methods demonstrated that PC-3 prostate cancer cells treated with EGFP-p53/PEI/PAH-Cit/AuNP-CS expressed higher levels of GFP than cells treated with EGFP-p53/PEI.	Cesium	186-188	P53	Homo sapiens	249-252
24411335-6	2014	Furthermore, PC-3 cells treated with EGFP-p53/PEI/PAH-Cit/AuNP-CS showed reduced cellular viability and increased nuclear fragmentation, consistent with elevated p53 expression.	p-Aminohippuric Acid	50-53	P53	Homo sapiens	42-45
24411335-6	2014	Furthermore, PC-3 cells treated with EGFP-p53/PEI/PAH-Cit/AuNP-CS showed reduced cellular viability and increased nuclear fragmentation, consistent with elevated p53 expression.	p-Aminohippuric Acid	50-53	P53	Homo sapiens	162-165
24411335-8	2014	Western blotting and caspase activation studies revealed that EGFP-p53/PEI/PAH-Cit/AuNP-CS complexes may induce PC-3 apoptosis via the mitochondria-mediated signaling pathway by up-regulation of Bax, down-regulation of Bcl-2, and activation of caspase-3.	p-Aminohippuric Acid	75-78	P53	Homo sapiens	67-70
26921248-3	2016	Here, we present data that define the first endogenous activation of the CS-pathway whereby, upon DNA damage, wild type p53 acts as an endogenous regulator of CHK1 levels that modulates caspase-2 activation.	Cesium	73-75	P53	Homo sapiens	120-123
24524627-13	2014	The multiplex mRNA expression study indicated that EADs-induced apoptosis was accompanied by upregulation of the expression of SOD1, SOD2, NF-kappaB, p53, p38 MAPK, and catalase, but downregulation of Akt1.	eads	51-55	P53	Homo sapiens	150-153
27073552-6	2016	Through upregulation in the expression of p53 and Bax, and downregulation in the expression of Bcl-2 and activation of caspase-3, costunolide-induced apoptosis was confirmed by western blot analysis.	costunolide	130-141	P53	Homo sapiens	42-45
24525232-5	2014	p53-like MIBCs were consistently resistant to neoadjuvant methotrexate, vinblastine, doxorubicin and cisplatin chemotherapy, and all chemoresistant tumors adopted a p53-like phenotype after therapy.	mibcs	9-14	P53	Homo sapiens	0-3
24525232-5	2014	p53-like MIBCs were consistently resistant to neoadjuvant methotrexate, vinblastine, doxorubicin and cisplatin chemotherapy, and all chemoresistant tumors adopted a p53-like phenotype after therapy.	mibcs	9-14	P53	Homo sapiens	165-168
27069137-8	2016	Moreover, depletion of PANDA prevented accumulation of p53 protein, as a result of DNA damage, induced by the genotoxic agent etoposide.	Etoposide	126-135	P53	Homo sapiens	55-58
25409339-4	2016	Simultaneous treatment of donor cells with TSA (50nM) and 5azadC (7.5nM) resulted in higher in vitro development to the blastocyst stage, reduction of the apoptotic index and the global level of H3K27 me3 and altered expression levels of HDAC1, P53, CASPASE3, CASPASE9 and DNMT3a in cloned blastocysts.	trichostatin A	43-46	P53	Homo sapiens	245-248
27069139-0	2016	Discovery of Novel (Imidazo[1,2-a]pyrazin-6-yl)ureas as Antiproliferative Agents Targeting P53 in Non-small Cell Lung Cancer Cell Lines.	(imidazo[1,2-a]pyrazin-6-yl)ureas	19-52	P53	Homo sapiens	91-94
26646449-12	2016	Furthermore, SIRT1 knockdown resulted in cell cycle arrest, induction of apoptosis and reduction of K562 cell proliferation accompanied by enhanced p53 and FOXO1 acetylation in K562 cells after etoposide treatment.	Etoposide	194-203	P53	Homo sapiens	148-151
23318437-10	2014	The regulation on p53 and MDM2 stability by RNF2 was also observed during the etoposide-induced DNA damage response.	Etoposide	78-87	P53	Homo sapiens	18-21
26883110-4	2016	The novel cyclometallated iridium(III) compound 1 [Ir(eppy)2(dcphen)](PF6) (where eppy = 2-(4-ethylphenyl)pyridine and dcphen = 4, 7-dichloro-1, 10-phenanthroline) blocked the interaction of p53/hDM2 in human amelanotic melanoma cells.	[ir(eppy)2(dcphen)](pf6	50-73	P53	Homo sapiens	191-194
24434508-6	2014	Investigation of the molecular mechanism of Roc-A-mediated protection revealed that Roc-A specifically blocks DNA damage-induced upregulation of the transcription factor p53 by inhibiting its protein synthesis.	roc-	44-48	P53	Homo sapiens	170-173
26871476-8	2016	The current study provides evidence that TP53 mutations are independently prognostic in MDS patients treated with HMA.	5-(N,N-hexamethylene)amiloride	114-117	P53	Homo sapiens	41-45
26871476-9	2016	While TP53-mutated MDS patients initially respond well to HMA, their duration of response is significantly shorter than WT patients.	5-(N,N-hexamethylene)amiloride	58-61	P53	Homo sapiens	6-10
28959565-5	2016	Molecular analysis of cells treated with ZnO chips revealed that zinc ions released from the chips increased cellular levels of reactive oxygen species, including hydrogen peroxide, which led to the down-regulation of anti-apoptotic molecules (such as HIF-1alpha, survivin, cIAP-2, claspin, p-53, and XIAP) and caspase-dependent apoptosis.	Zinc Oxide	41-44	P53	Homo sapiens	291-295
26771232-8	2016	Finally, shDlx-2 and Gln metabolism inhibition decreased Snail mRNA levels through p53-dependent upregulation of Snail-targeting microRNAs.	Glutamine	21-24	P53	Homo sapiens	83-86
26969379-2	2016	PURPOSE: In this study the effects of naturally occurring homochelidonine in comparison to chelidonine on cell cycle progression and cell death in leukemic T-cells with different p53 status are described.	chelidonine	62-73	P53	Homo sapiens	179-182
26699757-3	2016	Exposure of J/Neo cells to kaempeferol caused cytotoxicity and activation of the ATM/ATR-Chk1/Chk2 pathway, activating the phosphorylation of p53 (Ser-15), inhibitory phosphorylation of Cdc25C (Ser-216), and inactivation of cyclin-dependent kinase 1 (Cdk1), with resultant G2- arrest of the cell cycle.	kaempeferol	27-38	P53	Homo sapiens	142-145
26723900-0	2016	TP53 and lacZ mutagenesis induced by 3-nitrobenzanthrone in Xpa-deficient human TP53 knock-in mouse embryo fibroblasts.	3-nitrobenzanthrone	37-56	P53	Homo sapiens	0-4
26723900-0	2016	TP53 and lacZ mutagenesis induced by 3-nitrobenzanthrone in Xpa-deficient human TP53 knock-in mouse embryo fibroblasts.	3-nitrobenzanthrone	37-56	P53	Homo sapiens	80-84
26723900-10	2016	Thirty-two percent of 3-NBA-induced TP53 mutations occurred at CpG sites, all of which are hotspots for mutation in smokers" lung cancer (codons 157, 158, 175, 245, 248, 273, 282).	3-nitrobenzanthrone	22-27	P53	Homo sapiens	36-40
24427275-9	2014	This dysfunctional autophagy plays a pro-death role in GNA-treated cells by activating p53, Bax and cleaved caspase-3 while decreasing Bcl-2.	neo-gambogic acid	55-58	P53	Homo sapiens	87-90
26784190-7	2016	Metabolically stressed ob/ob mice and PA-treated HepG2 cells showed an increase in expression of endoplasmic reticulum (ER) stress markers and cytosolic p53.	Palmitates	38-40	P53	Homo sapiens	153-156
25169478-0	2014	Association of a miR-502-binding site single nucleotide polymorphism in the 3"-untranslated region of SET8 and the TP53 codon 72 polymorphism with cervical cancer in the Chinese population.	mir-502	17-24	P53	Homo sapiens	115-119
27085860-0	2016	Novel luminescent silica nanoparticles (LSN): p53 gene delivery system in breast cancer in vitro and in vivo.	Silicon Dioxide	18-24	P53	Homo sapiens	46-49
24795076-0	2016	p53 gene therapy of human breast carcinoma: using a transferrin-modified silica nanoparticles.	Silicon Dioxide	73-79	P53	Homo sapiens	0-3
26821367-15	2016	Expression of Bcl-2, survivin and p53 were reduced in LoVo cells co-cultured with TAMs, compared with the control group (P&lt;0.05), whereas Smac expression was increased in the co-culture groups (P&lt;0.01).	tams	82-86	P53	Homo sapiens	34-37
24899917-1	2014	The latest experimental evidence indicates that acetylation of p53 at K164 (lysine 164) and K120 may induce directly cell apoptosis under severe DNA damage.	5,6-dihydrothymine	70-74	P53	Homo sapiens	63-66
24795076-2	2016	In our study, we examined the efficacy of p53 gene therapy in human breast carcinoma (MCF-7) cells using silica nanoparticles (SiNPs) supplemented with transferrin.	Silicon Dioxide	105-111	P53	Homo sapiens	42-45
24795076-9	2016	CONCLUSION: These results suggest that p53 gene therapy via transferrin-modified silica nanoparticles is an effective strategy for treatment of breast carcinoma.	Silicon Dioxide	81-87	P53	Homo sapiens	39-42
24184596-9	2014	Taken together, these findings suggest that vanillin protects KSC from UVB irradiation and its effects may occur through the suppression of downstream step of MDM2 in UVB irradiation-induced p53 activation.	kappa-selenocarrageenan	62-65	P53	Homo sapiens	191-194
26812881-0	2016	Hydroxyurea synergizes with valproic acid in wild-type p53 acute myeloid leukaemia.	Hydroxyurea	0-11	P53	Homo sapiens	55-58
26521020-7	2016	Further, 0.45 and 4.5 muM of violacein increased apoptotic genes, such as Bax, p53, caspase 3, Fas, FADD and markedly reduced Bcl-2 and MDM2 expression levels to two fold when compared to control.	violacein	29-38	P53	Homo sapiens	79-82
26521020-10	2016	In conclusion, lower dose of violacein treatment induced apoptosis in human breast cancer MCF-7 cells through TNF-alpha and p53 dependent mitochondrial pathways.	violacein	29-38	P53	Homo sapiens	124-127
26585176-4	2016	In silico studies also performed to predict the binding mechanism of DHMA with MDM2-p53 protein.	dhma	69-73	P53	Homo sapiens	84-87
27750242-6	2016	For example, specific TP53 mutations frequently induced by aflatoxin B1 exposure might affect histone modifiers and nucleosome remodelers.	Aflatoxin B1	59-71	P53	Homo sapiens	22-26
26738694-0	2016	Effect of p53 Arg72Pro polymorphism on the induction of micronucleus by aflatoxin B1 in in vitro in human blood lymphocytes.	Aflatoxin B1	72-84	P53	Homo sapiens	10-13
26738694-3	2016	The aim of this study is to investigate association between p53 Arg72Pro polymorphism and the frequencies of spontaneous and AFB1-induced DNA damage in peripheral blood lymphocytes from 100 healthy individuals in Turkish population.	Aflatoxin B1	125-129	P53	Homo sapiens	60-63
26738694-7	2016	Moreover, genotype analysis revealed a statistically significant association between Pro/Pro genotype of p53 Arg72Pro polymorphism and increased frequencies of MN both spontaneous and AFB1-induced cultures when compared Arg/Arg genotype (0.69 +- 0.19 versus 0.46 +- 0.13, p &lt; 0.001; 1.59 +- 0.65 versus 1.01 +- 0.41 p &lt; 0.001; respectively).	Aflatoxin B1	184-188	P53	Homo sapiens	105-108
24128664-5	2014	When exposed to staurosporine, fibroblasts from patients also showed higher caspase-3 activity; a higher percentage of cells with translocated phosphatidylserine and condensed chromatin; and higher p53 expression compared to fibroblasts from controls.	Staurosporine	16-29	P53	Homo sapiens	198-201
24056736-3	2014	We exploited this system to examine select post-translational modifications (PTMs) present on a transcriptionally inert population of endogenous human p53, as well as on p53 activated in response to etoposide treatment of normal human fibroblasts.	Etoposide	199-208	P53	Homo sapiens	170-173
24056736-7	2014	Despite the differences in activity, including greater in vitro sequence-specific DNA binding activity exhibited by p53 isolated from etoposide-treated cells, few differences were observed in the location, nature, or relative frequencies of PTMs on the two populations of human p53.	Etoposide	134-143	P53	Homo sapiens	116-119
26738694-8	2016	Our data indicate that p53 Arg72Pro polymorphism plays a significant role in human sensitivity to the genotoxic effects of AFB1.	Aflatoxin B1	123-127	P53	Homo sapiens	23-26
26675484-10	2015	PS alone induced differentiation and expression of p21WAF1/CIP1 and p53 and decreased CHK1 in all three cell lines, with almost no further effect when combined with erlotinib.	Phosphorus	0-2	P53	Homo sapiens	68-71
26585176-8	2016	DHMA significantly increased the expression of anti-apoptotic protein such as p53, p21, Bax, and caspase-3 but downregulated the expression of NF-kappaB in NCI-H460 cell line.	dhma	0-4	P53	Homo sapiens	78-81
26585176-9	2016	In silico studies demonstrate that DHMA formed hydrogen bond interaction with key residues Trp26, Phe55 and Lys24 by which it disrupt the binding of p53 with MDM2 receptor.	dhma	35-39	P53	Homo sapiens	149-152
26585176-10	2016	These findings suggested that DHMA induces apoptosis in NCI-H460 via a p53-dependent pathway.	dhma	30-34	P53	Homo sapiens	71-74
26250460-0	2016	CP-31398 inhibits the growth of p53-mutated liver cancer cells in vitro and in vivo.	CP 31398	0-8	P53	Homo sapiens	32-35
26250460-2	2016	Previous studies demonstrated that CP-31398 restored the native conformation of mutant p53 and trans-activated p53 downstream genes in tumor cells.	CP 31398	35-43	P53	Homo sapiens	87-90
26250460-2	2016	Previous studies demonstrated that CP-31398 restored the native conformation of mutant p53 and trans-activated p53 downstream genes in tumor cells.	CP 31398	35-43	P53	Homo sapiens	111-114
26250460-4	2016	Here, we investigated the effects of CP-31398 on the phenotype of HCC cells carrying p53 mutation.	CP 31398	37-45	P53	Homo sapiens	85-88
26250460-5	2016	The effects of CP-31398 on the characteristic of p53-mutated HCC cells were evaluated through analyzing cell cycle, cell apoptosis, cell proliferation, and the expression of p53 downstream genes.	CP 31398	15-23	P53	Homo sapiens	49-52
26250460-6	2016	In tumor xenografts developed by PLC/PRF/5 cells, the inhibition of tumor growth by CP-31398 was analyzed through gross morphology, growth curve, and the expression of p53-related genes.	CP 31398	84-92	P53	Homo sapiens	168-171
26250460-7	2016	Firstly, we demonstrated that CP-31398 inhibited the growth of p53-mutated liver cancer cells in a dose-dependent and p53-dependent manner.	CP 31398	30-38	P53	Homo sapiens	63-66
26250460-7	2016	Firstly, we demonstrated that CP-31398 inhibited the growth of p53-mutated liver cancer cells in a dose-dependent and p53-dependent manner.	CP 31398	30-38	P53	Homo sapiens	118-121
26250460-8	2016	Then, further study showed that CP-31398 re-activated wild-type p53 function in p53-mutated HCC cells, which resulted in inhibitive response of cell proliferation and an induction of cell-cycle arrest and apoptosis.	CP 31398	32-40	P53	Homo sapiens	64-67
26250460-8	2016	Then, further study showed that CP-31398 re-activated wild-type p53 function in p53-mutated HCC cells, which resulted in inhibitive response of cell proliferation and an induction of cell-cycle arrest and apoptosis.	CP 31398	32-40	P53	Homo sapiens	80-83
26250460-9	2016	Finally, in vivo data confirmed that CP-31398 blocked the growth of xenografts tumors through transactivation of p53-responsive downstream molecules.	CP 31398	37-45	P53	Homo sapiens	113-116
26250460-10	2016	Our results demonstrated that CP-31398 induced desired phenotypic change of p53-mutated HCC cells in vitro and in vivo, which revealed that CP-31398 would be developed as a therapeutic candidate for HCC carrying p53 mutation.	CP 31398	30-38	P53	Homo sapiens	76-79
26250460-10	2016	Our results demonstrated that CP-31398 induced desired phenotypic change of p53-mutated HCC cells in vitro and in vivo, which revealed that CP-31398 would be developed as a therapeutic candidate for HCC carrying p53 mutation.	CP 31398	30-38	P53	Homo sapiens	212-215
26250460-10	2016	Our results demonstrated that CP-31398 induced desired phenotypic change of p53-mutated HCC cells in vitro and in vivo, which revealed that CP-31398 would be developed as a therapeutic candidate for HCC carrying p53 mutation.	CP 31398	140-148	P53	Homo sapiens	76-79
26250460-10	2016	Our results demonstrated that CP-31398 induced desired phenotypic change of p53-mutated HCC cells in vitro and in vivo, which revealed that CP-31398 would be developed as a therapeutic candidate for HCC carrying p53 mutation.	CP 31398	140-148	P53	Homo sapiens	212-215
26641105-2	2015	Site-specific synthesis of the C8-dG-ABA adduct in the oligodeoxynucleotide 5"-d(GTGCXTGTTTGT)-3":5"-d(ACAAACACGCAC)-3"; X = C8-dG-ABA adduct, including codons 272-275 of the p53 gene, has allowed for investigation into the structural and thermodynamic properties of this adduct.	Oligodeoxyribonucleotides	55-75	P53	Homo sapiens	175-178
26555243-5	2015	Furthermore, 11c simultaneously increased the acetylation of histone H3 and alpha-tubulin, enhanced expression of DNA damage markers histone H2AX phosphorylation and p-p53 (Ser15), and activated p53 signaling pathway in HCT116 cells.	Carbon-11	13-16	P53	Homo sapiens	168-171
26555243-5	2015	Furthermore, 11c simultaneously increased the acetylation of histone H3 and alpha-tubulin, enhanced expression of DNA damage markers histone H2AX phosphorylation and p-p53 (Ser15), and activated p53 signaling pathway in HCT116 cells.	Carbon-11	13-16	P53	Homo sapiens	195-198
26843455-6	2015	Using Western blot analysis, we found that Gaillardin upregulated the pro-apoptotic protein Bax and p53 and downregulated the anti-apoptotic protein Bcl-2.	gaillardin	43-53	P53	Homo sapiens	100-103
26354682-0	2015	Hypoxia Promotes Synergy between Mitomycin C and Bortezomib through a Coordinated Process of Bcl-xL Phosphorylation and Mitochondrial Translocation of p53.	Mitomycin	33-44	P53	Homo sapiens	151-154
26512780-9	2015	Furthermore, the combination of fatostatin and docetaxel resulted in greater proliferation inhibition and apoptosis induction compared with single agent treatment in PCa cells in vitro and in vivo, especially those with mutant p53s.	fatostatin	32-42	P53	Homo sapiens	227-230
26512780-10	2015	These data suggest for the first time that fatostatin alone or in combination with docetaxel could be exploited as a novel and promising therapy for metastatic PCa harboring p53 mutations.	fatostatin	43-53	P53	Homo sapiens	174-177
26453893-0	2015	Olaquindox induces DNA damage via the lysosomal and mitochondrial pathway involving ROS production and p53 activation in HEK293 cells.	olaquindox	0-10	P53	Homo sapiens	103-106
26453893-6	2015	The expression of p53 protein is increased in cells incubated with OLA.	olaquindox	67-70	P53	Homo sapiens	18-21
26453893-7	2015	The activation of p53 and ATM gene was assessed by exposure to OLA.	olaquindox	63-66	P53	Homo sapiens	18-21
26453893-9	2015	And desipramine significantly decreased AO fluorescence intensity and the expression of the p53 protein and gene.	Desipramine	4-15	P53	Homo sapiens	92-95
26453893-10	2015	These results support the assumption that OLA exerted genotoxic effects and induced DNA strand breaks in HEK293 cells, possibly through lysosomal-mitochondrial pathway involving ROS production and p53 activation.	olaquindox	42-45	P53	Homo sapiens	197-200
26517117-4	2015	Antroquinonol decreases anti-apoptotic proteins, whereas it increases p53 and pro-apoptotic proteins.	antroquinonol	0-13	P53	Homo sapiens	70-73
26431163-6	2015	We pretreated such cells with Nutlin-3a, a prototype inhibitor of the p53-antagonist Mdm2.	nutlin 3	30-39	P53	Homo sapiens	70-73
26469967-13	2015	Our results also suggest that genistein may be an effective agent for overcoming chemoresistance in cancers with dysfunctional Bax and p53.	Genistein	30-39	P53	Homo sapiens	135-138
26722448-8	2015	On the other hand, mefloquine treatment promoted the expression of p21WAF1/CIP1 and p53 at 40 muM concentration after 48 h. Therefore, mefloquine inhibits proliferation and induces cell cycle arrest in chondrocytes.	Mefloquine	19-29	P53	Homo sapiens	84-87
26722448-8	2015	On the other hand, mefloquine treatment promoted the expression of p21WAF1/CIP1 and p53 at 40 muM concentration after 48 h. Therefore, mefloquine inhibits proliferation and induces cell cycle arrest in chondrocytes.	Mefloquine	135-145	P53	Homo sapiens	84-87
24798859-8	2015	We found that (-)-epigallocatechin-3-gallate (EGCG), a constituent of green tea and a major component of the botanical drug Polyphenon  E, reduced the expression of four p53-targeting miRNAs, including miR-25, miR-92, miR-141, and miR-200a.	epigallocatechin gallate	14-44	P53	Homo sapiens	170-173
24798859-8	2015	We found that (-)-epigallocatechin-3-gallate (EGCG), a constituent of green tea and a major component of the botanical drug Polyphenon  E, reduced the expression of four p53-targeting miRNAs, including miR-25, miR-92, miR-141, and miR-200a.	epigallocatechin gallate	46-50	P53	Homo sapiens	170-173
26061814-3	2015	By repressing the expression of stearoyl-CoA desaturase 1, SCD, the enzyme that converts saturated to mono-unsaturated fatty acids, p53 causes a shift in the content of phospholipids with mono-unsaturated acyl chains towards more saturated phospholipid species, particularly of the phosphatidylinositol headgroup class.	Phosphatidylinositols	282-302	P53	Homo sapiens	132-135
25995247-3	2015	Oncomine data analysis of normal versus HCC tumors with the CHC background indicated a 4-fold increase in FBP1 expression with a concomitant 2.5-fold decrease in the expression of p53.	oncomine	0-8	P53	Homo sapiens	180-183
25954860-5	2015	It has been demonstrated that most chemotherapy drugs exert their anti-cancer effects via p53-mediated apoptosis, and in accordance, with this, the present study showed that treatment with etoposide significantly increased p53 levels.	Etoposide	189-198	P53	Homo sapiens	90-93
25954860-5	2015	It has been demonstrated that most chemotherapy drugs exert their anti-cancer effects via p53-mediated apoptosis, and in accordance, with this, the present study showed that treatment with etoposide significantly increased p53 levels.	Etoposide	189-198	P53	Homo sapiens	223-226
25954860-7	2015	This was further verified in CCRCC tissue specimens from patients The results of the present study suggested that loss of PTEN, which deactivated Akt/HDM2 signaling followed by degradation of p53, may contribute to the development of etoposide resistance in CCRCC.	Etoposide	234-243	P53	Homo sapiens	192-195
25964101-7	2015	In ovarian cancer cells, where &gt;90% have inactivated p53, Nutlin combined with the genotoxic agents, cisplatin or etoposide, had a cooperative lethal effect resulting in increased DNA damage and apoptosis.	Etoposide	117-126	P53	Homo sapiens	56-59
25792665-4	2015	Impaired mitophagy was attributed to reduced Parkin translocation to damaged mitochondria, which was due to CS-induced cytoplasmic p53 accumulation and its interaction with Parkin.	Cesium	108-110	P53	Homo sapiens	131-134
26077467-4	2015	Genetic deletion of PDCD5 abrogates etoposide (ET)-induced p53 stabilization and HDAC3 cleavage, indicating an essential role of PDCD5 in p53 activation.	Etoposide	36-45	P53	Homo sapiens	59-62
26077467-4	2015	Genetic deletion of PDCD5 abrogates etoposide (ET)-induced p53 stabilization and HDAC3 cleavage, indicating an essential role of PDCD5 in p53 activation.	Etoposide	36-45	P53	Homo sapiens	138-141
26077467-4	2015	Genetic deletion of PDCD5 abrogates etoposide (ET)-induced p53 stabilization and HDAC3 cleavage, indicating an essential role of PDCD5 in p53 activation.	Etoposide	47-49	P53	Homo sapiens	59-62
26077467-4	2015	Genetic deletion of PDCD5 abrogates etoposide (ET)-induced p53 stabilization and HDAC3 cleavage, indicating an essential role of PDCD5 in p53 activation.	Etoposide	47-49	P53	Homo sapiens	138-141
24379680-2	2013	Introduction of T-oligo, an eleven-base oligonucleotide homologous to the 3"-telomeric overhang, mimics telomere disruption and induces DNA damage responses through activation of p53, p73, p95/Nbs1, E2F1, pRb, and other DNA damage response proteins.	t-oligo	16-23	P53	Homo sapiens	179-182
24219989-2	2013	For example, activation of p53 by genotoxic agents, such as camptothecin (CPT), triggers apoptosis, while non-genotoxic activation of p53 by Nutlin-3 (Nut3) leads to cell-cycle arrest without significant apoptosis.	Camptothecin	60-72	P53	Homo sapiens	27-30
24219989-2	2013	For example, activation of p53 by genotoxic agents, such as camptothecin (CPT), triggers apoptosis, while non-genotoxic activation of p53 by Nutlin-3 (Nut3) leads to cell-cycle arrest without significant apoptosis.	Camptothecin	74-77	P53	Homo sapiens	27-30
24090840-4	2013	At low level of ZnO NMs induced ROS, p53 triggers expression of antioxidant genes such as SOD2, GPX1, SESN1, SESN2 and ALDH4A1 to restore oxidative homeostasis while at high concentration of ZnO NMs, the elevated level of intracellular ROS activated the apoptotic pathway through p53.	Zinc Oxide	16-19	P53	Homo sapiens	37-40
24090840-4	2013	At low level of ZnO NMs induced ROS, p53 triggers expression of antioxidant genes such as SOD2, GPX1, SESN1, SESN2 and ALDH4A1 to restore oxidative homeostasis while at high concentration of ZnO NMs, the elevated level of intracellular ROS activated the apoptotic pathway through p53.	Zinc Oxide	16-19	P53	Homo sapiens	280-283
24090840-4	2013	At low level of ZnO NMs induced ROS, p53 triggers expression of antioxidant genes such as SOD2, GPX1, SESN1, SESN2 and ALDH4A1 to restore oxidative homeostasis while at high concentration of ZnO NMs, the elevated level of intracellular ROS activated the apoptotic pathway through p53.	Zinc Oxide	191-194	P53	Homo sapiens	37-40
24090840-5	2013	The implication of our finding that p53 can function as an important regulator in determining ZnO induced cytotoxicity is highlighted by the differential action of ZnO on p53 deficient and proficient colorectal cell lines.	Zinc Oxide	94-97	P53	Homo sapiens	36-39
24090840-5	2013	The implication of our finding that p53 can function as an important regulator in determining ZnO induced cytotoxicity is highlighted by the differential action of ZnO on p53 deficient and proficient colorectal cell lines.	Zinc Oxide	164-167	P53	Homo sapiens	36-39
24090840-5	2013	The implication of our finding that p53 can function as an important regulator in determining ZnO induced cytotoxicity is highlighted by the differential action of ZnO on p53 deficient and proficient colorectal cell lines.	Zinc Oxide	164-167	P53	Homo sapiens	171-174
24090840-6	2013	p53 deficient cells cancer cells such as DLD-1 and SW480 are more susceptible to ZnO induced cell death compared to p53 proficient cells such as colon epithelial cells NCM460 and HCT116 cells in a ROS dependent manner.	Zinc Oxide	81-84	P53	Homo sapiens	0-3
24119020-3	2013	Additionally, by using the known inhibitor of p53-MDMX interaction, SJ-172550, the efficacy of a simplified yeast-based screening assay to search for inhibitors of p53-MDMX interaction is demonstrated for the first time.	SJ 172550	68-77	P53	Homo sapiens	46-49
24119020-3	2013	Additionally, by using the known inhibitor of p53-MDMX interaction, SJ-172550, the efficacy of a simplified yeast-based screening assay to search for inhibitors of p53-MDMX interaction is demonstrated for the first time.	SJ 172550	68-77	P53	Homo sapiens	164-167
24183976-0	2013	HZ08 reverse the aneuploidy-induced cisplatin-resistance in Gastric cancer by modulating the p53 pathway.	hz08	0-4	P53	Homo sapiens	93-96
24127627-1	2013	Chiral nonracemic cis-4,5-bis(aryl)imidazolines have emerged as a powerful platform for the development of cancer chemotherapeutics, stimulated by the Hoffmann-La Roche discovery that Nutlin-3 can restore apoptosis in cells with wild-type p53.	nutlin 3	184-192	P53	Homo sapiens	239-242
24179522-3	2013	EGCG treatment induced apoptosis in the presence of wild-type and mutant p53, indicating that a p53-independent pathway may contribute to EGCG-induced apoptosis in these cells.	epigallocatechin gallate	0-4	P53	Homo sapiens	73-76
24179522-3	2013	EGCG treatment induced apoptosis in the presence of wild-type and mutant p53, indicating that a p53-independent pathway may contribute to EGCG-induced apoptosis in these cells.	epigallocatechin gallate	0-4	P53	Homo sapiens	96-99
24179522-3	2013	EGCG treatment induced apoptosis in the presence of wild-type and mutant p53, indicating that a p53-independent pathway may contribute to EGCG-induced apoptosis in these cells.	epigallocatechin gallate	138-142	P53	Homo sapiens	96-99
24179522-4	2013	EGCG showed migration-suppressing effects, suggesting that this activity may also have p53-dependent and -independent components.	epigallocatechin gallate	0-4	P53	Homo sapiens	87-90
24179522-5	2013	The interaction between p53 and VEGF in the EGCG-treated cells was investigated using pifithrin-alpha.	epigallocatechin gallate	44-48	P53	Homo sapiens	24-27
24179522-6	2013	Notably, the suppression of p53 activity blocked the ability of EGCG to inhibit VEGF and MMP-9 in the cells expressing wild-type p53, but not mutant p53, indicating that the effects of EGCG on VEGF may be p53-dependent or -independent.	epigallocatechin gallate	64-68	P53	Homo sapiens	28-31
24179522-6	2013	Notably, the suppression of p53 activity blocked the ability of EGCG to inhibit VEGF and MMP-9 in the cells expressing wild-type p53, but not mutant p53, indicating that the effects of EGCG on VEGF may be p53-dependent or -independent.	epigallocatechin gallate	64-68	P53	Homo sapiens	129-132
24179522-6	2013	Notably, the suppression of p53 activity blocked the ability of EGCG to inhibit VEGF and MMP-9 in the cells expressing wild-type p53, but not mutant p53, indicating that the effects of EGCG on VEGF may be p53-dependent or -independent.	epigallocatechin gallate	64-68	P53	Homo sapiens	129-132
24179522-6	2013	Notably, the suppression of p53 activity blocked the ability of EGCG to inhibit VEGF and MMP-9 in the cells expressing wild-type p53, but not mutant p53, indicating that the effects of EGCG on VEGF may be p53-dependent or -independent.	epigallocatechin gallate	64-68	P53	Homo sapiens	129-132
24179522-6	2013	Notably, the suppression of p53 activity blocked the ability of EGCG to inhibit VEGF and MMP-9 in the cells expressing wild-type p53, but not mutant p53, indicating that the effects of EGCG on VEGF may be p53-dependent or -independent.	epigallocatechin gallate	185-189	P53	Homo sapiens	28-31
24055188-7	2013	P53 expression was up-regulated by resveratrol and etoposide and pre-incubation of both cells with resveratrol increased levels of etoposide-induced p53 expression.	Etoposide	51-60	P53	Homo sapiens	0-3
24055188-7	2013	P53 expression was up-regulated by resveratrol and etoposide and pre-incubation of both cells with resveratrol increased levels of etoposide-induced p53 expression.	Etoposide	131-140	P53	Homo sapiens	0-3
24055188-7	2013	P53 expression was up-regulated by resveratrol and etoposide and pre-incubation of both cells with resveratrol increased levels of etoposide-induced p53 expression.	Etoposide	131-140	P53	Homo sapiens	149-152
24055188-9	2013	It seems that resveratrol exerts differential synergistic effect with etoposide on proliferation of cancer cells from different origin which is mainly accompanied by p53 activation.	Etoposide	70-79	P53	Homo sapiens	166-169
24065519-0	2013	EGCG suppresses Fused Toes Homolog protein through p53 in cervical cancer cells.	epigallocatechin gallate	0-4	P53	Homo sapiens	51-54
24065519-8	2013	p53 silencing increased the expression of FTS and also decreased the reduction in the levels of FTS expression after EGCG treatment.	epigallocatechin gallate	117-121	P53	Homo sapiens	0-3
24065519-10	2013	Collectively, these results conclude that EGCG induced anti-proliferative action in the cervical cancer cell involves reduced mRNA expression of FTS through p53.	epigallocatechin gallate	42-46	P53	Homo sapiens	157-160
23817390-0	2013	Ceragenin CSA-13 induces cell cycle arrest and antiproliferative effects in wild-type and p53 null mutant HCT116 colon cancer cells.	Ceragenin CSA-13	10-16	P53	Homo sapiens	90-93
23817390-7	2013	Furthermore, cell cycle analysis showed that the cell cycle of CSA-13-treated wild-type and p53 null mutant HCT116 cells was arrested at the G1/S phase, indicating that CSA-13 affects the cell cycle by a p53-independent pathway.	Ceragenin CSA-13	63-69	P53	Homo sapiens	92-95
23817390-7	2013	Furthermore, cell cycle analysis showed that the cell cycle of CSA-13-treated wild-type and p53 null mutant HCT116 cells was arrested at the G1/S phase, indicating that CSA-13 affects the cell cycle by a p53-independent pathway.	Ceragenin CSA-13	63-69	P53	Homo sapiens	204-207
23817390-7	2013	Furthermore, cell cycle analysis showed that the cell cycle of CSA-13-treated wild-type and p53 null mutant HCT116 cells was arrested at the G1/S phase, indicating that CSA-13 affects the cell cycle by a p53-independent pathway.	Ceragenin CSA-13	169-175	P53	Homo sapiens	92-95
23881456-4	2013	Treatment with cudraflavone B triggered the mitochondrial apoptotic pathway (indicated by induction of the proapoptotic protein p53 and the p21 and p27 effector proteins), downregulation of cell cycle regulatory proteins (e.g., p-Rb, changing Bax/Bcl-2 ratios, cytochrome-c release), and caspase-3 activation.	cudraflavone B	15-29	P53	Homo sapiens	128-131
23881456-6	2013	SIRT1 activator, resveratrol, dose-dependently attenuated the growth-inhibitory and apoptosis-inducing effect of cudraflavone B and blocked cudraflavone B-induced regulatory protein expressions in the mitochondrial pathway such as p53, p21, p27, Bax, caspase-3, and cytochrome-c. Conversely, treatment with SIRT1 inhibitor sirtinol caused opposite effects.	cudraflavone B	113-127	P53	Homo sapiens	231-234
23977108-7	2013	Treatment of SK-N-DZ with PCI-24781 also induced cell cycle arrest in G2/M phase and activated apoptosis signaling pathways via the up-regulation of DR4, p21, p53 and caspase 3.	abexinostat	26-35	P53	Homo sapiens	159-162
23812671-8	2013	Suppression of p53 in melanoma cells abrogated Nt-3"s effects fully and vemurafenib"s effects partially.	nutlin 3	47-51	P53	Homo sapiens	15-18
23524907-2	2013	Preclinical studies suggest functional interactions between p53 and the BAF250a protein, the product of a tumor suppressor gene ARID1A (adenine-thymine (AT)-rich interactive domain containing protein 1A) that is frequently mutated in ovarian clear cell carcinoma.	adenine-thymine	136-151	P53	Homo sapiens	60-63
23474493-5	2013	CBX8 cooperated with SIRT1 for suppressing p53 acetylation induced by Sirtinol and etoposide/TSA.	sirtinol	70-78	P53	Homo sapiens	43-46
23474493-5	2013	CBX8 cooperated with SIRT1 for suppressing p53 acetylation induced by Sirtinol and etoposide/TSA.	Etoposide	83-92	P53	Homo sapiens	43-46
23474493-5	2013	CBX8 cooperated with SIRT1 for suppressing p53 acetylation induced by Sirtinol and etoposide/TSA.	trichostatin A	93-96	P53	Homo sapiens	43-46
23796712-3	2013	p53 has been emphasized as a metabolic regulator involved in glucose, glutamine, and purine metabolism.	Glutamine	70-79	P53	Homo sapiens	0-3
23758695-10	2013	Our data also suggested that inhibition of pAkt and activation of p53 pathway are the main molecular events involved in inhibitory effects of TSA.	trichostatin A	142-145	P53	Homo sapiens	66-69
23700428-7	2013	Mechanistically, FK-16 activated nuclear p53 to upregulate Bax and downregulate Bcl-2.	fk-16	17-22	P53	Homo sapiens	41-44
23700428-8	2013	Knockdown of p53, genetic ablation of Bax, or overexpression of Bcl-2 reversed FK-16-induced apoptosis and autophagy.	fk-16	79-84	P53	Homo sapiens	13-16
23700428-10	2013	Collectively, FK-16 induces caspase-independent apoptosis and autophagy through the common p53-Bcl-2/Bax cascade in colon cancer cells.	fk-16	14-19	P53	Homo sapiens	91-94
23536184-8	2013	Treatment with camptothecin, a topoisomerase I inhibitor, caused normal cells to down-regulate H2AX and become quiescent, a process mediated by both Arf and p53.	Camptothecin	15-27	P53	Homo sapiens	157-160
23545901-7	2013	In addition, p53 activity was validated with UV irradiation and siGABARBP.	sigabarbp	64-73	P53	Homo sapiens	13-16
25772545-0	2015	A novel dithiocarbamate derivative induces cell apoptosis through p53-dependent intrinsic pathway and suppresses the expression of the E6 oncogene of human papillomavirus 18 in HeLa cells.	Dithiocarbamate	8-23	P53	Homo sapiens	66-69
26024660-5	2015	Salinomycin induced p53 translocation to mitochondria, where it formed a complex with cyclophilin-D (CyPD).	salinomycin	0-11	P53	Homo sapiens	20-23
26024660-8	2015	Meanwhile, p53 stable knockdown alleviated salinomycin-induced necrosis in glioma cells.	salinomycin	43-54	P53	Homo sapiens	11-14
26024660-9	2015	Reactive oxygen species (ROS) production was required for salinomycin-induced p53 mitochondrial translocation, mPTP opening and necrosis, and anti-oxidants n-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) inhibited p53 translocation, mPTP opening and glioma cell death.	salinomycin	58-69	P53	Homo sapiens	78-81
26024660-9	2015	Reactive oxygen species (ROS) production was required for salinomycin-induced p53 mitochondrial translocation, mPTP opening and necrosis, and anti-oxidants n-acetylcysteine (NAC) and pyrrolidine dithiocarbamate (PDTC) inhibited p53 translocation, mPTP opening and glioma cell death.	salinomycin	58-69	P53	Homo sapiens	228-231
25724269-5	2015	Interestingly, selective inhibition of PP2A, by Okadaic acid at 5 nM, restored insulin induced phosphorylation of AKT, FOXO1, SIRT1 activity and p53 degradation.	Okadaic Acid	48-60	P53	Homo sapiens	145-148
25713207-8	2015	Finally, chromatin immunoprecipitation assays demonstrated p53 recruitment to the UGT2B7 p53 site upon exposure to mitomycin C, the most potent UGT2B7 inducer among the nine tested drugs.	Mitomycin	115-126	P53	Homo sapiens	59-62
25713207-8	2015	Finally, chromatin immunoprecipitation assays demonstrated p53 recruitment to the UGT2B7 p53 site upon exposure to mitomycin C, the most potent UGT2B7 inducer among the nine tested drugs.	Mitomycin	115-126	P53	Homo sapiens	89-92
24736102-10	2015	Finally, a R249S mutation of TP53, well-known hallmark of aflatoxin B1 exposure, was found.	Aflatoxin B1	58-70	P53	Homo sapiens	29-33
22290509-11	2013	We conclude that p53 independent apoptosis induced by combining curcumin and TSA involves JNK activation.	trichostatin A	77-80	P53	Homo sapiens	17-20
26475964-0	2015	Enhanced cytotoxicity of prenylated chalcone against tumour cells via disruption of the p53-MDM2 interaction.	Chalcone	36-44	P53	Homo sapiens	88-91
23483203-0	2013	Epigallocatechin gallate promotes p53 accumulation and activity via the inhibition of MDM2-mediated p53 ubiquitination in human lung cancer cells.	epigallocatechin gallate	0-24	P53	Homo sapiens	34-37
23483203-0	2013	Epigallocatechin gallate promotes p53 accumulation and activity via the inhibition of MDM2-mediated p53 ubiquitination in human lung cancer cells.	epigallocatechin gallate	0-24	P53	Homo sapiens	100-103
23483203-2	2013	Several studies have shown that p53 plays an important role in the activity of EGCG; however, the mechanism by which EGCG regulates p53 requires further investigation.	epigallocatechin gallate	79-83	P53	Homo sapiens	32-35
23483203-2	2013	Several studies have shown that p53 plays an important role in the activity of EGCG; however, the mechanism by which EGCG regulates p53 requires further investigation.	epigallocatechin gallate	117-121	P53	Homo sapiens	132-135
23483203-3	2013	In the present study, we showed that EGCG inhibits anchorage-independent growth of human lung cancer cells by upregulating p53 expression.	epigallocatechin gallate	37-41	P53	Homo sapiens	123-126
25898313-6	2015	The combined therapy with ISA27 produced a synergic effect on the inhibition of cell viability and on the reactivation of p53 pathway.	isa27	26-31	P53	Homo sapiens	122-125
25633416-9	2015	FOXM1 effector genes such as CDK4, p53 and cyclin D1 were downregulated in gastric cancer cells by combination treatment with DIM and paclitaxel.	3,3'-diindolylmethane	126-129	P53	Homo sapiens	35-38
23483203-4	2013	EGCG treatment can substantially increase p53 stability, promote nuclear localization of p53 and decrease nuclear accumulation of MDM2.	epigallocatechin gallate	0-4	P53	Homo sapiens	42-45
26446704-4	2015	The results of the present study showed that PKR can be specifically activated in PKR overexpressing beta-cells by a low dosage of the previously synthesized compound 1H-benzimidazole1-ethanol,2,3-dihydro-2-imino-a-(phenoxymethyl)-3-(phenylmethyl)-,monohydrochloride (BEPP), and this led to upregulation of P53 through sumoylation-dependent stability.	1h-benzimidazole1-ethanol	167-192	P53	Homo sapiens	307-310
23483203-4	2013	EGCG treatment can substantially increase p53 stability, promote nuclear localization of p53 and decrease nuclear accumulation of MDM2.	epigallocatechin gallate	0-4	P53	Homo sapiens	89-92
23483203-5	2013	We also found that EGCG increases the phosphorylation of p53 at Ser15 and Ser20 and enhances its transcriptional activity.	epigallocatechin gallate	19-23	P53	Homo sapiens	57-60
23483203-6	2013	Although EGCG promotes MDM2 expression in a p53-dependent manner, the interaction between MDM2 and p53 was significantly inhibited following EGCG treatment, which resulted in the inhibition of MDM2-mediated p53 ubiquitination.	epigallocatechin gallate	9-13	P53	Homo sapiens	44-47
25948191-0	2015	[2-methoxyestradiol induced apoptosis and expression of p53 gene in human acute T lymphoblastic leukemia cells].	2-Methoxyestradiol	1-19	P53	Homo sapiens	56-59
23266469-0	2013	Celastrol suppresses breast cancer MCF-7 cell viability via the AMP-activated protein kinase (AMPK)-induced p53-polo like kinase 2 (PLK-2) pathway.	celastrol	0-9	P53	Homo sapiens	108-111
26459497-6	2015	The results indicated that TAS9 inhibited SMMC-7721 cell growth by downregulating the signaling molecules protein kinase Cbeta (PKCbeta), Akt, mammalian target of rapamycin, mitogen-activated protein kinase kinase 2, RAF and c-Jun N-terminal kinase-1, and inhibiting SMMC-7721 cell migration by suppressing the expression of matrix metalloproteinase (MMP)-2, MMP-9, chemokine (C-X-C motif) receptor 4, nuclear factor kappaB, p38 and p53.	tas9	27-31	P53	Homo sapiens	433-436
23266469-5	2013	In addition, celastrol increased phosphorylation of the pro-apoptotic effector, p53.	celastrol	13-22	P53	Homo sapiens	80-83
23266469-6	2013	Inhibition of AMPK blocked celastrol-mediated p53 phosphorylation.	celastrol	27-36	P53	Homo sapiens	46-49
25568206-9	2015	However, expression of these genes did not attain the levels observed when p53 was activated in response to etoposide treatment and remained lower than those measured in mock-infected cells.	Etoposide	108-117	P53	Homo sapiens	75-78
26259609-0	2015	Etoposide Induces Necrosis Through p53-Mediated Antiapoptosis in Human Kidney Proximal Tubule Cells.	Etoposide	0-9	P53	Homo sapiens	35-38
25381309-5	2015	Using the differential expression analysis, we observed a significant (P &lt; 0.05) dose-dependent (10, 20 and 40 microg/ml for 6h) increase in the expression of tumour suppressor protein p53 (40, 60 and 110%); Ras p21 (30, 52 and 80%); c-Jun N-terminal kinases; JNKs) (28, 47 and 78%) in lung cancer patient samples treated with ZnO ENPs compared to healthy controls.	Zinc Oxide	330-333	P53	Homo sapiens	188-191
25381309-6	2015	A similar trend was also seen in COPD patient samples where a significant (P &lt; 0.05) dose-dependent increase in the expression of tumour suppressor protein p53 (26, 45 and 84%), Ras p21 (21, 40 and 77%), JNKs (17, 32 and 69%) was observed after 6h of ZnO ENPs treatment at the aforesaid concentrations.	Zinc Oxide	254-257	P53	Homo sapiens	159-162
23266469-7	2013	Moreover, celastrol increased the expression of tumor suppressor polo like kinase-2 (PLK-2) in a p53-dependent manner.	celastrol	10-19	P53	Homo sapiens	97-100
23266469-10	2013	Together, these results suggest that celastrol may have anti-tumor effects on MCF-7 cells via AMPK-induced p53 and PLK-2 pathways.	celastrol	37-46	P53	Homo sapiens	107-110
23398638-7	2013	The role of MDM2 binding was explored by inhibiting MDM2/p53 binding with nutlin-3.	nutlin 3	74-82	P53	Homo sapiens	57-60
26259609-7	2015	Thus, our study demonstrated that p53 protects against apoptosis, and leads to etoposide-induced necrosis.	Etoposide	79-88	P53	Homo sapiens	34-37
26408703-0	2015	Synthetic Bichalcone TSWU-BR23 Induces Apoptosis of Human Colon Cancer HT-29 Cells by p53-Mediated Mitochondrial Oligomerization of BAX/BAK and Lipid Raft Localization of CD95/FADD.	rhuschalcone-1	10-20	P53	Homo sapiens	86-89
23313858-7	2013	Interestingly, silencing of Sirt1 significantly enhances sensitivity of porcine preadipocytes to camptothecin, which may be due to upregulation of p53, acetylated p53, Bax, cleaved caspase-3 and downregulation of Bcl-2.	Camptothecin	97-109	P53	Homo sapiens	147-150
23313858-7	2013	Interestingly, silencing of Sirt1 significantly enhances sensitivity of porcine preadipocytes to camptothecin, which may be due to upregulation of p53, acetylated p53, Bax, cleaved caspase-3 and downregulation of Bcl-2.	Camptothecin	97-109	P53	Homo sapiens	163-166
25663867-0	2015	Liriodenine induces the apoptosis of human laryngocarcinoma cells via the upregulation of p53 expression.	liriodenine	0-11	P53	Homo sapiens	90-93
25663867-8	2015	The potential mechanism underlying the antitumor effects of liriodenine may result from an upregulative effect upon p53 expression, which ultimately induces cellular apoptosis.	liriodenine	60-71	P53	Homo sapiens	116-119
25663867-9	2015	By contrast, the downregulation of p53 significantly reduced the antitumor effects of liriodenine.	liriodenine	86-97	P53	Homo sapiens	35-38
25663867-10	2015	Together, these results suggest that liriodenine exhibits potent antitumor activities in laryngocarcinoma HEp-2 cells, in vitro and in vivo, via the upregulation of p53 expression.	liriodenine	37-48	P53	Homo sapiens	165-168
25623255-0	2015	Bone marrow stroma-derived PGE2 protects BCP-ALL cells from DNA damage-induced p53 accumulation and cell death.	bcp	41-44	P53	Homo sapiens	79-82
26189498-4	2015	We then synthesized stapled p53 mimetic analogues using pure hydrocarbon linkers and demonstrated their abilities to block the p53-MDM2 interaction and selectively kill p53 wild-type colorectal carcinoma HCT-116 cells but not p53 null cells.	Hydrocarbons	61-72	P53	Homo sapiens	28-31
25448276-8	2015	Finally, the effect of CHK1 inhibition on SM toxicity was much more marked in cells with non-functional p53.	Mustard Gas	42-44	P53	Homo sapiens	104-107
23187459-3	2013	Combined treatment with nutlin-3 and TRAIL markedly induces apoptosis in HCT116 cells (p53 wild type), but not in HCT116 p53-/- cells, suggesting that p53 is critical for the sensitizing effect of nutlin-3 on TRAIL-induced apoptosis.	nutlin 3	24-32	P53	Homo sapiens	87-90
23246812-0	2013	Functional characterisation of p53 mutants identified in breast cancers with suboptimal responses to anthracyclines or mitomycin.	Mitomycin	119-128	P53	Homo sapiens	31-34
23246812-2	2013	TP53 mutations, in particular those affecting the L2/L3 domains, are associated with resistance to anthracycline or mitomycin treatment in breast cancer patients.	Mitomycin	116-125	P53	Homo sapiens	0-4
26032169-0	2015	Genistein induces apoptosis by stabilizing intracellular p53 protein through an APE1-mediated pathway.	Genistein	0-9	P53	Homo sapiens	57-60
23161404-3	2013	In this study, we demonstrated that lithium and SB216763, which are pharmacological inhibitors of GSK3, attenuated p53 accumulation and caspase-3 activation, as shown by PARP cleavage induced by the DNA-damaging agents doxorubicin, etoposide and camptothecin.	SB 216763	48-56	P53	Homo sapiens	115-118
23161404-3	2013	In this study, we demonstrated that lithium and SB216763, which are pharmacological inhibitors of GSK3, attenuated p53 accumulation and caspase-3 activation, as shown by PARP cleavage induced by the DNA-damaging agents doxorubicin, etoposide and camptothecin.	Etoposide	232-241	P53	Homo sapiens	115-118
23161404-3	2013	In this study, we demonstrated that lithium and SB216763, which are pharmacological inhibitors of GSK3, attenuated p53 accumulation and caspase-3 activation, as shown by PARP cleavage induced by the DNA-damaging agents doxorubicin, etoposide and camptothecin.	Camptothecin	246-258	P53	Homo sapiens	115-118
23161404-7	2013	GSK3 inhibition also reduced the phosphorylation of wild-type p53 at serine 33, which is induced by doxorubicin, etoposide and camptothecin in the mitochondria.	Etoposide	113-122	P53	Homo sapiens	62-65
23161404-7	2013	GSK3 inhibition also reduced the phosphorylation of wild-type p53 at serine 33, which is induced by doxorubicin, etoposide and camptothecin in the mitochondria.	Camptothecin	127-139	P53	Homo sapiens	62-65
23161404-8	2013	Moreover, inhibition of GSK3 reduced etoposide-induced association of p53 with Bcl2 and Bax oligomerization.	Etoposide	37-46	P53	Homo sapiens	70-73
25543136-0	2015	p53 mutations change phosphatidylinositol acyl chain composition.	Phosphatidylinositols	21-41	P53	Homo sapiens	0-3
25543136-5	2015	We find that mutation of Trp53 results in PIs containing reduced-length fatty acid moieties.	Phosphatidylinositols	42-45	P53	Homo sapiens	25-30
26700591-0	2015	Upregulation of energy metabolism-related, p53-target TIGAR and SCO2 in HuH-7 cells with p53 mutation by geranylgeranoic acid treatment.	geranylgeranic acid	105-125	P53	Homo sapiens	43-46
26032169-4	2015	We initially showed that the p53 protein level was elevated in GEN-treated human non-small lung cancer A549 cells and cervical cancer HeLa cells.	Genistein	63-66	P53	Homo sapiens	29-32
26252178-2	2015	We determined the kinetics of the mitochondrial translocation of p53 in HCT-116 and PA-1 cells exposed to different genotoxic stresses (doxorubicin, camptothecin, UVB).	Camptothecin	149-161	P53	Homo sapiens	65-68
26277488-5	2015	In this study, one of the mutant p53 activators is suggested as an Hsp90 inhibitor according to a pyrazole scaffold.	pyrazole	98-106	P53	Homo sapiens	33-36
25483068-2	2015	Using genome-wide shRNA screening, we recently identified the ATM kinase as synthetic lethal with Nutlin-3, an MDM2 inhibitor that leads to non-genotoxic p53 activation.	nutlin 3	98-106	P53	Homo sapiens	154-157
26102294-3	2015	Previously, we showed that following etoposide (ETO) treatment embryonal carcinoma PA-1 cells undergo a p53-dependent upregulation of OCT4A and p21Cip1 (governing self-renewal and regulating cell cycle inhibition and senescence, respectively).	Etoposide	37-46	P53	Homo sapiens	104-107
26102294-3	2015	Previously, we showed that following etoposide (ETO) treatment embryonal carcinoma PA-1 cells undergo a p53-dependent upregulation of OCT4A and p21Cip1 (governing self-renewal and regulating cell cycle inhibition and senescence, respectively).	Etoposide	48-51	P53	Homo sapiens	104-107
22469985-3	2013	We have reported that p53 reactivation by an inhibitor of the p53-MDM2 interaction, Nutlin-3, induces selective and massive apoptosis in PEL cells leading to efficient anti-tumor activity in a subcutaneous xenograft model for PEL.	nutlin 3	84-92	P53	Homo sapiens	22-25
22469985-3	2013	We have reported that p53 reactivation by an inhibitor of the p53-MDM2 interaction, Nutlin-3, induces selective and massive apoptosis in PEL cells leading to efficient anti-tumor activity in a subcutaneous xenograft model for PEL.	nutlin 3	84-92	P53	Homo sapiens	62-65
22469985-5	2013	Interestingly, our results demonstrate that spontaneous induction of viral lytic replication in tumors could drastically attenuate the p53-dependent apoptotic response to Nutlin-3.	nutlin 3	171-179	P53	Homo sapiens	135-138
22469985-6	2013	Moreover, viral reactivation compromised p53-dependent apoptosis in PEL cells treated with genotoxic anti-cancer agents doxorubicin and etoposide.	Etoposide	136-145	P53	Homo sapiens	41-44
26277488-7	2015	Molecular dynamic simulations were also conducted to evaluate the obtained results on the other two pyrazole structures, one known as Hsp90 inhibitor and the other as the reported mutant p53 activator.	pyrazole	100-108	P53	Homo sapiens	187-190
23442930-6	2013	By western blot analysis, MAA was shown to suppress the expression of heat shock protein 27 and increase the expression of IkBalpha and p53.	methyl antcinate A	26-29	P53	Homo sapiens	136-139
26050209-8	2015	RESULTS: IC50 values for YH264, YH263, and WW751 against p53 wild-type HCT 116 cells after 72 h of incubation were 18.3 +- 2.3, 8.9 +- 0.6, and 3.1 +- 0.2 muM, respectively.	yh264	25-30	P53	Homo sapiens	57-60
23434831-0	2013	Asperolide A, a marine-derived tetranorditerpenoid, induces G2/M arrest in human NCI-H460 lung carcinoma cells, is mediated by p53-p21 stabilization and modulated by Ras/Raf/MEK/ERK signaling pathway.	asperolide A	0-12	P53	Homo sapiens	127-130
23434831-1	2013	Here we first demonstrate that asperolide A, a very recently reported marine-derived tetranorditerpenoid, leads to the inhibition of NCI-H460 lung carcinoma cell proliferation by G2/M arrest with the activation of the Ras/Raf/MEK/ERK signaling and p53-dependent p21 pathway.	asperolide A	31-43	P53	Homo sapiens	248-251
26835157-7	2015	To determine how p53 shapes the response of cells to NS depletion at the molecular level, we showed that p53 turns on the expression of reprimo and MDM2 in NS-deficient MEF cells.	ns	53-55	P53	Homo sapiens	17-20
25873070-8	2015	The results indicated that pamidronate decreased invasion, migration and Rho-A, c-Ha-ras, p53, Serpin-1, Caveolin-1, Bcl-xL and NFkappaB gene and protein expression.	Pamidronate	27-38	P53	Homo sapiens	90-93
23268733-0	2013	Siladenoserinols A-L: new sulfonated serinol derivatives from a tunicate as inhibitors of p53-Hdm2 interaction.	serinol	8-15	P53	Homo sapiens	90-93
26223322-8	2015	Inhibition of integrin beta4 and Akt signalling using blocking antibody and the inhibitor LY294002, respectively, significantly attenuated p53(R248)-mediated ovarian cancer-mesothelial adhesion.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	90-98	P53	Homo sapiens	139-142
25685256-0	2015	Naphthoquinone derivative PPE8 induces endoplasmic reticulum stress in p53 null H1299 cells.	Naphthoquinones	0-14	P53	Homo sapiens	71-74
25685256-7	2015	We synthesized a novel naphthoquinone derivative PPE8 and evaluated capacity to induce ER stress in p53 null H1299 and p53 wild-type A549 cells.	Naphthoquinones	23-37	P53	Homo sapiens	100-103
23287463-4	2013	Our previous work has demonstrated that chronic stimulation of a beta(2)AR-beta-arrestin-1-mediated signaling pathway by infusion of isoproterenol suppresses p53 levels and impairs genomic integrity.	Isoproterenol	133-146	P53	Homo sapiens	158-161
26288684-1	2015	A series of isatin Schiff base derivatives were identified during in silico screening of the small molecule library for novel activators of p53.	isatin schiff base	12-30	P53	Homo sapiens	140-143
25685256-7	2015	We synthesized a novel naphthoquinone derivative PPE8 and evaluated capacity to induce ER stress in p53 null H1299 and p53 wild-type A549 cells.	Naphthoquinones	23-37	P53	Homo sapiens	119-122
25490093-6	2014	Consistently, in p53siRNA transfected U2-OS cells we observed loss of miR-34a induction after etoposide exposure associated with a partial gain of gene methylation and cell cycle progress towards G2/M phase.	Etoposide	94-103	P53	Homo sapiens	17-20
25490093-8	2014	In conclusion, cell response to etoposide-induced DNA damage was not compromised in cells with dominant-negative p53 expression.	Etoposide	32-41	P53	Homo sapiens	113-116
23146022-3	2013	Here, a novel gene vector self-assembled through avidin-biotin interaction with optimized targeting functionality, biotinylated tumor-targeting peptide/avidin/biotinylated cell-penetrating peptide (TAC), was designed and prepared to mediate the in vitro and in vivo delivery of p53 gene.	avidin-biotin	49-62	P53	Homo sapiens	278-281
26095524-0	2015	XI-006 induces potent p53-independent apoptosis in Ewing sarcoma.	XI-006	0-6	P53	Homo sapiens	22-25
23054612-6	2013	Importantly, when p53 was activated following the administration of either of three different anticancer chemotherapeutic agents (cisplatin, etoposide or doxorubicin), it was able to induce CYP3A genes, which are the main factors in systemic clearance of these agents.	Etoposide	141-150	P53	Homo sapiens	18-21
25474278-0	2014	Prognostic value of microsatellite instability and p53 expression in metastatic colorectal cancer treated with oxaliplatin and fluoropyrimidine-based chemotherapy.	2-fluoropyrimidine	127-143	P53	Homo sapiens	51-54
26090895-5	2015	We predict that there could be a critical Deltatc induced by p53 via IRc, where, if Deltat(Deltatc the cell cycle may come back to normal state, otherwise it will go to cell cycle arrest (apoptosis).	deltatc	42-49	P53	Homo sapiens	61-64
25400509-5	2014	RESULTS: Here we report that phenoxodiol induces cell cycle arrest in the G1/S phase of the cell cycle, with the resultant arrest due to the upregulation of p21(WAF1) in all the cell lines in response to treatment, indicating that activation of p21(WAF1) and subsequent cell arrest was occurring via a p53 independent manner, with induction of cytotoxicity independent of caspase activation.	phenoxodiol	29-40	P53	Homo sapiens	302-305
23788960-12	2013	CONCLUSIONS: DNA damage provokes p53-mediated G2/M cell cycle arrest in oridonin-induced MCF-7 cells through the mechanism of CHK2 activation by activated ATM protein kinase, which is induced by oridonin.	oridonin	72-80	P53	Homo sapiens	33-36
25495205-10	2015	This segmental progeria differs from natural aging, and implicates p53 overexpression in the etiology of CS.	Cesium	105-107	P53	Homo sapiens	67-70
23788960-12	2013	CONCLUSIONS: DNA damage provokes p53-mediated G2/M cell cycle arrest in oridonin-induced MCF-7 cells through the mechanism of CHK2 activation by activated ATM protein kinase, which is induced by oridonin.	oridonin	195-203	P53	Homo sapiens	33-36
23149933-4	2013	Of the p53 target genes, the expression level and promoter activity of the DUSP1 gene, but not those of the p21 gene, were increased in H(2)O(2)-treated DJ-1(-/-) cells and were decreased in wild-type DJ-1- but not C106S DJ-1-transfected H1299 cells through sequestration of p53 from the DUSP1 promoter by DJ-1.	h(2)o	136-141	P53	Homo sapiens	7-10
23149933-4	2013	Of the p53 target genes, the expression level and promoter activity of the DUSP1 gene, but not those of the p21 gene, were increased in H(2)O(2)-treated DJ-1(-/-) cells and were decreased in wild-type DJ-1- but not C106S DJ-1-transfected H1299 cells through sequestration of p53 from the DUSP1 promoter by DJ-1.	h(2)o	136-141	P53	Homo sapiens	275-278
25400509-7	2014	CONCLUSIONS: Phenoxodiol demonstrates an ability in prostate cancer cells to induce significant cytotoxicity in cells by interacting with p21(WAF1) and inducing cell cycle arrest irrespective of p53 status or caspase pathway interactions.	phenoxodiol	13-24	P53	Homo sapiens	195-198
25294809-5	2014	SIGNIFICANCE: We have elucidated a novel mechanism to restore wild-type structure/function to mutant p53 using small molecules functioning as zinc-metallochaperones.	zinc-metallochaperones	142-164	P53	Homo sapiens	101-104
26024660-0	2015	ROS-p53-cyclophilin-D signaling mediates salinomycin-induced glioma cell necrosis.	salinomycin	41-52	P53	Homo sapiens	4-7
25933104-6	2015	Additionally, ARG induced apoptosis was accompanied by a deactivation of PI3K/p-Akt pathway, an accumulation of p53 protein and an inhibition of NF-kappaB nuclear translocation especially in Hep G2 cells, which might be the reason that Hep G2 was more sensitive than SMMC7721 cells to ARG treatment.	arctigenin	14-17	P53	Homo sapiens	112-115
25336953-12	2014	Cyclic pifithrin-alpha, an inhibitor of p53 transcriptional activity, enhanced CuONP-induced viability loss.	Pifithrin-Beta	0-22	P53	Homo sapiens	40-43
23062949-0	2013	p53-dependent radiobiological responses to internalised indium-111 in human cells.	Indium-111	56-66	P53	Homo sapiens	0-3
23062949-3	2013	This study investigated the role of p53 in the cellular response to the Auger-emitting radionuclide indium-111.	Indium-111	100-110	P53	Homo sapiens	36-39
25823924-5	2015	In addition, p53 and E-cadherin were decreased by silica-treatment.	Silicon Dioxide	50-56	P53	Homo sapiens	13-16
23342112-0	2013	Quercetin enhances the antitumor activity of trichostatin A through upregulation of p53 protein expression in vitro and in vivo.	trichostatin A	45-59	P53	Homo sapiens	84-87
23342112-2	2013	We first showed that quercetin (5 microM) significantly increased the growth arrest and apoptosis in A549 cells (expressing wild-type p53) induced by 25 ng/mL of (82.5 nM) TSA at 48 h by about 25% and 101%, respectively.	trichostatin A	172-175	P53	Homo sapiens	134-137
23342112-4	2013	In addition, quercetin significantly increased TSA-induced p53 expression in A549 cells.	trichostatin A	47-50	P53	Homo sapiens	59-62
23342112-11	2013	These data indicate that regulation of the expression of p53 by quercetin plays an important role in enhancing TSA-induced apoptosis in A549 cells.	trichostatin A	111-114	P53	Homo sapiens	57-60
25096914-2	2014	Through drug screening for novel anticancer therapeutics, we unexpectedly identified auranofin as a potent anticancer agent against a p53-null ovarian carcinoma SKOV3 cell line.	Auranofin	85-94	P53	Homo sapiens	134-137
25096914-9	2014	The observed upregulation of pro-apoptotic genes and apoptosis in cancer cells without p53 in response to auranofin suggests a novel p53-independent mechanism underlying auranofin-induced apoptosis in ovarian cancer cells.	Auranofin	106-115	P53	Homo sapiens	133-136
25103241-8	2014	Moreover, ATP-induced apoptosis and signaling-p53 increase, AMPK activation, and PARP cleavage-as well as autophagy induction were also inhibited by dipyridamole.	Dipyridamole	149-161	P53	Homo sapiens	46-49
25924011-12	2015	Conversely inhibition of SIRT1 and SIRT2 via siRNA or sirtinol treatment also induced senescence in BJ fibroblasts associated with increased SA-beta-gal activity, gamma-H2AX phosphorylation and p53, p21CIP1 and p16INK4A levels.	sirtinol	54-62	P53	Homo sapiens	194-197
25250818-5	2014	Treatment with etoposide, increased miR-34a levels in a p53-dependent fashion and the level of miR-34a transcription was correlated with the cell sensitivity to etoposide.	Etoposide	15-24	P53	Homo sapiens	56-59
23320119-6	2013	On the other hand, zebularine treatment downregulated CDK2 and the phosphorylation of retinoblastoma protein (Rb), and upregulated p21(WAF/CIP1) and p53.	pyrimidin-2-one beta-ribofuranoside	19-29	P53	Homo sapiens	149-152
25849487-3	2015	The purpose of our in vitro study was to evaluate the impact of p53 gene silencing in conjunction with the administration of a natural compound, epigallocatechingallate (EGCG).	epigallocatechin gallate	170-174	P53	Homo sapiens	64-67
24340645-8	2013	CONCLUSIONS: Legulation of apoptosis by cycloferon and remaxol mediated by external and p53-dependent pathway is confirmed by increased expression of CD95 and p53 protein.	10-carboxymethyl-9-acridanone	40-50	P53	Homo sapiens	88-91
24340645-8	2013	CONCLUSIONS: Legulation of apoptosis by cycloferon and remaxol mediated by external and p53-dependent pathway is confirmed by increased expression of CD95 and p53 protein.	10-carboxymethyl-9-acridanone	40-50	P53	Homo sapiens	159-162
25182732-5	2014	The collective application of polyunsaturated fatty acids (PUFAs) and irradiation significantly changed the expression of EGR1, TNF-alpha, NOTCH1, c-MYC, TP53, HMOX1, AKR1C1, NQO1, while up-regulation of GADD45A, EGR1, GRP78, DDIT3, c-MYC, FOSL1 were recorded both in response to PUFA treatment or irradiation alone.	Fatty Acids, Unsaturated	30-57	P53	Homo sapiens	154-158
24858802-3	2014	In the present study, we found that, in human colorectal cancer cells, low-dose camptothecin (CPT) simultaneously induced autophagy and premature senescence through AMPK-TSC2-mTOR pathway and ATM-Chk2-p53-p21 pathway respectively.	Camptothecin	80-92	P53	Homo sapiens	201-204
25849487-5	2015	Gene expression analysis revealed 28 genes were significantly altered (16 upregulated and 12 downregulated) in response to combined p53 siRNA and EGCG treatment.	epigallocatechin gallate	146-150	P53	Homo sapiens	132-135
24858802-3	2014	In the present study, we found that, in human colorectal cancer cells, low-dose camptothecin (CPT) simultaneously induced autophagy and premature senescence through AMPK-TSC2-mTOR pathway and ATM-Chk2-p53-p21 pathway respectively.	Camptothecin	94-97	P53	Homo sapiens	201-204
23351311-16	2012	Appropriate timing of administration and concentration of genistein determine the outcome of treatment and this method could potentially be developed as an alternative strategy for treatment of p53 defective cancer cells.	Genistein	58-67	P53	Homo sapiens	194-197
25821946-9	2015	Furthermore, phosphorylation of ATM targets, including gammaH2AX and serine 15 (S15) on p53, were increased in Rap1 silencing cells in response to etoposide.	Etoposide	147-156	P53	Homo sapiens	88-91
25750273-0	2015	The effect of silibinin in enhancing toxicity of temozolomide and etoposide in p53 and PTEN-mutated resistant glioma cell lines.	Etoposide	66-75	P53	Homo sapiens	79-82
23176676-15	2012	Lycorine treatment also significantly upregulated the expression of p53 and its target gene product, p21.	lycorine	0-8	P53	Homo sapiens	68-71
25036040-10	2014	Trichostatin A and MS-275 (both HDAC inhibitors) inhibited the downstream pathway of HDAC1 and caused cell growth arrest via activation of p53 and p21; the effects of digoxigenin were totally opposite.	trichostatin A	0-14	P53	Homo sapiens	139-142
25036040-11	2014	Staurosporine blocked the cell cycle via p53 and p21, but also promoted cell growth via activated HDAC1 and its downstream pathway.	Staurosporine	0-13	P53	Homo sapiens	41-44
24461059-2	2015	Chronic infection with hepatitis B virus (HBV) and exposure to aflatoxin B1 (AFB1) induces p53 mutations in hepatocellular carcinoma (HCC) tissue.	Aflatoxin B1	63-75	P53	Homo sapiens	91-94
25025378-8	2014	Moreover, combined positive expression of p53 and pAkt led to significantly increased PFS in subgroups carrying the XRCC1 Gln allele (HR 7.057; 95% CI 2.073-24.021; P = 0.002) or the ERCC1 Cys allele (HR 2.568; 95% CI 1.056-6.248; P = 0.038).	Glutamine	122-125	P53	Homo sapiens	42-45
22592924-1	2012	Increased expression of tumor suppressor protein p53 and of plasminogen activator inhibitor (PAI)-1 is associated with cigarette smoke (CS) exposure-induced lung epithelial injury.	Cesium	136-138	P53	Homo sapiens	49-52
22592924-4	2012	Here, we show that CS induces p53 and PAI-1 expression and apoptosis in cultured Beas2B and primary alveolar type (AT)II cells.	Cesium	19-21	P53	Homo sapiens	30-33
22592924-5	2012	CS exposure augmented binding of p53 protein with PAI-1 mRNA.	Cesium	0-2	P53	Homo sapiens	33-36
22592924-13	2012	This presents a novel link between p53-mediated PAI-1 expression and CS-induced ATII cell apoptosis.	Cesium	69-71	P53	Homo sapiens	35-38
24461059-2	2015	Chronic infection with hepatitis B virus (HBV) and exposure to aflatoxin B1 (AFB1) induces p53 mutations in hepatocellular carcinoma (HCC) tissue.	Aflatoxin B1	77-81	P53	Homo sapiens	91-94
25381309-0	2015	Zinc oxide nanoparticles affect the expression of p53, Ras p21 and JNKs: an ex vivo/in vitro exposure study in respiratory disease patients.	Zinc Oxide	0-10	P53	Homo sapiens	50-53
24989033-5	2014	Here, we show that the treatment of the novel small molecule, CG500354, into CD133-expressing human primary GBM cells induces growth arrest by cell cycle regulators, p53, p21, p27 and phase-specific cyclins, and neural differentiation, as confirmed by neural progenitor/precursor markers, nestin, GFAP and Tuj1.	CG500354	62-70	P53	Homo sapiens	166-169
22736505-3	2012	Here, we demonstrate that genistein inhibits the growth of glioblastoma multiforme and medulloblastoma cells with different TP53 mutations and radio-responses by arresting the cells at G2/M phase of the cell cycle.	Genistein	26-35	P53	Homo sapiens	124-128
25663456-0	2015	CP-31398 prevents the growth of p53-mutated colorectal cancer cells in vitro and in vivo.	CP 31398	0-8	P53	Homo sapiens	32-35
24789349-8	2014	Notably, FANCF shRNA was able to increase p53 levels through activation of the JNK pathway in MMC-treated breast cancer cells.	Mitomycin	94-97	P53	Homo sapiens	42-45
24789349-9	2014	Furthermore, p53 inhibition using pifithrin-alpha abolished the induction of caspase-3 and PARP by FANCF shRNA and MMC, indicating that MMC-induced apoptosis is substantially enhanced by FANCF shRNA via p53-dependent mechanisms.	Mitomycin	115-118	P53	Homo sapiens	13-16
24789349-9	2014	Furthermore, p53 inhibition using pifithrin-alpha abolished the induction of caspase-3 and PARP by FANCF shRNA and MMC, indicating that MMC-induced apoptosis is substantially enhanced by FANCF shRNA via p53-dependent mechanisms.	Mitomycin	115-118	P53	Homo sapiens	203-206
22936321-0	2012	Induction of apoptosis in human Hep3B hepatoma cells by norcantharidin through a p53 independent pathway via TRAIL/DR5 signal transduction.	norcantharidin	56-70	P53	Homo sapiens	81-84
22936321-1	2012	OBJECTIVE: To investigate the inhibitory activities of norcantharidin (NCTD), a demethylated analogue of cantharidin, on Hep3B cells (a human hepatoma cell line) with deficiency of p53.	norcantharidin	55-69	P53	Homo sapiens	181-184
25663456-2	2015	Small molecule CP-31398 was shown to restore mutant p53 tumor suppressor functions in cancer cells.	CP 31398	15-23	P53	Homo sapiens	52-55
25663456-3	2015	Here, we determined the effects of CP-31398 on the growth of p53-mutated colorectal cancer (CRC) cells in vitro and in vivo.	CP 31398	35-43	P53	Homo sapiens	61-64
22739265-6	2012	In addition, etoposide induced p53 phosphorylation and H2AX foci formation in proliferating SH-SY5Y cells but failed to do so in differentiated SH-SY5Y cells.	Etoposide	13-22	P53	Homo sapiens	31-34
25663456-7	2015	CP-31398 induced p53 downstream target molecules in cultured HT-29 cells, which resulted in the inhibition of CRC cell growth assessed by the determination of cell cycle, apoptosis, and cell proliferation.	CP 31398	0-8	P53	Homo sapiens	17-20
24817343-3	2014	We also demonstrate a K24R mutation, necessary for cellular activity in hydrocarbon-stapled p53 peptides, is not required for analogous "double-click" peptides.	Hydrocarbons	72-83	P53	Homo sapiens	92-95
25663456-9	2015	CP-31398 would be developed as a therapeutic candidate for p53-mutated CRC due to the restoration of mutant p53 tumor suppressor functions.	CP 31398	0-8	P53	Homo sapiens	59-62
25663456-9	2015	CP-31398 would be developed as a therapeutic candidate for p53-mutated CRC due to the restoration of mutant p53 tumor suppressor functions.	CP 31398	0-8	P53	Homo sapiens	108-111
25401976-8	2015	Furthermore, inhibition of Fhit loss-induced DNA damage via thymidine supplementation decreases the TP53 mutation burden in FHIT-low/APOBEC3B-high cells.	Thymidine	60-69	P53	Homo sapiens	100-104
25061640-0	2014	Reply to Liu: Amino acid 104 asparagine/glutamic acid of p53 is an adaptively selected site for extreme environments in mammals of the Tibet plateau.	Asparagine	29-39	P53	Homo sapiens	57-60
22395446-0	2012	3-Nitro-naphthalimide and nitrogen mustard conjugate NNM-25 induces hepatocellular carcinoma apoptosis via PARP-1/p53 pathway.	nnm-25	53-59	P53	Homo sapiens	114-117
22395446-7	2012	Inhibition of p53 by siRNA resulted in a significant decrease of NNM-25-induced apoptosis, which corroborated that p53 played a vital role in the cell apoptosis triggered by NNM-25.	nnm-25	65-71	P53	Homo sapiens	14-17
22395446-7	2012	Inhibition of p53 by siRNA resulted in a significant decrease of NNM-25-induced apoptosis, which corroborated that p53 played a vital role in the cell apoptosis triggered by NNM-25.	nnm-25	65-71	P53	Homo sapiens	115-118
22395446-7	2012	Inhibition of p53 by siRNA resulted in a significant decrease of NNM-25-induced apoptosis, which corroborated that p53 played a vital role in the cell apoptosis triggered by NNM-25.	nnm-25	174-180	P53	Homo sapiens	14-17
22395446-7	2012	Inhibition of p53 by siRNA resulted in a significant decrease of NNM-25-induced apoptosis, which corroborated that p53 played a vital role in the cell apoptosis triggered by NNM-25.	nnm-25	174-180	P53	Homo sapiens	115-118
25759589-4	2015	Treatment with EGCG activates the expression of the BAD, BAK, FAS, IGF1R, WNT11, and ZEB1 genes and inhibits CASP8, MYC, and TP53.	epigallocatechin gallate	15-19	P53	Homo sapiens	125-129
22395446-8	2012	NNM-25 inhibited the PARP-1 activity, AKT phosphorylation, up-regulated the protein expression of p53, Bad, and mTOR as well as down-regulating the protein expression of Bcl-2 and decreasing mitochondrial membrane potential.	nnm-25	0-6	P53	Homo sapiens	98-101
24902788-12	2014	Furthermore, oridonin markedly increased the expression of p14arf and p53.	oridonin	13-21	P53	Homo sapiens	70-73
24902788-13	2014	CONCLUSION: In NPM1c+ leukemia cells, oridonin induces NPM1c+ protein translocation into the nucleus possibly via nuclear accumulation of Crm1; the compound markedly increases p53 and p14arf expression, which may contribute to cell apoptosis.	oridonin	38-46	P53	Homo sapiens	176-179
25186437-11	2015	Also, CM-PFA-mediated delivery of p53 tumor suppressor promoted a decrease in tumor-spheroids volume.	Foscarnet	9-12	P53	Homo sapiens	34-37
24418072-2	2014	In this study, the alpha-helical conformation and structural stability of single and double stapled all-hydrocarbon cross-linked p53 peptides when bound and unbound to MDM2 are investigated.	Hydrocarbons	104-115	P53	Homo sapiens	129-132
22349266-4	2012	When treated with mitomycin C, p53-deficient cells, but not p53-expressing cells, showed a marked increase in ceramide levels.	Mitomycin	18-29	P53	Homo sapiens	31-34
22349266-7	2012	When inhibition of UGCG and treatment with mitomycin C were combined, p53-deficient, but not p53-expressing cells, showed a significant increase in cell death, suggesting that the regulation of sphingolipid metabolism could be used to sensitize cells to chemotherapeutic drugs.	Mitomycin	43-54	P53	Homo sapiens	70-73
22576012-5	2012	Inhibition of mitochondrial protein synthesis either by ERAL1 siRNA or chloramphenicol (CAP), a specific inhibitor of mitoribosomes, induced autophagy in HTC-116 TP53 (+/+)  cells, but not in HTC-116 TP53 (-/-)  cells, indicating that tumor protein 53 (TP53) is essential for the autophagy induction.	Chloramphenicol	71-86	P53	Homo sapiens	162-166
22576012-5	2012	Inhibition of mitochondrial protein synthesis either by ERAL1 siRNA or chloramphenicol (CAP), a specific inhibitor of mitoribosomes, induced autophagy in HTC-116 TP53 (+/+)  cells, but not in HTC-116 TP53 (-/-)  cells, indicating that tumor protein 53 (TP53) is essential for the autophagy induction.	Chloramphenicol	88-91	P53	Homo sapiens	162-166
22576012-5	2012	Inhibition of mitochondrial protein synthesis either by ERAL1 siRNA or chloramphenicol (CAP), a specific inhibitor of mitoribosomes, induced autophagy in HTC-116 TP53 (+/+)  cells, but not in HTC-116 TP53 (-/-)  cells, indicating that tumor protein 53 (TP53) is essential for the autophagy induction.	Chloramphenicol	88-91	P53	Homo sapiens	200-204
22576012-5	2012	Inhibition of mitochondrial protein synthesis either by ERAL1 siRNA or chloramphenicol (CAP), a specific inhibitor of mitoribosomes, induced autophagy in HTC-116 TP53 (+/+)  cells, but not in HTC-116 TP53 (-/-)  cells, indicating that tumor protein 53 (TP53) is essential for the autophagy induction.	Chloramphenicol	88-91	P53	Homo sapiens	235-251
22576012-5	2012	Inhibition of mitochondrial protein synthesis either by ERAL1 siRNA or chloramphenicol (CAP), a specific inhibitor of mitoribosomes, induced autophagy in HTC-116 TP53 (+/+)  cells, but not in HTC-116 TP53 (-/-)  cells, indicating that tumor protein 53 (TP53) is essential for the autophagy induction.	Chloramphenicol	88-91	P53	Homo sapiens	200-204
23821376-0	2014	Lack of KRAS, NRAS, BRAF and TP53 mutations improves outcome of elderly metastatic colorectal cancer patients treated with cetuximab, oxaliplatin and UFT.	Tegafur	150-153	P53	Homo sapiens	29-33
24989277-9	2014	Meanwhile, UA up-regulated the mRNA and protein levels of P53 in the same manner.	ursolic acid	11-13	P53	Homo sapiens	58-61
25312347-4	2015	In this work, we report the synthesis of nine enantiopure phenylalaninol-derived oxazolopyrrolidone lactams and the evaluation of their biological effects as p53-MDM2 interaction inhibitors.	phenylalaninol-derived oxazolopyrrolidone lactams	58-107	P53	Homo sapiens	158-161
24646317-8	2014	In particular, 2-(4-methoxyphenyl)-7-methyl-7H-pyrazolo[4,3-e][1,2,4]triazolo[1,5-c]pyrimidine resulted in a promising lead compound for further development of anti-AD agents in terms of neuroprotection, reducing the rate of NAC-induced cell death with an activity higher than that of pifithrin-beta, as a result of a more effective functional inhibition of p53 target gene transcription.	MLS-0146206.0001	15-94	P53	Homo sapiens	358-361
22773588-6	2012	BBN has a high propensity to induce mutations affecting the expression of genes such as p53, RAS and H19 among others.	Butylhydroxybutylnitrosamine	0-3	P53	Homo sapiens	88-91
25312347-6	2015	The molecular mechanism of oxazoloisoindolinone 3a was further validated in human colon adenocarcinoma HCT116 cells with wild-type p53 (HCT116 p53(+/+)) and in its isogenic derivative without p53 (HCT116 p53(-/-)).	oxazoloisoindolinone	27-47	P53	Homo sapiens	131-134
22552582-7	2012	The increased GTP/EGCG-mediated p53 acetylation enhanced its binding on the promoters of p21/waf1 and Bax, which was associated with increased accumulation of cells in the G0/G1 phase of the cell cycle and induction of apoptosis.	epigallocatechin gallate	14-17	P53	Homo sapiens	32-35
22552582-7	2012	The increased GTP/EGCG-mediated p53 acetylation enhanced its binding on the promoters of p21/waf1 and Bax, which was associated with increased accumulation of cells in the G0/G1 phase of the cell cycle and induction of apoptosis.	epigallocatechin gallate	18-22	P53	Homo sapiens	32-35
25312347-6	2015	The molecular mechanism of oxazoloisoindolinone 3a was further validated in human colon adenocarcinoma HCT116 cells with wild-type p53 (HCT116 p53(+/+)) and in its isogenic derivative without p53 (HCT116 p53(-/-)).	oxazoloisoindolinone	27-47	P53	Homo sapiens	143-146
22552582-8	2012	Our findings indicate that GTP/EGCG causes acetylation of p53 by inhibiting class I HDACs, a function that is likely to be part of the mechanisms that control the physiological activity of p53.	epigallocatechin gallate	27-30	P53	Homo sapiens	58-61
22552582-8	2012	Our findings indicate that GTP/EGCG causes acetylation of p53 by inhibiting class I HDACs, a function that is likely to be part of the mechanisms that control the physiological activity of p53.	epigallocatechin gallate	27-30	P53	Homo sapiens	189-192
24519527-3	2014	We recently demonstrated that a combination of sodium arsenite (NaAsO2) and hyperthermia sensitizes p53-expressing ovarian cancer cells to cisplatin by modulating DNA repair pathway and enhancing platinum accumulation.	sodium arsenite	47-62	P53	Homo sapiens	100-103
24519527-3	2014	We recently demonstrated that a combination of sodium arsenite (NaAsO2) and hyperthermia sensitizes p53-expressing ovarian cancer cells to cisplatin by modulating DNA repair pathway and enhancing platinum accumulation.	sodium arsenite	64-70	P53	Homo sapiens	100-103
22552582-8	2012	Our findings indicate that GTP/EGCG causes acetylation of p53 by inhibiting class I HDACs, a function that is likely to be part of the mechanisms that control the physiological activity of p53.	epigallocatechin gallate	31-35	P53	Homo sapiens	58-61
25312347-6	2015	The molecular mechanism of oxazoloisoindolinone 3a was further validated in human colon adenocarcinoma HCT116 cells with wild-type p53 (HCT116 p53(+/+)) and in its isogenic derivative without p53 (HCT116 p53(-/-)).	oxazoloisoindolinone	27-47	P53	Homo sapiens	143-146
22552582-8	2012	Our findings indicate that GTP/EGCG causes acetylation of p53 by inhibiting class I HDACs, a function that is likely to be part of the mechanisms that control the physiological activity of p53.	epigallocatechin gallate	31-35	P53	Homo sapiens	189-192
25312347-6	2015	The molecular mechanism of oxazoloisoindolinone 3a was further validated in human colon adenocarcinoma HCT116 cells with wild-type p53 (HCT116 p53(+/+)) and in its isogenic derivative without p53 (HCT116 p53(-/-)).	oxazoloisoindolinone	27-47	P53	Homo sapiens	143-146
25312347-7	2015	Indeed, using these cells, we demonstrated that oxazoloisoindolinone 3a exhibited a p53-dependent in vitro antitumor activity through induction of G0/G1-phase cell cycle arrest and apoptosis.	oxazoloisoindolinone	48-68	P53	Homo sapiens	84-87
25312347-8	2015	The selective activation of a p53-apoptotic pathway by oxazoloisoindolinone 3a was further supported by the occurrence of PARP cleavage only in p53-expressing HCT116 cells.	oxazoloisoindolinone	55-75	P53	Homo sapiens	30-33
24503697-5	2014	Treatment with momilactone B also increased the expression of cyclin-dependent kinase (Cdk) inhibitor p21Waf1/Cip1 in a p53-independent manner, without any noticeable changes in G1 cyclins and cyclin-dependent kinases (Cdks), except a slight decrease in cyclin E. Moreover, in vitro kinase assay indicated that momilactone B significantly decreased Cdk4- and Cdk6-associated kinase activities through a notably increased binding of p21 to Cdk4 and Cdk6.	momilactone	15-26	P53	Homo sapiens	120-123
24503697-5	2014	Treatment with momilactone B also increased the expression of cyclin-dependent kinase (Cdk) inhibitor p21Waf1/Cip1 in a p53-independent manner, without any noticeable changes in G1 cyclins and cyclin-dependent kinases (Cdks), except a slight decrease in cyclin E. Moreover, in vitro kinase assay indicated that momilactone B significantly decreased Cdk4- and Cdk6-associated kinase activities through a notably increased binding of p21 to Cdk4 and Cdk6.	momilactone B	15-28	P53	Homo sapiens	120-123
22904680-5	2012	In vitro, p53-72P was less effective than p53-72R in inducing apoptosis and inhibiting survival of p53-null LAN-1 cells treated with etoposide, topotecan, or ionizing radiation but not taxol.	Etoposide	133-142	P53	Homo sapiens	10-13
25312347-8	2015	The selective activation of a p53-apoptotic pathway by oxazoloisoindolinone 3a was further supported by the occurrence of PARP cleavage only in p53-expressing HCT116 cells.	oxazoloisoindolinone	55-75	P53	Homo sapiens	144-147
25312347-9	2015	Moreover, oxazoloisoindolinone 3a led to p53 protein stabilization and to the up-regulation of p53 transcriptional activity with increased expression levels of several p53 target genes, as p21(WAF1/CIP1), MDM2, BAX and PUMA, in p53(+/+) but not in p53(-/-) HCT116 cells.	oxazoloisoindolinone	10-30	P53	Homo sapiens	41-44
25312347-9	2015	Moreover, oxazoloisoindolinone 3a led to p53 protein stabilization and to the up-regulation of p53 transcriptional activity with increased expression levels of several p53 target genes, as p21(WAF1/CIP1), MDM2, BAX and PUMA, in p53(+/+) but not in p53(-/-) HCT116 cells.	oxazoloisoindolinone	10-30	P53	Homo sapiens	95-98
22431736-2	2012	We also show that at higher concentrations AEA induces normal human epidermal melanocyte apoptosis (~3-fold over controls at 5 muM) through a TRPV1-mediated pathway that increases DNA fragmentation and p53 expression.	anandamide	43-46	P53	Homo sapiens	202-205
24486906-6	2014	Bimodal p53 dynamics was largely influenced by cellular MDM2 and elevated p53/MDM2 ratios with increasing etoposide favor mono-ubiquitination.	Etoposide	106-115	P53	Homo sapiens	8-11
25312347-9	2015	Moreover, oxazoloisoindolinone 3a led to p53 protein stabilization and to the up-regulation of p53 transcriptional activity with increased expression levels of several p53 target genes, as p21(WAF1/CIP1), MDM2, BAX and PUMA, in p53(+/+) but not in p53(-/-) HCT116 cells.	oxazoloisoindolinone	10-30	P53	Homo sapiens	95-98
24486906-6	2014	Bimodal p53 dynamics was largely influenced by cellular MDM2 and elevated p53/MDM2 ratios with increasing etoposide favor mono-ubiquitination.	Etoposide	106-115	P53	Homo sapiens	74-77
22289577-5	2012	Diosmin showed strong HA22T cell viability inhibition in a dose dependent manner and significantly reduced the cell proliferative proteins as well as inducing cell cycle arrest in the G2/M phase through p53 activation and PI3K-Akt-MDM2 signaling pathway inhibition.	Diosmin	0-7	P53	Homo sapiens	203-206
25312347-9	2015	Moreover, oxazoloisoindolinone 3a led to p53 protein stabilization and to the up-regulation of p53 transcriptional activity with increased expression levels of several p53 target genes, as p21(WAF1/CIP1), MDM2, BAX and PUMA, in p53(+/+) but not in p53(-/-) HCT116 cells.	oxazoloisoindolinone	10-30	P53	Homo sapiens	95-98
24522962-3	2014	Here, we describe inhibition experiments on p53/Mdm2 interaction in Trichoplax adhaerens by applying the inhibitors nutlin-3 and roscovitine.	nutlin 3	116-124	P53	Homo sapiens	44-47
25312347-9	2015	Moreover, oxazoloisoindolinone 3a led to p53 protein stabilization and to the up-regulation of p53 transcriptional activity with increased expression levels of several p53 target genes, as p21(WAF1/CIP1), MDM2, BAX and PUMA, in p53(+/+) but not in p53(-/-) HCT116 cells.	oxazoloisoindolinone	10-30	P53	Homo sapiens	95-98
24366007-8	2014	Notably, the levels of nutlin-3-induced ROS were correlated with the mitochondrial translocation of p53 and this induction was prevented by PFT-mu, an inhibitor of the mitochondrial translocation of p53.	nutlin 3	23-31	P53	Homo sapiens	100-103
25312347-10	2015	Additionally, the ability of oxazoloisoindolinone 3a to block the p53-MDM2 interaction in HCT116 p53(+/+) cells was confirmed by co-immunoprecipitation.	oxazoloisoindolinone	29-49	P53	Homo sapiens	66-69
24366007-8	2014	Notably, the levels of nutlin-3-induced ROS were correlated with the mitochondrial translocation of p53 and this induction was prevented by PFT-mu, an inhibitor of the mitochondrial translocation of p53.	nutlin 3	23-31	P53	Homo sapiens	199-202
24366007-11	2014	Collectively, these results suggest that nutlin-3 induces HO-1 expression via the activation of both JNK which is dependent on ROS generated by p53 translocated to the mitochondria and p38 MAPK which appears to be stimulated by a ROS-independent mechanism, and this HO-1 induction may inhibit nutlin-3-induced apoptosis, constituting a negative feedback loop of p53-induced apoptosis.	nutlin 3	41-49	P53	Homo sapiens	144-147
21766316-0	2012	Effects of SiO2 nanoparticles on HFL-I activating ROS-mediated apoptosis via p53 pathway.	Silicon Dioxide	11-15	P53	Homo sapiens	77-80
25312347-10	2015	Additionally, the ability of oxazoloisoindolinone 3a to block the p53-MDM2 interaction in HCT116 p53(+/+) cells was confirmed by co-immunoprecipitation.	oxazoloisoindolinone	29-49	P53	Homo sapiens	97-100
24366007-11	2014	Collectively, these results suggest that nutlin-3 induces HO-1 expression via the activation of both JNK which is dependent on ROS generated by p53 translocated to the mitochondria and p38 MAPK which appears to be stimulated by a ROS-independent mechanism, and this HO-1 induction may inhibit nutlin-3-induced apoptosis, constituting a negative feedback loop of p53-induced apoptosis.	nutlin 3	41-49	P53	Homo sapiens	362-365
25312347-12	2015	Altogether, this work adds, for the first time, the oxazoloisoindolinone scaffold to the list of chemotypes activators of a wild-type p53-pathway with promising antitumor activity.	oxazoloisoindolinone	52-72	P53	Homo sapiens	134-137
25625511-9	2015	Treatment with EGCG was found to elevate the expression of p53 and p21, and eventually led to apoptosis of NPC cells via caspase 3 activation.	epigallocatechin gallate	15-19	P53	Homo sapiens	59-62
24297112-0	2014	Oridonin induces apoptosis in SW1990 pancreatic cancer cells via p53- and caspase-dependent induction of p38 MAPK.	oridonin	0-8	P53	Homo sapiens	65-68
24297112-4	2014	Additionally, cell apoptosis was markedly inhibited by PFT alpha (pifithrin alpha), a p53-specific inhibitor, which was applied to evaluate the function of p53, showing that p53 was responsible for the cytotoxity of oridonin.	oridonin	216-224	P53	Homo sapiens	156-159
24297112-4	2014	Additionally, cell apoptosis was markedly inhibited by PFT alpha (pifithrin alpha), a p53-specific inhibitor, which was applied to evaluate the function of p53, showing that p53 was responsible for the cytotoxity of oridonin.	oridonin	216-224	P53	Homo sapiens	156-159
24297112-5	2014	Moreover, oridonin increased the expression of p-p53 with a concomitant increase in p21 in the SW1990 cells.	oridonin	10-18	P53	Homo sapiens	49-52
25550551-7	2015	At the same time, S-petasin and iso-S-petasin increased mitochondrial membrane permeability and cytochrome c release from mitochondria to the cytosol via reducing the ratio of BCL2/BAX in DU145 and PC3 cells, and up-regulating the levels of p53 in DU145 cells but down-regulating it in PC3 cells.	petasin	18-27	P53	Homo sapiens	241-244
26700591-0	2015	Upregulation of energy metabolism-related, p53-target TIGAR and SCO2 in HuH-7 cells with p53 mutation by geranylgeranoic acid treatment.	geranylgeranic acid	105-125	P53	Homo sapiens	89-92
24246761-2	2014	We previously showed that the PAH prototype, benzo[a]pyrene (B[a]P), triggers apoptosis via DNA damage-induced p53 activation (genotoxic pathway) and via remodeling of the membrane cholesterol-rich microdomains called lipid rafts, leading to changes in pH homeostasis (non-genotoxic pathway).	Phosphorus	30-31	P53	Homo sapiens	111-114
26700591-3	2015	Here, we show that a branched-chain C-20 polyunsaturated fatty acid, geranylgeranoic acid (GGA), induces upregulation of the cellular protein levels of TP53-induced glycolysis and apoptosis regulator (TIGAR) and synthesis of cytochrome c oxidase 2 (SCO2) in human hepatoma-derived HuH-7cells harboring the mutant TP53 gene, suggesting that GGA may shift an energetic state of the tumor cells from aerobic glycolysis to mitochondrial respiration.	Fatty Acids, Unsaturated	41-67	P53	Homo sapiens	152-156
24052409-0	2014	Mahanine synergistically enhances cytotoxicity of 5-fluorouracil through ROS-mediated activation of PTEN and p53/p73 in colon carcinoma.	mahanine	0-8	P53	Homo sapiens	109-112
24052409-3	2014	We demonstrated that mahanine-induced apoptosis involved reactive oxygen species (ROS)-mediated nuclear accumulation of PTEN and its interaction with p53/p73.	mahanine	21-29	P53	Homo sapiens	150-153
26700591-3	2015	Here, we show that a branched-chain C-20 polyunsaturated fatty acid, geranylgeranoic acid (GGA), induces upregulation of the cellular protein levels of TP53-induced glycolysis and apoptosis regulator (TIGAR) and synthesis of cytochrome c oxidase 2 (SCO2) in human hepatoma-derived HuH-7cells harboring the mutant TP53 gene, suggesting that GGA may shift an energetic state of the tumor cells from aerobic glycolysis to mitochondrial respiration.	geranylgeranic acid	69-89	P53	Homo sapiens	152-156
26835157-7	2015	To determine how p53 shapes the response of cells to NS depletion at the molecular level, we showed that p53 turns on the expression of reprimo and MDM2 in NS-deficient MEF cells.	ns	53-55	P53	Homo sapiens	105-108
25179905-0	2014	Tumor suppressor protein p53 promotes 2-methoxyestradiol-induced activation of Bak and Bax, leading to mitochondria-dependent apoptosis in human colon cancer HCT116 cells.	2-Methoxyestradiol	38-56	P53	Homo sapiens	25-28
24268795-2	2014	We herein report the synthesis and evaluation of eighteen spiroisoxazoline oxindoles derivatives as p53-MDM2 interaction inhibitors.	spiroisoxazoline oxindoles	58-84	P53	Homo sapiens	100-103
24268795-3	2014	Seven compounds showed an antiproliferative profile superior to the p53-MDM2 interaction inhibitor nutlin-3, and induced cell death by apoptosis.	nutlin 3	99-107	P53	Homo sapiens	68-71
25179905-3	2014	These 2-MeO-E2-induced cellular changes, except for G2/M arrest, appeared to be more apparent in the presence of p53.	2-Methoxyestradiol	6-14	P53	Homo sapiens	113-116
24626184-8	2014	However, its recruitment is stimulated by etoposide in cells lacking p53, suggesting that p53 can oppose association of p68 with the PLK1 promoter.	Etoposide	42-51	P53	Homo sapiens	90-93
25490093-0	2014	p53-dependent activation of microRNA-34a in response to etoposide-induced DNA damage in osteosarcoma cell lines not impaired by dominant negative p53 expression.	Etoposide	56-65	P53	Homo sapiens	0-3
25490093-3	2014	In this study we evaluated the cascade of events determined by etoposide-induced DNA damage in OS cell lines with different p53 status focusing on methylation status and expression of miR-34a that modulate tumor cell growth and cell cycle progression.	Etoposide	63-72	P53	Homo sapiens	124-127
25490093-4	2014	Wild-type p53 U2-OS cells and U2-OS cells expressing dominant-negative form of p53 (U2- OS175) were more sensitive to etoposide than p53-deficient MG63 and Saos-2 cells, showing increased levels of unmethylated miR-34a, reduced expression of CDK4 and cell cycle arrest in G1 phase.	Etoposide	118-127	P53	Homo sapiens	10-13
25490093-4	2014	Wild-type p53 U2-OS cells and U2-OS cells expressing dominant-negative form of p53 (U2- OS175) were more sensitive to etoposide than p53-deficient MG63 and Saos-2 cells, showing increased levels of unmethylated miR-34a, reduced expression of CDK4 and cell cycle arrest in G1 phase.	Etoposide	118-127	P53	Homo sapiens	79-82
25490093-4	2014	Wild-type p53 U2-OS cells and U2-OS cells expressing dominant-negative form of p53 (U2- OS175) were more sensitive to etoposide than p53-deficient MG63 and Saos-2 cells, showing increased levels of unmethylated miR-34a, reduced expression of CDK4 and cell cycle arrest in G1 phase.	Etoposide	118-127	P53	Homo sapiens	79-82
24473562-2	2014	Therefore, the objective of the present study was to evaluate the in vitro effect of treatment with Nutlin-3, a small molecule inhibitor of the MDM2/p53 interaction, on the expression of the suppressor of cytokine signaling 1 in primary acute myeloid leukemia cells and in myeloid cell lines with differential p53 status.	nutlin 3	100-108	P53	Homo sapiens	149-152
24473562-2	2014	Therefore, the objective of the present study was to evaluate the in vitro effect of treatment with Nutlin-3, a small molecule inhibitor of the MDM2/p53 interaction, on the expression of the suppressor of cytokine signaling 1 in primary acute myeloid leukemia cells and in myeloid cell lines with differential p53 status.	nutlin 3	100-108	P53	Homo sapiens	310-313
25461359-5	2014	Increased gammaH2AX expression was observed in the pBSO and STICs compared with the controls whereas expression patterns of Ki67, p53 and bcl2 were low to moderate in the pBSO group.	pbso	171-175	P53	Homo sapiens	130-133
25745770-15	2014	The aim of the study was to investigate genistein as a potential inhibitor of CTGF and TGFbeta1, beta2 and beta3 isoforms expression and a potential regulator of p53.	Genistein	40-49	P53	Homo sapiens	162-165
24117366-7	2014	After analysing the p53 mRNA regulation by isoprenaline, we observed that only EAT p53 expression increased after adrenergic stimulation (1.63 +- 0.01 vs. 1.66 +- 0.02; P = 0.024).	Isoproterenol	43-55	P53	Homo sapiens	20-23
25107642-4	2014	AT9283 induced p53 expression, autophagy, and G2/M cell-cycle arrest, while combined treatment induced S phase arrest.	1-cyclopropyl-3-(3-(5-morpholin-4-ylmethyl-1H-benzoimidazol-2-yl)-1H-pyrazol-4-yl)urea	0-6	P53	Homo sapiens	15-18
25335230-0	2014	Acute L-glutamine deprivation affects the expression of TP53-related protein genes in U87 glioma cells.	Glutamine	6-17	P53	Homo sapiens	56-60
25335230-5	2014	Results of this investigation clearly demonstrate that the expression most of genes encoding TP53-related factors depends upon acute L-glutamine deprivation condition as well as upon ERN1, the major signaling system of the endoplasmic reticulum stress.	Glutamine	133-144	P53	Homo sapiens	93-97
24926617-2	2014	To investigate post-transcriptional controls as an additional dimension of p53-directed gene expression responses, we performed a translatome analysis through polysomal profiling on MCF7 cells upon 16 hours of doxorubicin or nutlin-3a treatment.	nutlin 3	225-234	P53	Homo sapiens	75-78
25431671-11	2014	Phosphorylation of p53 and Chk1 and expression of ATF4 and CHOP genes were detected in IS-, PCS-, and PhS-treated cells, but not in IAA-treated cells.	phenylsulfate	102-105	P53	Homo sapiens	19-22
24712372-7	2014	These results suggested that EGCG inhibited the expression of hsa-miR-98-5p, followed by an increase of p53, thus the efficacy of cisplatin was enhanced.	epigallocatechin gallate	29-33	P53	Homo sapiens	104-107
25078983-8	2014	LY294002 pre-treatment significantly alleviated Ang II-induced HUVEC senescence, and partly reversed the elevation of TERT, UCP2, p-Akt, c-myc and p53 protein levels.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	P53	Homo sapiens	147-150
24732641-0	2014	MDM2 rs2279744 and TP53 rs1042522 polymorphisms associated with etoposide- and cisplatin-induced grade III/IV neutropenia in Chinese extensive-stage small-cell lung cancer patients.	Etoposide	64-73	P53	Homo sapiens	19-23
24786831-5	2014	PELP1-depleted p53 (wild-type) breast cancer cells were less sensitive to various genotoxic agents including etoposide, camptothecin or gamma-radiation.	Etoposide	109-118	P53	Homo sapiens	15-18
24270847-2	2013	Using Brownian dynamics simulations, we show that the preferential binding of the MDM2 protein to the geometrical isomers of Nutlin-3, an effective anticancer lead that works by inhibiting the interaction between the proteins p53 and MDM2, can be explained by kinetic arguments related to the formation of the MDM2:Nutlin-3 encounter complex.	nutlin 3	125-133	P53	Homo sapiens	226-229
24270847-2	2013	Using Brownian dynamics simulations, we show that the preferential binding of the MDM2 protein to the geometrical isomers of Nutlin-3, an effective anticancer lead that works by inhibiting the interaction between the proteins p53 and MDM2, can be explained by kinetic arguments related to the formation of the MDM2:Nutlin-3 encounter complex.	nutlin 3	315-323	P53	Homo sapiens	226-229
24786831-5	2014	PELP1-depleted p53 (wild-type) breast cancer cells were less sensitive to various genotoxic agents including etoposide, camptothecin or gamma-radiation.	Camptothecin	120-132	P53	Homo sapiens	15-18
25047426-9	2014	In addition, hesperidin enhanced p53-p21 axis with concomitant decrease in cell cycle regulator.	Hesperidin	13-23	P53	Homo sapiens	33-36
24231949-5	2013	Here, we have reviewed existing cyclotherapy regimens using two well-known p53 activators, nutlin-3 and actinomycin D.	nutlin 3	91-99	P53	Homo sapiens	75-78
24071474-5	2013	Above results demonstrate that ursolic acid induces the activation of p53, NF-kappaB and Bax, leading to the enhancement of p21 transcriptional activity and activation of Caspase-9 and -3, thus finally induces apoptosis of SW480 cells.	ursolic acid	31-43	P53	Homo sapiens	70-73
25177931-8	2014	Only one patient had the homozygous TP53 248 genotype (Arg-Trp/Gln); all other patients were homozygous wild-type in both the control and endometriosis groups (P = 0.51; NS).	Glutamine	63-66	P53	Homo sapiens	36-40
24921920-2	2014	Nutlin-3, an MDM2-p53 antagonist, has previously been reported to be a competitive MDR-1 inhibitor.	nutlin 3	0-8	P53	Homo sapiens	18-21
24113549-3	2013	In this study, we evaluated the effects of a novel CHK1 inhibitor, MK-8776, in combination with pemetrexed (PMX) on cell proliferation and survival in a panel of p53 mutant non-small cell lung cancer (NSCLC) cell lines.	MK-8776	67-74	P53	Homo sapiens	162-165
23982736-8	2013	In addition, p53 siRNA transfection attenuated metformin-induced SA-beta-gal staining.	2-(2-quinolinyl)-1H-indene--1,3(2H)-dione-6'-sulfonic acid	65-76	P53	Homo sapiens	13-16
24179522-1	2013	The present study investigated the regulatory mechanisms by which epigallocatechin-3-gallate (EGCG) exerts vascular endothelial growth factor (VEGF)-, p53- and AMP-activated protein kinase (AMPK)-associated pro-apoptotic and migration-suppressing effects on colon cancer cells.	epigallocatechin gallate	66-92	P53	Homo sapiens	151-154
24179522-1	2013	The present study investigated the regulatory mechanisms by which epigallocatechin-3-gallate (EGCG) exerts vascular endothelial growth factor (VEGF)-, p53- and AMP-activated protein kinase (AMPK)-associated pro-apoptotic and migration-suppressing effects on colon cancer cells.	epigallocatechin gallate	94-98	P53	Homo sapiens	151-154
24921920-4	2014	RESULTS: Verapamil and the MDM2-p53 antagonists potentiated vincristine-mediated growth inhibition in a concentration-dependent manner when used in combination with high MDR-1-expressing p53 mutant neuroblastoma cell lines at concentrations that did not affect the viability of cells when given alone.	Verapamil	9-18	P53	Homo sapiens	187-190
24799378-0	2014	Oligosaccharide G19 inhibits U-87 MG human glioma cells growth in vitro and in vivo by targeting epidermal growth factor (EGF) and activating p53/p21 signaling.	oligosaccharide g19	0-19	P53	Homo sapiens	142-145
24205274-10	2013	Treatment with AG1024, an IGF-1R inhibitor, suppressed IR-induced upregulation of p53, p21/waf1, and SA-beta-gal.	tyrphostin AG 1024	15-21	P53	Homo sapiens	82-85
24867259-4	2014	We report on how nutlin-3-stimulated ERK1/2 activity inhibits p53-induced apoptosis.	nutlin 3	17-25	P53	Homo sapiens	62-65
23938948-5	2013	For the first time we showed that OKA/PN combination at subtoxic doses induces potent synergistic apoptotic effects accompanied by lowering in p-Akt levels, increasing in the stabilized forms of p53 and potent decrease in pS166-Mdm2.	oka/pn	34-40	P53	Homo sapiens	195-198
22270849-0	2012	P53-dependent antiproliferative and pro-apoptotic effects of trichostatin A (TSA) in glioblastoma cells.	trichostatin A	61-75	P53	Homo sapiens	0-3
24867259-12	2014	Collectively, these results suggest that nutlin-3-activated ERK1/2 may stimulate the transcription of BCL2A1 via the activation of ELK1, and BCL2A1 expression may contribute to the inhibitory effect of ERK1/2 on nutlin-3-induced apoptosis, thereby constituting a negative feedback loop of p53-induced apoptosis.	nutlin 3	41-49	P53	Homo sapiens	289-292
22270849-0	2012	P53-dependent antiproliferative and pro-apoptotic effects of trichostatin A (TSA) in glioblastoma cells.	trichostatin A	77-80	P53	Homo sapiens	0-3
22270849-8	2012	Characterizing the chromatin modulation around the p21(WAF1) promoter after TSA treatment using chromatin immunoprecipitation, we found (1) a release of HDAC1, (2) an increase of acetylated H4 binding, and (3) enhanced recruitment of p53.	trichostatin A	76-79	P53	Homo sapiens	234-237
22270849-12	2012	Furthermore, TSA-treated p53-mutant cell line U138 failed to show an induction in p21(WAF1), showed a deficient G2/M checkpoint, and underwent mitotic catastrophe.	trichostatin A	13-16	P53	Homo sapiens	25-28
24926563-8	2014	p53 mutation frequency was the lowest in the AB=0, CS=0 group, increased as AB and/or CS rose, and was significantly higher in the &gt;=1,000 AB, &gt;=25 CS group (p=0.039).	Cesium	51-53	P53	Homo sapiens	0-3
23954287-4	2013	Moreover, we showed that etoposide, a DNA damaging agent, activates p53 transcription through the E2F1 pathway.	Etoposide	25-34	P53	Homo sapiens	68-71
24926563-8	2014	p53 mutation frequency was the lowest in the AB=0, CS=0 group, increased as AB and/or CS rose, and was significantly higher in the &gt;=1,000 AB, &gt;=25 CS group (p=0.039).	Cesium	86-88	P53	Homo sapiens	0-3
24926563-8	2014	p53 mutation frequency was the lowest in the AB=0, CS=0 group, increased as AB and/or CS rose, and was significantly higher in the &gt;=1,000 AB, &gt;=25 CS group (p=0.039).	Cesium	86-88	P53	Homo sapiens	0-3
24996846-8	2014	Induction of gammaH2AX levels was chemotherapeutic dependent and correlated closely with potentiation of gemcitabine and camptothecin in p53 mutant colon cancer cells.	Camptothecin	121-133	P53	Homo sapiens	137-140
23908355-5	2013	p53 silencing or pharmacological inhibition of HMG-CoA reductase in these cells decreases protein isoprenylation from endogenously synthesized isoprenoids but enhances the use of exogenous isoprenols for this purpose, indicating that this latter process is regulated independently of the mevalonate pathway.	Terpenes	143-154	P53	Homo sapiens	0-3
23908355-5	2013	p53 silencing or pharmacological inhibition of HMG-CoA reductase in these cells decreases protein isoprenylation from endogenously synthesized isoprenoids but enhances the use of exogenous isoprenols for this purpose, indicating that this latter process is regulated independently of the mevalonate pathway.	isobutenylcarbinol	189-199	P53	Homo sapiens	0-3
22064349-0	2012	Synergistic induction of p53 mediated apoptosis by valproic acid and nutlin-3 in acute myeloid leukemia.	nutlin 3	69-77	P53	Homo sapiens	25-28
22064349-2	2012	We hypothesized that co-inhibition of MDM2 and HDACs, with nutlin-3 and valproic acid (VPA) would additively inhibit growth in leukemic cells expressing wild type TP53 and induce p53-mediated apoptosis.	nutlin 3	59-67	P53	Homo sapiens	163-167
22064349-2	2012	We hypothesized that co-inhibition of MDM2 and HDACs, with nutlin-3 and valproic acid (VPA) would additively inhibit growth in leukemic cells expressing wild type TP53 and induce p53-mediated apoptosis.	nutlin 3	59-67	P53	Homo sapiens	179-182
24742622-13	2014	CONCLUSIONS: Oridonin induces apoptosis and cell cycle arrest involving the p53-p21 pathway in HSC and appears to be nontoxic to hepatocytes.	oridonin	13-21	P53	Homo sapiens	76-79
22410117-3	2012	We found that rottlerin dramatically induced non-steroidal anti-inflammatory drug activated gene-1 (NAG-1) expression in both p53 wild-type and p53-null cancer cell lines, suggesting that NAG-1 upregulation is a common response to rottlerin that occurs independently of p53 in multiple cell lines.	rottlerin	14-23	P53	Homo sapiens	126-129
22410117-3	2012	We found that rottlerin dramatically induced non-steroidal anti-inflammatory drug activated gene-1 (NAG-1) expression in both p53 wild-type and p53-null cancer cell lines, suggesting that NAG-1 upregulation is a common response to rottlerin that occurs independently of p53 in multiple cell lines.	rottlerin	14-23	P53	Homo sapiens	144-147
22410117-3	2012	We found that rottlerin dramatically induced non-steroidal anti-inflammatory drug activated gene-1 (NAG-1) expression in both p53 wild-type and p53-null cancer cell lines, suggesting that NAG-1 upregulation is a common response to rottlerin that occurs independently of p53 in multiple cell lines.	rottlerin	14-23	P53	Homo sapiens	144-147
23896410-0	2013	The Src and c-Kit kinase inhibitor dasatinib enhances p53-mediated targeting of human acute myeloid leukemia stem cells by chemotherapeutic agents.	Dasatinib	35-44	P53	Homo sapiens	54-57
23896410-7	2013	Combined treatment using dasatinib and chemotherapy provides a novel approach to increasing p53 activity and enhancing targeting of AML stem cells.	Dasatinib	25-34	P53	Homo sapiens	92-95
24144307-5	2014	[Flu + Clo + Bu + SAHA] resulted in synergistic cytotoxicity, which can be attributed to (1) activated DNA-damage response and cell cycle checkpoint activation through the ATM-CHK2-P53 (or P73) pathway or ATM-CHK2-cdc25-cdc2 pathway, (2) histone modifications and (3) activated apoptosis pathway.	Clofarabine	7-10	P53	Homo sapiens	181-184
23977270-4	2013	We report that a new small-molecule inhibitor of MDM2 with a spirooxoindolepyrrolidine core structure, named ISA27, effectively reactivated p53 function and inhibited human GBM cell growth in vitro by inducing cell cycle arrest and apoptosis.	isa27	109-114	P53	Homo sapiens	140-143
23977270-5	2013	In immunoincompetent BALB/c nude mice bearing a human GBM xenograft, the administration of ISA27 in vivo activated p53, inhibited cell proliferation and induced apoptosis in tumor tissue.	isa27	91-96	P53	Homo sapiens	115-118
23977270-8	2013	In conclusion, our data show that ISA27 releases the powerful antitumor capacities of p53 in GBM cells.	isa27	34-39	P53	Homo sapiens	86-89
23648290-7	2013	Exposure of MM cells to [Gem+Clo] also decreased the level of ribosomal RNA (rRNA), which might have resulted in nucleolar stress, as reported previously, and caused a p53-dependent cell death.	Clofarabine	29-32	P53	Homo sapiens	168-171
22508727-0	2012	Mutant p53 cooperates with ETS2 to promote etoposide resistance.	Etoposide	43-52	P53	Homo sapiens	7-10
22420423-0	2012	Low expression levels of ATM may substitute for CHEK2 /TP53 mutations predicting resistance towards anthracycline and mitomycin chemotherapy in breast cancer.	Mitomycin	118-127	P53	Homo sapiens	55-59
22134502-0	2012	MDM2 SNP309 modifies the prognostic significance of the p53 mutational             status in patients with ovarian cancer.	snp309	5-11	P53	Homo sapiens	56-59
23648290-8	2013	A reduction by approximately 50% in the cytotoxicity of Gem and Clo was observed in the presence of pifithrin alpha, a p53 inhibitor.	Clofarabine	64-67	P53	Homo sapiens	119-122
26417293-7	2014	Western blotting with epitopespecific monoclonal antibody Pab240 strongly suggests that nuclear extracts from breast cancer cells express mutant forms of p53.	pab240	58-64	P53	Homo sapiens	154-157
23754252-6	2013	In combination with cerulenin and oxaliplatin, activation of the p53-p21 pathway and p38 occurred in a smaller concentration and finally induced caspase-3 cleavage in a smaller concentration of cerulenin and oxaliplatin.	Cerulenin	20-29	P53	Homo sapiens	65-68
23754252-6	2013	In combination with cerulenin and oxaliplatin, activation of the p53-p21 pathway and p38 occurred in a smaller concentration and finally induced caspase-3 cleavage in a smaller concentration of cerulenin and oxaliplatin.	Cerulenin	194-203	P53	Homo sapiens	65-68
24692054-0	2014	Isofraxidin, a potent reactive oxygen species (ROS) scavenger, protects human leukemia cells from radiation-induced apoptosis via ROS/mitochondria pathway in p53-independent manner.	isofraxidin	0-11	P53	Homo sapiens	158-161
23690541-7	2013	Unexpectedly, induction of p53 by etoposide was not inhibited by cordycepin, whereas (1) expression of Sp1 (required for the induction of p21(WAF1/CIP1) and activation of p16(INK4a) by genotoxic stress) was attenuated by cordycepin, (2) DNA binding activity of Sp1 was also inhibited, and (3) selective inhibition of Sp1 reproduced the suppressive effect of cordycepin on senescence.	Etoposide	34-43	P53	Homo sapiens	27-30
24736433-12	2014	Treatment with CP-31398, a p53 rescue compound, suppressed benzo[a]pyrene-mediated induction of CYP1A1 and CYP1B1 and the formation of DNA adducts.	CP 31398	15-23	P53	Homo sapiens	27-30
23523612-7	2013	Upon systemic injection, DMAB-NPs demonstrated a 4.6-fold increase in tumor accumulation compared to unmodified NPs which also correlated to improved efficacy of p53 gene therapy.	didodecyldimethylammonium	25-29	P53	Homo sapiens	162-165
24847310-1	2014	Physiological concentrations of the green tea extract epigallocatechin-3-gallate (EGCG) caused growth inhibition in estrogen receptor alpha (ERalpha)-positive MCF7 cells that was associated with down-regulation of the ERalpha and reduced insulin-like growth factor binding protein-2 abundance and increased protein abundance of the tumor suppressor genes p53/p21.	epigallocatechin gallate	54-80	P53	Homo sapiens	355-358
23686257-0	2013	Genistein induces G2/M cell cycle arrest and apoptosis via ATM/p53-dependent pathway in human colon cancer cells.	Genistein	0-9	P53	Homo sapiens	63-66
24847310-1	2014	Physiological concentrations of the green tea extract epigallocatechin-3-gallate (EGCG) caused growth inhibition in estrogen receptor alpha (ERalpha)-positive MCF7 cells that was associated with down-regulation of the ERalpha and reduced insulin-like growth factor binding protein-2 abundance and increased protein abundance of the tumor suppressor genes p53/p21.	epigallocatechin gallate	82-86	P53	Homo sapiens	355-358
23686257-11	2013	In addition, genistein caused cell cycle arrest in the G2/M phase, which was accompanied by activation of ATM/p53, p21waf1/cip1 and GADD45alpha as well as downregulation of cdc2 and cdc25A demonstrated by q-PCR and immunoblotting assay.	Genistein	13-22	P53	Homo sapiens	110-113
24847310-4	2014	EGCG significantly increased cell death in an ERalpha-negative cell line, MDA-MB-231 that also possesses mutant p53.	epigallocatechin gallate	0-4	P53	Homo sapiens	112-115
23686257-12	2013	Interestingly, genistein induced G2/M cell cycle arrest in a p53-dependent manner.	Genistein	15-24	P53	Homo sapiens	61-64
24627081-8	2014	Western blot analysis of oxidative stress pathway-related proteins demonstrated that oridonin treatment increased p-JNK, p-p38 and p-p53, and decreased Bcl-2 protein expression levels, promoted cytochrome c release, decreased mitochondrial membrane potential, and activated caspase-9 and caspase-3.	oridonin	85-93	P53	Homo sapiens	133-136
23686257-14	2013	The ATM/p53-p21 cross-regulatory network may play a crucial role in mediating the anticarcinogenic activities of genistein in colon cancer.	Genistein	113-122	P53	Homo sapiens	8-11
24676336-12	2014	For the TSA+DAC group, higher levels of p53, p21, cyclin B1 and Chk1 were detected, concomitant with lower levels of CDK1, when compared to the control group.	trichostatin A	8-11	P53	Homo sapiens	40-43
23425510-6	2013	Irradiation activates ATM kinase, and the level of p53 protein is increased due to its phosphorylation on serine15.	serine15	106-114	P53	Homo sapiens	51-54
24405416-4	2014	Herein we report the design, synthesis and optimization of YH239-EE (ethyl ester of the free carboxylic acid compound YH239), a potent p53-MDM2 antagonizing and apoptosis-inducing agent characterized by a number of leukemia cell lines as well as patient-derived AML blast samples.	yh239	59-64	P53	Homo sapiens	135-138
23745024-3	2013	Real time polymerase chain reaction and Western blotting were used to observe expression changes in p21, p53, Bax, Bcl-2, CDK2, and CyclinD1 in gastric cancer cells exposed to TSA.	trichostatin A	176-179	P53	Homo sapiens	105-108
23745024-7	2013	p21, p53 and Bax gene expression levels in AGS cells were increased with TSA treatment duration; Bcl-2, CDK2, and CyclinD1 gene expression levels were decreased with TSA treatment duration.	trichostatin A	73-76	P53	Homo sapiens	5-8
24405416-4	2014	Herein we report the design, synthesis and optimization of YH239-EE (ethyl ester of the free carboxylic acid compound YH239), a potent p53-MDM2 antagonizing and apoptosis-inducing agent characterized by a number of leukemia cell lines as well as patient-derived AML blast samples.	Carboxylic Acids	93-108	P53	Homo sapiens	135-138
24405416-4	2014	Herein we report the design, synthesis and optimization of YH239-EE (ethyl ester of the free carboxylic acid compound YH239), a potent p53-MDM2 antagonizing and apoptosis-inducing agent characterized by a number of leukemia cell lines as well as patient-derived AML blast samples.	yh239	118-123	P53	Homo sapiens	135-138
23017582-5	2013	Reporter assays, using the luciferase constructs containing the NAG-1 promoter, demonstrate that p53 is required for EGCG-mediated activation of NAG-1.	epigallocatechin gallate	117-121	P53	Homo sapiens	97-100
23017582-9	2013	Taken together, these results demonstrate for the first time that EGCG induces apoptosis via ATM/p53-dependent NAG-1 expression in HNSCC, providing an additional mechanistic explanation for the apoptotic activity of EGCG.	epigallocatechin gallate	66-70	P53	Homo sapiens	97-100
24405416-5	2014	The structural basis of the interaction between MDM2 (the p53 receptor) and YH239 is elucidated by a co-crystal structure.	yh239	76-81	P53	Homo sapiens	58-61
23017582-9	2013	Taken together, these results demonstrate for the first time that EGCG induces apoptosis via ATM/p53-dependent NAG-1 expression in HNSCC, providing an additional mechanistic explanation for the apoptotic activity of EGCG.	epigallocatechin gallate	216-220	P53	Homo sapiens	97-100
24451373-10	2014	Pharmacologic intervention with CP-31398, a p53 rescue agent, inhibited recruitment of Aha1 to Hsp90 and suppressed Wnt-mediated gene expression in colon cancer cells.	CP 31398	32-40	P53	Homo sapiens	44-47
23536721-2	2013	MK-8776 synergistically potentiated vorinostat-mediated apoptosis in various p53-wt or -deficient leukemia cell lines, whereas p53 knockdown by short hairpin RNA (shRNA) sensitized p53-wt cells to lethality of this regimen.	MK-8776	0-7	P53	Homo sapiens	77-80
23589839-4	2013	Here, we show that Myc-induced altered glutamine metabolism involves ATP depletion and activation of the energy sensor AMP-activated protein kinase (AMPK), which induces stabilizing phosphorylation of p53 at Ser15.	Glutamine	39-48	P53	Homo sapiens	201-204
24297112-9	2014	Collectively, these results suggest that p53-dependent and caspase-dependent induction of p38 MAPK directly participates in apoptosis induced by oridonin.	oridonin	145-153	P53	Homo sapiens	41-44
24871662-5	2014	Bufalin could activate phosphorylated p53 in NCI-H460 cells.	bufalin	0-7	P53	Homo sapiens	38-41
23406297-0	2013	ARHGDIA, a mutant TP53-associated Rho GDP dissociation inhibitor, is over-expressed in gene expression profiles of TP53 disrupted chronic lymphocytic leukaemia cells.	Guanosine Diphosphate	38-41	P53	Homo sapiens	18-22
23406297-0	2013	ARHGDIA, a mutant TP53-associated Rho GDP dissociation inhibitor, is over-expressed in gene expression profiles of TP53 disrupted chronic lymphocytic leukaemia cells.	Guanosine Diphosphate	38-41	P53	Homo sapiens	115-119
24239893-4	2014	Resveratrol, in combination with clofarabine, time-dependently induced a strong cytotoxic effect with the nuclear accumulation of phospho-p53 (p-p53) in MSTO-211H cells, but not in normal mesothelial MeT-5A cells.	Clofarabine	33-44	P53	Homo sapiens	138-141
24239893-4	2014	Resveratrol, in combination with clofarabine, time-dependently induced a strong cytotoxic effect with the nuclear accumulation of phospho-p53 (p-p53) in MSTO-211H cells, but not in normal mesothelial MeT-5A cells.	Clofarabine	33-44	P53	Homo sapiens	145-148
23463103-0	2013	Zinc(II) complexes containing bis-benzimidazole derivatives as a new class of apoptosis inducers that trigger DNA damage-mediated p53 phosphorylation in cancer cells.	bis-benzimidazole	30-47	P53	Homo sapiens	130-133
24239893-10	2014	Taken together, these results demonstrate that resveratrol and clofarabine synergistically elicit apoptotic signal via a p53-dependent pathway, and provide a scientific rationale for clinical evaluation of resveratrol as a promising chemopotentiator in MM.	Clofarabine	63-74	P53	Homo sapiens	121-124
24090840-0	2013	Effect of zinc oxide nanomaterials-induced oxidative stress on the p53 pathway.	Zinc Oxide	10-20	P53	Homo sapiens	67-70
23499005-0	2013	The B55alpha subunit of PP2A drives a p53-dependent metabolic adaptation to glutamine deprivation.	Glutamine	76-85	P53	Homo sapiens	38-41
24090840-3	2013	Here, using a BJ fibroblast p53 knockdown system, we showed that p53 may be implicated in playing a dual regulatory role to determine cell survivability in response to oxidative stress induced by ZnO NMs.	Zinc Oxide	196-199	P53	Homo sapiens	28-31
23499005-4	2013	Moreover, B55alpha is specifically induced upon glutamine deprivation in a ROS-dependent manner to activate p53 and promote cell survival.	Glutamine	48-57	P53	Homo sapiens	108-111
23499005-6	2013	Importantly, the B55alpha-EDD-p53 pathway is essential for cancer cell survival and tumor growth under low glutamine conditions in vitro and in vivo.	Glutamine	107-116	P53	Homo sapiens	30-33
24090840-3	2013	Here, using a BJ fibroblast p53 knockdown system, we showed that p53 may be implicated in playing a dual regulatory role to determine cell survivability in response to oxidative stress induced by ZnO NMs.	Zinc Oxide	196-199	P53	Homo sapiens	65-68
24071474-0	2013	Ursolic acid induces apoptosis of SW480 cells via p53 activation.	ursolic acid	0-12	P53	Homo sapiens	50-53
24071474-3	2013	Both the expression level and transcriptional activity of p53, an apoptotic protein, were remarkably up-regulated in cells treated with ursolic acid compared to blank group.	ursolic acid	136-148	P53	Homo sapiens	58-61
23426174-7	2013	Our study suggested that the apoptotic effect of 8-c can be attributed to the upregulation of p53, caspase-3, and cleaved poly(ADP-ribose) polymerase (PARP) and the downregulation of Bcl-2.	8-c	49-52	P53	Homo sapiens	94-97
24091633-4	2013	We explored tet-inducible miR-34a-expressing human p53 wild-type and R273H p53 mutant GBM cell lines, and found that miR-34a influences the broad spectrum of 53BP1-mediated DNA damage response.	tetramethylenedisulfotetramine	12-15	P53	Homo sapiens	51-54
23054209-1	2013	The effect of Nutlin-3, a small molecule inhibitor of the MDM2/p53 interaction, was investigated on the steady-state mRNA levels of the transcription factors E2F1 and E2F7 in a cohort of primary B-chronic lymphocytic leukemia (B-CLL) patient samples (n = 15) and normal peripheral blood mononuclear cells (PBMC).	nutlin 3	14-22	P53	Homo sapiens	63-66
24091633-4	2013	We explored tet-inducible miR-34a-expressing human p53 wild-type and R273H p53 mutant GBM cell lines, and found that miR-34a influences the broad spectrum of 53BP1-mediated DNA damage response.	tetramethylenedisulfotetramine	12-15	P53	Homo sapiens	75-78
23238993-3	2013	Here, we show that two of these compounds, CP-31398 and RITA, induce cell growth inhibition, apoptosis, and autophagy by activating p53/DNA binding and p53 phosphorylation (Ser15), without affecting the total p53 amount.	CP 31398	43-51	P53	Homo sapiens	132-135
24008518-9	2013	Protein levels of both p53 and glucosidase II were increased in response to UV irradiation but decreased in response to tunicamycin-induced ER stress.	Tunicamycin	120-131	P53	Homo sapiens	23-26
23238993-3	2013	Here, we show that two of these compounds, CP-31398 and RITA, induce cell growth inhibition, apoptosis, and autophagy by activating p53/DNA binding and p53 phosphorylation (Ser15), without affecting the total p53 amount.	CP 31398	43-51	P53	Homo sapiens	152-155
23238993-3	2013	Here, we show that two of these compounds, CP-31398 and RITA, induce cell growth inhibition, apoptosis, and autophagy by activating p53/DNA binding and p53 phosphorylation (Ser15), without affecting the total p53 amount.	CP 31398	43-51	P53	Homo sapiens	152-155
23988450-6	2013	We searched for compounds that can suppress excitotoxicity-induced neurodegeneration and found that CP-31398, a known compound that can rescue the structure and function of the tumor suppressor protein p53 mutant form and stabilize the active conformation of the p53 wild-type form, suppresses excitotoxicity-induced axon degeneration and cell body death.	CP 31398	100-108	P53	Homo sapiens	202-205
23255232-8	2013	p53-mediated downregulation of HMGB2 was confirmed by direct activation of p53 using Nutlin-3 or by inducing p53 expression using Tet-On system.	tetramethylenedisulfotetramine	130-133	P53	Homo sapiens	0-3
23808158-7	2013	Moreover, EGCG suppressed the high glucose-induced expression of c-fos, c-myc and p53.	epigallocatechin gallate	10-14	P53	Homo sapiens	82-85
23808158-8	2013	These findings suggest that EGCG protects HLEB-3 cells from high glucose-induced apoptosis by regulating the gene expression of the Bcl-2 family, c-fos, c-myc and p53.	epigallocatechin gallate	28-32	P53	Homo sapiens	163-166
22225791-9	2012	AMPKalpha(-/-)-MEFs showed increased basal levels of p53 and cyclin-dependent kinase inhibitors p21(cip1), but lack of response of both genes to IR.	(-/-)-mefs	9-19	P53	Homo sapiens	53-56
22104727-8	2012	The levels of Stat3 target oncogenes such as Bcl-2 and c-Myc were decreased with DPP, a Stat3 inhibitor, treatment, while the expression of tumor suppressor p53 was increased.	dipalmitoylphosphatidylserine	81-84	P53	Homo sapiens	157-160
23988450-6	2013	We searched for compounds that can suppress excitotoxicity-induced neurodegeneration and found that CP-31398, a known compound that can rescue the structure and function of the tumor suppressor protein p53 mutant form and stabilize the active conformation of the p53 wild-type form, suppresses excitotoxicity-induced axon degeneration and cell body death.	CP 31398	100-108	P53	Homo sapiens	263-266
23368735-0	2013	The contrasting activity of iodido versus chlorido ruthenium and osmium arene azo- and imino-pyridine anticancer complexes: control of cell selectivity, cross-resistance, p53 dependence, and apoptosis pathway.	iodido	28-34	P53	Homo sapiens	171-174
23208500-11	2013	Consistent with p53 derepression, NF90/NF45-depleted HeLa cells displayed elevated poly ADP-ribose polymerase (PARP) cleavage and susceptibility to camptothecin-induced apoptosis.	Camptothecin	148-160	P53	Homo sapiens	16-19
23287532-3	2013	To investigate these phenomena and their relationship to pluripotency and senescence, we examined the response of the TP53-competent embryonal carcinoma (EC) cell line PA-1 to etoposide-induced DNA damage.	Etoposide	176-185	P53	Homo sapiens	118-122
23434831-4	2013	Transfection of cells with dominant-negative Ras (RasN17) mutant genes up-regulated asperolide A-induced the decrease of cyclin B1 and CDC2, suppressed Raf, ERK activity and p53-p21 expression, and at last, abolished G2/M arrest.	asperolide A	84-96	P53	Homo sapiens	174-177
23434831-5	2013	This study indicates that asperolide A-induced G2/M arrest in human NCI-H460 lung carcinoma cells relys on the participation of the Ras/Raf/MEK/ERK signaling pathway in p53-p21 stabilization.	asperolide A	26-38	P53	Homo sapiens	169-172
21761401-11	2012	Knockdown of p53 or BAX in leukemia cells resulted in decreased apoptosis induced by ABT-737.	ABT-737	85-92	P53	Homo sapiens	13-16
21761401-12	2012	CONCLUSIONS: The current data indicated that p53 dysfunction may lead to decreased apoptosis induction by ABT-737.	ABT-737	106-113	P53	Homo sapiens	45-48
22112863-6	2012	Upon treatment with depsipeptide, p53 phosphorylation at threonine 18 (Thr18) was specifically induced.	Depsipeptides	20-32	P53	Homo sapiens	34-37
24066170-8	2013	Systematic analyses of the cytotoxic effects of 11a in NCI-60 cell lines revealed a strong positive correlation of cytotoxicity with p53 status, i.e., p53 wild type cell lines were significantly more sensitive to 11a than p53 mutated or null cell lines.	1-deamino-1-hydroxyxylostasin	48-51	P53	Homo sapiens	133-136
22112863-8	2012	Our results demonstrate that depsipeptide plays an anti-neoplastic role by generating ROS to elicit p53/p21 pathway activation.	Depsipeptides	29-41	P53	Homo sapiens	100-103
22076075-5	2012	Moreover, thioflavanone, but not thioflavone, induces apoptosis via p53-dependent expression of Bax.	thioflavanone	10-23	P53	Homo sapiens	68-71
24154492-4	2013	With this approach, we visualize the p53-HDM2 interaction in living cells and directly monitor the disruption of this interaction by Nutlin 3, a drug developed to boost p53 activity in cancer therapy.	nutlin 3	133-141	P53	Homo sapiens	37-40
24154492-4	2013	With this approach, we visualize the p53-HDM2 interaction in living cells and directly monitor the disruption of this interaction by Nutlin 3, a drug developed to boost p53 activity in cancer therapy.	nutlin 3	133-141	P53	Homo sapiens	169-172
24066170-8	2013	Systematic analyses of the cytotoxic effects of 11a in NCI-60 cell lines revealed a strong positive correlation of cytotoxicity with p53 status, i.e., p53 wild type cell lines were significantly more sensitive to 11a than p53 mutated or null cell lines.	1-deamino-1-hydroxyxylostasin	48-51	P53	Homo sapiens	151-154
24066170-8	2013	Systematic analyses of the cytotoxic effects of 11a in NCI-60 cell lines revealed a strong positive correlation of cytotoxicity with p53 status, i.e., p53 wild type cell lines were significantly more sensitive to 11a than p53 mutated or null cell lines.	1-deamino-1-hydroxyxylostasin	48-51	P53	Homo sapiens	151-154
22085531-0	2012	A butyrolactone derivative suppressed lipopolysaccharide-induced autophagic injury through inhibiting the autoregulatory loop of p8 and p53 in vascular endothelial cells.	4-Butyrolactone	2-15	P53	Homo sapiens	136-139
23922104-0	2013	Src kinases in chondrosarcoma chemoresistance and migration: dasatinib sensitises to doxorubicin in TP53 mutant cells.	Dasatinib	61-70	P53	Homo sapiens	100-104
22214764-8	2012	Functionally, the cytoplasmic accumulation of ZBP-89 by p53(G245D) significantly abrogated the induction of p21 caused by sodium butyrate (NaB) treatment and protected cells from TSA-induced death.	nab	139-142	P53	Homo sapiens	56-59
22214764-8	2012	Functionally, the cytoplasmic accumulation of ZBP-89 by p53(G245D) significantly abrogated the induction of p21 caused by sodium butyrate (NaB) treatment and protected cells from TSA-induced death.	trichostatin A	179-182	P53	Homo sapiens	56-59
23359208-0	2012	Anacardic acid (6-pentadecylsalicylic acid) induces apoptosis of prostate cancer cells through inhibition of androgen receptor and activation of p53 signaling.	anacardic acid	0-14	P53	Homo sapiens	145-148
23359208-0	2012	Anacardic acid (6-pentadecylsalicylic acid) induces apoptosis of prostate cancer cells through inhibition of androgen receptor and activation of p53 signaling.	anacardic acid	16-42	P53	Homo sapiens	145-148
23817390-7	2013	Furthermore, cell cycle analysis showed that the cell cycle of CSA-13-treated wild-type and p53 null mutant HCT116 cells was arrested at the G1/S phase, indicating that CSA-13 affects the cell cycle by a p53-independent pathway.	Ceragenin CSA-13	169-175	P53	Homo sapiens	204-207
22985798-0	2012	Cell death induced by 7-oxysterols via lysosomal and mitochondrial pathways is p53-dependent.	7-oxysterols	22-34	P53	Homo sapiens	79-82
22233735-4	2012	METHODS: We have analyzed uterine leiomyomas and matching normal tissue for the expression of p14Arf and used explants to see if reducing the MDM2 activity using the small-molecule inhibitor nutlin-3 can induce p53 and activate genes involved in senescence and/or apoptosis.	nutlin 3	191-199	P53	Homo sapiens	211-214
23835407-0	2013	miR-375 targets the p53 gene to regulate cellular response to ionizing radiation and etoposide in gastric cancer cells.	Etoposide	85-94	P53	Homo sapiens	20-23
21954050-0	2012	Exhaustive fluorine scanning toward potent p53-Mdm2 antagonists.	Fluorine	11-19	P53	Homo sapiens	43-46
22985798-4	2012	We show here that 7-oxysterols induce endogenous full-length p53 and phospho-p53 (p53-Ser15) in both nucleus and cytoplasm of THP1 and J774 cells, which is followed by cellular oxidative stress and apoptotic cell death.	7-oxysterols	18-30	P53	Homo sapiens	61-64
22985798-4	2012	We show here that 7-oxysterols induce endogenous full-length p53 and phospho-p53 (p53-Ser15) in both nucleus and cytoplasm of THP1 and J774 cells, which is followed by cellular oxidative stress and apoptotic cell death.	7-oxysterols	18-30	P53	Homo sapiens	77-80
22985798-4	2012	We show here that 7-oxysterols induce endogenous full-length p53 and phospho-p53 (p53-Ser15) in both nucleus and cytoplasm of THP1 and J774 cells, which is followed by cellular oxidative stress and apoptotic cell death.	7-oxysterols	18-30	P53	Homo sapiens	77-80
22985798-5	2012	The role of p53 in 7-oxysterol-mediated cell death is further investigated in temperature sensitive p53-transfected (M1-t-p53) and in p53-deficient (M1) cells.	7-oxysterol	19-30	P53	Homo sapiens	12-15
22985798-6	2012	These results reveal that 7-oxysterols induce induction and nuclear translocation of p53 in M1-t-p53 cells, which in turn enhances LMP, mitochondrial translocation of Bax, mitochondrial membrane permeabilization, cytosolic release of cytochrome c, and cell death.	7-oxysterols	26-38	P53	Homo sapiens	85-88
22985798-6	2012	These results reveal that 7-oxysterols induce induction and nuclear translocation of p53 in M1-t-p53 cells, which in turn enhances LMP, mitochondrial translocation of Bax, mitochondrial membrane permeabilization, cytosolic release of cytochrome c, and cell death.	7-oxysterols	26-38	P53	Homo sapiens	97-100
22985798-8	2012	The findings reveal that 7-oxysterol-induced cell death occurs via p53-dependent pathways.	7-oxysterol	25-36	P53	Homo sapiens	67-70
23351311-0	2012	Genistein abrogates G2 arrest induced by curcumin in p53 deficient T47D cells.	Genistein	0-9	P53	Homo sapiens	53-56
22715313-9	2012	Here, we have identified three drug-like compounds that are ZINC01019934, ZINC00624418 and ZINC00664532 adequate to interrupt stability of p53-mortalin complex that warrant for anticancer agent.	zinc00664532	91-103	P53	Homo sapiens	139-142
22065080-0	2012	Antitumor activity of NVP-BKM120--a selective pan class I PI3 kinase inhibitor showed differential forms of cell death based on p53 status of glioma cells.	NVP-BKM120	26-32	P53	Homo sapiens	128-131
22065080-13	2012	CONCLUSION: Our present findings establish that NVP-BKM120 inhibits the PI3K signaling pathways, leading to different forms of cell death on the basis of p53 statuses.	NVP-BKM120	52-58	P53	Homo sapiens	154-157
23835407-10	2013	These results demonstrate that miR-375 targets p53 to regulate the response to ionizing radiation and etoposide treatment.	Etoposide	102-111	P53	Homo sapiens	47-50
23184205-10	2012	Phosphatidylinositol 3-kinase CA exon 20 mutations were associated with poor overall survival and TP53 gene mutations.	Phosphatidylinositols	0-20	P53	Homo sapiens	98-102
25337549-7	2013	On the other hand, glutamine stimulates the activation of the tumor suppressor p53, which induces apoptosis and tumor regression.	Glutamine	19-28	P53	Homo sapiens	79-82
23058634-3	2012	Indeed, we showed that etoposide could influence transcription and was able to activate DDR in resting human T cells by inducing phosphorylation of ATM and its substrates, H2AX and p53.	Etoposide	23-32	P53	Homo sapiens	181-184
23251091-0	2012	Combining the chemotherapeutic effects of epigallocatechin 3-gallate with siRNA-mediated p53 knock-down results in synergic pro-apoptotic effects.	epigallocatechin gallate	42-68	P53	Homo sapiens	89-92
23720736-7	2013	RUNX2 protein levels decrease upon stabilization of p53 with the MDM2 inhibitor Nutlin-3.	nutlin 3	80-88	P53	Homo sapiens	52-55
23259030-0	2012	Preventive effects of epigallocatechin-3-O-gallate against replicative senescence associated with p53 acetylation in human dermal fibroblasts.	epigallocatechin gallate	22-50	P53	Homo sapiens	98-101
23259030-3	2012	The involvement of Sirt1 and acetylated p53 was examined as an underlying mechanism for the senescence preventive activity of EGCG in HDFs.	epigallocatechin gallate	126-130	P53	Homo sapiens	40-43
23259030-7	2012	Furthermore, EGCG was found to prevent serial passage- and H(2)O(2)-induced senescence in HDFs by suppressing p53 acetylation, but the Sirt1 activity was unaffected.	epigallocatechin gallate	13-17	P53	Homo sapiens	110-113
22948151-6	2012	Induction of p53 can be achieved by several means, such as UV radiation and treatment with anti-cancer agents (including doxorubicin, etoposide, roscovitine, flavopiridol, and nutlin-3).	Etoposide	134-143	P53	Homo sapiens	13-16
22948151-6	2012	Induction of p53 can be achieved by several means, such as UV radiation and treatment with anti-cancer agents (including doxorubicin, etoposide, roscovitine, flavopiridol, and nutlin-3).	nutlin 3	176-184	P53	Homo sapiens	13-16
23845085-5	2013	RESULTS: Cathinone, cathine and norephedrine generally reduced post-translational modifications of intracellular signal transducers in T-lymphocytes, B-lymphocytes, natural killer cells and monocytes, most prominently affecting c-Cbl (pTyr700), ERK1/2 (p-Thr202/p-Tyr204), p38 MAPK (p-Thr180/p-Tyr182) and p53 (both total p53 protein and p-Ser15).	cathinone	9-18	P53	Homo sapiens	306-309
22959527-0	2012	Synthesis of novel ursolic acid heterocyclic derivatives with improved abilities of antiproliferation and induction of p53, p21waf1 and NOXA in pancreatic cancer cells.	ursolic acid	19-31	P53	Homo sapiens	119-122
23300887-14	2012	Our studies demonstrate that terpenoids from SDGE mediate apoptosis by activating p53 and should be therefore be investigated as agents for the treatment of endometrial cancer.	Terpenes	29-39	P53	Homo sapiens	82-85
23845085-5	2013	RESULTS: Cathinone, cathine and norephedrine generally reduced post-translational modifications of intracellular signal transducers in T-lymphocytes, B-lymphocytes, natural killer cells and monocytes, most prominently affecting c-Cbl (pTyr700), ERK1/2 (p-Thr202/p-Tyr204), p38 MAPK (p-Thr180/p-Tyr182) and p53 (both total p53 protein and p-Ser15).	cathinone	9-18	P53	Homo sapiens	322-325
23236396-3	2012	It has been shown that DeltaNp73 has an inhibitory effect on the transactivation capacity of p53 and other p73 isoforms.	deltanp73	23-32	P53	Homo sapiens	93-96
23845085-10	2013	Cathinone, cathine and norephedrine reduced phosphorylation of c-Cbl, ERK1/2, p38 MAPK and p53(Ser15), and norephedrine induced T-lymphocyte proliferation.	cathinone	0-9	P53	Homo sapiens	91-94
23759586-8	2013	Use of antisense miR-125b transcripts enhanced expression of pro-apoptotic p53, repressed expression of anti-apoptotic SIRT1 and, importantly, significantly enhanced dexamethasone-induced cell death responses in MM.	125b	21-25	P53	Homo sapiens	75-78
22916232-5	2012	Simulations of arylamides in the p53 binding pocket of hDM2 are consistent with binding, exhibiting similar structural dynamics in the pocket as simulations of known hDM2 binders Nutlin-2 and a benzodiazepinedione compound.	benzodiazepinedione	194-213	P53	Homo sapiens	33-36
22765290-3	2012	In this review, we focus on highlighting several representative plant natural compounds such as curcumin, resveratrol, paclitaxel, oridonin, quercetin and plant lectin - that may lead to cancer cell death - for regulation of some core autophagic pathways, involved in Ras-Raf signalling, Beclin-1 interactome, BCR-ABL, PI3KCI/Akt/mTOR, FOXO1 signalling and p53.	oridonin	131-139	P53	Homo sapiens	357-360
22999639-4	2013	In U937 cells, 7beta-hydroxycholesterol and 7-ketocholesterol induced production of reactive oxygen species (ROS), transient up-regulation of Egr1 followed by late induction of p53 and apoptosis.	cholest-5-en-3 beta,7 alpha-diol	15-39	P53	Homo sapiens	177-180
22993307-0	2012	A new chalcone derivative (E)-3-(4-methoxyphenyl)-2-methyl-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-one suppresses prostate cancer involving p53-mediated cell cycle arrests and apoptosis.	Chalcone	6-14	P53	Homo sapiens	138-141
23019099-6	2012	This finding excluded that the individual p53 spots in 2D gels reflect charge isomers generated by phosphorylation, but rather suggest that they are due to conformational flexibility of urea-denatured monomeric p53 molecules or deamidation of asparagine and glutamine residues.	Glutamine	258-267	P53	Homo sapiens	42-45
22719951-11	2012	The use of small molecules that restore p53 activity, such as CP-31398 or Nutlin-3a, in association with TNF-alpha, potentiated the cell death of respectively TP53(Mut) and TP53(Wt)/MDM2(Ampl).	CP 31398	62-70	P53	Homo sapiens	40-43
22719951-11	2012	The use of small molecules that restore p53 activity, such as CP-31398 or Nutlin-3a, in association with TNF-alpha, potentiated the cell death of respectively TP53(Mut) and TP53(Wt)/MDM2(Ampl).	CP 31398	62-70	P53	Homo sapiens	159-163
22719951-11	2012	The use of small molecules that restore p53 activity, such as CP-31398 or Nutlin-3a, in association with TNF-alpha, potentiated the cell death of respectively TP53(Mut) and TP53(Wt)/MDM2(Ampl).	CP 31398	62-70	P53	Homo sapiens	173-177
22719951-12	2012	In particular, CP-31398 was able to induce p53 as well as some of its apoptotic target genes in TP53(Mut) cells.	CP 31398	15-23	P53	Homo sapiens	43-46
22719951-12	2012	In particular, CP-31398 was able to induce p53 as well as some of its apoptotic target genes in TP53(Mut) cells.	CP 31398	15-23	P53	Homo sapiens	96-100
22710877-5	2012	In vitro, oridonin inhibited the proliferation of the PaCa cell line, BxPC-3, potentiated the apoptosis induced by gemcitabine, induced G1 cell cycle arrest and activated p38 and p53; these results were significant when oridonin was combined with gemcitabine.	oridonin	10-18	P53	Homo sapiens	179-182
22999639-5	2013	Cells with nuclear fragmentation induced by 7-oxysterol or p53 showed increased levels of p53, but decreased levels of Egr1.	7-oxysterol	44-55	P53	Homo sapiens	90-93
22710877-7	2012	Tumors from nude mice injected with BxPC-3 PaCa cells and treated with a combination of oridonin and gemcitabine showed a significant upregulation in p38 and p53 activation (P&lt;0.05 vs. control, P&lt;0.05 vs. gemcitabine or oridonin alone).	oridonin	88-96	P53	Homo sapiens	158-161
22710877-8	2012	Taken together, our results demonstrate that oridonin can potentiate the effects of gemcitabine in PaCa through the mitogen-activated protein kinase (MAPK)-p38 signaling pathway, which is dependent on p53 activation.	oridonin	45-53	P53	Homo sapiens	201-204
22999639-7	2013	The late induced p53 by 7-oxysterols contributes to apoptotic cell death and is linked to the reduction of Egr1 levels, which resembles the differential expression of p53 and Egr1 in human atheroma progression.	7-oxysterols	24-36	P53	Homo sapiens	17-20
22319594-6	2012	By using a functional assay, the Functional Analysis of Separated Alleles in Yeast (FASAY), the present study depicts the mutational pattern of TP53 in normal human fibroblasts after in vitro exposure to well-known carcinogens: benzo[a]pyrene, aflatoxin B(1) and acetaldehyde.	Aflatoxin B1	244-255	P53	Homo sapiens	144-148
22999639-7	2013	The late induced p53 by 7-oxysterols contributes to apoptotic cell death and is linked to the reduction of Egr1 levels, which resembles the differential expression of p53 and Egr1 in human atheroma progression.	7-oxysterols	24-36	P53	Homo sapiens	167-170
23380026-8	2013	We also demonstrate that exogenous XOR is sufficient to increase p53 expression and induce apoptosis, suggesting that XOR is an upstream mediator of p53 in CS-induced EC apoptosis.	Cesium	156-158	P53	Homo sapiens	65-68
21703625-0	2011	Ursolic acid causes DNA-damage, p53-mediated, mitochondria- and caspase-dependent human endothelial cell apoptosis, and accelerates atherosclerotic plaque formation in vivo.	ursolic acid	0-12	P53	Homo sapiens	32-35
22751989-7	2012	As expected, sirtinol significantly increased the acetylation of p53, which has been reported to be a target of SIRT1/2.	sirtinol	13-21	P53	Homo sapiens	65-68
22763759-6	2012	However, the growth-inhibitory activity of vincristine, doxorubicin, carboplatin, etoposide, and temozolomide was significantly impaired by silencing of TP53.	Etoposide	82-91	P53	Homo sapiens	153-157
23380026-8	2013	We also demonstrate that exogenous XOR is sufficient to increase p53 expression and induce apoptosis, suggesting that XOR is an upstream mediator of p53 in CS-induced EC apoptosis.	Cesium	156-158	P53	Homo sapiens	149-152
21703625-4	2011	UA causes DNA-damage, followed by the activation of a p53-, BAK-, and caspase-dependent cell-death pathway.	ursolic acid	0-2	P53	Homo sapiens	54-77
23380026-10	2013	In conclusion, CS increases XOR expression, and the enzyme is both sufficient and necessary for p53 induction and CS-induced EC apoptosis.	Cesium	15-17	P53	Homo sapiens	96-99
23683164-6	2013	Synthetic oligodeoxynucleotide duplexes containing site-specific O(6)-POB-dG adducts within K-ras and p53 gene-derived DNA sequences were incubated with recombinant human AGT protein, and the kinetics of POB group transfer was monitored by isotope dilution HPLC-ESI(+)-MS/MS analysis of O(6)-POB-dG remaining in DNA over time.	Oligodeoxyribonucleotides	10-30	P53	Homo sapiens	102-105
21225623-8	2011	Further, stilbene-elicited signaling cascade leading to p53 activation was examined in MCF-7 cells and results showed that resveratrol and triacetyl-resveratrol induced both ERK and p38 phosphorylation, whereas only marginal changes in state of phosphorylation in these two kinases were observed in trimethoxy-resveratrol-treated cells.	trimethoxy resveratrol	299-321	P53	Homo sapiens	56-59
22979935-0	2012	Chelidonine isolated from ethanolic extract of Chelidonium majus promotes apoptosis in HeLa cells through p38-p53 and PI3K/AKT signalling pathways.	chelidonine	0-11	P53	Homo sapiens	110-113
22979935-10	2012	Studies of signalling pathway revealed that chelidonine could efficiently induce apoptosis through up-regulation of expressions of p38, p53 and other pro-apoptotic genes and down-regulation of expressions of AKT, PI3K, JAK3, STAT3, E6, E7 and other antiapoptotic genes.	chelidonine	44-55	P53	Homo sapiens	136-139
22979935-11	2012	CONCLUSION: Chelidonine isolated from Chelidonium majus efficiently induced apoptosis in HeLa cells through possible alteration of p38-p53 and AKT/PI3 kinase signalling pathways.	chelidonine	12-23	P53	Homo sapiens	135-138
23470959-6	2013	However, caspase-7 activation induced by camptothecin was regulated by DDX3 in a manner dependent on the functional status of p53.	Camptothecin	41-53	P53	Homo sapiens	126-129
22395444-8	2012	In addition, ZnO nanoparticles activated JNK, p38 and induced p53(Ser15) phosphorylation.	Zinc Oxide	13-16	P53	Homo sapiens	62-65
22785205-5	2012	In this study, we tested if combining Inauhzin with Nutlin-3, an inhibitor of MDM2-p53 binding, might synergistically activate p53 to suppress tumor growth.	nutlin 3	52-60	P53	Homo sapiens	83-86
22785205-5	2012	In this study, we tested if combining Inauhzin with Nutlin-3, an inhibitor of MDM2-p53 binding, might synergistically activate p53 to suppress tumor growth.	nutlin 3	52-60	P53	Homo sapiens	127-130
23470959-7	2013	Depletion of DDX3 abrogated camptothecin-induced caspase-7 activation in MCF-7 cells expressing functional wild-type p53, but oppositely potentiated camptothecin-mediated caspase activation in cells expressing mutant or non-functional p53, which was accompanied by increased activation of the extrinsic apoptotic signaling initiator caspase-8.	Camptothecin	28-40	P53	Homo sapiens	117-120
20857345-5	2011	Mechanistically, p53-siRNA inhibited phosphatidylinositol 3"-kinase/Akt signaling pathway, which might be responsible for the reduced proliferation and apoptosis induction.	Phosphatidylinositols	37-57	P53	Homo sapiens	17-20
23470959-8	2013	In MCF-7 cells, depletion of DDX3 reduced by more than 50% camptothecin-induced p53 accumulation, and this effect was blocked by inhibition of the proteasome with MG132, indicating that DDX3 regulates p53 not at expression level but rather its stabilization after DNA damage.	Camptothecin	59-71	P53	Homo sapiens	80-83
22481618-8	2012	The induction of apoptosis was inhibited in HCC cells precultured with p53 decoy oligodeoxynucleotide.	Oligodeoxyribonucleotides	81-101	P53	Homo sapiens	71-74
23470959-8	2013	In MCF-7 cells, depletion of DDX3 reduced by more than 50% camptothecin-induced p53 accumulation, and this effect was blocked by inhibition of the proteasome with MG132, indicating that DDX3 regulates p53 not at expression level but rather its stabilization after DNA damage.	Camptothecin	59-71	P53	Homo sapiens	201-204
23428467-3	2013	Using this approach, in association with a yeast p53 transactivation assay, the pyranoxanthone (3,4-dihydro-12-hydroxy-2,2-dimethyl-2H,6H-pyrano[3,2-b]xanthen-6-one) (1) was identified as a putative small-molecule inhibitor of p53-MDM2 interaction.	3,4-dihydro-12-hydroxy-2,2-dimethyl-2H,6H-pyrano(3,2-b)xanthen-6-one	96-164	P53	Homo sapiens	49-52
22357944-4	2012	We found that in untreated normal human cells these two nuclear proteins, p53 and RECQL4, instead colocalize in the mitochondrial nucleoids.	nucleoids	130-139	P53	Homo sapiens	74-77
21664489-0	2011	ZnO nanorod-induced apoptosis in human alveolar adenocarcinoma cells via p53, survivin and bax/bcl-2 pathways: role of oxidative stress.	Zinc Oxide	0-3	P53	Homo sapiens	73-76
21664489-5	2011	Western blot results showed that ZnO nanorods induced the expression of heat shock protein 70, a first-tier marker of cell damage and a cell-cycle checkpoint protein p53.	Zinc Oxide	33-36	P53	Homo sapiens	166-169
21664489-7	2011	In conclusion, our data demonstrates that ZnO nanorod induced apoptosis in A549 cells through ROS and oxidative stress via p53, survivin, bax/bcl-2 and caspase pathways.	Zinc Oxide	42-45	P53	Homo sapiens	123-126
22331493-10	2012	XPC siRNA transfection sensitized wild-type p53-expressing cells to cisplatin, suggesting that sodium arsenite +- hyperthermia attenuation of XPC is a mechanism by which wild-type p53-expressing cells are sensitized to cisplatin.	sodium arsenite	95-110	P53	Homo sapiens	180-183
23428467-3	2013	Using this approach, in association with a yeast p53 transactivation assay, the pyranoxanthone (3,4-dihydro-12-hydroxy-2,2-dimethyl-2H,6H-pyrano[3,2-b]xanthen-6-one) (1) was identified as a putative small-molecule inhibitor of p53-MDM2 interaction.	3,4-dihydro-12-hydroxy-2,2-dimethyl-2H,6H-pyrano(3,2-b)xanthen-6-one	96-164	P53	Homo sapiens	227-230
22331493-11	2012	Hyperthermia +- sodium arsenite enhanced cellular and DNA accumulation of platinum in wild-type p53-expressing cells.	sodium arsenite	16-31	P53	Homo sapiens	96-99
23483203-6	2013	Although EGCG promotes MDM2 expression in a p53-dependent manner, the interaction between MDM2 and p53 was significantly inhibited following EGCG treatment, which resulted in the inhibition of MDM2-mediated p53 ubiquitination.	epigallocatechin gallate	141-145	P53	Homo sapiens	99-102
22331493-13	2012	In conclusion, sodium arsenite +- hyperthermia sensitizes wild-type p53-expressing EOC cells to cisplatin by suppressing DNA repair protein XPC and increasing cellular and DNA platinum accumulation.	sodium arsenite	15-30	P53	Homo sapiens	68-71
22086402-0	2011	A triterpenoid from Thalictrum fortunei induces apoptosis in BEL-7402 cells through the P53-induced apoptosis pathway.	triterpenoid TP-222	2-14	P53	Homo sapiens	88-91
23483203-6	2013	Although EGCG promotes MDM2 expression in a p53-dependent manner, the interaction between MDM2 and p53 was significantly inhibited following EGCG treatment, which resulted in the inhibition of MDM2-mediated p53 ubiquitination.	epigallocatechin gallate	141-145	P53	Homo sapiens	99-102
21552291-7	2011	By contrast, p53(-/-) cells are expectedly resistant to cell death upon exposure to DNA-damaging agents such as cisplatin (CDDP) and etoposide.	Etoposide	133-142	P53	Homo sapiens	13-16
23483203-7	2013	Thus, our results suggest that the stabilization and activation of p53 may partly contribute to the anticancer activity of EGCG.	epigallocatechin gallate	123-127	P53	Homo sapiens	67-70
22294162-5	2012	N-acetylcysteine, a reactive oxygen species scavenger, not only blocked the oridonin-induced increase in hydrogen peroxide and glutathione depletion, but also blocked apoptosis and senescence induced by oridonin, as evidenced by the decrease in Annexin V and senescence-associated beta-galactosidase- positive cells and the inhibition of oridonin-induced upregulation of p53 and p16 and downregulation of c-Myc.	oridonin	76-84	P53	Homo sapiens	371-374
23622513-0	2013	The phosphatase PP2A links glutamine to the tumor suppressor p53.	Glutamine	27-36	P53	Homo sapiens	61-64
22103929-1	2012	BACKGROUND: To clarify the efficacy of grape seed procyanidin (GSP) on antiproliferative effects related to p53 functional status of oral squamous cell carcinoma (OSCC) for its chemoadjuvant potential.	gamma-Thio-GTP	63-66	P53	Homo sapiens	108-111
21567359-3	2011	Imbricatolic acid was evaluated for its ability to prevent cell cycle progression in p53-null CaLu-6 cells.	imbricatolic acid	0-17	P53	Homo sapiens	85-88
22331725-2	2011	The aim of this study was to analyse the impact of TP53 mutations, codon 72 polymorphism and human papillomavirus (HPV) infection on the response to platinum-taxane combination chemotherapy in patients with epithelial ovarian carcinomas.	platinum-taxane	149-164	P53	Homo sapiens	51-55
23622513-2	2013	(2013) show that glutamine withdrawal causes PP2A-mediated activation of p53 through its regulator EDD, linking levels of a critical metabolite to an important regulator of cell survival and proliferation.	Glutamine	17-26	P53	Homo sapiens	73-76
22331725-14	2011	Patients with mutations in TP53 gene, Arg/Arg genotype of codon 72 and absence of HPV infection experienced the highest tumor response rate to platinum-taxane chemotherapy.	platinum-taxane	143-158	P53	Homo sapiens	27-31
22331725-16	2011	CONCLUSION: Our results indicate that, based on the TP53 gene status and the presence/absence of HPV infection, the subgroups of patients having better initial response to platinum-taxane therapy could be distinguished.	platinum-taxane	172-187	P53	Homo sapiens	52-56
22260869-4	2012	Likewise, expression of either p53DD or knockdown of p53 prevented caspase-3/7 activation and chromatin fragmentation induced by nutlin-3, a compound that prevents the interaction between p53 and the E3 ubiquitin ligase MDM2.	nutlin 3	129-137	P53	Homo sapiens	31-34
23402389-7	2013	In addition, there was significant accumulation of nuclear p53, which showed that p53 itself might be a target for S-nitrosylation following the treatment with DETA/NO.	DEET	160-164	P53	Homo sapiens	59-62
22260869-4	2012	Likewise, expression of either p53DD or knockdown of p53 prevented caspase-3/7 activation and chromatin fragmentation induced by nutlin-3, a compound that prevents the interaction between p53 and the E3 ubiquitin ligase MDM2.	nutlin 3	129-137	P53	Homo sapiens	53-56
22307140-4	2012	Specifically, we focus on the functions of p53 in regulating aerobic glycolysis, oxidative phosphorylation, the pentose phosphate pathway, fatty acid synthesis and oxidation, and glutamine metabolism, and we discuss the therapeutic strategy whereby p53 helps to prevent malignant progression.	Glutamine	179-188	P53	Homo sapiens	43-46
21687937-3	2011	In this study, we studied cobalt-induced cell death in neuroblastoma cell lines carrying wild-type (WT) p53 ( SHSY5Y) and a mutated DNA-binding domain p53 [SKNBE(2c)].	Cobalt	26-32	P53	Homo sapiens	104-107
23402389-7	2013	In addition, there was significant accumulation of nuclear p53, which showed that p53 itself might be a target for S-nitrosylation following the treatment with DETA/NO.	DEET	160-164	P53	Homo sapiens	82-85
23357978-7	2013	The synergistic effect of combined HDACi/BTZ treatment was associated with the regulation of genes involved in cell cycle, JUN/MAPK, PI3K/AKT, p53, ubiquitin/proteasome, and NF-kappaB pathways.	btz	41-44	P53	Homo sapiens	143-146
24116292-5	2012	In A549, tetrazolium violet blocked the progression of the cell cycle at G1 phase by inducing p53 expression and further up-regulating p21/WAF1 expression.	tetrazolium violet	9-27	P53	Homo sapiens	94-97
24116292-7	2012	The conclusion of this study is that tetrazolium violet induced p53 expression which caused cell cycle arrest and apoptosis.	tetrazolium violet	37-55	P53	Homo sapiens	64-67
23382381-4	2013	Cellular responses to DNA damage induced by etoposide or doxorubicin include down-regulation of endogenous supervillin coincident with increases in p53.	Etoposide	44-53	P53	Homo sapiens	148-151
21455989-0	2012	The DNA methyltransferase inhibitors zebularine and decitabine induce mitochondria-mediated apoptosis and DNA damage in p53 mutant leukemic T cells.	pyrimidin-2-one beta-ribofuranoside	37-47	P53	Homo sapiens	120-123
21455989-11	2012	Our results suggest that the mitochondrial apoptotic pathway activated by decitabine and zebularine in p53 mutant leukemic T cells depends mainly on the induction of DNA damage.	pyrimidin-2-one beta-ribofuranoside	89-99	P53	Homo sapiens	103-106
23388203-6	2013	p53 regulates mitochondrial oxidative phosphorylation, glycolysis, glutamine metabolism, lipid metabolism, and antioxidant defense.	Glutamine	67-76	P53	Homo sapiens	0-3
22155302-0	2012	Withanone binds to mortalin and abrogates mortalin-p53 complex: computational and experimental evidence.	withanone	0-9	P53	Homo sapiens	51-54
22155302-5	2012	We found that withanone could bind to mortalin in a region, earlier predicted critical for binding to p53.	withanone	14-23	P53	Homo sapiens	102-105
22155302-8	2012	We also demonstrate the experimental evidence of abrogation of mortalin-p53 complex by withanone resulting in nuclear translocation and functional reactivation of p53 in human cancer cells.	withanone	87-96	P53	Homo sapiens	72-75
22155302-8	2012	We also demonstrate the experimental evidence of abrogation of mortalin-p53 complex by withanone resulting in nuclear translocation and functional reactivation of p53 in human cancer cells.	withanone	87-96	P53	Homo sapiens	163-166
23238817-8	2013	The BT-20-HNO cells were also more resistant to the apoptotic inducing agent salinomycin, which suggests that p53 may be mutated in these cells.	salinomycin	77-88	P53	Homo sapiens	110-113
22076446-3	2012	For the first time, we report p53 up-regulation in 9/14 and Fas up-regulation in 7/9 TCCB patients during intravesical MMC treatment.	Mitomycin	119-122	P53	Homo sapiens	30-33
23150668-9	2013	Furthermore, we showed that PHF1 regulates cell growth arrest and etoposide-induced apoptosis in a p53-dependent manner.	Etoposide	66-75	P53	Homo sapiens	99-102
22245848-7	2012	Quantitative real-time PCR and immunoblotting results showed that both the mRNA and protein expressions of cell cycle checkpoint gene p53 and apoptotic genes (bax and caspase-3) were up-regulated while the anti-apoptotic gene bcl-2 was down-regulated in silica nanoparticles treated cells.	Silicon Dioxide	254-260	P53	Homo sapiens	134-137
22245848-9	2012	Our data demonstrated that silica nanoparticles induced apoptosis in human liver cells, which is ROS mediated and regulated through p53, bax/bcl-2 and caspase pathways.	Silicon Dioxide	27-33	P53	Homo sapiens	132-135
24377536-0	2013	S-benzyl-cysteine-mediated cell cycle arrest and apoptosis involving activation of mitochondrial-dependent caspase cascade through the p53 pathway in human gastric cancer SGC-7901 cells.	S-benzylcysteine	2-17	P53	Homo sapiens	135-138
22002102-0	2012	p53-dependent regulation of Mcl-1 contributes to synergistic cell death by ionizing radiation and the Bcl-2/Bcl-XL inhibitor ABT-737.	ABT-737	125-132	P53	Homo sapiens	0-3
22002102-3	2012	Similarly, the relationship between p53 function and the pro-apoptotic effects of ABT-737 are still obscure.	ABT-737	82-89	P53	Homo sapiens	36-39
24460352-1	2013	BACKGROUND: A missense mutation in exon 7 (R249S) of the p53 tumor suppressor gene is characteristic of aflatoxin B1 (AFB1) exposure.	Aflatoxin B1	104-116	P53	Homo sapiens	57-60
21445621-0	2012	The citrus flavonoid hesperidin induces p53 and inhibits NF-kappaB activation in order to trigger apoptosis in NALM-6 cells: involvement of PPARgamma-dependent mechanism.	Hesperidin	21-31	P53	Homo sapiens	40-43
21445621-8	2012	RESULTS: Hesperidin induced the expression and transcriptional activity of PPARgamma and promoted p53 accumulation and downregulated constitutive NF-kappaB activity in a PPARgamma-dependent and PPARgamma-independent manner.	Hesperidin	9-19	P53	Homo sapiens	98-101
24460352-1	2013	BACKGROUND: A missense mutation in exon 7 (R249S) of the p53 tumor suppressor gene is characteristic of aflatoxin B1 (AFB1) exposure.	Aflatoxin B1	118-122	P53	Homo sapiens	57-60
23006513-0	2013	Topoisomerase degradation, DSB repair, p53 and IAPs in cancer cell resistance to camptothecin-like topoisomerase I inhibitors.	Camptothecin	81-93	P53	Homo sapiens	39-42
20953816-0	2012	Anti-leukemic activity of dasatinib in both p53(wild-type) and p53(mutated) B malignant cells.	Dasatinib	26-35	P53	Homo sapiens	44-47
20953816-0	2012	Anti-leukemic activity of dasatinib in both p53(wild-type) and p53(mutated) B malignant cells.	Dasatinib	26-35	P53	Homo sapiens	63-66
20953816-2	2012	Antibody phospho-kinase array analysis revealed that dasatinib inhibited the phosphorylation of various kinases, including ERK1/2 and p38/MAPK as well as of STAT3 transcription factors, in both p53(wild-type) and p53(mutated) cells.	Dasatinib	53-62	P53	Homo sapiens	194-197
20953816-2	2012	Antibody phospho-kinase array analysis revealed that dasatinib inhibited the phosphorylation of various kinases, including ERK1/2 and p38/MAPK as well as of STAT3 transcription factors, in both p53(wild-type) and p53(mutated) cells.	Dasatinib	53-62	P53	Homo sapiens	213-216
20953816-3	2012	Therefore, dasatinib might offer a novel therapeutic strategy not only for p53(wild-type), but also for p53(mutated) B malignancies that have the worst prognosis and urgently need innovative therapeutic approaches.	Dasatinib	11-20	P53	Homo sapiens	75-78
20953816-3	2012	Therefore, dasatinib might offer a novel therapeutic strategy not only for p53(wild-type), but also for p53(mutated) B malignancies that have the worst prognosis and urgently need innovative therapeutic approaches.	Dasatinib	11-20	P53	Homo sapiens	104-107
23781585-10	2013	The strengthening effect of growth inhibition and chemosensitivity to cisplatin of mifepristone are associated with down-regulating HPV E6 survivin protein and upregulating p53 protein.	Mifepristone	83-95	P53	Homo sapiens	173-176
22056254-7	2012	The (64)Cu from agonists (64)Cu-DOTA-Y3-TATE and (64)Cu-CB-TE2A-Y3-TATE showed greater nuclear localization at 24 h in p53 +/+ vs. -/- cells; however, there was no difference in the levels of (64)Cu from the antagonist based on p53 status.	cu-cb	53-58	P53	Homo sapiens	119-122
22056254-7	2012	The (64)Cu from agonists (64)Cu-DOTA-Y3-TATE and (64)Cu-CB-TE2A-Y3-TATE showed greater nuclear localization at 24 h in p53 +/+ vs. -/- cells; however, there was no difference in the levels of (64)Cu from the antagonist based on p53 status.	cu-cb	53-58	P53	Homo sapiens	228-231
22056254-9	2012	CONCLUSION: Based on these in vitro data, the agonist (64)Cu-CB-TE2A-Y3-TATE demonstrates the most promise as an agent for targeted radiotherapy in p53 positive, SSTr2-positive tumors.	cu-cb	58-63	P53	Homo sapiens	148-151
23200181-6	2013	Furthermore, the expression of p53, Fas, Bax and activated caspase-3 protein was significantly upregulated in cells treated with HMME-SDT and DOX, whereas Bcl-2 protein was downregulated.	hmme-sdt	129-137	P53	Homo sapiens	31-34
22123234-5	2012	A growing appreciation of the role of oncogenes and tumor suppressor genes in the Warburg effect was reflected in reports of the regulation of glutamine metabolism by p53, the role of c-Myc in the high glucose uptake of tumors, and the regulation of ectonucleoside triphosphate diphosphohydrolase 5 (ENTPD5) and ATP consumption by AKT.	Glutamine	143-152	P53	Homo sapiens	167-170
22982566-6	2012	Wt p53 MCF-7 cells responded to hypoxia by increasing superoxide dismutase and their reactivity with the PAb240 antibody, known to recognize conformationally-inactive p53.	pab240	105-111	P53	Homo sapiens	3-6
21954225-5	2012	METHODS: As-transformed p53lowHBECs were generated by exposing p53-knockdown HBECs to sodium arsenite (2.5 muM) for 16 weeks.	sodium arsenite	86-101	P53	Homo sapiens	24-27
22112837-5	2012	At the molecular level, AQ and AZ formed DNA adducts, generated free radicals, and upregulated pro-apoptotic signaling molecules (p53, caspases, PARP, death effectors).	aq	24-26	P53	Homo sapiens	130-133
23300887-0	2012	Terpenoids from Zingiber officinale (Ginger) induce apoptosis in endometrial cancer cells through the activation of p53.	Terpenes	0-10	P53	Homo sapiens	116-119
22982566-6	2012	Wt p53 MCF-7 cells responded to hypoxia by increasing superoxide dismutase and their reactivity with the PAb240 antibody, known to recognize conformationally-inactive p53.	pab240	105-111	P53	Homo sapiens	167-170
23187804-0	2012	p53 expression controls prostate cancer sensitivity to chemotherapy and the MDM2 inhibitor Nutlin-3.	nutlin 3	91-99	P53	Homo sapiens	0-3
23272236-4	2012	Etoposide-treated cells exhibited a senescent phenotype characterized by senile morphology, positive staining for senescence-associated beta-galactosidase, growth arrest and induction of p53 and p21(WAF1/CIP1).	Etoposide	0-9	P53	Homo sapiens	187-190
22773666-4	2012	By microarray analysis, we identified a palmitate-triggered ER stress gene expression signature and the induction of the BH3-only proteins death protein 5 (DP5) and p53-upregulated modulator of apoptosis (PUMA).	Palmitates	40-49	P53	Homo sapiens	165-168
21903158-0	2011	ZnO nanoparticles induce apoptosis in human dermal fibroblasts via p53 and p38 pathways.	Zinc Oxide	0-3	P53	Homo sapiens	67-70
22960751-3	2012	In the present study, our             results showed that genistein, an element found in soy, is an epigenetic modifier             able to decrease hypermethylation levels of CHD5, and enhances the expression             of CHD5 as well as p53, possibly contributing to inhibition of NB growth in vivo             and tumor microvessel formation.	Genistein	58-67	P53	Homo sapiens	241-244
21903158-3	2011	This study was designed to investigate the apoptosis induction by ZnO NPs via mitogen-activated protein kinase p38 and cell cycle checkpoint protein p53 pathways in human dermal fibroblasts.	Zinc Oxide	66-69	P53	Homo sapiens	149-152
21903158-6	2011	Furthermore, in ZnO NP exposed cells, p53 protein was phosphorylated at Ser33 and Ser46 sites known to be phosphorylated by p38.	Zinc Oxide	16-19	P53	Homo sapiens	38-41
21903158-7	2011	Our results suggest that ZnO NPs have the potential to induce apoptosis in human dermal fibroblasts via p53-p38 pathways.	Zinc Oxide	25-28	P53	Homo sapiens	104-107
21953469-4	2011	We found that K351N substitution abrogates the monoubiquitination of p53 induced by both Mdm2 and MSL2 E3-ligases.	k351n	14-19	P53	Homo sapiens	69-72
22244830-7	2012	Intriguingly, SU6656 abrogated the catalytic activities of Aurora kinases and led to the down-regulation of phosphorylated histone H3 coincidently with p53 accumulation, as did the Aurora kinase inhibitor VX-680.	SU 6656	14-20	P53	Homo sapiens	152-155
21927014-12	2011	CONCLUSION: Collectively, our data suggest that satraplatin induces apoptosis in CRC cells, which is preceded by cell cycle arrest at G(2)/M due to the effect of 14-3-3sigma and in a p53-p21(waf1/cip1)-independent manner.	satraplatin	48-59	P53	Homo sapiens	183-186
22895172-0	2012	Mitomycin C potentiates TRAIL-induced apoptosis through p53-independent upregulation of death receptors: evidence for the role of c-Jun N-terminal kinase activation.	Mitomycin	0-11	P53	Homo sapiens	56-59
21809047-0	2011	Camptothecin induces p53-dependent and -independent apoptogenic signaling in melanoma cells.	Camptothecin	0-12	P53	Homo sapiens	21-24
22895172-3	2012	We found that MMC not only potentiated TRAIL-induced apoptosis in HCT116 (p53-/-) colon cancer cells but also sensitized TRAIL-resistant colon cancer cells HT-29 to the cytokine both in vitro and in vivo.	Mitomycin	14-17	P53	Homo sapiens	74-77
23359343-9	2012	CONCLUSION: Both epigenetic reagents (5-Aza-Cdr/TSA) and Ad-p53 can suppress cell proliferation on Hep-2 in vivo and in vitro and there may be some antagonistic mechanism between Ad-p53 and epigenetic reagents (5-Aza-Cdr/ TSA).	trichostatin A	48-51	P53	Homo sapiens	182-185
23359343-9	2012	CONCLUSION: Both epigenetic reagents (5-Aza-Cdr/TSA) and Ad-p53 can suppress cell proliferation on Hep-2 in vivo and in vitro and there may be some antagonistic mechanism between Ad-p53 and epigenetic reagents (5-Aza-Cdr/ TSA).	trichostatin A	222-225	P53	Homo sapiens	60-63
21840268-6	2011	p53 was activated and phosphorylated at Serine15 followed by p21 gene activation through both p53-dependent and -independent pathways.	serine15	40-48	P53	Homo sapiens	0-3
23359343-9	2012	CONCLUSION: Both epigenetic reagents (5-Aza-Cdr/TSA) and Ad-p53 can suppress cell proliferation on Hep-2 in vivo and in vitro and there may be some antagonistic mechanism between Ad-p53 and epigenetic reagents (5-Aza-Cdr/ TSA).	trichostatin A	222-225	P53	Homo sapiens	182-185
22484386-0	2012	Mood stabilizers commonly restore staurosporine-induced increase of p53 expression and following decrease of Bcl-2 expression in SH-SY5Y cells.	Staurosporine	34-47	P53	Homo sapiens	68-71
21965740-9	2011	Genistein and quercetin induced extrinsic apoptosis pathway, up-regulating p53.	Genistein	0-9	P53	Homo sapiens	75-78
21708241-0	2011	Subamolide A, a component isolated from Cinnamomum subavenium, induces apoptosis mediated by mitochondria-dependent, p53 and ERK1/2 pathways in human urothelial carcinoma cell line NTUB1.	subamolide A	0-12	P53	Homo sapiens	117-120
22484386-8	2012	Therefore, p53 and Bcl-2 can be considered to mediate the common anti-apoptotic effects of Li, VPA, CBZ and LTG.	Carbamazepine	100-103	P53	Homo sapiens	11-14
21421594-6	2011	RESULTS: Periodic transfection of siRNA to a tumor suppressor p53 or a cyclin-dependent kinase inhibitor p16(INK4a) extended the lifespan by 33 and 63 PDs, respectively, in 3 months of culture.	3-{1-[3-(Dimethylamino)propyl]-2-Methyl-1h-Indol-3-Yl}-4-(2-Methyl-1h-Indol-3-Yl)-1h-Pyrrole-2,5-Dione	151-154	P53	Homo sapiens	62-65
21801448-0	2011	Essential role of caspase-8 in p53/p73-dependent apoptosis induced by etoposide in head and neck carcinoma cells.	Etoposide	70-79	P53	Homo sapiens	31-34
22573016-9	2012	Using RT-PCR, EGCG treatment induced a significant anti-apoptotic effect in injured muscle tissues by normalizing the Bax/Bcl-2 ratio back to baseline levels and inhibiting overexpression of the p53 apoptotic gene at days 3 and 7 post-surgery.	epigallocatechin gallate	14-18	P53	Homo sapiens	195-198
21801448-4	2011	RESULTS: We show that p53/p73-dependent caspase-8 activation is required for sensitizing etoposide-induced apoptosis by utilizing HOC313 cells carrying a temperature-sensitive p53G285K mutant.	Etoposide	89-98	P53	Homo sapiens	22-25
21801448-7	2011	In etoposide-sensitive Ca9-22 cells carrying a temperature-insensitive mutant p53, siRNA-based p73 knockdown blocked etoposide-induced apoptosis and procaspase-8 cleavage.	Etoposide	117-126	P53	Homo sapiens	78-81
21801448-9	2011	Finally, the caspase-9 inhibitor Ac-LEHD-CHO or caspase-9 siRNA blocked etoposide-induced caspase-8 activation, Bid cleavage, and apoptosis in both cell lines, indicating that p53/p73-dependent caspase-8 activation lies downstream of mitochondria.	Etoposide	72-81	P53	Homo sapiens	176-179
21801448-10	2011	CONCLUSIONS: we conclude that p53 and p73 can act as upstream regulators of caspase-8, and that caspase-8 is an essential mediator of the p53/p73-dependent apoptosis induced by etoposide in HNSCC cells.	Etoposide	177-186	P53	Homo sapiens	30-33
21801448-10	2011	CONCLUSIONS: we conclude that p53 and p73 can act as upstream regulators of caspase-8, and that caspase-8 is an essential mediator of the p53/p73-dependent apoptosis induced by etoposide in HNSCC cells.	Etoposide	177-186	P53	Homo sapiens	138-141
21801448-11	2011	Our data suggest the importance of caspase-8-mediated positive feedback amplification in the p53/p73-dependent apoptosis induced by etoposide in HNSCC cells.	Etoposide	132-141	P53	Homo sapiens	93-96
21549799-6	2011	Furthermore, we also found that olaquindox increased the expression of p53 protein and induced the release of cytochrome C from mitochondria to cytosol.	olaquindox	32-42	P53	Homo sapiens	71-74
21549799-7	2011	In conclusion, olaquindox induced apoptosis of HepG2 cells through a caspase-9 and -3 dependent mitochondrial pathway, involving p53, Bcl-2 family protein expression, Deltapsi(m) disruption and mPTP opening.	olaquindox	15-25	P53	Homo sapiens	129-132
21796156-4	2011	We previously showed that nutlin-3, an antagonist of MDM2, activates the p53 pathway in BL cell lines harboring wild-type p53.	nutlin 3	26-34	P53	Homo sapiens	73-76
21468663-4	2011	In this study, we showed that etoposide treatment activated caspase-8 and caspase-3, leading to cleavages of p53, Bid and PARP, which subsequently induced apoptosis.	Etoposide	30-39	P53	Homo sapiens	109-112
21468663-5	2011	Furthermore, p53 and Bid were accumulated in cytoplasm following etoposide treatment.	Etoposide	65-74	P53	Homo sapiens	13-16
21468663-9	2011	Moreover, the pretreatment with trichostatin A (TSA, a histone deacetylase inhibitor) or TSA in combination with etoposide significantly sensitized HCC cells to apoptosis by inhibiting ERK phosphorylation, reactivating caspases and PARP, and inducing translocation of p53 and Bid to cytoplasm.	trichostatin A	32-46	P53	Homo sapiens	268-271
21468663-9	2011	Moreover, the pretreatment with trichostatin A (TSA, a histone deacetylase inhibitor) or TSA in combination with etoposide significantly sensitized HCC cells to apoptosis by inhibiting ERK phosphorylation, reactivating caspases and PARP, and inducing translocation of p53 and Bid to cytoplasm.	trichostatin A	48-51	P53	Homo sapiens	268-271
21796156-4	2011	We previously showed that nutlin-3, an antagonist of MDM2, activates the p53 pathway in BL cell lines harboring wild-type p53.	nutlin 3	26-34	P53	Homo sapiens	122-125
21468663-9	2011	Moreover, the pretreatment with trichostatin A (TSA, a histone deacetylase inhibitor) or TSA in combination with etoposide significantly sensitized HCC cells to apoptosis by inhibiting ERK phosphorylation, reactivating caspases and PARP, and inducing translocation of p53 and Bid to cytoplasm.	trichostatin A	89-92	P53	Homo sapiens	268-271
21565980-7	2011	DNA-damaging chemotherapeutics, such as etoposide, activate a functional loop linking SIRT1 and p53 through the induction of miR-34a.	Etoposide	40-49	P53	Homo sapiens	96-99
22830357-6	2012	In accordance with this hypothesis, etoposide or nutlin-3 treatment or a small interfering RNA (siRNA) against BCL6 (B-cell lymphoma 6) inhibited the proliferation of DoHH2 cells by up-regulating p53 without affecting either miR-34a or c-MYC levels.	Etoposide	36-45	P53	Homo sapiens	196-199
21515331-1	2011	This study was designed to investigate the hypothesis that the toxic effects of di(2-ethylhexyl)phthalate (DEHP), the most abundantly used plasticizer and ubiquitous environmental contaminant that cause alterations in endocrine and spermatogenic functions in animals is mediated through the induction of reactive oxygen species (ROS) and activation of nuclear p53 and p21 proteins in LNCaP human prostate adenocarcinoma cell line.	Diethylhexyl Phthalate	80-105	P53	Homo sapiens	360-363
21515331-1	2011	This study was designed to investigate the hypothesis that the toxic effects of di(2-ethylhexyl)phthalate (DEHP), the most abundantly used plasticizer and ubiquitous environmental contaminant that cause alterations in endocrine and spermatogenic functions in animals is mediated through the induction of reactive oxygen species (ROS) and activation of nuclear p53 and p21 proteins in LNCaP human prostate adenocarcinoma cell line.	Diethylhexyl Phthalate	107-111	P53	Homo sapiens	360-363
21468663-9	2011	Moreover, the pretreatment with trichostatin A (TSA, a histone deacetylase inhibitor) or TSA in combination with etoposide significantly sensitized HCC cells to apoptosis by inhibiting ERK phosphorylation, reactivating caspases and PARP, and inducing translocation of p53 and Bid to cytoplasm.	Etoposide	113-122	P53	Homo sapiens	268-271
21411502-4	2011	Drug transport studies revealed that p53 inhibited both basal and PKCalpha-stimulated transport of glutathione conjugates of 4HNE (GSHNE) and doxorubicin.	gshne	131-136	P53	Homo sapiens	37-40
21619452-5	2011	MATERIALS AND METHODS: In cell cultures, we investigated the effects of forskolin/3-isobutyl-1-methylxanthine (IBMX) on stimulated p53 of ALL cell lines.	1-Methyl-3-isobutylxanthine	82-109	P53	Homo sapiens	131-134
21619452-5	2011	MATERIALS AND METHODS: In cell cultures, we investigated the effects of forskolin/3-isobutyl-1-methylxanthine (IBMX) on stimulated p53 of ALL cell lines.	1-Methyl-3-isobutylxanthine	111-115	P53	Homo sapiens	131-134
21570352-12	2011	In patients with TP53-mutated tumours, 5-year PFS was 59 5% (95% CI 53 4-65 1) in the T-ET group (n=326) and 55 3% (49 2-60 9) in the FEC group (n=318; hazard ratio 0 84, 98% CI 0 63-1 14; p=0 17).	tetramethylenedisulfotetramine	86-90	P53	Homo sapiens	17-21
21570352-13	2011	In patients with TP53 wild-type tumours, 5-year PFS was 66 8% (95% CI 61 4-71 6) in the T-ET group (n=398) and 64 7% (59 6-69 4) in the FEC group (n=427; 0 89, 98% CI 0 68-1 18; p=0 35).	tetramethylenedisulfotetramine	88-92	P53	Homo sapiens	17-21
22830357-6	2012	In accordance with this hypothesis, etoposide or nutlin-3 treatment or a small interfering RNA (siRNA) against BCL6 (B-cell lymphoma 6) inhibited the proliferation of DoHH2 cells by up-regulating p53 without affecting either miR-34a or c-MYC levels.	nutlin 3	49-57	P53	Homo sapiens	196-199
20955683-5	2011	The role of p53, C-MYC, Oct and RAS on the control of mitochondrial respiration and glutamine utilization has been explained recently on artificial models of tumorigenesis.	Glutamine	84-93	P53	Homo sapiens	12-15
22694121-5	2012	X-ray crystallographic studies validate (D)PMI-delta as an exceedingly potent inhibitor of the p53-MDM2 interaction, promising to be a highly attractive lead drug candidate for anticancer therapeutic development.	pmi-delta	43-52	P53	Homo sapiens	95-98
21636709-6	2011	We have examined inhibitors of the PI3K/Akt/mTOR signaling pathway and find that PI-103 and TCN show particular promise for inhibiting growth in Nf1 and Trp53 mutant astrocytoma cells.	triciribine	92-95	P53	Homo sapiens	153-158
21344307-0	2011	2ME and 2OHE2 exhibit growth inhibitory effects and cell cycle arrest at G2/M in RL95-2 human endometrial cancer cells through activation of p53 and Chk1.	2-Methoxyestradiol	0-3	P53	Homo sapiens	141-144
22552582-3	2012	In this study, we demonstrate that green tea polyphenols (GTPs) and their major constituent, (-) epigallocatechin-3-gallate (EGCG), activate p53 through acetylation at the Lys373 and Lys382 residues by inhibiting class I HDACs in LNCaP human prostate cancer cells.	epigallocatechin gallate	58-62	P53	Homo sapiens	141-144
21460101-0	2011	Functional analysis of the p53 pathway in neuroblastoma cells using the small-molecule MDM2 antagonist nutlin-3.	nutlin 3	103-111	P53	Homo sapiens	27-30
21396347-8	2011	In addition, overexpressing FAT10 in HEK293 cells also reduced the population of p53 which cross reacted with monoclonal anti-p53 antibody, PAB240, known to recognize only the transcriptionally inactive p53.	pab240	140-146	P53	Homo sapiens	81-84
21396347-8	2011	In addition, overexpressing FAT10 in HEK293 cells also reduced the population of p53 which cross reacted with monoclonal anti-p53 antibody, PAB240, known to recognize only the transcriptionally inactive p53.	pab240	140-146	P53	Homo sapiens	126-129
22552582-3	2012	In this study, we demonstrate that green tea polyphenols (GTPs) and their major constituent, (-) epigallocatechin-3-gallate (EGCG), activate p53 through acetylation at the Lys373 and Lys382 residues by inhibiting class I HDACs in LNCaP human prostate cancer cells.	epigallocatechin gallate	93-123	P53	Homo sapiens	141-144
21396347-8	2011	In addition, overexpressing FAT10 in HEK293 cells also reduced the population of p53 which cross reacted with monoclonal anti-p53 antibody, PAB240, known to recognize only the transcriptionally inactive p53.	pab240	140-146	P53	Homo sapiens	126-129
21482671-1	2011	DeltaNp73alpha, a dominant-negative inhibitor of p53 and p73, exhibits antiapoptotic and transforming activity in in vitro models and is often found to be upregulated in human cancers.	deltanp73alpha	0-14	P53	Homo sapiens	49-52
21380473-1	2011	The efficient formation of 5-methylcytosine glycol (mCg) and its facile deamination to thymine glycol (Tg) may account for the prevalent C   T transition mutation found at methylated CpG site (mCpG) in human p53 gene, a hallmark for many types of human tumors.	5-methylcytosine glycol	27-50	P53	Homo sapiens	208-211
21376104-0	2011	p53 in trichostatin A induced C6 glioma cell death.	trichostatin A	7-21	P53	Homo sapiens	0-3
22552582-3	2012	In this study, we demonstrate that green tea polyphenols (GTPs) and their major constituent, (-) epigallocatechin-3-gallate (EGCG), activate p53 through acetylation at the Lys373 and Lys382 residues by inhibiting class I HDACs in LNCaP human prostate cancer cells.	epigallocatechin gallate	125-129	P53	Homo sapiens	141-144
21376104-5	2011	RESULTS: TSA activated p38 mitogen-activated protein kinase (p38MAPK), leading to p53 phosphorylation and activation.	trichostatin A	9-12	P53	Homo sapiens	82-85
21480327-6	2011	Higher MYBL2/LINC activation in HCC with mutated p53 was in contrast with LINC inactivation in HCC harboring wildtype p53.	linc	13-17	P53	Homo sapiens	49-52
22552582-5	2012	Discontinuation of treatment with GTP/EGCG resulted in the loss of p53 acetylation at both the sites in these cells.	epigallocatechin gallate	34-37	P53	Homo sapiens	67-70
21376104-10	2011	CONCLUSIONS: TSA may cause C6 cell apoptosis through activating p38MAPK-p53 cascade resulting in Bax expression and survivin suppression.	trichostatin A	13-16	P53	Homo sapiens	72-75
21376104-12	2011	GENERAL SIGNIFICANCE: TSA-induced p53 activation may occur through p53 modification by phosphorylation or by acetylation via IKK inactivation.	trichostatin A	22-25	P53	Homo sapiens	34-37
22552582-5	2012	Discontinuation of treatment with GTP/EGCG resulted in the loss of p53 acetylation at both the sites in these cells.	epigallocatechin gallate	38-42	P53	Homo sapiens	67-70
21376104-12	2011	GENERAL SIGNIFICANCE: TSA-induced p53 activation may occur through p53 modification by phosphorylation or by acetylation via IKK inactivation.	trichostatin A	22-25	P53	Homo sapiens	67-70
22904680-6	2012	By contrast, p53-72P was more effective in promoting p21-dependent accelerated senescence, alone or in the presence of etoposide.	Etoposide	119-128	P53	Homo sapiens	13-16
21068437-5	2011	Pharmacologic inhibition of p53 rescued the erythroid defect, whereas nutlin-3, a compound that activates p53 through inhibition of HDM2, selectively impaired erythropoiesis.	nutlin 3	70-78	P53	Homo sapiens	106-109
22552631-0	2012	The histone deacetylase inhibitor trichostatin A induces cell cycle             arrest and apoptosis in colorectal cancer cells via p53-dependent and -independent             pathways.	trichostatin A	34-48	P53	Homo sapiens	132-135
21386967-5	2011	Direct or indirect activation of TP53 pathway with 5-aza-2"-deoxycitidine, Curcumin or Nutlin-3 induced an increase in apoptosis of ALL cells.	5-aza-2"-deoxycitidine	51-73	P53	Homo sapiens	33-37
21386967-5	2011	Direct or indirect activation of TP53 pathway with 5-aza-2"-deoxycitidine, Curcumin or Nutlin-3 induced an increase in apoptosis of ALL cells.	nutlin 3	87-95	P53	Homo sapiens	33-37
21386980-6	2011	Induction of DNA damage by UV, IR, etoposide and doxorubicin stabilizes p53 and induces DRAM expression, followed by VRK1 downregulation and a reduction in p53 Thr18 phosphorylation.	Etoposide	35-44	P53	Homo sapiens	72-75
21386980-6	2011	Induction of DNA damage by UV, IR, etoposide and doxorubicin stabilizes p53 and induces DRAM expression, followed by VRK1 downregulation and a reduction in p53 Thr18 phosphorylation.	Etoposide	35-44	P53	Homo sapiens	156-159
21504622-9	2011	RESULTS: Isochaihulactone caused cell cycle arrest at G2/M phase in LNCaP cells, which was correlated with an increase of p53 and p21 levels and downregulation of the checkpoint proteins cdc25c, cyclin B1, and cdc2.	isochaihulactone	9-25	P53	Homo sapiens	122-125
22552631-4	2012	Here, we report that, Trichostatin A (TSA), a             pan-HDAC inhibitor, could induce G2/M cell cycle arrest and apoptosis in both             colorectal cancer cell lines with wild-type p53 (HT116 cells) and mutant p53 (HT29             cells), although HCT116 cells had more apoptotic cells than HT29 cells.	trichostatin A	22-36	P53	Homo sapiens	192-195
22552631-4	2012	Here, we report that, Trichostatin A (TSA), a             pan-HDAC inhibitor, could induce G2/M cell cycle arrest and apoptosis in both             colorectal cancer cell lines with wild-type p53 (HT116 cells) and mutant p53 (HT29             cells), although HCT116 cells had more apoptotic cells than HT29 cells.	trichostatin A	22-36	P53	Homo sapiens	221-224
20390378-5	2011	The NaAsO2 treatment resulted in a marked increase in p53 protein as early as 4 h and in Bcl-2 protein level by 12 h. In addition, p53 downregulation accompanied the combined treatment of NaAsO2 and Na2SeO3.	sodium arsenite	4-10	P53	Homo sapiens	54-57
20390378-5	2011	The NaAsO2 treatment resulted in a marked increase in p53 protein as early as 4 h and in Bcl-2 protein level by 12 h. In addition, p53 downregulation accompanied the combined treatment of NaAsO2 and Na2SeO3.	sodium arsenite	4-10	P53	Homo sapiens	131-134
21156789-0	2011	Ursolic acid, a pentacyclin triterpene, potentiates TRAIL-induced apoptosis through p53-independent up-regulation of death receptors: evidence for the role of reactive oxygen species and JNK.	ursolic acid	0-12	P53	Homo sapiens	84-87
21156789-9	2011	Induction of DRs was independent of p53 because UA induced DR4 and DR5 in HCT116 p53(-/-) cells.	ursolic acid	48-50	P53	Homo sapiens	81-84
20390378-5	2011	The NaAsO2 treatment resulted in a marked increase in p53 protein as early as 4 h and in Bcl-2 protein level by 12 h. In addition, p53 downregulation accompanied the combined treatment of NaAsO2 and Na2SeO3.	sodium arsenite	188-194	P53	Homo sapiens	54-57
22552631-4	2012	Here, we report that, Trichostatin A (TSA), a             pan-HDAC inhibitor, could induce G2/M cell cycle arrest and apoptosis in both             colorectal cancer cell lines with wild-type p53 (HT116 cells) and mutant p53 (HT29             cells), although HCT116 cells had more apoptotic cells than HT29 cells.	trichostatin A	38-41	P53	Homo sapiens	192-195
20390378-5	2011	The NaAsO2 treatment resulted in a marked increase in p53 protein as early as 4 h and in Bcl-2 protein level by 12 h. In addition, p53 downregulation accompanied the combined treatment of NaAsO2 and Na2SeO3.	sodium arsenite	188-194	P53	Homo sapiens	131-134
20390378-6	2011	Thus, our results indicate upregulation of p53 and Bcl-2 play acrucial role in the NaAsO2-induced G1 arrest and apoptosis of A375 cells and that downregulation p53 appears to contribute to the inhibition by Na2SeO3 of the effects induced by NaAsO2.	sodium arsenite	83-89	P53	Homo sapiens	43-46
22552631-4	2012	Here, we report that, Trichostatin A (TSA), a             pan-HDAC inhibitor, could induce G2/M cell cycle arrest and apoptosis in both             colorectal cancer cell lines with wild-type p53 (HT116 cells) and mutant p53 (HT29             cells), although HCT116 cells had more apoptotic cells than HT29 cells.	trichostatin A	38-41	P53	Homo sapiens	221-224
20390378-6	2011	Thus, our results indicate upregulation of p53 and Bcl-2 play acrucial role in the NaAsO2-induced G1 arrest and apoptosis of A375 cells and that downregulation p53 appears to contribute to the inhibition by Na2SeO3 of the effects induced by NaAsO2.	sodium arsenite	83-89	P53	Homo sapiens	160-163
20390378-6	2011	Thus, our results indicate upregulation of p53 and Bcl-2 play acrucial role in the NaAsO2-induced G1 arrest and apoptosis of A375 cells and that downregulation p53 appears to contribute to the inhibition by Na2SeO3 of the effects induced by NaAsO2.	sodium arsenite	241-247	P53	Homo sapiens	43-46
21087144-5	2011	The current study demonstrates that DC cells signal a DNA damage response through p53 and its downstream mediator, p21(WAF/CIP), which is accompanied by an elevation in steady-state levels of superoxide and percent glutathione disulfide, both indicators of oxidative stress.	Glutathione Disulfide	215-236	P53	Homo sapiens	82-85
21106726-5	2011	At the molecular level, Dasatinib significantly counteracted the Nutlin-3-mediated induction of the p53 transcriptional targets MDM2 and p21 observed in p53(wild-type) leukemic cells.	Dasatinib	24-33	P53	Homo sapiens	153-156
21106726-8	2011	CONCLUSIONS: These findings suggest that Dasatinib + Nutlin-3 might represent an innovative therapeutic combination for both p53(wild-type) and p53(deleted/mutated) B-CLL.	Dasatinib	41-50	P53	Homo sapiens	125-128
21106726-8	2011	CONCLUSIONS: These findings suggest that Dasatinib + Nutlin-3 might represent an innovative therapeutic combination for both p53(wild-type) and p53(deleted/mutated) B-CLL.	Dasatinib	41-50	P53	Homo sapiens	144-147
22552631-8	2012	These             data suggest that TSA induces G2/M cell cycle arrest and Bax-dependent apoptosis             in colorectal cancer cells (HCT116 cells and HT29 cells) by both p53-dependent             and -independent mechanisms.	trichostatin A	36-39	P53	Homo sapiens	176-179
22552631-9	2012	However, cells with normal p53 function are more             sensitive to TSA-induced apoptosis.	trichostatin A	74-77	P53	Homo sapiens	27-30
21249311-7	2011	Moreover celastrol treatment increased p53 levels by phosphorylating Ser15 and Ser20 residues as well as by inhibiting its proteasomal degradation.	celastrol	9-18	P53	Homo sapiens	39-42
20812030-1	2011	Camptothecin (CPT) and Nutlin-3 caused apoptosis by increasing p53 protein and its activation in intestinal epithelial cells (IEC-6).	Camptothecin	0-12	P53	Homo sapiens	63-66
22511763-8	2012	Etoposide treatment also resulted in activation of the upstream promoter as well as nuclear accumulation of TLP and p53.	Etoposide	0-9	P53	Homo sapiens	116-119
20812030-1	2011	Camptothecin (CPT) and Nutlin-3 caused apoptosis by increasing p53 protein and its activation in intestinal epithelial cells (IEC-6).	Camptothecin	14-17	P53	Homo sapiens	63-66
20963498-0	2011	Apoptosis of human fibrosarcoma HT-1080 cells by epigallocatechin-3-O-gallate via induction of p53 and caspases as well as suppression of Bcl-2 and phosphorylated nuclear factor-kappaB.	epigallocatechin gallate	49-77	P53	Homo sapiens	95-98
21249311-8	2011	Celastrol may be considered an effective radiosensitizer acting as an inhibitor of Hsp90 and a p53 activator.	celastrol	0-9	P53	Homo sapiens	95-98
21106726-0	2011	Dasatinib plus Nutlin-3 shows synergistic antileukemic activity in both p53 wild-type and p53 mutated B chronic lymphocytic leukemias by inhibiting the Akt pathway.	Dasatinib	0-9	P53	Homo sapiens	72-75
21106726-0	2011	Dasatinib plus Nutlin-3 shows synergistic antileukemic activity in both p53 wild-type and p53 mutated B chronic lymphocytic leukemias by inhibiting the Akt pathway.	Dasatinib	0-9	P53	Homo sapiens	90-93
21106726-1	2011	PURPOSE: To analyze the effect of the combination of Dasatinib, a multikinase inhibitor, plus Nutlin-3, a nongenotoxic activator of the p53 pathway, in primary B chronic lymphocytic leukemia (B-CLL) patient samples and B leukemic cell line models.	nutlin 3	94-102	P53	Homo sapiens	136-139
21106726-4	2011	RESULTS: The combination of Dasatinib + Nutlin-3 exhibited a synergistic cytotoxicity in the majority (19 out of 20) of B-CLL samples, including patients carrying 17p- (n = 4), and in both p53(wild-type) and p53(deleted/mutated) B leukemic cell lines.	Dasatinib	28-37	P53	Homo sapiens	189-192
21106726-4	2011	RESULTS: The combination of Dasatinib + Nutlin-3 exhibited a synergistic cytotoxicity in the majority (19 out of 20) of B-CLL samples, including patients carrying 17p- (n = 4), and in both p53(wild-type) and p53(deleted/mutated) B leukemic cell lines.	Dasatinib	28-37	P53	Homo sapiens	208-211
21106726-5	2011	At the molecular level, Dasatinib significantly counteracted the Nutlin-3-mediated induction of the p53 transcriptional targets MDM2 and p21 observed in p53(wild-type) leukemic cells.	Dasatinib	24-33	P53	Homo sapiens	100-103
20963498-6	2011	Immunoblot analysis revealed that the expression of p53, caspase-7 and -9 as well as the ratio of Bax/Bcl-2 protein increased significantly with higher EGCG concentrations and longer incubation times.	epigallocatechin gallate	152-156	P53	Homo sapiens	52-55
20963498-10	2011	Taken together, our data indicate that HT-1080 apoptosis may be mediated through the induction of p53 and caspases by the pro-oxidant activity of internalized EGCG, as well as suppression of Bcl-2 and phosphorylated NF-kappaB by the antioxidant activity of EGCG.	epigallocatechin gallate	159-163	P53	Homo sapiens	98-101
22469844-5	2012	When MTS-p53 cells were treated with the nucleoside reverse transcriptase inhibitor (NRTI), 2",3"-dideoxycytidine or 2",3"-dideoxyinosine, mtDNA depletion that resembled untransfected controls was observed in both instances.	Didanosine	117-137	P53	Homo sapiens	9-12
22101376-8	2011	The individuals carrying the heterozygous genotype (Arg/Trp-Arg/Gln) in the p53 codon 248 polymorphism showed high BC risk (p &lt; 0.001).	Glutamine	64-67	P53	Homo sapiens	76-79
22101376-10	2011	The minor allele (Trp/Gln) carriers of the p53 codon 248 demonstrated a 1.7-fold risk for BC.	Glutamine	22-25	P53	Homo sapiens	43-46
21346816-6	2011	Culture of PBMC with TSA resulted in increased expression of p53 in HC but not in MS patients.	trichostatin A	21-24	P53	Homo sapiens	61-64
22493143-0	2012	Synergistic effect of p53 on TSA-induced stanniocalcin 1 expression in human nasopharyngeal carcinoma cells, CNE2.	trichostatin A	29-32	P53	Homo sapiens	22-25
21210663-4	2011	After a sandwich immunoreaction, the HRP-p53(392)Ab(2)-GO captured onto the electrode surface produced an amplified electrocatalytic response by the reduction of enzymatically oxidized thionine in the presence of hydrogen peroxide.	thionine	185-193	P53	Homo sapiens	41-44
20674019-0	2011	The role of p53 and autophagy in Dasatinib resistance of CLL lymphocytes.	Dasatinib	33-42	P53	Homo sapiens	12-15
22493143-5	2012	An activation of p53 (TP53) transcriptional activity in Dox- or Dox+TSA-treated cells was revealed by the increased expression levels of p53 mRNA/protein as well as p53-driven luciferase activities.	trichostatin A	68-71	P53	Homo sapiens	17-20
22493143-5	2012	An activation of p53 (TP53) transcriptional activity in Dox- or Dox+TSA-treated cells was revealed by the increased expression levels of p53 mRNA/protein as well as p53-driven luciferase activities.	trichostatin A	68-71	P53	Homo sapiens	22-26
22493143-5	2012	An activation of p53 (TP53) transcriptional activity in Dox- or Dox+TSA-treated cells was revealed by the increased expression levels of p53 mRNA/protein as well as p53-driven luciferase activities.	trichostatin A	68-71	P53	Homo sapiens	137-140
20931131-3	2011	This report describes a series of high-throughput LanthaScreen  time-resolved Forster resonance energy transfer (TR-FRET) immunoassays for detection of intracellular p53 phosphorylation of Ser15 and acetylation of Lys382 upon treatment with DNA damage agents, such as etoposide.	Etoposide	268-277	P53	Homo sapiens	166-169
20931131-5	2011	First, BacMam-mediated overexpression of SIRT1 resulted in dose-dependent deacetylation of GFP-p53 following etoposide treatment of U-2 OS cells, confirming that GFP-p53 serves as a SIRT1 substrate in this assay format.	Etoposide	109-118	P53	Homo sapiens	95-98
20858462-10	2011	The tumor suppressor p53 appeared as master regulator of these propapoptotic changes and is the transactivator of proapoptotic proteins which was upregulated by indirubin.	indirubin	161-170	P53	Homo sapiens	21-24
22493143-5	2012	An activation of p53 (TP53) transcriptional activity in Dox- or Dox+TSA-treated cells was revealed by the increased expression levels of p53 mRNA/protein as well as p53-driven luciferase activities.	trichostatin A	68-71	P53	Homo sapiens	137-140
22289577-7	2012	The HA22T-implanted nude mice model further confirmed that diosmin inhibited HA22T tumor cell growth and down regulated the PI3K-Akt-MDM2 signaling and cell cycle regulating proteins, as well as activating PP2A and p53 proteins.	Diosmin	59-66	P53	Homo sapiens	215-218
20840867-3	2011	This resulted in reduction of HU-induced phosphorylation of CHK1 S345 (serine 345), p53 S15, and H2AX S139.	Hydroxyurea	30-32	P53	Homo sapiens	84-87
21897876-0	2011	The combination of BH3-mimetic ABT-737 with the alkylating agent temozolomide induces strong synergistic killing of melanoma cells independent of p53.	ABT-737	31-38	P53	Homo sapiens	146-149
21897876-9	2011	Experiments with nutlin-3, a p53 inducer, demonstrated that p53 induction was sufficient for synergistic cell death with ABT-737 in a Noxa-dependent fashion.	ABT-737	121-128	P53	Homo sapiens	60-63
22708054-0	2011	Catalytic, Enantioselective Synthesis of Stilbene cis-Diamines: A Concise Preparation of (-)-Nutlin-3, a Potent p53/MDM2 Inhibitor.	nutlin 3	89-101	P53	Homo sapiens	112-115
22331493-0	2012	Sodium arsenite +- hyperthermia sensitizes p53-expressing human ovarian cancer cells to cisplatin by modulating platinum-DNA damage responses.	sodium arsenite	0-15	P53	Homo sapiens	43-46
22708054-3	2011	This method then became the lynchpin for an enantioselective synthesis of (-)-Nutlin-3 (Hoffmann-LaRoche), a potent cis-imidazoline small molecule inhibitor of p53-MDM2 used extensively as a probe of cell biology and currently in drug development.	nutlin 3	74-86	P53	Homo sapiens	160-163
20931131-5	2011	First, BacMam-mediated overexpression of SIRT1 resulted in dose-dependent deacetylation of GFP-p53 following etoposide treatment of U-2 OS cells, confirming that GFP-p53 serves as a SIRT1 substrate in this assay format.	Etoposide	109-118	P53	Homo sapiens	166-169
22331493-4	2012	In this study, we examined the role of p53 status in EOC response to a novel combination of cisplatin, sodium arsenite, and hyperthermia.	sodium arsenite	103-118	P53	Homo sapiens	39-42
20931131-9	2011	The effect of this compound was dramatically increased when used in combination with chemotherapeutic drug and/or the HDAC inhibitor Trichostatin A, confirming a proposed synergistic mechanism of p53 deacetylation by SIRT1 and Type I/II HDACs.	trichostatin A	133-147	P53	Homo sapiens	196-199
21159614-9	2010	Collectively, these results show that nutlin-3 may be a useful agent in combination with TRAIL and, importantly, uncover a novel regulatory effect of p53 on the expression of Mcl-1 in melanoma cells on treatment with nutlin-3, which may antagonize the therapeutic efficacy of other chemotherapeutic drugs in addition to docetaxel in melanoma.	nutlin 3	217-225	P53	Homo sapiens	150-153
22331493-5	2012	Human EOC cells were treated with cisplatin +- 20muM sodium arsenite at 37 C or 39 C for 1 h. Sodium arsenite +- hyperthermia sensitized wild-type p53-expressing (A2780, A2780/CP70, OVCA 420, OVCA 429, and OVCA 433) EOC cells to cisplatin.	sodium arsenite	94-109	P53	Homo sapiens	147-150
22331493-7	2012	P53 small interfering RNA (siRNA) transfection abrogated sodium arsenite sensitization effect.	sodium arsenite	57-72	P53	Homo sapiens	0-3
22331493-9	2012	Cotreatment with sodium arsenite +- hyperthermia attenuated cisplatin-induced XPC in wild-type p53-expressing cells.	sodium arsenite	17-32	P53	Homo sapiens	95-98
22331493-10	2012	XPC siRNA transfection sensitized wild-type p53-expressing cells to cisplatin, suggesting that sodium arsenite +- hyperthermia attenuation of XPC is a mechanism by which wild-type p53-expressing cells are sensitized to cisplatin.	sodium arsenite	95-110	P53	Homo sapiens	44-47
20926293-0	2010	Chalcone HTMC causes in vitro selective cytotoxicity, cell-cycle G1 phase arrest through p53-dependent pathway in human lung adenocarcinoma A549 cells, and in vivo tumor growth suppression.	Chalcone	0-8	P53	Homo sapiens	89-92
21173028-9	2011	Altogether, our data uncover a novel mechanism linking MYCN to apoptosis that can be triggered by the p53-reactivating compound Nutlin-3, supporting its use in the most difficult-to-treat subset of neuroblastoma.	nutlin 3	128-136	P53	Homo sapiens	102-105
22420423-11	2012	CONCLUSIONS: Our data indicate loss of function of the ATM-Chk2-p53 cascade to be strongly associated with resistance to anthracycline/mitomycin-containing chemotherapy in breast cancer.	Mitomycin	135-144	P53	Homo sapiens	64-67
22262850-5	2012	Herein, we describe the preparation and characterization of an oligodeoxynucleotide containing a CPD of a T(m)CG site, one of the major sites of C methylation and C-to-T mutations found in the p53 gene of basal and squamous cell cancers.	Oligodeoxyribonucleotides	63-83	P53	Homo sapiens	193-196
20850924-3	2010	In the bortezomib sensitive wild-type TP53 MCL cells, the Nutlin-3/bortezomib combination caused G0/G1 cell cycle arrest followed by the increase in apoptosis induction.	nutlin 3	58-66	P53	Homo sapiens	38-42
21088491-1	2010	Atomistic simulations of a set of stapled peptides derived from the transactivation domain of p53 (designed by Verdine &amp; colleagues, JACS 2007 129:2456) and complexed to MDM2 reveal that the good binders are uniquely characterized by higher helicity and by extensive interactions between the hydrocarbon staples and the MDM2 surface; in contrast the poor binders have reduced helicity and their staples are mostly solvent exposed.	Hydrocarbons	296-307	P53	Homo sapiens	94-97
20727582-9	2010	In summary, our findings demonstrated that silica nanoparticles could induce dysfunction of endothelial cells through oxidative stress via JNK, p53 and NF-kappaB pathways, suggesting that exposure to silica nanoparticles may be a significant risk for the development of cardiovascular diseases such as atherosclerosis and thrombus.	Silicon Dioxide	200-206	P53	Homo sapiens	144-147
21104938-6	2010	The combined treatment of FNQ with AG1478 (a specific EGFR inhibitor) significantly enhanced the G(2)/M arrest and apoptosis, and also led to up-regulation in Bax, p53, p21, p27, release of mitochondrial cytochrome c, and down-regulation of Bcl-2, XIAP, survivin, cyclin A, cyclin B, Cdk1, and Cdk2 in A549 cells.	RTKI cpd	35-41	P53	Homo sapiens	164-167
22341969-8	2012	The mutation did not lead to a reduction in ATR expression, but cultured fibroblasts showed lower p53 levels after activation of ATR with hydroxyurea than did normal control fibroblasts.	Hydroxyurea	138-149	P53	Homo sapiens	98-101
20840860-6	2010	Downregulation of p53 target genes BAX and/or GADD45 alpha led to decreased in PPP1R13L activation after adriamycin and/or etoposide treatments.	Etoposide	123-132	P53	Homo sapiens	18-21
20963488-8	2010	Bufalin induced the apoptosis and cell cycle arrest by affecting the protein expressions of Bcl-2/Bax, cytochrome c, caspase-3, PARP, p53, p21WAF1, cyclinD1, and COX-2 in A549 cells.	bufalin	0-7	P53	Homo sapiens	134-137
21080495-10	2010	We used this method to study differences in protein localization in HCT116 cells either with or without p53, and studied the differences in cellular response to DNA damage following treatment of HCT116 cells with etoposide in both p53 wild-type and null genetic backgrounds.	Etoposide	213-222	P53	Homo sapiens	231-234
20659543-10	2010	Caspase-8, caspase-3, Bax, P53 and P21 mRNAs as well as proteins were increased while Bcl-2 mRNA and protein were decreased significantly by 24 h of PE treatment.	pe	149-151	P53	Homo sapiens	27-30
20661218-9	2010	Restoration of p53 and silencing cyclin B1 render cervical carcinoma cells more susceptible to DNA damage agent camptothecin.	Camptothecin	112-124	P53	Homo sapiens	15-18
20851891-4	2010	Mutation or phosphorylation of p53 at Ser(269) attenuates binding of the p53-specific monoclonal antibody DO-12, identifying an assay for measuring Ser(269) phosphorylation of p53 in vivo.	do-12	106-111	P53	Homo sapiens	31-34
20851891-4	2010	Mutation or phosphorylation of p53 at Ser(269) attenuates binding of the p53-specific monoclonal antibody DO-12, identifying an assay for measuring Ser(269) phosphorylation of p53 in vivo.	do-12	106-111	P53	Homo sapiens	73-76
20851891-4	2010	Mutation or phosphorylation of p53 at Ser(269) attenuates binding of the p53-specific monoclonal antibody DO-12, identifying an assay for measuring Ser(269) phosphorylation of p53 in vivo.	do-12	106-111	P53	Homo sapiens	73-76
20851891-5	2010	The mAb DO-12 epitope of p53 is masked via phosphorylation in a range of human tumor cells with WT p53 status, as defined by increased mAb DO-12 binding to endogenous p53 after phosphatase treatment.	do-12	8-13	P53	Homo sapiens	25-28
20851891-5	2010	The mAb DO-12 epitope of p53 is masked via phosphorylation in a range of human tumor cells with WT p53 status, as defined by increased mAb DO-12 binding to endogenous p53 after phosphatase treatment.	do-12	8-13	P53	Homo sapiens	99-102
20682800-4	2010	Here, we show that CP-31398 blocks the growth of RMS cells that have either wild-type or mutant p53 status.	CP 31398	19-27	P53	Homo sapiens	96-99
22200537-0	2012	Liposomal formulations of Etoposide and Docetaxel for p53 mediated enhanced cytotoxicity in lung cancer cell lines.	Etoposide	26-35	P53	Homo sapiens	54-57
20682800-8	2010	Apoptosis induced by CP-31398 occurred with translocation of p53 to mitochondria, leading to altered mitochondrial membrane potential, cytochrome c release, and reactive oxygen species release.	CP 31398	21-29	P53	Homo sapiens	61-64
20682800-9	2010	In vivo, CP-31398 decreased the growth of tumor xenografts composed of wild-type or mutant p53 tumor cells, increasing tumor-free host survival.	CP 31398	9-17	P53	Homo sapiens	91-94
20682800-10	2010	Our findings indicate that the ability of CP-31398 to modulate wild-type and mutant p53 results in the inhibition of RMS growth and invasiveness.	CP 31398	42-50	P53	Homo sapiens	84-87
20466611-11	2010	CONCLUSIONS: Cholesterol and phytosterol treatment differentially regulated the growth of prostate cancer cells and the expression of p53 and cav-1, a gene that regulates androgen-regulated signals.	Phytosterols	29-40	P53	Homo sapiens	134-137
20810912-8	2010	Conversely, staurosporine, a kinase inhibitor, and nutlin-3, a drug that enhances p53 expression, both raised p53 levels and increased the rate of apoptosis in syncytiotrophoblasts compared with vehicle controls.	Staurosporine	12-25	P53	Homo sapiens	110-113
20978201-7	2010	Marked increase in p53, a downstream target of the activated ATM pathway, was detected only in response to camptothecin and doxorubicin.	Camptothecin	107-119	P53	Homo sapiens	19-22
20432447-6	2010	Tyr/Phe, Gln and Met restriction increase phosphorylation of GSK3beta-Ser(9), phosphorylation of p53-Ser(15) and reduce the mitochondrial localization of PDH.	Glutamine	9-12	P53	Homo sapiens	97-100
22200537-1	2012	The objective of present investigation was to develop and assess comparative enhancement in cytotoxicity of liposomal Etoposide and Docetaxel in non-small cell lung cancer cell lines after pre-treatment and co-administration of p53 tumor suppressor gene and to assess direct lung targeting of optimized formulations by dry powder inhaler technology.	Etoposide	118-127	P53	Homo sapiens	228-231
20432447-8	2010	In p53-null PC3 cells, Tyr/Phe, Gln and Met restriction decreases glucose consumption, reduces phosphorylation of Akt-Ser(473), and increases phosphorylation of GSK3beta-Ser(9).	Glutamine	32-35	P53	Homo sapiens	3-6
22172953-7	2012	LY294002 increased cytosolic p53 with a concomitant decrease in nuclear p53, suggesting transfer of p53 to the cytosol where apoptosis might be initiated via the intrinsic mitochondrial pathway.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	P53	Homo sapiens	29-32
20647331-8	2010	The importance of the p53 pathway to PIM1-driven cellular senescence was further shown by the observation that expression of dominant-negative p53 or shRNA targeting p21 blocked the PIM1-induced changes in the DNA damage response and increases in SA-beta-Gal activity.	2-(2-quinolinyl)-1H-indene--1,3(2H)-dione-6'-sulfonic acid	247-258	P53	Homo sapiens	22-25
20647331-8	2010	The importance of the p53 pathway to PIM1-driven cellular senescence was further shown by the observation that expression of dominant-negative p53 or shRNA targeting p21 blocked the PIM1-induced changes in the DNA damage response and increases in SA-beta-Gal activity.	2-(2-quinolinyl)-1H-indene--1,3(2H)-dione-6'-sulfonic acid	247-258	P53	Homo sapiens	143-146
20444544-0	2010	p53-Dependent p21-mediated growth arrest pre-empts and protects HCT116 cells from PUMA-mediated apoptosis induced by EGCG.	epigallocatechin gallate	117-121	P53	Homo sapiens	0-3
20444544-1	2010	The tumor suppressor protein p53 plays a key role in regulation of negative cellular growth in response to EGCG.	epigallocatechin gallate	107-111	P53	Homo sapiens	29-32
20444544-3	2010	Cells expressing p53 and p21 accumulate in G1 upon treatment with EGCG.	epigallocatechin gallate	66-70	P53	Homo sapiens	17-20
20444544-5	2010	Treatment with EGCG leads to induction of p53, p21 and PUMA in p21 wild-type, and p53 and PUMA in p21(-/-) cells.	epigallocatechin gallate	15-19	P53	Homo sapiens	42-45
20444544-5	2010	Treatment with EGCG leads to induction of p53, p21 and PUMA in p21 wild-type, and p53 and PUMA in p21(-/-) cells.	epigallocatechin gallate	15-19	P53	Homo sapiens	82-85
20798760-5	2010	Specifically, 2,7-DAM is not cytotoxic and does not activate the p53 pathway while MC and DMC are cytotoxic and able to activate the p53 pathway.	Mitomycin	83-85	P53	Homo sapiens	133-136
20444544-6	2010	Ablation of p53 by RNAi protects p21(-/-) cells, thus indicating a p53-dependent apoptosis by EGCG.	epigallocatechin gallate	94-98	P53	Homo sapiens	12-15
20798760-6	2010	DMC is more cytotoxic than MC and can also kill p53-deficient cells by inducing degradation of Checkpoint 1 protein, which is not seen with MC treatment of the p53-deficient cells.	Mitomycin	1-3	P53	Homo sapiens	48-51
22172953-7	2012	LY294002 increased cytosolic p53 with a concomitant decrease in nuclear p53, suggesting transfer of p53 to the cytosol where apoptosis might be initiated via the intrinsic mitochondrial pathway.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	P53	Homo sapiens	72-75
20444544-6	2010	Ablation of p53 by RNAi protects p21(-/-) cells, thus indicating a p53-dependent apoptosis by EGCG.	epigallocatechin gallate	94-98	P53	Homo sapiens	67-70
20444544-7	2010	Furthermore, analysis of cells lacking PUMA or Bax with or without p21 but with p53 reveals that all the cells expressing p53 and p21 survived after EGCG treatment.	epigallocatechin gallate	149-153	P53	Homo sapiens	80-83
20536192-1	2010	The mitomycin derivative 10-decarbamoyl mitomycin C (DMC) more rapidly activates a p53-independent cell death pathway than mitomycin C (MC).	Mitomycin	4-13	P53	Homo sapiens	83-86
22172953-7	2012	LY294002 increased cytosolic p53 with a concomitant decrease in nuclear p53, suggesting transfer of p53 to the cytosol where apoptosis might be initiated via the intrinsic mitochondrial pathway.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	P53	Homo sapiens	72-75
20536192-1	2010	The mitomycin derivative 10-decarbamoyl mitomycin C (DMC) more rapidly activates a p53-independent cell death pathway than mitomycin C (MC).	Mitomycin	40-51	P53	Homo sapiens	83-86
20536192-1	2010	The mitomycin derivative 10-decarbamoyl mitomycin C (DMC) more rapidly activates a p53-independent cell death pathway than mitomycin C (MC).	Mitomycin	54-56	P53	Homo sapiens	83-86
20444544-7	2010	Furthermore, analysis of cells lacking PUMA or Bax with or without p21 but with p53 reveals that all the cells expressing p53 and p21 survived after EGCG treatment.	epigallocatechin gallate	149-153	P53	Homo sapiens	122-125
20444544-10	2010	Furthermore, we find that p53-dependent activation of PUMA in response to EGCG directly leads to apoptosis with out requiring Bax as is the case in response to agents that induce DNA damage.	epigallocatechin gallate	74-78	P53	Homo sapiens	26-29
20962589-6	2010	Downregulation of PLK1 expression by p53 is relieved by the histone deacetylase inhibitor, trichostatin A, and involves recruitment of histone deacetylase to the vicinity of p53RE2, further supporting a transcriptional repression mechanism.	trichostatin A	91-105	P53	Homo sapiens	37-40
22172953-8	2012	Protein changes described here suggest that the anti-angiogenic effects of LY294002 may be related to p53; the mutational status of p53 in CRC may be an important determinant of the efficacy of PI3K inhibitors for treatment.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	75-83	P53	Homo sapiens	102-105
20819578-0	2010	Ursolic acid induces human hepatoma cell line SMMC-7721 apoptosis via p53-dependent pathway.	ursolic acid	0-12	P53	Homo sapiens	70-73
22184125-4	2012	We first show that both recombinant sAPPalpha and N1, but not its inactive parent fragment N2, reduce staurosporine-stimulated caspase-3 activation and TUNEL-positive cell death by lowering p53 promoter transactivation and activity in human cells.	Staurosporine	102-115	P53	Homo sapiens	190-193
20418912-4	2010	LY294002 (PI3-kinase inhibitor) pre-treatment altered the post-translational modifications and the sub-cellular localization of p53.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	P53	Homo sapiens	128-131
20418912-5	2010	Although LY294002 increased the chemosensitivity of cells to low concentrations of adriamycin (adriamycin-low), it protected the cells from cytotoxicity induced by high concentrations of adriamycin (adriamycin-high) in a p53-dependent manner.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	9-17	P53	Homo sapiens	221-224
20418912-6	2010	Further, we found that LY294002 completely abolished the activation of p53 target genes (particularly pro-apoptotic) under adriamycin-high conditions, whereas it only marginally repressed the p53 target genes under adriamycin-low conditions; in fact, it further activated the transcription of NOXA, HRK, APAF1 and CASP5 genes.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	23-31	P53	Homo sapiens	71-74
20655369-4	2010	Our results revealed a significant P53-induction by actinomycin D, methyl methanesulfonate and etoposide.	Etoposide	95-104	P53	Homo sapiens	35-38
20655369-7	2010	While cyclophosphamide showed an elevation of activated P53 in the presence of S9, 7,12-dimethylbenz[a]anthracene and aflatoxin B(1) responded without the MAS.	Aflatoxin B1	118-129	P53	Homo sapiens	56-59
20655369-8	2010	Inhibition of cellular CYP3A4 or CYP1A/1B suppressed the aflatoxin B(1)- and dimethylbenz[a]anthracene-mediated P53 response, respectively, indicating that HepG2 cells are capable of metabolizing these compounds in a CYP1A/B/3A4-dependent manner.	Aflatoxin B1	57-68	P53	Homo sapiens	112-115
21725357-0	2012	MYCN sensitizes neuroblastoma to the MDM2-p53 antagonists Nutlin-3 and MI-63.	nutlin 3	58-66	P53	Homo sapiens	42-45
20640432-8	2010	In addition, percentage of cells expressing p53 and p504S expression was higher in TSA than those of HP and SSA/SSP.	trichostatin A	83-86	P53	Homo sapiens	44-47
20219242-2	2010	In this paper, biotinylated transferrin/avidin/biotinylated disulfide containing PEI bioconjugates (TABP-SS) mediated p53 gene delivery system was formed attributed to the "avidin-biotin bridge".	avidin-biotin	173-186	P53	Homo sapiens	118-121
21725357-0	2012	MYCN sensitizes neuroblastoma to the MDM2-p53 antagonists Nutlin-3 and MI-63.	MI-63	71-76	P53	Homo sapiens	42-45
20811720-5	2010	In this study, we investigated the effect of trichostatin A or TSA (an HDAC inhibitor), and epoxomycin (a proteasome inhibitor) on MYCN and p53 expression in MYCN-amplified neuroblastoma cells.	trichostatin A	63-66	P53	Homo sapiens	140-143
22290291-0	2012	The dietary phytochemical 3,3"-diindolylmethane induces G2/M arrest and apoptosis in oral squamous cell carcinoma by modulating Akt-NF-kappaB, MAPK, and p53 signaling.	3,3'-diindolylmethane	26-47	P53	Homo sapiens	153-156
20811720-9	2010	Furthermore, Epoxomycin as a single agent and its combination with TSA enhance p53 expression in the MYCN-amplified neuroblastoma cell lines.	trichostatin A	67-70	P53	Homo sapiens	79-82
20356045-4	2010	6-DG also up-regulated Ser-15 phosphorylation and evoked p53 nuclear translocation.	6-dehydrogingerdione	0-4	P53	Homo sapiens	57-60
20356045-5	2010	Abrogation of p53 expression by p53 small interfering RNA significantly attenuated 6-DG-induced DR5 expression, thus rendering these cells resistant to TRAIL-induced apoptosis.	6-dehydrogingerdione	83-87	P53	Homo sapiens	14-17
20356045-5	2010	Abrogation of p53 expression by p53 small interfering RNA significantly attenuated 6-DG-induced DR5 expression, thus rendering these cells resistant to TRAIL-induced apoptosis.	6-dehydrogingerdione	83-87	P53	Homo sapiens	32-35
22056254-2	2012	Here we determine the effect of the tumor suppressor protein, p53, on trafficking (64)Cu to tumor cell nuclei from DOTA vs. CB-TE2A-conjugated agonist Y3-TATE and the antagonist (64)Cu-CB-TE2A-sst2-ANT in cell lines that are positive or negative for p53.	te2a	127-131	P53	Homo sapiens	62-65
20445579-9	2010	Thus, by coupling with bidirectional vector, controllable p53 transfer was achieved and the capability of fluoro-2-deoxy-D-glucose (FDG)-PET to assess the therapeutic response to p53 gene therapy was evidently confirmed, which may have an impact on the improvement of p53 gene therapy.	fluoro-2-deoxy-d-glucose	106-130	P53	Homo sapiens	58-61
20445579-9	2010	Thus, by coupling with bidirectional vector, controllable p53 transfer was achieved and the capability of fluoro-2-deoxy-D-glucose (FDG)-PET to assess the therapeutic response to p53 gene therapy was evidently confirmed, which may have an impact on the improvement of p53 gene therapy.	fluoro-2-deoxy-d-glucose	106-130	P53	Homo sapiens	179-182
20445579-9	2010	Thus, by coupling with bidirectional vector, controllable p53 transfer was achieved and the capability of fluoro-2-deoxy-D-glucose (FDG)-PET to assess the therapeutic response to p53 gene therapy was evidently confirmed, which may have an impact on the improvement of p53 gene therapy.	fluoro-2-deoxy-d-glucose	106-130	P53	Homo sapiens	179-182
20479887-5	2010	Camptothecin is a reported inhibitor of HIF-1alpha translation, while mitomycin C has been reported to induce p53-dependent HIF-1alpha degradation.	Mitomycin	70-81	P53	Homo sapiens	110-113
22056254-2	2012	Here we determine the effect of the tumor suppressor protein, p53, on trafficking (64)Cu to tumor cell nuclei from DOTA vs. CB-TE2A-conjugated agonist Y3-TATE and the antagonist (64)Cu-CB-TE2A-sst2-ANT in cell lines that are positive or negative for p53.	cu-cb	182-187	P53	Homo sapiens	62-65
20479887-6	2010	In this study we demonstrate that the inhibitory effect of mitomycin C on HIF-1alpha protein expression is not dependent on p53 and protein degradation, but also involves HIF-1alpha translational regulation.	Mitomycin	59-70	P53	Homo sapiens	124-127
21979946-0	2012	Germline SDHx variants modify breast and thyroid cancer risks in Cowden and Cowden-like syndrome via FAD/NAD-dependant destabilization of p53.	Flavin-Adenine Dinucleotide	101-104	P53	Homo sapiens	138-141
20143454-0	2010	Sulfur mustard induced cytokine production and cell death: investigating the potential roles of the p38, p53, and NF-kappaB signaling pathways with RNA interference.	Mustard Gas	0-14	P53	Homo sapiens	105-108
20662736-8	2010	Although mitoxantrone, ellipticine, camptothecin, and topotecan all exhibited concentration-dependent disruption of the p53-hDM2 PPIB, they were much less potent than Nutlin-3.	Camptothecin	36-48	P53	Homo sapiens	120-123
20422343-5	2010	To investigate their effects in combination, a p53-mutant cholangiocarcinoma line HuCCT1 was treated with Nutlin-3 and/or gemcitabine in the current study.	nutlin 3	106-114	P53	Homo sapiens	47-50
21979946-11	2012	This loss of p53 was regulated by MDM2-independent NADH quinone oxidoreductase 1-mediated protein degradation, likely due to the imbalance of flavin adenine dinucleotide/nicotinamide adenine dinucleotide in SDH(var+) cells.	Flavin-Adenine Dinucleotide	142-169	P53	Homo sapiens	13-16
20154087-7	2010	Induction of the death receptor by the triterpenoid was found to be p53-independent but required the induction of CAAT/enhancer-binding protein homologous protein (CHOP), inasmuch as gene silencing of CHOP abolished the induction of DR5 expression by celastrol and associated enhancement of TRAIL-induced apoptosis.	triterpenoid TP-222	39-51	P53	Homo sapiens	68-71
22277916-5	2012	RESULTS: CS correlates with several lung cancer risk factors, including histopathological grade, age, smoking status, and p53 and Ki67 immunostaining.	Cesium	9-11	P53	Homo sapiens	122-125
20080970-12	2010	When combined with selective MDM2 inhibitors, SJ-172550 may also be useful for treating tumors that express wild-type p53.	SJ 172550	46-55	P53	Homo sapiens	118-121
20406630-4	2010	(1) Sodium salicylate, a non-COX-selective NSAID, was shown to reduce DNA damage-induced RPA and p53 phosphorylation.	Sodium Salicylate	4-21	P53	Homo sapiens	97-100
20406630-8	2010	(5) The activation of ataxia telangiectasia mutated (ATM) kinase and DNA-dependent protein kinase (DNA-PK), two key signal transducers upstream of RPA and p53, was found to be significantly reduced with sodium salicylate treatment.	Sodium Salicylate	203-220	P53	Homo sapiens	155-158
20406630-11	2010	(7) Unexpectedly, sodium salicylate showed a p53-independent protection effect on topoisomerase-mediated cell killing.	Sodium Salicylate	18-35	P53	Homo sapiens	45-48
22090360-9	2012	Expression of disruptive TP53 mutations significantly decreased radiation-induced senescence, as measured by SA-beta-gal staining, p21 expression, and release of ROS.	2-(2-quinolinyl)-1H-indene--1,3(2H)-dione-6'-sulfonic acid	109-120	P53	Homo sapiens	25-29
20587660-0	2010	p53-independent induction of G1 arrest and p21WAF1/CIP1 expression by ascofuranone, an isoprenoid antibiotic, through downregulation of c-Myc.	Terpenes	87-97	P53	Homo sapiens	0-3
23251091-6	2012	p53siRNA promotes the convergence of the extrinsic and intrinsic pathways in a synergic manner with EGCG.	epigallocatechin gallate	100-104	P53	Homo sapiens	0-3
20499891-9	2010	Upregulation of pro-apoptotic proteins such as p53 and Bax and downregulation of antiapoptotic protein Bcl-2 were observed in PBQ-treated A549 cells.	1,3,4,6,7,11b-hexahydro-9,10-dimethoxy-2H-benzo(a)quinolizine-2-spiro-3'-(1'-phenyl)succinimide	126-129	P53	Homo sapiens	47-50
20530421-0	2010	Chronic exposure of colorectal cancer cells in culture to fluoropyrimidine analogs induces thymidylate synthase and suppresses p53.	2-fluoropyrimidine	58-74	P53	Homo sapiens	127-130
22393286-9	2012	CONCLUSION: Overall, our data demonstrated that ZnO NPs selectively induce apoptosis in cancer cells, which is likely to be mediated by reactive oxygen species via p53 pathway, through which most of the anticancer drugs trigger apoptosis.	Zinc Oxide	48-51	P53	Homo sapiens	164-167
19781850-5	2010	The levels of p53 were increased in the EGCG-treated cells, with a corresponding decrease in Bcl-2 and Bid protein levels as well as an increase in the Bax level.	epigallocatechin gallate	40-44	P53	Homo sapiens	14-17
20347026-7	2010	The complexes of PHEMA-g-(PEI-b-PEG) successfully induced elevated wild-type p53 expression in BT474 cells and led to enhanced apoptosis of BT474 cells.	Polyhydroxyethyl Methacrylate	17-22	P53	Homo sapiens	77-80
21918844-6	2012	The desipramine/cisplatin combination resulted in increased levels of p53 as well as mitochondrial damage, caspase activation, and poly(ADP ribose) polymerase cleavage, suggesting that desipramine may synergize with cisplatin more than with other platinum chemotherapeutics partly by activating distinct apoptotic pathways.	Desipramine	4-15	P53	Homo sapiens	70-73
24683262-4	2010	OBJECTIVE: The aim of this study was to examine the ability of the histone deacetylase inhibitor, sodium butyrate (NaB), to modulate the expression of p53.	nab	115-118	P53	Homo sapiens	151-154
24683262-10	2010	RESULTS: In the SW-1990 and JHP-1 cell lines, use of 1 mM NaB was found to induce histone acetylation and p53 expression compared with those not treated with NaB (P = 0.01 and P = 0.018, respectively).	nab	58-61	P53	Homo sapiens	106-109
24683262-14	2010	CONCLUSION: This in vitro study found that NaB induced p53 expression in 2 pancreatic cancer cell lines (SW-1990 and JHP-1).	nab	43-46	P53	Homo sapiens	55-58
20305378-0	2010	Inactivation of p53 signaling by p73 or PTEN ablation results in a transformed phenotype that remains susceptible to Nutlin-3 mediated apoptosis.	nutlin 3	117-125	P53	Homo sapiens	16-19
20299546-2	2010	In this study, we show that TCDD treatment counteracts the p53 activation (phosphorylation and acetylation) elicited by a genotoxic compound, etoposide, in the human hepatocarcinoma cell line HepG2 and we delineated the mechanisms of this interaction.	Etoposide	142-151	P53	Homo sapiens	59-62
21918844-6	2012	The desipramine/cisplatin combination resulted in increased levels of p53 as well as mitochondrial damage, caspase activation, and poly(ADP ribose) polymerase cleavage, suggesting that desipramine may synergize with cisplatin more than with other platinum chemotherapeutics partly by activating distinct apoptotic pathways.	Desipramine	185-196	P53	Homo sapiens	70-73
21523548-0	2012	Structural determinants of benzodiazepinedione/peptide-based p53-HDM2 inhibitors using 3D-QSAR, docking and molecular dynamics.	benzodiazepinedione	27-46	P53	Homo sapiens	61-64
21364648-0	2010	p53-mediated delayed NF-kappaB activity enhances etoposide-induced cell death in medulloblastoma.	Etoposide	49-58	P53	Homo sapiens	0-3
21364648-2	2010	Using several MB cell lines, we have demonstrated that the chemotherapeutic drug etoposide induces a p53- and caspase-dependent cell death.	Etoposide	81-90	P53	Homo sapiens	101-104
20356045-9	2010	Taken together, these data suggested that in addition to the mitochondrial- and Fas receptor-mediated apoptotic pathways involved, ROS-dependent and p53-regulated DR5 expression was also demonstrated to play a pivotal role in the synergistic enhancement of TRAIL-induced apoptosis instigated by 6-DG in Hep G2 cells.	6-dehydrogingerdione	295-299	P53	Homo sapiens	149-152
20404548-4	2010	Identification of guanidinoacetate methyltransferase (GAMT) as a new p53 target connects p53 to creatine metabolism critical in the regulation of ATP homeostasis.	Creatine	96-104	P53	Homo sapiens	69-72
23028738-0	2012	NVX-412, a new oncology drug candidate, induces S-phase arrest and DNA damage in cancer cells in a p53-independent manner.	pyrazine-2-carboxylic acid N'- (7-fluoropyrrolo(1,2-a)quinoxalin-4-yl)-hydrazide	0-7	P53	Homo sapiens	99-102
20404548-4	2010	Identification of guanidinoacetate methyltransferase (GAMT) as a new p53 target connects p53 to creatine metabolism critical in the regulation of ATP homeostasis.	Creatine	96-104	P53	Homo sapiens	89-92
20082627-9	2010	In addition, HL-60 cells were arrested in the G(0)/G(1) phase via the induction of p53/p21 by pipoxolan.	pipoxolan	94-103	P53	Homo sapiens	83-86
20351271-0	2010	Phosphate-activated glutaminase (GLS2), a p53-inducible regulator of glutamine metabolism and reactive oxygen species.	Glutamine	69-78	P53	Homo sapiens	42-45
20351271-1	2010	We identified a p53 target gene, phosphate-activated mitochondrial glutaminase (GLS2), a key enzyme in conversion of glutamine to glutamate, and thereby a regulator of glutathione (GSH) synthesis and energy production.	Glutamine	117-126	P53	Homo sapiens	16-19
20351271-9	2010	Thus, our results provide evidence for a unique metabolic role for p53, linking glutamine metabolism, energy, and ROS homeostasis, which may contribute to p53 tumor suppressor function.	Glutamine	80-89	P53	Homo sapiens	67-70
20351271-9	2010	Thus, our results provide evidence for a unique metabolic role for p53, linking glutamine metabolism, energy, and ROS homeostasis, which may contribute to p53 tumor suppressor function.	Glutamine	80-89	P53	Homo sapiens	155-158
22927971-6	2012	Furthermore, we identified p53 dependent premature senescence, a permanent cell cycle arrest, as the primary outcome in U87-MG cells after treatment with GC7.	2-(7-aminoheptyl)guanidine	154-157	P53	Homo sapiens	27-30
20371694-10	2010	Furthermore, in vivo delivery of anti-CK2alpha/alpha" oligodeoxynucleotide nanocapsules significantly suppressed tumor growth in HNSCC xenograft models, in association with modulation of CK2 and NF-kappaB regulated molecules, TP53 family proteins, and induction of apoptosis.	Oligodeoxyribonucleotides	54-74	P53	Homo sapiens	226-230
20068143-13	2010	High glucose and palmitate increased p53 acetylation and JNK phosphorylation; these effects were abolished in siRNA SIRT1-treated cells.	Palmitates	17-26	P53	Homo sapiens	37-40
22859938-6	2012	Tunicamycin or brefeldin A, two ER stress inducers, increased p53 expression in MCF-7 and Hela cells.	Tunicamycin	0-11	P53	Homo sapiens	62-65
20198331-4	2010	We showed that the killing efficacy of roscovitine and 16 other purines and potentiation of roscovitine-induced apoptosis by the PI3K inhibitor, LY294002, decreased with increasing corruption of the Rb and p53 pathways.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	145-153	P53	Homo sapiens	206-209
22860097-4	2012	Our results show that activation of the p14ARF-p53-p21-Rb pathway in the estrogen sensitive MCF-7 breast cancer cells induces many hallmarks of senescence including a large flat cell morphology, multinucleation, senescence-associated-beta-gal staining, and rapid G1 and G2/M phase cell cycle arrest.	beta-D-galactose	234-242	P53	Homo sapiens	47-50
20465947-0	2010	[Role of p53 in silica-induced cell cycle alternation and DNA double-strand break repair in human embryo lung fibroblasts].	Silicon Dioxide	16-22	P53	Homo sapiens	9-12
20465947-1	2010	OBJECTIVE: To study the role of p53 in silica-induced cell cycle alternation and DNA double strand breaks repair in human embryo lung fibroblasts (HELF).	Silicon Dioxide	39-45	P53	Homo sapiens	32-35
20465947-6	2010	RESULTS: After treatment with 200 microg/ml silica for different times (0, 1, 2, 6, 12 and 24 h), the expression levels and phosphorylation of p53 increased in a time-dependent manner, reaching maximum at 12 h and then decreasing at 24 h. After treatment with 0, 25, 50, 100, 200, 300 and 400 microg/ml silica for 12 h, the expression levels and phosphorylation of p53 increased in concentration-dependent manner.	Silicon Dioxide	44-50	P53	Homo sapiens	143-146
20465947-6	2010	RESULTS: After treatment with 200 microg/ml silica for different times (0, 1, 2, 6, 12 and 24 h), the expression levels and phosphorylation of p53 increased in a time-dependent manner, reaching maximum at 12 h and then decreasing at 24 h. After treatment with 0, 25, 50, 100, 200, 300 and 400 microg/ml silica for 12 h, the expression levels and phosphorylation of p53 increased in concentration-dependent manner.	Silicon Dioxide	44-50	P53	Homo sapiens	365-368
20465947-6	2010	RESULTS: After treatment with 200 microg/ml silica for different times (0, 1, 2, 6, 12 and 24 h), the expression levels and phosphorylation of p53 increased in a time-dependent manner, reaching maximum at 12 h and then decreasing at 24 h. After treatment with 0, 25, 50, 100, 200, 300 and 400 microg/ml silica for 12 h, the expression levels and phosphorylation of p53 increased in concentration-dependent manner.	Silicon Dioxide	303-309	P53	Homo sapiens	143-146
22044530-6	2011	In the presence of nutlin-3, an HDM2 inhibitor, TCDD was still able to suppress 1-NP-induced p53 expression.	nutlin 3	19-27	P53	Homo sapiens	93-96
20465947-7	2010	After p53 expression was inhibited, silica-induced DNA damage repair competence was markedly increased (DRC = 87.68%), compared with the negative control cell induced by silica (DRC = 57.19%).	Silicon Dioxide	36-42	P53	Homo sapiens	6-9
20465947-10	2010	CONCLUSION: The silica dramatically increases the expression levels and phosphorylation of p53.	Silicon Dioxide	16-22	P53	Homo sapiens	91-94
22077725-0	2011	Effects of estrogen metabolite 2-methoxyestradiol on tumor suppressor protein p53 and proliferation of breast cancer cells.	2-Methoxyestradiol	31-49	P53	Homo sapiens	78-81
20465947-11	2010	The increased expression of p53 mediates silica-induced cell cycle change and inhibits silica-induced DNA double strand breaks repair.	Silicon Dioxide	41-47	P53	Homo sapiens	28-31
20465947-11	2010	The increased expression of p53 mediates silica-induced cell cycle change and inhibits silica-induced DNA double strand breaks repair.	Silicon Dioxide	87-93	P53	Homo sapiens	28-31
20215548-5	2010	Knocking down p53 attenuated the effect of Nutlin-3 on DEK expression, whereas knocking down DEK significantly increased both spontaneous and Nutlin-3-induced apoptosis.	nutlin 3	43-51	P53	Homo sapiens	14-17
21927014-0	2011	Platinum-(IV)-derivative satraplatin induced G2/M cell cycle perturbation via p53-p21(waf1/cip1)-independent pathway in human colorectal cancer cells.	satraplatin	25-36	P53	Homo sapiens	78-81
21807406-0	2011	The role of the tumor suppressor p53 pathway in the cellular DNA damage response to zinc oxide nanoparticles.	Zinc Oxide	84-94	P53	Homo sapiens	33-36
22993551-4	2010	Treatment with thymoquinone-4-alpha-linolenoylhydrazone (TQ-H-10) or thymoquinone-4-palmitoylhydrazone (TQ-H-11) induced a cytostatic effect, particularly in p53-competent HCT116 cells, mediated by an up-regulation of p21(cip1/waf1) and a down-regulation of cyclin E, and associated with an S/G(2) arrest of the cell cycle.	thymoquinone-4-alpha-linolenoylhydrazone	15-55	P53	Homo sapiens	158-161
22993551-4	2010	Treatment with thymoquinone-4-alpha-linolenoylhydrazone (TQ-H-10) or thymoquinone-4-palmitoylhydrazone (TQ-H-11) induced a cytostatic effect, particularly in p53-competent HCT116 cells, mediated by an up-regulation of p21(cip1/waf1) and a down-regulation of cyclin E, and associated with an S/G(2) arrest of the cell cycle.	thymoquinone-4-palmitoylhydrazone	69-102	P53	Homo sapiens	158-161
21807406-1	2011	In this paper, we explored how ZnO nanoparticles cross-interact with a critical tumor suppressive pathway centered around p53, which is one of the most important known tumor suppressors that protects cells from developing cancer phenotypes through its control over major pathways like apoptosis, senescence and cell cycle progression.	Zinc Oxide	31-34	P53	Homo sapiens	122-125
21807406-2	2011	We showed that the p53 pathway was activated in BJ cells (skin fibroblasts) upon ZnO nanoparticles treatment with a concomitant decrease in cell numbers.	Zinc Oxide	81-84	P53	Homo sapiens	19-22
20178585-3	2010	The aim of this study was to selectively kill p53 deficient cells (FaDu and H1299) by taxol and to protect p53 wild type cells (A549) by the prior administration of nutlin-3 in comparison to certain known anticancer drugs (5-fluorouracil, camptothecin, roscovitine).	nutlin 3	165-173	P53	Homo sapiens	107-110
21807406-3	2011	This suggests that cellular responses like apoptosis in the presence of ZnO nanoparticles require p53 as the molecular master switch towards programmed cell death.	Zinc Oxide	72-75	P53	Homo sapiens	98-101
21807406-6	2011	These p53 knocked down BJ cells became more resistant to ZnO nanoparticles induced cell death and increased cell progression.	Zinc Oxide	57-60	P53	Homo sapiens	6-9
20086182-6	2010	Furthermore, the number of the CASP8 -652 6N del (but not 302H) variant allele tended to correlate with increased levels of camptothecin-induced p53-mediated apoptosis in T lymphocytes from 170 cancer-free controls.	Camptothecin	124-136	P53	Homo sapiens	145-148
21715570-7	2011	The p53 inhibitor pifithrin-alpha inhibited 3-NBA-induced apoptosis while small effects were seen using pifithrin-mu, suggesting that 3-NBA-induced cell death is a result of transcriptional activation of p53.	3-nitrobenzanthrone	44-49	P53	Homo sapiens	4-7
20126473-3	2010	Our study showed that p53 mitochondrial translocation was found in mitomycin C (MMC)-treated HepG2.	Mitomycin	67-78	P53	Homo sapiens	22-25
20126473-3	2010	Our study showed that p53 mitochondrial translocation was found in mitomycin C (MMC)-treated HepG2.	Mitomycin	80-83	P53	Homo sapiens	22-25
20126473-12	2010	In the low-dose MMC treatment, the increased mitochondrial p53, Bcl-xL, and Bcl-2 could attenuate apoptosis.	Mitomycin	16-19	P53	Homo sapiens	59-62
21715570-7	2011	The p53 inhibitor pifithrin-alpha inhibited 3-NBA-induced apoptosis while small effects were seen using pifithrin-mu, suggesting that 3-NBA-induced cell death is a result of transcriptional activation of p53.	3-nitrobenzanthrone	134-139	P53	Homo sapiens	4-7
20126473-13	2010	However, in the high-dose MMC treatment, only the p53 translocated to the mitochondria and resulted in apoptosis progression.	Mitomycin	26-29	P53	Homo sapiens	50-53
21715570-7	2011	The p53 inhibitor pifithrin-alpha inhibited 3-NBA-induced apoptosis while small effects were seen using pifithrin-mu, suggesting that 3-NBA-induced cell death is a result of transcriptional activation of p53.	3-nitrobenzanthrone	134-139	P53	Homo sapiens	204-207
21903579-4	2011	A focused real-time quantitative reverse transcription PCR array of known p53-regulated genes identified p21(WAF1) (CDKN1A) as the highest ranked gene to be differentially expressed between B-cell precursor (BCP)-ALL and T-ALL xenografts following exposure to the DNA-damaging drug etoposide.	Etoposide	282-291	P53	Homo sapiens	74-77
19994890-10	2010	Western blot data revealed that genistein (6) stimulated an increase in the protein expression of Fas, FasL, and p53.	Genistein	32-41	P53	Homo sapiens	113-116
21872575-11	2011	Furthermore, p53 siRNA and p21 siRNA transfection attenuated adriamycin-induced SA-beta-gal staining.	2-(2-quinolinyl)-1H-indene--1,3(2H)-dione-6'-sulfonic acid	80-91	P53	Homo sapiens	13-16
20048077-0	2010	Sodium orthovanadate inhibits p53-mediated apoptosis.	Sodium orthovanadate	0-20	P53	Homo sapiens	30-33
20048077-1	2010	Sodium orthovanadate (vanadate) inhibits the DNA-binding activity of p53, but its precise effects on p53 function have not been examined.	Sodium orthovanadate	0-20	P53	Homo sapiens	69-72
21460857-4	2011	In addition, ABT737 treatment dephosphorylates (and hence likewise inhibits) p53, glycogen synthase kinase-3 and Akt.	ABT-737	13-19	P53	Homo sapiens	77-80
20122668-0	2010	Influence of chemoresistance and p53 status on fluoro-2-deoxy-D-glucose incorporation in cancer.	fluoro-2-deoxy-d-glucose	47-71	P53	Homo sapiens	33-36
21892957-8	2011	An amino acid polymorphism in the ZANK region is identified in ZEBRA from tumor cell lines including Akata that could alter binding of Akata ZEBRA to the p53 tumor suppressor and other ankyrin binding protein, and a novel model of antagonistic binding interactions between ZANK and the DNA binding regions of ZEBRA is suggested that may be explored in further biochemical and molecular biological models of viral replication.	akata	101-106	P53	Homo sapiens	154-157
20023923-1	2009	Octahedral ruthenium complexes, capable of photodynamic singlet oxygen production at near 100% efficiency, were shown to cause light-dependent covalent crosslinking of p53 and PCNA subunits in mammalian cells and cell lysates.	Singlet Oxygen	56-70	P53	Homo sapiens	168-171
20023923-2	2009	Azide, a singlet oxygen quencher, greatly reduced the p53 photocrosslinking, consistent with the idea that singlet oxygen is the reactive oxygen species involved in p53 photocrosslinking.	Singlet Oxygen	9-23	P53	Homo sapiens	54-57
20023923-2	2009	Azide, a singlet oxygen quencher, greatly reduced the p53 photocrosslinking, consistent with the idea that singlet oxygen is the reactive oxygen species involved in p53 photocrosslinking.	Singlet Oxygen	107-121	P53	Homo sapiens	54-57
20023923-2	2009	Azide, a singlet oxygen quencher, greatly reduced the p53 photocrosslinking, consistent with the idea that singlet oxygen is the reactive oxygen species involved in p53 photocrosslinking.	Singlet Oxygen	107-121	P53	Homo sapiens	165-168
21708241-9	2011	Subamolide A increased Bax/Bcl-2 ratios, the amount of cytochrome c released from the mitochondria, caspase-3 and PARP cleavage, activated p53 and ERK1/2 and ultimately led to apoptosis in NTUB1 cells.	subamolide A	0-12	P53	Homo sapiens	139-142
19766654-6	2009	In fact, substitution of this Asn to Ala of CHC diminished its ability to interact with p53, leading to reduced activity to transactivate p53.	Asparagine	30-33	P53	Homo sapiens	88-91
21708241-11	2011	CONCLUSIONS: The current study demonstrated that subamolide A triggered the mitochondria-dependent apoptotic pathways and p53 and ERK1/2 activation in the human urothelial carcinoma cell line NTUB1.	subamolide A	49-61	P53	Homo sapiens	122-125
19715480-4	2009	We show that expression of wt-p53 from a recombinant adenovirus-p53 followed by treatment with 2-methoxyestradiol (2-ME), an endogenous, nontoxic, estrogenic metabolite, resulted in differential NF-kappaB activation and inhibitor kappaB alpha (IkappaB-alpha) degradation in three different human lung cancer cell lines with different p53 phenotypes.	2-Methoxyestradiol	115-119	P53	Homo sapiens	64-67
19715480-5	2009	The H322J cells, with mutant (Arg248Gln) p53, showed NF-kappaB activation and IkappaB-alpha degradation after adeno-p53 expression + 2-ME treatment; however, these conditions separately did not activate NF-kappaB, rather caused accumulation of IkappaB-alpha.	2-Methoxyestradiol	133-137	P53	Homo sapiens	41-44
19715480-6	2009	In contrast, either adeno-p53 expression or 2-ME treatment induced NF-kappaB activation in the p53-deleted H1299 cells, but H460 cells, containing wt-p53, did not show NF-kappaB activation under any of these conditions.	2-Methoxyestradiol	44-48	P53	Homo sapiens	95-98
19715480-6	2009	In contrast, either adeno-p53 expression or 2-ME treatment induced NF-kappaB activation in the p53-deleted H1299 cells, but H460 cells, containing wt-p53, did not show NF-kappaB activation under any of these conditions.	2-Methoxyestradiol	44-48	P53	Homo sapiens	95-98
19715480-7	2009	This shows p53-dependent differential signaling to NF-kappaB by 2-ME.	2-Methoxyestradiol	64-68	P53	Homo sapiens	11-14
19715480-8	2009	Since NF-kappaB activation inhibits apoptosis and causes resistance to chemotherapy, our study suggests the need to distinguish p53 phenotypes of tumors for p53 gene and 2-ME therapy.	2-Methoxyestradiol	170-174	P53	Homo sapiens	128-131
19917243-2	2009	(2009) have identified the enzyme guanidinoacetate methyltransferase (GAMT) that regulates creatine metabolism as a p53 target involved in apoptosis, reactive oxygen species (ROS), and fatty acid metabolism.	Creatine	91-99	P53	Homo sapiens	116-119
19917247-3	2009	Here we identify guanidinoacetate methyltransferase (GAMT), an enzyme involved in creatine synthesis, as a p53 target gene and a key downstream effector of adaptive response to nutrient stress.	Creatine	82-90	P53	Homo sapiens	107-110
19917247-7	2009	The p53--&gt;GAMT pathway represents a new link between cellular stress responses and processes of creatine synthesis and FAO, demonstrating a further role of p53 in cellular metabolism.	Creatine	99-107	P53	Homo sapiens	4-7
19917247-7	2009	The p53--&gt;GAMT pathway represents a new link between cellular stress responses and processes of creatine synthesis and FAO, demonstrating a further role of p53 in cellular metabolism.	Creatine	99-107	P53	Homo sapiens	159-162
19838062-6	2009	Similarly, the gold-based TrxR inhibitor auranofin induced apoptosis related to oxidative stress, but independently of p53 and without apparent induction of the approximately 130 kDa form of TrxR1.	Auranofin	41-50	P53	Homo sapiens	119-122
19656744-7	2009	DNA pull-down assays using a 7,8-dihydro-8-oxoguanine duplex oligonucleotide as a substrate found that RPS3 acted as a scaffold for the additional binding of MDM2 and p53, suggesting that RPS3 interacts with important proteins involved in maintaining genomic integrity.	7,8-dihydro-8-oxoguanine duplex oligonucleotide	29-76	P53	Homo sapiens	167-170
19646415-0	2009	NF-kappab facilitates oridonin-induced apoptosis and autophagy in HT1080 cells through a p53-mediated pathway.	oridonin	22-30	P53	Homo sapiens	89-92
19646415-3	2009	In addition, treatment with oridonin caused an increase in NF-kappaB and p53 activities in a time-dependent manner.	oridonin	28-36	P53	Homo sapiens	73-76
19646415-4	2009	Inhibition of NF-kappaB or p53 activation by its specific inhibitor PDTC or pifithrin-alpha respectively, significantly reduced both oridonin-induced apoptosis and autophagy accompanied by the decrease in Beclin 1 and LC3 levels.	oridonin	133-141	P53	Homo sapiens	27-30
19646415-5	2009	Further experiments confirmed that oridonin-induced p53 activation was reduced by the NF-kappaB inhibitor whereas the activation of NF-kappaB was not affected by p53 inhibition.	oridonin	35-43	P53	Homo sapiens	52-55
19646415-6	2009	Taken together, these results demonstrate that NF-kappaB promotes oridonin-induced apoptotic and autophagic cell death through regulating p53 activation in HT1080 cells.	oridonin	66-74	P53	Homo sapiens	138-141
19706754-5	2009	We also found that the enhanced activation of JNK by 2-ME is partially regulated by p53, highlighting the relationship of JNK and autophagy to p53 signaling pathway.	2-Methoxyestradiol	53-57	P53	Homo sapiens	84-87
19706754-5	2009	We also found that the enhanced activation of JNK by 2-ME is partially regulated by p53, highlighting the relationship of JNK and autophagy to p53 signaling pathway.	2-Methoxyestradiol	53-57	P53	Homo sapiens	143-146
19706754-6	2009	Furthermore, we showed that 2-ME up-regulates damage-regulated autophagy modulator (DRAM), a p53 target gene, in Ewing sarcoma cells through a mechanism that involves JNK activation.	2-Methoxyestradiol	28-32	P53	Homo sapiens	93-96
19458022-5	2009	Clinical importance of the polymorphic variants was evaluated in multivariate models on 69 patients treated with taxane-platinum chemotherapy, with respect to TP53 status.	taxane-platinum	113-128	P53	Homo sapiens	159-163
19524575-0	2009	In vitro recapitulating of TP53 mutagenesis in hepatocellular carcinoma associated with dietary aflatoxin B1 exposure.	Aflatoxin B1	96-108	P53	Homo sapiens	27-31
19524575-9	2009	CONCLUSIONS: In this model system, AFB(1)-induced DNA adduction and mutagenesis recapitulate the unique mutational features of TP53 in AFB(1)-associated human HCC.	Aflatoxin B1	35-41	P53	Homo sapiens	127-131
19421231-9	2009	Most BL patients with wild-type p53 tumors could therefore benefit from treatment with nutlin-3, after a careful determination of the latency pattern of EBV in infected patients.	nutlin 3	87-95	P53	Homo sapiens	32-35
19597154-4	2009	Functional assays revealed a specific dinucleotide core combination within the CWWG motif of the p53RE to be the key factor that determines whether p53 transcriptionally activates or represses a target gene.	Dinucleoside Phosphates	38-50	P53	Homo sapiens	97-100
19597154-4	2009	Functional assays revealed a specific dinucleotide core combination within the CWWG motif of the p53RE to be the key factor that determines whether p53 transcriptionally activates or represses a target gene.	Dinucleoside Phosphates	38-50	P53	Homo sapiens	148-151
19723057-0	2009	Effects of 15-deoxy-delta 12, 14-prostaglandin J2 on the expression of p53 in MCF-7 cells.	15-deoxy-delta 12	11-28	P53	Homo sapiens	71-74
19558638-0	2009	Effect of hydroxyurea on the promoter occupancy profiles of tumor suppressor p53 and p73.	Hydroxyurea	10-21	P53	Homo sapiens	77-80
19558638-4	2009	The goal of this study was to compare the promoter-binding activity of p53 and p73 at steady state and after genotoxic stress induced by hydroxyurea.	Hydroxyurea	137-148	P53	Homo sapiens	71-74
19558638-7	2009	We also found that after hydroxyurea treatment, the p53-bound promoters were still bound by p73, but p73 became associated with additional promoters that that did not bind p53.	Hydroxyurea	25-36	P53	Homo sapiens	52-55
19509161-0	2009	Restoration of p53 pathway by nutlin-3 induces cell cycle arrest and apoptosis in human rhabdomyosarcoma cells.	nutlin 3	30-38	P53	Homo sapiens	15-18
19411846-10	2009	Surprisingly, blocking the transcriptional arm of p53, either via alpha-Amanitin or the p53-specific transcriptional inhibitor Pifithrin alpha, not only fails to inhibit, but greatly potentiates Nutlin-induced apoptosis.	Alpha-Amanitin	66-80	P53	Homo sapiens	50-53
19411857-9	2009	Incubation with the phosphatase inhibitor okadaic acid produced more phosphorylation of CHK1 in UV-treated HPV16E6-expressing cells than in p53-H179Q-expressing cells suggesting that HPV16E6 may interfere with the recovery of coupled DNA replication at replication forks that are stalled at [6-4]pyrimidine-pyrimidone photoproducts and BPDE-DNA adducts.	Okadaic Acid	42-54	P53	Homo sapiens	140-143
19567200-6	2009	The up-regulations of Bcl-xL and IAP by CpG DNA were not inhibited when blocking PI3K by specific inhibitor Ly294002, while the inhibition of p53 by CpG DNA could be blocked by Ly294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	177-185	P53	Homo sapiens	142-145
19475715-5	2009	However, pifithrin alfa (PFT-alpha), an inhibitor of p53, fails to rescue the cells from the cadmium-induced cell cycle arrest but prevents Bcl-xl down-regulation and loss of Deltapsi(m), which indicates that there is an involvement of p53 in apoptosis.	pifithrin alfa	9-23	P53	Homo sapiens	53-56
19475715-5	2009	However, pifithrin alfa (PFT-alpha), an inhibitor of p53, fails to rescue the cells from the cadmium-induced cell cycle arrest but prevents Bcl-xl down-regulation and loss of Deltapsi(m), which indicates that there is an involvement of p53 in apoptosis.	pifithrin alfa	9-23	P53	Homo sapiens	236-239
19323449-2	2009	Here we study the effect of modifications of a p53 N-terminal fragment on its binding to MDM2, using implicit-solvent MD and MM-GB/SA calculations.	2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine	131-133	P53	Homo sapiens	47-50
19010591-4	2009	Subsequently, we found that PCL treatment abrogated glutathione antioxidant system and induced mitochondria to generate ROS accumulation, resulting in p38-p53 activation.	pcl	28-31	P53	Homo sapiens	155-158
19010591-6	2009	In conclusion, these results indicate that PCL induces apoptosis and autophagy via a mitochondrial-mediated ROS-p38-p53 pathway.	pcl	43-46	P53	Homo sapiens	116-119
19305157-0	2009	Diversity of DNA damage response of astrocytes and glioblastoma cell lines with various p53 status to treatment with etoposide and temozolomide.	Etoposide	117-126	P53	Homo sapiens	88-91
19060337-6	2009	In cells deficient in both Chk1 and p53, Cdc25A down-regulation upon camptothecin-induced DNA damage is completely abolished, leading to severe defects in cell cycle checkpoints and remarkable cell death in mitosis.	Camptothecin	69-81	P53	Homo sapiens	36-39
19155291-0	2009	Limits to thymidylate synthase and TP53 genes as predictive determinants for fluoropyrimidine sensitivity and further evidence for RNA-based toxicity as a major influence.	2-fluoropyrimidine	77-93	P53	Homo sapiens	35-39
19208740-0	2009	p53 mutant human glioma cells are sensitive to UV-C-induced apoptosis due to impaired cyclobutane pyrimidine dimer removal.	Cyclobutanes	86-97	P53	Homo sapiens	0-3
18765419-0	2009	The carcinogenic air pollutant 3-nitrobenzanthrone induces GC to TA transversion mutations in human p53 sequences.	3-nitrobenzanthrone	31-50	P53	Homo sapiens	100-103
19152081-3	2009	For the genetic changes closely related to etiology of liver cancer, the well-known cases include insertion and integration of the hepatitis B virus (HBV) DNA after infection, and mutations at site 249 of the tumor suppressor gene p53 induced by exposure to aflatoxin B1.	Aflatoxin B1	258-270	P53	Homo sapiens	231-234
20371709-7	2010	Consistently, Sirtinol and Salermide, but not EX527, treatment resulted in the in vivo acetylation of the SIRT1/2 target p53 and SIRT2 target tubulin in MCF-7 cells, suggesting that EX527 is ineffective in inhibiting SIRT2 and that p53 mediates the cytotoxic function of Sirtinol and Salermide.	sirtinol	14-22	P53	Homo sapiens	121-124
20371709-7	2010	Consistently, Sirtinol and Salermide, but not EX527, treatment resulted in the in vivo acetylation of the SIRT1/2 target p53 and SIRT2 target tubulin in MCF-7 cells, suggesting that EX527 is ineffective in inhibiting SIRT2 and that p53 mediates the cytotoxic function of Sirtinol and Salermide.	sirtinol	14-22	P53	Homo sapiens	232-235
20075077-4	2010	Treatment with the genotoxic agents, doxorubicin or etoposide, induced Foxp3 expression in p53-positive carcinoma cells, but not in cells lacking p53 function.	Etoposide	52-61	P53	Homo sapiens	91-94
20231502-3	2010	More recently, hydroxyurea-associated squamous dysplasia has been characterized as a premalignant precursor to hydroxyurea-associated nonmelanoma skin cancers and shown to manifest abnormal p53 expression.	Hydroxyurea	15-26	P53	Homo sapiens	190-193
20231502-7	2010	CONCLUSIONS: We suggest that dermatomyositis-like eruption and hydroxyurea-associated squamous dysplasia represent similar clinical manifestations of a common underlying chronic phototoxic process involving aberrant keratinocyte p53 expression mediated by hydroxyurea"s antimetabolite properties and UV radiation exposure.	Hydroxyurea	63-74	P53	Homo sapiens	229-232
19788889-7	2010	Although the HCT116 colon cancer cells did not mount a significant DNA damage response following Nutlin-3 treatment, Nutlin-3 enhanced the DNA damage response to the nucleotide synthesis inhibitor hydroxyurea in a p53-dependent manner.	nutlin 3	117-125	P53	Homo sapiens	214-217
19788889-7	2010	Although the HCT116 colon cancer cells did not mount a significant DNA damage response following Nutlin-3 treatment, Nutlin-3 enhanced the DNA damage response to the nucleotide synthesis inhibitor hydroxyurea in a p53-dependent manner.	Hydroxyurea	197-208	P53	Homo sapiens	214-217
19954744-5	2010	However, the role of SNP309 in hepatocarcinogenesis with respect to TP53 mutations is unknown.	snp309	21-27	P53	Homo sapiens	68-72
19880522-13	2010	Staurosporine stress of ID8 cells promoted endogenous Pyk2 nuclear accumulation and enhanced Pyk2 binding to p53.	Staurosporine	0-13	P53	Homo sapiens	109-112
19949306-3	2010	We showed that 2-methoxyestradiol (2-ME), an antitumoral compound, enhances autophagy and apoptosis in Ewing sarcoma cells through the activation of both p53 and JNK pathways.	2-Methoxyestradiol	15-33	P53	Homo sapiens	154-157
19949306-3	2010	We showed that 2-methoxyestradiol (2-ME), an antitumoral compound, enhances autophagy and apoptosis in Ewing sarcoma cells through the activation of both p53 and JNK pathways.	2-Methoxyestradiol	35-39	P53	Homo sapiens	154-157
19853978-0	2010	The role of p53 in the cellular toxicity by active trans-platinum complexes containing isopropylamine and hydroxymethylpyridine.	2-propylamine	87-101	P53	Homo sapiens	12-15
20185936-6	2010	PenA also protected against a CS-induced increase in carbonyls (oxidized proteins) and decrease in p53 levels (in the presence of saliva) and mitochondrial membrane potential (a hallmark of CS-induced apoptotic cell death).	Cesium	30-32	P53	Homo sapiens	99-102
20185936-7	2010	Malfunctioning p53 often characterizes carcinogenesis of CS-induced cancers.	Cesium	57-59	P53	Homo sapiens	15-18
20185936-8	2010	CONCLUSIONS: Redox-active iron and copper in pleural fluid and saliva, upon encounter with CS, may be responsible for this carcinogenesis, mediated via alteration of p53 function.	Cesium	91-93	P53	Homo sapiens	166-169
20681406-13	2010	The data suggest that ING1 contributes to TSA-induced apoptosis in GBM cells with deficient p53 and p14(ARF)/p16(INK4a) functions, possibly by regulating FADD/caspase 3 signaling.	trichostatin A	42-45	P53	Homo sapiens	92-95
19858204-6	2009	Additionally, cells treated with anti-cancer drug etoposide underwent apoptosis in association with the transcriptional enhancement of TAp63 in a p53-independent manner, and the knockdown of the endogenous TLP reduced etoposide-induced apoptosis through repression of TAp63 expression.	Etoposide	50-59	P53	Homo sapiens	146-149
19766654-6	2009	In fact, substitution of this Asn to Ala of CHC diminished its ability to interact with p53, leading to reduced activity to transactivate p53.	Asparagine	30-33	P53	Homo sapiens	138-141
19732843-7	2009	Moreover, genistein enhances the phosphorylation and activation of p53, while decreases the ratio of Bcl-2/Bax and Bcl-xL/Bax and the level of phosphorylated Akt, which result in cells undergoing apoptosis.	Genistein	10-19	P53	Homo sapiens	67-70
19857493-3	2009	In contrast to the wt p53 cell lines, the mt p53-R175H cell line was resistant to staurosporine (STS)-mediated detachment and caspase-3 activation.	Staurosporine	82-95	P53	Homo sapiens	45-48
19857493-3	2009	In contrast to the wt p53 cell lines, the mt p53-R175H cell line was resistant to staurosporine (STS)-mediated detachment and caspase-3 activation.	Staurosporine	97-100	P53	Homo sapiens	45-48
19457607-7	2009	The PI3K/Akt inhibitor LY294002 significantly increased the amount of p53 protein and ATO-induced apoptosis in both cell lines and decreased G2/M phase arrest of MGC803 cells.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	23-31	P53	Homo sapiens	70-73
19996705-11	2009	Moreover, both CS and PS induced expression of the p53 tumor suppressor gene and the Cdk inhibitor p21.	Cesium	15-17	P53	Homo sapiens	51-54
19459175-8	2009	Even though DATS treatment resulted in stabilization and Ser15 phosphorylation of p53, the knockdown of p53 protein failed to rescue DATS-induced mitotic arrest.	diallyl trisulfide	12-16	P53	Homo sapiens	82-85
21160963-5	2009	Interestingly, p53 expression was upregulated at the invasive stage of BilIN, but was low in noninvasive BilIN, while p53 expression was upregulated in IPN-B1 and reached a plateau in IPN-B2 and invasive ICC.	Bile Pigments	105-110	P53	Homo sapiens	15-18
19699254-4	2009	Capsaicin also induced degradation of tumor suppressor p53; this effect was enhanced by the ER stressor tunicamycin.	Tunicamycin	104-115	P53	Homo sapiens	55-58
19658174-6	2009	The CS-dose-dependent induction and increase in the extent of phosphorylation of ATM, Chk2, H2AX, and p53 were seen in both cell types.	Cesium	4-6	P53	Homo sapiens	102-105
18716605-4	2008	Genistein also decreased cisplatin-induced apoptosis by regulating p53 induction in kidney.	Genistein	0-9	P53	Homo sapiens	67-70
19010883-2	2008	We report here that treatment of cells with sodium arsenite at the concentrations close to environmental exposure is associated with the up-regulation of Hdm2 and the accumulation of p53 in the cytoplasm.	sodium arsenite	44-59	P53	Homo sapiens	183-186
18779328-5	2008	In addition, STX6 can be induced by DNA damage and Mdm2 inhibitor Nutlin-3 in a p53-dependent manner.	nutlin 3	66-74	P53	Homo sapiens	80-83
21739974-0	2011	4-acetylantroquinonol B isolated from Antrodia cinnamomea arrests proliferation of human hepatocellular carcinoma HepG2 cell by affecting p53, p21 and p27 levels.	4-acetylantroquinonol B	0-23	P53	Homo sapiens	138-141
18850315-6	2008	Transfection of HUVEC with dominant negative p53 cDNA prevented the progesterone-induced increases in p21 and p27 promoter activity and protein level, decreases in thymidine incorporation, and capillary-like tube formation.	Thymidine	164-173	P53	Homo sapiens	45-48
19794957-0	2009	Hypoxia-induced decrease in p53 protein level and increase in c-jun DNA binding activity results in cancer cell resistance to etoposide.	Etoposide	126-135	P53	Homo sapiens	28-31
19794957-4	2009	Whereas the profile of c-Myc and NF-kappaB activity did not fit the effect of hypoxia on caspase 3 activity, hypoxia decreased basal p53 abundance and DNA binding activity as well as p53 etoposide-induced activation.	Etoposide	187-196	P53	Homo sapiens	183-186
18822454-8	2008	Nevirapine treated cells strongly accumulated SA-b-Gal activity and also expressed increased levels of p53 and p21 when analyzed via RT-PCR.	Nevirapine	0-10	P53	Homo sapiens	103-106
21739974-4	2011	The protein levels of p53 and p21 proteins were also increased when the cells were treated with low dosage (0.1 mug/mL) of 4-acetylantroquinonol B.	4-acetylantroquinonol	123-144	P53	Homo sapiens	22-25
19794957-5	2009	Short interfering RNA (siRNA) silencing evidenced that p53 was required for etoposide-induced apoptosis under normoxia.	Etoposide	76-85	P53	Homo sapiens	55-58
19794957-12	2009	These data evidenced that hypoxia decreased the responsiveness of HepG2 cells to etoposide at least by two independent pathways involving p53 inhibition and c-jun activation.	Etoposide	81-90	P53	Homo sapiens	138-141
21739974-10	2011	Our finding suggested that the 4-acetylantroquinonol B inhibits proliferation of HepG2 cells via affecting p53, p21 and p27 proteins, and can be considered as a potential cancer drug.	4-acetylantroquinonol B	31-54	P53	Homo sapiens	107-110
18697203-3	2008	However, gradual induction of p53 in tet-onSAOS2 cells resulted in a transient increase of the PDGFRB-promoter activity and its expression.	tetramethylenedisulfotetramine	37-40	P53	Homo sapiens	30-33
18681908-8	2009	Activation of SIRT1 negatively regulates UV- and H(2)O(2)-induced p53 acetylation, because nicotinamide and sirtinol as well as SIRT1 siRNA enhance UV- and H(2)O(2)-induced p53 acetylation, whereas SIRT1 activator resveratrol inhibits it.	sirtinol	108-116	P53	Homo sapiens	66-69
18697203-9	2008	Mitomycin treatment of MEF induced similar epigenetic modification of p53 and its binding to the promoter chromatin.	Mitomycin	0-9	P53	Homo sapiens	70-73
21441950-8	2011	Instead, a natural antisense transcript of TP53, WRAP53, was strongly augmented by idarubicin and etoposide, but only less so by the other anthracyclines under study.	Etoposide	98-107	P53	Homo sapiens	43-47
18697203-10	2008	Addition of a PDGFR tyrosine-kinase inhibitor to p53-inducing tet-onSAOS2 increased the number of apoptotic cells.	tetramethylenedisulfotetramine	62-65	P53	Homo sapiens	49-52
18681908-8	2009	Activation of SIRT1 negatively regulates UV- and H(2)O(2)-induced p53 acetylation, because nicotinamide and sirtinol as well as SIRT1 siRNA enhance UV- and H(2)O(2)-induced p53 acetylation, whereas SIRT1 activator resveratrol inhibits it.	sirtinol	108-116	P53	Homo sapiens	173-176
19421231-4	2009	We show here that nutlin-3, a potent antagonist of MDM2, activates the p53 pathway in all BL cell lines harboring wild-type p53, regardless of EBV status.	nutlin 3	18-26	P53	Homo sapiens	71-74
19421231-4	2009	We show here that nutlin-3, a potent antagonist of MDM2, activates the p53 pathway in all BL cell lines harboring wild-type p53, regardless of EBV status.	nutlin 3	18-26	P53	Homo sapiens	124-127
21519790-0	2011	Histone deacetylase inhibitors, valproic acid and trichostatin-A induce apoptosis and affect acetylation status of p53 in ERG-positive prostate cancer cells.	trichostatin A	50-64	P53	Homo sapiens	115-118
19662644-0	2009	EGCG inhibits protein synthesis, lipogenesis, and cell cycle progression through activation of AMPK in p53 positive and negative human hepatoma cells.	epigallocatechin gallate	0-4	P53	Homo sapiens	103-106
19662644-1	2009	In the previous studies, (-)-epigallocatechin-3-gallate (EGCG) has been shown to have anticarcinogenic effects via modulation in protein expression of p53.	epigallocatechin gallate	25-55	P53	Homo sapiens	151-154
19662644-1	2009	In the previous studies, (-)-epigallocatechin-3-gallate (EGCG) has been shown to have anticarcinogenic effects via modulation in protein expression of p53.	epigallocatechin gallate	57-61	P53	Homo sapiens	151-154
18647660-0	2008	Differential expression of TP53 associated genes in Fanconi anemia cells after mitomycin C and hydroxyurea treatment.	Mitomycin	79-90	P53	Homo sapiens	27-31
18647660-0	2008	Differential expression of TP53 associated genes in Fanconi anemia cells after mitomycin C and hydroxyurea treatment.	Hydroxyurea	95-106	P53	Homo sapiens	27-31
18647660-8	2008	The MMC induced damage was correlated with a general increase in expression of TP53-modulated DNA damage stress response genes involved in processes such as DNA repair, cell cycle progression, and apoptosis.	Mitomycin	4-7	P53	Homo sapiens	79-83
19662644-2	2009	Using p53 positive Hep G2 and p53 negative Hep 3B cells, we found that treatment of EGCG resulted in dose-dependent inhibition of cellular proliferation, which suggests that the interaction of EGCG with p53 may not fully explain its inhibitory effect on proliferation.	epigallocatechin gallate	84-88	P53	Homo sapiens	6-9
21519790-11	2011	We found that VPA and TSA induce apoptosis, upregulate p21/Waf1/CIP1, repress TMPRSS2-ERG expression and affect acetylation status of p53 in VCaP cells.	trichostatin A	22-25	P53	Homo sapiens	134-137
19662644-2	2009	Using p53 positive Hep G2 and p53 negative Hep 3B cells, we found that treatment of EGCG resulted in dose-dependent inhibition of cellular proliferation, which suggests that the interaction of EGCG with p53 may not fully explain its inhibitory effect on proliferation.	epigallocatechin gallate	84-88	P53	Homo sapiens	30-33
19662644-2	2009	Using p53 positive Hep G2 and p53 negative Hep 3B cells, we found that treatment of EGCG resulted in dose-dependent inhibition of cellular proliferation, which suggests that the interaction of EGCG with p53 may not fully explain its inhibitory effect on proliferation.	epigallocatechin gallate	84-88	P53	Homo sapiens	30-33
18847459-11	2008	Furthermore, genistein induced the expression of apoptotic and anti-migratory proteins p53 and p38 in all cell lines.	Genistein	13-22	P53	Homo sapiens	87-90
21554433-8	2011	Both Odora cells (an olfactive cell line) and OM cells treated with etoposide, a p53 activity inducer, exhibited mitochondrial-dependent apoptosis that was inhibited by the pan-caspase inhibitor zVAD-fmk.	Etoposide	68-77	P53	Homo sapiens	81-84
18838865-3	2008	Here, we show by epistatic analysis that p53 inhibition results in a maximum level of autophagy that cannot be further enhanced by a variety of different autophagy inducers including lithium, tunicamycin-induced stress of the endoplasmic reticulum (ER) or inhibition of Bcl-2 and Bcl-X(L) with the BH3 mimetic ABT737.	Tunicamycin	192-203	P53	Homo sapiens	41-44
18838865-4	2008	Chemical inducers of autophagy (including rapamycin, lithium, tunicamycin and ABT737) induced rapid depletion of the p53 protein.	Tunicamycin	62-73	P53	Homo sapiens	117-120
18838865-4	2008	Chemical inducers of autophagy (including rapamycin, lithium, tunicamycin and ABT737) induced rapid depletion of the p53 protein.	ABT-737	78-84	P53	Homo sapiens	117-120
19662644-6	2009	Here, we showed that EGCG activated AMPK in both p53 positive and negative human hepatoma cells.	epigallocatechin gallate	21-25	P53	Homo sapiens	49-52
19662644-10	2009	In p53 positive Hep G2 cells, EGCG blocked the progression of cell cycle at G1 phase by inducing p53 expression and further up-regulating p21 expression.	epigallocatechin gallate	30-34	P53	Homo sapiens	3-6
19662644-10	2009	In p53 positive Hep G2 cells, EGCG blocked the progression of cell cycle at G1 phase by inducing p53 expression and further up-regulating p21 expression.	epigallocatechin gallate	30-34	P53	Homo sapiens	97-100
19662644-11	2009	However, EGCG inducted apoptosis in p53 negative Hep 3B cells.	epigallocatechin gallate	9-13	P53	Homo sapiens	36-39
19546226-3	2009	XCT790 induces, in a p53-independent manner, the expression of the cell cycle inhibitor p21(waf/cip)(1) at the protein, mRNA, and promoter level, leading to an accumulation of hypophosphorylated Rb.	XCT790	0-6	P53	Homo sapiens	21-24
20734047-9	2011	Satraplatin treatment induces p53-related genes and its direct microRNA target of miR-34a independently.	satraplatin	0-11	P53	Homo sapiens	30-33
19714248-5	2009	METHODOLOGY/PRINCIPAL FINDINGS: Upon exposure of colon and lung cancer cells to hypoxia, by either low oxygen or cobalt, HIPK2 function was impaired allowing for increased HIF-1alpha expression and inhibiting the p53-apoptotic response to drug.	Cobalt	113-119	P53	Homo sapiens	213-216
19723076-7	2009	Omega-3 fatty acids inhibited oxidative stress-induced cell death, DNA fragmentation, and induction of p53 and Bax of the cells.	Fatty Acids, Omega-3	0-19	P53	Homo sapiens	103-106
18571879-6	2008	We also analyzed the splice patterns of apoptosis-related genes in p53-deficient U2OS cells following treatment with the genotoxic drug mitomycin C.	Mitomycin	136-147	P53	Homo sapiens	67-70
18618574-10	2008	The p53 overexpression was associated with MDM2 SNP309.	snp309	48-54	P53	Homo sapiens	4-7
21120637-6	2011	Remarkably, the synergistic effect of 8-Br-cAMP and VPA on cellular reprogramming may be due to the transient decrease of p53 protein during the early stages of reprogramming.	8-Bromo Cyclic Adenosine Monophosphate	38-47	P53	Homo sapiens	122-125
18604159-6	2008	Several distinct autophagy inducers (e.g., starvation, rapamycin, lithium, tunicamycin and thapsigargin) stimulate the rapid degradation of p53.	Tunicamycin	75-86	P53	Homo sapiens	140-143
19638586-4	2009	We show that, along with p53 reactivation, the proapoptotic p53-activator HIPK2 is degraded by MDM2 in Nutlin-3-treated cells, but activated by transiently reduced MDM2 levels in RITA-treated ones.	nutlin 3	103-111	P53	Homo sapiens	25-28
19638586-4	2009	We show that, along with p53 reactivation, the proapoptotic p53-activator HIPK2 is degraded by MDM2 in Nutlin-3-treated cells, but activated by transiently reduced MDM2 levels in RITA-treated ones.	nutlin 3	103-111	P53	Homo sapiens	60-63
21120637-10	2011	In addition, 8-Br-cAMP and VPA have a synergistic effect on cellular reprogramming, which may be in part due to the transient down-regulation of the p53 signaling pathway during the early stages of reprogramming.	8-Bromo Cyclic Adenosine Monophosphate	13-22	P53	Homo sapiens	149-152
21508668-7	2011	Biochemical studies showed that zinc partly induced the transition of mutant p53 protein (reactive to conformation-sensitive PAb240 antibody for mutant conformation) into a functional conformation (reactive to conformation-sensitive PAb1620 antibody for wild-type conformation).	pab240	125-131	P53	Homo sapiens	77-80
19637078-6	2009	Other genes regulated by the transformation-related protein 53 (Trp53/p53) such as Bcl2-associated X protein (Bax) or etoposide-induced-2.4 (Ei24/PIG8) were not upregulated.	Etoposide	118-127	P53	Homo sapiens	29-62
18677110-1	2008	The cellular response to Nutlin-3, a small-molecule inhibitor of the p53 repressor MDM2, varies widely among human cancer-derived cell types.	nutlin 3	25-33	P53	Homo sapiens	69-72
19477925-3	2009	We find that in estrogen receptor (ER)-positive breast cancer cells, UV or ionizing radiation and hydroxyurea rapidly activate ATR-dependent phosphorylation of endogenous p53 and Chk1.	Hydroxyurea	98-109	P53	Homo sapiens	171-174
21454715-7	2011	A citrulline-mimicking Arg-NLS-Gln ING4 mutant, which has all Arg residues in the NLS mutated to Gln, loses its affinity for p53, can no longer promote p53 acetylation, and results in repression of downstream p21 expression.	Glutamine	31-34	P53	Homo sapiens	125-128
19536869-6	2009	The specific ATM inhibitor caffeine significantly decreased ISL-mediated G2/M arrest by inhibiting the phosphorylation of p53 (Serine15) and Chk2.	serine15	127-135	P53	Homo sapiens	122-125
18644983-7	2008	In addition, our data suggest that trichostatin A-induced p21(WAF1/Cip1) protein expression might be mediated through a p53-independent and HDAC deacetylase-independent pathway.	trichostatin A	35-49	P53	Homo sapiens	120-123
18645003-1	2008	Previous studies comparing the effects of two histone deacetylase (HDAC) inhibitors, trichostatin A (TSA) and CG-1521, have shown that these compounds selectively inhibit HDAC and induce differentially acetylated p53 isoforms and assembly of mutually exclusive transcriptional complexes on the p21 promoter.	trichostatin A	85-99	P53	Homo sapiens	213-216
18645003-1	2008	Previous studies comparing the effects of two histone deacetylase (HDAC) inhibitors, trichostatin A (TSA) and CG-1521, have shown that these compounds selectively inhibit HDAC and induce differentially acetylated p53 isoforms and assembly of mutually exclusive transcriptional complexes on the p21 promoter.	trichostatin A	101-104	P53	Homo sapiens	213-216
19558638-9	2009	CONCLUSION: These results suggest that hydroxyurea exerts differential effects on the promoter-binding functions of p53 and p73 and illustrate the power of model-based algorithm for promoter array in the analyses of promoter occupancy profiles of highly homologous transcription factors.	Hydroxyurea	39-50	P53	Homo sapiens	116-119
21454715-7	2011	A citrulline-mimicking Arg-NLS-Gln ING4 mutant, which has all Arg residues in the NLS mutated to Gln, loses its affinity for p53, can no longer promote p53 acetylation, and results in repression of downstream p21 expression.	Glutamine	31-34	P53	Homo sapiens	152-155
21292642-4	2011	We found that prolonged exposure of immortalized p53-knocked down human bronchial epithelial cells (p53(low)HBECs) to low levels of arsenite (NaAsO2, 2.5 muM) caused malignant transformation that was accompanied by epithelial to mesenchymal transition (EMT) and reduction in the levels of miR-200 family members.	sodium arsenite	142-148	P53	Homo sapiens	49-52
19216720-8	2009	Meanwhile, the use of 3-aminobenzamide, a PARP-1 inhibitor known to prevent AIF (apoptosis-inducing factor) release, significantly decreases staurosporine-induced death in these p53mt carcinoma cells, suggesting a preferential implication of caspase-independent apoptosis.	Staurosporine	141-154	P53	Homo sapiens	178-181
19216720-9	2009	On the other hand, we show that p53, whose activity is modulated by pifithrin-alpha, isolated as a suppressor of p53-mediated transactivation, or by PRIMA-1 (p53 reactivation and induction of massive apoptosis), that reactivates mutant p53, causes cytochrome c release as well as mitochondrio-nuclear AIF translocation in staurosporine-induced apoptosis of cervical carcinoma cells.	Staurosporine	322-335	P53	Homo sapiens	32-35
19216720-10	2009	CONCLUSIONS: The present paper highlights that staurosporine engages the intrinsic mitochondrial apoptotic pathway via caspase-8 or caspase-9 signalling cascades and via caspase-independent cell death, as well as through p53 activity.	Staurosporine	47-60	P53	Homo sapiens	221-224
19771878-7	2009	CONCLUSION: Oxymatrine could notably inhibit the HepG2 cells proliferation probably via upregulating the expression of the Bax and downregulating the expression of Bcl-2 and P53.	oxymatrine	12-22	P53	Homo sapiens	174-177
18492823-7	2008	Moreover, oxidized LDL increased luciferase activity of p53 in endothelial cells transfected with a p53 promoter construct, the increase of which was strikingly downregulated by EGCG and hesperetin.	epigallocatechin gallate	178-182	P53	Homo sapiens	56-59
18492823-7	2008	Moreover, oxidized LDL increased luciferase activity of p53 in endothelial cells transfected with a p53 promoter construct, the increase of which was strikingly downregulated by EGCG and hesperetin.	epigallocatechin gallate	178-182	P53	Homo sapiens	100-103
21972525-0	2011	[The roles of Ku80/p53 pathway in silica-induced cell cycle changes in human embryo lung fibroblasts].	Silicon Dioxide	34-40	P53	Homo sapiens	19-22
18092340-5	2008	Analysis of the gene expression profile of the p53-transcriptional targets showed distinct features between chlorambucil, Nutlin-3 and fludarabine, which likely account for their differential effect on cell cycle in SKW6.4 cells.	nutlin 3	122-130	P53	Homo sapiens	47-50
19211566-0	2009	Depletion of the poly(C)-binding proteins alphaCP1 and alphaCP2 from K562 cells leads to p53-independent induction of cyclin-dependent kinase inhibitor (CDKN1A) and G1 arrest.	Poly C	17-24	P53	Homo sapiens	89-92
21972525-1	2011	OBJECTIVE: To study the roles of Ku80/p53 pathway in silica-induced cell cycle changes in human embryo lung fibroblasts (HELF).	Silicon Dioxide	53-59	P53	Homo sapiens	38-41
19139275-3	2009	Experimentally, centrosome overduplication is observed in p53-deficient cells arrested in S phase with hydroxyurea.	Hydroxyurea	103-114	P53	Homo sapiens	58-61
18289623-7	2008	The RNA synthesis inhibitor alpha-amanitin induced similar to mafosfamide more apoptosis in p53(wt) than in p53(mt) cells.	Alpha-Amanitin	28-42	P53	Homo sapiens	92-95
18289623-7	2008	The RNA synthesis inhibitor alpha-amanitin induced similar to mafosfamide more apoptosis in p53(wt) than in p53(mt) cells.	Alpha-Amanitin	28-42	P53	Homo sapiens	108-111
21972525-7	2011	CONCLUSION: Ku80/p53 pathway plays a role in the cell cycle charges induced by silica in human embryo lung fibroblasts.	Silicon Dioxide	79-85	P53	Homo sapiens	17-20
19084536-6	2009	We systematically substituted a CpG dinucleotide at each position in the consensus p53 DNA binding sequence and identified substitutions tolerated by p53.	Dinucleoside Phosphates	36-48	P53	Homo sapiens	83-86
21524306-0	2011	The natural triterpene maslinic acid induces apoptosis in HT29 colon cancer cells by a JNK-p53-dependent mechanism.	Triterpenes	12-22	P53	Homo sapiens	91-94
19084536-6	2009	We systematically substituted a CpG dinucleotide at each position in the consensus p53 DNA binding sequence and identified substitutions tolerated by p53.	Dinucleoside Phosphates	36-48	P53	Homo sapiens	150-153
21510868-2	2011	We have recently shown that p53 is critical for the inhibitory effect of cAMP on genotoxic agents-mediated apoptosis in BCP-ALLs.	bcp-alls	120-128	P53	Homo sapiens	28-31
19188164-12	2009	CONCLUSION: These findings suggest that the MDM2 antagonist Nutlin-3 may be an effective agent in the treatment of MCL with or without wt-TP53.	nutlin 3	60-68	P53	Homo sapiens	138-142
21274505-6	2011	Furthermore, activation of p53 and AMPK was detected in etoposide-treated cells and inhibition of AMPK triggered apoptosis through suppression of autophagy.	Etoposide	56-65	P53	Homo sapiens	27-30
19091346-18	2009	CONCLUSIONS: Finasteride administered 30 days before surgery appears to decrease the apoptotic factors caspase-7 and IGFBP-3 in cancer cells, while having little to no effect on caspase-3, insulin growth factor-1, bcl-2, p53 and p21.	Finasteride	13-24	P53	Homo sapiens	221-224
21212274-2	2011	However, little is known about the regulation of the two other p53-family members, p63 and p73, by nitrogen oxides.	Nitrogen Oxides	99-114	P53	Homo sapiens	63-66
20077225-0	2009	The role of p53 in silica-induced cellular and molecular responses associated with carcinogenesis.	Silicon Dioxide	19-25	P53	Homo sapiens	12-15
21394211-3	2011	Here, we have analyzed the p53-regulated pathways induced by Actinomycin D and Etoposide treatment resulting in more growth arrested versus apoptotic cells respectively.	Etoposide	79-88	P53	Homo sapiens	27-30
20077225-3	2009	The goal of this study was to compare freshly fractured and aged silica-induced molecular alterations in human immortalized/transformed bronchial epithelial cells (BEAS-IIB) and lung cancer cells with altered (H460) or deficient (H1299) p53 expression.	Silicon Dioxide	65-71	P53	Homo sapiens	237-240
20077225-7	2009	p53 protein was present in the BEAS-IIB and was absent in cancer cell lines after silica exposure.	Silicon Dioxide	82-88	P53	Homo sapiens	0-3
20077225-8	2009	Exposure to freshly fractured silica also resulted in a rise in aneuploidy in cancer cells with a significantly greater increase in p53-deficient cells.	Silicon Dioxide	30-36	P53	Homo sapiens	132-135
21145583-7	2011	The expression of p53 increased in HeLa cell cultures treated with camptothecin (positive control) for 24h, and the formation of p53Ser15 and p53Ser46 was detected in cell nuclei by Western blotting.	Camptothecin	67-79	P53	Homo sapiens	18-21
20077225-10	2009	These results suggest that altered and deficient p53 affects the cellular response to freshly fractured silica exposure, and thereby enhances susceptibility and augments cell proliferation and lung cancer development.	Silicon Dioxide	104-110	P53	Homo sapiens	49-52
21145583-7	2011	The expression of p53 increased in HeLa cell cultures treated with camptothecin (positive control) for 24h, and the formation of p53Ser15 and p53Ser46 was detected in cell nuclei by Western blotting.	Camptothecin	67-79	P53	Homo sapiens	129-132
21145583-9	2011	Both camptothecin and TEGDMA increased p53 expression to some extent in the nuclear fraction in human transformed pulp-derived cells (tHPC), and similar effects were detected in RAW264.7 macrophages.	Camptothecin	5-17	P53	Homo sapiens	39-42
19373614-2	2009	Here we report two chemopreventive agents, selenite and genistein, that have synergistic effects on apoptosis, cell cycle arrest, and associated signaling pathways in p53-expressing LNCaP and p53-null PC3 prostate cancer cells.	Genistein	56-65	P53	Homo sapiens	167-170
21217086-2	2011	METHODS: We investigated associations between serum polyunsaturated fatty acid concentrations and p53 expression in normal skin, as a biomarker of early UV-induced carcinogenesis, in an unselected sample of Australian adults.	Fatty Acids, Unsaturated	52-78	P53	Homo sapiens	98-101
19373614-2	2009	Here we report two chemopreventive agents, selenite and genistein, that have synergistic effects on apoptosis, cell cycle arrest, and associated signaling pathways in p53-expressing LNCaP and p53-null PC3 prostate cancer cells.	Genistein	56-65	P53	Homo sapiens	192-195
19047160-9	2008	In contrast, dasatinib, a dual Bcr-Abl and Src kinase inhibitor, inhibited the phosphorylation of both BCR-ABL and Lyn, and induced apoptosis of the Bcr-Abl cell line overexpressing p53/56 Lyn.	Dasatinib	13-22	P53	Homo sapiens	182-185
21217086-5	2011	RESULTS: There was an inverse association, showing a dose-response relationship, between total n-3 fatty acid serum concentrations and p53 immunoreactivity in the whole epidermis and the basal layer.	Fatty Acids, Omega-3	95-109	P53	Homo sapiens	135-138
18971636-11	2008	This regulation is observed in a transgenic p53-inducible cell system as well as in cells with wild-type p53 treated with nutlin-3, doxorubicin or paclitaxel.	nutlin 3	122-130	P53	Homo sapiens	44-47
18971636-11	2008	This regulation is observed in a transgenic p53-inducible cell system as well as in cells with wild-type p53 treated with nutlin-3, doxorubicin or paclitaxel.	nutlin 3	122-130	P53	Homo sapiens	105-108
20963515-11	2011	The very low frequency of TP53 mutation suggests low levels of aflatoxin B1 exposure.	Aflatoxin B1	63-75	P53	Homo sapiens	26-30
18583568-2	2008	In HMCLs retaining a functional p53, PD treatment greatly enhances the ATO-induced p53 accumulation and p73, a p53 paralog, cooperates with p53 in caspase activation and apoptosis induction.	hmcls	3-8	P53	Homo sapiens	32-35
18583568-2	2008	In HMCLs retaining a functional p53, PD treatment greatly enhances the ATO-induced p53 accumulation and p73, a p53 paralog, cooperates with p53 in caspase activation and apoptosis induction.	hmcls	3-8	P53	Homo sapiens	83-86
18583568-2	2008	In HMCLs retaining a functional p53, PD treatment greatly enhances the ATO-induced p53 accumulation and p73, a p53 paralog, cooperates with p53 in caspase activation and apoptosis induction.	hmcls	3-8	P53	Homo sapiens	83-86
18583568-2	2008	In HMCLs retaining a functional p53, PD treatment greatly enhances the ATO-induced p53 accumulation and p73, a p53 paralog, cooperates with p53 in caspase activation and apoptosis induction.	hmcls	3-8	P53	Homo sapiens	83-86
21185854-0	2011	Dihydroptychantol A, a macrocyclic bisbibenzyl derivative, induces autophagy and following apoptosis associated with p53 pathway in human osteosarcoma U2OS cells.	dihydroptychantol A	0-19	P53	Homo sapiens	117-120
18707164-3	2008	The specific residues of MDM2 that have dominant binding interactions with p53 are specifically identified to be (51)Lys, (54)Leu, (62)Met, (67)Tyr, (72)Gln, (94)Lys, (96)His, and (100)Tyr.	Glutamine	153-156	P53	Homo sapiens	75-78
18550857-5	2008	In Mec1 and JVM-3 cell lines, dasatinib increased p53 protein levels and inhibited proliferation.	Dasatinib	30-39	P53	Homo sapiens	50-53
21185854-7	2011	Furthermore, p53 was shown to be involved in DHA-mediated autophagy and apoptosis.	dihydroptychantol A	45-48	P53	Homo sapiens	13-16
21185854-8	2011	In this connection, DHA increased nuclear expression of p53, induced p53 phosphorylation, and upregulated p53 target gene p21(Waf1/Cip1).	dihydroptychantol A	20-23	P53	Homo sapiens	56-59
21185854-8	2011	In this connection, DHA increased nuclear expression of p53, induced p53 phosphorylation, and upregulated p53 target gene p21(Waf1/Cip1).	dihydroptychantol A	20-23	P53	Homo sapiens	69-72
18384113-6	2008	The cell cycle arrest coincided with an increase in expression of the cell cycle markers p21, p27 and p53 proteins in 2-ME-treated osteosarcoma cells.	2-Methoxyestradiol	118-122	P53	Homo sapiens	102-105
21185854-8	2011	In this connection, DHA increased nuclear expression of p53, induced p53 phosphorylation, and upregulated p53 target gene p21(Waf1/Cip1).	dihydroptychantol A	20-23	P53	Homo sapiens	69-72
21185854-9	2011	In contrast, cytoplasmic p53 was reduced by DHA, which contributed to the stimulation of autophagy.	dihydroptychantol A	44-47	P53	Homo sapiens	25-28
18719315-0	2008	Reactive oxygen species mediate oridonin-induced HepG2 apoptosis through p53, MAPK, and mitochondrial signaling pathways.	oridonin	32-40	P53	Homo sapiens	73-76
21185854-13	2011	DHA-mediated autophagy and apoptosis are associated with the cytoplasmic and nuclear functions of p53.	dihydroptychantol A	0-3	P53	Homo sapiens	98-101
18719315-2	2008	p53, a specific inhibitor of pifithrin alpha (PFT alpha), markedly inhibited ROS generation and apoptosis, showing that p53 was responsible for the cytotoxity of oridonin through mediation by ROS.	oridonin	162-170	P53	Homo sapiens	0-3
18719315-2	2008	p53, a specific inhibitor of pifithrin alpha (PFT alpha), markedly inhibited ROS generation and apoptosis, showing that p53 was responsible for the cytotoxity of oridonin through mediation by ROS.	oridonin	162-170	P53	Homo sapiens	120-123
21149449-7	2011	Consistent with the ability of Ski to inactivate p53, overexpressing Ski desensitized cells to genotoxic drugs and Nutlin-3, a small-molecule antagonist of Mdm2 that stabilizes p53 and activates the p53 pathway, whereas knocking down Ski increased the cellular sensitivity to these agents.	nutlin 3	115-123	P53	Homo sapiens	49-52
21149449-7	2011	Consistent with the ability of Ski to inactivate p53, overexpressing Ski desensitized cells to genotoxic drugs and Nutlin-3, a small-molecule antagonist of Mdm2 that stabilizes p53 and activates the p53 pathway, whereas knocking down Ski increased the cellular sensitivity to these agents.	nutlin 3	115-123	P53	Homo sapiens	177-180
18625847-5	2008	Rather, p53 accumulation by either knockdown of Mdm2 or addition of an Mdm2 inhibitor, Nutlin-3, before irradiation strongly attenuated the UV-induced DDR and increased cell survival.	nutlin 3	87-95	P53	Homo sapiens	8-11
21149449-7	2011	Consistent with the ability of Ski to inactivate p53, overexpressing Ski desensitized cells to genotoxic drugs and Nutlin-3, a small-molecule antagonist of Mdm2 that stabilizes p53 and activates the p53 pathway, whereas knocking down Ski increased the cellular sensitivity to these agents.	nutlin 3	115-123	P53	Homo sapiens	177-180
20882314-0	2011	Therapeutic potential of antisense oligodeoxynucleotides in downregulating p53 oncogenic mutations in cancers.	Oligodeoxyribonucleotides	35-56	P53	Homo sapiens	75-78
22471459-0	2011	Jaceosidin induces p53-dependent G2/M phase arrest in U87 glioblastoma cells.	jaceosidin	0-10	P53	Homo sapiens	19-22
18594537-0	2008	Attenuated p53 activation in tumour-associated stromal cells accompanies decreased sensitivity to etoposide and vincristine.	Etoposide	98-107	P53	Homo sapiens	11-14
18426907-5	2008	NS binds to the central acidic domain of MDM2 and inhibits MDM2-mediated p53 ubiquitylation and degradation.	ns	0-2	P53	Homo sapiens	73-76
22471459-6	2011	The results demonstrated that jaceosidin-induced G2/M phase arrest in U87 cells is associated with DNA fragmentation, up-regulation of p53 and p21 and subsequent down-regulation of cyclin B1 and CDK1 expression at mRNA as well as at protein level.	jaceosidin	30-40	P53	Homo sapiens	135-138
18426907-9	2008	These results suggest that a p53-dependent cell cycle checkpoint monitors changes of cellular NS levels via the impediment of MDM2 function.	ns	94-96	P53	Homo sapiens	29-32
20336365-7	2011	The high frequency of spontaneous wt p53-reactive T cells detected in the peripheral blood of primary BCP with accumulation of p53 in tumor provides a rationale to consider DCs transfected with mRNA encoding wt p53 for clinical investigation in these patients.	bcp	102-105	P53	Homo sapiens	37-40
18519674-2	2008	Recent studies have revealed that EGCG triggers cancer cells undergoing apoptosis through p53-dependent pathway.	epigallocatechin gallate	34-38	P53	Homo sapiens	90-93
18519674-3	2008	How EGCG activates p53-dependent apoptosis is not fully understood.	epigallocatechin gallate	4-8	P53	Homo sapiens	19-22
18519674-4	2008	In the present study using JB6 cell as a model system, we have shown that EGCG can negatively regulate protein serine/threonine phosphatase-2A (PP-2A) to positively regulate p53-dependent apoptosis.	epigallocatechin gallate	74-78	P53	Homo sapiens	174-177
18519674-6	2008	Second, EGCG induces apoptosis of JB6 cells, which is associated with hyperphosphorylation of p53 and up-regulation of the proapoptotic gene, Bak.	epigallocatechin gallate	8-12	P53	Homo sapiens	94-97
18519674-8	2008	Knockdown of p53 and Bak expression with RNAi substantially inhibits EGCG-induced apoptosis.	epigallocatechin gallate	69-73	P53	Homo sapiens	13-16
18519674-12	2008	Finally, in the p53(-/-) H1299 and p53(+/+) H1080 cells, EGCG down-regulates PP-2A similarly but induces differential apoptosis.	epigallocatechin gallate	57-61	P53	Homo sapiens	16-19
20573397-0	2011	p53 and autophagy contribute to dasatinib resistance in primary CLL lymphocytes.	Dasatinib	32-41	P53	Homo sapiens	0-3
18519674-12	2008	Finally, in the p53(-/-) H1299 and p53(+/+) H1080 cells, EGCG down-regulates PP-2A similarly but induces differential apoptosis.	epigallocatechin gallate	57-61	P53	Homo sapiens	35-38
18519674-13	2008	In summary, our results show that (a) PP-2A directly dephosphorylates p53 at Ser-15; (b) P53 directly controls Bak expression; and (c) EGCG negatively regulates PP-2A.	epigallocatechin gallate	135-139	P53	Homo sapiens	70-73
18519674-14	2008	Together, our results show that EGCG-mediated negative regulation of PP-2A is an important molecular event for the activation of p53-dependent apoptosis during its chemoprevention.	epigallocatechin gallate	32-36	P53	Homo sapiens	129-132
20607720-7	2011	Cyclic pifithrin-alpha, an inhibitor of p53 transcriptional activity, blocked the decrease in mACON gene expression resulting from CPT treatment in LNCaP cells.	Pifithrin-Beta	0-22	P53	Homo sapiens	40-43
19383329-3	2008	Here we show that STIMA-1, a low molecular weight compound with some structural similarities to the previously identified molecule CP-31398, can stimulate mutant p53 DNA binding in vitro and induce expression of p53 target proteins and trigger apoptosis in mutant p53-expressing human tumor cells.	CP 31398	131-139	P53	Homo sapiens	162-165
19383329-3	2008	Here we show that STIMA-1, a low molecular weight compound with some structural similarities to the previously identified molecule CP-31398, can stimulate mutant p53 DNA binding in vitro and induce expression of p53 target proteins and trigger apoptosis in mutant p53-expressing human tumor cells.	CP 31398	131-139	P53	Homo sapiens	212-215
19383329-3	2008	Here we show that STIMA-1, a low molecular weight compound with some structural similarities to the previously identified molecule CP-31398, can stimulate mutant p53 DNA binding in vitro and induce expression of p53 target proteins and trigger apoptosis in mutant p53-expressing human tumor cells.	CP 31398	131-139	P53	Homo sapiens	212-215
20868669-4	2010	Trichostatin A induced nuclear damage, decreased Bid and Bcl-2 protein levels, increased in Bax levels, induced cytochrome c release, activated caspase-8, -9 and -3, and increased tumor suppressor p53 levels.	trichostatin A	0-14	P53	Homo sapiens	197-200
18516295-3	2008	In this study, we used cyclic pifithrin-alpha, a transcriptional inhibitor of p53, to further investigate the relevance of p53 function in the response of tumor cells to microtubule inhibitors.	Pifithrin-Beta	23-45	P53	Homo sapiens	78-81
19777160-0	2010	Synergistic efficacy of sorafenib and genistein in growth inhibition by down regulating angiogenic and survival factors and increasing apoptosis through upregulation of p53 and p21 in malignant neuroblastoma cells having N-Myc amplification or non-amplification.	Genistein	38-47	P53	Homo sapiens	169-172
17849423-1	2008	In hepatocellular carcinoma (HCC), hotspot mutation in codon 249 of the p53 gene has been associated with exposure to aflatoxin B1 (AFB1).	Aflatoxin B1	118-130	P53	Homo sapiens	72-75
17849423-5	2008	The HCC patients with XRCC1 genotypes with 399 Gln (namely: XRCC1-AG/GG) exhibited a significantly higher frequency of the p53 hotspot mutations in codon 249 than those with the wild-type homozygote of XRCC1 [namely: XRCC1-AA, adjusted odds ratio (OR) = 6.77, 95% confidence interval (CI) = 4.34-10.57].	Glutamine	47-50	P53	Homo sapiens	123-126
18413792-10	2008	In human cancer xenograft models, FK228 significantly increased the therapeutic effectiveness of p53 as well as p63 gene therapy.	romidepsin	34-39	P53	Homo sapiens	97-100
18358501-7	2008	Interestingly, 9 out of 14 (64.3%) tumors carrying p53 mutations displayed substitution of serine by arginine at codon 249, a characteristic change believed to be induced by aflatoxin-B1.	Aflatoxin B1	174-186	P53	Homo sapiens	51-54
20851891-5	2010	The mAb DO-12 epitope of p53 is masked via phosphorylation in a range of human tumor cells with WT p53 status, as defined by increased mAb DO-12 binding to endogenous p53 after phosphatase treatment.	do-12	8-13	P53	Homo sapiens	99-102
20727582-0	2010	Endothelial cells dysfunction induced by silica nanoparticles through oxidative stress via JNK/P53 and NF-kappaB pathways.	Silicon Dioxide	41-47	P53	Homo sapiens	95-98
18373075-5	2008	However, at a low dose of etoposide (repairable damage), Bid activated the S phase checkpoint through the up-regulation of p21 and p27, which are both p53-independent.	Etoposide	26-35	P53	Homo sapiens	151-154
18366759-6	2008	Of note is the inhibition of the etoposide-induced activation of p53 under hypoxia.	Etoposide	33-42	P53	Homo sapiens	65-68
20727582-7	2010	Silica nanoparticles also activated c-Jun N-terminal kinase (JNK), c-Jun, p53, caspase-3 and NF-kappaB, increased Bax expression and suppressed Bcl-2 protein.	Silicon Dioxide	0-6	P53	Homo sapiens	74-77
20727582-9	2010	In summary, our findings demonstrated that silica nanoparticles could induce dysfunction of endothelial cells through oxidative stress via JNK, p53 and NF-kappaB pathways, suggesting that exposure to silica nanoparticles may be a significant risk for the development of cardiovascular diseases such as atherosclerosis and thrombus.	Silicon Dioxide	43-49	P53	Homo sapiens	144-147
18366759-8	2008	Cluster analysis of data unravels several possible pathways involved in the hypoxia-induced protection against etoposide-induced apoptosis: one of them could be the inhibition of p53 activity under hypoxia since caspase 3 activity parallels Bax and Bak expression profile.	Etoposide	111-120	P53	Homo sapiens	179-182
20713149-11	2010	Furthermore, pretreatment with curculigoside decreased the activity of caspase-3 and p53 mRNA expression, which was known to play a key role in H(2)O(2)-induced cell apoptosis.	curculigoside	31-44	P53	Homo sapiens	85-88
18279445-6	2008	Leptin and fAd dose-dependently potentiated p53 expression in PC3 cells (P &lt; 0.001); leptin and gAd also increased p53 expression (P &lt; 0.05 and P &lt; 0.001).	Flavin-Adenine Dinucleotide	11-14	P53	Homo sapiens	44-47
20811720-5	2010	In this study, we investigated the effect of trichostatin A or TSA (an HDAC inhibitor), and epoxomycin (a proteasome inhibitor) on MYCN and p53 expression in MYCN-amplified neuroblastoma cells.	trichostatin A	45-59	P53	Homo sapiens	140-143
18409045-0	2008	A new triterpenoid from Panax ginseng exhibits cytotoxicity through p53 and the caspase signaling pathway in the HepG2 cell line.	triterpenoid TP-222	6-18	P53	Homo sapiens	68-71
21163061-8	2010	The bufalin-induced apoptosis was confirmed by increased expression of tumor suppressor protein p53, bax and decreased expression of bcl-2.	bufalin	4-11	P53	Homo sapiens	96-99
18206427-8	2008	Etoposide-induced phosphorylation of p53 relied mainly on RIP, whereas activation of Chk1, Chk2 depended largely on TIP.	Etoposide	0-9	P53	Homo sapiens	37-40
18206427-9	2008	Both RIP and TIP played roles in activating non-homologous end joining pathway, while only RIP modulated etoposide-induced cell killing in a p53-dependent manner.	Etoposide	105-114	P53	Homo sapiens	141-144
18418047-8	2008	However, HAUSP downregulation causes resistance to Camptothecin- and irradiation-induced apoptosis, which correlates with suppressed mitochondrial translocation of p53.	Camptothecin	51-63	P53	Homo sapiens	164-167
18026140-8	2008	p53 levels comparable to those found in induced mammalian cells confer synthetic sickness or lethality in combination with deletions in genes encoding transcription elongation factors; p53 likewise confers hypersensitivity to the anti-elongation drug 6-azauracil.	azauracil	251-262	P53	Homo sapiens	0-3
20622893-7	2010	BRCA1-IRIS abrogation of the homeostatic balance maintained by the p38MAPK-p53-WIP1 pathway suppressed cell death induced by a lethal dose of short-wavelength UV light, and high dosage of etoposide or H(2)O(2), and allowed cells to survive and proliferate post geno-/cell-toxic stresses.	Etoposide	188-197	P53	Homo sapiens	75-78
18026140-8	2008	p53 levels comparable to those found in induced mammalian cells confer synthetic sickness or lethality in combination with deletions in genes encoding transcription elongation factors; p53 likewise confers hypersensitivity to the anti-elongation drug 6-azauracil.	azauracil	251-262	P53	Homo sapiens	185-188
18296683-7	2008	We have applied this method to a mixed set of mutation spectra observed in exons 5, 7 and 8 of TP53 from cancers of brain, breast, skin, colon, oesophagus, liver, head and neck, stomach and lung (smokers and non-smokers) and spectra induced by benzo[a]pyrene diol epoxide, ultraviolet (UV) B, UVC, simulated sunlight and hydroxyl radicals in the cII, supF and yeast p53 model systems.	Hydroxyl Radical	321-338	P53	Homo sapiens	95-99
18292936-8	2008	Western blot analysis of apoptosis-related proteins demonstrated that treatment with MZ-5-156 (10(-6) M) for 48 h significantly increased the protein levels of Fas, phospho-p53 (Ser46), p53AIP1 (p53-regulated Apoptosis-Inducing Protein 1), and caspase-8, -9, and -3, and decreased the protein level of Bcl-2.	mz-5	85-89	P53	Homo sapiens	173-176
20664969-0	2010	Oridonin induces G2/M cell cycle arrest and apoptosis through MAPK and p53 signaling pathways in HepG2 cells.	oridonin	0-8	P53	Homo sapiens	71-74
18208837-4	2008	Time-dependent decrease was observed in APE1 mRNA and protein levels in the human colorectal cancer line HCT116 p53(+/+), but not in the isogenic p53 null mutant after treatment with camptothecin, a DNA topoisomerase I inhibitor.	Camptothecin	183-195	P53	Homo sapiens	112-115
17932621-11	2008	Under basal growth conditions and in response to the chemotherapeutic agent, etoposide, WIP1 antagonized p53-mediated apoptosis in medulloblastoma cell lines.	Etoposide	77-86	P53	Homo sapiens	105-108
18324703-2	2008	Using analysis of proteins related to cell cycle and apoptotic pathways, we confirmed an elevated level of p53 accompanying p21 Waf1/Cip1 protein in genistein-treated or genistin-treated A549 and WI-38 cells, but not in HeLa cells.	Genistein	149-158	P53	Homo sapiens	107-110
18324703-3	2008	In addition, a p53-upregulated modulator of apoptosis (Puma) protein accumulated significantly in genistein-treated A549 and WI-38 cells, but not in genistin-treated or beta-estradiol-treated cells, though the growth of any ingredient-treated cells was severely inhibited.	Genistein	98-107	P53	Homo sapiens	15-18
18324703-4	2008	Intriguingly, the caspase-3 activity of genistein-treated A549 cells, in which Puma or p53 expression was knocked-down by RNA interference (RNAi), remained unaltered compared to that in cells transfected with irrelevant RNAi.	Genistein	40-49	P53	Homo sapiens	87-90
20664969-7	2010	Immunoblot analysis demonstrated that oridonin treatment increased expression levels of p-JNK, p-p38, p-p53 and p21, elevated the level of cyclin B1/p-Cdc2 (Tyr15) complex, and inhibited the expression of p-ERK.	oridonin	38-46	P53	Homo sapiens	104-107
18357397-9	2008	There was an increase in the p53 and p21 levels in response to genistein.	Genistein	63-72	P53	Homo sapiens	29-32
18357397-13	2008	Moreover, the ectopic expression of temperature-sensitive p53V135A, which acts as a dominant-negative p53 mutant at 38.5 degrees C but assumes p53 wild-type properties at 32.5 degrees C, in LN-18 or LNT-229 cells, had no effect on genistein cytotoxicity at either temperature.	Genistein	231-240	P53	Homo sapiens	58-61
20664969-9	2010	In conclusion, oridonin induced G2/M cell cycle arrest and apoptosis in HepG2 cells through MAPK and p53 pathways, which advances our understanding on the molecular mechanisms of oridonin in hepatocarcinoma management.	oridonin	15-23	P53	Homo sapiens	101-104
18202783-3	2008	The data obtained show that normal human lymphocytes exposed in vitro to known DNA-damaging agents, e.g. H2O2, ionizing radiation and mitomycin C, exhibit an asynchronous replication of the genes TP53 and RB1.	Mitomycin	134-145	P53	Homo sapiens	196-200
20682800-3	2010	The small molecule CP-31398 modulates both the wild-type and the mutant p53 proteins.	CP 31398	19-27	P53	Homo sapiens	72-75
17942461-0	2008	Identification through microarray gene expression analysis of cellular responses to benzo(a)pyrene and its diol-epoxide that are dependent or independent of p53.	diol-epoxide	107-119	P53	Homo sapiens	157-160
18330473-0	2008	Class I phosphatidylinositol 3-kinase inhibitor LY294002 activates autophagy and induces apoptosis through p53 pathway in gastric cancer cell line SGC7901.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	48-56	P53	Homo sapiens	107-110
18087215-4	2007	When the H460 human lung cancer cell line was treated with hypoxia and etoposide, a chemotherapy agent that induces double-stranded DNA breaks, the dominant transcriptional response was regulated by DNA damage in a p53-dependent manner.	Etoposide	71-80	P53	Homo sapiens	215-218
20662736-7	2010	Anthracycline (topoisomerase II inhibitors such as mitoxantrone and ellipticine) and camptothecin (topoisomerase I inhibitor) derivatives including topotecan induce DNA double strand breaks, which activate the p53 pathway through the ataxia telangiectasia mutated-checkpoint kinase 2 (ATM-CHK2) DNA damage response pathway.	Camptothecin	85-97	P53	Homo sapiens	210-213
18330473-4	2008	LY294002 activated autophagy by activating p53 and caspase-3, and induced apoptosis by up-regulating p53 and p53-up-regulated modulator of apoptosis (PUMA).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	P53	Homo sapiens	43-46
18330473-4	2008	LY294002 activated autophagy by activating p53 and caspase-3, and induced apoptosis by up-regulating p53 and p53-up-regulated modulator of apoptosis (PUMA).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	P53	Homo sapiens	101-104
18330473-4	2008	LY294002 activated autophagy by activating p53 and caspase-3, and induced apoptosis by up-regulating p53 and p53-up-regulated modulator of apoptosis (PUMA).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	P53	Homo sapiens	101-104
18330473-5	2008	Therefore, LY294002 might induce cytotoxicity in SGC7901 cells through activation of p53 and the downstream point PUMA.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	11-19	P53	Homo sapiens	85-88
19002263-8	2008	Mucinous feature, signet ring cells, and p53-negativity were associated with CIMP-high in only univariate analysis.	cimp-high	77-86	P53	Homo sapiens	41-44
17897804-2	2007	The imidazoline compound (Nutlin-3) is a promising small molecule antagonist of the MDM2-p53 interaction.	nutlin 3	26-34	P53	Homo sapiens	89-92
18060027-3	2007	report on their study of a nonimmunodeficient mouse model of UVB-induced skin cancer and human skin carcinoma cells and show that the mutant p53 conformation-modifying drug CP-31398 not only treats these tumors but also prevents them (see the related article beginning on page 3753).	CP 31398	173-181	P53	Homo sapiens	141-144
18084622-8	2007	Moreover, we noted that in etoposide treated LNCaP cells p53 bound to the promoter region of the AR gene, which contains a potential p53 DNA-binding consensus sequence, in chromatin immunoprecipitation assays.	Etoposide	27-36	P53	Homo sapiens	57-60
18084622-8	2007	Moreover, we noted that in etoposide treated LNCaP cells p53 bound to the promoter region of the AR gene, which contains a potential p53 DNA-binding consensus sequence, in chromatin immunoprecipitation assays.	Etoposide	27-36	P53	Homo sapiens	133-136
18088187-7	2007	Chk1 phosphorylation was maintained only in the presence of staurosporine and UCN-01 in p53+/+ cells.	Staurosporine	60-73	P53	Homo sapiens	88-91
17945324-5	2007	These cells were treated with different doses of sodium arsenite (0, 0.1, 1, 5 and 10 microM) for 48 h. A greater reduction in cell viability was observed in the BEAS-2B cells vs. p53 compromised cells (H1355 or p53-inhibited BEAS-2B).	sodium arsenite	49-64	P53	Homo sapiens	180-183
17945324-5	2007	These cells were treated with different doses of sodium arsenite (0, 0.1, 1, 5 and 10 microM) for 48 h. A greater reduction in cell viability was observed in the BEAS-2B cells vs. p53 compromised cells (H1355 or p53-inhibited BEAS-2B).	sodium arsenite	49-64	P53	Homo sapiens	212-215
17726646-4	2007	Fusion of the p53 nuclear export signaling sequence MFRELNEALELK to NDelta19 (NDelta19NES) abolished its apoptosis promoting properties, while overexpression of NDelta19 significantly increased the susceptibility to apoptosis induction by the proteasome inhibitor PSI and by staurosporine.	Staurosporine	275-288	P53	Homo sapiens	14-17
17727682-7	2007	In addition, treatment with 30 microM genistein strongly induced phosphorylation of checkpoint kinase (CHK) 2 and p53 at serines 15, 20 and 37.	Genistein	38-47	P53	Homo sapiens	114-117
17727682-8	2007	Caffeine, an inhibitor of ataxia-telangiectasia mutated protein kinase, alleviated the genistein-induced p53 and CHK2 phosphorylation, suggesting the involvement of DNA damage at 30 microM.	Genistein	87-96	P53	Homo sapiens	105-108
17880120-5	2007	Application of SiO2-coated NW in discrimination of single base mismatches corresponding to a mutation of the p53 gene was also demonstrated.	Silicon Dioxide	15-19	P53	Homo sapiens	109-112
17681274-5	2007	Here, in p53 negative K562 myeloid leukemia cells, etoposide-induced mitotic catastrophe is shown to be time and/or concentration dependent.	Etoposide	51-60	P53	Homo sapiens	9-12
17636382-0	2007	New alternative phosphorylation sites on the cyclin dependent kinase 1/cyclin a complex in p53-deficient human cells treated with etoposide: possible association with etoposide-induced apoptosis.	Etoposide	130-139	P53	Homo sapiens	91-94
17636382-0	2007	New alternative phosphorylation sites on the cyclin dependent kinase 1/cyclin a complex in p53-deficient human cells treated with etoposide: possible association with etoposide-induced apoptosis.	Etoposide	167-176	P53	Homo sapiens	91-94
17636382-13	2007	These findings suggest novel Cdk1 phosphorylation sites, which appear to be associated with p53-independent cell death following etoposide treatment.	Etoposide	129-138	P53	Homo sapiens	92-95
17631051-5	2007	CD8(+) T cell precursors responsive to wt p53 epitopes were detected in the circulation of most subjects with early disease, and an elevated blood Tc(1)/Tc(2) ratio distinguished wt p53 peptide responders from non-responders.	tc(1)	147-152	P53	Homo sapiens	182-185
17624304-4	2007	EGCG has been demonstrated to inhibit the growth of a variety of cancer cells, induce apoptosis and regulate the expression of p53, myc, and ERK.	epigallocatechin gallate	0-4	P53	Homo sapiens	127-130
17958331-5	2007	TDB treatment also caused a marked increase in the level of p21WAF1/CIP1 protein in a p53-dependent manner.	TDB	0-3	P53	Homo sapiens	86-89
17310986-11	2007	This was shown by studying DNA damage-induced apoptosis in fibroblasts, the Fas death pathway in HeLa cells that do not express functional p53, and etoposide-induced apoptosis in breast carcinoma cells expressing mutant p53.	Etoposide	148-157	P53	Homo sapiens	220-223
17588343-0	2007	P53-mediated cell cycle arrest and apoptosis through a caspase-3- independent, but caspase-9-dependent pathway in oridonin-treated MCF-7 human breast cancer cells.	oridonin	114-122	P53	Homo sapiens	0-3
17504227-1	2007	To potentiate the response of acute myeloid leukemia (AML) to TRAIL cytotoxicity, we have adopted a strategy of combining nutlin-3, a potent non-genotoxic activator of the p53 pathway, with recombinant TRAIL.	nutlin 3	122-130	P53	Homo sapiens	172-175
17504227-6	2007	Moreover, while nutlin-3 up-regulated the expression of cyclin dependent kinase inhibitor p21, a p53-target gene mediating cell cycle block and showing anti-apoptotic activity, the simultaneous addition of TRAIL plus nutlin-3 induced the caspase-dependent cleavage of p21.	nutlin 3	16-24	P53	Homo sapiens	97-100
17230511-9	2007	p21 induction is closely associated with FK228 or TSA but not 5-Aza, which is mediated via p53-independent pathway.	romidepsin	41-46	P53	Homo sapiens	91-94
17230511-9	2007	p21 induction is closely associated with FK228 or TSA but not 5-Aza, which is mediated via p53-independent pathway.	trichostatin A	50-53	P53	Homo sapiens	91-94
17230511-12	2007	The elevated p21 level mediated via p53 independent pathway is a hallmark of FK228 mechanism of action.	romidepsin	77-82	P53	Homo sapiens	36-39
17276981-8	2007	Furthermore, the Aph-1- and Pen-2-associated reduction of staurosporine-induced caspase-3 activation was fully abolished by p53 deficiency.	Staurosporine	58-71	P53	Homo sapiens	124-127
17461764-9	2007	An extremely low concentration of cisplatin in addition to Ps-S-Oligos further up-regulated p53 activity, provoking massive apoptotic induction.	Phosphorus	59-63	P53	Homo sapiens	92-95
17461764-9	2007	An extremely low concentration of cisplatin in addition to Ps-S-Oligos further up-regulated p53 activity, provoking massive apoptotic induction.	2',5'-oligoadenylate	64-70	P53	Homo sapiens	92-95
17292432-4	2007	Treatment with other vanadate compounds, sodium orthovanadate (Na(3)VO(4)) and ammonium metavanadate (NH(4)VO(3)), also induced Ser15 phosphorylation and accumulation of p53 protein.	Sodium orthovanadate	41-61	P53	Homo sapiens	170-173
17372198-2	2007	We have investigated the effect of p53 activation on the proteome using 2D gel electrophoresis analysis of mitomycin C-treated HCT116 colon carcinoma cells carrying wild-type p53.	Mitomycin	107-118	P53	Homo sapiens	35-38
17372198-2	2007	We have investigated the effect of p53 activation on the proteome using 2D gel electrophoresis analysis of mitomycin C-treated HCT116 colon carcinoma cells carrying wild-type p53.	Mitomycin	107-118	P53	Homo sapiens	175-178
17218071-8	2007	PSC833 and verapamil also increased p53 protein expression at 48 h (p&lt;0.05).	Verapamil	11-20	P53	Homo sapiens	36-39
18032786-11	2007	Disruption of this regulation increases the proportions of PCs containing polyunsaturated fatty acids and activates the ATR-p53 signalling pathway.	Phosphatidylcholines	59-62	P53	Homo sapiens	124-127
18032786-11	2007	Disruption of this regulation increases the proportions of PCs containing polyunsaturated fatty acids and activates the ATR-p53 signalling pathway.	Fatty Acids, Unsaturated	74-101	P53	Homo sapiens	124-127
17850846-3	2007	Of the stress-related genes, the expressions of the aryl hydrocarbon receptor (AhR), cytochrome P450 (CYP) and p53 genes were most significantly induced by exposure to PCDDs/DFs.	aspartyl-phenylalanine	174-177	P53	Homo sapiens	111-114
17610503-4	2007	Here, we show that fusion of an 11-amino-acid region of the human immunodeficiency virus TAT protein transduction domain (PTD) to human p53 increases the solubility of the otherwise insoluble p53 protein and this rTAT-p53 protein can be transduced into human monocyte-derived dendritic cells (DCs).	11-amino-acid	32-45	P53	Homo sapiens	136-139
17610503-4	2007	Here, we show that fusion of an 11-amino-acid region of the human immunodeficiency virus TAT protein transduction domain (PTD) to human p53 increases the solubility of the otherwise insoluble p53 protein and this rTAT-p53 protein can be transduced into human monocyte-derived dendritic cells (DCs).	11-amino-acid	32-45	P53	Homo sapiens	192-195
17610503-4	2007	Here, we show that fusion of an 11-amino-acid region of the human immunodeficiency virus TAT protein transduction domain (PTD) to human p53 increases the solubility of the otherwise insoluble p53 protein and this rTAT-p53 protein can be transduced into human monocyte-derived dendritic cells (DCs).	11-amino-acid	32-45	P53	Homo sapiens	192-195
17916362-7	2007	Treatment with sirtinol or Sirt1 siRNA increased acetylation of p53, while p53 expression was unaltered.	sirtinol	15-23	P53	Homo sapiens	64-67
17942917-5	2007	Using this transformation model, we examined the sensitivity of the D1/CDK-expressing cells to Nutlin-3, an HDM2 antagonist that activates p53.	nutlin 3	95-103	P53	Homo sapiens	139-142
17709397-8	2007	The camptothecin effects on H-ras gene expression were p53 dependent and involved in part modulation of the SC35 splicing factor.	Camptothecin	4-16	P53	Homo sapiens	55-58
17709397-10	2007	Finally, Upf1, a major NMD effector, was necessary for optimal p53 activation by camptothecin, which is consistent with recent data showing that NMD effectors are required for genome stability.	Camptothecin	81-93	P53	Homo sapiens	63-66
17709487-10	2007	The effects of RSV infection are antagonized by Nutlin-3, a specific chemical inhibitor that prevents the Mdm2/p53 association.	nutlin 3	48-56	P53	Homo sapiens	111-114
21162257-4	2007	In contrast, tolbutamide (100 micromol/L), the K(ATP) channels antagonist, significantly rose p53 expression and the hypoxia-induced apoptosis, which could be reversed by p53 inhibitor TSA.	trichostatin A	185-188	P53	Homo sapiens	94-97
21162257-4	2007	In contrast, tolbutamide (100 micromol/L), the K(ATP) channels antagonist, significantly rose p53 expression and the hypoxia-induced apoptosis, which could be reversed by p53 inhibitor TSA.	trichostatin A	185-188	P53	Homo sapiens	171-174
17630856-0	2007	Absence of p53 enhances growth defects and etoposide sensitivity of human cells lacking the Bloom syndrome helicase BLM.	Etoposide	43-52	P53	Homo sapiens	11-14
17630856-5	2007	Our results suggest a direct, BLM-independent role for p53 in etoposide-induced, topoisomerase II-mediated DNA damage in human cells.	Etoposide	62-71	P53	Homo sapiens	55-58
17622845-0	2007	Detection of p53 protein in induced sputum after occupational exposure to crystalline silica.	Silicon Dioxide	86-92	P53	Homo sapiens	13-16
17622845-1	2007	OBJECTIVE: To examine the possibility of detecting p53 protein in the supernatant of induced sputum (IS) of workers exposed to crystalline silica.	Silicon Dioxide	139-145	P53	Homo sapiens	51-54
17694658-10	2007	At the same time of high expression of wt-P53 protein, the telomerase activity of KFBs in transfection group was significantly lower than that in the untransfection group (P &lt; 0.05).	kfbs	82-86	P53	Homo sapiens	42-45
17224908-5	2007	Disruption of transcription by actinomycin D, 5,6-dichloro-1-beta-D-ribofuranosyl-benzimadazole or alpha-amanitin leads to accumulation of cellular p53 protein.	5,6-dichloro-1-beta-d-ribofuranosyl-benzimadazole	46-95	P53	Homo sapiens	148-151
17224908-5	2007	Disruption of transcription by actinomycin D, 5,6-dichloro-1-beta-D-ribofuranosyl-benzimadazole or alpha-amanitin leads to accumulation of cellular p53 protein.	Alpha-Amanitin	99-113	P53	Homo sapiens	148-151
17530733-0	2007	Mitomycin-DNA adducts induce p53-dependent and p53-independent cell death pathways.	Mitomycin	0-9	P53	Homo sapiens	29-32
17530733-0	2007	Mitomycin-DNA adducts induce p53-dependent and p53-independent cell death pathways.	Mitomycin	0-9	P53	Homo sapiens	47-50
17530733-5	2007	In cell lines lacking wild-type p53, DMC was reproducibly more cytotoxic than MC, but it generated barely detectable signal transduction markers associated with apoptotic death.	Mitomycin	38-40	P53	Homo sapiens	32-35
17530733-8	2007	In cell lines with a functional p53 pathway, both MC and DMC induced apoptosis.	Mitomycin	50-52	P53	Homo sapiens	32-35
17530733-9	2007	In the presence of p53, both MC and DMC activate procaspases; however, the spectrum of procaspases involved differs for the two drugs, as does induction of p73.	Mitomycin	29-31	P53	Homo sapiens	19-22
17534142-8	2007	Activation of p53 signaling pathway leads to activation of caspases and caspases inhibitor VAD-fmk completely blocks low dose LDM induced apoptosis through the inhibition of mitochondria pathway.	VAD-fmk	91-98	P53	Homo sapiens	14-17
17317670-8	2007	DNA damage caused by camptothecin treatment increases mRNA and protein levels of CDA1, accompanied by induction of p53.	Camptothecin	21-33	P53	Homo sapiens	115-118
17363597-4	2007	The effect of SNP309 upon the p53-MDM2 oscillation was examined in various human cell lines and the oscillations were observed in the cells with at least one wild-type allele for SNP309 (T/T or T/G) but not in cells homozygous for SNP309 (G/G).	snp309	14-20	P53	Homo sapiens	30-33
17065198-3	2007	We detected 24 p53 mutations in 15/25 (60%) NMSCs, 1 deletion and 23 base substitutions, the majority (78%) being UV-specific C to T transitions at bipyrimidine sites.	2,2'-Bipyrimidine	148-160	P53	Homo sapiens	15-18
16870476-2	2007	The present in vitro study has primarily focused on the evaluation of the chemosensitising drug model, verapamil, as a P-glycoprotein antagonist not only to overcome chemoresistance in non-Hodgkin"s lymphoma (NHL) chemoresistant cells (p53(+) i.e. over-expressing p53 mutant protein NHL cells) but also to evaluate and suggest the use of the single cell gel electrophoresis (SCGE) assay in the clinical setting.	Verapamil	103-112	P53	Homo sapiens	236-239
16870476-2	2007	The present in vitro study has primarily focused on the evaluation of the chemosensitising drug model, verapamil, as a P-glycoprotein antagonist not only to overcome chemoresistance in non-Hodgkin"s lymphoma (NHL) chemoresistant cells (p53(+) i.e. over-expressing p53 mutant protein NHL cells) but also to evaluate and suggest the use of the single cell gel electrophoresis (SCGE) assay in the clinical setting.	Verapamil	103-112	P53	Homo sapiens	264-267
16870476-6	2007	RESULTS: Verapamil increased the tail moments induced by doxorubicin in all cell types over-expressing p53 mutant protein.	Verapamil	9-18	P53	Homo sapiens	103-106
17324262-8	2007	Most importantly, the antitumor effect of hydralazine and valproate in cervical cancer may at least partially depend on an up-regulating effect on p53 gene and on the valproate-induced hyperacetylation of p53 protein, protecting it from degradation by E6.	Hydralazine	42-53	P53	Homo sapiens	147-150
17324262-8	2007	Most importantly, the antitumor effect of hydralazine and valproate in cervical cancer may at least partially depend on an up-regulating effect on p53 gene and on the valproate-induced hyperacetylation of p53 protein, protecting it from degradation by E6.	Hydralazine	42-53	P53	Homo sapiens	205-208
17121856-3	2007	This study investigates the action of two HDAC inhibitors, CG-1521 and trichostatin A, which stabilize Ac-Lys-373 p53 and Ac-Lys-382 p53, respectively, in LNCaP prostate cancer cells.	trichostatin A	71-85	P53	Homo sapiens	114-117
17121856-3	2007	This study investigates the action of two HDAC inhibitors, CG-1521 and trichostatin A, which stabilize Ac-Lys-373 p53 and Ac-Lys-382 p53, respectively, in LNCaP prostate cancer cells.	trichostatin A	71-85	P53	Homo sapiens	133-136
17169477-0	2007	4-NQO induces apoptosis via p53-dependent mitochondrial signaling pathway.	4-Nitroquinoline-1-oxide	0-5	P53	Homo sapiens	28-31
17169477-5	2007	Further investigation showed that the apoptosis induced by 4-NQO was p53-dependent.	4-Nitroquinoline-1-oxide	59-64	P53	Homo sapiens	69-72
17169477-9	2007	The results indicated that 4-NQO arrested cell cycle in G(1) phase, thus allowing enough time for DNA repair; on the other hand, if the cellular DNA were not repaired, apoptosis may follow through the p53-dependent mitochondrial signaling pathway, and mechanism of apoptosis induced by 4-NQO is not exactly the same that induced by UV radiation, as the later induces apoptosis through death receptors and mitochondrial signaling pathway.	4-Nitroquinoline-1-oxide	27-32	P53	Homo sapiens	201-204
17169477-9	2007	The results indicated that 4-NQO arrested cell cycle in G(1) phase, thus allowing enough time for DNA repair; on the other hand, if the cellular DNA were not repaired, apoptosis may follow through the p53-dependent mitochondrial signaling pathway, and mechanism of apoptosis induced by 4-NQO is not exactly the same that induced by UV radiation, as the later induces apoptosis through death receptors and mitochondrial signaling pathway.	4-Nitroquinoline-1-oxide	286-291	P53	Homo sapiens	201-204
16926174-3	2007	Potassium diazoacetate (KDA) is a stable form of nitrosated glycine and its ability to induce mutations in the p53 gene in a functional yeast assay was studied.	KDA	24-27	P53	Homo sapiens	111-114
17255282-6	2007	CHIR-124 interacts synergistically with topoisomerase poisons (e.g., camptothecin or SN-38) in causing growth inhibition in several p53-mutant solid tumor cell lines as determined by isobologram or response surface analysis.	Camptothecin	69-81	P53	Homo sapiens	132-135
17274270-0	2007	Correlation of sulfur mustard exposure and tobacco use with expression (immunoreactivity) of p53 protein in bronchial epithelium of Iranian "mustard lung" patients.	Mustard Gas	15-29	P53	Homo sapiens	93-96
17172643-1	2007	Trichostatin A (TSA), a specific inhibitor of histone deacetylases (HDACs), induces acetylation of various non-histone proteins such as p53 and alpha-tubulin.	trichostatin A	0-14	P53	Homo sapiens	136-139
17172643-1	2007	Trichostatin A (TSA), a specific inhibitor of histone deacetylases (HDACs), induces acetylation of various non-histone proteins such as p53 and alpha-tubulin.	trichostatin A	16-19	P53	Homo sapiens	136-139
20226587-3	2010	Co-treatment of etoposide and KG-135 markedly elevated the expression and phosphorylation at the serine 15 residue of p53 as well as the cellular levels of Bax and p21(Waf1/Cip1).	Etoposide	16-25	P53	Homo sapiens	118-121
17138942-4	2007	Although nutlin-3 and doxorubicin induced a comparable p53 accumulation in endothelial cells, nutlin-3 was significantly more efficient than doxorubicin in upregulating the p53 target genes CDKN1A/p21, MDM2, and GDF-15, as well as in inhibiting cell cycle progression.	nutlin 3	9-17	P53	Homo sapiens	55-58
17404061-10	2007	Moreover, jaceosidin elevated the expression of p53 and p21, while the compound inhibited the activation of ERK1/2 that is an important component of cell survival signaling.	jaceosidin	10-20	P53	Homo sapiens	48-51
16620158-2	2007	These mutations also have another important characteristic of frequent occurrences at CpG dinucleotide sites, some of which actually show prominent hotspots in the p53 gene.	Dinucleoside Phosphates	90-102	P53	Homo sapiens	164-167
17534123-8	2007	Phosphatidylinositol 3-kinase (PI3K) inhibitors, wortmannin and LY294002 abolished the effect of RSVL on p53 activation.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	64-72	P53	Homo sapiens	105-108
20226587-6	2010	Our results indicate that etoposide-induced apoptosis in HeLa cells can be potentiated in the presence of KG-135 through a mechanism that involves the stabilization of p53 and the stimulation of Bax- and p21-mediated apoptotic signaling pathways.	Etoposide	26-35	P53	Homo sapiens	168-171
17077087-7	2006	Chromatin immunoprecipitation experiments support the hypothesis that this p53-dependent trans-repression is due to the direct interaction of p53 with the ARE-containing promoters.	ACARBOSE DERIVED PENTASACCHARIDE	155-158	P53	Homo sapiens	75-78
17077087-7	2006	Chromatin immunoprecipitation experiments support the hypothesis that this p53-dependent trans-repression is due to the direct interaction of p53 with the ARE-containing promoters.	ACARBOSE DERIVED PENTASACCHARIDE	155-158	P53	Homo sapiens	142-145
20554748-7	2010	Our findings provide support to GEN-induced PTEN as both a target and regulator of p53 action and offer a mechanistic basis for PTEN pathway activation to underlie the antitumor properties of dietary factors, with important implications for reducing breast cancer risk.	Genistein	32-35	P53	Homo sapiens	83-86
17112418-12	2006	N-demethyl-clarithromycin upregulated the expression ratio of mitochondrial Bax/Bcl-2, and significantly increased the expression of the p53 protein.	n-demethyl-clarithromycin	0-25	P53	Homo sapiens	137-140
17344317-7	2007	However, treatment with the histone deacetylase inhibitor trichostatin-A resulted in relief of mutant p53-mediated suppression, suggesting that mutant p53 may induce hypo-acetylation of target gene promoters leading to the suppressive effects.	trichostatin A	58-72	P53	Homo sapiens	102-105
17344317-7	2007	However, treatment with the histone deacetylase inhibitor trichostatin-A resulted in relief of mutant p53-mediated suppression, suggesting that mutant p53 may induce hypo-acetylation of target gene promoters leading to the suppressive effects.	trichostatin A	58-72	P53	Homo sapiens	151-154
20845286-7	2010	BRCA1-IRIS abrogation of the homeostatic balance maintained by p38MAPK-p53-WIP1 pathway suppressed cell death induced by a lethal dose of UVC, high dosages of etoposide or H2O2, and allowed cells to survive and proliferate post geno-/cell-toxic stresses.	Etoposide	159-168	P53	Homo sapiens	71-74
17341629-8	2006	Thus, beneficial effects of FK228 on human promyelocytic leukemia may be exerted through the induction of differentiation or apoptosis via histone modification and selective involvement of transcription factors, such as NF-kappaB and p53.	romidepsin	28-33	P53	Homo sapiens	234-237
16931776-10	2006	In vitro exposure of hMSCs to cisplatin, vincristine, and etoposide resulted in an increased p53 expression, independent of apoptosis induction.	Etoposide	58-67	P53	Homo sapiens	93-96
17045927-6	2006	Scavengers of singlet oxygen or NO could attenuate PDT-induced cell viability loss, nucleus morphology changes, cytochrome c release, mitochondria swelling, and apo-apoptosis gene p53 and p21 mRNA levels.	Singlet Oxygen	14-28	P53	Homo sapiens	180-183
20375332-9	2010	TSA induced caspase-mediated apoptotic pathways; caspase induction was accompanied by a decrease in endogenous DeltaNp63alpha and p53.	trichostatin A	0-3	P53	Homo sapiens	130-133
17030796-2	2006	The p53 binding pattern of carcinogenic polycyclic aromatic hydrocarbons (PAHs) found in CS coincides with the p53 mutational pattern found in lung cancer, and PAHs have thus been considered to be major culprits for lung cancer.	Cesium	89-91	P53	Homo sapiens	4-7
17030796-2	2006	The p53 binding pattern of carcinogenic polycyclic aromatic hydrocarbons (PAHs) found in CS coincides with the p53 mutational pattern found in lung cancer, and PAHs have thus been considered to be major culprits for lung cancer.	Cesium	89-91	P53	Homo sapiens	111-114
17030796-6	2006	These findings raise the question of whether Acr-DNA adducts are responsible for p53 mutations in CS-related lung cancer.	Cesium	98-100	P53	Homo sapiens	81-84
17030796-7	2006	To determine the role of Acr-DNA adducts in p53 mutagenesis in CS-related lung cancer we mapped the distribution of Acr-DNA adducts at the sequence level in the p53 gene of lung cells using the UvrABC incision method in combination with ligation-mediated PCR.	Cesium	63-65	P53	Homo sapiens	44-47
16872707-2	2006	It plays a crucial role in p53-dependent cellular response to DNA damage and oxidative stress by providing deoxyribonucleotides (dNTPs) to the DNA repair machinery and by scavenging reactive oxygen species (ROS).	dntps	129-134	P53	Homo sapiens	27-30
17079445-6	2006	The sequential treatment with nutlin-3 alone, followed by transient exposure to nutlin-3 plus gemcitabine, efficiently compromised the clonogenicity of tumor cells with deletions or mutations of p53 but largely spared the proliferation of nontransformed human keratinocytes.	nutlin 3	30-38	P53	Homo sapiens	195-198
17079445-6	2006	The sequential treatment with nutlin-3 alone, followed by transient exposure to nutlin-3 plus gemcitabine, efficiently compromised the clonogenicity of tumor cells with deletions or mutations of p53 but largely spared the proliferation of nontransformed human keratinocytes.	nutlin 3	80-88	P53	Homo sapiens	195-198
20432447-2	2010	This study shows that restriction of tyrosine and phenylalanine (Tyr/Phe), glutamine (Gln), or methionine (Met) differentially modulates glucose metabolism, glycogen synthase kinase 3beta (GSK3beta), p53, and pyruvate dehydrogenase (PDH) in these two cell lines.	Glutamine	75-84	P53	Homo sapiens	200-203
16882877-4	2006	The induction of WI38 cell senescence by Etop was associated with p53 activation and could be attenuated by down-regulation of p53 using alpha-pifithrin (alpha-PFT) or p53 small interference RNA (siRNA).	Etoposide	41-45	P53	Homo sapiens	66-69
16882877-4	2006	The induction of WI38 cell senescence by Etop was associated with p53 activation and could be attenuated by down-regulation of p53 using alpha-pifithrin (alpha-PFT) or p53 small interference RNA (siRNA).	Etoposide	41-45	P53	Homo sapiens	127-130
16882877-4	2006	The induction of WI38 cell senescence by Etop was associated with p53 activation and could be attenuated by down-regulation of p53 using alpha-pifithrin (alpha-PFT) or p53 small interference RNA (siRNA).	Etoposide	41-45	P53	Homo sapiens	127-130
17047058-5	2006	By contrast, etoposide activated p53 and down-regulated hTERT promoter activity in normal cells.	Etoposide	13-22	P53	Homo sapiens	33-36
19951064-8	2010	Hydroxyurea induced GPx1 expression in multiple cultured cell lines in a manner dependent on both p53 and NO-cGMP signaling pathways.	Hydroxyurea	0-11	P53	Homo sapiens	98-101
17040108-9	2006	The cytosine residue of the ACG sequence complementary to codon 273, well-known hotspots of the p53 gene, was cleaved with piperidine and Fpg treatments.	acceleratory factor from growth hormone	28-31	P53	Homo sapiens	96-99
16786570-10	2006	They further suggest that Sps1 and its reaction product selenophosphate might be involved in cancer prevention in a p53-dependent manner and could be applied to development of a novel cancer therapy.	selenophosphate	56-71	P53	Homo sapiens	116-119
16702947-7	2006	Finally, we show that Y276 phosphorylation stimulates interaction with ARF, leading to increased levels of nucleolar Hdm2 and decreased turnover of p53.	y276	22-26	P53	Homo sapiens	148-151
16702947-8	2006	These data establish Y276 as a physiological target of c-Abl that contributes functionally to the induction of p53.	y276	21-25	P53	Homo sapiens	111-114
20446899-2	2010	This study suggested that G2/M cell cycle arrest was triggered by ROS/NO productions with regulations of p53, p21, cell division cycle 25C (Cdc25C), Cdc2 and cyclin B1, which were able to be prevented by protein tyrosine kinase (PTK) activity inhibitor genistein or JNK inhibitor SP600125.	Genistein	253-262	P53	Homo sapiens	105-108
17034127-2	2006	Two of the most potent compounds, 2-benzyl-3-(4-chlorophenyl)-3-(3-hydroxypropoxy)-2,3-dihydroisoindol-1-one (76; IC(50) = 15.9 +/- 0.8 microM) and 3-(4-chlorophenyl)-3-(4-hydroxy-3,5-dimethoxybenzyloxy)-2-propyl-2,3-dihydroisoindol-1-one (79; IC(50) = 5.3 +/- 0.9 microM), induced p53-dependent gene transcription, in a dose-dependent manner, in the MDM2 amplified, SJSA human sarcoma cell line.	2-benzyl-3-(4-chlorophenyl)-3-(3-hydroxypropoxy)-2,3-dihydroisoindol-1-one	34-108	P53	Homo sapiens	282-285
16652373-6	2006	Cases with the XRCC1 codon 399 Gln/Gln genotype were positively associated with the presence of p53 transversions (OR = 4.8; 94% CI = 0.8-30).	Glutamine	31-34	P53	Homo sapiens	96-99
16652373-6	2006	Cases with the XRCC1 codon 399 Gln/Gln genotype were positively associated with the presence of p53 transversions (OR = 4.8; 94% CI = 0.8-30).	Glutamine	35-38	P53	Homo sapiens	96-99
16652373-7	2006	Cases with the XPD codon 751 Gln/Gln genotype were positively associated with the presence of p53 transitions (OR = 2.8; 95% CI = 0.8-9.3), in particular G:C-A:T transitions (OR = 3.7; 95% CI = 1.1-13).	Glutamine	29-32	P53	Homo sapiens	94-97
16652373-7	2006	Cases with the XPD codon 751 Gln/Gln genotype were positively associated with the presence of p53 transitions (OR = 2.8; 95% CI = 0.8-9.3), in particular G:C-A:T transitions (OR = 3.7; 95% CI = 1.1-13).	Glutamine	33-36	P53	Homo sapiens	94-97
20587666-6	2010	Exogenous E1A expression by SDION delivery significantly increased p53 expression, but inhibited HER-2/Neu expression in tumor tissue (P &lt; 0.05).	sdion	28-33	P53	Homo sapiens	67-70
16797759-3	2006	By Western blot, the expression of 14-3-3sigma, p53 and p21 was coordinately upregulated in astrocytes following exposure to hydrogen peroxide, 4-hydroxy-2-nonenal (4-HNE) or etoposide, a topoisomerase II inhibitor.	Etoposide	175-184	P53	Homo sapiens	48-51
16797759-6	2006	Microarray analysis of etoposide-treated astrocytes verified upregulation of p53-responsive genes and concurrent downregulation of mitotic checkpoint-regulatory genes.	Etoposide	23-32	P53	Homo sapiens	77-80
16514420-6	2006	In contrast, NPC death induced by staurosporine, a broad kinase inhibitor, is regulated by p53 in the absence of macromolecular synthesis.	Staurosporine	34-47	P53	Homo sapiens	91-94
20042274-7	2010	The susceptibility to camptothecin-induced apoptosis of A2780 cells was likely p53-dependent but not related to the activation of the ATM pathway.	Camptothecin	22-34	P53	Homo sapiens	79-82
16904205-1	2006	We present evidence that pyrrolidine dithiocarbamate (PDTC) inhibits growth of p53-negative pancreatic adenocarcinoma cell lines via cell cycle arrest in the S-phase, while it has no effect on primary fibroblast proliferation.	pyrrolidine dithiocarbamic acid	25-52	P53	Homo sapiens	79-82
16904205-1	2006	We present evidence that pyrrolidine dithiocarbamate (PDTC) inhibits growth of p53-negative pancreatic adenocarcinoma cell lines via cell cycle arrest in the S-phase, while it has no effect on primary fibroblast proliferation.	pyrrolidine dithiocarbamic acid	54-58	P53	Homo sapiens	79-82
16925398-1	2006	The most potent inhibitor of the p53-MDM2 interaction reported to date is an 8-mer p53 peptide analogue (Novartis peptide), which contains 6-chlorotryptophane (Cl-Trp) and phosphonomethylphenylalanine (Pmp) as key residues for the enhanced activity.	cl-trp	160-166	P53	Homo sapiens	33-36
16925398-1	2006	The most potent inhibitor of the p53-MDM2 interaction reported to date is an 8-mer p53 peptide analogue (Novartis peptide), which contains 6-chlorotryptophane (Cl-Trp) and phosphonomethylphenylalanine (Pmp) as key residues for the enhanced activity.	cl-trp	160-166	P53	Homo sapiens	83-86
16598770-8	2006	The over-expression of p53 protein in the etoposide treated cells indicated a significant level of DNA fragmentation and apoptosis.	Etoposide	42-51	P53	Homo sapiens	23-26
20423286-0	2010	Activation of p53 signaling by MI-63 induces apoptosis in acute myeloid leukemia cells.	MI-63	31-36	P53	Homo sapiens	14-17
16579792-5	2006	The extent of mutant p53(R175H) or p53(F270A) unfolding in cells as defined by exposure of the DO-12 epitope correlates with the extent of hyperubiquitination, suggesting a link between substrate conformation and E3 ligase function.	do-12	95-100	P53	Homo sapiens	21-24
16557586-0	2006	Aflatoxin-B exposure does not lead to p53 mutations but results in enhanced liver cancer of Hupki (human p53 knock-in) mice.	Aflatoxin B1	0-11	P53	Homo sapiens	105-108
16579792-5	2006	The extent of mutant p53(R175H) or p53(F270A) unfolding in cells as defined by exposure of the DO-12 epitope correlates with the extent of hyperubiquitination, suggesting a link between substrate conformation and E3 ligase function.	do-12	95-100	P53	Homo sapiens	35-38
20423286-2	2010	We report that treatment with MI-63, a novel inhibitor of MDM2, activates p53 signaling to induce apoptosis in AML cell lines and primary samples.	MI-63	30-35	P53	Homo sapiens	74-77
16607284-5	2006	We show that p53 synthesis increases dramatically in MCF-7 cells treated with etoposide.	Etoposide	78-87	P53	Homo sapiens	13-16
19781850-7	2010	Taken together, these findings indicate that the p53-mediated mitochondrial pathway and the nuclear translocation of AIF and EndoG play a crucial role in EGCG-induced apoptosis of human laryngeal epidermoid carcinoma Hep2 cells, which proceeds through a caspase-independent pathway.	epigallocatechin gallate	154-158	P53	Homo sapiens	49-52
16500682-6	2006	Treatment with sulforaphane (15 microM), PEITC (10 microM), indole-3-carbinol (10 microM) and 3,3"-diindolylmethane (10 microM) induced PARP cleavage after 24 and 48 h in both 40-16 and the 379.2 cell lines, suggestive of a p53-independent mechanism of apoptosis induction.	3,3'-diindolylmethane	94-115	P53	Homo sapiens	224-227
16818855-10	2006	CONCLUSION: A strong interaction between SNP309 status and tumor p53 status appears to modify the association between p53 status and breast cancer survival.	snp309	41-47	P53	Homo sapiens	65-68
16818855-10	2006	CONCLUSION: A strong interaction between SNP309 status and tumor p53 status appears to modify the association between p53 status and breast cancer survival.	snp309	41-47	P53	Homo sapiens	118-121
20060462-0	2010	Nano-SiO2 induces apoptosis via activation of p53 and Bax mediated by oxidative stress in human hepatic cell line.	Silicon Dioxide	5-9	P53	Homo sapiens	46-49
17041552-7	2006	In this study, nine colorectal carcinoma samples were used to establish a simple and sensitive strategy in the study on in vivo p53 expression by using realtime LightCycler SYBR Green I technology.	sybr green	173-183	P53	Homo sapiens	128-131
16554962-0	2006	Modulation of p53 transcriptional activity by PRIMA-1 and Pifithrin-alpha on staurosporine-induced apoptosis of wild-type and mutated p53 epithelial cells.	Staurosporine	77-90	P53	Homo sapiens	14-17
16154257-3	2006	Here, we report that hydroxyurea treatment induced centrosome amplification in both human fibroblasts expressing the HPV16 -E6-E7 oncoproteins, which act principally by targeting p53 and pRB, respectively, and in conditional pRB deficient mouse fibroblasts.	Hydroxyurea	21-32	P53	Homo sapiens	179-182
16154257-4	2006	Following hydroxyurea removal both normal and p53 deficient human fibroblasts arrested.	Hydroxyurea	10-21	P53	Homo sapiens	46-49
16554962-0	2006	Modulation of p53 transcriptional activity by PRIMA-1 and Pifithrin-alpha on staurosporine-induced apoptosis of wild-type and mutated p53 epithelial cells.	Staurosporine	77-90	P53	Homo sapiens	134-137
21787594-7	2010	Taken together, these data suggested that cell injuries were triggered by the generation of oxidative stress; p53 and p21 mediated G1 phase arrest is a potential mechanistic pathway of silica nanoparticles induced damage in H9c2(2-1) cells.	Silicon Dioxide	185-191	P53	Homo sapiens	110-113
16554962-1	2006	We recently argued for a major role of p53 in staurosporine(ST)-induced apoptosis of immortalized epithelial cells, depending on their p53 status.	Staurosporine	46-59	P53	Homo sapiens	39-42
16554962-1	2006	We recently argued for a major role of p53 in staurosporine(ST)-induced apoptosis of immortalized epithelial cells, depending on their p53 status.	Staurosporine	46-59	P53	Homo sapiens	135-138
16782091-1	2006	The plant homodomain (PHD) of ING2 was shown to regulate p53-dependent apoptosis through phosphoinositides signaling.	Phosphatidylinositols	89-106	P53	Homo sapiens	57-60
19889954-8	2010	Mechanistically, SAHA inhibited and TSA delayed p53 phosphorylation, acetylation, and activation during cisplatin incubation.	trichostatin A	36-39	P53	Homo sapiens	48-51
16986488-9	2006	Immunohistochemical staining with avidin-biotin was performed by using cytokeratin, vimentin, SMA, p53, Bcl 2, EMA, and CD10.	avidin-biotin	34-47	P53	Homo sapiens	99-102
16527552-9	2006	Phospho-ERK1/2, Akt activity and expression of c-Myc were significantly induced by etoposide in a time-dependent manner; moreover, there was a weak effect on the expression of p53 protein.	Etoposide	83-92	P53	Homo sapiens	176-179
19913028-4	2010	Recent structural evidence, however, suggests that DBDs may interact with each other in full-length tetrameric forms of p53.	4,4'-dibenzamido-2,2'-stilbenedisulfonic acid	51-55	P53	Homo sapiens	120-123
16307839-4	2006	Immunoblot assay showed that chalcone significantly decreased the expression of cyclin B1, cyclin A and Cdc2 protein, as well as increased the expression of p21 and p27 in a p53-independent manner, contributing to cell cycle arrest.	Chalcone	29-37	P53	Homo sapiens	174-177
16287077-9	2006	Cells treated with E2 or 4-OHE2 at doses of 0.007 nM and 70 nM and 2-OHE2 only at a higher dose (3.6 microM) exhibited a 5 bp deletion in p53 exon 4.	4-ohe2	25-31	P53	Homo sapiens	138-141
16773206-2	2006	Colony formation assays showed that LY294002 enhanced heat sensitivity in two human lung cancer cell lines; H1299/wild-type p53 (wtp53) and H1299/mutated p53 (mp53) cells.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	36-44	P53	Homo sapiens	124-127
16773206-2	2006	Colony formation assays showed that LY294002 enhanced heat sensitivity in two human lung cancer cell lines; H1299/wild-type p53 (wtp53) and H1299/mutated p53 (mp53) cells.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	36-44	P53	Homo sapiens	131-134
16773206-8	2006	LY294002 appears to be an attractive candidate for a p53-independent heat sensitizer in hyperthermic cancer therapy.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	P53	Homo sapiens	53-56
16824077-9	2006	The most sensitive cell line to 2-ME, SK-Hep1, showed an up-regulation of the p53 and p21 proteins.	2-Methoxyestradiol	32-36	P53	Homo sapiens	78-81
20505264-6	2010	We also observed that TSA-mediated radiosensitization was clearly influenced by p53 and ATM status of cells tested.	trichostatin A	22-25	P53	Homo sapiens	80-83
16474844-9	2006	Trichostatin A abolished the inhibitory effect of wt p53, suggesting the involvement of histone deacetylation in negative regulation of the heparanase promoter.	trichostatin A	0-14	P53	Homo sapiens	53-56
16314959-6	2006	Treatment of cells with TV at 15 microM for 24 h resulted in an increase in the activity of caspase-3, evidenced by colorimetric assay, and a dramatic up-regulation of p53, accompanied with a significant increase of Bax/Bcl-2 ratio, as evidenced by immunofluorescence assay.	tetrazolium violet	24-26	P53	Homo sapiens	168-171
16314959-7	2006	These results suggest that TV induces growth inhibition of C6 cells through p53-midiated apoptotic pathway and G0/G1 checkpoint mechanism.	tetrazolium violet	27-29	P53	Homo sapiens	76-79
16314959-8	2006	Although detailed mechanisms remain to be explored, selective blockage of tumor cells in G0/G1 phase accompanied by p53-associated apoptosis makes tetrazolium violet a promising anticancer agent, meriting further investigations.	Tetrazolium Salts	147-158	P53	Homo sapiens	116-119
19629643-5	2010	Here, we show that four of seven types of DNA damage signals we examined (induction by etoposide, doxorubicin, camptothecin and cisplatin treatment) resulted in significant Apak phosphorylation and dissociation of Apak from p53, releasing the inhibition of p53 transcriptional activity.	Etoposide	87-96	P53	Homo sapiens	224-227
16019139-6	2006	MMC treatment induced a reduction in the expressions of the E6 oncogene and IL-18, in a p53-independent manner.	Mitomycin	0-3	P53	Homo sapiens	88-91
19629643-5	2010	Here, we show that four of seven types of DNA damage signals we examined (induction by etoposide, doxorubicin, camptothecin and cisplatin treatment) resulted in significant Apak phosphorylation and dissociation of Apak from p53, releasing the inhibition of p53 transcriptional activity.	Etoposide	87-96	P53	Homo sapiens	257-260
19629643-5	2010	Here, we show that four of seven types of DNA damage signals we examined (induction by etoposide, doxorubicin, camptothecin and cisplatin treatment) resulted in significant Apak phosphorylation and dissociation of Apak from p53, releasing the inhibition of p53 transcriptional activity.	Camptothecin	111-123	P53	Homo sapiens	224-227
19629643-5	2010	Here, we show that four of seven types of DNA damage signals we examined (induction by etoposide, doxorubicin, camptothecin and cisplatin treatment) resulted in significant Apak phosphorylation and dissociation of Apak from p53, releasing the inhibition of p53 transcriptional activity.	Camptothecin	111-123	P53	Homo sapiens	257-260
16407843-2	2006	We report that defects of p21(CDKN1A) and p53 enhance camptothecin-induced histone H2AX phosphorylation (gammaH2AX), a marker for DNA DSBs.	Camptothecin	54-66	P53	Homo sapiens	42-45
16407843-3	2006	In human colon carcinoma HCT116 cells with wild-type (wt) p53, gammaH2AX reverses after camptothecin removal.	Camptothecin	88-100	P53	Homo sapiens	58-61
16498393-3	2006	All tested thimidine-containing PS-ODN, irrespective of their primary sequences, reduced the expression of Bcl-2 protein and increased the levels of the proapoptotic molecules p53, Bid, Bax in CLL cells.	thimidine	11-20	P53	Homo sapiens	176-179
16537920-0	2006	Acetylation of p53 at lysine 373/382 by the histone deacetylase inhibitor depsipeptide induces expression of p21(Waf1/Cip1).	Depsipeptides	74-86	P53	Homo sapiens	15-18
20053762-7	2010	This compound abrogates an etoposide-induced G(2) arrest with an IC(50) of 55 nmol/L in HT29 cells, and significantly enhances the cell killing of gemcitabine and SN38 by 3.0- to 29-fold in several colon tumor lines in vitro and in a p53-dependent fashion.	Etoposide	27-36	P53	Homo sapiens	234-237
16537920-2	2006	Here we found that an inhibitor of HDAC, depsipeptide (FR901228), but not trichostatin A (TSA), induces p21(Waf1/Cip1) expression through both p53 and Sp1/Sp3 pathways in A549 cells (which retain wild-type p53).	Depsipeptides	41-53	P53	Homo sapiens	143-146
16537920-2	2006	Here we found that an inhibitor of HDAC, depsipeptide (FR901228), but not trichostatin A (TSA), induces p21(Waf1/Cip1) expression through both p53 and Sp1/Sp3 pathways in A549 cells (which retain wild-type p53).	Depsipeptides	41-53	P53	Homo sapiens	206-209
16537920-2	2006	Here we found that an inhibitor of HDAC, depsipeptide (FR901228), but not trichostatin A (TSA), induces p21(Waf1/Cip1) expression through both p53 and Sp1/Sp3 pathways in A549 cells (which retain wild-type p53).	romidepsin	55-63	P53	Homo sapiens	143-146
16537920-2	2006	Here we found that an inhibitor of HDAC, depsipeptide (FR901228), but not trichostatin A (TSA), induces p21(Waf1/Cip1) expression through both p53 and Sp1/Sp3 pathways in A549 cells (which retain wild-type p53).	romidepsin	55-63	P53	Homo sapiens	206-209
16537920-8	2006	Furthermore, activity associated with the binding of the acetylated p53 at K373/K382 to the p21 promoter as well as p21(Waf1/Cip1) expression is significantly increased after depsipeptide treatment, as tested by chromatin immunoprecipitations and Western blotting, respectively.	Depsipeptides	175-187	P53	Homo sapiens	68-71
16537920-9	2006	In addition, p53 acetylation at K373/K382 is confirmed to be required for recruitment of p300 to the p21 promoter, and the depsipeptide-induced p53 acetylation at K373/K382 is unlikely to be dependent on p53 phosphorylation at Ser15, Ser20, and Ser392 sites.	Depsipeptides	123-135	P53	Homo sapiens	13-16
16537920-9	2006	In addition, p53 acetylation at K373/K382 is confirmed to be required for recruitment of p300 to the p21 promoter, and the depsipeptide-induced p53 acetylation at K373/K382 is unlikely to be dependent on p53 phosphorylation at Ser15, Ser20, and Ser392 sites.	Depsipeptides	123-135	P53	Homo sapiens	144-147
16537920-9	2006	In addition, p53 acetylation at K373/K382 is confirmed to be required for recruitment of p300 to the p21 promoter, and the depsipeptide-induced p53 acetylation at K373/K382 is unlikely to be dependent on p53 phosphorylation at Ser15, Ser20, and Ser392 sites.	Depsipeptides	123-135	P53	Homo sapiens	144-147
16537920-10	2006	Our data suggest that p53 acetylation at K373/K382 plays an important role in depsipeptide-induced p21(Waf1/Cip1) expression.	Depsipeptides	78-90	P53	Homo sapiens	22-25
16827139-7	2006	ZBP-89 potentiated p53-mediated cell death with 10 nM staurosporine and 100 nM etoposide, but did not in the presence of the R273H p53 mutation.	Staurosporine	54-67	P53	Homo sapiens	19-22
16827139-7	2006	ZBP-89 potentiated p53-mediated cell death with 10 nM staurosporine and 100 nM etoposide, but did not in the presence of the R273H p53 mutation.	Etoposide	79-88	P53	Homo sapiens	19-22
16458489-2	2006	To investigate the possible mechanism of oxymatrine"s role on cancer cells, in the present study, we examined further the effects of oxymatrine on the growth, proliferation, apoptosis and expression of bcl-2 and p53 gene in human hepatoma SMMC-7721 cells in vitro.	oxymatrine	41-51	P53	Homo sapiens	212-215
16458489-2	2006	To investigate the possible mechanism of oxymatrine"s role on cancer cells, in the present study, we examined further the effects of oxymatrine on the growth, proliferation, apoptosis and expression of bcl-2 and p53 gene in human hepatoma SMMC-7721 cells in vitro.	oxymatrine	133-143	P53	Homo sapiens	212-215
16458489-6	2006	Oxymatrine induce apoptosis of SMMC-7721 cells and apoptotic rate amount to about 60% after treatment with 1.0 mg/ml oxymatrine for 48 h. We also find that oxymatrine down-regulate expression of bcl-2 gene while up-regulate expression of p53 gene.	oxymatrine	0-10	P53	Homo sapiens	238-241
16458489-6	2006	Oxymatrine induce apoptosis of SMMC-7721 cells and apoptotic rate amount to about 60% after treatment with 1.0 mg/ml oxymatrine for 48 h. We also find that oxymatrine down-regulate expression of bcl-2 gene while up-regulate expression of p53 gene.	oxymatrine	117-127	P53	Homo sapiens	238-241
16458489-6	2006	Oxymatrine induce apoptosis of SMMC-7721 cells and apoptotic rate amount to about 60% after treatment with 1.0 mg/ml oxymatrine for 48 h. We also find that oxymatrine down-regulate expression of bcl-2 gene while up-regulate expression of p53 gene.	oxymatrine	156-166	P53	Homo sapiens	238-241
20429622-2	2010	A combination of camptothecin and etoposide (1 microg/ml + 10 microg/ml) proved to be efficient in both types of cell lines, although mutant p53 cells exhibited a higher resistance.	Camptothecin	17-29	P53	Homo sapiens	141-144
16458489-7	2006	These results demonstrate that oxymatrine inhibit the proliferation and induce apoptosis of human hepatoma SMMC-7721 cells, and suggest that this effect was mediated probably by a significant cell cycle blockage in G2/M and S phase, down-regulation of bcl-2 and up-regulation of p53.	oxymatrine	31-41	P53	Homo sapiens	279-282
16325212-0	2006	The p33ING1b tumor suppressor cooperates with p53 to induce apoptosis in response to etoposide in human osteosarcoma cells.	Etoposide	85-94	P53	Homo sapiens	46-49
16325212-4	2006	p33ING1b increased etoposide-induced growth inhibition and apoptosis to a much greater degree in p53+/+ U2OS cells than in p53-mutant MG63 cells.	Etoposide	19-28	P53	Homo sapiens	97-100
16410370-7	2006	Aflatoxin B1, hepatitis B virus, hepatitis C virus, and vinyl chloride all caused TP53 mutations in human liver tumors, but the mutation spectrum for each agent differed.	Aflatoxin B1	0-12	P53	Homo sapiens	82-86
20661829-0	2010	Protection of p53 wild type cells from taxol by genistein in the combined treatment of lung cancer.	Genistein	48-57	P53	Homo sapiens	14-17
16344270-9	2006	Violacein causes cell cycle block at G(1), upregulates p53, p27 and p21 levels and decreases the expression of cyclin D1.	violacein	0-9	P53	Homo sapiens	55-58
19996219-10	2009	SNP309 was significantly associated with increased sensitivity to alkylating agents and topoisomerase I inhibitors in the cells with wild-type TP53.	snp309	0-6	P53	Homo sapiens	143-147
16302260-3	2006	We recently identified a synthetic thiazolidin compound, 5-(2,4-dihydroxybenzylidene)-2-(phenylimino)-1,3-thiazolidione (DBPT), that induces apoptosis in human colon cancer cells, independent of p53 and P-glycoprotein status.	5-(2,4-dihydroxybenzylidene)-2-(phenylimino)-1,3-thiazolidione	57-119	P53	Homo sapiens	195-198
16325212-6	2006	Together, our data indicate that p33ING1b prominently enhances etoposide-induced apoptosis through p53-dependent pathways in human osteosarcoma cells.	Etoposide	63-72	P53	Homo sapiens	99-102
16378598-3	2006	Although a PI3 kinase inhibitor, LY294002, by itself does not induce apoptotic cell death, LY294002 selectively and markedly enhances the apoptosis-inducing efficacy of doxorubicin: such an enhanced cell death is only detected in tumor cells in which the PI3 kinase/Akt pathway is constitutively activated, and it is totally dependent on the functional p53 pathway.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	91-99	P53	Homo sapiens	353-356
16478747-2	2006	SNP309 induces an increase in the level of Mdm2 protein, which causes attenuation of the p53 pathway.	snp309	0-6	P53	Homo sapiens	89-92
16319068-4	2006	We had found that treatment of cells with camptothecin, a topoisomerase 1 inhibitor, led to the export of prohibitin and p53 from the nucleus to the mitochondria.	Camptothecin	42-54	P53	Homo sapiens	121-124
19751709-8	2009	This effect correlated with lowered basal levels of p53, as well as with an attenuated p53 response induced by etoposide and leptomycin B.	Etoposide	111-120	P53	Homo sapiens	87-90
16271357-0	2006	Erybraedin C and bitucarpin A, two structurally related pterocarpans purified from Bituminaria bituminosa, induced apoptosis in human colon adenocarcinoma cell lines MMR- and p53-proficient and -deficient in a dose-, time-, and structure-dependent fashion.	erybraedin C	0-12	P53	Homo sapiens	175-178
16271357-8	2006	Erybraedin C similarly affects the survival of HT29 (MMR +/+, p53 -/- and Bcl-2 +/+) and LoVo (MMR -/-, p53 +/+ and Bcl-2 -/-) cells (LD(50): 1.94 and 1.73 microg/ml, respectively).	erybraedin C	0-12	P53	Homo sapiens	62-65
16271357-8	2006	Erybraedin C similarly affects the survival of HT29 (MMR +/+, p53 -/- and Bcl-2 +/+) and LoVo (MMR -/-, p53 +/+ and Bcl-2 -/-) cells (LD(50): 1.94 and 1.73 microg/ml, respectively).	erybraedin C	0-12	P53	Homo sapiens	104-107
16513842-11	2006	The synergistic effect of simultaneous treatment with trichostatin A and doxorubicin is mediated via inhibition of AR expression, induction of protease activity, increased expression of p53, and proteolysis of p21.	trichostatin A	54-68	P53	Homo sapiens	186-189
16434701-1	2006	The main regulator of the human tumor suppresser gene p21(waf1/cip1) is the transcription factor p53, but more recently it has been suggested to be a primary anti-proliferative target for the nuclear receptor VDR in the presence of its ligand 1alpha,25-dihydroxyvitamin D3 (1alpha,25(OH)2D3).	25-dihydroxyvitamin d3	250-272	P53	Homo sapiens	97-100
19345001-3	2009	Aflatoxin B1, the most commonly occurring and potent of the aflatoxins is associated with a specific AGG to AGT transversion mutation at codon 249 of the p53 gene in human HCC, providing mechanistic support to a causal link between exposure and disease.	Aflatoxin B1	0-12	P53	Homo sapiens	154-157
16341031-0	2006	The p53 family inhibitor DeltaNp73 interferes with multiple developmental programs.	deltanp73	25-34	P53	Homo sapiens	4-7
16580789-3	2006	Moreover, oxidative stress by reactive oxygen species (ROS) such as the hydroxyl radical (*OH) produced by ionizing radiation (carcinogenic) triggers p53 activation in response to the damage of DNA (followed by initiation of DNA-repair mechanisms).	Hydroxyl Radical	72-88	P53	Homo sapiens	150-153
16432175-0	2006	Benzodiazepinedione inhibitors of the Hdm2:p53 complex suppress human tumor cell proliferation in vitro and sensitize tumors to doxorubicin in vivo.	benzodiazepinedione	0-19	P53	Homo sapiens	43-46
16219768-4	2005	Here, we determined that UV light, anisomycin, etoposide, and hypoxic stress rapidly induced phosphorylation of p53 at Ser46 and WOX1 at Tyr33 (phospho-WOX1) and their binding interactions in several tested cancer cells.	Etoposide	47-56	P53	Homo sapiens	112-115
16413759-2	2006	In order to identify new p53 downstream genes, we established a new system of p53 gene inducible expression, U251-pTet-p53 cell line, with the Tet-On Gene Expression System, in which exogenous p53 gene could overexpress in doxycycline (Dox) medium but not in the medium without Dox.	tetramethylenedisulfotetramine	115-118	P53	Homo sapiens	78-81
16467109-6	2006	Interestingly, radiosensitization by TSA in cell lines expressing p53 was more pronounced than in isogenic lines lacking p53.	trichostatin A	37-40	P53	Homo sapiens	66-69
16467109-7	2006	Radiosensitization of cells expressing p53 by TSA was reduced by pifithrin-alpha, a small-molecule inhibitor of p53.	trichostatin A	46-49	P53	Homo sapiens	39-42
16467109-7	2006	Radiosensitization of cells expressing p53 by TSA was reduced by pifithrin-alpha, a small-molecule inhibitor of p53.	trichostatin A	46-49	P53	Homo sapiens	112-115
19715480-0	2009	p53 gene expression and 2-methoxyestradiol treatment differentially induce nuclear factor kappa B activation in human lung cancer cells with different p53 phenotypes.	2-Methoxyestradiol	24-42	P53	Homo sapiens	151-154
16467399-5	2006	In JAR cells, etoposide increased expression of the proteins including IFNgammaR, p53 and pro-caspase 3 as well as IRF-1 mRNA and IFNgamma-pretreatment apparently promoted up-regulation of these molecules expression.	Etoposide	14-23	P53	Homo sapiens	82-85
19715480-4	2009	We show that expression of wt-p53 from a recombinant adenovirus-p53 followed by treatment with 2-methoxyestradiol (2-ME), an endogenous, nontoxic, estrogenic metabolite, resulted in differential NF-kappaB activation and inhibitor kappaB alpha (IkappaB-alpha) degradation in three different human lung cancer cell lines with different p53 phenotypes.	2-Methoxyestradiol	95-113	P53	Homo sapiens	30-33
19715480-4	2009	We show that expression of wt-p53 from a recombinant adenovirus-p53 followed by treatment with 2-methoxyestradiol (2-ME), an endogenous, nontoxic, estrogenic metabolite, resulted in differential NF-kappaB activation and inhibitor kappaB alpha (IkappaB-alpha) degradation in three different human lung cancer cell lines with different p53 phenotypes.	2-Methoxyestradiol	95-113	P53	Homo sapiens	64-67
15933740-0	2005	The PI3K inhibitor LY294002 prevents p53 induction by DNA damage and attenuates chemotherapy-induced apoptosis.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	19-27	P53	Homo sapiens	37-40
19715480-4	2009	We show that expression of wt-p53 from a recombinant adenovirus-p53 followed by treatment with 2-methoxyestradiol (2-ME), an endogenous, nontoxic, estrogenic metabolite, resulted in differential NF-kappaB activation and inhibitor kappaB alpha (IkappaB-alpha) degradation in three different human lung cancer cell lines with different p53 phenotypes.	2-Methoxyestradiol	95-113	P53	Homo sapiens	64-67
15933740-5	2005	We report here that exposure to LY294002, a potent PI3K inhibitor, aborts the activation of p53 by several drugs commonly used in cancer chemotherapy.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	32-40	P53	Homo sapiens	92-95
19715480-4	2009	We show that expression of wt-p53 from a recombinant adenovirus-p53 followed by treatment with 2-methoxyestradiol (2-ME), an endogenous, nontoxic, estrogenic metabolite, resulted in differential NF-kappaB activation and inhibitor kappaB alpha (IkappaB-alpha) degradation in three different human lung cancer cell lines with different p53 phenotypes.	2-Methoxyestradiol	115-119	P53	Homo sapiens	30-33
15933740-6	2005	Concomitantly, LY294002 attenuates p53-dependent, chemotherapy-induced apoptosis of cancer cells.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	15-23	P53	Homo sapiens	35-38
16280384-0	2006	Aflatoxin B1 alters the expression of p53 in cytochrome P450-expressing human lung cells.	Aflatoxin B1	0-12	P53	Homo sapiens	38-41
16280384-2	2006	Mutations (and altered expression) of the tumor suppresser gene p53 have been observed in liver tumors from patients exposed to high dietary AFB1.	Aflatoxin B1	141-145	P53	Homo sapiens	64-67
16280384-4	2006	We examined the effects of low concentrations of AFB1 on the expression of p53 and MDM2 in human bronchial epithelial cells (BEAS-2B) transfected with cDNA for either cytochrome P450 (CYP) 1A2 (B-CMV1A2) or CYP 3A4 (B3A4), two isozymes that are responsible for AFB1 activation in human liver and possibly the lung.	Aflatoxin B1	49-53	P53	Homo sapiens	75-78
19715480-4	2009	We show that expression of wt-p53 from a recombinant adenovirus-p53 followed by treatment with 2-methoxyestradiol (2-ME), an endogenous, nontoxic, estrogenic metabolite, resulted in differential NF-kappaB activation and inhibitor kappaB alpha (IkappaB-alpha) degradation in three different human lung cancer cell lines with different p53 phenotypes.	2-Methoxyestradiol	115-119	P53	Homo sapiens	64-67
16430208-7	2006	Flow cytometry results and transfection assays indicated that tetravalent decaarginyl peptides (10R-p53(tet) and NLS-10R-p53(tet)) were the peptides most efficiently routed into cells.	tetramethylenedisulfotetramine	62-65	P53	Homo sapiens	100-103
20025574-0	2009	Association of p53 with Bid induces cell death in response to etoposide treatment in hepatocellular carcinoma.	Etoposide	62-71	P53	Homo sapiens	15-18
16430208-7	2006	Flow cytometry results and transfection assays indicated that tetravalent decaarginyl peptides (10R-p53(tet) and NLS-10R-p53(tet)) were the peptides most efficiently routed into cells.	tetramethylenedisulfotetramine	62-65	P53	Homo sapiens	121-124
16298862-8	2005	PBN pre-treated cells showed significant inhibition of apoptotic features such as activation of caspase-3, up-regulation of Bax and p53, and down-regulation of Bcl-2 compared to control cells upon exposure to ionizing radiation.	phenyl-N-tert-butylnitrone	0-3	P53	Homo sapiens	132-135
20025574-6	2009	Here, we showed that etoposide-induced DNA damage could significantly induce p53 and Bid nuclear export.	Etoposide	21-30	P53	Homo sapiens	77-80
20025574-7	2009	When cells were stimulated by etoposide, p53 could, through the association with Bid, cause translocation of Bid from the nucleus to the cytoplasm and on to its ultimate location in the mitochondria.	Etoposide	30-39	P53	Homo sapiens	41-44
17080554-7	2006	These results suggest that EGCG may have an inhibitory effect on UVB-induced photo-damage and apoptosis by blocking the cytokine secretion and the mRNA expressions of p53, p21 and c-fos genes.	epigallocatechin gallate	27-31	P53	Homo sapiens	167-170
16170329-6	2005	Methyl jasmonate induced mostly apoptotic death in the wt p53-expressing cells, while no signs of early apoptosis were detected in mutant p53-expressing cells.	methyl jasmonate	0-16	P53	Homo sapiens	58-61
20025574-8	2009	p53 was physically associated with Bid, and both p53 and Bid cooperatively promoted cell death induced by etoposide.	Etoposide	106-115	P53	Homo sapiens	0-3
20025574-8	2009	p53 was physically associated with Bid, and both p53 and Bid cooperatively promoted cell death induced by etoposide.	Etoposide	106-115	P53	Homo sapiens	49-52
20025574-10	2009	These findings reveal a novel mechanism by which p53 is associated with Bid in the nucleus to facilitate exportation of Bid to the mitochondria and induce apoptosis in response to etoposide-induced DNA damage in HCC.	Etoposide	180-189	P53	Homo sapiens	49-52
16374552-2	2006	We have now investigated whether these parameters influence susceptibility to okadaic acid induced cell death in EGF-receptor overexpressing mutant p53 A431 human carcinoma.	Okadaic Acid	78-90	P53	Homo sapiens	148-151
16374552-3	2006	Exposure of these cells to 20 nM okadaic acid induced apoptosis-associated caspase 3 activation, DNA fragmentation, cleavage of Poly ADP-Ribose Polymerase (PARP), p53-independent expression of pro-apoptotic bax, and loss of proliferation-promoting cyclin D1.	Okadaic Acid	33-45	P53	Homo sapiens	163-166
16007163-4	2005	Blocking AKT with the PI3K/AKT inhibitor LY294002 or AKT SiRNA prevented NF-kappaB activation and inhibition of p53.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	41-49	P53	Homo sapiens	112-115
19641144-3	2009	Here we demonstrate for the first time increased DNA damage via 8-oxoguanine in the skin and plasma in association with epidermal up-regulated phosphorylated/acetylated p53 and high levels of the p53 antagonist p76(MDM2).	8-hydroxyguanine	64-76	P53	Homo sapiens	169-172
16007163-5	2005	Treatment of C81 cells with LY294002 resulted in an increase in the p53-responsive gene MDM2, suggesting a role for AKT in the Tax-mediated regulation of p53 transcriptional activity.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	28-36	P53	Homo sapiens	68-71
16007163-5	2005	Treatment of C81 cells with LY294002 resulted in an increase in the p53-responsive gene MDM2, suggesting a role for AKT in the Tax-mediated regulation of p53 transcriptional activity.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	28-36	P53	Homo sapiens	154-157
16007163-6	2005	Further, we show that LY294002 treatment of C81 cells abrogates in vitro IKKbeta phosphorylation of p65 and causes a reduction of p65 Ser-536 phosphorylation in vivo, steps critical to p53 inhibition.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	22-30	P53	Homo sapiens	185-188
17113242-1	2006	INTRODUCTION: The most frequent mutation in human hepatocellular carcinoma (HCC) in populations exposed to a high dietary intake of aflatoxin B1 (AFB1) is a mutation in codon 249 of the p53 gene.	Aflatoxin B1	132-144	P53	Homo sapiens	186-189
17113242-1	2006	INTRODUCTION: The most frequent mutation in human hepatocellular carcinoma (HCC) in populations exposed to a high dietary intake of aflatoxin B1 (AFB1) is a mutation in codon 249 of the p53 gene.	Aflatoxin B1	146-150	P53	Homo sapiens	186-189
17113242-3	2006	We hypothesized that the combination of schistosomiasis and aflatoxin B1 increases the incidence of p53 gene mutation.	Aflatoxin B1	60-72	P53	Homo sapiens	100-103
19641144-3	2009	Here we demonstrate for the first time increased DNA damage via 8-oxoguanine in the skin and plasma in association with epidermal up-regulated phosphorylated/acetylated p53 and high levels of the p53 antagonist p76(MDM2).	8-hydroxyguanine	64-76	P53	Homo sapiens	196-199
17113242-8	2006	CONCLUSION: These data suggest that schistosomiasis and exposure to aflatoxin B1 act synergistically to increase the incidence of p53 gene mutation.	Aflatoxin B1	68-80	P53	Homo sapiens	130-133
16227412-8	2005	The recruitment of the p53-dependent apoptosis pathway was suggested by the up-regulation of p53, p21, Bax, DR-4, DR-5, and p53 phosphorylated on Ser15; down-regulation of Bcl-2; and activation of caspase-8, -9, -7, and -3 in cells treated with 100 nmol/L WMC-79.	wmc	256-259	P53	Homo sapiens	23-26
21160963-4	2009	In both the BilIN and IPNB series, the expression of p21, p53, and cyclin D1 was upregulated with histological progression.	Bile Pigments	12-17	P53	Homo sapiens	58-61
21160963-5	2009	Interestingly, p53 expression was upregulated at the invasive stage of BilIN, but was low in noninvasive BilIN, while p53 expression was upregulated in IPN-B1 and reached a plateau in IPN-B2 and invasive ICC.	Bile Pigments	71-76	P53	Homo sapiens	15-18
20157557-0	2009	Reduced transcriptional activity in the p53 pathway of senescent cells revealed by the MDM2 antagonist nutlin-3.	nutlin 3	103-111	P53	Homo sapiens	40-43
16200332-6	2005	The expression of p53 was demonstrated using the avidin-biotin complex immunoperoxidase method and the monoclonal antibody DO7.	avidin-biotin	49-62	P53	Homo sapiens	18-21
16141004-3	2005	SNP309 was shown to result, via Sp1, in higher levels of MDM2 RNA and protein, and subsequent attenuation of the p53 pathway.	snp309	0-6	P53	Homo sapiens	113-116
16403018-7	2006	DNA adducts of trans-PtHMP also reduce the affinity of the p53 protein to its consensus DNA sequence.	trans-PtCl(2)NH(3)(4-hydroxymethylpyridine)	15-26	P53	Homo sapiens	59-62
16354677-5	2006	Acetyl-p53 was also increased by the histone deacetylase (HDAC) class I/II inhibitor trichostatin A (TSA).	trichostatin A	85-99	P53	Homo sapiens	7-10
16354677-5	2006	Acetyl-p53 was also increased by the histone deacetylase (HDAC) class I/II inhibitor trichostatin A (TSA).	trichostatin A	101-104	P53	Homo sapiens	7-10
16354677-6	2006	EX-527 and TSA acted synergistically to increase acetyl-p53 levels, confirming that p53 acetylation is regulated by both SIRT1 and HDACs.	trichostatin A	11-14	P53	Homo sapiens	56-59
16260623-3	2005	Compared to vector-transfected cells, H1299 cells expressing mutant p53 showed a survival advantage when treated with etoposide, a common chemotherapeutic agent; however, cells expressing the transactivation-deficient triple mutant p53-D281G (L22Q/W23S) had significantly lower resistance to etoposide.	Etoposide	118-127	P53	Homo sapiens	68-71
16177561-1	2005	CP-31398 activates wild-type p53 by a novel mechanism that does not involve phosphorylation of the amino-terminus of p53 and disassociation of MDM2.	CP 31398	0-8	P53	Homo sapiens	29-32
16177561-2	2005	To identify more potent CP-31398-like p53 activators, we synthesized 4 acridine derivatives with a similar structure to CP-31398.	CP 31398	24-32	P53	Homo sapiens	38-41
16177561-2	2005	To identify more potent CP-31398-like p53 activators, we synthesized 4 acridine derivatives with a similar structure to CP-31398.	CP 31398	120-128	P53	Homo sapiens	38-41
16260623-3	2005	Compared to vector-transfected cells, H1299 cells expressing mutant p53 showed a survival advantage when treated with etoposide, a common chemotherapeutic agent; however, cells expressing the transactivation-deficient triple mutant p53-D281G (L22Q/W23S) had significantly lower resistance to etoposide.	Etoposide	292-301	P53	Homo sapiens	68-71
16260623-6	2005	Treatment of H1299 cells expressing p53-R175H with small interfering RNA specific for NF-kappaB2 made these cells more sensitive to etoposide.	Etoposide	132-141	P53	Homo sapiens	36-39
16048565-1	2005	BACKGROUND AND AIMS: A specific mutation at codon 249 of the p53 tumor suppressor gene (guanine to thymine; arginine to serine [249(serine)p53]) is present in the cell-free plasma of 30-47% of patients with hepatocellular carcinoma (HCC) in regions with uniformly high levels of dietary exposure to the fungal toxin, aflatoxin B(1).	Aflatoxin B1	317-328	P53	Homo sapiens	61-64
19584398-9	2009	However, in p53-null K562 cells, phorbol esters induce miR-34a expression independently of p53 by activating an alternative phorbol ester-responsive promoter to produce a longer pri-miR-34a transcript.	Phorbol Esters	33-47	P53	Homo sapiens	12-15
16048565-1	2005	BACKGROUND AND AIMS: A specific mutation at codon 249 of the p53 tumor suppressor gene (guanine to thymine; arginine to serine [249(serine)p53]) is present in the cell-free plasma of 30-47% of patients with hepatocellular carcinoma (HCC) in regions with uniformly high levels of dietary exposure to the fungal toxin, aflatoxin B(1).	Aflatoxin B1	317-328	P53	Homo sapiens	139-142
16048565-9	2005	CONCLUSIONS: The 249(serine)p53 mutation is found less often in the serum of patients with HCC in a region with variable levels of exposure to aflatoxin B(1) than in those with uniformly high levels of exposure, but the mutation does occur in black Africans with presumed lower levels of exposure to the fungal toxin.	Aflatoxin B1	143-154	P53	Homo sapiens	28-31
15833387-0	2005	Liriodenine inhibits the proliferation of human hepatoma cell lines by blocking cell cycle progression and nitric oxide-mediated activation of p53 expression.	liriodenine	0-11	P53	Homo sapiens	143-146
19584398-9	2009	However, in p53-null K562 cells, phorbol esters induce miR-34a expression independently of p53 by activating an alternative phorbol ester-responsive promoter to produce a longer pri-miR-34a transcript.	Phorbol Esters	33-46	P53	Homo sapiens	12-15
15833387-2	2005	This study was designed to assess cell cycle arrest, the production of nitric oxide (NO) and p53 expression in liriodenine-treated human hepatoma cell lines, including wild-type p53 (Hep G2 and SK-Hep-1).	liriodenine	111-122	P53	Homo sapiens	93-96
15970518-6	2005	Interestingly, we have found that DTX reduces the expression of mutated p53 in HT-29 and increases the expression of wild type in KB and HCC1937 cells.	Digitoxigenin	34-37	P53	Homo sapiens	72-75
15970518-7	2005	Moreover, DTX reduces ubiquitination of the wild type p53 in KB and HCC1937 cells and increases the ubiquitin-conjugated form of mutated p53 in HT-29 cells.	Digitoxigenin	10-13	P53	Homo sapiens	54-57
16277093-0	2005	Expression of p53 protein and DNA flow cytometry in gastric adenocarcinoma: implications in patients treated with adjuvant etoposide, adriamycin and cisplatin.	Etoposide	123-132	P53	Homo sapiens	14-17
15970518-7	2005	Moreover, DTX reduces ubiquitination of the wild type p53 in KB and HCC1937 cells and increases the ubiquitin-conjugated form of mutated p53 in HT-29 cells.	Digitoxigenin	10-13	P53	Homo sapiens	137-140
19541822-0	2009	Forodesine has high antitumor activity in chronic lymphocytic leukemia and activates p53-independent mitochondrial apoptosis by induction of p73 and BIM.	forodesine	0-10	P53	Homo sapiens	85-88
16093994-0	2005	Differential regulation of p21waf-1/cip-1 and Mdm2 by etoposide: etoposide inhibits the p53-Mdm2 autoregulatory feedback loop.	Etoposide	54-63	P53	Homo sapiens	88-91
15958570-4	2005	Sublethal concentrations of camptothecin reduced the IC50 of agonistic anti-Fas antibody (CH-11) 10-fold, from 500 to 50 ng/mL, in human U87 glioblastoma cells (p53 wild-type).	Camptothecin	28-40	P53	Homo sapiens	161-164
15958570-4	2005	Sublethal concentrations of camptothecin reduced the IC50 of agonistic anti-Fas antibody (CH-11) 10-fold, from 500 to 50 ng/mL, in human U87 glioblastoma cells (p53 wild-type).	4-dimethylamino-3',4'-dimethoxychalcone	90-95	P53	Homo sapiens	161-164
19541822-7	2009	Forodesine induces transcriptional up-regulation of p73, a p53-related protein able to overcome the resistance to apoptosis of CLL cells lacking functional p53.	forodesine	0-10	P53	Homo sapiens	59-62
19541822-9	2009	In conclusion, forodesine induces apoptosis of CLL cells bypassing the DNA-damage/ATM/p53 pathway and might represent a novel chemotherapeutic approach that deserves clinical investigation.	forodesine	15-25	P53	Homo sapiens	86-89
19488905-2	2009	Etoposide initiated DNA-damage signaling via ATM kinase and activated p53 pathway and caspase-2.	Etoposide	0-9	P53	Homo sapiens	70-73
15896459-0	2005	Etoposide (VP-16) elicits apoptosis following prolonged G2-M cell arrest in p53-mutated human non-small cell lung cancer cells.	Etoposide	0-9	P53	Homo sapiens	76-79
15896459-1	2005	In this work, we described the proliferation of human non-small-cell-lung-cancer (NSCLC) cells H1437 harboring p53 alleles (proline-267) can be inhibited by low-dosage topoisomerase II inhibitor etoposide (VP-16) in vitro and in vivo.	Etoposide	195-204	P53	Homo sapiens	111-114
16120219-7	2005	Both etoposide and CLP induced an accumulation of p53 protein and upregulation of p53 transcriptional target genes.	Etoposide	5-14	P53	Homo sapiens	50-53
16120219-7	2005	Both etoposide and CLP induced an accumulation of p53 protein and upregulation of p53 transcriptional target genes.	Etoposide	5-14	P53	Homo sapiens	82-85
19406223-0	2009	Identification of epigallocatechin-3-gallate in green tea polyphenols as a potent inducer of p53-dependent apoptosis in the human lung cancer cell line A549.	epigallocatechin gallate	18-44	P53	Homo sapiens	93-96
16157026-6	2005	RT-PCR method was employed to detect the influence of EGCG on the expressions of hTERT, c-myc, p53 and mad1 genes in sensitive cancer cell line.	epigallocatechin gallate	54-58	P53	Homo sapiens	95-98
16157026-11	2005	After EGCG administration, the expression of hTERT and c-myc genes in MKN45 cells was decreased, that of the mad1 gene increased, and that of the p53 gene unchanged.	epigallocatechin gallate	6-10	P53	Homo sapiens	146-149
15941720-4	2005	Here, we report for the first time that during recovery from hydroxyurea treatment, the S100A2 protein translocated from the cytoplasm to the nucleus and co-localized with the tumor suppressor p53 in two different oral carcinoma cells (FADU and SCC-25).	Hydroxyurea	61-72	P53	Homo sapiens	193-196
15856030-6	2005	Using isogenic colon cancer cell lines that differ only by the presence of the mutant Ras allele, HCT116 and Hke-3 cells, we demonstrated that signaling by oncogenic Ras promotes both accumulation of p53 and its phosphorylation on serine15 in response to 5-FU, a situation that favors apoptosis over growth arrest.	serine15	231-239	P53	Homo sapiens	200-203
15892716-4	2005	We have studied the cellular effects of trichostatin A (TSA), a HDAC inhibitor, in a panel of melanoma cell lines and its mechanism of action in relation to p53.	trichostatin A	40-54	P53	Homo sapiens	157-160
15892716-5	2005	TSA stabilized wild-type p53, but p53 protein accumulation was overridden by simultaneous downregulation of p53 mRNA leading to a decrease in p53 protein.	trichostatin A	0-3	P53	Homo sapiens	25-28
19406223-6	2009	EGCg was a more potent inducer of p53-dependent transcription, and this induction was further supported by the induced level of p53 protein.	epigallocatechin gallate	0-4	P53	Homo sapiens	34-37
19406223-6	2009	EGCg was a more potent inducer of p53-dependent transcription, and this induction was further supported by the induced level of p53 protein.	epigallocatechin gallate	0-4	P53	Homo sapiens	128-131
15688418-2	2005	Sodium butyrate (NaB), a histone deacetylase inhibitor, has been shown to cause a G(1) cell cycle arrest by inducing p21(WAF1/CIP1) in a p53-independent manner.	nab	17-20	P53	Homo sapiens	137-140
19406223-7	2009	RNA interference (RNAi)-mediated p53 knockdown completely abolished EGCg-induced apoptosis.	epigallocatechin gallate	68-72	P53	Homo sapiens	33-36
15688418-3	2005	In this report, we present evidence for activation of p53 pathway by NaB and its role in the NaB-mediated growth suppression.	nab	69-72	P53	Homo sapiens	54-57
15905168-4	2005	Cellular levels of the p21(waf1/cip1) protein and p21(waf1/cip1) mRNA were increased through a p53-independent pathway, possibly because of the stabilization of p21(waf1/cip1) mRNA in chloramphenicol-treated cells.	Chloramphenicol	184-199	P53	Homo sapiens	95-98
15688418-3	2005	In this report, we present evidence for activation of p53 pathway by NaB and its role in the NaB-mediated growth suppression.	nab	93-96	P53	Homo sapiens	54-57
19406223-9	2009	Taken together, these results indicate that EGCg, among several green tea polyphenols, is a potent apoptosis inducer that functions exclusively through a p53-dependent pathway in A549 cells.	epigallocatechin gallate	44-48	P53	Homo sapiens	154-157
15688418-4	2005	Addition of NaB increased the levels of p53 involving a p14(ARF)-dependent post-transcriptional mechanism.	nab	12-15	P53	Homo sapiens	40-43
19398128-4	2009	RESULTS: p53 AAbs are associated with high grade, but not low grade ovarian carcinoma.	p-Aminoazobenzene	13-17	P53	Homo sapiens	9-12
15688418-5	2005	NaB induced p53 is functional as it activated p53-specific reporter, induced the level of p21(WAF1/CIP1), inhibited cellular DNA synthesis and induced apoptosis.	nab	0-3	P53	Homo sapiens	12-15
15688418-5	2005	NaB induced p53 is functional as it activated p53-specific reporter, induced the level of p21(WAF1/CIP1), inhibited cellular DNA synthesis and induced apoptosis.	nab	0-3	P53	Homo sapiens	46-49
15688418-6	2005	By using HPV 16 E6 stable transfectants as well as p53 null cancer cells, we show that NaB suppresses the growth of WT p53 containing cells more efficiently.	nab	87-90	P53	Homo sapiens	51-54
15688418-6	2005	By using HPV 16 E6 stable transfectants as well as p53 null cancer cells, we show that NaB suppresses the growth of WT p53 containing cells more efficiently.	nab	87-90	P53	Homo sapiens	119-122
15688418-7	2005	NaB inhibited DNA synthesis to similar extent both in the presence and absence of p53.	nab	0-3	P53	Homo sapiens	82-85
15688418-8	2005	However, NaB treatment lead to a major G(2)/M arrest of cells in the presence of p53, while cells without wild-type p53 accumulated mainly in G(1) phase of the cell cycle.	nab	9-12	P53	Homo sapiens	81-84
16024610-8	2005	NO treatment also induced the phosphorylation of p53 at Ser15; pretreatment with phosphoinositide-3 kinase (PI3K) family inhibitors, wortmannin, LY294002, and caffeine, blocked such phosphorylation, but the p38 mitogen-activated protein kinase inhibitor, SB203580, did not.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	145-153	P53	Homo sapiens	49-52
15896711-7	2005	These appear to be followed by the specific activation of AMPK and the up-regulation of p53, p21, and Bax by genistein.	Genistein	109-118	P53	Homo sapiens	88-91
19242657-0	2009	Tunicamycin suppresses cisplatin-induced HepG2 cell apoptosis via enhancing p53 protein nuclear export.	Tunicamycin	0-11	P53	Homo sapiens	76-79
15833387-4	2005	The p53, iNOS expression and intracellular NO level were markedly increased in Hep G2 cells after liriodenine treatment.	liriodenine	98-109	P53	Homo sapiens	4-7
15833387-5	2005	A NO inhibitor, carboxy-PTIO inhibited the p53 expression induced by liriodenine.	liriodenine	69-80	P53	Homo sapiens	43-46
15688418-10	2005	These results suggest that p53 pathway mediates in part growth suppression by NaB and the p53 status may be an important determinant of chemosensitivity in HDI based cancer chemotherapy.	nab	78-81	P53	Homo sapiens	27-30
19242657-4	2009	In order to further explore the mechanism underlying tumor resistance to cisplatin, we observed that increased nuclear export of endogenous p53 protein by pharmacological inducers of ER stress, such as tunicamycin, was associated with the suppression of cisplatin-induced apoptosis.	Tunicamycin	202-213	P53	Homo sapiens	140-143
15833387-7	2005	These results demonstrate that NO production and p53 expression are critical factors in liriodenine-induced growth inhibition in human wild-type p53 hepatoma cells.	liriodenine	88-99	P53	Homo sapiens	49-52
15833387-7	2005	These results demonstrate that NO production and p53 expression are critical factors in liriodenine-induced growth inhibition in human wild-type p53 hepatoma cells.	liriodenine	88-99	P53	Homo sapiens	145-148
19513516-0	2009	Trichostatin A with adenovirus-mediated p53 gene transfer synergistically induces apoptosis in breast cancer cell line MDA-MB-231.	trichostatin A	0-14	P53	Homo sapiens	40-43
15942663-3	2005	Here, we examined the molecular mechanisms whereby the PI3K inhibitor LY294002 sensitized p53- and Fas-deficient hepatoma cells to etoposide and camptothecin.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	70-78	P53	Homo sapiens	90-93
19216720-0	2009	Spatiotemporal activation of caspase-dependent and -independent pathways in staurosporine-induced apoptosis of p53wt and p53mt human cervical carcinoma cells.	Staurosporine	76-89	P53	Homo sapiens	111-114
19216720-0	2009	Spatiotemporal activation of caspase-dependent and -independent pathways in staurosporine-induced apoptosis of p53wt and p53mt human cervical carcinoma cells.	Staurosporine	76-89	P53	Homo sapiens	121-124
19216720-2	2009	Our laboratory has reported that p53 is a key contributor of mitochondrial apoptosis in cervical carcinoma cells after staurosporine exposure.	Staurosporine	119-132	P53	Homo sapiens	33-36
19519319-1	2009	By analyzing the cDNA obtained from 16 B-cell chronic lymphocytic leukemia (B-CLL) patient samples, we found that Nutlin-3, a small molecule inhibitor of MDM2/p53 interaction, induced a characteristic gene expression profile (GEP) signature in 13 out of 16 B-CLL samples.	nutlin 3	114-122	P53	Homo sapiens	159-162
15930285-7	2005	The DNA methyltransferase inhibitor zebularine reverses the methylation of the p53 promoter, allowing the resumption of its expression.	pyrimidin-2-one beta-ribofuranoside	36-46	P53	Homo sapiens	79-82
15930285-8	2005	However, when zebularine is withdrawn from the cells, the reestablishment of the original CpG island methylation within the p53 promoter does not occur in the absence of IL-6, and cells which do not receive IL-6 eventually die, as p53 expression continues unchecked by remethylation.	pyrimidin-2-one beta-ribofuranoside	14-24	P53	Homo sapiens	124-127
15930285-8	2005	However, when zebularine is withdrawn from the cells, the reestablishment of the original CpG island methylation within the p53 promoter does not occur in the absence of IL-6, and cells which do not receive IL-6 eventually die, as p53 expression continues unchecked by remethylation.	pyrimidin-2-one beta-ribofuranoside	14-24	P53	Homo sapiens	231-234
15930285-10	2005	Consistent with this model, when cells that express IL-6 in an autocrine fashion are subjected to identical treatment, p53 expression is reduced shortly after withdrawal of zebularine.	pyrimidin-2-one beta-ribofuranoside	173-183	P53	Homo sapiens	119-122
15870916-10	2005	Retinol significantly decreased (p&lt;0.05) invasive capabilities of cells across matrigel coated invasion chambers and significantly reduced (p&lt;0.05) PCNA, Fra-1, mutant p53 and increased Rb protein expression levels in comparison to non-retinol-treated ones when assayed using immunofluorescent staining coupled with confocal microscopy.	Vitamin A	0-7	P53	Homo sapiens	174-177
15892716-7	2005	Inhibiting p53 function by a dominant negative p53 (p53(175His)) confirmed that the HDAC inhibitor induced apoptosis was independent of wild-type p53, even though TSA slightly activated p53 in a reporter assay.	trichostatin A	163-166	P53	Homo sapiens	11-14
19445707-0	2009	Increased susceptibility of spinal muscular atrophy fibroblasts to camptothecin is p53-independent.	Camptothecin	67-79	P53	Homo sapiens	83-86
15753076-9	2005	Senescence induction, tested as staining for SA-beta-gal, in reoxygenated progenitor cells was closely correlated with extent of DNA damage and phosphorylation of ATM at Ser-1981 and p53 at Ser-15.	2-(2-quinolinyl)-1H-indene--1,3(2H)-dione-6'-sulfonic acid	45-56	P53	Homo sapiens	183-186
15909125-0	2005	Etoposide (VP-16) sensitizes p53-deficient human non-small cell lung cancer cells to caspase-7-mediated apoptosis.	Etoposide	0-9	P53	Homo sapiens	29-32
19445707-8	2009	Upon camptothecin treatment, levels of p53 were markedly increased.	Camptothecin	5-17	P53	Homo sapiens	39-42
19445707-9	2009	To determine if p53 plays a role in the increased sensitivity of SMA fibroblasts to camptothecin, we analyzed the sensitivity of SMA fibroblasts to another DNA topoisomerase I inhibitor, beta-lapachone.	Camptothecin	84-96	P53	Homo sapiens	16-19
19070402-2	2009	The thiosemicarbazones were cytotoxic against malignant RT2 glioblastoma cells (expressing p53 protein) with IC(50) values in the 7.3-360 microM range, and against malignant T98 glioblastoma cells (expressing mutant p53 protein) with IC(50) values in the 3.6-143 microM range.	Thiosemicarbazones	4-22	P53	Homo sapiens	91-94
15746940-4	2005	TSA stabilizes the acetylation of p53 at Lys382, elevating p21 levels and inducing cell cycle arrest, but does not induce Bax translocation or apoptosis.	trichostatin A	0-3	P53	Homo sapiens	34-37
19070402-2	2009	The thiosemicarbazones were cytotoxic against malignant RT2 glioblastoma cells (expressing p53 protein) with IC(50) values in the 7.3-360 microM range, and against malignant T98 glioblastoma cells (expressing mutant p53 protein) with IC(50) values in the 3.6-143 microM range.	Thiosemicarbazones	4-22	P53	Homo sapiens	216-219
15846088-5	2005	The cell line that showed greatest reduction (85-90%) of p53 expression showed decreased p21 promoter activation after DNA damage with camptothecin, etoposide and MMS.	Camptothecin	135-147	P53	Homo sapiens	57-60
15846088-5	2005	The cell line that showed greatest reduction (85-90%) of p53 expression showed decreased p21 promoter activation after DNA damage with camptothecin, etoposide and MMS.	Etoposide	149-158	P53	Homo sapiens	57-60
19123473-4	2009	Cantharidin and norcantharidin, a derivative with reduced toxicity, decreased HLF protein levels and induced apoptosis in the AML cell line MV4-11 by modulating the expression of several molecules that govern survival pathway, including HLF, SLUG, NFIL3 and c-myc, thereby inducing p53 and the mitochondrial caspase cascade.	norcantharidin	16-30	P53	Homo sapiens	282-285
19190243-8	2009	Therefore, therapeutic combinations of Nutlin-3 + gamma-secretase inhibitors might potentiate the cytotoxicity of Nutlin-3 in p53(wild-type) leukemic cells.	nutlin 3	39-47	P53	Homo sapiens	126-129
15764647-1	2005	Treatment with epigallocatechin-3-gallate (EGCG), a polyphenolic compound of green tea, results in activation of p53 and induction of apoptosis in prostate cancer LnCaP cells.	epigallocatechin gallate	15-41	P53	Homo sapiens	113-116
15764647-1	2005	Treatment with epigallocatechin-3-gallate (EGCG), a polyphenolic compound of green tea, results in activation of p53 and induction of apoptosis in prostate cancer LnCaP cells.	epigallocatechin gallate	43-47	P53	Homo sapiens	113-116
15764647-2	2005	However, no direct evidence has delineated the role of p53 and p53-dependent pathways in EGCG-mediated apoptosis.	epigallocatechin gallate	89-93	P53	Homo sapiens	63-66
15764647-4	2005	Treatment of the resultant cells, PC3-p53, with EGCG led to, as reported earlier in LnCaP cells, an increase in p53 protein, which exacerbated both G1 arrest and apoptosis.	epigallocatechin gallate	48-52	P53	Homo sapiens	38-41
15764647-4	2005	Treatment of the resultant cells, PC3-p53, with EGCG led to, as reported earlier in LnCaP cells, an increase in p53 protein, which exacerbated both G1 arrest and apoptosis.	epigallocatechin gallate	48-52	P53	Homo sapiens	112-115
19049493-8	2009	Reduction of Sp1 binding after activation of p53 with camptothecin was also observed in chromatin immunoprecipitation assays.	Camptothecin	54-66	P53	Homo sapiens	45-48
15764647-6	2005	The cells lacking p53 continued to cycle and did not undergo apoptosis upon treatment with similar concentrations of EGCG, thus establishing the action of EGCG in a p53-dependent manner.	epigallocatechin gallate	155-159	P53	Homo sapiens	18-21
15764647-6	2005	The cells lacking p53 continued to cycle and did not undergo apoptosis upon treatment with similar concentrations of EGCG, thus establishing the action of EGCG in a p53-dependent manner.	epigallocatechin gallate	155-159	P53	Homo sapiens	165-168
15764647-8	2005	Inactivation of p53 using small interfering RNA (siRNA) rendered these cells resistant to EGCG-mediated apoptosis.	epigallocatechin gallate	90-94	P53	Homo sapiens	16-19
15764647-13	2005	In summary, using isogenic cell lines and siRNA, we have clearly demonstrated that EGCG activates growth arrest and apoptosis primarily via p53-dependent pathway that involves the function of both p21 and Bax such that down-regulation of either molecule confers a growth advantage to the cells.	epigallocatechin gallate	83-87	P53	Homo sapiens	140-143
15833870-0	2005	Phenoxodiol, a novel isoflavone, induces G1 arrest by specific loss in cyclin-dependent kinase 2 activity by p53-independent induction of p21WAF1/CIP1.	phenoxodiol	0-11	P53	Homo sapiens	109-112
19261878-4	2009	Despite promoting nuclear p53 accumulation, Class I/II HDAC inhibitors (HDACIs) protected neurons from p53-dependent cell death induced by camptothecin, etoposide, heterologous p53 expression or the MDM2 inhibitor, nutlin-3a.	Camptothecin	139-151	P53	Homo sapiens	103-106
15809436-2	2005	NQO1 binds and stabilizes WT p53, whereas NQO1 inhibitors including dicoumarol and various other coumarins and flavones induce ubiquitin-independent proteasomal p53 degradation and thus inhibit p53-induced apoptosis.	Coumarins	97-106	P53	Homo sapiens	161-164
15809436-2	2005	NQO1 binds and stabilizes WT p53, whereas NQO1 inhibitors including dicoumarol and various other coumarins and flavones induce ubiquitin-independent proteasomal p53 degradation and thus inhibit p53-induced apoptosis.	Coumarins	97-106	P53	Homo sapiens	161-164
15746577-5	2005	Our study reports here for the first time that the induction of p53 and the activity of the Fas/FasL apoptotic system may participate in the antiproliferative activity of casuarinin in A549 cells.	casuarinin	171-181	P53	Homo sapiens	64-67
19261878-4	2009	Despite promoting nuclear p53 accumulation, Class I/II HDAC inhibitors (HDACIs) protected neurons from p53-dependent cell death induced by camptothecin, etoposide, heterologous p53 expression or the MDM2 inhibitor, nutlin-3a.	Camptothecin	139-151	P53	Homo sapiens	103-106
15827334-9	2005	Western immunoblot analysis indicated trichostatin A triggers apoptosis in resistant ovarian cancer cells via p53-independent activation of the intrinsic "mitochondrial" pathway, commensurate with induction of the Bcl-2-related protein Bad.	trichostatin A	38-52	P53	Homo sapiens	110-113
19261878-4	2009	Despite promoting nuclear p53 accumulation, Class I/II HDAC inhibitors (HDACIs) protected neurons from p53-dependent cell death induced by camptothecin, etoposide, heterologous p53 expression or the MDM2 inhibitor, nutlin-3a.	Etoposide	153-162	P53	Homo sapiens	103-106
19261878-4	2009	Despite promoting nuclear p53 accumulation, Class I/II HDAC inhibitors (HDACIs) protected neurons from p53-dependent cell death induced by camptothecin, etoposide, heterologous p53 expression or the MDM2 inhibitor, nutlin-3a.	Etoposide	153-162	P53	Homo sapiens	103-106
15670751-0	2005	Indole-3-carbinol and 3,3"-diindolylmethane induce expression of NAG-1 in a p53-independent manner.	3,3'-diindolylmethane	22-43	P53	Homo sapiens	76-79
19048622-5	2009	The TP53 wild-type tumor showed a strong early induction of senescence-like phenotype with overexpression of SA-beta-gal and p21(CIP1).	2-(2-quinolinyl)-1H-indene--1,3(2H)-dione-6'-sulfonic acid	109-120	P53	Homo sapiens	4-8
18951928-1	2009	We show that treatment with non-toxic doses of zinc in association to the ionophore compound pyrrolidine dithiocarbamate (PDTC) inhibits p53(-/-) pancreatic cancer cell growth much more efficiently than gemcitabine, the gold standard chemotherapeutic agent for pancreatic cancer.	pyrrolidine dithiocarbamic acid	93-120	P53	Homo sapiens	137-140
15557088-5	2005	Treatment of JB6 cells carrying a p53-luciferase reporter plasmid with silica caused dose-dependent p53 transactivation.	Silicon Dioxide	71-77	P53	Homo sapiens	34-37
18951928-1	2009	We show that treatment with non-toxic doses of zinc in association to the ionophore compound pyrrolidine dithiocarbamate (PDTC) inhibits p53(-/-) pancreatic cancer cell growth much more efficiently than gemcitabine, the gold standard chemotherapeutic agent for pancreatic cancer.	pyrrolidine dithiocarbamic acid	122-126	P53	Homo sapiens	137-140
15557088-5	2005	Treatment of JB6 cells carrying a p53-luciferase reporter plasmid with silica caused dose-dependent p53 transactivation.	Silicon Dioxide	71-77	P53	Homo sapiens	100-103
19064086-3	2009	In this paper, the polymer was introduced into 1-D chip for fluorescence detection of nucleic acids, and demonstrated its capability on rapid detection of p53 complementary DNA (cDNA) with different concentration.	Polymers	19-26	P53	Homo sapiens	155-158
15557088-7	2005	TUNEL and DNA fragmentation analysis show that silica caused apoptosis in both JB6 cells and wild-type p53 (p53+/+) fibroblasts but not in p53-deficient (p53-/-) fibroblasts.	Silicon Dioxide	47-53	P53	Homo sapiens	103-106
15557088-7	2005	TUNEL and DNA fragmentation analysis show that silica caused apoptosis in both JB6 cells and wild-type p53 (p53+/+) fibroblasts but not in p53-deficient (p53-/-) fibroblasts.	Silicon Dioxide	47-53	P53	Homo sapiens	108-111
15557088-7	2005	TUNEL and DNA fragmentation analysis show that silica caused apoptosis in both JB6 cells and wild-type p53 (p53+/+) fibroblasts but not in p53-deficient (p53-/-) fibroblasts.	Silicon Dioxide	47-53	P53	Homo sapiens	108-111
15592835-12	2005	Moreover, salvicine-induced apoptosis in MCF-7 subsequent to DNA damage seems to be mediated through a p53-independent pathway.	salvicine	10-19	P53	Homo sapiens	103-106
18937971-8	2009	CONCLUSION: Our results suggest that TP53, BCL-2 and BAX proteins carry some predictive potential in taxane-platinum-treated ovarian cancer patients, auxiliary to clinicopathological factors.	taxane-platinum	101-116	P53	Homo sapiens	37-41
15674351-11	2005	While RA alone had no effect on p53-NRD activity, cotreatment with RA and the histone deacetylase inhibitor trichostatin-A (TSA) completely relieved p53-NRD-mediated repression.	trichostatin A	108-122	P53	Homo sapiens	149-152
15674351-11	2005	While RA alone had no effect on p53-NRD activity, cotreatment with RA and the histone deacetylase inhibitor trichostatin-A (TSA) completely relieved p53-NRD-mediated repression.	trichostatin A	124-127	P53	Homo sapiens	149-152
19138738-8	2009	The results showed that genes presenting the epidermal growth factor (EGF)/MAP-kinase pathway were significantly over-represented by progesterone treatment, whereas, by Mifepristone treatment genes involved in the p53 pathway were also up-regulated (data not shown).	Mifepristone	169-181	P53	Homo sapiens	214-217
15647429-10	2005	Chondrocyte [(3)H]thymidine uptake correlated positively with Bcl-2 (r(s) = 0.62, p = 0.009) and correlated inversely with p53 levels (r(s) = -0.55, p = 0.02).	Thymidine	18-27	P53	Homo sapiens	123-126
18459128-4	2009	Further, the treatment of A549 cells with pifithrin-alpha, a specific inhibitor of p53, or transfection of A549 cells with a p53 antisense oligodeoxynucleotide resulted in a reduction in the berberine-induced inhibition of cell proliferation and apoptosis.	Oligodeoxyribonucleotides	139-159	P53	Homo sapiens	125-128
15713890-4	2005	Clusterin mRNA expression in PC3 cells was highly up-regulated by Ad5CMV-p53 treatment; however, antisense clusterin oligodeoxynucleotide treatment further suppressed clusterin expression in PC3 cells after Ad5CMV-p53 treatment.	Oligodeoxyribonucleotides	117-137	P53	Homo sapiens	214-217
15713890-5	2005	Antisense clusterin oligodeoxynucleotide treatment significantly enhanced the sensitivity of Ad5CMV-p53 in a dose-dependent manner, reducing the IC50 of Ad5CMV-p53 by 75%.	Oligodeoxyribonucleotides	20-40	P53	Homo sapiens	100-103
15713890-5	2005	Antisense clusterin oligodeoxynucleotide treatment significantly enhanced the sensitivity of Ad5CMV-p53 in a dose-dependent manner, reducing the IC50 of Ad5CMV-p53 by 75%.	Oligodeoxyribonucleotides	20-40	P53	Homo sapiens	160-163
18787402-3	2008	In p53(+/+) cells, the combination of Ly + Te + Ca (10(-3) M of each) caused significant accumulation of cells in PreG(1) (64% at 48 hours); less preG(1) increase was observed in response to Ly + Te (25%) or Ly + Ca (14%).	ly + te	38-45	P53	Homo sapiens	3-6
15829155-10	2005	Etoposide increased the expression of wild-type p53, activated CPP32 (but not ICE) activity, and induced apoptosis in these cells.	Etoposide	0-9	P53	Homo sapiens	48-51
19138991-3	2008	In a p53 wild-type, low-grade, and papillary bladder cancer cell line (RT4), flavokawain A increased p21/WAF1 and p27/KIP1, which resulted in a decrease in cyclin-dependent kinase-2 (CDK2) kinase activity and subsequent G(1) arrest.	flavokawain A	77-90	P53	Homo sapiens	5-8
15389812-3	2005	RESULTS: CDDP and DACH-Ac-Pt were equiactive against mutant p53 and androgen-independent DU-145 or PC-3 tumor cells.	dach-ac-pt	18-28	P53	Homo sapiens	60-63
15389812-6	2005	The greater potency of DACH-Ac-Pt than CDDP in wild-type p53 cells was not due to increased cellular drug uptake or increased adduct levels, but correlated with a lower tolerance to DNA damage.	dach-ac-pt	23-33	P53	Homo sapiens	57-60
15389812-10	2005	CONCLUSIONS: DACH-Ac-Pt is highly effective against wild-type p53 LNCaP and its LN3 variant, and this activity is androgen-independent.	dach-ac-pt	13-23	P53	Homo sapiens	62-65
15878336-9	2005	Moreover, TSA sensitization to UV-induced apoptosis is p53 dependent.	trichostatin A	10-13	P53	Homo sapiens	55-58
19138991-6	2008	In contrast, flavokawain A induced a G(2)-M arrest in six p53 mutant-type, high-grade bladder cancer cell lines (T24, UMUC3, TCCSUP, 5637, HT1376, and HT1197).	flavokawain A	13-26	P53	Homo sapiens	58-61
15832392-0	2005	Determination by asymmetric total synthesis of the absolute configuration of lucilactaene, a cell-cycle inhibitor in p53-transfected cancer cells.	lucilactaene	77-89	P53	Homo sapiens	117-120
19138991-8	2008	Suppression of p53 expression by small interfering RNA in RT4 cells restored Cdc25C expression and down-regulated p21/WAF1 expression, which allowed Cdc25C and CDK1 activation, which then led to a G(2)-M arrest and an enhanced growth-inhibitory effect by flavokawain A.	flavokawain A	255-268	P53	Homo sapiens	15-18
19138991-9	2008	Consistently, flavokawain A also caused a pronounced CDK1 activation and G(2)-M arrest in p53 knockout but not in p53 wild-type HCT116 cells.	flavokawain A	14-27	P53	Homo sapiens	90-93
15498771-1	2004	When added for a short period (2-4 h) to cells, the kinase inhibitor staurosporine (STS), can trigger double strand breaks, the formation of nuclear foci containing phosphorylated H2AX, Chk2, and p53, a decrease in transcription, and a minor degree of peripheral chromatin condensation.	Staurosporine	69-82	P53	Homo sapiens	196-199
19138991-10	2008	This selectivity of flavokawain A for inducing a G(2)-M arrest in p53-defective cells deserves further investigation as a new mechanism for the prevention and treatment of bladder cancer.	flavokawain A	20-33	P53	Homo sapiens	66-69
15498771-1	2004	When added for a short period (2-4 h) to cells, the kinase inhibitor staurosporine (STS), can trigger double strand breaks, the formation of nuclear foci containing phosphorylated H2AX, Chk2, and p53, a decrease in transcription, and a minor degree of peripheral chromatin condensation.	Staurosporine	84-87	P53	Homo sapiens	196-199
18557930-7	2008	On the other hand, p53 activator, etoposide, decreased the MMP-1 expression in both normal and p53-overexpressed cells.	Etoposide	34-43	P53	Homo sapiens	19-22
15595848-0	2004	Mutagenic potential of benzo[a]pyrene-derived DNA adducts positioned in codon 273 of the human P53 gene.	benzo[a	23-30	P53	Homo sapiens	95-98
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Hydroxyl Radical	45-61	P53	Homo sapiens	177-180
15489221-10	2004	In contrast, preincubation of cells with the hydroxyl radical scavenger, N-acetylcysteine, significantly attenuated the doxorubicin-mediated phosphorylation and accumulation of p53, p53-DNA binding, and the phosphorylation of H2AX, Nbs1, SMC1, Chk1, and Chk2, suggesting that hydroxyl radicals contribute to the doxorubicin-induced activation of ATM-dependent pathways.	Hydroxyl Radical	45-61	P53	Homo sapiens	182-185
18557930-7	2008	On the other hand, p53 activator, etoposide, decreased the MMP-1 expression in both normal and p53-overexpressed cells.	Etoposide	34-43	P53	Homo sapiens	95-98
15659824-9	2004	In the presence of estrogen, p21 and p53 protein expression were upregulated by high concentrations of genistein.	Genistein	103-112	P53	Homo sapiens	37-40
18949380-5	2008	In addition, TsA markedly down-regulated the expression of cyclin D1 and CDK4, up-regulated the expression of p21WAF1 and p53 and induced cell cycle arrest at the G1 phase in MCF10A-ras cells.	trichostatin A	13-16	P53	Homo sapiens	122-125
18725321-0	2008	Aflatoxin B1-induced TP53 mutational pattern in normal human cells using the FASAY (Functional Analysis of Separated Alleles in Yeast).	Aflatoxin B1	0-12	P53	Homo sapiens	21-25
15625017-5	2004	Blockage of PI3K pathway with its specific inhibitor LY294002 caused G1-S phase arrest, decreased cell growth rate and increased chemo- and radio-therapeutic sensitivity in MCF7 cells expressing wild-type p53.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	53-61	P53	Homo sapiens	205-208
18712872-1	2008	Chlorofusin is a recently isolated, naturally occurring inhibitor of p53-MDM2 complex formation whose structure is composed of a densely functionalized azaphilone-derived chromophore linked through the terminal amine of ornithine to a nine residue cyclic peptide.	azaphilone	152-162	P53	Homo sapiens	69-72
15548325-0	2004	CP-31398, a putative p53-stabilizing molecule tested in mammalian cells and in yeast for its effects on p53 transcriptional activity.	CP 31398	0-8	P53	Homo sapiens	21-24
15548325-0	2004	CP-31398, a putative p53-stabilizing molecule tested in mammalian cells and in yeast for its effects on p53 transcriptional activity.	CP 31398	0-8	P53	Homo sapiens	104-107
15548325-1	2004	BACKGROUND: CP-31398 is a small molecule that has been reported to stabilize the DNA-binding core domain of the human tumor suppressor protein p53 in vitro.	CP 31398	12-20	P53	Homo sapiens	143-146
18806879-10	2008	CONCLUSIONS: These results indicate that mitomycin-induced cellular apoptosis in corneal endothelial cells may be mediated through caspase-8, caspase-9, and the mitochondrial regulated pathways as well as through upregulation of p53-dependent and p21-dependent signal transduction pathways.	Mitomycin	41-50	P53	Homo sapiens	229-232
15345715-8	2004	Treatment of fibroblasts with etoposide, a potent inducer of cellular p53, abrogated TGF-beta stimulation of COL1A2 promoter activity and collagen synthesis in a p53-dependent manner.	Etoposide	30-39	P53	Homo sapiens	70-73
15345715-8	2004	Treatment of fibroblasts with etoposide, a potent inducer of cellular p53, abrogated TGF-beta stimulation of COL1A2 promoter activity and collagen synthesis in a p53-dependent manner.	Etoposide	30-39	P53	Homo sapiens	162-165
15505424-1	2004	In the p53-deficient human B lymphoma Namalwa cell line that quickly undergoes apoptosis after DNA topoisomerase I inhibitor (camptothecin, CPT) treatment, we observed rapid and slight induction of the pro-apoptotic BH3-only Bik, Bim-EL, Bim-L and Bim-S proteins.	Camptothecin	126-138	P53	Homo sapiens	7-10
18708766-4	2008	DP, TSA and SAHA inhibited Aurora A, Aurora B and survivin expression with kinetics that were remarkably similar within individual cell lines, and appeared to coincide with p53 expression status.	trichostatin A	4-7	P53	Homo sapiens	173-176
15542774-4	2004	An inhibitor of protein kinase C (PKC)-alpha, -beta, and -gamma (CGP41251) enhanced Ser15 phosphorylation of p53 by resveratrol in the absence of EGF and blocked EGF inhibition of the resveratrol effect.	midostaurin	65-73	P53	Homo sapiens	109-112
15475475-4	2004	Camptothecin activated p53 in A549 lung carcinoma cells pretreated with scrambled siRNA, exhibited concentration-dependent cell cycle blocks, and induced moderate microtubule stabilization.	Camptothecin	0-12	P53	Homo sapiens	23-26
15475475-5	2004	Knockdown of camptothecin-induced p53 protein expression with p53 siRNA inhibited the G1/S blocking activity of the drug and diminished its microtubule-stabilizing activity.	Camptothecin	13-25	P53	Homo sapiens	34-37
15475475-5	2004	Knockdown of camptothecin-induced p53 protein expression with p53 siRNA inhibited the G1/S blocking activity of the drug and diminished its microtubule-stabilizing activity.	Camptothecin	13-25	P53	Homo sapiens	62-65
18431742-3	2008	We tested the hypothesis that genistein activates expression of several aberrantly silenced tumor suppressor genes (TSGs) that have unmethylated promoters such as PTEN, CYLD, p53 and FOXO3a.	Genistein	30-39	P53	Homo sapiens	175-178
15492467-0	2004	Cytochrome c release from oridonin-treated apoptotic A375-S2 cells is dependent on p53 and extracellular signal-regulated kinase activation.	oridonin	26-34	P53	Homo sapiens	83-86
15492467-5	2004	The activation of p53 by oridonin was also blocked by wortmannin.	oridonin	25-33	P53	Homo sapiens	18-21
15492467-7	2004	Oridonin induced A375-S2 cell apoptosis by activating parallel p53 and ERK pathways, increasing the ratio of Bax/Bcl-xL protein expression, and promoting the release of cytochrome c into the cytosol, resulting in apoptotic cell death.	oridonin	0-8	P53	Homo sapiens	63-66
18594007-14	2008	Moreover, moscatilin induces DNA damage, phosphorylation of H2AX and p53, and up-regulation of p21.	dendrophenol	10-20	P53	Homo sapiens	69-72
15312684-8	2004	Treatment with 2ME induced upregulation of wild type p53 in one of the human glioblastoma cell lines as well as in proliferating adult rat astrocytes.	2-Methoxyestradiol	15-18	P53	Homo sapiens	53-56
21783897-1	2008	In A549 cells treated with zinc sulfate (ZnSO(4)), the levels of p53 phosphorylated at Ser15 and total p53 protein increased.	znso	41-45	P53	Homo sapiens	65-68
15302096-3	2004	NALM-6, which had a high expression level of p53, a tumor suppressor gene, was most susceptible to Ara-C.	nalm-6	0-6	P53	Homo sapiens	45-48
15763945-10	2004	Doxil minimally affected the expression levels of p53, whereas other anthracyclines induced p53 protein levels to a significant level, resulting in endothelial cell apoptosis.	liposomal doxorubicin	0-5	P53	Homo sapiens	50-53
21783897-1	2008	In A549 cells treated with zinc sulfate (ZnSO(4)), the levels of p53 phosphorylated at Ser15 and total p53 protein increased.	znso	41-45	P53	Homo sapiens	103-106
21783897-2	2008	Treatment with wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI3K)-related kinases, suppressed ZnSO(4)-induced phosphorylation and accumulation of p53 protein.	znso	108-112	P53	Homo sapiens	160-163
21783897-3	2008	Expression of cyclin-dependent kinase inhibitor p21, one of the genes regulated by p53, was up-regulated following exposure to ZnSO(4), and suppressed by preincubation with wortmannin.	znso	127-131	P53	Homo sapiens	83-86
15350370-10	2004	The continual expression in p21WAF1 suggests that EGCG acts in the same way with p53 proteins to facilitate apoptosis after EGCG treatment.	epigallocatechin gallate	124-128	P53	Homo sapiens	81-84
18511169-6	2008	Specific ATM inhibitor, caffeine, significantly decreased KTA-mediated G2/M arrest by inhibiting the phosphorylation of p53 (Serine15) and Chk2.	serine15	125-133	P53	Homo sapiens	120-123
14742315-5	2004	Consistent with the proposed role of p53 as a suppressor of error-prone recombination, both p53 proteins down-regulated recombination with most of the sequences tested, even with the MLL bcr after etoposide treatment.	Etoposide	197-206	P53	Homo sapiens	92-95
15363324-11	2004	When treated with LY294002 or U0126 for 24 hours, the amount of wild p53 protein in MCF7-neu3 cells was 1.7 or 1.5 times higher than those in DMSO treated cells.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	18-26	P53	Homo sapiens	69-72
15363324-12	2004	There were 4.7 or 5.3 times increase in the p53 protein when MCF7-neu3 cells were treated with LY294002 or U0126 for 48 hours (P &lt; 0.01).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	95-103	P53	Homo sapiens	44-47
18607537-7	2008	An IkappaB kinase 2 inhibitor, sc514, also strongly reduced IL-8 and significantly induced p53 protein levels.	SC 514	31-36	P53	Homo sapiens	91-94
15117953-3	2004	We report here that the BH3-only Bcl-2 family member Bid is required for mitochondrial permeabilization and apoptosis induction by etoposide and gamma-radiation in p53 mutant T leukemic cells.	Etoposide	131-140	P53	Homo sapiens	164-167
18200038-0	2008	A novel functional assay using etoposide plus nutlin-3a detects and distinguishes between ATM and TP53 mutations in CLL.	Etoposide	31-40	P53	Homo sapiens	98-102
15183489-0	2004	P53-independent thermosensitization by mitomycin C in human non-small-cell lung cancer cells.	Mitomycin	39-50	P53	Homo sapiens	0-3
15183489-1	2004	PURPOSE: To elucidate the relationship between p53 functions and the interactive effects of the combined treatment with mild hyperthermia and mitomycin C.	Mitomycin	142-153	P53	Homo sapiens	47-50
15183489-9	2004	CONCLUSION: Our findings demonstrate a p53-independent mechanism for an interactively cytotoxic enhancement by combined treatment with mild hyperthermia and mitomycin C.	Mitomycin	157-168	P53	Homo sapiens	39-42
18645022-1	2008	In the present article, we describe a mechanistic study of a novel derivative of N-amidino-substituted benzimidazo[1,2-alpha]quinoline in two human colorectal cancer cell lines differing in p53 gene status.	n-amidino-substituted benzimidazo[1,2-alpha]quinoline	81-134	P53	Homo sapiens	190-193
18405662-7	2008	However, we demonstrate that both staurosporine-stimulated caspase-3 activation, p53 and neprilysin expression and activity were not affected by TMP21 over-expression or depletion.	Staurosporine	34-47	P53	Homo sapiens	81-84
15201971-1	2004	We have previously shown that treatment of human glioma U87-MG cells expressing wild-type p53 with a DNA topoisomerase II inhibitor, etoposide resulted in ceramide-dependent apoptotic cell death.	Etoposide	133-142	P53	Homo sapiens	90-93
15731293-7	2005	In addition, AMPH also caused increased expression of p53 and Bax at both transcript and protein levels; in contrast, Bcl-2 levels were decreased after the AMPH injections.	Amphetamine	13-17	P53	Homo sapiens	54-57
18559532-4	2008	In this study, we show that Tax sensitizes p53-mutant cells to a broad range of DNA-damaging agents, including mitomycin C, a bifunctional alkylator, etoposide, a topoisomerase II drug, and UV light, but not ionizing radiation, a double-strand break agent, or vinblastine, a tubulin poison.	Mitomycin	111-122	P53	Homo sapiens	43-46
15130282-5	2004	Indeed, in addition to transition-type mutations at dipyrimidine sites, G:C to T:A transversions, which may be induced by the presence of 8-oxoguanine during DNA replication, are frequently observed in the ras oncogene and p53 tumor suppressor gene in human skin cancers of sun-exposed areas and in UV-induced mouse skin cancers.	8-hydroxyguanine	138-150	P53	Homo sapiens	223-226
15774934-13	2005	p53 as an antiproliferative drug has the potential to replace mitomycin C and 5-fluorouracil in glaucoma surgery.	Mitomycin	62-73	P53	Homo sapiens	0-3
18559532-4	2008	In this study, we show that Tax sensitizes p53-mutant cells to a broad range of DNA-damaging agents, including mitomycin C, a bifunctional alkylator, etoposide, a topoisomerase II drug, and UV light, but not ionizing radiation, a double-strand break agent, or vinblastine, a tubulin poison.	Etoposide	150-159	P53	Homo sapiens	43-46
15099969-3	2004	An association between endometrial cancer and the polymorphism at codon 31 (AGC/serine to AGA/arginine [Ser(31)Arg]) of the p21 gene, which is known to be a downstream mediator of p53, has also been reported.	agc	76-79	P53	Homo sapiens	180-183
18566213-7	2008	Pretreatment of resistant A2780 CIS cells with the histone deacetylase inhibitor trichostatin A overcomes apoptosis resistance to CDDP by restoring both p73 and Bax but not p53 expression.	trichostatin A	81-95	P53	Homo sapiens	173-176
14757171-7	2004	Caffeine, an ATM kinase inhibitor, inhibited these effects of genistein on Chk2, p53, and p21waf1/cip1.	Genistein	62-71	P53	Homo sapiens	81-84
15967108-6	2005	Significantly, p53-mediated SAK repression was largely reversed in a dose-dependent manner by Trichostatin A, a potent histone deacetylase (HDAC) inhibitor, suggesting an involvement of HDAC transcription repressors in SAK repression by p53.	trichostatin A	94-108	P53	Homo sapiens	15-18
15967108-6	2005	Significantly, p53-mediated SAK repression was largely reversed in a dose-dependent manner by Trichostatin A, a potent histone deacetylase (HDAC) inhibitor, suggesting an involvement of HDAC transcription repressors in SAK repression by p53.	trichostatin A	94-108	P53	Homo sapiens	237-240
16104504-12	2005	UA increased p 53 protein expression.	ursolic acid	0-2	P53	Homo sapiens	13-17
18193086-3	2008	Dipyridamole dramatically sensitized p53-mutant human cancer cell lines: SW480, MG63 and DU145, to the antitumor activity of TRAIL, as evidenced by enabling TRAIL to efficiently cleave initiator and executioner caspases.	Dipyridamole	0-12	P53	Homo sapiens	37-40
16104504-13	2005	CONCLUSION: The results suggest that UA evokes MCF-7 cell apoptosis is correlation with the up-regulation of p 53.	ursolic acid	37-39	P53	Homo sapiens	109-113
15611068-7	2005	Third, the IKKbeta-specific inhibitor SC-514 decreased the ability of Tax to inhibit p53.	SC 514	38-44	P53	Homo sapiens	85-88
15674334-6	2005	The camptothecin or etoposide-dependent p53-mediated repression was attenuated by trichostatin A (TSA), an inhibitor of histone deacetylases (HDACs).	Camptothecin	4-16	P53	Homo sapiens	40-43
15674334-6	2005	The camptothecin or etoposide-dependent p53-mediated repression was attenuated by trichostatin A (TSA), an inhibitor of histone deacetylases (HDACs).	Etoposide	20-29	P53	Homo sapiens	40-43
15674334-6	2005	The camptothecin or etoposide-dependent p53-mediated repression was attenuated by trichostatin A (TSA), an inhibitor of histone deacetylases (HDACs).	trichostatin A	82-96	P53	Homo sapiens	40-43
15674334-6	2005	The camptothecin or etoposide-dependent p53-mediated repression was attenuated by trichostatin A (TSA), an inhibitor of histone deacetylases (HDACs).	trichostatin A	98-101	P53	Homo sapiens	40-43
15674334-8	2005	The simultaneous formation of a camptothecin-dependent p53-SP1 complex indicated its occurrence outside of the RECQ4 promoter.	Camptothecin	32-44	P53	Homo sapiens	55-58
15868936-0	2005	Ellagic acid induced p53/p21 expression, G1 arrest and apoptosis in human bladder cancer T24 cells.	Ellagic Acid	0-12	P53	Homo sapiens	21-24
15713419-1	2005	A series of 2-N-alkyl-3-aryl-3-alkoxyisoindolinones has been synthesised and evaluated as inhibitors of the MDM2-p53 interaction.	2-n-alkyl-3-aryl-3-alkoxyisoindolinones	12-51	P53	Homo sapiens	113-116
15735102-0	2005	Ellagic acid potentiates the effect of quercetin on p21waf1/cip1, p53, and MAP-kinases without affecting intracellular generation of reactive oxygen species in vitro.	Ellagic Acid	0-12	P53	Homo sapiens	66-69
15649712-0	2005	Ethylnitrosourea induces neural progenitor cell apoptosis after S-phase accumulation in a p53-dependent manner.	Ethylnitrosourea	0-16	P53	Homo sapiens	90-93
15802022-0	2005	Therapeutic efficacy of adenoviral-mediated p53 gene transfer is synergistically enhanced by combined use of antisense oligodeoxynucleotide targeting clusterin gene in a human bladder cancer model.	Oligodeoxyribonucleotides	119-139	P53	Homo sapiens	44-47
15543231-8	2005	At the opposite, upon treatment with topoisomerase II inhibitors (doxorubicin or etoposide), the expression of TAp63 isoforms was clearly induced, independently of the TP53 status of cells.	Etoposide	81-90	P53	Homo sapiens	168-172
15583825-6	2005	Treatment with either cerulenin or C75 induced TP53 protein accumulation at 24 h in MCF-7 cells.	Cerulenin	22-31	P53	Homo sapiens	47-51
15583825-7	2005	To determine whether the up-regulation of TP53 following exposure to cerulenin or C75 was solely due to inhibition of endogenous fatty acid metabolism, we first evaluated the cytotoxic response to chemical FAS blockers on MCF-7 cells in which FAS gene expression was previously silenced by using the highly sequence-specific mechanism of RNA interference.	Cerulenin	69-78	P53	Homo sapiens	42-46
15456784-10	2004	Treatment with a specific p53 inhibitor, pifithrin-alpha, or transfection of a p53 antisense oligodeoxynucleotide enhanced the cytotoxicity of the quercetin-treated cells.	Oligodeoxyribonucleotides	93-113	P53	Homo sapiens	79-82
15475000-7	2004	Moreover, the overexpression of an inactivated GSK-3beta mutant counteracted the stimulatory effects of etoposide and camptothecin on a luciferase reporter plasmid driven by a p53-responsive sequence from the CD95 gene.	Etoposide	104-113	P53	Homo sapiens	176-179
15475000-7	2004	Moreover, the overexpression of an inactivated GSK-3beta mutant counteracted the stimulatory effects of etoposide and camptothecin on a luciferase reporter plasmid driven by a p53-responsive sequence from the CD95 gene.	Camptothecin	118-130	P53	Homo sapiens	176-179
20368822-9	2004	The continual expression in p21WAF1 suggests that EGCG acts in the same way with p53 proteins to facilitate apoptosis after EGCG treatment.	epigallocatechin gallate	124-128	P53	Homo sapiens	81-84
15485790-1	2004	OBJECTIVE: To investigate the mechanisms underlying the effect of selenium dioxide (SeO(2)) on the proliferation, apoptosis, and apoptosis-related gene expressions of Bcl-2 and p53 in 3 leukemia cell lines NB4, K562 and HL-60.	seo(2)	84-90	P53	Homo sapiens	177-180
15485790-2	2004	METHODS: The three leukemia cell lines were treated with 3, 10 and 30 mmol/L SeO(2) and apoptosis detected by flow cytometry and analysis of p53 and Bcl-2 expressions.	seo(2)	77-83	P53	Homo sapiens	141-144
15485790-5	2004	CONCLUSION: SeO(2) can induce apoptosis in NB4, K562 and HL-60 leukemia cells, involving the down-regulation of Bcl-2 and up-regulation of p53.	seo(2)	12-18	P53	Homo sapiens	139-142
15173313-4	2004	Treatment of HeLa cells with TPT-CuCl(2) rescues the accumulation of p53 from the suppression of human papilloma virus E6, resulting in a dramatic up-regulation of Bax and Bak and down-regulation of the antiapoptotic factor Survivin.	tpt-cucl	29-37	P53	Homo sapiens	69-72
15634518-6	2004	HER2/neu overexpressing MCF7 cells showed higher p-Akt expression and lower p53 expression than those of parental MCF7 cells, which could be abrogated by LY294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	154-162	P53	Homo sapiens	76-79
15199132-3	2004	Activation of p53 by the DNA damaging agent mitomycin C (MC) was accompanied by a potent repression of CAIX expression and the CA9 promoter in MCF-7 but not in Saos-2 cells.	Mitomycin	44-55	P53	Homo sapiens	14-17
15199132-3	2004	Activation of p53 by the DNA damaging agent mitomycin C (MC) was accompanied by a potent repression of CAIX expression and the CA9 promoter in MCF-7 but not in Saos-2 cells.	Mitomycin	57-59	P53	Homo sapiens	14-17
15199132-6	2004	Similarly, CA9 promoter activity was downregulated by MC in HCT 116 p53(+/+) but not the isogenic p53(-/-) cells.	Mitomycin	54-56	P53	Homo sapiens	68-71
15252149-6	2004	Selenite treatment led to a significant increase in p53 phosphorylation on Ser-15 (Ser15P).	ser15p	83-89	P53	Homo sapiens	52-55
15252149-7	2004	Time course experiments showed that p53 Ser15P occurred several hours before caspase activation and PARP cleavage.	ser15p	40-46	P53	Homo sapiens	36-39
15222051-2	2004	METHODS: After treatment with Ad-p53, LOVO/5-FU sensitivity to 5-Fu was investigated using tetrazolium dye assay.	Tetrazolium Salts	91-102	P53	Homo sapiens	33-36
15191662-11	2004	CONCLUSION: These observations suggest that p33(ING1b) up-regulates p53 protein, and cooperate with p53 in stimulating expression of p21(WAF1) and Bax gene, thus to enhance etoposide-induced apoptosis via p53-dependent pathways.	Etoposide	173-182	P53	Homo sapiens	100-103
15191662-11	2004	CONCLUSION: These observations suggest that p33(ING1b) up-regulates p53 protein, and cooperate with p53 in stimulating expression of p21(WAF1) and Bax gene, thus to enhance etoposide-induced apoptosis via p53-dependent pathways.	Etoposide	173-182	P53	Homo sapiens	100-103
15225412-0	2004	Induction of antiproliferative effect by diosgenin through activation of p53, release of apoptosis-inducing factor (AIF) and modulation of caspase-3 activity in different human cancer cells.	Diosgenin	41-50	P53	Homo sapiens	73-76
15225412-6	2004	Diosgenin treatment also induces p53 activation and cell cycle arrest in the different cell lines studied.	Diosgenin	0-9	P53	Homo sapiens	33-36
15064730-4	2004	Consistent with these observations, hMSH6 colocalized with BLM and phospho-ser15-p53 in hydroxyurea-induced RAD51 nuclear foci that may correspond to the sites of presumed stalled DNA replication forks and more likely the resultant DNA double-stranded breaks.	Hydroxyurea	88-99	P53	Homo sapiens	81-84
15258465-0	2004	Mitochondrial translocation of p53 and mitochondrial membrane potential (Delta Psi m) dissipation are early events in staurosporine-induced apoptosis of wild type and mutated p53 epithelial cells.	Staurosporine	118-131	P53	Homo sapiens	31-34
15258465-0	2004	Mitochondrial translocation of p53 and mitochondrial membrane potential (Delta Psi m) dissipation are early events in staurosporine-induced apoptosis of wild type and mutated p53 epithelial cells.	Staurosporine	118-131	P53	Homo sapiens	175-178
14990988-5	2004	Induction of wild-type p53 in a tet-off regulated human colon cell system leads to the reduction of Tcf-4 mRNA and protein levels.	tetramethylenedisulfotetramine	32-35	P53	Homo sapiens	23-26
15010835-4	2004	The photosensitizer accumulation was similar in both cell lines, and survival measurements using MTT test and clonogenic assays demonstrated that wt p53 transfected cells (HT29A4) were significantly more sensitive to chlorin e6-mediated PDT.	phytochlorin	217-227	P53	Homo sapiens	149-152
14639618-7	2004	p53 expression was confirmed using flow cytometry, using the DO1 pan-p53 Ab and the PAb240 anti-p53mut Ab.	pab240	84-90	P53	Homo sapiens	0-3
15009115-4	2004	In the first 8 h after retinol treatment the levels of p53 and Bax proteins as well as caspase 3 activity increased, suggesting apoptotic cell death during the first hours of treatment.	Vitamin A	23-30	P53	Homo sapiens	55-58
14707723-0	2004	Terminally modified oligodeoxynucleotides directed against p53 in an orthotopic xenograft model: a novel adjuvant treatment strategy for pancreatic ductal carcinoma.	Oligodeoxyribonucleotides	20-41	P53	Homo sapiens	59-62
14669279-9	2003	Positivity for Ki-67 and p53 was seen predominantly in the epithelium of inclusion cysts and deep invaginations, including those areas that had been identified as hyperplastic or dysplastic on routine hematoxylin and eosin-stained sections.	Eosine Yellowish-(YS)	217-222	P53	Homo sapiens	25-28
14695179-4	2003	Peroxynitrite (ONOO(-)) is a highly reactive molecule produced by excess NO and that can posttranslationally modify and inactivate proteins, especially zinc finger transcription factors such as p53.	onoo(-)	15-22	P53	Homo sapiens	194-197
14695212-2	2003	We, in the present study, first confirmed that some substantial extent of apoptotic cell death was seen when p53-deficient cells (KATO-III) were transfected with wild-type p53 and treated with sodium butyrate (SB) or trichostatin A.	trichostatin A	217-231	P53	Homo sapiens	109-112
14614447-0	2003	CP-31398, a novel p53-stabilizing agent, induces p53-dependent and p53-independent glioma cell death.	CP 31398	0-8	P53	Homo sapiens	18-21
14614447-0	2003	CP-31398, a novel p53-stabilizing agent, induces p53-dependent and p53-independent glioma cell death.	CP 31398	0-8	P53	Homo sapiens	49-52
14614447-0	2003	CP-31398, a novel p53-stabilizing agent, induces p53-dependent and p53-independent glioma cell death.	CP 31398	0-8	P53	Homo sapiens	49-52
14614447-1	2003	CP-31398 is a prototype small molecule that stabilizes the active conformation of p53 and promotes p53 activity in cancer cell lines with mutant or wild-type p53.	CP 31398	0-8	P53	Homo sapiens	82-85
14614447-1	2003	CP-31398 is a prototype small molecule that stabilizes the active conformation of p53 and promotes p53 activity in cancer cell lines with mutant or wild-type p53.	CP 31398	0-8	P53	Homo sapiens	99-102
14614447-1	2003	CP-31398 is a prototype small molecule that stabilizes the active conformation of p53 and promotes p53 activity in cancer cell lines with mutant or wild-type p53.	CP 31398	0-8	P53	Homo sapiens	99-102
14614447-2	2003	Here, we report that CP-31398 induces p53 reporter gene activity and p21 expression in all of 11 glioma cell lines harboring wild-type or mutant p53, but not in p53-null LN-308 cells.	CP 31398	21-29	P53	Homo sapiens	38-41
14614447-2	2003	Here, we report that CP-31398 induces p53 reporter gene activity and p21 expression in all of 11 glioma cell lines harboring wild-type or mutant p53, but not in p53-null LN-308 cells.	CP 31398	21-29	P53	Homo sapiens	145-148
14614447-2	2003	Here, we report that CP-31398 induces p53 reporter gene activity and p21 expression in all of 11 glioma cell lines harboring wild-type or mutant p53, but not in p53-null LN-308 cells.	CP 31398	21-29	P53	Homo sapiens	145-148
14614447-6	2003	These observations point out some of the liabilities of CP-31398 as a prototype p53-based therapeutic and define a rationale for further refinement of small molecules that specifically target the p53 pathway, but lack the p53-independent effects.	CP 31398	56-64	P53	Homo sapiens	80-83
14614447-6	2003	These observations point out some of the liabilities of CP-31398 as a prototype p53-based therapeutic and define a rationale for further refinement of small molecules that specifically target the p53 pathway, but lack the p53-independent effects.	CP 31398	56-64	P53	Homo sapiens	196-199
14614447-6	2003	These observations point out some of the liabilities of CP-31398 as a prototype p53-based therapeutic and define a rationale for further refinement of small molecules that specifically target the p53 pathway, but lack the p53-independent effects.	CP 31398	56-64	P53	Homo sapiens	196-199
14504477-2	2003	Chk1 has been shown to be transcriptionally down-regulated in response to cis-dichloro-diamino platinum treatment in a p53-dependent manner.	cis-dichloro-diamino platinum	74-103	P53	Homo sapiens	119-122
21432092-8	2003	Previously, we demonstrated that HDAC inhibitors, such as sodium butyrate and trichostatin A (TSA), transcriptionally induce the cyclin-dependent kinase inhibitor p21(WAF1/Cip1), a downstream target gene of p53, in a p53-independent manner.	trichostatin A	78-92	P53	Homo sapiens	207-210
21432092-8	2003	Previously, we demonstrated that HDAC inhibitors, such as sodium butyrate and trichostatin A (TSA), transcriptionally induce the cyclin-dependent kinase inhibitor p21(WAF1/Cip1), a downstream target gene of p53, in a p53-independent manner.	trichostatin A	78-92	P53	Homo sapiens	217-220
21432092-8	2003	Previously, we demonstrated that HDAC inhibitors, such as sodium butyrate and trichostatin A (TSA), transcriptionally induce the cyclin-dependent kinase inhibitor p21(WAF1/Cip1), a downstream target gene of p53, in a p53-independent manner.	trichostatin A	94-97	P53	Homo sapiens	207-210
21432092-8	2003	Previously, we demonstrated that HDAC inhibitors, such as sodium butyrate and trichostatin A (TSA), transcriptionally induce the cyclin-dependent kinase inhibitor p21(WAF1/Cip1), a downstream target gene of p53, in a p53-independent manner.	trichostatin A	94-97	P53	Homo sapiens	217-220
14583449-5	2003	Interestingly, ionizing radiation or etoposide, both of which stabilize and activate p53, diminished p53 binding in chromatin immunoprecipitation assays, concomitant with a 5-fold increase in Dnmt1 levels.	Etoposide	37-46	P53	Homo sapiens	85-88
14583449-5	2003	Interestingly, ionizing radiation or etoposide, both of which stabilize and activate p53, diminished p53 binding in chromatin immunoprecipitation assays, concomitant with a 5-fold increase in Dnmt1 levels.	Etoposide	37-46	P53	Homo sapiens	101-104
14728868-11	2003	Mifepristone up-regulated significantly the expression of p53 protein, but down-regulated the expression of bcl-2 protein (P &lt; 0.01).	Mifepristone	0-12	P53	Homo sapiens	58-61
14728868-12	2003	The expressive rates of p53 and bcl-2 proteins were (54.8 +/- 4.0)% and (10.1 +/- 1.2)%, respectively, when 3AO cells was cultured with mifepristone of 10 micro mol/L for 24 h. Compared with the expression rates of control group (27.1 +/- 3.3)% and (17.6 +/- 1.0)%, the difference was significant (P &lt; 0.01).	Mifepristone	136-148	P53	Homo sapiens	24-27
12876282-9	2003	Trichostatin A, a histone deacetylase inhibitor, relieved the p53 transrepression activity on MAD1.	trichostatin A	0-14	P53	Homo sapiens	62-65
12954772-8	2003	Treatment with trichostatin A, which is an inhibitor of histone deacetylase, or PML over-expression relieved Daxx-mediated transcriptional repression of p53.	trichostatin A	15-29	P53	Homo sapiens	153-156
12883741-0	2003	The alpha1-adrenoceptor antagonist terazosin induces prostate cancer cell death through a p53 and Rb independent pathway.	Terazosin	35-44	P53	Homo sapiens	90-93
12969763-7	2003	In addition, UVA-induced enhanced expression of p53, a hallmark of UV-induced DNA damage and cell death, was also significantly inhibited by pretreatment with asiatic acid or ursolic acid.	ursolic acid	175-187	P53	Homo sapiens	48-51
12794767-6	2003	Pretreatment of COLO 205 with p53-specific antisense oligodeoxynucleotide decreased the TB-induced elevations of p53 and p21/Cip1 proteins, which in turn led to arrest in the cell cycle at the G0/G1 phase.	Oligodeoxyribonucleotides	53-73	P53	Homo sapiens	30-33
12794767-6	2003	Pretreatment of COLO 205 with p53-specific antisense oligodeoxynucleotide decreased the TB-induced elevations of p53 and p21/Cip1 proteins, which in turn led to arrest in the cell cycle at the G0/G1 phase.	Oligodeoxyribonucleotides	53-73	P53	Homo sapiens	113-116
12767058-0	2003	Nonsteroidal anti-inflammatory drug-activated gene (NAG-1) is induced by genistein through the expression of p53 in colorectal cancer cells.	Genistein	73-82	P53	Homo sapiens	109-112
12767058-5	2003	The induction of p53 (3 hr) precedes the induction of NAG-1 (12 hr), suggesting that genistein-induced NAG-1 expression is mediated by p53.	Genistein	85-94	P53	Homo sapiens	17-20
12767058-5	2003	The induction of p53 (3 hr) precedes the induction of NAG-1 (12 hr), suggesting that genistein-induced NAG-1 expression is mediated by p53.	Genistein	85-94	P53	Homo sapiens	135-138
12767058-8	2003	The expression of p53 was critical for NAG-1 promoter activity since no promoter activity was observed with genistein treatment in HCT-15 cells.	Genistein	108-117	P53	Homo sapiens	18-21
12767058-9	2003	However, genistein-induced promoter activity was restored in HCT-15 cells by transfection with wild-type p53.	Genistein	9-18	P53	Homo sapiens	105-108
12874009-2	2003	Here, we investigate the role of p53 in the G(2) arrest that occurs in response to the topoisomerase inhibitors etoposide and merbarone.	Etoposide	112-121	P53	Homo sapiens	33-36
12874009-3	2003	In HT1080 cells expressing a dominant-negative form of p53, treatment with etoposide still caused G(2) arrest, but the arrest could be overcome by additional treatment with caffeine, which inhibits the damage-responsive kinases ataxia telangiectasia mutated (ATM) and atm and rad3-related (ATR).	Etoposide	75-84	P53	Homo sapiens	55-58
12874009-5	2003	We conclude that etoposide activates two pathways, one of which depends on p53 and the other of which is sensitive to caffeine, and that either pathway is sufficient to activate G(2) arrest.	Etoposide	17-26	P53	Homo sapiens	75-78
12807744-6	2003	Furthermore, caffeine also inhibited the accumulation of p53 by a variety of stress-inducing agents in vivo, such as 5-fluorouracil, doxorubicin, mitomycin C, camptothecin and roscovitine.	Mitomycin	146-157	P53	Homo sapiens	57-60
12807744-6	2003	Furthermore, caffeine also inhibited the accumulation of p53 by a variety of stress-inducing agents in vivo, such as 5-fluorouracil, doxorubicin, mitomycin C, camptothecin and roscovitine.	Camptothecin	159-171	P53	Homo sapiens	57-60
12792782-6	2003	During UA treatment, we also demonstrated that p53 was phosphorylated at serine 392 and translocated to the nucleus.	ursolic acid	7-9	P53	Homo sapiens	47-50
12767922-6	2003	These data suggest that both genistein and etoposide induce p21(WAF1/Cip1) expression in a p53-dependent manner.	Genistein	29-38	P53	Homo sapiens	91-94
12767922-6	2003	These data suggest that both genistein and etoposide induce p21(WAF1/Cip1) expression in a p53-dependent manner.	Etoposide	43-52	P53	Homo sapiens	91-94
12767922-7	2003	Genistein appears to stimulate p21(WAF1/Cip1) expression through p53 via ATM, whereas etoposide may activate both ATM and ATR pathways.	Genistein	0-9	P53	Homo sapiens	65-68
12807754-0	2003	Roles of p38- and c-jun NH2-terminal kinase-mediated pathways in 2-methoxyestradiol-induced p53 induction and apoptosis.	2-Methoxyestradiol	65-83	P53	Homo sapiens	92-95
12807754-3	2003	It was found that 2-ME mediates apoptosis through p53 induction.	2-Methoxyestradiol	18-22	P53	Homo sapiens	50-53
12807754-9	2003	The results suggest that not only p53 induction through p38/JNK-dependent NFkappaB/AP-1 activation but also JNK-dependent Bcl-2 phosphorylation are required for 2-ME-induced apoptosis; moreover, inhibition of these pathways may be involved in androgen-mediated resistance to apoptosis.	2-Methoxyestradiol	161-165	P53	Homo sapiens	34-37
12738983-7	2003	After genotoxic stress such as etoposide treatment, AS2 expressing cells readily progressed into apoptosis through p53 and caspase-3 activations.	Etoposide	31-40	P53	Homo sapiens	115-118
12712406-0	2003	c-Jun NH2-terminal kinase-dependent Fas activation contributes to etoposide-induced apoptosis in p53-mutated prostate cancer cells.	Etoposide	66-75	P53	Homo sapiens	97-100
15186734-3	2004	Our data also show that FL in synergy with TPO may inhibit apoptosis in megakaryocyte development by up-regulating bcl-2 and inducing conformational changes of p53, in MK progenitors.	fl	24-26	P53	Homo sapiens	160-163
14699137-3	2004	We report here that the tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate prevents DNA damage-induced up-regulation of p53 by down-regulating PKC delta.	Phorbol Esters	40-53	P53	Homo sapiens	136-139
14767544-16	2004	In SK-Br3 cells, cerulenin-induced inhibition of FAS activity resulted in down-regulation of p53, and up-regulation of cyclin-dependent kinase inhibitor (CDKi) p21WAF1/CIP1.	Cerulenin	17-26	P53	Homo sapiens	93-96
14757171-6	2004	Genistein enhanced the activity of the checkpoint kinase, Chk2, which phosphorylates/inactivates Cdc25C, induced accumulation of p53, and activated the ataxia-telangiectasia-mutated (ATM) gene.	Genistein	0-9	P53	Homo sapiens	129-132
14712319-4	2003	Antisense oligodeoxynucleotides (As-ODNs) were used to inhibit the p53 response in the cell lines H460 and A549 with functional p53.	Oligodeoxyribonucleotides	10-31	P53	Homo sapiens	67-70
14712319-4	2003	Antisense oligodeoxynucleotides (As-ODNs) were used to inhibit the p53 response in the cell lines H460 and A549 with functional p53.	Oligodeoxyribonucleotides	10-31	P53	Homo sapiens	128-131
14513366-5	2003	Although phosphorylation of p53 at Ser-392 was also observed in CDDP-treated sensitive and resistant cells, it was weak or absent in response to DACH-Ac-Pt.	ac-pt	150-155	P53	Homo sapiens	28-31
18495890-2	2008	Using the camptothecin-induced DNA damage model in neurons, we previously showed that cyclin D1-associated cell cycle cyclin-dependent kinases (Cdks) (Cdk4/6) and p53 activation are two major events leading to activation of the mitochondrial apoptotic pathway.	Camptothecin	10-22	P53	Homo sapiens	163-166
14666730-2	2003	We have reported that hypoxic cytotoxins, such as TX-1102, tirapazamine (TPZ) and TX-402, selectively induced tumor cells to p53-independent apoptosis under hypoxic conditions and inhibited angiogenesis.	Tirapazamine	59-71	P53	Homo sapiens	125-128
14666730-2	2003	We have reported that hypoxic cytotoxins, such as TX-1102, tirapazamine (TPZ) and TX-402, selectively induced tumor cells to p53-independent apoptosis under hypoxic conditions and inhibited angiogenesis.	Tirapazamine	73-76	P53	Homo sapiens	125-128
14981901-6	2003	Only one tumour, which previously had shown expression and mutation in the p53, had a point mutation at codon 117 of exon 2 of the p21 gene with a resulting Cys--&gt;Tyr amino acid substitution.	tyr amino acid	166-180	P53	Homo sapiens	75-78
12964003-7	2003	Interestingly, when p53 was suppressed by over-expression of E6 from human papilloma virus type 16 (HPV-16), these cells lost their sensitivity to oridonin-induced growth inhibition and apoptosis.	oridonin	147-155	P53	Homo sapiens	20-23
12538580-2	2003	Exposure of human neuroblastoma SH-SY5Y cells to the DNA-damaging agent camptothecin increased p53 levels, activated caspase-3, and caused cell death.	Camptothecin	72-84	P53	Homo sapiens	95-98
12612087-0	2003	Stabilization of p53 by CP-31398 inhibits ubiquitination without altering phosphorylation at serine 15 or 20 or MDM2 binding.	CP 31398	24-32	P53	Homo sapiens	17-20
12612087-1	2003	CP-31398, a styrylquinazoline, emerged from a high throughput screen for therapeutic agents that restore a wild-type-associated epitope (monoclonal antibody 1620) on the DNA-binding domain of the p53 protein.	CP 31398	0-8	P53	Homo sapiens	196-199
12612087-2	2003	We found that CP-31398 can not only restore p53 function in mutant p53-expressing cells but also significantly increase the protein level and promote the activity of wild-type p53 in multiple human cell lines, including ATM-null cells.	CP 31398	14-22	P53	Homo sapiens	44-47
12612087-2	2003	We found that CP-31398 can not only restore p53 function in mutant p53-expressing cells but also significantly increase the protein level and promote the activity of wild-type p53 in multiple human cell lines, including ATM-null cells.	CP 31398	14-22	P53	Homo sapiens	67-70
12612087-2	2003	We found that CP-31398 can not only restore p53 function in mutant p53-expressing cells but also significantly increase the protein level and promote the activity of wild-type p53 in multiple human cell lines, including ATM-null cells.	CP 31398	14-22	P53	Homo sapiens	67-70
12612087-4	2003	Further investigation showed that CP-31398 blocks the ubiquitination and degradation of p53 but not in human papillomavirus E6-expressing cells.	CP 31398	34-42	P53	Homo sapiens	88-91
12612087-7	2003	We found that CP-31398 could also stabilize exogenous p53 in p53 mutant, wild-type, and p53-null human cells, even in MDM2-null p53(-/-) mouse embryonic fibroblasts.	CP 31398	14-22	P53	Homo sapiens	54-57
12612087-7	2003	We found that CP-31398 could also stabilize exogenous p53 in p53 mutant, wild-type, and p53-null human cells, even in MDM2-null p53(-/-) mouse embryonic fibroblasts.	CP 31398	14-22	P53	Homo sapiens	61-64
12612087-7	2003	We found that CP-31398 could also stabilize exogenous p53 in p53 mutant, wild-type, and p53-null human cells, even in MDM2-null p53(-/-) mouse embryonic fibroblasts.	CP 31398	14-22	P53	Homo sapiens	61-64
12612087-7	2003	We found that CP-31398 could also stabilize exogenous p53 in p53 mutant, wild-type, and p53-null human cells, even in MDM2-null p53(-/-) mouse embryonic fibroblasts.	CP 31398	14-22	P53	Homo sapiens	61-64
12964003-8	2003	Taken together, oridonin inhibited the proliferation of cancer cells via apoptosis and cell cycle arrest with p53 playing a central role in several cancer types which express the wild-type p53 gene.	oridonin	16-24	P53	Homo sapiens	110-113
12964003-8	2003	Taken together, oridonin inhibited the proliferation of cancer cells via apoptosis and cell cycle arrest with p53 playing a central role in several cancer types which express the wild-type p53 gene.	oridonin	16-24	P53	Homo sapiens	189-192
18483381-4	2008	RESULTS: In this report, we show that the HDIs trichostatin A, sodium butyrate, and low nanomolar doses of LAQ824 combined with the glycolysis inhibitor 2-deoxy-d-glucose induce strong apoptosis in cancer cell lines of brain, breast, and cervix in a p53-independent manner.	trichostatin A	47-61	P53	Homo sapiens	250-253
14502645-2	2003	Accordingly, HDAC inhibitors such as trichostatin A (TSA) have potential utility in pancreatic cancer, as most of these tumors possess mutations in p53, which in fact is the main cause of chemoresistance to 5-fluorouracil.	trichostatin A	37-51	P53	Homo sapiens	148-151
14502645-2	2003	Accordingly, HDAC inhibitors such as trichostatin A (TSA) have potential utility in pancreatic cancer, as most of these tumors possess mutations in p53, which in fact is the main cause of chemoresistance to 5-fluorouracil.	trichostatin A	53-56	P53	Homo sapiens	148-151
14502645-6	2003	The expression of p21(WAF1/CIP1) normally induced at the transcriptional level by p53 was also strongly activated by TSA.	trichostatin A	117-120	P53	Homo sapiens	82-85
12793003-2	2003	Western Blot was used to detect the changes of the expression of p53 protein, Caspase-3 after SGC-7901 cells were exposed to genistein.	Genistein	125-134	P53	Homo sapiens	65-68
12592393-0	2003	Methylation of CpG dinucleotides and/or CCWGG motifs at the promoter of TP53 correlates with decreased gene expression in a subset of acute lymphoblastic leukemia patients.	Dinucleoside Phosphates	19-32	P53	Homo sapiens	72-76
12963117-0	2003	In vitro aflatoxin B1-induced p53 mutations.	Aflatoxin B1	9-21	P53	Homo sapiens	30-33
18362074-0	2008	Synthesis and discovery of a novel pyrazole derivative as an inhibitor of apoptosis through modulating integrin beta4, ROS, and p53 levels in vascular endothelial cells.	pyrazole	35-43	P53	Homo sapiens	128-131
12845670-2	2003	While the G--&gt;T p53 mutation at codon 249 has been identified as a genetic hallmark of HCC caused by aflatoxin B(1), the genetic profile associated with other etiologic factors appears to be less distinctive.	Aflatoxin B1	104-115	P53	Homo sapiens	19-22
12509267-10	2003	p53 deficient cells were cross-resistant to another topoisomerase II inhibitor etoposide, which also provoked increased DNA strand breakage in p53 wt cells.	Etoposide	79-88	P53	Homo sapiens	0-3
12509267-10	2003	p53 deficient cells were cross-resistant to another topoisomerase II inhibitor etoposide, which also provoked increased DNA strand breakage in p53 wt cells.	Etoposide	79-88	P53	Homo sapiens	143-146
14513722-2	2003	(1998) implicated the proline/argine polymorphism of the codon 72 of the tumor-suppressor gene p53 in the development of cervical cancer (CC) with the observation that the p53 protein is more efficiently inactivated by the E6 oncoprotein of human papillomavirus in p53 arginine as compared with its proline isoform.	argine	30-36	P53	Homo sapiens	95-98
14513722-2	2003	(1998) implicated the proline/argine polymorphism of the codon 72 of the tumor-suppressor gene p53 in the development of cervical cancer (CC) with the observation that the p53 protein is more efficiently inactivated by the E6 oncoprotein of human papillomavirus in p53 arginine as compared with its proline isoform.	argine	30-36	P53	Homo sapiens	172-175
14513722-2	2003	(1998) implicated the proline/argine polymorphism of the codon 72 of the tumor-suppressor gene p53 in the development of cervical cancer (CC) with the observation that the p53 protein is more efficiently inactivated by the E6 oncoprotein of human papillomavirus in p53 arginine as compared with its proline isoform.	argine	30-36	P53	Homo sapiens	172-175
12811820-1	2003	Methylxantine derivative, caffeine, is known to prevent the p53-dependent apoptosis pathway via inhibition of ATM (ataxia telangiectasia mutated) kinase, which activates p53 by phosphorylation of the Ser-15 residue.	methylxantine	0-13	P53	Homo sapiens	60-63
12811820-1	2003	Methylxantine derivative, caffeine, is known to prevent the p53-dependent apoptosis pathway via inhibition of ATM (ataxia telangiectasia mutated) kinase, which activates p53 by phosphorylation of the Ser-15 residue.	methylxantine	0-13	P53	Homo sapiens	170-173
18294283-6	2008	Intriguingly, reactivation of p53 was accompanied with a nuclear accumulation of p53 and the phosphorylated p53 at Serine15 was only detected in nuclear fraction, but not in cytosolic fraction of doxorubicin-treated ChangX-34 cells.	serine15	115-123	P53	Homo sapiens	30-33
12873973-2	2003	GCS inhibition, by both antisense and the specific inhibitor (D-threo)-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP), results in a drastic decrease of apoptosis induced by the p53-independent chemotherapeutic agent N-(4-hydroxyphenyl)retinamide in neuroepithelioma cells.	RV 538	61-119	P53	Homo sapiens	186-189
12873973-2	2003	GCS inhibition, by both antisense and the specific inhibitor (D-threo)-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP), results in a drastic decrease of apoptosis induced by the p53-independent chemotherapeutic agent N-(4-hydroxyphenyl)retinamide in neuroepithelioma cells.	RV 538	121-125	P53	Homo sapiens	186-189
14690797-7	2003	In all cell lines, p21 mRNA levels were immediately elevated after NaB exposure, and p21 protein levels were increased within 6 h. NaB increased p21 promoter activity in both Caco2 and Lovo, suggesting p53 independence.	nab	131-134	P53	Homo sapiens	202-205
12716906-5	2003	Treating human umbilical vein endothelial cells with trichostatin A (TSA), an HDAC inhibitor, abolished the flow-induced p53 deacetylation at Lys-320 and Lys-373.	trichostatin A	53-67	P53	Homo sapiens	121-124
18489080-10	2008	By contrast, micromolar concentrations of (+/-)- anti-BPDE generated (+)- trans- anti-BPDE-N (2)-dGuo adducts (detected by stable-isotope dilution LC/MS methodology) in p53 cDNA that correlated in a linear fashion with mutagenic frequency, but no 8-oxo-dGuo was detected.	(+)- trans- anti-bpde-n (2)-dguo	69-101	P53	Homo sapiens	169-172
12716906-5	2003	Treating human umbilical vein endothelial cells with trichostatin A (TSA), an HDAC inhibitor, abolished the flow-induced p53 deacetylation at Lys-320 and Lys-373.	trichostatin A	69-72	P53	Homo sapiens	121-124
12716906-6	2003	To investigate the role of the HDAC-deacetylated p53 in the flow activation of p21Waf1, we found that TSA inhibited the activation at both the mRNA and protein levels.	trichostatin A	102-105	P53	Homo sapiens	49-52
12716906-7	2003	Deletion and mutation analyses of the p21Waf1 promoter revealed that flow activated p21Waf1 through p53 and TSA abrogated this p53-dependent activation.	trichostatin A	108-111	P53	Homo sapiens	127-130
12767922-2	2003	Here we show that topoisomerase II inhibitors, genistein and etoposide, induce p21(WAF1/Cip1) expression mainly in a p53-dependent manner in human lung cancer cell line A549.	Genistein	47-56	P53	Homo sapiens	117-120
12767922-2	2003	Here we show that topoisomerase II inhibitors, genistein and etoposide, induce p21(WAF1/Cip1) expression mainly in a p53-dependent manner in human lung cancer cell line A549.	Etoposide	61-70	P53	Homo sapiens	117-120
12359354-4	2002	Treatment of CRC cells with 2-methoxyestradiol (2-MeOE(2)) increased expression of p53 and p21(WAF1/CIP1) proteins and induced apoptosis, but did not produce changes in expression of estrogen receptor (ER)alpha or ERbeta.	2-meoe	48-54	P53	Homo sapiens	83-86
12359354-5	2002	The finding that 2-MeOE(2) induces p53-mediated colon cell apoptosis in vitro supports a role for 2-MeOE(2) as an endogenous mediator of intestinal tumor suppression.	2-meoe	17-23	P53	Homo sapiens	35-38
12359354-5	2002	The finding that 2-MeOE(2) induces p53-mediated colon cell apoptosis in vitro supports a role for 2-MeOE(2) as an endogenous mediator of intestinal tumor suppression.	2-meoe	98-104	P53	Homo sapiens	35-38
12183079-0	2002	Asiatic acid, a triterpene, induces apoptosis through intracellular Ca2+ release and enhanced expression of p53 in HepG2 human hepatoma cells.	Triterpenes	16-26	P53	Homo sapiens	108-111
20731894-16	2008	The IC50 of pEGFP-p53(RS)-801D cell line to 5-Fluorouracil(5FU) is 2.08+/-0.18 mug/mL, which is obviously lower than that of 801D(4.90+/-1.12 mug/mL,P &lt;0.05) and pEGFP-801D(3.41+/-0.86 mug/mL,P &lt;0.05).	pegfp	12-17	P53	Homo sapiens	18-21
12445215-0	2002	The p53-stabilizing compound CP-31398 enhances ultraviolet-B-induced apoptosis in a human melanoma cell line MMRU.	CP 31398	29-37	P53	Homo sapiens	4-7
12813130-8	2003	MB-97 treatment also induced a higher level of apoptosis in p53-null cells relative to their p53-positive counterparts.	mb-97	0-5	P53	Homo sapiens	60-63
12813130-8	2003	MB-97 treatment also induced a higher level of apoptosis in p53-null cells relative to their p53-positive counterparts.	mb-97	0-5	P53	Homo sapiens	93-96
18358096-0	2008	LY294002 induces p53-dependent apoptosis of SGC7901 gastric cancer cells.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	P53	Homo sapiens	17-20
12773551-4	2003	p53 response to treatment with gamma irradiation or etoposide is lost due to a mutation at codon 242 of p53 (C--&gt;W).	Etoposide	52-61	P53	Homo sapiens	104-107
18358096-7	2008	Expression of p53 and PUMA was induced, and mitochondrial membrane potential collapsed after treatment with LY294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	108-116	P53	Homo sapiens	14-17
12419181-6	2002	Instead, cyclin E led to increased p53 serine15 phosphorylation that was sensitive to inhibitors of the ATM/ATR family.	serine15	39-47	P53	Homo sapiens	35-38
18358096-9	2008	CONCLUSION: Activation of the p53 pathway is involved in LY294002-induced SGC7901 cell death.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	57-65	P53	Homo sapiens	30-33
18646312-6	2008	Strikingly, the p53 G1 checkpoint in G/G cells was activated by Nutlin-3 but not by etoposide, whereas in other Mdm2-overexpressing cells, both drugs activated p53 and subsequent G1 arrest or apoptosis.	nutlin 3	64-72	P53	Homo sapiens	16-19
12508652-4	2002	MATERIALS AND METHODS: A p53 mutant human glioma cell line T98G and a p53 wild type human neuroblastoma cell line SKNSH were exposed to TSA.	trichostatin A	136-139	P53	Homo sapiens	70-73
12771025-6	2003	Furthermore, northern analysis showed that induction of this gene is independent of p53, as increased expression of the gene was observed in p53 null H1299/Neo control cells when the temperature was shifted to 32 degrees C. Moreover, a DNA damaging agent, etoposide, also induced beta1 subunit expression in multiple human tumor cells, regardless of p53 status.	Etoposide	256-265	P53	Homo sapiens	141-144
12771025-6	2003	Furthermore, northern analysis showed that induction of this gene is independent of p53, as increased expression of the gene was observed in p53 null H1299/Neo control cells when the temperature was shifted to 32 degrees C. Moreover, a DNA damaging agent, etoposide, also induced beta1 subunit expression in multiple human tumor cells, regardless of p53 status.	Etoposide	256-265	P53	Homo sapiens	141-144
12508652-7	2002	Expression patterns of accumulation of highly acetylated histone H3, H4; p53 and cell cycle-associated p21waf, p27 which were induced by TSA were determined by using Western blot analysis.	trichostatin A	137-140	P53	Homo sapiens	73-76
12771025-7	2003	Thus, the beta1 subunit of AMPK is not a p53 downstream target gene, but can be induced by cold shock or the chemotherapeutic drug, etoposide in a p53-independent manner.	Etoposide	132-141	P53	Homo sapiens	147-150
18419600-0	2008	Trichostatin A causes p53 to switch oxidative-damaged colorectal cancer cells from cell cycle arrest into apoptosis.	trichostatin A	0-14	P53	Homo sapiens	22-25
12730670-3	2003	Here, we report that 2-methoxy-estradiol (2-Me), a natural estrogen metabolite, induced a caspase-dependent apoptosis of Ewing sarcoma-derived cells independently of their p53 status.	2-Methoxyestradiol	42-46	P53	Homo sapiens	172-175
12702583-0	2003	A peroxisome proliferator-activated receptor-gamma agonist and the p53 rescue drug CP-31398 inhibit the spontaneous immortalization of breast epithelial cells.	CP 31398	83-91	P53	Homo sapiens	67-70
12376521-2	2002	A specific missense mutation resulting from a guanine to thymine transversion at the third position of codon 249 in the p53 tumor suppressor gene has been reported in 10-70% of HCCs from areas of high dietary exposure to aflatoxin B(1.)	Aflatoxin B1	221-232	P53	Homo sapiens	120-123
12389116-14	2002	Etoposide and vinblastine were found to effectively inactivate the androgen-independent cell lines, in which p53 is dysfunctional.	Etoposide	0-9	P53	Homo sapiens	109-112
18413792-0	2008	Histone deacetylase inhibitor FK228 enhances adenovirus-mediated p53 family gene therapy in cancer models.	romidepsin	30-35	P53	Homo sapiens	65-68
12556448-9	2003	We also demonstrate that the susceptibility to TSA- and SAHA-induced cell death is regulated by p53.	trichostatin A	47-50	P53	Homo sapiens	96-99
18413792-6	2008	Pretreatment with FK228 enhanced apoptosis in human cancer cells through enhanced transduction of Ad-p53.	romidepsin	18-23	P53	Homo sapiens	101-104
18413792-7	2008	FK228 also induced hyperacetylation of the p53 protein and specifically enhanced p53-mediated Noxa expression.	romidepsin	0-5	P53	Homo sapiens	43-46
18413792-7	2008	FK228 also induced hyperacetylation of the p53 protein and specifically enhanced p53-mediated Noxa expression.	romidepsin	0-5	P53	Homo sapiens	81-84
12181752-6	2002	The significance of the mitochondrial pathway for the cerulenin-mediated apoptosis was confirmed by the rapid mitochondrial release of cytochrome c both in wild-type p53 and mutant cell lines.	Cerulenin	54-63	P53	Homo sapiens	166-169
18377724-6	2008	CAS overexpression enhanced p53 accumulation induced by doxorubicin, 5-fluorouracil, cisplatin, tamoxifen, and etoposide.	Etoposide	111-120	P53	Homo sapiens	28-31
12646262-8	2003	The addition of butyrolactone I, which is an inhibitor of CDK1 and CDK2, to the p53-negative cells reduced the floating round cell population and induced the disappearance of cyclin B1.	4-Butyrolactone	16-29	P53	Homo sapiens	80-83
18507005-2	2008	The effectiveness of one of the novel HDACIs, FK228, was examined in adenovirus-mediated p53 gene therapy of esophageal squamous cell carcinoma (ESCC).	romidepsin	46-51	P53	Homo sapiens	89-92
12082608-3	2002	In an effort to shed light on consequences mediated by p53 inactivation in gliomas, we established the Tet-On system for p53 in the LN-Z308 glioblastoma cell line.	tetramethylenedisulfotetramine	103-106	P53	Homo sapiens	121-124
18507005-11	2008	CONCLUSION: Our findings suggest that FK228 has a potent ability to augment the effect of adenovirus-mediated p53 gene therapy in ESCC cells.	romidepsin	38-43	P53	Homo sapiens	110-113
12586742-6	2003	Treatment with 80 microg/ml EGCG induced the tumor suppressor p53, which was functional as judged by activation of the target cyclin-dependent kinase inhibitor p21CIP1.	epigallocatechin gallate	28-32	P53	Homo sapiens	62-65
12586742-10	2003	Thus, EGCG inhibits growth and induces death of SMCs in a p53- and NF-kappaB-dependent manner.	epigallocatechin gallate	6-10	P53	Homo sapiens	58-61
18334012-4	2008	P53 was overexpressed in a subset of CS-99 cells.	Cesium	37-39	P53	Homo sapiens	0-3
12690294-8	2003	Furthermore, examination of the levels of apoptosis regulatory proteins showed that, while levels of p53, Bax and p21 are higher, that of anti-apoptotic Bcl-2 is undetectable in cells treated with 2-ME compared with untreated controls.	2-Methoxyestradiol	197-201	P53	Homo sapiens	101-104
11923280-2	2002	Recent studies have reported that the phosphatidylinositol 3-OH-kinase-Akt pathway inhibits p53-mediated transcription and apoptosis, although the underlying mechanisms have yet to be determined.	Phosphatidylinositols	38-58	P53	Homo sapiens	92-95
11923280-8	2002	The serum-induced increase in p53 ubiquitination was blocked by LY294002, a phosphatidylinositol 3-OH-kinase inhibitor.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	64-72	P53	Homo sapiens	30-33
11923280-8	2002	The serum-induced increase in p53 ubiquitination was blocked by LY294002, a phosphatidylinositol 3-OH-kinase inhibitor.	Phosphatidylinositols	76-96	P53	Homo sapiens	30-33
12082016-11	2002	A reported clinical association of Tp53 immunopositive colorectal cancers with use of the antihypertensive agents was extended by the demonstration of hydralazine and nifedipine as Tp53-inducers.	Hydralazine	151-162	P53	Homo sapiens	35-39
12606585-3	2003	We show that p53 and BLM accumulated after hydroxyurea (HU) treatment, and physically associated and co-localized with each other and with RAD51 at sites of stalled DNA replication forks.	Hydroxyurea	43-54	P53	Homo sapiens	13-16
18224251-4	2008	In primary fibroblasts with mutations in the core complex FANCA protein, we discovered that basal expression and phosphorylation of ATM (ataxia telangiectasia mutated) and p53 induced by irradiation (IR) or mitomycin C (MMC) were upregulated.	Mitomycin	207-218	P53	Homo sapiens	172-175
12641444-7	2003	Of this group, arsenic trioxide was the strongest inducer of cellular p53, while dimethylarsinic acid, iododimethylarsine, and sodium arsenite also caused p53 induction in a dose- and time-dependent manner.	sodium arsenite	127-142	P53	Homo sapiens	155-158
12046074-1	2002	AIM: In hepatocellular carcinoma (HCC) prevalent areas of China, the point mutation of p53 exon7 is highly correlated with Hepatitis B virus(HBV) infection and aflatoxin B intake.	Aflatoxin B1	160-171	P53	Homo sapiens	87-90
11864976-0	2002	The course of etoposide-induced apoptosis from damage to DNA and p53 activation to mitochondrial release of cytochrome c.	Etoposide	14-23	P53	Homo sapiens	65-68
18224251-4	2008	In primary fibroblasts with mutations in the core complex FANCA protein, we discovered that basal expression and phosphorylation of ATM (ataxia telangiectasia mutated) and p53 induced by irradiation (IR) or mitomycin C (MMC) were upregulated.	Mitomycin	220-223	P53	Homo sapiens	172-175
11864976-3	2002	Etoposide caused the phosphorylation of p53 within 6 h, an effect prevented by wortmannin, an inhibitor of DNA-dependent protein kinase (DNA-PK).	Etoposide	0-9	P53	Homo sapiens	40-43
18191951-0	2008	Interferonalpha enhances etoposide-induced apoptosis in human osteosarcoma U2OS cells by a p53-dependent pathway.	Etoposide	25-34	P53	Homo sapiens	91-94
11864976-4	2002	The activation of p53 by etoposide resulted in the up-regulation of the pro-apoptotic protein Bax, a result that was prevented by the protein synthesis inhibitor cycloheximide.	Etoposide	25-34	P53	Homo sapiens	18-21
11980662-9	2002	Both inducible TS expression and the addition of exogenous thymidine (10 microM) blocked p53 and p21 induction by the antifolates but not by 5-FU in the M7TS90 cell line.	Thymidine	59-68	P53	Homo sapiens	89-92
12619109-3	2003	In populations exposed to dietary aflatoxin B1 with liver cancer (AFB1) and ultraviolet (UV)-radiation with skin cancer, a single specific-looking TP53 mutation has been described in some of the tumors.	Aflatoxin B1	34-46	P53	Homo sapiens	147-151
12609712-4	2003	Up-regulation of p53 coincided with accretion of 8-oxoguanine lesions.	8-hydroxyguanine	49-61	P53	Homo sapiens	17-20
18191951-4	2008	IFNalpha enhanced etoposide-induced growth inhibition and apoptosis in p53-wild U2OS cells but not p53-mutant MG63 cells in a dose- and time-dependent manner.	Etoposide	18-27	P53	Homo sapiens	71-74
11934438-0	2002	Role of P53 functionality in the genotoxicity of metronidazole and its hydroxy metabolite.	Metronidazole	49-62	P53	Homo sapiens	8-11
11948395-0	2002	Characterization of the p53-rescue drug CP-31398 in vitro and in living cells.	CP 31398	40-48	P53	Homo sapiens	24-27
11948395-1	2002	The Pfizer compound CP-31398 has been reported to stabilize the core domain of the tumour suppressor p53 in vitro and be an effective anti-cancer drug by virtue of rescuing destabilized mutants of p53.	CP 31398	20-28	P53	Homo sapiens	101-104
12468545-5	2003	After treatment with Vp16 or mitomycin C, control cells underwent apoptosis in a p53-dependent manner; however, overexpression of catalase inhibited this apoptosis.	Etoposide	21-25	P53	Homo sapiens	81-84
12468545-5	2003	After treatment with Vp16 or mitomycin C, control cells underwent apoptosis in a p53-dependent manner; however, overexpression of catalase inhibited this apoptosis.	Mitomycin	29-40	P53	Homo sapiens	81-84
12468545-6	2003	Basal levels as well as Vp16- or mitomycin C-stimulated levels of p53 and p21 protein were decreased in the catalase-overexpressing cells as compared with control cells; however, p53 mRNA levels were not decreased by catalase.	Mitomycin	33-44	P53	Homo sapiens	66-69
11948395-1	2002	The Pfizer compound CP-31398 has been reported to stabilize the core domain of the tumour suppressor p53 in vitro and be an effective anti-cancer drug by virtue of rescuing destabilized mutants of p53.	CP 31398	20-28	P53	Homo sapiens	197-200
18191951-9	2008	Thus we conclude that IFNalpha enhances etoposide-induced apoptosis in human osteosarcoma U2OS cells by a p53-dependent and caspase-activation pathway.	Etoposide	40-49	P53	Homo sapiens	106-109
11948395-6	2002	CP-31398 also decreased sequence-specific DNA binding of wild-type p53 and His-273 mutant p53.	CP 31398	0-8	P53	Homo sapiens	67-70
11948395-6	2002	CP-31398 also decreased sequence-specific DNA binding of wild-type p53 and His-273 mutant p53.	CP 31398	0-8	P53	Homo sapiens	90-93
12680200-3	2003	Since many chemotherapeutic drugs induce p53-dependent apoptosis, we sought to investigate if CP-31398 would enhance chemosensitivity in human melanoma cells by stabilizing p53.	CP 31398	94-102	P53	Homo sapiens	173-176
18245478-3	2008	In vitro treatment with etoposide only and in vivo treatment with either etoposide or mitoxantrone induces DNA damage, elevates expression (600-fold) and promotes nuclear translocation of p53, and results in apoptosis of leukemic clam hemocytes.	Etoposide	24-33	P53	Homo sapiens	188-191
13129816-5	2003	As(2)O(3)-induced apoptosis was associated with upregulation of p53 and caspase 3, whereas NaAsO(2)-induced apoptosis was associated with p53 upregulation.	sodium arsenite	91-99	P53	Homo sapiens	138-141
13129817-0	2003	Apoptosis mediated by phosphatidylcholine-specific phospholipase C is associated with cAMP, p53 level, and cell-cycle distribution in vascular endothelial cells.	Phosphatidylcholines	22-41	P53	Homo sapiens	92-95
14622914-6	2003	Treatments that modified the alkaloid-induced Ca2+ influx including tetrodotoxin or Ca2+ removal, prevented either veratridine-induced cell death or p53 immunoreactivity.	Tetrodotoxin	68-80	P53	Homo sapiens	149-152
11948395-7	2002	CP-31398 had a non-specific toxic effect independent of mutant p53 expression in several cell lines carrying Tet-regulated mutant p53.	CP 31398	0-8	P53	Homo sapiens	130-133
11948395-7	2002	CP-31398 had a non-specific toxic effect independent of mutant p53 expression in several cell lines carrying Tet-regulated mutant p53.	tetramethylenedisulfotetramine	109-112	P53	Homo sapiens	130-133
11948395-8	2002	CP-31398 caused a small increase in MDM-2 expression and a more pronounced p53-independent increase in Bax expression.	CP 31398	0-8	P53	Homo sapiens	75-78
11948395-9	2002	CP-31398 did, however, induce the PAb1620 epitope (characteristic of native p53) in cells expressing His-175 mutant p53.	CP 31398	0-8	P53	Homo sapiens	76-79
11948395-9	2002	CP-31398 did, however, induce the PAb1620 epitope (characteristic of native p53) in cells expressing His-175 mutant p53.	CP 31398	0-8	P53	Homo sapiens	116-119
11948395-10	2002	This was prevented by cycloheximide, suggesting that any stabilizing action of CP-31398 would have to be on newly synthesized p53.	CP 31398	79-87	P53	Homo sapiens	126-129
18245478-3	2008	In vitro treatment with etoposide only and in vivo treatment with either etoposide or mitoxantrone induces DNA damage, elevates expression (600-fold) and promotes nuclear translocation of p53, and results in apoptosis of leukemic clam hemocytes.	Etoposide	73-82	P53	Homo sapiens	188-191
11781135-0	2002	Activation of Erk1/Erk2 and transiently increased p53 levels together may account for p21 expression associated with phorbol ester-induced transient growth inhibition in HepG2 cells.	Phorbol Esters	117-130	P53	Homo sapiens	50-53
11781135-5	2002	Either the activation of PKC with phorbol ester or the addition of BIM to cells growing in serum induced a rapid but transient increase of p53 levels, which preceded growth inhibition.	Phorbol Esters	34-47	P53	Homo sapiens	139-142
18245478-4	2008	Pretreatment with wheat germ agglutinin followed by etoposide treatment induces DNA damage and elevates p53 expression (893-fold) but does not overcome cytoplasmic sequestration of p53 or induce apoptosis.	Etoposide	52-61	P53	Homo sapiens	104-107
11809417-9	2002	Pretreatment with pyrrolidine dithiocarbamate (PDTC), an inhibitor of the redox sensitive transcription factor NF-kappa B, abrogated the increased expression of p53 protein in response to H(2)O(2), and enhanced cell survival.	pyrrolidine dithiocarbamic acid	18-45	P53	Homo sapiens	161-164
12471108-2	2002	This repression is independent of the intrinsic transcriptional activity of p53 and is mediated by the Tax-responsive CD28RE-3"-12-O-tetradecanoylphorbol-13-acetate response element (AP1) element of the IL-2 promoter.	cd28re-3"-12-o-tetradecanoylphorbol-13-acetate	118-164	P53	Homo sapiens	76-79
11809417-9	2002	Pretreatment with pyrrolidine dithiocarbamate (PDTC), an inhibitor of the redox sensitive transcription factor NF-kappa B, abrogated the increased expression of p53 protein in response to H(2)O(2), and enhanced cell survival.	pyrrolidine dithiocarbamic acid	47-51	P53	Homo sapiens	161-164
18043262-6	2008	CP-31398 was the first small molecule identified with the ability to restore the wild-type conformation to mutant p53.	CP 31398	0-8	P53	Homo sapiens	114-117
12454767-10	2002	In conclusion, tumour stage, node stage, p53 gene status, and bcl-2 expression are independent predictors of tumour response to platin-fluorouracil in patients with squamous-cell carcinomas of the head and neck.	platin-fluorouracil	128-147	P53	Homo sapiens	41-44
12507920-8	2002	These results are also consistent with the hypothesis that BP (PAH) induce G:C to T:A transversion mutations in the hotspot codons of the p53 tumor suppressor gene and are thus involved in malignant transformation of the lung tissue of smokers.	p-Aminohippuric Acid	63-66	P53	Homo sapiens	138-141
18097557-2	2008	Trichostatin A (TSA), ITF2357 and suberoylanilide hydroxamic acid (SAHA), which were very effective agents, caused apoptotic effects after a lag phase of 12-16 h. In order to elucidate the mechanism of HDACIs action in HepG2 cells we have studied the effects of TSA, ITF2357 and SAHA on acetylation of p53 and histones H2A, H2B, H3 and H4.	trichostatin A	0-14	P53	Homo sapiens	302-305
12402298-6	2002	With formamidopyrimidine-DNA glycosylase treatment, N-OH-AF induced cleavage at guanine residues, especially of the ACG sequence complementary to codon 273, a well-known hot spot of the p53 gene.	acceleratory factor from growth hormone	116-119	P53	Homo sapiens	186-189
11818510-6	2002	Competition for coactivator CREB binding protein could not entirely account for the repression but trichostatin A, an inhibitor of histone deacetylase activity, could reverse p53-mediated repression of HNF4alpha1.	trichostatin A	99-113	P53	Homo sapiens	175-178
11818510-7	2002	In contrast, p53-mediated repression of transcriptional activation of the same promoter by another transcriptional activator, CCAAT/enhancer-binding protein-alpha, could not be reversed by the addition of trichostatin A.	trichostatin A	205-219	P53	Homo sapiens	13-16
11821962-5	2002	Mutant p53 stimulates recombination induced by the replication elongation inhibitors (aphidicolin, hydroxyurea and Ara-C) but is without effect on recombination induced by the initiation inhibitors (mimosine and ciclopirox olamine).	Hydroxyurea	99-110	P53	Homo sapiens	7-10
11791171-5	2002	In PA1-neo cells with wild-type p53, the activation of caspases including caspases 9, 8, 7 and 3 and cleavage of PARP were detected following adriamycin or etoposide treatment, whereas no such changes were observed in PA1-E6 cells whose p53 is degraded, suggesting that loss of p53 impairs caspase activation.	Etoposide	156-165	P53	Homo sapiens	32-35
11791171-5	2002	In PA1-neo cells with wild-type p53, the activation of caspases including caspases 9, 8, 7 and 3 and cleavage of PARP were detected following adriamycin or etoposide treatment, whereas no such changes were observed in PA1-E6 cells whose p53 is degraded, suggesting that loss of p53 impairs caspase activation.	Etoposide	156-165	P53	Homo sapiens	237-240
12421475-6	2002	The expression of G1 S checkpoint related proteins, p53, p21/WAF1, and p16/INK4, were up-regulated after MGC 803 cells were treated with isoverbascoside 20 micromol/L for 4-8 h. Contrarily, the expression of C-myc protein was suppressed after 8 h treatment.	isoacteoside	137-152	P53	Homo sapiens	52-55
11791171-5	2002	In PA1-neo cells with wild-type p53, the activation of caspases including caspases 9, 8, 7 and 3 and cleavage of PARP were detected following adriamycin or etoposide treatment, whereas no such changes were observed in PA1-E6 cells whose p53 is degraded, suggesting that loss of p53 impairs caspase activation.	Etoposide	156-165	P53	Homo sapiens	237-240
18097557-2	2008	Trichostatin A (TSA), ITF2357 and suberoylanilide hydroxamic acid (SAHA), which were very effective agents, caused apoptotic effects after a lag phase of 12-16 h. In order to elucidate the mechanism of HDACIs action in HepG2 cells we have studied the effects of TSA, ITF2357 and SAHA on acetylation of p53 and histones H2A, H2B, H3 and H4.	trichostatin A	16-19	P53	Homo sapiens	302-305
18032786-0	2007	The increase of cell-membranous phosphatidylcholines containing polyunsaturated fatty acid residues induces phosphorylation of p53 through activation of ATR.	Phosphatidylcholines	32-52	P53	Homo sapiens	127-130
12168779-0	2002	Expression of p53 and its transcriptional target genes mRNAs in the ethylnitrosourea-induced apoptosis and cell cycle arrest in the fetal central nervous system.	Ethylnitrosourea	68-84	P53	Homo sapiens	14-17
12642691-0	2002	The histone deacetylase inhibitor FR901228 (desipeptide) restores expression and function of pseudo-null p53.	romidepsin	34-42	P53	Homo sapiens	105-108
12642691-0	2002	The histone deacetylase inhibitor FR901228 (desipeptide) restores expression and function of pseudo-null p53.	desipeptide	44-55	P53	Homo sapiens	105-108
18032786-0	2007	The increase of cell-membranous phosphatidylcholines containing polyunsaturated fatty acid residues induces phosphorylation of p53 through activation of ATR.	Fatty Acids, Unsaturated	64-90	P53	Homo sapiens	127-130
12642691-2	2002	Here we demonstrated that treatment of SW-1736 cells with sub-cytotoxic concentrations of FR901228, a histone deacetylase (HDAC) inhibitor, results in marked induction of p53 mRNA and protein.	romidepsin	90-98	P53	Homo sapiens	171-174
12642691-3	2002	The p53 induced by FR901228 was functional as evidenced by mdm-2 and p21 transactivation, and its further accumulation following DNA damage by doxorubicin.	romidepsin	19-27	P53	Homo sapiens	4-7
18032786-8	2007	The time course of phosphorylation of Ser15 in p53 correlates with increasing levels of PCs containing polyunsaturated fatty acids.	Fatty Acids, Unsaturated	103-130	P53	Homo sapiens	47-50
12181752-2	2002	Here we report that cerulenin is an effective inducer of apoptosis in different wild-type p53 and mutant p53 tumor cell lines, whereas normal human keratinocytes and fibroblasts are resistant to the apoptotic effect.	Cerulenin	20-29	P53	Homo sapiens	90-93
17669439-6	2007	Elevated expressions of p53 and p21 with a decrease in cyclin-D level supported the observation on cell cycle arrest following TSA treatment.	trichostatin A	127-130	P53	Homo sapiens	24-27
12181752-2	2002	Here we report that cerulenin is an effective inducer of apoptosis in different wild-type p53 and mutant p53 tumor cell lines, whereas normal human keratinocytes and fibroblasts are resistant to the apoptotic effect.	Cerulenin	20-29	P53	Homo sapiens	105-108
11964141-0	2002	Copper uptake is required for pyrrolidine dithiocarbamate-mediated oxidation and protein level increase of p53 in cells.	pyrrolidine dithiocarbamic acid	30-57	P53	Homo sapiens	107-110
11964141-7	2002	Bathocuproinedisulphonic acid as well as the hydroxyl radical scavenger d-mannitol inhibited the PDTC-dependent increase in p53 protein and oxidation.	Hydroxyl Radical	45-61	P53	Homo sapiens	124-127
12462448-5	2002	Observations that mutations in gene p53 appear under conditions of occupational and environmental exposures to chemical and physical carcinogens, such as vinyl chloride, radon, or aflatoxin B1, have proved to be of enormous importance for the occupational and environmental health.	Aflatoxin B1	180-192	P53	Homo sapiens	36-39
11741290-0	2001	Camptothecin and Zeocin can increase p53 levels during all cell cycle stages.	Camptothecin	0-12	P53	Homo sapiens	37-40
11741290-7	2001	The p53 induced by both drugs was able to bind to DNA; however, only the p53 induced by camptothecin was phosphorylated at serine-392.	Camptothecin	88-100	P53	Homo sapiens	4-7
11741290-7	2001	The p53 induced by both drugs was able to bind to DNA; however, only the p53 induced by camptothecin was phosphorylated at serine-392.	Camptothecin	88-100	P53	Homo sapiens	73-76
12118068-6	2002	Fibroblasts from Alzheimer"s disease patients also have a profound impairment in the H(2)O(2)-activated, p53-dependent pathway, which results in a lack of activation of p53 or p53-target genes, including p21, GADD45 and bax.	h(2)o	85-90	P53	Homo sapiens	105-108
18088187-10	2007	Moreover, sustained phosphorylation of Chk1 in the presence of staurosporine and UCN-01 is strongly related to phosphorylation of p53.	Staurosporine	63-76	P53	Homo sapiens	130-133
17906315-10	2007	In conclusion, this study demonstrated that sodium arsenite is genotoxic to uroepithelial cells in vitro, and that it will induce expression of mutant p53 and COX-2 proteins, indicating a possible key event in carcinogenesis.	sodium arsenite	44-59	P53	Homo sapiens	151-154
12492119-4	2002	Rottlerin, a PKCdelta inhibitor that prevents CP-induced proteolytic activation of PKCdelta, caused an accumulation of p53 in HeLa cells when treated in conjunction with CP, but it had no additional effect in HeLa/CP cells.	rottlerin	0-9	P53	Homo sapiens	119-122
11704535-5	2001	The CS-induced apoptosis was associated with increased oxidative stress, Bax protein accumulation, mitochondrial dysfunction, and mitochondrial cytochrome c release but was independent of p53, Fas, and caspase activation.	Cesium	4-6	P53	Homo sapiens	188-191
11698292-9	2001	In contrast, in vitro treatment with cytarabine and etoposide induced p53 protein, CD95 receptor expression, CD95 sensitivity, and CD95 receptor-ligand interaction in stimulated cycling lymphocytes, but no such induction was seen in resting cells.	Etoposide	52-61	P53	Homo sapiens	70-73
12143201-15	2002	The expression of p53 oncogene and the PCNA were determined by immunohistochemical method, using avidin-biotin method (DAKO).	avidin-biotin	97-110	P53	Homo sapiens	18-21
17904593-3	2007	Our results suggest that the protective effects of esculin (10(-7), 10(-6) and 10(-5) M) on DA-induced cytotoxicity may be ascribed to its anti-oxidative properties by reducing ROS level, and its anti-apoptotic effect via protecting mitochondrion membrane potential (DeltaPsim), enhancing superoxide dismutaese (SOD) activity and reduced glutathione (GSH) levels, and regulating P53, Bax and Bcl-2 expression.	Esculin	51-58	P53	Homo sapiens	379-382
12187957-5	2002	Immunohistochemical variables differed between various subsets: the number of p53-positive tumors was found to be prevailed among the PGB, whereas the number of tumors with EGFR and mdm2 positivity was significantly greater in SGB.	Prostaglandins B	134-137	P53	Homo sapiens	78-81
12048243-3	2002	DNA damage induced by camptothecin, which activates the tumor suppressor p53, was found to activate GSK3beta.	Camptothecin	22-34	P53	Homo sapiens	73-76
11668507-11	2001	NaB was effective even in the cancer cells with mutant p53 and/or Rb genes by eliciting cell senescence.	nab	0-3	P53	Homo sapiens	55-58
19383392-0	2007	p53 is required for etoposide-induced apoptosis of human embryonic stem cells.	Etoposide	20-29	P53	Homo sapiens	0-3
11593403-3	2001	In contrast, agents that inhibit the elongation phase of transcription, such as UV light, camptothecin or actinomycin D, induced the accumulation of nuclear p53 proteins that were modified at both of these sites.	Camptothecin	90-102	P53	Homo sapiens	157-160
19383392-2	2007	Here we investigate the role of p53 in etoposide-induced apoptosis.	Etoposide	39-48	P53	Homo sapiens	32-35
12036943-7	2002	Subtoxic concentrations of camptothecin (which stabilizes topoisomerase I cleavage complexes, mediating nonhomologous recombination) produced a dose-dependent increase in PALA(R) colonies, and combining expression of mutant p53 with exposure to camptothecin produced a greater than additive increase in PALA(R) colony formation.	Camptothecin	27-39	P53	Homo sapiens	224-227
19383392-4	2007	Etoposide treatment results in a rapid and extensive induction of apoptosis and leads to a further increase in p53 and PUMA expression as well as Bax processing.	Etoposide	0-9	P53	Homo sapiens	111-114
11551522-4	2001	Wild-type p53 containing WMN Burkitt"s lymphoma cells and wild type p53-deficient CA46 exhibited similar sensitivities to miltefosine.	miltefosine	122-133	P53	Homo sapiens	10-13
19383392-6	2007	hESC stably transduced with p53 shRNA display 80% reduction of endogenous p53 and exhibit an 80% reduction in etoposide-induced apoptosis accompanied by constitutive downregulation of Bax and an attenuated upregulation of PUMA.	Etoposide	110-119	P53	Homo sapiens	28-31
19383392-8	2007	Our study demonstrates that p53 is required for etoposide-induced apoptosis of hESC and reveals, at least in part, the molecular mechanism of DNA-damage-induced apoptosis in hESC.	Etoposide	48-57	P53	Homo sapiens	28-31
12076704-3	2002	Mutational screening of the coding region of TP53 revealed an A>T transversion in codon 144 of exon 5 (CAG>CTG, Gln>Leu) in the germline of one of the three affected members, with loss of heterozygosity (LOH) in the tumour tissue.	Glutamine	112-115	P53	Homo sapiens	45-49
17894897-8	2007	Etoposide increased p53 activity in all cell lines while hypoxia alone decreased it only in HepG2 cells.	Etoposide	0-9	P53	Homo sapiens	20-23
12011430-1	2002	A G to T mutation has been observed at the third position of codon 249 of the p53 tumor-suppressor gene in over 50% of the hepatocellular carcinoma cases associated with high exposure to aflatoxin B(1) (AFB(1)).	Aflatoxin B1	187-198	P53	Homo sapiens	78-81
11507071-9	2001	Loss of p53 function was selectively achieved by transduction of human papillomavirus 16 E6 (which degrades p53) into two drug-sensitive neuroblastoma cell lines with intact p53, causing high-level drug resistance to L-PAM, carboplatin, and etoposide.	Etoposide	241-250	P53	Homo sapiens	8-11
11997093-5	2002	Expression of CDM2 was shown to be transcriptionally upregulated in the primary CEF cells where p53 was activated by either mitomycin C treatment or by the exogenous transfection of the chicken p53 cDNA.	Mitomycin	124-135	P53	Homo sapiens	96-99
17894897-10	2007	Using low density DNA arrays to detect the expression of genes involved in the regulation of apoptosis, etoposide and hypoxia were shown to each influence the expression of numerous genes, many of the ones influenced by etoposide being p53 target genes.	Etoposide	104-113	P53	Homo sapiens	236-239
11431359-14	2001	hMLH1-dependent responses to fluoropyrimidine treatment, which may involve the action of p53 and the formation of DSBs, clearly have clinical relevance for the use of this class of drugs in the treatment of tumors with MMR deficiencies.	2-fluoropyrimidine	29-45	P53	Homo sapiens	89-92
17894897-10	2007	Using low density DNA arrays to detect the expression of genes involved in the regulation of apoptosis, etoposide and hypoxia were shown to each influence the expression of numerous genes, many of the ones influenced by etoposide being p53 target genes.	Etoposide	220-229	P53	Homo sapiens	236-239
17894897-12	2007	CONCLUSION: These results evidenced that there was a striking parallelism between the effect of hypoxia on the etoposide-induced p53 stabilization as well as p53 target gene expression and its effect on the etoposide-induced apoptosis according to the cell type.	Etoposide	111-120	P53	Homo sapiens	129-132
11929951-4	2002	METHODS: Proliferation and apoptosis were assessed in a panel of NSCLC cell lines that vary in the expression of the growth-regulating proteins p53, pRb, and K-Ras treated with a clinically relevant dose of FK228 (25 ng/mL).	romidepsin	207-212	P53	Homo sapiens	144-147
17894897-12	2007	CONCLUSION: These results evidenced that there was a striking parallelism between the effect of hypoxia on the etoposide-induced p53 stabilization as well as p53 target gene expression and its effect on the etoposide-induced apoptosis according to the cell type.	Etoposide	207-216	P53	Homo sapiens	129-132
11929951-6	2002	RESULTS: FK228 treatment inhibited growth and induced apoptosis in NSCLC cells expressing wild-type or mutant p53.	romidepsin	9-14	P53	Homo sapiens	110-113
11929951-7	2002	FK228 treatment led to altered expression of cyclin A, cyclin E, and p21, and to reduced expression of mutant, but not wild-type, p53.	romidepsin	0-5	P53	Homo sapiens	130-133
11479920-10	2001	Examination of the signaling pathways that mediate 2-ME-induced apoptosis showed reduction in the level of p53 expression and its DNA-binding activity.	2-Methoxyestradiol	51-55	P53	Homo sapiens	107-110
17894897-12	2007	CONCLUSION: These results evidenced that there was a striking parallelism between the effect of hypoxia on the etoposide-induced p53 stabilization as well as p53 target gene expression and its effect on the etoposide-induced apoptosis according to the cell type.	Etoposide	207-216	P53	Homo sapiens	158-161
11479920-11	2001	Given the fact that p53 mutations are common in patients with metastatic prostate cancer, our finding that 2-ME-mediated growth inhibition of human prostate cancer cells occurred in a p53-independent manner has considerable clinical significance.	2-Methoxyestradiol	107-111	P53	Homo sapiens	20-23
11929951-9	2002	FK228 treatment also inhibited the binding of mutant p53 and Raf-1 to Hsp90; this inhibition was associated with acetylation of Hsp90.	romidepsin	0-5	P53	Homo sapiens	53-56
17767476-9	2007	Unlike PPI alone, rofecoxib + PPI was associated with an increase in the apoptotic cell index, a decrease in p53 cell staining and VEGF expression in mucosal vessels.	rofecoxib	18-27	P53	Homo sapiens	109-112
11960380-5	2002	Surprisingly, we found that hydroxyurea-treated BLM-deficient cells exhibit an intact S phase arrest, proper recovery from the S phase arrest, and intact p53 and p21 responses.	Hydroxyurea	28-39	P53	Homo sapiens	154-157
11935300-6	2002	RESULTS: Ex vivo chemosensitivity testing showed that tumors with p53 mutations were significantly more resistant to the cyclophosphamide/etoposide/epirubicin regimen than with normal p53 gene ( P = 0.012).	Etoposide	138-147	P53	Homo sapiens	66-69
11841447-4	2002	The p53-transfected cells showed a decreased ability to arrest in G2 and an increase in apoptosis in response to etoposide treatment, relative to the control mock-transfected cells.	Etoposide	113-122	P53	Homo sapiens	4-7
11841447-5	2002	p53-transfected and control cells were treated with etoposide and trapped at mitosis with nocodazole.	Etoposide	52-61	P53	Homo sapiens	0-3
11278647-5	2001	A differential modulation of the p53 target gene (p21/WAF, bax, thrombospondin-1, and mdm-2) transcription was observed upon Mts1 induction in tet-inducible cell lines expressing wild type p53.	tetramethylenedisulfotetramine	143-146	P53	Homo sapiens	33-36
11278647-5	2001	A differential modulation of the p53 target gene (p21/WAF, bax, thrombospondin-1, and mdm-2) transcription was observed upon Mts1 induction in tet-inducible cell lines expressing wild type p53.	tetramethylenedisulfotetramine	143-146	P53	Homo sapiens	189-192
11406538-10	2001	A more striking association was found in G:C to A:T transitions in non-CpG dinucleotides; 71% (12 of 17) of the total non-CpG transition mutations in p53 were observed in MGMT aberrantly methylated tumors (Fischer"s exact test, two-tailed; P = 0.008).	Dinucleoside Phosphates	75-88	P53	Homo sapiens	150-153
11482451-8	2001	In the TP53 mutant cell lines, DU145 and BM1604, dose enhancement factors (EFs) were found to be in the region of 4.20 for cisplatin, 3.70 for vinblastine, and 3.20 for etoposide.	Etoposide	169-178	P53	Homo sapiens	7-11
11482451-9	2001	In the TP53 wild-type cell line, LNCaP, the enhancement factors were low and in the region of 1.20 for cisplatin, vinblastine and etoposide.	Etoposide	130-139	P53	Homo sapiens	7-11
11841447-6	2002	The mitotic index of p53-transfected cells was higher than that of the control cells, which suggests that p53 abrogates the G2 checkpoint response to etoposide treatment in K562 cells.	Etoposide	150-159	P53	Homo sapiens	21-24
11841447-6	2002	The mitotic index of p53-transfected cells was higher than that of the control cells, which suggests that p53 abrogates the G2 checkpoint response to etoposide treatment in K562 cells.	Etoposide	150-159	P53	Homo sapiens	106-109
11841447-7	2002	We found that the expression of the cell cycle checkpoint protein Chk1 was reduced in the etoposide-treated p53-transfected cells by 24 h, and this correlated with a reduction in the extent of etoposide-induced phosphorylation of CDK1 at tyrosine 15 (Y15).	Etoposide	90-99	P53	Homo sapiens	108-111
17876055-6	2007	Mechanistic studies suggested roles for Akt, GSK-3beta, MDM2, and p53 in enterolactone-dependent apoptosis.	2,3-bis(3'-hydroxybenzyl)butyrolactone	73-86	P53	Homo sapiens	66-69
11791186-5	2002	The inhibitory effect of wild type p53 was undetectable in the presence of trichostatin A, suggesting the involvement of histone deacetylation in negative regulation of PSA promoter activity.	trichostatin A	75-89	P53	Homo sapiens	35-38
11279186-3	2001	DNA interactions of active wild-type human p53 protein with DNA fragments and oligodeoxyribonucleotide duplexes modified by antitumor cisplatin and its clinically ineffective trans isomer (transplatin) were investigated by using a gel mobility shift assay.	Oligodeoxyribonucleotides	78-102	P53	Homo sapiens	43-46
11316564-6	2001	In terms of changes in expression of p53-related proteins, increase in expression of Bax and decrease in that of Bcl-2 were observed in TE-2 but not in TE-1, suggesting that the main mode of cell death induced by genistein in a cell line with wild type p53 differed from that with mutant p53.	Genistein	213-222	P53	Homo sapiens	37-40
11316564-6	2001	In terms of changes in expression of p53-related proteins, increase in expression of Bax and decrease in that of Bcl-2 were observed in TE-2 but not in TE-1, suggesting that the main mode of cell death induced by genistein in a cell line with wild type p53 differed from that with mutant p53.	Genistein	213-222	P53	Homo sapiens	253-256
17286201-3	2007	LY294002 potentiated expression of p21WAF1/Cip1 via a p53-independent mechanism and did not affect mitogen activated protein kinase (MAPK) activation.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	P53	Homo sapiens	54-57
11316564-6	2001	In terms of changes in expression of p53-related proteins, increase in expression of Bax and decrease in that of Bcl-2 were observed in TE-2 but not in TE-1, suggesting that the main mode of cell death induced by genistein in a cell line with wild type p53 differed from that with mutant p53.	Genistein	213-222	P53	Homo sapiens	253-256
11300786-2	2001	Wild-type p53 was basally expressed after baculovirus infection while a parallel preparation was treated with the phosphatase inhibitor okadaic acid during the terminal stages of expression to create a hyperphosphorylated form of p53 known for its higher DNA binding and transcriptional activation.	Okadaic Acid	136-148	P53	Homo sapiens	230-233
11400161-9	2001	Induction of endogenous p53 expression by etoposide also inhibited promoter activity and minigene inducibility.	Etoposide	42-51	P53	Homo sapiens	24-27
11756188-3	2002	CDDO-Me decreased the viability of leukemic cell lines, including multidrug resistant (MDR)-1-overexpressing, p53(null) HL-60-Dox and of primary AML cells, and it was 3- to 5-fold more active than CDDO.	bardoxolone methyl	0-7	P53	Homo sapiens	110-113
11756188-10	2002	In conclusion, CDDO-Me is an MDR-1- and a p53-independent compound that exerts strong antiproliferative, apoptotic, and differentiating effects in myeloid leukemic cell lines and in primary AML samples when given in submicromolar concentrations.	bardoxolone methyl	15-22	P53	Homo sapiens	42-45
12429914-5	2002	BL also inhibited the p53-dependent increase of p21 protein expression in cells exposed to the DNA damag-ing agent etoposide, and favored a greater G2/M arrest as compared to the non-BL exposed cells.	Etoposide	115-124	P53	Homo sapiens	22-25
11400165-6	2001	In elucidating these findings, it was determined that after 2 days of incubation with genistein, MCF-7 but not MDA-MB-231 cells, had significantly higher levels of p53.	Genistein	86-95	P53	Homo sapiens	164-167
17515610-5	2007	p21CIP1 was found to be a critical p53 target for arrest induced by hydroxyurea or aphidicolin, but not etoposide, as judged by the ability of p21CIP1 suppression to mimic the effects of p53 disruption.	Hydroxyurea	68-79	P53	Homo sapiens	35-38
11400165-8	2001	Levels of p21 increased in both of the genistein-treated cell lines, suggesting that p21 gene expression was activated but in a p53-independent manner, whereas no significant changes in levels of the pro-apoptotic protein, Bax, were found.	Genistein	39-48	P53	Homo sapiens	128-131
11862321-4	2002	Cells with different states of p53 expression, either endogenously or ectopically, were exposed to hydroxyurea to induce an imbalance of cellular dNTP pools and cause replication errors.	Hydroxyurea	99-110	P53	Homo sapiens	31-34
11862321-6	2002	Incubation of cells with hydroxyurea induced a similar degree of dNTP pool imbalance in each cell line, but caused significantly more mutations in cells lacking p53 protein expression.	Hydroxyurea	25-36	P53	Homo sapiens	161-164
11594760-10	2001	Exploration of p53 fluorescence using potassium iodide as a quencher confirmed that these fluorophores are already substantially quenched in the native structure, and this quenching is not relieved during protein unfolding.	Potassium Iodide	38-54	P53	Homo sapiens	15-18
17515610-5	2007	p21CIP1 was found to be a critical p53 target for arrest induced by hydroxyurea or aphidicolin, but not etoposide, as judged by the ability of p21CIP1 suppression to mimic the effects of p53 disruption.	Hydroxyurea	68-79	P53	Homo sapiens	187-190
11556844-1	2001	The present study was performed to gain insight into the role of p53 on the cytotoxicity of tubulin-binding agents (TBA) on cancer cells.	tba	116-119	P53	Homo sapiens	65-68
11556844-9	2001	We conclude that the p53 status of cancer cells influences their sensitivity to TBA cytotoxicity.	tba	80-83	P53	Homo sapiens	21-24
11346470-5	2001	Treatment with etoposide increased expression of p53 and decreased expression of Bcl-X(L) in U-373MG cells which harbored mutant p53.	Etoposide	15-24	P53	Homo sapiens	49-52
11346470-5	2001	Treatment with etoposide increased expression of p53 and decreased expression of Bcl-X(L) in U-373MG cells which harbored mutant p53.	Etoposide	15-24	P53	Homo sapiens	129-132
17515610-6	2007	Suppression of Rad51 expression, required for homologous recombination repair, blocked the ability of mutant p53 to antagonize arrest induced by etoposide, but not aphidicolin.	Etoposide	145-154	P53	Homo sapiens	109-112
17515610-8	2007	However, when replication stress is associated with DNA strand breaks (such as with etoposide), up-regulation of homologous recombination repair in response to p53 disruption becomes important.	Etoposide	84-93	P53	Homo sapiens	160-163
11283670-4	2001	A specific HDAC inhibitor, trichostatin A (TSA), upregulated p53 and von Hippel-Lindau expression and downregulated hypoxia-inducible factor-1alpha and vascular endothelial growth factor.	trichostatin A	27-41	P53	Homo sapiens	61-64
11431470-6	2001	In addition, treatment of cells with the PKC activator phorbol ester stimulated the ubiquitination of p53 and reduced its ability to accumulate after stress.	Phorbol Esters	55-68	P53	Homo sapiens	102-105
11283670-4	2001	A specific HDAC inhibitor, trichostatin A (TSA), upregulated p53 and von Hippel-Lindau expression and downregulated hypoxia-inducible factor-1alpha and vascular endothelial growth factor.	trichostatin A	43-46	P53	Homo sapiens	61-64
17699715-4	2007	Etoposide-selective cytotoxicity in the Akt-myr-transduced cells was shown to be caused by nonapoptotic cell death and occurred in a p53-independent manner.	Etoposide	0-9	P53	Homo sapiens	133-136
11313875-5	2001	Nuclear accumulation of p53 was induced in NB cells using substances which disturb p53"s tertiary structure at its zinc finger motif, or by treatment with mitomycin C.	Mitomycin	155-166	P53	Homo sapiens	24-27
11313875-7	2001	Even though p53 showed DNA-binding capability after mitomycin C treatment of NB cells, the target gene products MDM2 and p21(WAF1,CIP1,SDI1) were not synthesized and no p53 transactivating activity measured in a reporter gene assay.	Mitomycin	52-63	P53	Homo sapiens	12-15
11313880-2	2001	Treatment of human glioma cells with etoposide caused apoptosis only in cells expressing functional p53.	Etoposide	37-46	P53	Homo sapiens	100-103
11313880-3	2001	p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2",7"-dichlorofluorescin (DCFH) into 2",7"-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase.	DCFH	233-237	P53	Homo sapiens	0-3
11526514-8	2001	Our data revealed a relationship between chromosome 16q homozygous deletions and R249S p53 mutations in tumors where the patient had been exposed to aflatoxin B1 (P=0.002).	Aflatoxin B1	149-161	P53	Homo sapiens	87-90
11375983-3	2001	When ectopic wild-type p53 expression was induced to a physiologically relevant level in "tet-off" cultured cells in which p53 expression was tightly regulated by tetracycline, it was found that POLD1 steady-state mRNA was repressed by about 65%.	tetramethylenedisulfotetramine	90-93	P53	Homo sapiens	23-26
11585319-8	2001	We further obtained evidence of the upregulation of the intracellular apoptotic signalling cascade, represented by bcl-2 and bax, the transcription factor p53 and the active form of caspase 3, after pretreatment with mitomycin C.	Mitomycin	217-228	P53	Homo sapiens	155-158
17555331-3	2007	First, a rapid and direct incorporation of biotinylated GSH or GSSG into the purified recombinant p53 protein was observed.	Glutathione Disulfide	63-67	P53	Homo sapiens	98-101
11462153-11	2001	Western blot analysis of p53 and p21 revealed a gradual increase in the level of these proteins when RPE cells were exposed to increasing concentrations of MMC.	Mitomycin	156-159	P53	Homo sapiens	25-28
17555331-7	2007	When tumor cells treated with camptothecin or cisplatin were subsequently exposed to glutathione-enhancing agents, p53 underwent dethiolation accompanied by detectable increases in the level of p21waf1 expression, relative to the DNA-damaging drugs alone.	Camptothecin	30-42	P53	Homo sapiens	115-118
17555331-9	2007	Biotinylated maleimide also reacted rapidly with Cys141, implying that this is the most reactive cysteine on the p53 surface.	biotinylated maleimide	0-22	P53	Homo sapiens	113-116
11438577-3	2001	Previous evidence has shown that the death of embryonic cortical neurons treated with the DNA-damaging agent camptothecin is dependent on the tumor suppressor p53 and cyclin-dependent kinase (CDK) activity and that the inhibition of either pathway alone leads to enhanced and prolonged survival.	Camptothecin	109-121	P53	Homo sapiens	159-162
21603516-1	2007	OBJECTIVE: We have previously reported that oligodeoxyribonucleotides, designed to bind in a triplex fashion to a specific p53 binding site homology, inhibit the proliferation of colon cancer cells in vitro and in vivo.	Oligodeoxyribonucleotides	44-69	P53	Homo sapiens	123-126
11457508-4	2001	Here we demonstrate increased expression and co-localization of p53 and Mdm2 in the nuclei of degenerating neurons following treatment with either the excitotoxin, kainic acid, or the topoisomerase I inhibitor, camptothecin.	Camptothecin	211-223	P53	Homo sapiens	64-67
11223035-3	2001	In this report, the DNA alkylating agents mitomycin C (MMC) and methylmethane sulfonate (MMS), as well as UV radiation, stabilized p53 in a manner independent of phosphorylation in p53 N-terminus.	Mitomycin	42-53	P53	Homo sapiens	131-134
11223035-3	2001	In this report, the DNA alkylating agents mitomycin C (MMC) and methylmethane sulfonate (MMS), as well as UV radiation, stabilized p53 in a manner independent of phosphorylation in p53 N-terminus.	Mitomycin	55-58	P53	Homo sapiens	131-134
11159535-5	2001	Results show that the mdm2 antisense oligodeoxynucleotide induces apoptosis of cells that express a high or low level of MDM2 protein, only if they contain wild-type p53.	Oligodeoxyribonucleotides	37-57	P53	Homo sapiens	166-169
17258428-6	2007	A screening study on 31 metal compounds, showed that the classified human carcinogens (NaAsO2, CdSO4 .8H2O, Na2CrO4 .4H2O, MnCl2, (NH4)2PtCl6) significantly increased cytotoxicity in p53-expressing cells compared to non-expressing cells, suggesting that their cytotoxicity was p53-mediated.	cdso4 .8h2o	95-106	P53	Homo sapiens	183-186
11159535-7	2001	Finally, the p53 antisense oligodeoxynucleotide, which inhibits the expression of wild-type p53, also induces a decrease of the MDM2 level in cells, whether or not they overexpress this protein, and causes apoptosis of these cells.	Oligodeoxyribonucleotides	27-47	P53	Homo sapiens	13-16
11159535-7	2001	Finally, the p53 antisense oligodeoxynucleotide, which inhibits the expression of wild-type p53, also induces a decrease of the MDM2 level in cells, whether or not they overexpress this protein, and causes apoptosis of these cells.	Oligodeoxyribonucleotides	27-47	P53	Homo sapiens	92-95
11172593-5	2001	Upon DNA damage by treatment with mitomycin C the DNA-binding activity was increased, as known for cells with wild-type p53.	Mitomycin	34-45	P53	Homo sapiens	120-123
11433418-8	2001	PEAZ-1 respond to ocadaic acid, a pro-apoptotic agent, by expression of p53.	Okadaic Acid	18-30	P53	Homo sapiens	72-75
11418138-1	2001	This paper studies the cytotoxic effect induced by the topoisomerase I inhibitor camptothecin in human osteosarcoma Saos-2 cells, which lack p53 and contain a non-functional form of the product of the retinoblastoma gene, pRb.	Camptothecin	81-93	P53	Homo sapiens	141-144
11498763-12	2001	In addition, we determined the effects of DNA damage produced by the DNA topoisomerase II inhibitor etoposide on wild-type p53 transfected lymphoma cells.	Etoposide	100-109	P53	Homo sapiens	123-126
11313973-9	2001	Moreover, the enhancement of hyperploid formation by staurosporine was also blocked by p53-dependent G1 checkpoint.	Staurosporine	53-66	P53	Homo sapiens	87-90
11299739-6	2001	We therefore concluded that immunohistochemical studies for p53 and p21 were useful for predicting the chemosensitivities of colon and gastric cancer to MMC and 5-FU.	Mitomycin	153-156	P53	Homo sapiens	60-63
11299740-7	2001	In addition, staurosporine or UCNO1 specifically sensitized p53 incompetent cells to adriamycin.	Staurosporine	13-26	P53	Homo sapiens	60-63
17258428-6	2007	A screening study on 31 metal compounds, showed that the classified human carcinogens (NaAsO2, CdSO4 .8H2O, Na2CrO4 .4H2O, MnCl2, (NH4)2PtCl6) significantly increased cytotoxicity in p53-expressing cells compared to non-expressing cells, suggesting that their cytotoxicity was p53-mediated.	cdso4 .8h2o	95-106	P53	Homo sapiens	277-280
17146434-6	2007	In the human dedifferentiated liposarcoma cell line (LS141) and the p53 wild-type HCT116 cells, Nutlin-3a induced downregulation of E2F1 and this effect appeared to be proteasome dependent.	nutlin 3	96-105	P53	Homo sapiens	68-71
11405176-0	2001	Mitomycin C and cisplatin enhanced the antitumor activity of p53-expressing adenovirus in cervical cancer cells.	Mitomycin	0-11	P53	Homo sapiens	61-64
11387205-2	2001	Here we provide evidence that overexpression of Gas2 efficiently increases cell susceptibility to apoptosis following UV irradiation, etoposide and methyl methanesulfonate treatments, and that these effects are dependent on increased p53 stability and transcription activity.	Etoposide	134-143	P53	Homo sapiens	234-237
11484935-2	2001	We found that four anticancer agents: etoposide, doxorubicin, bleomycin and paclitaxel induced apoptosis in human umbilical vein endothelial cells (HUVECs) (as judged by DNA fragmentation) with a time- and concentration-dependent decrease in bcl-2 protein but without the involvement of p53.	Etoposide	38-47	P53	Homo sapiens	287-290
17173070-1	2007	DDB2, a gene mutated in XPE patients, is involved in global genomic repair especially the repair of cyclobutane pyrimidine dimers (CPDs), and is regulated by p53 in human cells.	Cyclobutanes	100-111	P53	Homo sapiens	158-161
11295047-2	2001	A block of cell cycle checkpoint by dexamethasone and genistein correlates with a selective induction of cyclin-dependent kinase (Cdk) inhibitor p21WAF1/CIP1 in a tumor suppressor p53-independent manner and abolishment of Cdk2 phosphorylation.	Genistein	54-63	P53	Homo sapiens	180-183
11180394-9	2001	In MDA-MB-435 cells exposed to L-Ann or Dx, no change was observed in the expression of bax, but there was a p53-independent increase in p21(waf1) expression.	l-ann	31-36	P53	Homo sapiens	109-112
11180394-10	2001	In MCF7 cells, treatment with L-Ann or Dx induced an increase in p53 expression with a consequent transactivation of p21(waf1) and bax.	l-ann	30-35	P53	Homo sapiens	65-68
11180394-11	2001	Our results indicate that L-Ann is more cytotoxic than Dx in breast cancer cells and is able to induce apoptosis through p53-independent mechanisms.	l-ann	26-31	P53	Homo sapiens	121-124
17130833-10	2007	CP-31398, another p53 rescue drug, similarly reduced cell surface levels of CXCR4.	CP 31398	0-8	P53	Homo sapiens	18-21
11695553-7	2001	Overexpression of human c-Ha-ras gene or p53 gene knockout appeared to increase constitutive UGT activity toward 4-nitrophenol.	4-nitrophenol	113-126	P53	Homo sapiens	41-44
11695560-4	2001	Two hormones that are human tumorigens, diethylstilbestrol and 17beta-estradiol, gave positive and equivocal results, respectively, in the pituitary with p53-deficient mice showing a greater incidence of proliferative lesions than wild type.	Diethylstilbestrol	40-58	P53	Homo sapiens	154-157
11286989-5	2001	In addition, genistein enhanced the expression of the cell cycle inhibitor p21(waf/cip1) by 10- to 15-fold, increased p21(waf/cip1) association with Cdc2 by 2-fold, and increased the expression of the tumor suppressor p53 by 2.8-fold.	Genistein	13-22	P53	Homo sapiens	218-221
11313933-0	2001	Activation of the Fas pathway independently of Fas ligand during apoptosis induced by camptothecin in p53 mutant human colon carcinoma cells.	Camptothecin	86-98	P53	Homo sapiens	102-105
17097281-12	2007	After treatment with swainsonine at the concentrations of 0.5, 1.5 and 4.5 microg/ml for 24 h, the expression of apoptosis inhibiting gene p53 and bcl-2 decreases, and the apoptotic trigger gene c-myc increases markedly (p&lt;0.05), as well as [Ca2+]i overloading, SGC-7901 cell is induced to apoptosis in the end.	Swainsonine	21-32	P53	Homo sapiens	139-142
11333133-6	2001	When a p53 genetic suppressor element that encodes a dominant negative polypeptide (termed GSE56) was introduced into the CMN cells, the transfected cells were more sensitive to UV-induced DNA breakage.	gse56	91-96	P53	Homo sapiens	7-10
11090076-8	2000	These findings indicate that treatment with etoposide, Ara-C, or doxorubicin up-regulates DR5 levels in a p53-independent manner and sensitizes human acute leukemia cells to Apo-2L-induced apoptosis.	Etoposide	44-53	P53	Homo sapiens	106-109
11050162-7	2000	These results are consistent with the hypothesis that the generation of oxygen/nitrogen species and unsaturated aldehydes from iron and copper overload in hemochromatosis and WD causes mutations in the p53 tumor suppressor gene.	unsaturated aldehydes	100-121	P53	Homo sapiens	202-205
11401473-6	2001	Accumulation of P53 and its target gene bax then sensitized HeLa cells to cell-cycle arrest, cell death/apoptosis induced by cisplatin, and etoposide.	Etoposide	140-149	P53	Homo sapiens	16-19
11106264-0	2000	p53 dependence of Fas induction and acute apoptosis in response to 5-fluorouracil-leucovorin in human colon carcinoma cell lines.	5-fluorouracil-leucovorin	67-92	P53	Homo sapiens	0-3
17057733-7	2007	This transactivation was enhanced by etoposide, a DNA damaging agent that activates p53 and was completely blocked by a dominant-negative p53 mutant.	Etoposide	37-46	P53	Homo sapiens	84-87
11029511-0	2000	UCN-01 and camptothecin induce DNA double-strand breaks in p53 mutant tumor cells, but not in normal or p53 negative epithelial cells.	Camptothecin	11-23	P53	Homo sapiens	59-62
11029511-1	2000	Previous research has shown synergistic growth inhibition between UCN-01 and camptothecin (CPT) in tumor cells with mutant p53 versus tumor cells with wild-type p53.	Camptothecin	77-89	P53	Homo sapiens	123-126
11802967-13	2001	(4) The expression of p53 or Bax gene in salbutamol or 8-Br- cAMP group was significantly higher than that in control group, but the expression of BCl-2 gene was lower than that in control group.	Albuterol	41-51	P53	Homo sapiens	22-25
11802967-13	2001	(4) The expression of p53 or Bax gene in salbutamol or 8-Br- cAMP group was significantly higher than that in control group, but the expression of BCl-2 gene was lower than that in control group.	8-Bromo Cyclic Adenosine Monophosphate	55-65	P53	Homo sapiens	22-25
11313865-0	2001	p53 protein accumulation in addition to the transactivation activity is required for p53-dependent cell cycle arrest after treatment of cells with camptothecin.	Camptothecin	147-159	P53	Homo sapiens	0-3
11029511-1	2000	Previous research has shown synergistic growth inhibition between UCN-01 and camptothecin (CPT) in tumor cells with mutant p53 versus tumor cells with wild-type p53.	Camptothecin	91-94	P53	Homo sapiens	123-126
10998350-0	2000	p53 protein oxidation in cultured cells in response to pyrrolidine dithiocarbamate: a novel method for relating the amount of p53 oxidation in vivo to the regulation of p53-responsive genes.	pyrrolidine dithiocarbamic acid	55-82	P53	Homo sapiens	0-3
10998350-0	2000	p53 protein oxidation in cultured cells in response to pyrrolidine dithiocarbamate: a novel method for relating the amount of p53 oxidation in vivo to the regulation of p53-responsive genes.	pyrrolidine dithiocarbamic acid	55-82	P53	Homo sapiens	126-129
10998350-0	2000	p53 protein oxidation in cultured cells in response to pyrrolidine dithiocarbamate: a novel method for relating the amount of p53 oxidation in vivo to the regulation of p53-responsive genes.	pyrrolidine dithiocarbamic acid	55-82	P53	Homo sapiens	126-129
11313865-0	2001	p53 protein accumulation in addition to the transactivation activity is required for p53-dependent cell cycle arrest after treatment of cells with camptothecin.	Camptothecin	147-159	P53	Homo sapiens	85-88
11313865-2	2001	Several cell lines expressing wild-type p53 protein were treated with increasing concentrations of DNA-damaging drug camptothecin.	Camptothecin	117-129	P53	Homo sapiens	40-43
11313865-7	2001	We demonstrate here that transcriptional activation of p53 after the treatment of camptothecin is not sufficient to cause p53-dependent G1 cell cycle arrest.	Camptothecin	82-94	P53	Homo sapiens	55-58
10998350-3	2000	Treatment of MCF7 breast cancer cells with pyrrolidine dithiocarbamate (PDTC), a metal chelator, resulted in a minimum of 25% oxidation of p53.	pyrrolidine dithiocarbamic acid	43-70	P53	Homo sapiens	139-142
17057733-7	2007	This transactivation was enhanced by etoposide, a DNA damaging agent that activates p53 and was completely blocked by a dominant-negative p53 mutant.	Etoposide	37-46	P53	Homo sapiens	138-141
10998350-3	2000	Treatment of MCF7 breast cancer cells with pyrrolidine dithiocarbamate (PDTC), a metal chelator, resulted in a minimum of 25% oxidation of p53.	pyrrolidine dithiocarbamic acid	72-76	P53	Homo sapiens	139-142
10998350-8	2000	However, when cells were simultaneously treated with PDTC and actinomycin D, p53 accumulated in both the nucleus and the cytoplasm.	pyrrolidine dithiocarbamic acid	53-57	P53	Homo sapiens	77-80
11238924-8	2001	Using a monoclonal antibody (PAb240) that recognizes an epitope within the core domain of a subset of p53 mutants, we found a correlation between the ability of p53 proteins to be immunoprecipitated by this antibody and their ability to interact with p73 or p63 in vitro and in transfected cells.	pab240	29-35	P53	Homo sapiens	102-105
11238924-8	2001	Using a monoclonal antibody (PAb240) that recognizes an epitope within the core domain of a subset of p53 mutants, we found a correlation between the ability of p53 proteins to be immunoprecipitated by this antibody and their ability to interact with p73 or p63 in vitro and in transfected cells.	pab240	29-35	P53	Homo sapiens	161-164
17404287-0	2007	A critical role for p53 in the control of NF-kappaB-dependent gene expression in TLR4-stimulated dendritic cells exposed to Genistein.	Genistein	124-133	P53	Homo sapiens	20-23
11148027-5	2001	Here, we show by multidimensional NMR spectroscopy that chalcones (1,3-diphenyl-2-propen-1-ones) are MDM2 inhibitors that bind to a subsite of the p53 binding cleft of human MDM2.	Chalcone	67-95	P53	Homo sapiens	147-150
11005251-5	2000	In etoposide model with chip hybridization, we defined signaling pathways that mediate apoptosis in p53 dependent manner (through activation of p53 target genes such as Waf-1/p21, PCNA, GPX, S100A2 and PTGF-beta) as well as in p53-independent manner (through activation of ODC and TGF-beta receptor, among others).	Etoposide	3-12	P53	Homo sapiens	100-103
11005251-5	2000	In etoposide model with chip hybridization, we defined signaling pathways that mediate apoptosis in p53 dependent manner (through activation of p53 target genes such as Waf-1/p21, PCNA, GPX, S100A2 and PTGF-beta) as well as in p53-independent manner (through activation of ODC and TGF-beta receptor, among others).	Etoposide	3-12	P53	Homo sapiens	144-147
11005251-5	2000	In etoposide model with chip hybridization, we defined signaling pathways that mediate apoptosis in p53 dependent manner (through activation of p53 target genes such as Waf-1/p21, PCNA, GPX, S100A2 and PTGF-beta) as well as in p53-independent manner (through activation of ODC and TGF-beta receptor, among others).	Etoposide	3-12	P53	Homo sapiens	144-147
11313951-7	2001	Treatment of K562 cells with the histone deacetylase inhibitor, trichostatin A, resulted in an increase in bcl-2 promoter activity whether p53 was present or not.	trichostatin A	64-78	P53	Homo sapiens	139-142
17404287-9	2007	Moreover, analysis of IL-6 mRNA levels in bone marrow-derived p53 null vs wild-type dendritic cells confirms a role for p53 in the reduction of NF-kappaB-dependent gene expression, mediated by genistein.	Genistein	193-202	P53	Homo sapiens	120-123
17397945-6	2007	p53 siRNA prevented cisplatin-mediated up-regulation of FLJ11259 in NT2/D1 cells.	flj11259	56-64	P53	Homo sapiens	0-3
11129445-4	2000	Amplified mutant DNA PCR products were detected in SW480 cells using digoxigenin-labeled probes, visually identifying cells harboring specific mutations in the p53 gene.	Digoxigenin	69-80	P53	Homo sapiens	160-163
11006118-0	2000	Norcantharidin-induced post-G(2)/M apoptosis is dependent on wild-type p53 gene.	norcantharidin	0-14	P53	Homo sapiens	71-74
11006118-4	2000	Effort was made to investigate whether norcantharidin exerted its cytotoxicity through a p53-dependent or -independent mechanism.	norcantharidin	39-53	P53	Homo sapiens	89-92
11006118-8	2000	Restoring wild-type p53 gene function in the U251 cell line after adenoviral infections induced tumor cell cytotoxicity after exposure to norcantharidin.	norcantharidin	138-152	P53	Homo sapiens	20-23
11006118-9	2000	These results showed that norcantharidin kills tumor cells efficiently corresponding to their endogenous p53 gene status.	norcantharidin	26-40	P53	Homo sapiens	105-108
17397945-7	2007	Likewise in HCT116 p53+/+ cells and MCF10A cells, FLJ11259 is induced by cisplatin treatment but to a much lesser extent in isogenic p53-suppressed cells.	flj11259	50-58	P53	Homo sapiens	19-22
11006118-10	2000	The results also showed the feasibility of using adenoviral p53 gene therapy to enhance chemosensitivity of tumor cells to norcantharidin.	norcantharidin	123-137	P53	Homo sapiens	60-63
11428642-0	2000	Calmodulin, poly(ADP-ribose)polymerase and p53 are targets for modulating the effects of sulfur mustard.	Mustard Gas	89-103	P53	Homo sapiens	43-46
17397945-7	2007	Likewise in HCT116 p53+/+ cells and MCF10A cells, FLJ11259 is induced by cisplatin treatment but to a much lesser extent in isogenic p53-suppressed cells.	flj11259	50-58	P53	Homo sapiens	133-136
17364023-5	2007	Our results demonstrated that the KSHV latency-associated nuclear antigen (LANA) bound to both p53 and MDM2 and that the MDM2 inhibitor Nutlin-3a disrupted the p53-MDM2-LANA complex and selectively induced massive apoptosis in PEL cells.	nutlin 3	136-145	P53	Homo sapiens	160-163
11097865-5	2000	The ketoconazole-induced G0/G1 phase arrest in COLO 205 cells was attenuated by p53-specific antisense oligodeoxynucleotides (20 microM) treatment.	Oligodeoxyribonucleotides	103-124	P53	Homo sapiens	80-83
11205246-8	2000	These results demonstrated that induction of p53 by camptothecin treatment can lead to a decreased level of TOP2 alpha and should be considered in design of combination therapy.	Camptothecin	52-64	P53	Homo sapiens	45-48
10952788-5	2000	While it did not induce wt p53, FR901228 did induce p21(WAF1/CIP1)in a p53-independent manner.	romidepsin	32-40	P53	Homo sapiens	71-74
10952788-8	2000	Thus, FR901228, while not directly inhibiting kinase activity, causes cyclin D1 downregulation and a p53-independent p21 induction, leading to inhibition of CDK and dephosphorylation of Rb resulting in growth arrest in the early G1 phase.	romidepsin	6-14	P53	Homo sapiens	101-104
11126384-4	2000	Aflatoxin B1 exposure leads to mutations in the p53 tumor suppressor gene, most commonly a transversion in codon 249 that leads to a substitution of serine for arginine in the p53 protein.	Aflatoxin B1	0-12	P53	Homo sapiens	48-51
11126384-4	2000	Aflatoxin B1 exposure leads to mutations in the p53 tumor suppressor gene, most commonly a transversion in codon 249 that leads to a substitution of serine for arginine in the p53 protein.	Aflatoxin B1	0-12	P53	Homo sapiens	176-179
17406801-10	2007	Incubation of nonfunctional TP53 cells with genistein or estradiol increased radiosensitivity in both tested concentrations.	Genistein	44-53	P53	Homo sapiens	28-32
10949925-0	2000	Activation of the insulin-like growth factor II transcription by aflatoxin B1 induced p53 mutant 249 is caused by activation of transcription complexes; implications for a gain-of-function during the formation of hepatocellular carcinoma.	Aflatoxin B1	65-77	P53	Homo sapiens	86-89
17406801-13	2007	CONCLUSION: NSCLC cells with nonfunctional TP53 might be sensitized against radiation by genistein or estradiol.	Genistein	89-98	P53	Homo sapiens	43-47
10949925-1	2000	Aflatoxin B1 (AFB1) induced mutation of the p53 gene at codon 249 (p53mt249) is critical during the formation of hepatocellular carcinoma (HCC) following hepatitis B virus (HBV) infection.	Aflatoxin B1	0-12	P53	Homo sapiens	44-47
17242983-9	2007	In mammalian species, DeltaNp73 potently inhibits the tumor-suppressive function of p73 and p53, and its overexpression serves as a robust marker for mammalian cancer.	deltanp73	22-31	P53	Homo sapiens	92-95
10930016-8	2000	Etoposide significantly inhibited the growth of U-87MG and T-98G/p53 cells in a dose-dependent manner compared with the growth of the T-98G cells.	Etoposide	0-9	P53	Homo sapiens	65-68
10930016-9	2000	Treatment with low concentrations of etoposide resulted in the increased expression of wild-type p53; it also initiated CPP32 activity and induced apoptosis in the U-87MG cells.	Etoposide	37-46	P53	Homo sapiens	97-100
10930016-11	2000	Furthermore, low concentrations of etoposide also induced apoptosis in the T-98G/p53 cells by enhancing the expression of transfected wild-type p53, decreasing the expression of bcl-2, and activating CPP32 activity.	Etoposide	35-44	P53	Homo sapiens	81-84
17114299-3	2007	We assessed the effect of benzo[a]pyrene-7,8-dihydrodiol (BPD) on proliferation in p53-null bronchoalveolar carcinoma H358 cells.	benzo(a)pyrene 7,8-dihydrodiol	26-56	P53	Homo sapiens	83-86
10930016-11	2000	Furthermore, low concentrations of etoposide also induced apoptosis in the T-98G/p53 cells by enhancing the expression of transfected wild-type p53, decreasing the expression of bcl-2, and activating CPP32 activity.	Etoposide	35-44	P53	Homo sapiens	144-147
10930016-14	2000	CONCLUSIONS: These findings indicate that wild-type p53, CPP32, and bcl-2 may mediate apoptosis induced by etoposide.	Etoposide	107-116	P53	Homo sapiens	52-55
10930016-15	2000	Forced expression of wild-type p53 increases etoposide cytotoxicity in human glioma cells by inducing apoptosis and may have important therapeutic implications.	Etoposide	45-54	P53	Homo sapiens	31-34
17114299-3	2007	We assessed the effect of benzo[a]pyrene-7,8-dihydrodiol (BPD) on proliferation in p53-null bronchoalveolar carcinoma H358 cells.	benzo(a)pyrene 7,8-dihydrodiol	58-61	P53	Homo sapiens	83-86
10842192-1	2000	We have previously shown that bladder urothelium of people living in the cesium-137 ((137)Cs)-contaminated areas of Ukraine demonstrates accumulation of stable p53 and p53 mutational inactivation, preferentially through G:C to A:T transition mutations at CpG dinucleotides, with a codon 245 hot spot.	Cesium	90-92	P53	Homo sapiens	160-163
10842192-1	2000	We have previously shown that bladder urothelium of people living in the cesium-137 ((137)Cs)-contaminated areas of Ukraine demonstrates accumulation of stable p53 and p53 mutational inactivation, preferentially through G:C to A:T transition mutations at CpG dinucleotides, with a codon 245 hot spot.	Cesium	90-92	P53	Homo sapiens	168-171
17285122-3	2007	To study the genetic alterations of NDE in the multistep process of oesophageal carcinogenesis, we determined the relationship between p53 mutations and LULs-NDE.	NDE	36-39	P53	Homo sapiens	135-138
10811471-4	2000	Ad-p53 and DNA-damaging agents (cis-diamminedichloroplatinum(II), etoposide, and 7-ethyl-10-hydrocycamptothecin) showed synergistic effects in six of seven cell lines but additive effects against a p53-mutated cell line.	Etoposide	66-75	P53	Homo sapiens	3-6
17285122-11	2007	In biopsy samples from oesophageal cancer-free individuals, the p53 missense mutations containing a hotspot mutation were found in NDE, which was identified as an LUL.	NDE	131-134	P53	Homo sapiens	64-67
10739747-11	2000	Western blot analysis revealed that EGCG treatment resulted in (i) a dose-dependent increase of p53 in LNCaP cells (carrying wild-type p53), but not in DU145 cells (carrying mutant p53), and (ii) induction of cyclin kinase inhibitor WAF1/p21 in both cell types.	epigallocatechin gallate	36-40	P53	Homo sapiens	96-99
17121821-0	2007	The C-terminal products of cellular prion protein processing, C1 and C2, exert distinct influence on p53-dependent staurosporine-induced caspase-3 activation.	Staurosporine	115-128	P53	Homo sapiens	101-104
10739747-11	2000	Western blot analysis revealed that EGCG treatment resulted in (i) a dose-dependent increase of p53 in LNCaP cells (carrying wild-type p53), but not in DU145 cells (carrying mutant p53), and (ii) induction of cyclin kinase inhibitor WAF1/p21 in both cell types.	epigallocatechin gallate	36-40	P53	Homo sapiens	135-138
10739747-11	2000	Western blot analysis revealed that EGCG treatment resulted in (i) a dose-dependent increase of p53 in LNCaP cells (carrying wild-type p53), but not in DU145 cells (carrying mutant p53), and (ii) induction of cyclin kinase inhibitor WAF1/p21 in both cell types.	epigallocatechin gallate	36-40	P53	Homo sapiens	135-138
10739747-12	2000	These results suggest that EGCG negatively modulates PCA cell growth, by affecting mitogenesis as well as inducing apoptosis, in cell-type-specific manner which may be mediated by WAF1/p21-caused G(0)/G(1)-phase cell-cycle arrest, irrespective of the androgen association or p53 status of the cells.	epigallocatechin gallate	27-31	P53	Homo sapiens	275-278
17121821-7	2007	We show that C1 potentiates staurosporine-induced caspase-3 activation through a p53-dependent mechanism.	Staurosporine	28-41	P53	Homo sapiens	81-84
17159504-10	2007	15-Deoxy-Delta-prostaglandin J2+docetaxel showed a significant increase in apoptosis associated with inhibition of the Bcl2 and cyclin D1 expression and overexpression of caspase and p53 pathway genes.	15-deoxy-delta-prostaglandin j2	0-31	P53	Homo sapiens	183-186
12501603-3	2000	This exonuclease activity is intrinsic to wildtype P53 protein, dependent on Mg2+, and it can be inhibited by addition of 5 mmol/L nucleoside monophosphates.	nucleoside monophosphates	131-156	P53	Homo sapiens	51-54
17472413-52	2007	Introgen has a number of US patents that relate to the clinical use of adenoviral p53 gene therapy in cancer as monotherapy or in combination with one or more chemotherapeutic drugs, radiation therapies or other agents that have a damaging effect on the DNA or survival of (i.e. 2-methoxyestradiol, Patent No.	2-Methoxyestradiol	279-297	P53	Homo sapiens	82-85
10666172-2	2000	METHODS: Immunohistological expression of the p53 protein was studied using a streptavidin-biotin-peroxidase method and the monoclonal antibody DO-7, an antibody directed against both wild and mutant forms of p53 protein, in synovial tissues of RA patients (n=10) and from subjects with no known joint disease (n=4).	do-7	144-148	P53	Homo sapiens	46-49
10761703-7	2000	Genistein also induced the activation of a p21 promoter reporter construct, utilizing a sequence distinct from the p53-binding site.	Genistein	0-9	P53	Homo sapiens	115-118
10618379-5	2000	The p53 binding and transactivation of the PTGF-beta promoter was enhanced by etoposide, a p53 activator, and was largely blocked by a dominant negative p53 mutant.	Etoposide	78-87	P53	Homo sapiens	4-7
17051326-7	2006	Inhibition of Src by over-expression of C-terminal Src kinase (Csk) or treatment with Src family tyrosine kinase inhibitor SU-6656 diminished the ARV S1133-induced p53 expression, activation, and apoptosis.	SU 6656	123-130	P53	Homo sapiens	164-167
10618379-5	2000	The p53 binding and transactivation of the PTGF-beta promoter was enhanced by etoposide, a p53 activator, and was largely blocked by a dominant negative p53 mutant.	Etoposide	78-87	P53	Homo sapiens	91-94
10618379-5	2000	The p53 binding and transactivation of the PTGF-beta promoter was enhanced by etoposide, a p53 activator, and was largely blocked by a dominant negative p53 mutant.	Etoposide	78-87	P53	Homo sapiens	91-94
10618379-6	2000	Furthermore, expression of endogenous PTGF-beta was remarkably induced by etoposide in p53-positive, but not in p53-negative, cell lines.	Etoposide	74-83	P53	Homo sapiens	87-90
16971506-10	2006	p53 phosphorylation was induced by serum withdrawal and other chemotherapeutic reagents such as actinomycin D, doxorubicin, and etoposide.	Etoposide	128-137	P53	Homo sapiens	0-3
10612830-4	2000	For example, the p53 mutational spectrum reveals evidence for a direct causal effect of ultraviolet radiation in skin cancer, of aflatoxin B1 in liver cancer, and of tobacco smoke in lung cancer.	Aflatoxin B1	129-141	P53	Homo sapiens	17-20
16971507-0	2006	Proteasome inhibitors potentiate etoposide-induced cell death in human astrocytoma cells bearing a mutated p53 isoform.	Etoposide	33-42	P53	Homo sapiens	107-110
16865671-7	2006	However, patients with the XRCC1 399 Gln allele, that results in a lower base excision repair capacity, were more likely to have p53 mutations, compared with patients the wild-type Arg allele (P = 0.03).	Glutamine	37-40	P53	Homo sapiens	129-132
11023999-6	2000	Importantly, cells derived from WS patients exhibit an attenuated and delayed induction of p53 by UV or by the topoisomerase I inhibitor camptothecin.	Camptothecin	137-149	P53	Homo sapiens	91-94
11054676-5	2000	The YKL-1 and DNA damaging agent, camptothecin effectively induced p53 in H460 and HepG2 as well as in normal cells.	Camptothecin	34-46	P53	Homo sapiens	67-70
11072172-2	2000	METHODS AND MATERIALS: Two cancer cell lines with wild-type p53 status were exposed first to irradiation and then to an oral formulation of the nontoxic metabolite 2-methoxyestradiol (2ME) to stabilize p53 levels.	2-Methoxyestradiol	164-182	P53	Homo sapiens	202-205
20979724-2	2000	METHODS: The mutation of exon 5-8 of p53 gene and exon 1 of K-ras gene in cancer tissues and sputum cells was detected in 59 patients with lung cancer and in 14 patients with benign pulmonary lesions as control by PCR-SSCP-AgNO3 staining method.	Silver Nitrate	223-228	P53	Homo sapiens	37-40
11042688-0	2000	Differences in mutant p53 protein stability and functional activity in teniposide-sensitive and -resistant human leukemic CEM cells.	Teniposide	71-81	P53	Homo sapiens	22-25
11042688-2	2000	Although all cell lines contain the same p53 mutations at codons 175 (Arg--&gt;His) and 248 (Arg--&gt;Gln), the constitutive levels of p53 were progressively increased with the resistance of the cells to teniposide.	Glutamine	102-105	P53	Homo sapiens	135-138
11042688-2	2000	Although all cell lines contain the same p53 mutations at codons 175 (Arg--&gt;His) and 248 (Arg--&gt;Gln), the constitutive levels of p53 were progressively increased with the resistance of the cells to teniposide.	Teniposide	204-214	P53	Homo sapiens	135-138
11042688-8	2000	Specifically, while the mutant p53 was phosphorylated at serine-15 in response to ionizing radiation in all these cell lines, mutant p53 induction in response to teniposide or ionizing radiation and induction of the p53-target genes, p21 and GADD45 only occurred in the drug-sensitive CEM cells.	Teniposide	162-172	P53	Homo sapiens	31-34
11042688-8	2000	Specifically, while the mutant p53 was phosphorylated at serine-15 in response to ionizing radiation in all these cell lines, mutant p53 induction in response to teniposide or ionizing radiation and induction of the p53-target genes, p21 and GADD45 only occurred in the drug-sensitive CEM cells.	Teniposide	162-172	P53	Homo sapiens	133-136
11042688-8	2000	Specifically, while the mutant p53 was phosphorylated at serine-15 in response to ionizing radiation in all these cell lines, mutant p53 induction in response to teniposide or ionizing radiation and induction of the p53-target genes, p21 and GADD45 only occurred in the drug-sensitive CEM cells.	Teniposide	162-172	P53	Homo sapiens	133-136
10993652-4	2000	The p53(+)/RB(-)cells were susceptible to apoptosis under various experimental conditions: 1) incubation in serum-free culture for 72 h, 2) short-term (6 h) or long-term (48 h) exposure to etoposide, and 3) culturing in soft agar.	Etoposide	189-198	P53	Homo sapiens	4-7
11107048-7	2000	MKN-74 derived from moderately differentiated tubular adenocarcinoma has wild-type p53.	mkn-74	0-6	P53	Homo sapiens	83-86
10942736-0	2000	The role of hydroxyl radical as a messenger in Cr(VI)-induced p53 activation.	Hydroxyl Radical	12-28	P53	Homo sapiens	62-65
10942736-11	2000	Sodium formate and aspirin,.OH radical scavengers, also suppressed p53 activation.	formic acid	0-14	P53	Homo sapiens	67-70
11070791-4	2000	Restoration of p53 protein function in LN382 cells at 34 degrees C reduced the cytotoxicity of etoposide and paclitaxel, whereas that of cisplatin and ACNU was not affected.	Etoposide	95-104	P53	Homo sapiens	15-18
11070791-6	2000	Transduction of wild-type p53 in LN382 cells also reduced the sensitivity of the cells to etoposide.	Etoposide	90-99	P53	Homo sapiens	26-29
11070791-8	2000	These results indicate that cell cycle arrest induced by wild-type p53 function may abrogate the cytotoxic effects of etoposide and paclitaxel, which are dependent on G2M-associated apoptosis.	Etoposide	118-127	P53	Homo sapiens	67-70
10913345-0	2000	Activation of the tumor metastasis suppressor gene, KAI1, by etoposide is mediated by p53 and c-Jun genes.	Etoposide	61-70	P53	Homo sapiens	86-89
10978678-6	2000	These results suggest that a chronic hydroxyurea treatment induces the cellular senescence in association with the induction of p53 and p21(Waf1).	Hydroxyurea	37-48	P53	Homo sapiens	128-131
10891498-7	2000	Furthermore, we found that the level of the poly(C) binding MCG10 protein is increased in cells treated with the DNA-damaging agent camptothecin in a p53-dependent manner.	Poly C	44-51	P53	Homo sapiens	150-153
10891498-7	2000	Furthermore, we found that the level of the poly(C) binding MCG10 protein is increased in cells treated with the DNA-damaging agent camptothecin in a p53-dependent manner.	Camptothecin	132-144	P53	Homo sapiens	150-153
10737899-4	2000	We also demonstrate that treatment with p53/56(lyn) antisense oligodeoxynucleotides reverses the 1,25D(3)-induced G1/S block, and results in an accumulation of cells with S-phase DNA content.	Oligodeoxyribonucleotides	62-83	P53	Homo sapiens	40-43
10760566-3	2000	Upregulation of endogenous p53 by mitomycin C treatment in MaTu cells also had a profound effect on MN expression as well as the activity of MN promoter in a reporter construct.	Mitomycin	34-45	P53	Homo sapiens	27-30
10771089-7	2000	Wortmannin or LY294002 pretreatment reduces p53 expression after gamma-irradiation to a lesser degree than that of p21.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	14-22	P53	Homo sapiens	44-47
10786695-0	2000	Enhanced sensitivity to anti-benzo(a)pyrene-diol-epoxide DNA damage correlates with decreased global genomic repair attributable to abrogated p53 function in human cells.	pyrene-diol-epoxide	37-56	P53	Homo sapiens	142-145
10786695-4	2000	In this study, we have investigated the role of p53 protein in modulating nucleotide excision repair of anti-benzo-(a)pyrene-diol-epoxide (BPDE)-DNA adducts and related effects using human fibroblasts with normal (p53-WT) and altered p53 protein (p53Mut and p53-Null).	pyrene-diol-epoxide	118-137	P53	Homo sapiens	48-51
10786699-6	2000	1alpha,25-Dihydroxyvitamin D3 and EB1089 induced p53-independent apoptosis in adenoma and carcinoma cell lines in a dose-dependent manner between 10(-10) and 10(-6) M. EB1089, as well as inducing apoptosis, increased the proportion of cells in the G1 phase, particularly in the adenoma cell lines.	25-dihydroxyvitamin d3	7-29	P53	Homo sapiens	49-52
10739708-8	2000	RESULTS: The hormone antagonist RU486 reversed dexamethasone-dependent upregulation of E6/E7 mRNA and restored radiation-induced p53 expression, apoptosis, and clonogenic survival to levels similar to those observed following irradiation alone.	Mifepristone	32-37	P53	Homo sapiens	129-132
10739708-9	2000	CONCLUSION: RU486 reverses glucocorticoid-dependent upregulation of HPV E6/E7, which corresponds to restoration of p53 expression, and restores radiosensitivity and apoptosis following gamma-irradiation.	Mifepristone	12-17	P53	Homo sapiens	115-118
10767641-5	2000	Characteristic p53 mutation spectra have been associated with dietary aflatoxin B(1) (AFB(1)) exposure and hepatocellular carcinoma (HCC); sunlight exposure and skin cancer; and cigarette smoking and lung cancer.	Aflatoxin B1	70-84	P53	Homo sapiens	15-18
10767641-5	2000	Characteristic p53 mutation spectra have been associated with dietary aflatoxin B(1) (AFB(1)) exposure and hepatocellular carcinoma (HCC); sunlight exposure and skin cancer; and cigarette smoking and lung cancer.	Aflatoxin B1	86-92	P53	Homo sapiens	15-18
10767646-6	2000	This indicates that p53 mutation is associated with progression, rather than early development, of HCC in the low-aflatoxin B(1)-exposed region.	Aflatoxin B1	114-128	P53	Homo sapiens	20-23
10749144-3	2000	Activation of the gadd45 gene was observed when camptothecin was added to cells containing p53 in the absence of a further increase in the p53 level.	Camptothecin	48-60	P53	Homo sapiens	91-94
10749144-7	2000	Interestingly, after camptothecin treatment, increased DNase I sensitivity was detected at the gadd45 promoter, suggesting that an undetermined DNA damage signal is involved in inducing chromatin remodeling at the gadd45 promoter while cooperating with p53 to activate gadd45 transcription.	Camptothecin	21-33	P53	Homo sapiens	253-256
10616970-3	1999	RESULTS: P53 was expressed in 84.0% of esophagoscopy (EGD) biopsies; 71.4% of patients with metastasis of thoracoscopy/laparoscopy lymph nodes (TS/LS LN) identified by hematoxylin/eosin (H/E) were p53 (+); 14.2% of patients with negative TS/LS LN by H/E were p53 (+).	Eosine Yellowish-(YS)	180-185	P53	Homo sapiens	9-12
10698260-6	1999	Moreover, 200 nM staurosporine increased the expression of p53 and p21 proteins and inhibited the expression of cyclin E and cdk2 proteins, suggesting that the cells were arrested in the G1 phase of the next cycle.	Staurosporine	17-30	P53	Homo sapiens	59-62
10592324-1	1999	Mutations in the TP53 tumor suppressor gene are the most common alteration in cancer, and human primary liver cancers related to previous dietary exposure to the mycotoxin aflatoxin B1 (AFB1) exhibit a specific hot spot mutation at TP53 codon 249.	Aflatoxin B1	172-184	P53	Homo sapiens	17-21
17121917-6	2006	In line with our previous data, statins were found to attenuate the etoposide-induced p53 response.	Etoposide	68-77	P53	Homo sapiens	86-89
10592324-1	1999	Mutations in the TP53 tumor suppressor gene are the most common alteration in cancer, and human primary liver cancers related to previous dietary exposure to the mycotoxin aflatoxin B1 (AFB1) exhibit a specific hot spot mutation at TP53 codon 249.	Aflatoxin B1	172-184	P53	Homo sapiens	232-236
10592324-6	1999	The genotoxic action of AFB1 was completely different from that of the alkylating agent ethyl-methane-sulfonate, where 28/30 induced mutations were linked to the TP53 target gene.	Aflatoxin B1	24-28	P53	Homo sapiens	162-166
10536167-0	1999	Differences in induction of p53, p21WAF1 and apoptosis in relation to cell cycle phase of MCF-7 cells treated with camptothecin.	Camptothecin	115-127	P53	Homo sapiens	28-31
10699952-0	2000	UCN-01 selectively enhances mitomycin C cytotoxicity in p53 defective cells which is mediated through S and/or G(2) checkpoint abrogation.	Mitomycin	28-39	P53	Homo sapiens	56-59
10699952-3	2000	In this study, we report that UCN-01 selectively enhances the cytotoxicity of MMC in human p53 mutant cell lines.	Mitomycin	78-81	P53	Homo sapiens	91-94
10699952-6	2000	In p53 wild-type MCF-7 breast carcinoma cells, the cyclin-dependent kinase inhibitor protein p21/WAF1 was markedly induced after the treatment with MMC alone, although this response was significantly delayed from the time of MMC treatment.	Mitomycin	148-151	P53	Homo sapiens	3-6
10699952-6	2000	In p53 wild-type MCF-7 breast carcinoma cells, the cyclin-dependent kinase inhibitor protein p21/WAF1 was markedly induced after the treatment with MMC alone, although this response was significantly delayed from the time of MMC treatment.	Mitomycin	225-228	P53	Homo sapiens	3-6
10699952-7	2000	Detailed cell-cycle studies revealed that UCN-01 abrogated S and G(2) phase accumulation induced by MMC in p53 defective cells and to a lesser extent in p53 wild-type cell lines.	Mitomycin	100-103	P53	Homo sapiens	107-110
10536167-4	1999	The initial transient cell arrest at the G1 checkpoint seen at 8-16 h of treatment with 0.15 microM CPT was accompanied by the rapid accumulation of p53 (preventable by cycloheximide) in the nucleus; the rise (&gt;20-fold) in p53 was maximal for S phase cells.	Camptothecin	100-103	P53	Homo sapiens	149-152
10536167-4	1999	The initial transient cell arrest at the G1 checkpoint seen at 8-16 h of treatment with 0.15 microM CPT was accompanied by the rapid accumulation of p53 (preventable by cycloheximide) in the nucleus; the rise (&gt;20-fold) in p53 was maximal for S phase cells.	Camptothecin	100-103	P53	Homo sapiens	226-229
17029827-0	2006	Benzo[a]pyrene-induced DNA damage and p53 modulation in human hepatoma HepG2 cells for the identification of potential biomarkers for PAH monitoring and risk assessment.	p-Aminohippuric Acid	134-137	P53	Homo sapiens	38-41
10692111-0	2000	p53-dependent apoptosis in melanoma cells after treatment with camptothecin.	Camptothecin	63-75	P53	Homo sapiens	0-3
16930632-0	2006	Association of specific p53 polymorphisms with keratosis in individuals exposed to arsenic through drinking water in West Bengal, India.	Drinking Water	99-113	P53	Homo sapiens	24-27
10692111-8	2000	Our results indicate that overexpression of the mutant p53 increased the growth rate of MMAN cells, reduced the sensitivity to camptothecin, and lowered drug-induced apoptosis by 2-3-fold.	Camptothecin	127-139	P53	Homo sapiens	55-58
10692111-10	2000	Furthermore, camptothecin treatment reduced bcl-2 and P-glycoprotein expression in wild-type p53 MMAN cells, but not cells overexpressing mutant p53.	Camptothecin	13-25	P53	Homo sapiens	93-96
10657969-1	2000	Exposing the human bronchial epithelial cell line BEAS-2B to the nitric oxide (NO) donor sodium 1-(N,N-diethylamino)diazen-1-ium-1, 2-diolate (DEA/NO) at an initial concentration of 0.6 mM while generating superoxide ion at the rate of 1 microM/min with the hypoxanthine/xanthine oxidase (HX/XO) system induced C:G--&gt;T:A transition mutations in codon 248 of the p53 gene.	sodium 1-(n,n-diethylamino)diazen-1-ium-1, 2-diolate	89-141	P53	Homo sapiens	365-368
10761703-3	2000	In the present study, we have addressed the mechanism of action by which genistein suppressed the proliferation of p53-null human prostate carcinoma cells.	Genistein	73-82	P53	Homo sapiens	115-118
10761703-5	2000	The inhibitory effects of genistein on cell growth proliferation were associated with a G2/M arrest in cell cycle progression concomitant with a marked inhibition of cyclin B1 and an induction of Cdk inhibitor p21 (WAF1/CIP1) in a p53-independent manner.	Genistein	26-35	P53	Homo sapiens	231-234
10462699-9	1999	EGCG also induced the expression of the Cdk inhibitor p21 protein and this effect correlated with the increase in p53 levels.	epigallocatechin gallate	0-4	P53	Homo sapiens	114-117
12212278-1	1999	To investigate the expression of P53 protein in the premalignant lesion and carcinoma of laryngeal epithelium, the authors used DO-7, an antibody to wild and mutant type P53 protein.	do-7	128-132	P53	Homo sapiens	33-36
10458704-7	1999	To successfully prepare the site-specific adducts, the p53 oligodeoxyribonucleotide was annealed with either the blocking strand d(CTCCATTTTCCT) or d(CCTCCATTTTCCTC) to form the corresponding partial triplexes which targeted AFB(1) adduction either to G(4) or to G(5).	Oligodeoxyribonucleotides	59-83	P53	Homo sapiens	55-58
16865256-6	2006	TSA increases the expression of p21, p53, DAPK-1 and the DAPK-2 gene in both OCUM-8 and MKN-74 cells.	trichostatin A	0-3	P53	Homo sapiens	37-40
10639160-9	2000	p53-dependent cell death in the AGS human gastric cancer cell line after etoposide was similarly inhibited by transient expression of ITF but not a C-terminal truncation mutant of ITF, and it required functional phosphatidylinositol 3-kinase and EGF receptor.	Etoposide	73-82	P53	Homo sapiens	0-3
16865256-8	2006	The up-regulation of p53, p21, DAPK-1 and DAPK-2 might be associated with the synergistic effect of TSA.	trichostatin A	100-103	P53	Homo sapiens	21-24
10769650-4	2000	Induction of p53-dependent apoptosis was observed in the etoposide treatment group, the X-ray irradiation group, and the combined (etoposide + X-ray irradiation) group.	Etoposide	57-66	P53	Homo sapiens	13-16
10769650-4	2000	Induction of p53-dependent apoptosis was observed in the etoposide treatment group, the X-ray irradiation group, and the combined (etoposide + X-ray irradiation) group.	Etoposide	131-140	P53	Homo sapiens	13-16
10380883-9	1999	Nickel and cobalt ions inhibit binding of p53 to scDNA and to its consensus sequence in linear DNA fragments less efficiently than zinc; cobalt ions are least efficient, requiring &gt;100 microM Co2+ for full inhibition of p53 binding.	Cobalt	11-17	P53	Homo sapiens	42-45
10380883-9	1999	Nickel and cobalt ions inhibit binding of p53 to scDNA and to its consensus sequence in linear DNA fragments less efficiently than zinc; cobalt ions are least efficient, requiring &gt;100 microM Co2+ for full inhibition of p53 binding.	Cobalt	11-17	P53	Homo sapiens	223-226
16807237-5	2006	Furthermore, zebularine, a drug that selectively traps and depletes nuclear DNMT1 and DNMT3b, relieved p53-mediated repression of endogenous Cdc25C and Cdc2.	pyrimidin-2-one beta-ribofuranoside	13-23	P53	Homo sapiens	103-106
10380883-9	1999	Nickel and cobalt ions inhibit binding of p53 to scDNA and to its consensus sequence in linear DNA fragments less efficiently than zinc; cobalt ions are least efficient, requiring &gt;100 microM Co2+ for full inhibition of p53 binding.	Cobalt	137-143	P53	Homo sapiens	42-45
10339661-4	1999	However, the sensitivity to radiation was significantly improved by the transduction and T.Tn/p53 cells became markedly susceptible to cisplatin and etoposide compared with parental cells.	Etoposide	149-158	P53	Homo sapiens	94-97
10722231-4	2000	Interestingly, lymphoma cells were still sensitive to p53-mediated apoptosis induced by etoposide.	Etoposide	88-97	P53	Homo sapiens	54-57
16631372-1	2006	We describe the synthesis of derivatives of 4,11-diaminonaphtho[2,3-f]indole-5,10-dione and their cytotoxicity for human tumor cells that express major determinants of altered anticancer drug response, the efflux pump P-glycoprotein, and non-functional p53.	4,11-diaminonaphtho(2,3-f)indole-5,10-dione	44-87	P53	Homo sapiens	253-256
10642304-5	2000	The protein of p53 was potentiated by cilostazol as well as forskolin and 8-bromo-cAMP, whereas PDGF decreased p53 expression.	8-Bromo Cyclic Adenosine Monophosphate	74-86	P53	Homo sapiens	15-18
10644891-7	2000	The representative cell line NCI-H1437 cells transfected with wild-type p53 gene (H1437/wtp53) showed a dramatic increase in susceptibility to three anticancer agents (7-fold to cisplatin, 21-fold to etoposide, and 20-fold to camptothecin) compared to untransfected or neotransfected H1437 cells.	Etoposide	200-209	P53	Homo sapiens	72-75
10644891-7	2000	The representative cell line NCI-H1437 cells transfected with wild-type p53 gene (H1437/wtp53) showed a dramatic increase in susceptibility to three anticancer agents (7-fold to cisplatin, 21-fold to etoposide, and 20-fold to camptothecin) compared to untransfected or neotransfected H1437 cells.	Camptothecin	226-238	P53	Homo sapiens	72-75
10974929-1	2000	The purpose of the study was to assess the expression of p53 in non-small cell lung cancer (NSCLC) before and after treatment with cisplatin and vepeside (PE) and to define a relationship between p53 expression and responsiveness to chemotherapy prior to surgery.	pe	155-157	P53	Homo sapiens	57-60
10340389-7	1999	From these results, we conclude that genistein inhibits the growth of MDA-MB-231 breast cancer cells, regulates the expression of apoptosis-related genes, and induces apoptosis through a p53-independent pathway.	Genistein	37-46	P53	Homo sapiens	187-190
10223459-11	1999	CONCLUSIONS: The present study indicates that clotrimazole inhibits cell proliferation accompanied by morphological changes toward differentiation of glioblastoma cells and that this drug synergistically enhances the antitumor effect of cisplatin by inducing wild-type p53-mediated apoptosis.	Clotrimazole	46-58	P53	Homo sapiens	269-272
10349981-8	1999	All of the eight cases of NS showed diffuse positive membrane staining for Ber-EP4 and negative nuclear staining for p53.	ns	26-28	P53	Homo sapiens	117-120
16764954-5	2006	While p14(ARF) had no effect on the anchorage-dependent proliferation of p53(-/-) MEFs and Ras12V-transformed p53(-/-) MEFs, it inhibited the growth of Ras12V-transformed p53(-/-) MEFs in soft agar.	ras12v	91-97	P53	Homo sapiens	110-113
10096560-5	1999	Treatment of MALME-3M cells with 10 microM N1,N11-diethylnorspermine caused an increase in hypophosphorylated Rb, which correlated temporally with the onset of G1 arrest at 16-24 h. Rb hypophosphorylation was preceded by an increase in wild-type p53 (approximately 100-fold at maximum) and a concomitant increase in the cyclin-dependent kinase inhibitor, p21WAF1/CIP1 (p21; approximately 5-fold at maximum).	N(1),N(11)-diethylnorspermine	50-68	P53	Homo sapiens	246-249
10189126-10	1999	Among those patients whose tumors overexpressed p53, there was a trend toward improved outcome in the arm that received 5-FU and mitomycin-C compared with the arm that received 5-FU only.	Mitomycin	129-140	P53	Homo sapiens	48-51
10601022-0	1999	Serine15 phosphorylation stimulates p53 transactivation but does not directly influence interaction with HDM2.	serine15	0-8	P53	Homo sapiens	36-39
10502297-2	1999	The stable expression of wild-type p53 resulted in a significant increase in sensitivity to the topoisomerase II poisons etoposide and doxorubicin, but not to the topoisomerase II inhibitors razoxane and ADR-529.	Etoposide	121-130	P53	Homo sapiens	35-38
16764954-5	2006	While p14(ARF) had no effect on the anchorage-dependent proliferation of p53(-/-) MEFs and Ras12V-transformed p53(-/-) MEFs, it inhibited the growth of Ras12V-transformed p53(-/-) MEFs in soft agar.	ras12v	91-97	P53	Homo sapiens	110-113
10518116-9	1999	Retinoic acid increased Bcl-2 and decreased p53 levels, whereas staurosporine decreased Bcl-2 and increased p53 levels.	Staurosporine	64-77	P53	Homo sapiens	108-111
10518116-10	1999	The opposite alteration of Bcl-2 (anti-apoptotic) and p53 (apoptotic) contents in SH-SY5Y cells with retinoic acid and staurosporine are attributed to the changes in cell vulnerability.	Staurosporine	119-132	P53	Homo sapiens	54-57
10190556-11	1999	Mutations seen similarly in the human Ki-ras codon 12 or p53 codons 157, 248, and 273 of lung tumor were also found in the rpsL gene, and the mutations were suppressed by the EGCG treatment.	epigallocatechin gallate	175-179	P53	Homo sapiens	57-60
16847267-4	2006	Here we present evidence indicating that MageA2 protein, belonging to the MAGE-A subfamily, confers wild-type-p53-sensitive resistance to etoposide (ET) by inducing a novel p53 inhibitory loop involving recruitment of histone deacetylase 3 (HDAC3) to MageA2/p53 complex, thus strongly down-regulating p53 transactivation function.	Etoposide	138-147	P53	Homo sapiens	110-113
10355751-0	1999	p53/p21(WAF1/CIP1) expression and its possible role in G1 arrest and apoptosis in ellagic acid treated cancer cells.	Ellagic Acid	82-94	P53	Homo sapiens	0-3
10082308-3	1999	METHODS: We report here a parallel flow cytometric method for semiquantitative detection of p53 protein and apoptosis (percent of apoptotic cells) in a pre-B leukemic cell line (NALM-6) exposed to various antitumor agents (2.35 microg/ml etoposide; 0.175 microg/ml FCE296; 0.4 microg/ml FCE624; and 1.5 microg/ml L-PAM).	nalm-6	178-184	P53	Homo sapiens	92-95
10082308-3	1999	METHODS: We report here a parallel flow cytometric method for semiquantitative detection of p53 protein and apoptosis (percent of apoptotic cells) in a pre-B leukemic cell line (NALM-6) exposed to various antitumor agents (2.35 microg/ml etoposide; 0.175 microg/ml FCE296; 0.4 microg/ml FCE624; and 1.5 microg/ml L-PAM).	Etoposide	238-247	P53	Homo sapiens	92-95
10502735-6	1999	Intratumour density of TAMs was significantly associated with FIGO stage, histological type, histological grade, DNA index, estradiol receptor concentration, intratumour Ki-67 and p53 protein expression (all p &lt; 0.05).	tams	23-27	P53	Homo sapiens	180-183
10523305-8	1999	Finally, we observed that Ref-1 cooperates with a DNA-damaging compound, camptothecin, to stimulate the transcriptional activity of p53.	Camptothecin	73-85	P53	Homo sapiens	132-135
16847267-4	2006	Here we present evidence indicating that MageA2 protein, belonging to the MAGE-A subfamily, confers wild-type-p53-sensitive resistance to etoposide (ET) by inducing a novel p53 inhibitory loop involving recruitment of histone deacetylase 3 (HDAC3) to MageA2/p53 complex, thus strongly down-regulating p53 transactivation function.	Etoposide	138-147	P53	Homo sapiens	173-176
16847267-4	2006	Here we present evidence indicating that MageA2 protein, belonging to the MAGE-A subfamily, confers wild-type-p53-sensitive resistance to etoposide (ET) by inducing a novel p53 inhibitory loop involving recruitment of histone deacetylase 3 (HDAC3) to MageA2/p53 complex, thus strongly down-regulating p53 transactivation function.	Etoposide	138-147	P53	Homo sapiens	173-176
10521394-4	1999	We report that trichostatin A (TSA), an inhibitor of histone deacetylases (HDACs), abrogates the ability of p53 to repress the transcription of two genes that it negatively regulates, Map4 and stathmin.	trichostatin A	15-29	P53	Homo sapiens	108-111
10521394-4	1999	We report that trichostatin A (TSA), an inhibitor of histone deacetylases (HDACs), abrogates the ability of p53 to repress the transcription of two genes that it negatively regulates, Map4 and stathmin.	trichostatin A	31-34	P53	Homo sapiens	108-111
10448308-0	1999	Ginsenoside-Rs4, a new type of ginseng saponin concurrently induces apoptosis and selectively elevates protein levels of p53 and p21WAF1 in human hepatoma SK-HEP-1 cells.	ginsenoside-rs4	0-15	P53	Homo sapiens	121-124
16847267-4	2006	Here we present evidence indicating that MageA2 protein, belonging to the MAGE-A subfamily, confers wild-type-p53-sensitive resistance to etoposide (ET) by inducing a novel p53 inhibitory loop involving recruitment of histone deacetylase 3 (HDAC3) to MageA2/p53 complex, thus strongly down-regulating p53 transactivation function.	Etoposide	138-147	P53	Homo sapiens	173-176
10448308-1	1999	In this paper, we present evidence that ginsenoside-Rs4 (G-Rs4; an acetylated analogue of ginsenoside-Rg5), a new ginseng saponin isolated from Panax ginseng C. A. Meyer, elevates protein levels of p53 and p21WAF1, which are associated with the induction of apoptosis in SK-HEP-1 cells.	ginsenoside-rs4	40-55	P53	Homo sapiens	198-201
10448308-5	1999	We suggest that G-Rs4 induces apoptosis, the effect of which is closely related to the downregulation of both cyclins E- and A-dependent kinase activity as a consequence of selectively elevating protein levels of p53 and p21WAF1 in SK-HEP-1 cells.	g-rs4	16-21	P53	Homo sapiens	213-216
12712688-1	1999	The alteration of p53 and K-ras gene in 36 lung cancers of workers occupationally exposed to silica (LCWS) was studied.	Silicon Dioxide	93-99	P53	Homo sapiens	18-21
16847267-4	2006	Here we present evidence indicating that MageA2 protein, belonging to the MAGE-A subfamily, confers wild-type-p53-sensitive resistance to etoposide (ET) by inducing a novel p53 inhibitory loop involving recruitment of histone deacetylase 3 (HDAC3) to MageA2/p53 complex, thus strongly down-regulating p53 transactivation function.	Etoposide	149-151	P53	Homo sapiens	110-113
16847267-4	2006	Here we present evidence indicating that MageA2 protein, belonging to the MAGE-A subfamily, confers wild-type-p53-sensitive resistance to etoposide (ET) by inducing a novel p53 inhibitory loop involving recruitment of histone deacetylase 3 (HDAC3) to MageA2/p53 complex, thus strongly down-regulating p53 transactivation function.	Etoposide	149-151	P53	Homo sapiens	173-176
16847267-4	2006	Here we present evidence indicating that MageA2 protein, belonging to the MAGE-A subfamily, confers wild-type-p53-sensitive resistance to etoposide (ET) by inducing a novel p53 inhibitory loop involving recruitment of histone deacetylase 3 (HDAC3) to MageA2/p53 complex, thus strongly down-regulating p53 transactivation function.	Etoposide	149-151	P53	Homo sapiens	173-176
16847267-4	2006	Here we present evidence indicating that MageA2 protein, belonging to the MAGE-A subfamily, confers wild-type-p53-sensitive resistance to etoposide (ET) by inducing a novel p53 inhibitory loop involving recruitment of histone deacetylase 3 (HDAC3) to MageA2/p53 complex, thus strongly down-regulating p53 transactivation function.	Etoposide	149-151	P53	Homo sapiens	173-176
10051487-1	1999	A particular point mutation of the tumor suppressor gene p53, namely a G--&gt;T transversion at the third base of codon 249, is frequently detected in primary hepatocellular carcinomas from patients living in areas where the levels of dietary exposure to aflatoxin B1 and the rates of infection with the hepatitis B virus are very high.	Aflatoxin B1	255-267	P53	Homo sapiens	57-60
10051487-5	1999	Thus, these results strongly support the view that the mutation at codon 249 of the p53 gene may serve as a fingerprint for aflatoxin B1-induced hepatocellular carcinomas, but is not, by itself, sufficient to immortalize human liver cells.	Aflatoxin B1	124-136	P53	Homo sapiens	84-87
10505853-7	1999	Analysis of cell cycle and apoptosis in etoposide-treated cells corroborated the inability of NP-29 to die by apoptosis, suggesting that this wt p53 cell line lacks p53 downstream functions in the apoptosis pathway.	Etoposide	40-49	P53	Homo sapiens	145-148
16847267-7	2006	In addition, combined trichostatin A/ET treatment in melanoma cells expressing high MAGE-A levels reestablishes p53 response and reverts the chemoresistance.	trichostatin A	22-36	P53	Homo sapiens	112-115
10427135-3	1999	We have previously shown that genistein inhibits the growth of MDA-MB-231 breast cancer cells, regulates the expression of apoptosis-related genes, and induces apoptosis through a p53-independent pathway.	Genistein	30-39	P53	Homo sapiens	180-183
16847267-7	2006	In addition, combined trichostatin A/ET treatment in melanoma cells expressing high MAGE-A levels reestablishes p53 response and reverts the chemoresistance.	Etoposide	37-39	P53	Homo sapiens	112-115
10094469-5	1999	Furthermore, endogenous S100A2 mRNA expression is induced by etoposide in p53 positive, but not in p53 negative cells.	Etoposide	61-70	P53	Homo sapiens	74-77
16818668-0	2006	p53 expression after treatment with zebularine is not due to demethylation.	pyrimidin-2-one beta-ribofuranoside	36-46	P53	Homo sapiens	0-3
10094470-1	1999	DNA chip technology was used in an attempt to identify target genes responsible for apoptosis induced by etoposide, a p53 activating topoisomerase II inhibitor used clinically as an antitumor agent.	Etoposide	105-114	P53	Homo sapiens	118-121
10455888-11	1999	CONCLUSIONS: Treatment with CPT effectively inhibited the growth of the human gastric cancer SIIA; the mechanism involved was induction of apoptosis mediated by up-regulation of p53, p21Waf1/Cip1, and p27Kip1 and the down-regulation of Bcl-2 and Bcl-XL.	Camptothecin	28-31	P53	Homo sapiens	178-181
16547931-0	2006	The course of etoposide-induced apoptosis in Jurkat cells lacking p53 and Bax.	Etoposide	14-23	P53	Homo sapiens	66-69
10517975-8	1999	For example, exposure to ultraviolet light is correlated with transition mutations at dipyrimidine sites; aflatoxin B(1) exposure is correlated with a G:C to T:A transversion that leads to a serine substitution at residue 249 of p53 in hepatocellular carcinoma; and exposure to cigarette smoke is correlated with G:C to T:A transversions in lung carcinoma.	Aflatoxin B1	106-117	P53	Homo sapiens	229-232
9950253-1	1999	Expression of p53 protein was examined in oral squamous cell carcinoma (SCC) from patients who were areca quid (AQ) chewers and/or tobacco smokers, using anti-p53 antibodies with an immunoperoxidase technique.	aq	112-114	P53	Homo sapiens	14-17
9950253-3	1999	p53 overexpression was found to be higher in patients without AQ chewing and smoking habits than in patients with these two habits (80% vs 52%, P=0.076).	aq	62-64	P53	Homo sapiens	0-3
10391558-9	1999	p53 mutations were found in 4 of 16 GCCs (25%) and 8 of 18 TCs (44%).	9-ethyl-N-(3,4,5-trimethoxyphenyl)carbazole-3-sulfonamide	59-62	P53	Homo sapiens	0-3
16778203-8	2006	Furthermore, we provided evidence that inhibition of protein methyltransferases, especially arginine methyltransferases, relieve the repression of ECT2 induced by DNA damage or Nutlin-3 in a p53-dependent manner.	nutlin 3	177-185	P53	Homo sapiens	191-194
10391558-11	1999	CONCLUSIONS: p53 mutations appear to play a role in the pathogenesis of some GCCs and in approximately 50% of TCs of the appendix, whereas mutations in the K-ras oncogene do not appear to be important in the development of these tumors.	9-ethyl-N-(3,4,5-trimethoxyphenyl)carbazole-3-sulfonamide	110-113	P53	Homo sapiens	13-16
10381922-2	1999	Aflatoxin B1 causes a specific point mutation in the p53 tumor-suppressor gene in exposed individuals.	Aflatoxin B1	0-12	P53	Homo sapiens	53-56
10023685-0	1999	Differential regulation of p21waf-1/cip-1 and Mdm2 by etoposide: etoposide inhibits the p53-Mdm2 autoregulatory feedback loop.	Etoposide	54-63	P53	Homo sapiens	88-91
10023685-0	1999	Differential regulation of p21waf-1/cip-1 and Mdm2 by etoposide: etoposide inhibits the p53-Mdm2 autoregulatory feedback loop.	Etoposide	65-74	P53	Homo sapiens	88-91
10023685-9	1999	When cells are -treated with a pulse (1 h) of etoposide and reincubated in drug free medium, Mdm2 synthesis commences immediately after damage is repaired (3 h) and the p53 response is attenuated.	Etoposide	46-55	P53	Homo sapiens	169-172
9927204-6	1999	Moreover, p53His175 as well as p53His179 reduced substantially the rate of etoposide-induced apoptosis, whereas p53His273 and p53Trp248 had a much milder protective effect.	Etoposide	75-84	P53	Homo sapiens	31-34
10383145-5	1999	Either phosphatidylinositol (PI) 3-kinase or mitogen-activated protein kinase kinase (MEK) antagonized p53-induced apoptosis, and an additive preventive effect was observed when both kinases were activated.	Phosphatidylinositols	7-27	P53	Homo sapiens	103-106
16799873-11	2006	Cyclin A1 but not cyclin A2 was upregulated in etoposide-treated tumor cells undergoing p53-dependent apoptosis and mitotic catastrophe.	Etoposide	47-56	P53	Homo sapiens	88-91
14634277-6	1999	We conclude that high concentrations of L-745,337 and sodium salicylate inhibit colon cancer cell growth by a mechanism unrelated to cyclooxygenase inhibition that may involve p53-independent induction of the tumor suppressor p21WAF-1/cip1.	Sodium Salicylate	54-71	P53	Homo sapiens	176-179
10634308-0	1999	Effect of p53 tumor suppressor on nucleotide excision repair in human colon carcinoma cells treated with 4-nitroquinoline 1-oxide.	4-Nitroquinoline-1-oxide	105-129	P53	Homo sapiens	10-13
10634308-1	1999	In probing the mechanism of nucleotide excision repair (NER) in response to 4-nitroquinoline 1-oxide (4NQO)-induced DNA damage, the effect of p53 tumor suppressor was investigated.	4-Nitroquinoline-1-oxide	76-100	P53	Homo sapiens	142-145
10634308-4	1999	Compared to RKO cells having the wild-type p53 gene, increased cytotoxicity by 4NQO was observed in RKOmp53 cells with a mutation in p53 protein.	4-Nitroquinoline-1-oxide	79-83	P53	Homo sapiens	43-46
10634308-4	1999	Compared to RKO cells having the wild-type p53 gene, increased cytotoxicity by 4NQO was observed in RKOmp53 cells with a mutation in p53 protein.	4-Nitroquinoline-1-oxide	79-83	P53	Homo sapiens	104-107
10634308-6	1999	Also, the expression of p53 and p21 proteins was significantly increased in 4NQO-treated RKO cells.	4-Nitroquinoline-1-oxide	76-80	P53	Homo sapiens	24-27
10634308-8	1999	Our findings suggest that 4NQO-induced NER is p53-dependent and involves up-regulation of its downstream regulator, p21(Waf1/Cip1) proteins.	4-Nitroquinoline-1-oxide	26-30	P53	Homo sapiens	46-49
10207030-4	1999	This site bound to purified p53 as well as p53 in nuclear extract activated by etoposide.	Etoposide	79-88	P53	Homo sapiens	28-31
10207030-4	1999	This site bound to purified p53 as well as p53 in nuclear extract activated by etoposide.	Etoposide	79-88	P53	Homo sapiens	43-46
10207030-7	1999	The p53 binding and transactivation of the GPX promoter were enhanced by etoposide in p53-positive U2-OS cells.	Etoposide	73-82	P53	Homo sapiens	4-7
16684540-4	2006	PAF-induced increase in VEGF expression was correlated with decreased p53 activity.	Platelet Activating Factor	0-3	P53	Homo sapiens	70-73
10207030-7	1999	The p53 binding and transactivation of the GPX promoter were enhanced by etoposide in p53-positive U2-OS cells.	Etoposide	73-82	P53	Homo sapiens	86-89
10207030-8	1999	Etoposide-induced transactivation was blocked by a dominant negative p53 mutant, indicating that endogenous wild type p53, upon activation by etoposide, transactivated the GPX promoter.	Etoposide	0-9	P53	Homo sapiens	69-72
10327058-2	1999	We employ a tet-repressible system to show that, under conditions in which the WAF1 mRNA steady-state level is upregulated fourfold by p53, the SCL mRNA level is not altered.	tetramethylenedisulfotetramine	12-15	P53	Homo sapiens	135-138
10327058-3	1999	In a previous report, we demonstrated that p53 interactions with the SCL CS can upregulate downstream reporter gene activity 43-fold in transient reporter assays.	Cesium	73-75	P53	Homo sapiens	43-46
10327058-4	1999	This disparity prompted us to explore the differences between p53 regulation of SCL CS activity in organized (chromosomally integrated) and disorganized (non-replicating episomal plasmid) chromatin.	Cesium	84-86	P53	Homo sapiens	62-65
10022257-8	1998	For example, characteristic p53 mutation spectra have been associated with: dietary aflatoxin B1 exposure and hepatocellular carcinoma; sunlight exposure and skin carcinoma; and cigarette smoking and lung cancer.	Aflatoxin B1	84-96	P53	Homo sapiens	28-31
14646475-0	1998	Two-dimensional gel analysis of apoptosis-specific p53 isoforms induced by 2-methoxyestradiol in human lung cancer cells.	2-Methoxyestradiol	75-93	P53	Homo sapiens	51-54
14646475-1	1998	The natural metabolic byproduct of estradiol, 2-methoxyestradiol (2-MeOE2), induces apoptosis in human lung cancer cells by a p53-dependent mechanism.	2-Methoxyestradiol	46-64	P53	Homo sapiens	126-129
16426753-8	2006	Trichostatin (TSA), a p53 inhibitor, can block the effects of tolbutamide, lending further support for a role of p53 in mediating this process.	trichostatin A	0-12	P53	Homo sapiens	22-25
14646475-1	1998	The natural metabolic byproduct of estradiol, 2-methoxyestradiol (2-MeOE2), induces apoptosis in human lung cancer cells by a p53-dependent mechanism.	2-Methoxyestradiol	66-73	P53	Homo sapiens	126-129
14646475-4	1998	However, when H1299 cells transfected with p53 were treated with 2-MeOE2, they underwent rapid and extensive apoptosis.	2-Methoxyestradiol	65-72	P53	Homo sapiens	43-46
14646475-6	1998	Analysis of wild-type p53 phosphoisoforms in H1299 cells by two-dimensional gel electrophoresis revealed that 2-MeOE2 induced a unique group of acidic p53 isoforms.	2-Methoxyestradiol	110-117	P53	Homo sapiens	22-25
14646475-6	1998	Analysis of wild-type p53 phosphoisoforms in H1299 cells by two-dimensional gel electrophoresis revealed that 2-MeOE2 induced a unique group of acidic p53 isoforms.	2-Methoxyestradiol	110-117	P53	Homo sapiens	151-154
14646475-7	1998	Although most of the wild-type p53 in untreated H1299 cells migrated as at least five diffuse species with isoelectric points from pH 5.5-6.3, as many as nine additional forms migrating toward the acidic region with pI values from 4.4-5.3 were detected in 2-MeOE2-treated apoptotic cells.	2-Methoxyestradiol	256-263	P53	Homo sapiens	31-34
14646475-9	1998	The results indicated that the induction of apoptosis in H1299 cells by 2-MeOE2 is dependent on the upregulation of specific p53 isoforms.	2-Methoxyestradiol	72-79	P53	Homo sapiens	125-128
10203554-5	1999	Results obtained with diverse cell lines differing in ras and p53 status showed that the isoprenoid-mediated suppression of growth is independent of mutated ras and p53 functions.	Terpenes	89-99	P53	Homo sapiens	62-65
10363582-0	1999	p53 status predicts the efficacy of postoperative oral administration of tegafur for completely resected non-small cell lung cancer.	Tegafur	73-80	P53	Homo sapiens	0-3
12953991-0	1999	P53 gene of chang-liver cells (Atcc-Ccl13) exposed to aflatoxin B1 (Afb): the effect of lysine on mutation at codon 249 of exon 7.	Aflatoxin B1	54-66	P53	Homo sapiens	0-3
16426753-8	2006	Trichostatin (TSA), a p53 inhibitor, can block the effects of tolbutamide, lending further support for a role of p53 in mediating this process.	trichostatin A	0-12	P53	Homo sapiens	113-116
12953991-0	1999	P53 gene of chang-liver cells (Atcc-Ccl13) exposed to aflatoxin B1 (Afb): the effect of lysine on mutation at codon 249 of exon 7.	Aflatoxin B1	68-71	P53	Homo sapiens	0-3
12953991-1	1999	The effect of different regimes of lysine-pre treatment on mutation at the 3rd nucleotide base of codon 249 which is located at the 7th exon of p53 gene of Chang-liver cells (CCIL13) exposed to aflatoxin B1 (AFB1) has been investigated.	Aflatoxin B1	194-206	P53	Homo sapiens	144-147
16426753-8	2006	Trichostatin (TSA), a p53 inhibitor, can block the effects of tolbutamide, lending further support for a role of p53 in mediating this process.	trichostatin A	14-17	P53	Homo sapiens	22-25
9878214-5	1998	Camptothecin, but not beta-lapachone, induced accumulation of p53 and the major growth arrest-associated p53 response protein, p21.	Camptothecin	0-12	P53	Homo sapiens	62-65
16426753-8	2006	Trichostatin (TSA), a p53 inhibitor, can block the effects of tolbutamide, lending further support for a role of p53 in mediating this process.	trichostatin A	14-17	P53	Homo sapiens	113-116
9878214-5	1998	Camptothecin, but not beta-lapachone, induced accumulation of p53 and the major growth arrest-associated p53 response protein, p21.	Camptothecin	0-12	P53	Homo sapiens	105-108
11812373-2	1999	METHODS: The p16, p21 and p53 genes mediated by Stearylamine/DOPE (SA liposome) were introduced alone and jointly into the non-small cell lung cancer (NSCLC) cell line A549 and small cell lung cancer (SCLC) SH77.	2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine	67-69	P53	Homo sapiens	26-29
16545681-7	2006	GA was cytotoxic at 20 microM, inhibiting cell proliferation, and at 100 microM, induced p53 expression and caused apoptosis.	glycolaldehyde	0-2	P53	Homo sapiens	89-92
11812373-4	1999	RESULTS: The p16, p53 and p21 genes alone mediated by SA liposome can inhibit obviously the growth of NSCLC cell line A549 cells, while the genes were slightly effective on SCLC cell line SH77 cells at day 1, 3, 5 after transfecting the genes.	2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine	54-56	P53	Homo sapiens	18-21
10094469-1	1999	S100A2, a calcium binding protein of the EF-hand family, was recently identified to be inducible by etoposide, a p53 activator.	Etoposide	100-109	P53	Homo sapiens	113-116
10094469-2	1999	A potential p53 binding site was identified in the promoter of the S100A2 gene, which binds to purified p53 as well as p53 in nuclear extract activated by etoposide.	Etoposide	155-164	P53	Homo sapiens	12-15
10023317-4	1998	At 0.15 mM, genistein caused an increase in the steady-state levels of the wild-type tumour suppressor p53, which was attributed to stabilising the tumour suppressor protein, since p53 mRNA levels did not increase.	Genistein	12-21	P53	Homo sapiens	103-106
16545693-6	2006	N-OH-ABA induced DNA damage at cytosine and guanine residues of ACG sequence complementary to codon 273, a well-known hot spot of the p53 gene.	acceleratory factor from growth hormone	64-67	P53	Homo sapiens	134-137
10193333-7	1998	Immunohistochemistry using the avidin-biotin technique was applied for the expression of the markers p53 (D07), carcinoembryonic antigen (CEA), c-erbB-2, epithelial membrane antigen (EMA), and alpha-fetoprotein (AFP).	avidin-biotin	31-44	P53	Homo sapiens	101-104
9794234-4	1998	Forced expression of temperature-sensitive p53val135 in mutant conformation failed to prevent accumulation of endogenous wild-type p53 but acted in a transdominant negative manner to inhibit p53-mediated, camptothecin-induced p21WAF1/CIP1 expression.	Camptothecin	205-217	P53	Homo sapiens	43-46
10094469-2	1999	A potential p53 binding site was identified in the promoter of the S100A2 gene, which binds to purified p53 as well as p53 in nuclear extract activated by etoposide.	Etoposide	155-164	P53	Homo sapiens	104-107
10094469-2	1999	A potential p53 binding site was identified in the promoter of the S100A2 gene, which binds to purified p53 as well as p53 in nuclear extract activated by etoposide.	Etoposide	155-164	P53	Homo sapiens	104-107
10094469-4	1999	The p53-induced transactivation of the S100A2 promoter was enhanced by etoposide and blocked by a dominant negative p53 mutant.	Etoposide	71-80	P53	Homo sapiens	4-7
9668066-0	1998	Pyrrolidine dithiocarbamate prevents p53 activation and promotes p53 cysteine residue oxidation.	pyrrolidine dithiocarbamic acid	0-27	P53	Homo sapiens	37-40
16605112-3	2006	AAG to AGT transversion at codon 249 of the P53 gene arg-ser (249ser) has been identified as a hotspot, reflecting DNA damage caused by aflatoxin B1 metabolites in HCC.	Aflatoxin B1	136-148	P53	Homo sapiens	44-47
9668066-0	1998	Pyrrolidine dithiocarbamate prevents p53 activation and promotes p53 cysteine residue oxidation.	pyrrolidine dithiocarbamic acid	0-27	P53	Homo sapiens	65-68
9667752-4	1998	N-Methyl-N"-nitro-nitrosoguanidine and N-ethyl-N-nitrosourea, two direct-acting genotoxic (DNA-reactive) carcinogens, caused p53 induction as early as 2 h following treatment, with peak increases within 4-12 h. Aflatoxin B1 and 2-acetylaminofluorene, indirect-acting genotoxic carcinogens, caused a later induction of p53, with the peak increase appearing between 16 and 24 h following treatment.	Ethylnitrosourea	39-60	P53	Homo sapiens	125-128
9667752-4	1998	N-Methyl-N"-nitro-nitrosoguanidine and N-ethyl-N-nitrosourea, two direct-acting genotoxic (DNA-reactive) carcinogens, caused p53 induction as early as 2 h following treatment, with peak increases within 4-12 h. Aflatoxin B1 and 2-acetylaminofluorene, indirect-acting genotoxic carcinogens, caused a later induction of p53, with the peak increase appearing between 16 and 24 h following treatment.	Ethylnitrosourea	39-60	P53	Homo sapiens	318-321
9667752-4	1998	N-Methyl-N"-nitro-nitrosoguanidine and N-ethyl-N-nitrosourea, two direct-acting genotoxic (DNA-reactive) carcinogens, caused p53 induction as early as 2 h following treatment, with peak increases within 4-12 h. Aflatoxin B1 and 2-acetylaminofluorene, indirect-acting genotoxic carcinogens, caused a later induction of p53, with the peak increase appearing between 16 and 24 h following treatment.	Aflatoxin B1	211-223	P53	Homo sapiens	125-128
9667752-6	1998	Phenol, diethylstilbestrol and ethylacrylate also induced increases in cellular p53.	Diethylstilbestrol	8-26	P53	Homo sapiens	80-83
10071687-3	1999	Immunostaining for p53 protein was performed on paraffin and frozen sections from 61 patients with different grades of meningiomas using monoclonal antibodies (mAbs) DO-1 and pAb240.	pab240	175-181	P53	Homo sapiens	19-22
10226585-4	1999	Furthermore, 3H-thymidine incorporation in KOSC-3 cells, which display the p53 gene mutation, was inhibited by protons much more than by gamma-rays.	Thymidine	16-25	P53	Homo sapiens	75-78
9923540-10	1999	Our observations support the concept that cells carrying the wild-type p53 gene tend to be sensitive to etoposide and DXR and, in particular, deletion of the p53 function results in a greater resistance to anticancer agents.	Etoposide	104-113	P53	Homo sapiens	71-74
9923540-10	1999	Our observations support the concept that cells carrying the wild-type p53 gene tend to be sensitive to etoposide and DXR and, in particular, deletion of the p53 function results in a greater resistance to anticancer agents.	Etoposide	104-113	P53	Homo sapiens	158-161
16506813-7	2006	Pretreatment with green tea polyphenol epigallocatechin-3-gallate (EGCG) effectively blocked peroxynitrite-induced glutathione depletion, p53 accumulation, and apoptosis in both normal and G6PD-deficient cells.	epigallocatechin gallate	67-71	P53	Homo sapiens	138-141
9809972-2	1998	We asked whether combined treatment with 2-methoxyestradiol (2-Me), which increases levels of wild-type p53 protein in cancer cells, and the systemic administration of an adenoviral vector expressing wild-type p53 (Ad-p53) would inhibit the growth of human metastatic lung cancer cells in vivo.	2-Methoxyestradiol	41-59	P53	Homo sapiens	104-107
9809972-2	1998	We asked whether combined treatment with 2-methoxyestradiol (2-Me), which increases levels of wild-type p53 protein in cancer cells, and the systemic administration of an adenoviral vector expressing wild-type p53 (Ad-p53) would inhibit the growth of human metastatic lung cancer cells in vivo.	2-Methoxyestradiol	61-65	P53	Homo sapiens	104-107
9565608-6	1998	The polymer binding sites could be mapped to two amino acid sequences in the sequence-specific core DNA binding domain of p53 (amino acid positions 153-178 and 231-253) and another one in the oligomerization domain (amino acids 326-348).	Polymers	4-11	P53	Homo sapiens	122-125
9499438-0	1998	Upregulation of p21WAF1/CIP1 in human breast cancer cell lines MCF-7 and MDA-MB-468 undergoing apoptosis induced by natural product anticancer drugs 10-hydroxycamptothecin and camptothecin through p53-dependent and independent pathways.	Camptothecin	159-171	P53	Homo sapiens	197-200
9772293-4	1998	With the exception of the etoposide-effected G2/M arrest at high concentrations, which seems to depend on functional p53, since it did not occur in cells with inactive p53.	Etoposide	26-35	P53	Homo sapiens	117-120
16138109-0	2006	Sodium orthovanadate suppresses DNA damage-induced caspase activation and apoptosis by inactivating p53.	Sodium orthovanadate	0-20	P53	Homo sapiens	100-103
9772293-7	1998	The accumulated p53 was biochemically active, as measured in a transient transfection assay upon treatment with gemcitabine, cisplatin, etoposide, and Taxol.	Etoposide	136-145	P53	Homo sapiens	16-19
9586815-2	1998	We here demonstrate that the cell cycle was arrested in G2/M phase following supplementation with DZQ of human osteosarcoma Saos-2 cells (lacking both p53 and pRb) and HCT116 cells.	ethylenimine quinone	98-101	P53	Homo sapiens	151-154
16614702-4	2006	RESULTS: All the derivatives, except 3-isobutyl-methylxanthine, increased tumor cell sensitization to radiation by inducing apoptosis in the p53-null lung cancer cell line.	1-Methyl-3-isobutylxanthine	37-62	P53	Homo sapiens	141-144
9520163-0	1998	Inhibition of HIV-1 gp120-induced apoptosis in neuroblastoma SK-N-SH cells by an antisense oligodeoxynucleotide against p53.	Oligodeoxyribonucleotides	91-111	P53	Homo sapiens	120-123
9520163-6	1998	An antisense oligodeoxynucleotide against p53 was used to investigate the role of p53 in the gp120-induced apoptosis in these cells.	Oligodeoxyribonucleotides	13-33	P53	Homo sapiens	42-45
9520163-10	1998	The critical role of p53 was further illustrated by the effectiveness of a p53 antisense oligodeoxynucleotide to inhibit the gp120-induced apoptosis.	Oligodeoxyribonucleotides	89-109	P53	Homo sapiens	21-24
9520163-10	1998	The critical role of p53 was further illustrated by the effectiveness of a p53 antisense oligodeoxynucleotide to inhibit the gp120-induced apoptosis.	Oligodeoxyribonucleotides	89-109	P53	Homo sapiens	75-78
9822927-17	1998	Two malignant tumours showed increased expression of p53 protein, with approximately 50% of nuclei staining with DO-7.	do-7	113-117	P53	Homo sapiens	53-56
9743293-8	1998	Thus, although p53-dependent apoptosis is induced by camptothecin, topotecan and SN-38 in this human ovarian carcinoma cell line, these drugs induce p53-independent death, as measured by clonogenic assay.	Camptothecin	53-65	P53	Homo sapiens	15-18
16614702-6	2006	In contrast, 3-isobutyl-methylxanthine was more potent than the other derivatives in radiosensitization of normal lung epithelial cells and the lung carcinoma cells stably transfected with wild-type p53.	1-Methyl-3-isobutylxanthine	13-38	P53	Homo sapiens	199-202
9468185-5	1998	p53 gene transfer reduced thymidine incorporation of VSMCs stimulated by platelet-derived growth factor-BB (P&lt;.001).	Thymidine	26-35	P53	Homo sapiens	0-3
16614702-8	2006	CONCLUSION: Our results suggest that 3-isobutyl-methylxanthine might function through a p53-dependent mechanism.	1-Methyl-3-isobutylxanthine	37-62	P53	Homo sapiens	88-91
9508372-5	1998	After treatment with 40 nM, 200 nM or 1 microM of camptothecin the survival rates were, on average, 16%, 8% and 4% for the wild-type p53 melanoma cells, compared with 89%, 67% and 38% for the mutant p53 cells, respectively (P = 0.00004, P = 0.003 and P = 0.04, respectively).	Camptothecin	50-62	P53	Homo sapiens	133-136
9771945-6	1998	These data confirm our earlier results that p53 accumulation following UV treatment is directly related to the presence of unrepaired cyclobutane dimers on the transcribed strand of active genes.	Cyclobutanes	134-145	P53	Homo sapiens	44-47
9776455-4	1998	RESULTS: Proliferation and p53 expression of PancTu-I cells overexpressing mutant p53 protein were inhibited by antisense oligodeoxynucleotide treatment.	Oligodeoxyribonucleotides	122-142	P53	Homo sapiens	27-30
9508372-5	1998	After treatment with 40 nM, 200 nM or 1 microM of camptothecin the survival rates were, on average, 16%, 8% and 4% for the wild-type p53 melanoma cells, compared with 89%, 67% and 38% for the mutant p53 cells, respectively (P = 0.00004, P = 0.003 and P = 0.04, respectively).	Camptothecin	50-62	P53	Homo sapiens	199-202
9508372-8	1998	Cisplatin, camptothecin and vincristine all induced apoptosis in wild-type p53 melanoma cells, but not in mutant p53 cells.	Camptothecin	11-23	P53	Homo sapiens	75-78
9776455-4	1998	RESULTS: Proliferation and p53 expression of PancTu-I cells overexpressing mutant p53 protein were inhibited by antisense oligodeoxynucleotide treatment.	Oligodeoxyribonucleotides	122-142	P53	Homo sapiens	82-85
16489026-3	2006	Hydroxyurea triggered accumulation of p53 through an increase in protein stability.	Hydroxyurea	0-11	P53	Homo sapiens	38-41
9687575-8	1998	Importantly, we could show that MT1 cells are not deficient in the p53-dependent apoptosis pathway; treatment with etoposide, a topoisomerase II inhibitor, resulted in p53 and p21/waf-1 protein expression and apoptosis in both cell lines.	Etoposide	115-124	P53	Homo sapiens	168-171
16489026-9	2006	In contrast, induction of p53 by hydroxyurea was defective in cells lacking NBS1 and BLM.	Hydroxyurea	33-44	P53	Homo sapiens	26-29
16205639-9	2006	We show that DeltaNp73 antagonizes the repressive effect of the proapoptotic p53 family members on hTERT expression and, in addition, induces hTERT expression in telomerase-negative cells by interfering with E2F-RB-mediated repression of the hTERT core promoter.	deltanp73	13-22	P53	Homo sapiens	77-80
9726816-0	1998	Induction of apoptosis by thiuramdisulfides, the reactive metabolites of dithiocarbamates, through coordinative modulation of NFkappaB, c-fos/c-jun, and p53 proteins.	thiuramdisulfides	26-43	P53	Homo sapiens	153-156
9726816-5	1998	In contrast, PDTC, DDTC, and ammonium dithiocarbamate (ADTC) did not induce apoptosis; rather they led to the induction of p53 and p21 followed by G1/S arrest.	Ditiocarb	19-23	P53	Homo sapiens	123-126
9690517-8	1998	Restoration of wild type p53 status in HL60 myeloid leukemia cells significantly increases the cells" sensitivity to the cytotoxic effects of DZQ.	ethylenimine quinone	142-145	P53	Homo sapiens	25-28
9690520-3	1998	Here we report that exposure of macrophages to lipopolysaccharide/interferon-gamma or lipophilic cAMP analogs such as dibutyryl-cAMP or 8-bromo-cAMP for 15 h attenuated DNA fragmentation and accumulation of the tumor suppressor p53 in response to the chemotherapeutic agents cisplatin and etoposide, compared to cells that received chemotherapeutic agents only.	8-Bromo Cyclic Adenosine Monophosphate	136-148	P53	Homo sapiens	228-231
16413759-2	2006	In order to identify new p53 downstream genes, we established a new system of p53 gene inducible expression, U251-pTet-p53 cell line, with the Tet-On Gene Expression System, in which exogenous p53 gene could overexpress in doxycycline (Dox) medium but not in the medium without Dox.	tetramethylenedisulfotetramine	115-118	P53	Homo sapiens	25-28
9660477-9	1998	Camptothecin and etoposide increased the p53 level after 4 hours of treatment, before the onset of apoptosis.	Camptothecin	0-12	P53	Homo sapiens	41-44
9660477-9	1998	Camptothecin and etoposide increased the p53 level after 4 hours of treatment, before the onset of apoptosis.	Etoposide	17-26	P53	Homo sapiens	41-44
16413759-2	2006	In order to identify new p53 downstream genes, we established a new system of p53 gene inducible expression, U251-pTet-p53 cell line, with the Tet-On Gene Expression System, in which exogenous p53 gene could overexpress in doxycycline (Dox) medium but not in the medium without Dox.	tetramethylenedisulfotetramine	115-118	P53	Homo sapiens	78-81
16413759-2	2006	In order to identify new p53 downstream genes, we established a new system of p53 gene inducible expression, U251-pTet-p53 cell line, with the Tet-On Gene Expression System, in which exogenous p53 gene could overexpress in doxycycline (Dox) medium but not in the medium without Dox.	tetramethylenedisulfotetramine	115-118	P53	Homo sapiens	78-81
16356831-7	2006	Lower doses of 2-ME and paclitaxel resulted in G1 (but not G2/M) cell cycle arrest in the p53 wild type LNCaP cell line, but with minimal induction of apoptosis.	2-Methoxyestradiol	15-19	P53	Homo sapiens	90-93
9797738-8	1998	Large numbers of tumour cell nuclei were reactive with the anti-p53 antibody, DO-7, in contrast to the two previous resections.	do-7	78-82	P53	Homo sapiens	64-67
16354677-6	2006	EX-527 and TSA acted synergistically to increase acetyl-p53 levels, confirming that p53 acetylation is regulated by both SIRT1 and HDACs.	trichostatin A	11-14	P53	Homo sapiens	84-87
9719628-1	1998	A cationic polymer, Superfect, when complexed to the therapeutic genes, p53 and a TSP fragment, displays a much greater antitumor activity compared to cationic liposomes.	Polymers	11-18	P53	Homo sapiens	72-75
16568831-12	2006	Both cell lines exhibited high sensitivity to etoposide, classical inductor of unrepairable DSBs and p53.	Etoposide	46-55	P53	Homo sapiens	101-104
16365016-1	2005	A mutation in codon 249 of the TP53 gene (249(Ser)), related to aflatoxin B(1) exposure, has previously been associated with hepatocellular carcinoma risk.	Aflatoxin B1	64-75	P53	Homo sapiens	31-35
9647614-0	1998	Exploiting tumour hypoxia and overcoming mutant p53 with tirapazamine.	Tirapazamine	57-69	P53	Homo sapiens	48-51
9647614-4	1998	Tirapazamine is a novel bioreductive agent with selective cytotoxicity to hypoxic tumour cells, irrespective of their p53 status or apoptotic response, and acts synergistically with cisplatin.	Tirapazamine	0-12	P53	Homo sapiens	118-121
16287286-0	2005	Total synthesis of lucilactaene, a cell cycle inhibitor active in p53-inactive cells.	lucilactaene	19-31	P53	Homo sapiens	66-69
9635719-0	1998	The effect of activation of wild-type p53 function on fluoropyrimidine-mediated radiosensitization.	2-fluoropyrimidine	54-70	P53	Homo sapiens	38-41
16225598-0	2005	Mutant p53 melanoma cell lines respond differently to CP-31398-induced apoptosis.	CP 31398	54-62	P53	Homo sapiens	7-10
9673414-0	1998	Role of wild-type p53 in the enhancement of camptothecin cytotoxicity against human prostate tumor cells.	Camptothecin	44-56	P53	Homo sapiens	18-21
16225598-3	2005	Additionally, CP-31398 was found to be able to convert mutant p53 to wild-type conformation in several cell lines.	CP 31398	14-22	P53	Homo sapiens	62-65
9673414-1	1998	The role of wild-type human p53 protein in enhancing camptothecin cytotoxicity was examined by infecting human prostate PC3 cells with adenovirus expressing human wild-type p53 gene (Adwtp53).	Camptothecin	53-65	P53	Homo sapiens	28-31
9673414-4	1998	In the presence of camptothecin, an inhibitor of topoisomerase 1, significant increases in both p53 and p21 proteins were detected in Adwtp53-infected PC3 cells.	Camptothecin	19-31	P53	Homo sapiens	96-99
16225598-4	2005	OBJECTIVES: To examine if CP-31398 can revert all mutant p53 proteins to wild-type function.	CP 31398	26-34	P53	Homo sapiens	57-60
16225598-6	2005	RESULTS: Upon a moderate dose of CP-31398 treatment (15 microg mL(-1)), only the wild-type p53 MMRU and the single p53 point mutation MeWo cells exhibited apoptosis.	CP 31398	33-41	P53	Homo sapiens	91-94
16225598-6	2005	RESULTS: Upon a moderate dose of CP-31398 treatment (15 microg mL(-1)), only the wild-type p53 MMRU and the single p53 point mutation MeWo cells exhibited apoptosis.	CP 31398	33-41	P53	Homo sapiens	115-118
9563650-2	1998	When the p53 tumor suppressor gene was used, 4-nitro-2-aminophenol caused Cu(II)-dependent piperidine-labile sites at poly G sequences.	2-amino-4-nitrophenol	45-66	P53	Homo sapiens	9-12
16225598-8	2005	Although CP-31398 enhanced overall p53 protein level, its ability to promote proper folding of p53 protein was limited to CP-31398-sensitive MMRU and MeWo cells.	CP 31398	9-17	P53	Homo sapiens	35-38
11244964-3	1998	MDM2 and p53 genes were detected by digoxigenin labeling in situ hybridization-technique.	Digoxigenin	36-47	P53	Homo sapiens	9-12
16225598-8	2005	Although CP-31398 enhanced overall p53 protein level, its ability to promote proper folding of p53 protein was limited to CP-31398-sensitive MMRU and MeWo cells.	CP 31398	9-17	P53	Homo sapiens	95-98
9506540-3	1998	When p53 was expressed at sublethal levels, it sensitized cells to the DNA-damaging drugs Adriamycin, mitomycin C, actinomycin D, etoposide (VP16), cisplatin and CPT11.	Mitomycin	102-113	P53	Homo sapiens	5-8
9506540-3	1998	When p53 was expressed at sublethal levels, it sensitized cells to the DNA-damaging drugs Adriamycin, mitomycin C, actinomycin D, etoposide (VP16), cisplatin and CPT11.	Etoposide	130-139	P53	Homo sapiens	5-8
16225598-8	2005	Although CP-31398 enhanced overall p53 protein level, its ability to promote proper folding of p53 protein was limited to CP-31398-sensitive MMRU and MeWo cells.	CP 31398	122-130	P53	Homo sapiens	95-98
9506540-3	1998	When p53 was expressed at sublethal levels, it sensitized cells to the DNA-damaging drugs Adriamycin, mitomycin C, actinomycin D, etoposide (VP16), cisplatin and CPT11.	Etoposide	141-145	P53	Homo sapiens	5-8
16225598-12	2005	More studies are necessary, to further investigate the effect of CP-31398 on mutant p53 and its potential applications as an anticancer agent.	CP 31398	65-73	P53	Homo sapiens	84-87
16186332-8	2005	Treatment with mitomycin-C resulted in the increased expression of Fas, FasL, Bad, and phosphorylated p53 and a decreased level of phosphorylated AKT.	Mitomycin	15-26	P53	Homo sapiens	102-105
9482877-4	1998	Phorbol ester, a potent activator of PKC, significantly inhibited the accumulation of p53 after DNA damage.	Phorbol Esters	0-13	P53	Homo sapiens	86-89
16202244-3	2005	Here we showed that etoposide can induce the similar degree of cell death in p53-deficient HCT 116 cells, whereas 5"-FU-mediated cell death is strongly dependent on the existence of functional p53 in HCT 116 cells.	Etoposide	20-29	P53	Homo sapiens	77-80
9568504-1	1998	AIMS: Recent reports suggest that genetic examination of K-ras or p53 mutation is more sensitive for the detection of occult lymph node metastasis in colorectal carcinomas than conventional examination by haematoxylin and eosin (H &amp; E) staining or immunohistochemistry for gene products.	Eosine Yellowish-(YS)	222-227	P53	Homo sapiens	66-69
9464250-2	1998	We used doxorubicin (DOX) and sodium butyrate (NaB) to accumulate p53 protein.	nab	47-50	P53	Homo sapiens	66-69
16202244-5	2005	These data suggest that etoposide can directly induce the mitochondrial dysfunction irrespective of p53 status, and it may, at least in part, account for the p53-independent pathway in cell death induced by chemotherapeutic agents.	Etoposide	24-33	P53	Homo sapiens	158-161
16177181-5	2005	TSA-induced toxicity stimulates apoptosis and cell cycle checkpoint responses independent of p53, but does not increase phosphorylated histone H2AX (-H2AX) as compared with a clastogenic agent, camptothecin, indicating that the quantity of DSBs is not the primary cause of TSA-induced cell death.	trichostatin A	0-3	P53	Homo sapiens	93-96
9543255-5	1998	Teniposide enhanced CD95 expression in a glioma cell line with wild-type p53 (LN-229) but not in two p53 mutant cell lines (T98G, LN-308).	Teniposide	0-10	P53	Homo sapiens	73-76
9543255-6	1998	Forced expression of a transdominant negative p53 mutant prevented the teniposide induced augmentation of CD95 expression in LN-229 cells but did not prevent the synergy of CD95 ligand and teniposide.	Teniposide	71-81	P53	Homo sapiens	46-49
16121349-7	2005	The 249serine p53 gene mutation was detected in 27.2% of the hepatocellular carcinoma tissues but not in non-cancerous tissues.	249serine	4-13	P53	Homo sapiens	14-17
9773296-6	1998	The technique of microwave antigen retrieval gave crisp, clear immunohistochemical staining for p53 in tissues fixed in neutral buffered formalin or Bouin solution.	bouin	149-154	P53	Homo sapiens	96-99
15940259-8	2005	Interestingly, in p53 knockdown cells nearly the entire set of identified cisplatin targets fail to respond or have a diminished response to cisplatin, suggesting that many are new direct or indirect targets of p53 including GPR87, STK17A, INPP5D, FLJ11259, and EPS8L2.	flj11259	248-256	P53	Homo sapiens	18-21
10921048-11	1998	The close association of the hotspot mutation of p53 gene in Qidong HCC with the presence of HBVx gene sequence suggests that such mutation is the molecular footprint of the combined effect of aflatoxin B1 exposure and HBVx gene product.	Aflatoxin B1	193-205	P53	Homo sapiens	49-52
15940259-8	2005	Interestingly, in p53 knockdown cells nearly the entire set of identified cisplatin targets fail to respond or have a diminished response to cisplatin, suggesting that many are new direct or indirect targets of p53 including GPR87, STK17A, INPP5D, FLJ11259, and EPS8L2.	flj11259	248-256	P53	Homo sapiens	211-214
16093994-0	2005	Differential regulation of p21waf-1/cip-1 and Mdm2 by etoposide: etoposide inhibits the p53-Mdm2 autoregulatory feedback loop.	Etoposide	65-74	P53	Homo sapiens	88-91
9570360-2	1997	The most frequent p53 mutation has been found in HCCs in regions with high hepatitis B virus (HBV) infection and intake of aflatoxin B1 (AFB1).	Aflatoxin B1	123-135	P53	Homo sapiens	18-21
16103091-2	2005	We show that histone deacetylase inhibitors such as FR901228 and trichostatin A completely depleted mutant p53 in cancer cell lines.	romidepsin	52-60	P53	Homo sapiens	107-110
9405248-7	1997	These findings indicate that TSA induces the WAF1/Cip1 promoter through the typical Sp1 sites, in a p53-independent fashion.	trichostatin A	29-32	P53	Homo sapiens	100-103
16103091-2	2005	We show that histone deacetylase inhibitors such as FR901228 and trichostatin A completely depleted mutant p53 in cancer cell lines.	trichostatin A	65-79	P53	Homo sapiens	107-110
9434882-0	1997	Induction of p53 protein expression by sodium arsenite.	sodium arsenite	39-54	P53	Homo sapiens	13-16
15914462-8	2005	Treatment of colon and ovarian carcinoma cells with the anticancer genotoxic agent etoposide up-regulated both p53 and proline oxidase, activated calcineurin, and induced apoptosis.	Etoposide	83-92	P53	Homo sapiens	111-114
9434882-3	1997	Intrigued by these effects and based on the role of p53 on cell proliferation, we tested different concentrations of sodium arsenite for their ability to induce the expression of tumor suppressor gene p53 in different cell lines (HeLa, C-33A.	sodium arsenite	117-132	P53	Homo sapiens	52-55
9434882-3	1997	Intrigued by these effects and based on the role of p53 on cell proliferation, we tested different concentrations of sodium arsenite for their ability to induce the expression of tumor suppressor gene p53 in different cell lines (HeLa, C-33A.	sodium arsenite	117-132	P53	Homo sapiens	201-204
15908423-4	2005	Nuclear accumulation of p53 protein in mdm2 SNP309 cells results after 6 h of camptothecin, etoposide, or mitomycin C treatment, with the p53 protein phosphorylated at Ser15.	Camptothecin	78-90	P53	Homo sapiens	24-27
9434882-6	1997	Immunoblots showed an increased expression of p53 gene with 1 microM sodium arsenite in Jurkat cells and 10 microM sodium arsenite in HeLa and LCL-EBV cells.	sodium arsenite	69-84	P53	Homo sapiens	46-49
9434882-6	1997	Immunoblots showed an increased expression of p53 gene with 1 microM sodium arsenite in Jurkat cells and 10 microM sodium arsenite in HeLa and LCL-EBV cells.	sodium arsenite	115-130	P53	Homo sapiens	46-49
15908423-4	2005	Nuclear accumulation of p53 protein in mdm2 SNP309 cells results after 6 h of camptothecin, etoposide, or mitomycin C treatment, with the p53 protein phosphorylated at Ser15.	Etoposide	92-101	P53	Homo sapiens	24-27
9494534-8	1997	Levels of p53 mRNA decreased with increasing resistance to vindesine, etoposide and fotemustine.	Vindesine	59-68	P53	Homo sapiens	10-13
15908423-4	2005	Nuclear accumulation of p53 protein in mdm2 SNP309 cells results after 6 h of camptothecin, etoposide, or mitomycin C treatment, with the p53 protein phosphorylated at Ser15.	Mitomycin	106-117	P53	Homo sapiens	24-27
15832344-0	2005	JNK/p53 mediated cell death response in K562 exposed to etoposide-ionizing radiation combined treatment.	Etoposide	56-65	P53	Homo sapiens	4-7
9343394-6	1997	Treatment of U2-OS cells, a wild-type p53-containing osteogenic sarcoma line, with a common p53 inducer, etoposide, induced p53 DNA binding and transactivation activities in a time-dependent manner.	Etoposide	105-114	P53	Homo sapiens	38-41
11819223-1	1998	AIM:To study the p53 gene mutation and its relationship to aflatoxin B1 exposure in hepatocellular carcinoma (HCC).METHODS: Restriction fragment length polymorphism analysis method was used in 62 HCC samples, and DNA direct sequencing in another 45 HCC samples.RESULTS: In HCC and AFB1 high and low-risk areas, 36/52 (69%) and 2/10 (20%) cases were found losing the HaeIII allele respectively, suggesting one of the base G mutation at the p53 gene codon 249.	Aflatoxin B1	59-71	P53	Homo sapiens	17-20
9343394-6	1997	Treatment of U2-OS cells, a wild-type p53-containing osteogenic sarcoma line, with a common p53 inducer, etoposide, induced p53 DNA binding and transactivation activities in a time-dependent manner.	Etoposide	105-114	P53	Homo sapiens	92-95
15832344-5	2005	Moreover, p53 is a potential substrate for JNK and may act as a JNK target for etoposide and ionizing radiation.	Etoposide	79-88	P53	Homo sapiens	10-13
9343394-6	1997	Treatment of U2-OS cells, a wild-type p53-containing osteogenic sarcoma line, with a common p53 inducer, etoposide, induced p53 DNA binding and transactivation activities in a time-dependent manner.	Etoposide	105-114	P53	Homo sapiens	92-95
15833870-13	2005	Finally, induction of p21 by phenoxodiol is p53 independent, as phenoxodiol induced p21 in HCT116 lacking p53.	phenoxodiol	29-40	P53	Homo sapiens	44-47
9484835-12	1998	Of the tested inhibitors, only staurosporine, a known inhibitor of protein kinase C (PKC) and various other kinases, inhibited both p53 activation and accumulation, whereas specific PKC inhibitors, tyrosine kinase inhibitors and a serine/threonine kinase inhibitor did not.	Staurosporine	31-44	P53	Homo sapiens	132-135
9484835-14	1998	Kinetic studies showed that staurosporine-mediated inhibition of p53 function is an early event in cell damage response.	Staurosporine	28-41	P53	Homo sapiens	65-68
9484835-15	1998	Thus dual, kinetically different events, de novo protein synthesis and staurosporine-inhibited protein phosphorylation are required for p53 activation and accumulation in all phases of the cell cycle.	Staurosporine	71-84	P53	Homo sapiens	136-139
15833870-14	2005	These data therefore indicate that phenoxodiol promotes G(1)-S arrest by the specific loss in cdk2 activity due to p53-independent p21(WAF1) induction.	phenoxodiol	35-46	P53	Homo sapiens	115-118
9307289-0	1997	Abrogation of an S-phase checkpoint and potentiation of camptothecin cytotoxicity by 7-hydroxystaurosporine (UCN-01) in human cancer cell lines, possibly influenced by p53 function.	Camptothecin	56-68	P53	Homo sapiens	168-171
15805279-3	2005	We previously showed that infection by human cytomegalovirus (HCMV) induced drug resistance and altered p53- and p73-dependent apoptosis of infected cells through accumulation of DeltaN-p73alpha.	deltan-p73alpha	179-194	P53	Homo sapiens	104-107
9307289-2	1997	In this study, we found that nanomolar concentrations of camptothecin (CPT), a topoisomerase I inhibitor, arrest or delay cell cycle progression during the S and G2 phases in p53 mutant human colon carcinoma HT29 cells and that UCN-01 abrogates the S-phase arrest or delay induced by CPT.	Camptothecin	57-69	P53	Homo sapiens	175-178
9307289-2	1997	In this study, we found that nanomolar concentrations of camptothecin (CPT), a topoisomerase I inhibitor, arrest or delay cell cycle progression during the S and G2 phases in p53 mutant human colon carcinoma HT29 cells and that UCN-01 abrogates the S-phase arrest or delay induced by CPT.	Camptothecin	71-74	P53	Homo sapiens	175-178
10026991-8	1998	For example, characteristic p53 mutation spectra have been associated with: dietary aflatoxin B1 exposure and hepatocellular carcinoma; sunlight exposure and skin carcinoma; and cigarette smoking and lung cancer.	Aflatoxin B1	84-96	P53	Homo sapiens	28-31
15814660-0	2005	Tirapazamine cytotoxicity for neuroblastoma is p53 dependent.	Tirapazamine	0-12	P53	Homo sapiens	47-50
9815856-0	1997	Inactivation of p53 increases the cytotoxicity of camptothecin in human colon HCT116 and breast MCF-7 cancer cells.	Camptothecin	50-62	P53	Homo sapiens	16-19
15814660-5	2005	TPZ exhibited high cytotoxicity, especially in hypoxia (2% O2), for all four p53-functional neuroblastoma cell lines, achieving &gt;3 logs of cell kill (LC99 &lt; or = 0.7 microg/mL).	Tirapazamine	0-3	P53	Homo sapiens	77-80
15795422-6	2005	Micromolar (-)epigallocatechin gallate and quercetin partially eliminated the dichlorodihydrofluorescein (DCF) and phospho-p53 staining, suggesting that these flavonoids inhibited the accumulation of intracellular oxidants and nuclear transactivation of p53 in H2O2-exposed cells.	epigallocatechin gallate	11-38	P53	Homo sapiens	123-126
9285694-5	1997	Comparatively, a treatment of the cells with 100 nM 4OH-tamoxifen (OHT) decreased cell number to 40% of the control without a concomitant decrease in the p53 levels suggesting a differential ability of these antiestrogens to regulate p53 levels in cells cultured in whole serum.	4oh-tamoxifen	52-65	P53	Homo sapiens	154-157
9285694-5	1997	Comparatively, a treatment of the cells with 100 nM 4OH-tamoxifen (OHT) decreased cell number to 40% of the control without a concomitant decrease in the p53 levels suggesting a differential ability of these antiestrogens to regulate p53 levels in cells cultured in whole serum.	4oh-tamoxifen	52-65	P53	Homo sapiens	234-237
9437796-14	1997	Our studies show that exposure to phenolphthalein combined with a genetic predisposition to cancer can potentiate the carcinogenic process and cause p53 gene alterations, a gene alteration found in many human cancers.	Phenolphthalein	34-49	P53	Homo sapiens	149-152
9315628-0	1997	Regulation of p53 by metal ions and by antioxidants: dithiocarbamate down-regulates p53 DNA-binding activity by increasing the intracellular level of copper.	Dithiocarbamate	53-68	P53	Homo sapiens	14-17
9315628-0	1997	Regulation of p53 by metal ions and by antioxidants: dithiocarbamate down-regulates p53 DNA-binding activity by increasing the intracellular level of copper.	Dithiocarbamate	53-68	P53	Homo sapiens	84-87
9315628-3	1997	To address this question, we have analyzed the effect of pyrrolidine dithiocarbamate (PDTC) on p53 DNA-binding activity in cell lines expressing wild-type p53.	pyrrolidine dithiocarbamic acid	57-84	P53	Homo sapiens	95-98
9315628-3	1997	To address this question, we have analyzed the effect of pyrrolidine dithiocarbamate (PDTC) on p53 DNA-binding activity in cell lines expressing wild-type p53.	pyrrolidine dithiocarbamic acid	86-90	P53	Homo sapiens	95-98
9285062-7	1997	The results show that MMC treatment inhibited sod1 gene transcription through p53-mediated transcriptional repression.	Mitomycin	22-25	P53	Homo sapiens	78-81
15795422-6	2005	Micromolar (-)epigallocatechin gallate and quercetin partially eliminated the dichlorodihydrofluorescein (DCF) and phospho-p53 staining, suggesting that these flavonoids inhibited the accumulation of intracellular oxidants and nuclear transactivation of p53 in H2O2-exposed cells.	epigallocatechin gallate	11-38	P53	Homo sapiens	254-257
9212217-5	1997	The p53 mutational spectrum was 50% transitions (3 C-to-T and 1 G-to-A, all occurring at CpG dinucleotide sites) and 50% transversions (one each, C-to-G, G-to-T, T-to-G, and T-to-A).	Dinucleoside Phosphates	93-105	P53	Homo sapiens	4-7
9212237-8	1997	Treatment of both cell lines with mitomycin C (MMC), which acts with a mechanism different from CDDP, caused equal accumulation of p53 and induction of bax.	Mitomycin	34-45	P53	Homo sapiens	131-134
9212237-8	1997	Treatment of both cell lines with mitomycin C (MMC), which acts with a mechanism different from CDDP, caused equal accumulation of p53 and induction of bax.	Mitomycin	47-50	P53	Homo sapiens	131-134
15772596-8	2005	However, the staining rate of p53 in OLP was higher in areca quid (AQ) chewers compared to abstainers (P = .001), and the mean PCNA LI in atrophic cases was higher than that in hypertrophic cases (P = .029).	aq	67-69	P53	Homo sapiens	30-33
9812593-0	1997	[A preliminary study on p53 gene in lung cancer tissues of workers exposed to silica and welding fumes].	Silicon Dioxide	78-84	P53	Homo sapiens	24-27
9812593-1	1997	Mutations of suppressor gene p53 was studied in 36 cases of silica related lung cancer and 6 cases of welding fume related lung cancer with immunohistochemical and PCR-SSCP methods.	Silicon Dioxide	60-66	P53	Homo sapiens	29-32
9338145-0	1997	Immortalization of mutant p53-transfected human fibroblasts by treatment with either 4-nitroquinoline 1-oxide or X-rays.	4-Nitroquinoline-1-oxide	85-109	P53	Homo sapiens	26-29
9354939-3	1997	The effect of treatment with hyperthermia and verapamil on the expression of apoptosis-associated proteins including Bcl-2, p53, bax, and c-Myc was studied by Western blot analysis.	Verapamil	46-55	P53	Homo sapiens	124-127
9354939-9	1997	Also, apoptosis of HT-29 cells produced by hyperthermia in the presence of verapamil is a p53-independent process.	Verapamil	75-84	P53	Homo sapiens	90-93
9006107-0	1996	Absence of mutations in the p53 tumor suppressor gene in woodchuck hepatocellular carcinomas associated with hepadnavirus infection and intake of aflatoxin B1.	Aflatoxin B1	146-158	P53	Homo sapiens	28-31
15772596-9	2005	Interestingly, the staining rate of p53 and mean PCNA LI were significantly increased in AQ chewers with atrophic OLP (100%, 36.7% +/- 9.0%, respectively), which were similar to those in ED and SCC (all P &gt; .05).	aq	89-91	P53	Homo sapiens	36-39
8945622-4	1996	When exposed to DNA-damaging agents, cisplatin or mitomycin C, apoptosis was induced in RT4 with the wild-type (wt) p53/wt p21, whereas T24 with the p53 non-sense mutation/wt p21 was resistant.	Mitomycin	50-61	P53	Homo sapiens	116-119
15755327-0	2005	Activation of p53, inhibition of telomerase activity and induction of estrogen receptor beta are associated with the anti-growth effects of combination of ovarian hormones and retinoids in immortalized human mammary epithelial cells.	ovarian hormones	155-171	P53	Homo sapiens	14-17
8945622-4	1996	When exposed to DNA-damaging agents, cisplatin or mitomycin C, apoptosis was induced in RT4 with the wild-type (wt) p53/wt p21, whereas T24 with the p53 non-sense mutation/wt p21 was resistant.	Mitomycin	50-61	P53	Homo sapiens	149-152
8950211-4	1996	DDB (10(-4) M) could significantly increase the content of cAMP in Bel-7402 cells, and also enhance the expression of anti-oncogene p53.	ddb	0-3	P53	Homo sapiens	132-135
9816112-7	1996	We also find that induction of wild-type p53 potentiates the cytotoxicity of topotecan, a member of the camptothecin family of drugs that also has clinical activity against colon cancer.	Camptothecin	104-116	P53	Homo sapiens	41-44
9269997-2	1997	Similarly, upon treatment with S-nitroso-N-acetyl-DL-penicillamine (2-5 mM) or S-nitroso-glutathione (1-2 mM), human breast cancer cells (MCF-7), which express wild-type p53, rapidly accumulated p53 protein in the nuclei.	snap	31-66	P53	Homo sapiens	170-173
9269997-2	1997	Similarly, upon treatment with S-nitroso-N-acetyl-DL-penicillamine (2-5 mM) or S-nitroso-glutathione (1-2 mM), human breast cancer cells (MCF-7), which express wild-type p53, rapidly accumulated p53 protein in the nuclei.	snap	31-66	P53	Homo sapiens	195-198
9263993-13	1997	In contrast, cytokines in combination with pyrrolidine dithiocarbamate, which blocks endogenous superoxide dismutase, allowed p53 and Bax accumulation as well as DNA fragmentation.	pyrrolidine dithiocarbamic acid	43-70	P53	Homo sapiens	126-129
15701509-1	2005	It is well known that CpG dinucleotide steps in DNA, which are highly methylated at the 5-position of cytosine (meC) in human tissues, exhibit a disproportionate number of mutations within certain codons of the p53 gene.	Dinucleoside Phosphates	26-38	P53	Homo sapiens	211-214
9230270-1	1997	Epidemiological evidence has been supporting a relationship between dietary aflatoxin B1 (AFB1) exposure, development of human primary hepatocellular carcinoma (HCC) and mutations in the p53 tumor suppressor gene.	Aflatoxin B1	76-88	P53	Homo sapiens	187-190
9230270-1	1997	Epidemiological evidence has been supporting a relationship between dietary aflatoxin B1 (AFB1) exposure, development of human primary hepatocellular carcinoma (HCC) and mutations in the p53 tumor suppressor gene.	Aflatoxin B1	90-94	P53	Homo sapiens	187-190
9408079-0	1997	The mammalian metabolite, 2-methoxyestradiol, affects P53 levels and apoptosis induction in transformed cells but not in normal cells.	2-Methoxyestradiol	26-44	P53	Homo sapiens	54-57
8886839-7	1996	In vitro studies showed that cell growth, as measured by the thymidine incorporation assay, was inhibited in the C4-2, PC-3, and DU145 cells infected with wild-type p53 adenovirus in comparison to control viruses.	Thymidine	61-70	P53	Homo sapiens	165-168
21541495-1	1996	Gel fiberglass (GFG), a new affinity biosensor, was used to isolate human p53 antigen with rabbit anti-rat p53 IgG.	guanfu base G	16-19	P53	Homo sapiens	74-77
15557088-7	2005	TUNEL and DNA fragmentation analysis show that silica caused apoptosis in both JB6 cells and wild-type p53 (p53+/+) fibroblasts but not in p53-deficient (p53-/-) fibroblasts.	Silicon Dioxide	47-53	P53	Homo sapiens	108-111
21541495-1	1996	Gel fiberglass (GFG), a new affinity biosensor, was used to isolate human p53 antigen with rabbit anti-rat p53 IgG.	guanfu base G	16-19	P53	Homo sapiens	107-110
21541495-13	1996	Herein, we report for the first time the capability to isolate human p53 antigen using GFG columns with entrapped anti-rat p53 IgG.	guanfu base G	87-90	P53	Homo sapiens	69-72
8673929-4	1996	In vitro investigations have shown intact p53 to play a critical role executing cell death in response to treatment with cytotoxic drugs like 5-fluorouracil, etoposide and doxorubicin.	Etoposide	158-167	P53	Homo sapiens	42-45
9219564-3	1997	We found that exposure of human lung adenocarcinoma A549 cells to sodium arsenite (0.08-2 microM) or sodium arsenate (30-300 microM), but not dimethylarsenic acid (2-2000 microM), produced significant dose-responsive hypermethylation within a 341-base pair fragment of the promoter of p53.	sodium arsenite	66-81	P53	Homo sapiens	285-288
15868936-6	2005	Ellagic acid also increased p53 and p21 and decreased CDK2 gene expression, that may lead to the G0/G1 arrest of T24 cells.	Ellagic Acid	0-12	P53	Homo sapiens	28-31
9047387-7	1997	Inhibition of cellular DNA replication by hydroxyurea and AraC, in the presence or absence of DNA damage, also resulted in rapid p53 accumulation in repair-deficient cells.	Hydroxyurea	42-53	P53	Homo sapiens	129-132
14646555-4	1997	p53 and p21/waf1 protein levels were elevated in etoposide-treated cells, but not in cells subjected to serum with-drawal.	Etoposide	49-58	P53	Homo sapiens	0-3
8678559-4	1996	The immunohistochemical method was by the avidin-biotin complex method using anti-p53 protein monoclonal antibody.	avidin-biotin	42-55	P53	Homo sapiens	82-85
15703811-9	2005	Western blot analysis was used to determine the protein expression of cancer suppressor genes, p53 (wt) and Bax, and the proto-oncogene, Bcl-2 in LNCaP cells following treatment with oridonin.	oridonin	183-191	P53	Homo sapiens	95-98
8647635-0	1996	Mutation in p53 and de-regulation of p53-related gene expression in three human cell lines immortalized with 4-nitroquinoline 1-oxide or 60Co gamma rays.	4-Nitroquinoline-1-oxide	109-133	P53	Homo sapiens	12-15
8647635-0	1996	Mutation in p53 and de-regulation of p53-related gene expression in three human cell lines immortalized with 4-nitroquinoline 1-oxide or 60Co gamma rays.	4-Nitroquinoline-1-oxide	109-133	P53	Homo sapiens	37-40
8647635-4	1996	We detected expression of only mutated p53 mRNA by direct sequencing of the reverse-transcribed mRNA in 3 human cell lines immortalized either with 4-nitroquinoline 1-oxide or with 60Co gamma rays.	4-Nitroquinoline-1-oxide	148-172	P53	Homo sapiens	39-42
8950976-8	1996	Furthermore, a dominant-negative p53 mutant (introduced by retroviral transduction) rescued LacZ21 cells from senescence and generated colonies with extended lifespan in which beta-gal expression was totally abolished.	beta-D-galactose	176-184	P53	Homo sapiens	33-36
8982610-1	1996	The expression of p53 tumor suppressor protein isoforms in H460a cells induced to undergo apoptosis by 2-methoxyestradiol was investigated by two-dimensional gel electrophoresis.	2-Methoxyestradiol	103-121	P53	Homo sapiens	18-21
15703811-10	2005	Oridonin up-regulated p53 and Bax and down-regulated Bcl-2 expression in a dose-dependent manner.	oridonin	0-8	P53	Homo sapiens	22-25
8733762-3	1996	p53 nuclear staining was weakly positive in 21% of the TCs, whereas strong nuclear staining was seen in 64% of the ACs and 88% of the SCLCs (P = 0.0047).	9-ethyl-N-(3,4,5-trimethoxyphenyl)carbazole-3-sulfonamide	55-58	P53	Homo sapiens	0-3
15735102-4	2005	We found that quercetin and combinations of quercetin and ellagic acid nonsynergistically increased p53 protein levels.	Ellagic Acid	58-70	P53	Homo sapiens	100-103
8622872-2	1996	Cell type specific differences in p53-independent p21 expression and cell cycle arrest were found following treatment of human tumour cell lines with serum, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), or okadaic acid (OA).	Okadaic Acid	205-217	P53	Homo sapiens	34-37
8875976-7	1996	Moreover, when the DNA damage-inducing drugs etoposide or camptothecin were added to the cells, a further stimulation of kinase activity was observed following growth at 28 degrees C, but not 38 degrees C. These data are consistent with a regulatory model in which p53 is sensitive to stress or DNA damage through phosphorylation at its N-terminus.	Etoposide	45-54	P53	Homo sapiens	265-268
8875976-7	1996	Moreover, when the DNA damage-inducing drugs etoposide or camptothecin were added to the cells, a further stimulation of kinase activity was observed following growth at 28 degrees C, but not 38 degrees C. These data are consistent with a regulatory model in which p53 is sensitive to stress or DNA damage through phosphorylation at its N-terminus.	Camptothecin	58-70	P53	Homo sapiens	265-268
8622872-2	1996	Cell type specific differences in p53-independent p21 expression and cell cycle arrest were found following treatment of human tumour cell lines with serum, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), or okadaic acid (OA).	Okadaic Acid	219-221	P53	Homo sapiens	34-37
8895534-1	1996	AGG to AGT mutations in codon 249 of the p53 tumor-suppressor gene are frequently observed in hepatocellular carcinomas (HCC) from areas where exposure to aflatoxin B1 (AFB) occurs.	Aflatoxin B1	155-167	P53	Homo sapiens	41-44
15735102-5	2005	In contrast, ellagic acid potentiated the effects of quercetin for p21(cip1/waf1) protein levels and p53 phosphorylation at serine 15, possibly explaining the synergistic effect observed in apoptosis induction.	Ellagic Acid	13-25	P53	Homo sapiens	101-104
8895534-1	1996	AGG to AGT mutations in codon 249 of the p53 tumor-suppressor gene are frequently observed in hepatocellular carcinomas (HCC) from areas where exposure to aflatoxin B1 (AFB) occurs.	Aflatoxin B1	169-172	P53	Homo sapiens	41-44
15735102-10	2005	In summary, quercetin and ellagic acid combined increase the activation of p53 and p21(cip1/waf1) and the MAP kinases, JNK1,2 and p38, in a more than additive manner, suggesting a mechanism by which quercetin and ellagic acid synergistically induce apoptosis in cancer cells.	Ellagic Acid	26-38	P53	Homo sapiens	75-78
8790940-0	1996	Selective expression of mutated p53 in human cells immortalized with either 4-nitroquinoline 1-oxide or 60Co gamma rays.	4-Nitroquinoline-1-oxide	76-100	P53	Homo sapiens	32-35
15608686-5	2005	Similarly, constitutive hTERT expression inhibited wild-type p53-dependent apoptosis in response to mitomycin C or 5-fluorouracil in HCT116 colon carcinoma cells carrying endogenous p53.	Mitomycin	100-111	P53	Homo sapiens	61-64
8790940-2	1996	We immortalized three human cell lines by repeated treatment with either 60Co gamma rays or a chemical carcinogen, 4-nitroquinoline 1-oxide, and found that all three immortalized cell lines have mutations in the tumor suppressor gene, p53.	4-Nitroquinoline-1-oxide	115-139	P53	Homo sapiens	235-238
8706243-3	1996	Sublines that were resistant to melphalan, pyrazafurin, mitoxantrone, etoposide and PALA all retained expression of wild-type p53.	Etoposide	70-79	P53	Homo sapiens	126-129
15474986-3	2005	We found that hPCNA promoter was dose-dependently transactivated by 4-NQO under the concentration of 2 microM via a previously reported p53-binding element located from -236 to -217 upstream of the transcription start site.	4-Nitroquinoline-1-oxide	68-73	P53	Homo sapiens	136-139
8645592-2	1996	Alcohol use as well as medication with hydralazine-containing antihypertensive drugs, but not heredity were associated with p53 staining.	Hydralazine	39-50	P53	Homo sapiens	124-127
9816212-8	1996	Targeted loss of p53 protein in H460 lung cancer cells using HPV-16 E6 inhibited the etoposide-induced G1 checkpoint but did not decrease chemosensitivity.	Etoposide	85-94	P53	Homo sapiens	17-20
8655704-10	1996	CONCLUSIONS: The ELISA for anti-p53 is a convenient and specific tet for the detection of humoral response to alterations in p53 gene expression and could be of value in the diagnosis and characterisation of patients with hepatocellular carcinoma.	tetramethylenedisulfotetramine	65-68	P53	Homo sapiens	32-35
8655704-10	1996	CONCLUSIONS: The ELISA for anti-p53 is a convenient and specific tet for the detection of humoral response to alterations in p53 gene expression and could be of value in the diagnosis and characterisation of patients with hepatocellular carcinoma.	tetramethylenedisulfotetramine	65-68	P53	Homo sapiens	125-128
15474986-5	2005	It was observed that Staurosporine, a Ser/Thr kinase inhibitor, blocked the Ser15 phosphorylation of p53 and the hPCNA promoter response to 4-NQO simultaneously, suggesting that Ser15 phosphorylated p53 was the 4-NQO-responsive hPCNA regulator.	Staurosporine	21-34	P53	Homo sapiens	101-104
8564961-6	1996	Fluorescence-activated cell sorter analysis, continuous labeling with tritiated thymidine, and time-lapse videomicroscopy documented the first example of a prolonged p53-dependent G1 arrest induced by ionizing radiation during the first postirradiation cell cycle of tumor cells, suggesting a role for G1 arrest in determining the sensitivity of these cells to irradiation.	Tritiated thymidine	70-89	P53	Homo sapiens	166-169
16696067-1	1996	Aim-To study p53 expression in relation to proliferative status in normal and nondysplastic, dysplastic and malignant lesions of the oral mucosa.Method-The standard avidin-biotin complex (ABC) immunohistochemical staining method was used to study the expression of p53 and Ki67 on frozen sections of oral leukoplakias and carcinomas.Results-Of the leukoplakia and carcinoma samples, 70% expressed p53 in over 5% of cells.	avidin-biotin	165-178	P53	Homo sapiens	13-16
8762431-1	1996	An immunohistochemical method utilizing microwave oven treated avidin-biotin complex (ABC) technique was used in this study to detect P53 protein expression in 87 parafin-embedded fibrous neoplasm tissues.	avidin-biotin	63-76	P53	Homo sapiens	134-137
8832944-5	1996	RESULTS: Overexpression of p53 protein was detected in 6 (75%) of the cases examined with the D07 antibody and in 5 (62.5%) cases with BP53-12.	bp53-12	135-142	P53	Homo sapiens	27-30
15474986-5	2005	It was observed that Staurosporine, a Ser/Thr kinase inhibitor, blocked the Ser15 phosphorylation of p53 and the hPCNA promoter response to 4-NQO simultaneously, suggesting that Ser15 phosphorylated p53 was the 4-NQO-responsive hPCNA regulator.	Staurosporine	21-34	P53	Homo sapiens	199-202
15474986-5	2005	It was observed that Staurosporine, a Ser/Thr kinase inhibitor, blocked the Ser15 phosphorylation of p53 and the hPCNA promoter response to 4-NQO simultaneously, suggesting that Ser15 phosphorylated p53 was the 4-NQO-responsive hPCNA regulator.	4-Nitroquinoline-1-oxide	140-145	P53	Homo sapiens	199-202
21594347-0	1996	Phorbol ester stimulated Cip1 expression in p53-negative leukemic cells.	Phorbol Esters	0-13	P53	Homo sapiens	44-47
8668331-0	1996	Acute and delayed apoptosis induced by thymidine deprivation correlates with expression of p53 and p53-regulated genes in colon carcinoma cells.	Thymidine	39-48	P53	Homo sapiens	91-94
15474986-5	2005	It was observed that Staurosporine, a Ser/Thr kinase inhibitor, blocked the Ser15 phosphorylation of p53 and the hPCNA promoter response to 4-NQO simultaneously, suggesting that Ser15 phosphorylated p53 was the 4-NQO-responsive hPCNA regulator.	4-Nitroquinoline-1-oxide	211-216	P53	Homo sapiens	101-104
8668331-0	1996	Acute and delayed apoptosis induced by thymidine deprivation correlates with expression of p53 and p53-regulated genes in colon carcinoma cells.	Thymidine	39-48	P53	Homo sapiens	99-102
15474986-5	2005	It was observed that Staurosporine, a Ser/Thr kinase inhibitor, blocked the Ser15 phosphorylation of p53 and the hPCNA promoter response to 4-NQO simultaneously, suggesting that Ser15 phosphorylated p53 was the 4-NQO-responsive hPCNA regulator.	4-Nitroquinoline-1-oxide	211-216	P53	Homo sapiens	199-202
8619835-0	1996	DNA-dependent protein kinase inhibitor (OK-1035) suppresses p21 expression in HCT116 cells containing wild-type p53 induced by adriamycin.	3-cyano-5-(4-pyridyl)-6-hydrazonomethyl-2-pyridone	40-47	P53	Homo sapiens	112-115
15474986-7	2005	Taken together, our data indicate that after 4-NQO treatment hPCNA is transactivated by Ser15 phosphorylated p53, and participate in DNA repair.	4-Nitroquinoline-1-oxide	45-50	P53	Homo sapiens	109-112
8619835-3	1996	Using OK-1035, a selective inhibitor of DNA-dependent protein kinase (DNA-PK), we demonstrated the importance of the phosphorylation of wt-p53 by DNA-PK in the DNA damage-mediated expression of the p21 gene.	3-cyano-5-(4-pyridyl)-6-hydrazonomethyl-2-pyridone	6-13	P53	Homo sapiens	139-142
8619835-5	1996	By addition of OK-1035 to this culture, the induction of p21 protein was significantly decreased in a dose-dependent manner, whereas wt-p53 induction was not affected.	3-cyano-5-(4-pyridyl)-6-hydrazonomethyl-2-pyridone	15-22	P53	Homo sapiens	136-139
9552394-4	1996	In this article we review some of the emerging data that suggests the role of p53 in determining whether the cellular response to dThd deprivation is cytostasis or cytotoxicity (apoptosis).	Thymidine	130-134	P53	Homo sapiens	78-81
15671536-11	2005	As Adriamycin dose increased, radioiodide uptake was significantly correlated with activated p53 as well as total p53 protein level.	radioiodide	30-41	P53	Homo sapiens	93-96
7499360-6	1995	A 4-day treatment of cells with R5020 or RU486 lowered the p53 levels in cells grown in normal culturing conditions to 15 and 30% of control levels, respectively.	Mifepristone	41-46	P53	Homo sapiens	59-62
7499360-7	1995	R5020 and RU486 treatments also caused down-regulation and/or hyperphosphorylation of the progesterone receptor, which correlated with the down-regulation of p53.	Mifepristone	10-15	P53	Homo sapiens	158-161
15671536-11	2005	As Adriamycin dose increased, radioiodide uptake was significantly correlated with activated p53 as well as total p53 protein level.	radioiodide	30-41	P53	Homo sapiens	114-117
8622853-3	1996	The structure of the tet domain forms the basis for designing an active therapeutic p53 with an oligomerization domain which would not cross react with a DNA-binding mutant p53.	tetramethylenedisulfotetramine	21-24	P53	Homo sapiens	84-87
15657356-0	2005	Epigallocatechin-3-gallate induces apoptosis in estrogen receptor-negative human breast carcinoma cells via modulation in protein expression of p53 and Bax and caspase-3 activation.	epigallocatechin gallate	0-26	P53	Homo sapiens	144-147
8622853-3	1996	The structure of the tet domain forms the basis for designing an active therapeutic p53 with an oligomerization domain which would not cross react with a DNA-binding mutant p53.	tetramethylenedisulfotetramine	21-24	P53	Homo sapiens	173-176
8580407-3	1995	Six ducks with HCC, five of which were fed a diet containing aflatoxin B1 for 1-2 years, were analysed for the presence of point mutations at this codon of the p53 gene by polymerase chain reaction and direct nucleotide sequencing.	Aflatoxin B1	61-73	P53	Homo sapiens	160-163
15657356-5	2005	Induction of apoptosis by EGCG could be corroborated to the increased expression of tumor suppressor protein p53 and its phosphorylation at Ser 15 residue.	epigallocatechin gallate	26-30	P53	Homo sapiens	109-112
8774641-10	1996	The growth of the Ad5CMV-p53-infected cells was greatly suppressed as detected by both cell count and [3H]thymidine incorporation assay.	Thymidine	106-115	P53	Homo sapiens	25-28
15860933-8	2005	Moreover, overexpression of both wild-type p53 and exogenous PKCdelta in MKN28 increased cisplatin-induced cell death in MKN28.	mkn28	73-78	P53	Homo sapiens	43-46
8697089-2	1995	DDB at the concentration of 10(-4)M could significantly increase the content of cAMP in Bel-7402 cells, and also suppressed the expressions of oncogene c-myc and hepatocarcinoma marker AFP gene and enhanced the anti-oncogene p53 expression.	DDB	0-3	P53	Homo sapiens	225-228
15471885-6	2004	Comparison of the activity of unphosphorylated and phosphorylated p53 induced by the genotoxic drugs doxorubicin and etoposide in HCT116 and RKO cells revealed no difference in their sequence-specific DNA binding and ability to transactivate p53 target genes and to induce p53-dependent apoptosis.	Etoposide	117-126	P53	Homo sapiens	66-69
8796849-3	1996	For example, the p53 mutational spectrum reveals evidence for a direct causal effect of ultraviolet radiation in skin cancer, of aflatoxin B1 in liver cancer and of tobacco smoke in lung cancer.	Aflatoxin B1	129-141	P53	Homo sapiens	17-20
15534906-1	2004	AIM: To investigate p53 mutation and p21 expression in hepatocarcinogenesis induced by hepatitis B virus (HBV) and aflatoxin B(1) (AFB(1)) in tree shrews, and to reveal the role of these genes in hepatocarcinogenesis.	Aflatoxin B1	115-126	P53	Homo sapiens	20-23
7586148-4	1995	Two cell lines selected from V79/B7 for their resistance to phosphonacetyl-L-aspartate or methotrexate and previously shown to bear gene amplification, showed p53 expression.	phosphonacetyl-l-aspartate	60-86	P53	Homo sapiens	159-162
8526349-1	1995	Inhibition of expression of ras-p21 and p53 by sulindac during azoxymethane-induced colon carcinogenesis.	Azoxymethane	63-75	P53	Homo sapiens	40-43
15525476-9	2004	The expression levels of protein p53 and Bcl-2 decreased following 2-methoxyestradiol treatment in CNE2 cells, whereas Bax and p21(WAF1) protein expression were unaffected after treatment with 2-methoxyestradiol.	2-Methoxyestradiol	67-85	P53	Homo sapiens	33-36
7554056-0	1995	Nitric oxide and ethylnitrosourea: relative mutagenicity in the p53 tumor suppressor and hypoxanthine-phosphoribosyltransferase genes.	Ethylnitrosourea	17-33	P53	Homo sapiens	64-67
8547828-0	1995	Variation in the expression of p53, c-myc, and bcl-2 oncoproteins in individual patient cultures of normal urothelium exposed to cobalt 60 gamma-rays and N-nitrosodiethanolamine.	N-nitrosodiethanolamine	154-177	P53	Homo sapiens	31-34
8554597-0	1995	GM1492 human diploid skin fibroblasts lack the p53-dependent G1 cell-cycle checkpoint.	gm1492	0-6	P53	Homo sapiens	47-50
8599466-4	1995	We believe that the immunohistochemical detection of p53 protein with the use of monoclonal antibodies such as BP53-12 on paraffin sections, especially when strong nuclear reactivity is demonstrated, may prove to be an adjunctive tool in the histopathologic differentiation of MM from SN.	bp53-12	111-118	P53	Homo sapiens	53-56
9815936-0	1995	Expression of topoisomerase II, bcl-2, and p53 in three human brain tumor cell lines and their possible relationship to intrinsic resistance to etoposide.	Etoposide	144-153	P53	Homo sapiens	43-46
7488003-0	1995	Phorbol esters attenuate the expression of p53 in cells treated with doxorubicin and protect TS-P53/K562 from apoptosis.	Phorbol Esters	0-14	P53	Homo sapiens	43-46
7488003-0	1995	Phorbol esters attenuate the expression of p53 in cells treated with doxorubicin and protect TS-P53/K562 from apoptosis.	Phorbol Esters	0-14	P53	Homo sapiens	96-99
15520174-6	2004	Finally, using p53-null melanoma cell line and RNA interference in cells expressing wild-type p53 protein, we show that Bax induction and NaB-mediated apoptosis is p53 dependent.	nab	138-141	P53	Homo sapiens	15-18
7488003-1	1995	The induction of p53 by doxorubicin in normal human fibroblasts was completely reverted by TPA, a phorbol ester.	Phorbol Esters	98-111	P53	Homo sapiens	17-20
7478558-5	1995	Previous transfection of linear or circular, single- or ds, DNA, followed by mitomycin C-treatment, lead to a dramatic increase in nuclear p53 accumulation and p53 activity according to electrophoretic mobility shift analysis.	Mitomycin	77-88	P53	Homo sapiens	139-142
7478558-5	1995	Previous transfection of linear or circular, single- or ds, DNA, followed by mitomycin C-treatment, lead to a dramatic increase in nuclear p53 accumulation and p53 activity according to electrophoretic mobility shift analysis.	Mitomycin	77-88	P53	Homo sapiens	160-163
7560890-3	1995	In breast cancer, we observed a poor correlation (rs = 0.17) between P53 expression and proliferative activity evaluated as [3H]-thymidine ([3H]-dT) labeling index and an independent prognostic relevance of the two variables.	Thymidine	129-138	P53	Homo sapiens	69-72
7560890-3	1995	In breast cancer, we observed a poor correlation (rs = 0.17) between P53 expression and proliferative activity evaluated as [3H]-thymidine ([3H]-dT) labeling index and an independent prognostic relevance of the two variables.	Thymidine	145-147	P53	Homo sapiens	69-72
7560890-7	1995	A weak direct relation between P53 positivity and [3H]-dT incorporation (rs = 0.4) was observed on the overall series of P53+ tumors and was maintained in subgroups defined by several biological and pathological features, except for estrogen receptor-negative tumors.	Thymidine	55-57	P53	Homo sapiens	31-34
7560890-7	1995	A weak direct relation between P53 positivity and [3H]-dT incorporation (rs = 0.4) was observed on the overall series of P53+ tumors and was maintained in subgroups defined by several biological and pathological features, except for estrogen receptor-negative tumors.	Thymidine	55-57	P53	Homo sapiens	121-124
7656242-0	1995	Preferential promutagenic lesions at exons 7-8 of human p53 genomic DNA induced by the direct-acting hepatocarcinogens N-nitroso-2-acetylaminofluorene and N-acetoxy-2-acetylaminofluorene.	N-nitroso-N(2)-fluorenylacetamide	119-150	P53	Homo sapiens	56-59
7644500-9	1995	In contrast, two HPV immortalized cell lines in which p53 protein was destroyed by E6-modulated ubiquitinylation were highly sensitive to apoptosis induced by MMC.	Mitomycin	159-162	P53	Homo sapiens	54-57
7644500-12	1995	Thus, HPV 16E6 can sensitize mammary epithelial cells to MMC-induced apoptosis via a p53- and p21-independent pathway.	Mitomycin	57-60	P53	Homo sapiens	85-88
7766306-0	1995	Benzo[a]pyrene-induced mutagenesis of p53 hot-spot codons 248 and 249 in human hepatocytes.	benzo[a	0-7	P53	Homo sapiens	38-41
7766306-1	1995	Human tobacco-related cancers show a high frequency of G-to-T transversions in several mutation hot-spot regions of the p53 tumor suppressor gene, probably the result of specific mutagens in tobacco smoke, most notably benzo[a]pyrene.	benzo[a	219-226	P53	Homo sapiens	120-123
15520174-6	2004	Finally, using p53-null melanoma cell line and RNA interference in cells expressing wild-type p53 protein, we show that Bax induction and NaB-mediated apoptosis is p53 dependent.	nab	138-141	P53	Homo sapiens	94-97
7897229-10	1995	Third, p53-56lyn was probably activated after cell stimulation with zymosan, because the phosphorylation levels of a synthetic copolymer of glutamine-tyrosine were increased in Triton X-100-insoluble fraction.	Glutamine	140-149	P53	Homo sapiens	7-10
15520174-6	2004	Finally, using p53-null melanoma cell line and RNA interference in cells expressing wild-type p53 protein, we show that Bax induction and NaB-mediated apoptosis is p53 dependent.	nab	138-141	P53	Homo sapiens	94-97
7705936-0	1995	Transfected mutant p53 gene increases X-ray-induced cell killing and mutation in human fibroblasts immortalized with 4-nitroquinoline 1-oxide but does not induce neoplastic transformation of the cells.	4-Nitroquinoline-1-oxide	117-141	P53	Homo sapiens	19-22
21552884-2	1995	In all cell lines, the number of cell clones resistant to a neomycin analogue was strongly diminished when pCMVhup53 was cotransfected with the resistance plasmid pRSVneo as compared to cotransfection with either a plasmid vector, a p53 deletion and a mutant p53 expression vector.	Neomycin	60-68	P53	Homo sapiens	113-116
21552884-2	1995	In all cell lines, the number of cell clones resistant to a neomycin analogue was strongly diminished when pCMVhup53 was cotransfected with the resistance plasmid pRSVneo as compared to cotransfection with either a plasmid vector, a p53 deletion and a mutant p53 expression vector.	Neomycin	60-68	P53	Homo sapiens	233-236
15308639-0	2004	CP-31398 restores DNA-binding activity to mutant p53 in vitro but does not affect p53 homologs p63 and p73.	CP 31398	0-8	P53	Homo sapiens	49-52
7614480-0	1995	Base transitions at CpG dinucleotides in the p53 gene are common in esophageal adenocarcinoma.	Dinucleoside Phosphates	24-37	P53	Homo sapiens	45-48
7614480-7	1995	The tumors that were analyzed demonstrated a specific p53 mutation spectrum, with G:C to A:T base transitions at CpG dinucleotides accounting for 80% (8 of 10) of single-base substitutions.	Dinucleoside Phosphates	117-130	P53	Homo sapiens	54-57
7616356-8	1995	Tumours with p53 gene mutations at exon 5 had a higher median [3H]thymidine labelling index (17 per cent) than those with mutations at exons 6, 7, and 8 (11.8 per cent).	Thymidine	66-75	P53	Homo sapiens	13-16
7737156-6	1995	However, when we employed the phosphatase inhibitor okadaic acid, overall phosphorylation of p53 was drastically enhanced in a dose-dependent manner and resembled that of p53 from SV40-transformed rat cells.	Okadaic Acid	52-64	P53	Homo sapiens	93-96
7737156-6	1995	However, when we employed the phosphatase inhibitor okadaic acid, overall phosphorylation of p53 was drastically enhanced in a dose-dependent manner and resembled that of p53 from SV40-transformed rat cells.	Okadaic Acid	52-64	P53	Homo sapiens	171-174
7705850-0	1995	Polymorphism of the pentanucleotide repeat d(AAAAT) within intron 1 of the human tumor suppressor gene p53 (17p13.1).	pentanucleotide	20-35	P53	Homo sapiens	103-106
15308639-6	2004	Here we show that mutant p53, isolated from cells treated with CP-31398, is capable of binding to p53 response elements in vitro.	CP 31398	63-71	P53	Homo sapiens	25-28
7892276-1	1995	Aflatoxin B1 (AFB1) has been postulated to be a hepatocarcinogen in humans, possibly by causing p53 mutations at codon 249.	Aflatoxin B1	0-12	P53	Homo sapiens	96-99
15308639-6	2004	Here we show that mutant p53, isolated from cells treated with CP-31398, is capable of binding to p53 response elements in vitro.	CP 31398	63-71	P53	Homo sapiens	98-101
15308639-8	2004	In addition, using purified p53 core domain from two different hotspot mutants (R273H and R249S), we show that CP-31398 can restore DNA-binding activity in a dose-dependent manner.	CP 31398	111-119	P53	Homo sapiens	28-31
7889486-6	1995	Intranuclear accumulation of p53 protein was immunostained with the avidin-biotin complex method.	avidin-biotin	68-81	P53	Homo sapiens	29-32
15492260-4	2004	In two melanomas with wild-type p53 but with differential expression of APAF-1, treatment with camptothecin, celecoxib, or an nitric oxide synthase inhibitor (1400W) significantly modulated expression of 36 of 96 genes in an apoptosis-specific cDNA macroarray, but APAF-1 mRNA levels were not induced (in APAF-1(-) cells) nor up-regulated (in APAF-1(+) cells), a finding confirmed at the protein level.	Camptothecin	95-107	P53	Homo sapiens	32-35
7923176-11	1994	p53 allelic amino acid variation with sequences coding for aspartic acid or asparagine was present in codon 61 in the variable region of exon 4 in both HCCs and nonneoplastic tissues of ground squirrels.	Asparagine	76-86	P53	Homo sapiens	0-3
7931472-2	1994	MATERIALS AND METHODS: Paraffin sections from the primary tumors in 107 colorectal cancer patients who had preoperative serum carcinoembryonic antigen (CEA) levels less than five were examined for the expression of p53 nuclear protein by immunohistochemical staining using the monoclonal antibody PAb 1801.	4-Aminobenzoic Acid	297-300	P53	Homo sapiens	215-218
7883998-4	1995	Induced differentiation of the p53-deficient promyelocytic HL-60 cells along the monocytic lineage by phorbol ester or 1a,25 dihydroxyvitamin D3 resulted in a marked increase of both p21WAF1/CIP1/SDI1 mRNA and protein expression due to enhanced mRNA stability.	Phorbol Esters	102-115	P53	Homo sapiens	31-34
15492284-4	2004	We found that CDDO-Me not only activated caspase-8 but also induced expression of DRs, particularly DR5, in a p53-independent mechanism.	bardoxolone methyl	14-21	P53	Homo sapiens	110-113
7854771-5	1995	Under conditions of both serum deprivation and presence of hydroxyurea, p53 expression was decreased throughout the cell cycle, and the bivariate DNA/p53 distribution pattern during the cell cycle did not change.	Hydroxyurea	59-70	P53	Homo sapiens	72-75
7834638-4	1995	We show that p53-independent induction of WAF1/CIP1 occurs in human leukemia cells treated with 12-O-tetradecanoylphorbol-13-acetate, okadaic acid, or IFN-gamma but not with retinoic acid, vitamin D3, or DMSO.	Okadaic Acid	134-146	P53	Homo sapiens	13-16
8036011-7	1994	It is evident that H2O2/FeCl3 possesses essentially the same mutagenic specificity for codons 249 and 250 of p53 as bulky carcinogens such as aflatoxin B1, benzo(a)pyrene or heterocyclic amines.	Aflatoxin B1	142-154	P53	Homo sapiens	109-112
15486204-6	2004	This study, using gel-mobility-shift assays, was undertaken to examine the interactions of active and latent p53 protein with DNA fragments and oligodeoxyribonucleotide duplexes modified by BBR3464 in a cell free medium and to compare these results with those describing the interactions of these proteins with DNA modified by cisplatin.	Oligodeoxyribonucleotides	144-168	P53	Homo sapiens	109-112
15724841-3	2004	Subsequent studies from our laboratory also revealed that the combined use of both UCN-01 and camptothecin induced DNA double strand breaks in p53 mutant tumor cells but not in normal or p53 negative epithelial cells.	Camptothecin	94-106	P53	Homo sapiens	143-146
8061893-5	1994	IHC assays revealed nuclear p53 immunostaining in 53% of cases (32 of 60) with PAb1801, 38% (23 of 60) with PAb421, and 32% (19 of 60) with PAb240.	pab240	140-146	P53	Homo sapiens	28-31
8061893-10	1994	IHC with PAb240, which is thought to be specific for mutated p53, was positive in 9 cases with demonstrable p53 mutations and in 9 cases with no detectable mutations.	pab240	9-15	P53	Homo sapiens	61-64
8061893-10	1994	IHC with PAb240, which is thought to be specific for mutated p53, was positive in 9 cases with demonstrable p53 mutations and in 9 cases with no detectable mutations.	pab240	9-15	P53	Homo sapiens	108-111
8018565-0	1994	Tumor-promoting phorbol ester transiently down-modulates the p53 level and blocks the cell cycle.	Phorbol Esters	16-29	P53	Homo sapiens	61-64
8018565-1	1994	Activation of the protein kinase C signaling pathway by tumor-promoting phorbol esters, such as 4 beta-phorbol 12-myristate 13-acetate (PMA), induced a decrease in the level of p53 mRNA in several serum-starved human cell lines.	Phorbol Esters	72-86	P53	Homo sapiens	177-180
8018565-2	1994	Also, the tumor-promoting phosphatase inhibitor okadaic acid induced a decrease in the p53 mRNA level in the cell lines.	Okadaic Acid	48-60	P53	Homo sapiens	87-90
7530828-7	1995	We find that antibodies to two other discrete sites in the core can also, like PAb240, recognize cryptic epitopes and distinguish mutant from wild-type conformations implying that the point mutations found in p53 in human tumours have widespread effects on the folding pattern of the DNA binding domain.	pab240	79-85	P53	Homo sapiens	209-212
7970699-4	1994	The DNA damaging agent etoposide induced p53 accumulation only in cells harboring wild-type p53 yet it induced WAF1/Cip1 gene expression in cells carrying wild-type or mutant p53, suggesting the involvement of p53-dependent and independent signaling pathways in the regulation of WAF1/Cip1 gene expression.	Etoposide	23-32	P53	Homo sapiens	41-44
7970699-4	1994	The DNA damaging agent etoposide induced p53 accumulation only in cells harboring wild-type p53 yet it induced WAF1/Cip1 gene expression in cells carrying wild-type or mutant p53, suggesting the involvement of p53-dependent and independent signaling pathways in the regulation of WAF1/Cip1 gene expression.	Etoposide	23-32	P53	Homo sapiens	92-95
7970699-4	1994	The DNA damaging agent etoposide induced p53 accumulation only in cells harboring wild-type p53 yet it induced WAF1/Cip1 gene expression in cells carrying wild-type or mutant p53, suggesting the involvement of p53-dependent and independent signaling pathways in the regulation of WAF1/Cip1 gene expression.	Etoposide	23-32	P53	Homo sapiens	92-95
7970699-4	1994	The DNA damaging agent etoposide induced p53 accumulation only in cells harboring wild-type p53 yet it induced WAF1/Cip1 gene expression in cells carrying wild-type or mutant p53, suggesting the involvement of p53-dependent and independent signaling pathways in the regulation of WAF1/Cip1 gene expression.	Etoposide	23-32	P53	Homo sapiens	92-95
15371552-6	2004	Finally, this PNA acted cooperatively with camptothecin treatment both with regard to p53 activity induction as well as cell viability.	Camptothecin	43-55	P53	Homo sapiens	86-89
7923116-4	1994	Induction of p53 is also abnormal in AT cells following treatment with methylmethanesulfonate and bleomycin but appears relatively normal following treatment with UV-C irradiation or the topoisomerase inhibitors, etoposide and camptothecin.	Etoposide	213-222	P53	Homo sapiens	13-16
7923116-4	1994	Induction of p53 is also abnormal in AT cells following treatment with methylmethanesulfonate and bleomycin but appears relatively normal following treatment with UV-C irradiation or the topoisomerase inhibitors, etoposide and camptothecin.	Camptothecin	227-239	P53	Homo sapiens	13-16
7955081-4	1994	These results would indicate that BBN-induced rat urinary bladder carcinomas are similar to human urinary bladder carcinomas with respect to alterations in the p53 and H-ras genes and that p53 gene alterations are relatively early events in rat urinary bladder carcinogenesis induced by BBN treatment.	Butylhydroxybutylnitrosamine	34-37	P53	Homo sapiens	160-163
7955081-4	1994	These results would indicate that BBN-induced rat urinary bladder carcinomas are similar to human urinary bladder carcinomas with respect to alterations in the p53 and H-ras genes and that p53 gene alterations are relatively early events in rat urinary bladder carcinogenesis induced by BBN treatment.	Butylhydroxybutylnitrosamine	34-37	P53	Homo sapiens	189-192
8084605-0	1994	p56/p53lyn tyrosine kinase activation in mammalian cells treated with mitomycin C.	Mitomycin	70-81	P53	Homo sapiens	4-7
7903205-1	1994	Aflatoxin B1 has been suggested as a causative agent for a G to T mutation at codon 249 in the p53 gene in human hepatocellular carcinomas (HCC) from southern Africa and Qidong in China.	Aflatoxin B1	0-12	P53	Homo sapiens	95-98
15339383-9	2004	The protein level of Cdk4 protein increased at 3 h and then decreased gradually from 6 h, but it was still higher than that in the vehicle cultures at 12 h. The p53 level decreased obviously at 3 h after staurosporine treatment and then seemed to increase at 12 h, but remained lower than that of vehicle cultures.	Staurosporine	204-217	P53	Homo sapiens	161-164
8301066-8	1993	Although many HCC patients displaying P53 mutations also suffer from HBV infection, which itself can lead to rearrangements of P53 coding regions or induce the synthesis of viral proteins possibly interacting with p53, the specific G to T transversion within codon 249 of the P53 gene seems to directly reflect the extent of aflatoxin B1 exposure.	Aflatoxin B1	325-337	P53	Homo sapiens	38-41
8301066-8	1993	Although many HCC patients displaying P53 mutations also suffer from HBV infection, which itself can lead to rearrangements of P53 coding regions or induce the synthesis of viral proteins possibly interacting with p53, the specific G to T transversion within codon 249 of the P53 gene seems to directly reflect the extent of aflatoxin B1 exposure.	Aflatoxin B1	325-337	P53	Homo sapiens	214-217
8089212-10	1994	CONCLUSIONS: Immunostaining of wild type p53 is demonstrable not only in its nuclear form using antibody PAb240 but also in it common cytoplasmic-perinuclear localisation in normal tissues using the PAb248 monoclonal antibody.	pab240	105-111	P53	Homo sapiens	41-44
8208536-13	1994	In contrast, the p53 in cell lines with either homozygous 175His or 248His p53 mutations, were unable either to transactivate or bind to the p53 response element.	248his	68-74	P53	Homo sapiens	17-20
15289856-3	2004	Our results demonstrated that diosgenin induced G2/M arrest of cell cycle progression through p21 up-regulation in a p53-independent pathway and strong induction of apoptosis in HEL cells.	Diosgenin	30-39	P53	Homo sapiens	117-120
15208667-4	2004	We have studied here the p53 response to DNA-damaging agents (camptothecin, mitomycin C) in individual cells.	Camptothecin	62-74	P53	Homo sapiens	25-28
7907948-6	1994	In particular, we studied the mutability of codons 247-250 of p53 with the mycotoxin aflatoxin B1 (AFB1) in human hepatocytes.	Aflatoxin B1	85-97	P53	Homo sapiens	62-65
9419766-11	1994	Treatment of JEG-3 cells with 8-Br-cAMP, which induces genes characteristic of the syncytiotrophoblast, raised BCL-2 protein approximately twofold, whereas p53 mRNA declined.	8-Bromo Cyclic Adenosine Monophosphate	30-39	P53	Homo sapiens	156-159
15208667-4	2004	We have studied here the p53 response to DNA-damaging agents (camptothecin, mitomycin C) in individual cells.	Mitomycin	76-87	P53	Homo sapiens	25-28
15265702-2	2004	We have previously demonstrated that an inhibitor of HDAC, sodium butyrate (NaB), induces apoptosis of breast cancer cells in a P53-independent and P21(waf1)-dependent manner.	nab	76-79	P53	Homo sapiens	128-131
7905619-0	1994	Mutagenesis of codon 248 of the human p53 tumor suppressor gene by N-ethyl-N-nitrosourea.	Ethylnitrosourea	67-88	P53	Homo sapiens	38-41
8302577-2	1994	Cytoplasmic staining of p53 with the monoclonal antibody PAb240 was inhibited by the specific oligopeptide, NTFRHSVVVP, that corresponds to the amino acids between 210 and 219 in p53 and which includes the epitope domain for PAb240.	pab240	57-63	P53	Homo sapiens	24-27
15155752-4	2004	We have used the small molecule compound CP-31398 (Pfizer) to restore wild-type p53 function to the codon 248 mutant p53 present in WiT49 cells.	CP 31398	41-49	P53	Homo sapiens	80-83
8302577-2	1994	Cytoplasmic staining of p53 with the monoclonal antibody PAb240 was inhibited by the specific oligopeptide, NTFRHSVVVP, that corresponds to the amino acids between 210 and 219 in p53 and which includes the epitope domain for PAb240.	pab240	57-63	P53	Homo sapiens	179-182
8302577-2	1994	Cytoplasmic staining of p53 with the monoclonal antibody PAb240 was inhibited by the specific oligopeptide, NTFRHSVVVP, that corresponds to the amino acids between 210 and 219 in p53 and which includes the epitope domain for PAb240.	pab240	225-231	P53	Homo sapiens	24-27
8302577-2	1994	Cytoplasmic staining of p53 with the monoclonal antibody PAb240 was inhibited by the specific oligopeptide, NTFRHSVVVP, that corresponds to the amino acids between 210 and 219 in p53 and which includes the epitope domain for PAb240.	pab240	225-231	P53	Homo sapiens	179-182
7816989-2	1994	The mutation of an allele on the p53 gene with loss of the healthy allele, in different tissues such as lung, larynx, bladder, liver, skin, colon and breast, which may or may not be exposed to chemical or physical carcinogens (tobacco, radon, ultraviolet, aflatoxin B1), is associated with the occurrence of cancer.	Aflatoxin B1	256-268	P53	Homo sapiens	33-36
15155752-4	2004	We have used the small molecule compound CP-31398 (Pfizer) to restore wild-type p53 function to the codon 248 mutant p53 present in WiT49 cells.	CP 31398	41-49	P53	Homo sapiens	117-120
15155752-5	2004	In these cells, CP-31398 activated transcription of p53-regulated promoters and enhanced UV light-induced apoptosis without altering the overall p53 protein level.	CP 31398	16-24	P53	Homo sapiens	52-55
15155752-7	2004	Gene expression profiling of CP-31398-treated WiT49 cells revealed subsets of putative p53 target genes that were up- or down-regulated.	CP 31398	29-37	P53	Homo sapiens	87-90
15551755-0	2004	2-methoxyestradiol enhances p53 protein transduction therapy-associated inhibition of the proliferation of oral cancer cells through the suppression of NFkappaB activity.	2-Methoxyestradiol	0-18	P53	Homo sapiens	28-31
7690928-5	1993	Mutant p53 proteins were variably resistant to E6-mediated degradation, and this correlated with PAb 1620 reactivity.	4-Aminobenzoic Acid	97-100	P53	Homo sapiens	7-10
8397412-0	1993	Aflatoxin B1 induces the transversion of G--&gt;T in codon 249 of the p53 tumor suppressor gene in human hepatocytes.	Aflatoxin B1	0-12	P53	Homo sapiens	70-73
15551755-3	2004	However, the intracellular half-life of the delivered protein was less than 36 h. Previous studies also showed that 2-methoxyestradiol (2-ME), an endogenous non-toxic estrogenic metabolite, induces the stabilization of the wild-type p53 protein in human cancer cells posttranscriptionally.	2-Methoxyestradiol	116-134	P53	Homo sapiens	233-236
15551755-3	2004	However, the intracellular half-life of the delivered protein was less than 36 h. Previous studies also showed that 2-methoxyestradiol (2-ME), an endogenous non-toxic estrogenic metabolite, induces the stabilization of the wild-type p53 protein in human cancer cells posttranscriptionally.	2-Methoxyestradiol	136-140	P53	Homo sapiens	233-236
15551755-4	2004	In the present study, we examined whether 2-ME induced the stabilization of 11R-p53 and had an inhibitory effect on the proliferation of oral cancer cells.	2-Methoxyestradiol	42-46	P53	Homo sapiens	80-83
15551755-5	2004	The application of 2-ME significantly enhanced the inhibitory effect of 11R-p53 on the proliferation of oral cancer cells.	2-Methoxyestradiol	19-23	P53	Homo sapiens	76-79
15551755-8	2004	These results suggest that 2-ME synergistically enhances the 11R-p53-induced inhibition of the proliferation of oral cancer cells through the suppression of NFkB transcription.	2-Methoxyestradiol	27-31	P53	Homo sapiens	65-68
15242777-4	2004	Here, we have found that treatment of pyrrolidine dithiocarbamate (PDTC), a zinc ionophore, resulted in the accumulation of several proteasome substrates including p53 and p21 in HeLa cells.	pyrrolidine dithiocarbamic acid	38-65	P53	Homo sapiens	164-167
15242777-4	2004	Here, we have found that treatment of pyrrolidine dithiocarbamate (PDTC), a zinc ionophore, resulted in the accumulation of several proteasome substrates including p53 and p21 in HeLa cells.	pyrrolidine dithiocarbamic acid	67-71	P53	Homo sapiens	164-167
15252149-10	2004	Attenuating p53 by a chemical inhibitor pifithrin-alpha decreased the selenite-induced p53 Ser15P and led to concordant reductions of PARP cleavage and apoptosis.	ser15p	91-97	P53	Homo sapiens	12-15
15252149-10	2004	Attenuating p53 by a chemical inhibitor pifithrin-alpha decreased the selenite-induced p53 Ser15P and led to concordant reductions of PARP cleavage and apoptosis.	ser15p	91-97	P53	Homo sapiens	87-90
15252149-11	2004	In summary, selenite-induced p53 Ser15P appeared to be important for activating the caspase-mediated apoptosis involving both the caspase-8 and the caspase-9 pathways in the LNCaP cells.	ser15p	33-39	P53	Homo sapiens	29-32
14988151-6	2004	Furthermore, p53 gene silencing resulted in decreased p21 mRNA levels and reduced the sensitivity of CD34+ cells toward the cytotoxic drug etoposide.	Etoposide	139-148	P53	Homo sapiens	13-16
15149862-1	2004	Mutations in the WRN or the TP53 genes lead to spontaneous genetic instability, an elevated risk of tumor formation, and sensitivity to compounds that interfere with DNA replication, such as camptothecin and DNA interstrand cross-linking drugs.	Camptothecin	191-203	P53	Homo sapiens	28-32
15175154-3	2004	Both ATM and hSMG-1 phosphorylate Ser/Thr-Gln-containing target sequences in the checkpoint protein p53 and the nonsense-mediated mRNA decay (NMD) protein hUpf1.	Glutamine	42-45	P53	Homo sapiens	100-103
15178317-1	2004	Okadaic acid (OA) is a protein phosphatase (PP) inhibitor and induces hyperphosphorylation of p53.	Okadaic Acid	0-12	P53	Homo sapiens	94-97
15178317-1	2004	Okadaic acid (OA) is a protein phosphatase (PP) inhibitor and induces hyperphosphorylation of p53.	Okadaic Acid	14-16	P53	Homo sapiens	94-97
15179185-3	2004	TSA significantly induced protein expression of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) in a dose-dependent manner in all cell lines including those not expressing p21(WAF1/CIP1) constitutively, whereas the levels of both wild-type and mutated p53 protein were reduced.	trichostatin A	0-3	P53	Homo sapiens	257-260
15161716-10	2004	Lack of Fas up-regulation in the p53-null and -mutant lines abolished the synergistic interaction between 5-FU and CH-11.	4-dimethylamino-3',4'-dimethoxychalcone	115-120	P53	Homo sapiens	33-36
15161716-11	2004	Interestingly, synergy was still observed between the antifolates and CH-11 in the p53-null HCT116 and p53-mutant H630 cell lines, although this was significantly reduced compared with the p53 wild-type cell lines.	4-dimethylamino-3',4'-dimethoxychalcone	70-75	P53	Homo sapiens	83-86
15161716-11	2004	Interestingly, synergy was still observed between the antifolates and CH-11 in the p53-null HCT116 and p53-mutant H630 cell lines, although this was significantly reduced compared with the p53 wild-type cell lines.	4-dimethylamino-3',4'-dimethoxychalcone	70-75	P53	Homo sapiens	103-106
15161716-11	2004	Interestingly, synergy was still observed between the antifolates and CH-11 in the p53-null HCT116 and p53-mutant H630 cell lines, although this was significantly reduced compared with the p53 wild-type cell lines.	4-dimethylamino-3',4'-dimethoxychalcone	70-75	P53	Homo sapiens	103-106
15143945-6	2004	MKN45 that has wild-type p53 showed severe inhibition by irinotecan compared with MKN28, which has mutated p53.	mkn28	82-87	P53	Homo sapiens	107-110
14755248-2	2004	We found that supercoiled (sc) pBluescript DNAs with different inserted p53 target sequences were stronger competitors than a mixture of scDNA pBluescript with the given 20-mer target oligodeoxynucleotide.	Oligodeoxyribonucleotides	184-204	P53	Homo sapiens	72-75
14701864-4	2004	Treatment of co-transfected cells with phosphatidylinositol-specific phospholipase C liberated the complex of MT4-MMP and p68 ADAMTS4 from the cell membrane, but the p53 ADAMTS4 remained associated.	Phosphatidylinositols	39-59	P53	Homo sapiens	166-169
15177039-0	2004	The isoflavonoids genistein and quercetin activate different stress signaling pathways as shown by analysis of site-specific phosphorylation of ATM, p53 and histone H2AX.	Genistein	18-27	P53	Homo sapiens	149-152
15177039-3	2004	We previously showed that genistein, a naturally occurring isoflavonoid, induced increased ATM protein kinase activity, ATM-dependent phosphorylation of p53 on serine 15 and activation of the DNA-binding properties of p53.	Genistein	26-35	P53	Homo sapiens	153-156
15177039-3	2004	We previously showed that genistein, a naturally occurring isoflavonoid, induced increased ATM protein kinase activity, ATM-dependent phosphorylation of p53 on serine 15 and activation of the DNA-binding properties of p53.	Genistein	26-35	P53	Homo sapiens	218-221
15177039-4	2004	Here, we show that genistein also induces phosphorylation of p53 at serines 6, 9, 20, 46, and 392, and that genistein-induced accumulation and phosphorylation of p53 is reduced in two ATM-deficient human cell lines.	Genistein	19-28	P53	Homo sapiens	61-64
15177039-4	2004	Here, we show that genistein also induces phosphorylation of p53 at serines 6, 9, 20, 46, and 392, and that genistein-induced accumulation and phosphorylation of p53 is reduced in two ATM-deficient human cell lines.	Genistein	19-28	P53	Homo sapiens	162-165
15177039-4	2004	Here, we show that genistein also induces phosphorylation of p53 at serines 6, 9, 20, 46, and 392, and that genistein-induced accumulation and phosphorylation of p53 is reduced in two ATM-deficient human cell lines.	Genistein	108-117	P53	Homo sapiens	61-64
15177039-4	2004	Here, we show that genistein also induces phosphorylation of p53 at serines 6, 9, 20, 46, and 392, and that genistein-induced accumulation and phosphorylation of p53 is reduced in two ATM-deficient human cell lines.	Genistein	108-117	P53	Homo sapiens	162-165
15143984-6	2004	Median values and ranges of p53 protein expression were as follows: 0.0% (range, 0.0-1.8%) in NS, 0.0% (range, 0.0-6.5%) in PS, 9.2% (range, 0.0-24.0%) in KA, 19.3% (range, 0.0-48.1%) in BCC and 30.1% (range, 0.0-68.1%) in SCC.	ns	94-96	P53	Homo sapiens	28-31
14695155-2	2003	Importantly, the cytotoxic effects of thymidine deprivation induced by 5-fluorouracil (FUra) combined with leucovorin (LV) was enhanced by IFN-gamma, and the synergism was shown to be dependent on Fas, FUra-induced DNA damage, and independent of p53.	Thymidine	38-47	P53	Homo sapiens	246-249
14632576-8	2003	Three (25%) of 12 informative cases exhibited LOH at 17p for the dinucleotide repeat within the TP53 gene.	Dinucleoside Phosphates	65-77	P53	Homo sapiens	96-100
14660748-9	2003	Furthermore, we showed that c-myc-overexpressing cells retain a functional p53 pathway and thus respond to etoposide.	Etoposide	107-116	P53	Homo sapiens	75-78
14986813-6	2003	Hepatocyte necrosis and regeneration and the generation of oxygen and nitrogen reactive species resulting from chronic HBV infection increase the likelihood of the AFB1-induced p53 249ser and other mutations and the subsequent clonal expansion of cells containing these mutations.	nitrogen reactive species	70-95	P53	Homo sapiens	177-180
14654539-0	2003	TP53 gene mutations predict the response to neoadjuvant treatment with 5-fluorouracil and mitomycin in locally advanced breast cancer.	Mitomycin	90-99	P53	Homo sapiens	0-4
14654539-6	2003	CONCLUSION: This study revealed a significant association between lack of response to 5-fluorouracil and mitomycin and mutations affecting the L2/L3 domains of the p53 protein.	Mitomycin	105-114	P53	Homo sapiens	164-167
14583781-3	2003	Both camptothecin exposure and c-Myc overexpression in LoVo cells resulted in elevation of p53 protein levels, suggesting a role of p53 in the c-Myc-imposed sensitisation to the apoptotic effects of camptothecin.	Camptothecin	5-17	P53	Homo sapiens	91-94
14583781-3	2003	Both camptothecin exposure and c-Myc overexpression in LoVo cells resulted in elevation of p53 protein levels, suggesting a role of p53 in the c-Myc-imposed sensitisation to the apoptotic effects of camptothecin.	Camptothecin	5-17	P53	Homo sapiens	132-135
14583781-3	2003	Both camptothecin exposure and c-Myc overexpression in LoVo cells resulted in elevation of p53 protein levels, suggesting a role of p53 in the c-Myc-imposed sensitisation to the apoptotic effects of camptothecin.	Camptothecin	199-211	P53	Homo sapiens	91-94
14583781-3	2003	Both camptothecin exposure and c-Myc overexpression in LoVo cells resulted in elevation of p53 protein levels, suggesting a role of p53 in the c-Myc-imposed sensitisation to the apoptotic effects of camptothecin.	Camptothecin	199-211	P53	Homo sapiens	132-135
14583781-4	2003	This was confirmed by the ability of PFT-alpha, a specific inhibitor of p53, to attenuate camptothecin-induced apoptosis.	Camptothecin	90-102	P53	Homo sapiens	72-75
14612526-7	2003	Moreover, pretreatment with TSA also increased VP-16-induced apoptosis in a p53-dependent and -independent manner.	trichostatin A	28-31	P53	Homo sapiens	76-79
14599859-10	2003	Examination of signaling pathways that mediate 2-methoxyestradiol-induced apoptosis showed p53-independent growth inhibition.	2-Methoxyestradiol	47-65	P53	Homo sapiens	91-94
14599859-13	2003	Our finding that 2-methoxyestradiol-mediated growth inhibition of uterine sarcomatous cells occurred in a p53-independent manner may have considerable clinical significance.	2-Methoxyestradiol	17-35	P53	Homo sapiens	106-109
14586402-4	2003	We show here that it is also induced by a typical HDAC inhibitor, trichostatin A (TSA), through its promoter, in a p53-independent manner.	trichostatin A	66-80	P53	Homo sapiens	115-118
14586402-4	2003	We show here that it is also induced by a typical HDAC inhibitor, trichostatin A (TSA), through its promoter, in a p53-independent manner.	trichostatin A	82-85	P53	Homo sapiens	115-118
14583461-8	2003	The most striking p53-related effects are at K9, which is underacetylated in p53-/- cells under normal conditions of growth but which shows a dramatic increase in acetylation after combined treatment with UV plus TSA.	trichostatin A	213-216	P53	Homo sapiens	18-21
8334996-6	1993	Furthermore, the expression of the endogenous, chromosomally integrated GLN elements was significantly induced upon activation of wild type p53 in cells harboring a temperature sensitive p53 mutant.	Glutamine	72-75	P53	Homo sapiens	140-143
8334996-6	1993	Furthermore, the expression of the endogenous, chromosomally integrated GLN elements was significantly induced upon activation of wild type p53 in cells harboring a temperature sensitive p53 mutant.	Glutamine	72-75	P53	Homo sapiens	187-190
14583461-8	2003	The most striking p53-related effects are at K9, which is underacetylated in p53-/- cells under normal conditions of growth but which shows a dramatic increase in acetylation after combined treatment with UV plus TSA.	trichostatin A	213-216	P53	Homo sapiens	77-80
8485705-2	1993	Activation of p53-DNA binding was seen for treatment with radiation, hydrogen peroxide, actinomycin D, Adriamycin, etoposide, camptothecin, 5-fluorouracil, mitomycin C, and cisplatin.	Etoposide	115-124	P53	Homo sapiens	14-17
12844488-6	2003	Patients with the XPD codon 312 Asn allele were less likely to have p53 mutations (13.8%) than XPD 312 Asp/Asp (27.3%) [odds ratio (OR) 0.43, 95% confidence interval (CI) 0.20-0.89, P = 0.023].	Asparagine	32-35	P53	Homo sapiens	68-71
8485705-2	1993	Activation of p53-DNA binding was seen for treatment with radiation, hydrogen peroxide, actinomycin D, Adriamycin, etoposide, camptothecin, 5-fluorouracil, mitomycin C, and cisplatin.	Camptothecin	126-138	P53	Homo sapiens	14-17
8485705-2	1993	Activation of p53-DNA binding was seen for treatment with radiation, hydrogen peroxide, actinomycin D, Adriamycin, etoposide, camptothecin, 5-fluorouracil, mitomycin C, and cisplatin.	Mitomycin	156-167	P53	Homo sapiens	14-17
8485705-5	1993	The increase in p53 activation in camptothecin treated cells may result, at least in part, from an increased half-life of the protein and consequent increases in intracellular protein concentration.	Camptothecin	34-46	P53	Homo sapiens	16-19
12844488-8	2003	However, the p53 mutation frequency increased with the increased number of the combined genotypes among XPD 312WT (Asp/Asp), XPD 751VT (Lys/Gln or Gln/Gln) or XRCC1 399VT (Arg/Gln or Gln/Gln) (P = 0.01, trend test).	Glutamine	140-143	P53	Homo sapiens	13-16
12844488-8	2003	However, the p53 mutation frequency increased with the increased number of the combined genotypes among XPD 312WT (Asp/Asp), XPD 751VT (Lys/Gln or Gln/Gln) or XRCC1 399VT (Arg/Gln or Gln/Gln) (P = 0.01, trend test).	Glutamine	147-150	P53	Homo sapiens	13-16
7686255-9	1993	The RFLP/PCR protocol was successfully applied to the determination of N-ethyl-N-nitrosourea-induced mutations in codon 12 of c-H-ras1 (MspI site 1695-1698) and codon 248 of the p53 tumor suppressor gene (MspI site 14067-14070) in human skin fibroblasts.	Ethylnitrosourea	71-92	P53	Homo sapiens	178-181
12844488-8	2003	However, the p53 mutation frequency increased with the increased number of the combined genotypes among XPD 312WT (Asp/Asp), XPD 751VT (Lys/Gln or Gln/Gln) or XRCC1 399VT (Arg/Gln or Gln/Gln) (P = 0.01, trend test).	Glutamine	147-150	P53	Homo sapiens	13-16
8389256-1	1993	A G:C--&gt;T:A mutational hotspot at codon 249 of the p53 tumor suppressor gene has previously been identified in hepatocellular carcinoma (HCC) of patients from Qidong, China and southern Africa in which aflatoxin B1 (AFB1) and hepatitis B virus (HBV) are known synergistic risk factors.	Aflatoxin B1	205-217	P53	Homo sapiens	54-57
8477265-0	1993	Detection of point mutations in the p53 gene: comparison of single-strand conformation polymorphism, constant denaturant gel electrophoresis, and hydroxylamine and osmium tetroxide techniques.	Osmium Tetroxide	164-180	P53	Homo sapiens	36-39
12844488-8	2003	However, the p53 mutation frequency increased with the increased number of the combined genotypes among XPD 312WT (Asp/Asp), XPD 751VT (Lys/Gln or Gln/Gln) or XRCC1 399VT (Arg/Gln or Gln/Gln) (P = 0.01, trend test).	Glutamine	147-150	P53	Homo sapiens	13-16
1459195-3	1992	When a constitutively expressed wild-type p53 plasmid containing the neomycin resistance gene was transfected into these cells, no G418-resistant colonies contained the exogenous p53 cDNA even though the neomycin resistance gene was integrated.	Neomycin	69-77	P53	Homo sapiens	42-45
12844488-8	2003	However, the p53 mutation frequency increased with the increased number of the combined genotypes among XPD 312WT (Asp/Asp), XPD 751VT (Lys/Gln or Gln/Gln) or XRCC1 399VT (Arg/Gln or Gln/Gln) (P = 0.01, trend test).	Glutamine	147-150	P53	Homo sapiens	13-16
8417815-0	1993	Hyperphosphorylation of retinoblastoma protein and p53 by okadaic acid, a tumor promoter.	Okadaic Acid	58-70	P53	Homo sapiens	51-54
12844488-8	2003	However, the p53 mutation frequency increased with the increased number of the combined genotypes among XPD 312WT (Asp/Asp), XPD 751VT (Lys/Gln or Gln/Gln) or XRCC1 399VT (Arg/Gln or Gln/Gln) (P = 0.01, trend test).	Glutamine	147-150	P53	Homo sapiens	13-16
12869416-1	2003	A specific missense mutation in the p53 tumor gene at codon 249 has been reported in over 50% of hepatocellular carcinoma (HCC) tumors and in paired blood samples from areas of high dietary exposure to aflatoxin B1, including Qidong, People"s Republic of China.	Aflatoxin B1	202-214	P53	Homo sapiens	36-39
1630824-7	1992	The p53 protein from 32 of these 37 patients was immunoprecipitated by PAb240, which recognizes a conformation of p53 protein associated with point mutations.	pab240	71-77	P53	Homo sapiens	4-7
1303002-2	1992	The inhibition of p53 expression by a p53 antisense oligodeoxynucleotide lead to the significant decrease of formation of mature macrophages from U 937 cells in the presence of rhGM-CSF.	Oligodeoxyribonucleotides	52-72	P53	Homo sapiens	18-21
1303002-2	1992	The inhibition of p53 expression by a p53 antisense oligodeoxynucleotide lead to the significant decrease of formation of mature macrophages from U 937 cells in the presence of rhGM-CSF.	Oligodeoxyribonucleotides	52-72	P53	Homo sapiens	38-41
1303002-3	1992	By contrast, the p53 sense oligodeoxynucleotide had no any effect.	Oligodeoxyribonucleotides	27-47	P53	Homo sapiens	17-20
1630824-7	1992	The p53 protein from 32 of these 37 patients was immunoprecipitated by PAb240, which recognizes a conformation of p53 protein associated with point mutations.	pab240	71-77	P53	Homo sapiens	114-117
12907245-0	2003	The JNK, ERK and p53 pathways play distinct roles in apoptosis mediated by the antitumor agents vinblastine, doxorubicin, and etoposide.	Etoposide	126-135	P53	Homo sapiens	17-20
1630824-9	1992	Growth stimulation of normal lymphocytes also generated p53 which was immunoprecipitable by PAb240.	pab240	92-98	P53	Homo sapiens	56-59
1322785-5	1992	Furthermore, the incorporation of thymidine into DNA was reduced in cancer cells expressing the wild-type p53 gene.	Thymidine	34-43	P53	Homo sapiens	106-109
12894226-0	2003	Role of p53 and NF-kappaB in epigallocatechin-3-gallate-induced apoptosis of LNCaP cells.	epigallocatechin gallate	29-55	P53	Homo sapiens	8-11
1324739-7	1992	A mutational "hotspot" in the p53 gene in human hepatocellular carcinomas has been identified that could reflect exposure to a specific carcinogen, one candidate being aflatoxin B1.	Aflatoxin B1	168-180	P53	Homo sapiens	30-33
12894226-3	2003	In the present study, we report that EGCG-induced apoptosis in human prostate carcinoma LNCaP cells is mediated via modulation of two related pathways: (a) stabilization of p53 by phosphorylation on critical serine residues and p14ARF-mediated downregulation of murine double minute 2(MDM2) protein, and (b) negative regulation of NF-kappaB activity, thereby decreasing the expression of the proapoptotic protein Bcl-2.	epigallocatechin gallate	37-41	P53	Homo sapiens	173-176
1384667-4	1992	We report here the detection of loss of heterozygosity at the TP53 locus in various human cancers by using a highly informative dinucleotide repeat polymorphism.	Dinucleoside Phosphates	128-140	P53	Homo sapiens	62-66
12894226-4	2003	EGCG-induced stabilization of p53 caused an upregulation in its transcriptional activity, thereby resulting in activation of its downstream targets p21/WAF1 and Bax.	epigallocatechin gallate	0-4	P53	Homo sapiens	30-33
12894226-5	2003	Thus, EGCG had a concurrent effect on two important transcription factors p53 and NF-kappaB, causing a change in the ratio of Bax/Bcl-2 in a manner that favors apoptosis.	epigallocatechin gallate	6-10	P53	Homo sapiens	74-77
12750388-9	2003	The effect of p53 and p73alpha on cell migration was mediated through the activity of the phosphatidylinositol 3-kinase/Rac1 pathway.	Phosphatidylinositols	90-110	P53	Homo sapiens	14-17
1562724-5	1992	We have also found that the p53 immunologic subclass identified by PAb240 exists in normal human circulating lymphocytes either resting, serum starved, or PHA activated.	pab240	67-73	P53	Homo sapiens	28-31
1567424-4	1992	In addition, the Pro-17-Gly peptide competitively inhibited association between hsp70 and p53, an activity which was determined by immunoprecipitation with anti-p53 monoclonal antibody PAb240.	pab240	185-191	P53	Homo sapiens	90-93
1567424-4	1992	In addition, the Pro-17-Gly peptide competitively inhibited association between hsp70 and p53, an activity which was determined by immunoprecipitation with anti-p53 monoclonal antibody PAb240.	pab240	185-191	P53	Homo sapiens	161-164
1310637-0	1992	Low frequency of p53 gene mutation in tumors induced by aflatoxin B1 in nonhuman primates.	Aflatoxin B1	56-68	P53	Homo sapiens	17-20
1310637-1	1992	Aflatoxin B1 has been suggested as a causative agent for a G to T mutation at codon 249 in the p53 gene in human hepatocellular carcinomas from southern Africa and Qidong in China.	Aflatoxin B1	0-12	P53	Homo sapiens	95-98
1310637-7	1992	The occurrence of mutation in codon 249 of the p53 gene in selective samples of human hepatocellular cancers may indicate involvement of environmental carcinogens other than aflatoxin B1 or that hepatitis B virus-related hepatitis is a prerequisite for aflatoxin B1 induction of G to T transversion in codon 249.	Aflatoxin B1	174-186	P53	Homo sapiens	47-50
12721303-2	2003	Previous evidence has shown that apoptotic death of embryonic cortical neurons treated with the DNA damaging agent camptothecin is dependent upon the tumor suppressor p53, an upstream death mediator, and more distal death effectors such as caspases.	Camptothecin	115-127	P53	Homo sapiens	167-170
1565469-1	1992	We investigated the immunocytochemical staining and immunoblotting characteristics of 33 different p53 mutant proteins identified in lung cancer cell lines (18 small-cell lung cancer and 15 non-small-cell lung cancer) using monoclonal antibodies pAbs 240, 421 and 1801.	4-Aminobenzoic Acid	246-250	P53	Homo sapiens	99-102
12839945-4	2003	PTEN and LY294002 induced p53 activity in human brain endothelial cells, suggesting that PTEN and PI3K pathways can suppress the progression of cancer through direct actions on tumor and endothelial cells.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	9-17	P53	Homo sapiens	26-29
1332185-3	1992	Recent reports of a guanine to thymine mutation of the third base of codon 249 of the tumour suppressor gene, p53, in 50% of patients with hepatocellular carcinoma in regions of high aflatoxin exposure, and mutagenic experiments showing that aflatoxin B1 binds particularly to guanine residues in G-C-rich domains and that codon 249 is a preferred target have suggested a mechanism whereby aflatoxin might induce malignant transformation.	Aflatoxin B1	242-254	P53	Homo sapiens	110-113
1370482-3	1992	The fidelity of this mimicry by okadaic acid extends to the phosphorylation of the 27 hsp complex, stathmin, eIF-4E, myosin light chain, nucleolin, epidermal growth factor receptor, and other cdc2-kinase substrates (c-abl, RB, and p53).	Okadaic Acid	32-44	P53	Homo sapiens	231-234
1873816-7	1991	Immunocytochemical data indicate that prostate carcinoma cells expressing the transfected wild-type p53 gene are growth arrested because they exhibit a reduced level of thymidine incorporation into DNA.	Thymidine	169-178	P53	Homo sapiens	100-103
1923530-5	1991	PAb240 reacts exclusively with mutant p53.	pab240	0-6	P53	Homo sapiens	38-41
14508081-8	2003	High throughout screening of chemical libraries has led to the identification of a group of small synthetic molecules such as CP-31398, which can restore p53 function to mutant p53 by stabilizing the active conformation of the protein that is destabilized in many mutants.	CP 31398	126-134	P53	Homo sapiens	154-157
1923530-10	1991	Out of 15 BLs, nine (60%) carried mutant p53, as indicated by their reactivity with PAb240.	pab240	84-90	P53	Homo sapiens	41-44
33794285-0	2021	Effect of pharmacodynamical interaction between nutlin-3a and aspirin in the activation of p53.	nutlin 3	48-57	P53	Homo sapiens	91-94
33794285-4	2021	In the presented work, we have aimed to investigate the effect of pharmacodynamical interaction between two anti-cancer drugs, nutlin-3a and aspirin in the activation of p53 protein.	nutlin 3	127-136	P53	Homo sapiens	170-173
33812801-0	2021	Auranofin reveals therapeutic anticancer potential by triggering distinct molecular cell death mechanisms and innate immunity in mutant p53 non-small cell lung cancer.	Auranofin	0-9	P53	Homo sapiens	136-139
14508081-8	2003	High throughout screening of chemical libraries has led to the identification of a group of small synthetic molecules such as CP-31398, which can restore p53 function to mutant p53 by stabilizing the active conformation of the protein that is destabilized in many mutants.	CP 31398	126-134	P53	Homo sapiens	177-180
33804175-5	2021	Naturally-occurring carbazoles 1-3 and their amino derivatives were evaluated for their potential effect on wild-type and mutant p53 activity using a yeast screening assay and on human tumor cell lines.	Carbazoles	20-30	P53	Homo sapiens	129-132
33804175-6	2021	Naturally-occurring carbazoles 1-3 showed the most potent growth inhibitory effects on wild-type p53-expressing cells, being heptaphylline (1) the most promising in all the investigated cell lines.	Carbazoles	20-30	P53	Homo sapiens	97-100
33771885-8	2021	Implications: We identified common and reproducible genomic alterations in CTCs from AR-V7 negative mCRPC men associated with poor outcomes during enzalutamide/abiraterone treatment, including CNAs in genes linked to lineage plasticity and epigenetic signaling, DNA repair, AR, TP53/RB1, PTEN, and WNT pathways.	enzalutamide	147-159	P53	Homo sapiens	278-282
14508081-10	2003	Further understanding of the mechanisms by which CP-31398 and PRIMA-1 restore p53 activity may not only lead to discovery of more potent analogs but may also suggest new strategies for p53-targeting in tumor therapy.	CP 31398	49-57	P53	Homo sapiens	78-81
33804175-8	2021	Conversely, semi-synthetic aminocarbazole 1d showed an interesting growth inhibitory activity in tumor cells expressing both wild-type and mutant p53, exhibiting low growth inhibition on non-tumor cells.	9H-Carbazol-1-amine	27-41	P53	Homo sapiens	146-149
30578154-9	2019	The up-regulated miRNAs were mainly enriched in pathways as GO:0000122-negative regulation of transcription from RNA polymerase II promoter, phosphatidylinositol phosphorylation, MAPK signaling pathway, and Ras signaling pathway, etc., while the down-regulated miRNAs were enriched in pathways as, response to reactive oxygen species, p53 signaling pathway, calcium signaling pathway, etc.	Phosphatidylinositols	141-161	P53	Homo sapiens	335-338
14508081-10	2003	Further understanding of the mechanisms by which CP-31398 and PRIMA-1 restore p53 activity may not only lead to discovery of more potent analogs but may also suggest new strategies for p53-targeting in tumor therapy.	CP 31398	49-57	P53	Homo sapiens	185-188
12782403-5	2003	Pre-transfection of cultured hepatoma cells with p53mt249 resulted in a three to fourfold increase in IGF-IR phosphorylation and downstream mediator IRS-I phosphorylation but, enhanced more than 15-fold after IGF-II treatment, which coincides well with the cell growth and thymidine uptake results.	Thymidine	273-282	P53	Homo sapiens	49-52
34785441-6	2022	Interestingly MDA-MB-231 cells showed only cytostatic effects upon treatment with compound 4h due to defective p53 status.	4h	91-93	P53	Homo sapiens	111-114
34785441-7	2022	Toxicity study using overexpression of dominant-negative mutant p53 in MCF-7 cells (which have wild type functional p53) showed that anticancer potential of compound 4h is positively correlated with p53 expression.	4h	166-168	P53	Homo sapiens	116-119
34785441-7	2022	Toxicity study using overexpression of dominant-negative mutant p53 in MCF-7 cells (which have wild type functional p53) showed that anticancer potential of compound 4h is positively correlated with p53 expression.	4h	166-168	P53	Homo sapiens	199-202
24726431-6	2014	HaCaTs have impaired responses to p53/SIRT1/miR-34a axis manipulation which enhanced survival during exposure to the chemotherapeutic agent, camptothecin.	Camptothecin	141-153	P53	Homo sapiens	34-37
21380726-4	2011	Trichostatin A induced nuclear damage, decrease in Bid and Bcl-2 protein levels, increase in Bax levels, cytochrome c release, activation of caspases (8, 9, and 3) and increase in tumor suppressor p53 levels.	trichostatin A	0-14	P53	Homo sapiens	197-200
12750239-9	2003	The OSCC patients with a Gln/Gln genotype exhibited a significantly higher frequency of p53 mutation than those with an Arg/Gln and an Arg/Arg genotype.	Glutamine	25-28	P53	Homo sapiens	88-91
12750239-9	2003	The OSCC patients with a Gln/Gln genotype exhibited a significantly higher frequency of p53 mutation than those with an Arg/Gln and an Arg/Arg genotype.	Glutamine	29-32	P53	Homo sapiens	88-91
12750239-9	2003	The OSCC patients with a Gln/Gln genotype exhibited a significantly higher frequency of p53 mutation than those with an Arg/Gln and an Arg/Arg genotype.	Glutamine	29-32	P53	Homo sapiens	88-91
34798143-8	2022	Furthermore, NaAsO2 induced phosphorylation of p53 at Ser315, 376, 392, and Thr55, and acetylation of p53 at K370, 382 with a dose-response relationship, suggesting the contribution of PUMA up-regulation to p53 phosphorylation and acetylation.	sodium arsenite	13-19	P53	Homo sapiens	47-50
34798143-8	2022	Furthermore, NaAsO2 induced phosphorylation of p53 at Ser315, 376, 392, and Thr55, and acetylation of p53 at K370, 382 with a dose-response relationship, suggesting the contribution of PUMA up-regulation to p53 phosphorylation and acetylation.	sodium arsenite	13-19	P53	Homo sapiens	102-105
12750239-10	2003	After adjustment for age, cigarette smoking, areca quid chewing, and alcohol drinking, the Gln/Gln genotype still showed an independent association with the frequency of p53 mutation (odd ratio, 4.50; 95% confidence interval, 1.52-13.36).	Glutamine	91-94	P53	Homo sapiens	170-173
34798143-8	2022	Furthermore, NaAsO2 induced phosphorylation of p53 at Ser315, 376, 392, and Thr55, and acetylation of p53 at K370, 382 with a dose-response relationship, suggesting the contribution of PUMA up-regulation to p53 phosphorylation and acetylation.	sodium arsenite	13-19	P53	Homo sapiens	207-210
34798143-11	2022	To our knowledge, we first reported that NaAsO2 activated phosphorylation of p53 at Ser315, 376, and Thr55, as well as acetylation of p53 at K370.	sodium arsenite	41-47	P53	Homo sapiens	77-80
34945706-5	2021	GTE selectively targeted breast tumor cells without cytotoxic effect on non-tumoral cells and p53 inhibition led to an increase in viable cells, especially in MCF-7, suggesting the involvement of p53 in GTE-induced cytotoxicity.	epigallocatechin gallate	203-206	P53	Homo sapiens	94-97
34945706-5	2021	GTE selectively targeted breast tumor cells without cytotoxic effect on non-tumoral cells and p53 inhibition led to an increase in viable cells, especially in MCF-7, suggesting the involvement of p53 in GTE-induced cytotoxicity.	epigallocatechin gallate	203-206	P53	Homo sapiens	196-199
34945706-7	2021	An increment in p53 and p21 expression stimulated by GTE was observed in MCF-7, and the opposite phenomenon was found in MDA-MB-231 cells, with a redistribution of mutant-p53 from the nucleus and no differences in p21 levels.	epigallocatechin gallate	53-56	P53	Homo sapiens	16-19
34798143-11	2022	To our knowledge, we first reported that NaAsO2 activated phosphorylation of p53 at Ser315, 376, and Thr55, as well as acetylation of p53 at K370.	sodium arsenite	41-47	P53	Homo sapiens	134-137
34878630-6	2022	The treatment with 1 microM of staurosporine caused also a significant down-regulation of MEN1 and was able to restore the basal expression of TP53 only in QGP1 cells.	Staurosporine	31-44	P53	Homo sapiens	143-147
34945706-7	2021	An increment in p53 and p21 expression stimulated by GTE was observed in MCF-7, and the opposite phenomenon was found in MDA-MB-231 cells, with a redistribution of mutant-p53 from the nucleus and no differences in p21 levels.	epigallocatechin gallate	53-56	P53	Homo sapiens	171-174
12750239-10	2003	After adjustment for age, cigarette smoking, areca quid chewing, and alcohol drinking, the Gln/Gln genotype still showed an independent association with the frequency of p53 mutation (odd ratio, 4.50; 95% confidence interval, 1.52-13.36).	Glutamine	95-98	P53	Homo sapiens	170-173
34944489-7	2021	We found that EGCG (50 muM) significantly inhibited the aggregation of (i)sAPPbetaf, blocked p-TAU, increased  Psim, decreased oxidation of DJ-1 at residue Cys106-SH, and inhibited the activation of transcription factor c-JUN and P53, PUMA, and CASPASE-3 in mutant ChLNs compared to WT.	epigallocatechin gallate	14-18	P53	Homo sapiens	230-233
34085157-5	2021	Inhibition of collagen biosynthesis (proline utilizing process) by 2-methoxyestradiol (2ME) contributed to induction of apoptosis in MCF-7WT cells, as detected by increase in the expression of active caspase-3, -9 and p53.	2-Methoxyestradiol	67-85	P53	Homo sapiens	218-221
12678775-4	2003	Lucilactaene arrested cells at G1 phase through restoration of mutant p53.	lucilactaene	0-12	P53	Homo sapiens	70-73
34795783-6	2021	Low-dose oridonin induced GC cell cycle arrest at G0/G1 and cell senescence by suppressing the c-Myc-AP4 pathway and enhancing p53-p21 signaling.	oridonin	9-17	P53	Homo sapiens	127-130
34917264-8	2021	Additionally, KYP-2047 was able to increase Bax, Bad and caspase-3 expression, whereas Bcl-2 and p53 expression were reduced.	3-hydroxy-2-({4-[4-(pyrimidin-2-yl)piperazine-1-carbonyl]phenyl}methyl)-1-benzofuran-7-carboxamide	14-17	P53	Homo sapiens	97-100
34855076-1	2021	Incubation of primary culture of pulmonary fibroblasts with non-opiate analogue of leuenkephalin (NALE; Phe-D-Ala-Gly-Phe-Leu-Arg, 0.1 muM) reduced generation of superoxide anion-radical (by 20.7%) and decreased the number of p53+ cells (by 40.2%) induced by exposure to H2O2 (60 muM).	nale	98-102	P53	Homo sapiens	226-229
34855076-3	2021	Incubation of pulmonary fibroblasts culture with peptide G (Phe-D-Ala-Gly-Phe-Leu-Gly, 0.1 muM) also significantly reduced the damaging effect of H2O2: the number of p53+ cells decreased by 73.5%, the area of cell nuclei returned to normal, and generation of superoxide anion-radical decreased by 18.4%.	phe-d-ala-gly-phe-leu-gly	60-85	P53	Homo sapiens	166-169
34917611-9	2021	Compared to that in the wild type group, the TP53-mutant group showed a higher TMB value (P< 0.001), MSI value (p = 0.077), and TIDE value (p < 0.001) with respect to BC patient immunotherapy.	1,2,4,5-tetramethoxybenzene	79-82	P53	Homo sapiens	45-49
12684687-4	2003	We report that Brca1-deficiency in p53-null cells was associated with increased sensitivity to the topoisomerase I poisons camptothecin and topotecan, the topoisomerase II poisons doxorubicin, mitoxantrone and etoposide, and to the platinum compounds carboplatin and oxaliplatin, but not to the antimetabolites 5-fluorouracil and gemcitabine and the taxanes docetaxel and paclitaxel.	Camptothecin	123-135	P53	Homo sapiens	35-38
12684687-4	2003	We report that Brca1-deficiency in p53-null cells was associated with increased sensitivity to the topoisomerase I poisons camptothecin and topotecan, the topoisomerase II poisons doxorubicin, mitoxantrone and etoposide, and to the platinum compounds carboplatin and oxaliplatin, but not to the antimetabolites 5-fluorouracil and gemcitabine and the taxanes docetaxel and paclitaxel.	Etoposide	210-219	P53	Homo sapiens	35-38
12556443-0	2003	The C-terminal fragment of presenilin 2 triggers p53-mediated staurosporine-induced apoptosis, a function independent of the presenilinase-derived N-terminal counterpart.	Staurosporine	62-75	P53	Homo sapiens	49-52
34534740-10	2021	The novel crystal lattice of C-PC4 in presence of the peptide, the role of the disordered N-PC4 and the high throughput identification of potent small molecules will allow a better understanding and control of p53-PC4 interaction.	c-pc4	29-34	P53	Homo sapiens	210-213
34496154-9	2021	Overall, our results suggests that CBT suppresses colorectal cancer by upregulating the p53 pathway, and thus CBT may have potential as an alternative chemotherapeutic drug for colorectal cancer.	cabazitaxel	35-38	P53	Homo sapiens	88-91
12556448-0	2003	Role of caspases, Bid, and p53 in the apoptotic response triggered by histone deacetylase inhibitors trichostatin-A (TSA) and suberoylanilide hydroxamic acid (SAHA).	trichostatin A	101-115	P53	Homo sapiens	27-30
34745095-7	2021	Moreover, TP53 mutation correlated with TMB and the immune microenvironment.	1,2,4,5-tetramethoxybenzene	40-43	P53	Homo sapiens	10-14
34745095-9	2021	In summary, TP53 mutation is frequently mutated in AML, and its mutation is associated with dismal outcome, TMB, and immunological features, which may serve as a biomarker to predict immune response in AML.	1,2,4,5-tetramethoxybenzene	108-111	P53	Homo sapiens	12-16
34755922-6	2021	More intriguingly, this study demonstrates PDT-stimulated p53 can also re-educate TAMs, providing a combined strategy of using dual tumor microenvironment remodeling to achieve the synergistic effect in the transition from cold immunosuppressive to hot immunoresponsive tumor microenvironment.	tams	82-86	P53	Homo sapiens	58-61
12556448-0	2003	Role of caspases, Bid, and p53 in the apoptotic response triggered by histone deacetylase inhibitors trichostatin-A (TSA) and suberoylanilide hydroxamic acid (SAHA).	trichostatin A	117-120	P53	Homo sapiens	27-30
12628744-3	2003	Here we show that, in neuronal cells, divergent cellular insults, i.e. the exposure to glutamate, beta-amyloid (Abeta) or H(2)O(2), may converge to a common pathway that initiate with elevation of p53 protein levels.	h(2)o	122-127	P53	Homo sapiens	197-200
34769400-9	2021	Molecular analysis showed changes in BAX, BCL2, TP53, and CDKN1 expression in tested cell lines following incubation with ciprofloxacin and levofloxacin.	Levofloxacin	140-152	P53	Homo sapiens	48-52
12670900-4	2003	Both caspase-3 and caspase-8 activities were increased by anti-Fas antibody CH-11 only in cells at 32.5 degrees C with wild-type p53.	4-dimethylamino-3',4'-dimethoxychalcone	76-81	P53	Homo sapiens	129-132
34496154-0	2021	Cabazitaxel suppresses colorectal cancer cell growth via enhancing the p53 anti-tumor pathway.	cabazitaxel	0-11	P53	Homo sapiens	71-74
34496154-8	2021	Expression of several p53 downstream genes that are associated with cell cycle arrest, apoptosis and inhibition of angiogenesis and metastasis are induced by CBT in colorectal cancer cells.	cabazitaxel	158-161	P53	Homo sapiens	22-25
34496154-9	2021	Overall, our results suggests that CBT suppresses colorectal cancer by upregulating the p53 pathway, and thus CBT may have potential as an alternative chemotherapeutic drug for colorectal cancer.	cabazitaxel	110-113	P53	Homo sapiens	88-91
34620079-11	2021	The mutation status of ERBB4 and TP53 was tightly linked to DCB of ICIs treatment, PD-L1 expression, TMB value, and TIICs.	1,2,4,5-tetramethoxybenzene	101-104	P53	Homo sapiens	33-37
12644023-8	2003	CONCLUSION: p53, c-Myc, and BAFF pathways are main pathways utilized by CD34(+) cells to arrest cell-cycle progression at multiple checkpoints, to halt proliferation, and to induce apoptosis as part of their cellular response to etoposide.	Etoposide	229-238	P53	Homo sapiens	12-15
34411980-11	2021	Combination studies revealed that both compounds had synergistic effects (combination index CI < 1) on Cis and Eto through induction of apoptosis (p53 activation and up-regulation of BAX and p21 gene expression).	Etoposide	111-114	P53	Homo sapiens	147-150
34624459-6	2021	The knockdown of p53, a downstream effector of GSK3beta and an important regulator of cell senescence, repressed mitomycin-induced alveolar epithelial cell senescence.	Mitomycin	113-122	P53	Homo sapiens	17-20
34768862-3	2021	A reduction in p53 protein levels protects against poly-PR and partially against poly-GR neurotoxicity in cells.	poly-gr	81-88	P53	Homo sapiens	15-18
34452218-3	2021	This innovative approach explored the great capacity of both polyamidoamine (PAMAM)-paclitaxel (PTX) conjugate and polyethylenimine (PEI) polymers to complex a p53-encoding plasmid DNA (pDNA), highlighting the utility of considering two compacting agents.	Polymers	138-146	P53	Homo sapiens	160-163
34659550-0	2021	MIR-4507 Targets TP53 to Facilitate the Malignant Progression of Non-small-cell Lung Cancer.	mir-4507	0-8	P53	Homo sapiens	17-21
12595758-0	2003	Green tea constituent (-)-epigallocatechin-3-gallate inhibits Hep G2 cell proliferation and induces apoptosis through p53-dependent and Fas-mediated pathways.	epigallocatechin gallate	22-52	P53	Homo sapiens	118-121
34659550-7	2021	Subsequently, a luciferase activity assay was conducted to verify the regulation of the predicted gene target of miR-4507, namely, TP53.	mir-4507	113-121	P53	Homo sapiens	131-135
34659550-9	2021	Further, we co-transfected miR-4507 mimics and TP53 plasmids and found that TP53 overexpression could recover the effects of miR-4507 mimics on proliferation, migration, and the PI3K/AKT signal activation.	mir-4507	27-35	P53	Homo sapiens	76-80
34659550-9	2021	Further, we co-transfected miR-4507 mimics and TP53 plasmids and found that TP53 overexpression could recover the effects of miR-4507 mimics on proliferation, migration, and the PI3K/AKT signal activation.	mir-4507	125-133	P53	Homo sapiens	47-51
34659550-9	2021	Further, we co-transfected miR-4507 mimics and TP53 plasmids and found that TP53 overexpression could recover the effects of miR-4507 mimics on proliferation, migration, and the PI3K/AKT signal activation.	mir-4507	125-133	P53	Homo sapiens	76-80
34376212-9	2021	RESULTS: Bufalin upregulated the expression of cytochrome C, cleaved caspase 3, p-Chk1 and p-p53 proteins to induce U251 cell apoptosis and cycle arrest in the S phase.	bufalin	9-16	P53	Homo sapiens	93-96
12595758-5	2003	ELISA showed that EGCG significantly increased the expression of p53 and p21/WAF1 protein, and this contributed to cell cycle arrest.	epigallocatechin gallate	18-22	P53	Homo sapiens	65-68
34098386-11	2021	TP53 and LRP1B mutations were significantly associated with higher TMB (both p < 0.01), which may be potential markers of immunotherapy.	1,2,4,5-tetramethoxybenzene	67-70	P53	Homo sapiens	0-4
34448982-8	2021	The results obtained from the study indicate that the ZnO nanoparticles of Solanum nigrum possess a dose-dependent cytotoxic effect against HeLa cell lines through the inhibition of beta-catenin and increasing the levels of p53, caspase-3, and caspase-9.	Zinc Oxide	54-57	P53	Homo sapiens	224-227
12595758-7	2003	Taken together, our study suggests that the induction of p53 and the activity of the Fas/FasL apoptotic system play major roles in the antiproliferative activity of EGCG in Hep G2 cells.	epigallocatechin gallate	165-169	P53	Homo sapiens	57-60
12681064-1	2003	OBJECTIVE: To detect the expression and variation of p53 gene during tree shrews" hepatocarcinogenesis induced by hepatitis B virus (HBV) and aflatoxin B1 (AFB1).	Aflatoxin B1	142-154	P53	Homo sapiens	53-56
34512368-3	2021	In this review, we focus on summarizing some representative natural active compounds, mainly including curcumin, resveratrol, paclitaxel, Bufalin, and Ursolic acid that may ultimately trigger cancer cell death through the regulation of some key autophagic signaling pathways, such as RAS-RAF-MEK-ERK, PI3K-AKT-mTOR, AMPK, ULK1, Beclin-1, Atg5 and p53.	ursolic acid	151-163	P53	Homo sapiens	347-350
34205573-4	2021	PBM with both 635 and 808 nm at 4 J/cm2 increased the cell number, modulated extracellular oxidative stress and inflammation markers and decreased the susceptibility of human primary gingival fibroblasts to apoptosis through the downregulation of apoptotic-related genes (P53, CASP9, BAX).	pbm	0-3	P53	Homo sapiens	272-275
15314976-0	2003	Expression of p53 gene in stage IIIA non-small cell lung cancer in patients after neoadjuvant chemotherapy with Vepesid and Cisplatin.	Etoposide	112-119	P53	Homo sapiens	14-17
34141150-6	2021	Ursolic acid treatment downregulated the gene expression of survival factors BCL-2, SURVIVIN, NFKB and SP1, while upregulated the growth-restricting genes BAX, P21 and P53.	ursolic acid	0-12	P53	Homo sapiens	168-171
34383763-4	2021	In addition, norcycloartocarpin activated apoptosis caspase cascade associating with restoration of p53, down-regulated Bcl-2 and augmented Bax in A549 and H460 cells.	norcycloartocarpin	13-31	P53	Homo sapiens	100-103
34340691-14	2021	La3+, Ce3+, and F- are probably the main toxic substances in WSPM, and may be regulate the A549 cell cycle by affecting the expression of genes, such as MDM2, RB1, ATM, TP53, E2F1, CDK2 and CDK4.	Fluorine	16-17	P53	Homo sapiens	169-173
12359354-0	2002	2-Methoxyestradiol induces p53-associated apoptosis of colorectal cancer cells.	2-Methoxyestradiol	0-18	P53	Homo sapiens	27-30
12359354-4	2002	Treatment of CRC cells with 2-methoxyestradiol (2-MeOE(2)) increased expression of p53 and p21(WAF1/CIP1) proteins and induced apoptosis, but did not produce changes in expression of estrogen receptor (ER)alpha or ERbeta.	2-Methoxyestradiol	28-46	P53	Homo sapiens	83-86
34435054-11	2021	In Skov3 cells, the expression levels of p53 and p21 were downregulated, while those of Cyclin E, vascular endothelial growth factor (VEGF), matrix metallopeptidase 2 (MMP2), MMP9, signal transducers and activators of transcription 3 (Stat3), and p-Stat3 were upregulated by ATZ treatment.	Atrazine	275-278	P53	Homo sapiens	41-44
34324416-2	2021	CB002 and structural-analogs restore p53 signaling in tumors with mutant-p53 but we find that unlike other xanthines such as caffeine, pentoxifylline, and theophylline, they do not deregulate the G2 checkpoint.	CB002	0-5	P53	Homo sapiens	37-40
12183079-4	2002	In addition, AA profoundly increased protein level of p53, which was also inhibited by BAPTA/AM, an intracellular Ca(2+) chelator, TMB-8 and dantrolene.	Dantrolene	141-151	P53	Homo sapiens	54-57
34324416-2	2021	CB002 and structural-analogs restore p53 signaling in tumors with mutant-p53 but we find that unlike other xanthines such as caffeine, pentoxifylline, and theophylline, they do not deregulate the G2 checkpoint.	CB002	0-5	P53	Homo sapiens	73-76
12224020-3	2002	We reported that an adenoviral vector containing wt p53 significantly reduced [(3)H]thymidine uptake in melanoma cells containing mutant but not wt p53.	Thymidine	84-93	P53	Homo sapiens	52-55
34336006-8	2021	Data from Oncomine showed that the level of p53 mRNA was elevated in BCC (P < 0.05), and the Hsp70 mRNA was upregulated in SCC (P < 0.001).	oncomine	10-18	P53	Homo sapiens	44-47
34273265-7	2021	Platycodin D also increased caspase-9, caspase-8, caspase-3, and p53 expression and decreased Bcl-2 expression in tumour tissues.	platycodin D	0-12	P53	Homo sapiens	65-68
34485982-6	2021	Pharmacological-mediated increase of P53 protein levels with the Mdm2 inhibitor Nutlin-3a during early (mesoderm to cardiac mesoderm) stages of cardiogenesis resulted in a sizeable loss of cardiomyocytes due to increased apoptosis and cell cycle arrest.	nutlin 3	80-89	P53	Homo sapiens	37-40
12235210-0	2002	DeltaNp73, a dominant-negative inhibitor of wild-type p53 and TAp73, is up-regulated in human tumors.	deltanp73	0-9	P53	Homo sapiens	54-57
35584569-1	2022	Cathepsin K inhibitor (odanacatib; ODN) and cathepsin K knockdown (siRNA) enhance oxaliplatin-induced apoptosis through p53-dependent Bax upregulation.	odanacatib	23-33	P53	Homo sapiens	120-123
35489526-0	2022	Mogrol suppresses lung cancer cell growth by activating AMPK-dependent autophagic death and inducing p53-dependent cell cycle arrest and apoptosis.	MOGROL	0-6	P53	Homo sapiens	101-104
34298658-9	2021	Additionally, KYP-2047 at the concentrations of 50 microM and 100 microM was able to increase the pro-apoptotic protein Bax, p53 and caspase-3 expression whereas Bcl-2 expression was reduced.	3-hydroxy-2-({4-[4-(pyrimidin-2-yl)piperazine-1-carbonyl]phenyl}methyl)-1-benzofuran-7-carboxamide	14-17	P53	Homo sapiens	125-128
34285910-8	2021	Moreover, oridonin treatment significantly increased expression levels of p53 and cleaved caspase-3 and reduced expression of TRPM7, p-AKT, and p-ERK.	oridonin	10-18	P53	Homo sapiens	74-77
35489526-11	2022	In addition, mogrol induced a significant increase in p53 activity in lung cancer cells, accompanied with cell cycle arrest and apoptosis, which could be weakened by p53 silence.	MOGROL	13-19	P53	Homo sapiens	54-57
12235210-8	2002	Conversely, down-regulation of endogenous DeltaNp73 levels by antisense methods alleviates its suppressive action and enhances p53- and TAp73-mediated apoptosis.	deltanp73	42-51	P53	Homo sapiens	127-130
35489526-11	2022	In addition, mogrol induced a significant increase in p53 activity in lung cancer cells, accompanied with cell cycle arrest and apoptosis, which could be weakened by p53 silence.	MOGROL	13-19	P53	Homo sapiens	166-169
35489526-12	2022	Our results indicated that mogrol effectively suppressed lung cancer cells in vivo and in vitro by inducing the excessive autophagy and autophagic cell death via activating AMPK signaling pathway, as well as cell cycle arrest and apoptosis via activating p53 pathway.	MOGROL	27-33	P53	Homo sapiens	255-258
12202623-11	2002	As an example, using a second enzyme BbvI, a mutation frequently encountered in human cancers (G(14154)--&gt;A mutation, p53 codon 245, Arg--&gt;Gln) was detected in patient samples.	Glutamine	145-148	P53	Homo sapiens	121-124
34176787-4	2021	Molecular docking analysis indicated the binding efficacy of calycosin with three of the targets, namely TP53, AKT1, and VEGFA.	7,3'-dihydroxy-4'-methoxyisoflavone	61-70	P53	Homo sapiens	105-109
35421634-3	2022	Doxorubicin and etoposide were used to induce cell senescence as determined by the cessation of cell proliferation, augmented senescence-associated beta-galactosidase (SA-beta-Gal) staining, and increased p53 expression levels.	Etoposide	16-25	P53	Homo sapiens	205-208
35523729-4	2022	A combination of fluorine and sulfur substituents on an aromatic ring induces microdipoles that enhance cell uptake of 12-residue peptide inhibitors of p53-HDM2 interaction and of cell-penetrating cyclic peptides.	Fluorine	17-25	P53	Homo sapiens	152-155
12200149-1	2002	We determined the molecular mechanisms by which trichostatin A (TSA) induced insulin-like growth factor-binding protein 3 (IGFBP-3) gene expression in Hep3B cells, a p53-mutant human hepatocellular carcinoma (HCC) cell line.	trichostatin A	48-62	P53	Homo sapiens	166-169
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	phytochlorin	123-133	P53	Homo sapiens	65-68
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	phytochlorin	123-133	P53	Homo sapiens	101-104
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	phytochlorin	135-139	P53	Homo sapiens	65-68
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	phytochlorin	135-139	P53	Homo sapiens	101-104
35601155-8	2022	TMB-related DEGs were distinctly enriched in cancer- (MAPK, P53, PI3K-Akt, and Wnt pathways) and immune-related pathways (T cell selection and differentiation).	1,2,4,5-tetramethoxybenzene	0-3	P53	Homo sapiens	60-63
35513212-4	2022	The highly cytotoxic ROS was continuously produced via Fe2+-mediated and TA-assisted enhanced Fenton reaction as well as Ce6-induced photosensitive reaction, and meanwhile, the intratumoral upregulated p53 expression inactivated glutathione peroxidase 4 (GPX4) to suppress lipid peroxidation (LPO) resistance, thus resulting in amplified oxidative stress and intensified ferroptosis-apoptosis therapy.	phytochlorin	121-124	P53	Homo sapiens	202-205
12200149-1	2002	We determined the molecular mechanisms by which trichostatin A (TSA) induced insulin-like growth factor-binding protein 3 (IGFBP-3) gene expression in Hep3B cells, a p53-mutant human hepatocellular carcinoma (HCC) cell line.	trichostatin A	64-67	P53	Homo sapiens	166-169
12154028-3	2002	This study was designed to determine whether, and how, the cyclic Arg-Gly-Asp peptide Cilengitide (EMD 121974), which targets the alpha(v)beta(3) integrin receptor expressed on neovasculature, could increase systemic RIT efficacy of therapy in a human breast cancer tumor model having mutant p53 and expressing bcl-2.	peptide cilengitide	78-97	P53	Homo sapiens	292-295
35491653-7	2022	EXPERIMENTAL DESIGN: To gain insight into the relation of the interaction of TP53 and CDKN2A mutations with TMB in HNSCC, we have analyzed genomic data from 1,669 HPV-negative HNSCC tumors with multiple criteria proposed for assessing the damaging effect of TP53 mutations.	1,2,4,5-tetramethoxybenzene	108-111	P53	Homo sapiens	77-81
35491653-8	2022	RESULTS: Data analysis established the TP53 and CDKN2A mutation profiles in specific anatomic subsites and suggested that specific categories of TP53 mutations are more likely to associate with CDKN2A mutation or high TMB based on tumor subsite.	1,2,4,5-tetramethoxybenzene	218-221	P53	Homo sapiens	145-149
35491653-10	2022	CONCLUSIONS: These data emphasize the role of tumor subsite in evaluation of mutational profiles in HNSCC, and link defects in TP53 and CDKN2A to elevated TMB levels in some tumor subgroups.	1,2,4,5-tetramethoxybenzene	155-158	P53	Homo sapiens	127-131
35499148-0	2022	miRNA-34c-5p targets Fra-1 to inhibit pulmonary fibrosis induced by silica through p53 and PTEN/PI3K/Akt signaling pathway.	Silicon Dioxide	68-74	P53	Homo sapiens	83-86
35499148-8	2022	In addition, through interaction with PTEN/p53 it inhibits the proliferation and migration of human bronchial epithelial cells stimulated by silica, and promotes cell apoptosis, thereby preventing EMT.	Silicon Dioxide	141-147	P53	Homo sapiens	43-46
12492119-5	2002	The ability of rottlerin to prevent proteolytic activation of PKCdelta or to induce accumulation of p53 by CP was compromised in HeLa/CP cells.	rottlerin	15-24	P53	Homo sapiens	100-103
35478473-5	2022	In MCF-7 cells, atractylodin administration decreased Bcl-2 expression while activating the expression of p53, Bax, cleaved caspase-3, caspase-8, and caspase-9 apoptotic members.	atractylodin	16-28	P53	Homo sapiens	106-109
35468881-5	2022	Following overexpression or silencing of JMJD2C/MDM2/p53/IL5RA, the 50% concentration of inhibition (IC50) and the biological characteristics of MUM-2B and MUM-2B/CDDP cells were examined using CCK-8 assay, SA-beta-gal staining, fluorescence-activated cell sorting analysis, and Transwell assay.	2-(2-quinolinyl)-1H-indene--1,3(2H)-dione-6'-sulfonic acid	207-218	P53	Homo sapiens	53-56
35429966-5	2022	In addition, we observed that Triptolide and Nutlin-3a were also cooperative in part of p53 deficient cases.	nutlin 3	45-54	P53	Homo sapiens	88-91
35548580-5	2022	Moreover, it was also found that SIRT1 is down-regulated by EGCG, and the SIRT1-p53 signaling pathway participates in the effects of EGCG on CNE-2 and 5-8 F cells.	epigallocatechin gallate	133-137	P53	Homo sapiens	80-83
12492119-7	2002	Whereas the combination of rottlerin and CP increased the half-life of p53 in HeLa cells, CP alone was sufficient to stabilize p53 in HeLa/CP cells.	rottlerin	27-36	P53	Homo sapiens	71-74
35548580-6	2022	Taken together, the findings of this study provided evidence that EGCG could inhibit the growth of NPC cell lines and is linked with the inhibition of the SIRT1-p53 signaling pathway, suggesting the therapeutic potential of EGCG in human NPC.	epigallocatechin gallate	66-70	P53	Homo sapiens	161-164
35548580-6	2022	Taken together, the findings of this study provided evidence that EGCG could inhibit the growth of NPC cell lines and is linked with the inhibition of the SIRT1-p53 signaling pathway, suggesting the therapeutic potential of EGCG in human NPC.	epigallocatechin gallate	224-228	P53	Homo sapiens	161-164
35409358-8	2022	Immunofluorescence data affirmed the activation of P53, caspase 3 and 9 proteins in TEHP-treated cells.	tris(2-ethylhexyl)phosphate	84-88	P53	Homo sapiens	51-54
12416024-11	2002	We also observed that p53 status influenced correlations between ENT1 transporter gene RNA levels and sensitivity to the drugs tiazafurin, AZQ and 3-deazauridine.	tiazafurin	127-137	P53	Homo sapiens	22-25
35251293-0	2022	Metformin Bicarbonate-Mediated Efficient RNAi for Precise Targeting of TP53 Deficiency in Colon and Rectal Cancers.	metformin bicarbonate	0-21	P53	Homo sapiens	71-75
35251293-7	2022	Here, metformin bicarbonate (MetC) is synthesized to develop pH-responsive MetC-nanoparticles with a unique "bomb" for effective cytosolic delivery of POLR2A siRNA, which greatly facilitates its endo/lysosomal escape into the cytosol and augments its therapeutic efficacy of cancer harboring TP53 deficiency.	metformin bicarbonate	6-27	P53	Homo sapiens	292-296
35130342-4	2022	Across all but one molecular risk category (TP53-aneuploidy) and all co-mutated gene subgroups, higher pre-transplant response rates and longer overall survival (OS) were observed with gilteritinib versus SC.	gilteritinib	185-197	P53	Homo sapiens	44-48
12067251-0	2002	Reactive oxygen species generated by PAH o-quinones cause change-in-function mutations in p53.	pah o-quinones	37-51	P53	Homo sapiens	90-93
35478958-0	2022	Hesperidin Ameliorates Dexamethasone-Induced Osteoporosis by Inhibiting p53.	Hesperidin	0-10	P53	Homo sapiens	72-75
35478958-7	2022	Our in vitro results showed that hesperidin partially reversed dexamethasone-induced inhibition of osteogenic differentiation by suppressing the activation of p53, and suggest that hesperidin may be a promising candidate for the treatment against dexamethasone-induced osteoporosis.	Hesperidin	33-43	P53	Homo sapiens	159-162
35478958-7	2022	Our in vitro results showed that hesperidin partially reversed dexamethasone-induced inhibition of osteogenic differentiation by suppressing the activation of p53, and suggest that hesperidin may be a promising candidate for the treatment against dexamethasone-induced osteoporosis.	Hesperidin	181-191	P53	Homo sapiens	159-162
12067251-5	2002	We employed a yeast reporter system to determine whether PAH o-quinones or the ROS they generate cause change-in-function mutations in p53.	pah o-quinones	57-71	P53	Homo sapiens	135-138
35406381-7	2022	Dasatinib treatment also preferentially slowed the growth of gastric and mammary organoids harbouring both Cdh1 and Tp53 mutations.	Dasatinib	0-9	P53	Homo sapiens	116-120
12067251-10	2002	p53 mutagenesis by BP-7,8-dione was attenuated by ROS scavengers and completely abrogated by a combination of superoxide dismutase and catalase, indicating that both superoxide anion and hydroxyl radicals were the responsible mutagens.	Hydroxyl Radical	187-204	P53	Homo sapiens	0-3
35192728-4	2022	Together with extended tumor exposure to therapeutically effective drug levels via reversible conjugation to Pluronic F-108 (PF108), these features translated into rapid tumor regression and long-term survival in models of both ABCG2-overexpressing and p53-mutant high-risk neuroblastomas, in contrast to a marginal effect of the clinically used camptothecin derivative, irinotecan.	Poloxamer	125-130	P53	Homo sapiens	253-256
35192728-4	2022	Together with extended tumor exposure to therapeutically effective drug levels via reversible conjugation to Pluronic F-108 (PF108), these features translated into rapid tumor regression and long-term survival in models of both ABCG2-overexpressing and p53-mutant high-risk neuroblastomas, in contrast to a marginal effect of the clinically used camptothecin derivative, irinotecan.	Camptothecin	346-358	P53	Homo sapiens	253-256
35217496-9	2022	CONCLUSIONS: Taken together, we show that DLG2 over expression increases p53 mediated apoptosis in response to etoposide and UVC mediated genotoxicity and reduced DNA replication machinery.	Etoposide	111-120	P53	Homo sapiens	73-76
12067251-14	2002	Together these data suggest that PAH o-quinones generate an endogenous mutagen (ROS) which leads to p53 inactivation.	pah o-quinones	33-47	P53	Homo sapiens	100-103
12010862-0	2002	XRCC1 and CYP2E1 polymorphisms as susceptibility factors of plasma mutant p53 protein and anti-p53 antibody expression in vinyl chloride monomer-exposed polyvinyl chloride workers.	Polyvinyl Chloride	153-171	P53	Homo sapiens	74-77
35163524-6	2022	Herein, we report that EP4 receptor agonists PgE1-OH and L-902688 have exhibited enhanced cytotoxicity when applied together with anti-CD20 MAbs rituximab, ofatumumab and obinutuzumab in vitro in Burkitt lymphoma cells Ramos, as well as in p53-deficient chronic lymphocytic leukemia (CLL) cells MEC-1.	pge1-oh	45-52	P53	Homo sapiens	240-243
12010862-9	2002	Individuals having experienced a high VCM exposure and displaying a XRCC1 Gln-Gln genotype had a highest risk of p53 overexpression among those having different combinations of VCM exposure and XRCC1 genotypes (OR, 6.5; 95% CI, 1.7-24.2).	Glutamine	74-77	P53	Homo sapiens	113-116
12010862-9	2002	Individuals having experienced a high VCM exposure and displaying a XRCC1 Gln-Gln genotype had a highest risk of p53 overexpression among those having different combinations of VCM exposure and XRCC1 genotypes (OR, 6.5; 95% CI, 1.7-24.2).	Glutamine	78-81	P53	Homo sapiens	113-116
35007916-16	2022	The protein levels of P53 and Caspase 3 increased with BA, NaB and SPT treatment for 72 h. CONCLUSIONS: BA, NaB and SPT show anti-cancer activity in the DMS-114 cell line without damaging MRC-5 cells, and some of the molecular mechanisms are involved in apoptosis and cell cycle arrest.	nab	59-62	P53	Homo sapiens	22-25
11956160-12	2002	These regions contain consensus binding sites for p53 and GATA, respectively, but mutational analyses and gel shift assays suggested that, while the p53 response element is required for NaB responsiveness, neither p53 nor GATA are involved.	nab	186-189	P53	Homo sapiens	149-152
35007916-16	2022	The protein levels of P53 and Caspase 3 increased with BA, NaB and SPT treatment for 72 h. CONCLUSIONS: BA, NaB and SPT show anti-cancer activity in the DMS-114 cell line without damaging MRC-5 cells, and some of the molecular mechanisms are involved in apoptosis and cell cycle arrest.	nab	108-111	P53	Homo sapiens	22-25
35178190-0	2022	Etoposide-induced DNA damage is increased in p53 mutants: identification of ATR and other genes that influence effects of p53 mutations on Top2-induced cytotoxicity.	Etoposide	0-9	P53	Homo sapiens	45-48
35178190-4	2022	We assessed the impact of the loss of p53 function on the formation of DNA damage induced by the Top2 poison etoposide.	Etoposide	109-118	P53	Homo sapiens	38-41
35178190-5	2022	Using human HCT116 cells, we found resistance to etoposide in cell growth assays upon the functional loss of p53.	Etoposide	49-58	P53	Homo sapiens	109-112
35178190-6	2022	Nonetheless, cells lacking fully functional p53 were etoposide hypersensitive in clonogenic survival assays.	Etoposide	53-62	P53	Homo sapiens	44-47
35071802-8	2022	PfHz treatment for 24 h significantly altered expression for 14 genes: 12 were down-regulated (ANAPC11, BRCC3, CUL4B, FBXO4, MIB1, SKP2, TP53, UBA2, UBA3, UBE2G1, UBE2G2, and WWP1), while 2 were up-regulated (UBE2J1 and UBE2Z).	pfhz	0-4	P53	Homo sapiens	137-141
35178190-9	2022	Employing genome-wide siRNA screens, we identified a set of genes for which reduced expression resulted in enhanced synthetic lethality upon etoposide treatment of p53 defective cells.	Etoposide	141-150	P53	Homo sapiens	164-167
11956160-12	2002	These regions contain consensus binding sites for p53 and GATA, respectively, but mutational analyses and gel shift assays suggested that, while the p53 response element is required for NaB responsiveness, neither p53 nor GATA are involved.	nab	186-189	P53	Homo sapiens	149-152
35178190-10	2022	We focused on one hit from this screen, ATR, and showed that decreased expression sensitized the p53-defective cells to etoposide in all assays and generated elevated levels of Top2cc in both p53 proficient and deficient cells.	Etoposide	120-129	P53	Homo sapiens	97-100
12054599-0	2002	Restoration of p53 tumor suppressor pathway in human cervical carcinoma cells by sodium arsenite.	sodium arsenite	81-96	P53	Homo sapiens	15-18
35280362-13	2022	Conclusions: In contrast to most previous studies, we revealed TP53-MUT characteristic in NSCLC patients according to histology-specific differences and the association between TP53-MUT and the mutation landscape, the TMB, and the OS.	1,2,4,5-tetramethoxybenzene	218-221	P53	Homo sapiens	63-67
12054599-5	2002	Two p53-responsive genes, p21(waf1/cip1) and mdm2, were induced after SA treatment.	sodium arsenite	70-72	P53	Homo sapiens	4-7
12054599-7	2002	SA-induced apoptosis was greatly reduced by expression of a dominant-negative mutated p53.	sodium arsenite	0-2	P53	Homo sapiens	86-89
12054599-8	2002	In this study, we have first demonstrated that SA did repress E6 and E7 oncogenes, restore the p53 tumor suppressor pathway and induce apoptosis in SiHa cells.	sodium arsenite	47-49	P53	Homo sapiens	95-98
11896693-2	2002	A disproportionate number of mutations are found in certain codons of the p53 gene, mostly at CpG dinucleotide sequences, which are highly methylated in human tissues.	Dinucleoside Phosphates	98-110	P53	Homo sapiens	74-77
35111281-6	2022	TMB was associated with ALK (p = 0.01), EGFR (p < 0.01), and TP53 (p < 0.05) alterations.	1,2,4,5-tetramethoxybenzene	0-3	P53	Homo sapiens	61-65
11827710-0	2002	Pifithrin-alpha, an inhibitor of p53, enhances the genetic instability induced by etoposide (VP16) in human lymphoblastoid cells treated in vitro.	Etoposide	82-91	P53	Homo sapiens	33-36
11827710-0	2002	Pifithrin-alpha, an inhibitor of p53, enhances the genetic instability induced by etoposide (VP16) in human lymphoblastoid cells treated in vitro.	Etoposide	93-97	P53	Homo sapiens	33-36
11844817-5	2002	Induction of RNA and protein expression of the p53 target gene p21/WAF1 was demonstrated in samples from patients treated with SCH 58500 instillation at higher dose levels.	sch 58500	127-136	P53	Homo sapiens	47-50
11841447-7	2002	We found that the expression of the cell cycle checkpoint protein Chk1 was reduced in the etoposide-treated p53-transfected cells by 24 h, and this correlated with a reduction in the extent of etoposide-induced phosphorylation of CDK1 at tyrosine 15 (Y15).	Etoposide	193-202	P53	Homo sapiens	108-111
11841447-8	2002	We conclude, therefore, that p53 overrides the strong G2 checkpoint response to etoposide in K562 cells, by directly or indirectly downregulating Chk1 expression, which, in turn, contributes to the proapoptotic effect of p53.	Etoposide	80-89	P53	Homo sapiens	29-32
11841447-8	2002	We conclude, therefore, that p53 overrides the strong G2 checkpoint response to etoposide in K562 cells, by directly or indirectly downregulating Chk1 expression, which, in turn, contributes to the proapoptotic effect of p53.	Etoposide	80-89	P53	Homo sapiens	221-224
12174820-1	2002	CP-31398, a styrylquinazoline, emerged from a screen for therapeutic agents that restore a wild-type DNA-binding conformation of mutant p53 to suppress tumors in-vivo (Science 286, 2507, 1999).	CP 31398	0-8	P53	Homo sapiens	136-139
12174820-6	2002	Interestingly, we found that wild-type p53 protein is stabilized upon CP-31398 exposure.	CP 31398	70-78	P53	Homo sapiens	39-42
12174820-7	2002	p53 target genes such as p21WAF1/Cip1, and KILLER/DR5 were upregulated by CP-31398, but their expression did not correlate with arrest or apoptosis induction.	CP 31398	74-82	P53	Homo sapiens	0-3
12174820-8	2002	Combination of CP-31398 and TRAIL or chemotherapeutic agents enhanced cancer cell killing effect possibly through upregulation of p53-regulated genes such as KILLER/DR5.	CP 31398	15-23	P53	Homo sapiens	130-133
12174820-9	2002	Bax-/-, wild-type p53-expressing cells displayed reduced susceptibility to killing by CP-31398.	CP 31398	86-94	P53	Homo sapiens	18-21
12467212-11	2002	In addition, no correlation was found between cell sensitivity to CDDO-Me and p53 status, suggesting that CDDO-Me induce a p53-independent apoptosis.	bardoxolone methyl	106-113	P53	Homo sapiens	123-126
11741290-8	2001	This is the first demonstration that camptothecin and Zeocin can differentially signal for increased levels of modified p53 during all stages of the cell cycle.	Camptothecin	37-49	P53	Homo sapiens	120-123
11684284-0	2001	p53 and redox state in etoposide-induced acute myeloblastic leukemia cell death.	Etoposide	23-32	P53	Homo sapiens	0-3
11684284-1	2001	We investigated whether p53, being a redox-sensitive protein, has a role in the responsiveness of AML cells to etoposide.	Etoposide	111-120	P53	Homo sapiens	24-27
11684284-6	2001	After etoposide exposure for up to 24 hours, some nuclear accumulation of p53 was observed in the ER subclone, as analysed by Western blotting.	Etoposide	6-15	P53	Homo sapiens	74-77
11602746-6	2001	We demonstrate that p53 plays an essential role in the MVMp-induced cell cycle arrest in both S and G(2) by using p53 wild-type (+/+) and null (-/-) cells.	mvmp	55-59	P53	Homo sapiens	20-23
11602746-6	2001	We demonstrate that p53 plays an essential role in the MVMp-induced cell cycle arrest in both S and G(2) by using p53 wild-type (+/+) and null (-/-) cells.	mvmp	55-59	P53	Homo sapiens	114-117
11602746-8	2001	Together these results show that the MVMp-induced cell cycle arrest in S is p53 dependent but p21(cip1) independent, whereas the arrest in G(2) depends on both p53 and its downstream effector p21(cip1).	mvmp	37-41	P53	Homo sapiens	76-79
11602746-8	2001	Together these results show that the MVMp-induced cell cycle arrest in S is p53 dependent but p21(cip1) independent, whereas the arrest in G(2) depends on both p53 and its downstream effector p21(cip1).	mvmp	37-41	P53	Homo sapiens	160-163
11591730-5	2001	Induction of neuronal cell death by camptothecin, a DNA-damaging agent that functions through a p53-dependent mechanism, resulted in increased Apaf1 mRNA in p53-positive, but not p53-deficient neurons.	Camptothecin	36-48	P53	Homo sapiens	96-99
11591730-5	2001	Induction of neuronal cell death by camptothecin, a DNA-damaging agent that functions through a p53-dependent mechanism, resulted in increased Apaf1 mRNA in p53-positive, but not p53-deficient neurons.	Camptothecin	36-48	P53	Homo sapiens	157-160
11591730-5	2001	Induction of neuronal cell death by camptothecin, a DNA-damaging agent that functions through a p53-dependent mechanism, resulted in increased Apaf1 mRNA in p53-positive, but not p53-deficient neurons.	Camptothecin	36-48	P53	Homo sapiens	157-160
11576999-13	2001	Since over 50% of human tumors contain a functionally defective p53 that reduces sensitivity to commonly used chemotherapeutic agents, such as etoposide and cisplatin, the ability of tachpyridine to induce apoptosis independently of p53 may offer an advantage in anti-tumor therapy.	Etoposide	143-152	P53	Homo sapiens	64-67
11562347-3	2001	Dexamethasone (Dex) stimulates the degradation of endogenous GR and p53 by the proteasome pathway in HUVEC under hypoxia and mitomycin C treatments, and also in hepatoma cells (HepG2) under normoxia.	Mitomycin	125-136	P53	Homo sapiens	68-71
11427532-7	2001	In cells arrested in S phase with hydroxyurea, WRN exits the nucleolus and colocalizes with p53 in the nucleoplasm.	Hydroxyurea	34-45	P53	Homo sapiens	92-95
11522624-3	2001	In the present study, we have used a highly sensitive mutation assay to determine the p53 mutation load in nontumorous human lung and to study the mutability of p53 codons 157, 248, 249, and 250 to benzo(a)pyrene-diol-epoxide (BPDE), an active metabolite of BP in human bronchial epithelial BEAS-2B cells.	pyrene-diol-epoxide	206-225	P53	Homo sapiens	161-164
11555596-8	2001	Competition analysis with monoclonal antibodies showed that Fab binding could be inhibited most effectively with DO11 and, to a lesser extent, Pab240, indicating an epitope within or adjacent to residues 181-190 of p53.	pab240	143-149	P53	Homo sapiens	215-218
11602059-7	2001	Cytotoxicity assays revealed that the wt-p53 transfectants were more sensitive to doxorubicin and mitomycin compared with the pNeo transformants.	Mitomycin	98-107	P53	Homo sapiens	41-44
11479920-11	2001	Given the fact that p53 mutations are common in patients with metastatic prostate cancer, our finding that 2-ME-mediated growth inhibition of human prostate cancer cells occurred in a p53-independent manner has considerable clinical significance.	2-Methoxyestradiol	107-111	P53	Homo sapiens	184-187
11396965-3	2001	In stably transfected DLD-1 colorectal adenocarcinoma cells, cdc25C expression is down-regulated when p53 is induced from a (tet)-off-regulated system.	tetramethylenedisulfotetramine	125-128	P53	Homo sapiens	102-105
11423970-8	2001	Low concentrations of roscovitine cooperate with the DNA-damaging agent camptothecin to activate p53 in a synergistic fashion.	Camptothecin	72-84	P53	Homo sapiens	97-100
11350911-9	2001	Induction of wt p53 in these models led to a 3- and 2-fold increase in sensitivity to 1,3-bis(2-chloroethyl)-1-nitrosourea and temozolomide, respectively, which generate the MGMT-repairable O(6)-alkyl adducts in DNA.	o(6)-alkyl	190-200	P53	Homo sapiens	16-19
11706756-2	2001	The aim of this study was to determine the predictive value of p53 mutation or the expression of GML, a target of p53, for sensitivity to 5-FU and MMC.	Mitomycin	147-150	P53	Homo sapiens	63-66
11706756-2	2001	The aim of this study was to determine the predictive value of p53 mutation or the expression of GML, a target of p53, for sensitivity to 5-FU and MMC.	Mitomycin	147-150	P53	Homo sapiens	114-117
11706756-9	2001	CONCLUSION: GML expression and p53 mutation in colorectal cancer may be useful predictive genetic markers for sensitivity to MMC and 5-FU, respectively.	Mitomycin	125-128	P53	Homo sapiens	31-34
11306736-4	2001	When HL-60 cells, p53 null, were treated with etoposide, MDM2 was markedly decreased prior to caspase-3-dependent retinoblastoma tumor suppressor protein (pRb) and poly (ADP- ribose) polymerase (PARP) cleavages.	Etoposide	46-55	P53	Homo sapiens	18-21
11313880-7	2001	In contrast, human glioma cells lacking functional p53, either due to mutation or the expression of E6 protein of human papillomavirus, were highly resistant to etoposide and exhibited no significant change in the ceramide level.	Etoposide	161-170	P53	Homo sapiens	51-54
11267976-5	2001	The results suggest that NaB blocks the growth of both cell lines by induction of cyclin-dependent kinase inhibitors (in particular, p21(waf1) in NCI-H23 and p27(kip1) and p16(ink4) in NCI-H460) through a p53-dependent or p53-independent mechanism, and open up interesting perspectives for the use of NaB as an alternative or additional strategy in the treatment of non-small cell lung carcinoma.	nab	25-28	P53	Homo sapiens	205-208
11267976-5	2001	The results suggest that NaB blocks the growth of both cell lines by induction of cyclin-dependent kinase inhibitors (in particular, p21(waf1) in NCI-H23 and p27(kip1) and p16(ink4) in NCI-H460) through a p53-dependent or p53-independent mechanism, and open up interesting perspectives for the use of NaB as an alternative or additional strategy in the treatment of non-small cell lung carcinoma.	nab	25-28	P53	Homo sapiens	222-225
11342237-0	2001	SeO(2) induces apoptosis with down-regulation of Bcl-2 and up-regulation of P53 expression in both immortal human hepatic cell line and hepatoma cell line.	seo(2)	0-6	P53	Homo sapiens	76-79
11342237-3	2001	SeO(2) could also down-regulate the Bcl-2 level, greatly in HL-7702 and slightly in SMMC-7721 cells, but up-regulate wild type P53 level a little in HL-7702 and significantly in SMMC-7721 cells.	seo(2)	0-6	P53	Homo sapiens	127-130
11342237-4	2001	The Bcl-2/P53 value was closely correlated with the apoptotic rate as well as SeO(2) concentrations.	seo(2)	78-84	P53	Homo sapiens	10-13
11096068-5	2001	Here we show that genistein induces the up-regulation of p53 protein, phosphorylation of p53 at serine 15, activation of the sequence-specific DNA binding properties of p53, and phosphorylation of the hCds1/Chk2 protein kinase at threonine 68.	Genistein	18-27	P53	Homo sapiens	57-60
11096068-5	2001	Here we show that genistein induces the up-regulation of p53 protein, phosphorylation of p53 at serine 15, activation of the sequence-specific DNA binding properties of p53, and phosphorylation of the hCds1/Chk2 protein kinase at threonine 68.	Genistein	18-27	P53	Homo sapiens	89-92
11096068-5	2001	Here we show that genistein induces the up-regulation of p53 protein, phosphorylation of p53 at serine 15, activation of the sequence-specific DNA binding properties of p53, and phosphorylation of the hCds1/Chk2 protein kinase at threonine 68.	Genistein	18-27	P53	Homo sapiens	89-92
11096068-7	2001	In contrast, the topoisomerase II inhibitor etoposide induced phosphorylation of p53 and Chk2 in ATM-positive and ATM-deficient cells.	Etoposide	44-53	P53	Homo sapiens	81-84
11096068-9	2001	Together our data suggest that ATM is required for activation of a DNA damage-induced pathway that activates p53 and Chk2 in response to genistein.	Genistein	137-146	P53	Homo sapiens	109-112
11258706-1	2001	The N-terminal BOX-I domain of p53 containing a docking site for the negative regulator MDM2 and the positive effector p300, harbours two recently identified phosphorylation sites at Thr18 or Ser20O whose affect on p300 is undefined.	ser20o	192-198	P53	Homo sapiens	31-34
11158590-2	2001	We have examined the response to p53 when DNA synthesis is blocked by hydroxyurea (HU) or aphidicolin or when DNA is damaged by gamma IR.	Hydroxyurea	70-81	P53	Homo sapiens	33-36
11148027-0	2001	Chalcone derivatives antagonize interactions between the human oncoprotein MDM2 and p53.	Chalcone	0-8	P53	Homo sapiens	84-87
11013255-10	2001	Down-regulation of ADNP by antisense oligodeoxynucleotides up-regulated the tumor suppressor p53 and reduced the viability of intestinal cancer cells by 90%.	Oligodeoxyribonucleotides	37-58	P53	Homo sapiens	93-96
11299762-5	2001	Collectively, these observations suggest that growth inhibition by ellagic acid is mediated by signaling pathways that mediate DNA damage, triggers p53, which in turn activates p21 and at the same time alters the growth factor expression, resulting in the down regulation of IGF-II.	Ellagic Acid	67-79	P53	Homo sapiens	148-151
11196182-2	2001	A specific missense mutation resulting from a guanine to thymine transversion at the third position of codon 249 in the p53 tumor suppressor gene has been reported in 10-70% of HCCs from areas of high dietary exposure to aflatoxin B1.	Aflatoxin B1	221-233	P53	Homo sapiens	120-123
11140901-5	2001	A significant correlation was observed between MDM2 protein and p53 expression in 38 cases with an areca quid (AQ) chewing habit (P=0.032).	aq	111-113	P53	Homo sapiens	64-67
11125034-0	2001	MDM2 mediated nuclear exclusion of p53 attenuates etoposide-induced apoptosis in neuroblastoma cells.	Etoposide	50-59	P53	Homo sapiens	35-38
11125034-3	2001	Data presented here indicate that hyperactive nuclear export of p53 suppresses etoposide-induced apoptosis but does not prevent growth arrest.	Etoposide	79-88	P53	Homo sapiens	64-67
11125034-5	2001	Our data show etoposide induces complete trans-location of p53 to the nucleus and activation of apoptosis in the neuroblastic NB cell line SH-SY5Y (N-type), which expresses low levels of MDM2.	Etoposide	14-23	P53	Homo sapiens	59-62
11125034-11	2001	These results demonstrate for the first time that hyperactive nuclear export of p53 attenuates chemotherapy-induced apoptosis in NB cells, and our findings suggest that inhibitors of MDM2 may enhance the therapeutic efficacy of etoposide by promoting apoptosis rather than trans-differentiation.	Etoposide	228-237	P53	Homo sapiens	80-83
11093826-4	2000	TSA enhanced the protein expression of p21(WAF1), CREB-binding protein, cyclinE, cyclin A, Bak and Bax, while it reduced the expression of E2F-1, E2F-4, HDAC1, p53 and hyperphosphorylated form of Rb.	trichostatin A	0-3	P53	Homo sapiens	160-163
11329882-5	2000	These findings suggest that butyrolactone I prevents apoptosis by the direct inhibition of CDK and also, possibly, by CDK-inhibition through p53-independent p21-induction.	4-Butyrolactone	28-41	P53	Homo sapiens	141-144
11102893-8	2000	SDNA was greater in p53-positive and bcl-2-negative cases; SDNP was greater in p53-positive cases; SHF was lower in p53- and c-myc-positive cases.	sdnp	59-63	P53	Homo sapiens	79-82
11102893-8	2000	SDNA was greater in p53-positive and bcl-2-negative cases; SDNP was greater in p53-positive cases; SHF was lower in p53- and c-myc-positive cases.	sdnp	59-63	P53	Homo sapiens	79-82
11071927-5	2000	In DLD-1 colorectal adenocarcinoma cells (DLD-1-tet-off-p53) cyclin B1 and B2 mRNA levels drop after expression of wild-type p53 but not after induction of a DNA binding-deficient mutant of p53.	tetramethylenedisulfotetramine	48-51	P53	Homo sapiens	56-59
10884389-2	2000	In this study, we show that BRCA1 is initially up-regulated, followed by a reduction to below basal levels in response to treatment with the DNA-damaging agents adriamycin and mitomycin C, and that the reduction of BRCA1 expression is dependent on the presence of wild-type p53.	Mitomycin	176-187	P53	Homo sapiens	274-277
10996201-8	2000	Our findings suggest that down regulation of topo IIalpha in association with p53 deficiency can confer chromosomal instability in etoposide-resistant K562 cells.	Etoposide	131-140	P53	Homo sapiens	78-81
11070152-4	2000	Immunohistochemistry of FGF1, FGF2, FGFR1 and p53 used avidin-biotin detection of the primary antibody.	avidin-biotin	55-68	P53	Homo sapiens	46-49
10951577-7	2000	The antioxidant N-acetylcysteine and the Cu/Zn superoxide dismutase inhibitor diethyldithiocarbamic acid abolished the hypoxia-induced increases in ROS and p53 levels.	Ditiocarb	78-104	P53	Homo sapiens	156-159
10930016-0	2000	Wild-type p53-dependent etoposide-induced apoptosis mediated by caspase-3 activation in human glioma cells.	Etoposide	24-33	P53	Homo sapiens	10-13
10908664-4	2000	Derangement of its transcriptional activity manifested as inhibition of p53-mediated apoptosis by etoposide, a representative antineoplastic agent.	Etoposide	98-107	P53	Homo sapiens	72-75
10856831-2	2000	AGG to AGT transversion in codon 249 of exon 7 of the p53 gene occurs in over 50% of HCC from endemic regions, where both chronic infection with the hepatitis B virus (HBV) and exposure to carcinogens such as aflatoxin B1 (AFB1) prevail.	Aflatoxin B1	209-221	P53	Homo sapiens	54-57
10866313-7	2000	Perturbation of mitochondrial function mediated accumulation of wild-type p53 protein, since Bcl-2 overexpression, bongkrekic acid, or inhibition of mitochondrial protein synthesis with chloramphenicol strongly reduced TK/GCV-induced accumulation of wild-type p53 protein.	Chloramphenicol	186-201	P53	Homo sapiens	74-77
10863098-0	2000	Mutations in the p53 tumor suppressor gene in tree shrew hepatocellular carcinoma associated with hepatitis B virus infection and intake of aflatoxin B1.	Aflatoxin B1	140-152	P53	Homo sapiens	17-20
10959623-4	2000	At inhibitory concentrations (higher than 1 mM) NaB reduced cyclin D1 and p53 level in a dose-dependent manner and sustained the synthesis of p21waf1/cip1, probably in a p53-independent way, accounting for the G0/G1 block observed by flow cytometry.	nab	48-51	P53	Homo sapiens	74-77
10959623-4	2000	At inhibitory concentrations (higher than 1 mM) NaB reduced cyclin D1 and p53 level in a dose-dependent manner and sustained the synthesis of p21waf1/cip1, probably in a p53-independent way, accounting for the G0/G1 block observed by flow cytometry.	nab	48-51	P53	Homo sapiens	170-173
10842327-7	2000	P53 induction occurred in HPV-16 E6 and HPV-16 E6/E7 expressing cells after exposure to cisplatin or MMC, though never to levels found in normal untreated HKCs.	Mitomycin	101-104	P53	Homo sapiens	0-3
10757806-5	2000	Although normal cells and wild-type p53-expressing tumor cells showed similar responses to actinomycin D and camptothecin treatment, the transcriptional activity of stabilized p53 induced by deferoxamine mesylate, which mimics hypoxia, in normal cells was lost in all three tumor cell lines tested.	Camptothecin	109-121	P53	Homo sapiens	36-39
10738214-1	2000	BACKGROUND: Specific mutations of the p53 tumor suppressor gene in hepatocellular carcinoma (HCC) have been reported from several parts of the world, but to the authors" knowledge to date the status of this gene has not been studied in HCC patients in India, where HCC is one of the major cancers and the frequency of chronic hepatitis B virus (HBV) as well as hepatitis C virus (HCV) infection and exposure to dietary aflatoxin B(1) is very high.	Aflatoxin B1	419-430	P53	Homo sapiens	38-41
10699888-1	2000	BACKGROUND: This study examined the effect of tegafur, a depot of 5-fluorouracil, in human colorectal carcinomas in terms of apoptosis, cell proliferation, and expression of p53 gene and angiogenesis-related molecules.	Tegafur	46-53	P53	Homo sapiens	174-177
10741907-10	2000	Meanwhile, Ad-p53 gene transfer combined with taxol, cisplatin, doxorubicin or mitomycin C was shown to be even more effective in suppressing growth in the two cell lines.	Mitomycin	79-90	P53	Homo sapiens	14-17
10820956-1	2000	BACKGROUND AND PURPOSE: In our previous study, positive p53 staining was observed in 47 of 81 (58%) cases of oral squamous cell carcinoma associated with areca quid (AQ) chewing and cigarette smoking.	aq	166-168	P53	Homo sapiens	56-59
10820956-2	2000	This study looked for expression of p53 protein in premalignant oral lesions in patients who chewed AQ or smoked cigarettes, or both.	aq	100-102	P53	Homo sapiens	36-39
10820956-9	2000	CONCLUSIONS: These results demonstrate that p53 is often present in precancerous lesions of patients who chew AQ and smoke cigarettes.	aq	110-112	P53	Homo sapiens	44-47
10940651-2	2000	Although all the cell lines have a wild-type (wt) p53 gene, the protein is in a mutant conformation detectable by the anti-p53 antibody PAb 240.	4-Aminobenzoic Acid	136-139	P53	Homo sapiens	123-126
10940651-6	2000	The conformation of p53 remained unchanged, being detectable in flow cytometry by PAb 240, but not by PAb 1620 (an antibody which only detects p53 in wt conformation).	4-Aminobenzoic Acid	82-85	P53	Homo sapiens	20-23
10663644-5	2000	RESULTS: UCN-01, a specific inhibitor of protein kinase C (PKC) presently in clinical trials, abrogated CPT-induced activation of S and G(2) checkpoints in human MDA-MB-231 and GI 101A breast carcinoma cells, both of which are mutants for the p53 gene.	Camptothecin	104-107	P53	Homo sapiens	243-246
26368609-5	2000	Recent molecular studies of p53 tumor suppressor gene mutations and p53 protein expression in the lungs of patients with lung cancer and occupational exposure to crystalline silica and other dusts have been conducted.	Silicon Dioxide	174-180	P53	Homo sapiens	28-31
26368609-5	2000	Recent molecular studies of p53 tumor suppressor gene mutations and p53 protein expression in the lungs of patients with lung cancer and occupational exposure to crystalline silica and other dusts have been conducted.	Silicon Dioxide	174-180	P53	Homo sapiens	68-71
22607421-6	2000	Nickel and cobalt ions inhibited binding of p53 to scDNA and to p53CON in linear DNA fragments less efficiently than zinc.	Cobalt	11-17	P53	Homo sapiens	44-47
22607421-6	2000	Nickel and cobalt ions inhibited binding of p53 to scDNA and to p53CON in linear DNA fragments less efficiently than zinc.	Cobalt	11-17	P53	Homo sapiens	64-67
11173660-4	2000	Protein p53 accumulation was detected by the streptavidin-biotin method using DO-7 (Dako) antibody.	do-7	78-82	P53	Homo sapiens	8-11
10606504-2	1999	As a method for approaching the mechanism of tumor promoter function, the ability of oxidative DNA damage by BzPO was investigated by using (32)P-labeled DNA fragments obtained from the human p53 tumor suppressor gene and c-Ha-ras-1 protooncogene.	Benzoyl Peroxide	109-113	P53	Homo sapiens	192-195
10585266-5	1999	p53(V143A) inhibited the camptothecin-induced accumulation of p21(WAF1/CIP1) in cell lines with p53 functional wild-type activity, but not in cell lines lacking p53 activity, consistent with a transdominant-negative effect of p53(V143A).	Camptothecin	25-37	P53	Homo sapiens	0-3
10585266-5	1999	p53(V143A) inhibited the camptothecin-induced accumulation of p21(WAF1/CIP1) in cell lines with p53 functional wild-type activity, but not in cell lines lacking p53 activity, consistent with a transdominant-negative effect of p53(V143A).	Camptothecin	25-37	P53	Homo sapiens	96-99
10585266-5	1999	p53(V143A) inhibited the camptothecin-induced accumulation of p21(WAF1/CIP1) in cell lines with p53 functional wild-type activity, but not in cell lines lacking p53 activity, consistent with a transdominant-negative effect of p53(V143A).	Camptothecin	25-37	P53	Homo sapiens	96-99
10585266-5	1999	p53(V143A) inhibited the camptothecin-induced accumulation of p21(WAF1/CIP1) in cell lines with p53 functional wild-type activity, but not in cell lines lacking p53 activity, consistent with a transdominant-negative effect of p53(V143A).	Camptothecin	25-37	P53	Homo sapiens	96-99
10544021-3	1999	In the present study, we showed that the topoisomerase II inhibitor of widely used anticancer drugs etoposide and doxorubicin activated wt p53 in BL2, a Burkitt"s lymphoma cell line which overexpressed MDM2.	Etoposide	100-109	P53	Homo sapiens	139-142
10544021-8	1999	This p53 was co-immunoprecipitated with MDM2, but p53 activated by etoposide or doxorubicin barely complexed with MDM2.	Etoposide	67-76	P53	Homo sapiens	5-8
10544021-8	1999	This p53 was co-immunoprecipitated with MDM2, but p53 activated by etoposide or doxorubicin barely complexed with MDM2.	Etoposide	67-76	P53	Homo sapiens	50-53
10518116-8	1999	The expression of the proteins of the protooncogene Bcl-2 and the tumor suppressor gene p53 following staurosporine or retinoic acid treatment was assessed by Western blot and immunocytochemistry.	Staurosporine	102-115	P53	Homo sapiens	88-91
10529369-1	1999	Overexpression of the tumor suppressor p53 in HeLa cells leads to loss of the estradiol- and genistein-induced human estrogen receptor (ERalpha) transactivity.	Genistein	93-102	P53	Homo sapiens	39-42
10486243-4	1999	An in vitro study was carried out to determine whether p53 could be mutated at position 277 so that it binds preferentially to a sequence containing thymine or cytidine.	Cytidine	160-168	P53	Homo sapiens	55-58
11776565-4	1999	RESULTS: Genistein could inhibit proliferation of human breast carcinoma cells with different ER status and p53 status.	Genistein	9-18	P53	Homo sapiens	108-111
11776565-8	1999	CONCLUSION: The inhibitory effect of genistein on cell proliferation of breast cancer appears to be due to p21WAF1/CIP1 expression and apoptosis through mechanism independent of ER and p53.	Genistein	37-46	P53	Homo sapiens	185-188
10458704-0	1999	Site-specific synthesis of aflatoxin B(1) adducts within an oligodeoxyribonucleotide containing the human p53 codon 249 sequence.	Aflatoxin B1	27-38	P53	Homo sapiens	106-109
10458704-0	1999	Site-specific synthesis of aflatoxin B(1) adducts within an oligodeoxyribonucleotide containing the human p53 codon 249 sequence.	Oligodeoxyribonucleotides	60-84	P53	Homo sapiens	106-109
10402229-3	1999	A lower level of p53 was induced in CDK inhibitor-expressing etoposide-exposed cells suggesting that protection may be due to lower levels of DNA damage in the growth arrested cells.	Etoposide	61-70	P53	Homo sapiens	17-20
10389750-2	1999	The relation between aflatoxin B1 (AFB1 )-related hepatocellular carcinomas (HCCs) and hot spot at codon 249 of the p53 gene has received a great deal of attention, but its significance is still controversial.	Aflatoxin B1	21-33	P53	Homo sapiens	116-119
10389750-2	1999	The relation between aflatoxin B1 (AFB1 )-related hepatocellular carcinomas (HCCs) and hot spot at codon 249 of the p53 gene has received a great deal of attention, but its significance is still controversial.	Aflatoxin B1	35-39	P53	Homo sapiens	116-119
10421546-6	1999	The functional status of p53 in cells was assessed by thymidine and BrdU incorporation following exposure to ionizing radiation (4 Gy).	Thymidine	54-63	P53	Homo sapiens	25-28
10391688-0	1999	p53-Dependent growth arrest and altered p53-immunoreactivity following metabolic labelling with 32P ortho-phosphate in human fibroblasts.	32p ortho-phosphate	96-115	P53	Homo sapiens	0-3
10391688-0	1999	p53-Dependent growth arrest and altered p53-immunoreactivity following metabolic labelling with 32P ortho-phosphate in human fibroblasts.	32p ortho-phosphate	96-115	P53	Homo sapiens	40-43
10357771-0	1999	Inverse correlation between p53 protein levels and DNA repair efficiency in human fibroblast strains treated with 4-nitroquinoline 1-oxide: evidence that lesions other than DNA strand breaks trigger the p53 response.	4-Nitroquinoline-1-oxide	114-138	P53	Homo sapiens	28-31
10357771-0	1999	Inverse correlation between p53 protein levels and DNA repair efficiency in human fibroblast strains treated with 4-nitroquinoline 1-oxide: evidence that lesions other than DNA strand breaks trigger the p53 response.	4-Nitroquinoline-1-oxide	114-138	P53	Homo sapiens	203-206
10357771-3	1999	The aim of this study was to identify the triggering signal for induction of p53 in diploid human dermal fibroblasts treated with 4-nitroquinoline 1-oxide (4NQO), a model environmental carcinogen that produces both DNA strand breaks (like ionizing radiation) and alkali-stable bulky DNA lesions (like UV light).	4-Nitroquinoline-1-oxide	130-154	P53	Homo sapiens	77-80
10357771-4	1999	4NQO treatment of fibroblasts cultured from normal and AT donors and those from patients with the UV-hypersensitivity disorder xeroderma pigmentosum (XP, complementation groups A, E and G) resulted in up-regulation of p53 protein.	4-Nitroquinoline-1-oxide	0-4	P53	Homo sapiens	218-221
10357771-7	1999	XP cells with a severe deficiency in the nucleotide excision repair pathway showed abnormally high levels of p53 protein in response to 4NQO treatment, indicating that lesions other than incision-associated DNA strand breaks trigger p53 up-regulation.	4-Nitroquinoline-1-oxide	136-140	P53	Homo sapiens	109-112
10357771-7	1999	XP cells with a severe deficiency in the nucleotide excision repair pathway showed abnormally high levels of p53 protein in response to 4NQO treatment, indicating that lesions other than incision-associated DNA strand breaks trigger p53 up-regulation.	4-Nitroquinoline-1-oxide	136-140	P53	Homo sapiens	233-236
10357771-9	1999	Treatment with 0.12 microM 4NQO, for example, caused a &gt;2-fold up-regulation of p53 in excision repair-deficient (AT, XPA and XPG) strains without eliciting any effect on p53 levels in repair-proficient (normal and XPE) strains.	4-Nitroquinoline-1-oxide	27-31	P53	Homo sapiens	83-86
10357771-9	1999	Treatment with 0.12 microM 4NQO, for example, caused a &gt;2-fold up-regulation of p53 in excision repair-deficient (AT, XPA and XPG) strains without eliciting any effect on p53 levels in repair-proficient (normal and XPE) strains.	4-Nitroquinoline-1-oxide	27-31	P53	Homo sapiens	174-177
10341297-6	1999	Western blot analysis showed that auristatin-PE up-regulated the expression of wt-p53, p21WAF1 and Bax, and down-regulated Bcl-2 and cyclin B in HPAC cells, while only up-regulation of p21WAF1 and Bax was observed in PANC-1 cells.	pe	45-47	P53	Homo sapiens	82-85
10394883-2	1999	The incidence of p53 gene abnormalities in human hepatocellular carcinoma (HCC) varies in different geographical areas, being higher in regions where hepatitis virus infection and dietary exposure to aflatoxin B1 are the most common aetiological agents.	Aflatoxin B1	200-212	P53	Homo sapiens	17-20
10334204-0	1999	The level of DNA modification by (+)-syn-(11S,12R,13S,14R)- and (-)-anti-(11R,12S,13S,14R)-dihydrodiol epoxides of dibenzo[a,l]pyrene determined the effect on the proteins p53 and p21WAF1 in the human mammary carcinoma cell line MCF-7.	(-)-anti-(11r,12s,13s,14r)-dihydrodiol epoxides	64-111	P53	Homo sapiens	172-175
10223459-6	1999	Western immunoblot analysis revealed a marked increase in cellular glial fibrillary acidic protein and wild-type p53 and a decrease in c-myc and c-fos oncoproteins in both cell lines treated with clotrimazole.	Clotrimazole	196-208	P53	Homo sapiens	113-116
10206959-18	1999	The down-regulation of hMMP-1 gene expression by endogenous wt-p53 was shown by treatment of U2-OS cells, a wt-p53-containing osteogenic sarcoma line, and Saos-2 cells, a p53-negative osteogenic sarcoma line, with etoposide, a potent inducer of p53 expression.	Etoposide	214-223	P53	Homo sapiens	63-66
10206959-19	1999	p53, activated by etoposide, appears to block hMMP-1 promoter activity induced by etoposide in U2-OS cells.	Etoposide	18-27	P53	Homo sapiens	0-3
10206959-19	1999	p53, activated by etoposide, appears to block hMMP-1 promoter activity induced by etoposide in U2-OS cells.	Etoposide	82-91	P53	Homo sapiens	0-3
10207030-8	1999	Etoposide-induced transactivation was blocked by a dominant negative p53 mutant, indicating that endogenous wild type p53, upon activation by etoposide, transactivated the GPX promoter.	Etoposide	0-9	P53	Homo sapiens	118-121
10207030-8	1999	Etoposide-induced transactivation was blocked by a dominant negative p53 mutant, indicating that endogenous wild type p53, upon activation by etoposide, transactivated the GPX promoter.	Etoposide	142-151	P53	Homo sapiens	69-72
10207030-8	1999	Etoposide-induced transactivation was blocked by a dominant negative p53 mutant, indicating that endogenous wild type p53, upon activation by etoposide, transactivated the GPX promoter.	Etoposide	142-151	P53	Homo sapiens	118-121
10197633-5	1999	Thus, early mitochondria-associated events may play a key role in initiating and/or coordinating tributyrin-mediated growth arrest and apoptosis of wild-type p53 MCF-7 cells.	tributyrin	97-107	P53	Homo sapiens	158-161
10374839-3	1999	In vitro experiments using human cell line cells and aflatoxin B1 have demonstrated the induction of p53 mutations in codon 249 and adjacent codons.	Aflatoxin B1	53-65	P53	Homo sapiens	101-104
10374839-6	1999	In an in vivo rodent model systems using the aflatoxin B1-sensitive male F344 rat, previous studies have shown that hepatocarcinogenesis is accompanied by significant incidences of codon 12 mutations in K-ras and codon 13 mutations in N-ras genes, but in contrast to the human, apparently not by mutations in codon 243 of the p53 gene (which corresponds to codon 249 in the human gene).	Aflatoxin B1	45-57	P53	Homo sapiens	326-329
10037186-4	1999	Suppression of c-myc using antisense oligodeoxynucleotides (in the absence of p53) was sufficient to trigger apoptosis in Tu-138 cells, raising the possibility that the reduction of c-myc may be involved in at least one of the cell death pathways mediated by p53.	Oligodeoxyribonucleotides	37-58	P53	Homo sapiens	259-262
9880547-8	1999	These findings suggest a role for mitogen-activated protein kinase in the degradation of the DNA binding-impaired form of p53 protein and in the bryostatin-induced differentiation observed in this cell line.	Bryostatins	145-155	P53	Homo sapiens	122-125
9927204-5	1999	Clonogenic survival assays revealed that cells overexpressing the p53His175 mutant, but not the p53His273 mutant, recover preferentially from etoposide treatment.	Etoposide	142-151	P53	Homo sapiens	66-69
9927204-6	1999	Moreover, p53His175 as well as p53His179 reduced substantially the rate of etoposide-induced apoptosis, whereas p53His273 and p53Trp248 had a much milder protective effect.	Etoposide	75-84	P53	Homo sapiens	10-13
10667218-6	1999	This finding indicates that TSA activates the p21/WAF1/Cip1 promoter through the Sp1 sites in a p53-independent manner.	trichostatin A	28-31	P53	Homo sapiens	96-99
10368806-9	1999	Furthermore, cells treated with genistein showed an increased expression of endogenous wild-type p53, while the level of the mutant p53 protein remained unchanged.	Genistein	32-41	P53	Homo sapiens	97-100
10368806-10	1999	From these results, we conclude that genistein induces apoptosis in NSCLC cells through a p53-independent pathway and, thus, may act as an anticancer agent.	Genistein	37-46	P53	Homo sapiens	90-93
9769393-6	1998	On the other hand, an A to G substitution at codon 170 in exon 5 of p53 gene resulting in glutamic acid (ACG) to glycine (GCG) was detected in the DNA of her tongue cancer.	acceleratory factor from growth hormone	105-108	P53	Homo sapiens	68-71
9788435-3	1998	The effect of induced p53 and p21waf1 expression on the cytotoxic action of the anti-cancer drugs etoposide and cisplatin was also analysed.	Etoposide	98-107	P53	Homo sapiens	22-25
9770348-11	1998	An inhibitor of transcription, alpha-amanitin, dramatically induced wt p53 protein, whereas Mdm-2 protein was downregulated.	Alpha-Amanitin	31-45	P53	Homo sapiens	71-74
9766444-6	1998	The differentiation response to transfected p53 with or without INF-gamma was inhibited by cyclic adenosine monophosphate (cAMP)-inducing agents (dibutyryl cyclic adenosine 3":5"-monophosphate, forskolin, and 3-isobutyl-1-methylxanthine) in a dose-dependent manner.	1-Methyl-3-isobutylxanthine	209-236	P53	Homo sapiens	44-47
9690517-5	1998	Here we report that the induction of p21 by DZQ is regulated at the transcriptional level, and requires the activation of p53, a tumor suppressor protein.	ethylenimine quinone	44-47	P53	Homo sapiens	122-125
9690517-6	1998	In cells that lack functional p53 protein, DZQ-mediated p21 induction is greatly diminished.	ethylenimine quinone	43-46	P53	Homo sapiens	30-33
9690517-7	1998	However, the introduction of a wild type p53 gene into p53-negative cells restores the strong DZQ-inducibility of p21.	ethylenimine quinone	94-97	P53	Homo sapiens	41-44
9690517-7	1998	However, the introduction of a wild type p53 gene into p53-negative cells restores the strong DZQ-inducibility of p21.	ethylenimine quinone	94-97	P53	Homo sapiens	55-58
9674709-0	1998	Superinduction of wild-type p53 protein after 2-methoxyestradiol treatment of Ad5p53-transduced cells induces tumor cell apoptosis.	2-Methoxyestradiol	46-64	P53	Homo sapiens	28-31
9674709-1	1998	Because 2-methoxyestradiol (2-MeOE2) induces and stabilizes wild-type p53 protein (wt p53) in human lung cancer cell lines posttranscriptionally, we sought to study its effects on Ad5p53-transduced lung cancer cell lines at a low multiplicity of infection (1 MOI).	2-Methoxyestradiol	8-26	P53	Homo sapiens	70-73
9674709-1	1998	Because 2-methoxyestradiol (2-MeOE2) induces and stabilizes wild-type p53 protein (wt p53) in human lung cancer cell lines posttranscriptionally, we sought to study its effects on Ad5p53-transduced lung cancer cell lines at a low multiplicity of infection (1 MOI).	2-Methoxyestradiol	8-26	P53	Homo sapiens	86-89
9674709-1	1998	Because 2-methoxyestradiol (2-MeOE2) induces and stabilizes wild-type p53 protein (wt p53) in human lung cancer cell lines posttranscriptionally, we sought to study its effects on Ad5p53-transduced lung cancer cell lines at a low multiplicity of infection (1 MOI).	2-Methoxyestradiol	28-35	P53	Homo sapiens	70-73
9674709-1	1998	Because 2-methoxyestradiol (2-MeOE2) induces and stabilizes wild-type p53 protein (wt p53) in human lung cancer cell lines posttranscriptionally, we sought to study its effects on Ad5p53-transduced lung cancer cell lines at a low multiplicity of infection (1 MOI).	2-Methoxyestradiol	28-35	P53	Homo sapiens	86-89
9674709-2	1998	Treating these cells with 2-MeOE2 resulted in superinduction of wt p53 protein expression followed by apoptosis, as shown by terminal deoxynucleotidyl transferase (TdT) staining, and upregulation of wt p53 expression, as shown by Western blot analysis.	2-Methoxyestradiol	26-33	P53	Homo sapiens	67-70
9674709-2	1998	Treating these cells with 2-MeOE2 resulted in superinduction of wt p53 protein expression followed by apoptosis, as shown by terminal deoxynucleotidyl transferase (TdT) staining, and upregulation of wt p53 expression, as shown by Western blot analysis.	2-Methoxyestradiol	26-33	P53	Homo sapiens	202-205
9665463-3	1998	Phorbol ester induced p21WAF1 expression, which was maximal at 4 to 8 h with reduction back to baseline by 24 to 48 h. In contrast, increasing the extracellular Ca2+ concentration from 70 micromol/L to 1.5 mmol/L resulted in upregulation of p21WAF1 expression with a slower time course, with peak induction at 18 to 24 h. No parallel increase in p53 expression was observed in normal human keratinocytes.	Phorbol Esters	0-13	P53	Homo sapiens	346-349
9665463-4	1998	Up-regulation of p21WAF1 was also observed in response to phorbol ester in HaCaT cells, which carry homozygous and inactivating mutations for p53.	Phorbol Esters	58-71	P53	Homo sapiens	142-145
9665463-6	1998	The results demonstrate a differential time course of p21WAF1 protein up-regulation in response to phorbol ester and Ca2+, signals that result in keratinocyte differentiation, and suggest that induction of p21WAF1 in differentiating human keratinocytes occurs through protein kinase C-dependent and p53-independent mechanisms.	Phorbol Esters	99-112	P53	Homo sapiens	299-302
9650599-3	1998	The presence of the p53-expressing vector was toxic in both cell lines compared to control cells or to those containing the beta-gal vector.	beta-D-galactose	124-132	P53	Homo sapiens	20-23
10076525-0	1998	Effects of perturbations of pools of deoxyribonucleoside triphosphates on expression of ribonucleotide reductase, a G1/S transition state enzyme, in p53-mutated cells.	deoxyribonucleoside triphosphates	37-70	P53	Homo sapiens	149-152
10076525-9	1998	This suggests that in the presence of antimetabolite-induced depletion of dNTPs, SW480 cells, which lack a normal p53 gene, will proceed into S phase, and that this is associated with a rise in expression of the G1/S transition state enzyme, RR.	dntps	74-79	P53	Homo sapiens	114-117
9607592-3	1998	The sensitization ratio due to the transfected wt p53 varied from about 2-fold for cisplatin to over 50-fold for thymidine.	Thymidine	113-122	P53	Homo sapiens	50-53
9548807-10	1998	Thiotepa, a non-quinone aziridine-containing agent, and 1,4-benzoquinone (p-BQ), a redox cycling quinone, increased p53 levels.	1,3,4,6,7,11b-hexahydro-9,10-dimethoxy-2H-benzo(a)quinolizine-2-spiro-3'-(1'-phenyl)succinimide	74-78	P53	Homo sapiens	116-119
9513045-6	1998	The similar effects of genistein on a number of breast carcinoma cell lines with different ER and p53 status suggest that the actions of genistein reported here are mediated through ER and p53 independent mechanisms.	Genistein	137-146	P53	Homo sapiens	98-101
9513045-6	1998	The similar effects of genistein on a number of breast carcinoma cell lines with different ER and p53 status suggest that the actions of genistein reported here are mediated through ER and p53 independent mechanisms.	Genistein	137-146	P53	Homo sapiens	189-192
9648155-1	1998	Abnormalities of the p53 tumor suppressor gene were investigated in 22 foci from 14 adenoid cystic carcinomas (ACC) by polymerase chain reaction (PCR)-based assays for dinucleotide (CA)n and pentanucleotide (AAAAT)n repeat polymorphisms and by immunohistochemical staining for oncoprotein expression.	Dinucleoside Phosphates	168-180	P53	Homo sapiens	21-24
9648155-1	1998	Abnormalities of the p53 tumor suppressor gene were investigated in 22 foci from 14 adenoid cystic carcinomas (ACC) by polymerase chain reaction (PCR)-based assays for dinucleotide (CA)n and pentanucleotide (AAAAT)n repeat polymorphisms and by immunohistochemical staining for oncoprotein expression.	pentanucleotide	191-206	P53	Homo sapiens	21-24
9546425-1	1998	Using UvrABC incision in combination with ligation-mediated PCR (LMPCR) we have previously shown that benzo(a)pyrene diol epoxide (BPDE) adduct formation along the nontranscribed strand of the human p53 gene is highly selective; the preferential binding sites coincide with the major mutation hotspots found in human lung cancers.	lmpcr	65-70	P53	Homo sapiens	199-202
9719502-4	1998	In addition, p53 protein overexpression was assessed by immunohistochemistry using the monoclonal antibody DO-7 on paraffin-embedded tissue sections.	do-7	107-111	P53	Homo sapiens	13-16
9398050-6	1997	LN-229 cells which have partial p53-wild-type activity show enhanced expression of p53, p21 and bax protein, whereas bcl-2 levels decrease, after exposure to camptothecin.	Camptothecin	158-170	P53	Homo sapiens	32-35
9494534-8	1997	Levels of p53 mRNA decreased with increasing resistance to vindesine, etoposide and fotemustine.	Etoposide	70-79	P53	Homo sapiens	10-13
9264376-0	1997	Camptothecin-induced apoptosis in p53-null human leukemia HL60 cells and their isolated nuclei: effects of the protease inhibitors Z-VAD-fmk and dichloroisocoumarin suggest an involvement of both caspases and serine proteases.	Camptothecin	0-12	P53	Homo sapiens	34-37
9257692-7	1997	In this study I show that compounds that allow the accumulation of DNA single strand breaks, ara c and hydroxyurea, enhanced the UVC radiation (254 nm)-dependent increase in p53, but had no effect on the solar UV radiation-dependent increase.	Hydroxyurea	103-114	P53	Homo sapiens	174-177
9199206-4	1997	A region of the p53 promoter (from -199 to +142) containing 15 CpG dinucleotides was placed in a pCAT reporter plasmid and reporter activity was assessed in host CV-1 cells.	Dinucleoside Phosphates	67-80	P53	Homo sapiens	16-19
9203947-6	1997	Intranuclear p53 protein was immunostained by the avidin-biotin complex method.	avidin-biotin	50-63	P53	Homo sapiens	13-16
9168435-7	1997	DTctGMCSF also efficiently killed AML cells deficient in p53 expression, as well as radiation-resistant AML cells and mixed lineage leukemia cells expressing high levels of bcl-2.	dtctgmcsf	0-9	P53	Homo sapiens	57-60
21590066-4	1997	Although allelic imbalance in the p53 and DCC genes were observed in ten out of eleven primary tumors and all liver metastases using a dinucleotide repeat polymorphism, mutation was not detected in the DNA polymerase beta mRNA.	Dinucleoside Phosphates	135-147	P53	Homo sapiens	34-37
9332498-5	1997	These experiments demonstrated a decreased PAb 240 (mutant-specific) reactivity of nuclear p53(273.His) in EGF-treated cells, while that of PAb 1620 (wild-type specific) was enhanced.	4-Aminobenzoic Acid	43-46	P53	Homo sapiens	91-94
21533392-8	1997	Moreover, in the presence of okadaic acid, a potent inhibitor of protein phosphatase PP2a, phosphorylation of p53 is detectable early in G(1)-phase of the cell cycle.	Okadaic Acid	29-41	P53	Homo sapiens	110-113
9018125-1	1997	2-Methoxyestradiol (2-MeOE2) treatment caused significant growth inhibition of H460 and A549 human lung cancer cell lines which contain wild-type p53.	2-Methoxyestradiol	0-18	P53	Homo sapiens	146-149
9018125-1	1997	2-Methoxyestradiol (2-MeOE2) treatment caused significant growth inhibition of H460 and A549 human lung cancer cell lines which contain wild-type p53.	2-Methoxyestradiol	20-27	P53	Homo sapiens	146-149
9018125-3	1997	Western blot analysis indicated that 2-MeOE2 treatment resulted in an eightfold increase in the endogenous wild-type p53 protein, while the level of the mutant p53 protein remained unchanged.	2-Methoxyestradiol	37-44	P53	Homo sapiens	117-120
9018125-4	1997	TdT staining indicated that following 2-MeOE2-mediated increases in wildtype p53 protein, cells bypass the G1-S checkpoint of the cell cycle with 30 to 40% undergoing apoptosis.	2-Methoxyestradiol	38-45	P53	Homo sapiens	77-80
9018125-5	1997	Introduction of anti-sense wt-p53 into wt-p53 cells abrogated the 2-MeOE2 effect.	2-Methoxyestradiol	66-73	P53	Homo sapiens	30-33
9018125-5	1997	Introduction of anti-sense wt-p53 into wt-p53 cells abrogated the 2-MeOE2 effect.	2-Methoxyestradiol	66-73	P53	Homo sapiens	42-45
9018125-6	1997	A significant portion of lung cancer retains the wild-type p53 gene therefore, 2-MeOE2 may have therapeutic application.	2-Methoxyestradiol	79-86	P53	Homo sapiens	59-62
9184169-5	1997	Further support for this observation came from the stable transfection studies in which p53 transfectants expressing high levels of wild-type p53 became resistant to genistein.	Genistein	166-175	P53	Homo sapiens	88-91
9184169-5	1997	Further support for this observation came from the stable transfection studies in which p53 transfectants expressing high levels of wild-type p53 became resistant to genistein.	Genistein	166-175	P53	Homo sapiens	142-145
9329647-0	1997	Mutations, tissue accumulations, and serum levels of p53 in patients with occupational cancers from asbestos and silica exposure.	Silicon Dioxide	113-119	P53	Homo sapiens	53-56
9816160-8	1996	Conversely, the hazard increased with the increase of p53-positive cells only for tumors with a [3H]dT LI lower than 7.5%.	Thymidine	100-102	P53	Homo sapiens	54-57
8912651-8	1996	Western blot showed that wild-type p53 protein was unchanged after MCF-7 cells had been exposed to 50 microM 3,3"-diindolylmethane for 8 h. This study provides evidences that 3,3"-diindolylmethane induces apoptosis in human cancer cells and that the induction of apoptosis is independent of p53 pathway.	3,3'-diindolylmethane	109-130	P53	Homo sapiens	35-38
8912651-8	1996	Western blot showed that wild-type p53 protein was unchanged after MCF-7 cells had been exposed to 50 microM 3,3"-diindolylmethane for 8 h. This study provides evidences that 3,3"-diindolylmethane induces apoptosis in human cancer cells and that the induction of apoptosis is independent of p53 pathway.	3,3'-diindolylmethane	109-130	P53	Homo sapiens	291-294
8912651-8	1996	Western blot showed that wild-type p53 protein was unchanged after MCF-7 cells had been exposed to 50 microM 3,3"-diindolylmethane for 8 h. This study provides evidences that 3,3"-diindolylmethane induces apoptosis in human cancer cells and that the induction of apoptosis is independent of p53 pathway.	3,3'-diindolylmethane	175-196	P53	Homo sapiens	35-38
8912651-8	1996	Western blot showed that wild-type p53 protein was unchanged after MCF-7 cells had been exposed to 50 microM 3,3"-diindolylmethane for 8 h. This study provides evidences that 3,3"-diindolylmethane induces apoptosis in human cancer cells and that the induction of apoptosis is independent of p53 pathway.	3,3'-diindolylmethane	175-196	P53	Homo sapiens	291-294
8912537-5	1996	Immunohistochemical expression of p53 was investigated using a monoclonal anti-p53 antibody (DO-7).	do-7	93-97	P53	Homo sapiens	34-37
8912537-5	1996	Immunohistochemical expression of p53 was investigated using a monoclonal anti-p53 antibody (DO-7).	do-7	93-97	P53	Homo sapiens	79-82
8950479-5	1996	In vitro studies with a bladder carcinoma cell line containing a wild type p53 showed that it underwent a G1 checkpoint after etoposide, potentially allowing DNA damage repair, as well as apoptosis.	Etoposide	126-135	P53	Homo sapiens	75-78
8704210-8	1996	To analyze the possible interaction of FAC with the p53 pathway, we analyzed p53 induction in mock and corrected cell lines following exposure to MMC.	Mitomycin	146-149	P53	Homo sapiens	77-80
8806433-0	1996	DNA fragmentation induced by protease activation in p53-null human leukemia HL60 cells undergoing apoptosis following treatment with the topoisomerase I inhibitor camptothecin: cell-free system studies.	Camptothecin	163-175	P53	Homo sapiens	52-55
8806433-2	1996	HL60 cells are p53 null and extremely sensitive to a variety of apoptotic stimuli including DNA damage induced by the topoisomerase I inhibitor, camptothecin.	Camptothecin	145-157	P53	Homo sapiens	15-18
8707413-8	1996	Ad-p53-infected SKBr3 breast cancer cells were more sensitive to cytotoxicity of the DNA damaging drugs mitomycin C or Adriamycin, but not the M-phase specific drug vincristine.	Mitomycin	104-115	P53	Homo sapiens	3-6
8707413-9	1996	Our results suggest that Ad-p53 is capable of infecting and killing cancer cells of diverse tissue origins (including multi-drug resistant cancer cells), that p21WAFI/CIPI may be a useful marker of p53 infectivity and that there may be synergy between Ad-p53 and either mitomycin C or Adriamycin induced cell death in tumors with p53 mutations.	Mitomycin	270-281	P53	Homo sapiens	28-31
8651706-8	1996	Phosphatase digestion of immunoprecipitated p53 effectively removed phosphorous groups from the recombinant protein, reducing the number of isoforms from 11 to 2, demonstrating that phosphorylation is the major posttranslational event in the recombinant protein.	Phosphinidene	68-79	P53	Homo sapiens	44-47
8639538-1	1996	The tumor suppressor protein p53 plays a central role in the cellular response to genotoxic lesions and has been shown to be activated by most anticancer agents such as mitomycin C.	Mitomycin	169-180	P53	Homo sapiens	29-32
8639538-5	1996	In vitro experiments with purified recombinant proteins show that p53 increases the catalytic activities of topoisomerase I as measured by relaxation of supercoiled DNA, stabilization of the covalent topoisomerase I-DNA complex (in the presence of camptothecin), and phosphorylation of SR protein splicing factor ASF/SF2.	Camptothecin	248-260	P53	Homo sapiens	66-69
8640905-2	1996	The most frequent mutation in HCC in populations exposed to a high dietary intake of aflatoxin B1 (AFB1) is an AGGarg--&gt;AGTser missense mutation in codon 249 of the p53 gene.	Aflatoxin B1	85-97	P53	Homo sapiens	168-171
8634092-9	1996	The frequency of BPD-induced lesions in the p53 gene was sixfold to sevenfold greater than in the beta-globin gene and 200- to 300-fold greater than in bulk DNA.	benzo(a)pyrene 7,8-dihydrodiol	17-20	P53	Homo sapiens	44-47
9387565-2	1996	p53 protein was identified in all 17 cases (100%) of OCL, and 78% in control cases.	ocl	53-56	P53	Homo sapiens	0-3
8620501-0	1996	Hypersensitivity of human testicular tumors to etoposide-induced apoptosis is associated with functional p53 and a high Bax:Bcl-2 ratio.	Etoposide	47-56	P53	Homo sapiens	105-108
8620501-8	1996	First, they have functional p53: the product of the p53-dependent gene waf-1 was increased after etoposide treatment.	Etoposide	97-106	P53	Homo sapiens	28-31
8620501-8	1996	First, they have functional p53: the product of the p53-dependent gene waf-1 was increased after etoposide treatment.	Etoposide	97-106	P53	Homo sapiens	52-55
8608941-3	1996	However, we found that certain ribonucleotide biosynthesis inhibitors caused a p53-dependent G0 or early G1 arrest in the absence of replicative DNA synthesis or detectable DNA damage in normal human fibroblasts.	Ribonucleotides	31-45	P53	Homo sapiens	79-82
8829621-3	1996	On the other hand, significant induction of p53 message was demonstrated when Hela cells were exposed to genistein, a protein tyrosine kinase inhibitor.	Genistein	105-114	P53	Homo sapiens	44-47
8599578-0	1996	Diethylstilbestrol-induced immortalization of human endometrial cells: alterations in p53 and estrogen receptor.	Diethylstilbestrol	0-18	P53	Homo sapiens	86-89
8779543-1	1996	Mutations of the p53 tumour-suppressor gene in human hepatocellular carcinomas from certain geographic areas appear to be associated with high dietary exposure to aflatoxin B1 (AFB1).	Aflatoxin B1	163-175	P53	Homo sapiens	17-20
8779543-1	1996	Mutations of the p53 tumour-suppressor gene in human hepatocellular carcinomas from certain geographic areas appear to be associated with high dietary exposure to aflatoxin B1 (AFB1).	Aflatoxin B1	177-181	P53	Homo sapiens	17-20
8938795-0	1996	Differential GADD45, p21CIP1/WAF1, MCL-1 and topoisomerase II gene induction and secondary DNA fragmentation after camptothecin-induced DNA damage in two mutant p53 human colon cancer cell lines.	Camptothecin	115-127	P53	Homo sapiens	161-164
8979269-6	1996	A253-p53 cells could be distinguished from native A253 cells by prolonged doubling times (2-5 fold) and by a marked reduction of [3H]-thymidine uptake.	Thymidine	134-143	P53	Homo sapiens	5-8
8562479-3	1995	Flow cytometry, growth, and cytochemical analysis for alpha-napthyl butyrate esterase activity and nitroblue tetrazolium reduction indicated that wild-type p53 but not mutant p53 induced early monocytic differentiation in the transfected HL60 cells without terminal growth arrest.	Tetrazolium Salts	109-120	P53	Homo sapiens	156-159
8562479-5	1995	HL60 cells transfected with wild-type p53 were more sensitive to stress, such as growth in serum-depleted medium and exposure to a chemotherapeutic agent, etoposide.	Etoposide	155-164	P53	Homo sapiens	38-41
7563393-0	1995	Prognostic value of p53 nuclear overexpression in patients with invasive bladder cancer treated with neoadjuvant MVAC.	M-VAC protocol	113-117	P53	Homo sapiens	20-23
7623839-2	1995	We show that exposure of cells to various genotoxic agents, including anticancer drugs such as mitomycin and 5-fluorouracil, results in an increase in p53 mRNA levels and in p53 promoter activation, indicating that the p53 genotoxic stress response is partly regulated at the transcriptional level.	Mitomycin	95-104	P53	Homo sapiens	151-154
7623839-2	1995	We show that exposure of cells to various genotoxic agents, including anticancer drugs such as mitomycin and 5-fluorouracil, results in an increase in p53 mRNA levels and in p53 promoter activation, indicating that the p53 genotoxic stress response is partly regulated at the transcriptional level.	Mitomycin	95-104	P53	Homo sapiens	174-177
7623839-2	1995	We show that exposure of cells to various genotoxic agents, including anticancer drugs such as mitomycin and 5-fluorouracil, results in an increase in p53 mRNA levels and in p53 promoter activation, indicating that the p53 genotoxic stress response is partly regulated at the transcriptional level.	Mitomycin	95-104	P53	Homo sapiens	174-177
7750085-1	1995	Anticancer drugs etoposide and mitomycin C increased nuclear p53 protein and decreased proliferating cell nuclear antigen (PCNA) of PLC/PRF/5 human hepatoma cells.	Etoposide	17-26	P53	Homo sapiens	61-64
7750085-1	1995	Anticancer drugs etoposide and mitomycin C increased nuclear p53 protein and decreased proliferating cell nuclear antigen (PCNA) of PLC/PRF/5 human hepatoma cells.	Mitomycin	31-42	P53	Homo sapiens	61-64
7636632-7	1995	Moreover, mutations are targeted at py-py sequences in over 90% of skin tumors whereas in internal cancers the distribution is proportional to the frequency of bipyrimidine sequences in the p53 gene.	2,2'-Bipyrimidine	160-172	P53	Homo sapiens	190-193
7537340-1	1995	We previously described the use of a phage-displayed library of random hexapeptides to define and localise the epitope on the human tumor suppressor protein p53 recognised by the monoclonal antibody PAb240.	pab240	199-205	P53	Homo sapiens	157-160
7627557-2	1995	We have examined potential p53-mediated effects of metabolically labeling cultured mammalian cells with [35S]methionine and [3H]thymidine, methods that are commonly used to study the biochemical properties, synthesis, processing and degradation of proteins and the replication of DNA in proliferating cells.	Thymidine	128-137	P53	Homo sapiens	27-30
7790147-0	1995	Effect of orally administered antithyroid thioureylenes on PCNA and P53 expression in psoriatic lesions.	thioureylenes	42-55	P53	Homo sapiens	68-71
7854378-8	1995	Furthermore, 100 percent of the mutations in the patients who neither drank nor smoked occurred at sites containing cytidine phosphate guanosine dinucleotides (potentially representing endogenous mutations) within the p53 gene (5 of 5 mutations; 95 percent confidence interval, 48 to 100 percent), whereas only 23 percent of those in cigarette smokers consisted of such changes (12 of 53 mutations; 95 percent confidence interval, 12 to 36 percent; P = 0.001).	cytidine phosphate guanosine dinucleotides	116-158	P53	Homo sapiens	218-221
7896881-4	1995	Upon introduction of temperature-sensitive p53 into HC11 cells, which lack wild-type (wt) p53, PCD was observed after mitomycin treatment at 32 degrees, when the ts p53 protein is in wt conformation.	Mitomycin	118-127	P53	Homo sapiens	43-46
7896881-5	1995	Thus, wt p53 mediates activation of PCD in response to mitomycin in HC11 cells.	Mitomycin	55-64	P53	Homo sapiens	9-12
7835585-6	1995	Intranuclear p53 protein was immunostained by the avidin-biotin complex method.	avidin-biotin	50-63	P53	Homo sapiens	13-16
7824283-7	1995	Moreover, the same impairment in p53 induction is observed after exposure to mitomycin C, a chemical agent for which FA cells demonstrate a specific cellular and chromosomal hypersensitivity, as well as after u.v.-B irradiation, an agent known to cause oxidative stress.	Mitomycin	77-88	P53	Homo sapiens	33-36
7819056-5	1995	Sequencing analysis of the entire coding region of the p53 gene revealed that both alleles were expressed in the JEG-3 cell line, and one of the alleles contained a point mutation (G to T) in codon 167 (Gln to His).	Glutamine	203-206	P53	Homo sapiens	55-58
7718488-3	1995	Expression of p53 protein was characterized by biosynthetic labeling and immunoprecipitation with the monoclonal antibodies pAb 1801 (reacting with wild-type and mutant human p53), pAb 240 (reacting with mutant human p53) and pAb 1620 (reacting with wild-type human p53).	4-Aminobenzoic Acid	124-127	P53	Homo sapiens	14-17
7718488-3	1995	Expression of p53 protein was characterized by biosynthetic labeling and immunoprecipitation with the monoclonal antibodies pAb 1801 (reacting with wild-type and mutant human p53), pAb 240 (reacting with mutant human p53) and pAb 1620 (reacting with wild-type human p53).	4-Aminobenzoic Acid	181-184	P53	Homo sapiens	14-17
7718488-3	1995	Expression of p53 protein was characterized by biosynthetic labeling and immunoprecipitation with the monoclonal antibodies pAb 1801 (reacting with wild-type and mutant human p53), pAb 240 (reacting with mutant human p53) and pAb 1620 (reacting with wild-type human p53).	4-Aminobenzoic Acid	181-184	P53	Homo sapiens	14-17
7655736-6	1995	Additional immunostaining of the positive samples with mutant p53-specific Pab240 monoclonal antibody failed to detect immunopositive material.	pab240	75-81	P53	Homo sapiens	62-65
7713039-3	1994	This hypothesis has been supported by genetic evidence in liver tumors which has associated aflatoxin B1 exposure with the detection of inactivating DNA mutations within the human p53 tumor suppressor gene.	Aflatoxin B1	92-104	P53	Homo sapiens	180-183
7954409-1	1994	The present study assessed the role of the p53 tumor suppressor gene in cell cycle arrest and apoptosis following treatment of Burkitt"s lymphoma and lymphoblastoid cell lines with gamma-rays, etoposide, nitrogen mustard, and cisplatin.	Etoposide	193-202	P53	Homo sapiens	43-46
7954409-3	1994	We found that gamma-rays and etoposide induced a strong G1 arrest in the wild-type p53 lines while nitrogen mustard and cisplatin induced relatively little G1 arrest.	Etoposide	29-38	P53	Homo sapiens	83-86
7954409-5	1994	The degree of G1 arrest observed with these agents correlated with the rate of p53 and p21Waf1/Cip1 protein accumulation: gamma-rays and etoposide induced rapid accumulation of both p53 and p21Waf1/Cip1; nitrogen mustard and cisplatin induced slow accumulation of p53 and no major accumulation of the p21Waf1/Cip1 protein.	Etoposide	137-146	P53	Homo sapiens	79-82
7954409-5	1994	The degree of G1 arrest observed with these agents correlated with the rate of p53 and p21Waf1/Cip1 protein accumulation: gamma-rays and etoposide induced rapid accumulation of both p53 and p21Waf1/Cip1; nitrogen mustard and cisplatin induced slow accumulation of p53 and no major accumulation of the p21Waf1/Cip1 protein.	Etoposide	137-146	P53	Homo sapiens	182-185
7954409-5	1994	The degree of G1 arrest observed with these agents correlated with the rate of p53 and p21Waf1/Cip1 protein accumulation: gamma-rays and etoposide induced rapid accumulation of both p53 and p21Waf1/Cip1; nitrogen mustard and cisplatin induced slow accumulation of p53 and no major accumulation of the p21Waf1/Cip1 protein.	Etoposide	137-146	P53	Homo sapiens	182-185
7954409-8	1994	We also observed an inverse sensitivity relationship between nitrogen mustard/cisplatin and etoposide in the mutant p53 lines and this was found to correlate with topoisomerase II mRNA levels in the cells.	Etoposide	92-101	P53	Homo sapiens	116-119
7955036-2	1994	Our hypothesis is that lung cancers from MG workers contain mutations (G:C to A:T transitions) as the result of MG-produced DNA promutagenic adducts in the p53 tumor suppressor gene.	Mustard Gas	41-43	P53	Homo sapiens	156-159
7955036-9	1994	The p53 mutational frequency in the MG-exposed cases is similar to the non-exposed controls and the usual smoking-related lung cancers reported previously.	Mustard Gas	36-38	P53	Homo sapiens	4-7
8084582-9	1994	Inhibition of transcription with alpha-amanitin evokes nuclear accumulation of p53 both in normal cells and in XP cells.	Alpha-Amanitin	33-47	P53	Homo sapiens	79-82
8044794-0	1994	Hyperphosphorylation of p53 induced by okadaic acid attenuates its transcriptional activation function.	Okadaic Acid	39-51	P53	Homo sapiens	24-27
8044794-4	1994	Incubation of the transfected cells with okadaic acid, an inhibitor of serine phosphatases 2A and 1, induced hyperphosphorylation of p53 protein.	Okadaic Acid	41-53	P53	Homo sapiens	133-136
8044794-9	1994	These results suggest that the phosphorylation induced by okadaic acid may selectively modulate the transcription activation function of p53.	Okadaic Acid	58-70	P53	Homo sapiens	137-140
8207805-9	1994	In the ACH-2 cell line, which is now demonstrated to contain an endogenous mutant form of p53 (amino acid 248, Arg to Gln), additional mutant p53 proteins did not alter HIV-1 replication.	Glutamine	118-121	P53	Homo sapiens	90-93
8275497-1	1994	We investigated the expression of p53 in paraformaldehyde-lysine-periodate fixed normal and chronic myelogenous leukemia (CML) hemopoietic cells with flow cytometry and two monoclonal antibodies, PAb1801 and the mutant-conformation-associated PAb240.	paraform	41-57	P53	Homo sapiens	34-37
8275497-1	1994	We investigated the expression of p53 in paraformaldehyde-lysine-periodate fixed normal and chronic myelogenous leukemia (CML) hemopoietic cells with flow cytometry and two monoclonal antibodies, PAb1801 and the mutant-conformation-associated PAb240.	metaperiodate	65-74	P53	Homo sapiens	34-37
8275497-1	1994	We investigated the expression of p53 in paraformaldehyde-lysine-periodate fixed normal and chronic myelogenous leukemia (CML) hemopoietic cells with flow cytometry and two monoclonal antibodies, PAb1801 and the mutant-conformation-associated PAb240.	pab240	243-249	P53	Homo sapiens	34-37
8275497-3	1994	The expression of a p53 protein reactive with PAb240 was closely associated with CD34+/HLA-DR+ cells and with cells in active cell cycle, while the p53 protein recognized by PAb1801 was mainly found in CD34+/HLA-DR- cells and in cells in the G0/G1 phases of the cell cycle.	pab240	46-52	P53	Homo sapiens	20-23
8280176-0	1993	Okadaic acid inhibits dephosphorylation of cytoplasmic p53 during lymphocyte activation.	Okadaic Acid	0-12	P53	Homo sapiens	55-58
8280176-3	1993	Treatments of T cells with okadaic acid (1nM) prior to addition of Concanavalin-A/serum inhibited completely the dephosphorylation of cytosolic p53 observed to occur within 10-20min of stimulation.	Okadaic Acid	27-39	P53	Homo sapiens	144-147
8217600-6	1993	The remaining 31 samples expressed p53 detected by PAb240 which recognises mutant p53 and is predicted to recognise wild-type p53 in the promoter conformation.	pab240	51-57	P53	Homo sapiens	35-38
8217600-6	1993	The remaining 31 samples expressed p53 detected by PAb240 which recognises mutant p53 and is predicted to recognise wild-type p53 in the promoter conformation.	pab240	51-57	P53	Homo sapiens	82-85
8217600-6	1993	The remaining 31 samples expressed p53 detected by PAb240 which recognises mutant p53 and is predicted to recognise wild-type p53 in the promoter conformation.	pab240	51-57	P53	Homo sapiens	82-85
8096551-2	1993	Most of the mutations were G to T transversions in codon 249 of the p53 gene in HCCs in China and Mozambique, where aflatoxin B1 was a risk factor.	Aflatoxin B1	116-128	P53	Homo sapiens	68-71
8418091-14	1993	PAb240 may be a useful tool not only in screening point mutations of the p53 gene in osteosarcomas but also in the differential diagnosis between osteosarcomas and reactive bone-forming lesions.	pab240	0-6	P53	Homo sapiens	73-76
8380918-11	1993	Less frequent than the deamination of 5-methyl cytosine in CpG dinucleotides, mutations resulting in loss or gain of nucleotide base pairs may represent the second highest endogenous mutagenic event for p53 gene in human cancers.	Dinucleoside Phosphates	63-76	P53	Homo sapiens	203-206
1330291-1	1992	In order to clarify the significance of mutation of the p53 tumor suppressor gene in the genesis and development of human hepatocellular carcinoma (HCC) in an aflatoxin B1 low-exposure area, the spectrum, i.e., incidence, type, and site, of p53 gene mutations was examined in 169 tissue samples resected mainly from Japanese patients using single-strand conformation polymorphism analysis and direct sequencing.	Aflatoxin B1	159-171	P53	Homo sapiens	56-59
1358781-3	1992	Immunoreactive p53 was observed in the nuclei of tumor cells in 4% paraformaldehyde-fixed, frozen sections (12 of 15) and paraffin-embedded sections (11 of 15), but not in routinely processed (10% formalin-fixed) specimens.	paraform	67-83	P53	Homo sapiens	15-18
1406679-5	1992	Phosphorylation of the conserved serine 15 in human p53 peptides depended on the presence of an adjacent glutamine, and phosphorylation was inhibited by the presence of a nearby lysine.	Glutamine	105-114	P53	Homo sapiens	52-55
1644930-6	1992	The other nonhereditary p53 mutation was a transition at codon 248 (CGG to CAG, arginine to glutamine) found in the lymphoblasts of a patient with a preleukemic syndrome and acute lymphoblastic leukemia (ALL) whose brother is a long-term survivor of ALL.	Glutamine	92-101	P53	Homo sapiens	24-27
1685017-1	1991	p53 expression was studied in 111 primary breast cancers with a monoclonal antibody (PAb240) that reacts with an epitope in mutant p53.	pab240	85-91	P53	Homo sapiens	0-3
1685017-1	1991	p53 expression was studied in 111 primary breast cancers with a monoclonal antibody (PAb240) that reacts with an epitope in mutant p53.	pab240	85-91	P53	Homo sapiens	131-134
1958596-3	1991	One sample [human colon cancer (HCC) 278] was found to have a TP53 mutation altering the amino acid glutamine 167 in exon 5.	Glutamine	100-109	P53	Homo sapiens	62-66
1691710-5	1990	We have developed a monoclonal antibody to p53 designated PAb240 which does not immunoprecipitate wild type p53.	pab240	58-64	P53	Homo sapiens	43-46
1691710-6	1990	A series of different p53 mutants all react more strongly with PAb240 than with PAb246.	pab240	63-69	P53	Homo sapiens	22-25
1691710-7	1990	The PAb240 reactive form of p53 cannot bind to SV40 large T antigen but does bind to HSP70.	pab240	4-10	P53	Homo sapiens	28-31
1691710-9	1990	PAb240 recognizes all forms of p53 when they are denatured.	pab240	0-6	P53	Homo sapiens	31-34
1691710-11	1990	We propose that immunoprecipitation of p53 by PAb240 is diagnostic of mutation in both murine and human systems and suggest that the different point mutations which convert p53 from a recessive to a dominant oncogene exert a common conformational effect on the protein.	pab240	46-52	P53	Homo sapiens	173-176
33591325-6	2021	Serial molecular profiling revealed that clearance of TP53 mutations during HMA therapy was associated with superior OS (HR, 0.28; P = .001) and improved outcome in patients proceeding to allogeneic hematopoietic cell transplantation.	5-(N,N-hexamethylene)amiloride	76-79	P53	Homo sapiens	54-58
34785441-7	2022	Toxicity study using overexpression of dominant-negative mutant p53 in MCF-7 cells (which have wild type functional p53) showed that anticancer potential of compound 4h is positively correlated with p53 expression.	4h	166-168	P53	Homo sapiens	64-67
34728570-6	2022	Enzalutamide induced the expression of DNMT3A and DNMT3B in prostate cancer cells with a potential role of p53 and pRB in this process.	enzalutamide	0-12	P53	Homo sapiens	107-110
34661718-0	2022	Hydroxyurea-loaded Fe3O4/SiO2/chitosan-g-mPEG2000 nanoparticles; pH-dependent drug release and evaluation of cell cycle arrest and altering p53 and lincRNA-p21 genes expression.	Hydroxyurea	0-11	P53	Homo sapiens	140-143
34826742-5	2022	RESULTS: The most frequently mutated gene was TP53 in three cases of primary HAL and one case of metastatic HAL, with a mutation rate of 100%.	hal	77-80	P53	Homo sapiens	46-50
33901485-10	2021	Real time PCR analysis showed an increased transcription of p53 in MCF-7 cells, thus confirming the probable pro-apoptotic effect of the peptide BTM-P1.	btm-p1	145-151	P53	Homo sapiens	60-63
34826742-5	2022	RESULTS: The most frequently mutated gene was TP53 in three cases of primary HAL and one case of metastatic HAL, with a mutation rate of 100%.	hal	108-111	P53	Homo sapiens	46-50
34826742-8	2022	The TP53 mutation was related to the occurrence of HAL.	hal	51-54	P53	Homo sapiens	4-8
34826742-9	2022	CONCLUSION: HAL could be caused by genetic mutations and is closely related to TP53 mutation.	hal	12-15	P53	Homo sapiens	79-83
34595994-14	2021	In summary, LncRNA CASC9 played a regulative role in ovarian carcinoma by cyclinG1/TP53/MMP7 signaling via binding to miR-488-3p in vivo and in vitro.	mir-488-3p	118-128	P53	Homo sapiens	83-87
33667419-6	2021	Knockdown simulations identified AP1, ASK1, JNK, MEK47, p53, and ROS as positive functional regulators of sorafenib-induced apoptosis of cardiomyocytes.	Sorafenib	106-115	P53	Homo sapiens	56-59
34866972-9	2021	These chemotherapeutic and chemosensitising activities of hesperidin and hesperetin have been linked to several mechanisms, including the modulation of signalling pathways, glucose uptake, enzymes, miRNA expression, oxidative status, cell cycle regulatory proteins, tumour suppressor p53, plasma and liver lipid profiles as well as DNA repair mechanisms.	Hesperidin	58-68	P53	Homo sapiens	284-287
34055057-8	2021	Of note, hirsutanol A induced the expression of the tumor suppressor p53, whereas simultaneous treatment with pifithrin-alpha, an inhibitor of p53, significantly reduced Jurkat cell apoptosis induced by hirsutanol A.	pifithrin	110-125	P53	Homo sapiens	143-146
34799573-5	2021	The results of this approach closely reproduce the experimental data from recent literature on the binding of the ligand epigallocatechin gallate (EGCG) to the intrinsically disordered N-terminal domain of the tumor suppressor p53.	epigallocatechin gallate	121-145	P53	Homo sapiens	227-230
33965112-8	2021	Celastrol and Fe3O4/alpha-Fe2O3/CA-PEG-celastrol increased the production of reactive oxygen species in SMMC-7721 cells and promoted apoptosis and apoptosis-related proteins (p53, Bax, Bcl-2) were also changed.	ca-peg-celastrol	32-48	P53	Homo sapiens	175-178
34042457-6	2021	We investigated the dynamics of the p53 DNA-binding domain by 15N-NMR Carr-Purcell-Meiboom-Gill relaxation methods.	15n	62-65	P53	Homo sapiens	36-39
34799573-5	2021	The results of this approach closely reproduce the experimental data from recent literature on the binding of the ligand epigallocatechin gallate (EGCG) to the intrinsically disordered N-terminal domain of the tumor suppressor p53.	epigallocatechin gallate	147-151	P53	Homo sapiens	227-230
33652124-7	2021	Gliclazide did not affect 1.2B4 cell viability and Ca2+ concentration, however, it downregulated CASP-3 and upregulated TP53.	Gliclazide	0-10	P53	Homo sapiens	120-124
34743173-9	2021	p53 inactivation abrogated cell cycle arrest and reduced G4 accumulation in NGP clones.	Dichlorophen	57-59	P53	Homo sapiens	0-3
32789496-6	2021	Compared with previous established population-based signatures, PPS manifested superior ability to predict survival in TP53-mutant patients.	pps	64-67	P53	Homo sapiens	119-123
34019763-8	2021	Then, hepatitis B virus (HBV) and p53 gene were detected by this proposed method through introducing the Fe3O4 nanoparticles into the gene hybridization system.	ferryl iron	105-110	P53	Homo sapiens	34-37
33449813-0	2021	Eprenetapopt (APR-246) and Azacitidine in TP53-Mutant Myelodysplastic Syndromes.	Azacitidine	27-38	P53	Homo sapiens	42-46
33449813-13	2021	CONCLUSION: Combination treatment with eprenetapopt and azacitidine is well-tolerated yielding high rates of clinical response and molecular remissions in patients with TP53-mutant MDS and oligoblastic AML.	Azacitidine	56-67	P53	Homo sapiens	169-173
34739932-10	2021	PI3K/Akt signaling pathway, PI3K, AKT, tensin homolog deleted on chromosome 10 (PTEN), mechanistic target of rapamycin (mTOR) and p53 protein were all inhibited by PM10 exposure, and PI3K/Akt signaling pathway was inactivated.	pm10	164-168	P53	Homo sapiens	130-133
33625525-0	2021	P53-mediated in vitro inhibition of PhIP-induced oxidative damage by myricetin bulk and nano forms in healthy lymphocytes.	2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine	36-40	P53	Homo sapiens	0-3
34007049-15	2021	The iFCG regimen with only 3 cycles of chemotherapy is an effective, time-limited regimen for patients with CLL with mutated IGHV and without del(17p)/TP53 mutation.	ifcg	4-8	P53	Homo sapiens	151-155
34537213-0	2021	Sodium cantharidate induces apoptosis in breast cancer cells by regulating energy metabolism via the protein phosphatase 5-p53 axis.	sodium cantharidate	0-19	P53	Homo sapiens	123-126
33982403-6	2021	Supportive evidence indicated that MTX administration induced senescence and apoptosis of human GCs in vitro, and the effects were consistent with the high levels of p21, p53, and oxidative stress (OS).	Methotrexate	35-38	P53	Homo sapiens	171-174
33713969-0	2021	The DpdtbA induced EMT inhibition in gastric cancer cell lines was through ferritinophagy-mediated activation of p53 and PHD2/hif-1alpha pathway.	dpdtba	4-10	P53	Homo sapiens	113-116
33713969-9	2021	Taken together, All data supported that DpdtbA induced EMT inhibition was through activation of p53 and PHD2/hif-1alpha pathway.	dpdtba	40-46	P53	Homo sapiens	96-99
33913241-0	2021	Vanadium oxides modify the expression levels of the p21, p53, and Cdc25C proteins in human lymphocytes treated in vitro.	vanadium oxides	0-15	P53	Homo sapiens	57-60
33952867-2	2021	We previously showed that non-naturally occurring, stable helical trimers of bicyclic beta-amino acids (Abh) with all-trans amide bonds can block the p53-MDM2/MDMX alpha-helix-helix interaction, which plays a role in regulating p53 function.	beta-amino acids	86-102	P53	Homo sapiens	150-153
34004477-8	2021	gamma-Fe2O3 and Fe3O4 NPs could also cause mitochondrial fusion and fission dysregulation, activate lipid peroxidation and iron metabolism-related genes in a P53-dependent manner.	ferryl iron	16-21	P53	Homo sapiens	158-161
34537213-6	2021	Furthermore, bioinformatics analysis identified possible roles for p53 with respect to the effects of sodium cantharidate on breast cancer cells.	sodium cantharidate	102-121	P53	Homo sapiens	67-70
33952867-2	2021	We previously showed that non-naturally occurring, stable helical trimers of bicyclic beta-amino acids (Abh) with all-trans amide bonds can block the p53-MDM2/MDMX alpha-helix-helix interaction, which plays a role in regulating p53 function.	beta-amino acids	86-102	P53	Homo sapiens	228-231
34537213-7	2021	Western blot, docking, and phosphatase assays revealed that the regulation of p53 activity by sodium cantharidate was related to its inhibition of protein phosphatase 5 activity.	sodium cantharidate	94-113	P53	Homo sapiens	78-81
33918387-0	2021	Distinct Classes of Flavonoids and Epigallocatechin Gallate, Polyphenol Affects an Oncogenic Mutant p53 Protein, Cell Growth and Invasion in a TNBC Breast Cancer Cell Line.	Flavonoids	20-30	P53	Homo sapiens	100-103
34686652-3	2021	The regulatory roles of TAMs on miR-363/PDZD2 and the internal mechanism relating to long noncoding RNA p53 upregulated regulator of P53 levels (lncRNA PURPL) are examined in this study.	tams	24-28	P53	Homo sapiens	104-107
33639563-0	2021	Glutathionylation-dependent proteasomal degradation of wide-spectrum mutant p53 proteins by engineered zeolitic imidazolate framework-8.	imidazolate	112-123	P53	Homo sapiens	76-79
33984442-4	2021	To verify the biological effects of E6 polymorphisms towards p53 degradation, HPV16-E6 prototype and 7 variants isolated from cervical cancer biopsies of Moroccan women were evaluated for their activities by transient expression assays using pcDNA3.1-E6 constructs in C33A cell line.	Polyurethane Y-290	36-38	P53	Homo sapiens	61-64
33600210-0	2021	Eprenetapopt Plus Azacitidine in TP53-Mutated Myelodysplastic Syndromes and Acute Myeloid Leukemia: A Phase II Study by the Groupe Francophone des Myelodysplasies (GFM).	Azacitidine	18-29	P53	Homo sapiens	33-37
33600210-1	2021	PURPOSE: TP53-mutated (TP53m) myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) have very poor outcome irrespective of the treatment received, including 40% responses (20% complete remission [CR]) with azacitidine (AZA) alone, short response duration, and a median overall survival (OS) of approximately 6 months.	Azacitidine	217-228	P53	Homo sapiens	9-13
33600210-1	2021	PURPOSE: TP53-mutated (TP53m) myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) have very poor outcome irrespective of the treatment received, including 40% responses (20% complete remission [CR]) with azacitidine (AZA) alone, short response duration, and a median overall survival (OS) of approximately 6 months.	Azacitidine	217-228	P53	Homo sapiens	23-27
33600210-1	2021	PURPOSE: TP53-mutated (TP53m) myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) have very poor outcome irrespective of the treatment received, including 40% responses (20% complete remission [CR]) with azacitidine (AZA) alone, short response duration, and a median overall survival (OS) of approximately 6 months.	Azacitidine	230-233	P53	Homo sapiens	9-13
34686652-3	2021	The regulatory roles of TAMs on miR-363/PDZD2 and the internal mechanism relating to long noncoding RNA p53 upregulated regulator of P53 levels (lncRNA PURPL) are examined in this study.	tams	24-28	P53	Homo sapiens	133-136
33600210-1	2021	PURPOSE: TP53-mutated (TP53m) myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) have very poor outcome irrespective of the treatment received, including 40% responses (20% complete remission [CR]) with azacitidine (AZA) alone, short response duration, and a median overall survival (OS) of approximately 6 months.	Azacitidine	230-233	P53	Homo sapiens	23-27
33576462-3	2021	By conducting reverse transcription-quantitative polymerase chain reaction and Western blotting, relative levels of SIRT1 and p53 regulated by miR-138-5p were detected.	mir-138-5p	143-153	P53	Homo sapiens	126-129
34745455-6	2021	Mutations in GATA3 and MAP3K1 in beast invasive carcinoma (BRCA), TCF7L2 in colon adenocarcinoma (COAD), NFE2L2 in esophageal carcinoma (ESCA), CIC and IDH1 in brain lower grade glioma (LGG), CDH1 in stomach adenocarcinoma (STAD), and TP53 in uterine corpus endometrial carcinoma (UCEC) were demonstrated to be correlated with lower TMB.	1,2,4,5-tetramethoxybenzene	333-336	P53	Homo sapiens	235-239
33649861-2	2021	G-Rh2 exhibits anticancer activity in various human cancer cell lines both in vitro and in vivo by modulating several signaling pathways, such as those of PDZ-binding kinase/T-LAK cell-originated protein kinase, phosphatidylinositol 3-kinase, protein kinase B, mammalian target of rapamycin, epidermal growth factor receptor, p53, and reactive oxygen species.	ginsenoside Rh2	0-5	P53	Homo sapiens	326-329
33508133-0	2021	Broad-spectrum rescue compounds for structural p53 mutations: perspective on "Arsenic trioxide rescues structural p53 mutations through a cryptic allosteric site".	Arsenic Trioxide	78-94	P53	Homo sapiens	47-50
33508133-0	2021	Broad-spectrum rescue compounds for structural p53 mutations: perspective on "Arsenic trioxide rescues structural p53 mutations through a cryptic allosteric site".	Arsenic Trioxide	78-94	P53	Homo sapiens	114-117
34642468-3	2022	In the present study, an imipridone, ONC201, was combined with RG7112, an antagonist of MDM2, a p53 negative regulator, to activate downstream events of the p53 and TNF-related apoptosis-inducing ligand (TRAIL)/death receptor (DR) pathways.	RG7112	63-69	P53	Homo sapiens	96-99
33952503-6	2021	MLA exhibited the wild-type p53 expression pattern, whereas UC showed a uniform and strong p53 immunoreactivity.	CD63 protein, human	0-3	P53	Homo sapiens	28-31
33998890-8	2021	In astrocytes, CBG decreased levels of DNA damage proteins, including p53, whereas CBDV increased levels of DNA damage markers.	cannabigerol	15-18	P53	Homo sapiens	70-73
34642468-3	2022	In the present study, an imipridone, ONC201, was combined with RG7112, an antagonist of MDM2, a p53 negative regulator, to activate downstream events of the p53 and TNF-related apoptosis-inducing ligand (TRAIL)/death receptor (DR) pathways.	RG7112	63-69	P53	Homo sapiens	157-160
34642468-4	2022	As compared to treatment with the individual drugs, the combination of ONC201 and RG7112 promoted greater degrees of apoptosis of MF CD34+ cells through activation of both p53-dependent and -independent pathways.	RG7112	82-88	P53	Homo sapiens	172-175
33796223-3	2021	E6 effects this oncogenic phenotype in part through inhibitory protein-protein interactions (PPIs) and accelerated degradation of proteins with tumor suppressor properties, such as p53 and caspase 8.	Polyurethane Y-290	0-2	P53	Homo sapiens	181-184
33594879-6	2021	Cellular senescence-specific genes, such as p53 and p21, were downregulated on the PDA-coated substrate, while the stemness-related gene, OCT4, was upregulated.	polydopamine	83-86	P53	Homo sapiens	44-47
33967558-13	2021	CPI-455 significantly upregulated the ROS content, P53, Bax, Caspase-9, and Caspase-3 protein expression in Eca-109 cells, whereas KDM5C expression was downregulated.	CPI-455	0-7	P53	Homo sapiens	51-54
34639072-8	2021	Violacein induced nuclear condensation, dissipated mitochondrial membrane potential (MMP), increased generation of reactive oxygen species (ROS), activated the caspase cascade, and upregulated p53 and p21.	violacein	0-9	P53	Homo sapiens	193-196
33894275-4	2021	NADP formed, is rapidly converted to NADPH by glucose 6-phosphate dehydrogenase and malic enzymes, overexpressed in tumor cells with mutant p53.	NADP	0-4	P53	Homo sapiens	140-143
33549596-0	2021	Microvesicles mediate sorafenib resistance in liver cancer cells through attenuating p53 and enhancing FOXM1 expression.	Sorafenib	22-31	P53	Homo sapiens	85-88
33347603-0	2021	Quercetin Induces p53-independent Cancer Cell Death via TFEB-mediated Lysosome Activation and ROS-dependent Ferroptosis.	Quercetin	0-9	P53	Homo sapiens	18-21
33347603-5	2021	KEY RESULTS: Quercetin is able to promote p53-independent cell death in various cancer cell lines.	Quercetin	13-22	P53	Homo sapiens	42-45
33549596-8	2021	miR-25 in the cancer cell-secreted MVs was transferred to their host cells HepG2 and Huh7 cells and reversed the sorafenib induced expression of tumor suppressor p53.	Sorafenib	113-122	P53	Homo sapiens	162-165
34711017-0	2021	Anti-Proliferative and Pro-Apoptotic Activities of Synthesized 3,4,5 Tri-Methoxy Ciprofloxacin Chalcone Hybrid, through p53 Up-Regulation in HepG2 and MCF7 Cell Lines.	Chalcone	95-103	P53	Homo sapiens	120-123
33877544-12	2021	BOP1 silencing-induced suppression of cell proliferation was partly reversed by pifithrin-alpha (a p53 inhibitor).	pifithrin	80-95	P53	Homo sapiens	99-102
33668397-5	2021	In addition, pre-treatment with THF suppressed CoCl2-induced hypoxia-related genes including HIF1alpha, p53, VEGF, and GLUT1 at the mRNA and protein levels.	tetrahydrofuran	32-35	P53	Homo sapiens	104-107
34590505-8	2021	On a genetic basis, both agents engaged the BCL-2 family-regulated and caspase-dependent intrinsic apoptotic pathway, but EGCG and HNK triggered apoptosis via p53-independent and p53-dependent pathways, respectively.	epigallocatechin gallate	122-126	P53	Homo sapiens	159-162
33718183-0	2021	Advanced NSCLC Patients With EGFR T790M Harboring TP53 R273C or KRAS G12V Cannot Benefit From Osimertinib Based on a Clinical Multicentre Study by Tissue and Liquid Biopsy.	osimertinib	94-105	P53	Homo sapiens	50-54
33718183-13	2021	Moreover, we discovered two uncommon mutations, TP53 R273C and KRAS G12V, which attenuates the effectiveness of osimertinib.	osimertinib	112-123	P53	Homo sapiens	48-52
33620775-0	2021	Mutagenicity of N-hydroxy-4-aminobiphenyl in human TP53 knock-in (Hupki) mouse embryo fibroblasts.	N-hydroxy-4-aminobiphenyl	16-41	P53	Homo sapiens	51-55
33620775-6	2021	Here we studied the induction of mutations in human TP53 after treatment of primary HUFs with N-OH-4-ABP.	n-oh-4-abp	94-104	P53	Homo sapiens	52-56
34590505-8	2021	On a genetic basis, both agents engaged the BCL-2 family-regulated and caspase-dependent intrinsic apoptotic pathway, but EGCG and HNK triggered apoptosis via p53-independent and p53-dependent pathways, respectively.	epigallocatechin gallate	122-126	P53	Homo sapiens	179-182
33620775-8	2021	A total of 6% TP53-mutants were identified after treatment with 40 muM N-OH-4-ABP for 24 h (n = 150) with G > C/C > G transversion being the main mutation type.	n-oh-4-abp	71-81	P53	Homo sapiens	14-18
34524810-3	2021	Additionally, the limited quantity of target DNA (a fragment of p53 gene) could be transformed into abundant output DNA-SiO2 by employing the Nt BstNBI enzyme-assisted signal amplification procedure, leading to a highly improved detection sensitivity of the biosensor.	Silicon Dioxide	120-124	P53	Homo sapiens	64-67
33620775-9	2021	The mutation spectrum found in the TP53 gene of immortalised N-OH-4-ABP-treated HUFs was unlike the one found in human bladder cancer.	n-oh-4-abp	61-71	P53	Homo sapiens	35-39
33620775-12	2021	In conclusion, the observed difference in the N-OH-4-ABP-induced TP53 mutation spectrum to that observed in human bladder tumours do not support a role of 4-ABP in human bladder cancer development.	n-oh-4-abp	46-56	P53	Homo sapiens	65-69
33868388-3	2021	A major natural thiamine derivative, thiamine diphosphate (ThDP), is a coenzyme of central metabolism, also known to affect transcriptional activity of the master metabolic regulator and genome guardian p53.	Thiamine Pyrophosphate	37-57	P53	Homo sapiens	203-206
33628636-15	2021	In addition, quercetin, which has the most targets, can act on the main targets (BAX, CDK1, CCNB1, SERPINE1, CHEK2, and IGFBP3) of the P53 pathway to treat HCC.	Quercetin	13-22	P53	Homo sapiens	135-138
33561393-3	2021	discover a new role for an old drug, arsenic trioxide, in binding and stabilizing p53.	Arsenic Trioxide	37-53	P53	Homo sapiens	82-85
33868388-3	2021	A major natural thiamine derivative, thiamine diphosphate (ThDP), is a coenzyme of central metabolism, also known to affect transcriptional activity of the master metabolic regulator and genome guardian p53.	Thiamine Pyrophosphate	59-63	P53	Homo sapiens	203-206
34530900-8	2021	However, a deadly level of replicative stress was also observed in p53-deficient myeloma cells treated with UNC-0379, indicating that the cytotoxicity associated with SETD8 inhibition is not necessarily dependent on p53 activation.	6,7-dimethoxy-2-(pyrrolidin-1-yl)-N-(5-(pyrrolidin-1-yl)pentyl)quinazolin-4-amine	108-116	P53	Homo sapiens	67-70
33868388-10	2021	Correlation analysis of the p53 expression and enzymatic activities upon variations in cellular thiamine/ThDP levels indicates that p21 knockdown substitutes positive correlation of the p53 expression with the activity of 2-oxoglutarate dehydrogenase complex (OGDHC) for that with the activity of glutamate dehydrogenase (GDH).	Thiamine Pyrophosphate	105-109	P53	Homo sapiens	28-31
33868388-10	2021	Correlation analysis of the p53 expression and enzymatic activities upon variations in cellular thiamine/ThDP levels indicates that p21 knockdown substitutes positive correlation of the p53 expression with the activity of 2-oxoglutarate dehydrogenase complex (OGDHC) for that with the activity of glutamate dehydrogenase (GDH).	Thiamine Pyrophosphate	105-109	P53	Homo sapiens	186-189
33126266-10	2021	Together these findings indicate that CPUC002 induces apoptosis and G0/G1 cell cycle arrest in multiple myeloma cells by stabilizing p53 and inhibiting the STAT3 signaling pathway.	cpuc002	38-45	P53	Homo sapiens	133-136
33629325-5	2021	Besides, the expressions of GFP-LC3, p53, and Caspase in Sorafenib group and nano-ZnO group were significantly higher than that of control group, while their levels were highest in nano-ZnO group (p<0.05).	Sorafenib	57-66	P53	Homo sapiens	37-40
34511884-8	2021	ZJP may exert its inhibitory effects against pancreatic cancer by acting on key targets such as JUN, TP53, and MAPK1.	zjp	0-3	P53	Homo sapiens	101-105
33154093-7	2021	Combining INCB057643 with a MDM2-p53 inhibitor DS3032b significantly enhanced cytotoxicity in HGBCL-DH without TP53 mutation, while combining with the BCL-2 inhibitor venetoclax displayed potent therapeutic synergy in DLBCL/HGBCL cells with and without concurrent TP53 mutation.	ds3032b	47-54	P53	Homo sapiens	33-36
33154093-7	2021	Combining INCB057643 with a MDM2-p53 inhibitor DS3032b significantly enhanced cytotoxicity in HGBCL-DH without TP53 mutation, while combining with the BCL-2 inhibitor venetoclax displayed potent therapeutic synergy in DLBCL/HGBCL cells with and without concurrent TP53 mutation.	ds3032b	47-54	P53	Homo sapiens	111-115
33154093-7	2021	Combining INCB057643 with a MDM2-p53 inhibitor DS3032b significantly enhanced cytotoxicity in HGBCL-DH without TP53 mutation, while combining with the BCL-2 inhibitor venetoclax displayed potent therapeutic synergy in DLBCL/HGBCL cells with and without concurrent TP53 mutation.	ds3032b	47-54	P53	Homo sapiens	264-268
33732382-10	2021	Western blotting results also revealed the upregulation of p53 acetylation and p21, as well as the downregulation of Bcl-2 and cyclin D1 in cells treated with cambinol.	cambinol	159-167	P53	Homo sapiens	59-62
33732382-11	2021	In conclusion, the present results suggest that cambinol inhibits the proliferation and induces apoptosis in RPMI8226 and U266 cells by regulating acetylation of p53 via the targeting of SIRT1.	cambinol	48-56	P53	Homo sapiens	162-165
33850897-12	2021	Our results finally showed that high-risk cases were associated with cell proliferation and cell cycle related gene sets, high tumor protein P53 (TP53) mutation rate, suppressive immunity and increased sensitivity to cisplatin, gemcitabine and docetaxel.	Docetaxel	244-253	P53	Homo sapiens	141-144
33850897-12	2021	Our results finally showed that high-risk cases were associated with cell proliferation and cell cycle related gene sets, high tumor protein P53 (TP53) mutation rate, suppressive immunity and increased sensitivity to cisplatin, gemcitabine and docetaxel.	Docetaxel	244-253	P53	Homo sapiens	146-150
34511884-9	2021	Moreover, KEGG analysis indicated that the anti-pancreatic cancer effect of ZJP was mediated by multiple pathways, such as the PI3K-AKT, IL-17, TNF, HIF-1, and P53 signaling pathways.	zjp	76-79	P53	Homo sapiens	160-163
33416149-7	2021	Following garcinol treatment the expression levels of p53 and p21 were increased, while the expression levels of CDK2, CDK4, cyclin D1 and cyclin B1 were gradually decreased in a dose-dependent manner in both ISH and HEC-1B cells.	garcinol	10-18	P53	Homo sapiens	54-57
34315396-10	2022	Additionally, (Cu(phen)(L-tyr)Cl).3H20 induced apoptosis and cell cycle arrest towards MCF-7 and MDA-MB-231 breast cancer cells possibly via regulation of p53, Bax, caspase-9, caspase-3 and capase-7.	cu(phen)(l-tyr)cl	15-32	P53	Homo sapiens	155-158
33370709-11	2021	DHA also upregulated p53, CASP3, and cleaved-CASP3 and downregulated BCL2L1, MMP9, KDR, p-KDR, STAT1 and p-STAT1 in GC cell lines.	artenimol	0-3	P53	Homo sapiens	21-24
33370709-12	2021	In conclusion, DHA could suppress the tumorigenesis and invasion of GC by regulating STAT1/KDR/MMP9 and p53/BCL2L1/CASP3/7 pathways.	artenimol	15-18	P53	Homo sapiens	104-107
33274826-7	2021	We suggested that by reducing ETHE1, activation of the p53 pathway, and inhibiting mTOR pathways, DU might induce overactive autophagy, which affected the cytotoxicity.	du	98-100	P53	Homo sapiens	55-58
33360044-0	2021	Synergy between vinorelbine and afatinib in the inhibition of non-small cell lung cancer progression by EGFR and p53 signaling pathways.	Vinorelbine	16-27	P53	Homo sapiens	113-116
33360044-10	2021	The low doses of vinorelbine plus afatinib blocked the phosphorylation of AKT, ERK, JNK, and p38, but restored the expression of p53.	Vinorelbine	17-28	P53	Homo sapiens	129-132
34315396-10	2022	Additionally, (Cu(phen)(L-tyr)Cl).3H20 induced apoptosis and cell cycle arrest towards MCF-7 and MDA-MB-231 breast cancer cells possibly via regulation of p53, Bax, caspase-9, caspase-3 and capase-7.	3h20	34-38	P53	Homo sapiens	155-158
34309458-9	2022	The increase in p53, Bax, p38 MAPK, and PTEN gene expression levels compared to the control group was 1.71, 1.42, 3.26, and 3.29-fold with 5-FU + L treatment, respectively, while this increase was 8.43, 1.65, 3.55, and 3.54-fold with 5-FU + Q treatment, respectively.	Glutamine	241-242	P53	Homo sapiens	16-19
33520960-4	2020	It is suggested that enhancement of the p53 signaling pathway and weakening of the spindle assembly checkpoint are associated with the SP600125-induced cell cycle arrest.	pyrazolanthrone	135-143	P53	Homo sapiens	40-43
34169735-16	2021	Additionally, the p53 signaling pathway, platinum drug resistance, apoptosis, EGFR tyrosine kinase inhibitor resistance and ErbB signaling pathway may be critical pathways regulated by ARGs in CRC.	args	185-189	P53	Homo sapiens	18-21
33383327-7	2021	Mechanism study unfolded that, similar to niclosamide, 2 inhibited growth of cancer cells via p 53 activation and subsequent underwent cytochrome c dependent apoptosis.	Niclosamide	42-53	P53	Homo sapiens	94-98
33075425-1	2021	Most nucleoside anticancer drugs show a primary resistance to p53-deficient or p53-mutated cancer cells and are limited in the clinic to the treatment of hematological malignancies.	Nucleosides	5-15	P53	Homo sapiens	62-65
33075425-1	2021	Most nucleoside anticancer drugs show a primary resistance to p53-deficient or p53-mutated cancer cells and are limited in the clinic to the treatment of hematological malignancies.	Nucleosides	5-15	P53	Homo sapiens	79-82
35512188-3	2022	In a systematic analysis of 416 patients with t-MN and detailed prior exposure history, we found that TP53 mutations were significantly associated with prior treatment with thalidomide analogs, specifically lenalidomide.	Thalidomide	173-184	P53	Homo sapiens	102-106
32954996-11	2021	H2 also influences the crosstalk among the regulatory mechanisms of autophagy and apoptosis, which involve MAPKs, p53, Nrf2, NF-kappaB, p38 MAPK, mTOR, etc.	Deuterium	0-2	P53	Homo sapiens	114-117
35463672-8	2022	The effect of curaxins on p53 and NF-B (nuclear factor-kappaB), and their toxicity to cancer cells, is attributable to the FACT (facilitates chromatin transcription) complex"s chromatin trapping.	curaxins	14-22	P53	Homo sapiens	26-29
35410287-4	2022	RESULTS: By combining single-cell imaging and mathematical modeling of dose-dependent p53 dynamics induced by three chemotherapeutics of distinct mechanism-of-actions, including Etoposide, Nutlin-3a and 5-fluorouracil, and in five cancer cell types, we uncovered novel and highly variable p53 dynamic responses, in particular p53 transitional dynamics induced at intermediate drug concentrations, and identified the functional roles of distinct positive and negative feedback motifs of the p53 pathway in modulating the central p53-Mdm2 negative feedback to generate stimulus- and cell type-specific signaling responses.	Etoposide	178-187	P53	Homo sapiens	86-89
33189884-7	2021	TP53 mutations characteristic of those induced by N-OH-PhIP have been found in human tumours including breast and colorectal, which are cancer types that have been associated with PhIP exposure.	2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine	55-59	P53	Homo sapiens	0-4
35410287-4	2022	RESULTS: By combining single-cell imaging and mathematical modeling of dose-dependent p53 dynamics induced by three chemotherapeutics of distinct mechanism-of-actions, including Etoposide, Nutlin-3a and 5-fluorouracil, and in five cancer cell types, we uncovered novel and highly variable p53 dynamic responses, in particular p53 transitional dynamics induced at intermediate drug concentrations, and identified the functional roles of distinct positive and negative feedback motifs of the p53 pathway in modulating the central p53-Mdm2 negative feedback to generate stimulus- and cell type-specific signaling responses.	nutlin 3	189-198	P53	Homo sapiens	86-89
35410287-4	2022	RESULTS: By combining single-cell imaging and mathematical modeling of dose-dependent p53 dynamics induced by three chemotherapeutics of distinct mechanism-of-actions, including Etoposide, Nutlin-3a and 5-fluorouracil, and in five cancer cell types, we uncovered novel and highly variable p53 dynamic responses, in particular p53 transitional dynamics induced at intermediate drug concentrations, and identified the functional roles of distinct positive and negative feedback motifs of the p53 pathway in modulating the central p53-Mdm2 negative feedback to generate stimulus- and cell type-specific signaling responses.	nutlin 3	189-198	P53	Homo sapiens	289-292
33153480-9	2020	In addition, several other signaling pathways including the p53 and transforming growth factor-beta signaling pathways were also implicated in melphalan-induced cardiotoxicity according to the proteomic and transcriptomic analyses.	Melphalan	143-152	P53	Homo sapiens	60-63
35410287-4	2022	RESULTS: By combining single-cell imaging and mathematical modeling of dose-dependent p53 dynamics induced by three chemotherapeutics of distinct mechanism-of-actions, including Etoposide, Nutlin-3a and 5-fluorouracil, and in five cancer cell types, we uncovered novel and highly variable p53 dynamic responses, in particular p53 transitional dynamics induced at intermediate drug concentrations, and identified the functional roles of distinct positive and negative feedback motifs of the p53 pathway in modulating the central p53-Mdm2 negative feedback to generate stimulus- and cell type-specific signaling responses.	nutlin 3	189-198	P53	Homo sapiens	326-329
35410287-4	2022	RESULTS: By combining single-cell imaging and mathematical modeling of dose-dependent p53 dynamics induced by three chemotherapeutics of distinct mechanism-of-actions, including Etoposide, Nutlin-3a and 5-fluorouracil, and in five cancer cell types, we uncovered novel and highly variable p53 dynamic responses, in particular p53 transitional dynamics induced at intermediate drug concentrations, and identified the functional roles of distinct positive and negative feedback motifs of the p53 pathway in modulating the central p53-Mdm2 negative feedback to generate stimulus- and cell type-specific signaling responses.	nutlin 3	189-198	P53	Homo sapiens	490-493
35410287-4	2022	RESULTS: By combining single-cell imaging and mathematical modeling of dose-dependent p53 dynamics induced by three chemotherapeutics of distinct mechanism-of-actions, including Etoposide, Nutlin-3a and 5-fluorouracil, and in five cancer cell types, we uncovered novel and highly variable p53 dynamic responses, in particular p53 transitional dynamics induced at intermediate drug concentrations, and identified the functional roles of distinct positive and negative feedback motifs of the p53 pathway in modulating the central p53-Mdm2 negative feedback to generate stimulus- and cell type-specific signaling responses.	nutlin 3	189-198	P53	Homo sapiens	528-531
35385726-4	2022	AR blockade with enzalutamide induces (1) transcriptional silencing of TP53 and hence dedifferentiation to a hybrid epithelial and mesenchymal and stem-like state and (2) inhibition of BMP signaling, which promotes resistance to AR inhibition.	enzalutamide	17-29	P53	Homo sapiens	71-75
32911193-7	2020	Acyl-lysine peptide competition, pharmacological inhibition, and inhibitory post-translational modification of Sirt1 resulted in the loss of p53 ABP labeling both in vitro and in HEK293T cell lysates, consistent with the ABP measuring decreased Sirt1 activity.	abp	145-148	P53	Homo sapiens	141-144
32911193-7	2020	Acyl-lysine peptide competition, pharmacological inhibition, and inhibitory post-translational modification of Sirt1 resulted in the loss of p53 ABP labeling both in vitro and in HEK293T cell lysates, consistent with the ABP measuring decreased Sirt1 activity.	abp	221-224	P53	Homo sapiens	141-144
32901874-0	2020	Anti-proliferative effect of honokiol on SW620 cells through upregulating BMP7 expression via the TGF-beta1/p53 signaling pathway.	honokiol	29-37	P53	Homo sapiens	108-111
35114371-2	2022	Virtual screening identified N-(6-((4-bromobenzyl)amino)hexyl)-3,5-bis(trifluoromethyl)benzenesulfonamide (1) a lead compound that bound to the S100A2-p53 binding groove.	n-(6-((4-bromobenzyl)amino)hexyl)-3,5-bis(trifluoromethyl)benzenesulfonamide	29-105	P53	Homo sapiens	151-154
32602613-2	2020	Herein, we report the first rationally designed lasso proteins, or protein [1]rotaxanes, by using p53dim entwined dimer for intramolecular entanglement and SpyTag-SpyCatcher reaction for side-chain ring closure.	Rotaxanes	78-87	P53	Homo sapiens	98-101
35344507-6	2022	However, the genotype of TP53MUTBRAFWT in high-TMB status cohort have poorer response to ICI therapy than the genotype of BRAFMUTTP53WT in low-TMB status (Median, 18 months vs 47 month).	1,2,4,5-tetramethoxybenzene	47-50	P53	Homo sapiens	25-29
32988919-7	2020	CONCLUSION: Mutations in TP53 and PIK3CA hotspot at exon 9 may be potential negative predictors of ER+HER2+ BC treated with neoadjuvant letrozole and lapatinib, while MLL2 inactivating mutation might confer therapeutic benefit in these patients.	Lapatinib	150-159	P53	Homo sapiens	25-29
32881622-6	2020	This altered expression may account for differences between groups in timing of upregulation of some p53 targets such as apoptosis genes, and may account for the reduction in muscle loss in subjects receiving EAAs.	eaas	209-213	P53	Homo sapiens	101-104
35325405-10	2022	The gene expression of p16, p21, and p53 of smumf cells did not change until P10 and SA-beta-gal activity did not increase until P14.	2-(2-quinolinyl)-1H-indene--1,3(2H)-dione-6'-sulfonic acid	85-96	P53	Homo sapiens	37-40
32649952-5	2020	In the current study, based on 1H-15N HSQC NMR experiments and HADDOCK results, S100A4 interacts with the intrinsically unstructured transactivation domain (TAD) of the protein p53 and the pentamidine molecules in the presence of calcium ions.	15n	34-37	P53	Homo sapiens	177-180
35368662-12	2022	Further analysis showed that LGG patients with TP53 R273C mutation had higher M2 macrophage infiltration and tumor mutation burden (TMB) than that of TP53 wild-type LGG patients, and higher TMB indicates poor prognosis in LGG patients.	1,2,4,5-tetramethoxybenzene	132-135	P53	Homo sapiens	47-51
32978368-8	2020	Importantly, the antioxidant N-acetyl-cysteine and the p53 inhibitor pifithrin-alpha attenuated A1874-induced cell death and apoptosis in colon cancer cells.	pifithrin	69-84	P53	Homo sapiens	55-58
35368662-12	2022	Further analysis showed that LGG patients with TP53 R273C mutation had higher M2 macrophage infiltration and tumor mutation burden (TMB) than that of TP53 wild-type LGG patients, and higher TMB indicates poor prognosis in LGG patients.	1,2,4,5-tetramethoxybenzene	190-193	P53	Homo sapiens	47-51
32027454-7	2020	Dorsomorphin increased the production of intracellular reactive oxygen species (ROS) and induced ataxia telangiectasia mutated Ser1981 phosphorylation and p53 accumulation.	dorsomorphin	0-12	P53	Homo sapiens	155-158
35368662-13	2022	Furthermore, we identified genes which could be associated with higher M2 macrophage infiltration and TMB in LGG patients with TP53 R273C mutation.	1,2,4,5-tetramethoxybenzene	102-105	P53	Homo sapiens	127-131
35356272-13	2022	The frequency of TP53 mutation and copy number variation (CNV) were high in some LCGs.	lcgs	81-85	P53	Homo sapiens	17-21
35356282-5	2022	In some experiments, cells were pre-treated with rapamycin (an activator of autophagy), 3-MA (an inhibitor of autophagy), or cyclic pifithrin-alpha (PFT-alpha, an antagonist of p53), and then treated with AOPPs.	Pifithrin-Beta	125-147	P53	Homo sapiens	177-180
35204761-0	2022	Correlation of Occupational Exposure to Carcinogenic Polycyclic Aromatic Hydrocarbons (cPAHs) and Blood Levels of p53 and p21 Proteins.	cpahs	87-92	P53	Homo sapiens	114-117
32982737-0	2020	Theaflavin Induces Apoptosis of A375 Human Melanoma Cells and Inhibits Tumor Growth in Xenograft Zebrafishes Through P53- and JNK-Related Mechanism.	theaflavin	0-10	P53	Homo sapiens	117-120
35280362-10	2022	A higher TMB was significantly associated with TP53-MUTs in patients with LUAD but not in those with LUSC.	1,2,4,5-tetramethoxybenzene	9-12	P53	Homo sapiens	47-51
32822581-0	2020	Inositol Pyrophosphates Mediate the DNA-PK/ATM-p53 Cell Death Pathway by Regulating CK2 Phosphorylation of Tti1/Tel2.	inositol pyrophosphates	0-23	P53	Homo sapiens	47-50
32844143-0	2020	P53 is Subjected to Lipoteichoic Acid-Induced Phosphorylation in the Lungs.	lipoteichoic acid	20-37	P53	Homo sapiens	0-3
35242380-13	2022	The TMB value was significantly higher in those with P53 mutation than in P53 wild-type patients.	1,2,4,5-tetramethoxybenzene	4-7	P53	Homo sapiens	53-56
32884345-6	2020	Western blot analysis was used to detect the effect of allicin on the expression of intermediate-early gene 2 (IE2) and p53.	allicin	55-62	P53	Homo sapiens	120-123
32884345-12	2020	After treatment with allicin, p53 levels increased significantly, whereas expression of the inflammatory factors such as IL-6 and IFN-beta decreased.	allicin	21-28	P53	Homo sapiens	30-33
32884345-15	2020	Allicin also inhibited cytokine release, upregulated p53 activity, and increased the sensitivity of glioblastoma to radiotherapy.	allicin	0-7	P53	Homo sapiens	53-56
35242380-13	2022	The TMB value was significantly higher in those with P53 mutation than in P53 wild-type patients.	1,2,4,5-tetramethoxybenzene	4-7	P53	Homo sapiens	74-77
35005565-4	2022	Furthermore, TP53 mutation was more prevalent in smokers, and TP53-mutated tumor harbored more Massilia, as well as Acidovorax that was also capable of degrading PAH.	p-Aminohippuric Acid	162-165	P53	Homo sapiens	13-17
32823757-0	2020	Dietary Flavonoids in p53-Mediated Immune Dysfunctions Linking to Cancer Prevention.	Flavonoids	8-18	P53	Homo sapiens	22-25
32823757-8	2020	Recent studies have shown the ability of flavonoids to suppress chronic inflammation, specifically by modulating p53 responses.	Flavonoids	41-51	P53	Homo sapiens	113-116
35005565-4	2022	Furthermore, TP53 mutation was more prevalent in smokers, and TP53-mutated tumor harbored more Massilia, as well as Acidovorax that was also capable of degrading PAH.	p-Aminohippuric Acid	162-165	P53	Homo sapiens	62-66
33945996-8	2021	Additionally, the expression of these proteins can be reversed by the use of pifithrin-alpha (PFT-alpha), a p53 inhibitor.	pifithrin	77-92	P53	Homo sapiens	108-111
32417172-4	2020	Previously, we reported the tumor suppressor p53 could be O-GalNAc glycosylated in vitro.	o-galnac	58-66	P53	Homo sapiens	45-48
32417172-7	2020	Using mass spectrometry analysis and site-directed mutagenesis, we identified the glycosylated sites and studied the functions of O-GalNAc glycosylation on p53.	o-galnac	130-138	P53	Homo sapiens	156-159
32417172-10	2020	The O-GalNAc glycosylation at Ser121 was associated with the stability and activity of p53.	o-galnac	4-12	P53	Homo sapiens	87-90
32417172-11	2020	CONCLUSIONS: These results revealed that the O-GalNAc glycosylation was a novel modification on p53.	o-galnac	45-53	P53	Homo sapiens	96-99
32450254-0	2020	Oxygen-releasing Manganese clay Hybrid Complex triggers p53-mediated cancer cell death in hypoxia.	Manganese	17-26	P53	Homo sapiens	56-59
32664789-3	2020	Data from The Genomics of Drug Sensitivity in Cancer database showed that three drugs: (5Z)-7-oxozeaenol, dabrafenib and nutlin-3a (-), have shown more resistance in patients with TP53 mutation.	5-7-oxo-zeaenol	87-104	P53	Homo sapiens	180-184
32793462-8	2020	In the high-grade gliomas, the binary logistic regression revealed that the CHGMV can independently predict isocitrate dehydrogenase 1 (IDH1) and P53 mutations.	chgmv	76-81	P53	Homo sapiens	146-149
32628053-3	2022	OBJECTIVES: To evaluate the effectiveness of daylight photodynamic therapy (PDT) with methyl amino levulinate (MAL) based on clinical evaluation, histological examination and immunohistochemical expression of p53 and Ki67.	methyl amino levulinate	86-109	P53	Homo sapiens	209-212
32434944-8	2020	Complementing these data, we found that p53 deficiency or Bcl-2 overexpression reduced fluvastatin-induced apoptosis.	Fluvastatin	87-98	P53	Homo sapiens	40-43
32377702-0	2020	Juglone potentiates BRAF inhibitor-induced apoptosis in melanoma through reactive oxygen species and the p38-p53 pathway.	juglone	0-7	P53	Homo sapiens	109-112
32377702-7	2020	Moreover, juglone combined with PLX4032 markedly increased the intracellular level of reactive oxygen species (ROS) and activated p38 and p53, as compared with juglone alone or PLX4032 alone.	juglone	10-17	P53	Homo sapiens	138-141
32161142-6	2020	Tissue microarray (TMA) analysis identified a correlation between absent Rb and p53 expression and positive expression of Skp2.	tma	19-22	P53	Homo sapiens	80-83
32606738-9	2020	Moreover, a membrane-permeable N24 peptide enhanced p53-dependent apoptosis induced by methyl methanesulfonate.	Methyl Methanesulfonate	87-110	P53	Homo sapiens	52-55
32559584-2	2020	PURPOSE: We evaluated the cytotoxic potential of a naturally occurring N-acetylglycoside of oleanolic acid, aridanin, on 18 cancer cell lines, including sensitive and drug-resistant phenotypes mediated by P-glycoprotein, BCRP, p53 knockout, deletion-mutated EGFR, or BRAF mutations.	Oleanolic Acid	92-106	P53	Homo sapiens	227-230
32061892-7	2020	In general, cAT-stimulated ATM-dependent phosphorylation of Kap1 (Ser824) and p53 (Ser15) reflected best cAT-induced transcription blockage.	seryl-seryl-seryl-arginine	83-88	P53	Homo sapiens	78-81
32120128-3	2020	To strengthen the bioactivity of the scaffolds, pifithrin-alpha (PFTalpha), a p53 inhibitor that can reduce the repressive function of p53 in osteogenesis, was preloaded in the PLGA electrospinning solution.	pifithrin	48-63	P53	Homo sapiens	78-81
32120128-3	2020	To strengthen the bioactivity of the scaffolds, pifithrin-alpha (PFTalpha), a p53 inhibitor that can reduce the repressive function of p53 in osteogenesis, was preloaded in the PLGA electrospinning solution.	pifithrin	48-63	P53	Homo sapiens	135-138
32120128-3	2020	To strengthen the bioactivity of the scaffolds, pifithrin-alpha (PFTalpha), a p53 inhibitor that can reduce the repressive function of p53 in osteogenesis, was preloaded in the PLGA electrospinning solution.	pifithrin	65-73	P53	Homo sapiens	135-138
31488557-0	2020	Synergistic effects of PRIMA-1Met (APR-246) and Azacitidine in TP53-mutated myelodysplastic syndromes and acute myeloid leukemia.	Azacitidine	48-59	P53	Homo sapiens	63-67
31488557-1	2020	Myelodysplastic syndromes and acute myeloid leukemia with TP53 mutations are characterized by frequent relapses, poor or short responses, and poor survival with the currently available therapies including chemotherapy and 5-azacitidine.	Azacitidine	222-235	P53	Homo sapiens	58-62
31488557-3	2020	We show here that low doses of APR on its own or in combination with 5-azacitidine reactivate the p53 pathway and induce an apoptosis program.	Azacitidine	69-82	P53	Homo sapiens	98-101
31488557-4	2020	Functionally, we demonstrate that APR exerts these activities on its own and that it synergizes with 5-azacitidine in TP53-mutated Myelodysplastic syndromes / acute myeloid leukemia cell lines and in TP53-mutated primary cells from Myelodysplastic syndromes / acute myeloid leukemia patients.	Azacitidine	101-114	P53	Homo sapiens	118-122
32552932-8	2020	CONCLUSION: DHA can induce ROS production in Jurkat cells, which can cause DNA damage, activate the P53 apoptotic pathway, and promote apoptosis of cells.	artenimol	12-15	P53	Homo sapiens	100-103
32466567-2	2020	Thiamine diphosphate (ThDP, cocarboxylase) is an essential activator of the enzyme and inhibits p53-DNA binding in cancer cells.	Thiamine Pyrophosphate	0-20	P53	Homo sapiens	96-99
32466567-2	2020	Thiamine diphosphate (ThDP, cocarboxylase) is an essential activator of the enzyme and inhibits p53-DNA binding in cancer cells.	Thiamine Pyrophosphate	22-26	P53	Homo sapiens	96-99
32466567-5	2020	Molecular mechanisms of ThDP action on cellular viability and their interplay with the cisplatin and p53-p21 pathways are characterized.	Thiamine Pyrophosphate	24-28	P53	Homo sapiens	101-104
32466567-13	2020	High ThDP saturation of OGDHC compromises the redox state of A549 cells under the control of p53-p21 axes.	Thiamine Pyrophosphate	5-9	P53	Homo sapiens	93-96
32534357-10	2020	The apoptosis induced by EPI in MKN-45 cells would be effectively inhibited with the treatment of p53 siRNA and p53 inhibitor PFT-alpha.	pifithrin	126-135	P53	Homo sapiens	112-115
32457882-0	2020	beta-Elemene Reverses the Resistance of p53-Deficient Colorectal Cancer Cells to 5-Fluorouracil by Inducing Pro-death Autophagy and Cyclin D3-Dependent Cycle Arrest.	beta-elemene	0-12	P53	Homo sapiens	40-43
32457882-4	2020	This study aimed to investigate the effect of beta-elemene to 5-fluorouracil in drug-resistant p53-deficient colorectal cancer cells HCT116p53-/-, and determine the possible molecular mechanism of beta-elemene to reverse 5-fluorouracil resistance.	beta-elemene	46-58	P53	Homo sapiens	95-98
32457882-9	2020	Determine the role of Cyclin-related protein Cyclin D3 in beta-elemene reversing the resistance of HCT116p53-/- to 5-fluorouracil was detected by overexpression of Cyclin D3.	beta-elemene	58-70	P53	Homo sapiens	105-108
32457882-10	2020	The effect of beta-elemene on the tumorigenic ability of p53-deficient colorectal cancer cells was detected establishing HCT116p53-/- all line xenograft model.	beta-elemene	14-26	P53	Homo sapiens	57-60
32457882-12	2020	Conclusion: beta-elemene enhances the sensitivity of p53 wild-type cells to 5-fluorouracil, beta-elemene can reverse the resistance of HCT116p53-/- to 5-fluorouracil by inducing pro-death autophagy and Cyclin D3-dependent cycle arrest in p53-deficient colorectal cancer, which will provide a new method for the treatment of p53 deletion colorectal cancer patients.	beta-elemene	12-24	P53	Homo sapiens	53-56
32457882-12	2020	Conclusion: beta-elemene enhances the sensitivity of p53 wild-type cells to 5-fluorouracil, beta-elemene can reverse the resistance of HCT116p53-/- to 5-fluorouracil by inducing pro-death autophagy and Cyclin D3-dependent cycle arrest in p53-deficient colorectal cancer, which will provide a new method for the treatment of p53 deletion colorectal cancer patients.	beta-elemene	92-104	P53	Homo sapiens	141-144
32457882-12	2020	Conclusion: beta-elemene enhances the sensitivity of p53 wild-type cells to 5-fluorouracil, beta-elemene can reverse the resistance of HCT116p53-/- to 5-fluorouracil by inducing pro-death autophagy and Cyclin D3-dependent cycle arrest in p53-deficient colorectal cancer, which will provide a new method for the treatment of p53 deletion colorectal cancer patients.	beta-elemene	92-104	P53	Homo sapiens	141-144
32457882-12	2020	Conclusion: beta-elemene enhances the sensitivity of p53 wild-type cells to 5-fluorouracil, beta-elemene can reverse the resistance of HCT116p53-/- to 5-fluorouracil by inducing pro-death autophagy and Cyclin D3-dependent cycle arrest in p53-deficient colorectal cancer, which will provide a new method for the treatment of p53 deletion colorectal cancer patients.	beta-elemene	92-104	P53	Homo sapiens	141-144
32457871-3	2020	In this study, the Y220C-PhiKan5196 complex of p53 protein was adopted as a model, and the functions of three water molecules that formed hydrogen bonds with halogen atoms were analyzed by the simulation method governed by the hybrid quantum mechanical/molecular mechanical molecular dynamics.	Halogens	158-165	P53	Homo sapiens	47-50
32088177-5	2020	Mechanistically, BDMC attenuates cisplatin-induced apoptosis of renal tubular epithelial cells by inhibiting cisplatin-induced up-regulation of p53.	bisdemethoxycurcumin	17-21	P53	Homo sapiens	144-147
32123008-7	2020	Furthermore, protein stability and cell viability assays using two distinct proteasome inhibitor anticancer drugs, the 20S proteasome inhibitor bortezomib and the ubiquitin-activating enzyme E1 inhibitor TAK-243, show that the upregulation of the NRF3-POMP axis leads to ubiquitin-independent proteolysis of p53 and Rb and to impaired sensitivity to bortezomib but not TAK-243.	Bortezomib	144-154	P53	Homo sapiens	308-311
32325714-0	2020	Iron Oxide Nanoparticle-Induced Autophagic Flux Is Regulated by Interplay between p53-mTOR Axis and Bcl-2 Signaling in Hepatic Cells.	ferric oxide	0-10	P53	Homo sapiens	82-85
32112805-7	2020	In addition, ribavirin treatment (1, 5 and 10 muM) remarkably caused DNA damage which was shown by the increase of gammaH2AX-positive cells and upregulation of the p53 during the differentiation of hiPSCs from mesoderm to cardiac progenitor cells.	Ribavirin	13-22	P53	Homo sapiens	164-167
32112805-9	2020	In conclusion, our results suggest that ribavirin is detrimental in cardiac differentiation of hiPSCs, which may be associated with DNA damage, upregulated p53 and increased Gas5.	Ribavirin	40-49	P53	Homo sapiens	156-159
32017938-0	2020	Long non-coding RNA ROR confers arsenic trioxide resistance to HepG2 cells by inhibiting p53 expression.	Arsenic Trioxide	32-48	P53	Homo sapiens	89-92
32017938-4	2020	In this study, We found that cellular apoptosis was increased by arsenic trioxide in liver cancer HepG2 cells; P53 expression was also increased by arsenic trioxide at both mRNA level and protein level, indicating that P53-dependent apoptosis is the main mechanism for arsenic trioxide to induce cytotoxicity in liver cancer HepG2 cells.	Arsenic Trioxide	65-81	P53	Homo sapiens	219-222
32017938-4	2020	In this study, We found that cellular apoptosis was increased by arsenic trioxide in liver cancer HepG2 cells; P53 expression was also increased by arsenic trioxide at both mRNA level and protein level, indicating that P53-dependent apoptosis is the main mechanism for arsenic trioxide to induce cytotoxicity in liver cancer HepG2 cells.	Arsenic Trioxide	148-164	P53	Homo sapiens	111-114
32017938-4	2020	In this study, We found that cellular apoptosis was increased by arsenic trioxide in liver cancer HepG2 cells; P53 expression was also increased by arsenic trioxide at both mRNA level and protein level, indicating that P53-dependent apoptosis is the main mechanism for arsenic trioxide to induce cytotoxicity in liver cancer HepG2 cells.	Arsenic Trioxide	148-164	P53	Homo sapiens	219-222
32017938-4	2020	In this study, We found that cellular apoptosis was increased by arsenic trioxide in liver cancer HepG2 cells; P53 expression was also increased by arsenic trioxide at both mRNA level and protein level, indicating that P53-dependent apoptosis is the main mechanism for arsenic trioxide to induce cytotoxicity in liver cancer HepG2 cells.	Arsenic Trioxide	148-164	P53	Homo sapiens	111-114
32017938-4	2020	In this study, We found that cellular apoptosis was increased by arsenic trioxide in liver cancer HepG2 cells; P53 expression was also increased by arsenic trioxide at both mRNA level and protein level, indicating that P53-dependent apoptosis is the main mechanism for arsenic trioxide to induce cytotoxicity in liver cancer HepG2 cells.	Arsenic Trioxide	148-164	P53	Homo sapiens	219-222
32017938-7	2020	Through the knock-down of long non-coding RNA ROR by siRNA, we revealed that the activated long non-coding RNA ROR ameliorated arsenic trioxide-induced apoptosis by inhibiting P53 expression.	Arsenic Trioxide	127-143	P53	Homo sapiens	176-179
32017938-8	2020	Together, our study reported that long non-coding RNA ROR conferred arsenic trioxide resistance to liver cancer cells through inhibiting P53 expression, and long non-coding RNA ROR might be a novel sensitizing target for liver cancer treatment.	Arsenic Trioxide	68-84	P53	Homo sapiens	137-140
32147288-0	2020	Helveticoside Exhibited p53-dependent Anticancer Activity Against Colorectal Cancer.	helveticoside	0-13	P53	Homo sapiens	24-27
32147288-8	2020	Besides, using p53-knockout SW480 cells, the cytotoxic action of helveticoside was found to be p53-dependent.	helveticoside	65-78	P53	Homo sapiens	15-18
32147288-8	2020	Besides, using p53-knockout SW480 cells, the cytotoxic action of helveticoside was found to be p53-dependent.	helveticoside	65-78	P53	Homo sapiens	95-98
32218859-6	2020	In the present study, CP-31398, a p53-restoring agent, was used to improve the therapeutic efficacy of sorafenib in SW579 cells, an ATC cell line harboring p53 mutations.	Sorafenib	103-112	P53	Homo sapiens	34-37
32218859-6	2020	In the present study, CP-31398, a p53-restoring agent, was used to improve the therapeutic efficacy of sorafenib in SW579 cells, an ATC cell line harboring p53 mutations.	Sorafenib	103-112	P53	Homo sapiens	156-159
32235536-0	2020	Galangin, a Flavonoid from Lesser Galangal, Induced Apoptosis via p53-Dependent Pathway in Ovarian Cancer Cells.	Flavonoids	12-21	P53	Homo sapiens	66-69
32219038-9	2020	At molecular levels, cell cycle regulators cyclin D1, CDK4, CDK6, p21 and p53 were modulated in response to treatment with ICA.	icariin	123-126	P53	Homo sapiens	74-77
32256964-8	2020	As expected, an upregulation of p53 was observed after DpdtC insulting; however, the addition of a p53 inhibitor, PFT-alpha, could significantly attenuate the action of DpdtC on ferritinophagy induction and EMT inhibition.	pifithrin	114-123	P53	Homo sapiens	32-35
32256964-8	2020	As expected, an upregulation of p53 was observed after DpdtC insulting; however, the addition of a p53 inhibitor, PFT-alpha, could significantly attenuate the action of DpdtC on ferritinophagy induction and EMT inhibition.	pifithrin	114-123	P53	Homo sapiens	99-102
32001619-4	2020	Recently, we showed that KRAS depletion leads to P53 Ser-15 phosphorylation (P-P53) and increases the levels of P53 and its target P21/wild-type P53-activated fragment 1 (WAF1)/CIP1.	seryl-seryl-seryl-arginine	53-56	P53	Homo sapiens	49-52
32001619-4	2020	Recently, we showed that KRAS depletion leads to P53 Ser-15 phosphorylation (P-P53) and increases the levels of P53 and its target P21/wild-type P53-activated fragment 1 (WAF1)/CIP1.	seryl-seryl-seryl-arginine	53-56	P53	Homo sapiens	79-82
32138264-3	2020	Oncosuppressor TP53 may undergo inactivation following missense mutations within the DNA-binding domain (DBD), and mutant p53 (mutp53) proteins may acquire a misfolded conformation, often due to the loss of the DBD-bound zinc ion, leading to accumulation of hyperstable mutp53 proteins that correlates with more aggressive tumors, resistance to therapies, and poorer outcomes.	dbd	105-108	P53	Homo sapiens	15-19
32117586-3	2020	We investigated treatment response and resistance to AZD8055, an inhibitor of mammalian target of rapamycin (mTOR), in the K14-cre;Cdh1Flox/Flox;Trp53Flox/Flox (KEP) mouse model of metastatic ILC.	(5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol	53-60	P53	Homo sapiens	145-150
31665708-8	2020	Our results suggested ZH-BCDp-CPT inclusion complex induced cell apoptosis by up-regulation of Bax and P53 and down-regulation of Bcl-2, primarily involved in the mitochondrial pathways.	zh-bcdp	22-29	P53	Homo sapiens	103-106
32012207-0	2020	Retraction: Bak Compensated for Bax in p53-null Cells to Release Cytochrome c for the Initiation of Mitochondrial Signaling during Withanolide D-Induced Apoptosis.	withanolide D	131-144	P53	Homo sapiens	39-42
31631444-10	2020	Furthermore, the expressions of senescence markers, such as p21 and p53, were upregulated upon bleomycin treatment, thereby intensifying the fibrotic condition.	Bleomycin	95-104	P53	Homo sapiens	68-71
30856053-2	2020	The present study aimed to evaluate the interaction of saccharin (SA) and sodium saccharin (SSA) with the promoter of the human p53 gene.	Saccharin	55-64	P53	Homo sapiens	128-131
30856053-2	2020	The present study aimed to evaluate the interaction of saccharin (SA) and sodium saccharin (SSA) with the promoter of the human p53 gene.	Saccharin	66-68	P53	Homo sapiens	128-131
30856053-2	2020	The present study aimed to evaluate the interaction of saccharin (SA) and sodium saccharin (SSA) with the promoter of the human p53 gene.	Saccharin	74-90	P53	Homo sapiens	128-131
30856053-2	2020	The present study aimed to evaluate the interaction of saccharin (SA) and sodium saccharin (SSA) with the promoter of the human p53 gene.	Saccharin	92-95	P53	Homo sapiens	128-131
30856053-12	2020	This study could provide valuable insight into the binding mechanism of SA and its salt with p53 gene promoter as macromolecule at the molecular level in atomistic details.	Saccharin	72-74	P53	Homo sapiens	93-96
31689165-0	2020	Re: Dysregulation of p53-RBM25-Mediated circAMOTL1L Biogenesis Contributes to Prostate Cancer Progression through the circAMOTL1L-miR-193a-5p-Pcdha Pathway.	Rhenium	0-2	P53	Homo sapiens	21-24
31112799-6	2020	A role of cytoplasmic p53 in autophagy, pentose phosphate pathway, fatty acid synthesis and oxidation, and drug response has been proposed.	Pentosephosphates	40-57	P53	Homo sapiens	22-25
31707831-13	2020	Torin1 treatment increased protein expression of p53, and these effects were inhibited by pifithrin-alpha.	pifithrin	90-105	P53	Homo sapiens	49-52
31974452-0	2020	Pifithrin-alpha alters p53 post-translational modifications pattern and differentially inhibits p53 target genes.	pifithrin	0-15	P53	Homo sapiens	23-26
31974452-0	2020	Pifithrin-alpha alters p53 post-translational modifications pattern and differentially inhibits p53 target genes.	pifithrin	0-15	P53	Homo sapiens	96-99
31974452-1	2020	Pifithrin-alpha (PFT-alpha) is a small molecule which has been widely used as a specific inhibitor of p53 transcription activity.	pifithrin	0-15	P53	Homo sapiens	102-105
31974452-1	2020	Pifithrin-alpha (PFT-alpha) is a small molecule which has been widely used as a specific inhibitor of p53 transcription activity.	pifithrin	17-26	P53	Homo sapiens	102-105
31974452-3	2020	PFT-alpha has also been described to display potent p53-independent activity in cells.	pifithrin	0-9	P53	Homo sapiens	52-55
31974452-7	2020	PFT-alpha displayed a very limited effect on p53-dependent transcription upon its activation by Nutlin-3.	pifithrin	0-9	P53	Homo sapiens	45-48
31974452-8	2020	Moreover, PFT-alpha inhibitory effect on transcription was highly dependent on the nature of the p53 target gene.	pifithrin	10-19	P53	Homo sapiens	97-100
31974452-9	2020	PFT-alpha attenuated post-translational modifications of p53 without affecting total p53 protein level.	pifithrin	0-9	P53	Homo sapiens	57-60
31974452-10	2020	Finally, we found that PFT-alpha can decrease the level of intracellular reactive oxygen species through activation of an aryl hydrocarbon receptor (AHR)-Nrf2 axis in a p53-independent manner.	pifithrin	23-32	P53	Homo sapiens	169-172
31974452-11	2020	In conclusion, PFT-alpha inhibits only some aspects of p53 function, therefore it should be used with extreme caution to study p53-dependent processes.	pifithrin	15-24	P53	Homo sapiens	55-58
31974452-11	2020	In conclusion, PFT-alpha inhibits only some aspects of p53 function, therefore it should be used with extreme caution to study p53-dependent processes.	pifithrin	15-24	P53	Homo sapiens	127-130
31935871-7	2020	NPs of manganese (Mn and Mn3O4) induced the most remarkable ToxTracker response with activation of reporters for oxidative stress, DNA damage, protein unfolding and p53-related stress.	Manganese	7-16	P53	Homo sapiens	165-168
31733192-7	2020	Moreover, decreased phosphorylation of p53(Ser15) and NFkappaB(Ser536) was required for GV-induced cell death.	seryl-seryl-seryl-arginine	43-48	P53	Homo sapiens	39-42
32401925-4	2020	Results demonstrated that beta-elemene+paclitaxel induced apoptosis of SKOV3 cells, down-regulated anti-apoptotic Bcl-2 and Bcl-xl gene expression and up-regulated pro-apoptotic P53 and Apaf1 gene expression in SKOV3 cells.	beta-elemene	26-38	P53	Homo sapiens	178-181
31548614-7	2020	Disruption of DBT severely attenuates ERK/MAPK signaling, p53 activation, and apoptosis in melanocytes, at least in part due to accumulation of branched chain alpha-keto acids.	Keto Acids	159-175	P53	Homo sapiens	58-61
31911865-10	2019	Similarly, an MDM2 inhibitor, AMG-232, which induces p53 is active in early clinical trials of both liquid and advanced solid tumor patients.	2-(5-(3-chlorophenyl)-6-(4-chlorophenyl)-1-(1-(isopropylsulfonyl)-3-methylbutan-2-yl)-3-methyl-2-oxopiperidin-3-yl)acetic acid	30-37	P53	Homo sapiens	53-56
31335355-13	2019	Abnormal p53 status was associated with advanced Federation of Gynecology and Obstetrics stage, lymph node metastases, DFS and DSS (P<0.05, Fisher exact test).	dss	127-130	P53	Homo sapiens	9-12
31617338-0	2019	Dephosphorylation of p53 Ser 392 Enhances Trimethylation of Histone H3 Lys 9 via SUV39h1 Stabilization in CK2 Downregulation-Mediated Senescence.	seryl-seryl-seryl-arginine	25-28	P53	Homo sapiens	21-24
31617338-6	2019	Moreover, the dephosphorylation status of Ser 392 on p53, a possible CK2 target site, enhances the nuclear import and subsequent stabilization of SUV39h1 by inhibiting the interactions between p53, MDM2, and SUV39h1.	seryl-seryl-seryl-arginine	42-45	P53	Homo sapiens	53-56
31617338-6	2019	Moreover, the dephosphorylation status of Ser 392 on p53, a possible CK2 target site, enhances the nuclear import and subsequent stabilization of SUV39h1 by inhibiting the interactions between p53, MDM2, and SUV39h1.	seryl-seryl-seryl-arginine	42-45	P53	Homo sapiens	193-196
31617338-7	2019	Furthermore, p21Cip1/WAF1 is required for CK2 downregulation-mediated H3K9me3, and dephosphorylation of Ser 392 on p53 is important for efficient transcription of p21 Cip1/WAF1.	seryl-seryl-seryl-arginine	104-107	P53	Homo sapiens	115-118
31617338-8	2019	Taken together, these results suggest that CK2 downregulation induces dephosphorylation of Ser 392 on p53, which subsequently increases the stability of SUV39h1 and the expression of p21Cip1/WAF1, leading to H3K9me3 and SAHFs formation.	seryl-seryl-seryl-arginine	91-94	P53	Homo sapiens	102-105
31586554-0	2019	ERp29 inhibition attenuates TCA toxicity via affecting p38/p53- dependent pathway in human trophoblast HTR-8/SVeno cells.	Taurocholic Acid	28-31	P53	Homo sapiens	59-62
31827702-1	2019	A flavonoid antioxidant quercetin promotes dose-dependent activation of the ATM-CHK-p53 pathway, downregulation of antiapoptotic survivin, and upregulation of proapoptotic NOXA in human T cell acute lymphoblastic leukemia Jurkat clones (J/Neo and J/BCL-XL).	Flavonoids	2-11	P53	Homo sapiens	84-87
31827702-1	2019	A flavonoid antioxidant quercetin promotes dose-dependent activation of the ATM-CHK-p53 pathway, downregulation of antiapoptotic survivin, and upregulation of proapoptotic NOXA in human T cell acute lymphoblastic leukemia Jurkat clones (J/Neo and J/BCL-XL).	Quercetin	24-33	P53	Homo sapiens	84-87
31541852-5	2019	Presence of GMG-ITC prior to development of oxidative stress condition, downregulated the expression of cyt-c, p53, Apaf-1, Bax, CASP3, CASP8 and CASP9 genes with concurrent upregulation of Bcl-2 gene in mitochondrial apoptotic signalling pathway.	Isothiocyanates	12-19	P53	Homo sapiens	111-114
31541852-6	2019	Protein Multiplex revealed significant decreased in cyt-c, p53, Apaf-1, Bax, CASP8 and CASP9 due to GMG-ITC pre-treatment in oxidative stress condition.	Isothiocyanates	100-107	P53	Homo sapiens	59-62
30728460-4	2019	We found that 5-azacytidine (5-aza-CR) induces LOXL4 upregulation, with LOXL4 subsequently binding the basic domain of p53 via its low-isoelectric point region.	Azacitidine	14-27	P53	Homo sapiens	119-122
30728460-4	2019	We found that 5-azacytidine (5-aza-CR) induces LOXL4 upregulation, with LOXL4 subsequently binding the basic domain of p53 via its low-isoelectric point region.	Azacitidine	29-37	P53	Homo sapiens	119-122
30728460-8	2019	In conclusion, we found that 5-aza-CR-induced LOXL4 upregulation reactivates wild-type p53 and triggers cell death, which blocks liver cancer development.	Azacitidine	29-37	P53	Homo sapiens	87-90
31492752-2	2019	To examine the biochemical reaction in vitro, we established an efficient reconstitution system for the polyubiquitination of p53 by the E6AP-E6 complex.	Polyurethane Y-290	137-139	P53	Homo sapiens	126-129
31601054-6	2019	Furthermore, the effects of cell cycle arrest and apoptosis in A549 cells which were induced by actinomycin V could be reversed by the pifithrin-alpha, a specific inhibitor of p53 transcriptional activity.	pifithrin	135-150	P53	Homo sapiens	176-179
27025925-6	2019	Caspase-3 inhibitor (Ac-DEVD-CHO at concentrations between 10 to 20 mumol/L), p53 inhibitor (pifithrin-alpha at 5 mumol/L) and cyclosporin A can attenuate the apoptotic effect of psoralidin.	pifithrin	93-108	P53	Homo sapiens	78-81
31234033-6	2019	Alternatively, lapatinib amplified signals of TP53 gene effectively by raising the concentration.	Lapatinib	15-24	P53	Homo sapiens	46-50
31880513-4	2019	In this study, we determined the effect of Fentanyl on PANC-1 cells, by assessing the gene expression of cancer stem cell marker genes (Nanog, Oct4, and Sox2) and apoptosis-related genes (BAD, Bax, Bcl-2, and p53) by Quantitative RealTime PCR.	Fentanyl	43-51	P53	Homo sapiens	209-212
31283929-0	2019	ROS -mediated p53 activation by juglone enhances apoptosis and autophagy in vivo and in vitro.	juglone	32-39	P53	Homo sapiens	14-17
31482012-2	2019	In addition to doxorubicin, our results here indicated that camptothecin and bortezomib, which are a topoisomerase 1 poison and a 26 S proteasome inhibitor, respectively, could also induce apoptosis in a p53-dependent manner in prostate cancer.	Bortezomib	77-87	P53	Homo sapiens	204-207
31482012-5	2019	In contrast, p53-mediated apoptosis from bortezomib-induced stress is transcription-dependent.	Bortezomib	41-51	P53	Homo sapiens	13-16
31482012-7	2019	We then investigated the p53 ratio of nucleus to cytosol corresponding to low and high dose doxorubicin, camptothecin, or bortezomib treatment.	Bortezomib	122-132	P53	Homo sapiens	25-28
31388677-7	2019	Even when more abundantly present than after exposure to the radiomimetic bleomycin, Cr(VI)-stabilized p53 showed a much more limited activation of its target genes in two types of primary human cells.	Bleomycin	74-83	P53	Homo sapiens	103-106
31383247-6	2019	Regarding the underlying mechanisms, results showed that DHA induced cellular senescence by up-regulating expression levels of proteins such as p-ATM, p-ATR, gamma-H2AX, P53, and P21 involved in DNA damage response.	artenimol	57-60	P53	Homo sapiens	170-173
30981936-10	2019	These results suggest that aryl-PFRs (e.g., BDP, MDPP, CDP) cause oxidative stress-mediated DNA damage and mitochondrial impairment, and p53-dependent pathway was involved in the aryl-PFRs-induced DNA damage and cell cycle arrest.	diphenyl methyl phosphate	49-53	P53	Homo sapiens	137-140
31181622-4	2019	Albendazole and fenbendazole, two approved and commonly used benzimidazole anthelmintics, stimulated p53 activity and were selected for further studies.	Albendazole	0-11	P53	Homo sapiens	101-104
31181622-5	2019	The protein levels of p53 and p21 increased upon the treatment with albendazole and fenbendazole, indicating activation of the p53-p21 pathway, while the levels of Mdm2 and MdmX decreased in melanoma and breast cancer cells overexpressing these proteins.	Albendazole	68-79	P53	Homo sapiens	22-25
31181622-5	2019	The protein levels of p53 and p21 increased upon the treatment with albendazole and fenbendazole, indicating activation of the p53-p21 pathway, while the levels of Mdm2 and MdmX decreased in melanoma and breast cancer cells overexpressing these proteins.	Albendazole	68-79	P53	Homo sapiens	127-130
30921731-5	2019	Importantly, LProd potently inhibited tumor growth in a mouse model of human colon cancer through activating tumor suppressor protein p53 via MDM2/MDMX antagonism, while maintaining a highly favorable biosafety profile.	lprod	13-18	P53	Homo sapiens	134-137
30958996-0	2019	Quercetin enhances the antitumor activity of trichostatin A through up-regulation of p300 protein expression in p53 null cancer cells.	Quercetin	0-9	P53	Homo sapiens	112-115
30958996-1	2019	In the present study, we investigated the p53-independent mechanism by which quercetin (Q) increased apoptosis in human lung cancer H1299 cells exposed to trichostatin A (TSA), a histone deacetylase inhibitor.	Quercetin	77-86	P53	Homo sapiens	42-45
30853612-10	2019	More experiments showed GRh2-induced alterations of p53, phospho (p)-PI3K, p-AKT and p-mTOR were all reversed by miR-638 overexpression.	ginsenoside Rh2	24-28	P53	Homo sapiens	52-55
31039479-0	2019	Protective effects of novel derivatives of vitamin D3 and lumisterol against UVB-induced damage in human keratinocytes involve activation of Nrf2 and p53 defense mechanisms.	Ergosterol	58-68	P53	Homo sapiens	150-153
31041982-3	2019	In addition, compounds 14d-f, 14h and 14k are able to increase the p53 expression levels, activating also the apoptotic pathway.	N-[(1R,3R)-3-hydroxy-1-(hydroxymethyl)-3-phenylpropyl]tetradecanamide	30-33	P53	Homo sapiens	67-70
30802707-5	2019	Molecular modeling revealed that the compound 4d binds through hydrophobic-hydrophobic interactions with the essential amino acids (LEU: 57, GLY: 58, ILE: 61, and HIS: 96) in the p53-binding cleft, as a standard p53-MDM2 inhibitor (6SJ).	Leucine	132-135	P53	Homo sapiens	179-182
30924710-0	2019	Glyceollins Modulate Tumor Development and Growth in a Mouse Xenograft Model of Human Colon Cancer in a p53-Dependent Manner.	glyceollin	0-11	P53	Homo sapiens	104-107
30924710-5	2019	A high dose of glyceollins resulted in a significant increase in the average volume of p53 wild-type HCT116 xenografts, but not of p53 null HCT116 xenografts.	glyceollin	15-26	P53	Homo sapiens	87-90
30924710-7	2019	Interestingly, antioxidant enzymes, including heme oxygenase-1 (HO-1) and NAD(P)H: quinone oxidoreductase, were prominently induced by glyceollins in p53 wild-type xenografts, compared with p53 null xenografts.	glyceollin	135-146	P53	Homo sapiens	150-153
30924710-7	2019	Interestingly, antioxidant enzymes, including heme oxygenase-1 (HO-1) and NAD(P)H: quinone oxidoreductase, were prominently induced by glyceollins in p53 wild-type xenografts, compared with p53 null xenografts.	glyceollin	135-146	P53	Homo sapiens	190-193
30924710-8	2019	These results suggest that a high dose of glyceollins possibly promotes the growth of p53 wild-type colon cancer through activation of the Nrf2-mediated signaling pathway and, in particular, strong induction of HO-1 expression.	glyceollin	42-53	P53	Homo sapiens	86-89
30553920-7	2019	Our results indicate that the combined effect of pairwise PAHs of BaP with Benzo[b]fluoranthene (BbF) and Benz[a]anthracene (BaA) is synergistic on p53 pathway, and that the health risk of the such mixtures increases compared to that of the individual ones.	Polycyclic Aromatic Hydrocarbons	58-62	P53	Homo sapiens	148-151
30948782-8	2019	In this situation of metabolic stress, 17-AAG induces the binding of p53-R248Q to Hsc70 and the activation of Chaperone-Mediated Autophagy (CMA), leading to higher R248Q degradation than in non-stress conditions.	tanespimycin	39-45	P53	Homo sapiens	69-72
31001122-0	2019	Alkylaminophenol Induces G1/S Phase Cell Cycle Arrest in Glioblastoma Cells Through p53 and Cyclin-Dependent Kinase Signaling Pathway.	alkylaminophenol	0-16	P53	Homo sapiens	84-87
30936194-1	2019	KRAS G12D-mutant/p53-deficient non-small-cell lung cancer (NSCLC) models are dependent on the NF-kappaB pathway that can be down-regulated by the proteasome inhibitor bortezomib.	Bortezomib	167-177	P53	Homo sapiens	17-20
30883017-7	2019	In addition, delanzomib enhanced the Dox-induced phosphorylation of p38/JNK and the expression of transcriptional target proteins of p53, such as p21, p27, NOXA, and PUMA.	delanzomib	13-23	P53	Homo sapiens	133-136
30739913-6	2019	The clinical interest of the mechanism identified is underlined by our finding that p53 is activated in mastectomy patients undergoing intraoperative ketorolac, a treatment associated with decreased relapse risk and increased survival.	Ketorolac	150-159	P53	Homo sapiens	84-87
30554133-0	2019	In HPV-Positive HNSCC Cells, Functional Restoration of the p53/p21 Pathway by Proteasome Inhibitor Bortezomib Does Not Affect Radio- or Chemosensitivity.	Bortezomib	99-109	P53	Homo sapiens	59-62
30554133-6	2019	In HPV+ cells, BZM also restored the radiation-induced p53/p21 transactivation.	Bortezomib	15-18	P53	Homo sapiens	55-58
30808373-5	2019	METHODS: We used bioinformatics and molecular docking tools to investigate the structural changes between the wild type and mutant p53 proteins (p53V143A, p53R249S, p53R273H and p53Y220C) and explored the therapeutic potential of Withaferin A and Withanone for restoration of wild type p53 function in cancer cells.	withaferin A	230-242	P53	Homo sapiens	131-134
30808373-7	2019	RESULTS: We found that p53V143A mutation does not show any significant structural changes and was also refractory to the binding of withanolides.	Withanolides	132-144	P53	Homo sapiens	23-26
30808373-12	2019	Using human cell lines containing specific p53 mutant proteins, we demonstrated that Withaferin A, Withanone and the extract rich in these withanolides caused restoration of wild type p53 function in mutant p53Y220C cells.	withaferin A	85-97	P53	Homo sapiens	43-46
30808373-12	2019	Using human cell lines containing specific p53 mutant proteins, we demonstrated that Withaferin A, Withanone and the extract rich in these withanolides caused restoration of wild type p53 function in mutant p53Y220C cells.	withaferin A	85-97	P53	Homo sapiens	184-187
30808373-12	2019	Using human cell lines containing specific p53 mutant proteins, we demonstrated that Withaferin A, Withanone and the extract rich in these withanolides caused restoration of wild type p53 function in mutant p53Y220C cells.	Withanolides	139-151	P53	Homo sapiens	43-46
30808373-12	2019	Using human cell lines containing specific p53 mutant proteins, we demonstrated that Withaferin A, Withanone and the extract rich in these withanolides caused restoration of wild type p53 function in mutant p53Y220C cells.	Withanolides	139-151	P53	Homo sapiens	184-187
30813396-7	2019	On the other hand, the treatment with SFN alone seemed to exert a protective effect, increasing the level of p53, which can block the expansion of possible DNA damaged cells.	sulforaphane	38-41	P53	Homo sapiens	109-112
30834235-9	2019	Furthermore, co-treatment with IO and UCN-01 significantly increased cell death in primary cells expressing mutant p53.	7-hydroxystaurosporine	38-44	P53	Homo sapiens	115-118
30605652-9	2019	CAA45 also inhibited Akt, activated JNK and up-regulated p53 signals in A549 cells, which may serve as a modulator to induce apoptosis and autophagy in cancer cells.	caa45	0-5	P53	Homo sapiens	57-60
30741995-5	2019	p21 and PAI-1, which are two p53 downstream targets critical for senescence, were significantly induced in SK-N-SH cells subjected to either PRMT1-KD or inhibitor treatment.	sk-n	107-111	P53	Homo sapiens	29-32
30543781-7	2019	TCCP treatment caused endogenous ROS generation, increase in intracellular calcium and phosphorylation of p53 in a concentration-dependent manner, which was reverted upon pre-treatment with pifithrin-mu.	pifithrin	190-199	P53	Homo sapiens	106-109
30472223-0	2019	Pifithrin-alpha enhancing anticancer effect of topotecan on p53-expressing cancer cells.	pifithrin	0-9	P53	Homo sapiens	60-63
30472223-3	2019	In this study, pifithrin-alpha (PFTalpha), a p53 inhibitor, was used 2 h before treated with TPT on three kinds of cancer cell lines including MCF7, BGC823 and HepG2 cells.	pifithrin	15-30	P53	Homo sapiens	45-48
30472223-3	2019	In this study, pifithrin-alpha (PFTalpha), a p53 inhibitor, was used 2 h before treated with TPT on three kinds of cancer cell lines including MCF7, BGC823 and HepG2 cells.	pifithrin	32-40	P53	Homo sapiens	45-48
30472223-5	2019	It was demonstrated that PFTalpha decreases the p-p53 levels and p-p53 activity, not affects p53 expression in p53 positive tumor cells.	pifithrin	25-33	P53	Homo sapiens	50-53
30472223-5	2019	It was demonstrated that PFTalpha decreases the p-p53 levels and p-p53 activity, not affects p53 expression in p53 positive tumor cells.	pifithrin	25-33	P53	Homo sapiens	67-70
30472223-5	2019	It was demonstrated that PFTalpha decreases the p-p53 levels and p-p53 activity, not affects p53 expression in p53 positive tumor cells.	pifithrin	25-33	P53	Homo sapiens	67-70
30472223-5	2019	It was demonstrated that PFTalpha decreases the p-p53 levels and p-p53 activity, not affects p53 expression in p53 positive tumor cells.	pifithrin	25-33	P53	Homo sapiens	67-70
30472223-8	2019	Secondly, PFTalpha decreased formation of p53/mdm2 complex responsible for p53 degradation by inhibiting the protein expression of mdm2, so p53 degradation was decreased in cytoplasm and p53 accumulation was increased in nucleus, which induced more cells undergo apoptosis.	pifithrin	10-18	P53	Homo sapiens	42-45
30472223-8	2019	Secondly, PFTalpha decreased formation of p53/mdm2 complex responsible for p53 degradation by inhibiting the protein expression of mdm2, so p53 degradation was decreased in cytoplasm and p53 accumulation was increased in nucleus, which induced more cells undergo apoptosis.	pifithrin	10-18	P53	Homo sapiens	75-78
30350349-5	2019	Concurrent TP53 mutations and NFIB overexpression (z-scores &gt; 0) were observed in 77.9% of TNBCs, in contrast to 28.5% in non-TNBCs.	tnbcs	94-99	P53	Homo sapiens	11-15
30350349-6	2019	Depletion of NFIB in TP53-mutated TNBC cell lines promotes cell death, cell cycle arrest, and enhances sensitivity to docetaxel, a first-line chemotherapeutic drug in breast cancer treatment.	Docetaxel	118-127	P53	Homo sapiens	21-25
30458062-0	2019	Targeted Synthesis of Complex Spiro[3H-indole-3,2"-pyrrolidin]-2(1H)-ones by Intramolecular Cyclization of Azomethine Ylides: Highly Potent MDM2-p53 Inhibitors.	spiro(3H-indole-3,2'-pyrrolidin)-2(1H)-one	30-73	P53	Homo sapiens	145-148
29911263-0	2019	Novel Competitive Chemiluminescence DNA Assay Based on Fe3O4@SiO2@Au-Functionalized Magnetic Nanoparticles for Sensitive Detection of p53 Tumor Suppressor Gene.	ferryl iron	55-60	P53	Homo sapiens	134-137
29911263-1	2019	A simple, rapid response time and ultrahigh sensitive chemiluminescence (CL) DNA assay based on Fe3O4@SiO2@Au-functionalized magnetic nanoparticles (Au-MNPs) was developed for detection of p53 tumor suppressor gene.	ferryl iron	96-101	P53	Homo sapiens	189-192
29911263-2	2019	In this study, 2",6"-dimethylcarbonylphenyl-10-sulfopropyl acridinium-9-carboxylate 4"-NHS ester (NSP-DMAE-NHS), as a new kind of highly efficient luminescence reagent, was immobilized on the complementary sequence of the wild-type p53 (ssDNA) to improve the detection sensitivity.	2",6"-dimethylcarbonylphenyl-10-sulfopropyl acridinium-9-carboxylate 4"-nhs ester	15-96	P53	Homo sapiens	232-235
30551455-8	2019	Suppressing p53 expressions with its inhibitor, PFTalpha, blocked apoptotic response in JMJD5-silenced cells.	pifithrin	48-56	P53	Homo sapiens	12-15
30661409-1	2019	Quercetin, an antioxidant flavonoid, has been known that it can induce the cell cycle arrest and apoptosis of hepatocellular carcinoma (HCC) cells by the stabilization or induction of p53.	Quercetin	0-9	P53	Homo sapiens	184-187
30661409-1	2019	Quercetin, an antioxidant flavonoid, has been known that it can induce the cell cycle arrest and apoptosis of hepatocellular carcinoma (HCC) cells by the stabilization or induction of p53.	Flavonoids	26-35	P53	Homo sapiens	184-187
30661409-6	2019	This study demonstrates that the antiproliferative effect of quercetin on HCC cells can be mediated by reducing intracellular ROS, which is independent of p53 expression.	Quercetin	61-70	P53	Homo sapiens	155-158
30103008-11	2018	Both p53 inhibitor pifithrin-alpha and p53 siRNA significantly rescued costunolide suppression of GLS1 promoter activity and expression in HCT116 cells.	pifithrin	19-34	P53	Homo sapiens	5-8
30010803-0	2018	Selective killing of human breast cancer cells by the styryl lactone (R)-goniothalamin is mediated by glutathione conjugation, induction of oxidative stress and marked reactivation of the R175H mutant p53 protein.	styryl lactone	54-68	P53	Homo sapiens	201-204
30513611-9	2018	Additionally, 11-dehydrosinulariolide caused the accumulation of p53 and Bax, accompanied by the activation of DNA damage-inducing kinases, including ataxia-telangiectasia mutated (ATM) and checkpoint kinase 2 (CHK2).	11-dehydrosinulariolide	14-37	P53	Homo sapiens	65-68
30513611-13	2018	Together, the data indicate that 11-dehydrosinulariolide induces G (2)/M cell cycle arrest and apoptosis through various cellular processes, including the upregulation of p53 and Bax, activation of ATM and Chk2, activation of caspase-3 and -7, and accumulation of PTEN, leading to inhibition of the Akt pathway.	11-dehydrosinulariolide	33-56	P53	Homo sapiens	171-174
30420502-3	2018	Here we apply trans-intein splicing to generate segmentally 15N-labeled full-length p53 constructs in which only the resonances of the N-terminal transactivation domain (NTAD) are visible in NMR spectra, allowing us to observe this region of p53 with unprecedented detail within the tetramer.	15n	60-63	P53	Homo sapiens	84-87
30207732-6	2018	By eliminating the Ssd-induced increase of JNK/pJNK, additional SP600125 weakened the Ssd-induced apoptotic axis of TGFalpha-JNK-p53 and simultaneously abolished Ssd-induced apoptosis; (2) Ssd inhibited proliferation by the activation of two axes, TGFbeta-p53/p21/p27/p15/p16 and TGFalpha-Rassfia-cyclin D1.	pyrazolanthrone	64-72	P53	Homo sapiens	129-132
30207732-6	2018	By eliminating the Ssd-induced increase of JNK/pJNK, additional SP600125 weakened the Ssd-induced apoptotic axis of TGFalpha-JNK-p53 and simultaneously abolished Ssd-induced apoptosis; (2) Ssd inhibited proliferation by the activation of two axes, TGFbeta-p53/p21/p27/p15/p16 and TGFalpha-Rassfia-cyclin D1.	pyrazolanthrone	64-72	P53	Homo sapiens	256-259
30226534-10	2018	Sulforaphane inhibited multiple cancer-associated signaling pathways, including B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein, cytochrome c, Caspase-3, phosphorylated AKT, phosphorylated nuclear factor-kappaB, P53, P27, Cyclin-D1 and cMyc, and reduced the expression levels of human epidermal growth factor receptor 2 in human ovarian cancer cells.	sulforaphane	0-12	P53	Homo sapiens	218-221
29648492-0	2018	Azacitidine effectively reduces TP53-mutant leukemic cell burden in secondary acute myeloid leukemia after cord blood transplantation.	Azacitidine	0-11	P53	Homo sapiens	32-36
30303965-4	2018	Biological methods demonstrated the oxidative damage of P19 neurons and showed that quercetin improved neuronal survival by preventing H2O2-induced p53 and Bcl-2 down-regulation and modulated Akt and ERK1/2 signalling pathways.	Quercetin	84-93	P53	Homo sapiens	148-151
30287880-6	2018	In multivariate analysis, TP53 mutations in L3 and loop-sheet helix (LSH) associated with a risk ratio (RR) of disease-specific survival (DSS) of 8.779 (p = 0.022) and a RR of disease-free survival (DFS) of 10.498 (p = 0.011).	dss	138-141	P53	Homo sapiens	26-30
29802837-6	2018	The dissociation-induced increase of phosphorylated p53 Ser15 (p-p53) is suppressed by Pifithrin alpha which also rescues the elevated levels of pro-apoptotic proteins in mitochondrial pathway.	pifithrin	87-102	P53	Homo sapiens	52-55
29802837-6	2018	The dissociation-induced increase of phosphorylated p53 Ser15 (p-p53) is suppressed by Pifithrin alpha which also rescues the elevated levels of pro-apoptotic proteins in mitochondrial pathway.	pifithrin	87-102	P53	Homo sapiens	65-68
30088538-0	2018	Icariin reduces human colon carcinoma cell growth and metastasis by enhancing p53 activities.	icariin	0-7	P53	Homo sapiens	78-81
30088538-11	2018	Furthermore, the cytotoxicity of icariin was decreased after p53 knockdown or by using caspase inhibitors.	icariin	33-40	P53	Homo sapiens	61-64
30088538-13	2018	Icariin repressed colon carcinoma cell line HCT116 by enhancing p53 expression and activating p53 functions possibly through Bcl-2/Bax imbalance and caspase-9 and -3 regulation.	icariin	0-7	P53	Homo sapiens	64-67
30088538-13	2018	Icariin repressed colon carcinoma cell line HCT116 by enhancing p53 expression and activating p53 functions possibly through Bcl-2/Bax imbalance and caspase-9 and -3 regulation.	icariin	0-7	P53	Homo sapiens	94-97
29190376-0	2018	p53 promotes AKT and SP1-dependent metabolism through the pentose phosphate pathway that inhibits apoptosis in response to Nutlin-3a.	Pentosephosphates	58-75	P53	Homo sapiens	0-3
29935106-7	2018	Specifically, frataxin was lowered in the liver of HFD-fed mice or HepG2 cell incubated with oleate/palmitate but restored by quercetin, and quercetin"s regulation of frataxin may depend on p53.	Quercetin	141-150	P53	Homo sapiens	190-193
30073996-0	2018	TP53 polymorphisms in smokers" and nonsmokers" pericoronal follicles of asymptomatic impacted third molars.	pericoronal	47-58	P53	Homo sapiens	0-4
29738772-5	2018	Interestingly, co-treatment with DHA could effectively restore the anticancer effect of 5-FU against HCT116 TP53-/- cells, which manifested as the inhibition of proliferation and induction of reactive oxygen species (ROS)-mediated apoptosis and was accompanied by the upregulation of B-cell lymphoma 2 (BCL-2) and downregulation of the BCL-2-associated X protein (BAX).	artenimol	33-36	P53	Homo sapiens	108-112
29743236-4	2018	Mechanistically, 2-hydroxyglutarate (2-HG) stabilizes hypoxia-inducible factor-2alpha, which in turn activates the expression of miR-380-5p, a characterized microRNA against p53 expression.	alpha-hydroxyglutarate	17-35	P53	Homo sapiens	174-177
29525471-6	2018	Prolonged expression of p53 was responsible for melanocyte senescence and hyperpigmentation, and treatment with the p53-inhibitor pifithrin-alpha at 2-weeks post-UVB irradiation, but not at 48 h, significantly reduced melanin content along with decreases in tyrosinase levels.	pifithrin	130-145	P53	Homo sapiens	24-27
29525471-6	2018	Prolonged expression of p53 was responsible for melanocyte senescence and hyperpigmentation, and treatment with the p53-inhibitor pifithrin-alpha at 2-weeks post-UVB irradiation, but not at 48 h, significantly reduced melanin content along with decreases in tyrosinase levels.	pifithrin	130-145	P53	Homo sapiens	116-119
29425775-11	2018	A terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) assay revealed that the percentage of apoptotic coronary artery smooth muscle cells in the donor hearts was significantly increased in the Ad-P53 group compared to that in the Ad-LacZ group and the control group (P &lt; 0.01).	deoxyuridine triphosphate	40-44	P53	Homo sapiens	214-217
28659272-0	2018	p53/Drp1-dependent mitochondrial fission mediates aldosterone-induced podocyte injury and mitochondrial dysfunction.	Aldosterone	50-61	P53	Homo sapiens	0-3
28659272-10	2018	These findings implicated that aldosterone induced mitochondrial dysfunction and podocyte injury mediated by p53/Drp1-dependent mitochondrial fission, which may provide opportunities for therapeutic intervention for podocyte injury.	Aldosterone	31-42	P53	Homo sapiens	109-112
29471073-1	2018	Polycyclic aromatic hydrocarbons such as benzo[a]pyrene (BaP) can induce cytochrome P450 1A1 (CYP1A1) via a p53-dependent mechanism.	Polycyclic Aromatic Hydrocarbons	0-32	P53	Homo sapiens	108-111
29554943-10	2018	However, MTX treatment yielded significantly higher transcript levels of LBH, and of CDKN1A (p21) and TP53 (p53), compared to untreated samples upon mitogen stimulation.	Methotrexate	9-12	P53	Homo sapiens	102-106
29554943-10	2018	However, MTX treatment yielded significantly higher transcript levels of LBH, and of CDKN1A (p21) and TP53 (p53), compared to untreated samples upon mitogen stimulation.	Methotrexate	9-12	P53	Homo sapiens	108-111
29431732-6	2018	Upregulation of p53 in turn disrupted the pentose phosphate pathway, leading to excessive ROS production and dormant TRC death.	Pentosephosphates	42-59	P53	Homo sapiens	16-19
29363722-9	2018	Furthermore, the present study revealed that beta-elemene induced apoptosis in SiHa cells by enhancing the expression of p53 and Bax, and suppressing the expression of Bcl-2.	beta-elemene	45-57	P53	Homo sapiens	121-124
29440484-6	2018	Through gene expression profiling of p53R172H -mutant lymphomas, we identified retinoic acid receptor gamma (RARgamma) as an actionable target and demonstrated that pharmacological activation of RARgamma with a synthetic retinoid sensitizes resistant p53-mutant lymphomas to p53 restoration, while additively improving outcome and survival in inherently sensitive tumors.	Retinoids	221-229	P53	Homo sapiens	37-40
29440484-6	2018	Through gene expression profiling of p53R172H -mutant lymphomas, we identified retinoic acid receptor gamma (RARgamma) as an actionable target and demonstrated that pharmacological activation of RARgamma with a synthetic retinoid sensitizes resistant p53-mutant lymphomas to p53 restoration, while additively improving outcome and survival in inherently sensitive tumors.	Retinoids	221-229	P53	Homo sapiens	251-254
29467390-14	2018	Indeed, p53 accumulates at mitochondria upon etoposide treatment and inhibition of p53 mitochondrial localization using pifithrin-micro inhibits apoptosis of COV434 cells.	pifithrin	120-129	P53	Homo sapiens	83-86
29235570-6	2018	RESULTS: GSK2830371, at doses (&lt;=10 muM) that alone had no growth-inhibitory or cytotoxic effects on the cells, nevertheless significantly potentiated the growth-inhibitory and clonogenic cell killing effects of MDM2 inhibitors in p53WT but not p53MUT melanoma cells, indicating the potentiation worked in a p53-dependent manner.	GSK2830371	9-19	P53	Homo sapiens	234-237
29235570-8	2018	GSK2830371 increased p53 stabilisation through Ser15 phosphorylation and consequent Lys382 acetylation, and decreased ubiquitination and proteasome-dependent degradation when it was combined with MDM2 inhibitors.	GSK2830371	0-10	P53	Homo sapiens	21-24
29235570-10	2018	GSK2830371 enhanced the induction of p53 transcriptional target genes, cell cycle arrest and apoptosis.	GSK2830371	0-10	P53	Homo sapiens	37-40
29235570-11	2018	CONCLUSIONS: GSK2830371, a WIP1 inhibitor, at doses with no growth-inhibitory activity alone, potentiated the growth-inhibitory and cytotoxic activity of MDM2 inhibitors by increasing phosphorylation, acetylation and stabilisation of p53 in cutaneous melanoma cells in a functional p53-dependent manner.	GSK2830371	13-23	P53	Homo sapiens	234-237
29235570-11	2018	CONCLUSIONS: GSK2830371, a WIP1 inhibitor, at doses with no growth-inhibitory activity alone, potentiated the growth-inhibitory and cytotoxic activity of MDM2 inhibitors by increasing phosphorylation, acetylation and stabilisation of p53 in cutaneous melanoma cells in a functional p53-dependent manner.	GSK2830371	13-23	P53	Homo sapiens	282-285
29432478-0	2018	Correction: Apoptosis by [Pt(O,O"-acac)(gamma-acac)(DMS)] requires PKC-delta mediated p53 activation in malignant pleural mesothelioma.	gamma-acac	40-50	P53	Homo sapiens	86-89
29512370-4	2018	For this purpose, mixed lymphocyte reaction (MLR) was performed using the IDO inhibitor 1-DL-methyl-tryptophan and the p53 inhibitor pifithrin-alpha.	pifithrin	133-148	P53	Homo sapiens	119-122
28902433-0	2018	Curcumin alleviates IL-17A-mediated p53-PAI-1 expression in bleomycin-induced alveolar basal epithelial cells.	Bleomycin	60-69	P53	Homo sapiens	36-39
29260852-19	2018	Protection of backbone hydrogen bonds (BHBs) has been shown to be an important factor for the stability of amyloidogenic proteins and was employed to identify and stabilize the structural defect resulting from the p53 Y220C mutation.	bhbs	39-43	P53	Homo sapiens	214-217
30417784-7	2018	RESULTS: Treatment of BT-20 cells with vincristine, vinblastine, and/or vinorelbine resulted in upregulation of TP53 expression.	Vinblastine	52-63	P53	Homo sapiens	112-116
30417784-7	2018	RESULTS: Treatment of BT-20 cells with vincristine, vinblastine, and/or vinorelbine resulted in upregulation of TP53 expression.	Vinorelbine	72-83	P53	Homo sapiens	112-116
29269566-8	2018	Further analysis demonstrated that treatment with Bortezomib sensitized TC cells to Vemurafenib via mitochondrial dysregulation and apoptosis of TC cells, as evidenced by the increase in the expression of p53, Noxa protein, the loss of mitochondrial membrane potential, cytochrome c release and Poly (ADP-ribose) polymerase cleavage.	Bortezomib	50-60	P53	Homo sapiens	205-208
29275301-9	2018	p53 was activated in cells treated with cycloartobiloxanthone.	cycloartobiloxanthone	40-61	P53	Homo sapiens	0-3
29210587-0	2017	Organocatalytic Asymmetric Synthesis of Spiro-oxindole Piperidine Derivatives That Reduce Cancer Cell Proliferation by Inhibiting MDM2-p53 Interaction.	spiro-oxindole piperidine	40-65	P53	Homo sapiens	135-138
29371974-0	2017	Novel proteasome inhibitor delanzomib sensitizes cervical cancer cells to doxorubicin-induced apoptosis via stabilizing tumor suppressor proteins in the p53 pathway.	delanzomib	27-37	P53	Homo sapiens	153-156
29371974-7	2017	Additionally, delanzomib worked synergistically with Dox to further upregulate p53 and its downstream targets and enhanced Dox-induced p38 phosphorylation.	delanzomib	14-24	P53	Homo sapiens	79-82
29464049-0	2018	Inhibition of IAP"s and activation of p53 leads to caspase-dependent apoptosis in gastric cancer cells treated with Scutellarein.	scutellarein	116-128	P53	Homo sapiens	38-41
29039462-3	2017	In the present study, a dithiocarbamate derivative, di-2-pyridylhydrazone dithiocarbamate s-acetic acid (DpdtaA) was prepared to address the issue whether the molecular mechanism behind biological behavior showed by dithiocarbamate was p53 mediated.	di-2-pyridylhydrazone dithiocarbamate s-acetic acid	52-103	P53	Homo sapiens	236-239
29039462-3	2017	In the present study, a dithiocarbamate derivative, di-2-pyridylhydrazone dithiocarbamate s-acetic acid (DpdtaA) was prepared to address the issue whether the molecular mechanism behind biological behavior showed by dithiocarbamate was p53 mediated.	dpdtaa	105-111	P53	Homo sapiens	236-239
28128446-6	2017	AGE impairs autophagosomes" clearance in p53 negative cells as observed with an autophagosome maturation blocker-bafilomycinA1 treated cells.	bafilomycin A1	113-126	P53	Homo sapiens	41-44
29039537-10	2017	In conclusion, juglone potentiated TRAIL-induced apoptosis in melanoma cells, and these effects were partially mediated through the ROS-p38-p53 pathway.	juglone	15-22	P53	Homo sapiens	140-143
28928082-0	2017	miR-338-3p confers 5-fluorouracil resistance in p53 mutant colon cancer cells by targeting the mammalian target of rapamycin.	mir-338-3p	0-10	P53	Homo sapiens	48-51
29017950-8	2017	Downregulation of p53 occurred by VPA alone and fluvastatin alone, but not at their combined application; upregulation of p21 at the protein level was induced by each of the drugs alone and no further increase occurred at combined application.	Fluvastatin	48-59	P53	Homo sapiens	18-21
28944886-0	2017	Sulforaphane induces p53-deficient SW480 cell apoptosis via the ROS-MAPK signaling pathway.	sulforaphane	0-12	P53	Homo sapiens	21-24
28944886-2	2017	However, the detailed anticancer effects of SFN on p53-deficient colon cancer cells has yet to be clearly elucidated.	sulforaphane	44-47	P53	Homo sapiens	51-54
28944886-4	2017	The critical events leading to apoptosis were then evaluated in SFN-treated p53-deficient SW480 cells, by performing an MTT assay, flow cytometry, western blotting and ELISA.	sulforaphane	64-67	P53	Homo sapiens	76-79
28944886-10	2017	In conclusion, the results suggest that SFN may induce apoptosis in p53-deficient SW480 cells via p53/p73-independent and ROS-Erk/p38-dependent signaling pathways.	sulforaphane	40-43	P53	Homo sapiens	68-71
28944886-10	2017	In conclusion, the results suggest that SFN may induce apoptosis in p53-deficient SW480 cells via p53/p73-independent and ROS-Erk/p38-dependent signaling pathways.	sulforaphane	40-43	P53	Homo sapiens	98-101
29254178-4	2017	Here, we reveal that theophylline down-regulated SRSF3 expression and switched p53 from alpha into a beta isoform as caffeine did in HeLa and MCF-7 cells via the reverse-transcriptase polymerase chain reaction and Western blot analysis.	Theophylline	21-33	P53	Homo sapiens	79-82
28756530-0	2017	Intricatinol synergistically enhances the anticancerous activity of cisplatin in human A549 cells via p38 MAPK/p53 signalling.	intricatinol	0-12	P53	Homo sapiens	111-114
32719725-5	2017	Further study showed that TFS decreased mitochondrial membrane potential, activated Caspase-3/7, Caspase-8 and Caspase-9 activities, and that the p53 inhibitor PFT-alpha reversed the TFS-induced cell growth inhibition and apoptosis.	pifithrin	160-169	P53	Homo sapiens	146-149
28498781-12	2017	Preliminary results suggest that PIK3CA and TP53 mutations in circulating tumor DNA ( P = .013) rather than in archival tumor tissues ( P = .474) may predict the efficacy of pyrotinib.	pyrotinib	174-183	P53	Homo sapiens	44-48
28836764-2	2017	In this work, we studied the changes in the structure and dynamics of wild type p53DBD in comparison with two of its "hot-spot" DNA-contact mutants, R248Q and R273H, by analysis of backbone amide chemical shift perturbations and 15N spin relaxation measurements.	15n	229-232	P53	Homo sapiens	80-83
28709868-5	2017	Comparing with in p53 knockdown NP cells, relative high p53 expression in normal control NP cells inhibited autophagy and the pentose phosphate pathway.	Pentosephosphates	126-143	P53	Homo sapiens	56-59
28743509-8	2017	Such activities were absent in 3-(4-methoxyphenyl)propiophenone (SSE14106H2) demonstrating the importance of conjugated ketone for antiproliferative and p53 stabilizing activity of the chalcones.	Chalcones	185-194	P53	Homo sapiens	153-156
28743509-10	2017	These chalcones can, therefore, act as fragment leads for further structure optimization to obtain more potent p53 stabilizing agents with enhanced anti-proliferative activities.	Chalcones	6-15	P53	Homo sapiens	111-114
29135114-12	2017	Low percentage and weak intensity of p53-positive cells was detected mostly in OLP specimens with highly expressed civatte bodies (CB).	civatte	115-122	P53	Homo sapiens	37-40
28818808-1	2017	We have previously shown that givinostat can induce potent apoptosis in the BCR-ABL1-positive, TP53-wild type B-cell acute lymphoblastic leukemia (B-ALL) cell line SUP-B15.	givinostat	30-40	P53	Homo sapiens	95-99
28819586-0	2017	The cardiac glycoside convallatoxin inhibits the growth of colorectal cancer cells in a p53-independent manner.	Glycosides	12-21	P53	Homo sapiens	88-91
28528452-5	2017	RESULTS: Overexpression of wild-type p53 as a transgene or pharmacological activation by doxorubicin drug treatment shows significant suppression of NIS transcription in multiple BC cell types which also results in lowered NIS protein content and cellular iodide intake.	Iodides	256-262	P53	Homo sapiens	37-40
28714901-3	2017	Se-PPC markedly inhibited the growth of cancer cells via induction of apoptosis which was accompanied by the formation of apoptotic bodies, an increase in the population of apoptotic sub-G1 phase cells, upregulation of p53, and activation of caspase-3 in A549 cells.	se-ppc	0-6	P53	Homo sapiens	219-222
28431961-7	2017	Senescence was significantly inhibited by treatment with pifithrin-alpha, a p53 inhibitor, or by MnTBAP, a superoxide dismutase mimetic, validating those molecular actors in IR-induced endothelial cell aging.	pifithrin	57-66	P53	Homo sapiens	76-79
28592850-5	2017	We demonstrated for the first time that the activities and expression of SIRT1 were suppressed by reduction of intracellular NAD+ levels and the p53-microRNA-34a pathway in caerulein-induced AP.	Ceruletide	173-182	P53	Homo sapiens	145-148
28426525-6	2017	CONCLUSIONS: GSTT1 and GSTM1 may modulate DNA damage levels of p53 gene when exposed to polycyclic aromatic hydrocarbons.	Polycyclic Aromatic Hydrocarbons	88-120	P53	Homo sapiens	63-66
28233940-5	2017	The iron(II) complex activated p53-mediated mitochondrial dysfunction as can be seen by the upregulation in the expression of p53 and proapoptotic Bcl-2 family proteins, and downregulation in the expression of Bcl-2 family proteins.	ammonium ferrous sulfate	4-12	P53	Homo sapiens	31-34
28233940-5	2017	The iron(II) complex activated p53-mediated mitochondrial dysfunction as can be seen by the upregulation in the expression of p53 and proapoptotic Bcl-2 family proteins, and downregulation in the expression of Bcl-2 family proteins.	ammonium ferrous sulfate	4-12	P53	Homo sapiens	126-129
28476801-8	2017	These observations were accompanied by activation of ERK1/2 and p38MAPK, as well as up-regulation of BAX and P53 in the AzaC/Dox group.	Azacitidine	120-124	P53	Homo sapiens	109-112
28213783-7	2017	Notably, this association was limited to patients harboring TP53 wild-type tumors (RFS; p = 0.003, DSS; p = 0.009).	dss	99-102	P53	Homo sapiens	60-64
28384067-0	2017	miR-101 Enhances Cisplatin-Induced DNA Damage Through Decreasing Nicotinamide Adenine Dinucleotide Phosphate Levels by Directly Repressing Tp53-Induced Glycolysis and Apoptosis Regulator Expression in Prostate Cancer Cells.	NADP	65-108	P53	Homo sapiens	139-143
27053350-5	2017	Hck siRNA dramatically decrease hemin-induced expression of p53, Bax, and active caspase-3 as well as the amount of apoptotic SH-SY5Y cells in vitro.	Hemin	32-37	P53	Homo sapiens	60-63
28195382-0	2017	Contribution of ATM and ATR kinase pathways to p53-mediated response in etoposide and methyl methanesulfonate induced DNA damage.	Methyl Methanesulfonate	86-109	P53	Homo sapiens	47-50
28098861-10	2017	Treatment of HepG2 cells with p53 inhibitor, pifithrin-alpha prior to incubation with triptolide significantly prevented induction of cell apoptosis.	pifithrin	45-60	P53	Homo sapiens	30-33
28012015-0	2017	Modulation of cell death in human colorectal and breast cancer cells through a manganese chelate by involving GSH with intracellular p53 status.	Manganese	79-88	P53	Homo sapiens	133-136
28283087-7	2017	Our results indicate that BDMC stimulates the dephosphorylation and p53-binding activity of Bcl-2 and suggest that BDMC may induce a neutralization of Bcl-2"s anti-apoptotic function, thereby enhancing X-ray-induced apoptosis.	bisdemethoxycurcumin	26-30	P53	Homo sapiens	68-71
28280360-0	2017	Arenobufagin activates p53 to trigger esophageal squamous cell carcinoma cell apoptosis in vitro and in vivo.	arenobufagin	0-12	P53	Homo sapiens	23-26
27939741-4	2017	Herein, we identified GMP synthetase (GMPS), a key enzyme of de novo purine biosynthesis, as an important p53 repression target using a large-scale proteomics approach.	purine	69-75	P53	Homo sapiens	106-109
28143426-9	2017	The impact of functional p53 was investigated by siRNA gene silencing and the p53 inhibitor pifithrin-alpha.	pifithrin	92-107	P53	Homo sapiens	25-28
28143426-9	2017	The impact of functional p53 was investigated by siRNA gene silencing and the p53 inhibitor pifithrin-alpha.	pifithrin	92-107	P53	Homo sapiens	78-81
28035355-0	2017	Scutellarin suppresses growth and causes apoptosis of human colorectal cancer cells by regulating the p53 pathway.	scutellarin	0-11	P53	Homo sapiens	102-105
28035355-9	2017	Additionally, suppression of p53 using a specific inhibitor, pifithrin-alpha, abrogated the pro-apoptotic effects of Scutellarin in HCT-116 cells.	pifithrin	61-76	P53	Homo sapiens	29-32
28035355-9	2017	Additionally, suppression of p53 using a specific inhibitor, pifithrin-alpha, abrogated the pro-apoptotic effects of Scutellarin in HCT-116 cells.	scutellarin	117-128	P53	Homo sapiens	29-32
30428220-5	2017	In this study, we showed that the MeOH extract from R. sativus sprout exhibits significant but variable cytotoxic effects on human lung adenocarcinoma cells depending on their p53 status.	Methanol	34-38	P53	Homo sapiens	176-179
30428220-6	2017	The MeOH extract decreased the viability of p53-deleted human lung cancer cells (H1299 and Calu-6) by inducing apoptosis; this effect, however, did not occur for wild-type p53 cancer cells (A549), for cells expressing a p53 mutant lacking the C terminus (H1264), or for .	Methanol	4-8	P53	Homo sapiens	44-47
27791982-7	2017	Thus, our data suggest that mutant p53 sensitizes cancer cells to lapatinib via two complementary mechanisms: mutant p53 mediated amplification of ErbB2 signaling, and simultaneous annihilation of both potent oncogenic drivers, ErbB2 and mutant p53.	Lapatinib	66-75	P53	Homo sapiens	117-120
28102324-6	2017	PpIX-SDT caused cell membrane damage prior to mitochondria damage and upregulated the expression of Fas and Fas L, while the effect was suppressed if cells were pre-treated with p53 inhibitor.	ppix-sdt	0-8	P53	Homo sapiens	178-181
28102324-9	2017	Our data suggest that PpIX-SDT suppress the proliferation of SAS cells via arresting cell cycle at G2/M phase and activating the extrinsic Fas-mediated membrane receptor pathway to induce apoptosis, which is regulated by p53.	ppix-sdt	22-30	P53	Homo sapiens	221-224
28071670-4	2017	Mechanistically, BITC induces p73 expression in p53-mutant cells, disrupts the interaction of p73 and mutant-p53, thereby releasing p73 from sequestration and allowing it to be transcriptionally active.	benzyl isothiocyanate	17-21	P53	Homo sapiens	48-51
28071670-4	2017	Mechanistically, BITC induces p73 expression in p53-mutant cells, disrupts the interaction of p73 and mutant-p53, thereby releasing p73 from sequestration and allowing it to be transcriptionally active.	benzyl isothiocyanate	17-21	P53	Homo sapiens	109-112
28071670-5	2017	Furthermore, BITC-induced p53 and p73 axes converge on tumor-suppressor LKB1 which is transcriptionally upregulated by p53 and p73 in p53-wild-type and p53-mutant cells respectively; and in a feed-forward mechanism, LKB1 tethers with p53 and p73 to get recruited to p53-responsive promoters.	benzyl isothiocyanate	13-17	P53	Homo sapiens	26-29
28071670-5	2017	Furthermore, BITC-induced p53 and p73 axes converge on tumor-suppressor LKB1 which is transcriptionally upregulated by p53 and p73 in p53-wild-type and p53-mutant cells respectively; and in a feed-forward mechanism, LKB1 tethers with p53 and p73 to get recruited to p53-responsive promoters.	benzyl isothiocyanate	13-17	P53	Homo sapiens	119-122
28071670-5	2017	Furthermore, BITC-induced p53 and p73 axes converge on tumor-suppressor LKB1 which is transcriptionally upregulated by p53 and p73 in p53-wild-type and p53-mutant cells respectively; and in a feed-forward mechanism, LKB1 tethers with p53 and p73 to get recruited to p53-responsive promoters.	benzyl isothiocyanate	13-17	P53	Homo sapiens	119-122
28071670-5	2017	Furthermore, BITC-induced p53 and p73 axes converge on tumor-suppressor LKB1 which is transcriptionally upregulated by p53 and p73 in p53-wild-type and p53-mutant cells respectively; and in a feed-forward mechanism, LKB1 tethers with p53 and p73 to get recruited to p53-responsive promoters.	benzyl isothiocyanate	13-17	P53	Homo sapiens	119-122
28071670-5	2017	Furthermore, BITC-induced p53 and p73 axes converge on tumor-suppressor LKB1 which is transcriptionally upregulated by p53 and p73 in p53-wild-type and p53-mutant cells respectively; and in a feed-forward mechanism, LKB1 tethers with p53 and p73 to get recruited to p53-responsive promoters.	benzyl isothiocyanate	13-17	P53	Homo sapiens	119-122
28071670-5	2017	Furthermore, BITC-induced p53 and p73 axes converge on tumor-suppressor LKB1 which is transcriptionally upregulated by p53 and p73 in p53-wild-type and p53-mutant cells respectively; and in a feed-forward mechanism, LKB1 tethers with p53 and p73 to get recruited to p53-responsive promoters.	benzyl isothiocyanate	13-17	P53	Homo sapiens	119-122
28231749-0	2017	Flavonoids and Tannins from Smilax china L. Rhizome Induce Apoptosis Via Mitochondrial Pathway and MDM2-p53 Signaling in Human Lung Adenocarcinoma Cells.	Flavonoids	0-10	P53	Homo sapiens	104-107
28231749-8	2017	Moreover, MDM2 and p-MDM2 proteins were decreased, while p53 and p-p53 proteins were increased, both in a dose-dependent manner, after A549 treatment with total flavonoids and total tannins.	Flavonoids	161-171	P53	Homo sapiens	57-60
33488629-7	2020	Furthermore, ADV treatment induced DNA double-strand breaks (gammaH2AX foci expression), which led to an increase of p53-phospho-Ser15 expression.	adefovir dipivoxil	13-16	P53	Homo sapiens	117-120
33059259-10	2020	Loss of nuclear integrity and the upregulation of the p53 DNA damage response (DDR) pathway was revealed by DAPI staining, differential gene expression and IPA core analysis.	DAPI	108-112	P53	Homo sapiens	54-57
33140956-2	2020	Herein, we report the design and investigation of a series of right-handed helical heterogeneous 1:1 alpha/Sulfono-gamma-AA peptides as unprecedented inhibitors for p53-MDM2 and p53-MDMX.	alpha/sulfono-gamma-aa peptides	101-132	P53	Homo sapiens	165-168
33140956-2	2020	Herein, we report the design and investigation of a series of right-handed helical heterogeneous 1:1 alpha/Sulfono-gamma-AA peptides as unprecedented inhibitors for p53-MDM2 and p53-MDMX.	alpha/sulfono-gamma-aa peptides	101-132	P53	Homo sapiens	178-181
33140956-6	2020	Furthermore, effective cellular activity is achieved by the stapled 1:1 alpha/Sulfono-gamma-AA peptides, evidenced by significantly enhanced p53 transcriptional activity and much more induced level of MDM2 and p21.	alpha/sulfono-gamma-aa	72-94	P53	Homo sapiens	141-144
32530119-3	2020	As results, quercetin showed contrasting dose-response to cellular behaviors dependent on the ROS-regulated p53 signaling pathways.	Quercetin	12-21	P53	Homo sapiens	108-111
32901866-6	2020	Furthermore, the p53 inhibitor, Pifithrin-mu, diminished the augmentation in poly(ADP-ribose) polymerase (PARP) cleavage induced by OTS514 plus H2O2, while the Mdm2 antagonist, Nutlin 3, increased PARP cleavage.	pifithrin	32-41	P53	Homo sapiens	17-20
33138052-6	2020	In thirteen (second line) osimertinib-treated patients with a (plasma or tissue) concomitant TP53 mutation at baseline, PFS was significantly shorter compared to six wild-type cases; 8.8 vs. 18.8 months, p = 0.017.	osimertinib	26-37	P53	Homo sapiens	93-97
33108147-3	2020	We confirm that PhIP-induced apoptosis is p53 and caspase 3/7 dependent.	2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine	16-20	P53	Homo sapiens	42-45
33108147-4	2020	Interestingly, normal cells such as HaCaT, which lack functional p53 are more resistant to PhIP treatment.	2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine	91-95	P53	Homo sapiens	65-68
32621200-10	2020	ZNP concentration-dependently elevated mRNA expression and protein level of p53 and Bax while reduced the expression of Bcl-2 and ER-alpha.	znp	0-3	P53	Homo sapiens	76-79
32578917-0	2020	A synthetic coumarin derivative (4-flourophenylacetamide-acetyl coumarin) impedes cell cycle at G0/G1 stage, induces apoptosis, and inhibits metastasis via ROS-mediated p53 and AKT signaling pathways in A549 cells.	coumarin	12-20	P53	Homo sapiens	169-172
32945487-0	2020	Kevetrin induces apoptosis in TP53 wild-type and mutant acute myeloid leukemia cells.	KEVETRIN	0-8	P53	Homo sapiens	30-34
32945487-2	2020	Kevetrin exhibits p53-dependent as well as-independent activity in solid tumors, while its effects on leukemic cells remain unknown.	KEVETRIN	0-8	P53	Homo sapiens	18-21
32945487-8	2020	Kevetrin also displayed efficacy against TP53 wild-type and mutant primary AML, with a preferential cytotoxic activity against blast cells.	KEVETRIN	0-8	P53	Homo sapiens	41-45
32945487-10	2020	These findings suggest that kevetrin may be a promising therapeutic option for patients with both wild-type and TP53-mutant AML.	KEVETRIN	28-36	P53	Homo sapiens	112-116
32898154-8	2020	Accordingly, in utero treatment of TashT embryos with the p53 inhibitor pifithrin-alpha decreased Ddx3y expression and abolished the otherwise more severe ENS defect in TashT males.	pifithrin	72-87	P53	Homo sapiens	58-61
32687844-10	2020	DpdtC treatment resulted in upregulation of p53, but, the addition of p53 inhibitor, PFT-alpha could significantly neutralize the action of DpdtC on ferritinophagy induction and EMT inhibition.	pifithrin	85-94	P53	Homo sapiens	70-73
32648887-7	2020	The results indicate that DHA@ZIF-8 NPs modify the expression of 7090 genes in HepG2 cells, and the mechanism may be related to the induction of apoptosis through a p53-mediated mitochondrial pathway and the suppression of glycolysis by inhibiting the PI3K/AKT pathway.	artenimol	26-29	P53	Homo sapiens	165-168
32733640-5	2020	Western blot analysis revealed that quercetin reduced copper-induced increase in p53 upregulated modulator of apoptosis (PUMA) expression and promoted upregulation of nucleoside diphosphate kinase NME1.	Quercetin	36-45	P53	Homo sapiens	81-84
32650545-0	2020	Potential Metabolite Nymphayol Isolated from Water Lily (Nymphaea stellata) Flower Inhibits MCF-7 Human Breast Cancer Cell Growth via Upregulation of Cdkn2a, pRb2, p53 and Downregulation of PCNA mRNA Expressions.	nymphayol	21-30	P53	Homo sapiens	164-167
32630700-0	2020	The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis.	indicaxanthin	18-31	P53	Homo sapiens	130-133
33040724-3	2020	Thiamine diphosphate (ThDP), which is a major thiamine derivative, affects p53 binding to DNA.	Thiamine Pyrophosphate	0-20	P53	Homo sapiens	75-78
33040724-3	2020	Thiamine diphosphate (ThDP), which is a major thiamine derivative, affects p53 binding to DNA.	Thiamine Pyrophosphate	22-26	P53	Homo sapiens	75-78
32583791-6	2020	As main findings, phenolic compounds, saponins and alkaloids interfere with cancer progression by stimulating p53 expression, which can cause pro-apoptotic onset and restrict the anti-apoptotic activity, in addition to preventing telomerase enzyme activity.	Alkaloids	51-60	P53	Homo sapiens	110-113
32482751-0	2020	To target the untargetable: elucidation of synergy of APR-246 and azacitidine in TP53 mutant myelodysplastic syndromes and acute myeloid leukemia.	Azacitidine	66-77	P53	Homo sapiens	81-85
32427989-7	2020	However, depleting Mdm4 sensitized p53-/- cells to the nucleoside analog gemcitabine, raising the future perspective of using Mdm4 inhibitors as chemosensitizers.	Nucleosides	55-65	P53	Homo sapiens	35-38
32259553-0	2020	Ochratoxin a causes cell cycle arrest in G1 and G1/S phases through p53 in HK-2 cells.	ochratoxin A	0-12	P53	Homo sapiens	68-71
32455562-0	2020	Detection of Human p53 In-Vitro Expressed in a Transcription-Translation Cell-Free System by a Novel Conjugate Based on Cadmium Sulphide Nanoparticles.	cadmium sulfide	120-136	P53	Homo sapiens	19-22
32382022-7	2020	The administration of regular used in vitro dose (10 microM) in 3D and 2D cultures, as well as the dose-response analysis in 2D cultures showed Sorafenib and Regorafenib were increasingly effective in reducing cell proliferation, and inducing apoptosis in well-differentiated and expressing wild-type p53 in HCC cells.	Sorafenib	144-153	P53	Homo sapiens	301-304
32032660-1	2020	Actinomycin D and nutlin-3a (A + N) activate p53, partly through induction of phosphorylation on Ser392.	seryl-seryl-seryl-arginine	97-100	P53	Homo sapiens	45-48
31990086-8	2020	Decrease of TP53-mutated clone was correlated with response to AZA, confirming AZA efficacy in this subgroup.	Azacitidine	63-66	P53	Homo sapiens	12-16
31990086-8	2020	Decrease of TP53-mutated clone was correlated with response to AZA, confirming AZA efficacy in this subgroup.	Azacitidine	79-82	P53	Homo sapiens	12-16
31960917-7	2020	Quercetin down-regulated p53, Bax and cleaved-caspase-3 expression, while up-regulated CyclinD1, CDK4 and Bcl-2.	Quercetin	0-9	P53	Homo sapiens	25-28
32123008-7	2020	Furthermore, protein stability and cell viability assays using two distinct proteasome inhibitor anticancer drugs, the 20S proteasome inhibitor bortezomib and the ubiquitin-activating enzyme E1 inhibitor TAK-243, show that the upregulation of the NRF3-POMP axis leads to ubiquitin-independent proteolysis of p53 and Rb and to impaired sensitivity to bortezomib but not TAK-243.	Bortezomib	350-360	P53	Homo sapiens	308-311
32273511-0	2020	p53-mediated control of aspartate-asparagine homeostasis dictates LKB1 activity and modulates cell survival.	Aspartic Acid	24-33	P53	Homo sapiens	0-3
32273511-3	2020	Here, we report that p53 suppresses asparagine synthesis through the transcriptional downregulation of ASNS expression and disrupts asparagine-aspartate homeostasis, leading to lymphoma and colon tumour growth inhibition in vivo and in vitro.	Aspartic Acid	143-152	P53	Homo sapiens	21-24
32273511-5	2020	Mechanistically, asparagine and aspartate regulate AMPK-mediated p53 activation by physically binding to LKB1 and oppositely modulating LKB1 activity.	Aspartic Acid	32-41	P53	Homo sapiens	65-68
31838664-4	2020	Our observations suggest that P53 suppression by LPS, pifithrin, or small interfering RNA increased the expression of the redox marker malondialdehyde.	pifithrin	54-63	P53	Homo sapiens	30-33
32219038-11	2020	Further mechanical explorations showed that H19 knockdown resulted in alternative expressions levels of cyclin D1, CDK4, CDK6, p21 and p53 under ICA treatment.	icariin	145-148	P53	Homo sapiens	135-138
31876640-1	2020	In our proof-of-concept study of 1 patient with stage IIIC carcinosarcoma of the ovary, we discovered a rare mutation in the tumor suppressor, TP53, that results in the deletion of N131.	INT 131	181-185	P53	Homo sapiens	143-147
32114433-5	2020	We have also published that inhibition of basal activity of c-jun-NH2-terminal kinase (JNK) with JNK-specific inhibitor SP600125 represses PS1 transcription by reducing p-JNK and via p53 dependent mechanism.	pyrazolanthrone	120-128	P53	Homo sapiens	183-186
31953984-0	2020	Diepoxybutane induces the expression of a novel p53-target gene XCL1 that mediates apoptosis in exposed human lymphoblasts.	diepoxybutane	0-13	P53	Homo sapiens	48-51
31953984-3	2020	Our previous studies demonstrated that the X-C motif chemokine ligand 1 (XCL1) gene expression was upregulated 3.3-fold in a p53-dependent manner in TK6 lymphoblasts undergoing DEB-induced apoptosis.	diepoxybutane	177-180	P53	Homo sapiens	125-128
31839416-9	2020	Moreover, pathogenic mutations of TP53 were negatively related to the efficacy of osimertinib.	osimertinib	82-93	P53	Homo sapiens	34-38
31923958-2	2020	To this end, we constructed a novel UV-light cross-linked and pH de-cross-linked coumarin-decorated cationic copolymer functionalized mesoporous silica nanoparticles (MSN) for co-delivery of chemotherapeutic agent 5-FU and tumor suppresser p53 gene.	coumarin	81-89	P53	Homo sapiens	240-243
31815681-1	2020	We have recently described in this journal our detection of an anthropoid primate-specific, adrenal androgen-dependent, p53-mediated, "kill switch" tumor suppression mechanism that reached its fullest expression only in humans, as a result of human-specific exposure to polycyclic aromatic hydrocarbons caused by the harnessing of fire.	Polycyclic Aromatic Hydrocarbons	270-302	P53	Homo sapiens	120-123
31908078-6	2020	Mechanistically, the inhibitory phosphorylation of Drp1 Ser637 increased upon p53 expression, suppressing the translocation of Drp1 into mitochondria.	seryl-seryl-seryl-arginine	56-59	P53	Homo sapiens	78-81
31908078-8	2020	Protein kinase A (PKA) activity was responsible for p53-mediated Drp1 Ser637 phosphorylation and mitochondrial dysfunction.	seryl-seryl-seryl-arginine	70-73	P53	Homo sapiens	52-55
31645443-7	2020	Intriguingly, Cer-RUB nanomicelle treatments restored p53-dependent tumor suppression and sensitivity to cisplatin in OVCAR-3 ovarian cancer cells and xenograft tumors carrying p53 R248Q mutation.	rubusoside	18-21	P53	Homo sapiens	54-57
31645443-7	2020	Intriguingly, Cer-RUB nanomicelle treatments restored p53-dependent tumor suppression and sensitivity to cisplatin in OVCAR-3 ovarian cancer cells and xenograft tumors carrying p53 R248Q mutation.	rubusoside	18-21	P53	Homo sapiens	177-180
32016852-0	2020	Effect of new olivacine derivatives on p53 protein level.	olivacine	14-23	P53	Homo sapiens	39-42
32016852-6	2020	The cells were incubated with olivacine derivatives for 18 h and then assays were carried out: measurement of the amount of p53 and p21 proteins, detection of apoptosis, cell cycle analysis, and rhodamine 123 accumulation assay (evaluation of P-glycoprotein inhibition).	olivacine	30-39	P53	Homo sapiens	124-127
31841081-8	2020	When the p53 pathway of irradiated cells was inhibited by PFT-alpha, PFTmicro or p53 siRNA, the bystander damage to TK6 cells were clearly alleviated.	pifithrin	58-67	P53	Homo sapiens	9-12
31941067-8	2020	Accumulated evidence has revealed that Triphala modulates multiple cell signaling pathways including, ERK, MAPK, NF-kappaB, Akt, c-Myc, VEGFR, mTOR, tubulin, p53, cyclin D1, anti-apoptotic and pro-apoptotic proteins.	triphala	39-47	P53	Homo sapiens	158-161
33163985-2	2020	Methods: From our predictive synthetic lethality model used in SL-BioDP, we inferred TP53 mutation lead to potential synergistic drug combination of Bortezomib and Vorinostat.	Bortezomib	149-159	P53	Homo sapiens	85-89
32771207-6	2020	Inhibition of p53 by treated with pifithrin-alpha (PFTalpha) causing augments of osteoclastogenesis and bone resorption, also reversed OPG-mediated inhibition of osteoclastogenesis by reducing the expression of TSC2.	pifithrin	34-49	P53	Homo sapiens	14-17
32771207-6	2020	Inhibition of p53 by treated with pifithrin-alpha (PFTalpha) causing augments of osteoclastogenesis and bone resorption, also reversed OPG-mediated inhibition of osteoclastogenesis by reducing the expression of TSC2.	pifithrin	51-59	P53	Homo sapiens	14-17
31642121-5	2020	Using this tool, we have identified a putative domain enriched in hydrophilic and disorder-promoting residues (Pro, Ser, and Thr) and depleted in positive charges (Arg and Lys) bordering the folded DNA-binding domains of several transcription factors (p53, GCR, NAC46, MYB28, and MYB29).	pro	111-114	P53	Homo sapiens	252-255
32003702-5	2020	RESULTS: More than one hundred anticancer alkaloids were disclosed in Chinese patents and their mode of action referred to arresting cell cycle, inhibiting protein kinases, affecting DNA synthesis and p53 expression, etc.	Alkaloids	42-51	P53	Homo sapiens	201-204
31976328-0	2019	Dihydroartemisinin Sensitizes Mutant p53 (R248Q)-Expressing Hepatocellular Carcinoma Cells to Doxorubicin by Inhibiting P-gp Expression.	artenimol	0-18	P53	Homo sapiens	37-40
31976328-8	2019	However, combination of DHA and ADM treatment decreased cell viability and elevated cell apoptosis level in p53 (R248Q)-expressing Hep3B cells.	artenimol	24-27	P53	Homo sapiens	108-111
31976328-9	2019	Molecular dynamics simulations showed that DHA had the potential to bind with mutant p53 (R248Q) protein.	artenimol	43-46	P53	Homo sapiens	85-88
31976328-10	2019	Furthermore, DHA treatment decreased P-gp expression and inhibited phosphorylation levels of ERK1/2 and p65 in p53 (R248Q)-expressing Hep3B cells.	artenimol	13-16	P53	Homo sapiens	111-114
31976328-11	2019	Finally, DHA treatment could significantly reduce ADM efflux in p53 (R248Q)-expressing cells.	artenimol	9-12	P53	Homo sapiens	64-67
31976328-12	2019	Our results indicate that DHA could decrease P-gp expression via inhibiting the p53 (R248Q)-ERK1/2-NF-kappaB signaling pathway, which eventually confers sensitization of p53 (R248Q)-expressing HCC cells to ADM. Our study provides evidence for the potential application of DHA and ADM combination in treatment of mutant p53 (R248Q)-harbored HCC.	artenimol	26-29	P53	Homo sapiens	80-83
31976328-12	2019	Our results indicate that DHA could decrease P-gp expression via inhibiting the p53 (R248Q)-ERK1/2-NF-kappaB signaling pathway, which eventually confers sensitization of p53 (R248Q)-expressing HCC cells to ADM. Our study provides evidence for the potential application of DHA and ADM combination in treatment of mutant p53 (R248Q)-harbored HCC.	artenimol	26-29	P53	Homo sapiens	170-173
31976328-12	2019	Our results indicate that DHA could decrease P-gp expression via inhibiting the p53 (R248Q)-ERK1/2-NF-kappaB signaling pathway, which eventually confers sensitization of p53 (R248Q)-expressing HCC cells to ADM. Our study provides evidence for the potential application of DHA and ADM combination in treatment of mutant p53 (R248Q)-harbored HCC.	artenimol	26-29	P53	Homo sapiens	170-173
31976328-12	2019	Our results indicate that DHA could decrease P-gp expression via inhibiting the p53 (R248Q)-ERK1/2-NF-kappaB signaling pathway, which eventually confers sensitization of p53 (R248Q)-expressing HCC cells to ADM. Our study provides evidence for the potential application of DHA and ADM combination in treatment of mutant p53 (R248Q)-harbored HCC.	artenimol	272-275	P53	Homo sapiens	80-83
31763806-7	2019	Moreover, we demonstrate that the delivery of tumor suppressor p53 mRNA using PBA-BADP selectively prohibits cancer cell growth, while PBA-BADP/Cas9 mRNA NPs delivery knocks out gene expression of HeLa cancer cells in a much higher efficiency than non-cancer cells.	benzeneboronic acid	78-81	P53	Homo sapiens	63-66
31117836-0	2019	Antiproliferative activity and p53 upregulation effects of chalcones on human breast cancer cells.	Chalcones	59-68	P53	Homo sapiens	31-34
31608899-6	2019	RESULTS The most key anti-CRC targets of FN were identified as tumor protein p53 (TP53), cytochrome P450 3A4 (CYP3A4), ATP binding cassette subfamily G member 2 (ABCG2), tumor necrosis factor (TNF), epidermal growth factor receptor (EGFR), Erb-B2 receptor tyrosine kinase 2 (ERBB2), and cytochrome P450 1A1 (CYP1A1).	formononetin	41-43	P53	Homo sapiens	77-80
31608899-6	2019	RESULTS The most key anti-CRC targets of FN were identified as tumor protein p53 (TP53), cytochrome P450 3A4 (CYP3A4), ATP binding cassette subfamily G member 2 (ABCG2), tumor necrosis factor (TNF), epidermal growth factor receptor (EGFR), Erb-B2 receptor tyrosine kinase 2 (ERBB2), and cytochrome P450 1A1 (CYP1A1).	formononetin	41-43	P53	Homo sapiens	82-86
31601253-10	2019	We then showed that combination treatment with Cl-amidine and docetaxel enhanced p53 nuclear accumulation, which synergistically induced cell cycle arrest and apoptosis.	Docetaxel	62-71	P53	Homo sapiens	81-84
31155771-7	2019	Additionally, under the pretreatment of pifithrin-a (PFT-a, a p53 inhibitor), the magnolol-induced apoptosis was significantly reversed.	pifithrin	40-51	P53	Homo sapiens	62-65
31155771-7	2019	Additionally, under the pretreatment of pifithrin-a (PFT-a, a p53 inhibitor), the magnolol-induced apoptosis was significantly reversed.	pifithrin	53-58	P53	Homo sapiens	62-65
31546731-0	2019	p53-Mediated Oxidative Stress Enhances Indirubin-3"-Monoxime-Induced Apoptosis in HCT116 Colon Cancer Cells by Upregulating Death Receptor 5 and TNF-Related Apoptosis-Inducing Ligand Expression.	indirubin-3'-monoxime	39-60	P53	Homo sapiens	0-3
31546731-3	2019	However, this study demonstrated that HCT116 p53-/- cells were insensitive to I3M-mediated apoptosis, indicating that I3M-induced apoptosis depends on the p53 status of HCT116 cells.	indirubin-3'-monoxime	118-121	P53	Homo sapiens	45-48
31546731-3	2019	However, this study demonstrated that HCT116 p53-/- cells were insensitive to I3M-mediated apoptosis, indicating that I3M-induced apoptosis depends on the p53 status of HCT116 cells.	indirubin-3'-monoxime	118-121	P53	Homo sapiens	155-158
31546731-4	2019	Additionally, in HCT116 p53-/- cells, I3M significantly increased Ras expression, while in HCT116 p53+/+ cells, it reduced Ras expression.	indirubin-3'-monoxime	38-41	P53	Homo sapiens	24-27
31546731-5	2019	Furthermore, I3M remarkably increased the production of reactive oxygen species (ROS), which were reduced in transient p53 knockdown, indicating that I3M-mediated apoptosis was promoted by p53-mediated ROS production.	indirubin-3'-monoxime	13-16	P53	Homo sapiens	119-122
31546731-5	2019	Furthermore, I3M remarkably increased the production of reactive oxygen species (ROS), which were reduced in transient p53 knockdown, indicating that I3M-mediated apoptosis was promoted by p53-mediated ROS production.	indirubin-3'-monoxime	13-16	P53	Homo sapiens	189-192
31546731-5	2019	Furthermore, I3M remarkably increased the production of reactive oxygen species (ROS), which were reduced in transient p53 knockdown, indicating that I3M-mediated apoptosis was promoted by p53-mediated ROS production.	indirubin-3'-monoxime	150-153	P53	Homo sapiens	119-122
31546731-5	2019	Furthermore, I3M remarkably increased the production of reactive oxygen species (ROS), which were reduced in transient p53 knockdown, indicating that I3M-mediated apoptosis was promoted by p53-mediated ROS production.	indirubin-3'-monoxime	150-153	P53	Homo sapiens	189-192
31546731-8	2019	In summary, I3M potently enhances TRAIL-induced apoptosis by upregulating DR5 expression via p53-mediated ROS production in HCT116 p53+/+ cells.	indirubin-3'-monoxime	12-15	P53	Homo sapiens	93-96
31546731-9	2019	However, HCT116 p53-/- cells were less sensitive to I3M-mediated apoptosis, suggesting that I3M could be a promising anti-cancer candidate against TRAIL-resistant p53+/+ cancer cells.	indirubin-3'-monoxime	92-95	P53	Homo sapiens	16-19
31546731-9	2019	However, HCT116 p53-/- cells were less sensitive to I3M-mediated apoptosis, suggesting that I3M could be a promising anti-cancer candidate against TRAIL-resistant p53+/+ cancer cells.	indirubin-3'-monoxime	92-95	P53	Homo sapiens	163-166
31366730-3	2019	Here, we identified a relatively rare mutation leading to a proline to leucine substitution (P152L) in TP53 at the very end of its DNA-binding domain (DBD) in a sample from an Indian oral cancer patient.	Leucine	71-78	P53	Homo sapiens	103-107
31544060-0	2019	Activation of p53 Gene Expression and Synergistic Antiproliferative Effects of 5-Fluorouracil and beta-escin on MCF7 Cells.	Escin	98-108	P53	Homo sapiens	14-17
31544060-8	2019	The expression of p53 and apoptosis increased in the combination of 5-FU and beta-escin on MCF7 cells compared to that of control group (P &lt; 0.05).	Escin	77-87	P53	Homo sapiens	18-21
31544060-10	2019	The combination of 5-FU and beta-escin not only has synergistic effects by increasing cell apoptosis and p53 gene expression but also decreases Bcl-2 signaling protein in MCF7 cell lines.	Escin	28-38	P53	Homo sapiens	105-108
31438892-4	2019	METHODS: We monitored cell proliferation, in-vitro cell migration, wound healing, expression and activity of MMP-2, - 9 in A549 and p53-deficient H1299 cell lines exposed with 12C ion with and without PARP-1 inhibitor olaparib/DPQ.	12c	176-179	P53	Homo sapiens	132-135
31181181-0	2019	Probing direct interaction of oncomiR-21-3p with the tumor suppressor p53 by fluorescence, FRET and atomic force spectroscopy.	oncomir-21-	30-41	P53	Homo sapiens	70-73
31196710-0	2019	2,4,5-Tris(alkoxyaryl)imidazoline derivatives as potent scaffold for novel p53-MDM2 interaction inhibitors: Design, synthesis, and biological evaluation.	2,4,5-tris(alkoxyaryl)imidazoline	0-33	P53	Homo sapiens	75-78
31078603-6	2019	Furthermore, exposure to the Fe(II) complex led to excessive reactive oxygen species (ROS) accumulation by thioredoxin reductase (TrxR) inhibition and DNA double-strand breaks (DSBs), which in turn sequentially activated ATM, CHK1/2 and p53.	ammonium ferrous sulfate	29-35	P53	Homo sapiens	237-240
30628118-10	2019	The cytotoxic effects of solasonine correlated in part with its apoptotic properties and differed in the two HCC cell lines, being reversed by pifithrin-alpha, an inhibitor of p53 functions, in HepG2 cells but not in Hep3b cells.	pifithrin	143-158	P53	Homo sapiens	176-179
31276572-7	2019	Furthermore, a retinoid derivative and an endoplasmic reticulum stress inducer, fenretinide, induced NOXA, and combination of fenretinide and ABT-263 strongly induced apoptosis in HNSCC cells regardless of the HPV or p53 statuses.	Retinoids	15-23	P53	Homo sapiens	217-220
31354907-8	2019	In addition, DpdtbA also induced a downregulation of EGFR, p53, and AKT, which hinted that mutant p53 still played a role in the regulation of its downstream targets.	dpdtba	13-19	P53	Homo sapiens	59-62
31354907-8	2019	In addition, DpdtbA also induced a downregulation of EGFR, p53, and AKT, which hinted that mutant p53 still played a role in the regulation of its downstream targets.	dpdtba	13-19	P53	Homo sapiens	98-101
31354907-10	2019	Taken together, the DpdtbA-induced growth inhibition in a mechanism was through inactivating the p53/EGFR/AKT signal pathway.	dpdtba	20-26	P53	Homo sapiens	97-100
30904656-7	2019	Children with particle-bound PAH exposures have a relatively high health risk of aryl hydrocarbon receptor (AhR)-mediated adverse outcomes than adults, in particular in the winter period, while the activations of Nrf2 and p53 pathways are insignificant.	Polycyclic Aromatic Hydrocarbons	29-32	P53	Homo sapiens	222-225
31175839-5	2019	RESULTS Seven key target genes for formononetin in the treatment of patients with AD were identified, including estrogen receptor alpha (ESR1), peroxisome proliferator-activated receptor gamma (PPARG), tumor protein p53 (TP53), sirtuin 1 (SIRT1), tumor necrosis factor (TNF), cytochrome P450 19A1 (CYP19A1), and nuclear factor (erythroid-derived 2)-like 2 (NFE2L2).	formononetin	35-47	P53	Homo sapiens	216-219
31175839-5	2019	RESULTS Seven key target genes for formononetin in the treatment of patients with AD were identified, including estrogen receptor alpha (ESR1), peroxisome proliferator-activated receptor gamma (PPARG), tumor protein p53 (TP53), sirtuin 1 (SIRT1), tumor necrosis factor (TNF), cytochrome P450 19A1 (CYP19A1), and nuclear factor (erythroid-derived 2)-like 2 (NFE2L2).	formononetin	35-47	P53	Homo sapiens	221-225
31448047-0	2019	Correction: Artocarpin, an isoprenyl flavonoid, induces p53-dependent or independent apoptosis via ROS-mediated MAPKs and Akt activation in non-small cell lung cancer cells.	isoprenyl flavonoid	27-46	P53	Homo sapiens	56-59
30725256-10	2019	A potent, non-toxic benzodiazepine ("KRM-II-08") binds to the alpha5-GABAAR (0.8 microM EC50) enhancing a chloride-anion efflux that induces mitochondrial membrane depolarization and in response, TP53 upregulation and p53, constitutively phosphorylated at S392, cytoplasmic localization.	krm-ii-08	37-46	P53	Homo sapiens	196-200
30725256-10	2019	A potent, non-toxic benzodiazepine ("KRM-II-08") binds to the alpha5-GABAAR (0.8 microM EC50) enhancing a chloride-anion efflux that induces mitochondrial membrane depolarization and in response, TP53 upregulation and p53, constitutively phosphorylated at S392, cytoplasmic localization.	krm-ii-08	37-46	P53	Homo sapiens	218-221
31043658-0	2019	miR-150-5p represses TP53 tumor suppressor gene to promote proliferation of colon adenocarcinoma.	mir-150-5p	0-10	P53	Homo sapiens	21-25
31043658-8	2019	We further showed that inhibition of miR-150-5p increased TP53, and in turn, suppression of proliferation of colon adenocarcinoma.	mir-150-5p	37-47	P53	Homo sapiens	58-62
31043658-10	2019	Our results support that miR-150-5p-TP53 pathway plays an important role in regulation of proliferation, cell arrest, and apoptosis in colon cancer, and could be an attractive target for therapy.	mir-150-5p	25-35	P53	Homo sapiens	36-40
31022952-0	2019	p53-Dependent Apoptotic Effect of Puromycin via Binding of Ribosomal Protein L5 and L11 to MDM2 and its Combination Effect with RITA or Doxorubicin.	Puromycin	34-43	P53	Homo sapiens	0-3
31022952-2	2019	Here, the roles of RPL5 and RPL11 were investigated in association with p53/p21 signaling in the antitumor effect of puromycin mainly in HCT116 and H1299 cancer cells.	Puromycin	117-126	P53	Homo sapiens	72-75
31022952-4	2019	Puromycin exerted cytotoxic and anti-proliferative effects in p53 wild-type HCT116 more than in p53 null H1299 cells.	Puromycin	0-9	P53	Homo sapiens	62-65
31022952-8	2019	Also, puromycin enhanced the antitumor effect with reactivating p53 and inducing tumor apoptosis (RITA) or doxorubicin in HCT116 cells.	Puromycin	6-15	P53	Homo sapiens	64-67
31022952-9	2019	These findings suggest that puromycin induces p53-dependent apoptosis via upregulation of RPL5 or RPL11 for binding with MDM2, and so can be used more effectively in p53 wild-type cancers by combination with RITA or doxorubicin.	Puromycin	28-37	P53	Homo sapiens	46-49
31022952-9	2019	These findings suggest that puromycin induces p53-dependent apoptosis via upregulation of RPL5 or RPL11 for binding with MDM2, and so can be used more effectively in p53 wild-type cancers by combination with RITA or doxorubicin.	Puromycin	28-37	P53	Homo sapiens	166-169
31097990-3	2019	Library screening in assays that measure readthrough at a PTC in the TP53 gene in human HDQ-P1 cells identified six novel 2-aminothiazole-4-carboxamide derivatives that potentiate the PTC readthrough (PTCR) efficiency of G418 when used in combination.	2-aminothiazole-4-carboxamide	122-151	P53	Homo sapiens	69-73
30939155-5	2019	Our data showed that the statins-fluvastatin and lovastatin-induced p21 expression as general histone deacetylase inhibitors in a p53-independent manner, which is mediated through various pathways, such as apoptosis, autophagy, cell cycle progression, and DNA damage, to be involved in the function of p21 in HeLa cells.	Fluvastatin	33-44	P53	Homo sapiens	130-133
30885251-11	2019	Inhibiting CCDC106 phosphorylation by substituting both Ser-130 and Ser-147 with alanine or treating cells with the CK2 inhibitor CX-4945 abrogated CCDC106-induced p53 degradation and its oncogenic function in cells with wtp53.	silmitasertib	130-137	P53	Homo sapiens	164-167
30664221-0	2019	Quercetin induces G2 phase arrest and apoptosis with the activation of p53 in an E6 expression-independent manner in HPV-positive human cervical cancer-derived cells.	Quercetin	0-9	P53	Homo sapiens	71-74
30664221-7	2019	In the present study, it was demonstrated that quercetin induced G2 phase cell cycle arrest and apoptosis in both HeLa and SiHa cells, accompanied by an increase of p53 and its nuclear signal.	Quercetin	47-56	P53	Homo sapiens	165-168
30664221-8	2019	It was also observed that quercetin increased the level of the p21 transcript and the pro-apoptotic Bax protein, which are two p53-downstream effectors.	Quercetin	26-35	P53	Homo sapiens	127-130
30664221-9	2019	However, quercetin did not alter the expression of the HPV E6 protein in cervical cancer cells; therefore, the increase in p53 occurred in an E6 expression-independent manner.	Quercetin	9-18	P53	Homo sapiens	123-126
30664221-11	2019	These data suggest that quercetin increases the nuclear localization of p53 by interrupting E6/E6AP complex formation in cervical cancer cells.	Quercetin	24-33	P53	Homo sapiens	72-75
30873235-4	2019	Screening of the library for p53-MDM2 inhibition by fluorescence polarization and 1H,15N HSQC NMR measurements confirm MDM2 binding.	15n	85-88	P53	Homo sapiens	29-32
30744908-0	2019	Retraction notice to "Theaflavins induced apoptosis of LNCaP cells is mediated through induction of p53, down-regulation of NF-kappa B and mitogen-activated protein kinases pathways" [Life Sci.	theaflavin	22-33	P53	Homo sapiens	100-103
29769744-5	2019	Our present results demonstrated that NADPH inhibited the phosphorylation of p38MAPK, decreased the level of TP53 protein, and inhibited TP53 nuclear translocation in DA neurons of SNpc and in MES23.5 cells.	NADP	38-43	P53	Homo sapiens	109-113
29769744-5	2019	Our present results demonstrated that NADPH inhibited the phosphorylation of p38MAPK, decreased the level of TP53 protein, and inhibited TP53 nuclear translocation in DA neurons of SNpc and in MES23.5 cells.	NADP	38-43	P53	Homo sapiens	137-141
29769744-6	2019	Furthermore, NADPH decreased the protein level of TP53 target gene, Bax, cleavage of PARP, and nuclei condensation.	NADP	13-18	P53	Homo sapiens	50-54
29769744-7	2019	Taken together, NADPH abrogated MPTP-induced p38MAPK phosphorylation, TP53 nuclear translocation, and Bax induction, and finally, MPTP/MPP+-induced apoptosis of DA neurons.	NADP	16-21	P53	Homo sapiens	70-74
30472223-8	2019	Secondly, PFTalpha decreased formation of p53/mdm2 complex responsible for p53 degradation by inhibiting the protein expression of mdm2, so p53 degradation was decreased in cytoplasm and p53 accumulation was increased in nucleus, which induced more cells undergo apoptosis.	pifithrin	10-18	P53	Homo sapiens	75-78
30472223-8	2019	Secondly, PFTalpha decreased formation of p53/mdm2 complex responsible for p53 degradation by inhibiting the protein expression of mdm2, so p53 degradation was decreased in cytoplasm and p53 accumulation was increased in nucleus, which induced more cells undergo apoptosis.	pifithrin	10-18	P53	Homo sapiens	75-78
31223026-8	2019	The expression levels of BAD and p53 genes decreased by combined treatment with quercetin and selenium while showing synergistic effects in terms of gene expression.	Quercetin	80-89	P53	Homo sapiens	33-36
31495738-4	2019	Transfection with the p53 cDNA construct resulted in the accumulation of p53 and bax, in a reduced level of released PCNA and PGF, and in an increased PGE output.	Prostaglandins E	151-154	P53	Homo sapiens	22-25
31495738-6	2019	These observations are the first demonstration of the involvement of p53 in the control of healthy human ovarian cell functions, namely, in the downregulation of proliferation, in the upregulation of apoptosis, and in the alteration of PGF and PGE release, but not of P4, IGF-I, or OT.	Prostaglandins E	244-247	P53	Homo sapiens	69-72
30947605-6	2019	Quercetin did not have any influence on the number of granulosa cells containing caspase 3, but at the concentration 10 mumol L-1 it inhibited p53 occurrence.	Quercetin	0-9	P53	Homo sapiens	143-146
30947605-7	2019	Results confirm the safety of quercetin in porcine ovarian granulosa cell model and further suggest its possible concentration-dependent influence on ovarian functions through pathway that may involve progesterone, cyclin B1 and p53.	Quercetin	30-39	P53	Homo sapiens	229-232
30545932-8	2018	Correspondingly, embryos cultured with p53 transcriptional activity inhibitor pifithrin-alpha could overcome TPEN-induced apoptosis and failure of neural tube closure.	pifithrin	78-87	P53	Homo sapiens	39-42
30563120-12	2018	We observed that D2O cotreatment with BDMC significantly decreased cell proliferation compared to treatment with D2O alone, and this effect was accompanied by downregulation of HO-1 and an increase in p53 levels.	bisdemethoxycurcumin	38-42	P53	Homo sapiens	201-204
30240097-2	2018	It has been hypothesized that upregulation of nuclear FoxO transcription factors and p53 mediate isotretinoin-induced sebocyte apoptosis in vivo.	Isotretinoin	97-109	P53	Homo sapiens	85-88
29644528-0	2018	A novel, semi-synthetic diterpenoid 16(R and S)-phenylamino-cleroda-3,13(14), Z-dien-15,16 olide (PGEA-AN) inhibits the growth and cell survival of human neuroblastoma cell line SH-SY5Y by modulating P53 pathway.	pgea-an	98-105	P53	Homo sapiens	200-203
29644528-9	2018	PGEA-AN significantly increased expression of P53 and BAX with no or little effect on BCL2 shifting BAX/BCL2 towards BAX promoting apoptosis.	pgea-an	0-7	P53	Homo sapiens	46-49
29644528-12	2018	Based on these observations, we suggest that PGEA-AN modulates P53 system which further leads to the death of the neuroblastoma cells with no effect on renal system in vivo owing it to be a future prospect for development of anticancer moiety against neuroblastoma.	pgea-an	45-52	P53	Homo sapiens	63-66
30272369-5	2018	Subsequently, the expression trends of Bcl-2 and p53 were reversed after co-treatment with pifithrin-alpha (PFT-alpha, a p53 inhibitor).	pifithrin	91-106	P53	Homo sapiens	49-52
30272369-5	2018	Subsequently, the expression trends of Bcl-2 and p53 were reversed after co-treatment with pifithrin-alpha (PFT-alpha, a p53 inhibitor).	pifithrin	91-106	P53	Homo sapiens	121-124
30504836-6	2018	CXCR4 upregulation in radioresistant tumour ECs was highly associated with SDF-1+ TAM recruitment and M2 polarization of TAMs, which was suppressed by Trp53 deletion.	tam	82-85	P53	Homo sapiens	151-156
30207732-0	2018	Synergetic and Antagonistic Molecular Effects Mediated by the Feedback Loop of p53 and JNK between Saikosaponin D and SP600125 on Lung Cancer A549 Cells.	pyrazolanthrone	118-126	P53	Homo sapiens	79-82
30144329-7	2018	Isotretinoin enhanced FoxO1, p53 and p21 but inhibited p-FoxO1 and involucrin expression in HPKs.	Isotretinoin	0-12	P53	Homo sapiens	29-32
29986258-7	2018	The transfection of HeLa cells mediated by PEI/pDNA/MTX vectors leads to both the release of MTX and the p53 protein expression.	Methotrexate	52-55	P53	Homo sapiens	105-108
30214587-5	2018	c-Jun N-terminal kinase/p38-mitogen-activated protein kinase-induced endoplasmic reticulum (ER) stress through serial exposure to celecoxib and bortezomib may have induced the intracellular Ca2+ release, leading to the generation of autophagosomes in p53-expressing HCT-116 cells.	Bortezomib	144-154	P53	Homo sapiens	251-254
30214587-7	2018	Although p53-/- HCT-116 cells were less sensitive to sequential treatment with celecoxib and bortezomib, co-localization of autophagosomes was detected in the absence of CCAAT-enhancer-binding protein homologous protein expression.	Bortezomib	93-103	P53	Homo sapiens	9-12
30258081-3	2018	Here we identify niclosamide through a HTS screen for compounds selectively killing p53-deficient cells.	Niclosamide	17-28	P53	Homo sapiens	84-87
30258081-4	2018	Niclosamide impairs the growth of p53-deficient cells and of p53 mutant patient-derived ovarian xenografts.	Niclosamide	0-11	P53	Homo sapiens	34-37
30258081-4	2018	Niclosamide impairs the growth of p53-deficient cells and of p53 mutant patient-derived ovarian xenografts.	Niclosamide	0-11	P53	Homo sapiens	61-64
30258081-5	2018	Metabolome profiling reveals that niclosamide induces mitochondrial uncoupling, which renders mutant p53 cells susceptible to mitochondrial-dependent apoptosis through preferential accumulation of arachidonic acid (AA), and represents a first-in-class inhibitor of p53 mutant tumors.	Niclosamide	34-45	P53	Homo sapiens	101-104
30258081-5	2018	Metabolome profiling reveals that niclosamide induces mitochondrial uncoupling, which renders mutant p53 cells susceptible to mitochondrial-dependent apoptosis through preferential accumulation of arachidonic acid (AA), and represents a first-in-class inhibitor of p53 mutant tumors.	Niclosamide	34-45	P53	Homo sapiens	265-268
30258081-7	2018	Therefore, we propose a new paradigm for targeting cancers defective in the p53 pathway, by exploiting their vulnerability to niclosamide-induced mitochondrial uncoupling.	Niclosamide	126-137	P53	Homo sapiens	76-79
29944886-12	2018	Moreover, suppressing p53 expression with its inhibitor of PFTalpha abrogated the activity of LHPP to impede cell proliferation and metastasis, and to trigger apoptosis.	pifithrin	59-67	P53	Homo sapiens	22-25
29921695-6	2018	Importantly, YY1-mediated regulation of the pentose phosphate pathway in tumor cells occurred not through p53, but rather through direct activation of G6PD transcription by YY1.	Pentosephosphates	44-61	P53	Homo sapiens	106-109
30033448-8	2018	Mechanistically, ANGPTL3 bound to Focal Adhesion Kinase(FAK) and restained sorafenib induced nuclear translocation of FAK, leading to attenuate the ubiquitination of p53, which contributed to cellular apoptosis and enhanced sorafenib response.	Sorafenib	75-84	P53	Homo sapiens	166-169
30060617-6	2018	We verified that manzamine A induced cell cycle arrest at G0/G1 phase via inhibition of cyclin-dependent kinases by p53/p21/p27 and triggered a caspase-dependent apoptotic cell death through mitochondrial membrane potential depletion.	manzamine A	17-28	P53	Homo sapiens	116-119
30049386-11	2018	Repression of cIAP1 by a selective inhibitor, birinapant, promoted activation of the apoptosis induced by Pol I transcription inhibitor in p53 WT cancer cells.	birinapant	46-56	P53	Homo sapiens	139-142
29705383-11	2018	These findings suggest that endosulfan caused DNA damage response throughATM-p53 signaling pathway, implicating the potential correlation between endosulfan and leukemia.	Endosulfan	28-38	P53	Homo sapiens	77-80
29898731-12	2018	PCa cells with mutated p53 (DU-145) and increased ROS showed significant reduction in the activation of pro-survival Akt pathway while Raf/MEK were activated in response to quercetin.	Quercetin	173-182	P53	Homo sapiens	23-26
29571049-3	2018	Here we report the design of a fluorescent lanthanide oxyfluoride nanoparticle (LONp)-based multifunctional peptide drug delivery system for potential treatment of acute myeloid leukemia (AML) that commonly harbors wild type p53, high levels of MDM2 and/or MDMX, and an overexpressed cell surface receptor, CD33.	lanthanide oxyfluoride	43-65	P53	Homo sapiens	225-228
29512682-10	2018	Moreover, the p53-p21-retinoblastoma protein (Rb) pathway was activated by CMT to mediate the CMT-induced premature senescence of NP cells.	cmt	75-78	P53	Homo sapiens	14-17
29928326-8	2018	The results of the present study demonstrated that miltirone induces apoptosis in cisplatin-resistant lung cancer cells through ROS-p53, AIF, PARP and MMP2/9 signaling pathways.	miltirone	51-60	P53	Homo sapiens	132-135
29635169-6	2018	Furthermore, western blot assay demonstrated that 12c induced the intrinsic apoptotic mitochondrial pathway by upregulating protein expression of Bax, cytochrome c, caspase-3, -9 and p53, and downregulating the relative levels of Bcl-2.	5-(2-formyl-3-hydroxyphenoxy)pentanoic acid	50-53	P53	Homo sapiens	183-186
31938352-11	2018	The protein levels of bax and cl-caspase-3 were significantly decreased and the expression of bcl-2 was increased after pretreated with p53 specific inhibitor pifithrin-alpha.	pifithrin	159-174	P53	Homo sapiens	136-139
29599323-10	2018	In addition, p53 was shown to be involved in gallic acid-mediated Fas, FasL, and DR5 expression as well as cell apoptosis in AGS cells.	ammonium ferrous sulfate	66-69	P53	Homo sapiens	13-16
29382728-0	2018	The curcumin analog HO-3867 selectively kills cancer cells by converting mutant p53 protein to transcriptionally active wildtype p53.	(3,5-bis((4-fluorophenyl)methylidene)-1-((1-hydroxy-2,2,5,5-tetramethyl-2,5-dihydro-1H-pyrrol-3-yl)methyl)piperidin-4-one)	20-27	P53	Homo sapiens	80-83
29382728-0	2018	The curcumin analog HO-3867 selectively kills cancer cells by converting mutant p53 protein to transcriptionally active wildtype p53.	(3,5-bis((4-fluorophenyl)methylidene)-1-((1-hydroxy-2,2,5,5-tetramethyl-2,5-dihydro-1H-pyrrol-3-yl)methyl)piperidin-4-one)	20-27	P53	Homo sapiens	129-132
29358327-12	2018	In conclusion, we found that p53 plays an important role in warfarin induced pAVIC calcification, and increased slug transcription by p53 is required for p53-mediated pAVIC calcification.	Warfarin	60-68	P53	Homo sapiens	29-32
29470985-0	2018	Cytoplasmic p53 contributes to the removal of uracils misincorporated by HIV-1 reverse transcriptase.	Uracil	46-53	P53	Homo sapiens	12-15
29470985-5	2018	Since the presence of proofreading activity is essential for DNA synthesis accuracy, we elucidated the potential involvement of cytoplasmic p53 in the U-editing activities during insertion of dUTP into DNA by recombinant HIV-1 RT (using isogenic p53-proficient and -deficient HCT116 cells).	deoxyuridine triphosphate	192-196	P53	Homo sapiens	140-143
29470985-8	2018	Accordingly, the increased abundance of p53 in nutlin-treated cells correlates with enhanced error-correction functions, namely, removal of incorporated uracil.	Uracil	153-159	P53	Homo sapiens	40-43
29470985-9	2018	The data substantiate the significance of p53 as a potential proofreader for removal of non-canonical dUTP from HIV DNA, thus preventing the consequences of dUTP misincorporation in cell-type specific infectivity of HIV.	deoxyuridine triphosphate	102-106	P53	Homo sapiens	42-45
29470985-9	2018	The data substantiate the significance of p53 as a potential proofreader for removal of non-canonical dUTP from HIV DNA, thus preventing the consequences of dUTP misincorporation in cell-type specific infectivity of HIV.	deoxyuridine triphosphate	157-161	P53	Homo sapiens	42-45
29301793-6	2018	Thus, our study provides evidence to support a role for S284 O-GlcNAc as a critical block of FOXO3 to induce subsequent cancer cell growth via abrogation of the p53 regulatory circuit.Significance: These findings highlight a posttranslational mechanism for indirect abrogation of the p53 pathway, one that may occur with some frequency in human cancer cells.	s284 o-glcnac	56-69	P53	Homo sapiens	161-164
29301793-6	2018	Thus, our study provides evidence to support a role for S284 O-GlcNAc as a critical block of FOXO3 to induce subsequent cancer cell growth via abrogation of the p53 regulatory circuit.Significance: These findings highlight a posttranslational mechanism for indirect abrogation of the p53 pathway, one that may occur with some frequency in human cancer cells.	s284 o-glcnac	56-69	P53	Homo sapiens	284-287
29535630-7	2018	HCT-116 colon carcinoma p53-/- knockout cells were 7.16-fold resistant toward As2O3 compared to wild-type cells.	Arsenic Trioxide	78-83	P53	Homo sapiens	24-27
29487530-0	2018	Scutellarin Increases Cisplatin-Induced Apoptosis and Autophagy to Overcome Cisplatin Resistance in Non-small Cell Lung Cancer via ERK/p53 and c-met/AKT Signaling Pathways.	scutellarin	0-11	P53	Homo sapiens	135-138
29113888-2	2018	In this work, p53-antibody was immobilized onto a green and biocompatible nanocomposite containing poly l-cysteine (P-Cys) as conductive matrix and graphene quantum dots (GQDs)/gold nanoparticles (GNPs) as dual amplification elements.	poly l-cysteine	99-114	P53	Homo sapiens	14-17
29207130-10	2018	Furthermore, treatment or co-treatment with LY294002 (phosphoinositide-3-kinase/Akt inhibitor) or Pifithrin-alpha (p53 inhibitor) with CME resulted in CME-induced G1 arrest which occurred through the p53-independent signaling pathway in hepatocellular carcinoma cells.	pifithrin	98-113	P53	Homo sapiens	115-118
29207130-10	2018	Furthermore, treatment or co-treatment with LY294002 (phosphoinositide-3-kinase/Akt inhibitor) or Pifithrin-alpha (p53 inhibitor) with CME resulted in CME-induced G1 arrest which occurred through the p53-independent signaling pathway in hepatocellular carcinoma cells.	pifithrin	98-113	P53	Homo sapiens	200-203
29251333-9	2018	Additionally, analysis by FACS indicated that apoptosis was induced following ribavirin treatment and caspase cascade, downstream of the p53 pathway, which indicated the activation of both exogenous and endogenous apoptosis in both malignant glioma cell lines.	Ribavirin	78-87	P53	Homo sapiens	137-140
29050931-6	2018	In addition, to comprehensively clarify the mechanisms of teriflunomide in NSCLC, we explored a genome-wide transcriptomic analysis, and found that teriflunomide was involved in multiple signaling pathways and cellular processes, such as cell cycle, apoptosis, MAPK and p53 signaling pathway.	teriflunomide	148-161	P53	Homo sapiens	270-273
29737207-6	2018	Silencing LPL increased the expression levels of senescence proteins such as p16INK4A and p53 and silencing KCNE2 reversed gene expressions of EGR1 and p-ERK in quercetin-treated aged HDFs.	Quercetin	161-170	P53	Homo sapiens	90-93
28901264-14	2018	TQ mediated its anti-proliferative effect and apoptosis induction by an up-regulation of TGFbeta1, p53 and p21 and a down-regulation of TGF-alpha and Bcl-2alpha.	N-(6-methoxy-8-quinolyl)-4-toluenesulfonamide	0-2	P53	Homo sapiens	99-102
29282038-10	2017	The TP53 mutation group displayed significantly worse DSS and overall survival rates than the wild-type group (P = 0.01 and P = 0.007, respectively).	dss	54-57	P53	Homo sapiens	4-8
29295500-0	2017	Decitabine and Melphalan Fail to Reactivate p73 in p53 Deficient Myeloma Cells.	Melphalan	15-24	P53	Homo sapiens	51-54
29317830-0	2018	Quercetin suppresses DNA double-strand break repair and enhances the radiosensitivity of human ovarian cancer cells via p53-dependent endoplasmic reticulum stress pathway.	Quercetin	0-9	P53	Homo sapiens	120-123
29317830-2	2018	However, the role of tumor suppressor p53 on quercetin"s radiosensitization and regulation of endoplasmic reticulum (ER) stress response in this process remains obscure.	Quercetin	45-54	P53	Homo sapiens	38-41
29317830-3	2018	Here, quercetin exposure resulted in ER stress, prolonged DNA repair, and the expression of p53 protein; phosphorylation on serine 15 and 20 increased in combination with X-irradiation.	Quercetin	6-15	P53	Homo sapiens	92-95
29317830-6	2018	Knocking down of p53 could reverse all the above effects under quercetin in combination with radiation.	Quercetin	63-72	P53	Homo sapiens	17-20
29317830-8	2018	In human ovarian cancer xenograft model, combined treatment of quercetin and radiation significantly restrained the growth of tumors, accompanied with the activation of p53, CCAAT/enhancer-binding protein homologous protein, and gamma-H2AX.	Quercetin	63-72	P53	Homo sapiens	169-172
29317830-9	2018	Overall, these results indicated that quercetin acted as a promising radiosensitizer through p53-dependent ER stress signals.	Quercetin	38-47	P53	Homo sapiens	93-96
29383169-4	2017	administration of p53-derived hybrid peptides to activate p73 can induce apoptosis of SFs by using adenoviral vectors encoding 37 amino acid (Ad37AA), a p53-derived hybrid peptide capable of activating p73, to transduce SFs in vitro and inject collagen-induced arthritis (CIA) joints in vivo.	SFS	86-89	P53	Homo sapiens	18-21
29383169-4	2017	administration of p53-derived hybrid peptides to activate p73 can induce apoptosis of SFs by using adenoviral vectors encoding 37 amino acid (Ad37AA), a p53-derived hybrid peptide capable of activating p73, to transduce SFs in vitro and inject collagen-induced arthritis (CIA) joints in vivo.	SFS	86-89	P53	Homo sapiens	153-156
29383169-9	2017	administration of p53-derived hybrid peptides can activate p73 to induce apoptosis of SFs and ameliorate the rheumatoid joint, implicating an enhancement of the p73-dependent apoptotic mechanism as a pharmacological strategy in the RA therapy.	SFS	86-89	P53	Homo sapiens	18-21
29416681-3	2018	We show here that a metabolic switch to oxidative phosphorylation (OXPHOS), either by treating cells with dichloroacetate (DCA) or by changing the available substrates, reduced expression of ABCB1, ABCC1, ABCC5 and ABCG2 in wild-type p53-expressing cells.	Dichloroacetic Acid	106-121	P53	Homo sapiens	234-237
29416681-3	2018	We show here that a metabolic switch to oxidative phosphorylation (OXPHOS), either by treating cells with dichloroacetate (DCA) or by changing the available substrates, reduced expression of ABCB1, ABCC1, ABCC5 and ABCG2 in wild-type p53-expressing cells.	Dichloroacetic Acid	123-126	P53	Homo sapiens	234-237
29292794-7	2017	Our study highlights a role for p53 in regulating nutrient metabolism and provides insight into how iron and possibly other metals such as zinc and manganese could be regulated in p53-inactivated tumor cells.	Manganese	148-157	P53	Homo sapiens	180-183
29116749-0	2017	Direct LC-MS/MS Detection of Guanine Oxidations in Exon 7 of the p53 Tumor Suppressor Gene.	Guanine	29-36	P53	Homo sapiens	65-68
29116749-4	2017	We oxidized a 32 base pair (bp) double-stranded (ds) oligonucleotide representing exon 7 of the p53 gene.	(ds) oligonucleotide	48-68	P53	Homo sapiens	96-99
29031202-5	2017	We showed that niclosamide could inhibit OSCC cells proliferation through causing cell cycle arrest in G1 phase and promoting apoptosis, while the cell cycle-related proteins MCM2, MCM7, CDK2 and CDK4 were downregulated and the apoptosis-related proteins p53 and cleaved caspase-3 were upregulated.	Niclosamide	15-26	P53	Homo sapiens	255-258
29107083-4	2017	DNA-alkylating agent methyl methanesulfonate caused a reduction in CXCR5 expression not only in parental MCF-7 cells but also in MCF-7-p53off cells with CRISPR/Cas9-mediated inactivation of the p53 gene.	Methyl Methanesulfonate	21-44	P53	Homo sapiens	135-138
28990231-8	2017	Mechanistically, IFI16 could activate p53 at Ser15 to up-regulate the p21WAF1/CIP1 level to inhibit tumour growth and migration, which was restored by the p53 inhibitor Pifithrin-alpha (20 mumol/L).	pifithrin	169-184	P53	Homo sapiens	38-41
28990231-8	2017	Mechanistically, IFI16 could activate p53 at Ser15 to up-regulate the p21WAF1/CIP1 level to inhibit tumour growth and migration, which was restored by the p53 inhibitor Pifithrin-alpha (20 mumol/L).	pifithrin	169-184	P53	Homo sapiens	155-158
28774804-2	2017	In this work, biotin conjugated p53-antibody (anti-p53) was immobilized onto a green and biocompatible nanocomposite containing poly l-cysteine (P-Cys) as conductive matrix and 3D gold nanoparticles (GNPs) as signal amplification element.	poly l-cysteine	128-143	P53	Homo sapiens	32-35
28774804-2	2017	In this work, biotin conjugated p53-antibody (anti-p53) was immobilized onto a green and biocompatible nanocomposite containing poly l-cysteine (P-Cys) as conductive matrix and 3D gold nanoparticles (GNPs) as signal amplification element.	poly l-cysteine	128-143	P53	Homo sapiens	51-54
29039478-7	2017	In particular, inhibition of p53 by pifithrin-alpha, and upregulation of eIF2alpha phosphorylation by Sal003, reduced cisplatin-induced apoptosis.	pifithrin	36-45	P53	Homo sapiens	29-32
29123181-3	2017	Carnosol (CAR), a natural inhibitor of MDM2/p53 complex, has been attracted attention for its anti-cancer effects on several tumor types, including GBM.	carnosol	0-8	P53	Homo sapiens	44-47
29123181-3	2017	Carnosol (CAR), a natural inhibitor of MDM2/p53 complex, has been attracted attention for its anti-cancer effects on several tumor types, including GBM.	carnosol	10-13	P53	Homo sapiens	44-47
28755014-2	2017	Dexamethasone, one of the premedications of pemetrexed, may downregulate p53 through the glucocorticoid receptor (GR).	Pemetrexed	44-54	P53	Homo sapiens	73-76
28802167-10	2017	Induction of p53 by 5-Aza-dC was tested in vitro using cancer cells.	Azacitidine	20-25	P53	Homo sapiens	13-16
28731124-0	2017	BMP7 mediates the anticancer effect of honokiol by upregulating p53 in HCT116 cells.	honokiol	39-47	P53	Homo sapiens	64-67
30090552-3	2017	TBP and TBEP could induce both mitochondrial and p53 mediated apoptosis through different mitogen-activated protein kinase (MAPK) signal pathways.	tributyl phosphate	0-3	P53	Homo sapiens	49-52
28696098-0	2017	Enhanced Binding Affinity via Destabilization of the Unbound State: A Millisecond Hydrogen-Deuterium Exchange Study of the Interaction between p53 and a Pleckstrin Homology Domain.	Deuterium	91-100	P53	Homo sapiens	143-146
28798402-0	2017	Nutlin-3 enhances the bortezomib sensitivity of p53-defective cancer cells by inducing paraptosis.	Bortezomib	22-32	P53	Homo sapiens	48-51
28798402-3	2017	In this study, we show that treatment of various p53-defective bortezomib-resistant solid tumor cells with bortezomib plus nutlin-3 induces paraptosis, which is a cell death mode accompanied by dilation of the endoplasmic reticulum (ER) and mitochondria.	Bortezomib	63-73	P53	Homo sapiens	49-52
28798402-3	2017	In this study, we show that treatment of various p53-defective bortezomib-resistant solid tumor cells with bortezomib plus nutlin-3 induces paraptosis, which is a cell death mode accompanied by dilation of the endoplasmic reticulum (ER) and mitochondria.	Bortezomib	107-117	P53	Homo sapiens	49-52
28781658-12	2017	The present study reports a case of a sudden acceleration of DTC metastatic progression following sorafenib discontinuation, which could have been due to the emergence of sorafenib-resistant undifferentiated p53-positive tumor cell clones.	Sorafenib	98-107	P53	Homo sapiens	208-211
28781658-12	2017	The present study reports a case of a sudden acceleration of DTC metastatic progression following sorafenib discontinuation, which could have been due to the emergence of sorafenib-resistant undifferentiated p53-positive tumor cell clones.	Sorafenib	171-180	P53	Homo sapiens	208-211
29137381-6	2017	The marker genes/pathways are involved in the processes of purine nucleotide biosynthesis, ATP-binding, tetrahydrofolate metabolism, building mitochondrial matrix, biosynthesis of amino acids, tRNA aminoacylation and NADP-linked oxidation-reduction processes, as well as in the tyrosine phosphatase activity, p53 signaling, cell cycle progression and the G1/S and G2/M checkpoints.	purine	59-65	P53	Homo sapiens	309-312
28554861-4	2017	Abeta1-40-induced ROS production and p53 expression were increased as determined by DCF-derived fluorescence using flow cytometry and Western blotting and reduced in response to galantamine pretreatment.	Galantamine	178-189	P53	Homo sapiens	37-40
28505595-8	2017	Functional mapping of transcripts uniquely regulated by the azacitidine-panobinostat combination in MV4;11 cells identified p53 as an upstream regulator.	Azacitidine	60-71	P53	Homo sapiens	124-127
28505595-9	2017	A comparison of the uniquely modulated transcripts by azacitidine-panobinostat combination in MV4;11 cells versus AML-193 and THP-1 cells, bearing mutated p53, also revealed p53 as the topmost upstream regulator.	Azacitidine	54-65	P53	Homo sapiens	174-177
28505595-10	2017	Finally, expression of mutant p53 in MV4;11 cells reduced sensitivity to azacitidine-panobinostat combination, suggesting that p53 may be a predictor of response to epigenetic therapy in pediatric AML.	Azacitidine	73-84	P53	Homo sapiens	30-33
28505595-10	2017	Finally, expression of mutant p53 in MV4;11 cells reduced sensitivity to azacitidine-panobinostat combination, suggesting that p53 may be a predictor of response to epigenetic therapy in pediatric AML.	Azacitidine	73-84	P53	Homo sapiens	127-130
28535155-6	2017	RESULTS: Although APOBEC3B expression increased the incorporation of genomic uracil, invoked DDR biomarkers and caused cell cycle arrest, inactivation of p53 circumvented APOBEC3B-induced cell cycle arrest without reversing the increase in genomic uracil or DDR biomarkers.	Uracil	77-83	P53	Homo sapiens	154-157
28535155-6	2017	RESULTS: Although APOBEC3B expression increased the incorporation of genomic uracil, invoked DDR biomarkers and caused cell cycle arrest, inactivation of p53 circumvented APOBEC3B-induced cell cycle arrest without reversing the increase in genomic uracil or DDR biomarkers.	Uracil	248-254	P53	Homo sapiens	154-157
28465245-9	2017	Besides, mutp53 but not wild type p53 was essential for 1,25(OH)2D3-stimulated upregulation of p21 in gastric cancer cells.	(oh)2d3	60-67	P53	Homo sapiens	12-15
29100281-5	2017	The MMS-induced upregulation of RECQ1 expression is p53-dependent as it was observed in p53-proficient but not in isogenic p53-deficient cells.	Methyl Methanesulfonate	4-7	P53	Homo sapiens	52-55
29100281-5	2017	The MMS-induced upregulation of RECQ1 expression is p53-dependent as it was observed in p53-proficient but not in isogenic p53-deficient cells.	Methyl Methanesulfonate	4-7	P53	Homo sapiens	88-91
29100281-5	2017	The MMS-induced upregulation of RECQ1 expression is p53-dependent as it was observed in p53-proficient but not in isogenic p53-deficient cells.	Methyl Methanesulfonate	4-7	P53	Homo sapiens	88-91
28580174-2	2017	We inactivated TP53 and/or RB1 by siRNA mediated knockdown in breast cancer cell lines varying with respect to ER/PgR and Her-2 status as well as TP53 and RB1 mutation status (MCF-7, T47D, HTB-122 and CRL2324) and determined effects on cell cycle arrest, apoptosis and senescence with or without concomitant treatment with doxorubicin.	crl2324	201-208	P53	Homo sapiens	15-19
28607180-7	2017	This impact of p53 loss on 5-methylcytosine (5mC) heterogeneity was also evident in human ESCs and mouse embryos in vivo.	5-Methylcytosine	27-43	P53	Homo sapiens	15-18
28607180-7	2017	This impact of p53 loss on 5-methylcytosine (5mC) heterogeneity was also evident in human ESCs and mouse embryos in vivo.	5-Methylcytosine	45-48	P53	Homo sapiens	15-18
28476801-12	2017	CONCLUSION: AzaC significantly increases the sensitivity of MCF7 cells to Dox via activation of ERK1/2, P53, BAX and caspase-3.	Azacitidine	12-16	P53	Homo sapiens	104-107
28242062-5	2017	Anti-proliferative activity of seven novel racemic klavuzon derivatives were reported against MCF-7, PC3, HCT116 p53+/+ and HCT116 p53-/- cancer cell lines.	klavuzon	51-59	P53	Homo sapiens	113-116
28242062-5	2017	Anti-proliferative activity of seven novel racemic klavuzon derivatives were reported against MCF-7, PC3, HCT116 p53+/+ and HCT116 p53-/- cancer cell lines.	klavuzon	51-59	P53	Homo sapiens	131-134
28350084-13	2017	In conclusion, patients with TP53 mutations, RET mutations and sorafenib-targeted gene mutations were demonstrated to be associated with poor HCC prognosis, which suggests that both TP53 and RET may serve as biomarkers of prognostic evaluation and targeted therapy in HCC.	Sorafenib	63-72	P53	Homo sapiens	182-186
27919789-6	2017	Modulation of this network, by increasing the level of the novel p73-dependent target MIR3158, was found to induce anti-oncogenic/anti-invasive responses in p53-mutant cancer cells.	mir3158	86-93	P53	Homo sapiens	157-160
28195382-3	2017	This study evaluated chemical specificity of the p53 pathway response by manipulating p53 or its upstream kinases and assessing the effect on DNA damage and cellular responses to prototype chemicals: etoposide (ETP, topoisomerase II inhibitor) and methyl methane sulfonate (MMS, alkylating agent).	Methyl Methanesulfonate	248-272	P53	Homo sapiens	49-52
28195382-3	2017	This study evaluated chemical specificity of the p53 pathway response by manipulating p53 or its upstream kinases and assessing the effect on DNA damage and cellular responses to prototype chemicals: etoposide (ETP, topoisomerase II inhibitor) and methyl methane sulfonate (MMS, alkylating agent).	Methyl Methanesulfonate	274-277	P53	Homo sapiens	49-52
28199187-8	2017	Interestingly, the combined treatment with curcumin and docetaxel modulates the expression of RTKs, PI3K, phospho-AKT, NF-kappa B, p53, and COX-2.	Docetaxel	56-65	P53	Homo sapiens	131-134
28280414-9	2017	Knockdown of Foxo3a and inhibition of JNK activity reduced the signaling activities of p53, p21 and GADD45, triggered by quercetin.	Quercetin	121-130	P53	Homo sapiens	87-90
28283087-0	2017	Bisdemethoxycurcumin enhances X-ray-induced apoptosis possibly through p53/Bcl-2 pathway.	bisdemethoxycurcumin	0-20	P53	Homo sapiens	71-74
28283087-3	2017	Knockdown of p53 significantly attenuated the radiosensitizing effect of BDMC.	bisdemethoxycurcumin	73-77	P53	Homo sapiens	13-16
28283087-5	2017	On the other hand, BDMC promoted the X-ray-induced dephosphorylation at Ser 70 in Bcl-2"s flexible loop regulatory domain and Bcl-2 binding to p53.	bisdemethoxycurcumin	19-23	P53	Homo sapiens	143-146
28347251-8	2017	Meanwhile, knockdown of methyl methanesulfonate and ultraviolet-sensitive gene clone 81 activated the p53/Bcl-2 pathway in response to cisplatin.	Methyl Methanesulfonate	24-47	P53	Homo sapiens	102-105
28211885-10	2017	Our results indicate that PTC596 deserves further evaluation in clinical trials for refractory or relapsed AML patients, especially for those with unfavorable complex karyotype or therapy-related AML that are frequently associated with p53 mutations.	PTC596	26-32	P53	Homo sapiens	236-239
27943171-5	2017	In this review, we present a comprehensive account of the systematic development of and recent progress in diverse spiro-oxindole derivatives active as potent selective inhibitors of p53-MDM2 interaction with special emphasis on spiro-pyrrolidinyl oxindoles (the MI series), their mechanism of action, and structure-activity relationship.	spiro-oxindole	115-129	P53	Homo sapiens	183-186
27943171-5	2017	In this review, we present a comprehensive account of the systematic development of and recent progress in diverse spiro-oxindole derivatives active as potent selective inhibitors of p53-MDM2 interaction with special emphasis on spiro-pyrrolidinyl oxindoles (the MI series), their mechanism of action, and structure-activity relationship.	spiro-pyrrolidinyl oxindoles	229-257	P53	Homo sapiens	183-186
27943171-7	2017	Recent progress in spiro-oxindole derivatives as potent small molecule inhibitors of p53-MDM2 interaction, useful as anticancer agents, is described with reference to their mechanism of action and structure-activity relationship.	spiro-oxindole	19-33	P53	Homo sapiens	85-88
28129641-0	2017	The p53 protein plays a central role in the mechanism of action of epigentic drugs that alter the methylation of cytosine residues in DNA.	Cytosine	113-121	P53	Homo sapiens	4-7
28081035-10	2017	p53, by preferential removal of purine over pyrimidine ribonucleotides, may affect the ribonucleotide mutation spectra produced by HIV-1 reverse transcriptase.	purine	32-38	P53	Homo sapiens	0-3
27791982-0	2017	ErbB2 inhibition by lapatinib promotes degradation of mutant p53 protein in cancer cells.	Lapatinib	20-29	P53	Homo sapiens	61-64
27791982-5	2017	Here we report that pharmacological interception of this circuit by ErbB2 inhibitor lapatinib downregulates mutant p53 in vitro and in vivo.	Lapatinib	84-93	P53	Homo sapiens	115-118
27791982-6	2017	We found that ErbB2 inhibition by lapatinib inhibits transcription factor HSF1, and its target Hsp90, followed by mutant p53 degradation in MDM2 dependent manner.	Lapatinib	34-43	P53	Homo sapiens	121-124
27791982-7	2017	Thus, our data suggest that mutant p53 sensitizes cancer cells to lapatinib via two complementary mechanisms: mutant p53 mediated amplification of ErbB2 signaling, and simultaneous annihilation of both potent oncogenic drivers, ErbB2 and mutant p53.	Lapatinib	66-75	P53	Homo sapiens	35-38
27791982-7	2017	Thus, our data suggest that mutant p53 sensitizes cancer cells to lapatinib via two complementary mechanisms: mutant p53 mediated amplification of ErbB2 signaling, and simultaneous annihilation of both potent oncogenic drivers, ErbB2 and mutant p53.	Lapatinib	66-75	P53	Homo sapiens	117-120
28578643-0	2017	Glioblastoma Targeted Gene Therapy Based on pEGFP/p53-Loaded Superparamagnetic Iron Oxide Nanoparticles.	ferric oxide	79-89	P53	Homo sapiens	50-53
27865929-1	2017	Phosphanegold(I) thiolates, Ph3PAu[SC(OR)=NPh], R=Me (1), Et (2) and iPr (3), were previously shown to be significantly cytotoxic toward HT-29 cancer cells and to induce cell death by both intrinsic and extrinsic apoptotic pathways whereby 1 activated the p73 gene, and each of 2 and 3 activated p53; 2 also caused apoptotic cell death via the c-Jun N-terminal kinase/mitogen-activated protein kinase pathway.	thiolates	17-26	P53	Homo sapiens	296-299
27837434-7	2017	In contrast, only calcification, laterality, and lipid13 (lipid13/total Choline) were statistically significant parameters for differentiating TP53 wild-type and mutant in IDH mutant gliomas.	lipid13	49-56	P53	Homo sapiens	143-147
27837434-7	2017	In contrast, only calcification, laterality, and lipid13 (lipid13/total Choline) were statistically significant parameters for differentiating TP53 wild-type and mutant in IDH mutant gliomas.	lipid13	58-65	P53	Homo sapiens	143-147
28484169-8	2017	In the case of TP53 mutations, prognosis is poor for both hematopoietic stem cell transplantation and AZA treatment, although, patients with TP53 mutations have been shown to respond favorably to decitabine administration for 10 days.	Azacitidine	102-105	P53	Homo sapiens	15-19
27822577-0	2016	Combined bortezomib-based chemotherapy and p53 gene therapy using hollow mesoporous silica nanospheres for p53 mutant non-small cell lung cancer treatment.	Bortezomib	9-19	P53	Homo sapiens	107-110
27822577-2	2016	Then we found that the tumor-suppressing effect of BTZ or HMSNs-BTZ was compromised in p53 null/mutant NSCLC.	Bortezomib	51-54	P53	Homo sapiens	87-90
27822577-5	2016	Here, HMSN-based co-delivery of BTZ and the tumor-suppressor gene p53 was developed for p53 signal impaired NSCLC therapy.	Bortezomib	32-35	P53	Homo sapiens	66-69
27822577-5	2016	Here, HMSN-based co-delivery of BTZ and the tumor-suppressor gene p53 was developed for p53 signal impaired NSCLC therapy.	Bortezomib	32-35	P53	Homo sapiens	88-91
27822577-7	2016	Live/dead staining assay for treated H1299 cells exhibited wider distribution, and higher dead staining was prominent in the HMSNs-PEI-BTZ-p53 group when compared to that of the HMSNs-BTZ group with equivalent BTZ concentration, which was consistent with accumulated p53 expression.	Bortezomib	135-138	P53	Homo sapiens	139-142
27822577-7	2016	Live/dead staining assay for treated H1299 cells exhibited wider distribution, and higher dead staining was prominent in the HMSNs-PEI-BTZ-p53 group when compared to that of the HMSNs-BTZ group with equivalent BTZ concentration, which was consistent with accumulated p53 expression.	Bortezomib	135-138	P53	Homo sapiens	267-270
27822577-9	2016	Western blotting and real time PCR results showed that several p53 downstream genes responded strongly and synergistically to BTZ function and p53 restored expression (accumulation of p21 and bax, activation of caspase 3, down-regulation of Bcl-2, etc.).	Bortezomib	126-129	P53	Homo sapiens	63-66
27621033-14	2016	The expression level of LC3 and ERK as well as cytoplasm p53, cleaved Caspase-3 and PARP was positively correlated with the concentration of quercetin nanoparticle.	Quercetin	141-150	P53	Homo sapiens	57-60
27693638-0	2016	DNA-PKcs, a novel functional target of acriflavine, mediates acriflavine"s p53-dependent synergistic anti-tumor efficiency with melphalan.	Melphalan	128-137	P53	Homo sapiens	75-78
28231749-8	2017	Moreover, MDM2 and p-MDM2 proteins were decreased, while p53 and p-p53 proteins were increased, both in a dose-dependent manner, after A549 treatment with total flavonoids and total tannins.	Flavonoids	161-171	P53	Homo sapiens	67-70
28231749-10	2017	Our results indicated that total flavonoids and total tannins from SCR exerted a remarkable effect in reducing A549 growth through their action on mitochondrial pathway and disruption of MDM2-p53 balance.	Flavonoids	33-43	P53	Homo sapiens	192-195
28321407-7	2017	When using Pifithrin-alpha (one of p53 inhibitors), the level of p53-dependent apoptosis was significantly lower than untreated, which suggested that p53 was possibly involved in PTEN-dependent apoptosis.	pifithrin	11-26	P53	Homo sapiens	35-38
28321407-7	2017	When using Pifithrin-alpha (one of p53 inhibitors), the level of p53-dependent apoptosis was significantly lower than untreated, which suggested that p53 was possibly involved in PTEN-dependent apoptosis.	pifithrin	11-26	P53	Homo sapiens	65-68
28321407-7	2017	When using Pifithrin-alpha (one of p53 inhibitors), the level of p53-dependent apoptosis was significantly lower than untreated, which suggested that p53 was possibly involved in PTEN-dependent apoptosis.	pifithrin	11-26	P53	Homo sapiens	65-68
27029827-6	2017	The combination of Aza+SAHA significantly increased p53 protein binding to DNA in pax5 promoter region (p&lt;0.01).	Azacitidine	19-22	P53	Homo sapiens	52-55
27029827-7	2017	More efficient binding of the transcription factor p53 to pax5 promoter region is likely because SAHA increased accessibility of the chromatin conformation and Aza-demethylated DNA was more permissive, allowing transcription factors to bind.	Azacitidine	160-163	P53	Homo sapiens	51-54
27029827-8	2017	CONCLUSION: Our study not only explained an underlying mechanism, that pax5 re-expression was induced by Aza+SAHA combination in H460 cells via p53, but also demonstrated a pattern showing that the combination of demethylating agent and HDAC inhibitor can re-activate tumor suppressor gene (TSG) which is associated with the enhancement of transcription factors binding to the promoter region of the TSG.	Azacitidine	105-108	P53	Homo sapiens	144-147
27991505-0	2016	Wip1 inhibitor GSK2830371 inhibits neuroblastoma growth by inducing Chk2/p53-mediated apoptosis.	GSK2830371	15-25	P53	Homo sapiens	73-76
27991505-3	2016	Wip1 is a negative regulator of p53 and hindrance of Wip1 activity by novel inhibitor GSK2830371 is a potential strategy to activate p53"s tumor suppressing function in NB.	GSK2830371	86-96	P53	Homo sapiens	133-136
27991505-5	2016	Here we report that novel Wip1 inhibitor GSK2830371 induced Chk2/p53-mediated apoptosis in NB cells in a p53-dependent manner.	GSK2830371	41-51	P53	Homo sapiens	65-68
27991505-5	2016	Here we report that novel Wip1 inhibitor GSK2830371 induced Chk2/p53-mediated apoptosis in NB cells in a p53-dependent manner.	GSK2830371	41-51	P53	Homo sapiens	105-108
27991505-6	2016	In addition, GSK2830371 suppressed the colony-formation potential of p53 wild-type NB cell lines.	GSK2830371	13-23	P53	Homo sapiens	69-72
27991505-9	2016	Taken together, this study suggests that GSK2830371 induces Chk2/p53-mediated apoptosis both in vitro and in vivo in a p53 dependent manner.	GSK2830371	41-51	P53	Homo sapiens	65-68
27991505-9	2016	Taken together, this study suggests that GSK2830371 induces Chk2/p53-mediated apoptosis both in vitro and in vivo in a p53 dependent manner.	GSK2830371	41-51	P53	Homo sapiens	119-122
27591972-4	2016	RESULTS: The results showed that the cell line with p53 deleted the C-terminal sequences (p53(del)) was more sensitive to navelbine (NVB) compared to the cell line that carried the full length p53 (p53(wt)).	Vinorelbine	122-131	P53	Homo sapiens	52-55
27591972-4	2016	RESULTS: The results showed that the cell line with p53 deleted the C-terminal sequences (p53(del)) was more sensitive to navelbine (NVB) compared to the cell line that carried the full length p53 (p53(wt)).	Vinorelbine	122-131	P53	Homo sapiens	90-93
27591972-4	2016	RESULTS: The results showed that the cell line with p53 deleted the C-terminal sequences (p53(del)) was more sensitive to navelbine (NVB) compared to the cell line that carried the full length p53 (p53(wt)).	Vinorelbine	122-131	P53	Homo sapiens	90-93
27591972-4	2016	RESULTS: The results showed that the cell line with p53 deleted the C-terminal sequences (p53(del)) was more sensitive to navelbine (NVB) compared to the cell line that carried the full length p53 (p53(wt)).	Vinorelbine	122-131	P53	Homo sapiens	90-93
27941987-7	2016	Oncogene combination m-Ras/m-p53/m-PIK3CA efficiently transformed both K5+/K19- and K5+/K19+ cell lines in-vitro, as assessed by anchorage-independent soft agar colony formation assay.	Agar	156-160	P53	Homo sapiens	29-32
26920997-0	2016	Methotrexate selectively targets human proinflammatory macrophages through a thymidylate synthase/p53 axis.	Methotrexate	0-12	P53	Homo sapiens	98-101
26920997-8	2016	Furthermore, p53 activity was found to mediate the TS-dependent MTX-responsiveness of proinflammatory TS+ GM-MO.	Methotrexate	64-67	P53	Homo sapiens	13-16
26920997-10	2016	CONCLUSIONS: Macrophage response to MTX is polarisation-dependent and determined by the TS-p53 axis.	Methotrexate	36-39	P53	Homo sapiens	91-94
27588384-9	2016	Exposure to p-coumaric acid increased p53 and p21 expression but decreased CDK4 levels in both cell types, which could result in the observed G0/G1 arrest.	p-coumaric acid	12-27	P53	Homo sapiens	38-41
27710854-7	2016	Oxidative biomarkers (TBARS and protein carbonyl levels) and activity of antioxidant enzymes (CAT, SOD and GR) increased, and reduced glutathione (GSH) was depleted in animals treated with ABZ, indicating an oxidative stress condition, leading to a DNA damage causing phosphorylation of histone H2A variant, H2AX, and triggering apoptosis signaling, which was confirmed by increasing Bax/Bcl-xL rate, p53 and Bax expression.	Albendazole	189-192	P53	Homo sapiens	401-404
27965580-7	2016	The knockdown/over-expression of p53 was used to explain the differential sensitivity of HCC cell lines to sorafenib and/or OSU-2S.	Sorafenib	107-116	P53	Homo sapiens	33-36
27965580-13	2016	The p53 status in HCC cells predicts their sensitivity toward both sorafenib and OSU-2S.	Sorafenib	67-76	P53	Homo sapiens	4-7
27775892-0	2016	Discovery of Novel Spiro[3H-indole-3,2"-pyrrolidin]-2(1H)-one Compounds as Chemically Stable and Orally Active Inhibitors of the MDM2-p53 Interaction.	spiro(3H-indole-3,2'-pyrrolidin)-2(1H)-one	19-61	P53	Homo sapiens	134-137
27775892-1	2016	Scaffold modification based on Wang"s pioneering MDM2-p53 inhibitors led to novel, chemically stable spiro-oxindole compounds bearing a spiro[3H-indole-3,2"-pyrrolidin]-2(1H)-one scaffold that are not prone to epimerization as observed for the initial spiro[3H-indole-3,3"-pyrrolidin]-2(1H)-one scaffold.	spiro-oxindole	101-115	P53	Homo sapiens	54-57
27775892-1	2016	Scaffold modification based on Wang"s pioneering MDM2-p53 inhibitors led to novel, chemically stable spiro-oxindole compounds bearing a spiro[3H-indole-3,2"-pyrrolidin]-2(1H)-one scaffold that are not prone to epimerization as observed for the initial spiro[3H-indole-3,3"-pyrrolidin]-2(1H)-one scaffold.	spiro(3H-indole-3,2'-pyrrolidin)-2(1H)-one	136-178	P53	Homo sapiens	54-57
27638049-8	2016	Additionally, ATO treatment leads to p53-regulated mitochondrial apoptosis, where p53 phosphorylation plays a key role.	Arsenic Trioxide	14-17	P53	Homo sapiens	37-40
27638049-8	2016	Additionally, ATO treatment leads to p53-regulated mitochondrial apoptosis, where p53 phosphorylation plays a key role.	Arsenic Trioxide	14-17	P53	Homo sapiens	82-85
27573670-5	2016	The antiproliferative effect of GW501516 was directly linked to cell cycle arrest at the G0/G1 to S phase transition, which was followed by the down-regulation of cyclin-dependent kinase 4 along with increased levels of p21 and p53.	GW 501516	32-40	P53	Homo sapiens	228-231
27641669-0	2016	p53-dependent and -independent mechanisms are involved in (E)-1-(2-hydroxyphenyl)-3-(2-methoxynaphthalen-1-yl)prop-2-en-1-one (HMP)-induced apoptosis in HCT116 colon cancer cells.	(E)-1-(2-hydroxyphenyl)-3-(2-methoxynaphthalen-1-yl)prop-2-en-1-one	58-125	P53	Homo sapiens	0-3
27641669-0	2016	p53-dependent and -independent mechanisms are involved in (E)-1-(2-hydroxyphenyl)-3-(2-methoxynaphthalen-1-yl)prop-2-en-1-one (HMP)-induced apoptosis in HCT116 colon cancer cells.	(E)-1-(2-hydroxyphenyl)-3-(2-methoxynaphthalen-1-yl)prop-2-en-1-one	127-130	P53	Homo sapiens	0-3
27611952-3	2016	TP53 status was correlated to response to neoadjuvant anthracycline/taxane-based chemotherapy with or without carboplatin and trastuzumab/lapatinib in HER2-positive and bevacizumab in TNBC.	Lapatinib	138-147	P53	Homo sapiens	0-4
27270786-1	2016	TP53 abnormalities lead to resistance to purine analogues and are found in over 40% of patients with refractory chronic lymphocytic leukemia (CLL).	purine	41-47	P53	Homo sapiens	0-4
27774504-1	2016	This article contains raw and processed data related to a research, "Honokiol induces autophagic cell death in malignant glioma through reactive oxygen species-mediated regulation of the p53/PI3K/Akt/mTOR signaling pathway" (C.J.	honokiol	69-77	P53	Homo sapiens	187-190
27705786-2	2016	Here, we have identified an acetylation site at lysine K98 in mouse p53 (or K101 for human p53).	lysine k98	48-58	P53	Homo sapiens	91-94
27327234-6	2016	Pifithrin-alpha (PFT), an inhibitor of p53, significantly enhanced ARS-induced cytotoxicity in HepG2 cells, and the forced expression of wild-type p53 significantly enhanced ARS-induced cytotoxicity in Hep3B cells.	pifithrin	0-15	P53	Homo sapiens	39-42
27327234-6	2016	Pifithrin-alpha (PFT), an inhibitor of p53, significantly enhanced ARS-induced cytotoxicity in HepG2 cells, and the forced expression of wild-type p53 significantly enhanced ARS-induced cytotoxicity in Hep3B cells.	pifithrin	17-20	P53	Homo sapiens	39-42
27591796-8	2016	Increased Nrf2 expression and catalase activity at 40 C were inhibited by the antioxidant PEG-catalase and by p53 inhibitor pifithrin-alpha.	pifithrin	124-139	P53	Homo sapiens	110-113
28101201-10	2016	Notably, following treatment of HepG2 cells with the autophagy inhibitor, BA1, the expression of apoptosis-related proteins, including Bax, Bak and p53, were significantly decreased (P&lt;0.05), and cell viability was recovered to a certain extent.	bafilomycin A1	74-77	P53	Homo sapiens	148-151
27471307-9	2016	P53 and p21 expression were upregulated in MSC-ITP, but inhibition of p53 with pifithrin-alpha markedly inhibited apoptosis and senescence.	pifithrin	79-94	P53	Homo sapiens	70-73
27565221-9	2016	Ca-Asp also up-regulated the levels of caspase-3 and p53, but down regulated the level of cyclin D1, NF-kappaB, COX-2 and PGE2.	ca-asp	0-6	P53	Homo sapiens	53-56
26867804-5	2016	Here we demonstrate that the previously reported CDP-associated inhibition of bone repair can be modulated by the administration of a small molecule p53 inducer (nutlin-3).	Cytidine Diphosphate	49-52	P53	Homo sapiens	149-152
33945996-8	2021	Additionally, the expression of these proteins can be reversed by the use of pifithrin-alpha (PFT-alpha), a p53 inhibitor.	pifithrin	94-103	P53	Homo sapiens	108-111
26867804-9	2016	Collectively, these results demonstrate that the induction of p53 peri-operatively protects bone healing from the toxic effects of CDP, while maintaining OS toxicity.	Cytidine Diphosphate	131-134	P53	Homo sapiens	62-65
27846853-7	2016	Application of DGCA to the TCGA RNA-seq data in breast cancer not only identifies key changes in the regulatory relationships between TP53 and PTEN and their target genes in the presence of inactivating mutations, but also reveals an immune-related differential correlation module that is specific to triple negative breast cancer (TNBC).	dgca	15-19	P53	Homo sapiens	134-138
33990090-10	2021	AR amplification and TP53 and/or RB1 alterations were associated with resistance to abiraterone or docetaxel.	Docetaxel	99-108	P53	Homo sapiens	21-25
27543608-3	2016	Here, we report a rationally synthesized chalcone-based pyrido[ b ]indole, CPI-7c, as a unique small-molecule inhibitor of MDM2, which not only inhibited MDM2-p53 interaction but also promoted MDM2 degradation.	chalcone-based pyrido[ b ]indole	41-73	P53	Homo sapiens	159-162
27626308-6	2016	GSK2830371 inhibited the cell growth, being prominent in p53 wild-type cells.	GSK2830371	0-10	P53	Homo sapiens	57-60
27626308-9	2016	GSK2830371 increased the levels of total and Ser15-phosphorylated p53, and p53 targets p21 and PUMA.	GSK2830371	0-10	P53	Homo sapiens	66-69
27659302-5	2016	This high-throughput western blot approach allowed us to identify and characterize alterations in cellular signal transduction that occur during the development of resistance to the kinase inhibitor Lapatinib, revealing major changes in the activation state of Ephrin-mediated signalling and a central role for p53-controlled processes.	Lapatinib	199-208	P53	Homo sapiens	311-314
27626308-9	2016	GSK2830371 increased the levels of total and Ser15-phosphorylated p53, and p53 targets p21 and PUMA.	GSK2830371	0-10	P53	Homo sapiens	75-78
34035828-9	2021	Further analysis showed that the HGD activity of quercetin, formononetin, kaempferol, isorhamnetin, and beta-sitosterol ingredients is possible through VEGFA, IL6, TNF, AKT1, and TP53 targets involved in TNF, toll-like receptors, and MAPK-related pathways, which have anti-inflammatory, antiapoptosis, antioxidation, and autophagy effects, relieve renal fibrosis and renal cortex injury, and improve renal function, thus delaying the development of DN.	Quercetin	49-58	P53	Homo sapiens	179-183
27626308-10	2016	GSK2830371 and the MDM2 inhibitor Nutlin-3a acted synergistically in p53 wild-type cells.	GSK2830371	0-10	P53	Homo sapiens	69-72
27626308-11	2016	Interestingly, GSK2830371 sensitized MCL cells to bortezomib and doxorubicin in p53 wild-type and mutant cells; p38 signaling appeared to be involved in the GSK2830371/bortezomib lethality.	GSK2830371	15-25	P53	Homo sapiens	80-83
27626308-11	2016	Interestingly, GSK2830371 sensitized MCL cells to bortezomib and doxorubicin in p53 wild-type and mutant cells; p38 signaling appeared to be involved in the GSK2830371/bortezomib lethality.	Bortezomib	50-60	P53	Homo sapiens	80-83
27626308-11	2016	Interestingly, GSK2830371 sensitized MCL cells to bortezomib and doxorubicin in p53 wild-type and mutant cells; p38 signaling appeared to be involved in the GSK2830371/bortezomib lethality.	Bortezomib	168-178	P53	Homo sapiens	80-83
27515963-4	2016	AZD1152 treatment caused polyploidy and non-apoptotic cell death in all cell lines irrespective of p53 status and was accompanied by poly-merotelic kinetochore-microtubule attachments and DNA damage.	2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate	0-7	P53	Homo sapiens	99-102
27422117-2	2016	This is the first study on the interaction of wild-type p53 with guanine quadruplexes formed by the human telomere sequence.	Guanine	65-72	P53	Homo sapiens	56-59
27422117-5	2016	The presence of the quadruplex-stabilizing ligand, N-methyl mesoporphyrin IX (NMM), increases p53 recognition of G-quadruplexes in potassium.	N-methylmesoporphyrin IX	51-76	P53	Homo sapiens	94-97
27432655-11	2016	Furthermore, inhibition of NF-kappaB with Bay11-7082 decreased p53 expression in the MEG3-transfected cells.	3-(4-methylphenylsulfonyl)-2-propenenitrile	42-52	P53	Homo sapiens	63-66
27515963-8	2016	A concomitant increase of the activating natural killer (NK) cell ligand MIC A/B in p53-deficient cells and an induction of FAS/CD95 in cells containing p53 rendered AZD1152-treated cells more susceptible for NK-cell-mediated lysis.	2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate	166-173	P53	Homo sapiens	84-87
34035828-9	2021	Further analysis showed that the HGD activity of quercetin, formononetin, kaempferol, isorhamnetin, and beta-sitosterol ingredients is possible through VEGFA, IL6, TNF, AKT1, and TP53 targets involved in TNF, toll-like receptors, and MAPK-related pathways, which have anti-inflammatory, antiapoptosis, antioxidation, and autophagy effects, relieve renal fibrosis and renal cortex injury, and improve renal function, thus delaying the development of DN.	formononetin	60-72	P53	Homo sapiens	179-183
27515963-8	2016	A concomitant increase of the activating natural killer (NK) cell ligand MIC A/B in p53-deficient cells and an induction of FAS/CD95 in cells containing p53 rendered AZD1152-treated cells more susceptible for NK-cell-mediated lysis.	2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate	166-173	P53	Homo sapiens	153-156
27622714-7	2016	In contrast, in functional p53-impaired cells, this phytochemical exploits p53-paralogue p73, which up-regulates FAS to cleave BID through FAS-FADD-caspase-8-pathway.	ammonium ferrous sulfate	113-116	P53	Homo sapiens	27-30
27622714-7	2016	In contrast, in functional p53-impaired cells, this phytochemical exploits p53-paralogue p73, which up-regulates FAS to cleave BID through FAS-FADD-caspase-8-pathway.	ammonium ferrous sulfate	113-116	P53	Homo sapiens	75-78
27262408-0	2016	A new semisynthetic 1-O-acetyl-6-O-lauroylbritannilactone induces apoptosis of human laryngocarcinoma cells through p53-dependent pathway.	1-O-acetyl-6-O-lauroylbritannilactone	20-57	P53	Homo sapiens	116-119
34035828-10	2021	The molecular docking results showed that quercetin, formononetin, kaempferol, isorhamnetin, beta-sitosterol had a good binding activity with VEGFA, IL6, TNF, AKT1, and TP53.	Quercetin	42-51	P53	Homo sapiens	169-173
27545131-0	2016	[Icariin reduces S-nitrosogultathione induced endothelial cell apoptosis through modulating AKT/P53 pathway].	icariin	1-8	P53	Homo sapiens	96-99
27545131-13	2016	(7) The expression of P53 was significantly higher in GSNO group than in the blank control group (P&lt; 0.05), which could be significantly down regulated by pretreatment with high, medium and low concentration ICA in a concentration-dependent manner, above effects could be blocked by LY294002(all P&lt;0.05).	icariin	211-214	P53	Homo sapiens	22-25
34035828-10	2021	The molecular docking results showed that quercetin, formononetin, kaempferol, isorhamnetin, beta-sitosterol had a good binding activity with VEGFA, IL6, TNF, AKT1, and TP53.	formononetin	53-65	P53	Homo sapiens	169-173
27545131-16	2016	CONCLUSION: Icariin could reduce GSNO induced endothelial cell apoptosis through activating AKT pathway and downregulating P53 activity.	icariin	12-19	P53	Homo sapiens	123-126
27402273-12	2016	Pifithrin-alpha, a p53 inhibitor, slightly inhibited growth of A549 cells and under p53 inhibitory condition evodiamine-induced apoptosis could not be reversed.	pifithrin	0-15	P53	Homo sapiens	19-22
27402273-12	2016	Pifithrin-alpha, a p53 inhibitor, slightly inhibited growth of A549 cells and under p53 inhibitory condition evodiamine-induced apoptosis could not be reversed.	pifithrin	0-15	P53	Homo sapiens	84-87
34025442-8	2021	Results: In the initial small molecular inhibitor screening in KIT-independent GIST62, we found that bortezomib-mediated inhibition of the ubiquitin-proteasome machinery showed anti-proliferative effects of KIT-independent GIST cells via downregulation of cyclin D1 and induction of p53 and p21.	Bortezomib	101-111	P53	Homo sapiens	283-286
30034716-5	2016	The fluorene-linked DNA can be used as fluorescent probes for DNA-protein (p53) or DNA-lipid interactions, exerting significant color changes visible even to the naked eye.	fluorene	4-12	P53	Homo sapiens	75-78
27537898-4	2016	In this study, we observed that the selected marine life-derived compounds (Chromomycin A2, Psammaplin A, and Ilimaquinone) induce expression of several autophagic signaling intermediates in human squamous cell carcinoma, glioblastoma, and colorectal carcinoma cells in vitro through a transcriptional regulation by tumor protein (TP)-p53 family members.	Chromomycins	76-87	P53	Homo sapiens	335-338
33676681-4	2021	The Fe3O4@SiO2-NH2-Au@Pd0.30NPs-protG exhibited a high binding affinity for the captured anti-p53aAbs and high catalytic performance towards the oxidation of 3,3",5,5"-tetramethylbenzidine (TMB).	ferryl iron	4-9	P53	Homo sapiens	94-97
29029404-2	2017	In this context, we have reported that Quercetin (QC) induces cell death selectively in hESCs via p53 mitochondrial localization.	Quercetin	39-48	P53	Homo sapiens	98-101
27539542-4	2016	As a consequence, circANRIL induces nucleolar stress and p53 activation, resulting in the induction of apoptosis and inhibition of proliferation, which are key cell functions in atherosclerosis.	circanril	18-27	P53	Homo sapiens	57-60
27233942-5	2016	Stronger intracellular TrxR inhibition and higher accumulation of ROS (O2( -) and H2O2) are responsible for more effective S-phase arrest and mitochondria-mediated apoptotic induction of A549 cells by PL-CL than PLvia p53-p21-cyclinA/CDK2 and ASK1-JNK/p38 signaling cascade pathways, respectively.	pl-cl	201-206	P53	Homo sapiens	218-221
33676681-4	2021	The Fe3O4@SiO2-NH2-Au@Pd0.30NPs-protG exhibited a high binding affinity for the captured anti-p53aAbs and high catalytic performance towards the oxidation of 3,3",5,5"-tetramethylbenzidine (TMB).	protg	32-37	P53	Homo sapiens	94-97
27259808-0	2016	Indolo-pyrido-isoquinolin based alkaloid inhibits growth, invasion and migration of breast cancer cells via activation of p53-miR34a axis.	Alkaloids	32-40	P53	Homo sapiens	122-125
33676681-7	2021	The apparent binding affinity (KD) between the p53aAbs and Fe3O4@SiO2-NH2-Au@Pd0.30NPs-protG was 35.2 ng mL-1.	ferryl iron	59-64	P53	Homo sapiens	47-50
33676681-7	2021	The apparent binding affinity (KD) between the p53aAbs and Fe3O4@SiO2-NH2-Au@Pd0.30NPs-protG was 35.2 ng mL-1.	protg	87-92	P53	Homo sapiens	47-50
33894272-8	2021	KEY FINDINGS: Upon treatment with oleuropein, the expression of P21, P53, and TNFRSF10B increased while that of Bcl-2 and Mcl1 decreased.	oleuropein	34-44	P53	Homo sapiens	69-72
27079618-3	2016	Taking into account the antitumor activity of biflorin, a substance isolated from Capraria biflora L. roots that is cytotoxic in vitro and in vivo, this study aimed to demonstrate the action of biflorin against three established human melanoma cell lines that recapitulate the molecular landscape of the disease in terms of genetic alterations and mutations, such as the TP53, NRAS and BRAF genes.	biflorin	46-54	P53	Homo sapiens	371-375
27079618-3	2016	Taking into account the antitumor activity of biflorin, a substance isolated from Capraria biflora L. roots that is cytotoxic in vitro and in vivo, this study aimed to demonstrate the action of biflorin against three established human melanoma cell lines that recapitulate the molecular landscape of the disease in terms of genetic alterations and mutations, such as the TP53, NRAS and BRAF genes.	biflorin	194-202	P53	Homo sapiens	371-375
27233606-7	2016	In the presence of SP600125, expression of cleaved caspase-9/-3 and p53 as well as the ratio of Bax to Bcl-2 was significantly decreased compared to treatment with TNF-alpha alone.	pyrazolanthrone	19-27	P53	Homo sapiens	68-71
27236003-0	2016	Honokiol induces autophagic cell death in malignant glioma through reactive oxygen species-mediated regulation of the p53/PI3K/Akt/mTOR signaling pathway.	honokiol	0-8	P53	Homo sapiens	118-121
27236003-9	2016	Pretreatment with a p53 inhibitor or transfection with p53 small interfering (si)RNA suppressed honokiol-induced autophagy by reversing downregulation of p-Akt and p-mTOR expressions.	honokiol	96-104	P53	Homo sapiens	20-23
27236003-9	2016	Pretreatment with a p53 inhibitor or transfection with p53 small interfering (si)RNA suppressed honokiol-induced autophagy by reversing downregulation of p-Akt and p-mTOR expressions.	honokiol	96-104	P53	Homo sapiens	55-58
27236003-12	2016	Concurrently, honokiol-induced alterations in levels of p-p53, p53, p-Akt, and p-mTOR were attenuated following vitamin C administration.	honokiol	14-22	P53	Homo sapiens	58-61
27236003-12	2016	Concurrently, honokiol-induced alterations in levels of p-p53, p53, p-Akt, and p-mTOR were attenuated following vitamin C administration.	honokiol	14-22	P53	Homo sapiens	63-66
27236003-13	2016	Taken together, our data indicated that honokiol induced ROS-mediated autophagic cell death through regulating the p53/PI3K/Akt/mTOR signaling pathway.	honokiol	40-48	P53	Homo sapiens	115-118
27233606-8	2016	Our results therefore indicate that SP600125 improves the migration capacity of TNF-alpha-treated BMSCs and exerts a significant effect on the viability of TNF-alpha-treated BMSCs through reducing the up-regulation of p53, caspase-9/-3 and the Bcl-2 family induced by TNF-alpha.	pyrazolanthrone	36-44	P53	Homo sapiens	218-221
27283772-3	2016	Here, we demonstrate that the carriage of missense mutations in the TP53 DNA binding domain (DBD missense mutations) is associated with decreased disease-specific survival (DSS) compared with wild-type TP53 (P=0.002) in a cohort of 345 OSCC patients.	dss	173-176	P53	Homo sapiens	68-72
27283772-6	2016	When analyzed in combination with traditional clinicopathological factors, TP53 DBD missense mutations were an independent prognostic factor for shorter DSS (P=0.014) alongside with advanced AJCC T- and N-classifications and the presence of extracapsular spread.	dss	153-156	P53	Homo sapiens	75-79
27131434-14	2016	The cell cycle arrest in DCM-DS-treated MDA-MB-231 cells is possibly via p53-independent but p21-dependent pathway.	Deuterium	29-31	P53	Homo sapiens	73-76
33593530-0	2021	Chitooligosaccharides inhibit tumor progression and induce autophagy through the activation of the p53/mTOR pathway in osteosarcoma.	oligochitosan	0-21	P53	Homo sapiens	99-102
27174050-0	2016	Structural Determinants of p53-Independence in Anticancer Ruthenium-Arene Schiff-Base Complexes.	ruthenium-arene schiff-base	58-85	P53	Homo sapiens	27-30
27223263-5	2016	At the molecular level, aphidicolin enhanced purine analog-induced phosphorylation of p53 and accumulation of gammaH2AX, consistent with increase in DNA damage.	purine	45-51	P53	Homo sapiens	86-89
33593530-7	2021	We found that COS had significant effects on cell growth, metastasis inhibition, apoptosis and autophagy induction, and triggered pro-apoptosis autophagy through p53/mTOR signaling pathway in osteosarcoma cells.	oligochitosan	14-17	P53	Homo sapiens	162-165
27174050-5	2016	In the present study, we identified 9 Ru (II)-Arene Schiff-base (RAS) complexes able to induce p53-independent cytotoxicity and discuss structural features that are required for their p53-independent activity.	Schiff Bases	52-63	P53	Homo sapiens	95-98
33927966-8	2021	Folate receptor targeted MTX-GNPs showed significant cellular uptake in breast cancer cells along with significant down-regulation in expression of anti-apoptotic gene (Bcl-2) and up-regulation in expression of pro-apoptotic genes (Bax, Caspase-3, Caspase-9, APAF-1, p53).	Methotrexate	25-28	P53	Homo sapiens	267-270
27174050-5	2016	In the present study, we identified 9 Ru (II)-Arene Schiff-base (RAS) complexes able to induce p53-independent cytotoxicity and discuss structural features that are required for their p53-independent activity.	Schiff Bases	52-63	P53	Homo sapiens	184-187
27185843-10	2016	FAS and p53 were shown to be prognostic factors for PFS (7.0 months if FAS+ and p53-; 3.4 months if FAS+/p53+ or FAS-/p53-; and 0.7 months if FAS- and p53+; P &lt; .001) and for overall survival.	ammonium ferrous sulfate	71-74	P53	Homo sapiens	8-11
26433571-10	2016	DCA reactivated mitochondrial function (increased respiration, Krebs cycle metabolites such as alpha-ketoglutarate [cofactor of factor inhibiting HIF], and mitochondrial reactive oxygen species), increased p53 activity and apoptosis, and decreased proliferation in 786-O cells.	Dichloroacetic Acid	0-3	P53	Homo sapiens	206-209
32715386-0	2021	A natural flavonoid, apigenin isolated from Clerodendrum viscosum leaves, induces G2/M phase cell cycle arrest and apoptosis in MCF-7 cells through the regulation of p53 and caspase-cascade pathway.	Flavonoids	10-19	P53	Homo sapiens	166-169
25398514-6	2016	Bypass of the need for metabolic activation by treating cells with the corresponding reactive PAH-diol-epoxide metabolites resulted in similar adduct levels in all cell lines, which confirms that the influence of p53 is on the metabolism of the parent PAHs.	Polycyclic Aromatic Hydrocarbons	94-97	P53	Homo sapiens	213-216
27177208-0	2016	A novel all-trans retinoic acid derivative 4-amino-2-trifluoromethyl-phenyl retinate inhibits the proliferation of human hepatocellular carcinoma HepG2 cells by inducing G0/G1 cell cycle arrest and apoptosis via upregulation of p53 and ASPP1 and downregulation of iASPP.	2-octenal	12-17	P53	Homo sapiens	228-231
33868388-12	2021	Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment.	NADP	126-132	P53	Homo sapiens	8-11
26477317-8	2016	A fine characterization of the DNA deformation caused by p53 binding is obtained, with "static" deformations always present and measured by the slide parameter in the central thymine-adenine base pairs; we also detect "dynamic" deformations switched on and off by particular p53 tetrameric conformations and measured by the roll and twist parameters in the same base pairs.	Adenine	183-190	P53	Homo sapiens	57-60
26924930-0	2016	Agmatine Ameliorates High Glucose-Induced Neuronal Cell Senescence by Regulating the p21 and p53 Signaling.	Agmatine	0-8	P53	Homo sapiens	93-96
26924930-6	2016	Increased p21 and reduced p53 in high glucose conditioned cells were changed by agmatine.	Agmatine	80-88	P53	Homo sapiens	26-29
26924930-7	2016	Ultimately, agmatine inhibits the neuronal cell senescence through the activation of p53 and the inhibition of p21.	Agmatine	12-20	P53	Homo sapiens	85-88
33576462-6	2021	By recognizing and specifically targeting SIRT1 3"-untranslated region (3"-UTR), miR-138-5p decreased the translational level of SIRT1 and inhibited its enzyme activity, thereby decreasing the deacetylation level of p53.	mir-138-5p	81-91	P53	Homo sapiens	216-219
33576462-7	2021	Through downregulating SIRT1 and activating p53 signaling, miR-138-5p induced apoptosis in H2O2-induced AC-16 and HCM cells.	mir-138-5p	59-69	P53	Homo sapiens	44-47
27091351-11	2016	In summary, AZD1152 treatment led to endomitosis and polyploidy in TP53-mutated NB4 cells.	2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate	12-19	P53	Homo sapiens	67-71
33576462-10	2021	MiR-138-5p decreases the enzyme activity of SIRT1 by specifically targeting its 3"-UTR and activates p53 signaling, followed by triggering cardiomyocyte apoptosis during the process of HF.	mir-138-5p	0-10	P53	Homo sapiens	101-104
33710818-11	2021	PD166866 and RG7112, an MDM2/p53 inhibitor, cooperatively inhibited the colony formation and distal seeding of LSCC cells (P < 0.01), and upregulated the expression of p53 and p21.	PD 166866	0-8	P53	Homo sapiens	29-32
26794656-6	2016	Both compounds clearly inhibited the ability of E6 to bind in vitro to both caspase 8 and E6AP, the protein that mediates p53 degradation.	Polyurethane Y-290	48-50	P53	Homo sapiens	122-125
33710818-11	2021	PD166866 and RG7112, an MDM2/p53 inhibitor, cooperatively inhibited the colony formation and distal seeding of LSCC cells (P < 0.01), and upregulated the expression of p53 and p21.	PD 166866	0-8	P53	Homo sapiens	168-171
33613721-0	2021	Attenuating role of withaferin A in the proliferation and migration of lung cancer cells via a p53-miR-27a/miR-10b pathway.	withaferin A	20-32	P53	Homo sapiens	95-98
26783755-0	2016	Ceramide Synthase 6 Is a Novel Target of Methotrexate Mediating Its Antiproliferative Effect in a p53-Dependent Manner.	Methotrexate	41-53	P53	Homo sapiens	98-101
26783755-10	2016	The effect of MTX on CerS6 elevation was likely p53 dependent, which is in agreement with the hypothesis that the protein is a transcriptional target of p53.	Methotrexate	14-17	P53	Homo sapiens	48-51
26783755-10	2016	The effect of MTX on CerS6 elevation was likely p53 dependent, which is in agreement with the hypothesis that the protein is a transcriptional target of p53.	Methotrexate	14-17	P53	Homo sapiens	153-156
27376811-2	2016	The change from an arginine (Arg) to a proline (Pro) at codon 72 can influence the biological activity of p53, which predisposes to an increased risk of recurrent spontaneous abortion (RSA).	rabbit sperm membrane autoantigen	185-188	P53	Homo sapiens	106-109
27376811-12	2016	Our meta-analysis implied that p53 polymorphism at codon 72 carries high maternal risk of RSA.	rabbit sperm membrane autoantigen	90-93	P53	Homo sapiens	31-34
27064011-5	2016	Pifithrin-alpha (PFN-alpha), a p53 inhibitor, was pretreated into the cells.	pifithrin	0-15	P53	Homo sapiens	31-34
27064011-9	2016	Treatment of U87 MG cells with honokiol increased p53 phosphorylation and p21 levels.	honokiol	31-39	P53	Homo sapiens	50-53
27064011-11	2016	Pretreatment of U87 MG cells with PFN-alpha significantly reversed honokiol-induced p53 phosphorylation and p21 augmentation.	honokiol	67-75	P53	Homo sapiens	84-87
27064011-14	2016	In our in vivo model, administration of honokiol prolonged the survival rate of nude mice implanted with U87 MG cells and induced caspase-3 activation and chronological changes in p53, p21, CDK6, CDK4, cyclin D1, p-RB, and E2F1.	honokiol	40-48	P53	Homo sapiens	180-183
27064011-15	2016	CONCLUSIONS: Honokiol can repress human glioma growth by inducing apoptosis and cell cycle arrest in tumor cells though activating a p53/cyclin D1/CDK6/CDK4/E2F1-dependent pathway.	honokiol	13-21	P53	Homo sapiens	133-136
33357454-0	2021	Arsenic Trioxide Rescues Structural p53 Mutations through a Cryptic Allosteric Site.	Arsenic Trioxide	0-16	P53	Homo sapiens	36-39
26939786-0	2016	New insights into the anticancer activity of carnosol: p53 reactivation in the U87MG human glioblastoma cell line.	carnosol	45-53	P53	Homo sapiens	55-58
26985570-9	2016	The expression of p53 protein decreased in all of the cells that were treated with CAS.	castanospermine	83-86	P53	Homo sapiens	18-21
27099787-1	2016	This study was performed in order to reveal the effect of Noopept (ethyl ester of N-phenylacetyl-Lprolylglycine, GVS-111) on the DNA-binding activity of transcriptional factors (TF) in HEK293 cells transiently transfected with luciferase reporter constructs containing sequences for CREB, NFAT, NF-kappaB, p53, STAT1, GAS, VDR, HSF1, and HIF-1.	ethyl ester	67-78	P53	Homo sapiens	306-309
26537425-2	2016	Because the allowed conformational space of alpha-aminoisobutyric acid (Aib) is restricted to only the helical basin, Aib-containing helical mimics of p53 (binding epitope) are expected to inhibit interaction between p53 and Hdm2 with a much stronger affinity than the wild type p53 peptide (binding epitope), due to the entropic advantage associated with Aib.	2-aminoisobutyric acid	44-70	P53	Homo sapiens	151-154
26537425-2	2016	Because the allowed conformational space of alpha-aminoisobutyric acid (Aib) is restricted to only the helical basin, Aib-containing helical mimics of p53 (binding epitope) are expected to inhibit interaction between p53 and Hdm2 with a much stronger affinity than the wild type p53 peptide (binding epitope), due to the entropic advantage associated with Aib.	2-aminoisobutyric acid	44-70	P53	Homo sapiens	217-220
33357454-3	2021	Here we report the identification of small molecules, including arsenic trioxide (ATO), an established agent in treating acute promyelocytic leukemia, as cysteine-reactive compounds that rescue structural p53 mutations.	Arsenic Trioxide	64-80	P53	Homo sapiens	205-208
26537425-2	2016	Because the allowed conformational space of alpha-aminoisobutyric acid (Aib) is restricted to only the helical basin, Aib-containing helical mimics of p53 (binding epitope) are expected to inhibit interaction between p53 and Hdm2 with a much stronger affinity than the wild type p53 peptide (binding epitope), due to the entropic advantage associated with Aib.	2-aminoisobutyric acid	44-70	P53	Homo sapiens	217-220
26537425-2	2016	Because the allowed conformational space of alpha-aminoisobutyric acid (Aib) is restricted to only the helical basin, Aib-containing helical mimics of p53 (binding epitope) are expected to inhibit interaction between p53 and Hdm2 with a much stronger affinity than the wild type p53 peptide (binding epitope), due to the entropic advantage associated with Aib.	2-aminoisobutyric acid	72-75	P53	Homo sapiens	151-154
33357454-3	2021	Here we report the identification of small molecules, including arsenic trioxide (ATO), an established agent in treating acute promyelocytic leukemia, as cysteine-reactive compounds that rescue structural p53 mutations.	Arsenic Trioxide	82-85	P53	Homo sapiens	205-208
26537425-2	2016	Because the allowed conformational space of alpha-aminoisobutyric acid (Aib) is restricted to only the helical basin, Aib-containing helical mimics of p53 (binding epitope) are expected to inhibit interaction between p53 and Hdm2 with a much stronger affinity than the wild type p53 peptide (binding epitope), due to the entropic advantage associated with Aib.	2-aminoisobutyric acid	72-75	P53	Homo sapiens	217-220
26842845-5	2016	This inhibition was due to the Profilin mediated attenuation of IkappaBalpha degradation, thereby preventing p65 nuclear translocation and low NF-kappaB DNA binding activity.Moreover, Profilin increases level of p53 in the presence of known inducers, such as doxorubicin, vinblastine, and benzofuran.	Vinblastine	272-283	P53	Homo sapiens	212-215
26842845-5	2016	This inhibition was due to the Profilin mediated attenuation of IkappaBalpha degradation, thereby preventing p65 nuclear translocation and low NF-kappaB DNA binding activity.Moreover, Profilin increases level of p53 in the presence of known inducers, such as doxorubicin, vinblastine, and benzofuran.	benzofuran	289-299	P53	Homo sapiens	212-215
26537425-2	2016	Because the allowed conformational space of alpha-aminoisobutyric acid (Aib) is restricted to only the helical basin, Aib-containing helical mimics of p53 (binding epitope) are expected to inhibit interaction between p53 and Hdm2 with a much stronger affinity than the wild type p53 peptide (binding epitope), due to the entropic advantage associated with Aib.	2-aminoisobutyric acid	72-75	P53	Homo sapiens	217-220
26537425-6	2016	It was found that despite stabilizing a helical backbone in the unbound state, the Aib residues in Aib-p53 peptide arrested two functionally important side-chains (F19 and W23) in non-productive conformations, resulting in relative side-chain orientations of the binding triad F19-W23-L26 incompatible with the bound conformation.	2-aminoisobutyric acid	83-86	P53	Homo sapiens	103-106
33370709-0	2021	Dihydroartemisinin inhibits the tumorigenesis and invasion of gastric cancer by regulating STAT1/KDR/MMP9 and P53/BCL2L1/CASP3/7 pathways.	artenimol	0-18	P53	Homo sapiens	110-113
33370709-7	2021	The results indicated that the common targets of DHA and GC were enriched in multiple cancer-related pathways including KDR, STAT1 and apoptosis signaling pathways, where the core genes included KDR, MMP9, STAT1, TP53, CASP3/7 and BCL2L1.	artenimol	49-52	P53	Homo sapiens	213-217
27044814-0	2016	Tryptanthrin reduces mast cell proliferation promoted by TSLP through modulation of MDM2 and p53.	tryptanthrine	0-12	P53	Homo sapiens	93-96
33510228-0	2021	Sulforaphane induces S-phase arrest and apoptosis via p53-dependent manner in gastric cancer cells.	sulforaphane	0-12	P53	Homo sapiens	54-57
26684585-2	2016	It has recently been reported that p53 regulates glucose metabolism and that an increase in p53 protein level is induced after serum deprivation or treatments with a natural compound,trans-Resveratrol (Rsv).	Respiratory Syncytial Virus Vaccines	202-205	P53	Homo sapiens	35-38
26636375-3	2016	In the present study by using the specific inhibitors Ku55933 and Pifithrin-alpha, we confirmed implication of both ATM and p53 in H(2)O(2)-induced senescence of hMESCs.	pifithrin	66-75	P53	Homo sapiens	124-127
26684585-2	2016	It has recently been reported that p53 regulates glucose metabolism and that an increase in p53 protein level is induced after serum deprivation or treatments with a natural compound,trans-Resveratrol (Rsv).	Respiratory Syncytial Virus Vaccines	202-205	P53	Homo sapiens	92-95
27997894-11	2016	In addition, zedoarondiol activated AMPK and ACC, inhibited the phosphorylation of mTOR and p70S6K, increased the expression of p53 and p21, and decreased the expression of CDK2 and cyclin E. Compound C (an AMPK inhibitor) abrogated, whereas 5-aminoimidazole-4-carboxamide 1-beta-ribofuranoside (AICAR, an AMPK activator) enhanced zedoarondiol-mediated inhibition of VSMCs proliferation and DNA synthesis.	zedoarondiol	13-25	P53	Homo sapiens	128-131
26738694-2	2016	A common p53 Arg72Pro polymorphism resulting in the substitution of an arginine amino acid by proline amino acid in the transactivating domain has been demonstrated to affect p53 function.	arginine amino acid	71-90	P53	Homo sapiens	9-12
26738694-2	2016	A common p53 Arg72Pro polymorphism resulting in the substitution of an arginine amino acid by proline amino acid in the transactivating domain has been demonstrated to affect p53 function.	arginine amino acid	71-90	P53	Homo sapiens	175-178
33510228-7	2021	These results suggested that SFN-induced S phase cell cycle arrest and apoptosis through p53-dependent manner in GC cells, which suggested that SFN has a potential therapeutic application in the treatment and prevention of GC.	sulforaphane	29-32	P53	Homo sapiens	89-92
26459178-0	2016	Mithramycin Depletes Specificity Protein 1 and Activates p53 to Mediate Senescence and Apoptosis of Malignant Pleural Mesothelioma Cells.	Plicamycin	0-11	P53	Homo sapiens	57-60
33510838-7	2021	Knockdown ribosomal protein L11 (RPL11) by transfecting with siRNA or inhibiting p53 by pifithrin-alpha (PFT-alpha) partly reserved the biological effects induced by BOP1 knockdown.	pifithrin	88-103	P53	Homo sapiens	81-84
26459178-9	2016	Mithramycin depleted SP1 and activated p53, dramatically inhibiting proliferation and clonogenicity of MPM cells.	Plicamycin	0-11	P53	Homo sapiens	39-42
26459178-12	2016	The growth-inhibitory effects of mithramycin in MPM cells were recapitulated by combined SP1 knockdown/p53 overexpression.	Plicamycin	33-44	P53	Homo sapiens	103-106
26836165-5	2016	In the present study, we showed that Aluminum maltolate (Al-malt), a lipophilic Al complex which is a common component of human diet with the ability to facilitate the entry of Al into the brain, induced apoptosis in human neuroblastoma SH-SY5Y cells, along with downregulation of miR-19a/miR-19b, upregulation of miR-19-targeted PTEN, and alterations of its downstream apoptosis related proteins including AKT, p53, Bax, and Bcl-2.	aluminum maltolate	37-55	P53	Homo sapiens	412-415
33510838-7	2021	Knockdown ribosomal protein L11 (RPL11) by transfecting with siRNA or inhibiting p53 by pifithrin-alpha (PFT-alpha) partly reserved the biological effects induced by BOP1 knockdown.	pifithrin	105-114	P53	Homo sapiens	81-84
26832796-0	2016	Chemical Inhibition of Wild-Type p53-Induced Phosphatase 1 (WIP1/PPM1D) by GSK2830371 Potentiates the Sensitivity to MDM2 Inhibitors in a p53-Dependent Manner.	GSK2830371	75-85	P53	Homo sapiens	33-36
33469287-0	2021	p53 Promoted Ferroptosis in Ovarian Cancer Cells Treated with Human Serum Incubated-Superparamagnetic Iron Oxides.	ferric oxide	102-113	P53	Homo sapiens	0-3
26832796-7	2016	However, a non-growth-inhibitory dose of GSK2830371 markedly potentiated the response to MDM2 inhibitors in TP53 wild-type cell lines, most notably in those harboring PPM1D-activating mutations or copy number gain (up to 5.8-fold decrease in GI50).	GSK2830371	41-51	P53	Homo sapiens	108-112
25398514-0	2016	Carcinogenic polycyclic aromatic hydrocarbons induce CYP1A1 in human cells via a p53-dependent mechanism.	Polycyclic Aromatic Hydrocarbons	13-45	P53	Homo sapiens	81-84
25398514-2	2016	We have investigated the role of TP53 in cytochrome P450 (CYP)-mediated metabolic activation of three polycyclic aromatic hydrocarbons (PAHs) in a panel of isogenic colorectal HCT116 cells with differing TP53 status.	Polycyclic Aromatic Hydrocarbons	102-134	P53	Homo sapiens	33-37
25398514-2	2016	We have investigated the role of TP53 in cytochrome P450 (CYP)-mediated metabolic activation of three polycyclic aromatic hydrocarbons (PAHs) in a panel of isogenic colorectal HCT116 cells with differing TP53 status.	Polycyclic Aromatic Hydrocarbons	136-140	P53	Homo sapiens	33-37
26465677-8	2015	By inducing intracellular oxidative stress, Pt-1-DMCa potentiated platinum-induced DNA damage and led to enhanced p53 phosphorylation, followed by increased activation of both mitochondrial and death receptor pathways.	pt-1-dmca	44-53	P53	Homo sapiens	114-117
26354682-0	2015	Hypoxia Promotes Synergy between Mitomycin C and Bortezomib through a Coordinated Process of Bcl-xL Phosphorylation and Mitochondrial Translocation of p53.	Bortezomib	49-59	P53	Homo sapiens	151-154
26512780-3	2015	However, most mCRPC patients who receive docetaxel experience only transient benefits and rapidly develop incurable drug resistance, which is closely correlated with the p53 mutation status.	Docetaxel	41-50	P53	Homo sapiens	170-173
26512780-9	2015	Furthermore, the combination of fatostatin and docetaxel resulted in greater proliferation inhibition and apoptosis induction compared with single agent treatment in PCa cells in vitro and in vivo, especially those with mutant p53s.	Docetaxel	47-56	P53	Homo sapiens	227-230
26512780-10	2015	These data suggest for the first time that fatostatin alone or in combination with docetaxel could be exploited as a novel and promising therapy for metastatic PCa harboring p53 mutations.	Docetaxel	83-92	P53	Homo sapiens	174-177
32737944-1	2021	To search for novel p53 activators, four series of novel ( S )- and ( R )-tryptophanol-derived oxazoloisoindolinones have been straightforwardly synthesized and their antiproliferative activity evaluated in human colorectal cancer HCT116 cell line.	( r )-tryptophanol	68-86	P53	Homo sapiens	20-23
26556860-6	2015	Loss of nucleolin can activate Fas-mediated apoptosis, leading to the increase of pro-apoptotic proteins (BID, fas-associated factor-2) and subsequent apoptosis of p53-negative, 2-FaraA refractory CLL cells.	ammonium ferrous sulfate	31-34	P53	Homo sapiens	164-167
26651421-0	2016	A new prognostic index to make short-term prognoses in MDS patients treated with azacitidine: A combination of p53 expression and cytogenetics.	Azacitidine	81-92	P53	Homo sapiens	111-114
26651421-6	2016	Here, we propose a new prognostic index to make short-term prognoses of MDS patients in the era of Aza treatment; high: p53-positive and poor cytogenetics, low: p53-negative and absence of poor cytogenetics, and intermediate: the others.	Azacitidine	99-102	P53	Homo sapiens	120-123
26651421-8	2016	In conclusion, p53 expression was a significant prognostic factor in MDS patients treated with Aza.	Azacitidine	95-98	P53	Homo sapiens	15-18
32737944-2	2021	Structural optimization of the hit compound SLMP53-1 led to the identification of a ( R )-tryptophanol-derived isoindolinone 6-fold more active and with increased selectivity for colon cancer HCT116 cells with p53 and with low toxicity in normal cells.	( r )-tryptophanol	84-102	P53	Homo sapiens	210-213
26703711-4	2015	The application of pifithrin mu as an inhibitor of p53 shuttling to mitochondria reduced RV-induced cell death to an extent similar to that of the broad spectrum caspase inhibitor z-VAD-fmk (benzyloxycarbonyl-V-A-D-(OMe)-fmk).	pifithrin	19-28	P53	Homo sapiens	51-54
33254022-5	2021	In addition, we also observed that triptonide activated tumor suppressor p53.	triptonide	35-45	P53	Homo sapiens	73-76
26706021-1	2016	Flavonoid resveratrol modulates the transcription factor NF-kappaB; inhibits the cytochrome P450 isoenzyme CYP1 A1; suppresses the expression and activity of cyclooxygenase enzymes; and modulates Fas/Fas-ligand-mediated apoptosis, p53, mammalian target of rapamycin, and cyclins and various phosphodiesterases.	Flavonoids	0-9	P53	Homo sapiens	231-234
26917260-9	2016	Conversely, pretreated with salubrinal (a selective inhibition of protein phosphatase 1-mediated eIF2alpha dephosphorylation), JEG-3 cells were rescued from JMR-132-mediated cell growth inhibition, and abolished JMR-132-induced cleaved caspase-3, CHOP, phospho-p53, and ubiquitinated proteins accumulation.	salubrinal	28-38	P53	Homo sapiens	261-264
26391395-7	2015	Although both PTX and AICAR stabilized p53, only AICAR activated Chk2 phosphorylation, stimulating p53-dependent transcription.	Pemetrexed	14-17	P53	Homo sapiens	39-42
32420759-11	2021	Combination of quercetin and curcumin was effective on genes that were particularly related to p53, NF-kappaB and TGF-alpha pathways.	Quercetin	15-24	P53	Homo sapiens	95-98
26544558-8	2015	Mature miR-3151 level and p53 protein level were detected after HHT or Bortezomib treatment.	Bortezomib	71-81	P53	Homo sapiens	26-29
26483208-6	2016	The immunoblot analysis indicated that TVN efficiently regulated the cleavage of caspase family, p53, Bax and Bcl-2, all mediated by SIRT1.	N-{(2R)-4-(methylamino)-4-oxo-2-[4-(phosphonooxy)benzyl]butanoyl}-L-valyl-L-aspartamide	39-42	P53	Homo sapiens	97-100
33425890-9	2020	Finally, TP53 and TET1 were antagonistically regulated by DHRS4-AS1 and miR-224-3p in NSCLC cells.	mir-224-3p	72-82	P53	Homo sapiens	9-13
26556313-0	2016	Spiro-oxindole derivative 5-chloro-4",5"-diphenyl-3"-(4-(2-(piperidin-1-yl) ethoxy) benzoyl) spiro[indoline-3,2"-pyrrolidin]-2-one triggers apoptosis in breast cancer cells via restoration of p53 function.	spiro-oxindole	0-14	P53	Homo sapiens	192-195
32886933-0	2020	Induction of Cell Cycle Arrest in MKN45 Cells after Schiff Base Oxovanadium Complex Treatment Using Changes in Gene Expression of CdC25 and P53.	Schiff Bases	52-63	P53	Homo sapiens	140-143
26434996-6	2015	The energy metabolism phenotype of HeLa-H cells was reverted to that of HeLa-L cells by incubating with pifithrin-alpha, a p53-inhibitor.	pifithrin	104-119	P53	Homo sapiens	123-126
26438057-0	2015	Core domain mutant Y220C of p53 protein has a key role in copper homeostasis in case of free fatty acids overload.	Fatty Acids, Nonesterified	88-104	P53	Homo sapiens	28-31
31886905-5	2020	Western blot was used to measure the levels of p53 and its acetylated versions in cells treated with carboplatin and/or pifithrin-alpha.	pifithrin	120-135	P53	Homo sapiens	47-50
26400171-3	2015	Benzo[a]pyrene,diol epoxide (BPDE) is a potent cigarette smoke carcinogen that forms guanine adducts at TP53 CpG mutation hotspot sites including codons 157, 158, 245, 248 and 273.	Guanine	85-92	P53	Homo sapiens	104-108
32860803-8	2020	Exogenous H2S from sodium hydrosulfide, attenuated the efficacy of DIM in cancer cells by reducing the activation level of p38-p53 axis.	Deuterium	10-13	P53	Homo sapiens	127-130
32956986-11	2020	CONCLUSION: Concurrent aspirin use with osimertinib in EGFR-mutant NSCLC patients was associated with improved survival, regardless of lines of therapy, CNS metastatic status, EGFR mutation type, age, gender, TP53, and PD-L1 status.	osimertinib	40-51	P53	Homo sapiens	209-213
26485758-4	2015	Here, we reported that arenobufagin blocked the transition from G2 to M phase of cell cycle through inhibiting the activation of CDK1-Cyclin B1 complex; The tumor suppressor p53 contributed to sustaining arrest at the G2 phase of the cell cycle in hepatocellular carcinoma (HCC) cells.	arenobufagin	23-35	P53	Homo sapiens	174-177
26250568-5	2015	When cells were pretreated with a p53 inhibitor (pifithrin-a), followed by magnolol treatment, pifithrin-a blocked magnolol-induced apoptosis and G0 /G1 arrest.	pifithrin	49-60	P53	Homo sapiens	34-37
33052979-9	2020	In addition, our results indicated that the combination of anti-cancer drugs and quercetin down-regulated the expression of HIF-1alpha and increased the expression levels of the regulator of apoptosis p53.	Quercetin	81-90	P53	Homo sapiens	201-204
26417421-10	2015	Analysis of the adducted p53 fragment compared with unreacted fragment revealed guanines of codons 248 and 244 as most frequently targeted, which are also mutated with high frequency in human tumors.	Guanine	80-88	P53	Homo sapiens	25-28
24798859-0	2015	Regulation of p53-targeting microRNAs by polycyclic aromatic hydrocarbons: Implications in the etiology of multiple myeloma.	Polycyclic Aromatic Hydrocarbons	41-73	P53	Homo sapiens	14-17
33066414-9	2020	Schiff base complex treatment resulted in up-regulation of p53 and Bax genes expression and down-regulation of Bcl2 gene expression in SCCs paralleled with increased protein expression of caspase-3 and Bax and down-regulation of Bcl-2 protein.	Schiff Bases	0-11	P53	Homo sapiens	59-62
26387611-0	2015	The energy blockers bromopyruvate and lonidamine lead GL15 glioblastoma cells to death by different p53-dependent routes.	lonidamine	38-48	P53	Homo sapiens	100-103
26628835-0	2015	Fluorine-18 Fluorodeoxyglucose Uptake in Hepatocellular Carcinoma: Correlation with Glucose Transporters and p53 Expression.	18 fluorodeoxyglucose	9-30	P53	Homo sapiens	109-112
32945383-13	2020	Pifithrin-alpha, an inhibitor of p53, partially reduced RSV-induced apoptosis and autophagy.	pifithrin	0-15	P53	Homo sapiens	33-36
33001991-0	2020	Impact of TP53 mutations in acute myeloid leukemia patients treated with azacitidine.	Azacitidine	73-84	P53	Homo sapiens	10-14
26311153-0	2015	Anticarcinogenic action of quercetin by downregulation of phosphatidylinositol 3-kinase (PI3K) and protein kinase C (PKC) via induction of p53 in hepatocellular carcinoma (HepG2) cell line.	Quercetin	27-36	P53	Homo sapiens	139-142
33001991-2	2020	Recently, TP53 gene mutations have been described as a potential predictive biomarker of better outcome in patients treated with a ten-day decitabine regimen., However, functional characteristics of TP53 mutant are heterogeneous, as reflected in multiple functional TP53 classifications and their impact in patients treated with azacitidine is less clear.	Azacitidine	329-340	P53	Homo sapiens	10-14
25530422-6	2015	In the present study, we demonstrate that the proteasome inhibitor Bortezomib strongly inhibits ERalpha and HER2/neu expression, increases expression of cyclin-dependent kinase inhibitors, inhibits expression of multiple genes associated with poor prognosis in ERalpha+ breast cancer patients and induces cell death in ER+ breast cancer cells in both the presence and absence of functional p53.	Bortezomib	67-77	P53	Homo sapiens	390-393
33001991-2	2020	Recently, TP53 gene mutations have been described as a potential predictive biomarker of better outcome in patients treated with a ten-day decitabine regimen., However, functional characteristics of TP53 mutant are heterogeneous, as reflected in multiple functional TP53 classifications and their impact in patients treated with azacitidine is less clear.	Azacitidine	329-340	P53	Homo sapiens	199-203
25530422-7	2015	Although Bortezomib increased the levels of p53 and increased the expression of pro-apoptotic target genes in ERalpha+ breast cancer cells harboring wild-type p53, Bortezomib also exerts anti-tumoral effects on ERalpha+ breast cancer cells through suppression of ERalpha expression and inhibition of PI3K/Akt/mammalian target of rapamycin (mTOR) and ERK signaling independently of functional p53.	Bortezomib	9-19	P53	Homo sapiens	44-47
33001991-2	2020	Recently, TP53 gene mutations have been described as a potential predictive biomarker of better outcome in patients treated with a ten-day decitabine regimen., However, functional characteristics of TP53 mutant are heterogeneous, as reflected in multiple functional TP53 classifications and their impact in patients treated with azacitidine is less clear.	Azacitidine	329-340	P53	Homo sapiens	199-203
32899699-4	2020	ATS/DHA induces the expression of DR5 in a P53 dependent manner in HCT116 and DLD-1 cells.	artenimol	4-7	P53	Homo sapiens	43-46
26147621-8	2015	Interestingly, we were also able to describe a possible pathway that involves Hif-1alpha and p53 during DCA-induced loss of pluripotency.	Dichloroacetic Acid	104-107	P53	Homo sapiens	93-96
32899699-6	2020	We also demonstrate that DHA sensitizes HCT116 cells to DHER-induced apoptosis via P53 regulated DR5 expression in P53 knockdown assays.	artenimol	25-28	P53	Homo sapiens	83-86
32899699-6	2020	We also demonstrate that DHA sensitizes HCT116 cells to DHER-induced apoptosis via P53 regulated DR5 expression in P53 knockdown assays.	artenimol	25-28	P53	Homo sapiens	115-118
25955133-5	2015	Using the cell-based reporter assay, we identified several oncogenic pathways modulated by sulforaphane in hypoxia by activating anticancer responses (p53, ARE, IRF-1, Pax-6 and XRE) and suppressing responses supporting tumor progression (AP-1 and HIF-1).	sulforaphane	91-103	P53	Homo sapiens	151-154
32878802-5	2020	TMZ+AZD increased the expression of phospho-p53 (p-p53), p-p38 mitogen-activated protein kinase, and phosphatase and tensin homolog; and decreased the expression of p-extracellular signal-regulated kinase 1/2 and p-signal transducer and activator of transcription 3 in glioma cells.	azd	4-7	P53	Homo sapiens	44-47
25698149-3	2015	In a recent paper, we have provided evidence that p53 status is able to subdivide TNBCs into two distinct subgroups with different outcome, and consistent with basal- and normal-like phenotypes.	tnbcs	82-87	P53	Homo sapiens	50-53
32878802-5	2020	TMZ+AZD increased the expression of phospho-p53 (p-p53), p-p38 mitogen-activated protein kinase, and phosphatase and tensin homolog; and decreased the expression of p-extracellular signal-regulated kinase 1/2 and p-signal transducer and activator of transcription 3 in glioma cells.	azd	4-7	P53	Homo sapiens	51-54
32859641-9	2020	Two UEAs were found to have novel TP53 mutations.	ueas	4-8	P53	Homo sapiens	34-38
25955698-8	2015	Pre-treatment with the p53 inhibitor, pifithrin-alpha, prevented apoptosis and the changes in IGF-1R and IGFBP-3 elicited by doxorubicin.	pifithrin	38-47	P53	Homo sapiens	23-26
32504442-7	2020	The treatment of n-hexane fraction showed downregulation in the gene expression of Bcl-2 and upregulation in the expression level of p53, Bad, and caspase-3 genes analyzed using semi-quantitative RT-PCR in HeLa cells.	n-hexane	17-25	P53	Homo sapiens	133-136
25854514-2	2015	Layered double hydroxide nanoparticles are co-loaded with a Pt(IV) prodrug and a p53 activator.	hydroxide ion	15-24	P53	Homo sapiens	81-84
32467171-9	2020	These results demonstrate that DRS induced by a nucleoside analog-type chemotherapeutic drug suppresses tumor growth irrespective of p53 status by directing tumor cell fate toward cellular senescence or apoptotic cell death according to p53 status.	Nucleosides	48-58	P53	Homo sapiens	237-240
32922194-10	2020	Inhibition of p53 by pifithrin-alpha significantly reduced the levels of PUMA, Bax, and PTEN but restored AKT phosphorylation in SiHa cells exposed to sesamin.	pifithrin	21-36	P53	Homo sapiens	14-17
25938491-9	2015	Specific inhibition of p53 by pifithrin-alpha reduces the percentage of cells accumulated in S-phase, suggesting contribution of p53 to S-phase increase.	pifithrin	30-45	P53	Homo sapiens	23-26
32757802-7	2021	The synergistic antitumor effect of API and CDDP was blocked by addition of the p53 inhibitor Pifithrin-alpha, and siRNA targeting the p53 gene in A549R cells.	pifithrin	94-109	P53	Homo sapiens	80-83
25851939-3	2015	The results suggest that chromane containing glitazones are apoptic agonist (activating p53 by intrinsic pathway leading to the apoptosis) and those which do not contain the chromane are devoid of this.	Thiazolidinediones	45-55	P53	Homo sapiens	88-91
25851939-6	2015	Immunoblot analysis further confirm our hypothesis that troglitazone (chromane containing glitazone), but not rosiglitazone and pioglitazone (non-chromane containing glitazone) increased the levels of p53 in a time-dependent manner.	Troglitazone	56-68	P53	Homo sapiens	201-204
25851939-6	2015	Immunoblot analysis further confirm our hypothesis that troglitazone (chromane containing glitazone), but not rosiglitazone and pioglitazone (non-chromane containing glitazone) increased the levels of p53 in a time-dependent manner.	Thiazolidinediones	59-68	P53	Homo sapiens	201-204
25851939-6	2015	Immunoblot analysis further confirm our hypothesis that troglitazone (chromane containing glitazone), but not rosiglitazone and pioglitazone (non-chromane containing glitazone) increased the levels of p53 in a time-dependent manner.	Thiazolidinediones	90-99	P53	Homo sapiens	201-204
32798402-0	2020	[Clinical Efficacy and Prognosis of Double-Hit Multiple Myeloma Patients with Deletion P53 Treated with Regimen Based on Bortezomib].	Bortezomib	121-131	P53	Homo sapiens	87-90
25875800-8	2015	O-benzylguanine inhibits survivin and PCNA (proliferating cell nuclear antigen) at messenger RNA and protein levels in PANC-1 and L3.6pl cells and decreases survivin promoter activity via increased p53 recruitment to the survivin promoter.	o-benzylguanine	0-15	P53	Homo sapiens	198-201
32798402-1	2020	OBJECTIVE: To investigate the clinical efficacy and prognosis of double-hit multiple myeloma patients with deletion P53 treated with regimen based on bortezomib.	Bortezomib	150-160	P53	Homo sapiens	116-119
32683571-12	2020	Graphical abstract Schematic representation of the electrochemiluminescence sensor based on a Zn-MOF/GO nanocomposite, which can be applied to the determination of p53 antibody.	zn-mof	94-100	P53	Homo sapiens	164-167
26015807-11	2015	It also revealed overexpression of the ATM/p53/p21 pathway, which is activated in response to DNA damage and induces cell cycle arrest in thiopurine resistant LCLs.	2-mercaptopyrazine	138-148	P53	Homo sapiens	43-46
26015807-12	2015	Furthermore, overexpression of the p53 target gene TNFRSF10D or the negative cell cycle regulator CCNG2 induces cell cycle arrest and may also contribute to thiopurine resistance.	2-mercaptopyrazine	157-167	P53	Homo sapiens	35-38
32377702-9	2020	In conclusion, juglone potentiated BRAF inhibitor-induced apoptosis in resistant melanoma cells, and these effects occurred partially through ROS and the p38-p53 pathway, suggesting the potential of juglone as a sensitizer to BRAF inhibitors in the treatment of melanoma.	juglone	199-206	P53	Homo sapiens	158-161
32583791-4	2020	Some bioactive compounds, in particular phenolic compounds, saponins and alkaloids have revealed good abilities to affect p53 expression and indirectly control the telomere length.	Alkaloids	73-82	P53	Homo sapiens	122-125
32446382-8	2020	These results suggest that co-treatment with bortezomib and kuanoniamine C is a novel therapeutic strategy for the treatment of osteosarcoma that enhances bortezomib-dependent cell death by the downregulation of GRP78, and this combination selectively targets the major cell population of osteosarcoma, which expresses wild-type p53.	Bortezomib	45-55	P53	Homo sapiens	329-332
24882579-0	2015	miR-339-5p regulates the p53 tumor-suppressor pathway by targeting MDM2.	mir-339-5p	0-10	P53	Homo sapiens	25-28
24882579-5	2015	Using a high-throughput screening approach, we identified miR-339-5p as a regulator of the p53 pathway.	mir-339-5p	58-68	P53	Homo sapiens	91-94
24882579-6	2015	We demonstrate that this regulation occurs via the ability of miR-339-5p to target directly the 3"-untranslated region of MDM2 mRNA, reducing MDM2 expression and thus promoting p53 function.	mir-339-5p	62-72	P53	Homo sapiens	177-180
26497213-5	2015	In an expanded panel of ten NB cell lines, those with MYCN-amplification and wild-type TP53 were the most sensitive to low nanomolar concentrations of barasertib.	2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate	151-161	P53	Homo sapiens	87-91
26431163-11	2015	We conclude that the pre-activation of p53 through Mdm2 antagonists serves as a viable option to selectively protect p53-proficient cells against the cytotoxic effects of Wee1 inhibitors, especially when combined with a nucleoside analogue.	Nucleosides	220-230	P53	Homo sapiens	39-42
26485709-11	2015	According to the results, trabectedin induced cytotoxicity and apoptosis at the IC50 dose, resulting in a significant increase expression of caspase-3, caspase-8, caspase-9, p53 and decrease expression of bcl-2 in dose-dependent manner.	Trabectedin	26-37	P53	Homo sapiens	174-177
26722606-6	2015	Morphology observation, HE staining, and p53 and beta-catenin expression detection confirmed that drinking 3% DSS and 3% DSS combined with AOM intraperitoneal injection can successfully establish colitis and colitis associated colorectal cancer models.	dss	110-113	P53	Homo sapiens	41-44
26722606-6	2015	Morphology observation, HE staining, and p53 and beta-catenin expression detection confirmed that drinking 3% DSS and 3% DSS combined with AOM intraperitoneal injection can successfully establish colitis and colitis associated colorectal cancer models.	dss	121-124	P53	Homo sapiens	41-44
29308155-4	2015	Most significantly, selective inhibition of p53/hDM2 can be achieved against four other targets and the selectivity for p53/hDM2 inhibition versus Mcl-1/NOXA-B inhibition is critically dependent upon the stereochemistry of the helix mimetic.	noxa-b	153-159	P53	Homo sapiens	44-47
31792920-7	2020	Moreover, high glucose increased the protein levels of p53, acetyl-p53 and p21.	acetyl phosphate	60-66	P53	Homo sapiens	67-70
25689150-0	2015	Autophagy modulates the effects of bis-anthracycline WP631 on p53-deficient prostate cancer cells.	bis-anthracycline	35-52	P53	Homo sapiens	62-65
25689150-1	2015	Treatment of p53-deficient PC-3 human prostate carcinoma cells with nanomolar concentrations of bis-anthracycline WP631 induced changes in gene expression, which resulted in G2/M cell cycle arrest, autophagy and cell death.	bis-anthracycline	96-113	P53	Homo sapiens	13-16
24798859-9	2015	Collectively, these data implicate polycyclic aromatic hydrocarbons and AhR in the regulation of p53-targeting miRNAs in MM and identify a potential therapeutic and preventive agent to combat this deadly disease.	Polycyclic Aromatic Hydrocarbons	35-67	P53	Homo sapiens	97-100
26208523-11	2015	These data indicate that the DACH carrier ligand in oxaliplatin triggers signaling via the p53-miR-34a-E2F axis, leading to transcriptional regulation that ultimately results in accumulation of dUTP and reduced dTTP biosynthesis, potentially enhancing 5-FU cytotoxicity.	deoxyuridine triphosphate	194-198	P53	Homo sapiens	91-94
32319208-7	2020	Mechanistically, DHL is capable of inhibiting Hep-2 and TU212 cell viability via promoting p53 and P21 function, meanwhile DHL dose-dependently induces Hep-2 and TU212 cells apoptosis via activating mitochondrial apoptosis by inhibiting PI3K/Akt/Bad pathway and stimulating endoplasmic reticulum stress-mediated apoptosis pathway.	dehydrocostus lactone	17-20	P53	Homo sapiens	91-94
26302161-6	2015	Inhibition of p53 activity using either pifithrin-alpha or small interference RNA interference reduced OGD-induced cell death and pifithrin-alpha reversed OGD-induced impairment of glutamate uptake in astrocytes, suggesting that p53 might play a key role in mediating neurotoxicity and gliotoxicity in ischemic brain injury.	pifithrin	40-49	P53	Homo sapiens	14-17
26302161-6	2015	Inhibition of p53 activity using either pifithrin-alpha or small interference RNA interference reduced OGD-induced cell death and pifithrin-alpha reversed OGD-induced impairment of glutamate uptake in astrocytes, suggesting that p53 might play a key role in mediating neurotoxicity and gliotoxicity in ischemic brain injury.	pifithrin	130-139	P53	Homo sapiens	14-17
25595616-12	2015	However, p53 deficiency (using the TK6-isogenic cell line, NH32) increased sensitivity to MMS during chronic dosing, causing this LOGEL to equate to the acute treatment LOGEL.	Methyl Methanesulfonate	90-93	P53	Homo sapiens	9-12
32321249-0	2020	Design of hydrazide-bearing HDACIs based on panobinostat and their p53 and FLT3-ITD dependency in anti-leukemia activity.	hydrazide	10-19	P53	Homo sapiens	67-70
32403326-0	2020	Micheliolide Enhances Radiosensitivities of p53-Deficient Non-Small-Cell Lung Cancer via Promoting HIF-1alpha Degradation.	micheliolide	0-12	P53	Homo sapiens	44-47
25607831-8	2015	Pretreatment with N-acetyl-cysteine (NAC), the inhibitor of ROS, or with SP600125, the inhibitor of JNK, prevented the apoptosis and the high expression of p-JNK, p53, caspase-9 and caspase-3 in CDK5RAP1-deficient MCF-7 cells.	pyrazolanthrone	73-81	P53	Homo sapiens	163-166
25567764-1	2015	We report in this work that the Abeta peptide directly interacts with tubulin close to the vinblastine and GTP/GDP binding site, inhibits the tubulin polymerization rate, induces tubulin aggregation, causes cell shrinking, enhances Mad2, BubR1, p53, and p21 activation in MCF7 cells and induces the apoptotic death of A549, HeLa and MCF7 cells.	Vinblastine	91-102	P53	Homo sapiens	245-248
25544361-8	2015	These effects were blocked by pretreatment with pifithrin-alpha, a p53 inhibitor.	pifithrin	48-63	P53	Homo sapiens	67-70
26406246-6	2015	Nanocurcumin prevented translocation of p53 to mitochondria by stabilizing mitochondrial membrane potential and de-stressed hypertrophied HVCM cells by significant restoration in lactate, acetyl-coenzyme A, pyruvate and glucose content along with lactate dehydrogenase (LDH) and 5" adenosine monophosphate-activated protein kinase (AMPKalpha) activity.	nanocurcumin	0-12	P53	Homo sapiens	40-43
26406246-8	2015	Nanocurcumin prevented of mitochondrial stress as confirmed by c-fos/c-jun/p53 signalling.	nanocurcumin	0-12	P53	Homo sapiens	75-78
32382022-10	2020	Conclusions: Sorafenib and Regorafenib were especially active in well-differentiated cells, with wild-type p53 and increased mitochondrial respiration.	Sorafenib	13-22	P53	Homo sapiens	107-110
31781983-9	2020	Furthermore, Western blotting analysis showed that ABZ induced the apoptosis in MDA-MB-231 cells via GLUT1/AMPK/P53 signaling pathway.	Albendazole	51-54	P53	Homo sapiens	112-115
26378933-4	2015	In vitro analysis revealed a higher resistance to bortezomib possibly due to an altered gene expression profile caused by del(8)(p21) including genes such as TRAIL-R4, CCDC25, RHOBTB2, PTK2B, SCARA3, MYC, BCL2 and TP53.	Bortezomib	50-60	P53	Homo sapiens	214-218
25557114-0	2015	Sorafenib inhibits proliferation and invasion of human hepatocellular carcinoma cells via up-regulation of p53 and suppressing FoxM1.	Sorafenib	0-9	P53	Homo sapiens	107-110
25557114-9	2015	Furthermore, sorafenib (2-6 mumol/L) dose-dependently decreased the expression of FoxM1, MMP-2, and Ki-67, and up-regulated that of p53 in the cells.	Sorafenib	13-22	P53	Homo sapiens	132-135
25557114-10	2015	Silencing p53 abolished the decrease of FoxM1 and increase of p53 in sorafenib-treated cells.	Sorafenib	69-78	P53	Homo sapiens	10-13
25557114-10	2015	Silencing p53 abolished the decrease of FoxM1 and increase of p53 in sorafenib-treated cells.	Sorafenib	69-78	P53	Homo sapiens	62-65
32032660-9	2020	PKR was tested due to its ability to phosphorylate p53 on Ser392.	seryl-seryl-seryl-arginine	58-61	P53	Homo sapiens	51-54
26337976-11	2015	CONCLUSION: AARS, AURKA, AURKB, CENPA, CCNB1, CCNE2, and CDK may contribute to MTX resistance via aminoacyl-tRNA biosynthesis pathway, cell cycle pathway, or p53 signaling pathway.	Methotrexate	79-82	P53	Homo sapiens	158-161
25434456-9	2015	Further experiments showed that inhibition of cell proliferation by fluvastatin was associated with elevated IGFBP-6, p27, p53 levels and reduced survivin, cyclin B1, cyclin D1 and VEGF expression.	Fluvastatin	68-79	P53	Homo sapiens	123-126
32273511-6	2020	Thus, we found that p53 regulates asparagine metabolism and dictates cell survival by generating an auto-amplification loop via asparagine-aspartate-mediated LKB1-AMPK signalling.	Aspartic Acid	139-148	P53	Homo sapiens	20-23
25596743-10	2015	In addition, hsa-miR-526b overexpression or Ku80 knockdown increased p53 and p21CIP1/WAF1 expression.	Altretamine	13-16	P53	Homo sapiens	69-72
26151768-8	2015	Roscovitine led to a dose-dependent decrease of transcripts of p53, CDK 7 and cyclins A and E and an increase of &gt;4-fold of p21 in A172 cells.	Roscovitine	0-11	P53	Homo sapiens	63-66
32373219-5	2020	Patient-derived xenograft models were employed to determine the role of TP53 in response to sorafenib.	Sorafenib	92-101	P53	Homo sapiens	72-76
26231043-3	2015	We found that DCA induces the AMP-activated protein kinase (AMPK)/p53 pathway with increased efficacy in tumors expressing wild type (wt p53).	Dichloroacetic Acid	14-17	P53	Homo sapiens	66-69
26231043-3	2015	We found that DCA induces the AMP-activated protein kinase (AMPK)/p53 pathway with increased efficacy in tumors expressing wild type (wt p53).	Dichloroacetic Acid	14-17	P53	Homo sapiens	137-140
26231043-4	2015	Clinically relevant, low concentrations of doxorubicin synergize in vitro and in vivo with DCA to further enhance p53 activation and to block tumor progression.	Dichloroacetic Acid	91-94	P53	Homo sapiens	114-117
25510514-5	2015	The binding constants of 9 OPFRs with p53 DNA fragment were determined respectively, using ethidium bromide (EB) as fluorescence probe of DNA.	Ethidium	91-107	P53	Homo sapiens	38-41
25510514-5	2015	The binding constants of 9 OPFRs with p53 DNA fragment were determined respectively, using ethidium bromide (EB) as fluorescence probe of DNA.	Ethidium	109-111	P53	Homo sapiens	38-41
31278615-6	2020	Our study presents two preliminary findings: (a) in HaVSMCs, FOLFIRI treatment significantly induces oxidative damage to both DNA and protein, leading to a dramatic increase in caspase-dependent apoptotic death through P53-mediated Caspase3-dependent mitochondrial apoptosis, and results in TNF-alpha/Caspase8-mediated necrotic death, and (b) flavonoids not only regulate the expression of genes encoding antioxidant enzymes and increase DNA damage but also limit programmed and necrotic cell death processes in HaVSMCs.	Flavonoids	343-353	P53	Homo sapiens	219-222
25603347-0	2015	Activation of p53 with ilimaquinone and ethylsmenoquinone, marine sponge metabolites, induces apoptosis and autophagy in colon cancer cells.	ethylsmenoquinone	40-57	P53	Homo sapiens	14-17
25603347-2	2015	Here, we used a cell-based reporter system for the detection of p53 response transcription to identify the marine sponge metabolites, ilimaquinone and ethylsmenoquinone, as activators of the p53 pathway.	ethylsmenoquinone	151-168	P53	Homo sapiens	64-67
25603347-2	2015	Here, we used a cell-based reporter system for the detection of p53 response transcription to identify the marine sponge metabolites, ilimaquinone and ethylsmenoquinone, as activators of the p53 pathway.	ethylsmenoquinone	151-168	P53	Homo sapiens	191-194
25603347-3	2015	We demonstrated that ilimaquinone and ethylsmenoquinone efficiently stabilize the p53 protein through promotion of p53 phosphorylation at Ser15 in both HCT116 and RKO colon cancer cells.	ethylsmenoquinone	38-55	P53	Homo sapiens	82-85
25603347-3	2015	We demonstrated that ilimaquinone and ethylsmenoquinone efficiently stabilize the p53 protein through promotion of p53 phosphorylation at Ser15 in both HCT116 and RKO colon cancer cells.	ethylsmenoquinone	38-55	P53	Homo sapiens	115-118
25603347-7	2015	Our findings suggest that ilimaquinone and ethylsmenoquinone exert their anti-cancer activity by activation of the p53 pathway and may have significant potential as chemo-preventive and therapeutic agents for human colon cancer.	ethylsmenoquinone	43-60	P53	Homo sapiens	115-118
26251569-4	2015	METHODS: Here, we report the effects of several concentrations of zinc combined with docetaxel on p53-wild-type (A549) and p53-null (H1299) cells.	Docetaxel	85-94	P53	Homo sapiens	98-101
26170659-13	2015	Cells pretreated with pifithrin-alpha were protected from p53-mediated AgNPs-induced toxicity.	pifithrin	22-37	P53	Homo sapiens	58-61
32218859-0	2020	Potential synergistic effects of sorafenib and CP-31398 for treating anaplastic thyroid cancer with p53 mutations.	Sorafenib	33-42	P53	Homo sapiens	100-103
32218859-5	2020	Combined targeted therapy, including sorafenib, may be clinically significant for patients with ATC harboring p53 mutations.	Sorafenib	37-46	P53	Homo sapiens	110-113
31583975-7	2020	Then, both histidine-tagged proteins p53 and ERK1 were immobilized by the Ni-Co layer in a microarray format for subsequent immunoassay and fluorescence detection.	histidine-pyridine-histidine-3	11-20	P53	Homo sapiens	37-40
24994707-3	2015	Among them, spiro-pyrrolidinyl oxindoles have been extensively studied as potent inhibitors of p53-MDM2 interaction, finally leading to the identification of MI-888, which could achieve rapid, complete and durable tumor regression in xenograft models of human cancer with oral administration and is in advanced preclinical research for cancer therapy.	spiro-pyrrolidinyl oxindoles	12-40	P53	Homo sapiens	95-98
25820140-5	2015	At molecular level, PCN instigates apoptosis by mitochondrial intrinsic apoptotic pathway via the overexpression of p53, Bax, cytochrome C release and activation of caspase-3 with the inhibition of oncogenic anti-apoptotic proteins such as PARP and Bcl-2 family proteins (Bcl-2, Bcl-w and Bcl-xL).	Pregnenolone Carbonitrile	20-23	P53	Homo sapiens	116-119
26372775-2	2015	In the present study, we investigated the effects of sulforaphane (SFN), a phytochemical from cruciferous vegetables, on the methylation and expression of PTEN and RARbeta2 tumour suppressor genes as well as on the expression of regulators of DNA methylation reaction, DNMT1 , p53 , and p21 , in MCF-7 and MDA-MB-231 human breast cancer cells with different invasive potential.	sulforaphane	53-65	P53	Homo sapiens	277-280
26372775-2	2015	In the present study, we investigated the effects of sulforaphane (SFN), a phytochemical from cruciferous vegetables, on the methylation and expression of PTEN and RARbeta2 tumour suppressor genes as well as on the expression of regulators of DNA methylation reaction, DNMT1 , p53 , and p21 , in MCF-7 and MDA-MB-231 human breast cancer cells with different invasive potential.	sulforaphane	67-70	P53	Homo sapiens	277-280
32212969-6	2020	DNA fragmentation and up-regulated of caspase-3 and p53 had illustrated the apoptotic effect of MCF-7 treated with GEM-ANPS/CS.	gem-anps	115-123	P53	Homo sapiens	52-55
25947292-0	2015	PLGA-Loaded Gold-Nanoparticles Precipitated with Quercetin Downregulate HDAC-Akt Activities Controlling Proliferation and Activate p53-ROS Crosstalk to Induce Apoptosis in Hepatocarcinoma Cells.	Quercetin	49-58	P53	Homo sapiens	131-134
25354189-0	2014	Linear aliphatic dialkynes as alternative linkers for double-click stapling of p53-derived peptides.	aliphatic dialkynes	7-26	P53	Homo sapiens	79-82
32235770-8	2020	BTZ inhibited proliferation and induced apoptosis through the accumulation of p53 in three human Myc-ATRT cell lines (PDX-derived tumor cell line Re1-P6, BT-12 and CHLA-266).	Bortezomib	0-3	P53	Homo sapiens	78-81
25354189-1	2014	We investigated linear aliphatic dialkynes as a new structural class of i,i+7 linkers for the double-click stapling of p53-based peptides.	aliphatic dialkynes	23-42	P53	Homo sapiens	119-122
32121469-2	2020	Furthermore, all derivatives demonstrated promising activity upon evaluation of theirin vitroandin vivosuppression of p53 ubiquitination and inhibition assessment for LDHA kinase.	vitroandin	88-98	P53	Homo sapiens	118-121
25674209-7	2014	In addition, the expression level of p53 was dose-dependently upregulated after administration with formononetin.	formononetin	100-112	P53	Homo sapiens	37-40
25674209-8	2014	We also found that formononetin treatment increased the phosphorylation of p53 at Ser15 and Ser20 and enhances its transcriptional activity in a dose-dependent manner.	formononetin	19-31	P53	Homo sapiens	75-78
25743928-5	2015	Here we present the effects of tributyltin chloride (TBT-Cl) and triphenyltin chloride (TPT-Cl) on cell proliferation, expression of proapoptotic p53, Bax, and antiapoptotic Bcl-2 proteins in human breast cancer MCF-7 cell line.	tributyltin	31-51	P53	Homo sapiens	146-149
25743928-5	2015	Here we present the effects of tributyltin chloride (TBT-Cl) and triphenyltin chloride (TPT-Cl) on cell proliferation, expression of proapoptotic p53, Bax, and antiapoptotic Bcl-2 proteins in human breast cancer MCF-7 cell line.	tributyltin	53-59	P53	Homo sapiens	146-149
25743928-7	2015	Short time treatment with TBT-Cl displayed marked stimulation of p53 protein expression when compared to TPT-Cl.	tributyltin	26-32	P53	Homo sapiens	65-68
26109759-13	2015	CONCLUSION: These findings indicate that the methanol extract of wheatgrass inhibits human laryngeal cancer cell proliferation via cell cycle G1 arrest and p53 induction.	Methanol	45-53	P53	Homo sapiens	156-159
25279998-9	2014	Evaluation of the mutagenicity of anti-B[a]P-diol epoxide with B[a]P-7,8-dione on p53 showed that the o-quinone produced by AKRs was the more potent mutagen, provided that it was permitted to redox cycle, and that the mutations observed were G to T transversions, reminiscent of those observed in human lung cancer.	b[a]p-7,8-dione	63-78	P53	Homo sapiens	82-85
25713322-6	2015	A similar effect was induced by the p53 inhibitor pifithrin, which also potentiated the LPS-induced hyperpermeability in human lung microvascular endothelial cells (HLMVEC).	pifithrin	50-59	P53	Homo sapiens	36-39
25279998-9	2014	Evaluation of the mutagenicity of anti-B[a]P-diol epoxide with B[a]P-7,8-dione on p53 showed that the o-quinone produced by AKRs was the more potent mutagen, provided that it was permitted to redox cycle, and that the mutations observed were G to T transversions, reminiscent of those observed in human lung cancer.	2-benzoquinone	102-111	P53	Homo sapiens	82-85
32210718-10	2020	Western blot analysis showed that adenine reduced expression of cyclin A/D1 and cyclin-dependent kinase (CDK)2 and upregulated p53, p21, Bax, PUMA, and NOXA in HepG2 cell.	Adenine	34-41	P53	Homo sapiens	127-130
25437549-5	2014	DNA-damage-induced p53 interfered with chlamydial development through downregulation of the pentose phosphate pathway (PPP).	Pentosephosphates	92-109	P53	Homo sapiens	19-22
25489053-0	2015	A novel manganese-dependent ATM-p53 signaling pathway is selectively impaired in patient-based neuroprogenitor and murine striatal models of Huntington"s disease.	Manganese	8-17	P53	Homo sapiens	32-35
25489053-3	2015	We found that p53 phosphorylation at serine 15 is the most responsive cell signaling event to manganese exposure (of 18 tested) in human neuroprogenitors and a mouse striatal cell line.	Manganese	94-103	P53	Homo sapiens	14-17
32210718-11	2020	Moreover, adenine induced AMPK activation that was involved in the p53-associated apoptotic cascade in HepG2 cells.	Adenine	10-17	P53	Homo sapiens	67-70
32210718-13	2020	Conclusions: These findings reveal that adenine reduces the cell growth of HepG2 and SK-Hep-1 but not Hep3B cells, attributing to the AMPK/p53-mediated S phase arrest and apoptosis.	Adenine	40-47	P53	Homo sapiens	139-142
32210718-14	2020	It suggests that adenine has anticancer potential against p53-wild type HCC cells and may be beneficial as an adjuvant for HCC treatment.	Adenine	17-24	P53	Homo sapiens	58-61
25196217-9	2015	BIRC6 knockdown remarkably suppressed cell proliferation, caused G1/S arrest and sensitized hepatoma cells to sorafenib-induced apoptosis in hepatoma cells, which was partly reversed by RNA interference targeting p53.	Sorafenib	110-119	P53	Homo sapiens	213-216
24905183-0	2014	Expression of survivin and p53 modulates honokiol-induced apoptosis in colorectal cancer cells.	honokiol	41-49	P53	Homo sapiens	27-30
31952808-7	2020	[R273C]p53 aggregation is disulfide mediated, leading to cross-beta, thioflavin-T-positive aggregates, whereas hydrophobic interactions dominate self-assembly in [R273L]p53, leading to a mixture of amyloid and amorphous aggregates.	thioflavin T	69-81	P53	Homo sapiens	7-10
24905183-2	2014	Here, we show that survivin and p53 display the opposite role on the regulation of honokiol-induced apoptosis in the human colorectal cancer cells.	honokiol	83-91	P53	Homo sapiens	32-35
24905183-8	2014	Meantime, honokiol increased total p53 and the phosphorylated p53 proteins at Ser15 and Ser46.	honokiol	10-18	P53	Homo sapiens	35-38
24905183-8	2014	Meantime, honokiol increased total p53 and the phosphorylated p53 proteins at Ser15 and Ser46.	honokiol	10-18	P53	Homo sapiens	62-65
24905183-9	2014	The p53-wild type colorectal cancer cells were exhibited greater cytotoxicity, apoptosis and survivin reduction than the p53-null cancer cells after treatment with honokiol.	honokiol	164-172	P53	Homo sapiens	4-7
24905183-9	2014	The p53-wild type colorectal cancer cells were exhibited greater cytotoxicity, apoptosis and survivin reduction than the p53-null cancer cells after treatment with honokiol.	honokiol	164-172	P53	Homo sapiens	121-124
24905183-10	2014	Together, these findings demonstrate that the existence of survivin and p53 can modulate the honokiol-induced apoptosis in the human colorectal cancer cells.	honokiol	93-101	P53	Homo sapiens	72-75
26027393-4	2015	An immunohistochemical technique using mouse antibodies against p53 protein (&lt;&lt;DAKO&gt;&gt;, Denmark), stained with diaminobenzidine (DAB) chromogen, was employed to determine p53 protein.	4,4'-Dihydrazino-biphenyl	122-138	P53	Homo sapiens	64-67
31952808-7	2020	[R273C]p53 aggregation is disulfide mediated, leading to cross-beta, thioflavin-T-positive aggregates, whereas hydrophobic interactions dominate self-assembly in [R273L]p53, leading to a mixture of amyloid and amorphous aggregates.	thioflavin T	69-81	P53	Homo sapiens	169-172
25160801-4	2015	Here we show that MKs contact with OBs, via beta1 integrin, activate the p38/MAPKAPK2/p90RSK kinase cascade in the bone cells, which causes Mdm2 to neutralizes p53/Rb-mediated check point and allows progression through the G1/S.	obs	35-38	P53	Homo sapiens	160-163
31940492-4	2020	Mechanistically, DNA damage activates ATM to phosphorylate p53 on Ser33 and Ser37, which facilitates the FBXW7 binding and subsequent p53 degradation by SCFFBXW7.	seryl-seryl-seryl-arginine	66-69	P53	Homo sapiens	59-62
25350363-1	2014	2-Acetylpyridine acetylhydrazone (H2AcMe), 2-benzoylpyridine acetylhydrazone (H2BzMe) and complexes [Cu(H2AcMe)Cl2] (1) and [Cu(H2BzMe)Cl2] (2) were assayed for their cytotoxicity against wild type p53 U87 and mutant p53 T98 glioma cells, and against MRC-5 fibroblast cells.	2-acetylpyridine acetylhydrazone	0-32	P53	Homo sapiens	198-201
25350363-1	2014	2-Acetylpyridine acetylhydrazone (H2AcMe), 2-benzoylpyridine acetylhydrazone (H2BzMe) and complexes [Cu(H2AcMe)Cl2] (1) and [Cu(H2BzMe)Cl2] (2) were assayed for their cytotoxicity against wild type p53 U87 and mutant p53 T98 glioma cells, and against MRC-5 fibroblast cells.	2-acetylpyridine acetylhydrazone	0-32	P53	Homo sapiens	217-220
31940492-4	2020	Mechanistically, DNA damage activates ATM to phosphorylate p53 on Ser33 and Ser37, which facilitates the FBXW7 binding and subsequent p53 degradation by SCFFBXW7.	seryl-seryl-seryl-arginine	66-69	P53	Homo sapiens	134-137
31940492-4	2020	Mechanistically, DNA damage activates ATM to phosphorylate p53 on Ser33 and Ser37, which facilitates the FBXW7 binding and subsequent p53 degradation by SCFFBXW7.	seryl-seryl-seryl-arginine	76-79	P53	Homo sapiens	59-62
25371972-9	2015	Interestingly, both oxidative stress and p53 pathways were involved in GaM-induced cytotoxicity.	gallium maltolate	71-74	P53	Homo sapiens	41-44
25085902-6	2014	Enhanced cytotoxicities after treatment with the p53-inhibitory drug Pifithrinalpha further supported p53-mediated resistance to PARP inhibition.	pifithrin	69-83	P53	Homo sapiens	49-52
31940492-4	2020	Mechanistically, DNA damage activates ATM to phosphorylate p53 on Ser33 and Ser37, which facilitates the FBXW7 binding and subsequent p53 degradation by SCFFBXW7.	seryl-seryl-seryl-arginine	76-79	P53	Homo sapiens	134-137
25085902-6	2014	Enhanced cytotoxicities after treatment with the p53-inhibitory drug Pifithrinalpha further supported p53-mediated resistance to PARP inhibition.	pifithrin	69-83	P53	Homo sapiens	102-105
25714014-7	2015	In addition, transfection of miR-106b-5p antagomir resulted in the increased binding of H3K36me3 to the promoter of p53 and enhanced its activity, as well as upregulated the mRNA and protein levels of p53, and the effects were also abolished by cotransfection with si-SETD2.	CHEMBL3740941	38-40	P53	Homo sapiens	116-119
31958042-9	2020	Amygdalin treatment induced cell cycle arrest at G2/M and increased the levels of P53, Bax, cytochrome c, and caspase-3 significantly, while it decreased the level of anti-apoptotic Bcl2.	Amygdalin	0-9	P53	Homo sapiens	82-85
25714014-7	2015	In addition, transfection of miR-106b-5p antagomir resulted in the increased binding of H3K36me3 to the promoter of p53 and enhanced its activity, as well as upregulated the mRNA and protein levels of p53, and the effects were also abolished by cotransfection with si-SETD2.	CHEMBL3740941	38-40	P53	Homo sapiens	201-204
25544776-0	2015	The anti-leukemic activity of sodium dichloroacetate in p53mutated/null cells is mediated by a p53-independent ILF3/p21 pathway.	Dichloroacetic Acid	30-52	P53	Homo sapiens	56-59
25544776-0	2015	The anti-leukemic activity of sodium dichloroacetate in p53mutated/null cells is mediated by a p53-independent ILF3/p21 pathway.	Dichloroacetic Acid	30-52	P53	Homo sapiens	95-98
25544776-1	2015	B-chronic lymphocytic leukemia (B-CLL) patients harboring p53 mutations are invariably refractory to therapies based on purine analogues and have limited treatment options and poor survival.	purine	120-126	P53	Homo sapiens	58-61
25509266-11	2014	Western blot showed the expression of p53 and p21 protein could be increased by DHA combined irradiation, and the expression of Bcl-2 protein down-regulated (P &lt;0.01, P &lt;0.	artenimol	80-83	P53	Homo sapiens	38-41
25108166-6	2014	However, Quercetin decreased cell contents of HIF-1alpha, Foxo-3a and NICD as well as pro-apoptotic factors including p53 and Bax compared to H2O2-treated cells.	Quercetin	9-18	P53	Homo sapiens	118-121
25544776-2	2015	Having recently demonstrated that the mitochondria-targeting small molecule sodium dichloroacetate (DCA) exhibits anti-leukemic activity in p53wild-type B-CLL cells, the aim of this study was to evaluate the effect of DCA in p53mutated B-CLL cells and in p53mutated/null leukemic cell lines.	Dichloroacetic Acid	76-98	P53	Homo sapiens	140-143
32067620-9	2020	Also, P-3F and D-3F displayed most potent cytotoxicities against PLC/PRF/5 with p53-R249S and weakest inhibition of L02 (normal liver cell) growth.	Erythrosine	15-19	P53	Homo sapiens	80-83
25544776-2	2015	Having recently demonstrated that the mitochondria-targeting small molecule sodium dichloroacetate (DCA) exhibits anti-leukemic activity in p53wild-type B-CLL cells, the aim of this study was to evaluate the effect of DCA in p53mutated B-CLL cells and in p53mutated/null leukemic cell lines.	Dichloroacetic Acid	76-98	P53	Homo sapiens	225-228
25544776-2	2015	Having recently demonstrated that the mitochondria-targeting small molecule sodium dichloroacetate (DCA) exhibits anti-leukemic activity in p53wild-type B-CLL cells, the aim of this study was to evaluate the effect of DCA in p53mutated B-CLL cells and in p53mutated/null leukemic cell lines.	Dichloroacetic Acid	100-103	P53	Homo sapiens	140-143
25544776-2	2015	Having recently demonstrated that the mitochondria-targeting small molecule sodium dichloroacetate (DCA) exhibits anti-leukemic activity in p53wild-type B-CLL cells, the aim of this study was to evaluate the effect of DCA in p53mutated B-CLL cells and in p53mutated/null leukemic cell lines.	Dichloroacetic Acid	100-103	P53	Homo sapiens	225-228
25544776-3	2015	DCA exhibited comparable cytotoxicity in p53wild-type and p53mutated B-CLL patient cell cultures, as well as in p53mutated B leukemic cell lines (MAVER, MEC-1, MEC-2).	Dichloroacetic Acid	0-3	P53	Homo sapiens	41-44
24568186-11	2014	When MCF-7 cells were treated with the Fe(2+)-specific chelator phenanthroline, 15d-PGJ2-induced p53 expression was attenuated.	ammonium ferrous sulfate	39-45	P53	Homo sapiens	97-100
31747859-2	2020	Our previous study showed that CDK4/Cyclin D1 phosphorylates p53-RS at the cancer-derived Ser249 and promotes its interaction with c-Myc in the nucleus, consequently enhancing c-Myc-dependent ribosomal biogenesis and HCC cell proliferation.	seryl-seryl-seryl-arginine	90-93	P53	Homo sapiens	61-64
24308434-3	2014	Sensitivity of HMCLs to both drugs was correlated to p53: the BDM and melphalan median LD50 values of TP53(wild-type) HMCLs were more than two-fold lower than those of TP53(abnormal) HMCLs (p &lt; 0.001), and p53 silencing in TP53(wt) NCI-H929 cells inhibited BDM- and melphalan-induced cell death.	Melphalan	70-79	P53	Homo sapiens	53-56
25544776-3	2015	DCA exhibited comparable cytotoxicity in p53wild-type and p53mutated B-CLL patient cell cultures, as well as in p53mutated B leukemic cell lines (MAVER, MEC-1, MEC-2).	Dichloroacetic Acid	0-3	P53	Homo sapiens	58-61
25544776-3	2015	DCA exhibited comparable cytotoxicity in p53wild-type and p53mutated B-CLL patient cell cultures, as well as in p53mutated B leukemic cell lines (MAVER, MEC-1, MEC-2).	Dichloroacetic Acid	0-3	P53	Homo sapiens	58-61
25544776-8	2015	Taken together, our results emphasize that DCA is a small molecule that merits further evaluation as a therapeutic agent also for p53mutated leukemic cells, by acting through the induction of a p53-independent pathway.	Dichloroacetic Acid	43-46	P53	Homo sapiens	130-133
25544776-8	2015	Taken together, our results emphasize that DCA is a small molecule that merits further evaluation as a therapeutic agent also for p53mutated leukemic cells, by acting through the induction of a p53-independent pathway.	Dichloroacetic Acid	43-46	P53	Homo sapiens	194-197
24308434-3	2014	Sensitivity of HMCLs to both drugs was correlated to p53: the BDM and melphalan median LD50 values of TP53(wild-type) HMCLs were more than two-fold lower than those of TP53(abnormal) HMCLs (p &lt; 0.001), and p53 silencing in TP53(wt) NCI-H929 cells inhibited BDM- and melphalan-induced cell death.	Melphalan	70-79	P53	Homo sapiens	102-106
32907379-6	2020	ADAR1 and cyclin D1 protein levels were dramatically decreased, while p53 and p21 levels were increased after 8-Cl-Ado exposure.	8-chloroadenosine	110-118	P53	Homo sapiens	70-73
25118938-5	2014	Inhibition of p53 activity with pifithrin-alpha or inhibition of PI3K with LY294002 suppressed CdCl2-induced cellular damage and elevation of Notch1-NICD.	pifithrin	32-41	P53	Homo sapiens	14-17
25658320-7	2015	To a different extent, either the antioxidant N-acetyl-cysteine or the p53 inhibitor, Pifithrin-alpha, recover cell viability and decrease ROS formation.	pifithrin	86-101	P53	Homo sapiens	71-74
32907379-9	2020	Together, 8-Cl-Ado inhibits the cell proliferation, induces G1 phase arrest and apoptosis at least by targeting ADAR1/p53/p21 signaling pathway.	8-chloroadenosine	10-18	P53	Homo sapiens	118-121
25658463-5	2015	We therefore sought to determine whether inhibiting WIP1 with a selective antagonist, GSK2830371, can attenuate neuroblastoma cell growth through reactivation of p53 mediated tumor suppression.	GSK2830371	86-96	P53	Homo sapiens	162-165
32749126-6	2020	The effect of EGb761 on the p53 signaling pathway was further confirmed by adding pifithrin (PFT)-alpha, an inhibitor of p53.	pifithrin	82-91	P53	Homo sapiens	28-31
25658463-6	2015	Neuroblastoma cell lines with wild-type TP53 alleles were highly sensitive to GSK2830371 treatment, while cell lines with mutant TP53 were resistant to GSK2830371.	GSK2830371	78-88	P53	Homo sapiens	40-44
25658463-9	2015	Treatment of wild-type TP53 neuroblastoma cell lines with both GSK2830371 and either doxorubicin or carboplatin resulted in enhanced cell death, mediated through caspase 3/7 induction, as compared to either agent alone.	GSK2830371	63-73	P53	Homo sapiens	23-27
25474301-6	2015	In addition, some small molecule drugs, such as rapamycin and its derivatives, rottlerin, PP242 and AZD8055 (targeting PI3K/AKT/mTORC1), spautin-1, and tamoxifen, as well as oridonin and metformin (targeting p53), can modulate autophagic pathways in different types of cancer.	(5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol	100-107	P53	Homo sapiens	208-211
25116336-0	2014	Arsenic trioxide reactivates proteasome-dependent degradation of mutant p53 protein in cancer cells in part via enhanced expression of Pirh2 E3 ligase.	Arsenic Trioxide	0-16	P53	Homo sapiens	72-75
25116336-4	2014	Previously, we found that arsenic trioxide (ATO), a drug for acute promyelocytic leukemia, degrades mutant p53 protein through a proteasome pathway.	Arsenic Trioxide	26-42	P53	Homo sapiens	107-110
25116336-4	2014	Previously, we found that arsenic trioxide (ATO), a drug for acute promyelocytic leukemia, degrades mutant p53 protein through a proteasome pathway.	Arsenic Trioxide	44-47	P53	Homo sapiens	107-110
25116336-8	2014	We also found that knockdown of Pirh2 inhibits, whereas ectopic expression of Pirh2 enhances, ATO-induced degradation of mutant p53 protein.	Arsenic Trioxide	94-97	P53	Homo sapiens	128-131
25116336-10	2014	Interestingly, we found that ATO cooperates with HSP90 or HDAC inhibitor to promote mutant p53 degradation and growth suppression in tumor cells.	Arsenic Trioxide	29-32	P53	Homo sapiens	91-94
25116336-11	2014	Together, these data suggest that ATO promotes mutant p53 degradation in part via induction of the Pirh2-dependent proteasome pathway.	Arsenic Trioxide	34-37	P53	Homo sapiens	54-57
24374014-5	2015	p53 regulates many different aspects of metabolism, including glycolysis, mitochondrial oxidative phosphorylation, pentose phosphate pathway, fatty acid synthesis and oxidation, to maintain the homeostasis of cellular metabolism, which contributes to the role of p53 in tumor suppression.	Pentosephosphates	115-132	P53	Homo sapiens	0-3
32749126-6	2020	The effect of EGb761 on the p53 signaling pathway was further confirmed by adding pifithrin (PFT)-alpha, an inhibitor of p53.	pifithrin	82-91	P53	Homo sapiens	121-124
24374014-5	2015	p53 regulates many different aspects of metabolism, including glycolysis, mitochondrial oxidative phosphorylation, pentose phosphate pathway, fatty acid synthesis and oxidation, to maintain the homeostasis of cellular metabolism, which contributes to the role of p53 in tumor suppression.	Pentosephosphates	115-132	P53	Homo sapiens	263-266
25134538-5	2014	Furthermore, we assessed the expression of p53 and p73 isoforms in 5-aza-dC-treated T-47D cells and p53 knockout cells.	Azacitidine	67-72	P53	Homo sapiens	43-46
25134538-11	2014	We also demonstrate that p53 likely contributes to 5-aza-dC-induced DeltaNp73 transcriptional inactivation in breast cancer cells.	Azacitidine	51-56	P53	Homo sapiens	25-28
32749126-6	2020	The effect of EGb761 on the p53 signaling pathway was further confirmed by adding pifithrin (PFT)-alpha, an inhibitor of p53.	pifithrin	93-96	P53	Homo sapiens	28-31
32749126-6	2020	The effect of EGb761 on the p53 signaling pathway was further confirmed by adding pifithrin (PFT)-alpha, an inhibitor of p53.	pifithrin	93-96	P53	Homo sapiens	121-124
25623255-6	2015	We hypothesized that PGE(2) produced by stromal cells in the BM microenvironment could stimulate cAMP production and PKA activation in BCP-ALL cells, thereby suppressing p53 accumulation and promoting survival of the malignant cells.	Prostaglandins E	21-24	P53	Homo sapiens	170-173
31665549-6	2020	DNA damage induced by bleomycin dissociates MDM2 from the p53/HERC2/NEURL4 complex and increases the phosphorylation and acetylation of oligomeric p53 bound to HERC2 and NEURL4.	Bleomycin	22-31	P53	Homo sapiens	58-61
25623255-13	2015	CONCLUSIONS: Our findings support our hypothesis that BM-derived PGE(2), through activation of cAMP-PKA signalling in BCP-ALL blasts, can inhibit the tumour suppressive activity of wild type p53, thereby promoting leukaemogenesis and protecting against therapy-induced leukaemic cell death.	Prostaglandins E	65-69	P53	Homo sapiens	191-194
26119958-0	2015	Anti-Colon Cancer Effects of 6-Shogaol Through G2/M Cell Cycle Arrest by p53/p21-cdc2/cdc25A Crosstalk.	shogaol	29-38	P53	Homo sapiens	73-76
25033896-0	2014	Iodine-125 induces apoptosis via regulating p53, microvessel density, and vascular endothelial growth factor in colorectal cancer.	Iodine-125	0-10	P53	Homo sapiens	44-47
24921086-5	2014	The dA-AAI adduct induces AT to TA transversions in the tumor-suppressor TP53 gene in experimental systems, matching TP53 mutations observed in urothelial tumors from AAN cancer cases.	7-(deoxyadenosin-N(6)-yl)aristolactam I	4-10	P53	Homo sapiens	73-77
24921086-5	2014	The dA-AAI adduct induces AT to TA transversions in the tumor-suppressor TP53 gene in experimental systems, matching TP53 mutations observed in urothelial tumors from AAN cancer cases.	7-(deoxyadenosin-N(6)-yl)aristolactam I	4-10	P53	Homo sapiens	117-121
31665549-6	2020	DNA damage induced by bleomycin dissociates MDM2 from the p53/HERC2/NEURL4 complex and increases the phosphorylation and acetylation of oligomeric p53 bound to HERC2 and NEURL4.	Bleomycin	22-31	P53	Homo sapiens	147-150
26192233-0	2015	Bisindole-PBD regulates breast cancer cell proliferation via SIRT-p53 axis.	bisindole-pbd	0-13	P53	Homo sapiens	66-69
31597953-0	2020	Dichloroacetate restores colorectal cancer chemosensitivity through the p53/miR-149-3p/PDK2-mediated glucose metabolic pathway.	Dichloroacetic Acid	0-15	P53	Homo sapiens	72-75
31597953-4	2020	Using the microarray assay, we noted that miR-149-3p was involved in the chemoresistance of CRC, which was modulated by wild-type p53 after DCA treatment.	Dichloroacetic Acid	140-143	P53	Homo sapiens	130-133
31597953-9	2020	Taken together, we determined that the p53/miR-149-3p/PDK2 signaling pathway can potentially be targeted with DCA treatment to overcome chemoresistant CRC.	Dichloroacetic Acid	110-113	P53	Homo sapiens	39-42
25019218-6	2014	As to its cytotoxic mechanism, we found that sulforaphane creates an oxidative cellular environment that induces DNA damage and Bax and p53 gene activation, which in turn helps trigger apoptosis.	sulforaphane	45-57	P53	Homo sapiens	136-139
31905798-4	2019	Briefly, ent-kaur-15-en-17-al-18-oic acid protected cells from oxidative apoptosis associated with p53 and NF-kappaB pathways.	ent-kaur-15-en-17-al-18-oic acid	9-41	P53	Homo sapiens	99-102
24836762-0	2014	Prognostic value of TP53 gene mutations in myelodysplastic syndromes and acute myeloid leukemia treated with azacitidine.	Azacitidine	109-120	P53	Homo sapiens	20-24
24836762-2	2014	However, the impact of TP53 mutations in MDS treated with azacitidine (AZA) remains unclear.	Azacitidine	58-69	P53	Homo sapiens	23-27
25896587-6	2015	When inhibiting the miR-34a, the sensitivity of the cells to quercetin decreased and the expression of the SIRT1 was up-regulated, but the acetylation of p53 and the expression of some genes related to p53 down-regulated.	Quercetin	61-70	P53	Homo sapiens	202-205
25896587-7	2015	CONCLUSION: miR-34a plays an important role in the anti-tumor effects of querctin in HCC, miR-34a may be a tiemolecule between the p53 and SIRT1 and is composed of a p53/miR-34a/SIRT1 signal feedback loop, which could enhance apoptosis signal and significantly promote cell apoptosis.	querctin	73-81	P53	Homo sapiens	131-134
25896587-7	2015	CONCLUSION: miR-34a plays an important role in the anti-tumor effects of querctin in HCC, miR-34a may be a tiemolecule between the p53 and SIRT1 and is composed of a p53/miR-34a/SIRT1 signal feedback loop, which could enhance apoptosis signal and significantly promote cell apoptosis.	querctin	73-81	P53	Homo sapiens	166-169
25641429-5	2015	Furthermore, the enhancement of p53-dependent apoptosis by flavokawain B could be rescued by pifithrin-alpha, a pharmacological inhibitor of p53 transcriptional activity.	pifithrin	93-108	P53	Homo sapiens	32-35
25641429-5	2015	Furthermore, the enhancement of p53-dependent apoptosis by flavokawain B could be rescued by pifithrin-alpha, a pharmacological inhibitor of p53 transcriptional activity.	pifithrin	93-108	P53	Homo sapiens	141-144
25474278-9	2014	The post-progression survival (PPS) of p53-positive patients undergoing 2nd and/or 3rd line chemotherapy with irinotecan and/or cetuximab was significantly longer compared to p53-negative patients.	pps	31-34	P53	Homo sapiens	39-42
24836762-3	2014	We analyzed TP53 mutations in 62 patients with high risk MDS or AML treated with AZA.	Azacitidine	81-84	P53	Homo sapiens	12-16
24836762-9	2014	Thus, TP53 mutations strongly correlated with poorer survival in higher risk MDS and AML treated with AZA.	Azacitidine	102-105	P53	Homo sapiens	6-10
31654627-6	2019	Furthermore, methotrexate induced the down-regulation of the anti-apoptotic protein, MCL-1, DNA damage, and the activation of a p53 tumor suppressor, leading to apoptosis through the inhibition of STAT3.	Methotrexate	13-25	P53	Homo sapiens	128-131
24853816-6	2014	Greater p53 dissociation is observed from sequences containing low-redox potential purine regions, particularly guanine triplets.	purine	83-89	P53	Homo sapiens	8-11
24853816-6	2014	Greater p53 dissociation is observed from sequences containing low-redox potential purine regions, particularly guanine triplets.	Guanine	112-119	P53	Homo sapiens	8-11
24853816-11	2014	On the basis of our data, the guanine pattern within the purine region of each p53-binding site determines the response of p53 to DNA oxidation, yielding for some sequences the oxidative dissociation of p53 from a distance and thereby providing another potential role for DNA charge transport chemistry within the cell.	Guanine	30-37	P53	Homo sapiens	79-82
24853816-11	2014	On the basis of our data, the guanine pattern within the purine region of each p53-binding site determines the response of p53 to DNA oxidation, yielding for some sequences the oxidative dissociation of p53 from a distance and thereby providing another potential role for DNA charge transport chemistry within the cell.	Guanine	30-37	P53	Homo sapiens	123-126
24853816-11	2014	On the basis of our data, the guanine pattern within the purine region of each p53-binding site determines the response of p53 to DNA oxidation, yielding for some sequences the oxidative dissociation of p53 from a distance and thereby providing another potential role for DNA charge transport chemistry within the cell.	Guanine	30-37	P53	Homo sapiens	123-126
24853816-11	2014	On the basis of our data, the guanine pattern within the purine region of each p53-binding site determines the response of p53 to DNA oxidation, yielding for some sequences the oxidative dissociation of p53 from a distance and thereby providing another potential role for DNA charge transport chemistry within the cell.	purine	57-63	P53	Homo sapiens	79-82
24853816-11	2014	On the basis of our data, the guanine pattern within the purine region of each p53-binding site determines the response of p53 to DNA oxidation, yielding for some sequences the oxidative dissociation of p53 from a distance and thereby providing another potential role for DNA charge transport chemistry within the cell.	purine	57-63	P53	Homo sapiens	123-126
24853816-11	2014	On the basis of our data, the guanine pattern within the purine region of each p53-binding site determines the response of p53 to DNA oxidation, yielding for some sequences the oxidative dissociation of p53 from a distance and thereby providing another potential role for DNA charge transport chemistry within the cell.	purine	57-63	P53	Homo sapiens	123-126
25193633-3	2014	Recent studies demonstrate that the depletion of p53 and hypoxia-induced factor 1alpha proteins is caused by cardiac glycosides.	Glycosides	117-127	P53	Homo sapiens	49-52
25098371-5	2014	L-Leucine thus alleviates anaemia in RP-deficient cells in a TP53-independent manner.	Leucine	0-9	P53	Homo sapiens	61-65
31885624-0	2019	Palmitic Acid Methyl Ester Induces G2/M Arrest in Human Bone Marrow-Derived Mesenchymal Stem Cells via the p53/p21 Pathway.	methyl palmitate	0-26	P53	Homo sapiens	107-110
25158131-3	2014	Pifithrin-alpha, an inhibitor of p53 function, and knockdown of p53 decreased the level of frataxin mRNA in human kidney HEK 293T cells.	pifithrin	0-15	P53	Homo sapiens	33-36
24884809-3	2014	METHODS: Mutation detection of p53 gene in arsenic trioxide resistant HCC cell lines was performed.	Arsenic Trioxide	43-59	P53	Homo sapiens	31-34
24884809-6	2014	RESULTS: The acquisition of p53 mutation contributed to arsenic trioxide resistance and enhanced metastatic potential of HCC cells.	Arsenic Trioxide	56-72	P53	Homo sapiens	28-31
24884809-7	2014	Mutant p53 (Mutp53) silence could re-sensitize HCC resistant cells to arsenic trioxide and inhibit the metastatic activities, while mutp53 overexpression showed the opposite effects.	Arsenic Trioxide	70-86	P53	Homo sapiens	7-10
26027111-13	2014	The results of Western blot assay showed that this ratio of drugs could significantly increase the protein expression of Bax,P53 and P21 and decreased the expression of BCL-2, Casepase-3, p-Erk, p-Ras and p-c-Raf in SMMC-7721 cells.	smmc	216-220	P53	Homo sapiens	125-128
31885624-7	2019	Moreover, the level of Mdm2 protein decreased, while the levels of p21 and p53 protein increased in the PAME-treated hBM-MSCs.	methyl palmitate	104-108	P53	Homo sapiens	75-78
31885624-12	2019	Moreover, the half-life of p53 protein was prolonged in the PAME-treated hBM-MSCs.	methyl palmitate	60-64	P53	Homo sapiens	27-30
25019212-4	2014	This indicates p53-independent apoptotic pathway, because response of both p53 mutant and wild type cell line were found unaffected after treatment with pifithrin-alpha, an inhibitor of p53.	pifithrin	153-168	P53	Homo sapiens	15-18
24884809-11	2014	CONCLUSIONS: Acquisitions of p53 mutations contributed to the resistance of HCC to arsenic trioxide.	Arsenic Trioxide	83-99	P53	Homo sapiens	29-32
31885624-13	2019	Taken together, these results suggest that PAME induced p53 stabilization, which in turn increased the levels of p53/p21 proteins and decreased the levels of Cdk1/cyclin B1 proteins, thereby preventing the activation of Cdk1, and eventually caused cell cycle arrest at the G2/M phase.	methyl palmitate	43-47	P53	Homo sapiens	56-59
24632713-3	2014	The present results demonstrate that GO-203 and BTZ synergistically downregulate expression of the p53-inducible regulator of glycolysis and apoptosis (TIGAR), which promotes shunting of glucose-6-phosphate into the pentose phosphate pathway to generate reduced glutathione (GSH).	(arginine)9-cysteinyl-glutaminyl-cysteinyl-arginyl-arginyl-lysyl-asparagine	37-43	P53	Homo sapiens	99-102
24632713-3	2014	The present results demonstrate that GO-203 and BTZ synergistically downregulate expression of the p53-inducible regulator of glycolysis and apoptosis (TIGAR), which promotes shunting of glucose-6-phosphate into the pentose phosphate pathway to generate reduced glutathione (GSH).	Bortezomib	48-51	P53	Homo sapiens	99-102
31885624-13	2019	Taken together, these results suggest that PAME induced p53 stabilization, which in turn increased the levels of p53/p21 proteins and decreased the levels of Cdk1/cyclin B1 proteins, thereby preventing the activation of Cdk1, and eventually caused cell cycle arrest at the G2/M phase.	methyl palmitate	43-47	P53	Homo sapiens	113-116
24632713-3	2014	The present results demonstrate that GO-203 and BTZ synergistically downregulate expression of the p53-inducible regulator of glycolysis and apoptosis (TIGAR), which promotes shunting of glucose-6-phosphate into the pentose phosphate pathway to generate reduced glutathione (GSH).	Pentosephosphates	216-233	P53	Homo sapiens	99-102
25205311-10	2014	Pharmacological inhibition of mitochondrial p53 using pifithrin-mu abolished the detrimental effects of SI and reduced cell death.	pifithrin	54-63	P53	Homo sapiens	44-47
31472940-9	2019	Regarding DSS, pooled HR were 5.052 and 2.133 for p53mt group, 1.965 and 1.068 for MSI group, and 0.552 and 0.325 for POLEmt group at univariable and multivariable analyses, respectively.	dss	10-13	P53	Homo sapiens	50-53
25051404-6	2014	Moreover, we found that melphalan-induced apoptosis inversely correlated with the repair efficiency of the TS, with the duration of the inhibition of mRNA synthesis, phosphorylation of p53 at serine 15 and apoptosis rates being higher in responders than in non-responders (all P&lt;0.001).	Melphalan	24-33	P53	Homo sapiens	185-188
24833908-4	2014	In the cohort of patients with advanced localized or metastasized ccRCC, high staining of Ki67, p53 and nS predicted shorter DSS (Ki67: HR 1.07, 95% CI 1.02-1.11; p53: HR 1.05, 95% CI 1.01-1.09; nS: HR 1.08, 95% CI 1.02-1.14).	dss	125-128	P53	Homo sapiens	96-99
24849437-0	2014	[Effect of quercetin on glioma cell U87 apoptosis and feedback regulation of MDM2-p53].	Quercetin	11-20	P53	Homo sapiens	82-85
24849437-1	2014	OBJECTIVE: To investigate the effect of quercetin on apoptosis and feedback regulation of MDM2-p53 in multiform glioblastoma U87 cells in vitro.	Quercetin	40-49	P53	Homo sapiens	95-98
24726874-15	2014	Down-regulated the expression of tumor suppressor p53 by 10 muM pifithrin-alpha (PFTalpha) alone had no effect on adipose accumulation.	pifithrin	64-79	P53	Homo sapiens	50-53
31596196-3	2019	Therefore, HBx variants containing Ser-101 induced p53-dependent activation of PA28gamma expression in human hepatoma cells.	seryl-seryl-seryl-arginine	35-38	P53	Homo sapiens	51-54
24726874-15	2014	Down-regulated the expression of tumor suppressor p53 by 10 muM pifithrin-alpha (PFTalpha) alone had no effect on adipose accumulation.	pifithrin	81-89	P53	Homo sapiens	50-53
24849437-2	2014	METHODS: U87 cells exposed to different concentrations of quercetin (50, 100, and 150 micromol/L) were examined with flow cytometry, RT-PCR and Western blotting for detecting the cell apoptosis, MDM2 mRNA expression, and p53 and caspase-3 expressions.	Quercetin	58-67	P53	Homo sapiens	221-224
24849437-4	2014	Quercetin significantly increased the expressions of MDM2 mRNA and active caspase-3 protein but decreased the expression of p53 in the cells.	Quercetin	0-9	P53	Homo sapiens	124-127
24849437-5	2014	CONCLUSION: Quercetin promotes the apoptosis of multiform glioblastoma U87 cells mediated by caspase-3 and influences the feedback balance of MDM2-p53.	Quercetin	12-21	P53	Homo sapiens	147-150
25056872-4	2014	To detect the p53-bound osmium-labeled probes, we took advantage of a catalytic peak yielded by Os,bipy-modified DNA at the mercury-based electrodes, allowing facile determination of subnanogram quantities of the labeled oligonucleotides.	2,2'-Dipyridyl	99-103	P53	Homo sapiens	14-17
31596196-5	2019	The self-amplifying ability of HBx variants containing Ser-101 via a positive feedback loop involving p53 and PA28gamma was accurately reproduced in both a 1.2-mer HBV replicon and in vitro HBV infection systems, which also provided evidence for the stimulation of HBV replication by these HBx variants.	seryl-seryl-seryl-arginine	55-58	P53	Homo sapiens	102-105
24399651-0	2014	The impact of arsenic trioxide and all-trans retinoic acid on p53 R273H-codon mutant glioblastoma.	Arsenic Trioxide	14-30	P53	Homo sapiens	62-65
31596196-6	2019	In conclusion, the ability of HBx to upregulate PA28gamma levels via p53 activation, in a Ser-101-dependent pathway, is critical for the stimulation of HBV replication.	seryl-seryl-seryl-arginine	90-93	P53	Homo sapiens	69-72
24399651-6	2014	The results showed that U87-p53(R273H) cells generated more rapid neurosphere growth than U87-p53(wt) but inhibition of neurosphere proliferation was seen with both ATO and ATRA.	Arsenic Trioxide	165-168	P53	Homo sapiens	28-31
24399651-7	2014	U87-p53(R273H) neurospheres showed resistance to differentiation into glial cells and neuronal cells with ATO and ATRA exposure.	Arsenic Trioxide	106-109	P53	Homo sapiens	4-7
24952138-8	2014	The p53 inhibitor pifithrin-alpha and the antioxidants N-acetylcysteine and glutathione (GSH) protected the cells from PEITC-mediated apoptosis.	pifithrin	18-33	P53	Homo sapiens	4-7
31612057-5	2019	Treatment with PITC promoted total glutathione depletion in GC cell lines, leading to reactive oxygen species accumulation and DNA damage, which activated the mitochondria-dependent and p53 signaling pathways to trigger apoptosis in GC cells.	Isothiocyanates	15-19	P53	Homo sapiens	186-189
24939757-0	2014	Xylarianaphthol-1, a novel dinaphthofuran derivative, activates p21 promoter in a p53-independent manner.	xylarianaphthol-1	0-17	P53	Homo sapiens	82-85
24399651-8	2014	ATO was able to generate apoptosis at high doses and proliferation of U87-p53(wt) and U87-p53(R273H) cells was reduced with ATO and ATRA in a dose-dependent manner.	Arsenic Trioxide	0-3	P53	Homo sapiens	74-77
24399651-8	2014	ATO was able to generate apoptosis at high doses and proliferation of U87-p53(wt) and U87-p53(R273H) cells was reduced with ATO and ATRA in a dose-dependent manner.	Arsenic Trioxide	0-3	P53	Homo sapiens	90-93
24399651-8	2014	ATO was able to generate apoptosis at high doses and proliferation of U87-p53(wt) and U87-p53(R273H) cells was reduced with ATO and ATRA in a dose-dependent manner.	Arsenic Trioxide	124-127	P53	Homo sapiens	74-77
24399651-8	2014	ATO was able to generate apoptosis at high doses and proliferation of U87-p53(wt) and U87-p53(R273H) cells was reduced with ATO and ATRA in a dose-dependent manner.	Arsenic Trioxide	124-127	P53	Homo sapiens	90-93
24399651-9	2014	Elevated pERK1/2 and p53 expression was seen in U87-p53(R273H) neurospheres, which could be reduced with ATO and ATRA treatment.	Arsenic Trioxide	105-108	P53	Homo sapiens	21-24
24399651-9	2014	Elevated pERK1/2 and p53 expression was seen in U87-p53(R273H) neurospheres, which could be reduced with ATO and ATRA treatment.	Arsenic Trioxide	105-108	P53	Homo sapiens	52-55
31594538-4	2019	RESULTS: Here, we present data suggesting that LSH regulates p53 in cis through two pathways: prevention proteasomal degradation through its deubiquitination, which is achieved by reducing the lysine 11-linked, lysine 48-linked polyubiquitin chains (K11 and K48) on p53; and revival of the transcriptional activity of p53 by forming a complex with PKM2 (pyruvate kinase 2).	Pyruvates	354-362	P53	Homo sapiens	61-64
24685134-4	2014	Strikingly, the iron polyporphyrin heme binds to p53 protein, interferes with p53-DNA interactions, and triggers both nuclear export and cytosolic degradation of p53.	iron polyporphyrin heme	16-39	P53	Homo sapiens	49-52
24685134-4	2014	Strikingly, the iron polyporphyrin heme binds to p53 protein, interferes with p53-DNA interactions, and triggers both nuclear export and cytosolic degradation of p53.	iron polyporphyrin heme	16-39	P53	Homo sapiens	78-81
24685134-4	2014	Strikingly, the iron polyporphyrin heme binds to p53 protein, interferes with p53-DNA interactions, and triggers both nuclear export and cytosolic degradation of p53.	iron polyporphyrin heme	16-39	P53	Homo sapiens	78-81
24722580-0	2014	Gonadotropin-releasing hormone agonists sensitize, and resensitize, prostate cancer cells to docetaxel in a p53-dependent manner.	Docetaxel	93-102	P53	Homo sapiens	108-111
24905957-7	2014	VIP effects could be blocked by cell incubation with a specific p53 inhibitor, cyclin pifithrin-alpha hydrobromide (CPFT-alphaH).	pifithrin	86-114	P53	Homo sapiens	64-67
24913980-3	2014	Our findings indicate that sublethal doses of doxorubicin and melphalan initiate a DNA damage response (DDR) controlling ligand upregulation on MM cell lines and patient-derived malignant plasma cells in Chk1/2-dependent and p53-independent manner.	Melphalan	62-71	P53	Homo sapiens	225-228
24789349-9	2014	Furthermore, p53 inhibition using pifithrin-alpha abolished the induction of caspase-3 and PARP by FANCF shRNA and MMC, indicating that MMC-induced apoptosis is substantially enhanced by FANCF shRNA via p53-dependent mechanisms.	pifithrin	34-43	P53	Homo sapiens	13-16
24789349-9	2014	Furthermore, p53 inhibition using pifithrin-alpha abolished the induction of caspase-3 and PARP by FANCF shRNA and MMC, indicating that MMC-induced apoptosis is substantially enhanced by FANCF shRNA via p53-dependent mechanisms.	pifithrin	34-43	P53	Homo sapiens	203-206
24722580-4	2014	We demonstrated that, in p53-positive DU145 cells, GnRH agonists: a) increase the expression of the proapoptotic protein Bax; this effect is mediated by the phosphorylation (activation) of p53, triggered by the p38 MAPK; b) potentiate the antiproliferative/proapoptotic activity of docetaxel; c) resensitize docetaxel-resistant cells to the antitumor activity of the cytotoxic drug.	Docetaxel	282-291	P53	Homo sapiens	25-28
24722580-4	2014	We demonstrated that, in p53-positive DU145 cells, GnRH agonists: a) increase the expression of the proapoptotic protein Bax; this effect is mediated by the phosphorylation (activation) of p53, triggered by the p38 MAPK; b) potentiate the antiproliferative/proapoptotic activity of docetaxel; c) resensitize docetaxel-resistant cells to the antitumor activity of the cytotoxic drug.	Docetaxel	282-291	P53	Homo sapiens	189-192
31321604-7	2019	Of the twelve VUS (0.65%) identified in TP53, two were classified as likely pathogenic and two were classified as likely benign after re-evaluation, potentially resulting in significant management modification for the proband and relatives.	3-[(3~{a}~{S},4~{S},6~{a}~{R})-4-carboxy-2,3,4,5,6,6~{a}-hexahydro-1~{H}-pyrrolo[2,3-c]pyrrol-3~{a}-yl]propyl-$l^{3}-oxidanyl-bis(oxidanyl)boranuide	14-17	P53	Homo sapiens	40-44
24722580-4	2014	We demonstrated that, in p53-positive DU145 cells, GnRH agonists: a) increase the expression of the proapoptotic protein Bax; this effect is mediated by the phosphorylation (activation) of p53, triggered by the p38 MAPK; b) potentiate the antiproliferative/proapoptotic activity of docetaxel; c) resensitize docetaxel-resistant cells to the antitumor activity of the cytotoxic drug.	Docetaxel	308-317	P53	Homo sapiens	25-28
24722580-4	2014	We demonstrated that, in p53-positive DU145 cells, GnRH agonists: a) increase the expression of the proapoptotic protein Bax; this effect is mediated by the phosphorylation (activation) of p53, triggered by the p38 MAPK; b) potentiate the antiproliferative/proapoptotic activity of docetaxel; c) resensitize docetaxel-resistant cells to the antitumor activity of the cytotoxic drug.	Docetaxel	308-317	P53	Homo sapiens	189-192
24722580-8	2014	These results may provide a rationale for novel combination treatment strategies, especially for docetaxel-resistant CRPC patients expressing a functional p53 protein.	Docetaxel	97-106	P53	Homo sapiens	155-158
24962518-0	2014	Sodium dichloroacetate exhibits anti-leukemic activity in B-chronic lymphocytic leukemia (B-CLL) and synergizes with the p53 activator Nutlin-3.	Dichloroacetic Acid	0-22	P53	Homo sapiens	121-124
24380881-4	2014	BTZ-treated HTLA-230 cells down-regulated p53 and up-regulated p21, favoring cell survival.	Bortezomib	0-3	P53	Homo sapiens	42-45
31485626-4	2019	Result from the present study demonstrated that treatment with pemetrexed suppressed lung cancer cell proliferation, inhibited mRNA and protein expression levels of anti-apoptotic Bcl2, and increased the mRNA and the protein expression levels of pro-apoptotic p53 and apoptosis regulator BAX.	Pemetrexed	63-73	P53	Homo sapiens	260-263
24380881-5	2014	The inhibition of HO-1 activity obtained by Zinc (II) protoprophyrin IX (ZnPPIX) was able to significantly increase the pro-apoptotic effect of BTZ in a p53- and p21-independent way.	Bortezomib	144-147	P53	Homo sapiens	153-156
24760952-5	2014	Quercetin-induced cell apoptosis was shown to involve p53 and p21 up-regulation, Cyclin D1, Cdk2, and Cdk7 down-regulation.	Quercetin	0-9	P53	Homo sapiens	54-57
24760952-6	2014	These results suggested that the induction of G2/M arrest, apoptosis, and cell death by quercetin may associate with increased expression of p53 and p21, decrease of Cyclin D1, Cdk2, and Cdk7 levels, and generation of reactive oxygen species in cells.	Quercetin	88-97	P53	Homo sapiens	141-144
24646317-0	2014	p53 functional inhibitors behaving like pifithrin-beta counteract the Alzheimer peptide non-beta-amyloid component effects in human SH-SY5Y cells.	pifithrin	40-49	P53	Homo sapiens	0-3
24485799-4	2014	In this study, we investigate whether combined treatment with romidepsin and bortezomib would induce apoptosis in A549 NSCLC cells by activating cell cycle arrest, enhanced generation of p21 and p53, down-regulation of matrix metalloproteinases (MMPs) 2,9 also altering the acetylation status of histone proteins.	Bortezomib	77-87	P53	Homo sapiens	195-198
31414729-8	2019	Several possible osimertinib resistance associated mutations, including PIK3CA, BRAF and TP53 mutations, were detected by NGS in samples upon progression on osimertinib therapy.	osimertinib	17-28	P53	Homo sapiens	89-93
24485799-5	2014	Our data show that combination of romidepsin and bortezomib caused cell cycle arrest at Sub G0-G1 transition, up-regulation of cell cycle protein p21 and tumour suppressor protein p53.	Bortezomib	49-59	P53	Homo sapiens	180-183
24833880-1	2014	AIM: To investigate the changes in apoptosis in gastrointestinal cancer cells from patients with gastrointestinal cancers treated with arsenic trioxide (As2O3); and to study the possible molecular mechanisms of such changes by detecting the expression levels of p53 and Bcl-2.	Arsenic Trioxide	135-151	P53	Homo sapiens	262-265
23255470-3	2014	In the NuLi-1 immortalized human lung epithelial cell line with p53 and pRb deficiency, exposure to low doses of arsenic trioxide for 72 h promoted cell proliferation and upregulated the gene transcription levels of FOXM1, CDC6, CDC25A, and cyclin D1, which are both critical cell cycle regulatory genes and proto-oncogenes.	Arsenic Trioxide	113-129	P53	Homo sapiens	64-67
31636802-8	2019	The results indicate that the PMMA resin induced the intrinsic mitochondrial apoptosis as a consequence of p53 activation via the ATM pathway in response to oxidative DNA damage.	Polymethyl Methacrylate	30-34	P53	Homo sapiens	107-110
23255470-9	2014	These results showed for the first time that chronic exposure to low doses of arsenic trioxide promoted lung carcinogenicity, in part by aberrantly upregulating FOXM1 and its associated oncogenes, when the tumor suppressor genes p53 and pRb were inactivated.	Arsenic Trioxide	78-94	P53	Homo sapiens	229-232
24462521-9	2014	Consistent with the gene expression profiling and siRNA assays, the inhibition of MPS1 by SP600125 led to a reduction in cell viability and a significant increase in cell death, selectively in TP53-mutated BC cells.	pyrazolanthrone	90-98	P53	Homo sapiens	193-197
24481553-12	2014	Taken together, our study provides the first report that carnosol induced apoptosis in HCT116 cells via generation of ROS, induction of p53, activation of caspases and inhibition of STAT3 signaling pathway.	carnosol	57-65	P53	Homo sapiens	136-139
24535669-0	2014	Quercetin regulates the sestrin 2-AMPK-p38 MAPK signaling pathway and induces apoptosis by increasing the generation of intracellular ROS in a p53-independent manner.	Quercetin	0-9	P53	Homo sapiens	143-146
24535669-7	2014	We demonstrate that the increase in the expression of sestrin 2 by quercetin-generated intracellular ROS is p53-independent.	Quercetin	67-76	P53	Homo sapiens	108-111
24667842-0	2014	Sulforaphane induces oxidative stress and death by p53-independent mechanism: implication of impaired glutathione recycling.	sulforaphane	0-12	P53	Homo sapiens	51-54
25026697-3	2014	It has previously been reported that HER2/ERBB2, the estrogen receptor, progesterone receptor, and p53 were required for flavonoid induced cytotoxicity in breast cancer cell lines.	Flavonoids	121-130	P53	Homo sapiens	99-102
30879173-6	2019	The cytotoxicity of RH1 was inhibited in A549 cells treated with the p53-inhibitor pifithrin-alpha or transfected p53 siRNA and in human colon cancer HCT116 isogenic (p53-/-) cells.	pifithrin	83-98	P53	Homo sapiens	69-72
24657168-0	2014	Inositol pyrophosphates mediate the DNA-PK/ATM-p53 cell death pathway by regulating CK2 phosphorylation of Tti1/Tel2.	inositol pyrophosphates	0-23	P53	Homo sapiens	47-50
24657168-3	2014	The inositol pyrophosphates, such as 5-diphosphoinositol pentakisphosphate (IP7), are generated by a family of inositol hexakisphosphate kinases (IP6Ks), of which IP6K2 has been implicated in p53-associated cell death.	inositol pyrophosphates	4-27	P53	Homo sapiens	192-195
24667842-9	2014	In conclusion, SFN induced oxidative stress and apoptosis via a p53-independent mechanism.	sulforaphane	15-18	P53	Homo sapiens	64-67
24667845-5	2014	Using pifithrin-alpha(PFT), a p53"s mitochondrial translocation inhibitor, we found that pretreated with PFT, heat stress induced mitochondrial p53 translocation was significantly suppressed, accompanied by a significant alleviation in the loss of DeltaPsim, cytochrome c release and caspase-9 activation.	pifithrin	6-21	P53	Homo sapiens	30-33
24667845-5	2014	Using pifithrin-alpha(PFT), a p53"s mitochondrial translocation inhibitor, we found that pretreated with PFT, heat stress induced mitochondrial p53 translocation was significantly suppressed, accompanied by a significant alleviation in the loss of DeltaPsim, cytochrome c release and caspase-9 activation.	pifithrin	6-21	P53	Homo sapiens	144-147
24182986-5	2014	The primary objectives of the current study were to investigate the effects of haemanthamine and haemanthidine on the induction of apoptosis and the cell cycle regulatory pathway in p53-null Jurkat cells.	hemanthidine	97-110	P53	Homo sapiens	182-185
24343341-6	2014	The p53/Cyp-D mitochondrial complexation was prevented by CsA or Cyp-D silencing, or by p53 inhibitor pifithrin-alpha.	pifithrin	102-111	P53	Homo sapiens	4-7
31196889-6	2019	We explored the mechanism of this and found the reactive oxygen species (ROS) activity of ZMC1 negates the signal on p53 that is generated with chemotherapy and radiation.	NSC 319726	90-94	P53	Homo sapiens	117-120
24343341-6	2014	The p53/Cyp-D mitochondrial complexation was prevented by CsA or Cyp-D silencing, or by p53 inhibitor pifithrin-alpha.	pifithrin	102-111	P53	Homo sapiens	88-91
24667498-4	2014	We demonstrated that JMJD6 acts as an alpha-ketoglutarate- and Fe(II)-dependent lysyl hydroxylase to catalyze p53 hydroxylation.	ammonium ferrous sulfate	63-69	P53	Homo sapiens	110-113
31134974-4	2019	The p53-MDM2 complex was captured in one fluidic channel covered with consensus double-stranded (ds)-DNA, while the other channel was pre-immobilized with caspase-3-specific biotinylated DEVD-containing peptides.	DEVD	187-191	P53	Homo sapiens	4-7
24533688-0	2014	Induction of p21(Waf1/Cip1) by garcinol via downregulation of p38-MAPK signaling in p53-independent H1299 lung cancer.	garcinol	31-39	P53	Homo sapiens	84-87
24533688-4	2014	Treatments with garcinol for 24 h exhibited morphological changes and inhibited the proliferation of H460 (p53-wild type) and H1299 (p53-null) cells in dose- and time-dependent manners.	garcinol	16-24	P53	Homo sapiens	107-110
31334116-5	2019	In addition, co-treatment with a p53 inhibitor (cyclic pifithrin-alpha) and the ruthenium complexes significantly reduced the apoptosis rate in HCT116 cells, and increased phospho-p53 (S15) and phospho-histone H2AX (S139) expressions, indicating induction of DNA damage and p53-dependent apoptosis.	pifithrin	55-64	P53	Homo sapiens	33-36
24533688-4	2014	Treatments with garcinol for 24 h exhibited morphological changes and inhibited the proliferation of H460 (p53-wild type) and H1299 (p53-null) cells in dose- and time-dependent manners.	garcinol	16-24	P53	Homo sapiens	133-136
24411335-6	2014	Furthermore, PC-3 cells treated with EGFP-p53/PEI/PAH-Cit/AuNP-CS showed reduced cellular viability and increased nuclear fragmentation, consistent with elevated p53 expression.	aunp-cs	58-65	P53	Homo sapiens	42-45
24411335-6	2014	Furthermore, PC-3 cells treated with EGFP-p53/PEI/PAH-Cit/AuNP-CS showed reduced cellular viability and increased nuclear fragmentation, consistent with elevated p53 expression.	aunp-cs	58-65	P53	Homo sapiens	162-165
24411335-8	2014	Western blotting and caspase activation studies revealed that EGFP-p53/PEI/PAH-Cit/AuNP-CS complexes may induce PC-3 apoptosis via the mitochondria-mediated signaling pathway by up-regulation of Bax, down-regulation of Bcl-2, and activation of caspase-3.	aunp-cs	83-90	P53	Homo sapiens	67-70
24365254-7	2014	In our study, BDMC-A exerted more potent effect on the modulation of selective apoptotic markers (intrinsic pathway: p53, Bcl-2, Bax, cyt c, Apaf-1, caspase-9, 3, PARP; extrinsic pathway: FasL, caspase 8) compared to curcumin.	BDMC-A	14-20	P53	Homo sapiens	117-120
24293112-6	2014	After treating with DMPPQA, apoptosis-related protein expression of Bax, cytochrome c, caspase-9, caspase-3, PARP-1 and P53 increased and Bcl-2 protein expression decreased.	5,7-dimethoxy-2-phenyl-N-propylquinolin-4-amine	20-26	P53	Homo sapiens	120-123
31334116-5	2019	In addition, co-treatment with a p53 inhibitor (cyclic pifithrin-alpha) and the ruthenium complexes significantly reduced the apoptosis rate in HCT116 cells, and increased phospho-p53 (S15) and phospho-histone H2AX (S139) expressions, indicating induction of DNA damage and p53-dependent apoptosis.	pifithrin	55-64	P53	Homo sapiens	180-183
24522962-3	2014	Here, we describe inhibition experiments on p53/Mdm2 interaction in Trichoplax adhaerens by applying the inhibitors nutlin-3 and roscovitine.	Roscovitine	129-140	P53	Homo sapiens	44-47
31334116-5	2019	In addition, co-treatment with a p53 inhibitor (cyclic pifithrin-alpha) and the ruthenium complexes significantly reduced the apoptosis rate in HCT116 cells, and increased phospho-p53 (S15) and phospho-histone H2AX (S139) expressions, indicating induction of DNA damage and p53-dependent apoptosis.	pifithrin	55-64	P53	Homo sapiens	180-183
31048321-11	2019	Targeting CLPB synergizes with venetoclax and the venetoclax/azacitidine combination in AML in a p53-independent manner.See related commentary by Savona and Rathmell, p. 831.This article is highlighted in the In This Issue feature, p. 813.	Azacitidine	61-72	P53	Homo sapiens	97-100
23509992-8	2014	Analysis revealed a correlation between p53 protein overexpression and high CRS (P = 0.058).	3-cresol	76-79	P53	Homo sapiens	40-43
24037342-4	2014	We hypothesized that p53 function and therefore cell fate might be altered by the presence of Delta40p53, an embryonic isoform missing the first 40 N-terminal amino acids of the full-length protein including the transactivation and Mdm2-binding domains.	delta40p53	94-104	P53	Homo sapiens	21-24
23474763-3	2014	High-risk HPV E6 inactivates p53 through two distinct mechanisms; association with E6AP to degrade p53 and association with p300 to block p300-mediated p53 acetylation and activation.	e6ap	83-87	P53	Homo sapiens	29-32
23474763-3	2014	High-risk HPV E6 inactivates p53 through two distinct mechanisms; association with E6AP to degrade p53 and association with p300 to block p300-mediated p53 acetylation and activation.	e6ap	83-87	P53	Homo sapiens	99-102
23474763-3	2014	High-risk HPV E6 inactivates p53 through two distinct mechanisms; association with E6AP to degrade p53 and association with p300 to block p300-mediated p53 acetylation and activation.	e6ap	83-87	P53	Homo sapiens	99-102
24525232-5	2014	p53-like MIBCs were consistently resistant to neoadjuvant methotrexate, vinblastine, doxorubicin and cisplatin chemotherapy, and all chemoresistant tumors adopted a p53-like phenotype after therapy.	Methotrexate	58-70	P53	Homo sapiens	0-3
24456472-1	2014	We recently reported the discovery of AM-8553 (1), a potent and selective piperidinone inhibitor of the MDM2-p53 interaction.	2-(5-(3-chlorophenyl)-6-(4-chlorophenyl)-1-(2-hydroxypentan-3-yl)-3-methyl-2-oxopiperidin-3-yl)acetic acid	38-45	P53	Homo sapiens	109-112
31134745-8	2019	Torilin may covalently bind to Cys124 of p53 by 2-methyl-2-butenal (2M2B) group, as torilin derivatives, which do not contain the 2M2B group, were not able to increase the p53 transcription activity.	2-methyl-2-butenal	48-66	P53	Homo sapiens	41-44
24239715-10	2014	There were significant decreases in the expression levels of p53, p21, cyclin D1 and PCNA in AA SFs treated with rhEndostatin, and a significant increase in CDK4 expression.	SFS	96-99	P53	Homo sapiens	61-64
24738333-12	2014	Moreover, transcription and protein expression of bcl-2, NFKB, survivin, bax, p53 and caspase-3 of Raji cells were regulated at the most remarkable extent in ADM-As2O3, MNPs group as compared with other groups.	Arsenic Trioxide	162-167	P53	Homo sapiens	78-81
30821124-2	2019	Here we assessed the distribution of proliferating cells (PCs) and explored the possible occurrence of p53-upregulated cells in the NECS in a cohort of CoAs.	coas	152-156	P53	Homo sapiens	103-106
24246761-2	2014	We previously showed that the PAH prototype, benzo[a]pyrene (B[a]P), triggers apoptosis via DNA damage-induced p53 activation (genotoxic pathway) and via remodeling of the membrane cholesterol-rich microdomains called lipid rafts, leading to changes in pH homeostasis (non-genotoxic pathway).	Polycyclic Aromatic Hydrocarbons	30-33	P53	Homo sapiens	111-114
24465691-5	2014	Blocking GRP75 with its inhibitor MKT-077 potentiated the anti-tumor effects of 17-AAG by disrupting the formation of GRP75-p53 complexes, thereby facilitating translocation of p53 into the nuclei and leading to the induction of apoptosis-related genes.	MKT 077	34-41	P53	Homo sapiens	124-127
25379568-10	2014	Inhibiting p53 function with pifithrin alpha prevented the promotion of HRS by VorinostatSAHA.	pifithrin	29-44	P53	Homo sapiens	11-14
30821124-7	2019	In 30% of the 60 CoAs immunostained with p53 the NECS revealed haphazardly distributed p53-upregulated cells, singly or in clusters.	coas	17-21	P53	Homo sapiens	41-44
24465691-5	2014	Blocking GRP75 with its inhibitor MKT-077 potentiated the anti-tumor effects of 17-AAG by disrupting the formation of GRP75-p53 complexes, thereby facilitating translocation of p53 into the nuclei and leading to the induction of apoptosis-related genes.	MKT 077	34-41	P53	Homo sapiens	177-180
24465691-7	2014	In conclusion, the GRP75 inhibitor MKT-077 enhances 17-AAG-induced apoptosis in HCCs and increases p53-mediated inhibition of tumor growth in vivo.	MKT 077	35-42	P53	Homo sapiens	99-102
30821124-7	2019	In 30% of the 60 CoAs immunostained with p53 the NECS revealed haphazardly distributed p53-upregulated cells, singly or in clusters.	coas	17-21	P53	Homo sapiens	87-90
24120424-8	2014	OA-induced changes in cell viability and ATP production were rescued to control levels when cells were pretreated with pifithrin-alpha (PTA), a p53 inhibitor.	pifithrin	119-134	P53	Homo sapiens	144-147
31354907-0	2019	DpdtbA-Induced Growth Inhibition in Human Esophageal Cancer Cells Involved Inactivation of the p53/EGFR/AKT Pathway.	dpdtba	0-6	P53	Homo sapiens	95-98
31128451-9	2019	Further, we point out that structure guided optimization of PhiKan08 can lead to an improved drug that can interact favourably with yet another mutant, Y220 N. In addition, this study revealed that Y220H and other mutants including native p53 does not provide any favourable interaction with PhiKan08 which is in accord with the experimental findings.	phikan08	60-68	P53	Homo sapiens	239-242
24761888-0	2014	Impact of AhR, CYP1A1 and GSTM1 genetic polymorphisms on TP53 R273G mutations in individuals exposed to polycyclic aromatic hydrocarbons.	Polycyclic Aromatic Hydrocarbons	104-136	P53	Homo sapiens	57-61
24761888-1	2014	This study was to undertaken to investigate the impacts of AhR, CYP1A1, GSTM1 genetic polymorphisms on the R273G mutation in exon 8 of the tumor suppressor p53 gene (TP53) among polycyclic aromatic hydrocarbons (PAHs) exposed to coke-oven workers.	Polycyclic Aromatic Hydrocarbons	178-210	P53	Homo sapiens	156-159
24761888-1	2014	This study was to undertaken to investigate the impacts of AhR, CYP1A1, GSTM1 genetic polymorphisms on the R273G mutation in exon 8 of the tumor suppressor p53 gene (TP53) among polycyclic aromatic hydrocarbons (PAHs) exposed to coke-oven workers.	Polycyclic Aromatic Hydrocarbons	178-210	P53	Homo sapiens	166-170
24761888-1	2014	This study was to undertaken to investigate the impacts of AhR, CYP1A1, GSTM1 genetic polymorphisms on the R273G mutation in exon 8 of the tumor suppressor p53 gene (TP53) among polycyclic aromatic hydrocarbons (PAHs) exposed to coke-oven workers.	Polycyclic Aromatic Hydrocarbons	212-216	P53	Homo sapiens	156-159
24761888-1	2014	This study was to undertaken to investigate the impacts of AhR, CYP1A1, GSTM1 genetic polymorphisms on the R273G mutation in exon 8 of the tumor suppressor p53 gene (TP53) among polycyclic aromatic hydrocarbons (PAHs) exposed to coke-oven workers.	Polycyclic Aromatic Hydrocarbons	212-216	P53	Homo sapiens	166-170
24761888-7	2014	Our findings indicated that polymorphisms of PAH metabolic genes, such as AhR, CYP1A1, GSTM1 polymorphisms may interact with p53 genetic variants and may contribute to PAH related cancers.	Polycyclic Aromatic Hydrocarbons	45-48	P53	Homo sapiens	125-128
24716976-0	2014	Ubiquitination of p53 is involved in troglitazone induced apoptosis in cervical cancer cells.	Troglitazone	37-49	P53	Homo sapiens	18-21
24761888-7	2014	Our findings indicated that polymorphisms of PAH metabolic genes, such as AhR, CYP1A1, GSTM1 polymorphisms may interact with p53 genetic variants and may contribute to PAH related cancers.	Polycyclic Aromatic Hydrocarbons	168-171	P53	Homo sapiens	125-128
31033201-6	2019	PEM stimulation also augmented phosphorylation of AMPK, p70S6K, AKT and p53 in most cases.	Pemetrexed	0-3	P53	Homo sapiens	72-75
24190973-8	2014	The activation of p53 through AMPK-mediated MDMX phosphorylation and inactivation was further confirmed by using cell and animal model systems with two AMPK activators, metformin and salicylate (the active form of aspirin).	Salicylates	183-193	P53	Homo sapiens	18-21
24309939-10	2013	Molecular docking analysis suggested that WA could bind to HRas-GTP, causing accumulation of Ras-GTP and excessive activation of Raf/ERK/p53-p21.	ras-gtp	60-67	P53	Homo sapiens	137-140
24125776-7	2014	Finally, the tumor-suppressing effect of HMSNs-BTZ was enhanced in the presence of wild-type p53 signaling, suggesting a potential enhancement in clinical efficacy with combined p53 gene therapy and BTZ-based chemotherapy.	Bortezomib	47-50	P53	Homo sapiens	93-96
24125776-7	2014	Finally, the tumor-suppressing effect of HMSNs-BTZ was enhanced in the presence of wild-type p53 signaling, suggesting a potential enhancement in clinical efficacy with combined p53 gene therapy and BTZ-based chemotherapy.	Bortezomib	47-50	P53	Homo sapiens	178-181
24184596-7	2014	UVB-induced activation of p53 luciferase reporter was also significantly inhibited by vanillin.	vanillin	86-94	P53	Homo sapiens	26-29
24184596-9	2014	Taken together, these findings suggest that vanillin protects KSC from UVB irradiation and its effects may occur through the suppression of downstream step of MDM2 in UVB irradiation-induced p53 activation.	vanillin	44-52	P53	Homo sapiens	191-194
26629941-6	2014	Notably, these expression changes could be neutralized by PFTalpha, an inhibitor of p53 signaling pathway that could inhibit p53-dependent transactivation of p53-responsive genes.	pifithrin	58-66	P53	Homo sapiens	84-87
26629941-6	2014	Notably, these expression changes could be neutralized by PFTalpha, an inhibitor of p53 signaling pathway that could inhibit p53-dependent transactivation of p53-responsive genes.	pifithrin	58-66	P53	Homo sapiens	125-128
24307567-8	2014	We show that these features render the system applicable to biological data, exemplified by the high osmolarity glycerol system in yeast and the mammalian p53 system.	Glycerol	112-120	P53	Homo sapiens	155-158
26629941-6	2014	Notably, these expression changes could be neutralized by PFTalpha, an inhibitor of p53 signaling pathway that could inhibit p53-dependent transactivation of p53-responsive genes.	pifithrin	58-66	P53	Homo sapiens	125-128
31159174-8	2019	We also observed that p53 in vitro prefers binding to the Py-rich strand over the purine (Pu) rich strand in non-B DNA substrates formed by sequence derived from the first intron of the frataxin gene.	purine	82-88	P53	Homo sapiens	22-25
25552063-3	2014	In experimental studies it was showed that synthetic antineoplastons (A10-3-phenyl-acetyl-amino-2,6-piperidinedione and AS2-1--a mixture of phenylacetic acid and phenylacetylglutamine) were able to prevent the introduction of glutamine into the cell, to block the action of Bcl-2, to activate p53 and p21, to inhibit histone deacetylase, to induce apoptosis.	as2-1--a	120-128	P53	Homo sapiens	293-296
24379070-8	2013	CONCLUSIONS: The p53-CDKN1A and p53-Bax signaling pathways appear to be activated in RSA.	rabbit sperm membrane autoantigen	85-88	P53	Homo sapiens	17-20
24379070-8	2013	CONCLUSIONS: The p53-CDKN1A and p53-Bax signaling pathways appear to be activated in RSA.	rabbit sperm membrane autoantigen	85-88	P53	Homo sapiens	32-35
31138778-8	2019	The p53 inhibitor pifithrin-alpha attenuated the influences of ZCCHC10 overexpression on p53 pathway, cell cycle, apoptosis, and epithelial-mesenchymal transition, whereas the p53 activator Nutlin3 could reverse the effects of ZCCHC10 knockdown.	pifithrin	18-33	P53	Homo sapiens	4-7
24161692-9	2013	In addition, the protein levels of p53, p-p38 and p-JNK were increased in quinocetone-treated cells.	quinocetone	74-85	P53	Homo sapiens	35-38
24161692-10	2013	Taken together, quinocetone induced apoptosis in HepG2 cells via activation of caspase, interaction of TNF-alpha and TNFR1 and modulation of the protein levels of Bid, Bax and Bcl-2, involving the participation of p53, p38 and JNK.	quinocetone	16-27	P53	Homo sapiens	214-217
24055891-6	2013	We found that DMU-212 caused up-regulation of pro-apoptotic Bak1, Bok, Bik, Noxa, Bad, Bax, p53 and Apaf1 transcripts level in DLD-1 cell line, whereas anti-apoptotic Bcl-2, Bcl-xL and Bag1 mRNA expression was decreased.	dmu-212	14-21	P53	Homo sapiens	92-95
31138778-8	2019	The p53 inhibitor pifithrin-alpha attenuated the influences of ZCCHC10 overexpression on p53 pathway, cell cycle, apoptosis, and epithelial-mesenchymal transition, whereas the p53 activator Nutlin3 could reverse the effects of ZCCHC10 knockdown.	pifithrin	18-33	P53	Homo sapiens	89-92
31138778-8	2019	The p53 inhibitor pifithrin-alpha attenuated the influences of ZCCHC10 overexpression on p53 pathway, cell cycle, apoptosis, and epithelial-mesenchymal transition, whereas the p53 activator Nutlin3 could reverse the effects of ZCCHC10 knockdown.	pifithrin	18-33	P53	Homo sapiens	89-92
31121972-7	2019	These results demonstrated the potential usefulness of coupling amine-containing structural motifs of known MDM2-p53 disruptors into a 3,4-dioxygenated xanthone scaffold in the design of novel and potent p53 activators with antitumor activity and favorable drug-like properties.	Amines	64-69	P53	Homo sapiens	113-116
24085032-0	2013	Punicalagin, a polyphenol in pomegranate juice, downregulates p53 and attenuates hypoxia-induced apoptosis in cultured human placental syncytiotrophoblasts.	punicalagin	0-11	P53	Homo sapiens	62-65
24064862-4	2013	The tumor suppressor p53 regulates cellular migration, CXCL12 production and the promotion of tumor growth by carcinoma-associated fibroblasts (CAFs).	cafs	144-148	P53	Homo sapiens	21-24
24114842-3	2013	CQ accumulated the acetylation levels of several key proteins including histone H3 (H3), p53, HSP90, and alpha-tubulin.	Clioquinol	0-2	P53	Homo sapiens	89-92
24114842-8	2013	By inhibiting HDAC activity, CQ induced expression of p21, p27, and p53, cell cycle arrest at G1 phase, and cell apoptosis.	Clioquinol	29-31	P53	Homo sapiens	68-71
24182354-0	2013	The association of TP53 mutations with the resistance of colorectal carcinoma to the insulin-like growth factor-1 receptor inhibitor picropodophyllin.	picropodophyllin	133-149	P53	Homo sapiens	19-23
31121972-7	2019	These results demonstrated the potential usefulness of coupling amine-containing structural motifs of known MDM2-p53 disruptors into a 3,4-dioxygenated xanthone scaffold in the design of novel and potent p53 activators with antitumor activity and favorable drug-like properties.	Amines	64-69	P53	Homo sapiens	204-207
30926564-6	2019	Higher cytotoxicity of bleomycin occurred in cells with normal and shRNA-depleted p53.	Bleomycin	23-32	P53	Homo sapiens	82-85
21887816-5	2013	Comparison of genome-wide microarray expression profiles between a nonmutagenic and a mutagenic PAH-treated group revealed that xenobiotic response genes such as CYP1B1 were commonly upregulated in two groups and that DNA damage induced genes, especially p53-downstream genes such as p21 (CDKN1A) were upregulated only in the mutagenic PAH-treated group.	Polycyclic Aromatic Hydrocarbons	96-99	P53	Homo sapiens	255-258
23954467-0	2013	Teroxirone inhibited growth of human non-small cell lung cancer cells by activating p53.	teroxirone	0-10	P53	Homo sapiens	84-87
23954467-4	2013	Teroxirone caused transient elevation of p53 that activates downstream p21 and procaspase-3 cleavage.	teroxirone	0-10	P53	Homo sapiens	41-44
21887816-6	2013	Pretreatment with cytochrome P450 inhibitor alpha-naphthoflavone or p53 inhibitor pifithrin-alpha inhibited the benzo-[a]-pyrene-induced p21 expression.	pifithrin	82-91	P53	Homo sapiens	68-71
30660711-7	2019	In some assay p53 activity of NSCLC ( A549 and H460) cells were blocked with pifithrin-a, prior to treatment with ZQT.	pifithrin	77-88	P53	Homo sapiens	14-17
21887816-7	2013	These data suggest that when PAHs enter the cells, lung epithelium induces PAH metabolic activating enzymes, and then the DNA damages-recognition signal is converged with p53 downstream genes.	Polycyclic Aromatic Hydrocarbons	29-32	P53	Homo sapiens	171-174
24059278-0	2013	Allicin induces anti-human liver cancer cells through the p53 gene modulating apoptosis and autophagy.	allicin	0-7	P53	Homo sapiens	58-61
24127627-1	2013	Chiral nonracemic cis-4,5-bis(aryl)imidazolines have emerged as a powerful platform for the development of cancer chemotherapeutics, stimulated by the Hoffmann-La Roche discovery that Nutlin-3 can restore apoptosis in cells with wild-type p53.	cis-4,5-bis(aryl)imidazolines	18-47	P53	Homo sapiens	239-242
24179522-5	2013	The interaction between p53 and VEGF in the EGCG-treated cells was investigated using pifithrin-alpha.	pifithrin	86-95	P53	Homo sapiens	24-27
24059278-3	2013	Our earlier study indicated that allicin induced autophagic cell death in human HCC Hep G2 (p53(wild type)) cells, whereas in the present study, allicin induced apoptotic cell death through caspase-dependent and caspase-independent pathways by reactive oxygen species (ROS) overproduction in human HCC Hep 3B (p53(mutation)) cells.	allicin	145-152	P53	Homo sapiens	310-313
24059278-5	2013	Allicin treatment induced apoptotic cell death in p53 knocked down Hep G2 cells similar to that of Hep 3B cells.	allicin	0-7	P53	Homo sapiens	50-53
24135282-2	2013	Here, we show that DNp73, an inhibitor of the p53 tumor suppressor family, drives migration and invasion of nonmetastatic melanoma cells.	dnp73	19-24	P53	Homo sapiens	46-49
30531292-0	2019	Methotrexate-induced senescence of human colon cancer cells depends on p53 acetylation, but not genomic aberrations.	Methotrexate	0-12	P53	Homo sapiens	71-74
23964676-5	2013	Additionally, similar tumor suppressor activities of p53-CC and wt-p53 were detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), annexin-V, 7-aminoactinomycin D (7-AAD), and colony-forming assays.	deoxyuridine triphosphate	126-130	P53	Homo sapiens	53-56
23707715-6	2013	By docking of the ThTP molecule in the active site, we found that Trp-53 should interact with the thiazole part of the substrate molecule, thus playing a key role in substrate recognition and specificity.	Thiazoles	98-106	P53	Homo sapiens	66-72
30531292-8	2019	Although two p53 protein isoforms were detected in C85 cells, stabilization and acetylation of the full-length p53 isoform were shown to underpin progression of the cells into premature senescence upon methotrexate treatment.	Methotrexate	202-214	P53	Homo sapiens	13-16
24040102-7	2013	p53-knockdown experiment in C2C12 cells and experiment using p53-deficient HCT116 cells showed that splitomicin and resveratrol modulated apoptosis by p53-dependent and p53-independent pathways.	splitomicin	100-111	P53	Homo sapiens	61-64
24040102-7	2013	p53-knockdown experiment in C2C12 cells and experiment using p53-deficient HCT116 cells showed that splitomicin and resveratrol modulated apoptosis by p53-dependent and p53-independent pathways.	splitomicin	100-111	P53	Homo sapiens	61-64
30531292-8	2019	Although two p53 protein isoforms were detected in C85 cells, stabilization and acetylation of the full-length p53 isoform were shown to underpin progression of the cells into premature senescence upon methotrexate treatment.	Methotrexate	202-214	P53	Homo sapiens	111-114
23817390-0	2013	Ceragenin CSA-13 induces cell cycle arrest and antiproliferative effects in wild-type and p53 null mutant HCT116 colon cancer cells.	ceragenin	0-9	P53	Homo sapiens	90-93
23924947-7	2013	5-aza-dC induced p53-dependent tumor cell senescence and a high number of DNA double-strand breaks.	Azacitidine	0-5	P53	Homo sapiens	17-20
23924947-8	2013	In contrast, 5-aza-CR downregulated p53, induced caspase activation and apoptosis.	Azacitidine	13-21	P53	Homo sapiens	36-39
30770553-8	2019	Furthermore, we demonstrate that 8-Cl-Ado inhibits miR-155 expression levels accompanied by induction of DNA-damage and suppression of cell proliferation, through regulation of miR-155/ErbB3 binding protein 1(Ebp1)/p53/PCNA signaling.	8-chloroadenosine	33-41	P53	Homo sapiens	215-218
30743996-6	2019	Restoring wild type p53 activity either by transfection or by treatment with APR-246, a molecule which reactivates mutant p53, blocked lapatinib-induced senescence and caused increased cell death.	Lapatinib	135-144	P53	Homo sapiens	20-23
23723074-5	2013	We further revealed that miR-133a markedly increased p53 protein and induced p21(Cip1) transcription.	mir-133a	25-33	P53	Homo sapiens	53-56
23977343-8	2013	These data demonstrated firstly to our knowledge that IFN-beta produced synergistic anti-tumor effects with cisplatin or pemetrexed on mesothelioma through up-regulated p53 expression.	Pemetrexed	121-131	P53	Homo sapiens	169-172
30743996-6	2019	Restoring wild type p53 activity either by transfection or by treatment with APR-246, a molecule which reactivates mutant p53, blocked lapatinib-induced senescence and caused increased cell death.	Lapatinib	135-144	P53	Homo sapiens	122-125
30483736-0	2019	Attenuation of autophagy flux by 6-shogaol sensitizes human liver cancer cells to TRAIL-induced apoptosis via p53 and ROS.	shogaol	33-42	P53	Homo sapiens	110-113
22976055-5	2013	The p53 inhibitor pifithrin-alpha (PFT-alpha) knockdown of the signaling of p53 led vitexin to lose its antitumor effect and inhibited the expression of p53 downstream genes, p2(WAF1) and Bax.	pifithrin	18-27	P53	Homo sapiens	4-7
22976055-5	2013	The p53 inhibitor pifithrin-alpha (PFT-alpha) knockdown of the signaling of p53 led vitexin to lose its antitumor effect and inhibited the expression of p53 downstream genes, p2(WAF1) and Bax.	pifithrin	18-27	P53	Homo sapiens	76-79
22976055-5	2013	The p53 inhibitor pifithrin-alpha (PFT-alpha) knockdown of the signaling of p53 led vitexin to lose its antitumor effect and inhibited the expression of p53 downstream genes, p2(WAF1) and Bax.	pifithrin	18-27	P53	Homo sapiens	76-79
23796712-3	2013	p53 has been emphasized as a metabolic regulator involved in glucose, glutamine, and purine metabolism.	purine	85-91	P53	Homo sapiens	0-3
30483736-3	2019	The current study identified a potential pathway by revealing that TRAIL and 6-sho or chloroquine acted together to trigger reactive oxygen species (ROS) production, to upregulate tumor-suppressor protein 53 (p53) expression and to change the mitochondrial transmembrane potential (MTP).	shogaol	77-82	P53	Homo sapiens	209-212
30483736-6	2019	In conclusion, attenuation of 6-sho-induced autophagy flux sensitized cells to TRAIL-induced apoptosis via p53 and ROS, suggesting that the administration of TRAIL in combination with 6-sho may be a suitable therapeutic method for the treatment of TRAIL-resistant Huh7 liver cells.	shogaol	30-35	P53	Homo sapiens	107-110
30790509-14	2019	NTP induced apoptotic death in Huh7 liver cancer cells via simultaneous downregulation of mutated p53, pSTAT1 and STAT1.	ntp	0-3	P53	Homo sapiens	98-101
23640975-6	2013	In human HNSCC expressing PIK3CA and decreased wtTP53 and p73, PF-502 reciprocally enhanced TP53/p73 expression and growth inhibition, which was partially reversible by p53 inhibitor pifithrin-alpha.	pifithrin	183-192	P53	Homo sapiens	169-172
23802716-0	2013	Synthesis, in vitro, and in cell studies of a new series of [indoline-3,2"-thiazolidine]-based p53 modulators.	indoline-3,2"-thiazolidine	61-87	P53	Homo sapiens	95-98
30145226-6	2019	Treatment with pifithrin-alpha-HBr (PFTalpha), a specific blocker of p53-responsive gene transactivation, reduced the P4-increased p27 promoter activity and p27 protein expression.	pifithrin	36-44	P53	Homo sapiens	69-72
23478296-2	2013	A recent study published in Nature reveals a novel connection between p53 and metabolism: p53 transcriptionally represses the expression of malic enzymes and associated NADPH production, which in turn triggers a positive feedback loop resulting in sustained p53 activation, cellular senescence, and tumor suppression.	NADP	169-174	P53	Homo sapiens	70-73
23478296-2	2013	A recent study published in Nature reveals a novel connection between p53 and metabolism: p53 transcriptionally represses the expression of malic enzymes and associated NADPH production, which in turn triggers a positive feedback loop resulting in sustained p53 activation, cellular senescence, and tumor suppression.	NADP	169-174	P53	Homo sapiens	90-93
23478296-2	2013	A recent study published in Nature reveals a novel connection between p53 and metabolism: p53 transcriptionally represses the expression of malic enzymes and associated NADPH production, which in turn triggers a positive feedback loop resulting in sustained p53 activation, cellular senescence, and tumor suppression.	NADP	169-174	P53	Homo sapiens	90-93
30365089-3	2019	The mechanistic studies confirmed that the enhancement of Snail1 expression in bortezomib-resistant MMCs directly upregulated transcription of the intracellular MDR1 gene to immediately develop multiple drug resistance mechanisms and inhibited P53 protein expression through the Snail1/hsa-miRNA-22-3p/P53 pathway to inhibit tumor cell apoptosis.	Bortezomib	79-89	P53	Homo sapiens	244-247
23599745-7	2013	DNA adducts interact with the guanine bases of liver cell DNA and cause a mutational effect in the P53 tumor suppressor gene at the codon 249 hotspot in exon 7, which may lead to HCC.	Guanine	30-37	P53	Homo sapiens	99-102
30365089-3	2019	The mechanistic studies confirmed that the enhancement of Snail1 expression in bortezomib-resistant MMCs directly upregulated transcription of the intracellular MDR1 gene to immediately develop multiple drug resistance mechanisms and inhibited P53 protein expression through the Snail1/hsa-miRNA-22-3p/P53 pathway to inhibit tumor cell apoptosis.	Bortezomib	79-89	P53	Homo sapiens	302-305
23201752-5	2013	Cell exposure to pifithrin, an inhibitor of p53 transcriptional activity, reduced the caspase activity associated with decreased miR-21 expression.	pifithrin	17-26	P53	Homo sapiens	44-47
30365975-10	2019	Knockdown of p53 attenuated the ability of SNF to inhibit anoikis resistance and sphere formation in A549 cancer cells, suggesting that the presence of p53 in NSCLC cancer cells is involved in the sensitivity to SFN.	sulforaphane	212-215	P53	Homo sapiens	13-16
23059970-6	2013	Our results showed that 3,4-DMS exerted its anti-angiogenic effect likely through induction of endothelial cell apoptosis via a pathway involving p53, Bax, cytochrome c, and caspase proteases.	3,4-dms	24-31	P53	Homo sapiens	146-149
30365975-10	2019	Knockdown of p53 attenuated the ability of SNF to inhibit anoikis resistance and sphere formation in A549 cancer cells, suggesting that the presence of p53 in NSCLC cancer cells is involved in the sensitivity to SFN.	sulforaphane	212-215	P53	Homo sapiens	152-155
30591679-8	2018	RNA sequencing analysis suggested that sFRP4-mediated apoptosis is via the Fas-p53 pathway by activating the Wnt calcium and reactive oxygen species pathways.	ammonium ferrous sulfate	75-78	P53	Homo sapiens	79-82
22996738-0	2013	Functional p53 determines docetaxel sensitivity in prostate cancer cells.	Docetaxel	26-35	P53	Homo sapiens	11-14
22996738-5	2013	The potential role of p53 in docetaxel sensitivity in prostate cancer cells was tested by either p53 silencing using shRNA or p53 overexpression by introducing wild-type p53.	Docetaxel	29-38	P53	Homo sapiens	22-25
22996738-6	2013	RESULTS: We found that DU145 (mutant p53) and PC3 (p53 null) cells were less sensitive than LNCaP and C4-2 cells expressing functional p53 in response to docetaxel.	Docetaxel	154-163	P53	Homo sapiens	37-40
22996738-6	2013	RESULTS: We found that DU145 (mutant p53) and PC3 (p53 null) cells were less sensitive than LNCaP and C4-2 cells expressing functional p53 in response to docetaxel.	Docetaxel	154-163	P53	Homo sapiens	51-54
22996738-6	2013	RESULTS: We found that DU145 (mutant p53) and PC3 (p53 null) cells were less sensitive than LNCaP and C4-2 cells expressing functional p53 in response to docetaxel.	Docetaxel	154-163	P53	Homo sapiens	51-54
30555232-14	2018	DTX-loaded FA/PLGA NPs showed the highest apoptotic effect through the activation of Caspase-9, Caspase-3, and TP53 genes by 2.8-, 1.6-, and 1.86-fold, respectively.	Docetaxel	0-3	P53	Homo sapiens	111-115
22996738-8	2013	Docetaxel increases the levels of ser15 phosphorylation of p53 in a dose dependent manner in both LNCaP and C4-2 cells, while has no effect on the levels of ser15 phosphorylation of p53 in DU145 cells.	Docetaxel	0-9	P53	Homo sapiens	59-62
22996738-9	2013	These results suggest that p53 phosphorylation is associated with docetaxel sensitivity in prostate cancer cells.	Docetaxel	66-75	P53	Homo sapiens	27-30
22996738-10	2013	To further confirm whether p53 activation can induce cell sensitivity to docetaxel treatment, we used p53 shRNA to knock down p53 expression in C4-2 cells and determined the cells response to docetaxel treatment.	Docetaxel	73-82	P53	Homo sapiens	27-30
22996738-10	2013	To further confirm whether p53 activation can induce cell sensitivity to docetaxel treatment, we used p53 shRNA to knock down p53 expression in C4-2 cells and determined the cells response to docetaxel treatment.	Docetaxel	73-82	P53	Homo sapiens	102-105
22996738-10	2013	To further confirm whether p53 activation can induce cell sensitivity to docetaxel treatment, we used p53 shRNA to knock down p53 expression in C4-2 cells and determined the cells response to docetaxel treatment.	Docetaxel	73-82	P53	Homo sapiens	102-105
22996738-10	2013	To further confirm whether p53 activation can induce cell sensitivity to docetaxel treatment, we used p53 shRNA to knock down p53 expression in C4-2 cells and determined the cells response to docetaxel treatment.	Docetaxel	192-201	P53	Homo sapiens	27-30
30122553-3	2018	We show here that p53 promotes the expression of SLC1A3, an aspartate/glutamate transporter that allows the utilization of aspartate to support cells in the absence of extracellular glutamine.	Aspartic Acid	60-69	P53	Homo sapiens	18-21
22996738-11	2013	Knockdown of p53 significantly down regulated p53 phosphorylation and blocked docetaxel induced apoptotic cell death compared to the vector control.	Docetaxel	78-87	P53	Homo sapiens	13-16
22996738-13	2013	Down regulation of p53 in the stable p53 knock out C4-2 cells significantly inhibited docetaxel induced apoptotic cell death.	Docetaxel	86-95	P53	Homo sapiens	19-22
30080692-8	2018	We further found that pifithrin-alpha, a p53 inhibitor, attenuated the anticancer effects of VX-680 and downregulated the expression of apotosis-related proteins (Bax and caspase-9).	pifithrin	22-37	P53	Homo sapiens	41-44
22996738-13	2013	Down regulation of p53 in the stable p53 knock out C4-2 cells significantly inhibited docetaxel induced apoptotic cell death.	Docetaxel	86-95	P53	Homo sapiens	37-40
22996738-14	2013	We also used wild-type (WT) p53 to over express p53 in DU145 cells, and found that expression of WT-p53 in DU145 cells increased their sensitivity to docetaxel.	Docetaxel	150-159	P53	Homo sapiens	48-51
22996738-14	2013	We also used wild-type (WT) p53 to over express p53 in DU145 cells, and found that expression of WT-p53 in DU145 cells increased their sensitivity to docetaxel.	Docetaxel	150-159	P53	Homo sapiens	48-51
22996738-15	2013	CONCLUSIONS: These results demonstrate that docetaxel induces p53 phosphorylation and that p53 status is a crucial determinant of docetaxel sensitivity in prostate cancer cells.	Docetaxel	44-53	P53	Homo sapiens	62-65
22996738-15	2013	CONCLUSIONS: These results demonstrate that docetaxel induces p53 phosphorylation and that p53 status is a crucial determinant of docetaxel sensitivity in prostate cancer cells.	Docetaxel	130-139	P53	Homo sapiens	91-94
29569972-6	2018	Moreover, inhibition TRIM28 expression in B-NHL cells enhanced the sensibility to Bortezomib by regulating p53-mediated apoptosis pathway.	Bortezomib	82-92	P53	Homo sapiens	107-110
22430213-4	2013	In the complete absence of p53, cells treated with N-(phosphonacetyl)-L-aspartate (PALA) continue to synthesize DNA slowly and eventually progress through S-phase, suffering severe DNA damage that in turn triggers apoptosis, whereas cells with functional p53 undergo growth arrest.	sparfosic acid	51-81	P53	Homo sapiens	255-258
28978265-0	2018	Modulation of interaction of mutant TP53 and wild type BRCA1 by alkaloids: a computational approach towards targeting protein-protein interaction as a futuristic therapeutic intervention strategy for breast cancer impediment.	Alkaloids	64-73	P53	Homo sapiens	36-40
23395165-2	2013	A new study shows that, upon serine starvation, the tumor suppressor p53 activates p21 to shift metabolic flux from purine biosynthesis to glutathione production, which enhances cellular proliferation and viability by combating ROS (Maddocks et al., 2013).	purine	116-122	P53	Homo sapiens	69-72
22753261-5	2013	Remarkably, depletion of 15 out of 25 presumed passenger genes that interact with confirmed CAN-genes (60%) promoted soft agar growth in HCECs with TP53 knockdown compared to only 7 out of 55 (12.5%) of presumed passenger genes that do not interact.	Agar	122-126	P53	Homo sapiens	148-152
28978265-4	2018	Using computational approaches such as protein-protein docking, hot spot analyses, molecular docking and molecular dynamics simulation (MDS), stepwise analyses of the interactions of the wild type and mutant TP53 with that of wild type BRCA1 and their modulation by alkaloids were done.	Alkaloids	266-275	P53	Homo sapiens	208-212
30197676-9	2018	A pG13L (p53-responsive reporter plasmid) luciferase reporter and co-immunoprecipitation assay revealed that upregulation of RBEL1A led to an inhibition of the transcriptional activity of p53 or its target gene p21.	pg13l	2-7	P53	Homo sapiens	9-12
27481281-2	2013	Quercetin and taxifolin bind to p53 binding hydrophobic groove of MDM2, and alter the conformation of groove as evidenced by 65 ns molecular dynamics simulation.	Quercetin	0-9	P53	Homo sapiens	32-35
30235848-0	2018	Chalcone Derivatives 4"-Amino-1-Naphthyl-Chalcone (D14) and 4"-Amino-4-Methyl-1-Naphthyl-Chalcone (D15) Suppress Migration and Invasion of Osteosarcoma Cells Mediated by p53 Regulating EMT-Related Genes.	4"-amino-4-methyl-1-naphthyl-chalcone	60-97	P53	Homo sapiens	170-173
23266186-8	2013	Compound 4 combined with methyl methane sulfonate (MMS) treatment synergistically suppressed HCT116 p53(-/-) cell growth compared with MMS alone.	Methyl Methanesulfonate	25-49	P53	Homo sapiens	100-103
23266186-8	2013	Compound 4 combined with methyl methane sulfonate (MMS) treatment synergistically suppressed HCT116 p53(-/-) cell growth compared with MMS alone.	Methyl Methanesulfonate	51-54	P53	Homo sapiens	100-103
30235848-15	2018	These effects probably result from the induced increase of p53 protein expression by the two chalcones.	Chalcones	93-102	P53	Homo sapiens	59-62
30235848-16	2018	In conclusion, chalcones D14 and D15 have potential anti-metastatic activity mediated by p53 that can be exploited for OS treatment.	Chalcones	15-24	P53	Homo sapiens	89-92
23816816-9	2013	These effects were absent when the caspase inhibitor z-VAD-fmk or p53 inhibitor PFTalpha were applied, suggesting that casticin could trigger cell apoptosis in a caspase-3 and p53-dependent manner.	pifithrin	80-88	P53	Homo sapiens	66-69
29853027-0	2018	Highly sensitive fluorescent detection of p53 protein based on DNA functionalized Fe3O4 nanoparticles.	ferryl iron	82-87	P53	Homo sapiens	42-45
30166522-0	2018	TRMP, a p53-inducible long noncoding RNA, regulates G1/S cell cycle progression by modulating IRES-dependent p27 translation.	CHEMBL3144022	0-4	P53	Homo sapiens	8-11
23942225-3	2013	METHODS: In the present study, by using Z-VAD-fmk to inhibit caspase-3 in p53-deficient Hep3B cells, we explored the effect of Cr(VI) on apoptosis induction and the related mechanisms when the functions of p53 and caspase were simultaneously blocked.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	40-49	P53	Homo sapiens	74-77
30106986-8	2018	Boysenberry polyphenol also reduced ROS and p53 levels in cultured human umbilical vein endothelial cells (HUVECs), while increasing NO production.	boysenberry polyphenol	0-22	P53	Homo sapiens	44-47
30045945-6	2018	The combination of ATSP-7041 with P5091, GSK2830371, and chemotherapeutic agents showed synergistic action on the p53 pathway.	GSK2830371	41-51	P53	Homo sapiens	114-117
24059678-4	2013	In addition, while radiation-induced expression and phosphorylation of p53, inhibition of p53 function with pifithrin-alpha or transfection of cells with p53 siRNA significantly reduced the activation of both MMP2 and VEGF and resulted in a reduction of radiation-induced invasiveness.	pifithrin	108-123	P53	Homo sapiens	90-93
24059678-4	2013	In addition, while radiation-induced expression and phosphorylation of p53, inhibition of p53 function with pifithrin-alpha or transfection of cells with p53 siRNA significantly reduced the activation of both MMP2 and VEGF and resulted in a reduction of radiation-induced invasiveness.	pifithrin	108-123	P53	Homo sapiens	90-93
30033448-8	2018	Mechanistically, ANGPTL3 bound to Focal Adhesion Kinase(FAK) and restained sorafenib induced nuclear translocation of FAK, leading to attenuate the ubiquitination of p53, which contributed to cellular apoptosis and enhanced sorafenib response.	Sorafenib	224-233	P53	Homo sapiens	166-169
29908167-4	2018	The current study further affirmed that teroxirone inhibited the propagation of CSCs as enriched from NSCLC cells by inducing p53 that lead to ultimate apoptosis.	teroxirone	40-50	P53	Homo sapiens	126-129
23871989-0	2013	Dihydrotanshinone induces p53-independent but ROS-dependent apoptosis in colon cancer cells.	DIHYDROTANSHINONE	0-17	P53	Homo sapiens	26-29
23918355-7	2013	We found that quercetin-induced selective cell death is caused by mitochondrial accumulation of p53 and is sufficient to prevent teratoma formation after transplantation of hESC- or hiPSC-derived cells.	Quercetin	14-23	P53	Homo sapiens	96-99
30065615-0	2018	Impact of p53 arg72pro SNP on Breast Cancer Risk in North Indian Population.	arg72pro	14-22	P53	Homo sapiens	10-13
23652278-12	2013	An inhibitor of p53, pifithrin-alpha, attenuated the anticancer effects of OSU-03012 and downregulated the expression of Bax and cleaved caspase-9.	pifithrin	21-30	P53	Homo sapiens	16-19
23648290-8	2013	A reduction by approximately 50% in the cytotoxicity of Gem and Clo was observed in the presence of pifithrin alpha, a p53 inhibitor.	pifithrin	100-115	P53	Homo sapiens	119-122
29870655-3	2018	Taking advantage of surface roughness, near-infrared (NIR) responsiveness, and controlled release manner, AHPs were expected to realize the co-delivery of sorafenib (SF, a hydrophobic antiproliferative and antiangiogenic drug) and antioncogene p53 for malignant hepatocellular carcinoma treatment.	Sorafenib	155-164	P53	Homo sapiens	244-247
22789708-0	2013	Benzimidazole-2-one: a novel anchoring principle for antagonizing p53-Mdm2.	benzimidazole-2-one	0-19	P53	Homo sapiens	66-69
22789708-1	2013	Herein we propose the benzimidazole-2-one substructure as a suitable tryptophan mimic and thus a reasonable starting point for the design of p53 Mdm2 antagonists.	benzimidazole-2-one	22-41	P53	Homo sapiens	141-144
29910624-11	2018	Conclusion: The present results show that AZT could increase the sensitization of As2O3 for inhibiting proliferation and promoting apoptosis of HepG2 cells through regulating the expression of Egr-1, which may control the expression of p53 and caspase-3.	Zidovudine	42-45	P53	Homo sapiens	236-239
29910624-11	2018	Conclusion: The present results show that AZT could increase the sensitization of As2O3 for inhibiting proliferation and promoting apoptosis of HepG2 cells through regulating the expression of Egr-1, which may control the expression of p53 and caspase-3.	Arsenic Trioxide	82-87	P53	Homo sapiens	236-239
23856246-5	2013	Furthermore, we identify pharmacogenomic correlations between specific variants in genes such as TP53, BRAF, ERBBs, and ATAD5 and anticancer agents such as nutlin, vemurafenib, erlotinib, and bleomycin showing one of many ways the data could be used to validate and generate novel hypotheses for further investigation.	Bleomycin	192-201	P53	Homo sapiens	97-101
29928326-0	2018	Miltirone-induced apoptosis in cisplatin-resistant lung cancer cells through upregulation of p53 signaling pathways.	miltirone	0-9	P53	Homo sapiens	93-96
29928326-7	2018	It was also revealed that miltirone increased caspase-3/8 activity as well as B-cell lymphoma 2-associated X-protein, apoptosis-inducing factor (AIF), p53 and poly(ADP-ribose) polymerase (PARP) protein expression, whereas it inhibited mitochondrial reactive oxygen species (ROS) generation and matrix metalloproteinase (MMP)-2/9 protein expression in HCC827 and A549 platinum-resistant lung cancer cells.	miltirone	26-35	P53	Homo sapiens	151-154
23692869-1	2013	Our previous findings demonstrated that DNA damage by polynuclear aromatic hydrocarbons (PAHs) triggers a cellular protective response of growth inhibition (G1-S cell cycle arrest and inhibition of DNA synthesis) in human fibroblasts associated with accumulation of p53 protein, a growth-inhibitory transcription factor.	Polycyclic Aromatic Hydrocarbons	54-87	P53	Homo sapiens	266-269
23692869-1	2013	Our previous findings demonstrated that DNA damage by polynuclear aromatic hydrocarbons (PAHs) triggers a cellular protective response of growth inhibition (G1-S cell cycle arrest and inhibition of DNA synthesis) in human fibroblasts associated with accumulation of p53 protein, a growth-inhibitory transcription factor.	Polycyclic Aromatic Hydrocarbons	89-93	P53	Homo sapiens	266-269
29753331-1	2018	TIGAR is a p53 target gene that is known to protect cells from ROS-induced apoptosis by promoting the pentose phosphate pathway.	Pentosephosphates	102-119	P53	Homo sapiens	11-14
23701164-4	2013	The most abundant DNA adduct, 7-(deoxyadenosin-N6-yl)aristolactam I, causes characteristic AT TA transversions found in the TP53 tumor suppressor gene in tumors from AAN and BEN patients.	7-(deoxyadenosin-N(6)-yl)aristolactam I	30-67	P53	Homo sapiens	124-128
29662081-6	2018	We validated the assay by testing two small molecules, SAHA and RITA, reported to impair the E6-mediated p53 degradation.	Polyurethane Y-290	93-95	P53	Homo sapiens	105-108
23404993-0	2013	Inhibitory effect of oleanolic acid on hepatocellular carcinoma via ERK-p53-mediated cell cycle arrest and mitochondrial-dependent apoptosis.	Oleanolic Acid	21-35	P53	Homo sapiens	72-75
29555944-8	2018	Scoulerine was able to activate apoptosis, as determined by p53 upregulation, increase caspase activity, Annexin V and TUNEL labeling.	discretamine	0-10	P53	Homo sapiens	60-63
23563592-4	2013	In this study, we showed that p53 has a profound inhibitory effect on docetaxel (Doc)-induced apoptosis in prostate and colorectal cancer cells and that caspases play a critical role in this process.	Docetaxel	70-79	P53	Homo sapiens	30-33
23563592-4	2013	In this study, we showed that p53 has a profound inhibitory effect on docetaxel (Doc)-induced apoptosis in prostate and colorectal cancer cells and that caspases play a critical role in this process.	Docetaxel	81-84	P53	Homo sapiens	30-33
23563592-5	2013	Doc induced prostate cancer cell apoptosis at high levels in p53-null PC3 cells, at intermediate levels in p53-mutant DU145 cells and at low levels in p53 wild-type LNCaP cells.	Docetaxel	0-3	P53	Homo sapiens	61-64
23563592-5	2013	Doc induced prostate cancer cell apoptosis at high levels in p53-null PC3 cells, at intermediate levels in p53-mutant DU145 cells and at low levels in p53 wild-type LNCaP cells.	Docetaxel	0-3	P53	Homo sapiens	107-110
29358327-0	2018	Low-level overexpression of p53 promotes warfarin-induced calcification of porcine aortic valve interstitial cells by activating Slug gene transcription.	Warfarin	41-49	P53	Homo sapiens	28-31
23563592-5	2013	Doc induced prostate cancer cell apoptosis at high levels in p53-null PC3 cells, at intermediate levels in p53-mutant DU145 cells and at low levels in p53 wild-type LNCaP cells.	Docetaxel	0-3	P53	Homo sapiens	107-110
23563592-6	2013	While transient overexpression of p53 in PC3 cells suppressed Doc-induced apoptosis, knockdown of p53 in LNCaP cells increased apoptosis.	Docetaxel	62-65	P53	Homo sapiens	34-37
29358327-3	2018	Whether p53 participates in warfarin-induced AVIC calcification remains unknown.	Warfarin	28-36	P53	Homo sapiens	8-11
23563592-8	2013	To our knowledge, this is the first report describing that chemical or genetic knockout of p53 enhances the susceptibility of both prostate and colorectal cancer cells to Doc-induced apoptosis.	Docetaxel	171-174	P53	Homo sapiens	91-94
29358327-4	2018	In this study, we investigated the role of low-level p53 overexpression in warfarin-induced porcine AVIC (pAVIC) calcification.	Warfarin	75-83	P53	Homo sapiens	53-56
29358327-8	2018	Low-level overexpression of p53 in pAVICs via an adenovirus vector did not affect pAVIC apoptosis but promoted warfarin-induced calcium deposition and expression of osteogenic markers.	Warfarin	111-119	P53	Homo sapiens	28-31
28265856-0	2018	DRAM Is Involved in Regulating Nucleoside Analog-Induced Neuronal Autophagy in a p53-Independent Manner.	Nucleosides	31-41	P53	Homo sapiens	81-84
23635777-6	2013	Btz treatment led to caspase activation and induced DNA damage, as evidenced by the accumulation of phosphorylated gammaH2AX and p53.	Bortezomib	0-3	P53	Homo sapiens	129-132
23635777-7	2013	The addition of SAHA to Btz treatment was synergistic, as SAHA induced early acetylation of p53 and reduced interaction with its negative regulator MDM2, augmenting the effects of Btz.	Bortezomib	24-27	P53	Homo sapiens	92-95
29207126-7	2018	Specifically, docetaxel downregulated TP53, cyclin-dependent kinase inhibitor 1A (CDKN1A) and cadherin 13 (CDH13), and upregulated mucin 1 (MUC1), GATA binding protein 3 (GATA3) and c-MYC, whereas melatonin counteracted these effects.	Docetaxel	14-23	P53	Homo sapiens	38-42
23563597-4	2013	Ad5/F35-siAPE1 significantly enhanced the cytotoxic effect of SMMC-7721 cells to Ad-p53 in cell survival assays, associated with increased cell apoptosis.	smmc	62-66	P53	Homo sapiens	84-87
29117941-8	2018	In addition, sensitization is also observed with pemetrexed in p53 KO cells, but not with 5-FU, most likely due to RNA incorporation.	Pemetrexed	49-59	P53	Homo sapiens	63-66
23446853-4	2013	In cells carrying defective p53, the development of centrosome amplification also occurred following treatment with another DNA damaging agent, methotrexate.	Methotrexate	144-156	P53	Homo sapiens	28-31
29108775-3	2018	SK-N-SH cell treatment with a lethal concentration of PQ facilitated ROS production within 6 h. The treatment also promoted formation of 8-hydroxy-deoxyguanosine, p53 activation, elevation of Bax/Bcl-2 ratio, lowering of mitochondrial membrane potential, and resultant activation of caspase-9 and caspase-3, inferring that ROS production, DNA damage and mitochondrial dysfunction are crucial processes of the PQ-triggered SK-N-SH cell apoptosis.	sk-n	0-4	P53	Homo sapiens	163-166
23769286-3	2013	This study aimed to evaluate the efficacy of PDT with indocyanine green (ICG) through the investigation of TP53, HER-2 and TOP2A genes signals as breast cancer gene markers by interphase fluorescence in situ hybridization (nuc-FISH).	Indocyanine Green	54-71	P53	Homo sapiens	107-111
23769286-3	2013	This study aimed to evaluate the efficacy of PDT with indocyanine green (ICG) through the investigation of TP53, HER-2 and TOP2A genes signals as breast cancer gene markers by interphase fluorescence in situ hybridization (nuc-FISH).	Indocyanine Green	73-76	P53	Homo sapiens	107-111
29278895-5	2018	RESULTS: In cultures of myogenic cells from MDC1A donors, p53 accumulated in a subset of nuclei and aberrant caspase activation was inhibited by the p53 inhibitor pifithrin-alpha.	pifithrin	163-178	P53	Homo sapiens	58-61
23501101-8	2013	In the presence of specific DNA all p53 family core domains were partially protected against loss of DNA binding activity due to diamide treatment.	Diamide	129-136	P53	Homo sapiens	36-39
22983795-0	2013	p53 contributes to quercetin-induced apoptosis in human rheumatoid arthritis fibroblast-like synoviocytes.	Quercetin	19-28	P53	Homo sapiens	0-3
29278895-5	2018	RESULTS: In cultures of myogenic cells from MDC1A donors, p53 accumulated in a subset of nuclei and aberrant caspase activation was inhibited by the p53 inhibitor pifithrin-alpha.	pifithrin	163-178	P53	Homo sapiens	149-152
22983795-8	2013	Quercetin also elevated p53 phosphorylation at ser15.	Quercetin	0-9	P53	Homo sapiens	24-27
22983795-9	2013	Pretreatment with pifithrin-alpha, a p53 inhibitor, significantly diminished p53 phosphorylation at the concentration of 30 muM and abrogated quercetin-induced apoptosis in a dose-dependent manner.	pifithrin	18-33	P53	Homo sapiens	37-40
22983795-9	2013	Pretreatment with pifithrin-alpha, a p53 inhibitor, significantly diminished p53 phosphorylation at the concentration of 30 muM and abrogated quercetin-induced apoptosis in a dose-dependent manner.	pifithrin	18-33	P53	Homo sapiens	77-80
22983795-9	2013	Pretreatment with pifithrin-alpha, a p53 inhibitor, significantly diminished p53 phosphorylation at the concentration of 30 muM and abrogated quercetin-induced apoptosis in a dose-dependent manner.	Quercetin	142-151	P53	Homo sapiens	37-40
22983795-10	2013	Quercetin-induced apoptosis was also significantly blocked by p53 silencing, further suggesting the involvement of p53 in quercetin-induced apoptosis in RAFLSs.	Quercetin	0-9	P53	Homo sapiens	62-65
22983795-10	2013	Quercetin-induced apoptosis was also significantly blocked by p53 silencing, further suggesting the involvement of p53 in quercetin-induced apoptosis in RAFLSs.	Quercetin	0-9	P53	Homo sapiens	115-118
22983795-10	2013	Quercetin-induced apoptosis was also significantly blocked by p53 silencing, further suggesting the involvement of p53 in quercetin-induced apoptosis in RAFLSs.	Quercetin	122-131	P53	Homo sapiens	62-65
22983795-10	2013	Quercetin-induced apoptosis was also significantly blocked by p53 silencing, further suggesting the involvement of p53 in quercetin-induced apoptosis in RAFLSs.	Quercetin	122-131	P53	Homo sapiens	115-118
24171036-7	2013	TAM was more frequent in P53 negative tumors (P = 0.002).	tam	0-3	P53	Homo sapiens	25-28
29103773-11	2018	In conclusion, the expression of cyclin D, Ki-67, p53, mCEA and CA19-9 and KRAS mutation status are significantly correlated with histological grades of IPNBs.	ipnbs	153-158	P53	Homo sapiens	50-53
24319226-2	2013	For example, 5-azacytidine and decitabine produce remissions and better overall survival in MDS with high-risk chromosome abnormalities at a surprisingly high rate, consistent with experimental observations that noncytotoxic DNA methyltransferase depletion by 5-azacytidine/decitabine can trigger cell cycle exit independently of p53, thus circumventing a basis for resistance to apoptosis-based DNA-damaging therapy.	Azacitidine	13-26	P53	Homo sapiens	330-333
24319226-2	2013	For example, 5-azacytidine and decitabine produce remissions and better overall survival in MDS with high-risk chromosome abnormalities at a surprisingly high rate, consistent with experimental observations that noncytotoxic DNA methyltransferase depletion by 5-azacytidine/decitabine can trigger cell cycle exit independently of p53, thus circumventing a basis for resistance to apoptosis-based DNA-damaging therapy.	Azacitidine	260-273	P53	Homo sapiens	330-333
22983795-11	2013	Our study indicated that quercetin-induced apoptosis of RAFLSs is through mitochondrial pathway, in which p53 plays an important role.	Quercetin	25-34	P53	Homo sapiens	106-109
23421999-6	2013	Here, we demonstrate that siRNAs targeting the E6/E7 RNA, or treatment with the proteasome inhibitor bortezomib, resulted in upregulation of functional p53 and p53 gene targets in three HPV-positive HNSCC cell lines, but not in HPV-negative HNSCC cells.	Bortezomib	101-111	P53	Homo sapiens	152-155
23421999-6	2013	Here, we demonstrate that siRNAs targeting the E6/E7 RNA, or treatment with the proteasome inhibitor bortezomib, resulted in upregulation of functional p53 and p53 gene targets in three HPV-positive HNSCC cell lines, but not in HPV-negative HNSCC cells.	Bortezomib	101-111	P53	Homo sapiens	160-163
23421999-7	2013	Apoptosis induced by E6/E7 siRNA in HPV-positive cells was found to be dependent on p53, while bortezomib-induced cell death was modestly p53-dependent.	Bortezomib	95-105	P53	Homo sapiens	138-141
29416773-11	2018	Our in vitro and in vivo data demonstrate that DS-3032b reactivates TP53 signaling even in the presence of MYCN amplification in neuroblastoma cells, to reduce proliferative capacity and cause cytotoxicity.	Deuterium	47-49	P53	Homo sapiens	68-72
23807285-3	2013	We present examples for the 15N isotope-labeled N-terminal transactivation domain of human p53, which is either sequentially reacted with recombinant enzymes or directly added to mammalian cell extracts and phosphorylated by endogenous kinases.	15n	28-31	P53	Homo sapiens	91-94
29292794-7	2017	Our study highlights a role for p53 in regulating nutrient metabolism and provides insight into how iron and possibly other metals such as zinc and manganese could be regulated in p53-inactivated tumor cells.	Manganese	148-157	P53	Homo sapiens	32-35
29143344-5	2017	Cells transfected with siRNAs targeting p16 and MGMT as well as cells stimulated with 5-Aza-dC were arrested in S phase, and the expression of p53, p21, and Rb was up-regulated more significantly.	Azacitidine	86-91	P53	Homo sapiens	143-146
23530650-0	2013	Diallyl sulfide promotes cell-cycle arrest through the p53 expression and triggers induction of apoptosis via caspase- and mitochondria-dependent signaling pathways in human cervical cancer Ca Ski cells.	allyl sulfide	0-15	P53	Homo sapiens	55-58
23530650-6	2013	Western blotting showed that 75 muM of DAS-induced G0/G1 phase arrest was mediated through the increased expression of p21, p27, and p53 with a simultaneous decrease in CDK2, CDK6, and CHK2 expression.	allyl sulfide	39-42	P53	Homo sapiens	133-136
23354132-6	2013	Salubrinal, an inhibitor of the dephosphorylation             of eIF2alpha, suppressed the loss of mitochondrial membrane potential and the translocation             of stabilized p53 and Bax to the mitochondria; however, SP600125, a JNK kinase             inhibitor, did not exert this effect.	salubrinal	0-10	P53	Homo sapiens	180-183
23014341-7	2013	Independent treatment with DIDS, at concentrations that had no effect on thymine dimers, blocked UVR-induced upregulation of p53.	4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid	27-31	P53	Homo sapiens	125-128
28916527-4	2017	5-aza reduced expression of HPV genes, stabilized p53, and induced p53-dependent apoptosis in HNSCC cells and tumors.	Azacitidine	0-5	P53	Homo sapiens	50-53
23064281-7	2013	In addition, sequential or concomitant treatment of bortezomib and cisplatin             stimulated the expression of p53, hScrib and p21 and the stimulation was markedly             influenced by the order of drugs in HeLa cells.	Bortezomib	52-62	P53	Homo sapiens	118-121
23410627-1	2013	A novel electrochemical biosensor based on functional composite nanofibers for sensitive hybridization detection of p53 tumor suppressor using methylene blue (MB) as an electrochemical indicator is developed.	Methylene Blue	143-157	P53	Homo sapiens	116-119
28916527-4	2017	5-aza reduced expression of HPV genes, stabilized p53, and induced p53-dependent apoptosis in HNSCC cells and tumors.	Azacitidine	0-5	P53	Homo sapiens	67-70
23410627-1	2013	A novel electrochemical biosensor based on functional composite nanofibers for sensitive hybridization detection of p53 tumor suppressor using methylene blue (MB) as an electrochemical indicator is developed.	Methylene Blue	159-161	P53	Homo sapiens	116-119
23950593-8	2013	In addition, BDMC activated the pro-apoptotic protein p53 and its downstream effector p21 as well as the cell cycle regulatory proteins p16 and its downstream effector retinoblastoma protein (Rb).	bisdemethoxycurcumin	13-17	P53	Homo sapiens	54-57
29039537-0	2017	Juglone potentiates TRAIL-induced apoptosis in human melanoma cells via activating the ROS-p38-p53 pathway.	juglone	0-7	P53	Homo sapiens	95-98
23950593-10	2013	CONCLUSIONS: These results suggested that BDMC-induced ROS accumulation may contribute to its inhibitory effect on MCF-7 cell viability through regulation of p53/p21 and p16/Rb pathways.	bisdemethoxycurcumin	42-46	P53	Homo sapiens	158-161
23342112-0	2013	Quercetin enhances the antitumor activity of trichostatin A through upregulation of p53 protein expression in vitro and in vivo.	Quercetin	0-9	P53	Homo sapiens	84-87
23342112-2	2013	We first showed that quercetin (5 microM) significantly increased the growth arrest and apoptosis in A549 cells (expressing wild-type p53) induced by 25 ng/mL of (82.5 nM) TSA at 48 h by about 25% and 101%, respectively.	Quercetin	21-30	P53	Homo sapiens	134-137
23342112-4	2013	In addition, quercetin significantly increased TSA-induced p53 expression in A549 cells.	Quercetin	13-22	P53	Homo sapiens	59-62
23342112-7	2013	Transfection of p53 siRNA abolished such enhancing effects of quercetin.	Quercetin	62-71	P53	Homo sapiens	16-19
24280180-2	2013	p53 represses metabolic pathways that support tumor development (such as glycolysis and the pentose phosphate pathway (PPP)) and enhances metabolic pathways that are considered counter-tumorigenic such as fatty acid oxidation.	Pentosephosphates	92-109	P53	Homo sapiens	0-3
23342112-8	2013	However, quercetin increased the acetylation of histones H3 and H4 induced by TSA in A549 cells, even with p53 siRNA transfection as well as in H1299 cells.	Quercetin	9-18	P53	Homo sapiens	107-110
29039537-8	2017	However, exposure to TRAIL in combination with juglone markedly increased the production of ROS, activated p38 and increased p53, compared with the cells treated with either juglone or TRAIL alone.	juglone	47-54	P53	Homo sapiens	125-128
23342112-11	2013	These data indicate that regulation of the expression of p53 by quercetin plays an important role in enhancing TSA-induced apoptosis in A549 cells.	Quercetin	64-73	P53	Homo sapiens	57-60
29200826-6	2017	Results: At 3, 6, 12, and 24 microg/mL exposure, DEN and DEN-HPbetaCD complex significantly affected apoptosis in HT-29 cells through the down-regulation of Bcl-2 and cyclin A in turn, and up-regulation of Bax, p53, p21, cytochrome c at both protein and mRNA levels.	dentatin	49-52	P53	Homo sapiens	211-214
23342112-12	2013	However, p53-independent mechanisms may also contribute to the enhancing effect of quercetin.	Quercetin	83-92	P53	Homo sapiens	9-12
23349842-6	2013	A p53 inhibitor pifithrin-alpha inhibited the expression of p21(Cip1) and attenuated homocysteine-induced cell growth arrest.	pifithrin	16-31	P53	Homo sapiens	2-5
23267009-3	2013	Here, we demonstrate direct binding of both ssDNA and the transactivation domain 2 of p53 (p53TAD2) to DBD-F, as well as DBD-F-directed dsDNA strand separation by RPA, all of which are inhibited by fumaropimaric acid (FPA).	4-(N,N-dimethylaminosulfonyl)-7-fluoro-2,1,3-benzoxadiazole	103-108	P53	Homo sapiens	86-89
22982090-2	2013	The sestrin 2 gene, a p53-regulated member of the sestrins family, which lead to AMPK-dependent inhibition of TOR signaling, emerges as a novel player in autophagy induction.	Toremifene	110-113	P53	Homo sapiens	22-25
29200826-6	2017	Results: At 3, 6, 12, and 24 microg/mL exposure, DEN and DEN-HPbetaCD complex significantly affected apoptosis in HT-29 cells through the down-regulation of Bcl-2 and cyclin A in turn, and up-regulation of Bax, p53, p21, cytochrome c at both protein and mRNA levels.	den-hpbetacd	57-69	P53	Homo sapiens	211-214
29164574-12	2017	CONCLUSIONS: As2O3 can inhibit proliferation of glioma cells and induce its apoptosis, which may be correlated with down-regulation of expressions of apoptosis-related factors, Fas, FasL and Bax, and apoptosis-related proteins, p53, caspase-3 and caspase-9.	Arsenic Trioxide	13-18	P53	Homo sapiens	228-231
23228258-8	2013	RESULTS: CQ treatment suppressed the proliferation of DPSCs and induced the expression of p16(INK4A), p21(WAF1), and p53.	camphorquinone	9-11	P53	Homo sapiens	117-120
23185017-1	2012	The p53-inducible protein TIGAR (Tp53-induced Glycolysis and Apoptosis Regulator) functions as a fructose-2,6-bisphosphatase (Fru-2,6-BPase), and through promotion of the pentose phosphate pathway, increases NADPH production to help limit reactive oxygen species (ROS).	Pentosephosphates	171-188	P53	Homo sapiens	4-7
23185017-1	2012	The p53-inducible protein TIGAR (Tp53-induced Glycolysis and Apoptosis Regulator) functions as a fructose-2,6-bisphosphatase (Fru-2,6-BPase), and through promotion of the pentose phosphate pathway, increases NADPH production to help limit reactive oxygen species (ROS).	NADP	208-213	P53	Homo sapiens	4-7
28691888-10	2017	The p53 inhibitor, Pifithrin-alpha, blocked the gingipain-induced Bid.	pifithrin	19-34	P53	Homo sapiens	4-7
22886373-8	2012	ROS-mediated p53 activation was found to involve in Cr(VI)-induced cell cycle arrest, and p53 inhibitor Pifithrin-alpha (PFT-alpha) rescued Cr(VI)-induced reduction of check point proteins Mrc1 and BubR1, thus inhibiting cell cycle arrest.	pifithrin	104-113	P53	Homo sapiens	90-93
22006587-7	2013	Sorafenib and nutlin-3 decreased the phosphorylation of vascular endothelial growth factor receptor-2 (VEGFR-2) and ERK along with inducing p53 activity.	Sorafenib	0-9	P53	Homo sapiens	140-143
22006587-8	2013	The sorafenib and nutlin-3 co-treatment lead to enhanced levels of p53, p-p53, and increase in the levels of p53 pro-apoptotic effector PUMA, Bax, and decrease in the anti-apoptotic Bcl-2 levels.	Sorafenib	4-13	P53	Homo sapiens	67-70
22006587-8	2013	The sorafenib and nutlin-3 co-treatment lead to enhanced levels of p53, p-p53, and increase in the levels of p53 pro-apoptotic effector PUMA, Bax, and decrease in the anti-apoptotic Bcl-2 levels.	Sorafenib	4-13	P53	Homo sapiens	74-77
22006587-8	2013	The sorafenib and nutlin-3 co-treatment lead to enhanced levels of p53, p-p53, and increase in the levels of p53 pro-apoptotic effector PUMA, Bax, and decrease in the anti-apoptotic Bcl-2 levels.	Sorafenib	4-13	P53	Homo sapiens	74-77
23153533-2	2012	We found that the glycolytic enzyme phosphoglycerate mutase 1 (PGAM1), commonly upregulated in human cancers due to loss of TP53, contributes to biosynthesis regulation in part by controlling intracellular levels of its substrate, 3-phosphoglycerate (3-PG), and product, 2-phosphoglycerate (2-PG).	2-phosphoglycerate	271-289	P53	Homo sapiens	124-128
22006587-9	2013	Importantly, our studies revealed that sorafenib alone can activate p53 in a concentration dependent manner.	Sorafenib	39-48	P53	Homo sapiens	68-71
28849235-1	2017	Cellular tumor antigen p53 (p53) functions to maintain genomic stability and regulate cell apoptosis, while G protein-coupled receptor class C group 5 member A (GPCR5A) is a lung cancer suppressor gene whose expression is induced by retinoids.	Retinoids	233-242	P53	Homo sapiens	0-26
22006587-10	2013	Thus, co-treatment of nutlin-3 with sorafenib leads to increased half-life of p53, which in turn can be activated by sorafenib, to induce downstream pro-apoptotic and anti-proliferative effects.	Sorafenib	36-45	P53	Homo sapiens	78-81
22006587-10	2013	Thus, co-treatment of nutlin-3 with sorafenib leads to increased half-life of p53, which in turn can be activated by sorafenib, to induce downstream pro-apoptotic and anti-proliferative effects.	Sorafenib	117-126	P53	Homo sapiens	78-81
23117069-0	2012	Methyl methanesulfonate induces apoptosis in p53-deficient H1299 and Hep3B cells through a caspase 2- and mitochondria-associated pathway.	Methyl Methanesulfonate	0-23	P53	Homo sapiens	45-48
23117069-1	2012	Methyl methanesulfonate (MMS) has been shown to induce apoptosis in various cell types through p53-dependent pathways.	Methyl Methanesulfonate	0-23	P53	Homo sapiens	95-98
23117069-1	2012	Methyl methanesulfonate (MMS) has been shown to induce apoptosis in various cell types through p53-dependent pathways.	Methyl Methanesulfonate	25-28	P53	Homo sapiens	95-98
28901493-0	2017	High pemetrexed sensitivity of docetaxel-resistant A549 cells is mediated by TP53 status and downregulated thymidylate synthase.	Pemetrexed	5-15	P53	Homo sapiens	77-81
23117069-2	2012	Nevertheless, pharmacological and genetic blockade of p53 functions results in similar or delayed sensitivity to MMS treatment, suggesting the presence of p53-independent apoptotic mechanisms.	Methyl Methanesulfonate	113-116	P53	Homo sapiens	54-57
23117069-3	2012	To understand the p53-independent mechanisms that are engaged during MMS-induced apoptosis, we established MMS-induced apoptotic cell models using p53-deficient H1299 and Hep3B cells.	Methyl Methanesulfonate	107-110	P53	Homo sapiens	147-150
23117069-7	2012	These results demonstrated a p53- and p73-independent mechanism for MMS-induced apoptosis that involves the nuclear-cytosolic translocation of active caspase 2 as well as the mitochondria-mediated pathway.	Methyl Methanesulfonate	68-71	P53	Homo sapiens	29-32
23368925-11	2013	Our novel findings demonstrate that OL limits the growth and induces apoptosis in HT-29 cells via p53 pathway activation adapting the HIF-1alpha response to hypoxia.	oleuropein	36-38	P53	Homo sapiens	98-101
23859040-5	2013	The presence of pifithrin, an inhibitor of p53 function, blocked ECG-induced apoptosis as was manifested by restored cell viability and caspase-3 activity to control values and reestablished the balance among Bcl-2 anti- and proapoptotic protein levels.	pifithrin	16-25	P53	Homo sapiens	43-46
22689683-10	2012	CONCLUSIONS: Our data demonstrate that acute myeloid leukemia cells show a variable but overall good susceptibility to the innovative therapeutic combination of sorafenib+nutlin-3, which differentially involves the pro-apoptotic Bcl-2 family members Bax and Bak in p53(wild-type) and p53(deleted) cells.	Sorafenib	161-170	P53	Homo sapiens	265-268
28901493-0	2017	High pemetrexed sensitivity of docetaxel-resistant A549 cells is mediated by TP53 status and downregulated thymidylate synthase.	Docetaxel	31-40	P53	Homo sapiens	77-81
22689683-10	2012	CONCLUSIONS: Our data demonstrate that acute myeloid leukemia cells show a variable but overall good susceptibility to the innovative therapeutic combination of sorafenib+nutlin-3, which differentially involves the pro-apoptotic Bcl-2 family members Bax and Bak in p53(wild-type) and p53(deleted) cells.	Sorafenib	161-170	P53	Homo sapiens	284-287
24379902-2	2013	However, U373MG malignant glioma cells expressing mutant p53 are resistant to a 24 h quercetin treatment.	Quercetin	85-94	P53	Homo sapiens	57-60
24379902-5	2013	Furthermore, quercetin activated JNK and increased the expression of p53, which translocated to the mitochondria and simultaneously led to the release of cytochrome c from mitochondria to the cytosol.	Quercetin	13-22	P53	Homo sapiens	69-72
28901493-9	2017	The level of TS protein was significantly decreased in wild-type TP53-containing cells with DOC treatment; TS expression levels were not affected in mutant-TP53 and TP53-null cells under the same conditions.	Docetaxel	92-95	P53	Homo sapiens	65-69
29110583-10	2017	Meanwhile, at the protein level, beta-mangostin activated the formation of cleaved caspase-3 and caspase-9 and also upregulated the p53.	beta-Mangostin	33-47	P53	Homo sapiens	132-135
22893484-7	2012	5-AZA down-regulated MCL-1, known to mediate resistance to ABT-737, in a p53-independent manner.	Azacitidine	0-5	P53	Homo sapiens	73-76
23285810-2	2012	For the first time, our study indicated that neohesperidin also induces cell apoptosis in human breast adenocarcinoma MDA-MB-231 cells, which was possibly mediated by regulating the P53/Bcl-2/Bax pathway.	neohesperidin	45-58	P53	Homo sapiens	182-185
23091481-0	2012	Induction of p53-inducible microRNA miR-34 by gamma radiation and bleomycin are different.	Bleomycin	66-75	P53	Homo sapiens	13-16
29212215-5	2017	We examined the molecular mechanism of this cell death pathway, and found that B2 protein induces the P53/Bax-mediated apoptotic pathway in A549 cells, and that a P53 specific inhibitor (pifithrin-alpha) switches this response to RIP3-mediated necroptosis.	pifithrin	187-196	P53	Homo sapiens	102-105
29623239-5	2012	Forskolin treatment for up to 72 h resulted in 80% syncytialization, increased expression of Bcl-2 protein (P &lt; 0.01) and mRNA (P &lt; 0.05), and significantly decreased expression of protein and mRNA for Bax, p53, and caspases 3 and 8.	Colforsin	0-9	P53	Homo sapiens	213-216
23068099-6	2012	Although CAF-specific ER-activating abilities varied among individual cases, all CAFs maintained wild-type alleles for TP53 and PTEN.	cafs	81-85	P53	Homo sapiens	119-123
29212215-5	2017	We examined the molecular mechanism of this cell death pathway, and found that B2 protein induces the P53/Bax-mediated apoptotic pathway in A549 cells, and that a P53 specific inhibitor (pifithrin-alpha) switches this response to RIP3-mediated necroptosis.	pifithrin	187-196	P53	Homo sapiens	163-166
28573904-0	2017	Dichloroacetonitrile induces cytotoxicity through oxidative stress-mediated and p53-dependent apoptosis pathway in LO2 cells.	dichloroacetonitrile	0-20	P53	Homo sapiens	80-83
22922338-10	2012	Finally, capsazepine downregulated the expression of various antiapoptotic proteins (e.g., cFLIP and survivin) and increased the expression of proapoptotic proteins (e.g., Bax and p53).	capsazepine	9-20	P53	Homo sapiens	180-183
22948151-6	2012	Induction of p53 can be achieved by several means, such as UV radiation and treatment with anti-cancer agents (including doxorubicin, etoposide, roscovitine, flavopiridol, and nutlin-3).	Roscovitine	145-156	P53	Homo sapiens	13-16
22765290-3	2012	In this review, we focus on highlighting several representative plant natural compounds such as curcumin, resveratrol, paclitaxel, oridonin, quercetin and plant lectin - that may lead to cancer cell death - for regulation of some core autophagic pathways, involved in Ras-Raf signalling, Beclin-1 interactome, BCR-ABL, PI3KCI/Akt/mTOR, FOXO1 signalling and p53.	Quercetin	141-150	P53	Homo sapiens	357-360
22791815-0	2012	Chromium (VI) induces both bulky DNA adducts and oxidative DNA damage at adenines and guanines in the p53 gene of human lung cells.	Adenine	73-81	P53	Homo sapiens	102-105
22791815-0	2012	Chromium (VI) induces both bulky DNA adducts and oxidative DNA damage at adenines and guanines in the p53 gene of human lung cells.	Guanine	86-94	P53	Homo sapiens	102-105
22213398-8	2012	Finally, we isolated ursolic and oleanolic acids as the bioactive compounds able to upregulate p53 expression and inhibit breast cancer cell growth.	Oleanolic Acid	33-48	P53	Homo sapiens	95-98
22593008-3	2012	For this purpose, a amonafide analogue, 7-d (2-(3-(2-(Dimethylamino)ethylamino)propyl)-6-(dodecylamino)-1H-benzo[de]isoquinoline-1,3(2H)-dione) was screened, which exhibited high antitumor activity against p53-deficient human Chronic Myelogenous Leukemia (CML) K562 cells.	2-(3-(2-(dimethylamino)ethylamino)propyl)-6-(dodecylamino)-1H-benzo(de)isoquinoline-1,3(2H)-dione	45-142	P53	Homo sapiens	206-209
22791815-2	2012	However, both adenine (A) and guanine (G) mutations are found in the p53 gene in Cr exposure-related lung cancer.	Adenine	14-21	P53	Homo sapiens	69-72
28573904-7	2017	Therefore, we conclude that DCAN may activate apoptotic signals via p53 up-regulation and oxidative stress-mediated apoptosis in LO2 cells.	dichloroacetonitrile	28-32	P53	Homo sapiens	68-71
22791815-2	2012	However, both adenine (A) and guanine (G) mutations are found in the p53 gene in Cr exposure-related lung cancer.	Guanine	30-37	P53	Homo sapiens	69-72
22791815-5	2012	To understand the causes for these Cr-induced DNA damages, we mapped the distribution of BDA adducts and ODD in the p53 gene DNA fragments induced by Cr(III), Cr(VI) and Cr(V), the three major cellular Cr forms.	bda	89-92	P53	Homo sapiens	116-119
23017148-1	2012	BACKGROUND: Nucleoside analogs used in the chemotherapy of solid tumors, such as the capecitabine catabolite 5"-deoxy-5-fluorouridine (5"-DFUR) trigger a transcriptomic response that involves the aquaglyceroporin aquaporin 3 along with other p53-dependent genes.	Nucleosides	12-22	P53	Homo sapiens	242-245
22791815-9	2012	We propose that these Cr(VI)-induced BDA and ODD contribute to mutagenesis of the p53 gene that leads to lung carcinogenesis.	bda	37-40	P53	Homo sapiens	82-85
22993307-4	2012	Activation of p53 accounted for, at least in part, the growth inhibition by CHO27 in vitro.	cho27	76-81	P53	Homo sapiens	14-17
28927457-2	2017	All-trans retinoic acid (ATRA) and isotretinoin (13-cis retinoic acid) enhance p53 expression.	Isotretinoin	35-47	P53	Homo sapiens	79-82
22993307-6	2012	administration of CHO27 suppressed the growth of established PCa 22Rv1 xenograft tumors accompanied with p53 and p21(Cip1) induction.	cho27	18-23	P53	Homo sapiens	105-108
28927457-2	2017	All-trans retinoic acid (ATRA) and isotretinoin (13-cis retinoic acid) enhance p53 expression.	Isotretinoin	49-69	P53	Homo sapiens	79-82
22989009-0	2012	HDM2 antagonist MI-219 (spiro-oxindole), but not Nutlin-3 (cis-imidazoline), regulates p53 through enhanced HDM2 autoubiquitination and degradation in human malignant B-cell lymphomas.	spiro-oxindole	24-38	P53	Homo sapiens	87-90
28927457-7	2017	p53 induces FoxO1, FoxO3, p21 and sestrin 1, sestrin 2, and tumour necrosis factor-related apoptosis-inducing ligand (TRAIL), the key inducer of isotretinoin-mediated sebocyte apoptosis explaining isotretinoin"s sebum-suppressive effect.	Isotretinoin	145-157	P53	Homo sapiens	0-3
21633925-8	2012	Although not modulated, p53 appeared to enhance cells responsiveness to retinoid/ATRA combination.	Retinoids	72-80	P53	Homo sapiens	24-27
28927457-7	2017	p53 induces FoxO1, FoxO3, p21 and sestrin 1, sestrin 2, and tumour necrosis factor-related apoptosis-inducing ligand (TRAIL), the key inducer of isotretinoin-mediated sebocyte apoptosis explaining isotretinoin"s sebum-suppressive effect.	Isotretinoin	197-209	P53	Homo sapiens	0-3
28927105-5	2017	Subsequent to a 12 h treatment with low concentrations of teroxirone, MMP was suppressed, followed by ROS production and apoptosis in lung cancer cells carrying wild type p53.	teroxirone	58-68	P53	Homo sapiens	171-174
22734631-0	2012	An expeditious synthesis of the MDM2-p53 inhibitor AM-8553.	2-(5-(3-chlorophenyl)-6-(4-chlorophenyl)-1-(2-hydroxypentan-3-yl)-3-methyl-2-oxopiperidin-3-yl)acetic acid	51-58	P53	Homo sapiens	37-40
22723548-4	2012	Furthermore, Treg-mediated molecular control of senescence in responder T cells was associated with selective modulation of p38 and ERK1/2 signaling and cell-cycle-regulatory molecules p16, p21, and p53.	treg	13-17	P53	Homo sapiens	199-202
28478381-6	2017	Reduction in NADPH level leads to repression of HDAC1 activity and an increase in p53 acetylation.	NADP	13-18	P53	Homo sapiens	82-85
22627294-0	2012	Clioquinol induces DNA double-strand breaks, activation of ATM, and subsequent activation of p53 signaling.	Clioquinol	0-10	P53	Homo sapiens	93-96
22627294-6	2012	Activation of p53 by clioquinol was suggested, since clioquinol induced phosphorylation of p53 at Ser15 to enhance its stabilization.	Clioquinol	21-31	P53	Homo sapiens	14-17
22734631-1	2012	The development of the structurally complex MDM2/p53 inhibitor AM-8553 was impeded by the low yield of the initial synthesis.	2-(5-(3-chlorophenyl)-6-(4-chlorophenyl)-1-(2-hydroxypentan-3-yl)-3-methyl-2-oxopiperidin-3-yl)acetic acid	63-70	P53	Homo sapiens	49-52
28710427-5	2017	Transient resistance to bortezomib treatment was observed in p53-null cells that was later accompanied by an increase in levels and nuclear translocation of TAp73, an isoform of the p53-homologue p73, as well as induction of apoptosis.	Bortezomib	24-34	P53	Homo sapiens	61-64
22445862-0	2012	Docetaxel and 5-fluorouracil induce human p53 tumor suppressor gene transcription via a short sequence at core promoter element.	Docetaxel	0-9	P53	Homo sapiens	42-45
22445862-3	2012	Docetaxel (DOC), a member of the taxanes family that is widely used in cancer chemotherapy, activates p53 at the transcriptional level.	Docetaxel	0-9	P53	Homo sapiens	102-105
22445862-3	2012	Docetaxel (DOC), a member of the taxanes family that is widely used in cancer chemotherapy, activates p53 at the transcriptional level.	Docetaxel	11-14	P53	Homo sapiens	102-105
22445862-4	2012	We demonstrated that p53 is induced by low dose DOC treatment, resulting in MDR-1 gene suppression in human lung cancer cells.	Docetaxel	48-51	P53	Homo sapiens	21-24
22627294-6	2012	Activation of p53 by clioquinol was suggested, since clioquinol induced phosphorylation of p53 at Ser15 to enhance its stabilization.	Clioquinol	21-31	P53	Homo sapiens	91-94
22627294-6	2012	Activation of p53 by clioquinol was suggested, since clioquinol induced phosphorylation of p53 at Ser15 to enhance its stabilization.	Clioquinol	53-63	P53	Homo sapiens	14-17
22627294-6	2012	Activation of p53 by clioquinol was suggested, since clioquinol induced phosphorylation of p53 at Ser15 to enhance its stabilization.	Clioquinol	53-63	P53	Homo sapiens	91-94
22627294-9	2012	These results suggest that clioquinol-induced neurotoxicity is mediated by DSBs and subsequent activation of ATM/p53 signaling.	Clioquinol	27-37	P53	Homo sapiens	113-116
22736046-0	2012	The alpha-iso-cubebenol compound isolated from Schisandra chinensis induces             p53-independent pathway-mediated apoptosis in hepatocellular carcinoma cells.	alpha-iso-cubebenol	4-23	P53	Homo sapiens	88-91
28710427-5	2017	Transient resistance to bortezomib treatment was observed in p53-null cells that was later accompanied by an increase in levels and nuclear translocation of TAp73, an isoform of the p53-homologue p73, as well as induction of apoptosis.	Bortezomib	24-34	P53	Homo sapiens	182-185
28710427-8	2017	Thus, our results clearly demonstrated that TAp73 served as a substitute for p53 in bortezomib-induced apoptosis in p53-deficient or mutated cells, implicating that TAp73 could be a potential therapeutic target for treatment of CRCs, in particular those lacking functional p53.	Bortezomib	84-94	P53	Homo sapiens	116-119
22438244-2	2012	Using high-content videomicroscopy based on fluorescent TP53(+/+)  and TP53(-/-)  human colon carcinoma cells, we discovered that SP600125, a broad-spectrum serine/threonine kinase inhibitor, kills p53-deficient cells more efficiently than their p53-proficient counterparts, in vitro.	pyrazolanthrone	130-138	P53	Homo sapiens	56-60
22438244-2	2012	Using high-content videomicroscopy based on fluorescent TP53(+/+)  and TP53(-/-)  human colon carcinoma cells, we discovered that SP600125, a broad-spectrum serine/threonine kinase inhibitor, kills p53-deficient cells more efficiently than their p53-proficient counterparts, in vitro.	pyrazolanthrone	130-138	P53	Homo sapiens	71-75
22860996-0	2012	Allicin induces p53-mediated autophagy in Hep G2 human liver cancer cells.	allicin	0-7	P53	Homo sapiens	16-19
28710427-8	2017	Thus, our results clearly demonstrated that TAp73 served as a substitute for p53 in bortezomib-induced apoptosis in p53-deficient or mutated cells, implicating that TAp73 could be a potential therapeutic target for treatment of CRCs, in particular those lacking functional p53.	Bortezomib	84-94	P53	Homo sapiens	116-119
22860996-7	2012	Our results indicated that allicin induced p53-mediated autophagy and inhibited the viability of human hepatocellular carcinoma cell lines.	allicin	27-34	P53	Homo sapiens	43-46
22860996-8	2012	Using Western blotting, we observed that allicin decreased the level of cytoplasmic p53, the PI3K/mTOR signaling pathway, and the level of Bcl-2 and increased the expression of AMPK/TSC2 and Beclin-1 signaling pathways in Hep G2 cells.	allicin	41-48	P53	Homo sapiens	84-87
22438244-2	2012	Using high-content videomicroscopy based on fluorescent TP53(+/+)  and TP53(-/-)  human colon carcinoma cells, we discovered that SP600125, a broad-spectrum serine/threonine kinase inhibitor, kills p53-deficient cells more efficiently than their p53-proficient counterparts, in vitro.	pyrazolanthrone	130-138	P53	Homo sapiens	198-201
22438244-2	2012	Using high-content videomicroscopy based on fluorescent TP53(+/+)  and TP53(-/-)  human colon carcinoma cells, we discovered that SP600125, a broad-spectrum serine/threonine kinase inhibitor, kills p53-deficient cells more efficiently than their p53-proficient counterparts, in vitro.	pyrazolanthrone	130-138	P53	Homo sapiens	246-249
22519734-10	2012	Furthermore, blocking p53-mediated transcription using pifithrin significantly reduced apoptosis.	pifithrin	55-64	P53	Homo sapiens	22-25
28679691-0	2017	Metastatic triple-negative breast cancer patient with TP53 tumor mutation experienced 11 months progression-free survival on bortezomib monotherapy without adverse events after ending standard treatments with grade 3 adverse events.	Bortezomib	125-135	P53	Homo sapiens	54-58
22607268-5	2012	Inhibition of basal c-jun-NH2-terminal kinase (JNK) activity by JNK inhibitor SP600125 repressed PS1 transcription and PS1 protein expression by augmenting p53 protein level in SK-N-SH cells (Lee and Das 2008).	pyrazolanthrone	78-86	P53	Homo sapiens	156-159
21968939-6	2012	Apoptosis in lenalidomide/docetaxel-treated cells was increased by 2.2-fold over single agent docetaxel and a corresponding increase in p53, p38, and BAD activation was observed in Western blots (P &lt; 0.001).	Docetaxel	26-35	P53	Homo sapiens	136-139
28679691-10	2017	The success of bortezomib may be explained by the previously reported up-regulation of caspase-mediated apoptosis, which is p53-independent.	Bortezomib	15-25	P53	Homo sapiens	124-127
22507962-3	2012	The design of molecules based on this concept has allowed us to rapidly identify compounds having a 3-imidazolyl indole core structure as the first representatives of a new class of potent inhibitors of the p53-MDM2 interaction.	3-imidazolyl indole	100-119	P53	Homo sapiens	207-210
23150806-6	2012	The effect of NTP on the major stress-activated protein p53 was investigated.	ntp	14-17	P53	Homo sapiens	56-59
23150806-8	2012	NTP treatment caused an increase in the intracellular concentration of p53 and the induction of the p53-controlled regulon.	ntp	0-3	P53	Homo sapiens	71-74
23150806-8	2012	NTP treatment caused an increase in the intracellular concentration of p53 and the induction of the p53-controlled regulon.	ntp	0-3	P53	Homo sapiens	100-103
28498397-0	2017	Dihydroartemisinin inhibits the viability of cervical cancer cells by upregulating caveolin 1 and mitochondrial carrier homolog 2: Involvement of p53 activation and NAD(P)H:quinone oxidoreductase 1 downregulation.	artenimol	0-18	P53	Homo sapiens	146-149
23150806-9	2012	The p53-dependent accumulation of active proapoptotic caspase-3 was shown in NTP-treated cells.	ntp	77-80	P53	Homo sapiens	4-7
22509835-0	2012	Quercetin enhancement of arsenic-induced apoptosis via stimulating ROS-dependent p53 protein ubiquitination in human HaCaT keratinocytes.	Quercetin	0-9	P53	Homo sapiens	81-84
22509835-8	2012	QUE plus As(+3) stimulation of apoptosis in human HaCaT keratinocytes via activating ROS-dependent p53 protein ubiquitination may offer a rationale for the use of QUE to improve the clinical efficacy of arsenics in treating psoriasis.	Quercetin	0-3	P53	Homo sapiens	99-102
22103929-1	2012	BACKGROUND: To clarify the efficacy of grape seed procyanidin (GSP) on antiproliferative effects related to p53 functional status of oral squamous cell carcinoma (OSCC) for its chemoadjuvant potential.	procyanidin	50-61	P53	Homo sapiens	108-111
22570471-10	2012	GMX1778-mediated ROS induction is p53-dependent, suggesting that the status of both p53 and NAPRT1 might affect tumor apoptosis, as determined by annexin-V staining.	N-(6-chlorophenoxyhexyl)-N''-cyano-N''-4-pyridylguanidine	0-7	P53	Homo sapiens	34-37
22570471-10	2012	GMX1778-mediated ROS induction is p53-dependent, suggesting that the status of both p53 and NAPRT1 might affect tumor apoptosis, as determined by annexin-V staining.	N-(6-chlorophenoxyhexyl)-N''-cyano-N''-4-pyridylguanidine	0-7	P53	Homo sapiens	84-87
28498397-2	2017	Previous studies have revealed that the mechanisms involved in the inhibitory effects of DHA are based on theactivation of p53 and the mitochondrial-related cell death pathway.	artenimol	89-92	P53	Homo sapiens	123-126
28498397-6	2017	Moreover, we also found that the upregulation of Cav1 contributed to the DHA-mediated p53 activation and the downregulation of the redox enzyme, NAD(P)H:quinone oxidoreductase 1 (NQO1), which have been reported to contribute to the activation of the cell death pathway.	artenimol	73-76	P53	Homo sapiens	86-89
28498397-7	2017	Of note, we also found that DHA induced the nuclear translocation and accumulation of both Cav1 and p53, indicating a novel potential mechanism, namely the regulation of p53 activation by Cav1.	artenimol	28-31	P53	Homo sapiens	100-103
22183962-5	2012	The reduction in expression of mRNA for MAPK9, TP53, CDKN1A, and CDKN1B was greater in patients not receiving MTX than in those receiving low-dose MTX, with no difference in expression levels of CHEK2 and RANGAP1 mRNA between MTX-treated and non-MTX-treated patients.	Methotrexate	110-113	P53	Homo sapiens	47-51
22183962-5	2012	The reduction in expression of mRNA for MAPK9, TP53, CDKN1A, and CDKN1B was greater in patients not receiving MTX than in those receiving low-dose MTX, with no difference in expression levels of CHEK2 and RANGAP1 mRNA between MTX-treated and non-MTX-treated patients.	Methotrexate	147-150	P53	Homo sapiens	47-51
22160829-0	2012	Widdrol activates DNA damage checkpoint through the signaling Chk2-p53-Cdc25A-p21-MCM4 pathway in HT29 cells.	widdrol	0-7	P53	Homo sapiens	67-70
22160829-7	2012	Based on this result, the change of proteins related in checkpoint pathway was examined over a time course of 0.5-24 h. Treatment of HT29 cells with widdrol elicits the following: (1) phosphorylation of Chk2 and p53, (2) reduction of cell division cycle 25A (Cdc25A) expression, (3) increase of Cdk inhibitor p21 expression, and (4) decrease of the levels of Cdk2 and cyclin E expression in a time-dependent manner.	widdrol	149-156	P53	Homo sapiens	212-215
22183962-5	2012	The reduction in expression of mRNA for MAPK9, TP53, CDKN1A, and CDKN1B was greater in patients not receiving MTX than in those receiving low-dose MTX, with no difference in expression levels of CHEK2 and RANGAP1 mRNA between MTX-treated and non-MTX-treated patients.	Methotrexate	147-150	P53	Homo sapiens	47-51
28498397-7	2017	Of note, we also found that DHA induced the nuclear translocation and accumulation of both Cav1 and p53, indicating a novel potential mechanism, namely the regulation of p53 activation by Cav1.	artenimol	28-31	P53	Homo sapiens	170-173
22183962-5	2012	The reduction in expression of mRNA for MAPK9, TP53, CDKN1A, and CDKN1B was greater in patients not receiving MTX than in those receiving low-dose MTX, with no difference in expression levels of CHEK2 and RANGAP1 mRNA between MTX-treated and non-MTX-treated patients.	Methotrexate	147-150	P53	Homo sapiens	47-51
22307140-4	2012	Specifically, we focus on the functions of p53 in regulating aerobic glycolysis, oxidative phosphorylation, the pentose phosphate pathway, fatty acid synthesis and oxidation, and glutamine metabolism, and we discuss the therapeutic strategy whereby p53 helps to prevent malignant progression.	Pentosephosphates	112-129	P53	Homo sapiens	43-46
22183962-7	2012	In tissue culture, MTX induced expression of both p53 and p21 by JNK-2- and JNK-1-dependent mechanisms, respectively, while CHEK2 and RANGAP1 were not induced by MTX.	Methotrexate	19-22	P53	Homo sapiens	50-53
28398592-7	2017	TBT activated apoptosis in developing B cells at environmentally relevant concentrations (as low as 80 nM) in vitro, via a mechanism that is distinct from that induced by high dose (muM) TBT and that requires p53.	tributyltin	0-3	P53	Homo sapiens	209-212
22324515-7	2012	Bad, p53, p21 and p27 were downregulated by neuropeptides in PC-3, and these effects were reversed with the addition of bortezomib.	Bortezomib	120-130	P53	Homo sapiens	5-8
22012334-0	2012	Evidence supporting a role for dihydroorotate dehydrogenase, bioenergetics, and p53 in selective teriflunomide-induced apoptosis in transformed versus normal human keratinocytes.	teriflunomide	97-110	P53	Homo sapiens	80-83
22179765-8	2012	Furthermore, VI-16 could             significantly increase the loss of mitochondrial membrane potential and the expression             of p53.	vi-16	13-18	P53	Homo sapiens	139-142
21445621-0	2012	The citrus flavonoid hesperidin induces p53 and inhibits NF-kappaB activation in order to trigger apoptosis in NALM-6 cells: involvement of PPARgamma-dependent mechanism.	Flavonoids	11-20	P53	Homo sapiens	40-43
28658321-5	2017	RESULTS: STMN1 was downregulated and p53 was upregulated in the villus tissue from patients with RSA.	rabbit sperm membrane autoantigen	97-100	P53	Homo sapiens	37-40
21351099-8	2012	In vitro, low-dose DOC, which did not induce G2/M arrest, increased p53 and p21 and resulted in down-regulation of TS in C4-2 cells, and down-regulation of TS is considered to be responsible for the synergistic effect of S-1 in vivo.	Docetaxel	19-22	P53	Homo sapiens	68-71
22764405-0	2012	MR traceable delivery of p53 tumor suppressor gene by PEI-functionalized superparamagnetic iron oxide nanoparticles.	ferric oxide	91-101	P53	Homo sapiens	25-28
28476378-5	2017	Moreover, we found that the mechanism underlying NS-mediated sorafenib resistance involved dysregulated expression of p53, and downstream Bax and Bcl-2 proteins.	Sorafenib	61-70	P53	Homo sapiens	118-121
22491426-5	2012	Furthermore, rRNA fragmentation was suppressed by the p53 inhibitors pifithrin-alpha and pifithrin-mu as well as the pan caspase inhibitor Z-VAD-FMK.	pifithrin	69-78	P53	Homo sapiens	54-57
22491426-5	2012	Furthermore, rRNA fragmentation was suppressed by the p53 inhibitors pifithrin-alpha and pifithrin-mu as well as the pan caspase inhibitor Z-VAD-FMK.	pifithrin	89-98	P53	Homo sapiens	54-57
23038158-11	2012	CONCLUSIONS: These results suggest that the APE1 Asp/Asp genotype and the combination of the APE1 Asp/Asp and hOGG1-Cys variants are associated with increased risk of p53 mutation in non-small cell lung cancer.	Aspartic Acid	49-52	P53	Homo sapiens	167-170
23038158-11	2012	CONCLUSIONS: These results suggest that the APE1 Asp/Asp genotype and the combination of the APE1 Asp/Asp and hOGG1-Cys variants are associated with increased risk of p53 mutation in non-small cell lung cancer.	Aspartic Acid	53-56	P53	Homo sapiens	167-170
23038158-11	2012	CONCLUSIONS: These results suggest that the APE1 Asp/Asp genotype and the combination of the APE1 Asp/Asp and hOGG1-Cys variants are associated with increased risk of p53 mutation in non-small cell lung cancer.	Aspartic Acid	53-56	P53	Homo sapiens	167-170
23038158-11	2012	CONCLUSIONS: These results suggest that the APE1 Asp/Asp genotype and the combination of the APE1 Asp/Asp and hOGG1-Cys variants are associated with increased risk of p53 mutation in non-small cell lung cancer.	Aspartic Acid	53-56	P53	Homo sapiens	167-170
22427654-0	2012	Sulforaphane induction of p21(Cip1) cyclin-dependent kinase inhibitor expression requires p53 and Sp1 transcription factors and is p53-dependent.	sulforaphane	0-12	P53	Homo sapiens	90-93
28631571-14	2017	The above-mentioned characteristics were reverted by treatment of with pifithrin-a, a p53 inhibitor.	pifithrin	71-82	P53	Homo sapiens	86-89
22427654-0	2012	Sulforaphane induction of p21(Cip1) cyclin-dependent kinase inhibitor expression requires p53 and Sp1 transcription factors and is p53-dependent.	sulforaphane	0-12	P53	Homo sapiens	131-134
22103910-0	2012	Topical grape seed proanthocyandin extract reduces sunburn cells and mutant p53 positive epidermal cell formation, and prevents depletion of Langerhans cells in an acute sunburn model.	proanthocyandin	19-34	P53	Homo sapiens	76-79
23300844-3	2012	We show here that low-dose 5-aza treatment results in DNA damage and induction of p53 in NT2/D1 cells.	Azacitidine	27-32	P53	Homo sapiens	82-85
23300844-5	2012	Low-dose 5-aza induces a p53 transcriptional signature distinct from that induced with cisplatin in NT2/D1 cells and also uniquely downregulates genes associated with pluripotency including NANOG, SOX2, GDF3 and Myc target genes.	Azacitidine	9-14	P53	Homo sapiens	25-28
28153791-3	2017	In this study, we show that an HDAC6-selective inhibitor, A452, increased wild-type p53 levels by destabilizing MDM2, but decreased mutant p53 by inducing MDM2 and inhibiting Hsp90-mutant p53 complex formation.	Tetramethylammonium azide	58-62	P53	Homo sapiens	84-87
23300844-6	2012	Changes in the p53 and pluripotency signatures with 5-aza were to a large extent dependent on high levels of DNMT3B.	Azacitidine	52-57	P53	Homo sapiens	15-18
23300844-7	2012	In contrast to the majority of p53 target genes upregulated by 5-aza that did not show DNA hypomethylation, several other genes induced with 5-aza had corresponding decreases in promoter methylation.	Azacitidine	63-68	P53	Homo sapiens	31-34
23300844-9	2012	Our studies suggest that the hypersensitivity of NT2/D1 cells to low-dose 5-aza is multifactorial and involves the combined activation of p53 targets, repression of pluripotency genes, and activation of genes repressed by DNA methylation.	Azacitidine	74-79	P53	Homo sapiens	138-141
22655279-2	2012	Two most commonly studied polymorphisms that were shown to affect the biochemical functions of p53 protein are the exon 4 Arg72pro and Intron 3 16 bp Del/Ins polymorphisms.	arg72pro	122-130	P53	Homo sapiens	95-98
22537194-8	2012	We show that an increment of the intracellular reactive oxygen species (ROS) and p53 is required for MTA-induced cytotoxicity by utilizing N-Acetyl-L-Cysteine (NAC) to blockage of ROS and p53-defective H1299 NSCLC cell line.	Pemetrexed	101-104	P53	Homo sapiens	81-84
22537194-8	2012	We show that an increment of the intracellular reactive oxygen species (ROS) and p53 is required for MTA-induced cytotoxicity by utilizing N-Acetyl-L-Cysteine (NAC) to blockage of ROS and p53-defective H1299 NSCLC cell line.	Pemetrexed	101-104	P53	Homo sapiens	188-191
23251470-5	2012	The treatment of ALL leukemic cells with sulforaphane resulted in dose-dependent apoptosis and G2/M cell cycle arrest, which was associated with the activation of caspases (3, 8, and 9), inactivation of PARP, p53-independent upregulation of p21(CIP1/WAF1), and inhibition of the Cdc2/Cyclin B1 complex.	sulforaphane	41-53	P53	Homo sapiens	209-212
28153791-3	2017	In this study, we show that an HDAC6-selective inhibitor, A452, increased wild-type p53 levels by destabilizing MDM2, but decreased mutant p53 by inducing MDM2 and inhibiting Hsp90-mutant p53 complex formation.	Tetramethylammonium azide	58-62	P53	Homo sapiens	139-142
28153791-3	2017	In this study, we show that an HDAC6-selective inhibitor, A452, increased wild-type p53 levels by destabilizing MDM2, but decreased mutant p53 by inducing MDM2 and inhibiting Hsp90-mutant p53 complex formation.	Tetramethylammonium azide	58-62	P53	Homo sapiens	139-142
22445757-0	2012	The p53 inhibitor, pifithrin-alpha, suppresses self-renewal of embryonic stem cells.	pifithrin	19-34	P53	Homo sapiens	4-7
27903750-3	2017	Inhibition of CRM1, the nuclear export carrier protein, hampered protein export and synergistically enhanced the cytotoxic action of bortezomib on colon cancer cells containing wild-type p53, which underwent G2-M cell-cycle block and apoptosis.	Bortezomib	133-143	P53	Homo sapiens	187-190
22445757-3	2012	In this study, we investigated the effect of pifithrin (PFT)-alpha, an inhibitor of p53-dependent transcriptional activation, on self-renewal of ES cells.	pifithrin	45-54	P53	Homo sapiens	84-87
22353755-4	2012	We have previously shown that inhibition of basal activity of c-jun-NH2-terminal kinase (JNK) with JNK-specific inhibitor SP600125 represses the expression of PS1 and gamma-secretase activity by increasing p53 level in SK-N-SH cell line in vitro (Lee and Das, 2008, 2010).	pyrazolanthrone	122-130	P53	Homo sapiens	206-209
23226303-8	2012	Mechanistic studies of apoptotic pathways indicated that bortezomib induced activation of p53 and Bax, as well as cleavage of caspases and poly-ADP-ribose polymerase (PARP) in exposed chondrocytes.	Bortezomib	57-67	P53	Homo sapiens	90-93
22662219-7	2012	P53 reactivation substantially improved the apoptotic response after effective KIT inhibition with sunitinib and 17-AAG in IM-resistant cell lines.	tanespimycin	113-119	P53	Homo sapiens	0-3
27903750-5	2017	Moreover, knockdown of p53 significantly reduced the synergistic cytotoxic action of bortezomib and KPT330 on p53+/+ HCT116 cells.	Bortezomib	85-95	P53	Homo sapiens	23-26
22479585-0	2012	Bak compensated for Bax in p53-null cells to release cytochrome c for the initiation of mitochondrial signaling during Withanolide D-induced apoptosis.	Withanolides	119-130	P53	Homo sapiens	27-30
27903750-5	2017	Moreover, knockdown of p53 significantly reduced the synergistic cytotoxic action of bortezomib and KPT330 on p53+/+ HCT116 cells.	Bortezomib	85-95	P53	Homo sapiens	110-113
22479585-2	2012	Present study reports that Withanolide D (WithaD), a steroidal lactone isolated from Withania somnifera, induced cellular apoptosis in which mitochondria and p53 were intricately involved.	withanolide D	27-40	P53	Homo sapiens	158-161
22479585-2	2012	Present study reports that Withanolide D (WithaD), a steroidal lactone isolated from Withania somnifera, induced cellular apoptosis in which mitochondria and p53 were intricately involved.	withanolide D	42-48	P53	Homo sapiens	158-161
21915628-5	2012	In addition, flavonoids isolated from Velloziaceae showed an inhibitory effect on mutations in p53, which is mutated and nonfunctional in more than 50% of cases of human cancer.	Flavonoids	13-23	P53	Homo sapiens	95-98
27903750-7	2017	These results indicate that nuclear p53 is a major mediator in the synergistic antitumor effect of bortezomib and KPT330, and provides a rationale for the use of proteasome inhibitor together with nuclear export blocker in the treatment of colorectal cancer.	Bortezomib	99-109	P53	Homo sapiens	36-39
28349922-0	2017	Coumarin-chalcone hybrid instigates DNA damage by minor groove binding and stabilizes p53 through post translational modifications.	coumarin	0-8	P53	Homo sapiens	86-89
28336971-4	2017	A natural flavonoid acacetin is then identified to be capable of modulating RARgamma-dependent AKT-p53 network.	Flavonoids	10-19	P53	Homo sapiens	99-102
22223137-2	2012	We examined whether forced expression of p53 inhibited growth of mesothelioma cells and produced anti-tumor effects by a combination of cisplatin (CDDP) or pemetrexed (PEM), the first-line drugs for mesothelioma treatments.	Pemetrexed	168-171	P53	Homo sapiens	41-44
22223137-6	2012	Transduction with Ad-p53 suppressed viability of mesothelioma cells and augmented the growth inhibition by CDDP or PEM mostly in a synergistic manner.	Pemetrexed	115-118	P53	Homo sapiens	21-24
22276160-9	2012	Disruption of the JNK signal pathway by small interfering RNA (siRNA) against JNK or JNK specific inhibitor, SP-600125 inhibited the activation of p53 and attenuated apoptosis induced by RITA in myeloma cells carrying wild type p53.	pyrazolanthrone	109-118	P53	Homo sapiens	147-150
22276160-9	2012	Disruption of the JNK signal pathway by small interfering RNA (siRNA) against JNK or JNK specific inhibitor, SP-600125 inhibited the activation of p53 and attenuated apoptosis induced by RITA in myeloma cells carrying wild type p53.	pyrazolanthrone	109-118	P53	Homo sapiens	228-231
28024576-6	2017	We have found that apoptosis induced by RSV-DF was associated with the higher expression of p53, caspase-3, and BAX than the free RSV.	rsv-df	40-46	P53	Homo sapiens	92-95
23350039-7	2012	O-linked attachment of GlcNAc to Ser and Thr residues regulates a variety of intracellular proteins, including transcription factors such as NFkappaB, c-myc and p53.	Acetylglucosamine	23-29	P53	Homo sapiens	161-164
22010212-7	2011	In the subgroup of primary ALL cells, with low expression of caspase-8, methotrexate (MTX) upregulated the expression of caspase-8 mediated by the transcription factor p53, suggesting epigenetic silencing of caspase-8.	Methotrexate	72-84	P53	Homo sapiens	168-171
22283740-5	2012	Pifithrin-alpha (PFT-alpha), a specific inhibitor of p53, reduced ROS production and reversed silibinin"s growth-inhibitory effect.	pifithrin	0-15	P53	Homo sapiens	53-56
22225791-9	2012	AMPKalpha(-/-)-MEFs showed increased basal levels of p53 and cyclin-dependent kinase inhibitors p21(cip1), but lack of response of both genes to IR.	ampkalpha	0-9	P53	Homo sapiens	53-56
27846743-7	2017	RESULTS: We found altered expression of several proteins after enalapril treatment (decreased: NFkappaB, p = .043; NLRP3, p = .050; AMACR, p = .017; and caspase 3, p = .025; increased: p53, p = .050).	Enalapril	63-72	P53	Homo sapiens	185-188
21765469-0	2012	Inhibition of p53 expression by peptide-conjugated phosphorodiamidate morpholino oligomers sensitizes human cancer cells to chemotherapeutic drugs.	phosphorodiamidate morpholino	51-80	P53	Homo sapiens	14-17
22093905-3	2012	We showed a growth inhibition effect, which increased with the p53 protein expression level in recombinant Mut(s)  (methanol utilization slow) strain of Pichia.	Methanol	116-124	P53	Homo sapiens	63-66
21982800-5	2011	RCC patients with the p53Arg/Arg genotype had a signicantly low percentage of inorganic arsenic, a low percentage of monomethylarsonic acid (MMA), and a high percentage of dimethylarsinic acid (DMA), which indicates efcient arsenic methylation capacity.	Cacodylic Acid	172-192	P53	Homo sapiens	22-25
21982800-5	2011	RCC patients with the p53Arg/Arg genotype had a signicantly low percentage of inorganic arsenic, a low percentage of monomethylarsonic acid (MMA), and a high percentage of dimethylarsinic acid (DMA), which indicates efcient arsenic methylation capacity.	Cacodylic Acid	194-197	P53	Homo sapiens	22-25
28211885-0	2017	The novel BMI-1 inhibitor PTC596 downregulates MCL-1 and induces p53-independent mitochondrial apoptosis in acute myeloid leukemia progenitor cells.	PTC596	26-32	P53	Homo sapiens	65-68
28211885-7	2017	PTC596 induced apoptosis in a p53-independent manner.	PTC596	0-6	P53	Homo sapiens	30-33
24319543-2	2012	In the present investigation, we observed that C6-ceramide induces p53-dependent apoptosis and effectively killed the Astrocytoma grade4 (Glioblastoma Multiforme) HTB12 cell lines.	N-caproylsphingosine	47-58	P53	Homo sapiens	67-70
28028695-9	2017	An increase in p53 levels was detected following 5-FU treatment; pifithrin-alpha, an inhibitor of p53 activation, reversed 5-FU-induced SESN2 expression.	pifithrin	65-74	P53	Homo sapiens	15-18
21607615-2	2012	A guanine (G)/cytosine (C) common single nucleotide polymorphism (SNP) at second position of codon 72 in exon 4 of p53 gene determines a arginine (Arg) to proline (Pro) (Arg72Pro) aminoacidic substitution within the proline-rich domain of p53 protein.	Guanine	2-9	P53	Homo sapiens	115-118
21607615-2	2012	A guanine (G)/cytosine (C) common single nucleotide polymorphism (SNP) at second position of codon 72 in exon 4 of p53 gene determines a arginine (Arg) to proline (Pro) (Arg72Pro) aminoacidic substitution within the proline-rich domain of p53 protein.	Guanine	2-9	P53	Homo sapiens	239-242
21607615-2	2012	A guanine (G)/cytosine (C) common single nucleotide polymorphism (SNP) at second position of codon 72 in exon 4 of p53 gene determines a arginine (Arg) to proline (Pro) (Arg72Pro) aminoacidic substitution within the proline-rich domain of p53 protein.	Cytosine	14-22	P53	Homo sapiens	115-118
21196432-5	2011	Both strategies could use tyrosinase-mediated activation of quercetin, a dietary polyphenol that induces the expression of p53 and modulates reactive oxygen species.	Quercetin	60-69	P53	Homo sapiens	123-126
21196432-6	2011	In addition to antitumor signaling properties, activation of quercetin could complement conventional cancer therapy by the induction of phase II detoxification enzymes resulting in p53 stabilization and transduction of its downstream targets.	Quercetin	61-70	P53	Homo sapiens	181-184
22116673-8	2011	Furthermore, we showed that GTE inhibited Akt activation and the levels of mutant p53 protein, and induced apoptosis and growth suppression of the cells.	gte	28-31	P53	Homo sapiens	82-85
28028695-9	2017	An increase in p53 levels was detected following 5-FU treatment; pifithrin-alpha, an inhibitor of p53 activation, reversed 5-FU-induced SESN2 expression.	pifithrin	65-74	P53	Homo sapiens	98-101
22515118-0	2012	Geranylgeranylacetone attenuates cisplatin-induced reductions in cell viability by suppressing the elevation of intracellular p53 content without heat shock protein induction.	geranylgeranylacetone	0-21	P53	Homo sapiens	126-129
27637603-0	2017	The Presence of Serum p53 Antibody Predicts the Pathological Tumor Response to Neoadjuvant Chemotherapy with Docetaxel, Cisplatin and Fluorouracil (DCF) in Esophageal Squamous Cell Carcinoma.	Docetaxel	109-118	P53	Homo sapiens	22-25
22272214-0	2012	Cucurbitacin E Induces G(2)/M Phase Arrest through STAT3/p53/p21 Signaling and Provokes Apoptosis via Fas/CD95 and Mitochondria-Dependent Pathways in Human Bladder Cancer T24 Cells.	cucurbitacin E	0-14	P53	Homo sapiens	57-60
21331782-7	2011	In both MCC cell lines, we could detect a p53 missense mutation at codon 193 (exon 6) with a change in amino acids (His   Leu).	Leucine	122-125	P53	Homo sapiens	42-45
27936464-8	2017	Guadecitabine mediated transcriptional reprogramming of EC cells included induction of p53 targets and repression of pluripotency genes.	guadecitabine	0-13	P53	Homo sapiens	87-90
21859809-4	2011	Moreover, MCP-1 upregulated p53 expression of HUVECs and the p53-specific inhibitor pifithrin-alpha (PFTalpha) rescued the MCP-1-induced apoptosis of HUVECs.	pifithrin	84-99	P53	Homo sapiens	61-64
21859809-4	2011	Moreover, MCP-1 upregulated p53 expression of HUVECs and the p53-specific inhibitor pifithrin-alpha (PFTalpha) rescued the MCP-1-induced apoptosis of HUVECs.	pifithrin	101-109	P53	Homo sapiens	61-64
21965740-9	2011	Genistein and quercetin induced extrinsic apoptosis pathway, up-regulating p53.	Quercetin	14-23	P53	Homo sapiens	75-78
22202062-0	2012	Operation "p53 Hunt" to combat cancer: theaflavins in action.	theaflavin	39-50	P53	Homo sapiens	11-14
22202062-2	2012	Regulation of anti-tumor p53 functions by dietary plant polyphenols particularly black tea and its active component theaflavins has gained immense recognition from the point of view of both efficacy and safety.	theaflavin	116-127	P53	Homo sapiens	25-28
22202062-3	2012	This review highlights the complexities of p53 functions, molecular mechanisms of its inactivation in cancer, and therapeutic strategies for rescuing p53 dysfunction in tumors using theaflavins.	theaflavin	182-193	P53	Homo sapiens	150-153
27936464-11	2017	Genome-wide analysis indicated that in vivo antitumor activity was associated with activation of p53 and immune-related pathways and the antitumor effects of guadecitabine were dependent on p53, a gene rarely mutated in TGCTs.	guadecitabine	158-171	P53	Homo sapiens	190-193
22202062-4	2012	It describes how theaflavins, by steering a single molecular target - p53, regulate multiple hallmarks of carcinogenesis i.e., tumor glycolysis, angiogenesis, metastasis, apoptosis and drug resistance.	theaflavin	17-28	P53	Homo sapiens	70-73
22202062-5	2012	Additionally, considering the rising of the current concept of cancer stem cells (CSCs), the sole participant in tumor evolution, the review discusses about the possible role of theaflavin-p53 cross talk in targeting CSCs.	theaflavin	178-188	P53	Homo sapiens	189-192
28071670-0	2017	Benzyl Isothiocyanate potentiates p53 signaling and antitumor effects against breast cancer through activation of p53-LKB1 and p73-LKB1 axes.	benzyl isothiocyanate	0-21	P53	Homo sapiens	34-37
22202062-6	2012	Such attempts to target the complexities of p53 functions during neogenesis will be of immense help in developing a "new" strategy for successful cancer prevention and therapy by theaflavins.	theaflavin	179-190	P53	Homo sapiens	44-47
21557998-0	2011	Sulforaphane induces cytotoxicity and lysosome- and mitochondria-dependent cell death in colon cancer cells with deleted p53.	sulforaphane	0-12	P53	Homo sapiens	121-124
28071670-0	2017	Benzyl Isothiocyanate potentiates p53 signaling and antitumor effects against breast cancer through activation of p53-LKB1 and p73-LKB1 axes.	benzyl isothiocyanate	0-21	P53	Homo sapiens	114-117
28957796-0	2017	Wild-Type P53 Induces Sodium/Iodide Symporter Expression Allowing Radioiodide Therapy in Anaplastic Thyroid Cancer.	Iodides	29-35	P53	Homo sapiens	10-13
21654191-1	2011	The combined treatment with nanomolar doses of the PPARgamma ligand Rosiglitazone (BRL) and the RXR ligand 9-cis-retinoic acid (9RA) induces a p53-dependent apoptosis in MCF7, SKBR3 and T47D human breast cancer cells.	Alitretinoin	107-126	P53	Homo sapiens	143-146
23075517-8	2012	The 5-year DSS rate for patients with a p53 mutation was 84.4%, compared with 97.1% for patients without.	dss	11-14	P53	Homo sapiens	40-43
27721019-5	2016	BAY61-3606-induced the up-regulation of DR4 is p53-dependent.	2-(7-(3,4-dimethoxyphenyl)imidazo(1,2-c)pyrimidin-5-ylamino)nicotinamide	0-10	P53	Homo sapiens	47-50
23038158-0	2012	The APE1 Asp/Asp genotype and the combination of APE1 Asp/Asp and hOGG1-Cys variants are associated with increased p53 mutation in non-small cell lung cancer.	Aspartic Acid	9-12	P53	Homo sapiens	115-118
23038158-0	2012	The APE1 Asp/Asp genotype and the combination of APE1 Asp/Asp and hOGG1-Cys variants are associated with increased p53 mutation in non-small cell lung cancer.	Aspartic Acid	13-16	P53	Homo sapiens	115-118
23038158-0	2012	The APE1 Asp/Asp genotype and the combination of APE1 Asp/Asp and hOGG1-Cys variants are associated with increased p53 mutation in non-small cell lung cancer.	Aspartic Acid	13-16	P53	Homo sapiens	115-118
23038158-0	2012	The APE1 Asp/Asp genotype and the combination of APE1 Asp/Asp and hOGG1-Cys variants are associated with increased p53 mutation in non-small cell lung cancer.	Aspartic Acid	13-16	P53	Homo sapiens	115-118
23038158-9	2012	However, a higher risk of p53 mutation was found in participants with the APE1 Asp/Asp genotype than in those with the APE1-Glu allele (OR, 2.15; 95% CI, 1.19-3.87; P = 0.011).	Aspartic Acid	79-82	P53	Homo sapiens	26-29
21525791-0	2011	TOFA (5-tetradecyl-oxy-2-furoic acid) reduces fatty acid synthesis, inhibits expression of AR, neuropilin-1 and Mcl-1 and kills prostate cancer cells independent of p53 status.	5-(tetradecyloxy)-2-furancarboxylic acid	0-4	P53	Homo sapiens	165-168
21519792-0	2011	Lupulone triggers p38 MAPK-controlled activation of p53 and of the TRAIL receptor apoptotic pathway in human colon cancer-derived metastatic cells.	lupulon	0-8	P53	Homo sapiens	52-55
21519792-6	2011	In contrast to JNK and ERK inhibition, the specific inactivation of p38 inhibited the lupulone-triggered up-regulation of p53 and TRAIL-death receptor DR4/DR5 expression, and prevented DNA fragmentation.	lupulon	86-94	P53	Homo sapiens	122-125
23038158-9	2012	However, a higher risk of p53 mutation was found in participants with the APE1 Asp/Asp genotype than in those with the APE1-Glu allele (OR, 2.15; 95% CI, 1.19-3.87; P = 0.011).	Aspartic Acid	83-86	P53	Homo sapiens	26-29
23038158-10	2012	The risk of p53 mutation was also higher in participants with APE1 Asp/Asp plus hOGG1-Cys than in those with APE1-Glu plus hOGG1 Ser/Ser (OR, 3.72; 95% CI, 1.33-10.40; P = 0.012).	Aspartic Acid	67-70	P53	Homo sapiens	12-15
23038158-10	2012	The risk of p53 mutation was also higher in participants with APE1 Asp/Asp plus hOGG1-Cys than in those with APE1-Glu plus hOGG1 Ser/Ser (OR, 3.72; 95% CI, 1.33-10.40; P = 0.012).	Aspartic Acid	71-74	P53	Homo sapiens	12-15
23300887-13	2012	Inhibitor of p53, pifithrin-alpha, attenuated the anti-cancer effects of SDGE and apoptosis was also not observed in the p53(neg) SKOV-3 cells.	pifithrin	18-33	P53	Homo sapiens	13-16
21519792-9	2011	Our data support the view that the lupulone-triggered enhanced expression of p38 plays a major role in the activation of p53 and of the TRAIL-death receptor apoptotic pathway in SW620 human colon cancer-derived metastatic cells.	lupulon	35-43	P53	Homo sapiens	121-124
21619452-5	2011	MATERIALS AND METHODS: In cell cultures, we investigated the effects of forskolin/3-isobutyl-1-methylxanthine (IBMX) on stimulated p53 of ALL cell lines.	Colforsin	72-81	P53	Homo sapiens	131-134
21344307-0	2011	2ME and 2OHE2 exhibit growth inhibitory effects and cell cycle arrest at G2/M in RL95-2 human endometrial cancer cells through activation of p53 and Chk1.	2-hydroxyestradiol	8-13	P53	Homo sapiens	141-144
27721019-6	2016	Knockout of p53 decreased BAY61-3606-induced DR4 expression and inhibited the effect of BAY61-3606 on TRAIL-induced apoptosis.	2-(7-(3,4-dimethoxyphenyl)imidazo(1,2-c)pyrimidin-5-ylamino)nicotinamide	26-36	P53	Homo sapiens	12-15
26332341-6	2016	Confocal laser systems microscopy was used for examining the protein translocation and results show that BDMC increased the translocation of p-p53 and p-H2A.X (phospho Ser140) from cytosol to nuclei in NCI-H460 cells.	bisdemethoxycurcumin	105-109	P53	Homo sapiens	143-146
21459798-5	2011	In addition, bortezomib increases expression of p53 and Noxa.	Bortezomib	13-23	P53	Homo sapiens	48-51
22962590-9	2012	Compared to either ribavirin or IFN-alpha alone, ribavirin plus IFN-alpha resulted in greater p53 activation and HCV suppression.	Ribavirin	49-58	P53	Homo sapiens	94-97
22962590-10	2012	We further identified ERK1/2 that linked ribavirin signals to p53 activation.	Ribavirin	41-50	P53	Homo sapiens	62-65
22962590-11	2012	More importantly, knockdown of ERK1/2 and p53 partially mitigated the inhibitory effects of ribavirin on the HCV replication, indicating that ERK1/2-p53 pathway was involved in the anti-HCV effects of ribavirin.	Ribavirin	92-101	P53	Homo sapiens	42-45
22962590-11	2012	More importantly, knockdown of ERK1/2 and p53 partially mitigated the inhibitory effects of ribavirin on the HCV replication, indicating that ERK1/2-p53 pathway was involved in the anti-HCV effects of ribavirin.	Ribavirin	92-101	P53	Homo sapiens	149-152
22962590-11	2012	More importantly, knockdown of ERK1/2 and p53 partially mitigated the inhibitory effects of ribavirin on the HCV replication, indicating that ERK1/2-p53 pathway was involved in the anti-HCV effects of ribavirin.	Ribavirin	201-210	P53	Homo sapiens	42-45
22962590-11	2012	More importantly, knockdown of ERK1/2 and p53 partially mitigated the inhibitory effects of ribavirin on the HCV replication, indicating that ERK1/2-p53 pathway was involved in the anti-HCV effects of ribavirin.	Ribavirin	201-210	P53	Homo sapiens	149-152
22962590-12	2012	CONCLUSION: Ribavirin stimulates ERK1/2 and subsequently promotes p53 activity which at least partly contributes to the enhanced antiviral response of IFN-alpha plus ribavirin against HCV.	Ribavirin	12-21	P53	Homo sapiens	66-69
21481270-0	2011	Evaluation of HER2 and p53 expression in predicting response to docetaxel-based first-line chemotherapy in advanced breast cancer.	Docetaxel	64-73	P53	Homo sapiens	23-26
27432063-8	2016	These results indicated that over expression of miR-200c might enhance the sensitivity of A549 cells to methotrexate through the P53/P21 pathway.	Methotrexate	104-116	P53	Homo sapiens	129-132
21481270-2	2011	We explore the value of HER2 and p53 status to foretell docetaxel sensitivity in advanced breast cancer.	Docetaxel	56-65	P53	Homo sapiens	33-36
21278235-9	2011	Inhibition of ceramide synthase with fumonisin B1 prevented p53 reactivation induced by GCS silencing, whereas addition of exogenous C6-ceramide reactivated p53 function in p53-mutant cells.	N-caproylsphingosine	133-144	P53	Homo sapiens	157-160
21278235-9	2011	Inhibition of ceramide synthase with fumonisin B1 prevented p53 reactivation induced by GCS silencing, whereas addition of exogenous C6-ceramide reactivated p53 function in p53-mutant cells.	N-caproylsphingosine	133-144	P53	Homo sapiens	157-160
22962590-12	2012	CONCLUSION: Ribavirin stimulates ERK1/2 and subsequently promotes p53 activity which at least partly contributes to the enhanced antiviral response of IFN-alpha plus ribavirin against HCV.	Ribavirin	166-175	P53	Homo sapiens	66-69
22319594-0	2012	Benzo[a]pyrene, aflatoxine B1 and acetaldehyde mutational patterns in TP53 gene using a functional assay: relevance to human cancer aetiology.	aflatoxine	16-26	P53	Homo sapiens	70-74
22010212-7	2011	In the subgroup of primary ALL cells, with low expression of caspase-8, methotrexate (MTX) upregulated the expression of caspase-8 mediated by the transcription factor p53, suggesting epigenetic silencing of caspase-8.	Methotrexate	86-89	P53	Homo sapiens	168-171
27901115-0	2016	p53 coordinates DNA repair with nucleotide synthesis by suppressing PFKFB3 expression and promoting the pentose phosphate pathway.	Pentosephosphates	104-121	P53	Homo sapiens	0-3
21889927-6	2011	An M2 induced DDR in p53-defective MDA-MB-231 cells was abrogated by UCN-01, a ubiquitous inhibitor of kinases including Chk1, in a response associated with substantial mitotic catastrophe and strong synergy.	7-hydroxystaurosporine	69-75	P53	Homo sapiens	21-24
21479885-8	2011	Both flavonoids increased p53 expression in both cell lines, an effect particularly remarkable for Q.	Flavonoids	5-15	P53	Homo sapiens	26-29
21328450-1	2011	Roscovitine (ROSC), a selective cyclin-dependent kinase (CDK) inhibitor, arrests human estrogen receptor-alpha (ER-alpha) positive MCF-7 breast cancer cells in the G(2) phase of the cell cycle and concomitantly induces apoptosis via a p53-dependent pathway.	Roscovitine	0-11	P53	Homo sapiens	235-238
27901115-6	2016	Interestingly, although p53-mediated suppression of PFKFB3 could increase the two major PPP products, NADPH and nucleotides, only nucleotide production was essential to promote DDR.	NADP	102-107	P53	Homo sapiens	24-27
21266543-11	2011	The Pifithrin-alpha, an specific inhibitor of p53, inhibited the apoptosis and prevented the disruption of cytoskeleton induced by abnormal gravity.	pifithrin	4-14	P53	Homo sapiens	46-49
27895503-9	2016	Only in the choriocarcinoma cells, the expression of homologous recombination (HR) repair gene RAD51 was dramatically suppressed by MTX in a dose- and time-dependent manner, accompanied with the increase in p53.	Methotrexate	132-135	P53	Homo sapiens	207-210
22101337-3	2011	Using gene expression microarray analysis, we find that DNA damage response (DDR) pathways elicited by veliparib (ABT-888), a PARP inhibitor, plus topotecan comprise the G1/S checkpoint, ATM, and p53 signaling pathways in p53-wildtype cancer cell lines and BRCA1, BRCA2 and ATR pathway in p53-mutant lines.	veliparib	103-112	P53	Homo sapiens	196-199
22101337-3	2011	Using gene expression microarray analysis, we find that DNA damage response (DDR) pathways elicited by veliparib (ABT-888), a PARP inhibitor, plus topotecan comprise the G1/S checkpoint, ATM, and p53 signaling pathways in p53-wildtype cancer cell lines and BRCA1, BRCA2 and ATR pathway in p53-mutant lines.	veliparib	103-112	P53	Homo sapiens	222-225
22101337-3	2011	Using gene expression microarray analysis, we find that DNA damage response (DDR) pathways elicited by veliparib (ABT-888), a PARP inhibitor, plus topotecan comprise the G1/S checkpoint, ATM, and p53 signaling pathways in p53-wildtype cancer cell lines and BRCA1, BRCA2 and ATR pathway in p53-mutant lines.	veliparib	103-112	P53	Homo sapiens	222-225
22005259-0	2011	NF-kappaB, JNK and p53 pathways are involved in tubeimoside-1-induced apoptosis in HepG2 cells with oxidative stress and G2/M cell cycle arrest.	tubeimoside I	48-61	P53	Homo sapiens	19-22
20408963-13	2011	Molecular study did not indicate alterations of the INI-1 gene, whereas it showed the presence of Pro72Arg in exon 4 at heterozygous state in the TP53 gene.	pro72arg	98-106	P53	Homo sapiens	146-150
21214929-6	2011	Here we report on the reconstitution of the p53 tumor suppressor pathway in a p53-independent manner via p73 with combination treatments of alpha-TEA, a small bioactive lipid, plus DOXO or CDDP.	2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxy acetic acid	140-149	P53	Homo sapiens	44-47
21214929-6	2011	Here we report on the reconstitution of the p53 tumor suppressor pathway in a p53-independent manner via p73 with combination treatments of alpha-TEA, a small bioactive lipid, plus DOXO or CDDP.	2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxy acetic acid	140-149	P53	Homo sapiens	78-81
21214929-8	2011	RESULTS: Combination treatments of alpha-TEA plus DOXO or CDDP act cooperatively to induce apoptosis, caspase-8 and caspase-9 cleavage, p73, phospho-c-Ab1 and phospho-JNK protein expression, and increase expression of p53 downstream mediators; namely, death receptor-5, CD95/APO-1 (Fas), Bax and Noxa, as well as Yap nuclear translocation - plus reduce expression of Bcl-2.	2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxy acetic acid	35-44	P53	Homo sapiens	218-221
22005259-8	2011	Moreover, tubeimoside-1 induced accumulation of reactive oxygen species and arrested cell cycle at the G(2)/M phase, thus contributing to apoptosis, through signaling regulation by tumor necrosis factor alpha, nuclear factor kappaB (NF-kappaB), Jun N-terminal kinase (JNK) and p53.	tubeimoside I	10-23	P53	Homo sapiens	277-280
27689337-0	2016	p53 in the mitochondria, as a trans-acting protein, provides error-correction activities during the incorporation of non-canonical dUTP into DNA.	deoxyuridine triphosphate	131-135	P53	Homo sapiens	0-3
21225623-7	2011	Moreover, the different stilbenes also elicited diverse cellular and signaling responses in MCF-7 and MDA-MB-231 cells, as evidenced by analysis of colony formation, cell proliferation, cell cycle phase transition, the extent of phosphorylation of p53 at Ser15 and p53-inducible proteins, p21 and p53R2, respectively.	Stilbenes	24-33	P53	Homo sapiens	248-251
21225623-7	2011	Moreover, the different stilbenes also elicited diverse cellular and signaling responses in MCF-7 and MDA-MB-231 cells, as evidenced by analysis of colony formation, cell proliferation, cell cycle phase transition, the extent of phosphorylation of p53 at Ser15 and p53-inducible proteins, p21 and p53R2, respectively.	Stilbenes	24-33	P53	Homo sapiens	265-268
21225623-8	2011	Further, stilbene-elicited signaling cascade leading to p53 activation was examined in MCF-7 cells and results showed that resveratrol and triacetyl-resveratrol induced both ERK and p38 phosphorylation, whereas only marginal changes in state of phosphorylation in these two kinases were observed in trimethoxy-resveratrol-treated cells.	Stilbenes	9-17	P53	Homo sapiens	56-59
21139584-8	2011	Treatment with a combination of GUT-70 and bortezomib or doxorubicin had synergistic antiproliferative effects in MCL cells that were independent of p53 status.	Bortezomib	43-53	P53	Homo sapiens	149-152
21212516-2	2011	Pifithrin-alpha (PFT-alpha), a specific inhibitor of p53, reduced autophagy and reversed silibinin"s growth-inhibitory effect; besides, PFT-alpha decreased the activation of caspase-3, a crucial executor of apoptosis.	pifithrin	0-15	P53	Homo sapiens	53-56
27689337-4	2016	Here we demonstrate the impact of p53 on incorporation of uracil into DNA examined with mitochondrial fractions, as the source of polymerase gamma.	Uracil	58-64	P53	Homo sapiens	34-37
21212516-8	2011	However, activation of p53 was suppressed by SP600125; therefore the function of p53 was possibly controlled by JNK as well.	pyrazolanthrone	45-53	P53	Homo sapiens	23-26
21212516-8	2011	However, activation of p53 was suppressed by SP600125; therefore the function of p53 was possibly controlled by JNK as well.	pyrazolanthrone	45-53	P53	Homo sapiens	81-84
21602882-2	2011	Phosphorylation of p53 at S46, an apoptosis-specific p53 posttranslational modification, is the most characterized HIPK2 function in response to lethal doses of ultraviolet (UV), ionizing radiation or different anticancer drugs, such as cisplatin, roscovitine and doxorubicin (DOX).	Roscovitine	248-259	P53	Homo sapiens	19-22
21602882-2	2011	Phosphorylation of p53 at S46, an apoptosis-specific p53 posttranslational modification, is the most characterized HIPK2 function in response to lethal doses of ultraviolet (UV), ionizing radiation or different anticancer drugs, such as cisplatin, roscovitine and doxorubicin (DOX).	Roscovitine	248-259	P53	Homo sapiens	53-56
27689337-5	2016	p53 in mitochondria facilitates DNA damage repair functions resulting from uracil-DNA misincorporation.	Uracil	75-81	P53	Homo sapiens	0-3
27689337-7	2016	p53 in mitochondria can function as an exonuclease/proofreader for polymerase gamma by either decreasing the incorporation of non-canonical dUTP into DNA or by promoting the excision of incorporated nucleotide from nascent DNA, thus expanding the spectrum of DNA damage sites exploited for proofreading as a trans-acting protein.	deoxyuridine triphosphate	140-144	P53	Homo sapiens	0-3
27689337-8	2016	The data suggest that p53 may contribute to defense of the cells from consequences of dUTP misincorporation in both normal and tumor cells.	deoxyuridine triphosphate	86-90	P53	Homo sapiens	22-25
21903246-4	2011	Wild-type (wt) p53 was transiently transfected into the mutant p53 (m p53) SKOV3 cells which were treated with 5-azaC.	Azacitidine	111-117	P53	Homo sapiens	15-18
21903246-4	2011	Wild-type (wt) p53 was transiently transfected into the mutant p53 (m p53) SKOV3 cells which were treated with 5-azaC.	Azacitidine	111-117	P53	Homo sapiens	63-66
21273177-2	2011	In preclinical non-small-cell lung cancer (NSCLC) models, p53-dependent growth arrest after bortezomib treatment resulted in reduced cytotoxicity if bortezomib preceded docetaxel.	Bortezomib	92-102	P53	Homo sapiens	58-61
27122200-3	2016	Briefly, branched polyethylenimine (BPEI) was conjugated with beta-cyclodextrin hydrate (beta-CD) to form BPEI-beta-CD backbone, and p53 plasmid was condensed by positively charged BPEI via electrostatic interaction, while Dox was first conjugated with adamantine (AD) and then assembled with BPEI-beta-CD backbone via the host-guest interaction.	bpei-beta-cd	106-118	P53	Homo sapiens	133-136
21273177-2	2011	In preclinical non-small-cell lung cancer (NSCLC) models, p53-dependent growth arrest after bortezomib treatment resulted in reduced cytotoxicity if bortezomib preceded docetaxel.	Bortezomib	149-159	P53	Homo sapiens	58-61
21273177-2	2011	In preclinical non-small-cell lung cancer (NSCLC) models, p53-dependent growth arrest after bortezomib treatment resulted in reduced cytotoxicity if bortezomib preceded docetaxel.	Docetaxel	169-178	P53	Homo sapiens	58-61
21903246-4	2011	Wild-type (wt) p53 was transiently transfected into the mutant p53 (m p53) SKOV3 cells which were treated with 5-azaC.	Azacitidine	111-117	P53	Homo sapiens	63-66
22260024-8	2011	In addition, the cell growth inhibitory ratio and the apoptotic ratio of resveratrol-treated group decreased markedly by the p38 MAPK inhibitor SB203580 or p53 inhibitor pifithrin-alpha.	pifithrin	170-185	P53	Homo sapiens	156-159
21929745-8	2011	In responsive cell lines, the MI-319/sorafenib combination induced the disappearance of p53 from the nucleus, the down modulation of Bcl-2 and Bcl-xL, the translocation of p53 to the mitochondria and that of AIF to the nuclei.	Sorafenib	37-46	P53	Homo sapiens	88-91
21929745-8	2011	In responsive cell lines, the MI-319/sorafenib combination induced the disappearance of p53 from the nucleus, the down modulation of Bcl-2 and Bcl-xL, the translocation of p53 to the mitochondria and that of AIF to the nuclei.	Sorafenib	37-46	P53	Homo sapiens	172-175
21929745-13	2011	The data suggest that the ability of sorafenib to activate GSK-3beta and alter the intracellular distribution of p53 may be exploitable as an adjunct to agents that prevent the HDM2-dependent degradation of p53 in the treatment of melanoma.	Sorafenib	37-46	P53	Homo sapiens	113-116
21929745-13	2011	The data suggest that the ability of sorafenib to activate GSK-3beta and alter the intracellular distribution of p53 may be exploitable as an adjunct to agents that prevent the HDM2-dependent degradation of p53 in the treatment of melanoma.	Sorafenib	37-46	P53	Homo sapiens	207-210
21720516-3	2011	Standard ethidium bromide and acridine orange assays were used to detect apoptotic cells and indicated that a significantly larger percentage of the cells (approx 40%) were dead after 72 hours of exposure to f-SWCNTs-p53 as compared to the control cells, which were exposed to only p53 or f-SWCNTs, respectively.	Ethidium	9-25	P53	Homo sapiens	217-220
21275266-2	2011	In the present study we compared the effects of cisplatin (CP), a strong DNA damaging compound, with those of roscovitine (ROSC), a selective inhibitor of cyclin-dependent kinases (CDKs), on wt p53-positive human A549 lung adenocarcinoma cells harboring a mutated K-RAS gene.	Roscovitine	110-121	P53	Homo sapiens	194-197
27122200-3	2016	Briefly, branched polyethylenimine (BPEI) was conjugated with beta-cyclodextrin hydrate (beta-CD) to form BPEI-beta-CD backbone, and p53 plasmid was condensed by positively charged BPEI via electrostatic interaction, while Dox was first conjugated with adamantine (AD) and then assembled with BPEI-beta-CD backbone via the host-guest interaction.	bpei-beta-cd	293-305	P53	Homo sapiens	133-136
20850924-3	2010	In the bortezomib sensitive wild-type TP53 MCL cells, the Nutlin-3/bortezomib combination caused G0/G1 cell cycle arrest followed by the increase in apoptosis induction.	Bortezomib	67-77	P53	Homo sapiens	38-42
21699775-9	2011	Colitis induction with anti-CD3 or 3 cycles of DSS increased apoptosis and protein levels of p53 and PUMA in colonic crypt IECs.	Dextran Sulfate	47-50	P53	Homo sapiens	93-96
27748879-8	2016	Western blot analysis revealed that quercetin reduced the protein expression levels of phosphorylated-Akt and increased CSN6 protein degradation; therefore, affecting the expression levels of Myc, p53, B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated X protein.	Quercetin	36-45	P53	Homo sapiens	197-200
21810677-1	2011	INTRODUCTION: Retrospective studies suggest that p53 alteration is prognostic for recurrence in patients with urothelial bladder cancer and predictive for benefit from combination methotrexate, vinblastine, doxorubicin, and cisplatin (MVAC) adjuvant chemotherapy.	Methotrexate	180-192	P53	Homo sapiens	49-52
21810677-1	2011	INTRODUCTION: Retrospective studies suggest that p53 alteration is prognostic for recurrence in patients with urothelial bladder cancer and predictive for benefit from combination methotrexate, vinblastine, doxorubicin, and cisplatin (MVAC) adjuvant chemotherapy.	Vinblastine	194-205	P53	Homo sapiens	49-52
21810677-1	2011	INTRODUCTION: Retrospective studies suggest that p53 alteration is prognostic for recurrence in patients with urothelial bladder cancer and predictive for benefit from combination methotrexate, vinblastine, doxorubicin, and cisplatin (MVAC) adjuvant chemotherapy.	mvac	235-239	P53	Homo sapiens	49-52
20858478-0	2010	The flavonoid quercetin induces cell cycle arrest and mitochondria-mediated apoptosis in human cervical cancer (HeLa) cells through p53 induction and NF-kappaB inhibition.	Flavonoids	4-13	P53	Homo sapiens	132-135
20858478-0	2010	The flavonoid quercetin induces cell cycle arrest and mitochondria-mediated apoptosis in human cervical cancer (HeLa) cells through p53 induction and NF-kappaB inhibition.	Quercetin	14-23	P53	Homo sapiens	132-135
20858478-4	2010	The results demonstrate that quercetin suppressed the viability of HeLa cells in a dose-dependent manner by inducing G2/M phase cell cycle arrest and mitochondrial apoptosis through a p53-dependent mechanism.	Quercetin	29-38	P53	Homo sapiens	184-187
27555286-6	2016	Specific inhibition of p53 by pifithrin-alpha reversed the G2/M phase arrest induced by the 2b compound, suggesting contribution of p53 to increase.	pifithrin	30-39	P53	Homo sapiens	23-26
20953137-4	2010	In this study, the molecular mechanisms of ATO-induced myeloma apoptosis were explored on four myeloma cell lines of wild type or mutant p53 status and also on six primary myeloma cells.	Arsenic Trioxide	43-46	P53	Homo sapiens	137-140
20953137-7	2010	ATO treatment increased mRNA levels of interferon regulatory factor-1 and TRAIL, as well as protein levels of caspase 8 and cleaved caspase 3, indicating the involvement of the extrinsic apoptotic pathway in the mutated p53 myeloma cells.	Arsenic Trioxide	0-3	P53	Homo sapiens	220-223
20953137-8	2010	ATO also activated caspases 3 and 9, indicating involvement of the intrinsic apoptotic pathway in the wild type p53 myeloma cells.	Arsenic Trioxide	0-3	P53	Homo sapiens	112-115
21425328-10	2011	The cell growth inhibition by HMJ-30 was substantially attenuated either by the pre-incubation of U-2 OS cells with N-acetylcysteine (NAC, an antioxidant) and caffeine (an ATM kinase inhibitor) or by p53 knockdown via RNAi.	2-[(dibenzo[b,d]furan-2-yl)oxy]-N,N-dimethylethan-1-amine	30-33	P53	Homo sapiens	200-203
27633119-7	2016	Finally, we found that pretreatment with NAC prevented the JNK, p53, caspase-9 and -3 protein phosphorylation induced by the polysaccharide, however, pretreatment with SP600125 did not affect the generation of ROS, suggesting that ROS is upstream of JNK.	pyrazolanthrone	168-176	P53	Homo sapiens	64-67
21725213-4	2011	We show that quinacrine synergizes with 5-fluorouracil and significantly enhances the cytotoxicity of sorafenib in a panel of 10 human colorectal cancer cell lines, including those with KRAS mutations protein gel blot analysis confirmed that quinacrine"s anticancer activity partially arises from its ability to stabilize p53 and lower anti-apoptotic protein levels.	Sorafenib	102-111	P53	Homo sapiens	322-325
20953137-10	2010	Together, our data suggest that ATO induces apoptosis in MM through either extrinsic or intrinsic signaling pathway, depending on the p53 genetic background.	Arsenic Trioxide	32-35	P53	Homo sapiens	134-137
20947454-5	2010	In accordance with the dependence of ActD-induced apoptosis on a mitochondrial p53 function, in control T-cells specific inhibition of mitochondrial p53 translocation with mu pifithrin reduced apoptosis by 86%, whereas treatment with alpha pifithrin, which blocks p53-mediated transcription, had no effect.	pifithrin	175-184	P53	Homo sapiens	149-152
27229883-0	2016	beta-Ecdysterone Protects SH-SY5Y Cells Against 6-Hydroxydopamine-Induced Apoptosis via Mitochondria-Dependent Mechanism: Involvement of p38(MAPK)-p53 Signaling Pathway.	Ecdysterone	0-16	P53	Homo sapiens	147-150
20947454-5	2010	In accordance with the dependence of ActD-induced apoptosis on a mitochondrial p53 function, in control T-cells specific inhibition of mitochondrial p53 translocation with mu pifithrin reduced apoptosis by 86%, whereas treatment with alpha pifithrin, which blocks p53-mediated transcription, had no effect.	pifithrin	175-184	P53	Homo sapiens	149-152
21792014-7	2011	The contribution of YY1 to As2O3-induced p53 activation and apoptosis was also examined by Western blot and cell cycle analysis.	Arsenic Trioxide	27-32	P53	Homo sapiens	41-44
21457773-2	2011	The activation of benzo(a)pyrene (BP), a model compound of polycyclic aromatic hydrocarbons, to its genotoxic BP-diolepoxide (BPDE) and p53 response and cell viability after BP exposure, and the p53 status in these cell lines were analyzed.	Polycyclic Aromatic Hydrocarbons	59-91	P53	Homo sapiens	195-198
20824291-6	2010	TZDs induce apoptosis through increased levels of apoptotic molecules, such as p53 and PTEN and/or decreased level of anti-apoptotic molecules, such as Bcl-2 and survivin.	Thiazolidinediones	0-4	P53	Homo sapiens	79-82
20655369-4	2010	Our results revealed a significant P53-induction by actinomycin D, methyl methanesulfonate and etoposide.	Methyl Methanesulfonate	67-90	P53	Homo sapiens	35-38
27681719-10	2016	Quercetin more effectively induced p53-dependent apoptosis than isoliquiritigenin in EBV(+) human gastric carcinoma, and this induction was correlated with increased expressions of the cleaved forms of caspase-3, -9, and Parp.	Quercetin	0-9	P53	Homo sapiens	35-38
20811721-6	2010	Compound 5 (docosyl p-coumarate), which was the strongest inhibitor of topo II and cancer cell growth in the compounds tested, halted HCT116 p53(+/+) cells in G2/M phases, and induced apoptosis, although this compound did not affect the cell cycle of HCT116 p53(-/-) cells.	docosyl 4-coumarate	12-31	P53	Homo sapiens	141-144
20811721-6	2010	Compound 5 (docosyl p-coumarate), which was the strongest inhibitor of topo II and cancer cell growth in the compounds tested, halted HCT116 p53(+/+) cells in G2/M phases, and induced apoptosis, although this compound did not affect the cell cycle of HCT116 p53(-/-) cells.	docosyl 4-coumarate	12-31	P53	Homo sapiens	258-261
22848254-9	2011	Treatment of Caki-2/sh-A cells, but not Caki-2/C ones, with 5 nM docetaxel resulted in the induction of apoptotic cell death accompanying the induction of p53.	Docetaxel	65-74	P53	Homo sapiens	155-158
21297663-6	2011	As a result, in the presence of Myc, miR-34a inhibited p53-dependent bortezomib-induced apoptosis as efficiently as anti-p53 small interfering RNA.	Bortezomib	69-79	P53	Homo sapiens	55-58
27681719-11	2016	In EBV(-)human gastric carcinoma (MKN74), both quercetin and isoliquiritigenin induced the expressions of p53, Bax, and Puma and the cleaved forms of caspase-3 and -9 and Parp at similar levels.	Quercetin	47-56	P53	Homo sapiens	106-109
20348016-0	2010	Relation between DNA repair, apoptosis and chromosomal aberrations in presence of pifithrin-alpha, an inhibitor of p53.	pifithrin	82-97	P53	Homo sapiens	115-118
27600721-4	2016	Light scattering, thioflavin T (ThT) and high hydrostatic pressure (HHP) assays showed that p53 DBD aggregates faster and to a greater extent than p63 and p73 DBDs, and was more susceptible to denaturation.	thioflavin T	18-30	P53	Homo sapiens	92-95
20803121-8	2010	Quercetin caused S phase arrest by decreasing the protein expression of CDK2, cyclins A and B while increasing the p53 and p57 proteins.	Quercetin	0-9	P53	Homo sapiens	115-118
21424116-0	2011	Diallyl sulfide induces cell cycle arrest and apoptosis in HeLa human cervical cancer cells through the p53, caspase- and mitochondria-dependent pathways.	allyl sulfide	0-15	P53	Homo sapiens	104-107
21454520-5	2011	In this study, we found that wild type p53 is induced by arsenic trioxide in tumor cells, consistent with published studies.	Arsenic Trioxide	57-73	P53	Homo sapiens	39-42
21454520-7	2011	We also found that arsenic trioxide decreases the stability of mutant p53 protein through a proteasomal pathway, and blockage of mutant p53 nuclear export can alleviate the arsenic-induced mutant p53 degradation.	Arsenic Trioxide	19-35	P53	Homo sapiens	70-73
27600721-4	2016	Light scattering, thioflavin T (ThT) and high hydrostatic pressure (HHP) assays showed that p53 DBD aggregates faster and to a greater extent than p63 and p73 DBDs, and was more susceptible to denaturation.	thioflavin T	32-35	P53	Homo sapiens	92-95
21459798-7	2011	Knockdown of Bid, Noxa, or p53 significantly delays the kinetic of bortezomib- and TRAIL-induced apoptosis, whereas it does not confer long-term protection.	Bortezomib	67-77	P53	Homo sapiens	27-30
27600721-6	2016	Molecular Dynamics (MD) simulations indicated specific regions of structural heterogeneity unique to p53, which may be promoted by elevated incidence of exposed backbone hydrogen bonds (BHBs).	bhbs	186-190	P53	Homo sapiens	101-104
20653470-7	2010	SP600125 also attenuated Bax protein content and p53 nuclear accumulation induced by H(2)O(2).	pyrazolanthrone	0-8	P53	Homo sapiens	49-52
27533080-5	2016	The Bcl-2 inhibitor ABT-263 (navitoclax) increased sensitivity to the mTORC1/2 inhibitor AZD8055 in TP53 wild type GSCs, while sensitivity to AZD8055 in TP53 mutated GSCs remained unchanged.	(5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol	89-96	P53	Homo sapiens	100-104
20673369-11	2010	Additionally, we report that the upstream kinase cyclin dependent kinase 5 interacts with p53 to phosphorylate it at Serine20 and Serine46 residues thereby promoting its recruitment on p21 and bax promoters.	serine20	117-125	P53	Homo sapiens	90-93
21454483-9	2011	Furthermore, we show that the MDM2 inhibitor Nutlin cooperates with the proteasome inhibitor Bortezomib by stimulating p53 DNA binding and transcriptional activity, providing a rationale for combination therapy using proteasome and MDM2 inhibitors.	Bortezomib	93-103	P53	Homo sapiens	119-122
27533080-5	2016	The Bcl-2 inhibitor ABT-263 (navitoclax) increased sensitivity to the mTORC1/2 inhibitor AZD8055 in TP53 wild type GSCs, while sensitivity to AZD8055 in TP53 mutated GSCs remained unchanged.	(5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol	142-149	P53	Homo sapiens	153-157
27470413-10	2016	Moreover, the inhibiting effects and apoptotic related proteins responses to Ch-1 on Hela cells were abolished after pre-treated with Pifithrin-alpha (Pft-alpha), a p53 inhibitor.	pifithrin	134-149	P53	Homo sapiens	165-168
21234653-3	2011	This study aims to investigate the anti-tumor activity of DHA and the underlying mechanisms in human osteosarcoma cell lines with different p53 mutation statuses.	artenimol	58-61	P53	Homo sapiens	140-143
21234653-7	2011	P53 wild-type osteosarcoma cells were more sensitive to DHA.	artenimol	56-59	P53	Homo sapiens	0-3
21234653-11	2011	The p53 gene may play a certain role in the DHA-induced human osteosarcoma apoptosis and cell cycle arrest.	artenimol	44-47	P53	Homo sapiens	4-7
20230799-0	2010	Induction of p53-independent apoptosis by a novel synthetic hexahydrocannabinol analog is mediated via Sp1-dependent NSAID-activated gene-1 in colon cancer cells.	Hexahydrocannabinol	60-79	P53	Homo sapiens	13-16
20421341-0	2010	4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone [corrected] induces CRM1-dependent p53 nuclear accumulation in human bronchial epithelial cells.	4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone	0-46	P53	Homo sapiens	82-85
21478269-9	2011	Of note, 17AAG induces a stronger viability loss in mutant p53 than in wild-type p53 cancer cells.	tanespimycin	9-14	P53	Homo sapiens	59-62
20347026-7	2010	The complexes of PHEMA-g-(PEI-b-PEG) successfully induced elevated wild-type p53 expression in BT474 cells and led to enhanced apoptosis of BT474 cells.	pei-b-peg	26-35	P53	Homo sapiens	77-80
27368132-5	2016	Furthermore, it was shown that a combination of D5D knockdown along with DGLA treatment could also significantly sensitize BxPC-3 cells to various chemotherapy drugs, likely via a p53-independent pathway through downregulating of anti-apoptotic proteins (e.g., Bcl-2) and activating pro-apoptotic proteins (e.g., caspase 3, -9).	d5d	48-51	P53	Homo sapiens	180-183
20331637-0	2010	Low-dose mithramycin exerts its anticancer effect via the p53 signaling pathway and synergizes with nutlin-3 in gynecologic cancers.	Plicamycin	9-20	P53	Homo sapiens	58-61
20331637-5	2010	In gynecologic cancer cells expressing wild-type p53, mithramycin stabilized p53 and increased the expression of the p53 downstream target genes PUMA and p21, arrested the cell cycle, and induced apoptosis.	Plicamycin	54-65	P53	Homo sapiens	49-52
20331637-5	2010	In gynecologic cancer cells expressing wild-type p53, mithramycin stabilized p53 and increased the expression of the p53 downstream target genes PUMA and p21, arrested the cell cycle, and induced apoptosis.	Plicamycin	54-65	P53	Homo sapiens	77-80
20331637-5	2010	In gynecologic cancer cells expressing wild-type p53, mithramycin stabilized p53 and increased the expression of the p53 downstream target genes PUMA and p21, arrested the cell cycle, and induced apoptosis.	Plicamycin	54-65	P53	Homo sapiens	77-80
21478269-9	2011	Of note, 17AAG induces a stronger viability loss in mutant p53 than in wild-type p53 cancer cells.	tanespimycin	9-14	P53	Homo sapiens	81-84
21559393-0	2011	Molecular mode of action and role of TP53 in the sensitivity to the novel epothilone sagopilone (ZK-EPO) in A549 non-small cell lung cancer cells.	sagopilone	85-95	P53	Homo sapiens	37-41
21559393-0	2011	Molecular mode of action and role of TP53 in the sensitivity to the novel epothilone sagopilone (ZK-EPO) in A549 non-small cell lung cancer cells.	sagopilone	97-103	P53	Homo sapiens	37-41
21559393-11	2011	In contrast, treatment of A549 cells with a low concentration of sagopilone revealed an upregulation of direct transcriptional target genes of TP53, like CDKN1A, MDM2, GADD45A, FAS.	sagopilone	65-75	P53	Homo sapiens	143-147
21559393-12	2011	Knockdown of TP53, which inhibited the transcriptional induction of TP53 target genes, led to a significant increase in apoptosis induction in A549 cells when treated with a low concentration of sagopilone.	sagopilone	195-205	P53	Homo sapiens	13-17
21559393-12	2011	Knockdown of TP53, which inhibited the transcriptional induction of TP53 target genes, led to a significant increase in apoptosis induction in A549 cells when treated with a low concentration of sagopilone.	sagopilone	195-205	P53	Homo sapiens	68-72
21559393-13	2011	The results indicate that activation of TP53 and its downstream effectors like CDKN1A by low concentrations of sagopilone is responsible for the relative apoptosis resistance of A549 cells and might represent a mechanism of resistance to sagopilone.	sagopilone	111-121	P53	Homo sapiens	40-44
21559393-13	2011	The results indicate that activation of TP53 and its downstream effectors like CDKN1A by low concentrations of sagopilone is responsible for the relative apoptosis resistance of A549 cells and might represent a mechanism of resistance to sagopilone.	sagopilone	238-248	P53	Homo sapiens	40-44
20331637-6	2010	This activation of the p53 signaling pathway was a specific effect of MTH at concentrations &lt;50 nm.	Plicamycin	70-73	P53	Homo sapiens	23-26
20331637-10	2010	Although mithramycin activated p53 and suppressed the growth of human gynecologic cancer cell xenografts in mice, this was accompanied with a secondary up-regulation of MDM2.	Plicamycin	9-20	P53	Homo sapiens	31-34
27428957-0	2016	Methylsulfonylmethane Induces p53 Independent Apoptosis in HCT-116 Colon Cancer Cells.	dimethyl sulfone	0-21	P53	Homo sapiens	30-33
20460535-5	2010	We causally linked bortezomib-induced cell death to the accumulation of ASF1B, Myc, ODC1, Noxa, BNIP3, Gadd45alpha, p-SMC1A, SREBF1, and p53.	Bortezomib	19-29	P53	Homo sapiens	137-140
21532991-4	2011	Here we show that siRNA-mediated silencing of p53 is sufficient to completely abrogate hypersensitivity not only to Cisplatin but also to non-genotoxic inducers of p53 such as the Mdm2 antagonist Nutlin-3 and the proteasome inhibitor Bortezomib.	Bortezomib	234-244	P53	Homo sapiens	46-49
21459001-3	2011	Through the use of high-throughput screening of 1500 compounds, we have identified a small molecule inhibitor, 15-carboxy-13-isopropylatis-13-ene-17,18-dioic acid (NSC15520), that inhibited both the binding of Rad9-GST and p53-GST fusion proteins to the RPA N-terminal DNA binding domain (DBD), interactions that are essential for robust DNA damage signaling.	15-carboxy-13-isopropylatis-13-ene	111-145	P53	Homo sapiens	223-226
27428983-7	2016	Alkaloid 8 induced JNK1/2 (but not ERK1/2) activation leading to p53-independent cell death and strong suppression of AP-1 activity.	Alkaloids	0-8	P53	Homo sapiens	65-68
20484174-0	2010	p53-Independent apoptosis by benzyl isothiocyanate in human breast cancer cells is mediated by suppression of XIAP expression.	benzyl isothiocyanate	29-50	P53	Homo sapiens	0-3
27185843-10	2016	FAS and p53 were shown to be prognostic factors for PFS (7.0 months if FAS+ and p53-; 3.4 months if FAS+/p53+ or FAS-/p53-; and 0.7 months if FAS- and p53+; P &lt; .001) and for overall survival.	ammonium ferrous sulfate	0-3	P53	Homo sapiens	80-83
21130866-8	2011	FasL up-regulation; activation of caspases-8, -2, -9, and -3; and chromatin condensation were decreased by the p53 inhibitor pifithrin-alpha, implicating p53 as an upstream factor in the activation of death receptor-mediated apoptosis by H(2)O(2).	pifithrin	125-140	P53	Homo sapiens	111-114
21130866-8	2011	FasL up-regulation; activation of caspases-8, -2, -9, and -3; and chromatin condensation were decreased by the p53 inhibitor pifithrin-alpha, implicating p53 as an upstream factor in the activation of death receptor-mediated apoptosis by H(2)O(2).	pifithrin	125-140	P53	Homo sapiens	154-157
20473251-0	2010	The correlation of nitrous oxide of nNOS and p53 during developing brain.	Nitrous Oxide	19-32	P53	Homo sapiens	45-48
27185843-10	2016	FAS and p53 were shown to be prognostic factors for PFS (7.0 months if FAS+ and p53-; 3.4 months if FAS+/p53+ or FAS-/p53-; and 0.7 months if FAS- and p53+; P &lt; .001) and for overall survival.	ammonium ferrous sulfate	0-3	P53	Homo sapiens	80-83
27185843-10	2016	FAS and p53 were shown to be prognostic factors for PFS (7.0 months if FAS+ and p53-; 3.4 months if FAS+/p53+ or FAS-/p53-; and 0.7 months if FAS- and p53+; P &lt; .001) and for overall survival.	ammonium ferrous sulfate	0-3	P53	Homo sapiens	80-83
27185843-10	2016	FAS and p53 were shown to be prognostic factors for PFS (7.0 months if FAS+ and p53-; 3.4 months if FAS+/p53+ or FAS-/p53-; and 0.7 months if FAS- and p53+; P &lt; .001) and for overall survival.	ammonium ferrous sulfate	0-3	P53	Homo sapiens	80-83
21372157-3	2011	Moreover, the selective effect on erythropoiesis can be mimicked by activating p53 with the compound nutlin-3 and prevented by pifithrin-, an inhibitor of p53 activation.	pifithrin	127-136	P53	Homo sapiens	155-158
27185843-10	2016	FAS and p53 were shown to be prognostic factors for PFS (7.0 months if FAS+ and p53-; 3.4 months if FAS+/p53+ or FAS-/p53-; and 0.7 months if FAS- and p53+; P &lt; .001) and for overall survival.	ammonium ferrous sulfate	71-74	P53	Homo sapiens	8-11
21328450-1	2011	Roscovitine (ROSC), a selective cyclin-dependent kinase (CDK) inhibitor, arrests human estrogen receptor-alpha (ER-alpha) positive MCF-7 breast cancer cells in the G(2) phase of the cell cycle and concomitantly induces apoptosis via a p53-dependent pathway.	Roscovitine	13-17	P53	Homo sapiens	235-238
27185843-10	2016	FAS and p53 were shown to be prognostic factors for PFS (7.0 months if FAS+ and p53-; 3.4 months if FAS+/p53+ or FAS-/p53-; and 0.7 months if FAS- and p53+; P &lt; .001) and for overall survival.	ammonium ferrous sulfate	71-74	P53	Homo sapiens	8-11
19589203-11	2010	Significant proliferation of autologous PBLs and specific cytotoxicity against primary glioma cells were also induced by the infection of BB-102 in vitro, with the effect being more evident than that of Ad-p53.	bb-102	138-144	P53	Homo sapiens	206-209
27185843-10	2016	FAS and p53 were shown to be prognostic factors for PFS (7.0 months if FAS+ and p53-; 3.4 months if FAS+/p53+ or FAS-/p53-; and 0.7 months if FAS- and p53+; P &lt; .001) and for overall survival.	ammonium ferrous sulfate	71-74	P53	Homo sapiens	8-11
19828235-4	2010	Induction of G1 arrest by widdrol was correlated with induction of Chk2, p53 phosphorylation and CDK inhibitor p21 expression as well as inhibition of cyclin E, cyclin-dependent kinase (CDK2) and retinoblastoma protein (pRB).	widdrol	26-33	P53	Homo sapiens	73-76
21336302-3	2011	The tumour suppressor p53 has now been reported to block a metabolic pathway (the pentose phosphate pathway) that diverts glucose away from bioenergetic into biosynthetic routes.	Pentosephosphates	82-99	P53	Homo sapiens	22-25
21336310-4	2011	Here we show that the tumour suppressor p53, the most frequently mutated gene in human tumours, inhibits the pentose phosphate pathway (PPP).	Pentosephosphates	109-126	P53	Homo sapiens	40-43
27352049-9	2016	Increased expression of a p53 dimer in 3D-cultured LNCaP cells was correlated with increased resistance to Docetaxel.	Docetaxel	107-116	P53	Homo sapiens	26-29
21336310-5	2011	Through the PPP, p53 suppresses glucose consumption, NADPH production and biosynthesis.	NADP	53-58	P53	Homo sapiens	17-20
20198331-4	2010	We showed that the killing efficacy of roscovitine and 16 other purines and potentiation of roscovitine-induced apoptosis by the PI3K inhibitor, LY294002, decreased with increasing corruption of the Rb and p53 pathways.	Roscovitine	39-50	P53	Homo sapiens	206-209
20198331-4	2010	We showed that the killing efficacy of roscovitine and 16 other purines and potentiation of roscovitine-induced apoptosis by the PI3K inhibitor, LY294002, decreased with increasing corruption of the Rb and p53 pathways.	Roscovitine	92-103	P53	Homo sapiens	206-209
20064835-6	2010	Their bioinformatic analysis indicated that biological functions linked to immunity, inflammation, and cell death were among the most affected by BaP in human macrophages and that the AhR and p53 signaling pathways were the most significant canonical pathways activated by the PAH.	Polycyclic Aromatic Hydrocarbons	277-280	P53	Homo sapiens	192-195
21114963-0	2011	Methotrexate induces apoptosis through p53/p21-dependent pathway and increases E-cadherin expression through downregulation of HDAC/EZH2.	Methotrexate	0-12	P53	Homo sapiens	39-42
27058630-9	2016	The log10IC50 values for two out of 14 selected phytochemicals from these plants (acovenoside A and ouabain) of 60 tumor cell lines were correlated to the expression of ABC-transporters (ABCB1, ABCB5, ABCC1, ABCG2), oncogenes (EGFR, RAS) and tumor suppressors (TP53).	acovenoside A	82-95	P53	Homo sapiens	261-265
21114963-5	2011	Moreover, MTX promoted p53 phosphorylation at Ser15 and acetylaion at Lys373/382, which increase its stability and expression.	Methotrexate	10-13	P53	Homo sapiens	23-26
21114963-6	2011	The apoptosis and inhibition of cell viability induced by MTX were dependent on p53 and, partially, on p21.	Methotrexate	58-61	P53	Homo sapiens	80-83
21114963-8	2011	Therefore, the anticancer mechanism of MTX acts through initiation of p53-dependent apoptosis and restoration of E-cadherin expression by downregulation of HDAC/EZH2.	Methotrexate	39-42	P53	Homo sapiens	70-73
21163271-12	2011	p53-specific transcriptional inhibitor pifithrin-alpha or mitochondrial translocation inhibitor pifithrin-mu partially reversed solamargine-induced apoptosis.	pifithrin	39-48	P53	Homo sapiens	0-3
20064835-7	2010	AhR and p53 implications were moreover fully confirmed by the prevention of BaP-related upregulation of some selected target genes by AhR silencing or the use of pifithrin-alpha, an inhibitor of PAH bioactivation-related DNA damage/p53 pathways.	Polycyclic Aromatic Hydrocarbons	195-198	P53	Homo sapiens	8-11
20118233-5	2010	During DNA damage, the overall level of p53 modified at Lys(373)me2 does not increase, despite the dramatic increase in total p53, indicating that Lys(373)me2 correlates with inactive p53.	1-ETHOXY-2-(2-METHOXYETHOXY)ETHANE	64-67	P53	Homo sapiens	40-43
22993551-4	2010	Treatment with thymoquinone-4-alpha-linolenoylhydrazone (TQ-H-10) or thymoquinone-4-palmitoylhydrazone (TQ-H-11) induced a cytostatic effect, particularly in p53-competent HCT116 cells, mediated by an up-regulation of p21(cip1/waf1) and a down-regulation of cyclin E, and associated with an S/G(2) arrest of the cell cycle.	tq-h-10	57-64	P53	Homo sapiens	158-161
26827144-1	2016	A simple, rapid response time and ultrahigh sensitive electrochemiluminescence (ECL) immunosensor based on Ru(bpy)3(2+)doped silica doped AuNPs (Ru-Si@Au nanocomposite) was developed for detection of p53 protein, a well-known tumor suppressor.	ru(bpy)3	107-115	P53	Homo sapiens	200-203
21241062-0	2011	Selective depletion of mutant p53 by cancer chemopreventive isothiocyanates and their structure-activity relationships.	Isothiocyanates	60-75	P53	Homo sapiens	30-33
22993551-5	2010	Cells lacking p53 (HCT116(p53-/-)) or HepG2 liver cancer cells showed only a minor response to TQ-H-10.	tq-h-10	95-102	P53	Homo sapiens	14-17
27270209-8	2016	Inhibition of p53 by pifithrin-alpha, attenuates citral-mediated apoptosis.	pifithrin	21-36	P53	Homo sapiens	14-17
22993551-5	2010	Cells lacking p53 (HCT116(p53-/-)) or HepG2 liver cancer cells showed only a minor response to TQ-H-10.	tq-h-10	95-102	P53	Homo sapiens	26-29
20680693-6	2011	RESULTS: Kaplan-Meier analysis of survival revealed that no single alteration of the factors examined was associated with outcome, but tumors showing concomitant alteration of p16 and p53 were characterized by reduced MDFS and DSS (P = 0.01 and P &lt; 0.001, respectively).	dss	227-230	P53	Homo sapiens	184-187
20680693-8	2011	In multivariate analysis, altered p16/p53 remained the only parameter predictive of MDFS and DSS (P = 0.048, hazard ratio [HR] = 2.488, 95% confidence interval [95% CI] 1.006-5.116; P = 0.043, HR = 2.498, 95% CI 1.029-5.909, respectively).	dss	93-96	P53	Homo sapiens	38-41
27101893-0	2016	Discovery and optimization of new benzofuran derivatives against p53-independent malignant cancer cells through inhibition of HIF-1 pathway.	benzofuran	34-44	P53	Homo sapiens	65-68
21380817-0	2011	Role of nonsteroidal anti-inflammatory drug-activated gene-1 in docetaxel-induced cell death of human colorectal cancer cells with different p53 status.	Docetaxel	64-73	P53	Homo sapiens	141-144
21380817-5	2011	Although docetaxel induced an increase in NAG-1 and apoptosis in both HCT-116 (wild-type p53) and HT-29 (mutant p53) colon cancer cells, NAG-1 knockdown with siRNA prevented docetaxel-induced cell death in only HCT-116 cells.	Docetaxel	9-18	P53	Homo sapiens	89-92
21380817-5	2011	Although docetaxel induced an increase in NAG-1 and apoptosis in both HCT-116 (wild-type p53) and HT-29 (mutant p53) colon cancer cells, NAG-1 knockdown with siRNA prevented docetaxel-induced cell death in only HCT-116 cells.	Docetaxel	9-18	P53	Homo sapiens	112-115
21380817-6	2011	Docetaxel decreased Bcl-2 in HCT-116 cells, which have functionally active p53, according to luciferase reporter gene analyses, and docetaxel-induced cell death and changes in Bcl-2 and NAG-1 expression were blocked by PFT-alpha, a p53 inhibitor.	Docetaxel	0-9	P53	Homo sapiens	75-78
19931552-0	2010	Arsenite promotes centrosome abnormalities under a p53 compromised status induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK).	4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone	85-131	P53	Homo sapiens	51-54
19931552-0	2010	Arsenite promotes centrosome abnormalities under a p53 compromised status induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK).	4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone	133-136	P53	Homo sapiens	51-54
19969555-0	2010	Theaflavins target Fas/caspase-8 and Akt/pBad pathways to induce apoptosis in p53-mutated human breast cancer cells.	theaflavin	0-11	P53	Homo sapiens	78-81
19969555-2	2010	The present study revealed that theaflavins induced p53-mutated human breast cancer cell apoptosis.	theaflavin	32-43	P53	Homo sapiens	52-55
19969555-7	2010	Overexpression of either constitutively active myristylated-Akt (Myr-Akt) or Dn-caspase-8 partially blocked theaflavin-induced mitochondrial permeability transition and apoptosis of p53-mutated cells, whereas cotransfection of Myr-Akt and Dn-caspase-8 completely abolished theaflavin effect thereby negating the possibility of existence of third pathways.	theaflavin	108-118	P53	Homo sapiens	182-185
19969555-7	2010	Overexpression of either constitutively active myristylated-Akt (Myr-Akt) or Dn-caspase-8 partially blocked theaflavin-induced mitochondrial permeability transition and apoptosis of p53-mutated cells, whereas cotransfection of Myr-Akt and Dn-caspase-8 completely abolished theaflavin effect thereby negating the possibility of existence of third pathways.	theaflavin	273-283	P53	Homo sapiens	182-185
21380817-6	2011	Docetaxel decreased Bcl-2 in HCT-116 cells, which have functionally active p53, according to luciferase reporter gene analyses, and docetaxel-induced cell death and changes in Bcl-2 and NAG-1 expression were blocked by PFT-alpha, a p53 inhibitor.	Docetaxel	0-9	P53	Homo sapiens	232-235
21380817-6	2011	Docetaxel decreased Bcl-2 in HCT-116 cells, which have functionally active p53, according to luciferase reporter gene analyses, and docetaxel-induced cell death and changes in Bcl-2 and NAG-1 expression were blocked by PFT-alpha, a p53 inhibitor.	Docetaxel	132-141	P53	Homo sapiens	232-235
21380817-7	2011	In HT-29 cells with functionally inactive p53, the docetaxel-induced Bcl-xL decrease, NAG-1 increase, and cell death were not blocked by PFT-alpha.	Docetaxel	51-60	P53	Homo sapiens	42-45
21214929-10	2011	CONCLUSIONS: Data show that alpha-TEA in combination with DOXO or CDDP synergistically enhances apoptosis in TNBC via targeting p53-mediated genes in a p73-dependent manner, and that p73 responses are downstream of c-Abl, JNK and Yap.	2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxy acetic acid	28-37	P53	Homo sapiens	128-131
19969555-8	2010	These results and other biochemical correlates established the concept that two distinct signaling pathways were regulated by theaflavins to induce mitochondrial death cascade, eventually culminating to apoptosis of p53-mutated human breast cancer cells that are strongly resistant to conventional therapies.	theaflavin	126-137	P53	Homo sapiens	216-219
26876578-5	2016	Two p53 binding sites were mapped in the STAT5A gene and named PBS1 and PBS2; these sites were sufficient to confer p53 responsiveness in a luciferase reporter gene.	pbs1	63-67	P53	Homo sapiens	4-7
19948725-0	2010	A new isoquinolinium derivative, Cadein1, preferentially induces apoptosis in p53-defective cancer cells with functional mismatch repair via a p38-dependent pathway.	N-methylsalsolinium	6-20	P53	Homo sapiens	78-81
19948725-2	2010	A compound identified from this small molecule library, cadein1 (cancer-selective death inducer 1), an isoquinolinium derivative, effectively leads to a G(2)/M delay and caspase-dependent apoptosis in various carcinoma cells with non- functional p53.	N-methylsalsolinium	103-117	P53	Homo sapiens	246-249
21224072-4	2011	We found that well-known proteasome inhibitors such as MG132 and bortezomib, as well as the recently discovered proteasome inhibitor thiostrepton, induced p53-independent apoptosis in human cancer cell lines that correlated with p53-independent induction of proapoptotic Noxa but not Puma protein.	Bortezomib	65-75	P53	Homo sapiens	155-158
21224072-4	2011	We found that well-known proteasome inhibitors such as MG132 and bortezomib, as well as the recently discovered proteasome inhibitor thiostrepton, induced p53-independent apoptosis in human cancer cell lines that correlated with p53-independent induction of proapoptotic Noxa but not Puma protein.	Bortezomib	65-75	P53	Homo sapiens	229-232
26876578-5	2016	Two p53 binding sites were mapped in the STAT5A gene and named PBS1 and PBS2; these sites were sufficient to confer p53 responsiveness in a luciferase reporter gene.	pbs1	63-67	P53	Homo sapiens	116-119
26876578-5	2016	Two p53 binding sites were mapped in the STAT5A gene and named PBS1 and PBS2; these sites were sufficient to confer p53 responsiveness in a luciferase reporter gene.	pbs2	72-76	P53	Homo sapiens	4-7
20708607-11	2010	Inhibition of p53 expression by a specific p53 inhibitor pifithrin-alpha reduced the phosphorylated p38 MAP kinase and active caspase-3 proteins in the oxaliplatin-exposed RKO cells.	pifithrin	57-66	P53	Homo sapiens	14-17
20708607-11	2010	Inhibition of p53 expression by a specific p53 inhibitor pifithrin-alpha reduced the phosphorylated p38 MAP kinase and active caspase-3 proteins in the oxaliplatin-exposed RKO cells.	pifithrin	57-66	P53	Homo sapiens	43-46
26876578-5	2016	Two p53 binding sites were mapped in the STAT5A gene and named PBS1 and PBS2; these sites were sufficient to confer p53 responsiveness in a luciferase reporter gene.	pbs2	72-76	P53	Homo sapiens	116-119
21159614-9	2010	Collectively, these results show that nutlin-3 may be a useful agent in combination with TRAIL and, importantly, uncover a novel regulatory effect of p53 on the expression of Mcl-1 in melanoma cells on treatment with nutlin-3, which may antagonize the therapeutic efficacy of other chemotherapeutic drugs in addition to docetaxel in melanoma.	Docetaxel	320-329	P53	Homo sapiens	150-153
20005328-6	2010	Amplicons (PCR products) corresponding to the GC-rich p53 exon 5 containing cytosine and its methylated analogue, synthesized by substituting 60% of cytosine by 5-methyl-cytosine, were amplified and investigated electrochemically in the presence of SG and ethidium bromide (EtBr) by differential pulse voltammetry.	Cytosine	76-84	P53	Homo sapiens	54-57
26876578-6	2016	Chromatin immunoprecipitation experiments revealed that PBS2 has constitutive p53 bound to it, while p53 binding to PBS1 required DNA damage.	pbs2	56-60	P53	Homo sapiens	78-81
20005328-6	2010	Amplicons (PCR products) corresponding to the GC-rich p53 exon 5 containing cytosine and its methylated analogue, synthesized by substituting 60% of cytosine by 5-methyl-cytosine, were amplified and investigated electrochemically in the presence of SG and ethidium bromide (EtBr) by differential pulse voltammetry.	Cytosine	149-157	P53	Homo sapiens	54-57
20005328-6	2010	Amplicons (PCR products) corresponding to the GC-rich p53 exon 5 containing cytosine and its methylated analogue, synthesized by substituting 60% of cytosine by 5-methyl-cytosine, were amplified and investigated electrochemically in the presence of SG and ethidium bromide (EtBr) by differential pulse voltammetry.	5-Methylcytosine	161-178	P53	Homo sapiens	54-57
20005328-6	2010	Amplicons (PCR products) corresponding to the GC-rich p53 exon 5 containing cytosine and its methylated analogue, synthesized by substituting 60% of cytosine by 5-methyl-cytosine, were amplified and investigated electrochemically in the presence of SG and ethidium bromide (EtBr) by differential pulse voltammetry.	Ethidium	256-272	P53	Homo sapiens	54-57
20954859-1	2010	For repair of damaged DNA, cells increase de novo synthesis of deoxyribonucleotide triphosphates through the rate-limiting, p53-regulated ribonucleotide reductase (RNR) enzyme.	deoxyribonucleotide triphosphates	63-96	P53	Homo sapiens	124-127
20005328-6	2010	Amplicons (PCR products) corresponding to the GC-rich p53 exon 5 containing cytosine and its methylated analogue, synthesized by substituting 60% of cytosine by 5-methyl-cytosine, were amplified and investigated electrochemically in the presence of SG and ethidium bromide (EtBr) by differential pulse voltammetry.	Ethidium	274-278	P53	Homo sapiens	54-57
26876578-6	2016	Chromatin immunoprecipitation experiments revealed that PBS2 has constitutive p53 bound to it, while p53 binding to PBS1 required DNA damage.	pbs1	116-120	P53	Homo sapiens	101-104
19883646-0	2010	Theaflavins retard human breast cancer cell migration by inhibiting NF-kappaB via p53-ROS cross-talk.	theaflavin	0-11	P53	Homo sapiens	82-85
19883646-1	2010	The present study demonstrates that theaflavins exploit p53 to impede metastasis in human breast cancer cells.	theaflavin	36-47	P53	Homo sapiens	56-59
19883646-5	2010	These results indicate that inhibition of NF-kappaB via p53-ROS crosstalk is a pre-requisite for theaflavins to accomplish the anti-migratory effect in breast cancer cells.	theaflavin	97-108	P53	Homo sapiens	56-59
27383327-8	2016	Water-solvable vitamin E Trolox significantly promoted MCF7 cell proliferation in vitro, while reducing intracellular ROS level and p53 expression.	vitamin e trolox	15-31	P53	Homo sapiens	132-135
20036849-3	2010	Co-treatment of cells with SP600125 and p53 inhibitor, pifithrin-alpha, partially nullified the suppressive effects of SP610025 on PS1 expression and secreted Abeta40 level.	pifithrin	55-64	P53	Homo sapiens	40-43
20036849-3	2010	Co-treatment of cells with SP600125 and p53 inhibitor, pifithrin-alpha, partially nullified the suppressive effects of SP610025 on PS1 expression and secreted Abeta40 level.	sp610025	119-127	P53	Homo sapiens	40-43
20583997-1	2010	The beta-isoform of PIP4K (PtdIns5P-4-kinase) regulates the levels of nuclear PtdIns5P, which in turn modulates the acetylation of the tumour suppressor p53.	phosphatidylinositol 5-phosphate	27-35	P53	Homo sapiens	153-156
20492448-0	2010	1,4-Thienodiazepine-2,5-diones via MCR (I): synthesis, virtual space and p53-Mdm2 activity.	1,4-thienodiazepine-2,5-diones	0-30	P53	Homo sapiens	73-76
27183917-4	2016	When combining Nutlin-3a with the Wip1 inhibitor GSK2830371 in the treatment of p53-proficient but not p53-deficient cells, we observed enhanced phosphorylation (Ser 15) and acetylation (Lys 382) of p53, increased expression of p53 target gene products, and synergistic inhibition of cell proliferation.	GSK2830371	49-59	P53	Homo sapiens	80-83
20492448-4	2010	A small focused compound library of 1,4-thienodiazepine-2,5-diones has been screened for the activity against p53-Mdm2 interaction.	1,4-thienodiazepine-2,5-diones	36-66	P53	Homo sapiens	110-113
20493187-8	2010	Treatment with GA and 17-AAG led to growth arrests in G1 and S phases, increased sub-G1 hypodipoid cell population, induced apoptotic cell death, and upregulated P53 and P21 expression, although the drug-induced Bcl-2 upregulation cannot prevent cell death.	tanespimycin	22-28	P53	Homo sapiens	162-165
20013323-7	2010	Taken together, p53 plays an important role in AZD1152-HQPA-induced growth arrest and early onset of apoptosis in AML cells.	2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate	47-54	P53	Homo sapiens	16-19
27123085-7	2016	These results suggest that the 26S proteasome inhibitor bortezomib is more potent, compared with irinotecan and etoposide, in the androgen-insensitive and tumor protein p53-null cell line PC-3.	Bortezomib	56-66	P53	Homo sapiens	169-172
19895660-7	2010	The p53 transcription inhibitor, pifithrin-alpha, (10 microM) significantly reduced the expression of p53 in microglia and significantly modulated the levels of microglial apoptosis induced by activation.	pifithrin	33-48	P53	Homo sapiens	4-7
19895660-7	2010	The p53 transcription inhibitor, pifithrin-alpha, (10 microM) significantly reduced the expression of p53 in microglia and significantly modulated the levels of microglial apoptosis induced by activation.	pifithrin	33-48	P53	Homo sapiens	102-105
20639499-5	2010	The HCS campaign yielded 3 structurally related methylbenzo-naphthyridin-5-amine (MBNA) hits with IC(50)s between 30 and 50 microM in the p53-hDM2 PPIB.	methylbenzo-naphthyridin-5-amine	48-80	P53	Homo sapiens	138-141
26969764-11	2016	The pro-apoptotic activity of miltirone was p53- and ROS-dependent.	miltirone	30-39	P53	Homo sapiens	44-47
20302847-4	2010	Further, HMBA inhibited the progression of MCF-7 cells in mitosis and induced apoptotic cell death involving p53 pathway.	10-((3-hydroxy-4-methoxybenzylidene))-9(10H)-anthracenone	9-13	P53	Homo sapiens	109-112
19812371-11	2010	In U87MG (p53wt) cells cotreated with TPT and pifithrin-alpha, or transfected with p53-siRNA, caspase-2 and Bid were significantly cleaved and XIAP/survivin was degraded.	pifithrin	46-55	P53	Homo sapiens	10-13
26969764-15	2016	SIGNIFICANCE: In this study, ROS- and p53-dependent apoptosis induced by miltirone on colon cancer cells was firstly revealed.	miltirone	73-82	P53	Homo sapiens	38-41
20377131-4	2010	Flow cytometry analyses demonstrated an increase in apoptosis following combined treatment with As2O3 and Ad-PML for 24 h, which was correlated with increased p53 and decreased Bcl-2 expression.	Arsenic Trioxide	96-101	P53	Homo sapiens	159-162
20298761-8	2010	Eight genes showed a biologically relevant change (P&lt;0.05, &gt; or =2 fold change) after 3 h treatment with salicylate; seven genes (Tp53, Birc3, Tnfrsf5, Casp7, Nfkb1, Fas, Lta, Tnfsf10) were upregulated and one gene (Pycard) was downregulated.	Salicylates	111-121	P53	Homo sapiens	136-140
26511813-7	2016	DTX robustly enhanced Bcl-2 inactivation by CAV-1 in MDA-MB-231 cells, while p53-mediated cell cycle arrest by DTX was more pronounced in CAV-1-low but p53-functional MCF-7 cells.	Docetaxel	111-114	P53	Homo sapiens	77-80
20413784-8	2010	Promotion of CHIP function by heat shock protein (Hsp)90 inhibitor, 17-allylamino-17-demethoxy geldanamycin (17-AAG), also prevented p53 accumulation and cardiomyocyte apoptosis both in vitro and in vivo.	tanespimycin	68-107	P53	Homo sapiens	133-136
19906512-7	2009	Further, T-oligo increases cellular ROS levels via a p53-dependent pathway, and these increases are abrogated by the NAD(P)H oxidase inhibitor diphenyliodonium chloride.	diphenyliodonium	143-168	P53	Homo sapiens	53-56
26511813-7	2016	DTX robustly enhanced Bcl-2 inactivation by CAV-1 in MDA-MB-231 cells, while p53-mediated cell cycle arrest by DTX was more pronounced in CAV-1-low but p53-functional MCF-7 cells.	Docetaxel	111-114	P53	Homo sapiens	152-155
20413784-8	2010	Promotion of CHIP function by heat shock protein (Hsp)90 inhibitor, 17-allylamino-17-demethoxy geldanamycin (17-AAG), also prevented p53 accumulation and cardiomyocyte apoptosis both in vitro and in vivo.	tanespimycin	109-115	P53	Homo sapiens	133-136
20413784-9	2010	CHIP-mediated p53 degradation was at least one of the cardioprotective effects of 17-AAG.	tanespimycin	82-88	P53	Homo sapiens	14-17
26893131-7	2016	Agarol predominantly induced apoptosis in two p53-wild cell lines (A549 and MKN45) compared to the other p53-mutant cell lines (HSC-3 and HSC-4).	Agarol	0-6	P53	Homo sapiens	46-49
20331637-11	2010	Combined treatment with mithramycin and nutlin-3, a drug that inhibits MDM2-p53 interaction, overcame a secondary up-regulation of MDM2 and synergistically inhibited cancer cell growth by inducing apoptosis through activation of the p53 signaling pathway.	Plicamycin	24-35	P53	Homo sapiens	76-79
20331637-11	2010	Combined treatment with mithramycin and nutlin-3, a drug that inhibits MDM2-p53 interaction, overcame a secondary up-regulation of MDM2 and synergistically inhibited cancer cell growth by inducing apoptosis through activation of the p53 signaling pathway.	Plicamycin	24-35	P53	Homo sapiens	233-236
20221783-3	2010	The inhibitory effect of GW501516 on VSMC proliferation was associated with cell cycle arrest at the G1 to S phase transition, which was accompanied by the induction of p21 and p53 along with decreased cyclin-dependent kinase 4 expression.	GW 501516	25-33	P53	Homo sapiens	177-180
19929413-1	2009	Therapeutic ionizing radiation damages DNA, increasing p53-regulated ribonucleotide reductase (RNR) activity required for de novo synthesis of the deoxyribonucleotide triphosphates used during DNA repair.	deoxyribonucleotide triphosphates	147-180	P53	Homo sapiens	55-58
19939245-7	2009	Transcription factors Ets-2, phospho- p53, C/EBP epsilon, C/EBP lambda and AP-2 alpha bound to their respective binding sequences in response to Forskolin and the expressions of these transcription factors were all elevated in Forskolin- treated cells.	Colforsin	227-236	P53	Homo sapiens	38-41
19939245-8	2009	Inhibition of Ets-2 and p53 reduced MMP-2 expression, secretion and invasiveness of Forskolin treated cells.	Colforsin	84-93	P53	Homo sapiens	24-27
20307555-5	2010	This RAR could be slightly reduced by pifithrin-alpha, an inhibitor of P53, however it was completely suppressed by BAY11-7082, an inhibitor of nuclear factor-kappaB (NF-kappaB).	pifithrin	38-53	P53	Homo sapiens	71-74
26936104-0	2016	Paeoniflorin attenuates ultraviolet B-induced apoptosis in human keratinocytes by inhibiting the ROS-p38-p53 pathway.	peoniflorin	0-12	P53	Homo sapiens	105-108
20058240-1	2010	BACKGROUND: We previously described the identification of a transcriptional inhibitor ARC and FoxM1 inhibitors, thiazole antibiotics, Siomycin A and thiostrepton that were able to induce potent p53-independent apoptosis in cancer cell lines of different origin.	Thiazoles	112-120	P53	Homo sapiens	194-197
19580791-7	2009	Both bDMC and DAC impair correct spindles formation and induce a p53- and p21(CIP1/WAF1)-independent mitotic arrest, which is more stable and long-lasting for bDMC.	bisdemethoxycurcumin	5-9	P53	Homo sapiens	65-68
19580791-8	2009	A subsequent p53/p21(CIP1/WAF1)-dependent inhibition of G1 to S transition is triggered by Curcumin and DAC as a consequence of the mitotic slippage, preventing post-mitotic cells from re-entering the cell cycle.	diacetylcurcumin	104-107	P53	Homo sapiens	13-16
20024960-0	2009	Mechanism of diepoxybutane-induced p53 regulation in human cells.	diepoxybutane	13-26	P53	Homo sapiens	35-38
26883108-7	2016	In addition, combined treatment with GSK2830371 and doxorubicin or nutlin-3 potentiated cell death through a strong induction of p53 pathway and activation of caspase 9.	GSK2830371	37-47	P53	Homo sapiens	129-132
19731257-3	2009	The dependence of p53-mediated chemosensitivity on pRb status was first investigated in a prospective study on the prognostic relevance of p53 in breast cancer patients treated with adjuvant chemotherapy (5-fluorouracil, methotrexate and cyclophosphamide).	Methotrexate	221-233	P53	Homo sapiens	18-21
20067769-4	2010	Increased cytotoxicity of topoisomerase II inhibitor/NU1025 combinations was attributable to the re-activation of the p53 pathway in drug-treated HeLa cells.	NU 1025	53-59	P53	Homo sapiens	118-121
26883108-8	2016	We conclude that efficient inhibition of WIP1 by GSK2830371 sensitizes breast cancer cells with amplified PPM1D and wild type p53 to chemotherapy.	GSK2830371	49-59	P53	Homo sapiens	126-129
19731257-6	2009	We then studied the role of pRb status in the p53-mediated response to 5-fluorouracil and methotrexate or doxorubicin treatment in three human cancer cell lines.	Methotrexate	90-102	P53	Homo sapiens	46-49
26956619-6	2016	METHODS: In this study we have used p53 mutated and knock out colon cancer cells and xenograft tumours to study the role of p53 in apoptosis mediated by diaminothiazoles.	diaminothiazoles	153-169	P53	Homo sapiens	124-127
19444595-0	2009	Modulation of p53, c-fos, RARE, cyclin A, and cyclin D1 expression in human leukemia (HL-60) cells exposed to arsenic trioxide.	Arsenic Trioxide	110-126	P53	Homo sapiens	14-17
19643729-6	2009	We show that p53 is activated in response to diamide treatment by the oxidative induction of the Trx1/p38(MAPK) signaling pathway.	Diamide	45-52	P53	Homo sapiens	13-16
20200495-8	2010	Cleaved PARP was detected in HCT116(p53-/-) cells depleted of stathmin and cell death in stathmin-depleted HeLa cells was blocked by the caspase inhibitor Z-VAD-FMK, consistent with apoptotic death.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	155-164	P53	Homo sapiens	36-39
20208557-2	2010	In this study, treatment of human breast cancer cells (MCF-7) with 15d-PGJ(2) led to accumulation of p53 protein.	15d-pgj	67-74	P53	Homo sapiens	101-104
20208557-4	2010	15d-PGJ(2) directly modified p53 as verified by reacting recombinant p53 with biotinylated 15d-PGJ(2).	15d-pgj	0-7	P53	Homo sapiens	29-32
26883465-3	2016	The novel spiro-oxindole scaffold is validated as a new class of p53-MDM2 protein-protein interaction inhibitors with good antitumor activity.	spiro-oxindole	10-24	P53	Homo sapiens	65-68
20208557-4	2010	15d-PGJ(2) directly modified p53 as verified by reacting recombinant p53 with biotinylated 15d-PGJ(2).	15d-pgj	0-7	P53	Homo sapiens	69-72
20208557-4	2010	15d-PGJ(2) directly modified p53 as verified by reacting recombinant p53 with biotinylated 15d-PGJ(2).	15d-pgj	91-98	P53	Homo sapiens	29-32
20208557-4	2010	15d-PGJ(2) directly modified p53 as verified by reacting recombinant p53 with biotinylated 15d-PGJ(2).	15d-pgj	91-98	P53	Homo sapiens	69-72
20208557-6	2010	Moreover, by conducting an in vitro [(35)S]-labeled p53 translation assay, we identified cysteine 277 as a putative site of p53 modification by 15d-PGJ(2).	15d-pgj	144-151	P53	Homo sapiens	52-55
20208557-6	2010	Moreover, by conducting an in vitro [(35)S]-labeled p53 translation assay, we identified cysteine 277 as a putative site of p53 modification by 15d-PGJ(2).	15d-pgj	144-151	P53	Homo sapiens	124-127
20208557-8	2010	Likewise, p53 binding activity of biotinylated 15d-PGJ(2) was abolished in mutant cells.	15d-pgj	47-54	P53	Homo sapiens	10-13
19619545-0	2009	Ribavirin enhances interferon signaling via stimulation of mTOR and p53 activities.	Ribavirin	0-9	P53	Homo sapiens	68-71
19619545-2	2009	Here, we identified a novel role of ribavirin in the communication between p53 and the mammalian target of rapamycin (mTOR) signaling.	Ribavirin	36-45	P53	Homo sapiens	75-78
19619545-3	2009	Ribavirin activates p53 by stimulating mTOR and promoting the interaction between mTOR and p53.	Ribavirin	0-9	P53	Homo sapiens	20-23
26892186-7	2016	Furthermore, p53 decrease was observed along with VOA-induced apoptosis and autophagy in A172 cells.	voa	50-53	P53	Homo sapiens	13-16
19619545-3	2009	Ribavirin activates p53 by stimulating mTOR and promoting the interaction between mTOR and p53.	Ribavirin	0-9	P53	Homo sapiens	91-94
19619545-5	2009	Furthermore, ribavirin-induced activation of mTOR and p53 enhances IFN-dependent signaling for the IFN-alpha/ribavirin combined treatment.	Ribavirin	13-22	P53	Homo sapiens	54-57
19619545-5	2009	Furthermore, ribavirin-induced activation of mTOR and p53 enhances IFN-dependent signaling for the IFN-alpha/ribavirin combined treatment.	Ribavirin	109-118	P53	Homo sapiens	54-57
19619545-6	2009	We conclude that ribavirin enhances activities of mTOR and p53, which may account for its antiviral and antitumor effects.	Ribavirin	17-26	P53	Homo sapiens	59-62
20064791-0	2010	Associations between polycyclic aromatic hydrocarbon-related exposures and p53 mutations in breast tumors.	Polycyclic Aromatic Hydrocarbons	21-52	P53	Homo sapiens	75-78
19816711-6	2010	Western blotting also showed that cucurbitacin E treatment can inhibit STAT3 phosphorylation while upregulate p53 expression.	cucurbitacin E	34-48	P53	Homo sapiens	110-113
26892186-8	2016	VOA-induced autophagy was mediated through a p53/AMPK/mTOR signaling pathway in A172 cells, while an mTOR-independent signaling pathway in U251 cells.	voa	0-3	P53	Homo sapiens	45-48
19646415-4	2009	Inhibition of NF-kappaB or p53 activation by its specific inhibitor PDTC or pifithrin-alpha respectively, significantly reduced both oridonin-induced apoptosis and autophagy accompanied by the decrease in Beclin 1 and LC3 levels.	pifithrin	76-91	P53	Homo sapiens	27-30
26865041-5	2016	Furthermore, the perichondral spindle cells and marrow osteoblasts/fibroblasts of BPOP showed stronger immunoreaction of PCNA, p53, beta-catenin, BCL2, pAKT, survivin, 14-3-3, CEA, EMA, pan-K, and S-100 than the tumor cells of osteochondroma.	bpop	82-86	P53	Homo sapiens	127-130
19184017-7	2009	Importantly, pifithrin-alpha, a p53 inhibitor, protected against DOX-induced mitochondrial depolarization, caspase activation and cell death.	pifithrin	13-22	P53	Homo sapiens	32-35
19524575-2	2009	HCCs from AFB(1)-exposed individuals frequently have distinct TP53 mutations, such as G to T transversions in the second guanine of codon 249 (AGG to AGT), and a characteristic mutational spectrum predominated by G:C to T:A mutations.	Guanine	121-128	P53	Homo sapiens	62-66
19465072-4	2009	Effectiveness of the Pas segment in the intracellular delivery of bioactive peptides using arginine-rich CPPs was exemplified through the enhanced growth inhibition activity of the malignant glioma cells by a retro-inverso peptide derived from the p53 C-terminal 22-amino-acid segment (positions 361-382).	Aminosalicylic Acid	21-24	P53	Homo sapiens	248-251
20096120-9	2010	CONCLUSIONS: Our findings, for the first time, unify the current inconsistent findings for bortezomib treatment and survivin expression, and linked the effect of bortezomib on survivin expression, apoptosis induction and bortezomib resistance in the relationship with p53 status, which is independent of cancer cell types.	Bortezomib	162-172	P53	Homo sapiens	268-271
20096120-9	2010	CONCLUSIONS: Our findings, for the first time, unify the current inconsistent findings for bortezomib treatment and survivin expression, and linked the effect of bortezomib on survivin expression, apoptosis induction and bortezomib resistance in the relationship with p53 status, which is independent of cancer cell types.	Bortezomib	162-172	P53	Homo sapiens	268-271
19608275-7	2010	The enhanced cytotoxicity of ATO+bortezomib was associated with augmented STAT3 inhibition and JNK activation, up-regulation of Bim, p21, p27, p53 as well as down-regulation of Bcl-2.	Bortezomib	33-43	P53	Homo sapiens	143-146
26865836-11	2015	ICC analysis for bcl2 and p53 also confirmed our results; in treated samples for the dose of LD50 in 24 and 48 h of cisplatin and hypercin, more cells expressed p53 (guardian of cells in front of tumor formation/progression) and less expressed bcl2 (which has anti apoptotic activity) compared to untreated samples.	hypercin	130-138	P53	Homo sapiens	26-29
21499441-9	2010	Together this data indicate that the lack of PP1 activation in AT cells result in increased NPM and NCL protein levels which prevents p53 phosphorylation in response to bleomycin and contributes to a defective G2/M checkpoint.	Bleomycin	169-178	P53	Homo sapiens	134-137
19625696-5	2009	BCL2-related protein A1, hedgehog interacting protein, and p53 target zinc finger protein genes were downregulated to 26-52% of the control, because of methylselenol exposure.	methaneselenol	152-165	P53	Homo sapiens	59-62
19661301-7	2009	Stable down-regulation of p53 expression by siRNA led to attenuation of bortezomib effects, survivin down-regulation and p21 induction, suggesting that cellular effects are p53-dependent.	Bortezomib	72-82	P53	Homo sapiens	26-29
19661301-7	2009	Stable down-regulation of p53 expression by siRNA led to attenuation of bortezomib effects, survivin down-regulation and p21 induction, suggesting that cellular effects are p53-dependent.	Bortezomib	72-82	P53	Homo sapiens	173-176
19661301-8	2009	CONCLUSION: These results demonstrate that the antiproliferative effects of bortezomib in CCRCC cells are VHL independent and dependent on pathways regulated by p53.	Bortezomib	76-86	P53	Homo sapiens	161-164
26865836-11	2015	ICC analysis for bcl2 and p53 also confirmed our results; in treated samples for the dose of LD50 in 24 and 48 h of cisplatin and hypercin, more cells expressed p53 (guardian of cells in front of tumor formation/progression) and less expressed bcl2 (which has anti apoptotic activity) compared to untreated samples.	hypercin	130-138	P53	Homo sapiens	161-164
19723057-4	2009	In the present study, we examined the effects of 15d-PGJ(2) on activation of p53 tumor suppressor in human breast cancer (MCF-7) cells.	15d-pgj	49-56	P53	Homo sapiens	77-80
19723057-5	2009	MCF-7 cells treated with 15d-PGJ(2) exhibited elevated p53 protein expression in time- and concentration-related manners, whereas prostaglandin A(2) (PGA(2)) and the nonprostaglandin derivative 2-cyclopenten-1-one exerted an effect to a lesser extent than did 15d-PGJ(2).	15d-pgj	25-32	P53	Homo sapiens	55-58
19956882-0	2010	p53 independent radio-sensitization of human lymphoblastoid cell lines by Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin.	tanespimycin	90-128	P53	Homo sapiens	0-3
26523671-4	2016	We found that the expression level of miR-34a induced by the DNA damage agent adrmycin (ADR) was both p53- and time-dependent.	adrmycin	78-86	P53	Homo sapiens	102-105
21071999-0	2010	Pifithrin-alpha, an inhibitor of p53 transactivation, up-regulates COX-2 expression through an MAPK-dependent pathway.	pifithrin	0-15	P53	Homo sapiens	33-36
21071999-2	2010	In this study, we investigated the effect of pifithrin (PFT)-alpha, an inhibitor of p53 transactivation, on COX-2 expression in breast and fibrosarcoma cells.	pifithrin	45-54	P53	Homo sapiens	84-87
19497413-8	2009	Although both compounds are weakly but equally effective inhibitors of iNOS protein expression and activity, only Se-PBIT significantly enhanced the levels of p53, p38, p27 and p21 protein expression, reduced levels of phospholipase A2 (PLA2) but had no effect on cyclooxygenase-2 (COX-2) protein levels; such molecular targets are involved in cell growth inhibition, induction of apoptosis and cell cycle regulation.	se-pbit	114-121	P53	Homo sapiens	159-162
26694952-0	2016	ARTIK-52 induces replication-dependent DNA damage and p53 activation exclusively in cells of prostate and breast cancer origin.	ARTIK-52	0-8	P53	Homo sapiens	54-57
27997894-12	2016	CONCLUSION: Zedoarondiol inhibits PDGF-BB-induced VSMCs proliferation via AMPK-mediated down-regulation of the mTOR/p70S6K pathway and up-regulation of the p53/p21 pathway.	zedoarondiol	12-24	P53	Homo sapiens	156-159
19623560-6	2009	We also demonstrate that the levels of survivin and Bcl-2 protein expression in HepG2 cells decreased concurrently, and the levels of p53 protein increased significantly after treatment with quercetin by immunocytochemistry analysis.	Quercetin	191-200	P53	Homo sapiens	134-137
20041160-6	2009	We show that miR-24 regulates p53-independent cellular proliferation by regulating an S-phase enzyme, dihydrofolate reductase (DHFR) a target of the chemotherapeutic drug methotrexate (MTX).	Methotrexate	171-183	P53	Homo sapiens	30-33
20041160-6	2009	We show that miR-24 regulates p53-independent cellular proliferation by regulating an S-phase enzyme, dihydrofolate reductase (DHFR) a target of the chemotherapeutic drug methotrexate (MTX).	Methotrexate	185-188	P53	Homo sapiens	30-33
25808617-0	2016	Computational analysis of spiro-oxindole inhibitors of the MDM2-p53 interaction: insights and selection of novel inhibitors.	spiro-oxindole	26-40	P53	Homo sapiens	64-67
19804594-11	2009	RESULTS: Nicotinamide cooperated with ssUV to increase enzymes involved in cellular energy metabolism and p53, and significantly protected against immunosuppression caused by UVB, longwave UVA and single and repeated ssUV exposures.	ssuv	38-42	P53	Homo sapiens	106-109
19934289-0	2009	Interactions of the Hdm2/p53 and proteasome pathways may enhance the antitumor activity of bortezomib.	Bortezomib	91-101	P53	Homo sapiens	25-28
19513548-10	2009	The p53 inhibitor, pifithrin-alpha, was able to counteract the effect of Axin in C6 cells.	pifithrin	19-34	P53	Homo sapiens	4-7
19347880-4	2009	Treatment with a p53 specific inhibitor, pifithrin alpha, restored this resistant phenotype in the MCF-7 cell line.	pifithrin	41-50	P53	Homo sapiens	17-20
19531575-6	2009	Top-I, Sp1, and p53 expression modulated by 5-aza were measured by real-time PCR.	Azacitidine	44-49	P53	Homo sapiens	16-19
19531575-11	2009	In contrast, 5-aza down-regulated Top-I expression in the p53 wild-type LS174T cells in a p53-dependent manner, thereby reducing SN38 cytotoxicity.	Azacitidine	13-18	P53	Homo sapiens	58-61
19934289-8	2009	CONCLUSIONS: This differential response of MM versus epithelial carcinomas to combination of nutlin-3 with bortezomib sheds new light on the role of p53 in bortezomib-induced apoptosis.	Bortezomib	107-117	P53	Homo sapiens	149-152
25808617-5	2016	Based on this structure-function analysis, several novel spiro-oxindole derivatives were selected and evaluated for their ability to block the MDM2-p53 interaction in vitro.	spiro-oxindole	57-71	P53	Homo sapiens	148-151
19856920-3	2009	A high-throughput screening effort identified 6,7-bis(4-bromophenyl)-7,12-dihydro-6H-chromeno[4,3-d][1,2,4]triazolo[1,5-a]pyrimidine as a potent inhibitor of the MDM2-p53 protein-protein interaction.	CHEMBL584303	46-132	P53	Homo sapiens	167-170
19253369-1	2009	Ascochlorin, a prenylphenol antitumor antibiotic, profoundly increases the expression of endogenous p53 by increasing protein stability in the human osteosarcoma cells and human colon cancer cells.	o-Prenylphenol	15-27	P53	Homo sapiens	100-103
26414189-0	2016	Single nucleotide polymorphisms in TP53 but not KRAS or MDM2 are predictive of clinical outcome in multiple myeloma treated with high-dose melphalan and autologous stem cell support.	Melphalan	139-148	P53	Homo sapiens	35-39
19474676-11	2009	Only tumor size and nuclear p53 expression were found to be independent prognosticators for MPNST DSS in a multivariable analysis.	dss	98-101	P53	Homo sapiens	28-31
19411846-9	2009	Specific inhibition of mitochondrial p53 translocation by Pifithrin mu reduces the apoptotic Nutlin response by 2.5-fold, underlining the significance of p53"s mitochondrial program in Nutlin-induced apoptosis.	pifithrin	58-67	P53	Homo sapiens	37-40
19939245-6	2009	RESULTS: We found that Forskolin increased MMP-2 mRNA in JAR cells within 24 hours, and induced binding to p53, Ets, C/EBP and AP-2.	Colforsin	23-32	P53	Homo sapiens	107-110
19939245-7	2009	Transcription factors Ets-2, phospho- p53, C/EBP epsilon, C/EBP lambda and AP-2 alpha bound to their respective binding sequences in response to Forskolin and the expressions of these transcription factors were all elevated in Forskolin- treated cells.	Colforsin	145-154	P53	Homo sapiens	38-41
19457607-0	2009	Arsenic trioxide induces apoptosis and G2/M phase arrest by inducing Cbl to inhibit PI3K/Akt signaling and thereby regulate p53 activation.	Arsenic Trioxide	0-16	P53	Homo sapiens	124-127
19457607-4	2009	ATO-induced G2/M phase arrest and p53 degradation in gastric cancer MGC803 cells.	Arsenic Trioxide	0-3	P53	Homo sapiens	34-37
19652535-4	2009	We found that only normal cells that have wild-type p53 were resistant to the thiazole antibiotic, thiostrepton, suggesting that p53 plays an antiapoptotic role in normal cells.	Thiazoles	78-86	P53	Homo sapiens	52-55
19652535-4	2009	We found that only normal cells that have wild-type p53 were resistant to the thiazole antibiotic, thiostrepton, suggesting that p53 plays an antiapoptotic role in normal cells.	Thiazoles	78-86	P53	Homo sapiens	129-132
26440706-3	2016	Study objectives were to: 1) define the lowest safe dose of arsenic trioxide that transiently blocks p53 activation in patients and 2) assess the potential of LDA to decrease hematological toxicity from chemotherapy.	Arsenic Trioxide	60-76	P53	Homo sapiens	101-104
19706164-5	2009	Inhibition of p53 was achieved in U87MG cells transfected with E6 oncoprotein (U87MG-E6) and treated with pifithrin-alpha, a reversible inhibitor of p53 (U87MG-PFT).	pifithrin	106-121	P53	Homo sapiens	14-17
19706164-5	2009	Inhibition of p53 was achieved in U87MG cells transfected with E6 oncoprotein (U87MG-E6) and treated with pifithrin-alpha, a reversible inhibitor of p53 (U87MG-PFT).	pifithrin	106-121	P53	Homo sapiens	149-152
19428113-13	2009	The apoptosis induced by [Cu(N9-ABS)(phen)2].3.6H2O was associated with an increase in p53 protein levels while those of Bcl-2 were reduced.	3.6h2o	45-51	P53	Homo sapiens	87-90
19587434-6	2009	Effect of arsenic trioxide and adriamycin on the mutant p53 expression in Raji cells was detected by semi-quantitive RT-PCR.	Arsenic Trioxide	10-26	P53	Homo sapiens	56-59
26471831-5	2016	RESULTS: mTOR inhibitors AZD8055, RAD-001, rapamycin and BEZ235 induced synergistic cytotoxicity with the Chk1 inhibitor V158411 in p53 mutant colon cancer cells.	(5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol	25-32	P53	Homo sapiens	132-135
19203212-10	2009	Second, honokiol induces cyclophilin D, thus potentiating the mitochondrial permeability transition pore, and causing death in cells with wild-type p53.	honokiol	8-16	P53	Homo sapiens	148-151
19679550-0	2009	Cardiac glycosides inhibit p53 synthesis by a mechanism relieved by Src or MAPK inhibition.	Glycosides	8-18	P53	Homo sapiens	27-30
19679550-2	2009	We report here that p53, in multiple lines of human cancer cells, is down-regulated by cardiac glycoside drugs digoxin and ouabain, potent inhibitors of Na(+)/K(+)-ATPase.	Glycosides	95-104	P53	Homo sapiens	20-23
19679550-10	2009	This is the first report that cardiac glycoside drugs, by initiating the Src/MAPK signaling pathways, reduce the p53 levels via inhibition of p53 protein synthesis.	Glycosides	38-47	P53	Homo sapiens	113-116
19679550-10	2009	This is the first report that cardiac glycoside drugs, by initiating the Src/MAPK signaling pathways, reduce the p53 levels via inhibition of p53 protein synthesis.	Glycosides	38-47	P53	Homo sapiens	142-145
19373658-6	2009	Response to purine analogues was significantly higher in patients with long lymphocyte doubling time (LDT), few cells expressing CD38, normal karyotype or no p53 deletion, whereas there was no correspondence with ZAP-70 expression.	purine	12-18	P53	Homo sapiens	158-161
19661301-0	2009	Inhibition of proteasome activity by bortezomib in renal cancer cells is p53 dependent and VHL independent.	Bortezomib	37-47	P53	Homo sapiens	73-76
27169122-12	2016	CONCLUSION: The data suggests that there is a significant association of the P53 exon 5 deletion of cytosine in codon 168 with metastasis and staging of the disease.	Cytosine	100-108	P53	Homo sapiens	77-80
19723062-1	2009	Roscovitine (ROSC), a selective blocker of cyclin-dependent kinases (CDKs) efficiently inhibits proliferation of exponentially growing human MCF-7 breast cancer cells by induction of cell cycle arrest and p53-mediated apoptosis.	Roscovitine	0-11	P53	Homo sapiens	205-208
19723062-1	2009	Roscovitine (ROSC), a selective blocker of cyclin-dependent kinases (CDKs) efficiently inhibits proliferation of exponentially growing human MCF-7 breast cancer cells by induction of cell cycle arrest and p53-mediated apoptosis.	Roscovitine	13-17	P53	Homo sapiens	205-208
19541794-8	2009	Cells pretreatment with the p53 inhibitor pifithrin-alpha suggested that ZEN but not T-2 toxin triggered a p53-dependent mitochondrial apoptotic pathway.	pifithrin	42-51	P53	Homo sapiens	28-31
19059218-4	2009	In this study, we demonstrate that 8-Cl-Ado-induced DNA damage activates G2/M phase checkpoint, which is associated with ATM-activated CHK1-CDC25C-CDC2 pathway joined by BRCA1-CHK1 branch in apoptosis-resistant human myelocytic leukemia K562 (p53-null) cells.	8-chloroadenosine	35-43	P53	Homo sapiens	243-246
26658076-8	2015	CQ also activated ATM, Chk2, and p53 phosphorylation and GADD45alpha expression.	camphorquinone	0-2	P53	Homo sapiens	33-36
19088112-2	2009	Male germ cell apoptosis was initiated with doses as low as 0.1 Gy and was prevented by pifithrin alpha, a p53 inhibitor.	pifithrin	88-103	P53	Homo sapiens	107-110
19088112-7	2009	Inhibition of p53 with pifithrin alpha did not affect oogonia apoptosis following irradiation.	pifithrin	23-38	P53	Homo sapiens	14-17
19541794-8	2009	Cells pretreatment with the p53 inhibitor pifithrin-alpha suggested that ZEN but not T-2 toxin triggered a p53-dependent mitochondrial apoptotic pathway.	pifithrin	42-51	P53	Homo sapiens	107-110
19531575-11	2009	In contrast, 5-aza down-regulated Top-I expression in the p53 wild-type LS174T cells in a p53-dependent manner, thereby reducing SN38 cytotoxicity.	Azacitidine	13-18	P53	Homo sapiens	90-93
19531575-12	2009	In conclusion, 5-aza modulates Top-I expression by several mechanisms involving Sp1, p16, and p53.	Azacitidine	15-20	P53	Homo sapiens	94-97
19531575-13	2009	If confirmed in other models, these results suggest that p16 and p53 status affects the 5-aza-irinotecan interaction.	Azacitidine	88-93	P53	Homo sapiens	65-68
19428812-6	2009	Pifithrin-alpha (PFT), an inhibitor of p53, blocked these processes.	pifithrin	0-15	P53	Homo sapiens	39-42
19428812-6	2009	Pifithrin-alpha (PFT), an inhibitor of p53, blocked these processes.	pifithrin	17-20	P53	Homo sapiens	39-42
19131253-6	2009	Our data revealed that treatment of 293T cells with DC-81-enediyne resulted in a significant increase of annexin V binding, caspase-3 degradation, and p53 arrest to identify apoptotic cells than 6.	dc-81-enediyne	52-66	P53	Homo sapiens	151-154
26662407-9	2015	Pathway analysis showed that genes in 2 clusters were enriched in 3 pathways: purine metabolism, p53 signaling pathway, and melanogenesis.	purine	78-84	P53	Homo sapiens	97-100
19148545-6	2009	Following exposure to dehydrocostuslactone, there was a marked increase in the expression of the apoptotic protein Bax and the downstream target p53, a tumor suppressor transcription factor protein, causing the release of cytochrome c.	dehydrocostus lactone	22-42	P53	Homo sapiens	145-148
19389934-5	2009	The resultant V600E(+)/p53(sh) melanocytes grew anchorage-independently in soft agar, formed pigmented lesions reminiscent of in situ melanoma in artificial skin reconstructs, and were weakly tumorigenic in vivo.	Agar	80-84	P53	Homo sapiens	23-26
26342440-6	2015	The hydrophilic Fe(II) complex entered cancer cells through transferring receptor (TfR)-mediated endocytosis, and translocated to cell nucleus, where they induced S phase cell cycle arrest through triggering DNA damage-mediated p53 pathway.	ammonium ferrous sulfate	16-22	P53	Homo sapiens	228-231
19308936-0	2009	Functional p53 in cells contributes to the anticancer effect of the cyclin-dependent kinase inhibitor roscovitine.	Roscovitine	102-113	P53	Homo sapiens	11-14
19308936-8	2009	The results confirm that functional p53 protein may enhance the anticancer activity of roscovitine that could be beneficial for anticancer therapy.	Roscovitine	87-98	P53	Homo sapiens	36-39
18758819-0	2009	In vitro effect of radiation, antibody to epidermal growth factor receptor and Docetaxel in human head and neck squamous carcinoma cells with mutant P53 and over-expressed EGFR.	Docetaxel	79-88	P53	Homo sapiens	149-152
19580479-6	2009	The rapid increase in the nuclear PAb421 epitope was blocked by the protein serine phosphatase inhibitor calyculin A but was not blocked by the protein synthesis inhibitor cycloheximide, suggesting that serine 376 was dephosphorylated by protein serine phosphatase 1 or 2A acting on pre-existing p53 protein.	pab421	34-40	P53	Homo sapiens	296-299
26475964-9	2015	Furthermore, a correlation between the distinct cytotoxicity of chalcones 1 and 2 and their ability to disrupt the p53-MDM2 interaction was established.	Chalcones	64-73	P53	Homo sapiens	115-118
19127257-0	2009	Temozolomide- and fotemustine-induced apoptosis in human malignant melanoma cells: response related to MGMT, MMR, DSBs, and p53.	fotemustine	18-29	P53	Homo sapiens	124-127
26475964-10	2015	SIGNIFICANCE: This work shows that prenylation is a determinant factor for the enhancement of chalcones tumour cytotoxicity by improving their ability to disrupt the p53-MDM2 interaction.	Chalcones	94-103	P53	Homo sapiens	166-169
18820127-2	2009	Herein, we report that treatment with the 90-kDa heat shock protein (Hsp90) molecular chaperone inhibitor 17-allylamino-17-demethoxygeldanamycin (17AAG) selectively abrogates the G(2)/M checkpoint induced by 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of irinotecan, in p53-null compared with p53-intact HCT116 colon cancer cells.	tanespimycin	106-144	P53	Homo sapiens	287-290
26458285-6	2015	Further investigations indicated that the enhancement of CPPP-mediated antitumor effects by GRIM-19 may be associated with the upregulation of phosphorylated p53 and the downregulation of B cell lymphoma-2, cyclin D1, vascular endothelial growth factor, matrix metalloproteinase (MMP)-2 and MMP-9, the proteins of which are involved in the activation of signal transducer and activator of transcription 3.	4-carboxy-5-(pyridyloxy-5'-phosphate)proline	57-61	P53	Homo sapiens	158-161
18820127-2	2009	Herein, we report that treatment with the 90-kDa heat shock protein (Hsp90) molecular chaperone inhibitor 17-allylamino-17-demethoxygeldanamycin (17AAG) selectively abrogates the G(2)/M checkpoint induced by 7-ethyl-10-hydroxycamptothecin (SN-38), an active metabolite of irinotecan, in p53-null compared with p53-intact HCT116 colon cancer cells.	tanespimycin	106-144	P53	Homo sapiens	310-313
18820127-9	2009	The combination of SN-38 and 17AAG was shown to be synergistic in p53-null but not in parental HCT116 cells by median effect/combination index analysis.	tanespimycin	29-34	P53	Homo sapiens	66-69
18834919-7	2008	HepG2 cell treatment with the p53 inhibitor pifithrin-alpha (PFT) and western blot analysis suggested that both ZEN and OTA, but not T-2 toxin, trigger a p53-dependent apoptotic pathway.	pifithrin	44-59	P53	Homo sapiens	30-33
19417135-1	2009	The repair of melphalan-induced N-alkylpurine monoadducts and interstrand cross-links was examined in different repair backgrounds, focusing on four genes (beta-actin, p53, N-ras, and delta-globin) with dissimilar transcription activities.	Melphalan	14-23	P53	Homo sapiens	168-171
26415230-0	2015	SP600125 has a remarkable anticancer potential against undifferentiated thyroid cancer through selective action on ROCK and p53 pathways.	pyrazolanthrone	0-8	P53	Homo sapiens	124-127
19383849-3	2009	DHE suppresses the expression of cyclin D, cyclin A, cyclin-dependent kinase 2, and cdc25A and increases the amount of p53 and p21, resulting in G(0)/G(1)-S phase arrest in MCF-7 cells.	dehydrocostus lactone	0-3	P53	Homo sapiens	119-122
18834919-7	2008	HepG2 cell treatment with the p53 inhibitor pifithrin-alpha (PFT) and western blot analysis suggested that both ZEN and OTA, but not T-2 toxin, trigger a p53-dependent apoptotic pathway.	pifithrin	44-59	P53	Homo sapiens	154-157
26415230-2	2015	However, undifferentiated thyroid cancers are one of the most lethal human malignancies because of their invasiveness, metastatization and refractoriness even to the most recently developed therapies.In this study we show for the first time a significant hyperactivation of ROCK/HDAC6 pathway in thyroid cancer tissues, and its negative correlation with p53 DNA binding ability.We demonstrate that a small compound, SP600125 (SP), is able to induce cell death selectively in undifferentiated thyroid cancer cell lines by specifically acting on the pathogenic pathways of cancer development.	pyrazolanthrone	416-424	P53	Homo sapiens	354-357
18761329-3	2008	In this study we raised the question whether roscovitine (ROSC), an inhibitor of cyclin-dependent kinases (CDKs) with increased selectivity towards CDK2, could be able to affect human leukemia HL-60 cells in which the p53 gene is inactivated and whether ROSC-induced effects could be additionally modulated by compounds of natural origin, especially by polyphenols e.g. RES.	Roscovitine	45-56	P53	Homo sapiens	218-221
18761329-3	2008	In this study we raised the question whether roscovitine (ROSC), an inhibitor of cyclin-dependent kinases (CDKs) with increased selectivity towards CDK2, could be able to affect human leukemia HL-60 cells in which the p53 gene is inactivated and whether ROSC-induced effects could be additionally modulated by compounds of natural origin, especially by polyphenols e.g. RES.	Roscovitine	58-62	P53	Homo sapiens	218-221
19287302-0	2009	Excision of nucleoside analogs in mitochondria by p53 protein.	Nucleosides	12-22	P53	Homo sapiens	50-53
19287302-4	2009	In the present study, we investigated the ability of p53 to excise incorporated nucleoside analogs from DNA in mitochondria.	Nucleosides	80-90	P53	Homo sapiens	53-56
19287302-5	2009	DESIGN: The functional interaction of p53 and DNA polymerase gamma during the incorporation of nucleoside analog was examined in mitochondrial fractions of p53-null H1299 cells, as the source of DNA polymerase gamma.	Nucleosides	95-105	P53	Homo sapiens	38-41
19287302-7	2009	RESULTS: The results demonstrate that the excision of incorporated nucleoside analogs in mitochondrial fractions of H1299 cells increased in the presence of purified recombinant p53, or cytoplasmic extracts of large cell carcinoma 2 cells expressing endogenous wild-type p53 (but not specifically predepleted extracts) or cytoplasmic extracts of H1299 cells overexpressing wild-type p53, but not exonuclease-deficient mutant p53-R175H.	Nucleosides	67-77	P53	Homo sapiens	178-181
19287302-7	2009	RESULTS: The results demonstrate that the excision of incorporated nucleoside analogs in mitochondrial fractions of H1299 cells increased in the presence of purified recombinant p53, or cytoplasmic extracts of large cell carcinoma 2 cells expressing endogenous wild-type p53 (but not specifically predepleted extracts) or cytoplasmic extracts of H1299 cells overexpressing wild-type p53, but not exonuclease-deficient mutant p53-R175H.	Nucleosides	67-77	P53	Homo sapiens	271-274
19287302-7	2009	RESULTS: The results demonstrate that the excision of incorporated nucleoside analogs in mitochondrial fractions of H1299 cells increased in the presence of purified recombinant p53, or cytoplasmic extracts of large cell carcinoma 2 cells expressing endogenous wild-type p53 (but not specifically predepleted extracts) or cytoplasmic extracts of H1299 cells overexpressing wild-type p53, but not exonuclease-deficient mutant p53-R175H.	Nucleosides	67-77	P53	Homo sapiens	271-274
19287302-7	2009	RESULTS: The results demonstrate that the excision of incorporated nucleoside analogs in mitochondrial fractions of H1299 cells increased in the presence of purified recombinant p53, or cytoplasmic extracts of large cell carcinoma 2 cells expressing endogenous wild-type p53 (but not specifically predepleted extracts) or cytoplasmic extracts of H1299 cells overexpressing wild-type p53, but not exonuclease-deficient mutant p53-R175H.	Nucleosides	67-77	P53	Homo sapiens	271-274
18846503-0	2008	Roscovitine up-regulates p53 protein and induces apoptosis in human HeLaS(3) cervix carcinoma cells.	Roscovitine	0-11	P53	Homo sapiens	25-28
26415230-2	2015	However, undifferentiated thyroid cancers are one of the most lethal human malignancies because of their invasiveness, metastatization and refractoriness even to the most recently developed therapies.In this study we show for the first time a significant hyperactivation of ROCK/HDAC6 pathway in thyroid cancer tissues, and its negative correlation with p53 DNA binding ability.We demonstrate that a small compound, SP600125 (SP), is able to induce cell death selectively in undifferentiated thyroid cancer cell lines by specifically acting on the pathogenic pathways of cancer development.	pyrazolanthrone	416-418	P53	Homo sapiens	354-357
19189664-3	2008	The p53-expressing cells, SK-N-SH (IC50=37 microM) were more susceptible to berberine than the p53-deficient cells, SK-N-MC (IC50 &gt; or =100 microM) without cytotoxic effect on the cortical neuronal cells.	sk-n	26-30	P53	Homo sapiens	4-7
19189664-6	2008	Exploration of p53 siRNA or pifithrin-alpha (PFT-alpha), a p53 inhibitor, in the SK-N-SH cells resulted in increase of IC50 values for cell viability, and decreased apoptotic cell death, expression of p53 and activation of caspase-3.	sk-n	81-85	P53	Homo sapiens	15-18
19287302-8	2009	The amount of nucleoside analogs incorporated into the elongated DNA with mitochondrial fractions of human colon carcinoma 116 (HCT116)(p53+/+) cells was lower than that of HCT116(p53-/-) cells.	Nucleosides	14-24	P53	Homo sapiens	136-139
19287302-8	2009	The amount of nucleoside analogs incorporated into the elongated DNA with mitochondrial fractions of human colon carcinoma 116 (HCT116)(p53+/+) cells was lower than that of HCT116(p53-/-) cells.	Nucleosides	14-24	P53	Homo sapiens	180-183
19287302-9	2009	Furthermore, mitochondrion-localized elevation of p53 in HCT116(p53+/+) cells, following the irradiation-stress stimuli, correlates with the reduction in incorporation of nucleoside analogs and wrong nucleotides.	Nucleosides	171-181	P53	Homo sapiens	50-53
19189664-6	2008	Exploration of p53 siRNA or pifithrin-alpha (PFT-alpha), a p53 inhibitor, in the SK-N-SH cells resulted in increase of IC50 values for cell viability, and decreased apoptotic cell death, expression of p53 and activation of caspase-3.	sk-n	81-85	P53	Homo sapiens	59-62
19189664-6	2008	Exploration of p53 siRNA or pifithrin-alpha (PFT-alpha), a p53 inhibitor, in the SK-N-SH cells resulted in increase of IC50 values for cell viability, and decreased apoptotic cell death, expression of p53 and activation of caspase-3.	sk-n	81-85	P53	Homo sapiens	59-62
19287302-9	2009	Furthermore, mitochondrion-localized elevation of p53 in HCT116(p53+/+) cells, following the irradiation-stress stimuli, correlates with the reduction in incorporation of nucleoside analogs and wrong nucleotides.	Nucleosides	171-181	P53	Homo sapiens	64-67
26415230-5	2015	Moreover, SP exerts a preferential action on the mutant p53 by increasing its DNA binding ability.	pyrazolanthrone	10-12	P53	Homo sapiens	56-59
19287302-10	2009	CONCLUSION: p53 in mitochondria may functionally interact with DNA polymerase gamma, thus providing a proofreading function during mitochondrial DNA replication for excision of nucleoside analogs and polymerization errors.	Nucleosides	177-187	P53	Homo sapiens	12-15
26416354-5	2015	These findings were followed by acceleration of ubiquitin ligase CHIP-mediated mutant p53 (mut p53) degradation and subsequent down-regulation of P-gp in 17-AAG-treated MDR cancer cells expressing P-gp and mut p53 after inhibition of SIRT1.	tanespimycin	154-160	P53	Homo sapiens	86-89
19459735-0	2009	Enhancement of methyl methanesulfonate-induced base excision repair in the presence of selenomethionine on p53-dependent pathway.	Methyl Methanesulfonate	15-38	P53	Homo sapiens	107-110
18941194-11	2008	Troglitazone (a protein tyrosine phosphatase, PTP1B activator) phosphatase inhibited PSTAT3 and augmented p53 expression.	Troglitazone	0-12	P53	Homo sapiens	106-109
26416354-5	2015	These findings were followed by acceleration of ubiquitin ligase CHIP-mediated mutant p53 (mut p53) degradation and subsequent down-regulation of P-gp in 17-AAG-treated MDR cancer cells expressing P-gp and mut p53 after inhibition of SIRT1.	tanespimycin	154-160	P53	Homo sapiens	95-98
18676676-0	2008	Reactive oxygen species mediate p53 activation and apoptosis induced by sodium nitroprusside in SH-SY5Y cells.	Nitroprusside	72-92	P53	Homo sapiens	32-35
26416354-5	2015	These findings were followed by acceleration of ubiquitin ligase CHIP-mediated mutant p53 (mut p53) degradation and subsequent down-regulation of P-gp in 17-AAG-treated MDR cancer cells expressing P-gp and mut p53 after inhibition of SIRT1.	tanespimycin	154-160	P53	Homo sapiens	95-98
25944179-1	2015	ZMC1 {azetidinecarbothioic acid, [1-(2-pyridinyl) ethylidene] hydrazide} is a lead compound being developed as one of the first mutant p53 targeted anti-cancer drugs.	NSC 319726	0-4	P53	Homo sapiens	135-138
18718914-6	2008	Pretreatment with SP600125 partially prevented the phosphorylation of p53 at serines 33 and 392 induced by 15d-PGJ(2).	pyrazolanthrone	18-26	P53	Homo sapiens	70-73
18718914-6	2008	Pretreatment with SP600125 partially prevented the phosphorylation of p53 at serines 33 and 392 induced by 15d-PGJ(2).	15d-pgj	107-114	P53	Homo sapiens	70-73
18718914-10	2008	This is the first study that 15d-PGJ(2) induces vascular endothelial cell apoptosis through the signaling of JNK and p38 MAPK-mediated p53 activation both in vitro and in vivo, further establishing the potential of 15d-PGJ(2) as an anti-angiogenesis agent.	15d-pgj	29-36	P53	Homo sapiens	135-138
18718914-10	2008	This is the first study that 15d-PGJ(2) induces vascular endothelial cell apoptosis through the signaling of JNK and p38 MAPK-mediated p53 activation both in vitro and in vivo, further establishing the potential of 15d-PGJ(2) as an anti-angiogenesis agent.	15d-pgj	215-222	P53	Homo sapiens	135-138
18847491-11	2008	Pretreatment of cells with pifithrin-alpha or U0126, specific inhibitors of p53 or MEK-1/2, significantly attenuated Triphala-induced apoptosis.	pifithrin	27-42	P53	Homo sapiens	76-79
19225156-3	2009	Cells treated with AZD1152 progressed through mitosis with misaligned chromosomes and exited without cytokinesis and subsequently underwent endoreduplication of DNA despite activation of a p53-dependent pseudo G1 checkpoint.	2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate	19-26	P53	Homo sapiens	189-192
19188164-8	2009	The combination of Nutlin-3 with doxorubicin or bortezomib was synergistic in wt-TP53 MCL cells.	Bortezomib	48-58	P53	Homo sapiens	81-85
20067883-15	2009	beta-carotene, lycopene and all-trans retinoic acid alone and in combination with docetaxel were found to influence the expression of bcl-2 and p53 antigen in the cells examined.	Docetaxel	82-91	P53	Homo sapiens	144-147
25944179-1	2015	ZMC1 {azetidinecarbothioic acid, [1-(2-pyridinyl) ethylidene] hydrazide} is a lead compound being developed as one of the first mutant p53 targeted anti-cancer drugs.	[1-(2-pyridinyl) ethylidene] hydrazide	33-71	P53	Homo sapiens	135-138
20139052-9	2009	Concordance between the staining results of TMA and whole sections was good for PR (kappa=0.67) and ER (kappa=0.67) and very good for p53 (kappa=0.91) and HER2 (kappa=0.91), when all the 26 recipient blocks were included.	tma	44-47	P53	Homo sapiens	134-137
18628404-7	2008	Pifithrin-alpha, an inhibitor of the tumor suppressor protein p53, had no effect on ROS generation but did block alpha1D-AR-induced apoptosis.	pifithrin	0-15	P53	Homo sapiens	62-65
25968838-9	2015	The rAd-p53-based TACE treatment strategy improved the overall survival (hazard ratio: 0.58, 95% confidence interval: 0.35-0.96, P = 0.035), progression-free survival (hazard ratio: 0.60, 95% confidence interval: 0.37-0.97, P = 0.037), response rate (P = 0.047) compared with TACE monotherapy.	Chlorotrianisene	18-22	P53	Homo sapiens	8-11
18571879-7	2008	This analysis revealed that DNA damage resulted in changes in splicing activity that modified the splicing pattern of Fas, a key pro-apoptotic, p53-inducible death receptor.	ammonium ferrous sulfate	118-121	P53	Homo sapiens	144-147
19054132-4	2008	Moreover, we report, for the first time, that the human wt p53 induces yeast cell death with characteristic markers of apoptosis: exposure of phosphatidylserine and DNA strand cleavage as shown by Annexin V staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling assay, respectively.	deoxyuridine triphosphate	267-271	P53	Homo sapiens	59-62
18952844-6	2008	Interestingly, inhibition of Thr-55 phosphorylation by a dietary flavonoid, apigenin, specifically blocks the CRM1-p53 association, restores p53 nuclear localization, and sensitizes tumor cells with cytoplasm localized wild-type p53 to DNA damage.	Flavonoids	65-74	P53	Homo sapiens	115-118
18952844-6	2008	Interestingly, inhibition of Thr-55 phosphorylation by a dietary flavonoid, apigenin, specifically blocks the CRM1-p53 association, restores p53 nuclear localization, and sensitizes tumor cells with cytoplasm localized wild-type p53 to DNA damage.	Flavonoids	65-74	P53	Homo sapiens	141-144
18952844-6	2008	Interestingly, inhibition of Thr-55 phosphorylation by a dietary flavonoid, apigenin, specifically blocks the CRM1-p53 association, restores p53 nuclear localization, and sensitizes tumor cells with cytoplasm localized wild-type p53 to DNA damage.	Flavonoids	65-74	P53	Homo sapiens	141-144
18344010-5	2008	In addition to stimulating proteasome activity, glycerol led to an increased expression of the stress chaperone "mortalin" and decreased p53 function in human cells.	Glycerol	48-56	P53	Homo sapiens	137-140
26408703-0	2015	Synthetic Bichalcone TSWU-BR23 Induces Apoptosis of Human Colon Cancer HT-29 Cells by p53-Mediated Mitochondrial Oligomerization of BAX/BAK and Lipid Raft Localization of CD95/FADD.	fadd	176-180	P53	Homo sapiens	86-89
17960385-10	2008	An inhibitor of p53, pifithrin-alpha, antagonized the expression of the cleaved form of caspase-3 in MKN45 cells.	pifithrin	21-30	P53	Homo sapiens	16-19
26250568-5	2015	When cells were pretreated with a p53 inhibitor (pifithrin-a), followed by magnolol treatment, pifithrin-a blocked magnolol-induced apoptosis and G0 /G1 arrest.	pifithrin	95-106	P53	Homo sapiens	34-37
18058229-6	2008	However, combined analysis of the SNP"s showed that p53 (Arg/Arg and Arg/Pro) with TGFbeta1 (Pro/Pro and Leu/Pro) were associated with greater than 2 fold increased risk for breast cancer in Univariate (P=0.01) and Multivariate (P=0.003) analysis.	Leucine	105-108	P53	Homo sapiens	52-55
26208523-3	2015	In the p53-proficient colorectal cancer cell line HCT116, oxaliplatin represses the expression of deoxyuridine triphosphatase (dUTPase), a ubiquitous pyrophosphatase that catalyzes the hydrolysis of dUTP to dUMP and inhibits dUTP-mediated cytotoxicity.	deoxyuridine triphosphate	127-131	P53	Homo sapiens	7-10
18718914-4	2008	Moreover, 15d-PGJ(2) activated JNK and p38 MAPK while inducing p53 phosphorylation at sites responsible for p53 activity.	15d-pgj	10-17	P53	Homo sapiens	63-66
18718914-4	2008	Moreover, 15d-PGJ(2) activated JNK and p38 MAPK while inducing p53 phosphorylation at sites responsible for p53 activity.	15d-pgj	10-17	P53	Homo sapiens	108-111
18608579-0	2008	p53 status-dependent sensitization of human tumour cells to hyperthermia by plant flavonol.	3-hydroxyflavone	82-90	P53	Homo sapiens	0-3
18608579-1	2008	PURPOSE: Quercetin (QCT), an important flavonol, is known to sensitize tumour cells to hyperthermia by suppressing heat shock protein 72 (Hsp72) induction, and is also reported to inhibit p53 accumulation.	Quercetin	9-18	P53	Homo sapiens	188-191
26141594-2	2015	There are some factors that can help to predict effects of chemotherapy in chronic lymphocytic leukemia (CLL), such as presence of del17p, del11q, or TP53 gene mutations, which result in resistance to purine analogues and alkylating drugs.	purine	201-207	P53	Homo sapiens	150-154
18482988-0	2008	Arsenic trioxide augments Chk2/p53-mediated apoptosis by inhibiting oncogenic Wip1 phosphatase.	Arsenic Trioxide	0-16	P53	Homo sapiens	31-34
18482988-2	2008	It has been reported that arsenic trioxide (ATO), a potent cancer chemotherapeutic agent, in particular for acute promyelocytic leukemia, activates the Chk2/p53 pathway, leading to apoptosis.	Arsenic Trioxide	26-42	P53	Homo sapiens	157-160
18668508-8	2008	The marked correlation between ATO-induced mitotic arrest and apoptosis indicates that the induction of apoptosis by ATO was highly dependent on the functional activation of the spindle checkpoint in cancer cells lacking normal p53 function.	Arsenic Trioxide	31-34	P53	Homo sapiens	228-231
18668508-8	2008	The marked correlation between ATO-induced mitotic arrest and apoptosis indicates that the induction of apoptosis by ATO was highly dependent on the functional activation of the spindle checkpoint in cancer cells lacking normal p53 function.	Arsenic Trioxide	117-120	P53	Homo sapiens	228-231
18949611-7	2008	Cases with &gt;20%TP53-deleted cells had the worst prognosis in the LRF CLL4 trial.	cll4	72-76	P53	Homo sapiens	18-22
18486125-1	2008	We previously reported that 3,4,5,4"-tetramethoxy-trans-stilbene (MR-4) induces p53 and perinuclear mitochondrial clustering in cancer cells [Gosslau, A., Chen, M., Ho, C.-T., Chen, K.Y., 2005, A methoxy derivative of resveratrol analogue selectively induced activation of the mitochondrial apoptotic pathway in transformed fibroblasts.	mr-4	66-70	P53	Homo sapiens	80-83
26311153-12	2015	Additionally, QUE enhanced the expression of p53 and BAX in HepG2 cells.	Quercetin	14-17	P53	Homo sapiens	45-48
26050209-8	2015	RESULTS: IC50 values for YH264, YH263, and WW751 against p53 wild-type HCT 116 cells after 72 h of incubation were 18.3 +- 2.3, 8.9 +- 0.6, and 3.1 +- 0.2 muM, respectively.	yh263	32-37	P53	Homo sapiens	57-60
18601905-6	2008	The abrogation of apoptosis is completely reversed by specific COX-2 inhibition, suggesting that HBx blocks p53-induced apoptosis via activation of COX-2/PGE(2) pathway.	Prostaglandins E	154-157	P53	Homo sapiens	108-111
18583568-2	2008	In HMCLs retaining a functional p53, PD treatment greatly enhances the ATO-induced p53 accumulation and p73, a p53 paralog, cooperates with p53 in caspase activation and apoptosis induction.	Arsenic Trioxide	71-74	P53	Homo sapiens	83-86
18452313-11	2008	Mapping the sequence specificity of Cr(III)-GA 2- and Cr(III)-EGA 2-DNA formation in the human p53 gene sequence by UvrABC nuclease cutting, we found that the sequence specificity for both adducts is the same but is much more selective than Cr(III)-guanine-DNA adducts.	Guanine	249-256	P53	Homo sapiens	95-98
26010525-2	2015	In particular, G:C-T:A and G:C-C:G transversions are caused by oxidized guanine and have been observed in the p53 and K-ras genes.	Guanine	72-79	P53	Homo sapiens	110-113
18566224-3	2008	The spiro-oxindole MI-43, a small-molecule inhibitor of the MDM2-p53 interaction, was designed and examined for its cellular mechanism of action and therapeutic potential in colon cancer.	spiro-oxindole	4-18	P53	Homo sapiens	65-68
18566224-10	2008	This study suggests that p53 activation by a potent and specific spiro-oxindole MDM2 antagonist may represent a promising therapeutic strategy for the treatment of colon cancer and should be further evaluated in vivo and in the clinic.	spiro-oxindole	65-79	P53	Homo sapiens	25-28
18583568-2	2008	In HMCLs retaining a functional p53, PD treatment greatly enhances the ATO-induced p53 accumulation and p73, a p53 paralog, cooperates with p53 in caspase activation and apoptosis induction.	Arsenic Trioxide	71-74	P53	Homo sapiens	83-86
18583568-2	2008	In HMCLs retaining a functional p53, PD treatment greatly enhances the ATO-induced p53 accumulation and p73, a p53 paralog, cooperates with p53 in caspase activation and apoptosis induction.	Arsenic Trioxide	71-74	P53	Homo sapiens	83-86
18707136-2	2008	BDD electrodes were dipped into a 1% solution of polyethylenimine (PEI) to adsorb a thin layer of positively charged PEI on the surface of BDD, then PEI-modified BDD electrodes were used to immobilize negatively charged single-stranded PCR fragments from Exon 7 of human p53 gene.	7,7'-dimethoxy-(4,4'-bi-1,3-benzodioxole)-5,5'-dicarboxylic acid dimethyl ester	0-3	P53	Homo sapiens	271-274
18707164-2	2008	The result of the calculation, based on structures from nanosecond molecular dynamics simulation, revealed that (19)Phe, (22)Leu, and (23)Trp of p53 have the strongest binding interaction with MDM2 followed by (26)Leu and (27)Pro.	Leucine	125-128	P53	Homo sapiens	145-148
18707164-2	2008	The result of the calculation, based on structures from nanosecond molecular dynamics simulation, revealed that (19)Phe, (22)Leu, and (23)Trp of p53 have the strongest binding interaction with MDM2 followed by (26)Leu and (27)Pro.	Leucine	214-217	P53	Homo sapiens	145-148
18707164-3	2008	The specific residues of MDM2 that have dominant binding interactions with p53 are specifically identified to be (51)Lys, (54)Leu, (62)Met, (67)Tyr, (72)Gln, (94)Lys, (96)His, and (100)Tyr.	Leucine	126-129	P53	Homo sapiens	75-78
18727380-4	2008	The treatment of selective inhibitors JNK SP600125 and p38 ML3403 in vitro prevents peroxide-induced appearance of P53 and NF-kB in blood mononuclear cells, associated with increasing of their apoptotic activity.	pyrazolanthrone	42-50	P53	Homo sapiens	115-118
25939861-0	2015	Efficient one-pot synthesis of trans-Pt(II)(salicylaldimine)(4-picoline)Cl complexes: effective agents for enhanced expression of p53 tumor suppressor genes.	4-picoline)cl	61-74	P53	Homo sapiens	130-133
18342637-6	2008	All these effects were significantly blocked by pretreatment of cells with the antioxidant N-acetylcysteine, p53 inhibitor pifithrin-alpha, and enzyme catalase.	pifithrin	123-138	P53	Homo sapiens	109-112
18434081-0	2008	Cytotoxic activity of 3,3",4,4",5,5"-hexahydroxystilbene against breast cancer cells is mediated by induction of p53 and downregulation of mitochondrial superoxide dismutase.	3,3',4,4',5,5'-hexahydroxystilbene	22-56	P53	Homo sapiens	113-116
25914345-6	2015	In NB4 cells, vinblastine produces alteration of p53 and DNA fragmentation.	Vinblastine	14-25	P53	Homo sapiens	49-52
18391985-9	2008	Furthermore, Fbw7 expression regulates the p53-dependent induction of genes such as Lats2 and p21 in response to vinblastine.	Vinblastine	113-124	P53	Homo sapiens	43-46
18482988-2	2008	It has been reported that arsenic trioxide (ATO), a potent cancer chemotherapeutic agent, in particular for acute promyelocytic leukemia, activates the Chk2/p53 pathway, leading to apoptosis.	Arsenic Trioxide	44-47	P53	Homo sapiens	157-160
18482988-3	2008	ATO is also known to activate the p38 MAPK/p53 pathway.	Arsenic Trioxide	0-3	P53	Homo sapiens	43-46
18482988-7	2008	Importantly, this ATO-induced activation of Chk2/p53 and p38 MAPK/p53 apoptotic pathways can be enhanced by siRNA-mediated suppression of Wip1 expression, further indicating that ATO inhibits Wip1 phosphatase in vivo.	Arsenic Trioxide	18-21	P53	Homo sapiens	49-52
18482988-7	2008	Importantly, this ATO-induced activation of Chk2/p53 and p38 MAPK/p53 apoptotic pathways can be enhanced by siRNA-mediated suppression of Wip1 expression, further indicating that ATO inhibits Wip1 phosphatase in vivo.	Arsenic Trioxide	18-21	P53	Homo sapiens	66-69
18374905-11	2008	In this report we showed that p53 level was upregulated by SP600125 in SK-N-SH cell line.	pyrazolanthrone	59-67	P53	Homo sapiens	30-33
18374905-15	2008	Furthermore, p53 inhibitor pifithrin-alpha partially nullified the suppressive effects of SP600125 on PS1 expression.	pifithrin	27-42	P53	Homo sapiens	13-16
18374905-15	2008	Furthermore, p53 inhibitor pifithrin-alpha partially nullified the suppressive effects of SP600125 on PS1 expression.	pyrazolanthrone	90-98	P53	Homo sapiens	13-16
18374905-16	2008	We also showed that transfection of p53 was required for SP600125-mediated suppression of PS1 expression in p53-deficient PC3 cell line suggesting that inhibition of basal JNK activity suppresses PS1 expression through a p53-dependent mechanism.	pyrazolanthrone	57-65	P53	Homo sapiens	36-39
18374905-16	2008	We also showed that transfection of p53 was required for SP600125-mediated suppression of PS1 expression in p53-deficient PC3 cell line suggesting that inhibition of basal JNK activity suppresses PS1 expression through a p53-dependent mechanism.	pyrazolanthrone	57-65	P53	Homo sapiens	108-111
18374905-16	2008	We also showed that transfection of p53 was required for SP600125-mediated suppression of PS1 expression in p53-deficient PC3 cell line suggesting that inhibition of basal JNK activity suppresses PS1 expression through a p53-dependent mechanism.	pyrazolanthrone	57-65	P53	Homo sapiens	108-111
18082226-7	2008	Whereas the levels of phosphorylated p53 were elevated and remained unchanged at 2h and 6h postirradiation in irradiated cells, its levels rose at 6h postirradiation but not at 2h postirradiation in bystander cells, suggesting that bystander cells manifest delayed p53 phosphorylation.	Deuterium	81-83	P53	Homo sapiens	37-40
18482988-7	2008	Importantly, this ATO-induced activation of Chk2/p53 and p38 MAPK/p53 apoptotic pathways can be enhanced by siRNA-mediated suppression of Wip1 expression, further indicating that ATO inhibits Wip1 phosphatase in vivo.	Arsenic Trioxide	179-182	P53	Homo sapiens	49-52
18482988-7	2008	Importantly, this ATO-induced activation of Chk2/p53 and p38 MAPK/p53 apoptotic pathways can be enhanced by siRNA-mediated suppression of Wip1 expression, further indicating that ATO inhibits Wip1 phosphatase in vivo.	Arsenic Trioxide	179-182	P53	Homo sapiens	66-69
18414057-11	2008	Our results show that sulfinosine and curcumin overcome MDR in non-small cell lung carcinoma cell line (NSCLC), especially in combination despite the presence of a mutated p53 gene.	sulfinosine	22-33	P53	Homo sapiens	172-175
25818463-8	2015	Available evidence suggests that TBBPA may increase levels of circulating estrogens by a competitive inhibition of estrogen conjugation and produce uterine tumors by promoting pre-existing Tp53-mutations due to increased estrogen levels resulting in increased cell proliferation.	tetrabromobisphenol A	33-38	P53	Homo sapiens	189-193
18645026-7	2008	Pretreatment with an antioxidant (N-acetylcysteine) or a c-Jun NH(2)-terminal kinase inhibitor (SP600125) effectively prevented Andro-induced p53 activation and DR4 up-regulation and eventually blocked the Andro-induced sensitization on TRAIL-induced apoptosis.	pyrazolanthrone	96-104	P53	Homo sapiens	142-145
17390215-1	2008	The aim of this study was to evaluate the in vitro and in vivo effects of the new chemotherapy agent Casiopeina III-ia [(4,4"-dimethyl-2,2"-bipiridine)(acetylacetonate) Copper (II) nitrate] on HCT-15 (p53-/-) colon cellular line.	acetyl acetonate	152-167	P53	Homo sapiens	201-204
25934763-0	2015	Correction to "5-aza-Cytidine Is a Potent Inhibitor of DNA Methyltransferase 3a and Induces Apoptosis in HCT-116 Colon Cancer Cells via Gadd45- and p53-Dependent Mechanisms".	Azacitidine	15-29	P53	Homo sapiens	148-151
17968428-6	2007	To verify the role of p53, the assays were repeated in presence of pifithrin-alpha, an inhibitor of p53.	pifithrin	67-82	P53	Homo sapiens	100-103
18575717-9	2008	MDM2 SNP309 and p53 Arg72Pro polymorphisms might influence the clinical outcome of TCCB in a distinctive way between superficial TCCB and invasive TCCB.	tccb	83-87	P53	Homo sapiens	16-19
18575717-9	2008	MDM2 SNP309 and p53 Arg72Pro polymorphisms might influence the clinical outcome of TCCB in a distinctive way between superficial TCCB and invasive TCCB.	tccb	129-133	P53	Homo sapiens	16-19
18575717-9	2008	MDM2 SNP309 and p53 Arg72Pro polymorphisms might influence the clinical outcome of TCCB in a distinctive way between superficial TCCB and invasive TCCB.	tccb	129-133	P53	Homo sapiens	16-19
17849104-3	2007	Direct amplifications of p53 and K-ras (about 157 bp) gene segments from 0.5 microL blood samples were successfully demonstrated by a static PCR chip with an indium tin oxide glass substrate.	indium tin oxide	158-174	P53	Homo sapiens	25-28
26221255-0	2015	Honokiol induces cell cycle arrest and apoptosis via p53 activation in H4 human neuroglioma cells.	honokiol	0-8	P53	Homo sapiens	53-56
18225552-0	2007	P53 enhances ascorbyl stearate-induced G2/M arrest of human ovarian cancer cells.	ascorbyl monostearate	13-30	P53	Homo sapiens	0-3
18478141-1	2008	The newly synthesized water-soluble cyclodiphosphazane ligands and their gold(I) complexes inhibit HeLa cell proliferation by activating p53 protein and inducing apoptosis.	cyclodiphosphazane	36-54	P53	Homo sapiens	137-140
18084327-4	2008	Interestingly, more pronounced tumoricidal effects were observed in p53-deficient HCT116 and HT29 cells, as well as A549 cells treated with the p53 inhibitor cyclic pifithrin-alpha.	pifithrin	165-180	P53	Homo sapiens	68-71
18084327-4	2008	Interestingly, more pronounced tumoricidal effects were observed in p53-deficient HCT116 and HT29 cells, as well as A549 cells treated with the p53 inhibitor cyclic pifithrin-alpha.	pifithrin	165-180	P53	Homo sapiens	144-147
26221255-1	2015	OBJECTIVE: To investigate the signal pathway of honokiol-induced apoptosis in H4 human neuroglioma cells and to evaluate whether p53 signaling and cell cycle arrest were involved in honokiol-treated H4 human neuroglioma cells.	honokiol	182-190	P53	Homo sapiens	129-132
17849424-6	2008	Among patients with EADC, elevated levels of NTS immunoreactivity were more frequent in tumors with p53 mutations (11/21; 52%) compared with tumors with wild-type p53 (9/33; 27%; P = 0.063), and specifically in tumors with p53 mutations at CpG dinucleotides (10/12; 83%) compared with non-CpG p53 mutations (1/9; 11%; P = 0.008).	3-nitrotyrosine	45-48	P53	Homo sapiens	100-103
26221255-10	2015	Moreover, p53, p21 and Bax/Bcl-2 were significantly upregulated by honokiol treatment.	honokiol	67-75	P53	Homo sapiens	10-13
26221255-11	2015	CONCLUSIONS: These results confirmed that honokiol could induce apoptosis in human neuroglioma cells, the underlying molecular mechanisms, at least partially, through activation p53 signaling and induction of cell cycle arrest.	honokiol	42-50	P53	Homo sapiens	178-181
17849424-6	2008	Among patients with EADC, elevated levels of NTS immunoreactivity were more frequent in tumors with p53 mutations (11/21; 52%) compared with tumors with wild-type p53 (9/33; 27%; P = 0.063), and specifically in tumors with p53 mutations at CpG dinucleotides (10/12; 83%) compared with non-CpG p53 mutations (1/9; 11%; P = 0.008).	3-nitrotyrosine	45-48	P53	Homo sapiens	163-166
17849424-6	2008	Among patients with EADC, elevated levels of NTS immunoreactivity were more frequent in tumors with p53 mutations (11/21; 52%) compared with tumors with wild-type p53 (9/33; 27%; P = 0.063), and specifically in tumors with p53 mutations at CpG dinucleotides (10/12; 83%) compared with non-CpG p53 mutations (1/9; 11%; P = 0.008).	3-nitrotyrosine	45-48	P53	Homo sapiens	163-166
17221157-10	2007	Our study suggests that the type of TP53 mutation, especially missense mutation, is a strong prognostic indicator for DFS and DSS in node-negative breast cancer, particularly in combination with ERBB2 amplification.	dss	126-129	P53	Homo sapiens	36-40
17849424-6	2008	Among patients with EADC, elevated levels of NTS immunoreactivity were more frequent in tumors with p53 mutations (11/21; 52%) compared with tumors with wild-type p53 (9/33; 27%; P = 0.063), and specifically in tumors with p53 mutations at CpG dinucleotides (10/12; 83%) compared with non-CpG p53 mutations (1/9; 11%; P = 0.008).	3-nitrotyrosine	45-48	P53	Homo sapiens	163-166
25925024-8	2015	As the action of SMIFH2 may go beyond Formin inhibition, only short-term and low-dose SMIFH2 treatments minimize confounding effects induced by loss of p53 and cytotoxicity.	SMIFH2 compound	86-92	P53	Homo sapiens	152-155
17849424-8	2008	The highly significant association between NTS, reflecting chronic NO-induced cellular protein damage, and endogenous p53 mutations at CpG dinucleotides, provides further evidence for a molecular link between chronic inflammation and esophageal malignancy.	3-nitrotyrosine	43-46	P53	Homo sapiens	118-121
18096571-9	2008	Taken together, these data suggest that (1) Mdm2 is a sensitive biomarker for certain types of genotoxicity, and (2) that polycyclic aromatic hydrocarbons-induced Mdm2 binding to chromatin reflects repairable damage, whereas chromatin binding of p53 Ser15 and gammaH2AX indicates more persistent DNA damage.	Polycyclic Aromatic Hydrocarbons	122-154	P53	Homo sapiens	246-249
17938270-7	2007	Moreover, epothilone B and D increased the expressions of NF-kappaB-dependent apoptotic cell death regulatory genes, i.e., Bax, p53, and the active form of caspase-3, but reduced Bcl-2 expression, and these actions were partially reversed by salicylic acid.	Deuterium	27-28	P53	Homo sapiens	128-131
17914225-4	2007	By computing the free energies of wild-type and mutant p53c binding to DNA and decomposing them into contributions from individual residues, the DNA-binding loss upon charge/noncharge -conserving mutation of Arg 273 was attributed not only to the loss of DNA phosphate contacts, but also to longer-range structural changes caused by the loss of the Asp 281 salt-bridge.	Aspartic Acid	349-352	P53	Homo sapiens	55-58
17914225-5	2007	The results herein and in previous works suggest that Asp 281 plays a critical role in the sequence-specific DNA-binding function of p53c by (i)orienting Arg 273 and Arg 280 in an optimal position to interact with the phosphate and base groups of the consensus DNA, respectively, and (ii) helping to maintain the proper DNA-binding protein conformation.	Aspartic Acid	54-57	P53	Homo sapiens	133-136
18344606-0	2008	Trimidox-induced apoptosis is mediated through induction of p53 in NALM-6 cells.	3,4,5-trihydroxybenzamidoxime	0-8	P53	Homo sapiens	60-63
25793965-5	2015	The 1-induced degradation of beta-catenin was also abrogated in the presence of pifithrin-alpha, an inhibitor of p53 transcriptional activity.	pifithrin	80-95	P53	Homo sapiens	113-116
18344606-1	2008	We examined the effect of trimidox-induced apoptosis involvement of p53 in the NALM-6 cell line of acute lymphoblastic leukemia.	3,4,5-trihydroxybenzamidoxime	26-34	P53	Homo sapiens	68-71
18344606-2	2008	Trimidox has been shown to increase the induction of p53.	3,4,5-trihydroxybenzamidoxime	0-8	P53	Homo sapiens	53-56
18344606-4	2008	Pifithrin-alpha, a p53 inhibitor, significantly prevented trimidox-induced apoptotic characteristics, as detected by nuclear morphological observation and DNA fragmentation.	pifithrin	0-15	P53	Homo sapiens	19-22
18344606-4	2008	Pifithrin-alpha, a p53 inhibitor, significantly prevented trimidox-induced apoptotic characteristics, as detected by nuclear morphological observation and DNA fragmentation.	3,4,5-trihydroxybenzamidoxime	58-66	P53	Homo sapiens	19-22
18344606-5	2008	Trimidox-induced apoptosis was enhanced or attenuated by transfection with wild-type or dominant-negative p53 containing expression vectors, respectively.	3,4,5-trihydroxybenzamidoxime	0-8	P53	Homo sapiens	106-109
18344606-6	2008	These results indicate that one of the induction mechanisms of apoptosis by trimidox is the mediated augmentation of p53.	3,4,5-trihydroxybenzamidoxime	76-84	P53	Homo sapiens	117-120
18056705-10	2008	Furthermore, p53 promoter region responded to AMPKalpha and glucose deprivation as judged by luciferase reporter assay.	ampkalpha	46-55	P53	Homo sapiens	13-16
17482571-9	2007	In addition, tryptanthrin decreased the amount of mutant p53 protein with decreasing mutant p53 protein stability.	tryptanthrine	13-25	P53	Homo sapiens	57-60
17482571-9	2007	In addition, tryptanthrin decreased the amount of mutant p53 protein with decreasing mutant p53 protein stability.	tryptanthrine	13-25	P53	Homo sapiens	92-95
17672346-3	2007	RESULT: ASMq flavonoids significantly inhibited growth of HepG2 cells in vitro, arrested HepG2 in the sub-G, phase, induced cell apoptosis and significantly down-regulated expression level of Bcl-2 mRNA, and up-regulated expression of p53, p21, Bax gene mRNA expressions.	asmq flavonoids	8-23	P53	Homo sapiens	235-238
26131123-9	2015	P53 and p21 were significantly upregulated by honokiol treatment.	honokiol	46-54	P53	Homo sapiens	0-3
17499812-0	2007	Theaflavins induced apoptosis of LNCaP cells is mediated through induction of p53, down-regulation of NF-kappa B and mitogen-activated protein kinases pathways.	theaflavin	0-11	P53	Homo sapiens	78-81
17499812-3	2007	In the present study, we report that black tea polyphenol, Theaflavins (TF)-induced apoptosis in human prostate carcinoma, LNCaP cells is mediated via modulation of two related pathways: up-regulation of p53 and down-regulation of NF-kappa B activity, causing a change in the ratio of pro-and antiapoptotic proteins leading to apoptosis.	theaflavin	59-70	P53	Homo sapiens	204-207
18281755-8	2008	Recent studies in this area have demonstrated various mechanisms involved in the anti-tumor activity of docetaxel: (1) efflux (p-glycoprotein), (2) metabolism (CYP3A4), (3) beta-tubulin (isotype class I and III), (4) cell cycle (HER2, BRCA1), (5) apoptosis (p53, Bcl-2, thioredoxin), and (6) cell proliferation (MIB-1, nuclear grade).	Docetaxel	104-113	P53	Homo sapiens	258-261
17637740-2	2008	We found that the cytotoxic drugs methotrexate (MTX) and 5-fluorouracil (5-FU) were both able to sensitize resistant tumor cells for induction of apoptosis by p53-mediated upregulation of caspase-8.	Methotrexate	34-46	P53	Homo sapiens	159-162
26131123-11	2015	CONCLUSIONS: These results confirmed that honokiol could induce apoptosis and cell cycle arrest, the underlying molecular mechanisms, at least partially, through activation p53 signaling and downregulation CDC2/cdc25C expression.	honokiol	42-50	P53	Homo sapiens	173-176
17637740-2	2008	We found that the cytotoxic drugs methotrexate (MTX) and 5-fluorouracil (5-FU) were both able to sensitize resistant tumor cells for induction of apoptosis by p53-mediated upregulation of caspase-8.	Methotrexate	48-51	P53	Homo sapiens	159-162
25575314-3	2015	While pifithrin-alpha, a specific p53 inhibitor, induced cell cycle arrest in G1 phase.	pifithrin	6-21	P53	Homo sapiens	34-37
18160328-0	2008	Clioquinol inhibits peroxide-mediated toxicity through up-regulation of phosphoinositol-3-kinase and inhibition of p53 activity.	Clioquinol	0-10	P53	Homo sapiens	115-118
17340621-11	2007	In addition, inhibition of CD95/Fas receptor on the cell surface of MCF-EGFP cells by treatment with Pifithrin-alpha, a p53 specific transactivation inhibitor, partially abrogated the sensitivity of bystander MCF-EGFP cells.	pifithrin	101-116	P53	Homo sapiens	120-123
17406354-3	2007	Here, we show that the transient transfection of the proline allele in p53 null cancer cells exposed to low oxygen tension or to the hypoxia-mimetic drug Desferoxamine induces a higher amount of cell death than the arginine allele.	desferoxamine	154-167	P53	Homo sapiens	71-74
17276690-8	2007	Thus, our novel naphthoindole based derivative of tryptamine gained new activities important for anticancer therapy, namely, suppression of topoisomerase I and the ability to overcome resistance mediated by P-glycoprotein expression and p53 dysfunction.	naphthoindole	16-29	P53	Homo sapiens	237-240
25575314-4	2015	Although 1, 2 and pifithrin-alpha caused serious inhibition on p53, 1 and 2 significantly cause the loss of mitochondrial membrane potential and increase of the reactive oxygen species level, cytochrome c, apaf-1 and caspase-3/9 ratio in BEL-7404 cells.	pifithrin	18-27	P53	Homo sapiens	63-75
25767399-2	2015	METHODS: The expression level of p53 protein was detected by immunohistochemistry in primary early-stage ER-positive breast tumor specimens from 293 postmenopausal breast cancer patients who received first-line AI treatment (letrozole, anastrozole, or exemestane) until relapse, and analysis was performed to determine whether expression of p53 protein affected the response to endocrine therapy.	exemestane	252-262	P53	Homo sapiens	33-36
17235352-1	2007	In this report, the effects of a combined treatment with the proteasome inhibitor bortezomib and either a recombinant adeno-associated virus type 2 (rAAV-2)-mediated p53 gene transfer or chemotherapeutic agents, docetaxel and pemetrexed, were tested on p53 positive and p53negative non-small cell lung cancer (NSCLC) cell lines.	Bortezomib	82-92	P53	Homo sapiens	253-256
17235352-2	2007	The combination of bortezomib and rAAV-p53 led to a significant synergistic inhibition of cell growth between 62-82% depending on the p53 status of the cell line and drug concentration.	Bortezomib	19-29	P53	Homo sapiens	134-137
17235352-4	2007	Enhanced cell toxicity was associated with a 5.3-14.4-fold increase of the apoptotic rate and intracellular p53 level up to 50.4% following vector-mediated p53 restoration and bortezomib treatment.	Bortezomib	176-186	P53	Homo sapiens	108-111
18094076-0	2008	Induction of apoptosis by vinblastine via c-Jun autoamplification and p53-independent down-regulation of p21WAF1/CIP1.	Vinblastine	26-37	P53	Homo sapiens	70-73
18094076-8	2008	In KB-3 cells, which have compromised p53 function, and in p53-null cells but not in p53 wild-type cells, vinblastine caused down-regulation of p21 expression concomitant with increased c-Jun expression, suggesting a role for c-Jun in negative regulation of the p21 promoter independent of p53.	Vinblastine	106-117	P53	Homo sapiens	38-41
18094076-8	2008	In KB-3 cells, which have compromised p53 function, and in p53-null cells but not in p53 wild-type cells, vinblastine caused down-regulation of p21 expression concomitant with increased c-Jun expression, suggesting a role for c-Jun in negative regulation of the p21 promoter independent of p53.	Vinblastine	106-117	P53	Homo sapiens	59-62
18094076-8	2008	In KB-3 cells, which have compromised p53 function, and in p53-null cells but not in p53 wild-type cells, vinblastine caused down-regulation of p21 expression concomitant with increased c-Jun expression, suggesting a role for c-Jun in negative regulation of the p21 promoter independent of p53.	Vinblastine	106-117	P53	Homo sapiens	59-62
18094076-8	2008	In KB-3 cells, which have compromised p53 function, and in p53-null cells but not in p53 wild-type cells, vinblastine caused down-regulation of p21 expression concomitant with increased c-Jun expression, suggesting a role for c-Jun in negative regulation of the p21 promoter independent of p53.	Vinblastine	106-117	P53	Homo sapiens	59-62
25557114-13	2015	CONCLUSION: Sorafenib inhibits HCC proliferation and invasion by inhibiting MMP-2 and Ki-67 expression due to up-regulation of P53 and suppressing FoxM1.	Sorafenib	12-21	P53	Homo sapiens	127-130
17855337-6	2007	Furthermore, RNA interference-mediated lowering of the p53 protein in T1 cells or pifithrin-alpha-induced p53-specific inhibition activity significantly decreased CTL-induced target killing mediated by CTL or recombinant GrB.	pifithrin	82-91	P53	Homo sapiens	106-109
17855337-9	2007	Treatment of T1 cells with pifithrin-alpha resulted in inhibition of p53 phosphorylation at these residues and in a significant decrease in GrB-induced apoptotic T1 cell death.	pifithrin	27-36	P53	Homo sapiens	69-72
16821082-0	2007	Possible involvement of CCT5, RGS3, and YKT6 genes up-regulated in p53-mutated tumors in resistance to docetaxel in human breast cancers.	Docetaxel	103-112	P53	Homo sapiens	67-70
16821082-1	2007	BACKGROUND: Present study was aimed to investigate the relationship of p53 mutation status with response to docetaxel in breast cancers.	Docetaxel	108-117	P53	Homo sapiens	71-74
25444910-6	2015	By contrast, arsenic trioxide, which by inhibiting wild-type p53-induced phosphatase-1 that serves responses downstream of p53, and by depolymerizing tubulin, synergistically enhanced cisplatin cytotoxicity including loss of SP cells.	Arsenic Trioxide	13-29	P53	Homo sapiens	61-64
16821082-2	2007	In addition, attempts were made to identify the genes differentially expressed between p53-wild and p53-mutated breast tumors and to study their relationship with response to docetaxel.	Docetaxel	175-184	P53	Homo sapiens	100-103
16821082-3	2007	METHODS: Mutational analysis of p53 was done in 50 breast tumor samples obtained from primary breast cancer patients (n = 33) and locally recurrent breast cancer patients (n = 17) before docetaxel therapy.	Docetaxel	187-196	P53	Homo sapiens	32-35
16821082-8	2007	Of these 13 genes, mRNA expression of CCT5, RGS3, and YKT6 was significantly up-regulated in p53-mutated tumors and associated with a low response rate to docetaxel.	Docetaxel	155-164	P53	Homo sapiens	93-96
16821082-10	2007	CONCLUSIONS: CCT5, RGS3, and YKT6 mRNA expressions, which are up-regulated in p53-mutated breast tumors, might be implicated in resistance to docetaxel and clinically useful in identifying the subset of breast cancer patients who may or may not benefit from docetaxel treatment.	Docetaxel	142-151	P53	Homo sapiens	78-81
17900801-5	2007	Combining the Chk1 inhibitor UCN-01 dramatically enhanced the response to AG490 in p53-mutated or deleted glioma cells.	7-hydroxystaurosporine	29-35	P53	Homo sapiens	83-86
25453767-7	2015	However, the most pronounced anti-epileptic effect was observed in rosuvastatin-treated animals, which was associated with improved blood-brain barrier (BBB) integrity, increased expression of endothelial nitric oxide synthase (eNOS) mRNA and decreased expressions of pro-apoptotic p53, Bax and caspase-3 mRNAs.	Rosuvastatin Calcium	67-79	P53	Homo sapiens	282-285
17910628-6	2007	Bortezomib/PXD101 treatment markedly triggered reactive oxygen species (ROS) generation that was accompanied by p53, H2A.X and p38-mitogen-activated protein kinase phosphorylation.	Bortezomib	0-10	P53	Homo sapiens	112-115
16821082-10	2007	CONCLUSIONS: CCT5, RGS3, and YKT6 mRNA expressions, which are up-regulated in p53-mutated breast tumors, might be implicated in resistance to docetaxel and clinically useful in identifying the subset of breast cancer patients who may or may not benefit from docetaxel treatment.	Docetaxel	258-267	P53	Homo sapiens	78-81
17215292-11	2007	MTH-68/H thus selectively kills tumor cell cultures by inducing endoplasmic reticulum stress leading to p53-independent apoptotic cell death.	Plicamycin	0-3	P53	Homo sapiens	104-107
25453767-10	2015	Here, we provide evidence that among HMG-CoA reductase inhibitors, rosuvastatin was the most effective statin on the reduction of epileptiform activity, which was associated with improved BBB permeability, increased expression of eNOS and decreased expressions of pro-apoptotic p53, Bax and caspase-3.	Rosuvastatin Calcium	67-79	P53	Homo sapiens	278-281
17557903-13	2007	As observed in humans, p53 plays a protective role in colitis-associated neoplasia in the DSS model.	Dextran Sulfate	90-93	P53	Homo sapiens	23-26
26119958-7	2015	Using p53(-/-) and p53(+/+) HCT-116 cells, we confirmed that p53/p21 was the main pathway that contributed to the G2/M cell cycle arrest by 6-shogaol.	shogaol	140-149	P53	Homo sapiens	6-9
17224176-7	2007	Moreover, we compared side-by-side the activity of four prominent human 3"-5" exonucleases (WRN, APE1, TREX1, and p53) on substrates containing 3" phosphates, phosphoglycolates, and tyrosyl residues.	cyclo(tyrosyl-tyrosyl)	182-189	P53	Homo sapiens	114-117
26119958-7	2015	Using p53(-/-) and p53(+/+) HCT-116 cells, we confirmed that p53/p21 was the main pathway that contributed to the G2/M cell cycle arrest by 6-shogaol.	shogaol	140-149	P53	Homo sapiens	19-22
18024399-2	2007	DESIGN AND METHODS: Melphalan-induced damage formation and repair of monoadducts and interstrand cross-links in the p53 gene were studied in peripheral blood mononuclear cells obtained from 32 patients prior to therapy.	Melphalan	20-29	P53	Homo sapiens	116-119
18024399-9	2007	INTERPRETATION AND CONCLUSIONS: An in vitro assay to quantify melphalan-induced p53-specific damage formation/repair can be used to select those patients with MM who are more likely to benefit from HDM supported by ASCT.	Melphalan	62-71	P53	Homo sapiens	80-83
17191121-0	2007	NAG-1 up-regulation mediated by EGR-1 and p53 is critical for quercetin-induced apoptosis in HCT116 colon carcinoma cells.	Quercetin	62-71	P53	Homo sapiens	42-45
16926174-0	2007	Potassium diazoacetate-induced p53 mutations in vitro in relation to formation of O6-carboxymethyl- and O6-methyl-2"-deoxyguanosine DNA adducts: relevance for gastrointestinal cancer.	potassium diazoacetate	0-22	P53	Homo sapiens	31-34
17914583-7	2007	We showed that SFN induced the growth arrest and up-regulated the expression of p21(WAF1/CIP1) protein in a p53-independent manner in human osteosarcoma MG63 cells.	sulforaphane	15-18	P53	Homo sapiens	108-111
16926174-3	2007	Potassium diazoacetate (KDA) is a stable form of nitrosated glycine and its ability to induce mutations in the p53 gene in a functional yeast assay was studied.	potassium diazoacetate	0-22	P53	Homo sapiens	111-114
26119958-7	2015	Using p53(-/-) and p53(+/+) HCT-116 cells, we confirmed that p53/p21 was the main pathway that contributed to the G2/M cell cycle arrest by 6-shogaol.	shogaol	140-149	P53	Homo sapiens	19-22
26021729-8	2015	3-MA and Atg5 siRNA increased the ox-LDL-induced increases of the p53 protein level and the annexin V-positive staining, which was decreased by z-vad-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	144-153	P53	Homo sapiens	66-69
17174366-7	2007	Induction of apoptosis by the stilbene required Ser-15 phosphorylation of p53.	Stilbenes	30-38	P53	Homo sapiens	74-77
17681284-0	2007	GEA 3162, a peroxynitrite donor, induces Bcl-2-sensitive, p53-independent apoptosis in murine bone marrow cells.	gea	0-3	P53	Homo sapiens	58-61
17624472-6	2007	Furthermore, the inhibition of Sirt1 by ASODN greatly increased radiation-induced antiproliferation effects involving in increasing acetylation of tumour suppressor p53 and Bax expression in A549 lung cancer cells.	asodn	40-45	P53	Homo sapiens	165-168
25896587-0	2015	The p53/miR-34a/SIRT1 Positive Feedback Loop in Quercetin-Induced Apoptosis.	Quercetin	48-57	P53	Homo sapiens	4-7
17487067-12	2007	HepG2 cells exposed to arsenic trioxide and PFT-alpha showed expression of only the P53 and PCNA genes.	Arsenic Trioxide	23-39	P53	Homo sapiens	84-87
25896587-5	2015	RESULTS: miR-34a was up-regulated in HepG2 cells treated by quercetin exhibiting wild-type p53.	Quercetin	60-69	P53	Homo sapiens	91-94
17938262-5	2007	Exposure of PC-3 and LNCaP cells to honokiol resulted in the induction of p21 (PC-3 and LNCaP) and p53 protein expression (LNCaP).	honokiol	36-44	P53	Homo sapiens	99-102
28970873-5	2015	The transformation of the azidophenyl label to nitrophenyltriazole was used for electrochemical detection of DNA-protein interactions (p53 protein) since only those azidophenyl groups in the parts of the DNA not shielded by the bound p53 protein were transformed to nitrophenyltriazoles, whereas those covered by the protein were not.	nitrophenyltriazoles	266-286	P53	Homo sapiens	135-138
17611679-5	2007	Combinations of beta-elemene with docetaxel induced much stronger synergistic interactions in p53 mutant H23 cells and p53 null H358 cells than in p53 wild-type H460 and A549 cells.	beta-elemene	16-28	P53	Homo sapiens	94-97
17611679-5	2007	Combinations of beta-elemene with docetaxel induced much stronger synergistic interactions in p53 mutant H23 cells and p53 null H358 cells than in p53 wild-type H460 and A549 cells.	beta-elemene	16-28	P53	Homo sapiens	119-122
17611679-5	2007	Combinations of beta-elemene with docetaxel induced much stronger synergistic interactions in p53 mutant H23 cells and p53 null H358 cells than in p53 wild-type H460 and A549 cells.	beta-elemene	16-28	P53	Homo sapiens	119-122
18001220-7	2007	The increase in apoptosis following quercetin exposure was p53/Bax mediated and correlated with a decrease in GST-driven bioreduction capacity and an increase in ROS.	Quercetin	36-45	P53	Homo sapiens	59-62
17611679-5	2007	Combinations of beta-elemene with docetaxel induced much stronger synergistic interactions in p53 mutant H23 cells and p53 null H358 cells than in p53 wild-type H460 and A549 cells.	Docetaxel	34-43	P53	Homo sapiens	94-97
25737737-6	2015	Treatment of cells with pifithrin-alpha, a specific inhibitor of p53, suppressed shikonin-induced apoptosis and premature senescence, suggesting the role of p53 in mediating the actions of shikonin on regulation of lung cancer cell proliferation.	pifithrin	24-39	P53	Homo sapiens	65-68
17611679-5	2007	Combinations of beta-elemene with docetaxel induced much stronger synergistic interactions in p53 mutant H23 cells and p53 null H358 cells than in p53 wild-type H460 and A549 cells.	Docetaxel	34-43	P53	Homo sapiens	119-122
17611679-5	2007	Combinations of beta-elemene with docetaxel induced much stronger synergistic interactions in p53 mutant H23 cells and p53 null H358 cells than in p53 wild-type H460 and A549 cells.	Docetaxel	34-43	P53	Homo sapiens	119-122
17611679-8	2007	In H460 and A549 cells, dose-dependent upregulation of p53 protein expression was observed in cultures treated with docetaxel alone and with docetaxel plus beta-elemene, whereas no significant change in p53 expression was observed in any of the treatment groups in H23 cells.	Docetaxel	116-125	P53	Homo sapiens	55-58
17611679-8	2007	In H460 and A549 cells, dose-dependent upregulation of p53 protein expression was observed in cultures treated with docetaxel alone and with docetaxel plus beta-elemene, whereas no significant change in p53 expression was observed in any of the treatment groups in H23 cells.	Docetaxel	141-150	P53	Homo sapiens	55-58
17611679-8	2007	In H460 and A549 cells, dose-dependent upregulation of p53 protein expression was observed in cultures treated with docetaxel alone and with docetaxel plus beta-elemene, whereas no significant change in p53 expression was observed in any of the treatment groups in H23 cells.	beta-elemene	156-168	P53	Homo sapiens	55-58
17611679-11	2007	These results suggest that, although p53 plays an important role in taxane-induced cell death, apoptosis induced by beta-elemene or in combination with docetaxel thereof seems to be initiated through a p53- and Fas-independent pathway via mitochondria in our lung cancer cells.	beta-elemene	116-128	P53	Homo sapiens	202-205
16950207-6	2006	Combined sulindac/ATO treatment also activated p53 expression, and inhibition of p53 expression by small interfering RNA (siRNA) prevented sulindac/ATO-induced down-regulation of survivin, suggesting that survivin expression is negatively regulated by p53.	Arsenic Trioxide	18-21	P53	Homo sapiens	47-50
25737737-6	2015	Treatment of cells with pifithrin-alpha, a specific inhibitor of p53, suppressed shikonin-induced apoptosis and premature senescence, suggesting the role of p53 in mediating the actions of shikonin on regulation of lung cancer cell proliferation.	pifithrin	24-39	P53	Homo sapiens	157-160
17075316-2	2006	Here, we show that p53-defective HT-29 colon cancer cells overcome methotrexate-induced cell death owing to DNA damage checkpoint-mediated cell survival at the adaptive stage that precedes stable resistance acquisition.	Methotrexate	67-79	P53	Homo sapiens	19-22
17551498-5	2007	MCF-7 (oestrogen receptor (ER)+/p53 wild-type) was the most sensitive cell line to xanafide.	xanafide	83-91	P53	Homo sapiens	32-35
26089934-0	2015	The Flavonoid Apigenin Ameliorates Cisplatin-Induced Nephrotoxicity through Reduction of p53 Activation and Promotion of PI3K/Akt Pathway in Human Renal Proximal Tubular Epithelial Cells.	Flavonoids	4-13	P53	Homo sapiens	89-92
17096161-3	2007	We also tested whether bortezomib interactions with cytarabine and anthracyclines are affected by p53, because proteasome inhibition stabilizes p53 and may thus cause cell cycle arrest.	Bortezomib	23-33	P53	Homo sapiens	98-101
17630850-5	2007	The p53 inhibitor pifithrin did not block GSNO-induced cell death.	pifithrin	18-27	P53	Homo sapiens	4-7
17016641-0	2006	P53-dependent radiosensitizing effects of Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin on human oral squamous cell carcinoma cell lines.	tanespimycin	58-96	P53	Homo sapiens	0-3
17016641-9	2006	17-AAG enhanced the radiation sensitivity significantly and induced apoptosis in the SAS/neo cell which has a wild-type p53.	tanespimycin	0-6	P53	Homo sapiens	120-123
17016641-10	2006	But the radiation sensitizing effect of 17-AAG was limited in the SAS/Trp248 cell which has a mutated p53.	tanespimycin	40-46	P53	Homo sapiens	102-105
17030796-2	2006	The p53 binding pattern of carcinogenic polycyclic aromatic hydrocarbons (PAHs) found in CS coincides with the p53 mutational pattern found in lung cancer, and PAHs have thus been considered to be major culprits for lung cancer.	Polycyclic Aromatic Hydrocarbons	40-72	P53	Homo sapiens	4-7
17456577-13	2007	Finally, when we added pifithrin-alpha, a specific inhibitor of p53 functions, a significant decrease in irradiation-induced apoptosis in both germ and Sertoli cells was observed, indicating the involvement of the p53 pathway in irradiation-induced apoptosis.	pifithrin	23-38	P53	Homo sapiens	64-67
17030796-2	2006	The p53 binding pattern of carcinogenic polycyclic aromatic hydrocarbons (PAHs) found in CS coincides with the p53 mutational pattern found in lung cancer, and PAHs have thus been considered to be major culprits for lung cancer.	Polycyclic Aromatic Hydrocarbons	74-78	P53	Homo sapiens	4-7
17456577-13	2007	Finally, when we added pifithrin-alpha, a specific inhibitor of p53 functions, a significant decrease in irradiation-induced apoptosis in both germ and Sertoli cells was observed, indicating the involvement of the p53 pathway in irradiation-induced apoptosis.	pifithrin	23-38	P53	Homo sapiens	214-217
26374525-5	2015	However, the activation of a p63/p53-and PCNA-dependent DNA damage checkpoint, plays a major role in eliminating defective oocytes when they reach the diplotene stage.	diplotene	151-160	P53	Homo sapiens	33-36
17393435-0	2007	A plant lignan, 3"-O-methyl-nordihydroguaiaretic acid, suppresses papillomavirus E6 protein function, stabilizes p53 protein, and induces apoptosis in cervical tumor cells.	heminordihydroguaiaretic acid	16-53	P53	Homo sapiens	113-116
17030796-2	2006	The p53 binding pattern of carcinogenic polycyclic aromatic hydrocarbons (PAHs) found in CS coincides with the p53 mutational pattern found in lung cancer, and PAHs have thus been considered to be major culprits for lung cancer.	Polycyclic Aromatic Hydrocarbons	74-78	P53	Homo sapiens	111-114
17030796-2	2006	The p53 binding pattern of carcinogenic polycyclic aromatic hydrocarbons (PAHs) found in CS coincides with the p53 mutational pattern found in lung cancer, and PAHs have thus been considered to be major culprits for lung cancer.	Polycyclic Aromatic Hydrocarbons	160-164	P53	Homo sapiens	4-7
25597668-0	2015	Modulation of the DNA repair system and ATR-p53 mediated apoptosis is relevant for tributyltin-induced genotoxic effects in human hepatoma G2 cells.	tributyltin	83-94	P53	Homo sapiens	44-47
17035402-7	2006	Among patients with detectable LOH at the TP53 locus (on chromosome 17p), increasing bleomycin sensitivity was associated with increased risk of developing cancer (P(trend) &lt; 0.001) and aneuploidy (P(trend) = 0.005).	Bleomycin	85-94	P53	Homo sapiens	42-46
17040108-9	2006	The cytosine residue of the ACG sequence complementary to codon 273, well-known hotspots of the p53 gene, was cleaved with piperidine and Fpg treatments.	Cytosine	4-12	P53	Homo sapiens	96-99
17369602-0	2007	p-53 gene mutations as a predictive marker in a population of advanced breast cancer patients randomly treated with doxorubicin or docetaxel in the context of a phase III clinical trial.	Docetaxel	131-140	P53	Homo sapiens	0-4
17504512-4	2007	The polymorphism on p53, which encodes either a proline or an arginine amino acid residue at codon 72, has been reported as a possible risk factor for cervical disease.	arginine amino acid	62-81	P53	Homo sapiens	20-23
25597668-4	2015	We further demonstrated that TBT induced cell apoptosis via the p53-mediated pathway, which was most likely activated by the ataxia telangiectasia mutated and rad-3 related (ATR) protein kinase.	tributyltin	29-32	P53	Homo sapiens	64-67
25597668-7	2015	Then the generated DNA damage induced by TBT initiated ATR-p53-mediated apoptosis.	tributyltin	41-44	P53	Homo sapiens	59-62
25738310-12	2015	Sorafenib suppressed p53 expression at both mRNA and protein levels, which might contribute to cell cycle arrest and sensitize tumor cells to irinotecan.	Sorafenib	0-9	P53	Homo sapiens	21-24
17157427-8	2007	This damage was detected as an enhanced migration of TP53 signals into the comet tail in both cell types, which indicates a high susceptibility of this tumor relevant gene towards Fe-NTA.	ferric nitrilotriacetate	180-186	P53	Homo sapiens	53-57
16891316-9	2006	Based on this, we propose that a pathway composed of ATR, PML, Chk2, and p53 plays a role in ATO-mediated apoptosis, a notion that is consistent with the observation that Chk2 is genetically intact and mutations in the p53 gene are extremely rare in APL.	Arsenic Trioxide	93-96	P53	Homo sapiens	73-76
16891316-9	2006	Based on this, we propose that a pathway composed of ATR, PML, Chk2, and p53 plays a role in ATO-mediated apoptosis, a notion that is consistent with the observation that Chk2 is genetically intact and mutations in the p53 gene are extremely rare in APL.	Arsenic Trioxide	93-96	P53	Homo sapiens	219-222
17157427-9	2007	In conclusion, Fe-NTA acts genotoxic in non-transformed and in preneoplastic human colon cells, in which it also enhances migration of TP53 at relatively low concentrations.	ferric nitrilotriacetate	15-21	P53	Homo sapiens	135-139
25435953-15	2015	Subsequent to the use of Pifithrin-alpha, a specific inhibitor of p53 activation, increased MDM2 expression was observed in the LIRR1-overexpressing cells, suggesting that LIRR1 could mediate the DNA damage response (DDR) signaling in a p53-dependent manner.	pifithrin	25-40	P53	Homo sapiens	66-69
17230520-2	2007	Earlier studies have shown that selenite induces DNA single strand breaks (SSBs), reactive oxygen species (ROS), p53 Ser-15 phosphorylation and caspase-dependent and -independent apoptosis, whereas a methylselenol precursor methylseleninic acid (MSeA) induces caspase-mediated apoptosis regardless of p53 status.	methaneselenol	200-213	P53	Homo sapiens	301-304
20641411-10	2004	showed that the binding of resveratrol to integrin alphaVss3, principally to the ss3 monomer, was essential for transduction of the stilbene signal into p53-dependent apoptosis of breast cancer cells.	Stilbenes	132-140	P53	Homo sapiens	153-156
25435953-15	2015	Subsequent to the use of Pifithrin-alpha, a specific inhibitor of p53 activation, increased MDM2 expression was observed in the LIRR1-overexpressing cells, suggesting that LIRR1 could mediate the DNA damage response (DDR) signaling in a p53-dependent manner.	pifithrin	25-40	P53	Homo sapiens	237-240
16720286-9	2006	The three retinoids differentially affected p53, RARs, and JWA.	Retinoids	10-19	P53	Homo sapiens	44-47
25510742-8	2015	RESULTS: Anthocyanin treatment of DU-145 cells resulted in 1) significant increase in apoptosis in a dose-dependent manner, 2) significant decrease in p53 and Bcl-2 expressions (with increased Bax expression), and 3) significant decrease in PSA and AR expressions.	du	34-36	P53	Homo sapiens	151-154
16720314-7	2006	In all cell lines, quercetin decreased the expression of mutant P53 and Survivin proteins.	Quercetin	19-28	P53	Homo sapiens	64-67
16720314-11	2006	Quercetin-induced apoptosis might be associated with a decrease in mutant P53 and Survivin proteins.	Quercetin	0-9	P53	Homo sapiens	74-77
25523932-17	2014	CONCLUSIONS: HATi II inhibits proliferation and induces apoptosis via the caspase-dependent pathway in human glioma cell lines, possibly by activating the p53 signaling pathway.	hati ii	13-20	P53	Homo sapiens	155-158
16948901-6	2006	Expression of P53 and C-myc protein decreased following quercetin induction in a dose-dependent manner, whereas P16 expression increased significantly compared with that of the control group (P&lt;0.01).	Quercetin	56-65	P53	Homo sapiens	14-17
16632641-9	2006	SP600125 (anthra [1,9-cd]pyrazol-6(2H)-one-1,9-pyrazoloanthrone), a specific inhibitor of JNK, significantly decreased apoptosis by inhibiting the phosphorylation of p53 (serine 15) and subsequently increased the interaction of p53 and MDM2.	pyrazolanthrone	0-8	P53	Homo sapiens	166-169
25565771-9	2015	Pifithrin-alpha, a p53 inhibitor, blocked the modulation of As4S4 on AGS cells, but not on MGC803 cells.	pifithrin	0-15	P53	Homo sapiens	19-22
16632641-9	2006	SP600125 (anthra [1,9-cd]pyrazol-6(2H)-one-1,9-pyrazoloanthrone), a specific inhibitor of JNK, significantly decreased apoptosis by inhibiting the phosphorylation of p53 (serine 15) and subsequently increased the interaction of p53 and MDM2.	pyrazolanthrone	0-8	P53	Homo sapiens	228-231
16500682-6	2006	Treatment with sulforaphane (15 microM), PEITC (10 microM), indole-3-carbinol (10 microM) and 3,3"-diindolylmethane (10 microM) induced PARP cleavage after 24 and 48 h in both 40-16 and the 379.2 cell lines, suggestive of a p53-independent mechanism of apoptosis induction.	sulforaphane	15-27	P53	Homo sapiens	224-227
16500682-10	2006	Taken together, we demonstrated that the glucosinolate breakdown products investigated in this study have distinct profiles of cell growth inhibition, potential to induce p53-independent apoptosis and to modulate Bcl-2 family protein expression in human colon cancer cell lines.	Glucosinolates	41-54	P53	Homo sapiens	171-174
16714289-10	2006	PGE(2), overexpression of p53wt with PGE(2), or p53S15E abolished the MEKK1-induced MMP-1 promoter luciferase activity.	Prostaglandins E	37-40	P53	Homo sapiens	26-29
25495224-3	2014	RESULTS: The effect of IL-1beta, but not of TNF-alpha, on glutamate-mediated excitatory postsynaptic currents was blocked by pifithrin-alpha (PFT), inhibitor of p53.	pifithrin	125-140	P53	Homo sapiens	161-164
26579413-0	2014	ETME, a novel beta-elemene derivative, synergizes with arsenic trioxide in inducing apoptosis and cell cycle arrest in hepatocarcinoma cells via a p53-dependent pathway.	Arsenic Trioxide	55-71	P53	Homo sapiens	147-150
16765943-4	2006	Moreover, Western blot studies showed that (R)-roscovitine increased nutlin-3-mediated p53 stabilization.	Roscovitine	43-58	P53	Homo sapiens	87-90
16765943-5	2006	Therefore, we conclude the contribution of (R)-roscovitine to the synergism is basically the sensitization of SH-SY5Y cells to the action of nutlin-3 on p53.	Roscovitine	43-58	P53	Homo sapiens	153-156
16533604-3	2006	ET-743, a DNA minor groove binder, which blocks cell cycle progression in G2/M phase through a p53-independent apoptotic process, represents the most promising among novel compounds in STS, since recently completed phase II trials have consistently shown high survival, in spite of the relatively low incidence of major objective responses.	Trabectedin	0-6	P53	Homo sapiens	95-98
26579413-5	2014	The combination also decreased the MMP, down-regulated Bcl-2 and pro-proteins of the caspase family, and up-regulated Bax and BID, all of which were reversed by the p53 inhibitor, pifithrin-alpha.	pifithrin	180-189	P53	Homo sapiens	165-168
25412312-7	2014	On the other hand, when human colorectal cancer HCT-116 cells with wild-type p53 were treated with BITC, translocation of p65 to the nucleus was inhibited rather than enhanced.	benzyl isothiocyanate	99-103	P53	Homo sapiens	77-80
16735036-1	2006	Exposure of Jurkat T lymphocytes containing functional p53 to nanomolar concentrations of bisanthracycline WP631 resulted in arrest at the G2/M checkpoint and transient senescence-like phenotype in the presence of DNA synthesis.	bisanthracycline	90-106	P53	Homo sapiens	55-58
25098371-0	2014	L-Leucine improves the anaemia in models of Diamond Blackfan anaemia and the 5q- syndrome in a TP53-independent way.	Leucine	0-9	P53	Homo sapiens	95-99
25204604-0	2014	beta-Elemene against human lung cancer via up-regulation of P53 protein expression to promote the release of exosome.	beta-elemene	0-12	P53	Homo sapiens	60-63
16574813-8	2006	On the contrary, suppression of PTEN levels by RNA interference restores the enhanced expression of p53-dependent p21(WAF1) and p53-independent p27(kip1) through inactivating the effect of PTEN on PI-3K/AKT signaling modulated by ganglioside GM3.	Gangliosides	230-241	P53	Homo sapiens	100-103
16574813-8	2006	On the contrary, suppression of PTEN levels by RNA interference restores the enhanced expression of p53-dependent p21(WAF1) and p53-independent p27(kip1) through inactivating the effect of PTEN on PI-3K/AKT signaling modulated by ganglioside GM3.	Gangliosides	230-241	P53	Homo sapiens	128-131
16467208-6	2006	High doses of ATO induced p53 accumulation in 11 of 21 patients.	Arsenic Trioxide	14-17	P53	Homo sapiens	26-29
25204604-11	2014	The levels of the anti-apoptotic genes Bcl-2 and Bcl-xl in A549 cells decreased, while expression of P53 and production of exosomes increased after beta-elemene treatment.	beta-elemene	148-160	P53	Homo sapiens	101-104
16288207-9	2006	Pretreatment with the specific p53 inhibitor pifithrin or downregulation of p53 using a specific small inhibitory RNA significantly attenuated ODQ-induced apoptosis.	pifithrin	45-54	P53	Homo sapiens	31-34
25204604-12	2014	Further siRNA studies suggested that the effect of beta-elemene on A549 cells is dependent on P53 expression.	beta-elemene	51-63	P53	Homo sapiens	94-97
25204604-14	2014	The in vivo study demonstrated that beta-elemene inhibited tumor growth, and up-regulated the expression of P53 and the release of exosome.	beta-elemene	36-48	P53	Homo sapiens	108-111
16525665-9	2006	DHPLC demonstrated that 37.5% (3/8) of esophageal carcinomas and 44.4% (4/9) of gastric carcinomas have p53 mutations.	dhplc	0-5	P53	Homo sapiens	104-107
25204604-15	2014	CONCLUSION: Our results demonstrated beta-elemene acts on lung cancer cells in a P53 dependent manner and exosomes are involved in the regulation of cell proliferation.	beta-elemene	37-49	P53	Homo sapiens	81-84
24928376-9	2014	Quercetin also could increase p53 and Caspase-3 expression.	Quercetin	0-9	P53	Homo sapiens	30-33
16436374-3	2006	Mammalian cells contain three non-identical subunits of RNR; that is, one homodimeric large subunit, R1, carrying the catalytic site and two variants of the homodimeric small subunit, R2 and the p53-inducible p53R2, each containing a tyrosyl free radical essential for catalysis.	tyrosyl free radical	234-254	P53	Homo sapiens	195-198
24786831-4	2014	PELP1 is phosphorylated at Serine1033 by various DDR kinases like ataxia-telangiectasia mutated, ataxia telangiectasia and Rad3-related or DNAPKc and this phosphorylation of PELP1 is important for p53 coactivation functions.	serine1033	27-37	P53	Homo sapiens	197-200
16319070-7	2006	Furthermore, troglitazone induced Ser-392 phosphorylation of p53 via a PPARgamma-dependent pathway and up-regulation of Bax in a p53 wild-type glioma.	Troglitazone	13-25	P53	Homo sapiens	61-64
16319070-7	2006	Furthermore, troglitazone induced Ser-392 phosphorylation of p53 via a PPARgamma-dependent pathway and up-regulation of Bax in a p53 wild-type glioma.	Troglitazone	13-25	P53	Homo sapiens	129-132
24946211-9	2014	The anti-oxidant N-acetylcysteine (NAC), the P53 inhibitor pifithrin-alpha (PFTalpha) as well as P53 siRNA knockdown suppressed berberine-induced P53 mitochondrial translocation and Cyp-D association, thus inhibiting mitochondrial membrane potential (MMP) decrease and prostate cancer cell necrosis.	pifithrin	59-74	P53	Homo sapiens	45-48
16306425-7	2006	Taken together, these data suggest that the TRP53 protein influences the sensitivity of GC-2 cells to undergo FAS-mediated apoptosis by modulating the expression of FAS on their cell membranes and subsequently influencing the degradation of the antiapoptotic protein CFLAR (L).	ammonium ferrous sulfate	110-113	P53	Homo sapiens	44-49
16544944-9	2006	In TK6 cells (p53), the sublethal threshold dose induced DNA double-strand breaks, but nucleobase deamination products (xanthine, hypoxanthine, and uracil) in DNA were increased only modestly (&lt;50%) by toxic doses.	Uracil	148-154	P53	Homo sapiens	14-17
24928858-5	2014	p53 in which Ser15 is substituted by alanine (S15A) fails to mediate p53-dependent transcription or growth arrest but can be rescued by substitution with aspartate (S15D: a phospho-mimic).	Aspartic Acid	154-163	P53	Homo sapiens	0-3
16139849-0	2006	Role of the mismatch repair system and p53 in the clastogenicity and cytotoxicity induced by bleomycin.	Bleomycin	93-102	P53	Homo sapiens	39-42
16139849-2	2006	Aim of this study was to examine the effects of either MMR-deficiency or p53 inactivation, or both, on cellular responses to bleomycin.	Bleomycin	125-134	P53	Homo sapiens	73-76
24927258-0	2014	Increased growth-inhibitory and cytotoxic activity of arsenic trioxide in head and neck carcinoma cells with functional p53 deficiency and resistance to EGFR blockade.	Arsenic Trioxide	54-70	P53	Homo sapiens	120-123
16139849-11	2006	In conclusion, our data show that loss of MMR and p53 function exerts opposite and independent effects on apoptosis and chromosomal damage induced by bleomycin.	Bleomycin	150-159	P53	Homo sapiens	50-53
16170570-0	2006	p53-independent G1 cell cycle arrest of human colon carcinoma cells HT-29 by sulforaphane is associated with induction of p21CIP1 and inhibition of expression of cyclin D1.	sulforaphane	77-89	P53	Homo sapiens	0-3
24927258-4	2014	The causal relationship between p53 deficiency and ATO sensitivity was evaluated by reconstitution of wildtype p53 in p53-deficient SCCHN cells.	Arsenic Trioxide	51-54	P53	Homo sapiens	32-35
16467109-7	2006	Radiosensitization of cells expressing p53 by TSA was reduced by pifithrin-alpha, a small-molecule inhibitor of p53.	pifithrin	65-80	P53	Homo sapiens	39-42
24927258-4	2014	The causal relationship between p53 deficiency and ATO sensitivity was evaluated by reconstitution of wildtype p53 in p53-deficient SCCHN cells.	Arsenic Trioxide	51-54	P53	Homo sapiens	111-114
16467109-7	2006	Radiosensitization of cells expressing p53 by TSA was reduced by pifithrin-alpha, a small-molecule inhibitor of p53.	pifithrin	65-80	P53	Homo sapiens	112-115
24927258-4	2014	The causal relationship between p53 deficiency and ATO sensitivity was evaluated by reconstitution of wildtype p53 in p53-deficient SCCHN cells.	Arsenic Trioxide	51-54	P53	Homo sapiens	111-114
24927258-6	2014	RESULTS: Functional rather than structural defects in the p53 gene predisposed tumor cells to increased sensitivity to ATO.	Arsenic Trioxide	119-122	P53	Homo sapiens	58-61
24927258-7	2014	Reconstitution of wt p53 in p53-deficient SCCHN cells rendered them less sensitive to ATO treatment.	Arsenic Trioxide	86-89	P53	Homo sapiens	21-24
24927258-7	2014	Reconstitution of wt p53 in p53-deficient SCCHN cells rendered them less sensitive to ATO treatment.	Arsenic Trioxide	86-89	P53	Homo sapiens	28-31
24927258-9	2014	The inhibitory effect of ATO in p53-deficient tumor cells was mainly associated with DNA damage, G2/M arrest, upregulation of TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) receptors and apoptosis.	Arsenic Trioxide	25-28	P53	Homo sapiens	32-35
16505115-2	2006	However, it is also known that nucleosides are efficient activators of apoptosis in tumor cells that do not express a functional p53.	Nucleosides	31-42	P53	Homo sapiens	129-132
24927258-11	2014	CONCLUSIONS: Addition of ATO to treatment regimens for p53-deficient SCCHN and tumor recurrence after cetuximab-containing regimens might represent an attractive strategy in SCCHN.	Arsenic Trioxide	25-28	P53	Homo sapiens	55-58
16505115-11	2006	Together, these studies indicate that c-Abl-independent p73 stabilization pathways could account for the p53-independent mechanisms in nucleoside-induced apoptosis.	Nucleosides	135-145	P53	Homo sapiens	105-108
24841907-6	2014	Moreover, the p53 inhibitor pifithrin-alpha and the nuclear factor (NF)-kappaB inhibitor pyrrolidinedithiocarbamic acid (PDTC) clearly suppressed Beclin-1 and LC3-II and increased cytochrome c release, caspase-3 activation, and PARP cleavage.	pifithrin	28-37	P53	Homo sapiens	14-17
16582987-2	2006	We studied sequence-specific interaction of the vinyl-chloride metabolite CAA with human p53 gene exons 5-8, using DNA Polymerase Fingerprint Analysis (DPFA), and identified sites of the highest sensitivity.	chloroacetaldehyde	74-77	P53	Homo sapiens	89-92
16582987-3	2006	CAA-induced DNA damage was more extensive in p53 regions which revealed secondary structure perturbations, and were localized in regions of mutation hot-spots.	chloroacetaldehyde	0-3	P53	Homo sapiens	45-48
16582987-6	2006	A plasmid bearing full length cDNA of human p53 gene was modified in vitro with 360 mM CAA and transformed into E. coli DH5alpha strain, in which the adaptive response system had been induced by MMS treatment before the cells were made competent.	chloroacetaldehyde	87-90	P53	Homo sapiens	44-47
24736433-5	2014	The main objective of this study was to determine whether p53 modulated AhR-dependent gene expression and PAH metabolism.	Polycyclic Aromatic Hydrocarbons	106-109	P53	Homo sapiens	58-61
24736433-13	2014	Collectively, our results suggest that p53 affects AhR-dependent gene expression, PAH metabolism, and possibly carcinogenesis.	Polycyclic Aromatic Hydrocarbons	82-85	P53	Homo sapiens	39-42
24694947-11	2014	Our data show olaparib and veliparib differ in their off-target effects; olaparib, unlike veliparib, mitigates DNA damage repair activity via G(2) cell-cycle arrest-like effect in a p53-dependent manner.	veliparib	27-36	P53	Homo sapiens	182-185
24878898-8	2014	Phosphorylation of AMPK, ULK, JNK, c-jun, and p53 was increased significantly in response to KIOM-C treatment.	kiom-c	93-99	P53	Homo sapiens	46-49
24089038-4	2014	Following ex vivo treatment with melphalan, a gradual suppression of the apoptotic pathway occurred in samples collected at different stages of myelomagenesis, with the severity and duration of the inhibition of RNA synthesis, p53 phosphorylation at serine15 and induction of apoptosis being higher in MGUS than SMM and lowest in MM patients (all P&lt;0.0103).	Melphalan	33-42	P53	Homo sapiens	227-230
24462521-11	2014	Our results collectively demonstrate that TP53-correlated kinase MPS1, is a potential therapeutic target in BC patients with TP53 mutated tumors, and that SP600125 warrant further development in future clinical trials.	pyrazolanthrone	155-163	P53	Homo sapiens	42-46
24743574-12	2014	Moreover, Bcl-2 expression was completely reversed by treatment with pifithrin-alpha, a p53-specific inhibitor.	pifithrin	69-84	P53	Homo sapiens	88-91
24601644-0	2014	Novel inhibitors of the MDM2-p53 interaction featuring hydrogen bond acceptors as carboxylic acid isosteres.	carboxylic acid isosteres	82-107	P53	Homo sapiens	29-32
25237368-0	2014	Effect of boswellia thurifera gum methanol extract on cytotoxicity and p53 gene expression in human breast cancer cell line.	Methanol	34-42	P53	Homo sapiens	71-74
25237368-2	2014	The aim of this study was to evaluate the effect of the gum methanol extract of Boswellia thurifera on the viability and P53 gene expression of cultured breast cancer cells.	Methanol	60-68	P53	Homo sapiens	121-124
25237368-9	2014	This inductive effect in cells was higher after 12 h treatment than it was after 6 h. The results of the current study show that gum methanol extract of Boswellia thurifera has probably anti-cancer effects and could induce P53 gene transcription and toxicity in the cultured breast cancer cell line.	Methanol	133-141	P53	Homo sapiens	223-226
25237368-10	2014	The increase of P53 gene specific mRNA may be a mechanism of gum methanol extract induced cytotoxicity.	Methanol	65-73	P53	Homo sapiens	16-19
24736075-3	2014	As dexamethasone strongly regulates many genes including p53 through the glucocorticoid receptor (GR), we hypothesized that dexamethasone influences tumor response to pemetrexed.	Pemetrexed	167-177	P53	Homo sapiens	57-60
24405416-4	2014	Herein we report the design, synthesis and optimization of YH239-EE (ethyl ester of the free carboxylic acid compound YH239), a potent p53-MDM2 antagonizing and apoptosis-inducing agent characterized by a number of leukemia cell lines as well as patient-derived AML blast samples.	ethyl ester	69-80	P53	Homo sapiens	135-138
24576095-1	2014	TIGAR [TP53 (tumour protein 53)-induced glycolysis and apoptosis regulator] protein is known for its ability to inhibit glycolysis, shifting glucose consumption towards the pentose phosphate pathway to promote antioxidant protection of cancer cells.	Pentosephosphates	173-190	P53	Homo sapiens	7-11
24533688-14	2014	Accordingly, our data suggested that garcinol induced G1 cell cycle arrest and apoptosis in lung cancer cells under different p53 statuses.	garcinol	37-45	P53	Homo sapiens	126-129
24533688-15	2014	The p53-independent G1 cell cycle arrest induced by garcinol might be through upregulation of p21(Waf1/Cip1) triggered from p38-MAPK signaling inactivation.	garcinol	52-60	P53	Homo sapiens	4-7
24446736-0	2014	Induction of lung cancer cell apoptosis through a p53 pathway by [6]-shogaol and its cysteine-conjugated metabolite M2.	shogaol	65-76	P53	Homo sapiens	50-53
24525232-5	2014	p53-like MIBCs were consistently resistant to neoadjuvant methotrexate, vinblastine, doxorubicin and cisplatin chemotherapy, and all chemoresistant tumors adopted a p53-like phenotype after therapy.	Vinblastine	72-83	P53	Homo sapiens	0-3
24967384-0	2014	Estrogen-related receptor alpha confers methotrexate resistance via attenuation of reactive oxygen species production and P53 mediated apoptosis in osteosarcoma cells.	Methotrexate	40-52	P53	Homo sapiens	122-125
24967384-7	2014	In conclusion, this study demonstrated that ERR alpha plays an important role in the development of MTX resistance through blocking MTX-induced ROS production and attenuating the activation of p53 mediated apoptosis signaling pathway, and points to ERR alpha as a novel target for improving osteosarcoma therapy.	Methotrexate	100-103	P53	Homo sapiens	193-196
24967384-7	2014	In conclusion, this study demonstrated that ERR alpha plays an important role in the development of MTX resistance through blocking MTX-induced ROS production and attenuating the activation of p53 mediated apoptosis signaling pathway, and points to ERR alpha as a novel target for improving osteosarcoma therapy.	Methotrexate	132-135	P53	Homo sapiens	193-196
25485499-6	2014	Furthermore, for the first time we demonstrated that Arsenic trioxide, which was previously shown to suppress mutant p53 protein level, exhibits proteasome inhibitory activity.	Arsenic Trioxide	53-69	P53	Homo sapiens	117-120
24467530-4	2014	These pathways and targets that are affected by chalcones include MDM2/p53, tubulin, proteasome, NF-kappa B, TRIAL/death receptors and mitochondria mediated apoptotic pathways, cell cycle, STAT3, AP-1, NRF2, AR, ER, PPAR-gamma and beta-catenin/Wnt.	Chalcones	48-57	P53	Homo sapiens	71-74
25307014-7	2014	Treatment of the cells with the co-delivery of DDAB:DOPE liposome/p53 plasmid DNA complexes and DDAB:DOPE liposome/ bcl-2 AS ODN complexes inhibited cell growth to a greater degree than that with either DDAB:DOPE liposome/p53 plasmid DNA complexes or DDAB:DOPE liposome/bcl-2 AS ODN complexes alone.	dimethyldioctadecylammonium	47-51	P53	Homo sapiens	66-69
25307014-7	2014	Treatment of the cells with the co-delivery of DDAB:DOPE liposome/p53 plasmid DNA complexes and DDAB:DOPE liposome/ bcl-2 AS ODN complexes inhibited cell growth to a greater degree than that with either DDAB:DOPE liposome/p53 plasmid DNA complexes or DDAB:DOPE liposome/bcl-2 AS ODN complexes alone.	dimethyldioctadecylammonium	96-100	P53	Homo sapiens	222-225
25307014-7	2014	Treatment of the cells with the co-delivery of DDAB:DOPE liposome/p53 plasmid DNA complexes and DDAB:DOPE liposome/ bcl-2 AS ODN complexes inhibited cell growth to a greater degree than that with either DDAB:DOPE liposome/p53 plasmid DNA complexes or DDAB:DOPE liposome/bcl-2 AS ODN complexes alone.	dimethyldioctadecylammonium	96-100	P53	Homo sapiens	222-225
24900784-0	2014	Discovery of Potent and Orally Active p53-MDM2 Inhibitors RO5353 and RO2468 for Potential Clinical Development.	ro2468	69-75	P53	Homo sapiens	38-41
24900784-4	2014	Here we report two new potent, selective, and orally active p53-MDM2 antagonists, RO5353 and RO2468, as follow-ups with promising potential for clinical development.	ro2468	93-99	P53	Homo sapiens	60-63
24140468-5	2013	In addition, PBDE-47 activated the p53-dependent mitochondrial apoptotic pathway as evidenced by up-regulation of p53 and Bax, down-regulation of Bcl-2 and Bcl-2/Bax ration, enhancement of Cyt c release from mitochondria into the cytosol, activation of caspase-3 as well as ultrastructural abnormalities of mitochondria.	2,2',4,4'-tetrabromodiphenyl ether	13-20	P53	Homo sapiens	35-38
24140468-5	2013	In addition, PBDE-47 activated the p53-dependent mitochondrial apoptotic pathway as evidenced by up-regulation of p53 and Bax, down-regulation of Bcl-2 and Bcl-2/Bax ration, enhancement of Cyt c release from mitochondria into the cytosol, activation of caspase-3 as well as ultrastructural abnormalities of mitochondria.	2,2',4,4'-tetrabromodiphenyl ether	13-20	P53	Homo sapiens	114-117
24211095-0	2013	Arsenic trioxide induces apoptosis in B-cell chronic lymphocytic leukemic cells through down-regulation of survivin via the p53-dependent signaling pathway.	Arsenic Trioxide	0-16	P53	Homo sapiens	124-127
24211095-4	2013	WSU-CLL cells treated with 2muM As2O3 showed survivin down-regulation and p53 up-regulation.	Arsenic Trioxide	32-37	P53	Homo sapiens	74-77
24211095-6	2013	p53 inhibition by siRNA prevented the down-regulation of survivin by As2O3 and prevented the As2O3-induced cytotoxicity of WSU-CLL cells.	Arsenic Trioxide	69-74	P53	Homo sapiens	0-3
24211095-6	2013	p53 inhibition by siRNA prevented the down-regulation of survivin by As2O3 and prevented the As2O3-induced cytotoxicity of WSU-CLL cells.	Arsenic Trioxide	93-98	P53	Homo sapiens	0-3
23954467-6	2013	Furthermore, we showed the cytotoxicity of teroxirone in H1299 cells with stable ectopic expression of p53, but not those of mutant p53.	teroxirone	43-53	P53	Homo sapiens	103-106
24004656-3	2013	We used three human neuroblastoma cell lines (SH-SY5Y, IGR-N-91, LAN-1) that differ from their MYCN and p53 status to explore the intracellular events activated by As2O3 and involved in neurite outgrowth, a morphological marker of differentiation.	Arsenic Trioxide	164-169	P53	Homo sapiens	104-107
17019560-10	2007	TBT exposure alters neither pro-apoptotic proteins Bax and p53 nor anti-apoptotic protein Bcl-2 levels at any exposure studied.	tributyltin	0-3	P53	Homo sapiens	59-62
24030461-11	2013	SFN enhanced nuclear translocation of Nrf2 in FECD specimens and decreased p53 staining under oxidative stress.	sulforaphane	0-3	P53	Homo sapiens	75-78
16936710-6	2007	In addition, the increased expression of DR5 receptor after beta amyloid treatment was sustained by p53 transcriptional activity, as demonstrated by the data showing that the p53 inhibitor Pifithrin alpha prevented both beta amyloid-induced DR5 induction and cell death.	pifithrin	189-204	P53	Homo sapiens	100-103
16936710-6	2007	In addition, the increased expression of DR5 receptor after beta amyloid treatment was sustained by p53 transcriptional activity, as demonstrated by the data showing that the p53 inhibitor Pifithrin alpha prevented both beta amyloid-induced DR5 induction and cell death.	pifithrin	189-204	P53	Homo sapiens	175-178
17363600-0	2007	The proteasome inhibitor bortezomib acts independently of p53 and induces cell death via apoptosis and mitotic catastrophe in B-cell lymphoma cell lines.	Bortezomib	25-35	P53	Homo sapiens	58-61
17363600-3	2007	Bortezomib induced a time- and concentration-dependent reduction in cell viability in five lymphoma cell lines, with EC(50) values ranging from 6 nmol/L (DHL-7 cells) to 25 nmol/L (DHL-4 cells) after 72 h. Bortezomib cytotoxicity was independent of p53 function, as all cell lines exhibited mutations by sequence analysis.	Bortezomib	0-10	P53	Homo sapiens	249-252
17339891-4	2007	Lovo 175X2 cells (transfected with mt p53) were more resistant to 5-fluorouracil (5-FU; 2-fold), nolatrexed (3-fold), raltitrexed (3-fold) and pemetrexed (10-fold) in comparison with the wt p53 parental cells Lovo 92.	Pemetrexed	143-153	P53	Homo sapiens	38-41
24078862-7	2013	Further SAR studies demonstrated the requirement for the triarylpyrrole moiety for MDMX-p53 activity but not for MDM2-p53 inhibition.	triarylpyrrole	57-71	P53	Homo sapiens	88-91
16917513-6	2007	However, we found that Fas/CD95 was significantly induced in response to hypoxia in a p53-dependent manner, along with several novel p53 target genes including ANXA1, DDIT3/GADD153 (CHOP), SEL1L and SMURF1.	ammonium ferrous sulfate	23-26	P53	Homo sapiens	86-89
17263498-0	2007	6-shogaol (alkanone from ginger) induces apoptotic cell death of human hepatoma p53 mutant Mahlavu subline via an oxidative stress-mediated caspase-dependent mechanism.	shogaol	0-9	P53	Homo sapiens	80-83
17191121-4	2007	Reporter assays using the luciferase constructs containing NAG-1 promoter region demonstrate that early growth response-1 (EGR-1) and p53 are required for quercetin-mediated activation of the NAG-1 promoter.	Quercetin	155-164	P53	Homo sapiens	134-137
23895620-4	2013	Novel 3-(2-anilinoethyl)-substituted imidazotetrazines are reported that have activity independent of MGMT, MMR, and p53.	3-(2-anilinoethyl)-substituted imidazotetrazines	6-54	P53	Homo sapiens	117-120
16902184-0	2007	Pifithrin-alpha, an inhibitor of p53 transactivation, alters the inflammatory process and delays tendon healing following acute injury.	pifithrin	0-15	P53	Homo sapiens	33-36
16902184-2	2007	The goal of this study was to evaluate the effect of a p53 transactivation inhibitor, namely, pifithrin-alpha, on the pathophysiological sequence following collagenase-induced tendon injury.	pifithrin	94-109	P53	Homo sapiens	55-58
23859017-4	2013	Cytotoxic concentrations of the nitric oxide donor sodium nitroprusside activated several proapoptotic mechanisms, including stimulation of the stress kinase pathways mediated by c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), inhibition of the translation initiation factor eIF2alpha, induction and phosphorylation of the p53 protein, and inhibited Akt-mediated antiapoptotic signaling, independent of Ras function.	Nitroprusside	51-71	P53	Homo sapiens	354-357
17341629-6	2006	Pifithrin-alpha (PFT), an inhibitor of p53 transcriptional activity, protected only NB4 cells with functional p53 from FK228-induced apoptosis and did not interfere with antiproliferative activity in p53-negative HL-60 cells.	pifithrin	0-15	P53	Homo sapiens	39-42
17341629-6	2006	Pifithrin-alpha (PFT), an inhibitor of p53 transcriptional activity, protected only NB4 cells with functional p53 from FK228-induced apoptosis and did not interfere with antiproliferative activity in p53-negative HL-60 cells.	pifithrin	0-15	P53	Homo sapiens	110-113
17341629-6	2006	Pifithrin-alpha (PFT), an inhibitor of p53 transcriptional activity, protected only NB4 cells with functional p53 from FK228-induced apoptosis and did not interfere with antiproliferative activity in p53-negative HL-60 cells.	pifithrin	0-15	P53	Homo sapiens	110-113
23449393-8	2013	Our results present a previously unknown link between the RA and p53 pathways and provide a rationale to use retinoids to upregulate Stra6, and thus enhance the tumour suppressor functions of p53.	Retinoids	109-118	P53	Homo sapiens	192-195
16982703-10	2006	Pifithrin-alpha enhanced chemosensitivity by a mechanism independent of p53 and involving AhR and p38 MAPK deregulation of eIF-4E phosphorylation.	pifithrin	0-9	P53	Homo sapiens	72-75
16950207-6	2006	Combined sulindac/ATO treatment also activated p53 expression, and inhibition of p53 expression by small interfering RNA (siRNA) prevented sulindac/ATO-induced down-regulation of survivin, suggesting that survivin expression is negatively regulated by p53.	Arsenic Trioxide	148-151	P53	Homo sapiens	81-84
23564507-8	2013	Quercetin activated JNK and increased the expression levels of c-Jun and p53-dependent Bax.	Quercetin	0-9	P53	Homo sapiens	73-76
16950207-6	2006	Combined sulindac/ATO treatment also activated p53 expression, and inhibition of p53 expression by small interfering RNA (siRNA) prevented sulindac/ATO-induced down-regulation of survivin, suggesting that survivin expression is negatively regulated by p53.	Arsenic Trioxide	148-151	P53	Homo sapiens	81-84
16777994-5	2006	Pifithrin-alpha, a p53 inhibitor, reversed silibinin-induced caspase activation including caspase 2; however, caspase 2 inhibitor also reversed p53 phosphorylation suggesting a bidirectional regulation between them.	pifithrin	0-15	P53	Homo sapiens	19-22
23564507-9	2013	Blockade of JNK activation by overexpression of dominant negative JNK1 suppressed apoptosis by quercetin via inhibition of caspase-3 activation and reduction of p53 and Bax expression.	Quercetin	95-104	P53	Homo sapiens	161-164
17055606-3	2006	Additionally, after transfection of p53-expressing plasmid DNA by pullulan-spermine but not Lipofectamine 2000, the in vitro proliferation of T24 cells was significantly reduced.	pullulan-spermine	66-83	P53	Homo sapiens	36-39
23564507-13	2013	Taken together, the JNK-p53 pathway is involved in quercetin-induced apoptosis, and simultaneous inactivation of GSK-3beta can attenuate apoptosis in normal bronchial epithelial cells.	Quercetin	51-60	P53	Homo sapiens	24-27
23523585-7	2013	HMJ-38-influenced HUVECs were performed by determining the oxidative stress (ROS production) and ATM/p53-modulated Fas and DR4/DR5 signals that were examined by flow cytometry, Western blotting, siRNA and real-time RT-PCR analyses, respectively.	ammonium ferrous sulfate	115-118	P53	Homo sapiens	101-104
17050687-3	2006	In addition to its role in activating the G(1) and G(2) checkpoints, p53 also helps to protect cells in S phase when they are starved for DNA precursors by treatment with the specific aspartate transcarbamylase inhibitor N-phosphonacetyl-l-aspartate (PALA), which blocks the synthesis of pyrimidine nucleotides.	sparfosic acid	221-249	P53	Homo sapiens	69-72
17050687-3	2006	In addition to its role in activating the G(1) and G(2) checkpoints, p53 also helps to protect cells in S phase when they are starved for DNA precursors by treatment with the specific aspartate transcarbamylase inhibitor N-phosphonacetyl-l-aspartate (PALA), which blocks the synthesis of pyrimidine nucleotides.	sparfosic acid	251-255	P53	Homo sapiens	69-72
23688327-0	2013	Interferon-alpha (IFN-alpha) suppresses HTLV-1 gene expression and cell cycling, while IFN-alpha combined with zidovudine induces p53 signaling and apoptosis in HTLV-1-infected cells.	Zidovudine	111-121	P53	Homo sapiens	130-133
16646077-0	2006	Clinically tolerable concentrations of arsenic trioxide induce p53-independent cell death and repress NF-kappa B activation in Ewing sarcoma cells.	Arsenic Trioxide	39-55	P53	Homo sapiens	63-66
23688327-13	2013	AZT combined with IFN-alpha markedly induced cell apoptosis associated with phosphorylation of p53 and induction of p53-responsive genes in ILTs.	Zidovudine	0-3	P53	Homo sapiens	95-98
23688327-13	2013	AZT combined with IFN-alpha markedly induced cell apoptosis associated with phosphorylation of p53 and induction of p53-responsive genes in ILTs.	Zidovudine	0-3	P53	Homo sapiens	116-119
16849420-8	2006	Bortezomib inhibited NF-kappaB activity; increased p53, p21, and jun expression; and induced caspase-dependent apoptosis.	Bortezomib	0-10	P53	Homo sapiens	51-54
23688327-15	2013	In combination with AZT, IFN-alpha further induced p53 signaling and cell apoptosis in these cells.	Zidovudine	20-23	P53	Homo sapiens	51-54
23652204-8	2013	MDM2 inhibition overcame lapatinib resistance in cells with either wild-type or mutant p53 and in xenograft models.	Lapatinib	25-34	P53	Homo sapiens	87-90
17062352-2	2006	It was found that the p53 gene condon 282 mutation (Arg/Leu) may destabilize the H2 helix and DNA binding in the major groove by compromising the contacts of p53 protein with the beta-hairpin of DNA binding surface.	Leucine	56-59	P53	Homo sapiens	22-25
17062352-2	2006	It was found that the p53 gene condon 282 mutation (Arg/Leu) may destabilize the H2 helix and DNA binding in the major groove by compromising the contacts of p53 protein with the beta-hairpin of DNA binding surface.	Leucine	56-59	P53	Homo sapiens	158-161
16797627-5	2006	In this study, we show that AZT, cisplatin (CDDP) and docetaxel (DTX) all induce unique molecular responses in OVCAR-3 ovarian carcinoma cells carrying a mutated p53, while in A2780, ovarian carcinoma and MCF-7 breast carcinoma cells with wild type p53, all of these drugs cause similar p53 responses.	Zidovudine	28-31	P53	Homo sapiens	249-252
16797627-5	2006	In this study, we show that AZT, cisplatin (CDDP) and docetaxel (DTX) all induce unique molecular responses in OVCAR-3 ovarian carcinoma cells carrying a mutated p53, while in A2780, ovarian carcinoma and MCF-7 breast carcinoma cells with wild type p53, all of these drugs cause similar p53 responses.	Docetaxel	54-63	P53	Homo sapiens	162-165
16797627-5	2006	In this study, we show that AZT, cisplatin (CDDP) and docetaxel (DTX) all induce unique molecular responses in OVCAR-3 ovarian carcinoma cells carrying a mutated p53, while in A2780, ovarian carcinoma and MCF-7 breast carcinoma cells with wild type p53, all of these drugs cause similar p53 responses.	Docetaxel	54-63	P53	Homo sapiens	249-252
22841391-2	2013	In this study, we used a protein array which contained 112 different antibodies known to be involved in the p53 pathway to investigate the molecular targets of methylselenol in human HCT116 colon cancer cells.	methaneselenol	160-173	P53	Homo sapiens	108-111
16797627-5	2006	In this study, we show that AZT, cisplatin (CDDP) and docetaxel (DTX) all induce unique molecular responses in OVCAR-3 ovarian carcinoma cells carrying a mutated p53, while in A2780, ovarian carcinoma and MCF-7 breast carcinoma cells with wild type p53, all of these drugs cause similar p53 responses.	Docetaxel	54-63	P53	Homo sapiens	249-252
16797627-5	2006	In this study, we show that AZT, cisplatin (CDDP) and docetaxel (DTX) all induce unique molecular responses in OVCAR-3 ovarian carcinoma cells carrying a mutated p53, while in A2780, ovarian carcinoma and MCF-7 breast carcinoma cells with wild type p53, all of these drugs cause similar p53 responses.	Docetaxel	65-68	P53	Homo sapiens	162-165
16797627-5	2006	In this study, we show that AZT, cisplatin (CDDP) and docetaxel (DTX) all induce unique molecular responses in OVCAR-3 ovarian carcinoma cells carrying a mutated p53, while in A2780, ovarian carcinoma and MCF-7 breast carcinoma cells with wild type p53, all of these drugs cause similar p53 responses.	Docetaxel	65-68	P53	Homo sapiens	249-252
16797627-5	2006	In this study, we show that AZT, cisplatin (CDDP) and docetaxel (DTX) all induce unique molecular responses in OVCAR-3 ovarian carcinoma cells carrying a mutated p53, while in A2780, ovarian carcinoma and MCF-7 breast carcinoma cells with wild type p53, all of these drugs cause similar p53 responses.	Docetaxel	65-68	P53	Homo sapiens	249-252
23596569-8	2013	While the role of p53 in cancer cell metabolism in arresting glycolysis and inhibition of pentose phosphate pathway has come to be recognized, there are confusions in the literature on the role of FoxO and that of rictor.	Pentosephosphates	90-107	P53	Homo sapiens	18-21
16805818-8	2006	Various biological parameters have been studied clinically for their ability to predict response to docetaxel, such as parameters related to: (1) efflux (p-glycoprotein) and metabolism (CYP3A4); (2) beta-tubulin (somatic mutation of beta-tubulin and changes in beta-tubulin isotypes levels); (3) cell cycle (HER2, BRCA1 and Aurora-A); and (4) apoptosis (p53, BCL2 and thioredoxin).	Docetaxel	100-109	P53	Homo sapiens	354-357
23337567-8	2013	Additionally, these effects of ATO on gamma-H2AX, Chk1, Chk2, p53, and p21(waf1/cip1) were reduced by an ATM inhibitor.	Arsenic Trioxide	31-34	P53	Homo sapiens	62-65
16969115-4	2006	Here, we show that a short-term treatment with roscovitine is sufficient to inhibit DNA synthesis, and to activate a DNA damage checkpoint response, as indicated by phosphorylation of p53-Ser15, replication protein A, and histone H2AX.	Roscovitine	47-58	P53	Homo sapiens	184-187
16166592-0	2006	The proteasome inhibitor bortezomib induces apoptosis in mantle-cell lymphoma through generation of ROS and Noxa activation independent of p53 status.	Bortezomib	25-35	P53	Homo sapiens	139-142
16403018-0	2006	Recognition of DNA modified by trans-[PtClNH(4-hydroxymethylpyridine)] by tumor suppressor protein p53 and character of DNA adducts of this cytotoxic complex.	4-hydroxymethylpyridine	45-69	P53	Homo sapiens	99-102
16918599-10	2006	Similar to the primary tumour, the cell line showed p53 overexpression and had p53 mutation at codon 132: AAG (lys)--&gt;AAT (asp).	Aspartic Acid	126-129	P53	Homo sapiens	79-82
23241309-5	2013	In response to hydrogen peroxide (H2O2), we measured an increase in PtdIns5P in cells derived from human osteosarcoma, U2OS (5-fold); breast tumors, MDA-MB-468 (2-fold); and fibrosarcoma, HT1080 (3-fold); and in p53-null murine embryonic fibroblasts (8-fold).	phosphatidylinositol 5-phosphate	68-76	P53	Homo sapiens	212-215
16135398-5	2006	Moreover, TPL inhibited the clonogenic growth of MCF 7 cells, which was significantly recovered by pifithrin-alpha, the p53 inhibitor.	pifithrin	99-114	P53	Homo sapiens	120-123
17150856-4	2006	The discrimination of cytosine methylation status at the mutation hot spot in p53 gene was also executed using a well-designed fluorescent DNA probe.	Cytosine	22-30	P53	Homo sapiens	78-81
23667374-9	2013	Furthermore, pRb-inactivated cases showed better DSS (p=0.023), and p53-positive cases showed worse DSS (p=0.001).	dss	100-103	P53	Homo sapiens	68-71
18393778-7	2006	Finally, another new drug, ecteinascidin (ET-743), that blocks cell cycle progression in G2/M phase through a p53-independent apoptotic mechanism, has shown important preclinical and clinical activity against a number of human solid tumors, including GIST.	Trabectedin	27-40	P53	Homo sapiens	110-113
18393778-7	2006	Finally, another new drug, ecteinascidin (ET-743), that blocks cell cycle progression in G2/M phase through a p53-independent apoptotic mechanism, has shown important preclinical and clinical activity against a number of human solid tumors, including GIST.	Trabectedin	42-48	P53	Homo sapiens	110-113
16574813-5	2006	Moreover, the data herein clearly show that ganglioside GM3 induces p53-dependent transcriptional activity of p21(WAF1), as evidenced by the p21(WAF1) promoter-driven luciferase reporter plasmid (full-length p21(WAF1) promoter and a construct lacking the p53-binding sites).	Gangliosides	44-55	P53	Homo sapiens	68-71
16574813-5	2006	Moreover, the data herein clearly show that ganglioside GM3 induces p53-dependent transcriptional activity of p21(WAF1), as evidenced by the p21(WAF1) promoter-driven luciferase reporter plasmid (full-length p21(WAF1) promoter and a construct lacking the p53-binding sites).	Gangliosides	44-55	P53	Homo sapiens	255-258
16778187-8	2006	The p53 inhibitor, pifithrin-alpha, is able to attenuate the effect of proteasome inhibition.	pifithrin	19-34	P53	Homo sapiens	4-7
18528466-12	2006	We went on to show that p53 regulated the expression of MRP1 and that this produced resistance to doxorubicin and vinblastine.	Vinblastine	114-125	P53	Homo sapiens	24-27
18528468-6	2006	In the presence of E6, E6AP catalyses the ubiquitylation and proteolysis of p53.	Polyurethane Y-290	19-21	P53	Homo sapiens	76-79
16601678-3	2006	Early induced p53 allows caspase-mediated cleavage of HIPK2 following aspartic acids 916 and 977.	Aspartic Acid	70-84	P53	Homo sapiens	14-17
23537372-11	2013	CONCLUSIONS: These findings suggest that UCN-01 induces hepatoma cell growth inhibition by regulating the p53/p21(waf1) and CHK2/CDC25 pathways.	7-hydroxystaurosporine	41-47	P53	Homo sapiens	106-109
16169224-6	2005	Another trial (EORTC 10994) is conducted in order to show that in cases of p53 mutated tumors, neoadjuvant chemotherapy with docetaxel is more efficient than an anthracycline-containing regimen.	Docetaxel	125-134	P53	Homo sapiens	75-78
16170329-4	2005	Jasmonic acid and methyl jasmonate (0.25-3 mM) were each equally cytotoxic to both clones, whereas mutant p53-expressing cells were resistant to treatment with the radiomimetic agent neocarzinostatin and the chemotherapeutic agent bleomycin.	Bleomycin	231-240	P53	Homo sapiens	106-109
16582595-5	2006	A similar differential effect of these retinoids was observed for the induction of p53, which has been reported to regulate GDF-15 expression.	Retinoids	39-48	P53	Homo sapiens	83-86
16170329-5	2005	Neocarzinostatin and bleomycin induced an elevation in the p53 levels in wt p53-expressing cells, whereas methyl jasmonate did not.	Bleomycin	21-30	P53	Homo sapiens	59-62
23357978-0	2013	Synergistic activity of bortezomib and HDACi in preclinical models of B-cell precursor acute lymphoblastic leukemia via modulation of p53, PI3K/AKT, and NF-kappaB.	Bortezomib	24-34	P53	Homo sapiens	134-137
16170329-5	2005	Neocarzinostatin and bleomycin induced an elevation in the p53 levels in wt p53-expressing cells, whereas methyl jasmonate did not.	Bleomycin	21-30	P53	Homo sapiens	76-79
23482764-7	2013	Moreover, beta-elemene plus docetaxel induced elevated levels of caspase-9 and p53 proteins in A2780/CP70 cells, and the combination of beta-elemene plus a taxane caused marked cell-cycle arrest at the G2/M phase in these cells.	beta-elemene	10-22	P53	Homo sapiens	79-82
16211300-0	2005	Quercetin induces gadd45 expression through a p53-independent pathway.	Quercetin	0-9	P53	Homo sapiens	46-49
16618762-4	2006	Treatment of BCL6-expressing Burkitt lymphoma cells with cambinol as a single agent induced apoptosis, which was accompanied by hyperacetylation of BCL6 and p53.	cambinol	57-65	P53	Homo sapiens	157-160
16618762-5	2006	Because acetylation inactivates BCL6 and has the opposite effect on the function of p53 and other checkpoint pathways, the antitumor activity of cambinol in Burkitt lymphoma cells may be accomplished through a combined effect of BCL6 inactivation and checkpoint activation.	cambinol	145-153	P53	Homo sapiens	84-87
16287077-9	2006	Cells treated with E2 or 4-OHE2 at doses of 0.007 nM and 70 nM and 2-OHE2 only at a higher dose (3.6 microM) exhibited a 5 bp deletion in p53 exon 4.	2-hydroxyestradiol	67-73	P53	Homo sapiens	138-141
16211300-7	2005	Quercetin did not activate transcription through p53-binding sites in HeLa cells, although it up-regulated gadd45 in p53-inactivated tumor cells.	Quercetin	0-9	P53	Homo sapiens	117-120
16211300-8	2005	These results indicate that quercetin induces gadd45 expression in a p53-independent manner.	Quercetin	28-37	P53	Homo sapiens	69-72
23482764-7	2013	Moreover, beta-elemene plus docetaxel induced elevated levels of caspase-9 and p53 proteins in A2780/CP70 cells, and the combination of beta-elemene plus a taxane caused marked cell-cycle arrest at the G2/M phase in these cells.	Docetaxel	28-37	P53	Homo sapiens	79-82
16585172-10	2006	Recombinant p53 complemented p53-/- mitochondrial extract repair of uracil or 8-oxo-G-containing oligonucleotides.	Uracil	68-74	P53	Homo sapiens	12-15
23268708-10	2013	The IR-induced cell survival was significantly increased by Z-VAD-FMK and decreased by 3MA in H1299-P53 cells; IR- induced autophagy was significantly increased by Z-VAD-FMK in H1299-P53 cells (p &lt; 0.01), but not changed in H1299 cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	164-173	P53	Homo sapiens	183-186
16585172-10	2006	Recombinant p53 complemented p53-/- mitochondrial extract repair of uracil or 8-oxo-G-containing oligonucleotides.	Uracil	68-74	P53	Homo sapiens	29-32
16585172-11	2006	As a measure of DNA glycosylase activity, p53+/+ mitochondrial extracts more efficiently incised uracil or 8-oxo-G oligonucleotides, although recombinant p53 could not stimulate oligonucleotide incision.	Uracil	97-103	P53	Homo sapiens	42-45
15993080-3	2005	The introduced N at position 8 of the purine ring generally lowered CDK2 inhibitory activity of new 8-azapurines (1,2,3-triazolo[4,5-d]pyrimidines) in comparison to the model trisubstituted purines, whereas the antiproliferative potential of some derivatives remained very high, reflecting their ability to activate p53 tumor suppressor.	purine	38-44	P53	Homo sapiens	316-319
22860893-5	2013	IL-24-mediated apoptosis was also antagonized by pifithrin-alpha, an inhibitor of p53 transactivation.	pifithrin	49-64	P53	Homo sapiens	82-85
16481746-4	2006	Third, the molecular features of p53 residues 47-58 imitate those of single stranded DNA in their interaction with the oligonucleotide oliogsaccharide-binding (OB) fold of the N-terminal domain of RPA70.	oliogsaccharide	135-150	P53	Homo sapiens	33-36
16505115-1	2006	Nucleoside anticancer drugs like gemcitabine (2"-deoxy-2",2"-difluorocytidine) are potent inducers of p53, and ectopic expression of wild-type p53 sensitizes cells to these agents.	Nucleosides	0-10	P53	Homo sapiens	102-105
22749133-0	2013	The flavonoids diosmetin and luteolin exert synergistic cytostatic effects in human hepatoma HepG2 cells via CYP1A-catalyzed metabolism, activation of JNK and ERK and P53/P21 up-regulation.	Flavonoids	4-14	P53	Homo sapiens	167-174
16391851-8	2006	While TUNEL-positive cells and p53 immunoreactivity were detected in Docetaxel, Doxorubicin and Docetaxel/Doxorubicin groups, p53 immunoreactivity was not observed in the Docetaxel group.	Docetaxel	69-78	P53	Homo sapiens	31-34
16391851-8	2006	While TUNEL-positive cells and p53 immunoreactivity were detected in Docetaxel, Doxorubicin and Docetaxel/Doxorubicin groups, p53 immunoreactivity was not observed in the Docetaxel group.	Docetaxel	96-105	P53	Homo sapiens	31-34
16391851-8	2006	While TUNEL-positive cells and p53 immunoreactivity were detected in Docetaxel, Doxorubicin and Docetaxel/Doxorubicin groups, p53 immunoreactivity was not observed in the Docetaxel group.	Docetaxel	96-105	P53	Homo sapiens	31-34
16391851-13	2006	These findings suggest that the possible mechanism of cell death in Doxorubicin and Docetaxel/Doxorubicin treatment groups is related to apoptosis through the p53 pathway.	Docetaxel	84-93	P53	Homo sapiens	159-162
23356739-0	2013	Differential effects of garcinol and curcumin on histone and p53 modifications in tumour cells.	garcinol	24-32	P53	Homo sapiens	61-64
16436176-0	2006	The effect of ultra violet B (TL-01) phototherapy on epidermal expression of p53 protein in psoriatic plaques.	ultra violet b	14-28	P53	Homo sapiens	77-80
16436176-0	2006	The effect of ultra violet B (TL-01) phototherapy on epidermal expression of p53 protein in psoriatic plaques.	tl-01	30-35	P53	Homo sapiens	77-80
23356739-4	2013	In this study we assessed the effects of the phytocompounds garcinol and curcumin on histone and p53 modification in cancer cells, focussing on the breast tumour cell line MCF7.	garcinol	60-68	P53	Homo sapiens	97-100
23356739-12	2013	In addition to its effects on histone modifications, garcinol was found to block CBP/p300-mediated acetylation of the C-terminal activation domain of p53, but resulted in enhanced acetylation of p53K120, and accumulation of p53 in the cytoplasmic compartment.	garcinol	53-61	P53	Homo sapiens	150-153
16303758-7	2006	Further, troglitazone also induced p53 protein expression in HCT116 cells, which may be the possible mechanism for PPARgamma-independent POX activation, since POX has been shown to be a downstream mediator in p53-induced apoptosis.	Troglitazone	9-21	P53	Homo sapiens	35-38
16303758-7	2006	Further, troglitazone also induced p53 protein expression in HCT116 cells, which may be the possible mechanism for PPARgamma-independent POX activation, since POX has been shown to be a downstream mediator in p53-induced apoptosis.	Troglitazone	9-21	P53	Homo sapiens	209-212
23356739-12	2013	In addition to its effects on histone modifications, garcinol was found to block CBP/p300-mediated acetylation of the C-terminal activation domain of p53, but resulted in enhanced acetylation of p53K120, and accumulation of p53 in the cytoplasmic compartment.	garcinol	53-61	P53	Homo sapiens	195-198
23356739-15	2013	Garcinol treatment alters expression of chromatin modifying enzymes in MCF7 cells, resulting in reprogramming of key histone and p53 PTMs and growth arrest, underscoring its potential as a cancer chemopreventive agent.	garcinol	0-8	P53	Homo sapiens	129-132
23244159-0	2013	Electrochemical study on the effects of epigenetic cytosine methylation on anti-benzo[a]pyrene diol epoxide damage at TP53 oligomers.	Cytosine	51-59	P53	Homo sapiens	118-122
16080190-0	2006	Induction of tubulin by docetaxel is associated with p53 status in human non small cell lung cancer cell lines.	Docetaxel	24-33	P53	Homo sapiens	53-56
16080190-4	2006	The relationship between p53 function and DOC, acting through a microtubule-based mechanism, was examined.	Docetaxel	42-45	P53	Homo sapiens	25-28
16080190-5	2006	We found that after 18-hr treatment with DOC, beta-tubulin gene transcription was enhanced in p53-null H1299 cells but not in A549 cells.	Docetaxel	41-44	P53	Homo sapiens	94-97
16080190-8	2006	Further demonstrating an association of DOC treatment with p53 and beta-tubulin, inhibition of p53 expression by interference RNA in A549 cells showed increasing beta-tubulin gene expression with DOC treatment.	Docetaxel	40-43	P53	Homo sapiens	59-62
16080190-8	2006	Further demonstrating an association of DOC treatment with p53 and beta-tubulin, inhibition of p53 expression by interference RNA in A549 cells showed increasing beta-tubulin gene expression with DOC treatment.	Docetaxel	40-43	P53	Homo sapiens	95-98
23535401-8	2013	Furthermore, pretreatment with either p53 inhibitor pifithrin-alpha or calcium chelator BAPTA-AM effectively attenuated apoptosis induced by crotonaldehyde.	pifithrin	52-67	P53	Homo sapiens	38-41
16080190-8	2006	Further demonstrating an association of DOC treatment with p53 and beta-tubulin, inhibition of p53 expression by interference RNA in A549 cells showed increasing beta-tubulin gene expression with DOC treatment.	Docetaxel	196-199	P53	Homo sapiens	95-98
16080190-9	2006	We also selected a clone from the H1299 cells that stably expressed p53, examined the beta-tubulin expression after DOC treatment and found an inhibition of beta-tubulin induction in these p53-expressing cells.	Docetaxel	116-119	P53	Homo sapiens	189-192
16080190-10	2006	Our data suggest that the initial response of cells to DOC treatment involves p53; alternatively, in the absence of p53, tubulins may be transactivated.	Docetaxel	55-58	P53	Homo sapiens	78-81
16582987-0	2006	Sequence-specific p53 gene damage by chloroacetaldehyde and its repair kinetics in Escherichia coli.	chloroacetaldehyde	37-55	P53	Homo sapiens	18-21
23150443-7	2013	Furthermore, stable transfection of mutant p53-H179L into NIH3T3 fibroblasts was sufficient to allow anchorage-independent growth in soft agar.	Agar	138-142	P53	Homo sapiens	43-46
25049533-1	2012	The aim of this study was to investigate the impact of a reported p53 inhibitor, pifithrin-alpha (PFT-alpha), on preimplantation porcine in vitro fertilized (IVF) embryo development in culture.	pifithrin	81-90	P53	Homo sapiens	66-69
16213738-10	2006	The cell survival check protein p53 increased from 1.72- to 2.8-fold and 1.36- to 2.16-fold at concentrations of AZ-1 from 0.125 to 2.0 microM in a dose-dependently increasing manner on OEC-M1 as compared with control for 24 and48 h treatments, respectively.	2-aziridin-1-yl-3-((2-((2-(3-aziridin-1-yl-1,4-dioxo-1,4-dihydronaphthalen-2-yl)thio)ethoxy)ethyl)thio)naphthoquinone	113-117	P53	Homo sapiens	32-35
22964432-4	2012	We investigated the effects of bortezomib using a panel of six cancer cell lines with variable status of ERalpha or p53 and found that bortezomib inhibited the growth of all cell lines in the same concentration range irrespective of the ERalpha expression or the mutational status of p53.	Bortezomib	135-145	P53	Homo sapiens	116-119
16283431-0	2006	Opposite effect of ERK1/2 and JNK on p53-independent p21WAF1/CIP1 activation involved in the arsenic trioxide-induced human epidermoid carcinoma A431 cellular cytotoxicity.	Arsenic Trioxide	93-109	P53	Homo sapiens	37-40
16432159-0	2006	Restoration of p53 function for selective Fas-mediated apoptosis in human and rat glioma cells in vitro and in vivo by a p53 COOH-terminal peptide.	ammonium ferrous sulfate	42-45	P53	Homo sapiens	15-18
16432159-5	2006	Apoptosis induction by p53p-Ant was quantitated by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay and Annexin V staining in human glioma cells in vitro and in a syngeneic orthotopic 9L glioma rat model using convection-enhanced delivery in vivo.	deoxyuridine triphosphate	98-102	P53	Homo sapiens	23-27
16432159-8	2006	These data suggest that p53 function for inducing Fas-mediated apoptosis in gliomas, which express sufficient quantities of endogenous mutant or WT p53, may be restored or activated, respectively, by a cell-permeable peptide derived from the p53 COOH-terminal regulatory domain (p53p-Ant).	ammonium ferrous sulfate	50-53	P53	Homo sapiens	24-27
22964432-4	2012	We investigated the effects of bortezomib using a panel of six cancer cell lines with variable status of ERalpha or p53 and found that bortezomib inhibited the growth of all cell lines in the same concentration range irrespective of the ERalpha expression or the mutational status of p53.	Bortezomib	135-145	P53	Homo sapiens	284-287
16432159-8	2006	These data suggest that p53 function for inducing Fas-mediated apoptosis in gliomas, which express sufficient quantities of endogenous mutant or WT p53, may be restored or activated, respectively, by a cell-permeable peptide derived from the p53 COOH-terminal regulatory domain (p53p-Ant).	ammonium ferrous sulfate	50-53	P53	Homo sapiens	148-151
16432159-8	2006	These data suggest that p53 function for inducing Fas-mediated apoptosis in gliomas, which express sufficient quantities of endogenous mutant or WT p53, may be restored or activated, respectively, by a cell-permeable peptide derived from the p53 COOH-terminal regulatory domain (p53p-Ant).	ammonium ferrous sulfate	50-53	P53	Homo sapiens	148-151
22863952-2	2012	We previously showed that p53 is increased in crypt IECs in human colitis and is needed for IEC apoptosis in chronic dextran sulfate sodium-colitis.	Dextran Sulfate	117-139	P53	Homo sapiens	26-29
16432159-8	2006	These data suggest that p53 function for inducing Fas-mediated apoptosis in gliomas, which express sufficient quantities of endogenous mutant or WT p53, may be restored or activated, respectively, by a cell-permeable peptide derived from the p53 COOH-terminal regulatory domain (p53p-Ant).	ammonium ferrous sulfate	50-53	P53	Homo sapiens	279-283
16898267-0	2006	Quercetin induces p53-independent apoptosis in human prostate cancer cells by modulating Bcl-2-related proteins: a possible mediation by IGFBP-3.	Quercetin	0-9	P53	Homo sapiens	18-21
16898267-2	2006	We report insulin-like growth factor-binding protein-3 (IGFBP-3) as an effector of quercetin-induced apoptosis in human prostate cancer cell lines in a p53-independent manner.	Quercetin	83-92	P53	Homo sapiens	152-155
23156993-3	2012	It has previously been reported that HER2/ERBB2, the estrogen receptor, progesterone receptor, and p53 were required for flavonoid induced cytotoxicity in breast cancer cell lines.	Flavonoids	121-130	P53	Homo sapiens	99-102
15981203-7	2005	The higher expression of p53 and p21/WAF1 in skin after single topical application of AO or isolated sanguinarine further confirms the tumorigenic response.	argemone oil	86-88	P53	Homo sapiens	25-28
22491983-5	2012	Sodium nitroprusside (SNP), an NO donor, was found to induce the p53 protein and to inhibit proliferation of both PC12 and M-M17-26 cells, but failed to induce neuronal differentiation in these cell lines.	Nitroprusside	0-20	P53	Homo sapiens	65-68
16169939-0	2005	Ruthenium (II)-derived organometallic compounds induce cytostatic and cytotoxic effects on mammalian cancer cell lines through p53-dependent and p53-independent mechanisms.	ruthenium(2+)	0-14	P53	Homo sapiens	127-130
16169939-0	2005	Ruthenium (II)-derived organometallic compounds induce cytostatic and cytotoxic effects on mammalian cancer cell lines through p53-dependent and p53-independent mechanisms.	ruthenium(2+)	0-14	P53	Homo sapiens	145-148
22018604-7	2012	In addition, GCTI increased the expression of cell cycle inhibitory proteins (p21, p27 and p53) and the Bax-to-Bcl-2 ratio to induce apoptosis.	gcti	13-17	P53	Homo sapiens	91-94
16271620-6	2005	Surprisingly, juglone caused a drastic reduction of the basal level of p53 in human fibroblasts and this loss could not be fully rescued by proteasome and calpain I inhibitors.	juglone	14-21	P53	Homo sapiens	71-74
16170329-7	2005	In contrast, neocarzinostatin and bleomycin induced death only in wt p53-expressing cells, in an apoptotic mode.	Bleomycin	34-43	P53	Homo sapiens	69-72
22715097-5	2012	Full-length p53 aggregated into amyloid-like species that bound thioflavin T.	thioflavin T	64-76	P53	Homo sapiens	12-15
16178003-3	2005	Proteasome inhibition with bortezomib has specifically promoted apoptosis of tumor cells through the stabilization of p53, p21, p27, Bax, and IkappaBalpha, resulting in nuclear factor kappaB inhibition.	Bortezomib	27-37	P53	Homo sapiens	118-121
22653969-8	2012	In summary, the cytotoxic effects of bendamustine, melphalan and doxorubicin on p53-deficient multiple myeloma cell lines were enhanced by the coadministration of AZD7762.	Melphalan	51-60	P53	Homo sapiens	80-83
16096367-2	2005	TrxR1 can transduce regulatory redox signals through NADPH-dependent reduction of thioredoxin (Trx), which is able to reduce a broad spectrum of target enzymes and regulate the activity of several transcription factors (e.g., p53 and NF-kappaB).	NADP	53-58	P53	Homo sapiens	226-229
16204041-8	2005	Intact global NER was also confirmed in SCC25 cells possessing inactivating mutations in p53 as well as in cells treated with pifithrin-alpha, a chemical inhibitor of p53 that decreased sensitivity of cells to UV radiation.	pifithrin	126-141	P53	Homo sapiens	167-170
15983031-4	2005	Pancaspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone or p53 inhibitor pifithrin-alpha markedly prevented mitochondrial release of AIF, suggesting that caspases and p53 are involved in this release.	pifithrin	87-102	P53	Homo sapiens	73-76
15983031-4	2005	Pancaspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone or p53 inhibitor pifithrin-alpha markedly prevented mitochondrial release of AIF, suggesting that caspases and p53 are involved in this release.	pifithrin	87-102	P53	Homo sapiens	181-184
22395446-0	2012	3-Nitro-naphthalimide and nitrogen mustard conjugate NNM-25 induces hepatocellular carcinoma apoptosis via PARP-1/p53 pathway.	3-nitro-naphthalimide	0-21	P53	Homo sapiens	114-117
15983031-10	2005	The p53 inhibitor pifithrin-alpha or p53 siRNA prevented both cisplatin-induced caspase-2 activation and mitochondrial release of AIF.	pifithrin	18-27	P53	Homo sapiens	4-7
22438244-4	2012	Such a preferential cytotoxicity could be attributed to the failure of p53-deficient cells to undergo cell cycle arrest in response to SP600125.	pyrazolanthrone	135-143	P53	Homo sapiens	71-74
16140939-2	2005	We show that roscovitine, R-roscovitine, and CGP74514A (collectively referred to as CKIs) induce the apoptosis of LNCaP and LNCaP-Rf cells, both of which express wild-type p53.	Roscovitine	13-24	P53	Homo sapiens	172-175
22438244-5	2012	TP53(-/-)  (but not TP53(+/+) ) cells treated with SP600125 became polyploid upon mitotic abortion and progressively succumbed to mitochondrial apoptosis.	pyrazolanthrone	51-59	P53	Homo sapiens	0-4
22438244-6	2012	The expression of an SP600125-resistant variant of the mitotic kinase MPS1 in TP53(-/-)  cells reduced SP600125-induced polyploidization.	pyrazolanthrone	21-29	P53	Homo sapiens	78-82
16140939-2	2005	We show that roscovitine, R-roscovitine, and CGP74514A (collectively referred to as CKIs) induce the apoptosis of LNCaP and LNCaP-Rf cells, both of which express wild-type p53.	Roscovitine	26-39	P53	Homo sapiens	172-175
22438244-6	2012	The expression of an SP600125-resistant variant of the mitotic kinase MPS1 in TP53(-/-)  cells reduced SP600125-induced polyploidization.	pyrazolanthrone	103-111	P53	Homo sapiens	78-82
22405851-0	2012	p53-Independent expression of wild-type p53-induced phosphatase 1 (Wip1) in methylmethane sulfonate-treated cancer cell lines and human tumors.	Methyl Methanesulfonate	76-99	P53	Homo sapiens	0-3
16212876-7	2005	In addition, the same extent of TC-induced pRB-degradation was detected in the gastric tumor cells containing a p53 dominant-negative construct, indicating that this kind of pRB degradation is p53-independent.	tripchlorolide	32-34	P53	Homo sapiens	112-115
16212876-7	2005	In addition, the same extent of TC-induced pRB-degradation was detected in the gastric tumor cells containing a p53 dominant-negative construct, indicating that this kind of pRB degradation is p53-independent.	tripchlorolide	32-34	P53	Homo sapiens	193-196
16170037-7	2005	The use of the chemical inhibitor of p53, pifithrin alpha, excluded this possibility.	pifithrin	42-51	P53	Homo sapiens	37-40
16007224-6	2005	Treatment of Weri-Rb1 cell line by 5-Aza-dC induced an increase in expression level of pRb2/p130, E2F1, p73 and p53.	Azacitidine	35-40	P53	Homo sapiens	112-115
16127151-5	2005	A specific role for p53 in TRAIL-R2-mediated apoptosis was indicated by the ability of p53 siRNA to significantly reduce RASF apoptosis and by the reduced apoptosis of RASFs bearing p53 mutations on treatment with anti-DR5 antibody or anti-DR5 antibody plus lactacystin.	lactacystin	258-269	P53	Homo sapiens	20-23
16127151-5	2005	A specific role for p53 in TRAIL-R2-mediated apoptosis was indicated by the ability of p53 siRNA to significantly reduce RASF apoptosis and by the reduced apoptosis of RASFs bearing p53 mutations on treatment with anti-DR5 antibody or anti-DR5 antibody plus lactacystin.	lactacystin	258-269	P53	Homo sapiens	87-90
16127151-5	2005	A specific role for p53 in TRAIL-R2-mediated apoptosis was indicated by the ability of p53 siRNA to significantly reduce RASF apoptosis and by the reduced apoptosis of RASFs bearing p53 mutations on treatment with anti-DR5 antibody or anti-DR5 antibody plus lactacystin.	lactacystin	258-269	P53	Homo sapiens	87-90
15970518-0	2005	Docetaxel induces p53-dependent apoptosis and synergizes with farnesyl transferase inhibitor r115777 in human epithelial cancer cells.	Docetaxel	0-9	P53	Homo sapiens	18-21
21308489-0	2012	Arsenic trioxide induces apoptosis of p53 null osteosarcoma MG63 cells through the inhibition of catalase.	Arsenic Trioxide	0-16	P53	Homo sapiens	38-41
15843497-0	2005	The p53 inhibitor pifithrin-alpha is a potent agonist of the aryl hydrocarbon receptor.	pifithrin	18-33	P53	Homo sapiens	4-7
16093429-4	2005	Transient transfection of H460 lung cancer cells and human umbilical vascular endothelial cells (HUVEC) with antisense oligonucleotides (ASODN) against MDM2 resulted in a reduced level of MDM2 and increased levels of p21 and p53.	asodn	137-142	P53	Homo sapiens	225-228
15976193-6	2005	The p53 inhibitor PFTalpha reduced both DON-induced phosphorylation of p53 and p53 binding activity.	pifithrin	18-26	P53	Homo sapiens	4-7
15976193-6	2005	The p53 inhibitor PFTalpha reduced both DON-induced phosphorylation of p53 and p53 binding activity.	pifithrin	18-26	P53	Homo sapiens	71-74
15976193-6	2005	The p53 inhibitor PFTalpha reduced both DON-induced phosphorylation of p53 and p53 binding activity.	pifithrin	18-26	P53	Homo sapiens	71-74
21308489-1	2012	This study is aimed at investigating the effect of arsenic trioxide (ATO) on p53 null human osteosarcoma MG63 cells and the mechanisms underlying the effect.	Arsenic Trioxide	51-67	P53	Homo sapiens	77-80
21308489-1	2012	This study is aimed at investigating the effect of arsenic trioxide (ATO) on p53 null human osteosarcoma MG63 cells and the mechanisms underlying the effect.	Arsenic Trioxide	69-72	P53	Homo sapiens	77-80
16026868-4	2005	Specific depletion of JDP2 resulted in p53-independent cell death that resembles apoptosis and was evident at 72 h. The death mechanism was caspase dependent as the cells could be rescued by treatment with caspase inhibitor zVAD.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	224-228	P53	Homo sapiens	39-42
22441128-10	2012	The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect.	Iodized Oil	75-86	P53	Homo sapiens	18-21
16048565-1	2005	BACKGROUND AND AIMS: A specific mutation at codon 249 of the p53 tumor suppressor gene (guanine to thymine; arginine to serine [249(serine)p53]) is present in the cell-free plasma of 30-47% of patients with hepatocellular carcinoma (HCC) in regions with uniformly high levels of dietary exposure to the fungal toxin, aflatoxin B(1).	Guanine	88-95	P53	Homo sapiens	61-64
16048565-1	2005	BACKGROUND AND AIMS: A specific mutation at codon 249 of the p53 tumor suppressor gene (guanine to thymine; arginine to serine [249(serine)p53]) is present in the cell-free plasma of 30-47% of patients with hepatocellular carcinoma (HCC) in regions with uniformly high levels of dietary exposure to the fungal toxin, aflatoxin B(1).	Guanine	88-95	P53	Homo sapiens	139-142
15865929-3	2005	This strategy was validated by isolation and testing of small molecule p53 inhibitor pifithrin-alpha that demonstrated broad tissue protecting capacity.	pifithrin	85-100	P53	Homo sapiens	71-74
22441128-10	2012	The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect.	Iodized Oil	75-86	P53	Homo sapiens	125-128
15782134-2	2005	The Chk1 inhibitor, 7-hydroxystaurosporine (UCN-01), overcomes both S and G(2) arrest preferentially in cells mutated for p53, driving cells through a lethal mitosis and thereby enhancing cytotoxicity.	7-hydroxystaurosporine	20-42	P53	Homo sapiens	122-125
16030116-12	2005	The data on MGMT show that an inherited factor involving the repair of methylation and other alkylation damage, specifically to the O6 position of guanine, may be associated with the development of tumors that proceed in their development without TP53 mutations or accumulation of TP53 protein and possibly also those that do not involve amplification of the EGFR locus.	Guanine	147-154	P53	Homo sapiens	247-251
22441128-10	2012	The KI of the rAd/p53+5-FU group increased significantly at 24 h. 5-FU and iodized oil increase the anticancer effect of rAd/p53, and 5-FU combined with rAd/p53 has a synergistic anticancer effect.	Iodized Oil	75-86	P53	Homo sapiens	125-128
16030116-12	2005	The data on MGMT show that an inherited factor involving the repair of methylation and other alkylation damage, specifically to the O6 position of guanine, may be associated with the development of tumors that proceed in their development without TP53 mutations or accumulation of TP53 protein and possibly also those that do not involve amplification of the EGFR locus.	Guanine	147-154	P53	Homo sapiens	281-285
22559167-7	2012	The effects of rapamycin and/or bortezomib on the mRNA expression levels of p53, p27, p21 and Bcl-2 family in HCCLM3 cells were evaluated by RT-PCR.	Bortezomib	32-42	P53	Homo sapiens	76-79
15878162-0	2005	Icariin-mediated modulation of cell cycle and p53 during cardiomyocyte differentiation in embryonic stem cells.	icariin	0-7	P53	Homo sapiens	46-49
15878162-8	2005	Results showed p53 to be an important regulator in the differentiation in embryonic stem cells treated with 10(-7) M icariin, controlling or adjusting the balance between differentiated cells and cells undergoing apoptosis.	icariin	117-124	P53	Homo sapiens	15-18
15846088-5	2005	The cell line that showed greatest reduction (85-90%) of p53 expression showed decreased p21 promoter activation after DNA damage with camptothecin, etoposide and MMS.	Methyl Methanesulfonate	163-166	P53	Homo sapiens	57-60
15764647-0	2005	Ablation of either p21 or Bax prevents p53-dependent apoptosis induced by green tea polyphenol epigallocatechin-3-gallate.	polyphenol epigallocatechin-3-gallate	84-121	P53	Homo sapiens	39-42
15883412-0	2005	Extent of damage and repair in the p53 tumor-suppressor gene after treatment of myeloma patients with high-dose melphalan and autologous blood stem-cell transplantation is individualized and may predict clinical outcome.	Melphalan	112-121	P53	Homo sapiens	35-38
22342732-8	2012	Furthermore, p53 facilitated apoptosis caused by DHA.	artenimol	49-52	P53	Homo sapiens	13-16
15883412-2	2005	PATIENTS AND METHODS: The formation and subsequent repair of DNA damage (monoadducts and interstrand cross-links) in the p53 tumor-suppressor gene, the proto-oncogene N-ras, and the housekeeping gene beta-actin during the first 24 hours after treatment with high-dose melphalan (HDM; 200 mg/m2) supported by autologous blood stem-cell transplantation (ABSCT) was measured in blood leukocytes of 26 patients with MM.	Melphalan	268-277	P53	Homo sapiens	121-124
15975526-0	2005	Glycerol enhances radiosensitivity in a human oral squamous cell carcinoma cell line (Ca9-22) bearing a mutant p53 gene via Bax-mediated induction of apoptosis.	Glycerol	0-8	P53	Homo sapiens	111-114
15975526-3	2005	The addition of glycerol to the culture medium prior to irradiation of an oral squamous cell carcinoma cell line (Ca9-22) bearing a mutant p53 (mp53) gene was found to increase the radiosensitivity of these cells.	Glycerol	16-24	P53	Homo sapiens	139-142
15749705-10	2005	Without resveratrol, the coumarin of p53-AMC peptide is solvent-exposed and makes no significant contacts with SIRT1.	coumarin	25-33	P53	Homo sapiens	37-40
15710360-5	2005	Here, we show that treatment of the human colon carcinoma cell line HCT116 with different concentrations of R-flurbiprofen leads to an accumulation of p53 protein which is accompanied by an increase in phosphorylated p53 at serine 15.	tarenflurbil	108-122	P53	Homo sapiens	151-154
15710360-5	2005	Here, we show that treatment of the human colon carcinoma cell line HCT116 with different concentrations of R-flurbiprofen leads to an accumulation of p53 protein which is accompanied by an increase in phosphorylated p53 at serine 15.	tarenflurbil	108-122	P53	Homo sapiens	217-220
15710360-6	2005	Mutation of serine 15 to alanine by site directed mutagenesis and overexpression of the mutated p53 gene in HCT116 cells, revealed that these cells are significantly less sensitive to apoptosis induced by R-flurbiprofen than pcDNA control cells, as measured by PARP-cleavage and flow cytometry.	tarenflurbil	205-219	P53	Homo sapiens	96-99
15710360-9	2005	In conclusion, we were able to show that induction of apoptosis in HCT116 cells after R-flurbiprofen treatment is at least partly dependent on the tumor suppressor gene p53 and that mutation of p53 at serine 15 impairs the apoptotic potency of R-flurbiprofen.	tarenflurbil	86-100	P53	Homo sapiens	169-172
15710360-9	2005	In conclusion, we were able to show that induction of apoptosis in HCT116 cells after R-flurbiprofen treatment is at least partly dependent on the tumor suppressor gene p53 and that mutation of p53 at serine 15 impairs the apoptotic potency of R-flurbiprofen.	tarenflurbil	86-100	P53	Homo sapiens	194-197
15710360-9	2005	In conclusion, we were able to show that induction of apoptosis in HCT116 cells after R-flurbiprofen treatment is at least partly dependent on the tumor suppressor gene p53 and that mutation of p53 at serine 15 impairs the apoptotic potency of R-flurbiprofen.	tarenflurbil	244-258	P53	Homo sapiens	194-197
15975526-8	2005	A gel mobility-shift assay showed that glycerol restored the DNA-binding activity of mp53 for a p53-consensus sequence to levels similar to that of wild-type p53.	Glycerol	39-47	P53	Homo sapiens	86-89
15975526-8	2005	A gel mobility-shift assay showed that glycerol restored the DNA-binding activity of mp53 for a p53-consensus sequence to levels similar to that of wild-type p53.	Glycerol	39-47	P53	Homo sapiens	96-99
21373875-0	2012	TP53 genomics predict higher clinical and pathologic tumor response in operable early-stage breast cancer treated with docetaxel-capecitabine +- trastuzumab.	Docetaxel	119-128	P53	Homo sapiens	0-4
15692065-0	2005	A novel CDK inhibitor, CYC202 (R-roscovitine), overcomes the defect in p53-dependent apoptosis in B-CLL by down-regulation of genes involved in transcription regulation and survival.	Roscovitine	31-44	P53	Homo sapiens	71-74
15929791-4	2005	Exposure to bortezomib has been shown to stabilize p21, p27, and p53, as well as the proapoptotic Bid and Bax proteins, caveolin-1, and inhibitor kappaB-alpha, which prevents activation of nuclear factor kappaB-induced cell survival pathways.	Bortezomib	12-22	P53	Homo sapiens	65-68
15623356-8	2005	Moreover, p53 accumulation was three times lower in melanocytes than in unpigmented cells such as fibroblasts after SSUV exposure.	ssuv	116-120	P53	Homo sapiens	10-13
22387547-3	2012	METHODS: Human hepatoma cells (HepG2.2.15) were transfected with XPD expression vector, followed by incubation with Pifithrin-alpha (P53 inhibitor).	pifithrin	116-131	P53	Homo sapiens	133-136
15720190-10	2005	Small molecules that have been reported to disrupt the p53-MDM2 binding, thereby enhancing p53 activity to elicit anticancer effects include the following: synthetic chalcones, norbornane derivatives, cis-imidazoline derivatives (Nutlins), a pyrazolidinedione sulfonamide and 1,4-benzodiazepine-2,5-diones, as well as tryptophan derivatives.	Chalcones	166-175	P53	Homo sapiens	91-94
15904916-5	2005	Results also indicate that after arsenic trioxide treatment, p53 protein levels increased significantly and also could bind directly at the telomere t-loop junction.	Arsenic Trioxide	33-49	P53	Homo sapiens	61-64
22387547-8	2012	However, the inhibition of P53 by Pifithrin-alpha abolished the above-mentioned effects of XPD.	pifithrin	34-43	P53	Homo sapiens	27-30
15637397-5	2005	Retinoid-oral IEN studies (eg, of retinoic acid receptor-beta, p53, genetic instability, loss of heterozygosity, and cyclin D1) have advanced the overall understanding of the biology of intraepithelial carcinogenesis and of preventive agent molecular mechanisms and targets-important advances for monitoring preventive interventions and assessing cancer risk and pharmacogenomics.	Retinoids	0-8	P53	Homo sapiens	63-66
22425996-6	2012	Our studies demonstrate that concomitant loss of either p53 (also known as Tp53) or Lkb1 (also known as Stk11), two clinically relevant tumour suppressors, markedly impaired the response of Kras-mutant cancers to docetaxel monotherapy.	Docetaxel	213-222	P53	Homo sapiens	56-59
16122187-1	2005	PURPOSE: In this study the relationship between therapy with paclitaxel, cisplatin, vinorelbine and titanocene dichloride and of the expression of proliferation markers (ki67 and S-phase fraction) and tumour suppressor gene p53 was analyzed using a human ovarian cancer xenograft model.	Vinorelbine	84-95	P53	Homo sapiens	224-227
16122187-9	2005	The vinorelbine-group had the highest percentage of p53-positive specimens (60%), in both titanocene-groups no specimen showed a positive staining for p53 and in the control group 7.1% of the specimens were positively stained for p53.	Vinorelbine	4-15	P53	Homo sapiens	52-55
15869405-4	2005	However, addition of ethidium homodimer-1 and Annexin-V-FITC post-pulse demonstrated greater fluorescence in p53-/- versus p53+/+ cells, suggesting a postpulse p53-dependent biological effect at the plasma membrane.	Ethidium	21-29	P53	Homo sapiens	109-112
15869405-4	2005	However, addition of ethidium homodimer-1 and Annexin-V-FITC post-pulse demonstrated greater fluorescence in p53-/- versus p53+/+ cells, suggesting a postpulse p53-dependent biological effect at the plasma membrane.	Ethidium	21-29	P53	Homo sapiens	123-126
15869405-4	2005	However, addition of ethidium homodimer-1 and Annexin-V-FITC post-pulse demonstrated greater fluorescence in p53-/- versus p53+/+ cells, suggesting a postpulse p53-dependent biological effect at the plasma membrane.	Ethidium	21-29	P53	Homo sapiens	123-126
15793143-0	2005	Excision of nucleoside analogs from DNA by p53 protein, a potential cellular mechanism of resistance to inhibitors of human immunodeficiency virus type 1 reverse transcriptase.	Nucleosides	12-22	P53	Homo sapiens	43-46
15793143-1	2005	We investigated the ability of p53 in cytoplasm to excise nucleoside analogs (NAs).	Nucleosides	58-68	P53	Homo sapiens	31-34
22425996-6	2012	Our studies demonstrate that concomitant loss of either p53 (also known as Tp53) or Lkb1 (also known as Stk11), two clinically relevant tumour suppressors, markedly impaired the response of Kras-mutant cancers to docetaxel monotherapy.	Docetaxel	213-222	P53	Homo sapiens	75-79
15793143-2	2005	A decrease in incorporation of NAs by human immunodeficiency virus type 1 reverse transcriptase and their excision from DNA by p53, provided by the cytoplasmic fraction of LCC2 cells, suggest that p53 in cytoplasm may act as an external proofreader for NA incorporation.	Nucleosides	31-34	P53	Homo sapiens	197-200
15331571-6	2004	Treatment of nonluteinized macaque granulosa cells with hCG and the p53 inhibitor pifithrin-alpha (PFT) in vitro did not alter markers of the cell cycle, including proliferating cell nuclear antigen, p21, and human double minute (HDM)-2 expression compared with hCG alone.	pifithrin	82-97	P53	Homo sapiens	68-71
22200537-0	2012	Liposomal formulations of Etoposide and Docetaxel for p53 mediated enhanced cytotoxicity in lung cancer cell lines.	Docetaxel	40-49	P53	Homo sapiens	54-57
15648263-0	2004	Marine alkaloid polycarpine and its synthetic derivative dimethylpolycarpine induce apoptosis in JB6 cells through p53- and caspase 3-dependent pathways.	Alkaloids	7-15	P53	Homo sapiens	115-118
22200537-1	2012	The objective of present investigation was to develop and assess comparative enhancement in cytotoxicity of liposomal Etoposide and Docetaxel in non-small cell lung cancer cell lines after pre-treatment and co-administration of p53 tumor suppressor gene and to assess direct lung targeting of optimized formulations by dry powder inhaler technology.	Docetaxel	132-141	P53	Homo sapiens	228-231
15648263-0	2004	Marine alkaloid polycarpine and its synthetic derivative dimethylpolycarpine induce apoptosis in JB6 cells through p53- and caspase 3-dependent pathways.	dimethylpolycarpine	57-76	P53	Homo sapiens	115-118
15523690-0	2005	DHPLC is superior to SSCP in screening p53 mutations in esophageal cancer tissues.	dhplc	0-5	P53	Homo sapiens	39-42
15523690-8	2005	Thus, rates of p53 mutations and polymorphisms in esophageal cancer tissue in Chinese patients were 49% and 41% by DHPLC and SSCP, respectively.	dhplc	115-120	P53	Homo sapiens	15-18
16335246-3	2005	An increase in p53 protein expression was found in A549 and MCF7 (WT) cells treated with cisplatin, methotrexate, and doxorubicin, whereas the level of p53 was not statistically significantly changed in the MCF7 DOX/R cells.	Methotrexate	100-112	P53	Homo sapiens	15-18
22223137-0	2012	Upregulated p53 expression activates apoptotic pathways in wild-type p53-bearing mesothelioma and enhances cytotoxicity of cisplatin and pemetrexed.	Pemetrexed	137-147	P53	Homo sapiens	12-15
15547111-11	2005	Our data demonstrate that 5-aza-CR action in HCT-116 is mediated by p53 and its downstream effectors p21(WAF1) and GADD45.	Azacitidine	26-34	P53	Homo sapiens	68-71
15378026-7	2004	Activation of endogenous wt p53 in BLs and lymphoblastoid cell lines led to the induction of SAP and this was inhibited by the specific p53 inhibitor pifithrin-alpha.	pifithrin	150-165	P53	Homo sapiens	28-31
15378026-7	2004	Activation of endogenous wt p53 in BLs and lymphoblastoid cell lines led to the induction of SAP and this was inhibited by the specific p53 inhibitor pifithrin-alpha.	pifithrin	150-165	P53	Homo sapiens	136-139
22223137-2	2012	We examined whether forced expression of p53 inhibited growth of mesothelioma cells and produced anti-tumor effects by a combination of cisplatin (CDDP) or pemetrexed (PEM), the first-line drugs for mesothelioma treatments.	Pemetrexed	156-166	P53	Homo sapiens	41-44
22283740-10	2012	Activation of p53 was suppressed by SP600125 and expression of p-JNK was inhibited by PFT-alpha, therefore silibinin might activate a ROS-JNK-p53 cycle to induce cell death.	pyrazolanthrone	36-44	P53	Homo sapiens	14-17
15382061-4	2004	PARP cleavage and a decrease in S+G2 cells were evident after RuCl2(KTZ)2 treatment in genetically matched C8161 melanoma monolayers with unequal p53 functional status.	Ketoconazole	68-71	P53	Homo sapiens	146-149
15505427-0	2004	Sensitization by glycerol for CDDP-therapy against human cultured cancer cells and tumors bearing mutated p53 gene.	Glycerol	17-25	P53	Homo sapiens	106-109
15607904-4	2005	SK-N-BE human neuroblastoma cells express the three p53 family proteins and can be used for the study of their induction.	sk-n	0-4	P53	Homo sapiens	52-55
15607904-11	2005	Our results demonstrated that HNE inhibits SK-N-BE cell proliferation by increasing the expression of p53 family proteins and p53 target proteins which modulate cell cycle progression and apoptosis.	sk-n	43-47	P53	Homo sapiens	102-105
15505427-3	2004	When those cultured cells were pre-treated with glycerol, CDDP-induced apoptosis was enhanced by glycerol in SAS/m p53 cells but not in SAS/ neo cells.	Glycerol	48-56	P53	Homo sapiens	115-118
15607904-11	2005	Our results demonstrated that HNE inhibits SK-N-BE cell proliferation by increasing the expression of p53 family proteins and p53 target proteins which modulate cell cycle progression and apoptosis.	sk-n	43-47	P53	Homo sapiens	126-129
15505427-3	2004	When those cultured cells were pre-treated with glycerol, CDDP-induced apoptosis was enhanced by glycerol in SAS/m p53 cells but not in SAS/ neo cells.	Glycerol	97-105	P53	Homo sapiens	115-118
22301190-8	2012	In summary, we suggest that p53 has a novel function in regulating purine biosynthesis, aided by miR-34a-dependent IMPDH repression.	purine	67-73	P53	Homo sapiens	28-31
15492510-7	2004	Phosphatidylinositol-3 kinase-like protein kinases (ATR and also ATM) -dependent phosphorylation of p53-Ser15 residue was associated with the accumulation of p53, and stimulation of p21(Waf-1) and GADD45, resulting in G(2)/M delay in BCR/ABL cells after genotoxic treatment.	gadd45	197-203	P53	Homo sapiens	100-103
15492510-7	2004	Phosphatidylinositol-3 kinase-like protein kinases (ATR and also ATM) -dependent phosphorylation of p53-Ser15 residue was associated with the accumulation of p53, and stimulation of p21(Waf-1) and GADD45, resulting in G(2)/M delay in BCR/ABL cells after genotoxic treatment.	gadd45	197-203	P53	Homo sapiens	158-161
15685439-12	2005	TP53 mutations are significantly more frequent in low-grade astrocytomas with promoter methylation of the O(6)-methylguanine-DNA methyltransferase repair gene, suggesting that, in addition to deamination of 5-methylcytosine, exogenous or endogenous alkylation in the O(6) position of guanine may contribute to the formation of these mutations.	5-Methylcytosine	207-223	P53	Homo sapiens	0-4
15685439-12	2005	TP53 mutations are significantly more frequent in low-grade astrocytomas with promoter methylation of the O(6)-methylguanine-DNA methyltransferase repair gene, suggesting that, in addition to deamination of 5-methylcytosine, exogenous or endogenous alkylation in the O(6) position of guanine may contribute to the formation of these mutations.	Guanine	117-124	P53	Homo sapiens	0-4
22399804-8	2012	Consistent with a role for p53 in cell death in interphase, depletion of p53 renders cells less sensitive to vinorelbine, but only in the presence of wild-type APC.	Vinorelbine	109-120	P53	Homo sapiens	73-76
15642191-2	2005	This study was to observe the abrogation of radiation-induced G(2) phase arrest of p53 mutated human cancer cell lines by 7-hydroxystaurosporine (UCN-01), and explore the mechanism.	7-hydroxystaurosporine	122-144	P53	Homo sapiens	83-86
15931363-6	2004	Retinoid-oral IEN studies (e.g., retinoid acid receptor-beta, p53, genetic instability, loss of heterozygosity, and cyclin D1) have advanced the overall understanding of the biology of intraepithelial carcinogenesis and preventive agent molecular mechanisms and targets, important advances for monitoring preventive interventions, assessing cancer risk, and pharmacogenomics.	Retinoids	0-8	P53	Homo sapiens	62-65
22184125-5	2012	We demonstrate that N1 also lowers toxicity, cell death, and p53 pathway exacerbation triggered by Swedish mutated betaAPP overexpression in human cells.	4-(2-(4-isopropylbenzamido)ethoxy)benzoic acid	20-22	P53	Homo sapiens	61-64
15501776-0	2004	Role of protein tyrosine kinase p53/56lyn in diminished lipopolysaccharide priming of formylmethionylleucyl- phenylalanine-induced superoxide production in human newborn neutrophils.	N-Formylmethionine Leucyl-Phenylalanine	86-122	P53	Homo sapiens	32-35
15662128-5	2005	Apoptosis induced by Bortezomib was associated with inhibition of the classical and alternative NF-kappaB pathways, upregulation of p53, p21 and p27 and activation of caspase cascade.	Bortezomib	21-31	P53	Homo sapiens	132-135
21607615-2	2012	A guanine (G)/cytosine (C) common single nucleotide polymorphism (SNP) at second position of codon 72 in exon 4 of p53 gene determines a arginine (Arg) to proline (Pro) (Arg72Pro) aminoacidic substitution within the proline-rich domain of p53 protein.	Cytosine	14-22	P53	Homo sapiens	239-242
22213289-6	2012	In p53-null cells, the combination of low dose 5-FU with up to 6 muM quercetin promoted clonogenic survival.	Quercetin	69-78	P53	Homo sapiens	3-6
16190549-8	2005	CONCLUSIONS: Tissue p53 protein expression increase and bcl-2 decrease can be a prognostic marker as far as a positive effect of IFNa2b+RBV treatment and HCV elimination are concerned.	Ribavirin	136-139	P53	Homo sapiens	20-23
15308759-8	2004	The level of initially formed DNA adducts needed to cause elevation of p53 from a baseline level of 0.5 ng/mg total protein to 2 ng/mg was 5- to 8-fold higher for monohydroxymelphalan than melphalan.	Melphalan	174-183	P53	Homo sapiens	71-74
15361831-9	2004	The caspase inhibitor, Z-VAD-FMK, blocked the decrease in Mdm2 as well as the increase in p53 resulting from Survivin disruption, indicating that Survivin regulates Mdm2 at the post-translational level.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	23-32	P53	Homo sapiens	90-93
15456784-0	2004	Survivin and p53 modulate quercetin-induced cell growth inhibition and apoptosis in human lung carcinoma cells.	Quercetin	26-35	P53	Homo sapiens	13-16
15456784-2	2004	However, the regulation of survivin and p53 on the quercetin-induced cell growth inhibition and apoptosis in cancer cells remains unclear.	Quercetin	51-60	P53	Homo sapiens	40-43
22213289-7	2012	Treatment of p53-wild-type cells with 50 muM quercetin reduced drug-induced up-regulation of p53, p21 and BAX.	Quercetin	45-54	P53	Homo sapiens	13-16
15456784-3	2004	In this study, we investigated the roles of survivin and p53 in the quercetin-treated human lung carcinoma cells.	Quercetin	68-77	P53	Homo sapiens	57-60
15354323-0	2004	Induction of apoptosis in a non-small cell human lung cancer cell line by isothiocyanates is associated with P53 and P21.	Isothiocyanates	74-89	P53	Homo sapiens	109-112
15456784-9	2004	Subsequently, quercetin increased the levels of total p53 (DO-1), phospho-p53 (serine 15), and p21 proteins, which were translocated to the nuclei in A549 cells.	Quercetin	14-23	P53	Homo sapiens	54-57
22213289-7	2012	Treatment of p53-wild-type cells with 50 muM quercetin reduced drug-induced up-regulation of p53, p21 and BAX.	Quercetin	45-54	P53	Homo sapiens	93-96
15456784-9	2004	Subsequently, quercetin increased the levels of total p53 (DO-1), phospho-p53 (serine 15), and p21 proteins, which were translocated to the nuclei in A549 cells.	Quercetin	14-23	P53	Homo sapiens	74-77
15498930-8	2004	Furthermore, the low-dose hypersensitivity and Annexin V binding to irradiated A549 and T98G cells were eliminated by treating the cells with pifithrin, an inhibitor of p53.	pifithrin	142-151	P53	Homo sapiens	169-172
15456784-10	2004	Treatment with a specific p53 inhibitor, pifithrin-alpha, or transfection of a p53 antisense oligodeoxynucleotide enhanced the cytotoxicity of the quercetin-treated cells.	Quercetin	147-156	P53	Homo sapiens	26-29
22213289-9	2012	CONCLUSION: While high doses of quercetin synergize with DNA-damaging agents, the effect of drug combination with quercetin is influenced by the effective doses and the p53 status of the cells.	Quercetin	114-123	P53	Homo sapiens	169-172
15456784-10	2004	Treatment with a specific p53 inhibitor, pifithrin-alpha, or transfection of a p53 antisense oligodeoxynucleotide enhanced the cytotoxicity of the quercetin-treated cells.	Quercetin	147-156	P53	Homo sapiens	79-82
22901138-2	2012	METHODS: Stool DNA was isolated and tumor-associated high molecular weight DNA (1.476 kb fragment including exons 6-9 of the p53 gene) was amplified using PCR and visualized on ethidium bromide-stained agarose gels.	Ethidium	177-193	P53	Homo sapiens	125-128
15456784-12	2004	Together, our results suggest that survivin can reduce the cell growth inhibition and apoptosis, and p53 elevates the p21 level, which may attenuate the cell death in the quercetin-treated human lung carcinoma cells.	Quercetin	171-180	P53	Homo sapiens	101-104
15665582-4	2004	There are evidences to suggest that the base excision repair (BER) induced by the base-damaging agent methyl methanesulfonate (MMS) is partially deficient in cells lacking functional p53.	Methyl Methanesulfonate	102-125	P53	Homo sapiens	183-186
15544062-10	2004	HEM 25 microM and 30 microM significantly increased P53 protein expression 2.3-3.6-fold in SMMC-7721 and 3.0-5.7- fold in HO-8910 cells.	smmc	91-95	P53	Homo sapiens	52-55
15665582-4	2004	There are evidences to suggest that the base excision repair (BER) induced by the base-damaging agent methyl methanesulfonate (MMS) is partially deficient in cells lacking functional p53.	Methyl Methanesulfonate	127-130	P53	Homo sapiens	183-186
22415097-6	2012	The SKLB70359 induced G0/G1 cell cycle arrest was characterized by down-regulation of cyclin-dependent kinase 2 (CDK2), CDK4, CDK6 expression and up-regulation of p53, p21(WAF1).	3-amino-6-(3,4-dichlorophenyl)thieno(2,3-b)pyridine-2-carboxamide	4-13	P53	Homo sapiens	163-166
15638966-3	2004	Bortezomib targets pathways relevant to tumor progression and therapy resistance and can directly modulate expression of cyclins, p27kip1, p53, nuclear factor-kB, Bcl-2, and Bax.	Bortezomib	0-10	P53	Homo sapiens	139-142
15382061-8	2004	In studies with multicellular spheroids, which frequently are more resistant to cytotoxic anticancer drugs than monolayers, those from wt p53 C8161 melanoma underwent PARP fragmentation in response to RuCl2(KTZ)2.	Ketoconazole	207-210	P53	Homo sapiens	138-141
15239130-3	2004	For immunohistochemical analysis of p53 protein expression, we introduced tyramide signal amplification immunohistochemistry (TSA-IHC) on a tissue microarray.	tyramide	74-82	P53	Homo sapiens	36-39
15302096-7	2004	Pifithrin-alpha, a chemical inhibitor of wild-type p53, ameliorated the cytotoxicity of Ara-C in NALM-6 and MOLT-4, but not Jurkat, U937 or HL-60.	pifithrin	0-15	P53	Homo sapiens	51-54
22678405-3	2012	METHODS: Following our published data from S-adenosylmethionine (SAMe), oxaliplatin and sorafenib were further used to stimulate GADD45beta expression in cultured HepG2 (p53 wild type) and Hep3B (p53 null) hepatoma cells in vitro.	Sorafenib	88-97	P53	Homo sapiens	170-173
15460444-5	2004	These results suggest that activation of caspase-1 and -3 and the up-regulation of Bax are required in order for apoptotic death of SK-N-BE(2) cells to be induced by ginsenoside Rh2, and p53 plays an important role in the pathways to promote apoptosis.	sk-n-be	132-139	P53	Homo sapiens	187-190
15225615-0	2004	A P53 target gene, PIG11, contributes to chemosensitivity of cells to arsenic trioxide.	Arsenic Trioxide	70-86	P53	Homo sapiens	2-5
15308759-7	2004	Levels of p53 were quantified by sensitive fluorogenic enzyme-linked immunosorbent assay at intervals up to 24 h after exposure of cells to various concentrations of melphalan and monohydroxymelphalan.	Melphalan	166-175	P53	Homo sapiens	10-13
15375563-2	2004	PAb421 binding restores wild-type functions of some p53 mutants, including those of SW480 human colon cancer cells.	pab421	0-6	P53	Homo sapiens	52-55
15375563-6	2004	A single mutation in CDR1 of PAb421 VH eliminated binding of the Bs-scFv to p53 and abrogated cytotoxicity for SW480 cells without altering cellular penetration, further supporting the requirement of PAb421 binding to p53 for cytotoxicity.	pab421	29-35	P53	Homo sapiens	76-79
15375563-6	2004	A single mutation in CDR1 of PAb421 VH eliminated binding of the Bs-scFv to p53 and abrogated cytotoxicity for SW480 cells without altering cellular penetration, further supporting the requirement of PAb421 binding to p53 for cytotoxicity.	pab421	29-35	P53	Homo sapiens	218-221
15225615-3	2004	Recent data demonstrated that PIG11 was up-regulated markedly in arsenic trioxide induced apoptosis by DDRT-PCR, suggesting a new class of p53 target genes that sensitize cells to the effects of chemotherapeutic agents.	Arsenic Trioxide	65-81	P53	Homo sapiens	139-142
22678405-3	2012	METHODS: Following our published data from S-adenosylmethionine (SAMe), oxaliplatin and sorafenib were further used to stimulate GADD45beta expression in cultured HepG2 (p53 wild type) and Hep3B (p53 null) hepatoma cells in vitro.	Sorafenib	88-97	P53	Homo sapiens	196-199
15149862-3	2004	Loss of WRN or TP53 function resulted in induction of apoptosis and lesser proliferative survival in response to AraC and bleomycin.	Bleomycin	122-131	P53	Homo sapiens	15-19
15284338-3	2004	In cell culturing, the deuterium-labeled (heavy) amino acids were incorporated into the proteome of the induced DLD-1.p53 cells, whereas the DLD-1.vector cells were grown in the unlabeled medium.	Deuterium	23-32	P53	Homo sapiens	118-121
22096025-0	2012	Skin tumors induced by sorafenib; paradoxic RAS-RAF pathway activation and oncogenic mutations of HRAS, TP53, and TGFBR1.	Sorafenib	23-32	P53	Homo sapiens	104-108
15802048-0	2004	Loss of p53 function in colon cancer cells results in increased phosphocholine and total choline.	Phosphorylcholine	64-78	P53	Homo sapiens	8-11
15262986-4	2004	MDA, including epothilone B analogue (BMS-247550) and vinblastine, induced apoptosis of Bax-positive HCT116 cells in a p53-dependent manner; p53 was required for MDA-induced Bax conformational change.	Vinblastine	54-65	P53	Homo sapiens	119-122
15145520-9	2004	A triplex forming oligonucleotide directed at a p53 consensus binding site reduces tumor growth suggesting a novel method of tumor inhibition.	triplex forming oligonucleotide	2-33	P53	Homo sapiens	48-51
15163458-11	2004	CONCLUSIONS: This study provides evidence that redox-active (Fe2+), (Mn2+), (Cu2+), and (Zn2+) ion-induced apoptosis in PBL by (H2O2)/(.OH) generation, resulting in mitochondria depolarization, caspase-3 activation, and nuclear fragmentation independent of NF-kappaB and p53 transcription factors activation.	ammonium ferrous sulfate	61-65	P53	Homo sapiens	271-274
15262986-4	2004	MDA, including epothilone B analogue (BMS-247550) and vinblastine, induced apoptosis of Bax-positive HCT116 cells in a p53-dependent manner; p53 was required for MDA-induced Bax conformational change.	Vinblastine	54-65	P53	Homo sapiens	141-144
22272214-7	2012	Our findings provided the first evidence that STAT3/p53/p21 signaling, Fas/CD95 and mitochondria-dependent pathways play critical roles in cucurbitacin E-induced G(2)/M phase arrest and apoptosis of T24 cells.	cucurbitacin E	139-153	P53	Homo sapiens	52-55
22945568-8	2012	During the following DNA replication cycle, bulky PAH-DNA adducts may be converted into mutations, thereby affecting hot spot sites in regulatory important genes such as Ras, p53, and others.	Polycyclic Aromatic Hydrocarbons	50-53	P53	Homo sapiens	175-178
15259066-0	2004	Honokiol induces apoptosis through p53-independent pathway in human colorectal cell line RKO.	honokiol	0-8	P53	Homo sapiens	35-38
15259066-1	2004	AIM: To investigate the signal pathway of honokiol-induced apoptosis on human colorectal carcinoma RKO cells and to evaluate whether p53 and p53-related genes were involved in honokiol-treated RKO cells.	honokiol	176-184	P53	Homo sapiens	133-136
15259066-1	2004	AIM: To investigate the signal pathway of honokiol-induced apoptosis on human colorectal carcinoma RKO cells and to evaluate whether p53 and p53-related genes were involved in honokiol-treated RKO cells.	honokiol	176-184	P53	Homo sapiens	141-144
15259066-10	2004	CONCLUSION: Honokiol can induce RKO cells apoptosis through activating caspase cascade by p53-indepenent pathway.	honokiol	12-20	P53	Homo sapiens	90-93
15054096-8	2004	Further evidence was obtained using a p53 inhibitor, pifithrin-alpha.	pifithrin	53-68	P53	Homo sapiens	38-41
15131059-1	2004	PURPOSE: On the basis of clinical studies showing that arsenic trioxide (As(2)O(3)), via an apoptotic mechanism, and with minimal toxicity induces complete remission in patients with refractory acute promyelocytic leukemia and that multidrug-resistant and p53-mutated neuroblastoma cells are sensitive to As(2)O(3) both in vitro and in vivo, we searched for molecular mechanisms involved in the As(2)O(3)-induced neuroblastoma cell death.	Arsenic Trioxide	55-71	P53	Homo sapiens	256-259
15131059-1	2004	PURPOSE: On the basis of clinical studies showing that arsenic trioxide (As(2)O(3)), via an apoptotic mechanism, and with minimal toxicity induces complete remission in patients with refractory acute promyelocytic leukemia and that multidrug-resistant and p53-mutated neuroblastoma cells are sensitive to As(2)O(3) both in vitro and in vivo, we searched for molecular mechanisms involved in the As(2)O(3)-induced neuroblastoma cell death.	Arsenic Trioxide	73-82	P53	Homo sapiens	256-259
15054096-9	2004	Pifithrin-alpha completely suppressed DOX-induced activation of p53 in both normal and tumor cell lines and prevented apoptosis in tumor cell lines but not in endothelial cells and cardiomyocytes.	pifithrin	0-15	P53	Homo sapiens	64-67
15370294-6	2004	Fluvastatin did not regulate p21 and p27, but down-regulated Id3 and p53 slightly.	Fluvastatin	0-11	P53	Homo sapiens	69-72
22945568-9	2012	Depending on the degree of DNA distortion and cell cycle progression, PAH-DNA adducts trigger nucleotide excision repair (NER) and various DNA damage responses that might include TP53-dependent apoptosis in certain cell types.	Polycyclic Aromatic Hydrocarbons	70-73	P53	Homo sapiens	179-183
22945568-10	2012	In fact, cellular responses to bulky PAH-DNA damage are complex because distinct signaling branches such as ATM/ATR, NER, TP53, but also MAP kinases, interact and cooperate to determine the overall outcome to cellular injuries initiated by PAH-DNA adducts.	Polycyclic Aromatic Hydrocarbons	37-40	P53	Homo sapiens	122-126
22945568-10	2012	In fact, cellular responses to bulky PAH-DNA damage are complex because distinct signaling branches such as ATM/ATR, NER, TP53, but also MAP kinases, interact and cooperate to determine the overall outcome to cellular injuries initiated by PAH-DNA adducts.	Polycyclic Aromatic Hydrocarbons	240-243	P53	Homo sapiens	122-126
22862161-0	2012	Roscovitine-induced apoptosis of H1299 cells depends on functional status of p53.	Roscovitine	0-11	P53	Homo sapiens	77-80
14715658-0	2004	S-(2-chloroethyl)glutathione-generated p53 mutation spectra are influenced by differential repair rates more than sites of initial dna damage.	S-(2-chloroethyl)glutathione	0-28	P53	Homo sapiens	39-42
15007384-6	2004	The apoptosis induction due to As2O3 treatment of LNCaP cell correlated with the activation of JNK and p38 and induction of p53 protein.	Arsenic Trioxide	31-36	P53	Homo sapiens	124-127
14715658-4	2004	The synthetic analog S-(2-chloroethyl)glutathione was used to produce DNA damage; the damage to the p53 exons was analyzed using a new fluorescence-based modification of ligation-mediated polymerase chain reaction and an automated sequencer.	S-(2-chloroethyl)glutathione	21-49	P53	Homo sapiens	100-103
22862161-4	2012	In the presence of roscovitine, each cell line variant behaved in specific way reflecting activity of the p53 protein.	Roscovitine	19-30	P53	Homo sapiens	106-109
22862161-7	2012	The cell expressing partially and conditionally active p53 mutants responded to roscovitine less efficiently.	Roscovitine	80-91	P53	Homo sapiens	55-58
15285929-0	2004	Eicosapentaenoic acid induces Fas-mediated apoptosis through a p53-dependent pathway in hepatoma cells.	ammonium ferrous sulfate	30-33	P53	Homo sapiens	63-66
22862161-8	2012	The cells expressing p53 mutants A159V and Y234C were very sensitive to roscovitine but their response was clearly temperature-dependent.	Roscovitine	72-83	P53	Homo sapiens	21-24
22862161-9	2012	The cells expressing P98A, S215G and Y220C p53 mutants exhibited only weak sensitivity to roscovitine and underwent apoptosis in low frequency.	Roscovitine	90-101	P53	Homo sapiens	43-46
15052205-11	2004	The proteins p21 and p53 were stabilized after treatment with bortezomib, correlating with a G(2)/M cell-cycle arrest.	Bortezomib	62-72	P53	Homo sapiens	21-24
22862161-10	2012	In principle, each td p53 mutant responded to roscovitine in distinct way.	Roscovitine	46-57	P53	Homo sapiens	22-25
14527925-1	2004	Functional regulation of p53 protein, a critical regulator of cell cycle and apoptosis, was investigated in fiberoptic bronchoscopy biopsy samples taken from 23 patients suffering from recurrent squamous cell lung cancer by analyzing the expression and phosphorylation status of the p53 at Ser15 and Ser20 before and after treatment with radiotherapy/cisplatin/vinorelbine.	Vinorelbine	361-372	P53	Homo sapiens	25-28
22862161-11	2012	We showed clearly that the impact of roscovitine on H1299 cells depends on functional status of p53 they produce.	Roscovitine	37-48	P53	Homo sapiens	96-99
15003520-3	2004	We investigated the ability of nitrotyrosine and nitrotyrosine-containing peptides (nitroY-peptide) to induce DNA damage by the experiments using 32P-labeled DNA fragments obtained from the human p53 tumor suppressor gene and an HPLC-electrochemical detector.	3-nitrotyrosine	31-44	P53	Homo sapiens	196-199
22862161-12	2012	This suggests that patients with tumors exhibiting specific p53 variants can benefit from the roscovitine therapy.	Roscovitine	94-105	P53	Homo sapiens	60-63
14739660-6	2004	Our results demonstrated that high concentrations of MTBITC can also induce apoptosis, through an increase of p53 and bax, but not bcl-2, protein expression.	4-methylthiobutyl isothiocyanate	53-59	P53	Homo sapiens	110-113
22962590-0	2012	Ribavirin enhances the action of interferon-alpha against hepatitis C virus by promoting the p53 activity through the ERK1/2 pathway.	Ribavirin	0-9	P53	Homo sapiens	93-96
14987952-6	2004	Besides, HepG2/C3A cells were found to be arrested in G(2)/M phase after the cells were treated with 60 microM emodin for 48 h. Moreover, significant increase in the levels of apoptosis-related signals such as p53 (419.3 pg/ml), p21 (437.4 units/ml), Fas (6.6 units/ml), and caspase-3 (35.4 pmol/min) were observed in emodin treated HepG2/C3A cells.	ammonium ferrous sulfate	251-254	P53	Homo sapiens	210-213
15001399-6	2004	In contrast, in MCF-7 cells with wild type p53 and estrogen receptor, there was no change in Akt activation, while suppression of p53 activity by pifithrin-alpha increased phosphorylation of Akt after the treatment with copper.	pifithrin	146-155	P53	Homo sapiens	130-133
14726646-3	2004	We have previously shown that ATO is a potent inducer of apoptosis in myeloma cells expressing mutant p53 engaging both the intrinsic and extrinsic apoptotic pathways.	Arsenic Trioxide	30-33	P53	Homo sapiens	102-105
22962590-3	2012	We, therefore, decided to investigate whether and how ribavirin inhibits the replication of HCV by promoting the activity of p53.	Ribavirin	54-63	P53	Homo sapiens	125-128
22962590-4	2012	METHODS: HepG2 and HCV replicons (JFH1/HepG2) were utilized to study the relationship between ribavirin and p53.	Ribavirin	94-103	P53	Homo sapiens	108-111
15016328-4	2004	In this study, we found that PS-341 induced growth arrest and apoptosis of androgen-dependent human prostate cancer LNCaP cells in conjunction with markedly up-regulated levels of p21(waf1) and p53.	Bortezomib	29-35	P53	Homo sapiens	194-197
22962590-7	2012	By knocking down ERK1/ERK2 and p53 utilizing RNA interference strategy, we further assessed the role of ERK1/2 and p53 in the suppression of HCV replication by ribavirin in a HCV replicon system.	Ribavirin	160-169	P53	Homo sapiens	115-118
14975735-4	2004	Our data show that succinyl acetone-induced heme deficiency increases the protein levels of the tumor suppressor gene product p53 and CDK inhibitor p21, and decreases the protein levels of Cdk4, Cdc2, and cyclin D2.	succinylacetone	19-35	P53	Homo sapiens	126-129
22962590-8	2012	RESULTS: Using HepG2 and HCV replicons, we demonstrated that ribavirin caused the cell cycle arrest at G1 phase and stabilized and activated p53, which was associated with the antiviral activity of ribavirin.	Ribavirin	61-70	P53	Homo sapiens	141-144
22962590-8	2012	RESULTS: Using HepG2 and HCV replicons, we demonstrated that ribavirin caused the cell cycle arrest at G1 phase and stabilized and activated p53, which was associated with the antiviral activity of ribavirin.	Ribavirin	198-207	P53	Homo sapiens	141-144
14712481-5	2004	These effects, associated with an up-regulation of p53, p21 and bax, a shuttling of p53 protein into the nucleus and a down-regulation of bcl-2, survivin and p27 protein, were reversed by the simultaneous addition of guanine or guanosine and were more evident using nondialysed serum containing hypoxanthine.	Guanine	217-224	P53	Homo sapiens	51-54
14712481-5	2004	These effects, associated with an up-regulation of p53, p21 and bax, a shuttling of p53 protein into the nucleus and a down-regulation of bcl-2, survivin and p27 protein, were reversed by the simultaneous addition of guanine or guanosine and were more evident using nondialysed serum containing hypoxanthine.	Guanine	217-224	P53	Homo sapiens	84-87
14993250-6	2004	Microarrays revealed that most (85%) of the transcriptional effects of HIV-1 Env were blocked by the p53 inhibitor pifithrin-alpha.	pifithrin	115-130	P53	Homo sapiens	101-104
22905155-2	2012	This arrest can be abrogated in p53-defective cells by the Chk1 inhibitor 7-hydroxystaurosporine (UCN-01).	7-hydroxystaurosporine	74-96	P53	Homo sapiens	32-35
14767529-2	2004	In this report, we investigate the effects of quercetin on the growth of wild-type and mutant p53 nasopharyngeal carcinoma cell lines, HK1 and CNE2 respectively.	Quercetin	46-55	P53	Homo sapiens	94-97
22905155-2	2012	This arrest can be abrogated in p53-defective cells by the Chk1 inhibitor 7-hydroxystaurosporine (UCN-01).	7-hydroxystaurosporine	98-104	P53	Homo sapiens	32-35
14767529-3	2004	The wild-type p53 HK1 was more susceptible to growth inhibition by quercetin than the mutant p53 CNE2.	Quercetin	67-76	P53	Homo sapiens	14-17
15043303-15	2004	The 5-year PFS and DSS were significantly worse for carcinomas with a TP53 mutation (22.6% vs. 41.2% progressed [P = 0.04]; 21.7% vs. 24.7% died [P = 0.04]).	dss	19-22	P53	Homo sapiens	70-74
22859938-9	2012	ER stress-induced p53 expression was significantly inhibited by coincubation with the NF-kappaB inhibitor, Bay 11-7082 and downregulation of NF-kappaB p65 expression.	3-(4-methylphenylsulfonyl)-2-propenenitrile	107-118	P53	Homo sapiens	18-21
22815878-6	2012	In contrast, administration of pifithrin-alpha (a p53 activity inhibitor) during hypoxia resulted in protein levels that were similar to those of the control groups.	pifithrin	31-46	P53	Homo sapiens	50-53
14719107-0	2004	Induction of apoptosis by bleomycin in p53-null HL-60 leukemia cells.	Bleomycin	26-35	P53	Homo sapiens	39-42
14719118-7	2004	Subsequently, flow cytometric analysis revealed a 2- to 4-fold increase in surface Fas/CD95 expression following Ad-p53 infection in mutant-p53-containing cell lines.	ammonium ferrous sulfate	83-86	P53	Homo sapiens	116-119
14719118-7	2004	Subsequently, flow cytometric analysis revealed a 2- to 4-fold increase in surface Fas/CD95 expression following Ad-p53 infection in mutant-p53-containing cell lines.	ammonium ferrous sulfate	83-86	P53	Homo sapiens	140-143
14623946-0	2004	Central role of mitochondria and p53 in Fas-mediated apoptosis of rheumatoid synovial fibroblasts.	ammonium ferrous sulfate	40-43	P53	Homo sapiens	33-36
14719118-8	2004	Use of the protein transport inhibitor Brefeldin A significantly inhibited Ad-p53-induced surface Fas/CD95 expression, but only partially inhibited apoptosis in mutant-p53 cell lines.	ammonium ferrous sulfate	98-101	P53	Homo sapiens	78-81
22359675-0	2012	Critical role of p53 upregulated modulator of apoptosis in benzyl isothiocyanate-induced apoptotic cell death.	benzyl isothiocyanate	59-80	P53	Homo sapiens	17-20
14746616-8	2004	Two of 15 lesions examined presented p53 mutations located at nondipyrimidine sites.	nondipyrimidine	62-77	P53	Homo sapiens	37-40
14998682-0	2004	Diepoxybutane induces caspase and p53-mediated apoptosis in human lymphoblasts.	diepoxybutane	0-13	P53	Homo sapiens	34-37
22359675-4	2012	Instead, the BITC-treated MCF-7 and MDA-MB-231 cells exhibited upregulation of p53 upregulated modulator of apoptosis (PUMA) protein.	benzyl isothiocyanate	13-17	P53	Homo sapiens	79-82
22072715-4	2011	A marked increase in the levels of p53 and p21 induced by Ang II was blunted by the treatment with GW501516.	GW 501516	99-107	P53	Homo sapiens	35-38
14997055-10	2004	CONCLUSIONS: Breast-cancer-specific and all-cause mortality are increased in female breast cancer patients with the following p53 mutation characteristics: silent and missense mixed mutations, transitional mutations, mutations in which guanine changed, mutations on exon 7, or multiple mutations occurring within 60 codons.	Guanine	236-243	P53	Homo sapiens	126-129
14657672-2	2004	Two distinct synthetic CDK1/2 inhibitors, Roscovitine and NU2058, are pharmacologically distinct in their ability to modify p53-dependent transcription and perturb cell cycle progression.	Roscovitine	42-53	P53	Homo sapiens	124-127
14984262-12	2004	Moreover, DODC was found to induce the levels of p53 and an 18-kDa truncated Bax on mitochondria, which in turn potentiated the release of cytochrome c for activation of caspases.	3,3'-diethyloxadicarbocyanine	10-14	P53	Homo sapiens	49-52
14517211-0	2003	A defect in the p53 response pathway induced by de novo purine synthesis inhibition.	purine	56-62	P53	Homo sapiens	16-19
14517211-2	2003	We now report that the p53-dependent G1 checkpoint is blocked in human carcinoma cell lines after inhibition of de novo purine synthesis by folate analogs inhibitory to glycinamide ribonucleotide formyltransferase (GART).	purine	120-126	P53	Homo sapiens	23-26
22044530-5	2011	TCDD suppressed 1-NP- but not BaP-induced p53 activity, and in contrast, pifithrin-alpha (PFT-alpha), a p53 inhibitor, suppressed both 1-NP- and BaP-induced p53 activity.	pifithrin	73-82	P53	Homo sapiens	104-107
17564316-0	2004	Elimination of methyl methanesulfonate (MMS)-induced micronuclei (MNS) under mild hyperthermia via p53-dependent pathway in human lymphoid cells.	Methyl Methanesulfonate	15-38	P53	Homo sapiens	99-102
22044530-5	2011	TCDD suppressed 1-NP- but not BaP-induced p53 activity, and in contrast, pifithrin-alpha (PFT-alpha), a p53 inhibitor, suppressed both 1-NP- and BaP-induced p53 activity.	pifithrin	73-82	P53	Homo sapiens	104-107
17564316-0	2004	Elimination of methyl methanesulfonate (MMS)-induced micronuclei (MNS) under mild hyperthermia via p53-dependent pathway in human lymphoid cells.	Methyl Methanesulfonate	40-43	P53	Homo sapiens	99-102
14615974-6	2003	BA-3,4-dihydrodiol induced a double-base lesion of C and G at the 5"-ACG-3" sequence complementary to codon 273 of the human p53 tumor suppressor gene, which is known as a hotspot.	benz(a)anthracene-3,4-dihydrodiol	0-18	P53	Homo sapiens	125-128
17564316-4	2004	Here we first show the elimination of MMS-induced micronuclei (MN) as one of biomarkers of carcinogenic risk by p53 activation in human lymphoid cells in response to mild hyperthermia, strongly suggesting a possible protective role of mild hyperthermia in chromosomal stability against genotoxic stresses.	Methyl Methanesulfonate	38-41	P53	Homo sapiens	112-115
21685937-9	2011	Finally, we show that overexpression of SPARC renders cells more resistant to the p53-mediated cytotoxic effects of the DNA-damaging drug actinomycin-D.	Deuterium	120-121	P53	Homo sapiens	82-85
15033759-8	2003	Moreover, sulforaphane induced apoptosis (and also necrosis), mediated by an increase in the expression of p53, whereas it exerted little effect on bcl-2 and bax levels.	sulforaphane	10-22	P53	Homo sapiens	107-110
12888115-9	2003	However, dG-C8-AAF adducts produced greater p53 induction than dG-C8-AF adducts.	N-(deoxyguanosin-8-yl)acetylaminofluorene	9-18	P53	Homo sapiens	44-47
21479885-0	2011	Quercetin enhances 5-fluorouracil-induced apoptosis in MSI colorectal cancer cells through p53 modulation.	Quercetin	0-9	P53	Homo sapiens	91-94
12893292-8	2003	UVB-exposed AZT induced double base damage at the 5(")-ACG-3(") sequence, complementary to a hot spot of the p53 gene.	Zidovudine	12-15	P53	Homo sapiens	109-112
22101337-7	2011	We also show that the checkpoint kinase inhibitor UCN-01 abolishes the G2 arrest induced by the veliparib and topotecan combination and further increases cell death in both p53-wildtype and -mutant cells.	7-hydroxystaurosporine	50-56	P53	Homo sapiens	173-176
12712406-10	2003	CONCLUSIONS: These results suggest that, in p53-mutated prostate cancer, JNK-initiated Fas-mediated apoptotic signals may play an important role in chemosensitivity.	ammonium ferrous sulfate	87-90	P53	Homo sapiens	44-47
22101337-8	2011	Collectively, PARP inhibition by veliparib enhances DDR and cell death in BRCA-proficient cancer cells in a p53-dependent and -independent fashion.	veliparib	33-42	P53	Homo sapiens	108-111
14687474-4	2003	RESULTS: The combination of PCNA-ASO and Ad-p53 inhibited cell viability in both the EJ (89.3%) and BIU-87 (78.6%) cell lines.	biu	100-103	P53	Homo sapiens	44-47
21994207-0	2011	Enhancement of carboplatin- and quercetin-induced cell death by roscovitine is Akt dependent and p53 independent in hepatoma cells.	Quercetin	32-41	P53	Homo sapiens	97-100
14688479-5	2003	In this study, we investigated the role of p53 and its downstream targets in bortezomib-induced apoptosis in HCT116 human colon cancer cells.	Bortezomib	77-87	P53	Homo sapiens	43-46
14688479-6	2003	We demonstrated that bortezomib induced p53, and activated its downstream genes p21, PUMA and Bax in a p53-dependent fashion.	Bortezomib	21-31	P53	Homo sapiens	40-43
12531793-0	2003	Arsenic trioxide-induced apoptosis in myeloma cells: p53-dependent G1 or G2/M cell cycle arrest, activation of caspase-8 or caspase-9, and synergy with APO2/TRAIL.	Arsenic Trioxide	0-16	P53	Homo sapiens	53-56
12531793-4	2003	We tested the effect of ATO on 7 myeloma cell lines with varying p53 status and report that in cells with mutated p53, ATO induced rapid and extensive (more than 90%) apoptosis in a time- and dose-dependent manner concomitant with arrest of cells in G(2)/M phase of the cell cycle.	Arsenic Trioxide	119-122	P53	Homo sapiens	65-68
12531793-4	2003	We tested the effect of ATO on 7 myeloma cell lines with varying p53 status and report that in cells with mutated p53, ATO induced rapid and extensive (more than 90%) apoptosis in a time- and dose-dependent manner concomitant with arrest of cells in G(2)/M phase of the cell cycle.	Arsenic Trioxide	119-122	P53	Homo sapiens	114-117
12531793-5	2003	Myeloma cells with wild-type (wt) p53 were relatively resistant to ATO with maximal apoptosis of about 40% concomitant with partial arrest of cells in G(1) and up-regulation of p21.	Arsenic Trioxide	67-70	P53	Homo sapiens	34-37
14688479-6	2003	We demonstrated that bortezomib induced p53, and activated its downstream genes p21, PUMA and Bax in a p53-dependent fashion.	Bortezomib	21-31	P53	Homo sapiens	103-106
12531793-6	2003	The use of caspase blocking peptides, fluorescence-tagged caspase-specific substrate peptides, and Western immunoblotting confirmed the involvement of primarily caspase-8 and -3 in ATO-induced apoptosis in myeloma cells with mutated p53 and primarily caspase-9 and -3 in cells expressing wt p53.	Arsenic Trioxide	181-184	P53	Homo sapiens	233-236
14688479-11	2003	These results indicate that p53 downstream targets can collectively modulate apoptotic response to bortezomib and other proteasome inhibitors.	Bortezomib	99-109	P53	Homo sapiens	28-31
21438026-6	2011	MutHBx inhibited colony formation in p53-proficient cells (P &lt; 0.01), but not p53-deficient lines.	muthbx	0-6	P53	Homo sapiens	37-40
14682389-12	2003	The p53 protein was expressed in arsenic trioxide-treated cells, however, the densitometric analysis did not show any significant differences (p&lt;0.05) between treated and control cells.	Arsenic Trioxide	33-49	P53	Homo sapiens	4-7
12531793-6	2003	The use of caspase blocking peptides, fluorescence-tagged caspase-specific substrate peptides, and Western immunoblotting confirmed the involvement of primarily caspase-8 and -3 in ATO-induced apoptosis in myeloma cells with mutated p53 and primarily caspase-9 and -3 in cells expressing wt p53.	Arsenic Trioxide	181-184	P53	Homo sapiens	291-294
12734332-7	2003	Finally, in contrast to clonal deletion, PAH-induced pro/pre-B cell death was not dependent on p27(Kip1) or p21(WAF1) up-regulation but did coincide with p53 induction.	Polycyclic Aromatic Hydrocarbons	41-44	P53	Homo sapiens	154-157
21438026-9	2011	In clonogenic survival assays, MutHBx inhibited cell growth in p53-proficient cells rather than enhanced it.	muthbx	31-37	P53	Homo sapiens	63-66
12714698-0	2003	Simultaneous use of DGGE and DHPLC to screen TP53 mutations in cancers of the esophagus and cardia from a European high incidence area (Lower Normandy, France).	dhplc	29-34	P53	Homo sapiens	45-49
12698197-0	2003	Doxorubicin and vinorelbine act independently via p53 expression and p38 activation respectively in breast cancer cell lines.	Vinorelbine	16-27	P53	Homo sapiens	50-53
14562033-3	2003	In this study, the induction of p53 and p21 expression by vinorelbine (Navelbine) was compared between AD and AI cells in an attempt to understand the difference(s) in apoptotic signalling pathways in these cells.	Vinorelbine	58-69	P53	Homo sapiens	32-35
21438026-10	2011	This suggests that for MutHBx to behave oncogenically, the p53 pathway must be crippled or absent.	muthbx	23-29	P53	Homo sapiens	59-62
14562033-3	2003	In this study, the induction of p53 and p21 expression by vinorelbine (Navelbine) was compared between AD and AI cells in an attempt to understand the difference(s) in apoptotic signalling pathways in these cells.	Vinorelbine	71-80	P53	Homo sapiens	32-35
14562033-4	2003	Using a series of deletion of p21 reporter constructs, we found that vinorelbine mediated p21 induction in a p53-dependent manner in AD cells.	Vinorelbine	69-80	P53	Homo sapiens	109-112
14562033-5	2003	In contrast, p21 expression restored by vinorelbine in AI cells was found to be through both p53-dependent and-independent pathways.	Vinorelbine	40-51	P53	Homo sapiens	93-96
12698197-4	2003	The aim of this study was to establish the effects of doxorubicin and vinorelbine, as single agents, in combination, and as sequential treatments, on signal transduction and p53 in the breast cancer cell lines MCF-7 and MDA-MB-468.	Vinorelbine	70-81	P53	Homo sapiens	174-177
22070678-4	2011	Quercetin can also upregulate proteins that abrogate free radical damage, such as p53.	Quercetin	0-9	P53	Homo sapiens	82-85
12727806-4	2003	It has been reported that lung cancer from workers exposed to Cr(VI) has a high percentage of G to T transversion mutations in the non-transcribed strand of the p53 gene, a hallmark of PAH-induced mutation.	Polycyclic Aromatic Hydrocarbons	185-188	P53	Homo sapiens	161-164
12727806-6	2003	These results raise the possibility that Cr(VI) may enhance PAH binding at the p53 gene in lung tissue.	Polycyclic Aromatic Hydrocarbons	60-63	P53	Homo sapiens	79-82
12824901-6	2003	Western blot analysis revealed that p53 expression was increased by troglitazone in a time-dependent manner in MKN-74 cells, further suggesting that p53 may mediate the apoptotic process induced by troglitazone.	Troglitazone	68-80	P53	Homo sapiens	36-39
12824901-6	2003	Western blot analysis revealed that p53 expression was increased by troglitazone in a time-dependent manner in MKN-74 cells, further suggesting that p53 may mediate the apoptotic process induced by troglitazone.	Troglitazone	68-80	P53	Homo sapiens	149-152
12824901-6	2003	Western blot analysis revealed that p53 expression was increased by troglitazone in a time-dependent manner in MKN-74 cells, further suggesting that p53 may mediate the apoptotic process induced by troglitazone.	Troglitazone	198-210	P53	Homo sapiens	36-39
21889606-0	2011	Study on X-ray-induced apoptosis and chromosomal damage in G2 human lymphocytes in the presence of pifithrin-alpha, an inhibitor of p53.	pifithrin	99-114	P53	Homo sapiens	132-135
12824901-6	2003	Western blot analysis revealed that p53 expression was increased by troglitazone in a time-dependent manner in MKN-74 cells, further suggesting that p53 may mediate the apoptotic process induced by troglitazone.	Troglitazone	198-210	P53	Homo sapiens	149-152
12824901-8	2003	In the dominant-negative p53 mutant cells, troglitazone failed to induce apoptosis, strongly supporting the hypothesis that p53 indeed mediates the process of the troglitazone-induced apoptosis.	Troglitazone	163-175	P53	Homo sapiens	124-127
12824901-9	2003	In the dominant-negative p53 mutant cells, troglitazone significantly induced cell growth arrest and increased expression of p27(Kip1) protein, which is thought to be the key molecule to evoke growth arrest, suggesting that p53 is not involved in the growth inhibition by troglitazone.	Troglitazone	43-55	P53	Homo sapiens	25-28
22037577-7	2011	Additionally, cAMP-response element (CRE)- and p53-dependent transcriptional reporter activity was negatively regulated by vFLIP in the presence of bleomycin.	Bleomycin	148-157	P53	Homo sapiens	47-50
12660163-5	2003	Induction of ICAM-1 is abolished after treatment with the specific p53 inhibitor pifithrin-alpha and is abrogated in p53-deficient cell lines.	pifithrin	81-96	P53	Homo sapiens	67-70
22037577-8	2011	Interestingly, a negative regulatory phosphatase essential for G2 checkpoint recovery and for dephosphorylation of gamma-H2AX, Wip1/PPM1D, whose gene promoter is regulated by p53, CRE and NF-kappaB, was selectively downregulated in vFLIP-expressing cells after bleomycin treatment.	Bleomycin	261-270	P53	Homo sapiens	175-178
21715570-7	2011	The p53 inhibitor pifithrin-alpha inhibited 3-NBA-induced apoptosis while small effects were seen using pifithrin-mu, suggesting that 3-NBA-induced cell death is a result of transcriptional activation of p53.	pifithrin	18-33	P53	Homo sapiens	4-7
12631620-9	2003	CONCLUSIONS: Our data suggest that the PS-341-induced G(2)-M-phase arrest may be associated with the inhibition of degradation of cell cycle regulators and that the up-regulation of p21(cip/waf-1) expression may be via p53-dependent and/or -independent pathways.	Bortezomib	39-45	P53	Homo sapiens	219-222
21715570-7	2011	The p53 inhibitor pifithrin-alpha inhibited 3-NBA-induced apoptosis while small effects were seen using pifithrin-mu, suggesting that 3-NBA-induced cell death is a result of transcriptional activation of p53.	pifithrin	18-33	P53	Homo sapiens	204-207
12641444-7	2003	Of this group, arsenic trioxide was the strongest inducer of cellular p53, while dimethylarsinic acid, iododimethylarsine, and sodium arsenite also caused p53 induction in a dose- and time-dependent manner.	Arsenic Trioxide	15-31	P53	Homo sapiens	70-73
21557998-1	2011	Mechanisms and pathways responsible for cytotoxicity of sulforaphane (SF) in colon cancer cells with deleted p53 were investigated during 48 h of exposure.	sulforaphane	56-68	P53	Homo sapiens	109-112
12641444-7	2003	Of this group, arsenic trioxide was the strongest inducer of cellular p53, while dimethylarsinic acid, iododimethylarsine, and sodium arsenite also caused p53 induction in a dose- and time-dependent manner.	Arsenic Trioxide	15-31	P53	Homo sapiens	155-158
12641444-7	2003	Of this group, arsenic trioxide was the strongest inducer of cellular p53, while dimethylarsinic acid, iododimethylarsine, and sodium arsenite also caused p53 induction in a dose- and time-dependent manner.	Cacodylic Acid	81-101	P53	Homo sapiens	155-158
21557998-1	2011	Mechanisms and pathways responsible for cytotoxicity of sulforaphane (SF) in colon cancer cells with deleted p53 were investigated during 48 h of exposure.	sulforaphane	70-72	P53	Homo sapiens	109-112
21426305-5	2011	Thus, mt p53-R175H may desensitize tumours to Fas-mediated anchorage-independent death via a FAK-dependent mechanism.	ammonium ferrous sulfate	46-49	P53	Homo sapiens	9-12
12589822-7	2003	Treatment of quercetin, which induced a cell-cycle block in G1-phase, induced down-regulation of cyclins and CDKs and up-regulation of the CDK inhibitor p21 expression, whereas up-regulation of p27 or p53 by quercetin was not observed.	Quercetin	13-22	P53	Homo sapiens	201-204
12589822-7	2003	Treatment of quercetin, which induced a cell-cycle block in G1-phase, induced down-regulation of cyclins and CDKs and up-regulation of the CDK inhibitor p21 expression, whereas up-regulation of p27 or p53 by quercetin was not observed.	Quercetin	208-217	P53	Homo sapiens	201-204
21656826-0	2011	Resistance to docetaxel-induced apoptosis in prostate cancer cells by p38/p53/p21 signaling.	Docetaxel	14-23	P53	Homo sapiens	74-77
12473386-1	2003	The present study was performed to gain insight into the role of p53 and p21(WAF1) on the cytotoxicity of the purine analogue cladribine (2-CdA) on cancer cells.	purine	110-116	P53	Homo sapiens	65-68
21656826-8	2011	Knocking down p53 by small interference RNA (siRNA) sensitizes LNCaP cells to docetaxel treatment.	Docetaxel	78-87	P53	Homo sapiens	14-17
21656826-9	2011	Docetaxel stabilizes p53 protein level and upregulates p21 in a p53-dependent manner in LNCaP cells.	Docetaxel	0-9	P53	Homo sapiens	21-24
12517773-2	2003	We have reported that UCN-01 (7-hydroxystaurosporine) abrogates DNA damage-induced S and G(2) arrest and enhances cytotoxicity selectively in p53 mutant cells, thus providing a potential, tumor-targeted therapy.	7-hydroxystaurosporine	22-28	P53	Homo sapiens	142-145
12517773-2	2003	We have reported that UCN-01 (7-hydroxystaurosporine) abrogates DNA damage-induced S and G(2) arrest and enhances cytotoxicity selectively in p53 mutant cells, thus providing a potential, tumor-targeted therapy.	7-hydroxystaurosporine	30-52	P53	Homo sapiens	142-145
21656826-9	2011	Docetaxel stabilizes p53 protein level and upregulates p21 in a p53-dependent manner in LNCaP cells.	Docetaxel	0-9	P53	Homo sapiens	64-67
21656826-11	2011	Treatment with p38-specific inhibitor SB203580 or knocking down p38 by siRNA significantly impaired the upregulation of p53 and p21 by docetaxel.	Docetaxel	135-144	P53	Homo sapiens	120-123
12402298-6	2002	With formamidopyrimidine-DNA glycosylase treatment, N-OH-AF induced cleavage at guanine residues, especially of the ACG sequence complementary to codon 273, a well-known hot spot of the p53 gene.	Guanine	80-87	P53	Homo sapiens	186-189
21656826-13	2011	CONCLUSIONS: Stimulation of the p38/p53/p21 signaling axis could be important for regulating the susceptibility towards docetaxel in prostate cancer.	Docetaxel	120-129	P53	Homo sapiens	36-39
21763279-0	2011	p53 activation inhibits ochratoxin A-induced apoptosis in monkey and human kidney epithelial cells via suppression of JNK activation.	ochratoxin A	24-36	P53	Homo sapiens	0-3
12151394-3	2002	Recent evidence indicates that the monofunctional DNA alkylating agent N-methyl-N"-nitro-N- nitrosoguanidine (MNNG) also triggers up-regulation and phosphorylation of p53; however, the mechanism(s) responsible for this are unknown.	Methylnitronitrosoguanidine	71-108	P53	Homo sapiens	167-170
12151394-3	2002	Recent evidence indicates that the monofunctional DNA alkylating agent N-methyl-N"-nitro-N- nitrosoguanidine (MNNG) also triggers up-regulation and phosphorylation of p53; however, the mechanism(s) responsible for this are unknown.	Methylnitronitrosoguanidine	110-114	P53	Homo sapiens	167-170
21763279-4	2011	In the present study, we find that p53 activation exerts pro-survival function to inhibit apoptosis induction in MARC-145, Vero monkey kidney cells and HEK293 human kidney cells in response to ochratoxin A treatment.	ochratoxin A	193-205	P53	Homo sapiens	35-38
12151395-5	2002	Moreover, the role of p53 in activation of this pathway was demonstrated by the fact that inhibition of p53 activity by pifithrin-alpha reduced the sensitivity of HCT116/p21(-/-) cells to daunomycin-induced apoptosis and restored a Bax/Bcl-2 ratio similar to that observed in HCT116p21(+/+) cells.	pifithrin	120-135	P53	Homo sapiens	22-25
21586571-9	2011	Intermolecular nuclear Overhauser effect placed aspartate 76 in the vicinity of lysine 381, indicating that the region around residues 73-76 of PC4 is important for p53 recognition.	Aspartic Acid	48-57	P53	Homo sapiens	165-168
21458064-3	2011	Cationic beta-cyclodextrin-polyethylenimine-Dox (PC-Dox) conjugates were prepared for carrying wt p53 plasmid in the form of PC-Dox/p53 nanocomplexes to achieve synergistic cancer therapeutic effects of drug and gene therapies.	polyethylenimine-dox	27-47	P53	Homo sapiens	98-101
12231503-3	2002	We show here that a transgene with a dominant-negative mutant form of human p53 expressed from the surfactant protein C promoter sensitizes mice to bleomycin-induced lung injury.	Bleomycin	148-157	P53	Homo sapiens	76-79
11925449-5	2002	Mutation of conserved amino acids in the linker at Ser(261) and Leu(264), which bridges the S9-S10 beta-sheets, stimulated p53 activity from reporter templates and increased MDM2-dependent ubiquitination of p53.	Leucine	64-67	P53	Homo sapiens	123-126
21458064-3	2011	Cationic beta-cyclodextrin-polyethylenimine-Dox (PC-Dox) conjugates were prepared for carrying wt p53 plasmid in the form of PC-Dox/p53 nanocomplexes to achieve synergistic cancer therapeutic effects of drug and gene therapies.	polyethylenimine-dox	27-47	P53	Homo sapiens	132-135
11925449-5	2002	Mutation of conserved amino acids in the linker at Ser(261) and Leu(264), which bridges the S9-S10 beta-sheets, stimulated p53 activity from reporter templates and increased MDM2-dependent ubiquitination of p53.	Leucine	64-67	P53	Homo sapiens	207-210
11964141-2	2002	The p53 protein is vulnerable to oxidation at cysteine thiol groups.	cysteine thiol	46-60	P53	Homo sapiens	4-7
21554433-8	2011	Both Odora cells (an olfactive cell line) and OM cells treated with etoposide, a p53 activity inducer, exhibited mitochondrial-dependent apoptosis that was inhibited by the pan-caspase inhibitor zVAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	195-203	P53	Homo sapiens	81-84
21737649-4	2011	In three mutant forms of p53--S15A, S20A and S46A--serine was converted to alanine at these sites to prevent phosphorylation, and in two other mutant forms, S15D and S20D, serine was converted to aspartic acid to mimic phosphorylation.	Aspartic Acid	196-209	P53	Homo sapiens	25-28
12139723-0	2002	Superior effect of 9-cis retinoic acid (RA) compared with all-trans RA and 13-cis RA on the inhibition of clonogenic cell growth and the induction of apoptosis in OCI/AML-2 subclones: is the p53 pathway involved?	Alitretinoin	19-38	P53	Homo sapiens	191-194
12139723-4	2002	In addition, Western blotting revealed the most obvious translocation of p53 from cytosol to nucleus in the case of 9-cis RA, which was the only retinoid able to change the conformation of p53 from mutational to wild type, as demonstrated by flow cytometry.	Retinoids	145-153	P53	Homo sapiens	73-76
12139723-4	2002	In addition, Western blotting revealed the most obvious translocation of p53 from cytosol to nucleus in the case of 9-cis RA, which was the only retinoid able to change the conformation of p53 from mutational to wild type, as demonstrated by flow cytometry.	Retinoids	145-153	P53	Homo sapiens	189-192
21463108-6	2011	Both dATP and CdATP cause an initial accumulation of DNA strand breaks in lymphocytes and this results in the activation of p53, the release of cytochrome c from mitochondria, and apoptosis.	2'-deoxyadenosine triphosphate	5-9	P53	Homo sapiens	124-127
12071807-0	2002	7-Hydroxystaurosporine (UCN-01) preferentially sensitizes cells with a disrupted TP53 to gamma radiation in lung cancer cell lines.	7-hydroxystaurosporine	0-22	P53	Homo sapiens	81-85
21508668-7	2011	Biochemical studies showed that zinc partly induced the transition of mutant p53 protein (reactive to conformation-sensitive PAb240 antibody for mutant conformation) into a functional conformation (reactive to conformation-sensitive PAb1620 antibody for wild-type conformation).	pab1620	233-240	P53	Homo sapiens	77-80
12076704-3	2002	Mutational screening of the coding region of TP53 revealed an A>T transversion in codon 144 of exon 5 (CAG>CTG, Gln>Leu) in the germline of one of the three affected members, with loss of heterozygosity (LOH) in the tumour tissue.	Leucine	116-119	P53	Homo sapiens	45-49
21509038-7	2011	Importantly, an analogous Fas-dependent mechanism of apoptosis upon Nutlin-3 treatment is executed in wild-type p53 expressing Hodgkin lymphoma and acute myeloid leukaemia cell lines.	ammonium ferrous sulfate	26-29	P53	Homo sapiens	112-115
12009904-0	2002	N-hydroxy-4-aminobiphenyl-DNA binding in human p53 gene: sequence preference and the effect of C5 cytosine methylation.	Cytosine	98-106	P53	Homo sapiens	47-50
21417280-1	2011	Proteins which bind methylated lysines ("readers" of the histone code) are important components in the epigenetic regulation of gene expression and can also modulate other proteins that contain methyl-lysine such as p53 and Rb.	N(2)-methyl-L-lysine	194-207	P53	Homo sapiens	216-219
12432277-3	2002	In this study, we investigated the impact of Asp substitution at Thrl8 and Ser20 (p53Tl8D/S20D) on the functional regulation of p53.	Aspartic Acid	45-48	P53	Homo sapiens	82-85
12006519-0	2002	A Phase I/pilot study of sequential doxorubicin/vinorelbine: effects on p53 and microtubule-associated protein 4.	Vinorelbine	48-59	P53	Homo sapiens	72-75
21598493-4	2011	RESULTS: P53 protein and Bcl-2 protein can be combined with quantum dots fluorescent probes and specific fluorescene can be observed with ultraviolet light excited.	fluorescene	105-116	P53	Homo sapiens	9-12
21598493-6	2011	P53 protein and Bcl-2 protein can be combined with different particle size quantum dots fluorescent probes respectively in the same paraffin-embedded tissue section of human tongue squamous cell carcinoma and two kinds of fluorescene can be observed.	fluorescene	222-233	P53	Homo sapiens	0-3
12041674-0	2002	Epstein-Barr virus-associated B-cell type non-Hodgkin"s lymphoma with concurrent p53 protein expression in a rheumatoid arthritis patient treated with methotrexate.	Methotrexate	151-163	P53	Homo sapiens	81-84
21518493-5	2011	It is concluded that the combination treatment of MNP-Fe3O4 and daunorubicin efficiently inhibits growth and induces apoptosis in Raji cell line, while the activation of P53 and down-regulation of NF-kappaB may play important roles.	ferryl iron	54-59	P53	Homo sapiens	170-173
12041674-7	2002	This case suggests that concordant p53 expression and latent EBV infection may play an important role in the pathogenesis of lymphomas arising in patients with rheumatoid arthritis who are immunosuppressed with MTX.	Methotrexate	211-214	P53	Homo sapiens	35-38
21324703-2	2011	In an attempt to identify novel p53 inhibitors, a quality collection of compounds structurally related to pifithrin-beta were designed and synthesized as potential inhibitors of p53.	pifithrin	106-115	P53	Homo sapiens	32-35
11956312-6	2002	The mechanism of cell death appears to be p53 independent, and the cells are only partly rescued by incubation with the wide spectrum caspase inhibitor Z-VAD fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	152-161	P53	Homo sapiens	42-45
12918060-8	2003	Whereas SJ-N-KP cells were susceptible to a p53 transcription-dependent pathway of apoptosis, SK-N-BE(2c) cells underwent apoptosis with up-regulation of p53 expression but not of p53-target genes.	sk-n-be	94-101	P53	Homo sapiens	154-157
12918060-8	2003	Whereas SJ-N-KP cells were susceptible to a p53 transcription-dependent pathway of apoptosis, SK-N-BE(2c) cells underwent apoptosis with up-regulation of p53 expression but not of p53-target genes.	sk-n-be	94-101	P53	Homo sapiens	154-157
21324703-2	2011	In an attempt to identify novel p53 inhibitors, a quality collection of compounds structurally related to pifithrin-beta were designed and synthesized as potential inhibitors of p53.	pifithrin	106-115	P53	Homo sapiens	178-181
14580323-5	2003	Sulfite-mediated disulfide bond cleavage followed by reaction with 2-nitro-5-thiosulfobenzoate showed that oxidized p53 contains a single disulfide bond per monomer.	2-nitro-5-thiosulfobenzoate	67-94	P53	Homo sapiens	116-119
14580323-10	2003	The possibility that oxidized p53 contained significant amounts of sulfenic (-SOH), sulfinic (-SO2H), or sulfonic acid (-SO3H) was ruled out.	sulfenic	67-75	P53	Homo sapiens	30-33
21468572-10	2011	SFN treatment enhanced TRAIL-induced activation of proteins, including caspase-3 and p53.	sulforaphane	0-3	P53	Homo sapiens	85-88
14580323-10	2003	The possibility that oxidized p53 contained significant amounts of sulfenic (-SOH), sulfinic (-SO2H), or sulfonic acid (-SO3H) was ruled out.	-soh	77-81	P53	Homo sapiens	30-33
11916527-1	2002	The relationship between p53 gene status and the expression of DR5 and Fas was evaluated as a function of sensitivity of 11 acute lymphoblastic leukemia cell lines to adriamycin, etoposide, vincristine, methotrexate and dexamethasone.	Methotrexate	203-215	P53	Homo sapiens	25-28
14513055-6	2003	L-NAC also opposed bortezomib/HA14-1-mediated JNK activation, upregulation of p53 and Bax, and release of cytochrome c and Smac/DIABLO.	Bortezomib	19-29	P53	Homo sapiens	78-81
21148553-10	2011	Subsequent studies using p53(+/+) and p53(-/-) HCT116 cells established that lucanthone induced cathepsin D expression and reduced cancer cell viability independently of p53 status.	Lucanthone	77-87	P53	Homo sapiens	25-28
11965244-0	2002	Glycerol restores heat-induced p53-dependent apoptosis of human glioblastoma cells bearing mutant p53.	Glycerol	0-8	P53	Homo sapiens	31-34
11965244-0	2002	Glycerol restores heat-induced p53-dependent apoptosis of human glioblastoma cells bearing mutant p53.	Glycerol	0-8	P53	Homo sapiens	98-101
11965244-1	2002	BACKGROUND: We have previously reported that glycerol acts as a chemical chaperone to restore the expression of WAF1 in some human cancer cell lines bearing mutant p53.	Glycerol	45-53	P53	Homo sapiens	164-167
21148553-10	2011	Subsequent studies using p53(+/+) and p53(-/-) HCT116 cells established that lucanthone induced cathepsin D expression and reduced cancer cell viability independently of p53 status.	Lucanthone	77-87	P53	Homo sapiens	38-41
11965244-3	2002	The aim of the present study is to examine the restoration of heat-induced p53-dependent apoptosis by glycerol in human glioblastoma cells (A-172) transfected with a vector carrying a mutant p53 gene (A-172/mp53 cells) or neo control vector (A-172/neo cells).	Glycerol	102-110	P53	Homo sapiens	75-78
11965244-8	2002	CONCLUSION: These results suggest that glycerol is effective in inducing conformational change of phosphorylated p53 and restoring mp53 to wtp53 function, leading to enhanced heat sensitivity through the induction of apoptosis.	Glycerol	39-47	P53	Homo sapiens	113-116
12821677-11	2003	The transient transfection of wild type p53 in p53 null H358 cells caused stimulation of the bortezomib-induced apoptosis but failed to enhance ROS generation and Delta psi m increase.	Bortezomib	93-103	P53	Homo sapiens	40-43
12821677-11	2003	The transient transfection of wild type p53 in p53 null H358 cells caused stimulation of the bortezomib-induced apoptosis but failed to enhance ROS generation and Delta psi m increase.	Bortezomib	93-103	P53	Homo sapiens	47-50
21148553-10	2011	Subsequent studies using p53(+/+) and p53(-/-) HCT116 cells established that lucanthone induced cathepsin D expression and reduced cancer cell viability independently of p53 status.	Lucanthone	77-87	P53	Homo sapiens	38-41
21190955-4	2011	Aldosterone induced senescence-like changes in the kidney, exhibited by increased expression of the senescence-associated beta-galactosidase, overexpression of p53 and cyclin-dependent kinase inhibitor (p21), and decreased expression of SIRT1.	Aldosterone	0-11	P53	Homo sapiens	160-163
12851702-5	2003	In addition, 10 mM salicylate induced p53 tumor suppressor protein that plays an important role in cell cycle arrest or apoptosis and the induction seemed to be linked to its phosphorylation at Set 15.	Salicylates	19-29	P53	Homo sapiens	38-41
12874009-2	2003	Here, we investigate the role of p53 in the G(2) arrest that occurs in response to the topoisomerase inhibitors etoposide and merbarone.	merbarone	126-135	P53	Homo sapiens	33-36
11904448-6	2002	We also establish that wild-type- and mutated PS2-induced caspase activation is reduced by p53 antisense approach and by pifithrin-alpha, a chemical inhibitor of p53.	pifithrin	121-136	P53	Homo sapiens	162-165
11822871-3	2002	Fas-induced apoptosis and ceramide formation proceeded regardless of p53 status.	ammonium ferrous sulfate	0-3	P53	Homo sapiens	69-72
21274377-8	2011	We detected the effects of p53-mediated autophagy activation on the apoptosis of SGC7901 cells with the p53 inhibitor pifithrin-alpha.	pifithrin	118-133	P53	Homo sapiens	27-30
11977632-3	2002	The expressions of p53, p16 and cyclin D1 were stained by indirect immunofluorescence of fluorescein isothiocyanate(FTTC), which were detected by flow cytometry (FCM).	fttc	116-120	P53	Homo sapiens	19-22
12859901-6	2003	Further, we demonstrate that the ING2 PHD finger interacts with PtdIns(5)P in vivo and provide evidence that this interaction regulates the ability of ING2 to activate p53 and p53-dependent apoptotic pathways.	phosphatidylinositol 5-phosphate	64-74	P53	Homo sapiens	168-171
12859901-6	2003	Further, we demonstrate that the ING2 PHD finger interacts with PtdIns(5)P in vivo and provide evidence that this interaction regulates the ability of ING2 to activate p53 and p53-dependent apoptotic pathways.	phosphatidylinositol 5-phosphate	64-74	P53	Homo sapiens	176-179
12807744-6	2003	Furthermore, caffeine also inhibited the accumulation of p53 by a variety of stress-inducing agents in vivo, such as 5-fluorouracil, doxorubicin, mitomycin C, camptothecin and roscovitine.	Roscovitine	176-187	P53	Homo sapiens	57-60
21274377-8	2011	We detected the effects of p53-mediated autophagy activation on the apoptosis of SGC7901 cells with the p53 inhibitor pifithrin-alpha.	pifithrin	118-133	P53	Homo sapiens	104-107
21274377-13	2011	SN50-induced increases in PUMA, DRAM, LC3 and Beclin 1 and cell death were blocked by the p53 specific inhibitor pifithrin-alpha.	pifithrin	113-128	P53	Homo sapiens	90-93
12851490-0	2003	Arsenic trioxide selectively induces early and extensive apoptosis via the APO2/caspase-8 pathway engaging the mitochondrial pathway in myeloma cells with mutant p53.	Arsenic Trioxide	0-16	P53	Homo sapiens	162-165
11751391-0	2001	Interaction of p53 and DNA-PK in response to nucleoside analogues: potential role as a sensor complex for DNA damage.	Nucleosides	45-55	P53	Homo sapiens	15-18
22041910-0	2011	High dose of pyridoxine induces IGFBP-3 mRNA expression in MCF-7 cells and its induction is inhibited by the p53-specific inhibitor pifithrin-alpha.	pifithrin	132-141	P53	Homo sapiens	109-112
11751391-11	2001	These data suggest that DNA-PK and p53 may form a sensor complex that detects the disruption of DNA replication caused by nucleoside analogue incorporation and may subsequently signal for apoptosis.	Nucleosides	122-132	P53	Homo sapiens	35-38
11753641-7	2001	Analysis of mispair excision opposite the template adenine residue shows that p53 catalyzes 3" terminal mismatch excision with a specificity of A : G&gt;A : A&gt;A : C. Hence, the observed specificity of mismatch excision indicates that p53 exonucleolytic proofreading preferentially repairs transversion mutations.	Adenine	51-58	P53	Homo sapiens	78-81
11753641-7	2001	Analysis of mispair excision opposite the template adenine residue shows that p53 catalyzes 3" terminal mismatch excision with a specificity of A : G&gt;A : A&gt;A : C. Hence, the observed specificity of mismatch excision indicates that p53 exonucleolytic proofreading preferentially repairs transversion mutations.	Adenine	51-58	P53	Homo sapiens	237-240
12851490-2	2003	We have previously shown that ATO induces apoptosis in myeloma cells in two different modes depending on p53 status in the cells.	Arsenic Trioxide	30-33	P53	Homo sapiens	105-108
12851490-3	2003	In cells expressing mutated p53, ATO induced, G2/M arrest and activation caspase 8 and 3 and rapid and extensive apoptosis.	Arsenic Trioxide	33-36	P53	Homo sapiens	28-31
12884365-6	2003	Thus, we conclude that PFTalpha is not a specific p53 inhibitor in JB6 cells but is a potential activator of p53-mediated signaling and apoptosis.	pifithrin	23-31	P53	Homo sapiens	109-112
22041910-7	2011	The induction of IGFBP-3 by PN was inhibited by a p53-specific inhibitor, pifithrin-alpha, in a dose-dependent manner, but was not affected by PD169316 (MAPK inhibitor), AS601245 (c-Jun N-terminal kinase inhibitor) or SL327 (MEK1/2 inhibitor).	pifithrin	74-89	P53	Homo sapiens	50-53
20850924-0	2010	MDM2 antagonist Nutlin-3 enhances bortezomib-mediated mitochondrial apoptosis in TP53-mutated mantle cell lymphoma.	Bortezomib	34-44	P53	Homo sapiens	81-85
12794118-9	2003	The wt p53-induced optimization of tumor cell killing by specific CTL involves at least in part Fas-mediated pathway via induction of CD95 expression by tumor cells but does not appear to interfere with granzyme B cytotoxic pathway.	ammonium ferrous sulfate	96-99	P53	Homo sapiens	7-10
11562764-8	2001	We also found that quercetin markedly increased Cdk-inhibitor p21CIP1/WAF1 protein level after treatment for 48 h or longer, and the induction of p21CIP1/WAF1 increased its association with Cdc2-cyclin B1 complex, however, up-regulation of p53 by quercetin was not observed.	Quercetin	19-28	P53	Homo sapiens	240-243
20850924-2	2010	In the mutant TP53 MCL cells which are intrinsically resistant to bortezomib, the combination of Nutlin-3/bortezomib synergistically induced cytotoxicity through the mitochondrial apoptotic pathway mediated by transcription-independent upregulation of NOXA, sequestration of MCL-1, activation of BAX, BAK, caspase-9 and -3.	Bortezomib	106-116	P53	Homo sapiens	14-18
11470783-0	2001	p53 Phosphorylation at serine 15 is required for transcriptional induction of the plasminogen activator inhibitor-1 (PAI-1) gene by the alkylating agent N-methyl-N"-nitro-N-nitrosoguanidine.	Methylnitronitrosoguanidine	153-189	P53	Homo sapiens	0-3
20850924-3	2010	In the bortezomib sensitive wild-type TP53 MCL cells, the Nutlin-3/bortezomib combination caused G0/G1 cell cycle arrest followed by the increase in apoptosis induction.	Bortezomib	7-17	P53	Homo sapiens	38-42
11559534-0	2001	Lung tumor KRAS and TP53 mutations in nonsmokers reflect exposure to PAH-rich coal combustion emissions.	Polycyclic Aromatic Hydrocarbons	69-72	P53	Homo sapiens	20-24
12734658-8	2003	In the second case, in tumor samples from one hemisphere, nuclear accumulation of p53 was caused by a G--&gt;A transition in codon 244 (Gly--&gt;Asp).	Aspartic Acid	145-148	P53	Homo sapiens	82-85
21776480-10	2010	Our data suggest a promising therapeutic application of garcinol in p53-independent apoptosis in cancers.	garcinol	56-64	P53	Homo sapiens	68-71
12782597-3	2003	To determine the biological significance of this phenomenon, we analyzed p53 mutants, p53(223Leu) and p53(274Phe), from Fas-resistant prostate carcinoma cell line DU145.	ammonium ferrous sulfate	120-123	P53	Homo sapiens	73-76
12782597-6	2003	Whereas neither of the two mutants was found to be dominant-negative against wild-type p53, each neutralized the other"s growth-suppressive effects and, in combination, were capable of down-regulating Fas expression and converting Fas-sensitive prostate carcinoma cells PC3 into Fas-resistant ones.	ammonium ferrous sulfate	201-204	P53	Homo sapiens	87-90
11494044-10	2001	The MMS-induced phosphorylation of p53 correlates with our previous findings of p53"s ability for increased sequence-specific DNA-binding and transcriptional activity in the cells treated with DNA alkylating agents.	Methyl Methanesulfonate	4-7	P53	Homo sapiens	35-38
11494044-10	2001	The MMS-induced phosphorylation of p53 correlates with our previous findings of p53"s ability for increased sequence-specific DNA-binding and transcriptional activity in the cells treated with DNA alkylating agents.	Methyl Methanesulfonate	4-7	P53	Homo sapiens	80-83
11526498-4	2001	Here, we demonstrate that reintroduction of ATM into AT cells restores the activation of p53 by the radio-mimetic agent bleomycin.	Bleomycin	120-129	P53	Homo sapiens	89-92
11507071-3	2001	We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines.	Melphalan	93-102	P53	Homo sapiens	14-17
11507071-3	2001	We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines.	Melphalan	104-109	P53	Homo sapiens	14-17
11375983-2	2001	Northern blotting showed that a significantly decreased steady-state level of POLD1 mRNA was associated with increased wild-type p53 expression in cells treated with methyl methanesulfonate.	Methyl Methanesulfonate	166-189	P53	Homo sapiens	129-132
12963547-3	2003	RESULTS: On exposure to 5 Gy radiation, LNCaP cells demonstrated high sensitization to Fas-mediated apoptosis through increased Fas expression, stabilized p53 expression and binding to p53 response elements within the promoter and first intronic region of the Fas gene.	ammonium ferrous sulfate	87-90	P53	Homo sapiens	155-158
12963547-3	2003	RESULTS: On exposure to 5 Gy radiation, LNCaP cells demonstrated high sensitization to Fas-mediated apoptosis through increased Fas expression, stabilized p53 expression and binding to p53 response elements within the promoter and first intronic region of the Fas gene.	ammonium ferrous sulfate	87-90	P53	Homo sapiens	185-188
12963547-6	2003	CONCLUSIONS: Radiation-induced Fas sensitization in prostate cancer cell was mediated through p53-dependent transactivation of the Fas gene, which can be blocked by androgen stimulation mainly through induction of c-jun.	ammonium ferrous sulfate	31-34	P53	Homo sapiens	94-97
20533281-8	2010	However, DCA was found to have selective activity against rho(0) cells [mitochondrial DNA (mtDNA) deficient] and to synergize with 2-deoxyglucose in complex IV deficient HCT116 p53(-/-) cells.	Dichloroacetic Acid	9-12	P53	Homo sapiens	177-180
12750274-3	2003	Additional studies reported that roscovitine combined with cytotoxic agents can cooperate with DNA damage to activate p53 protein.	Roscovitine	33-44	P53	Homo sapiens	118-121
12750274-5	2003	In the breast cancer cell line MDA-MB 231, which lacks a functional p53 protein, we found a strong radiosensitization effect of roscovitine in vitro by clonogenic survival assay and in vivo in MDA-MB 231 xenograft model.	Roscovitine	128-139	P53	Homo sapiens	68-71
12750274-11	2003	In conclusion, we found a novel effect on DNA repair of the CDK inhibitor roscovitine, which acts as a radiosensitizer in vitro and in vivo in breast cancer cells lacking a functional p53.	Roscovitine	74-85	P53	Homo sapiens	184-187
12659718-10	2003	In these cells TP53 was more sensitive than global DNA for genotoxicity induced by trans-2-hexenal and H(2)O(2).	2-hexenal	83-98	P53	Homo sapiens	15-19
11489842-9	2001	These results demonstrate that a wild-type p53 cell line can be radiosensitized by dFdCyd, presumably because it was able to deplete dATP levels and progress through the cell cycle for at least 24 h after drug and radiation treatment.	2'-deoxyadenosine triphosphate	133-137	P53	Homo sapiens	43-46
11505223-7	2001	Thus, p53 accumulates in human skin and lymphocytes as a protective mechanism against polycyclic aromatic hydrocarbon induced DNA damage, and this is more pronounced in GSTM1(-/-) compared to GSTM1(+) individuals.	Polycyclic Aromatic Hydrocarbons	86-117	P53	Homo sapiens	6-9
11602056-1	2001	OBJECTIVE: To investigate the tumor suppressor activity of recombinant adenovirus vector expressing the human wild-type p53, GM-CSF, and B7-1 proteins (designated as BB-102) in human hepatocellular carcinoma cells (HCC) in vitro.	bb-102	166-172	P53	Homo sapiens	120-123
11602056-3	2001	Immunohistochemical assay was used to determine p53 expressed by BB-102.	bb-102	65-71	P53	Homo sapiens	48-51
19777160-0	2010	Synergistic efficacy of sorafenib and genistein in growth inhibition by down regulating angiogenic and survival factors and increasing apoptosis through upregulation of p53 and p21 in malignant neuroblastoma cells having N-Myc amplification or non-amplification.	Sorafenib	24-33	P53	Homo sapiens	169-172
11602056-4	2001	Tumor suppressor activity of the expressed p53 was identified by terminal deoxynucleotidy I transferase (TdT) assay in BB-102-infected HCC cell lines.	bb-102	119-125	P53	Homo sapiens	43-46
11602056-5	2001	RESULTS: p53 protein was found to express in a dose-dependent manner in BB-102-infected HCC cell lines.	bb-102	72-78	P53	Homo sapiens	9-12
12694301-5	2003	Radical (i.e., superoxide) (O2-) formation in response to oxLDL is associated with p53, as well as HIF-1 alpha accumulation in human macrophages, a process that is antagonized by NO.	radical	0-7	P53	Homo sapiens	83-86
11699407-2	2001	The effects of combining a phosphorothioate oligonucleotide OL(1) p53, which transiently down-regulates p53 levels, with an anthracycline, Idarubicin, on the growth of wild-type p53 WMN gene-expressing lymphoma cells was evaluated.	oligonucleotide ol	44-62	P53	Homo sapiens	66-69
12509264-1	2003	We investigated the effect of pifithrin-alpha (PFTalpha), a chemical inhibitor of p53, on DNA double-strand break (DSB) repair in mammalian chromosomes.	pifithrin	30-45	P53	Homo sapiens	82-85
11699407-2	2001	The effects of combining a phosphorothioate oligonucleotide OL(1) p53, which transiently down-regulates p53 levels, with an anthracycline, Idarubicin, on the growth of wild-type p53 WMN gene-expressing lymphoma cells was evaluated.	oligonucleotide ol	44-62	P53	Homo sapiens	104-107
21311676-9	2010	These effects were opposite to the expression of p-p53, p21, and MDM2 observed with SP600125 and SB202190 treatments.	pyrazolanthrone	84-92	P53	Homo sapiens	51-54
11699407-2	2001	The effects of combining a phosphorothioate oligonucleotide OL(1) p53, which transiently down-regulates p53 levels, with an anthracycline, Idarubicin, on the growth of wild-type p53 WMN gene-expressing lymphoma cells was evaluated.	oligonucleotide ol	44-62	P53	Homo sapiens	104-107
12509264-1	2003	We investigated the effect of pifithrin-alpha (PFTalpha), a chemical inhibitor of p53, on DNA double-strand break (DSB) repair in mammalian chromosomes.	pifithrin	47-55	P53	Homo sapiens	82-85
20945503-1	2010	Methylated cytosines within CpG dinucleotides (mCpGs) along the DNA-binding domain of the TP53 tumor suppressor gene (exons ~5-8) are the single most significant mutational target in human cancers.	Cytosine	11-20	P53	Homo sapiens	90-94
12538356-4	2003	Ultraviolet (UV) light from the sun and polycyclic aromatic hydrocarbons, such as benzo[a]pyrene, are strongly implicated in the spectrum of p53 mutations found in human non-melanoma skin cancers and smoking-associated lung cancers, respectively.	Polycyclic Aromatic Hydrocarbons	40-72	P53	Homo sapiens	141-144
11458984-0	2001	The effect of methyl methanesulfonate (MMS)-induced excision repair on p53-dependent apoptosis in human lymphoid cells.	Methyl Methanesulfonate	14-37	P53	Homo sapiens	71-74
11458984-0	2001	The effect of methyl methanesulfonate (MMS)-induced excision repair on p53-dependent apoptosis in human lymphoid cells.	Methyl Methanesulfonate	39-42	P53	Homo sapiens	71-74
11458984-5	2001	In addition, a clear p53-mediated contribution to apoptosis in MMS-induced cell death was observed.	Methyl Methanesulfonate	63-66	P53	Homo sapiens	21-24
21110861-8	2010	The Meq variants L-Meq and S-Meq, but not VS-Meq and  Meq, which were expressed in MD tumor cells and MDV-infected cells, exerted an inhibitory effect on p53 transcriptional activity.	s-meq	27-32	P53	Homo sapiens	154-157
11375905-7	2001	Both lactacystin, a specific inhibitor of the 26S proteasome, and leptomycin B, a specific inhibitor of the nuclear export protein CRM1, could block the effect that DCA had on p53 protein levels, suggesting that DCA suppressed p53 by stimulating the process of proteasome-mediated degradation of p53.	lactacystin	5-16	P53	Homo sapiens	176-179
11375905-7	2001	Both lactacystin, a specific inhibitor of the 26S proteasome, and leptomycin B, a specific inhibitor of the nuclear export protein CRM1, could block the effect that DCA had on p53 protein levels, suggesting that DCA suppressed p53 by stimulating the process of proteasome-mediated degradation of p53.	lactacystin	5-16	P53	Homo sapiens	227-230
11375905-7	2001	Both lactacystin, a specific inhibitor of the 26S proteasome, and leptomycin B, a specific inhibitor of the nuclear export protein CRM1, could block the effect that DCA had on p53 protein levels, suggesting that DCA suppressed p53 by stimulating the process of proteasome-mediated degradation of p53.	lactacystin	5-16	P53	Homo sapiens	227-230
11387205-2	2001	Here we provide evidence that overexpression of Gas2 efficiently increases cell susceptibility to apoptosis following UV irradiation, etoposide and methyl methanesulfonate treatments, and that these effects are dependent on increased p53 stability and transcription activity.	Methyl Methanesulfonate	148-171	P53	Homo sapiens	234-237
11484935-2	2001	We found that four anticancer agents: etoposide, doxorubicin, bleomycin and paclitaxel induced apoptosis in human umbilical vein endothelial cells (HUVECs) (as judged by DNA fragmentation) with a time- and concentration-dependent decrease in bcl-2 protein but without the involvement of p53.	Bleomycin	62-71	P53	Homo sapiens	287-290
12538456-7	2003	Quantitative reverse transcription-PCR analysis of the four p53 related genes [p21 (CDKN1A), FAS, BAK, and MDM2] revealed that Bak expression was increased significantly 24 h after Ad-p53 (INGN 201) injection and levels of CDKN1A and MDM2 expression were increased over the course of treatment.	ammonium ferrous sulfate	93-96	P53	Homo sapiens	60-63
12488329-7	2003	Moreover, in prostate cancer cells, the synergism between 1,25-(OH)(2)D(3) and 9-cis retinoic acid appears to be dependent on the presence of functional p53; however, 1,25-(OH)(2)D(3)-mediated induction of G(1) cell cycle accumulation and induction of apoptosis is not.	Isotretinoin	81-98	P53	Homo sapiens	153-156
12397013-0	2002	Hydrogen peroxide induces upregulation of Fas in human airway epithelial cells via the activation of PARP-p53 pathway.	ammonium ferrous sulfate	42-45	P53	Homo sapiens	106-109
12397013-11	2002	These results indicate that H(2)O(2) induces Fas upregulation by promoting cytoplasmic transport of Fas to the cell surface in human airway epithelial cells, and that the activation of the poly(ADP-ribose) polymerase-p53 pathway may be involved in this mechanism.	ammonium ferrous sulfate	45-48	P53	Homo sapiens	217-220
12530531-0	2002	Cyclin D3 and p53 mediate sulforaphane-induced cell cycle delay and apoptosis in non-transformed human T lymphocytes.	sulforaphane	26-38	P53	Homo sapiens	14-17
12530531-2	2002	Following our previous demonstration that sulforaphane induces cell cycle arrest and apoptosis in human T lymphoblastoid Jurkat leukemia cells and increases p53 and bax protein expression, we tested sulforaphane on non-transformed phytohemagglutinin-stimulated human lymphocytes.	sulforaphane	42-54	P53	Homo sapiens	157-160
11599886-0	2001	Fas-independent apoptosis induced by UVC in p53-mutated human epithelial tumor A431 cells through activation of caspase-8 and JNK/SAPK.	ammonium ferrous sulfate	0-3	P53	Homo sapiens	44-47
12530531-4	2002	Moreover, sulforaphane induced apoptosis (and also necrosis), mediated by an increase in the expression of p53.	sulforaphane	10-22	P53	Homo sapiens	107-110
21187919-8	2010	Furthermore, the combination of MNP-Fe3O4 with adriamycin or daunorubicin increased p53 protein levels and decreased NF-kappaB protein levels more than adriamycin or daunorubicin alone, indicating that MNP-Fe3O4 could enhance the effect of chemotherapeutic drugs on p53 and NF-kappaB.	ferryl iron	36-41	P53	Homo sapiens	84-87
12379456-1	2002	The high frequency of G--&gt;T transversions in the p53 gene is a distinctive feature of lung cancer patients with a smoking history and is commonly believed to reflect the direct mutagenic signature of polycyclic aromatic hydrocarbon (PAH) adducts along the gene.	Polycyclic Aromatic Hydrocarbons	203-234	P53	Homo sapiens	52-55
12578616-2	2001	The effects of exogenous wt-p53 gene on the proliferation and differentiation of K562 cells were studied by detection of cell growth curves, leukemic colony formation, cell cycle analysis and DNA fragmentation, TdT-mediated dUTP nick end labeling (TUNEL) and benzidine staining.	deoxyuridine triphosphate	224-228	P53	Homo sapiens	28-31
11279192-9	2001	However, the treatment of cells with DNA alkylating agents methylmethane sulfonate and N-methyl-N"-nitro-N-nitrosoguanidine, which cause phosphorylation of p53 at Ser(15) and Ser(392), induced pAPCP promoter activity in HCT-116(p53(+/+)) cells.	Methyl Methanesulfonate	59-82	P53	Homo sapiens	156-159
11279192-9	2001	However, the treatment of cells with DNA alkylating agents methylmethane sulfonate and N-methyl-N"-nitro-N-nitrosoguanidine, which cause phosphorylation of p53 at Ser(15) and Ser(392), induced pAPCP promoter activity in HCT-116(p53(+/+)) cells.	Methyl Methanesulfonate	59-82	P53	Homo sapiens	228-231
11279192-9	2001	However, the treatment of cells with DNA alkylating agents methylmethane sulfonate and N-methyl-N"-nitro-N-nitrosoguanidine, which cause phosphorylation of p53 at Ser(15) and Ser(392), induced pAPCP promoter activity in HCT-116(p53(+/+)) cells.	Methylnitronitrosoguanidine	87-123	P53	Homo sapiens	156-159
11279192-9	2001	However, the treatment of cells with DNA alkylating agents methylmethane sulfonate and N-methyl-N"-nitro-N-nitrosoguanidine, which cause phosphorylation of p53 at Ser(15) and Ser(392), induced pAPCP promoter activity in HCT-116(p53(+/+)) cells.	Methylnitronitrosoguanidine	87-123	P53	Homo sapiens	228-231
12379456-1	2002	The high frequency of G--&gt;T transversions in the p53 gene is a distinctive feature of lung cancer patients with a smoking history and is commonly believed to reflect the direct mutagenic signature of polycyclic aromatic hydrocarbon (PAH) adducts along the gene.	Polycyclic Aromatic Hydrocarbons	236-239	P53	Homo sapiens	52-55
11279192-10	2001	Other than p53-binding sites, using deletion mutation constructs, we have shown that N-methyl-N"-nitro-N-nitrosoguanidine-induced transcriptional activation of the pAPCP promoter in HCT-116(p53(+/+)) cells depended upon the Sp1-binding site and the E-box B site.	Methylnitronitrosoguanidine	85-121	P53	Homo sapiens	11-14
21187919-8	2010	Furthermore, the combination of MNP-Fe3O4 with adriamycin or daunorubicin increased p53 protein levels and decreased NF-kappaB protein levels more than adriamycin or daunorubicin alone, indicating that MNP-Fe3O4 could enhance the effect of chemotherapeutic drugs on p53 and NF-kappaB.	ferryl iron	36-41	P53	Homo sapiens	266-269
11279192-10	2001	Other than p53-binding sites, using deletion mutation constructs, we have shown that N-methyl-N"-nitro-N-nitrosoguanidine-induced transcriptional activation of the pAPCP promoter in HCT-116(p53(+/+)) cells depended upon the Sp1-binding site and the E-box B site.	Methylnitronitrosoguanidine	85-121	P53	Homo sapiens	190-193
21187919-8	2010	Furthermore, the combination of MNP-Fe3O4 with adriamycin or daunorubicin increased p53 protein levels and decreased NF-kappaB protein levels more than adriamycin or daunorubicin alone, indicating that MNP-Fe3O4 could enhance the effect of chemotherapeutic drugs on p53 and NF-kappaB.	ferryl iron	206-211	P53	Homo sapiens	266-269
11106643-2	2001	Activation of p53 in REH cells by treatment with daunorubicin was accompanied by decreased ( approximately 5-fold) levels of hRFC transcripts and methotrexate transport.	Methotrexate	146-158	P53	Homo sapiens	14-17
12379884-9	2002	Recent studies have indicated that there is a strong coincidence of G to T transversion hotspots in lung cancers and sites of preferential formation of PAH adducts along the p53 gene.	Polycyclic Aromatic Hydrocarbons	152-155	P53	Homo sapiens	174-177
20932552-0	2010	Evaluation of the noncovalent binding interactions between polycyclic aromatic hydrocarbon metabolites and human p53 cDNA.	Polycyclic Aromatic Hydrocarbons	59-90	P53	Homo sapiens	113-116
12423550-2	2002	The present study was designed to evaluate therapeutic effects of radiation by glycerol on p53-mutant anaplastic thyroid carcinoma cells (8305c cells).	Glycerol	79-87	P53	Homo sapiens	91-94
12423550-9	2002	CONCLUSION: These findings suggest that glycerol is effective against radiotherapy of p53-mutant thyroid carcinomas.	Glycerol	40-48	P53	Homo sapiens	86-89
12359750-4	2002	Reactive oxygen species apparently derived from a flavin-containing oxidase enzyme [presumably an NAD(P)H-oxidase] appeared to be major contributors to the bystander-induced up-regulation of p53 and p21(Waf1) as well as micronucleus formation, as evidenced by the inhibition of these effects with diphenyliodonium.	diphenyliodonium	297-313	P53	Homo sapiens	191-194
11106643-4	2001	p53 induction was accompanied by up to 3-fold decreases in hRFC transcripts transcribed from the upstream hRFC-B promoter and similar losses of hRFC protein and methotrexate uptake capacity.	Methotrexate	161-173	P53	Homo sapiens	0-3
11078726-6	2001	The treatment of cells with the cyclin-dependent protein kinase inhibitor Roscovitine promoted a reduction in the specific activity of endogenous p53 or ectopically expressed p53.	Roscovitine	74-85	P53	Homo sapiens	146-149
11078726-6	2001	The treatment of cells with the cyclin-dependent protein kinase inhibitor Roscovitine promoted a reduction in the specific activity of endogenous p53 or ectopically expressed p53.	Roscovitine	74-85	P53	Homo sapiens	175-178
11179763-9	2001	In conclusion, DHPLC screening appears to be a sensitive and effective test for genetic alterations in tumors with p53 involvement.	dhplc	15-20	P53	Homo sapiens	115-118
12376521-2	2002	A specific missense mutation resulting from a guanine to thymine transversion at the third position of codon 249 in the p53 tumor suppressor gene has been reported in 10-70% of HCCs from areas of high dietary exposure to aflatoxin B(1.)	Guanine	46-53	P53	Homo sapiens	120-123
20932552-2	2010	We investigated the noncovalent binding interactions between 11 PAH metabolites and human p53 complementary DNA (p53 cDNA) using the fluorescence displacement method and molecular docking analysis.	Polycyclic Aromatic Hydrocarbons	64-67	P53	Homo sapiens	90-93
20932552-2	2010	We investigated the noncovalent binding interactions between 11 PAH metabolites and human p53 complementary DNA (p53 cDNA) using the fluorescence displacement method and molecular docking analysis.	Polycyclic Aromatic Hydrocarbons	64-67	P53	Homo sapiens	113-116
20850841-3	2010	RESULTS: As expected, roscovitine caused dose and time dependent inhibition of cyclin dependent kinase 2 autophosphorylation, and of cyclin dependent kinase mediated Pol II phosphorylation in the ACHN (p53-wt) and 786-O (p53 inactive) renal cell carcinoma cell lines (ATCC ).	Roscovitine	22-33	P53	Homo sapiens	202-205
12431242-0	2002	Retinoid-induced apoptosis in B-cell chronic lymphocytic leukaemia cells is mediated through caspase-3 activation and is independent of p53, the retinoic acid receptor, and differentiation.	Retinoids	0-8	P53	Homo sapiens	136-139
12389116-14	2002	Etoposide and vinblastine were found to effectively inactivate the androgen-independent cell lines, in which p53 is dysfunctional.	Vinblastine	14-25	P53	Homo sapiens	109-112
11152598-0	2001	Similarities in sunlight-induced mutational spectra of CpG-methylated transgenes and the p53 gene in skin cancer point to an important role of 5-methylcytosine residues in solar UV mutagenesis.	5-Methylcytosine	143-159	P53	Homo sapiens	89-92
11152598-5	2001	A comparison of sunlight-induced mutational spectra of the cII and lacI transgenes, as well as the p53 gene in skin tumors, shows that 5-methylcytosine is involved in 25 to 40 % of all mutations in all three systems.	5-Methylcytosine	135-151	P53	Homo sapiens	99-102
11146441-0	2001	Arsenic trioxide induces apoptosis in human gastric cancer cells through up-regulation of p53 and activation of caspase-3.	Arsenic Trioxide	0-16	P53	Homo sapiens	90-93
11196182-2	2001	A specific missense mutation resulting from a guanine to thymine transversion at the third position of codon 249 in the p53 tumor suppressor gene has been reported in 10-70% of HCCs from areas of high dietary exposure to aflatoxin B1.	Guanine	46-53	P53	Homo sapiens	120-123
12171874-1	2002	Potentiation of 5-fluorouracil/leucovorin (FUra/LV) cytotoxicity by IFN-gamma in colon carcinoma cells is dependent on FUra-induced DNA damage, the Fas death receptor, and independent of p53 and RNA-mediated FUra toxicity, which occurs in normal gastrointestinal tissues.	fura	43-47	P53	Homo sapiens	187-190
20850841-3	2010	RESULTS: As expected, roscovitine caused dose and time dependent inhibition of cyclin dependent kinase 2 autophosphorylation, and of cyclin dependent kinase mediated Pol II phosphorylation in the ACHN (p53-wt) and 786-O (p53 inactive) renal cell carcinoma cell lines (ATCC ).	Roscovitine	22-33	P53	Homo sapiens	221-224
12171874-1	2002	Potentiation of 5-fluorouracil/leucovorin (FUra/LV) cytotoxicity by IFN-gamma in colon carcinoma cells is dependent on FUra-induced DNA damage, the Fas death receptor, and independent of p53 and RNA-mediated FUra toxicity, which occurs in normal gastrointestinal tissues.	fura	119-123	P53	Homo sapiens	187-190
20850841-8	2010	Partial restoration of roscovitine induced apoptosis in 786-O cells by the Mdm-2 inhibitor nutlin-3 (Sigma-Aldrich) suggests that the inactivating mutation of VHL in these cells and its destabilizing effect on p53 are responsible for the decreased sensitivity to apoptosis.	Roscovitine	23-34	P53	Homo sapiens	210-213
12131363-8	2002	The stilbene activated MAPK and caused increased abundance of p53 and serine-15 phosphorylated p53.	Stilbenes	4-12	P53	Homo sapiens	62-65
20850841-9	2010	CONCLUSIONS: Our data extend previous studies documenting the pro-apoptotic effect of roscovitine and to our knowledge show for the first time that this activity is restricted to a narrow dose range in renal cell carcinoma cells and partly depends on p53.	Roscovitine	86-97	P53	Homo sapiens	251-254
12131363-8	2002	The stilbene activated MAPK and caused increased abundance of p53 and serine-15 phosphorylated p53.	Stilbenes	4-12	P53	Homo sapiens	95-98
12131363-13	2002	Pifithrin-alpha (Calbiochem), a p53 inhibitor, blocked resveratrol induced serine-15 phosphorylation of p53 and p53 binding to DNA.	pifithrin	0-15	P53	Homo sapiens	32-35
11169523-6	2001	A positive correlation between Fas and p53 was demonstrated in RA ST.	ammonium ferrous sulfate	31-34	P53	Homo sapiens	39-42
20718603-2	2010	Pifithrin-alpha (PFT-alpha), a specific inhibitor of p53, has been suggested as a combinatory agent in the treatment of p53-deficient tumors in which inhibition of p53 would not compromise therapeutic efficacy but would decrease p53-mediated side effects in normal tissue.	pifithrin	0-10	P53	Homo sapiens	53-56
11156371-4	2000	In cancer cells, but not in normal cells, MKT-077 induced release of wild-type p53 from cytoplasmically sequestered p53-mot-2 complexes and rescued its transcriptional activation function.	MKT	42-45	P53	Homo sapiens	79-82
11156371-4	2000	In cancer cells, but not in normal cells, MKT-077 induced release of wild-type p53 from cytoplasmically sequestered p53-mot-2 complexes and rescued its transcriptional activation function.	MKT	42-45	P53	Homo sapiens	116-119
11104574-0	2000	Glycerol restores p53-dependent radiosensitivity of human head and neck cancer cells bearing mutant p53.	Glycerol	0-8	P53	Homo sapiens	18-21
11104574-0	2000	Glycerol restores p53-dependent radiosensitivity of human head and neck cancer cells bearing mutant p53.	Glycerol	0-8	P53	Homo sapiens	100-103
12131363-13	2002	Pifithrin-alpha (Calbiochem), a p53 inhibitor, blocked resveratrol induced serine-15 phosphorylation of p53 and p53 binding to DNA.	pifithrin	0-15	P53	Homo sapiens	104-107
12131363-13	2002	Pifithrin-alpha (Calbiochem), a p53 inhibitor, blocked resveratrol induced serine-15 phosphorylation of p53 and p53 binding to DNA.	pifithrin	0-15	P53	Homo sapiens	104-107
12126446-3	2002	Both alkaloids displayed a cytotoxic profile against a panel of HCT-116 colon carcinoma cells indicative of a p53 dependent mechanism.	Alkaloids	5-14	P53	Homo sapiens	110-113
11104574-3	2000	We examined the restoration of radiation-induced p53-dependent apoptosis by a chemical chaperone (glycerol) in human head and neck cancer cells (SAS cells, showing wild-type p53 phenotype).	Glycerol	98-106	P53	Homo sapiens	49-52
11104574-3	2000	We examined the restoration of radiation-induced p53-dependent apoptosis by a chemical chaperone (glycerol) in human head and neck cancer cells (SAS cells, showing wild-type p53 phenotype).	Glycerol	98-106	P53	Homo sapiens	174-177
20718603-2	2010	Pifithrin-alpha (PFT-alpha), a specific inhibitor of p53, has been suggested as a combinatory agent in the treatment of p53-deficient tumors in which inhibition of p53 would not compromise therapeutic efficacy but would decrease p53-mediated side effects in normal tissue.	pifithrin	0-10	P53	Homo sapiens	120-123
11104574-4	2000	SAS cells transfected with mutant p53 (SAS/m p53) showed radioresistance compared with SAS cells (SAS/ neo) transfected with neo vector as a control, but became radiosensitive when pre-treated with glycerol before X-ray irradiation.	Glycerol	198-206	P53	Homo sapiens	34-37
11104574-4	2000	SAS cells transfected with mutant p53 (SAS/m p53) showed radioresistance compared with SAS cells (SAS/ neo) transfected with neo vector as a control, but became radiosensitive when pre-treated with glycerol before X-ray irradiation.	Glycerol	198-206	P53	Homo sapiens	45-48
11953432-6	2002	In the p53 mutant cells, low concentrations of UCN-01 caused S phase cells to progress to G(2) before undergoing mitosis and death, whereas high concentrations caused rapid premature mitosis and death of S phase cells.	7-hydroxystaurosporine	47-53	P53	Homo sapiens	7-10
20718603-2	2010	Pifithrin-alpha (PFT-alpha), a specific inhibitor of p53, has been suggested as a combinatory agent in the treatment of p53-deficient tumors in which inhibition of p53 would not compromise therapeutic efficacy but would decrease p53-mediated side effects in normal tissue.	pifithrin	0-10	P53	Homo sapiens	120-123
11104574-5	2000	Apoptosis in the SAS/m p53 cells was induced by X-rays with glycerol pre-treatment, but not without glycerol pre-treatment, whereas apoptosis in the SAS/ neo cells was induced in both cases.	Glycerol	60-68	P53	Homo sapiens	23-26
11104574-7	2000	These results suggest that glycerol is effective in inducing a conformational change of p53 and restoring normal function to mp53, leading to enhanced radiosensitivity through the induction of apoptosis.	Glycerol	27-35	P53	Homo sapiens	88-91
21713362-6	2010	Activated p50/p65 and p53 forms were studied by ELISA and immunoblotting RESULTS: Pcy-triggered cell death was prevented by specific inhibitors of NF-kappaB and of p53: amino-4-(4-phenoxy-phenylethylamino) quinazoline (QNZ) and pifithrin alpha (Palpha), respectively.	amino-4-(4-phenoxy-phenylethylamino) quinazoline	169-217	P53	Homo sapiens	164-167
11072242-0	2000	Induction of apoptosis in head-and-neck squamous carcinoma cells by gamma-irradiation and bleomycin is p53-independent.	Bleomycin	90-99	P53	Homo sapiens	103-106
11102960-6	2000	Furthermore, 4H9 partially blocked the apoptosis induced by Ad5CMV-p53 in PC3 cells, but not in LNCaP and DU145 cells.	(5-Amino-1h-1,2,4-Triazol-1-Yl)(4-Methoxyphenyl)methanone	13-16	P53	Homo sapiens	67-70
12063549-8	2002	As2O3 induced an increase in p53 level and a decrease in level of cyclin B1 combined with cell arrest at G2/M in both cell lines.	Arsenic Trioxide	0-5	P53	Homo sapiens	29-32
12065694-7	2002	Treatment with the p53 inhibitor alpha-2-(2-imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone (PFT) before cisplatin exposure inhibited p53 nuclear expression at 4, 8, and 12 h and inhibited phosphatidylserine externalization and caspase 3 activation at 12 h. Neither DEVD-fmk nor ZVAD-fmk inhibited cisplatin-induced p53 nuclear expression.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	292-300	P53	Homo sapiens	19-22
12082016-10	2002	Flavonoids are known to have DNA topoisomerase activity, a Tp53-inducing activity that is confirmed in the assay.	Flavonoids	0-10	P53	Homo sapiens	59-63
11844800-9	2002	Because inhibition of p53 is a common theme in human cancer, our data strongly support a role of DeltaTA-p73 expression for tumor formation.	deltata	97-104	P53	Homo sapiens	22-25
11097865-3	2000	Our results revealed that ketoconazole-induced growth arrest was more profound in COLO 205 and Hep G2 (with wild-type p53) than in HT 29 (p53 His(273) mutant) and Hep 3B (with deleted p53) cells.	Ketoconazole	26-38	P53	Homo sapiens	118-121
20885891-0	2010	p53 Activates Either Survival or Apoptotic Signaling Responses in Lupulone-Treated Human Colon Adenocarcinoma Cells and Derived Metastatic Cells.	lupulon	66-74	P53	Homo sapiens	0-3
11097865-3	2000	Our results revealed that ketoconazole-induced growth arrest was more profound in COLO 205 and Hep G2 (with wild-type p53) than in HT 29 (p53 His(273) mutant) and Hep 3B (with deleted p53) cells.	Ketoconazole	26-38	P53	Homo sapiens	138-141
11097865-3	2000	Our results revealed that ketoconazole-induced growth arrest was more profound in COLO 205 and Hep G2 (with wild-type p53) than in HT 29 (p53 His(273) mutant) and Hep 3B (with deleted p53) cells.	Ketoconazole	26-38	P53	Homo sapiens	138-141
11097865-4	2000	The protein levels of p53, p21/Cip1, and p27/Kip1 were significantly elevated by ketoconazole (10 microM) treatment in COLO 205 but not in HT 29 cells.	Ketoconazole	81-93	P53	Homo sapiens	22-25
11097865-5	2000	The ketoconazole-induced G0/G1 phase arrest in COLO 205 cells was attenuated by p53-specific antisense oligodeoxynucleotides (20 microM) treatment.	Ketoconazole	4-16	P53	Homo sapiens	80-83
11097865-6	2000	These results suggested that the p53-associated signaling pathway is involved in the regulation of ketoconazole-induced cancer cell growth arrest.	Ketoconazole	99-111	P53	Homo sapiens	33-36
11042698-8	2000	The activity of p53 on pro-apoptotic genes expression in response to DNA damage induced by (-irradiation, was affected in the vinblastine (VLB) resistant cell line but not in CCRF-CEM sensitive cell line resulting in a much reduced apoptotic cell death of the multi-drug resistant cells.	Vinblastine	126-137	P53	Homo sapiens	16-19
11920959-4	2002	Assays using p53-null Saos2 cells were used to determine whether mammalian cells transfected with mutant p53 could up-regulate the MDR-1 or PCNA promoters, alter IL-6 expression or confer the ability to grow in soft agar.	Agar	216-220	P53	Homo sapiens	105-108
11042698-8	2000	The activity of p53 on pro-apoptotic genes expression in response to DNA damage induced by (-irradiation, was affected in the vinblastine (VLB) resistant cell line but not in CCRF-CEM sensitive cell line resulting in a much reduced apoptotic cell death of the multi-drug resistant cells.	Vinblastine	139-142	P53	Homo sapiens	16-19
20885891-5	2010	Because p53 plays a central role in the response to cellular stresses by upregulating the transcription of several genes controlling apoptosis, we aimed to study the involvement of p53 on lupulone-triggered apoptosis.	lupulon	188-196	P53	Homo sapiens	8-11
10993652-4	2000	The p53(+)/RB(-)cells were susceptible to apoptosis under various experimental conditions: 1) incubation in serum-free culture for 72 h, 2) short-term (6 h) or long-term (48 h) exposure to etoposide, and 3) culturing in soft agar.	Agar	225-229	P53	Homo sapiens	4-7
11839095-0	2002	Wild-type TP53 inhibits G(2)-phase checkpoint abrogation and radiosensitization induced by PD0166285, a WEE1 kinase inhibitor.	PD 0166285	91-100	P53	Homo sapiens	10-14
11839095-3	2002	To determine the role of TP53 in PD0166285-induced G(2)-phase checkpoint abrogation, human H1299 lung carcinoma cells expressing a temperature-sensitive TP53 were used.	PD 0166285	33-42	P53	Homo sapiens	25-29
11839095-5	2002	However, under permissive conditions (TP53 wild-type conformation), PD0166285 greatly inhibited the accumulation of cells in G(2) phase.	PD 0166285	68-77	P53	Homo sapiens	38-42
11839095-9	2002	To understand the potential mechanism(s) by which TP53 inhibits PD0166285-induced G(2)-phase checkpoint abrogation, two TP53 target proteins, 14-3-3rho and CDKN1A (also known as p21), that are known to be involved in G(2)-phase checkpoint control in other cell models were examined.	PD 0166285	64-73	P53	Homo sapiens	50-54
11839095-9	2002	To understand the potential mechanism(s) by which TP53 inhibits PD0166285-induced G(2)-phase checkpoint abrogation, two TP53 target proteins, 14-3-3rho and CDKN1A (also known as p21), that are known to be involved in G(2)-phase checkpoint control in other cell models were examined.	PD 0166285	64-73	P53	Homo sapiens	120-124
11073163-5	2000	Induction of apoptosis by lactacystin or ZLLLal was accompanied by cell cycle arrest at G2/M phase and by accumulation and stabilization of cyclin-dependent kinase inhibitor p21WAF1/Cip and tumor suppressor protein p53.	lactacystin	26-37	P53	Homo sapiens	215-218
11839095-12	2002	Thus inhibition of PD0166285-induced G(2)-phase checkpoint abrogation by TP53 was achieved at least in part through partial blockage of CDC2 dephosphorylation of Tyr15 and inhibition of cyclin B1 expression.	PD 0166285	19-28	P53	Homo sapiens	73-77
20885891-5	2010	Because p53 plays a central role in the response to cellular stresses by upregulating the transcription of several genes controlling apoptosis, we aimed to study the involvement of p53 on lupulone-triggered apoptosis.	lupulon	188-196	P53	Homo sapiens	181-184
11862326-0	2002	Proliferation-dependent induction of apoptosis by the retinoid CD437 in p53-mutated keratinocytes.	Retinoids	54-62	P53	Homo sapiens	72-75
11006407-6	2000	Wortmannin significantly increased the BLM-induced aberration frequencies in all but the ATM-/- cells, elevating the sensitivity of p53-/- cells to ATM-/- levels and that of wild-type cells to intermediate levels.	Bleomycin	39-42	P53	Homo sapiens	132-135
20885891-6	2010	Our data show that in SW620 cells, lupulone upregulated p53 gene expression and caused a cloistering of p53 in the nucleus, allowing p53 to play a proapoptotic role by activating the TRAIL-death receptor pathway.	lupulon	35-43	P53	Homo sapiens	56-59
10942736-13	2000	NADPH, which accelerated the one-electron reduction of Cr(VI) to Cr(V) and increased.OH radical generation, dramatically enhanced p53 activation.	NADP	0-5	P53	Homo sapiens	130-133
20885891-6	2010	Our data show that in SW620 cells, lupulone upregulated p53 gene expression and caused a cloistering of p53 in the nucleus, allowing p53 to play a proapoptotic role by activating the TRAIL-death receptor pathway.	lupulon	35-43	P53	Homo sapiens	104-107
20885891-6	2010	Our data show that in SW620 cells, lupulone upregulated p53 gene expression and caused a cloistering of p53 in the nucleus, allowing p53 to play a proapoptotic role by activating the TRAIL-death receptor pathway.	lupulon	35-43	P53	Homo sapiens	104-107
20885891-7	2010	In contrast, in lupulone-treated SW480 cells, p53 was translocated to the cytoplasm where it initiated a survival response associated with the up-regulation of antiapoptotic Bcl-2 and Mcl-1 proteins in an attempt to preserve mitochondrial integrity.	lupulon	16-24	P53	Homo sapiens	46-49
11719452-0	2001	Radiosensitization of p53 mutant cells by PD0166285, a novel G(2) checkpoint abrogator.	PD 0166285	42-51	P53	Homo sapiens	22-25
20885891-8	2010	These prosurvival effects of p53 in lupulone-treated SW480 cells were reversed by pifithrin-alpha, an inhibitor of p53 function, which caused a blocking of p53 in the nucleus leading to the down-regulation of Bcl-2 and Mcl-1, the up-regulation of proapoptotic Bax protein and TRAIL-death receptors leading to enhanced cell death.	lupulon	36-44	P53	Homo sapiens	29-32
11585742-2	2001	Previous studies have indicated that there is an association between G-to-T transversion hotspots in lung cancers and sites of preferential formation of polycyclic aromatic hydrocarbon adducts along the p53 gene.	Polycyclic Aromatic Hydrocarbons	153-184	P53	Homo sapiens	203-206
11068855-1	2000	The objective of the present work was to study the effects of 3"-azido-3"-deoxythymidine (azidothymidine, Zidovudine) on human breast cancer cells by using, as a model, the T47D cell line (typified as oestrogen-dependent and p53-mutated).	Zidovudine	90-104	P53	Homo sapiens	225-228
11068855-1	2000	The objective of the present work was to study the effects of 3"-azido-3"-deoxythymidine (azidothymidine, Zidovudine) on human breast cancer cells by using, as a model, the T47D cell line (typified as oestrogen-dependent and p53-mutated).	Zidovudine	106-116	P53	Homo sapiens	225-228
11585742-3	2001	p53 codons containing methylated CpG sequences are preferential targets for formation of adducts by (+/-) anti-7beta,8alpha-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE).	8alpha-dihydroxy-9alpha	117-140	P53	Homo sapiens	0-3
20885891-8	2010	These prosurvival effects of p53 in lupulone-treated SW480 cells were reversed by pifithrin-alpha, an inhibitor of p53 function, which caused a blocking of p53 in the nucleus leading to the down-regulation of Bcl-2 and Mcl-1, the up-regulation of proapoptotic Bax protein and TRAIL-death receptors leading to enhanced cell death.	lupulon	36-44	P53	Homo sapiens	115-118
10933801-4	2000	Phosphoamino acid analysis and manual Edman degradation of the isolated phosphopeptides enabled us to unequivocally identify Thr-55 as the major phosphorylation site on p53.	Phosphoamino Acids	0-17	P53	Homo sapiens	169-172
20885891-8	2010	These prosurvival effects of p53 in lupulone-treated SW480 cells were reversed by pifithrin-alpha, an inhibitor of p53 function, which caused a blocking of p53 in the nucleus leading to the down-regulation of Bcl-2 and Mcl-1, the up-regulation of proapoptotic Bax protein and TRAIL-death receptors leading to enhanced cell death.	lupulon	36-44	P53	Homo sapiens	115-118
11562441-0	2001	The cyclin-dependent kinase inhibitor roscovitine inhibits RNA synthesis and triggers nuclear accumulation of p53 that is unmodified at Ser15 and Lys382.	Roscovitine	38-49	P53	Homo sapiens	110-113
10945628-4	2000	Because poly(ADP-ribose) polymerase (PARP)-mediated NAD+/ATP depletion has been implicated in the nucleoside-induced killing of normal resting lymphocytes, we postulated that this mechanism might account for the p53-independent component of nucleoside cytotoxicity in CLL.	Nucleosides	98-108	P53	Homo sapiens	212-215
11562441-1	2001	Roscovitine has been shown to induce the accumulation of the tumor suppressor p53, to arrest cells in the G(1) and G(2)/M phases of the cell cycle, and to induce apoptosis in human cells.	Roscovitine	0-11	P53	Homo sapiens	78-81
20885891-9	2010	Our data support different functions of the same mutated p53 in colon adenocarcinoma and derived metastatic cells in response to the chemopreventive agent lupulone.	lupulon	155-163	P53	Homo sapiens	57-60
11562441-7	2001	Cells treated with roscovitine at doses that affected transcription were found to accumulate p53 in the nucleus; curiously, however, the nuclear accumulation of p53 was not accompanied by modifications at either the Ser15 or Lys382 sites of p53.	Roscovitine	19-30	P53	Homo sapiens	93-96
11562441-7	2001	Cells treated with roscovitine at doses that affected transcription were found to accumulate p53 in the nucleus; curiously, however, the nuclear accumulation of p53 was not accompanied by modifications at either the Ser15 or Lys382 sites of p53.	Roscovitine	19-30	P53	Homo sapiens	161-164
11562441-7	2001	Cells treated with roscovitine at doses that affected transcription were found to accumulate p53 in the nucleus; curiously, however, the nuclear accumulation of p53 was not accompanied by modifications at either the Ser15 or Lys382 sites of p53.	Roscovitine	19-30	P53	Homo sapiens	161-164
11562441-8	2001	We conclude that roscovitine is a potent inhibitor of RNA synthesis and that this inhibition may be responsible for the accumulation of nuclear p53.	Roscovitine	17-28	P53	Homo sapiens	144-147
10945628-4	2000	Because poly(ADP-ribose) polymerase (PARP)-mediated NAD+/ATP depletion has been implicated in the nucleoside-induced killing of normal resting lymphocytes, we postulated that this mechanism might account for the p53-independent component of nucleoside cytotoxicity in CLL.	Nucleosides	241-251	P53	Homo sapiens	212-215
10945628-10	2000	This indicates that PARP activity can occasionally be central to nucleoside-induced killing and that such PARP-mediated killing is p53 independent.	Nucleosides	65-75	P53	Homo sapiens	131-134
10825467-1	2000	The dietary isothiocyanates and cancer chemopreventive agents phenethyl isothiocyanate and allyl isothiocyanate and their cysteine conjugates inhibited the growth and induced apoptosis of human leukaemia HL60 (p53-) and human myeloblastic leukaemia-1 cells (p53+) in vitro.	Isothiocyanates	12-27	P53	Homo sapiens	210-213
10825467-1	2000	The dietary isothiocyanates and cancer chemopreventive agents phenethyl isothiocyanate and allyl isothiocyanate and their cysteine conjugates inhibited the growth and induced apoptosis of human leukaemia HL60 (p53-) and human myeloblastic leukaemia-1 cells (p53+) in vitro.	Isothiocyanates	12-27	P53	Homo sapiens	258-261
11507071-3	2001	We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines.	Melphalan	120-125	P53	Homo sapiens	14-17
11507071-3	2001	We determined p53 function by measuring induction of p21 and/or MDM2 proteins in response to melphalan (L-PAM) in seven L-PAM-sensitive and 11 L-PAM-resistant neuroblastoma cell lines.	Melphalan	120-125	P53	Homo sapiens	14-17
20844576-8	2010	Requirement for the cyclin dependent kinase (CDK) inhibitor p21 downstream of p53 suggests a pivotal role for CDKs in controlling IE gene repression in S/G2 and treatment of S/G2 cells with the CDK inhibitor roscovitine alleviates IE repression independently of p53.	Roscovitine	208-219	P53	Homo sapiens	78-81
11507071-9	2001	Loss of p53 function was selectively achieved by transduction of human papillomavirus 16 E6 (which degrades p53) into two drug-sensitive neuroblastoma cell lines with intact p53, causing high-level drug resistance to L-PAM, carboplatin, and etoposide.	Melphalan	217-222	P53	Homo sapiens	8-11
11577989-2	2001	The cyclin-dependent kinase inhibitor roscovitine has been shown to induce nuclear accumulation of wild-type p53 in human untransformed and tumour-derived cells.	Roscovitine	38-49	P53	Homo sapiens	109-112
11577989-3	2001	We analyzed the response of different human tumour cell lines to roscovitine treatment with respect to their p53 status.	Roscovitine	65-76	P53	Homo sapiens	109-112
10837373-0	2000	Polycyclic aromatic hydrocarbon carcinogens increase ubiquitination of p21 protein after the stabilization of p53 and the expression of p21.	Polycyclic Aromatic Hydrocarbons	0-31	P53	Homo sapiens	110-113
10837373-1	2000	Polycyclic aromatic hydrocarbon carcinogens (PAHs) and their metabolites have been found to result in a rapid accumulation of p53 gene product in human and mouse cells.	Polycyclic Aromatic Hydrocarbons	0-31	P53	Homo sapiens	126-129
10815933-3	2000	Notably, the Z-Phe-Gly-NHO-Bz-induced apoptosis exhibited independence of p53, caspases, and mitogen-activated protein (MAP) kinases.	phenylalanyl-glycyl-NHO-Bz	13-29	P53	Homo sapiens	74-77
11577989-4	2001	Striking induction of wild-type p53 protein and dramatic enhancement of p53-dependent transcription, coinciding with p21WAF1 induction, was observed in wildtype, but not mutant, p53-bearing tumour cells after treatment with roscovitine.	Roscovitine	224-235	P53	Homo sapiens	32-35
11577989-4	2001	Striking induction of wild-type p53 protein and dramatic enhancement of p53-dependent transcription, coinciding with p21WAF1 induction, was observed in wildtype, but not mutant, p53-bearing tumour cells after treatment with roscovitine.	Roscovitine	224-235	P53	Homo sapiens	72-75
20844576-8	2010	Requirement for the cyclin dependent kinase (CDK) inhibitor p21 downstream of p53 suggests a pivotal role for CDKs in controlling IE gene repression in S/G2 and treatment of S/G2 cells with the CDK inhibitor roscovitine alleviates IE repression independently of p53.	Roscovitine	208-219	P53	Homo sapiens	262-265
11577989-4	2001	Striking induction of wild-type p53 protein and dramatic enhancement of p53-dependent transcription, coinciding with p21WAF1 induction, was observed in wildtype, but not mutant, p53-bearing tumour cells after treatment with roscovitine.	Roscovitine	224-235	P53	Homo sapiens	72-75
11577989-5	2001	The transcriptional activity of p53 was substantially higher in roscovitine-treated cells than in cells irradiated with ultraviolet C or ionizing radiation, even though all these agents induced a similar amount of p53 accumulation.	Roscovitine	64-75	P53	Homo sapiens	32-35
20600834-5	2010	Untreated HCT116 cells showed low levels of glut-p53, which increased markedly after H(2)O(2), diamide, cisplatin, and doxorubicin treatments.	Diamide	95-102	P53	Homo sapiens	49-52
11577989-5	2001	The transcriptional activity of p53 was substantially higher in roscovitine-treated cells than in cells irradiated with ultraviolet C or ionizing radiation, even though all these agents induced a similar amount of p53 accumulation.	Roscovitine	64-75	P53	Homo sapiens	214-217
11577989-6	2001	These results highlight the therapeutic potential of roscovitine as an anticancer drug, especially in tumours retaining a functional wild-type p53 pathway.	Roscovitine	53-64	P53	Homo sapiens	143-146
10909873-0	2000	Sequence-specific 1H, 15N, and 13C assignment of the N-terminal domain of the human oncoprotein MDM2 that binds to p53.	15n	22-25	P53	Homo sapiens	115-118
20681654-4	2010	Notably, quercetin increased cell cycle arrest in the G1 phase and up-regulated apoptosis-related proteins, such as AMPK, p53, and p21, within 48 h. Furthermore, in vivo experiments showed that quercetin treatment resulted in a significant reduction in tumor volume over 6 weeks, and apoptosis-related protein induction by quercetin was significantly higher in the 100 mg/kg treated group compared to the control group.	Quercetin	9-18	P53	Homo sapiens	122-125
10766810-1	2000	Stimulation of transfected HepG2 cells (TFG2) with the alpha(1)-adrenergic agonist phenylephrine (PE) significantly activated p21(waf1/cip1) gene expression without affecting p53 gene expression.	Phenylephrine	83-96	P53	Homo sapiens	175-178
11389075-8	2001	We found that vinblastine treatment caused down-regulation of p53 and its target p21 and up-regulation of tumor necrosis factor alpha, Bak, and several other genes in control but not in KB3-TAM67 cells, identifying these genes as putative targets of vinblastine-inducible AP-1.	Vinblastine	14-25	P53	Homo sapiens	62-65
11465510-3	2001	In order to determine if the genotype of the p53 donor or the genotype of the sp donor determined the binding efficiency, p53 expression was induced by retinoic acid and sp synthesis by bleomycin.	Bleomycin	186-195	P53	Homo sapiens	45-48
10786699-6	2000	1alpha,25-Dihydroxyvitamin D3 and EB1089 induced p53-independent apoptosis in adenoma and carcinoma cell lines in a dose-dependent manner between 10(-10) and 10(-6) M. EB1089, as well as inducing apoptosis, increased the proportion of cells in the G1 phase, particularly in the adenoma cell lines.	1alpha	0-6	P53	Homo sapiens	49-52
11465510-3	2001	In order to determine if the genotype of the p53 donor or the genotype of the sp donor determined the binding efficiency, p53 expression was induced by retinoic acid and sp synthesis by bleomycin.	Bleomycin	186-195	P53	Homo sapiens	122-125
20681654-4	2010	Notably, quercetin increased cell cycle arrest in the G1 phase and up-regulated apoptosis-related proteins, such as AMPK, p53, and p21, within 48 h. Furthermore, in vivo experiments showed that quercetin treatment resulted in a significant reduction in tumor volume over 6 weeks, and apoptosis-related protein induction by quercetin was significantly higher in the 100 mg/kg treated group compared to the control group.	Quercetin	194-203	P53	Homo sapiens	122-125
11482451-8	2001	In the TP53 mutant cell lines, DU145 and BM1604, dose enhancement factors (EFs) were found to be in the region of 4.20 for cisplatin, 3.70 for vinblastine, and 3.20 for etoposide.	Vinblastine	143-154	P53	Homo sapiens	7-11
10773886-10	2000	Interestingly, accumulation of p53 in TNF-alpha-treated LNCaP cells was decreased in the presence of the caspase inhibitor Z-VAD-FMK, suggesting a new role of activated caspases in acceleration of p53 response.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	123-132	P53	Homo sapiens	31-34
10773886-10	2000	Interestingly, accumulation of p53 in TNF-alpha-treated LNCaP cells was decreased in the presence of the caspase inhibitor Z-VAD-FMK, suggesting a new role of activated caspases in acceleration of p53 response.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	123-132	P53	Homo sapiens	197-200
11482451-9	2001	In the TP53 wild-type cell line, LNCaP, the enhancement factors were low and in the region of 1.20 for cisplatin, vinblastine and etoposide.	Vinblastine	114-125	P53	Homo sapiens	7-11
20681654-4	2010	Notably, quercetin increased cell cycle arrest in the G1 phase and up-regulated apoptosis-related proteins, such as AMPK, p53, and p21, within 48 h. Furthermore, in vivo experiments showed that quercetin treatment resulted in a significant reduction in tumor volume over 6 weeks, and apoptosis-related protein induction by quercetin was significantly higher in the 100 mg/kg treated group compared to the control group.	Quercetin	194-203	P53	Homo sapiens	122-125
20681654-5	2010	All of these results indicate that quercetin induces apoptosis via AMPK activation and p53-dependent apoptotic cell death in HT-29 colon cancer cells and that it may be a potential chemopreventive or therapeutic agent against HT-29 colon cancer.	Quercetin	35-44	P53	Homo sapiens	87-90
20472557-0	2010	Novel derivative of benzofuran induces cell death mostly by G2/M cell cycle arrest through p53-dependent pathway but partially by inhibition of NF-kappaB.	benzofuran	20-30	P53	Homo sapiens	91-94
11328884-5	2001	In contrast, recombinant p53 bound strongly to the Mdm2 binding site in the absence of PAb421 antibody.	pab421	87-93	P53	Homo sapiens	25-28
10702305-5	2000	The addition of the broad-spectrum caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD-fmk) directly after transduction almost completely prevented p53-induced apoptotic cell death but did not inhibit mitochondrial cytochrome c release.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	104-112	P53	Homo sapiens	170-173
10702305-7	2000	Cytosolic extracts from Saos-2 cells transduced with p53, but not from Saos-2 cells transduced with the empty adenoviral vector, contained a cytochrome c-releasing activity in vitro, which was still active in the presence of zVAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	225-233	P53	Homo sapiens	53-56
20446899-2	2010	This study suggested that G2/M cell cycle arrest was triggered by ROS/NO productions with regulations of p53, p21, cell division cycle 25C (Cdc25C), Cdc2 and cyclin B1, which were able to be prevented by protein tyrosine kinase (PTK) activity inhibitor genistein or JNK inhibitor SP600125.	pyrazolanthrone	280-288	P53	Homo sapiens	105-108
10699952-2	2000	Subsequent studies from other laboratories revealed that UCN-01 could selectively enhance cytotoxicity of DNA damaging agents in p53 defective cells and that this was mediated by abrogation of S and /or G(2) arrest by UCN-01.	7-hydroxystaurosporine	57-63	P53	Homo sapiens	129-132
10699952-2	2000	Subsequent studies from other laboratories revealed that UCN-01 could selectively enhance cytotoxicity of DNA damaging agents in p53 defective cells and that this was mediated by abrogation of S and /or G(2) arrest by UCN-01.	7-hydroxystaurosporine	57-60	P53	Homo sapiens	129-132
11330409-4	2001	8-Cl-Adenosine inhibited growth by inducing a G1 cell cycle arrest that was associated with large (eightfold) increases in p21WAF1/Cip1 and p53 protein levels and a decrease in the phosphorylation status of the retinoblastoma protein.	8-chloroadenosine	0-14	P53	Homo sapiens	140-143
10699952-3	2000	In this study, we report that UCN-01 selectively enhances the cytotoxicity of MMC in human p53 mutant cell lines.	7-hydroxystaurosporine	30-36	P53	Homo sapiens	91-94
20135637-0	2010	Influence of p53 expression on sensitivity of cancer cells to bleomycin.	Bleomycin	62-71	P53	Homo sapiens	13-16
10699952-7	2000	Detailed cell-cycle studies revealed that UCN-01 abrogated S and G(2) phase accumulation induced by MMC in p53 defective cells and to a lesser extent in p53 wild-type cell lines.	7-hydroxystaurosporine	42-48	P53	Homo sapiens	107-110
11023067-7	2000	Mutations of p53 were present in 3 of 38 HPV-positive samples: one with an ATG--&gt;TTG transversion (Met--&gt;Leu) in codon 237 of exon 7; and the others with a TGC--&gt;TGG transversion (Cys--&gt;Trp) in codon 242 of exon 7, and a CGT--&gt;CCT transversion (Arg--&gt;Pro) in codon 273 of exon 8, respectively.	Leucine	111-114	P53	Homo sapiens	13-16
10751606-4	2000	The frequency of bleomycin-induced chromatid aberrations was significantly higher in p53-/- cells than wild-type cells in the absence of AraC.	Bleomycin	17-26	P53	Homo sapiens	85-88
11279278-2	2001	Based upon recent studies characterizing chemical inhibitors of p53 in preclinical studies in the cancer therapy field, we synthesized the compound pifithrin-alpha and evaluated its potential neuroprotective properties in experimental models relevant to the pathogenesis of stroke and neurodegenerative disorders.	pifithrin	148-163	P53	Homo sapiens	64-67
11313880-3	2001	p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2",7"-dichlorofluorescin (DCFH) into 2",7"-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase.	Ethidium	120-128	P53	Homo sapiens	0-3
11273776-3	2001	In this report, we describe an improved extruded DOTAP:cholesterol (DOTAP:Chol) cationic liposome that efficiently delivers therapeutic tumor suppressor genes p53 and FHIT, which are frequently altered in lung cancer, to localized human primary lung cancers and to experimental disseminated metastases.	1,2-dioleoyloxy-3-(trimethylammonium)propane	49-54	P53	Homo sapiens	159-162
11273776-3	2001	In this report, we describe an improved extruded DOTAP:cholesterol (DOTAP:Chol) cationic liposome that efficiently delivers therapeutic tumor suppressor genes p53 and FHIT, which are frequently altered in lung cancer, to localized human primary lung cancers and to experimental disseminated metastases.	1,2-dioleoyloxy-3-(trimethylammonium)propane	68-73	P53	Homo sapiens	159-162
11273776-5	2001	When treated with DOTAP:Chol-p53 and -FHIT complex, significant suppression was observed in both primary (P &lt; 0.02) and metastatic lung tumor growth (P &lt; 0.007).	1,2-dioleoyloxy-3-(trimethylammonium)propane	18-23	P53	Homo sapiens	29-32
10751606-5	2000	AraC treatment significantly increased the frequency of bleomycin-induced chromatid aberrations in p53+/+ MEF to the levels in p53-/- (no AraC) but had no effect in p53-/- MEF.	Bleomycin	56-65	P53	Homo sapiens	99-102
10664623-5	2000	Increased p53 staining was detected in 10 of 11 lymphomas arising in patients after methotrexate therapy vs 5 of 11 in patients not treated with methotrexate.	Methotrexate	84-96	P53	Homo sapiens	10-13
11182788-3	2001	Accumulation of TP53 and HSP72 in the wild-type TP53 cells was observed by cocultivation with irradiated mutant TP53 cells, and the accumulation was abolished by the addition of an inhibitor for inducible nitric oxide synthase, aminoguanidine, to the medium.	pimagedine	228-242	P53	Homo sapiens	16-20
10664623-5	2000	Increased p53 staining was detected in 10 of 11 lymphomas arising in patients after methotrexate therapy vs 5 of 11 in patients not treated with methotrexate.	Methotrexate	145-157	P53	Homo sapiens	10-13
11182788-3	2001	Accumulation of TP53 and HSP72 in the wild-type TP53 cells was observed by cocultivation with irradiated mutant TP53 cells, and the accumulation was abolished by the addition of an inhibitor for inducible nitric oxide synthase, aminoguanidine, to the medium.	pimagedine	228-242	P53	Homo sapiens	48-52
10664623-7	2000	Concordant p53 expression and latent EBV were detected in 5 of 7 lymphomas arising after treatment with methotrexate, including 1 that regressed after methotrexate therapy was withdrawn.	Methotrexate	104-116	P53	Homo sapiens	11-14
11182788-3	2001	Accumulation of TP53 and HSP72 in the wild-type TP53 cells was observed by cocultivation with irradiated mutant TP53 cells, and the accumulation was abolished by the addition of an inhibitor for inducible nitric oxide synthase, aminoguanidine, to the medium.	pimagedine	228-242	P53	Homo sapiens	48-52
20135637-1	2010	In this study, we determined whether p53 expression affected the sensitivity of non-small cell lung cancer (NSCLC) and colon cancer cells to bleomycin (BLM).	Bleomycin	141-150	P53	Homo sapiens	37-40
11223035-3	2001	In this report, the DNA alkylating agents mitomycin C (MMC) and methylmethane sulfonate (MMS), as well as UV radiation, stabilized p53 in a manner independent of phosphorylation in p53 N-terminus.	Methyl Methanesulfonate	64-87	P53	Homo sapiens	131-134
10664623-7	2000	Concordant p53 expression and latent EBV were detected in 5 of 7 lymphomas arising after treatment with methotrexate, including 1 that regressed after methotrexate therapy was withdrawn.	Methotrexate	151-163	P53	Homo sapiens	11-14
10696460-8	2000	In a p53-positive cell line (DU145), p53 was repressed by 70% and Fas elevated sixfold with 10 mM PB.	ammonium ferrous sulfate	66-69	P53	Homo sapiens	5-8
11223035-3	2001	In this report, the DNA alkylating agents mitomycin C (MMC) and methylmethane sulfonate (MMS), as well as UV radiation, stabilized p53 in a manner independent of phosphorylation in p53 N-terminus.	Methyl Methanesulfonate	89-92	P53	Homo sapiens	131-134
20135637-1	2010	In this study, we determined whether p53 expression affected the sensitivity of non-small cell lung cancer (NSCLC) and colon cancer cells to bleomycin (BLM).	Bleomycin	152-155	P53	Homo sapiens	37-40
20233844-4	2010	Using this approach, we quantified the site-specific cysteine oxidation status of endogenous p53 for the first time and found that Cys182 at the dimerization interface of the DNA binding domain is particularly susceptible to diamide oxidation intracellularly.	Diamide	225-232	P53	Homo sapiens	93-96
11172740-1	2001	We investigated the amplification of bleomycin-induced DNA cleavage by synthetic triamides containing N-methylpyrrole (Py) and/or N-methylimidazole (Im), PyPyPy, PyPyIm, PyImPy, and PyImIm, using 32P-labeled DNA fragments obtained from the human c-Ha-ras-1 and p53 genes.	Bleomycin	37-46	P53	Homo sapiens	261-264
10650940-0	2000	Iodide excess induces apoptosis in thyroid cells through a p53-independent mechanism involving oxidative stress.	Iodides	0-6	P53	Homo sapiens	59-62
20540768-4	2010	We have previously demonstrated that the bioflavonoid quercetin (Qct) promoted a p53-mediated response and sensitized melanoma to DTIC.	Flavonoids	41-53	P53	Homo sapiens	81-84
10636867-2	2000	Cells that acquire PAH-induced DNA damage undergo growth arrest in a p53-independent manner (Vaziri, C., and Faller, D. V. (1997) J. Biol.	Polycyclic Aromatic Hydrocarbons	19-22	P53	Homo sapiens	69-72
10642304-5	2000	The protein of p53 was potentiated by cilostazol as well as forskolin and 8-bromo-cAMP, whereas PDGF decreased p53 expression.	Colforsin	60-69	P53	Homo sapiens	15-18
11159751-8	2001	Polymerase arrest spectra thus obtained showed a preference for reaction with purine bases in the human p53 gene for both activated compounds.	purine	78-84	P53	Homo sapiens	104-107
11205742-4	2001	We report here that down-regulation of p53 resulted in conversion of SK-N-SH cells to the substrate-adherent fibroblast-like S-type cells.	sk-n	69-73	P53	Homo sapiens	39-42
20540768-4	2010	We have previously demonstrated that the bioflavonoid quercetin (Qct) promoted a p53-mediated response and sensitized melanoma to DTIC.	Quercetin	54-63	P53	Homo sapiens	81-84
10602500-2	1999	Novel potential functions of Cdk2 have been uncovered by using two potent and specific inhibitors of its kinase activity, roscovitine and olomoucine, on human wt p53-expresser untransformed and tumor-derived cells.	Roscovitine	122-133	P53	Homo sapiens	162-165
20456495-7	2010	Curcuminoids also promote the phosphorylation of p53 on serine 15 in a dose-dependent and p38-dependent manner, suggesting that these compounds may activate p53.	curcuminoids	0-12	P53	Homo sapiens	49-52
10543945-2	1999	Since CpGs are methylated along the p53 gene, these mutations may be derived from solar UV-induced pyrimidine dimers forming at sequences that contain 5-methylcytosine.	5-Methylcytosine	151-167	P53	Homo sapiens	36-39
10543945-9	1999	The data indicate that dipyrimidines that contain 5-methylcytosine are preferential targets for sunlight-induced mutagenesis in cultured mammalian cells, thus explaining the large proportion of p53 mutations at such sites in skin tumors in vivo.	5-Methylcytosine	50-66	P53	Homo sapiens	194-197
11165136-5	2001	ET-743 induced a significant increase in p53 levels in cell lines expressing wild-type (wt) (p53).	Trabectedin	0-6	P53	Homo sapiens	41-44
11165136-5	2001	ET-743 induced a significant increase in p53 levels in cell lines expressing wild-type (wt) (p53).	Trabectedin	0-6	P53	Homo sapiens	93-96
11146157-7	2000	The effect of Ad-p53 on colony-forming unit granulocyte-macrophage (CFU-GM) and burst-forming unit erythroid (BFU-E) colony formation in methylcellulose was tested on purified CD34(+) and CD34(-) cells to evaluate bone marrow toxicity.	Methylcellulose	137-152	P53	Homo sapiens	17-20
20456495-7	2010	Curcuminoids also promote the phosphorylation of p53 on serine 15 in a dose-dependent and p38-dependent manner, suggesting that these compounds may activate p53.	curcuminoids	0-12	P53	Homo sapiens	157-160
10488156-5	1999	For this purpose, we applied a recently developed random mutagenesis technique called DNA shuffling and screened for p53 variants that could retain reactivity to the native conformation-specific anti-p53 antibody PAb1620 upon thermal treatment.	pab1620	213-220	P53	Homo sapiens	117-120
10488156-5	1999	For this purpose, we applied a recently developed random mutagenesis technique called DNA shuffling and screened for p53 variants that could retain reactivity to the native conformation-specific anti-p53 antibody PAb1620 upon thermal treatment.	pab1620	213-220	P53	Homo sapiens	200-203
11096420-0	2000	Abrogation of G(2)/M-phase block enhances the cytotoxicity of daunorubicin, melphalan and cisplatin in TP53 mutant human tumor cells.	Melphalan	76-85	P53	Homo sapiens	103-107
11096420-3	2000	In the TP53-mutated cell lines MeWo and 4451, the survival ratio at 7 Gy measured by colony formation was 2.3-2.8, 8.6-85 and 52-74 for daunorubicin, melphalan and cisplatin, respectively.	Melphalan	150-159	P53	Homo sapiens	7-11
20456495-11	2010	Curcuminoids also synergize with UVB to enhance p53 phosphorylation.	curcuminoids	0-12	P53	Homo sapiens	48-51
11103825-6	2000	CD437 induced Fas expression in three NSCLC cell lines with wild-type p53 but not in six NSCLC cell lines containing mutant p53.	ammonium ferrous sulfate	14-17	P53	Homo sapiens	70-73
10520012-0	1999	The effect of p53 dysfunction on purine analogue cytotoxicity in chronic lymphocytic leukaemia.	purine	33-39	P53	Homo sapiens	14-17
10520012-1	1999	To clarify the role of p53 in the killing of chronic lymphocytic leukaemia (CLL) cells by purine analogues, we examined the cytotoxic effects of chlorodeoxyadenosine and fludarabine on CLL cells that had been characterized according to their p53 functional status.	purine	90-96	P53	Homo sapiens	23-26
20456495-12	2010	The findings provide a rationale for testing curcuminoids in disorders associated with impaired p53 function or in which UVB-treatment is efficacious.	curcuminoids	45-57	P53	Homo sapiens	96-99
10520012-2	1999	Cases of CLL with p53 dysfunction (n = 7) displayed slight, but significant, resistance to nucleoside-induced cell killing when compared with cases with functionally intact p53 (n = 12).	Nucleosides	91-101	P53	Homo sapiens	18-21
20515947-1	2010	Previously, we reported that the nucleoside analogue/transcriptional inhibitor ARC (4-amino-6-hydrazino-7-beta-D-ribofuranosyl-7H-pyrrolo(2,3-d)-pyrimidine-5-carboxamide) was able to induce p53-independent apoptosis in multiple cancer cell lines of different origins.	Nucleosides	33-43	P53	Homo sapiens	190-193
10520012-4	1999	These findings suggest that the poor therapeutic response to purine analogues observed in patients with p53 defects is likely to be caused by the emergence, on a background of genomic instability, of CLL-cell clones that are resistant to nucleoside-induced killing for reasons unrelated to p53.	purine	61-67	P53	Homo sapiens	104-107
10520012-4	1999	These findings suggest that the poor therapeutic response to purine analogues observed in patients with p53 defects is likely to be caused by the emergence, on a background of genomic instability, of CLL-cell clones that are resistant to nucleoside-induced killing for reasons unrelated to p53.	purine	61-67	P53	Homo sapiens	290-293
10520012-4	1999	These findings suggest that the poor therapeutic response to purine analogues observed in patients with p53 defects is likely to be caused by the emergence, on a background of genomic instability, of CLL-cell clones that are resistant to nucleoside-induced killing for reasons unrelated to p53.	Nucleosides	238-248	P53	Homo sapiens	104-107
10487521-0	1999	Induction of apoptosis by the p53-273L (Arg --&gt; Leu) mutant in HSC3 cells without transactivation of p21Waf1/Cip1/Sdi1 and bax.	Leucine	51-54	P53	Homo sapiens	30-33
10446979-9	1999	UV irradiation, bleomycin, and doxorubicin increased wild-type p53 expression and decreased MAP4 expression.	Bleomycin	16-25	P53	Homo sapiens	63-66
11050000-5	2000	Expression of wt p53 also leads to cell cycle arrest and protection from doxorubicin (Dox)- and melphalan (Mel)-induced apoptosis.	Melphalan	96-105	P53	Homo sapiens	17-20
11050000-5	2000	Expression of wt p53 also leads to cell cycle arrest and protection from doxorubicin (Dox)- and melphalan (Mel)-induced apoptosis.	Melphalan	107-110	P53	Homo sapiens	17-20
11106264-11	2000	Therefore, in colon carcinomas that express wtp53, the approach to sensitize tumors to Fas-mediated apoptosis may be further enhanced from the effect of FUra-LV in elevating Fas expression in a p53-dependent manner.	ammonium ferrous sulfate	87-90	P53	Homo sapiens	46-49
11106264-11	2000	Therefore, in colon carcinomas that express wtp53, the approach to sensitize tumors to Fas-mediated apoptosis may be further enhanced from the effect of FUra-LV in elevating Fas expression in a p53-dependent manner.	ammonium ferrous sulfate	174-177	P53	Homo sapiens	46-49
11029511-1	2000	Previous research has shown synergistic growth inhibition between UCN-01 and camptothecin (CPT) in tumor cells with mutant p53 versus tumor cells with wild-type p53.	7-hydroxystaurosporine	66-72	P53	Homo sapiens	123-126
10435597-6	1999	In the current study, we demonstrate that TRID gene expression is also induced by the genotoxic agents ionizing radiation and methyl methanesulfonate (MMS) in predominantly p53 wild-type cells, whereas UV-irradiation does not induce TRID gene expression.	Methyl Methanesulfonate	126-149	P53	Homo sapiens	173-176
20067769-10	2010	Finally, based on our studies we propose that NU1025 and possibly other inhibitors of PARP-1 may be used as non-genotoxic agents to activate p53 in tumor cells with non-functional p53 pathways.	NU 1025	46-52	P53	Homo sapiens	141-144
10435597-6	1999	In the current study, we demonstrate that TRID gene expression is also induced by the genotoxic agents ionizing radiation and methyl methanesulfonate (MMS) in predominantly p53 wild-type cells, whereas UV-irradiation does not induce TRID gene expression.	Methyl Methanesulfonate	151-154	P53	Homo sapiens	173-176
10944184-2	2000	A series of hydrophilic mutations at Met-340 and Leu-344 of human p53 were designed to disrupt the hydrophobic dimer-dimer interface of the tetrameric oligomerization domain of p53 (residues 325-355).	Leucine	49-52	P53	Homo sapiens	66-69
10944184-2	2000	A series of hydrophilic mutations at Met-340 and Leu-344 of human p53 were designed to disrupt the hydrophobic dimer-dimer interface of the tetrameric oligomerization domain of p53 (residues 325-355).	Leucine	49-52	P53	Homo sapiens	177-180
20067769-10	2010	Finally, based on our studies we propose that NU1025 and possibly other inhibitors of PARP-1 may be used as non-genotoxic agents to activate p53 in tumor cells with non-functional p53 pathways.	NU 1025	46-52	P53	Homo sapiens	180-183
20463368-7	2010	DCA therapy also inhibited the hypoxia-inducible factor-1alpha, promoted p53 activation, and suppressed angiogenesis both in vivo and in vitro.	Dichloroacetic Acid	0-3	P53	Homo sapiens	73-76
10891529-0	2000	Theophylline and cisplatin synergize in down regulation of BCL-2 induction of apoptosis in human granulosa cells transformed by a mutated p53 (p53 val135) and Ha-ras oncogene.	Theophylline	0-12	P53	Homo sapiens	138-141
10891529-0	2000	Theophylline and cisplatin synergize in down regulation of BCL-2 induction of apoptosis in human granulosa cells transformed by a mutated p53 (p53 val135) and Ha-ras oncogene.	Theophylline	0-12	P53	Homo sapiens	143-146
10891529-2	2000	We have examined the effect of cisplatin alone and in combination with theophylline, a phoshodiesterase inhibitor, on modulation of Bcl-2/Bax expression and induction of apoptosis in human granulosa cells transformed by stable transfection with mutant p53 plus Ha-ras.	Theophylline	71-83	P53	Homo sapiens	252-255
10405003-1	1999	PURPOSE: To investigate the ability of docetaxel (Taxotere) to radiosensitize human cell lines of differing malignant status, intrinsic radiosensitivity and p53 status.	Docetaxel	39-48	P53	Homo sapiens	157-160
10405003-1	1999	PURPOSE: To investigate the ability of docetaxel (Taxotere) to radiosensitize human cell lines of differing malignant status, intrinsic radiosensitivity and p53 status.	Docetaxel	50-58	P53	Homo sapiens	157-160
10405003-4	1999	RESULTS: The experiments indicate that docetaxel had the greatest cytotoxic and radiosensitizing effect on the SW48 (p53wt) cell line.	Docetaxel	39-48	P53	Homo sapiens	117-120
10449043-5	1999	In order to determine whether these conformational changes are consistent for other p53 mutants, we have now used molecular dynamics to determine the structure of the DNA-binding core domain of the Leu 179 p53 mutant.	Leucine	198-201	P53	Homo sapiens	84-87
10449043-5	1999	In order to determine whether these conformational changes are consistent for other p53 mutants, we have now used molecular dynamics to determine the structure of the DNA-binding core domain of the Leu 179 p53 mutant.	Leucine	198-201	P53	Homo sapiens	206-209
10449043-6	1999	The results indicate that the Leu 179 mutant differs substantially from the wild-type structure in certain discrete regions that are similar to those noted previously in the other p53 mutants.	Leucine	30-33	P53	Homo sapiens	180-183
10082548-5	1999	Treatment with lactacystin (an inhibitor of the proteasome) or heat shock leads to similar levels of p53 accumulation in normal and AT fibroblasts, but the p53 protein lacks a phosphorylated serine 15.	lactacystin	15-26	P53	Homo sapiens	101-104
10951228-4	2000	Recent evidence has shown that Fas-induced keratinocyte apoptosis in response to ultraviolet light, prevents the accumulation of pro-carcinogenic p53 mutations by deleting ultraviolet-mutated keratinocytes.	ammonium ferrous sulfate	31-34	P53	Homo sapiens	146-149
10082548-5	1999	Treatment with lactacystin (an inhibitor of the proteasome) or heat shock leads to similar levels of p53 accumulation in normal and AT fibroblasts, but the p53 protein lacks a phosphorylated serine 15.	lactacystin	15-26	P53	Homo sapiens	156-159
20372849-2	2010	Human head and neck squamous cell carcinoma (HNSCC) cells with different p53 status, and HSC4 (p53 wild-type) and CAL27 (p53 mutant type) cells were treated with docetaxel and irradiation using three schedules: i) concurrent treatment, ii) docetaxel pretreatment and iii) pre-radiation.	Docetaxel	162-171	P53	Homo sapiens	95-98
10082548-6	1999	Following microinjection of HaeIII into lactacystin-treated normal fibroblasts, lactacystin-induced p53 protein is phosphorylated at serine 15 and stabilized even in the presence of cycloheximide.	lactacystin	40-51	P53	Homo sapiens	100-103
10082548-6	1999	Following microinjection of HaeIII into lactacystin-treated normal fibroblasts, lactacystin-induced p53 protein is phosphorylated at serine 15 and stabilized even in the presence of cycloheximide.	lactacystin	80-91	P53	Homo sapiens	100-103
10327065-7	1999	In addition, an antagonistic anti-CD95 ligand antibody (4H9) that interfered with the CD95-receptor-ligand interaction partially reduced the apoptosis induced by the wild-type p53 gene transfer in H1299 cells, whereas apoptosis of DLD-1 and SW620 cells occurred in the presence of 4H9.	(5-Amino-1h-1,2,4-Triazol-1-Yl)(4-Methoxyphenyl)methanone	56-59	P53	Homo sapiens	176-179
10931684-2	2000	We wished to determine if TP53 function affected the response of cells to fluoropyrimidines and radiation, a combination used for tens of thousands of patients each year.	fluoropyrimidines	74-91	P53	Homo sapiens	26-30
10891461-7	2000	Nuclear wild-type p53 accumulated after lactacystin treatment used at the discriminating concentration in malignant, but not in normal, lymphocytes.	lactacystin	40-51	P53	Homo sapiens	18-21
10891461-10	2000	This could result in modification of apoptosis control, since in CLL-lymphocytes a highly upregulated ubiquitin-proteasome system, which controls p53 stability among other apoptotic factors, was correlated with an increased propensity of these cells to apoptosis triggered by lactacystin.	lactacystin	276-287	P53	Homo sapiens	146-149
10327065-7	1999	In addition, an antagonistic anti-CD95 ligand antibody (4H9) that interfered with the CD95-receptor-ligand interaction partially reduced the apoptosis induced by the wild-type p53 gene transfer in H1299 cells, whereas apoptosis of DLD-1 and SW620 cells occurred in the presence of 4H9.	(5-Amino-1h-1,2,4-Triazol-1-Yl)(4-Methoxyphenyl)methanone	281-284	P53	Homo sapiens	176-179
20372849-2	2010	Human head and neck squamous cell carcinoma (HNSCC) cells with different p53 status, and HSC4 (p53 wild-type) and CAL27 (p53 mutant type) cells were treated with docetaxel and irradiation using three schedules: i) concurrent treatment, ii) docetaxel pretreatment and iii) pre-radiation.	Docetaxel	162-171	P53	Homo sapiens	95-98
20175992-1	2010	Selective binding of the wild type tumor suppressor protein p53 to negatively and positively supercoiled (sc) DNA was studied using intercalative drugs chloroquine (CQ), ethidium bromide, acridine derivatives and doxorubicin as a modulators of the level of DNA supercoiling.	Ethidium	170-186	P53	Homo sapiens	60-63
10408175-3	1999	Quercetin, an inhibitor of heat-shock response, dose dependently suppressed the p53 accumulation induced by X-rays at more than 100 microM.	Quercetin	0-9	P53	Homo sapiens	80-83
10845931-10	2000	However, the MDM2 protein could be easily detected after treatment of cells with the specific proteasome inhibitor lactacystin, suggesting a normal regulation of the p53-MDM2 regulating loop.	lactacystin	115-126	P53	Homo sapiens	166-169
10747892-2	2000	Gadd45, a p53-regulated stress protein, plays an important role in the cell cycle G(2)-M checkpoint following exposure to certain types of DNA-damaging agents such as UV radiation and methylmethane sulfonate.	Methyl Methanesulfonate	184-207	P53	Homo sapiens	10-13
9920742-1	1999	The reactivity of guanines in an oligonucleotide containing mutational hot spots within the p53 gene (codons 248 and 249), 5"-CCG1G2AG3G4CCCA-3", toward dimethyl sulfate (DMS) and aflatoxin B1-8,9-epoxide (AFB1-8,9-epoxide) was investigated by a modified Maxam-Gilbert technique.	Guanine	18-26	P53	Homo sapiens	92-95
19739077-10	2010	The effect of MKT-077 on complement-mediated lysis of HCT116 p53(+/+) and p53(-/-) cells was found to be independent on the presence of p53.	MKT 077	14-21	P53	Homo sapiens	61-64
10527073-4	1999	Most of C6 cells infected in vitro with rVV-p53 expressing the tumor suppressor p53 protein showed apoptosis specific morphological changes in DAPI-stained nuclei and DNA fragmentation pattern on gel electrophoresis; infection with VV induced low level of cell apoptosis.	DAPI	143-147	P53	Homo sapiens	44-47
10527073-4	1999	Most of C6 cells infected in vitro with rVV-p53 expressing the tumor suppressor p53 protein showed apoptosis specific morphological changes in DAPI-stained nuclei and DNA fragmentation pattern on gel electrophoresis; infection with VV induced low level of cell apoptosis.	DAPI	143-147	P53	Homo sapiens	80-83
9823314-3	1998	Apoptosis was induced by exposing cells to 50 microM N-methyl-N"-nitro-N-nitrosoguanidine (MNNG) for increasing lengths of time and was confirmed by: (a) oligonucleosomal fragmentation of chromatin; (b) increase in p53 levels; and (c) degradation of PARP into the characteristic M(r) 85,000 (COOH-terminal catalytic domain) and M(r) 29,000 (DNA-binding domain) peptide fragments.	Methylnitronitrosoguanidine	53-89	P53	Homo sapiens	215-218
10814675-5	2000	METHODS: Here we have mapped the distribution of adducts induced by diol epoxides of additional PAHs: chrysene (CDE), 5-methylchrysene (5-MCDE), 6-methylchrysene (6-MCDE), benzo[c]phenanthrene (B[c]PDE), and benzo[g]chrysene (B[g]CDE) within exons 5, 7, and 8 of the p53 gene in human bronchial epithelial cells.	Polycyclic Aromatic Hydrocarbons	96-100	P53	Homo sapiens	267-270
10811471-5	2000	In contrast, Ad-p53 showed additive effects with the antitubulin agents (paclitaxel and docetaxel) in all four of the cell lines tested.	Docetaxel	88-97	P53	Homo sapiens	16-19
10767618-9	2000	With the advent of new techniques of molecular biology, mutations were investigated in the ras and p53 genes of tumors induced by vinyl chloride and urethane.	Urethane	149-157	P53	Homo sapiens	99-102
10767625-1	2000	About 23% of mutations in hereditary human diseases and 24% of mutations in p53 in human cancers are G to A transitions at sites of cytosine methylation suggesting that these sites are either foci for DNA damage, or foci for damage that is poorly repaired.	Cytosine	132-140	P53	Homo sapiens	76-79
20393600-10	2010	FasL upregulation and caspase-8 activation were decreased by p53 inhibitor pifithrin-alpha and antioxidant polyethylene glycol catalase.	pifithrin	75-90	P53	Homo sapiens	61-64
10788533-6	2000	Of the p53 functional mutations, a substitution of Gly at amino acid residue 245 to Asp (G245D) was identified in two patients in three subclones.	Aspartic Acid	84-87	P53	Homo sapiens	7-10
9735403-0	1998	Protein synthesis and transcriptional inhibitors control N-methyl-N"-nitro-N-nitrosoguanidine-induced levels of APC mRNA in a p53-dependent manner.	Methylnitronitrosoguanidine	57-93	P53	Homo sapiens	126-129
20179216-7	2010	Moreover, tumors with high expression of genes involved in cell adhesion/angiogenesis as well as of wild-type TP53 were more likely to be resistant to Sagopilone therapy.	sagopilone	151-161	P53	Homo sapiens	110-114
11245004-1	1998	OBJECTIVE: To establish a tetracycline-regulated expression model and to determine and verify whether a specific point mutant type p53 minigene, containing an Arg--&gt;Leu substitution at amino acid 172, possesses a suppressing effect on human lung cancer.	Leucine	168-171	P53	Homo sapiens	131-134
9733515-3	1998	Immunoprecipitated ATM had intrinsic protein kinase activity and phosphorylated p53 on serine-15 in a manganese-dependent manner.	Manganese	102-111	P53	Homo sapiens	80-83
9713990-6	1998	Under conditions of cellular stress (ultraviolet irradiation or exposure to bleomycin or cisplatin), expression of TP53TG1 was induced in a wild-type TP53-dependent manner, indicating that this gene is likely to play an important role in the signaling pathway of TP53 and may function in response to cellular damage.	Bleomycin	76-85	P53	Homo sapiens	115-119
10774750-4	2000	The alkylation sites observed in exon 9 of the p53 gene revealed that the most high reactivity sites for altromycin B were found to be N7 of guanine in a 5"-AG* sequence.	Guanine	141-148	P53	Homo sapiens	47-50
10751606-5	2000	AraC treatment significantly increased the frequency of bleomycin-induced chromatid aberrations in p53+/+ MEF to the levels in p53-/- (no AraC) but had no effect in p53-/- MEF.	Bleomycin	56-65	P53	Homo sapiens	127-130
10751606-5	2000	AraC treatment significantly increased the frequency of bleomycin-induced chromatid aberrations in p53+/+ MEF to the levels in p53-/- (no AraC) but had no effect in p53-/- MEF.	Bleomycin	56-65	P53	Homo sapiens	127-130
10751606-7	2000	Similar results were observed in p53-mutant WTK1 and wild-type TK6 human lymphoblast cells exposed to 0 to 3 microg/ml bleomycin in G(2).	Bleomycin	119-128	P53	Homo sapiens	33-36
9713990-6	1998	Under conditions of cellular stress (ultraviolet irradiation or exposure to bleomycin or cisplatin), expression of TP53TG1 was induced in a wild-type TP53-dependent manner, indicating that this gene is likely to play an important role in the signaling pathway of TP53 and may function in response to cellular damage.	Bleomycin	76-85	P53	Homo sapiens	150-154
9687575-10	1998	The results also suggest that p53 induction in response to O6-guanine methylation involves the mismatch repair system.	Guanine	62-69	P53	Homo sapiens	30-33
19676051-6	2010	Under conditions where single-agent treatment caused only antiproliferative effects, the combination of the atypical retinoid and HDAC inhibitor resulted in marked apoptotic cell death with a more rapid onset in wild-type p53 ovarian carcinoma cells.	Retinoids	117-125	P53	Homo sapiens	222-225
9726816-5	1998	In contrast, PDTC, DDTC, and ammonium dithiocarbamate (ADTC) did not induce apoptosis; rather they led to the induction of p53 and p21 followed by G1/S arrest.	AMMONIUM DITHIOCARBAMATE	29-53	P53	Homo sapiens	123-126
9690517-9	1998	Thus, our results indicate that the p53-p21 pathway may play a central role in mediating the gene-regulatory and cytotoxic effects of aziridinylbenzoquinones.	diaziquone	134-157	P53	Homo sapiens	36-39
9703875-0	1998	Increased p21/WAF-1 and p53 protein levels following sequential three drug combination regimen of fludarabine, cytarabine and docetaxel induces apoptosis in human leukemia cells.	Docetaxel	126-135	P53	Homo sapiens	24-27
9622079-1	1998	17-(Allylamino)-17-demethoxygeldanamycin (17AAG), a compound that is proposed for clinical development, shares the ability of geldanamycin to bind to heat shock protein 90 and GRP94, thereby depleting cells of p185erbB2, mutant p53, and Raf-1.	tanespimycin	0-40	P53	Homo sapiens	228-231
9622079-1	1998	17-(Allylamino)-17-demethoxygeldanamycin (17AAG), a compound that is proposed for clinical development, shares the ability of geldanamycin to bind to heat shock protein 90 and GRP94, thereby depleting cells of p185erbB2, mutant p53, and Raf-1.	tanespimycin	42-47	P53	Homo sapiens	228-231
9584191-7	1998	By comparison, the DNA-damaging drugs methotrexate and doxorubicin had no effect on Bcl2 hyperphosphorylation but induced p53 expression.	Methotrexate	38-50	P53	Homo sapiens	122-125
9619871-5	1998	p53, bax and bcl-xL were expressed at the same level in 4-pp-R and RVC cells.	4-pp	56-60	P53	Homo sapiens	0-3
9566927-3	1998	However, this conclusion derives from studies employing the UMP synthesis inhibitor N-phosphonacetyl-L-aspartate (PALA), which, in addition to selecting for cells containing extra copies of the CAD locus, enables p53-deficient cells to enter S phase and acquire the DNA breaks that initiate the amplification process.	sparfosic acid	84-112	P53	Homo sapiens	213-216
9566927-5	1998	The studies reported here assess whether p53 deficiency leads to spontaneous genetic instability by comparing cell cycle responses and amplification frequencies of the human fibrosarcoma cell line HT1080 when treated with PALA or with methotrexate, an antifolate that, under the conditions used, should not generate DNA breaks.	Methotrexate	235-247	P53	Homo sapiens	41-44
9591783-4	1998	Based on these results, we propose a mechanism by which PAb1620 can allosterically inhibit p53 binding to DNA through an indirect interaction between the antibody binding site and the L1 loop (amino acids 112-124) of p53, which is a component of the DNA binding region.	pab1620	56-63	P53	Homo sapiens	91-94
9548807-0	1998	Induction of p53 by the concerted actions of aziridine and quinone moieties of diaziquone.	diaziquone	79-89	P53	Homo sapiens	13-16
9548807-6	1998	Diaziquone (AZQ), an anticancer agent, and its derivatives, diaziridinequinone (DZQ) and methyldiaziridinequinone (MeDZQ), induced p53 in a dose- and time-dependent manner as measured by the electrophoretic mobility shift assay.	diaziquone	0-10	P53	Homo sapiens	131-134
9548807-6	1998	Diaziquone (AZQ), an anticancer agent, and its derivatives, diaziridinequinone (DZQ) and methyldiaziridinequinone (MeDZQ), induced p53 in a dose- and time-dependent manner as measured by the electrophoretic mobility shift assay.	diaziquone	12-15	P53	Homo sapiens	131-134
9548807-6	1998	Diaziquone (AZQ), an anticancer agent, and its derivatives, diaziridinequinone (DZQ) and methyldiaziridinequinone (MeDZQ), induced p53 in a dose- and time-dependent manner as measured by the electrophoretic mobility shift assay.	pycnogenols	80-83	P53	Homo sapiens	131-134
9502788-5	1998	Accordingly, bafilomycin A1-treated myocytes also showed increased accumulation of p53 protein and p53-dependent transactivation of gene expression, including a persistent upregulation of p21/wild-type p53 activated fragment 1/cyclin kinase inhibitor protein-1 mRNA.	bafilomycin A1	13-27	P53	Homo sapiens	83-86
9502788-5	1998	Accordingly, bafilomycin A1-treated myocytes also showed increased accumulation of p53 protein and p53-dependent transactivation of gene expression, including a persistent upregulation of p21/wild-type p53 activated fragment 1/cyclin kinase inhibitor protein-1 mRNA.	bafilomycin A1	13-27	P53	Homo sapiens	99-102
9502788-5	1998	Accordingly, bafilomycin A1-treated myocytes also showed increased accumulation of p53 protein and p53-dependent transactivation of gene expression, including a persistent upregulation of p21/wild-type p53 activated fragment 1/cyclin kinase inhibitor protein-1 mRNA.	bafilomycin A1	13-27	P53	Homo sapiens	99-102
9502788-6	1998	The bafilomycin A1-induced increase in p53 protein levels was accompanied by a marked increase in p53 mRNA accumulation.	bafilomycin	4-15	P53	Homo sapiens	39-42
9502788-6	1998	The bafilomycin A1-induced increase in p53 protein levels was accompanied by a marked increase in p53 mRNA accumulation.	bafilomycin	4-15	P53	Homo sapiens	98-101
9497376-4	1998	In vitro studies have shown that E6AP can form a high energy thiolester bond with ubiquitin and, in the presence of E6, transfer ubiquitin to p53.	Polyurethane Y-290	33-35	P53	Homo sapiens	142-145
9458377-5	1998	These findings suggest that Fas-mediated therapy could be a novel approach to RCC, if interferon- treatment is added according to the p53 gene status.	ammonium ferrous sulfate	28-31	P53	Homo sapiens	134-137
9649296-0	1998	Methotrexate resistance in human uroepithelial cells with p53 alterations.	Methotrexate	0-12	P53	Homo sapiens	58-61
9649296-3	1998	We tested if the status of p53 and/or pRb affects the development of MTX resistance in bladder epithelial cell lines.	Methotrexate	69-72	P53	Homo sapiens	27-30
9649296-7	1998	RESULTS: Two cell lines with both pRb and p53 alterations, alphaE6/E7-HUC and alphaE7-HUCp53mu, acquired the greatest resistance (750 nM) to MTX.	Methotrexate	141-144	P53	Homo sapiens	42-45
9649296-11	1998	In addition, two of five MTX resistant cell lines, both with altered p53, showed dihydrofolate reductase (DHFR) amplification.	Methotrexate	25-28	P53	Homo sapiens	69-72
9649296-12	1998	CONCLUSIONS: p53 alteration increases the risk for development of drug resistance by both DHFR amplification and altered MTX transport in transformed human bladder epithelial cell lines.	Methotrexate	121-124	P53	Homo sapiens	13-16
9463482-7	1998	The ellipticiniums, but not the ellipticines, were more potent on average against p53 mutant cells than against p53 wild-type ones (i.e., they seemed to be "p53-inverse") in this short term assay.	ellipticiniums	4-18	P53	Homo sapiens	82-85
9463482-7	1998	The ellipticiniums, but not the ellipticines, were more potent on average against p53 mutant cells than against p53 wild-type ones (i.e., they seemed to be "p53-inverse") in this short term assay.	ellipticiniums	4-18	P53	Homo sapiens	112-115
9463482-7	1998	The ellipticiniums, but not the ellipticines, were more potent on average against p53 mutant cells than against p53 wild-type ones (i.e., they seemed to be "p53-inverse") in this short term assay.	ellipticiniums	4-18	P53	Homo sapiens	112-115
9438391-2	1998	Using the proteasome-specific inhibitors, MG132 (N-acetyl-L-leucinyl-L-leucinal-L-leucinal) and lactacystin, here we show that the p53-response proteins, bax and mdm2 as well as p21, are degraded by the ubiquitin-proteasome pathway in HeLa cells.	lactacystin	96-107	P53	Homo sapiens	131-134
9516963-6	1998	Data demonstrated p53-dependent sensitization (&gt; or = 4-fold) to bleomycin, actinomycin D, and 5-fluorouracil and considerably less p53-dependence (&lt; or = 2-fold) for doxorubicin, topotecan, etoposide, and cisplatin in Cl.#27 compared to an equivalent clone containing the pGRE5-EBV vector alone (VC#3).	Bleomycin	68-77	P53	Homo sapiens	18-21
9447384-0	1997	Apoptosis occurs more frequently in intraductal carcinoma than in infiltrating duct carcinoma of human breast cancer and correlates with altered p53 expression: detected by terminal-deoxynucleotidyl-transferase-mediated dUTP-FITC nick end labelling (TUNEL).	dutp-fitc	220-229	P53	Homo sapiens	145-148
9307289-0	1997	Abrogation of an S-phase checkpoint and potentiation of camptothecin cytotoxicity by 7-hydroxystaurosporine (UCN-01) in human cancer cell lines, possibly influenced by p53 function.	7-hydroxystaurosporine	85-107	P53	Homo sapiens	168-171
9190897-5	1997	We found that this impairment of p53 turnover can be reversed by treatment of tumor cells with the benzoquinone ansamycin, geldanamycin, leading to a marked reduction in intracellular p53 levels.	benzoquinone ansamycin	99-121	P53	Homo sapiens	33-36
9190897-5	1997	We found that this impairment of p53 turnover can be reversed by treatment of tumor cells with the benzoquinone ansamycin, geldanamycin, leading to a marked reduction in intracellular p53 levels.	benzoquinone ansamycin	99-121	P53	Homo sapiens	184-187
9815762-0	1997	Accumulation of p53 protein and retinoic acid receptor beta in retinoid chemoprevention.	Retinoids	63-71	P53	Homo sapiens	16-19
9815762-8	1997	High p53 protein expression (LI &gt;/= 0.2) was detected in 25% of the lesions at baseline and in 18% of the lesions after isotretinoin therapy.	Isotretinoin	123-135	P53	Homo sapiens	5-8
21533491-7	1997	Induction of apoptosis in JCA-1 cells by treatment with the retinoid 4-HPR caused the virtual disappearance of p53, which coincided with specific processing of p53 into lower molecular weight 28 kD fragments.	Retinoids	60-68	P53	Homo sapiens	111-114
21533491-7	1997	Induction of apoptosis in JCA-1 cells by treatment with the retinoid 4-HPR caused the virtual disappearance of p53, which coincided with specific processing of p53 into lower molecular weight 28 kD fragments.	Retinoids	60-68	P53	Homo sapiens	160-163
9154813-4	1997	Treatment of cytoplasmic extracts with RNase or puromycin in the presence of high salt, both of which are known to disrupt ribosomal function, dissociated p53 polypeptide from the ribosomes.	Puromycin	48-57	P53	Homo sapiens	155-158
9136075-8	1997	Droloxifene, but not estrogen, induced p53 expression and apoptosis in MCF-7 cells.	droloxifene	0-11	P53	Homo sapiens	39-42
9022073-10	1997	These data suggest that apoptosis induced by bleomycin is mediated, at least in part, by p53-dependent stimulation of the CD95 receptor/ligand system.	Bleomycin	45-54	P53	Homo sapiens	89-92
15622746-5	1997	Furthermore, As2O3 effectively down-regulated the expression of bcl-2 gene without changing the mRNA levels of other apoptosis-associated genes (including p53, c-myc, bax and bcl-XL).	Arsenic Trioxide	13-18	P53	Homo sapiens	155-158
8956076-5	1996	Phosphoamino acid was incorporated into the N-terminal segment (1P315) at the residue corresponding to p53 serine 315 as Boc-Ser(PO3(Bzl)2)-OH during synthesis.	Phosphoamino Acids	0-17	P53	Homo sapiens	103-106
8895505-0	1996	Flavonoids activate wild-type p53.	Flavonoids	0-10	P53	Homo sapiens	30-33
8895505-4	1996	To further elucidate this dual role, we investigated the influence of apigenin, luteolin and quercetin on the tumour suppressor protein p53, regarding p53 accumulation, cell cycle arrest, apoptosis, and biological activity.	Quercetin	93-102	P53	Homo sapiens	136-139
8895505-5	1996	We found that incubation of the non-tumour cell line C3H10T1/2CL8 with these flavonoids resulted in induction of p53 accumulation and apoptosis.	Flavonoids	77-87	P53	Homo sapiens	113-116
8895505-8	1996	Differences between the flavonoids tested concerned p53 accumulation kinetics as well as the biological activity of accumulated p53 and might be due to different modes of flavonoid action.	Flavonoids	24-34	P53	Homo sapiens	52-55
8895505-8	1996	Differences between the flavonoids tested concerned p53 accumulation kinetics as well as the biological activity of accumulated p53 and might be due to different modes of flavonoid action.	Flavonoids	24-33	P53	Homo sapiens	52-55
8895505-9	1996	These data suggest that both aspects of flavonoid effects, i.e. inhibition of tumour growth through cell cycle arrest and induction of apoptosis, are functionally related to p53.	Flavonoids	40-49	P53	Homo sapiens	174-177
9031099-14	1996	Finally, whereas CLB and nucleoside analogs may produce cell death in CLL by a P53 dependent pathway other agents, such as dexamethasone or vincristine, may act through P53-independent pathways.	Nucleosides	25-35	P53	Homo sapiens	79-82
8845023-9	1996	Indeed it was found that TEC-induced apoptosis, led to the accumulation of p53 protein that preceded the step of DNA fragmentation in freshly isolated thymocytes as well as in a glucocorticoid resistant thymoma cell line.	Turpentine	25-28	P53	Homo sapiens	75-78
8822937-6	1996	For p53 we observed an overexpression in the presence of chlorambucil or both theophylline-chlorambucil and a decrease after theophylline incubation.	Theophylline	78-90	P53	Homo sapiens	4-7
8896794-7	1996	The dehydrating (coagulant) fixatives (e.g., ethanol and methanol) preserved immunorecognition of p53 and broad spectrum keratins best while the slow cross-linking fixatives (e.g., unbuffered zinc formalin) were best for demonstrating TGF alpha and p185erbB-2.	Methanol	57-65	P53	Homo sapiens	98-101
8787680-6	1996	To determine whether the lonidamine-induced apoptosis is mediated by p53 protein, we used cells lacking endogenous p53 and overexpressing either wild-type p53 or dominant-negative p53 mutant.	lonidamine	25-35	P53	Homo sapiens	69-72
8706003-0	1996	Separate pathways for p53 induction by ionizing radiation and N-(phosphonoacetyl)-L-aspartate.	sparfosic acid	62-93	P53	Homo sapiens	22-25
8706003-4	1996	Here, we demonstrate the existence of cell types in which the induction of p53 and associated G1 arrest by the antimetabolite, N-(phosphonoacetyl)-L-aspartate (PALA), is defective, whereas p53 induction and G1 arrest induced by ionizing radiation are intact.	sparfosic acid	127-158	P53	Homo sapiens	75-78
8761369-1	1996	The aim of this investigation was to examine the possibility of analysing TP53 mutations in archival paraffin-embedded material with the constant denaturant gel electrophoresis (CDGE) method.	cdge	178-182	P53	Homo sapiens	74-78
8757686-6	1996	Aberrant expression of p53 protein was documented in 48% of squamous cell carcinomas of skin, 29% of CRC, 22% of CIN and 23% of TCC.	Triclocarban	128-131	P53	Homo sapiens	23-26
8783012-7	1996	We suggest that these variants contained a gamma-N, N"-dimethylasparagine residue at position 83 and that one of them was additionally oxidized at Trp53 and Trp85.	gamma-n, n"-dimethylasparagine	43-73	P53	Homo sapiens	147-152
8790940-4	1996	Although the mutated p53 is selectively expressed in the immortalized cells, expression of the wild-type p53 was induced by treatment of the cells with a hypomethylating reagent, 5-azacytidine, indicating that the wild-type p53 allele might be inactivated by hypermethylation of DNA.	Azacitidine	179-192	P53	Homo sapiens	105-108
8790940-4	1996	Although the mutated p53 is selectively expressed in the immortalized cells, expression of the wild-type p53 was induced by treatment of the cells with a hypomethylating reagent, 5-azacytidine, indicating that the wild-type p53 allele might be inactivated by hypermethylation of DNA.	Azacitidine	179-192	P53	Homo sapiens	105-108
7478511-0	1995	Induction of Fas-mediated apoptosis in p53-transfected human colon carcinoma cells.	ammonium ferrous sulfate	13-16	P53	Homo sapiens	39-42
7478511-4	1995	The efficiency of colony formation in soft agar, however, was completely suppressed in two wild-type p53+ clones.	Agar	43-47	P53	Homo sapiens	101-104
7478511-7	1995	The findings suggest that a Fas-initiated pathway is incidentally linked to a p53-dependent apoptotic pathway through the reconstituted wild-type p53 gene in WiDr cells.	ammonium ferrous sulfate	28-31	P53	Homo sapiens	78-81
7478511-7	1995	The findings suggest that a Fas-initiated pathway is incidentally linked to a p53-dependent apoptotic pathway through the reconstituted wild-type p53 gene in WiDr cells.	ammonium ferrous sulfate	28-31	P53	Homo sapiens	146-149
7478567-4	1995	In contrast, the increase in p53 protein, WAF1/CIP1(p21) and GADD45 mRNA expression following exposure to the alkylating agent methylmethane sulphonate (25 and 100 micrograms ml-1) was similar in both cell types.	Methyl Methanesulfonate	127-151	P53	Homo sapiens	29-32
7586148-4	1995	Two cell lines selected from V79/B7 for their resistance to phosphonacetyl-L-aspartate or methotrexate and previously shown to bear gene amplification, showed p53 expression.	Methotrexate	90-102	P53	Homo sapiens	159-162
7605998-0	1995	Amplification of the dihydrofolate reductase gene is a mechanism of acquired resistance to methotrexate in patients with acute lymphoblastic leukemia and is correlated with p53 gene mutations.	Methotrexate	91-103	P53	Homo sapiens	173-176
7538902-3	1995	Following DNA strand break damage induced by bleomycin, both SDI1 induction and G1-S cell cycle arrest are p53 dependent, consistent with SDI1 being the key mediator.	Bleomycin	45-54	P53	Homo sapiens	107-110
7751883-0	1995	Prognostic value of p53 nuclear overexpression in patients with invasive bladder cancer treated with neoadjuvant MVAC.	mvac	113-117	P53	Homo sapiens	20-23
7622024-2	1995	It was shown that injection of a retroviral construction with p53His273 resulted in the accumulation of methotrexate-resistant variants with an increased number of dhfr copies in populations of recipient cells.	Methotrexate	104-116	P53	Homo sapiens	62-65
7783370-3	1995	The results of several fixation methods demonstrated that formalin and methanol, formalin and ethanol (1:9) and buffered formalin acetone gave good results for detecting p53 protein.	Methanol	71-79	P53	Homo sapiens	170-173
7897229-6	1995	First, the amount of immunoreactive p53-56lyn increased in Triton X-100-insoluble fraction as did zymosan-stimulated tyrosine phosphoproteins.	Octoxynol	59-71	P53	Homo sapiens	36-39
7897229-10	1995	Third, p53-56lyn was probably activated after cell stimulation with zymosan, because the phosphorylation levels of a synthetic copolymer of glutamine-tyrosine were increased in Triton X-100-insoluble fraction.	Octoxynol	177-189	P53	Homo sapiens	7-10
7567152-2	1995	Two 20-base oligomers complementary to bases 872-891 of human p53 cDNA with a single nucleotide difference in the third position of codon 249 were end-labelled with biotin-conjugated dATP using terminal deoxynucleotidyltransferase (TdT).	2'-deoxyadenosine triphosphate	183-187	P53	Homo sapiens	62-65
7888675-0	1995	p53 gene deletion predicts for poor survival and non-response to therapy with purine analogs in chronic B-cell leukemias.	purine	78-84	P53	Homo sapiens	0-3
7888675-12	1995	In conclusion, p53 gene deletion predicts for non-response to therapy with purine analogs and for poor survival in chronic B-cell leukemias.	purine	75-81	P53	Homo sapiens	15-18
7534296-5	1995	These effects are reversed by subsequent dephosphorylation of the protein kinase C-reactive site by protein phosphatases 1 (PP1) and 2A (PP2A), which restore the reactivity of p53 to PAb421 and regenerate the latent form of p53 lacking significant DNA binding activity.	pab421	183-189	P53	Homo sapiens	176-179
7534296-5	1995	These effects are reversed by subsequent dephosphorylation of the protein kinase C-reactive site by protein phosphatases 1 (PP1) and 2A (PP2A), which restore the reactivity of p53 to PAb421 and regenerate the latent form of p53 lacking significant DNA binding activity.	pab421	183-189	P53	Homo sapiens	224-227
7854771-6	1995	The expression of p53 was reduced to 60% for the first 4 h after the addition of cycloheximide, and showed no significant changes at least for 20 h. Treatment with Triton X-100 increased p53 immunoreactivity throughout the cell cycle.	Octoxynol	164-176	P53	Homo sapiens	18-21
7854771-6	1995	The expression of p53 was reduced to 60% for the first 4 h after the addition of cycloheximide, and showed no significant changes at least for 20 h. Treatment with Triton X-100 increased p53 immunoreactivity throughout the cell cycle.	Octoxynol	164-176	P53	Homo sapiens	187-190
7845670-8	1995	In both assays, complex formation with E6 was mediated through the amino-terminal 345 amino acids of p53 without a specific requirement for its C-terminus.	Polyurethane Y-290	39-41	P53	Homo sapiens	101-104
7597296-5	1995	Analysis of p53 gene showed mutation only in one case of mycosis fungoides in tumoral stage, at codon 163 of p53 gene (TAC--&gt;CAC; Tyr--&gt; Asp).	Aspartic Acid	143-146	P53	Homo sapiens	12-15
7597296-5	1995	Analysis of p53 gene showed mutation only in one case of mycosis fungoides in tumoral stage, at codon 163 of p53 gene (TAC--&gt;CAC; Tyr--&gt; Asp).	Aspartic Acid	143-146	P53	Homo sapiens	109-112
7923116-4	1994	Induction of p53 is also abnormal in AT cells following treatment with methylmethanesulfonate and bleomycin but appears relatively normal following treatment with UV-C irradiation or the topoisomerase inhibitors, etoposide and camptothecin.	Methyl Methanesulfonate	71-93	P53	Homo sapiens	13-16
7923116-4	1994	Induction of p53 is also abnormal in AT cells following treatment with methylmethanesulfonate and bleomycin but appears relatively normal following treatment with UV-C irradiation or the topoisomerase inhibitors, etoposide and camptothecin.	Bleomycin	98-107	P53	Homo sapiens	13-16
7926727-5	1994	Rather, the hydrophobic amino acid residues Leu-22 and Trp-23 of human p53 are both required for trans-activation activity, binding to the adenovirus E1B 55-kD protein and the human mdm-2-p53 protein in vitro.	Leucine	44-47	P53	Homo sapiens	71-74
7926727-5	1994	Rather, the hydrophobic amino acid residues Leu-22 and Trp-23 of human p53 are both required for trans-activation activity, binding to the adenovirus E1B 55-kD protein and the human mdm-2-p53 protein in vitro.	Leucine	44-47	P53	Homo sapiens	188-191
7926727-6	1994	In addition, hydrophobic residues Leu-14 and Phe-19 are crucial for the interactions between p53 and human mdm-2 (hdm-2).	Leucine	34-37	P53	Homo sapiens	93-96
8014109-6	1994	These data indicate that part of the IQ-induced HCCs in nonhuman primates may involve inactivation of the p53 gene and suggest that IQ and possibly other heterocyclic amines may participate in human carcinogenesis by a similar mechanism.	Amines	167-173	P53	Homo sapiens	106-109
8161788-5	1994	Morphological analysis, flow-cytometric determination of granulocytic or monocytic surface markers, and ability to reduce nitroblue tetrazolium (NBT) demonstrated that expression of exogenous wild-type p53 gene in HL-60 cells induces differentiation through the granulocytic pathway.	Nitroblue Tetrazolium	122-143	P53	Homo sapiens	202-205
8161788-5	1994	Morphological analysis, flow-cytometric determination of granulocytic or monocytic surface markers, and ability to reduce nitroblue tetrazolium (NBT) demonstrated that expression of exogenous wild-type p53 gene in HL-60 cells induces differentiation through the granulocytic pathway.	Nitroblue Tetrazolium	145-148	P53	Homo sapiens	202-205
8246608-2	1993	Sequencing of the p53 gene in the K562 cell line demonstrated a mutation in exon 5 characterized by a single base insertion (cytosine) between codons 135 and 136.	Cytosine	125-133	P53	Homo sapiens	18-21
1396069-0	1992	[Overexpression of p53 protein in human spontaneous esophageal carcinoma and fetal esophageal carcinoma induced by N-methyl-N-benzylnitrosamine (NMBzA)].	N-methyl-N-benzylnitrosamine	115-143	P53	Homo sapiens	19-22
1396069-0	1992	[Overexpression of p53 protein in human spontaneous esophageal carcinoma and fetal esophageal carcinoma induced by N-methyl-N-benzylnitrosamine (NMBzA)].	N-methyl-N-benzylnitrosamine	145-150	P53	Homo sapiens	19-22
1396069-7	1992	In addition, we found over expression of the p53 protein in the human fetal esophageal carcinoma induced by NMBzA, indicating that p53 gene mutation (s) might have occurred.	N-methyl-N-benzylnitrosamine	108-113	P53	Homo sapiens	45-48
1396069-7	1992	In addition, we found over expression of the p53 protein in the human fetal esophageal carcinoma induced by NMBzA, indicating that p53 gene mutation (s) might have occurred.	N-methyl-N-benzylnitrosamine	108-113	P53	Homo sapiens	131-134
1332185-3	1992	Recent reports of a guanine to thymine mutation of the third base of codon 249 of the tumour suppressor gene, p53, in 50% of patients with hepatocellular carcinoma in regions of high aflatoxin exposure, and mutagenic experiments showing that aflatoxin B1 binds particularly to guanine residues in G-C-rich domains and that codon 249 is a preferred target have suggested a mechanism whereby aflatoxin might induce malignant transformation.	Guanine	20-27	P53	Homo sapiens	110-113
1332185-3	1992	Recent reports of a guanine to thymine mutation of the third base of codon 249 of the tumour suppressor gene, p53, in 50% of patients with hepatocellular carcinoma in regions of high aflatoxin exposure, and mutagenic experiments showing that aflatoxin B1 binds particularly to guanine residues in G-C-rich domains and that codon 249 is a preferred target have suggested a mechanism whereby aflatoxin might induce malignant transformation.	Guanine	277-284	P53	Homo sapiens	110-113
1697983-0	1990	5-Methylcytosine as an endogenous mutagen in the human LDL receptor and p53 genes.	5-Methylcytosine	0-16	P53	Homo sapiens	72-75
1700664-1	1990	The effect of retinoid-induced suppression of in vitro invasive ability of A549 human lung carcinoma cells on p53 gene expression and cytokeratin (CK) 18 level was investigated.	Retinoids	14-22	P53	Homo sapiens	110-113
33804714-4	2021	Moreover, treatment with AI-EtE caused cell cycle arrest at the G1 phase in a p53-independent manner.	ai-ete	25-31	P53	Homo sapiens	78-81
33762927-5	2020	It was found that the combination of BoNT and MC obviously inhibits the inflammatory response and oxidative stress of glial cells, and notably activates SIRT1 and restrains pAKT, P53, and p-NF-KB.	Minocycline	46-48	P53	Homo sapiens	179-182
33762927-6	2020	Therefore, in the treatment of SCI-induced NP, the combination of BoNT and MC markedly improves the therapeutic effect of NP by promoting the SIRT1 expression, thereby inactivating NF-KB, P53, and PI3K/AKT signaling pathway, inhibiting inflammation and oxidative stress as well as relieving SCI-induced NP.	Minocycline	75-77	P53	Homo sapiens	188-191
34483003-5	2022	Furthermore, therapy-induced mutational signatures implicated in cancer progression have also been uncovered, including the identification of thiopurine-induced TP53 mutations in leukemia.	2-mercaptopyrazine	142-152	P53	Homo sapiens	161-165
34800879-6	2022	Generally, both cell lines treated with the combination of Flutamide and ATO showed a decrease in expression of KLK2, angiogenesis genes (VEGFA and VEGFC), and apoptosis gene (Bcl2), and an increase in expression of E-cadherin and P53 genes; however, contradictory findings were found regarding SNAIL expression in LNCaP and PC3 cells.	Flutamide	59-68	P53	Homo sapiens	231-234
34800879-6	2022	Generally, both cell lines treated with the combination of Flutamide and ATO showed a decrease in expression of KLK2, angiogenesis genes (VEGFA and VEGFC), and apoptosis gene (Bcl2), and an increase in expression of E-cadherin and P53 genes; however, contradictory findings were found regarding SNAIL expression in LNCaP and PC3 cells.	Arsenic Trioxide	73-76	P53	Homo sapiens	231-234
34951647-9	2021	ATRX loss enhanced the capacity of IDH1 R132H/p53mut cells to induce T-cell apoptosis, tumorigenic/anti-inflammatory macrophage polarization and Treg infiltration.	treg	145-149	P53	Homo sapiens	46-49
34986125-9	2021	Finally, the binding modes of EGFR, IL1B, NOS3 and TP53 with quercetin were visualized.	Quercetin	61-70	P53	Homo sapiens	51-55
34986125-10	2021	DISCUSSION AND CONCLUSION: Quercetin of Baiying Qinghou decoction showed therapeutic effect against laryngeal squamous cell carcinoma by regulating TP53, EGFR, NOS3 and IL1B involved with drug resistance and PI3K-AKT signaling pathway.	Quercetin	27-36	P53	Homo sapiens	148-152
34727807-0	2021	Carcinomatosis under control by osimertinib in EGFR and TP53 mutated lung adenocarcinoma.	osimertinib	32-43	P53	Homo sapiens	56-60
34825792-9	2021	Importantly, p53 mutant type as well as increased expression of Ki67 were detected in HPOE and HOSEpic cells when exposed to talcum powder.	Talc	125-131	P53	Homo sapiens	13-16
34832966-10	2021	Treatment with cisplatin, melphalan, or 9-cis RA decreased p53 expression levels in SK-N-FI cells but not in SK-N-Be (2).	Melphalan	26-35	P53	Homo sapiens	59-62
34832966-10	2021	Treatment with cisplatin, melphalan, or 9-cis RA decreased p53 expression levels in SK-N-FI cells but not in SK-N-Be (2).	sk-n	84-88	P53	Homo sapiens	59-62
34832966-14	2021	In conclusion, TP53 mutated SK-N-FI cells respond better to the retinoic isomers than TP53 wild-type SK-N-Be(2) cells.	sk-n-be	101-108	P53	Homo sapiens	86-90
34626309-0	2021	Allicin induces cell cycle arrest and apoptosis of breast cancer cells in vitro via modulating the p53 pathway.	allicin	0-7	P53	Homo sapiens	99-102
34626309-3	2021	However, whether allicin plays an anti-cancer role against breast cancer cells through the induction of p53-mediated apoptosis remains unknown.	allicin	17-24	P53	Homo sapiens	104-107
34626309-6	2021	Allicin activated p53 and caspase 3 expressions in both cells but produced different effects on the expression of p53-related biomarkers.	allicin	0-7	P53	Homo sapiens	18-21
34626309-6	2021	Allicin activated p53 and caspase 3 expressions in both cells but produced different effects on the expression of p53-related biomarkers.	allicin	0-7	P53	Homo sapiens	114-117
34626309-9	2021	Hence, allicin induces cell cycle arrest and apoptosis in breast cancer cells through p53 activation but it effects on the expression of p53-related biomarkers were dependent upon the specific type of breast cancer involved.	allicin	7-14	P53	Homo sapiens	86-89
34626309-9	2021	Hence, allicin induces cell cycle arrest and apoptosis in breast cancer cells through p53 activation but it effects on the expression of p53-related biomarkers were dependent upon the specific type of breast cancer involved.	allicin	7-14	P53	Homo sapiens	137-140
34626309-10	2021	CONCLUSIONS: These findings suggest that allicin induces apoptosis and regulates biomarker expression in breast cancer cell lines through modulating the p53 signaling pathway.	allicin	41-48	P53	Homo sapiens	153-156
34626309-11	2021	Furthermore, our results promote the utility of allicin as compound for further studies as an anticancer drug targeting p53.	allicin	48-55	P53	Homo sapiens	120-123
34743450-13	2021	The median docetaxel-PFS was 3.0 months in patients with TP53 mutation and 5.0 months in patients with TP53 wild-type.	Docetaxel	11-20	P53	Homo sapiens	57-61
34743450-13	2021	The median docetaxel-PFS was 3.0 months in patients with TP53 mutation and 5.0 months in patients with TP53 wild-type.	Docetaxel	11-20	P53	Homo sapiens	103-107
34743450-15	2021	Conclusions: TP53 mutations were associated with the presence of metastasis and castration resistance, and were also an independent prognostic factor for progression-free survival in patients treated with abiraterone and docetaxel.	Docetaxel	221-230	P53	Homo sapiens	13-17
34620048-5	2022	We selected the four currently most popular pathways for discussion and introduced the molecular mechanisms mediated by alkaloids in different signaling pathways, including the NF-kB signaling pathway, PI3K/AKT signaling pathway, MAPK signaling pathway, and P53 signaling pathway.	Alkaloids	120-129	P53	Homo sapiens	258-261
34608124-3	2021	In contrast, bortezomib and paclitaxel could drive U2OS or MG63 toward apoptosis effectively, suggesting that apoptosis induced by bortezomib or paclitaxel is p53-independent.	Bortezomib	13-23	P53	Homo sapiens	159-162
34608124-3	2021	In contrast, bortezomib and paclitaxel could drive U2OS or MG63 toward apoptosis effectively, suggesting that apoptosis induced by bortezomib or paclitaxel is p53-independent.	Bortezomib	131-141	P53	Homo sapiens	159-162
34608255-7	2021	Secondly, p53 silencing in H1975 cells enhanced the sensitivity to osimertinib through the emergence of mesenchymal-to-epithelial transition, and the emergence of acquired resistance to osimertinib in p53 knockout cells was much slower than in H1975 cells.	osimertinib	67-78	P53	Homo sapiens	10-13
34608255-7	2021	Secondly, p53 silencing in H1975 cells enhanced the sensitivity to osimertinib through the emergence of mesenchymal-to-epithelial transition, and the emergence of acquired resistance to osimertinib in p53 knockout cells was much slower than in H1975 cells.	osimertinib	67-78	P53	Homo sapiens	201-204
34608255-7	2021	Secondly, p53 silencing in H1975 cells enhanced the sensitivity to osimertinib through the emergence of mesenchymal-to-epithelial transition, and the emergence of acquired resistance to osimertinib in p53 knockout cells was much slower than in H1975 cells.	osimertinib	186-197	P53	Homo sapiens	10-13
34608255-7	2021	Secondly, p53 silencing in H1975 cells enhanced the sensitivity to osimertinib through the emergence of mesenchymal-to-epithelial transition, and the emergence of acquired resistance to osimertinib in p53 knockout cells was much slower than in H1975 cells.	osimertinib	186-197	P53	Homo sapiens	201-204
34255251-7	2021	Real-time RT-PCR indicated that the co-administration of Schiff base oxovanadium complex 40 microg/ml and arsenic trioxide 0.001 microM could increase the expression of P53 and P21 genes by 3.76 +- 0.19 and 6.57 +- 1.29 fold change, respectively to the control sample.	Arsenic Trioxide	106-122	P53	Homo sapiens	169-172
34577642-6	2021	Ovarian cancer cells OVCAR3 and ES-2, both harboring TP53 missense mutations, were treated with the p53 reactivator HO-3867.	(3,5-bis((4-fluorophenyl)methylidene)-1-((1-hydroxy-2,2,5,5-tetramethyl-2,5-dihydro-1H-pyrrol-3-yl)methyl)piperidin-4-one)	116-123	P53	Homo sapiens	100-103
34427098-9	2021	Furthermore, CDKL3 knockdown increases p53 expression and reduces cell viability, and these effects are significantly weakened by the p53 inhibitor, PFT-alpha.	pifithrin	149-158	P53	Homo sapiens	39-42
34427098-9	2021	Furthermore, CDKL3 knockdown increases p53 expression and reduces cell viability, and these effects are significantly weakened by the p53 inhibitor, PFT-alpha.	pifithrin	149-158	P53	Homo sapiens	134-137
34445227-5	2021	Osimertinib exerted significant inhibitory effects on cell growth and cell cycle progression by promoting the phosphorylation of p53 and p21 and decreasing cyclin D1 expression independently of EGFR.	osimertinib	0-11	P53	Homo sapiens	129-132
34243108-6	2021	Hemin caused upregulation of both P53 and beta-catenin gene and proteins expression in normal colonic cells with concomitant cell cycle arrest at G1(Gap 1) and G2/M (Gap 2/ Mitosis).	Hemin	0-5	P53	Homo sapiens	34-37
34359777-8	2021	Combination with GSK2830371 increased p53 phosphorylation, resulting in an increase in both p53 accumulation and p53-dependent trans-activation.	GSK2830371	17-27	P53	Homo sapiens	92-95
34359777-8	2021	Combination with GSK2830371 increased p53 phosphorylation, resulting in an increase in both p53 accumulation and p53-dependent trans-activation.	GSK2830371	17-27	P53	Homo sapiens	113-116
34359777-12	2021	CONCLUSION: The current study demonstrated that GSK2830371 enhanced the p53-dependent antiproliferative and cytotoxic effect of HDM201 on RBE and SK-Hep-1 cells, providing a novel strategy for potentiating the efficacy of targeting the p53 pathway in iCCA.	GSK2830371	48-58	P53	Homo sapiens	72-75
34359777-12	2021	CONCLUSION: The current study demonstrated that GSK2830371 enhanced the p53-dependent antiproliferative and cytotoxic effect of HDM201 on RBE and SK-Hep-1 cells, providing a novel strategy for potentiating the efficacy of targeting the p53 pathway in iCCA.	GSK2830371	48-58	P53	Homo sapiens	236-239
34362481-12	2021	At the same time, the protein level of P53 was significantly increased in KG1 and kG1a cells after treated by SFN(P<0.05).	sulforaphane	110-113	P53	Homo sapiens	39-42
34405020-8	2021	5-Aza also increased p53 and p21 transcription through promoter demethylation, and decreased the expression of oncogene c-Myc in 22RV1 and LNCaP cells.	Azacitidine	0-5	P53	Homo sapiens	21-24
34405020-11	2021	Thus, in responsible for its apoptotic induction and DNA damage, the mechanism of the antitumor activities of 5-Aza may involve in an increase of tumor suppressive maspin, upregulation of wild type p53-mediated p21 expression and a decrease of oncogene c-Myc level in 22RV1 and LNCaP cells, and enhancing the tumor suppressive maspin expression in DU145 cells.	Azacitidine	110-115	P53	Homo sapiens	198-201
34335587-12	2021	In the mechanistic study, we found that the induction of p53 deacetylation, due to either the resveratrol/quercetin -induced activation of the deacetylase Sirtuin 1 (Sirt1) or the mutation of the acetylated lysine site in p53, promoted RTEC autophagy and alleviated SAKI.	Quercetin	106-115	P53	Homo sapiens	57-60
34196654-8	2021	Cell experiments further confirmed that H2 could reverse MNU damage to CECs by decreasing oxidative stress injury, interfering with the NF-kappaB/NLRP3 pathway and the FOXO3a/p53/p21 pathway.	Deuterium	40-42	P53	Homo sapiens	175-178
34306252-10	2021	The main compounds of XYS include Quercetin, Naringenin, Isorhamnetin, and Stigmasterol, which mainly regulate the targets such as TP53, Akt1, and MYC and PI3K/Akt, p53, and cell cycle signal pathways.	Quercetin	34-43	P53	Homo sapiens	131-135
34306252-10	2021	The main compounds of XYS include Quercetin, Naringenin, Isorhamnetin, and Stigmasterol, which mainly regulate the targets such as TP53, Akt1, and MYC and PI3K/Akt, p53, and cell cycle signal pathways.	Quercetin	34-43	P53	Homo sapiens	165-168
34257824-5	2021	Dietary intake of flavonoids, a C15 group of polyphenols, is known to inhibit cancer progression and assist DNA repair through p53-mediated mechanisms in human cells via their antioxidant activities.	Flavonoids	18-28	P53	Homo sapiens	127-130
34257824-6	2021	For example, quercetin arrests human cervical cancer cell growth by blocking the G2/M phase cell cycle and inducing mitochondrial apoptosis through a p53-dependent mechanism.	Quercetin	13-22	P53	Homo sapiens	150-153
34202736-3	2021	E6 induces anti-apoptosis by degrading tumor suppressor proteins p53 (p53) via E6-E6-associated protein (E6AP)-mediated polyubiquitination.	Polyurethane Y-290	0-2	P53	Homo sapiens	65-68
34202736-3	2021	E6 induces anti-apoptosis by degrading tumor suppressor proteins p53 (p53) via E6-E6-associated protein (E6AP)-mediated polyubiquitination.	Polyurethane Y-290	0-2	P53	Homo sapiens	70-73
34202551-9	2021	Treatment Vero cells with the p53 inhibitor, PFT-alpha, could significantly inhibit PEDV-induced apoptosis.	pifithrin	45-54	P53	Homo sapiens	30-33
34094715-6	2021	Alternatively, binding interactions between TRMP-S and FUBP3 prevent p53 mRNA interactions with RPL26 ribosomal protein, the latter essential for promoting p53 translation with ensuing suppression of p53 translation limiting p27 expression.	trmp-s	44-50	P53	Homo sapiens	69-72
34094715-6	2021	Alternatively, binding interactions between TRMP-S and FUBP3 prevent p53 mRNA interactions with RPL26 ribosomal protein, the latter essential for promoting p53 translation with ensuing suppression of p53 translation limiting p27 expression.	trmp-s	44-50	P53	Homo sapiens	156-159
34094715-6	2021	Alternatively, binding interactions between TRMP-S and FUBP3 prevent p53 mRNA interactions with RPL26 ribosomal protein, the latter essential for promoting p53 translation with ensuing suppression of p53 translation limiting p27 expression.	trmp-s	44-50	P53	Homo sapiens	200-203
34094715-7	2021	Significantly, as TRMP-S is itself transactivated by p53, this identifies negative feedback regulation between p53 and TRMP-S.	trmp-s	18-24	P53	Homo sapiens	53-56
34094715-7	2021	Significantly, as TRMP-S is itself transactivated by p53, this identifies negative feedback regulation between p53 and TRMP-S.	trmp-s	18-24	P53	Homo sapiens	111-114
34094715-7	2021	Significantly, as TRMP-S is itself transactivated by p53, this identifies negative feedback regulation between p53 and TRMP-S.	trmp-s	119-125	P53	Homo sapiens	53-56
34094715-7	2021	Significantly, as TRMP-S is itself transactivated by p53, this identifies negative feedback regulation between p53 and TRMP-S.	trmp-s	119-125	P53	Homo sapiens	111-114
35576022-0	2022	Selinexor synergizes with azacitidine to eliminate myelodysplastic syndrome cells through p53 nuclear accumulation.	Azacitidine	26-37	P53	Homo sapiens	90-93
35532255-7	2022	By constructing the disease-common target-compound network, five ingredients (quercetin, arachidonate, beta-sitosterol, beta-carotene, and cholesterol) were selected out as the key ingredients of YJD, which can interact with the 10 hub genes (VEGFA, AKT1, TP53, ALB, TNF, PIK3CA, IGF1, INS, IL1B, PTEN) against PCOS.	Quercetin	78-87	P53	Homo sapiens	256-260
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	imidazolate	194-205	P53	Homo sapiens	65-68
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	imidazolate	194-205	P53	Homo sapiens	101-104
35513212-4	2022	The highly cytotoxic ROS was continuously produced via Fe2+-mediated and TA-assisted enhanced Fenton reaction as well as Ce6-induced photosensitive reaction, and meanwhile, the intratumoral upregulated p53 expression inactivated glutathione peroxidase 4 (GPX4) to suppress lipid peroxidation (LPO) resistance, thus resulting in amplified oxidative stress and intensified ferroptosis-apoptosis therapy.	ammonium ferrous sulfate	55-59	P53	Homo sapiens	202-205
35383482-4	2022	Results: The study found that FHS-1 detects H2S levels with high selectivity and pH stability and that H2S may regulate apoptosis in MCF-7 cells through the p53/mTOR/STAT3 pathway.	Deuterium	103-106	P53	Homo sapiens	157-160
35337799-7	2022	The results show that P53 mediates the dissociation induced-ferroptosis in hESCs which is suppressed by Pifithrin alpha.	pifithrin	104-119	P53	Homo sapiens	22-25
35530310-1	2022	Dienone compounds have been demonstrated to display tumor-selective anti-cancer activity independently of the mutational status of TP53.	dienone	0-7	P53	Homo sapiens	131-135
35530319-10	2022	Knockdown of p53 or inhibition of p53"s transcriptional activity by addition of its specific inhibitor PFT-alpha decreased expression of ALKBH5 and CSCs" malignancies, including proliferation, invasion, and tumor formation ability, indicating that p53 may partially regulate CSC"s malignancies via ALKBH5.	pifithrin	103-112	P53	Homo sapiens	13-16
35129780-0	2022	MALAT-1/p53/miR-155/miR-146a ceRNA circuit tuned by methoxylated quercitin glycoside alters immunogenic and oncogenic profiles of breast cancer.	quercitin glycoside	65-84	P53	Homo sapiens	8-11
35418961-9	2022	The treatment of PFT-alpha (p53 inhibitor) significantly suppressed the expression of cleaved caspase 9 and caspase 3, leading to the decrease of apoptosis.	pifithrin	17-26	P53	Homo sapiens	28-31
35025136-5	2022	Here, we combined genetic code expansion with oxime ligation to generate p53 site-specifically mono-ubiquitylated at position 120.	Oximes	46-51	P53	Homo sapiens	73-76
35326597-5	2022	Herein, we report that 8-Cl-Ado inhibits ribosomal RNA (rRNA) synthesis through the downregulation of transcription initiation factor TIF-IA that is associated with increasing levels of p53.	8-chloroadenosine	23-31	P53	Homo sapiens	186-189
35326597-6	2022	Paradoxically, 8-Cl-Ado-induced p53 increased FAO and OXPHOS, thereby self-limiting the activity of 8-Cl-Ado on LSCs.	8-chloroadenosine	15-23	P53	Homo sapiens	32-35
35326597-6	2022	Paradoxically, 8-Cl-Ado-induced p53 increased FAO and OXPHOS, thereby self-limiting the activity of 8-Cl-Ado on LSCs.	8-chloroadenosine	100-108	P53	Homo sapiens	32-35
35326597-7	2022	Since VEN inhibits amino acid-driven OXPHOS, the addition of VEN significantly enhanced the activity of 8-Cl-Ado by counteracting the self-limiting effect of p53 on FAO and OXPHOS.	8-chloroadenosine	104-112	P53	Homo sapiens	158-161
35356282-14	2022	Pre-treatment with rapamycin or PFT-alpha significantly down-regulated the levels of SA beta-Gal, SAHF, p-p53, p21, autophagy related protein p62, the percentage of cells in the G0/G1 phase, and significantly up-regulated DeltaPsim, autophagy related protein BECN1, autophagosomes and autolysosomes compared with cells only treated with AOPPs.	pifithrin	32-41	P53	Homo sapiens	106-109
35227162-4	2022	Following 30 microM 8-Cl-Ado treatment, RNA synthesis was inhibited, p53 protein was stabilized, and p21 expression was activated.	8-chloroadenosine	20-28	P53	Homo sapiens	69-72
35163828-3	2022	The TP53-Induced Glycolysis and Apoptosis Regulator (TIGAR) is an important regulator of glycolysis and the pentose phosphate pathway that was described as a p53 response gene, yet TIGAR expression is detected in p53-null tumors.	Pentosephosphates	108-125	P53	Homo sapiens	158-161
35228743-0	2022	Malic enzyme 2 maintains protein stability of mutant p53 through 2-hydroxyglutarate.	alpha-hydroxyglutarate	65-83	P53	Homo sapiens	53-56
35242623-0	2022	TP53 co-mutations as an independent prognostic factor in 2nd and further line therapy-EGFR mutated non-small cell lung cancer IV patients treated with osimertinib.	osimertinib	151-162	P53	Homo sapiens	0-4
35242623-12	2022	Conclusions: TP53 mt+ have a negative impact on PFS and OS in a group of patients carrying a sensitizing EGFR mt+ and a T790M resistance mutation treated with Osimertinib.	osimertinib	159-170	P53	Homo sapiens	13-17
10682666-1	2000	The purpose of this work was to analyse the ability of p53 and thymidilate synthase (TS) primary tumour expression to retrospectively predict clinical response to chemotherapy and long-term prognosis in patients with advanced colorectal cancers homogeneously treated by methotrexate (MTX)-modulated-5-fluorouracil (5-FU-FA).	Methotrexate	270-282	P53	Homo sapiens	55-58
10682666-1	2000	The purpose of this work was to analyse the ability of p53 and thymidilate synthase (TS) primary tumour expression to retrospectively predict clinical response to chemotherapy and long-term prognosis in patients with advanced colorectal cancers homogeneously treated by methotrexate (MTX)-modulated-5-fluorouracil (5-FU-FA).	Methotrexate	284-287	P53	Homo sapiens	55-58
10631110-4	2000	Western blot analyses of immunoprecipitates for p53 or for nitrotyrosine revealed low levels of nitrotyrosine in p53 from untreated cells.	3-nitrotyrosine	96-109	P53	Homo sapiens	48-51
10631110-4	2000	Western blot analyses of immunoprecipitates for p53 or for nitrotyrosine revealed low levels of nitrotyrosine in p53 from untreated cells.	3-nitrotyrosine	96-109	P53	Homo sapiens	113-116
10631110-5	2000	Incubation with 2 mM S-nitrosoglutathione induced a significant increase in the nitrotyrosine level in p53 protein compared to nontreated cells.	3-nitrotyrosine	80-93	P53	Homo sapiens	103-106
22607421-15	2000	Binding of C-terminal anti-p53 antibody also protected bacterially expressed protein against irreversible loss of activity due to diamide oxidation.	Diamide	130-137	P53	Homo sapiens	27-30
10982614-6	2000	Investigation of K-ras mutation and overexpression of p53 protein was performed using an enriched polymerase chain reaction (PCR) and enzyme-linked mini-sequence assay (ELMA), and by the streptavidin-biotin (SAB) method, using DO-7 antibodies, respectively.	sab	208-211	P53	Homo sapiens	54-57
10772725-6	2000	The hypothesis on an important role of the 3"-to-5" exonuclease activity of p53 protein in the action of nucleoside analogs was proposed.	Nucleosides	105-115	P53	Homo sapiens	76-79
10656489-0	1999	5-methylcytosine at HpaII sites in p53 is not hypermutable after UVC irradiation.	5-Methylcytosine	0-16	P53	Homo sapiens	35-38
10464313-3	1999	Here we compare the effects of oxidation of p53 by azodicarboxylic acid bis[dimethylamide] (diamide) and other agents on p53 binding to p53CON and to scDNA.	Diamide	51-90	P53	Homo sapiens	44-47
10464313-3	1999	Here we compare the effects of oxidation of p53 by azodicarboxylic acid bis[dimethylamide] (diamide) and other agents on p53 binding to p53CON and to scDNA.	Diamide	51-90	P53	Homo sapiens	121-124
10464313-3	1999	Here we compare the effects of oxidation of p53 by azodicarboxylic acid bis[dimethylamide] (diamide) and other agents on p53 binding to p53CON and to scDNA.	Diamide	51-90	P53	Homo sapiens	121-124
10464313-3	1999	Here we compare the effects of oxidation of p53 by azodicarboxylic acid bis[dimethylamide] (diamide) and other agents on p53 binding to p53CON and to scDNA.	Diamide	92-99	P53	Homo sapiens	44-47
10464313-3	1999	Here we compare the effects of oxidation of p53 by azodicarboxylic acid bis[dimethylamide] (diamide) and other agents on p53 binding to p53CON and to scDNA.	Diamide	92-99	P53	Homo sapiens	121-124
10464313-3	1999	Here we compare the effects of oxidation of p53 by azodicarboxylic acid bis[dimethylamide] (diamide) and other agents on p53 binding to p53CON and to scDNA.	Diamide	92-99	P53	Homo sapiens	121-124
10628338-3	1999	Lactacystin increased the cellular level of p53 and cdk2-associated p21WAF1/CIP1 leading to cdk2 inactivation.	lactacystin	0-11	P53	Homo sapiens	44-47
10628338-5	1999	Lactacystin induced p53-dependent p21WAF1/CIP1 expression at lower concentrations in HUVECs than in other cells.	lactacystin	0-11	P53	Homo sapiens	20-23
10496344-6	1999	Moreover, studies in vitro and in vivo indicate that p53 mutants with intact conformational structure (as determined by immunoreactivity with PAb246 and PAb1620) retain the ability to undergo proteolytic cleavage similar, if not identical, to the wild-type p53 protein.	pab246	142-148	P53	Homo sapiens	53-56
10496344-6	1999	Moreover, studies in vitro and in vivo indicate that p53 mutants with intact conformational structure (as determined by immunoreactivity with PAb246 and PAb1620) retain the ability to undergo proteolytic cleavage similar, if not identical, to the wild-type p53 protein.	pab1620	153-160	P53	Homo sapiens	53-56
10490506-14	1999	In p53 and ras genes, the frequency of methylation of guanines parallels the frequency of mutations of those same guanines in lung cancer.	Guanine	54-62	P53	Homo sapiens	3-6
10490506-14	1999	In p53 and ras genes, the frequency of methylation of guanines parallels the frequency of mutations of those same guanines in lung cancer.	Guanine	114-122	P53	Homo sapiens	3-6
10487521-2	1999	We have previously reported that a mutation at codon 273, p53-273L (Arg --&gt; Leu), suppresses cell growth despite its having no p53-specific transactivation activity.	Leucine	79-82	P53	Homo sapiens	58-61
10446162-2	1999	It has recently been shown that BPDE preferentially modifies the guanine in methylated 5"-CpG-3" sequences in the human p53 gene, providing one explanation for why these sites are mutational hot spots.	Guanine	65-72	P53	Homo sapiens	120-123
10470656-8	1999	However, in the p53 negative subgroup (n = 36), AI and BAX scores were higher and BCL-2 scores lower in the 5"-DFUR group than in the control group (P = 0.006, 0.008 and 0.050, respectively).	5"-dfur	108-115	P53	Homo sapiens	16-19
10470656-12	1999	CONCLUSIONS: Preoperative treatment with 5"-DFUR induced apoptosis and changes in BCL-2 and BAX expression in p53 negative breast cancers.	5"-dfur	41-48	P53	Homo sapiens	110-113
10383141-0	1999	Implication of p53 in growth arrest and apoptosis induced by the synthetic retinoid CD437 in human lung cancer cells.	Retinoids	75-83	P53	Homo sapiens	15-18
10403664-0	1999	Methyl methanesulfonate and hydrogen peroxide differentially regulate p53 accumulation in hepatoblastoma cells.	Methyl Methanesulfonate	0-23	P53	Homo sapiens	70-73
10403664-3	1999	Since the mechanisms by which cellular DNA damaged by different DNA-damaging chemicals may not be the same, we studied the involvement of p53, Bcl-2 and Bax in apoptosis induced by methyl methanesulfonate (MMS) and hydrogen peroxide (H2O2).	Methyl Methanesulfonate	206-209	P53	Homo sapiens	138-141
10403664-5	1999	At non-lethal doses, both H2O2 and MMS induced high level of p53 protein accumulation.	Methyl Methanesulfonate	35-38	P53	Homo sapiens	61-64
10226945-3	1999	One tumor sample (case 23) showed a mis-sense point mutation at codon 177, changing CCC to CTC, which resulted in a substitution of proline to leucine in the p53 protein.	Leucine	143-150	P53	Homo sapiens	158-161
10096970-1	1999	BACKGROUND: The cytotoxic effects of cisplatin and anthracyclins have been attributed to apoptosis induction, which has been recognized as a major function of the TP53 gene.	anthracyclins	51-64	P53	Homo sapiens	163-167
10190503-0	1999	Restoration of mutant TP53 to normal TP53 function by glycerol as a chemical chaperone.	Glycerol	54-62	P53	Homo sapiens	22-26
10190503-0	1999	Restoration of mutant TP53 to normal TP53 function by glycerol as a chemical chaperone.	Glycerol	54-62	P53	Homo sapiens	37-41
10190503-5	1999	We examined whether glycerol can act as a chemical chaperone to correct the mutant TP53 conformation.	Glycerol	20-28	P53	Homo sapiens	83-87
10190503-9	1999	These cells showed similar CDKN1A expression when heated in the presence of glycerol at 0.6 or 1.2 M. These results suggest that glycerol is effective in restoring several TP53 mutants to normal TP53 function, leading to normal CDKN1A expression after heat stress.	Glycerol	129-137	P53	Homo sapiens	172-176
10190503-9	1999	These cells showed similar CDKN1A expression when heated in the presence of glycerol at 0.6 or 1.2 M. These results suggest that glycerol is effective in restoring several TP53 mutants to normal TP53 function, leading to normal CDKN1A expression after heat stress.	Glycerol	129-137	P53	Homo sapiens	195-199
10096571-4	1999	Fas-mediated cell death in these cell lines is p53-independent.	ammonium ferrous sulfate	0-3	P53	Homo sapiens	47-50
10082992-4	1999	Northern blot analysis revealed that quercetin induced the increases in c-fos and p21WAF1CIP1 mRNA levels within 2 h. The expression of p21 protein was also enhanced, while p53 mRNA and protein levels were not affected by quercetin.	Quercetin	37-46	P53	Homo sapiens	173-176
10082992-5	1999	These results suggest that quercetin-induced apoptosis is associated with the increase in c-fos mRNA level and the upregulation of p21 mRNA and protein expression, probably in a p53-independent pathway.	Quercetin	27-36	P53	Homo sapiens	178-181
9927185-3	1999	When treated with N-(phosphonacetyl)-L-aspartate (PALA), which inhibits pyrimidine nucleotide synthesis, leading to synthesis of damaged DNA from highly unbalanced dNTP pools, p53-null cells enter mitosis after they have completed DNA replication, but cells with wild-type p53 do not, revealing that p53 also mediates a checkpoint that monitors the quality of newly replicated DNA.	sparfosic acid	18-48	P53	Homo sapiens	176-179
9927185-3	1999	When treated with N-(phosphonacetyl)-L-aspartate (PALA), which inhibits pyrimidine nucleotide synthesis, leading to synthesis of damaged DNA from highly unbalanced dNTP pools, p53-null cells enter mitosis after they have completed DNA replication, but cells with wild-type p53 do not, revealing that p53 also mediates a checkpoint that monitors the quality of newly replicated DNA.	sparfosic acid	18-48	P53	Homo sapiens	273-276
9927185-3	1999	When treated with N-(phosphonacetyl)-L-aspartate (PALA), which inhibits pyrimidine nucleotide synthesis, leading to synthesis of damaged DNA from highly unbalanced dNTP pools, p53-null cells enter mitosis after they have completed DNA replication, but cells with wild-type p53 do not, revealing that p53 also mediates a checkpoint that monitors the quality of newly replicated DNA.	sparfosic acid	18-48	P53	Homo sapiens	273-276
10412949-9	1999	RESULTS: p53 Ad combined with cisplatin, doxorubicin, 5-fluorouracil, methotrexate, or etoposide inhibited cell proliferation more effectively than chemotherapy alone in SCC-9 head and neck, SCC-15 head and neck, SCC-25 head and neck, SK-OV-3 ovarian, DU-145 prostate, MDA-MB-468 breast, and MDA-MB-231 breast tumor cells.	Methotrexate	70-82	P53	Homo sapiens	9-12
10626228-0	1999	Localization of chloroacetaldehyde-induced DNA damage in human p53 gene by DNA polymerase fingerprint analysis.	chloroacetaldehyde	16-34	P53	Homo sapiens	63-66
10626228-1	1999	Chloroacetaldehyde (CAA) reacts with DNA bases, forming hydroxyethano derivatives of different stability, which are subsequently converted into etheno (epsilon) adducts: epsilon A, epsilon C, epsilon G. DNA polymerase fingerprint analysis was used to study the distribution of CAA-induced modifications in the p53 sequence.	chloroacetaldehyde	0-18	P53	Homo sapiens	310-313
10626228-1	1999	Chloroacetaldehyde (CAA) reacts with DNA bases, forming hydroxyethano derivatives of different stability, which are subsequently converted into etheno (epsilon) adducts: epsilon A, epsilon C, epsilon G. DNA polymerase fingerprint analysis was used to study the distribution of CAA-induced modifications in the p53 sequence.	chloroacetaldehyde	20-23	P53	Homo sapiens	310-313
10626228-2	1999	A plasmid bearing cDNA containing the human p53 gene was reacted in vitro with CAA, then dehydrated for conversion of hydroxyethano into etheno adducts, and primer extension by T7 DNA polymerase in the presence of four dNTPs was performed.	chloroacetaldehyde	79-82	P53	Homo sapiens	44-47
10626228-9	1999	In exons 5-8 of p53, 143 out of 500 sites appeared to be damaged by CAA, with four particularly densely modified regions between codons 135-147, 218-222, 234-255 and 284-292.	chloroacetaldehyde	68-71	P53	Homo sapiens	16-19
11601009-10	1999	CONCLUSION: Codon 172 mutant (Arg--&gt;Leu) p53 genomic DNA exhibited a strong suppressive transfecting effects on carcinoma cell, so it is a possible candidate to be used in cancer gene therapy.	Leucine	39-42	P53	Homo sapiens	44-47
9875290-6	1998	We found that DU-86, a duocarmycin derivative which alkylates DNA, bound ssDNA and enhanced the DNA binding activity of the p53 C-terminus.	du	14-16	P53	Homo sapiens	124-127
9875290-7	1998	DU-86 weakened p53-mediated catalysis of complementary ssDNA renaturation.	du	0-2	P53	Homo sapiens	15-18
9881702-1	1998	Sequence-dependent formation and lack of repair of polycyclic aromatic hydrocarbon-induced DNA adducts correlates well with the positions of p53 mutational hotspots in smoking-related lung cancers (Denissenko et al, 1996, 1998).	Polycyclic Aromatic Hydrocarbons	51-82	P53	Homo sapiens	141-144
14646475-8	1998	Two other agents known to induce apoptosis, vinblastine and actinomycin D, induced a similar pattern of acidic p53 species as that observed for 2-MeOE2.	Vinblastine	44-55	P53	Homo sapiens	111-114
9823951-15	1998	In contrast, four of five Fas+/Fas-resistant (R) lines were wt-p53+/Bcl-2+; the exception was p53-null/Bcl-2- but expressed a low level of Fas (150 MESF).	ammonium ferrous sulfate	26-29	P53	Homo sapiens	63-66
9823951-15	1998	In contrast, four of five Fas+/Fas-resistant (R) lines were wt-p53+/Bcl-2+; the exception was p53-null/Bcl-2- but expressed a low level of Fas (150 MESF).	ammonium ferrous sulfate	31-34	P53	Homo sapiens	63-66
9823951-15	1998	In contrast, four of five Fas+/Fas-resistant (R) lines were wt-p53+/Bcl-2+; the exception was p53-null/Bcl-2- but expressed a low level of Fas (150 MESF).	ammonium ferrous sulfate	31-34	P53	Homo sapiens	63-66
9823951-18	1998	These results suggest that some pediatric ALL cells expressing mt-p53+ may be sensitive to Fas-mediated apoptosis due to high levels of Fas expression and lack of Bcl-2, and further suggest that molecular methods of activating Fas may be useful for therapy of refractory ALL with the Fas+/mt-p53+ phenotype.	ammonium ferrous sulfate	91-94	P53	Homo sapiens	66-69
9823951-18	1998	These results suggest that some pediatric ALL cells expressing mt-p53+ may be sensitive to Fas-mediated apoptosis due to high levels of Fas expression and lack of Bcl-2, and further suggest that molecular methods of activating Fas may be useful for therapy of refractory ALL with the Fas+/mt-p53+ phenotype.	ammonium ferrous sulfate	91-94	P53	Homo sapiens	292-295
9765154-5	1998	p53 also induced Fas-FADD binding and transiently sensitized cells to Fas-induced apoptosis.	ammonium ferrous sulfate	17-20	P53	Homo sapiens	0-3
9879152-0	1998	13-cis-retinoic acid and interferon-alpha 2a therapy in locally advanced squamous cell carcinoma of the cervix: p53 alteration, proliferating cell nuclear antigen expression and angiogenesis response.	Isotretinoin	0-20	P53	Homo sapiens	112-115
9771923-10	1998	The status of the tumor suppressor gene p53 was analyzed in methotrexate sensitive and resistant clones.	Methotrexate	60-72	P53	Homo sapiens	40-43
9771923-11	1998	In all the methotrexate resistant clones analyzed, the western blots indicated that the p53 protein was still present and transcriptionally competent, as measured by its capacity to stimulate transcription of the p21waf1/cip1 gene following UVB irradiation.	Methotrexate	11-23	P53	Homo sapiens	88-91
9771923-13	1998	However, this induction of p53 accumulation by estrogens failed to stimulate the transcription of p21waf1/cip1, which indicates that a transcriptionally inactive form of p53 accumulated in methotrexate resistant cells.	Methotrexate	189-201	P53	Homo sapiens	170-173
9790785-8	1998	Exons 2 through 11 of the p53 gene were analyzed by direct DNA sequencing, revealing a homozygous mutation at codon 281 in exon 8, GAC to CAC (Asp--&gt;His).	Aspartic Acid	143-146	P53	Homo sapiens	26-29
9719464-5	1998	This apoptotic cell death with p21 induction was also observed in the Hep 3B cells lacking functional p53 after exposure to C6-ceramide.	N-caproylsphingosine	124-135	P53	Homo sapiens	102-105
9610721-5	1998	The initial analysis showed NY-CO-13 to be a mutated version of the p53 tumor suppressor gene.	ny-co-13	28-36	P53	Homo sapiens	68-71
9605744-3	1998	Using a UvrABC incision method, we have found that cytosine methylation greatly enhances guanine alkylation at all CpG sites in the p53 gene by a variety of carcinogens, including benzo(a)pyrene diol epoxide, benzo(g)chrysene diol epoxide, aflatoxin B1 8,9-epoxide, and N-acetoxy-2-acetylaminofluorene.	Cytosine	51-59	P53	Homo sapiens	132-135
9605744-3	1998	Using a UvrABC incision method, we have found that cytosine methylation greatly enhances guanine alkylation at all CpG sites in the p53 gene by a variety of carcinogens, including benzo(a)pyrene diol epoxide, benzo(g)chrysene diol epoxide, aflatoxin B1 8,9-epoxide, and N-acetoxy-2-acetylaminofluorene.	Guanine	89-96	P53	Homo sapiens	132-135
9591783-4	1998	Based on these results, we propose a mechanism by which PAb1620 can allosterically inhibit p53 binding to DNA through an indirect interaction between the antibody binding site and the L1 loop (amino acids 112-124) of p53, which is a component of the DNA binding region.	pab1620	56-63	P53	Homo sapiens	217-220
9528853-5	1998	By 8 days after a brief exposure to DNA strand breaking agents, bleomycin or actinomycin D, p53 protein is at baseline levels, while the p53 transactivation level is only slightly above its baseline.	Bleomycin	64-73	P53	Homo sapiens	92-95
9448010-4	1998	OA also induced RER accumulation of the IC protein p53/p58 via an IC-RER recycling pathway which was resistant to OA and inhibited by the G protein activator aluminium fluoride.	aluminum fluoride	158-176	P53	Homo sapiens	51-54
9388195-0	1997	Activation of adenomatous polyposis coli (APC) gene expression by the DNA-alkylating agent N-methyl-N"-nitro-N-nitrosoguanidine requires p53.	Methylnitronitrosoguanidine	91-127	P53	Homo sapiens	137-140
9365236-9	1997	The result was repeated with two additional human colon adenocarcinoma cell lines with the different p53 status, mutant p53-expressing DLD-1 and wild-type p53-expressing LoVo, suggesting that this phemonenon is a general event among human cancer cells.	phemonenon	197-207	P53	Homo sapiens	101-104
9365236-9	1997	The result was repeated with two additional human colon adenocarcinoma cell lines with the different p53 status, mutant p53-expressing DLD-1 and wild-type p53-expressing LoVo, suggesting that this phemonenon is a general event among human cancer cells.	phemonenon	197-207	P53	Homo sapiens	120-123
9365236-9	1997	The result was repeated with two additional human colon adenocarcinoma cell lines with the different p53 status, mutant p53-expressing DLD-1 and wild-type p53-expressing LoVo, suggesting that this phemonenon is a general event among human cancer cells.	phemonenon	197-207	P53	Homo sapiens	120-123
9321401-2	1997	Undifferentiated ES cells express high levels of p53 exclusively in the wild-type conformation, immunoprecipitable by monoclonal antibody PAb246, and p53 was found to be functionally active as determined by its ability to bind DNA specifically and to activate transcription of target genes.	pab246	138-144	P53	Homo sapiens	49-52
9368180-0	1997	Ex vivo treatment of bone marrow with phosphorothioate oligonucleotide OL(1)p53 for autologous transplantation in acute myelogenous leukemia and myelodysplastic syndrome.	oligonucleotide ol	55-73	P53	Homo sapiens	76-79
9380510-9	1997	Addition of anti-p53 antibody PAb421 (epitope 372-381 amino acids) inhibited the interaction with hRad51.	pab421	30-36	P53	Homo sapiens	17-20
9380755-6	1997	Enhanced mdr1a gene expression in the TDN p53 cells was not secondary to mdr1 gene amplification and Pgp was functional as demonstrated by the decreased uptake of vinblastine.	Vinblastine	163-174	P53	Homo sapiens	42-45
9389932-8	1997	Both m-AMCA and amsacrine induced p53 protein expression in proliferating but not in non-proliferating H460 cells, and induced p21WAF1 regardless of proliferation status.	methyl-N-(4-(9-acridinylamino)-2-methoxyphenyl)carbamate	5-11	P53	Homo sapiens	34-37
9308722-5	1997	Only 2 of 22 (9%) patients harbored a p53 mutation (which, interestingly, were identical and consisted of a codon 259 Asp --&gt; His exchange), despite diffuse overexpression of high levels of nuclear p53 protein in most cases.	Aspartic Acid	118-121	P53	Homo sapiens	38-41
9266962-0	1997	Transcriptional squelching by ectopic expression of E2F-1 and p53 is alleviated by proteasome inhibitors MG-132 and lactacystin.	lactacystin	116-127	P53	Homo sapiens	62-65
9266962-3	1997	Although the proteasome inhibitors MG-132 and lactacystin markedly increased the level of expression of E2F-1 and p53, these inhibitors completely alleviated squelching by both proteins.	lactacystin	46-57	P53	Homo sapiens	114-117
9244359-9	1997	Activation of p53 by PAb421 also results in enhanced transactivation in vitro.	pab421	21-27	P53	Homo sapiens	14-17
9815762-13	1997	Eighty-three percent of patients having low p53 expression had up-regulation of RAR-beta mRNA after isotretinoin therapy, compared with 22% of patients with high p53 expression (P = 0.003).	Isotretinoin	100-112	P53	Homo sapiens	44-47
9815762-14	1997	We correlated baseline p53 protein expression with RAR-beta modulation and clinical responses to isotretinoin therapy.	Isotretinoin	97-109	P53	Homo sapiens	23-26
9815762-17	1997	The patients with high p53 protein expression and either no change or down-regulation of RAR-beta had a response rate of only 14% to isotretinoin therapy.	Isotretinoin	133-145	P53	Homo sapiens	23-26
9219564-0	1997	Arsenic alters cytosine methylation patterns of the promoter of the tumor suppressor gene p53 in human lung cells: a model for a mechanism of carcinogenesis.	Cytosine	15-23	P53	Homo sapiens	90-93
9108075-0	1997	Cytosine methylation determines hot spots of DNA damage in the human P53 gene.	Cytosine	0-8	P53	Homo sapiens	69-72
9108075-2	1997	We have previously mapped the distribution of (+/-) anti-7beta,8alpha-dihydroxy-9alpha,10alpha-epoxy -7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE) adducts along the human P53 gene [Denissenko, M. F., Pao, A., Tang, M.-s. &amp; Pfeifer, G. P. (1996) Science 274, 430-432].	8alpha-dihydroxy-9alpha	63-86	P53	Homo sapiens	167-170
10763010-7	1997	CONCLUSIONS: Molecular studies of loss of heterozygosity and p53 gene mutations are advancing our understanding of field carcinogenesis and the biology, pharmacology, and effects of the retinoids used in cancer prevention.	Retinoids	186-195	P53	Homo sapiens	61-64
9112432-5	1997	Treatment of these drug-resistant cells with non-toxic doses of the resistance-inducing drug vinblastin induced a strong increase in p53 protein and mRNA but was ineffective on mdm2 protein expression, or mdr1 mRNA expression.	Vinblastine	93-103	P53	Homo sapiens	133-136
9008206-4	1997	Using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling, internucleosomal DNA ladders and flow cytometry, we correlated observed changes in p53 expression with the induction of apoptosis at low, intermediate and high doses of UVB radiation.	deoxyuridine triphosphate	53-78	P53	Homo sapiens	181-184
9107076-0	1997	Bcl-2 protein expression and p53 gene mutation in chronic lymphocytic leukemia: correlation with in vitro sensitivity to chlorambucil and purine analogs.	purine	138-144	P53	Homo sapiens	29-32
9038605-4	1996	In 4 cases, the mutations lead to distinct changes in the primary or secondary structure of the protein (cysteine--&gt;tyrosine, proline--&gt;leucine) and were associated with marked accumulation of p53 protein.	Leucine	142-149	P53	Homo sapiens	199-202
9042236-0	1996	Effects of microtubule inhibitors-taxol, vinblastine and estramustine on the growth and p53 gene expression in the hormone independent human prostatic JCA-1 cells.	Vinblastine	41-52	P53	Homo sapiens	88-91
19727814-0	2010	P53 and p38 MAPK pathways are involved in MONCPT-induced cell cycle G2/M arrest in human non-small cell lung cancer A549.	10-methoxy-9-nitrocamptothecin	42-48	P53	Homo sapiens	0-3
8900110-7	1996	Cells lacking the c-abl gene also responded to ara-C and MMS with increases in p53 levels and induction of p21.	Methyl Methanesulfonate	57-60	P53	Homo sapiens	79-82
19727814-8	2010	Moreover, down-regulation of p-AKT in A549 cells was seen after treated with 100.0 nM MONCPT for 12-48 h. Over-expression of p53 and p21 in A549 cells treated with MONCPT was observed in time-dependent manner.	10-methoxy-9-nitrocamptothecin	86-92	P53	Homo sapiens	125-128
19727814-8	2010	Moreover, down-regulation of p-AKT in A549 cells was seen after treated with 100.0 nM MONCPT for 12-48 h. Over-expression of p53 and p21 in A549 cells treated with MONCPT was observed in time-dependent manner.	10-methoxy-9-nitrocamptothecin	164-170	P53	Homo sapiens	125-128
8824527-12	1996	At this passage, mutation of the p53 gene was detected at codon 273 of exon 8, with G to T conversion (Arg to Leu).	Leucine	110-113	P53	Homo sapiens	33-36
19727814-9	2010	When wild type p53 expression was specifically inhibited by RNA-interference, A549 cells treated with MONCPT delayed the onset of G2/M arrest; meanwhile p-ERK and Cdc2 were up-regulated while p21 and CDK7 were down-regulated in A549 cells treated with MONCPT and p53 SiRNA transfection in contrast to cells treated with 100.0 nM MONCPT alone.	10-methoxy-9-nitrocamptothecin	102-108	P53	Homo sapiens	15-18
8763853-0	1996	The interaction of taxol and vinblastine with radiation induction of p53 and p21 WAF1/CIP1.	Vinblastine	29-40	P53	Homo sapiens	69-72
19727814-9	2010	When wild type p53 expression was specifically inhibited by RNA-interference, A549 cells treated with MONCPT delayed the onset of G2/M arrest; meanwhile p-ERK and Cdc2 were up-regulated while p21 and CDK7 were down-regulated in A549 cells treated with MONCPT and p53 SiRNA transfection in contrast to cells treated with 100.0 nM MONCPT alone.	10-methoxy-9-nitrocamptothecin	102-108	P53	Homo sapiens	263-266
8763853-4	1996	We examined the induction of p53 and its downstream target, p21WAF1/CIP1, by the microtubule active agents taxol and vinblastine with radiation.	Vinblastine	117-128	P53	Homo sapiens	29-32
8763853-5	1996	An increase in induction of both p53 and p21 WAF1/CIP1 was demonstrated when radiation was added to either taxol or vinblastine treatment.	Vinblastine	116-127	P53	Homo sapiens	33-36
19727814-9	2010	When wild type p53 expression was specifically inhibited by RNA-interference, A549 cells treated with MONCPT delayed the onset of G2/M arrest; meanwhile p-ERK and Cdc2 were up-regulated while p21 and CDK7 were down-regulated in A549 cells treated with MONCPT and p53 SiRNA transfection in contrast to cells treated with 100.0 nM MONCPT alone.	10-methoxy-9-nitrocamptothecin	252-258	P53	Homo sapiens	15-18
8706243-3	1996	Sublines that were resistant to melphalan, pyrazafurin, mitoxantrone, etoposide and PALA all retained expression of wild-type p53.	Melphalan	32-41	P53	Homo sapiens	126-129
19727814-9	2010	When wild type p53 expression was specifically inhibited by RNA-interference, A549 cells treated with MONCPT delayed the onset of G2/M arrest; meanwhile p-ERK and Cdc2 were up-regulated while p21 and CDK7 were down-regulated in A549 cells treated with MONCPT and p53 SiRNA transfection in contrast to cells treated with 100.0 nM MONCPT alone.	10-methoxy-9-nitrocamptothecin	252-258	P53	Homo sapiens	15-18
8706243-4	1996	Methotrexate-resistant MCF-7 cells were unusual heterozygotes that expressed a wild-type and dominant, in-frame p53 deletion mutant and the doxorubicin-resistant cells expressed only mutant p53.	Methotrexate	0-12	P53	Homo sapiens	112-115
8706243-4	1996	Methotrexate-resistant MCF-7 cells were unusual heterozygotes that expressed a wild-type and dominant, in-frame p53 deletion mutant and the doxorubicin-resistant cells expressed only mutant p53.	Methotrexate	0-12	P53	Homo sapiens	190-193
19727814-11	2010	Treatment with p38 mitogen-activated protein kinase (MAPK) SiRNA obviously inhibited p38 MAPK and delayed the G2/M arrest induced by 50.0 nM MONCPT after 48 h. CONCLUSION: Cell cycle regulators, AKT, p53, and MAPK, as therapeutic targets for MONCPT to induce cell cycle G2/M arrest in the context of anticancer therapy.	10-methoxy-9-nitrocamptothecin	141-147	P53	Homo sapiens	200-203
19892797-7	2010	Cokeoven workers were heavily exposed to PAHs (79% exceeded the urinary 1-pyrenol biological exposure index) and exhibited lower TL (P = 0.038) than controls, as well as higher levels of genetic and chromosomal alterations [i.e. anti-BPDE-DNA adduct and MN (P &lt; 0.0001)] and epigenetic changes [i.e. p53 gene-specific promoter and global methylation (P &lt;or= 0.001)].	Polycyclic Aromatic Hydrocarbons	41-45	P53	Homo sapiens	303-306
8800591-6	1996	Alterations in exons 4, 5 and 7 of the p53 gene in patients with functional adrenal tumours, including aldosterone-producing adenomas, have recently been described.	Aldosterone	103-114	P53	Homo sapiens	39-42
8666362-6	1996	Three (50%) BPB and WDFA stained for p53 and five (83%) for MDM2.	bpb	12-15	P53	Homo sapiens	37-40
20465648-9	2010	Slight but significant difference between A/B for p53 with major reduction post isotretinoin [0.66+/-0.31 vs. 0.94+/-0.34 respectively (P = 0.04) was observed.	Isotretinoin	80-92	P53	Homo sapiens	50-53
8669168-8	1996	RESULTS: Freeze substituted cells that were fixed with methanol/ether and stored for more than six months retained strong p53 positivity, as strong as that of the control cells, which had been fixed and stored in methanol.	Methanol	55-63	P53	Homo sapiens	122-125
8669168-8	1996	RESULTS: Freeze substituted cells that were fixed with methanol/ether and stored for more than six months retained strong p53 positivity, as strong as that of the control cells, which had been fixed and stored in methanol.	Ether	64-69	P53	Homo sapiens	122-125
20465648-12	2010	The role of ultra-violet induced p53 mutation in skin carcinogenesis reinforces retinoids chemoprevention.	Retinoids	80-89	P53	Homo sapiens	33-36
8622881-3	1996	A specific incorporation of the p53 gene with ACN53 reduced 3 (deleted p53 gene) cells was observed.	acn53	46-51	P53	Homo sapiens	32-35
19913028-8	2010	Destabilizing mutations cause DBD to misfold when it is part of the p53 tetramer, but not when it is monomeric.	dbd	30-33	P53	Homo sapiens	68-71
8622881-3	1996	A specific incorporation of the p53 gene with ACN53 reduced 3 (deleted p53 gene) cells was observed.	acn53	46-51	P53	Homo sapiens	71-74
19955567-6	2010	Furthermore, we characterize for the first time the binding behavior of Pifithrin-mu, a specific small molecule inhibitor of the p53-BclxL interaction, and present a structural model of the protein-ligand complex.	pifithrin	72-81	P53	Homo sapiens	129-132
8590759-1	1995	The effects of exogenous human p53 and its various mutants (Ala-141, His-175, His-194, Trp-248, His-273) on two key enzymes of purine uptake, adenosine deaminase (AD) and hypoxanthine phosphoribosyl transferase (HPRT), has been studied in Rat 1 immortalized fibroblasts and their sublines transformed by N-RAS or v-mos oncogenes.	purine	127-133	P53	Homo sapiens	31-34
20006625-10	2010	Results of FAK promoter activity and ChIP assays in A549 and H1299 cells indicated that bortezomib suppressed FAK activity through a p53-independent pathway.	Bortezomib	88-98	P53	Homo sapiens	133-136
7586163-5	1995	The results in Salmonella are consistent with a role for the PAH component of cigarette smoke in the base-substitution specificity found in the p53 gene of smoking-associated lung tumors.	Polycyclic Aromatic Hydrocarbons	61-64	P53	Homo sapiens	144-147
20096120-0	2010	Cancer cell sensitivity to bortezomib is associated with survivin expression and p53 status but not cancer cell types.	Bortezomib	27-37	P53	Homo sapiens	81-84
8579493-1	1995	The ability of exogenous p53 tumor-suppressor and activated N-PAS oncogene to influence differentiation state of human colon carcinoma LIM 1215 cells and their derivatives with acquired resistance to actinomycin D or methotrexate was analysed Introduction of retroviral construct expressing human wild-type (wt) p53 into LIM 1215 cells induced electron microscopic manifestations of enterocytic differentiation, i.e. caused an increase in the numbers of cells with microvilli, desmosomes and glandular-like lumens.	Methotrexate	217-229	P53	Homo sapiens	25-28
20096120-5	2010	RESULTS: We found that cancer cells with wild type p53 show a low level expression of survivin and are sensitive to treatment with bortezomib, while cancer cells with a mutant or null p53 show a high level expression of survivin and are resistant to bortezomib-mediated apoptosis induction.	Bortezomib	131-141	P53	Homo sapiens	51-54
8579493-7	1995	Comparison of expression of different electron microscopic features of cell differentiation and CEA expression in cell sublines selected for methotrexate-resistance and/or expressing exogenous constructs allows to suppose that p53 tumor-suppressor, PAS oncogene and dhfr gene amplification may lead to somewhat distinct differentiation states.	Methotrexate	141-153	P53	Homo sapiens	227-230
20096120-5	2010	RESULTS: We found that cancer cells with wild type p53 show a low level expression of survivin and are sensitive to treatment with bortezomib, while cancer cells with a mutant or null p53 show a high level expression of survivin and are resistant to bortezomib-mediated apoptosis induction.	Bortezomib	250-260	P53	Homo sapiens	51-54
20096120-7	2010	We further noted that modulation of survivin expression by bortezomib is dependent on p53 status but independent of cancer cell types.	Bortezomib	59-69	P53	Homo sapiens	86-89
19629643-3	2010	After treatment of cells with methyl methanesulfonate (MMS), Apak is phosphorylated by ATM kinase and dissociates from p53, resulting in p53 activation and induction of apoptosis.	Methyl Methanesulfonate	30-53	P53	Homo sapiens	119-122
19629643-3	2010	After treatment of cells with methyl methanesulfonate (MMS), Apak is phosphorylated by ATM kinase and dissociates from p53, resulting in p53 activation and induction of apoptosis.	Methyl Methanesulfonate	30-53	P53	Homo sapiens	137-140
7630633-0	1995	p53 independent G0/G1 arrest and apoptosis induced by a novel retinoid in human breast cancer cells.	Retinoids	62-70	P53	Homo sapiens	0-3
19629643-3	2010	After treatment of cells with methyl methanesulfonate (MMS), Apak is phosphorylated by ATM kinase and dissociates from p53, resulting in p53 activation and induction of apoptosis.	Methyl Methanesulfonate	55-58	P53	Homo sapiens	119-122
7630633-8	1995	Thus AHPN represents a novel retinoid that induces G0/G1 arrest and apoptosis via a unique pathway which appears to involve activation of known downstream effectors of p53 in a p53-independent manner.	Retinoids	29-37	P53	Homo sapiens	168-171
19629643-3	2010	After treatment of cells with methyl methanesulfonate (MMS), Apak is phosphorylated by ATM kinase and dissociates from p53, resulting in p53 activation and induction of apoptosis.	Methyl Methanesulfonate	55-58	P53	Homo sapiens	137-140
7790313-3	1995	Immunostaining revealed nuclear accumulation of p53 within 6 h after various stresses [heat shock, osmotic shock, heavy metal (Cd), blockers of the cellular respiratory system (NaN3), amino acid analogues (azetidine and canavanine), an inhibitor of protein synthesis (puromycin), and oxygen free radicals (H2O2)].	Puromycin	268-277	P53	Homo sapiens	48-51
21499441-6	2010	Both, NPM and NCL interact with p53 and hinder its phosphorylation at Serine 15 in response to bleomycin.	Bleomycin	95-104	P53	Homo sapiens	32-35
19934289-8	2009	CONCLUSIONS: This differential response of MM versus epithelial carcinomas to combination of nutlin-3 with bortezomib sheds new light on the role of p53 in bortezomib-induced apoptosis.	Bortezomib	156-166	P53	Homo sapiens	149-152
19548002-0	2009	Adenovirally mediated p53 overexpression diversely influence the cell cycle of HEp-2 and CAL 27 cell lines upon cisplatin and methotrexate treatment.	Methotrexate	126-138	P53	Homo sapiens	22-25
7805028-2	1995	These p53 analyses were included in a prospective trial of the retinoid isotretinoin (1.5 mg/kg/day for 3 months) in 40 patients (45 oral premalignant lesions).	Retinoids	63-71	P53	Homo sapiens	6-9
7805028-8	1995	An inverse relationship occurred between the levels of accumulated p53 protein and response to isotretinoin (P = 0.006).	Isotretinoin	95-107	P53	Homo sapiens	67-70
19548002-7	2009	RESULTS: In CAL 27 cells overexpression of p53 completely abrogated high S phase content observed in methotrexate-treated cells into a G1 and slight G2 arrest, while it sustained G2 arrest of the cells treated with cisplatin, along with the reduction of DNA synthesis and cyclin B1 expression.	Methotrexate	101-113	P53	Homo sapiens	43-46
19548002-8	2009	On the other hand, in HEp-2 cell line p53 overexpression slightly slowed down the progression through S phase in cells treated with methotrexate, decreased the cyclin B1 expression only after 24 h, and failed to sustain the G2 arrest after treatment with cisplatin alone.	Methotrexate	132-144	P53	Homo sapiens	38-41
7966288-5	1994	Two conformation-specific anti-p53 monoclonal antibodies were used to dissect the phage-p53 interaction, the phage were found to preferentially bind the PAb1620-p53 conformation rather than the PAb240-p53 conformation.	pab1620	153-160	P53	Homo sapiens	31-34
7966288-5	1994	Two conformation-specific anti-p53 monoclonal antibodies were used to dissect the phage-p53 interaction, the phage were found to preferentially bind the PAb1620-p53 conformation rather than the PAb240-p53 conformation.	pab1620	153-160	P53	Homo sapiens	88-91
7966288-5	1994	Two conformation-specific anti-p53 monoclonal antibodies were used to dissect the phage-p53 interaction, the phage were found to preferentially bind the PAb1620-p53 conformation rather than the PAb240-p53 conformation.	pab1620	153-160	P53	Homo sapiens	88-91
7966288-5	1994	Two conformation-specific anti-p53 monoclonal antibodies were used to dissect the phage-p53 interaction, the phage were found to preferentially bind the PAb1620-p53 conformation rather than the PAb240-p53 conformation.	pab1620	153-160	P53	Homo sapiens	88-91
19548002-10	2009	CONCLUSIONS: This study demonstrates that adenovirally mediated p53 overexpression at sub-cytotoxic levels enhanced the activity of low doses of cisplatin and methotrexate in HEp-2 and CAL 27 cells through changes in the cell cycle.	Methotrexate	159-171	P53	Homo sapiens	64-67
19555669-0	2009	Transcriptional down-regulation of Bcl-2 by vinorelbine: identification of a novel binding site of p53 on Bcl-2 promoter.	Vinorelbine	44-55	P53	Homo sapiens	99-102
7923176-11	1994	p53 allelic amino acid variation with sequences coding for aspartic acid or asparagine was present in codon 61 in the variable region of exon 4 in both HCCs and nonneoplastic tissues of ground squirrels.	Aspartic Acid	59-72	P53	Homo sapiens	0-3
8036011-0	1994	Oxy-radical induced mutagenesis of hotspot codons 248 and 249 of the human p53 gene.	oxy-radical	0-11	P53	Homo sapiens	75-78
19555669-5	2009	We report here that p53 contributes to vinorelbine-induced Bcl-2 down-regulation.	Vinorelbine	39-50	P53	Homo sapiens	20-23
19713938-1	2009	The p53-inducible TIGAR protein functions as a fructose-2,6-bisphosphatase, promoting the pentose phosphate pathway and helping to lower intracellular reactive oxygen species (ROS).	Pentosephosphates	90-107	P53	Homo sapiens	4-7
7946294-1	1994	A procedure for direct sequencing of the human p53 gene based on micro-dissection of frozen tumor tissue stained with methylene blue without prior fixation is described.	Methylene Blue	118-132	P53	Homo sapiens	47-50
8061893-5	1994	IHC assays revealed nuclear p53 immunostaining in 53% of cases (32 of 60) with PAb1801, 38% (23 of 60) with PAb421, and 32% (19 of 60) with PAb240.	pab421	108-114	P53	Homo sapiens	28-31
18930193-1	2009	OBJECTIVE: To determine whether the p53 codon 72 single nucleotide polymorphism, a change of the amino acid arginine (Arg) to proline (Pro) resulting from a single nucleotide mutation of guanine (G) to cytosine (C), has a clinically significant effect on implantation rate in fresh IVF cycles.	Guanine	187-194	P53	Homo sapiens	36-39
8162591-0	1994	Quercetin mediates the down-regulation of mutant p53 in the human breast cancer cell line MDA-MB468.	Quercetin	0-9	P53	Homo sapiens	49-52
8162591-4	1994	We have correlated these effects on cell proliferation with the observation that quercetin strongly inhibited, in a time- and dose-dependent fashion, the expression of the mutated p53 protein, which is the only form present at high levels in this cell line.	Quercetin	81-90	P53	Homo sapiens	180-183
8162591-6	1994	Quercetin did not affect the steady-state mRNA levels of p53, but prevented the accumulation of newly synthesized p53 protein.	Quercetin	0-9	P53	Homo sapiens	114-117
8162591-7	1994	This quercetin action appeared to be somewhat specific for p53 because the drug did not alter the amount of other proteins present in MDA-MB468 cells such as P-glycoprotein and did not prevent the induction of the synthesis of epidermal growth factor receptor in response to epidermal growth factor.	Quercetin	5-14	P53	Homo sapiens	59-62
18930193-1	2009	OBJECTIVE: To determine whether the p53 codon 72 single nucleotide polymorphism, a change of the amino acid arginine (Arg) to proline (Pro) resulting from a single nucleotide mutation of guanine (G) to cytosine (C), has a clinically significant effect on implantation rate in fresh IVF cycles.	Cytosine	202-210	P53	Homo sapiens	36-39
19452524-9	2009	The associations between lutein and tocopherol and TP53 and KRAS2 mutations were modified by IL6 genotype.	Tocopherols	36-46	P53	Homo sapiens	51-55
8114714-4	1994	We exposed human cell lines containing wild-type p53 alleles to several different DNA-damaging agents and found that agents which rapidly induce DNA strand breaks, such as ionizing radiation, bleomycin, and DNA topoisomerase-targeted drugs, rapidly triggered p53 protein elevations.	Bleomycin	192-201	P53	Homo sapiens	49-52
8114714-4	1994	We exposed human cell lines containing wild-type p53 alleles to several different DNA-damaging agents and found that agents which rapidly induce DNA strand breaks, such as ionizing radiation, bleomycin, and DNA topoisomerase-targeted drugs, rapidly triggered p53 protein elevations.	Bleomycin	192-201	P53	Homo sapiens	259-262
20448956-0	2009	Oligobenzamide proteomimetic inhibitors of the p53-hDM2 protein-protein interaction.	oligobenzamide	0-14	P53	Homo sapiens	47-50
8114714-6	1994	Furthermore, treatment of cells with the antimetabolite N(phosphonoacetyl)-L-aspartate (PALA) did not cause rapid p53 protein increases but resulted in delayed increases in p53 protein levels temporally correlated with the appearance of DNA strand breaks.	sparfosic acid	56-86	P53	Homo sapiens	173-176
8108114-5	1994	T402DE-induced NHDF foci senesced at the same time as untransfected cells, but the equivalent LFS foci all had increased proliferative potentials, with the greatest increase being seen in clones that lost the wt p53 allele.	t402de	0-6	P53	Homo sapiens	212-215
20448956-1	2009	Oligobenzamide inhibitors of the p53-hDM2 protein-protein interaction are described.	oligobenzamide	0-14	P53	Homo sapiens	33-36
19579043-3	2009	At 5-10 muM concentrations, rhizochalin was effective as an inhibitor of the malignant transformation of JB6 P(+) Cl 41 cells or colony formation of human tumor cells, which exerted its action, at least in part, through the induction of p53-dependent apoptosis.	rhizochalin	28-39	P53	Homo sapiens	237-240
7849743-4	1994	The high incidence of C-to-T transitions found in the p53 tumor-suppressor gene is attributed to the spontaneous deamination of 5-methylcytosine residues.	5-Methylcytosine	128-144	P53	Homo sapiens	54-57
19531487-2	2009	In the present study, a mass spectrometry-based approach was used to analyze the effects of cytosine methylation on the kinetics of AGT repair of O(6)-methyldeoxyguanosine (O(6)-Me-dG) adducts placed within frequently mutated 5"-CG-3" dinucleotides of the p53 tumor suppressor gene.	Cytosine	92-100	P53	Homo sapiens	256-259
8302593-9	1994	The first detected electromobility shift of 32P-labelled DNA and was carried out in the presence of PAb421, which stabilises and supershifts p53-DNA complexes.	pab421	100-106	P53	Homo sapiens	141-144
19531487-7	2009	In contrast, cytosine methylation within p53 codon 158 slightly increased the rate of O(6)-Me-dG repair by AGT.	Cytosine	13-21	P53	Homo sapiens	41-44
19328766-4	2009	Deneddylase-1 (DEN1/NEDP1/SENP8) features a selective peptidase activity converting the proNEDD8 precursor to its mature form and an isopeptidase activity deconjugating NEDD8 from substrates such as cullins and p53.	pronedd8	88-96	P53	Homo sapiens	211-214
8321226-4	1993	IR, UV radiation, and methylmethane sulfonate were found to induce p53 activity when a stably integrated reporter construct containing functional p53-binding sites was used and also in mobility shift assays with a p53-binding site from the GADD45 gene, and IR-inducible gene previously associated with growth arrest.	Methyl Methanesulfonate	22-45	P53	Homo sapiens	67-70
8321226-4	1993	IR, UV radiation, and methylmethane sulfonate were found to induce p53 activity when a stably integrated reporter construct containing functional p53-binding sites was used and also in mobility shift assays with a p53-binding site from the GADD45 gene, and IR-inducible gene previously associated with growth arrest.	Methyl Methanesulfonate	22-45	P53	Homo sapiens	146-149
8321226-4	1993	IR, UV radiation, and methylmethane sulfonate were found to induce p53 activity when a stably integrated reporter construct containing functional p53-binding sites was used and also in mobility shift assays with a p53-binding site from the GADD45 gene, and IR-inducible gene previously associated with growth arrest.	Methyl Methanesulfonate	22-45	P53	Homo sapiens	146-149
8477265-0	1993	Detection of point mutations in the p53 gene: comparison of single-strand conformation polymorphism, constant denaturant gel electrophoresis, and hydroxylamine and osmium tetroxide techniques.	Hydroxylamine	146-159	P53	Homo sapiens	36-39
19337030-3	2009	Our study showed that the proteasome inhibitor lactacystin induced an increase in p53 level and autophagy activity, whereas inhibition of p53 by pifithrin-alpha or small interference RNA (siRNA) of p53 attenuated the autophagy induction and increased protein aggregation.	lactacystin	47-58	P53	Homo sapiens	82-85
1995413-2	1991	This p53val135 mutant is temperature sensitive for a conformational change detected by the binding of a monoclonal antibody, PAb246, which recognizes the wild-type protein or the great majority of p53val135 at 32.5 degrees C. At 37 degrees C, both mutant and wild-type p53 conformational forms co-exist in the cells, while at 39.5 degrees C, the majority of the p53val135 in the cell is in a mutant conformation not recognized by PAb246 antibody.	pab246	125-131	P53	Homo sapiens	5-8
1995413-2	1991	This p53val135 mutant is temperature sensitive for a conformational change detected by the binding of a monoclonal antibody, PAb246, which recognizes the wild-type protein or the great majority of p53val135 at 32.5 degrees C. At 37 degrees C, both mutant and wild-type p53 conformational forms co-exist in the cells, while at 39.5 degrees C, the majority of the p53val135 in the cell is in a mutant conformation not recognized by PAb246 antibody.	pab246	125-131	P53	Homo sapiens	197-200
1995413-2	1991	This p53val135 mutant is temperature sensitive for a conformational change detected by the binding of a monoclonal antibody, PAb246, which recognizes the wild-type protein or the great majority of p53val135 at 32.5 degrees C. At 37 degrees C, both mutant and wild-type p53 conformational forms co-exist in the cells, while at 39.5 degrees C, the majority of the p53val135 in the cell is in a mutant conformation not recognized by PAb246 antibody.	pab246	430-436	P53	Homo sapiens	5-8
19337030-3	2009	Our study showed that the proteasome inhibitor lactacystin induced an increase in p53 level and autophagy activity, whereas inhibition of p53 by pifithrin-alpha or small interference RNA (siRNA) of p53 attenuated the autophagy induction and increased protein aggregation.	lactacystin	47-58	P53	Homo sapiens	138-141
19337030-3	2009	Our study showed that the proteasome inhibitor lactacystin induced an increase in p53 level and autophagy activity, whereas inhibition of p53 by pifithrin-alpha or small interference RNA (siRNA) of p53 attenuated the autophagy induction and increased protein aggregation.	lactacystin	47-58	P53	Homo sapiens	138-141
19337030-7	2009	Further autophagy induction with rapamycin protects DA neurons from lactacystin-mediated cell death by downregulating p53 and its related apoptotic pathways and by inducing autophagy to degrade aggregated proteins.	lactacystin	68-79	P53	Homo sapiens	118-121
19217709-6	2009	We report herein that lung cancer cell lines expressing wild-type p53, when exposed to cisplatin treatment, induced COX-2 (mRNA and protein), with concurrent synthesis of prostaglandins (PGE(2)).	Prostaglandins E	187-190	P53	Homo sapiens	66-69
19216720-7	2009	Attenuation of PARP-1 [poly(ADP-ribose) polymerase-1] cleavage as well as oligonucleosomal DNA fragmentation in the presence of z-VAD-fmk points toward a major involvement of a caspase-dependent pathway in staurosporine-induced apoptosis in p53wt HeLa cells, which is not the case in p53mt C-33A cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	128-137	P53	Homo sapiens	241-244
19216720-7	2009	Attenuation of PARP-1 [poly(ADP-ribose) polymerase-1] cleavage as well as oligonucleosomal DNA fragmentation in the presence of z-VAD-fmk points toward a major involvement of a caspase-dependent pathway in staurosporine-induced apoptosis in p53wt HeLa cells, which is not the case in p53mt C-33A cells.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	128-137	P53	Homo sapiens	284-287
19424582-5	2009	From 117 kinds of chemicals (34 kinds of natural compounds that are obtained from herbal plants, 53 kinds of flavonoid, and 31 kinds of phenolic compounds), we find that quercetin works as an activator of p53 in K-Ras mutated cells but not in wild-type cells.	Quercetin	170-179	P53	Homo sapiens	205-208
19424582-6	2009	Treatment with quercetin can induce p53 target genes such as PUMA and p21.	Quercetin	15-24	P53	Homo sapiens	36-39
19424582-7	2009	These results suggest that although quercetin has limitations for use as a therapeutic drug due to its broad effects, specific function of it on K-Ras-p53 may be useful for K-Ras-induced cancer prevention and therapy through further development.	Quercetin	36-45	P53	Homo sapiens	151-154
19549370-6	2009	The expression of NF-kappaB mRNA and p53 mRNA decreased after treatment with bortezomib.	Bortezomib	77-87	P53	Homo sapiens	37-40
19549370-8	2009	NF-kappaB and p53 gene are supposed to participate in the bortezomib induced apoptosis of Raji cells.	Bortezomib	58-68	P53	Homo sapiens	14-17
19135778-6	2009	Apoptosis caused by honokiol was also concomitant with the cleavage of caspases (caspase-3, -8, and -9) and Bid along with the suppressive expression of Bcl-2, but it was independent on the expression of Bax and p53.	honokiol	20-28	P53	Homo sapiens	212-215
19362839-0	2009	Protective effects of a benzoxazine derivative against oxidized LDL-induced apoptosis and the increases of integrin beta4, ROS, NF-kappaB and P53 in human umbilical vein endothelial cells.	Benzoxazines	24-35	P53	Homo sapiens	142-145
19439228-9	2009	In parallel, p53 is activated, leading to a range of regulations typical for cell-cycle-arrested cells such as upregulation of CDKN1A, induction of GADD45, inhibition of eIF5A maturation, and reduced phosphorylation of stathmin.	gadd45	148-154	P53	Homo sapiens	13-16
19287975-7	2009	In RT112 cells, which express high levels of ErbB receptors and harbour wild-type p53, combined GTC/lapatinib treatment resulted in the phosphorylation of p53 at Ser46 and accumulation of sub-G1 cell populations.	Lapatinib	100-109	P53	Homo sapiens	82-85
19287975-7	2009	In RT112 cells, which express high levels of ErbB receptors and harbour wild-type p53, combined GTC/lapatinib treatment resulted in the phosphorylation of p53 at Ser46 and accumulation of sub-G1 cell populations.	Lapatinib	100-109	P53	Homo sapiens	155-158
19153082-2	2009	The p53 residues Leu(26), Trp(23), and Phe(19) are crucial to mediate these interactions.	Leucine	17-20	P53	Homo sapiens	4-7
18718551-0	2009	Selenocystine induces caspase-independent apoptosis in MCF-7 human breast carcinoma cells with involvement of p53 phosphorylation and reactive oxygen species generation.	selenocystine	0-13	P53	Homo sapiens	110-113
18472237-0	2009	p53 expression in concurrent chemoradiotherapy with docetaxel for head and neck squamous cell carcinoma.	Docetaxel	52-61	P53	Homo sapiens	0-3
18472237-1	2009	BACKGROUND: The current study aimed to evaluate the significance of an immunohistochemical assessment of tumor suppressor p53 as a prognostic marker in head and neck squamous cell carcinoma (HNSCC) patients treated with docetaxel and radiotherapy.	Docetaxel	220-229	P53	Homo sapiens	122-125
18472237-2	2009	METHODS: The expression of tumor suppressor p53 and its phosphorylated form at the Ser392 residue was retrospectively evaluated by immunohistochemistry in 51 Stage T1-3N0-2M0 (except T1N0 glottis) HNSCC patients who were treated with 10mg/m(2)/week docetaxel four to six times and received concurrent chemoradiotherapy.	Docetaxel	249-258	P53	Homo sapiens	44-47
19267667-1	2009	Pifithrin alpha (PFTalpha), one of the first known low molecular weight modulators of activity of tumor suppressor p53, increases survival of hemopoietic clonogenic cells (evaluated by the criterion of formation of endogenous spleen CFU-C8 colonies in irradiated animals).	pifithrin	0-15	P53	Homo sapiens	115-118
19267667-1	2009	Pifithrin alpha (PFTalpha), one of the first known low molecular weight modulators of activity of tumor suppressor p53, increases survival of hemopoietic clonogenic cells (evaluated by the criterion of formation of endogenous spleen CFU-C8 colonies in irradiated animals).	pifithrin	17-25	P53	Homo sapiens	115-118
19068089-5	2009	In addition, among the members of the BH3-only family, upregulation of Noxa was consistently seen at both the transcriptional and protein levels in a p53-independent manner after exposure to bortezomib.	Bortezomib	191-201	P53	Homo sapiens	150-153
19127257-16	2009	Melanoma lines expressing p53 wild-type were more resistant to TMZ and fotemustine than p53 mutant melanoma lines, which is in marked contrast to previous data reported for glioma cells treated with TMZ.	fotemustine	71-82	P53	Homo sapiens	26-29
19147762-7	2009	Treatment of cervical cancer cells with bortezomib elevated the level of p53 but not hDlg, hScribble or hMAGI.	Bortezomib	40-50	P53	Homo sapiens	73-76
19275612-3	2009	Immunoblot assay showed that chalcones significantly decreased the expression of cyclin Bl, cyclin A and Cdc2 protein, as well as increased the expression of p21 and p27 in a p53-independent manner, contributing to cell cycle arrest.	Chalcones	29-38	P53	Homo sapiens	175-178
18459128-4	2009	Further, the treatment of A549 cells with pifithrin-alpha, a specific inhibitor of p53, or transfection of A549 cells with a p53 antisense oligodeoxynucleotide resulted in a reduction in the berberine-induced inhibition of cell proliferation and apoptosis.	pifithrin	42-51	P53	Homo sapiens	83-86
18459128-4	2009	Further, the treatment of A549 cells with pifithrin-alpha, a specific inhibitor of p53, or transfection of A549 cells with a p53 antisense oligodeoxynucleotide resulted in a reduction in the berberine-induced inhibition of cell proliferation and apoptosis.	pifithrin	42-51	P53	Homo sapiens	125-128
19088023-11	2008	Endogenous miR-192 expression was increased in HCT-116 (wt-p53) and RKO (wt-p53) cells treated with methotrexate, which caused an induction of p53 expression.	Methotrexate	100-112	P53	Homo sapiens	59-62
19088023-11	2008	Endogenous miR-192 expression was increased in HCT-116 (wt-p53) and RKO (wt-p53) cells treated with methotrexate, which caused an induction of p53 expression.	Methotrexate	100-112	P53	Homo sapiens	76-79
19088023-11	2008	Endogenous miR-192 expression was increased in HCT-116 (wt-p53) and RKO (wt-p53) cells treated with methotrexate, which caused an induction of p53 expression.	Methotrexate	100-112	P53	Homo sapiens	76-79
18703674-7	2008	Over-expression of p53 resulted in reduced accumulation of a marker of proliferation (cyclin B1), P(4), and PGF secretion and increased OT and PGE secretion.	Prostaglandins E	143-146	P53	Homo sapiens	19-22
18813780-11	2008	Incubation with either the irreversible pan-caspase inhibitors Z-VAD-FMK, or SP600125, a selective inhibitor of JNK, or pifithrin alpha, a potent p53 inhibitor, significantly inhibited the effects induced by PTX.	pyrazolanthrone	77-85	P53	Homo sapiens	146-149
1853683-8	1991	These data suggest that IP staining with PAb421 can be used to demonstrate high p53 expression in B cell leukemias.	pab421	41-47	P53	Homo sapiens	80-83
18813780-11	2008	Incubation with either the irreversible pan-caspase inhibitors Z-VAD-FMK, or SP600125, a selective inhibitor of JNK, or pifithrin alpha, a potent p53 inhibitor, significantly inhibited the effects induced by PTX.	pifithrin	120-135	P53	Homo sapiens	146-149
18813348-6	2008	Suppression of Hsf1 in A1-5 cells with quercetin or an Hsf1 siRNA reduced p53 nuclear importation and inhibited p53-mediated activation of a p21 reporter.	Quercetin	39-48	P53	Homo sapiens	74-77
1844242-0	1991	5-Methylcytosine as an endogenous mutagen in the p53 tumor suppressor gene.	5-Methylcytosine	0-16	P53	Homo sapiens	49-52
1844242-7	1991	The results suggest that 5mC may play a substantial role as an endogenous mutagen in the p53 gene and that the generation of these mutations does not require the direct interaction of a carcinogen with DNA.	5-Methylcytosine	25-28	P53	Homo sapiens	89-92
1844242-11	1991	Assessment of the proportion of 5mC induced mutations in the p53 gene therefore allows for an estimate of the relative importance of endogenous and exogenous mechanisms of carcinogenesis.	5-Methylcytosine	32-35	P53	Homo sapiens	61-64
18712872-1	2008	Chlorofusin is a recently isolated, naturally occurring inhibitor of p53-MDM2 complex formation whose structure is composed of a densely functionalized azaphilone-derived chromophore linked through the terminal amine of ornithine to a nine residue cyclic peptide.	Amines	211-216	P53	Homo sapiens	69-72
17530438-0	2008	Arsenic trioxide induces different gene expression profiles of genes related to growth and apoptosis in glioma cells dependent on the p53 status.	Arsenic Trioxide	0-16	P53	Homo sapiens	134-137
2254323-7	1990	N alpha-Acetyl[D-Phe45, Arg47] hirudin45-65 (P53) emerged as a pure competitive inhibitor with a Ki = 2.8 +/- 0.9 nM and IC50 = 4.0 +/- 0.8 nM (human alpha-thrombin) and is designated as a "bifunctional" inhibitor.	d-phe45	15-22	P53	Homo sapiens	45-48
18790767-3	2008	Mechanistically, bortezomib induced a G2-M-phase cell cycle arrest and p53-independent apoptosis associated with caspase cleavage and Noxa induction.	Bortezomib	17-27	P53	Homo sapiens	71-74
33817171-4	2019	The activation of AMPKalpha induced changes of downstream proteins, including increase of P53 phosphorylation and P21 production, as well as decrease of mTOR phosphorylation, that eventually inhibited C6 cells growth.	ampkalpha	18-27	P53	Homo sapiens	90-93
18790779-2	2008	Here, we show that treatment of HCT-116 (p53+/+) colon carcinoma cells with the novel antitumor antibiotic mithramycin SK (MSK) results in polyploidization and mitotic catastrophe, which occurs after a transient halt in G1 phase followed by the overtaking of the G2-M checkpoint when treated cells are incubated in a fresh drug-free medium.	Plicamycin	107-118	P53	Homo sapiens	41-44
18446786-4	2008	Stilbene-induced apoptosis was concentration-dependent, and associated with ERK1/2 activation, serine-15 p53 phosphorylation and nuclear accumulation of these proteins.	Stilbenes	0-8	P53	Homo sapiens	105-108
34958576-4	2022	Hoping to create a novel class of membrane-permeable PPI inhibitors, the phenylalanine, tryptophan, and leucine residues that play a critical role in inhibiting the p53-HDM2 interaction were grafted into the framework of CADY2 a cell-penetrating peptide (CPP) having a helical propensity.	Leucine	104-111	P53	Homo sapiens	165-168
34945706-4	2021	MDA-MB-231 (p53-p.R280K mutant) and MCF-7 (wild-type p53) breast tumor cells and MCF-10A non-tumoral cells were exposed to GTE for 24-48 h and cell viability was assessed in the presence of p53 inhibitor pifithrin-alpha.	pifithrin	204-219	P53	Homo sapiens	190-193
34959709-8	2021	Moreover, treatment with the p53 inhibitor pifithrin-alpha (PFT-alpha) inhibited autophagy and increased apoptotic response in MLPE-treated HepG2 cells.	pifithrin	43-58	P53	Homo sapiens	29-32
34959709-8	2021	Moreover, treatment with the p53 inhibitor pifithrin-alpha (PFT-alpha) inhibited autophagy and increased apoptotic response in MLPE-treated HepG2 cells.	pifithrin	60-69	P53	Homo sapiens	29-32
34959709-10	2021	Thus, co-treatment with MLPE and PFT-alpha significantly increased caspase-3, caspase-8, and cytochrome c release, indicating that p53 deficiency caused the apoptosis.	pifithrin	33-42	P53	Homo sapiens	131-134
18547707-10	2008	Pifithrin alpha, a p53 transcriptional inhibitor, increases Cr (VI) cytotoxicity, suggesting a role of p53 as a survival molecule.	pifithrin	0-15	P53	Homo sapiens	19-22
34959382-3	2021	Cell cycle analysis proved that Pt-8AQ significantly affected the cell cycle pattern by increasing the apoptotic cells represented by the sub G0/G1 region related with a downregulation of p53 and Bcl-2.	pt-8aq	32-38	P53	Homo sapiens	188-191
34967559-4	2021	Therefore, this study aimed to investigate XPD Lys751Gln and TP53 Arg72Pro polymorphisms on the risk of platinum-based chemotherapy-induced toxicity in lung cancer patients in the Bangladeshi population.	arg72pro	66-74	P53	Homo sapiens	61-65
18547707-10	2008	Pifithrin alpha, a p53 transcriptional inhibitor, increases Cr (VI) cytotoxicity, suggesting a role of p53 as a survival molecule.	pifithrin	0-15	P53	Homo sapiens	103-106
34967559-9	2021	Similar results were found between neutropenia, leukopenia, thrombocytopenia and gastrointestinal toxicities and XPD Lys751Gln or TP53 Arg72Pro genetic polymorphisms.	arg72pro	135-143	P53	Homo sapiens	130-134
18642443-1	2008	We have previously shown that tetraploid cancer cells succumb through a p53-dependent apoptotic pathway when checkpoint kinase 1 (Chk1) is depleted by small interfering RNAs (siRNAs) or inhibited with 7-hydroxystaurosporine (UCN-01).	7-hydroxystaurosporine	201-223	P53	Homo sapiens	72-75
34832966-9	2021	Treatment of SK-N-FI and SK-N-Be(2) cells with doxorubicin, etoposide, cisplatin, and melphalan increased apoptosis and blocked the cycle in G2/M, while retinoic acid isomers induced apoptosis and decreased the percentage of cells in S phase in TP53 mutated SK-N-FI cells, but not in TP53 wild-type SK-N-Be(2) cells.	sk-n-be	25-32	P53	Homo sapiens	245-249
18439434-6	2008	In this report, we studied by means of immunoprecipitation analysis, the levels of markers of protein oxidation, 3-nitrotyrosine (3-NT) and protein carbonyls, in p53 in a specific region of the cerebral cortex, namely the inferior parietal lobule, in MCI and AD compared to control brains.	3-nitrotyrosine	130-134	P53	Homo sapiens	162-165
34759291-7	2021	We observed that a combination of AZD5363 and AZD8055 treatment synergizes antiproliferative activity on p53 mutated or wild-type HCC cell lines and induces apoptotic cell death.	(5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol	46-53	P53	Homo sapiens	105-108
34759291-8	2021	Mechanistic insights indicate that a combination of AZD5363 and AZD8055 activated FOXO3a to induce Bim-associated apoptosis in p53 mutated HCC cells, whereas cells retaining functional p53 enhanced Bax.	(5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol	64-71	P53	Homo sapiens	127-130
18474878-9	2008	The combination of low p53 and high Bcl-xL expression was associated with poor OS (P = .005) and DSS (P = .002).	dss	97-100	P53	Homo sapiens	23-26
34711990-4	2022	Focusing on cancers driven by HER2 amplification, we find that TFOs targeting HER2 induce copy number-dependent DNA double-strand breaks (DSBs) and activate p53-independent apoptosis in HER2-positive cancer cells and human tumor xenografts via a mechanism that is independent of HER2 cellular function.	tfos	63-67	P53	Homo sapiens	157-160
34707773-7	2021	More importantly, STAT3 overexpression, SLC7A11 overexpression, and pretreatment with pifithrin-alpha (P53 inhibitor) rescued OS cell ferroptosis induced by bavachin.	pifithrin	86-101	P53	Homo sapiens	103-106
18559532-4	2008	In this study, we show that Tax sensitizes p53-mutant cells to a broad range of DNA-damaging agents, including mitomycin C, a bifunctional alkylator, etoposide, a topoisomerase II drug, and UV light, but not ionizing radiation, a double-strand break agent, or vinblastine, a tubulin poison.	Vinblastine	260-271	P53	Homo sapiens	43-46
18353898-6	2008	Abolishment of the increase in p53 protein in ZS cells with transfection of p53 siRNA normalized the elevated p21 protein to a similar level as in ZN control cells, which demonstrated that the p21 induction is p53 dependent.	Zinc	147-149	P53	Homo sapiens	31-34
34660782-11	2021	This study revealed that SZRD has the characteristics and advantages of "multicomponent, multitarget, and multipathway" in the treatment of PDSD; among these, the combination of the main active components of quercetin and kaempferol with the key targets of AKT1, IL6, MAPK1, TP53, and VEGFA may be one of the important mechanisms.	Quercetin	208-217	P53	Homo sapiens	275-279
18353898-6	2008	Abolishment of the increase in p53 protein in ZS cells with transfection of p53 siRNA normalized the elevated p21 protein to a similar level as in ZN control cells, which demonstrated that the p21 induction is p53 dependent.	Zinc	147-149	P53	Homo sapiens	76-79
18353898-6	2008	Abolishment of the increase in p53 protein in ZS cells with transfection of p53 siRNA normalized the elevated p21 protein to a similar level as in ZN control cells, which demonstrated that the p21 induction is p53 dependent.	Zinc	147-149	P53	Homo sapiens	76-79
18448277-5	2008	Inhibition of p53 by either its inhibitor pifithrin-alpha or p53 siRNA markedly increased B(a)P-induced the activation of c-Jun, Akt and ERK in this context.	pifithrin	42-51	P53	Homo sapiens	14-17
34469060-12	2021	Inhibition of p53 by PFT-alpha partially restored the levels of PD-L1 and miR-34a-5p.	pifithrin	21-30	P53	Homo sapiens	14-17
34589431-0	2021	Four and a Half LIM Domains Protein 2 Mediates Bortezomib-Induced Osteogenic Differentiation of Mesenchymal Stem Cells in Multiple Myeloma Through p53 Signaling and beta-Catenin Nuclear Enrichment.	Bortezomib	47-57	P53	Homo sapiens	147-150
18084327-0	2008	Enhancement of radiation response in p53-deficient cancer cells by the Aurora-B kinase inhibitor AZD1152.	2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphate	97-104	P53	Homo sapiens	37-40
34589431-12	2021	In conclusion, FHL2 is critical for Bzb-induced osteoblast differentiation of MM-MSCs and promotes the osteogenesis, through p53 signaling and beta-catenin activation.	Bortezomib	36-39	P53	Homo sapiens	125-128
18483253-5	2008	We present evidence that zinc supplementation to HIPK2i cells increased p53 reactivity to conformation-sensitive PAb1620 (wild-type conformation) antibody and restored p53 sequence-specific DNA binding in vivo and transcription of target genes in response to Adriamycin treatment.	pab1620	113-120	P53	Homo sapiens	72-75
18451217-2	2008	Epigenetic alterations affect genetic events: Loss of MGMT via hypermethylation reportedly predisposes to guanine-to-adenine or cytosine-to-thymine (G:C--&gt;A:T) transition mutations in KRAS and P53, and silencing of hMLH1 leads to high levels of microsatellite instability (MSI-H)/mutator phenotype, suggesting that epigenetic-genetic subtypes exist.	Guanine	106-113	P53	Homo sapiens	196-199
34258884-6	2021	Additionally, mechanistic investigations reveal that pulsed triboelectric stimulation by P-TENG rejuvenates senescent BMSCs by enhancing MDM2-dependent p53 degradation, which is demonstrated by loss-of-function studies of MDM2 and p53.	p-teng	89-95	P53	Homo sapiens	152-155
34258884-6	2021	Additionally, mechanistic investigations reveal that pulsed triboelectric stimulation by P-TENG rejuvenates senescent BMSCs by enhancing MDM2-dependent p53 degradation, which is demonstrated by loss-of-function studies of MDM2 and p53.	p-teng	89-95	P53	Homo sapiens	231-234
34688317-9	2021	We demonstrated that PC-CP had a more significant alteration effect on mTOR, P-Ak, LC3 and P53.	pc-cp	21-26	P53	Homo sapiens	91-94
18451217-2	2008	Epigenetic alterations affect genetic events: Loss of MGMT via hypermethylation reportedly predisposes to guanine-to-adenine or cytosine-to-thymine (G:C--&gt;A:T) transition mutations in KRAS and P53, and silencing of hMLH1 leads to high levels of microsatellite instability (MSI-H)/mutator phenotype, suggesting that epigenetic-genetic subtypes exist.	Cytosine	128-136	P53	Homo sapiens	196-199
34659819-0	2021	miR-488-5p promotes esophageal squamous cell carcinoma progression by suppressing the P53 pathway.	mir-488-5p	0-10	P53	Homo sapiens	86-89
34659819-12	2021	Similarly, the miR-488-5p inhibitor induced the expression of P53 and P21 than normal control (NC) group in which miR-488-5p expression was normal, while P53 KD prevented the effects of the miR-488-5p inhibitor in KYSE-150 cells.	mir-488-5p	15-25	P53	Homo sapiens	62-65
18489080-12	2008	However, mutations at guanine bases observed with either PAH-treatment occurred randomly throughout the DNA-binding domain of p53.	Guanine	22-29	P53	Homo sapiens	126-129
34659819-12	2021	Similarly, the miR-488-5p inhibitor induced the expression of P53 and P21 than normal control (NC) group in which miR-488-5p expression was normal, while P53 KD prevented the effects of the miR-488-5p inhibitor in KYSE-150 cells.	mir-488	190-197	P53	Homo sapiens	154-157
34659819-12	2021	Similarly, the miR-488-5p inhibitor induced the expression of P53 and P21 than normal control (NC) group in which miR-488-5p expression was normal, while P53 KD prevented the effects of the miR-488-5p inhibitor in KYSE-150 cells.	CHEMBL3740941	198-200	P53	Homo sapiens	154-157
34659819-15	2021	Conclusions: Our results suggest that miR-488-5p promotes ESCC progression by suppressing the P53 pathway.	mir-488-5p	38-48	P53	Homo sapiens	94-97
18434539-3	2008	p53 is activated in normal cells starved for pyrimidine nucleotides by treatment with N-(phosphonacetyl)-l-aspartate (PALA).	sparfosic acid	86-116	P53	Homo sapiens	0-3
18434539-9	2008	We propose that p53 is activated by stimulation of mismatch repair in response to the misincorporation of deoxynucleotides into newly synthesized DNA, long before the lack of pyrimidine nucleoside triphosphates causes the rate of DNA synthesis to slow appreciably.	pyrimidine nucleoside triphosphates	175-210	P53	Homo sapiens	16-19
34476069-0	2021	Arsenic trioxide targets Hsp60, triggering degradation of p53 and survivin.	Arsenic Trioxide	0-16	P53	Homo sapiens	58-61
18323654-0	2008	Stabilization of p53 is involved in quercetin-induced cell cycle arrest and apoptosis in HepG2 cells.	Quercetin	36-45	P53	Homo sapiens	17-20
34476069-7	2021	Significantly, the binding of ATO to Hsp60 disrupts the formation of Hsp60-p53 and Hsp60-survivin complexes, resulting in degradation of p53 and survivin.	Arsenic Trioxide	30-33	P53	Homo sapiens	75-78
34476069-7	2021	Significantly, the binding of ATO to Hsp60 disrupts the formation of Hsp60-p53 and Hsp60-survivin complexes, resulting in degradation of p53 and survivin.	Arsenic Trioxide	30-33	P53	Homo sapiens	137-140
34205698-7	2021	To support these data, Western blot analysis was performed to analyze glucose-6-phosphate dehydrogenase (G6PD), TP53-induced glycolysis and the apoptosis regulator (TIGAR), and the glutamate cysteine ligase catalytic (GCLC) subunit, as they represent the main regulators of the pentose phosphate pathway (PPP) and glutathione synthesis, respectively.	Pentosephosphates	278-295	P53	Homo sapiens	112-116
18323654-3	2008	In the present study, we attempted to reactivate p53 in HepG2 retaining wild-type p53 by quercetin, an ubiquitous bioactive plant flavonoid.	Quercetin	89-98	P53	Homo sapiens	49-52
18323654-3	2008	In the present study, we attempted to reactivate p53 in HepG2 retaining wild-type p53 by quercetin, an ubiquitous bioactive plant flavonoid.	Quercetin	89-98	P53	Homo sapiens	82-85
18323654-3	2008	In the present study, we attempted to reactivate p53 in HepG2 retaining wild-type p53 by quercetin, an ubiquitous bioactive plant flavonoid.	Flavonoids	130-139	P53	Homo sapiens	49-52
34126912-2	2022	Among similar compounds, monastrol being the most prominent due to cell-permeant inhibitor of mitosis therefore, we investigated the new Pyrimidine-5-carbonitrile as a cytotoxic agent for p53 pathway.	5-Cyanopyrimidine	137-162	P53	Homo sapiens	188-191
18323654-5	2008	Molecular data revealed that quercetin induced p53 phosphorylation and total p53 protein, but that it did not up-regulate p53 mRNA at the transcription level.	Quercetin	29-38	P53	Homo sapiens	47-50
18323654-5	2008	Molecular data revealed that quercetin induced p53 phosphorylation and total p53 protein, but that it did not up-regulate p53 mRNA at the transcription level.	Quercetin	29-38	P53	Homo sapiens	77-80
18323654-5	2008	Molecular data revealed that quercetin induced p53 phosphorylation and total p53 protein, but that it did not up-regulate p53 mRNA at the transcription level.	Quercetin	29-38	P53	Homo sapiens	77-80
18323654-8	2008	Interestingly, quercetin inhibited p53 ubiquitination and extended the half-life (t(1/2)) of p53 from 74 to 184 min.	Quercetin	15-24	P53	Homo sapiens	35-38
18323654-8	2008	Interestingly, quercetin inhibited p53 ubiquitination and extended the half-life (t(1/2)) of p53 from 74 to 184 min.	Quercetin	15-24	P53	Homo sapiens	93-96
34073459-0	2021	Pt(II)-Thiocarbohydrazone Complex as Cytotoxic Agent and Apoptosis Inducer in Caov-3 and HT-29 Cells through the P53 and Caspase-8 Pathways.	pt(ii)-thiocarbohydrazone	0-25	P53	Homo sapiens	113-116
18323654-9	2008	Quercetin also inhibited p53 mRNA degradation at the post-transcription stage.	Quercetin	0-9	P53	Homo sapiens	25-28
34073459-4	2021	Results demonstrated that the cytotoxic effect of the Pt(II)-thiocarbohydrazone complexes against Caov-3 and HT-29 cells was highly significant, and this effect triggered the activation of the p53 and caspase-8 pathways.	thiocarbohydrazone	61-79	P53	Homo sapiens	193-196
18323654-11	2008	Taken together, our data demonstrate that quercetin stabilized p53 at both the mRNA and protein levels to reactivate p53-dependent cell cycle arrest and apoptosis in HepG2 cells.	Quercetin	42-51	P53	Homo sapiens	63-66
18323654-11	2008	Taken together, our data demonstrate that quercetin stabilized p53 at both the mRNA and protein levels to reactivate p53-dependent cell cycle arrest and apoptosis in HepG2 cells.	Quercetin	42-51	P53	Homo sapiens	117-120
18212337-10	2008	Within cohort A, phosphorylated (p) HER-3 and lack of p53 expression predicted for response to lapatinib (P &lt; .05).	Lapatinib	95-104	P53	Homo sapiens	54-57
34113336-2	2021	TP53 mutation is an independently poor progonistic indicator in patients with THL, hence novel therapeutic strategies are needed for these patients.	Orlistat	78-81	P53	Homo sapiens	0-4
17965848-5	2008	Consequential decrease in cell viability was in part prevented by the p53 inhibitor pifithrin-alpha, suggesting that p53 translocation contributes to QD-induced cytotoxicity.	pifithrin	84-99	P53	Homo sapiens	70-73
34070172-8	2021	In the subgroup analyses, patients with mutated TP53 (HR, 4.71, p = 0.009) showed a better RFS in the azacytidine arm.	Azacitidine	102-113	P53	Homo sapiens	48-52
17965848-5	2008	Consequential decrease in cell viability was in part prevented by the p53 inhibitor pifithrin-alpha, suggesting that p53 translocation contributes to QD-induced cytotoxicity.	pifithrin	84-99	P53	Homo sapiens	117-120
34093867-5	2021	Results: This approach significantly improved p53 activation and inhibition of lung and colorectal cancer cell growth by n-INZ-C in vitro and in vivo while it displayed a minimal effect on normal human Wi38 and mouse MEF cells.	n-inz-c	121-128	P53	Homo sapiens	46-49
35460941-8	2022	To sum up, we developed a new, safe strategy for melanoma treatment by using low doses of niclosamide and quinacrine to treat melanoma; and found a novel mechanism by which the combination application of low doses of niclosamide and quinacrine exerts an efficient anti-melanoma effect through activation of autophagy-mediated p53-dependent apoptosis.	Niclosamide	90-101	P53	Homo sapiens	326-329
35460941-8	2022	To sum up, we developed a new, safe strategy for melanoma treatment by using low doses of niclosamide and quinacrine to treat melanoma; and found a novel mechanism by which the combination application of low doses of niclosamide and quinacrine exerts an efficient anti-melanoma effect through activation of autophagy-mediated p53-dependent apoptosis.	Niclosamide	217-228	P53	Homo sapiens	326-329
18281560-7	2008	RESULTS: Exposure of human prostate cancer cells (PC-3, LNCaP, and C4-2) to honokiol resulted in apoptotic DNA fragmentation in a concentration- and time-dependent manner irrespective of their androgen responsiveness or p53 status.	honokiol	76-84	P53	Homo sapiens	220-223
35294085-0	2022	beta-Elemene induces apoptosis by activating the P53 pathway in human hypertrophic scar fibroblasts.	beta-elemene	0-12	P53	Homo sapiens	49-52
17975552-0	2008	R-Roscovitine simultaneously targets both the p53 and NF-kappaB pathways and causes potentiation of apoptosis: implications in cancer therapy.	Roscovitine	0-13	P53	Homo sapiens	46-49
35294085-8	2022	The results of our study indicates that beta-Elemene induced hHSFs to undergo apoptosis though ERS pathway in a P53-dependent manner, which means that our research provided a new strategy for the development of drugs for the treatment of HS.	beta-elemene	40-52	P53	Homo sapiens	112-115
35487055-9	2022	Generally, both cell lines treated with the combination of Curcumin and As2O3 displayed decreased angiogenesis genes (VEGFA and VEGFC), apoptosis genes (BAX and Bcl2), and prostate cancer marker (KLK2), the zinc-finger protein (SNAIL); and an increase in expression (P < 0.05) of cell-cell adhesion molecule (E-cadherin) and tumor suppressor gene (P53) genes.	Arsenic Trioxide	72-77	P53	Homo sapiens	348-351
17975552-3	2008	Activation of p53-dependent transcription is not compromised when R-Roscovitine is combined with TNFalpha.	Roscovitine	66-79	P53	Homo sapiens	14-17
35600955-8	2022	Results: The network pharmacology analysis showed that quercetin, luteolin, and kaempferol are the most significant active components in BHHD; STAT3, Jun, AKT1, MAPK3, MAPK1, and TP53 are the most critical drug targets; regulating hormones, reversing insulin (INS) resistance, exerting anti-inflammatory effects, and improving fertility might be the most important mechanisms of BHHD in the treatment of PCOS.	Quercetin	55-64	P53	Homo sapiens	179-183
17975552-8	2008	Based on these results, we suggest the potential use of R-Roscovitine as a bitargeted anticancer drug that functions by simultaneously causing p53 activation and NF-kappaB suppression.	Roscovitine	56-69	P53	Homo sapiens	143-146
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	ammonium ferrous sulfate	158-162	P53	Homo sapiens	65-68
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	ammonium ferrous sulfate	158-162	P53	Homo sapiens	101-104
17846083-5	2008	Apoptosis was prevented by the p53 inhibitor pifithrin and by p53 antisense oligonucleotides, indicating dependency of force-induced apoptosis on p53.	pifithrin	45-54	P53	Homo sapiens	31-34
35530319-10	2022	Knockdown of p53 or inhibition of p53"s transcriptional activity by addition of its specific inhibitor PFT-alpha decreased expression of ALKBH5 and CSCs" malignancies, including proliferation, invasion, and tumor formation ability, indicating that p53 may partially regulate CSC"s malignancies via ALKBH5.	pifithrin	103-112	P53	Homo sapiens	34-37
35530319-10	2022	Knockdown of p53 or inhibition of p53"s transcriptional activity by addition of its specific inhibitor PFT-alpha decreased expression of ALKBH5 and CSCs" malignancies, including proliferation, invasion, and tumor formation ability, indicating that p53 may partially regulate CSC"s malignancies via ALKBH5.	pifithrin	103-112	P53	Homo sapiens	248-251
17977830-2	2008	However, whether cellular responses to nucleoside analogue-induced DNA damage also operate through p53 posttranslational modification has not been reported.	Nucleosides	39-49	P53	Homo sapiens	99-102
35501643-3	2022	Significant differences in quantitative yield of residual gammaH2AX foci between wild-type and p53-deficient cell lines were observed only after exposure to subpicosecond, but not quasi-continuous beams of accelerated electrons.	subpicosecond	157-170	P53	Homo sapiens	95-98
18095870-6	2008	Cells expressing the p53 mutants were either more sensitive to cisplatin and melphalan or more resistant than the untransfected cells, depending on the mutation.	Melphalan	77-86	P53	Homo sapiens	21-24
35103478-11	2022	Notably, P53 activation with Nutilin3 significantly weakened the epithelial-mesenchymal transformation (EMT) promotion effect of ASF1B, while P53 inhibition with pifithrin-alpha significantly enhanced the EMT promotion effect of sh-ASF1B.	pifithrin	162-177	P53	Homo sapiens	142-145
17984113-1	2008	The stilbene resveratrol (RV) initiates p53-dependent apoptosis via plasma membrane integrin alphaVbeta3 in human cancer cells.	Stilbenes	4-12	P53	Homo sapiens	40-43
35216478-10	2022	Among a number of non-canonical approaches to TP53-mutated AML, the anti-CD47 antibody magrolimab in combination with azacitidine showed promising results in a phase 1b trial.	Azacitidine	118-129	P53	Homo sapiens	46-50
18791269-0	2008	Tyrosinase overexpression promotes ATM-dependent p53 phosphorylation by quercetin and sensitizes melanoma cells to dacarbazine.	Quercetin	72-81	P53	Homo sapiens	49-52
35215593-2	2022	In this work, polyethylenimine (PEI) has been used to complex p53 encoded plasmid DNA (pDNA), and the anticancer drug methotrexate (MTX) has also been loaded into the vectors.	Methotrexate	132-135	P53	Homo sapiens	62-65
35228743-3	2022	Here we show that cancer-associated mutant p53 protein is stabilized by 2-hydroxyglutarate generated by malic enzyme 2.	alpha-hydroxyglutarate	72-90	P53	Homo sapiens	43-46
18097557-5	2008	Experiments performed using pifithrin-alpha, a reversible inhibitor of p53, showed a correlation between acetylation of p53 and induction of apoptosis.	pifithrin	28-43	P53	Homo sapiens	71-74
35228743-6	2022	We further show that 2-hydroxyglutarate binds directly to mutant p53, which reduces Mdm2-mediated mutant p53 ubiquitination and degradation.	alpha-hydroxyglutarate	21-39	P53	Homo sapiens	65-68
35228743-6	2022	We further show that 2-hydroxyglutarate binds directly to mutant p53, which reduces Mdm2-mediated mutant p53 ubiquitination and degradation.	alpha-hydroxyglutarate	21-39	P53	Homo sapiens	105-108
18097557-5	2008	Experiments performed using pifithrin-alpha, a reversible inhibitor of p53, showed a correlation between acetylation of p53 and induction of apoptosis.	pifithrin	28-43	P53	Homo sapiens	120-123
35228743-7	2022	2-Hydroxyglutarate supplementation is sufficient for maintaining mutant p53 protein stability in malic enzyme 2-depleted cells, and restores tumour growth of malic enzyme 2-ablated cells, but not of cells that lack mutant p53.	alpha-hydroxyglutarate	0-18	P53	Homo sapiens	72-75
35228743-8	2022	Our findings reveal the previously unrecognized versatility of malic enzyme 2 catalytic functions, and uncover a role for mutant p53 in sensing cellular 2-hydroxyglutarate levels, which contribute to the stabilization of mutant p53 and tumour growth.	alpha-hydroxyglutarate	153-171	P53	Homo sapiens	129-132
35228743-8	2022	Our findings reveal the previously unrecognized versatility of malic enzyme 2 catalytic functions, and uncover a role for mutant p53 in sensing cellular 2-hydroxyglutarate levels, which contribute to the stabilization of mutant p53 and tumour growth.	alpha-hydroxyglutarate	153-171	P53	Homo sapiens	228-231
18167198-0	2007	Effects of HBV X gene and arsenic trioxide on the expression of p53 in cultured HepG2 cells.	Arsenic Trioxide	26-42	P53	Homo sapiens	64-67
35064206-8	2022	These findings indicate that alphaalpha-syn is a functional tumor suppressor that can inhibit the proliferation of BCa cells by activating the p53/p21 signaling pathway.	-syn	39-43	P53	Homo sapiens	143-146
35070983-13	2021	The KEGG pathway analysis revealed that quercetin and cisplatin may affect cervical cancer through platinum drug resistance and the p53 and HIF-1 pathways.	Quercetin	40-49	P53	Homo sapiens	132-135
18167198-2	2007	In recent years, effects of arsenic trioxide (As2O3) on the expression of p53 protein have been widely studied, while little is known about the activity of p53 protein.	Arsenic Trioxide	28-44	P53	Homo sapiens	74-77
35071005-6	2021	Third, treatments that specifically affect HPV+ cancer cells by targeting the viral enzymes E6/E7 which are responsible for the breakdown of p53 such as Ad-E6/E7-As and bortezomib.	Bortezomib	169-179	P53	Homo sapiens	141-144
18167198-2	2007	In recent years, effects of arsenic trioxide (As2O3) on the expression of p53 protein have been widely studied, while little is known about the activity of p53 protein.	Arsenic Trioxide	46-51	P53	Homo sapiens	74-77
18167198-3	2007	This study was undertaken to delineate the effect of HBV X gene and As2O3 on p53 protein expression (level and activity) in HepG2 cells by small hairpin RNA (shRNA)-mediated RNA interference (RNAi) technique.	Arsenic Trioxide	68-73	P53	Homo sapiens	77-80
35005656-3	2022	Here, we present a case of spontaneous transformation from EGFR-mutant LUAD with loss of p53 and RB to EGFR expression-positive SCLC and neuroendocrine-differentiated LUAD, which was successfully treated with osimertinib.	osimertinib	209-220	P53	Homo sapiens	89-92
18167198-9	2007	The effect of As2O3 on p53 protein expression and activity was re-observed.	Arsenic Trioxide	14-19	P53	Homo sapiens	23-26
18167198-10	2007	RESULTS: Total p53 protein level was up-regulated and its relative activity ratio was enhanced by As2O3 in HepG2 and HepG2-X cells.	Arsenic Trioxide	98-103	P53	Homo sapiens	15-18
18167198-11	2007	The total p53 protein level induced by As2O3 was up-regulated by HBV X gene expression, while its relative activity was significantly suppressed.	Arsenic Trioxide	39-44	P53	Homo sapiens	10-13
18167198-13	2007	CONCLUSIONS: As2O3 up-regulates p53 protein expression and enhance its activity.	Arsenic Trioxide	13-18	P53	Homo sapiens	32-35
18167198-14	2007	HBV X up-regulates As2O3 induced-p53 protein expression while suppresses its activity.	Arsenic Trioxide	19-24	P53	Homo sapiens	33-36
17853924-5	2007	The cellular growth inhibition and apoptosis of HPhA-mediated p53 transfection were assessed by XTT (sodium 3"-[1-(phenylaminocarbonyl)-3,4-tetrazolium]-bis(4-methoxy-6-nitro)benzene sulfonic acid hydrate) assay and annexin V-FITC (fluorescein isothiocyanate) staining, respectively.	hpha	48-52	P53	Homo sapiens	62-65
17855051-3	2007	In this study, we show that Bax translocation, caspase-3 activation and cell death by UV irradiation are not affected by Z-IETD-fmk (caspase-8 inhibitor), but delayed by Pifithrin-alpha (p53 inhibitor), although Bid cleavage could be completely abolished by Z-IETD-fmk.	pifithrin	170-179	P53	Homo sapiens	187-190
17904874-4	2007	Moreover, the effect of SP600125 on the expression of cell cycle related proteins was an upregulation of p53 protein accompanied by an increase in its molecular mass.	pyrazolanthrone	24-32	P53	Homo sapiens	105-108
17904874-5	2007	Prolonged SP600125 treatment downregulated p21, Bax and Mdm2 expression, but increased the level of the cellular p53-Mdm2 complex.	pyrazolanthrone	10-18	P53	Homo sapiens	113-116
17904874-6	2007	Taken together, we show that SP600125 could induce G2/M cell cycle arrest and endoreduplication in a p21 independent manner, and that SP600125 could also post-translationally modify p53 to modify its function.	pyrazolanthrone	134-142	P53	Homo sapiens	182-185
17673346-2	2007	The aim of this study was to investigate the effect of pifithrin-alpha (PFTalpha; a specific p53 inhibitor) and mitogen-activated protein kinases (MAPKs) inhibitors [namely SP600125 (a specific JNK inhibitor), SB203580 (a specific p38 inhibitor) and PD98059 (a specific ERK inhibitor)] on apoptotic signaling transduction mechanism induced by Cin in human hepatoma PLC/PRF/5 (CD95-negative) cells.	pifithrin	72-80	P53	Homo sapiens	93-96
18088187-9	2007	The pathway of Chk1 phosphorylation --&gt; Cdc25A degradation --&gt; inhibition of cyclin B1/Cdk1 activity --&gt; G2 arrest is accordingly resistant to staurosporine and UCN-01 in p53+/+ cells.	7-hydroxystaurosporine	170-176	P53	Homo sapiens	180-183
17929901-0	2007	Method for lipidomic analysis: p53 expression modulation of sulfatide, ganglioside, and phospholipid composition of U87 MG glioblastoma cells.	Gangliosides	71-82	P53	Homo sapiens	31-34
17929901-9	2007	Also, a decrease in the longer chain gangliosides, GD1 and GM1b, is observed in wild-type p53 (treated) cells.	Gangliosides	37-49	P53	Homo sapiens	90-93
17653713-10	2007	In contrast, an excess of the GSTM1 null (45.1 vs 17.2%, P = 0.009), the P53 PP+AP (70.4 vs 44.8%, P = 0.041) and the GSTM1 null plus P53 PP+AP (29.6 vs 10.3%, P = 0.004) genotypes were seen in MM patients at stage III compared with those at stages I + II.	N-(3-phenyl-n-propyl)-1-phenyl-2-aminopropane	77-82	P53	Homo sapiens	73-76
17940011-1	2007	A recently discovered phosphatidylinositol monophosphate, phosphatidylinositol 5-phosphate (PtdIns-5-P), plays an important role in nuclear signaling by influencing p53-dependent apoptosis.	phosphatidylinositol 5-phosphate	58-90	P53	Homo sapiens	165-168
17940011-1	2007	A recently discovered phosphatidylinositol monophosphate, phosphatidylinositol 5-phosphate (PtdIns-5-P), plays an important role in nuclear signaling by influencing p53-dependent apoptosis.	phosphatidylinositol 5-phosphate	92-102	P53	Homo sapiens	165-168
17940011-8	2007	This enzyme therefore controls nuclear levels of PtdIns-5-P and thereby p53-dependent apoptosis.	phosphatidylinositol 5-phosphate	49-59	P53	Homo sapiens	72-75
17698841-5	2007	Ubiquitination of p53 in mock-infected LU cells was sensitive to inhibition by trans-4-iodo, 4"-boranyl-chalcone, consistent with HDM2-catalyzing ubiquitination of p53.	4'-boranyl-chalcone	93-112	P53	Homo sapiens	18-21
17505786-5	2007	Moreover, the presence of pifithrin-alpha, an inhibitor of p53 transcriptional activity, blocked cisplatin-induced apoptosis, reduced the generation of ROS produced upon cisplatin treatment.	pifithrin	26-41	P53	Homo sapiens	59-62
17356895-0	2007	Caspase-independent death of human osteosarcoma cells by flavonoids is driven by p53-mediated mitochondrial stress and nuclear translocation of AIF and endonuclease G.	Flavonoids	57-67	P53	Homo sapiens	81-84
17695548-4	2007	RESULTS: FAS was statistically associated with p53 (p = 0.002), Ki-67 (p = 0.003), higher histological grade (p = 0.001 and recurrence and overall survival (p = 0.001).	ammonium ferrous sulfate	9-12	P53	Homo sapiens	47-50
17408702-1	2007	We analyzed the effect of exposure to carcinogenic polycyclic aromatic hydrocarbons (c-PAHs) in ambient air on the plasma levels of p53 and p21(WAF1) proteins among city policemen, bus drivers and controls in three European cities: Prague (Czech Republic), Kosice (Slovakia) and Sofia (Bulgaria).	Polycyclic Aromatic Hydrocarbons	51-83	P53	Homo sapiens	132-135
17547405-1	2007	Photosensitized one-electron oxidation was applied to discriminate a specific base site of 5-methylcytosine (mC) generated in DNA possessing a partial sequence of naturally occurring p53 gene, using a sensitizing 2-methyl-1,4-naphthoquinone (NQ) chromophore tethered to an interior of oligodeoxynucleotide (ODN) strands.	5-Methylcytosine	91-107	P53	Homo sapiens	183-186
17547405-1	2007	Photosensitized one-electron oxidation was applied to discriminate a specific base site of 5-methylcytosine (mC) generated in DNA possessing a partial sequence of naturally occurring p53 gene, using a sensitizing 2-methyl-1,4-naphthoquinone (NQ) chromophore tethered to an interior of oligodeoxynucleotide (ODN) strands.	5-Methylcytosine	109-111	P53	Homo sapiens	183-186
17547405-7	2007	Thus, photosensitization by an NQ-tethered ODN led to one-electron oxidative strand cleavage exclusively at the target mC site, providing a convenient method of discriminating mC in naturally occurring DNA such as human p53 gene as a positive band on a sequencing gel.	5-Methylcytosine	119-121	P53	Homo sapiens	220-223
17547405-7	2007	Thus, photosensitization by an NQ-tethered ODN led to one-electron oxidative strand cleavage exclusively at the target mC site, providing a convenient method of discriminating mC in naturally occurring DNA such as human p53 gene as a positive band on a sequencing gel.	5-Methylcytosine	176-178	P53	Homo sapiens	220-223
17349663-11	2007	Fe-NTA enhanced the migration of TP53 signals into the comet tail of human leucocytes, indicating a high susceptibility of this tumour-relevant gene towards DNA damage induced by iron overload.	ferric nitrilotriacetate	0-6	P53	Homo sapiens	33-37
17499812-3	2007	In the present study, we report that black tea polyphenol, Theaflavins (TF)-induced apoptosis in human prostate carcinoma, LNCaP cells is mediated via modulation of two related pathways: up-regulation of p53 and down-regulation of NF-kappa B activity, causing a change in the ratio of pro-and antiapoptotic proteins leading to apoptosis.	theaflavin	72-74	P53	Homo sapiens	204-207
17376296-10	2007	The anti-apoptotic protein (Bcl-2) expression in H460 cells altered by 39% with downregulation, and the p53 protein by 25% with upregulation after being cultured with 2.0 micromol/L AZ4 for 48 h. In a time-dependent manner, the expression of the p53 and p21 proteins were increased to the maximum at 24 h, and then decreased at 48.	az4	182-185	P53	Homo sapiens	104-107
17332940-0	2007	Arsenic trioxide induces p53-dependent apoptotic signals in myeloma cells with SiRNA-silenced p53: MAP kinase pathway is preferentially activated in cells expressing inactivated p53.	Arsenic Trioxide	0-16	P53	Homo sapiens	25-28
17332940-0	2007	Arsenic trioxide induces p53-dependent apoptotic signals in myeloma cells with SiRNA-silenced p53: MAP kinase pathway is preferentially activated in cells expressing inactivated p53.	Arsenic Trioxide	0-16	P53	Homo sapiens	94-97
17332940-0	2007	Arsenic trioxide induces p53-dependent apoptotic signals in myeloma cells with SiRNA-silenced p53: MAP kinase pathway is preferentially activated in cells expressing inactivated p53.	Arsenic Trioxide	0-16	P53	Homo sapiens	94-97
17520098-6	2007	Furthermore, the results indicate that quercetin increased the content of Cdk inhibitor p21 protein, which was correlated with the elevation in p53 levels during 12 h of incubation.	Quercetin	39-48	P53	Homo sapiens	144-147
17520098-8	2007	From our results it can be concluded that quercetin blocks cell cycle progression at G(1) phase and exerts its growth-inhibitory effect through the increase of Cdk inhibitors p21 and p27 and tumor suppressor p53 in HepG2.	Quercetin	42-51	P53	Homo sapiens	208-211
17192950-5	2007	RESULTS: A guanine to adenine substitution occurred in CGC, codon 175 of exon 5 in p53 gene, to CAC in the tumor sample of Case 1.	Guanine	11-18	P53	Homo sapiens	83-86
17192950-5	2007	RESULTS: A guanine to adenine substitution occurred in CGC, codon 175 of exon 5 in p53 gene, to CAC in the tumor sample of Case 1.	Adenine	22-29	P53	Homo sapiens	83-86
17192950-6	2007	Likewise, a thymine to cytosine substitution occurred in TTT, codon 270 of exon 8 in p53 gene, to TCT in tumor sample of Case 2.	Cytosine	23-31	P53	Homo sapiens	85-88
17326668-8	2007	In contrast, 3H-thymidine incorporation revealed a significantly more efficient block of DNA synthesis in p53 wild-type as compared to knock-out cells.	3h-thymidine	13-25	P53	Homo sapiens	106-109
17471156-3	2007	In addition, the improved effectiveness of guanine cytosine (GC)-clamped DHPLC for TP53 screening is detailed.	dhplc	73-78	P53	Homo sapiens	83-87
17523278-11	2007	P53 nuclear immunopositivity was observed in 12 GSC (71%) and 15 IPGC (60%).	ipgc	65-69	P53	Homo sapiens	0-3
17194597-4	2007	The discrimination of the cytosine methylation status at a methylation hot spot in the p53 gene was also executed using a well-designed fluorescent DNA probe.	Cytosine	26-34	P53	Homo sapiens	87-90
16888811-0	2007	Extreme sensitivity to Yondelis (Trabectedin, ET-743) in low passaged sarcoma cell lines correlates with mutated p53.	Trabectedin	46-52	P53	Homo sapiens	113-116
17159504-10	2007	15-Deoxy-Delta-prostaglandin J2+docetaxel showed a significant increase in apoptosis associated with inhibition of the Bcl2 and cyclin D1 expression and overexpression of caspase and p53 pathway genes.	Docetaxel	32-41	P53	Homo sapiens	183-186
17508926-1	2007	This article describes recent progress in the development of small molecule protein-protein inhibitors of the p53-MDM2 (purine double minute 2, or HDM2 for the human congener) protein-protein interaction, with special attention to the diversity of chemotypes reported to disrupt this protein-protein interaction.	purine	120-126	P53	Homo sapiens	110-113
17577621-9	2007	p53 expression was more frequent in the tumors of male patients (55% vs 27%); in poorly differentiated TAs (60% vs 47% in well-to-moderately differentiated TAs); in smaller tumors (&lt; or = 3 cm, 72% vs 43%-50% in larger tumors); in patients with a prominent inflammatory response (61% vs 21%; P &lt; 0.02); and in patients with lymphatic vessel invasion (77% vs 34%; P &lt; 0.02).	Tantalum	103-106	P53	Homo sapiens	0-3
17662641-3	2007	We show that bleomycin-treated A549 cells exhibit: senescence-like cell morphology; a senescence-associated increase in SA-beta-galactosidase activity; cell cycle arrest; and upregulation of p53 and p21.	Bleomycin	13-22	P53	Homo sapiens	191-194
17662641-6	2007	Our results support the hypothesis that downregulation of caveolin-1 expression affects bleomycin-induced cell cycle arrest and subsequent cellular senescence that is driven by p53 and p21.	Bleomycin	88-97	P53	Homo sapiens	177-180
17319790-11	2007	In the younger women group, the p53 BstUI polymorphism genotype frequencies were 6.2% for BstUIPro/Pro, 31.0% for BstUIArg/Pro and 62.8% for BstUIArg/Arg in controls and 11.11 %, 40.74% and 48.15% in cases respectively.	bstuipro	90-98	P53	Homo sapiens	32-35
17127074-4	2007	We also evaluated, the influence of TPT+/-NU1025 treatment on PARP-1 and p53 activity.	NU 1025	42-48	P53	Homo sapiens	73-76
17143939-8	2006	Troglitazone induced p53 expression in HCT-116 cells, but not in HCT-15 cells.	Troglitazone	0-12	P53	Homo sapiens	21-24
17143939-12	2006	Troglitazone may induce p53-independent apoptosis and p53-dependent expression of p21 and p27.	Troglitazone	0-12	P53	Homo sapiens	24-27
17143939-12	2006	Troglitazone may induce p53-independent apoptosis and p53-dependent expression of p21 and p27.	Troglitazone	0-12	P53	Homo sapiens	54-57
17384267-1	2006	We have recently observed activation of wild-type (wt) p53 protein in human MCF-7 breast cancer cells upon treatment with roscovitine (ROSC), a potent cyclin-dependent kinase inhibitor.	Roscovitine	122-133	P53	Homo sapiens	55-58
17384267-1	2006	We have recently observed activation of wild-type (wt) p53 protein in human MCF-7 breast cancer cells upon treatment with roscovitine (ROSC), a potent cyclin-dependent kinase inhibitor.	Roscovitine	135-139	P53	Homo sapiens	55-58
17157164-7	2006	At the molecular level, 17-AAG induced degradation of ALK and Akt proteins, dephosphorylated extracellular signal-regulated kinase, and degraded the cell-cycle regulatory protein cyclin D1 and its cyclin-dependent kinases, CDK4 and CDK6, but had a differential effect on p27 and p53 proteins.	tanespimycin	24-30	P53	Homo sapiens	279-282
16971506-7	2006	The p53 inhibitor pifithrin-alpha protects HepG2 cells against apoptosis induced by serum withdrawal.	pifithrin	18-33	P53	Homo sapiens	4-7
16797627-4	2006	However, the knowledge of the relationship between AZT and cellular pathways, e.g. p53 pathway, is very limited.	Zidovudine	51-54	P53	Homo sapiens	83-86
16797627-5	2006	In this study, we show that AZT, cisplatin (CDDP) and docetaxel (DTX) all induce unique molecular responses in OVCAR-3 ovarian carcinoma cells carrying a mutated p53, while in A2780, ovarian carcinoma and MCF-7 breast carcinoma cells with wild type p53, all of these drugs cause similar p53 responses.	Zidovudine	28-31	P53	Homo sapiens	162-165
16797627-5	2006	In this study, we show that AZT, cisplatin (CDDP) and docetaxel (DTX) all induce unique molecular responses in OVCAR-3 ovarian carcinoma cells carrying a mutated p53, while in A2780, ovarian carcinoma and MCF-7 breast carcinoma cells with wild type p53, all of these drugs cause similar p53 responses.	Zidovudine	28-31	P53	Homo sapiens	249-252
17064470-0	2006	[Study of effects of HBV X gene and As2O3 on expression and activity of p53 in HepG2 cells with shRNA].	Arsenic Trioxide	36-41	P53	Homo sapiens	72-75
16844116-1	2006	Ionizing radiation (IR) is known to upregulate cell surface Fas through p53 activation in various cells.	ammonium ferrous sulfate	60-63	P53	Homo sapiens	72-75
16844116-6	2006	Pretreatment with p53 inhibitor pifithrin alpha cancelled the IR-induced downregulation of FAP-1 mRNA.	pifithrin	32-41	P53	Homo sapiens	18-21
16844116-7	2006	These results suggest that IR-induced p53 activation may upregulate cell surface Fas via the down-modulation of FAP-1.	ammonium ferrous sulfate	81-84	P53	Homo sapiens	38-41
16790523-9	2006	In conclusion, binding of resveratrol to integrin alphaVbeta3, principally to the beta3 monomer, is essential for transduction of the stilbene signal into p53-dependent apoptosis of breast cancer cells.	Stilbenes	134-142	P53	Homo sapiens	155-158
16714289-4	2006	PGE(2) induced a time-dependent increase in p53 Ser(15) phosphorylation, with no discernible change in overall p53 levels.	Prostaglandins E	0-3	P53	Homo sapiens	44-47
16462765-3	2006	A polymorphic site at codon 72 in exon 4 encodes either an arginine amino acid (Trp53(72R)) or a proline residue (Trp53(72P)).	arginine amino acid	59-78	P53	Homo sapiens	80-85
16759106-3	2006	Here, we report the design, synthesis, and biological evaluation of novel p53 inhibitors based on the imino-tetrahydrobenzothiazole scaffold.	imino-tetrahydrobenzothiazole	102-131	P53	Homo sapiens	74-77
16651619-6	2006	In addition, treatment of leukemic clam hemocytes with MKT-077, a cationic inhibitor of mortalin, disrupts the interaction of mortalin and p53 proteins, resulting in translocation of some p53 to the nucleus.	MKT 077	55-62	P53	Homo sapiens	139-142
16651619-6	2006	In addition, treatment of leukemic clam hemocytes with MKT-077, a cationic inhibitor of mortalin, disrupts the interaction of mortalin and p53 proteins, resulting in translocation of some p53 to the nucleus.	MKT 077	55-62	P53	Homo sapiens	188-191
16636310-3	2006	Nuclear p53 levels were almost 100% and 40% higher in ZD0.2 and ZD0.4 cells, respectively, than in ZN cells.	Zinc	99-101	P53	Homo sapiens	8-11
16636310-5	2006	In addition, the observed reductions of nuclear c-Abl in ZD0.2 and ZD0.4 cells to 50% and 60% of ZN cells, respectively, may be a cellular response attempting to normalize nuclear p53 accumulation because nuclear c-Abl is known to down-regulate ubiquitination and nuclear export of p53.	Zinc	97-99	P53	Homo sapiens	180-183
16518418-3	2006	In FaDu xenografts, a poorly differentiated tumor-expressing mutant p53, the cure rate was increased from 30% with irinotecan alone to 100% with the combination of irinotecan and MSC.	fadu	3-7	P53	Homo sapiens	68-71
16545693-6	2006	N-OH-ABA induced DNA damage at cytosine and guanine residues of ACG sequence complementary to codon 273, a well-known hot spot of the p53 gene.	Cytosine	31-39	P53	Homo sapiens	134-137
16545693-6	2006	N-OH-ABA induced DNA damage at cytosine and guanine residues of ACG sequence complementary to codon 273, a well-known hot spot of the p53 gene.	Guanine	44-51	P53	Homo sapiens	134-137
16506813-7	2006	Pretreatment with green tea polyphenol epigallocatechin-3-gallate (EGCG) effectively blocked peroxynitrite-induced glutathione depletion, p53 accumulation, and apoptosis in both normal and G6PD-deficient cells.	polyphenol epigallocatechin-3-gallate	28-65	P53	Homo sapiens	138-141
16461914-4	2006	The NMR spectrum (15N,1H transverse relaxation optimized spectroscopy) of full-length p53 was close to that expected from the sum of the spectra of isolated individual domains.	15n	18-21	P53	Homo sapiens	86-89
16343421-8	2006	Soft-agar colony formation activity of p53-knockout MEF was increased by wild-type Mdm2 but not mutant Mdm2.	Agar	5-9	P53	Homo sapiens	39-42
16427050-0	2006	Activation of p53 as a causal step for atherosclerosis induced by polycyclic aromatic hydrocarbons.	Polycyclic Aromatic Hydrocarbons	66-98	P53	Homo sapiens	14-17
16427050-1	2006	This study was performed to prove our hypothesis that the metabolite(s) of polycyclic aromatic hydrocarbons (PAHs) caused the activation or phosphorylation of p53 via DNA damage to suppress the liver X receptor (LXR)-mediated signal transductions as a probably more direct mechanism.	Polycyclic Aromatic Hydrocarbons	75-107	P53	Homo sapiens	159-162
16427050-1	2006	This study was performed to prove our hypothesis that the metabolite(s) of polycyclic aromatic hydrocarbons (PAHs) caused the activation or phosphorylation of p53 via DNA damage to suppress the liver X receptor (LXR)-mediated signal transductions as a probably more direct mechanism.	Polycyclic Aromatic Hydrocarbons	109-113	P53	Homo sapiens	159-162
16505115-1	2006	Nucleoside anticancer drugs like gemcitabine (2"-deoxy-2",2"-difluorocytidine) are potent inducers of p53, and ectopic expression of wild-type p53 sensitizes cells to these agents.	Nucleosides	0-10	P53	Homo sapiens	143-146
17065086-1	2006	Previously, we have found that activation of deoxycytidine kinase elicited by various DNA-damaging chemical agents could be prevented by BAPTA-AM, a cell-permeable calcium chelator or by pifithrin-alpha, a pharmacological inhibitor of p53.	pifithrin	187-202	P53	Homo sapiens	235-238
15908180-7	2005	This synergistic activation of JNK/SAPK by TNF-alpha/IFN-gamma was also induced in insulin-expressing pancreatic islet cells, and increased ROS production and p53 level, which was significantly inhibited by SP600125.	pyrazolanthrone	207-215	P53	Homo sapiens	159-162
16332175-2	2005	In the AD patients the increased levels of oxidized guanine were demonstrated in DNA, accompanied by the elevated expression of p53, Bax, PARP, and of a 85-kDa protein subunit as well as an augmented ratio of Bax:Bcl-2.	Guanine	52-59	P53	Homo sapiens	128-131
16226226-10	2005	In contrast, p53 mutated Huh-7 hepatocellular cancer cells proved to be less sensitive towards cetuximab, but when combined with TKIs or fluvastatin or doxorubicin a pronounced reduction of cell growth was observed.	Fluvastatin	137-148	P53	Homo sapiens	13-16
16382051-4	2005	Colon cancer cell lines lacking p53 or Bax were sensitized by bortezomib, suggesting that neither p53 nor Bax levels were crucial for sensitization.	Bortezomib	62-72	P53	Homo sapiens	32-35
16091363-9	2005	More importantly, small interfering RNA knockdown of ASPP2/(53BP2L) levels attenuated bortezomib-induced apoptosis, and this effect was greater in wild-type p53 cells.	Bortezomib	86-96	P53	Homo sapiens	157-160
16204064-7	2005	Treatment of p53 wild-type cells with pifithrin-alpha, an inhibitor of the trans-activating activity of p53, caused reversal of the phenotype, making wild-type cells more sensitive to topotecan.	pifithrin	38-53	P53	Homo sapiens	13-16
16204064-7	2005	Treatment of p53 wild-type cells with pifithrin-alpha, an inhibitor of the trans-activating activity of p53, caused reversal of the phenotype, making wild-type cells more sensitive to topotecan.	pifithrin	38-53	P53	Homo sapiens	104-107
16204068-3	2005	In contrast, irinotecan (CPT-11) and tomudex sensitized p53 WT, mutant, and null cells to Fas-mediated cell death.	ammonium ferrous sulfate	90-93	P53	Homo sapiens	56-59
16051302-7	2005	A proteasome inhibitor, lactacystin, enhances TNFalpha cytotoxicity in p53-positive and -negative cells, suggesting that accumulation of cellular proteins other than p53 might also regulate the cellular response to TNFalpha signaling.	lactacystin	24-35	P53	Homo sapiens	71-74
15879012-4	2005	In this study, we report a 23 year old patient with recurrent HCC who was treated with the p53 gene (Gendicine) combining TACE, which resulted in a good clinical prognosis.	Chlorotrianisene	122-126	P53	Homo sapiens	91-94
16005638-6	2005	Moreover, gp120 neurotoxicity is markedly reduced by the p53-inhibitor, pifithrin-alpha.	pifithrin	72-87	P53	Homo sapiens	57-60
15800902-1	2005	Pifithrin-alpha (PFTalpha) is a small molecule inhibitor of p53.	pifithrin	0-15	P53	Homo sapiens	60-63
15800902-1	2005	Pifithrin-alpha (PFTalpha) is a small molecule inhibitor of p53.	pifithrin	17-25	P53	Homo sapiens	60-63
15800902-5	2005	We observed that exposure of U87MG cells to PFTalpha before cytotoxic chemotherapy attenuated p53-mediated induction of p21WAF1 protein levels, sensitizing U87MG cells to BCNU and TMZ.	pifithrin	44-52	P53	Homo sapiens	94-97
15800902-7	2005	Our findings suggest that in addition to protecting normal cells from the toxic effects of radiation and chemotherapy, small molecule inhibitors of p53, like PFTalpha, might play a role in clinical oncology by sensitizing certain resistant cancers to cytotoxic chemotherapies.	pifithrin	158-166	P53	Homo sapiens	148-151
16123139-7	2005	These retinoids were partially dependent on p53 and transforming growth factor beta to exert their radiosensitizing effects.	Retinoids	6-15	P53	Homo sapiens	44-47
16123139-9	2005	Taken together, these data suggest that sensitization of the mammary epithelium to p53-dependent apoptosis is a common pathway, which is engaged by retinoids as well as ovarian hormones.	Retinoids	148-157	P53	Homo sapiens	83-86
16009942-7	2005	The UVB-induced lesions detected by terminal transferase-PCR were almost exclusively mapped to pyrimidine-rich sequences; however, the UVA1-induced lesions were mapped to purine- and pyrimidine-containing sequences along the p53 gene.	purine	171-177	P53	Homo sapiens	225-228
16002925-9	2005	The p53 and phospho-p53 proteins were significantly increased in LCW samples (56,536.8 +/- 4,629 densitometry units [DU] and 58,244.8 +/- 7,492 DU, respectively [+/- SD]), in comparison with the other groups.	du	117-119	P53	Homo sapiens	4-7
16002925-9	2005	The p53 and phospho-p53 proteins were significantly increased in LCW samples (56,536.8 +/- 4,629 densitometry units [DU] and 58,244.8 +/- 7,492 DU, respectively [+/- SD]), in comparison with the other groups.	du	117-119	P53	Homo sapiens	20-23
16002925-9	2005	The p53 and phospho-p53 proteins were significantly increased in LCW samples (56,536.8 +/- 4,629 densitometry units [DU] and 58,244.8 +/- 7,492 DU, respectively [+/- SD]), in comparison with the other groups.	du	144-146	P53	Homo sapiens	4-7
16002925-9	2005	The p53 and phospho-p53 proteins were significantly increased in LCW samples (56,536.8 +/- 4,629 densitometry units [DU] and 58,244.8 +/- 7,492 DU, respectively [+/- SD]), in comparison with the other groups.	du	144-146	P53	Homo sapiens	20-23
15905035-5	2005	Treatment with CoQs having shorter isoprenoid chains, especially CoQ2, induced apoptosis in p53-point mutated BALL-1 cells, whereas treatment with longer isoprenoid chains did not.	coqs	15-19	P53	Homo sapiens	92-95
15605368-3	2005	Benzyl isothiocyanate (BITC) treatment down-regulates cyclins and CDKs and up-regulates the expression of the CDK inhibitor p21, but up-regulation of p27 or p53 was not detected.	benzyl isothiocyanate	23-27	P53	Homo sapiens	157-160
15965099-8	2005	In conclusion, these data suggest that thallium acetate inhibits cell cycle progression at G2/M phase by suppressing CDK activity through the p53-mediated induction of the CDK inhibitor p21(Cip1).	thallium acetate	39-55	P53	Homo sapiens	142-145
15916722-2	2005	Our present works show that the expression of E6/E7 oncogenes of human papillomavirus in HeLa cells is inhibited in the presence of anti-tumor reagent tripchlorolide (TC), which results in the up-regulation of p53 in HeLa cells.	tripchlorolide	151-165	P53	Homo sapiens	210-213
15916722-2	2005	Our present works show that the expression of E6/E7 oncogenes of human papillomavirus in HeLa cells is inhibited in the presence of anti-tumor reagent tripchlorolide (TC), which results in the up-regulation of p53 in HeLa cells.	tripchlorolide	167-169	P53	Homo sapiens	210-213
15916722-3	2005	Interestingly, under the same TC-treatment, the cells at the early S-phase are more susceptible to apoptosis than those at the middle S-phase although p53 protein is stabilized to the same level in both situations.	tripchlorolide	30-32	P53	Homo sapiens	151-154
15916722-5	2005	Further analysis demonstrates that anti-apoptotic gene survivin is up-regulated by p53 in the TC-treated middle-S cells, whereas it is down-regulated by p53 in the TC-treated early-S cells.	tripchlorolide	94-96	P53	Homo sapiens	83-86
15916722-5	2005	Further analysis demonstrates that anti-apoptotic gene survivin is up-regulated by p53 in the TC-treated middle-S cells, whereas it is down-regulated by p53 in the TC-treated early-S cells.	tripchlorolide	164-166	P53	Homo sapiens	153-156
15795422-6	2005	Micromolar (-)epigallocatechin gallate and quercetin partially eliminated the dichlorodihydrofluorescein (DCF) and phospho-p53 staining, suggesting that these flavonoids inhibited the accumulation of intracellular oxidants and nuclear transactivation of p53 in H2O2-exposed cells.	Quercetin	43-52	P53	Homo sapiens	123-126
15795422-6	2005	Micromolar (-)epigallocatechin gallate and quercetin partially eliminated the dichlorodihydrofluorescein (DCF) and phospho-p53 staining, suggesting that these flavonoids inhibited the accumulation of intracellular oxidants and nuclear transactivation of p53 in H2O2-exposed cells.	Quercetin	43-52	P53	Homo sapiens	254-257
15795422-6	2005	Micromolar (-)epigallocatechin gallate and quercetin partially eliminated the dichlorodihydrofluorescein (DCF) and phospho-p53 staining, suggesting that these flavonoids inhibited the accumulation of intracellular oxidants and nuclear transactivation of p53 in H2O2-exposed cells.	Flavonoids	159-169	P53	Homo sapiens	123-126
15795422-6	2005	Micromolar (-)epigallocatechin gallate and quercetin partially eliminated the dichlorodihydrofluorescein (DCF) and phospho-p53 staining, suggesting that these flavonoids inhibited the accumulation of intracellular oxidants and nuclear transactivation of p53 in H2O2-exposed cells.	Flavonoids	159-169	P53	Homo sapiens	254-257
15748635-4	2005	Since 5"-CG sequences are methylated along the p53 coding sequence in human cells, these mutations may be derived from sunlight-induced pyrimidine dimers forming at sequences that contain 5-methylcytosine.	5-Methylcytosine	188-204	P53	Homo sapiens	47-50
15755327-0	2005	Activation of p53, inhibition of telomerase activity and induction of estrogen receptor beta are associated with the anti-growth effects of combination of ovarian hormones and retinoids in immortalized human mammary epithelial cells.	Retinoids	176-185	P53	Homo sapiens	14-17
15755327-7	2005	In addition, our results showed that both E/P and retinoid treatments resulted in increased RARE and p53 gene activity.	Retinoids	50-58	P53	Homo sapiens	101-104
15755327-8	2005	We further demonstrated that p53 and p21 protein expression were induced following the E/P and retinoid treatments.	Retinoids	95-103	P53	Homo sapiens	29-32
15701509-1	2005	It is well known that CpG dinucleotide steps in DNA, which are highly methylated at the 5-position of cytosine (meC) in human tissues, exhibit a disproportionate number of mutations within certain codons of the p53 gene.	Cytosine	102-110	P53	Homo sapiens	211-214
15735102-0	2005	Ellagic acid potentiates the effect of quercetin on p21waf1/cip1, p53, and MAP-kinases without affecting intracellular generation of reactive oxygen species in vitro.	Quercetin	39-48	P53	Homo sapiens	66-69
15735102-4	2005	We found that quercetin and combinations of quercetin and ellagic acid nonsynergistically increased p53 protein levels.	Quercetin	14-23	P53	Homo sapiens	100-103
15735102-4	2005	We found that quercetin and combinations of quercetin and ellagic acid nonsynergistically increased p53 protein levels.	Quercetin	44-53	P53	Homo sapiens	100-103
15735102-10	2005	In summary, quercetin and ellagic acid combined increase the activation of p53 and p21(cip1/waf1) and the MAP kinases, JNK1,2 and p38, in a more than additive manner, suggesting a mechanism by which quercetin and ellagic acid synergistically induce apoptosis in cancer cells.	Quercetin	12-21	P53	Homo sapiens	75-78
15564291-2	2005	Previous studies of lung tumors from both non-smoking women and smoking men in this region showed high frequencies of mutations, consisting mostly of G--&gt;T transversions in the p53 tumor suppressor gene and K-ras oncogene, suggesting that these mutations were caused primarily by polycyclic aromatic hydrocarbons.	Polycyclic Aromatic Hydrocarbons	283-315	P53	Homo sapiens	180-183
15474986-0	2005	p53 protein activates the transcription of human proliferating cell nuclear antigen in response to 4-nitroquinoline N-oxide treatment.	n-oxide	116-123	P53	Homo sapiens	0-3
15547111-0	2005	5-Aza-cytidine is a potent inhibitor of DNA methyltransferase 3a and induces apoptosis in HCT-116 colon cancer cells via Gadd45- and p53-dependent mechanisms.	Azacitidine	0-14	P53	Homo sapiens	133-136
15547111-4	2005	In this study, we investigated the p53 dependence of apoptotic, cell cycle, and growth inhibitory effects of 5-aza-CR, as well as the influence on the expression level of DNMT1, DNMT3a, and DNMT3b in the colon cancer cell line HCT-116.	Azacitidine	109-117	P53	Homo sapiens	35-38
15547111-5	2005	Exposure to 5-aza-CR induced the up-regulation of genes promoting cell cycle arrest and DNA repair (p21(WAF1) and GADD45) or apoptosis (p53, RIPK2, Bak1, caspase 5, and caspase 6).	Azacitidine	12-20	P53	Homo sapiens	136-139
15547111-7	2005	Co-incubation with pifithrin-alpha (PFT-alpha), a selective p53 inhibitor, restored GADD45, Bcl2, cyclin B1, and p21(WAF1) expression levels and almost completely reversed the growth inhibitory, cell cycle, and apoptotic effects of 5-aza-CR.	pifithrin	19-28	P53	Homo sapiens	60-63
15680394-0	2005	Altered trafficking of Fas and subsequent resistance to Fas-mediated apoptosis occurs by a wild-type p53 independent mechanism in esophageal adenocarcinoma.	ammonium ferrous sulfate	23-26	P53	Homo sapiens	101-104
15680394-0	2005	Altered trafficking of Fas and subsequent resistance to Fas-mediated apoptosis occurs by a wild-type p53 independent mechanism in esophageal adenocarcinoma.	ammonium ferrous sulfate	56-59	P53	Homo sapiens	101-104
15680394-9	2005	CONCLUSIONS: These data suggest that decreased cell-surface expression of Fas and resistance to Fas-mediated apoptosis may occur independently of loss of wt p53 expression.	ammonium ferrous sulfate	74-77	P53	Homo sapiens	157-160
15548639-9	2005	Pifithrin-alpha, a synthetic inhibitor of p53 activity, abolished both S-phase arrest and apoptosis induced by genotoxic PAHs, and it potentiated the proliferative effect of BaP.	pifithrin	0-15	P53	Homo sapiens	42-45
15830705-0	2005	Intracellular inhibitory effects of Velcade correlate with morphoproteomic expression of phosphorylated-nuclear factor-kappaB and p53 in breast cancer cell lines.	Bortezomib	36-43	P53	Homo sapiens	130-133
15830705-1	2005	Velcade, a proteasome inhibitor, has been shown to inhibit DNA binding activity of nuclear factor-kappaB (NF-kappaB) and to stabilize p53 in vitro.	Bortezomib	0-7	P53	Homo sapiens	134-137
15830705-9	2005	Velcade treatment resulted in cleaved caspase-3 expression in MDA-231 cells and in the overexpression of p53 and p21WAF1 in all 3 cell lines, as evaluated using Western blotting.	Bortezomib	0-7	P53	Homo sapiens	105-108
15830705-10	2005	In summary, morphoproteomic analysis of p-NF-kappaB and p53 can be correlated with the inhibitory effect of Velcade in vitro.	Bortezomib	108-115	P53	Homo sapiens	56-59
15642166-15	2005	CONCLUSIONS: The AZ-1-induced cell death of BC-M1 cells mediating the apoptosis pathway might be associated with p53 protein expression, and AZ-1 could have the chance to be a candidate drug for anti-breast cancer following more experimental evidence, such as animal models.	2-aziridin-1-yl-3-((2-((2-(3-aziridin-1-yl-1,4-dioxo-1,4-dihydronaphthalen-2-yl)thio)ethoxy)ethyl)thio)naphthoquinone	17-21	P53	Homo sapiens	113-116
15657359-2	2005	After roscovitine treatment, the level of wild-type p53 protein strongly increased and p53 was accumulated in the nucleus.	Roscovitine	6-17	P53	Homo sapiens	52-55
15657359-2	2005	After roscovitine treatment, the level of wild-type p53 protein strongly increased and p53 was accumulated in the nucleus.	Roscovitine	6-17	P53	Homo sapiens	87-90
15657359-3	2005	Here, we raised the question of which pathway would be involved in roscovitine-induced apoptosis in MCF-7 cells, which are known to be caspase-3-deficient, and whether roscovitine-mediated activation of p53 protein might positively affect the execution of cell death.	Roscovitine	168-179	P53	Homo sapiens	203-206
15657359-5	2005	Interestingly, roscovitine stimulated a site-specific phosphorylation of wild-type p53 protein in a time-dependent manner.	Roscovitine	15-26	P53	Homo sapiens	83-86
15657359-9	2005	We compared the kinetics of roscovitine-mediated p53 activation between caspase-3-deficient parental MCF-7 cells and cells reconstituted with caspase-3.	Roscovitine	28-39	P53	Homo sapiens	49-52
15589979-0	2005	The monofunctional alkylating agent N-methyl-N"-nitro-N-nitrosoguanidine triggers apoptosis through p53-dependent and -independent pathways.	Methylnitronitrosoguanidine	36-72	P53	Homo sapiens	100-103
15589979-5	2005	The S(N)1 DNA alkylating agent N-methyl-N"-nitro-N-nitrosoguanidine (MNNG) triggers apoptosis and the upregulation/phosphorylation of p53; however, the mechanism(s) governing MNNG-induced cell death remain unresolved.	Methylnitronitrosoguanidine	31-67	P53	Homo sapiens	134-137
15592306-6	2004	The apoptotic index was reduced by &gt;/=30% ( P &lt;.001), and the expression of p53 was 2-fold lower ( P &lt;.02) in troglitazone-exposed cells under hypoxia for &lt;/=16 hours but not different after &gt;24 hours of low oxygen.	Troglitazone	119-131	P53	Homo sapiens	82-85
15547693-8	2004	DNA sequencing in FaDu cells showed a G/T point mutation at codon 248 in exon 7 of p53 gene, resulting in an arginine-to-leucine substitution.	Leucine	121-128	P53	Homo sapiens	83-86
15450935-0	2004	Influence of p53 and caspase 3 activity on cell death and senescence in response to methotrexate in the breast tumor cell.	Methotrexate	84-96	P53	Homo sapiens	13-16
15450935-2	2004	In p53 wild-type, but caspase 3 deficient MCF-7 breast tumor cells, death of approximately 40% of the cell population was observed immediately after acute exposure to 10 microM methotrexate (the IC80 value for a 2 h drug exposure).	Methotrexate	177-189	P53	Homo sapiens	3-6
15450935-5	2004	The response to methotrexate in MCF-7/E6 cells with attenuated p53 function was also primarily growth arrest--but lacking characteristics of senescence.	Methotrexate	16-28	P53	Homo sapiens	63-66
15450935-7	2004	DNA fragmentation indicative of apoptosis was also detected after exposure to methotrexate in p53 mutant MDA-MB231 breast tumor cells which also express caspase 3.	Methotrexate	78-90	P53	Homo sapiens	94-97
15450935-8	2004	Methotrexate-induced both p53 and p21waf1/cip1 in MCF-7 cells within 6 h; however, no significant DNA strand breakage was evident before 18 h, suggesting that the induction of p53 reflects a response to cellular stress other than DNA damage, such as nucleotide depletion.	Methotrexate	0-12	P53	Homo sapiens	26-29
15450935-8	2004	Methotrexate-induced both p53 and p21waf1/cip1 in MCF-7 cells within 6 h; however, no significant DNA strand breakage was evident before 18 h, suggesting that the induction of p53 reflects a response to cellular stress other than DNA damage, such as nucleotide depletion.	Methotrexate	0-12	P53	Homo sapiens	176-179
15450935-9	2004	Overall, these studies suggest that the nature of the cellular response to methotrexate depends, in large part, on p53 and caspase function.	Methotrexate	75-87	P53	Homo sapiens	115-118
15450935-10	2004	p53 appears to be required for methotrexate-induced senescence, but not apoptosis, caspase 3 is required for DNA fragmentation and the morphological changes associated with apoptosis, while neither p53 nor caspase 3 are required for methotrexate-induced growth arrest.	Methotrexate	31-43	P53	Homo sapiens	0-3
15450935-10	2004	p53 appears to be required for methotrexate-induced senescence, but not apoptosis, caspase 3 is required for DNA fragmentation and the morphological changes associated with apoptosis, while neither p53 nor caspase 3 are required for methotrexate-induced growth arrest.	Methotrexate	233-245	P53	Homo sapiens	0-3
15510008-0	2004	Enhancement of Ad-p53 therapy with docetaxel in head and neck cancer.	Docetaxel	35-44	P53	Homo sapiens	18-21
15510008-1	2004	OBJECTIVE: The objective of this project was to determine the mechanisms in which docetaxel enhances Ad-p53 tumor suppressive effects in head and neck cancer.	Docetaxel	82-91	P53	Homo sapiens	104-107
15510008-11	2004	Pretreatment with docetaxel enhanced Ad-p53-induced apoptosis through increased expression of exogenous p53.	Docetaxel	18-27	P53	Homo sapiens	40-43
15510008-11	2004	Pretreatment with docetaxel enhanced Ad-p53-induced apoptosis through increased expression of exogenous p53.	Docetaxel	18-27	P53	Homo sapiens	104-107
15510008-12	2004	Together, the combination of docetaxel and Ad-p53 altered expression of key regulators in the cell cycle, apoptosis and signal transduction pathways with an increase in the expression of p53, bax, cleaved PARP, cleaved caspase-3 and phosphorylation of c-Jun at position at Ser.	Docetaxel	29-38	P53	Homo sapiens	187-190
15510008-14	2004	When comparing the docetaxel-resistant to sensitive cell lines, the altered expression of p27 and skp1 by docetaxel and Ad-p53 were dissimilar between these cell lines.	Docetaxel	19-28	P53	Homo sapiens	123-126
15510008-15	2004	CONCLUSIONS: Docetaxel enhanced Ad-p53 transduction and increased expression of exogenous p53 gene transfer, apoptosis, and antitumor mechanisms.	Docetaxel	13-22	P53	Homo sapiens	35-38
15510008-15	2004	CONCLUSIONS: Docetaxel enhanced Ad-p53 transduction and increased expression of exogenous p53 gene transfer, apoptosis, and antitumor mechanisms.	Docetaxel	13-22	P53	Homo sapiens	90-93
15542774-9	2004	The stilbene promoted p53-dependent apoptosis, whereas EGF opposed induction of apoptosis by resveratrol via a PKC-alpha-mediated mechanism.	Stilbenes	4-12	P53	Homo sapiens	22-25
15720807-3	2004	In this study, we found that exposure of human lung cancer cell lines A549 (p53-wt) and H1299 (p53-depleted) to 8-Cl-Ado induced cell arrest in the G2/M phase, which was accompanied by accumulation of binucleated and polymorphonucleated cells resulting from aberrant mitosis and failed cytokinesis.	8-chloroadenosine	112-120	P53	Homo sapiens	76-79
15720807-3	2004	In this study, we found that exposure of human lung cancer cell lines A549 (p53-wt) and H1299 (p53-depleted) to 8-Cl-Ado induced cell arrest in the G2/M phase, which was accompanied by accumulation of binucleated and polymorphonucleated cells resulting from aberrant mitosis and failed cytokinesis.	8-chloroadenosine	112-120	P53	Homo sapiens	95-98
15450401-2	2004	By removing alkyl groups from the O6-position in guanine, MGMT can prevent G:C to A:T transition mutations, a type of variation frequently involving TP53 mutations in brain tumors.	Guanine	49-56	P53	Homo sapiens	149-153
15450419-0	2004	A mixture of isothiocyanates induces cyclin B1- and p53-mediated cell-cycle arrest and apoptosis of human T lymphoblastoid cells.	Isothiocyanates	13-28	P53	Homo sapiens	52-55
15464472-13	2004	Combined gemcitabine and bortezomib enhanced p21 and p53 expression and induced S-phase and G2/M cell-cycle arrests, respectively.	Bortezomib	25-35	P53	Homo sapiens	53-56
15466201-5	2004	Sensitization to IR-induced apoptosis by caffeine or UCN-01 was abrogated neither by cycloheximide nor by pifithrin-alpha, an inhibitor of the transcriptional activity of p53.	7-hydroxystaurosporine	53-59	P53	Homo sapiens	171-174
15724841-1	2004	We previously reported (Cancer Chemother Pharmacol 45: 252-258, 2000) that UCN-01 (7-hydroxystaurosporine), a protein kinase inhibitor, which is under clinical trials as an anti-cancer agent in the USA and Japan, enhanced camptothecin-induced cytotoxicity in breast cancer cells that lack p53 function.	7-hydroxystaurosporine	75-81	P53	Homo sapiens	289-292
15724841-1	2004	We previously reported (Cancer Chemother Pharmacol 45: 252-258, 2000) that UCN-01 (7-hydroxystaurosporine), a protein kinase inhibitor, which is under clinical trials as an anti-cancer agent in the USA and Japan, enhanced camptothecin-induced cytotoxicity in breast cancer cells that lack p53 function.	7-hydroxystaurosporine	83-105	P53	Homo sapiens	289-292
15724841-9	2004	Detailed cell-cycle analyses revealed that UCN-01 abrogated S-phase accumulation induced by topotecan treatment in p53 defective MDA231 tumor cells and HMEC/E6 cells.	7-hydroxystaurosporine	43-49	P53	Homo sapiens	115-118
15724841-12	2004	These data indicate that UCN-01 selectively enhances topotecan cytotoxicity in p53 defective cells through the induction of apoptotic signaling pathway(s), although the time course for the induction of cell death is not the same.	7-hydroxystaurosporine	25-31	P53	Homo sapiens	79-82
16200870-6	2004	There was a significant correlation between p53 mutation with simultaneous expression of Pgp and MRP1 and drug-resistance to either vinorelbine or carboplatin.	Vinorelbine	132-143	P53	Homo sapiens	44-47
15374966-0	2004	Retinoic acid increases the expression of p53 and proapoptotic caspases and sensitizes keratinocytes to apoptosis: a possible explanation for tumor preventive action of retinoids.	Retinoids	169-178	P53	Homo sapiens	42-45
15374966-8	2004	Inhibition of p53 and caspases with alpha-pifithrin and z-Val-Ala-Asp-fluoromethyl ketone, respectively, blocked UVB- and doxorubicin-induced apoptosis in ATRA-treated KCs.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	56-89	P53	Homo sapiens	14-17
15388804-5	2004	While an increase in intrachromosomal recombination induced by both UV radiation and methylmethane sulphonate (MMS) was observed in yeast cells carrying the void plasmid, p53 expression significantly reduced recombination frequency.	Methyl Methanesulfonate	111-114	P53	Homo sapiens	171-174
15169778-1	2004	The tumor suppressor p53 is commonly inhibited under conditions in which the phosphatidylinositide 3"-OH kinase/protein kinase B (PKB)Akt pathway is activated.	phosphatidylinositide	77-98	P53	Homo sapiens	21-24
15219939-1	2004	The pro-apoptotic ability of (Z)-3,5,4"-Tri-O-methyl-resveratrol (R3) was investigated in vitro on the human lymphoblastoid cell line TK6 and its p53-knockout counterpart (NH32).	(z)-3,5,4"-tri-o-methyl-resveratrol	29-64	P53	Homo sapiens	146-149
15145929-1	2004	Pifithrin-alpha (PFTalpha) was originally thought to be a specific inhibitor of signaling by the tumor suppressor protein p53.	pifithrin	0-15	P53	Homo sapiens	122-125
15145929-1	2004	Pifithrin-alpha (PFTalpha) was originally thought to be a specific inhibitor of signaling by the tumor suppressor protein p53.	pifithrin	17-25	P53	Homo sapiens	122-125
15252149-10	2004	Attenuating p53 by a chemical inhibitor pifithrin-alpha decreased the selenite-induced p53 Ser15P and led to concordant reductions of PARP cleavage and apoptosis.	pifithrin	40-49	P53	Homo sapiens	12-15
15252149-10	2004	Attenuating p53 by a chemical inhibitor pifithrin-alpha decreased the selenite-induced p53 Ser15P and led to concordant reductions of PARP cleavage and apoptosis.	pifithrin	40-49	P53	Homo sapiens	87-90
15147952-4	2004	Using the proteasome-specific inhibitors, MG132 and lactacystin, we show that the p53, the cdk inhibitors p21 and p27, and cyclin A are degraded by the ubiquitin-proteasome pathway in human osteosarcoma cells.	lactacystin	52-63	P53	Homo sapiens	82-85
15149862-0	2004	Distinct functions for WRN and TP53 in a shared pathway of cellular response to 1-beta-D-arabinofuranosylcytosine and bleomycin.	Bleomycin	118-127	P53	Homo sapiens	31-35
15144874-0	2004	The role of p53-induced apoptosis in cerebral ischemia: effects of the p53 inhibitor pifithrin alpha.	pifithrin	85-100	P53	Homo sapiens	71-74
15144874-4	2004	Pifithrin alpha reduced the number of apoptotic cells in the ischemic brain by inhibiting the binding of p53 to its DNA sites as it reduced the expression of the p53-related gene p21(WAF) without changing the amount of p53 protein itself.	pifithrin	0-15	P53	Homo sapiens	105-108
15144874-4	2004	Pifithrin alpha reduced the number of apoptotic cells in the ischemic brain by inhibiting the binding of p53 to its DNA sites as it reduced the expression of the p53-related gene p21(WAF) without changing the amount of p53 protein itself.	pifithrin	0-15	P53	Homo sapiens	162-165
15144874-4	2004	Pifithrin alpha reduced the number of apoptotic cells in the ischemic brain by inhibiting the binding of p53 to its DNA sites as it reduced the expression of the p53-related gene p21(WAF) without changing the amount of p53 protein itself.	pifithrin	0-15	P53	Homo sapiens	162-165
15161716-0	2004	The roles of thymidylate synthase and p53 in regulating Fas-mediated apoptosis in response to antimetabolites.	ammonium ferrous sulfate	56-59	P53	Homo sapiens	38-41
15042566-5	2004	In DNA from the breast and liver tumors the authors showed the same missense mutation in codon 245 (GGC--&gt;GAC; Gly--&gt;Asp) of exon 7 of p53.	Aspartic Acid	123-126	P53	Homo sapiens	141-144
15059920-4	2004	PG(13)-Luc activity, which was used as a positive control for functional p53 expression, was increased up to approximately 250-fold by coexpression of wild-type p53.	pg(13)	0-6	P53	Homo sapiens	73-76
15059920-4	2004	PG(13)-Luc activity, which was used as a positive control for functional p53 expression, was increased up to approximately 250-fold by coexpression of wild-type p53.	pg(13)	0-6	P53	Homo sapiens	161-164
15034932-9	2004	Also, apoptosis was observed to be induced by SP600125, concomitant with the increase in c-myc, p53, and bax protein level.	pyrazolanthrone	46-54	P53	Homo sapiens	96-99
15034932-11	2004	When the cells were treated with NDGA or SP600125 in the presence of antisense c-myc oligonucleotides, apoptosis was not observed and an increase of c-myc, p53, and bax proteins was not manifested.	Masoprocol	33-37	P53	Homo sapiens	156-159
15034932-11	2004	When the cells were treated with NDGA or SP600125 in the presence of antisense c-myc oligonucleotides, apoptosis was not observed and an increase of c-myc, p53, and bax proteins was not manifested.	pyrazolanthrone	41-49	P53	Homo sapiens	156-159
15177039-0	2004	The isoflavonoids genistein and quercetin activate different stress signaling pathways as shown by analysis of site-specific phosphorylation of ATM, p53 and histone H2AX.	Quercetin	32-41	P53	Homo sapiens	149-152
15177039-7	2004	Like genistein, quercetin induced phosphorylation of ATM on serine 1981, and ATM-dependent phosphorylation of histone H2AX on serine 139; however, p53 accumulation and phosphorylation on serines 6, 9, 15, 20, 46, and 392 occurred in ATM-deficient cells, indicating that ATM is not required for quercetin-induced phosphorylation of p53.	Quercetin	16-25	P53	Homo sapiens	331-334
14965369-3	2004	In this study, we found that PS-341 induced growth arrest and apoptosis of NCI-H520 and -H460 non-small cell lung cancer (NSCLC) cells in conjunction with markedly up-regulated levels of p21(waf1) and p53, and down-regulation of bcl-2 protein in these cells.	Bortezomib	29-35	P53	Homo sapiens	201-204
14965369-5	2004	Interestingly, when the JNK/c-Jun/AP-1 signal pathway was disrupted by the JNK inhibitor SP600125, the ability of PS-341 to inhibit the growth of NSCLC cells and to up-regulate the levels of p21(waf1) in these cells was blunted, but the expression of p53 was sustained at a high level, suggesting that the JNK/c-Jun/AP-1 signal pathway might mediate the anti-lung cancer effects of PS-341, with p21(waf1) playing the central role.	pyrazolanthrone	89-97	P53	Homo sapiens	251-254
14965369-5	2004	Interestingly, when the JNK/c-Jun/AP-1 signal pathway was disrupted by the JNK inhibitor SP600125, the ability of PS-341 to inhibit the growth of NSCLC cells and to up-regulate the levels of p21(waf1) in these cells was blunted, but the expression of p53 was sustained at a high level, suggesting that the JNK/c-Jun/AP-1 signal pathway might mediate the anti-lung cancer effects of PS-341, with p21(waf1) playing the central role.	Bortezomib	114-120	P53	Homo sapiens	251-254
14965371-0	2004	p53-independent anti-tumor effects of the nitrogen-containing bisphosphonate zoledronic acid.	Diphosphonates	62-76	P53	Homo sapiens	0-3
14751514-12	2004	The other 50% was attributed to the p53-dependent permanent G1 arrest, because cells lacking in functional p53 (LFS2800, FaDu, CHO) showed a ratio of LE:CA = 1.01 +/- 0.02:1.	fadu	121-125	P53	Homo sapiens	36-39
14751514-12	2004	The other 50% was attributed to the p53-dependent permanent G1 arrest, because cells lacking in functional p53 (LFS2800, FaDu, CHO) showed a ratio of LE:CA = 1.01 +/- 0.02:1.	fadu	121-125	P53	Homo sapiens	107-110
14743382-6	2004	When their DNA is damaged, p53-defective tumor cells preferentially arrest in S or G2 phase where they are susceptible to checkpoint inhibitors such as caffeine and UCN-01.	7-hydroxystaurosporine	165-171	P53	Homo sapiens	27-30
15515172-7	2004	In contrast to L5178Y cells, the response of TK6 cells to MMS and bleomycin was characterized by the induction of p53-dependent genes that are involved in DNA repair, cell cycle regulation, and apoptosis.	Methyl Methanesulfonate	58-61	P53	Homo sapiens	114-117
15515172-7	2004	In contrast to L5178Y cells, the response of TK6 cells to MMS and bleomycin was characterized by the induction of p53-dependent genes that are involved in DNA repair, cell cycle regulation, and apoptosis.	Bleomycin	66-75	P53	Homo sapiens	114-117
14634213-4	2003	We now show that, like dicoumarol, several other coumarin and flavone inhibitors of NQO1 activity, which compete with NAD(P)H for binding to NQO1, induced ubiquitin-independent p53 degradation and inhibited wild-type p53-mediated apoptosis.	coumarin	49-57	P53	Homo sapiens	177-180
14634213-4	2003	We now show that, like dicoumarol, several other coumarin and flavone inhibitors of NQO1 activity, which compete with NAD(P)H for binding to NQO1, induced ubiquitin-independent p53 degradation and inhibited wild-type p53-mediated apoptosis.	coumarin	49-57	P53	Homo sapiens	217-220
14636064-2	2003	We have previously shown that 15d-PGJ(2) potently induces apoptosis of SH-SY5Y human neuroblastoma cells via accumulation of the tumor suppressor gene product p53.	15d-pgj	30-37	P53	Homo sapiens	159-162
14636064-5	2003	In addition, exposure of the cells to 15d-PGJ(2) resulted in an accumulation of ubiquitinated proteins and in a significant inhibition of proteasome activities, suggesting that 15d-PGJ(2) acted on the ubiquitin-proteasome pathway, a regulatory mechanism of p53 turnover.	15d-pgj	38-45	P53	Homo sapiens	257-260
14636064-5	2003	In addition, exposure of the cells to 15d-PGJ(2) resulted in an accumulation of ubiquitinated proteins and in a significant inhibition of proteasome activities, suggesting that 15d-PGJ(2) acted on the ubiquitin-proteasome pathway, a regulatory mechanism of p53 turnover.	15d-pgj	177-184	P53	Homo sapiens	257-260
14636064-7	2003	These data suggest that the modulation of proteasome activity may be involved in the mechanism responsible for the accumulation of p53 and subsequent induction of apoptotic cell death induced by 15d-PGJ(2).	15d-pgj	195-202	P53	Homo sapiens	131-134
14654783-7	2003	Substitution of S407 with aspartate (S407D), but not with alanine (S407A), promotes nuclear localization of p53.	Aspartic Acid	26-35	P53	Homo sapiens	108-111
14612532-0	2003	The proteasome inhibitor bortezomib stabilizes a novel active form of p53 in human LNCaP-Pro5 prostate cancer cells.	Bortezomib	25-35	P53	Homo sapiens	70-73
14612532-4	2003	Bortezomib induced strong stabilization of p53, but it did not promote phosphorylation on serines 15 and 20, and p53 remained bound to its inhibitor, mdm2.	Bortezomib	0-10	P53	Homo sapiens	43-46
14612532-5	2003	Nonetheless, bortezomib stimulated p53 translocation to the nucleus (not mitochondria) and enhanced p53 DNA binding, accumulation of p53-dependent transcripts, and activation of a p53-responsive reporter gene.	Bortezomib	13-23	P53	Homo sapiens	35-38
14612532-5	2003	Nonetheless, bortezomib stimulated p53 translocation to the nucleus (not mitochondria) and enhanced p53 DNA binding, accumulation of p53-dependent transcripts, and activation of a p53-responsive reporter gene.	Bortezomib	13-23	P53	Homo sapiens	100-103
14612532-5	2003	Nonetheless, bortezomib stimulated p53 translocation to the nucleus (not mitochondria) and enhanced p53 DNA binding, accumulation of p53-dependent transcripts, and activation of a p53-responsive reporter gene.	Bortezomib	13-23	P53	Homo sapiens	100-103
14612532-5	2003	Nonetheless, bortezomib stimulated p53 translocation to the nucleus (not mitochondria) and enhanced p53 DNA binding, accumulation of p53-dependent transcripts, and activation of a p53-responsive reporter gene.	Bortezomib	13-23	P53	Homo sapiens	100-103
14612532-6	2003	Furthermore, stable LNCaP-Pro5 transfectants of LNCaP-Pro5 expressing the p53 inhibitor human papillomavirus-E6 displayed reduced bortezomib-induced p53 activation and cell death.	Bortezomib	130-140	P53	Homo sapiens	74-77
14612532-6	2003	Furthermore, stable LNCaP-Pro5 transfectants of LNCaP-Pro5 expressing the p53 inhibitor human papillomavirus-E6 displayed reduced bortezomib-induced p53 activation and cell death.	Bortezomib	130-140	P53	Homo sapiens	149-152
14612532-7	2003	Together, our data demonstrate that bortezomib stimulates p53 activation via a novel mechanism.	Bortezomib	36-46	P53	Homo sapiens	58-61
12844488-8	2003	However, the p53 mutation frequency increased with the increased number of the combined genotypes among XPD 312WT (Asp/Asp), XPD 751VT (Lys/Gln or Gln/Gln) or XRCC1 399VT (Arg/Gln or Gln/Gln) (P = 0.01, trend test).	Aspartic Acid	115-118	P53	Homo sapiens	13-16
12844488-8	2003	However, the p53 mutation frequency increased with the increased number of the combined genotypes among XPD 312WT (Asp/Asp), XPD 751VT (Lys/Gln or Gln/Gln) or XRCC1 399VT (Arg/Gln or Gln/Gln) (P = 0.01, trend test).	Aspartic Acid	119-122	P53	Homo sapiens	13-16
12844488-9	2003	These results suggest that individuals who smoke and have the XPD codon 312 Asp/Asp genotype may be at a greater risk of p53 mutations, especially if combined with other polymorphisms that may result in deficient DNA repair.	Aspartic Acid	76-79	P53	Homo sapiens	121-124
12844488-9	2003	These results suggest that individuals who smoke and have the XPD codon 312 Asp/Asp genotype may be at a greater risk of p53 mutations, especially if combined with other polymorphisms that may result in deficient DNA repair.	Aspartic Acid	80-83	P53	Homo sapiens	121-124
14555520-4	2003	RESULTS: When lymphocytes were treated in vitro with biologically relevant doses of melphalan, monoadducts accumulated rapidly in both p53 and N-ras genes, reaching maximal levels within 2 h, whereas the highest interstrand cross-link levels were found within 8 h. Thereafter, the adducts were repaired with half-lives of 14.5 +/- 0.3 h (p53) or 18.8 +/- 1.5 h (N-ras) for monoadducts and 12.4 +/- 0.8 h (p53) or 14.1 +/- 2.2 h (N-ras) for interstrand cross-links.	Melphalan	84-93	P53	Homo sapiens	135-138
14555520-4	2003	RESULTS: When lymphocytes were treated in vitro with biologically relevant doses of melphalan, monoadducts accumulated rapidly in both p53 and N-ras genes, reaching maximal levels within 2 h, whereas the highest interstrand cross-link levels were found within 8 h. Thereafter, the adducts were repaired with half-lives of 14.5 +/- 0.3 h (p53) or 18.8 +/- 1.5 h (N-ras) for monoadducts and 12.4 +/- 0.8 h (p53) or 14.1 +/- 2.2 h (N-ras) for interstrand cross-links.	Melphalan	84-93	P53	Homo sapiens	338-341
14555520-4	2003	RESULTS: When lymphocytes were treated in vitro with biologically relevant doses of melphalan, monoadducts accumulated rapidly in both p53 and N-ras genes, reaching maximal levels within 2 h, whereas the highest interstrand cross-link levels were found within 8 h. Thereafter, the adducts were repaired with half-lives of 14.5 +/- 0.3 h (p53) or 18.8 +/- 1.5 h (N-ras) for monoadducts and 12.4 +/- 0.8 h (p53) or 14.1 +/- 2.2 h (N-ras) for interstrand cross-links.	Melphalan	84-93	P53	Homo sapiens	338-341
12915590-4	2003	Cellular stress and DNA damage caused by UV-radiation, downregulation of the proteasome and arsenic trioxide promoted Mdm2 and PML damage-specific nuclear relocalization and interaction in a p53-independent manner.	Arsenic Trioxide	92-108	P53	Homo sapiens	191-194
12860987-1	2003	Modification-specific antibodies were used to characterize the phosphorylation and acetylation of human p53 in response to genotoxic (UV, IR, and adriamycin) and non-genotoxic (PALA, taxol, nocodazole) stress in cultured human cells at 14 known modification sites.	sparfosic acid	177-181	P53	Homo sapiens	104-107
12967348-0	2003	The p53-inhibitor pifithrin-alpha inhibits firefly luciferase activity in vivo and in vitro.	pifithrin	18-33	P53	Homo sapiens	4-7
12967348-2	2003	It has been proposed that the use of pifithrin-alpha in conjunction with chemotherapeutic and radiation therapies for cancer will reduce the side effects of these treatments in normal tissue that still contains wild type p53.	pifithrin	37-46	P53	Homo sapiens	221-224
12967348-3	2003	In addition, pifithrin-alpha provides a useful tool in the laboratory to investigate the function of p53 in model systems.	pifithrin	13-22	P53	Homo sapiens	101-104
12883691-3	2003	In this study, we found PIG11, a p53-induced gene, was upregulated markedly by As2O3 using the technique of differential display reverse transcriptase PCR (DDRT-PCR).	Arsenic Trioxide	79-84	P53	Homo sapiens	33-36
12893085-0	2003	Inhibition of p53, p21 and Bax by pifithrin-alpha does not affect UV induced apoptotic response in CS-B cells.	pifithrin	34-49	P53	Homo sapiens	14-17
12948823-3	2003	Procarbazine plus Cu(II) induced piperidine-labile and formamidopyrimidine-DNA glycosylase-sensitive lesions at the 5"-ACG-3" sequence, complementary to a hotspot of the p53 gene, and the 5"-TG-3" sequence.	Procarbazine	0-12	P53	Homo sapiens	170-173
12907245-0	2003	The JNK, ERK and p53 pathways play distinct roles in apoptosis mediated by the antitumor agents vinblastine, doxorubicin, and etoposide.	Vinblastine	96-107	P53	Homo sapiens	17-20
12907245-9	2003	Vinblastine induced p53 downregulation, and chemical inhibition of p53 potentiated vinblastine-induced cell death, suggesting a protective effect of p53.	Vinblastine	0-11	P53	Homo sapiens	20-23
12907245-9	2003	Vinblastine induced p53 downregulation, and chemical inhibition of p53 potentiated vinblastine-induced cell death, suggesting a protective effect of p53.	Vinblastine	83-94	P53	Homo sapiens	67-70
12907245-9	2003	Vinblastine induced p53 downregulation, and chemical inhibition of p53 potentiated vinblastine-induced cell death, suggesting a protective effect of p53.	Vinblastine	83-94	P53	Homo sapiens	67-70
12821135-5	2003	HCT116 p53-/- cells expressing p53 mutant, in which serine residues at 6, 9, 46, 376, and 378 were replaced by aspartic acids, were resistant to TPCK-induced apoptosis suggesting the requirement of dephosphorylation of p53 on serine residues during TPCK-induced apoptosis.	Aspartic Acid	111-125	P53	Homo sapiens	31-34
12821135-5	2003	HCT116 p53-/- cells expressing p53 mutant, in which serine residues at 6, 9, 46, 376, and 378 were replaced by aspartic acids, were resistant to TPCK-induced apoptosis suggesting the requirement of dephosphorylation of p53 on serine residues during TPCK-induced apoptosis.	Aspartic Acid	111-125	P53	Homo sapiens	31-34
12971634-9	2003	CONCLUSION: Our results suggest that in NSCLC, there was a weak correlation between higher 201Tl ratios and positive response to chemotherapy, absence of distant metastasis, and p53(-) status.	Thallium-201	91-96	P53	Homo sapiens	178-181
12829999-9	2003	Furthermore, cells treated with 15d-PGJ(2) and troglitazone showed elevated expression of p53 and two p53-controlled downstream genes, GADD45 and p21(WAF1/Cip1).	15d-pgj	32-39	P53	Homo sapiens	90-93
12829999-9	2003	Furthermore, cells treated with 15d-PGJ(2) and troglitazone showed elevated expression of p53 and two p53-controlled downstream genes, GADD45 and p21(WAF1/Cip1).	15d-pgj	32-39	P53	Homo sapiens	102-105
12829999-9	2003	Furthermore, cells treated with 15d-PGJ(2) and troglitazone showed elevated expression of p53 and two p53-controlled downstream genes, GADD45 and p21(WAF1/Cip1).	Troglitazone	47-59	P53	Homo sapiens	90-93
12829999-9	2003	Furthermore, cells treated with 15d-PGJ(2) and troglitazone showed elevated expression of p53 and two p53-controlled downstream genes, GADD45 and p21(WAF1/Cip1).	Troglitazone	47-59	P53	Homo sapiens	102-105
12829999-10	2003	Dominant negative inhibition of p53 in SG231 cells significantly blocked the 15d-PGJ(2) and troglitazone-induced growth inhibition, G2/M arrest, and GADD45/p21 induction.	15d-pgj	77-84	P53	Homo sapiens	32-35
12829999-10	2003	Dominant negative inhibition of p53 in SG231 cells significantly blocked the 15d-PGJ(2) and troglitazone-induced growth inhibition, G2/M arrest, and GADD45/p21 induction.	Troglitazone	92-104	P53	Homo sapiens	32-35
12884365-1	2003	Recently, blockage of p53-dependent transcriptional activation and apoptosis by pifithrin-alpha (PFTalpha) has been reported to be useful for reducing the side effects of cancer therapy and the compound is thus thought to be a specific inhibitor of p53 [Komarov et al., Science 1999;285:1733-1737].	pifithrin	80-95	P53	Homo sapiens	22-25
12884365-1	2003	Recently, blockage of p53-dependent transcriptional activation and apoptosis by pifithrin-alpha (PFTalpha) has been reported to be useful for reducing the side effects of cancer therapy and the compound is thus thought to be a specific inhibitor of p53 [Komarov et al., Science 1999;285:1733-1737].	pifithrin	80-95	P53	Homo sapiens	249-252
12884365-1	2003	Recently, blockage of p53-dependent transcriptional activation and apoptosis by pifithrin-alpha (PFTalpha) has been reported to be useful for reducing the side effects of cancer therapy and the compound is thus thought to be a specific inhibitor of p53 [Komarov et al., Science 1999;285:1733-1737].	pifithrin	97-105	P53	Homo sapiens	22-25
12884365-1	2003	Recently, blockage of p53-dependent transcriptional activation and apoptosis by pifithrin-alpha (PFTalpha) has been reported to be useful for reducing the side effects of cancer therapy and the compound is thus thought to be a specific inhibitor of p53 [Komarov et al., Science 1999;285:1733-1737].	pifithrin	97-105	P53	Homo sapiens	249-252
12884365-3	2003	Instead, p53-dependent activation and apoptosis were not only induced by PFTalpha itself but were also enhanced by a combination of PFTalpha with UVB or Dox.	pifithrin	73-81	P53	Homo sapiens	9-12
12884365-4	2003	Furthermore, PFTalpha-induced apoptosis was mediated through p53-dependent and -independent signaling pathways.	pifithrin	13-21	P53	Homo sapiens	61-64
12884365-5	2003	Extracellular signal-regulated kinases and p38 kinase, but not c-jun N-terminal kinases (JNKs), were activated, and these activations were required for phosphorylation and accumulation of p53 in the cellular apoptotic response to PFTalpha.	pifithrin	230-238	P53	Homo sapiens	188-191
12700230-9	2003	Drugs such as CDB3, which rescue the conformation of unstable mutants of p53, have to act during or immediately after biosynthesis.	cdb3	14-18	P53	Homo sapiens	73-76
12753897-3	2003	However, the substitution of the serine residues with the aspartic acid (S116/127D) abolished p53 DNA binding and led to protein stabilization.	Aspartic Acid	58-71	P53	Homo sapiens	94-97
12697268-5	2003	Furthermore, annonacin activated p21 in a p53-independent manner and arrested T24 cells at the G1 phase.	annonacin	13-22	P53	Homo sapiens	42-45
12684687-4	2003	We report that Brca1-deficiency in p53-null cells was associated with increased sensitivity to the topoisomerase I poisons camptothecin and topotecan, the topoisomerase II poisons doxorubicin, mitoxantrone and etoposide, and to the platinum compounds carboplatin and oxaliplatin, but not to the antimetabolites 5-fluorouracil and gemcitabine and the taxanes docetaxel and paclitaxel.	Docetaxel	358-367	P53	Homo sapiens	35-38
12711114-1	2003	The p53 gene is frequently mutated in lung tumors, and mutations may be caused by both polycyclic aromatic hydrocarbons (PAHs) and nitrosamines found in tobacco smoke.	Polycyclic Aromatic Hydrocarbons	87-119	P53	Homo sapiens	4-7
12711114-1	2003	The p53 gene is frequently mutated in lung tumors, and mutations may be caused by both polycyclic aromatic hydrocarbons (PAHs) and nitrosamines found in tobacco smoke.	Polycyclic Aromatic Hydrocarbons	121-125	P53	Homo sapiens	4-7
12711114-12	2003	These results suggest that p53 mutations in both types of lung tumors may arise from adduction by both PAHs and nitrosamines.	Polycyclic Aromatic Hydrocarbons	103-107	P53	Homo sapiens	27-30
12556443-8	2003	Interestingly, CTF-PS2-induced caspase 3 activation is prevented by pifithrin-alpha, a selective blocker of p53 transcriptional activity.	pifithrin	68-77	P53	Homo sapiens	108-111
12670900-0	2003	Fas-mediated apoptosis is dependent on wild-type p53 status in human cancer cells expressing a temperature-sensitive p53 mutant alanine-143.	ammonium ferrous sulfate	0-3	P53	Homo sapiens	49-52
12670900-0	2003	Fas-mediated apoptosis is dependent on wild-type p53 status in human cancer cells expressing a temperature-sensitive p53 mutant alanine-143.	ammonium ferrous sulfate	0-3	P53	Homo sapiens	117-120
12670900-5	2003	Our results demonstrated that Fas-mediated apoptosis in H1299 and PC-3 cells expressing p53 mutant 143Ala occurred only with the wild-type p53 phenotype.	ammonium ferrous sulfate	30-33	P53	Homo sapiens	88-91
12670900-5	2003	Our results demonstrated that Fas-mediated apoptosis in H1299 and PC-3 cells expressing p53 mutant 143Ala occurred only with the wild-type p53 phenotype.	ammonium ferrous sulfate	30-33	P53	Homo sapiens	139-142
12670900-6	2003	These results support the hypothesis that Fas-mediated apoptosis is dependent, at least partially, on the presence of a functional wild-type p53 state.	ammonium ferrous sulfate	42-45	P53	Homo sapiens	141-144
12634062-2	2003	Circular dichroism, Fourier transform infrared spectroscopy and staining with Congo red and thioflavin T showed that p53tet-wt and p53tet-R337H adopt an alternative beta-sheet conformation (p53tet-wt-beta and p53tet-R337H-beta, respectively), characteristic of amyloid-like fibrils, when incubated at pH 4.0 and elevated temperatures.	thioflavin T	92-104	P53	Homo sapiens	117-120
12634062-2	2003	Circular dichroism, Fourier transform infrared spectroscopy and staining with Congo red and thioflavin T showed that p53tet-wt and p53tet-R337H adopt an alternative beta-sheet conformation (p53tet-wt-beta and p53tet-R337H-beta, respectively), characteristic of amyloid-like fibrils, when incubated at pH 4.0 and elevated temperatures.	thioflavin T	92-104	P53	Homo sapiens	131-134
12393500-4	2003	We here demonstrate molecular mechanisms whereby PS-341 mediates anti-MM activity by inducing p53 and MDM2 protein expression; inducing the phosphorylation (Ser15) of p53 protein; activating c-Jun NH(2)-terminal kinase (JNK), caspase-8, and caspase-3; and cleaving the DNA protein kinase catalytic subunit, ATM, and MDM2.	Bortezomib	49-55	P53	Homo sapiens	94-97
12393500-4	2003	We here demonstrate molecular mechanisms whereby PS-341 mediates anti-MM activity by inducing p53 and MDM2 protein expression; inducing the phosphorylation (Ser15) of p53 protein; activating c-Jun NH(2)-terminal kinase (JNK), caspase-8, and caspase-3; and cleaving the DNA protein kinase catalytic subunit, ATM, and MDM2.	Bortezomib	49-55	P53	Homo sapiens	167-170
12628584-6	2003	Further, we found that nitric oxide synthase inhibitor N(G)-nitro-L-arginine prevented deltamethrin-induced neuronal apoptosis and altered expression of p53, Bax, and Bcl-2.	Nitroarginine	55-76	P53	Homo sapiens	153-156
12469188-0	2003	Restoration of p53 gene function in 12-O-tetradecanoylphorbor 13-acetate-resistant human leukemia K562/TPA cells.	12-o-tetradecanoylphorbor 13-acetate	36-72	P53	Homo sapiens	15-18
12393870-7	2002	In addition, down-regulation of the pro-apoptotic tumor suppressor protein, p53, via PKB-mediated phosphorylation of MDM2 might also play a role in partially protecting beta-cells from FFA-induced apoptosis.	Fatty Acids, Nonesterified	185-188	P53	Homo sapiens	76-79
12393870-8	2002	Adenoviral mediated expression of wild type p53 potentiated FFA-induced beta-cell apoptosis, whereas expression of a dominant negative p53 partly inhibited beta-cell apoptosis by approximately 50%.	Fatty Acids, Nonesterified	60-63	P53	Homo sapiens	44-47
12221076-4	2002	With the loss of the p53 gene, the levels of phosphorylation of Ser-63 of c-Jun and Thr-183/Tyr-185 of JNK1/2 in p53-/- cells did not increase as markedly as in p53+/+ cells in response to a 1-h treatment with nocodazole or other microtubule-disrupting drugs such as vinblastine and colchicine.	Vinblastine	267-278	P53	Homo sapiens	21-24
12221076-4	2002	With the loss of the p53 gene, the levels of phosphorylation of Ser-63 of c-Jun and Thr-183/Tyr-185 of JNK1/2 in p53-/- cells did not increase as markedly as in p53+/+ cells in response to a 1-h treatment with nocodazole or other microtubule-disrupting drugs such as vinblastine and colchicine.	Vinblastine	267-278	P53	Homo sapiens	113-116
12221076-4	2002	With the loss of the p53 gene, the levels of phosphorylation of Ser-63 of c-Jun and Thr-183/Tyr-185 of JNK1/2 in p53-/- cells did not increase as markedly as in p53+/+ cells in response to a 1-h treatment with nocodazole or other microtubule-disrupting drugs such as vinblastine and colchicine.	Vinblastine	267-278	P53	Homo sapiens	113-116
12221076-6	2002	However, arsenate-induced JNK activation in p53-/- cells was preserved.	arsenic acid	9-17	P53	Homo sapiens	44-47
12221076-8	2002	Surprisingly, cotransfection of p53+/+ cells with dominant negative mutants of JNK isoforms and treatment of p53+/+ cells with the JNK inhibitor SP600125 actually further enhanced apoptosis in p53+/+ cells by up to 2-fold in response to nocodazole.	pyrazolanthrone	145-153	P53	Homo sapiens	32-35
12221076-8	2002	Surprisingly, cotransfection of p53+/+ cells with dominant negative mutants of JNK isoforms and treatment of p53+/+ cells with the JNK inhibitor SP600125 actually further enhanced apoptosis in p53+/+ cells by up to 2-fold in response to nocodazole.	pyrazolanthrone	145-153	P53	Homo sapiens	109-112
12221076-8	2002	Surprisingly, cotransfection of p53+/+ cells with dominant negative mutants of JNK isoforms and treatment of p53+/+ cells with the JNK inhibitor SP600125 actually further enhanced apoptosis in p53+/+ cells by up to 2-fold in response to nocodazole.	pyrazolanthrone	145-153	P53	Homo sapiens	109-112
12490120-0	2002	[Arsenic trioxide induced apoptosis and expression of p53 and bcl-2 genes in human small cell lung cancer cells].	Arsenic Trioxide	1-17	P53	Homo sapiens	54-57
12151395-5	2002	Moreover, the role of p53 in activation of this pathway was demonstrated by the fact that inhibition of p53 activity by pifithrin-alpha reduced the sensitivity of HCT116/p21(-/-) cells to daunomycin-induced apoptosis and restored a Bax/Bcl-2 ratio similar to that observed in HCT116p21(+/+) cells.	pifithrin	120-135	P53	Homo sapiens	104-107
12107073-6	2002	In addition, p21 mRNA abundance, a downstream target of p53 protein, was increased in the ZS cells compared with both the ZN control and ZD cells.	Zinc	122-124	P53	Homo sapiens	56-59
12130688-6	2002	Shikoccin (a diterpene), dibenzylideneacetone, and curcumin fit the pharmacophore hypothesis, inhibit cellular isopeptidases, and cause cell death independently of p53 in isogenic pairs of RKO and HCT 116 cells with differential p53 status.	Shikoccin	0-9	P53	Homo sapiens	229-232
12430174-6	2002	Protein levels of p53 and cleavage of poly(ADP)-ribose polymerase were increased in a dose-dependent manner following treatment of As2O3.	Arsenic Trioxide	131-136	P53	Homo sapiens	18-21
12416024-11	2002	We also observed that p53 status influenced correlations between ENT1 transporter gene RNA levels and sensitivity to the drugs tiazafurin, AZQ and 3-deazauridine.	diaziquone	139-142	P53	Homo sapiens	22-25
12067251-8	2002	Treatment of p53 cDNA with micromolar concentrations of (+/-)-anti-7,8-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydro-benzo[a]pyrene, (anti-BPDE, an ultimate carcinogen) or sub-micromolar concentrations of BP-7,8-dione in the presence of redox-cycling conditions (NADPH and CuCl(2)) also caused p53 mutations in a dose-dependent manner.	NADP	268-273	P53	Homo sapiens	13-16
12082016-8	2002	Tp53 was also strongly induced by an N-oxide of quinoline and by dabequine, an experimental antimalarial evaluated in humans; dabequine was reported to be negative in other screens of mutagenicity and clastogenicity but carcinogenic in animal studies.	n-oxide	37-44	P53	Homo sapiens	0-4
12011992-10	2002	The KOSCC-11 cell line contained a frameshift mutation and the other cell lines harbored an identical p53 mutation at codon 175 from CGC (Arg) to CTC (Leu).	Leucine	151-154	P53	Homo sapiens	102-105
11986953-1	2002	The retinoid, N-(4-hydroxyphenyl)retinamide (4-HPR), mediates p53-independent cytotoxicity and can increase reactive oxygen species and ceramide in solid tumor cell lines.	Retinoids	4-12	P53	Homo sapiens	62-65
11890931-4	2002	MMS induces phosphorylation of p53 on Ser15 and Ser392 in a dose- and time-dependent manner.	Methyl Methanesulfonate	0-3	P53	Homo sapiens	31-34
11890931-5	2002	MMS-induced p53 phosphorylation is independent of DNA mismatch repair (MMR) activity.	Methyl Methanesulfonate	0-3	P53	Homo sapiens	12-15
11854596-7	2002	In addition, a new p53 mutation not previously reported in ET/pPNET involving exon 5 codon 138: GCC to GAC (Ala/Asp) was detected.	Aspartic Acid	112-115	P53	Homo sapiens	19-22
11889192-4	2002	Addition of pifithrin-alpha, a specific inhibitor of p53, or transfection of p53 antisense oligonucleotides caused decreased RV-induced p53 and p21 expression in PTC and FTC cells.	pifithrin	12-27	P53	Homo sapiens	53-56
11827710-0	2002	Pifithrin-alpha, an inhibitor of p53, enhances the genetic instability induced by etoposide (VP16) in human lymphoblastoid cells treated in vitro.	pifithrin	0-15	P53	Homo sapiens	33-36
11992635-0	2002	Monoamine neurotoxins-induced apoptosis in lymphocytes by a common oxidative stress mechanism: involvement of hydrogen peroxide (H(2)O(2)), caspase-3, and nuclear factor kappa-B (NF-kappaB), p53, c-Jun transcription factors.	monoamine	0-9	P53	Homo sapiens	191-194
11799138-9	2002	The truncated p53 was not immunohistochemically detected in three cases with the DO-7 antibody and in five cases with the G59-12 antibody, giving false-negative results in 25% or 40%, respectively, of all tumor cell lines examined.	g59-12	122-128	P53	Homo sapiens	14-17
11782540-8	2002	CDB3 may act as a "chaperone" that maintains existing or newly synthesized destabilized p53 mutants in a native conformation and then allows transfer to specific DNA, which binds more tightly.	cdb3	0-4	P53	Homo sapiens	88-91
11850804-10	2002	Western analysis of p53 was supplemented with its cytolocalization by immuno-labeling using laser scanning confocal fluorescence microscopy, which revealed an ICI-sensitive increase in the abundance of p53 in hormone-treated cells.	ici	159-162	P53	Homo sapiens	20-23
11850804-10	2002	Western analysis of p53 was supplemented with its cytolocalization by immuno-labeling using laser scanning confocal fluorescence microscopy, which revealed an ICI-sensitive increase in the abundance of p53 in hormone-treated cells.	ici	159-162	P53	Homo sapiens	202-205
11859874-10	2002	A non-significant increased risk of breast cancer was observed in the highest exposure level of dieldrin and polychlorinated biphenyls among women who developed a tumor with mutant p53 (odds ratio (OR) = 3.53, 95% confidence interval (CI) = 0.79-15.79 and OR = 3.00, 95% CI = 0.66-13.62).	Dieldrin	96-104	P53	Homo sapiens	181-184
11859874-11	2002	There was no clear difference in overall survival between breast cancer cases with "wild-type" and mutant p53, although a significant dose-response relationship appeared for dieldrin exposure in tumors with "wild-type" p53.	Dieldrin	174-182	P53	Homo sapiens	219-222
11815972-3	2002	METHODS: The p53 gene was overexpressed in IHGK (immortalized human gingival keratinocyte), IHGKN [4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, (NNK)]-carcinogen transformed keratinocytes, and two head and neck squamous carcinoma (HNSCC) cell lines, HN30 and HN12.	4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone	99-145	P53	Homo sapiens	13-16
11740818-6	2001	PS-341 inhibits p44/42 mitogen-activated protein kinase (MAPK) growth signaling triggered by IL-6 and induces apoptosis, despite induction of p21 and p27, in p53 wild-type and p53 mutant MM cells.	Bortezomib	0-6	P53	Homo sapiens	158-161
11740818-6	2001	PS-341 inhibits p44/42 mitogen-activated protein kinase (MAPK) growth signaling triggered by IL-6 and induces apoptosis, despite induction of p21 and p27, in p53 wild-type and p53 mutant MM cells.	Bortezomib	0-6	P53	Homo sapiens	176-179
11593402-1	2001	Two specific inhibitors of cyclin-dependent kinase 2 (Cdk2), roscovitine and olomoucine, have been shown recently to induce nuclear accumulation of wt p53 and nucleolar unravelling in interphase human untransformed IMR-90 and breast tumor-derived MCF-7 cells.	Roscovitine	61-72	P53	Homo sapiens	151-154
11593402-4	2001	Cells exposed to the two types of protein kinase inhibitors for longer times keep exhibiting altered nucleolar and wt p53 features, yet they strikingly differentiate in that most roscovitine-treated cells fail to ever accumulate high levels of p21(WAF1/CIP1) in contrast with DRB-treated ones.	Roscovitine	179-190	P53	Homo sapiens	118-121
11559355-1	2001	We have analysed the hydrogen/deuterium exchange of the tetramerization domain of human tumour suppressor p53 under mild chemical denaturation conditions, and at different temperatures.	Deuterium	30-39	P53	Homo sapiens	106-109
11494044-3	2001	In the present study, we have examined the effect of methylmethane sulfonate (MMS) to HCT-116 human colon cancer cells on the phosphorylation of p53.	Methyl Methanesulfonate	53-76	P53	Homo sapiens	145-148
11494044-3	2001	In the present study, we have examined the effect of methylmethane sulfonate (MMS) to HCT-116 human colon cancer cells on the phosphorylation of p53.	Methyl Methanesulfonate	78-81	P53	Homo sapiens	145-148
11494044-4	2001	Results show that p53 protein becomes phosphorylated at serine 15 (Ser15) and Ser392 residues after treatment with MMS in a time-dependent manner.	Methyl Methanesulfonate	115-118	P53	Homo sapiens	18-21
11494044-5	2001	Increased levels of phospho-p53(Ser15) and phospho-p53(Ser392) were maintained up to 50 h of the MMS treatment.	Methyl Methanesulfonate	97-100	P53	Homo sapiens	28-31
11494044-5	2001	Increased levels of phospho-p53(Ser15) and phospho-p53(Ser392) were maintained up to 50 h of the MMS treatment.	Methyl Methanesulfonate	97-100	P53	Homo sapiens	51-54
11494044-6	2001	We also examined the involvement of probable kinase(s), which could be responsible for MMS-induced phosphorylation of p53 at Ser15 and Ser392.	Methyl Methanesulfonate	87-90	P53	Homo sapiens	118-121
11494044-7	2001	In vitro phosphorylation assay, carried out with the immunoprecipates of MMS-treated cells, showed an increased phosphorylation of p53 by c-Jun kinase 1 (JNK1) at early time points (2.5 h).	Methyl Methanesulfonate	73-76	P53	Homo sapiens	131-134
11496322-7	2001	The tumor suppressor p53 and Cdk inhibitor p21, a known downstream effector of the p53, and association of p21 with Cdk2 were markedly induced in DHF-treated cells.	dhf	146-149	P53	Homo sapiens	21-24
11496322-7	2001	The tumor suppressor p53 and Cdk inhibitor p21, a known downstream effector of the p53, and association of p21 with Cdk2 were markedly induced in DHF-treated cells.	dhf	146-149	P53	Homo sapiens	83-86
11522376-0	2001	Induction of apoptotic cell death by a p53-independent pathway in neuronal SK-N-MC cells after treatment with 2,2",5,5"-tetrachlorobiphenyl.	2,5,2',5'-tetrachlorobiphenyl	110-139	P53	Homo sapiens	39-42
11397792-6	2001	The simplified reaction recapitulates the ubiquitination of p53 observed with individual components and the p53-Ub((n)) is qualitatively similar to p53-Ub((n)) detected in lactacystin-treated cells.	lactacystin	172-183	P53	Homo sapiens	60-63
11397792-6	2001	The simplified reaction recapitulates the ubiquitination of p53 observed with individual components and the p53-Ub((n)) is qualitatively similar to p53-Ub((n)) detected in lactacystin-treated cells.	lactacystin	172-183	P53	Homo sapiens	108-111
11397792-6	2001	The simplified reaction recapitulates the ubiquitination of p53 observed with individual components and the p53-Ub((n)) is qualitatively similar to p53-Ub((n)) detected in lactacystin-treated cells.	lactacystin	172-183	P53	Homo sapiens	108-111
11397792-7	2001	Surprisingly, we find that p53 is modified with multiple mono-ubiquitin moieties as opposed to a poly-ubiquitin chain.	mono-ubiquitin	57-71	P53	Homo sapiens	27-30
11602056-7	2001	CONCLUSIONS: Besides the expression of B7-1 and GM-CSF, BB-102 is able to express p53 protein in independent manner and exerts its anti-tumor activity, which suggests that BB-102 may be useful for gene therapy against HCC in vivo.	bb-102	56-62	P53	Homo sapiens	82-85
11602056-7	2001	CONCLUSIONS: Besides the expression of B7-1 and GM-CSF, BB-102 is able to express p53 protein in independent manner and exerts its anti-tumor activity, which suggests that BB-102 may be useful for gene therapy against HCC in vivo.	bb-102	172-178	P53	Homo sapiens	82-85
11464290-0	2001	Modulation of p53 dependent gene expression and cell death through thioredoxin-thioredoxin reductase by the Interferon-Retinoid combination.	Retinoids	119-127	P53	Homo sapiens	14-17
11408351-4	2001	However, in cells transformed but non-tumorigenic, p53 protein is elevated and transcriptionally activated in response to quercetin or other DNA damaging stimuli, but the cells bypass quercetin-induced G1 arrest likely due to E7 expression.	Quercetin	122-131	P53	Homo sapiens	51-54
11408351-4	2001	However, in cells transformed but non-tumorigenic, p53 protein is elevated and transcriptionally activated in response to quercetin or other DNA damaging stimuli, but the cells bypass quercetin-induced G1 arrest likely due to E7 expression.	Quercetin	184-193	P53	Homo sapiens	51-54
11408351-5	2001	In transformed tumorigenic cells, p53 is elevated in response to quercetin but its transcriptional activity is inhibited due to mutation, and the cells fail to stop in G1 in the presence of quercetin.	Quercetin	65-74	P53	Homo sapiens	34-37
11408351-5	2001	In transformed tumorigenic cells, p53 is elevated in response to quercetin but its transcriptional activity is inhibited due to mutation, and the cells fail to stop in G1 in the presence of quercetin.	Quercetin	190-199	P53	Homo sapiens	34-37
11423970-0	2001	Activation of p53 by roscovitine-mediated suppression of MDM2 expression.	Roscovitine	21-32	P53	Homo sapiens	14-17
11423970-3	2001	We found that treatment with roscovitine and olomoucin, which were originally developed as cyclin-dependent kinase (CDK) inhibitors, can efficiently stabilize and activate nuclear p53 in tumor cells with MDM2 amplification or cytoplasmic p53.	Roscovitine	29-40	P53	Homo sapiens	180-183
11423970-3	2001	We found that treatment with roscovitine and olomoucin, which were originally developed as cyclin-dependent kinase (CDK) inhibitors, can efficiently stabilize and activate nuclear p53 in tumor cells with MDM2 amplification or cytoplasmic p53.	Roscovitine	29-40	P53	Homo sapiens	238-241
11423970-5	2001	Roscovitine also induces stabilization of the p53 Ala-315 mutant, indicating that it does not act by regulating the CDK phosphorylation of serine 315.	Roscovitine	0-11	P53	Homo sapiens	46-49
11423970-7	2001	Ectopic expression of MDM2 can abrogate the ability of roscovitine to induce p53 stabilization.	Roscovitine	55-66	P53	Homo sapiens	77-80
11423970-8	2001	Low concentrations of roscovitine cooperate with the DNA-damaging agent camptothecin to activate p53 in a synergistic fashion.	Roscovitine	22-33	P53	Homo sapiens	97-100
11345135-4	2001	Flow cytometric analysis demonstrated that all pancreatic cancer cell lines studied responded with cell surface CD95R and CD95L upregulation to bleomycin treatment, and PANC1 (mt p53) cells demonstrated a dose-dependent response to interferon gamma and bleomycin treatment with CD95R and CD95L up-regulation.	Bleomycin	144-153	P53	Homo sapiens	179-182
21044462-9	2001	The different biological effect between 172Leu and 172His shows that some p53 variants such as 172 Arg-&gt;Leu may act as wild-type p53.	Leucine	43-46	P53	Homo sapiens	74-77
21044462-9	2001	The different biological effect between 172Leu and 172His shows that some p53 variants such as 172 Arg-&gt;Leu may act as wild-type p53.	Leucine	43-46	P53	Homo sapiens	132-135
11150309-0	2001	Opposite effect of NF-kappa B and c-Jun N-terminal kinase on p53-independent GADD45 induction by arsenite.	Arsenic Trioxide	97-105	P53	Homo sapiens	61-64
11150309-2	2001	Using cells derived from human bronchial epithelial cells, we demonstrate that NF-kappaB and c-Jun N-terminal kinase (JNK) reciprocally regulate arsenic trioxide (arsenite)-induced, p53-independent expression of GADD45 protein, a cell cycle checkpoint protein that arrests cells at the G(2)/M phase transition.	Arsenic Trioxide	145-161	P53	Homo sapiens	182-185
11150309-2	2001	Using cells derived from human bronchial epithelial cells, we demonstrate that NF-kappaB and c-Jun N-terminal kinase (JNK) reciprocally regulate arsenic trioxide (arsenite)-induced, p53-independent expression of GADD45 protein, a cell cycle checkpoint protein that arrests cells at the G(2)/M phase transition.	Arsenic Trioxide	163-171	P53	Homo sapiens	182-185
11306489-3	2001	In this study, we demonstrate that the proteasome inhibitor PS-341 directly inhibits proliferation and induces apoptosis of human MM cell lines and freshly isolated patient MM cells; inhibits mitogen-activated protein kinase growth signaling in MM cells; induces apoptosis despite induction of p21 and p27 in both p53 wild-type and p53 mutant MM cells; overcomes drug resistance; adds to the anti-MM activity of dexamethasone; and overcomes the resistance to apoptosis in MM cells conferred by interleukin-6.	Bortezomib	60-66	P53	Homo sapiens	314-317
11306489-3	2001	In this study, we demonstrate that the proteasome inhibitor PS-341 directly inhibits proliferation and induces apoptosis of human MM cell lines and freshly isolated patient MM cells; inhibits mitogen-activated protein kinase growth signaling in MM cells; induces apoptosis despite induction of p21 and p27 in both p53 wild-type and p53 mutant MM cells; overcomes drug resistance; adds to the anti-MM activity of dexamethasone; and overcomes the resistance to apoptosis in MM cells conferred by interleukin-6.	Bortezomib	60-66	P53	Homo sapiens	332-335
11277927-7	2001	The results demonstrate that p53 exhibits mispair excision with a specificity of A:A &gt; A:G &gt; A:C opposite the template adenine residue and with a specificity of G:A &gt; G:G &gt; G:T opposite the template guanine residue.	Adenine	125-132	P53	Homo sapiens	29-32
11277927-7	2001	The results demonstrate that p53 exhibits mispair excision with a specificity of A:A &gt; A:G &gt; A:C opposite the template adenine residue and with a specificity of G:A &gt; G:G &gt; G:T opposite the template guanine residue.	Guanine	211-218	P53	Homo sapiens	29-32
11325644-8	2001	RESULTS: TA was detected in 93% of HG-NHL and tended to be higher in p53+ lymphomas.	Tantalum	9-11	P53	Homo sapiens	69-72
11238174-4	2001	Previous studies have indicated that there is a good correlation between G--&gt;T transversion hotspots in lung cancers and sites of preferential formation of polycyclic aromatic hydrocarbon (PAH) adducts along the p53 gene.	Polycyclic Aromatic Hydrocarbons	159-190	P53	Homo sapiens	215-218
11238174-4	2001	Previous studies have indicated that there is a good correlation between G--&gt;T transversion hotspots in lung cancers and sites of preferential formation of polycyclic aromatic hydrocarbon (PAH) adducts along the p53 gene.	Polycyclic Aromatic Hydrocarbons	192-195	P53	Homo sapiens	215-218
11096068-0	2001	The plant isoflavenoid genistein activates p53 and Chk2 in an ATM-dependent manner.	isoflavenoid	10-22	P53	Homo sapiens	43-46
11158615-6	2001	This reduction was prevented by the proteasome inhibitors MG132 and lactacystin, suggesting enhanced p53 degradation in the presence of dicoumarol.	lactacystin	68-79	P53	Homo sapiens	101-104
11148027-5	2001	Here, we show by multidimensional NMR spectroscopy that chalcones (1,3-diphenyl-2-propen-1-ones) are MDM2 inhibitors that bind to a subsite of the p53 binding cleft of human MDM2.	Chalcones	56-65	P53	Homo sapiens	147-150
11162500-4	2001	However, in an in vitro transcription assay with partially purified basal transcription factors, p53 only partially activated transcription from the same binding site and required PAb421 for full activation.	pab421	180-186	P53	Homo sapiens	97-100
11205907-9	2001	By contrast with camptothecin, these lesions persisted for several hours after drug removal and were not formed at 4 degrees C. Et743 treatment induced transient p53 elevation, dose-dependent cell cycle accumulation in G2-M and in G1- and S-phase, and inhibition of DNA synthesis.	Trabectedin	128-133	P53	Homo sapiens	162-165
11107118-4	2000	RESULTS: Loss of p53 function (p53-LOF), defined as a failure to induce p21 and/or MDM2 in response to melphalan, was seen in 1/8 drug-sensitive and 6/10 drug-resistant cell lines.	Melphalan	103-112	P53	Homo sapiens	17-20
11107118-4	2000	RESULTS: Loss of p53 function (p53-LOF), defined as a failure to induce p21 and/or MDM2 in response to melphalan, was seen in 1/8 drug-sensitive and 6/10 drug-resistant cell lines.	Melphalan	103-112	P53	Homo sapiens	31-34
11071927-4	2000	We show that upon treatment of HepG2 cells with 5-fluorouracil or methotrexate, p53 levels increase while concentrations of cyclin B2 mRNA, measured by RT-PCR with the LightCycler system, are reduced.	Methotrexate	66-78	P53	Homo sapiens	80-83
11029509-7	2000	Tumor B18 exhibited two novel mutations in the p53 gene, ATGright curved arrow GTG (Metright curved arrow Val) at codon 237 and AATright curved arrow GAT (Asnright curved arrow Asp) at codon 263.	Aspartic Acid	177-180	P53	Homo sapiens	47-50
11034086-10	2000	Like other antimicrotubule agents, the sulfamoylated estrone derivatives induced BCL-2 and BCL-XL phosphorylation and increased p53 expression.	Estrone	53-60	P53	Homo sapiens	128-131
10994962-3	2000	PCR products of the proline [5"-x(G17)-x(C38)x-3"] and arginine variants [(5"-x(Gl7)-x(G38)x-3"] of the p53 gene are distinguished by an SNP (cytosine or guanine) and were discriminated using both quadrupole and quadrupole ion trap MS analysis.	Cytosine	142-150	P53	Homo sapiens	104-107
10994962-3	2000	PCR products of the proline [5"-x(G17)-x(C38)x-3"] and arginine variants [(5"-x(Gl7)-x(G38)x-3"] of the p53 gene are distinguished by an SNP (cytosine or guanine) and were discriminated using both quadrupole and quadrupole ion trap MS analysis.	Guanine	154-161	P53	Homo sapiens	104-107
11798837-2	2000	METHODS: Human lung adenocarcinoma cell line GLC-82 was transfected with adenovirus-mediated p53 gene (Ad-p53) combining with administration of either kind of chemotherapeutic agents-cisplatin (CDDP) and arsenic trioxide (As(2)O(3)).	Arsenic Trioxide	204-220	P53	Homo sapiens	93-96
10951576-4	2000	The mechanism of ionizing radiation-dependent activation of p53-dependent transcription using DRB is more likely due to inhibition of gene transcription rather than prolonged DNA damage, as the non-genotoxic and general transcription inhibitor Roscovitine also synergistically activates p53 function in ionizing irradiated cells.	Roscovitine	244-255	P53	Homo sapiens	60-63
10951576-4	2000	The mechanism of ionizing radiation-dependent activation of p53-dependent transcription using DRB is more likely due to inhibition of gene transcription rather than prolonged DNA damage, as the non-genotoxic and general transcription inhibitor Roscovitine also synergistically activates p53 function in ionizing irradiated cells.	Roscovitine	244-255	P53	Homo sapiens	287-290
10945628-3	2000	Whereas p53 can contribute to the nucleoside-induced killing of CLL cells, recent work from this laboratory and elsewhere has shown that such killing can also occur by p53-independent mechanisms.	Nucleosides	34-44	P53	Homo sapiens	8-11
10713094-4	2000	Serine 15 of p53 is phosphorylated in vivo in response to ionizing radiation, and antibodies to ATM immunoprecipitate a protein kinase activity that, in the presence of manganese, phosphorylates p53 at serine 15.	Manganese	169-178	P53	Homo sapiens	13-16
10713094-4	2000	Serine 15 of p53 is phosphorylated in vivo in response to ionizing radiation, and antibodies to ATM immunoprecipitate a protein kinase activity that, in the presence of manganese, phosphorylates p53 at serine 15.	Manganese	169-178	P53	Homo sapiens	195-198
10699891-11	2000	The mutation pattern of p53 with a nearly equal rate of incidence of transitions and transversions and a high rate of incidence of mutations at CpG sites may reflect endogenous mechanisms (e.g., deamination of 5-methylcytosine) rather than exogenous carcinogens.	5-Methylcytosine	210-226	P53	Homo sapiens	24-27
10663644-1	2000	PURPOSE: To determine the ability of UCN-01 to abrogate the cell cycle arrest induced by camptothecin (CPT) in tumor cells that lack p53 function, and therefore enhance the cytotoxicity of CPT in these cells in relation to normal cells with wild-type p53.	7-hydroxystaurosporine	37-43	P53	Homo sapiens	251-254
10663644-14	2000	Our findings suggest potential usefulness of combining UCN-01 in topoisomerase I inhibitor-based drug therapy for the treatment of breast cancer with a dysfunctional p53 gene.	7-hydroxystaurosporine	55-61	P53	Homo sapiens	166-169
22607421-11	2000	p53 with diamide was irreversible and was not reverted by an excess of DTT.	Diamide	9-16	P53	Homo sapiens	0-3
10618704-2	1999	Several forms of DNA damage have been shown to activate p53, including those generated by ionising radiation (IR), radio-mimetic drugs, ultraviolet light (UV) and chemicals such as methyl methane sulfonate (MMS).	Methyl Methanesulfonate	181-205	P53	Homo sapiens	56-59
10618704-2	1999	Several forms of DNA damage have been shown to activate p53, including those generated by ionising radiation (IR), radio-mimetic drugs, ultraviolet light (UV) and chemicals such as methyl methane sulfonate (MMS).	Methyl Methanesulfonate	207-210	P53	Homo sapiens	56-59
10545114-6	1999	Nevertheless, p53-induced apoptosis is still caspase dependent because it could be abolished by z-VAD-fmk.	benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone	96-105	P53	Homo sapiens	14-17
10531375-4	1999	Cadmium at 10-30 microM impairs the p53 induction in response to DNA-damaging agents such as actinomycin D, methylmethane sulfonate, and hydrogen peroxide.	Methyl Methanesulfonate	108-131	P53	Homo sapiens	36-39
10535931-3	1999	Furthermore, treatment of human cells with the S(N)1 DNA methylators N-methyl-N-nitrosourea or N-methyl-N"-nitro-N-nitrosoguanidine results in p53 phosphorylation on serine residues 15 and 392, and these phosphorylation events depend on the presence of functional hMutSalpha and hMutLalpha.	Methylnitronitrosoguanidine	95-131	P53	Homo sapiens	143-146
10421649-6	1999	In Fas-positive HCC cases (n = 15), the intrahepatic metastatic foci was less (P =.037), apoptosis of tumor cells was more (P =.004), the disease-free survival rate was higher (P =.004), and p53-positive cases were less (P =.003), compared with Fas-negative cases.	ammonium ferrous sulfate	3-6	P53	Homo sapiens	191-194
10360831-1	1999	Lonidamine (LND), a selective inhibitor of the energy metabolism of tumor cells, induces apoptosis, independently of the p53 gene, in the adriamycin(ADR)-resistant MCF7 breast-cancer cell line (MCF7 ADR).	lonidamine	0-10	P53	Homo sapiens	121-124
10380883-3	1999	Using immunoblotting with the antibody DO-1, we show that the bands obtained correspond to ethidium-stained DNA, suggesting that each band of the ladder contains a DNA-p53 complex.	Ethidium	91-99	P53	Homo sapiens	168-171
10389864-14	1999	We have also shown that Fas levels are significantly increased in response to irradiation in a wt p53 line.	ammonium ferrous sulfate	24-27	P53	Homo sapiens	98-101
10408853-8	1999	The mean in vitro bleomycin-induced breaks per cell (a marker of cancer susceptibility) was significantly higher (0.92) for patients who overexpressed p53 in lung tumour tissue than that for patients with no detectable p53 expression in lung tumour tissue (0.65).	Bleomycin	18-27	P53	Homo sapiens	151-154
10408853-8	1999	The mean in vitro bleomycin-induced breaks per cell (a marker of cancer susceptibility) was significantly higher (0.92) for patients who overexpressed p53 in lung tumour tissue than that for patients with no detectable p53 expression in lung tumour tissue (0.65).	Bleomycin	18-27	P53	Homo sapiens	219-222
10080943-3	1999	Here, we report that although Fas induction is closely linked to the expression of wild type p53, it is not correlated with JNK activation induced by apoptotic stimuli.	ammonium ferrous sulfate	30-33	P53	Homo sapiens	93-96
10087941-9	1999	Homozygous deletion in p16INK4A/p15INK4B genes and a codon 259 missense point mutation (GAC--&gt;TAC; Asp--&gt;Tyr) in the TP53 gene were observed in one human papilloma positive scrotal carcinoma case.	Aspartic Acid	102-105	P53	Homo sapiens	123-127
11812373-2	1999	METHODS: The p16, p21 and p53 genes mediated by Stearylamine/DOPE (SA liposome) were introduced alone and jointly into the non-small cell lung cancer (NSCLC) cell line A549 and small cell lung cancer (SCLC) SH77.	dioleoyl phosphatidylethanolamine	61-65	P53	Homo sapiens	26-29
9989601-1	1999	The proteasome inhibitors lactacystin and AcLLNal induced p53-independent apoptosis in two human glioma cell lines, and the apoptosis was accompanied by up-regulation of immunoreactive wild-type p53, p21Waf1, Mdm2, and p27Kip1.	lactacystin	26-37	P53	Homo sapiens	58-61
9989601-1	1999	The proteasome inhibitors lactacystin and AcLLNal induced p53-independent apoptosis in two human glioma cell lines, and the apoptosis was accompanied by up-regulation of immunoreactive wild-type p53, p21Waf1, Mdm2, and p27Kip1.	lactacystin	26-37	P53	Homo sapiens	195-198
10369188-2	1999	The accumulation of hsp72 and p53 was observed in A-172 cells cocultivated with heat-shocked T98G cells, which was suppressed by the addition of aminoguanidine to the medium.	pimagedine	145-159	P53	Homo sapiens	30-33
9823951-0	1998	Sensitivity to Fas-mediated apoptosis in pediatric acute lymphoblastic leukemia is associated with a mutant p53 phenotype and absence of Bcl-2 expression.	ammonium ferrous sulfate	15-18	P53	Homo sapiens	108-111
9823951-3	1998	We therefore investigated the relationship between sensitivity to Fas-mediated apoptosis and (1) Fas expression, (2) p53 status, and (3) Bcl-2 protein levels in pediatric ALL cell lines and primary leukemic cells.	ammonium ferrous sulfate	66-69	P53	Homo sapiens	117-120
9823951-13	1998	Sensitivity to Fas-mediated apoptosis was associated with a mt-p53 phenotype and absence of Bcl-2 expression.	ammonium ferrous sulfate	15-18	P53	Homo sapiens	63-66
9875298-0	1998	Ketoconazole-induced apoptosis through P53-dependent pathway in human colorectal and hepatocellular carcinoma cell lines.	Ketoconazole	0-12	P53	Homo sapiens	39-42
9766444-6	1998	The differentiation response to transfected p53 with or without INF-gamma was inhibited by cyclic adenosine monophosphate (cAMP)-inducing agents (dibutyryl cyclic adenosine 3":5"-monophosphate, forskolin, and 3-isobutyl-1-methylxanthine) in a dose-dependent manner.	Colforsin	194-203	P53	Homo sapiens	44-47
9690517-0	1998	Role of p53 in aziridinylbenzoquinone-induced p21waf1 expression.	diaziquone	15-37	P53	Homo sapiens	8-11
9647183-9	1998	Transfection with p53 had only a minor effect on the plating efficiency of nonirradiated U87MG cells, reducing the plating efficiency from 0.23 +/- 0.01 in DMEM to 0.22 +/- 0.04 after addition of Ad5CMV-p53.	dmem	156-160	P53	Homo sapiens	18-21
9647183-20	1998	Infection of U87MG cells with Ad5CMV-p53 only resulted in an increase in p21 compared with DMEM- and dl312-treated cells.	dmem	91-95	P53	Homo sapiens	37-40
9681674-9	1998	Immunohistochemical overexpression of p53 was detected in the basal layer of the cultures treated with methotrexate.	Methotrexate	103-115	P53	Homo sapiens	38-41
9548807-6	1998	Diaziquone (AZQ), an anticancer agent, and its derivatives, diaziridinequinone (DZQ) and methyldiaziridinequinone (MeDZQ), induced p53 in a dose- and time-dependent manner as measured by the electrophoretic mobility shift assay.	2,5-dimethyl-3,6-diaziridinyl-1,4-benzoquinone	89-113	P53	Homo sapiens	131-134
9548807-6	1998	Diaziquone (AZQ), an anticancer agent, and its derivatives, diaziridinequinone (DZQ) and methyldiaziridinequinone (MeDZQ), induced p53 in a dose- and time-dependent manner as measured by the electrophoretic mobility shift assay.	2,5-dimethyl-3,6-diaziridinyl-1,4-benzoquinone	115-120	P53	Homo sapiens	131-134
9548807-7	1998	Wild type p53 induction by AZQ was suppressed when DT-diaphorase activity was inhibited by pretreating the cells with dicumarol.	diaziquone	27-30	P53	Homo sapiens	10-13
9548807-9	1998	Inhibition of ROS production by the antioxidant enzyme catalase reduced AZQ- and DZQ-mediated p53 induction by about 45%.	diaziquone	72-75	P53	Homo sapiens	94-97
9548807-9	1998	Inhibition of ROS production by the antioxidant enzyme catalase reduced AZQ- and DZQ-mediated p53 induction by about 45%.	pycnogenols	81-84	P53	Homo sapiens	94-97
9548807-12	1998	On the basis of these data, we propose that the bioreductive activation of AZQ is a prerequisite for p53 induction.	diaziquone	75-78	P53	Homo sapiens	101-104
9548807-13	1998	Moreover, the induction of p53 by AZQ requires both the quinone and the aziridine moieties of the AZQ molecule.	diaziquone	34-37	P53	Homo sapiens	27-30
9548807-13	1998	Moreover, the induction of p53 by AZQ requires both the quinone and the aziridine moieties of the AZQ molecule.	diaziquone	98-101	P53	Homo sapiens	27-30
9548807-14	1998	Although AZQ and its analogues increased p53 levels in MCF-7 cells, p53 induction in these cells may not be responsible for the apoptosis seen upon treatment of MCF-7 cells with these agents.	diaziquone	9-12	P53	Homo sapiens	41-44
9579370-8	1998	The known tumor suppressor genes retinoblastoma (RB) and p53 showed loss of expression in GMTT compared with NBT.	Nitroblue Tetrazolium	109-112	P53	Homo sapiens	57-60
15281315-8	1998	With new technology for cytological screening techniques using dot ELISA and evidence of differences in TP53 mutations that support the involvement of nitrous oxide, it is clear that there is more to learn from study of this tumour type that may be of general interest in understanding the clonal development of cancer.	Nitrous Oxide	151-164	P53	Homo sapiens	104-108
9718082-8	1998	An increase in the level of immunophenotypic expression of wild type p53 was also noted after treatment with all trans retinoic acid and 9-cis retinoic acid.	2-octenal	113-118	P53	Homo sapiens	69-72
9718082-8	1998	An increase in the level of immunophenotypic expression of wild type p53 was also noted after treatment with all trans retinoic acid and 9-cis retinoic acid.	Alitretinoin	137-156	P53	Homo sapiens	69-72
9718082-10	1998	In addition, they may be inducing a p53 dependent cell cycle arrest and thus suggests that all-trans and 9-cis retinoic acid may have a cytostatic effect rather than a cytotoxic effect on CaSki cells.	Alitretinoin	105-124	P53	Homo sapiens	36-39
9718082-11	1998	The increased expression of p53 positive cells and the inhibition of E6/E7 transcription after treatment with these retinoids may indicate the potential role of all trans and 9-cis retinoic acid as a cell cycle regulator and an antiviral chemoprevention agent.	Retinoids	116-125	P53	Homo sapiens	28-31
9395460-1	1997	We previously demonstrated that the anticancer agent and protein kinase C (PKC) inhibitor 7-hydroxystaurosporine (UCN-01) induces apoptosis independently of p53 and protein synthesis in HL60 cells.	7-hydroxystaurosporine	90-112	P53	Homo sapiens	157-160
9395460-1	1997	We previously demonstrated that the anticancer agent and protein kinase C (PKC) inhibitor 7-hydroxystaurosporine (UCN-01) induces apoptosis independently of p53 and protein synthesis in HL60 cells.	7-hydroxystaurosporine	114-120	P53	Homo sapiens	157-160
9388195-2	1997	In this study we treated the HCT-116 colon cancer cell line with alkylating agents including N-methyl-N"-nitro-N-nitrosoguanidine (MNNG),which is known to cause colon cancer in animals, and examined the expression of both APC and p53 genes.	Methylnitronitrosoguanidine	131-135	P53	Homo sapiens	230-233
9494534-8	1997	Levels of p53 mRNA decreased with increasing resistance to vindesine, etoposide and fotemustine.	fotemustine	84-95	P53	Homo sapiens	10-13
9367071-6	1997	The most common p53 mutations in these tumors were guanine to adenine (G--&gt;A) transitions (10 of 20 tumors; 50%).	Guanine	51-58	P53	Homo sapiens	16-19
9367071-6	1997	The most common p53 mutations in these tumors were guanine to adenine (G--&gt;A) transitions (10 of 20 tumors; 50%).	Adenine	62-69	P53	Homo sapiens	16-19
9815601-11	1997	p53 wild-type cells seem to be more sensitive to the cytotoxic effects of the combination of UCN-01 + CDDP than the p53 mutant cells.	7-hydroxystaurosporine	93-99	P53	Homo sapiens	0-3
9271379-7	1997	In contrast, exposure to the alkylating agent methyl methanesulfonate results in similar increases of p53 and p21(WAF1/CIP1) mRNA in both cell types.	Methyl Methanesulfonate	46-69	P53	Homo sapiens	102-105
9266938-0	1997	Alterations of p53 and Rb genes in a novel human GM-CSF-dependent myeloid cell line (OHN-GM) established from therapy-related leukaemia.	ohn-gm	85-91	P53	Homo sapiens	15-18
9595771-4	1997	The reaction with DNA occurs with guanines in the codon 249 of tumor suppressor gene p53.	Guanine	34-42	P53	Homo sapiens	85-88
9199206-5	1997	We show for the first time that transcriptional activation of the p53 tumor suppressor gene, as assessed by a reporter plasmid construct, can be down-regulated by cytosine methylation in the basal promoter region.	Cytosine	163-171	P53	Homo sapiens	66-69
9135020-5	1997	Using Western blot analysis, we found abundant expression of p53 in the cytoplasm of two Fas-resistant cell lines, DU145 and ND1, and did not find p53 in two Fas-sensitive cell lines, PC3 and ALVA31.	ammonium ferrous sulfate	89-92	P53	Homo sapiens	61-64
9139842-4	1997	The results showed that 2% of ACs, 4% of ATL patients and 6% of HAM/TSP patients had anti-p53 antibody.	Aminocaproic Acid	30-33	P53	Homo sapiens	90-93
9105409-13	1997	Finally, western analysis revealed that a 24-hr exposure to 5000 IU/mL rIFN-alpha 2a (+/-20 microM AZT) significantly reduced wild-type p53 expression compared with AZT-exposed cells.	Zidovudine	99-102	P53	Homo sapiens	136-139
9105409-14	1997	We conclude that rIFN-alpha 2a enhances AZT-induced tumor cell growth inhibition by (i) increasing AZT metabolism, and (ii) inhibiting DNA repair and p53-mediated cell cycle control processes.	Zidovudine	40-43	P53	Homo sapiens	150-153
9029132-2	1997	To identify proteins present in complexes with Src family kinases, we subjected p58(c-fgr) or p53/56(lyn) immunoprecipitates from Triton X-100 lysates of PMN incubated on fibrinogen-coated surfaces to in vitro kinase assays.	Octoxynol	130-142	P53	Homo sapiens	94-97
9022073-3	1997	At concentrations present in the sera of patients during therapy, bleomycin induced transient accumulation of nuclear wild-type (wt) p53 and upregulated expression of cell surface CD95 (APO-1/Fas) receptor in hepatoma cells carrying wt p53 (HepG2).	Bleomycin	66-75	P53	Homo sapiens	133-136
9022073-3	1997	At concentrations present in the sera of patients during therapy, bleomycin induced transient accumulation of nuclear wild-type (wt) p53 and upregulated expression of cell surface CD95 (APO-1/Fas) receptor in hepatoma cells carrying wt p53 (HepG2).	Bleomycin	66-75	P53	Homo sapiens	236-239
9137531-1	1997	PURPOSE: Recently, it has been shown that geldanamycin (GA), a benzoquinone ansamycin, is able to deplete mutant p53, p185erbB2 and Raf-1 proteins in cancer cells.	benzoquinone ansamycin	63-85	P53	Homo sapiens	113-116
8895764-3	1996	In this report, we describe the mechanism by which the retinoid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid (CD437) induces p21WAF1/CIP1 in breast carcinoma cells possessing either a wild-type (MCF-7 cells) or mutated (MDA-MB-468 cells) p53.	Retinoids	55-63	P53	Homo sapiens	259-262
8878553-2	1996	We found that the proteasome-specific inhibitor lactacystin (LC) induced expression of the cell cycle inhibitor p21WAF1/CIP1 in human cancer cells regardless of their p53 status.	lactacystin	48-59	P53	Homo sapiens	167-170
8892753-3	1996	In contrast, the gadd gene stress response to base-damaging agents, such as methylmethane sulfonate (MMS) or UV radiation, or medium depletion (starvation) occurs in all mammalian cells examined to date regardless of p53 status for both GADD45 and also GADD153, which is not IR-responsive in many lines with functional p53.	Methyl Methanesulfonate	101-104	P53	Homo sapiens	319-322
8692233-11	1996	We found a weak association between total PAH-DNA adduct levels in lung tissue and TP53 mutations.	Polycyclic Aromatic Hydrocarbons	42-45	P53	Homo sapiens	83-87
8676917-0	1996	p53 accumulates in micronuclei after treatment with a DNA breaking chemical, methylnitrosourea, and with the spindle poison, vinblastine.	Vinblastine	125-136	P53	Homo sapiens	0-3
8676920-7	1996	The induction pattern of the three p53 effector genes by the alkylating agent methylmethane sulfonate (MMS) was also attenuated in WI-L2-NS cells.	Methyl Methanesulfonate	78-101	P53	Homo sapiens	35-38
8676920-7	1996	The induction pattern of the three p53 effector genes by the alkylating agent methylmethane sulfonate (MMS) was also attenuated in WI-L2-NS cells.	Methyl Methanesulfonate	103-106	P53	Homo sapiens	35-38
8649776-2	1996	By using recombination PCR in vitro mutagenesis, we introduced point mutations into the codon 273 of wild-type (wt) p53 (pC53-SN3) from Arg to His (pC53-273H [273H]), Asp (273D), Pro (273P), Lys (273K), Leu (273L) or Thr (273T), and compared their biological and biochemical activities with wt p53 and cancer-derived 175H, 248W and 273H/309S.	Aspartic Acid	167-170	P53	Homo sapiens	116-119
8649776-2	1996	By using recombination PCR in vitro mutagenesis, we introduced point mutations into the codon 273 of wild-type (wt) p53 (pC53-SN3) from Arg to His (pC53-273H [273H]), Asp (273D), Pro (273P), Lys (273K), Leu (273L) or Thr (273T), and compared their biological and biochemical activities with wt p53 and cancer-derived 175H, 248W and 273H/309S.	Leucine	203-206	P53	Homo sapiens	116-119
8603385-0	1996	Effects of sodium saccharin and linoleic acid on mRNA levels of Her2/neu and p53 in a human breast epithelial cell line.	Saccharin	11-27	P53	Homo sapiens	77-80
8603385-1	1996	The effects of two food-related chemicals (sodium saccharin and linoleic acid) on the levels of Her2/neu and p53 mRNA in a non-cancerous human breast epithelial cell line (HBL-100) were tested in comparison with the effects of the known tumor promoter phorbol 12-myristate 13-acetate (TPA).	Saccharin	43-59	P53	Homo sapiens	109-112
8814703-6	1996	The wild-type TP53+ cells were morphologically flat and enlarged when cultured in vitro, and were less able to form colonies in soft agar.	Agar	133-137	P53	Homo sapiens	14-18
8603737-1	1996	Evidence that p58C-FGR and p53/56LYN redistributed to a Triton X-100-insoluble cytoskeletal fraction, also enriched in the caveolar protein caveolin, display an enhanced kinase activity.	Octoxynol	56-68	P53	Homo sapiens	27-30
8603737-4	1996	Moreover, we found that up to about 20% of p58c-fgr and p53/56lyn redistribute to a Triton X-100-insoluble fraction after PMA stimulation, and it is this fraction of the two kinases which diplays an increased activity.	Octoxynol	84-96	P53	Homo sapiens	56-59
8944328-3	1996	TP53 mutations were identified in four out of 30 (13%) DCIS by constant denaturant gel electrophoresis (CDGE).	cdge	104-108	P53	Homo sapiens	0-4
8521385-0	1995	Microtubule-active drugs taxol, vinblastine, and nocodazole increase the levels of transcriptionally active p53.	Vinblastine	32-43	P53	Homo sapiens	108-111
8521385-2	1995	We examined the ability of three microtubule-active agents, taxol, vinblastine, and nocodazole, to increase p53 levels and activate p53-dependent processes.	Vinblastine	67-78	P53	Homo sapiens	108-111
8521385-2	1995	We examined the ability of three microtubule-active agents, taxol, vinblastine, and nocodazole, to increase p53 levels and activate p53-dependent processes.	Vinblastine	67-78	P53	Homo sapiens	132-135
7586518-0	1995	Direct solid-phase sequence analysis of the human p53 gene by use of multiplex polymerase chain reaction and alpha-thiotriphosphate nucleotides.	alpha-thiotriphosphate nucleotides	109-143	P53	Homo sapiens	50-53
7563172-0	1995	Accumulation of p53 protein as a possible predictor of response to adjuvant combination chemotherapy with cyclophosphamide, methotrexate, fluorouracil, and prednisone for breast cancer.	Methotrexate	124-136	P53	Homo sapiens	16-19
7627952-0	1995	Microinjection of monoclonal antibody PAb421 into human SW480 colorectal carcinoma cells restores the transcription activation function to mutant p53.	pab421	38-44	P53	Homo sapiens	146-149
7596441-2	1995	p53 response elements contain two or more copies of a somewhat promiscuous consensus sequence: 5"-XXXC(A,T)(T,A)GYY-3" (where X is a purine and Y is a pyrimidine) (ref.	purine	133-139	P53	Homo sapiens	0-3
7587888-2	1995	The results showed that in 40.9% (9/22) of the specimen examined, the mutation spectrum of p53 in primary EC was similar to that in the esophageal epithelium of human fetus (in vitro) and monkey (in vivo) treated with NMBzA.	N-methyl-N-benzylnitrosamine	218-223	P53	Homo sapiens	91-94
7784087-2	1995	It has recently been shown (Lin et al., 1994b) that the transcriptional activator domain of the p53 protein contains two amino acids, leu-22 and trp-23, which are required by the wild-type p53 protein for transcriptional activity.	Leucine	134-137	P53	Homo sapiens	96-99
7784087-2	1995	It has recently been shown (Lin et al., 1994b) that the transcriptional activator domain of the p53 protein contains two amino acids, leu-22 and trp-23, which are required by the wild-type p53 protein for transcriptional activity.	Leucine	134-137	P53	Homo sapiens	189-192
7663341-0	1995	Backbone dynamics of the oligomerization domain of p53 determined from 15N NMR relaxation measurements.	15n	71-74	P53	Homo sapiens	51-54
7663341-1	1995	The backbone dynamics of the tetrameric p53 oligomerization domain (residues 319-360) have been investigated by two-dimensional inverse detected heteronuclear 1H-15N NMR spectroscopy at 500 and 600 MHz.	15n	162-165	P53	Homo sapiens	40-43
7537340-5	1995	Finally, we employed all three libraries to reveal the distinct mechanisms by which PAb421 and PAb122, two monoclonal antibodies that allosterically activate sequence-specific DNA binding by p53, react specifically with the same positively-charged C-terminal segment.	pab421	84-90	P53	Homo sapiens	191-194
7882284-4	1995	Specimens containing p53 mutations tended to exhibit an increased growth delay in procarbazine-treated xenografts and lower amounts of AT.	Procarbazine	82-94	P53	Homo sapiens	21-24
7882284-5	1995	CONCLUSIONS: p53 mutations in brain tumors may contribute to procarbazine sensitivity by failing to induce arrest at the G1/S cell-cycle checkpoint, thereby preventing the repair of procarbazine-induced genetic alterations.	Procarbazine	61-73	P53	Homo sapiens	13-16
7882284-5	1995	CONCLUSIONS: p53 mutations in brain tumors may contribute to procarbazine sensitivity by failing to induce arrest at the G1/S cell-cycle checkpoint, thereby preventing the repair of procarbazine-induced genetic alterations.	Procarbazine	182-194	P53	Homo sapiens	13-16
7727133-2	1995	A nuclear phosphoprotein, p53, was isolated by immunoprecipitation after biosynthetic labeling with 35S, 32P or 33P in cultured human cells.	Phosphorus-33	112-115	P53	Homo sapiens	26-29
7727133-7	1995	The relative phosphorylation of each p53 isoform was estimated by normalizing 33P or 32P isoform volumes with the corresponding 35S volume and showed progressive phosphorylation of acidic isoforms.	Phosphorus-33	78-81	P53	Homo sapiens	37-40
7955057-3	1994	Only one case of hydatidiform mole was found to have a missense point mutation (codon 295, CCT--&gt;CTT, i.e. proline to leucine) of the p53 gene.	Leucine	121-128	P53	Homo sapiens	137-140
8275462-1	1994	The ability of cloned human O6-methylguanine-DNA methyltransferase to repair a methylated guanine in a CpG-containing sequence, i.e., island, was studied by using a synthetic double-stranded 20-mer oligonucleotide from codon 248 of the p53 gene and another designed sequence.	Guanine	37-44	P53	Homo sapiens	236-239
8275462-6	1994	These results suggest that O6-methylation of the guanine moiety at CpG islands may not be efficiently repaired when normal 5mC is present and this may contribute significantly to an increase in mutagenesis of p53 and like molecules.	Guanine	49-56	P53	Homo sapiens	209-212
8275462-6	1994	These results suggest that O6-methylation of the guanine moiety at CpG islands may not be efficiently repaired when normal 5mC is present and this may contribute significantly to an increase in mutagenesis of p53 and like molecules.	5-Methylcytosine	123-126	P53	Homo sapiens	209-212
8517643-5	1993	Immunoreactive p53 was observed in the nuclei of the cancer cells in 15/33 (45%) by pAbDO-7, 11/26 (42%) by pAb1801, and 16/33 (48%) by pAbCM-1.	pabdo-7	84-91	P53	Homo sapiens	15-18
8380918-11	1993	Less frequent than the deamination of 5-methyl cytosine in CpG dinucleotides, mutations resulting in loss or gain of nucleotide base pairs may represent the second highest endogenous mutagenic event for p53 gene in human cancers.	5-Methylcytosine	38-55	P53	Homo sapiens	203-206
1895390-9	1991	That p53 was stabilized because of association with LPV T antigen and not because of mutation was demonstrated with the p53 conformation-dependent monoclonal antibody PAb246.	pab246	167-173	P53	Homo sapiens	5-8
1895390-9	1991	That p53 was stabilized because of association with LPV T antigen and not because of mutation was demonstrated with the p53 conformation-dependent monoclonal antibody PAb246.	pab246	167-173	P53	Homo sapiens	120-123
1895390-11	1991	Sequential immunoprecipitation showed all detectable p53 to be of the PAb246+ class in each LPV-transformed cell line, suggesting that the stable p53 was indeed wild type.	pab246	70-76	P53	Homo sapiens	53-56
1924299-3	1991	We have developed a modification of denaturing gradient gel electrophoresis termed "constant denaturant gel electrophoresis" (CDGE), which provides a rapid and sensitive method to screen the four conserved regions within the p53 gene where the majority of p53 mutations have been reported.	cdge	126-130	P53	Homo sapiens	225-228
1924299-3	1991	We have developed a modification of denaturing gradient gel electrophoresis termed "constant denaturant gel electrophoresis" (CDGE), which provides a rapid and sensitive method to screen the four conserved regions within the p53 gene where the majority of p53 mutations have been reported.	cdge	126-130	P53	Homo sapiens	256-259
1924299-10	1991	We conclude that CDGE is a rapid and effective technique to screen for p53 mutations.	cdge	17-21	P53	Homo sapiens	71-74
1707233-7	1991	The improved morphologic resolution available in periodate lysine paraformaldehyde dichromate (PLPD)-fixed, paraffin-embedded tissue permitted several conclusions to be made: p53 is confined to neoplastic nuclei; staining in positive tumors is heterogeneous and often more marked at the infiltrative margins; and staining intensity is dramatically reduced in mitotic cells.	plpd	95-99	P53	Homo sapiens	175-178
1986144-4	1991	On Northern, Southern, and Western blot analysis, the p53 gene and its product appear to be normal in DU-145.	du	102-104	P53	Homo sapiens	54-57
2259385-8	1990	This mutation leads to substitution of aspartic acid for glycine in one of the regions identified as a frequent target of point mutations in p53.	Aspartic Acid	39-52	P53	Homo sapiens	141-144
2141685-6	1990	Phosphoamino acid analysis of in vitro phosphorylated p53 revealed a phosphorylation predominantly on serine residues similar to p53 phosphorylated in vivo.	Phosphoamino Acids	0-17	P53	Homo sapiens	54-57
1691710-6	1990	A series of different p53 mutants all react more strongly with PAb240 than with PAb246.	pab246	80-86	P53	Homo sapiens	22-25
2139577-4	1990	For example, activated mutant p53 fails to react with PAb246 (p53-246 degrees).	pab246	54-60	P53	Homo sapiens	30-33
33803928-6	2021	Proteome-based mechanistic analysis revealed that inhibition of ganglioside synthesis downregulated the expression of AURKA, AURKB, TTK, and NDC80 involved in the regulation of kinetochore metaphase signaling, which is essential for chromosome segregation and mitotic progression and probably under the control of activation of TP53-dependent cell cycle arrest.	Gangliosides	64-75	P53	Homo sapiens	328-332
11931974-9	2002	Addition of pifithrin-alpha (PFT), a specific inhibitor of p53, reduced the activation of p53 with a concomitant decrease in growth arrest at S phase.	pifithrin	12-27	P53	Homo sapiens	59-62
11931974-9	2002	Addition of pifithrin-alpha (PFT), a specific inhibitor of p53, reduced the activation of p53 with a concomitant decrease in growth arrest at S phase.	pifithrin	12-27	P53	Homo sapiens	90-93
34947951-7	2021	Puromycin screening revealed that 75.0% (21/28) and 68.7% (22/32) of cell colonies contained a P53 mutation at sgRNA-Exon5 and sgRNA-Exon4, respectively.	Puromycin	0-9	P53	Homo sapiens	95-98
34909835-0	2021	Alterations in APC, BECN1, and TP53 gene expression levels in colon cancer cells caused by monosodium glutamate.	Sodium Glutamate	91-111	P53	Homo sapiens	31-35
34909835-7	2021	In the present study, the effect of MSG on cell viability and its effect on expression of APC, BECN1, and TP53 genes in SW620 and SW480 colon cancer cell lines were studied.	Sodium Glutamate	36-39	P53	Homo sapiens	106-110
34880920-15	2021	In the arsenic trioxide-target-pathway-HCC network, targets such as AKT1, RAF1, RELA, TP53, and PTEN had a higher degree.	Arsenic Trioxide	7-23	P53	Homo sapiens	86-90
34785649-5	2021	However, recent data suggests that STRA6 may not function merely as a retinoid transporter but also act as a complex signalling hub in its own right, being able to affect cell fate through the integration of retinoid signalling with other key pathways, such as those involving p53, JAK/STAT, Wnt/beta catenin and calcium.	Retinoids	208-216	P53	Homo sapiens	277-280
34343634-9	2021	Moreover, RRP15 depletion in p53-mutant PLC5 and p53-deleted Hep3B cells induced metabolic shift from the glycolytic pentose-phosphate to mitochondrial oxidative phosphorylation via regulating a series of key genes such as HK2 and TIGAR, and thus, promoted the generation of ROS and apoptosis.	Pentosephosphates	117-134	P53	Homo sapiens	29-32
34343634-9	2021	Moreover, RRP15 depletion in p53-mutant PLC5 and p53-deleted Hep3B cells induced metabolic shift from the glycolytic pentose-phosphate to mitochondrial oxidative phosphorylation via regulating a series of key genes such as HK2 and TIGAR, and thus, promoted the generation of ROS and apoptosis.	Pentosephosphates	117-134	P53	Homo sapiens	49-52
34768330-0	2021	Lymphocytic Infiltrate and p53 Protein Expression as Predictive Markers of Response and Outcome in Myelodysplastic Syndromes Treated with Azacitidine.	Azacitidine	138-149	P53	Homo sapiens	27-30
34768330-8	2021	Our results suggest the possible role of lymphocytic infiltrate and p53+ elements as predictive markers in MDS treated with azacitidine, disclosing new chapters in the understanding of MDS evolution and treatment.	Azacitidine	124-135	P53	Homo sapiens	68-71
34768743-0	2021	Bcl-2 Modulation in p53 Signaling Pathway by Flavonoids: A Potential Strategy towards the Treatment of Cancer.	Flavonoids	45-55	P53	Homo sapiens	20-23
34768743-8	2021	Flavonoids inhibit B-cell lymphoma 2 (Bcl-2) via the p53 signaling pathway, which is a significant apoptotic target in many cancer types, hence suppressing a major dysregulated pathway in cancer.	Flavonoids	0-10	P53	Homo sapiens	53-56
34768743-9	2021	To date, there have been no studies reported which extensively highlight the role of flavonoids and especially the different classes of flavonoids in the modulation of Bcl-2 in the P53 signaling pathway.	Flavonoids	85-95	P53	Homo sapiens	181-184
34768743-9	2021	To date, there have been no studies reported which extensively highlight the role of flavonoids and especially the different classes of flavonoids in the modulation of Bcl-2 in the P53 signaling pathway.	Flavonoids	136-146	P53	Homo sapiens	181-184
34768743-10	2021	Herein, we discuss the modulation of Bcl-2 in the p53 signaling pathway by different classes of flavonoids and highlight different mechanisms through which this modulation can occur.	Flavonoids	96-106	P53	Homo sapiens	50-53
34644781-9	2021	RESULTS: In our results, 6-shogaol not only suppressed proliferation and anchorage-independent cell growth in OSCC cells, but also induced apoptosis by regulating the apoptosis-associated factors such as p53, Bax, Bcl-2, and cleaved caspase-3.	shogaol	25-34	P53	Homo sapiens	204-207
34711017-7	2021	RESULTS: CCH caused concentration and time-dependent reduction in the viability of human HepG2 and MCF7 cells, pre-G1 apoptosis and cell cycle arrest at G2/M stage, significantly higher P53 and TNF-alpha mRNA and protein expression levels but significantly lower COX2 mRNA and protein expression levels.	1-acetyl-2-(coumariniminecarboxamide-3-yl)hydrazine	9-12	P53	Homo sapiens	186-189
34638761-3	2021	Previously, we reported that niclosamide targets a metabolic vulnerability in p53-deficient tumours, providing a basis for patient stratification and personalised treatment strategies.	Niclosamide	29-40	P53	Homo sapiens	78-81
34638761-8	2021	Notably, quantitative scoring of drug sensitivity suggests that elimination of its nitro group enhanced the target selectivity of niclosamide against p53 deficiency.	Niclosamide	130-141	P53	Homo sapiens	150-153
34577642-9	2021	We conclude that the use of HO-3867 as an adjuvant to conventional therapeutics in ovarian cancers harboring TP53 missense mutations could improve patient outcomes.	(3,5-bis((4-fluorophenyl)methylidene)-1-((1-hydroxy-2,2,5,5-tetramethyl-2,5-dihydro-1H-pyrrol-3-yl)methyl)piperidin-4-one)	28-35	P53	Homo sapiens	109-113
34530900-12	2021	Moreover, we provide evidences that myeloma cells are dependent on SETD8 activity and its pharmacological inhibition synergizes with melphalan, which could be beneficial to improve MM treatment in high-risk patients whatever their status for p53.	Melphalan	133-142	P53	Homo sapiens	242-245
34082063-4	2021	TP53-induced glycolysis and apoptotic regulators (TIGAR) may facilitate the production of nicotinamide adenine dinucleotide phosphoric acid (NADPH) via the pentose phosphate pathway (PPP) to inhibit oxidative stress and neuroinflammation.	NADP	141-146	P53	Homo sapiens	0-4
34082063-4	2021	TP53-induced glycolysis and apoptotic regulators (TIGAR) may facilitate the production of nicotinamide adenine dinucleotide phosphoric acid (NADPH) via the pentose phosphate pathway (PPP) to inhibit oxidative stress and neuroinflammation.	Pentosephosphates	156-173	P53	Homo sapiens	0-4
34224824-5	2021	Isotretinoin is associated with pro-apoptotic signaling in sebaceous glands through upregulated expression of p53, forkhead box O transcription factors (FOXO1, FOXO3), and tumor necrosis factor-related apoptosis inducing ligand (TRAIL).	Isotretinoin	0-12	P53	Homo sapiens	110-113
34224824-6	2021	Two literature searches including clinical and experimental studies respectively support the hypothesis that isotretinoin s toxicological mode of action on the pituitary-ovarian axis might be caused by over-expressed p53/FOXO1 signaling resulting in gonadotropin suppression and granulosa cell apoptosis.	Isotretinoin	109-121	P53	Homo sapiens	217-220
34353269-0	2022	A Novel Imidazo(1,2-a)pyridine Compound Reduces Cell Viability and Induces Apoptosis of HeLa Cells by p53/Bax-Mediated Activation of Mitochondrial Pathway.	imidazo(1,2-a)pyridine	8-30	P53	Homo sapiens	102-105
34353269-12	2022	CONCLUSION: The novel imidazo(1,2-a)pyridine compound, La23, was synthesized and suppressed cell growth by inducing cell apoptosis via the p53/Bax mitochondrial apoptotic pathway.	imidazo(1,2-a)pyridine	22-44	P53	Homo sapiens	139-142
34359777-0	2021	WIP1 Inhibition by GSK2830371 Potentiates HDM201 through Enhanced p53 Phosphorylation and Activation in Liver Adenocarcinoma Cells.	GSK2830371	19-29	P53	Homo sapiens	66-69
34359777-8	2021	Combination with GSK2830371 increased p53 phosphorylation, resulting in an increase in both p53 accumulation and p53-dependent trans-activation.	GSK2830371	17-27	P53	Homo sapiens	38-41
34244426-2	2021	Here, we show that the mitochondrial methylenetetrahydrofolate dehydrogenase (MTHFD2) is transcriptionally suppressed by p53, and its up-regulation by p53 inactivation leads to increased folate metabolism, de novo purine synthesis, and tumor growth in vivo and in vitro.	purine	214-220	P53	Homo sapiens	121-124
34244426-2	2021	Here, we show that the mitochondrial methylenetetrahydrofolate dehydrogenase (MTHFD2) is transcriptionally suppressed by p53, and its up-regulation by p53 inactivation leads to increased folate metabolism, de novo purine synthesis, and tumor growth in vivo and in vitro.	purine	214-220	P53	Homo sapiens	151-154
34256525-7	2021	TA also down-regulated antiapoptotic proteins and induced p53 in colon cancer cells.	Tantalum	0-2	P53	Homo sapiens	58-61
34172723-3	2021	Screening an oligopyridylamide library, previously shown to inhibit amyloid formation associated with Alzheimer"s disease and type II diabetes, identified a tripyridylamide, ADH-6, that abrogates self-assembly of the aggregation-nucleating subdomain of mutant p53 DBD.	tripyridylamide	157-172	P53	Homo sapiens	260-263
34208730-8	2021	Examination of the NAG-1 promoter activity showed that p53, C/EBPalpha, or C/EBPdelta played a role in quercetin-induced NAG-1 expression.	Quercetin	103-112	P53	Homo sapiens	55-58
35504052-14	2022	Moreover, we further articulate the molecular mechanism of action for SN and, reveal that SN promotes the expression of cell cycle-dependent kinase inhibitory protein p21 Waf1/Cip1 through targeting Grp94 and then inhibiting PI3K/AKT signaling pathway as well as up-regulating p53 to disrupt the progression of HONE1 cells.	Tin	90-92	P53	Homo sapiens	277-280
35460941-0	2022	Low doses of niclosamide and quinacrine combination yields synergistic effect in melanoma via activating autophagy-mediated p53-dependent apoptosis.	Niclosamide	13-24	P53	Homo sapiens	124-127
35460941-5	2022	The results showed, briefly, an exposure to niclosamide and quinacrine led to an increased apoptosis-related protein p53, cleaved caspase-3 and cleaved PARP and autophagy-related protein LC3B expression, and a decreased expression of autophagy-related protein p62, finally leading to cell apoptosis and autophage.	Niclosamide	44-55	P53	Homo sapiens	117-120
35526567-0	2022	Sampsonione F suppresses adipogenesis via activating p53 pathway during the mitotic clonal expansion progression of adipocyte differentiation.	Sampsonione F	0-13	P53	Homo sapiens	53-56
35526567-8	2022	Our data support that sampsonione F suppressed adipogenesis by activating p53 pathway, regulating cyclins, and resulting in G1/S phase arrest during the MCE progression of adipogenesis.	Sampsonione F	22-35	P53	Homo sapiens	74-77
35461040-11	2022	MiR-377-3p facilitates the proliferation and suppresses the cell cycle arrest and apoptosis in HCC by affecting transcription factor EGR1-mediated p53 activation.	mir-377-3p	0-10	P53	Homo sapiens	147-150
35626421-5	2022	Here, we describe a case report of a patient with metastatic NSCLC harboring EGFR mutation who developed two independent resistance mechanisms (EGFR-T790M and TP53 + RB1 mutations) to dacomitinib.	dacomitinib	184-195	P53	Homo sapiens	159-163
35626421-6	2022	Osimertinib given as a second-line treatment eliminated the EGFR-T790M population and simultaneously consolidated the proliferation of the TP53 + RB1 clone that eventually led to the histologic transformation to small-cell lung cancer (SCLC).	osimertinib	0-11	P53	Homo sapiens	139-143
35510223-13	2022	The molecular docking results showed that there was a certain affinity between the main compounds (kaempferol, quercetin, beta-sitosterol, naringenin) and core target genes (PTGS2, CASP3, MAPK1, MAPK3, TP53).	Quercetin	111-120	P53	Homo sapiens	202-206
35564499-6	2022	Probes associated with established tumor suppressor genes (ATM, BRCA1, PALB2, and TP53) were hypermethylated among WTC-exposed breast cancer cases compared to the unexposed group.	CHEMBL572934	115-118	P53	Homo sapiens	82-86
35435229-0	2022	Malic enzyme 2 as a therapeutic target for cancer: comments on "Malic enzyme 2 maintains protein stability of mutant p53 through 2-hydroxyglutarate".	alpha-hydroxyglutarate	129-147	P53	Homo sapiens	117-120
35368106-7	2022	Notably, 6 of 7 pts (86%) who received either allo-SCT3 or a combination therapy of DLIs, 5-azacytidine and venetoclax achieved CR despite poor cytogenetics post-allo-SCT2 (e.g. TP53).	Azacitidine	90-103	P53	Homo sapiens	178-182
35356282-5	2022	In some experiments, cells were pre-treated with rapamycin (an activator of autophagy), 3-MA (an inhibitor of autophagy), or cyclic pifithrin-alpha (PFT-alpha, an antagonist of p53), and then treated with AOPPs.	pifithrin	149-158	P53	Homo sapiens	177-180
35088582-6	2022	In contrast, delivery of wild type p53 and suppression of NEK2 in TP53-/- MM cell lines inhibit tumor formation and enhance the effect of Bortezomib against MM.	Bortezomib	138-148	P53	Homo sapiens	35-38
35088582-6	2022	In contrast, delivery of wild type p53 and suppression of NEK2 in TP53-/- MM cell lines inhibit tumor formation and enhance the effect of Bortezomib against MM.	Bortezomib	138-148	P53	Homo sapiens	66-70
35215995-9	2022	The ROS scavenger N-acetyl-l-cysteine (NAC) and the p53 specific inhibitor Pifithrin-alpha (PFT-alpha) suppressed PEDV-induced apoptosis and impeded viral replication, suggesting that ROS and p53 play an important role in PEDV-induced apoptosis and viral replication.	pifithrin	75-90	P53	Homo sapiens	52-55
35215995-9	2022	The ROS scavenger N-acetyl-l-cysteine (NAC) and the p53 specific inhibitor Pifithrin-alpha (PFT-alpha) suppressed PEDV-induced apoptosis and impeded viral replication, suggesting that ROS and p53 play an important role in PEDV-induced apoptosis and viral replication.	pifithrin	75-90	P53	Homo sapiens	192-195
35215995-9	2022	The ROS scavenger N-acetyl-l-cysteine (NAC) and the p53 specific inhibitor Pifithrin-alpha (PFT-alpha) suppressed PEDV-induced apoptosis and impeded viral replication, suggesting that ROS and p53 play an important role in PEDV-induced apoptosis and viral replication.	pifithrin	92-101	P53	Homo sapiens	52-55
35215995-9	2022	The ROS scavenger N-acetyl-l-cysteine (NAC) and the p53 specific inhibitor Pifithrin-alpha (PFT-alpha) suppressed PEDV-induced apoptosis and impeded viral replication, suggesting that ROS and p53 play an important role in PEDV-induced apoptosis and viral replication.	pifithrin	92-101	P53	Homo sapiens	192-195
35204761-0	2022	Correlation of Occupational Exposure to Carcinogenic Polycyclic Aromatic Hydrocarbons (cPAHs) and Blood Levels of p53 and p21 Proteins.	Polycyclic Aromatic Hydrocarbons	53-85	P53	Homo sapiens	114-117
35038960-6	2022	The results showed that I125 seed stent implantation combined with TACE in the treatment of patients with cholangiocarcinoma can play an obvious clinical effect, effectively reduce the level of tumor markers and p53, reduce tumor lesions, improve the survival rate of patients, and play an important role in tumor treatment.	Chlorotrianisene	67-71	P53	Homo sapiens	212-215
35105987-8	2022	Our results identify cGAMP uptake through LRRC8C and STING-p53 signaling as a new inhibitory signaling pathway in T cells and adaptive immunity.	cyclic guanosine monophosphate-adenosine monophosphate	21-26	P53	Homo sapiens	59-62
34854834-6	2022	Early phase clinical trials combining the anti-CD47 mAb magrolimab with the hypomethylating agent azacitidine have showed synergistic activities, deep and durable responses, as well as a tolerable safety profile in these patients, including those with TP53 mutations.	Azacitidine	98-109	P53	Homo sapiens	252-256
11892796-5	1983	PAb1101 reacts far more weakly with rodent p53 than with primate p53.	pab1101	0-7	P53	Homo sapiens	43-46
11892796-5	1983	PAb1101 reacts far more weakly with rodent p53 than with primate p53.	pab1101	0-7	P53	Homo sapiens	65-68
34055057-9	2021	In summary, the present study suggested that hirsutanol A inhibited Jurkat cell viability through induction of cell cycle arrest and p53-dependent initiation of apoptosis, thus hirsutanol may serve as a promising compound for the treatment of T-ALL.	hirsutanol	45-55	P53	Homo sapiens	133-136
32008465-7	2021	In cancer cells, Vit C, in a pharmacological dose, decreased cell proliferation through an inhibitory effect on cyclin-dependent kinase 2 (CDK2) (4.4-fold; p &lt; 0.01), mainly due to the stimulatory effect on the expression of cyclin-dependent kinase (CDK) inhibitors, such as p21 and p53 (3.2- and 2.8-fold, respectively; p &lt; 0.001), but not caspase pathway.	Ascorbic Acid	17-22	P53	Homo sapiens	286-289
33880579-8	2021	Therefore, the results of the present study demonstrated that GM induced lung cancer cell apoptosis and cell cycle arrest via the Akt/MDM2/p53 signaling pathway.	germacrone	62-64	P53	Homo sapiens	139-142
34043149-7	2021	Upregulation of DUXAP8 and FOXD2-AS1 was significantly associated with progesterone receptor-positive (PR+) and p53 protein expression in luminal BC patients, respectively.	Phenobarbital	138-145	P53	Homo sapiens	112-115
33990090-10	2021	AR amplification and TP53 and/or RB1 alterations were associated with resistance to abiraterone or docetaxel.	abiraterone	84-95	P53	Homo sapiens	21-25
34035828-9	2021	Further analysis showed that the HGD activity of quercetin, formononetin, kaempferol, isorhamnetin, and beta-sitosterol ingredients is possible through VEGFA, IL6, TNF, AKT1, and TP53 targets involved in TNF, toll-like receptors, and MAPK-related pathways, which have anti-inflammatory, antiapoptosis, antioxidation, and autophagy effects, relieve renal fibrosis and renal cortex injury, and improve renal function, thus delaying the development of DN.	kaempferol	74-84	P53	Homo sapiens	179-183
34035828-10	2021	The molecular docking results showed that quercetin, formononetin, kaempferol, isorhamnetin, beta-sitosterol had a good binding activity with VEGFA, IL6, TNF, AKT1, and TP53.	kaempferol	67-77	P53	Homo sapiens	169-173
33556560-0	2021	Phenanthroline impairs betaAPP processing and expression, increases p53 protein levels and induces cell cycle arrest in human neuroblastoma cells.	Phenanthrolines	0-14	P53	Homo sapiens	68-71
33556560-6	2021	We establish that, beyond the ability of all inhibitors to affect sAPPalpha production to varying degrees, phenanthroline specifically and dose-dependently lessened betaAPP expression, a phenomenon that correlated with a strong increase in p53 protein levels and a concomitant decrease of the p53-degrading calpain protease.	Phenanthrolines	107-121	P53	Homo sapiens	240-243
33556560-6	2021	We establish that, beyond the ability of all inhibitors to affect sAPPalpha production to varying degrees, phenanthroline specifically and dose-dependently lessened betaAPP expression, a phenomenon that correlated with a strong increase in p53 protein levels and a concomitant decrease of the p53-degrading calpain protease.	Phenanthrolines	107-121	P53	Homo sapiens	293-296
33556560-8	2021	Altogether, our results identify new roles of phenanthroline in perturbing betaAPP, p53 and calpain biology, and suggest that the use of this compound and its derivatives as antimicrobial and anti-cancer therapies might trigger Alzheimer"s disease pathogenesis.	Phenanthrolines	46-60	P53	Homo sapiens	84-87
33995088-6	2021	TB treatment caused the downregulating of c-myc, cyclin D, CDK2, and CDK4 and upregulating of p21 and p27 in the HOG cell, while TB increased P53, p21, and p27 levels and decreased the levels of cell cycle regulator proteins such as CDK and cyclin A/B in the U251 cells.	theabrownin	0-2	P53	Homo sapiens	142-145
33995088-6	2021	TB treatment caused the downregulating of c-myc, cyclin D, CDK2, and CDK4 and upregulating of p21 and p27 in the HOG cell, while TB increased P53, p21, and p27 levels and decreased the levels of cell cycle regulator proteins such as CDK and cyclin A/B in the U251 cells.	theabrownin	129-131	P53	Homo sapiens	142-145
33925065-0	2021	Potential Antitumor Effects of 6-Gingerol in p53-Dependent Mitochondrial Apoptosis and Inhibition of Tumor Sphere Formation in Breast Cancer Cells.	gingerol	31-41	P53	Homo sapiens	45-48
33925065-7	2021	6-Gingerol induced cellular and mitochondrial ROS that elevated DDR through ataxia-telangiectasia mutated and p53 activation.	gingerol	0-10	P53	Homo sapiens	110-113
33925065-10	2021	EGFR/Src/STAT3 signaling was also determined to be responsible for p53 activation and that 6-gingerol induced p53-dependent intrinsic apoptosis in breast cancer cells.	gingerol	91-101	P53	Homo sapiens	110-113
33923162-5	2021	In addition, we showed that pentamidine treatment of ZR-75-1 breast cancer cells resulted in reduced proliferation and increased p53 and p21 protein levels, indicating that pentamidine is an effective antagonist that interferes with the S100P-p53 interaction, leading to re-activation of the p53-21 pathway and inhibition of cancer cell proliferation.	Pentamidine	28-39	P53	Homo sapiens	129-132
33923162-5	2021	In addition, we showed that pentamidine treatment of ZR-75-1 breast cancer cells resulted in reduced proliferation and increased p53 and p21 protein levels, indicating that pentamidine is an effective antagonist that interferes with the S100P-p53 interaction, leading to re-activation of the p53-21 pathway and inhibition of cancer cell proliferation.	Pentamidine	28-39	P53	Homo sapiens	243-246
33923162-5	2021	In addition, we showed that pentamidine treatment of ZR-75-1 breast cancer cells resulted in reduced proliferation and increased p53 and p21 protein levels, indicating that pentamidine is an effective antagonist that interferes with the S100P-p53 interaction, leading to re-activation of the p53-21 pathway and inhibition of cancer cell proliferation.	Pentamidine	28-39	P53	Homo sapiens	243-246
33923162-5	2021	In addition, we showed that pentamidine treatment of ZR-75-1 breast cancer cells resulted in reduced proliferation and increased p53 and p21 protein levels, indicating that pentamidine is an effective antagonist that interferes with the S100P-p53 interaction, leading to re-activation of the p53-21 pathway and inhibition of cancer cell proliferation.	Pentamidine	173-184	P53	Homo sapiens	129-132
33923162-5	2021	In addition, we showed that pentamidine treatment of ZR-75-1 breast cancer cells resulted in reduced proliferation and increased p53 and p21 protein levels, indicating that pentamidine is an effective antagonist that interferes with the S100P-p53 interaction, leading to re-activation of the p53-21 pathway and inhibition of cancer cell proliferation.	Pentamidine	173-184	P53	Homo sapiens	243-246
33923162-5	2021	In addition, we showed that pentamidine treatment of ZR-75-1 breast cancer cells resulted in reduced proliferation and increased p53 and p21 protein levels, indicating that pentamidine is an effective antagonist that interferes with the S100P-p53 interaction, leading to re-activation of the p53-21 pathway and inhibition of cancer cell proliferation.	Pentamidine	173-184	P53	Homo sapiens	243-246
33923162-6	2021	Collectively, our findings suggest that blocking the association between S100P and p53 by pentamidine will prevent cancer progression and, therefore, provide a new avenue for cancer therapy by targeting the S100P-p53 interaction.	Pentamidine	90-101	P53	Homo sapiens	83-86
33923162-6	2021	Collectively, our findings suggest that blocking the association between S100P and p53 by pentamidine will prevent cancer progression and, therefore, provide a new avenue for cancer therapy by targeting the S100P-p53 interaction.	Pentamidine	90-101	P53	Homo sapiens	213-216
33678118-5	2021	miR-129 directly targeted MDM2/4 to inhibit expression, therefore counteracting MDM2/4-mediated p53 signaling suppression and modulating RB cell proliferation and apoptosis.	mir-129	0-7	P53	Homo sapiens	96-99
33125183-6	2021	At nontoxic concentration, IP-Se-06 decreased the protein levels of Bcl-xL and increased the levels of p53, leading to inhibition of cell proliferation and apoptosis.	ip-se-06	27-35	P53	Homo sapiens	103-106
33538587-0	2021	Benzothiazolyl and Benzoxazoyl Hydrazones Function as Zinc Metallochaperones to Reactivate Mutant p53.	benzothiazolyl	0-14	P53	Homo sapiens	98-101
33538587-0	2021	Benzothiazolyl and Benzoxazoyl Hydrazones Function as Zinc Metallochaperones to Reactivate Mutant p53.	zinc metallochaperones	54-76	P53	Homo sapiens	98-101
33538587-1	2021	We identified a set of thiosemicarbazone (TSC) metal ion chelators that reactivate specific zinc-deficient p53 mutants using a mechanism called zinc metallochaperones (ZMCs) that restore zinc binding by shuttling zinc into cells.	zinc metallochaperones	144-166	P53	Homo sapiens	107-110
33664742-0	2021	Therapeutic Effects of (5R)-5-Hydroxytriptolide on Fibroblast-Like Synoviocytes in Rheumatoid Arthritis via lncRNA WAKMAR2/miR-4478/E2F1/p53 Axis.	5alpha-Hydroxytriptolide	23-47	P53	Homo sapiens	137-140
33566220-10	2021	Subsequently, the upregulated p53 facilitated SAT1 transcription and enhanced SAT1-catalyzed spermine metabolism, which further resulted in trophoblastic cell apoptosis and induced miscarriage.	Spermine	93-101	P53	Homo sapiens	30-33
33566220-15	2021	P53 promotes SAT1 transcription and reduces its cellular spermine content, resulting in cell apoptosis.	Spermine	57-65	P53	Homo sapiens	0-3
33486250-5	2021	We hypothesized that curcumin attenuates fluoride toxicity through modulation of Ac-p53.	Fluorides	41-49	P53	Homo sapiens	84-87
33486250-6	2021	Here we investigated how curcumin affects the p53-p21 pathway in fluoride toxicity.	Fluorides	65-73	P53	Homo sapiens	46-49
32737944-0	2021	Potency and selectivity optimization of tryptophanol-derived oxazoloisoindolinones: novel p53 activators in human colorectal cancer.	tryptophanol	40-52	P53	Homo sapiens	90-93
33365081-0	2021	Proliferation, migration and invasion of triple negative breast cancer cells are suppressed by berbamine via the PI3K/Akt/MDM2/p53 and PI3K/Akt/mTOR signaling pathways.	berbamine	95-104	P53	Homo sapiens	127-130
34055057-8	2021	Of note, hirsutanol A induced the expression of the tumor suppressor p53, whereas simultaneous treatment with pifithrin-alpha, an inhibitor of p53, significantly reduced Jurkat cell apoptosis induced by hirsutanol A.	hirsutanol	9-19	P53	Homo sapiens	69-72
33318190-4	2020	Here, we identified sulfated GAGs as molecules that mediate prion-like behavior of p53 aggregates.	Glycosaminoglycans	29-33	P53	Homo sapiens	83-86
33880579-0	2021	Germacrone induces lung cancer cell apoptosis and cell cycle arrest via the Akt/MDM2/p53 signaling pathway.	germacrone	0-10	P53	Homo sapiens	85-88
33880579-6	2021	GM also significantly altered the expression levels of Akt/MDM2/p53 signaling pathway-related proteins compared with the control group.	germacrone	0-2	P53	Homo sapiens	64-67
33318190-5	2020	Sulfated GAGs at the cell surface were required for cellular uptake of recombinant and cancer cell-derived p53 aggregates and extracellular release of p53 from cancer cells.	Glycosaminoglycans	9-13	P53	Homo sapiens	107-110
33318190-5	2020	Sulfated GAGs at the cell surface were required for cellular uptake of recombinant and cancer cell-derived p53 aggregates and extracellular release of p53 from cancer cells.	Glycosaminoglycans	9-13	P53	Homo sapiens	151-154
2834865-6	1988	Equivalent amounts of p53 were immunoprecipitated with the anti-T-antigen antibodies PAb416, PAb419, and PAb101, suggesting that in vitro made p53 complexed mostly to a population of T-antigen molecules that had matured at least 15 min in the cell.	pab416	85-91	P53	Homo sapiens	22-25
2834865-6	1988	Equivalent amounts of p53 were immunoprecipitated with the anti-T-antigen antibodies PAb416, PAb419, and PAb101, suggesting that in vitro made p53 complexed mostly to a population of T-antigen molecules that had matured at least 15 min in the cell.	pab416	85-91	P53	Homo sapiens	143-146
33727227-8	2021	The expression of TP53 and BRCA1 was decreased in luminal progenitor cells from normal breast tissue in BRCA1 mutation carriers, which might trigger the basal/mesenchymal transition of luminal progenitors and might result in basal-like tumor development.	Phenobarbital	50-57	P53	Homo sapiens	18-22
33318190-7	2020	Finally, sulfated GAG-dependent cellular uptake of p53 aggregates was critical for subsequent extracellular release of the aggregates and gain of oncogenic function in recipient cells.	Glycosaminoglycans	18-21	P53	Homo sapiens	51-54
33727227-8	2021	The expression of TP53 and BRCA1 was decreased in luminal progenitor cells from normal breast tissue in BRCA1 mutation carriers, which might trigger the basal/mesenchymal transition of luminal progenitors and might result in basal-like tumor development.	Phenobarbital	185-192	P53	Homo sapiens	18-22
33318190-8	2020	Our work provides a mechanism of prion-like behavior of p53 aggregates and will shed light on sulfated GAGs as a common mediator of prions.	Glycosaminoglycans	103-107	P53	Homo sapiens	56-59
33209128-2	2020	In the present study, the small molecule 2-[1-(4-(benzyloxy)phenyl)-3-oxoisoindolin-2-yl)-2-(4-methoxyphenyl)] acetic acid (CDS-3078) significantly increased p53 mRNA expression levels in a dose-dependent manner.	2-[1-(4-(benzyloxy)phenyl)-3-oxoisoindolin-2-yl)-2-(4-methoxyphenyl)] acetic acid	41-122	P53	Homo sapiens	158-161
33662352-6	2021	In addition, perifosine enhanced the cytotoxicity of the 5-FU and L-OHP combination, inhibited Akt activation and the expression of Survivin, Bcl-2, and Bcl-xL, and increased the expression of Puma, phospho-p53, and p53 in DLD-1 cells.	perifosine	13-23	P53	Homo sapiens	207-210
33662352-6	2021	In addition, perifosine enhanced the cytotoxicity of the 5-FU and L-OHP combination, inhibited Akt activation and the expression of Survivin, Bcl-2, and Bcl-xL, and increased the expression of Puma, phospho-p53, and p53 in DLD-1 cells.	perifosine	13-23	P53	Homo sapiens	216-219
34047071-1	2021	In silico approaches identified 1 , N -(6-((4-bromo- benzyl)amino)hexyl)-3,5-bis(trifluoromethyl)benzene sulfonamide, as a potential inhibitor of S100A2-p53 protein-protein interaction, a validated pancreatic cancer drug target.	1 , n -(6-((4-bromo- benzyl)amino)hexyl)-3,5-bis(trifluoromethyl)benzene sulfonamide	32-116	P53	Homo sapiens	153-156
33449813-1	2021	PURPOSE: Approximately 20% of patients with TP53-mutant myelodysplastic syndromes (MDS) achieve complete remission (CR) with hypomethylating agents.	hypomethylating agents	125-147	P53	Homo sapiens	44-48
33299560-8	2020	Lower mRNA TP53 expression correlated with shorter time to CRPC among patients treated with ADT (p = 0.006).	adt	92-95	P53	Homo sapiens	11-15
33834390-0	2022	Lead Borate Nanoparticles Induce Apoptotic Gene Activity in P53 Mutant Cancer Cells.	Lead metaborate	0-11	P53	Homo sapiens	60-63
33834390-5	2022	In this current study, lead borate nanoparticles (LB-Np) have been synthesized, and their effects on P53 mutant cancer cells were investigated.	Lead metaborate	23-34	P53	Homo sapiens	101-104
33970096-0	2021	Rapid Response of a BRCA2/TP53/PTEN-Deleted Metastatic Uterine Leiomyosarcoma to Olaparib: A Case Report.	olaparib	81-89	P53	Homo sapiens	26-30
33923162-4	2021	Our experimental analysis indicates that the S100P-53 complex formation is successfully disrupted by pentamidine, since S100P shares the same binding site for p53 and pentamidine.	Pentamidine	101-112	P53	Homo sapiens	159-162
33299560-10	2020	Conclusions: Low expression of mRNA of RB1 and TP53 has been shown to be a potential marker of shorter time to develop CRPC in patients with advanced stages of prostate cancer treated with ADT.	adt	189-192	P53	Homo sapiens	47-51
33047953-3	2020	Additionally, with the assistance of Nt.BstNBI enzyme-assisted target cycling process, a limited amount of target DNA (a fragment of p53 gene) could be converted into extensive output DNA, which could hybridize with capture DNA to yield abundant DNA duplex for loading mimetic enzyme manganese porphyrin (MnPP).	manganese porphyrin	284-303	P53	Homo sapiens	133-136
32898442-5	2021	When inhibiting the expression of SIRT1 by EX527, our results showed that TSG reversed the effect of EX527, by promoting the expression level of SIRT1, reducing the expression of SA-beta-gal positive cell and the expression level of p53 and PAI-1 proteins.	2',3',4',5'-tetrahydroxystilbene-2-O-beta-D-glucoside	74-77	P53	Homo sapiens	233-236
33476981-3	2021	Pharmacological inhibition of TLR4 signaling by TAK242 or its siRNA-mediated knockdown in p53 mutant or wild-type glioma cells resulted in either increased or decreased SOCS1 expression and promoter activity, respectively.	ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate	48-54	P53	Homo sapiens	90-93
33851623-13	2021	Interestingly, xanthoceraside also downregulated the expression of p-PI3K and p-Akt, and upregulated P53.	xanthoceraside	15-29	P53	Homo sapiens	101-104
33860088-3	2021	Our recent study revealed that sulfated glycosaminoglycans, especially highly sulfated domains of heparan sulfate (heparan sulfate S-domains), participate in cancer pathology by mediating transcellular propagation of p53 aggregates.	Glycosaminoglycans	40-58	P53	Homo sapiens	217-220
33139695-9	2020	Copanlisib-mediated chemosensitization seemed to involve the concurrent induction of PUMA expression via mechanisms that were both dependent and independent of p53.	copanlisib	0-10	P53	Homo sapiens	160-163
33860088-3	2021	Our recent study revealed that sulfated glycosaminoglycans, especially highly sulfated domains of heparan sulfate (heparan sulfate S-domains), participate in cancer pathology by mediating transcellular propagation of p53 aggregates.	Heparitin Sulfate	98-113	P53	Homo sapiens	217-220
33860088-3	2021	Our recent study revealed that sulfated glycosaminoglycans, especially highly sulfated domains of heparan sulfate (heparan sulfate S-domains), participate in cancer pathology by mediating transcellular propagation of p53 aggregates.	Heparitin Sulfate	115-130	P53	Homo sapiens	217-220
33472889-6	2021	For all tissues combined, hierarchical clustering of subtype gene expression revealed three subtypes: "luminal," "basal," and a "luminal p53-/ extracellular matrix (ECM)-like" phenotype of ECM-related genes enriched in tumor-associated urothelium, non-invasive urothelial lesions, and CIS, but rarely invasive carcinomas.	Phenobarbital	129-136	P53	Homo sapiens	137-140
33472889-8	2021	A PanCancer Progression Panel of 681 genes unveiled pathways specific for the luminal p53-/ECM-like cluster, e.g., ECM remodeling, angiogenesis, epithelial to mesenchymal transition (EMT), cellular discohesion, cell motility involved in tumor progression; and cell proliferation and oncogenic ERBB2/ERBB3 signaling for invasive carcinomas.	Phenobarbital	78-85	P53	Homo sapiens	86-89
33668397-5	2021	In addition, pre-treatment with THF suppressed CoCl2-induced hypoxia-related genes including HIF1alpha, p53, VEGF, and GLUT1 at the mRNA and protein levels.	cobaltous chloride	47-52	P53	Homo sapiens	104-107
32871626-9	2020	Furthermore, TP53 was most frequently mutated in patients who progressed on crizotinib, and TP53 mutations were significantly associated with shorter crizotinib PFS.	Crizotinib	76-86	P53	Homo sapiens	13-17
33356180-0	2021	Diclofenac Sodium Triggers p53-Dependent Apoptosis in Human Corneal Epithelial Cells via ROS-Mediated Crosstalk.	Diclofenac	0-17	P53	Homo sapiens	27-30
33743824-6	2021	The combination of AUY922 with VE821 led to strong apoptosis induction independent of the cellular p53 status, yet based on different molecular mechanisms.	5-(2,4-dihydroxy-5-isopropylphenyl)-4-(4-morpholin-4-ylmethylphenyl)isoxazole-3-carboxylic acid ethylamide	19-25	P53	Homo sapiens	99-102
33356180-10	2021	Additionally, the DFS-induced apoptosis was alleviated by p53 inhibitor.	Diclofenac	18-21	P53	Homo sapiens	58-61
33704017-9	2021	Docking study of isoleucine sulfonamide analogues (I1-I6) were carried out to determine the possible interaction sites of the analogues with p53 tumor suppressor-DNA complex and demonstrate that the analogues confirmed binding and inhibition with the most mutated residues of p53.	isoleucine sulfonamide	17-39	P53	Homo sapiens	141-144
32871626-9	2020	Furthermore, TP53 was most frequently mutated in patients who progressed on crizotinib, and TP53 mutations were significantly associated with shorter crizotinib PFS.	Crizotinib	150-160	P53	Homo sapiens	92-96
33704017-9	2021	Docking study of isoleucine sulfonamide analogues (I1-I6) were carried out to determine the possible interaction sites of the analogues with p53 tumor suppressor-DNA complex and demonstrate that the analogues confirmed binding and inhibition with the most mutated residues of p53.	isoleucine sulfonamide	17-39	P53	Homo sapiens	276-279
32649952-9	2020	We found that the presence of a pentamidine molecule results in higher p53 activity, which is also reflected in less cell proliferation.	Pentamidine	32-43	P53	Homo sapiens	71-74
33631963-6	2021	Next-generation sequencing (NGS) was performed on formalin-fixed paraffin-embedded tumor tissue, revealing one mutation in exon 5, TP53: p.A159 V, which may be associated with chemo-resistance.	Formaldehyde	50-58	P53	Homo sapiens	131-135
32986365-0	2020	Ki67 and P53 Expression in Relation to Clinicopathological Features in Phyllodes Tumour of the Breast.	phyllodes	71-80	P53	Homo sapiens	9-12
33481236-4	2021	Importantly, we have specifically detected the PLA signal between PtdIns(4,5)P2 and its binding effector p53 in the nucleus.	Phosphatidylinositol 4,5-Diphosphate	66-79	P53	Homo sapiens	105-108
33310890-7	2021	In subcutaneous tumor models, combination of ixazomib and alectinib prominently induced tumor regression and apoptosis even though the tumors were generated from ALK-rearranged NSCLC cells with non-functional p53.	ixazomib	45-53	P53	Homo sapiens	209-212
32638267-7	2020	Moreover, we found that hypo-DNA methylation, DNA amplification, and TP53 mutation were contributing to the high expression levels of pyrimidine metabolic rate-limiting enzymes in lung cancer cells.	pyrimidine	134-144	P53	Homo sapiens	69-73
33529089-5	2021	Among the 10 resveratrol analogues, Pts and Pts nicotinate attenuated the expression of senescence-associated beta-galactosidase, downregulated p21 and p53, and increased the production of NO in both angiotensin II and H2O2-induced endothelial senescence models.	Niacin	48-58	P53	Homo sapiens	152-155
33416166-7	2021	The p53 activator Mithramycin A stimulated p53 and miR-3184-5p expression, thereby lowering the levels of ERBB2 and attenuating proliferation, migration and sphere-formation of cervical cancer cells.	mithramycin A	18-31	P53	Homo sapiens	4-7
33416166-7	2021	The p53 activator Mithramycin A stimulated p53 and miR-3184-5p expression, thereby lowering the levels of ERBB2 and attenuating proliferation, migration and sphere-formation of cervical cancer cells.	mithramycin A	18-31	P53	Homo sapiens	43-46
33416166-9	2021	Treatment of cervical cancer cells with the p53 activator Mithramycin A restored the levels of the endogenous ERBB2 inhibitor miR-3184-5p and may represent a novel treatment strategy for cervical cancer.	mithramycin A	58-71	P53	Homo sapiens	44-47
31562955-3	2021	The anticancer potential of quinacrine was discovered in a screen for small molecule activators of p53, and was specifically shown to inhibit NFkappaB suppression of p53.	Quinacrine	28-38	P53	Homo sapiens	99-102
33326188-4	2021	Therefore, a CD44-targeted delivery system is designed and constructed by self-assembly of tyrosine (Tyr)-hyaluronic acid (HA)-polyethyleneimine (PEI), which can radiolabel 131/125 I and load a p53 mutant restoring regent, Prima-1.	Hyaluronic Acid	123-125	P53	Homo sapiens	194-197
31562955-3	2021	The anticancer potential of quinacrine was discovered in a screen for small molecule activators of p53, and was specifically shown to inhibit NFkappaB suppression of p53.	Quinacrine	28-38	P53	Homo sapiens	166-169
32872120-5	2020	Nevertheless, TP53 co-mutations are relatively frequent and are associated with adverse outcome of crizotinib treatment, whereas utility of next-generation ALK inhibitors in TP53-mutant tumors is still unknown.	Crizotinib	99-109	P53	Homo sapiens	14-18
31562955-4	2021	However, quinacrine can cause cell death in cells that lack p53 or have p53 mutations, which is a common occurrence in many malignant tumors including high grade serous ovarian cancer.	Quinacrine	9-19	P53	Homo sapiens	60-63
31562955-4	2021	However, quinacrine can cause cell death in cells that lack p53 or have p53 mutations, which is a common occurrence in many malignant tumors including high grade serous ovarian cancer.	Quinacrine	9-19	P53	Homo sapiens	72-75
33302638-0	2021	Ligustrazine induces the colorectal cancer cells apoptosis via p53-dependent mitochondrial pathway and cell cycle arrest at the G0/G1 phase.	tetramethylpyrazine	0-12	P53	Homo sapiens	63-66
33580460-7	2021	Overall, our data suggests that p53 is a potent transcriptional repressor of SVCT2, a critical transporter of diet-derived ascorbic acid, across the plasma membranes of numerous essential tissue cell types.	Ascorbic Acid	123-136	P53	Homo sapiens	32-35
32846494-8	2020	The C-CD/TiO2 group showed up-regulation of the pro-apoptotic markers such as P53 and BAX in tumor.	titanium dioxide	9-13	P53	Homo sapiens	78-81
33297189-7	2021	Notably, the molecular docking findings indicated that TP53, MAPK1, and ESR1 were potent pharmacological targets of VC against PFOS-associated leukemia.	Ascorbic Acid	116-118	P53	Homo sapiens	55-59
33297189-7	2021	Notably, the molecular docking findings indicated that TP53, MAPK1, and ESR1 were potent pharmacological targets of VC against PFOS-associated leukemia.	perfluorooctane sulfonic acid	127-131	P53	Homo sapiens	55-59
33297189-10	2021	The validated genes of TP53, MAPK1, ESR1 may become potential biomarkers for monitoring and treating PFOS-associated leukemia.	perfluorooctane sulfonic acid	101-105	P53	Homo sapiens	23-27
32950498-0	2020	Tetrandrine enhances antitumor effects of the histone deacetylase inhibitor MS-275 in human cancer in a Bax- and p53-dependent manner.	tetrandrine	0-11	P53	Homo sapiens	113-116
32950498-8	2020	Moreover, molecular assays indicated that Bax and p53 were the key regulators of MS-275/tetrandrine induced apoptosis.	tetrandrine	88-99	P53	Homo sapiens	50-53
32950498-10	2020	Based on our findings, tetrandrine enhanced the antitumor effects of MS-275 in a Bax- and p53-dependent manner.	tetrandrine	23-34	P53	Homo sapiens	90-93
32765594-5	2020	We show here that topotecan treatment significantly down-regulated estrogen receptor alpha (ERalpha/ESR1) and antiapoptotic BCL2 genes in addition to many other p53-regulated genes.	Topotecan	18-27	P53	Homo sapiens	161-164
33097607-6	2020	Therefore, taken together with the previous report, we conclude that both IKKalpha- and CHK1-dependent p53 phosphorylation and acetylation contribute to mediating selective autophagy targeting feedback degradation of IKKalpha in arsenite-induced proapoptotic responses.	arsenite	229-237	P53	Homo sapiens	103-106
32700164-2	2020	Here, we demonstrate that exposure to PFOS (10 microM) and PFOA (100 microM)-two contaminants ubiquitously found in human blood-for 72 h induced breast epithelial cell (MCF-10A cell line) proliferation and alteration of regulatory cell-cycle proteins (cyclin D1, CDK6, p21, p53, p27, ERK 1/2 and p38) that persisted after a multitude of cell divisions.	perfluorooctane sulfonic acid	38-42	P53	Homo sapiens	274-277
33035554-5	2021	At the same time, EPZ015666 regulated cell cycle related protein (P53, P21, P27, CDK2) expression.	GSK3235025	18-27	P53	Homo sapiens	66-69
33035554-6	2021	In brief, our study showed that PRMT5 promoted retinoblastoma growth, the PRMT5 inhibitor EPZ015666 inhibited retinoblastoma in vitro by regulating P53-P21/P27-CDK2 signaling pathways and slowed retinoblastoma growth in a xenograft model.	GSK3235025	90-99	P53	Homo sapiens	148-151
33189884-0	2021	Mutagenicity of 2-hydroxyamino-1-methyl-6-phenylimidazo[4,5-b]pyridine (N-OH-PhIP) in human TP53 knock-in (Hupki) mouse embryo fibroblasts.	2-hydroxyamino-1-methyl-6-phenylimidazo(4,5-b)pyridine	16-70	P53	Homo sapiens	92-96
33189884-0	2021	Mutagenicity of 2-hydroxyamino-1-methyl-6-phenylimidazo[4,5-b]pyridine (N-OH-PhIP) in human TP53 knock-in (Hupki) mouse embryo fibroblasts.	2-hydroxyamino-1-methyl-6-phenylimidazo(4,5-b)pyridine	72-81	P53	Homo sapiens	92-96
32700164-2	2020	Here, we demonstrate that exposure to PFOS (10 microM) and PFOA (100 microM)-two contaminants ubiquitously found in human blood-for 72 h induced breast epithelial cell (MCF-10A cell line) proliferation and alteration of regulatory cell-cycle proteins (cyclin D1, CDK6, p21, p53, p27, ERK 1/2 and p38) that persisted after a multitude of cell divisions.	perfluorooctanoic acid	59-63	P53	Homo sapiens	274-277
33189884-3	2021	Here, we studied N-OH-PhIP-induced whole genome mutagenesis in human TP53 knock-in (Hupki) mouse embryo fibroblasts (HUFs) immortalised and subjected to whole genome sequencing (WGS).	2-hydroxyamino-1-methyl-6-phenylimidazo(4,5-b)pyridine	17-26	P53	Homo sapiens	69-73
32765594-7	2020	The differential expression of these genes was observed in a wild-type p53-containing breast ZR-75-1 tumor cell line following topotecan treatment.	Topotecan	127-136	P53	Homo sapiens	71-74
33189884-7	2021	TP53 mutations characteristic of those induced by N-OH-PhIP have been found in human tumours including breast and colorectal, which are cancer types that have been associated with PhIP exposure.	2-hydroxyamino-1-methyl-6-phenylimidazo(4,5-b)pyridine	50-59	P53	Homo sapiens	0-4
32209732-0	2020	Econazole Induces p53-Dependent Apoptosis and Decreases Metastasis Ability in Gastric Cancer Cells.	Econazole	0-9	P53	Homo sapiens	18-21
33437202-10	2021	After comparing high- and low-risk groups separated by CDCA risk scores, the activated pathways were revealed and included the cell cycle, DNA repair, P53, MYC-targets, E2F-targets and PI3K pathways.	Chenodeoxycholic Acid	55-59	P53	Homo sapiens	151-154
33238796-8	2020	Western blotting revealed that Bcl-2 and p53 expression were significantly lower in the salidroside group than in the other groups, whereas Bax and caspase 3 (17 kDa) expression were increased.	rhodioloside	88-99	P53	Homo sapiens	41-44
33001126-0	2020	Fabrication of aminated poly(glycidyl methacrylate)-based polymers for co-delivery of anticancer drugs and the p53 gene.	aminated poly(glycidyl methacrylate)-based polymers	15-66	P53	Homo sapiens	111-114
33108147-0	2020	Resveratrol enhances apoptosis induced by the heterocyclic aromatic amines in p53-wt LoVo cells, but not in p53-deficient HaCaT cells.	aromatic amines	59-74	P53	Homo sapiens	78-81
33437202-12	2021	The cell cycle, DNA repair, E2F, P53 and PI3K signaling pathways, in which CDCAs are involved, impact the tumorigenesis of PAAD.	Chenodeoxycholic Acid	75-80	P53	Homo sapiens	33-36
33040459-7	2021	In Ba/F3 cells transformed by NPM-ALK and Ki-JK cells, p53 activation induced by knockdown of EBP2 was significantly inhibited by Akt inhibitor GDC-0068, mTORC1 inhibitor rapamycin, and knockdown of Raptor, an essential component of mTORC1.	ipatasertib	144-152	P53	Homo sapiens	55-58
32209732-4	2020	Using the gastric cancer cell lines AGS and SNU1 expressing wild-type p53 we demonstratedthat econazole could significantly reduce cell viability and colony-forming (tumorigenesis) ability.	Econazole	94-103	P53	Homo sapiens	70-73
32209732-8	2020	The protein level of p53 was significantly elevated after econazole treatmentof AGS and SNU1 cells.	Econazole	58-67	P53	Homo sapiens	21-24
32209732-9	2020	However, apoptosis was blocked in econazole-treated cells exposed to a p53-specific small-interferingRNA (siRNA) to eliminate p53 expression.	Econazole	34-43	P53	Homo sapiens	71-74
33145357-6	2020	Apoptotic genes that indicating a marked increase in expression are Caspase 3, p53, and Bax, while Bcl2 and AFP showed a downregulation of expression after treatment of HepG2 cells with lectin-loaded chitosan-TPP nanoparticles.	Chitosan	200-208	P53	Homo sapiens	79-82
32209732-9	2020	However, apoptosis was blocked in econazole-treated cells exposed to a p53-specific small-interferingRNA (siRNA) to eliminate p53 expression.	Econazole	34-43	P53	Homo sapiens	126-129
33238842-7	2021	Mutant p53 reactivation with a new class of zinc metallochaperones (ZMC) that restore WT p53 structure and function by restoring Zn2+ to Zn2+ deficient mutant p53.	zinc metallochaperones	44-66	P53	Homo sapiens	7-10
32334110-3	2020	4-nerolidylcathecol (4-NC), a natural product extracted from Pothomorphe umbellata, induces apoptosis in melanoma cells by ROS production, DNA damage and increased p53 expression, in addition to inhibiting invasion in reconstructed skin.	4-nerolidylcathecol	0-19	P53	Homo sapiens	164-167
33238842-7	2021	Mutant p53 reactivation with a new class of zinc metallochaperones (ZMC) that restore WT p53 structure and function by restoring Zn2+ to Zn2+ deficient mutant p53.	zinc metallochaperones	44-66	P53	Homo sapiens	89-92
33238842-7	2021	Mutant p53 reactivation with a new class of zinc metallochaperones (ZMC) that restore WT p53 structure and function by restoring Zn2+ to Zn2+ deficient mutant p53.	zinc metallochaperones	44-66	P53	Homo sapiens	89-92
33328303-8	2020	In addition to its effect of KSHV reactivation, this study revealed that SBHA induces apoptosis in PEL cells in a dose-dependent manner, inducing acetylation and phosphorylation of p53, cleavage of caspases, and expression of pro-apoptotic factors such as Bim and Bax.	suberoyl bis-hydroxamic acid	73-77	P53	Homo sapiens	181-184
32738393-15	2020	Therefore, we speculated that TMF-induced apoptosis might be achieved by regulating the p53-Bcl-2/Bax-caspase-3 pathways.	triflumuron	30-33	P53	Homo sapiens	88-91
33028529-3	2020	Here, we found that DSBs in oxygen/glucose-deprived (OGD) neurons spatiotemporally correlated with the up-regulation of WRAP53 (WD40-encoding p53-antisense RNA), which translocated to the nucleus to activate the DSB repair response.	dsbs	20-24	P53	Homo sapiens	142-145
32976294-14	2020	Null p53 helped distinguish dVIN from VAM and dermatoses.	METHYL 4-O-(4-THIO-BETA-D-GLUCOPYRANOSYL)-BETA-D-GLUCOPYRANOSIDE	38-41	P53	Homo sapiens	5-8
32386222-8	2020	The CPO-A treatment attenuated or restored (P < 0.05) these changes and inhibited (P < 0.05) the MPTP-induced activation of P38 mitogen-activated protein kinase (P38MAPK) and P53, along with the downstream expression of BCL-2 associated X protein (BAX) in the SN.	cpo-a	4-9	P53	Homo sapiens	175-178
32915786-8	2020	ZnO-NP treatment reduced the basal levels of reactive oxygen species and Bax/Bcl-2 mRNA ratios; in addition, ZnO-NP decreased the 6-OHDA-induced ROS production, p53 expression, and cell death.	Oxidopamine	130-136	P53	Homo sapiens	161-164
33178028-8	2020	Further study disclosed that UDCA significantly inhibited As(III)-induced apoptosis through increasing the expression of Bcl-2 and decreasing the expression of Bax, p53, Cyt C, Cleaved caspase-3 and 9.	Ursodeoxycholic Acid	29-33	P53	Homo sapiens	165-168
32609349-0	2020	Detection of TP53 Clonal Variants in Papanicolaou Test Samples Collected up to 6 Years Prior to High-Grade Serous Epithelial Ovarian Cancer Diagnosis.	papanicolaou	37-49	P53	Homo sapiens	13-17
33017467-4	2020	The cytotoxic effect of talazoparib on Moloney MuLV-induced T-cell lymphoma (MBL2) cells was a result of G2/M cell cycle arrest via the upregulation of p53.	talazoparib	24-35	P53	Homo sapiens	152-155
32878784-0	2020	Inhibition of Retinoblastoma Cell Growth by CEP1347 Through Activation of the P53 Pathway.	3,9-bis((ethylthio)methyl)-K-252a	44-51	P53	Homo sapiens	78-81
32878784-3	2020	The role of the P53 pathway in CEP1347-induced growth inhibition was also investigated.	3,9-bis((ethylthio)methyl)-K-252a	31-38	P53	Homo sapiens	16-19
32878786-5	2020	In contrast, CDKN1A gene expression was significantly increased by both SBHA and SAHA treatment of TP53-mutated RPMI8226 cells.	rpmi8226	112-120	P53	Homo sapiens	99-103
32451170-4	2020	MATERIALS AND METHODS: TP53 was PCR amplified using the genomic DNA extracted from peripheral blood mononuclear cells and formalin-fixed, paraffin-embedded tissue sections from the tumor site of the patient, and was sequenced.	Formaldehyde	122-130	P53	Homo sapiens	23-27
32609349-2	2020	Objective: To determine whether the presence of the clonal pathogenic TP53 variant detected in matched primary tumor biopsies can be identified in DNA purified from Papanicolaou test samples collected from women with HGS-EOC years before the diagnosis.	papanicolaou	165-177	P53	Homo sapiens	70-74
32649952-0	2020	Pentamidine inhibit S100A4 - p53 interaction and decreases cell proliferation activity.	Pentamidine	0-11	P53	Homo sapiens	29-32
32589431-5	2020	DMSN showed in vitro and in vivo p53-dependent antiproliferative activity, and augmented antitumor immunity elicited by anti-PD1 therapy.	dmsn	0-4	P53	Homo sapiens	33-36
32609349-8	2020	Results: Among 17 included patients (median [interquartile range] age at diagnosis, 60 [53-69] years), Papanicolaou tests withdrawn before diagnosis presented tumor-matched TP53 variants in 11 patients (64%).	papanicolaou	103-115	P53	Homo sapiens	173-177
32609349-9	2020	In 2 patients for whom longitudinal Papanicolaou tests were available, including 1 patient with Papanicolaou tests from 25 and 49 months before diagnosis and 1 patient with Papanicolaou tests from 27 and 68 months before diagnosis, the TP53 clonal variant was detected at all time points.	papanicolaou	36-48	P53	Homo sapiens	236-240
32590072-4	2020	Sappanchalcone triggered phosphorylation of p53, which is involved in the activation of caspases and increased expression of Bax in HCT116 cells.	sappanchalcone	0-14	P53	Homo sapiens	44-47
32609349-9	2020	In 2 patients for whom longitudinal Papanicolaou tests were available, including 1 patient with Papanicolaou tests from 25 and 49 months before diagnosis and 1 patient with Papanicolaou tests from 27 and 68 months before diagnosis, the TP53 clonal variant was detected at all time points.	papanicolaou	96-108	P53	Homo sapiens	236-240
32526907-4	2020	Our aim is to compare mechanisms of resistance to the PARP inhibitor olaparib in these two main molecular categories of HGSOC and investigate a way to overcome resistance that we considered particularly suited to a cancer like HGSOC, where there is a very high incidence of TP53 gene mutation, making HGSOC cells heavily reliant on the G2 checkpoint for repair of DNA damage and survival.	olaparib	69-77	P53	Homo sapiens	274-278
32801647-0	2020	Nano-Graphene Oxide-supported APTES-Spermine, as Gene Delivery System, for Transfection of pEGFP-p53 into Breast Cancer Cell Lines.	Spermine	36-44	P53	Homo sapiens	97-100
32470748-6	2020	Remarkably, P53, P21, BAX, and SMAD4 were significantly upregulated after PL treatment whereas; BCL2 and SURVIVIN were down-regulated.	piperlonguminine	74-76	P53	Homo sapiens	12-15
32315827-8	2020	Recombinant human PEDF treatment (100 nM) prevented the toxic effects of arsenite (50 muM) on endothelial cells in vitro by increasing NO content, decreasing reactive oxygen species (ROS) levels, and inhibiting apoptosis, as well as increasing cell viability and decreasing levels of P53 and phospho-p38.	arsenite	73-81	P53	Homo sapiens	284-287
32775440-1	2020	RRM2B gene encodes ribonucleoside-diphosphate reductase subunit M2 B, the p53-inducible small subunit (p53R2) of ribonucleotide reductase (RNR), an enzyme catalyzing dNTP synthesis for mitochondrial DNA.	Parathion	166-170	P53	Homo sapiens	74-77
32072678-9	2020	Specifically, the combination of ART and CBP at a lower concentration suppressed cell clone numbers, promoted cell cycle arrest at the G2 /M phase, and induced the expression of the cell cycle and apoptosis related proteins BAX, p21, p53, and Caspae-3, while decreasing Bcl-2 and CyclinB1 expression.	artesunate	33-36	P53	Homo sapiens	234-237
32774710-0	2020	Downregulation of LINC01021 by curcumin analog Da0324 inhibits gastric cancer progression through activation of P53.	Da0324	47-53	P53	Homo sapiens	112-115
32774710-6	2020	Da0324 treatment or knockdown of LINC01021 by antisense oligos significantly inhibited gastric cancer cell growth, and also up-regulated P53 expression and down-regulated Bcl-2 expression in vitro and in vivo.	Da0324	0-6	P53	Homo sapiens	137-140
32377702-7	2020	Moreover, juglone combined with PLX4032 markedly increased the intracellular level of reactive oxygen species (ROS) and activated p38 and p53, as compared with juglone alone or PLX4032 alone.	Vemurafenib	32-39	P53	Homo sapiens	138-141
33680018-0	2020	Inhibition of Cyclin-dependent Kinase (CDK) Decreased Survival of NB4 Leukemic Cells: Proposing a p53-Independent Sensitivity of Leukemic Cells to Multi-CDKs Inhibitor AT7519.	4-(2,6-dichlorobenzoylamino)-1H-pyrazole-3-carboxylic acid piperidin-4-ylamide	168-174	P53	Homo sapiens	98-101
32572160-9	2020	B02 further synergized with clinically relevant topotecan (TPT) to engage this pathway, activating p53-BAX mediated killing of RB but not human retinal progenitor cells.	Topotecan	48-57	P53	Homo sapiens	99-102
32483405-0	2020	Bioinformatics and experimental studies of anti-leukemic activity from 6-gingerol demonstrate its role in p53 mediated apoptosis pathway.	gingerol	71-81	P53	Homo sapiens	106-109
32373892-0	2020	Linc-ROR promotes arsenite-transformed keratinocyte proliferation by inhibiting P53 activity.	arsenite	18-26	P53	Homo sapiens	80-83
32424350-0	2020	Cas9 activates the p53 pathway and selects for p53-inactivating mutations.	cas9	0-4	P53	Homo sapiens	19-22
32424350-0	2020	Cas9 activates the p53 pathway and selects for p53-inactivating mutations.	cas9	0-4	P53	Homo sapiens	47-50
32373892-6	2020	We further demonstrated that linc-ROR down-regulation by siRNA significantly inhibited the cellular proliferation and restored P53 activity in arsenite-transformed HaCaT cells, suggesting that linc-ROR promotes proliferation of arsenite-transformed HaCaT cells by inhibiting P53 activity.	arsenite	143-151	P53	Homo sapiens	127-130
32373892-6	2020	We further demonstrated that linc-ROR down-regulation by siRNA significantly inhibited the cellular proliferation and restored P53 activity in arsenite-transformed HaCaT cells, suggesting that linc-ROR promotes proliferation of arsenite-transformed HaCaT cells by inhibiting P53 activity.	arsenite	228-236	P53	Homo sapiens	127-130
32483405-9	2020	Moreover, it was found that 6-gingerol could increase the levels of p53 mRNA in all leukemic cell lines.	gingerol	28-38	P53	Homo sapiens	68-71
32373892-6	2020	We further demonstrated that linc-ROR down-regulation by siRNA significantly inhibited the cellular proliferation and restored P53 activity in arsenite-transformed HaCaT cells, suggesting that linc-ROR promotes proliferation of arsenite-transformed HaCaT cells by inhibiting P53 activity.	arsenite	228-236	P53	Homo sapiens	275-278
32373892-7	2020	Moreover, linc-ROR siRNA also down-regulated the PI3K/AKT pathway in arsenite-transformed HaCaT cells, and treatment with AKT inhibitor wortmannin restored P53 activity, implying that linc-ROR inhibits P53 activity by activating the PI3K/AKT pathway.	arsenite	69-77	P53	Homo sapiens	202-205
32380113-0	2020	Modification-free amperometric biosensor for the detection of wild-type p53 protein based on the in situ formation of silver nanoparticle networks for signal amplification.	Silver	118-124	P53	Homo sapiens	72-75
32373892-8	2020	Taken together, the present study shows that linc-ROR promotes arsenite-transformed keratinocyte proliferation by inhibiting P53 activity through activating PI3K/AKT, providing a novel carcinogenic mechanism of arsenite-induced skin cancer.	arsenite	63-71	P53	Homo sapiens	125-128
32595984-10	2020	Unlike with chronic viral infections, MDM2-p53 axis might play a dual role in glucolipid metabolism of hepatocytes, which presented with enhancing glucolipid catabolism, but promoting hepatocyte injury at the early and late stages of glucolipid metabolism disorder.	glucolipid	78-88	P53	Homo sapiens	43-46
32428701-0	2020	miRNA-98-5p Targeting IGF2BP1 Induces Mesenchymal Stem Cell Apoptosis by Modulating PI3K/Akt and p53 in Immune Thrombocytopenia.	mirna-98-5p	0-11	P53	Homo sapiens	97-100
31254176-4	2020	The cytotoxicity of a panel of vitamin K3 analogs was screened against 10 doxorubicin-sensitive and -resistant cancer cell lines overexpressing ATP-binding cassette transporters (P-glycoprotein, ABCB5, BCRP) or oncogenes (DeltaEGFR) or with knockout of tumor suppressors (p53), Cell cycle arrest, apoptosis, cell migration, and microtubule formation were further investigated.	Vitamin K 3	31-41	P53	Homo sapiens	272-275
32380113-2	2020	Herein, a modification-free amperometric biosensor was proposed for sensitive detection of wild-type p53 protein by the signal amplification of silver nanoparticles (AgNPs) networks preformed in situ on electrode surface.	Silver	144-150	P53	Homo sapiens	101-104
32366419-8	2020	p53 and Bax proteins were overexpressed, while p21 and bcl2 gene expression was decreased after treatment with the ciprofloxacin derivative.	Ciprofloxacin	115-128	P53	Homo sapiens	0-3
32367104-5	2020	A key feature of this 1,3-dipolar cycloaddition is the wide substrate applicability, even with alkyl aldehyde-derived azomethine ylide; thus it has streamlined a highly enantioselective access to a new class of antiproliferative agents, MDM2-p53.	alkyl aldehyde	95-109	P53	Homo sapiens	242-245
32534357-10	2020	The apoptosis induced by EPI in MKN-45 cells would be effectively inhibited with the treatment of p53 siRNA and p53 inhibitor PFT-alpha.	epiberberine	25-28	P53	Homo sapiens	112-115
32512936-13	2020	CUR-PEI-K14/p53 can be used as an effective strategy to enhance the sensitivity of drug-resistant ovarian cancer cells to DDP.	cur-pei	0-7	P53	Homo sapiens	12-15
31112603-4	2020	We demonstrate that the selective cytotoxicity of the combination, called CucWi-N, to cancer cells is mediated by induction of cellular senescence that was characterized by decrease in Lamin A/C, CDK2, CDK4, Cyclin D, Cyclin E, phosphorylated RB, mortalin and increase in p53 and CARF proteins.	cucwi-n	74-81	P53	Homo sapiens	272-275
31959058-0	2020	MiR-219a-2-3p suppresses cell proliferation and promotes apoptosis by targeting MDM2/p53 in pituitary adenomas cells.	mir-219a-2-3p	0-13	P53	Homo sapiens	85-88
32534357-10	2020	The apoptosis induced by EPI in MKN-45 cells would be effectively inhibited with the treatment of p53 siRNA and p53 inhibitor PFT-alpha.	epiberberine	25-28	P53	Homo sapiens	98-101
32393310-11	2020	The expression of P53 and phosphokinases including CHK1, CHK2, PLK1, and Aurora A increased after CoCl2 treatment.	cobaltous chloride	98-103	P53	Homo sapiens	18-21
32403433-5	2020	Amuc_1434* also blocked the G0/G1 phase of the cell cycle of LS174T cells and upregulated the expression of tumor protein 53 (p53), which is a cell cycle-related protein.	amuc_1434	0-9	P53	Homo sapiens	108-124
32403433-5	2020	Amuc_1434* also blocked the G0/G1 phase of the cell cycle of LS174T cells and upregulated the expression of tumor protein 53 (p53), which is a cell cycle-related protein.	amuc_1434	0-9	P53	Homo sapiens	126-129
32253666-3	2020	The aim of therapy for CLL patients has been to control the disease; however, FCR (fludarabine, cyclophosphamide, rituximab) has improved outcomes and reduced the high incidence of undetectable minimum/measurable residual disease (MRD) in previously untreated CLL patients with no 17p deletion/TP53 disruption and mutated immunoglobulin heavy chain gene (IGHV).	fludarabine	83-94	P53	Homo sapiens	294-298
32260165-10	2020	CPS correlated with strong nuclear or null p53 staining in AC, NOS but not in other SGCs.	cps	0-3	P53	Homo sapiens	43-46
32369692-8	2020	RESULTS: The enhanced pro-apoptotic and anti-proliferative properties of Tacrolimus versus mTOR inhibitors were associated with increased protein kinase RNA-like endoplasmic reticulum kinase (PERK)-related ER stress, Ser15P-p53/p53 ratio and p21 protein expression that may counterbalance the risk of proliferative upregulation caused by enhanced Thr172P-Cdk4/Cdk4 activation in liver cancer cells.	Tacrolimus	73-83	P53	Homo sapiens	224-227
32369692-8	2020	RESULTS: The enhanced pro-apoptotic and anti-proliferative properties of Tacrolimus versus mTOR inhibitors were associated with increased protein kinase RNA-like endoplasmic reticulum kinase (PERK)-related ER stress, Ser15P-p53/p53 ratio and p21 protein expression that may counterbalance the risk of proliferative upregulation caused by enhanced Thr172P-Cdk4/Cdk4 activation in liver cancer cells.	Tacrolimus	73-83	P53	Homo sapiens	228-231
32369692-13	2020	CONCLUSION: The more potent pro-apoptotic and anti-proliferative properties of Tacrolimus versus mTOR inhibitors were associated with an increased activation of PERK and p53 signaling, and p21 protein expression.	Tacrolimus	79-89	P53	Homo sapiens	170-173
32483402-9	2020	While perifosine+vitamin D combinations increased P53 mRNA expression in HEC-1A cells we did not find any significant change in BCL2, BAX mRNA expression levels.	perifosine	6-16	P53	Homo sapiens	50-53
32290083-7	2020	Taken together, our findings identify p53-independent and uL3-dependent nucleolar stress as a novel stress response pathway activated by a specific G-quadruplex TBA derivative.	thrombin aptamer	161-164	P53	Homo sapiens	38-41
31931413-0	2020	N6-methyladenosine mediates arsenite-induced human keratinocyte transformation by suppressing p53 activation.	arsenite	28-36	P53	Homo sapiens	94-97
32265434-6	2020	Taken together, we conclude that IKKalpha attenuates arsenite-induced apoptosis by inducing p53-dependent autophagy, and then selective feedback degradation of IKKalpha by autophagy contributes to the cytotoxic response induced by arsenite.	arsenite	53-61	P53	Homo sapiens	92-95
32385658-0	2020	Zn(II)-Based Coordination Polymer for Detection of Picric Acid in Aqueous Media and Treatment Effect against Deep Vein Thrombosis by Reducing P-ERK2 and p53 Expression.	picric acid	51-62	P53	Homo sapiens	153-156
31931413-10	2020	Taken together, our study revealed the novel role of m6A in mediating arsenite-induced human keratinocyte transformation by suppressing p53 activation.	arsenite	70-78	P53	Homo sapiens	136-139
32200264-10	2020	We also found that pinitol could inhibit TNF-alpha-induced increased telomerase activity and expression of p16 and p53.	pinitol	19-26	P53	Homo sapiens	115-118
32045602-0	2020	Vitexin protects against ethanol-induced liver injury through Sirt1/p53 signaling pathway.	vitexin	0-7	P53	Homo sapiens	68-71
32045602-11	2020	Vitexin supplement restored the decrease of Sirt1/Bcl-2 expression, restrained the elevation of caspase3, cleaved caspse-3, p53 and ac-p53 expression in vivo and in vitro.	vitexin	0-7	P53	Homo sapiens	124-127
32045602-11	2020	Vitexin supplement restored the decrease of Sirt1/Bcl-2 expression, restrained the elevation of caspase3, cleaved caspse-3, p53 and ac-p53 expression in vivo and in vitro.	vitexin	0-7	P53	Homo sapiens	135-138
32045602-12	2020	Vitexin has a protective effect against ethanol-induced liver damage, and the underlying mechanism is probably through Sirt1/p53 mediated mitochondrial apoptotic pathway.	vitexin	0-7	P53	Homo sapiens	125-128
31822380-8	2020	However, TP53 GOF mutations had a positive association with prior abiraterone/enzalutamide therapy (P = .047).	abiraterone	66-77	P53	Homo sapiens	9-13
32027103-0	2020	The PI3K/mTOR dual inhibitor NVP-BEZ235 stimulates mutant p53 degradation to exhibit anti-tumor effect on triple-negative breast cancer cells.	dactolisib	29-39	P53	Homo sapiens	58-61
32193421-2	2020	We previously found that IGFBP-3 exerts its cytotoxic effects on A549 (p53 wild-type) cell survival through a mechanism that depends on hyaluronan-CD44 interactions.	Hyaluronic Acid	136-146	P53	Homo sapiens	71-74
32241181-9	2021	In conclusion, the C. densiflorus essential oil presents antitumor effects on TP53 wild-type and mutated bladder cancer cells, however, the mechanism of action is TP53 status-dependent.	densiflorus essential oil	22-47	P53	Homo sapiens	78-82
32241181-9	2021	In conclusion, the C. densiflorus essential oil presents antitumor effects on TP53 wild-type and mutated bladder cancer cells, however, the mechanism of action is TP53 status-dependent.	densiflorus essential oil	22-47	P53	Homo sapiens	163-167
31289209-6	2020	Interestingly, we observed that higher levels of HIF-1A mRNA correlate with a lower susceptibility of leukemic cells to spontaneous apoptosis, and associate with the fludarabine resistance that mainly characterizes TP53dis tumour cells.	fludarabine	166-177	P53	Homo sapiens	215-219
32193421-8	2020	Taken together, our results show that IGFBP-3 or its peptide blocks hyaluronan-CD44 signaling via a mechanism that depends on both p53 and acetylcholinesterase.	Hyaluronic Acid	68-78	P53	Homo sapiens	131-134
31289209-8	2020	BAY87-2243 also overcomes the constitutive fludarabine resistance of TP53dis leukemic cells and elicits a strongly synergistic cytotoxic effect in combination with ibrutinib, thus providing preclinical evidences for its further investigation as a potential new drug in chronic lymphocytic leukemia.	fludarabine	43-54	P53	Homo sapiens	69-73
32072836-0	2021	Ingenol mebutate treatment for actinic cheilitis: clinical, histopathological and p53 profile of 14 cases.	3-ingenyl angelate	0-16	P53	Homo sapiens	82-85
32097779-4	2020	We found that triterpenoid alkaloids extracted from Buxus sinica found in the Yunnan Province exhibit anticancer activity by depleting mutant p53 levels in colon cancer cells.	triterpenoid alkaloids	14-36	P53	Homo sapiens	142-145
33224241-8	2020	The essential oil inhibited the growth of HeLa cells and increased the expression of p21 and p53.	Oils, Volatile	4-17	P53	Homo sapiens	93-96
31834974-1	2020	The tumor suppressor gene p53 encodes a transcriptional activator that has two transactivation domains (TADs) located in its amino terminus.	Amino Acids	125-130	P53	Homo sapiens	26-29
32235536-0	2020	Galangin, a Flavonoid from Lesser Galangal, Induced Apoptosis via p53-Dependent Pathway in Ovarian Cancer Cells.	galangin	0-8	P53	Homo sapiens	66-69
32235536-8	2020	By down-regulating the level of p53 with 20 muM pifithrin-alpha (PFT-alpha), the apoptotic rates of OVCAR-3 cells induced by galangin treatment (40 muM) were significantly decreased from 18.2% to 10.2%, indicating that p53 is a key regulatory protein in galangin-induced apoptosis in ovarian cancer cells.	galangin	125-133	P53	Homo sapiens	32-35
32235536-8	2020	By down-regulating the level of p53 with 20 muM pifithrin-alpha (PFT-alpha), the apoptotic rates of OVCAR-3 cells induced by galangin treatment (40 muM) were significantly decreased from 18.2% to 10.2%, indicating that p53 is a key regulatory protein in galangin-induced apoptosis in ovarian cancer cells.	galangin	125-133	P53	Homo sapiens	219-222
32235536-8	2020	By down-regulating the level of p53 with 20 muM pifithrin-alpha (PFT-alpha), the apoptotic rates of OVCAR-3 cells induced by galangin treatment (40 muM) were significantly decreased from 18.2% to 10.2%, indicating that p53 is a key regulatory protein in galangin-induced apoptosis in ovarian cancer cells.	galangin	254-262	P53	Homo sapiens	32-35
32001619-9	2020	Consistent with this, the IKK inhibitor BAY11-7085 and dominant-negative mutant IkappaBalphaM inhibited NFkappaB activity and increased P-P53, P53, and P21/WAF1/CIP1 levels in a ROS-dependent manner.	BAY 11-7085	40-50	P53	Homo sapiens	138-141
32034120-2	2020	Here we demonstrate that inhibition of dihydroorotate dehydrogenase (DHODH), a key enzyme of the de novo pyrimidine synthesis pathway, effectively decreases proliferation of cancer cells via induction of replication and ribosomal stress in a p53- and checkpoint kinase 1 (Chk1)-dependent manner.	pyrimidine	105-115	P53	Homo sapiens	242-245
31776133-8	2020	Staining of p53 and PARP1 in breast cancer TMAs and comparison with the TCGA database indicated a higher double-positive signal in basal-like breast cancer than in luminal A or luminal B subtypes.	Phenobarbital	164-171	P53	Homo sapiens	12-15
32231713-0	2020	Riluzole Enhances the Response of Human Nasopharyngeal Carcinoma Cells to Ionizing Radiation via ATM/P53 Signalling Pathway.	Riluzole	0-8	P53	Homo sapiens	101-104
32093976-8	2020	Enrichment analysis showed that these hub genes were primarily accumulated in "cell cycle", "p53 signaling pathway", "viral carcinogenesis", "pyrimidine metabolism" and "ubiquitin mediated proteolysis".	pyrimidine	142-152	P53	Homo sapiens	93-96
32231713-9	2020	P53 silencing reduced cell reactiveness to riluzole therapy.	Riluzole	43-51	P53	Homo sapiens	0-3
32231713-10	2020	These observations demonstrate that the riluzole-activated ATM/P53 pathway is directly involved in radiation-induced apoptosis of NPC cells.	Riluzole	40-48	P53	Homo sapiens	63-66
32013615-6	2022	In addition, APAP overdose induced the tissue expression of the apoptotic biomarker, p53, and caused profound kidney damage as demonstrated by substantial alterations to the glomerular basement membrane, podocytes, endothelial cells, widening of Bowman"s space, and vacuolation of the cells lining the parietal layer, which were substantially protected by RES + QUR.	Acetaminophen	13-17	P53	Homo sapiens	85-88
31566298-6	2020	Furthermore, aging markers such as senescence-associated beta-galactosidase p53, p21Cip1/WAF1 , and p16INK4A were upregulated under H2 O2 exposure and galangin could reverse its effects.	galangin	151-159	P53	Homo sapiens	76-79
31535397-6	2020	The results of this study propose a mechanistic pathway by which the inhibition of TLR4 using TAK-242 could augment apoptotic cell death through the alteration of both nuclear factor-kB- and p53-related apoptosis genes in breast cancer cells, especially cells with overexpression of TLR4.	ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate	94-101	P53	Homo sapiens	191-194
32067620-9	2020	Also, P-3F and D-3F displayed most potent cytotoxicities against PLC/PRF/5 with p53-R249S and weakest inhibition of L02 (normal liver cell) growth.	Phlorhizin	6-10	P53	Homo sapiens	80-83
31841081-8	2020	When the p53 pathway of irradiated cells was inhibited by PFT-alpha, PFTmicro or p53 siRNA, the bystander damage to TK6 cells were clearly alleviated.	pftmicro	69-77	P53	Homo sapiens	9-12
31285544-0	2020	The antimalarial drug amodiaquine stabilizes p53 through ribosome biogenesis stress, independently of its autophagy-inhibitory activity.	Amodiaquine	22-33	P53	Homo sapiens	45-48
31536751-3	2020	Recently, we have reported the (S)-tryptophanol-derived oxazoloisoindolinone SLMP53-1 as a new reactivator of wt and mutp53 R280K with in vitro and in vivo p53-dependent antitumor activity.	tryptophanol	31-47	P53	Homo sapiens	120-123
31285544-3	2020	Amodiaquine triggers degradation of the catalytic subunit of RNA polymerase I (Pol I), with ensuing RPL5/RPL11-dependent stabilization of p53.	Amodiaquine	0-11	P53	Homo sapiens	138-141
31963392-2	2020	Herein, we unveiled that p53 activation by (S)-tryptophanol-derived oxazoloisoindolinone (SLMP53-1) mediated the reprograming of glucose metabolism in cancer cells and xenograft human tumor tissue, interfering with angiogenesis and migration.	tryptophanol	43-59	P53	Homo sapiens	25-28
31952105-8	2020	Furthermore, casticin increased p-ATM at 6 h and increased p-ATR and BRCA1 at 6-24 h treatment but decreased p-ATM at 24-48 h, as well as decreased p-ATR and BRCA1 at 48 h. Furthermore, casticin decreased p-p53 at 6-24 h but increased at 48 h. Casticin increased p-H2A.X and MDC1 at 6-48 h treatment.	casticin	13-21	P53	Homo sapiens	207-210
31747859-0	2020	Co-targeting p53-R249S and CDK4 synergistically suppresses survival of hepatocellular carcinoma cells.	12-(4'-azido-2'-nitrophenoxy)dodecanoyl-coenzyme A	0-2	P53	Homo sapiens	13-16
31935871-7	2020	NPs of manganese (Mn and Mn3O4) induced the most remarkable ToxTracker response with activation of reporters for oxidative stress, DNA damage, protein unfolding and p53-related stress.	manganese oxide	25-30	P53	Homo sapiens	165-168
32974616-8	2020	Signalling pathway analysis revealed the top five pathways to be metabolic, pyrimidine metabolism, protein processing in endoplasmic reticulum, phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signalling and p53 signalling.	pyrimidine	76-86	P53	Homo sapiens	217-220
33345608-6	2020	These genes were enriched in cell cycle, MAPK signaling, JAK-STAT signaling, pyrimidine metabolism, arachidonic acid metabolism, and P53 signaling pathway activity, all of which are directly linked with the development of cancer.	pyrimidine	77-87	P53	Homo sapiens	133-136
31804169-5	2020	It has been observed that nickel exposure induces the generation of reactive oxygen species which leads to the increased expression of p53, NF-kbeta, AP-1, and MAPK.	Nickel	26-32	P53	Homo sapiens	135-138
31892709-7	2019	Significantly higher levels of cellular apoptosis, inhibited cell growth, and regulated lipid raft content were observed in mutant p53 lung cancer cells treated with simvastatin.	Simvastatin	166-177	P53	Homo sapiens	131-134
31581548-0	2019	Clonal Evolution of TP53 c.375+1G>A Mutation in Pre- and Post- Neo-Adjuvant Chemotherapy (NACT) Tumor Samples in High-Grade Serous Ovarian Cancer (HGSOC).	nact	90-94	P53	Homo sapiens	20-24
31680191-6	2020	Specifically, lysine 370/372/373 and 381/382/386 mutations decreased p53 stability, and lysine 305 mutation reduced p53 phosphorylation level at serine 15, while lysine 120 and 164 mutations decreased p53 acetylation level at lysine 382.	tyrosyl-lysine	14-20	P53	Homo sapiens	69-72
31203647-4	2019	RESULTS: Alantolactone induced apoptosis of gastric cancer cells by regulating the expression of Bax, Bcl-2, and p53, which related to intrinsic apoptotic pathway, and suppressed colony formation, migration, and invasion by mediating the expression of matrix metalloproteinase (MMP)-2, MMP-7, and MMP-9.	alantolactone	9-22	P53	Homo sapiens	113-116
31892709-8	2019	Further, simvastatin increased the caspase-dependent apoptotic pathway, promotes mutant p53 protein degradation, and decreased motile activity in lung cancer cells with p53 missense mutations.	Simvastatin	9-20	P53	Homo sapiens	88-91
31892709-8	2019	Further, simvastatin increased the caspase-dependent apoptotic pathway, promotes mutant p53 protein degradation, and decreased motile activity in lung cancer cells with p53 missense mutations.	Simvastatin	9-20	P53	Homo sapiens	169-172
31984217-5	2019	Then, we reactivated the SOCS1-p53 tumor suppressor axis with the SFK inhibitor dasatinib in combination with the p53 activating compound PRIMA.	dasatinib	80-89	P53	Homo sapiens	31-34
31680191-6	2020	Specifically, lysine 370/372/373 and 381/382/386 mutations decreased p53 stability, and lysine 305 mutation reduced p53 phosphorylation level at serine 15, while lysine 120 and 164 mutations decreased p53 acetylation level at lysine 382.	tyrosyl-lysine	88-94	P53	Homo sapiens	116-119
31098781-0	2019	ASO Author Reflections: Precise p53 Analysis in Formalin-Fixed Paraffin-Embedded Specimens Can Predict Head and Neck Squamous Cell Carcinoma Outcomes.	Formaldehyde	48-56	P53	Homo sapiens	32-35
31326626-5	2019	The goal of our study was to establish if cells differing in EGFR, KRAS, p53 mutation status and VDR polymorphism were sensitive to antiproliferative activity of selected vitamin D derivatives (VDDs).	vdds	194-198	P53	Homo sapiens	73-76
31326626-13	2019	Lack of KRAS and p53 mutations in HCC827 cells may be, therefore, responsible for the higher antiproliferative activity of VDDs, while the presence of KRAS and/or p53 mutations in other cell lines might prevent antiproliferative activity even though the VDDs were transcriptionally active as assessed on increased CYP24A1 expression.	vdds	123-127	P53	Homo sapiens	17-20
31680191-6	2020	Specifically, lysine 370/372/373 and 381/382/386 mutations decreased p53 stability, and lysine 305 mutation reduced p53 phosphorylation level at serine 15, while lysine 120 and 164 mutations decreased p53 acetylation level at lysine 382.	tyrosyl-lysine	88-94	P53	Homo sapiens	116-119
31680191-6	2020	Specifically, lysine 370/372/373 and 381/382/386 mutations decreased p53 stability, and lysine 305 mutation reduced p53 phosphorylation level at serine 15, while lysine 120 and 164 mutations decreased p53 acetylation level at lysine 382.	tyrosyl-lysine	88-94	P53	Homo sapiens	116-119
31680191-6	2020	Specifically, lysine 370/372/373 and 381/382/386 mutations decreased p53 stability, and lysine 305 mutation reduced p53 phosphorylation level at serine 15, while lysine 120 and 164 mutations decreased p53 acetylation level at lysine 382.	tyrosyl-lysine	88-94	P53	Homo sapiens	116-119
31680191-6	2020	Specifically, lysine 370/372/373 and 381/382/386 mutations decreased p53 stability, and lysine 305 mutation reduced p53 phosphorylation level at serine 15, while lysine 120 and 164 mutations decreased p53 acetylation level at lysine 382.	tyrosyl-lysine	88-94	P53	Homo sapiens	116-119
31680191-6	2020	Specifically, lysine 370/372/373 and 381/382/386 mutations decreased p53 stability, and lysine 305 mutation reduced p53 phosphorylation level at serine 15, while lysine 120 and 164 mutations decreased p53 acetylation level at lysine 382.	tyrosyl-lysine	88-94	P53	Homo sapiens	116-119
31478534-0	2019	Organocatalytic diastereoselective [3+2] cyclization of MBH carbonates with dinucleophiles: synthesis of bicyclic imidazoline derivatives that inhibit MDM2-p53 interaction.	mbh carbonates	56-70	P53	Homo sapiens	156-159
31863007-0	2019	PBRM1 acts as a p53 lysine-acetylation reader to suppress renal tumor growth.	tyrosyl-lysine	20-26	P53	Homo sapiens	16-19
31255635-6	2019	As the important markers of apoptosis, p53 and Bax were both upregulated by the treatment of TET and CEP.	tetrandrine	93-96	P53	Homo sapiens	39-42
31222582-4	2019	Here, based on the hybrid model I, we computationally searched all the parameters and parameter combinations in the parameter space to identify those that could alter the natural preferential response of p53 when SSBs and DSBs coexist.	dsbs	222-226	P53	Homo sapiens	204-207
31795610-7	2019	RESULTS: Our data showed that CoCl2 induced cytotoxicity and changes of hypoxia-inducible factor-1alpha (HIF-1alpha) and p53 expression in SH-SY5Y cells.	cobaltous chloride	30-35	P53	Homo sapiens	121-124
31607444-5	2019	In contrast, P53 induction by Nutlin and Hsp90 inhibitor AUY922 enhanced the BBB function.	5-(2,4-dihydroxy-5-isopropylphenyl)-4-(4-morpholin-4-ylmethylphenyl)isoxazole-3-carboxylic acid ethylamide	57-63	P53	Homo sapiens	13-16
31863007-4	2019	Here, we identify PBRM1 as a reader for p53 acetylation on lysine 382 (K382Ac) through its bromodomain 4 (BD4).	tyrosyl-lysine	59-65	P53	Homo sapiens	40-43
31795610-8	2019	However, pretreatment with NRG1 inhibited CoCl2-induced accumulation of HIF-1alpha and p53 stability.	cobaltous chloride	42-47	P53	Homo sapiens	87-90
31682411-7	2019	Using thioacylated lysine residues in p53-derived peptides we optimized substrates for HDAC8 with catalytic efficiency over 250,000 M-1s-1, which are more than 100-fold more effective than most of the known substrates.	tyrosyl-lysine	6-25	P53	Homo sapiens	38-41
31983107-4	2019	RESULTS: P53 expression was the lowest in Luminal A subtype and similar in human epidermal growth factor receptor 2 (HER-2)-overexpression subtype and triple-negative subtype, with higher expression rates than those in other molecular subtypes.	Phenobarbital	42-49	P53	Homo sapiens	9-12
31226417-0	2019	Entinostat combined with Fludarabine synergistically enhances the induction of apoptosis in TP53 mutated CLL cells via the HDAC1/HO-1 pathway.	fludarabine	25-36	P53	Homo sapiens	92-96
31226417-2	2019	Worse still, CLL patients with TP53 mutation are associated with poor efficacy to current chemotherapeutic, such as Fludarabine.	fludarabine	116-127	P53	Homo sapiens	31-35
31226417-4	2019	Subsequently, we demonstrated Entinostat (HDAC1 inhibitor) combination with Fludarabine significantly induced apoptosis in TP53 mutations CLL cells.	fludarabine	76-87	P53	Homo sapiens	123-127
31226417-8	2019	Finally, combining vitro and vivo experiments, we presented the first demonstration that Entinostat combination with Fludarabine had a synergistic effect on the induction of apoptosis in TP53 mutations CLL cells.	fludarabine	117-128	P53	Homo sapiens	187-191
31434476-10	2019	Codelivery of functional gene (pCEP4-p53) and drug (doxorubicin) was accomplished in vitro and in vivo with the chitosan-pyridine imine vector, (py)CS(CH2COOH), and the newly synthesized doxorubicin oxime ether, CS(Dox).	Chitosan	112-120	P53	Homo sapiens	37-40
31970141-0	2019	The molecular targets of diclofenac differs from ibuprofen to induce apoptosis and epithelial mesenchymal transition due to alternation on oxidative stress management p53 independently in PC3 prostate cancer cells.	Diclofenac	25-35	P53	Homo sapiens	167-170
31434476-10	2019	Codelivery of functional gene (pCEP4-p53) and drug (doxorubicin) was accomplished in vitro and in vivo with the chitosan-pyridine imine vector, (py)CS(CH2COOH), and the newly synthesized doxorubicin oxime ether, CS(Dox).	pyridine	144-148	P53	Homo sapiens	37-40
31418442-5	2019	To demonstrate their extensive utility, we applied our novel dialkynes to a double strain-promoted macrocyclisation strategy to generate functionalised p53-based stapled peptides for inhibiting the oncogenic p53-MDM2 interaction.	dialkynes	61-70	P53	Homo sapiens	152-155
31418442-5	2019	To demonstrate their extensive utility, we applied our novel dialkynes to a double strain-promoted macrocyclisation strategy to generate functionalised p53-based stapled peptides for inhibiting the oncogenic p53-MDM2 interaction.	dialkynes	61-70	P53	Homo sapiens	208-211
31970141-3	2019	We evaluated the effects of ectopic expression of p53 on the biological functions of ibuprofen and diclofenac.	Diclofenac	99-109	P53	Homo sapiens	50-53
31388677-4	2019	We examined Cr(VI) effects on the p53 pathway in human cells with restored levels of ascorbate that acts as a principal reducer of Cr(VI) in vivo but is nearly absent in standard cell cultures.	Ascorbic Acid	85-94	P53	Homo sapiens	34-37
31388677-5	2019	Ascorbate-restored H460 and primary human cells treated with Cr(VI) contained higher levels of p53 and its Ser15 phosphorylation, which were induced by ATR kinase.	Ascorbic Acid	0-9	P53	Homo sapiens	95-98
31388677-9	2019	A weak transcription activity of Cr(VI)-upregulated p53 was associated with its low lysine acetylation in the regulatory C-terminal domain, resulting from the inability of Cr(VI) to activate ATM in ascorbate-restored cells.	Ascorbic Acid	198-207	P53	Homo sapiens	52-55
31388677-10	2019	Thus, p53 activation by ascorbate-metabolized Cr(VI) represents a limited genome-protective response that is defective in upregulation of DNA repair genes and proapoptotic transcripts for elimination of damaged cells.	Ascorbic Acid	24-33	P53	Homo sapiens	6-9
32184862-10	2019	P53 expression levels in captopril and BTX-A treated DU145 cells were elevated by 4 and 2.5 folds, respectively, while lower level of apoptosis induction in HCT116 cells was observed.	Captopril	25-34	P53	Homo sapiens	0-3
31558316-8	2019	In addition, NAC can block the up-regulation of p53/PUMA induced by combined treatment with ipatasertib and TRAIL.	ipatasertib	92-103	P53	Homo sapiens	48-51
31162820-7	2019	Compared with the control cells, brefeldin A significantly inhibited the expression of PSMD4 and increased the expression of p53-upregulated modulator of apoptosis.	Brefeldin A	33-44	P53	Homo sapiens	125-128
31158748-6	2019	The results suggest that styrylquinolines induce cell cycle arrest and activate a p53-independent apoptosis.	styrylquinoline	25-41	P53	Homo sapiens	82-85
31088908-0	2019	HIF Inactivation of p53 in Ovarian Cancer Can Be Reversed by Topotecan, Restoring Cisplatin and Paclitaxel Sensitivity.	Topotecan	61-70	P53	Homo sapiens	20-23
31558316-10	2019	In conclusion, p53 and PUMA may play a pivotal role in sensitizing colon cancer cell to TRAIL-induced apoptosis by sub-toxic doses of ipatasertib treatment.	ipatasertib	134-145	P53	Homo sapiens	15-18
31088908-12	2019	TPT-mediated downregulation of HIF1alpha in hypoxic cells required TOPO1 resident on HIF1alpha mRNA, restored p53 transcriptional activity, downregulated ABCB1/ABCB5 cell surface expression, and reversed hypoxia-related cisplatin and paclitaxel resistance.	Topotecan	0-3	P53	Homo sapiens	110-113
31088908-13	2019	IMPLICATIONS: TPT-mediated reduction of HIF1alpha accumulation in hypoxic ovarian cancer cell lines restores p53 tumor-suppressor function, offering a novel approach to reverse chemoresistance.	Topotecan	14-17	P53	Homo sapiens	109-112
31253693-3	2019	Our previous efforts to identify novel radiosensitizers, using high-throughput screening targeting p53 and Nrf2 revealed a promising N-phenylpyrimidin-2-amine (PPA) lead compound.	ppa	160-163	P53	Homo sapiens	99-102
31446323-0	2019	Loading of some quinoxaline derivatives in poly (l-lactic) acid/Pluronic  F-127 nanofibers enhances their anticancer efficiency and induces a p53 and p21 apoptotic-signaling pathway.	Quinoxalines	16-27	P53	Homo sapiens	142-145
31452815-0	2019	Phenylhexyl isothiocyanate suppresses cell proliferation and promotes apoptosis via repairing mutant P53 in human myeloid leukemia M2 cells.	6-phenylhexyl isothiocyanate	0-26	P53	Homo sapiens	101-104
31555522-13	2019	Under hypoxic conditions, apatinib could not inhibit the protein expression of VEGFR and HIF-alpha in both cell lines; however, apatinib decreased the expression of cyclin D1 and P53 significantly.	apatinib	128-136	P53	Homo sapiens	179-182
30628118-0	2019	In silico analysis of the binding properties of solasonine to mortalin and p53, and in vitro pharmacological studies of its apoptotic and cytotoxic effects on human HepG2 and Hep3b hepatocellular carcinoma cells.	alpha-solamargine	48-58	P53	Homo sapiens	75-78
31450059-2	2019	Chitosan-grafted poly-(N-3-carbobenzyloxy-lysine) (CCL) decorated with human immunodeficiency virus-1 transactivator of transcription (TAT) can co-deliver p53 and doxorubicin into the nucleus simultaneously, such that their antitumor functions are exerted.	Chitosan	0-8	P53	Homo sapiens	155-158
30628118-6	2019	In silico screening of a database of 354 natural compounds identified solasonine, a steroidal glycoalkaloid from Solanaceae, as a potent inhibitor of p53-mortalin interactions.	alpha-solamargine	70-80	P53	Homo sapiens	150-153
30628118-7	2019	Pharmacological studies confirmed that solasonine was able to inhibit efficiently mortalin-p53 interaction in HCC HepG2 cell line that expresses both mortalin and p53.	alpha-solamargine	39-49	P53	Homo sapiens	91-94
30628118-7	2019	Pharmacological studies confirmed that solasonine was able to inhibit efficiently mortalin-p53 interaction in HCC HepG2 cell line that expresses both mortalin and p53.	alpha-solamargine	39-49	P53	Homo sapiens	163-166
30628118-9	2019	Solasonine-induced apoptosis and cell death of HCC cell lines either expressing p53 (HepG2) or not (Hep3b), indicating that apoptotic activities of solasonine can be mediated not only through p53-dependent but also p53-independent pathways.	alpha-solamargine	0-10	P53	Homo sapiens	80-83
30628118-9	2019	Solasonine-induced apoptosis and cell death of HCC cell lines either expressing p53 (HepG2) or not (Hep3b), indicating that apoptotic activities of solasonine can be mediated not only through p53-dependent but also p53-independent pathways.	alpha-solamargine	0-10	P53	Homo sapiens	192-195
30628118-9	2019	Solasonine-induced apoptosis and cell death of HCC cell lines either expressing p53 (HepG2) or not (Hep3b), indicating that apoptotic activities of solasonine can be mediated not only through p53-dependent but also p53-independent pathways.	alpha-solamargine	0-10	P53	Homo sapiens	192-195
30981936-0	2019	Aryl-phosphorus-containing flame retardants induce oxidative stress, the p53-dependent DNA damage response and mitochondrial impairment in A549 cells.	aryl-phosphorus	0-15	P53	Homo sapiens	73-76
31253862-6	2019	NMR spectroscopy and molecular dynamics simulation revealed that DP6 selectively binds to the vicinity of the target sequence in the C-terminal domain of p53.	5-diphosphomevalonic acid	65-68	P53	Homo sapiens	154-157
31253862-7	2019	DP6 inhibits the nonspecific DNA binding of a tetrameric form of the p53 C-terminal domain, but does not significantly affect the specific DNA binding of a tetrameric form of the p53 core domain.	5-diphosphomevalonic acid	0-3	P53	Homo sapiens	69-72
30628118-9	2019	Solasonine-induced apoptosis and cell death of HCC cell lines either expressing p53 (HepG2) or not (Hep3b), indicating that apoptotic activities of solasonine can be mediated not only through p53-dependent but also p53-independent pathways.	alpha-solamargine	148-158	P53	Homo sapiens	80-83
30628118-9	2019	Solasonine-induced apoptosis and cell death of HCC cell lines either expressing p53 (HepG2) or not (Hep3b), indicating that apoptotic activities of solasonine can be mediated not only through p53-dependent but also p53-independent pathways.	alpha-solamargine	148-158	P53	Homo sapiens	192-195
31594538-4	2019	RESULTS: Here, we present data suggesting that LSH regulates p53 in cis through two pathways: prevention proteasomal degradation through its deubiquitination, which is achieved by reducing the lysine 11-linked, lysine 48-linked polyubiquitin chains (K11 and K48) on p53; and revival of the transcriptional activity of p53 by forming a complex with PKM2 (pyruvate kinase 2).	tyrosyl-lysine	193-199	P53	Homo sapiens	61-64
30628118-9	2019	Solasonine-induced apoptosis and cell death of HCC cell lines either expressing p53 (HepG2) or not (Hep3b), indicating that apoptotic activities of solasonine can be mediated not only through p53-dependent but also p53-independent pathways.	alpha-solamargine	148-158	P53	Homo sapiens	192-195
30628118-10	2019	The cytotoxic effects of solasonine correlated in part with its apoptotic properties and differed in the two HCC cell lines, being reversed by pifithrin-alpha, an inhibitor of p53 functions, in HepG2 cells but not in Hep3b cells.	alpha-solamargine	25-35	P53	Homo sapiens	176-179
31239671-0	2019	In vitro cytotoxicity and transfection efficiency of pDNA encoded p53 gene-loaded chitosan-sodium deoxycholate nanoparticles.	Chitosan	82-90	P53	Homo sapiens	66-69
31239671-1	2019	Purpose: The objective of this work was to formulate a delivery system of pDNA encoded p53 gene-loaded chitosan-sodium deoxycholate (CS-DS) nanoparticles, and to evaluate their influence on in vitro cytotoxicity and transfection efficiency of p53 gene.	Chitosan	103-111	P53	Homo sapiens	87-90
31594538-4	2019	RESULTS: Here, we present data suggesting that LSH regulates p53 in cis through two pathways: prevention proteasomal degradation through its deubiquitination, which is achieved by reducing the lysine 11-linked, lysine 48-linked polyubiquitin chains (K11 and K48) on p53; and revival of the transcriptional activity of p53 by forming a complex with PKM2 (pyruvate kinase 2).	tyrosyl-lysine	211-217	P53	Homo sapiens	61-64
31331066-0	2019	Effect of Vasicinone against Paraquat-Induced MAPK/p53-Mediated Apoptosis via the IGF-1R/PI3K/AKT Pathway in a Parkinson"s Disease-Associated SH-SY5Y Cell Model.	Paraquat	29-37	P53	Homo sapiens	51-54
32274404-0	2019	Achillea Wilhelmsii C. KochHydroalcoholic Extract Induces Apoptosis and Alters LIN28B and p53 Gene Expression in Hela Cervical Cancer Cells.	kochhydroalcoholic extract	23-49	P53	Homo sapiens	90-93
31239643-12	2019	Furthermore, notopterol induced the G0/G1 cell-cycle arrest as determined using flow cytometry, which may be related to the regulation of cell-cycle-related proteins p53, CDK2, CDK4, Cyclin D1, Cyclin E, and survivin.	notopterol	13-23	P53	Homo sapiens	166-169
30932278-2	2019	Here, we identified protopine, an isoquinoline alkaloid isolated from Nandina domestica, as an activator of the p53 pathway from cell-based natural compound screening based on p53-responsive transcription.	Tubocurarine	34-55	P53	Homo sapiens	112-115
30742880-10	2019	Interestingly, HMGB1 rather than p53 plays a primary role in 5 muM of PCB29-pQ-induced autophagy in the nucleus; however, p53 promoted apoptosis to a great extent in the cytosol at the dose of 15 muM PCB29-pQ.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	200-208	P53	Homo sapiens	122-125
31289894-0	2019	Functional mismatch repair and inactive p53 drive sensitization of colorectal cancer cells to irinotecan via the IAP antagonist BV6.	BV6	128-131	P53	Homo sapiens	40-43
30724592-11	2019	Further, RG7112 restores p53 and p21 protein levels in IMR5 and LAN-5 in a dose-dependent manner.	lan-5	64-69	P53	Homo sapiens	25-28
31244286-4	2019	Thisstudy aimed to investigate the effect of metfomin on expression of cyclin D1 and p53 and apoptosis in HeLa cancer cellline.	metfomin	45-53	P53	Homo sapiens	85-88
31159174-0	2019	p53 Binds Preferentially to Non-B DNA Structures Formed by the Pyrimidine-Rich Strands of GAA TTC Trinucleotide Repeats Associated with Friedreich"s Ataxia.	pyrimidine	63-73	P53	Homo sapiens	0-3
31159174-0	2019	p53 Binds Preferentially to Non-B DNA Structures Formed by the Pyrimidine-Rich Strands of GAA TTC Trinucleotide Repeats Associated with Friedreich"s Ataxia.	ttc trinucleotide	94-111	P53	Homo sapiens	0-3
31159174-6	2019	We demonstrate that p53 binds to all studied non-B DNA structures, with a preference for non-B DNA structures formed by pyrimidine (Py) rich strands.	pyrimidine	120-130	P53	Homo sapiens	20-23
30725256-10	2019	A potent, non-toxic benzodiazepine ("KRM-II-08") binds to the alpha5-GABAAR (0.8 microM EC50) enhancing a chloride-anion efflux that induces mitochondrial membrane depolarization and in response, TP53 upregulation and p53, constitutively phosphorylated at S392, cytoplasmic localization.	Chlorides	106-114	P53	Homo sapiens	196-200
30725256-10	2019	A potent, non-toxic benzodiazepine ("KRM-II-08") binds to the alpha5-GABAAR (0.8 microM EC50) enhancing a chloride-anion efflux that induces mitochondrial membrane depolarization and in response, TP53 upregulation and p53, constitutively phosphorylated at S392, cytoplasmic localization.	Chlorides	106-114	P53	Homo sapiens	218-221
31339741-0	2019	Recombinant Pierisin-5 Induces Apoptosis and Differential Expression of Bcl-2, Bax, and p53 in Human Cancer Cells.	pierisin-5	12-22	P53	Homo sapiens	88-91
30843662-0	2019	Concomitant TP53 mutations with response to crizotinib treatment in patients with ALK-rearranged non-small-cell lung cancer.	Crizotinib	44-54	P53	Homo sapiens	12-16
30833076-0	2019	Kruppel-like factor 2 mediated anti-proliferative and anti-metastasis effects of simvastatin in p53 mutant colon cancer.	Simvastatin	81-92	P53	Homo sapiens	96-99
30553920-7	2019	Our results indicate that the combined effect of pairwise PAHs of BaP with Benzo[b]fluoranthene (BbF) and Benz[a]anthracene (BaA) is synergistic on p53 pathway, and that the health risk of the such mixtures increases compared to that of the individual ones.	benzo(b)fluoranthene	75-95	P53	Homo sapiens	148-151
30553920-7	2019	Our results indicate that the combined effect of pairwise PAHs of BaP with Benzo[b]fluoranthene (BbF) and Benz[a]anthracene (BaA) is synergistic on p53 pathway, and that the health risk of the such mixtures increases compared to that of the individual ones.	benzo(b)fluoranthene	97-100	P53	Homo sapiens	148-151
30843662-4	2019	The clinicopathologic features of the TP53 mutations and its impact on the effect of crizotinib treatment were analyzed.	Crizotinib	85-95	P53	Homo sapiens	38-42
31196889-0	2019	Combinatorial Therapy of Zinc Metallochaperones with Mutant p53 Reactivation and Diminished Copper Binding.	zinc metallochaperones	25-47	P53	Homo sapiens	60-63
30843662-11	2019	CONCLUSIONS: TP53 mutations, especially nondisruptive mutations, negatively affected the response to crizotinib and correlated with shorter PFS in ALK-rearranged NSCLC patients.	Crizotinib	101-111	P53	Homo sapiens	13-17
31196889-3	2019	Zinc metallochaperones (ZMC) are a new class of mutant p53 reactivators that restore WT structure and function to zinc-deficient p53 mutants.	zinc metallochaperones	0-22	P53	Homo sapiens	55-58
30952724-8	2019	Furthermore, casticin decreased expression of p-ATM, p-ATR, MDC1 and MGMT levels after 48 h of treatment, however, it increased p-ATR and MGMT levels after 12 h. In contrast, casticin increased the levels of p-p53, p-H2A.X, and PARP after 48 h of treatment.	casticin	13-21	P53	Homo sapiens	210-213
30952724-8	2019	Furthermore, casticin decreased expression of p-ATM, p-ATR, MDC1 and MGMT levels after 48 h of treatment, however, it increased p-ATR and MGMT levels after 12 h. In contrast, casticin increased the levels of p-p53, p-H2A.X, and PARP after 48 h of treatment.	casticin	175-183	P53	Homo sapiens	210-213
31196889-3	2019	Zinc metallochaperones (ZMC) are a new class of mutant p53 reactivators that restore WT structure and function to zinc-deficient p53 mutants.	zinc metallochaperones	0-22	P53	Homo sapiens	129-132
30952724-9	2019	As shown by confocal microscopy, casticin affected the translocation of DNA-PKcs and p-p53 to the nucleus of TSGH-8301 cells.	casticin	33-41	P53	Homo sapiens	87-90
31334116-0	2019	Ruthenium Complexes With Piplartine Cause Apoptosis Through MAPK Signaling by a p53-Dependent Pathway in Human Colon Carcinoma Cells and Inhibit Tumor Development in a Xenograft Model.	piplartine	25-35	P53	Homo sapiens	80-83
30822424-9	2019	Meanwhile, down-regulation of Cyclin D1, MMP-2 and Vimentin, up-regulations of p53 and p21, as well as cleavage of caspase-3 and -9 were observed in Salidroside-treated cell.	rhodioloside	149-160	P53	Homo sapiens	79-82
31055607-0	2019	Chrysophanol, an anthraquinone from AST2017-01, possesses the anti-proliferative effect through increasing p53 protein levels in human mast cells.	chrysophanic acid	0-12	P53	Homo sapiens	107-110
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	p-cso-sa	292-300	P53	Homo sapiens	80-83
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	p-cso-sa	292-300	P53	Homo sapiens	99-102
30554333-3	2019	In this study, we aimed to further clarify the mechanism of inactivation of TP53 in GAED in the light of promoter methylation of TP53, and expression of methylation-associated proteins such as Ten-eleven translocation (TET) 1 and 5-hydroxymethylcytosine (5-hmc) in addition to ATM mutations.	tet	219-222	P53	Homo sapiens	76-80
30862347-0	2019	Salidroside Reduces PDE2A Expression by Down-regulating p53 in Human Embryonic Lung Fibroblasts.	rhodioloside	0-11	P53	Homo sapiens	56-59
30886346-4	2019	Here, we demonstrate that the stability of stress-induced wild-type and mutant p53 is regulated by the type I phosphatidylinositol phosphate kinase (PIPKI-alpha (also known as PIP5K1A)) and its product phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2).	Phosphatidylinositol 4,5-Diphosphate	202-239	P53	Homo sapiens	79-82
30886346-4	2019	Here, we demonstrate that the stability of stress-induced wild-type and mutant p53 is regulated by the type I phosphatidylinositol phosphate kinase (PIPKI-alpha (also known as PIP5K1A)) and its product phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2).	Phosphatidylinositol 4,5-Diphosphate	241-254	P53	Homo sapiens	79-82
30886346-5	2019	Nuclear PIPKI-alpha binds to p53 upon stress, resulting in the production and association of PtdIns(4,5)P2 with p53.	Phosphatidylinositol 4,5-Diphosphate	93-106	P53	Homo sapiens	29-32
30886346-5	2019	Nuclear PIPKI-alpha binds to p53 upon stress, resulting in the production and association of PtdIns(4,5)P2 with p53.	Phosphatidylinositol 4,5-Diphosphate	93-106	P53	Homo sapiens	112-115
30886346-6	2019	PtdIns(4,5)P2 binding promotes the interaction between p53 and the small heat shock proteins HSP27 (also known as HSPB1) and alphaB-crystallin (also known as HSPB5), which stabilize nuclear p53.	Phosphatidylinositol 4,5-Diphosphate	0-13	P53	Homo sapiens	55-58
30886346-6	2019	PtdIns(4,5)P2 binding promotes the interaction between p53 and the small heat shock proteins HSP27 (also known as HSPB1) and alphaB-crystallin (also known as HSPB5), which stabilize nuclear p53.	Phosphatidylinositol 4,5-Diphosphate	0-13	P53	Homo sapiens	190-193
30886346-7	2019	Moreover, inhibition of PIPKI-alpha or PtdIns(4,5)P2 association results in p53 destabilization.	Phosphatidylinositol 4,5-Diphosphate	39-52	P53	Homo sapiens	76-79
30521886-8	2019	Treating U2OS and MG63 cells with the p53 inhibitor alpha-pifithrin or the p38alpha MAPK inhibitor SB203580 led to higher cell survival and proliferation and lower cell apoptosis, compared with the pcDNA3.1-HOXA5 group.	alpha-pifithrin	52-67	P53	Homo sapiens	38-41
31055607-7	2019	AST2017-01 and chrysophanol enhanced expressions of p53 and Bax, whereas inhibited expression of Bcl-2.	chrysophanic acid	15-27	P53	Homo sapiens	52-55
30801837-0	2019	Ingenol mebutate-mediated reduction in p53-positive keratinocytes in skin cancerization field directly correlates with clinical response in patients with multiple actinic keratoses.	3-ingenyl angelate	0-16	P53	Homo sapiens	39-42
30209161-0	2019	TP53 Outperforms Other Androgen Receptor Biomarkers to Predict Abiraterone or Enzalutamide Outcome in Metastatic Castration-Resistant Prostate Cancer.	abiraterone	63-74	P53	Homo sapiens	0-4
30599074-5	2019	This cytotoxicity resulted from TTO induced apoptosis in both A-375 and HEp-2 cell lines as evidenced by morphological features of apoptosis and Annexin V/PI staining results in addition to the activation of caspase-3/7 and -9, upregulation of pro-apoptotic genes (P53 and BAX) and downregulation of the anti-apoptotic gene BCL-2.	Tea Tree Oil	32-35	P53	Homo sapiens	265-268
30723502-5	2019	The presence of R273H-P53 conferred the cancer cells with drug resistance not only against the widely used chemotherapeutic agents like cisplatin (CDDP) or 5-flurouracil (5-FU) but also against potent alternative modes of therapy like proteasomal inhibition.	5-flurouracil	156-169	P53	Homo sapiens	22-25
30801837-3	2019	AIMS: Analysis of ingenol mebutate gel (150 and 500 mcg/g) effects in the reduction in "p53 patches" inside skin cancerization field (CF) in patients with multiple AKs of face/scalp or trunk/extremities, in order to investigate whether the expected reduction in p53+ keratinocytes might have a direct role in the long-term AK reduction in treated areas.	3-ingenyl angelate	18-34	P53	Homo sapiens	88-91
30881947-3	2019	Aim: To evaluate the prognostic value of p53 and p53 phosphorylation at serine 15 (p53 Ser15-P) in patients with HCC.	ser15-p	87-94	P53	Homo sapiens	49-52
30801837-3	2019	AIMS: Analysis of ingenol mebutate gel (150 and 500 mcg/g) effects in the reduction in "p53 patches" inside skin cancerization field (CF) in patients with multiple AKs of face/scalp or trunk/extremities, in order to investigate whether the expected reduction in p53+ keratinocytes might have a direct role in the long-term AK reduction in treated areas.	3-ingenyl angelate	18-34	P53	Homo sapiens	262-265
30881947-3	2019	Aim: To evaluate the prognostic value of p53 and p53 phosphorylation at serine 15 (p53 Ser15-P) in patients with HCC.	ser15-p	87-94	P53	Homo sapiens	49-52
30881947-5	2019	Results: Stratifying by the expression of p53 Ser15-P (P = 0.016), but not by p53 (P = 0.301), revealed significantly different survival outcomes in patients with HCC.	ser15-p	46-53	P53	Homo sapiens	42-45
30370860-12	2019	We also observed that both compounds up-regulated the p53 expression where Emodin causes nuclear p53 localization, which leads to down-regulation in mTOR expression and induces autophagy while Chrysophanol inhibits p53 translocation into nucleus, up-regulates mTOR expression and inhibits autophagy.	chrysophanic acid	193-205	P53	Homo sapiens	54-57
30801837-11	2019	Ingenol mebutate is able to reduce p53+ keratinocytes with variable efficacy, this reduction degree directly correlating with clinical efficacy.	3-ingenyl angelate	0-16	P53	Homo sapiens	35-38
30881947-7	2019	Conclusions: P53 Ser15-P is associated with poor outcomes in patients with HCC, and this prognostic marker is useful for predicting the survival of patients with PCNA-positive HCC.	ser15-p	17-24	P53	Homo sapiens	13-16
31046065-0	2019	Androgen Receptor Burden and Poor Response to Abiraterone or Enzalutamide in TP53 Wild-Type Metastatic Castration-Resistant Prostate Cancer.	abiraterone	46-57	P53	Homo sapiens	77-81
30543781-0	2019	A new pyrrole based small molecule from Tinospora cordifolia induces apoptosis in MDA-MB-231 breast cancer cells via ROS mediated mitochondrial damage and restoration of p53 activity.	Pyrroles	6-13	P53	Homo sapiens	170-173
30472223-0	2019	Pifithrin-alpha enhancing anticancer effect of topotecan on p53-expressing cancer cells.	Topotecan	47-56	P53	Homo sapiens	60-63
30697266-12	2019	Co-treatment with captopril and the AKT inhibitor MK-2206 reduced the H2O2-induced P53 and ICAM-1 protein expression (p &lt; 0.05).	Captopril	18-27	P53	Homo sapiens	83-86
32042864-4	2019	PRMT5 can also methylate nonhistone proteins such as the transcription factors p53, E2F1 and p65.	potassium methylate	15-24	P53	Homo sapiens	79-82
30642546-12	2019	Concomitant TP53 mutation correlated to unfavorable survival when receiving a single TKI crizotinib.	Crizotinib	89-99	P53	Homo sapiens	12-16
30868056-5	2019	HDAC2 gene silencing significantly decreased the sensitivity of U2OS cells to ADR and attenuated p53-dependent DNA damage responses, such as ADR-mediated phosphorylation of ataxia telangiectasia mutated (ATM) and p53, as well as accumulation of gammaH2AX and cleaved poly (ADP-ribose) polymerase.	gammah2ax	245-254	P53	Homo sapiens	97-100
30634697-6	2019	Furthermore, molecular mechanisms of cytotoxicity of [4-NH2-2-Me(Q)H][VO(bcma)(H2O)]2H2O (T1) were dependent on antiproliterative activity, increased ROS generation, cell cycle arrest in G2/M phase with simultaneous triggering of the p53/p21 pathway, binucleation, and induction of autophagy.	bcma)(h2o)]2h2o	73-88	P53	Homo sapiens	234-237
31099374-10	2019	These results suggested that PaH was a promising sensitizer that can be combined with light to produce significant anti-tumor effects in oral squamous cell carcinoma via enhanced ROS production and up-regulated expression of p53.	palmatine	29-32	P53	Homo sapiens	225-228
30634697-6	2019	Furthermore, molecular mechanisms of cytotoxicity of [4-NH2-2-Me(Q)H][VO(bcma)(H2O)]2H2O (T1) were dependent on antiproliterative activity, increased ROS generation, cell cycle arrest in G2/M phase with simultaneous triggering of the p53/p21 pathway, binucleation, and induction of autophagy.	titanium silicide	90-92	P53	Homo sapiens	234-237
30458062-0	2019	Targeted Synthesis of Complex Spiro[3H-indole-3,2"-pyrrolidin]-2(1H)-ones by Intramolecular Cyclization of Azomethine Ylides: Highly Potent MDM2-p53 Inhibitors.	azomethine ylides	107-124	P53	Homo sapiens	145-148
30370860-12	2019	We also observed that both compounds up-regulated the p53 expression where Emodin causes nuclear p53 localization, which leads to down-regulation in mTOR expression and induces autophagy while Chrysophanol inhibits p53 translocation into nucleus, up-regulates mTOR expression and inhibits autophagy.	chrysophanic acid	193-205	P53	Homo sapiens	97-100
30370860-12	2019	We also observed that both compounds up-regulated the p53 expression where Emodin causes nuclear p53 localization, which leads to down-regulation in mTOR expression and induces autophagy while Chrysophanol inhibits p53 translocation into nucleus, up-regulates mTOR expression and inhibits autophagy.	chrysophanic acid	193-205	P53	Homo sapiens	97-100
30177839-0	2019	Transcriptional repression of IKKbeta by p53 in arsenite-induced GADD45alpha accumulation and apoptosis.	arsenite	48-56	P53	Homo sapiens	41-44
30177839-4	2019	Arsenite stimulation induced transactivation of p53, which formed a complex with its downstream target, Ets-1, and then synergistically repressed IKKbeta transcription, reduced MDM2 stability, and ultimately removed the inhibitory effect of MDM2 on GADD45alpha induction.	arsenite	0-8	P53	Homo sapiens	48-51
30316840-0	2018	1,3-Dichloro-2-Propanol inhibits autophagy via P53/AMPK/mTOR pathway in HepG2 cells.	1,3-dichloro-2-propanol	0-23	P53	Homo sapiens	47-50
31239671-1	2019	Purpose: The objective of this work was to formulate a delivery system of pDNA encoded p53 gene-loaded chitosan-sodium deoxycholate (CS-DS) nanoparticles, and to evaluate their influence on in vitro cytotoxicity and transfection efficiency of p53 gene.	Chitosan	103-111	P53	Homo sapiens	243-246
30973113-8	2019	Using flow cytometry to determine cell cycle analysis and determination the possible mechanisms of action for apoptosis revealed that ME-GA arrested the cell cycle at G2/M that lead to inhibition of hepatocellular carcinoma and induced apoptosis via the extrinsic pathway and its ability to increase p53 transactivation.	me-ga	134-139	P53	Homo sapiens	300-303
31159174-6	2019	We demonstrate that p53 binds to all studied non-B DNA structures, with a preference for non-B DNA structures formed by pyrimidine (Py) rich strands.	pyrimidine	132-134	P53	Homo sapiens	20-23
30177839-6	2019	Subsequent studies further revealed that the activation of the DAPK1/p53/Ets-1/IKKbeta/MDM2/GADD45alpha cascade was a common signaling event in mediating apoptosis of diverse cancer cells induced by arsenite and other tumor therapeutic agents.	arsenite	199-207	P53	Homo sapiens	69-72
30406888-3	2018	In this study, our aim to understand the potential molecular targets of diclofenac, which may propose new therapeutic targets in HCT 116 (wt p53) and SW480 (mutant p53R273H) colon cancer cells.	Diclofenac	72-82	P53	Homo sapiens	141-144
30272369-0	2018	JIB-04 induces cell apoptosis via activation of the p53/Bcl-2/caspase pathway in MHCC97H and HepG2 cells.	JIB-04	0-6	P53	Homo sapiens	52-55
30742880-8	2019	HMGB1 and p53 both serve as transcription factors that play crucial roles in the regulation of PCB29-pQ-induced autophagy and apoptosis.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	95-103	P53	Homo sapiens	10-13
30742880-9	2019	PCB29-pQ not only enhanced the expression of HMGB1 and p53 but also promoted their binding and cytosolic translocation.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	0-8	P53	Homo sapiens	55-58
30742880-10	2019	Interestingly, HMGB1 rather than p53 plays a primary role in 5 muM of PCB29-pQ-induced autophagy in the nucleus; however, p53 promoted apoptosis to a great extent in the cytosol at the dose of 15 muM PCB29-pQ.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	70-78	P53	Homo sapiens	122-125
30526032-0	2018	One-pot synthesis of spiro(indoline-3,4"-pyrazolo[3,4-b]pyridine)-5"-carbonitriles as p53-MDM2 interaction inhibitors.	spiro(indoline-3,4"-pyrazolo[3,4-b]pyridine)-5"-carbonitriles	21-82	P53	Homo sapiens	86-89
30742880-11	2019	Together, HMGB1 and p53 provided a subtle balance between autophagy and apoptosis, thus determining the fate of PCB29-pQ-treated cells.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	112-120	P53	Homo sapiens	20-23
30717558-14	2018	L-TP could delay HGMCs senescence through regulating STAT3/miR-126 expressions and inhibiting the telomere-p53-p21-Rb signaling pathway activation.	l-tp	0-4	P53	Homo sapiens	107-110
31191795-0	2019	p53-Mediated PI3K/AKT/mTOR Pathway Played a Role in PtoxDpt-Induced EMT Inhibition in Liver Cancer Cell Lines.	ptoxdpt	52-59	P53	Homo sapiens	0-3
30212393-12	2018	The immunolabeling of invasive PDAC and COD for p53 and Smad4 supports the high prevalence of COD observed on hematoxylin and eosin and highlights the utility of p53 and Smad4 immunolabeling in differentiating COD and HG-PanIN.	Hematoxylin	110-121	P53	Homo sapiens	48-51
29552710-0	2018	Gold and Silver Nanoparticles Biomimetically Synthesized Using Date Palm Pollen Extract-Induce Apoptosis and Regulate p53 and Bcl-2 Expression in Human Breast Adenocarcinoma Cells.	Silver	9-15	P53	Homo sapiens	118-121
30833076-5	2019	Our data demonstrated that suppression of mevalonate pathway by simvastatin significantly upregulated Kruppel-like factor 2 (KLF2) and p21WAF1/CIP1 expression in mutp53 colon cancer cells SW1116 but not in p53 wild type cells HCT116.	Simvastatin	64-75	P53	Homo sapiens	165-168
30833076-10	2019	These data provide strong evidences for clinical application of simvastatin in treatment of colon cancer with p53 mutation.	Simvastatin	64-75	P53	Homo sapiens	110-113
30217415-1	2018	Small molecule inhibitors of the p53-MDM2 protein complex are under intense investigation in clinical trials as anti-cancer agents, including our first generation inhibitor NVP-CGM097.	NVP-CGM097	177-183	P53	Homo sapiens	33-36
31105826-12	2019	TMPP increased SOD, GSH-Px, and bFGF, and reduced MDA, ROS, p53, and caspase-3 levels.	TMPP	0-4	P53	Homo sapiens	60-63
30361551-6	2018	Results: Exposure to increasing concentrations of TiO2 NPs enhanced overall cell survivalof HCT116 cells and reduced the Bcl-2 and Caspase 3 expression while the ratio of Bax/Bcl-2 was down-regulated.TiO2 NPs at 400 and 50 mug/ml concentrations suppressed cell proliferation and induced apoptosis of HT29 cells andalso up-regulated P53 and Bax at the mRNA level, enhanced the Bax/Bcl-2 ratio and eventually up-regulated Caspase3 mRNA.	titanium dioxide	50-54	P53	Homo sapiens	332-335
30361551-6	2018	Results: Exposure to increasing concentrations of TiO2 NPs enhanced overall cell survivalof HCT116 cells and reduced the Bcl-2 and Caspase 3 expression while the ratio of Bax/Bcl-2 was down-regulated.TiO2 NPs at 400 and 50 mug/ml concentrations suppressed cell proliferation and induced apoptosis of HT29 cells andalso up-regulated P53 and Bax at the mRNA level, enhanced the Bax/Bcl-2 ratio and eventually up-regulated Caspase3 mRNA.	titanium dioxide	200-204	P53	Homo sapiens	332-335
30215795-0	2018	The impact of p53 function on the metabolic activation of the carcinogenic air pollutant 3-nitrobenzanthrone and its metabolites 3-aminobenzanthrone and N-hydroxy-3-aminobenzanthrone in human cells.	N-hydroxy-3-aminobenzanthrone	153-182	P53	Homo sapiens	14-17
30239626-0	2018	A molecular mechanism of nickel (II): reduction of nucleotide excision repair activity by structural and functional disruption of p53.	Nickel	25-31	P53	Homo sapiens	130-133
30395490-0	2018	Modulating Survivin as a Radioresistant Factor, Caspase-3, and Apoptosis by Omega-3 Docosahexaenoic Acid Sensitizes Mutant-p53 Colorectal Cancer Cells to gamma-Irradiation.	omega-3 docosahexaenoic acid	76-104	P53	Homo sapiens	123-126
30993195-6	2019	Zinc metallochaperones (ZMCs) are a new class of anti-cancer drugs that specifically reactivate zinc-deficient mutant p53 by restoring zinc binding.	zinc metallochaperones	0-22	P53	Homo sapiens	118-121
30344715-6	2018	The results demonstrate that apatinib significantly inhibited cell proliferation and colony formation through promoting cell apoptosis in p53- and EGFR-mutated and wild-type glioma cells.	apatinib	29-37	P53	Homo sapiens	138-141
30015828-4	2018	Alantolactone induced apoptosis of MCF-7 cells by regulating the protein expression levels of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein, p53, caspase-3 and caspase-12, which are associated with the apoptotic pathway, and suppressed colony formation and migration by regulating the protein expression of matrix metalloproteinase (MMP)-2, MMP-7 and MMP-9.	alantolactone	0-13	P53	Homo sapiens	149-152
30297838-0	2018	C16-ceramide is a natural regulatory ligand of p53 in cellular stress response.	N-palmitoylsphingosine	0-12	P53	Homo sapiens	47-50
30297838-2	2018	Here we report the mechanism for activation of p53 tumor suppressor by C16-ceramide.	N-palmitoylsphingosine	71-83	P53	Homo sapiens	47-50
30297838-3	2018	C16-ceramide tightly binds within the p53 DNA-binding domain (Kd ~ 60 nM), in close vicinity to the Box V motif.	N-palmitoylsphingosine	0-12	P53	Homo sapiens	38-41
30297838-8	2018	Our study establishes C16-ceramide as a natural small molecule activating p53 through the direct binding.	N-palmitoylsphingosine	22-34	P53	Homo sapiens	74-77
30905619-4	2019	p53-mediated DDR pathway activation was the predominant response to even single-nuclease-induced DSBs across all HSPC subtypes analyzed.	dsbs	97-101	P53	Homo sapiens	0-3
30214587-8	2018	Treatment of p53-/- HCT-116 cells with BAPTA-AM did not inhibit apoptosis following serial treatment with celecoxib and bortezomib.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	39-47	P53	Homo sapiens	13-16
30211553-6	2018	Likewise, pancaspase inhibitor z-vad-fmk, p38 MAPK inhibitor SB203580, and p53 depletion blocked PARP and caspase-3 in Kaempferol treated HCT116 colorectal cancer cells.	kaempferol	119-129	P53	Homo sapiens	75-78
30211553-7	2018	Therefore, these findings provide novel insight that ROS and p53 signalings mediate p38 phosphorylation and caspase activation in Kaempferol stimulated apoptosis in CRCs.	kaempferol	130-140	P53	Homo sapiens	61-64
30753858-3	2019	In cell model, scandenolone suppressed the breast cancer MCF-7 cells viability, ceased mitotic cell cycle, decreased mitochondrial membrane potential, up-regulated cleaved caspase-3 and promoted the phosphorylation of p53.	warangalone	15-27	P53	Homo sapiens	218-221
30176902-11	2018	Treatment with XWL-1-48 caused ROS generation and triggered DNA damage through induction of gamma-H2AX and activation of ATM/p53/p21 pathway.	xwl-1-48	15-23	P53	Homo sapiens	125-128
29800662-6	2018	The critical groups and significant binding sites for the interaction between alisol monomers and p53DNA include C19-OH and C22-OH of the alisols; N2 and H21 of the guanine deoxynucleotide (DG8), N2-H21 of the DG7, O4" of the DG9 in the f-chain of p53DNA; and C2-O2 of the cytosine deoxynucleotide (DC16) in the e-chain of p53DNA.	DG9	226-229	P53	Homo sapiens	98-101
30250566-0	2018	Erianin inhibits human cervical cancer cell through regulation of tumor protein p53 via the extracellular signal-regulated kinase signaling pathway.	Erianin	0-7	P53	Homo sapiens	80-83
30211553-0	2018	Reactive Oxygen Species and p53 Mediated Activation of p38 and Caspases is Critically Involved in Kaempferol Induced Apoptosis in Colorectal Cancer Cells.	kaempferol	98-108	P53	Homo sapiens	28-31
30211553-4	2018	Also, Kaempferol increased the PARP cleavages and activation of caspase-8, -9, and -3, phospho-p38 MAPK, p53, and p21 in HCT116 and HCT15 cells.	kaempferol	6-16	P53	Homo sapiens	105-108
30936832-11	2019	In conclusion, this integrative pharmacology-based analysis revealed the anti-NPC effects of RO might be related to its regulatory impact via the PI3K-AKT signaling pathway, the Wnt signaling pathway, and the cAMP signaling pathway by targeting VEGFA, TP53, and HSPA8.	ro	93-95	P53	Homo sapiens	252-256
30100398-4	2018	We observed that hypo-methylated DMR near CREB5 recruited transcription factors binding, such as P53 and SP1, and in turn upregulated CREB5.	aspartylmethionylarginine	33-36	P53	Homo sapiens	97-100
29800662-6	2018	The critical groups and significant binding sites for the interaction between alisol monomers and p53DNA include C19-OH and C22-OH of the alisols; N2 and H21 of the guanine deoxynucleotide (DG8), N2-H21 of the DG7, O4" of the DG9 in the f-chain of p53DNA; and C2-O2 of the cytosine deoxynucleotide (DC16) in the e-chain of p53DNA.	alisols	138-145	P53	Homo sapiens	98-101
29997221-4	2018	CLL high-risk-I, CIT-resistant is defined by clinically CIT-resistant disease with TP53 aberrations, but fully responsive to PI.	cit	17-20	P53	Homo sapiens	83-87
29997221-4	2018	CLL high-risk-I, CIT-resistant is defined by clinically CIT-resistant disease with TP53 aberrations, but fully responsive to PI.	cit	56-59	P53	Homo sapiens	83-87
30899200-6	2019	However, apoptotic responses to trametinib and vemurafenib were greater in WM35 than WM35-R, evidenced by FACS analysis and caspase 3/7 activity, indicating that these MAPK inhibitors acted on the cells partially through p53-regulated pathways.	Vemurafenib	47-58	P53	Homo sapiens	221-224
29702192-8	2018	Moreover, PAB depleted intracellular GSH via p53-mediated xCT pathway, which further exacerbated accumulation of H2O2 and lipid peroxides.	Lipid Peroxides	122-137	P53	Homo sapiens	45-48
29668064-10	2018	Multiparametric analysis demonstrates a strong correlation between gammaH2AX and p-p53(S15) for clastogen compounds.	gammah2ax	67-76	P53	Homo sapiens	83-86
30116169-7	2018	The results demonstrate that the bile acids, ursodeoxycholate and tauroursodeoxycholate, exhibit selective cytotoxicity toward nonfunctional p53 cell lines suggesting a p53-mediated role in inhibition of cell clonogenicity and potential chemopreventative properties.	Ursodeoxycholic Acid	45-61	P53	Homo sapiens	141-144
30116169-7	2018	The results demonstrate that the bile acids, ursodeoxycholate and tauroursodeoxycholate, exhibit selective cytotoxicity toward nonfunctional p53 cell lines suggesting a p53-mediated role in inhibition of cell clonogenicity and potential chemopreventative properties.	Ursodeoxycholic Acid	45-61	P53	Homo sapiens	169-172
29980405-6	2018	Likewise, the sensitivity to drugs used to treat other cancers such as: doxorubicin, mitoxantrone, and 4 hydroxy tamoxifen (4HT) also increased upon introduction of WT-TP53 into MIA-PaCa-2 cells.	4 hydroxy tamoxifen	103-122	P53	Homo sapiens	168-172
29892062-6	2018	The toxic response to DSBs was P53/TP53-dependent, such that the efficiency of precise genome engineering in hPSCs with a wild-type P53 gene was severely reduced.	dsbs	22-26	P53	Homo sapiens	31-34
30899200-7	2019	SiRNA mediated p53 knockdown in WM35 replicated the same pattern of response to trametinib and vemurafenib as seen in WM35-R, confirming that p53 plays a role in trametinib and vemurafenib induced apoptosis.	Vemurafenib	95-106	P53	Homo sapiens	15-18
29892062-6	2018	The toxic response to DSBs was P53/TP53-dependent, such that the efficiency of precise genome engineering in hPSCs with a wild-type P53 gene was severely reduced.	dsbs	22-26	P53	Homo sapiens	35-39
29892062-6	2018	The toxic response to DSBs was P53/TP53-dependent, such that the efficiency of precise genome engineering in hPSCs with a wild-type P53 gene was severely reduced.	dsbs	22-26	P53	Homo sapiens	36-39
30899200-7	2019	SiRNA mediated p53 knockdown in WM35 replicated the same pattern of response to trametinib and vemurafenib as seen in WM35-R, confirming that p53 plays a role in trametinib and vemurafenib induced apoptosis.	Vemurafenib	177-188	P53	Homo sapiens	15-18
29525471-6	2018	Prolonged expression of p53 was responsible for melanocyte senescence and hyperpigmentation, and treatment with the p53-inhibitor pifithrin-alpha at 2-weeks post-UVB irradiation, but not at 48 h, significantly reduced melanin content along with decreases in tyrosinase levels.	Melanins	218-225	P53	Homo sapiens	24-27
28920465-0	2018	Fish-oil-derived eicosapentaenoic acid decreases survivin expression and induces wt-p53 accumulation with caspase-3 activation in acute lymphoblastic leukemia cells.	Eicosapentaenoic Acid	17-38	P53	Homo sapiens	84-87
30899200-7	2019	SiRNA mediated p53 knockdown in WM35 replicated the same pattern of response to trametinib and vemurafenib as seen in WM35-R, confirming that p53 plays a role in trametinib and vemurafenib induced apoptosis.	Vemurafenib	177-188	P53	Homo sapiens	142-145
28920465-3	2018	Here, we investigated if in vitro eicosapentaenoic acid (EPA) concentrations equal to human plasma levels are able to target wt-p53 and survivin.	Eicosapentaenoic Acid	34-55	P53	Homo sapiens	128-131
29525471-6	2018	Prolonged expression of p53 was responsible for melanocyte senescence and hyperpigmentation, and treatment with the p53-inhibitor pifithrin-alpha at 2-weeks post-UVB irradiation, but not at 48 h, significantly reduced melanin content along with decreases in tyrosinase levels.	Melanins	218-225	P53	Homo sapiens	116-119
28920465-3	2018	Here, we investigated if in vitro eicosapentaenoic acid (EPA) concentrations equal to human plasma levels are able to target wt-p53 and survivin.	Eicosapentaenoic Acid	57-60	P53	Homo sapiens	128-131
30740957-0	2019	Olaparib induced senescence under P16 or P53 dependent manner in ovarian cancer.	olaparib	0-8	P53	Homo sapiens	41-44
28920465-7	2018	EPA induced 1.3-6 and 1.9-20-fold increases in caspase-3 activation and wt-p53 accumulation, respectively.	Eicosapentaenoic Acid	0-3	P53	Homo sapiens	75-78
28920465-10	2018	CONCLUSION: EPA induces strongly wt-p53 with a remarkable decrease in survivin expression, representing an attractive compound to modulate wt-p53 and survivin in ALL cells.	Eicosapentaenoic Acid	12-15	P53	Homo sapiens	36-39
28920465-10	2018	CONCLUSION: EPA induces strongly wt-p53 with a remarkable decrease in survivin expression, representing an attractive compound to modulate wt-p53 and survivin in ALL cells.	Eicosapentaenoic Acid	12-15	P53	Homo sapiens	142-145
29571049-3	2018	Here we report the design of a fluorescent lanthanide oxyfluoride nanoparticle (LONp)-based multifunctional peptide drug delivery system for potential treatment of acute myeloid leukemia (AML) that commonly harbors wild type p53, high levels of MDM2 and/or MDMX, and an overexpressed cell surface receptor, CD33.	lonp	80-84	P53	Homo sapiens	225-228
29348462-6	2018	Interestingly, PL-sensitized HNSCC cells to APR-246 are TP53 mutation-independent.	piperlonguminine	15-17	P53	Homo sapiens	56-60
30740957-9	2019	The expression of P16 and retinoblastoma protein (p-RB) were significantly enhanced in SKOV3 cells under olaparib treated, meanwhile, the expression of P53 and p-RB were upregulated in A2780 cells.	olaparib	105-113	P53	Homo sapiens	152-155
30740957-12	2019	CONCLUSION: Continuous low dosage administration of olaparib induced senescence under P16 or P53 dependent manner in ovarian cancer.	olaparib	52-60	P53	Homo sapiens	93-96
30778058-4	2019	Mechanistically, miR-135 accumulates specifically in response to glutamine deprivation and requires ROS-dependent activation of mutant p53, which directly promotes miR-135 expression.	mir-135	17-24	P53	Homo sapiens	135-138
29783721-7	2018	Moreover, the combination of AZD1775 with olaparib or gemcitabine is synergistic in cells with mutant p53 and constitutes a new approach that should be considered in the treatment of advanced and recurrent gynecologic cancer.	olaparib	42-50	P53	Homo sapiens	102-105
29532860-0	2018	Ciprofloxacin triggers the apoptosis of human triple-negative breast cancer MDA-MB-231 cells via the p53/Bax/Bcl-2 signaling pathway.	Ciprofloxacin	0-13	P53	Homo sapiens	101-104
29545477-0	2018	Therapeutic Effect of Quinacrine, an Antiprotozoan Drug, by Selective Suppression of p-CHK1/2 in p53-Negative Malignant Cancers.	Quinacrine	22-32	P53	Homo sapiens	97-100
29549167-8	2018	Given that loss of p53 is associated with progression of prostate cancer to CRPC and NEPC, our results show that TET, by acting as a TRAIL-sensitizing agent in prostate cancer, could serve as a potential therapeutic agent in CRPC and NEPC, for which there is no cure to date.	tetrandrine	113-116	P53	Homo sapiens	19-22
30778058-4	2019	Mechanistically, miR-135 accumulates specifically in response to glutamine deprivation and requires ROS-dependent activation of mutant p53, which directly promotes miR-135 expression.	mir-135	164-171	P53	Homo sapiens	135-138
29302046-0	2018	p53 status in the primary tumor predicts efficacy of subsequent abiraterone and enzalutamide in castration-resistant prostate cancer.	abiraterone	64-75	P53	Homo sapiens	0-3
30591552-2	2019	In this study, we show that synthetic peptides corresponding to the binding interface between Rbm38 and eIF4E, including an 8 amino acid peptide (Pep8) derived from Rbm38, are effective in relieving Rbm38-mediated repression of p53.	amino acid peptide	126-144	P53	Homo sapiens	228-231
30132214-6	2019	PI3 K inhibitor LY294002 and MDM2 inhibitor Nutlin-3a block Pgp3-induced inhibition of HeLa cell apoptosis, suggesting a critical role for the PI3K/AKT pathway and its effect on the MDM2-p53 axis in Pgp3 anti-apoptotic activity.	pgp3	60-64	P53	Homo sapiens	187-190
29616120-0	2018	Salidroside induces apoptosis in human ovarian cancer SKOV3 and A2780 cells through the p53 signaling pathway.	rhodioloside	0-11	P53	Homo sapiens	88-91
29616120-6	2018	Salidroside activated the caspase-dependent pathway in SKOV3 and A2780 cells, upregulating p53, p21Cip1/Waf1 and p16INK4a.	rhodioloside	0-11	P53	Homo sapiens	91-94
29616120-7	2018	These results suggest that the p53/p21Cip1/Waf1/p16INK4a pathway may serve a key function in salidroside-mediated effects on SKOV3 and A2780 cells.	rhodioloside	93-104	P53	Homo sapiens	31-34
29843463-3	2018	We are currently developing a new class of mutant p53 reactivators called zinc metallochaperones (ZMCs) and, here, we review our current understanding of them.	zinc metallochaperones	74-96	P53	Homo sapiens	50-53
30960044-4	2019	Doxorubicin (DOX) could be loaded into the cavity of CD polymers to form DOX-loaded nanoparticles (DOX-NPs) and the p53 gene could be subsequently condensed by DOX-NPs.	cyclodextrin polymer	53-64	P53	Homo sapiens	116-119
29691156-1	2018	Five lactam chemotypes amenable by the Castagnoli-Cushman reaction of imines and cyclic anhydrides have been investigated for their ability to activate p53 tumor suppressing transcription factor thus induce apoptosis in p53+ cancer cells.	Lactams	5-11	P53	Homo sapiens	152-155
29691156-1	2018	Five lactam chemotypes amenable by the Castagnoli-Cushman reaction of imines and cyclic anhydrides have been investigated for their ability to activate p53 tumor suppressing transcription factor thus induce apoptosis in p53+ cancer cells.	Lactams	5-11	P53	Homo sapiens	220-223
29720963-4	2018	Multiple oncogenic signaling pathways, such as c-Myc, p53, and mTORC1 feed into dNTP metabolism, and there is a clear role for dNTP imbalances in cancer initiation and progression.	Parathion	80-84	P53	Homo sapiens	54-57
29624044-2	2018	Herein, a dual-color ECL strategy is proposed by transferring ECL to two PMTs in a waveband-resolved way via dichroic mirror, simultaneously detecting wild-type p53 (WTp53) in near-infrared wavebands with CdTe (lambdamax = 782 nm) nanocrystals as tag and mutant p53 (MUp53) in eye-visible wavebands with CdSe (lambdamax = 554 nm) nanocrystals as tag.	cadmium telluride	205-209	P53	Homo sapiens	161-164
29624044-2	2018	Herein, a dual-color ECL strategy is proposed by transferring ECL to two PMTs in a waveband-resolved way via dichroic mirror, simultaneously detecting wild-type p53 (WTp53) in near-infrared wavebands with CdTe (lambdamax = 782 nm) nanocrystals as tag and mutant p53 (MUp53) in eye-visible wavebands with CdSe (lambdamax = 554 nm) nanocrystals as tag.	cadmium telluride	205-209	P53	Homo sapiens	168-171
30642546-10	2019	Additionally, concurrent TP53 mutation demonstrated significantly shorter progression-free survival (PFS) compared with TP53 wildtype in crizotinib-alone group (median PFS: 8 vs 13 months, Hazard Ratio = 1.494, P = 0.019).	Crizotinib	137-147	P53	Homo sapiens	25-29
32123827-5	2019	Attempts to preserve p53 proteins by treating cells with the calpain inhibitor E64d for 6 hours before harvesting increased the sensitivity of p53 to calpain cleavage.	aloxistatin	79-83	P53	Homo sapiens	21-24
29695998-3	2018	However, p53 has a number of other functions that recent data strongly implicate in tumor suppression, particularly with regard to the control of metabolism and ferroptosis (iron- and lipid-peroxide-mediated cell death) by p53.	Peroxides	190-198	P53	Homo sapiens	9-12
29695998-3	2018	However, p53 has a number of other functions that recent data strongly implicate in tumor suppression, particularly with regard to the control of metabolism and ferroptosis (iron- and lipid-peroxide-mediated cell death) by p53.	Peroxides	190-198	P53	Homo sapiens	223-226
29609003-8	2018	In addition, fluoride inhibited the deacetylase activity of SIRT1 and increased p53 (acetyl K382) level in SH-SY5Y cells.	Fluorides	13-21	P53	Homo sapiens	80-83
29609003-9	2018	Apoptosis and upregulation of cleaved caspase-3, cleaved PARP and p53 (acetyl K382) induced by fluoride could be ameliorated by SIRT1 overexpression or its activator resveratrol in SH-SY5Y cells.	acetyl k382	71-82	P53	Homo sapiens	66-69
29609003-9	2018	Apoptosis and upregulation of cleaved caspase-3, cleaved PARP and p53 (acetyl K382) induced by fluoride could be ameliorated by SIRT1 overexpression or its activator resveratrol in SH-SY5Y cells.	Fluorides	95-103	P53	Homo sapiens	66-69
29609003-10	2018	Taken together, our study demonstrates that fluoride induces apoptosis by inhibiting the deacetylase activity of SIRT1 to activate mitochondrial p53 pathway in SH-SY5Y cells, which depends on p53 transcriptional activity.	Fluorides	44-52	P53	Homo sapiens	145-148
29609003-10	2018	Taken together, our study demonstrates that fluoride induces apoptosis by inhibiting the deacetylase activity of SIRT1 to activate mitochondrial p53 pathway in SH-SY5Y cells, which depends on p53 transcriptional activity.	Fluorides	44-52	P53	Homo sapiens	192-195
29356571-10	2018	In addition, EO-PCL-PEG electrospun nanofibrous mats significantly upregulated the expression levels of cell cycle regulated genes (Cyclin D1, pRb, and P53) and stemness markers (Nanog, OCT-4, Rex-1, and Sox-2) than PCL-PEG nanofiber and tissue culture polystyrene in 7 and 14 days of cell culture.	eo-pcl-peg	13-23	P53	Homo sapiens	152-155
32123827-5	2019	Attempts to preserve p53 proteins by treating cells with the calpain inhibitor E64d for 6 hours before harvesting increased the sensitivity of p53 to calpain cleavage.	aloxistatin	79-83	P53	Homo sapiens	143-146
29511347-9	2018	Consistent with the role of TP53 in ROS regulation, loss of p53 function enhanced radiosensitization by olaparib in non-isogenic and isogenic cell line models and was associated with increased PARP-1 expression in bladder cancer cell lines and tumors.	olaparib	104-112	P53	Homo sapiens	60-63
28374118-4	2018	Diol-epoxides of DBP and BP were found to bind to p53 with tighter interaction than MDM2 and p53-MDM2 complex.	diol-epoxides	0-13	P53	Homo sapiens	50-53
29736211-12	2018	Vemurafenib treatment also increased the level of P53 protein in GNCs.	Vemurafenib	0-11	P53	Homo sapiens	50-53
29386219-1	2018	Purpose: We aimed to investigate the therapeutic efficacy of single agent and the combination of quinacrine and suberoylanilide hydroxamic acid (SAHA) in wt- and mut-p53 upper gastrointestinal cancer (UGC) cell models.Experimental Design: ATP-Glo, clonogenic cell survival, Annexin V, comet, DNA double-strand breaks (DSBs), qPCR, and Western blot analysis assays were utilized.Results: Using clonogenic cell survival, ATP-Glo cell viability, Annexin V, and sub-G0 population analysis, we demonstrated that a combination of quinacrine and SAHA significantly decreased colony formation and increased cancer cell death (range, 4-20 fold) in six UGC cell models, as compared with single-agent treatments, irrespective of the p53 status (P < 0.01).	Quinacrine	97-107	P53	Homo sapiens	166-169
29636995-5	2018	As2S2 upregulated pro-apoptotic proteins like p53 and PARP in MCF-7 cells.	Arsenic(II) sulfide	0-5	P53	Homo sapiens	46-49
29185024-0	2018	Sirt1 overexpression suppresses fluoride-induced p53 acetylation to alleviate fluoride toxicity in ameloblasts responsible for enamel formation.	Fluorides	32-40	P53	Homo sapiens	49-52
29386219-4	2018	Of note, although quinacrine treatment induced expression of wt-p53 protein, the combination of quinacrine and SAHA substantially decreased the levels of both wt-P53 and mut-P53.	Quinacrine	18-28	P53	Homo sapiens	64-67
29185024-0	2018	Sirt1 overexpression suppresses fluoride-induced p53 acetylation to alleviate fluoride toxicity in ameloblasts responsible for enamel formation.	Fluorides	78-86	P53	Homo sapiens	49-52
29386219-4	2018	Of note, although quinacrine treatment induced expression of wt-p53 protein, the combination of quinacrine and SAHA substantially decreased the levels of both wt-P53 and mut-P53.	Quinacrine	96-106	P53	Homo sapiens	162-165
29185024-4	2018	Here, we demonstrate that fluoride induced p53 acetylation (Ac-p53) [Lys379], which is a SIRT1 deacetylation target, in ameloblast-derived LS8 cells in vitro and in enamel organ in vivo.	Fluorides	26-34	P53	Homo sapiens	43-46
28374118-4	2018	Diol-epoxides of DBP and BP were found to bind to p53 with tighter interaction than MDM2 and p53-MDM2 complex.	diol-epoxides	0-13	P53	Homo sapiens	93-96
29185024-4	2018	Here, we demonstrate that fluoride induced p53 acetylation (Ac-p53) [Lys379], which is a SIRT1 deacetylation target, in ameloblast-derived LS8 cells in vitro and in enamel organ in vivo.	Fluorides	26-34	P53	Homo sapiens	63-66
29386219-4	2018	Of note, although quinacrine treatment induced expression of wt-p53 protein, the combination of quinacrine and SAHA substantially decreased the levels of both wt-P53 and mut-P53.	Quinacrine	96-106	P53	Homo sapiens	174-177
29386219-6	2018	Tumor xenograft data confirmed that a combination of quinacrine and SAHA is more effective than a single-agent treatment in abrogating tumor growth in vivo (P < 0.01).Conclusions: Our novel findings show that the combination of quinacrine and SAHA promotes DNA damage and is effective in inducing cancer cell death, irrespective of p53 status and resistance to CDDP or gefitinib in UGC models.	Quinacrine	53-63	P53	Homo sapiens	332-335
29386219-6	2018	Tumor xenograft data confirmed that a combination of quinacrine and SAHA is more effective than a single-agent treatment in abrogating tumor growth in vivo (P < 0.01).Conclusions: Our novel findings show that the combination of quinacrine and SAHA promotes DNA damage and is effective in inducing cancer cell death, irrespective of p53 status and resistance to CDDP or gefitinib in UGC models.	Quinacrine	228-238	P53	Homo sapiens	332-335
29185024-5	2018	Here we assessed SIRT1 function on fluoride-induced Ac-p53 formation using CRISPR/Cas9-mediated Sirt1 knockout (LS8Sirt/KO) cells or CRISPR/dCas9/SAM-mediated Sirt1 overexpressing (LS8Sirt1/over) cells.	Fluorides	35-43	P53	Homo sapiens	55-58
29185024-7	2018	However, fluoride-induced Ac-p53 was suppressed by the SIRT1 activator resveratrol (50 microM).	Fluorides	9-17	P53	Homo sapiens	29-32
29185024-9	2018	Fluoride-induced Ac-p53 formation was also suppressed in LS8Sirt1/over cells.	Fluorides	0-8	P53	Homo sapiens	20-23
29185024-14	2018	Our results suggest that SIRT1 deacetylates Ac-p53 to mitigate fluoride-induced cell growth inhibition, mitochondrial damage, DNA damage and apoptosis.	Fluorides	63-71	P53	Homo sapiens	47-50
29185024-15	2018	This is the first report implicating Ac-p53 in fluoride toxicity.	Fluorides	47-55	P53	Homo sapiens	40-43
29595201-3	2018	Herein, an acetyllysine mimic has been exploited for detecting the conformational changes of acetylated p53-protein/DNA interactions by genetic code expansion and 19F NMR.	N-epsilon-Acetyl-L-lysine	11-23	P53	Homo sapiens	104-107
30574046-4	2018	Nobiletin induced apoptosis of breast cancer MCF-7 cells via regulating the protein expression of Bax, Bcl-2, cleaved caspase-3, and p53.	nobiletin	0-9	P53	Homo sapiens	133-136
29881420-0	2018	Silver Nanoparticles Synthesized Coating with Zataria Multiflora Leaves Extract Induced Apoptosis in HeLa Cells Through p53 Activation.	Silver	0-6	P53	Homo sapiens	120-123
29496041-4	2018	Formalin-fixed, paraffin-embedded cancer tissues were subjected to histopathological evaluation, DNA quality control, HPV-DNA detection, and p16INK4a/pRb/p53/Cyclin-D1 immunohistochemistry.	Formaldehyde	0-8	P53	Homo sapiens	154-157
30574046-5	2018	The expression of Bcl-2 decreased, while the expression of Bax and p53 increased in MCF-7 cells treated with nobiletin.	nobiletin	109-118	P53	Homo sapiens	67-70
29665004-6	2018	Our initial studies suggested that mutant p53 degradation post THSP treatment was carried out by BAG3 mediated autophagy, based on the evidence of BAG1 to BAG3 switching.	thsp	63-67	P53	Homo sapiens	42-45
28830984-7	2018	However, ADT caused a significant radiosensitization that was more pronounced in a GBM cell model with p53 loss of function as compared with its p53-wildtype counterpart.	adt	9-12	P53	Homo sapiens	103-106
28830984-10	2018	Although the underlying mechanism is still ambiguous, the observation of ADT-induced radiosensitization is of great clinical interest, in particular for patients with GBM showing high radioresistance and/or p53 loss of function.	adt	73-76	P53	Homo sapiens	207-210
29493465-9	2018	RESULT: At the molecular level, we found that these cells treated with Riluzole had a decrease of Cyclin B and an increase of p21 Waf1/Cip1 and p53 expression.	Riluzole	71-79	P53	Homo sapiens	144-147
29665004-9	2018	Further, localization of p53 into the lysosome upon THSP treatment substantiated our findings that mutant p53 was degraded by an autopahgic process.	thsp	52-56	P53	Homo sapiens	25-28
29665004-9	2018	Further, localization of p53 into the lysosome upon THSP treatment substantiated our findings that mutant p53 was degraded by an autopahgic process.	thsp	52-56	P53	Homo sapiens	106-109
27871087-0	2018	The HDM2 (MDM2) Inhibitor NVP-CGM097 Inhibits Tumor Cell Proliferation and Shows Additive Effects with 5-Fluorouracil on the p53-p21-Rb-E2F1 Cascade in the p53wild type Neuroendocrine Tumor Cell Line GOT1.	NVP-CGM097	30-36	P53	Homo sapiens	156-159
28949066-1	2018	In previous work, we presented experimental and theoretical evidence that D-3F or 4-N-(2-Amino-3-fluoropyridine)-4-deoxidation-4"-demethylepipofophyllotoxin induced G2 /M phase arrest and apoptosis, purportedly by increasing the expression of P53.	d-3f	74-78	P53	Homo sapiens	243-246
29931256-0	2018	A molecular mechanism of nickel (II): reduction of nucleotide excision repair activity by structural and functional disruption of p53.	Nickel	25-31	P53	Homo sapiens	130-133
29078261-9	2017	Collectively, our data suggest that citral induced p53 and ROS-mediated mitochondrial-mediated apoptosis in human colorectal cancer HCT116 and HT29 cells.	citral	36-42	P53	Homo sapiens	51-54
29257079-8	2017	Consistently, sulfuretin decreased p53 expression and the Bax/Bcl-2 ratio.	sulfuretin	14-24	P53	Homo sapiens	35-38
29931256-3	2018	Here, we investigated whether low concentrations of nickel would affect p53-mediated DNA repair, especially nucleotide excision repair.	Nickel	52-58	P53	Homo sapiens	72-75
29931256-4	2018	Our results showed that nickel inhibited the promoter binding activity of p53 on the downstream gene GADD45A, as a result of the disturbance of p53 oligomerization by nickel.	Nickel	24-30	P53	Homo sapiens	74-77
29074359-5	2017	Further investigation on Cdc25C/CDK1/CyclinB1 signaling cascade in the absence or presence of pharmacological DDR inhibitors showed that xanthatin directly destabilized the protein levels of Cdc25C, and recovery of p53 expression in p53-deficient H1299 cells further intensified xanthatin-mediated inhibition of Cdc25C, suggesting p53-dependent regulation of Cdc25C in a DDR machinery.	xanthatin	137-146	P53	Homo sapiens	215-218
29089230-6	2017	Valine and phenylglycine ester derivatives were identified as potentially active MDM2-p53 inhibitors.	Valine	0-6	P53	Homo sapiens	86-89
29074359-5	2017	Further investigation on Cdc25C/CDK1/CyclinB1 signaling cascade in the absence or presence of pharmacological DDR inhibitors showed that xanthatin directly destabilized the protein levels of Cdc25C, and recovery of p53 expression in p53-deficient H1299 cells further intensified xanthatin-mediated inhibition of Cdc25C, suggesting p53-dependent regulation of Cdc25C in a DDR machinery.	xanthatin	137-146	P53	Homo sapiens	233-236
29931256-4	2018	Our results showed that nickel inhibited the promoter binding activity of p53 on the downstream gene GADD45A, as a result of the disturbance of p53 oligomerization by nickel.	Nickel	24-30	P53	Homo sapiens	144-147
29074359-5	2017	Further investigation on Cdc25C/CDK1/CyclinB1 signaling cascade in the absence or presence of pharmacological DDR inhibitors showed that xanthatin directly destabilized the protein levels of Cdc25C, and recovery of p53 expression in p53-deficient H1299 cells further intensified xanthatin-mediated inhibition of Cdc25C, suggesting p53-dependent regulation of Cdc25C in a DDR machinery.	xanthatin	137-146	P53	Homo sapiens	233-236
29931256-4	2018	Our results showed that nickel inhibited the promoter binding activity of p53 on the downstream gene GADD45A, as a result of the disturbance of p53 oligomerization by nickel.	Nickel	167-173	P53	Homo sapiens	74-77
29931256-4	2018	Our results showed that nickel inhibited the promoter binding activity of p53 on the downstream gene GADD45A, as a result of the disturbance of p53 oligomerization by nickel.	Nickel	167-173	P53	Homo sapiens	144-147
29372687-5	2017	Instead of this, we have shown that treatment of HT29 cells with SU9516 is associated with decreased expression of tumour suppressor protein p53.	SU 9516	65-71	P53	Homo sapiens	141-144
28913568-8	2017	Increased p21 via the p53-independent pathway in PL-treated CCA cells led to G2/M phase arrest and cell apoptosis.	piperlonguminine	49-51	P53	Homo sapiens	22-25
29931256-6	2018	These results imply that inhibition of p53-mediated DNA repair can be considered a potential carcinogenic mechanism of nickel at low concentrations.	Nickel	119-125	P53	Homo sapiens	39-42
30235848-0	2018	Chalcone Derivatives 4"-Amino-1-Naphthyl-Chalcone (D14) and 4"-Amino-4-Methyl-1-Naphthyl-Chalcone (D15) Suppress Migration and Invasion of Osteosarcoma Cells Mediated by p53 Regulating EMT-Related Genes.	D15	99-102	P53	Homo sapiens	170-173
28370377-0	2017	Analysis of apoptosis-associated molecules Erythroid differentiation regulator 1, bcl-2 and p53 in actinic keratosis after treatment with ingenol mebutate.	3-ingenyl angelate	138-154	P53	Homo sapiens	92-95
29712686-5	2018	Finally, the anti-HPV effect of FIT-039 was further examined in vivo, using HPV+ cervical cancer xenografts.Results: FIT-039 inhibits HPV replication and expression of E6 and E7 viral oncogenes, restoring tumor suppressors p53 and pRb in HPV+ cervical cancer cells.	FIT-039	117-124	P53	Homo sapiens	223-226
28370377-7	2017	The purpose of this study was to investigate whether the expression of apoptosis-associated molecules such as Erdr1, p53 and bcl-2 was affected by the treatment of ingenol mebutate in AK.	3-ingenyl angelate	164-180	P53	Homo sapiens	117-120
29073938-8	2017	Importantly, we found that p53 decreases the expression of MSI-2 through elevating miR-143/miR-107 levels, and treatment with a natural antibiotic Mithramycin A increased p53 and miR-143/miR-107 expression and reduced MSI-2 expression, resulting in the inhibition of CC cell proliferation, invasion and sphere formation.	mithramycin A	147-160	P53	Homo sapiens	171-174
29073938-9	2017	CONCLUSIONS: These results suggest that MSI-2 plays a crucial role in promoting the aggressive phenotypes of CC cells, and restoration of miR-143/miR-107 by Mithramycin A via activation of p53 may represent a novel therapeutic approach for CC.	mithramycin A	157-170	P53	Homo sapiens	189-192
28892665-6	2017	On the other hand, significantly greater GPBB immunoreactivity was observed in the basal and parabasal layers of iodine-unstained epithelium, where higher positivity for p53 and Ki67 was also showed.	Iodine	113-119	P53	Homo sapiens	170-173
28821555-3	2017	Moreover, p53 reactivation via RG7388, a second-generation MDM2 inhibitor, strongly enhances the in vivo antitumor activity of temsirolimus.	temsirolimus	127-139	P53	Homo sapiens	10-13
30181332-0	2018	Retraction: gamma-Tocotrienol Promotes TRAIL-Induced Apoptosis through Reactive Oxygen Species/Extracellular Signal-Regulated Kinase/p53-Mediated Upregulation of Death Receptors.	plastochromanol 8	12-29	P53	Homo sapiens	133-136
28901519-0	2017	Salidroside, a scavenger of ROS, enhances the radioprotective effect of Ex-RAD  via a p53-dependent apoptotic pathway.	rhodioloside	0-11	P53	Homo sapiens	86-89
28901519-4	2017	Sal downregulated the expression of Bax and p53 and increased the ratio of Bcl-2/Bax, which indicated that Sal inhibited the radiation-induced apoptosis through p53-dependent pathways.	rhodioloside	0-3	P53	Homo sapiens	44-47
28901519-4	2017	Sal downregulated the expression of Bax and p53 and increased the ratio of Bcl-2/Bax, which indicated that Sal inhibited the radiation-induced apoptosis through p53-dependent pathways.	rhodioloside	0-3	P53	Homo sapiens	161-164
28901519-4	2017	Sal downregulated the expression of Bax and p53 and increased the ratio of Bcl-2/Bax, which indicated that Sal inhibited the radiation-induced apoptosis through p53-dependent pathways.	rhodioloside	107-110	P53	Homo sapiens	44-47
28901519-4	2017	Sal downregulated the expression of Bax and p53 and increased the ratio of Bcl-2/Bax, which indicated that Sal inhibited the radiation-induced apoptosis through p53-dependent pathways.	rhodioloside	107-110	P53	Homo sapiens	161-164
28619518-0	2017	In vitro cytotoxic potential of friedelin in human MCF-7 breast cancer cell: Regulate early expression of Cdkn2a and pRb1, neutralize mdm2-p53 amalgamation and functional stabilization of p53.	friedelin	32-41	P53	Homo sapiens	139-142
28619518-0	2017	In vitro cytotoxic potential of friedelin in human MCF-7 breast cancer cell: Regulate early expression of Cdkn2a and pRb1, neutralize mdm2-p53 amalgamation and functional stabilization of p53.	friedelin	32-41	P53	Homo sapiens	188-191
28619518-8	2017	In conclusion, friedelin effectively inhibit breast cancer MCF-7 cell growth, it was associated with early expression of Cdkn1a, pRb2 and activation of p53 and caspases.	friedelin	15-24	P53	Homo sapiens	152-155
29096508-8	2017	In this particular case, ff15ipq-Qsolv increases stability in a number of alpha-helices, correctly obtaining 70% helical character in the K19 system at 275 K and showing appropriately diminishing content up to 325 K, but overestimating the helical fraction of AAQAA3 by 50% or more, forming long-lived alpha-helices in simulations of a beta-hairpin, and increasing the likelihood that the disordered p53 N-terminal peptide will also form a helix.	ff15ipq-qsolv	25-38	P53	Homo sapiens	400-403
28888100-5	2017	In contrast to their wt counterparts, the p53- or p21-deficient cells treated with SCH900776 and cisplatin or LA-12 enter mitosis and become polyploid, and the senescence phenotype is strongly suppressed.	UNII-37WM0V5E17	110-115	P53	Homo sapiens	42-45
30103421-7	2018	Therefore, our findings support a potential selective role of these structurally simplified, reversine-related molecules in p53-defective cancer cells.	2-(4-morpholinoanilino)-6-cyclohexylaminopurine	93-102	P53	Homo sapiens	124-127
28743509-7	2017	Further analysis of these compounds revealed that (E)-3-(4-chlorophenyl)-1-phenylprop-2-en-1-one (SSE14105) and (E)-3-(4-methoxyphenyl)-1-phenylprop-2-en-1-one (SSE14106) caused rapid (4 and 8-h post-treatment) accumulation of p53 in HCT116 cells similar to its induction by positive control, Nutlin-3.	4-Chlorochalcone	50-96	P53	Homo sapiens	227-230
28743509-8	2017	Such activities were absent in 3-(4-methoxyphenyl)propiophenone (SSE14106H2) demonstrating the importance of conjugated ketone for antiproliferative and p53 stabilizing activity of the chalcones.	Ketones	120-126	P53	Homo sapiens	153-156
28937626-4	2017	Aspalathin, a polyphenolic dihydrochalcone C-glucoside has been shown to activate AMPK while decreasing the expression of p53.	polyphenolic dihydrochalcone c-glucoside	14-54	P53	Homo sapiens	122-125
30045945-6	2018	The combination of ATSP-7041 with P5091, GSK2830371, and chemotherapeutic agents showed synergistic action on the p53 pathway.	ATSP-7041	19-28	P53	Homo sapiens	114-117
28576074-9	2017	Additional qRT-PCR data suggest that TiO2 nanostructures induced the upregulation of tumor suppressor genes p53, MDA7, TRAIL and transcription factor STAT3, which suggests the probable mechanism for the anticancer activity of TiO2 nanostructures.	titanium dioxide	37-41	P53	Homo sapiens	108-111
30013227-5	2018	We also found that the frequency of circulating tet+ CD8+ T cells negatively correlated with p53 expression in tumor tissues and tumor stage.	tet	48-51	P53	Homo sapiens	93-96
28576074-9	2017	Additional qRT-PCR data suggest that TiO2 nanostructures induced the upregulation of tumor suppressor genes p53, MDA7, TRAIL and transcription factor STAT3, which suggests the probable mechanism for the anticancer activity of TiO2 nanostructures.	titanium dioxide	226-230	P53	Homo sapiens	108-111
28714021-2	2017	We found that iodine-131 reduced cell proliferation, induced apoptosis, induced p53, PIDD, t-BID (mitochondria) protein expression, suppressed cytochrome c (mitochondria) protein expression, and increased Bax protein expression, and promoted caspase-2, -3 and -9 expression levels in human cardiac muscle cells.	Iodine	14-20	P53	Homo sapiens	80-83
28714021-3	2017	Meanwhile, si-p53 inhibited the effects of iodine-131 on the reduction in cell proliferation and induction of apoptosis in human cardiac muscle cells through regulation of Bax/cytochrome c/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway.	Iodine	43-49	P53	Homo sapiens	14-17
30090552-3	2017	TBP and TBEP could induce both mitochondrial and p53 mediated apoptosis through different mitogen-activated protein kinase (MAPK) signal pathways.	tris(2-butoxyethyl) phosphate	8-12	P53	Homo sapiens	49-52
28745887-0	2017	Phthalazino[1,2-b]quinazolinones as p53 Activators: Cell Cycle Arrest, Apoptotic Response and Bak-Bcl-xl Complex Reorganization in Bladder Cancer Cells.	phthalazino[1,2-b]quinazolinones	0-32	P53	Homo sapiens	36-39
28745887-2	2017	It is therefore highly desirable to develop anticancer agents by restoring p53 function.1 Herein the synthesized phthalazino[1,2-b]quinazolinones were discovered as p53 activators in bladder cancer cells.	phthalazino[1,2-b]quinazolinones	113-145	P53	Homo sapiens	75-78
28745887-2	2017	It is therefore highly desirable to develop anticancer agents by restoring p53 function.1 Herein the synthesized phthalazino[1,2-b]quinazolinones were discovered as p53 activators in bladder cancer cells.	phthalazino[1,2-b]quinazolinones	113-145	P53	Homo sapiens	165-168
28745887-6	2017	Molecular mechanism studies suggested that accumulation of phospho-p53 in mitochondria after 5da treatment resulted in conformational activation of Bak, thereby evoking cell apoptosis, finally leading to irreversible cancer cell inhibition.	1-[(4s)-4-(4-{4-[4-(5,5'-Dimethyl-2,4'-Bi-1,3-Oxazol-2'-Yl)-1,3-Thiazol-2-Yl]-5-Methyl-1,3-Oxazol-2-Yl}-1,3-Thiazol-2-Yl)-4-(Methylamino)butyl]guanidine	93-96	P53	Homo sapiens	67-70
28745887-7	2017	Our present studies furnish new insights into the molecular interactions and anticancer mechanisms of phospho-p53-dependent quinazolinone compound.	Quinazolinones	124-137	P53	Homo sapiens	110-113
30013227-6	2018	Our findings support further clinical-based investigations to define the frequencies and phenotypes of wt sequence p53 peptide-specific CD8+ T cells to predict disease severity, enhance selection of patients for inclusion in vaccination trials and highlight prerequisites to enhance immune susceptibility by activation of inactive naive tet+ T cells and/or enhancing circulating effector T cell activity by checkpoint blockage.	tet	337-340	P53	Homo sapiens	115-118
29635125-6	2018	In the present study, NOB selectively suppressed the growth and proliferation of human SKOV3/TAX cells, inducing G0/G1 phase arrest and reducing G2/M phase, along with the increase of p53 and p21.	nobiletin	22-25	P53	Homo sapiens	184-187
28785074-7	2017	In addition, treatment of PD98059 reversed low-dose arsenite-induced MDM2 expression, and the inhibition of ERK2 expression could significantly block MDM2 expression as a consequence, and p53 expression automatically was increased.	arsenite	52-60	P53	Homo sapiens	188-191
28785074-9	2017	Taken together, our results demonstrated that low-dose arsenite-induced resistance to apoptosis through p53 mediated by MDM2 in keratinocytes.	arsenite	55-63	P53	Homo sapiens	104-107
28597880-2	2017	In its active form p53 is a tetramer, with each monomer organised in domains with different degrees of structural stability, ranging from the well folded DNA-binding domain (DBD) and tetramerization domain (TET), to the intrinsically disordered transactivation domain (TAD), and extreme C-terminal domain (CTD).	tet	207-210	P53	Homo sapiens	19-22
28785074-0	2017	Low dose arsenite confers resistance to UV induced apoptosis via p53-MDM2 pathway in ketatinocytes.	arsenite	9-17	P53	Homo sapiens	65-68
28785074-4	2017	We found that the cell apoptosis induced by UV exposure was significantly attenuated after exposure to low-dose arsenite, and knockdown of p53 could block UV-induced apoptosis indicating that this phenomenon depended on p53.	arsenite	112-120	P53	Homo sapiens	139-142
28785074-4	2017	We found that the cell apoptosis induced by UV exposure was significantly attenuated after exposure to low-dose arsenite, and knockdown of p53 could block UV-induced apoptosis indicating that this phenomenon depended on p53.	arsenite	112-120	P53	Homo sapiens	220-223
28528452-4	2017	The relation of NIS and p53 in clinical samples was judged by TCGA data analysis and immunohistochemistry.	Nickel	16-19	P53	Homo sapiens	24-27
29874795-4	2018	The study demonstrated that luteoloside could inhibit proliferation remarkably; promote apoptosis and cytochrome C release; decrease the mitochondrial membrane potential and reactive oxygen species level; upregulate the expression of Fas, Bax, p53, phospho-p38, phospho-JNK, and cleaved PARP; downregulate the expression of Bcl-2 and phospho-mTOR; activate caspase-3 and caspase-8; change the nuclear morphology, and fragmentate DNA in Hela cells.	luteolin-7-glucoside	28-39	P53	Homo sapiens	244-247
28528452-5	2017	RESULTS: Overexpression of wild-type p53 as a transgene or pharmacological activation by doxorubicin drug treatment shows significant suppression of NIS transcription in multiple BC cell types which also results in lowered NIS protein content and cellular iodide intake.	Nickel	149-152	P53	Homo sapiens	37-40
28528452-5	2017	RESULTS: Overexpression of wild-type p53 as a transgene or pharmacological activation by doxorubicin drug treatment shows significant suppression of NIS transcription in multiple BC cell types which also results in lowered NIS protein content and cellular iodide intake.	Nickel	223-226	P53	Homo sapiens	37-40
28528452-6	2017	NIS repression by activated p53 is further confirmed by non-invasive bioluminescence imaging in live cell and orthotropic tumor model.	Nickel	0-3	P53	Homo sapiens	28-31
28528452-10	2017	CONCLUSION: Our data for the first time highlight the role of p53 as a negative regulator of functional NIS expression in BC, where the latter is a potential targeted radioiodine therapy candidate.	Nickel	104-107	P53	Homo sapiens	62-65
28835017-6	2017	Preceding these changes, a cariporide-induced p-AKT down-regulation, a p53 up-regulation, an ROS accumulation, and the depolarization of the mitochondrial-membrane potential were observed.	cariporide	27-37	P53	Homo sapiens	71-74
28781658-12	2017	The present study reports a case of a sudden acceleration of DTC metastatic progression following sorafenib discontinuation, which could have been due to the emergence of sorafenib-resistant undifferentiated p53-positive tumor cell clones.	dtc	61-64	P53	Homo sapiens	208-211
29874795-7	2018	Furthermore, the luteoloside-induced apoptosis in Hela cells is mediated by both intrinsic and extrinsic pathways and the effects of luteoloside may be regulated by the mitogen-activated protein kinases and mTOR signaling pathways via p53.	luteolin-7-glucoside	17-28	P53	Homo sapiens	235-238
28631436-9	2017	However, functional evaluation showed that only one of the analogs BL140 ubiquitously inhibited AKT phosphorylation in all CRPC cell lines tested with diverse genetic abnormalities including AR, PTEN, and p53 status.	bl140	67-72	P53	Homo sapiens	205-208
28223274-8	2017	In the olaparib LT group, 244 genetic alterations were detected, with TP53, BRCA1, and BRCA2 mutations being most common (90%, 25%, and 35%, respectively).	olaparib	7-15	P53	Homo sapiens	70-74
29874795-7	2018	Furthermore, the luteoloside-induced apoptosis in Hela cells is mediated by both intrinsic and extrinsic pathways and the effects of luteoloside may be regulated by the mitogen-activated protein kinases and mTOR signaling pathways via p53.	luteolin-7-glucoside	133-144	P53	Homo sapiens	235-238
29843366-4	2018	The major causes of excessive DSBs in H1299 cells are as follows: First, defect of p53-p21 signal and phosphorylation of SMC1 increase S phase cells, where replication of DNA containing single-strand DNA break (SSB) produces more DSBs in H1299 cells.	dsbs	30-34	P53	Homo sapiens	83-86
28536076-0	2017	Polyarginine and its analogues inhibit p53 mutant aggregation and cancer cell proliferation in vitro.	polyarginine	0-12	P53	Homo sapiens	39-42
28536076-6	2017	Here in this study we focus on the inhibitory effects of polyarginine and its analogues polyornithine, canavanine, and citrulline on the inhibition of p53 mutant peptide aggregation, and p53 mutant cancer cell proliferation inhibition in vitro.	polyarginine	57-69	P53	Homo sapiens	151-154
28536076-6	2017	Here in this study we focus on the inhibitory effects of polyarginine and its analogues polyornithine, canavanine, and citrulline on the inhibition of p53 mutant peptide aggregation, and p53 mutant cancer cell proliferation inhibition in vitro.	polyarginine	57-69	P53	Homo sapiens	187-190
28536076-8	2017	The results show that polyarginine, and polyornithine, in micromolar concentrations, significantly inhibits p53 conserved peptide aggregation, and the cell proliferation of p53 mutant cancer cells.	polyarginine	22-34	P53	Homo sapiens	108-111
28536076-8	2017	The results show that polyarginine, and polyornithine, in micromolar concentrations, significantly inhibits p53 conserved peptide aggregation, and the cell proliferation of p53 mutant cancer cells.	polyarginine	22-34	P53	Homo sapiens	173-176
28790851-13	2017	It exerted anticancer effects through targeting the expression of DEGs, such as HSPA6, APCDD1, TP53, and JUN, and affecting the signaling pathways including apoptosis and cell cycle pathway, which demonstrated the promising potential of ixazomib for CRC therapy.	ixazomib	237-245	P53	Homo sapiens	95-99
28705212-13	2017	Finally, MAC was found to trigger apoptotic death pathway (based on expression levels of cleaved-caspase 3, Bax/Bcl-2 balance, p53 and p21).	mac	9-12	P53	Homo sapiens	127-130
29789497-9	2018	Recent studies using polyarginine analogues and designer peptides for inhibiting p53 aggregation and tumor growth gives further encouragement in treating cancer as a protein aggregation disease.	polyarginine	21-33	P53	Homo sapiens	81-84
28190297-0	2017	Elevated PRC1 in gastric carcinoma exerts oncogenic function and is targeted by piperlongumine in a p53-dependent manner.	piperlonguminine	80-94	P53	Homo sapiens	100-103
28320780-0	2017	Thiosemicarbazones Functioning as Zinc Metallochaperones to Reactivate Mutant p53.	zinc metallochaperones	34-56	P53	Homo sapiens	78-81
28405933-0	2017	Detection of p53 Gene Mutation (Single-Base Mismatch) Using a Fluorescent Silver Nanoclusters.	Silver	74-80	P53	Homo sapiens	13-16
29609003-0	2018	Fluoride induces apoptosis via inhibiting SIRT1 activity to activate mitochondrial p53 pathway in human neuroblastoma SH-SY5Y cells.	Fluorides	0-8	P53	Homo sapiens	83-86
28320780-2	2017	We previously discovered that small-molecule zinc chelators called zinc metallochaperones (ZMCs) reactivate mutant p53 by restoring zinc binding to zinc-deficient p53 mutants.	zinc metallochaperones	67-89	P53	Homo sapiens	115-118
28320780-2	2017	We previously discovered that small-molecule zinc chelators called zinc metallochaperones (ZMCs) reactivate mutant p53 by restoring zinc binding to zinc-deficient p53 mutants.	zinc metallochaperones	67-89	P53	Homo sapiens	163-166
29609003-6	2018	Meanwhile, fluoride increased p53 nuclear translocation, cyto c release from mitochondria to cytoplasm and mitochondrial translocation of Bax in SH-SY5Y cells.	Fluorides	11-19	P53	Homo sapiens	30-33
29609003-7	2018	Fluoride-induced increases of apoptotic rates and apoptosis-related protein levels were significantly attenuated by inhibiting p53 transcriptional activity with pifithrin-alpha.	Fluorides	0-8	P53	Homo sapiens	127-130
29997966-0	2018	TP53 mutations predict for poor survival in ALK rearrangement lung adenocarcinoma patients treated with crizotinib.	Crizotinib	104-114	P53	Homo sapiens	0-4
28440512-0	2017	Astemizole protects against human umbilical vein endothelial cell injury induced by hydrogen peroxide via the p53 signaling pathway.	Astemizole	0-10	P53	Homo sapiens	110-113
28440512-5	2017	Additionally, the protein expression of p53, p21Cip1/Waf1 and p16INK4a was measured by western blot analysis The results demonstrated that astemizole (0.5-1 microM) was able to significantly restore the viability of HUVECs under oxidative stress and scavenge intracellular ROS induced by H2O2.	Astemizole	139-149	P53	Homo sapiens	40-43
28440512-7	2017	In addition, astemizole significantly increased p53, p21Cip1/Waf1 and p16INK4a protein expression.	Astemizole	13-23	P53	Homo sapiens	48-51
28440512-8	2017	In conclusion, astemizole effectively protected endothelial cells against oxidative stress induced by H2O2, a function that may involve ROS/p53/p21Cip1/Waf1/ p16INK4a signaling pathways.	Astemizole	15-25	P53	Homo sapiens	140-143
28808400-12	2017	FKC induced cell cycle arrest at the G1 and G2/M phases via upregulation of p21 and p27 in a p53-independent manner.	flavokawain C	0-3	P53	Homo sapiens	93-96
28718371-11	2017	These results demonstrated that the messenger RNA expression levels of p53 and p21 may have a relationship with the changes in telomere length induced by omethoate and provided strong evidence for the mechanism of canceration induced by poison.	dimethoxon	154-163	P53	Homo sapiens	71-74
29997966-2	2018	We analyze the impact of TP53 mutations on response to crizotinib in patients with ALK rearrangement NSCLC.	Crizotinib	55-65	P53	Homo sapiens	25-29
29997966-10	2018	Conclusions: TP53 mutations reduce responsiveness to crizotinib and worsen prognosis in ALK rearrangement NSCLC patients.	Crizotinib	53-63	P53	Homo sapiens	13-17
28469202-5	2017	The TBP-p53Tet peptide caps the surface of the silver crystals, which enhances crystal growth on specific faces and thereby regulates silver nanostructure formation in a catalytic fashion.	Silver	47-53	P53	Homo sapiens	8-11
29565448-3	2018	Our previous study revealed that kaempferol triggered apoptosis in human umbilical vein endothelial cells (HUVECs) by ROS-mediated p53/ATM/death receptor signaling.	kaempferol	33-43	P53	Homo sapiens	131-134
28469202-5	2017	The TBP-p53Tet peptide caps the surface of the silver crystals, which enhances crystal growth on specific faces and thereby regulates silver nanostructure formation in a catalytic fashion.	Silver	134-140	P53	Homo sapiens	8-11
28112451-3	2017	Although EBR has been shown to affect survival and mitochondria-mediated apoptosis pathways in a p53-independent manner, the exact molecular targets of EBR are still under investigation.	EBR	9-12	P53	Homo sapiens	97-100
29634060-4	2018	The cellular mechanism of action studies show that the most effective cobalt(ii) complex, 2, enters U2OS cells, penetrates the nucleus, induces genomic DNA damage, and triggers caspase-dependent apoptosis in a p53-independent manner.	Cobalt(2+)	70-80	P53	Homo sapiens	210-213
29955707-8	2017	Tumor suppressor p53 (p53), mitochondrial transcription factor A (TFAM), and cytochrome c oxidase subunit IV (COXIV) expression was greater for CON than for CHO+EAA treatments (drink main effect, P &lt; 0.05).	CAV protocol	157-160	P53	Homo sapiens	17-20
29955707-8	2017	Tumor suppressor p53 (p53), mitochondrial transcription factor A (TFAM), and cytochrome c oxidase subunit IV (COXIV) expression was greater for CON than for CHO+EAA treatments (drink main effect, P &lt; 0.05).	CAV protocol	157-160	P53	Homo sapiens	22-25
28324749-11	2017	Treatment with SAR405838 was associated with increased plasma MIC-1, reflecting p53 pathway activation.	SAR405838	15-24	P53	Homo sapiens	80-83
29508534-1	2018	The total synthesis of siladenoserinol A, an inhibitor of the p53-Hdm2 interaction, has been achieved.	siladenoserinol a	23-40	P53	Homo sapiens	62-65
28529565-9	2017	These observations demonstrate that p53 is a mediator of OPA and PPA-induced apoptosis in OVCAR-3 cells.	ppa	65-68	P53	Homo sapiens	36-39
28182994-7	2017	Moreover, HCT116 cells are sensitive to olaparib in combination with the ATM inhibitor KU55933, and sensitivity is enhanced by deletion of p53.	olaparib	40-48	P53	Homo sapiens	139-142
28496125-6	2017	These hurdles were overcome by successfully identifying a pyridinium-based cationic lipid formulation, which significantly improved the activity of the stapled peptide in a p53 reporter cell line, principally through increased vesicular escape.	pyridine	58-68	P53	Homo sapiens	173-176
29719590-9	2018	2HF activated TP53 and inhibited TGFbeta1 canonical pathway in MCF7 and MDA-MB-231 BC cells.	2'-hydroxyflavanone	0-3	P53	Homo sapiens	14-18
28415717-4	2017	For the first time we demonstrate that the tumor suppressor, p53 plays a key role in cell fate determination after C-1311 treatment.	C 1311	115-121	P53	Homo sapiens	61-64
28415717-7	2017	C-1311 also induced autophagy in a non-p53-dependent manner.	C 1311	0-6	P53	Homo sapiens	39-42
28415717-8	2017	Cells in hypoxic conditions also responded to C-1311 in a p53-dependent manner, suggesting that our observations are physiologically relevant.	C 1311	46-52	P53	Homo sapiens	58-61
28069876-7	2017	In BRCA1 wild-type C4-2 cells, Plk1 inhibition also significantly increases the efficacy of olaparib in the presence of p53 inhibitor.	olaparib	92-100	P53	Homo sapiens	120-123
28280360-11	2017	Taken together, these results demonstrate the p53-targeting therapeutic potential of bufadienolides against ESCC.	Bufanolides	85-99	P53	Homo sapiens	46-49
29719590-10	2018	2HF also regulated the expression of a number of critical prognostic genes of MammaPrint panel and their upstream targets including TP53, CDKN2A and MYC.	2'-hydroxyflavanone	0-3	P53	Homo sapiens	132-136
29491062-0	2018	Galangin Induces p53-independent S-phase Arrest and Apoptosis in Human Nasopharyngeal Carcinoma Cells Through Inhibiting PI3K-AKT Signaling Pathway.	galangin	0-8	P53	Homo sapiens	17-20
27998772-7	2017	p53 was induced after CIZAR treatment and p53-dependent apoptosis did not occur after knock down by p53 siRNA.	cizar	22-27	P53	Homo sapiens	0-3
27998772-8	2017	In cervical carcinoma cells, regardless of HPV-infection, CIZAR induces apoptosis by the activation of the p53-independent pathways through the up-regulation of p21waf1, the down-regulation of c-Myc, and by decreasing the Bcl-2/Bax ratio.	cizar	58-63	P53	Homo sapiens	107-110
27998772-9	2017	CONCLUSIONS: CIZAR induces apoptosis not only through the restoration of p53/Rb-dependent pathways in HPV-positive cells, but also through the activation of p53/Rb-independent pathways and the mitochondrial death-signal pathway in cervical carcinoma cells regardless of HPV-infection.	cizar	13-18	P53	Homo sapiens	73-76
28504908-1	2017	and Triana Fruit Extract Induces Cell Death in the Human Colon Cancer Cell Line, SW480, via Mitochondria-Related Apoptosis and Activation of p53.	triana fruit	4-16	P53	Homo sapiens	141-144
28361937-3	2017	We then established that the two p53 isoforms exerted opposite effects on regulating NF-kappaB induced antimicrobial peptides (AMPs) and white spot syndrome virus (WSSV) immediate-early (IE) genes expression, suggesting there could be a crosstalk between p53 and NF-kappaB pathways.	Adenylyl sulfate	127-131	P53	Homo sapiens	33-36
29491062-8	2018	CONCLUSION: Galangin effects on apoptosis and S-phase arrest in NPC cells are mediated via interfering with the PI3K-AKT signaling pathway in a p53-independent manner.	galangin	12-20	P53	Homo sapiens	144-147
27345397-5	2017	Mitochondrial dysfunction induced by mitochondrial ionophore, carbonyl cyanide m-chlorophenyl hydrazone and other respiratory inhibitors, which perturb the transmembrane potential, were equally efficient in inducing the expression of p53 and downregulation of MDM2.	Carbonyl Cyanide m-Chlorophenyl Hydrazone	62-103	P53	Homo sapiens	234-237
28102315-3	2017	Here we describe the first restriction-enzyme-assisted LC-MS/MS sequencing study of the influence of methyl cytosines (MeC) on kinetics of p53 gene adduction by model metabolite benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE), using methodology applicable to correlate gene damage sites for drug and pollutant metabolites with mutation sites.	mec	119-122	P53	Homo sapiens	139-142
29126924-1	2018	INTRODUCTION: p53R2 is a p53-inducible protein that contributes to DNA repair by providing dNTPs in response to DNA damage.	Parathion	91-96	P53	Homo sapiens	14-17
28102324-7	2017	Additionally, we examined the SDT-induced cell apoptosis in two cell lines with different p53 status.	3,4-Dihydroxy-9,10-secoandrosta-1,3,5(10)-triene-9,17-dione	30-33	P53	Homo sapiens	90-93
28102324-8	2017	The increases of p53 expression and apoptosis rate in wild-type p53 SAS cells were found in the SDT group, while p53-mutated HSC-3 cells did not show such increase.	3,4-Dihydroxy-9,10-secoandrosta-1,3,5(10)-triene-9,17-dione	96-99	P53	Homo sapiens	17-20
28102324-8	2017	The increases of p53 expression and apoptosis rate in wild-type p53 SAS cells were found in the SDT group, while p53-mutated HSC-3 cells did not show such increase.	3,4-Dihydroxy-9,10-secoandrosta-1,3,5(10)-triene-9,17-dione	96-99	P53	Homo sapiens	64-67
28102324-8	2017	The increases of p53 expression and apoptosis rate in wild-type p53 SAS cells were found in the SDT group, while p53-mutated HSC-3 cells did not show such increase.	3,4-Dihydroxy-9,10-secoandrosta-1,3,5(10)-triene-9,17-dione	96-99	P53	Homo sapiens	64-67
28068628-0	2017	Epoxy clerodane diterpene inhibits MCF-7 human breast cancer cell growth by regulating the expression of the functional apoptotic genes Cdkn2A, Rb1, mdm2 and p53.	epoxy clerodane	0-15	P53	Homo sapiens	158-161
29063134-8	2018	In addition, PFOS exposure increased CDK4 and decreased p27, p21, and p53 levels in the cells.	perfluorooctane sulfonic acid	13-17	P53	Homo sapiens	70-73
28338113-10	2017	Similarly, the expression level of p53 was significant decreased in HepG2 lines treated with lidocaine as compared with control and LX2 (p = 0.0241).	Lidocaine	93-102	P53	Homo sapiens	35-38
27998772-9	2017	CONCLUSIONS: CIZAR induces apoptosis not only through the restoration of p53/Rb-dependent pathways in HPV-positive cells, but also through the activation of p53/Rb-independent pathways and the mitochondrial death-signal pathway in cervical carcinoma cells regardless of HPV-infection.	cizar	13-18	P53	Homo sapiens	157-160
28163043-2	2017	Here, we tested the effects of a single extra-copy of p53 on the function of CPCs in the presence of oxidative stress mediated by doxorubicin in vitro and type-1 diabetes in vivo.	cpcs	77-81	P53	Homo sapiens	54-57
27717875-10	2017	Further studies indicated that TMP promoted the expression of P53 through a YAP inhibition-dependent mechanism.	tetramethylpyrazine	31-34	P53	Homo sapiens	62-65
28004113-0	2017	Suberoyl bis-hydroxamic acid activates Notch1 signaling and induces apoptosis in anaplastic thyroid carcinoma through p53.	suberoyl bis-hydroxamic acid	0-28	P53	Homo sapiens	118-121
29434780-0	2018	Berbamine induces SMMC-7721 cell apoptosis via upregulating p53, downregulating survivin expression and activating mitochondria signaling pathway.	berbamine	0-9	P53	Homo sapiens	60-63
28004113-3	2017	Interesting, suberoyl bis-hydroxamic acid (SBHA) administration could induce Notch1 intracellular domain levels in a dose-dependent manner, coupled with the increase of p53 and p21.	suberoyl bis-hydroxamic acid	13-41	P53	Homo sapiens	169-172
28004113-3	2017	Interesting, suberoyl bis-hydroxamic acid (SBHA) administration could induce Notch1 intracellular domain levels in a dose-dependent manner, coupled with the increase of p53 and p21.	suberoyl bis-hydroxamic acid	43-47	P53	Homo sapiens	169-172
28004113-4	2017	Furthermore, ectopic expression of Notch1 or deletion of p53 with small-interfering RNA was able to abolish the effects of SBHA to elevation of Notch1 and p53 in ATC cells.	suberoyl bis-hydroxamic acid	123-127	P53	Homo sapiens	57-60
28004113-4	2017	Furthermore, ectopic expression of Notch1 or deletion of p53 with small-interfering RNA was able to abolish the effects of SBHA to elevation of Notch1 and p53 in ATC cells.	suberoyl bis-hydroxamic acid	123-127	P53	Homo sapiens	155-158
28004113-6	2017	These results indicate that SBHA may play antitumor functions via regulating Notch1/p53 signals, and highlight that SBHA could have clinical potential to benefit the therapy of ATC patients.	suberoyl bis-hydroxamic acid	28-32	P53	Homo sapiens	84-87
27764791-0	2016	Novel MDM2 inhibitor SAR405838 (MI-773) induces p53-mediated apoptosis in neuroblastoma.	SAR405838	21-30	P53	Homo sapiens	48-51
27764791-0	2016	Novel MDM2 inhibitor SAR405838 (MI-773) induces p53-mediated apoptosis in neuroblastoma.	SAR405838	32-38	P53	Homo sapiens	48-51
28163043-5	2017	With doxorubicin, a larger fraction of CPCs carrying an extra-copy of the p53 allele recruited gammaH2A.X reestablishing DNA integrity.	cpcs	39-43	P53	Homo sapiens	74-77
27380217-5	2017	The top two compounds, DTOM (ZINC 28639308) and TTOM (ZINC 38143676) with Glide score of -12.27 and -12.16, respectively, were identified with the potential to abrogate mortalin-p53 interaction.	dtom	23-27	P53	Homo sapiens	178-181
27717875-8	2017	We further demonstrated that P53 siRNA or P53 pharmacological inhibitor PFT-alpha abrogated the TMP-induced HSC senescence in vitro.	tetramethylpyrazine	96-99	P53	Homo sapiens	29-32
27717875-8	2017	We further demonstrated that P53 siRNA or P53 pharmacological inhibitor PFT-alpha abrogated the TMP-induced HSC senescence in vitro.	tetramethylpyrazine	96-99	P53	Homo sapiens	42-45
29434780-12	2018	Berbamine (10, 20, 40 micromol/l) significantly enhanced Bax and p53 levels and decreased Bcl-2 and survivin levels compared with control group, according to RT-sqPCR and western blot assay findings.	berbamine	0-9	P53	Homo sapiens	65-68
28232952-11	2017	To target the mutant p53- poly ADP-ribose polymerase-minichromosome maintenance axis we treated cells with the poly ADP-ribose polymerase inhibitor talazoparib and the alkylating agent temozolomide and detected synergistic activation of apoptosis only in the presence of mutant p53.	talazoparib	148-159	P53	Homo sapiens	21-24
28232952-11	2017	To target the mutant p53- poly ADP-ribose polymerase-minichromosome maintenance axis we treated cells with the poly ADP-ribose polymerase inhibitor talazoparib and the alkylating agent temozolomide and detected synergistic activation of apoptosis only in the presence of mutant p53.	talazoparib	148-159	P53	Homo sapiens	278-281
27765850-6	2016	This study provides a preclinical rationale for evaluation of MI-77301 or other MDM2 inhibitors as a new therapeutic strategy for the treatment of endocrine-resistant breast cancer retaining wild-type p53.	SAR405838	62-70	P53	Homo sapiens	201-204
29434780-13	2018	In conclusion, berbamine induced SMMC-7721 cell apoptosis, through upregulating p53 expression and downregulating survivin expression, which further triggered mitochondria signaling pathway-mediated apoptosis.	berbamine	15-24	P53	Homo sapiens	80-83
29434851-0	2018	Bufadienolides induce p53-mediated apoptosis in esophageal squamous cell carcinoma cells in vitro and in vivo.	Bufanolides	0-14	P53	Homo sapiens	22-25
28002389-0	2016	Transglutaminase 2 Inhibitor KCC009 Induces p53-Independent Radiosensitization in Lung Adenocarcinoma Cells.	KCC 009	29-35	P53	Homo sapiens	44-47
27822577-2	2016	Then we found that the tumor-suppressing effect of BTZ or HMSNs-BTZ was compromised in p53 null/mutant NSCLC.	hmsns-btz	58-67	P53	Homo sapiens	87-90
27822577-7	2016	Live/dead staining assay for treated H1299 cells exhibited wider distribution, and higher dead staining was prominent in the HMSNs-PEI-BTZ-p53 group when compared to that of the HMSNs-BTZ group with equivalent BTZ concentration, which was consistent with accumulated p53 expression.	-pei	130-134	P53	Homo sapiens	139-142
27686740-0	2016	Efficacy of poly (ADP-ribose) polymerase inhibitor olaparib against head and neck cancer cells: Predictions of drug sensitivity based on PAR-p53-NF-kappaB interactions.	olaparib	51-59	P53	Homo sapiens	141-144
29434851-7	2018	In addition, treatment of ESCC cells with bufotalin markedly activated tumor protein p53 (p53) phosphorylation.	bufotalin	42-51	P53	Homo sapiens	85-88
27686740-10	2016	As interference with p53 expression led to NF-kappaB reactivation, we concluded that elevated basal PAR and NF-kappaB levels are predictive of olaparib responsiveness in HNC cells; in addition, olaparib inhibits HNC cells via PAR-p53-NF-kappaB interactions.	olaparib	143-151	P53	Homo sapiens	21-24
27686740-10	2016	As interference with p53 expression led to NF-kappaB reactivation, we concluded that elevated basal PAR and NF-kappaB levels are predictive of olaparib responsiveness in HNC cells; in addition, olaparib inhibits HNC cells via PAR-p53-NF-kappaB interactions.	olaparib	194-202	P53	Homo sapiens	21-24
27822577-7	2016	Live/dead staining assay for treated H1299 cells exhibited wider distribution, and higher dead staining was prominent in the HMSNs-PEI-BTZ-p53 group when compared to that of the HMSNs-BTZ group with equivalent BTZ concentration, which was consistent with accumulated p53 expression.	-pei	130-134	P53	Homo sapiens	267-270
27686740-10	2016	As interference with p53 expression led to NF-kappaB reactivation, we concluded that elevated basal PAR and NF-kappaB levels are predictive of olaparib responsiveness in HNC cells; in addition, olaparib inhibits HNC cells via PAR-p53-NF-kappaB interactions.	olaparib	194-202	P53	Homo sapiens	230-233
29434851-7	2018	In addition, treatment of ESCC cells with bufotalin markedly activated tumor protein p53 (p53) phosphorylation.	bufotalin	42-51	P53	Homo sapiens	90-93
29434851-8	2018	Transfection of cells with p53 small interfering RNA markedly inhibited bufotalin-induced p53 phosphorylation and significantly inhibited bufotalin-induced cell apoptosis.	bufotalin	72-81	P53	Homo sapiens	27-30
27997533-5	2016	Patient-specific TP53 assays were developed for 31 unique mutations identified in formalin-fixed paraffin-embedded tumour DNA from these patients.	Formaldehyde	82-90	P53	Homo sapiens	17-21
29434851-8	2018	Transfection of cells with p53 small interfering RNA markedly inhibited bufotalin-induced p53 phosphorylation and significantly inhibited bufotalin-induced cell apoptosis.	bufotalin	72-81	P53	Homo sapiens	90-93
27764791-6	2016	SAR405838 caused significantly decreased cell viability of p53 wild-type NB cells and induced p53-mediated apoptosis, as well as augmenting the cytotoxic effects of doxorubicin (Dox).	SAR405838	0-9	P53	Homo sapiens	59-62
27764791-6	2016	SAR405838 caused significantly decreased cell viability of p53 wild-type NB cells and induced p53-mediated apoptosis, as well as augmenting the cytotoxic effects of doxorubicin (Dox).	SAR405838	0-9	P53	Homo sapiens	94-97
27473386-6	2016	Apigenin attenuated the proteasome inhibitors (MG132 and MG115)-induced decrease in the levels of Bid and Bcl-2, increase in the levels of Bax and p53, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), cleavage of PARP-1 and cell death in both cell lines.	carbobenzoxy-leucyl-leucyl-norvalinal	57-62	P53	Homo sapiens	147-150
27764791-8	2016	In summary, our data strongly suggest that MDM2-specific inhibitors like SAR405838 may serve not only as a stand-alone therapy, but also as an effective adjunct to current chemotherapeutic regimens for treating NB with an intact MDM2-p53 axis.	SAR405838	73-82	P53	Homo sapiens	234-237
29434851-8	2018	Transfection of cells with p53 small interfering RNA markedly inhibited bufotalin-induced p53 phosphorylation and significantly inhibited bufotalin-induced cell apoptosis.	bufotalin	138-147	P53	Homo sapiens	27-30
27705786-2	2016	Here, we have identified an acetylation site at lysine K98 in mouse p53 (or K101 for human p53).	THIAMINE HYDROCHLORIDE	76-80	P53	Homo sapiens	91-94
27229883-8	2016	These data provide the first evidence that beta-Ecd protects SH-SY5Y cells against 6-OHDA-induced apoptosis, possibly through mitochondria protection and p53 modulation via ROS-dependent ASK1-p38(MAPK) pathways.	Oxidopamine	83-89	P53	Homo sapiens	154-157
27994550-9	2016	The real time PCR assay demonstrated that TB down-regulated the expression of TOPO I, TOPO II, and BCL-2, and up-regulated the expression of E2F1, P53, GADD45, BAX, BIM, and CASP 3,7,8,9, which suggests an activation of P53-mediated apoptotic (caspase-dependent) pathway in response to TB treatment.	theabrownin	42-44	P53	Homo sapiens	147-150
29434851-10	2018	Collectively, the results from the present study suggested that bufadienolides exert anticancer effects against ESCC by regulating the p53 signaling pathway.	Bufanolides	64-78	P53	Homo sapiens	135-138
27871087-0	2018	The HDM2 (MDM2) Inhibitor NVP-CGM097 Inhibits Tumor Cell Proliferation and Shows Additive Effects with 5-Fluorouracil on the p53-p21-Rb-E2F1 Cascade in the p53wild type Neuroendocrine Tumor Cell Line GOT1.	NVP-CGM097	30-36	P53	Homo sapiens	125-128
27693458-0	2016	2-Methoxy-5((3,4,5-trimethosyphenyl)seleninyl) phenol inhibits MDM2 and induces apoptosis in breast cancer cells through a p53-independent pathway.	2-methoxy-5-((3,4,5-trimethosyphenyl)seleninyl)phenol	0-53	P53	Homo sapiens	123-126
27339904-0	2016	Combined treatment with vitamin C and sulindac synergistically induces p53- and ROS-dependent apoptosis in human colon cancer cells.	Ascorbic Acid	24-33	P53	Homo sapiens	71-74
29078261-0	2017	Antiproliferative and apoptosis inducing effects of citral via p53 and ROS-induced mitochondrial-mediated apoptosis in human colorectal HCT116 and HT29 cell lines.	citral	52-58	P53	Homo sapiens	63-66
27339904-0	2016	Combined treatment with vitamin C and sulindac synergistically induces p53- and ROS-dependent apoptosis in human colon cancer cells.	Sulindac	38-46	P53	Homo sapiens	71-74
27339904-8	2016	Taken together, our results demonstrate that combination therapy with sulindac and vitamin C could be a novel anti-cancer therapeutic strategy for p53 wild type colon cancers.	Sulindac	70-78	P53	Homo sapiens	147-150
27339904-8	2016	Taken together, our results demonstrate that combination therapy with sulindac and vitamin C could be a novel anti-cancer therapeutic strategy for p53 wild type colon cancers.	Ascorbic Acid	83-92	P53	Homo sapiens	147-150
27074052-7	2016	Diclofenac treatment was associated with increased activity of caspases 3, 7, and 8 and induction of p53 transcriptional target genes.	Diclofenac	0-10	P53	Homo sapiens	101-104
29078261-8	2017	Citral induced the phosphorylation of p53 protein and the expression of Bax while decreasing Bc-2 and Bcl-xL expression which promoted the cleavage of caspase-3.	citral	0-6	P53	Homo sapiens	38-41
28743575-6	2017	Similarly transfection studies carried out with p53 plasmid also revealed that PPI derivatives promote more apoptosis in both C6 and HeLa cell lines as compared to that of DPI derivatives.	ppi	79-82	P53	Homo sapiens	48-51
27832134-0	2016	Comparison of the QuantiGene 2.0 Assay and Real-Time RT-PCR in the Detection of p53 Isoform mRNA Expression in Formalin-Fixed Paraffin-Embedded Tissues- A Preliminary Study.	Formaldehyde	111-119	P53	Homo sapiens	80-83
27584794-0	2016	Nuclear translocation of annexin 1 following oxygen-glucose deprivation-reperfusion induces apoptosis by regulating Bid expression via p53 binding.	oxygen-glucose	45-59	P53	Homo sapiens	135-138
27832134-4	2016	However, there are serious limitations when detecting p53 isoforms using this method, particularly for formalin-fixed paraffin-embedded (FFPE) tissues.	Formaldehyde	103-111	P53	Homo sapiens	54-57
28270077-0	2017	Combined Treatment with CCI779 and SB203580 Induces Cellular Senescence in Renal Cell Carcinoma Cell Line via p53 Pathway.	temsirolimus	24-30	P53	Homo sapiens	110-113
27853385-3	2016	In particular, ultraviolet B radiation causes direct damage to the DNA, producing pyrimidine dimers that suppress the protective role of p53.	pyrimidine	82-92	P53	Homo sapiens	137-140
27414741-0	2016	ROS-mediated apoptosis of HAPI microglia through p53 signaling following PFOS exposure.	perfluorooctane sulfonic acid	73-77	P53	Homo sapiens	49-52
27414741-4	2016	The results showed that PFOS could significantly reduce the cell viability and mediate cell apoptosis in HAPI microglia, which was closely accompanied with ROS production and p53 overexpression.	perfluorooctane sulfonic acid	24-28	P53	Homo sapiens	175-178
27414741-5	2016	Moreover, p53 interference significantly ameliorated PFOS-triggered cytotoxic effects in HAPI microglia, including the downregulation of cleaved PARP and cleaved caspase 3.	perfluorooctane sulfonic acid	53-57	P53	Homo sapiens	10-13
27414741-7	2016	Taken together, these findings suggest that upregulated production of ROS plays a vital role in PFOS-mediated apoptosis in HAPI microglia via the modulation of p53 signaling.	perfluorooctane sulfonic acid	96-100	P53	Homo sapiens	160-163
27236003-12	2016	Concurrently, honokiol-induced alterations in levels of p-p53, p53, p-Akt, and p-mTOR were attenuated following vitamin C administration.	Ascorbic Acid	112-121	P53	Homo sapiens	58-61
29036263-0	2017	Effects of 12C6+ heavy ion beam irradiation on the p53 signaling pathway in HepG2 liver cancer cells.	12c6	11-15	P53	Homo sapiens	51-54
27236003-12	2016	Concurrently, honokiol-induced alterations in levels of p-p53, p53, p-Akt, and p-mTOR were attenuated following vitamin C administration.	Ascorbic Acid	112-121	P53	Homo sapiens	63-66
27453171-12	2016	Furthermore, thioridazine and irradiation treatment inhibited the PI3K-AKT-mTOR pathway and up-regulated the expression of p53.	Thioridazine	13-25	P53	Homo sapiens	123-126
27640744-5	2016	In ZR-75-1 cells, cytochalasin B triggered G2/M phase arrest through the modulation of CDK1, cyclin B1, p53, p27 and p21 expressions.	Cytochalasin B	18-32	P53	Homo sapiens	104-107
27462923-0	2016	Delphinidin induces apoptosis via cleaved HDAC3-mediated p53 acetylation and oligomerization in prostate cancer cells.	delphinidin	0-11	P53	Homo sapiens	57-60
27462923-4	2016	We found that treatment of LNCaP cells (a p53 wild-type, human prostate cancer cell line) with delphinidin increased caspase-3, -7, and -8 activity, whereas it decreased histone deacetylase activity.	delphinidin	95-106	P53	Homo sapiens	42-45
28370377-10	2017	Upregulation of Erdr1 and a significant decrease in expression of p53 and bcl-2 were observed after treatment with ingenol mebutate.	3-ingenyl angelate	115-131	P53	Homo sapiens	66-69
27462923-6	2016	Moreover, the induction of apoptosis by delphinidin was dependent on caspase-mediated cleavage of HDAC3, which results in the acetylation and stabilization of p53.	delphinidin	40-51	P53	Homo sapiens	159-162
27462923-7	2016	We also observed that delphinidin potently upregulated pro-apoptotic genes that are positively regulated by p53, and downregulated various anti-apoptotic genes.	delphinidin	22-33	P53	Homo sapiens	108-111
27462923-8	2016	Taken together, these results show that delphinidin induces p53-mediated apoptosis by suppressing HDAC activity and activating p53 acetylation in human prostate cancer LNCaP cells.	delphinidin	40-51	P53	Homo sapiens	60-63
28370377-11	2017	Ingenol mebutate treatment for AK resulted in the modulation of apoptosis-associated molecules with an increase in the expression of Erdr1 and a decrease in the expression of p53 and bcl-2.	3-ingenyl angelate	0-16	P53	Homo sapiens	175-178
27462923-8	2016	Taken together, these results show that delphinidin induces p53-mediated apoptosis by suppressing HDAC activity and activating p53 acetylation in human prostate cancer LNCaP cells.	delphinidin	40-51	P53	Homo sapiens	127-130
27154500-0	2016	Synthesis of intracellular reduction-sensitive amphiphilic polyethyleneimine and poly(epsilon-caprolactone) graft copolymer for on-demand release of doxorubicin and p53 plasmid DNA.	polycaprolactone	81-107	P53	Homo sapiens	165-168
26833899-0	2016	A protease-activated receptor 2 agonist (AC-264613) suppresses interferon regulatory factor 5 and decreases interleukin-12p40 production by lipopolysaccharide-stimulated macrophages: Role of p53.	AC 264613	41-50	P53	Homo sapiens	191-194
27501149-0	2016	Minnelide/Triptolide Impairs Mitochondrial Function by Regulating SIRT3 in P53-Dependent Manner in Non-Small Cell Lung Cancer.	14-O-phosphonooxymethyltriptolide disodium salt	0-9	P53	Homo sapiens	75-78
28973015-9	2017	We, therefore, hypothesized that enoxacin could, by modulating miRNAs targeting splicing machinery, activate p53 in melanoma cells overexpressing MdmX.	Enoxacin	33-41	P53	Homo sapiens	109-112
27304668-0	2016	Glaucarubinone sensitizes KB cells to paclitaxel by inhibiting ABC transporters via ROS-dependent and p53-mediated activation of apoptotic signaling pathways.	glaucarubinone	0-14	P53	Homo sapiens	102-105
27304668-9	2016	Importantly, GLU and/or PTX triggered apoptosis through the activation of pro-apoptotic proteins such as p53, Bax, and caspase-9.	glaucarubinone	13-16	P53	Homo sapiens	105-108
27304668-10	2016	Our findings demonstrated for the first time that GLU causes cell death in human oral cancer cells via the ROS-dependent suppression of MDR transporters and p53-mediated activation of the intrinsic mitochondrial pathway of apoptosis.	glaucarubinone	50-53	P53	Homo sapiens	157-160
26833899-7	2016	Incubation of macrophages with a PAR-2 agonist, AC-264613, caused a decrease of IRF5 expression and also significantly reduced p53 protein expression.	AC 264613	48-57	P53	Homo sapiens	127-130
26975633-5	2016	We observed that APR-246 synergistically enhanced the cytotoxic response of olaparib in TP53 mutant non-small cell lung cancer cell lines, resulting in a strong apoptotic response.	olaparib	76-84	P53	Homo sapiens	88-92
26975633-8	2016	The combined treatment of APR-246 and olaparib induced cell death that was associated with increased ROS production, accumulation of DNA damage and translocation of p53 to the mitochondria.	olaparib	38-46	P53	Homo sapiens	165-168
26975633-9	2016	Out data suggest a promising targeted combination strategy in which the response to olaparib is synergistically enhanced by the addition of APR-246, especially in a TP53 mutant background.	olaparib	84-92	P53	Homo sapiens	165-169
28973015-10	2017	We found that enoxacin and ciprofloxacin, a related fluoroquinolone capable of promoting microRNA processing, but not ofloxacin, strongly activated wild type p53-dependent transcription in A375 melanoma without causing significant DNA damage.	Enoxacin	14-22	P53	Homo sapiens	158-161
28973015-10	2017	We found that enoxacin and ciprofloxacin, a related fluoroquinolone capable of promoting microRNA processing, but not ofloxacin, strongly activated wild type p53-dependent transcription in A375 melanoma without causing significant DNA damage.	Ciprofloxacin	27-40	P53	Homo sapiens	158-161
28973015-10	2017	We found that enoxacin and ciprofloxacin, a related fluoroquinolone capable of promoting microRNA processing, but not ofloxacin, strongly activated wild type p53-dependent transcription in A375 melanoma without causing significant DNA damage.	Fluoroquinolones	52-67	P53	Homo sapiens	158-161
26914593-7	2016	FR180204, a specific inhibitor of ERK1/2 phosphorylation, slightly attenuated the effect of Ca(2+) on the expression of differentiation markers and p53 and the activation of Notch1.	FR 180204	0-8	P53	Homo sapiens	148-151
27179035-0	2016	Antihepatocellular Carcinoma Potential of Tetramethylpyrazine Induces Cell Cycle Modulation and Mitochondrial-Dependent Apoptosis: Regulation of p53 Signaling Pathway in HepG2 Cells In Vitro.	tetramethylpyrazine	42-61	P53	Homo sapiens	145-148
28849003-9	2017	Chrysophanol nanoparticles induced apoptosis in LNCap cells by promoting p53/ROS crosstalk to prevent proliferation.	chrysophanic acid	0-12	P53	Homo sapiens	73-76
27179035-7	2016	Moreover, TMP altered expression of p53 and the Bcl-2/Bax protein ratio, which revealed that TMP induced cell cycle arrest and caspase-dependent mitochondrial apoptosis in HepG2 cells in vitro.	tetramethylpyrazine	10-13	P53	Homo sapiens	36-39
27179035-7	2016	Moreover, TMP altered expression of p53 and the Bcl-2/Bax protein ratio, which revealed that TMP induced cell cycle arrest and caspase-dependent mitochondrial apoptosis in HepG2 cells in vitro.	tetramethylpyrazine	93-96	P53	Homo sapiens	36-39
27127046-5	2016	Here, DCA-PEI was utilized to effectively condense the p53 plasmid, to incorporate the plasmid into rHDL and to act as an antitumor drug to inhibit tumor cell growth.	dca-pei	6-13	P53	Homo sapiens	55-58
27821721-10	2017	Furthermore, CoQ0 induced apoptosis in MCF-7 cells, which was associated with PARP degradation, Bcl-2/Bax dysregulation, and p53 expression as shown by western blot.	ubiquinone-O	13-17	P53	Homo sapiens	125-128
27314292-5	2016	The relationship between the combined expression of HER2 and P53 and the efficacy of NACT was further analyzed by chi-square test.	nact	85-89	P53	Homo sapiens	61-64
27041463-0	2016	Hyaluronan suppresses lidocaine-induced apoptosis of human chondrocytes in vitro by inhibiting the p53-dependent mitochondrial apoptotic pathway.	Hyaluronic Acid	0-10	P53	Homo sapiens	99-102
27041463-0	2016	Hyaluronan suppresses lidocaine-induced apoptosis of human chondrocytes in vitro by inhibiting the p53-dependent mitochondrial apoptotic pathway.	Lidocaine	22-31	P53	Homo sapiens	99-102
27041463-11	2016	Furthermore, co-treatment with lidocaine and hyaluronan significantly decreased the levels of p53 and its transcription targets Bax and p21 in SW1353 cells, although treatment with lidocaine alone did not significantly change these proteins.	Lidocaine	31-40	P53	Homo sapiens	94-97
27041463-11	2016	Furthermore, co-treatment with lidocaine and hyaluronan significantly decreased the levels of p53 and its transcription targets Bax and p21 in SW1353 cells, although treatment with lidocaine alone did not significantly change these proteins.	Hyaluronic Acid	45-55	P53	Homo sapiens	94-97
27041463-11	2016	Furthermore, co-treatment with lidocaine and hyaluronan significantly decreased the levels of p53 and its transcription targets Bax and p21 in SW1353 cells, although treatment with lidocaine alone did not significantly change these proteins.	Lidocaine	181-190	P53	Homo sapiens	94-97
28851987-2	2017	Here we describe p53-dependent control of the rate-limiting enzyme in the pyrimidine catabolic pathway, dihydropyrimidine dehydrogenase (DPYD) and its effect on pharmacokinetics of and response to 5-fluorouracil (5-FU).	pyrimidine	74-84	P53	Homo sapiens	17-20
27041463-13	2016	CONCLUSION: Hyaluronan suppresses lidocaine-induced apoptosis of human chondrocytes in vitro through inhibiting the p53-dependent mitochondrial apoptotic pathway.	Hyaluronic Acid	12-22	P53	Homo sapiens	116-119
27041463-13	2016	CONCLUSION: Hyaluronan suppresses lidocaine-induced apoptosis of human chondrocytes in vitro through inhibiting the p53-dependent mitochondrial apoptotic pathway.	Lidocaine	34-43	P53	Homo sapiens	116-119
28851987-6	2017	In-vivo, liver specific Tp53 loss increases the conversion of 5-FU to 5-FUH2 in plasma and elicits a diminished 5-FU therapeutic response in a syngeneic colorectal tumor model consistent with increased DPYD-activity.	5-fuh2	70-76	P53	Homo sapiens	24-28
27035541-5	2016	These events were p53-independent in the case of RAP, but were accompanied by an increase in p53 levels in the case of TRP.	tryptophanol	119-122	P53	Homo sapiens	93-96
28851987-7	2017	Our data suggest that p53 plays an important role in controlling pyrimidine catabolism through repression of DPYD expression, following metabolic stress imposed by nucleotide imbalance.	pyrimidine	65-75	P53	Homo sapiens	22-25
26739061-0	2016	Astemizole-Histamine induces Beclin-1-independent autophagy by targeting p53-dependent crosstalk between autophagy and apoptosis.	Astemizole	0-10	P53	Homo sapiens	73-76
28718729-0	2017	The novel autophagy inhibitor elaiophylin exerts antitumor activity against multiple myeloma with mutant TP53 in part through endoplasmic reticulum stress-induced apoptosis.	elaiophylin	30-41	P53	Homo sapiens	105-109
26790143-0	2016	p53 Reactivation by PRIMA-1(Met) (APR-246) sensitises (V600E/K)BRAF melanoma to vemurafenib.	Vemurafenib	80-91	P53	Homo sapiens	0-3
28718729-3	2017	This study aimed to assess the effect of elaiophylin on MM cells with mutant TP53 and the possible molecular mechanism.	elaiophylin	41-52	P53	Homo sapiens	77-81
28718729-9	2017	Taken together, our data are the first to demonstrate that exposure of human MM cells with mutant TP53 to elaiophylin blocked autophagy flux and thus induced cell death, which partially involved ER stress-associated apoptosis.	elaiophylin	106-117	P53	Homo sapiens	98-102
28671946-5	2017	Forced depletion of mutant p53 stimulated SAHA-mediated cell death of MiaPaCa-2 cells, which was accomapanied by a further accumulation of gammaH2AX and cleaved PARP.	gammah2ax	139-148	P53	Homo sapiens	27-30
25727911-10	2016	Furthermore, simvastatin effectively reduced the expression of p53 and p21.	Simvastatin	13-24	P53	Homo sapiens	63-66
28918747-0	2017	Omega-3 Polyunsaturated Fatty Acids Eicosapentaenoic Acid and Docosahexaenoic Acid Enhance Dexamethasone Sensitivity in Multiple Myeloma Cells by the p53/miR-34a/Bcl-2 Axis.	Eicosapentaenoic Acid	36-57	P53	Homo sapiens	150-153
27455620-0	2016	Biodegradable Poly(aminoester)-Mediated p53 Gene Delivery for Cancer Therapy.	poly(aminoester)	14-30	P53	Homo sapiens	40-43
26848703-14	2016	In conclusion, thymoquinone increased the effectiveness of the chemotherapeutic reagent topotecan by inhibiting proliferation and lowering toxicity through p53- and Bax/Bcl2-independent mechanisms.	Topotecan	88-97	P53	Homo sapiens	156-159
28411207-7	2017	These findings underscore principal roles for TP53 and PTEN inactivation in abiraterone resistance and progression from adenocarcinoma to CRPC-NE by transdifferentiation.Significance: Understanding adverse treatment response and identifying patients likely to fail treatment represent fundamental clinical challenges.	abiraterone	76-87	P53	Homo sapiens	46-50
26735173-2	2016	Herein, we report the identification of the enantiopure tryptophanol-derived oxazoloisoindolinone SLMP53-1 as a novel reactivator of wild-type (wt) and mut p53, using a yeast-based screening strategy.	tryptophanol	56-68	P53	Homo sapiens	156-159
26735173-8	2016	Collectively, besides the potential use of SLMP53-1 as anticancer drug, the tryptophanol-derived oxazoloisoindolinone scaffold represents a promissing starting point for the development of effective p53-reactivating drugs.	tryptophanol	76-88	P53	Homo sapiens	199-202
26735629-0	2016	CSL-p53: From senescence to CAF activation.	cafestol palmitate	28-31	P53	Homo sapiens	4-7
28693277-0	2017	Curcumol triggers apoptosis of p53 mutant triple-negative human breast cancer MDA-MB 231 cells via activation of p73 and PUMA.	curcumol	0-8	P53	Homo sapiens	31-34
26900800-4	2016	Herein, SIRT1 inhibitor Tenovin-1 and polo-like kinase 1 (Plk1) inhibitor BI2536 were used to stabilize p53.	BI 2536	74-80	P53	Homo sapiens	104-107
28693277-6	2017	The present study aimed to investigate the anticancer effects of curcumol in the human p53 mutant TNBC MDA-MB-231 cell line and its underlying mechanisms.	curcumol	65-73	P53	Homo sapiens	87-90
28693277-12	2017	Curcumol treatment also resulted in the suppression of xenograft growth in vivo (100 or 200 microg/kg for 21 days), as well as G1 phase arrest and an apoptotic response, which were accompanied by the upregulation of p73 expression and the activation of the expression of p53 upregulated modulator of apoptosis (PUMA) and Bcl-2 antagonistic killer (Bak).	curcumol	0-8	P53	Homo sapiens	271-274
26942868-5	2016	EPA/DHA significantly induced PPARgamma and p53 overexpression as observed in immunoblotting assay and the induction of p53 by EPA/DHA was abolished by GW9662.	Eicosapentaenoic Acid	0-3	P53	Homo sapiens	44-47
28693277-14	2017	To the best of our knowledge, the present data demonstrate for the first time that curcumol inhibits the growth of MDA-MB-231 cells and triggers p53-independent apoptosis, which may be mediated by the p73-PUMA/Bak signaling pathway.	curcumol	83-91	P53	Homo sapiens	145-148
26942868-5	2016	EPA/DHA significantly induced PPARgamma and p53 overexpression as observed in immunoblotting assay and the induction of p53 by EPA/DHA was abolished by GW9662.	Eicosapentaenoic Acid	0-3	P53	Homo sapiens	120-123
26942868-5	2016	EPA/DHA significantly induced PPARgamma and p53 overexpression as observed in immunoblotting assay and the induction of p53 by EPA/DHA was abolished by GW9662.	Eicosapentaenoic Acid	127-130	P53	Homo sapiens	120-123
28498808-7	2017	The novel MDM2-p53 interaction antagonist APG115 is an analogue of SAR405838, and is being tested in a phase I clinical trial.	SAR405838	67-76	P53	Homo sapiens	15-18
28591603-2	2017	To elucidate how p53 maintains efficient target search at different concentrations of divalent cations such as Ca2+ and Mg2+, we prepared two mutants of p53, each possessing one of its two DNA-binding domains, the CoreTet mutant having the structured core domain plus the tetramerization (Tet) domain, and the TetCT mutant having Tet plus the disordered C-terminal domain.	tet	218-221	P53	Homo sapiens	17-20
26539646-7	2015	Proliferating CLL cells (including those with p53 or ATM loss) are highly sensitive to the PARP inhibitor talazoparib.	talazoparib	106-117	P53	Homo sapiens	46-49
28296148-4	2017	Here, we describe the synthesis of the new tryptophanol-derived oxazoloisoindolinone DIMP53-1 and identify its activity as a dual inhibitor of the p53-MDM2/X interactions using a yeast-based assay.	tryptophanol	43-55	P53	Homo sapiens	147-150
28529565-8	2017	The knockdown of p53 by specific small interfering RNA resulted in the depletion of p53, and inhibited the OPA and PPA treatment-induced increases in p53, which led to a decrease in the expression of p21, DR5, Fas, PUMA and phosphatase and tensin homolog proteins.	ppa	115-118	P53	Homo sapiens	17-20
26451628-8	2015	Moreover, p53 plays a pivotal role in PCB29-pQ-induced cell cycle arrest and apoptosis via the activation of ATM/Chk2 and ATR/Chk1 checkpoints.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	38-46	P53	Homo sapiens	10-13
28197638-0	2017	Cobalt chloride treatment induces autophagic apoptosis in human glioma cells via a p53-dependent pathway.	cobaltous chloride	0-15	P53	Homo sapiens	83-86
26488797-5	2015	p53 signaling was identified as an important pathway modulated by both arene ruthenium compounds.	arene	71-76	P53	Homo sapiens	0-3
28197638-13	2017	Therefore, the present study shows that CoCl2 treatment can induce autophagy of human glioma cells and subsequent autophagic apoptosis via a p53-dependent pathway.	cobaltous chloride	40-45	P53	Homo sapiens	141-144
28044473-3	2017	In our study, the nanotheranostic agent was fabricated through filling perfluoropropane (C3F8) into poly(d,l-lactic-co-glycolic acid) nanoparticles (PLGA NPs), followed by the formation of gold nanoshell on the surface, then conjugated with anti p53 antibody which has high specificity with the p53 protein overexpressing in breast cancer.	perflutren	89-93	P53	Homo sapiens	246-249
26205328-5	2015	Here, we describe recent work defining a new class of drugs termed zinc metallochaperones that restore WT p53 structure and function by restoring Zn(2+) to Zn(2+)-deficient mutant p53.	zinc metallochaperones	67-89	P53	Homo sapiens	106-109
26205328-5	2015	Here, we describe recent work defining a new class of drugs termed zinc metallochaperones that restore WT p53 structure and function by restoring Zn(2+) to Zn(2+)-deficient mutant p53.	zinc metallochaperones	67-89	P53	Homo sapiens	180-183
26319366-5	2015	This toxicity can be produced by numerous Hedgehog antagonists (vismodegib, cyclopamine, and jervine) and is Bax/Bak dependent but p53 independent.	cyclopamine	76-87	P53	Homo sapiens	131-134
28044473-3	2017	In our study, the nanotheranostic agent was fabricated through filling perfluoropropane (C3F8) into poly(d,l-lactic-co-glycolic acid) nanoparticles (PLGA NPs), followed by the formation of gold nanoshell on the surface, then conjugated with anti p53 antibody which has high specificity with the p53 protein overexpressing in breast cancer.	perflutren	89-93	P53	Homo sapiens	295-298
27550999-3	2017	Here, we evaluated the antitumor effect of a novel small-molecule inhibitor of the MDM2-p53 interaction (MI-773) combined with cisplatin in patient-derived xenograft (PDX) ACC tumors.Experimental Design: Therapeutic strategies with MI-773 and/or cisplatin were evaluated in SCID mice harboring PDX ACC tumors (UM-PDX-HACC-5) and in low passage primary human ACC cells (UM-HACC-2A, -2B, -5, -6) in vitro The effect of therapy on the fraction of cancer stem cells (CSC) was determined by flow cytometry for ALDH activity and CD44 expression.Results: Combined therapy with MI-773 with cisplatin caused p53 activation, induction of apoptosis, and regression of ACC PDX tumors.	SAR405838	105-111	P53	Homo sapiens	88-91
26206331-0	2015	Inhibition of Wild-Type p53-Expressing AML by the Novel Small Molecule HDM2 Inhibitor CGM097.	NVP-CGM097	86-92	P53	Homo sapiens	24-27
26206331-4	2015	Here, we investigated the ability of the novel HDM2 inhibitor CGM097 to potently and selectively kill WT p53-expressing AML cells.	NVP-CGM097	62-68	P53	Homo sapiens	105-108
26206331-6	2015	CGM097 potently and selectively inhibited the proliferation of human AML cell lines and the majority of primary AML cells expressing WT p53, but not mutant p53, in a target-specific manner.	NVP-CGM097	0-6	P53	Homo sapiens	136-139
26206331-10	2015	These data suggest that CGM097 is a promising treatment for AML characterized as harboring WT p53 as a single agent, as well as in combination with other therapies targeting oncogene-activated pathways that drive AML.	NVP-CGM097	24-30	P53	Homo sapiens	94-97
27743086-7	2017	The expression of CoCl2-induced HIF-1alpha was inhibited by BP-1T in various p53 (WT)-expressing cancer cells, including A549, MCF-7 and DLA, but not in mutant p53-expressing SCC-9 cells.	cobaltous chloride	18-23	P53	Homo sapiens	77-80
26194454-0	2015	Quantitative phosphoproteomic analysis reveals gamma-bisabolene inducing p53-mediated apoptosis of human oral squamous cell carcinoma via HDAC2 inhibition and ERK1/2 activation.	gamma-bisabolene	47-63	P53	Homo sapiens	73-76
27387714-0	2017	Polyvinyl pyrrolidone-coated silver nanoparticles in a human lung cancer cells: time- and dose-dependent influence over p53 and caspase-3 protein expression and epigenetic effects.	Silver	29-35	P53	Homo sapiens	120-123
26665397-13	2015	Cell cycle regulatory genes (TP53, CDKN1A) expression and protein products of genes involved in mitochondial apoptosis pathway (BAX, BCL-2) expression are changed by the presence of phenothiazine derivatives during culturing.	phenothiazine	182-195	P53	Homo sapiens	29-33
25966046-7	2015	The mRNA levels for the tumor suppressor gene p53 and the apoptotic genes bax, CASP3 and CASP9 were up-regulated, while the anti-apoptotic gene bcl-2 was down-regulated following nickel ferrite NP exposure.	Nickel	179-185	P53	Homo sapiens	46-49
28357076-5	2017	The distribution frequency of p53 sites of arginine (Arg)/Arg, Arg/proline (Pro), Pro/Pro were 18.4, 48.8 and 32.8% in the control group, as compared with 18.7, 49.9 and 31.4% in the case group, which indicated that there was no difference between two groups (chi2=0.14; P=0.93).	arginylproline	76-79	P53	Homo sapiens	30-33
28721806-3	2017	We hypothesized that L-THP, being an isoquinoline alkaloid, could be a potential molecule against acute lymphoblastic leukemia (ALL), in this study, we evaluate L-THP against p53 deficient leukemia EU-4 cell lines in vitro.	tetrahydropalmatine	21-26	P53	Homo sapiens	175-178
24604693-7	2015	Moreover, PCB29-pQ exposure induced B-cell lymphoma 2 (Bcl-2) downregulation and Bcl-2-associated X (Bax) upregulation, poly(ADP-ribose) polymerase cleavage, accompanied with the increased caspase-3/9 and p53 expressions.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	10-18	P53	Homo sapiens	205-208
28721806-8	2017	RESULTS: Outcomes of the study suggested that L-THP caused p53-indipendent apoptosis mediated by XIAP in EU-4 cells.	tetrahydropalmatine	46-51	P53	Homo sapiens	59-62
26026961-1	2015	We recently reported that nickel accumulation in lung tissues may be associated with an increased in p53 mutation risk via reduced DNA repair activity.	Nickel	26-32	P53	Homo sapiens	101-104
28721806-12	2017	CONCLUSION: Findings of the study confirm that L-THP resulted in p53 independent apoptosis via down-regulating XIAP protein by inhibiting MDM2 associated with proteasome-dependent pathway and increased sensitivity of EU-4 cells against doxorubicin.	tetrahydropalmatine	47-52	P53	Homo sapiens	65-68
28721806-13	2017	L-THP caused activation of caspase and resulted in apoptosis, L-THP may be a novel molecule for inducing apoptosis specifically in p53 null leukemia EU-4 cells.	tetrahydropalmatine	0-5	P53	Homo sapiens	131-134
28721806-13	2017	L-THP caused activation of caspase and resulted in apoptosis, L-THP may be a novel molecule for inducing apoptosis specifically in p53 null leukemia EU-4 cells.	tetrahydropalmatine	62-67	P53	Homo sapiens	131-134
27841435-0	2016	Autophagy and apoptosis: studies on the effects of bisthiosemicarbazone copper(ii) complexes on p53 and p53-null tumour cell lines.	bisthiosemicarbazone	51-71	P53	Homo sapiens	96-99
26550410-9	2015	After bioinformatic analysis of significantly regulated signaling pathways, we found these transcripts may target 35 gene pathways, including p53 signaling, glioma, ubiquitin-mediated proteolysis, insulin signaling, cell cycle, inositol phosphate metabolism, mTOR signaling, and MAPK signaling.	Inositol Phosphates	228-246	P53	Homo sapiens	142-145
25193344-0	2016	Assessment of lipid peroxidation and p53 as a biomarker of carcinogenesis among workers exposed to formaldehyde in the cosmetic industry.	Formaldehyde	99-111	P53	Homo sapiens	37-40
25193344-2	2016	Our study aimed at assessing the effect of formaldehyde on lipid peroxidation and verifying the susceptibility to carcinogenesis using p53 as a biomarker among workers exposed to formaldehyde in cosmetic industry.	Formaldehyde	179-191	P53	Homo sapiens	135-138
27841435-0	2016	Autophagy and apoptosis: studies on the effects of bisthiosemicarbazone copper(ii) complexes on p53 and p53-null tumour cell lines.	bisthiosemicarbazone	51-71	P53	Homo sapiens	104-107
27994550-9	2016	The real time PCR assay demonstrated that TB down-regulated the expression of TOPO I, TOPO II, and BCL-2, and up-regulated the expression of E2F1, P53, GADD45, BAX, BIM, and CASP 3,7,8,9, which suggests an activation of P53-mediated apoptotic (caspase-dependent) pathway in response to TB treatment.	theabrownin	42-44	P53	Homo sapiens	220-223
26002572-5	2015	Subunit silencing (RNAi) or pharmacological antagonism (using myriocin) of serine palmitoyltransferase (SPT; catalyzing the first committed step of SL biosynthesis) reduced proliferation of p53(wt) but not p53(mut) GBM cells.	thermozymocidin	62-70	P53	Homo sapiens	190-193
27994550-12	2016	Our results indicate that TB exhibits its anti-NSCLC activity via a P53-dependent mechanism, which may be a promising candidate of natural product for anti-cancer drug development in the treatment of NSCLC.	theabrownin	26-28	P53	Homo sapiens	68-71
25840356-8	2015	However, overexpression of SIRT1 through resveratrol treatment or transfection clearly attenuated the NiONPs-induced apoptosis and activation of p53 and Bax.	nionps	102-108	P53	Homo sapiens	145-148
27109480-7	2016	Both CQ and AQ elevated the transcription level of p21 though the activation of p53, but also blocked p21 protein degradation in the presence of cycloheximide, causing p21 protein accumulation mainly in the nucleus.	Amodiaquine	12-14	P53	Homo sapiens	80-83
27613187-0	2016	Vitamin C in synergism with cisplatin induces cell death in cervical cancer cells through altered redox cycling and p53 upregulation.	Ascorbic Acid	0-9	P53	Homo sapiens	116-119
26984266-11	2016	Based on these results, kaempferol-induced HUVEC apoptosis was involved in an ROS-mediated p53/ATM/death receptor signaling.	kaempferol	24-34	P53	Homo sapiens	91-94
26426889-0	2015	Synthesis of androstanopyridine and pyrimidine compounds as novel activators of the tumor suppressor protein p53.	pyrimidine	36-46	P53	Homo sapiens	109-112
26756900-0	2016	COX-2 inhibitor NS-398 suppresses doxorubicin-induced p53 accumulation through inhibition of ROS-mediated Jnk activation.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	16-22	P53	Homo sapiens	54-57
26070072-11	2015	Interestingly, SAR405838 can still effectively activate p53 in all sublines containing a single heterozygous C176F mutation, with a moderately reduced potency as compared to that in the parental cell line.	SAR405838	15-24	P53	Homo sapiens	56-59
26848023-0	2016	Piperlongumine exerts cytotoxic effects against cancer cells with mutant p53 proteins at least in part by restoring the biological functions of the tumor suppressor.	piperlonguminine	0-14	P53	Homo sapiens	73-76
26848023-2	2016	Since p53 is a redox-sensitive protein, we hypothesized that the redox imbalance induced by PL may affect the structure and/or function of the mutant p53 protein and promote cell death.	piperlonguminine	92-94	P53	Homo sapiens	6-9
26848023-2	2016	Since p53 is a redox-sensitive protein, we hypothesized that the redox imbalance induced by PL may affect the structure and/or function of the mutant p53 protein and promote cell death.	piperlonguminine	92-94	P53	Homo sapiens	150-153
26848023-10	2016	These clinically-relevant findings suggest that PL-induced oxidative milieu facilitates a weak functional restoration of mutant p53 through protein glutathionylation and contributes to the increased drug sensitivity.	piperlonguminine	48-50	P53	Homo sapiens	128-131
26070072-12	2015	Consistently, SAR405838 is 3-5 times less effective in all the in vivo derived sublines containing a single heterozygous C176F p53 mutation than in the SJSA-1 parental cell line in assays of cell growth and apoptosis.	SAR405838	14-23	P53	Homo sapiens	127-130
26756900-4	2016	In this study, we investigated the effect of NS-398, a COX-2 inhibitor, on modulation of doxorubicin (DOX)-induced p53 accumulation.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	45-51	P53	Homo sapiens	115-118
25938491-0	2015	Novel Pactamycin Analogs Induce p53 Dependent Cell-Cycle Arrest at S-Phase in Human Head and Neck Squamous Cell Carcinoma (HNSCC) Cells.	Pactamycin	6-16	P53	Homo sapiens	32-35
25938491-7	2015	The pactamycin analogs induce expression of cell cycle regulatory proteins including master regulator p53, its downstream target p21Cip1/WAF1, p27kip21, p19, cyclin E, total and phospho Cdc2 (Tyr15) and Cdc25C.	Pactamycin	4-14	P53	Homo sapiens	102-105
26686386-3	2016	Systemic plasmid DNA delivery with dual CD44/EGFR-targeted hyaluronic acid (HA)-based nanoparticles (NPs) resulted in a 2- to 20-fold increase in wt-p53 and miR-125b gene expression in SK-LU-1 cells.	Hyaluronic Acid	59-74	P53	Homo sapiens	149-152
26686386-3	2016	Systemic plasmid DNA delivery with dual CD44/EGFR-targeted hyaluronic acid (HA)-based nanoparticles (NPs) resulted in a 2- to 20-fold increase in wt-p53 and miR-125b gene expression in SK-LU-1 cells.	Hyaluronic Acid	76-78	P53	Homo sapiens	149-152
25938491-10	2015	Altogether, our results demonstrate that Pactamycin analogs TM-025 and TM-026 induce senescence and inhibit proliferation of HNSCC cells via accumulation in S-phase through possible contribution of p53.	Pactamycin	41-51	P53	Homo sapiens	198-201
28105206-0	2016	Curcumin enhances temsirolimus-induced apoptosis in human renal carcinoma cells through upregulation of YAP/p53.	temsirolimus	18-30	P53	Homo sapiens	108-111
26718266-6	2016	Simultaneously, selenite induced DNA damage in treated cells with activation of p53, PARP-1 and JNK and suppressed autophagy.	Selenious Acid	16-24	P53	Homo sapiens	80-83
28105206-5	2016	Co-treatment with temsirolimus and curcumin led to the activation of cleaved poly ADP-ribose polymerase and caspase 3, upregulation of p53 expression and nuclear translocation, and downregulation of B-cell lymphoma 2 protein expression.	temsirolimus	18-30	P53	Homo sapiens	135-138
25586269-0	2015	SIAH1-induced p34SEI-1 polyubiquitination/degradation mediates p53 preferential vitamin C cytotoxicity.	Ascorbic Acid	80-89	P53	Homo sapiens	63-66
25586269-3	2015	Our previous and current data reveal that p53 tumor suppressor is the prerequisite factor for stronger anticancer effects of vitamin C.	Ascorbic Acid	125-134	P53	Homo sapiens	42-45
28105206-7	2016	In conclusion, the present results indicate that combined curcumin and temsirolimus treatment has a synergistic effect on apoptosis in human RCC cells, through the activation of p53.	temsirolimus	71-83	P53	Homo sapiens	178-181
25586269-8	2015	In summary, vitamin C increases cancer cell death by inducing SIAH1-mediated polyubiquitination/degradation of the p34SEI-1 oncoprotein in a p53-dependent manner.	Ascorbic Acid	12-21	P53	Homo sapiens	141-144
27122200-0	2016	Investigation of the Sequential Actions of Doxorubicin and p53 on Tumor Cell Growth Via Branched Polyethylenimine-beta-cyclodextrin Conjugates.	betadex	114-131	P53	Homo sapiens	59-62
27551505-7	2016	Taken together, our data indicate that pan-nuclear gammaH2AX response represents an apoptotic signal that is triggered by the transient pan-nuclear ATM and DNA-PKcs activation, and mediated by p53 and pan-caspases in X-irradiated HPBLs, and that caspase inhibitors are better than ATM/DNA-PKcs inhibitors and p53 inhibitors to block pan-nuclear gammaH2AX response/apoptosis and protect HPBLs from IR.	gammah2ax	51-60	P53	Homo sapiens	193-196
27551505-7	2016	Taken together, our data indicate that pan-nuclear gammaH2AX response represents an apoptotic signal that is triggered by the transient pan-nuclear ATM and DNA-PKcs activation, and mediated by p53 and pan-caspases in X-irradiated HPBLs, and that caspase inhibitors are better than ATM/DNA-PKcs inhibitors and p53 inhibitors to block pan-nuclear gammaH2AX response/apoptosis and protect HPBLs from IR.	gammah2ax	51-60	P53	Homo sapiens	309-312
27551505-7	2016	Taken together, our data indicate that pan-nuclear gammaH2AX response represents an apoptotic signal that is triggered by the transient pan-nuclear ATM and DNA-PKcs activation, and mediated by p53 and pan-caspases in X-irradiated HPBLs, and that caspase inhibitors are better than ATM/DNA-PKcs inhibitors and p53 inhibitors to block pan-nuclear gammaH2AX response/apoptosis and protect HPBLs from IR.	gammah2ax	345-354	P53	Homo sapiens	193-196
27122200-2	2016	In this work, p53/BPEI-beta-CD/AD-dox complex was fabricated and employed to investigate the interaction manner between p53 and doxorubicin (Dox).	betadex	23-30	P53	Homo sapiens	14-17
27551505-7	2016	Taken together, our data indicate that pan-nuclear gammaH2AX response represents an apoptotic signal that is triggered by the transient pan-nuclear ATM and DNA-PKcs activation, and mediated by p53 and pan-caspases in X-irradiated HPBLs, and that caspase inhibitors are better than ATM/DNA-PKcs inhibitors and p53 inhibitors to block pan-nuclear gammaH2AX response/apoptosis and protect HPBLs from IR.	gammah2ax	345-354	P53	Homo sapiens	309-312
25593054-9	2015	CPC senescence resulting from NS loss is partially p53 dependent and is rescued by concurrent silencing of p53.	cpc	0-3	P53	Homo sapiens	51-54
25593054-9	2015	CPC senescence resulting from NS loss is partially p53 dependent and is rescued by concurrent silencing of p53.	cpc	0-3	P53	Homo sapiens	107-110
27122200-2	2016	In this work, p53/BPEI-beta-CD/AD-dox complex was fabricated and employed to investigate the interaction manner between p53 and doxorubicin (Dox).	betadex	23-30	P53	Homo sapiens	120-123
25446071-3	2015	Here we report for the first time that cadmium, nickel and cobalt, which have already been shown to disturb various DNA repair mechanisms, can also influence p63 and p73 sequence-specific DNA binding activity and transactivation of p53 family target genes.	Nickel	48-54	P53	Homo sapiens	232-235
27114909-0	2016	Transcriptome profiling identifies genes and pathways deregulated upon floxuridine treatment in colorectal cancer cells harboring GOF mutant p53.	Floxuridine	71-82	P53	Homo sapiens	141-144
25446071-9	2015	Nickel and cobalt abolished DNA-p53 interaction at sub-millimolar concentrations while inhibition of p63 and p73 DNA binding was observed at millimolar concentrations.	Nickel	0-6	P53	Homo sapiens	32-35
27114909-4	2016	To identify a potential gene expression signature of GOF mutant p53-driven acquired chemoresistance in CRC, we performed transcriptome profiling of floxuridine (FUdR) treated SW480 cells expressing mutant p53(R273H) (GEO#: GSE77533).	Floxuridine	148-159	P53	Homo sapiens	64-67
27122200-3	2016	Briefly, branched polyethylenimine (BPEI) was conjugated with beta-cyclodextrin hydrate (beta-CD) to form BPEI-beta-CD backbone, and p53 plasmid was condensed by positively charged BPEI via electrostatic interaction, while Dox was first conjugated with adamantine (AD) and then assembled with BPEI-beta-CD backbone via the host-guest interaction.	betadex	89-96	P53	Homo sapiens	133-136
27114909-4	2016	To identify a potential gene expression signature of GOF mutant p53-driven acquired chemoresistance in CRC, we performed transcriptome profiling of floxuridine (FUdR) treated SW480 cells expressing mutant p53(R273H) (GEO#: GSE77533).	Floxuridine	148-159	P53	Homo sapiens	205-208
27122200-5	2016	Moreover, p53/BPEI-beta-CD/AD-dox complex released Dox and enabled the expression of p53 gene in a sequential manner, and the released Dox and expressed p53 gene showed successive inhibition of the growth of HeLa cells in vitro.	betadex	19-26	P53	Homo sapiens	10-13
27114909-4	2016	To identify a potential gene expression signature of GOF mutant p53-driven acquired chemoresistance in CRC, we performed transcriptome profiling of floxuridine (FUdR) treated SW480 cells expressing mutant p53(R273H) (GEO#: GSE77533).	Floxuridine	161-165	P53	Homo sapiens	64-67
27114909-4	2016	To identify a potential gene expression signature of GOF mutant p53-driven acquired chemoresistance in CRC, we performed transcriptome profiling of floxuridine (FUdR) treated SW480 cells expressing mutant p53(R273H) (GEO#: GSE77533).	Floxuridine	161-165	P53	Homo sapiens	205-208
27122200-5	2016	Moreover, p53/BPEI-beta-CD/AD-dox complex released Dox and enabled the expression of p53 gene in a sequential manner, and the released Dox and expressed p53 gene showed successive inhibition of the growth of HeLa cells in vitro.	betadex	19-26	P53	Homo sapiens	85-88
25835179-6	2015	Significant association was found between variant genotype of codon 72 of TP53 gene and young age group, female gender, urban dwellers, non-smokers and patients with elevated TSH levels (P &lt; 0.05).	Thyrotropin	175-178	P53	Homo sapiens	74-78
25835179-7	2015	CONCLUSION: It is evident from our study that Arg72Pro SNP of TP53 gene is connected with higher susceptibility to thyroid cancer especially in young age group, female gender, non-smokers and patients with elevated TSH levels, hence, implicated in thyroid carcinogenesis.	Thyrotropin	215-218	P53	Homo sapiens	62-66
27122200-5	2016	Moreover, p53/BPEI-beta-CD/AD-dox complex released Dox and enabled the expression of p53 gene in a sequential manner, and the released Dox and expressed p53 gene showed successive inhibition of the growth of HeLa cells in vitro.	betadex	19-26	P53	Homo sapiens	85-88
27229883-0	2016	beta-Ecdysterone Protects SH-SY5Y Cells Against 6-Hydroxydopamine-Induced Apoptosis via Mitochondria-Dependent Mechanism: Involvement of p38(MAPK)-p53 Signaling Pathway.	Oxidopamine	48-65	P53	Homo sapiens	147-150
27053954-0	2016	Tetrahydroanthraquinone Derivative (+-)-4-Deoxyaustrocortilutein Induces Cell Cycle Arrest and Apoptosis in Melanoma Cells via Upregulation of p21 and p53 and Downregulation of NF-kappaB.	tetrahydroanthraquinone	0-23	P53	Homo sapiens	151-154
27229883-5	2016	In the present study, pretreatment with beta-Ecd significantly reduced 6-OHDA-induced apoptosis of SH-SY5Y cells by a mitochondria-dependent pathway, as indicated by downregulation of Bax and PUMA (p53 upregulated modulator of apoptosis) expression, suppressing DeltaPsim loss, inhibiting cytochrome c release, and attenuating caspase-9 activation.	Oxidopamine	71-77	P53	Homo sapiens	198-201
27665737-9	2016	Our results therefore suggest that cSCCHN with clinical PNI may be more likely to contain alterations in the p53 pathway, compared to cSCCHN without PNI.	cscchn	35-41	P53	Homo sapiens	109-112
26754547-10	2016	BI-2536 treatment resulted in a decrease in mutant p53 protein in SW-13 cells but had no effect on wild-type p53 protein levels in H295R cells.	BI 2536	0-7	P53	Homo sapiens	51-54
25395102-7	2015	In addition, we have found that PES induces a severe oxidative stress and the activation of p53.	polyether sulfone	32-35	P53	Homo sapiens	92-95
25765771-4	2016	METHODS: The RDP-p53 fusion proteins are expressed in Escherichia coli, and they are labeled with FITC and rhodamine B by chemical modification.	rhodamine B	107-118	P53	Homo sapiens	17-20
25877312-9	2015	Jaridonin resulted in extensive p53 up-regulation in the EC-1 cells.	jaridonin	0-9	P53	Homo sapiens	32-35
25877312-10	2015	More importantly, the p53 up-regulation occurred as early as 2 h after Jaridonin incubation, and in a time-dependent manner (P &lt; 0.05).	jaridonin	71-80	P53	Homo sapiens	22-25
25877312-11	2015	p53 siRNA transfection inhibited apoptosis in the EC-1 cells, and the Jaridonin-induced apoptosis rate was reduced from 38.5% to 8.8%.	jaridonin	70-79	P53	Homo sapiens	0-3
26773499-6	2016	6-OHDA-induced intracellular generation of ROS and mitochondrial dysfunctions, release of cytochrome c, imbalance of Bax/Bcl-2, cleaved caspase-9/caspase-9 and cleaved caspase-3/caspase-3 ratio, and p-p53 activation were strikingly attenuated by SJP pretreatment.	Oxidopamine	0-6	P53	Homo sapiens	201-204
27576846-0	2016	TP53 mutations emerge with HDM2 inhibitor SAR405838 treatment in de-differentiated liposarcoma.	SAR405838	42-51	P53	Homo sapiens	0-4
26727270-1	2016	The drug pentamidine inhibits calcium-dependent complex formation with p53 ((Ca)S100B p53) in malignant melanoma (MM) and restores p53 tumor suppressor activity in vivo.	Pentamidine	9-20	P53	Homo sapiens	71-74
26727270-1	2016	The drug pentamidine inhibits calcium-dependent complex formation with p53 ((Ca)S100B p53) in malignant melanoma (MM) and restores p53 tumor suppressor activity in vivo.	Pentamidine	9-20	P53	Homo sapiens	86-89
26727270-1	2016	The drug pentamidine inhibits calcium-dependent complex formation with p53 ((Ca)S100B p53) in malignant melanoma (MM) and restores p53 tumor suppressor activity in vivo.	Pentamidine	9-20	P53	Homo sapiens	86-89
26727270-5	2016	The (Ca)S100B 17 structure illustrates, for the first time, a pentamidine analog capable of binding the "open" form of the "FF-gate" and provides a means to block all three "hot spots" on (Ca)S100B, which will impact next generation (Ca)S100B p53 inhibitor design.	Pentamidine	62-73	P53	Homo sapiens	243-246
27109154-7	2016	The induced G2/M phase arrest indicated by the Western blotting assay showed that casticin promoted the expression of p53, p21 and CHK-1 proteins and inhibited the protein levels of Cdc25c, CDK-1, Cyclin A and B.	casticin	82-90	P53	Homo sapiens	118-121
25384157-0	2014	Discovery of AM-7209, a potent and selective 4-amidobenzoic acid inhibitor of the MDM2-p53 interaction.	am-7209	13-20	P53	Homo sapiens	87-90
25384157-0	2014	Discovery of AM-7209, a potent and selective 4-amidobenzoic acid inhibitor of the MDM2-p53 interaction.	4-amidobenzoic acid	45-64	P53	Homo sapiens	87-90
25531293-5	2014	In the p53-/- cells, carbon-ion beam irradiation, but not X-ray irradiation, markedly induced mitotic catastrophe that was associated with premature mitotic entry with harboring long-retained DSBs at 24 h post-irradiation.	dsbs	192-196	P53	Homo sapiens	7-10
27383270-0	2016	Inactivation of oncogenic cAMP-specific phosphodiesterase 4D by miR-139-5p in response to p53 activation.	mir-139-5p	64-74	P53	Homo sapiens	90-93
27039820-7	2016	The fact that bromodeoxyuridine had the strongest effects on growth inhibition and senescence induction implies that senescence in cholangiocarcinoma cells is likely controlled by DNA damage response pathways relating to the p53/p21 signaling.	Bromodeoxyuridine	14-31	P53	Homo sapiens	225-228
25214240-7	2014	Furthermore, EBR treatment was also induced apoptosis in both LNCaP(wt p53) and DU 145 (mt p53)cells, respectively.	EBR	13-16	P53	Homo sapiens	71-74
27383270-2	2016	Here, we report miR-139-5p as another new p53 microRNA target.	mir-139-5p	16-26	P53	Homo sapiens	42-45
25214240-7	2014	Furthermore, EBR treatment was also induced apoptosis in both LNCaP(wt p53) and DU 145 (mt p53)cells, respectively.	EBR	13-16	P53	Homo sapiens	91-94
27231022-0	2016	Vitamin C promotes the proliferation of human adipose-derived stem cells via p53-p21 pathway.	Ascorbic Acid	0-9	P53	Homo sapiens	77-80
25214240-8	2014	These all findings verified that EBR-induced apoptosis regardless of p53 expression.	EBR	33-36	P53	Homo sapiens	69-72
25214240-11	2014	CONCLUSIONS: Therefore, we concluded that EBR-induced apoptosis was mainly related with PA catabolic pathway and independent from p53 expression.	EBR	42-45	P53	Homo sapiens	130-133
27889776-9	2016	The western blot analysis results showed that KLF6, Fas-L, Bax, P53 and caspase-3 protein expression was drastically increased in the CNE2 cells after treatment with 2 mmol/L CINN, whereas Bcl-2 and cyclin D1 protein expression was markedly reduced.	cinnamic acid	175-179	P53	Homo sapiens	64-67
26942868-5	2016	EPA/DHA significantly induced PPARgamma and p53 overexpression as observed in immunoblotting assay and the induction of p53 by EPA/DHA was abolished by GW9662.	2-chloro-5-nitrobenzanilide	152-158	P53	Homo sapiens	120-123
27231022-9	2016	Western blot analysis indicated that vitamin C treatment up-regulated the expression levels of cyclin E1 and CDK2, but down-regulated p53 and p21 proteins expression, which contributed to cell proliferation and cell cycle progression.	Ascorbic Acid	37-46	P53	Homo sapiens	134-137
27231022-11	2016	These findings suggest that vitamin C can promote the proliferation and cell cycle progression in the ADSCs possibly through regulation of p53-p21 signal pathway.	Ascorbic Acid	28-37	P53	Homo sapiens	139-142
25429619-6	2014	Collectively, our results show that ROS inhibited autophagy by downregulating the p70S6K/p53/ULK1 axis in selenite-treated NB4 cells.	Selenious Acid	106-114	P53	Homo sapiens	89-92
26980146-7	2016	In addition, T4-suppressed mRNA expressions of pro-apoptotic genes p53 and RRM2B could be significantly elevated by the combination of NDAT and cetuximab compared to cetuximab alone.	ndat	135-139	P53	Homo sapiens	67-70
26641105-2	2015	Site-specific synthesis of the C8-dG-ABA adduct in the oligodeoxynucleotide 5"-d(GTGCXTGTTTGT)-3":5"-d(ACAAACACGCAC)-3"; X = C8-dG-ABA adduct, including codons 272-275 of the p53 gene, has allowed for investigation into the structural and thermodynamic properties of this adduct.	acaaacacgcac	103-115	P53	Homo sapiens	175-178
26641105-2	2015	Site-specific synthesis of the C8-dG-ABA adduct in the oligodeoxynucleotide 5"-d(GTGCXTGTTTGT)-3":5"-d(ACAAACACGCAC)-3"; X = C8-dG-ABA adduct, including codons 272-275 of the p53 gene, has allowed for investigation into the structural and thermodynamic properties of this adduct.	aminobenzanthrone	37-40	P53	Homo sapiens	175-178
25289068-6	2014	Furthermore, the results from the western blot analysis demonstrated that augmenting ADR treatment with germacrone resulted in a reduction of anti-apoptotic protein expression levels (bcl-2) and enhancement of pro-apoptotic protein expression levels (p53 and bax) in MCF-7/ADR cells compared with the levels achieved by treatment with ADR alone.	germacrone	104-114	P53	Homo sapiens	251-254
27390612-3	2016	Herein, we designed a chimeric p53 protein flanked with the MyoD N-terminal transcriptional activation domain (amino acids 1-62, called M3) and a poly-arginine (R12) cell penetrating signal in its N-and C-termini respectively.	polyarginine	146-159	P53	Homo sapiens	31-34
25336953-0	2014	Activation of Erk and p53 regulates copper oxide nanoparticle-induced cytotoxicity in keratinocytes and fibroblasts.	cupric oxide	36-48	P53	Homo sapiens	22-25
26597381-7	2015	Western blot analysis revealed that severe p53-K382ac activation was promoted by benzylester 5.	benzylester 5	81-94	P53	Homo sapiens	43-46
27291325-0	2016	Silver nanoparticles defeat p53-positive and p53-negative osteosarcoma cells by triggering mitochondrial stress and apoptosis.	Silver	0-6	P53	Homo sapiens	28-31
26500073-0	2015	Sedanolide induces autophagy through the PI3K, p53 and NF-kappaB signaling pathways in human liver cancer cells.	neocnidilide	0-10	P53	Homo sapiens	47-50
26556860-8	2015	These results provide valuable insight into the synergistic mechanism between SNX-7081 and 2-FaraA that may provide an alternative treatment for CLL patients with p53 mutations, for whom therapeutic options are currently limited.	2-faraa	91-98	P53	Homo sapiens	163-166
25086499-3	2014	Furthermore, while p53R2, a p53-inducible peptide involved in the synthesis of dNTPs normally works toward suppression of cancer through elimination of reactive oxygen species (ROS), inhibition of MAPK/ERK pathway and providing dNTPs for DNA repair, the overexpression of p53R2 is reported to be associated with cancer progression and resistance to therapy.	Parathion	228-233	P53	Homo sapiens	19-22
27291325-0	2016	Silver nanoparticles defeat p53-positive and p53-negative osteosarcoma cells by triggering mitochondrial stress and apoptosis.	Silver	0-6	P53	Homo sapiens	45-48
27270209-3	2016	In p53 expressing ECC-1 and OVCAR-3 but not in p53-deficient SKOV-3 cells, citral induces G1/S cell cycle arrest and apoptosis as determined by Annexin V staining and increased cleaved caspase3 and Bax and decreased Bcl-2.	citral	75-81	P53	Homo sapiens	3-6
25198897-0	2014	Design, synthesis and biological evaluation of sulfamide and triazole benzodiazepines as novel p53-MDM2 inhibitors.	triazole benzodiazepines	61-85	P53	Homo sapiens	95-98
27270209-6	2016	In p53-expressing cells, citral increases phosphorylation of serine-15 of p53.	citral	25-31	P53	Homo sapiens	3-6
27270209-6	2016	In p53-expressing cells, citral increases phosphorylation of serine-15 of p53.	citral	25-31	P53	Homo sapiens	74-77
24967548-6	2014	In addition, p53 protein inexpression, mediated by rhodamine nanoparticles, demonstrates the ability of the proposed system to target mitochondria; due to the different genetic code in mitochondria, p53 protein cannot be expressed.	Rhodamines	51-60	P53	Homo sapiens	13-16
26462022-5	2015	Herein, we report that the cell penetrating peptide (polyarginine, R11)-conjugated p53C can exhibit a preferential uptake and growth inhibit of UCB cells expressing either mutant or wild-type TP53 by the activation of p53-dependent pathway.	polyarginine	53-65	P53	Homo sapiens	192-196
26462022-5	2015	Herein, we report that the cell penetrating peptide (polyarginine, R11)-conjugated p53C can exhibit a preferential uptake and growth inhibit of UCB cells expressing either mutant or wild-type TP53 by the activation of p53-dependent pathway.	polyarginine	53-65	P53	Homo sapiens	83-86
24568186-0	2014	15-deoxy-Delta12,14-prostaglandin J2 induces p53 expression through Nrf2-mediated upregulation of heme oxygenase-1 in human breast cancer cells.	14-prostaglandin j2	17-36	P53	Homo sapiens	45-48
24568186-11	2014	When MCF-7 cells were treated with the Fe(2+)-specific chelator phenanthroline, 15d-PGJ2-induced p53 expression was attenuated.	Phenanthrolines	64-78	P53	Homo sapiens	97-100
27270209-8	2016	Inhibition of p53 by pifithrin-alpha, attenuates citral-mediated apoptosis.	citral	49-55	P53	Homo sapiens	14-17
26492315-4	2015	Our results suggest that combined treatment with rosiglitazone and LA-12 might be promising anticancer strategy in colon-derived tumours regardless of their p53 status, and also favourable in those defective in PTEN function.	UNII-37WM0V5E17	67-72	P53	Homo sapiens	157-160
27270209-9	2016	Citral increases intracellular oxygen radicals and this leads to activation of p53.	citral	0-6	P53	Homo sapiens	79-82
27270209-11	2016	Pretreatment with N-acetylcysteine decreases phosphorylation of p53 in citral-treated ECC-1 and OVCAR-3.	citral	71-77	P53	Homo sapiens	64-67
25091696-12	2014	Different driver mutations were associated with distinct patterns of specific metabolites, such as lower levels of several lipid-glycerophosphocholines in tumors with mutated TP53.	Glycerylphosphorylcholine	129-151	P53	Homo sapiens	175-179
27270209-12	2016	These results define a p53-dependent, and in the absence of p53, ER stress-dependent mode of action of citral.	citral	103-109	P53	Homo sapiens	23-26
24926563-10	2014	Combined effects of asbestos and smoking were suggested by LOH and p53 analyses.	Asbestos	20-28	P53	Homo sapiens	67-70
27507190-9	2016	When combined with AEB071, the two agents CGM097 (p53-MDM2 inhibitor) and RAD001 (mTORC1 inhibitor) demonstrated greater activity than single agents, with tumor regression observed in several UM PDXs.	NVP-CGM097	42-48	P53	Homo sapiens	50-53
24926563-11	2014	Sole exposure to asbestos did not increase LOH frequency but increased non-specific p53 mutations.	Asbestos	17-25	P53	Homo sapiens	84-87
25033896-11	2014	CONCLUSIONS: The inhibitory mechanisms of iodine on CRC acted through an increase in the level of p53 and a decrease in the level of VEGF, resulting in a decrease of MVD.	Iodine	42-48	P53	Homo sapiens	98-101
26181229-0	2015	Cell cycle arrest and apoptosis induced by aspidin PB through the p53/p21 and mitochondria-dependent pathways in human osteosarcoma cells.	aspidin PB	43-53	P53	Homo sapiens	66-69
26181229-2	2015	We reported that aspidin PB induced cell cycle arrest and apoptosis through the p53/p21 and mitochondria-dependent pathways in human osteosarcoma cells.	aspidin PB	17-27	P53	Homo sapiens	80-83
26181229-4	2015	Aspidin PB induced changes in the cell cycle regulators (cyclin A, pRb, CDK2, p53, and p21), which caused cell cycle arrest in the S phase.	aspidin PB	0-10	P53	Homo sapiens	78-81
26181229-5	2015	We also explored the role of siRNA targeted to p53; it led to a dose-dependent attenuation of aspidin PB-induced apoptosis signaling.	aspidin PB	94-104	P53	Homo sapiens	47-50
26208523-10	2015	Consequently, oxaliplatin significantly decreased the level of dTTP in the dNTP pool in a p53-dependent manner.	thymidine 5'-triphosphate	63-67	P53	Homo sapiens	90-93
26841929-0	2016	Sponges against miR-19 and miR-155 reactivate the p53-Socs1 axis in hematopoietic cancers.	mir-19	16-22	P53	Homo sapiens	50-53
26208523-10	2015	Consequently, oxaliplatin significantly decreased the level of dTTP in the dNTP pool in a p53-dependent manner.	Parathion	75-79	P53	Homo sapiens	90-93
26208523-11	2015	These data indicate that the DACH carrier ligand in oxaliplatin triggers signaling via the p53-miR-34a-E2F axis, leading to transcriptional regulation that ultimately results in accumulation of dUTP and reduced dTTP biosynthesis, potentially enhancing 5-FU cytotoxicity.	thymidine 5'-triphosphate	211-215	P53	Homo sapiens	91-94
26194454-4	2015	Phosphoproteome profiling revealed that gamma-bisabolene increased the phosphorylation of ERK1/2, protein phosphatases 1 (PP1), and p53, as well as decreased the phosphorylation of histone deacetylase 2 (HDAC2) in the process of apoptosis induction.	gamma-bisabolene	40-56	P53	Homo sapiens	132-135
26194454-5	2015	Protein-protein interaction network analysis proposed the involvement of PP1-HDAC2-p53 and ERK1/2-p53 pathways in gamma-bisabolene-induced apoptosis.	gamma-bisabolene	114-130	P53	Homo sapiens	83-86
24956278-5	2014	The quinic acid derivative KZ-41 lessened leukocyte adhesion and paxillin-dependent proliferation via inhibition of p38MAPK-p53-ICAM-1 signaling.	kz-41	27-32	P53	Homo sapiens	124-127
26194454-5	2015	Protein-protein interaction network analysis proposed the involvement of PP1-HDAC2-p53 and ERK1/2-p53 pathways in gamma-bisabolene-induced apoptosis.	gamma-bisabolene	114-130	P53	Homo sapiens	98-101
24922640-3	2014	RESULTS: Significant differences were observed in the p53 expression between the different groups: NN and CIN I (p=0.010); NN and CIN II (p&lt;0.00001); CIN II and CIN III (p=0.02); CIN II and CIS (p=0.0220); CIN II and CEC (p=0.010).	cin ii	130-136	P53	Homo sapiens	54-57
27144436-7	2016	Both NR4A1 knockdown and treatment with DIM-C-pPhOH and DIM-C-pPhCO2Me also induced ROS which activated stress genes and induced sestrin 2 which activated AMPK and inhibited mTOR in the mutant p53 RMS cells.	p-carboxymethylphenyl 1,1-bis(3'-indolyl)-1-(p-carboxymethylphenyl)methane	56-70	P53	Homo sapiens	193-196
24922640-3	2014	RESULTS: Significant differences were observed in the p53 expression between the different groups: NN and CIN I (p=0.010); NN and CIN II (p&lt;0.00001); CIN II and CIN III (p=0.02); CIN II and CIS (p=0.0220); CIN II and CEC (p=0.010).	cin ii	153-159	P53	Homo sapiens	54-57
24114315-9	2014	Regarding the TP53 Arg72Pro, we showed statistical significance for ProPro + ProArg comparing to ArgArg (OR 2.34, 95 %, CI 1.17-4.70) in hereditary compared to sporadic group.	arginylarginine	97-103	P53	Homo sapiens	14-18
26194454-6	2015	Subsequent assays indicated gamma-bisabolene eliciting p53 acetylation that enhanced the expression of p53-regulated apoptotic genes.	gamma-bisabolene	28-44	P53	Homo sapiens	55-58
26194454-6	2015	Subsequent assays indicated gamma-bisabolene eliciting p53 acetylation that enhanced the expression of p53-regulated apoptotic genes.	gamma-bisabolene	28-44	P53	Homo sapiens	103-106
26194454-7	2015	PP1 inhibitor-2 restored the status of HDAC2 phosphorylation, reducing p53 acetylation and PUMA mRNA expression in gamma-bisabolene-treated Ca9-22 and SAS cells.	gamma-bisabolene	115-131	P53	Homo sapiens	71-74
26194454-9	2015	Notably, the results ascertained the involvement of PP1-HDAC2-p53 and ERK1/2-p53 pathways in mitochondria-mediated apoptosis of gamma-bisabolene-treated cells.	gamma-bisabolene	128-144	P53	Homo sapiens	62-65
26194454-9	2015	Notably, the results ascertained the involvement of PP1-HDAC2-p53 and ERK1/2-p53 pathways in mitochondria-mediated apoptosis of gamma-bisabolene-treated cells.	gamma-bisabolene	128-144	P53	Homo sapiens	77-80
26302161-5	2015	We showed that p53 is activated in ischemic brains and in oxygen-glucose deprivation (OGD)-induced cell death in neurons and astrocytes.	oxygen-glucose	58-72	P53	Homo sapiens	15-18
27164076-0	2016	Anticancer Activity of gamma-Bisabolene in Human Neuroblastoma Cells via Induction of p53-Mediated Mitochondrial Apoptosis.	gamma-bisabolene	23-39	P53	Homo sapiens	86-89
26527121-8	2015	P53 expression in the HuH7 and HepG2 cell lines increased after internal and external irradiation with iodine-131.	Iodine	103-109	P53	Homo sapiens	0-3
26061814-3	2015	By repressing the expression of stearoyl-CoA desaturase 1, SCD, the enzyme that converts saturated to mono-unsaturated fatty acids, p53 causes a shift in the content of phospholipids with mono-unsaturated acyl chains towards more saturated phospholipid species, particularly of the phosphatidylinositol headgroup class.	Fatty Acids, Monounsaturated	102-130	P53	Homo sapiens	132-135
26061814-3	2015	By repressing the expression of stearoyl-CoA desaturase 1, SCD, the enzyme that converts saturated to mono-unsaturated fatty acids, p53 causes a shift in the content of phospholipids with mono-unsaturated acyl chains towards more saturated phospholipid species, particularly of the phosphatidylinositol headgroup class.	mono-unsaturated acyl chains	188-216	P53	Homo sapiens	132-135
24959385-10	2014	Importantly, inhibition of these target genes and of tumor growth by FL118 is independent of p53 status (wild type, mutant or null), although mechanisms of action may be distinct among cells with different p53 status.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	69-74	P53	Homo sapiens	206-209
24959385-11	2014	Therefore, FL118 may effectively control cancer that loses functional p53, in which most DNA damage drugs (if not all) show a marked lack of efficiency.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	11-16	P53	Homo sapiens	70-73
24642253-8	2014	In addition, over-expression of ChDFFA inhibited the transcriptional activities of p53/p21-Luc reporter genes in HEK293T cells.	chdffa	32-38	P53	Homo sapiens	83-86
24743574-0	2014	Curcumin significantly enhances dual PI3K/Akt and mTOR inhibitor NVP-BEZ235-induced apoptosis in human renal carcinoma Caki cells through down-regulation of p53-dependent Bcl-2 expression and inhibition of Mcl-1 protein stability.	dactolisib	69-75	P53	Homo sapiens	157-160
24743574-11	2014	Combined treatment with NVP-BEZ235 and curcumin reduced Bcl-2 expression in wild-type p53 HCT116 human colon carcinoma cells but not p53-null HCT116 cells.	dactolisib	28-34	P53	Homo sapiens	86-89
27164076-7	2016	Moreover, gamma-bisabolene increased p53 phosphorylation and up-regulated p53-mediated apoptotic genes Bim and PUMA, as well as decreased the mRNA and protein levels of CK2alpha.	gamma-bisabolene	10-26	P53	Homo sapiens	37-40
27164076-7	2016	Moreover, gamma-bisabolene increased p53 phosphorylation and up-regulated p53-mediated apoptotic genes Bim and PUMA, as well as decreased the mRNA and protein levels of CK2alpha.	gamma-bisabolene	10-26	P53	Homo sapiens	74-77
25308476-5	2015	We further demonstrate that CtIP expression is repressed by miR-19 during continuous genotoxic stress in a p53-dependent manner.	mir-19	60-66	P53	Homo sapiens	107-110
27164076-8	2016	Notably, the results indicated the involvement of CK2alpha-p53 pathways in mitochondria-mediated apoptosis of human neuroblastoma cells treated with gamma-bisabolene.	gamma-bisabolene	149-165	P53	Homo sapiens	59-62
26984266-0	2016	Kaempferol induces ATM/p53-mediated death receptor and mitochondrial apoptosis in human umbilical vein endothelial cells.	kaempferol	0-10	P53	Homo sapiens	23-26
24764719-3	2014	Here, we report the case of a woman with TP53 mutation who was treated with adjuvant pelvic rt for stage ib uterine leiomyosarcoma in 2000, with radioactive iodine for papillary thyroid cancer in 2001, and with palliative rt to the humerus in 2010 for metastatic uterine leiomyosarcoma.	Iodine	157-163	P53	Homo sapiens	41-45
26984266-10	2016	We further investigated the upstream extrinsic pathway and showed that kaempferol stimulated death receptor signals [Fas/CD95, death receptor 4 (DR4) and DR5] through increasing the levels of phosphorylated p53 and phosphorylated ATM pathways in HUVECs, which can be individually confirmed by N-acetylcysteine (NAC), ATM specific inhibitor (caffeine) and p53 siRNA.	kaempferol	71-81	P53	Homo sapiens	207-210
25980497-9	2015	Furthermore, PYR-41-mediated PMTRPM8 activity was accompanied by enhanced activation of p53 and Caspase-9.	4(4-(5-nitro-furan-2-ylmethylene)-3,5-dioxo-pyrazolidin-1-yl)-benzoic acid ethyl ester	13-19	P53	Homo sapiens	88-91
26984266-10	2016	We further investigated the upstream extrinsic pathway and showed that kaempferol stimulated death receptor signals [Fas/CD95, death receptor 4 (DR4) and DR5] through increasing the levels of phosphorylated p53 and phosphorylated ATM pathways in HUVECs, which can be individually confirmed by N-acetylcysteine (NAC), ATM specific inhibitor (caffeine) and p53 siRNA.	kaempferol	71-81	P53	Homo sapiens	355-358
27563220-12	2016	OSEO has the ability to up-regulate the apoptotic genes p53 and Bid and as well as elevates the ratio of Bax/Bcl-2.	oseo	0-4	P53	Homo sapiens	56-59
26170659-0	2015	Comparative assessment of the apoptotic potential of silver nanoparticles synthesized by Bacillus tequilensis and Calocybe indica in MDA-MB-231 human breast cancer cells: targeting p53 for anticancer therapy.	Silver	53-59	P53	Homo sapiens	181-184
26062895-3	2015	One mechanism of regulation is acetylation of p53 on lysine K120 by the histone-acetyltransferase Tip60, resulting in preferential transcription of proapoptotic target genes.	lysine k120	53-64	P53	Homo sapiens	46-49
24464432-2	2014	In response to DSBs, the ATM kinase is activated and subsequently phosphorylates numerous downstream substrates, including p53, Chk2, BRCA1, and KAP1, which affect processes such as cell cycle progression and DNA repair.	dsbs	15-19	P53	Homo sapiens	123-126
24413339-1	2014	Recently, it has been reported that anti-viral drugs, such as indinavir and lopinavir (originally targeted for HIV), also inhibit E6-mediated proteasomal degradation of mutant p53 in E6-transfected C33A cells.	Indinavir	62-71	P53	Homo sapiens	176-179
27165078-0	2016	p53- and Caspase-3-Independent Mechanism of Acetaminophen Effect on Human Neural Cells.	Acetaminophen	44-57	P53	Homo sapiens	0-3
24169260-3	2014	PATIENTS AND METHODS: Mutations in TP53 (exons 4-9), KRAS (exon 1), and EGFR (exons 18-21) were identified by direct sequencing of DNA from formalin-fixed, paraffin-embedded resected tumors.	Formaldehyde	140-148	P53	Homo sapiens	35-39
25965911-5	2015	NVP-BEZ235 effectively up-regulated PUMA expression, mainly through inactivation of PI3K/Akt and activation of FOXO3a, leading to cell apoptosis even in the p53-/- HCT-116 cells.	dactolisib	4-10	P53	Homo sapiens	157-160
26475335-0	2016	SAR405838: A Novel and Potent Inhibitor of the MDM2:p53 Axis for the Treatment of Dedifferentiated Liposarcoma.	SAR405838	0-9	P53	Homo sapiens	52-55
25882531-0	2015	Discovery of DS-5272 as a promising candidate: A potent and orally active p53-MDM2 interaction inhibitor.	DS-5272	13-20	P53	Homo sapiens	74-77
24421392-2	2014	We have shown that ursodeoxycholic acid, a hydrophilic bile acid, counteracts the miR-34a/sirtuin 1 (SIRT1)/p53 pathway, activated in the liver of nonalcoholic steatohepatitis (NASH) patients.	Ursodeoxycholic Acid	19-39	P53	Homo sapiens	108-111
26475335-7	2016	RESULTS: SAR405838 effectively stabilized p53 and activated the p53 pathway, resulting in abrogated cellular proliferation, cell-cycle arrest, and apoptosis.	SAR405838	9-18	P53	Homo sapiens	42-45
25828929-0	2015	Distinct novel quinazolinone exhibits selective inhibition in MGC-803 cancer cells by dictating mutant p53 function.	Quinazolinones	15-28	P53	Homo sapiens	103-106
25828929-1	2015	The mutant p53 proteins and their corresponding cellular response can be manipulated by novel quinazolinone derivatives 4-8 (a-i) in p53 mutant cancer cells.	Quinazolinones	94-107	P53	Homo sapiens	11-14
25828929-1	2015	The mutant p53 proteins and their corresponding cellular response can be manipulated by novel quinazolinone derivatives 4-8 (a-i) in p53 mutant cancer cells.	Quinazolinones	94-107	P53	Homo sapiens	133-136
25828929-6	2015	To the best of our knowledge, 6c is the first quinazolinone derivative to dictate mutant p53 function for apoptotic cell death.	Quinazolinones	46-59	P53	Homo sapiens	89-92
24514456-0	2014	A dual-targeting, p53-independent, apoptosis-inducing platinum(II) anticancer complex, [Pt(BDI(QQ))]Cl.	platinum(ii)	54-66	P53	Homo sapiens	18-21
26475335-7	2016	RESULTS: SAR405838 effectively stabilized p53 and activated the p53 pathway, resulting in abrogated cellular proliferation, cell-cycle arrest, and apoptosis.	SAR405838	9-18	P53	Homo sapiens	64-67
24858040-11	2015	Our findings suggest that the p53-SLC2A9 pathway is a novel antioxidant mechanism that uses uric acid to maintain ROS homeostasis and prevent accumulation of ROS-associated damage that potentially contributes to cancer development.	Uric Acid	92-101	P53	Homo sapiens	30-33
23396362-3	2014	We found that the deletion of p50 (p50-/-) impaired arsenite-induced p53 protein expression, which could be restored after reconstitutive expression of HA-p50 in p50-/- cells, p50-/-(Ad-HA-p50).	arsenite	52-60	P53	Homo sapiens	69-72
26475335-10	2016	Microarray analyses revealed genes enriching the p53 signaling pathway as well as genomic stability and DNA damage following SAR405838 treatment.	SAR405838	125-134	P53	Homo sapiens	49-52
26892186-0	2016	Volatile Oil of Acori Graminei Rhizoma-Induced Apoptosis and Autophagy are dependent on p53 Status in Human Glioma Cells.	Oils, Volatile	0-12	P53	Homo sapiens	88-91
26699757-6	2016	Together these results demonstrate that kaempferol-mediated antitumor activity toward Jurkat T cells was attributable to G2-checkpoint activation, which caused not only G2-arrest of the cell cycle but also activating phosphorylation of p53 (Ser-15) and subsequent induction of mitochondriadependent apoptotic events, including Bak and PUMA upregulation, Bak activation, Deltapsim loss, and caspase cascade activation.	kaempferol	40-50	P53	Homo sapiens	236-239
24368590-13	2014	The lomeguatrib-TMZ combination did not have any effect on the cell cycle and caused apoptosis by increasing p53 expression and decreasing MGMT expression.	lomeguatrib-tmz	4-19	P53	Homo sapiens	109-112
25780433-4	2015	The results indicated that piperlongumine promoted doxorubicin sensitivity, apoptosis, the intracellular accumulation of rhodamine-123, the activities of caspase-3 and -8, and the expression of reactive oxygen species, p53, p27 and p-PTEN.	piperlonguminine	27-41	P53	Homo sapiens	219-222
26400731-0	2016	Formaldehyde-induced paxillin-tyrosine phosphorylation and paxillin and P53 downexpression in Hela cells.	Formaldehyde	0-12	P53	Homo sapiens	72-75
25515142-12	2015	In addition, iodine-131 may upregulate GADD45 mRNA expression in HTori-3 cells, resulting in G2/M phase arrest in a p53-independent pathway.	Iodine	13-19	P53	Homo sapiens	116-119
26016020-2	2015	An increase in the IL-6, IL-8, TNF-alpha and p53 genes expression in the concentration range of silver and titanium dioxide nanoparticles of 10-40 muk g/ml was found.	Silver	96-102	P53	Homo sapiens	45-48
24475287-4	2014	It has been recently proposed that tyrosinase related protein 2 (TRP2), a protein involved in melanin synthesis, may act as suppressor of the p53 pathway in melanoma.	Melanins	94-101	P53	Homo sapiens	142-145
26016020-2	2015	An increase in the IL-6, IL-8, TNF-alpha and p53 genes expression in the concentration range of silver and titanium dioxide nanoparticles of 10-40 muk g/ml was found.	titanium dioxide	107-123	P53	Homo sapiens	45-48
26824362-10	2016	Consistent with the potential inhibition of ATM by squalene, IR-induced phosphorylation of ATM effectors such as p53 (Ser15) and Chk1 (Ser317) was inhibited by cell treatment with squalene.	Squalene	51-59	P53	Homo sapiens	113-116
25469820-7	2015	EPA inhibited SNP-induced chondrocyte apoptosis, caspase 3 and poly(ADP-ribose) polymerase cleavage, phosphorylation of p38 MAPK and p53, and expression of MMP3 and MMP13.	Eicosapentaenoic Acid	0-3	P53	Homo sapiens	133-136
24247248-6	2014	Whereas hirsutenone treatment activated p53, its modest efficacy in p53-mutant and -null cell lines suggested the existence of a p53-independent mode of action.	hirsutenone	8-19	P53	Homo sapiens	40-43
24761875-8	2014	p53 PIN3 genotype was determined using electrophoresis of PCR products on 8% non-denaturing polyacrylamide gels and silver staining.	Silver	116-122	P53	Homo sapiens	0-3
24125776-7	2014	Finally, the tumor-suppressing effect of HMSNs-BTZ was enhanced in the presence of wild-type p53 signaling, suggesting a potential enhancement in clinical efficacy with combined p53 gene therapy and BTZ-based chemotherapy.	hmsns-btz	41-50	P53	Homo sapiens	93-96
26824362-10	2016	Consistent with the potential inhibition of ATM by squalene, IR-induced phosphorylation of ATM effectors such as p53 (Ser15) and Chk1 (Ser317) was inhibited by cell treatment with squalene.	Squalene	180-188	P53	Homo sapiens	113-116
24125776-7	2014	Finally, the tumor-suppressing effect of HMSNs-BTZ was enhanced in the presence of wild-type p53 signaling, suggesting a potential enhancement in clinical efficacy with combined p53 gene therapy and BTZ-based chemotherapy.	hmsns-btz	41-50	P53	Homo sapiens	178-181
26358421-7	2016	Malignant pleural mesothelioma (MPM) is an aggressive asbestos-related tumor where wild-type p53 might be present.	Asbestos	54-62	P53	Homo sapiens	93-96
24189097-8	2014	Therefore, the multifunctional gamma-CD-OEI-SS-FA/PTX self-assembly system with the synergistic effects of redox-sensitive FA-targeted and PTX-enhanced p53 gene delivery may be promising for cancer therapeutic application.	gamma-cyclodextrin	31-39	P53	Homo sapiens	152-155
25958121-6	2015	Moreover, treatment of ascorbic acid inhibited p53 accumulation at 3 days after irradiation.	Ascorbic Acid	23-36	P53	Homo sapiens	47-50
25647416-5	2015	On the contrary, when the CTDBS was blocked by antibody used for immunoprecipitation, all p53-DNA complexes were completely dissociated from the p53 protein in KCl concentrations&gt;=200 mM under the same conditions.	ctdbs	26-31	P53	Homo sapiens	90-93
25647416-5	2015	On the contrary, when the CTDBS was blocked by antibody used for immunoprecipitation, all p53-DNA complexes were completely dissociated from the p53 protein in KCl concentrations&gt;=200 mM under the same conditions.	ctdbs	26-31	P53	Homo sapiens	145-148
25647416-6	2015	These observations suggest: (a) different ways for association and dissociation of the p53-DNA complexes in the presence of the CTDBS; and (b) a critical role for a sliding mechanism, mediated by the C-terminal domain, in the dissociation process.	ctdbs	128-133	P53	Homo sapiens	87-90
24940695-4	2014	We have demonstrated using the human Burkitt"s lymphoma B-cell line, Raji, that p53, p63 and p73 all accumulate in the nucleus, following treatment of cells with fludarabine nucleoside (2-FaraA).	2-faraa	186-193	P53	Homo sapiens	80-83
26599530-0	2016	Design and synthesis of a C7-aryl piperlongumine derivative with potent antimicrotubule and mutant p53-reactivating properties.	piperlonguminine	34-48	P53	Homo sapiens	99-102
25147862-4	2014	Further results indicated that Vit C caused the dysregulation of some stress responses factors (SIRT1, p53 and FOXO3) in ARPE-19 cells response to H2O2.	Ascorbic Acid	31-36	P53	Homo sapiens	103-106
25505174-4	2015	Mechanistically, we found that co-treatment with BI2536 and metformin induced p53-dependent apoptosis and further activated the p53/Redd-1 pathway.	BI 2536	49-55	P53	Homo sapiens	78-81
25772694-10	2016	Pretreatment of cells with meloxicam blocked the translocation of p53 from the cytosol to the nucleus.	Meloxicam	27-36	P53	Homo sapiens	66-69
25505174-4	2015	Mechanistically, we found that co-treatment with BI2536 and metformin induced p53-dependent apoptosis and further activated the p53/Redd-1 pathway.	BI 2536	49-55	P53	Homo sapiens	128-131
26434906-0	2015	Induction of Apoptosis by Eugenol and Capsaicin in Human Gastric Cancer AGS Cells--Elucidating the Role of p53.	Eugenol	26-33	P53	Homo sapiens	107-110
26434906-3	2015	The aim of the study was to elucidate the role of p53 in the induction of apoptosis by eugenol and capsaicin in a human gastric cancer cell line, AGS.	Eugenol	87-94	P53	Homo sapiens	50-53
26434906-9	2015	CONCLUSIONS: Unlike capsaicin, eugenol could induce apoptosis both in presence and absence of functional p53.	Eugenol	31-38	P53	Homo sapiens	105-108
24035753-0	2013	Perfluorooctanoic acid induces apoptosis through the p53-dependent mitochondrial pathway in human hepatic cells: a proteomic study.	perfluorooctanoic acid	0-22	P53	Homo sapiens	53-56
24035753-7	2013	Induction of apoptosis via the p53-dependent mitochondrial pathway is further suggested as one of the key toxicological events occurring in L-02 cells under PFOA stress.	perfluorooctanoic acid	157-161	P53	Homo sapiens	31-34
24179531-5	2013	Immunohistochemically, EVNs are characterized by the robust expression of synaptophysin, but with a lack of oligodendrocyte transcription factor 2, isocitrate dehydrogenase enzyme isoform 1 (IDH1) R132/IDH2 R172 mutations and p53 immunoexpression.	evns	23-27	P53	Homo sapiens	226-229
23820125-2	2013	Serdemetan induced a dose-dependent inhibition of proliferation in both wild-type (wt) and mutant (mut) p53 cell lines, with IC50 values from 0.25 to 3 muM/l, in association with an S phase cell cycle arrest.	JNJ 26854165	0-10	P53	Homo sapiens	104-107
25772694-11	2016	Together, these data suggest that meloxicam may exert anti-apoptotic effects against FPN-induced cytotoxicity by both attenuating oxidative stress and inhibiting the inflammatory cascade via inactivation of MAPK and p53 signaling.	Meloxicam	34-43	P53	Homo sapiens	216-219
25333296-0	2015	Icariside II inhibits cell proliferation and induces cell cycle arrest through the ROS-p38-p53 signaling pathway in A375 human melanoma cells.	icariside	0-9	P53	Homo sapiens	91-94
26471831-5	2016	RESULTS: mTOR inhibitors AZD8055, RAD-001, rapamycin and BEZ235 induced synergistic cytotoxicity with the Chk1 inhibitor V158411 in p53 mutant colon cancer cells.	dactolisib	57-63	P53	Homo sapiens	132-135
23821658-0	2013	NOTCH1, SF3B1, and TP53 mutations in fludarabine-refractory CLL patients treated with alemtuzumab: results from the CLL2H trial of the GCLLSG.	fludarabine	37-48	P53	Homo sapiens	19-23
23821658-1	2013	We studied the incidences, associations, and prognostic roles of NOTCH1 and SF3B1 mutations (NOTCH1(mut), SF3B1(mut)) as compared with TP53(mut) in fludarabine-refractory chronic lymphocytic leukemia (CLL) patients treated with alemtuzumab in the CLL2H trial.	fludarabine	148-159	P53	Homo sapiens	135-139
27178816-0	2016	Radiosensitization of Non-Small Cell Lung Cancer Cells by Inhibition of TGF-beta1 Signaling With SB431542 Is Dependent on p53 Status.	4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide	97-105	P53	Homo sapiens	122-125
25512388-0	2014	FL118 induces p53-dependent senescence in colorectal cancer cells by promoting degradation of MdmX.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	0-5	P53	Homo sapiens	14-17
25512388-4	2014	Here, we report that FL118 activates tumor suppressor p53 as a novel MOA in p53 wild-type cancer cells.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	21-26	P53	Homo sapiens	54-57
27178816-7	2016	To study whether the radiosensitizing effect of SB431542 was associated with p53 status of cancer cells, the p53 of H460 cells was silenced using shRNA transfection.	4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide	48-56	P53	Homo sapiens	77-80
25512388-4	2014	Here, we report that FL118 activates tumor suppressor p53 as a novel MOA in p53 wild-type cancer cells.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	21-26	P53	Homo sapiens	76-79
25512388-6	2014	FL118 inhibits p53 polyubiquitination and monoubiquitination by Mdm2-MdmX E3 complex in cells and in cell-free systems.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	0-5	P53	Homo sapiens	15-18
23812671-8	2013	Suppression of p53 in melanoma cells abrogated Nt-3"s effects fully and vemurafenib"s effects partially.	Vemurafenib	72-83	P53	Homo sapiens	15-18
23812671-11	2013	CONCLUSION: These results show preclinical feasibility for overcoming primary vemurafenib resistance by restoring p53 function.	Vemurafenib	78-89	P53	Homo sapiens	114-117
27178816-12	2016	Thus, we concluded that the radiosensitizing effect of inhibition of TGF-beta1 signaling in NSCLC cells by SB431542 was p53 dependent, suggesting that using TGF-beta1 inhibitor in radiotherapy may be more complicated than previously thought and may need further investigation.	4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide	107-115	P53	Homo sapiens	120-123
23802716-1	2013	Analogues of the previously described spiro[imidazo[1,5-c]thiazole-3,3"-indoline]-2",5,7(6H,7aH)-trione p53 modulators were prepared to explore new structural requirements at the thiazolidine domain for the antiproliferative activity and p53 modulation.	spiro[imidazo[1,5-c]thiazole-3,3"-indoline]-2",5,7(6h,7ah)-trione	38-103	P53	Homo sapiens	104-107
25512388-8	2014	Coimmunoprecipitation revealed that FL118 slightly decreases Mdm2-p53 interactions and moderately increases Mdm2-MdmX interactions, suggesting a change of targeting specificity of Mdm2-MdmX E3 complex from p53 to MdmX, resulting in accelerated MdmX degradation.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	36-41	P53	Homo sapiens	66-69
25512388-8	2014	Coimmunoprecipitation revealed that FL118 slightly decreases Mdm2-p53 interactions and moderately increases Mdm2-MdmX interactions, suggesting a change of targeting specificity of Mdm2-MdmX E3 complex from p53 to MdmX, resulting in accelerated MdmX degradation.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	36-41	P53	Homo sapiens	206-209
25512388-10	2014	Activation of the p53 pathway by FL118 induces p53-dependent senescence in colorectal cancer cells.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	33-38	P53	Homo sapiens	18-21
26584879-0	2015	2,30-Bis(10H-indole) heterocycles: New p53/MDM2/MDMX antagonists.	2,30-bis(10h-indole)	0-20	P53	Homo sapiens	39-42
25512388-10	2014	Activation of the p53 pathway by FL118 induces p53-dependent senescence in colorectal cancer cells.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	33-38	P53	Homo sapiens	47-50
25512388-11	2014	However, in the absence of p53 or in the presence of MdmX overexpression, FL118 promotes p53-independent apoptosis.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	74-79	P53	Homo sapiens	89-92
25490748-0	2014	Mimulone-induced autophagy through p53-mediated AMPK/mTOR pathway increases caspase-mediated apoptotic cell death in A549 human lung cancer cells.	mimulone	0-8	P53	Homo sapiens	35-38
23417568-6	2013	We also observed that menadione induced JNK-dependent p53 expression and apoptotic death in SK-N-MC cells while H2O2-induced JNK activation was p53 independent.	Vitamin K 3	22-31	P53	Homo sapiens	54-57
26330291-7	2015	We found that FK866 induced cell senescence and diminished cellular NAD(+) levels and SIRT1 activity (detected by acetylation of p53), and these effects were dramatically antagonized by co-treatment with nicotinic acid, nicotinamide, or NAD(+).	Niacin	204-218	P53	Homo sapiens	129-132
23794094-0	2013	A TP53 founder mutation, p.R337H, is associated with phyllodes breast tumors in Brazil.	phyllodes	53-62	P53	Homo sapiens	2-6
23794094-1	2013	A few studies have reported phyllodes tumors (PT) of the breast with germline TP53 mutations.	phyllodes	28-37	P53	Homo sapiens	78-82
24301089-7	2014	Furthermore, the proteomic results especially proposed that the inhibition of HNRNPC, HUWE1 and UBQLN1, as well as the induction of PAF1 is involved in the activation of the p53 and c-myc signaling pathways, which then trigger the apoptotic process in L-02 cells exposed to PFOS.	perfluorooctane sulfonic acid	274-278	P53	Homo sapiens	174-177
27093815-0	2015	[Pacilitaxel induces human nasopharyngeal carcinoma cell line CNE2 apoptosis and growth inhibition by suppressing PI3K/AKT/p53 signaling pathway].	pacilitaxel	1-12	P53	Homo sapiens	123-126
25145672-9	2014	Our findings provide a preclinical basis upon which to evaluate SAR405838 as a therapeutic agent in patients whose tumors retain wild-type p53.	SAR405838	64-73	P53	Homo sapiens	139-142
23525490-9	2013	The results suggest that the anti-cancer effect of tetrandrine in Huh-7 cells may be mediated by p53-independent pathways.	tetrandrine	51-62	P53	Homo sapiens	97-100
26451628-10	2015	Taken together, these results demonstrate that PCB29-pQ induces oxidative stress and promotes p53-dependent DNA damage checkpoint activation, S-phase cycle arrest, and extrinsic apoptosis in HepG2 cells.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	47-55	P53	Homo sapiens	94-97
23608376-14	2013	No correlation was found between cell sensitivity to casticin and that to p53 status, suggesting that casticin induce a p53-independent apoptosis.	casticin	102-110	P53	Homo sapiens	120-123
25294809-0	2014	Small molecule restoration of wildtype structure and function of mutant p53 using a novel zinc-metallochaperone based mechanism.	zinc-metallochaperone	90-111	P53	Homo sapiens	72-75
26465338-3	2015	Fibroblasts cultured on commercial tissue culture polystyrene (TCPS) entered senescence after 55-60 population doublings (PDs), and were accompanied by larger cell shape, higher senescence-associated beta-galactosidase (SA beta-gal) activity, lower proliferation capacity, and upregulation of senescence-associated molecular markers p21, p53, retinoblastoma (pRB), and p16.	tcps	63-67	P53	Homo sapiens	338-341
24499675-0	2014	Arsenite induces premature senescence via p53/p21 pathway as a result of DNA damage in human malignant glioblastoma cells.	arsenite	0-8	P53	Homo sapiens	42-45
24499675-1	2014	In this study, we investigate whether arsenite-induced DNA damage leads to p53-dependent premature senescence using human glioblastoma cells with p53-wild type (U87MG-neo) and p53 deficient (U87MG-E6).	arsenite	38-46	P53	Homo sapiens	75-78
24499675-5	2014	This suggests that arsenite induces premature senescence as a result of DNA damage with heterochromatin forming through a p53/p21 dependent pathway.	arsenite	19-27	P53	Homo sapiens	122-125
24499675-7	2014	Taken together, arsenite reduces cell growth independently of p53 and induces premature senescence via p53/p21-dependent pathway following DNA damage.	arsenite	16-24	P53	Homo sapiens	62-65
23545901-6	2013	The p53 and p21 promoter luciferase activities were induced by GABARBP, whereas there was no effect on the p53-/- and p21-/- system.	gabarbp	63-70	P53	Homo sapiens	4-7
23545901-8	2013	Taken together, our results indicate that GABARBP can regulate the pro-apoptotic activity of cisplatin via the upregulation of p53 expression.	gabarbp	42-49	P53	Homo sapiens	127-130
24499675-7	2014	Taken together, arsenite reduces cell growth independently of p53 and induces premature senescence via p53/p21-dependent pathway following DNA damage.	arsenite	16-24	P53	Homo sapiens	103-106
26459859-8	2015	All these parameters conclude that elevated unconjugated bilirubin causes thrombocytopenia by stimulating platelet apoptosis via mitochondrial ROS-induced p38 and p53 activation.	Bilirubin	57-66	P53	Homo sapiens	163-166
25086499-3	2014	Furthermore, while p53R2, a p53-inducible peptide involved in the synthesis of dNTPs normally works toward suppression of cancer through elimination of reactive oxygen species (ROS), inhibition of MAPK/ERK pathway and providing dNTPs for DNA repair, the overexpression of p53R2 is reported to be associated with cancer progression and resistance to therapy.	Parathion	79-84	P53	Homo sapiens	19-22
23380477-0	2013	Autophagy takes place in mutated p53 neuroblastoma cells in response to hypoxia mimetic CoCl(2).	cobaltous chloride	88-95	P53	Homo sapiens	33-36
23380477-5	2013	We focused on CoCl2-induced cell death in a DNA-binding mutated p53 neuroblastoma cell line (SKNBE(2c)).	cobaltous chloride	14-19	P53	Homo sapiens	64-67
23380477-6	2013	An autophagic signaling was evidenced by an increase of Beclin-1, ATG 5-12, and LC3-II expression whereas the p53(mut) presence decreased with CoCl2 time exposure.	cobaltous chloride	143-148	P53	Homo sapiens	110-113
26427060-0	2015	Design, Synthesis and Evaluation of 2,5-Diketopiperazines as Inhibitors of the MDM2-p53 Interaction.	2,5-dioxopiperazine	36-57	P53	Homo sapiens	84-87
23015227-4	2013	Perifosine blocks Akt/mTOR complex 1 (mTORC1) signaling, while promoting caspase-3, c-Jun N-terminal kinases (JNK), and p53 activation.	perifosine	0-10	P53	Homo sapiens	120-123
24997481-5	2014	In addition, CPC/wt-p53 complexes co-delivering CD and wild type p53 (wt-p53) gene achieved synergistic angiogenesis suppression by more effectively downregulating the expression of vascular endothelial growth factor (VEGF) mRNA and protein via different pathways in vitro, as compared to mono-delivery and mixed-delivery systems.	candesartan	48-50	P53	Homo sapiens	20-23
26427060-3	2015	We have designed and synthesised two series of 2,5-diketopiperazines as inhibitors of the MDM2-p53 interaction.	2,5-dioxopiperazine	47-68	P53	Homo sapiens	95-98
25003641-4	2014	Recently developed specific ATR inhibitor, VE-821 (3-amino-6-(4-(methylsulfonyl)phenyl)-N-phenylpyrazine-2-carboxamide), has been reported to have a significant radio- and chemo-sensitizing effect delimited to cancer cells (largely p53-deficient) without affecting normal cells.	3-amino-6-(4-(methylsulfonyl)phenyl)-N-phenylpyrazine-2-carboxamide	43-49	P53	Homo sapiens	232-235
23184052-7	2013	Subgroup analyses by ethnicity showed that TP53 Arg72Pro polymorphism contributed to bladder cancer risk in East Asians in three genetic models (For Pro vs. Arg, Fixed-effects OR 1.18, 95 % CI 1.05-1.32; For ProPro vs. ArgArg, Fixed-effects OR 1.40, 95 % CI 1.11-1.77; For ProPro vs. ArgPro/ArgArg, Fixed-effects OR 1.32, 95 % CI 1.07-1.62).	prolyl-proline	208-214	P53	Homo sapiens	43-47
26472972-9	2015	Curcumin and citral generated ROS and activated p53 and poly (ADP-ribose) polymerase-1 mediated apoptotic pathways.	citral	13-19	P53	Homo sapiens	48-51
23184052-7	2013	Subgroup analyses by ethnicity showed that TP53 Arg72Pro polymorphism contributed to bladder cancer risk in East Asians in three genetic models (For Pro vs. Arg, Fixed-effects OR 1.18, 95 % CI 1.05-1.32; For ProPro vs. ArgArg, Fixed-effects OR 1.40, 95 % CI 1.11-1.77; For ProPro vs. ArgPro/ArgArg, Fixed-effects OR 1.32, 95 % CI 1.07-1.62).	arginylarginine	219-225	P53	Homo sapiens	43-47
23184052-7	2013	Subgroup analyses by ethnicity showed that TP53 Arg72Pro polymorphism contributed to bladder cancer risk in East Asians in three genetic models (For Pro vs. Arg, Fixed-effects OR 1.18, 95 % CI 1.05-1.32; For ProPro vs. ArgArg, Fixed-effects OR 1.40, 95 % CI 1.11-1.77; For ProPro vs. ArgPro/ArgArg, Fixed-effects OR 1.32, 95 % CI 1.07-1.62).	prolyl-proline	273-279	P53	Homo sapiens	43-47
23184052-7	2013	Subgroup analyses by ethnicity showed that TP53 Arg72Pro polymorphism contributed to bladder cancer risk in East Asians in three genetic models (For Pro vs. Arg, Fixed-effects OR 1.18, 95 % CI 1.05-1.32; For ProPro vs. ArgArg, Fixed-effects OR 1.40, 95 % CI 1.11-1.77; For ProPro vs. ArgPro/ArgArg, Fixed-effects OR 1.32, 95 % CI 1.07-1.62).	arginylproline	284-290	P53	Homo sapiens	43-47
23184052-7	2013	Subgroup analyses by ethnicity showed that TP53 Arg72Pro polymorphism contributed to bladder cancer risk in East Asians in three genetic models (For Pro vs. Arg, Fixed-effects OR 1.18, 95 % CI 1.05-1.32; For ProPro vs. ArgArg, Fixed-effects OR 1.40, 95 % CI 1.11-1.77; For ProPro vs. ArgPro/ArgArg, Fixed-effects OR 1.32, 95 % CI 1.07-1.62).	arginylarginine	291-297	P53	Homo sapiens	43-47
23247439-0	2013	Tetramethylpyrazine induces G0/G1 cell cycle arrest and stimulates mitochondrial-mediated and caspase-dependent apoptosis through modulating ERK/p53 signaling in hepatic stellate cells in vitro.	tetramethylpyrazine	0-19	P53	Homo sapiens	145-148
25003641-4	2014	Recently developed specific ATR inhibitor, VE-821 (3-amino-6-(4-(methylsulfonyl)phenyl)-N-phenylpyrazine-2-carboxamide), has been reported to have a significant radio- and chemo-sensitizing effect delimited to cancer cells (largely p53-deficient) without affecting normal cells.	3-amino-6-(4-(methylsulfonyl)phenyl)-N-phenylpyrazine-2-carboxamide	51-118	P53	Homo sapiens	232-235
25003641-9	2014	Taken together, our data indicates that ATR kinase has multiple roles in response to DNA damage throughout the cell cycle and that its inhibitor VE-821 is a potent radiosensitizing agent for p53-negative HL-60 cells.	3-amino-6-(4-(methylsulfonyl)phenyl)-N-phenylpyrazine-2-carboxamide	145-151	P53	Homo sapiens	191-194
24841907-0	2014	Isoorientin induces apoptosis and autophagy simultaneously by reactive oxygen species (ROS)-related p53, PI3K/Akt, JNK, and p38 signaling pathways in HepG2 cancer cells.	homoorientin	0-11	P53	Homo sapiens	100-103
23247439-9	2013	Mechanistic investigations revealed that TMP selectively blocked the extracellular signal-regulated kinase (ERK) signaling and activated p53, which was required for TMP induction of caspase-dependent mitochondrial apoptosis in HSCs.	tetramethylpyrazine	41-44	P53	Homo sapiens	137-140
26143716-8	2015	These results demonstrated clearly that the 1D sliding dynamics of p53 is strongly dependent on the concentration of Mg(2+) and Ca(2+), which maintains the search distance of p53 along DNA in cells that lost homeostatic control of the divalent cations.	mg(2+	117-122	P53	Homo sapiens	67-70
23247439-9	2013	Mechanistic investigations revealed that TMP selectively blocked the extracellular signal-regulated kinase (ERK) signaling and activated p53, which was required for TMP induction of caspase-dependent mitochondrial apoptosis in HSCs.	tetramethylpyrazine	165-168	P53	Homo sapiens	137-140
23247439-12	2013	These data collectively revealed that TMP modulation of ERK/p53 signaling led to mitochondrial-mediated and caspase-dependent apoptosis in HSCs in vitro.	tetramethylpyrazine	38-41	P53	Homo sapiens	60-63
27481281-2	2013	Quercetin and taxifolin bind to p53 binding hydrophobic groove of MDM2, and alter the conformation of groove as evidenced by 65 ns molecular dynamics simulation.	taxifolin	14-23	P53	Homo sapiens	32-35
23816816-9	2013	These effects were absent when the caspase inhibitor z-VAD-fmk or p53 inhibitor PFTalpha were applied, suggesting that casticin could trigger cell apoptosis in a caspase-3 and p53-dependent manner.	casticin	119-127	P53	Homo sapiens	66-69
23816816-9	2013	These effects were absent when the caspase inhibitor z-VAD-fmk or p53 inhibitor PFTalpha were applied, suggesting that casticin could trigger cell apoptosis in a caspase-3 and p53-dependent manner.	casticin	119-127	P53	Homo sapiens	176-179
24709078-0	2014	Lidamycin regulates p53 expression by repressing Oct4 transcription.	C 1027	0-9	P53	Homo sapiens	20-23
24657168-3	2014	The inositol pyrophosphates, such as 5-diphosphoinositol pentakisphosphate (IP7), are generated by a family of inositol hexakisphosphate kinases (IP6Ks), of which IP6K2 has been implicated in p53-associated cell death.	pentakisphosphate	57-74	P53	Homo sapiens	192-195
26143716-8	2015	These results demonstrated clearly that the 1D sliding dynamics of p53 is strongly dependent on the concentration of Mg(2+) and Ca(2+), which maintains the search distance of p53 along DNA in cells that lost homeostatic control of the divalent cations.	mg(2+	117-122	P53	Homo sapiens	175-178
24286312-0	2014	Nutlin-3 downregulates p53 phosphorylation on serine392 and induces apoptosis in hepatocellular carcinoma cells.	serine392	46-55	P53	Homo sapiens	23-26
25818601-5	2015	Our data illustrated that PCB29-pQ induces the phosphorylation of p53, which was mediated by ataxia telangiectasia mutated (ATM) protein kinase.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	26-34	P53	Homo sapiens	66-69
24249420-1	2014	Time-resolved fluorescence anisotropy spectroscopy was applied to study the interaction between a peptide truncated from the binding site of tumor suppressor p53 protein and the DNAs covalently labeled with 6-carboxyfluorescein (FAM) dye.	6-carboxyfluorescein	207-227	P53	Homo sapiens	158-161
23012397-6	2013	Moreover, at both these sites, PAb416 expression was significantly associated with p53 nuclear accumulation.	pab416	31-37	P53	Homo sapiens	83-86
25914192-0	2015	Rational Design of Ruthenium Complexes Containing 2,6-Bis(benzimidazolyl)pyridine Derivatives with Radiosensitization Activity by Enhancing p53 Activation.	2,6-bis(benzimidazolyl)pyridine	50-81	P53	Homo sapiens	140-143
22953760-8	2013	Differential expressions of proteins such as p53, Bax, caspase-3, and caspase-9 were significantly up-regulated in PFOS-exposed hosts, whereas Bcl-2 expression was significantly down-regulated.	perfluorooctane sulfonic acid	115-119	P53	Homo sapiens	45-48
24375191-7	2014	Subgroup analysis by race showed that TP53 Arg72Pro polymorphism was associated with thyroid carcinoma in Caucasians (ProPro vs. ArgArg/ArgPro, OR = 2.31, 95% CI 1.08 to 4.93, P = 0.03).	prolyl-proline	118-124	P53	Homo sapiens	38-42
24375191-7	2014	Subgroup analysis by race showed that TP53 Arg72Pro polymorphism was associated with thyroid carcinoma in Caucasians (ProPro vs. ArgArg/ArgPro, OR = 2.31, 95% CI 1.08 to 4.93, P = 0.03).	arginylarginine	129-135	P53	Homo sapiens	38-42
25754349-5	2015	RS4;11 and MV4;11 tumors treated with SAR405838 acquire resistance to the drug by mutation of the TP53 gene or compromise of p53 protein function.	SAR405838	38-47	P53	Homo sapiens	98-102
24375191-7	2014	Subgroup analysis by race showed that TP53 Arg72Pro polymorphism was associated with thyroid carcinoma in Caucasians (ProPro vs. ArgArg/ArgPro, OR = 2.31, 95% CI 1.08 to 4.93, P = 0.03).	arginylproline	136-142	P53	Homo sapiens	38-42
24189165-0	2014	Activation of p53 by spermine mediates induction of autophagy in HT1080 cells.	Spermine	21-29	P53	Homo sapiens	14-17
24189165-2	2014	The efficacy of spermine was investigated on induction of autophagy through histone deacetylation and p53 activation in human fibrosarcoma cell line, HT1080.	Spermine	16-24	P53	Homo sapiens	102-105
24225580-5	2013	DynaMine provides molecular biologists with an important new method that grasps the dynamical characteristics of any protein of interest, as we show here for human p53 and E1A from human adenovirus 5.	Amifampridine	0-8	P53	Homo sapiens	164-167
24340645-8	2013	CONCLUSIONS: Legulation of apoptosis by cycloferon and remaxol mediated by external and p53-dependent pathway is confirmed by increased expression of CD95 and p53 protein.	Remaxol	55-62	P53	Homo sapiens	88-91
24340645-8	2013	CONCLUSIONS: Legulation of apoptosis by cycloferon and remaxol mediated by external and p53-dependent pathway is confirmed by increased expression of CD95 and p53 protein.	Remaxol	55-62	P53	Homo sapiens	159-162
24189165-7	2014	In addition, the expression levels of protein such as acetyl-p53, p-p53, Bcl-2 and caspase-9 inducing apoptosis were increased in the presence of spermine.	Spermine	146-154	P53	Homo sapiens	61-64
24189165-7	2014	In addition, the expression levels of protein such as acetyl-p53, p-p53, Bcl-2 and caspase-9 inducing apoptosis were increased in the presence of spermine.	Spermine	146-154	P53	Homo sapiens	68-71
24189165-9	2014	These results suggest that activation of HAT in the presence of spermine promotes the induction of autophagy in HT1080 cells through the enhanced activity of p-p53 and acetyl p53.	Spermine	64-72	P53	Homo sapiens	160-163
24189165-9	2014	These results suggest that activation of HAT in the presence of spermine promotes the induction of autophagy in HT1080 cells through the enhanced activity of p-p53 and acetyl p53.	Spermine	64-72	P53	Homo sapiens	175-178
23041153-0	2012	Cleistanthoside A tetraacetate-induced DNA damage leading to cell cycle arrest and apoptosis with the involvement of p53 in lung cancer cells.	cleistanthoside A tetraacetate	0-30	P53	Homo sapiens	117-120
25754349-5	2015	RS4;11 and MV4;11 tumors treated with SAR405838 acquire resistance to the drug by mutation of the TP53 gene or compromise of p53 protein function.	SAR405838	38-47	P53	Homo sapiens	125-128
25839657-5	2015	When the antioxidant ascorbic acid was used to eliminate excess ROS, the levels of antioxidant enzymes (catalase, SOD1 and 2, p-FOXO1, and p53) were partly restored.	Ascorbic Acid	21-34	P53	Homo sapiens	139-142
22937789-6	2012	Both S-MDM4 and MDM2 expressions were significantly increased after fludarabine treatment of CLL cells without p53 aberrations (P = 0.013 and P = 0.030).	fludarabine	68-79	P53	Homo sapiens	111-114
25965177-0	2015	A distinct p53 target gene set predicts for response to the selective p53-HDM2 inhibitor NVP-CGM097.	NVP-CGM097	93-99	P53	Homo sapiens	11-14
23052131-0	2012	Expression level of DEK in chronic lymphocytic leukemia is regulated by fludarabine and Nutlin-3 depending on p53 status.	fludarabine	72-83	P53	Homo sapiens	110-113
23052131-6	2012	Both fludarabine and Nutlin-3 significantly downregulated DEK in the primary CLL cells which were with normal function of p53, or without deletion or mutation of p53 (p = 0.042, p = 0.038; p = 0.021, p = 0.017; p = 0.037, p = 0.017).	fludarabine	5-16	P53	Homo sapiens	122-125
25965177-0	2015	A distinct p53 target gene set predicts for response to the selective p53-HDM2 inhibitor NVP-CGM097.	NVP-CGM097	93-99	P53	Homo sapiens	70-73
23052131-8	2012	These data show that DEK might be applied for the assessment of prognosis in patients with CLL, and fludarabine and Nutlin-3 regulate DEK expression depended on p53 status.	fludarabine	100-111	P53	Homo sapiens	161-164
26019998-4	2015	Additionally, the molecular mechanisms of lappaconitine"s analgesic effects may be related to affect the expression levels of endogenous opioid system genes (POMC, PENK and MOR), as well as apoptosis-related genes (Xiap, Smac, Bim, NF-kappaB and p53).	lappaconitine	42-55	P53	Homo sapiens	246-249
22981429-5	2012	THSG weekly activated SIRT1 activity, stimulated eNOS promoter reporter gene activity, and ameliorated H(2)O(2)-induced cellular senescence and K373 acetylation of p53 in cultured human umbilical vein endothelial cells (HUVECs).	2,3,5,4'-tetrahydroxystilbene 2-O-glucopyranoside	0-4	P53	Homo sapiens	164-167
22981429-6	2012	CONCLUSIONS: THSG improves blood flow and ameliorates vascular senescence by increasing eNOS expression and Sirt1 activity and decreasing acetylation of p53 at K373 site, at least in part, both in vitro and in vivo.	2,3,5,4'-tetrahydroxystilbene 2-O-glucopyranoside	13-17	P53	Homo sapiens	153-156
25829127-1	2015	In this paper, N-isopropylacrylamide-modified polyethylenimine (PEN) was constructed through Michael addition and employed as a carrier to achieve the p53 gene delivery, using HeLa (p53wt) and PC-3 cells (p53null) as models.	n-isopropylacrylamide-modified polyethylenimine	15-62	P53	Homo sapiens	151-154
22841670-5	2012	Further mechanistic studies revealed that bufotalin treatment induced cell cycle arrest at G(2)/M phase through down-regulation of Aurora A, CDC25, CDK1, cyclin A and cyclin B1, as well as up-regulation of p53 and p21.	bufotalin	42-51	P53	Homo sapiens	206-209
25829127-1	2015	In this paper, N-isopropylacrylamide-modified polyethylenimine (PEN) was constructed through Michael addition and employed as a carrier to achieve the p53 gene delivery, using HeLa (p53wt) and PC-3 cells (p53null) as models.	n-isopropylacrylamide-modified polyethylenimine	15-62	P53	Homo sapiens	182-185
25814188-3	2015	Herein, we report the identification of a dual inhibitor of the p53 interaction with MDM2 and MDMX, the (S)-tryptophanol derivative OXAZ-1, from the screening of a small library of enantiopure tryptophanol-derived oxazolopiperidone lactams, using a yeast-based assay.	tryptophanol	104-120	P53	Homo sapiens	64-67
22939915-10	2012	In addition, dioscin inhibited APAP-induced activation and expression of CYP2E1, up-regulated the expression of Bcl-2 and Bid, and inhibited the expression of Bax, Bak and p53.	Acetaminophen	31-35	P53	Homo sapiens	172-175
25814188-3	2015	Herein, we report the identification of a dual inhibitor of the p53 interaction with MDM2 and MDMX, the (S)-tryptophanol derivative OXAZ-1, from the screening of a small library of enantiopure tryptophanol-derived oxazolopiperidone lactams, using a yeast-based assay.	tryptophanol	108-120	P53	Homo sapiens	64-67
23168703-6	2012	Mutational analysis of TP53 was done in DNA extracted from formalin fixed paraffin embedded tissue of 80 CaP and 24 BPH cases.	Formaldehyde	59-67	P53	Homo sapiens	23-27
24858040-5	2015	Here, we reported a first beneficial link between p53 and uric acid.	Uric Acid	58-67	P53	Homo sapiens	50-53
24858040-6	2015	We identified the uric acid transporter SLC2A9 (also known as GLUT9) as a direct p53 target gene and a key downstream effector in the reduction of reactive oxygen species (ROS) through transporting uric acid as a source of antioxidant.	Uric Acid	18-27	P53	Homo sapiens	81-84
25667043-7	2015	Moreover, TPT as single agent stimulates p53(ser15) phosphorylation, p53 PARylation and occupancy of the p21WAF promoter by p53 resulting in an increase of p21WAF expression.	Topotecan	10-13	P53	Homo sapiens	41-44
22829200-9	2012	Interestingly, alpha-tocopherol (vitamin E) treatment, but not other antioxidants, rescued SDH(var+) cells from apoptosis resistance and protected SDH(var+) cells from oxidative damage such as decreased lipid peroxidation as well as partially recovered p53 expression and NAD/NADH levels.	alpha-Tocopherol	15-31	P53	Homo sapiens	253-256
25667043-7	2015	Moreover, TPT as single agent stimulates p53(ser15) phosphorylation, p53 PARylation and occupancy of the p21WAF promoter by p53 resulting in an increase of p21WAF expression.	Topotecan	10-13	P53	Homo sapiens	69-72
22584119-2	2012	Perifosine inhibited UVB-induced pro-survival Akt/mammalian target of rapamycin (mTOR) and ERK activation, while facilitating pro-apoptotic AMP-activated protein kinas (AMPK), c-Jun-NH(2)-kinase (JNK), and p53 activation; these signaling changes together promoted a striking increase in skin cell apoptosis and a significantly reduced amount of DNA damages.	perifosine	0-10	P53	Homo sapiens	206-209
25667043-7	2015	Moreover, TPT as single agent stimulates p53(ser15) phosphorylation, p53 PARylation and occupancy of the p21WAF promoter by p53 resulting in an increase of p21WAF expression.	Topotecan	10-13	P53	Homo sapiens	69-72
25667043-8	2015	Interestingly, PJ34 in combination with TPT enhances p53 occupancy at the BAX promoter and is associated with increased BAX protein level.	Topotecan	40-43	P53	Homo sapiens	53-56
25821946-9	2015	Furthermore, phosphorylation of ATM targets, including gammaH2AX and serine 15 (S15) on p53, were increased in Rap1 silencing cells in response to etoposide.	gammah2ax	55-64	P53	Homo sapiens	88-91
22504106-7	2012	Asbestos exposure significantly correlated with p53, p21(waf) and mdm2 aberrations (p=0.001, p=0.03, p=0.02).	Asbestos	0-8	P53	Homo sapiens	48-51
22797300-7	2012	Our identification of HCLK2 as a substrate of PHD3 reveals the mechanism through which hypoxia inhibits the DDR, suggesting hydroxylation of HCLK2 is a potential therapeutic target for regulating the ATR/CHK1/p53 pathway.	hclk2	141-146	P53	Homo sapiens	209-212
22348919-7	2012	Notably, 5-epi-sinuleptolide up-regulated p53 and p21 expression and inhibited G2/M phase regulators of cyclin B1 and cyclin-dependent kinease 1 (CDK1) in SCC25 cells.	5-episinuleptolide	9-28	P53	Homo sapiens	42-45
25412322-6	2015	In addition, reverse transcription quantitative polymerase chain reaction and western blot analysis revealed that simvastatin-treated cells exhibited increased expression levles of Notch1, p53, and Bax, as well as decreased expression levels of B cell lymphoma 2; furthermore, Notch1 upregulation resulted in the inhibition of Akt phosphorylation.	Simvastatin	114-125	P53	Homo sapiens	189-192
22722496-0	2012	S-phase sensing of DNA-protein crosslinks triggers TopBP1-independent ATR activation and p53-mediated cell death by formaldehyde.	Formaldehyde	116-128	P53	Homo sapiens	89-92
25663901-7	2015	Ad-p53 infusion via IIHTBA promoted the protein expression levels of p53, however, it inhibited the protein expression levels of MMP2 and VEGF, indirectly indicating that the gene may inhibit the growth of liver cancer.	iihtba	20-26	P53	Homo sapiens	3-6
25663901-7	2015	Ad-p53 infusion via IIHTBA promoted the protein expression levels of p53, however, it inhibited the protein expression levels of MMP2 and VEGF, indirectly indicating that the gene may inhibit the growth of liver cancer.	iihtba	20-26	P53	Homo sapiens	69-72
22464689-7	2012	The transcriptional activity of NF-kB, an upstream activator of p53 is suppressed in both cell lines when treated with anethole.	anethole	119-127	P53	Homo sapiens	64-67
25779644-12	2015	Protein translocation was examined by confocal laser microscopy, and we found that kaempferol increased the levels of p-H2AX and p-p53 in HL-60 cells.	kaempferol	83-93	P53	Homo sapiens	131-134
22447124-0	2012	Blockade of p53 by HIF-2alpha, but not HIF-1alpha, is involved in arsenite-induced malignant transformation of human bronchial epithelial cells.	arsenite	66-74	P53	Homo sapiens	12-15
22447124-12	2012	Thus, our studies show that blockade of p53 function by inhibiting the ubiquitin-mediated proteasome degradation of HIF-2alpha, but not that of HIF-1alpha, is involved in arsenite-induced proliferation and neoplastic transformation of HBE cells.	arsenite	171-179	P53	Homo sapiens	40-43
25550551-7	2015	At the same time, S-petasin and iso-S-petasin increased mitochondrial membrane permeability and cytochrome c release from mitochondria to the cytosol via reducing the ratio of BCL2/BAX in DU145 and PC3 cells, and up-regulating the levels of p53 in DU145 cells but down-regulating it in PC3 cells.	iso-s-petasin	32-45	P53	Homo sapiens	241-244
22592527-6	2012	Videomicroscopy-based cell fate profiling revealed that, in response to high-dose reversine, TP53 (-/-)  (but not TP53 (+/+) ) cells undergo several consecutive rounds of abortive mitosis, resulting in the generation of hyperpolyploid cells that are prone to succumb to apoptosis upon the activation of mitotic catastrophe.	2-(4-morpholinoanilino)-6-cyclohexylaminopurine	82-91	P53	Homo sapiens	93-97
22592527-7	2012	In line with this notion, the depletion of anti-apoptotic proteins of the BCL-2 family sensitized TP53 (-/-)  cells to the toxic effects of high-dose reversine.	2-(4-morpholinoanilino)-6-cyclohexylaminopurine	150-159	P53	Homo sapiens	98-102
22592527-9	2012	Altogether, these results suggest that p53-deficient cells are particularly sensitive to the simultaneous inhibition of multiple kinases, including MPS1, as it occurs in response to high-dose reversine.	2-(4-morpholinoanilino)-6-cyclohexylaminopurine	192-201	P53	Homo sapiens	39-42
25528022-7	2015	BAY 80-6946 inhibited PI3K signalling and was effective in cells regardless of their PI3K, P53 or PTEN status.	copanlisib	0-11	P53	Homo sapiens	91-94
22641291-1	2012	PURPOSE: Human Raji cells treated with fludarabine nucleoside (2-FaraA, 3 muM) undergo apoptosis with accumulation of p53 in the nuclei as multiple phosphorylated isoforms and C-terminal truncated derivatives.	fludarabine	63-70	P53	Homo sapiens	118-121
22641291-8	2012	CONCLUSIONS AND CLINICAL RELEVANCE: Comprehensive information on the subcellular distributions and responses of p53, p63 and p73 to 2-FaraA provides additional insight into mechanisms for induction of apoptosis in the treatment of B-lymphoproliferative disorders with fludarabine.	fludarabine	132-139	P53	Homo sapiens	112-115
25338966-2	2015	We screened a library of 7920 chemical compounds for the p53 activator and identified N-[2-(dimethylamino)ethyl]-2,3-dimethyl-4-oxo-4H-pyrido[1,2-a]thieno[2,3-d]pyrimidine-9-carboxamide (PTP), which significantly increased p53-mediated reporter activity in colorectal cancer cells.	N-(2-(dimethylamino)ethyl)-2,3-dimethyl-4-oxo-4H-pyrido(1,2-a)thieno(2,3-d)pyrimidine-9-carboxamide	86-185	P53	Homo sapiens	57-60
22366412-0	2012	DNA-PKcs-mediated stabilization of p53 by JNK2 is involved in arsenite-induced DNA damage and apoptosis in human embryo lung fibroblast cells.	arsenite	62-70	P53	Homo sapiens	35-38
22366412-6	2012	Knockdown of DNA-PKcs/JNK2 signal pathway or p53 reduces apoptosis but elevates the DNA damage induced by a high level of arsenite.	arsenite	122-130	P53	Homo sapiens	45-48
25338966-2	2015	We screened a library of 7920 chemical compounds for the p53 activator and identified N-[2-(dimethylamino)ethyl]-2,3-dimethyl-4-oxo-4H-pyrido[1,2-a]thieno[2,3-d]pyrimidine-9-carboxamide (PTP), which significantly increased p53-mediated reporter activity in colorectal cancer cells.	N-(2-(dimethylamino)ethyl)-2,3-dimethyl-4-oxo-4H-pyrido(1,2-a)thieno(2,3-d)pyrimidine-9-carboxamide	86-185	P53	Homo sapiens	223-226
22366412-7	2012	These results suggest that DNA-PKcs-mediated stabilization of p53 by JNK2 is involved in arsenite-induced DNA damage and apoptosis.	arsenite	89-97	P53	Homo sapiens	62-65
25338966-2	2015	We screened a library of 7920 chemical compounds for the p53 activator and identified N-[2-(dimethylamino)ethyl]-2,3-dimethyl-4-oxo-4H-pyrido[1,2-a]thieno[2,3-d]pyrimidine-9-carboxamide (PTP), which significantly increased p53-mediated reporter activity in colorectal cancer cells.	N-(2-(dimethylamino)ethyl)-2,3-dimethyl-4-oxo-4H-pyrido(1,2-a)thieno(2,3-d)pyrimidine-9-carboxamide	187-190	P53	Homo sapiens	57-60
25338966-2	2015	We screened a library of 7920 chemical compounds for the p53 activator and identified N-[2-(dimethylamino)ethyl]-2,3-dimethyl-4-oxo-4H-pyrido[1,2-a]thieno[2,3-d]pyrimidine-9-carboxamide (PTP), which significantly increased p53-mediated reporter activity in colorectal cancer cells.	N-(2-(dimethylamino)ethyl)-2,3-dimethyl-4-oxo-4H-pyrido(1,2-a)thieno(2,3-d)pyrimidine-9-carboxamide	187-190	P53	Homo sapiens	223-226
27905780-2	2014	According to this approval of idelalisib, the G-BA distinguished between 2 subindications within the therapeutic indication CLL: pretreated patients and treatment-naive patients with 17p deletion and/or TP53 mutation.	g-ba	46-50	P53	Homo sapiens	203-207
22450794-8	2012	However, the interaction between p53 and T antigen was inhibited at a TBT or TPT concentration of 10-9 M, respectively.	tbt	70-73	P53	Homo sapiens	33-36
21765469-4	2012	In this study, we use cell penetrating peptide conjugates of phosphorodiamidate morpholino oligomers (PPMOs) to inhibit p53 expression.	DIAMIDOPHOSPHATE	61-79	P53	Homo sapiens	120-123
25214240-4	2014	RESULTS: To better understand the apoptotic effect of EBR, we aimed to investigate the cellular responses in p53 null, PC3 prostate cancer cells.	EBR	54-57	P53	Homo sapiens	109-112
22138446-6	2012	We show that concurrent treatment with GA and TPT is able to reverse TPT induced up-regulation of the anti-apoptotic protein Bcl2 in both p53+/+ and p53-/- HCT116 cells.	tpt	46-49	P53	Homo sapiens	138-141
22138446-6	2012	We show that concurrent treatment with GA and TPT is able to reverse TPT induced up-regulation of the anti-apoptotic protein Bcl2 in both p53+/+ and p53-/- HCT116 cells.	tpt	46-49	P53	Homo sapiens	149-152
22138446-6	2012	We show that concurrent treatment with GA and TPT is able to reverse TPT induced up-regulation of the anti-apoptotic protein Bcl2 in both p53+/+ and p53-/- HCT116 cells.	tpt	69-72	P53	Homo sapiens	138-141
22138446-6	2012	We show that concurrent treatment with GA and TPT is able to reverse TPT induced up-regulation of the anti-apoptotic protein Bcl2 in both p53+/+ and p53-/- HCT116 cells.	tpt	69-72	P53	Homo sapiens	149-152
25214240-5	2014	We showed that EBR induced mitochondria-mediated and caspase-dependent apoptosis in wt and p53 stable transfected PC3 cells, which suggesting that EBR-induced apoptosis regardless of p53 expression.	EBR	15-18	P53	Homo sapiens	91-94
25214240-5	2014	We showed that EBR induced mitochondria-mediated and caspase-dependent apoptosis in wt and p53 stable transfected PC3 cells, which suggesting that EBR-induced apoptosis regardless of p53 expression.	EBR	147-150	P53	Homo sapiens	91-94
25568812-0	2014	Rapid and Sensitive Detection of p53 Based on DNA-Protein Binding Interactions Using Silver Nanoparticle Films and Microwave Heating.	Silver	85-91	P53	Homo sapiens	33-36
22256804-2	2012	METHODS: We performed a molecular analysis to identify oncogenic mutations (HRAS, KRAS, NRAS, CDKN2A, and TP53) in the lesions from patients treated with the BRAF inhibitor vemurafenib.	Vemurafenib	173-184	P53	Homo sapiens	106-110
25182801-8	2014	These effects were influenced by the p53 activity: cells carrying an active p53 were more sensitive to the combination of PARP inhibitor and RT, while cells carrying an inactive p53 displayed a higher sensitivity to the combination of PARP inhibitor and TPT.	Topotecan	254-257	P53	Homo sapiens	37-40
22715313-9	2012	Here, we have identified three drug-like compounds that are ZINC01019934, ZINC00624418 and ZINC00664532 adequate to interrupt stability of p53-mortalin complex that warrant for anticancer agent.	zinc01019934	60-72	P53	Homo sapiens	139-142
25182801-8	2014	These effects were influenced by the p53 activity: cells carrying an active p53 were more sensitive to the combination of PARP inhibitor and RT, while cells carrying an inactive p53 displayed a higher sensitivity to the combination of PARP inhibitor and TPT.	Topotecan	254-257	P53	Homo sapiens	76-79
25182801-8	2014	These effects were influenced by the p53 activity: cells carrying an active p53 were more sensitive to the combination of PARP inhibitor and RT, while cells carrying an inactive p53 displayed a higher sensitivity to the combination of PARP inhibitor and TPT.	Topotecan	254-257	P53	Homo sapiens	76-79
22719783-8	2012	In addition, 6-gingerol treatment elevated intracellular reactive oxygen species (ROS) and phosphorylation level of p53.	gingerol	13-23	P53	Homo sapiens	116-119
25182801-9	2014	Our study suggests that p53 activity influences the differential sensitivity of GBM cells to combined treatments of TPT, RT, and PARP inhibitors.	Topotecan	116-119	P53	Homo sapiens	24-27
22719783-9	2012	These findings indicate that exposure of 6-gingerol may induce intracellular ROS and upregulate p53, p27(Kip1), and p21(Cip1) levels leading to consequent decrease of CDK1, cyclin A, and cyclin B1 as result of cell cycle arrest in LoVo cells.	gingerol	41-51	P53	Homo sapiens	96-99
25263558-7	2014	Furthermore, Blm-s is a direct target gene of p53 and AP1 via the ataxia telangiectasia mutated (ATM)- and c-Jun N-terminal kinase (JNK)-signaling pathways activated by DSBs.	dsbs	169-173	P53	Homo sapiens	46-49
23056207-9	2012	Also, decreased androgen receptor, prostate specific antigen, p53 and p21 protein levels were demonstrated in response to treatment with NU9056.	1,2-bis(isothiazol-5-yl)disulfane	137-143	P53	Homo sapiens	62-65
24454781-10	2014	The increased binding of the H-Ras transcriptional regulator p53 to its consensus sequence within the intronic CpG island further confirmed the effect of EPA as demethylating agent.	Eicosapentaenoic Acid	154-157	P53	Homo sapiens	61-64
24711049-0	2014	Nickel accumulation in lung tissues is associated with increased risk of p53 mutation in lung cancer patients.	Nickel	0-6	P53	Homo sapiens	73-76
24275138-7	2014	However, combining the latter with 100muM CoCl2 was preferentially toxic for mutant p53 C8161 melanoma, and was enhanced by catalase in wt p53 C8161 cells.	cobaltous chloride	42-47	P53	Homo sapiens	84-87
24275138-7	2014	However, combining the latter with 100muM CoCl2 was preferentially toxic for mutant p53 C8161 melanoma, and was enhanced by catalase in wt p53 C8161 cells.	cobaltous chloride	42-47	P53	Homo sapiens	139-142
23029106-8	2012	Although the survivin promoter-reporter system was used for the identification of FL118, our studies revealed that FL118 not only inhibits survivin expression but also selectively and independently inhibits three additional cancer-associated survival genes (Mcl-1, XIAP and cIAP2) in a p53 status-independent manner, while showing no inhibitory effects on control genes.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	115-120	P53	Homo sapiens	286-289
24711049-3	2014	This study assessed whether nickel exposure increased the occurrence of p53 mutations due to DNA repair inhibition by nickel.	Nickel	28-34	P53	Homo sapiens	72-75
24772329-4	2014	The p53 activation induced in response to the inhibition of the electron transport chain complex III has been shown to be triggered by the impairment of the de novo pyrimidine biosynthesis due to the suppression of DHODH.	pyrimidine	165-175	P53	Homo sapiens	4-7
24711049-3	2014	This study assessed whether nickel exposure increased the occurrence of p53 mutations due to DNA repair inhibition by nickel.	Nickel	118-124	P53	Homo sapiens	72-75
23024792-2	2012	In this study, sensitising topotecan to colon cancer cells with different P53 status via modulation of autophagy was examined.	Topotecan	27-36	P53	Homo sapiens	74-77
24711049-5	2014	Nickel levels in p53 mutant patients were significantly higher than those in p53 wild-type patients.	Nickel	0-6	P53	Homo sapiens	17-20
23024792-3	2012	METHODOLOGY/PRINCIPAL FINDINGS: The DNA damage induced by topotecan treatment resulted in cytoprotective autophagy in colon cancer cells with wild-type p53.	Topotecan	58-67	P53	Homo sapiens	152-155
24711049-6	2014	When patients were divided into high- and low-nickel subgroups by median nickel level, the high-nickel subgroup of patients had an odds ratio (OR) of 3.25 for p53 mutation risk relative to the low-nickel subgroup patients.	Nickel	46-52	P53	Homo sapiens	159-162
23024792-4	2012	However, in cells with mutant p53 or p53 knockout, treatment with topotecan induced autophagy-associated cell death.	Topotecan	66-75	P53	Homo sapiens	30-33
23024792-4	2012	However, in cells with mutant p53 or p53 knockout, treatment with topotecan induced autophagy-associated cell death.	Topotecan	66-75	P53	Homo sapiens	37-40
23024792-5	2012	In wild-type p53 colon cancer cells, topotecan treatment activated p53, upregulated the expression of sestrin 2, induced the phosphorylation of the AMPKalpha subunit at Thr172, and inhibited the mTORC1 pathway.	Topotecan	37-46	P53	Homo sapiens	13-16
24641404-0	2014	D-pinitol promotes apoptosis in MCF-7 cells via induction of p53 and Bax and inhibition of Bcl-2 and NF-kappaB.	pinitol	0-9	P53	Homo sapiens	61-64
24641404-9	2014	The results revealed that D-pinitol significantly inhibited the proliferation of MCF-7 cells in a concentration-dependent manner, while upregulating the expression of p53, Bax and down regulating Bcl-2 and NF-kB.	pinitol	26-35	P53	Homo sapiens	167-170
24841718-0	2014	Low ATM protein expression and depletion of p53 correlates with olaparib sensitivity in gastric cancer cell lines.	olaparib	64-72	P53	Homo sapiens	44-47
24841718-6	2014	Moreover, reducing ATM kinase activity using a small-molecule inhibitor (KU55933) or shRNA-mediated depletion of ATM protein enhanced olaparib sensitivity in gastric cancer cell lines with depletion or inactivation of p53.	olaparib	134-142	P53	Homo sapiens	218-221
23024792-5	2012	In wild-type p53 colon cancer cells, topotecan treatment activated p53, upregulated the expression of sestrin 2, induced the phosphorylation of the AMPKalpha subunit at Thr172, and inhibited the mTORC1 pathway.	Topotecan	37-46	P53	Homo sapiens	67-70
23024792-6	2012	Furthermore, the inhibition of autophagy enhanced the anti-tumour effect of topotecan treatment in wild-type p53 colon cancer cells but alleviated the anti-tumour effect of topotecan treatment in p53 knockout cells in vivo.	Topotecan	76-85	P53	Homo sapiens	109-112
23024792-6	2012	Furthermore, the inhibition of autophagy enhanced the anti-tumour effect of topotecan treatment in wild-type p53 colon cancer cells but alleviated the anti-tumour effect of topotecan treatment in p53 knockout cells in vivo.	Topotecan	173-182	P53	Homo sapiens	196-199
23024792-7	2012	CONCLUSIONS/SIGNIFICANCE: These results imply that the wild-type p53-dependent induction of cytoprotective autophagy is one of the cellular responses that determines the cellular sensitivity to the DNA-damaging drug topotecan.	Topotecan	216-225	P53	Homo sapiens	65-68
25147862-7	2014	Interestingly, data also revealed the dysregulation of p53 and FOXO3 was dependent on the regulation of SIRT1 rather than Vit C.	Ascorbic Acid	122-127	P53	Homo sapiens	55-58
24711049-6	2014	When patients were divided into high- and low-nickel subgroups by median nickel level, the high-nickel subgroup of patients had an odds ratio (OR) of 3.25 for p53 mutation risk relative to the low-nickel subgroup patients.	Nickel	73-79	P53	Homo sapiens	159-162
24711049-6	2014	When patients were divided into high- and low-nickel subgroups by median nickel level, the high-nickel subgroup of patients had an odds ratio (OR) of 3.25 for p53 mutation risk relative to the low-nickel subgroup patients.	Nickel	73-79	P53	Homo sapiens	159-162
24711049-6	2014	When patients were divided into high- and low-nickel subgroups by median nickel level, the high-nickel subgroup of patients had an odds ratio (OR) of 3.25 for p53 mutation risk relative to the low-nickel subgroup patients.	Nickel	73-79	P53	Homo sapiens	159-162
22916232-0	2012	Modeling of arylamide helix mimetics in the p53 peptide binding site of hDM2 suggests parallel and anti-parallel conformations are both stable.	arylamide	12-21	P53	Homo sapiens	44-47
24711049-7	2014	The OR for p53 mutation risk of lifetime non-smokers, particularly females, in the high-nickel subgroup was greater than that in the low-nickel subgroup.	Nickel	88-94	P53	Homo sapiens	11-14
22916232-4	2012	Results from both docking and molecular dynamics simulations are consistent with the arylamides binding in the p53 peptide binding pocket.	arylamides	85-95	P53	Homo sapiens	111-114
24330704-11	2013	Moreover, eugenol up-regulated the versatile cyclin-dependent kinase inhibitor p21WAF1 protein, and inhibited the proliferation of breast cancer cells in a p53-independent manner.	Eugenol	10-17	P53	Homo sapiens	156-159
22916232-5	2012	Simulations of arylamides in the p53 binding pocket of hDM2 are consistent with binding, exhibiting similar structural dynamics in the pocket as simulations of known hDM2 binders Nutlin-2 and a benzodiazepinedione compound.	arylamides	15-25	P53	Homo sapiens	33-36
24711049-7	2014	The OR for p53 mutation risk of lifetime non-smokers, particularly females, in the high-nickel subgroup was greater than that in the low-nickel subgroup.	Nickel	137-143	P53	Homo sapiens	11-14
22916232-8	2012	In the first, the arylamide compound lies parallel to the observed p53 helix.	arylamide	18-27	P53	Homo sapiens	67-70
22916232-9	2012	In the second class, not previously identified or proposed, the arylamide compound lies anti-parallel to the p53 helix.	arylamide	64-73	P53	Homo sapiens	109-112
24711049-10	2014	Therefore, increased risk of p53 mutation due to defective DNA repair caused by high nickel levels in lung tissues may be one mechanism by which nickel exposure contributes to lung cancer development, especially in lifetime female non-smokers.	Nickel	85-91	P53	Homo sapiens	29-32
24711049-10	2014	Therefore, increased risk of p53 mutation due to defective DNA repair caused by high nickel levels in lung tissues may be one mechanism by which nickel exposure contributes to lung cancer development, especially in lifetime female non-smokers.	Nickel	145-151	P53	Homo sapiens	29-32
24954032-9	2014	Our data indicate interplay between p53, FoxO3a and 14-3-3 leading to an attenuated BaP induced apoptosis in cells co-exposed to TCDD, PCB 153 or estradiol.	2,2',4,4',5,5'-Hexachlorobiphenyl	135-142	P53	Homo sapiens	36-39
21937165-1	2011	Serdemetan (JNJ-26854165) is a novel tryptamine compound with antiproliferative activity in various p53 wild-type (WT) tumor cell lines.	JNJ 26854165	0-10	P53	Homo sapiens	100-103
21937165-5	2011	At 2Gy, surviving fractions were 0.72 and 0.97 for p53-WT HCT116 and p53-null cells exposed to 0.5muM of Serdemetan, respectively (p&lt;0.05).	JNJ 26854165	105-115	P53	Homo sapiens	51-54
21937165-5	2011	At 2Gy, surviving fractions were 0.72 and 0.97 for p53-WT HCT116 and p53-null cells exposed to 0.5muM of Serdemetan, respectively (p&lt;0.05).	JNJ 26854165	105-115	P53	Homo sapiens	69-72
23911866-0	2013	A ruthenium(II) beta-carboline complex induced p53-mediated apoptosis in cancer cells.	ruthenium(ii) beta-carboline	2-30	P53	Homo sapiens	47-50
24802382-0	2014	Ciprofloxacin as a potential radio-sensitizer to tumor cells and a radio-protectant for normal cells: differential effects on gamma-H2AX formation, p53 phosphorylation, Bcl-2 production, and cell death.	Ciprofloxacin	0-13	P53	Homo sapiens	148-151
24164297-4	2013	Since p53-Delta30 was efficiently labeled, poly(ADP-ribosyl)ation target site(s) of wt-p53 must reside outside its carboxy-terminal-domain.	poly(adp-ribosyl)	43-60	P53	Homo sapiens	87-90
24121233-1	2013	A novel series of 3-methyl-1-benzofuran derivatives were synthesized and screened in vitro for their antiproliferative activity against two human NSCLC cell lines (NSCLC-N6 mutant p53 and A549 wild type p53).	3-Methylbenzofuran	18-39	P53	Homo sapiens	180-183
22134241-3	2011	Thus, we hypothesized that inhibition of HRR (mediated by Chk1 via AZD7762) and PARP1 [via olaparib (AZD2281)] would selectively sensitize p53 mutant pancreatic cancer cells to radiation.	olaparib	101-108	P53	Homo sapiens	139-142
22134241-6	2011	We found that the combination of AZD7762 and olaparib produced significant radiosensitization in p53 mutant pancreatic cancer cells and in all of the isogenic cancer cell lines.	olaparib	45-53	P53	Homo sapiens	97-100
22134241-7	2011	The magnitude of radiosensitization by AZD7762 and olaparib was greater in p53 mutant cells compared with p53 wild type cells.	olaparib	51-59	P53	Homo sapiens	75-78
24121233-1	2013	A novel series of 3-methyl-1-benzofuran derivatives were synthesized and screened in vitro for their antiproliferative activity against two human NSCLC cell lines (NSCLC-N6 mutant p53 and A549 wild type p53).	3-Methylbenzofuran	18-39	P53	Homo sapiens	203-206
22134241-7	2011	The magnitude of radiosensitization by AZD7762 and olaparib was greater in p53 mutant cells compared with p53 wild type cells.	olaparib	51-59	P53	Homo sapiens	106-109
24802382-8	2014	CIP pretreatment reduced Bcl-2 production but promoted p53 phosphorylation, caspase-3 activation and cell death.	Ciprofloxacin	0-3	P53	Homo sapiens	55-58
22101337-3	2011	Using gene expression microarray analysis, we find that DNA damage response (DDR) pathways elicited by veliparib (ABT-888), a PARP inhibitor, plus topotecan comprise the G1/S checkpoint, ATM, and p53 signaling pathways in p53-wildtype cancer cell lines and BRCA1, BRCA2 and ATR pathway in p53-mutant lines.	Topotecan	147-156	P53	Homo sapiens	196-199
22101337-3	2011	Using gene expression microarray analysis, we find that DNA damage response (DDR) pathways elicited by veliparib (ABT-888), a PARP inhibitor, plus topotecan comprise the G1/S checkpoint, ATM, and p53 signaling pathways in p53-wildtype cancer cell lines and BRCA1, BRCA2 and ATR pathway in p53-mutant lines.	Topotecan	147-156	P53	Homo sapiens	222-225
22101337-3	2011	Using gene expression microarray analysis, we find that DNA damage response (DDR) pathways elicited by veliparib (ABT-888), a PARP inhibitor, plus topotecan comprise the G1/S checkpoint, ATM, and p53 signaling pathways in p53-wildtype cancer cell lines and BRCA1, BRCA2 and ATR pathway in p53-mutant lines.	Topotecan	147-156	P53	Homo sapiens	222-225
22101337-4	2011	In contrast, topotecan alone induces the G1/S checkpoint pathway in p53-wildtype lines and not in p53-mutant cells.	Topotecan	13-22	P53	Homo sapiens	68-71
22829208-8	2013	Iodine-negative epithelium presented significantly higher immunoreactions for P53 and GLUT 1 in basal, parabasal, and superficial layers, respectively, whereas the reaction for Ki67 in the superficial layer was higher than that in iodine-positive epithelium (Wilcoxon signed-rank test, P &lt; 0.05).	Iodine	0-6	P53	Homo sapiens	78-81
24802382-10	2014	In normal healthy human PBMCs, CIP failed to block the radiation-induced gamma-H2AX increase but effectively increased Bcl-2 production, but blocked the phospho-p53 increase and subsequent cell death.	Ciprofloxacin	31-34	P53	Homo sapiens	161-164
24040331-1	2013	Serdemetan (JNJ-26854165), an antagonist to Mdm2, was anticipated to promote the activation of p53.	JNJ 26854165	0-10	P53	Homo sapiens	95-98
24889088-5	2014	Flow cytometric analysis and DNA fragmentation revealed that germacrone promoted apoptosis of glioma cells, associated with an increased expression of p53 and bax and decreased expression of bcl-2.	germacrone	61-71	P53	Homo sapiens	151-154
24040331-1	2013	Serdemetan (JNJ-26854165), an antagonist to Mdm2, was anticipated to promote the activation of p53.	JNJ 26854165	12-24	P53	Homo sapiens	95-98
21963806-3	2011	Sappanchalcone-treated oral cancer cells showed an increased cytosolic level of cytochrome c, downregulated Bcl-2 expression, upregulated Bax and p53 expression, caspase-3 and -9 activation, and poly (ADP-ribose) polymerase cleavage.	sappanchalcone	0-14	P53	Homo sapiens	146-149
23583370-0	2013	Simvastatin induced HCT116 colorectal cancer cell apoptosis through p38MAPK-p53-survivin signaling cascade.	Simvastatin	0-11	P53	Homo sapiens	76-79
25119920-9	2014	Among 20 patients who received fludarabine therapy, the overall remission rate for those with p53 gene deletion (20%) was lower than those without (75%) (P&lt;0.05).	fludarabine	31-42	P53	Homo sapiens	94-97
23583370-9	2013	Simvastatin"s actions on p21(cip/Waf1), survivin and apoptosis were reduced in p53 null HCT116 cells.	Simvastatin	0-11	P53	Homo sapiens	79-82
23583370-10	2013	Simvastatin caused an increase in p53 phosphorylation and acetylation.	Simvastatin	0-11	P53	Homo sapiens	34-37
23583370-11	2013	In addition, simvastatin activated p38 mitogen-activated protein kinase (p38MAPK), whereas an inhibitor of p38MAPK signaling abrogated simvastatin"s effects of increasing p53 and p21(cip/Waf1) promoter luciferase activity.	Simvastatin	135-146	P53	Homo sapiens	171-174
23583370-13	2013	Furthermore, Sp1 binding to the survivin promoter region decreased while p53 and p63 binding to the promoter region increased after simvastatin exposure.	Simvastatin	132-143	P53	Homo sapiens	73-76
21818781-6	2011	Upregulation of the p53 protein in benzidine-treated cells suggests the induction of the p53 DNA damage signaling pathway.	benzidine	35-44	P53	Homo sapiens	20-23
21818781-6	2011	Upregulation of the p53 protein in benzidine-treated cells suggests the induction of the p53 DNA damage signaling pathway.	benzidine	35-44	P53	Homo sapiens	89-92
23583370-14	2013	CONCLUSIONS: Simvastatin activates the p38MAPK-p53-survivin cascade to cause HCT116 colorectal cancer cell apoptosis.	Simvastatin	13-24	P53	Homo sapiens	47-50
25119920-14	2014	High-level ZAP-70 expression and the presence of p53 deletion are associated with shorter survival and poor response to fludarabine containing therapy.	fludarabine	120-131	P53	Homo sapiens	49-52
24996846-8	2014	Induction of gammaH2AX levels was chemotherapeutic dependent and correlated closely with potentiation of gemcitabine and camptothecin in p53 mutant colon cancer cells.	gammah2ax	13-22	P53	Homo sapiens	137-140
23696216-0	2013	Deubiquitinase inhibition of 19S regulatory particles by 4-arylidene curcumin analog AC17 causes NF-kappaB inhibition and p53 reactivation in human lung cancer cells.	4-arylidene curcumin	57-77	P53	Homo sapiens	122-125
21846830-6	2011	The ovarian cancer cell line A2780 and the p53-null lung cancer cell line H1299 were particularly sensitive to MCI13E treatment, with IC(50) values less than 3 mumol/L.	mci13e	111-117	P53	Homo sapiens	43-46
21687937-0	2011	The cell death response to the ROS inducer, cobalt chloride, in neuroblastoma cell lines according to p53 status.	cobaltous chloride	44-59	P53	Homo sapiens	102-105
21687937-4	2011	CoCl2 induced an upregulation of p53, p21 and PUMA expression in WT cells but not in SKNBE(2c).	cobaltous chloride	0-5	P53	Homo sapiens	33-36
24144307-5	2014	[Flu + Clo + Bu + SAHA] resulted in synergistic cytotoxicity, which can be attributed to (1) activated DNA-damage response and cell cycle checkpoint activation through the ATM-CHK2-P53 (or P73) pathway or ATM-CHK2-cdc25-cdc2 pathway, (2) histone modifications and (3) activated apoptosis pathway.	fludarabine	1-4	P53	Homo sapiens	181-184
21687937-5	2011	In SHSY5Y cells, p53 serine-15 phosphorylation appeared early (6 h) in the mitochondria, and also in the nucleus after 12 h. In contrast, in SKNBE(2c) cells, the slight nuclear signal disappeared with CoCl2 treatment.	cobaltous chloride	201-206	P53	Homo sapiens	17-20
21687937-9	2011	Finally, CoCl2 induced time-dependent canonical p53 mitochondrial apoptosis in the WT p53 cell line, and caspase-independent cell death in cells with a mutated or KO p53.	cobaltous chloride	9-14	P53	Homo sapiens	48-51
21687937-9	2011	Finally, CoCl2 induced time-dependent canonical p53 mitochondrial apoptosis in the WT p53 cell line, and caspase-independent cell death in cells with a mutated or KO p53.	cobaltous chloride	9-14	P53	Homo sapiens	86-89
21687937-9	2011	Finally, CoCl2 induced time-dependent canonical p53 mitochondrial apoptosis in the WT p53 cell line, and caspase-independent cell death in cells with a mutated or KO p53.	cobaltous chloride	9-14	P53	Homo sapiens	86-89
21425328-0	2011	Novel quinazoline HMJ-30 induces U-2 OS human osteogenic sarcoma cell apoptosis through induction of oxidative stress and up-regulation of ATM/p53 signaling pathway.	Quinazolines	6-17	P53	Homo sapiens	143-146
23856246-5	2013	Furthermore, we identify pharmacogenomic correlations between specific variants in genes such as TP53, BRAF, ERBBs, and ATAD5 and anticancer agents such as nutlin, vemurafenib, erlotinib, and bleomycin showing one of many ways the data could be used to validate and generate novel hypotheses for further investigation.	Vemurafenib	164-175	P53	Homo sapiens	97-101
23684722-0	2013	Physalin A induces apoptosis via p53-Noxa-mediated ROS generation, and autophagy plays a protective role against apoptosis through p38-NF-kappaB survival pathway in A375-S2 cells.	physalin A	0-10	P53	Homo sapiens	33-36
23684722-7	2013	Moreover, physalin A-induced apoptosis was triggered by activation of p53-Noxa pathway and intracellular reactive oxygen species (ROS) generation.	physalin A	10-20	P53	Homo sapiens	70-73
23861960-2	2013	Also PRODH2, which degrades 4-hydroxy-L-proline, a product of protein (e.g. collagen) catabolism, was recently described as a p53 target.	Hydroxyproline	28-47	P53	Homo sapiens	126-129
21663398-0	2011	Geldanamycin analog 17-DMAG limits apoptosis in human peripheral blood cells by inhibition of p53 activation and its interaction with heat-shock protein 90 kDa after exposure to ionizing radiation.	geldanamycin	0-12	P53	Homo sapiens	94-97
26417293-11	2014	The expression of mutant p53 is correlated to increased lipid peroxides (0.346, p&lt;0.05 ) and lowered antioxidant activity of CAT (- 0.437, p&lt;0.01) in the breast cancer patients.	Lipid Peroxides	56-71	P53	Homo sapiens	25-28
21725212-2	2011	We find that quinacrine stabilizes p53 and induces p53-dependent and independent cell death.	Quinacrine	13-23	P53	Homo sapiens	35-38
21725212-2	2011	We find that quinacrine stabilizes p53 and induces p53-dependent and independent cell death.	Quinacrine	13-23	P53	Homo sapiens	51-54
21725212-6	2011	While the synergistic effect of quinacrine with TRAIL appears to be in part independent of p53, knockdown of p53 in HepG2 cells by siRNA results in more cell death after treatment by quinacrine and TRAIL.	Quinacrine	183-193	P53	Homo sapiens	109-112
21725213-4	2011	We show that quinacrine synergizes with 5-fluorouracil and significantly enhances the cytotoxicity of sorafenib in a panel of 10 human colorectal cancer cell lines, including those with KRAS mutations protein gel blot analysis confirmed that quinacrine"s anticancer activity partially arises from its ability to stabilize p53 and lower anti-apoptotic protein levels.	Quinacrine	13-23	P53	Homo sapiens	322-325
23559539-6	2013	Intranuclear p53 protein levels were increased by ACA but decreased by sodium butyrate alone or combined treatment with ACA and sodium butyrate.	Acetates	50-53	P53	Homo sapiens	13-16
24932611-7	2014	Furthermore, CoCl2 treatment effectively induced the stabilization of HIF-1alpha, the differential expression of a truncated form of p53 (p47) and decreased levels of cyclin D1, indicating molecular mechanisms associated with cell cycle arrest at G2.	cobaltous chloride	13-18	P53	Homo sapiens	133-136
23771657-7	2013	The results showed that germacrone exposure decreased p-STAT3 and p-JAK2 and regulated expression of p53 and Bcl-2 family members at the same time.	germacrone	24-34	P53	Homo sapiens	101-104
21693655-3	2011	PATIENTS AND METHODS: Epithelial p53 expression was evaluated using two immunohistochemical antibodies (DO7 and 1801) in formalin-fixed, paraffin-embedded tissue from patients with node-positive breast cancer who were randomized to four cycles of cyclophosphamide and one of three doses of doxorubicin (60, 75, or 90 mg/m(2); AC) and to receive four subsequent cycles of paclitaxel (T) or not.	Formaldehyde	121-129	P53	Homo sapiens	33-36
24841907-8	2014	Furthermore, ISO-induced apoptosis by activating the Fas receptor-mediated apoptotic pathway and suppressing the p53 and PI3K/Akt-dependent NF-kappaB signaling pathway, with the subsequent increase in the release of cytochrome c, caspase-3 activation, and PARP cleavage.	homoorientin	13-16	P53	Homo sapiens	113-116
21521181-0	2011	A pilot monocentric analysis of efficacy and safety of Fludarabine-Campath combination (Flucam) as first line treatment in elderly patients with chronic lymphocytic leukaemia and Tp53 disfunction.	fludarabine	55-66	P53	Homo sapiens	179-183
24918290-4	2014	The results revealed that EPA attenuated PA-induced cell death and activation of apoptosis-related proteins, such as caspase-3, p53 and Bax.	Eicosapentaenoic Acid	26-29	P53	Homo sapiens	128-131
21464199-0	2011	Cyclopentenyl cytosine induces senescence in breast cancer cells through the nucleolar stress response and activation of p53.	cyclopentenyl cytosine	0-22	P53	Homo sapiens	121-124
21464199-2	2011	We have demonstrated that depletion of CTP induced by cyclopentenyl cytosine (CPEC; NSC 375575), a specific inhibitor of the enzyme CTP synthetase, induces irreversible growth arrest and senescence characterized by altered morphology and expression of senescence-associated beta-galactosidase activity in MCF-7 breast cancer cells expressing wild-type p53.	cyclopentenyl cytosine	54-76	P53	Homo sapiens	352-355
21464199-2	2011	We have demonstrated that depletion of CTP induced by cyclopentenyl cytosine (CPEC; NSC 375575), a specific inhibitor of the enzyme CTP synthetase, induces irreversible growth arrest and senescence characterized by altered morphology and expression of senescence-associated beta-galactosidase activity in MCF-7 breast cancer cells expressing wild-type p53.	cyclopentenyl cytosine	78-82	P53	Homo sapiens	352-355
24010301-9	2013	CONCLUSION: Curcumol can inhibit the proliferation of HepG2 cells in vitro and induce G1 arrest of cell cycle through mechanisms activating p53 and pRB pathways that involve genes of cyclin A1, CDK2, CDK8, p21WAF1 and p27KIP1.	curcumol	12-20	P53	Homo sapiens	140-143
23667851-5	2013	Germline TP53 mutation c.566C&gt;T results in the missense mutation GCC (Ala) to GTC (Val) at codon 189 (A189V) and has been reported in a case of multiple primary colon tumors.	Valine	86-89	P53	Homo sapiens	9-13
24684237-5	2014	The predicted targets of these miRNAs are clearly enriched in genes involved in heparan-sulfate biosynthesis, extracellular matrix-receptor interaction, carbohydrate digestion and absorption, p53 signaling, and cytokine-cytokine-receptor interaction.	Heparitin Sulfate	80-95	P53	Homo sapiens	192-195
23376119-2	2013	Our previous findings showed that the hydrophilic PARP inhibitor PJ34 enhances the sensitivity of p53 proficient MCF7 breast carcinoma cells to topotecan, a DNA Topoisomerase I (TOP 1) inhibitor.	Topotecan	144-153	P53	Homo sapiens	98-101
21620802-5	2011	The SUAM-14746-induced growth inhibition in NB-1 cells was associated with pronounced G(0)/G(1) arrest and reduced levels of phosphorylated retinoblastoma protein (pRb), cyclin E, and cyclin dependent kinase (CDK) 2, and increased levels of the CDK inhibitor p27(kip1) and the tumor suppressor p53.	3-((4-(2-styrylphenoxy)butanoyl)-4-hydroxyprolyl)thiazolidine	4-14	P53	Homo sapiens	294-297
24849675-0	2014	Silver nanoparticles induce p53-mediated apoptosis in human bronchial epithelial (BEAS-2B) cells.	Silver	0-6	P53	Homo sapiens	28-31
21626703-5	2011	The biophysical study of the interaction between a designed flexible tetraguanidinium-calix[4]arene and the tetramerization domain of protein p53 (p53TD) and its natural mutant p53TD-R337H shows how the floppy mutant domain interacts more tightly with the ligand than the well-packed wild-type protein.	tetraguanidinium-calix[4]arene	69-99	P53	Homo sapiens	142-145
23364526-2	2013	The aim of the present study was to test the hypothesis that reduced CHO availability enhances p53 signaling and expression of genes associated with regulation of mitochondrial biogenesis and substrate utilization in human skeletal muscle.	CAV protocol	69-72	P53	Homo sapiens	95-98
23364526-8	2013	We conclude that the exercise-induced increase in p53 phosphorylation is enhanced in conditions of reduced CHO availability, which may be related to upstream signaling through AMPK.	CAV protocol	107-110	P53	Homo sapiens	50-53
21626703-5	2011	The biophysical study of the interaction between a designed flexible tetraguanidinium-calix[4]arene and the tetramerization domain of protein p53 (p53TD) and its natural mutant p53TD-R337H shows how the floppy mutant domain interacts more tightly with the ligand than the well-packed wild-type protein.	tetraguanidinium-calix[4]arene	69-99	P53	Homo sapiens	147-150
24694947-9	2014	Lack of the same effect in p53-null H1299(DR-GFP) cells suggested that olaparib"s effect is p53 related, which was confirmed in p53-depleted U2OS(DR-GFP) and p53-null HCT116 cells.	olaparib	71-79	P53	Homo sapiens	92-95
21569639-3	2011	In particular, quinacrine"s role on the NF-kappaB, p53, and AKT pathways are summarized.	Quinacrine	15-25	P53	Homo sapiens	51-54
22981708-6	2013	A significant increase in the number of pan-gammaH2AX-staining apoptotic cells was observed only in p53-deficient cell lines.	gammah2ax	44-53	P53	Homo sapiens	100-103
23422857-0	2013	A low-carb diet kills tumor cells with a mutant p53 tumor suppressor gene: the Atkins diet suppresses tumor growth.	carb	6-10	P53	Homo sapiens	48-51
23354132-2	2013	We previously reported that simvastatin             triggered the mitochondrial apoptotic pathway in MethA fibrosarcoma cells, which             was accompanied by the translocation of stabilized p53 to the mitochondria.	Simvastatin	28-39	P53	Homo sapiens	196-199
24694947-9	2014	Lack of the same effect in p53-null H1299(DR-GFP) cells suggested that olaparib"s effect is p53 related, which was confirmed in p53-depleted U2OS(DR-GFP) and p53-null HCT116 cells.	olaparib	71-79	P53	Homo sapiens	92-95
23364682-5	2013	Iodinin also successfully induced cell death in patient-derived leukemia cells or cell lines with  features associated with poor prognostic such as FLT3 internal tandem duplications or mutated/deficient p53.	iodinin	0-7	P53	Homo sapiens	203-206
21518868-1	2011	Quinacrine, a drug with antimalarial and anticancer activities that inhibits NF-kappaB and activates p53, has progressed into phase II clinical trials in cancer.	Quinacrine	0-10	P53	Homo sapiens	101-104
24694947-9	2014	Lack of the same effect in p53-null H1299(DR-GFP) cells suggested that olaparib"s effect is p53 related, which was confirmed in p53-depleted U2OS(DR-GFP) and p53-null HCT116 cells.	olaparib	71-79	P53	Homo sapiens	92-95
24694947-11	2014	Our data show olaparib and veliparib differ in their off-target effects; olaparib, unlike veliparib, mitigates DNA damage repair activity via G(2) cell-cycle arrest-like effect in a p53-dependent manner.	olaparib	14-22	P53	Homo sapiens	182-185
24694947-11	2014	Our data show olaparib and veliparib differ in their off-target effects; olaparib, unlike veliparib, mitigates DNA damage repair activity via G(2) cell-cycle arrest-like effect in a p53-dependent manner.	olaparib	73-81	P53	Homo sapiens	182-185
24480460-5	2014	Treatment of cells overexpressing Aurora-A and ATM/Chk2 with the ATM specific inhibitor KU-55933 increased the cell sensitivity to cisplatin and irradiation through increasing the phosphorylation of p53 at Ser15 and inhibiting the expression of Chk2, gammaH2AX (Ser319), and RAD51.	gammah2ax	251-260	P53	Homo sapiens	199-202
21382360-5	2011	6-OHDA-induced IkappaB-alpha degradation, NF-kappaB p65 nuclear translocation, p53 and PUMA expression were partially blocked by Z-FY(t-Bu)-DMK.	Oxidopamine	0-6	P53	Homo sapiens	79-82
23841076-0	2013	The omega-3 polyunsaturated fatty acid DHA induces simultaneous apoptosis and autophagy via mitochondrial ROS-mediated Akt-mTOR signaling in prostate cancer cells expressing mutant p53.	omega-3 polyunsaturated fatty acid	4-38	P53	Homo sapiens	181-184
24743574-15	2014	Taken together, combined treatment with NVP-BEZ235 and curcumin induces apoptosis through p53-dependent Bcl-2 mRNA down-regulation at the transcriptional level and Mcl-1 protein down-regulation at the post-transcriptional level.	dactolisib	44-50	P53	Homo sapiens	90-93
23165143-10	2013	Sertraline and thioridazine interfere with this repressive feedback by targeting directly TPT1/TCTP and inhibiting its binding to MDM2, restoring wildtype p53 function.	Thioridazine	15-27	P53	Homo sapiens	155-158
21216846-6	2011	p-HPEA-EDA-induced activation of caspase-3 and poly-adenosine diphosphate-ribose polymerase, phosphorylation of p53 (Ser15) and DNA fragmentation in HT-29 cells, leading to apoptosis.	HPEA	2-6	P53	Homo sapiens	112-115
24717393-5	2014	Our results further demonstrated that this antitumor activity was caused by the activation of the p53-dependent apoptosis pathway via p53 phosphorylation at serine (15Ser).	15ser	165-170	P53	Homo sapiens	98-101
21199873-0	2011	Simvastatin prevents skeletal metastasis of breast cancer by an antagonistic interplay between p53 and CD44.	Simvastatin	0-11	P53	Homo sapiens	95-98
23063592-4	2013	It was observed that CPs caused the increased in Bax/Bcl-2 ratio and triggered the activation of Cleaved-caspase-3, p53 in HepG2 cells.	cps	21-24	P53	Homo sapiens	116-119
24717393-5	2014	Our results further demonstrated that this antitumor activity was caused by the activation of the p53-dependent apoptosis pathway via p53 phosphorylation at serine (15Ser).	15ser	165-170	P53	Homo sapiens	134-137
21145583-14	2011	The present study provides experimental evidence that TEGDMA interferes with the regulation of cellular pathways through transcription factors activated as a consequence of DNA damage like p53 or initiated downstream of MAPK (mitogen-activated protein kinases) like c-Jun, ATF-2 and ATF-3.	triethylene glycol dimethacrylate	54-60	P53	Homo sapiens	189-192
26580383-5	2014	Depending on its sequence, presence of staple, and/or a C-terminal tail, the peptide approaches MDM2 differently and not exclusively via the crack propagation mechanism proposed previously for p53.	Cocaine	141-146	P53	Homo sapiens	193-196
21429301-0	2011	Vitamin C increases the apoptosis via up-regulation p53 during cisplatin treatment in human colon cancer cells.	Ascorbic Acid	0-9	P53	Homo sapiens	52-55
24082817-14	2013	TMA analysis showed p53 overexpression in 25.7% of SA and 0% RAA, high Ki-67 in 35.3% of SA and 44.4% RAA, and hTERT expression in 100% of SA and RAA.	alpha-L-Rhamnose	61-64	P53	Homo sapiens	20-23
24082817-15	2013	TP53 mutations were detected in 13.5% of SA and 11.1% RAA.	alpha-L-Rhamnose	54-57	P53	Homo sapiens	0-4
24691273-6	2014	Our results demonstrate that metallic nickel nanoparticles caused higher activation of AP-1 and NF-kappaB, and a greater decrease of p53 transcription activity than fine particles.	Nickel	38-44	P53	Homo sapiens	133-136
23205301-0	2012	dNTP Supply Gene Expression Patterns after P53 Loss.	Parathion	0-4	P53	Homo sapiens	43-46
21263216-4	2011	BrdU photolysis resulted in well-controlled, dose- dependent generation of DSBs equivalent to radiation doses between 0.2 - 20 Gy, as determined by pulsed-field gel electrophoresis, and accompanied by dose-dependent ATM (ser-1981), H2AX (ser-139), Chk2 (thr-68), and p53 (ser-15) phosphorylation.	dsbs	75-79	P53	Homo sapiens	267-270
24637250-8	2014	The results indicated that CIT inhibited HUVECs proliferation and the cells were arrested at G0/G1 phase, which is associated with decreased levels of cyclinD1 and increased expression of p53 and p21.	citreoviridin	27-30	P53	Homo sapiens	188-191
21194611-4	2011	Previous studies have shown that uranyl acetate and uranyl nitrate are capable of inducing DNA strand breaks and potentially of inducing oxidative stress through free radical generation, two potential mechanisms for activation of p53.	uranyl acetate	33-47	P53	Homo sapiens	230-233
21194611-5	2011	Based on these studies, we hypothesized that either uranyl acetate or uranyl nitrate could act as an activator of p53.	uranyl acetate	52-66	P53	Homo sapiens	114-117
22865487-5	2012	Radicicol and geldanamycin induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels, an increase in Bax levels, the mitochondrial transmembrane potential loss, cytochrome c release, activation of caspases (-8, -9, and -3), cleavage of PARP-1, and an increase in the tumor suppressor p53 levels.	geldanamycin	14-26	P53	Homo sapiens	295-298
23003675-6	2012	Sedimentation field-flow fractionation (SdFFF) was first used to monitor physical parameter changes due to the hypoxia mimetic CoCl(2) in the p53 mutated SKNBE2(c) human neuroblastoma cell line.	cobaltous chloride	127-134	P53	Homo sapiens	142-145
21304979-7	2011	Simvastatin concomitantly increased p53-dependent expression of p53 up-regulated modulator of apoptosis (PUMA), NOXA, and damage-regulated autophagy modulator (DRAM).	Simvastatin	0-11	P53	Homo sapiens	36-39
21304979-7	2011	Simvastatin concomitantly increased p53-dependent expression of p53 up-regulated modulator of apoptosis (PUMA), NOXA, and damage-regulated autophagy modulator (DRAM).	Simvastatin	0-11	P53	Homo sapiens	64-67
23073516-1	2014	BACKGROUND: Investigation of p53 immunoreactivity in formalin-fixed paraffin-embedded tissues of normal renal tissue and renal cell carcinoma with respect to histopathologic subtype and nuclear grade of RCC.	Formaldehyde	53-61	P53	Homo sapiens	29-32
20875401-7	2011	Furthermore, TPT-dependent induction of p53, p21 and apoptosis were found 24-72h after treatment and were increased by PJ34 both in PARP-1 proficient and silenced cells.	Topotecan	13-16	P53	Homo sapiens	40-43
22940704-1	2012	In order to discuss the structure-activity relationship (SAR) of the thio-benzodiazepine compounds which showed excellent activity against p53-MDM2 protein-protein interaction, we designed and synthesized twenty compounds with electrophilic and nucleophilic groups on the benzene ring.	thio-benzodiazepine	69-88	P53	Homo sapiens	139-142
24118195-3	2013	We have compared ability of oxaliplatin and a novel platinum(IV) complex, LA-12, to modulate the cell cycle and induce apoptosis in human colon adenocarcinoma HCT116 wt and p53/p21 null cells, and have investigated molecular mechanisms involved.	UNII-37WM0V5E17	74-79	P53	Homo sapiens	173-176
21376265-5	2011	Subgroup analyses showed that P53 Arg72Pro was associated with risk of gallbladder and pancreatic cancer (OR [95% CI]: 1.44 [1.13-1.83] for Pro carriers vs. ArgArg).	arginylarginine	157-163	P53	Homo sapiens	30-33
24118195-7	2013	RESULTS: Our results highlight the outstanding ability of LA-12 to induce effective elimination of colon cancer cells independently of p53/p21, and in significantly lower doses compared to oxaliplatin.	UNII-37WM0V5E17	58-63	P53	Homo sapiens	135-138
21454974-4	2011	Further experiments revealed that DMFC induced apoptosis in HepG2 cells through both extrinsic and intrinsic apoptotic pathways in a p53-dependent manner.	3,5-dimethyl-7H-furo(3,2-g)chromen-7-one	34-38	P53	Homo sapiens	133-136
23933099-0	2013	Simvastatin rises reactive oxygen species levels and induces senescence in human melanoma cells by activation of p53/p21 pathway.	Simvastatin	0-11	P53	Homo sapiens	113-116
21144624-5	2011	The anthra[2,3-b]furan-5,10-dione 9 with distal methylamino groups was markedly potent against drug-resistant cell lines with P-glycoprotein overexpression or p53 gene deletion.	methylamino	48-59	P53	Homo sapiens	159-162
23933099-4	2013	Also, the main pathways leading to cell senescence were examined in simvastatin-treated human melanoma cells, and the expression levels of phospho-p53 and p21 were upregulated by simvastatin, suggesting that cell cycle regulators and DNA damage pathways are involved in the onset of senescence.	Simvastatin	68-79	P53	Homo sapiens	147-150
23933099-4	2013	Also, the main pathways leading to cell senescence were examined in simvastatin-treated human melanoma cells, and the expression levels of phospho-p53 and p21 were upregulated by simvastatin, suggesting that cell cycle regulators and DNA damage pathways are involved in the onset of senescence.	Simvastatin	179-190	P53	Homo sapiens	147-150
22242209-2	2011	We assessed the immunohistochemical expression of p53 and P-gp using formalin-fixed, paraffin-embedded specimens in 108 patients diagnosed with de novo DLBC.	Formaldehyde	69-77	P53	Homo sapiens	50-53
23933099-7	2013	Collectively, our results demonstrated that simvastatin can induce senescence in human melanoma cells by activation of p53/p21 pathway, and that oxidative stress may be related to this process.	Simvastatin	44-55	P53	Homo sapiens	119-122
23938375-11	2013	The association with dMMR in HGEC with ARID1A/PTEN alterations, TP53 wild type expression pattern and unfavorable outcome suggests that different oncogenetic pathways within HGEC are present.	dmmr	21-25	P53	Homo sapiens	64-68
21088491-1	2010	Atomistic simulations of a set of stapled peptides derived from the transactivation domain of p53 (designed by Verdine &amp; colleagues, JACS 2007 129:2456) and complexed to MDM2 reveal that the good binders are uniquely characterized by higher helicity and by extensive interactions between the hydrocarbon staples and the MDM2 surface; in contrast the poor binders have reduced helicity and their staples are mostly solvent exposed.	Verdine	111-118	P53	Homo sapiens	94-97
23860250-9	2013	We further hypothesize that the higher binding affinity of the novel Geldanamycin analogue for hsp90 alpha triggers the degradation of nonfunctional mutant p53 by cellular proteasomes.	geldanamycin	69-81	P53	Homo sapiens	156-159
20727621-3	2010	For instance, the Ru(II)(p-cymene)(isonicotinate)Cl(2) complex 6a of the known 4-(3,4,5-trimethoxyphenyl)-5-(3-hydroxy-4-methoxyphenyl)-oxazole 4a was far more active than the latter against cells of the p53-competent wild-type form of HCT-116 colon carcinoma at low 0.01 muM concentrations.	4-(3,4,5-trimethoxyphenyl)-5-(3-hydroxy-4-methoxyphenyl)-oxazole	79-143	P53	Homo sapiens	204-207
20727621-5	2010	The Ru(arene) complexes 6a-c were also more efficacious against combretastatin-refractory p53(+) cells of human HT-29 colon carcinoma when compared to their parent 4-(3,4-dimethoxy-5-methoxy/halo-phenyl)-5-(3-hydroxy-4-methoxyphenyl)-oxazoles 4a-c.	arene	7-12	P53	Homo sapiens	90-93
23495037-4	2013	Blockade of cyclooxygenase-2 (COX-2) activity by siRNA or NS398 correspondingly inhibited ceramide-induced p53 Ser-15 phosphorylation and apoptosis; thus COX-2 appears at the apex of the p38 kinase-mediated signaling cascade induced by ceramide.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	58-63	P53	Homo sapiens	107-110
20686355-3	2010	In the latter case, Ets1 molecules bind to palindromic sequences in which two Ets-binding sites (EBS) are separated by four base pairs, for example in the promoters of stromelysin-1 and p53.	ethylbenzene	97-100	P53	Homo sapiens	186-189
20493187-8	2010	Treatment with GA and 17-AAG led to growth arrests in G1 and S phases, increased sub-G1 hypodipoid cell population, induced apoptotic cell death, and upregulated P53 and P21 expression, although the drug-induced Bcl-2 upregulation cannot prevent cell death.	geldanamycin	15-17	P53	Homo sapiens	162-165
23514434-0	2013	Silver-based nanoparticles induce apoptosis in human colon cancer cells mediated through p53.	Silver	0-6	P53	Homo sapiens	89-92
20148857-5	2010	Our study reports here for the first time that the induction of p53 and the activity of Fas/Fas ligand apoptotic system may participate in the anti-proliferative activity of asperfuranone in A549 cells.	asperfuranone	174-187	P53	Homo sapiens	64-67
23684722-12	2013	CONCLUSIONS: Physalin A induced apoptotic cell death via p53-Noxa-mediated ROS generation, and autophagy played a protective role against apoptosis through up-regulating the p38-NF-kappaB survival pathway in A375-S2 cells.	physalin A	13-23	P53	Homo sapiens	57-60
20199942-0	2010	mot-2-Mediated cross talk between nuclear factor-B and p53 is involved in arsenite-induced tumorigenesis of human embryo lung fibroblast cells.	arsenite	74-82	P53	Homo sapiens	55-58
20199942-1	2010	BACKGROUND: Inactivation of p53 is involved in arsenite-induced tumorigenesis; however, the molecular mechanisms remain poorly understood.	arsenite	47-55	P53	Homo sapiens	28-31
20199942-2	2010	OBJECTIVE: We investigated the molecular mechanisms underlying the inactivation of p53 and neoplastic transformation induced by arsenite in human embryo lung fibroblast (HELF) cells.	arsenite	128-136	P53	Homo sapiens	83-86
23523585-0	2013	Newly synthesized quinazolinone HMJ-38 suppresses angiogenetic responses and triggers human umbilical vein endothelial cell apoptosis through p53-modulated Fas/death receptor signaling.	Quinazolinones	18-31	P53	Homo sapiens	142-145
20199942-4	2010	We determined the levels and functions of p53, nuclear factor-kappa B (NF-B; a key transcriptional regulator), and mot-2 (a p53 inhibitor) and their relationships in arsenite-induced transformed HELF cells by two-dimensional electrophoresis, reverse-transcriptase polymerase chain reaction, Western blot, immunofluorescence, and co-immunoprecipitation assays.	arsenite	166-174	P53	Homo sapiens	42-45
20199942-4	2010	We determined the levels and functions of p53, nuclear factor-kappa B (NF-B; a key transcriptional regulator), and mot-2 (a p53 inhibitor) and their relationships in arsenite-induced transformed HELF cells by two-dimensional electrophoresis, reverse-transcriptase polymerase chain reaction, Western blot, immunofluorescence, and co-immunoprecipitation assays.	arsenite	166-174	P53	Homo sapiens	124-127
20199942-13	2010	CONCLUSIONS: mot-2-mediated cross talk between NF-B and p53 appears to be involved in arsenite-induced tumorigenesis of HELF cells.	arsenite	86-94	P53	Homo sapiens	56-59
23455057-0	2013	Microwave-assisted synthesis of arene ruthenium(II) complexes that induce S-phase arrest in cancer cells by DNA damage-mediated p53 phosphorylation.	arene	32-37	P53	Homo sapiens	128-131
21787621-9	2010	Furthermore, 2-TeCD blocks the accumulation of wild-type-p53 (wt-p53) tumor-suppressor gene product caused by UV-B radiation.	2-tecd	13-19	P53	Homo sapiens	57-60
21787621-9	2010	Furthermore, 2-TeCD blocks the accumulation of wild-type-p53 (wt-p53) tumor-suppressor gene product caused by UV-B radiation.	2-tecd	13-19	P53	Homo sapiens	65-68
23455057-6	2013	In conclusion, the synthetic arene Ru(II) complexes could serve as novel p53 activator with potential application in cancer chemotherapy.	arene	29-34	P53	Homo sapiens	73-76
23435014-8	2013	Significant enhancement of TP53 G:C to T:A transversions was found in NSCLC from asbestos-exposed patients when compared with unexposed patients (P = 0.037).	Asbestos	81-89	P53	Homo sapiens	27-31
20353787-0	2010	ROS leads to MnSOD upregulation through ERK2 translocation and p53 activation in selenite-induced apoptosis of NB4 cells.	Selenious Acid	81-89	P53	Homo sapiens	63-66
23435014-9	2013	Interestingly, TP53 polymorphisms in intron 7 (rs12947788 and rs12951053) were more frequently identified in asbestos-exposed NSCLC (P = 0.046) and MPM patients than in unexposed patients (P &lt; 0.001 and P = 0.012, respectively).	Asbestos	109-117	P53	Homo sapiens	15-19
23406775-13	2013	CONCLUSION: Our study established a novel TP53-associated pediatric ACC xenograft and identified topotecan as a potentially effective agent for treating children with this disease.	Topotecan	97-106	P53	Homo sapiens	42-46
20421506-3	2010	We found that the transactivation domain of p53 made specific interactions with the C-terminal oligonucleotide/oligosaccharide-binding-fold domains of BRCA2 (BRCA2(CTD)).	Oligosaccharides	111-126	P53	Homo sapiens	44-47
20459648-3	2010	The expressions of IDH1 and p53 in formalin-fixed paraffin-embedded tissue sections from 44 osteosarcoma patients were determined by immunohistochemistry, and the correlation between them and clinicopagthological features were analyzed.	Formaldehyde	35-43	P53	Homo sapiens	28-31
23117090-6	2013	In the meantime, the up-regulation of p53 and reactive oxygen species increase were observed, which suggested that germacrone might be a new potent chemopreventive drug candidate for liver cancer via regulating the expression of proteins related to G2/M cell cycle and apoptosis, and p53 and oxidative damage may play important roles in the inhibition of human hepatoma cells growth by germacrone.	germacrone	115-125	P53	Homo sapiens	38-41
19941079-7	2010	RESULTS: Transcriptional activity of the MDM2 promoter containing the SNP309 GG genotype was significantly lower than that containing the TT genotype in p53-null lung cancer cells cotransfected with wild-type p53 expression plasmid under mithramycin A treatment.	mithramycin A	238-251	P53	Homo sapiens	209-212
23117090-6	2013	In the meantime, the up-regulation of p53 and reactive oxygen species increase were observed, which suggested that germacrone might be a new potent chemopreventive drug candidate for liver cancer via regulating the expression of proteins related to G2/M cell cycle and apoptosis, and p53 and oxidative damage may play important roles in the inhibition of human hepatoma cells growth by germacrone.	germacrone	115-125	P53	Homo sapiens	284-287
24175842-4	2013	Menadione treatment increased the expression of pro-apoptotic proteins, Bax and p53, with a concurrent decrease in anti-apoptotic proteins, Bcl-2 and p65.	Vitamin K 3	0-9	P53	Homo sapiens	80-83
20450732-0	2010	[Vitexicarpin affects proliferation and apoptosis in mutated p53 breast cancer cell].	casticin	1-13	P53	Homo sapiens	61-64
20450732-1	2010	OBJECTIVE: To elucidate the effect of proliferation and apoptosis induced by vitexicarpin in mutated p53 Hs578T cell line and study the expression of c-Myc, p21 and Bcl-2 protein in Hs578T and wild p53 MCF-7 cell pre-treated with vitexicarpin.	casticin	77-89	P53	Homo sapiens	101-104
23803025-3	2013	We recently investigated the genetic status of p53 and H-ras, which are known to be frequently mutated in Indian oral carcinomas in GO tissues and found them to only contain wild type sequences, which suggested a non-neoplastic nature of phenytoin induced GO.	Phenytoin	238-247	P53	Homo sapiens	47-50
20036271-10	2010	Our results suggest that arsenite"s interference with activation of P53 via poly(ADP-ribosyl)ation may play a role in the comutagenic and cocarcinogenic effects of arsenite.	arsenite	164-172	P53	Homo sapiens	68-71
23150440-2	2013	Here, we describe a detailed protocol to identify small molecules capable of targeting p53-MDM2/MDMX interactions using a fluorescence polarization assay with Rhodamine-labeled p53 peptides.	Rhodamines	159-168	P53	Homo sapiens	87-90
23150440-2	2013	Here, we describe a detailed protocol to identify small molecules capable of targeting p53-MDM2/MDMX interactions using a fluorescence polarization assay with Rhodamine-labeled p53 peptides.	Rhodamines	159-168	P53	Homo sapiens	177-180
23441616-0	2013	Nobiletin induces apoptosis and potentiates the effects of the anticancer drug 5-fluorouracil in p53-mutated SNU-16 human gastric cancer cells.	nobiletin	0-9	P53	Homo sapiens	97-100
20054683-6	2010	RESULTS: Within 2-4 hr, lidocaine and procaine (&gt; or = 1 mM) induced massive cell vacuolization, a response abated by the V-ATPase inhibitor, bafilomycin A1, and activated macroautophagic signalling (LC3 II formation) but not other stress signalling (p38, ERK1/2, p53, no influence on serum-controlled Akt phosphorylation).	Lidocaine	24-33	P53	Homo sapiens	267-270
23441616-1	2013	Nobiletin is a typical polymethoxyl flavone from citrus fruits that has anticancer properties, but the molecular mechanism of its inhibitory effects on the growth of p53-mutated SNU-16 human gastric cancer cells has not been explored.	nobiletin	0-9	P53	Homo sapiens	166-169
23441616-7	2013	The results of this study suggest the potential application of nobiletin to the enhancement of 5-FU efficiency in p53 mutant tumors.	nobiletin	63-72	P53	Homo sapiens	114-117
25198662-4	2013	Selenite induced phosphorylation of p53 at the vital site Ser15 via p38MAPK and ERK.	Selenious Acid	0-8	P53	Homo sapiens	36-39
20043868-0	2010	Stabilization and translocation of p53 to mitochondria is linked to Bax translocation to mitochondria in simvastatin-induced apoptosis.	Simvastatin	105-116	P53	Homo sapiens	35-38
25198662-8	2013	Furthermore, in p53 mutant U937 leukemia cells, selenite could not elicit such a switch from autophagy to apoptosis, laying emphasis on the crucial role p53 played in this process.	Selenious Acid	48-56	P53	Homo sapiens	16-19
23124131-8	2013	RESULTS: CO(2) incubation was associated with an increase in ROS production (p &lt; 0.01), cell DNA damage mainly after 24 h (12 % increase of tail DNA content and 4-fold increase of tail length) and a significant up-regulation in p53 expression at 24 h with an intense nuclear staining.	co(2)	9-14	P53	Homo sapiens	231-234
20043868-4	2010	Interestingly, the simvastatin-induced apoptosis was accompanied by p53 stabilization involving Mdm2 degradation.	Simvastatin	19-30	P53	Homo sapiens	68-71
20043868-7	2010	Moreover, knockdown or deficiency of p53 expression reduced both Bax translocation to mitochondria and MMP disruption in simvastatin-induced apoptosis.	Simvastatin	121-132	P53	Homo sapiens	37-40
20043868-8	2010	Taken together, these all indicate that stabilization and translocation of p53 to mitochondria is involved in Bax translocation to mitochondria in simvastatin-induced apoptosis.	Simvastatin	147-158	P53	Homo sapiens	75-78
23124131-10	2013	CONCLUSIONS: In vitro-simulated pneumoperitoneum environment with CO(2) induces oxidative stress and cell DNA damage, leading to p53 up-regulation involved in cell-cycle arrest of neuroblastoma cells.	co(2)	66-71	P53	Homo sapiens	129-132
20085733-3	2010	Vitamin C can alleviate cell senescence by p53 repression and may accelerate reprogramming by synergizing with epigenetic regulators.	Ascorbic Acid	0-9	P53	Homo sapiens	43-46
22286760-0	2012	Poly(ADP-ribosyl)ation of p53 induces gene-specific transcriptional repression of MTA1.	poly(adp-ribosyl)	0-17	P53	Homo sapiens	26-29
20010306-3	2010	Mutation analysis of TP53 Exons 4 to 9 on DNA from formalin-fixed, paraffin-embedded specimens was performed by bidirectional DNA sequencing.	Formaldehyde	51-59	P53	Homo sapiens	21-25
22944355-4	2012	Based on this rationale, Cenersen, a phosphorothioate oligonucleotide antisense to p53-mRNA was synthesized and tested in clinical trials for patients with acute myeloid leukemia (AML).	Phosphorothioate Oligonucleotides	37-69	P53	Homo sapiens	83-86
23205301-4	2012	We also found compensatory increases in cytosolic deoxycytidine kinase (dCK) and thymidine kinase 1 (TK1) and in mitochondrial deoxyguanosine kinase (dGK), all of the salvage dNTP supply system; in contrast, the remaining mitochondrial salvage enzyme thymidine kinase 2 (TK2) decreased with p53 loss.	Parathion	175-179	P53	Homo sapiens	291-294
22705848-8	2012	Besides the topoisomerase inhibitor doxorubicin known for its cardiotoxicity, we show that the mitochondria-specific inhibitor menadione is able to activate p53 and to kill effectively myotubes.	Vitamin K 3	127-136	P53	Homo sapiens	157-160
22920218-1	2012	We use molecular docking and free energy calculations to estimate the relative free energy of binding of six arylamide compounds designed to inhibit the hDM2-p53 interaction.	arylamide	109-118	P53	Homo sapiens	158-161
22920218-2	2012	We show that using docking methods to predict or rank the binding affinity of a series of arylamide inhibitors of the hDM2-p53 interaction is problematic.	arylamide	90-99	P53	Homo sapiens	123-126
22706169-0	2012	Opposed arsenite-mediated regulation of p53-survivin is involved in neoplastic transformation, DNA damage, or apoptosis in human keratinocytes.	arsenite	8-16	P53	Homo sapiens	40-43
22721982-9	2012	In addition, a significant and progressive increase in the level of p53 protein in alantolactone-treated cells was observed.	alantolactone	83-96	P53	Homo sapiens	68-71
22706169-3	2012	Our present study shows that, for human keratinocytes (HaCaT) cells, a low concentration of arsenite activates extracellular signal-regulated kinases (ERKs), which leads to up-regulation of nuclear factor kappaB (NF-kappaB) binding to DNA and to elevated, NF-kappaB-dependent expression of mot-2 (a p53 inhibitor) and survivin (an inhibitor of apoptosis).	arsenite	92-100	P53	Homo sapiens	299-302
22706169-9	2012	By identifying a mechanism whereby ERKs and JNKs-mediated regulation of the p53-survivin signal pathway is involved in the biphasic effects of arsenite on human keratinocytes, our data expand understanding of arsenite-induced cell proliferation, neoplastic transformation, DNA damage, and apoptosis.	arsenite	143-151	P53	Homo sapiens	76-79
22706169-9	2012	By identifying a mechanism whereby ERKs and JNKs-mediated regulation of the p53-survivin signal pathway is involved in the biphasic effects of arsenite on human keratinocytes, our data expand understanding of arsenite-induced cell proliferation, neoplastic transformation, DNA damage, and apoptosis.	arsenite	209-217	P53	Homo sapiens	76-79
22638860-6	2012	We demonstrated that co-infusion of 6-OHDA with adenovirus expressing siRNA of iNOS blocked the activation of microglia, iNOS transcription, and p53-Bax-CC3 apoptotic cascade as well as significantly blocking 6-OHDA-induced decreases in DA, DOPAC, HVA, and TH levels and effectively decreased rotation number.	Oxidopamine	36-42	P53	Homo sapiens	145-148
22638860-7	2012	Our study highlighted the role of iNOS in the neurodegeneration of nigrostriatal dopaminergic neurons in the 6-OHDA animal model of PD and suggested that the microglial activation-iNOS-p53-Bax-CC3 apoptotic pathway plays a key role in the neurodegeneration in the 6-OHDA model.	Oxidopamine	109-115	P53	Homo sapiens	185-188
22892142-0	2012	Enhanced antitumor activity of vitamin C via p53 in cancer cells.	Ascorbic Acid	31-40	P53	Homo sapiens	45-48
22638860-7	2012	Our study highlighted the role of iNOS in the neurodegeneration of nigrostriatal dopaminergic neurons in the 6-OHDA animal model of PD and suggested that the microglial activation-iNOS-p53-Bax-CC3 apoptotic pathway plays a key role in the neurodegeneration in the 6-OHDA model.	Oxidopamine	264-270	P53	Homo sapiens	185-188
22797300-7	2012	Our identification of HCLK2 as a substrate of PHD3 reveals the mechanism through which hypoxia inhibits the DDR, suggesting hydroxylation of HCLK2 is a potential therapeutic target for regulating the ATR/CHK1/p53 pathway.	hclk2	22-27	P53	Homo sapiens	209-212
22892142-4	2012	Because p53 is activated by DNA-damaging stress and then regulates various cellular conditions, we hypothesized that p53 can sensitize cancer cells to ascorbate.	Ascorbic Acid	151-160	P53	Homo sapiens	8-11
22892142-4	2012	Because p53 is activated by DNA-damaging stress and then regulates various cellular conditions, we hypothesized that p53 can sensitize cancer cells to ascorbate.	Ascorbic Acid	151-160	P53	Homo sapiens	117-120
22892142-5	2012	Using isogenic cancer cells, we observed that the presence of p53 can affect ascorbate cytotoxicity, and also reactivation of p53 can make cancer cells sensitive to ascorbate.	Ascorbic Acid	77-86	P53	Homo sapiens	62-65
22149137-0	2012	The Hsp90 inhibitor SNX-7081 synergizes with and restores sensitivity to fludarabine in chronic lymphocytic leukemia cells with lesions in the TP53 pathway: a potential treatment strategy for fludarabine refractory disease.	fludarabine	73-84	P53	Homo sapiens	143-147
22892142-5	2012	Using isogenic cancer cells, we observed that the presence of p53 can affect ascorbate cytotoxicity, and also reactivation of p53 can make cancer cells sensitive to ascorbate.	Ascorbic Acid	165-174	P53	Homo sapiens	126-129
22149137-0	2012	The Hsp90 inhibitor SNX-7081 synergizes with and restores sensitivity to fludarabine in chronic lymphocytic leukemia cells with lesions in the TP53 pathway: a potential treatment strategy for fludarabine refractory disease.	fludarabine	192-203	P53	Homo sapiens	143-147
22149137-4	2012	In seven cell lines and 23 patient samples synergy between SNX-7081 and fludarabine (2-FaraA) was apparent in the three TP53 mutated cell lines and at significantly lower concentrations in TP53 or ATM dysfunctional patient cells.	fludarabine	72-83	P53	Homo sapiens	120-124
22892142-6	2012	p53-dependent enhancement of ascorbate cytotoxicity is caused by increased reactive oxygen species generation via a differentially regulated p53 transcriptional network.	Ascorbic Acid	29-38	P53	Homo sapiens	0-3
22149137-4	2012	In seven cell lines and 23 patient samples synergy between SNX-7081 and fludarabine (2-FaraA) was apparent in the three TP53 mutated cell lines and at significantly lower concentrations in TP53 or ATM dysfunctional patient cells.	fludarabine	85-92	P53	Homo sapiens	120-124
22614867-0	2012	Nano-TiO2-induced apoptosis by oxidative stress-mediated DNA damage and activation of p53 in human embryonic kidney cells.	titanium dioxide	5-9	P53	Homo sapiens	86-89
22892142-6	2012	p53-dependent enhancement of ascorbate cytotoxicity is caused by increased reactive oxygen species generation via a differentially regulated p53 transcriptional network.	Ascorbic Acid	29-38	P53	Homo sapiens	141-144
22614867-9	2012	In conclusion, ROS-mediated oxidative stress, the activation of p53, Bax, caspase-3 and oxidative DNA damage are involved in the mechanistic pathways of nano-TiO(2)-induced apoptosis in HEK-293 cells.	titanium dioxide	158-164	P53	Homo sapiens	64-67
22892142-7	2012	We also found that transcriptionally activated p53 was derived from MDM2 ubiquitination by ascorbate and subsequently its signaling network renders cancer cells more susceptible to oxidative stress.	Ascorbic Acid	91-100	P53	Homo sapiens	47-50
22892142-8	2012	Similar to the p53 effect on in vitro ascorbate cytotoxicity, inhibition of tumor growth is also stronger in p53-expressing tumors than in p53-deficient ones in vivo.	Ascorbic Acid	38-47	P53	Homo sapiens	15-18
22592527-3	2012	We found that low doses (~0.5 microM) of reversine, which selectively inhibit MPS1 and hence impair the spindle assembly checkpoint, kill human TP53 (-/-)  colon carcinoma cells less efficiently than their wild-type counterparts.	2-(4-morpholinoanilino)-6-cyclohexylaminopurine	41-50	P53	Homo sapiens	144-148
22892142-8	2012	Similar to the p53 effect on in vitro ascorbate cytotoxicity, inhibition of tumor growth is also stronger in p53-expressing tumors than in p53-deficient ones in vivo.	Ascorbic Acid	38-47	P53	Homo sapiens	109-112
22892142-8	2012	Similar to the p53 effect on in vitro ascorbate cytotoxicity, inhibition of tumor growth is also stronger in p53-expressing tumors than in p53-deficient ones in vivo.	Ascorbic Acid	38-47	P53	Homo sapiens	109-112
22416035-2	2012	Here, we show that mantle cell lymphoma (MCL) cells deficient in both ATM and p53 are more sensitive to the PARP inhibitor olaparib than cells lacking ATM function alone.	olaparib	123-131	P53	Homo sapiens	78-81
22416035-3	2012	In ATM-deficient MCL cells, olaparib induced DNA-PK-dependent phosphorylation and stabilization of p53 as well as expression of p53-responsive cell cycle checkpoint regulators, and inhibition of DNA-PK reduced the toxicity of olaparib in ATM-deficient MCL cells.	olaparib	28-36	P53	Homo sapiens	99-102
22892142-9	2012	This is the first observation that ascorbate cytotoxicity is positively related to p53 expression, activating its transcriptional network to worsen intracellular oxidative stress and consequently enhancing its cytotoxicity.	Ascorbic Acid	35-44	P53	Homo sapiens	83-86
22416035-3	2012	In ATM-deficient MCL cells, olaparib induced DNA-PK-dependent phosphorylation and stabilization of p53 as well as expression of p53-responsive cell cycle checkpoint regulators, and inhibition of DNA-PK reduced the toxicity of olaparib in ATM-deficient MCL cells.	olaparib	28-36	P53	Homo sapiens	128-131
22416035-4	2012	Thus, both DNA-PK and p53 regulate the response of ATM-deficient MCL cells to olaparib.	olaparib	78-86	P53	Homo sapiens	22-25
22892142-10	2012	Based on our study, reactivation of p53 may help to achieve more consistent cytotoxic effects of ascorbate in cancer therapies.	Ascorbic Acid	97-106	P53	Homo sapiens	36-39
21912889-0	2012	Therapeutic reactivation of mutant p53 protein by quinazoline derivatives.	Quinazolines	50-61	P53	Homo sapiens	35-38
22673830-10	2012	Significant increases in expression of bax/bcl2 and p53 proteins confirmed that volatile oil induces apoptosis.	Oils, Volatile	80-92	P53	Homo sapiens	52-55
22507962-0	2012	The central valine concept provides an entry in a new class of non peptide inhibitors of the p53-MDM2 interaction.	Valine	12-18	P53	Homo sapiens	93-96
21912889-2	2012	Several drugs including the quinazoline derivative 1 (CP-31398) have been reported to restore p53 activity in mutant cells.	Quinazolines	28-39	P53	Homo sapiens	94-97
22507962-2	2012	In our search for non peptide inhibitors of this protein-protein interaction, we have devised a ligand design concept exploiting the central position of Val 93 in the p53 binding pocket of MDM2.	Valine	153-156	P53	Homo sapiens	167-170
22922335-1	2012	The influence of the surface chemistry of silver nanoparticles (AgNPs) on p53 mediated cell death was evaluated using human dermal fibroblast (HDF) and lung cancer (A549) cells.	Silver	42-48	P53	Homo sapiens	74-77
22439615-4	2012	From screening of HEFLibs and subsequent structure-guided design, we developed substituted 2-(aminomethyl)-4-ethynyl-6-iodophenols as p53-Y220C stabilizers.	2-(aminomethyl)-4-ethynyl-6-iodophenols	91-130	P53	Homo sapiens	134-137
22433057-4	2012	Geldanamycin induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels; an increase in Bax and tumour suppressor p53 levels; loss of the mitochondrial transmembrane potential; cytochrome c release; activation of caspases (-8, -9 and -3); cleavage of PARP-1; and increase in the reactive oxygen species formation.	geldanamycin	0-12	P53	Homo sapiens	124-127
21544805-1	2012	The small molecule Quinacrine (QC, a derivative of 9-aminoacridine), an anti-malaria drug, displays activity against cancer cell lines and can simultaneously suppress nuclear factor-kappaB (NF-kappaB) and activate p53 signaling.	Quinacrine	19-29	P53	Homo sapiens	214-217
22608759-10	2012	The canonical pathways associated with these genes were in relation to pyrimidine metabolism, G2/M damage checkpoint regulation and p53 signaling (FDR&lt;=0.05).	pyrimidine	71-81	P53	Homo sapiens	132-135
22260869-0	2012	Arsenite-induced apoptosis of human neuroblastoma cells requires p53 but occurs independently of c-Jun.	arsenite	0-8	P53	Homo sapiens	65-68
22260869-1	2012	Arsenite treatment of human SH-SY5Y neuroblastoma cells leads to an upregulation of caspase-3/7 activity and to the fragmentation of chromatin that is accompanied by elevated p53 and c-Jun levels.	arsenite	0-8	P53	Homo sapiens	175-178
22260869-2	2012	Expression of a truncated mutant of p53, p53DD, which interfered with the oligomerization of p53, suppressed the arsenite-induced upregulation of caspase-3/7 activity and the fragmentation of chromatin, indicating that p53 is required for arsenite-induced cell death.	arsenite	113-121	P53	Homo sapiens	36-39
22260869-2	2012	Expression of a truncated mutant of p53, p53DD, which interfered with the oligomerization of p53, suppressed the arsenite-induced upregulation of caspase-3/7 activity and the fragmentation of chromatin, indicating that p53 is required for arsenite-induced cell death.	arsenite	113-121	P53	Homo sapiens	41-44
22260869-2	2012	Expression of a truncated mutant of p53, p53DD, which interfered with the oligomerization of p53, suppressed the arsenite-induced upregulation of caspase-3/7 activity and the fragmentation of chromatin, indicating that p53 is required for arsenite-induced cell death.	arsenite	113-121	P53	Homo sapiens	41-44
22260869-2	2012	Expression of a truncated mutant of p53, p53DD, which interfered with the oligomerization of p53, suppressed the arsenite-induced upregulation of caspase-3/7 activity and the fragmentation of chromatin, indicating that p53 is required for arsenite-induced cell death.	arsenite	239-247	P53	Homo sapiens	36-39
22945197-8	2012	Haloperidol, of the typical antipsychotics, causes neuron apoptosis by a free radical induced mechanism, involving Bcl-XS, P53, cytochrome c translocation and caspase 3 activation.	Haloperidol	0-11	P53	Homo sapiens	123-126
22260869-2	2012	Expression of a truncated mutant of p53, p53DD, which interfered with the oligomerization of p53, suppressed the arsenite-induced upregulation of caspase-3/7 activity and the fragmentation of chromatin, indicating that p53 is required for arsenite-induced cell death.	arsenite	239-247	P53	Homo sapiens	41-44
22260869-2	2012	Expression of a truncated mutant of p53, p53DD, which interfered with the oligomerization of p53, suppressed the arsenite-induced upregulation of caspase-3/7 activity and the fragmentation of chromatin, indicating that p53 is required for arsenite-induced cell death.	arsenite	239-247	P53	Homo sapiens	41-44
22260869-5	2012	Transcriptional upregulation of a chromatin-embedded p53-responsive reporter gene in either arsenite or nutlin-3 stimulated neuroblastoma cells revealed that the transcriptional activity of p53 was increased under these conditions.	arsenite	92-100	P53	Homo sapiens	53-56
22260869-5	2012	Transcriptional upregulation of a chromatin-embedded p53-responsive reporter gene in either arsenite or nutlin-3 stimulated neuroblastoma cells revealed that the transcriptional activity of p53 was increased under these conditions.	arsenite	92-100	P53	Homo sapiens	190-193
22260869-9	2012	Together, these data show that the upregulation of p53 is causally linked with arsenite-induced cell death in neuroblastoma cells, whereas the upregulation of c-Jun is not part of this apoptotic signaling cascade.	arsenite	79-87	P53	Homo sapiens	51-54
22200533-5	2012	Thus the aim of this study was to investigate in detail mechanisms, relationship and crosstalk between apoptosis and autophagy in Se-treated HCT-116 cancer cells differing in p53 status since p53 has been shown to play a well-known role in apoptosis but dichotomous role in autophagy.	Selenious Acid	130-132	P53	Homo sapiens	175-178
22693169-6	2012	METHODS: The peptide was bioinformatically modelled on the critical region of the p53 protein associated with DNA binding and fluorescently labeled with a terminal rhodamine B dye.	rhodamine B	164-175	P53	Homo sapiens	82-85
22200533-5	2012	Thus the aim of this study was to investigate in detail mechanisms, relationship and crosstalk between apoptosis and autophagy in Se-treated HCT-116 cancer cells differing in p53 status since p53 has been shown to play a well-known role in apoptosis but dichotomous role in autophagy.	Selenious Acid	130-132	P53	Homo sapiens	192-195
22200533-6	2012	We report that the absence of p53 in malignant colonocytes changes patterns of response to Se-induced stress which include differential activation of MAP kinases (p38 - HCT-116 and JNK - HCT-116 p53KO) including their respective roles in the process of apoptosis and autophagy as well as the involvement of mTOR or PI3K signaling.	Selenious Acid	91-93	P53	Homo sapiens	30-33
22138446-4	2012	Lack of p53 is associated with an increase in sensitivity to the combination treatment; p53+/+ cells treated with the topoisomerase I poison topotecan (TPT) arrest at G2, whereas in p53-/- cells the additional presence of the Hsp90 inhibitor geldanamycin (GA) selectively abrogates the G2M checkpoint.	Topotecan	141-150	P53	Homo sapiens	8-11
22138446-4	2012	Lack of p53 is associated with an increase in sensitivity to the combination treatment; p53+/+ cells treated with the topoisomerase I poison topotecan (TPT) arrest at G2, whereas in p53-/- cells the additional presence of the Hsp90 inhibitor geldanamycin (GA) selectively abrogates the G2M checkpoint.	Topotecan	141-150	P53	Homo sapiens	88-91
22138446-4	2012	Lack of p53 is associated with an increase in sensitivity to the combination treatment; p53+/+ cells treated with the topoisomerase I poison topotecan (TPT) arrest at G2, whereas in p53-/- cells the additional presence of the Hsp90 inhibitor geldanamycin (GA) selectively abrogates the G2M checkpoint.	Topotecan	141-150	P53	Homo sapiens	88-91
22138446-4	2012	Lack of p53 is associated with an increase in sensitivity to the combination treatment; p53+/+ cells treated with the topoisomerase I poison topotecan (TPT) arrest at G2, whereas in p53-/- cells the additional presence of the Hsp90 inhibitor geldanamycin (GA) selectively abrogates the G2M checkpoint.	tpt	152-155	P53	Homo sapiens	8-11
22138446-4	2012	Lack of p53 is associated with an increase in sensitivity to the combination treatment; p53+/+ cells treated with the topoisomerase I poison topotecan (TPT) arrest at G2, whereas in p53-/- cells the additional presence of the Hsp90 inhibitor geldanamycin (GA) selectively abrogates the G2M checkpoint.	tpt	152-155	P53	Homo sapiens	88-91
22138446-4	2012	Lack of p53 is associated with an increase in sensitivity to the combination treatment; p53+/+ cells treated with the topoisomerase I poison topotecan (TPT) arrest at G2, whereas in p53-/- cells the additional presence of the Hsp90 inhibitor geldanamycin (GA) selectively abrogates the G2M checkpoint.	tpt	152-155	P53	Homo sapiens	88-91
22904680-5	2012	In vitro, p53-72P was less effective than p53-72R in inducing apoptosis and inhibiting survival of p53-null LAN-1 cells treated with etoposide, topotecan, or ionizing radiation but not taxol.	Topotecan	144-153	P53	Homo sapiens	10-13
22138446-4	2012	Lack of p53 is associated with an increase in sensitivity to the combination treatment; p53+/+ cells treated with the topoisomerase I poison topotecan (TPT) arrest at G2, whereas in p53-/- cells the additional presence of the Hsp90 inhibitor geldanamycin (GA) selectively abrogates the G2M checkpoint.	geldanamycin	242-254	P53	Homo sapiens	8-11
22138446-4	2012	Lack of p53 is associated with an increase in sensitivity to the combination treatment; p53+/+ cells treated with the topoisomerase I poison topotecan (TPT) arrest at G2, whereas in p53-/- cells the additional presence of the Hsp90 inhibitor geldanamycin (GA) selectively abrogates the G2M checkpoint.	geldanamycin	256-258	P53	Homo sapiens	8-11
22138446-6	2012	We show that concurrent treatment with GA and TPT is able to reverse TPT induced up-regulation of the anti-apoptotic protein Bcl2 in both p53+/+ and p53-/- HCT116 cells.	geldanamycin	39-41	P53	Homo sapiens	138-141
23360043-4	2012	Immunohistochemical staining for p53 was performed on formalin fixed paraffin embedded tissue sections with appropriate positive and negative control.	Formaldehyde	54-62	P53	Homo sapiens	33-36
22138446-6	2012	We show that concurrent treatment with GA and TPT is able to reverse TPT induced up-regulation of the anti-apoptotic protein Bcl2 in both p53+/+ and p53-/- HCT116 cells.	geldanamycin	39-41	P53	Homo sapiens	149-152
22441128-3	2012	Whether the chemotherapeutic agent or the iodized oil affects exogenous wt-p53 activity remains poorly understood.	Oils	50-53	P53	Homo sapiens	75-78
22078465-0	2012	CYR61 controls p53 and NF-kappaB expression through PI3K/Akt/mTOR pathways in carboplatin-induced ovarian cancer cells.	cyr61	0-5	P53	Homo sapiens	15-18
22551203-11	2012	Short-term in vitro arsenite treatment in lymphoblastoid cells clearly demonstrated a significant global hypomethylation, determined as reduction in LINE-1 methylation and total 5-MedC content, and p53 hypermethylation (p &lt; 0.05).	arsenite	20-28	P53	Homo sapiens	198-201
22130551-4	2012	Functional studies showed that AQP3 and AQP9 can inhibit cell apoptosis induced by arsenite through down-regulating p53 and up-regulating Bcl-2 and XIAP.	arsenite	83-91	P53	Homo sapiens	116-119
19728742-3	2009	But rather than cyclic dNTP synthesis, hp53R2 has been shown to supply dNTPs for DNA repair to cells in G0-G1 in a p53-dependent fashion.	Parathion	71-76	P53	Homo sapiens	40-43
20946258-4	2012	Our previous study has demonstrated that simvastatin inhibits VSMC proliferation in high glucose status without dyslipidemia, inducing a G0/G1 phase cell cycle growth arrest by acting on multiple steps upstream of pRb, including inhibition of CDK2/4 expression and upregulation of p53, p21, p16, and p27.	Simvastatin	41-52	P53	Homo sapiens	281-284
19801972-4	2009	First, parkin prevented 6-hydroxydopamine-induced caspase-3 activation in a p53-dependent manner.	Oxidopamine	24-41	P53	Homo sapiens	76-79
22076938-0	2012	5-Aminoimidazole-4-carboxyamide ribonucleoside induces G(1)/S arrest and Nanog downregulation via p53 and enhances erythroid differentiation.	5-aminoimidazole-4-carboxyamide ribonucleoside	0-46	P53	Homo sapiens	98-101
22189786-0	2012	Ingenol mebutate field-directed treatment of UVB-damaged skin reduces lesion formation and removes mutant p53 patches.	3-ingenyl angelate	0-16	P53	Homo sapiens	106-109
23317213-0	2012	Lack of mutation in p53 and H-ras genes in phenytoin induced gingival overgrowth suggests its non cancerous nature.	Phenytoin	43-52	P53	Homo sapiens	20-23
23317213-2	2012	However, a detailed analysis for the presence of mutations in p53 and ras genes, which are the two most frequently mutated genes in cancers, in phenytoin induced gingival overgrowth tissues has hitherto not been performed.	Phenytoin	144-153	P53	Homo sapiens	62-65
23317213-6	2012	CONCLUSION: Our result indicates that mutational alteration of p53 and H-ras genes is infrequent in phenytoin induced gingival growth, which thus suggests a non malignant nature of this pathology.	Phenytoin	100-109	P53	Homo sapiens	63-66
19559674-4	2009	AC-93253 significantly enhanced acetylation of tubulin, p53, and histone H4, confirming SIRT2 and SIRT1 as its cellular targets.	AC 93253	0-8	P53	Homo sapiens	56-59
19468714-8	2009	Differential expression of genes, such as p53, Bcl-2, caspase-9, was evident in PFOA or PFOS exposure groups.	perfluorooctanoic acid	80-84	P53	Homo sapiens	42-45
19468714-8	2009	Differential expression of genes, such as p53, Bcl-2, caspase-9, was evident in PFOA or PFOS exposure groups.	perfluorooctane sulfonic acid	88-92	P53	Homo sapiens	42-45
22189786-4	2012	Ingenol mebutate treatment also reduced the number of mutant p53 keratinocyte patches by  70%.	3-ingenyl angelate	0-16	P53	Homo sapiens	61-64
22308293-0	2012	Disruption of BIRC3 associates with fludarabine chemorefractoriness in TP53 wild-type chronic lymphocytic leukemia.	fludarabine	36-47	P53	Homo sapiens	71-75
19725468-10	2009	High expressions of SIRT1 and Akt were found in colon carcinoma HCT116 p53 knock-out cells exposed to lidamycin.	C 1027	102-111	P53	Homo sapiens	71-74
19725468-11	2009	Degradation of PARP and p53 by lidamycin as a substitute for SIRT1 and Akt was confirmed with caspase inhibitor Q-VD-OPh and proteasome inhibitor MG132.	C 1027	31-40	P53	Homo sapiens	24-27
23193914-0	2012	Quinacrine-mediated autophagy and apoptosis in colon cancer cells is through a p53- and p21-dependent mechanism.	Quinacrine	0-10	P53	Homo sapiens	79-82
23193914-1	2012	We previously showed that quinacrine (QC), a small molecule antimalarial agent, also presented anticancer activity in breast cancer cells through activation of p53, p21, and inhibition of topoisomerase activity.	Quinacrine	26-36	P53	Homo sapiens	160-163
23133524-6	2012	Our study is of interest because fluoroquinolones have the ability to penetrate pancreatic tissue which can be very effective in combating pancreatic cancers that are usually associated with loss or downregulation of CDK inhibitors p21/p27 as well as mutational inactivation of p53.	Fluoroquinolones	33-49	P53	Homo sapiens	278-281
19397590-5	2009	Flow cytometry and fluorescence microscopy revealed that although As(2)O(3) alone caused a moderate level of mitotic arrest, it greatly attenuated paclitaxel-induced mitotic arrest in cells with p53 deficiency.	(2)o(3)	68-75	P53	Homo sapiens	195-198
22470341-6	2012	Bilirubin-mediated inhibition of neointimal thickening was associated with a significant decrease in ERK activity and cyclin D1 and A protein expression, and an increase in p21 and p53 protein expression in injured blood vessels.	Bilirubin	0-9	P53	Homo sapiens	181-184
19139269-4	2009	Exposure to capsaicin or DHC caused induction of p53, p21, and G(0)/G(1) arrest.	dihydrocapsaicin	25-28	P53	Homo sapiens	49-52
22509368-3	2012	We demonstrate that treatment of cancer cells with a newly described synthetic ROR agonist, SR1078, leads to p53 stabilization and induction of apoptosis.	SR 1078	92-98	P53	Homo sapiens	109-112
21765463-11	2012	Nutlin-3, RITA and Topotecan lead to comparable p53 activation and growth inhibition under normoxia and hypoxia.	Topotecan	19-28	P53	Homo sapiens	48-51
19180570-0	2009	Cyr61 is up-regulated in prostate cancer and associated with the p53 gene status.	cyr61	0-5	P53	Homo sapiens	65-68
21765463-13	2012	Also Topotecan, alone or in combination with Nutlin-3, reduced HIF-1alpha protein levels, suggesting that a certain level of DNA damage response is required for p53-mediated downregulation of HIF-1alpha.	Topotecan	5-14	P53	Homo sapiens	161-164
19180570-7	2009	In addition, our analysis based on published data and data present in this report indicted that levels of Cyr61 expression associated with the status of the tumor suppressor gene p53 in 32 cancer cell lines analyzed, high levels of Cyr61 expression were found in cell lines with mutant or null p53 gene, whereas lower expression levels of Cyr61 in the cell lines with wild-type p53.	cyr61	106-111	P53	Homo sapiens	179-182
22039264-4	2011	In fludarabine-refractory CLL, SF3B1 mutations and TP53 disruption distributed in a mutually exclusive fashion (P = .046).	fludarabine	3-14	P53	Homo sapiens	51-55
19180570-7	2009	In addition, our analysis based on published data and data present in this report indicted that levels of Cyr61 expression associated with the status of the tumor suppressor gene p53 in 32 cancer cell lines analyzed, high levels of Cyr61 expression were found in cell lines with mutant or null p53 gene, whereas lower expression levels of Cyr61 in the cell lines with wild-type p53.	cyr61	106-111	P53	Homo sapiens	294-297
22052376-0	2012	The pleiotropic effects of statins in the prevention of atherosclerosis : Editorial to: "Simvastatin suppresses apoptosis in vulnerable atherosclerotic plaques through regulating the expression of p53, Bcl-2 en Bcl-xL" by Weiwei Qin et al.	Simvastatin	89-100	P53	Homo sapiens	197-200
19180570-7	2009	In addition, our analysis based on published data and data present in this report indicted that levels of Cyr61 expression associated with the status of the tumor suppressor gene p53 in 32 cancer cell lines analyzed, high levels of Cyr61 expression were found in cell lines with mutant or null p53 gene, whereas lower expression levels of Cyr61 in the cell lines with wild-type p53.	cyr61	106-111	P53	Homo sapiens	294-297
19180570-7	2009	In addition, our analysis based on published data and data present in this report indicted that levels of Cyr61 expression associated with the status of the tumor suppressor gene p53 in 32 cancer cell lines analyzed, high levels of Cyr61 expression were found in cell lines with mutant or null p53 gene, whereas lower expression levels of Cyr61 in the cell lines with wild-type p53.	cyr61	232-237	P53	Homo sapiens	179-182
19180570-7	2009	In addition, our analysis based on published data and data present in this report indicted that levels of Cyr61 expression associated with the status of the tumor suppressor gene p53 in 32 cancer cell lines analyzed, high levels of Cyr61 expression were found in cell lines with mutant or null p53 gene, whereas lower expression levels of Cyr61 in the cell lines with wild-type p53.	cyr61	232-237	P53	Homo sapiens	294-297
19180570-7	2009	In addition, our analysis based on published data and data present in this report indicted that levels of Cyr61 expression associated with the status of the tumor suppressor gene p53 in 32 cancer cell lines analyzed, high levels of Cyr61 expression were found in cell lines with mutant or null p53 gene, whereas lower expression levels of Cyr61 in the cell lines with wild-type p53.	cyr61	232-237	P53	Homo sapiens	294-297
19180570-7	2009	In addition, our analysis based on published data and data present in this report indicted that levels of Cyr61 expression associated with the status of the tumor suppressor gene p53 in 32 cancer cell lines analyzed, high levels of Cyr61 expression were found in cell lines with mutant or null p53 gene, whereas lower expression levels of Cyr61 in the cell lines with wild-type p53.	cyr61	232-237	P53	Homo sapiens	179-182
19180570-7	2009	In addition, our analysis based on published data and data present in this report indicted that levels of Cyr61 expression associated with the status of the tumor suppressor gene p53 in 32 cancer cell lines analyzed, high levels of Cyr61 expression were found in cell lines with mutant or null p53 gene, whereas lower expression levels of Cyr61 in the cell lines with wild-type p53.	cyr61	232-237	P53	Homo sapiens	294-297
19180570-7	2009	In addition, our analysis based on published data and data present in this report indicted that levels of Cyr61 expression associated with the status of the tumor suppressor gene p53 in 32 cancer cell lines analyzed, high levels of Cyr61 expression were found in cell lines with mutant or null p53 gene, whereas lower expression levels of Cyr61 in the cell lines with wild-type p53.	cyr61	232-237	P53	Homo sapiens	294-297
19180570-8	2009	We further show that over-expression of dominant negative p53 or down-expression of endogenous wild-type p53 resulted in up-regulation of Cyr61 expression, suggesting a functional link between Cyr61 and p53 in cancers.	cyr61	138-143	P53	Homo sapiens	58-61
19180570-8	2009	We further show that over-expression of dominant negative p53 or down-expression of endogenous wild-type p53 resulted in up-regulation of Cyr61 expression, suggesting a functional link between Cyr61 and p53 in cancers.	cyr61	138-143	P53	Homo sapiens	105-108
22028325-8	2011	Although the overall contribution of miR-194 to neoplastic growth is context dependent, p53-induced activation of this GI tract-specific miRNA during ischemia could promote angiogenesis and facilitate tissue repair.	mir-194	37-44	P53	Homo sapiens	88-91
22134241-3	2011	Thus, we hypothesized that inhibition of HRR (mediated by Chk1 via AZD7762) and PARP1 [via olaparib (AZD2281)] would selectively sensitize p53 mutant pancreatic cancer cells to radiation.	olaparib	91-99	P53	Homo sapiens	139-142
22009179-4	2011	Importantly, radiation enhancement by BEZ235 coincides with a prominent p53-dependent accelerated senescence phenotype characterized by positive beta-galactosidase staining, G(2)-M cell-cycle arrest, enlarged and flattened cellular morphology, and increased p21 expression and senescence-associated cytokine secretion.	dactolisib	38-44	P53	Homo sapiens	72-75
21963806-6	2011	These results provide the first evidence that sappanchalcone suppresses oral cancer cell growth and induces apoptosis through the activation of p53-dependent mitochondrial, p38, ERK, JNK, and NF-kappaB signaling.	sappanchalcone	46-60	P53	Homo sapiens	144-147
19180570-8	2009	We further show that over-expression of dominant negative p53 or down-expression of endogenous wild-type p53 resulted in up-regulation of Cyr61 expression, suggesting a functional link between Cyr61 and p53 in cancers.	cyr61	138-143	P53	Homo sapiens	105-108
19180570-8	2009	We further show that over-expression of dominant negative p53 or down-expression of endogenous wild-type p53 resulted in up-regulation of Cyr61 expression, suggesting a functional link between Cyr61 and p53 in cancers.	cyr61	193-198	P53	Homo sapiens	58-61
22004065-5	2012	We report herein a class of natural product derived Chk2 inhibitors, exemplified by indoloazepine 1, that elicit a strong ATM-dependent Chk2-mediated radioprotection effect in normal cells and p53 wt cells, but not p53 mutant cells (&gt;50% of all cancers).	indoloazepine	84-97	P53	Homo sapiens	193-196
19180570-8	2009	We further show that over-expression of dominant negative p53 or down-expression of endogenous wild-type p53 resulted in up-regulation of Cyr61 expression, suggesting a functional link between Cyr61 and p53 in cancers.	cyr61	193-198	P53	Homo sapiens	105-108
19180570-8	2009	We further show that over-expression of dominant negative p53 or down-expression of endogenous wild-type p53 resulted in up-regulation of Cyr61 expression, suggesting a functional link between Cyr61 and p53 in cancers.	cyr61	193-198	P53	Homo sapiens	105-108
22027149-2	2011	Previously, we showed that molecular Iodine (I(2)) induces apoptosis in hormone responsive MCF-7 breast cancer cells, and non-apoptotic cell death in ER(-ve)-p53 mutant MDA-MB231 cells (Shrivastava, 2006).	Iodine	37-43	P53	Homo sapiens	158-161
22265415-5	2012	Statins and sterol biosynthesis intermediates reveal that this pathway is both necessary and sufficient for the phenotypic effects of mutant p53 on breast tissue architecture.	Sterols	12-18	P53	Homo sapiens	141-144
21996465-1	2011	A series of thio-benzodiazepine p53-MDM2 inhibitors were designed and synthesized based on the principle of bioisosterism.	thio-benzodiazepine	12-31	P53	Homo sapiens	32-35
19137016-3	2009	The small molecule 9-aminoacridine (9AA) and its derivative, the antimalaria drug quinacrine, have selective toxicity for tumor cells and can simultaneously suppress nuclear factor-kappaB (NF-kappaB) and activate p53 signaling.	Quinacrine	82-92	P53	Homo sapiens	213-216
22265415-7	2012	Finally, p53 mutation correlates with highly expressed sterol biosynthesis genes in human breast tumors.	Sterols	55-61	P53	Homo sapiens	9-12
19280470-8	2009	CONCLUSIONS: 1-MTX significantly increased the radiosensitivity of RKO human colorectal cancer cells carrying wild type p53 mainly by inhibiting the repair of radiation-induced DNA DSB without causing significant alteration in radiation-induced G2/M arrest.	1-methylxanthine	13-18	P53	Homo sapiens	120-123
22693688-7	2012	Vanadium compounds inhibit p53-dependent apoptosis and promote entry into the S phase of cells containing functional p53 protein.	Vanadium Compounds	0-18	P53	Homo sapiens	27-30
21625365-0	2011	Kaempferol induces apoptosis in ovarian cancer cells through activating p53 in the intrinsic pathway.	kaempferol	0-10	P53	Homo sapiens	72-75
22693688-7	2012	Vanadium compounds inhibit p53-dependent apoptosis and promote entry into the S phase of cells containing functional p53 protein.	Vanadium Compounds	0-18	P53	Homo sapiens	117-120
21625365-7	2011	Western blot analysis revealed that protein levels of Bcl-x(L) were decreased in ovarian cancer cells, while p53, Bad, and Bax proteins were up-regulated by kaempferol treatment.	kaempferol	157-167	P53	Homo sapiens	109-112
19408145-6	2009	Berbamine treatment increased the expression level of Fas and P53, caused depolarization of mitochondrial membrane and decrease of membrane potential, and activated caspase-3, -8, and -9 in HepG2 cells.	berbamine	0-9	P53	Homo sapiens	62-65
22972485-0	2012	Involvement of p53 and nuclear factor-kappaB signaling pathway for the induction of G1-phase cell cycle arrest of cholangiocarcinoma cell lines by isomorellin.	isomorellin	147-158	P53	Homo sapiens	15-18
19408145-9	2009	These studies suggest that berbamine exerts anticancer effects on human HCC HepG2 cells in vivo and in vitro, the induction of p53 and the activity of the Fas apoptotic system may participate in the anticancer activity of berbamine in HepG2 cells.	berbamine	27-36	P53	Homo sapiens	127-130
19183832-5	2009	The bile duct cancer revealed a well-differentiated adenocarcinoma without mutation of the K-ras gene and with p53 miss-sense mutation of GTG (Val) to GAG (Glu) on codon 272 in exon 8.	Valine	143-146	P53	Homo sapiens	111-114
19183832-5	2009	The bile duct cancer revealed a well-differentiated adenocarcinoma without mutation of the K-ras gene and with p53 miss-sense mutation of GTG (Val) to GAG (Glu) on codon 272 in exon 8.	Glycosaminoglycans	151-154	P53	Homo sapiens	111-114
19373614-2	2009	Here we report two chemopreventive agents, selenite and genistein, that have synergistic effects on apoptosis, cell cycle arrest, and associated signaling pathways in p53-expressing LNCaP and p53-null PC3 prostate cancer cells.	Selenious Acid	43-51	P53	Homo sapiens	167-170
19373614-2	2009	Here we report two chemopreventive agents, selenite and genistein, that have synergistic effects on apoptosis, cell cycle arrest, and associated signaling pathways in p53-expressing LNCaP and p53-null PC3 prostate cancer cells.	Selenious Acid	43-51	P53	Homo sapiens	192-195
21671008-6	2011	Importantly, alpha-PGG"s ability to elevate p53 was diminished by IR inhibitor and IR-siRNA, suggesting a non-conventional role of IR as being involved in p53 induction.	alphaPGG	13-22	P53	Homo sapiens	44-47
21671008-6	2011	Importantly, alpha-PGG"s ability to elevate p53 was diminished by IR inhibitor and IR-siRNA, suggesting a non-conventional role of IR as being involved in p53 induction.	alphaPGG	13-22	P53	Homo sapiens	155-158
21671008-8	2011	Blocking MEK significantly suppressed alpha-PGG-induced p53 and Bax elevation.	alphaPGG	38-47	P53	Homo sapiens	56-59
21671008-9	2011	All these results suggested that alpha-PGG induced p53, Bax, and apoptosis through the IR-MEK signaling pathway.	alphaPGG	33-42	P53	Homo sapiens	51-54
21620827-0	2011	The labdane diterpene sclareol (labd-14-ene-8, 13-diol) induces apoptosis in human tumor cell lines and suppression of tumor growth in vivo via a p53-independent mechanism of action.	labdane	4-11	P53	Homo sapiens	146-149
22972485-6	2012	Our research suggests that isomorellin induces cell cycle arrest and apoptosis in CCA cell lines through p53 and the NF-kappaB-signaling pathway.	isomorellin	27-38	P53	Homo sapiens	105-108
18929532-4	2008	In this study, the wild-type p53 (wt-p53) gene was transfected into human hepatocellular carcinoma cell line HepG(2) using the urocanic acid-modified chitosan (UAC) as a nonviral vector, and transfection efficiency was determined by FACS analysis.	uac	160-163	P53	Homo sapiens	29-32
22962562-4	2012	In this pilot study, changes in p53 and its transcriptional targets, p21/waf1 and MDM2 were analyzed by immunoblotting and densitometry in CLL cells from 10 patients immediately prior to the start of chemotherapy, and after culture for 24 hours (h) with fludarabine (n=7) or chlorambucil (n=3).	fludarabine	254-265	P53	Homo sapiens	32-35
18929532-4	2008	In this study, the wild-type p53 (wt-p53) gene was transfected into human hepatocellular carcinoma cell line HepG(2) using the urocanic acid-modified chitosan (UAC) as a nonviral vector, and transfection efficiency was determined by FACS analysis.	uac	160-163	P53	Homo sapiens	37-40
18929532-5	2008	UAC-mediated p53 transfection in HepG(2) cells resulted in high expression levels of wt-p53 mRNA and protein and significant cellular growth inhibition.	uac	0-3	P53	Homo sapiens	13-16
18929532-5	2008	UAC-mediated p53 transfection in HepG(2) cells resulted in high expression levels of wt-p53 mRNA and protein and significant cellular growth inhibition.	uac	0-3	P53	Homo sapiens	88-91
18929532-6	2008	DAPI staining and Annexin V/PI double-staining assay revealed apoptosis occurrence in HepG(2) cells after treatment with UAC/pEGFP-p53 complexes.	uac	121-124	P53	Homo sapiens	131-134
18929532-8	2008	These results demonstrated that UAC-mediated efficient p53 gene transfer could induce apoptosis thereby significantly inhibiting the growth of HepG(2) cells in vitro and in vivo, and suggested that UAC-mediated p53 gene delivery might be a promising approach for HCC gene therapy.	uac	32-35	P53	Homo sapiens	55-58
21980285-11	2011	Consequently, TAp63beta is the only p63 isoform suppressed by E6 in cervical carcinoma as demonstrated previously for p53.	tap63beta	14-23	P53	Homo sapiens	118-121
22507894-0	2012	Galangin induces autophagy through upregulation of p53 in HepG2 cells.	galangin	0-8	P53	Homo sapiens	51-54
21663643-11	2011	Nonetheless, in two p53-deficient SLGC lines examined gammaIR-induced apoptosis even correlated with EGF/FGF-induced proliferation and mitotic catastrophe.	gammair	54-61	P53	Homo sapiens	20-23
18929532-8	2008	These results demonstrated that UAC-mediated efficient p53 gene transfer could induce apoptosis thereby significantly inhibiting the growth of HepG(2) cells in vitro and in vivo, and suggested that UAC-mediated p53 gene delivery might be a promising approach for HCC gene therapy.	uac	32-35	P53	Homo sapiens	211-214
18929532-8	2008	These results demonstrated that UAC-mediated efficient p53 gene transfer could induce apoptosis thereby significantly inhibiting the growth of HepG(2) cells in vitro and in vivo, and suggested that UAC-mediated p53 gene delivery might be a promising approach for HCC gene therapy.	uac	198-201	P53	Homo sapiens	55-58
18929532-8	2008	These results demonstrated that UAC-mediated efficient p53 gene transfer could induce apoptosis thereby significantly inhibiting the growth of HepG(2) cells in vitro and in vivo, and suggested that UAC-mediated p53 gene delivery might be a promising approach for HCC gene therapy.	uac	198-201	P53	Homo sapiens	211-214
21382431-8	2011	Quantitative real-time PCR analysis demonstrated that following the exposure of A549 cells to nickel ferrite nanoparticles, the level of mRNA expressions of cell cycle checkpoint protein p53 and apoptotic proteins (bax, caspase-3 and caspase-9) were significantly up-regulated, whereas the expression of anti-apoptotic proteins (survivin and bcl-2) were down-regulated.	Nickel	94-100	P53	Homo sapiens	187-190
23029106-0	2012	A novel small molecule FL118 that selectively inhibits survivin, Mcl-1, XIAP and cIAP2 in a p53-independent manner, shows superior antitumor activity.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	23-28	P53	Homo sapiens	92-95
21382431-10	2011	To the best of our knowledge this is the first report showing that nickel ferrite nanoparticles induced apoptosis in A549 cells through ROS generation and oxidative stress via p53, survivin, bax/bcl-2 and caspase pathways.	Nickel	67-73	P53	Homo sapiens	176-179
19026165-0	2008	Suberoyl bis-hydroxamic acid induces p53-dependent apoptosis of MCF-7 breast cancer cells.	suberoyl bis-hydroxamic acid	0-28	P53	Homo sapiens	37-40
23029106-7	2012	Moreover, FL118 selectively inhibited survivin promoter activity and gene expression also in a p53 status-independent manner.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	10-15	P53	Homo sapiens	95-98
19026165-6	2008	The expressions of p53, p21, Bax, and PUMA were induced, and DeltaPsim collapsed after treatment with SBHA.	suberoyl bis-hydroxamic acid	102-106	P53	Homo sapiens	19-22
21376392-9	2011	With no significant changes in the mRNA levels of p53, the increase in overall p53 protein levels and its post-translational modification by phosphorylation at Ser-15 are induced by CdTe QD treatment.	cadmium telluride	182-186	P53	Homo sapiens	79-82
22859938-6	2012	Tunicamycin or brefeldin A, two ER stress inducers, increased p53 expression in MCF-7 and Hela cells.	Brefeldin A	15-26	P53	Homo sapiens	62-65
20390378-5	2011	The NaAsO2 treatment resulted in a marked increase in p53 protein as early as 4 h and in Bcl-2 protein level by 12 h. In addition, p53 downregulation accompanied the combined treatment of NaAsO2 and Na2SeO3.	na2seo3	199-206	P53	Homo sapiens	54-57
19026165-8	2008	CONCLUSION: The activation of the p53 pathway is involved in SBHA-induced apoptosis in MCF-7 cells.	suberoyl bis-hydroxamic acid	61-65	P53	Homo sapiens	34-37
20390378-5	2011	The NaAsO2 treatment resulted in a marked increase in p53 protein as early as 4 h and in Bcl-2 protein level by 12 h. In addition, p53 downregulation accompanied the combined treatment of NaAsO2 and Na2SeO3.	na2seo3	199-206	P53	Homo sapiens	131-134
22859938-10	2012	The role of p53 in mediating Brefeldin A-induced apoptosis was also investigated.	Brefeldin A	29-40	P53	Homo sapiens	12-15
21462329-3	2011	METHODS AND RESULTS: Annexin V/PI co-staining assay demonstrated that 5HHMF and 5HTMF significantly induced apoptosis in HCT116 (p53(+/+) ) cells but not in HCT116 (p53(-/-) ) cells.	5-hydroxy-6,7,8,4'-tetramethoxyflavone	80-85	P53	Homo sapiens	129-132
19010883-3	2008	Through the mitogen-activated protein kinase pathway, arsenite stimulates the P2 promoter-mediated expression of Hdm2, which then promotes p53 nuclear export.	arsenite	54-62	P53	Homo sapiens	139-142
22859938-11	2012	Induction of p53 expression by Brefeldin A was correlated to Brefeldin A-induced apoptosis.	Brefeldin A	31-42	P53	Homo sapiens	13-16
18818525-12	2008	Collectively, DHC activates autophagy in a p53-independent manner and that may contribute to cytotoxicity of DHC.	dihydrocapsaicin	14-17	P53	Homo sapiens	43-46
21462329-3	2011	METHODS AND RESULTS: Annexin V/PI co-staining assay demonstrated that 5HHMF and 5HTMF significantly induced apoptosis in HCT116 (p53(+/+) ) cells but not in HCT116 (p53(-/-) ) cells.	5-hydroxy-6,7,8,4'-tetramethoxyflavone	80-85	P53	Homo sapiens	165-168
21462329-5	2011	All three 5OH-PMFs increased G0/G1 cell population of HCT116 (p53(+/+) ) cells, and these effects were abolished in HCT116 (p53(-/-) ) and HCT116 (p21(-/-) ) cells.	5oh	10-13	P53	Homo sapiens	62-65
22859938-11	2012	Induction of p53 expression by Brefeldin A was correlated to Brefeldin A-induced apoptosis.	Brefeldin A	61-72	P53	Homo sapiens	13-16
21462329-5	2011	All three 5OH-PMFs increased G0/G1 cell population of HCT116 (p53(+/+) ) cells, and these effects were abolished in HCT116 (p53(-/-) ) and HCT116 (p21(-/-) ) cells.	5oh	10-13	P53	Homo sapiens	124-127
21462329-7	2011	CONCLUSION: Our results demonstrated that 5OH-PMFs, especially 5HHMF and 5HTMF, induce apoptosis and cell-cycle arrest by p53-, Bax- and p21-dependent mechanism.	5oh-pmfs	42-50	P53	Homo sapiens	122-125
22859938-12	2012	Furthermore, downregulation of p53 expression by p53 siRNA significantly reduced Brefeldin A-induced apoptosis in MCF-7 cells.	Brefeldin A	81-92	P53	Homo sapiens	31-34
21462329-7	2011	CONCLUSION: Our results demonstrated that 5OH-PMFs, especially 5HHMF and 5HTMF, induce apoptosis and cell-cycle arrest by p53-, Bax- and p21-dependent mechanism.	5-hydroxy-6,7,8,4'-tetramethoxyflavone	73-78	P53	Homo sapiens	122-125
22859938-12	2012	Furthermore, downregulation of p53 expression by p53 siRNA significantly reduced Brefeldin A-induced apoptosis in MCF-7 cells.	Brefeldin A	81-92	P53	Homo sapiens	49-52
18787402-2	2008	Here we show that combining the three sage bioactive compounds, Linalyl acetate (Ly), Terpeniol (Te) and Camphor (Ca), caused synergistic inhibition of the growth of two isogenic human colon cancer cell lines HCT-116 (p53(+/+) and p53(-/-)) and had no effect on growth of FHs74Int normal human intestinal cell line.	terpeniol	86-95	P53	Homo sapiens	218-221
18787402-2	2008	Here we show that combining the three sage bioactive compounds, Linalyl acetate (Ly), Terpeniol (Te) and Camphor (Ca), caused synergistic inhibition of the growth of two isogenic human colon cancer cell lines HCT-116 (p53(+/+) and p53(-/-)) and had no effect on growth of FHs74Int normal human intestinal cell line.	terpeniol	86-95	P53	Homo sapiens	231-234
22044530-9	2011	beta-Naphthoflavon (beta-NF), an aryl hydrocarbon receptor (AHR) agonist, mimicked TCDD"s action and abolished 1-NP-induced p53 expression.	beta-naphthoflavon	0-18	P53	Homo sapiens	124-127
22047690-0	2011	Conjugation of spermine enhances cellular uptake of the stapled peptide-based inhibitors of p53-Mdm2 interaction.	Spermine	15-23	P53	Homo sapiens	92-95
18720420-8	2008	Finally, ascorbic acid could also protect SY5Y cells from DA-induced cellular apoptotic signal changes including PARP and P53.	Ascorbic Acid	9-22	P53	Homo sapiens	122-125
18554781-2	2008	The present study was undertaken to examine whether HS-1200 had an anticancer effect on HepG2 (wild-type p53) and Hep3B (p53 deleted) human hepatoma cells.	HS 1200	52-59	P53	Homo sapiens	105-108
21115943-3	2011	The results showed that PFOS could reduce the cell viability significantly, and the cellular apoptosis induced by PFOS was closely accompanied with dissipation of mitochondria membrane potential, upregulation messenger RNAs (mRNAs) of p53, Bax, caspase 9, and caspase 3, and decreased expression of Bcl-2 mRNA.	perfluorooctane sulfonic acid	24-28	P53	Homo sapiens	235-238
21115943-3	2011	The results showed that PFOS could reduce the cell viability significantly, and the cellular apoptosis induced by PFOS was closely accompanied with dissipation of mitochondria membrane potential, upregulation messenger RNAs (mRNAs) of p53, Bax, caspase 9, and caspase 3, and decreased expression of Bcl-2 mRNA.	perfluorooctane sulfonic acid	114-118	P53	Homo sapiens	235-238
21468351-0	2011	A label-free biosensor based on silver nanoparticles array for clinical detection of serum p53 in head and neck squamous cell carcinoma.	Silver	32-38	P53	Homo sapiens	91-94
18554781-2	2008	The present study was undertaken to examine whether HS-1200 had an anticancer effect on HepG2 (wild-type p53) and Hep3B (p53 deleted) human hepatoma cells.	HS 1200	52-59	P53	Homo sapiens	121-124
18554781-7	2008	HS-1200 treatment also caused an increase in the expression levels of p21 WAF1/CIP1 in HepG2 cells in a p53-dependent manner and in Hep3B cells in a p53-independent manner.	HS 1200	0-7	P53	Homo sapiens	104-107
22047690-1	2011	We report the first synthesis of the C-terminally spermine-conjugated stapled peptide-based inhibitors of the p53-Mdm2 interaction.	Spermine	50-58	P53	Homo sapiens	110-113
18554781-7	2008	HS-1200 treatment also caused an increase in the expression levels of p21 WAF1/CIP1 in HepG2 cells in a p53-dependent manner and in Hep3B cells in a p53-independent manner.	HS 1200	0-7	P53	Homo sapiens	149-152
18554781-10	2008	Furthermore, HS-1200 treatment markedly induced the Egr-1 expression at an early time point, and the increased expression levels of p53, p21 WAF1/CIP1, p27 KIP1, and COX-2 after treatment with HS-1200 were completely inhibited in HepG2 cells and partially inhibited in Hep3B cells by silencing of Egr-1, respectively.	HS 1200	13-20	P53	Homo sapiens	132-135
20717878-9	2011	These findings indicate that araliadiol exhibits its growth-inhibitory effects on MCF-7 cells through downregulation of cdk4 and cyclin D (3), and upregulation of p21 (WAF-1/Cip1) by a p53-independent mechanism.	Araliadiol	29-39	P53	Homo sapiens	185-188
21995630-2	2011	The human p53 3"-untranslated region (3"-UTR) contains two regions similar to cytoplasmic polyadenylation elements (CPEs) just upstream of the poly(A) hexanucleotide.	poly(a) hexanucleotide	143-165	P53	Homo sapiens	10-13
21655246-12	2011	Moreover, these findings place h-eag1 in the p53-miR-34-E2F1-h-eag1 pathway with h-eag as a terminal effecter component and with miR-34 (and E2F1) as a linker between p53 and h-eag1.	h-eag	31-36	P53	Homo sapiens	45-48
18554781-10	2008	Furthermore, HS-1200 treatment markedly induced the Egr-1 expression at an early time point, and the increased expression levels of p53, p21 WAF1/CIP1, p27 KIP1, and COX-2 after treatment with HS-1200 were completely inhibited in HepG2 cells and partially inhibited in Hep3B cells by silencing of Egr-1, respectively.	HS 1200	193-200	P53	Homo sapiens	132-135
18446786-8	2008	Activation of p53 and p53-dependent apoptosis were blocked by the COX-2 inhibitor, NS398, and by transfection of cells with COX-2-siRNA.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	83-88	P53	Homo sapiens	14-17
18446786-8	2008	Activation of p53 and p53-dependent apoptosis were blocked by the COX-2 inhibitor, NS398, and by transfection of cells with COX-2-siRNA.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	83-88	P53	Homo sapiens	22-25
21655246-12	2011	Moreover, these findings place h-eag1 in the p53-miR-34-E2F1-h-eag1 pathway with h-eag as a terminal effecter component and with miR-34 (and E2F1) as a linker between p53 and h-eag1.	h-eag	31-36	P53	Homo sapiens	167-170
21092078-6	2010	Furthermore, the role of p53 in flavopiridol- and 4OH-Tam-mediated induction of cell cycle arrest and apoptosis was characterized using RNA interference (siRNA) analysis.	Estetrol	50-53	P53	Homo sapiens	25-28
18379194-8	2008	Taken together, these results suggest that Nobiletin could induce p53-mediated cell cycle arrest and apoptosis via modulated the Bax:Bcl-2 protein ratio, is effective as a potent antitumor agent on lung tumors.	nobiletin	43-52	P53	Homo sapiens	66-69
21092078-11	2010	Abrogation of p53 by siRNA abolished flavopiridol-induced G2 arrest, but enhanced flavopiridol- (but not 4OH-Tam-) mediated apoptosis, by enhancing caspase 2 and 3 activities.	4oh-tam	105-112	P53	Homo sapiens	14-17
21831953-1	2011	PURPOSE: Originally isolated on the basis of its ability to induce p53, serdemetan showed potent activity in various preclinical models, inducing S-phase arrest and apoptosis in TP53 wild-type and mutant tumors.	JNJ 26854165	72-82	P53	Homo sapiens	67-70
21078189-0	2010	Cell death by the quinoxaline dioxide DCQ in human colon cancer cells is enhanced under hypoxia and is independent of p53 and p21.	Quinoxalines	18-29	P53	Homo sapiens	118-121
20655369-7	2010	While cyclophosphamide showed an elevation of activated P53 in the presence of S9, 7,12-dimethylbenz[a]anthracene and aflatoxin B(1) responded without the MAS.	s9, 7,12-dimethylbenz[a	79-102	P53	Homo sapiens	56-59
18452313-11	2008	Mapping the sequence specificity of Cr(III)-GA 2- and Cr(III)-EGA 2-DNA formation in the human p53 gene sequence by UvrABC nuclease cutting, we found that the sequence specificity for both adducts is the same but is much more selective than Cr(III)-guanine-DNA adducts.	tris(1,10-phenanthroline)chromium(III) chloride	36-43	P53	Homo sapiens	95-98
18452313-11	2008	Mapping the sequence specificity of Cr(III)-GA 2- and Cr(III)-EGA 2-DNA formation in the human p53 gene sequence by UvrABC nuclease cutting, we found that the sequence specificity for both adducts is the same but is much more selective than Cr(III)-guanine-DNA adducts.	tris(1,10-phenanthroline)chromium(III) chloride	54-61	P53	Homo sapiens	95-98
18331475-0	2008	Anti-apoptotic effect of Mao-B inhibitor PF9601N [N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine] is mediated by p53 pathway inhibition in MPP+-treated SH-SY5Y human dopaminergic cells.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	41-48	P53	Homo sapiens	117-120
18331475-0	2008	Anti-apoptotic effect of Mao-B inhibitor PF9601N [N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine] is mediated by p53 pathway inhibition in MPP+-treated SH-SY5Y human dopaminergic cells.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	50-100	P53	Homo sapiens	117-120
21831953-1	2011	PURPOSE: Originally isolated on the basis of its ability to induce p53, serdemetan showed potent activity in various preclinical models, inducing S-phase arrest and apoptosis in TP53 wild-type and mutant tumors.	JNJ 26854165	72-82	P53	Homo sapiens	178-182
21831953-12	2011	CONCLUSIONS: Serdemetan treatment was associated with p53 induction in both tumor and surrogate tissue pharmacodynamic studies and modest clinical activity.	JNJ 26854165	13-23	P53	Homo sapiens	54-57
20467885-10	2011	Irinotecan and simvastatin combination treatment of A549 and H460 cells increased G(1) phase arrest, which was associated with up-regulation of p21(WAF1/CIP) and p53 compared with irinotecan alone.	Simvastatin	15-26	P53	Homo sapiens	162-165
18400537-0	2008	De novo N-palmitoylsphingosine synthesis is the major biochemical mechanism of ceramide accumulation following p53 up-regulation.	N-palmitoylsphingosine	8-30	P53	Homo sapiens	111-114
20702613-4	2010	RESULTS: EZN-2208 was about 100-fold more potent than CPT-11 in vitro, by inducing apoptosis/necrosis and p53 expression and by reducing hypoxia-inducible factor (HIF)-1alpha/HIF-2alpha expression.	EZN-2208	9-17	P53	Homo sapiens	106-109
18400537-5	2008	In both Molt-4 LXSN leukemia cells exposed to gamma-irradiation and in EB-1 colon cancer cells treated with ZnCl(2), p53 up-regulation led to de novo ceramide synthesis with predominance of N-palmitoylsphingosine (C16-ceramide) synthesis.	N-palmitoylsphingosine	190-212	P53	Homo sapiens	117-120
21809836-2	2011	After metabolic activation, some NOCs can induce carboxymethylation of nucleobases through a diazoacetate intermediate, which could give rise to p53 mutations similar to those seen in human gastrointestinal cancers.	diazoacetate	93-105	P53	Homo sapiens	145-148
18400537-5	2008	In both Molt-4 LXSN leukemia cells exposed to gamma-irradiation and in EB-1 colon cancer cells treated with ZnCl(2), p53 up-regulation led to de novo ceramide synthesis with predominance of N-palmitoylsphingosine (C16-ceramide) synthesis.	N-palmitoylsphingosine	214-226	P53	Homo sapiens	117-120
18358838-2	2008	Here we studied whether p53 mitochondrial translocation and subsequent apoptosis were affected by blocking mitochondrial permeability transition pore using cyclosporine A (CsA) and bongkrekic acid (BA) in skin epidermal JB6 cells and skin tissues.	Bongkrekic Acid	181-196	P53	Homo sapiens	24-27
18358838-2	2008	Here we studied whether p53 mitochondrial translocation and subsequent apoptosis were affected by blocking mitochondrial permeability transition pore using cyclosporine A (CsA) and bongkrekic acid (BA) in skin epidermal JB6 cells and skin tissues.	Bongkrekic Acid	198-200	P53	Homo sapiens	24-27
20558185-7	2010	While the benzofurylquinazolines increased the expression level of the pro-inflammatory gene IL1-alpha as well as p21 and p53 in the PC3 cell line, a phenylpyrrolocarbazole had the converse effect on p53 expression.	phenylpyrrolocarbazole	150-172	P53	Homo sapiens	200-203
21671008-5	2011	alpha-PGG induced apoptosis in RKO cells through p53, Bax and caspase 3.	alphaPGG	0-9	P53	Homo sapiens	49-52
20700496-0	2010	Lysine120 interactions with p53 response elements can allosterically direct p53 organization.	lysine120	0-9	P53	Homo sapiens	28-31
21067279-5	2011	Both types of TiO2 nanoparticles transiently upregulated mRNA expression of p53 and its downstream regulated DNA damage responsive genes (mdm2, gadd45alpha, p21), providing additional evidence that TiO2 nanoparticles are genotoxic.	titanium dioxide	14-18	P53	Homo sapiens	76-79
20700496-0	2010	Lysine120 interactions with p53 response elements can allosterically direct p53 organization.	lysine120	0-9	P53	Homo sapiens	76-79
20662736-8	2010	Although mitoxantrone, ellipticine, camptothecin, and topotecan all exhibited concentration-dependent disruption of the p53-hDM2 PPIB, they were much less potent than Nutlin-3.	Topotecan	54-63	P53	Homo sapiens	120-123
18358838-3	2008	Our results demonstrated that CsA and BA blocked TPA-induced p53 translocation, leading to protection against the loss of mitochondrial membrane potential and Complex I activity, and eventually suppression of apoptosis.	Bongkrekic Acid	38-40	P53	Homo sapiens	61-64
17982489-7	2008	GA also produced a p53/ATM-independent increase in the levels of p21-a potent inducer of cell-cycle arrest.	geldanamycin	0-2	P53	Homo sapiens	19-22
20605095-0	2010	Enhancement of transcriptional activity of mutant p53 tumor suppressor protein through stabilization of tetramer formation by calix[6]arene derivatives.	arene	134-139	P53	Homo sapiens	50-53
21067279-5	2011	Both types of TiO2 nanoparticles transiently upregulated mRNA expression of p53 and its downstream regulated DNA damage responsive genes (mdm2, gadd45alpha, p21), providing additional evidence that TiO2 nanoparticles are genotoxic.	titanium dioxide	198-202	P53	Homo sapiens	76-79
20605095-5	2010	In this study, we report, for the first time, the enhancement of the in vivo transcriptional activity of the most common Li-Fraumeni p53 mutant by imidazole-calix[6]arene through stabilization of the oligomer formation.	imidazole-calix[6]	147-165	P53	Homo sapiens	133-136
20605095-5	2010	In this study, we report, for the first time, the enhancement of the in vivo transcriptional activity of the most common Li-Fraumeni p53 mutant by imidazole-calix[6]arene through stabilization of the oligomer formation.	arene	165-170	P53	Homo sapiens	133-136
18201741-9	2008	Furthermore, arsenite and hyperthermia treatments activated a p53/p21 pathway associated with apoptosis induction, whereas vincristine did not activate this pathway.	arsenite	13-21	P53	Homo sapiens	62-65
21614555-4	2011	Western blot analysis of phosphorylated proteins showed that exposure to prazosin increased the levels of phospho-p53 and phospho-adenosine monophosphate-activated protein kinase (AMPK) but dramatically decreased the levels of phospho-mammalian target of rapamycin (mTOR), phospho-protein kinase B (Akt), and phospho-ribosomal protein S6 kinase (p70S6K).	Prazosin	73-81	P53	Homo sapiens	114-117
17728781-0	2008	Multiple forms of nuclear p53 formed in human Raji and MEC1 cells treated with fludarabine.	fludarabine	79-90	P53	Homo sapiens	26-29
18365879-8	2008	We provide evidence that PQ induces apoptosis in lymphocytes in a concentration- and time-dependent fashion by an oxidative stress mechanism involving O(2)( radical - ), H(2)O(2)/(( radical)OH) generation, simultaneous activation of NF-kappaB/p53/c-Jun transcription factors, mitochondrial depolarization and caspase-3 activation leading to morphological apoptosis.	Paraquat	25-27	P53	Homo sapiens	243-246
19499188-0	2010	The effect of cellular environment and p53 status on the mode of action of the platinum derivative LA-12.	UNII-37WM0V5E17	99-104	P53	Homo sapiens	39-42
19499188-3	2010	LA-12 induces weak accumulation of both transcriptionally active p53 tumor suppressor and of p21(WAF1/CIP1) protein.	UNII-37WM0V5E17	0-5	P53	Homo sapiens	65-68
19499188-5	2010	LA-12 induces higher apoptosis levels in comparison with those induced by cisplatin, especially in p53-deficient H1299 cells and in MCF-7DD cells with transcriptionally inactive p53.	UNII-37WM0V5E17	0-5	P53	Homo sapiens	99-102
19499188-5	2010	LA-12 induces higher apoptosis levels in comparison with those induced by cisplatin, especially in p53-deficient H1299 cells and in MCF-7DD cells with transcriptionally inactive p53.	UNII-37WM0V5E17	0-5	P53	Homo sapiens	178-181
19499188-7	2010	This confirms the therapeutic potential of LA-12 as a more potent cytostatic agent for both tumor cells expressing wild type p53 and for p53-deficient or mutant cells.	UNII-37WM0V5E17	43-48	P53	Homo sapiens	125-128
19499188-7	2010	This confirms the therapeutic potential of LA-12 as a more potent cytostatic agent for both tumor cells expressing wild type p53 and for p53-deficient or mutant cells.	UNII-37WM0V5E17	43-48	P53	Homo sapiens	137-140
21458064-3	2011	Cationic beta-cyclodextrin-polyethylenimine-Dox (PC-Dox) conjugates were prepared for carrying wt p53 plasmid in the form of PC-Dox/p53 nanocomplexes to achieve synergistic cancer therapeutic effects of drug and gene therapies.	betadex	9-26	P53	Homo sapiens	98-101
20682650-0	2010	Gamma-tocotrienol promotes TRAIL-induced apoptosis through reactive oxygen species/extracellular signal-regulated kinase/p53-mediated upregulation of death receptors.	plastochromanol 8	0-17	P53	Homo sapiens	121-124
18042465-7	2008	Based on these results, we conclude that HO activity is involved in the regulation of p53 expression in a ROS-independent mechanism, and also suggest that the expression of p53 in ARPE-19 cells is associated with heme metabolites such as biliverdin/bilirubin, carbon monoxide, and iron produced by the activity of HO.	Bilirubin	249-258	P53	Homo sapiens	173-176
21458064-3	2011	Cationic beta-cyclodextrin-polyethylenimine-Dox (PC-Dox) conjugates were prepared for carrying wt p53 plasmid in the form of PC-Dox/p53 nanocomplexes to achieve synergistic cancer therapeutic effects of drug and gene therapies.	betadex	9-26	P53	Homo sapiens	132-135
18160328-0	2008	Clioquinol inhibits peroxide-mediated toxicity through up-regulation of phosphoinositol-3-kinase and inhibition of p53 activity.	Peroxides	20-28	P53	Homo sapiens	115-118
21458064-3	2011	Cationic beta-cyclodextrin-polyethylenimine-Dox (PC-Dox) conjugates were prepared for carrying wt p53 plasmid in the form of PC-Dox/p53 nanocomplexes to achieve synergistic cancer therapeutic effects of drug and gene therapies.	pc-dox	49-55	P53	Homo sapiens	98-101
21458064-3	2011	Cationic beta-cyclodextrin-polyethylenimine-Dox (PC-Dox) conjugates were prepared for carrying wt p53 plasmid in the form of PC-Dox/p53 nanocomplexes to achieve synergistic cancer therapeutic effects of drug and gene therapies.	pc-dox	49-55	P53	Homo sapiens	132-135
20371239-7	2010	Western blot analysis indicated that BTZQ may up-regulate expression of cyclin B, p21, p53 and cytochrome c, but down-regulate cdk1 expression in a dose-dependent manner, leading to apoptosis of BC-M1 cells.	btzq	37-41	P53	Homo sapiens	87-90
21458064-4	2011	Such PC-Dox/p53 nanocomplexes ensure that both drug and gene can be delivered to the same cancer cells.	pc-dox	5-11	P53	Homo sapiens	12-15
18348409-1	2007	OBJECTIVE: To assess the ability of tetrandrine (Tet) to enhance the sensitivity to irradiation and its mechanism in cell lines of human breast cancer p53-mutant MCF-7/ADR, p53-wild-type MCF-7 and human colon carcinoma p53-mutant HT-29 as well as in C26 colorectal carcinoma-bearing BALB/c mice.	tetrandrine	36-47	P53	Homo sapiens	151-154
20230799-4	2010	LYR-8 dramatically induced NAG-1 expression and apoptosis in HCT116 (wild-type p53) and HT29 (mutant p53) colon cancer cells.	1-(1-hydroxy-6,6,9-trimethyl-6a,7,8,9,10,10a-hexahydro-6H-benzo(c)chromen-2-yl)ethanone	0-5	P53	Homo sapiens	79-82
21458064-7	2011	By investigating anticancer efficacy via multi-drug resistant MCF-7/Adr breast cancer cells, it was found that PC-Dox/wt p53 complexes promoted the inhibition of tumor growth in vivo and prolonged the survival time of tumor-bearing mice.	pc-dox	111-117	P53	Homo sapiens	121-124
20230799-4	2010	LYR-8 dramatically induced NAG-1 expression and apoptosis in HCT116 (wild-type p53) and HT29 (mutant p53) colon cancer cells.	1-(1-hydroxy-6,6,9-trimethyl-6a,7,8,9,10,10a-hexahydro-6H-benzo(c)chromen-2-yl)ethanone	0-5	P53	Homo sapiens	101-104
18348409-1	2007	OBJECTIVE: To assess the ability of tetrandrine (Tet) to enhance the sensitivity to irradiation and its mechanism in cell lines of human breast cancer p53-mutant MCF-7/ADR, p53-wild-type MCF-7 and human colon carcinoma p53-mutant HT-29 as well as in C26 colorectal carcinoma-bearing BALB/c mice.	tetrandrine	36-47	P53	Homo sapiens	173-176
18348409-1	2007	OBJECTIVE: To assess the ability of tetrandrine (Tet) to enhance the sensitivity to irradiation and its mechanism in cell lines of human breast cancer p53-mutant MCF-7/ADR, p53-wild-type MCF-7 and human colon carcinoma p53-mutant HT-29 as well as in C26 colorectal carcinoma-bearing BALB/c mice.	tetrandrine	36-47	P53	Homo sapiens	173-176
18348409-1	2007	OBJECTIVE: To assess the ability of tetrandrine (Tet) to enhance the sensitivity to irradiation and its mechanism in cell lines of human breast cancer p53-mutant MCF-7/ADR, p53-wild-type MCF-7 and human colon carcinoma p53-mutant HT-29 as well as in C26 colorectal carcinoma-bearing BALB/c mice.	tetrandrine	49-52	P53	Homo sapiens	173-176
20230799-8	2010	Knockdown of NAG-1 using siRNA significantly reversed LYR-8-induced cell death in both wild-type and mutant p53-expressing colon cancer cells.	1-(1-hydroxy-6,6,9-trimethyl-6a,7,8,9,10,10a-hexahydro-6H-benzo(c)chromen-2-yl)ethanone	54-59	P53	Homo sapiens	108-111
20230799-10	2010	These results suggest that induction of NAG-1 via Sp1 activation is a promising therapeutic approach in cancer treatment, and that a novel compound like LYR-8 could be a potent chemotherapeutic agent for colon cancers including p53-mutated cancer.	1-(1-hydroxy-6,6,9-trimethyl-6a,7,8,9,10,10a-hexahydro-6H-benzo(c)chromen-2-yl)ethanone	153-158	P53	Homo sapiens	228-231
20375080-10	2010	Together, the results suggest that the repressive effect of NF-kappaB on p53 by mot-2 leads to genomic instability, which is involved in arsenite-induced malignant transformation of human keratinocytes.	arsenite	137-145	P53	Homo sapiens	73-76
18348409-1	2007	OBJECTIVE: To assess the ability of tetrandrine (Tet) to enhance the sensitivity to irradiation and its mechanism in cell lines of human breast cancer p53-mutant MCF-7/ADR, p53-wild-type MCF-7 and human colon carcinoma p53-mutant HT-29 as well as in C26 colorectal carcinoma-bearing BALB/c mice.	tetrandrine	49-52	P53	Homo sapiens	173-176
18348409-7	2007	RESULTS: Clonogenic assay showed that tetrandrine markedly enhanced the lethal effect of X-rays on p53-mutant MCF-7/ADR and HT-29 cells and the sensitization enhancement ratio (SER) of tetrandrine was 1.51 and 1.63, but its SER was only 1.1 in p53-wt MCF-7 cells.	tetrandrine	38-49	P53	Homo sapiens	99-102
18348409-7	2007	RESULTS: Clonogenic assay showed that tetrandrine markedly enhanced the lethal effect of X-rays on p53-mutant MCF-7/ADR and HT-29 cells and the sensitization enhancement ratio (SER) of tetrandrine was 1.51 and 1.63, but its SER was only 1.1 in p53-wt MCF-7 cells.	tetrandrine	38-49	P53	Homo sapiens	244-247
21663679-3	2011	RESULTS: It is shown that vitamin K3- or vitamin C- induced apoptosis in leukemia cells by oxidative stress mechanism involving superoxide anion radical and hydrogen peroxide generation, activation of NF-kappaB, p53, c-Jun, protease caspase-3 activation and mitochondria depolarization leading to nuclei fragmentation.	Vitamin K 3	26-36	P53	Homo sapiens	212-215
17914575-6	2007	A comparison with the wild-type after 1 nano-second molecular dynamic simulation analysis revealed a significant structural change (over 4A displacement) in the contact loop Lys-Ser-Val which lies upstream and next to the mutated site in the TP53, that sterically prevents its DNA-binding activity.	Valine	182-185	P53	Homo sapiens	242-246
20504344-7	2010	After performing messenger RNA expression profile of the same patients, the activation of p53-responsive genes was detected in fludarabine responsive cases only, therefore suggesting a possible mechanism linked to microRNA deregulation in non-responder patients.	fludarabine	127-138	P53	Homo sapiens	90-93
20504344-8	2010	Importantly, inhibition of miR-21 and miR-222 by anti-miRNA oligonucleotides induced a significant increase in caspase activity in fludarabine-treated p53-mutant MEG-01 cells, suggesting that miR-21 and miR-222 up-regulation may be involved in the establishment of fludarabine resistance.	fludarabine	131-142	P53	Homo sapiens	151-154
20504344-8	2010	Importantly, inhibition of miR-21 and miR-222 by anti-miRNA oligonucleotides induced a significant increase in caspase activity in fludarabine-treated p53-mutant MEG-01 cells, suggesting that miR-21 and miR-222 up-regulation may be involved in the establishment of fludarabine resistance.	fludarabine	265-276	P53	Homo sapiens	151-154
21663679-3	2011	RESULTS: It is shown that vitamin K3- or vitamin C- induced apoptosis in leukemia cells by oxidative stress mechanism involving superoxide anion radical and hydrogen peroxide generation, activation of NF-kappaB, p53, c-Jun, protease caspase-3 activation and mitochondria depolarization leading to nuclei fragmentation.	Ascorbic Acid	41-50	P53	Homo sapiens	212-215
17496931-5	2007	We demonstrate that in addition to topotecan (TPT), a known inhibitor of HIF-1alpha, UVC, but not other DNA damaging agents (cisplatin, ionizing radiation and doxorubicin), inhibited HIF-1alpha protein accumulation in a dose-dependent, p53-independent fashion.	Topotecan	46-49	P53	Homo sapiens	236-239
23556086-11	2011	The only group that can be clearly identified pretreatment for whom conventional fludarabine-based therapies produce significantly inferior response rates, PFS and overall survival are the patients who harbour a genetic fault; deletion or mutation or a combination of deletion and mutation of tumour protein p53 (TP53).	fludarabine	81-92	P53	Homo sapiens	308-311
17610067-5	2007	In the sensitive cell line an upregulation of multiple E2F1- and p53-inducible proapaptotic and cell-cycle regulating target genes by Topotecan as well as TRAIL was observed.	Topotecan	134-143	P53	Homo sapiens	65-68
21162257-3	2007	RESULTS: In the group of a 12 h long exposure to oxygen concentration of 0%, diazoxide (100 micromol/L), the K(ATP) channels agonist, reduced p53 expression and the hypoxia-induced apoptosis.	Diazoxide	77-86	P53	Homo sapiens	142-145
21162257-4	2007	In contrast, tolbutamide (100 micromol/L), the K(ATP) channels antagonist, significantly rose p53 expression and the hypoxia-induced apoptosis, which could be reversed by p53 inhibitor TSA.	Tolbutamide	13-24	P53	Homo sapiens	94-97
21162257-4	2007	In contrast, tolbutamide (100 micromol/L), the K(ATP) channels antagonist, significantly rose p53 expression and the hypoxia-induced apoptosis, which could be reversed by p53 inhibitor TSA.	Tolbutamide	13-24	P53	Homo sapiens	171-174
19960411-4	2010	In addition, 24-hydroxyursolic acid induced cellular apoptosis by activation of poly(ADP-ribose) polymerase (PARP), caspase-3, and phosphorylation of p53 at Ser15.	24-hydroxyursolic acid	13-35	P53	Homo sapiens	150-153
23556086-11	2011	The only group that can be clearly identified pretreatment for whom conventional fludarabine-based therapies produce significantly inferior response rates, PFS and overall survival are the patients who harbour a genetic fault; deletion or mutation or a combination of deletion and mutation of tumour protein p53 (TP53).	fludarabine	81-92	P53	Homo sapiens	313-317
23556086-12	2011	TP53 inactivation is a less common finding at first treatment but becomes much more common in fludarabine-refractory patients.	fludarabine	94-105	P53	Homo sapiens	0-4
21277290-8	2011	As for the 47 IotaIotaIota stage NSCLC treated with NACT, s-p53 Abs and CA12-5 remarkably decreased after NACT treatment (P=0.034 and P=0.007) and pre-NACT low s-p53 Abs correlated with high objective chemoresponse rate (P=0.016).	nact	52-56	P53	Homo sapiens	60-63
20045437-6	2010	Simvastatin increased expression of Bax, oligomerization of Bax and Bak, and expression of BH3-only p53-dependent genes, PUMA and NOXA.	Simvastatin	0-11	P53	Homo sapiens	100-103
20045437-7	2010	Inhibition of p53 and silencing of p53 unregulated modulator of apoptosis (PUMA) expression partly counteracted simvastatin-induced cell death, suggesting a role for p53-independent mechanisms.	Simvastatin	112-123	P53	Homo sapiens	35-38
20045437-7	2010	Inhibition of p53 and silencing of p53 unregulated modulator of apoptosis (PUMA) expression partly counteracted simvastatin-induced cell death, suggesting a role for p53-independent mechanisms.	Simvastatin	112-123	P53	Homo sapiens	35-38
20045437-10	2010	Thus, simvastatin activates novel apoptosis pathways in lung mesenchymal cells involving p53, IAP inhibitor release, and disruption of mitochondrial fission.	Simvastatin	6-17	P53	Homo sapiens	89-92
20535395-7	2007	Further western blot analysis showed that ascorbic acid treatment decreased levels of p53, phospho-p53 at ser 15, and p21, indicating that ascorbic acid relieved senescence-related G1 arrest.	Ascorbic Acid	42-55	P53	Homo sapiens	86-89
20535395-7	2007	Further western blot analysis showed that ascorbic acid treatment decreased levels of p53, phospho-p53 at ser 15, and p21, indicating that ascorbic acid relieved senescence-related G1 arrest.	Ascorbic Acid	42-55	P53	Homo sapiens	99-102
20535395-7	2007	Further western blot analysis showed that ascorbic acid treatment decreased levels of p53, phospho-p53 at ser 15, and p21, indicating that ascorbic acid relieved senescence-related G1 arrest.	Ascorbic Acid	139-152	P53	Homo sapiens	86-89
17534142-0	2007	P53 dependent and independent apoptosis induced by lidamycin in human colorectal cancer cells.	C 1027	51-60	P53	Homo sapiens	0-3
17534142-3	2007	Here we reported the involvement of p53 signaling pathway in apoptosis induction by lidamycin (LDM), a member of the enediyne antibiotic family.	C 1027	84-93	P53	Homo sapiens	36-39
17230520-9	2007	Furthermore a p53-dominant negative mutant attenuated selenite-induced ROS, leading to a proportionate protection against apoptosis.	Selenious Acid	54-62	P53	Homo sapiens	14-17
17230520-10	2007	The results support the p53-mitochondria axis in a feedback loop for sustaining superoxide production to lead to efficient caspase-mediated apoptosis by selenite.	Selenious Acid	153-161	P53	Homo sapiens	24-27
20062073-0	2010	HSP72 depletion suppresses gammaH2AX activation by genotoxic stresses via p53/p21 signaling.	gammah2ax	27-36	P53	Homo sapiens	74-77
21277290-8	2011	As for the 47 IotaIotaIota stage NSCLC treated with NACT, s-p53 Abs and CA12-5 remarkably decreased after NACT treatment (P=0.034 and P=0.007) and pre-NACT low s-p53 Abs correlated with high objective chemoresponse rate (P=0.016).	nact	52-56	P53	Homo sapiens	162-165
21277290-8	2011	As for the 47 IotaIotaIota stage NSCLC treated with NACT, s-p53 Abs and CA12-5 remarkably decreased after NACT treatment (P=0.034 and P=0.007) and pre-NACT low s-p53 Abs correlated with high objective chemoresponse rate (P=0.016).	nact	106-110	P53	Homo sapiens	60-63
19963248-2	2010	The transduction of p53 using poly-arginine is useful for targeting and suppressing the growth of bladder cancer cells.	polyarginine	30-43	P53	Homo sapiens	20-23
21277290-10	2011	S-p53 Abs level correlates with cancer patients" clinicalpathological parameters and can predict the chemoresponse of IotaIotaIota stage NSCLC patients during MCV-based NACT treatment.	nact	169-173	P53	Homo sapiens	2-5
20036271-0	2010	Arsenite induced poly(ADP-ribosyl)ation of tumor suppressor P53 in human skin keratinocytes as a possible mechanism for carcinogenesis associated with arsenic exposure.	arsenite	0-8	P53	Homo sapiens	60-63
17505702-4	2007	Formalin-fixed, paraffin-embedded archival tissue was immunostained for p53 and proliferation cell nuclear antigen.	Formaldehyde	0-8	P53	Homo sapiens	72-75
20036271-6	2010	This laboratory demonstrated earlier that in cells treated with arsenite, the P53-dependent increase in p21(WAF1/CIP1) expression, normally a block to cell cycle progression after DNA damage, is deficient.	arsenite	64-72	P53	Homo sapiens	78-81
21292642-4	2011	We found that prolonged exposure of immortalized p53-knocked down human bronchial epithelial cells (p53(low)HBECs) to low levels of arsenite (NaAsO2, 2.5 muM) caused malignant transformation that was accompanied by epithelial to mesenchymal transition (EMT) and reduction in the levels of miR-200 family members.	arsenite	132-140	P53	Homo sapiens	49-52
20036271-7	2010	Here we show that although long-term exposure of human keratinocytes (HaCaT) to a nontoxic concentration (0.1 microM) of arsenite decreases the level of global protein poly(ADP-ribosyl)ation, it increases poly(ADP-ribosyl)ation of P53 protein and PARP-1 protein abundance.	arsenite	121-129	P53	Homo sapiens	231-234
20036271-10	2010	Our results suggest that arsenite"s interference with activation of P53 via poly(ADP-ribosyl)ation may play a role in the comutagenic and cocarcinogenic effects of arsenite.	arsenite	25-33	P53	Homo sapiens	68-71
19931552-0	2010	Arsenite promotes centrosome abnormalities under a p53 compromised status induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK).	arsenite	0-8	P53	Homo sapiens	51-54
19931552-7	2010	NNK treatment could also reduce arsenite-induced G2/M cell cycle arrest and apoptosis, these cellular effects were found to be correlated with p53 dysfunction.	arsenite	32-40	P53	Homo sapiens	143-146
19931552-10	2010	Arsenite would act specifically on this p53 compromised status to induce centrosomal abnormality and colony formation.	arsenite	0-8	P53	Homo sapiens	40-43
17150195-13	2007	Collectively, we conclude that D-501036 induces cellular apoptosis through the p53-associated mitochondrial pathway.	2,5-bis(5-hydroxymethyl-2-selenienyl)-3-hydroxymethyl-N-methylpyrrole	31-39	P53	Homo sapiens	79-82
17263498-0	2007	6-shogaol (alkanone from ginger) induces apoptotic cell death of human hepatoma p53 mutant Mahlavu subline via an oxidative stress-mediated caspase-dependent mechanism.	alkanone	11-19	P53	Homo sapiens	80-83
21292642-4	2011	We found that prolonged exposure of immortalized p53-knocked down human bronchial epithelial cells (p53(low)HBECs) to low levels of arsenite (NaAsO2, 2.5 muM) caused malignant transformation that was accompanied by epithelial to mesenchymal transition (EMT) and reduction in the levels of miR-200 family members.	arsenite	132-140	P53	Homo sapiens	100-103
21292642-6	2011	Moreover, stably expressing miR-200b alone in parental nontransformed p53(low)HBECs was sufficient to completely prevent arsenite exposure from inducing EMT and malignant transformation.	arsenite	121-129	P53	Homo sapiens	70-73
20130960-0	2011	Perifosine selectively induces cell cycle block and modulates retinoblastoma and E2F1 protein levels in p53 mutated leukemic cell lines.	perifosine	0-10	P53	Homo sapiens	104-107
17234448-4	2007	9-HSA administration to U2OS, an osteosarcoma cell line p53 wt, induces a growth arrest of the cells in G2/M and apoptosis via a mitochondrial pathway.	9-hydroxystearic acid	0-5	P53	Homo sapiens	56-59
17234448-5	2007	In particular hyperacetylation of p53 induced by the HDAC1 inhibitory activity of 9-HSA has been demonstrated to increase Bax synthesis both at the transcriptional and the translational level.	9-hydroxystearic acid	82-87	P53	Homo sapiens	34-37
17234448-7	2007	Our data demonstrate that the effects of 9-HSA on U2OS correlate with posttranslational modifications of p53.	9-hydroxystearic acid	41-46	P53	Homo sapiens	105-108
17325891-8	2007	In conclusion, 17p deletion, which causes loss of p53 gene, is associated with resistance to fludarabine-induced apoptosis in vitro.	fludarabine	93-104	P53	Homo sapiens	50-53
19966562-1	2010	Pentamidine is a small molecule inhibitor of the Ca(+)-binding protein S100B and disrupts the S100B-p53 protein-protein interaction; this is thought to restore wild-type p53 tumour suppressor function in melanoma.	Pentamidine	0-11	P53	Homo sapiens	100-103
19966562-1	2010	Pentamidine is a small molecule inhibitor of the Ca(+)-binding protein S100B and disrupts the S100B-p53 protein-protein interaction; this is thought to restore wild-type p53 tumour suppressor function in melanoma.	Pentamidine	0-11	P53	Homo sapiens	170-173
20130960-2	2011	Perifosine promoted cytotoxicity with a combination of apoptosis induction in all cell lines and cell cycle block at the G(2)M checkpoint, which was selectively observed in p53(mutated) BJAB and MAVER cell lines.	perifosine	0-10	P53	Homo sapiens	173-176
19727716-15	2010	Transfection of the NIS gene into human anaplastic thyroid cancer induced the accumulation of beta-emitter radionuclides, and cotransfection with a wt-p53 gene enhanced the cytotoxic effect.	Nickel	20-23	P53	Homo sapiens	151-154
17135250-6	2007	Moreover, HCT116 colon cancer cells exhibited a p53-dependent sensitivity to PpIX in a dose-dependent manner, as was demonstrated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and fluorescence-activated cell sorter (FACS) analysis of cell cycle profiles.	thiazolyl blue	136-196	P53	Homo sapiens	48-51
20130960-3	2011	At the molecular level, perifosine induced hypophosphorylation of retinoblastoma protein and the degradation of E2F1 protein in p53(mutated) but not in p53(wild-type) cells.	perifosine	24-34	P53	Homo sapiens	128-131
20130960-4	2011	These data indicate that perifosine potentially represents an innovative therapeutic approach for p53(mutated) hematological malignancies.	perifosine	25-35	P53	Homo sapiens	98-101
17182066-0	2007	Taiwanin A induced cell cycle arrest and p53-dependent apoptosis in human hepatocellular carcinoma HepG2 cells.	taiwanin A	0-10	P53	Homo sapiens	41-44
19933157-6	2010	Binding of the probe bis-ANS (bis-8-anilinonaphthalene-1-sulfonate) indicates that there is an increase in the exposure of hydrophobic pockets for both wt and mutant p53C at low pH.	bis-8-anilinonaphthalene-1-sulfonate	30-66	P53	Homo sapiens	166-169
21030860-5	2011	p53 and phospho-Histone3 (mitotic marker) showed increased staining in higher grade phyllodes tumors.	phyllodes	84-93	P53	Homo sapiens	0-3
20048077-3	2010	We compared the effects of vanadate to PFTalpha and PFTmicro, an inhibitor of transcription-independent apoptosis by p53.	pftmicro	52-60	P53	Homo sapiens	117-120
20500145-8	2010	Finally, ursodeoxycholic acid (UDCA), an endogenous bile acid used to treat cholestatic liver diseases, was recently described as a fine modulator of the complex control of p53 by Mdm-2.	Ursodeoxycholic Acid	9-29	P53	Homo sapiens	173-176
19812371-0	2010	Topotecan triggers apoptosis in p53-deficient cells by forcing degradation of XIAP and survivin thereby activating caspase-3-mediated Bid cleavage.	Topotecan	0-9	P53	Homo sapiens	32-35
17352246-6	2007	RESULTS: Ascorbic acid was found to reduce the proliferation of cells and induce apoptosis by the modulation of p53, p21, Bcl-2 and Bax.	Ascorbic Acid	9-22	P53	Homo sapiens	112-115
17136320-6	2007	Most importantly, sulindac-derived ROS activated p38 mitogen-activated protein kinase and p53.	Sulindac	18-26	P53	Homo sapiens	90-93
17136320-7	2007	SB203580, a p38 mitogen-activated protein kinase inhibitor, and RNA inhibition of p53 inhibited the sulindac-induced apoptosis.	Sulindac	100-108	P53	Homo sapiens	82-85
19812371-2	2010	We previously showed that TPT-induced apoptosis depends on p53 with p53 wild-type (wt) cells being more resistant because of p53-controlled degradation of topoisomerase I.	Topotecan	26-29	P53	Homo sapiens	59-62
21145583-8	2011	TEGDMA (3 mm) appeared to stimulate p53 expression only slightly, but increased p21 expression was found in cell nuclei and cytoplasm.	triethylene glycol dimethacrylate	0-6	P53	Homo sapiens	36-39
19812371-2	2010	We previously showed that TPT-induced apoptosis depends on p53 with p53 wild-type (wt) cells being more resistant because of p53-controlled degradation of topoisomerase I.	Topotecan	26-29	P53	Homo sapiens	68-71
19812371-2	2010	We previously showed that TPT-induced apoptosis depends on p53 with p53 wild-type (wt) cells being more resistant because of p53-controlled degradation of topoisomerase I.	Topotecan	26-29	P53	Homo sapiens	68-71
19812371-13	2010	Overall, the data show that p53-deficient/depleted cells are hypersensitive to TPT because they down-regulate XIAP and survivin, and thus amplify the intrinsic apoptotic pathway via caspase-3-mediated Bid cleavage.	Topotecan	79-82	P53	Homo sapiens	28-31
17136320-8	2007	Furthermore, p53, Bax, and Bak accumulated in mitochondria during sulindac-induced apoptosis.	Sulindac	66-74	P53	Homo sapiens	13-16
17136320-10	2007	Our results demonstrate a novel mechanism of sulindac-induced apoptosis in human MM cells, namely, accumulation of p53, Bax, and Bak in mitochondria mediated by p38 MAPK activation downstream of ROS production.	Sulindac	45-53	P53	Homo sapiens	115-118
19812371-14	2010	Therefore, in gliomas harboring wild-type p53, TPT-based therapy might be improved by targeted down-regulation of XIAP and survivin.	Topotecan	47-50	P53	Homo sapiens	42-45
21145583-9	2011	Both camptothecin and TEGDMA increased p53 expression to some extent in the nuclear fraction in human transformed pulp-derived cells (tHPC), and similar effects were detected in RAW264.7 macrophages.	triethylene glycol dimethacrylate	22-28	P53	Homo sapiens	39-42
20974702-5	2011	This is because the effect of p53 in CoCl(2)-treated monocytes is counteracted by the antiapoptotic activity of cytoplasmic p21(Cip1/WAF1), the activation of nuclear factor kappaB, and the inflammasome danger signaling pathway leading to the production of proinflammatory cytokines.	cobaltous chloride	37-44	P53	Homo sapiens	30-33
19744477-5	2009	Pre-treating cells with the antioxidant ascorbic acid not only prohibited the induction of reactive oxygen species by emodin, but also inhibited the up-regulation of p53.	Ascorbic Acid	40-53	P53	Homo sapiens	166-169
17245120-7	2007	We also analyzed the antiproliferative effects of the bile pigments in an in vitro system where bilirubin/biliverdin caused p53 dependent cell cycle arrest by hypophosphorylation of the retinoblastoma tumor suppressor protein in growth factor stimulated VSMCs.	Bilirubin	96-105	P53	Homo sapiens	124-127
21304979-8	2011	Notably both mevalonate cascade inhibition-induced autophagy and apoptosis were p53 dependent: simvastatin increased nuclear p53 accumulation, and both cyclic pifithrin-alpha and p53 shRNAi partially inhibited NOXA, PUMA expression and caspase-3/7 cleavage (apoptosis) and DRAM expression, Atg5-12 complex formation, LC3 lipidation, and autophagosome formation (autophagy).	Simvastatin	95-106	P53	Homo sapiens	80-83
17060456-11	2007	These studies demonstrate that activation of PI3K signaling by mutations in PTEN or PIK3CA can lead to activation of p53-mediated growth suppression in human cells, indicating that p53 can function as a brake on phosphatidylinositol (3,4,5)-triphosphate-induced mitogenesis during human cancer pathogenesis.	phosphatidylinositol 3,4,5-triphosphate	212-253	P53	Homo sapiens	117-120
17060456-11	2007	These studies demonstrate that activation of PI3K signaling by mutations in PTEN or PIK3CA can lead to activation of p53-mediated growth suppression in human cells, indicating that p53 can function as a brake on phosphatidylinositol (3,4,5)-triphosphate-induced mitogenesis during human cancer pathogenesis.	phosphatidylinositol 3,4,5-triphosphate	212-253	P53	Homo sapiens	181-184
19787260-0	2009	Organophosphorous pesticides and estrogen induce transformation of breast cells affecting p53 and c-Ha-ras genes.	organophosphorous	0-17	P53	Homo sapiens	90-93
19787260-13	2009	It can be concluded that the organophosphorous pesticides parathion and malathion induced malignant transformation of breast cells through genomic instability altering p53 and c-Ha-ras, considered pivotal to cancer process.	organophosphorous	29-46	P53	Homo sapiens	168-171
21304979-8	2011	Notably both mevalonate cascade inhibition-induced autophagy and apoptosis were p53 dependent: simvastatin increased nuclear p53 accumulation, and both cyclic pifithrin-alpha and p53 shRNAi partially inhibited NOXA, PUMA expression and caspase-3/7 cleavage (apoptosis) and DRAM expression, Atg5-12 complex formation, LC3 lipidation, and autophagosome formation (autophagy).	Simvastatin	95-106	P53	Homo sapiens	125-128
19787260-13	2009	It can be concluded that the organophosphorous pesticides parathion and malathion induced malignant transformation of breast cells through genomic instability altering p53 and c-Ha-ras, considered pivotal to cancer process.	Parathion	58-67	P53	Homo sapiens	168-171
19787260-13	2009	It can be concluded that the organophosphorous pesticides parathion and malathion induced malignant transformation of breast cells through genomic instability altering p53 and c-Ha-ras, considered pivotal to cancer process.	Malathion	72-81	P53	Homo sapiens	168-171
21304979-8	2011	Notably both mevalonate cascade inhibition-induced autophagy and apoptosis were p53 dependent: simvastatin increased nuclear p53 accumulation, and both cyclic pifithrin-alpha and p53 shRNAi partially inhibited NOXA, PUMA expression and caspase-3/7 cleavage (apoptosis) and DRAM expression, Atg5-12 complex formation, LC3 lipidation, and autophagosome formation (autophagy).	Simvastatin	95-106	P53	Homo sapiens	125-128
19822456-3	2009	In addition, recent work has provided new insights into mechanisms underlying the antiapoptotic functions of the endogenous bile acid ursodeoxycholic acid (UDCA), suggesting that the finely tuned, complex control of p53 by Mdm2 is a key step in the UDCA modulation of deregulated, p53-triggered apoptosis.	Ursodeoxycholic Acid	134-154	P53	Homo sapiens	216-219
17119452-11	2006	The increased expressions of p53 and p21, and the decreased expressions of cyclin A, cyclin E, CDK2 and CDK4, indicated the cell cycle arrest at G1/S phase after the cells had been treated with sodium ascorbate.	Ascorbic Acid	194-210	P53	Homo sapiens	29-32
17119452-12	2006	Induction of apoptosis involved an increase in the levels of p53, p21 and cellular Ca, and a decrease in mitochondrial membrane potential and activation of caspase 3 before culminating in apoptosis in sodium ascorbate-treated A375.S2 cells.	Ascorbic Acid	201-217	P53	Homo sapiens	61-64
19822456-3	2009	In addition, recent work has provided new insights into mechanisms underlying the antiapoptotic functions of the endogenous bile acid ursodeoxycholic acid (UDCA), suggesting that the finely tuned, complex control of p53 by Mdm2 is a key step in the UDCA modulation of deregulated, p53-triggered apoptosis.	Ursodeoxycholic Acid	134-154	P53	Homo sapiens	281-284
21261644-7	2011	NS-398, a specific pharmacologic inhibitor of COX-2, prevents resveratrol-induced complexing of nuclear ERK1/2 with COX-2 and with pSer-15-p53 and subsequent apoptosis; cyclooxygenase enzyme activity is not involved.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	0-6	P53	Homo sapiens	139-142
19643983-0	2009	Detailed analysis of p53 pathway defects in fludarabine-refractory chronic lymphocytic leukemia (CLL): dissecting the contribution of 17p deletion, TP53 mutation, p53-p21 dysfunction, and miR34a in a prospective clinical trial.	fludarabine	44-55	P53	Homo sapiens	21-24
19723057-0	2009	Effects of 15-deoxy-delta 12, 14-prostaglandin J2 on the expression of p53 in MCF-7 cells.	14-prostaglandin j2	30-49	P53	Homo sapiens	71-74
16741250-5	2006	Transduction of CLL cells with an adenovirus encoding p73 also induced Bid and CD95 and enhanced the sensitivity to F-ara-A of p53-deficient CLL cells.	fludarabine	116-123	P53	Homo sapiens	127-130
16950207-6	2006	Combined sulindac/ATO treatment also activated p53 expression, and inhibition of p53 expression by small interfering RNA (siRNA) prevented sulindac/ATO-induced down-regulation of survivin, suggesting that survivin expression is negatively regulated by p53.	Sulindac	139-147	P53	Homo sapiens	81-84
16950207-6	2006	Combined sulindac/ATO treatment also activated p53 expression, and inhibition of p53 expression by small interfering RNA (siRNA) prevented sulindac/ATO-induced down-regulation of survivin, suggesting that survivin expression is negatively regulated by p53.	Sulindac	139-147	P53	Homo sapiens	81-84
16882877-4	2006	The induction of WI38 cell senescence by Etop was associated with p53 activation and could be attenuated by down-regulation of p53 using alpha-pifithrin (alpha-PFT) or p53 small interference RNA (siRNA).	alpha-pifithrin	137-152	P53	Homo sapiens	127-130
16882877-4	2006	The induction of WI38 cell senescence by Etop was associated with p53 activation and could be attenuated by down-regulation of p53 using alpha-pifithrin (alpha-PFT) or p53 small interference RNA (siRNA).	alpha-pifithrin	137-152	P53	Homo sapiens	127-130
21220492-4	2011	In this study, we report that pancratistatin decreased mitochondrial membrane potential and induced apoptotic nuclear morphology in p53-mutant (HT-29) and wild-type p53 (HCT116) colorectal carcinoma cell lines, but not in noncancerous colon fibroblast (CCD-18Co) cells.	pancratistatin	30-44	P53	Homo sapiens	132-135
16979516-13	2006	Lipofuscin probably indicates slow cellular turnover as suggested by the low proliferation rate and p53 expression.	Lipofuscin	0-10	P53	Homo sapiens	100-103
19470404-1	2009	Arsenite effects on the benzo[a]pyrene diol epoxide (BPDE)-DNA adduct-induced mutation were evaluated in three human lung cell-lines--A549 (wild-type p53), WI38-VA13 (p53 inhibited by SV40 large-T antigen), and H1299 (p53-null)--by using the pSP189 shuttle vector, which carries a mutation target supF gene.	arsenite	0-8	P53	Homo sapiens	167-170
19470404-1	2009	Arsenite effects on the benzo[a]pyrene diol epoxide (BPDE)-DNA adduct-induced mutation were evaluated in three human lung cell-lines--A549 (wild-type p53), WI38-VA13 (p53 inhibited by SV40 large-T antigen), and H1299 (p53-null)--by using the pSP189 shuttle vector, which carries a mutation target supF gene.	arsenite	0-8	P53	Homo sapiens	167-170
19470404-5	2009	These results suggest that arsenite potentiates the BPDE-induced supF mutation via a p53-independent mechanism.	arsenite	27-35	P53	Homo sapiens	85-88
21220492-4	2011	In this study, we report that pancratistatin decreased mitochondrial membrane potential and induced apoptotic nuclear morphology in p53-mutant (HT-29) and wild-type p53 (HCT116) colorectal carcinoma cell lines, but not in noncancerous colon fibroblast (CCD-18Co) cells.	pancratistatin	30-44	P53	Homo sapiens	165-168
21110861-8	2010	The Meq variants L-Meq and S-Meq, but not VS-Meq and  Meq, which were expressed in MD tumor cells and MDV-infected cells, exerted an inhibitory effect on p53 transcriptional activity.	l-meq	17-22	P53	Homo sapiens	154-157
19435284-2	2009	The p53 antibody molecules immobilized on an (R)-lipo-diaza-18-crown-6 self-assembled monolayer (SAM)-modified gold disk electrode were shown to effectively capture the p53 protein by Western blot, quartz crystal microbalance, and electrochemical impedance experiments.	(r)-lipo-diaza-18-crown-6	45-70	P53	Homo sapiens	4-7
16598789-7	2006	As observed with 10 nM OA, both phospho-ser15-p53 levels and p53 activity were increased by 10 microM fostriecin or SV40 small t-antigen.	fostriecin	102-112	P53	Homo sapiens	46-49
16598789-7	2006	As observed with 10 nM OA, both phospho-ser15-p53 levels and p53 activity were increased by 10 microM fostriecin or SV40 small t-antigen.	fostriecin	102-112	P53	Homo sapiens	61-64
19435284-2	2009	The p53 antibody molecules immobilized on an (R)-lipo-diaza-18-crown-6 self-assembled monolayer (SAM)-modified gold disk electrode were shown to effectively capture the p53 protein by Western blot, quartz crystal microbalance, and electrochemical impedance experiments.	(r)-lipo-diaza-18-crown-6	45-70	P53	Homo sapiens	169-172
20380827-4	2010	Specifically, we focus on the role of asbestos in augmenting AEC apoptosis by the mitochondria- and p53-regulated death pathways that result from the production of iron-derived reactive oxygen species (ROS) and DNA damage.	Asbestos	38-46	P53	Homo sapiens	100-103
19587434-12	2009	CONCLUSION: As(2)O(3) and ADM alone or combined can inhibit the proliferation, induce cell apoptosis, and downregulate the expression of mutant p53 in vitro.	(2)o(3)	14-21	P53	Homo sapiens	144-147
16945145-5	2006	A variety of data has revealed a critical role for p53-binding protein 1 (53BP1) in the cellular response to DSBs including various aspects of p53 function.	dsbs	109-113	P53	Homo sapiens	51-54
20708793-0	2010	The effect of triethylene glycol dimethacrylate on p53-dependent G2 arrest in human gingival fibroblasts.	triethylene glycol dimethacrylate	14-47	P53	Homo sapiens	51-54
16814620-13	2006	Moreover, cells from this panel with wild-type p53 showed a significantly lower background level of gammaH2AX than cells with mutant p53.	gammah2ax	100-109	P53	Homo sapiens	47-50
16814620-15	2006	Again, higher gammaH2AX expression was found in SKOV3 cell lines expressing mutant p53 compared to wild-type p53.	gammah2ax	14-23	P53	Homo sapiens	83-86
19100681-8	2009	Increased PDF mRNA stability in response to hypoxia and cobalt chloride, but not doxorubicin, indicates that p53-dependent induction of PDF expression occurs via diverse mechanisms.	cobaltous chloride	56-71	P53	Homo sapiens	109-112
19417156-7	2009	Saq-NO blocked the proliferation of C6 and B16 cells, up-regulated p53 expression, and promoted the differentiation of these two cell types into oligodendrocytes or Schwann-like cells, respectively.	saq-no	0-6	P53	Homo sapiens	67-70
16814620-15	2006	Again, higher gammaH2AX expression was found in SKOV3 cell lines expressing mutant p53 compared to wild-type p53.	gammah2ax	14-23	P53	Homo sapiens	109-112
16574813-4	2006	Results from our current study show that GM3 treatment dramatically increases cyclin-dependent kinase (CDK) inhibitor (CKI) p21(WAF1) expression through the accumulation of p53 protein by the PTEN-mediated inhibition of the PI-3K/AKT/MDM2 survival signaling in HCT116 colon cancer cells.	gm3	41-44	P53	Homo sapiens	173-176
16574813-5	2006	Moreover, the data herein clearly show that ganglioside GM3 induces p53-dependent transcriptional activity of p21(WAF1), as evidenced by the p21(WAF1) promoter-driven luciferase reporter plasmid (full-length p21(WAF1) promoter and a construct lacking the p53-binding sites).	gm3	56-59	P53	Homo sapiens	68-71
21035481-3	2010	We found that salidroside considerably reversed senescence-like phenotypes in the oxidant challenged model, including alterations of morphology, cell cycle, SA-beta-gal staining, DNA damage, as well as related molecules expression such as p53, p21 and p16.	rhodioloside	14-25	P53	Homo sapiens	239-242
16614167-0	2006	p53 suppression of arsenite-induced mitotic catastrophe is mediated by p21CIP1/WAF1.	arsenite	19-27	P53	Homo sapiens	0-3
16614167-3	2006	Arsenite sensitivity correlates with deficient p53 pathways in multiple cell lines.	arsenite	0-8	P53	Homo sapiens	47-50
16614167-4	2006	The role of p53 in preventing arsenite-induced mitotic arrest-associated apoptosis (MAAA), a form of mitotic catastrophe, was examined in TR9-7 cells, a model cell line with p53 exogenously regulated in a tetracycline-off expression system.	arsenite	30-38	P53	Homo sapiens	12-15
19331830-4	2009	Two human p14ARF residues (Ala(14) and Thr(31)) were found to destabilize the protein while two others (Val(24) and Ala(41)) promoted more efficient p53 stabilization and activation.	Valine	104-107	P53	Homo sapiens	149-152
19331830-7	2009	Val(24) was required for p53-independent growth suppression whereas multiple residues (Val(24), Thr(31), Ala(41) and His(60)) enabled p14ARF to block or reverse the inherent chromosomal instability of p53-null MEFs.	Valine	0-3	P53	Homo sapiens	25-28
20619728-7	2010	The mRNA and protein level of p53 was significantly higher in high fluoride+high selenium group than that in other two groups.	Fluorides	67-75	P53	Homo sapiens	30-33
19243593-4	2009	However, both p53-positive and -negative cells arrest in mitosis if treated with low doses of siRNA against NEDD1 combined with low doses of the inhibitor BI2536 against the mitotic kinase Plk1.	BI 2536	155-161	P53	Homo sapiens	14-17
19155291-1	2009	The major determinants of 5-flurouracil (5-FU) response would seem, based on accumulated literature, to be thymidylate synthase (TYMS, TS) expression levels, TS gene modifications, and TP53 status.	5-flurouracil	26-39	P53	Homo sapiens	185-189
19155295-6	2009	Down-regulation of CtBPs mediated by some tumor suppressors results in p53-independent apoptosis and reduced tumor cell migration and invasion.	ctbps	19-24	P53	Homo sapiens	71-74
16443387-5	2006	Trypan blue and acridine orange/ethidium bromide staining were carried out, as well as quantitative analysis of the apoptotic signal of P53 and BAX induction caused by the cis-Pt(II) complex of 3-aminoflavone in comparison with cis-DDP.	3-aminoflavone	194-208	P53	Homo sapiens	136-139
16585172-11	2006	As a measure of DNA glycosylase activity, p53+/+ mitochondrial extracts more efficiently incised uracil or 8-oxo-G oligonucleotides, although recombinant p53 could not stimulate oligonucleotide incision.	8-oxo-g oligonucleotides	107-131	P53	Homo sapiens	42-45
19155295-8	2009	The results discussed here suggest that CtBPs may constitute a novel p53-independent anticancer target.	ctbps	40-45	P53	Homo sapiens	69-72
20662736-7	2010	Anthracycline (topoisomerase II inhibitors such as mitoxantrone and ellipticine) and camptothecin (topoisomerase I inhibitor) derivatives including topotecan induce DNA double strand breaks, which activate the p53 pathway through the ataxia telangiectasia mutated-checkpoint kinase 2 (ATM-CHK2) DNA damage response pathway.	Topotecan	148-157	P53	Homo sapiens	210-213
16533058-2	2006	However, we previously showed that cells lacking ATM robustly activate p53 in response to DNA strand breaks induced by the radiomimetic enediyne C-1027.	C 1027	145-151	P53	Homo sapiens	71-74
25961194-3	2010	The cells grown in charcoal-treated serum were treated with 1 nM E2 or different concentrations of LY117018 for 24 h. E2 or LY117018 treatments caused a 2- to 3-fold increase in the level of p53 and hyperphosphorylation of pRb.	LY 117018	99-107	P53	Homo sapiens	191-194
16582987-2	2006	We studied sequence-specific interaction of the vinyl-chloride metabolite CAA with human p53 gene exons 5-8, using DNA Polymerase Fingerprint Analysis (DPFA), and identified sites of the highest sensitivity.	Chlorides	54-62	P53	Homo sapiens	89-92
19042973-3	2009	The remarkable similarity in p53 mutations found in human gastrointestinal tumors and in shuttle vector studies, where the human p53 gene-containing vector was treated with diazoacetate and propagated in yeast cells, suggests that diazoacetate might be an important etiological agent for human gastrointestinal tumors.	diazoacetate	173-185	P53	Homo sapiens	129-132
19042973-3	2009	The remarkable similarity in p53 mutations found in human gastrointestinal tumors and in shuttle vector studies, where the human p53 gene-containing vector was treated with diazoacetate and propagated in yeast cells, suggests that diazoacetate might be an important etiological agent for human gastrointestinal tumors.	diazoacetate	231-243	P53	Homo sapiens	29-32
19042973-3	2009	The remarkable similarity in p53 mutations found in human gastrointestinal tumors and in shuttle vector studies, where the human p53 gene-containing vector was treated with diazoacetate and propagated in yeast cells, suggests that diazoacetate might be an important etiological agent for human gastrointestinal tumors.	diazoacetate	231-243	P53	Homo sapiens	129-132
17310826-6	2006	In conclusion, these data show that specific HIV PIs such as lopinavir and possibly indinavir, can induce selective toxicity of HPV-transformed cervical carcinoma cells expressing wild-type p53 and may form the basis of a topically applied alternative to surgery for the treatment of HPV-related premalignant lesions of the cervix.	Monothiopyrophosphoric acid	49-52	P53	Homo sapiens	190-193
17310826-6	2006	In conclusion, these data show that specific HIV PIs such as lopinavir and possibly indinavir, can induce selective toxicity of HPV-transformed cervical carcinoma cells expressing wild-type p53 and may form the basis of a topically applied alternative to surgery for the treatment of HPV-related premalignant lesions of the cervix.	Indinavir	84-93	P53	Homo sapiens	190-193
25961194-3	2010	The cells grown in charcoal-treated serum were treated with 1 nM E2 or different concentrations of LY117018 for 24 h. E2 or LY117018 treatments caused a 2- to 3-fold increase in the level of p53 and hyperphosphorylation of pRb.	LY 117018	124-132	P53	Homo sapiens	191-194
25961194-6	2010	Thus, LY117018 treatment induces changes in the level/activity of p53 and pRb and ultrastructure of T47D cells.	LY 117018	6-14	P53	Homo sapiens	66-69
19950227-6	2010	Risk of TP53 mutation was significantly increased in association with duration (&gt; or =24 years, OR 5.1, 95% CI, 1.5-17.1), average level (&gt;2 mg/m(3); OR 3.6, 95% CI, 1.2-10.8) and cumulative level (&gt; or =30 mg/m(3) x years; OR 3.5, 95% CI, 1.2-10.7) of wood-dust exposure; adjustment for formaldehyde affected the ORs only slightly.	Formaldehyde	297-309	P53	Homo sapiens	8-12
16297852-6	2006	However, mutant p53(143ala) increased the sensitivity of MRC-5 to C(2)-ceramide-induced apoptosis by markedly downregulating Bcl-2, pointing to a role for p53.	A(2)C	66-70	P53	Homo sapiens	16-19
19028473-0	2009	Kaempferol induces apoptosis in human HCT116 colon cancer cells via the Ataxia-Telangiectasia Mutated-p53 pathway with the involvement of p53 Upregulated Modulator of Apoptosis.	kaempferol	0-10	P53	Homo sapiens	102-105
19028473-0	2009	Kaempferol induces apoptosis in human HCT116 colon cancer cells via the Ataxia-Telangiectasia Mutated-p53 pathway with the involvement of p53 Upregulated Modulator of Apoptosis.	kaempferol	0-10	P53	Homo sapiens	138-141
19028473-3	2009	In the human HCT116 colon cancer cell line, kaempferol induced p53-dependent growth inhibition and apoptosis.	kaempferol	44-54	P53	Homo sapiens	63-66
16889904-0	2006	Correlation of p53 and MIB-1 expression with both the systemic recurrence and survival in cases of phyllodes tumors of the breast.	phyllodes	99-108	P53	Homo sapiens	15-18
19022222-4	2009	Here we show that Ets-1 also binds cooperatively to the EBS palindrome of the human p53 promoter, despite the presence of a degenerate EBS to which Ets-1 cannot otherwise bind.	ethylbenzene	56-59	P53	Homo sapiens	84-87
20566882-0	2010	Pyrimidine biosynthesis links mitochondrial respiration to the p53 pathway.	pyrimidine	0-10	P53	Homo sapiens	63-66
16889904-9	2006	Positive staining for p53 was seen in 10 phyllodes tumors (24%), and the median MIB-1 index was 10%.	phyllodes	41-50	P53	Homo sapiens	22-25
20566882-8	2010	The results establish the deficiency in pyrimidine biosynthesis as the cause of p53 response in the cells with impaired mitochondrial respiration.	pyrimidine	40-50	P53	Homo sapiens	80-83
16157218-1	2005	Recently, we have reported that a synthetic derivative of ursodeoxycholic acid (UDCA), HS-1183, and those of chenodeoxycholic acid (CDCA), HS-1199 and HS-1200, induced apoptosis in human breast carcinoma cells through a p53-independent pathway.	Ursodeoxycholic Acid	58-78	P53	Homo sapiens	220-223
16157218-1	2005	Recently, we have reported that a synthetic derivative of ursodeoxycholic acid (UDCA), HS-1183, and those of chenodeoxycholic acid (CDCA), HS-1199 and HS-1200, induced apoptosis in human breast carcinoma cells through a p53-independent pathway.	Ursodeoxycholic Acid	80-84	P53	Homo sapiens	220-223
19778838-2	2009	Dysfunction of p53 leads to resistance to fludarabine-based therapies.	fludarabine	42-53	P53	Homo sapiens	15-18
20657652-4	2010	METHODOLOGY/PRINCIPAL FINDINGS: In this study, we show that DCB-3503 suppresses the expression of pro-oncogenic or pro-survival proteins with short half-lives, including cyclin D1, survivin, beta-catenin, p53, and p21, without decreasing their mRNA levels.	DCB 3503	60-68	P53	Homo sapiens	205-208
19062342-4	2008	In contrast, chlorambucil and fludarabine resistance correlated with basal p53 protein levels.	fludarabine	30-41	P53	Homo sapiens	75-78
16157218-1	2005	Recently, we have reported that a synthetic derivative of ursodeoxycholic acid (UDCA), HS-1183, and those of chenodeoxycholic acid (CDCA), HS-1199 and HS-1200, induced apoptosis in human breast carcinoma cells through a p53-independent pathway.	Chenodeoxycholic Acid	132-136	P53	Homo sapiens	220-223
16225864-3	2005	The data showed that safrole oxide induced apoptosis by increasing the expressions of Fas, integrin beta4 and P53, and depressing the activity of Ca(2+)-independent phosphatidylcholine-specific phospholipase C and intracellular reactive oxygen species levels in VECs.	safrole oxide	21-34	P53	Homo sapiens	110-113
20375080-0	2010	The repressive effect of NF-kappaB on p53 by mot-2 is involved in human keratinocyte transformation induced by low levels of arsenite.	arsenite	125-133	P53	Homo sapiens	38-41
20375080-5	2010	In arsenite-exposed cells, the levels of phospho-p53, p21, and mdm2 increase at early times after exposure.	arsenite	3-11	P53	Homo sapiens	49-52
16107721-9	2005	In addition, depolarization of the mitochondrial membrane by mitochondrial inhibitors such as rotenone or antimycin A led colorectal cancer cells into p53-dependent senescence.	Antimycin A	106-117	P53	Homo sapiens	151-154
18945750-8	2008	CONCLUSIONS: We demonstrate a correlation between the recently described p53-inducible apoptosis gene TIGAR and both sensitivity to fludarabine and hENT2 expression in chronic lymphocytic leukemia cells.	fludarabine	132-143	P53	Homo sapiens	73-76
20375080-8	2010	Blockage of NF-kappaB prevents the increases of arsenite-induced mot-2 levels, and knockdown of mot-2 facilitates the nuclear translocation of p53, indicating that, in HaCaT cells exposed to arsenite, NF-kappaB inhibits p53 function by mot-2.	arsenite	191-199	P53	Homo sapiens	143-146
16177561-4	2005	We also found that several randomly chosen acridine derivatives, including 9-aminoacridine, amsacrine, quinacrine and acridine orange, induced p53 transcriptional activity.	Quinacrine	103-113	P53	Homo sapiens	143-146
16177561-8	2005	In addition, in vivo delivery of quinacrine and amsacrine induced p53 transcriptional activity in tumor xenografts.	Quinacrine	33-43	P53	Homo sapiens	66-69
20375080-8	2010	Blockage of NF-kappaB prevents the increases of arsenite-induced mot-2 levels, and knockdown of mot-2 facilitates the nuclear translocation of p53, indicating that, in HaCaT cells exposed to arsenite, NF-kappaB inhibits p53 function by mot-2.	arsenite	191-199	P53	Homo sapiens	220-223
20171194-2	2010	iPLA2 inhibition using siRNA, or the selective inhibitor bromoenol lactone (BEL) and it"s enantiomers, decreased growth in LNCaP (p53 positive) and PC-3 (p53 negative) human prostate cancer cells.	6-(bromomethylene)tetrahydro-3-(1-naphthaleneyl)-2H-pyran-2-one	57-74	P53	Homo sapiens	130-133
16001656-6	2005	The immunohistochemical method determined protein p53 in formalin-fixed, paraffin-embedded liver tissue sections.	Formaldehyde	57-65	P53	Homo sapiens	50-53
19015526-1	2008	Ribonucleotide reductase small subunit p53R2 was identified as a p53 target gene that provides dNTP for DNA damage repair.	Parathion	95-99	P53	Homo sapiens	39-42
18949386-10	2008	Therefore, it is suggested that vitamin C inhibits p53-induced senescence by preventing ROS generation, which in turn leads to the activation of p38 MAPKinase.	Ascorbic Acid	32-41	P53	Homo sapiens	51-54
20171194-2	2010	iPLA2 inhibition using siRNA, or the selective inhibitor bromoenol lactone (BEL) and it"s enantiomers, decreased growth in LNCaP (p53 positive) and PC-3 (p53 negative) human prostate cancer cells.	6-(bromomethylene)tetrahydro-3-(1-naphthaleneyl)-2H-pyran-2-one	57-74	P53	Homo sapiens	154-157
19031258-10	2008	Collectively, the data demonstrated that baicalin-induced apoptotic cell death in the breast cancer cells involves the up-regulation of proapoptotic p53 and bax, implying potential crucial roles of bax and p53 in the baicalin-induced apoptosis.	baicalin	41-49	P53	Homo sapiens	149-152
19031258-10	2008	Collectively, the data demonstrated that baicalin-induced apoptotic cell death in the breast cancer cells involves the up-regulation of proapoptotic p53 and bax, implying potential crucial roles of bax and p53 in the baicalin-induced apoptosis.	baicalin	41-49	P53	Homo sapiens	206-209
15622519-2	2005	About 5% and 3% of the PTTs and 4.5% and 6.8% of BBTs showed alterations in HER2 and p53 expression, respectively.	ptts	23-27	P53	Homo sapiens	85-88
20550649-4	2010	RESULTS: LA-12 disrupts cellular proliferation regardless of the p53 status in the cells, however the potency of the drug is greatly enhanced by the presence of a functional p53, indicating several mechanisms of action.	UNII-37WM0V5E17	9-14	P53	Homo sapiens	174-177
16158967-0	2005	Xanthorrhizol induces apoptosis via the up-regulation of bax and p53 in HeLa cells.	xanthorrhizol	0-13	P53	Homo sapiens	65-68
16158967-6	2005	Western blot analysis, which was further confirmed by the immunostaining results, implied an up-regulation of tumor suppressor protein p53 and the pro-apoptotic protein Bax, following the treatment with xanthorrhizol.	xanthorrhizol	203-216	P53	Homo sapiens	135-138
16158967-8	2005	Hence, xanthorrhizol is a promising antiproliferative and anticancer agent which induces p53 and Bax-dependent apoptosis in HeLa cervical cancer cells.	xanthorrhizol	7-20	P53	Homo sapiens	89-92
18193228-0	2008	7-Chloro-6-piperidin-1-yl-quinoline-5,8-dione (PT-262), a novel synthetic compound induces lung carcinoma cell death associated with inhibiting ERK and CDC2 phosphorylation via a p53-independent pathway.	7-chloro-6-piperidin-1-ylquinoline-5,8-dione	0-45	P53	Homo sapiens	179-182
18802408-6	2008	In the nuclei of cells treated with TPT or MXT, the expression of p53-Ser15(P) appeared as closely packed foci of intense IF.	Topotecan	36-39	P53	Homo sapiens	66-69
18802408-7	2008	Following TPT treatment, the induction of p53-Ser15(P) was most pronounced in S-phase cells while no significant cell cycle phase differences were seen in cells treated with MXT.	Topotecan	10-13	P53	Homo sapiens	42-45
18802408-8	2008	The maximal increase in p53-Ser15(P) expression, rising up to 2.5-fold above the level of its constitutive expression, was observed in cells treated with TPT or MXT for 4-6 h. This maximum expression of p53-Ser15(P) coincided in time with the peak of Chk2 activation but not with ATM activation and H2AX phosphorylation, both of which crested 1-2 h after the treatment with TPT or MXT.	Topotecan	154-157	P53	Homo sapiens	24-27
18802408-8	2008	The maximal increase in p53-Ser15(P) expression, rising up to 2.5-fold above the level of its constitutive expression, was observed in cells treated with TPT or MXT for 4-6 h. This maximum expression of p53-Ser15(P) coincided in time with the peak of Chk2 activation but not with ATM activation and H2AX phosphorylation, both of which crested 1-2 h after the treatment with TPT or MXT.	Topotecan	154-157	P53	Homo sapiens	203-206
18802408-8	2008	The maximal increase in p53-Ser15(P) expression, rising up to 2.5-fold above the level of its constitutive expression, was observed in cells treated with TPT or MXT for 4-6 h. This maximum expression of p53-Ser15(P) coincided in time with the peak of Chk2 activation but not with ATM activation and H2AX phosphorylation, both of which crested 1-2 h after the treatment with TPT or MXT.	Topotecan	374-377	P53	Homo sapiens	24-27
18802408-8	2008	The maximal increase in p53-Ser15(P) expression, rising up to 2.5-fold above the level of its constitutive expression, was observed in cells treated with TPT or MXT for 4-6 h. This maximum expression of p53-Ser15(P) coincided in time with the peak of Chk2 activation but not with ATM activation and H2AX phosphorylation, both of which crested 1-2 h after the treatment with TPT or MXT.	Topotecan	374-377	P53	Homo sapiens	203-206
20550649-7	2010	An inhibitory effect of LA-12 on Hsp90 chaperoning function was shown by decrease of Hsp90-assisted wild-type p53 binding to p21WAF1 promoter sequence in vitro and by accelerated ubiqutination and degradation of primarily unfolded mutant p53 proteins in cells exposed to LA-12.	UNII-37WM0V5E17	24-29	P53	Homo sapiens	110-113
20550649-7	2010	An inhibitory effect of LA-12 on Hsp90 chaperoning function was shown by decrease of Hsp90-assisted wild-type p53 binding to p21WAF1 promoter sequence in vitro and by accelerated ubiqutination and degradation of primarily unfolded mutant p53 proteins in cells exposed to LA-12.	UNII-37WM0V5E17	24-29	P53	Homo sapiens	238-241
20456495-9	2010	Both curcuminoids induced G2/M block and inhibited keratinocyte growth, and THC increased cellular levels of p21, a known p53 transcriptional target.	tetrahydrocurcumin	76-79	P53	Homo sapiens	122-125
20515774-4	2010	In vitro, two cell lines exhibiting a similar sensitivity towards Topotecan-induced cell death revealed a similar induction of p53 target genes but strongly differed in their extent of apoptosis.	Topotecan	66-75	P53	Homo sapiens	127-130
18504430-0	2008	Geldanamycin promotes premature mitotic entry and micronucleation in irradiated p53/p21 deficient colon carcinoma cells.	geldanamycin	0-12	P53	Homo sapiens	80-83
18504430-3	2008	We show that GA treatment abrogates IR-induced G(2)-phase arrest in cells null or mutant for p53.	geldanamycin	13-15	P53	Homo sapiens	93-96
18504430-5	2008	Cells expressing wild-type p53 were resistant to GA-induced G(2) checkpoint abrogation.	geldanamycin	49-51	P53	Homo sapiens	27-30
18504430-8	2008	Clonogenic survival studies demonstrated higher sensitivity to GA alone or combination IR plus GA treatment in p53 and p21-null cells.	geldanamycin	63-65	P53	Homo sapiens	111-114
20515947-1	2010	Previously, we reported that the nucleoside analogue/transcriptional inhibitor ARC (4-amino-6-hydrazino-7-beta-D-ribofuranosyl-7H-pyrrolo(2,3-d)-pyrimidine-5-carboxamide) was able to induce p53-independent apoptosis in multiple cancer cell lines of different origins.	4-amino-6-hydrazino-7-beta-D-ribofuranosyl-7H-pyrrolo(2,3-d)-pyrimidine-5-carboxamide	84-169	P53	Homo sapiens	190-193
18712872-1	2008	Chlorofusin is a recently isolated, naturally occurring inhibitor of p53-MDM2 complex formation whose structure is composed of a densely functionalized azaphilone-derived chromophore linked through the terminal amine of ornithine to a nine residue cyclic peptide.	Peptides, Cyclic	248-262	P53	Homo sapiens	69-72
20138958-0	2010	Iodine induces apoptosis via regulating MAPKs-related p53, p21, and Bcl-xL in thyroid cancer cells.	Iodine	0-6	P53	Homo sapiens	54-57
18804536-0	2008	Simvastatin inhibits cell cycle progression in glucose-stimulated proliferation of aortic vascular smooth muscle cells by up-regulating cyclin dependent kinase inhibitors and p53.	Simvastatin	0-11	P53	Homo sapiens	175-178
18804536-8	2008	We also found that simvastatin inhibited phosphorylation of Rb, promoted expression of p53, p16, p21, p27 and decreased CDK2/4 activity.	Simvastatin	19-30	P53	Homo sapiens	87-90
18804536-9	2008	In conclusion, simvastatin inhibits VSMC proliferation in high glucose status, mimicking diabetes, inducing a G0/G1 phase cell cycle growth arrest by acting on multiple steps upstream of pRb, including inhibition of CDK2/4 expression and up-regulation of p53, p21, p16, and p27.	Simvastatin	15-26	P53	Homo sapiens	255-258
20138958-6	2010	Iodine treatment decreased the level of mutant p53 including the R273H mutant that possesses anti-apoptotic features, but increased the p21 level.	Iodine	0-6	P53	Homo sapiens	47-50
20138958-8	2010	Moreover, iodine transiently activated the subfamily members of mitogen activated protein kinases (MAPKs) (ERK1/2, p38 and JNK1/2) which contribute to modulate p53, p21 and Bcl-xL expression.	Iodine	10-16	P53	Homo sapiens	160-163
18401588-7	2008	Compared with UVB irradiated cells, UVB-induced p53 accumulation was less pronounced in Baicalin-treated cells.	baicalin	88-96	P53	Homo sapiens	48-51
20138958-10	2010	Collectively, iodine-induced apoptotic pathway is involved in the activation of MAPKs-related p21, Bcl-xL and mutant p53 regulation.	Iodine	14-20	P53	Homo sapiens	117-120
20160501-7	2010	This inhibitory effect was not dependent on the status of p53 and p21 although GDP366 potently increased p53 and p21 levels.	GDP 366	79-85	P53	Homo sapiens	105-108
18452313-11	2008	Mapping the sequence specificity of Cr(III)-GA 2- and Cr(III)-EGA 2-DNA formation in the human p53 gene sequence by UvrABC nuclease cutting, we found that the sequence specificity for both adducts is the same but is much more selective than Cr(III)-guanine-DNA adducts.	tris(1,10-phenanthroline)chromium(III) chloride	54-61	P53	Homo sapiens	95-98
18266926-4	2008	We recently reported that PQ induces neuronal apoptosis through Bak activation, in contrast to MPP(+), the toxic metabolite of MPTP, which relies on Bax and p53.	Paraquat	26-28	P53	Homo sapiens	157-160
18727380-4	2008	The treatment of selective inhibitors JNK SP600125 and p38 ML3403 in vitro prevents peroxide-induced appearance of P53 and NF-kB in blood mononuclear cells, associated with increasing of their apoptotic activity.	Peroxides	84-92	P53	Homo sapiens	115-118
19728331-0	2010	Ursodeoxycholic acid switches oxaliplatin-induced necrosis to apoptosis by inhibiting reactive oxygen species production and activating p53-caspase 8 pathway in HepG2 hepatocellular carcinoma.	Ursodeoxycholic Acid	0-20	P53	Homo sapiens	136-139
18071310-0	2008	Hsp90-inhibitor geldanamycin abrogates G2 arrest in p53-negative leukemia cell lines through the depletion of Chk1.	geldanamycin	16-28	P53	Homo sapiens	52-55
20450732-14	2010	CONCLUSION: The suppressing mechanism of vitexicarpin for malignant tumors is through c-Myc in p53 mutated Hs578T cells.	casticin	41-53	P53	Homo sapiens	95-98
18092340-2	2008	Exposure to chlorambucil, fludarabine, and Nutlin-3 induced p53 accumulation and variably affected cell cycle progression in SKW6.4 lymphoblastoid cells.	fludarabine	26-37	P53	Homo sapiens	60-63
20038611-7	2010	Finally, we show that the combination of L-asparaginase (by specifically down-regulating Mcl-1 protein levels), topotecan (by activating p53 via DNA damage), and ABT-737 (by inhibiting antiapoptotic Bcl-2 family members) caused profound synergistic antileukemic efficacy both in vitro and in vivo.	Topotecan	112-121	P53	Homo sapiens	137-140
18092340-5	2008	Analysis of the gene expression profile of the p53-transcriptional targets showed distinct features between chlorambucil, Nutlin-3 and fludarabine, which likely account for their differential effect on cell cycle in SKW6.4 cells.	fludarabine	135-146	P53	Homo sapiens	47-50
20067818-8	2010	The antioxidant ascorbic acid inhibited BrO(3)(-)-induced p38 activation, G2/M arrest, p-p53, p21 and cyclin B1 expression; however, ascorbic acid had no effect on BrO(3)(-)-induced formation of 8-OHdG, a marker of DNA oxidative damage, whose increases preceded cell death by 24h.	Ascorbic Acid	16-29	P53	Homo sapiens	89-92
18316341-5	2008	The enhanced expression of PTEN by GM3 in both HCT116 and p53-null HCT116 cells has been shown to be not associated with p53 function.	gm3	35-38	P53	Homo sapiens	58-61
20000476-0	2010	Suppression of p53 and p21CIP1/WAF1 reduces arsenite-induced aneuploidy.	arsenite	44-52	P53	Homo sapiens	15-18
18348286-2	2008	We have developed a high-throughput scanning assay with automatic calling to detect TP53 mutations in DNA from fresh frozen (FF) and formalin-fixed paraffin-embedded (FFPE) tissues.	Formaldehyde	133-141	P53	Homo sapiens	84-88
17849503-7	2008	Moreover, arsenite induced the translocation of Bax and p53 to the mitochondria and the activation-associated oligomerization of Bax, and these crucial events were reduced by inhibition of GSK3, indicating that GSK3 promotes arsenite-induced apoptosis by facilitating signals leading to mitochondrial apoptotic events.	arsenite	10-18	P53	Homo sapiens	56-59
20000476-7	2010	Although suppression of p53 increased the fraction of arsenite-treated cells with MN, it caused a decrease in the fraction with centromeric DNA.	arsenite	54-62	P53	Homo sapiens	24-27
20557688-9	2010	In conclusion, the release of ROS by PU- or PTFE-treated THP-1 cells may induce iNOS expression and cause apoptosis in HUVECs via the p53, Bax and Bcl-2 proteins.	Polyurethanes	37-39	P53	Homo sapiens	134-137
18226502-2	2008	OBJECTIVE: We aimed to investigate (1) the UV transmission through tacrolimus ointment and (2) the impact of topical exposure to tacrolimus on the protein expression of thymine dimers (TD) and p53 in human skin.	Tacrolimus	129-139	P53	Homo sapiens	193-196
20211059-8	2010	NT4-p53(N15)-Ant on HepG2 cells was measured by a colorimetric 3-[4,5-dimethyl thiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay.	thiazolyl blue	63-124	P53	Homo sapiens	4-7
18504176-0	2008	[Construction and expression of different mutants of human p53 and their effects on arsenite-induced cell apoptosis].	arsenite	84-92	P53	Homo sapiens	59-62
18504176-6	2008	The apoptotic ratio of p53(WT)-transfected cells induced by arsenite increased and that of p53(S15A)-transfected cells decreased significantly after arsenite stimulation, but no significant changes occurred in the apoptosis of p53(S46A)-transfected cells.	arsenite	60-68	P53	Homo sapiens	23-26
18504176-6	2008	The apoptotic ratio of p53(WT)-transfected cells induced by arsenite increased and that of p53(S15A)-transfected cells decreased significantly after arsenite stimulation, but no significant changes occurred in the apoptosis of p53(S46A)-transfected cells.	arsenite	149-157	P53	Homo sapiens	91-94
18504176-6	2008	The apoptotic ratio of p53(WT)-transfected cells induced by arsenite increased and that of p53(S15A)-transfected cells decreased significantly after arsenite stimulation, but no significant changes occurred in the apoptosis of p53(S46A)-transfected cells.	arsenite	149-157	P53	Homo sapiens	91-94
18504176-7	2008	CONCLUSION: The phosphorylation on Ser15 of p53 plays an important role in mediating arsenite-induced cell apoptosis.	arsenite	85-93	P53	Homo sapiens	44-47
19009304-0	2009	Establishment of ponasterone A-inducible the wild-type p53 protein-expressing clones from HSC-1 cells, cell growth suppression by p53 expression and the suppression mechanism.	ponasterone A	17-30	P53	Homo sapiens	55-58
18347187-7	2008	Cellular levels of ceramide, sphingomyelinase activity, caspase-3, and p53 were elevated with increasing time of exposure to alpha-TOS.	alpha-tos	125-134	P53	Homo sapiens	71-74
15890420-1	2005	BACKGROUND AND PURPOSE: To elucidate the role of TP53 on differential effects of topoisomerase I inhibitor topotecan (Hycamtin on radiation sensitivity.	Topotecan	107-116	P53	Homo sapiens	49-53
15890420-1	2005	BACKGROUND AND PURPOSE: To elucidate the role of TP53 on differential effects of topoisomerase I inhibitor topotecan (Hycamtin on radiation sensitivity.	Topotecan	118-126	P53	Homo sapiens	49-53
15890420-4	2005	Phosphorylation of TP53 and expression of p21(WAF1/CIP1) was induced by IR and/or topotecan in CCD32 cells, and in U118 cells after topotecan treatment, accompanied by cyclin B degradation.	Topotecan	82-91	P53	Homo sapiens	19-23
15890420-4	2005	Phosphorylation of TP53 and expression of p21(WAF1/CIP1) was induced by IR and/or topotecan in CCD32 cells, and in U118 cells after topotecan treatment, accompanied by cyclin B degradation.	Topotecan	132-141	P53	Homo sapiens	19-23
15890420-5	2005	In U87 cells only 1 microM topotecan generated phosphorylation of TP53 and p21(WAF1/CIP1) expression; 0.05 microM caused stabilization of cyclin B.	Topotecan	27-36	P53	Homo sapiens	66-70
15890420-7	2005	Thus, the impact of TP53 on the topotecan response remains indistinct, and is obviously influenced by other genomic alterations acquired by tumor cells.	Topotecan	32-41	P53	Homo sapiens	20-24
16104504-7	2005	p 53 protein expression was analyzed by fluorescence immunohistochemical method (SABC-Cy3).	sabc-cy3	81-89	P53	Homo sapiens	0-4
15713419-2	2005	The most potent compound, 3-(4-chlorophenyl)-3-(4-hydroxy-3,5-dimethoxybenzyloxy)-2-propyl-2,3-dihydroisoindol-1-one (NU8231), exhibited an IC50 of 5.3 +/- 0.9 microM in an ELISA assay, and induced p53-dependent gene transcription in a dose-dependent manner, in the SJSA human sarcoma cell line.	3-(4-chlorophenyl)-3-(4-hydroxy-3,5-dimethoxybenzyloxy)-2-propyl-2,3-dihydroisoindol-1-one	26-116	P53	Homo sapiens	198-201
15713419-2	2005	The most potent compound, 3-(4-chlorophenyl)-3-(4-hydroxy-3,5-dimethoxybenzyloxy)-2-propyl-2,3-dihydroisoindol-1-one (NU8231), exhibited an IC50 of 5.3 +/- 0.9 microM in an ELISA assay, and induced p53-dependent gene transcription in a dose-dependent manner, in the SJSA human sarcoma cell line.	3-(4-chlorophenyl)-3-(4-hydroxy-3,5-dimethoxybenzyloxy)-2-propyl-2,3-dihydroisoindol-1-one	118-124	P53	Homo sapiens	198-201
15546879-4	2005	Our results showed that simultaneous 5-FU and DENSPM, a spermine analogue, synergistically increased transcript levels of the polyamine catabolism enzyme spermidine/spermine N1-acetyltransferase, depleted spermine and spermidine, increased acetylated spermidine, and produced synergistic tumor cell apoptosis in both p53 wild-type and p53-null variants.	Spermine	56-64	P53	Homo sapiens	317-320
15546879-4	2005	Our results showed that simultaneous 5-FU and DENSPM, a spermine analogue, synergistically increased transcript levels of the polyamine catabolism enzyme spermidine/spermine N1-acetyltransferase, depleted spermine and spermidine, increased acetylated spermidine, and produced synergistic tumor cell apoptosis in both p53 wild-type and p53-null variants.	Spermine	56-64	P53	Homo sapiens	335-338
15652229-12	2005	In spite of the low rate of apoptosis, LA-12 caused increase of p53 level and cell cycle perturbations in the ovarian cancer cell lines studied.	UNII-37WM0V5E17	39-44	P53	Homo sapiens	64-67
16127286-1	2005	OBJECTIVE: Since the p53 gene has been identified as a determinant of response to chemotherapy in ovarian carcinoma in previous studies, we investigated the significance of the p53 status in response to topotecan as second-line therapy.	Topotecan	203-212	P53	Homo sapiens	177-180
16127286-4	2005	RESULTS: Wild-type p53 tumors responsive to first-line therapy maintained substantial responsiveness to topotecan.	Topotecan	104-113	P53	Homo sapiens	19-22
16127286-7	2005	This outcome is consistent with the clinical observation that the efficacy of topotecan in the treatment of relapsed ovarian carcinoma patients is dependent on platinum sensitivity, because platinum-sensitive tumors are expected to carry wild-type p53.	Topotecan	78-87	P53	Homo sapiens	248-251
15604277-0	2004	Tetrandrine induces early G1 arrest in human colon carcinoma cells by down-regulating the activity and inducing the degradation of G1-S-specific cyclin-dependent kinases and by inducing p53 and p21Cip1.	tetrandrine	0-11	P53	Homo sapiens	186-189
15604277-8	2004	Third, tetrandrine increases the expression of p53 and p21(Cip1) in wild-type p53 HCT116 cells.	tetrandrine	7-18	P53	Homo sapiens	47-50
15604277-8	2004	Third, tetrandrine increases the expression of p53 and p21(Cip1) in wild-type p53 HCT116 cells.	tetrandrine	7-18	P53	Homo sapiens	78-81
15604277-9	2004	Collectively, these results show that tetrandrine arrests cells in G(1) by convergent mechanisms, including down-regulation of E2F1 and up-regulation of p53/p21(Cip1).	tetrandrine	38-49	P53	Homo sapiens	153-156
15489892-0	2004	Inhibition of p53-mediated transcriptional responses by mithramycin A.	mithramycin A	56-69	P53	Homo sapiens	14-17
15489892-1	2004	In the present work, we show that mithramycin A, a drug that is currently used for the treatment of patients with Paget"s disease of the bone as well as with several forms of cancer, is a strong activator of the tumor suppressor p53 protein in human hepatoma cells.	mithramycin A	34-47	P53	Homo sapiens	229-232
15489892-2	2004	The time course of p53 activation by mithramycin A was similar to the known chemotherapeutic compound 5-fluorouracil (5-FU).	mithramycin A	37-50	P53	Homo sapiens	19-22
15382140-5	2004	For example, bromodomains of Gcn5, PCAF, TAF1 and CBP are able to recognize acetyllysine residues in histones, HIV Tat, p53, c-Myb or MyoD.	N-epsilon-Acetyl-L-lysine	76-88	P53	Homo sapiens	120-123
15466212-7	2004	A substantial correlation with gammaH2AX loss half-time measured over the first 4 hours was seen only when cervical cell lines were included in a larger series of p53-deficient cell lines.	gammah2ax	31-40	P53	Homo sapiens	163-166
15466212-8	2004	Interestingly, p53 wild-type cell lines consistently showed faster gammaH2AX loss half-times than p53-deficient cell lines.	gammah2ax	67-76	P53	Homo sapiens	15-18
15138159-0	2004	Fludarabine treatment of patients with chronic lymphocytic leukemia induces a p53-dependent gene expression response.	fludarabine	0-11	P53	Homo sapiens	78-81
15138159-4	2004	Many of the fludarabine signature genes were known p53 target genes and genes involved in DNA repair.	fludarabine	12-23	P53	Homo sapiens	51-54
15138159-6	2004	Using isogenic p53 wild-type and null lymphoblastoid cell lines, we confirmed that many of the fludarabine signature genes were also p53 target genes.	fludarabine	95-106	P53	Homo sapiens	15-18
15138159-6	2004	Using isogenic p53 wild-type and null lymphoblastoid cell lines, we confirmed that many of the fludarabine signature genes were also p53 target genes.	fludarabine	95-106	P53	Homo sapiens	133-136
15138159-7	2004	Because in vivo treatment with fludarabine induces a p53-dependent gene expression response, fludarabine treatment has the potential to select p53-mutant CLL cells, which are more drug resistant and associated with an aggressive clinical course.	fludarabine	31-42	P53	Homo sapiens	53-56
15138159-7	2004	Because in vivo treatment with fludarabine induces a p53-dependent gene expression response, fludarabine treatment has the potential to select p53-mutant CLL cells, which are more drug resistant and associated with an aggressive clinical course.	fludarabine	31-42	P53	Homo sapiens	143-146
15138159-7	2004	Because in vivo treatment with fludarabine induces a p53-dependent gene expression response, fludarabine treatment has the potential to select p53-mutant CLL cells, which are more drug resistant and associated with an aggressive clinical course.	fludarabine	93-104	P53	Homo sapiens	53-56
15138159-7	2004	Because in vivo treatment with fludarabine induces a p53-dependent gene expression response, fludarabine treatment has the potential to select p53-mutant CLL cells, which are more drug resistant and associated with an aggressive clinical course.	fludarabine	93-104	P53	Homo sapiens	143-146
15524402-6	2004	Taken together, these results revealed that safrole oxide could induce apoptosis of A549 cells and suggested that safrole oxide might perform its function by blocking cells completely at G1 phase and partly at G(2)-M phase, and also by up-regulating the expression of P53 protein.	safrole oxide	44-57	P53	Homo sapiens	268-271
15524402-6	2004	Taken together, these results revealed that safrole oxide could induce apoptosis of A549 cells and suggested that safrole oxide might perform its function by blocking cells completely at G1 phase and partly at G(2)-M phase, and also by up-regulating the expression of P53 protein.	safrole oxide	114-127	P53	Homo sapiens	268-271
15260130-4	2004	However, pre-treatment with FK506 and V10367 significantly prevented any increase in this ratio or p53 mRNA expression.	Tacrolimus	28-33	P53	Homo sapiens	99-102
15207728-7	2004	Molecular analysis indicates that induction of p53 and p21, and suppression of pRB are associated with apoptosis induced by 5-FUdR and may partly explain the hypersensitivity of E6E7/OSE cells to low-dose 5-FUdR.	Floxuridine	124-130	P53	Homo sapiens	47-50
15207728-7	2004	Molecular analysis indicates that induction of p53 and p21, and suppression of pRB are associated with apoptosis induced by 5-FUdR and may partly explain the hypersensitivity of E6E7/OSE cells to low-dose 5-FUdR.	Floxuridine	205-211	P53	Homo sapiens	47-50
15252149-0	2004	Selenite-induced p53 Ser-15 phosphorylation and caspase-mediated apoptosis in LNCaP human prostate cancer cells.	Selenious Acid	0-8	P53	Homo sapiens	17-20
15252149-2	2004	We and others have shown that selenite induces apoptotic DNA laddering in the p53-mutant DU145 prostate cancer cells and the p53-null HL60 leukemia cells without the cleavage of poly(ADP-ribose) polymerase (PARP; i.e., caspase-independent apoptosis), whereas selenium compounds leading to the formation of methylselenol induce caspase-mediated apoptosis in these cells.	Selenious Acid	30-38	P53	Homo sapiens	78-81
15252149-2	2004	We and others have shown that selenite induces apoptotic DNA laddering in the p53-mutant DU145 prostate cancer cells and the p53-null HL60 leukemia cells without the cleavage of poly(ADP-ribose) polymerase (PARP; i.e., caspase-independent apoptosis), whereas selenium compounds leading to the formation of methylselenol induce caspase-mediated apoptosis in these cells.	Selenious Acid	30-38	P53	Homo sapiens	125-128
15461257-0	2004	[Effects on DNA damage and apoptosis and p53 protein expression induced by fluoride in human embryo hepatocytes].	Fluorides	75-83	P53	Homo sapiens	41-44
15312403-2	2004	METHODS: The status of p53 gene mutation of the tumor tissues and corresponding fecal specimens was analyzed by polymerase chain reaction-single strand configuration polymorphism with EB staining in 40 CRC, 20 colorectal adenoma and 15 gastrocarcinoma.	ethylbenzene	184-186	P53	Homo sapiens	23-26
15096505-10	2004	The findings provide evidence that R2-RNR can be employed to supply dNTPs for the repair of DNA damage in cells with an impaired p53-dependent induction of p53R2.	Parathion	68-73	P53	Homo sapiens	129-132
15107830-7	2004	Most cells exhibited elevated levels of p53 in response to hypoxia mimetics such as deferoxamine mesylate and CoCl(2), regardless of their HIF-alpha protein expression profile.	cobaltous chloride	110-117	P53	Homo sapiens	40-43
15122344-3	2004	Subsequently, we found that 2,3-DCPE could induce S-phase arrest and upregulate p21 but not p27 at a time- and dose-dependent but p53-dispensable manner in DLD-1 human colon cancer cells.	2-((3-(2,3-dichlorophenoxy)propyl)amino)ethanol	28-36	P53	Homo sapiens	130-133
18270365-6	2008	The authors identified 1 natural product, sempervirine, that inhibited MDM2 auto-ubiquitination, MDM2-mediated p53 degradation, and led to accumulation of p53 in cells.	sempervirine	42-54	P53	Homo sapiens	111-114
18270365-6	2008	The authors identified 1 natural product, sempervirine, that inhibited MDM2 auto-ubiquitination, MDM2-mediated p53 degradation, and led to accumulation of p53 in cells.	sempervirine	42-54	P53	Homo sapiens	155-158
18270365-7	2008	Sempervirine preferentially induced apoptosis in transformed cells expressing wild-type p53, suggesting that it could be a potential lead for anticancer therapeutics.	sempervirine	0-12	P53	Homo sapiens	88-91
19009304-0	2009	Establishment of ponasterone A-inducible the wild-type p53 protein-expressing clones from HSC-1 cells, cell growth suppression by p53 expression and the suppression mechanism.	ponasterone A	17-30	P53	Homo sapiens	130-133
15269478-6	2004	MATERIALS AND METHODS: p53 protein expression was evaluated on formalin-fixed paraffin-embedded sections using streptavidin biotin immunoperoxidase technique after high temperature antigen retrieval.	Formaldehyde	63-71	P53	Homo sapiens	23-26
19452524-7	2009	Ibuprofen-type drugs, IL6 polymorphisms (rs1800796) and dietary alpha-tocopherol and lycopene significantly altered likelihood of having a TP53 mutation.	alpha-Tocopherol	64-80	P53	Homo sapiens	139-143
18067855-0	2008	Chloride ions control the G1/S cell-cycle checkpoint by regulating the expression of p21 through a p53-independent pathway in human gastric cancer cells.	Chlorides	0-8	P53	Homo sapiens	99-102
19452524-8	2009	This was especially true for TP53 transversion mutations and dietary antioxidants (OR for beta-carotene 0.51 95% CI 0.27, 0.97, p trend 0.03; alpha-tocopherol 0.41 95% CI 0.20, 0.84, p trend 0.02) Beta-carotene and ibuprofen significantly altered risk of KRAS2 tumors.	alpha-Tocopherol	142-158	P53	Homo sapiens	29-33
18067855-5	2008	These observations indicate that chloride ions play important roles in cell-cycle progression by regulating the expression of p21 through a p53-independent pathway in human gastric cancer cells, leading to a novel, unique therapeutic strategy for gastric cancer treatment via control of [Cl(-)](i).	Chlorides	33-41	P53	Homo sapiens	140-143
15081867-2	2004	Tachpyridine induces apoptosis in cultured cancer cells by triggering a mitochondrial pathway of cell death that is p53-independent.	tachpyr	0-12	P53	Homo sapiens	116-119
19796081-0	2009	Oligonucleotide probe array for p53 gene alteration analysis in DNA from formalin-fixed paraffin-embedded breast cancer tissues.	Formaldehyde	73-81	P53	Homo sapiens	32-35
15285929-0	2004	Eicosapentaenoic acid induces Fas-mediated apoptosis through a p53-dependent pathway in hepatoma cells.	Eicosapentaenoic Acid	0-21	P53	Homo sapiens	63-66
15285929-7	2004	We also observed that EPA induced transient nuclear accumulation of P53 protein that subsequently up-regulated the expression of Fas messenger RNA and protein in HepG2 cells.	Eicosapentaenoic Acid	22-25	P53	Homo sapiens	68-71
18059176-5	2008	Treatment of TK6 cells (wild-type p53) with 100 microg/ml CPFX for 2-10 h produced no increase in gammaH2AX; to the contrary, its level in S phase cells was reduced at 10 h compared to controls.	Ciprofloxacin	58-62	P53	Homo sapiens	34-37
15039212-1	2004	The allele constitution at codon 72 of the p53 gene (CGC-arginine or CCC-proline) plays a major role in inducing apoptosis in p53 mutant cells.	ccc-proline	69-80	P53	Homo sapiens	43-46
19830854-6	2009	RESULT: The growth of RPMI 8226 cells was suppressed in a dose-dependent manner after treatment with BBM(P&lt;0.05), and its IC(50) value was 3.83 microg/ml at 48 h. Both DNA ladder and FCM results showed that BBM induced apoptosis of RPMI 8226 cells with concomitant increase of activated p53, p21 and GADD45gamma mRNA.	berbamine	101-104	P53	Homo sapiens	290-293
15039212-1	2004	The allele constitution at codon 72 of the p53 gene (CGC-arginine or CCC-proline) plays a major role in inducing apoptosis in p53 mutant cells.	ccc-proline	69-80	P53	Homo sapiens	126-129
20016737-7	2008	The kaempferol-induced apoptosis was associated with the up-regulation of p53.	kaempferol	4-14	P53	Homo sapiens	74-77
20016737-8	2008	In addition, the phosphorylation of p53 at the Ser-15 residue was observed with kaempferol.	kaempferol	80-90	P53	Homo sapiens	36-39
20016737-9	2008	Kaempferol inhibits cell proliferation by disrupting the cell cycle, which is strongly associated with the induction of arrest at G2/M phase and may induce apoptosis via p53 phosphorylation in human breast carcinoma MDA-MB-453 cells.	kaempferol	0-10	P53	Homo sapiens	170-173
17945324-7	2007	TUNEL analysis confirmed that there was indeed a significantly reduced arsenite-induced apoptosis found in p53-compromised cells.	arsenite	71-79	P53	Homo sapiens	107-110
19502782-0	2009	Knockdown of Chk1 sensitizes human colon carcinoma HCT116 cells in a p53-dependent manner to lidamycin through abrogation of a G2/M checkpoint and induction of apoptosis.	C 1027	93-102	P53	Homo sapiens	69-72
17945324-9	2007	In our present study, reduced p21 and Gadd45a expressions and increased centrosomal abnormality (atopic and multiple centrosomes) were observed in both arsenite-treated H1355 and p53-inhibited BEAS-2B cells as compared with similarly treated BEAS-2B cells.	arsenite	152-160	P53	Homo sapiens	179-182
18006756-0	2007	Deficient TP53 expression, function, and cisplatin sensitivity are restored by quinacrine in head and neck cancer.	Quinacrine	79-89	P53	Homo sapiens	10-14
18006756-3	2007	The genotoxic drug doxorubicin and the anti-inflammatory and antimalarial drug quinacrine, previously identified as inducers of TP53, were used to examine the nature and potential reversibility of deficient TP53 expression and function.	Quinacrine	79-89	P53	Homo sapiens	128-132
18006756-7	2007	Although doxorubicin failed to induce TP53 expression or functional activity, quinacrine induced TP53 mRNA and protein expression, increased TP53 reporter activity and p21 protein expression, and induced growth inhibition in these wild-type TP53 cell lines.	Quinacrine	78-88	P53	Homo sapiens	97-101
18006756-7	2007	Although doxorubicin failed to induce TP53 expression or functional activity, quinacrine induced TP53 mRNA and protein expression, increased TP53 reporter activity and p21 protein expression, and induced growth inhibition in these wild-type TP53 cell lines.	Quinacrine	78-88	P53	Homo sapiens	97-101
18006756-7	2007	Although doxorubicin failed to induce TP53 expression or functional activity, quinacrine induced TP53 mRNA and protein expression, increased TP53 reporter activity and p21 protein expression, and induced growth inhibition in these wild-type TP53 cell lines.	Quinacrine	78-88	P53	Homo sapiens	97-101
18006756-8	2007	Quinacrine-induced TP53 reporter activity and growth suppression were attenuated by pifithrin-alpha and TP53 short hairpin RNA knockdown.	Quinacrine	0-10	P53	Homo sapiens	19-23
18006756-8	2007	Quinacrine-induced TP53 reporter activity and growth suppression were attenuated by pifithrin-alpha and TP53 short hairpin RNA knockdown.	Quinacrine	0-10	P53	Homo sapiens	104-108
18006756-10	2007	CONCLUSIONS: Deficient TP53 mRNA and protein expression underlies decreased function in a subset of HNSCC with wild-type TP53 and can be restored together with cisplatin sensitization by quinacrine.	Quinacrine	187-197	P53	Homo sapiens	23-27
14737002-5	2004	On the other hand, cell cycle progression that is closely connected to p53 was affected by 2,2",4,6,6"-PeCB, resulting in mitotic arrest.	2,2",4,6,6"-pecb	91-107	P53	Homo sapiens	71-74
14737002-8	2004	These results imply that 2,2",4,6,6"-PeCB induces mitotic arrest by interfering with mitotic spindle assembly, followed by genetic instability which triggers p53-activating signals to prevent further polyploidization.	2,2",4,6,6"-pecb	25-41	P53	Homo sapiens	158-161
14737002-9	2004	Taking these findings together, we suggest that 2,2",4,6,6"-PeCB could be involved in cancer development by causing genetic instability through mitotic spindle damage, which brings about aneuploidy in p53-deficient tumor cells.	2,2",4,6,6"-pecb	48-64	P53	Homo sapiens	201-204
14719118-8	2004	Use of the protein transport inhibitor Brefeldin A significantly inhibited Ad-p53-induced surface Fas/CD95 expression, but only partially inhibited apoptosis in mutant-p53 cell lines.	Brefeldin A	39-50	P53	Homo sapiens	78-81
14719118-8	2004	Use of the protein transport inhibitor Brefeldin A significantly inhibited Ad-p53-induced surface Fas/CD95 expression, but only partially inhibited apoptosis in mutant-p53 cell lines.	Brefeldin A	39-50	P53	Homo sapiens	168-171
15651660-2	2004	The functional oligonucleotide polymorphism of the p53 gene causes the substitution of arginine (Arg) for praline (Pro) in the codon 72.	praline	106-113	P53	Homo sapiens	51-54
14666730-2	2003	We have reported that hypoxic cytotoxins, such as TX-1102, tirapazamine (TPZ) and TX-402, selectively induced tumor cells to p53-independent apoptosis under hypoxic conditions and inhibited angiogenesis.	tx-1102	50-57	P53	Homo sapiens	125-128
19373929-6	2009	Exposure to DCV also led to an increase in the level of activated ATM and Chk2 as well as of phosphorylated p53 and accumulation of cells in G(2)M and S phase.	DyeCycle Violet	12-15	P53	Homo sapiens	108-111
14676405-2	2003	Previously we reported that the accumulation of inducible nitric oxide (NO) synthase (iNOS) was induced only in human glioblastoma mutant (m) p53 cells by acute irradiation with X-rays, suggesting a suppression of iNOS induction after acute irradiation with X-rays in wtp53 cells.	nitric	58-64	P53	Homo sapiens	142-145
17726646-4	2007	Fusion of the p53 nuclear export signaling sequence MFRELNEALELK to NDelta19 (NDelta19NES) abolished its apoptosis promoting properties, while overexpression of NDelta19 significantly increased the susceptibility to apoptosis induction by the proteasome inhibitor PSI and by staurosporine.	ndelta19nes	78-89	P53	Homo sapiens	14-17
19373929-8	2009	The data indicate that supravital use of Ho 42, DRAQ5, and DCV induces various degrees of DDR, including activation of ATM, Chk2 and p53, which may have significant consequences on regulatory cell cycle pathways and apoptosis.	DyeCycle Violet	59-62	P53	Homo sapiens	133-136
17704656-6	2007	Sublethal concentrations of BrdU evoke a DNA damage response in these cells that involves the activation of Chk1, Chk2 and p53.	Bromodeoxyuridine	28-32	P53	Homo sapiens	123-126
12948852-5	2003	Treatment of cells with tetrandrine caused the upregulation of p53, downregulation of Bcl-X(L), cleavage of Bid and Bax, and release of cytochrome c, which were accompanied by activation of caspases 9, 3 and 8.	tetrandrine	24-35	P53	Homo sapiens	63-66
19197159-7	2009	Binding of Cep164 to the region of exon 4 to intron 9 within p53 gene, known as a pyrimidine-rich region as well as a photoproduct formation region upon UV damage, increases 2.5-fold upon UV irradiation.	pyrimidine	82-92	P53	Homo sapiens	61-64
12810654-8	2003	In these cells too, the GA analogues antagonized DDP, suggesting a role for p53 in the observed effects.	geldanamycin	24-26	P53	Homo sapiens	76-79
17971903-5	2007	In p53-null PC-3 cells, prazosin induced an increase in DNA strand breaks and ATM/ATR checkpoint pathways, leading to the activation of downstream signaling cascades, including Cdc25c phosphorylation at Ser216, nuclear export of Cdc25c, and cyclin-dependent kinase (Cdk) 1 phosphorylation at Tyr15.	Prazosin	24-32	P53	Homo sapiens	3-6
19018867-6	2009	RESULTS AND CONCLUSIONS: At the clinically relevant concentration of fludarabine, TP53-abnormal samples exhibited markedly higher resistance to fludarabine than the remaining CLL samples (P = 0.012); cohort with ATM deletion was not more resistant than wt cells.	fludarabine	69-80	P53	Homo sapiens	82-86
17636258-5	2007	Topotecan- and paclitaxel-resistant prostate cancer lines were as sensitive to p53p-Ant-induced targeted necrosis as parental lines.	Topotecan	0-9	P53	Homo sapiens	79-83
17301063-10	2007	Thus, mismatch repair-mediated enhancement of Cr(VI) cytotoxicity by Asc should promote the selection of MSI+/wt-p53 phenotype found among chromate-induced human lung cancers.	Ascorbic Acid	69-72	P53	Homo sapiens	113-116
12771037-9	2003	Moreover, UVR-induced skin p53 expression, assessed immunohistochemically at 24 h post-UVR exposure, fell from a mean of 16 (SD 5) positive cells/100 epidermal cells at baseline to 8 (4) after EPA supplementation, P &lt; 0.01.	Eicosapentaenoic Acid	193-196	P53	Homo sapiens	27-30
12771037-13	2003	Reduction in this range of early markers, i.e. sunburn, UVR-induced p53 in skin and strand breaks in PBL, indicate protection by dietary EPA against acute UVR-induced genotoxicity; longer-term supplementation might reduce skin cancer in humans.	Eicosapentaenoic Acid	137-140	P53	Homo sapiens	68-71
12698201-5	2003	Topotecan caused pan-cycle induction and activation of p53.	Topotecan	0-9	P53	Homo sapiens	55-58
12719725-4	2003	p53 mutations resulted not only in a shorter survival but, notably also in selective resistance to alkylating agents, fludarabine and gamma-irradiation.	fludarabine	118-129	P53	Homo sapiens	0-3
12586742-0	2003	Green tea polyphenol epigallocatechin-3 gallate induces apoptosis of proliferating vascular smooth muscle cells via activation of p53.	polyphenol epigallocatechin-3 gallate	10-47	P53	Homo sapiens	130-133
19018867-6	2009	RESULTS AND CONCLUSIONS: At the clinically relevant concentration of fludarabine, TP53-abnormal samples exhibited markedly higher resistance to fludarabine than the remaining CLL samples (P = 0.012); cohort with ATM deletion was not more resistant than wt cells.	fludarabine	144-155	P53	Homo sapiens	82-86
19148495-9	2009	In addition, up-regulated p21WAF/CIP1 was accompanied by reduction of phosphorylation on retinoblastoma (Rb) protein in p53-null cells, implying that p21WAF/CIP1 might in part account for the molecular regulation of cytochalasin B induced G1 phase arrest.	Cytochalasin B	216-230	P53	Homo sapiens	120-123
12532420-5	2003	The mutation status of exons 5-8 of p53 was analyzed by denaturing high pressure liquid chromatography (DHPLC) in formalin-fixed, paraffin-embedded tumor sections, followed by direct sequencing of cases with aberrant chromatographic patterns.	Formaldehyde	114-122	P53	Homo sapiens	36-39
17718196-8	2007	Western blotting results showed that TPT caused an obvious increase of p53 expression and a decline of ERK expression in EA.hy926 cells.	Topotecan	37-40	P53	Homo sapiens	71-74
17125918-0	2007	Simvastatin induces apoptosis in human breast cancer cells: p53 and estrogen receptor independent pathway requiring signalling through JNK.	Simvastatin	0-11	P53	Homo sapiens	60-63
12795334-10	2003	An inhibitor of PKC, GF 109203X inhibited EGF-mediated suppression of TNF-alpha-induced accumulation of p53, p21 and induction of apoptosis.	bisindolylmaleimide I	21-31	P53	Homo sapiens	104-107
19025975-0	2009	Activity of cladribine combined with cyclophosphamide in frontline therapy for chronic lymphocytic leukemia with 17p13.1/TP53 deletion: report from the Polish Adult Leukemia Group.	Cladribine	12-22	P53	Homo sapiens	121-125
17550442-7	2007	RESULTS: Both CO(2) and Er:YAG lasers were found to induce a significant decrease in p53 expression in biopsies obtained after 3 months (p=.0004 and .002, respectively) followed by gradual increase (p=.01 in both groups).	co(2)	14-19	P53	Homo sapiens	85-88
17550442-10	2007	CONCLUSION: The decrease in epidermal p53 expression after CO(2) and Er:YAG lasers may account for some of the benefits of resurfacing on the epidermis, as well as prevention of actinic neoplasia by adjusting any disturbance in the proliferation/apoptosis balance observed in photoaged facial skin.	co(2)	59-64	P53	Homo sapiens	38-41
12427754-7	2003	Inhibition of hsp90-p53 interaction by geldanamycin prevented p53 accumulation partially in ATM-wild type cells and completely in ATM-deficient cells.	geldanamycin	39-51	P53	Homo sapiens	20-23
18822392-9	2009	Finally, the sustained p53 activation in SWI/SNF-defective cells was accompanied by accumulation of unrepaired DSBs owing to inefficient DNA repair.	dsbs	111-115	P53	Homo sapiens	23-26
12427754-7	2003	Inhibition of hsp90-p53 interaction by geldanamycin prevented p53 accumulation partially in ATM-wild type cells and completely in ATM-deficient cells.	geldanamycin	39-51	P53	Homo sapiens	62-65
12424231-4	2003	We report that electrophilic cyclopentenone prostaglandins covalently modify and inhibit thioredoxin reductase, a selenoprotein that governs p53 and other redox-sensitive transcription factors.	cyclopentenone prostaglandins	29-58	P53	Homo sapiens	141-144
17226861-5	2007	In vitro resistance to fludarabine was greatest in B-CLL cells with deletions of p53, a cytogenetic abnormality that is almost invariably associated with a poor therapeutic response clinically.	fludarabine	23-34	P53	Homo sapiens	81-84
17230520-2	2007	Earlier studies have shown that selenite induces DNA single strand breaks (SSBs), reactive oxygen species (ROS), p53 Ser-15 phosphorylation and caspase-dependent and -independent apoptosis, whereas a methylselenol precursor methylseleninic acid (MSeA) induces caspase-mediated apoptosis regardless of p53 status.	Selenious Acid	32-40	P53	Homo sapiens	113-116
12473386-1	2003	The present study was performed to gain insight into the role of p53 and p21(WAF1) on the cytotoxicity of the purine analogue cladribine (2-CdA) on cancer cells.	Cladribine	126-136	P53	Homo sapiens	65-68
17230520-2	2007	Earlier studies have shown that selenite induces DNA single strand breaks (SSBs), reactive oxygen species (ROS), p53 Ser-15 phosphorylation and caspase-dependent and -independent apoptosis, whereas a methylselenol precursor methylseleninic acid (MSeA) induces caspase-mediated apoptosis regardless of p53 status.	Selenious Acid	32-40	P53	Homo sapiens	301-304
19037992-10	2008	Downregulation of p53 by antisense TP53 restored the cell viability suppressed by bufalienolides.	bufalienolides	82-96	P53	Homo sapiens	18-21
17390078-8	2007	There was also an increase in c-kit, Trio, Rho-A, Rac-3, EGFR, Notch-4, Dvl-2, Ezrin, beta catenin and mutant p53 protein expression in the parathion-treated cells.	Parathion	140-149	P53	Homo sapiens	110-113
13129816-5	2003	As(2)O(3)-induced apoptosis was associated with upregulation of p53 and caspase 3, whereas NaAsO(2)-induced apoptosis was associated with p53 upregulation.	(2)o(3)	2-9	P53	Homo sapiens	64-67
14689061-1	2003	The aim of this study was to assess the possible relationship between the silver stained nucleolar organizer regions (AgNOR) and immunocytochemically detected p53 and bcl-2 proteins in ALL, AML, B-CLL and CML patients (adults and children) at the initial presentation.	Silver	74-80	P53	Homo sapiens	159-162
14622914-8	2003	Treatments of neuronal cultures with the permeability transitory pore blockers cyclosporin A and bongkrekic acid prevented veratridine-induced p53 immunoreactivity and neuronal death, placing mitochondria upstream of veratridine-induced p53 immunoreactivity.	Bongkrekic Acid	97-112	P53	Homo sapiens	143-146
19037992-10	2008	Downregulation of p53 by antisense TP53 restored the cell viability suppressed by bufalienolides.	bufalienolides	82-96	P53	Homo sapiens	35-39
14622914-8	2003	Treatments of neuronal cultures with the permeability transitory pore blockers cyclosporin A and bongkrekic acid prevented veratridine-induced p53 immunoreactivity and neuronal death, placing mitochondria upstream of veratridine-induced p53 immunoreactivity.	Bongkrekic Acid	97-112	P53	Homo sapiens	237-240
17204746-9	2007	Thus, disruption of p53/p90RSK-mediated NF-kappaB signaling and activation of ARE/EpRE pathways may be effective strategies to delineate mechanisms of action of BFA-induced inflammation and cell death signaling in immortalized versus normal skin systems.	O(4)-benzylfolic acid	161-164	P53	Homo sapiens	20-23
19189638-6	2008	Conversely, RKO cells expressing wildtype p53, proteolytically activated caspase-8, -9, -7 and -3 and unmethylated caspase-8 were more responsive to 5-FU and selenous acid-induced apoptosis.	Selenious Acid	158-171	P53	Homo sapiens	42-45
12091392-7	2002	Bis IX induced p53 accumulation in LNCaP (lymph node carcinoma of prostate), which expresses wild-type p53 that was not accompanied by the induction of p53-responsive genes, p21/WAF1, and Mdm2.	bisindolylmaleimide IX	0-6	P53	Homo sapiens	15-18
12091392-7	2002	Bis IX induced p53 accumulation in LNCaP (lymph node carcinoma of prostate), which expresses wild-type p53 that was not accompanied by the induction of p53-responsive genes, p21/WAF1, and Mdm2.	bisindolylmaleimide IX	0-6	P53	Homo sapiens	103-106
12091392-7	2002	Bis IX induced p53 accumulation in LNCaP (lymph node carcinoma of prostate), which expresses wild-type p53 that was not accompanied by the induction of p53-responsive genes, p21/WAF1, and Mdm2.	bisindolylmaleimide IX	0-6	P53	Homo sapiens	103-106
18949386-0	2008	Vitamin C inhibits p53-induced replicative senescence through suppression of ROS production and p38 MAPK activity.	Ascorbic Acid	0-9	P53	Homo sapiens	19-22
17431114-9	2007	Interestingly, TAE226 treatment of tumor cells containing wild-type p53 mainly exhibited G(2)-M arrest, whereas tumor cells bearing mutant p53 underwent apoptosis.	TAE226	15-21	P53	Homo sapiens	68-71
18949386-3	2008	Vitamin C was found to inhibit p53-induced senescence in human bladder cancer EJ cells.	Ascorbic Acid	0-9	P53	Homo sapiens	31-34
18949386-7	2008	We found that vitamin C inhibited this p53-induced ROS generation.	Ascorbic Acid	14-23	P53	Homo sapiens	39-42
12176904-6	2002	Fludarabine and FCM induce p53 stabilization, but do not seem to be essential in inducing Bax and Bak conformational changes, as they are also observed in dexamethasone-treated CLL cells.	fludarabine	0-11	P53	Homo sapiens	27-30
17465228-0	2007	Regulation of p53-, Bcl-2- and caspase-dependent signaling pathway in xanthorrhizol-induced apoptosis of HepG2 hepatoma cells.	xanthorrhizol	70-83	P53	Homo sapiens	14-17
17465228-6	2007	The apoptosis mediated by xanthorrhizol in the HepG2 cells was associated with the activation of tumor suppressor p53 and down-regulation of antiapoptotic Bcl-2 protein expression, but not Bax.	xanthorrhizol	26-39	P53	Homo sapiens	114-117
12496485-1	2002	In this study, we investigated the influence of Bcl-2 overexpression on the radiosensitizing potential of Didox (DX; 3,4-Dihydroxybenzohydroxamic acid), a novel ribonucleotide reductase inhibitor, in p53-null prostate cancer cell line PC-3.	3,4-dihydroxybenzohydroxamic acid	117-150	P53	Homo sapiens	200-203
18959823-0	2008	P53 transcription-independent activity mediates selenite-induced acute promyelocytic leukemia NB4 cell apoptosis.	Selenious Acid	48-56	P53	Homo sapiens	0-3
12118111-0	2002	Increased p53 protein expression in malignant mammary phyllodes tumors.	phyllodes	54-63	P53	Homo sapiens	10-13
17169329-0	2007	The expression of phosphatidic acid phosphatase 2a, which hydrolyzes lipids to generate diacylglycerol, is regulated by p73, a member of the p53 family.	Diglycerides	88-102	P53	Homo sapiens	141-144
17189187-7	2006	Furthermore, the acetyllysine 120 (acetyl-K120) form of p53 specifically accumulates at proapoptotic target genes.	N-epsilon-Acetyl-L-lysine	17-29	P53	Homo sapiens	56-59
17189187-7	2006	Furthermore, the acetyllysine 120 (acetyl-K120) form of p53 specifically accumulates at proapoptotic target genes.	acetyl-k120	35-46	P53	Homo sapiens	56-59
12012007-3	2002	In this study, we investigated particularly the effect of 100 microM NS-398 on p53 and p21 expression, caspase activities and nuclear factor-kappaB (NF-kappaB).	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	69-75	P53	Homo sapiens	79-82
18959823-5	2008	Immunofluorescent and Western blot procedures revealed selenite-induced p53 translocation to mitochondria.	Selenious Acid	55-63	P53	Homo sapiens	72-75
18959823-9	2008	Taken together, these results indicate that p53 involves selenite-induced NB4 cell apoptosis by translocation to mitochondria and activation mitochondrial apoptosis pathway in a transcription-independent manner.	Selenious Acid	57-65	P53	Homo sapiens	44-47
18460348-0	2008	Novel nitric oxide-donating compound (S,R)-3-phenyl-4,5-dihydro-5-isoxazole acetic acid-nitric oxide (GIT-27NO) induces p53 mediated apoptosis in human A375 melanoma cells.	3-phenyl-4,5-dihydro-5-isoxazole acetic acid	37-87	P53	Homo sapiens	120-123
11884368-6	2002	However, p53 induced profoundly different biological effects in r-VSMCs versus n-VSMCs, causing growth arrest and apoptosis in r-VSMCs only.	r-vsmcs	64-71	P53	Homo sapiens	9-12
11884368-6	2002	However, p53 induced profoundly different biological effects in r-VSMCs versus n-VSMCs, causing growth arrest and apoptosis in r-VSMCs only.	r-vsmcs	127-134	P53	Homo sapiens	9-12
11884368-7	2002	In addition, dominant-negative p53 promoted cell proliferation and apoptosis in r-VSMCs but not n-VSMCs.	r-vsmcs	80-87	P53	Homo sapiens	31-34
17213797-3	2006	BaP 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of BaP, attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 mutations.	benzylaminopurine	0-3	P53	Homo sapiens	129-132
16950207-6	2006	Combined sulindac/ATO treatment also activated p53 expression, and inhibition of p53 expression by small interfering RNA (siRNA) prevented sulindac/ATO-induced down-regulation of survivin, suggesting that survivin expression is negatively regulated by p53.	Sulindac	9-17	P53	Homo sapiens	47-50
18780655-1	2008	AIM: To examine by means of immunohistochemistry the expression of the tumor suppressing gene p53 and gene p21 in cells of malignant melanoma of the uvea from formalin-paraffin material from patients, who were during the period 2000 - 2006 surgically treated due to malignant melanoma of the uvea at the Department of Ophthalmology in the University Hospital in Brno (Brunn), Czech Republic, E.U., and to correlate the results of the immunohistochemical detection with clinical signs of the tumor of each patient.	Formaldehyde	159-167	P53	Homo sapiens	94-97
17201174-7	2006	The level of p53 was greatly increased, whilst PARP-1 was cleaved to 85 kDa subunits, following the treatment with xanthorrhizol at a dose-dependent manner.	xanthorrhizol	115-128	P53	Homo sapiens	13-16
17201174-8	2006	These results, thereby, suggest that xanthorrhizol has antiproliferative effects on MCF-7 cells by inducing apoptosis through the modulation of bcl-2, p53 and PARP-1 protein levels.	xanthorrhizol	37-50	P53	Homo sapiens	151-154
11888912-0	2002	Perifosine, a novel alkylphospholipid, induces p21(WAF1) expression in squamous carcinoma cells through a p53-independent pathway, leading to loss in cyclin-dependent kinase activity and cell cycle arrest.	perifosine	0-10	P53	Homo sapiens	106-109
11888912-12	2002	These data, therefore, indicate that perifosine blocks cell cycle progression of head and neck squamous carcinoma cells at G(1)-S and G(2)-M by inducing p21(WAF1), irrespective of p53 function, and may be exploited clinically because the majority of human malignancies harbor p53 mutations.	perifosine	37-47	P53	Homo sapiens	276-279
11888918-11	2002	In the latter case, &gt; or = 80% of the PEN-induced apoptosis was dependent on the presence of wild-type p53.	Penicillamine	41-44	P53	Homo sapiens	106-109
18445521-5	2008	In contrast to irinotecan, ST1968 still showed an excellent, persisting activity in models less susceptible to apoptosis induction (KB, Caski and SiHa), in which drug treatment elicited a persistent DNA damage response, as documented by phosphorylation of p53, RPA-2 and histone H2AX, resulting in delayed apoptosis and senescence.	namitecan	27-33	P53	Homo sapiens	256-259
11850838-5	2002	Adenoviral delivery of p53 resulted in potent inhibition in production of proMMP-13 (by 71 to 92%) and collagenase-1 (MMP-1) (by 27 to 93%) by all cell lines in 24 h, whereas production of gelatinase-A (MMP-2) and gelatinase-B (MMP-9) was not altered.	prommp-13	74-83	P53	Homo sapiens	23-26
11862321-4	2002	Cells with different states of p53 expression, either endogenously or ectopically, were exposed to hydroxyurea to induce an imbalance of cellular dNTP pools and cause replication errors.	Parathion	146-150	P53	Homo sapiens	31-34
12065876-2	2002	METHODS: The expression of p53 and mdm2 was analyzed by an immunohistochemical assay in 80 formalin-fixed paraffin embedded primary tumour samples and related to the clinical response to 5-fluorouracil therapy and to the prognosis of the patients.	Formaldehyde	91-99	P53	Homo sapiens	27-30
16624386-13	2006	CIZAR increased the expression of p21(waf1) which is a part of p53-independent pathway and induced reduction of telomerase activity.	cizar	0-5	P53	Homo sapiens	63-66
18598164-7	2008	Up-regulation of p21(CIP1/WAF1) was found to be mediated by a p53-dependent pathway in EAPP-induced G(1)-arrested A172 cells.	eapp	87-91	P53	Homo sapiens	62-65
16826403-10	2006	CONCLUSION: The AN-7 combined with doxorubicin overcame drug resistance; at least in part by the intracellularly releasable formaldehyde that augmented formation of doxorubicin-DNA adducts and butyric acid that induced histone and p53 acetylation.	Formaldehyde	124-136	P53	Homo sapiens	231-234
17050670-5	2006	We show that p53 binds to a 10-bp perfect palindromic decanucleotide (GTGACGTCAC) in the ECK promoter, activates the ECK promoter, and increases the transcription of ECK.	decanucleotide	54-68	P53	Homo sapiens	13-16
11696352-0	2001	Transcriptional repression of the human p53 gene by cobalt chloride mimicking hypoxia.	cobaltous chloride	52-67	P53	Homo sapiens	40-43
11696352-2	2001	We herein report that the transcription of the human p53 gene was repressed by treatment with a hypoxia-mimicking concentration of cobalt chloride and alone by hypoxia-inducible factor 1alpha.	cobaltous chloride	131-146	P53	Homo sapiens	53-56
17094452-8	2006	Silvestrol caused a dose-dependent decrease in p53 protein within 30 min of exposure with no p53 detectable after 6 h. Down-regulation of p53 by silvestrol was associated with down-regulation of MDM2 and not prevented by lactacystin suggesting that silvestrol-induced degradation of p53 is not mediated by the proteasome.	silvestrol	0-10	P53	Homo sapiens	47-50
11710597-1	2001	PURPOSE: To establish the relationship between the number and site of p53 genomic mutations in metastatic colorectal cancer, and the response to hepatic arterial floxuridine.	Floxuridine	162-173	P53	Homo sapiens	70-73
18400537-10	2008	These studies indicate that p53 specifically drives de novo ceramide synthesis by activation of a ceramide synthase that favors the synthesis of N-palmitoylsphingosine.	N-palmitoylsphingosine	145-167	P53	Homo sapiens	28-31
17094452-10	2006	These data demonstrate that cytotoxicity induced by silvestrol in LNCaP cells is associated with a block in the cell cycle at the G2/M checkpoint and alterations in the expression of genes regulating apoptosis and cell cycle in a manner independent of p53.	silvestrol	52-62	P53	Homo sapiens	252-255
16574813-5	2006	Moreover, the data herein clearly show that ganglioside GM3 induces p53-dependent transcriptional activity of p21(WAF1), as evidenced by the p21(WAF1) promoter-driven luciferase reporter plasmid (full-length p21(WAF1) promoter and a construct lacking the p53-binding sites).	gm3	56-59	P53	Homo sapiens	255-258
18071310-10	2008	These results suggest that abrogation of G2 checkpoint by GM may play a central role in sensitizing p53-negative tumor cells to DNA-damaging and decatenation-inhibiting agents.	geldanamycin	58-60	P53	Homo sapiens	100-103
16574813-8	2006	On the contrary, suppression of PTEN levels by RNA interference restores the enhanced expression of p53-dependent p21(WAF1) and p53-independent p27(kip1) through inactivating the effect of PTEN on PI-3K/AKT signaling modulated by ganglioside GM3.	gm3	242-245	P53	Homo sapiens	100-103
16574813-8	2006	On the contrary, suppression of PTEN levels by RNA interference restores the enhanced expression of p53-dependent p21(WAF1) and p53-independent p27(kip1) through inactivating the effect of PTEN on PI-3K/AKT signaling modulated by ganglioside GM3.	gm3	242-245	P53	Homo sapiens	128-131
21059310-4	2001	p53 genemutation was detected by polymerase chain reaction ( PCR)-single strand conformation polymorphism ( SSCP)-silver staining technique and the mutated p53 gene specimen was analysed by DNA-sequencing .	Silver	114-120	P53	Homo sapiens	0-3
18489080-10	2008	By contrast, micromolar concentrations of (+/-)- anti-BPDE generated (+)- trans- anti-BPDE-N (2)-dGuo adducts (detected by stable-isotope dilution LC/MS methodology) in p53 cDNA that correlated in a linear fashion with mutagenic frequency, but no 8-oxo-dGuo was detected.	(+/-)- anti-	42-54	P53	Homo sapiens	169-172
11526536-4	2001	PNP/fludarabine induced strong p53 accumulation and a more rapid onset of apoptosis in p53-positive HepG2 cells as compared with p53-negative Hep3B cells, but efficiency of tumor cell killing was similar in both cell lines.	fludarabine	4-15	P53	Homo sapiens	31-34
11526536-4	2001	PNP/fludarabine induced strong p53 accumulation and a more rapid onset of apoptosis in p53-positive HepG2 cells as compared with p53-negative Hep3B cells, but efficiency of tumor cell killing was similar in both cell lines.	fludarabine	4-15	P53	Homo sapiens	87-90
16614167-6	2006	Cyclin B/CDC2(CDK1) stabilization and caspase-3 activation persisted in arsenite-treated p53- cells consistent with MAAA/mitotic catastrophe.	arsenite	72-80	P53	Homo sapiens	89-92
11526536-4	2001	PNP/fludarabine induced strong p53 accumulation and a more rapid onset of apoptosis in p53-positive HepG2 cells as compared with p53-negative Hep3B cells, but efficiency of tumor cell killing was similar in both cell lines.	fludarabine	4-15	P53	Homo sapiens	87-90
18454047-0	2008	The novel platinum(IV) complex LA-12 induces p53 and p53/47 responses that differ from the related drug, cisplatin.	UNII-37WM0V5E17	31-36	P53	Homo sapiens	45-48
11521201-4	2001	We observed that an unmodified C-terminus was required for the suppression of apoptosis by the p53 135(Ala to Val) oncogenic p53 mutant.	Valine	110-113	P53	Homo sapiens	95-98
11521201-4	2001	We observed that an unmodified C-terminus was required for the suppression of apoptosis by the p53 135(Ala to Val) oncogenic p53 mutant.	Valine	110-113	P53	Homo sapiens	125-128
16614167-9	2006	CDC2-Y15-P was transiently elevated in arsenite-treated p53+ cells but persisted in p53- cells.	arsenite	39-47	P53	Homo sapiens	56-59
16614167-10	2006	Arsenite induced p53-S15-P and p21CIP1/WAF1 only in p53+ cells.	arsenite	0-8	P53	Homo sapiens	17-20
16614167-10	2006	Arsenite induced p53-S15-P and p21CIP1/WAF1 only in p53+ cells.	arsenite	0-8	P53	Homo sapiens	52-55
16702812-0	2006	Octahedral Pt(IV) complex K101 induces apoptosis via ERK1/2 activation and the p53 pathway in human colon cancer cells.	THIAMINE HYDROCHLORIDE	26-30	P53	Homo sapiens	79-82
18454047-0	2008	The novel platinum(IV) complex LA-12 induces p53 and p53/47 responses that differ from the related drug, cisplatin.	UNII-37WM0V5E17	31-36	P53	Homo sapiens	53-56
18454047-3	2008	We tested the effects of LA-12 on the p53 response and demonstrate that LA-12 induces unique changes in the profile of gene expression compared with cisplatin and doxorubicin.	UNII-37WM0V5E17	72-77	P53	Homo sapiens	38-41
16407843-3	2006	In human colon carcinoma HCT116 cells with wild-type (wt) p53, gammaH2AX reverses after camptothecin removal.	gammah2ax	63-72	P53	Homo sapiens	58-61
11489357-1	2001	In a previous study we reported that methylation within the promoter region of p53 was altered in human lung A549 cells exposed to arsenite over a 2-week period in culture.	arsenite	131-139	P53	Homo sapiens	79-82
18454047-4	2008	Furthermore, the ability of LA-12 to disrupt cellular proliferation is greatly enhanced by the expression of p53 and p53/47 indicating both p53-dependent and p53-independent effects of LA-12.	UNII-37WM0V5E17	28-33	P53	Homo sapiens	109-112
11699407-2	2001	The effects of combining a phosphorothioate oligonucleotide OL(1) p53, which transiently down-regulates p53 levels, with an anthracycline, Idarubicin, on the growth of wild-type p53 WMN gene-expressing lymphoma cells was evaluated.	Parathion	27-43	P53	Homo sapiens	104-107
18454047-4	2008	Furthermore, the ability of LA-12 to disrupt cellular proliferation is greatly enhanced by the expression of p53 and p53/47 indicating both p53-dependent and p53-independent effects of LA-12.	UNII-37WM0V5E17	28-33	P53	Homo sapiens	117-120
11699407-2	2001	The effects of combining a phosphorothioate oligonucleotide OL(1) p53, which transiently down-regulates p53 levels, with an anthracycline, Idarubicin, on the growth of wild-type p53 WMN gene-expressing lymphoma cells was evaluated.	Parathion	27-43	P53	Homo sapiens	104-107
16445975-13	2006	Statistical analyses showed significant positive correlations (p &lt; 0.001) between the presence of polyethylene and metal debris and the expression of BAK and p53.	Polyethylene	101-113	P53	Homo sapiens	161-164
18454047-4	2008	Furthermore, the ability of LA-12 to disrupt cellular proliferation is greatly enhanced by the expression of p53 and p53/47 indicating both p53-dependent and p53-independent effects of LA-12.	UNII-37WM0V5E17	28-33	P53	Homo sapiens	117-120
18454047-4	2008	Furthermore, the ability of LA-12 to disrupt cellular proliferation is greatly enhanced by the expression of p53 and p53/47 indicating both p53-dependent and p53-independent effects of LA-12.	UNII-37WM0V5E17	28-33	P53	Homo sapiens	117-120
11406180-0	2001	Effects of arsenite on p53, p21 and cyclin D expression in normal human fibroblasts -- a possible mechanism for arsenite"s comutagenicity.	arsenite	112-120	P53	Homo sapiens	23-26
11406180-3	2001	To determine whether arsenite affects signaling which might alter DNA repair, this study assesses the effect of arsenite on p53-related signal transduction pathways after ionizing radiation.	arsenite	112-120	P53	Homo sapiens	124-127
11406180-4	2001	Long-term (14 day) low dose (0.1 microM) arsenite caused a modest increase in p53 expression in WI38 normal human fibroblasts, while only toxic (50 microM) concentrations increased p53 levels after short-term (18 h) exposure.	arsenite	41-49	P53	Homo sapiens	78-81
11406180-8	2001	These results show that in cells treated with arsenite, p53-dependent increase in p21 expression, normally a block to cell cycle progression after DNA damage, is deficient.	arsenite	46-54	P53	Homo sapiens	56-59
16700663-5	2006	An immunohistochemical method was used to investigate the expression of COX-2 and p53 proteins on formalin-fixed, paraffin-embedded tissue specimens of squamous cell carcinomas (SCC), basal cell carcinomas (BCC), Bowen"s disease (BD), actinic keratosis (AK) and porokeratosis.	Formaldehyde	98-106	P53	Homo sapiens	82-85
11406180-10	2001	We suggest that the absence of normal p53 functioning, along with increased positive growth signaling in the presence of DNA damage may result in defective DNA repair and account for the comutagenic effects of arsenite.	arsenite	210-218	P53	Homo sapiens	38-41
18454047-5	2008	Exposure of the human cancer cell lines H1299, A2780, BT549 and BT474 to LA-12 alters the expression of p53 and p53/47 in both a time-dependent and dose-dependent manner.	UNII-37WM0V5E17	73-78	P53	Homo sapiens	104-107
18454047-5	2008	Exposure of the human cancer cell lines H1299, A2780, BT549 and BT474 to LA-12 alters the expression of p53 and p53/47 in both a time-dependent and dose-dependent manner.	UNII-37WM0V5E17	73-78	P53	Homo sapiens	112-115
16682816-1	2006	The effect of poly(ADP-ribosyl)ation on the stability of p53 in SK-HEP1 cells treated with UV light was examined.	poly(adp-ribosyl)	14-31	P53	Homo sapiens	57-60
11429707-0	2001	Contrasting roles of NF-kappaB and JNK in arsenite-induced p53-independent expression of GADD45alpha.	arsenite	42-50	P53	Homo sapiens	59-62
18454047-7	2008	The distinct p53 activation profile of LA-12 compared with cisplatin and doxorubicin provides a molecular explanation for the ability of this drug to treat cisplatin-resistant cells and indicates its potential usefulness as an alternative antitumour agent in first-line therapy or as a second-line therapy in patients with acquired cisplatin resistance.	UNII-37WM0V5E17	39-44	P53	Homo sapiens	13-16
11429707-2	2001	We report here that arsenite induces GADD45alpha expression in a p53-independent fashion and that this GADD45alpha induction by arsenite is regulated by NF-kappaB and c-Jun-N-terminal kinase (JNK) oppositely.	arsenite	20-28	P53	Homo sapiens	65-68
11429707-6	2001	Analysis of GADD45alpha expression in both wild-type and p53-/- fibroblasts indicated that the induction of GADD45alpha by arsenite was independent of the status of p53 protein.	arsenite	123-131	P53	Homo sapiens	57-60
16288207-6	2006	Suppression of sGC activity with the specific inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) lowered cGMP content, and increased p53 protein content and induced apoptosis in three ovarian cancer cell lines, effects which were attenuated by the cGMP analog 8-Br-cGMP and by Atrial Natriuretic Factor, an activator of particulate guanylyl cyclase, which circumvent the inhibition of sGC.	1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one	56-99	P53	Homo sapiens	142-145
16288207-6	2006	Suppression of sGC activity with the specific inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) lowered cGMP content, and increased p53 protein content and induced apoptosis in three ovarian cancer cell lines, effects which were attenuated by the cGMP analog 8-Br-cGMP and by Atrial Natriuretic Factor, an activator of particulate guanylyl cyclase, which circumvent the inhibition of sGC.	1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one	101-104	P53	Homo sapiens	142-145
16288207-9	2006	Pretreatment with the specific p53 inhibitor pifithrin or downregulation of p53 using a specific small inhibitory RNA significantly attenuated ODQ-induced apoptosis.	1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one	143-146	P53	Homo sapiens	31-34
16288207-9	2006	Pretreatment with the specific p53 inhibitor pifithrin or downregulation of p53 using a specific small inhibitory RNA significantly attenuated ODQ-induced apoptosis.	1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one	143-146	P53	Homo sapiens	76-79
12578616-2	2001	The effects of exogenous wt-p53 gene on the proliferation and differentiation of K562 cells were studied by detection of cell growth curves, leukemic colony formation, cell cycle analysis and DNA fragmentation, TdT-mediated dUTP nick end labeling (TUNEL) and benzidine staining.	benzidine	259-268	P53	Homo sapiens	28-31
17610029-8	2008	We conclude that selenite induces caspase-independent apoptosis in cervical carcinoma cells mostly by oxidative stress-mediated activation of p53 and p38 pathways, but other selenite-mediated effects, in particular mitochondria-specific ones, are also involved.	Selenious Acid	17-25	P53	Homo sapiens	142-145
16288207-10	2006	Moreover, ODQ-induced upregulation of p21 and Bax and ODQ-induced apoptosis were significantly reduced in a p53 mutant cell line relative to the wild-type parental cell line.	1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one	10-13	P53	Homo sapiens	108-111
16288207-10	2006	Moreover, ODQ-induced upregulation of p21 and Bax and ODQ-induced apoptosis were significantly reduced in a p53 mutant cell line relative to the wild-type parental cell line.	1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one	54-57	P53	Homo sapiens	108-111
11358811-3	2001	We identified mutations in exons 5-8 of p53 using DNA extracted from formalin-fixed paraffin-embedded tissue blocks from 146 whites and 26 non-whites with astrocytic glioma by PCR-single-strand conformation polymorphism and direct sequencing.	Formaldehyde	69-77	P53	Homo sapiens	40-43
17554785-3	2008	Sequence analysis of the patient"s p53 gene revealed a novel germline three base-pair deletion (339_341delCTT) in exon 4, resulting in removal of an evolutionarily conserved phenylalanine amino acid residue at codon 113.	phenylalanine amino acid	174-198	P53	Homo sapiens	35-38
11340094-6	2001	Treatment of Hep G2 cells with increasing concentrations of the copper chelator tetraethylenepentamine (TEPA, 0-50 micromol/L, 48 h) reduced cellular copper and increased mean p53 mRNA abundance by over fourfold with nuclear translocation of the wild-type protein.	tetraethylenepentamine	80-102	P53	Homo sapiens	176-179
11340094-6	2001	Treatment of Hep G2 cells with increasing concentrations of the copper chelator tetraethylenepentamine (TEPA, 0-50 micromol/L, 48 h) reduced cellular copper and increased mean p53 mRNA abundance by over fourfold with nuclear translocation of the wild-type protein.	tetraethylenepentamine	104-108	P53	Homo sapiens	176-179
16529749-0	2006	Alpha-tocopheryl succinate induces DR4 and DR5 expression by a p53-dependent route: implication for sensitisation of resistant cancer cells to TRAIL apoptosis.	alpha-Tocopherol	0-26	P53	Homo sapiens	63-66
16529749-2	2006	We show that alpha-TOS activates expression of DR4/DR5 in a p53-dependent manner and re-establishes sensitivity of resistant MM cells to TRAIL-mediated apoptosis, as documented in p53wt MM cells but not in their p53null counterparts.	alpha-Tocopherol	13-22	P53	Homo sapiens	60-63
16529749-2	2006	We show that alpha-TOS activates expression of DR4/DR5 in a p53-dependent manner and re-establishes sensitivity of resistant MM cells to TRAIL-mediated apoptosis, as documented in p53wt MM cells but not in their p53null counterparts.	alpha-Tocopherol	13-22	P53	Homo sapiens	180-183
16529749-2	2006	We show that alpha-TOS activates expression of DR4/DR5 in a p53-dependent manner and re-establishes sensitivity of resistant MM cells to TRAIL-mediated apoptosis, as documented in p53wt MM cells but not in their p53null counterparts.	alpha-Tocopherol	13-22	P53	Homo sapiens	180-183
16501812-0	2006	Fludarabine induces apoptosis in chronic lymphocytic leukemia--the role of P53, Bcl-2, Bax, Mcl-1, and Bag-1 proteins.	fludarabine	0-11	P53	Homo sapiens	75-78
11401473-7	2001	Increasing drug sensitivity of cervical carcinoma cells by stabilizing P53 using vitamin C is a novel approach and has potential clinical relevance.	Ascorbic Acid	81-90	P53	Homo sapiens	71-74
18506998-11	2008	Immunohistochemical staining showed increased expression of p65 after paclitaxel treatment, while paclitaxel in combination with AdIkappaBalpha intratumoral injection eliminated this expression accompanied by the slightly reduced expression of VEGF, with stable p53 status.	adikappabalpha	129-143	P53	Homo sapiens	262-265
11160753-5	2001	DNA-PKcs that was bound to EBNA-LP phosphorylated p53 or EBNA-LP in vitro, and the phosphorylation of EBNA-LP was inhibited by Wortmannin, a specific in vitro inhibitor of DNA-PKcs.	ebna-lp	27-34	P53	Homo sapiens	50-53
16338954-10	2006	Arsenite raised the levels of phospho-p53 (serine-15) and p53 (DO-1) proteins in both the securin-wild-type and -null cells.	arsenite	0-8	P53	Homo sapiens	38-41
18630678-10	2008	CONCLUSION: The telomerase activation and mutant P53 expression in MDA-MB-435s cells are related to HSP90 function, of which the inhibition with GA can decrease the telomerase activity and the protein expression of mutant P53, and further repress the proliferation of MDA-MB-435s cells.	geldanamycin	145-147	P53	Homo sapiens	49-52
16338954-10	2006	Arsenite raised the levels of phospho-p53 (serine-15) and p53 (DO-1) proteins in both the securin-wild-type and -null cells.	arsenite	0-8	P53	Homo sapiens	58-61
16338954-11	2006	The p53-functional cells were more susceptible than the p53-mutational cells to arsenite on the cytotoxicity and apoptosis.	arsenite	80-88	P53	Homo sapiens	4-7
16338954-11	2006	The p53-functional cells were more susceptible than the p53-mutational cells to arsenite on the cytotoxicity and apoptosis.	arsenite	80-88	P53	Homo sapiens	56-59
16338954-12	2006	Besides, arsenite decreased the levels of securin proteins to a similar degree in both the p53-functional and -mutational cells.	arsenite	9-17	P53	Homo sapiens	91-94
16338954-13	2006	Together, it is the first time to demonstrate that the inhibition of securin expression induced by arsenite increases the chromosomal instability and apoptosis via a p53-independent pathway.	arsenite	99-107	P53	Homo sapiens	166-169
16489034-0	2006	Expression of p53 enhances selenite-induced superoxide production and apoptosis in human prostate cancer cells.	Selenious Acid	27-35	P53	Homo sapiens	14-17
11166732-4	2001	High p53 protein levels, but not genetic or functional p53 status, were associated with increased topotecan-induced DNA/topoisomerase I complex formation.	Topotecan	98-107	P53	Homo sapiens	5-8
11146441-10	2001	Co-incubation with p53 anti-sense oligo-nucleotide suppressed As(2)O(3)-induced intracellular p53 over-expression and apoptosis.	(2)o(3)	64-71	P53	Homo sapiens	19-22
11146441-10	2001	Co-incubation with p53 anti-sense oligo-nucleotide suppressed As(2)O(3)-induced intracellular p53 over-expression and apoptosis.	(2)o(3)	64-71	P53	Homo sapiens	94-97
11146441-13	2001	As(2)O(3) inhibits cell growth and induces apoptosis in gastric cancer cells, involving p53 over-expression and activation of caspase-3.	(2)o(3)	2-9	P53	Homo sapiens	88-91
16489034-3	2006	In the present study, we showed that selenite-induced apoptosis was superoxide mediated and p53 dependent via mitochondrial pathways.	Selenious Acid	37-45	P53	Homo sapiens	92-95
18630678-10	2008	CONCLUSION: The telomerase activation and mutant P53 expression in MDA-MB-435s cells are related to HSP90 function, of which the inhibition with GA can decrease the telomerase activity and the protein expression of mutant P53, and further repress the proliferation of MDA-MB-435s cells.	geldanamycin	145-147	P53	Homo sapiens	222-225
16489034-4	2006	In addition, we also showed that superoxide production by selenite was p53 dependent.	Selenious Acid	58-66	P53	Homo sapiens	71-74
17984113-9	2008	NS-398, a COX-2 inhibitor, did not affect ERK1/2 activation, but reduced the nuclear abundance of COX-2 protein and the formation of complexes of nuclear COX-2 and activated ERK1/2 that are required for p53-dependent apoptosis in RV-treated cells.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	0-6	P53	Homo sapiens	203-206
16489034-5	2006	Our study showed that wild-type p53-expressing LNCaP cells were more sensitive to selenite-induced apoptosis than p53-null PC3 cells.	Selenious Acid	82-90	P53	Homo sapiens	32-35
16489034-8	2006	The effects of selenite were suppressed by pretreatment with a synthetic superoxide dismutase mimic or by knockdown of p53 via RNA interference.	Selenious Acid	15-23	P53	Homo sapiens	119-122
11752901-0	2001	Bromodeoxyuridine induces p53-dependent and -independent cell cycle arrests in human gastric carcinoma cell lines.	Bromodeoxyuridine	0-17	P53	Homo sapiens	26-29
11752901-6	2001	CONCLUSIONS: These data suggested that the BrdU-induced growth suppression of the cell lines examined was mainly caused by cell cycle arrest rather than cell death, and that the cell cycle arrests in the first S and G(1) phases (elicited by BrdU in the single DNA strand) and those in the second S, G(2) and G(1) phases (elicited by BrdU in the double DNA strands) were mediated by p53-dependent and -independent pathways, respectively.	Bromodeoxyuridine	43-47	P53	Homo sapiens	382-385
18403247-8	2008	We found that oncogenes c-myc, c-fos and tumor suppressor genes, P53, Rb were regulated by ginsenoside Rg1, cinnamic acid, and tanshinone IIA as well.	cinnamic acid	108-121	P53	Homo sapiens	65-68
11134551-7	2001	Exposure to 250 microM or 1000 microM phenytoin also elicited a relatively minor (less than 2-fold) but significant increase in p53 steady-state mRNA expression.	Phenytoin	38-47	P53	Homo sapiens	128-131
16489034-9	2006	LNCaP cells treated with selenite also showed p53 translocation to mitochondria, cytochrome c release into the cytosol, and activation of caspase-9.	Selenious Acid	25-33	P53	Homo sapiens	46-49
16489034-11	2006	These results suggest that selenite induces apoptosis by producing superoxide to activate p53 and to induce p53 mitochondrial translocation.	Selenious Acid	27-35	P53	Homo sapiens	90-93
16489034-11	2006	These results suggest that selenite induces apoptosis by producing superoxide to activate p53 and to induce p53 mitochondrial translocation.	Selenious Acid	27-35	P53	Homo sapiens	108-111
16489034-12	2006	Activation of p53 in turn synergistically enhances superoxide production and apoptosis induced by selenite.	Selenious Acid	98-106	P53	Homo sapiens	14-17
18253895-0	2008	Paraquat-induced apoptosis in human neuroblastoma SH-SY5Y cells: involvement of p53 and mitochondria.	Paraquat	0-8	P53	Homo sapiens	80-83
16273229-3	2005	There is evidence that non-steroidal anti-inflammatory drugs, e.g. sulindac, have some anti-proliferative effects on various tumors involving altered p53 function.	Sulindac	67-75	P53	Homo sapiens	150-153
16273229-5	2005	Therefore, the present study was undertaken to analyze the differentially expressed genes of the p53 signaling pathway by means of a gene array for the immortalized human breast epithelial cell line, MCF-10F, treated with sulindac.	Sulindac	222-230	P53	Homo sapiens	97-100
16273229-11	2005	The alteration of p53 signaling pathway gene markers by sulindac treatment can give us valuable information about the response to drug treatments in a proliferative cell population.	Sulindac	56-64	P53	Homo sapiens	18-21
11133809-0	2000	Differential gene expression in p53-mediated G(1) arrest of human fibroblasts after gamma-irradiation or N-phosphoacetyl-L-aspartate treatment.	n-phosphoacetyl-l-aspartate	105-132	P53	Homo sapiens	32-35
11103796-0	2000	Arsenite induces p53 accumulation through an ATM-dependent pathway in human fibroblasts.	arsenite	0-8	P53	Homo sapiens	17-20
11103796-3	2000	Because p53 plays a guarding role in maintaining genome integrity and accuracy of chromosome segregation, the mechanistic effects of arsenite on p53 activation were analyzed.	arsenite	133-141	P53	Homo sapiens	145-148
11103796-5	2000	Accompanying the appearance of DNA strand breaks was a significant accumulation of p53 in arsenite-treated HFW cells, as demonstrated by immunoblotting and immunofluorescence techniques.	arsenite	90-98	P53	Homo sapiens	83-86
11103796-6	2000	p53 downstream proteins, such as p21 and the human homologue of murine double minute-2, were also significantly induced by arsenite treatment.	arsenite	123-131	P53	Homo sapiens	0-3
11268475-3	2000	PATIENTS AND METHODS: Nuclear immunohistochemical expression of p53 protein was determined in formalin-fixed paraffin-embedded archival tumor tissue samples from 190 primary colorectal adenocarcinomas.	Formaldehyde	94-102	P53	Homo sapiens	64-67
16287968-3	2005	Among the compounds isolated were derivatives of 9-aminoacridine (9AA), including the antimalaria drug quinacrine, which strongly induced p53 function in RCC and other types of cancer cells.	Quinacrine	103-113	P53	Homo sapiens	138-141
16287968-8	2005	The results demonstrate, in principle, the possibility to kill cancer cells selectively through simultaneous inhibition of NF-kappaB and activation of p53 by a single small molecule and suggest anticancer applications for the well known antimalaria drug quinacrine.	Quinacrine	254-264	P53	Homo sapiens	151-154
18253895-4	2008	Based on reported evidence that paraquat increases p53 protein levels and inhibits mitochondrial function, it was hypothesized that paraquat induces cell death in dopaminergic neurons through a mechanism in which p53 and mitochondrial apoptotic pathway are linked.	Paraquat	32-40	P53	Homo sapiens	51-54
16507397-0	2005	Study of COX-2, Ki67, and p53 expression to predict effectiveness of 5-flurouracil, epirubicin and cyclophosphamide with celecoxib treatment in breast cancer patients.	5-flurouracil	69-82	P53	Homo sapiens	26-29
18253895-4	2008	Based on reported evidence that paraquat increases p53 protein levels and inhibits mitochondrial function, it was hypothesized that paraquat induces cell death in dopaminergic neurons through a mechanism in which p53 and mitochondrial apoptotic pathway are linked.	Paraquat	32-40	P53	Homo sapiens	213-216
10880954-5	2000	When the responses of the tumour suppressors p53 and RB were analysed, it was found that TNF-alpha and C8-ceramide induced increased expression of p53.	2,3-N-octanoylsphingosine	103-114	P53	Homo sapiens	45-48
10880954-5	2000	When the responses of the tumour suppressors p53 and RB were analysed, it was found that TNF-alpha and C8-ceramide induced increased expression of p53.	2,3-N-octanoylsphingosine	103-114	P53	Homo sapiens	147-150
18253895-4	2008	Based on reported evidence that paraquat increases p53 protein levels and inhibits mitochondrial function, it was hypothesized that paraquat induces cell death in dopaminergic neurons through a mechanism in which p53 and mitochondrial apoptotic pathway are linked.	Paraquat	132-140	P53	Homo sapiens	51-54
10880954-6	2000	Treatment with TNF-alpha or C8-ceramide lead to a significant decrease in total retinoblastoma protein (RB) content that correlated with high levels of p53.	2,3-N-octanoylsphingosine	28-39	P53	Homo sapiens	152-155
15905198-0	2005	Novel genotoxicity assays identify norethindrone to activate p53 and phosphorylate H2AX.	Norethindrone	35-48	P53	Homo sapiens	61-64
18253895-4	2008	Based on reported evidence that paraquat increases p53 protein levels and inhibits mitochondrial function, it was hypothesized that paraquat induces cell death in dopaminergic neurons through a mechanism in which p53 and mitochondrial apoptotic pathway are linked.	Paraquat	132-140	P53	Homo sapiens	213-216
15905198-2	2005	We applied a novel and particularly sensitive method to screen for DNA damage with special attention to double-strand breaks (DSBs) and identified norethindrone to be likely genotoxic and therefore potentially mutagenic: a p53-reporter assay served as a first, high-throughput screening method and was followed by the immunofluorescent detection of phosphorylated H2AX as a sensitive assay for the presence of DSBs.	Norethindrone	147-160	P53	Homo sapiens	223-226
15905198-3	2005	Norethindrone at concentrations of 2-100 microg/ml activated p53 and phosphorylated H2AX specifically and in a dose-dependent manner.	Norethindrone	0-13	P53	Homo sapiens	61-64
18253895-11	2008	These findings support the conclusion that paraquat produced apoptosis in SY5Y cells through the mitochondrial intrinsic pathway associated with p53.	Paraquat	43-51	P53	Homo sapiens	145-148
18089819-9	2007	Therefore, functional p53 seems to stimulate the repair of CNU-induced cross-links and/or DSBs generated from CNU-induced lesions.	1-(2-chloroethyl)-1-nitrosourea	59-62	P53	Homo sapiens	22-25
15993080-3	2005	The introduced N at position 8 of the purine ring generally lowered CDK2 inhibitory activity of new 8-azapurines (1,2,3-triazolo[4,5-d]pyrimidines) in comparison to the model trisubstituted purines, whereas the antiproliferative potential of some derivatives remained very high, reflecting their ability to activate p53 tumor suppressor.	triazolopyrimidinone	100-112	P53	Homo sapiens	316-319
16109309-8	2005	The peroxide-resistant cells are diploid rather than aneuploid, show fundamental changes in the cytoskeletal cellular structure, suggesting less rigid more flexible cells, express a new lower molecular mass of p53, a key stress protein responder involved in adaptation, and finally have an immunochemical modification in alphaA-crystallin, a small heat-shock protein.	Peroxides	4-12	P53	Homo sapiens	210-213
10850547-2	2000	A novel polymerase chain reaction (PCR) approach for the analysis of the entire p53 coding and splice site regions from microdissected, formalin-fixed, paraffin-embedded tumor tissues has been developed which allows multiple genetic analyses to be performed from one primary amplification reaction.	Formaldehyde	136-144	P53	Homo sapiens	80-83
18089819-9	2007	Therefore, functional p53 seems to stimulate the repair of CNU-induced cross-links and/or DSBs generated from CNU-induced lesions.	1-(2-chloroethyl)-1-nitrosourea	110-113	P53	Homo sapiens	22-25
10874665-6	2000	Mdm2 and p53 were demonstrated by immunohistology on formalin-fixed and paraffin-embedded tumor tissue.	Formaldehyde	53-61	P53	Homo sapiens	9-12
17906315-8	2007	In addition, the expression of mutant p53 increased in parallel with comet scores, and the maximal expression of mutant p53 was observed at 4 microM arsenite.	arsenite	149-157	P53	Homo sapiens	38-41
10897337-3	2000	This is a highly selective approach, whereby immunostained sections of formalin fixed, paraffin wax embedded tissue are exposed to ultraviolet irradiation to damage the DNA in p53 negative cells.	Formaldehyde	71-79	P53	Homo sapiens	176-179
15946692-3	2005	This study was undertaken to dissect the molecular mechanism underlying sulindac-induced apoptosis in human colon cancer cell line HT-29 (mutant p53), focusing on nuclear translocation of AIF, DFF and endonuclease G.	Sulindac	72-80	P53	Homo sapiens	145-148
15950406-0	2005	Effects on protein and mRNA expression levels of p53 induced by fluoride in human embryonic hepatocytes.	Fluorides	64-72	P53	Homo sapiens	49-52
10815759-2	2000	Therefore, we investigated the utility of new heterodinucleoside phosphate dimers of 5-fluorodeoxyuridine (5-FdUrd) in p53-mutated and androgen-independent DU-145 human prostate tumour cells.	Floxuridine	85-105	P53	Homo sapiens	119-122
17906315-8	2007	In addition, the expression of mutant p53 increased in parallel with comet scores, and the maximal expression of mutant p53 was observed at 4 microM arsenite.	arsenite	149-157	P53	Homo sapiens	120-123
10815759-2	2000	Therefore, we investigated the utility of new heterodinucleoside phosphate dimers of 5-fluorodeoxyuridine (5-FdUrd) in p53-mutated and androgen-independent DU-145 human prostate tumour cells.	Floxuridine	107-114	P53	Homo sapiens	119-122
15950406-1	2005	We investigated the effects of protein and mRNA expression levels on p53 induced by fluoride in human embryo hepatocyte L-02 cells.	Fluorides	84-92	P53	Homo sapiens	69-72
15950406-2	2005	The protein and mRNA levels of p53 in L-02 cells were measured after in vitro cultured L-02 was exposed to sodium fluoride at different doses (40, 80, and 160 microg/ml) for 24 h. The results showed that the cell survival rate of L-02 cells in the high dose fluoride group was significantly lower than that of the control group.	Fluorides	114-122	P53	Homo sapiens	31-34
15950406-3	2005	The protein expression levels of p53 in the middle and high dose fluoride group were significantly higher than in the control group and elevated with increasing fluoride concentration.	Fluorides	65-73	P53	Homo sapiens	33-36
15950406-3	2005	The protein expression levels of p53 in the middle and high dose fluoride group were significantly higher than in the control group and elevated with increasing fluoride concentration.	Fluorides	161-169	P53	Homo sapiens	33-36
15950406-4	2005	The mRNA expression levels of p53 in the fluoride groups were markedly higher than in the control group.	Fluorides	41-49	P53	Homo sapiens	30-33
15950406-5	2005	The mRNA expression level of p53 in the high dose fluoride group was however lower compared to the middle dose fluoride group, but similar to the low dose fluoride group.	Fluorides	50-58	P53	Homo sapiens	29-32
10799338-6	2000	During the same time period lower concentrations of DBC (&lt;10 microM) induced the formation of DBC-DNA adducts and increased p53 protein levels followed by apoptotic cell death.	7H-dibenzo(c,g)carbazole	52-55	P53	Homo sapiens	127-130
15950406-5	2005	The mRNA expression level of p53 in the high dose fluoride group was however lower compared to the middle dose fluoride group, but similar to the low dose fluoride group.	Fluorides	111-119	P53	Homo sapiens	29-32
10799338-7	2000	However, increasing the concentration of DBC to 80 microM led to lower DNA adduct and p53 protein levels.	7H-dibenzo(c,g)carbazole	41-44	P53	Homo sapiens	86-89
17906315-11	2007	This study provides us with knowledge of the relationship between p53 and COX-2 over-expression in arsenite-treated urothelial cells and suggests a potential therapeutic role of COX-2 inhibitors in human urothelial malignancies.	arsenite	99-107	P53	Homo sapiens	66-69
10786699-6	2000	1alpha,25-Dihydroxyvitamin D3 and EB1089 induced p53-independent apoptosis in adenoma and carcinoma cell lines in a dose-dependent manner between 10(-10) and 10(-6) M. EB1089, as well as inducing apoptosis, increased the proportion of cells in the G1 phase, particularly in the adenoma cell lines.	seocalcitol	34-40	P53	Homo sapiens	49-52
15950406-5	2005	The mRNA expression level of p53 in the high dose fluoride group was however lower compared to the middle dose fluoride group, but similar to the low dose fluoride group.	Fluorides	111-119	P53	Homo sapiens	29-32
15950406-6	2005	These finding suggest that fluoride can decrease the L-02 cells survival rate and induce protein and mRNA expressions of p53; however, there is no consistency between the protein expression level of p53 and the mRNA expression level.	Fluorides	27-35	P53	Homo sapiens	121-124
17624594-8	2007	Western blot analyses showed that while pretreatment of TEA and Tet produced an increase in expressions of p53, p21, and Bax, pretreatment of these two agents led to a decrease in expressions of heat shock protein (hsp)90alpha, hsp90beta, and hsp70.	tetrandrine	64-67	P53	Homo sapiens	107-110
10751531-3	2000	Silver staining PCR-SSCP method was used to detect mutations in exons 5, 6, 7, 8 of p53 gene and MSI at 4 loci on chromosomes 2, 5, 17 in the 73 paraffin-embedded biopsy specimens, and the relationship between them was studied further.	Silver	0-6	P53	Homo sapiens	84-87
17909057-13	2007	Furthermore, PYR-41 inhibits degradation of p53 and activates the transcriptional activity of this tumor suppressor.	4(4-(5-nitro-furan-2-ylmethylene)-3,5-dioxo-pyrazolidin-1-yl)-benzoic acid ethyl ester	13-19	P53	Homo sapiens	44-47
10718209-7	2000	In the present study the authors optimized a polymerase chain reaction-based mutation screening method, fluorescence-single strand conformation polymorphism (F-SSCP), that allows p53 status to be assessed accurately and reproducibly in routinely handled, formalin-fixed and paraffin-embedded tumor specimens.	Formaldehyde	255-263	P53	Homo sapiens	179-182
15716589-1	2005	Recent studies have shown that an endogenous lipoperoxidation product, 9-hydroxystearic acid (9-HSA), acts in colon carcinoma cells (HT29) as a growth inhibitor by inducing p21(WAF1) in an immediate-early, p53-independent manner and that p21(WAF1) is required for 9-HSA-mediated growth arrest in HT29 cells.	9-hydroxystearic acid	71-92	P53	Homo sapiens	206-209
15716589-1	2005	Recent studies have shown that an endogenous lipoperoxidation product, 9-hydroxystearic acid (9-HSA), acts in colon carcinoma cells (HT29) as a growth inhibitor by inducing p21(WAF1) in an immediate-early, p53-independent manner and that p21(WAF1) is required for 9-HSA-mediated growth arrest in HT29 cells.	9-hydroxystearic acid	94-99	P53	Homo sapiens	206-209
15904897-8	2005	Our results also show that preincubation of HepG2 cells with vitamin C decreased the expression of p53 and bax and inhibited the release of cytochrome c, activation of downstream caspase and the cleavage of poly(ADP-ribose) polymerase, thus inhibiting the apoptosis inducing effect of 6ME.	Ascorbic Acid	61-70	P53	Homo sapiens	99-102
17666403-4	2007	In cells under elevated temperatures that contained a higher level of p53 mutant phenotype, CHIP restored the native-like conformation of p53 in the presence of geldanamycin, whereas CHIP-small interfering RNA considerably increased the mutant form.	geldanamycin	161-173	P53	Homo sapiens	138-141
15625077-8	2005	Thus, in HepG2 cells pravastatin and simvastatin pretreatment attenuated the p53 response to DNA damage induced by 5-fluorouracil and benzo(a)pyrene.	Simvastatin	37-48	P53	Homo sapiens	77-80
10690553-7	2000	This change resulted in a Val to Phe substitution and was associated with a constitutive production of high levels of p53, which was inactive as a transcriptional activator of bax and p21.	Valine	26-29	P53	Homo sapiens	118-121
17627614-0	2007	CR229, a novel derivative of beta-carbolin-1-one, induces cell cycle arrest and apoptosis in HeLa cells via p53 activation.	6-bromo-2,3,4,9-tetrahydrocarbolin-1-one	0-5	P53	Homo sapiens	108-111
11193587-0	2000	p53-independent apoptosis induced by menadione in the human colon carcinoma cell line Caco-2.	Vitamin K 3	37-46	P53	Homo sapiens	0-3
10618603-4	2000	Immunohistochemical expression of nuclear p53 protein was assessed in formalin fixed, paraffin embedded archival tumor tissue.	Formaldehyde	70-78	P53	Homo sapiens	42-45
15941514-4	2005	Streptavidin-peroxidase immunohistochemical technique was used to detect the expression of p53, C-erbB-2, nm23-H(1) and Ras on formalin-fixed, paraffin embedded sections of CRC from the 120 patients.	Formaldehyde	127-135	P53	Homo sapiens	91-94
15613472-7	2005	Mutant reactivation is enhanced by simultaneous treatment with agents that stabilize the reactivated protein and is blocked by geldanamycin, a specific inhibitor of Hsp90 activity, indicating that Hsp90 antagonist therapy and therapies that act to reactivate mutant p53 will be incompatible.	geldanamycin	127-139	P53	Homo sapiens	266-269
10543945-1	1999	In human skin cancers, more than 30 % of all mutations in the p53 gene are transitions at dipyrimidines within the sequence context CpG, i.e. 5"-TCG and 5"-CCG, found at several mutational hotspots.	dipyrimidines	90-103	P53	Homo sapiens	62-65
10543945-2	1999	Since CpGs are methylated along the p53 gene, these mutations may be derived from solar UV-induced pyrimidine dimers forming at sequences that contain 5-methylcytosine.	pyrimidine	99-109	P53	Homo sapiens	36-39
10543945-9	1999	The data indicate that dipyrimidines that contain 5-methylcytosine are preferential targets for sunlight-induced mutagenesis in cultured mammalian cells, thus explaining the large proportion of p53 mutations at such sites in skin tumors in vivo.	dipyrimidines	23-36	P53	Homo sapiens	194-197
15748509-0	2005	[Expression of protein p53 in workers occupationally exposed to benzidine and bladder cancer patients.].	benzidine	64-73	P53	Homo sapiens	23-26
15748509-1	2005	OBJECTIVE: To study expression of mutant p53 protein in workers occupationally exposed to benzidine and bladder cancer patients.	benzidine	90-99	P53	Homo sapiens	41-44
15748509-2	2005	METHODS: Mutant p53 protein in serum from the workers occupationally exposed to benzidine and bladder cancer patients were determined with Immuno-PCR, while exfoliated urothelial cells in the urine samples were classified with Papanicolau grading.	benzidine	80-89	P53	Homo sapiens	16-19
15748509-3	2005	RESULTS: Positive rate of mutant p53 protein increased with the exposed intensity index in workers occupationally exposed to benzidine.	benzidine	125-134	P53	Homo sapiens	33-36
17627614-3	2007	Analysis of flow cytometry and western blots of HeLa cells treated with 2.5 microM CR229 revealed an appreciable cell cycle arrest in the G1, G2/M phase and apoptotic induction via the p53-dependent pathway.	6-bromo-2,3,4,9-tetrahydrocarbolin-1-one	83-88	P53	Homo sapiens	185-188
15748509-9	2005	CONCLUSION: The increase of exposed intensity may not only result in the positive rate of mutant p53 protein, but also the quantity of mutant p53 protein in serum within the low range of benzidine exposure.	benzidine	187-196	P53	Homo sapiens	97-100
15748509-9	2005	CONCLUSION: The increase of exposed intensity may not only result in the positive rate of mutant p53 protein, but also the quantity of mutant p53 protein in serum within the low range of benzidine exposure.	benzidine	187-196	P53	Homo sapiens	142-145
10557093-7	1999	Second, geldanamycin also induced mt p53 destabilization through the dissociation of the protein from hsp90 but not through the restoration of wt p53 function.	geldanamycin	8-20	P53	Homo sapiens	37-40
17531965-5	2007	CONCLUSION: These results suggest that the Val allele of CYP1A1 Ile462Val polymorphism and the Pro allele of TP53 Arg72Pro polymorphism contribute to an increased risk of GBC among Japanese women and men, respectively.	Valine	43-46	P53	Homo sapiens	109-113
10560525-4	1999	Formalin-fixed, paraffin-embedded tissue sections were immunostained with a monoclonal antibody against p53 protein using an avidin-streptavidin method.	Formaldehyde	0-8	P53	Homo sapiens	104-107
15748509-11	2005	There was tight correlation between Papanicolau grade of exfoliated urothelial cells and the positive rate or the quantity of mutant p53 protein for the higher benzidine exposure intensity.	benzidine	160-169	P53	Homo sapiens	133-136
15489892-3	2004	Both 5-FU and mithramycin A induced site-specific phosphorylation of p53 at serine 15.	mithramycin A	14-27	P53	Homo sapiens	69-72
15489892-5	2004	Using transactivation assays in Sp1-deficient cells, we showed that mithramycin A inhibited the transcriptional activation of the p21Cip1 and PUMA promoters by Sp1 and p53.	mithramycin A	68-81	P53	Homo sapiens	168-171
15489892-7	2004	Mithramycin A also enhanced the recruitment of p53 to the distal p21Cip1 promoter but totally blocked the recruitment of Sp1 to the proximal p21Cip1 promoter.	mithramycin A	0-13	P53	Homo sapiens	47-50
15489892-8	2004	Our findings suggest that inhibition of Sp1 binding to the promoters of several p53 target genes, such as the p21Cip1 gene as well as certain proapoptotic genes, by mithramycin A, prevents the transcriptional induction of these genes by p53 and propose a mechanism that could account for some of the tumor suppressing and antiapoptotic effects of mithramycin A.	mithramycin A	165-178	P53	Homo sapiens	80-83
15489892-8	2004	Our findings suggest that inhibition of Sp1 binding to the promoters of several p53 target genes, such as the p21Cip1 gene as well as certain proapoptotic genes, by mithramycin A, prevents the transcriptional induction of these genes by p53 and propose a mechanism that could account for some of the tumor suppressing and antiapoptotic effects of mithramycin A.	mithramycin A	165-178	P53	Homo sapiens	237-240
10427139-5	1999	Sequence analysis of exons 5 through 8 of p53 was performed on subcloned PCR-amplified DNA, extracted from formalin-fixed, paraffin-embedded tumors.	Formaldehyde	107-115	P53	Homo sapiens	42-45
17690521-0	2007	Detection of mutant p53 protein in workers occupationally exposed to benzidine.	benzidine	69-78	P53	Homo sapiens	20-23
10606186-4	1999	Immunohistochemical staining for mutant p53 was performed on formalin fixed transurethral resection specimens of 31 patients who underwent radical cystectomy.	Formaldehyde	61-69	P53	Homo sapiens	40-43
15489892-8	2004	Our findings suggest that inhibition of Sp1 binding to the promoters of several p53 target genes, such as the p21Cip1 gene as well as certain proapoptotic genes, by mithramycin A, prevents the transcriptional induction of these genes by p53 and propose a mechanism that could account for some of the tumor suppressing and antiapoptotic effects of mithramycin A.	mithramycin A	347-360	P53	Homo sapiens	80-83
15489892-8	2004	Our findings suggest that inhibition of Sp1 binding to the promoters of several p53 target genes, such as the p21Cip1 gene as well as certain proapoptotic genes, by mithramycin A, prevents the transcriptional induction of these genes by p53 and propose a mechanism that could account for some of the tumor suppressing and antiapoptotic effects of mithramycin A.	mithramycin A	347-360	P53	Homo sapiens	237-240
15459092-0	2004	Additional data for oligonucleotide arrays of the p53 gene in DNA from formalin-fixed, paraffin-embedded tissue.	Formaldehyde	71-79	P53	Homo sapiens	50-53
17690521-1	2007	To investigate the expression of mutant p53 protein in workers occupationally exposed to benzidine, we detected mutant p53 protein by immuno-PCR assay in the serum of 331 benzidine-exposed healthy workers, while we classified exfoliated urothelial cells in urine samples with Papanicoloau"s grading (PG).	benzidine	89-98	P53	Homo sapiens	40-43
15648263-0	2004	Marine alkaloid polycarpine and its synthetic derivative dimethylpolycarpine induce apoptosis in JB6 cells through p53- and caspase 3-dependent pathways.	polycarpine	16-27	P53	Homo sapiens	115-118
17690521-7	2007	Detection of mutant p53 protein in conjunction with benzidine exposure level and Papanicoloau"s gradings of exfoliated urothelial cells could provide more information to help us elevate surveillance efficiency and diagnose bladder cancer in the early period.	benzidine	52-61	P53	Homo sapiens	20-23
15648263-9	2004	Furthermore, polycarpines were unable to induce apoptosis in p53-deficient MEFs in contrast to a strong induction of apoptosis in wild type MEFs, suggesting that p53 is involved in apoptosis induced by polycarpines.	polycarpine	202-214	P53	Homo sapiens	162-165
10505042-4	1999	The cytotoxicities of topotecan and gemcitabine on the human lung cancer cell lines H460 (wild-type-p53) and H322 (mutant p53 were determined after 72 h drug exposure employing the MTT assay.	Topotecan	22-31	P53	Homo sapiens	100-103
10505042-4	1999	The cytotoxicities of topotecan and gemcitabine on the human lung cancer cell lines H460 (wild-type-p53) and H322 (mutant p53 were determined after 72 h drug exposure employing the MTT assay.	Topotecan	22-31	P53	Homo sapiens	122-125
15648263-12	2004	Evidence also supports a proapoptotic role of the JNKs signaling pathway in vivo and clearly indicates that JNKs are required for phosphorylation of c-Jun, activation of p53, and subsequent apoptosis induced by polycarpines.	polycarpine	211-223	P53	Homo sapiens	170-173
15450952-6	2004	Interestingly, 6-hydroxymelatonin strongly damaged G and C of the 5"-ACG-3" sequence complementary to codon 273 of the p53 gene.	6-hydroxymelatonin	15-33	P53	Homo sapiens	119-122
20535395-7	2007	Further western blot analysis showed that ascorbic acid treatment decreased levels of p53, phospho-p53 at ser 15, and p21, indicating that ascorbic acid relieved senescence-related G1 arrest.	Ascorbic Acid	139-152	P53	Homo sapiens	99-102
10378792-0	1999	Wild-type p53 protein potentiates phototoxicity of 2-BA-2-DMHA in HT29 cells expressing endogenous mutant p53.	2-butylamino-2-demethoxy-hypocrellin A	51-62	P53	Homo sapiens	10-13
17547405-1	2007	Photosensitized one-electron oxidation was applied to discriminate a specific base site of 5-methylcytosine (mC) generated in DNA possessing a partial sequence of naturally occurring p53 gene, using a sensitizing 2-methyl-1,4-naphthoquinone (NQ) chromophore tethered to an interior of oligodeoxynucleotide (ODN) strands.	Vitamin K 3	213-240	P53	Homo sapiens	183-186
10378792-0	1999	Wild-type p53 protein potentiates phototoxicity of 2-BA-2-DMHA in HT29 cells expressing endogenous mutant p53.	2-butylamino-2-demethoxy-hypocrellin A	51-62	P53	Homo sapiens	106-109
10378792-2	1999	The influence of p53 status on the sensitivity induced by 2-butylamino-2-demethoxy-hypocrellin A (2-BA-2-DMHA) photosensitization was then examined.	2-butylamino-2-demethoxy-hypocrellin A	58-96	P53	Homo sapiens	17-20
10378792-2	1999	The influence of p53 status on the sensitivity induced by 2-butylamino-2-demethoxy-hypocrellin A (2-BA-2-DMHA) photosensitization was then examined.	2-butylamino-2-demethoxy-hypocrellin A	98-109	P53	Homo sapiens	17-20
15284248-4	2004	We have found that the level of p53 is elevated with the decline of Hsp90 in UV-irradiated cells and that malfunction of Hsp90, as inhibited by geldanamycin, enhances the p53-involved UV irradiation-induced apoptosis.	geldanamycin	144-156	P53	Homo sapiens	32-35
15284248-4	2004	We have found that the level of p53 is elevated with the decline of Hsp90 in UV-irradiated cells and that malfunction of Hsp90, as inhibited by geldanamycin, enhances the p53-involved UV irradiation-induced apoptosis.	geldanamycin	144-156	P53	Homo sapiens	171-174
15724841-0	2004	Implications of p53 in growth arrest and apoptosis on combined treatment of human Mammary epithelial cells with topotecan and UCN-01.	Topotecan	112-121	P53	Homo sapiens	16-19
10378792-4	1999	At a concentration of 5 microM 2-BA-2-DMHA with a red light of 18 J/cm2 (lambda = 600-700 nm), the survival is reduced from 58.72% in HT29 cells to 13.49% in wild-type p53-infected HT29 cells.	2-butylamino-2-demethoxy-hypocrellin A	31-42	P53	Homo sapiens	168-171
10378792-6	1999	These findings suggest that although wild-type p53 is, by itself, insufficient to induce apoptosis in cells with p53 mutation, it enhances the photosensitivity of 2-BA-2-DMHA by strongly potentiating the induction of apoptosis.	2-butylamino-2-demethoxy-hypocrellin A	163-174	P53	Homo sapiens	47-50
17204746-7	2007	CAPE disrupted BFA-induced phosphorylation of p53 and p90 ribosomal S6 kinase (p90RSK) in both cell lines.	O(4)-benzylfolic acid	15-18	P53	Homo sapiens	46-49
17268519-3	2007	Cells with mutant p53 are resistant to nutlin-3, but sensitive to geldanamycin, a pharmacologic inhibitor of heat shock 90 kDa protein (HSP90), indicating that HSP90 inhibition can induce apoptosis in a p53-independent manner.	geldanamycin	66-78	P53	Homo sapiens	18-21
10100998-9	1999	The frequency of p53 mutations was 39% (13 of 33) among the asbestos-exposed cases, as compared with 54% (29 of 54) among the nonexposed cases; the difference was not significant, however.	Asbestos	60-68	P53	Homo sapiens	17-20
9894613-5	1998	CEP1612-induced apoptosis is p53-independent, inhibitable by a tetrapeptide caspase inhibitor, and associated with accumulation of the cyclin-dependent kinase inhibitors p21 and p27.	CEP 1612	0-7	P53	Homo sapiens	29-32
15568402-2	2004	STUDY DESIGN: Polymerase chain reaction (PCR) was used to amplify DNA sequences of the viruses and PCR-single-strand conformation polymorphism analysis to screen for p53 gene mutations in exons 5-8 from formalin-fixed, paraffin-embedded blocks including 10 undifferentiated vulvar intraepithelial neoplasia (VIN) specimens.	Formaldehyde	203-211	P53	Homo sapiens	166-169
15313404-7	2004	In addition, eupatilin treatment led to elevated expression of p53 and p27Kip1 that act as Cdk inhibitors.	eupatilin	13-22	P53	Homo sapiens	63-66
17268519-3	2007	Cells with mutant p53 are resistant to nutlin-3, but sensitive to geldanamycin, a pharmacologic inhibitor of heat shock 90 kDa protein (HSP90), indicating that HSP90 inhibition can induce apoptosis in a p53-independent manner.	geldanamycin	66-78	P53	Homo sapiens	203-206
15254427-6	2004	Increased signal from the phosphorothioate-modified p21-beacon in doxorubicin-treated cells likely resulted from sequence-specific hybridization as well as sequence-independent cleavage that may occur due to p53-dependent activation of endonucleases during apoptosis.	Parathion	26-42	P53	Homo sapiens	208-211
17268519-4	2007	Conversely, cells with defects in the HSP90/nuclear factor-kappa B pathway expressing wild-type p53 are more resistant to geldanamycin, but still sensitive to nutlin-3.	geldanamycin	122-134	P53	Homo sapiens	96-99
9865315-0	1998	In vitro transcription and translation of the tumour suppressor protein P53: qualitative and quantitative effects of FK506 and rapamycin.	Tacrolimus	117-122	P53	Homo sapiens	72-75
15064747-0	2004	Limited role of N-terminal phosphoserine residues in the activation of transcription by p53.	Phosphoserine	27-40	P53	Homo sapiens	88-91
17293044-4	2007	Treatment of the cells with all trans retinoic acid (RA) generates a neuron-like, morphological change of differentiation, and results in the activation of ERK and Akt pathways, an inhibition of the nuclear translocation of p53 induced by GA, and induces higher resistance to the GA-induced apoptosis.	geldanamycin	239-241	P53	Homo sapiens	224-227
15285929-11	2004	It appears that the effects of EPA on hepatoma cells are determined by the status of p53 and that wild-type p53 is a prerequisite for the anticancer effect of EPA.	Eicosapentaenoic Acid	159-162	P53	Homo sapiens	108-111
15131059-1	2004	PURPOSE: On the basis of clinical studies showing that arsenic trioxide (As(2)O(3)), via an apoptotic mechanism, and with minimal toxicity induces complete remission in patients with refractory acute promyelocytic leukemia and that multidrug-resistant and p53-mutated neuroblastoma cells are sensitive to As(2)O(3) both in vitro and in vivo, we searched for molecular mechanisms involved in the As(2)O(3)-induced neuroblastoma cell death.	(2)o(3)	75-82	P53	Homo sapiens	256-259
17293044-5	2007	These results provide the first evidence for the requirement of p53 nucleation in SH-SY5Y cells to counteract GA in neuron survival.	geldanamycin	110-112	P53	Homo sapiens	64-67
9828101-1	1998	Brefeldin A (BFA) has recently been shown to induce apoptosis in human tumor cells in a p53-independent fashion.	Brefeldin A	0-11	P53	Homo sapiens	88-91
9828101-1	1998	Brefeldin A (BFA) has recently been shown to induce apoptosis in human tumor cells in a p53-independent fashion.	Brefeldin A	13-16	P53	Homo sapiens	88-91
17285122-3	2007	To study the genetic alterations of NDE in the multistep process of oesophageal carcinogenesis, we determined the relationship between p53 mutations and LULs-NDE.	luls-nde	153-161	P53	Homo sapiens	135-138
9823314-7	1998	Therefore, we next examined p53 as a covalent target for poly(ADP-ribosyl)ation.	poly(adp-ribosyl)	57-74	P53	Homo sapiens	28-31
9811465-5	1998	A significant decrease in the G1/S arrest assayed by bromodeoxyuridine and PI staining (cell cycle/proliferation assay) was also observed in response to irradiation and cisplatin in cell lines expressing either of the mutant p53 constructs.	Bromodeoxyuridine	53-70	P53	Homo sapiens	225-228
15130753-6	2004	The selective COX-2 inhibitor, NS-398, can inhibit the senescence-associated increases of COX-2, PGE(2), p53 and MMP-1 expression, and the senescence-associated decreases of PCNA, TIMP-1 and procollagen expression.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	31-37	P53	Homo sapiens	105-108
17285122-8	2007	The p53 mutation was detected in five of 137 samples with LULs-NDE (4%) and in five of 15 samples with dysplasia (33%).	luls-nde	58-66	P53	Homo sapiens	4-7
15124906-7	2004	p56lck, p59fyn and p53/56lyn are mediators of caspase-3 activation during Cr(III) exposure.	tris(1,10-phenanthroline)chromium(III) chloride	74-81	P53	Homo sapiens	19-22
9796984-4	1998	The inhibition of cell growth in FUdR-treated cells by PB was more sustained in U4 than U9 cells and was associated with an increased and sustained expression of p21waf1 protein, secretion of transforming growth factor beta1, mediators of p53-dependent or -independent G1 cell cycle arrest, and an increase in the alkaline phosphatase activity as well, considered a marker of differentiation in colon carcinoma cells.	Floxuridine	33-37	P53	Homo sapiens	239-242
17196878-0	2007	Conjugated EPA activates mutant p53 via lipid peroxidation and induces p53-dependent apoptosis in DLD-1 colorectal adenocarcinoma human cells.	Eicosapentaenoic Acid	11-14	P53	Homo sapiens	32-35
9773930-0	1998	Advantages of immunostaining over DNA analysis using PCR amplification to detect p53 abnormality in long-term formalin-fixed tissues of human colorectal carcinomas.	Formaldehyde	110-118	P53	Homo sapiens	81-84
15124906-8	2004	Collectively, our findings support a plausible mechanism in which Cr(III) mediates ROS generation that precedes the up-regulation of p56lck, p59fyn and p53/56lyn which eventually activates caspase-3 to promote apoptotic cell death of lymphocytes.	tris(1,10-phenanthroline)chromium(III) chloride	66-73	P53	Homo sapiens	152-155
14701864-5	2004	Specific glycosaminoglycan lyase digestions, followed by product analyses using fluorescence-assisted carbohydrate electrophoresis and immunoprecipitation experiments, showed that the p53 form is associated with syndecan-1 through both chondroitin sulfate and heparan sulfate.	Heparitin Sulfate	260-275	P53	Homo sapiens	184-187
17196878-0	2007	Conjugated EPA activates mutant p53 via lipid peroxidation and induces p53-dependent apoptosis in DLD-1 colorectal adenocarcinoma human cells.	Eicosapentaenoic Acid	11-14	P53	Homo sapiens	71-74
14726466-0	2004	Evaluation of oligonucleotide arrays for sequencing of the p53 gene in DNA from formalin-fixed, paraffin-embedded breast cancer specimens.	Formaldehyde	80-88	P53	Homo sapiens	59-62
17210678-2	2007	The ability of p53R2 to supply dNTPs for repairing DNA damages requires the presence of a functional p53 tumor suppressor.	Parathion	31-36	P53	Homo sapiens	15-18
14726466-2	2004	The purpose of this study was to determine whether a p53 microarray could be used to sequence the p53 gene in DNA extracted from formalin-fixed, paraffin-embedded (FFPE) tissues.	Formaldehyde	129-137	P53	Homo sapiens	53-56
14726466-2	2004	The purpose of this study was to determine whether a p53 microarray could be used to sequence the p53 gene in DNA extracted from formalin-fixed, paraffin-embedded (FFPE) tissues.	Formaldehyde	129-137	P53	Homo sapiens	98-101
17966099-7	2007	Therapy increased p53 expression and p53 phosphorylation at Ser392 and Ser20, and these changes correlated with poly-ADP-ribose levels and Ki-67 expression.	poly-adp	112-120	P53	Homo sapiens	18-21
14759370-3	2004	This bromodomain/acetyl-lysine binding is responsible for p53 acetylation-dependent coactivator recruitment after DNA damage, a step essential for p53-induced transcriptional activation of the cyclin-dependent kinase inhibitor p21 in G1 cell cycle arrest.	N(alpha)-acetyllysine	17-30	P53	Homo sapiens	58-61
14759370-3	2004	This bromodomain/acetyl-lysine binding is responsible for p53 acetylation-dependent coactivator recruitment after DNA damage, a step essential for p53-induced transcriptional activation of the cyclin-dependent kinase inhibitor p21 in G1 cell cycle arrest.	N(alpha)-acetyllysine	17-30	P53	Homo sapiens	147-150
17213797-3	2006	BaP 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of BaP, attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 mutations.	benzylaminopurine	60-63	P53	Homo sapiens	129-132
14639618-12	2004	For example, of the 4 lines, the p53wt transfectant was the most resistant to topotecan and the 143mut was the most resistant to carboplatin.	Topotecan	78-87	P53	Homo sapiens	33-36
16645841-6	2006	We found that this arsenite-induced G2/M phase arrest was accompanied by accumulation and/or phosphorylation of checkpoint-related molecules, including p53, Cdc25B, Cdc25C, and securin.	arsenite	19-27	P53	Homo sapiens	152-155
12959929-2	2004	Although H2O2 and other peroxides have been shown to induce ataxia telangiectasia-mutated (ATM)-dependent p53 phosphorylation in response to DNA damage, the signal transduction mechanisms in response to hyperoxia are currently unknown.	Peroxides	24-33	P53	Homo sapiens	106-109
16645841-8	2006	Our data suggest that the DNA damage responsive kinases ATM (ataxia-telangiectasia mutated) and ATR (ATM and Rad3-related) play critical roles in arsenite-induced G2/M phase arrest in aortic endothelial cells possibly via regulation of checkpoint-related signaling molecules including p53, Cdc25B, Cdc25C, and securin.	arsenite	146-154	P53	Homo sapiens	285-288
17066513-0	2006	[6]-Gingerol induces cell cycle arrest and cell death of mutant p53-expressing pancreatic cancer cells.	gingerol	4-12	P53	Homo sapiens	64-67
14695607-0	2004	A tetraguanidinium ligand binds to the surface of the tetramerization domain of protein P53.	tetraguanidinium	2-18	P53	Homo sapiens	88-91
17066513-3	2006	The purpose of this study was to investigate the action of [6]-gingerol on two human pancreatic cancer cell lines, HPAC expressing wild- type (wt) p53 and BxPC-3 expressing mutated p53.	gingerol	59-71	P53	Homo sapiens	181-184
15162845-0	2004	The involvement of p53 in paraquat-induced apoptosis in human lung epithelial-like cells.	Paraquat	26-34	P53	Homo sapiens	19-22
17066513-7	2006	p53 expression was decreased by [6]-gingerol treatment in both cell lines suggesting that the induction of Cyclin-dependent kinase inhibitor, p21cip1, was p53-independent.	gingerol	36-44	P53	Homo sapiens	0-3
15162845-1	2004	To investigate the possible role of p53 in the progression of paraquat-induced apoptosis, the authors used two cell lines that were wild-type p53-expressing human lung epithelial-like cell line (L132) and a p53-deficient human promyelocytic leukemia cell line (U937) and explored the linkage between p53, DNA damage, and apoptosis.	Paraquat	62-70	P53	Homo sapiens	36-39
17066513-8	2006	[6]-Gingerol induced mostly apoptotic death in the mutant p53-expressing cells, while no signs of early apoptosis were detected in wild type p53-expressing cells and this was related to the increased phosphorylation of AKT.	gingerol	4-12	P53	Homo sapiens	58-61
15162845-2	2004	Following paraquat exposure to L132 cells, the percentage of S-phase cells decreased significantly and the expression of p53 protein increased, suggesting that entry into S phase from G1 phase was blocked.	Paraquat	10-18	P53	Homo sapiens	121-124
15162845-5	2004	These results suggest that paraquat-induced DNA damage caused G1 arrest and apoptosis only in L132 cells, and that p53 protein accumulation is required for the induction of apoptosis by paraquat.	Paraquat	186-194	P53	Homo sapiens	115-118
17066513-9	2006	These results suggest that [6]-gingerol can circumvent the resistance of mutant p53- expressing cells towards chemotherapy by inducing apoptotic cell death while it exerts cytostatic effect on wild type p53- expressing cells by inducing temporal growth arrest.	gingerol	27-39	P53	Homo sapiens	80-83
17066513-9	2006	These results suggest that [6]-gingerol can circumvent the resistance of mutant p53- expressing cells towards chemotherapy by inducing apoptotic cell death while it exerts cytostatic effect on wild type p53- expressing cells by inducing temporal growth arrest.	gingerol	27-39	P53	Homo sapiens	203-206
14669279-9	2003	Positivity for Ki-67 and p53 was seen predominantly in the epithelium of inclusion cysts and deep invaginations, including those areas that had been identified as hyperplastic or dysplastic on routine hematoxylin and eosin-stained sections.	Hematoxylin	201-212	P53	Homo sapiens	25-28
16966095-0	2006	Exit from arsenite-induced mitotic arrest is p53 dependent.	arsenite	10-18	P53	Homo sapiens	45-48
14695179-6	2003	Here we show that both authentic peroxynitrite and SIN-1 (3-morpholinosydnonimine hydrochloride), a molecule that decomposes into NO and to form peroxynitrite, can inhibit wild-type p53 function in malignant glioma cells.	linsidomine	58-95	P53	Homo sapiens	182-185
14623330-0	2003	Involvement of p53 in alpha4beta1 integrin-mediated resistance of B-CLL cells to fludarabine.	fludarabine	81-92	P53	Homo sapiens	15-18
14623330-4	2003	Parallel to this different viability, fludarabine increased p53 expression on pLys-cultured cells and this increase was significantly reduced (P&lt;or=0.05) on cells cultured on H/89.	fludarabine	38-49	P53	Homo sapiens	60-63
16966095-2	2006	Using a model cell line in which p53 expression is regulated exogenously in a tetracycline-off system (TR9-7 cells) , our laboratory has shown that arsenite disrupts mitosis and that p53-deficient cells [p53(-)], in contrast to p53-expressing cells [p53(+)], display greater sensitivity to arsenite-induced mitotic arrest and apoptosis.	arsenite	148-156	P53	Homo sapiens	33-36
16966095-3	2006	OBJECTIVE: Our goal was to examine the role p53 plays in protecting cells from arsenite-induced mitotic arrest.	arsenite	79-87	P53	Homo sapiens	44-47
16966095-5	2006	RESULTS: Mitotic index analysis demonstrated that arsenite treatment delayed exit from G2 in p53(+) and p53(-) cells.	arsenite	50-58	P53	Homo sapiens	93-96
16966095-5	2006	RESULTS: Mitotic index analysis demonstrated that arsenite treatment delayed exit from G2 in p53(+) and p53(-) cells.	arsenite	50-58	P53	Homo sapiens	104-107
14981925-7	2003	Apoptosis induced by CAPE or CAO is associated with increased expression of p53, p21 and c-Jun.	cao	29-32	P53	Homo sapiens	76-79
16966095-6	2006	Arsenite-treated p53(+) cells exited mitosis normally, whereas p53(-) cells exited mitosis with delayed kinetics.	arsenite	0-8	P53	Homo sapiens	17-20
16966095-7	2006	Microarray analysis performed on mRNAs of cells exposed to arsenite for 0 and 3 hr after release from G2 phase synchrony showed that arsenite induced inhibitor of DNA binding-1 (ID1) differentially in p53(+) and p53(-) cells.	arsenite	59-67	P53	Homo sapiens	201-204
16966095-7	2006	Microarray analysis performed on mRNAs of cells exposed to arsenite for 0 and 3 hr after release from G2 phase synchrony showed that arsenite induced inhibitor of DNA binding-1 (ID1) differentially in p53(+) and p53(-) cells.	arsenite	59-67	P53	Homo sapiens	212-215
16966095-7	2006	Microarray analysis performed on mRNAs of cells exposed to arsenite for 0 and 3 hr after release from G2 phase synchrony showed that arsenite induced inhibitor of DNA binding-1 (ID1) differentially in p53(+) and p53(-) cells.	arsenite	133-141	P53	Homo sapiens	201-204
12907684-5	2003	CD also suppressed activation of downstream signaling of p38 kinase and PKC, such as NF-kappaB activation, p53 accumulation, and caspase-3 activation, which are necessary for NO-induced apoptosis.	Cytochalasin D	0-2	P53	Homo sapiens	107-110
16966095-7	2006	Microarray analysis performed on mRNAs of cells exposed to arsenite for 0 and 3 hr after release from G2 phase synchrony showed that arsenite induced inhibitor of DNA binding-1 (ID1) differentially in p53(+) and p53(-) cells.	arsenite	133-141	P53	Homo sapiens	212-215
16966095-9	2006	CONCLUSIONS: p53 promotes mitotic exit and leads to more extensive ID1 induction by arsenite.	arsenite	84-92	P53	Homo sapiens	13-16
16966095-11	2006	ID1 may play a role in the survival of arsenite-treated p53(+) cells and contribute to arsenic carcinogenicity.	arsenite	39-47	P53	Homo sapiens	56-59
16865270-2	2006	We treated a human gastric carcinoma cell line, MKN-1 (mutant P53), with 500 microM CoCl(2).	cobaltous chloride	84-91	P53	Homo sapiens	62-65
12912974-0	2003	Activation of a p53-mediated apoptotic pathway in quiescent lymphocytes after the inhibition of DNA repair by fludarabine.	fludarabine	110-121	P53	Homo sapiens	16-19
16543464-7	2006	Combination treatment of Nutlin-3a and fludarabine synergistically increased p53 levels, and induced conformational change of Bax and apoptosis in wild-type p53 cells but not in cells with mutant p53.	fludarabine	39-50	P53	Homo sapiens	77-80
12912974-11	2003	CONCLUSIONS: These results suggest that inhibition of UV-induced DNA repair by F-ara-A is critical for cytotoxicity and that induction of apoptosis may be conducted by a p53-mediated signaling mechanism to the Fas death pathway.	fludarabine	79-86	P53	Homo sapiens	170-173
12859744-5	2003	Formalin-fixed, paraffin-embedded archival tissue from these cases was immunostained for p53 and used for DNA extraction for the analysis of p53 mutations by polymerase chain reaction and single-strand conformation polymorphism.	Formaldehyde	0-8	P53	Homo sapiens	89-92
16543464-7	2006	Combination treatment of Nutlin-3a and fludarabine synergistically increased p53 levels, and induced conformational change of Bax and apoptosis in wild-type p53 cells but not in cells with mutant p53.	fludarabine	39-50	P53	Homo sapiens	157-160
16543464-7	2006	Combination treatment of Nutlin-3a and fludarabine synergistically increased p53 levels, and induced conformational change of Bax and apoptosis in wild-type p53 cells but not in cells with mutant p53.	fludarabine	39-50	P53	Homo sapiens	157-160
16928824-7	2006	A specific inhibitor of COX-2, NS398, and small interfering RNA knockdown of COX-2 were associated with reduced p53 phosphorylation and consequent decrease in p53-dependent apoptosis in resveratrol-treated cells.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	31-36	P53	Homo sapiens	112-115
12843186-8	2003	In the FTC-133 cell line, geldanamycin treatment decreased clonogenicity by 21% at a concentration of 50 nM; geldanamycin induced apoptosis and down-regulated c-Raf-1, mutant p53, and epidermal growth factor (EGF) receptor expression; geldanamycin inhibited EGF-stimulated invasion.	geldanamycin	26-38	P53	Homo sapiens	175-178
16928824-7	2006	A specific inhibitor of COX-2, NS398, and small interfering RNA knockdown of COX-2 were associated with reduced p53 phosphorylation and consequent decrease in p53-dependent apoptosis in resveratrol-treated cells.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	31-36	P53	Homo sapiens	159-162
12843186-8	2003	In the FTC-133 cell line, geldanamycin treatment decreased clonogenicity by 21% at a concentration of 50 nM; geldanamycin induced apoptosis and down-regulated c-Raf-1, mutant p53, and epidermal growth factor (EGF) receptor expression; geldanamycin inhibited EGF-stimulated invasion.	geldanamycin	109-121	P53	Homo sapiens	175-178
12843186-8	2003	In the FTC-133 cell line, geldanamycin treatment decreased clonogenicity by 21% at a concentration of 50 nM; geldanamycin induced apoptosis and down-regulated c-Raf-1, mutant p53, and epidermal growth factor (EGF) receptor expression; geldanamycin inhibited EGF-stimulated invasion.	geldanamycin	109-121	P53	Homo sapiens	175-178
16364413-12	2006	Overall, LA-12 but not its reduced Pt(II) counterpart LA-9 is the compound effective in p53 null human ovarian cancer cells and it is able to overcome intrinsic cisplatin resistance in these cells.	UNII-37WM0V5E17	9-14	P53	Homo sapiens	88-91
12823592-10	2003	Alimentary history documented that patients with a p53 over-expression had a lower intake of total calories, monounsaturated fatty acids, vitamin C and riboflavin.	Fatty Acids, Monounsaturated	109-136	P53	Homo sapiens	51-54
12823592-10	2003	Alimentary history documented that patients with a p53 over-expression had a lower intake of total calories, monounsaturated fatty acids, vitamin C and riboflavin.	Ascorbic Acid	138-147	P53	Homo sapiens	51-54
16891474-6	2006	Selenite induced a rapid generation of superoxide and p53 Ser(15) phosphorylation and increased Bax abundance and translocation into the mitochondria.	Selenious Acid	0-8	P53	Homo sapiens	54-57
12787880-2	2003	Cells were stably transfected with a plasmid containing a chimeric DNA construct encoding a temperature-sensitive p53 variant (135(ala--&gt;val)), which transactivates at 32 degrees but is non-functional at 37 degrees.	Valine	140-143	P53	Homo sapiens	114-117
16891474-8	2006	Inactivating p53 with a dominant-negative mutant abolished apoptosis without affecting superoxide generation, whereas a superoxide dismutase mimetic agent blocked p53 activation, Bax translocation to mitochondria, cytochrome c release, and apoptosis induced by selenite/TRAIL.	Selenious Acid	261-269	P53	Homo sapiens	13-16
12781329-7	2003	p27(Kip) and p21(Cip), inhibitors of cyclin/CDK complexes in G1-phase, were gradually increased after 5GG treatment in a time-dependent manner and the induction of p21(Cip) was correlated with an increase in p53 levels.	pentagalloylglucose	102-105	P53	Homo sapiens	208-211
16891474-10	2006	Taken together, the results indicate that selenite induces a rapid superoxide burst and p53 activation, leading to Bax up-regulation and translocation into mitochondria, which restores the cross-talk with stalled TRAIL signaling for a synergistic caspase-9/3 cascade-mediated apoptosis execution.	Selenious Acid	42-50	P53	Homo sapiens	88-91
16426753-6	2006	The inhibition of apoptosis is mediated through diazoxide"s ability to reduce p53 expression.	Diazoxide	48-57	P53	Homo sapiens	78-81
12782583-1	2003	To uncover transcriptional stress responses related to p53, we used cDNA microarrays (National Cancer Institute Oncochips comprising 6500 different genes) to characterize the gene expression profiles of wild-type p53 HCT-116 cells and an isogenic p53 knockout counterpart after treatment with topotecan, a specific topoisomerase I inhibitor.	Topotecan	293-302	P53	Homo sapiens	55-58
12782583-5	2003	Approximately 10% of the transcripts were up- or down-regulated in response to topotecan in the p53+/+ cells, whereas only 1% of the transcripts changed in the p53-/- cells, indicating that p53 has a broad effect on the transcriptional response to this stress.	Topotecan	79-88	P53	Homo sapiens	96-99
16426753-7	2006	On the other hand, tolbutamide, a KATP channels antagonist which blocks the cellular sulphonylureas receptor, significantly increases p53 expression and apoptosis under hypoxic/anoxic conditions.	Tolbutamide	19-30	P53	Homo sapiens	134-137
16426753-8	2006	Trichostatin (TSA), a p53 inhibitor, can block the effects of tolbutamide, lending further support for a role of p53 in mediating this process.	Tolbutamide	62-73	P53	Homo sapiens	22-25
12945745-0	2003	Increased p53 levels without caspase-3 activity and change of cell viability in 6-hydroxydopamine-treated CV1-P cells.	Oxidopamine	80-97	P53	Homo sapiens	10-13
16426753-8	2006	Trichostatin (TSA), a p53 inhibitor, can block the effects of tolbutamide, lending further support for a role of p53 in mediating this process.	Tolbutamide	62-73	P53	Homo sapiens	113-116
12945745-4	2003	Interestingly, in the fibroblasts at the low 6-OHDA concentrations, p53 remained high during the whole experiment, and there was neither significant caspase-3 activity nor cell death.	Oxidopamine	45-51	P53	Homo sapiens	68-71
16545693-6	2006	N-OH-ABA induced DNA damage at cytosine and guanine residues of ACG sequence complementary to codon 273, a well-known hot spot of the p53 gene.	N-hydroxy-3-aminobenzanthrone	0-8	P53	Homo sapiens	134-137
12945745-7	2003	In contrast to some earlier reports, we have shown that the actual 6-OHDA sensitivity of nonneuronal cells may be equal or even higher than that in neuronal cells if the enhancement of p53 levels is used as a criterion for the response.	Oxidopamine	67-73	P53	Homo sapiens	185-188
16251206-0	2006	Sequence specificity of Cr(III)-DNA adduct formation in the p53 gene: NGG sequences are preferential adduct-forming sites.	tris(1,10-phenanthroline)chromium(III) chloride	24-31	P53	Homo sapiens	60-63
12771391-0	2003	DNA-protein crosslinks and p53 protein expression in relation to occupational exposure to formaldehyde.	Formaldehyde	90-102	P53	Homo sapiens	27-30
12750285-3	2003	Colocalization was observed with the phosphoserine-15 form of p53 at presumed DNA processing sites after the induction of DNA breaks.	Phosphoserine	37-50	P53	Homo sapiens	62-65
16251206-7	2006	We have found that the sequence specificities of Cr(III)-DNA and Cr(III)-histidine-DNA adducts in the p53 gene sequence are identical and that both types of adducts are preferentially formed at -NGG- sequences, including codons 245, 248 and 249, the mutational hotspots in human lung cancer.	tris(1,10-phenanthroline)chromium(III) chloride	49-56	P53	Homo sapiens	102-105
16251206-7	2006	We have found that the sequence specificities of Cr(III)-DNA and Cr(III)-histidine-DNA adducts in the p53 gene sequence are identical and that both types of adducts are preferentially formed at -NGG- sequences, including codons 245, 248 and 249, the mutational hotspots in human lung cancer.	tris(1,10-phenanthroline)chromium(III) chloride	65-72	P53	Homo sapiens	102-105
16251206-9	2006	Therefore, these results suggest that Cr(III)-DNA adduct formation contributes to the p53 gene mutations in lung carcinogenesis.	tris(1,10-phenanthroline)chromium(III) chloride	38-45	P53	Homo sapiens	86-89
12642506-11	2003	Treatment with a beta1-integrin-blocking antibody or integrin signaling inhibitor cytochalasin B but not growth factor receptor inhibitor suramin abrogated both stretch-induced phosphorylation of p38 MAPK and p53 expression.	Cytochalasin B	82-96	P53	Homo sapiens	209-212
16300733-6	2006	Blocking of the p53 CTDBS by a monoclonal antibody Bp53-10.1 resulted in abolishment of the isolated CTD binding to the cisPt-DNA.	ctdbs	20-25	P53	Homo sapiens	16-19
12642506-12	2003	Akin to the inhibition of p38 MAPK-p53 signaling, pretreatment with a beta1-integrin-blocking antibody or cytochalasin B but not suramin inhibited stretch-induced apoptosis on collagen plates.	Cytochalasin B	106-120	P53	Homo sapiens	35-38
16405733-11	2006	To this end, tacrolimus has been shown to have an impact on cancer signalling pathways such as the MAPK and the p53 pathway.	Tacrolimus	13-23	P53	Homo sapiens	112-115
12628922-4	2003	Whereas levels of p53, phosphoserine-15 p53, p21, ARF and Bcl-X(L) were increased in response to exogenous overexpression of activated DDR1, dominant-negative DDR1 inhibited irradiation-induced MAPK activation and p53, phosphoserine-15 p53, as well as induced p21 and DDR1 levels, suggesting that DDR1 functions in a feedforward loop to increase p53 levels and at least some of its effectors.	Phosphoserine	23-36	P53	Homo sapiens	40-43
12628922-4	2003	Whereas levels of p53, phosphoserine-15 p53, p21, ARF and Bcl-X(L) were increased in response to exogenous overexpression of activated DDR1, dominant-negative DDR1 inhibited irradiation-induced MAPK activation and p53, phosphoserine-15 p53, as well as induced p21 and DDR1 levels, suggesting that DDR1 functions in a feedforward loop to increase p53 levels and at least some of its effectors.	Phosphoserine	23-36	P53	Homo sapiens	40-43
12628922-4	2003	Whereas levels of p53, phosphoserine-15 p53, p21, ARF and Bcl-X(L) were increased in response to exogenous overexpression of activated DDR1, dominant-negative DDR1 inhibited irradiation-induced MAPK activation and p53, phosphoserine-15 p53, as well as induced p21 and DDR1 levels, suggesting that DDR1 functions in a feedforward loop to increase p53 levels and at least some of its effectors.	Phosphoserine	23-36	P53	Homo sapiens	40-43
12628922-4	2003	Whereas levels of p53, phosphoserine-15 p53, p21, ARF and Bcl-X(L) were increased in response to exogenous overexpression of activated DDR1, dominant-negative DDR1 inhibited irradiation-induced MAPK activation and p53, phosphoserine-15 p53, as well as induced p21 and DDR1 levels, suggesting that DDR1 functions in a feedforward loop to increase p53 levels and at least some of its effectors.	Phosphoserine	23-36	P53	Homo sapiens	40-43
12424231-1	2003	Tumor suppressor p53 exhibits an enigmatic phenotype in cells exposed to electrophilic, cyclopentenone prostaglandins of the A and J series.	cyclopentenone prostaglandins	88-117	P53	Homo sapiens	17-20
12473386-0	2003	Influence of p53 and p21(WAF1) expression on sensitivity of cancer cells to cladribine.	Cladribine	76-86	P53	Homo sapiens	13-16
16426974-4	2006	Structural characterization shows that these chemicals inhibit CBP/p53 association by binding to the acetyl-lysine binding site of the bromodomain.	N(alpha)-acetyllysine	101-114	P53	Homo sapiens	67-70
12759546-6	2003	Since p53 expression was not modified after BFA exposure, BFA-induced apoptosis may follow a p53-independent pathway, as already reported.	Brefeldin A	58-61	P53	Homo sapiens	93-96
16702019-5	2006	To understand the possible mechanism of safrole oxide acting, we first examined the phosphorylation of Akt and the activity of nitric oxide synthase (NOS); secondly, we analyzed the expressions and distributions of Fas and P53; then we measured the activity of phosphatidylcholine specific phospholipase C (PC-PLC) in the VECs treated with and without safrole oxide.	safrole oxide	40-53	P53	Homo sapiens	223-226
12411481-6	2002	Also, a selective Cox-2 inhibitor, NS-398, significantly enhanced genotoxic stress-induced apoptosis in several types of p53+/+ normal human cells, through a caspase-dependent pathway.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	35-41	P53	Homo sapiens	121-124
16702019-9	2006	The data suggested that safrole oxide effectively inhibited angiogenesis and triggered VEC apoptosis in the presence of FGF-2 and serum, and it might perform its functions by suppressing Akt/NOS signal pathway, upregulating the expressions of Fas and P53 and modifying the distributing pattern of Fas in VEC.	safrole oxide	24-37	P53	Homo sapiens	251-254
17120736-6	2006	It is concluded that MDM2 specific antisense oligonucletides can inhibit the expression of MDM2, induce the expression of P53 and increase the apoptosis of leukemia cells after chemotherapy.	oligonucletides	45-60	P53	Homo sapiens	122-125
17065086-1	2006	Previously, we have found that activation of deoxycytidine kinase elicited by various DNA-damaging chemical agents could be prevented by BAPTA-AM, a cell-permeable calcium chelator or by pifithrin-alpha, a pharmacological inhibitor of p53.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	137-145	P53	Homo sapiens	235-238
12208600-3	2002	The reduction of Cr(VI) to Cr(III) results in the formation of reactive intermediates that together with oxidative stress oxidative tissue damage and a cascade of cellular events including modulation of apoptosis regulatory gene p53, contribute to the cytotoxicity, genotoxicity and carcinogenicity of Cr(VI)-containing compounds.	tris(1,10-phenanthroline)chromium(III) chloride	27-34	P53	Homo sapiens	229-232
16375215-4	2005	Immunostaining for p53 protein was performed on formalin-fixed, paraffin-embedded tissue sections, using the alkaline phosphatase antialkaline phosphatase (APAAP) method.	Formaldehyde	48-56	P53	Homo sapiens	19-22
12359050-5	2002	Sequencing of all coding exons of the p53 gene demonstrated only a neutral genetic polymorphism, i.e. a G-to-A substitution (GAG to GAA) at nucleotide position 13 432.	Glycosaminoglycans	125-128	P53	Homo sapiens	38-41
15887239-3	2005	We demonstrated that vitamin C inhibits DNA synthesis in HeLa cells and, mainly the form of dehydroascorbic acid (DHA), delays the entry of p53-deficient synchronized HeLa and T98G cancer cells into mitosis.	Ascorbic Acid	21-30	P53	Homo sapiens	140-143
12126965-5	2002	Addition of alpha-tocopherol before arsenite treatment abolished the transient increase in superoxide formation, lipid peroxidation, intracellular [Ca(2+)] levels and p53 gene expression, and furthermore could significantly inhibited the arsenite-induced apoptosis of MGC-803 cells.	alpha-Tocopherol	12-28	P53	Homo sapiens	167-170
9773930-1	1998	To study the appropriate period for formalin fixation in order to detect p53 abnormalities in formalin-fixed tissue, we used seven surgically resected human colorectal cancer specimens.	Formaldehyde	36-44	P53	Homo sapiens	73-76
9773930-1	1998	To study the appropriate period for formalin fixation in order to detect p53 abnormalities in formalin-fixed tissue, we used seven surgically resected human colorectal cancer specimens.	Formaldehyde	94-102	P53	Homo sapiens	73-76
9773930-6	1998	PCR amplification for p53 at exon 8 and K-ras at codon 12 was successful until 1 day and 2 weeks, respectively, of formalin-fixation for the specimens of all seven cases.	Formaldehyde	115-123	P53	Homo sapiens	22-25
9773930-9	1998	These results suggest that to detect p53 abnormality in specimens that have been formalin-fixed for long periods, immunohistochemical staining may have advantages over DNA analysis with PCR amplification.	Formaldehyde	81-89	P53	Homo sapiens	37-40
9743293-8	1998	Thus, although p53-dependent apoptosis is induced by camptothecin, topotecan and SN-38 in this human ovarian carcinoma cell line, these drugs induce p53-independent death, as measured by clonogenic assay.	Topotecan	67-76	P53	Homo sapiens	15-18
16234232-5	2005	The H2 helix of p53 structurally mimics the binding of ssDNA to the oligonucleotide/oligosaccharide-binding fold.	Oligosaccharides	84-99	P53	Homo sapiens	16-19
9705861-4	1998	We show here that chronic treatment of human fibroblast with DAG induces p53 down-regulation and inhibition of p53 functional activity, and protection from UV-induced apoptosis.	Diglycerides	61-64	P53	Homo sapiens	111-114
12085225-8	2002	In the PRI cells fludarabine activated p53, but not in the BL2.B95.8 cells in which the p53 pathway is inactivated.	fludarabine	17-28	P53	Homo sapiens	39-42
12082016-9	2002	Further exploration of antimalarial compounds identified the common medicinals chloroquine, quinacrine, and amodiaquine as Tp53-inducers.	Quinacrine	92-102	P53	Homo sapiens	123-127
12082016-9	2002	Further exploration of antimalarial compounds identified the common medicinals chloroquine, quinacrine, and amodiaquine as Tp53-inducers.	Amodiaquine	108-119	P53	Homo sapiens	123-127
16204064-0	2005	Topotecan-triggered degradation of topoisomerase I is p53-dependent and impacts cell survival.	Topotecan	0-9	P53	Homo sapiens	54-57
12046070-2	2002	METHODS: Two hundreds and forty-four formalin-fixed paraffin-embedded tumor samples of the patients with HCC receiving liver resection were detected for nuclear accumulation of p53.	Formaldehyde	37-45	P53	Homo sapiens	177-180
9705861-5	1998	As PKC phosphorylation is necessary for p53 functional activity, we propose that chronic DAG treatment mimics the same event occurring in vivo for the effect of glycolysis in tumor progression.	Diglycerides	89-92	P53	Homo sapiens	40-43
16204064-7	2005	Treatment of p53 wild-type cells with pifithrin-alpha, an inhibitor of the trans-activating activity of p53, caused reversal of the phenotype, making wild-type cells more sensitive to topotecan.	Topotecan	184-193	P53	Homo sapiens	13-16
9743466-7	1998	Chimeric methylphosphonate-phosphodiester oligodeoxynucleotide antisense to a point mutation in KYO-1 p53 mRNA efficiently reduced target mRNA expression, but only small, transient reductions in p53 protein expression were observed.	methylphosphonate-phosphodiester oligodeoxynucleotide	9-62	P53	Homo sapiens	102-105
11880381-7	2002	Finally, stable expression of the HPV16 E6 oncogene or dominant negative p53 peptide, GSE-22, both of which inhibit p53 function, delayed entry into quiescence following growth factor withdrawal.	GSH monoMe ester	86-89	P53	Homo sapiens	73-76
9743466-8	1998	However, a chimeric methylphosphonate-phosphorothioate oligodeoxynucleotide targeted to the same site reduced p53 protein to 30% of control levels over a 48-hour period.	methylphosphonate-phosphorothioate oligodeoxynucleotide	20-75	P53	Homo sapiens	110-113
11880381-7	2002	Finally, stable expression of the HPV16 E6 oncogene or dominant negative p53 peptide, GSE-22, both of which inhibit p53 function, delayed entry into quiescence following growth factor withdrawal.	GSH monoMe ester	86-89	P53	Homo sapiens	116-119
16204064-7	2005	Treatment of p53 wild-type cells with pifithrin-alpha, an inhibitor of the trans-activating activity of p53, caused reversal of the phenotype, making wild-type cells more sensitive to topotecan.	Topotecan	184-193	P53	Homo sapiens	104-107
16204064-11	2005	U138 cells (p53 mutated) were significantly more sensitive to topotecan than U87 cells (p53 wild-type).	Topotecan	62-71	P53	Homo sapiens	12-15
16204064-14	2005	The data suggests that p53 causes resistance of cells to topo I inhibitors due to stimulation of topotecan-triggered topo I degradation which may impact topotecan-based cancer therapy.	Topotecan	97-106	P53	Homo sapiens	23-26
9679939-0	1998	Alterations of the p53 gene in occupational bladder cancer in workers exposed to aromatic amines.	aromatic amines	81-96	P53	Homo sapiens	19-22
16204064-14	2005	The data suggests that p53 causes resistance of cells to topo I inhibitors due to stimulation of topotecan-triggered topo I degradation which may impact topotecan-based cancer therapy.	Topotecan	153-162	P53	Homo sapiens	23-26
12003538-10	2002	Moreover, it turned out that these phosmidosine derivatives showed characteristic inhibitory activities against cancer cells independent of their p53 phenotypes.	phosmidosine	35-47	P53	Homo sapiens	146-149
9687575-10	1998	The results also suggest that p53 induction in response to O6-guanine methylation involves the mismatch repair system.	6-Oxamyristic acid	59-61	P53	Homo sapiens	30-33
15914462-4	2005	Both proline oxidase- and p53-induced activation of NFAT were sensitive to the calcineurin inhibitors cyclosporin A and FK-506, to scavengers of ROS, and to inhibitors of calcium mobilization.	Tacrolimus	120-126	P53	Homo sapiens	26-29
9726816-0	1998	Induction of apoptosis by thiuramdisulfides, the reactive metabolites of dithiocarbamates, through coordinative modulation of NFkappaB, c-fos/c-jun, and p53 proteins.	dithiocarbamates	73-89	P53	Homo sapiens	153-156
16012788-0	2005	Enhanced P53 and BAX gene expression and apoptosis in A549 cells by cis-Pt(II) complex of 3-aminoflavone in comparison with cis-DDP.	3-aminoflavone	90-104	P53	Homo sapiens	9-12
9726816-10	1998	These results suggested that PTDS and DTDS induced p53-dependent apoptosis, whereas PDTC, DDTC, and ADTC induced G1/S arrest.	ptds	29-33	P53	Homo sapiens	51-54
9726816-10	1998	These results suggested that PTDS and DTDS induced p53-dependent apoptosis, whereas PDTC, DDTC, and ADTC induced G1/S arrest.	5'-O-(4,4'-dimethoxytrityl)thymidine-3'-O-(2,4-dinitrophenyl) succinate	38-42	P53	Homo sapiens	51-54
9703875-0	1998	Increased p21/WAF-1 and p53 protein levels following sequential three drug combination regimen of fludarabine, cytarabine and docetaxel induces apoptosis in human leukemia cells.	fludarabine	98-109	P53	Homo sapiens	24-27
9698472-2	1998	Immunostaining for p53 protein was performed on formalin-fixed, paraffin-embedded sections from 158 patients with verified uterine sarcomas using monoclonal p53 antibody (DO-1).	Formaldehyde	48-56	P53	Homo sapiens	19-22
9622079-1	1998	17-(Allylamino)-17-demethoxygeldanamycin (17AAG), a compound that is proposed for clinical development, shares the ability of geldanamycin to bind to heat shock protein 90 and GRP94, thereby depleting cells of p185erbB2, mutant p53, and Raf-1.	geldanamycin	28-40	P53	Homo sapiens	228-231
12094375-8	2002	Nuclear p53 immunostaining was detected in 30% of IPN-L as a whole and increased in tandem with the progression of IPN-L (P &lt; 0.01).	isoamyl nitrite	50-53	P53	Homo sapiens	8-11
11929820-6	2002	We have designed allele-specific phosphorothioate ODNs against the gene of the large subunit of RNA polymerase II (POLR2A), a gene located in close proximity to the tumor suppressor gene p53, which frequently shows LOH in cancer cells.	Parathion	33-49	P53	Homo sapiens	187-190
15996664-1	2005	Protein transduction therapy using poly-arginine can deliver the bioactive p53 protein into cancer cells and inhibits the proliferation of the cells.	polyarginine	35-48	P53	Homo sapiens	75-78
11917017-9	2002	The non-detectable DNA binding of the 273H p53-CD is due mainly to the disruption of a hydrogen-bonding network involving R273, D281 and R280, leading to a loss of major groove binding by R280 and K120.	273h	38-42	P53	Homo sapiens	43-46
9635828-7	1998	The valine 272 residue may thus be crucial for properties (other than sequence-specific DNA binding) that are important for p53 function(s) in vivo.	Valine	4-10	P53	Homo sapiens	124-127
9482877-1	1998	Treatment of mouse or human cells with the protein kinase C (PKC) inhibitors H7 or bisindolylmaleimide I induced an increase in the lifetime of p53, leading to its accumulation.	bisindolylmaleimide I	83-104	P53	Homo sapiens	144-147
11912124-7	2002	These results indicate that the combination of TRAIL/Apo2L with either irradiation or sulindac may be highly effective against both p53-proficient and p53-deficient colorectal cancers; however, BAX-deficient tumors may evade elimination by TRAIL/Apo2L-based regimens.	Sulindac	86-94	P53	Homo sapiens	132-135
16009942-7	2005	The UVB-induced lesions detected by terminal transferase-PCR were almost exclusively mapped to pyrimidine-rich sequences; however, the UVA1-induced lesions were mapped to purine- and pyrimidine-containing sequences along the p53 gene.	pyrimidine	183-193	P53	Homo sapiens	225-228
11912124-7	2002	These results indicate that the combination of TRAIL/Apo2L with either irradiation or sulindac may be highly effective against both p53-proficient and p53-deficient colorectal cancers; however, BAX-deficient tumors may evade elimination by TRAIL/Apo2L-based regimens.	Sulindac	86-94	P53	Homo sapiens	151-154
9562963-3	1998	Compared to BAP-p53, the BAP-TSPf group had a similar antitumor efficacy.	benzylaminopurine	12-15	P53	Homo sapiens	16-19
11870884-4	2002	This cell line contains a mutation in codon 272 of p53 (p53(V272M), with methionine instead of a valine), conferring temperature-sensitive properties to the p53 protein.	Valine	97-103	P53	Homo sapiens	51-54
15905035-9	2005	An antioxidant, l-ascorbic acid, inhibited CoQ2-induced p53 phosphorylation and further apoptotic stimuli.	Ascorbic Acid	16-31	P53	Homo sapiens	56-59
11870884-4	2002	This cell line contains a mutation in codon 272 of p53 (p53(V272M), with methionine instead of a valine), conferring temperature-sensitive properties to the p53 protein.	Valine	97-103	P53	Homo sapiens	56-59
11870884-4	2002	This cell line contains a mutation in codon 272 of p53 (p53(V272M), with methionine instead of a valine), conferring temperature-sensitive properties to the p53 protein.	Valine	97-103	P53	Homo sapiens	56-59
9562963-4	1998	More importantly, liposomes complexed with BAP-TSPf and BAP-p53 synergistically decreased the growth of MDA-MB-435 tumors when compared to either BAP-p53 or BAP-TSPf alone.	benzylaminopurine	43-46	P53	Homo sapiens	150-153
9562963-4	1998	More importantly, liposomes complexed with BAP-TSPf and BAP-p53 synergistically decreased the growth of MDA-MB-435 tumors when compared to either BAP-p53 or BAP-TSPf alone.	benzylaminopurine	56-59	P53	Homo sapiens	60-63
9562963-4	1998	More importantly, liposomes complexed with BAP-TSPf and BAP-p53 synergistically decreased the growth of MDA-MB-435 tumors when compared to either BAP-p53 or BAP-TSPf alone.	benzylaminopurine	56-59	P53	Homo sapiens	150-153
9562963-4	1998	More importantly, liposomes complexed with BAP-TSPf and BAP-p53 synergistically decreased the growth of MDA-MB-435 tumors when compared to either BAP-p53 or BAP-TSPf alone.	benzylaminopurine	56-59	P53	Homo sapiens	60-63
9562963-4	1998	More importantly, liposomes complexed with BAP-TSPf and BAP-p53 synergistically decreased the growth of MDA-MB-435 tumors when compared to either BAP-p53 or BAP-TSPf alone.	benzylaminopurine	56-59	P53	Homo sapiens	150-153
15780621-1	2005	Crystallographic analysis of ligands bound to HDM2 suggested that 7-substituted 1,4-diazepine-2,5-diones could mimic the alpha-helix of p53 peptide and may represent a promising scaffold to develop HDM2-p53 antagonists.	7-substituted 1,4-diazepine-2,5-diones	66-104	P53	Homo sapiens	136-139
9773296-6	1998	The technique of microwave antigen retrieval gave crisp, clear immunohistochemical staining for p53 in tissues fixed in neutral buffered formalin or Bouin solution.	Formaldehyde	137-145	P53	Homo sapiens	96-99
11786354-3	2002	We propose a method for the determination of traces of GST in the p53 C-terminus based on the constant current chronopotentiometric stripping analysis (CPSA) with hanging mercury drop electrode (HMDE).	hmde	195-199	P53	Homo sapiens	66-69
11898040-10	2002	MSI appears to contribute to carcinogenesis in the biliary tract mucosa of PBM patients, and p53 mutations may be related to the development of GB cancer in the CCD group.	ccd	161-164	P53	Homo sapiens	93-96
15780621-1	2005	Crystallographic analysis of ligands bound to HDM2 suggested that 7-substituted 1,4-diazepine-2,5-diones could mimic the alpha-helix of p53 peptide and may represent a promising scaffold to develop HDM2-p53 antagonists.	7-substituted 1,4-diazepine-2,5-diones	66-104	P53	Homo sapiens	203-206
9498829-8	1998	Cell labeling by staining with bromodeoxiuridine indicated that p53 is an important factor in modulating growth in NSCLC tumors.	bromodeoxiuridine	31-48	P53	Homo sapiens	64-67
15748635-3	2005	In human skin cancers, about 35% of all mutations in the p53 gene are transitions at dipyrimidines within the sequence 5"-TCG and 5"-CCG, and these are localized at several mutational hotspots.	dipyrimidines	85-98	P53	Homo sapiens	57-60
15748635-4	2005	Since 5"-CG sequences are methylated along the p53 coding sequence in human cells, these mutations may be derived from sunlight-induced pyrimidine dimers forming at sequences that contain 5-methylcytosine.	pyrimidine	136-146	P53	Homo sapiens	47-50
15707991-5	2005	Furthermore, COX-2 interacted with p53 in vitro and in vivo, which was inhibited by the treatment with NS-398.	N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide	103-109	P53	Homo sapiens	35-38
15678854-6	1998	Immunohistochemical determination of p53 protein was performed on tissular samples formalin fixed and paraffin embedded, using mouse monoclonal antibody DAKO--p53 DO 7 p53 human antiprotein.	Formaldehyde	83-91	P53	Homo sapiens	37-40
9407038-7	1997	Low levels of phosphoserine-15 p53 are detectable within 6 hr after IR in AT cells, whereas lymphoblasts from normal individuals exhibit this modification within 1 hr.	Phosphoserine	14-27	P53	Homo sapiens	31-34
11747348-5	2001	Western blot analysis indicated that Tyrphostin AG 1024-induced apoptosis was associated with a downregulation of expression of phospho-Akt1, increased expression of Bax, p53 and p21, and a decreased expression of bcl-2 expression, especially when combined with irradiation.	Tyrphostins	37-47	P53	Homo sapiens	171-174
11554448-6	2001	Furthermore, we also review the available evidence on the role of p53 as a transactivator or transrepressor of genes involved in the production and control of reactive oxygen intermediates.	reactive oxygen	159-174	P53	Homo sapiens	66-69
15715472-10	2005	The butyric acid and formaldehyde induced cell differentiation and increased p53 and p21 levels, suggesting that both affect cancer cells, the acid by inhibiting HDAC and the aldehyde by an as yet unknown mechanism.	Formaldehyde	21-33	P53	Homo sapiens	77-80
11523059-10	2001	It is concluded that sennosides acutely induce apoptosis of colonic epithelial cells, presumably by a p53, p21/WAF-mediated pathway, resulting in shorter crypts.	senokot	21-31	P53	Homo sapiens	102-105
9499672-17	1997	Finally, p53 tumor suppressor gene has been associated with resistance to therapy with fludarabine.	fludarabine	87-98	P53	Homo sapiens	9-12
9267568-0	1997	Diagnostic implications of p53 protein reactivity in nasal mucosa of nickel workers.	Nickel	69-75	P53	Homo sapiens	27-30
15720815-6	2005	GSP-induced apoptosis in JB6 C141 cells was associated with increased expression of the tumor-suppressor protein, p53, and its phosphorylation at Ser15.	Grape Seed Proanthocyanidins	0-3	P53	Homo sapiens	114-117
9267568-1	1997	OBJECTIVE: To investigate whether the quantitation of p53 protein reactivity in nasal biopsies could be related to nickel exposure by comparing nickel workers with various control groups.	Nickel	115-121	P53	Homo sapiens	54-57
9267568-5	1997	RESULTS: p53 Protein reactivity was found in 54% (49/93) of nickel workers, 50% (17/34) of office staff members, 67% (4/6) of hospital attendants.	Nickel	60-66	P53	Homo sapiens	9-12
9267568-11	1997	CONCLUSION: Accumulation of p53 protein in nickel workers seems not to be attributable to nickel exposure.	Nickel	43-49	P53	Homo sapiens	28-31
11466694-6	2001	RESULTS: In the NSCLC specimens, anticancer agents, including TZT-1027, showed strong antitumor activity against 50--75% of specimens with the wild type p53 gene.	soblidotin	62-70	P53	Homo sapiens	153-156
11466694-11	2001	Therefore, TZT-1027 is expected to show similar antitumor activity against tumors with a loss of p53 function as well as those with normal function of p53 in clinical fields.	soblidotin	11-19	P53	Homo sapiens	97-100
15576237-7	2004	Interestingly, CYP2D6-treated eugenol strongly damaged C and G of the 5"-ACG-3" sequence complementary to codon 273 of the p53 gene.	Eugenol	30-37	P53	Homo sapiens	123-126
11451905-0	2001	Enhancement of fibrogenesis by the p53 tumor suppressor protein in asbestos-exposed rodents.	Asbestos	67-75	P53	Homo sapiens	35-38
11453316-1	2001	The aim of this study is to investigate immunoreactivity for p53, p21 and metallothionein in diffuse malignant pleural mesothelioma (DMPM) and to determine the relationships between the age, sex, asbestos exposure time, survival of DMPM patients with environmental asbestos exposure and immunoreactivity to p53, p21 and metallothionein.	dmpm	133-137	P53	Homo sapiens	61-64
9389352-8	1997	Treatment of CLL cells having wild type p53 with CdA, F-ara-A or CLB produced an increase in p53 protein and mdm-2 mRNA.	Cladribine	49-52	P53	Homo sapiens	40-43
9389352-8	1997	Treatment of CLL cells having wild type p53 with CdA, F-ara-A or CLB produced an increase in p53 protein and mdm-2 mRNA.	Cladribine	49-52	P53	Homo sapiens	93-96
9389352-8	1997	Treatment of CLL cells having wild type p53 with CdA, F-ara-A or CLB produced an increase in p53 protein and mdm-2 mRNA.	fludarabine	54-61	P53	Homo sapiens	40-43
9389352-8	1997	Treatment of CLL cells having wild type p53 with CdA, F-ara-A or CLB produced an increase in p53 protein and mdm-2 mRNA.	fludarabine	54-61	P53	Homo sapiens	93-96
9389352-11	1997	Treatment of CLL cells containing a wild type p53 gene with CdA, F-ara-A, or CLB, did not produce any consistent changes in bax or bcl-2.	Cladribine	60-63	P53	Homo sapiens	46-49
9389352-12	1997	Thus, CdA, F-ara-A and CLB appear to act in CLL cells through a p53-dependent pathway, whereas this does not occur with dexamethasone or vincristine.	Cladribine	6-9	P53	Homo sapiens	64-67
9812577-2	1997	Results showed that fragment of exon 7 or 8 of p53 gene in four cases was positive in silver-staining analysis of PCR-SSCP.	Silver	86-92	P53	Homo sapiens	47-50
9812584-3	1997	Lanthanum chloride, cerium chloride and mixed rare-earth chloride at levels of 0.5 to 1.5 mmol/L could inhibit obviously growth of cancer cells and change cell morphology and microtubule structure of PAMC82, similar to that of normal cells, their colony-forming ability lowered in soft agar, and expression of tumor suppressor gene p53, p16 and p21 increased and that of gene nm23 lowered.	Chlorides	10-18	P53	Homo sapiens	332-335
11358908-10	2001	All tumour regions showed a point mutation in p53 gene at exon 7 (GGC (glycine)--&gt;GTC (valine) at codon 245).	Valine	90-96	P53	Homo sapiens	46-49
11358908-11	2001	The distal portion of the duodenal tumour showed an additional point mutation in p53 gene at exon 5 (GCC (alanine)--&gt;GTC (valine) at codon 129).	Valine	125-131	P53	Homo sapiens	81-84
11494111-0	2001	Poly(ADP-ribosyl)ation of p53 in vitro and in vivo modulates binding to its DNA consensus sequence.	poly(adp-ribosyl)	0-17	P53	Homo sapiens	26-29
9190897-0	1997	Geldanamycin-stimulated destabilization of mutated p53 is mediated by the proteasome in vivo.	geldanamycin	0-12	P53	Homo sapiens	51-54
15547693-4	2004	The p53-mutated status of FaDu human pharynx carcinoma cell line was first assessed by DNA sequencing and the cells were transfected using tetraglucosylated polyethylenimine (PEI-Glu4) in conjunction with photochemical internalisation (PCI).	pei-glu4	175-183	P53	Homo sapiens	4-7
9190897-5	1997	We found that this impairment of p53 turnover can be reversed by treatment of tumor cells with the benzoquinone ansamycin, geldanamycin, leading to a marked reduction in intracellular p53 levels.	geldanamycin	123-135	P53	Homo sapiens	33-36
9190897-5	1997	We found that this impairment of p53 turnover can be reversed by treatment of tumor cells with the benzoquinone ansamycin, geldanamycin, leading to a marked reduction in intracellular p53 levels.	geldanamycin	123-135	P53	Homo sapiens	184-187
9190897-6	1997	Finally, using cells which over-express a mutant p53 protein, we were able to demonstrate that restoration of proteasome-mediated degradation by geldanamycin is accompanied by p53 polyubiquitination.	geldanamycin	145-157	P53	Homo sapiens	49-52
11289281-4	2001	METHODS: Mutation screening of the hot spots of the K-ras gene and of the evolutionarily conserved regions of the TP53 gene was performed by denaturing gradient gel electrophoresis technique in formalin-fixed paraffin-embedded specimens of 55 consecutive patients with Dukes C colon cancer treated with adjuvant 5-fluorouracil-based chemotherapy.	Formaldehyde	194-202	P53	Homo sapiens	114-118
15358769-2	2004	We show that geldanamycin or radicicol, specific inhibitors of Hsp90, diminish specific wild-type p53 binding to the p21 promoter sequence.	geldanamycin	13-25	P53	Homo sapiens	98-101
11273776-3	2001	In this report, we describe an improved extruded DOTAP:cholesterol (DOTAP:Chol) cationic liposome that efficiently delivers therapeutic tumor suppressor genes p53 and FHIT, which are frequently altered in lung cancer, to localized human primary lung cancers and to experimental disseminated metastases.	chol	74-78	P53	Homo sapiens	159-162
11273776-5	2001	When treated with DOTAP:Chol-p53 and -FHIT complex, significant suppression was observed in both primary (P &lt; 0.02) and metastatic lung tumor growth (P &lt; 0.007).	chol	24-28	P53	Homo sapiens	29-32
11797833-0	2001	Low levels of p53 mutations in Indian patients with osteosarcoma and the correlation with fluoride levels in bone.	Fluorides	90-98	P53	Homo sapiens	14-17
11797833-3	2001	We were interested in exploring the possible relationship between fluoride bone content and p53 mutations.	Fluorides	66-74	P53	Homo sapiens	92-95
9190897-6	1997	Finally, using cells which over-express a mutant p53 protein, we were able to demonstrate that restoration of proteasome-mediated degradation by geldanamycin is accompanied by p53 polyubiquitination.	geldanamycin	145-157	P53	Homo sapiens	176-179
9190897-7	1997	Although much remains to be learned about the mechanisms involved, our data demonstrate that selective de-stabilization of mutant transforming proteins such as p53 can be achieved pharmacologically with agents such as geldanamycin which modify the function of molecular chaperone proteins within tumor cells.	geldanamycin	218-230	P53	Homo sapiens	160-163
9815713-8	1997	Growth of NPC cells treated with Ad5CMV-p53 was observed to be significantly inhibited when determined by either the 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide or clonogenic assay.	thiazolyl blue	117-178	P53	Homo sapiens	40-43
15358769-11	2004	Consistent with our in vivo results, geldanamycin can suppress Hsp90 ability to regulate in vitro p53 DNA binding to the promoter sequence.	geldanamycin	37-49	P53	Homo sapiens	98-101
15217838-8	2004	Nuclear translocation of p53 after fludarabine treatment was decreased when STAT1beta was overexpressed, and it was increased when STAT1alpha was induced.	fludarabine	35-46	P53	Homo sapiens	25-28
9260591-4	1997	The expression of the proteins p53 and mdm2 was determined immunohistochemically using formalin-fixed, paraffin-embedded material.	Formaldehyde	87-95	P53	Homo sapiens	31-34
8967975-1	1996	With the use of clonogenic survival assays, we show that wild-type p53-expressing A2780 human ovarian cell lines transfected with a dominant negative mutant p53 gene (codon 143, valine to alanine) acquired cross-resistance to ionizing radiation, cisplatin, doxorubicin, and 1-beta-D-arabinofuranosylcytosine.	Valine	178-184	P53	Homo sapiens	67-70
8967975-1	1996	With the use of clonogenic survival assays, we show that wild-type p53-expressing A2780 human ovarian cell lines transfected with a dominant negative mutant p53 gene (codon 143, valine to alanine) acquired cross-resistance to ionizing radiation, cisplatin, doxorubicin, and 1-beta-D-arabinofuranosylcytosine.	Valine	178-184	P53	Homo sapiens	157-160
11351862-5	2000	The Northern blot analysis revealed marked up-regulation of p53, p16(MTS1), p21 (WAF1) gene expressions in PAMC82 cells treated with lanthanum chloride and cerium chloride, as compared to control PAMC82 cells.	cerous chloride	156-171	P53	Homo sapiens	60-63
11029511-10	2000	These data indicate that synergistic growth inhibition by UCN-01 and CPT against p53 mutant MDA-MB-231 tumor cells may be due to induction of DSBs however the loss of p53 function alone does not sensitize normal cells to the combination of both drugs.	dsbs	142-146	P53	Homo sapiens	81-84
15217838-10	2004	Our results show that imbalance between the antiproliferative/proapoptotic isoform STAT1alpha and the proliferative isoform STAT1beta is likely to play a crucial role in the regulation of proliferation and apoptosis and that STAT1alpha may regulate p53 activity and sensitize B cells to fludarabine-induced apoptosis.	fludarabine	287-298	P53	Homo sapiens	249-252
11079153-2	2000	Clonogenic survival studies indicate that EB 1089 shifts the dose-response curve for sensitivity to adriamycin by approximately six-fold in p53 wild-type MCF-7 cells; comparative studies in MCF-7 cells with a temperature-sensitive dominant negative p53 mutation show less than a two-fold shift in adriamycin sensitivity in the presence of EB 1089.	ethylbenzene	42-44	P53	Homo sapiens	140-143
11079153-2	2000	Clonogenic survival studies indicate that EB 1089 shifts the dose-response curve for sensitivity to adriamycin by approximately six-fold in p53 wild-type MCF-7 cells; comparative studies in MCF-7 cells with a temperature-sensitive dominant negative p53 mutation show less than a two-fold shift in adriamycin sensitivity in the presence of EB 1089.	ethylbenzene	42-44	P53	Homo sapiens	249-252
9387525-2	1996	METHODS: Mutations in exons 5-8 of p53 gene in 41 patients with primary ovarian cancer were screened by polymerase chain reaction-single strand conformation polymorphism analysis with non-isotopic silver staining method.	Silver	197-203	P53	Homo sapiens	35-38
8870682-4	1996	With the use of S-nitroglutathione (GSNO) we correlated a dose-dependent p53 up-regulation to DNA fragmentation measured after 4 h and 8 h, respectively.	S-nitroglutathione	16-34	P53	Homo sapiens	73-76
15456252-6	2004	An NMR-docked model of one such inhibitor, pentamidine, bound to Ca(2+)-loaded S100B was calculated using intermolecular NOE data between S100B and the drug, and indicates that pentamidine binds into the p53 binding site on S100B defined by helices 3 and 4 and loop 2 (termed the hinge region).	Pentamidine	43-54	P53	Homo sapiens	204-207
9816112-7	1996	We also find that induction of wild-type p53 potentiates the cytotoxicity of topotecan, a member of the camptothecin family of drugs that also has clinical activity against colon cancer.	Topotecan	77-86	P53	Homo sapiens	41-44
10953164-0	2000	Brefeldin A induces p53-independent apoptosis in primary cultures of human prostatic cancer cells.	Brefeldin A	0-11	P53	Homo sapiens	20-23
10953164-5	2000	Immunoblots were used to monitor p53 and pRB expression in response to BFA.	Brefeldin A	71-74	P53	Homo sapiens	33-36
10953164-12	2000	CONCLUSIONS: BFA is a potent inducer of apoptosis in prostatic cancer cells via a p53-independent mechanism.	Brefeldin A	13-16	P53	Homo sapiens	82-85
10953164-14	2000	Since p53-mediated pathways of apoptosis may frequently be abrogated in prostatic cancer cells, agents such as BFA that induce p53-independent cell death may be promising candidates for chemotherapeutic agents.	Brefeldin A	111-114	P53	Homo sapiens	6-9
10953164-14	2000	Since p53-mediated pathways of apoptosis may frequently be abrogated in prostatic cancer cells, agents such as BFA that induce p53-independent cell death may be promising candidates for chemotherapeutic agents.	Brefeldin A	111-114	P53	Homo sapiens	127-130
8855263-0	1996	p53-dependent cell cycle arrest induced by N-acetyl-L-leucinyl-L-leucinyl-L-norleucinal in platelet-derived growth factor-stimulated human fibroblasts.	n-acetyl-l-leucinyl-l-leucinyl	43-73	P53	Homo sapiens	0-3
15456252-6	2004	An NMR-docked model of one such inhibitor, pentamidine, bound to Ca(2+)-loaded S100B was calculated using intermolecular NOE data between S100B and the drug, and indicates that pentamidine binds into the p53 binding site on S100B defined by helices 3 and 4 and loop 2 (termed the hinge region).	Pentamidine	177-188	P53	Homo sapiens	204-207
15373832-2	2004	Using p53 deletion mutants, we have previously shown that the p53 C-terminal DNA-binding site (CTDBS) is critical for this binding.	ctdbs	95-100	P53	Homo sapiens	6-9
8831555-6	1996	BFA-induced apoptosis is p53-independent as HL60 and K562 cells are p53 null and HT-29 are p53 mutant cells.	Brefeldin A	0-3	P53	Homo sapiens	25-28
8831555-6	1996	BFA-induced apoptosis is p53-independent as HL60 and K562 cells are p53 null and HT-29 are p53 mutant cells.	Brefeldin A	0-3	P53	Homo sapiens	68-71
10910962-1	2000	Simultaneous labelling of 17cen and the p53 locus by multicolour FISH was used to monitor radioactive iodine-induced structural and numerical chromosome abnormalities in buccal cells from 29 hyperthyroidism and thyroid cancer patients sampled before and after therapeutic treatment.	Iodine	102-108	P53	Homo sapiens	40-43
8831555-6	1996	BFA-induced apoptosis is p53-independent as HL60 and K562 cells are p53 null and HT-29 are p53 mutant cells.	Brefeldin A	0-3	P53	Homo sapiens	68-71
15373832-2	2004	Using p53 deletion mutants, we have previously shown that the p53 C-terminal DNA-binding site (CTDBS) is critical for this binding.	ctdbs	95-100	P53	Homo sapiens	62-65
15724841-4	2004	In this study, we report the implication of p53 on growth arrest and apoptosis following the combined treatment of human mammary epithelial cells with topotecan, a specific topoisomerase I inhibitor, and UCN-01.	Topotecan	151-160	P53	Homo sapiens	44-47
10972990-3	2000	In this study, we demonstrate that the deficiency of wild-type p53 protein may allow unrepaired DSBs to initiate chromosomal instability.	dsbs	96-100	P53	Homo sapiens	63-66
10972990-11	2000	In wild-type p53 cells, spontaneous DSBs appear to be promptly repaired through recombination between homologous chromosomes.	dsbs	36-40	P53	Homo sapiens	13-16
15724841-9	2004	Detailed cell-cycle analyses revealed that UCN-01 abrogated S-phase accumulation induced by topotecan treatment in p53 defective MDA231 tumor cells and HMEC/E6 cells.	Topotecan	92-101	P53	Homo sapiens	115-118
10930428-2	2000	Several attempts to generate an antibody to p53 phosphorylated at Ser(6) using a phosphoserine-containing peptide as an immunogen were unsuccessful; however, phosphorylation-specific antibodies were produced by using the phosphoserine mimetic, l-2-amino-4-phosphono-4, 4-difluorobutanoic acid (F(2)Pab), in place of phosphoserine.	Phosphoserine	81-94	P53	Homo sapiens	44-47
8875051-1	1996	It has been demonstrated that temperature-sensitive mutant p53 (val--&gt;ala143) inhibits cell-proliferation at the permissive temperature, albeit to a lesser extent than wild-type p53 (Zhang et al.	Valine	64-67	P53	Homo sapiens	59-62
10930428-2	2000	Several attempts to generate an antibody to p53 phosphorylated at Ser(6) using a phosphoserine-containing peptide as an immunogen were unsuccessful; however, phosphorylation-specific antibodies were produced by using the phosphoserine mimetic, l-2-amino-4-phosphono-4, 4-difluorobutanoic acid (F(2)Pab), in place of phosphoserine.	Phosphoserine	221-234	P53	Homo sapiens	44-47
15724841-12	2004	These data indicate that UCN-01 selectively enhances topotecan cytotoxicity in p53 defective cells through the induction of apoptotic signaling pathway(s), although the time course for the induction of cell death is not the same.	Topotecan	53-62	P53	Homo sapiens	79-82
10930428-2	2000	Several attempts to generate an antibody to p53 phosphorylated at Ser(6) using a phosphoserine-containing peptide as an immunogen were unsuccessful; however, phosphorylation-specific antibodies were produced by using the phosphoserine mimetic, l-2-amino-4-phosphono-4, 4-difluorobutanoic acid (F(2)Pab), in place of phosphoserine.	l-2-amino-4-phosphono-4, 4-difluorobutanoic acid	244-292	P53	Homo sapiens	44-47
10930428-2	2000	Several attempts to generate an antibody to p53 phosphorylated at Ser(6) using a phosphoserine-containing peptide as an immunogen were unsuccessful; however, phosphorylation-specific antibodies were produced by using the phosphoserine mimetic, l-2-amino-4-phosphono-4, 4-difluorobutanoic acid (F(2)Pab), in place of phosphoserine.	Phosphoserine	221-234	P53	Homo sapiens	44-47
15724841-13	2004	UCN-01 may, therefore, provide a new modality for topotecan-based therapy, particularly in p53 defective cancer patients.	Topotecan	50-59	P53	Homo sapiens	91-94
8879300-2	1996	The accumulation of p53 protein was studied immunohistochemically using monoclonal antibody BP53-12 on formalin-fixed paraffin-embedded sections of 36 KS lesions, of which 14 were classified histologically as early type and 22 as spindle-cell or mixed type.	Formaldehyde	103-111	P53	Homo sapiens	20-23
15374966-8	2004	Inhibition of p53 and caspases with alpha-pifithrin and z-Val-Ala-Asp-fluoromethyl ketone, respectively, blocked UVB- and doxorubicin-induced apoptosis in ATRA-treated KCs.	alpha-pifithrin	36-51	P53	Homo sapiens	14-17
10884347-4	2000	Peptide competition studies have localized a cyclin A interaction site to a Lys381Lys382Leu383Met384Phe385 sequence within C-terminal negative regulatory domain of human p53.	lys381lys382leu383met384phe385	76-106	P53	Homo sapiens	170-173
8782209-10	1996	We used the DO-7 monoclonal antibody reactive for the N-terminal of the p53 protein on formalin-fixed paraffin-embedded tissue.	Formaldehyde	87-95	P53	Homo sapiens	72-75
15551755-2	2004	A previous study showed that 11 poly-arginine fused p53 protein (11R-p53) effectively penetrated across the plasma membrane and inhibited the proliferation of oral cancer cells.	polyarginine	32-45	P53	Homo sapiens	52-55
15551755-2	2004	A previous study showed that 11 poly-arginine fused p53 protein (11R-p53) effectively penetrated across the plasma membrane and inhibited the proliferation of oral cancer cells.	polyarginine	32-45	P53	Homo sapiens	69-72
10903257-8	2000	p53 expression evaluated by immunohistochemistry was frequently observed in dysplasias from pneumoconiosis with DIF, although it was not significantly different compared with that in dysplasias from pneumoconiosis without DIF (5 [50%] of 10 versus 12 [38%] of 32).	Diclofenac	112-115	P53	Homo sapiens	0-3
15252149-10	2004	Attenuating p53 by a chemical inhibitor pifithrin-alpha decreased the selenite-induced p53 Ser15P and led to concordant reductions of PARP cleavage and apoptosis.	Selenious Acid	70-78	P53	Homo sapiens	12-15
10918568-8	2000	Secondly, azadeoxycytidine reactivation of the silent hMLH1 gene or expression of a transfected hMLH1 cDNA sensitized the doubly hMLH1/p53 deficient cells only slightly to cisplatin.	azadeoxycytidine	10-26	P53	Homo sapiens	135-138
8787547-11	1996	Together with earlier results showing downmodulation for IL-8 receptor type A expression in cultured KC treated with FK506, these results suggest that both the mitogenic IL-8/IL-8R system and the cell cycle inhibitor p53 represent potential targets for the antipsoriatic action of the drug, whereas protooncogenes acting downstream in mitogenic signal transduction cascades are unaffected.	Tacrolimus	117-122	P53	Homo sapiens	217-220
15252149-10	2004	Attenuating p53 by a chemical inhibitor pifithrin-alpha decreased the selenite-induced p53 Ser15P and led to concordant reductions of PARP cleavage and apoptosis.	Selenious Acid	70-78	P53	Homo sapiens	87-90
15252149-11	2004	In summary, selenite-induced p53 Ser15P appeared to be important for activating the caspase-mediated apoptosis involving both the caspase-8 and the caspase-9 pathways in the LNCaP cells.	Selenious Acid	12-20	P53	Homo sapiens	29-32
10929428-14	2000	Mutant p53 expression was more decreased in the EJ cells treated with RA or Ni(RA)2.3H2O than in the control.	ni(ra)2.3h2o	76-88	P53	Homo sapiens	7-10
15461257-1	2004	OBJECTIVE: To study the effects of DNA damage and apoptosis and p53 expression, and to explore the relationship between apoptosis and p53 expression in human embryo hepatocytes induced by fluoride.	Fluorides	188-196	P53	Homo sapiens	134-137
8691338-2	1996	Stabilization of the p53 gene product was analysed by immunohistochemistry and proliferative activity was determined flow cytometrically and by silver staining of nucleolar organizer regions (AgNORs).	Silver	144-150	P53	Homo sapiens	21-24
15461257-7	2004	CONCLUSION: Fluoride can increase the rate of DNA damage, and induce apoptosis and expression of p53 in human embryo hepatocytes.	Fluorides	12-20	P53	Homo sapiens	97-100
15461257-8	2004	Furthermore, both apoptosis and the level of p53 expression, there exists a rise tendency with the increase concentration of fluoride.	Fluorides	125-133	P53	Homo sapiens	45-48
14751514-12	2004	The other 50% was attributed to the p53-dependent permanent G1 arrest, because cells lacking in functional p53 (LFS2800, FaDu, CHO) showed a ratio of LE:CA = 1.01 +/- 0.02:1.	CAV protocol	127-130	P53	Homo sapiens	36-39
8606380-5	1996	METHODS: Immunohistochemical analysis with a monoclonal antibody (DO7) specific for p53 protein was used to detect expression of the protein in formalin-fixed, paraffin-embedded tumor samples from 69 head and neck cancer patients treated with definitive local therapy (surgery and/or radiotherapy) between January 1980 and October 1983 at The University of Texas M. D. Anderson Cancer Center.	Formaldehyde	144-152	P53	Homo sapiens	84-87
14751514-12	2004	The other 50% was attributed to the p53-dependent permanent G1 arrest, because cells lacking in functional p53 (LFS2800, FaDu, CHO) showed a ratio of LE:CA = 1.01 +/- 0.02:1.	CAV protocol	127-130	P53	Homo sapiens	107-110
8648390-2	1996	In vitro incubation of acute myelogenous leukemia with OL(1)p53, a 20-mer phosphorothioate oligonucleotide complementary to p53 mRNA, results in leukemic cell death.	Parathion	74-90	P53	Homo sapiens	60-63
14744793-4	2004	We have shown previously that perifosine induces p21(waf1/cip1) in a p53-independent fashion and that induction of p21(waf1/cip1) is required for the perifosine-induced cell cycle arrest because cell lines lacking p21(waf1/cip1) are refractory to perifosine.	perifosine	30-40	P53	Homo sapiens	69-72
8648390-2	1996	In vitro incubation of acute myelogenous leukemia with OL(1)p53, a 20-mer phosphorothioate oligonucleotide complementary to p53 mRNA, results in leukemic cell death.	Parathion	74-90	P53	Homo sapiens	124-127
8648390-13	1996	CONCLUSION: A phosphorothioate oligonucleotide, OL(1)p53, can be administered systemically without complications.	Phosphorothioate Oligonucleotides	14-46	P53	Homo sapiens	53-56
8733010-7	1996	Omitting the cAMP stimulus prevents the p53-induced apoptosis in these cells, suggesting cross-talk between p53 and c-AMP-generated signals in the induction of apoptosis.	c-amp	116-121	P53	Homo sapiens	40-43
14744793-7	2004	Using several p21(waf1/cip1) promoter-driven luciferase reporter plasmids, we observed that perifosine activates the 2.4-kb full-length p21(waf1/cip1) promoter as well as a p21 promoter construct lacking p53-binding sites, suggesting that perifosine activates the p21(waf1/cip1) promoter independent of p53.	perifosine	92-102	P53	Homo sapiens	204-207
14744793-7	2004	Using several p21(waf1/cip1) promoter-driven luciferase reporter plasmids, we observed that perifosine activates the 2.4-kb full-length p21(waf1/cip1) promoter as well as a p21 promoter construct lacking p53-binding sites, suggesting that perifosine activates the p21(waf1/cip1) promoter independent of p53.	perifosine	92-102	P53	Homo sapiens	303-306
14698413-10	2004	Based on the results from Tester Strain TA7005, it indicate that BPT and its most mutagenic metabolite BPT sulfoxide induce predominantly CG --&gt; AT transversion, which is observed as the most frequent base substitution mutation of p53 tumor-suppressor gene in human lung cancer.	bpt sulfoxide	103-116	P53	Homo sapiens	234-237
8649821-0	1996	ETS1 and ETS2 in p53 regulation: spatial separation of ETS binding sites (EBS) modulate protein: DNA interaction.	ethylbenzene	74-77	P53	Homo sapiens	17-20
8600043-10	1996	p53 staining was associated with juvenile type GCTs (P&lt;.001) and higher Ki67PI (P&lt;.005).	ki67pi	75-81	P53	Homo sapiens	0-3
14682762-0	2003	Solid-phase synthesis of the cyclic peptide portion of chlorofusin, an inhibitor of p53-MDM2 interactions.	Peptides, Cyclic	29-43	P53	Homo sapiens	84-87
14637186-11	2003	The expression of p53, phospho-serine 15 of p53, and Bax, and inactivate form of CPP32 was suppressed by a pretreatment of a specific p38 MAPK inhibitor, SB203580.	Phosphoserine	23-37	P53	Homo sapiens	44-47
8846164-0	1996	The induction of p53 and WAF1/CIP1 in chronic lymphocytic leukemia cells treated with 2-chlorodeoxyadenosine.	Cladribine	86-108	P53	Homo sapiens	17-20
8846164-3	1996	In this report we describe the induction of p53 and WAF1/CIP1 in the apoptotic chronic lymphocytic leukemia cells after exposure to 2-chlorodeoxyadenosine.	Cladribine	132-154	P53	Homo sapiens	44-47
8832944-4	1996	OBJECTIVE AND METHODS: The aim of the present study is to examine the frequency of immunohistochemically detectable p53 protein by using two monoclonal antibodies (D07 and BP53-12) in 8 cases of formalin-fixed and paraffin-embedded specimens of verrucous skin carcinoma.	Formaldehyde	195-203	P53	Homo sapiens	116-119
14617782-4	2003	Recent studies have identified that perifosine could cause cell cycle arrest with induction of p21(WAF1/CIP1) in a p53-independent fashion; however, the basis for that effect is not known.	perifosine	36-46	P53	Homo sapiens	115-118
9163103-6	1996	In conditions that do not lead to apoptosis, the expression of ts-wt-p53 was accompanied by dramatic increase in the number of cells containing glycophorin A (GlycPhA) and "antigen of erythroblasts"--specific markers of erythroid differentiation.	erythroid	220-229	P53	Homo sapiens	69-72
8732103-0	1996	[Detection of point mutation of p53 gene by silver staining PCR-SSCP in paraffin-embedded malignant fibrous histiocytoma].	Silver	44-50	P53	Homo sapiens	32-35
8732103-1	1996	Silver staining PCR-SSCP method was used to detect point mutation of p53 gene in paraffin-embedded malignant fibrous histiocytoma (MFH) tissues.	Silver	0-6	P53	Homo sapiens	69-72
14559983-6	2003	P53 protein expression showed a positive correlation with microvessel density, suggesting possible overlap in the underlying mechanism of these two factors in the pathogenesis of phyllodes tumors.	phyllodes	179-188	P53	Homo sapiens	0-3
7493974-2	1995	We found that DEM-induced oxidative stress reduced the ability of p53 to bind its consensus recognition sequence and to activate transcription of a p53-specific reporter gene.	diethyl maleate	14-17	P53	Homo sapiens	66-69
7493974-2	1995	We found that DEM-induced oxidative stress reduced the ability of p53 to bind its consensus recognition sequence and to activate transcription of a p53-specific reporter gene.	diethyl maleate	14-17	P53	Homo sapiens	148-151
14559983-8	2003	We conclude that microvessel density and p53 are useful as independent criteria in evaluating malignancy in phyllodes tumors.	phyllodes	108-117	P53	Homo sapiens	41-44
14508081-7	2003	The activity of the mutant p53 in tumor cells is restorable based on the fact that PAb241 antibody against the carboxy-terminus of p53 and peptides corresponding to the p53 carboxy-terminus can restore specific DNA-binding ability to some mutant p53 proteins.	pab241	83-89	P53	Homo sapiens	27-30
8640471-0	1995	Immunohistochemical detection of p53 overexpression in formalin-fixed, paraffin-embedded sections of endometrial carcinoma.	Formaldehyde	55-63	P53	Homo sapiens	33-36
8640471-2	1995	However using CM1 and an enhanced method based on microwave heating and protease digestion enabled the immunohistochemical detection of p53 overexpression in formalin-fixed, paraffin-embedded sections of endometrial carcinoma, although very few positive stainings were obtained without such an enhanced treatment.	Formaldehyde	158-166	P53	Homo sapiens	136-139
14508081-7	2003	The activity of the mutant p53 in tumor cells is restorable based on the fact that PAb241 antibody against the carboxy-terminus of p53 and peptides corresponding to the p53 carboxy-terminus can restore specific DNA-binding ability to some mutant p53 proteins.	pab241	83-89	P53	Homo sapiens	131-134
14508081-7	2003	The activity of the mutant p53 in tumor cells is restorable based on the fact that PAb241 antibody against the carboxy-terminus of p53 and peptides corresponding to the p53 carboxy-terminus can restore specific DNA-binding ability to some mutant p53 proteins.	pab241	83-89	P53	Homo sapiens	131-134
14508081-7	2003	The activity of the mutant p53 in tumor cells is restorable based on the fact that PAb241 antibody against the carboxy-terminus of p53 and peptides corresponding to the p53 carboxy-terminus can restore specific DNA-binding ability to some mutant p53 proteins.	pab241	83-89	P53	Homo sapiens	131-134
12826255-5	2003	Pretreatment of neurons with alpha-pifithrin, a specific p53 inhibitor, resulted in a 50-60% prevention of Abeta induced apoptosis.	alpha-pifithrin	29-44	P53	Homo sapiens	57-60
8524262-4	1995	A temperature-sensitive p53 allele (Val-135) was introduced into the Friend erythroleukemia cell line (DP-16) which lacks endogenous p53 expression.	Valine	36-39	P53	Homo sapiens	24-27
12738038-3	2003	ELISA assay demonstrated that tetrandrine significantly increased the expression of p53 and p21/WAF1 protein, which caused cell cycle arrest.	tetrandrine	30-41	P53	Homo sapiens	84-87
8521821-0	1995	Loss of p53 function through PAX-mediated transcriptional repression.	pax	29-32	P53	Homo sapiens	8-11
8521821-4	1995	The human p53 gene harbours a PAX binding site within its untranslated first exon that is conserved throughout evolution.	pax	30-33	P53	Homo sapiens	10-13
12738038-5	2003	Taken together, p53 and Fas/FasL apoptotic system possibly participated in the antiproliferative activity of tetrandrine in Hep G2 cells.	tetrandrine	109-120	P53	Homo sapiens	16-19
8533158-2	1995	In normal cells, the induction of p53 by dNTP starvation serves a protective role, mediating rapid, reversible cell-cycle arrest without DNA damage.	Parathion	41-45	P53	Homo sapiens	34-37
12684687-4	2003	We report that Brca1-deficiency in p53-null cells was associated with increased sensitivity to the topoisomerase I poisons camptothecin and topotecan, the topoisomerase II poisons doxorubicin, mitoxantrone and etoposide, and to the platinum compounds carboplatin and oxaliplatin, but not to the antimetabolites 5-fluorouracil and gemcitabine and the taxanes docetaxel and paclitaxel.	Topotecan	140-149	P53	Homo sapiens	35-38
12659945-9	2003	We demonstrated an antisense ODN of p53 delivered by PEI/DOTAP-Chol combination effectively inhibited the biosynthesis of p53 protein in HepG2 (68% inhibiton) and 2.2.15 cells (43% inhibition).	dotap-chol	57-67	P53	Homo sapiens	36-39
8526349-1	1995	Inhibition of expression of ras-p21 and p53 by sulindac during azoxymethane-induced colon carcinogenesis.	Sulindac	47-55	P53	Homo sapiens	40-43
12659945-9	2003	We demonstrated an antisense ODN of p53 delivered by PEI/DOTAP-Chol combination effectively inhibited the biosynthesis of p53 protein in HepG2 (68% inhibiton) and 2.2.15 cells (43% inhibition).	dotap-chol	57-67	P53	Homo sapiens	122-125
7472782-3	1995	p53 expression was evaluated by immunohistochemistry in formalin-fixed, paraffin-embedded tissue from 23 leiomyosarcomas, 10 tumours of uncertain malignant potential (TUMPs), and 18 leiomyomas.	Formaldehyde	56-64	P53	Homo sapiens	0-3
12446453-0	2003	The vitamin D3 analog EB1089 induces apoptosis via a p53-independent mechanism involving p38 MAP kinase activation and suppression of ERK activity in B-cell chronic lymphocytic leukemia cells in vitro.	seocalcitol	22-28	P53	Homo sapiens	53-56
8697968-3	1995	The expression of p53 protein was also immunohistochemically studied in formalin-fixed paraffin embedded specimens of 76 colorectal adenocarcinomas and 112 colorectal polyps.	Formaldehyde	72-80	P53	Homo sapiens	18-21
12729255-8	2003	For example, both nickel compounds activated a number of transcription factors including hypoxia-inducible factor I (HIF-1) and p53.	Nickel	18-24	P53	Homo sapiens	128-131
7656242-2	1995	Two "hot regions" at codons 223-250 and 257-283 of the p53 gene were easily attacked by nitroso-2-acetylaminofluorene or acetoxy-2-acetylaminofluorene.	1-Acetoxy-2-acetylaminofluorene	121-150	P53	Homo sapiens	55-58
12729255-10	2003	The obtained data are in agreement with our previous observations that acute nickel exposure activates HIF-1 and p53 transcription factors and in nickel-transformed cells, the ratio of HIF-I activity to p53 activity was shifted towards high HIF-I activity.	Nickel	77-83	P53	Homo sapiens	113-116
21552845-5	1995	p53 aberrations (gene mutation and/or protein overexpression) were observed in 1 (12%) of 8 DCIS, 1 (11%) of 9 DCIC (&lt;20%), 3 (23%) of 13 DCIC (20%-50%), and 13 (28%) of 47 DCIC (&gt;50%).	dcic	111-115	P53	Homo sapiens	0-3
21552845-5	1995	p53 aberrations (gene mutation and/or protein overexpression) were observed in 1 (12%) of 8 DCIS, 1 (11%) of 9 DCIC (&lt;20%), 3 (23%) of 13 DCIC (20%-50%), and 13 (28%) of 47 DCIC (&gt;50%).	dcic	141-145	P53	Homo sapiens	0-3
21552845-5	1995	p53 aberrations (gene mutation and/or protein overexpression) were observed in 1 (12%) of 8 DCIS, 1 (11%) of 9 DCIC (&lt;20%), 3 (23%) of 13 DCIC (20%-50%), and 13 (28%) of 47 DCIC (&gt;50%).	dcic	141-145	P53	Homo sapiens	0-3
12729255-10	2003	The obtained data are in agreement with our previous observations that acute nickel exposure activates HIF-1 and p53 transcription factors and in nickel-transformed cells, the ratio of HIF-I activity to p53 activity was shifted towards high HIF-I activity.	Nickel	77-83	P53	Homo sapiens	203-206
12729255-10	2003	The obtained data are in agreement with our previous observations that acute nickel exposure activates HIF-1 and p53 transcription factors and in nickel-transformed cells, the ratio of HIF-I activity to p53 activity was shifted towards high HIF-I activity.	Nickel	146-152	P53	Homo sapiens	203-206
7477776-1	1995	Mutations of the p53 tumor-suppressor gene, as determined by the immunohistochemistry of archival formalin-fixed specimens, have been correlated with the prognosis for patients with many different types of malignancy.	Formaldehyde	98-106	P53	Homo sapiens	17-20
12640128-8	2003	We found that centrosomal p53 is poly(ADP-ribosyl)ated in vivo and centrosomal PARP-1 directly catalyzes poly(ADP-ribosyl)ation of p53 in vitro.	poly(adp-ribosyl)	33-50	P53	Homo sapiens	26-29
9816045-7	1995	p53 gene and its protein product were examined in formalin-fixed and fresh-frozen tumor tissues using immunohistochemistry, PCR-single-strand conformational polymorphism, and sequencing.	Formaldehyde	50-58	P53	Homo sapiens	0-3
12524418-1	2003	During a search for causative genes in patients with concurrent multiple primary colon tumours, we found a novel case with a germline mutation of the p53 gene, from GCC (Ala) to GTC (Val) at codon 189.	Valine	183-186	P53	Homo sapiens	150-153
7674092-2	1995	The TP53 gene mutation pattern in prostatic cancer was examined in relation to progression and survival, using archival formalin-fixed pre- and post-treatment tumour specimens from 84 prostatic cancer patients.	Formaldehyde	120-128	P53	Homo sapiens	4-8
12532223-5	2003	Fifty-seven ACT (21 from children and 36 from adults) were evaluated for p53 expression by immunohistochemistry in formalin-fixed paraffin-embedded tissue and analyzed in terms of outcome.	Formaldehyde	115-123	P53	Homo sapiens	73-76
10824754-5	2000	Formalin-fixed, paraffin-embedded tissue was processed for ploidy, S phase fraction, and immunohistochemical detection of estrogen and progesterone receptors plus expression of p53 and erbB-2 protein.	Formaldehyde	0-8	P53	Homo sapiens	177-180
10682666-3	2000	Immunohistochemical p53 (pAb 1801 mAb) and TS (TS106 mAb) expression on formalin-fixed paraffin-embedded primary tumour specimens was related to probability of clinical response to chemotherapy, time to progression and overall survival.	Formaldehyde	72-80	P53	Homo sapiens	20-23
7753561-9	1995	Induction of growth arrest and terminal differentiation in H0-1 human melanoma cells by IFN-beta + MEZ results in a temporal decrease in wild-type p53 protein levels with a corresponding increase in p21 levels.	beta + mez	92-102	P53	Homo sapiens	147-150
12607601-10	2002	In addition, expression of Ki-67 in all four groups paralleled p53 expression.	ki-67	27-32	P53	Homo sapiens	63-66
7783370-3	1995	The results of several fixation methods demonstrated that formalin and methanol, formalin and ethanol (1:9) and buffered formalin acetone gave good results for detecting p53 protein.	Formaldehyde	58-66	P53	Homo sapiens	170-173
7783370-3	1995	The results of several fixation methods demonstrated that formalin and methanol, formalin and ethanol (1:9) and buffered formalin acetone gave good results for detecting p53 protein.	Formaldehyde	81-89	P53	Homo sapiens	170-173
10605931-2	2000	Reactive oxygen intermediates (ROI) play several distinct roles in the p53 pathway.	reactive oxygen	0-15	P53	Homo sapiens	71-74
10772725-5	2000	The affinity of p53 protein for an beta-L-nucleotide terminated primer was 5 fold lower compared to non-modified primer.	beta-l-nucleotide	35-52	P53	Homo sapiens	16-19
12183079-5	2002	Treatment with A23187, a Ca(2+) ionophore, or thapsigargin, a Ca(2+)-ATPase inhibitor, alone enhanced p53 nuclear accumulation, indicating that p53 accumulation is dependent on intracellular Ca(2+) increase.	Calcimycin	15-21	P53	Homo sapiens	102-105
8867696-5	1995	The low proliferation rate of the tumor together with immunohistochemical evidence of inactivation of p53 protein suggest a delayed turnover of neoplastic cells as a possible source of lipofuscin accumulation.	Lipofuscin	185-195	P53	Homo sapiens	102-105
10606817-6	1999	Sequence analysis of exons 5 through 8 of p53 was performed on cloned PCR-amplified DNA of formalin-fixed, paraffin-embedded tumors.	Formaldehyde	91-99	P53	Homo sapiens	42-45
12183079-5	2002	Treatment with A23187, a Ca(2+) ionophore, or thapsigargin, a Ca(2+)-ATPase inhibitor, alone enhanced p53 nuclear accumulation, indicating that p53 accumulation is dependent on intracellular Ca(2+) increase.	Calcimycin	15-21	P53	Homo sapiens	144-147
12490121-7	2002	CONCLUSIONS: Detection of p53 gene mutation with PCR-SSCP-silver stain combined with cytological examination of sputum samples can improve the diagnosis of lung cancer.	Silver	58-64	P53	Homo sapiens	26-29
10604414-4	1999	OBJECTIVE: To determine the association of p53 expression with chemotherapy response rates and disease-free survival rates in 62 patients with locally advanced pharyngeal cancer treated with induction cisplatin-5-fluorouracil chemotherapy between 1983 and 1995.	cisplatin-5-fluorouracil	201-225	P53	Homo sapiens	43-46
7704245-1	1995	The expression of p53 protein was studied in formalin-fixed paraffin-embedded specimens of 41 well-differentiated adenocarcinomas of the gall-bladder, six cases of acute cholecystitis and 23 cases of chronic cholecystitis, using a monoclonal p53 (PAb 1801) antibody and streptavidin-biotin.	Formaldehyde	45-53	P53	Homo sapiens	18-21
12372430-3	2002	In Saos-2 cells harboring the temperature-sensitive mutant p53(Val-138), the expression of ATF3 gene was more significant at permissive temperature of 32.5 degrees C than at non-permissive 37.5 degrees C. Reporter assay of the human ATF3 gene promoter identified two p53-responsive elements at -379 to -370 and -351 to -342 from the transcriptional start site.	Valine	63-66	P53	Homo sapiens	59-62
7876377-2	1994	METHODS: Immunocytochemistry for p53 was performed in 65 specimens of formalin fixed, paraffin wax embedded cervical tissue using a polyclonal antibody against recombinant p53.	Formaldehyde	70-78	P53	Homo sapiens	33-36
10616970-3	1999	RESULTS: P53 was expressed in 84.0% of esophagoscopy (EGD) biopsies; 71.4% of patients with metastasis of thoracoscopy/laparoscopy lymph nodes (TS/LS LN) identified by hematoxylin/eosin (H/E) were p53 (+); 14.2% of patients with negative TS/LS LN by H/E were p53 (+).	Hematoxylin	168-179	P53	Homo sapiens	9-12
12372430-3	2002	In Saos-2 cells harboring the temperature-sensitive mutant p53(Val-138), the expression of ATF3 gene was more significant at permissive temperature of 32.5 degrees C than at non-permissive 37.5 degrees C. Reporter assay of the human ATF3 gene promoter identified two p53-responsive elements at -379 to -370 and -351 to -342 from the transcriptional start site.	Valine	63-66	P53	Homo sapiens	267-270
10547570-11	1999	It is concluded that p53 gene status and an accumulation of BAX, both involved in the same apoptosis-controlling pathway, may be of prognostic relevance in phyllodes tumours.	phyllodes	156-165	P53	Homo sapiens	21-24
10518106-5	1999	METHODS: p53 expression in formalin-fixed, paraffin-embedded samples of 239 patients with primary esophageal squamous cell carcinoma (TNM stage I:79 cases, stage II: 82 cases, stage III: 78 cases), who underwent esophageal resection without additional treatment, were analyzed by immunohistochemical staining using a polyclonal antibody, RSP53.	Formaldehyde	27-35	P53	Homo sapiens	9-12
7959668-1	1994	Immunohistochemical expression of the cellular phosphoprotein p53 was investigated in archival, formalin-fixed, and paraffin-embedded surgical breast tissue specimens from 543 patients using the polyclonal antibody CM-1.	Formaldehyde	96-104	P53	Homo sapiens	62-65
7922972-6	1994	METHODS: p53 expression in formalin fixed, paraffin embedded samples of 204 patients with primary squamous cell carcinoma of the esophagus, who underwent esophageal resection, were analyzed immunohistochemically with DO-1, a monoclonal antibody that detects wild-type and mutant forms of p53.	Formaldehyde	27-35	P53	Homo sapiens	9-12
12160929-6	2002	Cotreatment of p53-WT H460 cells with free radical scavengers, such as D-mannitol, uric acid, and sodium selenite, significantly attenuated the TCE- or PERC-induced lipid peroxidation.	Uric Acid	83-92	P53	Homo sapiens	15-18
12130688-4	2002	Our recent investigations with electrophilic prostaglandins enabled us to devise a pharmacophore and mechanism of action hypothesis relevant to this problem: a cross-conjugated alpha,beta-unsaturated dienone with two sterically accessible electrophilic beta-carbons is a molecular determinant that confers activity among this class of ubiquitin isopeptidases inhibitors, and that inhibitors of ubiquitin isopeptidases cause cell death in vitro independently of p53.	beta-	183-188	P53	Homo sapiens	461-464
7937752-3	1994	Using conformational energy analysis based on ECEPP (Empirical Conformational Energy for Peptides Program), we have determined the low-energy three-dimensional structures for this dodecapeptide sequence for the human wild-type p53 protein and three environmentally induced, cancer-related mutant p53 proteins with His-151, Ser-152, and Val-154, respectively.	Valine	336-339	P53	Homo sapiens	227-230
10491313-4	1999	Arsenite reduced p53 levels while concomitantly increasing the p53 regulatory protein mdm2 levels in a dose- and time-dependent manner.	arsenite	0-8	P53	Homo sapiens	17-20
10491313-4	1999	Arsenite reduced p53 levels while concomitantly increasing the p53 regulatory protein mdm2 levels in a dose- and time-dependent manner.	arsenite	0-8	P53	Homo sapiens	63-66
12190289-5	2002	p53 immunoreactive cells were randomly distributed in invasive carcinoma, confined to the lower third of the epithelium in CIN I, reached the middle third in 20% of CIN II and upper third in 16.6% of CIN III.	cin ii	165-171	P53	Homo sapiens	0-3
10380883-9	1999	Nickel and cobalt ions inhibit binding of p53 to scDNA and to its consensus sequence in linear DNA fragments less efficiently than zinc; cobalt ions are least efficient, requiring &gt;100 microM Co2+ for full inhibition of p53 binding.	Nickel	0-6	P53	Homo sapiens	42-45
10380883-9	1999	Nickel and cobalt ions inhibit binding of p53 to scDNA and to its consensus sequence in linear DNA fragments less efficiently than zinc; cobalt ions are least efficient, requiring &gt;100 microM Co2+ for full inhibition of p53 binding.	Nickel	0-6	P53	Homo sapiens	223-226
10380883-9	1999	Nickel and cobalt ions inhibit binding of p53 to scDNA and to its consensus sequence in linear DNA fragments less efficiently than zinc; cobalt ions are least efficient, requiring &gt;100 microM Co2+ for full inhibition of p53 binding.	Cobalt(2+)	195-199	P53	Homo sapiens	42-45
10380883-9	1999	Nickel and cobalt ions inhibit binding of p53 to scDNA and to its consensus sequence in linear DNA fragments less efficiently than zinc; cobalt ions are least efficient, requiring &gt;100 microM Co2+ for full inhibition of p53 binding.	Cobalt(2+)	195-199	P53	Homo sapiens	223-226
8030271-4	1994	Thus, the present study was designed to investigate the presence of HPV and p53 gene mutations in 17 formalin-fixed, paraffin-embedded KS [7 acquired immunodeficiency syndrome-KS (AIDS-KS) and 10 classic KS] specimens.	Formaldehyde	101-109	P53	Homo sapiens	76-79
8049841-7	1994	Abnormal accumulation of p53 protein was found in 36 tumors (51%), more often in patients exposed to asbestos than in patients without exposure (67% versus 40%, p = 0.027).	Asbestos	101-109	P53	Homo sapiens	25-28
10397512-0	1999	Expression of p53 protein and Ki-67 antigen in gingival hyperplasia induced by nifedipine and phenytoin.	Phenytoin	94-103	P53	Homo sapiens	14-17
12023887-6	2002	The increased sensitivity to cisplatin observed in ascorbate-loaded cells appeared to be dependent exclusively on MLH1 and c-Abl expression, and independent of p53.	Ascorbic Acid	51-60	P53	Homo sapiens	160-163
10397512-4	1999	RESULTS: Two specimens out of 4 nifedipine-induced and 4 out of 7 phenytoin-induced hyperplastic gingival tissues revealed the expression of p53 protein in the nuclei of epithelial cells, while no expression of p53 protein was observed in the epithelia of the 5 non-hyperplastic control tissues.	Phenytoin	66-75	P53	Homo sapiens	141-144
10349985-4	1999	bcl-2 and p53 protein expression were demonstrated by immunohistochemical methods, using formalin-fixed, paraffin-embedded biopsy tissues.	Formaldehyde	89-97	P53	Homo sapiens	10-13
10348343-8	1999	In addition, p53 may function as a substrate of PKR since phosphorylation of human p53 on serine392 is induced by activated PKR in vitro.	serine392	90-99	P53	Homo sapiens	13-16
7708439-9	1994	P53 was investigated by immunohistochemistry, using a monoclonal anti-p53 antibody (DO-7), on formalin fixed, paraffin embedded tissue.	Formaldehyde	94-102	P53	Homo sapiens	0-3
12045262-9	2002	CD2-activated LPTs displayed a striking upregulation of p53, whose blockade by antisense oligonucleotides accelerated their S phase transit time to that of CD3-activated PBTs.	pbts	170-174	P53	Homo sapiens	56-59
7913577-10	1994	Both p53 protein and p185 antibodies work well on routine, formalin-fixed, paraffin-embedded tissue and are easily used in routine diagnostic procedures.	Formaldehyde	59-67	P53	Homo sapiens	5-8
10348343-8	1999	In addition, p53 may function as a substrate of PKR since phosphorylation of human p53 on serine392 is induced by activated PKR in vitro.	serine392	90-99	P53	Homo sapiens	83-86
11240754-4	1999	We examined p53 accumulation in formalin-fixed, paraffin-embedded archival sections in 19 cases previously shown to have mutations in the p53 gene and performed semi-quantitative analysis of the intensity of staining and relative density of positive cells and stromal and glandular elements.	Formaldehyde	32-40	P53	Homo sapiens	12-15
11877452-4	2002	Here we report that KChAP induces apoptosis in the prostate cancer cell line, LNCaP, which expresses both K(+) currents and wild-type p53.	kchap	20-25	P53	Homo sapiens	134-137
10626228-2	1999	A plasmid bearing cDNA containing the human p53 gene was reacted in vitro with CAA, then dehydrated for conversion of hydroxyethano into etheno adducts, and primer extension by T7 DNA polymerase in the presence of four dNTPs was performed.	Parathion	219-224	P53	Homo sapiens	44-47
8028344-0	1994	High proliferative rates demonstrated by bromodeoxyuridine labeling index in breast carcinomas with p53 overexpression.	Bromodeoxyuridine	41-58	P53	Homo sapiens	100-103
8028344-3	1994	We determined the extent to which p53 abnormality was associated with proliferation by measuring p53 immunohistochemically with a polyclonal antibody and monoclonal PAb1801 in invasive carcinomas of known S-phase fraction (SPF) assessed histologically by bromodeoxyuridine incorporation.	Bromodeoxyuridine	255-272	P53	Homo sapiens	34-37
8200229-3	1994	METHODS: IgG1 monoclonal antibody to human p53 protein (PAb 1801) was used to detect p53 in formalin-fixed, paraffin-embedded archival tumors resected from 84 patients with tumor limited to the bowel wall.	Formaldehyde	92-100	P53	Homo sapiens	43-46
10079373-3	1999	Therefore, to assess the alterations in the conjoint expression of Rb and p53 proteins in formalin fixed paraffin embedded sections, 64 astrocytic tumors were studied (16 astrocytomas,7 gemistocytic astrocytomas, 19 anaplastic astrocytomas and 22 glioblastomas) using the avidin biotin immunoperoxidase technique.	Formaldehyde	90-98	P53	Homo sapiens	74-77
9875290-0	1998	The C-terminal domain of p53 catalyzes DNA-renaturation and strand exchange toward annealing between intact ssDNAs and toward eliminating damaged ssDNA from duplex formation through preferential recognition of damaged DNA by a duocarmycin.	duocarmycin	227-238	P53	Homo sapiens	25-28
9875290-6	1998	We found that DU-86, a duocarmycin derivative which alkylates DNA, bound ssDNA and enhanced the DNA binding activity of the p53 C-terminus.	duocarmycin	23-34	P53	Homo sapiens	124-127
8200229-3	1994	METHODS: IgG1 monoclonal antibody to human p53 protein (PAb 1801) was used to detect p53 in formalin-fixed, paraffin-embedded archival tumors resected from 84 patients with tumor limited to the bowel wall.	Formaldehyde	92-100	P53	Homo sapiens	85-88
12064559-0	2002	Assessment of the mutations of p53 suppressor gene and Ha- and Ki-ras oncogenes in malignant mesothelioma in relation to asbestos exposure: a study of 12 American patients.	Asbestos	121-129	P53	Homo sapiens	31-34
8152811-4	1994	We therefore introduced the pC53-SCX3 143 (Val-Ala) p53 mutation into a non tumorigenic adenoma derived cell line, AA/C1, which contained a truncating APC mutation, activating K-ras mutation but was wild-type for the p53 protein.	Valine	43-46	P53	Homo sapiens	52-55
9886570-3	1998	Exons 5-8 of the p53 gene were examined for mutations by the polymerase chain reaction-single strand conformation polymorphism technique and DNA sequencing, using DNA from formalin-fixed paraffin-embedded tissues.	Formaldehyde	172-180	P53	Homo sapiens	17-20
12064559-7	2002	Further studies are needed to examine whether the observed mutation of the p53 suppressor gene is due to the combined effects of asbestos and smoking or to other unknown factors.	Asbestos	129-137	P53	Homo sapiens	75-78
9732400-6	1998	Transfer of a mutant p53 gene enhanced topotecan sensitivity in wild-type p53 LN-229 but not mutant p53 LN-18 cells.	Topotecan	39-48	P53	Homo sapiens	74-77
8043159-9	1994	Since p53 (PAb 1801) expression can withstand formalin fixation and pepsin treatment of paraffin-embedded tissues, flow cytometric analysis of archival specimens is feasible, and clinical correlations such as these may be carried out in retrospective studies of other tumors.	Formaldehyde	46-54	P53	Homo sapiens	6-9
18968561-1	2002	Single nucleotide polymorphisms (SNPs) of cancer repression gene p53 were analyzed electrochemically with ferrocenyl naphthalene diimide (1) as a hybridization indicator.	ferrocenylnaphthalene diimide	106-136	P53	Homo sapiens	65-68
8156496-3	1994	METHODS: The status of the p53 gene was studied by immunohistochemistry of formalin-fixed paraffin-embedded biopsy samples from 72 patients with atypical endometrial hyperplasia or endometrioid carcinoma who underwent hysterectomy immediately after biopsy and from 5 patients with benign endometria.	Formaldehyde	75-83	P53	Homo sapiens	27-30
9668066-4	1998	In this communication, we report that PDTC inhibits the activation of temperature-sensitive murine p53(Val-135) (TSp53) in the transformed rat embryo fibroblast line, A1-5, as well as wild-type human p53 in the normal diploid fibroblast line, WS1neo.	Valine	103-106	P53	Homo sapiens	115-118
9688570-0	1998	Disruption of actin microfilaments by cytochalasin D leads to activation of p53.	Cytochalasin D	38-52	P53	Homo sapiens	76-79
9688570-2	1998	We investigated whether p53 is activated upon disruption of actin microfilaments, caused by cytochalasin D (CD).	Cytochalasin D	92-106	P53	Homo sapiens	24-27
11867746-7	2002	Inhibitors of heat shock protein 90 (hsp90), radicicol and geldanamycin, induced degradation of p53 and suppressed p53-induced apoptosis in normal thymocytes and myeloid leukemic cells.	geldanamycin	59-71	P53	Homo sapiens	96-99
9688948-2	1998	Mesothelioma, an asbestos-induced tumor, is highly resistant to therapy but generally expresses wild-type p53.	Asbestos	17-25	P53	Homo sapiens	106-109
7823583-9	1994	A study employing image analysis to detect and quantitate androgen receptors and p53 in formalin-fixed, paraffin-embedded prostate cancer biopsies is underway to determine the utility of androgen receptors in predicting response to hormonal therapy.	Formaldehyde	88-96	P53	Homo sapiens	81-84
11867746-7	2002	Inhibitors of heat shock protein 90 (hsp90), radicicol and geldanamycin, induced degradation of p53 and suppressed p53-induced apoptosis in normal thymocytes and myeloid leukemic cells.	geldanamycin	59-71	P53	Homo sapiens	115-118
8158458-1	1993	The expression of the nuclear protein p53 in oligodendrogliomas was investigated by immunohistochemistry, using a monoclonal anti-p53 antibody (DO-7) on formalin-fixed, paraffin-embedded material in 84 histologically verified cases, and compared with the histopathological grade and survival.	Formaldehyde	153-161	P53	Homo sapiens	38-41
9626464-3	1998	The expression of p53, bcl-2, thymidylate synthase (TS), glutathione S-transferase pi (GST-pi), and vascular endothelial growth factor (VEGF) in the formalin-fixed biopsy samples of primary tumors before chemotherapy was examined immunohistochemically.	Formaldehyde	149-157	P53	Homo sapiens	18-21
11864911-1	2002	We have investigated the mechanism of S-phase arrest elicited by the carcinogen benzo(a)pyrene dihydrodiol epoxide (BPDE) in p53-deficient cells.	pyrene dihydrodiol epoxide	88-114	P53	Homo sapiens	125-128
9610736-2	1998	We now show that UV irradiation of B16 melanoma after prior exposure to the radiation sensitizer, bromodeoxyuridine (BUdR) leads to induction of p53 and DNA fragmentation, and concomitant decreases in Rb, E2F, cyclin D1, and cell viability, with no comparable effects on irradiated unsensitized cells.	Bromodeoxyuridine	98-115	P53	Homo sapiens	145-148
7901994-13	1993	We conclude that the immunohistochemical detection of p53 nuclear accumulation in formalin-fixed, paraffin-embedded tissue is highly associated with mutations in the p53 gene; this association has now been demonstrated in a large number of tumors.	Formaldehyde	82-90	P53	Homo sapiens	54-57
7901994-13	1993	We conclude that the immunohistochemical detection of p53 nuclear accumulation in formalin-fixed, paraffin-embedded tissue is highly associated with mutations in the p53 gene; this association has now been demonstrated in a large number of tumors.	Formaldehyde	82-90	P53	Homo sapiens	166-169
11815995-0	2002	Immunoreactivity of p53, Ki-67, and c-erbB-2 in phyllodes tumors of the breast in correlation with clinical and morphologic features.	phyllodes	48-57	P53	Homo sapiens	20-23
7692889-1	1993	OBJECTIVES: To improve the detection of p53 protein in formalin-fixed, paraffin-embedded head and neck tumor tissues.	Formaldehyde	55-63	P53	Homo sapiens	40-43
7692889-8	1993	RESULTS: An antigen retrieval method facilitated the unmasking of previously inaccessible p53 antigenic determinants in formalin-fixed, paraffin-embedded tissues.	Formaldehyde	120-128	P53	Homo sapiens	90-93
7692889-11	1993	CONCLUSIONS: Antigen retrieval method in formalin-fixed, paraffin-embedded tissue demonstrated a significant increase in p53 immunostaining.	Formaldehyde	41-49	P53	Homo sapiens	121-124
9540056-5	1998	Four recurrent meningiomas with high p53 PIs were analyzed by the polymerase chain reaction-single strand conformation polymorphism method to detect p53 gene mutations, but none were found in exons 4-8 of this gene.	Monothiopyrophosphoric acid	41-44	P53	Homo sapiens	37-40
9609668-0	1998	Simultaneous detection of p53 nuclear protein and chromosome aberrations on sections from formalin-fixed, paraffin-embedded breast cancer tissue.	Formaldehyde	90-98	P53	Homo sapiens	26-29
9535218-6	1998	These results indicate that in oxLDL-induced apoptosis, a concomitant induction of p53 and MnSOD is critical, and suggest that it is at least in part due to an enhancement of the sphingomyelin/ceramide pathway.	Sphingomyelins	179-192	P53	Homo sapiens	83-86
8252351-3	1993	Positive staining for p53 protein was detected in ten of 77 (13 per cent) of these tumours using polyclonal CM1 antibody on formalin-fixed tissue.	Formaldehyde	124-132	P53	Homo sapiens	22-25
8406999-8	1993	Transfection of a mutant p53 gene construct (containing a mutation at codon 143, val to ala) into the A2780/cp70 resistant cells conferred a significantly increased sensitivity to cisplatin, suggesting that p53 is a direct determinant of cisplatin resistance in these cells.	Valine	81-84	P53	Homo sapiens	25-28
8406999-8	1993	Transfection of a mutant p53 gene construct (containing a mutation at codon 143, val to ala) into the A2780/cp70 resistant cells conferred a significantly increased sensitivity to cisplatin, suggesting that p53 is a direct determinant of cisplatin resistance in these cells.	Valine	81-84	P53	Homo sapiens	207-210
11779115-7	2002	Using this assay, we have demonstrated that a peptide with a nonhydrolyzable beta-amino acid substitution binds DM2 with an affinity comparable to a p53 peptide that is composed of only alpha-amino acids.	Amino Acids	186-203	P53	Homo sapiens	149-152
8222064-0	1993	p53 mutations in phenacetin-associated human urothelial carcinomas.	Phenacetin	17-27	P53	Homo sapiens	0-3
9473858-0	1998	Assessment of mutations of Ha- and Ki-ras oncogenes and the p53 suppressor gene in seven malignant mesothelioma patients exposed to asbestos--PCR-SSCP and sequencing analyses of paraffin-embedded primary tumors.	Asbestos	132-140	P53	Homo sapiens	60-63
15678851-4	1998	In this study we analyzed the expression of p53 protein in a variety of salivary gland malignant tumors fixed in formalin and included in paraffin, using the method of immunohistochemical coloring with the anti-p53 DO-7 antibody.	Formaldehyde	113-121	P53	Homo sapiens	44-47
12174262-5	1998	p53 protein was highly purified with either of the two columns, as indicated by silver staining and Western blot analysis.	Silver	80-86	P53	Homo sapiens	0-3
11813266-5	2002	P53, p21, and MDM2 were induced in E6-transfected TK6 cells, as well as in parental TK6 cells after arsenite treatment.	arsenite	100-108	P53	Homo sapiens	0-3
9417863-0	1997	Geldanamycin prevents nuclear translocation of mutant p53.	geldanamycin	0-12	P53	Homo sapiens	54-57
8347496-1	1993	The expression of p53 protein was immunohistochemically studied in formalin-fixed paraffin-embedded biopsy specimens of 203 colorectal carcinomas by use of a monoclonal antibody specific for the p53 protein.	Formaldehyde	67-75	P53	Homo sapiens	18-21
9417863-9	1997	Treatment of transformed cells with geldanamycin (GA), a small molecule that binds hsp90, causes a rapid destabilization of p53 by 50%.	geldanamycin	36-48	P53	Homo sapiens	124-127
11813266-7	2002	It indicated that arsenite, but not X-ray, could suppress the transcription of E6 gene and therefore activate the p53 tumor suppressor pathway in TK6-E6 cells.	arsenite	18-26	P53	Homo sapiens	114-117
9417863-9	1997	Treatment of transformed cells with geldanamycin (GA), a small molecule that binds hsp90, causes a rapid destabilization of p53 by 50%.	geldanamycin	50-52	P53	Homo sapiens	124-127
9417863-12	1997	Although GA appears to dramatically alter the translocating properties of mutant p53 it does not dissociate the p53-hsp90 complex.	geldanamycin	9-11	P53	Homo sapiens	81-84
8392933-3	1993	These results suggest that GM-CSF can stimulate formation of protein tyrosine kinase co-ordinated signalling complexes, that contain p53/p56lyn, p62c-yes and an activated PtdInsP2 directed phosphoinositide 3OH-kinase, which can drive the accumulation of the putative second-messenger PtdIns(3,4,5)P3.	phosphatidylinositol 3,4,5-triphosphate	284-299	P53	Homo sapiens	133-136
12199376-5	2002	Cells that became de-attached and floated in the medium after treatment with growth inhibitory concentrations of daidzein or biochanin A, showed higher P53 levels than cells that remained attached.	daidzein	113-121	P53	Homo sapiens	152-155
32370448-2	1993	In the present study, p53 immunoreactivity was investigated in formalin-fixed, paraffin-embedded tissues from human and animal pituitary tumors, using the avidin-biotin-peroxidase complex technique.	Formaldehyde	63-71	P53	Homo sapiens	22-25
9417863-13	1997	We suggest that a second chaperone protein, called p23, which we show also binds p53, may play an important role in these GA-mediated effects.	geldanamycin	122-124	P53	Homo sapiens	81-84
9368180-0	1997	Ex vivo treatment of bone marrow with phosphorothioate oligonucleotide OL(1)p53 for autologous transplantation in acute myelogenous leukemia and myelodysplastic syndrome.	Parathion	38-54	P53	Homo sapiens	76-79
9368180-2	1997	In preliminary studies, OL(1)p53, a 20-mer phosphorothioate oligonucleotide directed against p53 mRNA, decreased the number of acute myelogenous leukemia (AML) cells in vitro, suggesting a possible role for OL(1)p53 in purging bone marrow harvests of leukemia cells.	Phosphorothioate Oligonucleotides	43-75	P53	Homo sapiens	29-32
9368180-2	1997	In preliminary studies, OL(1)p53, a 20-mer phosphorothioate oligonucleotide directed against p53 mRNA, decreased the number of acute myelogenous leukemia (AML) cells in vitro, suggesting a possible role for OL(1)p53 in purging bone marrow harvests of leukemia cells.	Phosphorothioate Oligonucleotides	43-75	P53	Homo sapiens	93-96
9368180-2	1997	In preliminary studies, OL(1)p53, a 20-mer phosphorothioate oligonucleotide directed against p53 mRNA, decreased the number of acute myelogenous leukemia (AML) cells in vitro, suggesting a possible role for OL(1)p53 in purging bone marrow harvests of leukemia cells.	Phosphorothioate Oligonucleotides	43-75	P53	Homo sapiens	93-96
11745874-4	2001	PROCEDURE: Ninety-seven WT were evaluated for p53 expression by immunohistochemistry in formalin-fixed paraffin-embedded tissue and correlated with outcome.	Formaldehyde	88-96	P53	Homo sapiens	46-49
9380022-0	1997	Prevention of fluorodeoxyuridine-induced cytotoxicity and DNA damage in HT29 colon carcinoma cells by conditional expression of wild-type p53 phenotype.	Floxuridine	14-32	P53	Homo sapiens	138-141
8387645-6	1993	Promoters whose accurate transcription is directed by a pyrimidine-rich initiator element, however, are immune to the effects of p53.	pyrimidine	56-66	P53	Homo sapiens	129-132
11576999-0	2001	p53-independent apoptosis mediated by tachpyridine, an anti-cancer iron chelator.	tachpyr	38-50	P53	Homo sapiens	0-3
7684193-2	1993	Immunohistochemical staining with a monoclonal antibody (DO-7) and a polyclonal antibody (CM-1) to p53 protein (both wild type and mutant) on formalin-fixed paraffin sections showed a strong correlation with malignancy grade.	Formaldehyde	142-150	P53	Homo sapiens	99-102
21528215-6	1997	The incidence of p53 gene mutation CYP1A1; Val/Val (60.0%), CYP1A1; C (50.0%) tended to be higher than those of CYPIAI; Ile/Ile and Ile/Val (40.4%) or CYP1A1; A and B (40.5%).	Valine	43-46	P53	Homo sapiens	17-20
21528215-6	1997	The incidence of p53 gene mutation CYP1A1; Val/Val (60.0%), CYP1A1; C (50.0%) tended to be higher than those of CYPIAI; Ile/Ile and Ile/Val (40.4%) or CYP1A1; A and B (40.5%).	Valine	47-50	P53	Homo sapiens	17-20
11576999-7	2001	Although immunoblotting revealed rapid accumulation of p53 following treatment with tachpyridine, p21(WAF1) was not induced.	tachpyr	84-96	P53	Homo sapiens	55-58
9213225-10	1997	The sensitivity of cells to atractyloside-induced apoptosis was found to be: HPV 16 E6-J2-3T3 &gt; CaSki &gt; normal-J2-3T3 cells approximately ts p53-J2-3T3 approximately vector-J2-3T3 cells &gt; Hela &gt; SiHa &gt; C33A approximately C33A 16 E6.	Atractyloside	28-41	P53	Homo sapiens	147-150
8456936-2	1993	The polyclonal antibody used (CM-1) is directed against the wild-type p53 protein, but also recognizes the mutated p53 in formalin-fixed and paraffin-embedded sections.	Formaldehyde	122-130	P53	Homo sapiens	115-118
9234928-4	1997	METHODS: Phosphorothioate oligonucleotides were used to target p53-related sequences in two p53-mutant/overexpressing endometrial cancer cell lines (KLE and RL95-2) and a normal fibroblast control.	Phosphorothioate Oligonucleotides	9-42	P53	Homo sapiens	63-66
7509541-1	1993	Overexpression of p53 and erbB-2 was studied by immunohistochemistry in formalin-fixed tissue samples of 179 patients with transitional cell carcinoma of the urinary bladder.	Formaldehyde	72-80	P53	Homo sapiens	18-21
11576999-9	2001	p53 null human lung cancer H1299 cells transfected with an ecdysone-inducible p53 exhibited equivalent sensitivity to tachpyridine in the presence and absence of p53, demonstrating the lack of requirement for p53 in an isogenic cell system.	tachpyr	118-130	P53	Homo sapiens	0-3
9234928-4	1997	METHODS: Phosphorothioate oligonucleotides were used to target p53-related sequences in two p53-mutant/overexpressing endometrial cancer cell lines (KLE and RL95-2) and a normal fibroblast control.	Phosphorothioate Oligonucleotides	9-42	P53	Homo sapiens	92-95
9234928-18	1997	CONCLUSION: Phosphorothioate oligos directed against p53 sequences in two p53-mutant endometrial cancer cell lines demonstrated antiproliferative effects.	Parathion	12-28	P53	Homo sapiens	53-56
11576999-9	2001	p53 null human lung cancer H1299 cells transfected with an ecdysone-inducible p53 exhibited equivalent sensitivity to tachpyridine in the presence and absence of p53, demonstrating the lack of requirement for p53 in an isogenic cell system.	tachpyr	118-130	P53	Homo sapiens	78-81
9234928-18	1997	CONCLUSION: Phosphorothioate oligos directed against p53 sequences in two p53-mutant endometrial cancer cell lines demonstrated antiproliferative effects.	Parathion	12-28	P53	Homo sapiens	74-77
7511292-0	1993	[p53 mutation in phenacetin-induced urothelial carcinomas].	Phenacetin	17-27	P53	Homo sapiens	1-4
11576999-9	2001	p53 null human lung cancer H1299 cells transfected with an ecdysone-inducible p53 exhibited equivalent sensitivity to tachpyridine in the presence and absence of p53, demonstrating the lack of requirement for p53 in an isogenic cell system.	tachpyr	118-130	P53	Homo sapiens	78-81
11576999-9	2001	p53 null human lung cancer H1299 cells transfected with an ecdysone-inducible p53 exhibited equivalent sensitivity to tachpyridine in the presence and absence of p53, demonstrating the lack of requirement for p53 in an isogenic cell system.	tachpyr	118-130	P53	Homo sapiens	78-81
11576999-10	2001	Further, time-lapse video microscopy and TUNEL assays demonstrated that both p53 null and p53 wild-type cells underwent apoptotic cell death in response to tachpyridine.	tachpyr	156-168	P53	Homo sapiens	77-80
9204056-4	1997	OBJECTIVE: Our purpose was to investigate the immunohistochemical expression of p53 protein in premalignant and malignant cutaneous lesions in kidney transplant recipients and the effect of low-dose etretinate on p53 expression.	Etretinate	199-209	P53	Homo sapiens	213-216
1279244-8	1992	Additionally, we showed the applicability of immunohistochemical detection of p53 protein in endoscopic biopsy material routinely formalin-fixed.	Formaldehyde	130-138	P53	Homo sapiens	78-81
11576999-10	2001	Further, time-lapse video microscopy and TUNEL assays demonstrated that both p53 null and p53 wild-type cells underwent apoptotic cell death in response to tachpyridine.	tachpyr	156-168	P53	Homo sapiens	90-93
11576999-11	2001	In addition, in 55 human cancer cell lines the mean GI(50) of tachpyridine in cells with mutant p53 was virtually identical to the GI(50) in cells with wild-type p53.	tachpyr	62-74	P53	Homo sapiens	96-99
11480026-1	1997	After obtaining the results of p53 gene mutation by a silver staining method to polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis, P53 protein staining and proliferation cell nuclear antigen (PCNA) index by double-blind method, multivariate correlation analysis two by two showed that PCR-SSCP, P53 positive protein staining and PCNA index had markedly correlation not only in oral precancerous lesions (OPL) but also in primary sites and regional metastatic lymph nodes of oral squamous cell carcinomas (OSCC).	Silver	54-60	P53	Homo sapiens	31-34
11576999-13	2001	Since over 50% of human tumors contain a functionally defective p53 that reduces sensitivity to commonly used chemotherapeutic agents, such as etoposide and cisplatin, the ability of tachpyridine to induce apoptosis independently of p53 may offer an advantage in anti-tumor therapy.	tachpyr	183-195	P53	Homo sapiens	64-67
1319835-9	1992	Also, carcinoma cells with p53 mutations existing within adenoma tissues are detectable by immunostaining, even in formalin-fixed, paraffin-embedded specimens.	Formaldehyde	115-123	P53	Homo sapiens	27-30
11406618-7	2001	Encapsulated phosphorothioate p53 antisense oligonucleotides were neuroprotective at 5-10-fold lower concentrations than when unencapsulated.	Parathion	13-29	P53	Homo sapiens	30-33
12114668-5	1997	Immunohistochemical staining for p53 was performed on paraffin sections of formalin-fixed tumor tissue.	Formaldehyde	75-83	P53	Homo sapiens	33-36
11493433-4	2001	These pathways are themselves influenced by a number of lipid products (diacylglycerol, sphingosine-1 phosphate, and glucosyl ceramide), reactive oxygen species, oncogenes (such as the tumor suppressor gene p53), protein kinases (protein kinase C and phosphoinositide-3 kinase), and external stimuli (hematopoietic growth factors and the extracellular matrix).	Diglycerides	72-86	P53	Homo sapiens	207-210
9331847-5	1997	In 34 patients who had tumors designated p53-/p21+ or p53+/p21+, CHPP reduced the percentage of patients who died from recurrence of cancer from 10/20 (50%) to 3/14 (21.4%, P = 0.184).	chpp	65-69	P53	Homo sapiens	41-44
9331847-5	1997	In 34 patients who had tumors designated p53-/p21+ or p53+/p21+, CHPP reduced the percentage of patients who died from recurrence of cancer from 10/20 (50%) to 3/14 (21.4%, P = 0.184).	chpp	65-69	P53	Homo sapiens	54-57
1607637-0	1992	p53 overexpression in formalin-fixed, paraffin-embedded tissue detected by immunohistochemistry.	Formaldehyde	22-30	P53	Homo sapiens	0-3
11780329-10	2001	CONCLUSION: Detection of p53 gene alterations in sputum samples by PCR-SSCP-silver stain can be used as a follow-up surveillance index for the early diagnosis of lung cancer in suspicious patients.	Silver	76-82	P53	Homo sapiens	25-28
1347094-3	1992	Mutations were not found in Ki-ras, but 9 p53 mutations, including 2 deletions, were found in 7 patients by direct DNA sequencing after polymerase chain reaction amplification of DNA from formalin-fixed, paraffin-embedded tissue.	Formaldehyde	188-196	P53	Homo sapiens	42-45
11511362-3	2001	Overexpression of p53DINP1 and DNA damage by DSBs synergistically enhanced Ser46 phosphorylation of p53, induction of p53AIP1 expression, and apoptotic cell death.	dsbs	45-49	P53	Homo sapiens	18-21
1727381-0	1992	Altered p53 gene structure and expression in human epithelial cells after exposure to nickel.	Nickel	86-92	P53	Homo sapiens	8-11
1727381-3	1992	Immunocytochemistry and sequence analysis of DNA from the nickel-immortalized cells revealed abnormal p53 expression and a T----C transition mutation in codon 238.	Nickel	58-64	P53	Homo sapiens	102-105
9138481-0	1997	Immunohistochemical detection of p21WAF1/CIP1 and p53 proteins in formalin-fixed paraffin-embedded tissue sections of squamous cell carcinoma of the skin.	Formaldehyde	66-74	P53	Homo sapiens	50-53
9047387-0	1997	Modulation of (+/-)-anti-BPDE mediated p53 accumulation by inhibitors of protein kinase C and poly(ADP-ribose) polymerase.	(+/-)-anti	14-24	P53	Homo sapiens	39-42
9047387-2	1997	In order to gain insights on the biochemical pathways leading to p53 stabilization, the effect of (+/-) 7,8-dihydroxy-anti-9, 10-epoxy-7,8,9,10-tetrahydrobenzo(a)-pyrene [(+/-)-anti-BPDE] induced DNA damage on p53 protein levels was investigated in various repair-proficient and repair-deficient human cells.	7,8-dihydroxy-anti-9, 10-epoxy-7,8,9,10-tetrahydrobenzo(a)-pyrene	104-169	P53	Homo sapiens	210-213
9058631-4	1997	METHODS: The p53 expression in tumour tissue was studied by immunohistochemistry using CM1 polyclonal rabbit antibody and formalin-fixed, paraffin-embedded material.	Formaldehyde	122-130	P53	Homo sapiens	13-16
1569122-5	1992	Most importantly, they also permit the detection of p53 in archival tumour material that has been conventionally fixed in formalin and embedded in paraffin wax.	Formaldehyde	122-130	P53	Homo sapiens	52-55
11313463-3	2001	p53-DNA complexes were cross-linked in vivo by treating the cells with formaldehyde and processed by chromatin immunoprecipitation-PCR.	Formaldehyde	71-83	P53	Homo sapiens	0-3
1528930-5	1992	In most cases, the mutations in ras and p53 genes are localized to pyrimidine-rich sequences, particularly C-C sequences, which indicates that these sites are probably the targets for UV-induced DNA damage and subsequent mutation and transformation.	pyrimidine	67-77	P53	Homo sapiens	40-43
21044462-9	2001	The different biological effect between 172Leu and 172His shows that some p53 variants such as 172 Arg-&gt;Leu may act as wild-type p53.	172leu	40-46	P53	Homo sapiens	74-77
9400941-3	1997	The potential of CdA to induce the p53-dependent DNA damage response was assessed in resting and phytohaemagglutinine (PHA)-activated peripheral blood mononuclear cells (PBMCs) and compared with cisplatin (DDP), a cell cycle-dependent and DNA-damaging agent that is mainly used in the treatment of solid tumours.	Cladribine	17-20	P53	Homo sapiens	35-38
9400941-9	1997	Activation of the p53-dependent DNA damage response seems to be an important component of the toxic effect of CdA.	Cladribine	110-113	P53	Homo sapiens	18-21
21044462-9	2001	The different biological effect between 172Leu and 172His shows that some p53 variants such as 172 Arg-&gt;Leu may act as wild-type p53.	172leu	40-46	P53	Homo sapiens	132-135
11401473-0	2001	Vitamin C augments chemotherapeutic response of cervical carcinoma HeLa cells by stabilizing P53.	Ascorbic Acid	0-9	P53	Homo sapiens	93-96
1959638-4	1991	The purified protease processed the natural substrate gag precursor (p53) to form gag p19 and gag p24.	Glycosaminoglycans	54-57	P53	Homo sapiens	69-72
1959638-4	1991	The purified protease processed the natural substrate gag precursor (p53) to form gag p19 and gag p24.	Glycosaminoglycans	82-85	P53	Homo sapiens	69-72
9868114-2	1997	The results showed that overexpression of p53 was detected in 54.8% (23/42) of L-GSCC and 20% (5/25) of hyperlasia epithelia, respectively.	l-gscc	79-85	P53	Homo sapiens	42-45
1959638-4	1991	The purified protease processed the natural substrate gag precursor (p53) to form gag p19 and gag p24.	Glycosaminoglycans	82-85	P53	Homo sapiens	69-72
11401473-4	2001	Our findings show that vitamin C downregulates the redox sensitive transcription factor AP-1 and decreases one of its transcription targets HPV E6, and stabilizes P53.	Ascorbic Acid	23-32	P53	Homo sapiens	163-166
11125034-7	2001	Notably, when MDM2 expression is inhibited in S-type cells, with a phosphorothioated antisense oligonucleotide (AS5), then p53 accumulates in the nucleus and the SH-EP1 cells undergo apoptosis.	AS5	112-115	P53	Homo sapiens	123-126
9342752-6	1997	Our results indicate that IHC could be applied for studies of p53 protein accumulation in archival formalin fixed, paraffin-embedded bladder tumours.	Formaldehyde	99-107	P53	Homo sapiens	62-65
11311793-0	2001	Inhibition of 6-hydroxydopamine-induced p53 expression and survival of neuroblastoma cells following interaction with astrocytes.	Oxidopamine	14-31	P53	Homo sapiens	40-43
9592339-0	1996	[Detection of p53 gene mutation in bronchial biopsy samples from lung cancer patients with polymerase chain reaction-single strand conformation polymorphism-silver staining method].	Silver	157-163	P53	Homo sapiens	14-17
11311793-8	2001	Western blot analysis demonstrated that 6-hydroxydopamine significantly increased p53 protein in monolayer SH-SY5Y cells grown in either regular medium or conditioned medium from astrocytes.	Oxidopamine	40-57	P53	Homo sapiens	82-85
8810317-1	1996	We have examined in detail the DNA binding properties of several immunopurified tumor-derived mutant p53 proteins (Val-143 --&gt; Ala, Arg-175 --&gt; His, Arg-248 --&gt; Trp, Arg-249 --&gt; Ser, and Arg-273 --&gt; His).	Valine	115-118	P53	Homo sapiens	101-104
1793482-4	1991	Because the mutations in the p53 tumor suppressor gene in both tumors were located opposite potential pyrimidine dimer sites (C-C), it is consistent with these mutations having been induced by the ultraviolet radiation present in sunlight.	pyrimidine	102-112	P53	Homo sapiens	29-32
8875976-5	1996	Similarly, multiple p53NK activities were detected in the MethAp53(ts) cell line (which expresses the valine 135 temperature-sensitive p53 protein).	Valine	102-108	P53	Homo sapiens	20-23
11311793-11	2001	The enhanced resistance of the co-cultured SH-SY5Y cells to the toxicity of 6-hydroxydopamine is attributed to the ability of astrocytes to prevent the increase of p53 induced by this toxin.	Oxidopamine	76-93	P53	Homo sapiens	164-167
8875976-5	1996	Similarly, multiple p53NK activities were detected in the MethAp53(ts) cell line (which expresses the valine 135 temperature-sensitive p53 protein).	Valine	102-108	P53	Homo sapiens	63-66
11103796-8	2000	Wortmannin, an inhibitor of phosphatidylinositol 3-kinases, inhibited arsenite- or X-ray irradiation-induced p53 accumulation but did not alter UV irradiation- or N-acetyl-Leu-Leu-norleucinal-induced p53 accumulation.	arsenite	70-78	P53	Homo sapiens	109-112
11103796-9	2000	p53 phosphorylation on serine 15 was also confirmed by immunoblotting technique in arsenite- and X-ray-treated HFW cells but was not observed in UV- or N-acetyl-Leu-Leu-norleucinal-treated HFW cells.	arsenite	83-91	P53	Homo sapiens	0-3
11103796-10	2000	These results suggest the involvement of a phosphatidylinositol 3-kinase-related protein kinase in arsenite-induced p53 accumulation.	arsenite	99-107	P53	Homo sapiens	116-119
8931502-2	1996	METHOD: A dexamethazone-inducible wt-p53 cDNA was introduced into two cervical carcinoma cell lines (TMCC-1 and ME180) and morphological changes were examined under a phase contrast microscope and following Papanicolaou staining.	papanicolaou	207-219	P53	Homo sapiens	37-40
33824293-6	2021	Furthermore, ASP4132 treatment in NSCLC cells induced programmed necrosis, causing mitochondrial p53-cyclophilin D (CyPD)-adenine nucleotide translocase 1 (ANT1) association, mitochondrial depolarization and medium lactate dehydrogenase release.	4-(4-dimethylaminostyryl)-1-methylpyridinium	13-20	P53	Homo sapiens	97-100
11103796-13	2000	Together, these findings infer that arsenite-induced DNA strand breaks may lead to p53 phosphorylation and accumulation through an ataxia telangiectasia mutated-dependent pathway in HFW cells.	arsenite	36-44	P53	Homo sapiens	83-86
11029509-7	2000	Tumor B18 exhibited two novel mutations in the p53 gene, ATGright curved arrow GTG (Metright curved arrow Val) at codon 237 and AATright curved arrow GAT (Asnright curved arrow Asp) at codon 263.	Valine	106-109	P53	Homo sapiens	47-50
33808343-6	2021	Treatment of differentiated SH-SY5Y cells with 6-OHDA brought cell death, and specifically, apoptosis, which was significantly inhibited by the preincubation with MJe through caspase 3 blockage and the modulation of p53, Bax, and Bcl-2 genes.	Oxidopamine	47-53	P53	Homo sapiens	216-219
9389053-4	1996	Comparison of these positive results of p53 gene mutation detected by silver staining method with the results by polymerase chain reaction-single strand conformation polymorphism analysis did not reveal matched results, especially during the precancerous period.	Silver	70-76	P53	Homo sapiens	40-43
11195849-0	2000	The phototumorigenic fluoroquinolone, lomefloxacin, photosensitises p53 accumulation and transcriptional activity in human skin cells.	Fluoroquinolones	21-36	P53	Homo sapiens	68-71
9064332-6	1996	BA is also an efficient inhibitor of p53-dependent thymocyte apoptosis induced by DNA damage.	Bongkrekic Acid	0-2	P53	Homo sapiens	37-40
12545812-5	2000	The results showed that the prevalence of p53 mutations in LSCC subjected to silver staining PCR-SSCP test were 50% (30/60) in exon 5, 11.67%(7/60) in exon 6, 41.6%(25/60) in exon 7, and 25%(15/60) in exon 8.	Silver	77-83	P53	Homo sapiens	42-45
8764107-13	1996	Because these cell lines have the same p53 mutation, these findings suggest that there is a p53-independent G1-S checkpoint that mediates radiosensitization produced by fluorodeoxyuridine.	Floxuridine	169-187	P53	Homo sapiens	92-95
33801507-2	2021	Previously, we demonstrated the ability of tryptophanol-derived polycyclic compounds to activate the tumor suppressor protein p53, a relevant therapeutic target in cancer.	tryptophanol	43-55	P53	Homo sapiens	126-129
10953132-2	2000	MATERIALS AND METHODS: Immunohistochemical staining for p53 was semiquantitatively scored in archival formalin fixed, paraffin embedded tumor tissue obtained at diagnosis in 221 patients with prostate cancer.	Formaldehyde	102-110	P53	Homo sapiens	56-59
33236159-0	2021	PARP inhibitor resistance and TP53 mutations in patients treated with olaparib for BRCA-mutated cancer: Four case reports.	olaparib	70-78	P53	Homo sapiens	30-34
8780893-0	1996	Expression of memory, differentiation, and repression of c-myc and p53 genes in human RD/TE-671 cells induced by a ureido-derivative of pyridine (UDP-4).	pyridine	136-144	P53	Homo sapiens	67-70
11798837-2	2000	METHODS: Human lung adenocarcinoma cell line GLC-82 was transfected with adenovirus-mediated p53 gene (Ad-p53) combining with administration of either kind of chemotherapeutic agents-cisplatin (CDDP) and arsenic trioxide (As(2)O(3)).	as(2)o	222-228	P53	Homo sapiens	93-96
8787547-0	1996	Antioncogene P53 and mitogenic cytokine interleukin-8 aberrantly expressed in psoriatic skin are inversely regulated by the antipsoriatic drug tacrolimus (FK506).	Tacrolimus	143-153	P53	Homo sapiens	13-16
8787547-0	1996	Antioncogene P53 and mitogenic cytokine interleukin-8 aberrantly expressed in psoriatic skin are inversely regulated by the antipsoriatic drug tacrolimus (FK506).	Tacrolimus	155-160	P53	Homo sapiens	13-16
8787547-8	1996	Interestingly, p53 transcription was clearly induced by FK506 treatment.	Tacrolimus	56-61	P53	Homo sapiens	15-18
33236159-10	2021	Exome analyses following olaparib treatment identified de novo TP53 mutations, as well as increased frequencies of pre-existing TP53 mutations compared with the primary tumor.	olaparib	25-33	P53	Homo sapiens	63-67
33236159-10	2021	Exome analyses following olaparib treatment identified de novo TP53 mutations, as well as increased frequencies of pre-existing TP53 mutations compared with the primary tumor.	olaparib	25-33	P53	Homo sapiens	128-132
33236159-11	2021	In HCT116 TP53-/- cells carrying BRCA2 pathogenic mutations, TP53 inactivating mutations were associated with lower sensitivity to olaparib in vitro.	olaparib	131-139	P53	Homo sapiens	61-65
33236159-12	2021	Thus, inactivating TP53 mutations may be associated to olaparib resistance in the presence of BRCA mutations.	olaparib	55-63	P53	Homo sapiens	19-23
10953344-5	2000	In this study, we attempted to establish a polymerase chain reaction (PCR)-based assay for assessing the possibility of early detection of p53 mutation in archival Papanicolaou-stained cytologic sputum smears.	papanicolaou	164-176	P53	Homo sapiens	139-142
8695259-1	1996	The expression of mutated p53 protein was studied in paraffin-embedded, formalin-fixed tumour specimens from 183 women with endometrial carcinoma.	Formaldehyde	72-80	P53	Homo sapiens	26-29
10232607-0	1999	Poly(ADP-ribosyl)ation of p53 during apoptosis in human osteosarcoma cells.	poly(adp-ribosyl)	0-17	P53	Homo sapiens	26-29
10863160-0	2000	Analysis of K-ras and p53 mutations in mesotheliomas from humans and rats exposed to asbestos.	Asbestos	85-93	P53	Homo sapiens	22-25
8691320-1	1996	To examine the expression of p53 protein and gene alterations in oral epithelial lesions including epithelial dysplasias and primary squamous cell carcinomas, immunohistochemical and temperature gradient gel electrophoresis (TGGE) methods were applied to formalin-fixed and paraffin-embedded tissues.	Formaldehyde	255-263	P53	Homo sapiens	29-32
34951009-0	2022	Prognostic impact of TP53 mutation in newly diagnosed diffuse large B-cell lymphoma patients treated in the FIL-DLCL04 trial.	dlcl04	112-118	P53	Homo sapiens	21-25
10866313-7	2000	Perturbation of mitochondrial function mediated accumulation of wild-type p53 protein, since Bcl-2 overexpression, bongkrekic acid, or inhibition of mitochondrial protein synthesis with chloramphenicol strongly reduced TK/GCV-induced accumulation of wild-type p53 protein.	Bongkrekic Acid	115-130	P53	Homo sapiens	74-77
8857671-4	1996	In this report, we present the effects of tumor suppressor p53 protein in tyrosinase gene expression and melanin synthesis in human melanoma.	Melanins	105-112	P53	Homo sapiens	59-62
8857671-9	1996	These data suggest that in human melanoma p53 down-regulates the tissue-specific expression of tyrosinase gene and subsequent melanin synthesis.	Melanins	126-133	P53	Homo sapiens	42-45
10857993-6	2000	Our results show that: 1) Sequential TPT --&gt; G2/M-active drugs are synergistic when administration overlapped the maximum percentage of TPT-induced G2/M-phase cell arrest interval in all three mutated p53 cell lines; 2) the reverse sequential schedule (G2/M-active drug --&gt; TPT) was antagonistic, and being only additive for Etoposide --&gt; TPT association.	Topotecan	37-40	P53	Homo sapiens	204-207
8711933-3	1996	In this study, we investigated the immunohistochemical expression of p53 in formalin fixed paraffin embedded archival specimens of 36 extrahepatic bile duct cancers in which p53 expression was found in eighteen (50%) cases.	Formaldehyde	76-84	P53	Homo sapiens	69-72
8615678-10	1996	Contrary, massive damage initiated by a 1-h exposure to DEA-NO is irreversible, with persistent p53 levels.	1,1-Diethyl-2-hydroxy-2-nitrosohydrazine	56-62	P53	Homo sapiens	96-99
8778328-2	1996	This immunohistochemical study on formalin-fixed, paraffin-embedded material found p53 expression in 43 per cent (n = 51) of carcinomas using a monoclonal antibody (DO-1), whereas no immunoreactivity for p53 was present in tumour-associated non-neoplastic gastric mucosa or tumour stroma.	Formaldehyde	34-42	P53	Homo sapiens	83-86
8633403-3	1996	METHODS: Immunohistochemical staining for mutant p53 was performed on 40 formalin-fixed radical prostatectomy specimens.	Formaldehyde	73-81	P53	Homo sapiens	49-52
8599864-0	1996	Cell-cycle arrest and p53 accumulation induced by geldanamycin in human ovarian tumour cells.	geldanamycin	50-62	P53	Homo sapiens	22-25
8599864-3	1996	After a 3-h exposure to 0.1 microM geldanamycin, the cells show an increase in accumulation of p53 protein that is maximal at 24 h after drug exposure.	geldanamycin	35-47	P53	Homo sapiens	95-98
8599864-5	1996	Using dominant negative mutant TP53 transfectants of A2780 we have analysed the possible dependence of geldanamycin-induced cell-cycle arrests on the presence of functional p53.	geldanamycin	103-115	P53	Homo sapiens	31-35
8599864-5	1996	Using dominant negative mutant TP53 transfectants of A2780 we have analysed the possible dependence of geldanamycin-induced cell-cycle arrests on the presence of functional p53.	geldanamycin	103-115	P53	Homo sapiens	173-176
8599864-8	1996	These results suggest that geldanamycin can induce increased p53 protein by a mechanism not involving DNA damage.	geldanamycin	27-39	P53	Homo sapiens	61-64
8634780-10	1995	The results of our investigation demonstrate that nonradioactive silver-stained SSCP is a sensitive, rapid, and simple technique to detect p53 mutations, even in formalin-fixed tissues, and could be easily used to investigate large series of patients to assess the clinical significance of p53 mutations in human tumors.	Silver	65-71	P53	Homo sapiens	139-142
8634780-10	1995	The results of our investigation demonstrate that nonradioactive silver-stained SSCP is a sensitive, rapid, and simple technique to detect p53 mutations, even in formalin-fixed tissues, and could be easily used to investigate large series of patients to assess the clinical significance of p53 mutations in human tumors.	Silver	65-71	P53	Homo sapiens	290-293
8634783-0	1995	A universal method for the mutational analysis of K-ras and p53 gene in non-small-cell lung cancer using formalin-fixed paraffin-embedded tissue.	Formaldehyde	105-113	P53	Homo sapiens	60-63
8822113-1	1995	The expression of p53 and bcl-2 was immunohistochemically investigated in 61 formalin-fixed, paraffin-embedded invasive breast carcinomas.	Formaldehyde	77-85	P53	Homo sapiens	18-21
8745488-3	1995	The structure of p53 gene (exons 6-8) was also analyzed by PCR-SSCP silver staining method.	Silver	68-74	P53	Homo sapiens	17-20
7490678-1	1995	A rapid non-isotopic PCR-SSCP (polymerase chain reaction-single-stranded conformation polymorphism) method was developed in this study to detect polymorphism and loss of heterozygosity (LOH) of p53 in formalin-fixed and paraffin-embedded samples of normal breast tissue and of breast cancer.	Formaldehyde	201-209	P53	Homo sapiens	194-197
8771158-3	1995	Tumor p53 protein expression was detected by means of immunohistochemistry using the monoclonal antibody D07 on formalin fixed paraffin-embedded tissue sections.	Formaldehyde	112-120	P53	Homo sapiens	6-9
7675452-0	1995	Geldanamycin selectively destabilizes and conformationally alters mutated p53.	geldanamycin	0-12	P53	Homo sapiens	74-77
7675452-3	1995	We sought to examine whether geldanamycin, a drug capable of destabilizing several oncogene and proto-oncogene products, could alter the stability and DNA binding characteristics of several mutated p53 proteins.	geldanamycin	29-41	P53	Homo sapiens	198-201
7672694-4	1995	In this study we examined 88 formalin-fixed paraffin-embedded clinical specimens of cervix for the presence of HPV and p53 expression.	Formaldehyde	29-37	P53	Homo sapiens	119-122
7786800-0	1995	Modulation of cell kinetics and cell cycle status by treating CD34+ chronic myeloid leukaemia cells with p53 antisense phosphorothioate oligonucleotides.	Phosphorothioate Oligonucleotides	119-152	P53	Homo sapiens	105-108
7547494-1	1995	Expression of c-erbB-2 and p53 protein was analysed retrospectively by immunohistochemistry in formalin-fixed tissue samples from 293 patients with colorectal adenocarcinoma.	Formaldehyde	95-103	P53	Homo sapiens	27-30
7726729-0	1995	A microwave method that enhances detection of aberrant p53 expression in formalin-fixed, paraffin-embedded tissues.	Formaldehyde	73-81	P53	Homo sapiens	55-58
7726729-10	1995	CONCLUSIONS: Microwave pretreatment in conjunction with the use of either PAb1801 or DO7 is highly efficacious in the immunohistochemical detection of aberrant p53 expression in formalin-fixed, paraffin-embedded tissues.	Formaldehyde	178-186	P53	Homo sapiens	160-163
7556591-6	1995	Nuclear p53 immunoreactivity was assessed using a monoclonal antibody, DO-1, on Formalin-fixed paraffin-embedded specimens.	Formaldehyde	80-88	P53	Homo sapiens	8-11
8529093-5	1995	The mdm-2 protein binds to both leucine-tryptophan residues at amino acids 22 and 23, from the amino terminal end of the protein, and in so doing, prevents all p53 functions.	leucine-tryptophan	32-50	P53	Homo sapiens	160-163
7957681-5	1994	The ethylene glycol fraction contained a number of p53 binding proteins, and this fraction showed a DNA helicase activity measured by the displacement of DNA fragment from partially duplexed M13 DNA.	Ethylene Glycol	4-19	P53	Homo sapiens	51-54
7530851-8	1994	Fixation-induced loss of p53 immunoreactivity was minimal for formalin (two of 10 tumors for one antibody each), more significant for Bouin (six of 10 tumors for one to five antibodies).	Formaldehyde	62-70	P53	Homo sapiens	25-28
8036011-7	1994	It is evident that H2O2/FeCl3 possesses essentially the same mutagenic specificity for codons 249 and 250 of p53 as bulky carcinogens such as aflatoxin B1, benzo(a)pyrene or heterocyclic amines.	heterocyclic amines	174-193	P53	Homo sapiens	109-112
21567003-10	1994	to-ether with other factors like p53 and nm23.	to-ether	0-8	P53	Homo sapiens	33-36
8058709-8	1994	When bromodeoxyuridine was administered either in vivo (n = 93) or in vitro (n = 79), p53 accumulation was only marginally related to proliferative fraction (P = 0.067 by chi 2; P = 0.055 by Mann-Whitney).	Bromodeoxyuridine	5-22	P53	Homo sapiens	86-89
8128225-0	1994	Slow repair of pyrimidine dimers at p53 mutation hotspots in skin cancer.	pyrimidine	15-25	P53	Homo sapiens	36-39
8238731-3	1993	The goal of this study was to determine the frequency and relationship of p53 gene alterations and hepatitis B in formalin-fixed, paraffin-embedded HCCs resected in the United States.	Formaldehyde	114-122	P53	Homo sapiens	74-77
8283348-6	1993	Overexpression of the p53 protein was found by immunostaining of sections from formalin-fixed, paraffin-embedded material in 55 per cent (51/92) of the tumours.	Formaldehyde	79-87	P53	Homo sapiens	22-25
8283352-0	1993	Immunocytochemical p53 detection by microwave oven heating of routinely formalin-fixed paraffin sections.	Formaldehyde	72-80	P53	Homo sapiens	19-22
8155979-6	1993	Hence, a phosphorothioate oligonucleotide complementary to p53 mRNA can be administered at this dose level to humans without major toxicity.	Phosphorothioate Oligonucleotides	9-41	P53	Homo sapiens	59-62
1382834-3	1992	Teleocidin transiently increased the levels of c-fos and p53 mRNAs measured by reverse transcription and polymerase chain reaction.	teleocidins	0-10	P53	Homo sapiens	57-60
1382834-6	1992	Sequential alterations of the expression of c-fos, p53, c-myc and cytokeratin genes induced by teleocidin may be responsible for the morphological and functional changes of hepatoma cells induced by this tumor promoter.	teleocidins	95-105	P53	Homo sapiens	51-54
1606969-2	1992	The activity was analyzed by autoprocessing of the protease itself or by processing of the gag p53 precursor.	Glycosaminoglycans	91-94	P53	Homo sapiens	95-98
1317462-3	1992	METHODS: IgG1 monoclonal antibody to human p53 protein (PAb 1801) and immunohistochemical methods were used to detect p53 protein accumulation in archival formalin-fixed, paraffin-embedded, randomly selected carcinomas.	Formaldehyde	155-163	P53	Homo sapiens	118-121
1324804-4	1992	Signal transduction following binding of AMF to its receptor, a cell surface glycoprotein of 78 kD (gp78) homologous to p53, is mediated by a pertussis toxin sensitive G protein, inositol phosphate production and the phosphorylation of gp78.	Inositol Phosphates	179-197	P53	Homo sapiens	120-123
1413493-1	1992	The expression of the p53 gene product was investigated immunocytochemically in a retrospective series of 164 formalin-fixed paraffin-embedded invasive breast carcinomas with pathologically proven negative lymph nodes.	Formaldehyde	110-118	P53	Homo sapiens	22-25
33771885-6	2021	After progression on abiraterone/enzalutamide, we observed clonal-evolution of CTCs harboring TP53 mutations and gain of ATM, KDM6A, and MYC, and loss of NCOR1, PTEN, RB1, and RUNX2.	abiraterone	21-32	P53	Homo sapiens	94-98
33771885-8	2021	Implications: We identified common and reproducible genomic alterations in CTCs from AR-V7 negative mCRPC men associated with poor outcomes during enzalutamide/abiraterone treatment, including CNAs in genes linked to lineage plasticity and epigenetic signaling, DNA repair, AR, TP53/RB1, PTEN, and WNT pathways.	abiraterone	160-171	P53	Homo sapiens	278-282
25311433-4	2014	The aim of this study was to investigate whether a novel compound derived from diterpene triepoxide (Minnelide ) can reactivate wild-type p53 function in HPV-positive HNSCC.	14-O-phosphonooxymethyltriptolide disodium salt	101-110	P53	Homo sapiens	138-141
25311433-8	2014	RESULTS: In HPV-positive HNSCC, Minnelide reactivated p53 by suppressing E6 oncoprotein.	14-O-phosphonooxymethyltriptolide disodium salt	32-41	P53	Homo sapiens	54-57
25311433-10	2014	In 2 preclinical HNSCC animal models (a subcutaneous xenograft model and a patient-derived tumor xenograft model), Minnelide reactivated p53 function and significantly decreased tumor progression and tumor volume.	14-O-phosphonooxymethyltriptolide disodium salt	115-124	P53	Homo sapiens	137-140
25311433-11	2014	CONCLUSION: Triptolide and Minnelide caused cell death in vitro and in vivo in HPV-positive HNSCC by reactivating wild-type p53 and thus inducing apoptosis.	14-O-phosphonooxymethyltriptolide disodium salt	27-36	P53	Homo sapiens	124-127
34970530-4	2021	The adducts mimic the thematic features of the chemically stable potent spiro (3H-indole-3,2"-pyrrolidin)-2(1H)-ones p53-MDM2 inhibitors, while installing a pyrrole ring via a carbonyl spacer inspired by the natural marine or synthetic products that efficiently inhibit Bcl2 family functions.	Pyrroles	157-164	P53	Homo sapiens	117-120
34886743-2	2022	Results from our laboratory indicate that 2-FaraAMP (fludarabine) has multiple mechanisms of cytotoxicity that include accumulation of isoforms and phosphorylated derivatives of p53, and induction of the unfolded protein response (UPR).	fludarabine	53-64	P53	Homo sapiens	178-181
34886743-3	2022	Using protein pull-downs with Dynabeads coated with p53 antibody, we have found that 2-FaraA (fludarabine nucleoside) induces major changes in the p53 interactome in human Raji lymphoma and IM9 multiple myeloma cells.	fludarabine	85-92	P53	Homo sapiens	52-55
34886743-3	2022	Using protein pull-downs with Dynabeads coated with p53 antibody, we have found that 2-FaraA (fludarabine nucleoside) induces major changes in the p53 interactome in human Raji lymphoma and IM9 multiple myeloma cells.	fludarabine	85-92	P53	Homo sapiens	147-150
34886886-8	2021	Mechanistic studies showed that increased p53 and its downstream proteins, and disrupted MMP with increased intracellular peroxide production participated in EVO-induced apoptosis and G2/M arrest of SW1736 cells.	Peroxides	122-130	P53	Homo sapiens	42-45
34417893-11	2021	Given that cocaine-induced p53 PARylation is an energy-dependent process, we observed that cocaine-induced PARP-1/p53/POX axes alters cellular energy metabolism.	Cocaine	91-98	P53	Homo sapiens	114-117
34762985-10	2021	Gene expression analyses revealed pathways differently regulated in the PFOS-treated groups compared to the controls, which were related to cell death and survival through e.g., P38 mitogen-activated protein kinases and signal transducer and activator of transcription 3, which in turn activates tumour protein 53 (TP53).	perfluorooctane sulfonic acid	72-76	P53	Homo sapiens	315-319
34840582-0	2021	A Metabolomic Investigation of Eugenol on Colorectal Cancer Cell Line HT-29 by Modifying the Expression of APC, p53, and KRAS Genes.	Eugenol	31-38	P53	Homo sapiens	112-115
34840582-5	2021	The purpose of this research was to investigate the anticancer effects of eugenol and variations in p53, KRAS, and APC gene expression and metabolic changes associated with the abovementioned gene expressions using 1HNMR spectroscopy.	Eugenol	74-81	P53	Homo sapiens	100-103
34840582-7	2021	After treating HT-29 cells with IC50 concentration of eugenol, RNA was extracted and cDNA was obtained from them and the expression of p53, KRAS, and APC genes was measured using the qRT-PCR technique.	Eugenol	54-61	P53	Homo sapiens	135-138
34840582-11	2021	The observed IC50 for eugenol was 500 muM, and the relative expression of APC and p53 genes in the treated cells increased compared to the control group, and the expression of KRAS oncogene gene decreased significantly.	Eugenol	22-29	P53	Homo sapiens	82-85
34769400-9	2021	Molecular analysis showed changes in BAX, BCL2, TP53, and CDKN1 expression in tested cell lines following incubation with ciprofloxacin and levofloxacin.	Ciprofloxacin	122-135	P53	Homo sapiens	48-52
34183353-6	2021	Luminal A/B to HER2-Enriched switching was associated with TP53 and/or PIK3CA mutations.	Phenobarbital	0-7	P53	Homo sapiens	59-63
34771553-5	2021	Herein, we discuss the features of monoallelic and biallelic TP53 mutations within MDS, their corresponding carcinogenic mechanisms, their predictive value in current standard treatments including hypomethylating agents, allogeneic hematopoietic stem cell transplantation, and lenalidomide, together with the latest progress in TP53-targeted therapy strategies, especially MDS clinical trial data.	hypomethylating agents	197-219	P53	Homo sapiens	61-65
34660782-11	2021	This study revealed that SZRD has the characteristics and advantages of "multicomponent, multitarget, and multipathway" in the treatment of PDSD; among these, the combination of the main active components of quercetin and kaempferol with the key targets of AKT1, IL6, MAPK1, TP53, and VEGFA may be one of the important mechanisms.	kaempferol	222-232	P53	Homo sapiens	275-279
34638899-9	2021	The present results indicate a shift towards synergism in cells with mutant or null p53, treated with olaparib combined with metformin, providing a new approach to the treatment of gynecologic cancers.	olaparib	102-110	P53	Homo sapiens	84-87
34560639-12	2021	Additionally, H3 K27M-mutant DMG frequently demonstrated overexpression of p53.	dimethylglycine	29-32	P53	Homo sapiens	75-78
34552337-6	2021	The effect of the TP53 G245S mutation on crizotinib sensitivity was tested in H3122 cells.	Crizotinib	41-51	P53	Homo sapiens	18-22
34552337-11	2021	H3122 cells with TP53 mutant were more sensitive to crizotinib compared with control cells.	Crizotinib	52-62	P53	Homo sapiens	17-21
34552337-12	2021	Conclusion: A higher mutation burden and mutations in DNA repair gene, including TP53, were potentially associated with primary resistance to crizotinib in ALK-rearranged NSCLC.	Crizotinib	142-152	P53	Homo sapiens	81-85
34502536-0	2021	Fe-N Co-Doped Titanium Dioxide Nanoparticles Induce Cell Death in Human Lung Fibroblasts in a p53-Independent Manner.	titanium dioxide	14-30	P53	Homo sapiens	94-97
34502536-4	2021	Long-term exposure to TiO2 nanoparticles co-doped with 1% of iron and nitrogen led to the alteration of p53 protein activity and the gene expression controlled by this suppressor (NF-kB and mdm2), DNA damage, cell cycle disruptions at the G2/M and S phases, and lysosomal membrane permeabilization and the subsequent release of cathepsin B, triggering the intrinsic pathway of apoptosis in a Bax- and p53-independent manner.	titanium dioxide	22-26	P53	Homo sapiens	104-107
34502536-4	2021	Long-term exposure to TiO2 nanoparticles co-doped with 1% of iron and nitrogen led to the alteration of p53 protein activity and the gene expression controlled by this suppressor (NF-kB and mdm2), DNA damage, cell cycle disruptions at the G2/M and S phases, and lysosomal membrane permeabilization and the subsequent release of cathepsin B, triggering the intrinsic pathway of apoptosis in a Bax- and p53-independent manner.	titanium dioxide	22-26	P53	Homo sapiens	401-404
34571936-7	2021	Pathways of necroptosis, ferroptosis, p53, NRF2, ATF4, WNT, MAPK, NF-kappaB, EGFR, and ERK may be connected to the tumor suppressive effect caused by pretreatment of DHA/EPA prior to bortezomib.	Eicosapentaenoic Acid	170-173	P53	Homo sapiens	38-41
34097952-8	2021	Interestingly, PQ induced unfolded protein response (UPR), p53, Irf and DC maturation genes in DCcd34, responses absent in MCcd34.	Paraquat	15-17	P53	Homo sapiens	59-62
34149899-6	2021	Compared with the PBS control group, the A549, A549/DDP and A549/Taxol cells treated with NaI131, GA or a combination of the drugs exhibited G2/M arrest and increased percentages of total apoptotic cells, as well as significantly decreased protein levels of CDK1, cyclin B, mtp53, HSP90, Bcl-2 and P-gp, increased protein levels of Bax and decreased mRNA levels of p53 and HSP90.	pbs	18-21	P53	Homo sapiens	365-368
34161403-4	2021	First, the p53 expression plasmid (p53 DNA) was ultrasonically sprayed on a polycaprolactone (PCL) microneedle patch (D@MNP).	polycaprolactone	76-92	P53	Homo sapiens	11-14
34188682-13	2021	bcl-2 (protein) and p53 significantly correlated with Luminal B and TNBC (p < 0.01).	Phenobarbital	54-61	P53	Homo sapiens	20-23
34476443-9	2021	CONCLUSIONS: ki-67 and p53 protein are lowly expressed in OSCC patients with the habit of betel nut chewing, suggesting that clinicopathologic factors such as the proliferation activity, malignancy, differentiation and prognosis of tumor are much better.	betel	90-95	P53	Homo sapiens	23-26
34093867-0	2021	Nanoparticle encapsulation of non-genotoxic p53 activator Inauhzin-C for improved therapeutic efficacy.	inauhzin-c	58-68	P53	Homo sapiens	44-47
34062962-6	2021	We therefore determined how modulation of C16-ceramide, either through CerS6 or p53, a known PGCC suppressor and enhancer of CerS6-derived C16-ceramide, affected PGCC progeny formation.	N-palmitoylsphingosine	42-54	P53	Homo sapiens	80-83
34062962-6	2021	We therefore determined how modulation of C16-ceramide, either through CerS6 or p53, a known PGCC suppressor and enhancer of CerS6-derived C16-ceramide, affected PGCC progeny formation.	N-palmitoylsphingosine	139-151	P53	Homo sapiens	80-83
35605655-5	2022	In addition, the downregulation of PICT1 was required to enhancement of p53 stability, resulted from its promoting the nucleoplasmic translocation of RPL11 to bind to Mdm2 following D-3F treatment.	d-3f	182-186	P53	Homo sapiens	72-75
35460941-8	2022	To sum up, we developed a new, safe strategy for melanoma treatment by using low doses of niclosamide and quinacrine to treat melanoma; and found a novel mechanism by which the combination application of low doses of niclosamide and quinacrine exerts an efficient anti-melanoma effect through activation of autophagy-mediated p53-dependent apoptosis.	Quinacrine	106-116	P53	Homo sapiens	326-329
35460941-8	2022	To sum up, we developed a new, safe strategy for melanoma treatment by using low doses of niclosamide and quinacrine to treat melanoma; and found a novel mechanism by which the combination application of low doses of niclosamide and quinacrine exerts an efficient anti-melanoma effect through activation of autophagy-mediated p53-dependent apoptosis.	Quinacrine	233-243	P53	Homo sapiens	326-329
35271947-6	2022	The in vivo efficacy of TB on p53-deficient NSCLC (H1299) cells and p53-wild type NSCLC (A549) cells NSCLC cells were determined, and its mechanism of action was explored.	theabrownin	24-26	P53	Homo sapiens	30-33
35600955-8	2022	Results: The network pharmacology analysis showed that quercetin, luteolin, and kaempferol are the most significant active components in BHHD; STAT3, Jun, AKT1, MAPK3, MAPK1, and TP53 are the most critical drug targets; regulating hormones, reversing insulin (INS) resistance, exerting anti-inflammatory effects, and improving fertility might be the most important mechanisms of BHHD in the treatment of PCOS.	kaempferol	80-90	P53	Homo sapiens	179-183
35510223-13	2022	The molecular docking results showed that there was a certain affinity between the main compounds (kaempferol, quercetin, beta-sitosterol, naringenin) and core target genes (PTGS2, CASP3, MAPK1, MAPK3, TP53).	kaempferol	99-109	P53	Homo sapiens	202-206
35404445-4	2022	Lastly, the inhibitory effects of ketorolac tromethamine on the activation of beta-galactosidase and the upregulation of p21 and p53 were greatly abolished by the overexpression of COX-2.	Ketorolac Tromethamine	34-56	P53	Homo sapiens	129-132
35223357-4	2022	The computational docking and molecular dynamics simulation of FDA-approved drugs followed by an in vitro experimental validation identified acarbose, an anti-diabetic medication and caloric restriction mimetic as a potential inhibitor of DAPK1-p53 interaction.	Acarbose	141-149	P53	Homo sapiens	245-248
35223357-7	2022	The reduced fluorescence emission in cells stained with pS20 supported the potential of acarbose in inhibiting the DAPK1-p53 interaction.	Acarbose	88-96	P53	Homo sapiens	121-124
35173185-7	2022	In the ER+/PR+/HER2-negative subset (n = 356) of The Cancer Genome Atlas, the non-luminal A intrinsic subtype was more prevalent in the group with mutant TP53.	Phenobarbital	82-89	P53	Homo sapiens	154-158
35223843-0	2022	Harpagoside Protects Against Doxorubicin-Induced Cardiotoxicity via P53-Parkin-Mediated Mitophagy.	harpagoside	0-11	P53	Homo sapiens	68-71
34932948-4	2021	The clearance of EpiSCs with DSBs is caused by selective differentiation and delamination through the DNA damage response (DDR)-p53-Notch/p21 axis, with the downregulation of ITGB1.	dsbs	29-33	P53	Homo sapiens	128-131
34905275-1	2021	OBJECTIVE: Elevated p53 promote oxidative stress and production of proinflammatory cytokines in liposaccharide (LPS)-treated healthy human gingival fibroblasts (HGFs).	liposaccharide	96-110	P53	Homo sapiens	20-23
34829934-5	2021	We found that BETi, similar to ATO + ATRA, induced differentiation and apoptosis which was TP53 independent in the NPM1c cell line OCI-AML3 and primary cells.	beti	14-18	P53	Homo sapiens	91-95
34743450-12	2021	The median abiraterone-PFS was 4.7 months for patients with TP53 mutation and 11.0 months for TP53 wild-type patients.	abiraterone	11-22	P53	Homo sapiens	60-64
34743450-12	2021	The median abiraterone-PFS was 4.7 months for patients with TP53 mutation and 11.0 months for TP53 wild-type patients.	abiraterone	11-22	P53	Homo sapiens	94-98
34743450-14	2021	TP53 mutation was the undependent prognosis factor of PFS in patients treated with abiraterone(HR=2.23, 95%CI: 1.26 to 3.94, P=0.006) and docetaxel(HR=1.92, 95%CI: 1.01 to 3.66, P=0.047) had significant differences in PFS.	abiraterone	83-94	P53	Homo sapiens	0-4
34743450-15	2021	Conclusions: TP53 mutations were associated with the presence of metastasis and castration resistance, and were also an independent prognostic factor for progression-free survival in patients treated with abiraterone and docetaxel.	abiraterone	205-216	P53	Homo sapiens	13-17
34599843-3	2022	Objective of this study is to investigate whether combined treatment of p53 agonist, Nutlin3a, and HIF-2alpha antagonist, PT2385, confers advanced efficacy than monotreatment strategies, based on a cell type-divergent regulation.	PT2385	122-128	P53	Homo sapiens	72-75
34610483-10	2021	CONCLUSION: MiR-146b-5p is a cholangiocarcinoma suppressor by inhibiting cell proliferation and promoting cell apoptosis with targeting TRAF6, possibly via modulating p53 translocation to mitochondria.	mir-146b-5p	12-23	P53	Homo sapiens	167-170
34324743-0	2021	A rohitukine derivative IIIM-290 induces p53 dependent mitochondrial apoptosis in acute lymphoblastic leukemia cells.	IIIM-290	24-32	P53	Homo sapiens	41-44
34324743-6	2021	Interestingly, the elevation in proapoptotic markers was p53 dependent-the silencing of p53 abrogated apoptosis (programmed cell death) triggered by IIIM-290 in MOLT-4 cells.	IIIM-290	149-157	P53	Homo sapiens	57-60
34324743-6	2021	Interestingly, the elevation in proapoptotic markers was p53 dependent-the silencing of p53 abrogated apoptosis (programmed cell death) triggered by IIIM-290 in MOLT-4 cells.	IIIM-290	149-157	P53	Homo sapiens	88-91
34594342-9	2021	Interestingly, gammaH2AX induction level correlated inversely with ATM-dependent p-CHK2 and p53 responses.	gammah2ax	15-24	P53	Homo sapiens	92-95
34392440-0	2021	Ursodeoxycholic acid shows antineoplastic effects in bile duct cancer cells via apoptosis induction; p53 activation; and EGFR-ERK, COX-2, and PI3K-AKT pathway inhibition.	Ursodeoxycholic Acid	0-20	P53	Homo sapiens	101-104
34392440-8	2021	In cultured bile duct cancer cells, UDCA suppressed cell proliferation in bile duct cancer cells by inducing apoptosis and p53 activation, blocking deoxycholic acid (DCA)-induced activated EGFR-ERK signaling and COX-2, inhibiting DCA-induced activated PI3K-AKT signaling, and suppressing the invasiveness of bile duct cancer cells.	Ursodeoxycholic Acid	36-40	P53	Homo sapiens	123-126
34425169-9	2021	A common element in the changing response of cells to arsenite over time appears to involve up-regulation of MDM2 by inflammatory signaling (through AP-1 and NF-kappaB), leading to inhibition of P53 function.	arsenite	54-62	P53	Homo sapiens	195-198
34488591-10	2022	Based on the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses, we found that p53-related signaling played an important role in xanthatin-treated HT-29 colon cancer cells.	xanthatin	153-162	P53	Homo sapiens	103-106
34445495-3	2021	Previously, we have demonstrated that the combined inhibition of EGFR and MDM2-p53 pathways, by gefitinib and JNJ-26854165, exerts a strong synergistic lethal effect on HGSOC cells.	JNJ 26854165	110-122	P53	Homo sapiens	79-82
34140638-1	2021	BACKGROUND: CGM097 inhibits the p53-HDM2 interaction leading to downstream p53 activation.	NVP-CGM097	12-18	P53	Homo sapiens	32-35
34140638-1	2021	BACKGROUND: CGM097 inhibits the p53-HDM2 interaction leading to downstream p53 activation.	NVP-CGM097	12-18	P53	Homo sapiens	75-78
34440719-0	2021	Enzymatic Spermine Metabolites Induce Apoptosis Associated with Increase of p53, caspase-3 and miR-34a in Both Neuroblastoma Cells, SJNKP and the N-Myc-Amplified Form IMR5.	Spermine	10-18	P53	Homo sapiens	76-79
34337018-12	2021	KEGG pathway analysis further suggested that the p53 signalling pathway was involved in the baicalin-induced antitumour effect on SGC-7901 cells.	baicalin	92-100	P53	Homo sapiens	49-52
34158560-10	2021	Finally, anethole treatment inhibits the expression of oncogenes (cyclin D1) and up-regulated cyclin-dependent kinase inhibitor (p21WAF1), increases the expression of p53 gene, but inhibits the epithelial-mesenchymal transition markers.	anethole	9-17	P53	Homo sapiens	167-170
34109737-6	2022	In luminal A MCF-7 cells, the selection of a drug-resistant subline from parental cells with deregulation of p53 pathways occurred.	Phenobarbital	3-10	P53	Homo sapiens	109-112
34621341-9	2021	Additionally, the levels of wt-p53 in EW and EEEP were lower than controls, while OGG1 activity in EEEP was higher.	eeep	45-49	P53	Homo sapiens	31-34
34094678-0	2021	Minnelide, a prodrug, inhibits cervical cancer growth by blocking HPV-induced changes in p53 and pRb.	14-O-phosphonooxymethyltriptolide disodium salt	0-9	P53	Homo sapiens	89-92
34194837-10	2021	Conclusion: We conclude that thrombin is an important factor in the pathogenesis of CDDP kidney toxicity via activation of ERK1/2, P53 and caspase-3 pathway, which can be effectively blocked by Dab.	Dabigatran	194-197	P53	Homo sapiens	131-134
34570571-5	2021	In the patients with a stable disease, strong significant negative correlations between Cho/Cr and Cho/NAA with p53 mutation (-0.945 and -0.812 respectively, p < 0.05) and between Cho/Cr and IDH1, 2 mutation (-0.796, p < 0.05) were found.	CAV protocol	88-91	P53	Homo sapiens	112-115
34570571-5	2021	In the patients with a stable disease, strong significant negative correlations between Cho/Cr and Cho/NAA with p53 mutation (-0.945 and -0.812 respectively, p < 0.05) and between Cho/Cr and IDH1, 2 mutation (-0.796, p < 0.05) were found.	CAV protocol	99-102	P53	Homo sapiens	112-115
34570571-6	2021	In the patients with tumour progression, a significant positive correlation of NAA/Cr with 1p19q codeletion (0.486, p < 0.05) and of Cho/Cr and Cho/NAA values with p53 mutation (0.477 and 0.416, p < 0.05) were identified.	CAV protocol	133-136	P53	Homo sapiens	164-167
34570571-6	2021	In the patients with tumour progression, a significant positive correlation of NAA/Cr with 1p19q codeletion (0.486, p < 0.05) and of Cho/Cr and Cho/NAA values with p53 mutation (0.477 and 0.416, p < 0.05) were identified.	CAV protocol	144-147	P53	Homo sapiens	164-167
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	N-methyl-valyl-amiclenomycin	246-250	P53	Homo sapiens	160-163
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	N-methyl-valyl-amiclenomycin	246-250	P53	Homo sapiens	165-168
35344833-12	2022	ALOX15B and lipid peroxides obtained feedback from the p38-p53 pathway.	Lipid Peroxides	12-27	P53	Homo sapiens	59-62
35189247-4	2022	Out of these, the most prominent genetic alterations (PRKAR-1A, CTNNB1, ZNRF3, TP53, CCNE1 and TERF2 genes) are linked with a glycolytic enzyme pyruvate kinase M2 (PKM2), which converts phosphoenolpyruvate (PEP) to pyruvate in the glycolytic pathway.	Phosphoenolpyruvate	207-210	P53	Homo sapiens	79-83
35634298-11	2022	Overall, pharmacologic induction of mitophagy by inhibiting p53 may be a promising therapeutic approach for HS-ALI treatment.	hs-ali	108-114	P53	Homo sapiens	60-63
35566044-8	2022	A real-time PCR study showed that 6-Gingerol induces the simultaneous transcription of Bax with TP53 genes in large excess to BCL-2.	gingerol	34-44	P53	Homo sapiens	96-100
35086956-5	2022	In LNCaP and C4-2B cells, we found that olaparib induces massive DNA damage, leading to activation of the G2/M checkpoint, activation of p53, and cell cycle arrest.	olaparib	40-48	P53	Homo sapiens	137-140
35360199-8	2022	Furthermore, IP-Se-06 induced apoptosis by decreasing levels of Bcl-xL while increasing levels of gamma-H2AX and p53 proteins.	ip-se-06	13-21	P53	Homo sapiens	113-116
35406150-9	2022	Zn-BTC@CS stimulated the apoptotic process through up-regulating P53 expression and down-regulating Bcl-2 expression.	Chitosan	7-9	P53	Homo sapiens	65-68
35326597-6	2022	Paradoxically, 8-Cl-Ado-induced p53 increased FAO and OXPHOS, thereby self-limiting the activity of 8-Cl-Ado on LSCs.	fao	46-49	P53	Homo sapiens	32-35
35309342-7	2022	Moreover, uric acid upregulated autophagy via promoting the p53 pathway.	Uric Acid	10-19	P53	Homo sapiens	60-63
35134436-5	2022	The transcriptome analysis shows that the p53 signaling pathway is the most enriched cellular pathway and EG affects the proliferation of HCT 116 cells through modulating cell cycle related genes, such as CDKN1A and Cyclin-dependent kinases (CDKs).	anthraglycoside B	106-108	P53	Homo sapiens	42-45
35269669-5	2022	Furthermore, qRT-PCR revealed that olaparib inhibited the mRNA expression of markers associated with tumorigenesis and EMT, notably Ki67, Vimentin, beta-catenin, MMP2, MMP9, p53, and integrin alpha2 and beta1, while E-Cadherin was upregulated.	olaparib	35-43	P53	Homo sapiens	174-177
35121390-10	2022	RESULTS: Pachymic acid, shionone, peiminine and astragaloside A was verified as therapeutic agents for improving the condition of COPD by acting on the EGFR, ERK1, PAI-1 and p53 target, respectively.	astragaloside A	48-63	P53	Homo sapiens	174-177
35078476-11	2022	CONCLUSIONS: To sum up, TB exerted tumor-inhibitory, pro-senescent and pro-apoptotic effects on SK-Hep-1 cells through ATM-Chk2-p53 signaling axis in accompany with JNK bypass regulation.	theabrownin	24-26	P53	Homo sapiens	128-131
35078476-12	2022	This is the first report on the pro-senescent effect and multi-target (p53 and JNK) mechanism of TB on HCC cells, providing new insights into the underlying mechanisms of TB"s anti-HCC efficacy.	theabrownin	97-99	P53	Homo sapiens	71-74
35078476-12	2022	This is the first report on the pro-senescent effect and multi-target (p53 and JNK) mechanism of TB on HCC cells, providing new insights into the underlying mechanisms of TB"s anti-HCC efficacy.	theabrownin	171-173	P53	Homo sapiens	71-74
34969758-9	2022	Treatment with eupatilin induced p21 expression but inhibited the expression of mutated p53.	eupatilin	15-24	P53	Homo sapiens	88-91
35163037-0	2022	Sesquiterpene Lactones Potentiate Olaparib-Induced DNA Damage in p53 Wildtype Cancer Cells.	olaparib	34-42	P53	Homo sapiens	65-68
35163037-2	2022	In this work, we show that the two structurally-related sesquiterpene lactones, a 2-bromobenzyloxy derivative of dehydrosantonin (BdS) and alantolactone (ATL) sensitise p53 wildtype, homologous recombination-proficient cancer cells to low-dose treatment with the PARP inhibitor, olaparib.	alantolactone	139-152	P53	Homo sapiens	169-172
35163037-2	2022	In this work, we show that the two structurally-related sesquiterpene lactones, a 2-bromobenzyloxy derivative of dehydrosantonin (BdS) and alantolactone (ATL) sensitise p53 wildtype, homologous recombination-proficient cancer cells to low-dose treatment with the PARP inhibitor, olaparib.	olaparib	279-287	P53	Homo sapiens	169-172
35045964-0	2022	Correction: SAR405838: A Novel and Potent Inhibitor of the MDM2:p53 Axis for the Treatment of Dedifferentiated Liposarcoma.	SAR405838	12-21	P53	Homo sapiens	64-67
35008945-0	2022	Exposure of Toluene Diisocyanate Induces DUSP6 and p53 through Activation of TRPA1 Receptor.	Toluene 2,4-Diisocyanate	12-32	P53	Homo sapiens	51-54
10857993-6	2000	Our results show that: 1) Sequential TPT --&gt; G2/M-active drugs are synergistic when administration overlapped the maximum percentage of TPT-induced G2/M-phase cell arrest interval in all three mutated p53 cell lines; 2) the reverse sequential schedule (G2/M-active drug --&gt; TPT) was antagonistic, and being only additive for Etoposide --&gt; TPT association.	Topotecan	139-142	P53	Homo sapiens	204-207
10857993-6	2000	Our results show that: 1) Sequential TPT --&gt; G2/M-active drugs are synergistic when administration overlapped the maximum percentage of TPT-induced G2/M-phase cell arrest interval in all three mutated p53 cell lines; 2) the reverse sequential schedule (G2/M-active drug --&gt; TPT) was antagonistic, and being only additive for Etoposide --&gt; TPT association.	Topotecan	139-142	P53	Homo sapiens	204-207
10857993-6	2000	Our results show that: 1) Sequential TPT --&gt; G2/M-active drugs are synergistic when administration overlapped the maximum percentage of TPT-induced G2/M-phase cell arrest interval in all three mutated p53 cell lines; 2) the reverse sequential schedule (G2/M-active drug --&gt; TPT) was antagonistic, and being only additive for Etoposide --&gt; TPT association.	Topotecan	139-142	P53	Homo sapiens	204-207
11322510-4	2000	We also report on the permissive effects of Vitamin D3 and the Vitamin D3 analog EB 1089 in the promotion of apoptosis in p53-wild-type cells.	ethylbenzene	81-83	P53	Homo sapiens	122-125
22607421-6	2000	Nickel and cobalt ions inhibited binding of p53 to scDNA and to p53CON in linear DNA fragments less efficiently than zinc.	Nickel	0-6	P53	Homo sapiens	44-47
22607421-6	2000	Nickel and cobalt ions inhibited binding of p53 to scDNA and to p53CON in linear DNA fragments less efficiently than zinc.	Nickel	0-6	P53	Homo sapiens	64-67
10640990-6	2000	This study shows that the promoters of the genes coding for the enzymes crucial in melanin biosynthesis, namely tyrosinase and tyrosinase-related protein-1 (TRP-1), are activated by wild-type p53.	Melanins	83-90	P53	Homo sapiens	192-195
10574264-2	1999	Immunohistochemical analysis of p53 was performed on formalin-fixed, paraffin-embedded specimens from 168 primary ovarian carcinomas by using the DO-7 monoclonal antibody.	Formaldehyde	53-61	P53	Homo sapiens	32-35
10469629-0	1999	Nickel-induced transformation shifts the balance between HIF-1 and p53 transcription factors.	Nickel	0-6	P53	Homo sapiens	67-70
10484981-7	1999	In the analyses of tumor tissues from the propositus and his daughter, a P16INK4A codon 94 missense point mutation (GCG-->GAG; Ala-->Glu) was observed with the hereditary TP53 mutation.	Glycosaminoglycans	122-125	P53	Homo sapiens	171-175
10458704-1	1999	This work describes the preparation of the cationic trans-8, 9-dihydro-8-(N7-guanyl)-9-hydroxyaflatoxin B(1) ((AFB)G) adducts at the positions corresponding to G(746) or G(747), within the oligodeoxyribonucleotide d(GGAGGCCT) containing the codon 249 sequence (underlined) of the p53 gene, using DNA triplexes to target adduction at the desired site.	trans-8, 9-dihydro-8-(n7-guanyl)-9-hydroxyaflatoxin b	52-105	P53	Homo sapiens	280-283
10483067-2	1999	MATERIALS AND METHODS: The expression of p53 and MDM2 proteins was determined immunohistochemically in 51 formalin-fixed, paraffin embedded specimens of odontogenic cysts and tumours.	Formaldehyde	106-114	P53	Homo sapiens	41-44
10341297-3	1999	In this study, we investigated the molecular mechanisms by which auristatin-PE, a newly developed experimental agent, and gemcitabine, a commercially available anti-cancer agent, exert their inhibitory effects on pancreatic cancer cell lines containing wild-type p53 (HPAC) and mutant p53 (PANC-1).	soblidotin	65-78	P53	Homo sapiens	263-266
10341297-3	1999	In this study, we investigated the molecular mechanisms by which auristatin-PE, a newly developed experimental agent, and gemcitabine, a commercially available anti-cancer agent, exert their inhibitory effects on pancreatic cancer cell lines containing wild-type p53 (HPAC) and mutant p53 (PANC-1).	soblidotin	65-78	P53	Homo sapiens	285-288
10341297-7	1999	These results suggest that auristatin-PE may induce apoptosis and p21WAF1 expression through p53-dependent or independent pathways, and that up-regulation of p21WAF1 and Bax and down-regulation of Bcl-2 may be the molecular mechanism through which auristatin-PE inhibits cell growth and induces apoptosis.	soblidotin	27-40	P53	Homo sapiens	93-96
10621852-9	1999	For the formalin-fixed tissue specimens, 62% (13/21) and 90% (19/21) expressed p53 and PCNA, respectively.	Formaldehyde	8-16	P53	Homo sapiens	79-82
10233583-0	1999	Brefeldin A-induced apoptosis in prostatic cancer DU-145 cells: a possible p53-independent death pathway.	Brefeldin A	0-11	P53	Homo sapiens	75-78
10233583-7	1999	Western blots showed that the expression of cell cycle-dependent kinases (cdk2 and cdk4), cyclin D1 and p53 was significantly reduced, while WAF1 was increased, after BFA treatment.	Brefeldin A	167-170	P53	Homo sapiens	104-107
10051470-11	1999	The p53 polymorphism also interacted with the cytochrome P450 1A1 and carotenoid levels in smoking-related hepatocarcinogenesis.	Carotenoids	70-80	P53	Homo sapiens	4-7
9747866-10	1998	An interaction was also observed between p53 immunopositivity and CAF dose.	cafestol palmitate	66-69	P53	Homo sapiens	41-44
9732400-6	1998	Transfer of a mutant p53 gene enhanced topotecan sensitivity in wild-type p53 LN-229 but not mutant p53 LN-18 cells.	Topotecan	39-48	P53	Homo sapiens	21-24
9732400-6	1998	Transfer of a mutant p53 gene enhanced topotecan sensitivity in wild-type p53 LN-229 but not mutant p53 LN-18 cells.	Topotecan	39-48	P53	Homo sapiens	74-77
9972170-3	1998	The objective of this study was to investigate the immunodetection of p53 and PCNA in IPHP, and to correlate these results with the degree of epithelial hyperplasia and inflammatory infiltrate.	iphp	86-90	P53	Homo sapiens	70-73
9705861-0	1998	Chronic treatment of human fibroblasts cultures with diacylglycerol induces down-regulation of p53 functional activity.	Diglycerides	53-67	P53	Homo sapiens	95-98
9705861-4	1998	We show here that chronic treatment of human fibroblast with DAG induces p53 down-regulation and inhibition of p53 functional activity, and protection from UV-induced apoptosis.	Diglycerides	61-64	P53	Homo sapiens	73-76
9655287-4	1998	Histopathologic/genetic analysis of p53 was performed on formalin fixed, paraffin embedded tissues.	Formaldehyde	57-65	P53	Homo sapiens	36-39
9797697-4	1998	Immunohistochemical expression of p53 protein was evaluated in formalin-fixed paraffin-embedded sections of CRC liver metastases using the monoclonal antibodies (MAbs) D01 and Pab 1801.	Formaldehyde	63-71	P53	Homo sapiens	34-37
9607618-9	1998	p53 mutant status was assessed immunohistochemically from sections of the formalin-fixed, paraffin-embedded pretreatment biopsy and the resected specimen.	Formaldehyde	74-82	P53	Homo sapiens	0-3
9548807-10	1998	Thiotepa, a non-quinone aziridine-containing agent, and 1,4-benzoquinone (p-BQ), a redox cycling quinone, increased p53 levels.	Thiotepa	0-8	P53	Homo sapiens	116-119
9548807-11	1998	The nonalkylator oxygen-radical-generating agent menadione (MD) caused p53 induction only when MCF-7 cells were allowed to recover in drug-free media.	Vitamin K 3	49-58	P53	Homo sapiens	71-74
9548807-15	1998	The uncoupling of p53 induction and apoptosis is evidenced by the generation of nucleosomal DNA laddering in aziridinequinone-treated T47D cells, a breast cancer cell line bearing a p53 mutation.	aziridinequinone	109-125	P53	Homo sapiens	18-21
9548807-15	1998	The uncoupling of p53 induction and apoptosis is evidenced by the generation of nucleosomal DNA laddering in aziridinequinone-treated T47D cells, a breast cancer cell line bearing a p53 mutation.	aziridinequinone	109-125	P53	Homo sapiens	182-185
9488468-0	1998	The physical association of multiple molecular chaperone proteins with mutant p53 is altered by geldanamycin, an hsp90-binding agent.	geldanamycin	96-108	P53	Homo sapiens	78-81
9488468-8	1998	To examine the effect of directly disrupting chaperone interactions with mutant p53, we made use of geldanamycin (GA), a selective hsp90-binding agent which has been shown to alter the chaperone associations regulating the function of unliganded steroid receptors.	geldanamycin	100-112	P53	Homo sapiens	80-83
9488468-8	1998	To examine the effect of directly disrupting chaperone interactions with mutant p53, we made use of geldanamycin (GA), a selective hsp90-binding agent which has been shown to alter the chaperone associations regulating the function of unliganded steroid receptors.	geldanamycin	114-116	P53	Homo sapiens	80-83
9488468-9	1998	GA treatment of cells altered heteroprotein complex formation with several different mutant p53 species.	geldanamycin	0-2	P53	Homo sapiens	92-95
9740272-3	1998	One case harbored a p53 gene mutation in codon 282 in exon 8, CGG (arginine) to TGG (tryptophan), but the mutation was not found in other patient"s tissues with similar histological features.	GAMMA-GLUTAMYL-S-(1,2-DICARBOXYETHYL)CYSTEINYLGLYCINE	80-83	P53	Homo sapiens	20-23
9510313-3	1998	METHODS: p53 and p21/WAF1 expressions in formalin fixed, paraffin-embedded, preradiation biopsy samples from 49 patients with primary rectal carcinoma were analyzed immunohistochemically.	Formaldehyde	41-49	P53	Homo sapiens	9-12
10069444-5	1998	In one case, p53 codon 282 mutation (CGG--&gt;TGG; arg--&gt;trp) were observed in initial diagnosis.	GAMMA-GLUTAMYL-S-(1,2-DICARBOXYETHYL)CYSTEINYLGLYCINE	46-49	P53	Homo sapiens	13-16
9426406-0	1997	Alterations of the p53 gene in occupational bladder cancer in workers exposed to aromatic amines.	aromatic amines	81-96	P53	Homo sapiens	19-22
9426406-2	1997	In the present study, p53 gene mutations in 26 patients with bladder lesions occupationally exposed to aromatic amines were examined by single-strand conformation polymorphism analysis of PCR-amplified DNA segments, followed by direct sequencing.	aromatic amines	103-118	P53	Homo sapiens	22-25
9366263-3	1997	Both apoptosis triggered by the purine analog 2-chlorodeoxyadenosine (CdA) and growth stimulation by the mitogen phytohemagglutinin (PHA) induced a comparable level and time course of p53 mRNA expression.	Cladribine	70-73	P53	Homo sapiens	184-187
9368590-0	1997	Immunohistochemical detection of p53 in archival formalin-fixed tissues of lip and intraoral squamous cell carcinomas from Norway.	Formaldehyde	49-57	P53	Homo sapiens	33-36
9368590-1	1997	We investigated the expression of p53 in 82 formalin-fixed, paraffin-embedded archival tissue specimens of lip and intraoral squamous cell carcinomas (SCCs) from the period 1930-1995, by immunohistochemistry using three monoclonal antibodies (MAbs DO-7, DO-1 and 1801).	Formaldehyde	44-52	P53	Homo sapiens	34-37
9365042-7	1997	p53 antibody positivity was associated with bilirubin and the number of tumors (p=0.027 and p=0.018, respectively).	Bilirubin	44-53	P53	Homo sapiens	0-3
9350037-10	1997	Phenanthroline treatment (&gt; 2 mM) caused a complete down-regulation of PR and the tumor suppressor protein, p53.	Phenanthrolines	0-14	P53	Homo sapiens	111-114
9350037-12	1997	We propose that the inhibition of T47D cell proliferation by phenanthroline, Rifampicin and ATA results from a number of cellular changes that include regulation of p53 and PR.	Phenanthrolines	61-75	P53	Homo sapiens	165-168
21590166-5	1997	carcinomas of female breast with and without lymph node metastasis for p53 protein overexpression by immunohistochemistry on formalin-fixed, paraffin-embedded tissue sections to ascertain if p53 positive tumors have greater metastatic potential than p53 negative tumors.	Formaldehyde	125-133	P53	Homo sapiens	71-74
10325638-1	1997	To explore the carcinogenic effect of asbestos at molecular level, we directly analyzed the mutations of exon 5, 7 and 8 of anti-oncogene p53 in paraffin-embedded human lung tissue affected by asbestos for the first time.	Asbestos	38-46	P53	Homo sapiens	138-141
9257692-5	1997	Simulated solar UV radiation increased p53, and agents that scavenge active oxygen species, N-acetylcysteine, ascorbate and alpha-tocopherol, inhibited the increase.	Ascorbic Acid	110-119	P53	Homo sapiens	39-42
9257692-5	1997	Simulated solar UV radiation increased p53, and agents that scavenge active oxygen species, N-acetylcysteine, ascorbate and alpha-tocopherol, inhibited the increase.	alpha-Tocopherol	124-140	P53	Homo sapiens	39-42
9192825-3	1997	In this study, we characterized the growth-inhibitory effects of active metabolites of sulindac in cultured colon adenocarcinoma cells by determining the contribution of apoptosis and cell cycle arrest and the requirement for cyclooxygenase (COX) inhibition and p53 involvement and compared the effects of sulindac metabolites with the chemotherapeutic drug, 5-fluorouracil (5-FU).	Sulindac	87-95	P53	Homo sapiens	262-265
9192825-12	1997	Saos-2 cells, which lack p53, responded to sulindac metabolites but not 5-FU.	Sulindac	43-51	P53	Homo sapiens	25-28
9071734-0	1997	A rapid and nonisotopic method for the screening and sequencing of p53 gene mutations in formalin-fixed, paraffin-embedded tumors.	Formaldehyde	89-97	P53	Homo sapiens	67-70
9071734-2	1997	In this study, we describe a sensitive, rapid, nonisotopic and inexpensive procedure for the polymerase chain reaction (PCR)-single-stranded conformational polymorphism (SSCP) detection and subsequent sequencing of p53 mutations in formalin-fixed and paraffin-embedded tumor (PET) samples.	Formaldehyde	232-240	P53	Homo sapiens	215-218
8980360-3	1997	Genomic p53 was amplified with the polymerase chain reaction (PCR) from formalin-fixed, paraffin-embedded tissues.	Formaldehyde	72-80	P53	Homo sapiens	8-11
9137531-0	1997	Depletion of p185erbB2, Raf-1 and mutant p53 proteins by geldanamycin derivatives correlates with antiproliferative activity.	geldanamycin	57-69	P53	Homo sapiens	41-44
9137531-1	1997	PURPOSE: Recently, it has been shown that geldanamycin (GA), a benzoquinone ansamycin, is able to deplete mutant p53, p185erbB2 and Raf-1 proteins in cancer cells.	geldanamycin	42-54	P53	Homo sapiens	113-116
9137531-1	1997	PURPOSE: Recently, it has been shown that geldanamycin (GA), a benzoquinone ansamycin, is able to deplete mutant p53, p185erbB2 and Raf-1 proteins in cancer cells.	geldanamycin	56-58	P53	Homo sapiens	113-116
9137531-13	1997	CONCLUSIONS: These findings suggest that GA and its derivatives are cytostatic/cytotoxic at concentrations that also downregulate Raf-1, p185erbB2 and mutant p53, and raise the possibility that depletion of these proteins and the antiproliferative activities of GA have a common mechanism.	geldanamycin	41-43	P53	Homo sapiens	158-161
9042262-3	1996	The expression of p53 and bcl-2 gene products was studied immunohistochemically using formalin-fixed paraffinembedded tumor samples of 31 locally confined RCC of patients treated with radical nephrectomy.	Formaldehyde	86-94	P53	Homo sapiens	18-21
8798554-1	1996	Evidence that reactive oxygen intermediates produced by adherent neutrophils increase the activity of the p58c-fgr and p53/56lyn tyrosine kinases.	reactive oxygen	14-29	P53	Homo sapiens	119-122
8841466-8	1996	Addition of the purified fatty acids, comprising the diglyceride fraction, indicated that the fatty acids, 16:1, 18:0, and 18:1, induced the most significant increases in p53 expression by HT-29 cells.	Diglycerides	53-64	P53	Homo sapiens	171-174
8881915-2	1996	METHODS: Expression of p53 was evaluated immunocytochemically in a retrospective study of formalin fixed, paraffin wax embedded tissue.	Formaldehyde	90-98	P53	Homo sapiens	23-26
8663952-2	1996	OBJECTIVE: To demonstrate how the detection of p53 protein in formaldehyde-fixed, paraffin-embedded oropharyngeal carcinoma may be used as a factor in estimating prognosis.	Formaldehyde	62-74	P53	Homo sapiens	47-50
8674115-1	1996	Highly purified p53 protein from different sources was able to degrade DNA with a 3"-to-5" polarity, yielding deoxynucleoside monophosphates as reaction products.	deoxynucleoside monophosphates	110-140	P53	Homo sapiens	16-19
10330207-3	1996	Mutational analysis of p53 was performed retrospectively by means of topographic genotyping (TG), using formalin-fixed, paraffin-embedded tissue of the primary and recurrent tumor.	Formaldehyde	104-112	P53	Homo sapiens	23-26
8616846-5	1996	Because p53 is inducible by ionizing radiation, we propose that existing cancer therapy regimens that combine radiotherapy with CENU chemotherapy may be improved by altering scheduling and allowing enough time between the two therapies for the relatively stable MGMT protein to degrade.	1-(2-chloroethyl)-1-nitrosourea	128-132	P53	Homo sapiens	8-11
8612815-2	1996	With the use of NO donors such as S-nitrosoglutathione or spermine-NO we established that PARP digestion occurs in parallel with DNA fragmentation, and is preceded by accumulation of the tumor suppressor gene product p53.	Spermine	58-66	P53	Homo sapiens	217-220
8822203-0	1996	p53-independent increase in p21WAF1 and reciprocal down-regulation of cyclin A and proliferating cell nuclear antigen in bromodeoxyuridine-mediated growth arrest of human melanoma cells.	Bromodeoxyuridine	121-138	P53	Homo sapiens	0-3
16696044-1	1996	Aims-To study the possible accumulation of p53 protein in inverted papilloma of the urinary bladder.Methods-Formalin fixed, paraffin wax embedded sections from 14 cases of inverted papilloma of the urinary bladder were studied retrospectively.	Formaldehyde	108-116	P53	Homo sapiens	43-46
9431695-1	1996	Detection of various epitopes of the p53 and MDM-2 proteins, using new antibodies was performed on formalin-fixed and paraffin-embedded tissue samples from breast cancer and compared with results obtained using well-characterized antibodies.	Formaldehyde	99-107	P53	Homo sapiens	37-40
7487899-6	1995	Addition of 2-chlorodeoxyadenosine induced an increase in the amount of p53 in human thymocytes, while 2-chloroadenosine had no effect.	Cladribine	12-34	P53	Homo sapiens	72-75
7557622-13	1995	Phosphorothioate oligos directed against c-myc and p53 in different cell lines were shown to have both antiproliferative and stimulatory activity, as single agents and in combination, at concentrations that are achievable in vivo.	Parathion	0-16	P53	Homo sapiens	51-54
7559091-4	1995	The molecular weight of p53 protein in SAOS-MC43 was lower than that in SAOS-MC11, SAOS-MC11 and SAOS-MC43 were more sensitive and more resistant, respectively, to ionizing radiation than the parental SAOS-2.	saos-mc43	39-48	P53	Homo sapiens	24-27
7596441-2	1995	p53 response elements contain two or more copies of a somewhat promiscuous consensus sequence: 5"-XXXC(A,T)(T,A)GYY-3" (where X is a purine and Y is a pyrimidine) (ref.	pyrimidine	151-161	P53	Homo sapiens	0-3
7624116-1	1995	A human p53 mutant, p53Val-138 (amino acid 138, Alanine--&gt;Valine), generated by in vitro mutagenesis was introduced into Saos-2 human osteosarcoma and Jurkat acute T-lymphoblastic leukemia cell lines, both lacking p53 protein expression.	Valine	61-67	P53	Homo sapiens	8-11
7624116-1	1995	A human p53 mutant, p53Val-138 (amino acid 138, Alanine--&gt;Valine), generated by in vitro mutagenesis was introduced into Saos-2 human osteosarcoma and Jurkat acute T-lymphoblastic leukemia cell lines, both lacking p53 protein expression.	Valine	61-67	P53	Homo sapiens	20-23
7549812-9	1995	Interestingly, we also found that p53 mutations occurred significantly more frequently in patients with a history of occupational exposure to asbestos [3 of 60 (5%) for patients without p53 mutations versus 5 of 25 (20%) of those with p53 mutations; P &lt; 0.05].	Asbestos	142-150	P53	Homo sapiens	34-37
7549812-9	1995	Interestingly, we also found that p53 mutations occurred significantly more frequently in patients with a history of occupational exposure to asbestos [3 of 60 (5%) for patients without p53 mutations versus 5 of 25 (20%) of those with p53 mutations; P &lt; 0.05].	Asbestos	142-150	P53	Homo sapiens	186-189
7549812-9	1995	Interestingly, we also found that p53 mutations occurred significantly more frequently in patients with a history of occupational exposure to asbestos [3 of 60 (5%) for patients without p53 mutations versus 5 of 25 (20%) of those with p53 mutations; P &lt; 0.05].	Asbestos	142-150	P53	Homo sapiens	186-189
7750085-3	1995	Teleocidin antagonized both apoptosis and alterations of nuclear p53 protein and PCNA induced by these anticancer drugs.	teleocidins	0-10	P53	Homo sapiens	65-68
7720110-3	1994	The result showed that mutation of both cell lines occurred on the 154th codon in exon5 of p53 gene, where GGC was displaced by GTC resulting a substitution of Val for Gly, nevertheless, N-ras oncogene and the exon7 of p53 gene are normal.	Valine	160-163	P53	Homo sapiens	91-94
7720110-3	1994	The result showed that mutation of both cell lines occurred on the 154th codon in exon5 of p53 gene, where GGC was displaced by GTC resulting a substitution of Val for Gly, nevertheless, N-ras oncogene and the exon7 of p53 gene are normal.	Valine	160-163	P53	Homo sapiens	219-222
7580888-2	1994	Sequences of the p53 gene have been obtained from DNA extracted from frozen and formalin-fixed paraffin-embedded cancer tissues.	Formaldehyde	80-88	P53	Homo sapiens	17-20
8168507-7	1994	Using metal affinity chromatography, we have established that pure p53 binds the immobilised divalent ions Zn2+, Ni2+ and Co2+ with high affinity.	Cobalt(2+)	122-126	P53	Homo sapiens	67-70
8139558-6	1994	Rodent cells transformed with E1A plus the p53(Val-135) temperature-sensitive mutant are transformed at the restrictive temperature and undergo rapid and complete apoptosis at the permissive temperature when p53 adopts the wild-type conformation.	Valine	47-50	P53	Homo sapiens	43-46
8139558-6	1994	Rodent cells transformed with E1A plus the p53(Val-135) temperature-sensitive mutant are transformed at the restrictive temperature and undergo rapid and complete apoptosis at the permissive temperature when p53 adopts the wild-type conformation.	Valine	47-50	P53	Homo sapiens	208-211
8176513-1	1994	Serum levels of p53 protein were examined in 23 cases of lung cancer (many with potential asbestos exposure), 23 unexposed matched hospital control subjects, 58 unmatched general population control subjects, and 4 people with nonmalignant lung disease using an enzyme-linked immunosorbent assay and Western immunoblotting.	Asbestos	90-98	P53	Homo sapiens	16-19
8008749-1	1994	p53 expression in formalin-fixed, paraffin-embedded archival specimens of intrahepatic cholangiocarcinoma: retrieval of p53 antigenicity by microwave oven heating of tissue sections.	Formaldehyde	18-26	P53	Homo sapiens	0-3
8008749-4	1994	We investigated expression of p53 in formalin-fixed, paraffin-embedded archival specimens of 40 CCs (22 autopsy cases and 18 surgical cases) by immunohistochemistry using four antibodies (PAb1801, DO-7, BP53-12, CM1).	Formaldehyde	37-45	P53	Homo sapiens	30-33
8008749-10	1994	These results shows that a pretreatment of tissue sections by microwave oven heating is a very good method for demonstrating p53 protein in formalin-fixed, paraffin-embedded archival materials and that DO-7, BP53-12, and CM1 are useful antibodies for detection of p53 in formalin-fixed, paraffin-embedded archival materials.	Formaldehyde	140-148	P53	Homo sapiens	125-128
8261448-5	1994	Forty-four % (16 of 36) of BCCs had a mutated p53 allele, usually opposite pyrimidine tracts, which is consistent with UV-induced mutations.	pyrimidine	75-85	P53	Homo sapiens	46-49
7533993-3	1994	81.7% of AK, 100% of SCC, 73.8% of BCC as well as 29.2% of BEN, 37.5% of REH, and 26.9% of NE showed p53 positivity.	benzamidine	59-62	P53	Homo sapiens	101-104
8112175-1	1993	Expression of P53 protein was detected immunohistochemically in formalin-fixed, paraffin-embedded tissues from 67 patients with bladder carcinoma and 6 normal bladder controls.	Formaldehyde	64-72	P53	Homo sapiens	14-17
8325885-4	1993	The p53 mutants Val-135 and Phe-132 up-regulated IL-6 promoter activity in these cells at both 32.5 and 37 degrees C. The temperature-sensitive Val-135 mutant was not only not inhibitory or "wt-like" at the lower temperature, but had gained a transcriptional activator phenotype which was temperature-independent in HeLa cells.	Valine	16-19	P53	Homo sapiens	4-7
8325885-4	1993	The p53 mutants Val-135 and Phe-132 up-regulated IL-6 promoter activity in these cells at both 32.5 and 37 degrees C. The temperature-sensitive Val-135 mutant was not only not inhibitory or "wt-like" at the lower temperature, but had gained a transcriptional activator phenotype which was temperature-independent in HeLa cells.	Valine	144-147	P53	Homo sapiens	4-7
8325885-5	1993	The functional DNA target for transcriptional modulation of the IL-6 promoter by p53 species included the multiple cytokine- and second messenger-response element (-173 to -145); point mutations in the transcription factor C/EBP beta-binding site within the second messenger-response element largely blocked the ability of p53 mutants Val-135 and Phe-132 to up-regulate this promoter.	Valine	335-338	P53	Homo sapiens	81-84
8325885-7	1993	In contrast, the p53 mutants Val-135 and Phe-132 further enhanced C/EBP beta-mediated up-regulation of IL-6 promoter constructs.	Valine	29-32	P53	Homo sapiens	17-20
8415589-1	1993	The p53 gene was examined in a series of formalin-fixed paraffin-embedded astrocytic neoplasms of various types by polymerase chain reaction (PCR), single-strand conformation polymorphism analysis (SSCP), and direct sequencing of amplified DNA.	Formaldehyde	41-49	P53	Homo sapiens	4-7
8390283-8	1993	The 12th mutation GTG--&gt;GGG (valine--&gt;glycine) at codon 216 was expressed in line SCC-12 clone B along with an apparently normal p53 allele and is to our knowledge a novel mutation.	Valine	32-38	P53	Homo sapiens	135-138
8392521-3	1993	METHODS: The presence and localisation of the p53 protein in formalin fixed, paraffin wax embedded specimens of anal squamous epithelium (normal and neoplastic) was examined using immunohistochemical staining with a panel of two monoclonal antibodies (DO-1, DO-7) and one polyclonal antibody (CM-1).	Formaldehyde	61-69	P53	Homo sapiens	46-49
8384406-1	1993	Striking differences were found between different histological types of breast cancer when 263 invasive breast carcinomas were tested for nuclear p53 accumulation in formaldehyde-fixed paraffin sections.	Formaldehyde	166-178	P53	Homo sapiens	146-149
8384408-1	1993	The spectrum of p53 gene mutations was determined in formalin-fixed, paraffin-embedded samples of small-cell lung cancer derived from 28 patients.	Formaldehyde	53-61	P53	Homo sapiens	16-19
8506620-2	1993	Using a microwave oven heating method, we have detected over-expression of p53 in buffered-formalin fixed, paraffin-embedded sections of oesophageal carcinomas immunohistochemically and examined the relationship between the p53 over-expression and postoperative survival.	Formaldehyde	91-99	P53	Homo sapiens	75-78
1484319-0	1992	p53 immunostaining in the distinction between benign and malignant mesothelial proliferations using formalin-fixed paraffin sections.	Formaldehyde	100-108	P53	Homo sapiens	0-3
1484319-2	1992	The object of this study was to examine the frequency of immunohistochemically detectable p53 overexpression in routinely processed, paraffin-embedded tissue from pleural mesotheliomas and from pleura showing reactive mesothelial hyperplasia, using a polyclonal antibody to formalin-resistant p53 epitopes, and to consider the diagnostic utility of this antibody in the distinction between mesothelioma and reactive mesothelium in pleural biopsy specimens.	Formaldehyde	274-282	P53	Homo sapiens	90-93
1484319-6	1992	In conclusion, this study suggests that p53 immunostaining can help to distinguish epithelial or biphasic mesothelioma from reactive mesothelial hyperplasia in formalin-fixed, paraffin-embedded pleural biopsy specimens.	Formaldehyde	160-168	P53	Homo sapiens	40-43
1358781-3	1992	Immunoreactive p53 was observed in the nuclei of tumor cells in 4% paraformaldehyde-fixed, frozen sections (12 of 15) and paraffin-embedded sections (11 of 15), but not in routinely processed (10% formalin-fixed) specimens.	Formaldehyde	197-205	P53	Homo sapiens	15-18
1406686-7	1992	The covalence of the p53-5.8S rRNA linkage was demonstrated by the following findings: (i) p53 and the linked 5.8S rRNA comigrated in SDS-PAGE; (ii) only after treatment of the p53-RNA complex with proteinase K did the 5.8S rRNA migrate differently from p53-linked 5.8S rRNA; and (iii) this isolated RNA was found linked to phosphoserine, presumably at the 5" end.	Phosphoserine	324-337	P53	Homo sapiens	21-24
1406686-7	1992	The covalence of the p53-5.8S rRNA linkage was demonstrated by the following findings: (i) p53 and the linked 5.8S rRNA comigrated in SDS-PAGE; (ii) only after treatment of the p53-RNA complex with proteinase K did the 5.8S rRNA migrate differently from p53-linked 5.8S rRNA; and (iii) this isolated RNA was found linked to phosphoserine, presumably at the 5" end.	Phosphoserine	324-337	P53	Homo sapiens	91-94
1406686-7	1992	The covalence of the p53-5.8S rRNA linkage was demonstrated by the following findings: (i) p53 and the linked 5.8S rRNA comigrated in SDS-PAGE; (ii) only after treatment of the p53-RNA complex with proteinase K did the 5.8S rRNA migrate differently from p53-linked 5.8S rRNA; and (iii) this isolated RNA was found linked to phosphoserine, presumably at the 5" end.	Phosphoserine	324-337	P53	Homo sapiens	91-94
1406686-7	1992	The covalence of the p53-5.8S rRNA linkage was demonstrated by the following findings: (i) p53 and the linked 5.8S rRNA comigrated in SDS-PAGE; (ii) only after treatment of the p53-RNA complex with proteinase K did the 5.8S rRNA migrate differently from p53-linked 5.8S rRNA; and (iii) this isolated RNA was found linked to phosphoserine, presumably at the 5" end.	Phosphoserine	324-337	P53	Homo sapiens	91-94
1764370-4	1991	One of the antibodies, CM1, recognises p53 in formalin-fixed, paraffin-embedded archival material and using this reagent we found immunodetectable p53 in 28 of 124 (23%) pancreatic cancers.	Formaldehyde	46-54	P53	Homo sapiens	39-42
1918170-4	1991	We previously identified a case of human acute myelogenous leukemia (AML) in which both alleles of the p53 gene had undergone independent missense mutations (at codons 135 cys to ser and 246 met to val).	Valine	198-201	P53	Homo sapiens	103-106
2137009-1	1990	p53 messenger RNA expression was examined using a cDNA probe in 76 fresh primary breast tumour specimens, 15 of which came from patients treated with toxoxifen prior to surgery.	toxoxifen	150-159	P53	Homo sapiens	0-3
33773191-0	2021	Bibenzyl analogue DS-1 inhibits MDM2-mediated p53 degradation and sensitizes apoptosis in lung cancer cells.	Bibenzyls	0-8	P53	Homo sapiens	46-49
33773191-4	2021	PURPOSE: The present study aimed to investigate the effect of 3,4-dihydroxy-5,4"-dimethoxybibenzyl (DS-1) on targeting MDM2 and restoring p53 function in lung cancer cells.	3,4-dihydroxy-5,4"-dimethoxybibenzyl	62-98	P53	Homo sapiens	138-141
34417893-7	2021	Exposure of differentiated SH-SY5Y cells to varying concentrations of cocaine resulted in the induction of PARP-1 dependent PARylation of p53 tumor suppressor.	Cocaine	70-77	P53	Homo sapiens	138-141
34417893-8	2021	Further analysis revealed that PARylation of p53 by cocaine treatment resulted in nuclear accumulation of p53.	Cocaine	52-59	P53	Homo sapiens	45-48
34417893-8	2021	Further analysis revealed that PARylation of p53 by cocaine treatment resulted in nuclear accumulation of p53.	Cocaine	52-59	P53	Homo sapiens	106-109
34417893-10	2021	Interestingly, cocaine-induced p53 PARylation resulted in the induction of proline oxidase (POX)-a p53 responsive gene involved in cellular metabolism.	Cocaine	15-22	P53	Homo sapiens	31-34
34417893-11	2021	Given that cocaine-induced p53 PARylation is an energy-dependent process, we observed that cocaine-induced PARP-1/p53/POX axes alters cellular energy metabolism.	Cocaine	11-18	P53	Homo sapiens	27-30
34417893-11	2021	Given that cocaine-induced p53 PARylation is an energy-dependent process, we observed that cocaine-induced PARP-1/p53/POX axes alters cellular energy metabolism.	Cocaine	11-18	P53	Homo sapiens	114-117
34417893-11	2021	Given that cocaine-induced p53 PARylation is an energy-dependent process, we observed that cocaine-induced PARP-1/p53/POX axes alters cellular energy metabolism.	Cocaine	91-98	P53	Homo sapiens	27-30
34343636-8	2021	The AKT1/FOXP3 axis mediated the CerS6 expression and promoted p53 mutant pancreatic tumorigenesis by producing excessive C16-ceramide, which induced the accumulation of mutant p53.	N-palmitoylsphingosine	122-134	P53	Homo sapiens	63-66
34343636-8	2021	The AKT1/FOXP3 axis mediated the CerS6 expression and promoted p53 mutant pancreatic tumorigenesis by producing excessive C16-ceramide, which induced the accumulation of mutant p53.	N-palmitoylsphingosine	122-134	P53	Homo sapiens	177-180
34850229-8	2022	MON 52276 and glyphosate altered the expression of genes in liver reflecting TP53 activation by DNA damage and circadian rhythm regulation.	mon 52276	0-9	P53	Homo sapiens	77-81
34680379-10	2021	Lastly, vemurafenib-resistant melanoma cells showed an altered expression of p53 and p73 isoforms, namely an increased expression of potentially pro-oncogenic Delta40p53beta and a decrease in tumor-suppressive TAp73beta.	Vemurafenib	8-19	P53	Homo sapiens	77-80
34711017-0	2021	Anti-Proliferative and Pro-Apoptotic Activities of Synthesized 3,4,5 Tri-Methoxy Ciprofloxacin Chalcone Hybrid, through p53 Up-Regulation in HepG2 and MCF7 Cell Lines.	3,4,5 tri-methoxy ciprofloxacin	63-94	P53	Homo sapiens	120-123
34226168-8	2021	Treatment response to CR or PR and TP53 mutation were 2 prognostic factor for OS and PFS in decitabine with CEG regimen.	Cephaloglycin	108-111	P53	Homo sapiens	35-39
34497762-0	2021	Ascorbate Inhibits Proliferation and Promotes Myeloid Differentiation in TP53-Mutant Leukemia.	Ascorbic Acid	0-9	P53	Homo sapiens	73-77
34497762-10	2021	Collectively, these data suggest that ascorbate could exert a beneficial anti-proliferative effect on AML cells harboring both TET2 and TP53 mutations whilst not interfering with targeted cytotoxic therapies such as Prima-1Met.	Ascorbic Acid	38-47	P53	Homo sapiens	136-140
34338098-9	2022	Thus, we summarized some of the sterol-related signaling pathways in glioma and how they can be associated with other signaling pathways, including EGFR/PI3K/Akt/mTOR, P53, and retinoblastoma protein.	Sterols	32-38	P53	Homo sapiens	168-171
34377229-5	2021	This finding suggests that both KrasG12V and KrasG12D are required for showing higher FL118 efficacy, while the presence of KrasG13D could somehow decrease FL118 efficacy under the defined p53/APC genetic status.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	156-161	P53	Homo sapiens	189-192
34377229-10	2021	These findings would be useful for predicting FL118 sensitivity to patients" CRC tumors with the defined Kras mutation subtypes under the defined p53/APC genetic status.	7-ethyl-7-hydroxy-10H-1,3-Dioxolo(4,5-g)pyrano(3',4':6,7)indolizino(1,2-b)quinoline-8,11(7H,12H)-dione	46-51	P53	Homo sapiens	146-149
35460941-0	2022	Low doses of niclosamide and quinacrine combination yields synergistic effect in melanoma via activating autophagy-mediated p53-dependent apoptosis.	Quinacrine	29-39	P53	Homo sapiens	124-127
35460941-5	2022	The results showed, briefly, an exposure to niclosamide and quinacrine led to an increased apoptosis-related protein p53, cleaved caspase-3 and cleaved PARP and autophagy-related protein LC3B expression, and a decreased expression of autophagy-related protein p62, finally leading to cell apoptosis and autophage.	Quinacrine	60-70	P53	Homo sapiens	117-120
35217253-8	2022	Biotin-C3 peptide characterized luminal BC according to p53 status and to HER2 expression, being the biosensor a better strategy when compared to ELISA test.	Phenobarbital	32-39	P53	Homo sapiens	56-59
35189247-4	2022	Out of these, the most prominent genetic alterations (PRKAR-1A, CTNNB1, ZNRF3, TP53, CCNE1 and TERF2 genes) are linked with a glycolytic enzyme pyruvate kinase M2 (PKM2), which converts phosphoenolpyruvate (PEP) to pyruvate in the glycolytic pathway.	Phosphoenolpyruvate	186-205	P53	Homo sapiens	79-83
35626649-6	2022	Here, we employed the prime editing tool to revert a TP53 missense C > T mutation (L194F) in a T47D luminal A breast cancer cell line.	Phenobarbital	100-107	P53	Homo sapiens	53-57
35367334-0	2022	Induction of p53 mediated mitochondrial apoptosis and cell cycle arrest in human breast cancer cells by plant mediated synthesis of silver nanoparticles from Bergenia ligulata (Whole plant).	Silver	132-138	P53	Homo sapiens	13-16
35489754-0	2022	The MDM2 and CDKN2A Copy-number-variation Influence the TP53-signature-score in Wild-type TP53 Luminal Type Breast Cancer.	Phenobarbital	95-102	P53	Homo sapiens	56-60
35489754-0	2022	The MDM2 and CDKN2A Copy-number-variation Influence the TP53-signature-score in Wild-type TP53 Luminal Type Breast Cancer.	Phenobarbital	95-102	P53	Homo sapiens	90-94
35038965-2	2022	INTRODUCTION: The most common altered signaling found in aggressive iodine-refractory thyroid cancers derived from follicular cells (RAI-TC) are RTK, MAPK, PI3K, WNT, BRAF, RAS, RET, and TP53.	Iodine	68-74	P53	Homo sapiens	187-191
35085581-0	2022	Piperlongumine induces ROS mediated apoptosis by transcriptional regulation of SMAD4/P21/P53 genes and synergizes with doxorubicin in osteosarcoma cells.	piperlonguminine	0-14	P53	Homo sapiens	89-92
35085581-7	2022	Piperlongumine treatment significantly upregulated the expression of genes BAX, P21, P53, and SMAD4; while the BCL-2, SURVIVIN, TNFA, and NFKB genes expression was found down-regulated.	piperlonguminine	0-14	P53	Homo sapiens	85-88
35209068-7	2022	The expression of tumor protein p53 and microphthalmia-associated transcription factor and tyrosinase activity decreased in response to HQ, PDRN, and PVN, and this decrease was accompanied by decreased melanin content in the skin.	Melanins	202-209	P53	Homo sapiens	32-35
35211418-4	2022	Longitudinal analysis before and after fludarabine based on NGS sequencing demonstrated that low-burden TP53 mutations were present before the onset of treatment and expanded at relapse to become the predominant clone.	fludarabine	39-50	P53	Homo sapiens	104-108
35012638-7	2022	Based on recent reports of frequent defects in the homologous recombination (HR) pathway in EC, we assessed mutational signatures and HR deficiency scores and correlated these with in vivo responses to the PARP inhibitor (PARPi) talazoparib in six PDXs representing the copy number high/p53-mutant and mismatch-repair deficient molecular subtypes of EC.	talazoparib	229-240	P53	Homo sapiens	287-290
33905708-6	2021	RESULTS: Heme supports carcinogenesis via modulation of immune cell function, promoting inflammation and gut dysbiosis, impeding tumour suppressive potential of P53 gene, promoting cellular cytotoxicity and reactive oxygen species generation and modulating Nfr2 /HO-1 axis.	Heme	9-13	P53	Homo sapiens	161-164
3025664-10	1986	This sequence difference resulted in an arginine being coded for in clone p53-H-1 and a proline being coded for at the equivalent position in clone p53-H-19.	Proline	88-95	P53	Homo sapiens	148-151
33932899-8	2021	In human podocyte, inhibition of AGE formation by pyridoxamine prevented miR-34a dependent repression of SIRT1, p53 acetylation and activate podocyte autophagy in a dose-dependent manner.	Pyridoxamine	50-62	P53	Homo sapiens	112-115
33965112-8	2021	Celastrol and Fe3O4/alpha-Fe2O3/CA-PEG-celastrol increased the production of reactive oxygen species in SMMC-7721 cells and promoted apoptosis and apoptosis-related proteins (p53, Bax, Bcl-2) were also changed.	alpha-fe2o3	20-31	P53	Homo sapiens	175-178
34039253-7	2021	Considering the important role played by MAPK and p53 signaling pathways in cell-cycle arrest, we explored their potential involvement in STE-induced cell-cycle arrest by using specific inhibitors.	Sterigmatocystin	138-141	P53	Homo sapiens	50-53
34039253-8	2021	The inhibition of JNK and ERK resulted to attenuate S and G2/M arrest, whereas the inhibition of p38 and p53 attenuated only STE-induced S phase arrest.	Sterigmatocystin	125-128	P53	Homo sapiens	105-108
34039253-9	2021	In conclusion, the present study demonstrates that STE induced DNA damage and triggered MAPK and p53 pathways activation, resulting in cell-cycle arrest at the S and the G2/M phase.	Sterigmatocystin	51-54	P53	Homo sapiens	97-100
32480415-8	2021	Interestingly, patients with mutated allele rs1229984 in ADH1B had lower level of signature J while mutated allele rs671 in ALDH2 exhibited higher signature J abundance, suggesting acetaldehyde is one cause of signature J. Intriguingly, somatic mutations of three potential cancer driver genes (TP53, CUL3 and NSD1) were found the critical contributors for increased mutational load of signature J in alcohol consumption patients.	Acetaldehyde	181-193	P53	Homo sapiens	295-299
34004477-8	2021	gamma-Fe2O3 and Fe3O4 NPs could also cause mitochondrial fusion and fission dysregulation, activate lipid peroxidation and iron metabolism-related genes in a P53-dependent manner.	gamma-fe2o3	0-11	P53	Homo sapiens	158-161
33987018-15	2021	Western blot results revealed that the expression of p53, p27, p21, CDK4, cyclin D1, CDK2, cyclin E, pRb, E2F1 and c-myc decreased after CENPN knockdown, but there was no significant change in total Rb levels.	Rubidium	102-104	P53	Homo sapiens	53-56
33858805-0	2021	Expression of p53 is associated with microbial acetaldehyde production in oralsquamous cell carcinoma.	Acetaldehyde	47-59	P53	Homo sapiens	14-17
33858805-1	2021	OBJECTIVES: The objective of this study was to investigate the association between p53 expression and microbial acetaldehyde production in patients with oral squamous cell carcinoma (OSCC).	Acetaldehyde	112-124	P53	Homo sapiens	83-86
33858805-6	2021	A significant positive correlation between microbial acetaldehyde production and p53 expression levels in OSCC samples was seen in the intermediate and superficial layers of the epithelium of the infiltrative zone (P = .0005 and P = .0004, respectively) and in the superficial layer of the healthy appearing mucosa next to the tumor (P = .0391).	Acetaldehyde	53-65	P53	Homo sapiens	81-84
33858805-8	2021	CONCLUSIONS: Our results show an association between microbial acetaldehyde production and immunostaining of p53 in OSCC samples.	Acetaldehyde	63-75	P53	Homo sapiens	109-112
33881209-7	2021	Tumor tissue was examined for biomarkers (CHK1 and TP53) of prexasertib activity.	prexasertib	60-71	P53	Homo sapiens	51-55
33823140-5	2021	p53-regulated speckle association did not depend on p53 transactivation functions but required an intact proline-rich domain and direct DNA binding, providing mechanisms within p53 for regulating gene-speckle association.	Proline	105-112	P53	Homo sapiens	0-3
33924734-7	2021	The uptake of [18F]1 in these cells could be modulated using 100 microM SP-141, potentially reflecting changes in MDM2 expression because of p53 activation by SP-141.	6-methoxy-1-(naphthalen-1-yl)-9H-pyrido(3,4-b)indole	159-165	P53	Homo sapiens	141-144
33486761-9	2021	The beneficial effects of CX-5461 in vivo and in vitro were associated with increased activation (phosphorylation) of p53.	CX 5461	26-33	P53	Homo sapiens	118-121
33916029-5	2021	SLMP53-2 inhibited the growth of human melanoma cells in a p53-dependent manner through induction of cell cycle arrest and apoptosis.	slmp53-2	0-8	P53	Homo sapiens	59-62
33868388-0	2021	Interplay Between Thiamine and p53/p21 Axes Affects Antiproliferative Action of Cisplatin in Lung Adenocarcinoma Cells by Changing Metabolism of 2-Oxoglutarate/Glutamate.	Ketoglutaric Acids	145-159	P53	Homo sapiens	31-34
33868388-9	2021	Analysis of the associated metabolic changes in the cells indicates that (i) p21 knockdown restricts the production of 2-oxoglutarate via glutamate oxidation, stimulating that within the tricarboxylic acid (TCA) cycle; (ii) cellular cisplatin sensitivity is associated with a 4-fold upregulation of glutamic-oxaloacetic transaminase (GOT2) by cisplatin; (iii) cellular cisplatin resistance is associated with a 2-fold upregulation of p53 by cisplatin.	Ketoglutaric Acids	119-133	P53	Homo sapiens	434-437
33790890-3	2021	Idelalisib is a highly selective inhibitor of the PI3K p110  isoform and is approved for the treatment of CLL in patients with relapsed/refractory disease or in those harboring 17p deletions or tp53 mutations.	idelalisib	0-10	P53	Homo sapiens	194-198
33326188-4	2021	Therefore, a CD44-targeted delivery system is designed and constructed by self-assembly of tyrosine (Tyr)-hyaluronic acid (HA)-polyethyleneimine (PEI), which can radiolabel 131/125 I and load a p53 mutant restoring regent, Prima-1.	pei	146-149	P53	Homo sapiens	194-197
33576217-0	2021	Effect of Valproic Acid on the Class I Histone Deacetylase 1, 2 and 3, Tumor Suppressor Genes p21WAF1/CIP1 and p53, and Intrinsic Mitochondrial Apoptotic Pathway, Pro- (Bax, Bak, and Bim) and anti- (Bcl-2, Bcl-xL, and Mcl-1) Apoptotic Genes Expression, Cell Viability, and Apoptosis Induction in Hepatocellular Carcinoma HepG2 Cell Line.	Valproic Acid	10-23	P53	Homo sapiens	111-114
33098492-4	2021	Furthermore, TPEN induced oxidation of hydrogen peroxide (H2O2) sensor protein DJ-1, induced up-regulation of BH3-only pro-apoptotic protein PUMA, transcription factor p53 and activated the executor protease CASPASE-3 as apoptosis markers, and reduced the reactivity of the cellular proliferating marker Ki-67 in all acute leukemic groups, and reduced the phosphorylation of c-ABL protein signal in an AML case.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	13-17	P53	Homo sapiens	168-171
33290860-4	2021	We found that while EVOO treatment increases BMI1 levels, p53 levels drop in MCI patient serum after EVOO treatment for 12 months.	evoo	101-105	P53	Homo sapiens	58-61
33002289-0	2021	Gallic acid potentiates the apoptotic effect of paclitaxel and carboplatin via overexpression of Bax and P53 on the MCF-7 human breast cancer cell line.	Gallic Acid	0-11	P53	Homo sapiens	105-108
33492639-11	2021	ZINC10157406 (2 x IC50) downregulated TCTP expression by 86.70 +- 0.44% and upregulated p53 expression by 177.60 +- 12.46%.	6-(4-fluorophenyl)-2-[(8-methoxy-4-methyl-2-quinazolinyl)amino]-4(3H)-pyrimidinone	0-12	P53	Homo sapiens	88-91
33492639-12	2021	We validated ZINC10157406 binding to the p53 interaction site of TCTP and replacing p53 by co-immunoprecipitation.	6-(4-fluorophenyl)-2-[(8-methoxy-4-methyl-2-quinazolinyl)amino]-4(3H)-pyrimidinone	13-25	P53	Homo sapiens	41-44
32865667-5	2021	Further DAPI staining has revealed wikstromol at 10 muM induced apoptosis of cancer cells, which was associated with the activation of caspase-3 following down-regulation of Bcl-2 as well as up-regulation of Bax, cleaved PARP and phosphorylated p53.	nortrachelogenin	35-45	P53	Homo sapiens	245-248
33283112-0	2020	The Inhibition of H1N1 Influenza Virus-Induced Apoptosis by Surface Decoration of Selenium Nanoparticles with beta-Thujaplicin through Reactive Oxygen Species-Mediated AKT and p53 Signaling Pathways.	Selenium	82-90	P53	Homo sapiens	176-179
33165811-11	2021	Further docking studies revealed the different binding fates of sodium cantharidinate to activate wild-type p53 function.	sodium cantharidinate	64-85	P53	Homo sapiens	108-111
32572277-0	2020	Manumycin polyketides act as molecular glues between UBR7 and P53.	manumycin polyketides	0-21	P53	Homo sapiens	62-65
32738659-5	2020	Meanwhile, the intracellular ROS-P53 crosstalk can be upregulated by diallyl disulfide (up to 8-fold increase of ROS) and valproate (up to 18-fold increase of P53) to enhance early apoptosis.	Valproic Acid	122-131	P53	Homo sapiens	33-36
32738659-5	2020	Meanwhile, the intracellular ROS-P53 crosstalk can be upregulated by diallyl disulfide (up to 8-fold increase of ROS) and valproate (up to 18-fold increase of P53) to enhance early apoptosis.	Valproic Acid	122-131	P53	Homo sapiens	159-162
32973496-8	2020	Real-Time PCR results verified that GA significantly promoted Caspase-3, Bax, P53, and Cyt-c genes expression, and inhibited Bcl-2, PI3K, Akt, and NF-kappaB p65 genes expression (p < 0.001).	Gallic Acid	36-38	P53	Homo sapiens	78-81
32782319-2	2020	Herein, we determined the effect of O6-methylguanine (O6-meG) on transcription and subsequent transactivation activity of p53 in human lung H1299 cells.	O-(6)-methylguanine	36-52	P53	Homo sapiens	122-125
32339497-7	2020	Our findings suggest that intermediate cells as well as basal cells also can give rise to basal-like MIBC, with pre-induction of Trp53 mutation accelerating MIBC.	4-METHYL-2-PENTANOL	157-161	P53	Homo sapiens	129-134
32339497-8	2020	Thus, in BBN chemical carcinogenesis, pre-induction of Trp53 mutation in basal cells facilitates efficient modeling of the basal squamous subtype of human MIBC.	4-METHYL-2-PENTANOL	155-159	P53	Homo sapiens	55-60
32020421-0	2020	Decylubiquinone suppresses breast cancer growth and metastasis by inhibiting angiogenesis via the ROS/p53/ BAI1 signaling pathway.	2,3-dimethoxy-5-methyl-6-decyl-1,4-benzoquinone	0-15	P53	Homo sapiens	102-105
32020421-10	2020	Further studies demonstrate that DUb suppresses the formation of tubular structures by regulating the reactive oxygen species (ROS)/p53/BAI1 signaling pathway.	2,3-dimethoxy-5-methyl-6-decyl-1,4-benzoquinone	33-36	P53	Homo sapiens	132-135
32727419-8	2020	CONCLUSIONS: This pilot study suggests that both the Arg/Arg and Arg/Pro genotypes of p53 codon 72 polymorphism may have value as independent prognostic or predictive parameters for bevacizumab treatment response and failure.	Proline	69-72	P53	Homo sapiens	86-89
32722430-0	2020	Downregulation of the DNA Repair Gene DDB2 by Arecoline Is through p53"s DNA-Binding Domain and Is Correlated with Poor Outcome of Head and Neck Cancer Patients with Betel Quid Consumption.	Arecoline	46-55	P53	Homo sapiens	67-70
32722430-3	2020	Previously, we have reported that arecoline (0.3 mM) is able to inhibit DNA repair in a p53-dependent pathway, but the underlying mechanism is unclear.	Arecoline	34-43	P53	Homo sapiens	88-91
32722430-4	2020	Here we demonstrated that arecoline suppressed the expression of DDB2, which is transcriptionally regulated by p53 and is required for nucleotide excision repair (NER).	Arecoline	26-35	P53	Homo sapiens	111-114
32678213-8	2020	We found that dihydrotanshinone-I (DHTS-I), a plant-derived product which prevents HuR binding to specific RNAs, prevented HuR-mediated upregulation of TRIM21, while increasing the HuR-mediated upregulation of p53.	dhts	14-33	P53	Homo sapiens	210-213
32714975-7	2020	Pathway enrichment analyses revealed that DEGs were mainly enriched in 36 pathways, such as the proteasome, p53, and beta-alanine metabolism pathways.	beta-Alanine	117-129	P53	Homo sapiens	108-111
32630235-5	2020	Treatment with SP-141 resulted in diminished MDM2 and increased p53 and p21cip1 levels, G2/M cell cycle arrest, and marked apoptosis.	6-methoxy-1-(naphthalen-1-yl)-9H-pyrido(3,4-b)indole	15-21	P53	Homo sapiens	64-67
32630235-6	2020	In intracranial xenograft models of U87MG glioblastoma (wt p53) and DAOY medulloblastoma (mutant p53) expressing luciferase, treatment with SP-141 caused a significant 4- to 9-fold decrease in tumor growth in the absence of discernible toxicity.	6-methoxy-1-(naphthalen-1-yl)-9H-pyrido(3,4-b)indole	140-146	P53	Homo sapiens	59-62
32630235-6	2020	In intracranial xenograft models of U87MG glioblastoma (wt p53) and DAOY medulloblastoma (mutant p53) expressing luciferase, treatment with SP-141 caused a significant 4- to 9-fold decrease in tumor growth in the absence of discernible toxicity.	6-methoxy-1-(naphthalen-1-yl)-9H-pyrido(3,4-b)indole	140-146	P53	Homo sapiens	97-100
32229503-8	2020	Collectively, our findings reveal the potential role of the PPM1D-p53 signaling axis in the regulation of HR-mediated DNA repair and provide preclinical evidence demonstrating that combined inhibition of PPM1D and PARP1/2 may be a promising therapeutic combination for targeting PPM1D-mutant DIPG tumors.	Dipinacoline glutamate	292-296	P53	Homo sapiens	66-69
32605139-6	2020	Our results show that treatment of HCT-116 colon cancer cells with the deoxyhypusine (DHS) inhibitor N1-guanyl-1,7-diamineheptane (GC7) caused both inhibition of eIF5A hypusination and a significant reduction of p53 expression in UV-treated cells, and that eIF5A controls p53 expression at the level of protein synthesis.	deoxyhypusine	71-84	P53	Homo sapiens	212-215
32605139-6	2020	Our results show that treatment of HCT-116 colon cancer cells with the deoxyhypusine (DHS) inhibitor N1-guanyl-1,7-diamineheptane (GC7) caused both inhibition of eIF5A hypusination and a significant reduction of p53 expression in UV-treated cells, and that eIF5A controls p53 expression at the level of protein synthesis.	deoxyhypusine	71-84	P53	Homo sapiens	272-275
32605139-6	2020	Our results show that treatment of HCT-116 colon cancer cells with the deoxyhypusine (DHS) inhibitor N1-guanyl-1,7-diamineheptane (GC7) caused both inhibition of eIF5A hypusination and a significant reduction of p53 expression in UV-treated cells, and that eIF5A controls p53 expression at the level of protein synthesis.	deoxyhypusine	86-89	P53	Homo sapiens	212-215
32605139-6	2020	Our results show that treatment of HCT-116 colon cancer cells with the deoxyhypusine (DHS) inhibitor N1-guanyl-1,7-diamineheptane (GC7) caused both inhibition of eIF5A hypusination and a significant reduction of p53 expression in UV-treated cells, and that eIF5A controls p53 expression at the level of protein synthesis.	deoxyhypusine	86-89	P53	Homo sapiens	272-275
32161142-8	2020	Inhibition of Skp2 using the neddylation-activating enzyme (NAE) inhibitor pevonedistat decreased growth of Rb/p53-negative patient-derived cell lines and mouse xenografts.	pevonedistat	75-87	P53	Homo sapiens	111-114
32540853-2	2020	It has been noted that MFS and UPS frequently lose function of the tumor suppressor genes RB1 and TP53 In this issue of Cancer Research, Li and colleagues demonstrate that proliferation in RB1- and TP53-deficient MFS and UPS depends on SKP2; inhibiting SKP2 with the neddylation inhibitor, pevonedistat, halts tumor growth in a panel of patient-derived xenografts.	pevonedistat	290-302	P53	Homo sapiens	98-102
32272181-10	2020	TQ alone or in combination activated p53 in HTLV-1 positive cell lines.	thymoquinone	0-2	P53	Homo sapiens	37-40
32606738-9	2020	Moreover, a membrane-permeable N24 peptide enhanced p53-dependent apoptosis induced by methyl methanesulfonate.	n24 peptide	31-42	P53	Homo sapiens	52-55
32424519-5	2020	The results indicate that the TP53 Arg/Pro heterozygosity (adjusted OR   2.32, 95% CI  1.28-4.34, p = 0.01), Pro/Pro mutant homozygosity (adjusted OR  4.15, 95% CI  1.75-9.86, p = 0.001), along with the combined genotype (Arg/Pro + Pro/Pro) (adjusted OR  2.83, 95% CI  1.61-4.97, p < 0.001) significantly increases the risk of cervical cancer.	Proline	39-42	P53	Homo sapiens	30-34
32424519-6	2020	Moreover, the cervical cancer patients with a first-degree relative cancer patient possesses 4.45 folds more risk (p = 0.019) of carrying a proline allele in codon 72 of the TP53 gene compared to those patients who do not have any first-degree relative with cancer.	Proline	140-147	P53	Homo sapiens	174-178
32435647-13	2020	DNA damage was induced by IS stimulation as confirmed by elevated protein level of p-ATM, p-ATR, p-BRCA1, and p-p53 in T cells.	Indican	26-28	P53	Homo sapiens	112-115
32179165-0	2020	The gut microbiota metabolite urolithin A, but not other relevant urolithins, induces p53-dependent cellular senescence in human colon cancer cells.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	30-41	P53	Homo sapiens	86-89
32266639-6	2020	Moreover, GSPE was able to avoid mitochondria dysfunction and the increased in p53 and poly-(ADP-ribose) polymerase expression induced by high glucose exposition.	gspe	10-14	P53	Homo sapiens	79-82
32313423-5	2020	Conclusion: In low-grade gliomas, mutations in IDH1, IDH2, and TP53 may be the key to tumor progression because they have an effect on the function of the protein such as mutations R132H in IDH1 and R172M in IDH2, which change the function of the enzyme alpha-ketoglutarate, or R158G in TP53, which affects the structure of the generated protein, thus their importance in understanding gliomagenesis and for more accurate diagnosis complementary to the anatomical pathology tests.	Ketoglutaric Acids	254-273	P53	Homo sapiens	63-67
32313423-5	2020	Conclusion: In low-grade gliomas, mutations in IDH1, IDH2, and TP53 may be the key to tumor progression because they have an effect on the function of the protein such as mutations R132H in IDH1 and R172M in IDH2, which change the function of the enzyme alpha-ketoglutarate, or R158G in TP53, which affects the structure of the generated protein, thus their importance in understanding gliomagenesis and for more accurate diagnosis complementary to the anatomical pathology tests.	Ketoglutaric Acids	254-273	P53	Homo sapiens	287-291
32035620-4	2020	Surprisingly this crotonylation targets serine 46, instead of any predicted lysine residues, of p53, as detected in TCEP-probe labeled crotonylation and anti-crotonylated peptide antibody reaction assays.	tris(2-carboxyethyl)phosphine	116-120	P53	Homo sapiens	96-99
32052927-8	2020	Inc-MST1P2/miR-133b axis affected the resistance of bladder cancer cells to DDP via Sirt1/p53 signaling.	2-dimethylaminoethyl(dimethylamido)phosphonofluoridate	76-79	P53	Homo sapiens	90-93
32052927-10	2020	MST1P2/miR-133b axis affects the resistance of bladder cancer cells to DDP via downstream Sirt1/p53 signaling.	2-dimethylaminoethyl(dimethylamido)phosphonofluoridate	71-74	P53	Homo sapiens	96-99
32235535-6	2020	Norhierridin B (10) interfered with several p53 transcriptional targets, increasing p21, Bax, and MDM2, while decreasing Bcl-2 protein levels, which suggested the potential activation of a p53 pathway.	norhierridin b	0-14	P53	Homo sapiens	44-47
32235535-6	2020	Norhierridin B (10) interfered with several p53 transcriptional targets, increasing p21, Bax, and MDM2, while decreasing Bcl-2 protein levels, which suggested the potential activation of a p53 pathway.	norhierridin b	0-14	P53	Homo sapiens	189-192
32182802-6	2020	In addition, EPS increases p53 accumulation and expression of its downstream targets.	eps	13-16	P53	Homo sapiens	27-30
32182802-7	2020	In p53 knockout (KO) iPSCs, the EPS did not induce apoptosis, indicating that EPS-mediated apoptosis of USCs was p53-dependent.	eps	78-81	P53	Homo sapiens	113-116
32182802-9	2020	EPS treatment before injection efficiently prevented in ovo teratoma formation of p53 wild-type (WT) iPSCs but not p53KO iPSCs.	eps	0-3	P53	Homo sapiens	82-85
31867678-7	2020	Observations of this investigation suggest that LPA supports survival of T lymphoma cells via altering apoptosis and glucose metabolism through changing the level of reactive species, namely nitric oxide and reactive oxygen species along with expression of various survival and glucose metabolism regulatory molecules, including hypoxia-inducible factor 1-alpha, p53, Bcl2, and glucose transporter 3, hexokinase II, pyruvate kinase muscle isozyme 2, monocarboxylate transporter 1, pyruvate dehydrogenase kinase 1.	lysophosphatidic acid	48-51	P53	Homo sapiens	363-366
31676337-5	2020	Furthermore, BAX, TP53 and ATM were found to be upregulated in DU145 and MCF7 treated with RuPro and RuThr, in which, a higher ASCT2 gene expression was also observed.	Ruthenium	91-96	P53	Homo sapiens	18-22
31668372-7	2020	What is more, circ_0001546 inhibits the chemoresistance of HGC-27 cells to L-OPH (Oxaliplatin) may through the activation of the ATM/checkpoint kinase 2 (Chk2)/p53-dependent signaling pathway.	oxaliplatin	82-93	P53	Homo sapiens	160-163
32564014-8	2020	In conclusion, the results clearly demonstrate that THC possesses anti-inflammatory properties by increasing SIRT1 expression and subsequent suppression of p53 activation in LPS-challenged HUVECs.	Dronabinol	52-55	P53	Homo sapiens	156-159
31308078-6	2019	Additionally, bioinformatical analysis of indomethacin treated resistant cells revealed that indomethacin significantly activates the unfolded protein response (UPR), p53 and apoptosis pathways, and suppresses cell cycle, Myc and AR/ARV7 pathways.	Indomethacin	93-105	P53	Homo sapiens	167-170
31478534-0	2019	Organocatalytic diastereoselective [3+2] cyclization of MBH carbonates with dinucleophiles: synthesis of bicyclic imidazoline derivatives that inhibit MDM2-p53 interaction.	Imidazolines	114-125	P53	Homo sapiens	156-159
31301771-7	2019	Furthermore, our results indicated that the NEDD8-conjugating E2 enzyme UBE2M was essential for E4orf6-mediated p53 degradation and that its dominant negative mutant UBE2M C111S dramatically blocked E4orf6 functions.	e4orf6	96-102	P53	Homo sapiens	112-115
31301771-8	2019	The Nedd8-activating enzyme inhibitor MLN4924 decreased E4orf6-induced neddylation of the cullin5 protein and subsequently suppressed p53 degradation.	pevonedistat	38-45	P53	Homo sapiens	134-137
31301771-8	2019	The Nedd8-activating enzyme inhibitor MLN4924 decreased E4orf6-induced neddylation of the cullin5 protein and subsequently suppressed p53 degradation.	e4orf6	56-62	P53	Homo sapiens	134-137
31534224-0	2019	alpha-Ketoglutarate links p53 to cell fate during tumour suppression.	Ketoglutaric Acids	0-19	P53	Homo sapiens	26-29
31405162-0	2019	Synthesis, Biological and In Silico Evaluation of Pure Nucleobase-Containing Spiro (Indane-Isoxazolidine) Derivatives as Potential Inhibitors of MDM2-p53 Interaction.	indane-isoxazolidine	84-104	P53	Homo sapiens	150-153
31388677-0	2019	p53 activation by Cr(VI): a transcriptionally limited response induced by ATR kinase in S-phase.	Chromium	18-20	P53	Homo sapiens	0-3
31388677-5	2019	Ascorbate-restored H460 and primary human cells treated with Cr(VI) contained higher levels of p53 and its Ser15 phosphorylation, which were induced by ATR kinase.	Chromium	61-63	P53	Homo sapiens	95-98
31388677-9	2019	A weak transcription activity of Cr(VI)-upregulated p53 was associated with its low lysine acetylation in the regulatory C-terminal domain, resulting from the inability of Cr(VI) to activate ATM in ascorbate-restored cells.	Chromium	33-35	P53	Homo sapiens	52-55
31388677-10	2019	Thus, p53 activation by ascorbate-metabolized Cr(VI) represents a limited genome-protective response that is defective in upregulation of DNA repair genes and proapoptotic transcripts for elimination of damaged cells.	Chromium	46-48	P53	Homo sapiens	6-9
30912145-6	2019	Then, we found that the pretreatment with nicotine and PNU-282987 showed the neuroprotective antiapoptotic effects via activating the alpha7-nAChRs/MAPK/p53 axis.	PNU-282987	55-65	P53	Homo sapiens	153-156
31369573-5	2019	RESULTS: The allele frequency of TP53 codon 72 in our cohort was 37, 42, and 21% for Arg/Arg, Arg/Pro, and Pro/Pro, respectively.	Proline	98-101	P53	Homo sapiens	33-37
31369573-5	2019	RESULTS: The allele frequency of TP53 codon 72 in our cohort was 37, 42, and 21% for Arg/Arg, Arg/Pro, and Pro/Pro, respectively.	Proline	107-110	P53	Homo sapiens	33-37
31369573-5	2019	RESULTS: The allele frequency of TP53 codon 72 in our cohort was 37, 42, and 21% for Arg/Arg, Arg/Pro, and Pro/Pro, respectively.	Proline	107-110	P53	Homo sapiens	33-37
31228347-9	2019	Moreover, diosmetin treatment significantly downregulated the expression levels of Bcl-2 and Cyclin D1, and upregulated that of p53, Bax, caspase 3, cleaved caspase 9, and cleaved caspase 3.	diosmetin	10-19	P53	Homo sapiens	128-131
31181622-4	2019	Albendazole and fenbendazole, two approved and commonly used benzimidazole anthelmintics, stimulated p53 activity and were selected for further studies.	Fenbendazole	16-28	P53	Homo sapiens	101-104
31181622-5	2019	The protein levels of p53 and p21 increased upon the treatment with albendazole and fenbendazole, indicating activation of the p53-p21 pathway, while the levels of Mdm2 and MdmX decreased in melanoma and breast cancer cells overexpressing these proteins.	Fenbendazole	84-96	P53	Homo sapiens	22-25
31181622-5	2019	The protein levels of p53 and p21 increased upon the treatment with albendazole and fenbendazole, indicating activation of the p53-p21 pathway, while the levels of Mdm2 and MdmX decreased in melanoma and breast cancer cells overexpressing these proteins.	Fenbendazole	84-96	P53	Homo sapiens	127-130
30921731-3	2019	Here, we describe the design, via assembly of a p53-activating peptide termed PMI, functionalized PEG and fluorescent lanthanide oxyfluoride nanocrystals, of a novel nanotheranostic shaped in flexible rods.	Lanthanoid Series Elements	118-128	P53	Homo sapiens	48-51
30892621-0	2019	Interactions of p53 with poly(ADP-ribose) and DNA induce distinct changes in protein structure as revealed by ATR-FTIR spectroscopy.	Poly Adenosine Diphosphate Ribose	25-41	P53	Homo sapiens	16-19
30892621-2	2019	Here, we applied a novel attenuated total reflection Fourier transform infrared (ATR-FTIR) spectroscopic approach to investigate changes in secondary structure of full-length p53 induced by non-covalent interactions with DNA and poly(ADP-ribose) (PAR).	Poly Adenosine Diphosphate Ribose	229-245	P53	Homo sapiens	175-178
30892621-2	2019	Here, we applied a novel attenuated total reflection Fourier transform infrared (ATR-FTIR) spectroscopic approach to investigate changes in secondary structure of full-length p53 induced by non-covalent interactions with DNA and poly(ADP-ribose) (PAR).	Poly Adenosine Diphosphate Ribose	247-250	P53	Homo sapiens	175-178
30892621-7	2019	Finally, temperature-induced melting experiments via CD spectroscopy show that DNA binding stabilizes the structure of p53, while PAR binding can shift the irreversible formation of insoluble p53 aggregates to higher temperatures.	Poly Adenosine Diphosphate Ribose	130-133	P53	Homo sapiens	192-195
30796178-12	2019	IMPLICATIONS: The identification of a novel apoptotic pathway triggered by the temozolomide-induced DNA damage O6 -methylguanine supports the role of p53 in the decision between survival and death and suggests SIAH1 and HIPK2 as new therapeutic targets.	O-(6)-methylguanine	111-128	P53	Homo sapiens	150-153
30988205-3	2019	The p53 N terminus (NT) contains two transactivation domains (TAD1 and TAD2), a proline-rich region (PRR), and multiple phosphorylation sites.	Proline	80-87	P53	Homo sapiens	4-7
30843693-6	2019	The Pearson"s correlation coefficient test elucidated that inorganics (EC), organics (OC, PAHs, and alkane), and metals (Cr, Mn, and Sb) were significantly correlated to the dysregulated oncoproteins (VEGF, IL6, MDM2, AKT1, STAT, and P53).	Chromium	121-123	P53	Homo sapiens	234-237
31001122-5	2019	Upon prolonged exposer to THTMP, all glioma cell lines undergo p53 and cyclin-dependent kinase mediated cell death with the IC50 concentration of 26.5 and 75.4 muM in LN229 and Snb19, respectively.	thtmp	26-31	P53	Homo sapiens	63-66
31001122-9	2019	Further, a transcriptional analysis (RNA-seq) revealed that THTMP targeted the p53 signaling pathway specific genes causing DNA damage and cell cycle arrest at G1/S phase explained by the decrease of cyclin-dependent kinase 1, cyclin A2, cyclin E1 and E2 in glioma cells.	thtmp	60-65	P53	Homo sapiens	79-82
30837643-5	2019	Moreover, CHK1 knockdown or addition of a CHK1 inhibitor such as MK-8776, rabusertib or prexasertib enhances CPX-351-induced apoptosis in multiple TP53-null and TP53-wildtype AML cell lines.	LY2603618	74-84	P53	Homo sapiens	147-151
30837643-5	2019	Moreover, CHK1 knockdown or addition of a CHK1 inhibitor such as MK-8776, rabusertib or prexasertib enhances CPX-351-induced apoptosis in multiple TP53-null and TP53-wildtype AML cell lines.	LY2603618	74-84	P53	Homo sapiens	161-165
30837643-5	2019	Moreover, CHK1 knockdown or addition of a CHK1 inhibitor such as MK-8776, rabusertib or prexasertib enhances CPX-351-induced apoptosis in multiple TP53-null and TP53-wildtype AML cell lines.	prexasertib	88-99	P53	Homo sapiens	147-151
30837643-5	2019	Moreover, CHK1 knockdown or addition of a CHK1 inhibitor such as MK-8776, rabusertib or prexasertib enhances CPX-351-induced apoptosis in multiple TP53-null and TP53-wildtype AML cell lines.	prexasertib	88-99	P53	Homo sapiens	161-165
30863051-1	2019	Background: An amphiphilic cationic copolymer cholesterol-g-poly(amine-co-ester), namely Chol-g-PMSC-PPDL synthesized in a chemoenzymatic route has been utilized as a carrier for p53 gene delivery to check its antitumor efficacy, using human prostate cancer cell line PC-3 (p53 null) as a model.	copolymer	36-45	P53	Homo sapiens	179-182
30863051-1	2019	Background: An amphiphilic cationic copolymer cholesterol-g-poly(amine-co-ester), namely Chol-g-PMSC-PPDL synthesized in a chemoenzymatic route has been utilized as a carrier for p53 gene delivery to check its antitumor efficacy, using human prostate cancer cell line PC-3 (p53 null) as a model.	copolymer	36-45	P53	Homo sapiens	274-277
30863051-1	2019	Background: An amphiphilic cationic copolymer cholesterol-g-poly(amine-co-ester), namely Chol-g-PMSC-PPDL synthesized in a chemoenzymatic route has been utilized as a carrier for p53 gene delivery to check its antitumor efficacy, using human prostate cancer cell line PC-3 (p53 null) as a model.	cholesterol-g-poly(amine-co-ester	46-79	P53	Homo sapiens	179-182
30863051-1	2019	Background: An amphiphilic cationic copolymer cholesterol-g-poly(amine-co-ester), namely Chol-g-PMSC-PPDL synthesized in a chemoenzymatic route has been utilized as a carrier for p53 gene delivery to check its antitumor efficacy, using human prostate cancer cell line PC-3 (p53 null) as a model.	cholesterol-g-poly(amine-co-ester	46-79	P53	Homo sapiens	274-277
30578766-6	2019	Conversely, either silencing METTL3 expression by using small interfering RNA (siRNA) or inhibiting RNA methylation with neplanocin A suppressed m6A formation in p53 pre-mRNA, and substantially increased the level of phosphorylated p53 protein (Ser15) and its function in cells heterozygously carrying the R273H mutation, thereby re-sensitizing these cells to anticancer drugs.	neplanocin A	121-133	P53	Homo sapiens	162-165
29911263-2	2019	In this study, 2",6"-dimethylcarbonylphenyl-10-sulfopropyl acridinium-9-carboxylate 4"-NHS ester (NSP-DMAE-NHS), as a new kind of highly efficient luminescence reagent, was immobilized on the complementary sequence of the wild-type p53 (ssDNA) to improve the detection sensitivity.	NSP-DMAE-NHS	98-110	P53	Homo sapiens	232-235
30318011-1	2019	BACKGROUND: Treatment of hematological malignancies with conventional DNA-damaging drugs, such as chlorambucil (CLB), commonly results in p53-dependent chemo-resistance.	Chlorambucil	98-110	P53	Homo sapiens	138-141
30318011-1	2019	BACKGROUND: Treatment of hematological malignancies with conventional DNA-damaging drugs, such as chlorambucil (CLB), commonly results in p53-dependent chemo-resistance.	Chlorambucil	112-115	P53	Homo sapiens	138-141
30278899-4	2018	The addition of the mutant p53 gene causes the disassembly of the THC probes with the release of the Fc-tagged sequence and the folding of the MB-labeled sequence into a hairpin structure, causing the change in the current response ratio of MB to Fc for monitoring the mutant p53 gene.	Dronabinol	66-69	P53	Homo sapiens	27-30
30278899-4	2018	The addition of the mutant p53 gene causes the disassembly of the THC probes with the release of the Fc-tagged sequence and the folding of the MB-labeled sequence into a hairpin structure, causing the change in the current response ratio of MB to Fc for monitoring the mutant p53 gene.	Dronabinol	66-69	P53	Homo sapiens	276-279
30278899-6	2018	With the significant signal amplification and the advantageous specificity of the THC probes, sub-femtomolar detection limit and a highly enhanced SNP discrimination factor for the mutant p53 gene can be obtained.	Dronabinol	82-85	P53	Homo sapiens	188-191
30473536-5	2018	Our observations are consistent with a model in which alpha-pinene inhibits miR221 expression, which leads to G2/M-phase arrest and activation of CDKN1B/p27-CDK1 and ATM-p53-Chk2 pathways that suppress human hepatoma tumor progression.	alpha-pinene	54-66	P53	Homo sapiens	170-173
30348117-14	2018	Inhibition of miR-28-5p or miR-650 could induce more apoptosis in CLL cells with germline TP53.	mir-28-5p	14-23	P53	Homo sapiens	90-94
30096294-0	2018	PIM2 survival kinase is upregulated in a p53-dependent manner in cells treated with camptothecin or co-treated with actinomycin D and nutlin-3a.	Dactinomycin	116-129	P53	Homo sapiens	41-44
30096294-2	2018	In a previous study, we found that actinomycin D and nutlin-3a (A + N) synergistically activate p53.	Dactinomycin	35-48	P53	Homo sapiens	96-99
29753810-6	2018	Cell viability measurements demonstrated that DNC suppresses the proliferation of MDA-MB-231 cells in a time- and dose-dependent mode and exogenous p53 elevates the sensitivity of cells to DNC-mediated cytotoxic effects.	dnc	189-192	P53	Homo sapiens	148-151
30221528-15	2018	Therefore, it is of great importance to consider that hypericin would have better impact on cells or tumors with wild type P53.	hypericin	54-63	P53	Homo sapiens	123-126
29800662-6	2018	The critical groups and significant binding sites for the interaction between alisol monomers and p53DNA include C19-OH and C22-OH of the alisols; N2 and H21 of the guanine deoxynucleotide (DG8), N2-H21 of the DG7, O4" of the DG9 in the f-chain of p53DNA; and C2-O2 of the cytosine deoxynucleotide (DC16) in the e-chain of p53DNA.	cytosine deoxynucleotide	273-297	P53	Homo sapiens	98-101
29931810-0	2018	A Cu2+ complex induces the aggregation of human papillomavirus oncoprotein E6 and stabilizes p53.	cupric ion	2-6	P53	Homo sapiens	93-96
29931810-5	2018	The Cu2+ complex interacts with E6 at the E6AP and p53 binding sites.	cupric ion	4-8	P53	Homo sapiens	51-54
30108509-0	2018	Cisatracurium Retards Cell Migration and Invasion Upon Upregulation of p53 and Inhibits the Aggressiveness of Colorectal Cancer.	cisatracurium	0-13	P53	Homo sapiens	71-74
30108509-7	2018	Cisatracurium caused upregulation of p53 and its down-stream genes and proteins known to regulate proliferation and metastasis in vitro and in vivo.	cisatracurium	0-13	P53	Homo sapiens	37-40
30108509-10	2018	Together, the findings demonstrate that elevation of p53 upon cisatracurium-induced genomic injury, represent a potential mechanism by which cisatracurium result in the suppression of CRC progression and metastasis.	cisatracurium	62-75	P53	Homo sapiens	53-56
30108509-10	2018	Together, the findings demonstrate that elevation of p53 upon cisatracurium-induced genomic injury, represent a potential mechanism by which cisatracurium result in the suppression of CRC progression and metastasis.	cisatracurium	141-154	P53	Homo sapiens	53-56
29863754-0	2018	Ruthenium-Containing Linear Helicates and Mesocates with Tuneable p53-Selective Cytotoxicity in Colorectal Cancer Cells.	Ruthenium	0-9	P53	Homo sapiens	66-69
30011295-3	2018	Arecoline arrested preadipocyte growth in the G2/M phase of the cell cycle; decreased the total levels of cyclin-dependent kinase 1 (CDK1), p21, and p27 proteins; increased p53 and cyclin B1 protein levels; and had no effect on CDK2 protein levels.	Arecoline	0-9	P53	Homo sapiens	173-176
29778287-5	2018	One of the underlying mechanisms of the anti-cancer effect exerted by PGG, was owing to the induction p53 expression, a well-known tumor suppressor, and increased in P21, the representative target gene of p53.	beta-penta-O-galloyl-glucose	70-73	P53	Homo sapiens	102-105
29778287-5	2018	One of the underlying mechanisms of the anti-cancer effect exerted by PGG, was owing to the induction p53 expression, a well-known tumor suppressor, and increased in P21, the representative target gene of p53.	beta-penta-O-galloyl-glucose	70-73	P53	Homo sapiens	205-208
32254384-0	2018	A synergistic polyphosphoester-based co-delivery system of the anticancer drug doxorubicin and the tumor suppressor gene p53 for lung cancer therapy.	polyphosphoester	14-30	P53	Homo sapiens	121-124
29440146-5	2018	High expression of both cytoplasmic DDX31 and p53 proteins correlated with poor prognosis in patients with MIBC, and blocking the DDX31/NCL interaction resulted in downregulation of EGFR/Akt signaling, eliciting an in vivo antitumor effect against bladder cancer.	4-METHYL-2-PENTANOL	107-111	P53	Homo sapiens	46-49
29545144-0	2018	The G2 phase arrest induced by sterigmatocystin is dependent on hMLH1- ERK/p38-p53 pathway in human esophageal epithelium cells in vitro.	Sterigmatocystin	31-47	P53	Homo sapiens	79-82
28389531-12	2018	CONCLUSIONS: LY2606368 selectively eliminates replication-stressed, p53-deficient and hyperdiploid CRC-SCs independently of RAS mutational status.	prexasertib	13-22	P53	Homo sapiens	68-71
29731965-10	2018	In this study, the presence of both TP53 mutation and 17p/TP53 deletion, but not the individual variants, was associated with poor prognosis in DLBCL patients after treatment with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) or similar regimens.	Vincristine	222-233	P53	Homo sapiens	36-40
29731965-10	2018	In this study, the presence of both TP53 mutation and 17p/TP53 deletion, but not the individual variants, was associated with poor prognosis in DLBCL patients after treatment with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) or similar regimens.	Vincristine	222-233	P53	Homo sapiens	58-62
28550687-0	2018	Tanshinone Suppresses Arecoline-Induced Epithelial-Mesenchymal Transition in Oral Submucous Fibrosis by Epigenetically Reactivating the p53 Pathway.	Arecoline	22-31	P53	Homo sapiens	136-139
28550687-7	2018	In addition, p53 and its downstream molecules were decreased by arecoline treatment in oral mucosal fibroblasts, which was reversed by treatment with TSN in a dose-dependent manner.	Arecoline	64-73	P53	Homo sapiens	13-16
28550687-8	2018	Our results also revealed that arecoline stimulation resulted in hypermethylation of the promoter of TP53 and subsequent downregulation of p53 levels, which was reversed by TSN.	Arecoline	31-40	P53	Homo sapiens	101-105
28550687-8	2018	Our results also revealed that arecoline stimulation resulted in hypermethylation of the promoter of TP53 and subsequent downregulation of p53 levels, which was reversed by TSN.	Arecoline	31-40	P53	Homo sapiens	139-142
29261364-1	2018	BACKGROUND: The TP53 codon 72 Proline-Arginine polymorphism (TP53 P72R) is the most widely studied candidate among those evaluated for a putative association between impaired apoptosis and glaucoma.	Proline	30-37	P53	Homo sapiens	16-20
29261364-1	2018	BACKGROUND: The TP53 codon 72 Proline-Arginine polymorphism (TP53 P72R) is the most widely studied candidate among those evaluated for a putative association between impaired apoptosis and glaucoma.	Proline	30-37	P53	Homo sapiens	61-65
29185024-6	2018	NaF (5 mM) induced Ac-p53 formation and increased cell cycle arrest via Cdkn1a/p21 expression in Wild-type (WT) cells.	Sodium Fluoride	0-3	P53	Homo sapiens	22-25
29435010-5	2018	The inhibition of autophagy by CQ enhanced sunitinib-induced apoptosis, which was characterized by the activation of caspase-3, caspase-9, Bcl-2 and p53.	Chloroquine	31-33	P53	Homo sapiens	149-152
28971495-3	2018	Herein, we described the first report of a patient with relapsed chronic lymphocytic leukaemia harbouring TP53 abnormalities who developed, histologically proven, systemic light chain amyloidosis who was treated with the PI3K inhibitor, idelalisib, and rituximab.	idelalisib	237-247	P53	Homo sapiens	106-110
29281902-19	2018	Local application of rAd-p53 combined with local injection of bleomycin and intravenous infusion of cisplatin, epirubicin and isocyclophosphamide was effective for treatment of uterine sarcoma, especially for patients with liver metastases.	isocyclophosphamide	126-145	P53	Homo sapiens	25-28
29434892-0	2018	Effects of harmaline on cell growth of human liver cancer through the p53/p21 and Fas/FasL signaling pathways.	Harmaline	11-20	P53	Homo sapiens	70-73
29434892-5	2018	Harmaline significantly increased p53, p21, Fas and FasL protein expression in HepG2 cells.	Harmaline	0-9	P53	Homo sapiens	34-37
29434892-7	2018	The results from the present study suggest that harmaline suppresses the viability, but induces the apoptosis, of human liver carcinoma cells through upregulation of the p53/p21 and Fas/FasL signaling pathways.	Harmaline	48-57	P53	Homo sapiens	170-173
29174979-9	2018	MiR-30e-5p inhibited SIRT1 expression and increased expression of p53 and the phosphorylated form of STAT3 (pSTAT3).	mir-30e-5p	0-10	P53	Homo sapiens	66-69
30417784-7	2018	RESULTS: Treatment of BT-20 cells with vincristine, vinblastine, and/or vinorelbine resulted in upregulation of TP53 expression.	Vincristine	39-50	P53	Homo sapiens	112-116
2905688-4	1988	Molecular cloning and sequencing of both the alleles of p53 gene revealed a base-pair change in codon 72 causing arginine----proline substitution in the allele with the additional BglII site.	Proline	125-132	P53	Homo sapiens	56-59
33982778-0	2021	Isoquercitrin protects HUVECs against high glucose-induced apoptosis through regulating p53 proteasomal degradation.	isoquercitrin	0-13	P53	Homo sapiens	88-91
33982778-11	2021	Moreover, under HG stress, IQC treatment markedly inhibited the increased expression levels of the pro-apoptotic proteins p53, Bax and C-caspase3, and increased the expression levels of the anti-apoptotic protein Bcl-2 in HUVECs.	isoquercitrin	27-30	P53	Homo sapiens	122-125
33857626-0	2021	Sodium fluoride activates the extrinsic apoptosis via regulating NOX4/ROS-mediated p53/DR5 signaling pathway in lung cells both in vitro and in vivo.	Sodium Fluoride	0-15	P53	Homo sapiens	83-86
33952867-0	2021	Elaboration of non-naturally occurring helical tripeptides as p53-MDM2/MDMX interaction inhibitors.	tripeptides	47-58	P53	Homo sapiens	62-65
33073884-2	2021	Alongside clinical platinum drugs, these bimetallic ruthenium-iron complexes have been screened for their cytotoxicity against MIA PaCa-2 (human pancreatic carcinoma), HCT116 p53+/+ (human colon carcinoma, p53-wild type) and ARPE-19 (human retinal pigment epithelial) cell lines.	Ruthenium	52-61	P53	Homo sapiens	175-178
33073884-2	2021	Alongside clinical platinum drugs, these bimetallic ruthenium-iron complexes have been screened for their cytotoxicity against MIA PaCa-2 (human pancreatic carcinoma), HCT116 p53+/+ (human colon carcinoma, p53-wild type) and ARPE-19 (human retinal pigment epithelial) cell lines.	Ruthenium	52-61	P53	Homo sapiens	206-209
33576217-10	2021	RESULTS: VPA downregulated class I histone deacetylase (HDAC) 1, 2, and 3, Bcl-2, Bcl-xL, and Mcl-1 and upregulated p21, p53, Bax, Bak, and Bim resulting in apoptosis induction.	Valproic Acid	9-12	P53	Homo sapiens	121-124
33576217-11	2021	CONCLUSION: VPA can induce apoptosis via activation of the intrinsic mitochondrial apoptotic pathway and also epigenetic reactivation of p21 and p53 through inhibition of class I HDAC 1, 2 and 3, activity.<br />.	Valproic Acid	12-15	P53	Homo sapiens	145-148
33253914-7	2021	We will also provide insights on the integrative role of p53 with the lysophosphatidic acid (LPA) signaling pathway in cancer progression and TME regulation.	lysophosphatidic acid	70-91	P53	Homo sapiens	57-60
33253914-7	2021	We will also provide insights on the integrative role of p53 with the lysophosphatidic acid (LPA) signaling pathway in cancer progression and TME regulation.	lysophosphatidic acid	93-96	P53	Homo sapiens	57-60
33747489-4	2021	Thymoquinone as phytochemical also downregulated the Rac1 expression, mediated the miR-34a upregulation, and increased the levels of miR-34a through p53, as well as also regulated the pro- and antiapoptotic genes and decreased the phosphorylation of NF-kappaB and IKKalpha/beta.	thymoquinone	0-12	P53	Homo sapiens	149-152
33221336-10	2021	Moreover, triggering nucleolar stress by the chemotherapeutic agents ActinomycinD or the RNA polymeraseI inhibitor CX-5461 stimulates expression of Wnt/beta-Catenin targets, which is followed by the p53 target CDKN1A(p21).	Dactinomycin	69-81	P53	Homo sapiens	199-202
33221336-10	2021	Moreover, triggering nucleolar stress by the chemotherapeutic agents ActinomycinD or the RNA polymeraseI inhibitor CX-5461 stimulates expression of Wnt/beta-Catenin targets, which is followed by the p53 target CDKN1A(p21).	CX 5461	115-122	P53	Homo sapiens	199-202
32347047-10	2021	Results: Arbutin pre-treatment increased the total antioxidative power and cell viability in the MTT assay and reduced BAX/BCL-2 ratio, P53 mRNA expression and necrosis in fibroblasts exposed to the oxidative agent (P<0.001).	Arbutin	9-16	P53	Homo sapiens	136-139
33574643-12	2021	Seven (46.6%) of the Vietnam era veterans with potential exposure to Agent Orange were positive for Tp53 mutations irrespective of the cancer type.	Agent Orange	69-81	P53	Homo sapiens	100-104
33723162-9	2021	Furthermore, after 24 h of exposure to hypericin with IC50 concentration, the expression of P53 and Bax genes increased and the expression of the Bcl2, Myc, and Mdm2 gene decreased.	hypericin	39-48	P53	Homo sapiens	92-95
32964394-11	2021	The gene expression analysis conducted with RT-PCR device and immunocytochemical analysis revealed that beta-arbutin at LD50 dose induced apoptosis in MCF-7 cells via p53 and Caspase 3.	Arbutin	104-116	P53	Homo sapiens	167-170
32964394-13	2021	Considering that arbutin increased the activation of apoptotic Caspase 3 through p53, which was stimulated by genotoxic and inflammatory effects at LD50 dose in MCF-7 cells.	Arbutin	17-24	P53	Homo sapiens	81-84
33186920-8	2020	We found that activation of autophagy could promote MEndT and increase cytoplasmic and total expression of p53, that but nuclear p53 expression was decreased, and that inhibition of autophagy activation could reverse the effect of EBSS.	ebss	231-235	P53	Homo sapiens	107-110
33186920-8	2020	We found that activation of autophagy could promote MEndT and increase cytoplasmic and total expression of p53, that but nuclear p53 expression was decreased, and that inhibition of autophagy activation could reverse the effect of EBSS.	ebss	231-235	P53	Homo sapiens	129-132
33165811-0	2021	Sodium cantharidinate, a novel anti-pancreatic cancer agent that activates functional p53.	sodium cantharidinate	0-21	P53	Homo sapiens	86-89
33165811-3	2021	In this study, we identified sodium cantharidinate as a novel, potential anti-pancreatic cancer agent that activates p53 function.	sodium cantharidinate	29-50	P53	Homo sapiens	117-120
33165811-6	2021	Furthermore, proteome-wide sequencing analysis detected a marked perturbation in p53 signaling pathway on PANC-1 cells upon sodium cantharidinate.	sodium cantharidinate	124-145	P53	Homo sapiens	81-84
33165811-8	2021	The p53-activating effect of sodium cantharidinate was strongly abrogated by treatment with TP53-targeting shRNA.	sodium cantharidinate	29-50	P53	Homo sapiens	4-7
33165811-8	2021	The p53-activating effect of sodium cantharidinate was strongly abrogated by treatment with TP53-targeting shRNA.	sodium cantharidinate	29-50	P53	Homo sapiens	92-96
33165811-9	2021	Moreover, sodium cantharidinate inhibited neoplasm growth via the JAK2-STAT3 pathway, which was inhibited by shRNA-TP53 and triggered by combination with gemcitabine.	sodium cantharidinate	10-31	P53	Homo sapiens	115-119
33001126-6	2020	The PCL-ss-P(PEGMA-co-GHA) amphiphilic copolymer could self-assemble into nanoparticles, which could be used to encapsulate anticancer drug doxorubicin (DOX) and compress the p53 gene to form the DOX-loaded PCL-ss-P(PEGMA-co-GHA)/p53 complex (abbreviated as DPGHAP/p53).	pcl-ss-p	4-12	P53	Homo sapiens	175-178
33001126-6	2020	The PCL-ss-P(PEGMA-co-GHA) amphiphilic copolymer could self-assemble into nanoparticles, which could be used to encapsulate anticancer drug doxorubicin (DOX) and compress the p53 gene to form the DOX-loaded PCL-ss-P(PEGMA-co-GHA)/p53 complex (abbreviated as DPGHAP/p53).	pcl-ss-p	4-12	P53	Homo sapiens	230-233
33001126-6	2020	The PCL-ss-P(PEGMA-co-GHA) amphiphilic copolymer could self-assemble into nanoparticles, which could be used to encapsulate anticancer drug doxorubicin (DOX) and compress the p53 gene to form the DOX-loaded PCL-ss-P(PEGMA-co-GHA)/p53 complex (abbreviated as DPGHAP/p53).	pcl-ss-p	4-12	P53	Homo sapiens	258-269
33001126-6	2020	The PCL-ss-P(PEGMA-co-GHA) amphiphilic copolymer could self-assemble into nanoparticles, which could be used to encapsulate anticancer drug doxorubicin (DOX) and compress the p53 gene to form the DOX-loaded PCL-ss-P(PEGMA-co-GHA)/p53 complex (abbreviated as DPGHAP/p53).	copolymer	39-48	P53	Homo sapiens	175-178
33001126-6	2020	The PCL-ss-P(PEGMA-co-GHA) amphiphilic copolymer could self-assemble into nanoparticles, which could be used to encapsulate anticancer drug doxorubicin (DOX) and compress the p53 gene to form the DOX-loaded PCL-ss-P(PEGMA-co-GHA)/p53 complex (abbreviated as DPGHAP/p53).	copolymer	39-48	P53	Homo sapiens	230-233
33001126-6	2020	The PCL-ss-P(PEGMA-co-GHA) amphiphilic copolymer could self-assemble into nanoparticles, which could be used to encapsulate anticancer drug doxorubicin (DOX) and compress the p53 gene to form the DOX-loaded PCL-ss-P(PEGMA-co-GHA)/p53 complex (abbreviated as DPGHAP/p53).	copolymer	39-48	P53	Homo sapiens	258-269
33177794-12	2020	CONCLUSION: APC, KRAS, PIK3CA, SMAD4, and TP53 mutations can be predicted from H&E pathology images using deep learning-based classifiers, demonstrating the potential for deep learning-based mutation prediction in the CRC tissue slides.	h&e	79-82	P53	Homo sapiens	42-46
33145353-0	2020	Amarogentin Inhibits Liver Cancer Cell Angiogenesis after Insufficient Radiofrequency Ablation via Affecting Stemness and the p53-Dependent VEGFA/Dll4/Notch1 Pathway.	amarogentin	0-11	P53	Homo sapiens	126-129
33145353-9	2020	Inversely, the antiangiogenesis effect of amarogentin was counteracted after p53 silencing in the iRFA cell models.	amarogentin	42-53	P53	Homo sapiens	77-80
33145353-10	2020	Conclusion: Amarogentin prevents the malignant transformation of liver cancer after iRFA via affecting stemness and the p53-dependent VEGFA/Dll4/Notch1 pathway to inhibit cancer cell angiogenesis.	amarogentin	12-23	P53	Homo sapiens	120-123
32946762-3	2020	The switch of p53 from tumor suppressor to oncogene is location-dependent and is impacted by microbially derived gallic acid.	Gallic Acid	113-124	P53	Homo sapiens	14-17
32942535-5	2020	Using H1299 cells, which are null for TP53, we generated cell lines expressing either a tetracycline inducible wild-type (WT) TP53 gene, or a representative mutated TP53 gene from six exemplary "hotspot" mutations in the DNA binding domain (R273H, R248Q, R282W, R175H, G245S, and R249S).	Tetracycline	88-100	P53	Homo sapiens	126-130
32942535-5	2020	Using H1299 cells, which are null for TP53, we generated cell lines expressing either a tetracycline inducible wild-type (WT) TP53 gene, or a representative mutated TP53 gene from six exemplary "hotspot" mutations in the DNA binding domain (R273H, R248Q, R282W, R175H, G245S, and R249S).	Tetracycline	88-100	P53	Homo sapiens	126-130
32915786-8	2020	ZnO-NP treatment reduced the basal levels of reactive oxygen species and Bax/Bcl-2 mRNA ratios; in addition, ZnO-NP decreased the 6-OHDA-induced ROS production, p53 expression, and cell death.	zno-np	0-6	P53	Homo sapiens	161-164
32915786-8	2020	ZnO-NP treatment reduced the basal levels of reactive oxygen species and Bax/Bcl-2 mRNA ratios; in addition, ZnO-NP decreased the 6-OHDA-induced ROS production, p53 expression, and cell death.	zno-np	109-115	P53	Homo sapiens	161-164
32641480-3	2020	DFO and MLN-4924, but not FG-4592, induced accumulation of both lytic EBV proteins and phosphorylated p53 in cell lines that contain a wild-type p53 gene.	pevonedistat	8-16	P53	Homo sapiens	102-105
32641480-3	2020	DFO and MLN-4924, but not FG-4592, induced accumulation of both lytic EBV proteins and phosphorylated p53 in cell lines that contain a wild-type p53 gene.	pevonedistat	8-16	P53	Homo sapiens	145-148
32722430-6	2020	Mechanistically, arecoline inhibited p53-induced DDB2 promoter activity through the DNA-binding but not the transactivation domain of p53.	Arecoline	17-26	P53	Homo sapiens	37-40
32722430-9	2020	These data uncover one of mechanisms underlying arecoline-mediated carcinogenicity through inhibiting p53-regulated DDB2 expression and DNA repair.	Arecoline	48-57	P53	Homo sapiens	102-105
32714568-3	2020	In an effort to understand MLN4924-induced cell death in CRC, we identified p53 as an important mediator of the apoptotic response to MLN4924.	pevonedistat	27-34	P53	Homo sapiens	76-79
32714568-3	2020	In an effort to understand MLN4924-induced cell death in CRC, we identified p53 as an important mediator of the apoptotic response to MLN4924.	pevonedistat	134-141	P53	Homo sapiens	76-79
32714568-5	2020	Depletion of the anti-apoptotic protein FLIP, which we identify as a novel mediator of resistance to MLN4924, enhanced apoptosis in a p53-, TRAIL-R2/DR5-, and caspase-8-dependent manner.	pevonedistat	101-108	P53	Homo sapiens	134-137
32714568-8	2020	The cell death induced by MLN4924/SN38 combination was dependent on activation of mitochondria through BAX/BAK, but in a p53-independent manner, an important observation given the high frequency of TP53 mutation(s) in advanced CRC.	pevonedistat	26-33	P53	Homo sapiens	121-124
32714568-8	2020	The cell death induced by MLN4924/SN38 combination was dependent on activation of mitochondria through BAX/BAK, but in a p53-independent manner, an important observation given the high frequency of TP53 mutation(s) in advanced CRC.	pevonedistat	26-33	P53	Homo sapiens	198-202
33102192-7	2020	The activation level of tumor suppressor protein (p53) increased after PTX treatment in MCF-7, but no changes observed in HT-29 might be due to hereditary mutations.	ptx	71-74	P53	Homo sapiens	50-53
33680035-9	2020	Real-time PCR showed that expression level of Bax, p53 and Bax genes increases and Bcl2 gene decreases in AGS cell lines after treatment by hypericin.	hypericin	140-149	P53	Homo sapiens	51-54
32566012-6	2020	These analyses along with reactome pathway enrichment analyses indicated that the genes upregulated in the ASR488-treated cells are involved in focal adhesion, neurotrophin signaling, p53 signaling, endoplasmic reticulum functioning in terms of protein processing, and pathways related to bladder cancer.	asr488	107-113	P53	Homo sapiens	184-187
32583791-6	2020	As main findings, phenolic compounds, saponins and alkaloids interfere with cancer progression by stimulating p53 expression, which can cause pro-apoptotic onset and restrict the anti-apoptotic activity, in addition to preventing telomerase enzyme activity.	phenolic compounds	18-36	P53	Homo sapiens	110-113
31177307-0	2020	Urolithin A induces prostate cancer cell death in p53-dependent and in p53-independent manner.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	0-11	P53	Homo sapiens	50-53
31177307-0	2020	Urolithin A induces prostate cancer cell death in p53-dependent and in p53-independent manner.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	0-11	P53	Homo sapiens	71-74
31177307-4	2020	The purpose of this study was to investigate the influence of UA on the p53-MDM2 interaction pathway in prostate cancer cell lines.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	62-64	P53	Homo sapiens	72-75
31177307-10	2020	Co-immunoprecipitation-immunoblotting was used to assess the inhibition of interactions between p53 and MDM2 and to assess the effect of UA on MDM2-mediated p53 polyubiquitination.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	137-139	P53	Homo sapiens	157-160
31177307-13	2020	In addition, UA increased the p53 proapoptotic proteins PUMA and NOXA.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	13-15	P53	Homo sapiens	30-33
31177307-14	2020	Moreover, UA inhibited the interaction between p53 and MDM2 and inhibited MDM2-mediated p53 polyubiquitination.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	10-12	P53	Homo sapiens	47-50
31177307-14	2020	Moreover, UA inhibited the interaction between p53 and MDM2 and inhibited MDM2-mediated p53 polyubiquitination.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	10-12	P53	Homo sapiens	88-91
31177307-16	2020	CONCLUSION: The influencing of UA on p53-MDM2 pathway may partly contribute to its anticancer effect.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	31-33	P53	Homo sapiens	37-40
32233050-8	2020	Women harbouring the variant G allele of the TP53 rs1042522 were at increased risk of cervical cancer in allelic (G vs. C; OR = 1.30, 95% Cl = 1.12-1.50), homozygous (GG vs. CC; OR=1.62, 95% CI = 1.20-2.19), and recessive (GG vs.CG+GG; OR=1.74, 95% CI = 1.34-2.25) genetic models.	cysteinylglycine	229-231	P53	Homo sapiens	45-49
31980261-0	2020	Purification of supercoiled p53-encoding plasmid using an arginine-modified macroporous support.	Arginine Vasopressin	58-66	P53	Homo sapiens	28-31
32032660-0	2020	Synergistic activation of p53 by actinomycin D and nutlin-3a is associated with the upregulation of crucial regulators and effectors of innate immunity.	Dactinomycin	33-46	P53	Homo sapiens	26-29
32032660-1	2020	Actinomycin D and nutlin-3a (A + N) activate p53, partly through induction of phosphorylation on Ser392.	Dactinomycin	0-13	P53	Homo sapiens	45-48
32691575-9	2020	Meanwhile, Baicalein treatment downregulated CyclinD1 and CDK4, while upregulating P53 and P21.	baicalein	11-20	P53	Homo sapiens	83-86
32385658-0	2020	Zn(II)-Based Coordination Polymer for Detection of Picric Acid in Aqueous Media and Treatment Effect against Deep Vein Thrombosis by Reducing P-ERK2 and p53 Expression.	zn(ii)-based coordination polymer	0-33	P53	Homo sapiens	153-156
32345994-5	2020	Previously, we demonstrated that the treatment of hepatoma cells with alpha-LA induced apoptosis, which was preceded by the generation of reactive oxygen species (ROS) and activation of the p53 protein, a known inducer of mitochondria-mediated apoptosis.	Thioctic Acid	70-78	P53	Homo sapiens	190-193
32164385-9	2020	Gene expression profiling characterize THTMP as an inhibitor of the p53 signaling pathway causing DNA damage and cell cycle arrest in CSC population.	thtmp	39-44	P53	Homo sapiens	68-71
31923958-2	2020	To this end, we constructed a novel UV-light cross-linked and pH de-cross-linked coumarin-decorated cationic copolymer functionalized mesoporous silica nanoparticles (MSN) for co-delivery of chemotherapeutic agent 5-FU and tumor suppresser p53 gene.	copolymer	109-118	P53	Homo sapiens	240-243
32097779-5	2020	PURPOSE: To explore the anticancer mechanism of action of the triterpenoid alkaloid KBA01 compound by targeting mutant p53 degradation.	kba01	84-89	P53	Homo sapiens	119-122
32097779-11	2020	KBA01 decreases the stability of DNA contact mutant p53 proteins through the proteasomal pathway with minimal effects on p53 mutant protein conformation.	kba01	0-5	P53	Homo sapiens	52-55
32097779-13	2020	In addition, KBA01 disrupts the HSF1-mutant p53-Hsp90 complex and releases mutant p53 to enable its MDM2- and CHIP-mediated degradation.	kba01	13-18	P53	Homo sapiens	44-47
32097779-13	2020	In addition, KBA01 disrupts the HSF1-mutant p53-Hsp90 complex and releases mutant p53 to enable its MDM2- and CHIP-mediated degradation.	kba01	13-18	P53	Homo sapiens	82-85
31815681-0	2020	A lex naturalis delineates components of a human-specific, adrenal androgen-dependent, p53-mediated "kill switch" tumor suppression mechanism.	Androgens	67-75	P53	Homo sapiens	87-90
31815681-1	2020	We have recently described in this journal our detection of an anthropoid primate-specific, adrenal androgen-dependent, p53-mediated, "kill switch" tumor suppression mechanism that reached its fullest expression only in humans, as a result of human-specific exposure to polycyclic aromatic hydrocarbons caused by the harnessing of fire.	Androgens	100-108	P53	Homo sapiens	120-123
31939089-6	2020	Actinomycin D was utilized to examine the stability of p53 mRNA.	Dactinomycin	0-13	P53	Homo sapiens	55-58
31812668-2	2020	In this study, we used wild-type (A375) and mutant p53 (MeWo) melanoma cell lines to assess the regulation of the mitochondrial antioxidant manganese superoxide dismutase (MnSOD) by mutant p53.	dimethylcuprate(I)	56-60	P53	Homo sapiens	51-54
31897241-10	2020	In summary, we showed that genipin increases the oxaliplatin-induced cell death via p53-DRAM autophagy.	oxaliplatin	49-60	P53	Homo sapiens	84-87
31781989-0	2020	Simulation of MDM2 N-terminal domain conformational lability in the presence of imidazoline based inhibitors of MDM2-p53 protein-protein interaction.	Imidazolines	80-91	P53	Homo sapiens	117-120
32564014-7	2020	Among the downstream molecular targets of SIRT1, the level of LPS-induced acetylated p53 was significantly decreased by THC treatment, whereas no noticeable change was observed in the levels of forkhead box O3 and peroxisome proliferator activated receptor gamma coactivator 1 alpha.	Dronabinol	120-123	P53	Homo sapiens	85-88
31861721-0	2019	Peroxiredoxin 5 Silencing Sensitizes Dopaminergic Neuronal Cells to Rotenone via DNA Damage-Triggered ATM/p53/PUMA Signaling-Mediated Apoptosis.	Rotenone	68-76	P53	Homo sapiens	106-109
31861721-7	2019	Furthermore, Prx5 knockdown enhanced the induction of PUMA by rotenone through a p53-dependent mechanism.	Rotenone	62-70	P53	Homo sapiens	81-84
31861721-11	2019	These findings provided a novel link between Prx5 and DNA damage-triggered ATM/p53/PUMA signaling in a rotenone-induced PD model.	Rotenone	103-111	P53	Homo sapiens	79-82
31222582-4	2019	Here, based on the hybrid model I, we computationally searched all the parameters and parameter combinations in the parameter space to identify those that could alter the natural preferential response of p53 when SSBs and DSBs coexist.	ssbs	213-217	P53	Homo sapiens	204-207
31578743-9	2019	CONCLUSIONS: The TP53 codon 72 Pro/Pro polymorphism may isolate a relatively high-risk patient group in T1N1M0/T2N0M0/T3N0M0 gastric cancer.	Proline	31-34	P53	Homo sapiens	17-21
31578743-9	2019	CONCLUSIONS: The TP53 codon 72 Pro/Pro polymorphism may isolate a relatively high-risk patient group in T1N1M0/T2N0M0/T3N0M0 gastric cancer.	Proline	35-38	P53	Homo sapiens	17-21
31563649-5	2019	Further studies revealed that nitidine chloride inhibited HaCaT proliferation and induced S phase cell cycle arrest; these effects were associated with reduced DNA synthesis, decreased Ki67, cyclin A, and cyclin D1 levels, and increased p53 protein expression.	nitidine	30-47	P53	Homo sapiens	237-240
31698450-2	2019	We previously showed that the cyclooxygenase (COX) inhibitor indomethacin prevents the ability of stromal cells to diminish p53-mediated killing of cocultured ALL cells in vitro, possibly by blocking the production of prostaglandin E2 (PGE2).	Indomethacin	61-73	P53	Homo sapiens	124-127
31698450-6	2019	The indomethacin treatment increased the level of p53 in the leukemic cells, implying that COX inhibition might reduce progression of ALL by attenuating protective paracrine PGE2 signaling from bone marrow stroma to leukemic cells.	Indomethacin	4-16	P53	Homo sapiens	50-53
31685796-2	2019	In this study, we report that the haplo-insufficient tumor suppressor ASPP2, a p53 activator, negatively regulates the mevalonate pathway to mediate its inhibitory effect on tumor growth in hepatocellular carcinoma (HCC).	Mevalonic Acid	119-129	P53	Homo sapiens	79-82
30521787-1	2019	Cabazitaxel as microtubule inhibitor and thymoquinone as HDAC inhibitor affects the important genes like p53, STAT3, Bax, BCL-2, p21 and down regulation of NF-kappaB are reported for potential activity against breast tumors.	thymoquinone	41-53	P53	Homo sapiens	105-108
31731474-5	2019	These actions may be mediated by oxidative stress induced by selenium compounds, leading to the activation of p53, proapoptotic proteins and caspases.	Selenium	61-69	P53	Homo sapiens	110-113
31467081-8	2019	We also found that PI3Kdelta inactivation through two approaches, CRISPR/Cas9-mediated depletion and a PI3Kdelta specific inhibitor (idelalisib) not only blocks vitreous-induced activation of AKT and MDM2 but also abrogates a vitreous-stimulated decrease in p53.	idelalisib	133-143	P53	Homo sapiens	258-261
31631976-0	2019	Erratum: 20(S)-Ginsenoside Rg3 Promotes Senescence And Apoptosis In Gallbladder Cancer Cells Via The P53 Pathway [Corrigendum].	ginsenoside Rg3	9-30	P53	Homo sapiens	101-104
31783991-3	2019	RESULTS: The essential nodes of the apoptotic pathways, TP53, and CASP3, were identified in both, Paclitaxel and Vincristine networks, but the intrinsic pathway markers BCL2, BAX, and BCL2L1 were identified as hub nodes only in the Paclitaxel network.	Vincristine	113-124	P53	Homo sapiens	56-60
31433961-8	2019	Treatment of A431 cells with TQ-induced apoptosis, which was associated with the induction of p53 and Bax, inhibition of Mdm2, Bcl-2, and Bcl-xl expression, and activation of caspase-9, -7, and -3.	thymoquinone	29-31	P53	Homo sapiens	94-97
31308078-6	2019	Additionally, bioinformatical analysis of indomethacin treated resistant cells revealed that indomethacin significantly activates the unfolded protein response (UPR), p53 and apoptosis pathways, and suppresses cell cycle, Myc and AR/ARV7 pathways.	Indomethacin	42-54	P53	Homo sapiens	167-170
31425749-0	2019	An oral 2-hydroxypropyl-beta-cyclodextrin-loaded spirooxindole-pyrrolizidine derivative restores p53 activity via targeting MDM2 and JNK1/2 in hepatocellular carcinoma.	2-Hydroxypropyl-beta-cyclodextrin	8-41	P53	Homo sapiens	97-100
31425749-0	2019	An oral 2-hydroxypropyl-beta-cyclodextrin-loaded spirooxindole-pyrrolizidine derivative restores p53 activity via targeting MDM2 and JNK1/2 in hepatocellular carcinoma.	PYRROLIZIDINE	63-76	P53	Homo sapiens	97-100
31325764-7	2019	We found that both TP53 Arg72Pro (CG/GG vs. CC: adjusted OR = 0.82, 95% CI = 0.69-0.98) and miR-34b/c rs4938723 (TC/CC vs. TT: adjusted OR = 0.64, 95% CI = 0.54-0.75) were associated with decreased neuroblastoma susceptibility.	cysteinylglycine	34-36	P53	Homo sapiens	19-23
31366730-3	2019	Here, we identified a relatively rare mutation leading to a proline to leucine substitution (P152L) in TP53 at the very end of its DNA-binding domain (DBD) in a sample from an Indian oral cancer patient.	Proline	60-67	P53	Homo sapiens	103-107
31158746-11	2019	Moreover, it was shown that an interaction of 1,4-quinone fragment with the hydrophobic matrix of the active site near Tyr128, Phe178, Trp105 and FAD cofactor could explain the observed increase of TP53 gene expression.	1,4-quinone	46-57	P53	Homo sapiens	198-202
31150783-7	2019	Furthermore, DMC increased p53 level and inhibited NF-kappaB nuclear-localization via suppression of PI3K/AKT signaling axis, which might be the underlying mechanism of DMC-induced apoptosis and cell cycle arrest in BEL-7402/5-FU cells.	2',4'-dihydroxy-6'-methoxy-3',5'-dimethylchalcone	13-16	P53	Homo sapiens	27-30
31150783-7	2019	Furthermore, DMC increased p53 level and inhibited NF-kappaB nuclear-localization via suppression of PI3K/AKT signaling axis, which might be the underlying mechanism of DMC-induced apoptosis and cell cycle arrest in BEL-7402/5-FU cells.	2',4'-dihydroxy-6'-methoxy-3',5'-dimethylchalcone	169-172	P53	Homo sapiens	27-30
31387680-5	2019	Herein, we report a one-step method to conjugate lanthanide-doped nanoparticles with p53-activating peptide (PMI: TSFAEYWALLSP), Bcl2-blocking peptide (BIM: IWIAQELRRIGDEFNAYYARR) and CD13-binding peptide (iNGR: CRNGRGPDC) by mercaptogenic self-assembly.	Lanthanoid Series Elements	49-59	P53	Homo sapiens	85-88
31296660-2	2019	KAISO potently stimulates apoptosis in cells expressing WT p53, but not in p53-mutant or p53-null cells.	kaiso	0-5	P53	Homo sapiens	59-62
31441737-10	2019	Predicting the cardiotoxicity of chemotherapy using the polymorphism of the p53 gene is an effective measure of early pre-symptom diagnosis of an increased risk of anthracyclineinduced cardiotoxicity.	anthracyclineinduced	164-184	P53	Homo sapiens	76-79
31196710-1	2019	Imidazoline-based small molecule inhibitors of p53-MDM2 interaction intended for the treatment of p53 wild-type tumors are the promising structures for design of anticancer drugs.	Imidazolines	0-11	P53	Homo sapiens	47-50
31196710-1	2019	Imidazoline-based small molecule inhibitors of p53-MDM2 interaction intended for the treatment of p53 wild-type tumors are the promising structures for design of anticancer drugs.	Imidazolines	0-11	P53	Homo sapiens	98-101
31016752-7	2019	Additionally, we confirmed 0.1 mum BBP-induced cell proliferation caused the arrest of cells in S phase and inhibited apoptosis, which might be partially explained by the decreased expression of p53, the increased expression of proliferating cell nuclear antigen, Bcl-2 and cell cycle regulator cyclin-D1, and the activation of aromatase.	butylbenzyl phthalate	35-38	P53	Homo sapiens	195-198
31276572-7	2019	Furthermore, a retinoid derivative and an endoplasmic reticulum stress inducer, fenretinide, induced NOXA, and combination of fenretinide and ABT-263 strongly induced apoptosis in HNSCC cells regardless of the HPV or p53 statuses.	Fenretinide	80-91	P53	Homo sapiens	217-220
31276572-7	2019	Furthermore, a retinoid derivative and an endoplasmic reticulum stress inducer, fenretinide, induced NOXA, and combination of fenretinide and ABT-263 strongly induced apoptosis in HNSCC cells regardless of the HPV or p53 statuses.	Fenretinide	126-137	P53	Homo sapiens	217-220
31276572-7	2019	Furthermore, a retinoid derivative and an endoplasmic reticulum stress inducer, fenretinide, induced NOXA, and combination of fenretinide and ABT-263 strongly induced apoptosis in HNSCC cells regardless of the HPV or p53 statuses.	navitoclax	142-149	P53	Homo sapiens	217-220
31171918-6	2019	Results: Our results revealed that the highest cytotoxic effect, the highest induction of apoptosis and significant elevation in P53 and Caspase 3 levels was seen in Paclitaxel/Gallic acid combination.	Gallic Acid	177-188	P53	Homo sapiens	129-132
30982228-5	2019	MCF7 mammary carcinoma cells harboring wild-type p53 (WT-p53) and LA/C responded to RS by transition to senescence with a significant reduction of lamin B receptor and LB1 proteins.	rs	84-86	P53	Homo sapiens	49-52
30725256-10	2019	A potent, non-toxic benzodiazepine ("KRM-II-08") binds to the alpha5-GABAAR (0.8 microM EC50) enhancing a chloride-anion efflux that induces mitochondrial membrane depolarization and in response, TP53 upregulation and p53, constitutively phosphorylated at S392, cytoplasmic localization.	Benzodiazepines	20-34	P53	Homo sapiens	196-200
30725256-10	2019	A potent, non-toxic benzodiazepine ("KRM-II-08") binds to the alpha5-GABAAR (0.8 microM EC50) enhancing a chloride-anion efflux that induces mitochondrial membrane depolarization and in response, TP53 upregulation and p53, constitutively phosphorylated at S392, cytoplasmic localization.	Benzodiazepines	20-34	P53	Homo sapiens	218-221
29715507-3	2019	However, p38 mediated activation of p53 was found to play a pivotal role in governing the apoptotic activity of embelin due to the following observations: a time-dependent activation of p53 and apoptosis by embelin; selective inhibition of p38 inhibited embelin-induced p53 levels.	embelin	112-119	P53	Homo sapiens	36-39
29715507-3	2019	However, p38 mediated activation of p53 was found to play a pivotal role in governing the apoptotic activity of embelin due to the following observations: a time-dependent activation of p53 and apoptosis by embelin; selective inhibition of p38 inhibited embelin-induced p53 levels.	embelin	112-119	P53	Homo sapiens	186-189
29715507-3	2019	However, p38 mediated activation of p53 was found to play a pivotal role in governing the apoptotic activity of embelin due to the following observations: a time-dependent activation of p53 and apoptosis by embelin; selective inhibition of p38 inhibited embelin-induced p53 levels.	embelin	112-119	P53	Homo sapiens	186-189
29715507-3	2019	However, p38 mediated activation of p53 was found to play a pivotal role in governing the apoptotic activity of embelin due to the following observations: a time-dependent activation of p53 and apoptosis by embelin; selective inhibition of p38 inhibited embelin-induced p53 levels.	embelin	207-214	P53	Homo sapiens	36-39
30651598-2	2019	Human epidemiological studies reveal that a p53 single-nucleotide polymorphism (SNP) at codon 72, encoding proline (P72) or arginine (R72), is associated with differential risk of several cancers, including BrCa.	Proline	107-114	P53	Homo sapiens	44-47
30710454-10	2019	Dioscin induced cell apoptosis, autophagy, and DNA damage via increasing expression levels of p53, cleaved PARP, Bax, cleaved caspase-3/9, Beclin-1, and LC3 and suppressing those of Bcl-2, p-Akt, p-mammalian target of rapamycin (mTOR), CDK5, p-ataxia telangiectasia-mutated gene (ATM).	dioscin	0-7	P53	Homo sapiens	94-97
30171603-8	2019	Finally, the combination of DMY, OND, and ADR led to G2/M cell cycle arrest and apoptosis via resuming P53 function and restraining relevant proteins expression.	dihydromyricetin	28-31	P53	Homo sapiens	103-106
29687302-4	2019	Recently, we have described that PC-mediated neuroprotection against ischemic insult is promoted by p53 destabilization, which is mediated by its main regulator MDM2.	pc	33-35	P53	Homo sapiens	100-103
29687302-6	2019	Here, we studied the contribution of the human Tp53 Arg72Pro SNP on PC-induced neuroprotection after ischemia.	pc	68-70	P53	Homo sapiens	47-51
29687302-7	2019	Our results showed that cortical neurons expressing the Pro72-p53 variant exhibited higher PC-mediated neuroprotection as compared with Arg72-p53 neurons.	pc	91-93	P53	Homo sapiens	62-65
29687302-8	2019	PC prevented ischemia-induced nuclear and cytosolic p53 stabilization in Pro72-p53 neurons.	pc	0-2	P53	Homo sapiens	52-55
29687302-8	2019	PC prevented ischemia-induced nuclear and cytosolic p53 stabilization in Pro72-p53 neurons.	pc	0-2	P53	Homo sapiens	79-82
29687302-10	2019	Furthermore, PC promoted neuroprotection against ischemia by controlling the p53/active caspase-3 pathway in Pro72-p53, but not in Arg72-p53 neurons.	pc	13-15	P53	Homo sapiens	77-80
29687302-10	2019	Furthermore, PC promoted neuroprotection against ischemia by controlling the p53/active caspase-3 pathway in Pro72-p53, but not in Arg72-p53 neurons.	pc	13-15	P53	Homo sapiens	115-118
29687302-10	2019	Furthermore, PC promoted neuroprotection against ischemia by controlling the p53/active caspase-3 pathway in Pro72-p53, but not in Arg72-p53 neurons.	pc	13-15	P53	Homo sapiens	115-118
30610102-2	2019	A new study suggests that mutation of TP53 supersedes AR in predicting mCRPC survival.	Argon	54-56	P53	Homo sapiens	38-42
29468637-0	2019	Idelalisib-rituximab induces durable remissions in TP53 disrupted B-PLL but results in significant toxicity: updated results of the UK-wide compassionate use programme.	idelalisib	0-10	P53	Homo sapiens	51-55
30655700-13	2019	HCEE promoted cell cycle arrest at G1 phase in HeLa cells by upregulating the levels of p53 and p21 and downregulating the levels of cyclin D1, CDK-4, and CDK-6.	hcee	0-4	P53	Homo sapiens	88-91
31223026-8	2019	The expression levels of BAD and p53 genes decreased by combined treatment with quercetin and selenium while showing synergistic effects in terms of gene expression.	Selenium	94-102	P53	Homo sapiens	33-36
31359386-5	2019	We recently reported that acacetin could antagonize the non-genomic action of RARgamma via tipping the balance of AKT-p53 driven by RARgamma from tumor promoting to tumor suppressive effect.	acacetin	26-34	P53	Homo sapiens	118-121
30316750-2	2018	Here, we studied the interaction between the transactivation domain peptide of cancer suppressor protein p53 and its negative regulator Mdm2 using a novel protein-protein interaction assay, based on the modified FlimPIA using the streptavidin-biotin interaction to link the p53 peptide and the probe enzyme.	Biotin	243-249	P53	Homo sapiens	105-108
30545932-4	2018	TPEN-induced p53 protein stabilization in vivo and in neuroepithelial cell cultures and apoptosis was dependent on p53.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	0-4	P53	Homo sapiens	13-16
30545932-4	2018	TPEN-induced p53 protein stabilization in vivo and in neuroepithelial cell cultures and apoptosis was dependent on p53.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	0-4	P53	Homo sapiens	115-118
30545932-6	2018	Overexpression of human CHIP, a zinc-independent E3 ubiquitin ligase that targets p53, relieved TPEN-induced p53 stabilization and reduced apoptosis.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	96-100	P53	Homo sapiens	82-85
30545932-6	2018	Overexpression of human CHIP, a zinc-independent E3 ubiquitin ligase that targets p53, relieved TPEN-induced p53 stabilization and reduced apoptosis.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	96-100	P53	Homo sapiens	109-112
30545932-8	2018	Correspondingly, embryos cultured with p53 transcriptional activity inhibitor pifithrin-alpha could overcome TPEN-induced apoptosis and failure of neural tube closure.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	109-113	P53	Homo sapiens	39-42
30563120-3	2018	After D2O treatment, the p53-cyclin-dependent kinase (CDK) pathway was stimulated, leading to inhibition of the proliferation of HSCs and an increase in the [ATP]/[ADP] ratio.	Deuterium Oxide	6-9	P53	Homo sapiens	25-28
30563120-12	2018	We observed that D2O cotreatment with BDMC significantly decreased cell proliferation compared to treatment with D2O alone, and this effect was accompanied by downregulation of HO-1 and an increase in p53 levels.	Deuterium Oxide	17-20	P53	Homo sapiens	201-204
29644528-0	2018	A novel, semi-synthetic diterpenoid 16(R and S)-phenylamino-cleroda-3,13(14), Z-dien-15,16 olide (PGEA-AN) inhibits the growth and cell survival of human neuroblastoma cell line SH-SY5Y by modulating P53 pathway.	(r and s)-phenylamino-cleroda-3,13	38-72	P53	Homo sapiens	200-203
30501707-11	2018	The ORR in patients with TP53 mutation was high (P=0.04), moreover the patients with TP53 mutation more easily gained CR (P&lt;0.001).	Chromium	118-120	P53	Homo sapiens	25-29
30501707-11	2018	The ORR in patients with TP53 mutation was high (P=0.04), moreover the patients with TP53 mutation more easily gained CR (P&lt;0.001).	Chromium	118-120	P53	Homo sapiens	85-89
30265530-8	2018	Additionally, the activated P53 pathway, hyperactivated Akt, and apoptosis were found in L02 cells after incubation with 100 muM cyadox.	cyadox	129-135	P53	Homo sapiens	28-31
30265530-10	2018	Thus, the present study revealed that N-O reduction of cyadox and ROS-mediated AKT/FOXO1 and AKT/P53 pathways were involved in growth promotion and cytotoxicity of cyadox.	cyadox	55-61	P53	Homo sapiens	97-100
30265530-10	2018	Thus, the present study revealed that N-O reduction of cyadox and ROS-mediated AKT/FOXO1 and AKT/P53 pathways were involved in growth promotion and cytotoxicity of cyadox.	cyadox	164-170	P53	Homo sapiens	97-100
30396948-0	2018	Phoyunnanin E Induces Apoptosis of Non-small Cell Lung Cancer Cells via p53 Activation and Down-regulation of Survivin.	phoyunnanin E	0-13	P53	Homo sapiens	72-75
30774789-2	2018	Our research was aimed to study p53 protein codon 72 polymorphism, a single base pair change of either arginine (Arg; CGC) or proline (Pro; CCC) that creates 3 distinct genotypes in reticular oral lichen planus (OLP) in comparison to oral SCC which is the most common oral mucosal malignancy as positive control and inflammatory fibrous hyperplasia (IFH) lesion as negative control.	Proline	126-133	P53	Homo sapiens	32-35
30774789-2	2018	Our research was aimed to study p53 protein codon 72 polymorphism, a single base pair change of either arginine (Arg; CGC) or proline (Pro; CCC) that creates 3 distinct genotypes in reticular oral lichen planus (OLP) in comparison to oral SCC which is the most common oral mucosal malignancy as positive control and inflammatory fibrous hyperplasia (IFH) lesion as negative control.	Proline	135-138	P53	Homo sapiens	32-35
29498006-7	2018	Furthermore, nimesulide with MPTP increased apoptotic protein cleaved caspase-3 and also induced expression of p53 gene.	nimesulide	13-23	P53	Homo sapiens	111-114
30214601-8	2018	Western blot and reverse transcription-quantitative polymerase chain reaction analyses suggested that chaetominine treatment facilitated the expression of p53, p21, checkpoint kinase 2 (Chk2) and phosphorylated ataxia telangiectasia mutated (p-ATM) and caused a reduction in the mRNA levels of cyclin E and cyclin-dependent kinases (CDKs) 2 and 4.	chaetominine	102-114	P53	Homo sapiens	155-158
30214601-9	2018	These results suggest that chaetominine may be involved in the regulation of p53/p21 and ATM and Rad3-related (ATM)/Chk2 signaling in SW1116 cells.	chaetominine	27-39	P53	Homo sapiens	77-80
30250619-6	2018	Thus, wild-type p53 was overexpressed in A549/VCR cells and it reversed vincristine resistance of A549/VCR cells via the inhibition of survivin expression.	Vincristine	72-83	P53	Homo sapiens	16-19
30250619-9	2018	These results suggested that survivin expression regulated by p53 may serve an important role in drug resistance in A549/VCR cells and may be a potential target for enhancing vincristine sensitivity in A549 lung cancer cells.	Vincristine	175-186	P53	Homo sapiens	62-65
29255172-4	2018	By investigating the cellular pathways that induce protection of mutant p53 from ubiquitin-mediated proteolysis, we found that HDAC6/Hsp90-dependent mutant p53 accumulation is sustained by RhoA geranylgeranylation downstream of the mevalonate pathway, as well as by RhoA- and actin-dependent transduction of mechanical inputs, such as the stiffness of the extracellular environment.	Mevalonic Acid	232-242	P53	Homo sapiens	156-159
29222481-6	2017	Furthermore, HIF-P4H-1 inactivation increases p53 activity and stability and hydroxylation of proline 142 in p53 has an important role in this regulation.	Proline	94-101	P53	Homo sapiens	109-112
29207594-3	2017	Ectopic expression of RPL22/eL22 suppressed the colony formation of cancer cells in a p53-dependent manner, whereas knockdown of RPL22/eL22 significantly compromised p53 activation by Actinomycin D, rescuing p53-induced G1/G0 cell cycle arrest.	Dactinomycin	184-197	P53	Homo sapiens	166-169
29207594-3	2017	Ectopic expression of RPL22/eL22 suppressed the colony formation of cancer cells in a p53-dependent manner, whereas knockdown of RPL22/eL22 significantly compromised p53 activation by Actinomycin D, rescuing p53-induced G1/G0 cell cycle arrest.	Dactinomycin	184-197	P53	Homo sapiens	166-169
29308362-6	2017	Molecular analysis of p53 codon 72 gene polymorphism was performed by polymerase chain reaction - restriction fragment length polymorphism for Arg/Arg, Arg/Pro, and Pro/Pro.	Proline	156-159	P53	Homo sapiens	22-25
29308362-6	2017	Molecular analysis of p53 codon 72 gene polymorphism was performed by polymerase chain reaction - restriction fragment length polymorphism for Arg/Arg, Arg/Pro, and Pro/Pro.	Proline	165-168	P53	Homo sapiens	22-25
29308362-6	2017	Molecular analysis of p53 codon 72 gene polymorphism was performed by polymerase chain reaction - restriction fragment length polymorphism for Arg/Arg, Arg/Pro, and Pro/Pro.	Proline	165-168	P53	Homo sapiens	22-25
27402632-0	2017	Amarogentin Induces Apoptosis of Liver Cancer Cells via Upregulation of p53 and Downregulation of Human Telomerase Reverse Transcriptase in Mice.	amarogentin	0-11	P53	Homo sapiens	72-75
27402632-2	2017	We attempted to elucidate the roles of p53-associated apoptosis pathways in the chemopreventive mechanism of amarogentin.	amarogentin	109-120	P53	Homo sapiens	39-42
27402632-7	2017	The gene and protein expression of p53-associated molecules, such as Akt, human telomerase reverse transcriptase, RelA, and p38, was detected by real-time quantitative polymerase chain reaction, Western blotting, and immunohistochemical staining in liver cancer cells and mouse tumor tissues after treatment with amarogentin.	amarogentin	313-324	P53	Homo sapiens	35-38
27402632-11	2017	CONCLUSION: The results of our study suggest that amarogentin promotes apoptosis of liver cancer cells by the upregulation of p53 and downregulation of human telomerase reverse transcriptase and prevents the malignant transformation of these cells.	amarogentin	50-61	P53	Homo sapiens	126-129
29033852-3	2017	Small interfering RNA (siRNA)-mediated suppression of BIK inhibited GA-induced oligomeric complex of BAX/BAK in the ER and mitochondria, increase of cytosolic Ca++ and ROS, and apoptosis, but did not attenuate the increase in the level of Ser 15-phosphated p53 induced by GA. Blockade of p53 expression by short hairpin RNA suppressed BAX/BAK oligomerization and ER Ca++-ROS-associated apoptosis induced by GA but did not affect GA-induced phospho-BIK (Thr 33/Ser 35) levels.	Gallic Acid	68-70	P53	Homo sapiens	257-260
29033852-3	2017	Small interfering RNA (siRNA)-mediated suppression of BIK inhibited GA-induced oligomeric complex of BAX/BAK in the ER and mitochondria, increase of cytosolic Ca++ and ROS, and apoptosis, but did not attenuate the increase in the level of Ser 15-phosphated p53 induced by GA. Blockade of p53 expression by short hairpin RNA suppressed BAX/BAK oligomerization and ER Ca++-ROS-associated apoptosis induced by GA but did not affect GA-induced phospho-BIK (Thr 33/Ser 35) levels.	Gallic Acid	68-70	P53	Homo sapiens	288-291
28782884-14	2017	Patients with a del(17p) or TP53 mutation can be treated with ibrutinib, venetoclax, or a combination of idelalisib and rituximab.	idelalisib	105-115	P53	Homo sapiens	28-32
28628491-5	2017	Furthermore, we found that TopBP1, which we previously showed was involved in doxorubicin resistance through upregulation of aberrant p53, was involved in calcein-AM-mediated increased doxorubicin sensitivity.	calcein AM	155-165	P53	Homo sapiens	134-137
28628491-7	2017	Calcein-AM repressed the expression of TopBP1, which resulted in reduced expression of aberrant p53 and disrupted the antiapoptotic activity mediated by the TopBP1/mutp53 pathway in NSCLC.	calcein AM	0-10	P53	Homo sapiens	96-99
28583901-8	2017	In addition, encapsulating BA-TPQ in the hydrogels amplifies the potency of the drug via down-regulation of MDM2 oncogenic protein and upregulation of p53 (a tumor suppressor) and p21 (cell proliferation suppressor) expression in HepG2 liver cancer cells.	7-(benzylamino)-1,3,4,8-tetrahydropyrrolo(4,3,2-de)quinolin-8(1H)-one	27-33	P53	Homo sapiens	151-154
28714573-8	2017	Furthermore, 53 chemical substructures associated with genotoxicity were enriched in certain classes of p53 actives, for example, anthracyclines (antineoplastics) and vinca alkaloids (tubulin disruptors).	Vinca Alkaloids	167-182	P53	Homo sapiens	104-107
28726723-7	2017	Moreover, mertensene-induced G2/M cell cycle arrest was associated with a decrease in the phosphorylated forms of the anti-tumor transcription factor p53, retinoblastoma protein (Rb), cdc2 and chkp2.	Mertensene	10-20	P53	Homo sapiens	150-153
28475405-3	2017	A common coding region variant at amino acid 72 of p53 encodes either proline (P72) or arginine (R72).	Proline	70-77	P53	Homo sapiens	51-54
28618944-6	2017	The combination of ultraviolet radiation B irradiation with demethoxycurcumin synergistically induced apoptotic cell death in A431 and HaCaT cells through activation of p53 and caspase pathways, as well as through upregulation of Bax and p-p65 expression and downregulation of Bcl-2, Mcl-1, and nuclear factor-kappaB expression.	demethoxycurcumin	60-77	P53	Homo sapiens	169-172
29029384-3	2017	We demonstrated that p53 increases the intracellular IP3 and Ca2+ levels and decreases the LC3 protein levels through its target gene Rap2B, suggesting that p53 can inhibit the autophagic response triggered by starvation via upregulation of the Rap2B-PLCepsilon-IP3-Ca2+ pathway.	Inositol 1,4,5-Trisphosphate	53-56	P53	Homo sapiens	21-24
29029384-3	2017	We demonstrated that p53 increases the intracellular IP3 and Ca2+ levels and decreases the LC3 protein levels through its target gene Rap2B, suggesting that p53 can inhibit the autophagic response triggered by starvation via upregulation of the Rap2B-PLCepsilon-IP3-Ca2+ pathway.	Inositol 1,4,5-Trisphosphate	53-56	P53	Homo sapiens	157-160
29029384-3	2017	We demonstrated that p53 increases the intracellular IP3 and Ca2+ levels and decreases the LC3 protein levels through its target gene Rap2B, suggesting that p53 can inhibit the autophagic response triggered by starvation via upregulation of the Rap2B-PLCepsilon-IP3-Ca2+ pathway.	Inositol 1,4,5-Trisphosphate	262-265	P53	Homo sapiens	21-24
29029384-3	2017	We demonstrated that p53 increases the intracellular IP3 and Ca2+ levels and decreases the LC3 protein levels through its target gene Rap2B, suggesting that p53 can inhibit the autophagic response triggered by starvation via upregulation of the Rap2B-PLCepsilon-IP3-Ca2+ pathway.	Inositol 1,4,5-Trisphosphate	262-265	P53	Homo sapiens	157-160
28214592-4	2017	We found that the polymorphism rs1042522:C &gt; G in codon 72 of exon 4 of the TP53 gene, whose C variant produces a proline and is more common in most ethnicities, has a G variant producing an arginine in 79.8% of NFPAs (n = 42; p &lt; 1.411 x 10-18 vs. 1000 Genomes database), causing patients to present a decade earlier with symptomatic NFPAs.	Proline	117-124	P53	Homo sapiens	79-83
30116169-7	2018	The results demonstrate that the bile acids, ursodeoxycholate and tauroursodeoxycholate, exhibit selective cytotoxicity toward nonfunctional p53 cell lines suggesting a p53-mediated role in inhibition of cell clonogenicity and potential chemopreventative properties.	ursodoxicoltaurine	66-87	P53	Homo sapiens	141-144
30116169-7	2018	The results demonstrate that the bile acids, ursodeoxycholate and tauroursodeoxycholate, exhibit selective cytotoxicity toward nonfunctional p53 cell lines suggesting a p53-mediated role in inhibition of cell clonogenicity and potential chemopreventative properties.	ursodoxicoltaurine	66-87	P53	Homo sapiens	169-172
29980405-6	2018	Likewise, the sensitivity to drugs used to treat other cancers such as: doxorubicin, mitoxantrone, and 4 hydroxy tamoxifen (4HT) also increased upon introduction of WT-TP53 into MIA-PaCa-2 cells.	Mitoxantrone	85-97	P53	Homo sapiens	168-172
28679068-2	2018	In present study, berberine hydrochloride (BER) triggered proliferative inhibition and G2/M arrest in AGS cells, down-regulated protein expression of cyclin B1, Bcl-2, up-regulated expression of p21, p53 and cleaved caspase 3, but showed no effect on protein expression of CHOP, Bip, and caspase 4.	berberine chloride	18-41	P53	Homo sapiens	200-203
33781788-0	2021	T-17, a spirostanol saponin, inhibits p53-independent proliferation and p53-dependent migration of gastric cancer cells.	spirostanol saponin	8-27	P53	Homo sapiens	38-41
30067985-0	2018	PHD3 Regulates p53 Protein Stability by Hydroxylating Proline 359.	Proline	54-61	P53	Homo sapiens	15-18
30067985-3	2018	Here, we show that PHD3 hydroxylates p53 at proline 359, a residue that is in the p53-DUB binding domain.	Proline	44-51	P53	Homo sapiens	37-40
30067985-3	2018	Here, we show that PHD3 hydroxylates p53 at proline 359, a residue that is in the p53-DUB binding domain.	Proline	44-51	P53	Homo sapiens	82-85
30067985-4	2018	Hydroxylation of p53 upon proline 359 regulates its interaction with USP7 and USP10, and its inhibition decreases the association of p53 with USP7/USP10, increases p53 ubiquitination, and rapidly reduces p53 protein levels independently of mRNA expression.	Proline	26-33	P53	Homo sapiens	17-20
30067985-4	2018	Hydroxylation of p53 upon proline 359 regulates its interaction with USP7 and USP10, and its inhibition decreases the association of p53 with USP7/USP10, increases p53 ubiquitination, and rapidly reduces p53 protein levels independently of mRNA expression.	Proline	26-33	P53	Homo sapiens	133-136
30067985-4	2018	Hydroxylation of p53 upon proline 359 regulates its interaction with USP7 and USP10, and its inhibition decreases the association of p53 with USP7/USP10, increases p53 ubiquitination, and rapidly reduces p53 protein levels independently of mRNA expression.	Proline	26-33	P53	Homo sapiens	133-136
30067985-4	2018	Hydroxylation of p53 upon proline 359 regulates its interaction with USP7 and USP10, and its inhibition decreases the association of p53 with USP7/USP10, increases p53 ubiquitination, and rapidly reduces p53 protein levels independently of mRNA expression.	Proline	26-33	P53	Homo sapiens	133-136
28436480-0	2017	Dihydromyricetin Induces Apoptosis and Reverses Drug Resistance in Ovarian Cancer Cells by p53-mediated Downregulation of Survivin.	dihydromyricetin	0-16	P53	Homo sapiens	91-94
28436480-5	2017	Survivin, an inhibitor of apoptosis (IAPs) family member, exhibited a decreased expression level after DHM treatment, which may be attributed to the activation of p53.	dihydromyricetin	103-106	P53	Homo sapiens	163-166
28125433-4	2017	CAL-101 also leads to induction of caspase-dependent apoptosis probably through reactive oxygen species-dependent upregulation of FOXO3a and subsequent induction of the proapoptotic target genes of p53.	idelalisib	0-7	P53	Homo sapiens	198-201
33781788-0	2021	T-17, a spirostanol saponin, inhibits p53-independent proliferation and p53-dependent migration of gastric cancer cells.	spirostanol saponin	8-27	P53	Homo sapiens	72-75
30603472-0	2017	Valproic Acid Modulates the Multipotency in Periodontal Ligament Stem Cells via p53-Mediated Cell Cycle.	Valproic Acid	0-13	P53	Homo sapiens	80-83
30140694-6	2018	Govaniadine-induced apoptosis was also accompanied by upregulation of Bax, p53, and Survivin mRNA expression as assessed by real time PCR analysis.	govaniadine	0-11	P53	Homo sapiens	75-78
33961435-0	2021	Adamantyl Isothiocyanates as Mutant p53 Rescuing Agents and Their Structure-Activity Relationships.	adamantyl isothiocyanate	0-25	P53	Homo sapiens	36-39
30011295-6	2018	Pre-treatment with the antioxidant, N-acetylcysteine, prevented the actions of arecoline on cell viability, G2/M growth arrest, reactive oxygen species (ROS) production, and the levels of CDK1, p21, p27, p53, cyclin B1, and phospho-AMPK proteins.	Arecoline	79-88	P53	Homo sapiens	204-207
29665353-0	2018	Tripartite motif 31 promotes resistance to anoikis of hepatocarcinoma cells through regulation of p53-AMPK axis.	tripartite	0-10	P53	Homo sapiens	98-101
28131902-0	2017	CQ synergistically sensitizes human colorectal cancer cells to SN-38/CPT-11 through lysosomal and mitochondrial apoptotic pathway via p53-ROS cross-talk.	Chloroquine	0-2	P53	Homo sapiens	134-137
28131902-4	2017	Notably, another autophagy inhibitor chloroquine (CQ) synergistically enhanced the anti-tumor activity of SN-38 in CRC cells with wild type (WT) p53.	Chloroquine	37-48	P53	Homo sapiens	145-148
28131902-4	2017	Notably, another autophagy inhibitor chloroquine (CQ) synergistically enhanced the anti-tumor activity of SN-38 in CRC cells with wild type (WT) p53.	Chloroquine	50-52	P53	Homo sapiens	145-148
28131902-5	2017	Subsequently, we identified a potential mechanism of this cooperative interaction by showing that CQ and SN-38 acted together to trigger reactive oxygen species (ROS) burst, upregulate p53 expression, elicit the loss of lysosomal membrane potential (LMP) and mitochondrial membrane potential ( psim).	Chloroquine	98-100	P53	Homo sapiens	185-188
33961435-2	2021	In this structure-activity relationship study, we examined a series of adamantyl isothiocyanates (Ad-ITCs) to discover novel agents as therapeutics by targeting mutant p53.	adamantyl isothiocyanate	71-96	P53	Homo sapiens	168-171
28131902-6	2017	In addition, ROS induced by CQ plus SN-38 upregulated p53 levels by activating p38, conversely, p53 stimulated ROS.	Chloroquine	28-30	P53	Homo sapiens	54-57
29936711-4	2018	Researchers observed thata protective genetic variant TP53 codon 72 proline allele was more commonly found in this population and appear tobe over-transmitted compared to others known for their high rate of cervical cancer.	Proline	68-75	P53	Homo sapiens	54-58
33990623-8	2021	ADPE upregulated the p53, Bax and cleaved caspase-3, thereby leading to the downregulation of Bcl-2 and AKT/mTOR pathway.	adpe	0-4	P53	Homo sapiens	21-24
29571049-0	2018	Lanthanide-doped nanoparticles conjugated with an anti-CD33 antibody and a p53-activating peptide for acute myeloid leukemia therapy.	Lanthanoid Series Elements	0-10	P53	Homo sapiens	75-78
28131902-9	2017	Altogether, all results suggested that CQ synergistically sensitized human CRC cells with WT p53 to SN-38 through lysosomal and mitochondrial apoptotic pathway via p53-ROS cross-talk.	Chloroquine	39-41	P53	Homo sapiens	93-96
28131902-9	2017	Altogether, all results suggested that CQ synergistically sensitized human CRC cells with WT p53 to SN-38 through lysosomal and mitochondrial apoptotic pathway via p53-ROS cross-talk.	Chloroquine	39-41	P53	Homo sapiens	164-167
34035828-9	2021	Further analysis showed that the HGD activity of quercetin, formononetin, kaempferol, isorhamnetin, and beta-sitosterol ingredients is possible through VEGFA, IL6, TNF, AKT1, and TP53 targets involved in TNF, toll-like receptors, and MAPK-related pathways, which have anti-inflammatory, antiapoptosis, antioxidation, and autophagy effects, relieve renal fibrosis and renal cortex injury, and improve renal function, thus delaying the development of DN.	3-methylquercetin	86-98	P53	Homo sapiens	179-183
34035828-10	2021	The molecular docking results showed that quercetin, formononetin, kaempferol, isorhamnetin, beta-sitosterol had a good binding activity with VEGFA, IL6, TNF, AKT1, and TP53.	3-methylquercetin	79-91	P53	Homo sapiens	169-173
28279036-9	2017	Patients with TP53 gene mutation were more likely to receive CR, 10 of 15 patients with TP53 mutations achieved CR.	Chromium	61-63	P53	Homo sapiens	14-18
28681618-9	2018	Prodigiosin induced remarkably p53 accumulation and increased p53/survivin and caspase-3/survivin ratios by 6.1 to 11.3 and 10.3 to 47.5-fold at 100 to 600 nM, respectively.	Prodigiosin	0-11	P53	Homo sapiens	31-34
28681618-9	2018	Prodigiosin induced remarkably p53 accumulation and increased p53/survivin and caspase-3/survivin ratios by 6.1 to 11.3 and 10.3 to 47.5-fold at 100 to 600 nM, respectively.	Prodigiosin	0-11	P53	Homo sapiens	62-65
28279036-9	2017	Patients with TP53 gene mutation were more likely to receive CR, 10 of 15 patients with TP53 mutations achieved CR.	Chromium	112-114	P53	Homo sapiens	14-18
33958632-5	2021	Differences in Abeta levels might be accounted for, in part, by p53 since blocking p53 function in A549 cells resulted in decreased Abeta levels, increased MMP2/9 levels, increased PI3K/AKT activities and the phospho/total NFkappaB ratio.	UNII-042A8N37WH	15-20	P53	Homo sapiens	64-67
28279036-9	2017	Patients with TP53 gene mutation were more likely to receive CR, 10 of 15 patients with TP53 mutations achieved CR.	Chromium	112-114	P53	Homo sapiens	88-92
29854877-3	2018	For initial screening, we screened 5,000 genes through selection of shRNAs in p53 wild-type tumor cells that altered sensitivity to the p53 activator actinomycin D (ActD) to identify p53 regulatory genes; shRNAs targeting 322 genes were obtained.	Dactinomycin	150-163	P53	Homo sapiens	136-139
33958632-5	2021	Differences in Abeta levels might be accounted for, in part, by p53 since blocking p53 function in A549 cells resulted in decreased Abeta levels, increased MMP2/9 levels, increased PI3K/AKT activities and the phospho/total NFkappaB ratio.	UNII-042A8N37WH	15-20	P53	Homo sapiens	83-86
29854877-3	2018	For initial screening, we screened 5,000 genes through selection of shRNAs in p53 wild-type tumor cells that altered sensitivity to the p53 activator actinomycin D (ActD) to identify p53 regulatory genes; shRNAs targeting 322 genes were obtained.	Dactinomycin	150-163	P53	Homo sapiens	136-139
28055238-3	2017	VPA treatment (1.5, 3.0, or 4.5 mM) altered (p &lt; 0.05) the growth characteristics and relative expression level of HDAC1, DNMT1, DNMT3a, P53, and CASPASE3, and the global level of H3K9/14ac, H4K5ac, and H3K18ac but not H3K27me3 in the cells.	Valproic Acid	0-3	P53	Homo sapiens	140-143
28102315-0	2017	Methyl-Cytosine-Driven Structural Changes Enhance Adduction Kinetics of an Exon 7 fragment of the p53 Gene.	methyl-cytosine	0-15	P53	Homo sapiens	98-101
33958632-5	2021	Differences in Abeta levels might be accounted for, in part, by p53 since blocking p53 function in A549 cells resulted in decreased Abeta levels, increased MMP2/9 levels, increased PI3K/AKT activities and the phospho/total NFkappaB ratio.	UNII-042A8N37WH	132-137	P53	Homo sapiens	64-67
29599323-6	2018	To determine the pathway and relevant components by which gallic acid-induced apoptosis is mediated through, cells were transfected with siRNA (Fas, FasL, DR5, p53) using Lipofectamine 2000.	Gallic Acid	58-69	P53	Homo sapiens	160-163
29599323-10	2018	In addition, p53 was shown to be involved in gallic acid-mediated Fas, FasL, and DR5 expression as well as cell apoptosis in AGS cells.	Gallic Acid	45-56	P53	Homo sapiens	13-16
33958632-5	2021	Differences in Abeta levels might be accounted for, in part, by p53 since blocking p53 function in A549 cells resulted in decreased Abeta levels, increased MMP2/9 levels, increased PI3K/AKT activities and the phospho/total NFkappaB ratio.	UNII-042A8N37WH	132-137	P53	Homo sapiens	83-86
33666815-0	2021	Urolithin A induces cell cycle arrest and apoptosis by inhibiting Bcl-2, increasing p53-p21 proteins and reactive oxygen species production in colorectal cancer cells.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	0-11	P53	Homo sapiens	84-87
29552154-3	2018	The status of P53 may determine the effect of TAp73 on angiogenesis.	tap73	46-51	P53	Homo sapiens	14-17
28076793-4	2017	CQ induces Par-4 secretion via the classical secretory pathway that requires the activation of p53.	Chloroquine	0-2	P53	Homo sapiens	95-98
28076793-6	2017	Our findings indicate that CQ induces p53- and Rab8b-dependent Par-4 secretion from normal cells for Par-4-dependent inhibition of metastatic tumor growth.	Chloroquine	27-29	P53	Homo sapiens	38-41
29511341-0	2018	The stiff RhoAd from mevalonate to mutant p53.	Mevalonic Acid	21-31	P53	Homo sapiens	42-45
34056355-2	2021	A survey of the mutation spectra of the p53 tumor suppressor gene in these cancers suggested that the types of mutations and the hot spots are similar to those induced by acetaldehyde (AcAld) in an in vitro p53 mutation analysis system.	Acetaldehyde	171-183	P53	Homo sapiens	40-43
29221641-9	2018	In outcome-models including further well-established histo-pathological factors, p53-expression dichotomized at 20% independently impacted DP (HR = 4.13; P = 0.004) and CSM (HR = 3.74; P = 0.033), while no significant PA gain was achieved.	Protactinium	218-220	P53	Homo sapiens	81-84
27810593-0	2017	Novel phenylenediamine bridged mixed ligands dimetallic square planner Pt(II) complex inhibits MMPs expression via p53 and caspase-dependent signaling and suppress cancer metastasis and invasion.	Phenylenediamines	6-22	P53	Homo sapiens	115-118
34056355-2	2021	A survey of the mutation spectra of the p53 tumor suppressor gene in these cancers suggested that the types of mutations and the hot spots are similar to those induced by acetaldehyde (AcAld) in an in vitro p53 mutation analysis system.	Acetaldehyde	171-183	P53	Homo sapiens	207-210
29333597-2	2017	TP53 codon 72 polymorphism (P72R) results in proline (P) or arginine (R) at 72 amino acid position, which causes synthesis of proteins with distinct functions.	Proline	45-52	P53	Homo sapiens	0-4
33953676-6	2021	The results showed that astragalin significantly inhibited the proliferation and diffusion of HCT116 cells by induced apoptosis (by modulation of Bax, Bcl-2, P53, caspase-3, caspase 6, caspase 7, caspase 8, caspase 9 protein express) and cell cycle arrest (by modulation of Cyclin D1, Cyclin E, P21, P27, CDK2, CDK4 protein express).	astragalin	24-34	P53	Homo sapiens	158-161
28240161-0	2017	Dihydromyricetin Reduces TGF-beta Via P53 Activation-dependent Mechanism in Hepatocellular Carcinoma HepG2 Cells.	dihydromyricetin	0-16	P53	Homo sapiens	38-41
29069577-3	2018	The 2-sulfonylpyrimidine compound, PK11007, preferentially decreases viability in p53-compromised cancer cell lines.	2-sulfonylpyrimidine	4-24	P53	Homo sapiens	82-85
33852837-3	2021	Here, we disclose the p53-activating anticancer drug (3S)-6,7-bis(hydroxymethyl)-5-methyl-3-phenyl-1H,3H-pyrrolo[1,2-c]thiazole (MANIO).	manio	129-134	P53	Homo sapiens	22-25
29274324-7	2018	The results demonstrate that two AHR antagonists, alpha-naphthoflavone (alpha-NF) and resveratrol, decreased cell proliferation, arrested cells in the gap 1/synthesis (G1/S) phases, and increased p53 levels and apoptosis.	alpha-naphthoflavone	50-70	P53	Homo sapiens	196-199
29274324-7	2018	The results demonstrate that two AHR antagonists, alpha-naphthoflavone (alpha-NF) and resveratrol, decreased cell proliferation, arrested cells in the gap 1/synthesis (G1/S) phases, and increased p53 levels and apoptosis.	alpha-naphthoflavone	72-80	P53	Homo sapiens	196-199
29113888-0	2018	Ultrasensitive electrochemical immunosensing of tumor suppressor protein p53 in unprocessed human plasma and cell lysates using a novel nanocomposite based on poly-cysteine/graphene quantum dots/gold nanoparticle.	polycysteine	159-172	P53	Homo sapiens	73-76
28033105-6	2016	Multivariate analysis showed a significant association with NSCLC for the combination between the TP53 codon72 Arg/Pro and the Pro/Pro genotypes (OR 2.21, 95 % CI 1.390-3.51; p=0.001).	Proline	115-118	P53	Homo sapiens	98-102
28096969-7	2016	Apoptosis evaluation revealed that p53 overexpression accompanied by DNC treatment can act in a synergistic manner to significantly enhance the number of apoptotic cells (90%) compared with their application alone (15% and 38% for p53 overexpression and DNC, respectively).	dnc	69-72	P53	Homo sapiens	35-38
28096969-7	2016	Apoptosis evaluation revealed that p53 overexpression accompanied by DNC treatment can act in a synergistic manner to significantly enhance the number of apoptotic cells (90%) compared with their application alone (15% and 38% for p53 overexpression and DNC, respectively).	dnc	69-72	P53	Homo sapiens	231-234
33948573-4	2021	By focusing on Juberg-Marsidi syndrome (JMS), one of the severest XLIDs, we show that increased p53 signaling results from p53 accumulation caused by HUWE1 p.G4310R destabilization.	g4310r	158-164	P53	Homo sapiens	96-99
28101238-0	2016	Diosmetin triggers cell apoptosis by activation of the p53/Bcl-2 pathway and inactivation of the Notch3/NF-kappaB pathway in HepG2 cells.	diosmetin	0-9	P53	Homo sapiens	55-58
28101238-5	2016	Western blotting was performed to evaluate cell apoptosis and survival-associated proteins, and the results demonstrated that DIOS treatment resulted in the activation of the p53-dependent apoptosis pathway.	diosmetin	126-130	P53	Homo sapiens	175-178
27765352-0	2016	Dioscin suppresses hepatocellular carcinoma tumor growth by inducing apoptosis and regulation of TP53, BAX, BCL2 and cleaved CASP3.	dioscin	0-7	P53	Homo sapiens	97-101
29434841-8	2018	In addition, A172 cells treated with SB exhibited positivity for senescence-associated (SA) beta-galactosidase (gal) staining and elevated protein expression of p53 and p21 in a time- and dose-dependent manner, whereas the expression of p21 mRNA decreased.	Butyric Acid	37-39	P53	Homo sapiens	161-164
29343717-7	2018	Significant upregulations of the mRNAs of enzymes degrading heme, of ANXA1, ANXA2, CTGF, CAV2 and ICAM1, as well as of FAS, Casp8, BAX, p53, CYC1 and PARP1 were observed in MCS cells as compared with 1g-control and AD cells.	Heme	60-64	P53	Homo sapiens	136-139
27765352-14	2016	Moreover, we demonstrated that Dioscin displayed anticancer activity via up-regulating expression of TP53, BAX and CASP3 protein, as well as down-regulating BCL2 in Bel-7402 cells.	dioscin	31-38	P53	Homo sapiens	101-105
27765352-16	2016	CONCLUSIONS: Dioscin inhibited tumor growth via inducing apoptosis, which was accompanied by altered expression of apoptotic pathway proteins, such as TP53, BAX, BCL2 and CASP3.	dioscin	13-20	P53	Homo sapiens	151-155
29483824-5	2018	Mechanistically, dioscin may down-regulate the expression of SH2 domain-containing phosphatase-2 (SHP2) at the transcription level by increasing p53 binding to the SHP2 promoter due to reactive oxygen species (ROS).	dioscin	17-24	P53	Homo sapiens	145-148
33948573-4	2021	By focusing on Juberg-Marsidi syndrome (JMS), one of the severest XLIDs, we show that increased p53 signaling results from p53 accumulation caused by HUWE1 p.G4310R destabilization.	g4310r	158-164	P53	Homo sapiens	123-126
27379929-0	2016	KSP inhibitor SB743921 inhibits growth and induces apoptosis of breast cancer cells by regulating p53, Bcl-2, and DTL.	SB 743921	14-22	P53	Homo sapiens	98-101
33868388-12	2021	Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment.	Ketoglutaric Acids	80-94	P53	Homo sapiens	8-11
33868388-12	2021	Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment.	Ketoglutaric Acids	157-171	P53	Homo sapiens	8-11
28901264-0	2018	Inhibition of Proliferation and Induction of Apoptosis by Thymoquinone via Modulation of TGF Family, p53, p21 and Bcl-2alpha in Leukemic Cells.	thymoquinone	58-70	P53	Homo sapiens	101-104
33181285-0	2021	Antrodia camphorata extract (ACE)-induced apoptosis is associated with BMP4 expression and p53-dependent ROS generation in human colon cancer cells.	Acetaldehyde	29-32	P53	Homo sapiens	91-94
28960612-0	2018	Triggering p53 activation is essential in ziyuglycoside I-induced human retinoblastoma WERI-Rb-1 cell apoptosis.	ziyuglycoside I	42-57	P53	Homo sapiens	11-14
28960612-5	2018	Furthermore, Ziyu I treatment increased p53 expression as well as improved p53 stabilization through downregulation of pS166-Mdm2 and upregulation of phosphorylated- and acetylated-p53.	ziyuglycoside I	13-19	P53	Homo sapiens	40-43
27601129-0	2016	p53, Bcl-2 and cox-2 are involved in berberine hydrochloride-induced apoptosis of HeLa229 cells.	berberine chloride	37-60	P53	Homo sapiens	0-3
27601129-5	2016	Berberine hydrochloride upregulated the mRNA expression levels of p53, and downregulated mRNA expression levels of Bcl-2 and cox-2, in a dose-dependent manner.	berberine chloride	0-23	P53	Homo sapiens	66-69
27601129-6	2016	In conclusion, berberine hydrochloride inhibited the proliferation and induced apoptosis of HeLa229 cells, potentially via the upregulation of p53 and the downregulation of Bcl-2 and cox-2 mRNA expression levels.	berberine chloride	15-38	P53	Homo sapiens	143-146
27698880-7	2016	In addition, treatment with DPPT markedly downregulated the levels of phosphorylated Akt and activated the p53/B-cell lymphoma 2 associated X protein (Bax)/phosphatase and tensin homolog (PTEN) signaling pathway in DU-145 cells, suggesting that caspase-mediated pathways were involved in DPPT-induced apoptosis.	deoxypodophyllotoxin	28-32	P53	Homo sapiens	107-110
28960612-5	2018	Furthermore, Ziyu I treatment increased p53 expression as well as improved p53 stabilization through downregulation of pS166-Mdm2 and upregulation of phosphorylated- and acetylated-p53.	ziyuglycoside I	13-19	P53	Homo sapiens	75-78
28960612-5	2018	Furthermore, Ziyu I treatment increased p53 expression as well as improved p53 stabilization through downregulation of pS166-Mdm2 and upregulation of phosphorylated- and acetylated-p53.	ziyuglycoside I	13-19	P53	Homo sapiens	75-78
33656867-2	2021	DMSe has been recently revealed as a precursor of secondary organic aerosol (SOA), and its resultant SOA possesses strong oxidizing capability toward thiol groups that can perturb several major biological pathways in human airway epithelial cells and is linked to genotoxicity, DNA damage, and p53-mediated stress responses.	dimethylselenide	0-4	P53	Homo sapiens	294-297
28960612-7	2018	Our findings demonstrate that Ziyu I exhibits excellent anticancer effect on human RB WERI-Rb-1 cells by triggering p53 activation, and imply Ziyu I as a potential compound for chemotherapy of human RB.	ziyuglycoside I	30-36	P53	Homo sapiens	116-119
29255172-0	2018	Mechanical cues control mutant p53 stability through a mevalonate-RhoA axis.	Mevalonic Acid	55-65	P53	Homo sapiens	31-34
29255172-4	2018	By investigating the cellular pathways that induce protection of mutant p53 from ubiquitin-mediated proteolysis, we found that HDAC6/Hsp90-dependent mutant p53 accumulation is sustained by RhoA geranylgeranylation downstream of the mevalonate pathway, as well as by RhoA- and actin-dependent transduction of mechanical inputs, such as the stiffness of the extracellular environment.	Mevalonic Acid	232-242	P53	Homo sapiens	72-75
27599722-8	2016	METHODS: p53 levels were analysed by western blot upon capsaicin treatment in the presence of the autophagy inhibitor chloroquine.	Chloroquine	118-129	P53	Homo sapiens	9-12
27422117-4	2016	Further, p53 strongly favors G-quadruplexes folded in potassium over those formed in sodium, thus indicating the telomeric G-quadruplex conformational selectivity of p53.	Potassium	54-63	P53	Homo sapiens	9-12
27422117-4	2016	Further, p53 strongly favors G-quadruplexes folded in potassium over those formed in sodium, thus indicating the telomeric G-quadruplex conformational selectivity of p53.	Potassium	54-63	P53	Homo sapiens	166-169
29222275-7	2017	TP53 disruption by gene mutation and/or deletion associates with chemoimmunotherapy failure and mandates treatment with innovative drugs, including ibrutinib, idelalisib, or venetoclax.	idelalisib	159-169	P53	Homo sapiens	0-4
33484475-4	2021	Previously, serine deprivation has been connected to the action of the tumor suppressor p53, and we have previously published on a role for p53 regulating sphingosine kinase 1 (SK1), an enzyme that phosphorylates sphingosine to form sphingosine-1-phosphate (S1P).	sphingosine 1-phosphate	233-256	P53	Homo sapiens	140-143
29333130-3	2017	Here, curcumin, flavokawain B, and alpinetin were docked against the crystal structure of R273H mutant p53 in silico.	alpinetin	35-44	P53	Homo sapiens	103-106
29333130-4	2017	Consequently, all the compounds bind to the cavity of R273H mutant p53 with a dissociation constant estimated to have 36.57, 70.77, and 75.11 microM for curcumin, flavokawain B, and alpinetin, respectively.	alpinetin	182-191	P53	Homo sapiens	67-70
27259808-0	2016	Indolo-pyrido-isoquinolin based alkaloid inhibits growth, invasion and migration of breast cancer cells via activation of p53-miR34a axis.	indolo-pyrido-isoquinolin	0-25	P53	Homo sapiens	122-125
33197601-0	2021	Flubendazole, FDA-approved anthelmintic, Elicits Valid Antitumor Effects by Targeting P53 and Promoting Ferroptosis in Castration-resistant Prostate Cancer.	flubendazole	0-12	P53	Homo sapiens	86-89
27738496-11	2016	Amitriptyline also induced cell death in hepatoma cells lines with mutated p53 and non-sense p53 mutation.	Amitriptyline	0-13	P53	Homo sapiens	75-78
27738496-11	2016	Amitriptyline also induced cell death in hepatoma cells lines with mutated p53 and non-sense p53 mutation.	Amitriptyline	0-13	P53	Homo sapiens	93-96
27738496-12	2016	Our results support the hypothesis that Amitriptyline-induced mitochondrial dysfunction can be a useful therapeutic strategy for HCC treatment, especially in tumors showing p53 mutations and/or resistant to genotoxic treatments.	Amitriptyline	40-53	P53	Homo sapiens	173-176
29212503-5	2017	RESULTS: Combined treatment with equipotent doses of VPA and 5"-DFUR resulted in synergistic effects in CRC lines expressing p53 (wild-type or mutant).	Valproic Acid	53-56	P53	Homo sapiens	125-128
29089230-6	2017	Valine and phenylglycine ester derivatives were identified as potentially active MDM2-p53 inhibitors.	phenylglycine ester	11-30	P53	Homo sapiens	86-89
28774804-2	2017	In this work, biotin conjugated p53-antibody (anti-p53) was immobilized onto a green and biocompatible nanocomposite containing poly l-cysteine (P-Cys) as conductive matrix and 3D gold nanoparticles (GNPs) as signal amplification element.	Biotin	14-20	P53	Homo sapiens	32-35
28774804-2	2017	In this work, biotin conjugated p53-antibody (anti-p53) was immobilized onto a green and biocompatible nanocomposite containing poly l-cysteine (P-Cys) as conductive matrix and 3D gold nanoparticles (GNPs) as signal amplification element.	Biotin	14-20	P53	Homo sapiens	51-54
27271587-8	2016	In addition, dioscin significantly up-regulated the protein levels of Bak, Bax, Bid, p53, caspase-3, caspase-9, and down-regulated the protein levels of Bcl-2 and Bcl-xl.	dioscin	13-20	P53	Homo sapiens	85-88
33197601-7	2021	In addition, we reported that flubendazole induced the expression of P53, which partly accounted for the G2/M phase arrest and led to inhibition of the transcription of SLC7A11, and then downregulated the GPX4, which is a major ferroptosis-related gene.	flubendazole	30-42	P53	Homo sapiens	69-72
33197601-9	2021	This study provides biological evidence that flubendazole is a novel P53 inducer which exerts anti-proliferation and pro-apoptosis effects in CRPC through hindering the cell cycle and activating the ferroptosis, and indicates that a novel utilization of flubendazole in neoadjuvant chemotherapy of CRPC.	flubendazole	45-57	P53	Homo sapiens	69-72
32737944-0	2021	Potency and selectivity optimization of tryptophanol-derived oxazoloisoindolinones: novel p53 activators in human colorectal cancer.	oxazoloisoindolinones	61-82	P53	Homo sapiens	90-93
27304453-10	2016	The results revealed that (1) homozygosity of the Pro72 variant of p53 was present in 26 laryngeal carcinoma patients (65%), (2) heterozygosity for the Pro/Arg genotype was present in 13 patients (32.5%), and (3) the Arg72 variant of the p53 allele was present in 1 patient (2.5%) before treatment.	Proline	50-53	P53	Homo sapiens	67-70
32737944-1	2021	To search for novel p53 activators, four series of novel ( S )- and ( R )-tryptophanol-derived oxazoloisoindolinones have been straightforwardly synthesized and their antiproliferative activity evaluated in human colorectal cancer HCT116 cell line.	Sulfur	57-63	P53	Homo sapiens	20-23
28733702-8	2017	Finally, we tested the ability of CXCR4 and FAK inhibitors (WZ811 and PF-573228, respectively) to suppress the migratory and invasive potential of p53/PTEN deficient NSCLC cells, in vitro and in vivo using metastatic models of human NSCLC.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	70-79	P53	Homo sapiens	147-150
32737944-1	2021	To search for novel p53 activators, four series of novel ( S )- and ( R )-tryptophanol-derived oxazoloisoindolinones have been straightforwardly synthesized and their antiproliferative activity evaluated in human colorectal cancer HCT116 cell line.	oxazoloisoindolinones	95-116	P53	Homo sapiens	20-23
26996126-7	2016	From this result, we tested the effect of ABT-263 (Navitoclax), the specific inhibitor of Bcl-2 and Bcl-XL, but not Mcl-1, and found that ABT-263 synergistically enhanced cisplatin-induced apoptosis in NSCLC cells in the presence or absence of p53.	navitoclax	51-61	P53	Homo sapiens	244-247
33281970-0	2021	Antitumor effects of dioscin in A431 cells via adjusting ATM/p53-mediated cell apoptosis, DNA damage and migration.	dioscin	21-28	P53	Homo sapiens	61-64
27141285-0	2016	Effect of Thymoquinone on P53 Gene Expression and Consequence Apoptosis in Breast Cancer Cell Line.	thymoquinone	10-22	P53	Homo sapiens	26-29
29196570-0	2017	Reactivation of mutant p53 and induction of apoptosis in human tumor cells by maleimide analogs.	maleimide	78-87	P53	Homo sapiens	23-26
33281970-7	2021	Investigations into the mechanism revealed that the expression levels of phosphorylated Ataxia telangiectasia-mutated (ATM) were considerably activated by dioscin, which significantly upregulated the expression levels of p53 to activate mitochondrial apoptosis signaling.	dioscin	155-162	P53	Homo sapiens	221-224
27141285-4	2016	Hereby, this study reports the potency of TQ on expression of tumor suppressor gene P53 and apoptosis induction in breast cancer cell line Michigan Cancer Foundation-7 (MCF-7).	thymoquinone	42-44	P53	Homo sapiens	84-87
33281970-10	2021	In addition, p53-small interfering RNA transfection experiments indicated that dioscin exhibited excellent activity against skin cancer in vitro by decreasing p53 expression.	dioscin	79-86	P53	Homo sapiens	13-16
33281970-10	2021	In addition, p53-small interfering RNA transfection experiments indicated that dioscin exhibited excellent activity against skin cancer in vitro by decreasing p53 expression.	dioscin	79-86	P53	Homo sapiens	159-162
33281970-11	2021	Overall, the present results suggested that dioscin inhibited skin cancer cell proliferation via adjusting ATM/p53-mediated cell apoptosis, migration and DNA damage, which should be considered as a potential option for future treatments of skin cancer.	dioscin	44-51	P53	Homo sapiens	111-114
26759239-6	2016	Consistently, prodigiosin induced activation of a p53-responsive luciferase reporter in colonospheres, Aldefluor(+) cells, and tumor xenografts.	Prodigiosin	14-25	P53	Homo sapiens	50-53
28802253-0	2017	The Combination of Metformin and Valproic Acid Induces Synergistic Apoptosis in the Presence of p53 and Androgen Signaling in Prostate Cancer.	Valproic Acid	33-46	P53	Homo sapiens	96-99
33323544-2	2020	The status of TP53 mutations played an essential role in the progression and the prognosis of MIBC.	4-METHYL-2-PENTANOL	94-98	P53	Homo sapiens	14-18
29200992-10	2017	On the other hand, O-TFDG induced HCT116 cells apoptosis mainly by increasing the expression of p53, p21, and cleaved caspase-3.	o-tfdg	19-25	P53	Homo sapiens	96-99
27053954-10	2016	In particular, 4-DACL treatment induced mitochondrial ROS, reduced NF-kappaB signaling activity and increased up-regulation of the cell cycle inhibitors cyclin-dependent kinase inhibitor p21 (p21(WAF1/Cip1)) and the tumor suppressor protein p53 in a dose-dependent manner, which was accompanied by decreased cell proliferation and apoptosis via the intrinsic pathway.	4-dacl	15-21	P53	Homo sapiens	241-244
26812881-0	2016	Hydroxyurea synergizes with valproic acid in wild-type p53 acute myeloid leukaemia.	Valproic Acid	28-41	P53	Homo sapiens	55-58
33323544-3	2020	The present study proposed to investigate the association between TP53 mutations and immunophenotype in MIBC.	4-METHYL-2-PENTANOL	104-108	P53	Homo sapiens	66-70
29126407-7	2017	RESULTS: Patients with Arg/Arg and Arg/Pro at codon 72 of TP53 had a higher complete response rate (61% vs. 44%, P = 0.007) than those with Pro/Pro.	Proline	39-42	P53	Homo sapiens	58-62
33321563-8	2021	In addition, ALA significantly enhanced radiation-induced cellular senescence, which was shown by increased HMGB1 expression in the cytosol fraction compared to the control, increased p53 expression compared to the control, activation of p38 as well as NF-kappaB, and G2/M cell cycle arrest.	Thioctic Acid	13-16	P53	Homo sapiens	184-187
28988496-7	2017	In addition, DNA damage-associated proteins (p53 and p-Chk2 (T68)) were significantly increased by the treatment of MEHP.	mono-(2-ethylhexyl)phthalate	116-120	P53	Homo sapiens	45-48
26718886-9	2016	The patients with a proline (Pro) polymorphism in SNP72 of TP53 showed significantly higher PrP-positive rates than those with arginine (Arg).	Proline	20-27	P53	Homo sapiens	59-63
26718886-9	2016	The patients with a proline (Pro) polymorphism in SNP72 of TP53 showed significantly higher PrP-positive rates than those with arginine (Arg).	Proline	29-32	P53	Homo sapiens	59-63
26728659-4	2016	METHODS: Neuroblastoma cell lines with different p53 genetic background were employed to determine the response on cell viability and apoptosis of low-dose of actinomycin D.	Dactinomycin	159-172	P53	Homo sapiens	49-52
33322048-5	2020	LCTP also induced the cell cycle arrest in G2/M phase, confirmed by decrease of CDK2 protein and increase of p53 and p21.	intybin	0-4	P53	Homo sapiens	109-112
26728659-6	2016	RESULTS: Low-dose actinomycin D treatment causes a reduction of cell viability in neuroblastoma cell lines and that this effect is stronger in cells that are wild-type for p53.	Dactinomycin	18-31	P53	Homo sapiens	172-175
26738694-2	2016	A common p53 Arg72Pro polymorphism resulting in the substitution of an arginine amino acid by proline amino acid in the transactivating domain has been demonstrated to affect p53 function.	proline amino acid	94-112	P53	Homo sapiens	9-12
26738694-2	2016	A common p53 Arg72Pro polymorphism resulting in the substitution of an arginine amino acid by proline amino acid in the transactivating domain has been demonstrated to affect p53 function.	proline amino acid	94-112	P53	Homo sapiens	175-178
28618116-0	2017	Differences in p53 status significantly influence the cellular response and cell survival to 1,25-dihydroxyvitamin D3-metformin cotreatment in colorectal cancer cells.	1,25-dihydroxyvitamin d3-metformin	93-127	P53	Homo sapiens	15-18
33302580-6	2020	The aim of our studies was to investigate the influence of low, non-toxic doses of diphenyleneiodonium chloride (DPI), a potent inhibitor of flavoenzymes including NADPH oxidases, on p53-proficient and p53-deficient HCT116 human colon cancer cells and MCF-7 breast cancer cells.	diphenyleneiodonium	83-111	P53	Homo sapiens	183-186
28797774-0	2017	Design, synthesis and biological evaluation of novel antitumor spirotetrahydrothiopyran-oxindole derivatives as potent p53-MDM2 inhibitors.	spirotetrahydrothiopyran-oxindole	63-96	P53	Homo sapiens	119-122
28797774-2	2017	Previously, we identified a new class of spirotetrahydrothiopyran-oxindole p53-MDM2 inhibitors by novel organocatalytic enantioselective cascade reactions.	spirotetrahydrothiopyran-oxindole	41-74	P53	Homo sapiens	75-78
26836165-5	2016	In the present study, we showed that Aluminum maltolate (Al-malt), a lipophilic Al complex which is a common component of human diet with the ability to facilitate the entry of Al into the brain, induced apoptosis in human neuroblastoma SH-SY5Y cells, along with downregulation of miR-19a/miR-19b, upregulation of miR-19-targeted PTEN, and alterations of its downstream apoptosis related proteins including AKT, p53, Bax, and Bcl-2.	Aluminum	37-39	P53	Homo sapiens	412-415
26836165-5	2016	In the present study, we showed that Aluminum maltolate (Al-malt), a lipophilic Al complex which is a common component of human diet with the ability to facilitate the entry of Al into the brain, induced apoptosis in human neuroblastoma SH-SY5Y cells, along with downregulation of miR-19a/miR-19b, upregulation of miR-19-targeted PTEN, and alterations of its downstream apoptosis related proteins including AKT, p53, Bax, and Bcl-2.	Aluminum	57-59	P53	Homo sapiens	412-415
33302580-6	2020	The aim of our studies was to investigate the influence of low, non-toxic doses of diphenyleneiodonium chloride (DPI), a potent inhibitor of flavoenzymes including NADPH oxidases, on p53-proficient and p53-deficient HCT116 human colon cancer cells and MCF-7 breast cancer cells.	diphenyleneiodonium	83-111	P53	Homo sapiens	202-205
29085386-5	2017	Dose-Time Network Identification (DTNI) was applied to gene sets from exposed primary human hepatocytes using four stress pathways, namely endoplasmic reticulum (ER), NF-kappaB, NRF2, and TP53.	dtni	34-38	P53	Homo sapiens	188-192
33302580-6	2020	The aim of our studies was to investigate the influence of low, non-toxic doses of diphenyleneiodonium chloride (DPI), a potent inhibitor of flavoenzymes including NADPH oxidases, on p53-proficient and p53-deficient HCT116 human colon cancer cells and MCF-7 breast cancer cells.	diphenyleneiodonium	113-116	P53	Homo sapiens	183-186
33302580-6	2020	The aim of our studies was to investigate the influence of low, non-toxic doses of diphenyleneiodonium chloride (DPI), a potent inhibitor of flavoenzymes including NADPH oxidases, on p53-proficient and p53-deficient HCT116 human colon cancer cells and MCF-7 breast cancer cells.	diphenyleneiodonium	113-116	P53	Homo sapiens	202-205
26785263-1	2016	BACKGROUND: In human papillomavirus (HPV)-induced carcinogenesis, the arginine (Arg) allele of the TP53 codon 72 polymorphism binds more efficiently to the HPV E6 oncoprotein than the proline (Pro) allele.	Proline	184-191	P53	Homo sapiens	99-103
33302580-7	2020	We demonstrated that the temporal treatment of HCT116 and MCF-7 cancer cells (both p53 wild-type) with DPI caused induction of senescence, that was correlated with decreased level of ROS and upregulation of p53/p21 proteins.	diphenyleneiodonium	103-106	P53	Homo sapiens	83-86
26785263-1	2016	BACKGROUND: In human papillomavirus (HPV)-induced carcinogenesis, the arginine (Arg) allele of the TP53 codon 72 polymorphism binds more efficiently to the HPV E6 oncoprotein than the proline (Pro) allele.	Proline	193-196	P53	Homo sapiens	99-103
28791403-10	2017	Among DLBCL cases, the TP53 mutations shortened both OS and PFS of patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) and decreased both OS and PFS of patients with secondary DLBCL disease.	Vincristine	139-150	P53	Homo sapiens	23-27
33302580-7	2020	We demonstrated that the temporal treatment of HCT116 and MCF-7 cancer cells (both p53 wild-type) with DPI caused induction of senescence, that was correlated with decreased level of ROS and upregulation of p53/p21 proteins.	diphenyleneiodonium	103-106	P53	Homo sapiens	207-210
32886187-0	2020	Mutagenicity of acrylamide and glycidamide in human TP53 knock-in (Hupki) mouse embryo fibroblasts.	glycidamide	31-42	P53	Homo sapiens	52-56
29212196-5	2017	Juglanin promoted apoptosis in lung cancer cells through increasing Caspase-3 and poly ADP-ribose polymerase (PARP) cleavage, which is regulated by TNF-related apoptosis-inducing ligand/Death receptors (TRAIL/DRs) relied on p53 activation.	juglanin	0-8	P53	Homo sapiens	224-227
27019558-13	2016	CONCLUSIONS: These results indicated that treatment with LER-induced cell death in mitochondrial apoptosis pathway by regulating pro-apoptotic proteins via the up regulation of the p53 protein.	ler	57-60	P53	Homo sapiens	181-184
29299182-3	2017	In this study, we report 3 cases of elderly patients with treatment-naive, TP53 un-mutated HCLv, who were effectively treated with four cycles of bendamustine plus rituximab.	Bendamustine Hydrochloride	146-158	P53	Homo sapiens	75-79
32886187-7	2020	Mutations induced by glycidamide occurred at specific TP53 codons that have also been found to be mutated in human tumours (i.e., breast, ovary, colorectal, and lung) previously associated with acrylamide exposure.	glycidamide	21-32	P53	Homo sapiens	54-58
29299182-7	2017	In this work, bendamustine plus rituximab proved to be an effective and feasible first-line treatment strategy for elderly patients with TP53 un-mutated HCLv.	Bendamustine Hydrochloride	14-26	P53	Homo sapiens	137-141
32886187-8	2020	The spectrum of TP53 mutations was further reflected by the mutations detected by whole-genome sequencing (WGS) and a distinct WGS mutational signature was found in HUF clones treated with glycidamide that was again characterised by A > G/T > C and A > T/T > A mutations.	glycidamide	189-200	P53	Homo sapiens	16-20
28937626-0	2017	Aspalathin Reverts Doxorubicin-Induced Cardiotoxicity through Increased Autophagy and Decreased Expression of p53/mTOR/p62 Signaling.	aspalathin	0-10	P53	Homo sapiens	110-113
28937626-4	2017	Aspalathin, a polyphenolic dihydrochalcone C-glucoside has been shown to activate AMPK while decreasing the expression of p53.	aspalathin	0-10	P53	Homo sapiens	122-125
25975351-5	2015	Our data show that BI 2536 and GSK461364 increased the population of cells in the G2/M phase compared with controls, while treatment with poloxin and thymoquinone increased cell population in the S phase as well as in G2/M, in a p53-independent manner.	thymoquinone	150-162	P53	Homo sapiens	229-232
32950500-0	2020	Targeting DNA and mutant p53 by a naphthalimide derivative, NA20, exhibits selective inhibition in gastric tumorigenesis by blocking mutant p53-EGFR signaling pathway.	na20	60-64	P53	Homo sapiens	25-28
26520021-8	2015	The support l-tyrosine Sepharose used in chromatographic experiments promotes the separation of native pVAX1-LacZ and pcDNA3-FLAG-p53 samples (oc+sc) by decreasing the salt concentration.	Sepharose	23-32	P53	Homo sapiens	130-133
26556860-0	2015	The Hsp90 inhibitor SNX-7081 is synergistic with fludarabine nucleoside via DNA damage and repair mechanisms in human, p53-negative chronic lymphocytic leukemia.	SNX-7081	20-28	P53	Homo sapiens	119-122
26556860-0	2015	The Hsp90 inhibitor SNX-7081 is synergistic with fludarabine nucleoside via DNA damage and repair mechanisms in human, p53-negative chronic lymphocytic leukemia.	fludarabine nucleoside	49-71	P53	Homo sapiens	119-122
26556860-2	2015	We previously showed that the Hsp90 inhibitor, SNX-7081, synergizes with and restores sensitivity to fludarabine nucleoside (2-FaraA) in human chronic lymphocytic leukemia (CLL) cells with lesions in the p53 pathway (Best OG, et al., Leukemia Lymphoma 53:1367-75, 2012).	SNX-7081	47-55	P53	Homo sapiens	204-207
26556860-8	2015	These results provide valuable insight into the synergistic mechanism between SNX-7081 and 2-FaraA that may provide an alternative treatment for CLL patients with p53 mutations, for whom therapeutic options are currently limited.	SNX-7081	78-86	P53	Homo sapiens	163-166
28771332-6	2017	To address these problems, we have constructed a PA platform consisting of cathepsin-B cleavable PAs in which a selective p53-based inhibitory peptide is cleaved from its lipid tail within endosomes, allowing for intracellular peptide accumulation and extracellular recycling of the lipid moiety.	Protactinium	49-51	P53	Homo sapiens	122-125
26208523-11	2015	These data indicate that the DACH carrier ligand in oxaliplatin triggers signaling via the p53-miR-34a-E2F axis, leading to transcriptional regulation that ultimately results in accumulation of dUTP and reduced dTTP biosynthesis, potentially enhancing 5-FU cytotoxicity.	1,2-cyclohexanediamine	29-33	P53	Homo sapiens	91-94
28870911-7	2017	Mechanistically, blocking of de novo RNA synthesis by actinomycin D significantly inhibited sunitinib-induced expression of p53 mRNA, but not that of caspase-3, indicating involvement of a transcriptional mechanism.	Dactinomycin	54-67	P53	Homo sapiens	124-127
32950500-0	2020	Targeting DNA and mutant p53 by a naphthalimide derivative, NA20, exhibits selective inhibition in gastric tumorigenesis by blocking mutant p53-EGFR signaling pathway.	na20	60-64	P53	Homo sapiens	140-143
32950500-3	2020	We show here that gain-of-function p53 mutation in gastric cancer cells promotes tumorigenesis by enhancing p53-EGFR (epidermal growth factor receptor) signaling pathway, and such process can be blocked by small molecule NA20, a naphthalimide derivative that exhibited selective inhibition in p53 mutant gastric cancer cell lines.	na20	221-225	P53	Homo sapiens	35-38
32950500-3	2020	We show here that gain-of-function p53 mutation in gastric cancer cells promotes tumorigenesis by enhancing p53-EGFR (epidermal growth factor receptor) signaling pathway, and such process can be blocked by small molecule NA20, a naphthalimide derivative that exhibited selective inhibition in p53 mutant gastric cancer cell lines.	na20	221-225	P53	Homo sapiens	108-111
32950500-3	2020	We show here that gain-of-function p53 mutation in gastric cancer cells promotes tumorigenesis by enhancing p53-EGFR (epidermal growth factor receptor) signaling pathway, and such process can be blocked by small molecule NA20, a naphthalimide derivative that exhibited selective inhibition in p53 mutant gastric cancer cell lines.	na20	221-225	P53	Homo sapiens	108-111
28463795-0	2017	Cisatracurium-induced proliferation impairment and death of colorectal cancer cells, HCT116 is mediated by p53 dependent intrinsic apoptotic pathway in vitro.	cisatracurium	0-13	P53	Homo sapiens	107-110
26090767-12	2015	CONCLUSION: The p53-related apoptosis pathway and transforming growth factor-beta1-mediated signaling may be important factors used to predict and evaluate the treatment outcomes of 5-aminolevulinic acid-based photodynamic therapy used in hypertrophic scar patients.	5-amino levulinic acid	182-203	P53	Homo sapiens	16-19
32950500-4	2020	We found that targeting DNA and blocking the mutant p53-drived carcinogenicity accounted for the primary antitumor effect of NA20 in gastric tumor models.	na20	125-129	P53	Homo sapiens	52-55
28463795-8	2017	Western blot analysis indicated remarkable concentration dependent alterations in the expression of proliferation and survival proteins CD1, E2F, CE1, p53, p21, BAX, BCL-2, cytochrome C and cleaved PARP in cisatracurium-treated groups as compared with the untreated group.	cisatracurium	206-219	P53	Homo sapiens	151-154
28463795-10	2017	Thus, cisatracurium effectively inhibited proliferation and induced apoptosis of HCT116 cells in vitro at least via alteration of p53-dependent apoptotic pathway.	cisatracurium	6-19	P53	Homo sapiens	130-133
33220534-4	2020	In the presence of target gene (mutant human p53 gene fragment), the H-bonds between fullerenol and ssDNA were competitively depleted during the base pairing process of complete hybridization between ssDNA and target, making double-stranded DNA-AuNPs (dsDNA-AuNPs) depart so that the photocurrent powerfully recovered.	fullerenol	85-95	P53	Homo sapiens	45-48
28498637-7	2017	Our data suggest that the p53-dependent, chemotherapeutics-induced cytotoxicity in cervical cancer cells may be compromised by catecholamines-induced upregulation of the Sirt1 expression through activating the beta2-AR signaling.	Catecholamines	127-141	P53	Homo sapiens	26-29
26384650-5	2015	An increase of phospho-Thr in the p53 TXR motif was confirmed in the cells overexpressing G2019S, and human induced pluripotent stem (iPS) cells of a G2019S carrier.	Phosphothreonine	15-26	P53	Homo sapiens	34-37
33224889-0	2020	Beyond the Mevalonate Pathway: Control of Post-Prenylation Processing by Mutant p53.	Mevalonic Acid	11-21	P53	Homo sapiens	80-83
26347142-7	2015	Up-regulation of apoptotic genes (e.g. p53, bax/bcl2 ratio, caspase-3 &amp;caspase-9) along with loss of mitochondrial membrane potential suggested that Al-doped ZnO nanoparticles induced apoptosis in MCF-7 cells through mitochondrial pathway.	Aluminum	153-155	P53	Homo sapiens	39-42
28402954-8	2017	Interestingly, inhibition of lysosomal degradation using hydroxychloroquine (HCQ) induced expression of the tumor suppressor p53, promoted apoptosis, and inhibited HCC growth, whereas activation of autophagy using an mTOR inhibitor (Torin1) promoted HCC growth.	Hydroxychloroquine	57-75	P53	Homo sapiens	125-128
28402954-8	2017	Interestingly, inhibition of lysosomal degradation using hydroxychloroquine (HCQ) induced expression of the tumor suppressor p53, promoted apoptosis, and inhibited HCC growth, whereas activation of autophagy using an mTOR inhibitor (Torin1) promoted HCC growth.	Hydroxychloroquine	77-80	P53	Homo sapiens	125-128
33224889-3	2020	An unexpected aspect of mutant p53 function was uncovered by showing that some mutants can increase the malignant phenotype of tumor cells through alteration of the mevalonate pathway.	Mevalonic Acid	165-175	P53	Homo sapiens	31-34
28410239-0	2017	Homoharringtonine suppresses imatinib resistance via the Bcl-6/p53 pathway in chronic myeloid leukemia cell lines.	Homoharringtonine	0-17	P53	Homo sapiens	63-66
26183023-8	2015	While KAISO enhances p53-dependent apoptosis by increasing APAF1 gene expression, RelA/p65 decreases apoptosis by blocking interaction between KAISO and p53.	kaiso	6-11	P53	Homo sapiens	21-24
33224889-7	2020	Instead, wild type p53 acts in the opposite way, downregulating mevalonate pathway genes and ICMT.	Mevalonic Acid	64-74	P53	Homo sapiens	19-22
33216844-2	2020	In published xenograft studies, TRC102 enhanced the antitumor effect of temozolomide regardless of cell line genetic characteristics, e.g., O6-methylguanine DNA methyltransferase (MGMT), mismatch repair (MMR), or p53 status.	methoxyamine	32-38	P53	Homo sapiens	213-216
26116623-0	2015	C6 ceramide dramatically increases vincristine sensitivity both in vivo and in vitro, involving AMP-activated protein kinase-p53 signaling.	Vincristine	35-46	P53	Homo sapiens	125-128
26116623-3	2015	In vitro, C6 and vincristine coadministration induced substantial necrosis and apoptosis in multiple human cancer cell lines, which were accompanied by a profound AMP-activated protein kinase (AMPK) activation, subsequent p53 activation, mTORC1 inactivation and Bcl-2/HIF-1alpha downregulation.	Vincristine	17-28	P53	Homo sapiens	222-225
26116623-8	2015	Together, C6 sensitizes vincristine-induced anticancer activity in vivo and in vitro, involving activating AMPK-p53 signaling.	Vincristine	24-35	P53	Homo sapiens	112-115
28366825-0	2017	Novel quinuclidinone derivatives induced apoptosis in human breast cancer via targeting p53.	1-azabicyclo[2.2.2]octan-2-one	6-20	P53	Homo sapiens	88-91
32947166-8	2020	Moreover, the acetazolamide/cisplatin combination could decrease the level of PCNA but increase the level of p53; decrease the ratio of Bcl-2/Bax and increase the expression of caspase-3 compared with the single drug treated group.	Acetazolamide	14-27	P53	Homo sapiens	109-112
26113084-9	2015	Taken together, our findings highlight p53 status in pancreatic cancer as a biomarker to predict sensitivity to LDH-A inhibition, with regard to both real-time noninvasive imaging by 13C MRS as well as therapeutic response.	13c	183-186	P53	Homo sapiens	39-42
33079785-13	2022	CONCLUSION: P53 may serve as a diagnostic marker for de-novo HCC after DAAs therapy.	daas	71-75	P53	Homo sapiens	12-15
25991017-0	2015	Rotenone affects p53 transcriptional activity and apoptosis via targeting SIRT1 and H3K9 acetylation in SH-SY5Y cells.	Rotenone	0-8	P53	Homo sapiens	17-20
25991017-3	2015	In this study, we found that rotenone treatment decreased cell viability, induced apoptosis, reduced SIRT1 level, and promoted p53 expression.	Rotenone	29-37	P53	Homo sapiens	127-130
32896741-9	2020	In addition, our data revealed that our novel efficiently damage the genomic DNA of colorectal cells involving P53 dependent mechanism using DPA assay.	dpa	141-144	P53	Homo sapiens	111-114
26060937-5	2015	Notably, all new compounds were more toxic than their cyclometallated precursor bearing two chlorido ligands, and the derivative bearing one phosphane ligand presented the most promising toxicity profile in our in vitro screening, displaying a p53 dependent activity in colorectal cancer HCT116 cells.	phosphine	141-150	P53	Homo sapiens	244-247
32431164-0	2020	Apoptotic and cell cycle response to homoharringtonine and harringtonine in wild and mutant p53 hepatocarcinoma cells.	Homoharringtonine	37-54	P53	Homo sapiens	92-95
25232917-8	2015	Patients with homozygous Arg/arg at codon 72 of P53 had a better median OS months than Arg/Pro and Pro/Pro (13.4 vs. 8.4 vs. 1.5 months, respectively; P = 0.045).	Proline	91-94	P53	Homo sapiens	48-51
25232917-8	2015	Patients with homozygous Arg/arg at codon 72 of P53 had a better median OS months than Arg/Pro and Pro/Pro (13.4 vs. 8.4 vs. 1.5 months, respectively; P = 0.045).	Proline	99-102	P53	Homo sapiens	48-51
25232917-8	2015	Patients with homozygous Arg/arg at codon 72 of P53 had a better median OS months than Arg/Pro and Pro/Pro (13.4 vs. 8.4 vs. 1.5 months, respectively; P = 0.045).	Proline	99-102	P53	Homo sapiens	48-51
33041795-0	2020	Thymoquinone Selectively Induces Hepatocellular Carcinoma Cell Apoptosis in Synergism With Clinical Therapeutics and Dependence of p53 Status.	thymoquinone	0-12	P53	Homo sapiens	131-134
25818185-11	2015	Finally, pretreatment of cells with DMY prior to H2O2 exposure resulted in the inhibition of p53 activation, followed by the regulation of the expression of Bcl-2 and Bax, the release of cytochrome c, the cleavage (activation) of caspase-9 and caspase-3, and then the suppression of PARP cleavage in H2O2-induced HUVECs.	dihydromyricetin	36-39	P53	Homo sapiens	93-96
25743928-5	2015	Here we present the effects of tributyltin chloride (TBT-Cl) and triphenyltin chloride (TPT-Cl) on cell proliferation, expression of proapoptotic p53, Bax, and antiapoptotic Bcl-2 proteins in human breast cancer MCF-7 cell line.	triphenyltin chloride	65-86	P53	Homo sapiens	146-149
25743928-5	2015	Here we present the effects of tributyltin chloride (TBT-Cl) and triphenyltin chloride (TPT-Cl) on cell proliferation, expression of proapoptotic p53, Bax, and antiapoptotic Bcl-2 proteins in human breast cancer MCF-7 cell line.	triphenyltin chloride	88-94	P53	Homo sapiens	146-149
33041795-10	2020	Furthermore, TQ-stimulated increase of reactive oxygen species (ROS) in p53-depleted cells was more pronounced than that in cells with intact p53.	thymoquinone	13-15	P53	Homo sapiens	72-75
33041795-10	2020	Furthermore, TQ-stimulated increase of reactive oxygen species (ROS) in p53-depleted cells was more pronounced than that in cells with intact p53.	thymoquinone	13-15	P53	Homo sapiens	142-145
32467171-0	2020	DNA replication stress induced by trifluridine determines tumor cell fate according to p53 status.	Trifluridine	34-46	P53	Homo sapiens	87-90
32640976-13	2020	Furthermore, chloroquine inhibited proliferation and promoted apoptosis and oxidative stress of SRA01/04 cells by activating ATM/p53 signaling pathway.	Chloroquine	13-24	P53	Homo sapiens	129-132
32711437-12	2020	Significant increased risk of lung cancer was found with Arg/Pro genotypes of TP53, Lys/Gln and Gln/Gln variants of XPD in individuals with family history of cancer (OR=3.44; 95% CI=1.36-8.72; p=0.011; OR=3.17; 95% CI=1.20-8.39; p=0.024; OR=16.35; 95% CI=0.92-289.5; p=0.007, respectively).	Proline	61-64	P53	Homo sapiens	78-82
32592343-1	2020	BACKGROUND: A transversion missense polymorphism of the TP53 tumor suppressor gene at the codon 72 codes proline instead of arginine causes an altered p53 protein expression and has been found to be associated with an elevated risk of various cancer; especially breast and lung cancer.	Proline	105-112	P53	Homo sapiens	56-60
32592343-1	2020	BACKGROUND: A transversion missense polymorphism of the TP53 tumor suppressor gene at the codon 72 codes proline instead of arginine causes an altered p53 protein expression and has been found to be associated with an elevated risk of various cancer; especially breast and lung cancer.	Proline	105-112	P53	Homo sapiens	151-154
32547191-11	2020	Western blot results showed that DIOS significantly suppressed the expression levels of Bcl-2, cdc2, cyclinB1, and promoted the expression levels of Bax, cleaved-caspase3, cleaved-caspase8, cleaved-PARP, Bak, P53, and P21.	diosmetin	33-37	P53	Homo sapiens	209-212
32391458-10	2020	Experimental data suggest that CeO2 treatment causes DNA fragmentation through enhanced generation of ROS, which ultimately leads to cellular apoptosis through the p53-dependent mitochondrial signaling pathway.	ceric oxide	31-35	P53	Homo sapiens	164-167
32213586-4	2020	Intriguingly, expressions of proline biosynthesis PYCR gene and proline degradation PRODH gene are up-regulated directly by c-Myc oncoprotein and p53 tumor suppressor, respectively, suggesting that the proline-P5C metabolic axis is a key checkpoint for tumor cell growth.	Proline	29-36	P53	Homo sapiens	146-149
32213586-4	2020	Intriguingly, expressions of proline biosynthesis PYCR gene and proline degradation PRODH gene are up-regulated directly by c-Myc oncoprotein and p53 tumor suppressor, respectively, suggesting that the proline-P5C metabolic axis is a key checkpoint for tumor cell growth.	Proline	64-71	P53	Homo sapiens	146-149
32213586-4	2020	Intriguingly, expressions of proline biosynthesis PYCR gene and proline degradation PRODH gene are up-regulated directly by c-Myc oncoprotein and p53 tumor suppressor, respectively, suggesting that the proline-P5C metabolic axis is a key checkpoint for tumor cell growth.	Proline	64-71	P53	Homo sapiens	146-149
31707450-12	2020	P53 protein expression in AGS cells also decreased significantly with FLX treatment.	Fluoxetine	70-73	P53	Homo sapiens	0-3
31682781-6	2020	In the current study, treatment of A594 cells with Pb significantly induced cell apoptosis as evidenced by increased the percentage of cells underwent apoptosis determined by flow cytometry and increased p53 mRNA and induced oxidative stress by increasing the formation of reactive oxygen species and decreasing GSTA1 mRNA levels.	Lead	51-53	P53	Homo sapiens	204-207
32110174-12	2020	Moreover, Sirt1 knockdown abolished these ameliorative effects of PSPC on apoptosis and P53 acetylation and protein expression in PA-treated L02 cells.	Protactinium	130-132	P53	Homo sapiens	88-91
31855686-4	2020	More importantly, then UCNPs(BTZ)@mSiO2-H2A/p53 induced specific and efficient apoptotic cell death in p53-null cancer cells and restored the functional activity of tumor suppressor p53 by the success of co-delivery of BTZ/p53.	bortezomib	29-32	P53	Homo sapiens	44-47
31855686-4	2020	More importantly, then UCNPs(BTZ)@mSiO2-H2A/p53 induced specific and efficient apoptotic cell death in p53-null cancer cells and restored the functional activity of tumor suppressor p53 by the success of co-delivery of BTZ/p53.	bortezomib	29-32	P53	Homo sapiens	103-106
31855686-4	2020	More importantly, then UCNPs(BTZ)@mSiO2-H2A/p53 induced specific and efficient apoptotic cell death in p53-null cancer cells and restored the functional activity of tumor suppressor p53 by the success of co-delivery of BTZ/p53.	bortezomib	29-32	P53	Homo sapiens	103-106
31855686-4	2020	More importantly, then UCNPs(BTZ)@mSiO2-H2A/p53 induced specific and efficient apoptotic cell death in p53-null cancer cells and restored the functional activity of tumor suppressor p53 by the success of co-delivery of BTZ/p53.	bortezomib	29-32	P53	Homo sapiens	103-106
31855686-4	2020	More importantly, then UCNPs(BTZ)@mSiO2-H2A/p53 induced specific and efficient apoptotic cell death in p53-null cancer cells and restored the functional activity of tumor suppressor p53 by the success of co-delivery of BTZ/p53.	bortezomib	219-222	P53	Homo sapiens	44-47
31855686-4	2020	More importantly, then UCNPs(BTZ)@mSiO2-H2A/p53 induced specific and efficient apoptotic cell death in p53-null cancer cells and restored the functional activity of tumor suppressor p53 by the success of co-delivery of BTZ/p53.	bortezomib	219-222	P53	Homo sapiens	103-106
31855686-4	2020	More importantly, then UCNPs(BTZ)@mSiO2-H2A/p53 induced specific and efficient apoptotic cell death in p53-null cancer cells and restored the functional activity of tumor suppressor p53 by the success of co-delivery of BTZ/p53.	bortezomib	219-222	P53	Homo sapiens	103-106
31855686-4	2020	More importantly, then UCNPs(BTZ)@mSiO2-H2A/p53 induced specific and efficient apoptotic cell death in p53-null cancer cells and restored the functional activity of tumor suppressor p53 by the success of co-delivery of BTZ/p53.	bortezomib	219-222	P53	Homo sapiens	103-106
31855686-5	2020	Moreover, the transfection with UCNPs(BTZ)@mSiO2-H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO2/p53.	bortezomib	38-41	P53	Homo sapiens	53-56
31855686-5	2020	Moreover, the transfection with UCNPs(BTZ)@mSiO2-H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO2/p53.	bortezomib	38-41	P53	Homo sapiens	60-63
31855686-5	2020	Moreover, the transfection with UCNPs(BTZ)@mSiO2-H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO2/p53.	bortezomib	38-41	P53	Homo sapiens	60-63
31855686-5	2020	Moreover, the transfection with UCNPs(BTZ)@mSiO2-H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO2/p53.	bortezomib	38-41	P53	Homo sapiens	60-63
31855686-5	2020	Moreover, the transfection with UCNPs(BTZ)@mSiO2-H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO2/p53.	bortezomib	205-208	P53	Homo sapiens	53-56
28328238-5	2017	Western blot results showed that the expression of p53 protein was increased following treatment with VPA.	Valproic Acid	102-105	P53	Homo sapiens	51-54
31855686-5	2020	Moreover, the transfection with UCNPs(BTZ)@mSiO2-H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO2/p53.	bortezomib	205-208	P53	Homo sapiens	60-63
31855686-5	2020	Moreover, the transfection with UCNPs(BTZ)@mSiO2-H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO2/p53.	bortezomib	205-208	P53	Homo sapiens	60-63
31855686-5	2020	Moreover, the transfection with UCNPs(BTZ)@mSiO2-H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO2/p53.	bortezomib	205-208	P53	Homo sapiens	60-63
31855686-5	2020	Moreover, the transfection with UCNPs(BTZ)@mSiO2-H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO2/p53.	bortezomib	205-208	P53	Homo sapiens	53-56
31855686-5	2020	Moreover, the transfection with UCNPs(BTZ)@mSiO2-H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO2/p53.	bortezomib	205-208	P53	Homo sapiens	60-63
27061924-0	2017	Idelalisib-Rituximab induces clinical remissions in patients with TP53 disrupted B cell prolymphocytic leukaemia.	idelalisib	0-10	P53	Homo sapiens	66-70
31855686-5	2020	Moreover, the transfection with UCNPs(BTZ)@mSiO2-H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO2/p53.	bortezomib	205-208	P53	Homo sapiens	60-63
31855686-5	2020	Moreover, the transfection with UCNPs(BTZ)@mSiO2-H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO2/p53.	bortezomib	205-208	P53	Homo sapiens	60-63
31855686-7	2020	The results here suggested that the as-developed UCNPs(BTZ)@mSiO2-H2A/p53 nanoplatform with coordinating biocompatibility, UCL image, and sustained release manner might be desirable gene/drug codelivery nanocarrier for clinical cancer therapy.	bortezomib	55-58	P53	Homo sapiens	70-73
28140474-13	2017	PL significantly reduced the p53 (-80%), p21 (-84%), and Ki-67 (-48%) positive cells.	pl	0-2	P53	Homo sapiens	29-32
32039016-15	2019	Apoptosis of BTZ-sensitive cells was correlating with induction of p53 and NOXA.	bortezomib	13-16	P53	Homo sapiens	67-70
28400988-7	2017	More importantly, we found that Delta133p53 played a negative role in p53 stimulation of DNA pol gamma activity when studied in d4T-treated and d4T-untreated mitochondrial extracts.	Stavudine	128-131	P53	Homo sapiens	40-43
28400988-7	2017	More importantly, we found that Delta133p53 played a negative role in p53 stimulation of DNA pol gamma activity when studied in d4T-treated and d4T-untreated mitochondrial extracts.	Stavudine	144-147	P53	Homo sapiens	40-43
28258507-7	2017	Herein we report on the effect of unmodified and neutron activated phosphine ruthenium II complexes on glioblastoma cell lines carrying wild-type and mutated p53 tumor suppressor gene.	phosphine	67-76	P53	Homo sapiens	158-161
28258507-9	2017	The phosphine ruthenium II complexes tested were highly active against glioblastoma cell lines inducing cell death both through apoptosis and autophagy in a p53 independent fashion.	phosphine	4-13	P53	Homo sapiens	157-160
32039016-17	2019	Conclusions: We identified low sXBP1 levels and TP53 abnormalities as factors correlating with bortezomib resistance in MM.	bortezomib	95-105	P53	Homo sapiens	48-52
32039016-18	2019	Therefore, determination of sXBP1 levels and TP53 status prior to BTZ treatment in MM may be beneficial to predict BTZ resistance.	bortezomib	115-118	P53	Homo sapiens	45-49
31690451-1	2020	The p53 protein plays a number of roles in protecting organisms from different genotoxic stresses and this includes DNA damage induced by acetaldehyde, a metabolite of alcohol.	Acetaldehyde	138-150	P53	Homo sapiens	4-7
28004224-10	2017	Moreover, TBBE and TBWE treated MCF-7, HeLa and U87 cells showed upregulation of p53 and p21 proteins.	tbwe	19-23	P53	Homo sapiens	81-84
28336971-8	2017	When bound to RARgamma, acacetin prevents RARgamma from its activation of AKT followed by recovery of the normal p53 signaling.	acacetin	24-32	P53	Homo sapiens	113-116
32223728-0	2020	Diosmetin Induces Apoptosis by Downregulating AKT Phosphorylation via P53 Activation in Human Renal Carcinoma ACHN Cells.	diosmetin	0-9	P53	Homo sapiens	70-73
28250973-8	2017	Although MPP+-induced death and ferroptosis shared some features, such as occurrence of lipid peroxidation and inhibition by Fer-1, MPP+-induced death seemed to be distinct from ferroptosis because MPP+-induced death (but not ferroptosis) was inhibited by Nec-1, was independent of p53, and was accompanied by ATP depletion and mitochondrial swelling.	mangion-purified polysaccharide (Candida albicans)	132-136	P53	Homo sapiens	282-285
32223728-8	2020	In addition, it was observed that the anticancer effect of DIOS was significantly enhanced by the p53 activator, but inhibited by the p53 inhibitor.	diosmetin	59-63	P53	Homo sapiens	98-101
32223728-8	2020	In addition, it was observed that the anticancer effect of DIOS was significantly enhanced by the p53 activator, but inhibited by the p53 inhibitor.	diosmetin	59-63	P53	Homo sapiens	134-137
32223728-9	2020	CONCLUSION: Our data suggested that DIOS induced apoptosis in renal carcinoma ACHN cells by reducing AKT phosphorylation through p53 upregulation.	diosmetin	36-40	P53	Homo sapiens	129-132
31863007-4	2019	Here, we identify PBRM1 as a reader for p53 acetylation on lysine 382 (K382Ac) through its bromodomain 4 (BD4).	Potassium	71-77	P53	Homo sapiens	40-43
28081035-11	2017	CONCLUSION: The data implies that p53 can excise incorrect sugar in addition to base mispairs, thereby expanding the role of p53 in the repair of nucleic acids replication errors.	Sugars	59-64	P53	Homo sapiens	34-37
28081035-11	2017	CONCLUSION: The data implies that p53 can excise incorrect sugar in addition to base mispairs, thereby expanding the role of p53 in the repair of nucleic acids replication errors.	Sugars	59-64	P53	Homo sapiens	125-128
31863007-5	2019	Notably, mutations on key residues of BD4 disrupt recognition of p53 K382Ac.	Potassium	69-75	P53	Homo sapiens	65-68
31751125-7	2019	Utilizing RNA-Seq techniques, gene expression profiling followed by pathway enrichment analysis revealed several major biological pathways perturbed by DMSe-derived SOA, including elevated genotoxicity, DNA damage, and p53-mediated stress responses, as well as downregulated cholesterol biosynthesis, glycolysis and interleukin IL-4/IL-13 signaling.	dimethylselenide	152-156	P53	Homo sapiens	219-222
27993707-10	2017	Moreover, MDM2 knockdown or p53 over-expression could induce the cleaved Caspase 3 expression and blocked the protective effects of PC in primary cultured spinal cord neurons against OGD-reperfusion injury.	pc	132-134	P53	Homo sapiens	28-31
27993707-11	2017	In conclusion, our work demonstrated that MDM2-p53 pathway plays a pivotal role in the protective effect of PC against OGD-reperfusion injury and PC may be a feasible therapy strategy in the treatment for spinal cord I/R injury.	pc	108-110	P53	Homo sapiens	47-50
31777420-6	2019	We also found that NC significantly affected the p53/Bim signaling axis, which was accompanied by mitochondrial membrane depolarization and cytochrome c release from the mitochondria into the cytosol.	nitidine	19-21	P53	Homo sapiens	49-52
27604683-4	2017	METHOD: Here, p53 mutant/Wild-type cells were employed to study the toxicity of DNC using MTT assay, Flow cytometry and Annexin-V, Real-time PCR and Western blot were used to analyze p53, BAX, Bcl-2, p21 and Noxa changes after treatment.	dnc	80-83	P53	Homo sapiens	14-17
31683960-7	2019	Treatment of MDA-MB-231 cells with fruit ethyl acetate fraction (RSF EtOAc) increased expression 11of P53, Bax and activation of caspase 3/7.	ethyl acetate	41-54	P53	Homo sapiens	102-105
27768124-5	2017	The human Tp53 gene harbors a common single-nucleotide polymorphism (SNP) at codon 72, which yields an arginine-to-proline amino-acidic substitution (Arg72Pro) that modulates the apoptotic activity of the p53 protein.	Proline	115-122	P53	Homo sapiens	10-14
27768124-5	2017	The human Tp53 gene harbors a common single-nucleotide polymorphism (SNP) at codon 72, which yields an arginine-to-proline amino-acidic substitution (Arg72Pro) that modulates the apoptotic activity of the p53 protein.	Proline	115-122	P53	Homo sapiens	11-14
31612051-9	2019	When assessing the underlying molecular mechanism, it was revealed that PPI and PPVII enhanced DDP-induced apoptosis in A549/DDP cells via p53 upregulation and the caspase-dependent pathway.	2-dimethylaminoethyl(dimethylamido)phosphonofluoridate	95-98	P53	Homo sapiens	139-142
28848088-6	2017	In the present paper we aim to characterize the combined effects of 64CuCl2 and SI113 on human GBM cell lines with variable p53 expression.	CHEMBL1775042	80-85	P53	Homo sapiens	124-127
31525915-3	2019	In a malignant breast cancer cell line, it can be observed that oxidative stress-triggered nuclear co-translocations of heme and ferritin may lead to direct molecular contact of ferritin with p53, to pass heme to p53, which subsequently sequestered into the cytoplasm, therefore forming a possible new route of tumor survival under oxidative stress, by using the stress to circumvent oxidative stress-induced apoptosis.	Heme	120-124	P53	Homo sapiens	192-195
27813686-0	2017	The Telomerase Activity of Selenium-Induced Human Umbilical Cord Mesenchymal Stem Cells Is Associated with Different Levels of c-Myc and p53 Expression.	Selenium	27-35	P53	Homo sapiens	137-140
27813686-3	2017	Here, we find out whether the effect of sodium selenite and selenomethionine on telomerase activity in human umbilical cord-derived mesenchymal stem cells (hUCMSCs) is associated with different levels of c-Myc and p53 expression.	Selenomethionine	60-76	P53	Homo sapiens	214-217
27813686-4	2017	The use of different staining methods including ethidium bromide/acridine orange and DAPI in addition to telomeric repeat amplification protocol assay and real-time PCR indicated that different forms of selenium have opposite impacts on c-Myc and p53 expressions in both hUCMSCs and AGS, a gastric adenocarcinoma cell line, as a positive control.	Selenium	203-211	P53	Homo sapiens	247-250
27814589-6	2017	Our results indicate that Parathion causes ER stress, up regulates the expression of GRP78, leads to nuclear localization of p53 and induces autophagy while Rotenone down regulates GRP78, causes cytoplasmic localization of p53 and inhibits autophagy.	Rotenone	157-165	P53	Homo sapiens	223-226
27822577-6	2016	The result of the cell viability assay on p53-mutant H1299 cells showed that the half-maximum inhibiting concentration (IC50) of HMSN-PEI-BTZ-p53 was 51% or 25% of that for HMSN-BTZ in 72 or 96 h treatment, respectively.	hmsn-btz	173-181	P53	Homo sapiens	42-45
27822577-6	2016	The result of the cell viability assay on p53-mutant H1299 cells showed that the half-maximum inhibiting concentration (IC50) of HMSN-PEI-BTZ-p53 was 51% or 25% of that for HMSN-BTZ in 72 or 96 h treatment, respectively.	hmsn-btz	173-181	P53	Homo sapiens	142-145
31525915-3	2019	In a malignant breast cancer cell line, it can be observed that oxidative stress-triggered nuclear co-translocations of heme and ferritin may lead to direct molecular contact of ferritin with p53, to pass heme to p53, which subsequently sequestered into the cytoplasm, therefore forming a possible new route of tumor survival under oxidative stress, by using the stress to circumvent oxidative stress-induced apoptosis.	Heme	120-124	P53	Homo sapiens	213-216
31525915-4	2019	The observed peroxidase-like activity of ferritin-heme and p53-heme complexes may also contribute to survival.	Heme	63-67	P53	Homo sapiens	59-62
31581454-7	2019	GS treatment also induced expression of p53 protein while p21 expression was unaltered with no cell cycle arrest.	pregna-4,17-diene-3,16-dione	0-2	P53	Homo sapiens	40-43
27784901-0	2016	Targeting mutant p53 through the mevalonate pathway.	Mevalonic Acid	33-43	P53	Homo sapiens	17-20
27784901-2	2016	Inhibition of the mevalonate pathway is now shown to promote degradation of select oncogenic mutant p53 proteins, indicating that destabilization of mutant p53 could be a promising therapeutic strategy.	Mevalonic Acid	18-28	P53	Homo sapiens	100-103
27784901-2	2016	Inhibition of the mevalonate pathway is now shown to promote degradation of select oncogenic mutant p53 proteins, indicating that destabilization of mutant p53 could be a promising therapeutic strategy.	Mevalonic Acid	18-28	P53	Homo sapiens	156-159
31546954-0	2019	Proteomic Analysis of miR-195 and miR-497 Replacement Reveals Potential Candidates that Increase Sensitivity to Oxaliplatin in MSI/P53wt Colorectal Cancer Cells.	oxaliplatin	112-123	P53	Homo sapiens	131-134
27464825-6	2016	The GABN model of the p53-signaling pathway in response to gamma-irradiation has also been simulated in the current paper to provide an indirect validation of the proposed schema.	gabn	4-8	P53	Homo sapiens	22-25
31546954-6	2019	Cell viability analysis of transfected cells revealed increased sensitivity to oxaliplatin in microsatellite instable (MSI)/P53 wild-type HCT116 and RKO cells.	oxaliplatin	79-90	P53	Homo sapiens	124-127
31546954-10	2019	In conclusion, miR-195-5p and miR-497-5p replacement enhanced sensitivity to oxaliplatin in treatment naive MSI/P53 wild-type CRC cells.	oxaliplatin	77-88	P53	Homo sapiens	112-115
31518420-0	2019	An oral second-generation proteasome inhibitor oprozomib significantly inhibits lung cancer in a p53 independent manner in vitro.	ONX 0912	47-56	P53	Homo sapiens	97-100
27686769-8	2016	Further, in the exposed group, the MN frequencies were lower in TP53 rs1042522 CG and CG+GG genotype carriers((3.63+-2.61)% and(3.66+-2.61)%, respectively)than in TP53 rs1042522 CC genotype carriers(3.95+-3.06)%(FR=0.87 and 0.90; 95% CI: 0.83-0.96 and 0.84-0.97, respectively).	cysteinylglycine	79-81	P53	Homo sapiens	64-68
27686769-8	2016	Further, in the exposed group, the MN frequencies were lower in TP53 rs1042522 CG and CG+GG genotype carriers((3.63+-2.61)% and(3.66+-2.61)%, respectively)than in TP53 rs1042522 CC genotype carriers(3.95+-3.06)%(FR=0.87 and 0.90; 95% CI: 0.83-0.96 and 0.84-0.97, respectively).	cysteinylglycine	86-88	P53	Homo sapiens	163-167
31399545-5	2019	TP53 facilitated ARF6 activation by platelet-derived growth factor (PDGF), via its known function to promote the expression of PDGF receptor beta (PDGFRbeta) and enzymes of the mevalonate pathway (MVP).	Mevalonic Acid	177-187	P53	Homo sapiens	0-4
27698449-7	2016	A tetracycline-inducible lentiviral expression system containing shRNA to p53 was used to knockout p53.	Tetracycline	2-14	P53	Homo sapiens	74-77
27698449-7	2016	A tetracycline-inducible lentiviral expression system containing shRNA to p53 was used to knockout p53.	Tetracycline	2-14	P53	Homo sapiens	99-102
31047842-12	2019	Upon restoration of WT-TP53 activity in MIA-PaCa-2 cells, an altered sensitivity to the combination of certain NAX compounds and metformin was observed compared to the parental cells which normally lack WT-TP53.	nax compounds	111-124	P53	Homo sapiens	23-27
31366086-0	2019	Lipoic Acid Synergizes with Antineoplastic Drugs in Colorectal Cancer by Targeting p53 for Proteasomal Degradation.	Thioctic Acid	0-11	P53	Homo sapiens	83-86
27651634-8	2016	The present study of p53 gene regulation analyzed the expression of 279-bp bands on 1.5 agarose gel.	Sepharose	88-95	P53	Homo sapiens	21-24
27698880-8	2016	The present study suggested the role of DPPT as a novel chemotherapeutic drug for human PCa, which may function through the Akt/p53/Bax/PTEN signaling pathway.	deoxypodophyllotoxin	40-44	P53	Homo sapiens	128-131
31260310-5	2019	Treatment with jorunnamycin A (0.05-0.5 muM) altered the expression of p53 and Bcl-2 family proteins, particularly causing the down-regulation of antiapoptosis Bcl-2 and Mcl-1 proteins.	jorunnamycin A	15-29	P53	Homo sapiens	71-74
27729773-0	2016	Andrographolide promotes vincristine-induced SK-NEP-1 tumor cell death via PI3K-AKT-p53 signaling pathway.	Vincristine	25-36	P53	Homo sapiens	84-87
31354481-0	2019	A Novel Indolizine Derivative Induces Apoptosis Through the Mitochondria p53 Pathway in HepG2 Cells.	indolizine	8-18	P53	Homo sapiens	73-76
27267810-0	2016	Harnessing Fluorine-Sulfur Contacts and Multipolar Interactions for the Design of p53 Mutant Y220C Rescue Drugs.	Sulfur	20-26	P53	Homo sapiens	82-85
31334116-0	2019	Ruthenium Complexes With Piplartine Cause Apoptosis Through MAPK Signaling by a p53-Dependent Pathway in Human Colon Carcinoma Cells and Inhibit Tumor Development in a Xenograft Model.	Ruthenium	0-9	P53	Homo sapiens	80-83
31334116-5	2019	In addition, co-treatment with a p53 inhibitor (cyclic pifithrin-alpha) and the ruthenium complexes significantly reduced the apoptosis rate in HCT116 cells, and increased phospho-p53 (S15) and phospho-histone H2AX (S139) expressions, indicating induction of DNA damage and p53-dependent apoptosis.	Ruthenium	80-89	P53	Homo sapiens	33-36
27302066-7	2016	Treatment of cells with Nutlin-3 or low concentrations of actinomycin D resulted in a strong elevation of CerS6 mRNA and protein, thus demonstrating that CerS6 is a component of the non-genotoxic p53-dependent cellular stress response.	Dactinomycin	58-71	P53	Homo sapiens	196-199
31334116-5	2019	In addition, co-treatment with a p53 inhibitor (cyclic pifithrin-alpha) and the ruthenium complexes significantly reduced the apoptosis rate in HCT116 cells, and increased phospho-p53 (S15) and phospho-histone H2AX (S139) expressions, indicating induction of DNA damage and p53-dependent apoptosis.	Ruthenium	80-89	P53	Homo sapiens	180-183
27154500-0	2016	Synthesis of intracellular reduction-sensitive amphiphilic polyethyleneimine and poly(epsilon-caprolactone) graft copolymer for on-demand release of doxorubicin and p53 plasmid DNA.	copolymer	114-123	P53	Homo sapiens	165-168
27154500-10	2016	Finally, the co-delivery of Dox and p53-pDNA using the copolymer displayed greater cytotoxic effect compared with the Dox-loaded nanoparticle counterpart as revealed by cell viability and Caspase 3 expression assay.	copolymer	55-64	P53	Homo sapiens	36-39
27154500-16	2016	In addition, the co-delivery of doxorubicin and p53 plasmid DNA using the new copolymer displayed greater cytotoxic effect compared with single agent (i.e. Dox) loaded counterpart, which indicated the significance of rapid dissociation of therapeutic agents from the carrier for synergistic cytotoxic effects on cancer cells.	copolymer	78-87	P53	Homo sapiens	48-51
27283770-6	2016	Moreover, MGCD-induced apoptosis was decreased by inhibition of p53 using short interfering RNA (siRNA), suggesting that p53 was required for MGCD-induced cell apoptosis.	mocetinostat	10-14	P53	Homo sapiens	64-67
31334116-5	2019	In addition, co-treatment with a p53 inhibitor (cyclic pifithrin-alpha) and the ruthenium complexes significantly reduced the apoptosis rate in HCT116 cells, and increased phospho-p53 (S15) and phospho-histone H2AX (S139) expressions, indicating induction of DNA damage and p53-dependent apoptosis.	Ruthenium	80-89	P53	Homo sapiens	180-183
27283770-6	2016	Moreover, MGCD-induced apoptosis was decreased by inhibition of p53 using short interfering RNA (siRNA), suggesting that p53 was required for MGCD-induced cell apoptosis.	mocetinostat	10-14	P53	Homo sapiens	121-124
31128065-0	2019	TP53 Gene 72 Arg/Pro (rs1042522) Single Nucleotide Polymorphism Contribute to Increase the Risk of B-Chronic Lymphocytic Leukemia in the Sudanese Population Objective: This study aimed at exploring the association of TP53 72Arg/Pro polymorphism and Risk of ChronicLymphocytic Leukemia and to assess the correlation between TP53 72Arg/Pro polymorphism and clinical parameter,hematological profile and some biological prognostic markers among Sudanese patients with chronic lymphocyticleukemia.	Proline	17-20	P53	Homo sapiens	0-4
27283770-6	2016	Moreover, MGCD-induced apoptosis was decreased by inhibition of p53 using short interfering RNA (siRNA), suggesting that p53 was required for MGCD-induced cell apoptosis.	mocetinostat	142-146	P53	Homo sapiens	64-67
27283770-6	2016	Moreover, MGCD-induced apoptosis was decreased by inhibition of p53 using short interfering RNA (siRNA), suggesting that p53 was required for MGCD-induced cell apoptosis.	mocetinostat	142-146	P53	Homo sapiens	121-124
27283770-8	2016	Collectively, our data revealed that MGCD induced p53-dependent cell apoptosis following formation of multipolar spindles in NPC cells, suggesting the therapeutic potential of combinations of HDACs and MDM2 inhibitors for NPC treatment.	mocetinostat	37-41	P53	Homo sapiens	50-53
27445491-0	2016	Histone deacetylase inhibitor sodium butyrate suppresses proliferation and promotes apoptosis in osteosarcoma cells by regulation of the MDM2-p53 signaling.	Butyric Acid	30-45	P53	Homo sapiens	142-145
31128065-0	2019	TP53 Gene 72 Arg/Pro (rs1042522) Single Nucleotide Polymorphism Contribute to Increase the Risk of B-Chronic Lymphocytic Leukemia in the Sudanese Population Objective: This study aimed at exploring the association of TP53 72Arg/Pro polymorphism and Risk of ChronicLymphocytic Leukemia and to assess the correlation between TP53 72Arg/Pro polymorphism and clinical parameter,hematological profile and some biological prognostic markers among Sudanese patients with chronic lymphocyticleukemia.	Proline	17-20	P53	Homo sapiens	217-221
31128065-0	2019	TP53 Gene 72 Arg/Pro (rs1042522) Single Nucleotide Polymorphism Contribute to Increase the Risk of B-Chronic Lymphocytic Leukemia in the Sudanese Population Objective: This study aimed at exploring the association of TP53 72Arg/Pro polymorphism and Risk of ChronicLymphocytic Leukemia and to assess the correlation between TP53 72Arg/Pro polymorphism and clinical parameter,hematological profile and some biological prognostic markers among Sudanese patients with chronic lymphocyticleukemia.	Proline	17-20	P53	Homo sapiens	217-221
31210846-8	2019	The RNA polymerase I inhibitor cx-5461 induced apoptosis, ROS production, and proliferative inhibition in the HASMCs, which was partly attenuated by p53 knockout.	CX 5461	31-38	P53	Homo sapiens	149-152
27317992-6	2016	Furthermore, dioscin significantly decreased the expression levels of FasL, Fas, p53, Bak, Caspase-3/9, and upregulated Bcl-2 level through decreasing IRF9 level against apoptosis.	dioscin	13-20	P53	Homo sapiens	81-84
31015501-7	2019	A radiation resistance mutation in cep-1, the p53 orthologue, that is deficient in double strand break repair of DNA and is also deficient in apoptosis causes radiation-resistance results but sensitivity toward phosphine.	phosphine	211-220	P53	Homo sapiens	46-49
27176768-3	2016	The present study observed that cell proliferation of HepG2 cells was inhibited by Dio treatment and tumor protein p53 was significantly increased following Dio treatment.	diosmetin	157-160	P53	Homo sapiens	115-118
27376811-2	2016	The change from an arginine (Arg) to a proline (Pro) at codon 72 can influence the biological activity of p53, which predisposes to an increased risk of recurrent spontaneous abortion (RSA).	Proline	39-46	P53	Homo sapiens	106-109
27376811-2	2016	The change from an arginine (Arg) to a proline (Pro) at codon 72 can influence the biological activity of p53, which predisposes to an increased risk of recurrent spontaneous abortion (RSA).	Proline	48-51	P53	Homo sapiens	106-109
27376811-7	2016	There was a significant association between p53 polymorphism at codon 72 and RSA in recessive model (Pro/Pro vs. Pro/Arg+Arg/Arg; OR=1.60, 95% CI: 1.14-2.24) and co-dominant model (Pro/Pro vs. Arg/Arg; OR=1.47, 95% CI: 1.02-2.12) whether the study that was deviated from HWE was eliminated or not.	Proline	101-104	P53	Homo sapiens	44-47
27376811-7	2016	There was a significant association between p53 polymorphism at codon 72 and RSA in recessive model (Pro/Pro vs. Pro/Arg+Arg/Arg; OR=1.60, 95% CI: 1.14-2.24) and co-dominant model (Pro/Pro vs. Arg/Arg; OR=1.47, 95% CI: 1.02-2.12) whether the study that was deviated from HWE was eliminated or not.	Proline	105-108	P53	Homo sapiens	44-47
27376811-7	2016	There was a significant association between p53 polymorphism at codon 72 and RSA in recessive model (Pro/Pro vs. Pro/Arg+Arg/Arg; OR=1.60, 95% CI: 1.14-2.24) and co-dominant model (Pro/Pro vs. Arg/Arg; OR=1.47, 95% CI: 1.02-2.12) whether the study that was deviated from HWE was eliminated or not.	Proline	105-108	P53	Homo sapiens	44-47
27376811-7	2016	There was a significant association between p53 polymorphism at codon 72 and RSA in recessive model (Pro/Pro vs. Pro/Arg+Arg/Arg; OR=1.60, 95% CI: 1.14-2.24) and co-dominant model (Pro/Pro vs. Arg/Arg; OR=1.47, 95% CI: 1.02-2.12) whether the study that was deviated from HWE was eliminated or not.	Proline	105-108	P53	Homo sapiens	44-47
30833076-2	2019	Recent findings suggested that the mutation of tumor suppressor gene p53 promoted lipids synthesis and mutant p53 (mutp53) was essential for regulating mevalonate pathway for cholesterol synthesis.	Mevalonic Acid	152-162	P53	Homo sapiens	69-72
27376811-7	2016	There was a significant association between p53 polymorphism at codon 72 and RSA in recessive model (Pro/Pro vs. Pro/Arg+Arg/Arg; OR=1.60, 95% CI: 1.14-2.24) and co-dominant model (Pro/Pro vs. Arg/Arg; OR=1.47, 95% CI: 1.02-2.12) whether the study that was deviated from HWE was eliminated or not.	Proline	105-108	P53	Homo sapiens	44-47
30833076-2	2019	Recent findings suggested that the mutation of tumor suppressor gene p53 promoted lipids synthesis and mutant p53 (mutp53) was essential for regulating mevalonate pathway for cholesterol synthesis.	Mevalonic Acid	152-162	P53	Homo sapiens	110-113
27136267-8	2016	Masking H3.3 Ser31P by antibody microinjection prevents nuclear p53 accumulation in the aneuploid daughters.	ser31p	13-19	P53	Homo sapiens	64-67
30833076-5	2019	Our data demonstrated that suppression of mevalonate pathway by simvastatin significantly upregulated Kruppel-like factor 2 (KLF2) and p21WAF1/CIP1 expression in mutp53 colon cancer cells SW1116 but not in p53 wild type cells HCT116.	Mevalonic Acid	42-52	P53	Homo sapiens	165-168
27109480-7	2016	Both CQ and AQ elevated the transcription level of p21 though the activation of p53, but also blocked p21 protein degradation in the presence of cycloheximide, causing p21 protein accumulation mainly in the nucleus.	Chloroquine	5-7	P53	Homo sapiens	80-83
30378157-3	2019	Cell viability assay showed that GA-DM was relatively more toxic to LNCaP cells than to PC-3 cells (IC50 s ranged 45-55 microM for PC-3, and 20-25 microM for LNCaP), which may have occurred due to differential expression of p53.	3,7-dioxolanosta-8,24-dien-26-oic acid	33-38	P53	Homo sapiens	224-227
26619844-5	2016	Increased cervical cancer risks were also found in the TP53 Arg72Pro under a heterozygous comparison and overdominant model (CG vs. GG: adjusted OR = 1.44, 95 % CI = 1.06-1.95; CG vs. GG/CC: adjusted OR = 1.47, 95 % CI = 1.12-1.94, respectively).	cysteinylglycine	125-127	P53	Homo sapiens	55-59
26619844-5	2016	Increased cervical cancer risks were also found in the TP53 Arg72Pro under a heterozygous comparison and overdominant model (CG vs. GG: adjusted OR = 1.44, 95 % CI = 1.06-1.95; CG vs. GG/CC: adjusted OR = 1.47, 95 % CI = 1.12-1.94, respectively).	cysteinylglycine	177-179	P53	Homo sapiens	55-59
26619844-8	2016	Combined analysis revealed that the genotypes of rs4938723 CT/CC and TP53 Arg72Pro CG/CC had an increased cervical cancer risk (OR = 2.21, 95 % CI = 1.38-3.53).	cysteinylglycine	83-85	P53	Homo sapiens	69-73
30542116-5	2019	Treatment of neuroblastoma cells with quarfloxin or CX-5461, two small molecule inhibitors of RNA polymerase I, suppressed MycN expression, induced DNA damage, and activated p53 followed by cell cycle arrest or apoptosis.	CX 5461	52-59	P53	Homo sapiens	174-177
26773055-5	2016	Here we show that accumulation of unrepaired SSBs triggers a p53/Sp1-dependent downregulation of APE1, the endonuclease responsible for the DNA incision during BER.	ssbs	45-49	P53	Homo sapiens	61-64
30418550-0	2019	Urolithin A gains in antiproliferative capacity by reducing the glycolytic potential via the p53/TIGAR axis in colon cancer cells.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	0-11	P53	Homo sapiens	93-96
27040702-5	2016	Patients with a del(17p) or TP53 mutation should be treated with the kinase inhibitors ibrutinib or a combination of idelalisib and rituximab.	idelalisib	117-127	P53	Homo sapiens	28-32
30418550-5	2019	Urolithin A induced p53 stabilization and p53 target gene expression, and absence of p53 significantly dampened the antiproliferative effect of urolithin A (IC50(p53-/-) = 38 microM).	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	0-11	P53	Homo sapiens	20-23
30418550-5	2019	Urolithin A induced p53 stabilization and p53 target gene expression, and absence of p53 significantly dampened the antiproliferative effect of urolithin A (IC50(p53-/-) = 38 microM).	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	0-11	P53	Homo sapiens	42-45
26934645-5	2016	Furthermore, SKi or ABC294640 or fenretinide increase the expression of the senescence markers, p53 and p21 in LNCaP-AI prostate cancer cells.	Fenretinide	33-44	P53	Homo sapiens	96-99
30418550-5	2019	Urolithin A induced p53 stabilization and p53 target gene expression, and absence of p53 significantly dampened the antiproliferative effect of urolithin A (IC50(p53-/-) = 38 microM).	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	0-11	P53	Homo sapiens	42-45
26848703-14	2016	In conclusion, thymoquinone increased the effectiveness of the chemotherapeutic reagent topotecan by inhibiting proliferation and lowering toxicity through p53- and Bax/Bcl2-independent mechanisms.	thymoquinone	15-27	P53	Homo sapiens	156-159
30418550-5	2019	Urolithin A induced p53 stabilization and p53 target gene expression, and absence of p53 significantly dampened the antiproliferative effect of urolithin A (IC50(p53-/-) = 38 microM).	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	0-11	P53	Homo sapiens	42-45
30418550-7	2019	Moreover, extracellular flux analyses and knockdown approaches uncovered a reduced glycolytic potential via the p53/TIGAR axis which was linked to the higher susceptibility of wildtype cells to urolithin A.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	194-205	P53	Homo sapiens	112-115
30765875-6	2019	RESULTS: Using a proteomic approach, we have shown that Notch3 is strongly involved in brivanib resistance through a p53-dependent regulation of enzymes of the tricarboxylic acid (TCA), both in vitro and in vivo.	brivanib	87-95	P53	Homo sapiens	117-120
26440049-0	2016	Alpha-linolenic acid regulates Cox2/VEGF/MAP kinase pathway and decreases the expression of HPV oncoproteins E6/E7 through restoration of p53 and Rb expression in human cervical cancer cell lines.	alpha-Linolenic Acid	0-20	P53	Homo sapiens	138-141
26440049-6	2016	Most importantly, ALA reduced the expression of HPV onco-proteins E6 and E7, resulting into restoration of expression of tumor suppressor proteins, p53 and Rb.	alpha-Linolenic Acid	18-21	P53	Homo sapiens	148-151
30782173-10	2019	In a luciferase assay, hypericin-PDT treatment was able to activate the promoter activity of Bax and p53, resulting in enhanced expression of Bax and p53 proteins.	hypericin	23-32	P53	Homo sapiens	101-104
30782173-10	2019	In a luciferase assay, hypericin-PDT treatment was able to activate the promoter activity of Bax and p53, resulting in enhanced expression of Bax and p53 proteins.	hypericin	23-32	P53	Homo sapiens	150-153
30465996-1	2019	We have successfully encapsulated two proteins, bovine serum albumin (BSA) and p53, in chitosan-tripolyphosphate (TPP) nanoparticles at various pH values from 5.5 to 6.5 and delivered the particles to human melanoma cells.	chitosan-tripolyphosphate	114-117	P53	Homo sapiens	79-82
30465996-5	2019	The method we describe appears to be a general method for delivery of proteins to cells using chitosan-TPP nanoparticles as a drug delivery system, since structurally unrelated proteins such as BSA and p53 with different isoelectrical points can be encapsulated in the chitosan-TPP nanoparticles and be effectively internalized by the cells.	chitosan-tripolyphosphate	103-106	P53	Homo sapiens	202-205
30465996-5	2019	The method we describe appears to be a general method for delivery of proteins to cells using chitosan-TPP nanoparticles as a drug delivery system, since structurally unrelated proteins such as BSA and p53 with different isoelectrical points can be encapsulated in the chitosan-TPP nanoparticles and be effectively internalized by the cells.	chitosan-tripolyphosphate	278-281	P53	Homo sapiens	202-205
30483736-3	2019	The current study identified a potential pathway by revealing that TRAIL and 6-sho or chloroquine acted together to trigger reactive oxygen species (ROS) production, to upregulate tumor-suppressor protein 53 (p53) expression and to change the mitochondrial transmembrane potential (MTP).	Chloroquine	86-97	P53	Homo sapiens	209-212
30261716-0	2019	Cis-3-O-p-hydroxycinnamoyl Ursolic Acid Induced ROS-Dependent p53-Mediated Mitochondrial Apoptosis in Oral Cancer Cells.	DTXSID80639812	0-39	P53	Homo sapiens	62-65
25961931-4	2016	In the present study we exposed a series of p53 wild-type human cancer cell lines to drugs such as actinomycin D (ActD), doxorubicin, 5-fluorouracil and CX-5461, which hinder ribosomal RNA (rRNA) synthesis.	Dactinomycin	99-112	P53	Homo sapiens	44-47
25961931-4	2016	In the present study we exposed a series of p53 wild-type human cancer cell lines to drugs such as actinomycin D (ActD), doxorubicin, 5-fluorouracil and CX-5461, which hinder ribosomal RNA (rRNA) synthesis.	Dactinomycin	114-118	P53	Homo sapiens	44-47
26768586-10	2016	Over-expression of p53 suppressed the inhibitory effects of GB on NOX4 and p66(shc) expression and superoxide generation and the protective effects of GB on loss of cell viability and apoptosis associated with cisplatin.	ginkgolide B	151-153	P53	Homo sapiens	19-22
26768586-12	2016	GB significantly increased miR214 expression and inhibition of miR214 suppressed the inhibitory effects of GB on p53, NOX4 and p66(shc) expression and superoxide generation and the protective effects of GB against cisplatin-induced cytotoxicity.	ginkgolide B	107-109	P53	Homo sapiens	113-116
26768586-12	2016	GB significantly increased miR214 expression and inhibition of miR214 suppressed the inhibitory effects of GB on p53, NOX4 and p66(shc) expression and superoxide generation and the protective effects of GB against cisplatin-induced cytotoxicity.	ginkgolide B	107-109	P53	Homo sapiens	113-116
26768586-13	2016	We demonstrate that GB decreases superoxide generation and the subsequent apoptosis through reduction of p53-mediated NOX4/p66(shc) pathway via up-regulation of miR214, resulting in attenuation of cisplatin-induced cytotoxicity.	ginkgolide B	20-22	P53	Homo sapiens	105-108
30289354-0	2019	Alpha ketoglutarate levels, regulated by p53 and OGDH, determine autophagy and cell fate/apoptosis in response to Nutlin-3a.	Ketoglutaric Acids	0-19	P53	Homo sapiens	41-44
27075390-5	2016	Also the expression of P53 becomes upregulated with time of DPCPX treatment.	1,3-dipropyl-8-cyclopentylxanthine	60-65	P53	Homo sapiens	23-26
27075390-7	2016	CONCLUSION: DPCPX can induce P53 expression which consequently promotes the cell apoptosis in MCF-7.	1,3-dipropyl-8-cyclopentylxanthine	12-17	P53	Homo sapiens	29-32
30607176-8	2018	The genotypic distribution at codon 72 of TP53 in control group was 20%, 62.4% and 16.6% for Arg (wildtype), Arg/Pro (heterozygous) and Pro (homozygous variant) respectively.	Proline	113-116	P53	Homo sapiens	42-46
26188904-0	2015	TLR2 22 (-196-174) significantly increases the risk of breast cancer in females carrying proline allele at codon 72 of TP53 gene: a case-control study from four ethnic groups of North Eastern region of India.	Proline	89-96	P53	Homo sapiens	119-123
30218352-7	2018	The data showed that ALA treatment promoted a dose-dependent increase of p53 expression, downregulation of Bcl-2, HMG-CoA reductase and OGG1 and an increase in lipoperoxidation.	5-amino levulinic acid	21-24	P53	Homo sapiens	73-76
26469958-0	2015	p53 regulates the mevalonate pathway in human glioblastoma multiforme.	Mevalonic Acid	18-28	P53	Homo sapiens	0-3
26312825-0	2015	AMPK/p53 Axis Is Essential for alpha-Lipoic Acid-Regulated Metastasis in Human and Mouse Colon Cancer Cells.	Thioctic Acid	31-48	P53	Homo sapiens	5-8
30265530-0	2018	N-O Reduction and ROS-Mediated AKT/FOXO1 and AKT/P53 Pathways Are Involved in Growth Promotion and Cytotoxicity of Cyadox.	cyadox	115-121	P53	Homo sapiens	49-52
26312825-8	2015	Finally, we observed that ALA activates p53 and AMPK signaling pathways in human and mouse colon cancer cells.	Thioctic Acid	26-29	P53	Homo sapiens	40-43
26312825-9	2015	We found for the first time that ALA suppresses cell proliferation and malignant potential via p53 and AMPK signaling pathways in human and mouse colon cancer cells.	Thioctic Acid	33-36	P53	Homo sapiens	95-98
29524194-12	2018	Moreover, a low-Se diet downregulated (P &lt; 0.05) the level of Bcl-2 and upregulated (P &lt; 0.05) the levels of Bax, Bak, Cyt-C, Caspase-9, Caspase-3, and p53.	Selenium	16-18	P53	Homo sapiens	158-161
30555549-5	2018	Using a D-peptide p53 activator (DPA) as a proof of concept, we synthesized, functionalized and characterized gold- and DPA-based nanoparticles termed AuNP-DPA.	dpa	33-36	P53	Homo sapiens	18-21
26320861-2	2015	A cell-based, high-throughput small-molecule screen identified chetomin (CTM) as a mutant p53 R175H reactivator.	chetomin	63-71	P53	Homo sapiens	90-93
26320861-2	2015	A cell-based, high-throughput small-molecule screen identified chetomin (CTM) as a mutant p53 R175H reactivator.	chetomin	73-76	P53	Homo sapiens	90-93
26320861-3	2015	CTM enabled p53 to transactivate target genes, restored MDM2 negative regulation, and selectively inhibited the growth of cancer cells harboring mutant p53 R175H in vitro and in vivo.	chetomin	0-3	P53	Homo sapiens	12-15
26320861-3	2015	CTM enabled p53 to transactivate target genes, restored MDM2 negative regulation, and selectively inhibited the growth of cancer cells harboring mutant p53 R175H in vitro and in vivo.	chetomin	0-3	P53	Homo sapiens	152-155
30555549-5	2018	Using a D-peptide p53 activator (DPA) as a proof of concept, we synthesized, functionalized and characterized gold- and DPA-based nanoparticles termed AuNP-DPA.	dpa	120-123	P53	Homo sapiens	18-21
26320861-4	2015	We found that CTM binds to Hsp40 and increases the binding capacity of Hsp40 to the p53 R175H mutant protein, causing a potential conformational change to a wild-type-like p53.	chetomin	14-17	P53	Homo sapiens	84-87
26320861-4	2015	We found that CTM binds to Hsp40 and increases the binding capacity of Hsp40 to the p53 R175H mutant protein, causing a potential conformational change to a wild-type-like p53.	chetomin	14-17	P53	Homo sapiens	172-175
30555549-5	2018	Using a D-peptide p53 activator (DPA) as a proof of concept, we synthesized, functionalized and characterized gold- and DPA-based nanoparticles termed AuNP-DPA.	dpa	120-123	P53	Homo sapiens	18-21
26320861-5	2015	Thus, CTM acts as a specific reactivator of the p53 R175H mutant form through Hsp40.	chetomin	6-9	P53	Homo sapiens	48-51
30243491-9	2018	Parent genes of these DEAS play a important role in regulating CRC-related processes such as protein kinase activity (FDR&lt;0.0001), PI3K-Akt signaling pathway (FDR = 0.0024) and p53 signaling pathway (FDR = 0.0143).	Diethyl 2-acetylsuccinate	22-26	P53	Homo sapiens	180-183
26405550-6	2015	Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P&lt;0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC.	Proline	262-269	P53	Homo sapiens	40-43
30066888-3	2018	CTB-1-treated DLD-1, COLO 201 and HCT-116 (WT p53 and p53 null) colon cancer cells and CCD 841 CoN normal colon epithelial cells were assessed for changes in survival using MTT assay.	cinnamtannin B-1	0-5	P53	Homo sapiens	46-49
26345416-10	2015	Overall, this study suggested caspase-dependent activation of both the intrinsic and extrinsic signaling pathways, probably through blockade of the SIRT1/p53-mediated mitochondrial and Akt pathways to exert the proapoptotic effect of CCF-NLs in DBTRG-05MG GBM cells.	dbtrg	245-250	P53	Homo sapiens	154-157
30066888-3	2018	CTB-1-treated DLD-1, COLO 201 and HCT-116 (WT p53 and p53 null) colon cancer cells and CCD 841 CoN normal colon epithelial cells were assessed for changes in survival using MTT assay.	cinnamtannin B-1	0-5	P53	Homo sapiens	54-57
26070487-3	2015	Through an unbiased genome-wide ChIP-seq analysis, we have found that 5-lipoxygenase (ALOX5, 5-LO) which is a key enzyme of leukotriene (LT) biosynthesis, is a direct target gene of p53 and its expression is induced by genotoxic stress via actinomycin D (Act.D) or etoposide (Eto) treatment.	Dactinomycin	240-253	P53	Homo sapiens	182-185
29665004-5	2018	Combined treatment of thiostrepton and cycloheximide/chloroquine prevented the degradation of mutant p53 protein, reinforcing autophagy as the means of mutant p53 destabilization.	Chloroquine	53-64	P53	Homo sapiens	101-104
25991017-6	2015	In conclusion, our data indicate that rotenone promotes p53 transcription and apoptosis through targeting SIRT1 and H3K9.	Rotenone	38-46	P53	Homo sapiens	56-59
29665004-5	2018	Combined treatment of thiostrepton and cycloheximide/chloroquine prevented the degradation of mutant p53 protein, reinforcing autophagy as the means of mutant p53 destabilization.	Chloroquine	53-64	P53	Homo sapiens	159-162
30197671-10	2018	Zerumbone can inhibit the proliferation and induce apoptosis of esophageal cancer EC-109 cells, and its induction of apoptosis may be realized through upregulating the mRNA expression of P53 and downregulating the mRNA expression of Bcl-2, and upregulating the protein expression of P53 and downregulating the protein expression of Bcl-2.	zerumbone	0-9	P53	Homo sapiens	187-190
26196503-3	2015	Especially basic esters, which are positively charged under physiological conditions, were in the crystal violet and the MTT assay up to approximately 100 times more effective than bendamustine, paralleled by a higher fraction of early apoptotic cancer cells and increased expression of p53.	Esters	17-23	P53	Homo sapiens	287-290
26196503-3	2015	Especially basic esters, which are positively charged under physiological conditions, were in the crystal violet and the MTT assay up to approximately 100 times more effective than bendamustine, paralleled by a higher fraction of early apoptotic cancer cells and increased expression of p53.	Bendamustine Hydrochloride	181-193	P53	Homo sapiens	287-290
26070072-13	2015	Computational modeling suggested that a p53 tetramer containing two wild-type p53 molecules and two C176F mutated molecules can maintain the structural stability and interactions with DNA by formation of additional hydrophobic and cation-pi interactions which compensate for the loss of sulphur-zinc coordination.	Sulfur	287-294	P53	Homo sapiens	40-43
30197671-10	2018	Zerumbone can inhibit the proliferation and induce apoptosis of esophageal cancer EC-109 cells, and its induction of apoptosis may be realized through upregulating the mRNA expression of P53 and downregulating the mRNA expression of Bcl-2, and upregulating the protein expression of P53 and downregulating the protein expression of Bcl-2.	zerumbone	0-9	P53	Homo sapiens	283-286
25964547-4	2015	Western blotting indicated that DMC suppressed the protein levels associated with DNA damage and repair, such as 14-3-3sigma (an important checkpoint keeper of DNA damage response), DNA repair proteins breast cancer 1, early onset (BRCA1), O6-methylguanine-DNA methyltransferase (MGMT), mediator of DNA damage checkpoint 1 (MDC1), and p53 (tumor suppressor protein).	demethoxycurcumin	32-35	P53	Homo sapiens	335-338
25964547-5	2015	DMC activated phosphorylated p53 and p-H2A.X (phospho Ser140) in NCI-H460 cells.	demethoxycurcumin	0-3	P53	Homo sapiens	29-32
30106571-9	2018	p53-dependence of Ru-NO complexes [3]Cl2 and [4]Cl2 was studied and p53-independent mode of action was confirmed.	ru-no	18-23	P53	Homo sapiens	0-3
25964547-7	2015	The results showed that DMC promotes the translocation of p-p53 and p-H2A.X from the cytosol to the nuclei in NCI-H460 cells.	demethoxycurcumin	24-27	P53	Homo sapiens	60-63
30106571-9	2018	p53-dependence of Ru-NO complexes [3]Cl2 and [4]Cl2 was studied and p53-independent mode of action was confirmed.	[3]cl2	34-40	P53	Homo sapiens	0-3
30221528-12	2018	Moreover, after 24 hours of exposure to hypericin with MDA- MB-231 IC50 concentration, the expression of P53 and P21 genes upregulated in MDA-MB-175-VII much more than MDA-MB-231 when both cell lines were treated with 24 hours IC50 dose of MDA-MB-231.	hypericin	40-49	P53	Homo sapiens	105-108
25681668-0	2015	The synergistic effect of combination temozolomide and chloroquine treatment is dependent on autophagy formation and p53 status in glioma cells.	Chloroquine	55-66	P53	Homo sapiens	117-120
25681668-2	2015	The late autophagy inhibitor chloroquine (CQ) inhibits glioblastoma tumors in a p53-independent and p53-dependent manner.	Chloroquine	29-40	P53	Homo sapiens	80-83
30221528-14	2018	CONCLUSION: The results of this study demonstrated that hypericin"s apoptotic and cytotoxic effects on cancer cells may be mediated via P53 overexpression, cell cycle arrest and the subsequent apoptosis.	hypericin	56-65	P53	Homo sapiens	136-139
25681668-2	2015	The late autophagy inhibitor chloroquine (CQ) inhibits glioblastoma tumors in a p53-independent and p53-dependent manner.	Chloroquine	29-40	P53	Homo sapiens	100-103
29842899-4	2018	To stimulate p53 in synergistic fashion, we exposed A549 lung cancer cells to actinomycin D and nutlin-3a (A + N).	Dactinomycin	78-91	P53	Homo sapiens	13-16
25681668-2	2015	The late autophagy inhibitor chloroquine (CQ) inhibits glioblastoma tumors in a p53-independent and p53-dependent manner.	Chloroquine	42-44	P53	Homo sapiens	80-83
25681668-2	2015	The late autophagy inhibitor chloroquine (CQ) inhibits glioblastoma tumors in a p53-independent and p53-dependent manner.	Chloroquine	42-44	P53	Homo sapiens	100-103
25681668-4	2015	Combination treatment of U87 cell (wild type p53) with TMZ and CQ synergistically reduced cell proliferation and enhanced apoptosis, with increased sub-G1 hypodiploid cells and caspase activation.	Chloroquine	63-65	P53	Homo sapiens	45-48
25681668-12	2015	Our data support the beneficial effect of combination treatment with TMZ and CQ in glioma via differential autophagy-associated mechanisms, depending on p53 status.	Chloroquine	77-79	P53	Homo sapiens	153-156
29785653-0	2018	Valproic acid treatment response in vitro is determined by TP53 status in medulloblastoma.	Valproic Acid	0-13	P53	Homo sapiens	59-63
25734693-8	2015	Chloroquine has been shown to stabilize p53 and induce p53-dependent apoptosis or cell cycle arrest.	Chloroquine	0-11	P53	Homo sapiens	40-43
25734693-8	2015	Chloroquine has been shown to stabilize p53 and induce p53-dependent apoptosis or cell cycle arrest.	Chloroquine	0-11	P53	Homo sapiens	55-58
30288482-4	2018	Objective: This study was designed to examine associations of TP53 72 Arg&gt;Pro (rs1042522), and MDM2 309 T&gt;G (rs937283) polymorphisms with spermatogenetic failure in Iranian population.	Proline	77-80	P53	Homo sapiens	62-66
30288482-6	2018	The two polymorphisms, 72 Arg&gt;Pro in TP53 and 309 T&gt;G in MDM2, were genotyped using PCR-RFLP and ARMS-PCR respectively.	Proline	33-36	P53	Homo sapiens	40-44
29656006-0	2018	Par-4-dependent p53 up-regulation plays a critical role in thymoquinone-induced cellular senescence in human malignant glioma cells.	thymoquinone	59-71	P53	Homo sapiens	16-19
25915649-0	2015	Dihydromyricetin Enhances the Chemo-Sensitivity of Nedaplatin via Regulation of the p53/Bcl-2 Pathway in Hepatocellular Carcinoma Cells.	dihydromyricetin	0-16	P53	Homo sapiens	84-87
25915649-9	2015	Furthermore, we demonstrated that the combination of DHM and NDP activated the p53/Bcl-2 signaling pathway, which resulted in mitochondrial dysfunction and induced cell death and growth inhibition in HCC cells.	dihydromyricetin	53-56	P53	Homo sapiens	79-82
29656006-6	2018	Altogether, we describe a novel mechanism of cross talk between Par-4 and p53, that plays a critical role in TQ-induced senescence in human malignant glioma cells.	thymoquinone	109-111	P53	Homo sapiens	74-77
25437011-5	2015	Activation of the Wnt pathway by treatment with Wnt3a-conditioned medium or glycogen synthase kinase 3beta inhibitors, such as SB-216763 and 6-bromoindirubin-3"-oxime, delays the progression of cellular senescence as shown by the decrease in the senescence effectors p53 and pRb, lowered senescence-associated beta-galactosidase activity, and increased telomerase activity.	6-bromoindirubin-3'-oxime	141-166	P53	Homo sapiens	267-270
29899832-2	2018	Here we developed a sensitive quantification method for MIBC subclassification (luminal, basal, p53-like).	4-METHYL-2-PENTANOL	56-60	P53	Homo sapiens	96-99
25430047-1	2015	This study aimed to clarify the association between the TP53 rs1625895 polymorphism and the efficiency of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) therapy in 106 patients with diffuse large B cell lymphoma (DLBCL).	Vincristine	156-167	P53	Homo sapiens	56-60
25700705-0	2015	Trifluridine Induces p53-Dependent Sustained G2 Phase Arrest with Its Massive Misincorporation into DNA and Few DNA Strand Breaks.	Trifluridine	0-12	P53	Homo sapiens	21-24
29323455-10	2018	These results indicated that SeC had the potential to inhibit human osteosarcoma cells growth in vitro and in vivo through triggering mitochondrial dysfunction and ROS-mediated p53 phosphorylation, which validated the potential application of Se-containing compounds in treatment of human osteosarcoma.	Selenium	29-31	P53	Homo sapiens	177-180
26064201-1	2015	BACKGROUND: The polymorphism of TP53 codon 72, a transversion of G to C (Arg to Pro), has been demonstrated to be associated with the risk for lung cancer.	Proline	80-83	P53	Homo sapiens	32-36
29143969-0	2018	The molecular basis of cytotoxicity of alpha-spinasterol from Ganoderma resinaceum: Induction of apoptosis and overexpression of p53 in breast and ovarian cancer cell lines.	spinasterol	39-56	P53	Homo sapiens	129-132
25444916-8	2015	Conditional knockdown of p53 by tetracycline inducible expression system significantly abrogated curcumin-induced miR-192-5p/215 upregulation in the p53 wild-type H460, A427 and A549 cells.	Tetracycline	32-44	P53	Homo sapiens	25-28
25444916-8	2015	Conditional knockdown of p53 by tetracycline inducible expression system significantly abrogated curcumin-induced miR-192-5p/215 upregulation in the p53 wild-type H460, A427 and A549 cells.	Tetracycline	32-44	P53	Homo sapiens	149-152
29143969-9	2018	A significant increase in the expression of p53 and Bax was observed in cells treated with alpha-spinasterol, while cdk4/6 were significantly down-regulated upon exposure to alpha-spinasterol.	spinasterol	91-108	P53	Homo sapiens	44-47
29143969-9	2018	A significant increase in the expression of p53 and Bax was observed in cells treated with alpha-spinasterol, while cdk4/6 were significantly down-regulated upon exposure to alpha-spinasterol.	spinasterol	174-191	P53	Homo sapiens	44-47
29666243-0	2018	O6-methylguanine-induced transcriptional mutagenesis reduces p53 tumor-suppressor function.	O-(6)-methylguanine	0-16	P53	Homo sapiens	61-64
25404486-9	2015	We propose that abrogating the expression of the stemness regulators is a prerequisite for rooperol to fully exert its pro-apoptotic properties on wild-type p53-bearing CSCs.	rooperol	91-99	P53	Homo sapiens	157-160
29666243-4	2018	In this study, the impact of O6-methylguanine on the transcription fidelity of p53 and the subsequent effects on the protein"s function as a regulator of cell death and cell-cycle arrest were examined in human cells.	O-(6)-methylguanine	29-45	P53	Homo sapiens	79-82
29593334-3	2018	We identified a small molecule called MCB-613 to cause rapid ubiquitination, nuclear export, and degradation of p53-R175H through a lysosome-mediated pathway, leading to catastrophic cancer cell death.	4-ethyl-2,6-bispyridin-3-ylmethylenecyclohexanone	38-45	P53	Homo sapiens	112-115
25256710-2	2015	Several genetic polymorphisms exist in TP53, including a proline to arginine variant at amino acid 72 (P72 and R72, respectively); this polymorphism alters p53 function.	Proline	57-64	P53	Homo sapiens	39-43
25256710-2	2015	Several genetic polymorphisms exist in TP53, including a proline to arginine variant at amino acid 72 (P72 and R72, respectively); this polymorphism alters p53 function.	Proline	57-64	P53	Homo sapiens	156-159
25446071-7	2015	Furthermore, we detected partial reversibility of cadmium inhibition for all p53 family members by EDTA.	Edetic Acid	99-103	P53	Homo sapiens	77-80
29557783-3	2018	In humans, single nucleotide polymorphism (SNP) with either arginine (R72) or proline (P72) at codon 72 influences p53 activity; the P72 allele has a weaker p53 activity and function in tumor suppression.	Proline	78-85	P53	Homo sapiens	115-118
26745067-4	2015	In HeLa S3 cells treated with siRNA for HPV E6, adenovirus-mediated transduction was enhanced by an upstream ERE linked to a p53 gene carrying a proline variant at codon 72, but not for a p53 gene with arginine variant at codon 72.	Proline	145-152	P53	Homo sapiens	125-128
29557783-3	2018	In humans, single nucleotide polymorphism (SNP) with either arginine (R72) or proline (P72) at codon 72 influences p53 activity; the P72 allele has a weaker p53 activity and function in tumor suppression.	Proline	78-85	P53	Homo sapiens	157-160
29563788-1	2018	Introduction: The nucleobase 2-amino-6-chloropurine-modified polyamidoamine (AP-PAMAM) was used as a carrier for p53 gene delivery to achieve the antitumor effects.	ap-pamam	77-85	P53	Homo sapiens	113-116
26333122-6	2015	The p53 protein was activated and phosphorylated at serines 15 and 392 and accumulated in the nucleus after 24 and 48 h. The Mdm2 protein was present in the cytoplasm with its maximal level after 8 and 16 h. The p21 protein was detected in the nucleus after 24 and 48 h. Increased levels of phosphorylated Chk2 at threonine 68 were observed in the cytoplasmic fraction after 24 and 48 h of mitoxantrone treatment.	Mitoxantrone	390-402	P53	Homo sapiens	4-7
26062943-6	2015	Fortunately, significant progress in the understanding of CLL biology has enabled the development of new molecular drugs targeting the B-cell receptor signaling pathway, such as ibrutinib and idelalisib, which have shown impressive results in patients with relapsed/refractory disease or with TP53 mutation/deletion.	idelalisib	192-202	P53	Homo sapiens	293-297
29563788-6	2018	AP-PAMAM-mediated p53 delivery could achieve stronger antiproliferative effect than PAMAM/p53.	ap-pamam	0-8	P53	Homo sapiens	18-21
24836118-13	2014	Moreover, Riccardin D induced p53-proficient MCF-7 cells to arrest in G1 phase and p53-deficient MDA-MB-231 cells to arrest in G2/M phase.	riccardin D	10-21	P53	Homo sapiens	30-33
24836118-13	2014	Moreover, Riccardin D induced p53-proficient MCF-7 cells to arrest in G1 phase and p53-deficient MDA-MB-231 cells to arrest in G2/M phase.	riccardin D	10-21	P53	Homo sapiens	83-86
29563788-6	2018	AP-PAMAM-mediated p53 delivery could achieve stronger antiproliferative effect than PAMAM/p53.	ap-pamam	0-8	P53	Homo sapiens	90-93
29563788-8	2018	Additionally, AP-PAMAM/p53 transfection has been found to suppress the cell migration and invasion of cancer cells.	ap-pamam	14-22	P53	Homo sapiens	23-26
28264628-4	2018	This work explores the changes in efficacy of the four HDAC inhibitors SAHA, MS-275, valproic acid and sodium butyrate on a panel of colon cancer cell lines - HCT116 (p53 wt), HCT116 p53-/-, HT29 and SW480 (with mutations in p53).	Butyric Acid	103-118	P53	Homo sapiens	167-170
25220870-11	2014	There was increased p53 and Bax expression and ROS production in zerumbone-treated cells.	zerumbone	65-74	P53	Homo sapiens	20-23
25220870-13	2014	Combinational treatment with zerumbone and cisplatin significantly accelerated apoptosis and promoted p53 expression and ROS production in NSCLC cells, compared with each alone.	zerumbone	29-38	P53	Homo sapiens	102-105
25220870-14	2014	These findings demonstrate that zerumbone induces mitochondrial apoptosis and enhances the susceptibility to cisplatin in NSCLC cells, which are, at least partially, mediated through activation of p53 signaling and promotion of ROS generation.	zerumbone	32-41	P53	Homo sapiens	197-200
29745082-13	2018	Cho/NAA and Cho/Cr in the tumor were positively correlated with p53 in the tumor, but negatively correlated with PTEN in the tumor.	N-acetylaspartate	4-7	P53	Homo sapiens	64-67
24115240-1	2014	BACKGROUND: The TP53 single nucleotide polymorphism (SNP) rs1042522 encodes arginine (Arg) or proline (Pro).	Proline	94-101	P53	Homo sapiens	16-20
24115240-1	2014	BACKGROUND: The TP53 single nucleotide polymorphism (SNP) rs1042522 encodes arginine (Arg) or proline (Pro).	Proline	103-106	P53	Homo sapiens	16-20
27308524-0	2016	The heme-p53 interaction: Linking iron metabolism to p53 signaling and tumorigenesis.	Heme	4-8	P53	Homo sapiens	9-12
27308524-0	2016	The heme-p53 interaction: Linking iron metabolism to p53 signaling and tumorigenesis.	Heme	4-8	P53	Homo sapiens	53-56
27308524-1	2016	Recently, we reported that heme binds to tumor suppressor p53 protein (TP53, best known as p53) and promotes its nuclear export and cytosolic degradation, whereas iron chelation stabilizes p53 protein and suppresses tumors in a p53-dependent manner.	Heme	27-31	P53	Homo sapiens	58-61
27308524-1	2016	Recently, we reported that heme binds to tumor suppressor p53 protein (TP53, best known as p53) and promotes its nuclear export and cytosolic degradation, whereas iron chelation stabilizes p53 protein and suppresses tumors in a p53-dependent manner.	Heme	27-31	P53	Homo sapiens	71-75
29531815-8	2018	Consistently, Flubendazole induced P53 expression and reduced Cyclin B1 and p-cdc2 expression in glioma cells.	flubendazole	14-26	P53	Homo sapiens	35-38
27308524-1	2016	Recently, we reported that heme binds to tumor suppressor p53 protein (TP53, best known as p53) and promotes its nuclear export and cytosolic degradation, whereas iron chelation stabilizes p53 protein and suppresses tumors in a p53-dependent manner.	Heme	27-31	P53	Homo sapiens	91-94
27308524-1	2016	Recently, we reported that heme binds to tumor suppressor p53 protein (TP53, best known as p53) and promotes its nuclear export and cytosolic degradation, whereas iron chelation stabilizes p53 protein and suppresses tumors in a p53-dependent manner.	Heme	27-31	P53	Homo sapiens	91-94
27308524-1	2016	Recently, we reported that heme binds to tumor suppressor p53 protein (TP53, best known as p53) and promotes its nuclear export and cytosolic degradation, whereas iron chelation stabilizes p53 protein and suppresses tumors in a p53-dependent manner.	Heme	27-31	P53	Homo sapiens	91-94
25129649-8	2014	Moreover, OA and ALA up-regulated tumor suppressor genes (p53, p21, and p27) and these effects are abolished by AMPK siRNA administration.	alpha-Linolenic Acid	17-20	P53	Homo sapiens	58-61
29334217-3	2018	Using a combination of nuclear magnetic resonance (NMR) titration, isothermal titration calorimetry, fluorescence anisotropy, and native agarose gel electrophoresis, we have identified a direct interaction between the p53 DBD and Hsp90 co-chaperone p23 that occurs in the absence of Hsp90.	Sepharose	137-144	P53	Homo sapiens	218-221
29334217-5	2018	We show by NMR and native agarose gel electrophoresis that a p53-specific double-stranded DNA sequence competes successfully with p23 for binding to the p53 DBD.	Sepharose	26-33	P53	Homo sapiens	61-64
29334217-5	2018	We show by NMR and native agarose gel electrophoresis that a p53-specific double-stranded DNA sequence competes successfully with p23 for binding to the p53 DBD.	Sepharose	26-33	P53	Homo sapiens	153-156
24292333-7	2014	The N+&amp;C+ group was associated with larger tumor size, higher grade, negativity for estrogen and progesterone receptors, HER2 positivity, high Ki-67 index, p53 positivity, and triple negative breast cancer.	n+&amp	4-10	P53	Homo sapiens	160-163
29479097-9	2018	CONCLUSIONS: In Pakistani women the association of TP53 gene codon 72 arginine/proline polymorphism was present..	Proline	79-86	P53	Homo sapiens	51-55
24913304-7	2014	Furthermore, p53(mut_c) cells exhibited a pronounced side population that could be suppressed by RNAi knockdown of ABCG2 as well as treatment with the ATP-binding-cassette transporter inhibitors imatinib, MK571 and tariquidar.	verlukast	205-210	P53	Homo sapiens	13-16
29216473-8	2018	Besides inhibition of ERK1/2 phosphorylation, estafiatin also inhibited phosphorylation of p53, AMPKalpha1, CREB, and p27 elicited by TCR activation in Jurkat cells, but it did not bind to any of 95 kinases evaluated.	Estafiatin	46-56	P53	Homo sapiens	91-94
24308434-0	2014	Bendamustine and melphalan kill myeloma cells similarly through reactive oxygen species production and activation of the p53 pathway and do not overcome resistance to each other.	Bendamustine Hydrochloride	0-12	P53	Homo sapiens	121-124
25536560-2	2014	To set of p53-mediated apoptosis gene polymorphisms (TP53 codon 72 Arg/Pro, r21 codon 31 Ser/Arg, MDM2 SNP309) for the occurrence of CLL in patients who were exposed to ionizing radiation (IR) from the Chornobyl accident.	Proline	71-74	P53	Homo sapiens	10-13
29302672-3	2018	Interestingly, the oxindoles displayed moderate to good in vitro antitumor activities and were validated as p53-MDM2 inhibitors, which represented promising lead compounds for antitumor drug discovery.	Oxindoles	19-28	P53	Homo sapiens	108-111
24862437-0	2014	Selective purification of supercoiled p53-encoding pDNA with L-methionine-agarose matrix.	Sepharose	74-81	P53	Homo sapiens	38-41
29362398-0	2018	A novel ruthenium complex with xanthoxylin induces S-phase arrest and causes ERK1/2-mediated apoptosis in HepG2 cells through a p53-independent pathway.	Ruthenium	8-17	P53	Homo sapiens	128-131
23475592-2	2014	This SNP encodes either an arginine or proline at position 72 (R72P) of the p53 protein, which can alter the apoptotic activity of p53 via transcriptional and non-transcriptional mechanisms.	Proline	39-46	P53	Homo sapiens	76-79
29362398-0	2018	A novel ruthenium complex with xanthoxylin induces S-phase arrest and causes ERK1/2-mediated apoptosis in HepG2 cells through a p53-independent pathway.	xanthoxyline	31-42	P53	Homo sapiens	128-131
23475592-2	2014	This SNP encodes either an arginine or proline at position 72 (R72P) of the p53 protein, which can alter the apoptotic activity of p53 via transcriptional and non-transcriptional mechanisms.	Proline	39-46	P53	Homo sapiens	131-134
29108775-3	2018	SK-N-SH cell treatment with a lethal concentration of PQ facilitated ROS production within 6 h. The treatment also promoted formation of 8-hydroxy-deoxyguanosine, p53 activation, elevation of Bax/Bcl-2 ratio, lowering of mitochondrial membrane potential, and resultant activation of caspase-9 and caspase-3, inferring that ROS production, DNA damage and mitochondrial dysfunction are crucial processes of the PQ-triggered SK-N-SH cell apoptosis.	9,10-phenanthrenequinone	54-56	P53	Homo sapiens	163-166
30244250-11	2018	CONCLUSION: Baicalein repressed proliferation of human colorectal cancer cells HCT116 and blocked cell cycle through downregulating Ezrin and upregulating P53 pathway-related proteins.	baicalein	12-21	P53	Homo sapiens	155-158
25261644-0	2014	The effects of hypericin on ADAMTS and p53 gene expression in MCF-7 breast cancer cells.	hypericin	15-24	P53	Homo sapiens	39-42
25261644-1	2014	PURPOSE: The purpose of this study was to determine the effects of hypericin on MCF-7 (Michigan Cancer Foundation- 7) breast cancer cells, as it is known to exert an antitumor effect on the expression and regulation of ADAMTS1, 3, 10 and the p53 gene in breast cancer cells.	hypericin	67-76	P53	Homo sapiens	242-245
28844940-1	2018	Normal sun-exposed skin contains numerous epidermal patches that stain positive for p53 protein (p53 immunopositive patches, PIPs), which are considered potential early precursors of skin cancer.	piperidine	125-129	P53	Homo sapiens	84-87
24915467-0	2014	Rapamycin prevents strong phosphorylation of p53 on serine 46 and attenuates activation of the p53 pathway in A549 lung cancer cells exposed to actinomycin D.	Dactinomycin	144-157	P53	Homo sapiens	45-48
24915467-0	2014	Rapamycin prevents strong phosphorylation of p53 on serine 46 and attenuates activation of the p53 pathway in A549 lung cancer cells exposed to actinomycin D.	Dactinomycin	144-157	P53	Homo sapiens	95-98
24915467-1	2014	The activation of the p53 pathway by 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), a molecule that mimics metabolic stress, is attenuated by rapamycin, an inhibitor of mTOR kinase, immunosuppressant, and cancer drug.	acadesine	37-82	P53	Homo sapiens	22-25
24915467-3	2014	Because AICAR is a relatively weak activator of p53, we investigated whether stimulation of p53 by the strong activator actinomycin D is also sensitive to the inhibitory effect of rapamycin.	Dactinomycin	120-133	P53	Homo sapiens	92-95
24915467-4	2014	In A549 lung cancer cells, activation of p53 by actinomycin D was associated with phosphorylation of p53 on Ser46.	Dactinomycin	48-61	P53	Homo sapiens	41-44
24915467-4	2014	In A549 lung cancer cells, activation of p53 by actinomycin D was associated with phosphorylation of p53 on Ser46.	Dactinomycin	48-61	P53	Homo sapiens	101-104
24793306-13	2014	In addition, we found that AR-mediated CSPCs enrichment was accompanied by down-regulation of p53 and p16.	Argon	27-29	P53	Homo sapiens	94-97
28844940-2	2018	Although the TP53 gene is mutated in many PIPs, it is unclear whether PIPs contain any other cancer-related mutations.	piperidine	42-46	P53	Homo sapiens	13-17
28844940-3	2018	Here we report that PIPs, predominantly &lt;3,000 p53 immunopositive cells in size, within normal chronically exposed skin contain mutations in multiple genes that are mutated in cutaneous squamous cell cancers.	piperidine	20-24	P53	Homo sapiens	50-53
29233996-4	2017	PEPD binds to the proline-rich domain in p53, which inhibits phosphorylation of nuclear p53 and MDM2-mediated mitochondrial translocation of nuclear and cytoplasmic p53.	Proline	18-25	P53	Homo sapiens	41-44
24474455-8	2014	The Arg72Pro-p53 polymorphism showed for the genotypes Arg/Pro and Pro/Pro, and for the Pro allele, a significant association only to the risk for CIN (p&lt;0.03).	Proline	9-12	P53	Homo sapiens	13-16
24474455-8	2014	The Arg72Pro-p53 polymorphism showed for the genotypes Arg/Pro and Pro/Pro, and for the Pro allele, a significant association only to the risk for CIN (p&lt;0.03).	Proline	59-62	P53	Homo sapiens	13-16
24474455-8	2014	The Arg72Pro-p53 polymorphism showed for the genotypes Arg/Pro and Pro/Pro, and for the Pro allele, a significant association only to the risk for CIN (p&lt;0.03).	Proline	59-62	P53	Homo sapiens	13-16
24922640-3	2014	RESULTS: Significant differences were observed in the p53 expression between the different groups: NN and CIN I (p=0.010); NN and CIN II (p&lt;0.00001); CIN II and CIN III (p=0.02); CIN II and CIS (p=0.0220); CIN II and CEC (p=0.010).	nn	99-101	P53	Homo sapiens	54-57
24922640-3	2014	RESULTS: Significant differences were observed in the p53 expression between the different groups: NN and CIN I (p=0.010); NN and CIN II (p&lt;0.00001); CIN II and CIN III (p=0.02); CIN II and CIS (p=0.0220); CIN II and CEC (p=0.010).	chlorethylclonidine	220-223	P53	Homo sapiens	54-57
29233996-4	2017	PEPD binds to the proline-rich domain in p53, which inhibits phosphorylation of nuclear p53 and MDM2-mediated mitochondrial translocation of nuclear and cytoplasmic p53.	Proline	18-25	P53	Homo sapiens	88-91
24878590-8	2014	Overall our findings suggest that Al induces ER stress and ROS generation which compromises the antioxidant defenses of neuronal cells thereby promoting neuronal apoptosis in p53 independent pathway.	Aluminum	34-36	P53	Homo sapiens	175-178
29233996-4	2017	PEPD binds to the proline-rich domain in p53, which inhibits phosphorylation of nuclear p53 and MDM2-mediated mitochondrial translocation of nuclear and cytoplasmic p53.	Proline	18-25	P53	Homo sapiens	88-91
29250930-7	2017	In the relapsed or refractory setting, patients with del(17p) or TP53 aberrations should be offered treatment with a novel agent, such as ibrutinib, idelalisib-rituximab or venetoclax.	idelalisib	149-159	P53	Homo sapiens	65-69
24727941-15	2014	CONCLUSION: The synergistic anticancer effect of LDM and CQ in vitro results from activation of a caspase-dependent and p53-independent apoptosis pathway as well as inhibition of cytoprotective autophagy.	Chloroquine	57-59	P53	Homo sapiens	120-123
24685134-0	2014	Iron metabolism regulates p53 signaling through direct heme-p53 interaction and modulation of p53 localization, stability, and function.	Heme	55-59	P53	Homo sapiens	26-29
29141234-4	2017	Our data showed that miR-302 directly suppresses the tumor suppressor p53, which is modestly upregulated in Dgcr8-/- ESCs and serves as a barrier restricting neural differentiation.	mir-302	21-28	P53	Homo sapiens	70-73
24685134-0	2014	Iron metabolism regulates p53 signaling through direct heme-p53 interaction and modulation of p53 localization, stability, and function.	Heme	55-59	P53	Homo sapiens	60-63
24685134-0	2014	Iron metabolism regulates p53 signaling through direct heme-p53 interaction and modulation of p53 localization, stability, and function.	Heme	55-59	P53	Homo sapiens	60-63
24685134-6	2014	Our findings thus identify a direct link between iron/heme homeostasis and the regulation of p53 signaling, which not only provides mechanistic insights into iron-excess-associated tumorigenesis but may also help predict and improve outcomes in iron-deprivation-based chemotherapy.	Heme	54-58	P53	Homo sapiens	93-96
28465189-0	2017	P53 tumor suppressor is required for efficient execution of the death program following treatment with a cytotoxic limonoid obtained from Melia azedarach.	Limonins	115-123	P53	Homo sapiens	0-3
24530425-6	2014	Our results show that gestational exposure to CrVI resulted in (i) increased Cr concentration in the placenta, (ii) increased germ cell apoptosis by up-regulating p53/p27-Bax-caspase-3 proteins and by increasing p53-SOD-2 co-localization; (iii) accelerated germ cell cyst (GCC) breakdown; (iv) advanced primordial follicle assembly and primary follicle transition and (v) down regulation of p-AKT, p-ERK and XIAP.	Chromium	46-48	P53	Homo sapiens	163-166
24530425-6	2014	Our results show that gestational exposure to CrVI resulted in (i) increased Cr concentration in the placenta, (ii) increased germ cell apoptosis by up-regulating p53/p27-Bax-caspase-3 proteins and by increasing p53-SOD-2 co-localization; (iii) accelerated germ cell cyst (GCC) breakdown; (iv) advanced primordial follicle assembly and primary follicle transition and (v) down regulation of p-AKT, p-ERK and XIAP.	Chromium	46-48	P53	Homo sapiens	212-215
24667845-5	2014	Using pifithrin-alpha(PFT), a p53"s mitochondrial translocation inhibitor, we found that pretreated with PFT, heat stress induced mitochondrial p53 translocation was significantly suppressed, accompanied by a significant alleviation in the loss of DeltaPsim, cytochrome c release and caspase-9 activation.	bentiromide	22-25	P53	Homo sapiens	30-33
24667845-5	2014	Using pifithrin-alpha(PFT), a p53"s mitochondrial translocation inhibitor, we found that pretreated with PFT, heat stress induced mitochondrial p53 translocation was significantly suppressed, accompanied by a significant alleviation in the loss of DeltaPsim, cytochrome c release and caspase-9 activation.	bentiromide	22-25	P53	Homo sapiens	144-147
24514456-6	2014	[Pt(BDI(QQ))]Cl induces DNA damage, leading to p53 enrichment, mitochondrial membrane potential depolarisation, and caspase-mediated apoptosis.	pt(bdi(qq))]cl	1-15	P53	Homo sapiens	47-50
28973015-10	2017	We found that enoxacin and ciprofloxacin, a related fluoroquinolone capable of promoting microRNA processing, but not ofloxacin, strongly activated wild type p53-dependent transcription in A375 melanoma without causing significant DNA damage.	Ofloxacin	31-40	P53	Homo sapiens	158-161
28927457-5	2017	Azelaic acid leads to mitochondrial damage associated with increased release of reactive oxygen species inducing p53.	azelaic acid	0-12	P53	Homo sapiens	113-116
24247721-3	2014	Prodigiosin and its structural analogue (compound R) induced the expression of p53 target genes accompanied by cell-cycle arrest and apoptosis in p53-deficient cancer cells.	Prodigiosin	0-11	P53	Homo sapiens	79-82
24247721-4	2014	Prodigiosin restored p53 signaling in cancer cells harboring hotspot TP53 mutations, with little to no detectable cytotoxicity in normal human fibroblasts and with no genotoxicity.	Prodigiosin	0-11	P53	Homo sapiens	21-24
24247721-4	2014	Prodigiosin restored p53 signaling in cancer cells harboring hotspot TP53 mutations, with little to no detectable cytotoxicity in normal human fibroblasts and with no genotoxicity.	Prodigiosin	0-11	P53	Homo sapiens	69-73
24247721-5	2014	Prodigiosin induced the expression of p73 and disrupted its interaction with mutant p53, thereby rescuing p53 pathway deficiency and promoting antitumor effects.	Prodigiosin	0-11	P53	Homo sapiens	84-87
24247721-5	2014	Prodigiosin induced the expression of p73 and disrupted its interaction with mutant p53, thereby rescuing p53 pathway deficiency and promoting antitumor effects.	Prodigiosin	0-11	P53	Homo sapiens	106-109
28962183-9	2017	These results suggested that MTE inhibited growth and exhibited pro-apoptotic effects in Bel-7402 cells, which was mediated by downregulation of the MDM2-induced p53-dependent mitochondrial apoptosis pathway and blocking the NF-kappaB pathway.	methylthioethanol	29-32	P53	Homo sapiens	162-165
24247721-8	2014	In exhibiting this capability, prodigiosin and its analogue provide lead compounds to rescue deficiencies in the p53 pathway in cancer cells by upregulating p73 and targeting mutant p53/p73 interaction there.	Prodigiosin	31-42	P53	Homo sapiens	113-116
24247721-8	2014	In exhibiting this capability, prodigiosin and its analogue provide lead compounds to rescue deficiencies in the p53 pathway in cancer cells by upregulating p73 and targeting mutant p53/p73 interaction there.	Prodigiosin	31-42	P53	Homo sapiens	182-185
28789369-5	2017	Notably, the Pro72 allele was significantly enriched in patients with ESCC compared with its abundance in the healthy control group, and the genotype of Pro/Arg on p53 codon 72 was confirmed to exhibit a significant correlation with ESCC in Mongolian patients.	Proline	13-16	P53	Homo sapiens	164-167
24269727-0	2014	ROS and RNS induced apoptosis through p53 and iNOS mediated pathway by a dibasic hydroxamic acid molecule in leukemia cells.	Radon	8-11	P53	Homo sapiens	38-41
28789369-7	2017	Mongolian patients who carry the partocular genotype of Arg/Pro or Pro/Pro on p53 codon 72 may be more likely to develop ESCC.	Proline	60-63	P53	Homo sapiens	78-81
24120424-0	2014	Role of p53 in the cellular response following oleic acid accumulation in Chang liver cells.	Oleic Acid	47-57	P53	Homo sapiens	8-11
28789369-7	2017	Mongolian patients who carry the partocular genotype of Arg/Pro or Pro/Pro on p53 codon 72 may be more likely to develop ESCC.	Proline	67-70	P53	Homo sapiens	78-81
24120424-8	2014	OA-induced changes in cell viability and ATP production were rescued to control levels when cells were pretreated with pifithrin-alpha (PTA), a p53 inhibitor.	pta	136-139	P53	Homo sapiens	144-147
28789369-7	2017	Mongolian patients who carry the partocular genotype of Arg/Pro or Pro/Pro on p53 codon 72 may be more likely to develop ESCC.	Proline	67-70	P53	Homo sapiens	78-81
28498637-1	2017	It has been suggested that beta2-adrenergic receptor (beta2-AR)-mediated signaling induced by catecholamines regulates the degradation of p53.	Catecholamines	94-108	P53	Homo sapiens	138-141
24403501-9	2014	Plasma concentration of DCP prototype was 17.1 mug/ml 2h after administration, with a peak concentration of 26.9 mug/ml at 0.5 h. Immunoblotting showed DCP-induced activation of DNA damage pathways, including double-phosphorylated checkpoint kinase 2 (CHK2) and breast cancer 1 (BRCA1) and triple-phosphorylated p53, compared to controls.	diammine(1,1-cyclobutanedicarboxylate)platinum(II)	24-27	P53	Homo sapiens	312-315
28498637-4	2017	Catecholamines inhibited doxorubicin (DOX)-induced p53 acetylation and transcription-activation activities by inducing the expression of Sirt1.	Catecholamines	0-14	P53	Homo sapiens	51-54
28245756-0	2017	Diosmetin Induces Cell Apoptosis by Regulating CYP1A1/CYP1A2 Due to p53 Activation in HepG2 Cells.	diosmetin	0-9	P53	Homo sapiens	68-71
24121312-1	2014	OBJECTIVE: We evaluated tumor hypoxia using F-fluoromisonidazole (F-FMISO) PET in relation to the expression of hypoxia-inducible factor-1alpha (HIF-1alpha) and p53 in patients with head and neck cancer and compared the results with those obtained using 2-deoxy-2-F-fluoro-D-glucose (F-FDG) PET.	f-fluoromisonidazole	44-64	P53	Homo sapiens	161-164
24940695-4	2014	We have demonstrated using the human Burkitt"s lymphoma B-cell line, Raji, that p53, p63 and p73 all accumulate in the nucleus, following treatment of cells with fludarabine nucleoside (2-FaraA).	fludarabine nucleoside	162-184	P53	Homo sapiens	80-83
28245756-5	2017	Meanwhile, when cells were co-treated with Dios and PFT-alpha, P53 was down-regulated and CYP1A1/CYP1A2 up-regulated controlled with that of Dios treated cells.	dios	43-47	P53	Homo sapiens	63-66
25552063-3	2014	In experimental studies it was showed that synthetic antineoplastons (A10-3-phenyl-acetyl-amino-2,6-piperidinedione and AS2-1--a mixture of phenylacetic acid and phenylacetylglutamine) were able to prevent the introduction of glutamine into the cell, to block the action of Bcl-2, to activate p53 and p21, to inhibit histone deacetylase, to induce apoptosis.	a10-3-phenyl-acetyl-amino-2,6-piperidinedione	70-115	P53	Homo sapiens	293-296
28245756-6	2017	The data reveal the new evidence that cytochrome P450 CYP1A regulation by P53 enzyme plays an important role in Diosmetin anti-cancer activity of HepG2 cells.	diosmetin	112-121	P53	Homo sapiens	74-77
28521469-8	2017	Furthermore, treatment with Lico-E increased the expression of pro-apoptotic factors, including apoptosis regulator BAX, Bcl-2-associated agonist of cell death, apoptotic protease-activating factor 1, caspase-9 and tumor suppressor p53, while decreasing the expression of anti-apoptotic factors, including apoptosis regulator Bcl-2 and Bcl-2-like protein 1 in FaDu cells.	licochalcone E	28-34	P53	Homo sapiens	232-235
24113239-1	2013	Based on previous reports of certain 5-deazaflavin derivatives being capable of activating the tumour suppressor p53 in cancer cells through inhibition of the p53-specific ubiquitin E3 ligase HDM2, we have conducted an structure-activity relationship (SAR) analysis through systematic modification of the 5-deazaflavin template.	5-deazaflavin	305-318	P53	Homo sapiens	113-116
28369725-4	2017	CX-5461 induced significant growth inhibition in wild-type (WT) and mutant TP53 myeloma cell lines and primary samples, in association with increases in downstream markers of apoptosis.	CX 5461	0-7	P53	Homo sapiens	75-79
24223706-0	2013	Dihydromyricetin reduced Bcl-2 expression via p53 in human hepatoma HepG2 cells.	dihydromyricetin	0-16	P53	Homo sapiens	46-49
24223706-3	2013	In this study, we investigated whether p53 is involved in DHM-triggered viability inhibition and apoptosis induction in cancer cells.	dihydromyricetin	58-61	P53	Homo sapiens	39-42
24223706-8	2013	P53 expression was significantly increased after DHM treatment, whereas Bcl-2 was reduced potently.	dihydromyricetin	49-52	P53	Homo sapiens	0-3
24223706-11	2013	These findings defined and supported a novel function that DHM could induce human hepatocellular carcinoma HepG2 cells apoptosis by up-regulating Bax/Bcl-2 expression via p53 signal pathway.	dihydromyricetin	59-62	P53	Homo sapiens	171-174
28160167-6	2017	As underlying molecular events, we found that ERK1/2 was de-phosphorylated and that the c-Myc and mutant p53 protein levels were reduced after VPA and, to a lesser extent, after TSA treatment.	Valproic Acid	143-146	P53	Homo sapiens	105-108
28454438-0	2017	CHK2 is involved in the p53-independent radiosensitizing effects of valproic acid.	Valproic Acid	68-81	P53	Homo sapiens	24-27
23959424-0	2013	Upregulation of sestrin-2 expression via P53 protects against 1-methyl-4-phenylpyridinium (MPP+) neurotoxicity.	mangion-purified polysaccharide (Candida albicans)	91-95	P53	Homo sapiens	41-44
25606382-2	2013	Polymorphism of p53 gene codon 72 Arg/Pro (rs1042522) may influence the function of p53 protein and then affect the processing of carcinogenesis.	Proline	38-41	P53	Homo sapiens	16-19
25606382-2	2013	Polymorphism of p53 gene codon 72 Arg/Pro (rs1042522) may influence the function of p53 protein and then affect the processing of carcinogenesis.	Proline	38-41	P53	Homo sapiens	84-87
25606382-3	2013	It has been suggested that p53 codon 72 Arg/Pro polymorphism is associated with susceptibility to hepatocellular carcinoma (HCC).	Proline	44-47	P53	Homo sapiens	27-30
28454438-6	2017	Notably, treatment with valproic acid also induced increases in the level of p21 protein levels and CHK2 activity in p53-null colon cancer HCT116 cells.	Valproic Acid	24-37	P53	Homo sapiens	117-120
25606382-10	2013	CONCLUSIONS/SIGNIFICANCE: This meta-analysis suggests that p53 codon 72 Arg/Pro polymorphism may be associated with the risk of HCC, especially in subgroup analysis of Asian and Caucasian population, hospital-based population, the female, and the individuals infected with hepatitis virus.	Proline	76-79	P53	Homo sapiens	59-62
28454438-8	2017	The results of the present study reveal that valproic acid may exhibit clinical utility with respect to increasing the anticancer efficacy of radiotherapy by affecting the level of p53.	Valproic Acid	45-58	P53	Homo sapiens	181-184
28234008-5	2017	(+)-Strebloside potently inhibited mutant p53 expression through the induction of ERK pathways and inhibited NF-kappaB activity in human ovarian cancer cells.	strebloside-	0-15	P53	Homo sapiens	42-45
24109558-6	2013	Our data indicate that harmine exhibits a pronounced cytotoxicity and induces an anti-proliferation state in MCF-7 cells which is accompanied by a significant inhibition of telomerase activity and an induction of an accelerated senescence phenotype by over-expressing elements of the p53/p21 pathway.	Harmine	23-30	P53	Homo sapiens	284-287
28336971-4	2017	A natural flavonoid acacetin is then identified to be capable of modulating RARgamma-dependent AKT-p53 network.	acacetin	20-28	P53	Homo sapiens	99-102
28336971-7	2017	Acacetin induces cancer cell apoptosis through antagonizing the non-genomic effect of RARgamma on AKT and p53.	acacetin	0-8	P53	Homo sapiens	106-109
28187444-6	2017	Idelalisib enhanced the bendamustine-mediated DNA damage/repair response, indicated by the phosphorylation of ATM, Chk2, and p53.	idelalisib	0-10	P53	Homo sapiens	125-128
23715779-9	2013	Concerning the histological types of lung cancer, the p53 codon 72 variant exerts risk effect on the lung carcinogenesis in patients with adenocarcinoma (OR Arg/Pro vs. Arg/Arg = 1.10, 95 % CI = 1.00-1.22, P OR = 0.048).	Proline	161-164	P53	Homo sapiens	54-57
23715779-10	2013	Additionally, subgroup analysis by the smoking status demonstrated that the p53 codon 72 variant seemed to play a protective role in lung carcinogenesis among the non-smokers but not the smokers in the contrast model of Arg/Pro vs. Arg/Arg (OR Arg/Pro vs. Arg/Arg = 0.71, 95 % CI = 0.50-1.00, P OR = 0.049).	Proline	224-227	P53	Homo sapiens	76-79
28187444-6	2017	Idelalisib enhanced the bendamustine-mediated DNA damage/repair response, indicated by the phosphorylation of ATM, Chk2, and p53.	Bendamustine Hydrochloride	24-36	P53	Homo sapiens	125-128
28357076-5	2017	The distribution frequency of p53 sites of arginine (Arg)/Arg, Arg/proline (Pro), Pro/Pro were 18.4, 48.8 and 32.8% in the control group, as compared with 18.7, 49.9 and 31.4% in the case group, which indicated that there was no difference between two groups (chi2=0.14; P=0.93).	Proline	67-74	P53	Homo sapiens	30-33
24023291-0	2013	Enhanced redox factor 1 (REF1)-modulated p53 stabilization and JNK1 dissociation in response to selenomethionine.	Selenomethionine	96-112	P53	Homo sapiens	41-44
28102346-0	2017	Human p53 interacts with the elongating RNAPII complex and is required for the release of actinomycin D induced transcription blockage.	Dactinomycin	90-103	P53	Homo sapiens	6-9
27888799-0	2017	New bipyridine gold(III) dithiocarbamate-containing complexes exerted a potent anticancer activity against cisplatin-resistant cancer cells independent of p53 status.	bipyridine gold(iii) dithiocarbamate	4-40	P53	Homo sapiens	155-158
23483183-9	2013	RESULTS: The distribution of Arg/Arg, Arg/Pro, and Pro/Pro genotypes of codon 72 of TP53 gene was: 63.3, 34.7, and 2.0 % in the cervical carcinomas and 58.1, 33.8, and 8.1 % in the control group.	Proline	42-45	P53	Homo sapiens	84-88
26478521-7	2017	RESULTS: DHTI treatment inhibited the proliferation of 143B cells in a dose- and time-dependent manner through arresting cells in G1 phase by reducing the expression of cyclin D1, cyclin E1, CDK2, CDK4, CDK6, p-Rb, E2F1, SKP2 and increasing the expression of P53, P21cip1, P27kip1.	dhts	9-13	P53	Homo sapiens	259-262
23758064-11	2013	Finally, DAB treatment disrupted the cell cycle in response to increased p53 and activation of ATM.	1,4-diaminobutanone	9-12	P53	Homo sapiens	73-76
27960113-7	2017	Briefly, these results suggest that tebufenozide- induces cell cycle arrest and apoptosis through activating p53 protein in a Bax- and Bcl-2-triggered mitochondrial pathway.	tebufenozide	36-48	P53	Homo sapiens	109-112
23880760-0	2013	Regulation of hypoxia-inducible factor 1alpha (HIF-1alpha) by lysophosphatidic acid is dependent on interplay between p53 and Kruppel-like factor 5.	lysophosphatidic acid	62-83	P53	Homo sapiens	118-121
23880760-6	2013	HIF-1alpha induction was observed in cells expressing WT p53, where LPA decreased p53 expression.	lysophosphatidic acid	68-71	P53	Homo sapiens	57-60
23880760-6	2013	HIF-1alpha induction was observed in cells expressing WT p53, where LPA decreased p53 expression.	lysophosphatidic acid	68-71	P53	Homo sapiens	82-85
23880760-8	2013	A decrease in p53 expression was dependent on induction of p53-specific E3 ubiquitin ligase Mdm2 by LPA.	lysophosphatidic acid	100-103	P53	Homo sapiens	14-17
23880760-8	2013	A decrease in p53 expression was dependent on induction of p53-specific E3 ubiquitin ligase Mdm2 by LPA.	lysophosphatidic acid	100-103	P53	Homo sapiens	59-62
23880760-13	2013	LPA increased the occupancy of the Hif1alpha promoter by KLF5, while decreasing p53 binding.	lysophosphatidic acid	0-3	P53	Homo sapiens	80-83
23880760-15	2013	These results identify KLF5 as a transactivator of HIF-1alpha and show that LPA regulates HIF-1alpha by dynamically modulating its interaction with KLF5 and p53.	lysophosphatidic acid	76-79	P53	Homo sapiens	157-160
28240165-0	2017	Diosmetin, a Potential p53 Activator, Performs Anticancer Effect by Regulating Cell Cycling and Cell Proliferation in HepG2 Cells.	diosmetin	0-9	P53	Homo sapiens	23-26
28240165-4	2017	Meanwhile, Dios-induced liver cancer cell apoptosis was related with the p53 activation.	diosmetin	11-15	P53	Homo sapiens	73-76
27912880-15	2016	CONCLUSION: HCPT and BA, a new and effective combination therapy, synergistically target Topo I and up-regulate p53 to induce cell apoptosis and cell cycle arrest.	baicalein	21-23	P53	Homo sapiens	112-115
23899521-5	2013	SL-01 modulated the expressions of p-ATM, p53 and p21 and decrease of cyclin D1 in MCF-7 cells.	dodecyl-3-((1-(3,3-difluoro-4-hydroxy-5-(hydroxymethyl)-tetrahydrofuran-2-yl)-2-oxo-1,2-dihydropyrimidin-4-yl)carbamoyl)pyrazine-2-carboxylate	0-5	P53	Homo sapiens	42-45
27841435-0	2016	Autophagy and apoptosis: studies on the effects of bisthiosemicarbazone copper(ii) complexes on p53 and p53-null tumour cell lines.	cupric ion	72-82	P53	Homo sapiens	96-99
23977108-7	2013	Treatment of SK-N-DZ with PCI-24781 also induced cell cycle arrest in G2/M phase and activated apoptosis signaling pathways via the up-regulation of DR4, p21, p53 and caspase 3.	sk-n-dz	13-20	P53	Homo sapiens	159-162
27841435-0	2016	Autophagy and apoptosis: studies on the effects of bisthiosemicarbazone copper(ii) complexes on p53 and p53-null tumour cell lines.	cupric ion	72-82	P53	Homo sapiens	104-107
27735058-1	2016	The C-terminal domain (CTD) of tumor suppressor protein p53 is an intrinsically disordered region that binds to various partner proteins, where lysine of CTD is acetylated/nonacetylated and histidine neutralized/non-neutralized.	3-deazacytidine	23-26	P53	Homo sapiens	56-59
23684542-5	2013	Furthermore, sprengerinin C induced HepG-2/BEL7402 cell apoptosis by activating NADPH oxidase/reactive oxygen species-dependent caspase apoptosis pathway and suppressed HepG-2/BEL7402 cell growth through p53-mediated G2/M-phase arrest.	sprengerinin C	13-27	P53	Homo sapiens	204-207
21763161-1	2013	OBJECTIVE: To understand developmental characteristics of urinary bladder carcinomas (UBC) by evaluating genomic alterations and p53 protein expression in primary tumors, their recurrences, and in the morphologically normal urothelium of UBC patients.	1-(2-amino-2-carboxyethyl)-3-(2-carboxybenzyl)pyrimidine-2,4-dione	86-89	P53	Homo sapiens	129-132
27913471-7	2016	These recently approved drugs (ibrutinib, idelalisib, and venetoclax) are reporting excellent outcomes, including patients with high-risk disease such as 17p deletion (17p-) or TP53 mutations (TP53mut).	idelalisib	42-52	P53	Homo sapiens	177-181
21763161-11	2013	Biopsies taken during the follow-up of patients with history of previously resected UBC revealed that 5/15 patients with no histologic alterations had more than 25% of urothelial cells expressing the p53 protein, suggesting that the apparently normal urothelium was genomically unstable.	1-(2-amino-2-carboxyethyl)-3-(2-carboxybenzyl)pyrimidine-2,4-dione	84-87	P53	Homo sapiens	200-203
23802716-1	2013	Analogues of the previously described spiro[imidazo[1,5-c]thiazole-3,3"-indoline]-2",5,7(6H,7aH)-trione p53 modulators were prepared to explore new structural requirements at the thiazolidine domain for the antiproliferative activity and p53 modulation.	Thiazolidines	179-191	P53	Homo sapiens	104-107
27693049-6	2016	Based on in vivo studies, the growth of breast tumor and expression of CD31, Bcl-2 and nonfunctional p53 were inhibited more effectively by ES-R than by ES-Zn.	Erbium	140-144	P53	Homo sapiens	101-104
23515910-9	2013	The similar correlation between the wild-type form p53 and response to therapy were also detected in subgroup analyses (total MR, pathological MR, and total CR in chemoradiotherapy subgroup; total MR in chemotherapy subgroup; total MR and pathological CR in esophageal squamous cell carcinoma [ESCC]).	Chromium	157-159	P53	Homo sapiens	51-54
27654922-6	2016	Compared to untreated glioblastoma cells TPEN treatment or expression of ZIP9 results in activation of the tumor suppressor p53 by phosphorylation at serine residue 46 (Ser46) and in inactivation of the migration relevant glycogen synthase kinase 3 beta (GSK-3beta) by phosphorylation at serine residue 9 (Ser9).	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	41-45	P53	Homo sapiens	124-127
23558054-7	2013	There is evidence of premalignant changes (e.g. p53 inactivation) in morphologically normal OSE and of rare but definitive dysplastic and early preinvasive lesions in OSE-lined inclusion cysts.	serine O-sulfate	92-95	P53	Homo sapiens	48-51
27879682-0	2016	Ziyuglycoside I Inhibits the Proliferation of MDA-MB-231 Breast Carcinoma Cells through Inducing p53-Mediated G2/M Cell Cycle Arrest and Intrinsic/Extrinsic Apoptosis.	ziyuglycoside I	0-15	P53	Homo sapiens	97-100
23297003-0	2013	HDAC inhibitor DWP0016 activates p53 transcription and acetylation to inhibit cell growth in U251 glioblastoma cells.	dwp0016	15-22	P53	Homo sapiens	33-36
23297003-9	2013	Conclusively, our results show DWP0016 is a potent HDAC inhibitor and the anti-tumor activity is consistent with its intended p53 activation mechanisms.	dwp0016	31-38	P53	Homo sapiens	126-129
27736799-7	2016	TM5441 exerts its inhibitory effect on Doxorubicin-induced cellular senescence by decreasing reactive oxygen species generation, induction of antioxidants like catalase and suppression of stress-induced senescence cadre p53, p21, p16, PAI-1 and IGFBP3.	TM5441	0-6	P53	Homo sapiens	220-223
23360684-4	2013	The cleavage of caspases and PARP, activation of p53 and mitochondrial-mediated apoptosis pathways induced by cisplatin were effectively blocked by cyanidin.	cyanidin	148-156	P53	Homo sapiens	49-52
27122200-3	2016	Briefly, branched polyethylenimine (BPEI) was conjugated with beta-cyclodextrin hydrate (beta-CD) to form BPEI-beta-CD backbone, and p53 plasmid was condensed by positively charged BPEI via electrostatic interaction, while Dox was first conjugated with adamantine (AD) and then assembled with BPEI-beta-CD backbone via the host-guest interaction.	ADAMANTANE	253-263	P53	Homo sapiens	133-136
27122200-3	2016	Briefly, branched polyethylenimine (BPEI) was conjugated with beta-cyclodextrin hydrate (beta-CD) to form BPEI-beta-CD backbone, and p53 plasmid was condensed by positively charged BPEI via electrostatic interaction, while Dox was first conjugated with adamantine (AD) and then assembled with BPEI-beta-CD backbone via the host-guest interaction.	ad	265-267	P53	Homo sapiens	133-136
23519841-10	2013	The combination of TMZ and lomeguatrib in primary GBM cell cultures and glioma cell lines decreased MGMT expression, increased p53 expression, and did not change MGMT methylation.	lomeguatrib	27-38	P53	Homo sapiens	127-130
27775703-0	2016	DNAJA1 controls the fate of misfolded mutant p53 through the mevalonate pathway.	Mevalonic Acid	61-71	P53	Homo sapiens	45-48
23564481-0	2013	Association between the p53 codon 72 Arg/Pro polymorphism and hepatocellular carcinoma risk.	Proline	41-44	P53	Homo sapiens	24-27
23564481-1	2013	Previous studies regarding the association of p53 codon 72 Arg/Pro polymorphism with hepatocellular carcinoma (HCC) risk have provided conflicting and inconclusive findings.	Proline	63-66	P53	Homo sapiens	46-49
23564481-4	2013	The strength of the association of p53 codon 72 Arg/Pro polymorphism with HCC risk was estimated by the pooled odds ratio (OR) with its corresponding 95 % confidence interval (95 % CI).	Proline	52-55	P53	Homo sapiens	35-38
27775703-7	2016	Our study reveals that DNAJA1 controls the fate of misfolded mutp53, provides insights into potential strategies to deplete mutp53 through the mevalonate pathway-DNAJA1 axis, and highlights the significance of p53 status in impacting statins" efficacy on cancer therapy.	Mevalonic Acid	143-153	P53	Homo sapiens	64-67
27817864-1	2016	The aim of this study was to investigate the cytotoxic effect of mitoxantrone on two human non-small cell lung cancer cell lines, A549 (p53+) and H1299 (p53-).	Mitoxantrone	65-77	P53	Homo sapiens	136-139
23058179-7	2013	Treatment with 0.1 and 1 muM of gallic acid also resulted in a significant increase in caspase-3 activity and regulated the productions of Bcl-2, Bax, p53 and pAkt.	Gallic Acid	32-43	P53	Homo sapiens	151-154
27817864-1	2016	The aim of this study was to investigate the cytotoxic effect of mitoxantrone on two human non-small cell lung cancer cell lines, A549 (p53+) and H1299 (p53-).	Mitoxantrone	65-77	P53	Homo sapiens	153-156
27681719-11	2016	In EBV(-)human gastric carcinoma (MKN74), both quercetin and isoliquiritigenin induced the expressions of p53, Bax, and Puma and the cleaved forms of caspase-3 and -9 and Parp at similar levels.	isoliquiritigenin	61-78	P53	Homo sapiens	106-109
27565728-3	2016	Here we found that four nucleocytoplasmic-shuttling RNA-binding proteins and p53 interact specifically with the YB-NLS and co-accumulate with YB-1 in the nucleus of actinomycin D-treated cells.	Dactinomycin	165-178	P53	Homo sapiens	77-80
23506195-0	2013	C2-streptavidin mediates the delivery of biotin-conjugated tumor suppressor protein p53 into tumor cells.	Biotin	41-47	P53	Homo sapiens	84-87
23506195-3	2013	In the present study, we used the C2-streptavidin transporter to introduce biotin-conjugated p53 protein into various mammalian cell lines.	Biotin	75-81	P53	Homo sapiens	93-96
23506195-5	2013	Recombinant p53 was expressed in insect cells and biotin-labeled.	Biotin	50-56	P53	Homo sapiens	12-15
23506195-6	2013	Biotin-p53 retained its specific high-affinity DNA-binding as revealed by gel-shift analysis.	Biotin	0-6	P53	Homo sapiens	7-10
23506195-9	2013	Using cell fractionation, the cytosolic translocation of biotin-p53 was detected in Vero cells as well as in HeLa cervix carcinoma cells.	Biotin	57-63	P53	Homo sapiens	64-67
23506195-10	2013	In line with this finding, confocal microscopy displayed cytoplasmic staining of biotin-p53 in HeLa and HL60 leukemia cells.	Biotin	81-87	P53	Homo sapiens	88-91
23506195-12	2013	In conclusion, our results demonstrate the successful conjugation of biotin-p53 to C2-streptavidin and its subsequent receptor-mediated endocytosis into different human tumor cell lines.	Biotin	69-75	P53	Homo sapiens	76-79
27556362-0	2016	Low-dose Actinomycin-D treatment re-establishes the tumoursuppressive function of P53 in RELA-positive ependymoma.	Dactinomycin	9-22	P53	Homo sapiens	82-85
23186127-9	2013	Antitumour effects of Vinca alkaloids in the presence of cytostatic drugs were restored by caffeine, which maintained active cell cycling, or by knockdown of p53, which prevented drug-induced cell cycle arrest.	Vinca Alkaloids	22-37	P53	Homo sapiens	158-161
27556362-6	2016	Among the p53-positive ependymomas, the vast majority exhibited a RELA fusion leading to the hypothesis that p53 inactivation might be linked to RELA positivity.In order to assess the potential of p53 reactivation through MDM2 inhibition in ependymoma, we evaluated the effects of Actinomycin-D and Nutlin-3 treatment in two preclinical ependymoma models representing the high-risk subtypes PF-EPN-A and ST-EPN-RELA.	Dactinomycin	281-294	P53	Homo sapiens	109-112
27556362-6	2016	Among the p53-positive ependymomas, the vast majority exhibited a RELA fusion leading to the hypothesis that p53 inactivation might be linked to RELA positivity.In order to assess the potential of p53 reactivation through MDM2 inhibition in ependymoma, we evaluated the effects of Actinomycin-D and Nutlin-3 treatment in two preclinical ependymoma models representing the high-risk subtypes PF-EPN-A and ST-EPN-RELA.	Dactinomycin	281-294	P53	Homo sapiens	109-112
27556362-9	2016	At the protein level, we validated the Actinomycin-D induced upregulation of PUMA, and of p53 interaction partners MDM2 and p21.	Dactinomycin	39-52	P53	Homo sapiens	90-93
23376438-10	2013	Collectively, these results suggest that the activation of p53, JNK or p38 kinase by ZEN metabolites is the main upstream signal required for the mitochondrial alteration of Bcl-2/Bax signaling pathways and intracellular ROS generation, while MMP loss and nuclear translocation of AIF are the critical downstream events for ZEN metabolite-mediated apoptosis in macrophages.	Zearalenone	85-88	P53	Homo sapiens	59-62
27556362-11	2016	Thus, Actinomycin-D could constitute a promising therapeutic option for ST-EPN-RELA ependymoma patients, whose tumours frequently exhibit p53 inactivation.	Dactinomycin	6-19	P53	Homo sapiens	138-141
23376438-10	2013	Collectively, these results suggest that the activation of p53, JNK or p38 kinase by ZEN metabolites is the main upstream signal required for the mitochondrial alteration of Bcl-2/Bax signaling pathways and intracellular ROS generation, while MMP loss and nuclear translocation of AIF are the critical downstream events for ZEN metabolite-mediated apoptosis in macrophages.	Zearalenone	324-327	P53	Homo sapiens	59-62
27533080-5	2016	The Bcl-2 inhibitor ABT-263 (navitoclax) increased sensitivity to the mTORC1/2 inhibitor AZD8055 in TP53 wild type GSCs, while sensitivity to AZD8055 in TP53 mutated GSCs remained unchanged.	navitoclax	20-27	P53	Homo sapiens	100-104
27533080-5	2016	The Bcl-2 inhibitor ABT-263 (navitoclax) increased sensitivity to the mTORC1/2 inhibitor AZD8055 in TP53 wild type GSCs, while sensitivity to AZD8055 in TP53 mutated GSCs remained unchanged.	navitoclax	20-27	P53	Homo sapiens	153-157
27445491-6	2016	In addition, SB enhanced p53 expression and decreased MDM2 expression, indicating that SB can regulate MDM2-p53 feedback loop.	Butyric Acid	13-15	P53	Homo sapiens	25-28
23319609-3	2013	Polyamide treatment activates p53 signaling in LNCaP prostate cancer cells without detectable DNA damage.	Nylons	0-9	P53	Homo sapiens	30-33
27445491-6	2016	In addition, SB enhanced p53 expression and decreased MDM2 expression, indicating that SB can regulate MDM2-p53 feedback loop.	Butyric Acid	13-15	P53	Homo sapiens	108-111
27445491-7	2016	p53 inhibited proliferation and promoted apoptosis, whereas MDM2 promoted proliferation and suppressed apoptosis, which indicated that functional effect of SB on OS cell lines at least in part depended on the MDM2-p53 signaling.	Butyric Acid	156-158	P53	Homo sapiens	0-3
27445491-7	2016	p53 inhibited proliferation and promoted apoptosis, whereas MDM2 promoted proliferation and suppressed apoptosis, which indicated that functional effect of SB on OS cell lines at least in part depended on the MDM2-p53 signaling.	Butyric Acid	156-158	P53	Homo sapiens	214-217
23092908-7	2013	RESULTS: The distribution of Arg/Arg, Arg/Pro and Pro/Pro genotypes of codon 72 of the TP53 gene was: 46.8%, 46.8% and 6.4%, respectively in the ovarian carcinomas and 64.3%, 31.4% and 4.3%, respectively in the control group.	Proline	50-53	P53	Homo sapiens	87-91
28911558-4	2016	Western blotting assay indicated that ZTP induced cell-cycle arrest by upregulation of p53 and reduced the expression of CDK2 in MCF-7 cells.	ztp	38-41	P53	Homo sapiens	87-90
23710242-0	2013	A Phenylbutenoid Dimer, cis-3-(3",4"-Dimethoxyphenyl)-4-[(E)-3""",4"""-Dimethoxystyryl] Cyclohex-1-ene, Exhibits Apoptogenic Properties in T-Acute Lymphoblastic Leukemia Cells via Induction of p53-Independent Mitochondrial Signalling Pathway.	phenylbutenoid	2-16	P53	Homo sapiens	193-196
27176768-0	2016	Diosmetin induces apoptosis by upregulating p53 via the TGF-beta signal pathway in HepG2 hepatoma cells.	diosmetin	0-9	P53	Homo sapiens	44-47
23149933-3	2013	In this study, we found that DJ-1 bound to the DNA-binding region of p53 in a manner dependent on the oxidation of C106.	(+)-Nicotine (+)-di-p-toluoyl tartrate	115-119	P53	Homo sapiens	69-72
27330773-10	2016	The p53 LIs were 24.5+-19.9, 25.7+-16.9 and 19.8+-13.8 in the CR, PR and SD/PD groups, respectively (P&gt;0.05).	Chromium	62-64	P53	Homo sapiens	4-7
24381593-4	2013	The combination of BIBF1120, an investigational VEGFR, PDGFR, and FGFR multityrosine kinase inhibitor with established anti-angiogenic activity, with paclitaxel abrogated the G2/M checkpoint in p53-null endometrial cancer cells via modulation of G2/M checkpoint regulators followed by induction of mitotic cell death.	nintedanib	19-27	P53	Homo sapiens	194-197
24381593-5	2013	In endometrial cancer cells harboring an oncogenic gain-of-function p53 mutation, synthetic lethality was created by combining paclitaxel with BIBF1120 and a histone deacetylase inhibitor, which serves to destabilize mutant p53.	nintedanib	143-151	P53	Homo sapiens	68-71
24381593-5	2013	In endometrial cancer cells harboring an oncogenic gain-of-function p53 mutation, synthetic lethality was created by combining paclitaxel with BIBF1120 and a histone deacetylase inhibitor, which serves to destabilize mutant p53.	nintedanib	143-151	P53	Homo sapiens	224-227
24381593-7	2013	These findings reveal that, in addition to antiangiogenic activity, the angiokinase inhibitor BIBF1120 can be used to restore sensitivity to paclitaxel and induce mitotic cell death in endometrial cancer cells with non-functional p53.	nintedanib	94-102	P53	Homo sapiens	230-233
22862424-0	2013	The p53-dependent expression of frataxin controls 5-aminolevulinic acid-induced accumulation of protoporphyrin IX and photo-damage in cancerous cells.	5-amino levulinic acid	50-71	P53	Homo sapiens	4-7
27651810-4	2016	Our findings indicated that DPCPX significantly induced apoptosis in MCF-7 cells while the cell viability was reduced specially 72 h after the treatment and the expression of p53 gene and caspase expressions was dramatically up-regulated.	1,3-dipropyl-8-cyclopentylxanthine	28-33	P53	Homo sapiens	175-178
22886373-0	2012	Hexavalent chromium induces energy metabolism disturbance and p53-dependent cell cycle arrest via reactive oxygen species in L-02 hepatocytes.	Chromium	11-19	P53	Homo sapiens	62-65
22939915-10	2012	In addition, dioscin inhibited APAP-induced activation and expression of CYP2E1, up-regulated the expression of Bcl-2 and Bid, and inhibited the expression of Bax, Bak and p53.	dioscin	13-20	P53	Homo sapiens	172-175
27651810-7	2016	Furthermore, DPCPX induced p53 and caspase 3, 8 and 9 expressions that consequently promotes the cell apoptosis in MCF-7 cells.	1,3-dipropyl-8-cyclopentylxanthine	13-18	P53	Homo sapiens	27-30
27221738-0	2016	miR-30c and miR-181a synergistically modulate p53-p21 pathway in diabetes induced cardiac hypertrophy.	mir-181a	12-20	P53	Homo sapiens	46-49
22692362-7	2012	The treatment of HOS cells with dicumarol, a NQO1 inhibitor, caused a dose-dependent decline in p53 protein levels, proving the effect of an antioxidant enzyme on p53 expression and, potentially, down-stream processes.	Dicumarol	32-41	P53	Homo sapiens	96-99
22692362-7	2012	The treatment of HOS cells with dicumarol, a NQO1 inhibitor, caused a dose-dependent decline in p53 protein levels, proving the effect of an antioxidant enzyme on p53 expression and, potentially, down-stream processes.	Dicumarol	32-41	P53	Homo sapiens	163-166
27159678-3	2016	Single-nucleotide polymorphism of p53 at codon72 leading to substitution of proline (Pro) in place of arginine (Arg) has been identified as a risk factor for development of many cancers, including nasopharyngeal carcinoma (NPC).	Proline	76-83	P53	Homo sapiens	34-37
22796327-3	2012	PRODH expression is inducible by p53, leading to increased proline oxidation, reactive oxygen species formation, and induction of apoptosis.	Proline	59-66	P53	Homo sapiens	33-36
27159678-3	2016	Single-nucleotide polymorphism of p53 at codon72 leading to substitution of proline (Pro) in place of arginine (Arg) has been identified as a risk factor for development of many cancers, including nasopharyngeal carcinoma (NPC).	Proline	85-88	P53	Homo sapiens	34-37
29931964-2	2016	METHODS: Human breast cancer MCF-7 cells were treated with arecoline at the concentrations of 0,10,30,50, 100,300,500mumol/L, the cell proliferation were detected by MTT assay, cell apoptosis were analyzed by Hoechst 33342 staining and flow cy-tometry, the protein expression of Bax,Bcl-2 and P53 were detected by Western blot.	Arecoline	59-68	P53	Homo sapiens	293-296
22700474-0	2012	Anthranilamide-pyrazolo[1,5-a]pyrimidine conjugates as p53 activators in cervical cancer cells.	anthranilamide-pyrazolo[1,5-a]pyrimidine	0-40	P53	Homo sapiens	55-58
22700474-1	2012	A library of new anthranilamide-pyrazolo[1,5-a]pyrimidine conjugates were designed, synthesized, and evaluated for their anticancer activity in cervical cancer cells such as HeLa and SiHa that possess low levels of p53.	anthranilamide-pyrazolo[1,5-a]pyrimidine	17-57	P53	Homo sapiens	215-218
29931964-4	2016	However, high concentration(100,300,500mumol/L) arecoline inhibited proliferation and induced apoptosis of MCF-7 cells in a concentration-dependent manner, arecoline also significantly increased P53 and Bax protein expression and decreased Bcl-2 protein expression.	Arecoline	156-165	P53	Homo sapiens	195-198
29931964-5	2016	CONCLUSIONS: High concentration arecoline inhibited the proliferation and induced the apoptosis of MCF-7 cells, the mechanism was probably corrected with increasing P53 and Bax protein expression and decreasing Bcl-2 pro-tein expression.	Arecoline	32-41	P53	Homo sapiens	165-168
22052810-2	2012	A single nucleotide polymorphism of TP53 encoding either arginine or proline at codon 72 is suggested to alter in vitro p53 behavior.	Proline	69-76	P53	Homo sapiens	36-40
27209699-5	2016	Of them, dual-specificity protein phosphatase 26 (DUSP26), which inhibits mitogen-activated protein kinase (MAPK) and p53 tumor suppressor and is known to be overexpressed in anaplastic thyroid carcinoma, was inhibited by ethyl-3,4-dephostatin in a concentration-dependent manner.	ethyl-3,4-dephostatin	222-243	P53	Homo sapiens	118-121
22052810-2	2012	A single nucleotide polymorphism of TP53 encoding either arginine or proline at codon 72 is suggested to alter in vitro p53 behavior.	Proline	69-76	P53	Homo sapiens	120-123
27209699-7	2016	Moreover, ethyl-3,4-dephostatin protects DUSP26-mediated dephosphorylation of p38, a member of the MAPK family, and p53.	ethyl-3,4-dephostatin	10-31	P53	Homo sapiens	116-119
22542555-0	2012	MEHP-induced oxidative DNA damage and apoptosis in HepG2 cells correlates with p53-mediated mitochondria-dependent signaling pathway.	mono-(2-ethylhexyl)phthalate	0-4	P53	Homo sapiens	79-82
26849940-4	2016	Mechanism investigation showed that dioscin markedly up-regulated p53 level, and down-regulated cyclin-dependent kinase 2 (CDK2) and Cyclin A levels.	dioscin	36-43	P53	Homo sapiens	66-69
22542555-6	2012	These findings indicated that MEHP induced oxidative DNA damage and apoptosis in HepG2 cells, and p53 and its downstream proteins were involved in mitochondria- and caspase-mediated apoptosis induced by MEHP.	mono-(2-ethylhexyl)phthalate	203-207	P53	Homo sapiens	98-101
22356895-9	2012	In contrast, the predictive utility of the 72 Arg/Pro SNP in p53 requires mutational analysis of p53, limiting its routine clinical use.	Proline	50-53	P53	Homo sapiens	61-64
22356895-9	2012	In contrast, the predictive utility of the 72 Arg/Pro SNP in p53 requires mutational analysis of p53, limiting its routine clinical use.	Proline	50-53	P53	Homo sapiens	97-100
26883465-0	2016	Meeting Organocatalysis with Drug Discovery: Asymmetric Synthesis of 3,3"-Spirooxindoles Fused with Tetrahydrothiopyrans as Novel p53-MDM2 Inhibitors.	tetrahydrothiopyrans	100-120	P53	Homo sapiens	130-133
22641291-0	2012	Fludarabine nucleoside induces accumulations of p53, p63 and p73 in the nuclei of human B-lymphoid cell lines, with cytosolic and mitochondrial increases in p53.	fludarabine nucleoside	0-22	P53	Homo sapiens	48-51
22641291-0	2012	Fludarabine nucleoside induces accumulations of p53, p63 and p73 in the nuclei of human B-lymphoid cell lines, with cytosolic and mitochondrial increases in p53.	fludarabine nucleoside	0-22	P53	Homo sapiens	157-160
22641291-1	2012	PURPOSE: Human Raji cells treated with fludarabine nucleoside (2-FaraA, 3 muM) undergo apoptosis with accumulation of p53 in the nuclei as multiple phosphorylated isoforms and C-terminal truncated derivatives.	fludarabine nucleoside	39-61	P53	Homo sapiens	118-121
26909997-6	2016	TP53*72 showed genotypic distribution: in the control group, there was 16.10% homozygous Pro, and 42.44% heterozygous and 41.46% homozygous Arg; in the BC group, there was 15.43% homozygous Pro, and 42.55% heterozygous and 42.02% homozygous Arg.	Proline	89-92	P53	Homo sapiens	0-4
22074401-0	2012	Gallium compound GaQ(3) -induced Ca(2+)  signalling triggers p53-dependent and -independent apoptosis in cancer cells.	tris(8-quinolinolato)gallium (III)	17-23	P53	Homo sapiens	61-64
22074401-4	2012	Here, we have explored the mechanism(s) of GaQ(3) -induced apoptosis in cancer cells, focusing on p53 and intracellular Ca(2+)  signalling.	tris(8-quinolinolato)gallium (III)	43-49	P53	Homo sapiens	98-101
22074401-5	2012	EXPERIMENTAL APPROACH GaQ(3) -induced cytotoxicity and apoptosis were determined in cancer cell lines, with different p53 status (p53(+/+) , p53(-/-)  and p53 mutant).	tris(8-quinolinolato)gallium (III)	22-28	P53	Homo sapiens	118-121
22074401-5	2012	EXPERIMENTAL APPROACH GaQ(3) -induced cytotoxicity and apoptosis were determined in cancer cell lines, with different p53 status (p53(+/+) , p53(-/-)  and p53 mutant).	tris(8-quinolinolato)gallium (III)	22-28	P53	Homo sapiens	130-133
22074401-5	2012	EXPERIMENTAL APPROACH GaQ(3) -induced cytotoxicity and apoptosis were determined in cancer cell lines, with different p53 status (p53(+/+) , p53(-/-)  and p53 mutant).	tris(8-quinolinolato)gallium (III)	22-28	P53	Homo sapiens	130-133
22074401-5	2012	EXPERIMENTAL APPROACH GaQ(3) -induced cytotoxicity and apoptosis were determined in cancer cell lines, with different p53 status (p53(+/+) , p53(-/-)  and p53 mutant).	tris(8-quinolinolato)gallium (III)	22-28	P53	Homo sapiens	130-133
22074401-8	2012	Ca(2+)  signalling, p53, p300 and ROS were serially knocked down to study Ca(2+) -p53-ROS ineractions in GaQ(3) -induced apoptosis.	tris(8-quinolinolato)gallium (III)	105-111	P53	Homo sapiens	82-85
22074401-9	2012	KEY RESULTS GaQ(3)  triggered intracellular Ca(2+)  release stabilizing p53-p300 complex and recruited p53 to p53 promoter, leading to p53 mRNA and protein synthesis.	tris(8-quinolinolato)gallium (III)	12-18	P53	Homo sapiens	72-75
22074401-9	2012	KEY RESULTS GaQ(3)  triggered intracellular Ca(2+)  release stabilizing p53-p300 complex and recruited p53 to p53 promoter, leading to p53 mRNA and protein synthesis.	tris(8-quinolinolato)gallium (III)	12-18	P53	Homo sapiens	103-106
26909997-6	2016	TP53*72 showed genotypic distribution: in the control group, there was 16.10% homozygous Pro, and 42.44% heterozygous and 41.46% homozygous Arg; in the BC group, there was 15.43% homozygous Pro, and 42.55% heterozygous and 42.02% homozygous Arg.	Proline	190-193	P53	Homo sapiens	0-4
22074401-9	2012	KEY RESULTS GaQ(3)  triggered intracellular Ca(2+)  release stabilizing p53-p300 complex and recruited p53 to p53 promoter, leading to p53 mRNA and protein synthesis.	tris(8-quinolinolato)gallium (III)	12-18	P53	Homo sapiens	103-106
22074401-9	2012	KEY RESULTS GaQ(3)  triggered intracellular Ca(2+)  release stabilizing p53-p300 complex and recruited p53 to p53 promoter, leading to p53 mRNA and protein synthesis.	tris(8-quinolinolato)gallium (III)	12-18	P53	Homo sapiens	103-106
26668309-5	2016	Moreover, NA-17 showed p53-dependent inhibition selectivity in different NSCLC cell lines due to the activation state of endogenous p53 in the background level.	na-17	10-15	P53	Homo sapiens	23-26
22481236-0	2012	Zoledronic acid produces antitumor effects on mesothelioma through apoptosis and S-phase arrest in p53-independent and Ras prenylation-independent manners.	Zoledronic Acid	0-15	P53	Homo sapiens	99-102
26668309-5	2016	Moreover, NA-17 showed p53-dependent inhibition selectivity in different NSCLC cell lines due to the activation state of endogenous p53 in the background level.	na-17	10-15	P53	Homo sapiens	132-135
22064349-0	2012	Synergistic induction of p53 mediated apoptosis by valproic acid and nutlin-3 in acute myeloid leukemia.	Valproic Acid	51-64	P53	Homo sapiens	25-28
22064349-2	2012	We hypothesized that co-inhibition of MDM2 and HDACs, with nutlin-3 and valproic acid (VPA) would additively inhibit growth in leukemic cells expressing wild type TP53 and induce p53-mediated apoptosis.	Valproic Acid	72-85	P53	Homo sapiens	163-167
26768586-0	2016	miR214-regulated p53-NOX4/p66shc pathway plays a crucial role in the protective effect of Ginkgolide B against cisplatin-induced cytotoxicity in HEI-OC1 cells.	ginkgolide B	90-102	P53	Homo sapiens	17-20
22064349-2	2012	We hypothesized that co-inhibition of MDM2 and HDACs, with nutlin-3 and valproic acid (VPA) would additively inhibit growth in leukemic cells expressing wild type TP53 and induce p53-mediated apoptosis.	Valproic Acid	72-85	P53	Homo sapiens	179-182
22064349-2	2012	We hypothesized that co-inhibition of MDM2 and HDACs, with nutlin-3 and valproic acid (VPA) would additively inhibit growth in leukemic cells expressing wild type TP53 and induce p53-mediated apoptosis.	Valproic Acid	87-90	P53	Homo sapiens	163-167
22064349-2	2012	We hypothesized that co-inhibition of MDM2 and HDACs, with nutlin-3 and valproic acid (VPA) would additively inhibit growth in leukemic cells expressing wild type TP53 and induce p53-mediated apoptosis.	Valproic Acid	87-90	P53	Homo sapiens	179-182
26768586-9	2016	GB significantly decreased p53 expression and p53-binding of the promoters of NOX4 and p66(shc).	ginkgolide B	0-2	P53	Homo sapiens	27-30
26768586-9	2016	GB significantly decreased p53 expression and p53-binding of the promoters of NOX4 and p66(shc).	ginkgolide B	0-2	P53	Homo sapiens	46-49
26768586-10	2016	Over-expression of p53 suppressed the inhibitory effects of GB on NOX4 and p66(shc) expression and superoxide generation and the protective effects of GB on loss of cell viability and apoptosis associated with cisplatin.	ginkgolide B	60-62	P53	Homo sapiens	19-22
22301280-7	2012	Deazaflavin analogs therefore function to activate p53 through a novel mechanism, by inhibiting the E3 ligase activity of MDM2 in a manner that involves binding to the MDM2 RING.	5-deazaflavin	0-11	P53	Homo sapiens	51-54
25867069-0	2016	The NEDD8 inhibitor MLN4924 increases the size of the nucleolus and activates p53 through the ribosomal-Mdm2 pathway.	pevonedistat	20-27	P53	Homo sapiens	78-81
22285236-8	2012	Based on the detection of protein expression (PARP, p53, Bcl-2/Bcl-xL, Bax, p38, pp38) we found that usnic acid and atranorin are activators of programmed cell death in A2780 and HT-29, probably through the mitochondrial pathway.	atranorin	116-125	P53	Homo sapiens	52-55
26985323-3	2016	Further investigation of the Leu26 pocket resulted in potent, novel substituted piperidine inhibitors of the HDM2-p53 interaction that demonstrated tumor regression in several human cancer xenograft models in mice.	piperidine	80-90	P53	Homo sapiens	114-117
22450794-8	2012	However, the interaction between p53 and T antigen was inhibited at a TBT or TPT concentration of 10-9 M, respectively.	9 alpha,11 alpha,15 alpha-trihydroxy-16-phenoxy-17,18,19,20-tetranorprosta-4,5,13-trienoic acid	77-80	P53	Homo sapiens	33-36
22159450-6	2012	In contrast, CG-1521             significantly induces the expression of several p53 target genes associated with             apoptosis including Bnip3/Bnip3L, p21/p21B and Gdf15.	cysteinylglycine	13-15	P53	Homo sapiens	81-84
27551490-7	2016	DBME induced G2/M phase arrest and apoptosis in MCF-7 cells by suppressing the expression of cyclin A1, cyclin B1 and Cdk-1 and increasing the expression of p53, Bax/Bcl-2 ratio leading to activation of caspases and PARP degradation.	dbme	0-4	P53	Homo sapiens	157-160
22172427-5	2012	Furthermore, PGG suppressed PARP cleavage and caspase-3 activation, cytochrome c release, up-regulation of bax and p53 in cisplatin-treated HRCs.	beta-penta-O-galloyl-glucose	13-16	P53	Homo sapiens	115-118
26608553-0	2016	Synthesis, characterization and biological evaluation of anti-cancer indolizine derivatives via inhibiting beta-catenin activity and activating p53.	indolizine	69-79	P53	Homo sapiens	144-147
22027089-15	2012	The enhanced sensitivity of PCa cells to ZP and the apparent ability of ZP and TPEN to kill quiescent and rapidly dividing cells in a p53-independent manner suggest that ZP/TPEN might be used to develop adjunct treatments for PCa.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	79-83	P53	Homo sapiens	134-137
27168690-12	2016	Thus, it is possible to conclude that 1-(3,4,5-trihydroxyphenyl)-dodecylbenzoate induces apoptosis by inhibiting the antiapoptotic protein Bcl-2 and by increasing the release of AIF, Bax and p53.	1-(3,4,5-trihydroxyphenyl)-dodecylbenzoate	38-80	P53	Homo sapiens	191-194
22051195-4	2012	In this study, we found that Mdm2 was stabilized and upregulated upon Actinomycin D (ActD) treatment in the p53-deficient H1299 cell line.	Dactinomycin	70-83	P53	Homo sapiens	108-111
22051195-4	2012	In this study, we found that Mdm2 was stabilized and upregulated upon Actinomycin D (ActD) treatment in the p53-deficient H1299 cell line.	Dactinomycin	85-89	P53	Homo sapiens	108-111
25908509-14	2015	Patients with a del(17p) or TP53 mutation can be treated with ibrutinib or a combination of idelalisib and rituximab.	idelalisib	92-102	P53	Homo sapiens	28-32
26782376-10	2015	Analysis of p53 gene polymorphisms showed a higher frequency for the genotype Arg/Pro (66%) and a lower frequency for the Arg/Arg (23%) and Pro/Pro (11%) genotypes.	Proline	82-85	P53	Homo sapiens	12-15
25633658-7	2015	Herein, we showed that Naph treatment enhances IR-induced cell cycle arrest and death in MCF-7 human breast cancer cells through the p53-dependent p21 activation mechanism.	naphthazarin	23-27	P53	Homo sapiens	133-136
25633658-8	2015	These results suggest that Naph might sensitize breast cancer cells to radiotherapy by enhancing the p53-p21 mechanism activity.	naphthazarin	27-31	P53	Homo sapiens	101-104
21717444-1	2012	BACKGROUND: The p53 antisense oligonucleotide cenersen has been shown to sensitize acute myeloid leukemia (AML) stem cells to DNA damaging agents.	oligonucleotide cenersen	30-54	P53	Homo sapiens	16-19
22214764-8	2012	Functionally, the cytoplasmic accumulation of ZBP-89 by p53(G245D) significantly abrogated the induction of p21 caused by sodium butyrate (NaB) treatment and protected cells from TSA-induced death.	Butyric Acid	122-137	P53	Homo sapiens	56-59
26782376-10	2015	Analysis of p53 gene polymorphisms showed a higher frequency for the genotype Arg/Pro (66%) and a lower frequency for the Arg/Arg (23%) and Pro/Pro (11%) genotypes.	Proline	140-143	P53	Homo sapiens	12-15
26782376-10	2015	Analysis of p53 gene polymorphisms showed a higher frequency for the genotype Arg/Pro (66%) and a lower frequency for the Arg/Arg (23%) and Pro/Pro (11%) genotypes.	Proline	140-143	P53	Homo sapiens	12-15
25226867-7	2015	TP53 sequence analysis of the index patient revealed the germline mutation c.1025G &gt; C in a heterozygous state, resulting in an amino acid exchange from arginine to proline (p.Arg342Pro) in the tetramerization domain of p53.	Proline	168-175	P53	Homo sapiens	0-4
26634523-0	2015	Dihydromyricetin induces cell apoptosis via a p53-related pathway in AGS human gastric cancer cells.	dihydromyricetin	0-16	P53	Homo sapiens	46-49
25226867-7	2015	TP53 sequence analysis of the index patient revealed the germline mutation c.1025G &gt; C in a heterozygous state, resulting in an amino acid exchange from arginine to proline (p.Arg342Pro) in the tetramerization domain of p53.	Proline	168-175	P53	Homo sapiens	223-226
25530218-0	2015	Nitidine chloride induces apoptosis in human hepatocellular carcinoma cells through a pathway involving p53, p21, Bax and Bcl-2.	nitidine	0-17	P53	Homo sapiens	104-107
25404486-0	2015	Selective ROS-dependent p53-associated anticancer effects of the hypoxoside derivative rooperol on human teratocarcinomal cancer stem-like cells.	rooperol	87-95	P53	Homo sapiens	24-27
25404486-4	2015	Accordingly, rooperol only eliminates colon carcinoma cells expressing p53.	rooperol	13-21	P53	Homo sapiens	71-74
22502699-2	2012	A common single nucleotide polymorphism located within the proline rich region of TP53 gene at codon 72 in exon 4 encodes either proline or arginine.	Proline	59-66	P53	Homo sapiens	82-86
22502699-2	2012	A common single nucleotide polymorphism located within the proline rich region of TP53 gene at codon 72 in exon 4 encodes either proline or arginine.	Proline	129-136	P53	Homo sapiens	82-86
22502699-3	2012	TP53 Arg 72 is more active than TP53 Pro 72 in inducing apoptosis.	Proline	37-40	P53	Homo sapiens	0-4
25404486-6	2015	Rooperol-induced apoptosis was associated with activation of p53 and concentration-dependent changes of the expression levels of both caspase 3 and poly ADP ribose polymerase type 1 cleaved subunits.	rooperol	0-8	P53	Homo sapiens	61-64
26634523-6	2015	Furthermore, DHM also regulated the expression of apoptotic genes such as p53 and B-cell lymphoma-2 (bcl-2) in a dose- and time-dependent manner.	dihydromyricetin	13-16	P53	Homo sapiens	74-77
22454691-0	2012	Zerumbone, a Southeast Asian Ginger Sesquiterpene, Induced Apoptosis of Pancreatic Carcinoma Cells through p53 Signaling Pathway.	zerumbone	0-9	P53	Homo sapiens	107-110
26628631-7	2015	Ibrutinib and idelalisib are active in patients with high-risk features, achieving superior disease control in difficult-to-treat patients than prior best therapy, making them the preferred agents for chronic lymphocytic leukemia with TP53 aberrations and for patients resistant to chemoimmunotherapy.	idelalisib	14-24	P53	Homo sapiens	235-239
22613405-1	2012	OBJECTIVE: The association between codon 72 polymorphism of the tumour protein p53 (TP53) gene - which results in a missense mutation of arginine (R) to proline (P) - and susceptibility to hepatocellular carcinoma (HCC) is controversial.	Proline	153-160	P53	Homo sapiens	79-82
22613405-1	2012	OBJECTIVE: The association between codon 72 polymorphism of the tumour protein p53 (TP53) gene - which results in a missense mutation of arginine (R) to proline (P) - and susceptibility to hepatocellular carcinoma (HCC) is controversial.	Proline	153-160	P53	Homo sapiens	84-88
25261582-2	2015	The tumour-suppressor p53 protein presents a proline-rich region that is crucial for regulating apoptosis by connecting the p53 with a complex protein network.	Proline	45-52	P53	Homo sapiens	22-25
25261582-2	2015	The tumour-suppressor p53 protein presents a proline-rich region that is crucial for regulating apoptosis by connecting the p53 with a complex protein network.	Proline	45-52	P53	Homo sapiens	124-127
25261582-5	2015	In this article, we analyse the binding of the p53 proline-rich region with a pool of selected polyproline binding domains (i.e. SH3 and WW), and we present the first demonstration that the purified SH3 domains of the CD2AP/Cin85 protein family are able to directly bind the p53 protein, and to discriminate between the two polymorphic variants P72R.	Proline	51-58	P53	Homo sapiens	47-50
27093815-5	2015	RESULT: The results showed that PTX could increase the apoptosis and the expression of Caspase3, PARP, CytC, AIF and Bax and reduce the proliferation, membrane potential and the expression of PI3K, p-AKT, p53, p21, Cleavage-PARP, Cleavage-Caspase3 and Bcl-2 in CNE2 cell in a concentration-dependent manner.	ptx	32-35	P53	Homo sapiens	205-208
26637744-5	2015	New B-cell receptor inhibitors, such as ibrutinib and idelalisib, may have a role in the management of B-PLL, especially for the patients harboring abnormalities of TP53.	idelalisib	54-64	P53	Homo sapiens	165-169
23152837-4	2012	Besides, some apoptosis related events were observed after treatment with dicycloplatin, including increase of reactive oxygen species (ROS), collapse of mitochondrial membrane potential (Deltapsim), release of cytochrome c from the mitochondria to the cytosol, upregulation of p53, which were accompanied by activation of caspase-9, caspase-3, caspase-8, and poly (ADP-ribose) polymerase cleavage in a concentration-dependent manner.	diammine(1,1-cyclobutanedicarboxylate)platinum(II)	74-87	P53	Homo sapiens	278-281
27093815-7	2015	CONCLUSION: PTX can promote apoptosis and growth inhibition of human nasopharyngeal cancer cell line CNE2 and the mechanism involves suppressing PI3K/AKT/p53 signaling pathway.	ptx	12-15	P53	Homo sapiens	154-157
26637745-6	2015	Ibrutinib and idelalisib are currently approved for the treatment of relapsed or refractory CLL or frontline treatment of 17p-/TP53mut CLL regardless of fitness.	idelalisib	14-24	P53	Homo sapiens	127-131
22319594-0	2012	Benzo[a]pyrene, aflatoxine B1 and acetaldehyde mutational patterns in TP53 gene using a functional assay: relevance to human cancer aetiology.	Acetaldehyde	34-46	P53	Homo sapiens	70-74
26322477-0	2015	Induction of apoptosis in cancer cells through N-acetyl-l-leucine-modified polyethylenimine-mediated p53 gene delivery.	acetylleucine	47-65	P53	Homo sapiens	101-104
22319594-6	2012	By using a functional assay, the Functional Analysis of Separated Alleles in Yeast (FASAY), the present study depicts the mutational pattern of TP53 in normal human fibroblasts after in vitro exposure to well-known carcinogens: benzo[a]pyrene, aflatoxin B(1) and acetaldehyde.	Acetaldehyde	263-275	P53	Homo sapiens	144-148
25502079-3	2015	A common polymorphism of the p53 codon 72 in exon 4 with two alleles encoding arginine or proline is known at this locus.	Proline	90-97	P53	Homo sapiens	29-32
25220870-0	2014	Promotion of p53 expression and reactive oxidative stress production is involved in zerumbone-induced cisplatin sensitization of non-small cell lung cancer cells.	zerumbone	84-93	P53	Homo sapiens	13-16
21879111-11	2011	Cd(2+) strongly induced damages and altered the function of p53, while Cu(2+), followed by Cr(3+), showed lower percentages of p53-mutant colonies.	cupric ion	71-77	P53	Homo sapiens	127-130
26322477-1	2015	Herein, N-acetyl-L-leucine-modified polyethylenimine was successfully constructed through the EDC/NHS-mediated coupling reaction and employed as vectors to accomplish p53 gene delivery using HeLa (p53wt) and PC-3 cells (p53null) as models.	acetylleucine	8-26	P53	Homo sapiens	167-170
25526924-0	2015	Lipoic acid induces p53-independent cell death in colorectal cancer cells and potentiates the cytotoxicity of 5-fluorouracil.	Thioctic Acid	0-11	P53	Homo sapiens	20-23
21893155-0	2011	Differential programming of p53-deficient embryonic cells during rotenone block.	Rotenone	65-73	P53	Homo sapiens	28-31
25244701-4	2014	Using the intrinsically disordered N-terminal region of the p53 protein as an experimental model, a set of proline (PRO) and alanine (ALA) to glycine (GLY) substitution variants were designed to modulate backbone conformational propensities without introducing non-native intramolecular interactions.	Proline	107-114	P53	Homo sapiens	60-63
25244701-4	2014	Using the intrinsically disordered N-terminal region of the p53 protein as an experimental model, a set of proline (PRO) and alanine (ALA) to glycine (GLY) substitution variants were designed to modulate backbone conformational propensities without introducing non-native intramolecular interactions.	Proline	116-119	P53	Homo sapiens	60-63
25641576-4	2015	SCOPE OF REVIEW: p53 family proteins have unique structural and functional plasticity, and here we discuss the relevance of prolyl-isomerization to actively shape these features.	Peptide oostatic hormone	124-130	P53	Homo sapiens	17-20
25242120-6	2014	The results indicated that silymarin effectively suppressed cell growth in a dose- and time-dependent manner, and arrested cell cycle progression at G1/S phase in A2780s and PA-1 cells via up-regulation of p53, p21, and p27 protein expression, and down-regulation of CDK2 protein expression.	Silymarin	27-36	P53	Homo sapiens	206-209
21973212-0	2011	Role for p53 in selenium-induced senescence.	Selenium	16-24	P53	Homo sapiens	9-12
21973212-3	2011	Here, the shRNA knockdown approach and other DNA damage assays are employed to test the hypothesis that p53 plays a role in selenium-induced senescence.	Selenium	124-132	P53	Homo sapiens	104-107
21973212-6	2011	These results suggest that p53 is critical for senescence induction in the response of MRC-5 noncancerous cells to selenium compounds.	Selenium	115-123	P53	Homo sapiens	27-30
26208523-0	2015	The 1,2-Diaminocyclohexane Carrier Ligand in Oxaliplatin Induces p53-Dependent Transcriptional Repression of Factors Involved in Thymidylate Biosynthesis.	1,2-cyclohexanediamine	4-26	P53	Homo sapiens	65-68
26420962-4	2015	A single nucleotide polymorphism (SNP) in the TP53 gene resulting in the presence of either arginine (Arg) or proline (Pro) or both at codon 72 was shown to alter TP53 tumor-suppressor properties.	Proline	110-117	P53	Homo sapiens	46-50
21595775-4	2011	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in EC were 39.4%, 45.6%, and 15.0%, respectively; frequencies in the controls were 43.2%, 45.6%, and 11.2%, respectively.	Proline	60-63	P53	Homo sapiens	19-22
21595775-4	2011	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in EC were 39.4%, 45.6%, and 15.0%, respectively; frequencies in the controls were 43.2%, 45.6%, and 11.2%, respectively.	Proline	69-72	P53	Homo sapiens	19-22
21595775-4	2011	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in EC were 39.4%, 45.6%, and 15.0%, respectively; frequencies in the controls were 43.2%, 45.6%, and 11.2%, respectively.	Proline	69-72	P53	Homo sapiens	19-22
25368817-9	2014	CONCLUSIONS: CD34 and p53 IHC stains of BMC or BMB provide useful information for differentiating between hMDS and AA.	bmc	40-43	P53	Homo sapiens	22-25
25712892-1	2014	AIM: Arg72Pro is a polymorphism commonly occurring in the proline-rich domain of Tp53.	Proline	58-65	P53	Homo sapiens	81-85
26420962-4	2015	A single nucleotide polymorphism (SNP) in the TP53 gene resulting in the presence of either arginine (Arg) or proline (Pro) or both at codon 72 was shown to alter TP53 tumor-suppressor properties.	Proline	110-117	P53	Homo sapiens	163-167
26420962-4	2015	A single nucleotide polymorphism (SNP) in the TP53 gene resulting in the presence of either arginine (Arg) or proline (Pro) or both at codon 72 was shown to alter TP53 tumor-suppressor properties.	Proline	119-122	P53	Homo sapiens	46-50
25241984-5	2014	Moreover, quantitative PCR revealed that TQ induced apoptosis in Siha cells through p53-dependent pathway as shown by elevated level of p53-mediated apoptosis target genes, whereas apoptosis in C33A cells was mainly associated with the activation of caspase-3.	thymoquinone	41-43	P53	Homo sapiens	84-87
25241984-5	2014	Moreover, quantitative PCR revealed that TQ induced apoptosis in Siha cells through p53-dependent pathway as shown by elevated level of p53-mediated apoptosis target genes, whereas apoptosis in C33A cells was mainly associated with the activation of caspase-3.	thymoquinone	41-43	P53	Homo sapiens	136-139
21841506-7	2011	Pairwise combination analysis showed that patients carrying the variant P53 Pro/Pro-P73 GC/GC or P53 Pro/Pro-MDM2 GG genotypes had survival time only half of that for those carrying the wild-type genotypes, with hazard ratio being 2.47 (95% CI, 1.20-5.10) and 2.00 (95% CI, 1.15-3.46), respectively.	Proline	76-79	P53	Homo sapiens	72-75
26420962-4	2015	A single nucleotide polymorphism (SNP) in the TP53 gene resulting in the presence of either arginine (Arg) or proline (Pro) or both at codon 72 was shown to alter TP53 tumor-suppressor properties.	Proline	119-122	P53	Homo sapiens	163-167
26091798-13	2015	These results demonstrate that p53 is able to respond to exposure of arsenic or Cr(VI), suggesting that BEAS-2B cells are an appropriate in vitro model to investigate arsenic or Cr(VI) induced lung cancer.	Chromium	80-82	P53	Homo sapiens	31-34
21875801-1	2011	Structure-activity relationships for the MDM2-p53 inhibitory activity of a series of A-ring substituted 2-N-benzyl-3-(4-chlorophenyl)-3-(1-(hydroxymethyl)cyclopropyl)methoxy)isoindolinones have been investigated, giving rise to compounds with improved potency over their unsubstituted counterparts.	2-n-benzyl-3-(4-chlorophenyl)-3-(1-(hydroxymethyl)cyclopropyl)methoxy)isoindolinones	104-188	P53	Homo sapiens	46-49
25108128-9	2014	It was resulted that F0/1-HCV patients have significant differences of P53 at 72 (Pro/Pro and Arg/Arg) genotypes and dominant/recessive genetic models as well as APO-1 -670 A/A genotype and dominant genetic model as compared to F3/4-HCV patients.	Proline	82-85	P53	Homo sapiens	71-74
25202384-8	2014	Furthermore, it was found that DHM induced cell apoptosis in a p53-dependent manner.	dihydromyricetin	31-34	P53	Homo sapiens	63-66
25202384-9	2014	DHM upregulated p53 expression, and the upregulation of p53 increased the levels of the cleaved caspase-3 protein, directly inducing cell apoptosis.	dihydromyricetin	0-3	P53	Homo sapiens	16-19
20443084-11	2011	Our data show that proline homozygosity at p53 codon 72 is associated with decreased breast cancer risk in Arab women.	Proline	19-26	P53	Homo sapiens	43-46
26091798-13	2015	These results demonstrate that p53 is able to respond to exposure of arsenic or Cr(VI), suggesting that BEAS-2B cells are an appropriate in vitro model to investigate arsenic or Cr(VI) induced lung cancer.	Chromium	178-180	P53	Homo sapiens	31-34
21663398-0	2011	Geldanamycin analog 17-DMAG limits apoptosis in human peripheral blood cells by inhibition of p53 activation and its interaction with heat-shock protein 90 kDa after exposure to ionizing radiation.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	20-27	P53	Homo sapiens	94-97
21663398-2	2011	We tested the effect of 17-dimethylamino-ethylamino-17-demethoxygeldanamycin (17-DMAG) on p53 expression and function after radiation exposure.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	24-76	P53	Homo sapiens	90-93
26405550-6	2015	Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P&lt;0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC.	Proline	271-274	P53	Homo sapiens	40-43
21663398-2	2011	We tested the effect of 17-dimethylamino-ethylamino-17-demethoxygeldanamycin (17-DMAG) on p53 expression and function after radiation exposure.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	78-85	P53	Homo sapiens	90-93
21663398-7	2011	Analysis of p53-Hsp90 interaction in ex vivo cell lysates indicated that the binding between the two molecules occurred after irradiation but 17-DMAG prevented the binding.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	142-149	P53	Homo sapiens	12-15
25034526-6	2014	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in lung cancer were 25.5, 37.7, and 36.8 %, respectively; frequencies in the controls were 53.4, 30.2, and 16.4 %, respectively (p &lt; 0.01).	Proline	60-63	P53	Homo sapiens	19-22
25034526-6	2014	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in lung cancer were 25.5, 37.7, and 36.8 %, respectively; frequencies in the controls were 53.4, 30.2, and 16.4 %, respectively (p &lt; 0.01).	Proline	69-72	P53	Homo sapiens	19-22
25034526-6	2014	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in lung cancer were 25.5, 37.7, and 36.8 %, respectively; frequencies in the controls were 53.4, 30.2, and 16.4 %, respectively (p &lt; 0.01).	Proline	69-72	P53	Homo sapiens	19-22
26405550-6	2015	Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P&lt;0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC.	Proline	276-279	P53	Homo sapiens	40-43
26405550-6	2015	Conversely, the interaction between the p53 and p21 polymorphisms significantly decreased the risk of prostate cancer, with the odds ratio (OR) being 0.49 [95% confidence interval (CI), 0.27-0.86; P&lt;0.05] for subjects carrying the p53 codon 72 arginine (Arg)/proline (Pro)+Pro/Pro and p21 C98A CA genotypes compared to the combined reference genotypes p53 codon 72 Arg/Arg and p21 C98A CC.	Proline	276-279	P53	Homo sapiens	40-43
21857681-8	2011	Here we elucidate a molecular mechanism by which beta-adrenergic catecholamines, acting through both Gs-PKA and beta-arrestin-mediated signalling pathways, trigger DNA damage and suppress p53 levels respectively, thus synergistically leading to the accumulation of DNA damage.	Catecholamines	65-79	P53	Homo sapiens	188-191
25989210-0	2015	Actinomycin D and nutlin-3a synergistically promote phosphorylation of p53 on serine 46 in cancer cell lines of different origin.	Dactinomycin	0-13	P53	Homo sapiens	71-74
24928205-5	2014	A marked induction of DDR, including the phosphorylation of ATM, Chk2, p53 and histone H2AX, was observed after LY2603618 treatment.	LY2603618	112-121	P53	Homo sapiens	71-74
25989210-5	2015	Actinomycin D promotes phosphorylation and accumulation of p53 via a mechanism that involves high expression of MDM2.	Dactinomycin	0-13	P53	Homo sapiens	59-62
21570478-9	2011	Within the regulatory network affected by crocidolite, p53 and NF-kappaB complex are the most important regulators.	Asbestos, Crocidolite	42-53	P53	Homo sapiens	55-58
25989210-6	2015	We hypothesized that co-treatment of cells with actinomycin D and nutlin-3a would lead to synergistic activation of p53 by stimulating kinases and preventing accumulated MDM2 from binding to p53.	Dactinomycin	48-61	P53	Homo sapiens	116-119
24832164-9	2014	Our series of IC-PBL and PT-PBL cases revealed differential expression of CD10 (0% vs. 42%, respectively), CD56 (22% vs. 42%, respectively), TP53 (67% vs. 8%, respectively), and BCL2 (88% vs. 25%, respectively).	pt-pbl	25-31	P53	Homo sapiens	141-145
25989210-6	2015	We hypothesized that co-treatment of cells with actinomycin D and nutlin-3a would lead to synergistic activation of p53 by stimulating kinases and preventing accumulated MDM2 from binding to p53.	Dactinomycin	48-61	P53	Homo sapiens	191-194
25989210-7	2015	Indeed, co-treatment of various cell lines with actinomycin D and nutlin-3a resulted in a synergistic increase of p53 phosphorylation on serine 46.	Dactinomycin	48-61	P53	Homo sapiens	114-117
21772120-10	2011	Taken together, our results demonstrate that the loss of Spn induces a proliferative response by increasing Rb phosphorylation, which, in turn, activates p53, thereby neutralizing the proliferative response.	Rubidium	108-110	P53	Homo sapiens	154-157
24706461-0	2015	Mono(2-ethylhexyl) phthalate induces apoptosis in p53-silenced L02 cells via activation of both mitochondrial and death receptor pathways.	mono-(2-ethylhexyl)phthalate	0-28	P53	Homo sapiens	50-53
21461655-5	2011	RESULTS: The frequencies of Arg/Arg, Arg/Pro, and Pro/Pro genotypes of the p53 codon 72 polymorphism were 43.3, 42.0, and 13.0% in the gastric cancer patients; 40.5, 45.0, and 14.0% in the colorectal cancer patients; and 43.2, 45.6, and 11.2% in the controls, respectively.	Proline	41-44	P53	Homo sapiens	75-78
24359220-2	2014	Although high levels of ROS/RNS mainly causes cell death, low levels of free radicals directly modulate the activities of transcriptional factors, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB), p53, and nuclear factor (erythroid-derived) 2-like (Nrf2), and regulate numerous protein kinase cascades that participate in the regulation of the cross talk between autophagy and apoptosis.	Free Radicals	72-85	P53	Homo sapiens	223-226
24859470-6	2014	Actinomycin D (ActD), an activator of p53, induces the promoter and protein activities of HspB2/alphaB-crystallin.	Dactinomycin	0-13	P53	Homo sapiens	38-41
24706461-3	2015	MEHP-induced apoptosis is mediated by either p53-dependent or -independent pathway.	mono-(2-ethylhexyl)phthalate	0-4	P53	Homo sapiens	45-48
21515331-0	2011	Induction of ROS, p53, p21 in DEHP- and MEHP-exposed LNCaP cells-protection by selenium compounds.	Selenium	79-87	P53	Homo sapiens	18-21
21454683-3	2011	The arginine form (p53-72R) shows significantly enhanced phosphorylation at Ser-6 and Ser-20 compared with the proline form (p53-72P).	Proline	111-118	P53	Homo sapiens	19-22
24852275-0	2014	Design, synthesis and in vitro and in vivo antitumour activity of 3-benzylideneindolin-2-one derivatives, a novel class of small-molecule inhibitors of the MDM2-p53 interaction.	3-BENZYLIDENEINDOLIN-2-ONE	66-92	P53	Homo sapiens	161-164
24706461-5	2015	In this study, immortalized normal human liver cell line L02 was chosen, as an in vitro model of nonmalignant liver, to elucidate the role of p53 in MEHP-induced apoptosis.	mono-(2-ethylhexyl)phthalate	149-153	P53	Homo sapiens	142-145
26194899-4	2015	In further experiments, p53 protein expression was increased, and H2AX phosphorylation and p21 protein expression were induced after treatment with 3EZ, 20Ac-ingenol.	3EZ	148-151	P53	Homo sapiens	24-27
24793593-5	2014	In fact, the hexamethylbenzene-ruthenium complexes activated caspase activity, with consequent DNA fragmentation, accumulation of pro-apoptotic proteins (p27, p53, p89 PARP fragments), and the concomitant down-regulation of antiapoptotic protein Bcl-2.	Ruthenium	31-40	P53	Homo sapiens	159-162
24710610-2	2014	A common polymorphism of the encoding TP53 gene (codon 72, Pro &gt; Arg, rs1042522) is associated with susceptibility to virus-related and other cancers.	Proline	59-62	P53	Homo sapiens	38-42
21490429-3	2011	Here we analyze and compare the effects of nutlin-3, tenovin-6 and low doses of actinomycin-D on p53 and its main negative regulator, mdm2.	Dactinomycin	80-93	P53	Homo sapiens	97-100
21380473-1	2011	The efficient formation of 5-methylcytosine glycol (mCg) and its facile deamination to thymine glycol (Tg) may account for the prevalent C   T transition mutation found at methylated CpG site (mCpG) in human p53 gene, a hallmark for many types of human tumors.	thymine glycol	87-101	P53	Homo sapiens	208-211
26402809-8	2015	Significantly increased PTC susceptibility was also associated with the TP-53 Arg72Pro CC and CG/CC genotypes compared with the GG genotype (CC vs GG: adjusted OR = 2.04, 95%CI = 1.54-2.70; CG/CC vs GG: adjusted OR = 1.35, 95%CI = 1.11-1.67, respectively).	cysteinylglycine	190-192	P53	Homo sapiens	72-77
21380473-1	2011	The efficient formation of 5-methylcytosine glycol (mCg) and its facile deamination to thymine glycol (Tg) may account for the prevalent C   T transition mutation found at methylated CpG site (mCpG) in human p53 gene, a hallmark for many types of human tumors.	thymine glycol	103-105	P53	Homo sapiens	208-211
24789439-6	2014	DHM increased the production of p53 and p21 proteins and downregulated the production of Cdc25A, Cdc2 and P-Cdc2 proteins, which induced cell cycle arrest.	dihydromyricetin	0-3	P53	Homo sapiens	32-35
26236013-0	2015	Pin1-Induced Proline Isomerization in Cytosolic p53 Mediates BAX Activation and Apoptosis.	Proline	13-20	P53	Homo sapiens	48-51
24835245-6	2014	We also found that HIF-1alpha does not contribute to the protection against DNA damage that can be observed in low oxygen environments, and that there are certain DNA damaging agents, such as doxorubicin and actinomycin D, that prevent HIF-1alpha induction independently of p53.	Dactinomycin	208-221	P53	Homo sapiens	274-277
24787013-6	2014	EBV sensitized TP53-mutated BL cells to all spindle poisons tested, including vincristine and taxol, an effect that was systematically downmodulated by pretreatment of cells with inhibitors of p38 and c-Jun N-terminal kinase (JNK) mitogen-activated protein kinases.	Vincristine	78-89	P53	Homo sapiens	15-19
21303901-0	2011	Low-dose valproic acid enhances radiosensitivity of prostate cancer through acetylated p53-dependent modulation of mitochondrial membrane potential and apoptosis.	Valproic Acid	9-22	P53	Homo sapiens	87-90
21357744-3	2011	The p53 tumor suppressor protein, an important transcriptional regulator of apoptosis, naturally occurs in humans in two variants with single nucleotide polymorphisms resulting in Arg or Pro at residue 72.	Proline	187-190	P53	Homo sapiens	4-7
26236013-3	2015	We observed that cis-trans isomerization of proline 47 (Pro47) within p53, an inherently rare molecular event, was required for BAX activation.	Proline	44-51	P53	Homo sapiens	70-73
26287184-3	2015	Culture studies found that methyl sartortuoate inhibited colon cancer cell (LoVo and RKO) growth and caused apoptotic death in a concentration- and time-dependent manner, by activation of caspase-8, caspase-9, caspase-3, p53 and Bax, and inactivation of B-cell lymphoma 2 (Bcl-2) apoptosis regulating proteins.	methyl sartortuoate	27-46	P53	Homo sapiens	221-224
21223980-0	2011	Involvement of p53 in cell death following cell cycle arrest and mitotic catastrophe induced by rotenone.	Rotenone	96-104	P53	Homo sapiens	15-18
21223980-4	2011	The tumor suppressor p53 is involved in rotenone-induced cell death, since the drug treatment results in increased expression, phosphorylation and nuclear localization of the protein.	Rotenone	40-48	P53	Homo sapiens	21-24
21223980-5	2011	The evaluation of the effects of rotenone on a p53-deficient cell line revealed that although not required for the promotion of mitotic catastrophe, functional p53 appears to be essential for the extensive cell death that occurs afterwards.	Rotenone	33-41	P53	Homo sapiens	160-163
26287184-4	2015	Methyl sartortuoate treatment led to reduced expression of cdc2 and up-regulated p21 and p53, suggesting that Methyl sartortuoate induced G2-M arrest through modulation of p53/p21/cdc2 pathways.	methyl sartortuoate	0-19	P53	Homo sapiens	89-92
21043833-10	2011	Interactions of betel quid with p53 genotypes in lung cancer showed significant increase for all the three genotypes, indicating a major role of betel quid (OR=5.90, CI=1.67-20.81, p=0.006; OR=5.44, CI=1.67-17.75, p=0.005; and OR=5.84, CI=1.70-19.97, p=0.005 for Arg/Arg, Arg/Pro, and Pro/Pro, respectively).	Proline	276-279	P53	Homo sapiens	32-35
26287184-4	2015	Methyl sartortuoate treatment led to reduced expression of cdc2 and up-regulated p21 and p53, suggesting that Methyl sartortuoate induced G2-M arrest through modulation of p53/p21/cdc2 pathways.	methyl sartortuoate	0-19	P53	Homo sapiens	172-175
21043833-10	2011	Interactions of betel quid with p53 genotypes in lung cancer showed significant increase for all the three genotypes, indicating a major role of betel quid (OR=5.90, CI=1.67-20.81, p=0.006; OR=5.44, CI=1.67-17.75, p=0.005; and OR=5.84, CI=1.70-19.97, p=0.005 for Arg/Arg, Arg/Pro, and Pro/Pro, respectively).	Proline	285-288	P53	Homo sapiens	32-35
26287184-4	2015	Methyl sartortuoate treatment led to reduced expression of cdc2 and up-regulated p21 and p53, suggesting that Methyl sartortuoate induced G2-M arrest through modulation of p53/p21/cdc2 pathways.	methyl sartortuoate	110-129	P53	Homo sapiens	89-92
21043833-10	2011	Interactions of betel quid with p53 genotypes in lung cancer showed significant increase for all the three genotypes, indicating a major role of betel quid (OR=5.90, CI=1.67-20.81, p=0.006; OR=5.44, CI=1.67-17.75, p=0.005; and OR=5.84, CI=1.70-19.97, p=0.005 for Arg/Arg, Arg/Pro, and Pro/Pro, respectively).	Proline	285-288	P53	Homo sapiens	32-35
26287184-4	2015	Methyl sartortuoate treatment led to reduced expression of cdc2 and up-regulated p21 and p53, suggesting that Methyl sartortuoate induced G2-M arrest through modulation of p53/p21/cdc2 pathways.	methyl sartortuoate	110-129	P53	Homo sapiens	172-175
26287184-9	2015	Taken together, these findings suggest that methyl sartortuoate is capable of leading to activation of caspase-8, -9, -3, increasing p53 and Bax/Bcl-2 ratio apoptosis through MAPK-dependent apoptosis and results in G2-M phase arrest in LoVo and RKO cells.	methyl sartortuoate	44-63	P53	Homo sapiens	133-136
25910917-7	2015	UA also increased protein expression of p53, p38-MAPK and caspase-3, but suppressed expression of NF-kappaB p65 and other inflammatory mediators.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	0-2	P53	Homo sapiens	40-43
21300767-2	2011	Of all the extracts tested, chloroform and ethyl acetate extracts of M piperita showed significant dose- and time-dependent anticarcinogenic activity leading to G1 cell cycle arrest and mitochondrial-mediated apoptosis, perturbation of oxidative balance, upregulation of Bax gene, elevated expression of p53 and p21 in the treated cells, acquisition of senescence phenotype, while inducing pro-inflammatory cytokines response.	Chloroform	28-38	P53	Homo sapiens	304-307
21300767-2	2011	Of all the extracts tested, chloroform and ethyl acetate extracts of M piperita showed significant dose- and time-dependent anticarcinogenic activity leading to G1 cell cycle arrest and mitochondrial-mediated apoptosis, perturbation of oxidative balance, upregulation of Bax gene, elevated expression of p53 and p21 in the treated cells, acquisition of senescence phenotype, while inducing pro-inflammatory cytokines response.	ethyl acetate	43-56	P53	Homo sapiens	304-307
21194611-2	2011	Previous studies have demonstrated that arsenic and chromium complexes are able to activate p53, but there is a dearth of data investigating whether uranium complexes exhibit similar effects.	Chromium	52-60	P53	Homo sapiens	92-95
21247336-0	2011	Effect of G-rich oligonucleotides on the proliferation of leukemia cells and its relationship with p53 expression.	rich oligonucleotides	12-33	P53	Homo sapiens	99-102
25697053-7	2015	Our data provide evidence that 7-ketocholesterol and 5,6-secosterol are efficient instigators of apoptosis, which for 5,6-secosterol is associated to PKC and p53 up-regulation.	5,6-secosterol	53-67	P53	Homo sapiens	158-161
21304979-8	2011	Notably both mevalonate cascade inhibition-induced autophagy and apoptosis were p53 dependent: simvastatin increased nuclear p53 accumulation, and both cyclic pifithrin-alpha and p53 shRNAi partially inhibited NOXA, PUMA expression and caspase-3/7 cleavage (apoptosis) and DRAM expression, Atg5-12 complex formation, LC3 lipidation, and autophagosome formation (autophagy).	Mevalonic Acid	13-23	P53	Homo sapiens	80-83
21304979-8	2011	Notably both mevalonate cascade inhibition-induced autophagy and apoptosis were p53 dependent: simvastatin increased nuclear p53 accumulation, and both cyclic pifithrin-alpha and p53 shRNAi partially inhibited NOXA, PUMA expression and caspase-3/7 cleavage (apoptosis) and DRAM expression, Atg5-12 complex formation, LC3 lipidation, and autophagosome formation (autophagy).	Mevalonic Acid	13-23	P53	Homo sapiens	125-128
21304979-8	2011	Notably both mevalonate cascade inhibition-induced autophagy and apoptosis were p53 dependent: simvastatin increased nuclear p53 accumulation, and both cyclic pifithrin-alpha and p53 shRNAi partially inhibited NOXA, PUMA expression and caspase-3/7 cleavage (apoptosis) and DRAM expression, Atg5-12 complex formation, LC3 lipidation, and autophagosome formation (autophagy).	Mevalonic Acid	13-23	P53	Homo sapiens	125-128
25697053-7	2015	Our data provide evidence that 7-ketocholesterol and 5,6-secosterol are efficient instigators of apoptosis, which for 5,6-secosterol is associated to PKC and p53 up-regulation.	5,6-secosterol	118-132	P53	Homo sapiens	158-161
22393962-7	2011	CONCLUSIONS: Our results suggest that the codon 72 SNP which results in amino acid substitution of Arginine to Proline in cell cycle regulatory gene P53, is associated with sporadic CRC risk and carriers of Pro/Pro genotype and more than 50 years old may have high susceptibility.	Proline	111-118	P53	Homo sapiens	149-152
26123760-10	2015	However, a significant association between p53 Arg72Pro polymorphism and the risk of oral cancer with HPV infection was detected in the Arg/Arg vs. Arg/Pro + Pro/Pro model.	Proline	52-55	P53	Homo sapiens	43-46
21467739-8	2011	We next investigated the involvement of the transcription-independent function of p53 using an RNA synthesis inhibitor, actinomycin D (ActD), and a protein synthesis inhibitor, cycloheximide (CHX), and found that the apoptosis was suppressed by CHX but not by ActD.	Dactinomycin	120-133	P53	Homo sapiens	82-85
26123760-10	2015	However, a significant association between p53 Arg72Pro polymorphism and the risk of oral cancer with HPV infection was detected in the Arg/Arg vs. Arg/Pro + Pro/Pro model.	Proline	152-155	P53	Homo sapiens	43-46
26123760-10	2015	However, a significant association between p53 Arg72Pro polymorphism and the risk of oral cancer with HPV infection was detected in the Arg/Arg vs. Arg/Pro + Pro/Pro model.	Proline	152-155	P53	Homo sapiens	43-46
20861261-2	2010	During viral infection, E1B-55K and E4orf6 substitute for the substrate-binding subunits of the host cell cullin 5 class of ubiquitin ligases, resulting in p53 polyubiquitinylation and proteasomal degradation.	e4orf6	36-42	P53	Homo sapiens	156-159
25939861-0	2015	Efficient one-pot synthesis of trans-Pt(II)(salicylaldimine)(4-picoline)Cl complexes: effective agents for enhanced expression of p53 tumor suppressor genes.	trans-pt(ii)	31-43	P53	Homo sapiens	130-133
20727621-3	2010	For instance, the Ru(II)(p-cymene)(isonicotinate)Cl(2) complex 6a of the known 4-(3,4,5-trimethoxyphenyl)-5-(3-hydroxy-4-methoxyphenyl)-oxazole 4a was far more active than the latter against cells of the p53-competent wild-type form of HCT-116 colon carcinoma at low 0.01 muM concentrations.	ru(ii)(p-cymene)(isonicotinate)cl(2)	18-54	P53	Homo sapiens	204-207
25840370-0	2015	The cis conformation of proline leads to weaker binding of a p53 peptide to MDM2 compared to trans.	Proline	24-31	P53	Homo sapiens	61-64
21384570-2	2010	The p53 gene is characterized by Arg/Pro polymorphism in codon 72 whose alleles exhibit differential functional activity.	Proline	37-40	P53	Homo sapiens	4-7
25840370-3	2015	In this study, computer simulations were used to calculate the absolute binding affinity for a p53 peptide (residues 17-29) to MDM2 for both cis and trans isomers of the p53 proline in position 27.	Proline	174-181	P53	Homo sapiens	95-98
25840370-3	2015	In this study, computer simulations were used to calculate the absolute binding affinity for a p53 peptide (residues 17-29) to MDM2 for both cis and trans isomers of the p53 proline in position 27.	Proline	174-181	P53	Homo sapiens	170-173
25914192-0	2015	Rational Design of Ruthenium Complexes Containing 2,6-Bis(benzimidazolyl)pyridine Derivatives with Radiosensitization Activity by Enhancing p53 Activation.	Ruthenium	19-28	P53	Homo sapiens	140-143
20594980-3	2010	The effects of 24R,25(OH)(2)D(3) are mediated by activation of phospholipase D (PLD), resulting in increased production of lysophosphatidic acid (LPA) and LPA-mediated proliferation, maturation, inhibition of Pi-induced apoptosis, and reduction of p53.	lysophosphatidic acid	123-144	P53	Homo sapiens	248-251
20594980-3	2010	The effects of 24R,25(OH)(2)D(3) are mediated by activation of phospholipase D (PLD), resulting in increased production of lysophosphatidic acid (LPA) and LPA-mediated proliferation, maturation, inhibition of Pi-induced apoptosis, and reduction of p53.	lysophosphatidic acid	155-158	P53	Homo sapiens	248-251
25663373-7	2015	Quantitative real-time PCR data demonstrated that the mRNA level of tumor suppressor gene p53 and apoptotic genes (bax, CASP3 and CASP9) were up-regulated whereas the anti-apoptotic gene bcl-2 was down-regulated in HEp2 and HepG2 cells exposed to dolomite NPs.	calcium magnesium carbonate	247-255	P53	Homo sapiens	90-93
20594980-8	2010	Moreover, LPA induced increased mdm2 phosphorylation, a negative regulator of p53.	lysophosphatidic acid	10-13	P53	Homo sapiens	78-81
25981639-9	2015	DL-TBOA did not significantly alter cellular levels of p21, cleaved PARP-1, or phospho-Retinoblastoma protein, yet altered SLC1A1 subcellular localization, and reduced chemotherapy-induced p53 induction.	benzyloxyaspartate	0-7	P53	Homo sapiens	189-192
20667493-6	2010	A significant increase in the phosphorylation of DNA damage response proteins (ATM, ATR, H2AX and p53) in OHBI in comparison to controls suggested that OHBI induces DNA damage in peripheral blood lymphocytes and elicit a PI3 kinase mediated cellular response.	ohbi	106-110	P53	Homo sapiens	98-101
20667493-6	2010	A significant increase in the phosphorylation of DNA damage response proteins (ATM, ATR, H2AX and p53) in OHBI in comparison to controls suggested that OHBI induces DNA damage in peripheral blood lymphocytes and elicit a PI3 kinase mediated cellular response.	ohbi	152-156	P53	Homo sapiens	98-101
19936915-9	2010	Our preclinical data indicate that BA-TPQ is a potential therapeutic agent for breast cancer that has multiple hormone-, Her2-, and p53-independent mechanisms of action, providing a basis for further development of the compound as a novel anticancer agent.	7-(benzylamino)-1,3,4,8-tetrahydropyrrolo(4,3,2-de)quinolin-8(1H)-one	35-41	P53	Homo sapiens	132-135
25981639-11	2015	Importantly, the non-selective glutamate transporter inhibitor DL-TBOA reduces chemotherapy-induced p53 induction and augments CRC cell death induced by SN38, while attenuating that induced by oxaliplatin.	benzyloxyaspartate	63-70	P53	Homo sapiens	100-103
25814188-3	2015	Herein, we report the identification of a dual inhibitor of the p53 interaction with MDM2 and MDMX, the (S)-tryptophanol derivative OXAZ-1, from the screening of a small library of enantiopure tryptophanol-derived oxazolopiperidone lactams, using a yeast-based assay.	oxaz-1	132-138	P53	Homo sapiens	64-67
20630574-8	2010	However, a significantly decreased risk of bladder cancer was associated with TP53 genotypes for Arg/Arg versus Pro/Pro (odds ratio 0.74, 95% confidence interval 0.55-0.99) and Arg/Arg plus Arg/Pro versus Pro/Pro (odds ratio 0.77, 95% confidence interval 0.59-1.00) in Asians.	Proline	112-115	P53	Homo sapiens	78-82
25814188-5	2015	In fact, OXAZ-1 induced p53 stabilization, up-regulated p53 transcription targets, such as MDM2, MDMX, p21, Puma and Bax, and led to PARP cleavage, in p53(+/+), but not in p53(-/-), HCT116 cells.	oxaz-1	9-15	P53	Homo sapiens	24-27
20630574-8	2010	However, a significantly decreased risk of bladder cancer was associated with TP53 genotypes for Arg/Arg versus Pro/Pro (odds ratio 0.74, 95% confidence interval 0.55-0.99) and Arg/Arg plus Arg/Pro versus Pro/Pro (odds ratio 0.77, 95% confidence interval 0.59-1.00) in Asians.	Proline	116-119	P53	Homo sapiens	78-82
20630574-8	2010	However, a significantly decreased risk of bladder cancer was associated with TP53 genotypes for Arg/Arg versus Pro/Pro (odds ratio 0.74, 95% confidence interval 0.55-0.99) and Arg/Arg plus Arg/Pro versus Pro/Pro (odds ratio 0.77, 95% confidence interval 0.59-1.00) in Asians.	Proline	116-119	P53	Homo sapiens	78-82
20630574-8	2010	However, a significantly decreased risk of bladder cancer was associated with TP53 genotypes for Arg/Arg versus Pro/Pro (odds ratio 0.74, 95% confidence interval 0.55-0.99) and Arg/Arg plus Arg/Pro versus Pro/Pro (odds ratio 0.77, 95% confidence interval 0.59-1.00) in Asians.	Proline	116-119	P53	Homo sapiens	78-82
25814188-5	2015	In fact, OXAZ-1 induced p53 stabilization, up-regulated p53 transcription targets, such as MDM2, MDMX, p21, Puma and Bax, and led to PARP cleavage, in p53(+/+), but not in p53(-/-), HCT116 cells.	oxaz-1	9-15	P53	Homo sapiens	56-59
20630574-8	2010	However, a significantly decreased risk of bladder cancer was associated with TP53 genotypes for Arg/Arg versus Pro/Pro (odds ratio 0.74, 95% confidence interval 0.55-0.99) and Arg/Arg plus Arg/Pro versus Pro/Pro (odds ratio 0.77, 95% confidence interval 0.59-1.00) in Asians.	Proline	116-119	P53	Homo sapiens	78-82
25814188-5	2015	In fact, OXAZ-1 induced p53 stabilization, up-regulated p53 transcription targets, such as MDM2, MDMX, p21, Puma and Bax, and led to PARP cleavage, in p53(+/+), but not in p53(-/-), HCT116 cells.	oxaz-1	9-15	P53	Homo sapiens	56-59
25814188-5	2015	In fact, OXAZ-1 induced p53 stabilization, up-regulated p53 transcription targets, such as MDM2, MDMX, p21, Puma and Bax, and led to PARP cleavage, in p53(+/+), but not in p53(-/-), HCT116 cells.	oxaz-1	9-15	P53	Homo sapiens	56-59
25814188-7	2015	In HCT116 p53(+/+) cells, the disruption of the p53 interaction with MDMs by OXAZ-1 was further confirmed by co-immunoprecipitation.	oxaz-1	77-83	P53	Homo sapiens	10-13
20600004-3	2010	Our results demonstrated that wild-type p53 markedly suppressed BCRP activity and enhanced the chemosensitivity of cells to mitoxantrone, whereas mutant p53 had little inhibitory effect.	Mitoxantrone	124-136	P53	Homo sapiens	40-43
25814188-7	2015	In HCT116 p53(+/+) cells, the disruption of the p53 interaction with MDMs by OXAZ-1 was further confirmed by co-immunoprecipitation.	oxaz-1	77-83	P53	Homo sapiens	48-51
20600004-5	2010	Following knockdown of endogenous p53, BCRP and p50 expressions were increased, and the chemosensitivity of the cells to mitoxantrone was decreased.	Mitoxantrone	121-133	P53	Homo sapiens	34-37
25814188-8	2015	It was also shown that OXAZ-1 potently triggered a p53-dependent mitochondria-mediated apoptosis, characterized by reactive oxygen species generation, mitochondrial membrane potential dissipation, Bax translocation to mitochondria, and cytochrome c release, and exhibited a p53-dependent synergistic effect with conventional chemotherapeutic drugs.	oxaz-1	23-29	P53	Homo sapiens	51-54
25814188-8	2015	It was also shown that OXAZ-1 potently triggered a p53-dependent mitochondria-mediated apoptosis, characterized by reactive oxygen species generation, mitochondrial membrane potential dissipation, Bax translocation to mitochondria, and cytochrome c release, and exhibited a p53-dependent synergistic effect with conventional chemotherapeutic drugs.	oxaz-1	23-29	P53	Homo sapiens	274-277
25814188-10	2015	Moreover, OXAZ-1 may represent a promising starting scaffold to search for new dual inhibitors of the p53-MDMs interaction.	oxaz-1	10-16	P53	Homo sapiens	102-105
20380571-4	2010	The frequencies of Arg/Arg, Arg/Pro, and Pro/Pro genotypes for P53 codon 72 were 51.7%, 41.4%, and 6.9% in patients and 42.6%, 47.3%, and 10.1% in controls, respectively.	Proline	32-35	P53	Homo sapiens	63-66
20380571-4	2010	The frequencies of Arg/Arg, Arg/Pro, and Pro/Pro genotypes for P53 codon 72 were 51.7%, 41.4%, and 6.9% in patients and 42.6%, 47.3%, and 10.1% in controls, respectively.	Proline	41-44	P53	Homo sapiens	63-66
25156865-7	2015	TP53mut patients had lower response rates (22% compared with 76% CR in TP53 wild-type (wt) patients, P &lt; 0.001) and reduced OS (2 and 16 months, respectively, P &lt; 0.001).	Chromium	65-67	P53	Homo sapiens	0-4
20514405-7	2010	In addition, possible mechanisms involved in the antiproliferative activity of 2-Fluoro-ara-AMP, such as the effects on cell cycle progression, p53 expression and STAT1 pathway activation in ER+ and ER- cancer cell lines, are proposed.	fludarabine phosphate	79-95	P53	Homo sapiens	144-147
25156865-7	2015	TP53mut patients had lower response rates (22% compared with 76% CR in TP53 wild-type (wt) patients, P &lt; 0.001) and reduced OS (2 and 16 months, respectively, P &lt; 0.001).	Chromium	65-67	P53	Homo sapiens	71-75
25407160-10	2015	In addition, TUDCA decreased cellular senescence by reducing levels of p53, p21, and reactive oxygen species and increased nitric oxide.	ursodoxicoltaurine	13-18	P53	Homo sapiens	71-74
20050848-3	2010	FLX-induced increase in mitochondrial Bax levels, decrease in cytosolic Bid and Bcl-2 levels, loss of the mitochondrial transmembrane potential, cytochrome c release, caspase-3 activation and up-regulation of p53.	Fluoxetine	0-3	P53	Homo sapiens	209-212
25312347-0	2015	Oxazoloisoindolinones with in vitro antitumor activity selectively activate a p53-pathway through potential inhibition of the p53-MDM2 interaction.	oxazoloisoindolinones	0-21	P53	Homo sapiens	78-81
20428765-4	2010	Here we report that incubation of LNCaP human prostate cancer cells (p53 +/+) with a natural form of selenium triggers rapid transcriptional activation of p53, and up-regulation of the expression of p53-target genes as well as induction of miR-34 class of microRNAs.	Selenium	101-109	P53	Homo sapiens	69-72
20428765-4	2010	Here we report that incubation of LNCaP human prostate cancer cells (p53 +/+) with a natural form of selenium triggers rapid transcriptional activation of p53, and up-regulation of the expression of p53-target genes as well as induction of miR-34 class of microRNAs.	Selenium	101-109	P53	Homo sapiens	155-158
20428765-4	2010	Here we report that incubation of LNCaP human prostate cancer cells (p53 +/+) with a natural form of selenium triggers rapid transcriptional activation of p53, and up-regulation of the expression of p53-target genes as well as induction of miR-34 class of microRNAs.	Selenium	101-109	P53	Homo sapiens	155-158
20428765-5	2010	Moreover, blocking p53 function by transfection of cells with a dominant-negative, mutated p53 gene, or by siRNA, significantly reduced selenium-induced expression of p53-target genes and induction of apoptosis.	Selenium	136-144	P53	Homo sapiens	19-22
20428765-5	2010	Moreover, blocking p53 function by transfection of cells with a dominant-negative, mutated p53 gene, or by siRNA, significantly reduced selenium-induced expression of p53-target genes and induction of apoptosis.	Selenium	136-144	P53	Homo sapiens	91-94
25312347-0	2015	Oxazoloisoindolinones with in vitro antitumor activity selectively activate a p53-pathway through potential inhibition of the p53-MDM2 interaction.	oxazoloisoindolinones	0-21	P53	Homo sapiens	126-129
20428765-5	2010	Moreover, blocking p53 function by transfection of cells with a dominant-negative, mutated p53 gene, or by siRNA, significantly reduced selenium-induced expression of p53-target genes and induction of apoptosis.	Selenium	136-144	P53	Homo sapiens	91-94
20428765-6	2010	Since majority of the early-stage human prostate cancers bear functional p53 gene (p53+/+), our findings indicate that the anticancer action of selenium may involve transactivation of p53 as a potential mechanism, and suggest that selenite may be useful not only for prevention but also for treatment of human prostate cancer.	Selenium	144-152	P53	Homo sapiens	73-76
25312347-5	2015	Using a yeast-based screening assay, two oxazoloisoindolinones, compounds 1b and 3a, were identified as potential p53-MDM2 interaction inhibitors.	oxazoloisoindolinones	41-62	P53	Homo sapiens	114-117
20428765-6	2010	Since majority of the early-stage human prostate cancers bear functional p53 gene (p53+/+), our findings indicate that the anticancer action of selenium may involve transactivation of p53 as a potential mechanism, and suggest that selenite may be useful not only for prevention but also for treatment of human prostate cancer.	Selenium	144-152	P53	Homo sapiens	83-86
20428765-6	2010	Since majority of the early-stage human prostate cancers bear functional p53 gene (p53+/+), our findings indicate that the anticancer action of selenium may involve transactivation of p53 as a potential mechanism, and suggest that selenite may be useful not only for prevention but also for treatment of human prostate cancer.	Selenium	144-152	P53	Homo sapiens	83-86
26745067-5	2015	Expression levels of p53 mRNA and Coxsackie/adenovirus receptor (CAR) mRNA after adenovirus-mediated transfer of an ERE-linked p53 gene (proline variant at codon 72) were higher compared with those after non-ERE-linked p53 gene transfer in siRNA-treated HeLa S3 cells.	Proline	137-144	P53	Homo sapiens	21-24
26745067-5	2015	Expression levels of p53 mRNA and Coxsackie/adenovirus receptor (CAR) mRNA after adenovirus-mediated transfer of an ERE-linked p53 gene (proline variant at codon 72) were higher compared with those after non-ERE-linked p53 gene transfer in siRNA-treated HeLa S3 cells.	Proline	137-144	P53	Homo sapiens	127-130
26745067-5	2015	Expression levels of p53 mRNA and Coxsackie/adenovirus receptor (CAR) mRNA after adenovirus-mediated transfer of an ERE-linked p53 gene (proline variant at codon 72) were higher compared with those after non-ERE-linked p53 gene transfer in siRNA-treated HeLa S3 cells.	Proline	137-144	P53	Homo sapiens	127-130
26745067-6	2015	Western blot analysis showed lower beta-tubulin levels and comparatively higher p53/beta-tubulin or CAR /beta-tubulin ratios in siRNA-treated HeLa S3 cells after adenovirus-mediated ERE-linked p53 gene (proline variant at codon 72) transfer compared with those in non-siRNA-treated cells.	Proline	203-210	P53	Homo sapiens	193-196
20067769-0	2010	Increased cytotoxicity of an unusual DNA topoisomerase II inhibitor compound C-1305 toward HeLa cells with downregulated PARP-1 activity results from re-activation of the p53 pathway and modulation of mitotic checkpoints.	C 1305	77-83	P53	Homo sapiens	171-174
26745067-7	2015	Apoptosis, as measured by annexin V binding, was higher after adenovirus-mediated ERE-linked p53 gene (proline variant at codon 72) transfer compared with that after non-ERE-linked p53 gene transfer in siRNA-treated cells.	Proline	103-110	P53	Homo sapiens	93-96
25338966-0	2015	A novel pyrido-thieno-pyrimidine derivative activates p53 through induction of phosphorylation and acetylation in colorectal cancer cells.	pyrido-thieno-pyrimidine	8-32	P53	Homo sapiens	54-57
25605490-3	2015	Recently, the association between the p53 gene encoding for proline at codon 72 and primary open-angle glaucoma (POAG) has been studied in some ethnic groups.	Proline	60-67	P53	Homo sapiens	38-41
20212049-7	2010	Furthermore, we showed that deletion of the basic domain enhances, whereas a mutation in activation domains 1-2 and deletion of the proline-rich domain abolish mutant p53 to regulate Gro1 and Id2, both of which are regulated by and mediate endogenous mutant p53 gain of function.	Proline	132-139	P53	Homo sapiens	167-170
25178583-8	2014	RESULTS: While blood cells isolated from K3EDTA tubes showed significant changes in cellular mRNA concentrations for GAPDH, c-fos, and p53, these mRNAs concentrations were stable in blood drawn into RNA-BCT.	k3edta	41-47	P53	Homo sapiens	135-138
20406898-0	2010	Chloroquine-induced autophagic vacuole accumulation and cell death in glioma cells is p53 independent.	Chloroquine	0-11	P53	Homo sapiens	86-89
20406898-4	2010	We and others have shown that CQ-mediated cell death may be p53-dependent and at least in part due to the intrinsic apoptotic death pathway.	Chloroquine	30-32	P53	Homo sapiens	60-63
20406898-9	2010	Thus, CQ can induce p53-independent death in gliomas that do not require caspase-mediated apoptosis.	Chloroquine	6-8	P53	Homo sapiens	20-23
25217526-5	2014	Rubone activated miR34a expression in HCC cells with wild-type or mutated p53 but not in cells with p53 deletions.	2'-hydroxy-2,4,4',5,6'-pentamethylchalcone	0-6	P53	Homo sapiens	74-77
20378837-7	2010	Consistent with these functions of GLS2, the activation of p53 increases the levels of glutamate and alpha-ketoglutarate, mitochondrial respiration rate, and GSH levels and decreases reactive oxygen species (ROS) levels in cells.	Ketoglutaric Acids	101-120	P53	Homo sapiens	59-62
25096910-3	2014	Our study revealed that treatment with CAY10598 significantly reduced the cell viability and induced apoptosis in HCT116 cells, as evidenced by the induction of p53 and Bax, release of cytochrome c, cleavage of caspase-9, -7, and -3, and PARP, and the inhibition of Bcl-2, Bcl-xL and survivin expression.	CAY10598	39-47	P53	Homo sapiens	161-164
20308316-0	2010	Chloroquine activates the p53 pathway and induces apoptosis in human glioma cells.	Chloroquine	0-11	P53	Homo sapiens	26-29
20308316-4	2010	We show that the quinoline derivative chloroquine activates the p53 pathway and suppresses growth of glioma cells in vitro and in vivo in an orthotopic (U87MG) human glioblastoma mouse model.	Chloroquine	38-49	P53	Homo sapiens	64-67
20308316-6	2010	siRNA-mediated downregulation of p53 in wild-type but not mutant p53 glioblastoma cells substantially impaired chloroquine-induced apoptosis.	Chloroquine	111-122	P53	Homo sapiens	33-36
20308316-7	2010	In addition to its p53-activating effects, chloroquine may also inhibit glioma cell growth via p53-independent mechanisms.	Chloroquine	43-54	P53	Homo sapiens	95-98
25313037-4	2014	XAF1 binds directly to the N-terminal proline-rich domain of p53 and thus interferes with E3 ubiquitin ligase MDM2 binding and ubiquitination of p53.	Proline	38-45	P53	Homo sapiens	61-64
19918261-7	2010	Moreover, DNA-PKc physically interacts with ARHGEF6 and p53 mostly in the nucleus of Cbl-treated cells, whereas in Cbl(cos)-treated cells, its interactions are mostly in the cytoplasm.	Chlorambucil	85-88	P53	Homo sapiens	56-59
25277183-3	2014	Herein, we reported that 3,3"-diselenodipropionic acid (DSeA), a Selenocysteine derivative, could synergistically enhance the growth inhibitory effect of TRAIL on A375 melanoma cells though induction of ROS-dependent apoptosis with involvement of PTEN-mediated Akt inactivation and DNA damage-mediated p53 phosphorylation, which subsequently activated mitochondrial and death receptor apoptotic pathways.	3,3'-diselenodipropionic acid	25-54	P53	Homo sapiens	302-305
19583730-0	2010	Dicoumarol enhances doxorubicin-induced cytotoxicity in p53 wild-type urothelial cancer cells through p38 activation.	Dicumarol	0-10	P53	Homo sapiens	56-59
19583730-3	2010	Then, dicoumarol-mediated enhancement of doxorubicin-induced cytotoxicity was screened in urothelial cancer cell lines with different p53 statuses or RT112 stable transfectants with a dominant-negative mutant of p53 (p53DN).	Dicumarol	6-16	P53	Homo sapiens	134-137
19583730-3	2010	Then, dicoumarol-mediated enhancement of doxorubicin-induced cytotoxicity was screened in urothelial cancer cell lines with different p53 statuses or RT112 stable transfectants with a dominant-negative mutant of p53 (p53DN).	Dicumarol	6-16	P53	Homo sapiens	212-215
19583730-4	2010	To clarify the importance of the modification of p53 function by dicoumarol to enhance doxorubicin toxicity, the change in the p53-p21 pathway and mitogen-activated protein kinase (MAPK)-mitochondria pathway by the combined treatment were elucidated by Western blot analysis.	Dicumarol	65-75	P53	Homo sapiens	49-52
19583730-7	2010	Dicoumarol (100 microm) also enhanced the cytotoxicity of doxorubicin in other bladder cancer cell lines with wild-type p53 (wt-p53; three times in 253J and 13 times in KK47), but not in those with mutant-type p53 (TCCsup, J82 and EJ) or in RT112 p53DN.	Dicumarol	0-10	P53	Homo sapiens	120-123
19583730-7	2010	Dicoumarol (100 microm) also enhanced the cytotoxicity of doxorubicin in other bladder cancer cell lines with wild-type p53 (wt-p53; three times in 253J and 13 times in KK47), but not in those with mutant-type p53 (TCCsup, J82 and EJ) or in RT112 p53DN.	Dicumarol	0-10	P53	Homo sapiens	128-131
19583730-7	2010	Dicoumarol (100 microm) also enhanced the cytotoxicity of doxorubicin in other bladder cancer cell lines with wild-type p53 (wt-p53; three times in 253J and 13 times in KK47), but not in those with mutant-type p53 (TCCsup, J82 and EJ) or in RT112 p53DN.	Dicumarol	0-10	P53	Homo sapiens	128-131
19583730-8	2010	The combined treatment with dicoumarol suppressed p53/p21 induction by doxorubicin and resulted in sequential p38 MAPK activation, myeloid cell leukaemia 1 suppression and caspase cleavage.	Dicumarol	28-38	P53	Homo sapiens	50-53
25277183-3	2014	Herein, we reported that 3,3"-diselenodipropionic acid (DSeA), a Selenocysteine derivative, could synergistically enhance the growth inhibitory effect of TRAIL on A375 melanoma cells though induction of ROS-dependent apoptosis with involvement of PTEN-mediated Akt inactivation and DNA damage-mediated p53 phosphorylation, which subsequently activated mitochondrial and death receptor apoptotic pathways.	3,3'-diselenodipropionic acid	56-60	P53	Homo sapiens	302-305
19583730-10	2010	CONCLUSION: These results suggest that concomitant use of dicoumarol could enhance the cytotoxicity of doxorubicin in urothelial cancer cells with wt-p53 through the p53/p21/p38 MAPK pathways.	Dicumarol	58-68	P53	Homo sapiens	150-153
19583730-10	2010	CONCLUSION: These results suggest that concomitant use of dicoumarol could enhance the cytotoxicity of doxorubicin in urothelial cancer cells with wt-p53 through the p53/p21/p38 MAPK pathways.	Dicumarol	58-68	P53	Homo sapiens	166-169
25177931-6	2014	TP53 72 showed the following genotypic distribution: the control group was 29.75% homozygous wild-type (Arg), 47.11% heterozygous (Arg-Pro), and 23.14% homozygous variant (Pro).	Proline	135-138	P53	Homo sapiens	0-4
24921920-4	2014	RESULTS: Verapamil and the MDM2-p53 antagonists potentiated vincristine-mediated growth inhibition in a concentration-dependent manner when used in combination with high MDR-1-expressing p53 mutant neuroblastoma cell lines at concentrations that did not affect the viability of cells when given alone.	Vincristine	60-71	P53	Homo sapiens	32-35
21133638-5	2010	OBJECTIVE: The purpose of this study was to investigate the p53 polymorphism at codon 72 which results in encoding of either proline or arginine.	Proline	125-132	P53	Homo sapiens	60-63
24921920-4	2014	RESULTS: Verapamil and the MDM2-p53 antagonists potentiated vincristine-mediated growth inhibition in a concentration-dependent manner when used in combination with high MDR-1-expressing p53 mutant neuroblastoma cell lines at concentrations that did not affect the viability of cells when given alone.	Vincristine	60-71	P53	Homo sapiens	187-190
19874289-3	2010	Since insulin-like growth factor-1 (IGF-1) interferes with a cell"s apoptotic machinery when subjected to several stressful conditions, it is demonstrated here for the first time that IGF-1 effectively protects lymphocytes against rotenone through PI-3K/Akt activation, down-regulation of p53 and maintenance of mitochondrial membrane potential independently of ROS generation.	Rotenone	231-239	P53	Homo sapiens	289-292
24942866-4	2014	Recent understanding of the p53 pathway and other family members reveals a broad interaction with inflammatory elements such as reactive oxygen and nitrogen species, cytokines, infectious agents and major immune-regulatory pathways like nuclear factor-kappaB.	reactive oxygen and nitrogen species	128-164	P53	Homo sapiens	28-31
20809980-9	2010	Higher levels of PGG induced more caspase-mediated apoptosis in MCF-7, in strong association with induction of P53 Ser(15) phosphorylation, than in MDA-MB-231 cells.	beta-penta-O-galloyl-glucose	17-20	P53	Homo sapiens	111-114
24939851-2	2014	In this report, we demonstrate that the stress response gene ATF3 is required for endoplasmic reticulum stress-mediated DR5 induction upon zerumbone (ZER) and celecoxib (CCB) in human p53-deficient colorectal cancer cells.	zerumbone	139-148	P53	Homo sapiens	184-187
19853978-3	2010	In the present work, we have studied the biochemical properties of the trans-[PtCl2(isopropylamine)(L)] complexes (where L is 3- or 4-(hydroxymethyl)-pyridine) against several cell lines and the relationship between cytotoxicity and the protein p53.	l	100-101	P53	Homo sapiens	245-248
25017623-1	2014	The finding by scientists at Hoffmann-La Roche that cis-imidazolines could disrupt the protein-protein interaction between p53 and MDM2, thereby inducing apoptosis in cancer cells, raised considerable interest in this scaffold over the past decade.	cis-imidazolines	52-68	P53	Homo sapiens	123-126
20414935-14	2010	Distribution of p53 gene mutations between Pro/Pro genotype and Arg/Pro plus Arg/Arg genotypes was not statistically significant.	Proline	43-46	P53	Homo sapiens	16-19
24958857-3	2014	Here, we identify apoptosis-stimulating protein of p53 with signature sequences of ankyrin repeat-, SH3 domain-, and proline-rich region-containing protein 2 (ASPP2), a haploinsufficient tumor suppressor, activator of p53, and regulator of cell polarity, as a transcriptional target of signal transducer and activator of transcription 1 (STAT1).	Proline	117-124	P53	Homo sapiens	51-54
20369465-5	2010	RESULTS: The rSIFN-co demonstrated a efficiency of inhibiting the cell proliferation, induce apoptosis of both MCF-7 cells and MCF-7/ADR cells, which was stronger than that of infergen in the same concentration; rSIFN-co combined with epirubicin has a synergistic action in inhibiting cell proliferation, inducing apoptosis of both type of breast cancer cells; rSIFN-co can also decrease the expression level of P53 and CerbB-2, increase the expression of Bcl-2 in both cell lines.	rsifn	13-18	P53	Homo sapiens	412-415
24804820-8	2014	Furthermore, as shown by our results, the inhibition of gemcitabine-induced autophagy by chloroquine shifts the expression of the p53 protein, Bcl-2 family proteins and the relative Bax/Bcl-xL ratio in favor of promoting apoptosis.	Chloroquine	89-100	P53	Homo sapiens	130-133
20664183-6	2010	RESULTS: p53 codon 72 GG genotype was associated with increased biochemical recurrence compared with CG+CC genotypes and poorer PSA-free survival.	cysteinylglycine	101-103	P53	Homo sapiens	9-12
24819061-9	2014	In addition, activation of the redox-sensitive anticancer drug EO9 was enhanced selectively in p53(+/+) cancer cells, attributable to increased activity of NAD(P)H-dependent oxidoreductase NQO1 (NAD(P)H quinone oxidoreductase 1).	apaziquone	63-66	P53	Homo sapiens	95-98
19718045-5	2009	The proline-rich region (amino acids 64-91) of p53 was most likely responsible for the observed binding because a synthetic peptide comprising amino acids 68-81 of p53 inhibited this interaction, and a p53 variant containing a proline residue at position 72 (p53(P72)) interacted with Cyp18 more effectively than the corresponding p53(R72) variant.	Proline	4-11	P53	Homo sapiens	47-50
19718045-5	2009	The proline-rich region (amino acids 64-91) of p53 was most likely responsible for the observed binding because a synthetic peptide comprising amino acids 68-81 of p53 inhibited this interaction, and a p53 variant containing a proline residue at position 72 (p53(P72)) interacted with Cyp18 more effectively than the corresponding p53(R72) variant.	Proline	4-11	P53	Homo sapiens	164-167
19718045-5	2009	The proline-rich region (amino acids 64-91) of p53 was most likely responsible for the observed binding because a synthetic peptide comprising amino acids 68-81 of p53 inhibited this interaction, and a p53 variant containing a proline residue at position 72 (p53(P72)) interacted with Cyp18 more effectively than the corresponding p53(R72) variant.	Proline	4-11	P53	Homo sapiens	164-167
19718045-5	2009	The proline-rich region (amino acids 64-91) of p53 was most likely responsible for the observed binding because a synthetic peptide comprising amino acids 68-81 of p53 inhibited this interaction, and a p53 variant containing a proline residue at position 72 (p53(P72)) interacted with Cyp18 more effectively than the corresponding p53(R72) variant.	Proline	4-11	P53	Homo sapiens	164-167
24819061-10	2014	Suppressing LDH-A increased EO9-induced DNA damage in p53(+/+) cancer cells, but importantly had no additive effect in non-cancer cells.	apaziquone	28-31	P53	Homo sapiens	54-57
19718045-5	2009	The proline-rich region (amino acids 64-91) of p53 was most likely responsible for the observed binding because a synthetic peptide comprising amino acids 68-81 of p53 inhibited this interaction, and a p53 variant containing a proline residue at position 72 (p53(P72)) interacted with Cyp18 more effectively than the corresponding p53(R72) variant.	Proline	4-11	P53	Homo sapiens	164-167
19718045-5	2009	The proline-rich region (amino acids 64-91) of p53 was most likely responsible for the observed binding because a synthetic peptide comprising amino acids 68-81 of p53 inhibited this interaction, and a p53 variant containing a proline residue at position 72 (p53(P72)) interacted with Cyp18 more effectively than the corresponding p53(R72) variant.	Proline	227-234	P53	Homo sapiens	47-50
24656661-1	2014	The discovery of 3,3-disubstituted piperidine 1 as novel p53-HDM2 inhibitors prompted us to implement subsequent SAR follow up directed towards piperidine core modifications.	piperidine	35-45	P53	Homo sapiens	57-60
24717393-0	2014	Dihydromyricetin promotes hepatocellular carcinoma regression via a p53 activation-dependent mechanism.	dihydromyricetin	0-16	P53	Homo sapiens	68-71
19693773-7	2009	Taken together, our results suggest that JNK activation is involved in the TB-induced inhibition of ERK phosphorylation, p53 and p21 up-regulation and DNA synthesis inhibition in HUVEC.	Terbinafine	75-77	P53	Homo sapiens	121-124
24114124-10	2014	Consistent with abrogation of the Chk1 and p53-dependent G2/M checkpoint, mutant TP53 HT-29 colon cancer cells were more sensitive to gemcitabine when also treated with LY2603618, while wild-type TP53 HCT116 cells were not sensitized by LY2603618 to gemcitabine.	LY2603618	169-178	P53	Homo sapiens	43-46
19423162-2	2009	A G-C exchange at p53 codon 72 polymorphism results in a substitution of proline (Pro) for arginine (Arg) in the transactivation domain, which was shown to alter the primary structure of the p53 protein.	Proline	73-80	P53	Homo sapiens	18-21
24150971-7	2014	The simulation data also predicted that proline content contributed minimally to the native Rh of p53(1-93), which was confirmed by measuring Rh for a substitution variant that had all 22 proline residues changed for glycine.	Proline	40-47	P53	Homo sapiens	98-101
19423162-2	2009	A G-C exchange at p53 codon 72 polymorphism results in a substitution of proline (Pro) for arginine (Arg) in the transactivation domain, which was shown to alter the primary structure of the p53 protein.	Proline	73-80	P53	Homo sapiens	191-194
19423162-2	2009	A G-C exchange at p53 codon 72 polymorphism results in a substitution of proline (Pro) for arginine (Arg) in the transactivation domain, which was shown to alter the primary structure of the p53 protein.	Proline	82-85	P53	Homo sapiens	18-21
19423162-2	2009	A G-C exchange at p53 codon 72 polymorphism results in a substitution of proline (Pro) for arginine (Arg) in the transactivation domain, which was shown to alter the primary structure of the p53 protein.	Proline	82-85	P53	Homo sapiens	191-194
24451377-0	2014	The Chinese herb isolate yuanhuacine (YHL-14) induces G2/M arrest in human cancer cells by up-regulating p21 protein expression through an p53 protein-independent cascade.	Yuanhuacin	25-36	P53	Homo sapiens	139-142
19862414-0	2009	The role of p53 in the efficiency of photodynamic therapy with hypericin and subsequent long-term survival of colon cancer cells.	hypericin	63-72	P53	Homo sapiens	12-15
24451377-0	2014	The Chinese herb isolate yuanhuacine (YHL-14) induces G2/M arrest in human cancer cells by up-regulating p21 protein expression through an p53 protein-independent cascade.	Yuanhuacin	38-44	P53	Homo sapiens	139-142
19597352-5	2009	Furthermore, downregulation of EMMPRIN by p53 can be rescued by chloroquine, a lysosome inhibitor, but not by MG132, a proteasome inhibitor, suggesting an involvement of the lysosomal pathway in the p53-regulated degradation of EMMPRIN.	Chloroquine	64-75	P53	Homo sapiens	42-45
24596384-1	2014	Previously, our laboratory reported on novel quinuclidinone derivatives that cause cytotoxicity in human non-small lung carcinoma epithelial cells null for p53 (H1299).	1-azabicyclo[2.2.2]octan-2-one	45-59	P53	Homo sapiens	156-159
19657224-0	2009	Specific activation of the p53 pathway by low dose actinomycin D: a new route to p53 based cyclotherapy.	Dactinomycin	51-64	P53	Homo sapiens	27-30
19657224-0	2009	Specific activation of the p53 pathway by low dose actinomycin D: a new route to p53 based cyclotherapy.	Dactinomycin	51-64	P53	Homo sapiens	81-84
19657224-7	2009	We show here that low doses of actinomycin D mimic nutlin-3 in the highly specific activation of p53 dependant transcription, in the induction of a reversible protective growth arrest in normal cells and in the enhancement of the activity of chemotherapeutic drug induced killing of p53 positive human tumor cells.	Dactinomycin	31-44	P53	Homo sapiens	97-100
19657224-7	2009	We show here that low doses of actinomycin D mimic nutlin-3 in the highly specific activation of p53 dependant transcription, in the induction of a reversible protective growth arrest in normal cells and in the enhancement of the activity of chemotherapeutic drug induced killing of p53 positive human tumor cells.	Dactinomycin	31-44	P53	Homo sapiens	283-286
19654292-3	2009	Proline oxidase (POX), catalyzing the first step in proline catabolism, is induced by p53 and can regulate cell survival as well as mediate programmed cell death.	Proline	52-59	P53	Homo sapiens	86-89
24155029-7	2014	Increased expression of ATG5, p53 and DRAM, along with an increase in BCLN1/Bcl-2 ratio, indicated that acetazolamide inhibited the proliferation of T-47D cells by inducing autophagy.	Acetazolamide	104-117	P53	Homo sapiens	30-33
19654295-9	2009	Zerumbone also induced the p53 tumor suppressor gene but was found to be optional for DR induction or for enhancement of TRAIL-induced apoptosis.	zerumbone	0-9	P53	Homo sapiens	27-30
19723050-5	2009	We found that beta-carotene (100 micromol/L) induced apoptosis (determined by cell viability), DNA fragmentation, and the protein levels of p53 and Bcl-2 in AGS cells.	beta Carotene	14-27	P53	Homo sapiens	140-143
19723050-7	2009	beta-Carotene-induced alterations, including an increase in DNA fragmentation and p53 levels and a decrease in nuclear ATM and cellular Bcl-2 levels, were inhibited in the cells transfected with full-length ATM cDNA compared to wild-type cells or the cells transfected with control vector plasmid control DNA vector (pcDNA).	beta Carotene	0-13	P53	Homo sapiens	82-85
19723050-8	2009	In conclusion, beta-carotene induces apoptosis by increasing apoptotic protein p53 and decreasing anti-apoptotic Bcl-2 as well as nuclear ATM in AGS cells.	beta Carotene	15-28	P53	Homo sapiens	79-82
24155029-9	2014	Collectively the results indicate that autophagy is an adequate mechanism mediating the anti-cancer effects of acetazolamide in T-47D cells through engagement of p53/DRAM pathway and attenuation of Akt survival signalling.	Acetazolamide	111-124	P53	Homo sapiens	162-165
25422197-11	2014	The analysis of p53 72 SNP revealed that p53 (Arg/Arg), (Pro /Arg) variant are higher (40.59% and 33.66%) as compared to p53 pro/pro variant (25.74%) in the healthy population.	Proline	57-60	P53	Homo sapiens	16-19
19448667-6	2009	We found a proline-rich region unique to BRG1 was required for binding to the histone acetyl transferase protein, CBP, as well as to p53.	Proline	11-18	P53	Homo sapiens	133-136
19448667-7	2009	Ectopic expression of a proline-rich region deletion mutant BRG1 that is defective for CBP binding inhibited p53 destabilization.	Proline	24-31	P53	Homo sapiens	109-112
25482947-6	2014	We found that inhibitors of the mTOR pathway including rapamycin, wortmannin, and caffeine blunted the p53 response to nucleolar stress induced by actinomycin D.	Dactinomycin	147-160	P53	Homo sapiens	103-106
19409917-3	2009	In the present study, the mechanism of action of ovatodiolide was further investigated in the p53 mutant OSCC cell line Ca9-22.	ovatodiolide	49-61	P53	Homo sapiens	94-97
19536869-0	2009	Shallot and licorice constituent isoliquiritigenin arrests cell cycle progression and induces apoptosis through the induction of ATM/p53 and initiation of the mitochondrial system in human cervical carcinoma HeLa cells.	isoliquiritigenin	33-50	P53	Homo sapiens	133-136
25482947-7	2014	Synthetic inhibitors of mTOR (temsirolimus, LY294.002 and PP242) also impaired actinomycin D triggered p53 stabilization and induction of p21.	PP242	58-63	P53	Homo sapiens	103-106
25482947-7	2014	Synthetic inhibitors of mTOR (temsirolimus, LY294.002 and PP242) also impaired actinomycin D triggered p53 stabilization and induction of p21.	Dactinomycin	79-92	P53	Homo sapiens	103-106
24161784-6	2013	Cell viability assays and cytometric analysis of p53 and p21 null cells indicated that BBR3610-DACH-induced cell cycle arrest was p21-dependent and partially p53-dependent.	1,2-cyclohexanediamine	95-99	P53	Homo sapiens	49-52
19269999-1	2009	We have recently shown that penta-1,2,3,4,6-O-galloyl-beta-D-glucose (PGG), a naturally occurring hydrolyzable gallotannin, inhibited the in vivo growth of human androgen-independent p53-mutant DU145 prostate cancer (PCa) xenograft in athymic nude mice without adverse effect on their body weight.	beta-penta-O-galloyl-glucose	28-68	P53	Homo sapiens	183-186
19269999-1	2009	We have recently shown that penta-1,2,3,4,6-O-galloyl-beta-D-glucose (PGG), a naturally occurring hydrolyzable gallotannin, inhibited the in vivo growth of human androgen-independent p53-mutant DU145 prostate cancer (PCa) xenograft in athymic nude mice without adverse effect on their body weight.	beta-penta-O-galloyl-glucose	70-73	P53	Homo sapiens	183-186
19269999-2	2009	We have also shown that PGG induced caspase-mediated apoptosis in the DU145 cells and the androgen-dependent human p53-wild-type LNCaP cells.	beta-penta-O-galloyl-glucose	24-27	P53	Homo sapiens	115-118
24161784-6	2013	Cell viability assays and cytometric analysis of p53 and p21 null cells indicated that BBR3610-DACH-induced cell cycle arrest was p21-dependent and partially p53-dependent.	1,2-cyclohexanediamine	95-99	P53	Homo sapiens	158-161
24000115-6	2013	Real-time PCR analyses showed that berberine, NAX012 and NAX014 compounds increased the expression of some cell-cycle checkpoint molecules involved in cell senescence such as p53, p21(WAF1) , p16(INK4a) , and PAI-1, already after 24 h of 50 microM treatments.	nax012	46-52	P53	Homo sapiens	175-178
19434769-4	2009	p53 protein contains a transactivation domain, a sequence-specific DNA binding domain, a tetramerization domain, a non-specific DNA binding domain that recognizes damaged DNA, and a later identified proline-rich domain.	Proline	199-206	P53	Homo sapiens	0-3
24002546-3	2013	DHM induced G2/M cell-cycle arrest in HepG2 and Hep3B cells by altering the expression of cell cycle proteins such as cyclin A, cyclin B1, Cdk1, p53, Cdc25c, p-Cdc25c Chk1 and Chk, which are critical for G2/M transition.	dihydromyricetin	0-3	P53	Homo sapiens	145-148
19317806-7	2009	Silymarin also decreased mitochondrial transmembrane potential of the cells, thereby increasing levels of cytosolic cytochrome c while up-regulating expression of pro-apoptotic proteins (such as p53, Bax, APAF-1 and caspase-3) with concomitant decrease in anti-apoptotic proteins (Bcl-2 and survivin) and proliferation-associated proteins (beta-catenin, cyclin D1, c-Myc and PCNA).	Silymarin	0-9	P53	Homo sapiens	195-198
23992861-0	2013	Novel anthranilamide-pyrazolo[1,5-a]pyrimidine conjugates modulate the expression of p53-MYCN associated micro RNAs in neuroblastoma cells and cause cell cycle arrest and apoptosis.	anthranilamide-pyrazolo[1,5-a]pyrimidine	6-46	P53	Homo sapiens	85-88
19459735-0	2009	Enhancement of methyl methanesulfonate-induced base excision repair in the presence of selenomethionine on p53-dependent pathway.	Selenomethionine	87-103	P53	Homo sapiens	107-110
19459735-1	2009	Selenomethionine (SeMet) has been identified as a chemopreventive antioxidant to activate p53-mediated nucleotide excision repair.	Selenomethionine	0-16	P53	Homo sapiens	90-93
19459735-1	2009	Selenomethionine (SeMet) has been identified as a chemopreventive antioxidant to activate p53-mediated nucleotide excision repair.	Selenomethionine	18-23	P53	Homo sapiens	90-93
19459742-0	2009	Protective effects of selenomethionine against ionizing radiation under the modulation of p53 tumor suppressor.	Selenomethionine	22-38	P53	Homo sapiens	90-93
19459742-5	2009	In addition, our data showed that p53 functional activity was significantly reduced against IR in the cells expressing a mutant form of redox factor 1 (Ref-1) contrast with Ref-1 wild-type cells treated with SeMet, suggesting that p53 activation under the modulation of Ref-1 might play an important role in IR-treated cells in the presence of SeMet.	Selenomethionine	208-213	P53	Homo sapiens	34-37
19459742-5	2009	In addition, our data showed that p53 functional activity was significantly reduced against IR in the cells expressing a mutant form of redox factor 1 (Ref-1) contrast with Ref-1 wild-type cells treated with SeMet, suggesting that p53 activation under the modulation of Ref-1 might play an important role in IR-treated cells in the presence of SeMet.	Selenomethionine	208-213	P53	Homo sapiens	231-234
19459742-5	2009	In addition, our data showed that p53 functional activity was significantly reduced against IR in the cells expressing a mutant form of redox factor 1 (Ref-1) contrast with Ref-1 wild-type cells treated with SeMet, suggesting that p53 activation under the modulation of Ref-1 might play an important role in IR-treated cells in the presence of SeMet.	Selenomethionine	344-349	P53	Homo sapiens	34-37
19459742-5	2009	In addition, our data showed that p53 functional activity was significantly reduced against IR in the cells expressing a mutant form of redox factor 1 (Ref-1) contrast with Ref-1 wild-type cells treated with SeMet, suggesting that p53 activation under the modulation of Ref-1 might play an important role in IR-treated cells in the presence of SeMet.	Selenomethionine	344-349	P53	Homo sapiens	231-234
23992861-1	2013	It has previously been shown that anthranilamide-pyrazolo[1,5-a]pyrimidine conjugates activate p53 and cause apoptosis in cervical cancer cells such as HeLa and SiHa.	anthranilamide-pyrazolo[1,5-a]pyrimidine	34-74	P53	Homo sapiens	95-98
23837945-8	2013	RESULTS: Patients carrying p53 Arg/Arg or Arg/Pro had a higher risk of esophageal SCC (P&lt;0.001, Odds ratio [OR] 4.98, 95% confidential interval [CI] 3.46-7.17), however, not found in MDM2 rs937283.	Proline	46-49	P53	Homo sapiens	27-30
19244175-11	2009	The increase in the mean percentage of p53-positive tumor cells in the selenium-treated group (26.3%), compared with that in the placebo-treated group (5%), showed borderline statistical significance (difference = 21.3%; 95% CI = 0.7 to 41.8; P = .051).	Selenium	71-79	P53	Homo sapiens	39-42
24518718-9	2013	CONCLUSIONS: 2-DG could be considered as a potential therapeutic agent that induces cell death (which could be linked to induced oxidative stress) selectively in tumors with p53 mutations (particularly in the proline rich region).	Proline	209-216	P53	Homo sapiens	174-177
19142877-5	2009	RESULTS: The positivity for total p53, RARbeta, cyclin D1, and PCNA was nonsignificantly lower among lung cancer patients who were assigned to receive beta-carotene than those who were assigned to receive beta-carotene placebo.	beta Carotene	151-164	P53	Homo sapiens	34-37
19263299-0	2009	Bendamustine-containing immunochemotherapy is active in transformed follicular lymphoma with overexpression of p53.	Bendamustine Hydrochloride	0-12	P53	Homo sapiens	111-114
23846616-0	2013	A novel chemopreventive mechanism of selenomethionine: enhancement of APE1 enzyme activity via a Gadd45a, PCNA and APE1 protein complex that regulates p53-mediated base excision repair.	Selenomethionine	37-53	P53	Homo sapiens	151-154
19116135-5	2009	61 (2001) 1957-1963; W. Roos, M. Baumgartner, B. Kaina, Apoptosis triggered by DNA damage O6-methylguanine in human lymphocytes requires DNA replication and is mediated by p53 and Fas/CD95/Apo-1, Oncogene 23 (2004) 359-367].	O-(6)-methylguanine	90-106	P53	Homo sapiens	172-175
23846616-2	2013	Our previous study showed that selenomethionine (SeMet) induces p53 activation without genotoxic effects including apoptosis and cell cycle arrest.	Selenomethionine	31-47	P53	Homo sapiens	64-67
23846616-2	2013	Our previous study showed that selenomethionine (SeMet) induces p53 activation without genotoxic effects including apoptosis and cell cycle arrest.	Selenomethionine	49-54	P53	Homo sapiens	64-67
23846616-3	2013	In this study, we investigated the mechanism by which organic selenium compounds promote p53-mediated base excision repair (BER) activity.	Selenium	62-70	P53	Homo sapiens	89-92
20067883-15	2009	beta-carotene, lycopene and all-trans retinoic acid alone and in combination with docetaxel were found to influence the expression of bcl-2 and p53 antigen in the cells examined.	beta Carotene	0-13	P53	Homo sapiens	144-147
23846616-4	2013	Our data demonstrated for the first time that the interaction between growth arrest and DNA damage-inducible protein 45A (Gadd45a), which is a p53-activated downstream gene, and two BER-mediated repair proteins, proliferating cell nuclear antigen (PCNA) and apurinic/apyrimidinic endonuclease (APE1/Ref-1), was significantly increased in a p53-dependent manner following treatment with organic selenium compounds.	Selenium	394-402	P53	Homo sapiens	143-146
23846616-4	2013	Our data demonstrated for the first time that the interaction between growth arrest and DNA damage-inducible protein 45A (Gadd45a), which is a p53-activated downstream gene, and two BER-mediated repair proteins, proliferating cell nuclear antigen (PCNA) and apurinic/apyrimidinic endonuclease (APE1/Ref-1), was significantly increased in a p53-dependent manner following treatment with organic selenium compounds.	Selenium	394-402	P53	Homo sapiens	340-343
23846616-5	2013	Furthermore, we observed that the activity of APE1 was significantly increased in a p53-dependent manner in response to the organic selenium compounds.	Selenium	132-140	P53	Homo sapiens	84-87
23846616-7	2013	We propose that p53-dependent BER activity is a distinct chemopreventive mechanism mediated by organic selenium compounds, and that this may provide insight into the development of effective chemopreventive strategies against various oxidative stresses that contribute to a variety of human diseases, particularly cancer.	Selenium	103-111	P53	Homo sapiens	16-19
19093259-2	2008	Correlations between enhanced Ki67 and enhanced p53 and TUNEL and heparanase staining levels were significant.	ki67	30-34	P53	Homo sapiens	48-51
23965518-6	2013	P53 mediated-apoptosis and impairment of survival were reverted by treatment with Zofenoprilat.	zofenoprilate	82-94	P53	Homo sapiens	0-3
18058229-6	2008	However, combined analysis of the SNP"s showed that p53 (Arg/Arg and Arg/Pro) with TGFbeta1 (Pro/Pro and Leu/Pro) were associated with greater than 2 fold increased risk for breast cancer in Univariate (P=0.01) and Multivariate (P=0.003) analysis.	Proline	73-76	P53	Homo sapiens	52-55
23860773-0	2013	P53 codon 72 Arg/Pro polymorphism and glioma risk: an updated meta-analysis.	Proline	17-20	P53	Homo sapiens	0-3
18583539-3	2008	Also, selenium-treated ATSCs significantly downregulated p53 and p21 tumor suppressor gene products.	Selenium	6-14	P53	Homo sapiens	57-60
23860773-1	2013	P53 codon 72 Arg/Pro is a C/G variation upstream of the p53 gene on human chromosome 17p13.	Proline	17-20	P53	Homo sapiens	0-3
23860773-1	2013	P53 codon 72 Arg/Pro is a C/G variation upstream of the p53 gene on human chromosome 17p13.	Proline	17-20	P53	Homo sapiens	56-59
23860773-9	2013	Our study suggests that the polymorphism of p53 codon 72 Arg/Pro may play a protective role in the development of glioblastoma.	Proline	61-64	P53	Homo sapiens	44-47
23085759-3	2013	Here, we show that the p53 family member p73 is able to interact with the CDL4A complex through its direct binding to the receptor subunit DNA-binding protein 1 (DDB1).	cdl4a	74-79	P53	Homo sapiens	23-26
18781154-2	2008	Specifically, two polymorphisms in p53, c.97-147ins16bp and p.Arg72Pro have been analysed as putative breast cancer susceptibility variants, and it has been recently reported that a p53 haplotype combining the absence of the 16-bp insertion and the presence of proline at codon 72 (No Ins-72Pro) was associated with an earlier age at the onset of the first primary tumour in BRCA2 mutation carriers in the Spanish population.	Proline	261-268	P53	Homo sapiens	35-38
18781154-2	2008	Specifically, two polymorphisms in p53, c.97-147ins16bp and p.Arg72Pro have been analysed as putative breast cancer susceptibility variants, and it has been recently reported that a p53 haplotype combining the absence of the 16-bp insertion and the presence of proline at codon 72 (No Ins-72Pro) was associated with an earlier age at the onset of the first primary tumour in BRCA2 mutation carriers in the Spanish population.	Proline	261-268	P53	Homo sapiens	182-185
24078862-0	2013	Diaryl- and triaryl-pyrrole derivatives: inhibitors of the MDM2-p53 and MDMX-p53 protein-protein interactions Electronic supplementary information (ESI) available: Experimental details for compound synthesis, analytical data for all compounds and intermediates.	diaryl- and triaryl-pyrrole	0-27	P53	Homo sapiens	64-67
18521083-5	2008	It can also be activated independently from p53 by sodium butyrate, which leads to the differentiation events very similar to the ones induced by p53.	Butyric Acid	51-66	P53	Homo sapiens	44-47
18521083-5	2008	It can also be activated independently from p53 by sodium butyrate, which leads to the differentiation events very similar to the ones induced by p53.	Butyric Acid	51-66	P53	Homo sapiens	146-149
18707164-2	2008	The result of the calculation, based on structures from nanosecond molecular dynamics simulation, revealed that (19)Phe, (22)Leu, and (23)Trp of p53 have the strongest binding interaction with MDM2 followed by (26)Leu and (27)Pro.	Proline	226-229	P53	Homo sapiens	145-148
24213373-7	2014	Induction of the DR5 by indomethacin was found to be p53 independent but dependent on the induction of CCAAT/enhancer-binding protein homologous protein (CHOP).	Indomethacin	24-36	P53	Homo sapiens	53-56
24078862-0	2013	Diaryl- and triaryl-pyrrole derivatives: inhibitors of the MDM2-p53 and MDMX-p53 protein-protein interactions Electronic supplementary information (ESI) available: Experimental details for compound synthesis, analytical data for all compounds and intermediates.	diaryl- and triaryl-pyrrole	0-27	P53	Homo sapiens	77-80
24114124-10	2014	Consistent with abrogation of the Chk1 and p53-dependent G2/M checkpoint, mutant TP53 HT-29 colon cancer cells were more sensitive to gemcitabine when also treated with LY2603618, while wild-type TP53 HCT116 cells were not sensitized by LY2603618 to gemcitabine.	LY2603618	169-178	P53	Homo sapiens	81-85
23708819-4	2013	Molecular pathological analysis showed that amitriptyline induced p53, activated caspase-3, and decreased antiapoptotic Bcl-2 and Mcl-1 in tumor tissues.	Amitriptyline	44-57	P53	Homo sapiens	66-69
24114124-10	2014	Consistent with abrogation of the Chk1 and p53-dependent G2/M checkpoint, mutant TP53 HT-29 colon cancer cells were more sensitive to gemcitabine when also treated with LY2603618, while wild-type TP53 HCT116 cells were not sensitized by LY2603618 to gemcitabine.	LY2603618	237-246	P53	Homo sapiens	81-85
24114124-11	2014	Treatment of Calu-6 human mutant TP53 lung cancer cell xenografts with gemcitabine resulted in a stimulation of Chk1 kinase activity that was inhibited by co-administration of LY2603618.	LY2603618	176-185	P53	Homo sapiens	33-37
18625218-10	2008	Thus we conclude that pinocembrin exerts its neuroprotective effects in glutamate injury model partly by inhibiting p53 expression, thus Bax-Bcl-2 ratio, and the release of cytochrome c.	pinocembrin	22-33	P53	Homo sapiens	116-119
23612009-14	2013	Furthermore, EFV led to an activating phosphorylation of the tumour suppressor protein p53 going in line with earlier reports that EFV may be antitumourigenic and a potential cytostatic drug.	efavirenz	13-16	P53	Homo sapiens	87-90
18630942-6	2008	Sixteen differentially expressed proteins exhibited interaction network linked to the downstream regulations of p53 tumor suppressor and cell apoptosis, which may lead to suppress the melanogenesis and tumorigenesis of kojic acid treated A375 cells.	kojic acid	219-229	P53	Homo sapiens	112-115
23368763-0	2014	Evaluation of naproxen and cromolyn activities against cancer cells viability, proliferation, apoptosis, p53 and gene expression of survivin and caspase-3.	Naproxen	14-22	P53	Homo sapiens	105-108
24326769-0	2014	The association between polymorphism of P53 Codon72 Arg/Pro and hepatocellular carcinoma susceptibility: evidence from a meta-analysis of 15 studies with 3,704 cases.	Proline	56-59	P53	Homo sapiens	40-43
24326769-2	2014	Polymorphism of p53 gene codon72 arginine (Arg)/proline (Pro) (rs1042522) may influence the function of p53 protein and then affect the processing of carcinogenesis.	Proline	48-55	P53	Homo sapiens	16-19
18701478-4	2008	In the present work, we isolated PAs able to interact more efficiently with p53 conformational mutants compared with wild-type p53.	Protactinium	33-36	P53	Homo sapiens	76-79
23612009-14	2013	Furthermore, EFV led to an activating phosphorylation of the tumour suppressor protein p53 going in line with earlier reports that EFV may be antitumourigenic and a potential cytostatic drug.	efavirenz	131-134	P53	Homo sapiens	87-90
18701478-4	2008	In the present work, we isolated PAs able to interact more efficiently with p53 conformational mutants compared with wild-type p53.	Protactinium	33-36	P53	Homo sapiens	127-130
24326769-2	2014	Polymorphism of p53 gene codon72 arginine (Arg)/proline (Pro) (rs1042522) may influence the function of p53 protein and then affect the processing of carcinogenesis.	Proline	48-55	P53	Homo sapiens	104-107
24326769-2	2014	Polymorphism of p53 gene codon72 arginine (Arg)/proline (Pro) (rs1042522) may influence the function of p53 protein and then affect the processing of carcinogenesis.	Proline	57-60	P53	Homo sapiens	16-19
24326769-2	2014	Polymorphism of p53 gene codon72 arginine (Arg)/proline (Pro) (rs1042522) may influence the function of p53 protein and then affect the processing of carcinogenesis.	Proline	57-60	P53	Homo sapiens	104-107
22334414-8	2013	Increased mRNA expression of p53 was also found in dioscin-treated SGC-7901 cells, and the activation of caspase-3 and -8 was also observed.	dioscin	51-58	P53	Homo sapiens	29-32
24326769-3	2014	It has been suggested that p53 codon72 Arg/Pro polymorphism is associated with susceptibility to hepatocellular carcinoma (HCC).	Proline	43-46	P53	Homo sapiens	27-30
24326769-10	2014	This meta-analysis suggests that p53 codon72 Arg/Pro polymorphism may be associated with the risk of HCC, especially in subgroup analysis of Asian and Caucasian population, hospital-based population, the female, and the individuals infected with hepatitis virus.	Proline	49-52	P53	Homo sapiens	33-36
24667498-4	2014	We demonstrated that JMJD6 acts as an alpha-ketoglutarate- and Fe(II)-dependent lysyl hydroxylase to catalyze p53 hydroxylation.	Ketoglutaric Acids	38-57	P53	Homo sapiens	110-113
18510673-6	2008	RESULTS: We found that the p53 Proline (Pro) allele was positively associated with childhood tanning response only among black/dark brown-haired women.	Proline	31-38	P53	Homo sapiens	27-30
23683469-5	2013	The p53 gene contains a single nucleotide polymorphism at codon 72 of exon 4 which encodes either proline (Pro) or arginine (Arg).	Proline	98-105	P53	Homo sapiens	4-7
18636204-1	2008	In this study, we aimed at evaluating the possible enhancing effect exerted by the combined use of sodium butyrate (SB) and X-rays on eradicating the human colorectal cancer cell line HCT 116 containing wild-type p53.	Butyric Acid	99-114	P53	Homo sapiens	213-216
18636204-1	2008	In this study, we aimed at evaluating the possible enhancing effect exerted by the combined use of sodium butyrate (SB) and X-rays on eradicating the human colorectal cancer cell line HCT 116 containing wild-type p53.	Butyric Acid	116-118	P53	Homo sapiens	213-216
18594537-0	2008	Attenuated p53 activation in tumour-associated stromal cells accompanies decreased sensitivity to etoposide and vincristine.	Vincristine	112-123	P53	Homo sapiens	11-14
24242917-8	2014	However, in colon carcinoma (Caco-2) cells with mutant p53, treatment with either AZD5438 or NU6140 blocked proliferation, albeit more robustly with AZD5438.	4-(6-cyclohexylmethoxy-9H-purin-2-ylamino)-N,N-diethylbenzamide	93-99	P53	Homo sapiens	55-58
24366026-2	2014	The polymorphism in the p53 72nd codon involves a proline to arginine substitution, leading to changes in gene transcription activity, interaction with other proteins and modulation of apoptosis.	Proline	50-57	P53	Homo sapiens	24-27
23683469-5	2013	The p53 gene contains a single nucleotide polymorphism at codon 72 of exon 4 which encodes either proline (Pro) or arginine (Arg).	Proline	107-110	P53	Homo sapiens	4-7
24525337-0	2014	AKT mediates actinomycin D-induced p53 expression.	Dactinomycin	13-26	P53	Homo sapiens	35-38
18331475-0	2008	Anti-apoptotic effect of Mao-B inhibitor PF9601N [N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine] is mediated by p53 pathway inhibition in MPP+-treated SH-SY5Y human dopaminergic cells.	mangion-purified polysaccharide (Candida albicans)	143-147	P53	Homo sapiens	117-120
23869224-9	2013	The anti-fibrotic action of rupatadine might relate to its attenuation of BLM- or PAF-induced premature senescence because rupatadine treatment protected against the in vivo and in vitro activation of the p53/p21-dependent senescence pathway.	rupatadine	28-38	P53	Homo sapiens	205-208
18272192-3	2008	RT-PCR analysis demonstrated that the mRNA levels of p21 and p53 were increased in the TB-treated HUVEC.	Terbinafine	87-89	P53	Homo sapiens	61-64
24525337-1	2014	At high cytotoxic concentrations, actinomycin D (ActD) blocks transcription, decreasing levels of MDM2 and thus causing p53 stabilization.	Dactinomycin	34-47	P53	Homo sapiens	120-123
24174547-8	2014	Longer treatment of actinomycin D increases RPL6 ubiquitination and destabilizes RPL6, and thereby putatively attenuates p53 response until the level of L6 subsides.	Dactinomycin	20-33	P53	Homo sapiens	121-124
23869224-9	2013	The anti-fibrotic action of rupatadine might relate to its attenuation of BLM- or PAF-induced premature senescence because rupatadine treatment protected against the in vivo and in vitro activation of the p53/p21-dependent senescence pathway.	rupatadine	123-133	P53	Homo sapiens	205-208
24275138-4	2014	p53 Silencing decreased survival of glucose-starved C8161 melanoma with pyruvate supplementation under hypoxia (&lt;=1% oxygen), but increased resistance to glycolytic inhibitors oxamate and 2-deoxyglucose in 5mM glucose, preferentially under normoxia.	Oxamic Acid	179-186	P53	Homo sapiens	0-3
18355840-9	2008	In p53 codon72 Arg/Pro + Pro/Pro carriers the frequency of the AG + GG genotype of MSH3 exon23 was significantly increased in patients compared to controls (OR 2.1, 95% CI 1.05-4.34).	Proline	19-22	P53	Homo sapiens	3-6
23845085-5	2013	RESULTS: Cathinone, cathine and norephedrine generally reduced post-translational modifications of intracellular signal transducers in T-lymphocytes, B-lymphocytes, natural killer cells and monocytes, most prominently affecting c-Cbl (pTyr700), ERK1/2 (p-Thr202/p-Tyr204), p38 MAPK (p-Thr180/p-Tyr182) and p53 (both total p53 protein and p-Ser15).	norpseudoephedrine	20-27	P53	Homo sapiens	306-309
18355840-9	2008	In p53 codon72 Arg/Pro + Pro/Pro carriers the frequency of the AG + GG genotype of MSH3 exon23 was significantly increased in patients compared to controls (OR 2.1, 95% CI 1.05-4.34).	Proline	25-28	P53	Homo sapiens	3-6
18355840-9	2008	In p53 codon72 Arg/Pro + Pro/Pro carriers the frequency of the AG + GG genotype of MSH3 exon23 was significantly increased in patients compared to controls (OR 2.1, 95% CI 1.05-4.34).	Proline	25-28	P53	Homo sapiens	3-6
23845085-5	2013	RESULTS: Cathinone, cathine and norephedrine generally reduced post-translational modifications of intracellular signal transducers in T-lymphocytes, B-lymphocytes, natural killer cells and monocytes, most prominently affecting c-Cbl (pTyr700), ERK1/2 (p-Thr202/p-Tyr204), p38 MAPK (p-Thr180/p-Tyr182) and p53 (both total p53 protein and p-Ser15).	norpseudoephedrine	20-27	P53	Homo sapiens	322-325
25551567-7	2014	The administration of the autophagy inhibitor chloroquine significantly increased the expression of proapoptotic genes (Trp53, Bax, Bak1, Pmaip1, Bcl2l11, Cdkn1a, and Cdkn1b) and DNA fragmentation in the frontal brain region of olanzapine-exposed animals.	Chloroquine	46-57	P53	Homo sapiens	120-125
23845085-10	2013	Cathinone, cathine and norephedrine reduced phosphorylation of c-Cbl, ERK1/2, p38 MAPK and p53(Ser15), and norephedrine induced T-lymphocyte proliferation.	norpseudoephedrine	11-18	P53	Homo sapiens	91-94
23837445-0	2013	Induction of apoptosis in melanoma A375 cells by a chloroform fraction of Centratherum anthelminticum (L.) seeds involves NF-kappaB, p53 and Bcl-2-controlled mitochondrial signaling pathways.	Chloroform	51-61	P53	Homo sapiens	133-136
24387312-8	2014	As a result MDM2-p53 interaction inhibitors, including cis-imidazolines analogs (Nutlins), are potentially very effective agents in neuroblastoma and sarcomas.	cis-imidazolines	55-71	P53	Homo sapiens	17-20
18215142-0	2008	The 7-amino-acid site in the proline-rich region of the N-terminal domain of p53 is involved in the interaction with FAK and is critical for p53 functioning.	Proline	29-36	P53	Homo sapiens	77-80
18058069-10	2008	Furthermore, we have shown that vincristine and lomustine up-regulated p21 protein level in a p53-independent manner.	Vincristine	32-43	P53	Homo sapiens	94-97
23705030-0	2013	Sterigmatocystin-induced DNA damage triggers G2 arrest via an ATM/p53-related pathway in human gastric epithelium GES-1 cells in vitro.	Sterigmatocystin	0-16	P53	Homo sapiens	66-69
18242117-0	2008	Acetaldehyde-induced mutational pattern in the tumour suppressor gene TP53 analysed by use of a functional assay, the FASAY (functional analysis of separated alleles in yeast).	Acetaldehyde	0-12	P53	Homo sapiens	70-74
18242117-3	2008	As mutations in the tumour suppressor gene TP53 are the most common genetic alterations involved in human cancers, especially esophageal tumours, the aim of this work was to establish the mutational pattern induced by acetaldehyde in vitro on the TP53 gene, and to compare this pattern with that found in human alcohol-related tumours.	Acetaldehyde	218-230	P53	Homo sapiens	43-47
24231363-4	2013	DPMA inhibited microtubule formation and induced expression of Bax, cleaved caspase-3, p53 and ROS, and inhibited Bcl-2 expression.	CGS 24012	0-4	P53	Homo sapiens	87-90
23663243-1	2013	BACKGROUND: Codon 72 (Arg/Pro), the most frequently studied single nucleotide polymorphism (SNP) of p53 to date, is associated with the ability of the gene to induce cell apoptosis.	Proline	26-29	P53	Homo sapiens	100-103
23983135-9	2013	Heme iron intake was positively associated with the risk of P53 overexpressed tumors but not with tumors without P53 overexpression (Pheterogeneity = 0.12).	Heme	0-4	P53	Homo sapiens	60-63
23983135-10	2013	Heme iron intake was associated with an increased risk of colorectal tumors harboring G&gt;A transitions in KRAS and APC and overexpression of P53.	Heme	0-4	P53	Homo sapiens	143-146
18242117-3	2008	As mutations in the tumour suppressor gene TP53 are the most common genetic alterations involved in human cancers, especially esophageal tumours, the aim of this work was to establish the mutational pattern induced by acetaldehyde in vitro on the TP53 gene, and to compare this pattern with that found in human alcohol-related tumours.	Acetaldehyde	218-230	P53	Homo sapiens	247-251
18242117-10	2008	These results support the notion that acetaldehyde plays a role in TP53 mutations in esophageal cancers.	Acetaldehyde	38-50	P53	Homo sapiens	67-71
18260647-4	2008	Without a water channel, the substrate p53-Lys4-N(Me)H is not available because the proton dissociation p53-Lys4-N(Me)H 2 (+) --&gt; p53-Lys4-N(Me)H + H (+) does not occur.	lys4-n	43-49	P53	Homo sapiens	39-42
18260647-4	2008	Without a water channel, the substrate p53-Lys4-N(Me)H is not available because the proton dissociation p53-Lys4-N(Me)H 2 (+) --&gt; p53-Lys4-N(Me)H + H (+) does not occur.	lys4-n	43-49	P53	Homo sapiens	104-107
24057326-11	2013	These results suggest that (a) BRAF-KIAA1549 fusion may be common in PAs with atypical clinicoradiologic and histologic features, including those at extracerebellar sites, (b) BRAF V600E mutation is uncommon in extracerebellar PAs, and (c) TP53 mutation analysis remains a valuable tool in identifying childhood gliomas that will likely behave in a malignant fashion.	Protactinium	69-72	P53	Homo sapiens	240-244
23597199-6	2013	The detailed in vitro and in vivo study on the molecular mechanisms of this compound demonstrated that IVHD-valtrate exposure modulated the expression of numerous molecules involved in cell cycle progression and apoptosis regardless of p53 status, leading to increase the level of p53, Rb, p21, p27 and decrease Mdm2, E2F1, Cyclin B1, Cdc25C and Cdc2.	valtrate	108-116	P53	Homo sapiens	236-239
23963993-8	2013	The data obtain in this study indicate that rotenone-induced cytotoxicity in HepG2 cells via ROS-induced oxidative stress and mitochondria-mediated apoptosis involving p53, Bax/Bcl-2, and caspase-3.	Rotenone	44-52	P53	Homo sapiens	168-171
24113239-0	2013	5-Deazaflavin derivatives as inhibitors of p53 ubiquitination by HDM2.	5-deazaflavin	0-13	P53	Homo sapiens	43-46
24113239-1	2013	Based on previous reports of certain 5-deazaflavin derivatives being capable of activating the tumour suppressor p53 in cancer cells through inhibition of the p53-specific ubiquitin E3 ligase HDM2, we have conducted an structure-activity relationship (SAR) analysis through systematic modification of the 5-deazaflavin template.	5-deazaflavin	37-50	P53	Homo sapiens	113-116
24113239-1	2013	Based on previous reports of certain 5-deazaflavin derivatives being capable of activating the tumour suppressor p53 in cancer cells through inhibition of the p53-specific ubiquitin E3 ligase HDM2, we have conducted an structure-activity relationship (SAR) analysis through systematic modification of the 5-deazaflavin template.	5-deazaflavin	37-50	P53	Homo sapiens	159-162
18267949-6	2008	We have used a (32)P-postlabelling method to monitor the removal of GpG- and ApG-intrastrand cross links from two human cell models (the 041TR system, in which p53 is regulated by a tetracycline-inducible promoter, together with WI38 fibroblasts and the SV40-transformed derivative VA13) that each differ in p53 status.	Tetracycline	182-194	P53	Homo sapiens	160-163
18179182-4	2008	In this work, double-stranded (ds-) oligonucleotides (ODNs) containing the consensus site are immobilized onto gold electrodes to capture wild-type p53.	odns	54-58	P53	Homo sapiens	148-151
23597199-6	2013	The detailed in vitro and in vivo study on the molecular mechanisms of this compound demonstrated that IVHD-valtrate exposure modulated the expression of numerous molecules involved in cell cycle progression and apoptosis regardless of p53 status, leading to increase the level of p53, Rb, p21, p27 and decrease Mdm2, E2F1, Cyclin B1, Cdc25C and Cdc2.	valtrate	108-116	P53	Homo sapiens	281-284
23639512-3	2013	The wild-type p53 codon has two common polymorphic variants from a single-base-pair substitution at codon 72, where either C-C-C encodes proline (p53-p72) or C-G-C encodes arginine (p53-R72).	Proline	137-144	P53	Homo sapiens	14-17
17653574-0	2008	Bendamustine induces G2 cell cycle arrest and apoptosis in myeloma cells: the role of ATM-Chk2-Cdc25A and ATM-p53-p21-pathways.	Bendamustine Hydrochloride	0-12	P53	Homo sapiens	110-113
17637756-3	2008	When these cells were allowed to proliferate by subculture in DPI-free medium, an extensive G(1) delay was observed with concomitant activation of p53/p21(Waf1) signaling and reduced phosphorylation of mitogen-activated kinases.	diphenyleneiodonium	62-65	P53	Homo sapiens	147-150
24136223-0	2013	The p90 ribosomal S6 kinase (RSK) inhibitor BI-D1870 prevents gamma irradiation-induced apoptosis and mediates senescence via RSK- and p53-independent accumulation of p21WAF1/CIP1.	BI D1870	44-52	P53	Homo sapiens	135-138
23812725-0	2013	P53 codon 72 Arg/Pro polymorphism and lung cancer risk in Asians: an updated meta-analysis.	Proline	17-20	P53	Homo sapiens	0-3
23812725-1	2013	The polymorphism of p53 codon 72, a transversion of G to C (Arg to Pro), has been demonstrated to be associated with the risk for lung cancer.	Proline	67-70	P53	Homo sapiens	20-23
17637756-5	2008	Whereas the DPI-induced G(1) checkpoint was completely dependent on PHOX91, ATM and WAF1, it was only partially dependent on P53.	diphenyleneiodonium	12-15	P53	Homo sapiens	125-128
23533280-1	2013	B-cell translocation gene 3 (BTG3) is a member of the antiproliferative BTG/ Transducer of ErbB2 gene family and is induced by genotoxic stress in a p53- and Checkpoint kinase 1 (CHK1)-dependent manner.	beta-2'-deoxythioguanosine	29-32	P53	Homo sapiens	149-152
17938576-7	2008	However, nuclear localization of (64)Cu-DOTA-cetuximab showed increased uptake in the nuclei of HCT 116 +/+ cells as early as 4 h. These data demonstrate that (64)Cu is delivered to tumor cell nuclei in a p53 positive cell line in significantly greater amounts than in p53 negative cells by both non-specific and receptor-mediated uptake mechanisms.	1,4,7,10-tetraazacyclododecane- 1,4,7,10-tetraacetic acid	37-44	P53	Homo sapiens	205-208
17938576-7	2008	However, nuclear localization of (64)Cu-DOTA-cetuximab showed increased uptake in the nuclei of HCT 116 +/+ cells as early as 4 h. These data demonstrate that (64)Cu is delivered to tumor cell nuclei in a p53 positive cell line in significantly greater amounts than in p53 negative cells by both non-specific and receptor-mediated uptake mechanisms.	1,4,7,10-tetraazacyclododecane- 1,4,7,10-tetraacetic acid	37-44	P53	Homo sapiens	269-272
23812725-3	2013	Thus, we performed a meta-analysis by pooling all currently available case-control studies to estimate the effect of p53 codon 72 Arg/Pro polymorphism on the development of lung cancer.	Proline	134-137	P53	Homo sapiens	117-120
23812725-10	2013	The updated meta-analysis suggests that the p53 codon 72 Arg/Pro polymorphism is a risk factor for lung cancer in the Asian population.	Proline	61-64	P53	Homo sapiens	44-47
23860773-10	2013	The relationship of p53 codon 72 Arg/Pro polymorphism with the susceptibility to glioma needs further estimation by more individual studies with high quality across ethnicities.	Proline	37-40	P53	Homo sapiens	20-23
20306673-8	2008	In contrast to overexpression of MDM-2, the mutation of p53 was detected in 6 (13%) out of 46 ALL patients at the initial time of diagnosis, 3 of them (10.3%) were out of 29 cases of CR and the other 3 cases (17.6%) were out of 17 of relapsed group, which is significantly higher than CR group (P &lt; 0.05).	Chromium	183-185	P53	Homo sapiens	56-59
23458665-1	2013	The proteomic effects of the Hsp90 inhibitor, SNX-7081, have been determined on the p53-mutated B-cell chronic lymphocytic leukemia (CLL) cell line, MEC1.	SNX-7081	46-54	P53	Homo sapiens	84-87
20306673-8	2008	In contrast to overexpression of MDM-2, the mutation of p53 was detected in 6 (13%) out of 46 ALL patients at the initial time of diagnosis, 3 of them (10.3%) were out of 29 cases of CR and the other 3 cases (17.6%) were out of 17 of relapsed group, which is significantly higher than CR group (P &lt; 0.05).	Chromium	285-287	P53	Homo sapiens	56-59
18551893-1	2008	Hypericin (HY) is an interesting photosensitizer with dark activity and photodynamic therapy (PDT) effects via p53-independent pathway.	hypericin	0-9	P53	Homo sapiens	111-114
23908355-4	2013	Mutational activation of p53 in MDA-MB-231 breast cancer cells up-regulates the mevalonate pathway to promote tumor invasiveness.	Mevalonic Acid	80-90	P53	Homo sapiens	25-28
23908355-5	2013	p53 silencing or pharmacological inhibition of HMG-CoA reductase in these cells decreases protein isoprenylation from endogenously synthesized isoprenoids but enhances the use of exogenous isoprenols for this purpose, indicating that this latter process is regulated independently of the mevalonate pathway.	Mevalonic Acid	288-298	P53	Homo sapiens	0-3
23871989-7	2013	DHTS induced a selective cytotoxicity and apoptosis in both HCT116 p53(-/-) and HCT116 p53(+/+) colon cancer cells.	dhts	0-4	P53	Homo sapiens	67-70
23871989-7	2013	DHTS induced a selective cytotoxicity and apoptosis in both HCT116 p53(-/-) and HCT116 p53(+/+) colon cancer cells.	dhts	0-4	P53	Homo sapiens	87-90
23871989-13	2013	SIGNIFICANCE: We report for the first time that DHTS induces apoptosis in colon cancer cells through a p53-independent pathway.	dhts	48-52	P53	Homo sapiens	103-106
19013355-13	2008	Selenium induces apoptosis by producing superoxide that activates p53.	Selenium	0-8	P53	Homo sapiens	66-69
23450436-2	2013	The combination of bendamustine and cytarabine has demonstrated distinct and synergistic mechanisms of action in preclinical studies on cell lines and primary tumor cells of several B-cell lymphomas, including 17p deleted or TP53 mutated CLL.	Bendamustine Hydrochloride	19-31	P53	Homo sapiens	225-229
17989425-9	2007	The authors describe the development, validation, and execution of a high-throughput screening measuring the ubiquitination of p53 by mdm2, with p53 labeled with europium and the other substrate (Ub-UbcH5b) labeled with a Cy5 on the ubiquitin.	cyanine dye 5	222-225	P53	Homo sapiens	127-130
24019961-2	2013	We previously reported that the proline 72 polymorphic variant of p53 (P72) demonstrates increased ability to transactivate a subset of genes, relative to arginine 72 (R72); one of these genes is macrophage colony stimulating factor (CSF1).	Proline	32-39	P53	Homo sapiens	66-69
23204505-6	2013	Selenium, therefore, may be protective by preventing DNA damage from occurring as well as by increasing the activity of repair enzymes such as DNA glycosylases and DNA damage repair pathways that involve p53, BRCA1 and Gadd45.	Selenium	0-8	P53	Homo sapiens	204-207
23986050-0	2013	[Bendamustine-rituximab therapy is effective for transformed follicular lymphoma with significant expression of p53].	Bendamustine Hydrochloride	1-13	P53	Homo sapiens	112-115
23986050-9	2013	Subsequently, she was treated with five courses of BR therapy, because bendamustine had been reported to be effective for p53 gene-deficient B cell neoplasms.	Bendamustine Hydrochloride	71-83	P53	Homo sapiens	122-125
17900801-5	2007	Combining the Chk1 inhibitor UCN-01 dramatically enhanced the response to AG490 in p53-mutated or deleted glioma cells.	alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide	74-79	P53	Homo sapiens	83-86
23393342-6	2013	The underlying mechanism was investigated and it was found that ET-770 sensitized the cells by activating the p53 protein, which in turn down-regulated anti-apoptotic myeloid cell leukemia sequence-1 (MCL1) and up-regulated BCL2-associated X protein (BAX) proteins.	ecteinascidin 770	64-70	P53	Homo sapiens	110-113
18210755-4	2007	RESULTS: Our results showed that baicalein promoted the levels of p53, BAX, cytochrome c, capase-3 and -9 and reduced the level of BCL-2, which were associated with the induction of apoptotic cell death of SCC-4 cells.	baicalein	33-42	P53	Homo sapiens	66-69
23775793-6	2013	Unexpectedly, the solvent dimethylsulphoxide (DMSO) alone induced p53 binding to many sites common to DXR; however, this binding had no effect on target gene expression.	Dimethyl Sulfoxide	26-44	P53	Homo sapiens	66-69
23775793-6	2013	Unexpectedly, the solvent dimethylsulphoxide (DMSO) alone induced p53 binding to many sites common to DXR; however, this binding had no effect on target gene expression.	Dimethyl Sulfoxide	46-50	P53	Homo sapiens	66-69
23861960-1	2013	The tumor suppressor p53 was previously shown to markedly up-regulate the expression of the PRODH gene, encoding the proline dehydrogenase (PRODH) enzyme, which catalyzes the first step in proline degradation.	Proline	117-124	P53	Homo sapiens	21-24
23861960-11	2013	This supports a deeper link between proteins of the p53-family and metabolic pathways, as PRODH modulates the balance of proline and glutamate levels and those of their derivative alpha-keto-glutarate (alpha-KG) under normal and pathological (tumor) conditions.	Proline	121-128	P53	Homo sapiens	52-55
23393342-9	2013	CONCLUSION: The present results reveal for the first time that ET-770 can sensitize anoikis through the p53 pathway and further development of this compound for therapeutic use is warranted.	ecteinascidin 770	63-69	P53	Homo sapiens	104-107
23861960-11	2013	This supports a deeper link between proteins of the p53-family and metabolic pathways, as PRODH modulates the balance of proline and glutamate levels and those of their derivative alpha-keto-glutarate (alpha-KG) under normal and pathological (tumor) conditions.	Ketoglutaric Acids	180-200	P53	Homo sapiens	52-55
23861960-11	2013	This supports a deeper link between proteins of the p53-family and metabolic pathways, as PRODH modulates the balance of proline and glutamate levels and those of their derivative alpha-keto-glutarate (alpha-KG) under normal and pathological (tumor) conditions.	Ketoglutaric Acids	202-210	P53	Homo sapiens	52-55
22749133-0	2013	The flavonoids diosmetin and luteolin exert synergistic cytostatic effects in human hepatoma HepG2 cells via CYP1A-catalyzed metabolism, activation of JNK and ERK and P53/P21 up-regulation.	diosmetin	15-24	P53	Homo sapiens	167-174
23599020-0	2013	alpha-Lipoic acid prevents p53 degradation in colon cancer cells by blocking NF-kappaB induction of RPS6KA4.	Thioctic Acid	0-17	P53	Homo sapiens	27-30
18025263-0	2007	Lysophosphatidic acid decreases the nuclear localization and cellular abundance of the p53 tumor suppressor in A549 lung carcinoma cells.	lysophosphatidic acid	0-21	P53	Homo sapiens	87-90
18025263-2	2007	Here, we provide the first evidence that LPA reduces the cellular abundance of the tumor suppressor p53 in A549 lung carcinoma cells, which express endogenous LPA receptors.	lysophosphatidic acid	41-44	P53	Homo sapiens	100-103
18025263-4	2007	Inhibition of phosphatidylinositol 3-kinase protected cells from the LPA-induced reduction of p53, which implicates this signaling pathway in the mechanism of LPA-induced loss of p53.	lysophosphatidic acid	69-72	P53	Homo sapiens	94-97
18025263-4	2007	Inhibition of phosphatidylinositol 3-kinase protected cells from the LPA-induced reduction of p53, which implicates this signaling pathway in the mechanism of LPA-induced loss of p53.	lysophosphatidic acid	69-72	P53	Homo sapiens	179-182
18025263-4	2007	Inhibition of phosphatidylinositol 3-kinase protected cells from the LPA-induced reduction of p53, which implicates this signaling pathway in the mechanism of LPA-induced loss of p53.	lysophosphatidic acid	159-162	P53	Homo sapiens	94-97
18025263-4	2007	Inhibition of phosphatidylinositol 3-kinase protected cells from the LPA-induced reduction of p53, which implicates this signaling pathway in the mechanism of LPA-induced loss of p53.	lysophosphatidic acid	159-162	P53	Homo sapiens	179-182
18025263-5	2007	LPA partially protected A549 cells from actinomycin D induction of both apoptosis and increased p53 abundance.	Dactinomycin	40-53	P53	Homo sapiens	96-99
18025263-6	2007	Expression of LPA(1), LPA(2), and LPA(3) receptors in HepG2 hepatoma cells, which normally do not respond to LPA, also decreased p53 expression and p53-dependent transcription.	lysophosphatidic acid	14-17	P53	Homo sapiens	129-132
18025263-6	2007	Expression of LPA(1), LPA(2), and LPA(3) receptors in HepG2 hepatoma cells, which normally do not respond to LPA, also decreased p53 expression and p53-dependent transcription.	lysophosphatidic acid	14-17	P53	Homo sapiens	148-151
18025263-8	2007	These results identify p53 as a target of LPA action and provide a new dimension for understanding how LPA stimulates cancer cell division, protects against apoptosis, and thereby promotes tumor progression.	lysophosphatidic acid	42-45	P53	Homo sapiens	23-26
23559539-6	2013	Intranuclear p53 protein levels were increased by ACA but decreased by sodium butyrate alone or combined treatment with ACA and sodium butyrate.	Butyric Acid	71-86	P53	Homo sapiens	13-16
23559539-6	2013	Intranuclear p53 protein levels were increased by ACA but decreased by sodium butyrate alone or combined treatment with ACA and sodium butyrate.	Butyric Acid	128-143	P53	Homo sapiens	13-16
23559539-7	2013	In contrast, p53 acetylation was promoted by sodium butyrate and the ACA and sodium butyrate combination.	Butyric Acid	45-60	P53	Homo sapiens	13-16
23559539-7	2013	In contrast, p53 acetylation was promoted by sodium butyrate and the ACA and sodium butyrate combination.	Butyric Acid	77-92	P53	Homo sapiens	13-16
23559539-11	2013	The combined ACA and sodium butyrate treatment synergistically upregulated phase II enzyme activities through AMPK activation and p53 acetylation.	Butyric Acid	21-36	P53	Homo sapiens	130-133
23563240-4	2013	EFV treatment led to cell proliferation arrest and cell death of the NHKs by inducing autophagy mediated by proteasome-dependent degradation of p53.	efavirenz	0-3	P53	Homo sapiens	144-147
17678638-0	2007	Effects of the environmental mammary carcinogen 6-nitrochrysene on p53 and p21(Cip1) protein expression and cell cycle regulation in MCF-7 and MCF-10A cells.	6-nitrochrysene	48-63	P53	Homo sapiens	67-70
22749133-8	2013	More importantly, induction of G2/M arrest and p53 and p-ERK up-regulation were reversed by the application of the CYP1 inhibitor alpha-naphthoflavone.	alpha-naphthoflavone	130-150	P53	Homo sapiens	47-50
23192640-1	2013	The genetic polymorphism of p53 codon 72 Arg/Pro has been implicated in oral cancer risk, but the results of previous studies remain controversial and ambiguous.	Proline	45-48	P53	Homo sapiens	28-31
17486059-6	2007	Rb depletion after DNA damage did not occur in the absence of p21, and it was reduced when p21 induction was inhibited by p21-targeting short hairpin RNA or by a transdominant inhibitor of p53.	Rubidium	0-2	P53	Homo sapiens	189-192
17891139-5	2007	PARP-1 becomes super-activated by binding to damaged DNA, which in turn poly(ADP-ribosyl)ates p53.	poly(adp-ribosyl)ates	72-93	P53	Homo sapiens	94-97
23504554-5	2013	The gene-gene interaction of miR-34b/c rs4938723 and TP-53 Arg72-Pro showed that the combined genotypes of rs4938723CT/CC and TP-53CG/CC increased the risk of NPC (rs4938723CT/CC + TP-53CG/CC vs. rs4938723 TT+TP-53 CG/CC: OR=1.58, 95 % CI 1.04-2.42, p=0.03).	cysteinylglycine	131-133	P53	Homo sapiens	53-58
23238815-13	2013	Taken collectively, this data provides evidence that cancer cells subjected to HNO concentrations become resistant to free radicals such as NO via up-regulated cellular defense mechanisms, including p53 and GST-pi.	Free Radicals	118-131	P53	Homo sapiens	199-202
23629966-6	2013	IFN-gamma-induced interaction of HDAC1 and p53 resulted in the deacetylation of p53 and suppression of Bmf expression independent of p53"s proline-rich domain.	Proline	139-146	P53	Homo sapiens	43-46
24083726-5	2013	After inhibition of autophagy by chloroquine, the rates of cell apoptosis were increased to (30.16+-3.54)%, and the level of Caspase-3 and P53 protein were increased, and Bcl-2 protein was decreased.	Chloroquine	33-44	P53	Homo sapiens	139-142
23942225-5	2013	CONCLUSION: Our research has disclosed the mechanism involved in Cr(VI)-induced cytotoxicity following the loss of p53 and caspase-3 functions and shed light on the importance of using antioxidants for primary and secondary prevention in Cr(VI) occupational exposure populations.	Chromium	65-67	P53	Homo sapiens	115-118
23756401-10	2013	MTX provokes the activation of p53-p21(WAF1/Cip1) pathway in both cell types and activates cell-cycle inhibitor p16(INK4a) in HDFs, but not in DPSCs.	Mitoxantrone	0-3	P53	Homo sapiens	31-34
23238993-6	2013	The protective role of autophagy in cell growth inhibition by CP-31398 and RITA is supported by the finding that the AMPK inhibitor compound C or the autophagy inhibitors chloroquine or 3-methyladenine sensitize both pancreatic adenocarcinoma cell lines to the apoptotic response induced by p53-reactivating molecules.	Chloroquine	171-182	P53	Homo sapiens	291-294
22864686-7	2013	LUN-induced cellular apoptosis, akin to GEN, was mediated by PTEN, but unlike that for GEN, was p53-independent.	(5-Fluoro-1h-Indol-2-Yl)[(3r)-1'-[(3r)-Piperidin-3-Yl]spiro[indole-3,3'-Pyrrolidin]-1(2h)-Yl]methanone	0-3	P53	Homo sapiens	96-99
23092908-7	2013	RESULTS: The distribution of Arg/Arg, Arg/Pro and Pro/Pro genotypes of codon 72 of the TP53 gene was: 46.8%, 46.8% and 6.4%, respectively in the ovarian carcinomas and 64.3%, 31.4% and 4.3%, respectively in the control group.	Proline	42-45	P53	Homo sapiens	87-91
23092908-7	2013	RESULTS: The distribution of Arg/Arg, Arg/Pro and Pro/Pro genotypes of codon 72 of the TP53 gene was: 46.8%, 46.8% and 6.4%, respectively in the ovarian carcinomas and 64.3%, 31.4% and 4.3%, respectively in the control group.	Proline	50-53	P53	Homo sapiens	87-91
22286760-7	2012	Interestingly, p53 was poly(ADP-ribose)ylated by PARP-1, and the p53-mediated transrepression of the MTA1 gene required poly(ADP-ribose)ylation of p53.	Poly Adenosine Diphosphate Ribose	23-38	P53	Homo sapiens	15-18
22286760-7	2012	Interestingly, p53 was poly(ADP-ribose)ylated by PARP-1, and the p53-mediated transrepression of the MTA1 gene required poly(ADP-ribose)ylation of p53.	Poly Adenosine Diphosphate Ribose	23-39	P53	Homo sapiens	15-18
23278893-8	2013	Further evidences of AzA anti-senescence effect were repression of p53 and p21, increase in type I pro-collagen and abrogation of the enhanced expression of growth factors, such as HGF and SCF.	azelaic acid	21-24	P53	Homo sapiens	67-70
22286760-7	2012	Interestingly, p53 was poly(ADP-ribose)ylated by PARP-1, and the p53-mediated transrepression of the MTA1 gene required poly(ADP-ribose)ylation of p53.	Poly Adenosine Diphosphate Ribose	23-39	P53	Homo sapiens	65-68
22286760-7	2012	Interestingly, p53 was poly(ADP-ribose)ylated by PARP-1, and the p53-mediated transrepression of the MTA1 gene required poly(ADP-ribose)ylation of p53.	Poly Adenosine Diphosphate Ribose	23-39	P53	Homo sapiens	65-68
22286760-8	2012	In summary, we report a novel function for poly(ADP-ribose)ylation of p53 in the gene-specific regulation of the transcriptional mode of p53 on the promoter of MTA1.	Poly Adenosine Diphosphate Ribose	43-59	P53	Homo sapiens	70-73
22286760-8	2012	In summary, we report a novel function for poly(ADP-ribose)ylation of p53 in the gene-specific regulation of the transcriptional mode of p53 on the promoter of MTA1.	Poly Adenosine Diphosphate Ribose	43-59	P53	Homo sapiens	137-140
23991369-2	2013	In human populations, the p53 gene contains a common single nucleotide polymorphism (SNP) affecting codon 72 that determines whether a proline (P72) or an arginine (R72) is present at this amino acid position of the polypeptide.	Proline	135-142	P53	Homo sapiens	26-29
22743622-0	2012	Actinomycin D induces p53-independent cell death and prolongs survival in high-risk chronic lymphocytic leukemia.	Dactinomycin	0-13	P53	Homo sapiens	22-25
23124863-1	2013	The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene in association with human papillomavirus (HPV) 16 E6 variants has been implicated as a risk marker in cervical neoplasia.	Proline	32-35	P53	Homo sapiens	66-69
23124863-1	2013	The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene in association with human papillomavirus (HPV) 16 E6 variants has been implicated as a risk marker in cervical neoplasia.	Proline	39-42	P53	Homo sapiens	66-69
23124863-1	2013	The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene in association with human papillomavirus (HPV) 16 E6 variants has been implicated as a risk marker in cervical neoplasia.	Proline	39-42	P53	Homo sapiens	66-69
23555949-0	2013	Zoledronic acid produces combinatory anti-tumor effects with cisplatin on mesothelioma by increasing p53 expression levels.	Zoledronic Acid	0-15	P53	Homo sapiens	101-104
22743622-4	2012	In an extensive screen for p53-independent apoptosis inducers, actinomycin D was identified from 1496 substances and shown to induce apoptosis in primary CLL cells derived from high-risk patients including those with aberrant p53, revealing a novel p53-independent mechanism of action.	Dactinomycin	63-76	P53	Homo sapiens	27-30
23555949-5	2013	ZOL-treated cells as well as CDDP-treated cells induced p53 phosphorylation at Ser 15, a marker of p53 activation, and up-regulated p53 protein expression levels.	Zoledronic Acid	0-3	P53	Homo sapiens	56-59
23555949-5	2013	ZOL-treated cells as well as CDDP-treated cells induced p53 phosphorylation at Ser 15, a marker of p53 activation, and up-regulated p53 protein expression levels.	Zoledronic Acid	0-3	P53	Homo sapiens	99-102
22743622-4	2012	In an extensive screen for p53-independent apoptosis inducers, actinomycin D was identified from 1496 substances and shown to induce apoptosis in primary CLL cells derived from high-risk patients including those with aberrant p53, revealing a novel p53-independent mechanism of action.	Dactinomycin	63-76	P53	Homo sapiens	226-229
23555949-5	2013	ZOL-treated cells as well as CDDP-treated cells induced p53 phosphorylation at Ser 15, a marker of p53 activation, and up-regulated p53 protein expression levels.	Zoledronic Acid	0-3	P53	Homo sapiens	99-102
23555949-6	2013	Down-regulation of p53 levels with siRNA however did not influence the ZOL-mediated cytotoxicity but negated the combinatory effects by ZOL and CDDP.	Zoledronic Acid	136-139	P53	Homo sapiens	19-22
22743622-4	2012	In an extensive screen for p53-independent apoptosis inducers, actinomycin D was identified from 1496 substances and shown to induce apoptosis in primary CLL cells derived from high-risk patients including those with aberrant p53, revealing a novel p53-independent mechanism of action.	Dactinomycin	63-76	P53	Homo sapiens	226-229
23555949-8	2013	These data demonstrated that ZOL-mediated augmentation of p53, which was not linked with ZOL-induced cytotoxicity, played a role in the combinatory effects with a p53 up-regulating agent, and suggests a possible clinical use of ZOL to mesothelioma with anti-cancer agents.	Zoledronic Acid	29-32	P53	Homo sapiens	58-61
23555949-8	2013	These data demonstrated that ZOL-mediated augmentation of p53, which was not linked with ZOL-induced cytotoxicity, played a role in the combinatory effects with a p53 up-regulating agent, and suggests a possible clinical use of ZOL to mesothelioma with anti-cancer agents.	Zoledronic Acid	29-32	P53	Homo sapiens	163-166
23053979-0	2012	p53 Codon 72 arginine/proline polymorphism and cancer in Sudan.	Proline	22-29	P53	Homo sapiens	0-3
22886373-9	2012	In summary, the present study provides experimental evidence that Cr(VI) leads to energy metabolism disturbance and p53-dependent cell cycle arrest via ROS in L-02 hepatocytes.	Chromium	66-68	P53	Homo sapiens	116-119
22955915-1	2012	TP53 mutation is an independent marker of poor prognosis in patients with diffuse large B-cell lymphoma (DLBCL) treated with cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone (CHOP) therapy.	Vincristine	164-175	P53	Homo sapiens	0-4
23053979-1	2012	The aim of this report is to determine frequencies and associations of p53 codon 72 arg/pro polymorphism with different types of cancer in Sudan.	Proline	88-91	P53	Homo sapiens	71-74
23053979-8	2012	We concluded that p53 arg/pro polymorphism has different pattern of frequency in different types of cancer among Sudanese patients, indicating perhaps different etiology and biology of these tumours.	Proline	26-29	P53	Homo sapiens	18-21
22992837-6	2012	The results indicated that baicalein             induced apoptosis via Akt activation in a p53-dependent manner in the HT-29 colon             cancer cells and that it may serve as a chemopreventive or therapeutic agent for             HT-29 colon cancer.	baicalein	27-36	P53	Homo sapiens	91-94
22892830-8	2012	In addition, a higher frequency of cytogenetic aberrations was observed in p53 variants having the homozygous proline genotype compared to variants having other genotypes both in patients and healthy individuals.	Proline	110-117	P53	Homo sapiens	75-78
22915551-4	2012	p53 is a well-studied transcription factor that has a proline-rich N-terminal ID region containing two activation domains.	Proline	54-61	P53	Homo sapiens	0-3
22929231-4	2012	Compound 3a [(Z)-2-(5-bromo-2-hydroxybenzylidene) benzofuran-3(2H)-one] was identified as a potent inhibitor of SIRT1 (IC(50)=1muM) which showed a dose dependent increase in the acetylation of p53 resulting in induction of apoptosis.	(z)-2-(5-bromo-2-hydroxybenzylidene) benzofuran-3(2h)-one	13-70	P53	Homo sapiens	193-196
22624727-6	2012	Bendamustine activated p53 in Granta 519 tumours, concurrent with activation of caspase 3.	Bendamustine Hydrochloride	0-12	P53	Homo sapiens	23-26
22915551-5	2012	High proline content is a property commonly associated with ID, and thus p53 may be a good model system for investigating the biochemical importance of ID.	Proline	5-12	P53	Homo sapiens	73-76
22791815-2	2012	However, both adenine (A) and guanine (G) mutations are found in the p53 gene in Cr exposure-related lung cancer.	Chromium	81-83	P53	Homo sapiens	69-72
22995316-6	2012	Microarray analysis showed that ISL-treated LCLs represented gene expression changes in cell cycle and p53 signaling pathway, having a potential as regulators in LCL survival and sensitivity to ISL-induced cytotoxicity.	isoliquiritigenin	32-35	P53	Homo sapiens	103-106
22791815-5	2012	To understand the causes for these Cr-induced DNA damages, we mapped the distribution of BDA adducts and ODD in the p53 gene DNA fragments induced by Cr(III), Cr(VI) and Cr(V), the three major cellular Cr forms.	Chromium	35-37	P53	Homo sapiens	116-119
22791815-5	2012	To understand the causes for these Cr-induced DNA damages, we mapped the distribution of BDA adducts and ODD in the p53 gene DNA fragments induced by Cr(III), Cr(VI) and Cr(V), the three major cellular Cr forms.	Chromium	150-152	P53	Homo sapiens	116-119
22791815-5	2012	To understand the causes for these Cr-induced DNA damages, we mapped the distribution of BDA adducts and ODD in the p53 gene DNA fragments induced by Cr(III), Cr(VI) and Cr(V), the three major cellular Cr forms.	Chromium	150-152	P53	Homo sapiens	116-119
22791815-5	2012	To understand the causes for these Cr-induced DNA damages, we mapped the distribution of BDA adducts and ODD in the p53 gene DNA fragments induced by Cr(III), Cr(VI) and Cr(V), the three major cellular Cr forms.	Chromium	150-152	P53	Homo sapiens	116-119
22791815-5	2012	To understand the causes for these Cr-induced DNA damages, we mapped the distribution of BDA adducts and ODD in the p53 gene DNA fragments induced by Cr(III), Cr(VI) and Cr(V), the three major cellular Cr forms.	Chromium	150-152	P53	Homo sapiens	116-119
23182046-6	2012	Quinuclidinone derivative 6 increased expression levels of p53 and Bax at  both protein and mRNA levels and reduced expression level of Mdm2, Bcl2, Akt and Bcl-XL It also increased mitochondrial apoptotic pathways by activating release of cytochrome c which is consistent with activation of caspase-9 as confirmed by caspase-9 inhibitor LEHD-CHO.	1-azabicyclo[2.2.2]octan-2-one	0-14	P53	Homo sapiens	59-62
22894610-2	2012	Using a coprecipitation method, doxorubicin hydrochloride (DOX), an antitumor drug, and p53 expression plasmid were encapsulated in alginate/CaCO(3)/DNA/DOX nanoparticles with high encapsulation efficiency.	Alginates	132-140	P53	Homo sapiens	88-91
22549660-6	2012	Our findings indicated that by synergism with anticancer drugs, FLX modulation of apoptosis via targeting p53 and Bcl-2 expression, FLX reverse the breast cancer cell"s resistance and enhance the chemosensitivity to ADM and PTX.	Fluoxetine	64-67	P53	Homo sapiens	106-109
22982226-9	2012	In conclusion, our finding demonstrates that H(2)S/CSE pathway plays a radioprotection role by inhibiting radiation-induced ROS production, P53 phosphorylation, NF-kappaB activation and decrease of Bcl-2/Bax, indicating that modulation of H(2)S may be a novel protection strategy for liver radiation injury in radiotherapy.	h(2)	45-49	P53	Homo sapiens	140-143
22903472-5	2012	A non-significant trend towards a good pathological response was shown in patients carrying the Arg/Arg or Arg/Pro TP53 codon 72 gene variant compared to those harboring the Pro/Pro variant (17.6 or 37.9 % vs. 0; p = 0.071).	Proline	111-114	P53	Homo sapiens	115-119
22960073-3	2012	Cell viability assays showed that TQ killed T-47D, MDA-MB-231, and MDA-MB-468 cells via p53-independent induction of apoptosis; however, MCF-7 cells were refractory to the cytotoxic action of TQ.	thymoquinone	34-36	P53	Homo sapiens	88-91
22763759-6	2012	However, the growth-inhibitory activity of vincristine, doxorubicin, carboplatin, etoposide, and temozolomide was significantly impaired by silencing of TP53.	Vincristine	43-54	P53	Homo sapiens	153-157
21881978-4	2012	The strong correlations of lower CR rate with advanced Binet stage, unmutated IGHV, cytogenetic abnormalities of del(17p13) or del(11q23), and p53 mutations were observed by univariable analyses.	Chromium	33-35	P53	Homo sapiens	143-146
22869710-4	2012	EDTA removes Zn(2+) to generate apo-p53, which aggregated faster than holo-p53.	Edetic Acid	0-4	P53	Homo sapiens	36-39
22249977-0	2012	Impact of codon 72 Arg &gt; Pro single nucleotide polymorphism in TP53 gene in the risk of kangri cancer: a case control study in Kashmir.	Proline	28-31	P53	Homo sapiens	66-70
22751434-0	2012	p53 and cancer stem cells: the mevalonate connexion.	Mevalonic Acid	31-41	P53	Homo sapiens	0-3
22529099-3	2012	This concept is strongly supported by the recent finding that mutant p53, which is present in more than half of all human cancers, can significantly upregulate mevalonate metabolism and protein prenylation in carcinoma cells.	Mevalonic Acid	160-170	P53	Homo sapiens	69-72
22149137-0	2012	The Hsp90 inhibitor SNX-7081 synergizes with and restores sensitivity to fludarabine in chronic lymphocytic leukemia cells with lesions in the TP53 pathway: a potential treatment strategy for fludarabine refractory disease.	SNX-7081	20-28	P53	Homo sapiens	143-147
22149137-4	2012	In seven cell lines and 23 patient samples synergy between SNX-7081 and fludarabine (2-FaraA) was apparent in the three TP53 mutated cell lines and at significantly lower concentrations in TP53 or ATM dysfunctional patient cells.	SNX-7081	59-67	P53	Homo sapiens	120-124
22483234-8	2012	We noted that the favorable histology Wilms tumors with a proline residue at position 72 of TP53 tended to have higher immunoexpression of GLUT1, although this immunoexpression did not reach statistical significance in this small set of cases.	Proline	58-65	P53	Homo sapiens	92-96
22561874-0	2012	Eriocalyxin B induces apoptosis and cell cycle arrest in pancreatic adenocarcinoma cells through caspase- and p53-dependent pathways.	eriocalyxin B	0-13	P53	Homo sapiens	110-113
22737668-5	2012	The discovery that proline degradation is activated by p53 directed our attention to the initiation of apoptosis by proline oxidase/dehydrogenase.	Proline	19-26	P53	Homo sapiens	55-58
22081073-3	2012	We show that the RPL11 is rapidly but transiently recruited at promoter sites of p53-regulated genes upon nucleolar stress induced by actinomycin D (ActD).	Dactinomycin	134-147	P53	Homo sapiens	81-84
22509835-6	2012	L-Buthionine sulphoximine (BSO) enhanced the cytotoxicity of As(+3) against the viability of HaCaT cells with reduced p53 protein through inducing protein ubiquitination and reactive oxygen species (ROS) production, and disrupting the mitochondrial membrane potential in HaCaT cells.	l-buthionine sulphoximine	0-25	P53	Homo sapiens	118-121
22504299-4	2012	The IFN-gamma-dependent poly(ADP-ribosyl)ation of DNA-PKcs (which activates its kinase function) and concomitant activation of the tumor suppressor p53 were specifically prevented by Trp-SA, an analog of Trp-AMP that disrupted the TrpRS-DNA-PKcs-PARP-1 complex.	tryptophanyl-5'-adenosine monophosphate	204-211	P53	Homo sapiens	148-151
22265823-8	2012	Collectively, these data suggest that the activation of PI3K/Akt pathway is involved in the protective effect of puerarin against MPP(+)-induced neuroblastoma SH-SY5Y cell death through inhibiting nuclear p53 accumulation and subsequently caspase-3-dependent PCD.	mangion-purified polysaccharide (Candida albicans)	130-136	P53	Homo sapiens	205-208
22293494-0	2012	The induction of polyploidy or apoptosis by the Aurora A kinase inhibitor MK8745 is p53-dependent.	MK-8745	74-80	P53	Homo sapiens	84-87
22293494-5	2012	MK8745 induced apoptotic cell death in a p53-dependent manner when tested in vitro in cell lines of multiple lineages.	MK-8745	0-6	P53	Homo sapiens	41-44
22310775-9	2012	We also found that the levels of pro-apoptotic proteins, including phospho-p53 (Ser 15), Bad, Bax, and cleaved caspase-3 were significantly increased in the IC/PBS bladders.	Lead	160-163	P53	Homo sapiens	75-78
22525470-0	2012	Different responses to 5-fluoraouracil in mutagenicity and gene expression between two human lymphoblastoid cell lines with or without TP53 mutation.	5-fluoraouracil	23-38	P53	Homo sapiens	135-139
22631671-0	2012	Pro variant of TP53 Arg72Pro contributes to gastric cancer risk in Asians: evidence from a meta-analysis.	Proline	0-3	P53	Homo sapiens	15-19
22687398-0	2012	Effects of the ethylacetate extract of Orostachys japonicus on induction of apoptosis through the p53-mediated signaling pathway in human gastric cancer cells.	ethyl acetate	15-27	P53	Homo sapiens	98-101
22844323-7	2012	Moreover, a significant gene interaction of the carriers with the combined genotypes of miR-34b/c rs4938723CC and TP53 Arg72Pro CG/CC/GG had a decreased risk of IA, compared with those carrying miR-34b/c rs4938723CT/TT+TP53 Arg72Pro GG/CG/CC combined genotypes.	cysteinylglycine	128-130	P53	Homo sapiens	114-118
22844323-7	2012	Moreover, a significant gene interaction of the carriers with the combined genotypes of miR-34b/c rs4938723CC and TP53 Arg72Pro CG/CC/GG had a decreased risk of IA, compared with those carrying miR-34b/c rs4938723CT/TT+TP53 Arg72Pro GG/CG/CC combined genotypes.	cysteinylglycine	128-130	P53	Homo sapiens	219-223
22210716-9	2012	Our study indicated that a high prevalence of the genotype Arg/Pro at the p53 codon 72 may contribute to susceptibility to OSCC, especially in combination with the use of carcinogenic tobacco-specific nitrosamine (TSNA)-rich toombak.	Proline	63-66	P53	Homo sapiens	74-77
22199295-7	2011	Individuals with the C (Pro) allele at p53 codon 72 had a 1.6-fold increased odds ratio of endometriosis, and those with Arg/Pro and Pro/Pro genotypes for p53 codon 72 had a 1.84- and 2.74-fold (95% confidence interval=1.17-2.92 and 1.58-4.74) increased risk of endometriosis compared to those with Arg/Arg, respectively.	Proline	24-27	P53	Homo sapiens	39-42
21880715-4	2011	We have solved the high resolution crystal structures of the full-length SMYD2 protein in binary complex with its cofactor S-adenosylmethionine and in ternary complex with cofactor product S-adenosylhomocysteine and p53 substrate peptide (residues 368-375), respectively.	Sulfur	73-74	P53	Homo sapiens	216-219
21316118-4	2011	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in LC were 37.0%, 46.2%, and 16.7%, respectively; frequencies in the controls were 43.2%, 45.6%, and 11.2%, respectively (p&lt;0.01).	Proline	60-63	P53	Homo sapiens	19-22
21316118-4	2011	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in LC were 37.0%, 46.2%, and 16.7%, respectively; frequencies in the controls were 43.2%, 45.6%, and 11.2%, respectively (p&lt;0.01).	Proline	69-72	P53	Homo sapiens	19-22
21316118-4	2011	The frequencies of p53 codon 72 polymorphisms (Arg/Arg, Arg/Pro, and Pro/Pro) in LC were 37.0%, 46.2%, and 16.7%, respectively; frequencies in the controls were 43.2%, 45.6%, and 11.2%, respectively (p&lt;0.01).	Proline	69-72	P53	Homo sapiens	19-22
21843334-1	2011	BACKGROUND: Single-nucleotide polymorphisms within TP53 gene (codon 72 exon 4, rs1042522, encoding either arginine or proline) and MDM2 promoter (SNP309; rs2279744), have been independently associated with increased risk of several cancer types.	Proline	118-125	P53	Homo sapiens	51-55
21659383-0	2011	Baicalein potently suppresses angiogenesis induced by vascular endothelial growth factor through the p53/Rb signaling pathway leading to G1/S cell cycle arrest.	baicalein	0-9	P53	Homo sapiens	101-104
21402718-3	2011	By using human p53 knockin (Hupki) mice carrying a single nucleotide polymorphism (SNP) at codon 72 (arginine/proline), the arginine allele was demonstrated to produce higher uterine LIF levels during implantation than the proline allele.	Proline	110-117	P53	Homo sapiens	15-18
21411502-2	2011	Our studies on the drug-resistant p53-mutant as compared with drug-resistant p53 wild-type neuroblastoma revealed a novel mechanism for resistance to apoptosis: a direct role of p53 in regulating the cellular concentration of proapoptotic alkenals by functioning as a specific and saturable allosteric inhibitor of the alkenal-glutathione conjugate transporter, RLIP76.	alkenal	239-246	P53	Homo sapiens	34-37
21411502-2	2011	Our studies on the drug-resistant p53-mutant as compared with drug-resistant p53 wild-type neuroblastoma revealed a novel mechanism for resistance to apoptosis: a direct role of p53 in regulating the cellular concentration of proapoptotic alkenals by functioning as a specific and saturable allosteric inhibitor of the alkenal-glutathione conjugate transporter, RLIP76.	alkenal	239-246	P53	Homo sapiens	77-80
21411502-2	2011	Our studies on the drug-resistant p53-mutant as compared with drug-resistant p53 wild-type neuroblastoma revealed a novel mechanism for resistance to apoptosis: a direct role of p53 in regulating the cellular concentration of proapoptotic alkenals by functioning as a specific and saturable allosteric inhibitor of the alkenal-glutathione conjugate transporter, RLIP76.	alkenal	239-246	P53	Homo sapiens	77-80
21120637-10	2011	In addition, 8-Br-cAMP and VPA have a synergistic effect on cellular reprogramming, which may be in part due to the transient down-regulation of the p53 signaling pathway during the early stages of reprogramming.	Valproic Acid	27-30	P53	Homo sapiens	149-152
21454683-1	2011	The common polymorphism of p53 at codon 72, either encoding proline or arginine, has drawn attention as a genetic factor associated with clinical outcome or cancer risk for the last 2 decades.	Proline	60-67	P53	Homo sapiens	27-30
21530747-7	2011	Reactive oxygen and nitrogen species produced by inflammatory cells can affect regulation of genes that encode factors that prevent carcinogenesis (such as p53, DNA mismatch repair proteins, and DNA base excision-repair proteins), transcription factors (such as nuclear factor-kappaB), or signaling proteins (such as cyclooxygenases).	reactive oxygen and nitrogen species	0-36	P53	Homo sapiens	156-159
21385899-8	2011	In HepG2 epithelial cells, LPA-stimulated AKT phosphorylation and EMT features reached maximum when both RKTG and p53 were simultaneously silenced.	lpa	27-30	P53	Homo sapiens	114-117
21401896-8	2011	The Western blot showed that increasing the concentration of HCPT resulted in a higher expression level of p-JNK, P53, ubiquitin, GADD 153 and Grp78/Bip in the Ufd1 knockdown cells than that in the control cells.	hydroxycamptothecinum	61-65	P53	Homo sapiens	114-117
21498708-1	2011	Novel quinuclidinone derivatives that cause cytotoxicity in human non-small lung carcinoma epithelial cells null for p53 (H1299) have been previously reported.	1-azabicyclo[2.2.2]octan-2-one	6-20	P53	Homo sapiens	117-120
21078359-5	2011	The tryptophan environment of the molten globule beta-fragment has been probed by selective modification with N-bromosuccinimide (NBS), which shows that two tryptophans, possibly Trp 53 and Trp 152 are oxidized while the other Trp 128 remains resistant to oxidation.	Bromosuccinimide	110-128	P53	Homo sapiens	179-185
21165656-0	2011	CITED2 is activated in ulcerative colitis and induces p53-dependent apoptosis in response to butyric acid.	Butyric Acid	93-105	P53	Homo sapiens	54-57
21165656-1	2011	BACKGROUND: In ulcerative colitis (UC), Fusobacterium varium is significantly detected in patients" mucosa, and butyric acid (BA), abundantly produced by the bacterium, activates the p53 system and induces epithelial apoptosis, as we previously reported.	Butyric Acid	112-124	P53	Homo sapiens	183-186
21165656-1	2011	BACKGROUND: In ulcerative colitis (UC), Fusobacterium varium is significantly detected in patients" mucosa, and butyric acid (BA), abundantly produced by the bacterium, activates the p53 system and induces epithelial apoptosis, as we previously reported.	Butyric Acid	0-2	P53	Homo sapiens	183-186
21165656-8	2011	BA-dependent apoptosis was suppressed by an inhibitor of monocarboxylate transporter-1 and an siRNA for p53.	Butyric Acid	0-2	P53	Homo sapiens	104-107
21262846-1	2011	The inositol pyrophosphate, diphosphoinositol pentakisphosphate, regulates p53 and protein kinase Akt signaling, and its aberrant increase in cells has been implicated in apoptosis and insulin resistance.	inositol pyrophosphate	4-26	P53	Homo sapiens	75-78
21262846-2	2011	Inositol hexakisphosphate kinase-2 (IP6K2), one of the major inositol pyrophosphate synthesizing enzymes, mediates p53-linked apoptotic cell death.	inositol pyrophosphate	61-83	P53	Homo sapiens	115-118
20419384-4	2011	PCR amplification for the analysis of p53 codon 72 arginine/proline alleles was carried out in a separate reaction.	Proline	60-67	P53	Homo sapiens	38-41
21598212-6	2011	PCR amplification of TP53 codon 72 polymorphism: TP53 codon 72 genotypes were detected by PCR using specific primer pairs for amplifying the proline or the arginine Alleles.	Proline	141-148	P53	Homo sapiens	21-25
21598212-6	2011	PCR amplification of TP53 codon 72 polymorphism: TP53 codon 72 genotypes were detected by PCR using specific primer pairs for amplifying the proline or the arginine Alleles.	Proline	141-148	P53	Homo sapiens	49-53
21598212-13	2011	In control samples, the genotype distribution for TP53 polymorphism showed 30.4%, 45.2% and 24.4% for the arginine/arginine, arginine/proline and proline/proline genotypes, respectively.	Proline	134-141	P53	Homo sapiens	50-54
21598212-13	2011	In control samples, the genotype distribution for TP53 polymorphism showed 30.4%, 45.2% and 24.4% for the arginine/arginine, arginine/proline and proline/proline genotypes, respectively.	Proline	146-153	P53	Homo sapiens	50-54
21598212-13	2011	In control samples, the genotype distribution for TP53 polymorphism showed 30.4%, 45.2% and 24.4% for the arginine/arginine, arginine/proline and proline/proline genotypes, respectively.	Proline	146-153	P53	Homo sapiens	50-54
21359449-6	2011	p53 positivity was observed in 93.3% of PMD, in 63.3% of OSCC and in 80% of OEH.	OEH	76-79	P53	Homo sapiens	0-3
20807569-2	2011	Others and we have previously reported that TQ acts as agent that triggers cell cycle arrest and apoptosis through either a p53- or p73-dependent pathway.	thymoquinone	44-46	P53	Homo sapiens	124-127
21720516-0	2011	Ethylenediamine functionalized-single-walled nanotube (f-SWNT)-assisted in vitro delivery of the oncogene suppressor p53 gene to breast cancer MCF-7 cells.	ethylenediamine	0-15	P53	Homo sapiens	117-120
21720516-1	2011	A gene delivery concept based on ethylenediamine-functionalized single-walled carbon nanotubes (f-SWCNTs) using the oncogene suppressor p53 gene as a model gene was successfully tested in vitro in MCF-7 breast cancer cells.	ethylenediamine	33-48	P53	Homo sapiens	136-139
20549306-1	2010	In fibroblasts, beryllium salt causes activation of the p53 transcription factor and induction of a senescence-like state.	UNII-1757C4Y7HM	16-30	P53	Homo sapiens	56-59
20705543-11	2010	Crocidolite and Libby amphibole similarly activated the p53 pathway.	Asbestos, Crocidolite	0-11	P53	Homo sapiens	56-59
21199742-7	2010	Caffeic acid decreased levels of uncleaved caspase-3 and Bcl-2, and induced cleaved caspase-3 and p53.	caffeic acid	0-12	P53	Homo sapiens	98-101
20947454-1	2010	We have previously shown that whereas T-cells from normal individuals undergo accumulation of p53 and apoptosis when treated with the genotoxic agent Actinomycin D (ActD), those from Ataxia Telangiectasia (AT) and Nijmegen Breakage Syndrome (NBS) patients resist ActD-induced apoptosis [1].	Dactinomycin	150-163	P53	Homo sapiens	94-97
20878062-9	2010	P53 staining was decreased, while PCNA and TGFbeta3 staining were increased by indomethacin in tumor areas with high presence of COX-2, which correlated to staining of BAX, TUNEL, Bcl-2, c-jun, p21, p27, p53 and NM23.	Indomethacin	79-91	P53	Homo sapiens	204-207
20655369-4	2010	Our results revealed a significant P53-induction by actinomycin D, methyl methanesulfonate and etoposide.	Dactinomycin	52-65	P53	Homo sapiens	35-38
20732856-4	2010	We observed an increased risk of cervical cancer associated with the p53 Arg/Arg (OR, 2.25; 95% CI, 1.11-4.54) or p21 Ser/Ser (OR, 2.09; 95% CI, 1.04-4.19) genotype, compared with the p53 Pro/Pro or p21 Arg/Arg genotype, respectively.	Proline	188-191	P53	Homo sapiens	69-72
20732856-4	2010	We observed an increased risk of cervical cancer associated with the p53 Arg/Arg (OR, 2.25; 95% CI, 1.11-4.54) or p21 Ser/Ser (OR, 2.09; 95% CI, 1.04-4.19) genotype, compared with the p53 Pro/Pro or p21 Arg/Arg genotype, respectively.	Proline	192-195	P53	Homo sapiens	69-72
20472715-8	2010	While in GBM cells treated with the chemotherapeutic agent 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), HDMX appears to stabilize p53 and promote phosphorylation of the DNA double-stranded break repair protein H2AX, up-regulate the DNA repair gene VPX, stimulate DNA repair, and confer resistance to BCNU.	Carmustine	59-95	P53	Homo sapiens	130-133
21103216-5	2010	Proline to alanine substitutions at P53, P481, P484, and P485 in the V42C background, as well as P53, P481, and P484 in the G489C background, exhibited decreased nucleotidase activities.	Proline	0-7	P53	Homo sapiens	36-39
20415579-3	2010	Matrix metalloproteinases degrading collagen are activated during stress to make proline available, and proline oxidase, the first enzyme in proline degradation, is induced by p53, peroxisome proliferator-activated receptor gamma (PPARgamma) and its ligands, and by AMP-activated protein kinase downregulating mTOR.	Proline	104-111	P53	Homo sapiens	176-179
20435884-3	2010	Losses of TP53 and CDKN2A, observed in 8% and 35% of patients, respectively, were significantly associated with a shorter survival after rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) treatment, independently of the International Prognostic Index and of the cell of origin.	Vincristine	179-190	P53	Homo sapiens	10-14
20673369-11	2010	Additionally, we report that the upstream kinase cyclin dependent kinase 5 interacts with p53 to phosphorylate it at Serine20 and Serine46 residues thereby promoting its recruitment on p21 and bax promoters.	serine46	130-138	P53	Homo sapiens	90-93
20389250-0	2010	Pro variant of TP53 Arg72Pro contributes to esophageal squamous cell carcinoma risk: evidence from a meta-analysis.	Proline	0-3	P53	Homo sapiens	15-19
24683262-4	2010	OBJECTIVE: The aim of this study was to examine the ability of the histone deacetylase inhibitor, sodium butyrate (NaB), to modulate the expression of p53.	Butyric Acid	98-113	P53	Homo sapiens	151-154
19948747-4	2010	Since mutations in the p53 gene are present in approximately 40% of all human lung cancers and are more common in smokers than in nonsmokers, we aimed to detect the status of p53 at codon 72 for Arg/Arg or Arg/Pro or Pro/Pro allele polymorphism and p53 codon 249 mutation in smokers and nonsmokers of South India.	Proline	210-213	P53	Homo sapiens	175-178
19948747-4	2010	Since mutations in the p53 gene are present in approximately 40% of all human lung cancers and are more common in smokers than in nonsmokers, we aimed to detect the status of p53 at codon 72 for Arg/Arg or Arg/Pro or Pro/Pro allele polymorphism and p53 codon 249 mutation in smokers and nonsmokers of South India.	Proline	210-213	P53	Homo sapiens	175-178
20512840-3	2010	Actually, polymorphic variants Arg and Pro were found to have different properties of regulation of TP53-dependent DNA repair target genes, that can effect various levels of chromosome aberrations in cancer patients with these genotypes.	Proline	39-42	P53	Homo sapiens	100-104
20428827-6	2010	Similarly, BCL2 and E2F3 were down-regulated when P53 expression was elevated by ASO treatment.	Oligonucleotides, Antisense	81-84	P53	Homo sapiens	50-53
20480521-13	2010	However, gemcitabine and dicoumarol combination induced increased p53 and decreased Bcl-(XL) levels in KKU-100, but not in KKU-M214 cells.	Dicumarol	25-35	P53	Homo sapiens	66-69
20658010-1	2010	UNLABELLED: p53 tumoral suppressor gene harbors a functional polymorphism which codes either arginine (Arg) or proline (Pro) in the protein p53 of codon 72.	Proline	111-118	P53	Homo sapiens	12-15
20658010-1	2010	UNLABELLED: p53 tumoral suppressor gene harbors a functional polymorphism which codes either arginine (Arg) or proline (Pro) in the protein p53 of codon 72.	Proline	111-118	P53	Homo sapiens	140-143
20658010-1	2010	UNLABELLED: p53 tumoral suppressor gene harbors a functional polymorphism which codes either arginine (Arg) or proline (Pro) in the protein p53 of codon 72.	Proline	120-123	P53	Homo sapiens	12-15
20658010-1	2010	UNLABELLED: p53 tumoral suppressor gene harbors a functional polymorphism which codes either arginine (Arg) or proline (Pro) in the protein p53 of codon 72.	Proline	120-123	P53	Homo sapiens	140-143
20406950-3	2010	It is known that the interaction of the vitamin D metabolite 1,25-dihydroxyvitamin D(3) (1,25D) with its functional vitamin D receptor leads to differentiation, G(1) arrest, and increased cell survival in p53-null AML cells.	1,25-dihydroxyvitamin D	61-84	P53	Homo sapiens	205-208
19922265-9	2010	The CUVA treatment may represent a novel mechanism-based protocol for increasing the efficacy of coralyne in inducing apoptosis in both p53 wild-type and mutant tumor cells.	cuva	4-8	P53	Homo sapiens	136-139
20221258-8	2010	Our PPI inhibitor profiler is challenged on the experimental screening results of 11 different PPIs among which the p53/MDM2 interaction screened within our own CDithem platform, that in addition to the validation of our concept led to the identification of 4 novel p53/MDM2 inhibitors.	cdithem	161-168	P53	Homo sapiens	116-119
20221258-8	2010	Our PPI inhibitor profiler is challenged on the experimental screening results of 11 different PPIs among which the p53/MDM2 interaction screened within our own CDithem platform, that in addition to the validation of our concept led to the identification of 4 novel p53/MDM2 inhibitors.	cdithem	161-168	P53	Homo sapiens	266-269
20193851-1	2010	Polymorphism at codon 72 of TP53, resulting in either the arginine (Arg) or proline (Pro) form of p53 (R72P), has been associated with the susceptibility to different cancers.	Proline	76-83	P53	Homo sapiens	28-32
20193851-1	2010	Polymorphism at codon 72 of TP53, resulting in either the arginine (Arg) or proline (Pro) form of p53 (R72P), has been associated with the susceptibility to different cancers.	Proline	76-83	P53	Homo sapiens	98-101
20193851-1	2010	Polymorphism at codon 72 of TP53, resulting in either the arginine (Arg) or proline (Pro) form of p53 (R72P), has been associated with the susceptibility to different cancers.	Proline	85-88	P53	Homo sapiens	28-32
20193851-1	2010	Polymorphism at codon 72 of TP53, resulting in either the arginine (Arg) or proline (Pro) form of p53 (R72P), has been associated with the susceptibility to different cancers.	Proline	85-88	P53	Homo sapiens	98-101
22993551-6	2010	These findings demonstrate that derivatives of TQ inhibit cell proliferation dependent on p53 status by activating the cell cycle inhibitor p21(cip1/waf1) at lower concentrations than unmodified TQ.	thymoquinone	47-49	P53	Homo sapiens	90-93
20150224-0	2010	Apoptotic effects of Physalis minima L. chloroform extract in human breast carcinoma T-47D cells mediated by c-myc-, p53-, and caspase-3-dependent pathways.	Chloroform	40-50	P53	Homo sapiens	117-120
20150224-4	2010	The c-myc was significantly induced by the chloroform extract at the earlier phase of treatment, followed by p53 and caspase-3.	Chloroform	43-53	P53	Homo sapiens	109-112
20150224-7	2010	Thus, the results from this study strongly suggest that the chloroform extract of P. minima induced apoptotic cell death via p53-, caspase-3-, and c-myc-dependent pathways.	Chloroform	60-70	P53	Homo sapiens	125-128
20008555-2	2010	Here, we show that PolH, a target of the p53 tumor suppressor, is a short-half-life protein.	polh	19-23	P53	Homo sapiens	41-44
19786980-7	2010	Severe neutropenia was associated with the TP53 72 Pro/Pro, XPD 312 Asp/Asn and XRCC1 399 Arg/Arg genotypes.	Proline	51-54	P53	Homo sapiens	43-47
19616373-6	2010	In addition, DPPT causes p53 and Bax to accumulate, accompanied by activation of DNA damage-sensing kinases, including ataxia-telangiectasia mutated (ATM) kinase and Chk2.	deoxypodophyllotoxin	13-17	P53	Homo sapiens	25-28
19616373-9	2010	Together, these data suggest that DPPT induces G(2)/M cell-cycle arrest followed by apoptosis through multiple cellular processes, involving the activation of ATM, upregulation of p53 and Bax, activation of caspase-3 and -7, and accumulation of PTEN resulting in the inhibition of the Akt pathway.	deoxypodophyllotoxin	34-38	P53	Homo sapiens	180-183
20082853-2	2010	To investigate the frequency of proline and arginine alleles of TP53 codon 72, the present study analyzed the DNA from blood samples of 30 Iranian women with endometrial cancer, in comparison with 32 healthy women.	Proline	32-39	P53	Homo sapiens	64-68
19874289-2	2010	The present work shows that rotenone, a mitochondrial complex I inhibitor, induced time- and concentration-dependent apoptosis in lymphocytes which was mediated by anion superoxide radicals (O(2)*(-))/hydrogen peroxide, depolarization of mitochondria, caspase-3 activation, concomitantly with the nuclear translocation of transcription factors such as NF-kappaB, p53, c-Jun and nuclei fragmentation.	Rotenone	28-36	P53	Homo sapiens	363-366
20130515-5	2010	RESULTS: Women homozygous for the p53 codon 72 Arg genotype were at a 5.6-fold higher risk for developing cervical intraepithelial neoplasia (CIN) 2 or 3 compared with those showing homozygosity for the Pro genotype or heterozygosity for the Pro/Arg genotype.	Proline	203-206	P53	Homo sapiens	34-37
20023923-1	2009	Octahedral ruthenium complexes, capable of photodynamic singlet oxygen production at near 100% efficiency, were shown to cause light-dependent covalent crosslinking of p53 and PCNA subunits in mammalian cells and cell lysates.	Ruthenium	11-20	P53	Homo sapiens	168-171
19764997-6	2009	Single nucleotide polymorphisms (SNPs) in TP53 (codon 72, arginine &gt; proline) and MDM2 (SNP309, T &gt; G) were genotyped using PCR-RFLP, and nuclear expression levels of p53 were examined using immunohistochemistry.	Proline	72-79	P53	Homo sapiens	42-46
19941740-4	2009	p53 mutation was detected in six out of 46 patients at initial diagnosis, three of them were out of 29 cases achieving complete remission (CR) and the other three cases were out of 17 of relapsed patients, which is significantly higher than CR group (P&lt;0.05).	Chromium	139-141	P53	Homo sapiens	0-3
19941740-4	2009	p53 mutation was detected in six out of 46 patients at initial diagnosis, three of them were out of 29 cases achieving complete remission (CR) and the other three cases were out of 17 of relapsed patients, which is significantly higher than CR group (P&lt;0.05).	Chromium	241-243	P53	Homo sapiens	0-3
17767549-0	2007	Predisposition to HPV16/18-related cervical cancer because of proline homozygosity at codon 72 of p53 among Indian women is influenced by HLA-B*07 and homozygosity of HLA-DQB1*03.	Proline	62-69	P53	Homo sapiens	98-101
17544621-6	2007	HOC1-induced apoptosis in BEC in a dose-dependent fashion increased the activity of caspase-3 and the expression of p53 and p-JNK.	hoc1	0-4	P53	Homo sapiens	116-119
17224908-5	2007	Disruption of transcription by actinomycin D, 5,6-dichloro-1-beta-D-ribofuranosyl-benzimadazole or alpha-amanitin leads to accumulation of cellular p53 protein.	Dactinomycin	31-44	P53	Homo sapiens	148-151
17492690-2	2007	The TP53 polymorphism, in which an arginine (R) is changed to proline (P) at codon 72, is functionally significant and could therefore be a predisposing genetic defect.	Proline	62-69	P53	Homo sapiens	4-8
17113707-2	2007	Parental p53+/pRb+ U2-OS, p53-mutant U2-OS (U2-OS/175) and p53-/pRb- SAOS were sensitive to zoledronic acid with no significant differences in IC50 values.	Zoledronic Acid	92-107	P53	Homo sapiens	9-12
17113707-2	2007	Parental p53+/pRb+ U2-OS, p53-mutant U2-OS (U2-OS/175) and p53-/pRb- SAOS were sensitive to zoledronic acid with no significant differences in IC50 values.	Zoledronic Acid	92-107	P53	Homo sapiens	26-29
17113707-2	2007	Parental p53+/pRb+ U2-OS, p53-mutant U2-OS (U2-OS/175) and p53-/pRb- SAOS were sensitive to zoledronic acid with no significant differences in IC50 values.	Zoledronic Acid	92-107	P53	Homo sapiens	26-29
17300219-6	2007	The N-terminal domain of MAML1 contains a proline repeat motif (PXPAAPAP) that was previously shown to be present in p53 and important for the p300-p53 interaction.	Proline	42-49	P53	Homo sapiens	117-120
17504512-4	2007	The polymorphism on p53, which encodes either a proline or an arginine amino acid residue at codon 72, has been reported as a possible risk factor for cervical disease.	Proline	48-55	P53	Homo sapiens	20-23
17383050-6	2007	Taurolidine but not PVP-I treatment resulted in p53 activation in 2/3 MPM cell lines and a decrease in the protein levels of survivin, Bcl-2 and Mcl-1.	taurolidine	0-11	P53	Homo sapiens	48-51
17383050-10	2007	Taurolidine induces apoptosis and necrosis, activates p53 and sensitizes cells to cisplatin, whereas PVP-I inhibits cell growth via necrosis.	taurolidine	0-11	P53	Homo sapiens	54-57
17371838-8	2007	Although comparable in level to that achieved by treatment with the p53 activators actinomycin D and nutlin-3, the increases in p53 and p21 after downregulation of Mdm2 were not sufficient to trigger cell cycle arrest.	Dactinomycin	83-96	P53	Homo sapiens	68-71
17403527-1	2007	A very common polymorphism of p53, that of codon 72, codes either for a proline (P72) or an arginine (R72).	Proline	72-79	P53	Homo sapiens	30-33
17631738-2	2007	The wild type p53 protein presents a common polymorphism at position 72 resulting in either a proline or an arginine residue at this position, leading to differences between the two variants in the induction of apoptosis.	Proline	94-101	P53	Homo sapiens	14-17
17230520-12	2007	Since p53 is frequently mutated or deleted in prostate cancer and many other cancers, our results suggest that genotoxic vs. nongenotoxic classes of selenium may exert differential apoptosis efficacy depending on the p53 status of the cancer cells.	Selenium	149-157	P53	Homo sapiens	6-9
17230520-12	2007	Since p53 is frequently mutated or deleted in prostate cancer and many other cancers, our results suggest that genotoxic vs. nongenotoxic classes of selenium may exert differential apoptosis efficacy depending on the p53 status of the cancer cells.	Selenium	149-157	P53	Homo sapiens	217-220
17407577-10	2007	CONCLUSION: Therefore, zerumbone was found to induce the apoptotic process in HepG2 cells through the up and down regulation of Bax/Bcl-2 protein independently of functional p53 activity.	zerumbone	23-32	P53	Homo sapiens	174-177
17363597-7	2007	Furthermore, using the H1299-HW24 cells expressing wild-type p53 under a tetracycline-regulated promoter, the p53-MDM2 oscillation was observed only when p53 levels were in a specific range, and DNA damage was found to be necessary for triggering the p53-MDM2 oscillation.	Tetracycline	73-85	P53	Homo sapiens	61-64
17363597-7	2007	Furthermore, using the H1299-HW24 cells expressing wild-type p53 under a tetracycline-regulated promoter, the p53-MDM2 oscillation was observed only when p53 levels were in a specific range, and DNA damage was found to be necessary for triggering the p53-MDM2 oscillation.	Tetracycline	73-85	P53	Homo sapiens	110-113
17363597-7	2007	Furthermore, using the H1299-HW24 cells expressing wild-type p53 under a tetracycline-regulated promoter, the p53-MDM2 oscillation was observed only when p53 levels were in a specific range, and DNA damage was found to be necessary for triggering the p53-MDM2 oscillation.	Tetracycline	73-85	P53	Homo sapiens	110-113
17363597-7	2007	Furthermore, using the H1299-HW24 cells expressing wild-type p53 under a tetracycline-regulated promoter, the p53-MDM2 oscillation was observed only when p53 levels were in a specific range, and DNA damage was found to be necessary for triggering the p53-MDM2 oscillation.	Tetracycline	73-85	P53	Homo sapiens	110-113
18853251-1	2009	The p53 tumor suppressor gene has a central role in the defense against cancer, including breast cancer, and contains a polymorphic variant (Arg/Pro) at codon 72 that has been shown to have different biological properties regarding apoptosis and cell cycle arrest.	Proline	145-148	P53	Homo sapiens	4-7
19521721-5	2009	Similarly, the alleles of rs1042522 in TP53 that encode arginine (G-allele) or proline (C-allele) at codon 72, which cause increased pro-apoptotic (G-allele) or cell-cycle arrest activities (C-allele), respectively, may moderate p53"s ability to prevent DNA damage.	Proline	79-86	P53	Homo sapiens	39-43
19521721-5	2009	Similarly, the alleles of rs1042522 in TP53 that encode arginine (G-allele) or proline (C-allele) at codon 72, which cause increased pro-apoptotic (G-allele) or cell-cycle arrest activities (C-allele), respectively, may moderate p53"s ability to prevent DNA damage.	Proline	79-86	P53	Homo sapiens	229-232
19705844-6	2009	The specific ATM inhibitor caffeine significantly decreased tricetin-mediated G2/M arrest by inhibiting the phosphorylation of p53 (serine 15) and Chk2.	tricetin	60-68	P53	Homo sapiens	127-130
22120717-7	2012	An SCO2 transgene reverted the metabolic phenotype and restored resistance towards hypoxia in p53-depleted and p53 mutant glioma cells in a rotenone-sensitive manner, demonstrating that this effect was dependent on intact oxidative phosphorylation.	Rotenone	140-148	P53	Homo sapiens	111-114
21475903-4	2009	Polymorphisms of TP53 include codon 72 containing either arginine (CGC) or proline (CCC).	Proline	75-82	P53	Homo sapiens	17-21
17256875-0	2007	Multiplexed p53 mutation detection by free-solution conjugate microchannel electrophoresis with polyamide drag-tags.	Nylons	96-105	P53	Homo sapiens	12-15
22715097-11	2012	We conclude that aggregation of p53 into a mixture of oligomers and fibrils sequestrates the native protein into an inactive conformation that is typical of a prionoid.	prionoid	159-167	P53	Homo sapiens	32-35
17216584-4	2007	Knockdown of p53 by RNA interference (RNAi) demonstrated upregulation of Noxa protein levels in response to fenretinide was p53-independent, although evidence suggested that Noxa may be transcriptionally regulated by p53.	Fenretinide	108-119	P53	Homo sapiens	13-16
17216584-4	2007	Knockdown of p53 by RNA interference (RNAi) demonstrated upregulation of Noxa protein levels in response to fenretinide was p53-independent, although evidence suggested that Noxa may be transcriptionally regulated by p53.	Fenretinide	108-119	P53	Homo sapiens	124-127
17216584-4	2007	Knockdown of p53 by RNA interference (RNAi) demonstrated upregulation of Noxa protein levels in response to fenretinide was p53-independent, although evidence suggested that Noxa may be transcriptionally regulated by p53.	Fenretinide	108-119	P53	Homo sapiens	124-127
19723085-7	2009	DHA and ALA inhibited DNA fragmentation, inhibited the decrease in cell viability, and inhibited the expression of apoptotic genes (p53, Bax, apoptosis-inducing factor) induced by hydrogen peroxide in pancreatic acinar cells.	alpha-Linolenic Acid	8-11	P53	Homo sapiens	132-135
19397953-4	2009	RESULTS: We show that p53 and damage-specific DNA binding protein 2 (ddb2) genes are up-regulated by morphine in a naloxone-sensitive manner.	Naloxone	115-123	P53	Homo sapiens	22-25
19397953-5	2009	Furthermore, the results indicate that DNA damage, quantified by apurinic-apyrimidinic site counting assay and phosphorylation of Ser-15 in P53 protein, is induced in CD3+ T cells by morphine in a naloxone-sensitive manner.	Naloxone	197-205	P53	Homo sapiens	140-143
22653969-8	2012	In summary, the cytotoxic effects of bendamustine, melphalan and doxorubicin on p53-deficient multiple myeloma cell lines were enhanced by the coadministration of AZD7762.	Bendamustine Hydrochloride	37-49	P53	Homo sapiens	80-83
19602589-5	2009	To investigate the role of GPR87 in the p53 pathway, we generated multiple RKO and MCF7 cell lines in that GPR87 can be inducibly overexpressed or knocked down by a tetracycline-inducible system.	Tetracycline	165-177	P53	Homo sapiens	40-43
17050058-10	2007	Baicalein-induced apoptosis were also accompanied by decreasing in Bcl-2 and proform of caspase-3 and increasing p53 and Bax protein levels.	baicalein	0-9	P53	Homo sapiens	113-116
22689577-5	2012	Transient transfection of tenocytes with ASO against Sirt-1 induced expression of Bax and other proteins involved in apoptosis (cleaved caspase-3 and poly(ADP-ribose)polymerase), acetylation of tumor suppressor p53, and mitochondrial degradation.	Oligonucleotides, Antisense	41-44	P53	Homo sapiens	211-214
17324262-8	2007	Most importantly, the antitumor effect of hydralazine and valproate in cervical cancer may at least partially depend on an up-regulating effect on p53 gene and on the valproate-induced hyperacetylation of p53 protein, protecting it from degradation by E6.	Valproic Acid	58-67	P53	Homo sapiens	147-150
17324262-8	2007	Most importantly, the antitumor effect of hydralazine and valproate in cervical cancer may at least partially depend on an up-regulating effect on p53 gene and on the valproate-induced hyperacetylation of p53 protein, protecting it from degradation by E6.	Valproic Acid	58-67	P53	Homo sapiens	205-208
17324262-8	2007	Most importantly, the antitumor effect of hydralazine and valproate in cervical cancer may at least partially depend on an up-regulating effect on p53 gene and on the valproate-induced hyperacetylation of p53 protein, protecting it from degradation by E6.	Valproic Acid	167-176	P53	Homo sapiens	205-208
19509161-12	2009	A combination of vincristine or actinomycin D with nutlin-3 enhanced the antitumor activity in RMS cell lines with wild-type p53.	Vincristine	17-28	P53	Homo sapiens	125-128
19509161-12	2009	A combination of vincristine or actinomycin D with nutlin-3 enhanced the antitumor activity in RMS cell lines with wild-type p53.	Dactinomycin	32-45	P53	Homo sapiens	125-128
19091459-4	2009	Antioxidant N-acetyl-l-aspartate (NAC) decreased vessels number in tumors formed by cells with inactivated p53 and inhibited their growth.	N-acetylaspartate	12-32	P53	Homo sapiens	107-110
19091459-4	2009	Antioxidant N-acetyl-l-aspartate (NAC) decreased vessels number in tumors formed by cells with inactivated p53 and inhibited their growth.	N-acetylaspartate	34-37	P53	Homo sapiens	107-110
17121856-3	2007	This study investigates the action of two HDAC inhibitors, CG-1521 and trichostatin A, which stabilize Ac-Lys-373 p53 and Ac-Lys-382 p53, respectively, in LNCaP prostate cancer cells.	cysteinylglycine	59-61	P53	Homo sapiens	114-117
17121856-3	2007	This study investigates the action of two HDAC inhibitors, CG-1521 and trichostatin A, which stabilize Ac-Lys-373 p53 and Ac-Lys-382 p53, respectively, in LNCaP prostate cancer cells.	cysteinylglycine	59-61	P53	Homo sapiens	133-136
22833097-0	2012	D(-)lentiginosine-induced apoptosis involves the intrinsic pathway and is p53-independent.	lentiginosine	4-17	P53	Homo sapiens	74-77
17121856-3	2007	This study investigates the action of two HDAC inhibitors, CG-1521 and trichostatin A, which stabilize Ac-Lys-373 p53 and Ac-Lys-382 p53, respectively, in LNCaP prostate cancer cells.	ac-lys	103-109	P53	Homo sapiens	114-117
17218778-0	2007	Lack of p53 augments thymoquinone-induced apoptosis and caspase activation in human osteosarcoma cells.	thymoquinone	21-33	P53	Homo sapiens	8-11
18996230-7	2009	In addition, three upregulated proteins (14-3-3G, VDAC-1 and p53) and five downregulated proteins (ENPL, ENOA, IMDH2, PRDX1 and VIME) in arbutin-treated A375 cells were validated by RT-PCR analysis.	Arbutin	137-144	P53	Homo sapiens	61-64
22716215-11	2012	The combination of 5-FU and chloroquine induced G1 arrest, up-regulation of p27 and p53, and down-regulation of CDK2 and cyclin D1.	Chloroquine	28-39	P53	Homo sapiens	84-87
19208740-1	2009	The p53 protein is a key regulator of cell responses to DNA damage, and it has been shown that it sensitizes glioma cells to the alkylating agent temozolomide by up-regulating the extrinsic apoptotic pathway, whereas it increases the resistance to chloroethylating agents, such as ACNU and BCNU, probably by enhancing the efficiency of DNA repair.	Carmustine	290-294	P53	Homo sapiens	4-7
17218778-1	2007	We have recently shown that thymoquinone (TQ) is an antineoplastic drug that induces p53-dependent apoptosis in human colon cancer cells.	thymoquinone	28-40	P53	Homo sapiens	85-88
17218778-1	2007	We have recently shown that thymoquinone (TQ) is an antineoplastic drug that induces p53-dependent apoptosis in human colon cancer cells.	thymoquinone	42-44	P53	Homo sapiens	85-88
17218778-12	2007	Collectively, these findings show that TQ induces p53-independent apoptosis in human osteosarcoma cells.	thymoquinone	39-41	P53	Homo sapiens	50-53
19042971-4	2009	We show that upregulation of IRF2BP2 after treatment with actinomycin D (Act.D) is dependent on functional p53 in different cell lines.	Dactinomycin	58-71	P53	Homo sapiens	107-110
22735455-7	2012	These PIMT effects on p53 stability and activity are attributed to the PIMT-mediated methylation of p53 at isoaspartate residues 29 and 30.	Isoaspartic Acid	107-119	P53	Homo sapiens	22-25
19291875-2	2009	The p53 codon 72 Arg-Pro (CGC to CCC) polymorphism of exon 4 affects various biological properties; recently, it was reported that this polymorphism affects the ability to induce apoptosis in vitro.	Proline	21-24	P53	Homo sapiens	4-7
19940524-1	2009	OBJECTIVES: Several studies have examined the association of codon 72 polymorphism of the TP53 gene, encoding either arginine or proline, in several tumor types but none have investigated its role in Kaposi"s sarcoma (KS) development.	Proline	129-136	P53	Homo sapiens	90-94
19062342-4	2008	In contrast, chlorambucil and fludarabine resistance correlated with basal p53 protein levels.	Chlorambucil	13-25	P53	Homo sapiens	75-78
19012502-9	2008	The cis-imidazolines were the first reported potent, selective small-molecule inhibitors of the p53-MDM2 interaction, and continue to show therapeutic potential.	cis-imidazolines	4-20	P53	Homo sapiens	96-99
23675098-3	2008	The TP53 codon 72 polymorphism is a single-nucleotide polymorphism (SNP) in exon 4, resulting in the expression of either arginine (CGC) or proline (CCC) residues.	Proline	140-147	P53	Homo sapiens	4-8
18980985-0	2008	Bendamustine is effective in p53-deficient B-cell neoplasms and requires oxidative stress and caspase-independent signaling.	Bendamustine Hydrochloride	0-12	P53	Homo sapiens	29-32
18980985-6	2008	Bendamustine was found to act synergistically with nucleoside analogues in both CLL and MCL, this combination being effective in p53 mutated cases resistant to standard chemotherapy.	Bendamustine Hydrochloride	0-12	P53	Homo sapiens	129-132
18980985-8	2008	CONCLUSIONS: Our findings support the use of bendamustine as a therapeutic agent, alone or in combination, for CLL and MCL with p53 alterations and describe the molecular basis of its activity in these entities.	Bendamustine Hydrochloride	45-57	P53	Homo sapiens	128-131
19148357-5	2008	Hematoxylin-eosin-stained sections were submitted to histopathological analysis and the immunohistochemical expression of COX-1, COX-2 and p53 was evaluated by the streptavidin-biotin-peroxidase method.	Biotin	177-183	P53	Homo sapiens	139-142
18802408-6	2008	In the nuclei of cells treated with TPT or MXT, the expression of p53-Ser15(P) appeared as closely packed foci of intense IF.	Mitoxantrone	43-46	P53	Homo sapiens	66-69
18802408-8	2008	The maximal increase in p53-Ser15(P) expression, rising up to 2.5-fold above the level of its constitutive expression, was observed in cells treated with TPT or MXT for 4-6 h. This maximum expression of p53-Ser15(P) coincided in time with the peak of Chk2 activation but not with ATM activation and H2AX phosphorylation, both of which crested 1-2 h after the treatment with TPT or MXT.	Mitoxantrone	161-164	P53	Homo sapiens	24-27
18802408-8	2008	The maximal increase in p53-Ser15(P) expression, rising up to 2.5-fold above the level of its constitutive expression, was observed in cells treated with TPT or MXT for 4-6 h. This maximum expression of p53-Ser15(P) coincided in time with the peak of Chk2 activation but not with ATM activation and H2AX phosphorylation, both of which crested 1-2 h after the treatment with TPT or MXT.	Mitoxantrone	161-164	P53	Homo sapiens	203-206
18619459-0	2008	Folate and vitamin B6 intake and risk of colon cancer in relation to p53 expression.	Vitamin B 6	11-21	P53	Homo sapiens	69-72
18790750-0	2008	Penta-1,2,3,4,6-O-galloyl-beta-D-glucose induces p53 and inhibits STAT3 in prostate cancer cells in vitro and suppresses prostate xenograft tumor growth in vivo.	beta-penta-O-galloyl-glucose	0-40	P53	Homo sapiens	49-52
18790750-3	2008	Here, we investigated the cell death signaling mechanisms induced by PGG in human prostate cancer cells of different p53 functional status.	beta-penta-O-galloyl-glucose	69-72	P53	Homo sapiens	117-120
18790750-5	2008	In LNCaP cells, caspase-mediated apoptosis induction by PGG was associated with and mediated in major part by activation of p53 as established through small interfering RNA knockdown and dominant-negative mutant approaches.	beta-penta-O-galloyl-glucose	56-59	P53	Homo sapiens	124-127
18790750-10	2008	Our data support PGG as a multitargeting agent for chemoprevention and therapy of prostate cancer by activating the p53 tumor suppressor pathway and by inhibiting STAT3 oncogenic signaling.	beta-penta-O-galloyl-glucose	17-20	P53	Homo sapiens	116-119
18619950-11	2008	These results suggested Andro can inhibit Lovo cell growth by G1-S phase arrest, and was exerted by inducing the expression of p53, p21 and p16 that, in turn, repressed the activity of Cyclin D1/Cdk4 and/or Cyclin A/Cdk2, as well as Rb phosphorylation.	Rubidium	233-235	P53	Homo sapiens	127-130
18632613-3	2008	The p53 wild-type (wt) status correlated with more pronounced DNA damage and higher apoptosis after thymoquinone treatment.	thymoquinone	100-112	P53	Homo sapiens	4-7
18632613-4	2008	A significant up-regulation of the survival gene CHEK1 was observed in p53-/- cells in response to thymoquinone due to the lack of transcriptional repression of p53.	thymoquinone	99-111	P53	Homo sapiens	71-74
18632613-7	2008	Immunofluorescence analysis revealed that the apoptosis resistance in p53-/- cells after thymoquinone treatment might be conveyed by shuttling of CHEK1 into the nucleus.	thymoquinone	89-101	P53	Homo sapiens	70-73
18490454-6	2008	Moreover, Cdk5 (cyclin-dependent kinase 5), a proline-directed Ser/Thr kinase, additionally increases p53 stability via post-translational modification of p53 in response to hydrogen peroxide.	Proline	46-53	P53	Homo sapiens	102-105
18490454-6	2008	Moreover, Cdk5 (cyclin-dependent kinase 5), a proline-directed Ser/Thr kinase, additionally increases p53 stability via post-translational modification of p53 in response to hydrogen peroxide.	Proline	46-53	P53	Homo sapiens	155-158
18645003-1	2008	Previous studies comparing the effects of two histone deacetylase (HDAC) inhibitors, trichostatin A (TSA) and CG-1521, have shown that these compounds selectively inhibit HDAC and induce differentially acetylated p53 isoforms and assembly of mutually exclusive transcriptional complexes on the p21 promoter.	cysteinylglycine	110-112	P53	Homo sapiens	213-216
18645003-5	2008	These data show that the selective effects of CG-1521 and TSA on the assembly of transcription complexes are not unique to the p21 gene and suggest that selective inhibition of HDAC can lead to significant changes in gene expression through the acetylation of transcription factors including but not limited to p53.	cysteinylglycine	46-48	P53	Homo sapiens	311-314
18402771-5	2008	Furthermore, p53 protein and its downstream pro-apoptotic target, Bax, were induced in SAS cells after treatment with rotenone.	Rotenone	118-126	P53	Homo sapiens	13-16
18486125-1	2008	We previously reported that 3,4,5,4"-tetramethoxy-trans-stilbene (MR-4) induces p53 and perinuclear mitochondrial clustering in cancer cells [Gosslau, A., Chen, M., Ho, C.-T., Chen, K.Y., 2005, A methoxy derivative of resveratrol analogue selectively induced activation of the mitochondrial apoptotic pathway in transformed fibroblasts.	3,4,5,4"-tetramethoxy-trans-stilbene	28-64	P53	Homo sapiens	80-83
18390844-7	2008	Multivariate analysis for the presence of HCC revealed that the odds ratio (OR) for MDM2 G/G over T/T was 4.89 (P &lt; 0.001) and that of p53 Pro/Pro over Arg/Arg was 3.03 (P = 0.006).	Proline	142-145	P53	Homo sapiens	138-141
18315559-8	2008	Also, the general transcription inhibitor actinomycin D triggered nucleolar stress and activated p53.	Dactinomycin	42-55	P53	Homo sapiens	97-100
18474530-3	2008	In a genome-wide tiling ChIP-on-chip approach, we have identified and characterized 1546 binding sites of p53 upon Actinomycin D treatment.	Dactinomycin	115-128	P53	Homo sapiens	106-109
18092340-2	2008	Exposure to chlorambucil, fludarabine, and Nutlin-3 induced p53 accumulation and variably affected cell cycle progression in SKW6.4 lymphoblastoid cells.	Chlorambucil	12-24	P53	Homo sapiens	60-63
18092340-5	2008	Analysis of the gene expression profile of the p53-transcriptional targets showed distinct features between chlorambucil, Nutlin-3 and fludarabine, which likely account for their differential effect on cell cycle in SKW6.4 cells.	Chlorambucil	108-120	P53	Homo sapiens	47-50
18272192-5	2008	Transfection of HUVEC with p53 dominant negative (DN) abolished the TB-induced increases of p21 promoter activity and protein level, suggesting that the TB-induced increase of p21 is p53-dependent.	Terbinafine	68-70	P53	Homo sapiens	27-30
18272192-5	2008	Transfection of HUVEC with p53 dominant negative (DN) abolished the TB-induced increases of p21 promoter activity and protein level, suggesting that the TB-induced increase of p21 is p53-dependent.	Terbinafine	68-70	P53	Homo sapiens	183-186
18272192-5	2008	Transfection of HUVEC with p53 dominant negative (DN) abolished the TB-induced increases of p21 promoter activity and protein level, suggesting that the TB-induced increase of p21 is p53-dependent.	Terbinafine	153-155	P53	Homo sapiens	27-30
18272192-5	2008	Transfection of HUVEC with p53 dominant negative (DN) abolished the TB-induced increases of p21 promoter activity and protein level, suggesting that the TB-induced increase of p21 is p53-dependent.	Terbinafine	153-155	P53	Homo sapiens	183-186
18272192-7	2008	Over-expression of mitogen-activated protein kinase (MEK)-1, the immediate upstream activator kinase of ERK, abolished the TB-induced increases of p21 and p53 protein and decrease of thymidine incorporation.	Terbinafine	123-125	P53	Homo sapiens	155-158
18272192-11	2008	Taken together, our results suggest that TB might cause a decrease of MEK, which in turn up-regulates p53 through the inhibition of ERK phosphorylation, and finally causes an increase of p21 expression and cell-cycle arrest.	Terbinafine	41-43	P53	Homo sapiens	102-105
17668440-6	2008	Both the levels of p53 and p16 proteins were raised after diorganotin(IV) treatment and such induction was maximum in the OTC-3 treated samples.	diorganotin	58-69	P53	Homo sapiens	19-22
18423915-4	2008	A G-to-C SNP at p53 codon 72 results in an Arg/Pro polymorphism, which is associated with apoptosis induction potential and p53 mutation status.	Proline	47-50	P53	Homo sapiens	16-19
18423915-4	2008	A G-to-C SNP at p53 codon 72 results in an Arg/Pro polymorphism, which is associated with apoptosis induction potential and p53 mutation status.	Proline	47-50	P53	Homo sapiens	124-127
17998932-1	2008	Codon 72 of human p53 gene is polymorphic, encoding arginine or proline.	Proline	64-71	P53	Homo sapiens	18-21
18342333-4	2008	Ectopic and endogenous expression of TAp73 leads to a significant downregulation of cp/EII activity in p53-deficient hepatoma cell lines.	tap73	37-42	P53	Homo sapiens	103-106
18414047-8	2008	An association has been reported between women carrying the p53 codon 72 polymorphism (a proline to arginine change) with recurrent implantation failure, suggesting a similar function for p53 in humans.	Proline	89-96	P53	Homo sapiens	60-63
18414047-8	2008	An association has been reported between women carrying the p53 codon 72 polymorphism (a proline to arginine change) with recurrent implantation failure, suggesting a similar function for p53 in humans.	Proline	89-96	P53	Homo sapiens	188-191
18272203-2	2008	In humans, we recently found that a TP53 codon 72 Arginine (Arg) to Proline (Pro) polymorphism affected both cancer incidence and longevity as well.	Proline	68-75	P53	Homo sapiens	36-40
18272203-2	2008	In humans, we recently found that a TP53 codon 72 Arginine (Arg) to Proline (Pro) polymorphism affected both cancer incidence and longevity as well.	Proline	68-71	P53	Homo sapiens	36-40
18260647-4	2008	Without a water channel, the substrate p53-Lys4-N(Me)H is not available because the proton dissociation p53-Lys4-N(Me)H 2 (+) --&gt; p53-Lys4-N(Me)H + H (+) does not occur.	lys4-n	43-49	P53	Homo sapiens	104-107
18260647-4	2008	Without a water channel, the substrate p53-Lys4-N(Me)H is not available because the proton dissociation p53-Lys4-N(Me)H 2 (+) --&gt; p53-Lys4-N(Me)H + H (+) does not occur.	lys4-n	108-114	P53	Homo sapiens	39-42
18260647-4	2008	Without a water channel, the substrate p53-Lys4-N(Me)H is not available because the proton dissociation p53-Lys4-N(Me)H 2 (+) --&gt; p53-Lys4-N(Me)H + H (+) does not occur.	lys4-n	108-114	P53	Homo sapiens	104-107
18260647-4	2008	Without a water channel, the substrate p53-Lys4-N(Me)H is not available because the proton dissociation p53-Lys4-N(Me)H 2 (+) --&gt; p53-Lys4-N(Me)H + H (+) does not occur.	lys4-n	108-114	P53	Homo sapiens	104-107
18260647-4	2008	Without a water channel, the substrate p53-Lys4-N(Me)H is not available because the proton dissociation p53-Lys4-N(Me)H 2 (+) --&gt; p53-Lys4-N(Me)H + H (+) does not occur.	lys4-n	108-114	P53	Homo sapiens	39-42
18260647-4	2008	Without a water channel, the substrate p53-Lys4-N(Me)H is not available because the proton dissociation p53-Lys4-N(Me)H 2 (+) --&gt; p53-Lys4-N(Me)H + H (+) does not occur.	lys4-n	108-114	P53	Homo sapiens	104-107
18260647-4	2008	Without a water channel, the substrate p53-Lys4-N(Me)H is not available because the proton dissociation p53-Lys4-N(Me)H 2 (+) --&gt; p53-Lys4-N(Me)H + H (+) does not occur.	lys4-n	108-114	P53	Homo sapiens	104-107
18260647-5	2008	The lack of formation of a water channel is due to the positioning of the methyl substituent of the SET7/9.p53-Lys4-N(Me)H 2 (+).AdoMet complex.	lys4-n	111-117	P53	Homo sapiens	107-110
17159502-6	2007	Western blot analysis further showed down-regulation of procaspase-3, X-linked inhibitor of apoptosis protein and poly(ADP-ribose) polymerase cleavage in Bel-7402 cells treated with 15 mumol/l fenretinide for 48 h. Overexpression of p53 was observed in a time-dependent manner, along with a decrease in the Bcl-2/Bax ratio.	Fenretinide	193-204	P53	Homo sapiens	233-236
17182797-9	2007	The caspase-8 inhibitor Z-IETD-FMK attenuated the DIM-induced apoptosis, indicating that increased activation of this enzyme contributed to the increase in p53-independent apoptosis that was observed in colon cancer cells.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	24-34	P53	Homo sapiens	156-159
17050806-0	2007	Zoledronic acid activates the DNA S-phase checkpoint and induces osteosarcoma cell death characterized by apoptosis-inducing factor and endonuclease-G translocation independently of p53 and retinoblastoma status.	Zoledronic Acid	0-15	P53	Homo sapiens	182-185
17050806-9	2007	Therefore, zoledronic acid may be considered as an effective therapeutic agent in clinical trials of osteosarcoma in which mutation for p53 and Rb very often occur, and where current treatment with traditional chemotherapeutic agents is ineffective.	Zoledronic Acid	11-26	P53	Homo sapiens	136-139
17170001-2	2007	Comparing p53 and p73beta proteins, our data show that zinc chelation by EDTA is significantly more detrimental to the ability of p73beta than of p53 to bind DNA, most likely due to the greater effect that the loss of zinc has on the conformation of the DNA-binding domain of p73.	Edetic Acid	73-77	P53	Homo sapiens	10-13
17170001-2	2007	Comparing p53 and p73beta proteins, our data show that zinc chelation by EDTA is significantly more detrimental to the ability of p73beta than of p53 to bind DNA, most likely due to the greater effect that the loss of zinc has on the conformation of the DNA-binding domain of p73.	Edetic Acid	73-77	P53	Homo sapiens	146-149
17056014-4	2006	KAP1 reduction markedly enhanced the induction of p21, a product of the p53 target gene, after treatment with actinomycin D or gamma-irradiation, but not with camptothecin.	Dactinomycin	110-123	P53	Homo sapiens	72-75
17056014-5	2006	Treatment with actinomycin D, but not with camptothecin, augmented the interaction of p53 with Mdm2 and KAP1.	Dactinomycin	15-28	P53	Homo sapiens	86-89
17341630-6	2006	During first hours after the beginning of cultivation with VA in both studied concentrations (2 and 4 mM) an increase of p53 and its phosphorylation on serine 392 is detected, as well as a phosphorylation of Mdm2 on serine 166.	Valproic Acid	59-61	P53	Homo sapiens	121-124
17100737-0	2006	Selenomethionine inhibits ultraviolet radiation-induced p53 transactivation.	Selenomethionine	0-16	P53	Homo sapiens	56-59
17100737-3	2006	Selenium protects cells from UVB-induced cell death and apoptosis by mechanisms which are unclear, although recent reports suggest that selenium protects against UV-induced cell damage by inducing DNA repair enzymes and transactivating p53.	Selenium	136-144	P53	Homo sapiens	236-239
17100737-4	2006	METHODS: We examined whether selenomethionine could protect human skin cells from UV radiation-induced p53 transactivation, using a pRGCDeltafos-lacZ p53-dependent reporter construct stably transfected in an amelanotic melanoma cell line (Arn-8) which expresses wild-type p53.	Selenomethionine	29-45	P53	Homo sapiens	103-106
17100737-7	2006	Treatment with 50 microM selenomethionine for 24 h both pre- and post-irradiation, significantly diminished p53 activation by 30-43% across the UV dose range (P=0.0085, n=5 independent experiments) and decreased UV-induced p53 protein accumulation as assessed by Western blotting.	Selenomethionine	25-41	P53	Homo sapiens	108-111
17100737-7	2006	Treatment with 50 microM selenomethionine for 24 h both pre- and post-irradiation, significantly diminished p53 activation by 30-43% across the UV dose range (P=0.0085, n=5 independent experiments) and decreased UV-induced p53 protein accumulation as assessed by Western blotting.	Selenomethionine	25-41	P53	Homo sapiens	223-226
17100737-8	2006	CONCLUSIONS: We conclude that selenomethionine inhibits broad band UVB-induced p53 transactivation and protein accumulation and that this effect correlates with reported protective effects of selenium against UV-induced DNA damage.	Selenomethionine	30-46	P53	Homo sapiens	79-82
16931776-10	2006	In vitro exposure of hMSCs to cisplatin, vincristine, and etoposide resulted in an increased p53 expression, independent of apoptosis induction.	Vincristine	41-52	P53	Homo sapiens	93-96
17123452-6	2006	When evaluated by several pathway and biological process analysis programs, these proteins are demonstrated to be involved with a high degree of confidence (p values &lt; 2.0 E-05) in glycolysis, propanoate metabolism, pyruvate metabolism, urea cycle and arginine/proline metabolism, as well as in the non-metabolic p53 and FAS pathways.	Proline	264-271	P53	Homo sapiens	316-319
17085670-0	2006	Schedule-dependent synergy between the heat shock protein 90 inhibitor 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin and doxorubicin restores apoptosis to p53-mutant lymphoma cell lines.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	71-124	P53	Homo sapiens	163-166
17085670-13	2006	Administration of DMAG before doxorubicin resulted in G1-S arrest and protection from apoptosis, leading to additive or antagonistic interactions that were exacerbated by p53 mutation.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	18-22	P53	Homo sapiens	171-174
17085670-14	2006	CONCLUSIONS: Administration of DMAG to doxorubicin-primed cells induced premature mitosis and had a synergistic effect on apoptosis regardless of p53 status.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	31-35	P53	Homo sapiens	146-149
16887109-5	2006	Cr(VI) (50, 10 and 1 microM) was found to produce time- and dose-dependent cytotoxicity resulting in oxidative stress, suppression of antioxidant systems and activation of p53-dependent apoptosis which is reported for the first time in this model in relation to environmental Cr(VI).	Chromium	0-2	P53	Homo sapiens	172-175
16887109-5	2006	Cr(VI) (50, 10 and 1 microM) was found to produce time- and dose-dependent cytotoxicity resulting in oxidative stress, suppression of antioxidant systems and activation of p53-dependent apoptosis which is reported for the first time in this model in relation to environmental Cr(VI).	Chromium	276-278	P53	Homo sapiens	172-175
16923170-0	2006	Tauroursodeoxycholic acid modulates p53-mediated apoptosis in Alzheimer"s disease mutant neuroblastoma cells.	ursodoxicoltaurine	0-25	P53	Homo sapiens	36-39
16923170-3	2006	Tauroursodeoxycholic acid (TUDCA) modulates exogenous Abeta-induced apoptosis by interfering with E2F-1/p53/Bax.	ursodoxicoltaurine	0-25	P53	Homo sapiens	104-107
16917215-1	2006	BBR 3464 is a novel triplatinum compound that has exhibited anti-tumor activity in both cisplatin-sensitive and cisplatin-resistant, as well as in p53 mutant tumor models.	bbr	0-3	P53	Homo sapiens	147-150
16786124-1	2006	The TP53 polymorphism occurs at codon 72 of exon 4 with two alleles encoding either arginine or proline.	Proline	96-103	P53	Homo sapiens	4-8
16633920-2	2006	Unrepaired O6-methylguanines result in G:C to A:T transitions in mutated K-ras and p53 in colorectal tumors.	O-(6)-methylguanine	11-28	P53	Homo sapiens	83-86
16700548-4	2006	Dicoumarol also disrupts the binding of NQO1 to p53, p73, and ODC and induces their ubiquitin-independent proteasomal degradation.	Dicumarol	0-10	P53	Homo sapiens	48-51
16684279-2	2006	In the present study, we compared the effects of calcipotriol and methylprednisolone aseponate (MPA) treatments on bcl-2, p53 and ki-67 expressions in psoriatic patients in order to define a relationship between regulation of apoptosis and healing process in psoriasis.	mpa	96-99	P53	Homo sapiens	122-125
16585172-10	2006	Recombinant p53 complemented p53-/- mitochondrial extract repair of uracil or 8-oxo-G-containing oligonucleotides.	8-oxo-g	78-85	P53	Homo sapiens	12-15
16585172-10	2006	Recombinant p53 complemented p53-/- mitochondrial extract repair of uracil or 8-oxo-G-containing oligonucleotides.	8-oxo-g	78-85	P53	Homo sapiens	29-32
16499995-11	2006	Somatic TP53 mutations were found in 62 out of 240 NSCLC patients (26%), more frequently in Pro carriers (31%) than in Arg homozygotes (20%, p = 0.06).	Proline	92-95	P53	Homo sapiens	8-12
16648559-9	2006	However, a larger population of senescence-activated beta-galactosidase-positive cells was seen in IUdR/methoxyamine/ionizing radiation-treated cells, which was correlated with the increased activation of the senescence factors p53 and pRb.	methoxyamine	104-116	P53	Homo sapiens	228-231
16206288-6	2006	In vitro treatment with butyrate or propionic acid, but not succinic acid, elicited a positive response in the p53-p53R2 system.	propionic acid	36-50	P53	Homo sapiens	111-114
16206288-7	2006	Moreover, p53-dependent DNA repair, investigated by radioactive nucleotide incorporation, was induced by butyric acid and inhibited by short-interfering p53 and p53R2 RNAs.	Butyric Acid	105-117	P53	Homo sapiens	10-13
16206288-8	2006	Therefore, it was concluded that the p53-p53R2-dependent DNA repair system is constitutively stimulated by butyric acid, which accumulates in UC inflammatory lesions.	Butyric Acid	107-119	P53	Homo sapiens	37-40
16619485-1	2006	Selenium, in the form of seleno-L-methionine (SeMet), induced Redox-factor-1 (Ref1) and p53 proteins in normal human and mouse fibroblasts.	Selenomethionine	25-44	P53	Homo sapiens	88-91
16619485-1	2006	Selenium, in the form of seleno-L-methionine (SeMet), induced Redox-factor-1 (Ref1) and p53 proteins in normal human and mouse fibroblasts.	Selenomethionine	46-51	P53	Homo sapiens	88-91
16611213-0	2006	Substituted 1,4-benzodiazepine-2,5-diones as alpha-helix mimetic antagonists of the HDM2-p53 protein-protein interaction.	Bz-423	12-41	P53	Homo sapiens	89-92
16611213-3	2006	We present an analysis of how molecules based on the 1,4-benzodiazepine-2,5-dione scaffold serve to mimic the side-chains presented by the hydrophobic face of two turns of an alpha-helix derived from the tumor suppressor protein p53, and thus antagonize the HDM2-p53 protein-protein binding interaction.	Bz-423	53-81	P53	Homo sapiens	229-232
16611213-3	2006	We present an analysis of how molecules based on the 1,4-benzodiazepine-2,5-dione scaffold serve to mimic the side-chains presented by the hydrophobic face of two turns of an alpha-helix derived from the tumor suppressor protein p53, and thus antagonize the HDM2-p53 protein-protein binding interaction.	Bz-423	53-81	P53	Homo sapiens	263-266
16646561-2	2006	The codon 72 polymorphism on exon 4 in the p53 gene produces variant proteins with either arginine (Arg) or proline (Pro), and is associated with an increased susceptibility of cancers of the lung, esophagus, breast, cervix and nasopharynx on a genetic basis.	Proline	108-115	P53	Homo sapiens	43-46
16646561-2	2006	The codon 72 polymorphism on exon 4 in the p53 gene produces variant proteins with either arginine (Arg) or proline (Pro), and is associated with an increased susceptibility of cancers of the lung, esophagus, breast, cervix and nasopharynx on a genetic basis.	Proline	117-120	P53	Homo sapiens	43-46
16498444-3	2006	The identification of a new family of proteins, known as ASPPs (ankyrin-repeat-, SH3-domain- and proline-rich-region-containing proteins), has led to the discovery of a novel mechanism that selectively regulates the apoptotic function, but not the cell-cycle-arrest function, of p53, and gives an insight into how p53 responds to different stress signals.	Proline	97-104	P53	Homo sapiens	279-282
16498444-3	2006	The identification of a new family of proteins, known as ASPPs (ankyrin-repeat-, SH3-domain- and proline-rich-region-containing proteins), has led to the discovery of a novel mechanism that selectively regulates the apoptotic function, but not the cell-cycle-arrest function, of p53, and gives an insight into how p53 responds to different stress signals.	Proline	97-104	P53	Homo sapiens	314-317
16251187-3	2006	To identify an oxidized lipid that induces p53 phosphorylation, we conducted a screening of lipid peroxidation products in human neuroblastoma SH-SY5Y cells and identified 4-oxo-2-nonenal (ONE), a recently identified aldehyde originating from the peroxidation of omega6 polyunsaturated fatty acids, as a potential inducer of the p53 phosphorylation.	4-oxo-2-nonenal	172-187	P53	Homo sapiens	329-332
16251187-3	2006	To identify an oxidized lipid that induces p53 phosphorylation, we conducted a screening of lipid peroxidation products in human neuroblastoma SH-SY5Y cells and identified 4-oxo-2-nonenal (ONE), a recently identified aldehyde originating from the peroxidation of omega6 polyunsaturated fatty acids, as a potential inducer of the p53 phosphorylation.	omega6 polyunsaturated fatty acids	263-297	P53	Homo sapiens	43-46
16326430-9	2005	The levels of p53, bcl-2, and 8-OHdG were concomitantly changed by alcohol and acetaldehyde treatment in midbrain cells.	Acetaldehyde	79-91	P53	Homo sapiens	14-17
16362078-4	2005	DHC exposure in the human TK6 lymphoblastoid cell line also caused concentration-dependent increases in p53 acetylation and cytotoxicity.	3,4-dihydrocoumarin	0-3	P53	Homo sapiens	104-107
16362078-6	2005	Thus, DHC inhibits both yeast Sir2p and human SIRT1 deacetylases and increases p53 acetylation and apoptosis, a phenotype associated with senescence and aging.	3,4-dihydrocoumarin	6-9	P53	Homo sapiens	79-82
16307686-2	2005	Furthermore, the polymorphism at codon 72 (encoding either arginine or proline) of the p53 tumor-suppressor gene is discussed as a possible determinant for cancer risk.	Proline	71-78	P53	Homo sapiens	87-90
16120440-2	2005	To study the function of p53 in a keratinocyte background, a tetracycline-controlled p53 transgene was introduced into a human SCC cell line (SCC15), lacking endogenous p53.	Tetracycline	61-73	P53	Homo sapiens	85-88
16120440-2	2005	To study the function of p53 in a keratinocyte background, a tetracycline-controlled p53 transgene was introduced into a human SCC cell line (SCC15), lacking endogenous p53.	Tetracycline	61-73	P53	Homo sapiens	85-88
16120440-3	2005	Conditional expression of wild-type p53 protein upon withdrawal of tetracycline was accompanied with increased expression of p21(WAF1/Cip1) resulting in reduced cell proliferation.	Tetracycline	67-79	P53	Homo sapiens	36-39
15905205-7	2005	Importantly, patient survival did significantly differ: those patients having a TP53 mutation on the proline allele had the worst survival outcomes (hazards ratio = 2.6, P &lt; 0.03).	Proline	101-108	P53	Homo sapiens	80-84
15905205-9	2005	Our data suggest that there are selective pressures for loss of the TP53 proline allele in non-small cell lung cancer.	Proline	73-80	P53	Homo sapiens	68-72
18315954-8	2008	Moreover, pretreatment with FeSO4 and the carbon monoxide donor CORM-2, but not biliverdin, significantly protected p53-deficient cells from SNAP-induced cell death compared with normal cells.	ferrous sulfate	28-33	P53	Homo sapiens	116-119
18024214-7	2008	2D gel analysis revealed p53 patterns in p21-/- cells were distinct from those in wild-type cells before and after chromium exposure.	Chromium	115-123	P53	Homo sapiens	25-28
17653574-15	2008	CONCLUSION: Bendamustine induces ATM-Chk2-Cdc2-mediated G2 arrest and p53 mediated apoptosis.	Bendamustine Hydrochloride	12-24	P53	Homo sapiens	70-73
17847033-0	2008	Dulxanthone A induces cell cycle arrest and apoptosis via up-regulation of p53 through mitochondrial pathway in HepG2 cells.	Dulxanthone A	0-13	P53	Homo sapiens	75-78
17847033-4	2008	Furthermore, p53 was dramatically up-regulated, leading to altered expression of downstream proteins upon dulxanthone A treatment.	Dulxanthone A	106-119	P53	Homo sapiens	13-16
17847033-10	2008	Concurrently, Apaf-1 was stimulated with p53 by dulxanthone A.	Dulxanthone A	48-61	P53	Homo sapiens	41-44
17847033-13	2008	Moreover, cell cycle arrest and apoptosis in HepG2 cells induced by dulxanthone A were markedly inhibited by siRNA knockdown of p53.	Dulxanthone A	68-81	P53	Homo sapiens	128-131
18803266-0	2008	p53 codon 72 proline/arginine polymorphism and autoimmune thyroid diseases.	Proline	13-20	P53	Homo sapiens	0-3
18803266-8	2008	The p53 codon 72 proline/arginine polymorphism may be a genetic marker to predict the increased susceptibility of development of HT.	Proline	17-24	P53	Homo sapiens	4-7
18003626-5	2008	Two cell models were selected: 041 TR fibroblasts in which the expression of p53 is regulated by a tetracycline-inducible promoter, and WI38 primary lung fibroblasts together with their isogenic derivative VA13, in which p53 is abrogated post-translationally by SV40 transformation.	Tetracycline	99-111	P53	Homo sapiens	77-80
22735455-7	2012	These PIMT effects on p53 stability and activity are attributed to the PIMT-mediated methylation of p53 at isoaspartate residues 29 and 30.	Isoaspartic Acid	107-119	P53	Homo sapiens	100-103
16179969-1	2005	We recently identified two thiazolidin compounds, 5-[(4-methylphenyl)methylene]-2-(phenylamino)-4(5H)-thiazolone (MMPT) and 5-(2,4-dihydroxybenzylidene)-2-(phenylimino)-1,3-thiazolidin (DBPT), that inhibit the growth of human non-small-cell lung and colon cancer cells independent of P-glycoprotein and p53 status.	5-(2,4-dihydroxybenzylidene)-2-(phenylimino)-1,3-thiazolidin	124-184	P53	Homo sapiens	303-306
22717582-4	2012	In proof-of-principle studies, betulinic acid, doxorubicin and vincristine induced cell death in a p53- and NOXA-independent pathway involving mitochondrial pore formation, release of cytochrome c and caspase activation.	Vincristine	63-74	P53	Homo sapiens	99-102
16140998-8	2005	CONCLUSIONS: The p53 codon 72 Arg/Pro polymorphism is not associated with age of onset or severity of glaucoma.	Proline	34-37	P53	Homo sapiens	17-20
16107721-9	2005	In addition, depolarization of the mitochondrial membrane by mitochondrial inhibitors such as rotenone or antimycin A led colorectal cancer cells into p53-dependent senescence.	Rotenone	94-102	P53	Homo sapiens	151-154
18612219-1	2008	BACKGROUND: The p53 codon 72 polymorphism, which results in either an arginine or proline residue, plays a different role in vitro and in vivo in cell survival and drug resistance.	Proline	82-89	P53	Homo sapiens	16-19
22717582-5	2012	In contrast, when betulinic acid was combined with either doxorubicine or vincristine, cell death signaling changed considerably; the drug combinations clearly depended on both p53 and NOXA.	Vincristine	74-85	P53	Homo sapiens	177-180
17897804-2	2007	The imidazoline compound (Nutlin-3) is a promising small molecule antagonist of the MDM2-p53 interaction.	Imidazolines	4-15	P53	Homo sapiens	89-92
22493262-9	2012	AL-DNA adducts were present in the renal cortex of 83% of patients with A:T to T:A mutations in TP53, FGFR3, or HRAS.	Aluminum	0-2	P53	Homo sapiens	96-100
18089834-6	2007	Using a human nontumorigenic mammary gland epithelial cell line, MCF10A, we confirm that in the absence of detectable DNA damage, chloroquine activates the tumor-suppressor p53 and the p53 downstream target gene p21, resulting in G(1) cell cycle arrest.	Chloroquine	130-141	P53	Homo sapiens	173-176
18089834-6	2007	Using a human nontumorigenic mammary gland epithelial cell line, MCF10A, we confirm that in the absence of detectable DNA damage, chloroquine activates the tumor-suppressor p53 and the p53 downstream target gene p21, resulting in G(1) cell cycle arrest.	Chloroquine	130-141	P53	Homo sapiens	185-188
18089834-7	2007	p53 activation occurs at a posttranslational level via chloroquine-dependent phosphorylation of the checkpoint protein kinase, ataxia telangiectasia-mutated (ATM), leading to ATM-dependent phosphorylation of p53.	Chloroquine	55-66	P53	Homo sapiens	0-3
15896459-1	2005	In this work, we described the proliferation of human non-small-cell-lung-cancer (NSCLC) cells H1437 harboring p53 alleles (proline-267) can be inhibited by low-dosage topoisomerase II inhibitor etoposide (VP-16) in vitro and in vivo.	Proline	124-131	P53	Homo sapiens	111-114
15688418-0	2005	Role of p53 status in chemosensitivity determination of cancer cells against histone deacetylase inhibitor sodium butyrate.	Butyric Acid	107-122	P53	Homo sapiens	8-11
15688418-2	2005	Sodium butyrate (NaB), a histone deacetylase inhibitor, has been shown to cause a G(1) cell cycle arrest by inducing p21(WAF1/CIP1) in a p53-independent manner.	Butyric Acid	0-15	P53	Homo sapiens	137-140
18089834-7	2007	p53 activation occurs at a posttranslational level via chloroquine-dependent phosphorylation of the checkpoint protein kinase, ataxia telangiectasia-mutated (ATM), leading to ATM-dependent phosphorylation of p53.	Chloroquine	55-66	P53	Homo sapiens	208-211
22074401-11	2012	In p53(-/-)  and p53 mutant cells, GaQ(3) -induced Ca(2+) -signalling generated ROS.	tris(8-quinolinolato)gallium (III)	35-41	P53	Homo sapiens	3-6
15809436-2	2005	NQO1 binds and stabilizes WT p53, whereas NQO1 inhibitors including dicoumarol and various other coumarins and flavones induce ubiquitin-independent proteasomal p53 degradation and thus inhibit p53-induced apoptosis.	Dicumarol	68-78	P53	Homo sapiens	161-164
22074401-11	2012	In p53(-/-)  and p53 mutant cells, GaQ(3) -induced Ca(2+) -signalling generated ROS.	tris(8-quinolinolato)gallium (III)	35-41	P53	Homo sapiens	17-20
22517433-7	2012	In contrast, pre-incubation of p53-mutant cells with tenovin-6 or leptomycin B reduces the efficacy of vinca alkaloids, suggesting that these p53 activators could be effective as chemoprotectants if combined with S- but not M-phase poisons.	Vinca Alkaloids	103-118	P53	Homo sapiens	31-34
15846102-6	2005	We then injected Ad-p53 into subcutaneous tumors of KATO-III and HuH7 combined with intraperitoneal administration of SB and found a significantly higher growth suppressive effect than single treatments of each.	Butyric Acid	118-120	P53	Homo sapiens	20-23
15846102-10	2005	This was further supported by the finding that BAI-1 (brain specific angiogenesis inhibitor-1), an inhibitor of vascularization, was induced by SB treatment in KATO-III and HuH7 cells transfected with Ad-p53.	Butyric Acid	144-146	P53	Homo sapiens	204-207
15846102-11	2005	Thus SB was shown to be an efficient potentiator of p53 gene therapy for cancer.	Butyric Acid	5-7	P53	Homo sapiens	52-55
15814626-0	2005	The p53 codon 72 proline allele is associated with p53 gene mutations in non-small cell lung cancer.	Proline	17-24	P53	Homo sapiens	4-7
15814626-0	2005	The p53 codon 72 proline allele is associated with p53 gene mutations in non-small cell lung cancer.	Proline	17-24	P53	Homo sapiens	51-54
16973256-1	2007	OBJECTIVE: To compare the mechanism of action of raloxifene and gosereline induced shrinkage of leiomyomas via estrogen receptor, progesterone receptor, bcl-2 and p53 expression immunohistochemically.	Raloxifene Hydrochloride	49-59	P53	Homo sapiens	163-166
18025273-8	2007	In a cell death ELISA, 17-DMAG markedly induced apoptosis in both p53-wt and p53-deficient cells.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	23-30	P53	Homo sapiens	66-69
18025273-8	2007	In a cell death ELISA, 17-DMAG markedly induced apoptosis in both p53-wt and p53-deficient cells.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	23-30	P53	Homo sapiens	77-80
18025273-11	2007	Importantly, combining oxaliplatin with 17-DMAG in vivo significantly improved growth inhibitory and proapoptotic effects on p53-deficient cells, compared with either substance alone.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	40-47	P53	Homo sapiens	125-128
17906639-5	2007	Accordingly, tumor-associated mutations at Pin1-binding residues within the p53 proline-rich domain hamper acetylation of p53 by p300.	Proline	80-87	P53	Homo sapiens	76-79
22517433-7	2012	In contrast, pre-incubation of p53-mutant cells with tenovin-6 or leptomycin B reduces the efficacy of vinca alkaloids, suggesting that these p53 activators could be effective as chemoprotectants if combined with S- but not M-phase poisons.	Vinca Alkaloids	103-118	P53	Homo sapiens	142-145
17906639-5	2007	Accordingly, tumor-associated mutations at Pin1-binding residues within the p53 proline-rich domain hamper acetylation of p53 by p300.	Proline	80-87	P53	Homo sapiens	122-125
15733860-1	2005	In this study, we demonstrated that Ent-11alpha-hydroxy-15-oxo-kaur-16-en-19-oic-acid (5F) had stronger cytotoxicity against MKN-45, a gastric cancer cell line bearing wild-type p53 than MKN-28, another gastric cancer cell line containing missense mutation in p53.	ent-11alpha-hydroxy-15-oxo-kaur-16-en-19-oic-acid	36-85	P53	Homo sapiens	178-181
22521640-0	2012	WITHDRAWN: Hexavalent chromium induces premature senescence through reactive oxygen species-mediated p53 pathway in L-02 hepatocytes.	Chromium	22-30	P53	Homo sapiens	101-104
15733860-1	2005	In this study, we demonstrated that Ent-11alpha-hydroxy-15-oxo-kaur-16-en-19-oic-acid (5F) had stronger cytotoxicity against MKN-45, a gastric cancer cell line bearing wild-type p53 than MKN-28, another gastric cancer cell line containing missense mutation in p53.	ent-11alpha-hydroxy-15-oxo-kaur-16-en-19-oic-acid	36-85	P53	Homo sapiens	260-263
15686411-11	2005	On the other hand, the results showed that acacetin-induced apoptosis was accompanied by up-regulation of Bax and p53, down-regulation of Bcl-2, and cleavage of Bad.	acacetin	43-51	P53	Homo sapiens	114-117
17685632-5	2007	Western blot data revealed that gallic acid stimulated an increase in the protein expression of Fas, FasL, and p53.	Gallic Acid	32-43	P53	Homo sapiens	111-114
17113707-9	2007	Present findings indicate occurrence of sensitization to cisplatin by zoledronic acid in wild-type p53 osteosarcoma cells but not in p53-null cells nor in cells expressing a dominant-negative form of p53, supporting that wild-type p53 is required for synergistic interaction of cisplatin and zoledronic acid.	Zoledronic Acid	70-85	P53	Homo sapiens	99-102
22262850-5	2012	Herein, we describe the preparation and characterization of an oligodeoxynucleotide containing a CPD of a T(m)CG site, one of the major sites of C methylation and C-to-T mutations found in the p53 gene of basal and squamous cell cancers.	cysteinylglycine	110-112	P53	Homo sapiens	193-196
17428792-5	2007	Using potent PARP inhibitors and PARP-1 knock-out cells, we demonstrate a functional interplay between ATM and poly(ADP-ribose) that is important for the phosphorylation of p53, SMC1, and H2AX.	Poly Adenosine Diphosphate Ribose	111-127	P53	Homo sapiens	173-176
16285571-3	2005	These experiments led us to identify ingenol-20-benzoate (11) as a promising antitumour compound characterized by a relevant inhibition of cell growth and apoptotic cell death involving a p53-mediated pathway.	ingenol-20-benzoate	37-56	P53	Homo sapiens	188-191
22223356-8	2012	These results suggest that aluminium is not generically mutagenic, but similar to an activated oncogene, it induces proliferation stress, DSBs and senescence in normal mammary epithelial cells; and that long-term exposure to AlCl(3) generates and selects for cells able to bypass p53/p21(Waf1) -mediated cellular senescence.	Aluminum	27-36	P53	Homo sapiens	280-283
15638997-0	2005	Microarray analysis of bicalutamide action on telomerase activity, p53 pathway and viability of prostate carcinoma cell lines.	bicalutamide	23-35	P53	Homo sapiens	67-70
15638997-4	2005	Response to bicalutamide in LNCaP cells was represented by downregulation of androgen-regulated genes, activation of the p53 pathway and inhibition of telomerase, which was associated with downregulation of v-myc avian myelocytomatosis viral oncogene homologue (MYC) and telomerase reverse transcriptase subunit.	bicalutamide	12-24	P53	Homo sapiens	121-124
15638997-6	2005	In conclusion, we provide an explanation for telomerase inhibition after androgen receptor blockade in LNCaP cells and we also report activation of the p53 pathway in LNCaP cells and in-vitro sensitivity to bicalutamide of low confluent androgen-insensitive DU145 cells.	bicalutamide	207-219	P53	Homo sapiens	152-155
15638997-8	2005	In particular, activation of the p53 pathway after treatment with 80 microM bicalutamide could justify usage of bicalutamide dosages higher than 150 mg daily in androgen-sensitive carcinoma therapy.	bicalutamide	76-88	P53	Homo sapiens	33-36
17631738-7	2007	All of the RA patients and controls were genotyped by the polymerase chain reaction and allele-specific oligonucleotide techniques for p53 gene polymorphism Arg/Pro at codon 72.	Proline	161-164	P53	Homo sapiens	135-138
15638997-8	2005	In particular, activation of the p53 pathway after treatment with 80 microM bicalutamide could justify usage of bicalutamide dosages higher than 150 mg daily in androgen-sensitive carcinoma therapy.	bicalutamide	112-124	P53	Homo sapiens	33-36
22357201-2	2012	Among TP53 gene polymorphisms, the most studied is the G to C transversion in exon 4 at codon 72, which results in three distinct genotypes, Arg/Arg, Pro/Pro and Arg/Pro, each one encoding different p53 isoforms.	Proline	150-153	P53	Homo sapiens	6-10
17599946-1	2007	A TP53 gene polymorphism, resulting in an arginine (R) to proline (P) at codon 72 (TP53 R72P), has been associated with the susceptibility to various cancers.	Proline	58-65	P53	Homo sapiens	2-6
17599946-1	2007	A TP53 gene polymorphism, resulting in an arginine (R) to proline (P) at codon 72 (TP53 R72P), has been associated with the susceptibility to various cancers.	Proline	58-65	P53	Homo sapiens	83-87
17406354-0	2007	The p53 codon 72 proline allele is endowed with enhanced cell-death inducing potential in cancer cells exposed to hypoxia.	Proline	17-24	P53	Homo sapiens	4-7
17406354-1	2007	The preferential retention of the arginine allele at the p53 codon 72 locus is commonly observed in tumours from arginine/proline heterozygotes.	Proline	122-129	P53	Homo sapiens	57-60
15355990-3	2004	Etk is physically associated with p53 through its Src homology 3 domain and the proline-rich domain of p53.	Proline	80-87	P53	Homo sapiens	34-37
17406354-2	2007	Considering that cancer cells are harboured in a hypoxic environment in vivo, we here tested the hypothesis that the p53 codon 72 proline allele confers a survival disadvantage in presence of hypoxia.	Proline	130-137	P53	Homo sapiens	117-120
17406354-3	2007	Here, we show that the transient transfection of the proline allele in p53 null cancer cells exposed to low oxygen tension or to the hypoxia-mimetic drug Desferoxamine induces a higher amount of cell death than the arginine allele.	Proline	53-60	P53	Homo sapiens	71-74
17406354-6	2007	These data indicate that the p53 codon 72 proline allele is less permissive for the growth of cancer cells in a hypoxic environment, and suggest that the preferential retention of the arginine allele in the tumour tissues of arginine/proline heterozygous patients may depend upon its lowered capacity to induce cell death in a hypoxic tumour environment.	Proline	42-49	P53	Homo sapiens	29-32
15355990-3	2004	Etk is physically associated with p53 through its Src homology 3 domain and the proline-rich domain of p53.	Proline	80-87	P53	Homo sapiens	103-106
17406354-6	2007	These data indicate that the p53 codon 72 proline allele is less permissive for the growth of cancer cells in a hypoxic environment, and suggest that the preferential retention of the arginine allele in the tumour tissues of arginine/proline heterozygous patients may depend upon its lowered capacity to induce cell death in a hypoxic tumour environment.	Proline	234-241	P53	Homo sapiens	29-32
22357201-2	2012	Among TP53 gene polymorphisms, the most studied is the G to C transversion in exon 4 at codon 72, which results in three distinct genotypes, Arg/Arg, Pro/Pro and Arg/Pro, each one encoding different p53 isoforms.	Proline	154-157	P53	Homo sapiens	6-10
22357201-2	2012	Among TP53 gene polymorphisms, the most studied is the G to C transversion in exon 4 at codon 72, which results in three distinct genotypes, Arg/Arg, Pro/Pro and Arg/Pro, each one encoding different p53 isoforms.	Proline	154-157	P53	Homo sapiens	6-10
17332930-0	2007	Involvement of Bcl-2 family members, phosphatidylinositol 3"-kinase/AKT and mitochondrial p53 in curcumin (diferulolylmethane)-induced apoptosis in prostate cancer.	diferulolylmethane	107-125	P53	Homo sapiens	90-93
15479836-7	2004	Analysis of c-Myc- and E2F1-mediated inhibition of a panel of Zta mutants shows parallel genetics and inhibition maps to a small bipartite sequence located between amino acids 29 and 53 of Zta, containing homology to the proline-rich domain of the tumor suppressor protein p53.	Proline	221-228	P53	Homo sapiens	273-276
22142888-0	2012	Akt and p53 are potential mediators of reduced mammary tumor growth by cloroquine and the mTOR inhibitor RAD001.	Chloroquine	71-81	P53	Homo sapiens	8-11
15672606-0	2004	A new set of monoclonal antibodies directed to proline-rich and central regions of p53.	Proline	47-54	P53	Homo sapiens	83-86
15672606-5	2004	The H53C2 and H53C3 MAbs are against different epitopes within the proline-rich region of p53.	Proline	67-74	P53	Homo sapiens	90-93
17292432-4	2007	Treatment with other vanadate compounds, sodium orthovanadate (Na(3)VO(4)) and ammonium metavanadate (NH(4)VO(3)), also induced Ser15 phosphorylation and accumulation of p53 protein.	na(3)vo	63-70	P53	Homo sapiens	170-173
17292432-4	2007	Treatment with other vanadate compounds, sodium orthovanadate (Na(3)VO(4)) and ammonium metavanadate (NH(4)VO(3)), also induced Ser15 phosphorylation and accumulation of p53 protein.	ammonium metavanadate	79-100	P53	Homo sapiens	170-173
22142888-4	2012	We previously showed that the anti-malarial Chloroquine, a 4-alkylamino substituted quinoline, is a p53 activator and reduced the incidence of breast tumors in animal models.	Chloroquine	44-55	P53	Homo sapiens	100-103
22273545-0	2012	Design, synthesis and CoMFA studies of N1-amino acid substituted 2,4,5-triphenyl imidazoline derivatives as p53-MDM2 binding inhibitors.	2,4,5-triphenyl imidazoline	65-92	P53	Homo sapiens	108-111
17311614-2	2007	MATERIALS AND METHODS: The optimal uptake of photosensitizer ALA in HepG2 (p53 wild) cells was investigated by means of spectrometric measurement.	5-amino levulinic acid	61-64	P53	Homo sapiens	75-78
17311614-13	2007	ALA-PDT induces apoptosis in the HepG2 cell line that may be mediated by a p53-dependent pathway.	5-amino levulinic acid	0-3	P53	Homo sapiens	75-78
15173313-5	2004	Apoptotic induction by TPT-CuCl(2) was shown to mediate in a p53-depedent manner; loss of p53 impairs the release of cytochrome c and Smac/DIABLO from mitochondria to cytosol.	tpt-cucl(2)	23-34	P53	Homo sapiens	61-64
15262986-9	2004	Together, these findings suggest that p53 acts upstream of Bax to promote MDA-mediated cell death in a proline-rich domain-dependent manner through both transcription-dependent (by up-regulating PUMA expression) and -independent mechanisms in human colon cancer HCT116 cells.	Proline	103-110	P53	Homo sapiens	38-41
17283151-8	2007	In the stable H1299 cell line with tetracycline-inducible p53 expression, induced p53 enhanced growth inhibition and apoptosis by gefitinib through the up-regulation of Fas and restoration of caspase activation.	Tetracycline	35-47	P53	Homo sapiens	58-61
17283151-8	2007	In the stable H1299 cell line with tetracycline-inducible p53 expression, induced p53 enhanced growth inhibition and apoptosis by gefitinib through the up-regulation of Fas and restoration of caspase activation.	Tetracycline	35-47	P53	Homo sapiens	82-85
22184120-7	2012	BI 2356, a selective Plk1 inhibitor, however, prevented Cep55 accumulation in p53 knockdown cells while persistently keeping Plk1 levels elevated.	bi 2356	0-7	P53	Homo sapiens	78-81
17235397-7	2007	Inhibition of autophagy with either chloroquine or ATG5 short hairpin RNA (shRNA) enhanced the ability of either p53 activation or alkylating drug therapy to induce tumor cell death.	Chloroquine	36-47	P53	Homo sapiens	113-116
15381546-0	2004	Effect of carbon dioxide laser resurfacing on epidermal p53 immunostaining in photodamaged skin.	Carbon Dioxide	10-24	P53	Homo sapiens	56-59
15381546-1	2004	OBJECTIVE: To quantitatively examine changes in p53 tumor suppressor gene immunostaining after carbon dioxide (CO(2)) laser resurfacing of photodamaged skin to assess the potential value of this treatment in reducing the risk of progression to cutaneous carcinoma.	Carbon Dioxide	95-109	P53	Homo sapiens	48-51
21607615-2	2012	A guanine (G)/cytosine (C) common single nucleotide polymorphism (SNP) at second position of codon 72 in exon 4 of p53 gene determines a arginine (Arg) to proline (Pro) (Arg72Pro) aminoacidic substitution within the proline-rich domain of p53 protein.	Proline	155-162	P53	Homo sapiens	115-118
21607615-2	2012	A guanine (G)/cytosine (C) common single nucleotide polymorphism (SNP) at second position of codon 72 in exon 4 of p53 gene determines a arginine (Arg) to proline (Pro) (Arg72Pro) aminoacidic substitution within the proline-rich domain of p53 protein.	Proline	155-162	P53	Homo sapiens	239-242
15246561-5	2004	Taken together, p53 and Fas/FasL apoptotic system may participate in the antiproliferative activity of acacetin in A549 cells.	acacetin	103-111	P53	Homo sapiens	16-19
17184774-0	2007	Diphenyleneiodonium induces ROS-independent p53 expression and apoptosis in human RPE cells.	diphenyleneiodonium	0-19	P53	Homo sapiens	44-47
17184774-4	2007	In addition, DPI significantly induced the expression and phosphorylation of p53, which induces proapoptotic genes in response to DNA damage or irreparable cell cycle arrest.	diphenyleneiodonium	13-16	P53	Homo sapiens	77-80
21607615-2	2012	A guanine (G)/cytosine (C) common single nucleotide polymorphism (SNP) at second position of codon 72 in exon 4 of p53 gene determines a arginine (Arg) to proline (Pro) (Arg72Pro) aminoacidic substitution within the proline-rich domain of p53 protein.	Proline	164-167	P53	Homo sapiens	115-118
17184774-8	2007	Although there was increase in ROS level from cells treated for 24h with DPI, it was not detectable at early time points, required to induce p53 expression.	diphenyleneiodonium	73-76	P53	Homo sapiens	141-144
17184774-9	2007	And DPI-induced p53 expression was not affected by the ROS scavenger NAC.	diphenyleneiodonium	4-7	P53	Homo sapiens	16-19
17184774-10	2007	We conclude that DPI induces the expression of p53 by ROS-independent mechanism in ARPE-19 cells, and renders cells sensitive to drug-induced apoptosis by induction of p53 expression.	diphenyleneiodonium	17-20	P53	Homo sapiens	47-50
17184774-10	2007	We conclude that DPI induces the expression of p53 by ROS-independent mechanism in ARPE-19 cells, and renders cells sensitive to drug-induced apoptosis by induction of p53 expression.	diphenyleneiodonium	17-20	P53	Homo sapiens	168-171
15319038-4	2004	Coinfection of Ad vectors containing the siRNA expression system under the control of the Dox-inducible H1 promoter and Ad vectors expressing a tetracycline repressor inhibited the expression levels of p53 and c-Myc in a dose-dependent manner with both Dox and viral dose.	Tetracycline	144-156	P53	Homo sapiens	202-205
21607615-2	2012	A guanine (G)/cytosine (C) common single nucleotide polymorphism (SNP) at second position of codon 72 in exon 4 of p53 gene determines a arginine (Arg) to proline (Pro) (Arg72Pro) aminoacidic substitution within the proline-rich domain of p53 protein.	Proline	164-167	P53	Homo sapiens	239-242
17064912-0	2007	Synthesis of 5-deazaflavin derivatives and their activation of p53 in cells.	5-deazaflavin	13-26	P53	Homo sapiens	63-66
21607615-2	2012	A guanine (G)/cytosine (C) common single nucleotide polymorphism (SNP) at second position of codon 72 in exon 4 of p53 gene determines a arginine (Arg) to proline (Pro) (Arg72Pro) aminoacidic substitution within the proline-rich domain of p53 protein.	Proline	216-223	P53	Homo sapiens	115-118
15240786-6	2004	RESULTS: Acrylamide and glycidamide formed DNA adducts at similar specific locations within TP53 and cII, and DNA adduct formation was more pronounced after glycidamide treatment than after acrylamide treatment at all doses tested.	glycidamide	24-35	P53	Homo sapiens	92-96
21607615-2	2012	A guanine (G)/cytosine (C) common single nucleotide polymorphism (SNP) at second position of codon 72 in exon 4 of p53 gene determines a arginine (Arg) to proline (Pro) (Arg72Pro) aminoacidic substitution within the proline-rich domain of p53 protein.	Proline	216-223	P53	Homo sapiens	239-242
15240786-6	2004	RESULTS: Acrylamide and glycidamide formed DNA adducts at similar specific locations within TP53 and cII, and DNA adduct formation was more pronounced after glycidamide treatment than after acrylamide treatment at all doses tested.	glycidamide	157-168	P53	Homo sapiens	92-96
22056254-2	2012	Here we determine the effect of the tumor suppressor protein, p53, on trafficking (64)Cu to tumor cell nuclei from DOTA vs. CB-TE2A-conjugated agonist Y3-TATE and the antagonist (64)Cu-CB-TE2A-sst2-ANT in cell lines that are positive or negative for p53.	1,4,7,10-tetraazacyclododecane- 1,4,7,10-tetraacetic acid	115-119	P53	Homo sapiens	62-65
17237295-6	2007	Our results show that prodigiosin triggers accumulation of the DNA-damage response tumor-suppressor protein p53 but that NAG-1 induction was independent of p53 accumulation.	Prodigiosin	22-33	P53	Homo sapiens	108-111
22265415-0	2012	Mutant p53 disrupts mammary tissue architecture via the mevalonate pathway.	Mevalonic Acid	56-66	P53	Homo sapiens	7-10
17056014-7	2006	Thus, the reduction of KAP1 levels promotes p53-dependent p21 induction and inhibits cell proliferation in actinomycin D-treated cells.	Dactinomycin	107-120	P53	Homo sapiens	44-47
15257943-1	2004	A single nucleotide polymorphism at TP53 codon 72 means that two alleles exist: A1 (proline residue, Pro72) and A2 (arginine residue, Arg72).	Proline	84-91	P53	Homo sapiens	36-40
22265415-4	2012	Genome-wide expression analysis identified the mevalonate pathway as significantly upregulated by mutant p53.	Mevalonic Acid	47-57	P53	Homo sapiens	105-108
15252149-1	2004	The issue of p53 requirement for the caspase-mediated apoptosis induced by selenium in a cancer chemoprevention or chemotherapy context has not been critically addressed.	Selenium	75-83	P53	Homo sapiens	13-16
22265415-8	2012	These findings implicate the mevalonate pathway as a therapeutic target for tumors bearing mutations in p53.	Mevalonic Acid	29-39	P53	Homo sapiens	104-107
22108589-6	2012	In addition, arecoline induced progressive and sustained accumulation of BCC-1/KMC cells in G2/M phase as a result of reducing checkpoint Cdc2 activity by decreasing Cdc25C phosphatase levels and increasing p53 levels.	Arecoline	13-22	P53	Homo sapiens	207-210
15152193-3	2004	In search of mechanisms controlling L11-HDM2 interaction, we found that the induction of p53 under growth inhibitory conditions, such as low dose of actinomycin D or serum depletion, can be significantly attenuated by knocking down L11, indicating the importance of L11 in mediating these growth inhibitory signals to p53.	Dactinomycin	149-162	P53	Homo sapiens	89-92
17164358-1	2006	O6-methylguanine, a methylated damage lesion in DNA, correlates with spontaneous G:C --&gt; A:T transition mutations and leads to activation of oncogene K-ras or dysfunction of the tumor suppressor gene p53.	O-(6)-methylguanine	0-16	P53	Homo sapiens	203-206
17172431-0	2006	Apoptosis induced by selenomethionine and methioninase is superoxide mediated and p53 dependent in human prostate cancer cells.	Selenomethionine	21-37	P53	Homo sapiens	82-85
17172431-11	2006	These results suggest that superoxide and p53 may play a role in cancer chemoprevention by selenium.	Selenium	91-99	P53	Homo sapiens	42-45
22108589-8	2012	This study demonstrates that arecoline has potential for preventing BCC tumorigenesis by reducing levels of the tumor cell survival factor IL-6, increasing levels of the tumor suppressor factor p53, and eliciting cell cycle arrest, followed by apoptosis.	Arecoline	29-38	P53	Homo sapiens	194-197
15169974-9	2004	Oxoguanine adducts persisted and CA-125 (a phenotype of metaplastic transformation) was expressed in cultures of cells that were distressed by ovulation in which p53 synthesis was inhibited.	oxoguanine	0-10	P53	Homo sapiens	162-165
22289634-1	2012	Human TP53 gene is characterised by a polymorphism at codon 72 leading to an Arginine-to-Proline (R/P) substitution.	Proline	89-96	P53	Homo sapiens	6-10
15269478-6	2004	MATERIALS AND METHODS: p53 protein expression was evaluated on formalin-fixed paraffin-embedded sections using streptavidin biotin immunoperoxidase technique after high temperature antigen retrieval.	Biotin	124-130	P53	Homo sapiens	23-26
16763664-0	2006	A multifunctional PEI-based cationic polyplex for enhanced systemic p53-mediated gene therapy.	pei	18-21	P53	Homo sapiens	68-71
22901126-2	2012	Ser/Cys polymorphism in hOGG1 and Arg/Pro polymorphism in p53 among 124 patients with lung cancer and 128 normal people were detected using PCR-RFLP.	Proline	38-41	P53	Homo sapiens	58-61
16721787-3	2006	Among 856 colorectal adenoma cases and 1,184 controls, we observed a modest association with p53 Arg72Pro genotype (multivariate odds ratio (OR) = 1.25, 95% confidence interval (CI) = 1.04-1.50 for Arg/Pro and Pro/Pro vs. Arg/Arg).	Proline	102-105	P53	Homo sapiens	93-96
16721787-3	2006	Among 856 colorectal adenoma cases and 1,184 controls, we observed a modest association with p53 Arg72Pro genotype (multivariate odds ratio (OR) = 1.25, 95% confidence interval (CI) = 1.04-1.50 for Arg/Pro and Pro/Pro vs. Arg/Arg).	Proline	202-205	P53	Homo sapiens	93-96
16721787-3	2006	Among 856 colorectal adenoma cases and 1,184 controls, we observed a modest association with p53 Arg72Pro genotype (multivariate odds ratio (OR) = 1.25, 95% confidence interval (CI) = 1.04-1.50 for Arg/Pro and Pro/Pro vs. Arg/Arg).	Proline	202-205	P53	Homo sapiens	93-96
15077186-1	2004	A single-nucleotide polymorphism (SNP) in exon 4 results in expression of either arginine (72R) or proline (72P) at codon 72 of p53.	Proline	99-106	P53	Homo sapiens	128-131
14527925-4	2004	p53 phosphorylated on Ser20 was also increased by approximately 57% in radiotherapy/chemotherapy patients, and these changes correlated with Ki-67 proliferation and with elevated (by 69%; P &lt; 0.01) poly(ADP-ribose) levels.	Poly Adenosine Diphosphate Ribose	201-217	P53	Homo sapiens	0-3
15041222-4	2004	The TP53 gene has a single polymorphism at codon 72 of exon 4 that encodes either arginine (Arg) or proline (Pro).	Proline	100-107	P53	Homo sapiens	4-8
15041222-4	2004	The TP53 gene has a single polymorphism at codon 72 of exon 4 that encodes either arginine (Arg) or proline (Pro).	Proline	109-112	P53	Homo sapiens	4-8
17040108-9	2006	The cytosine residue of the ACG sequence complementary to codon 273, well-known hotspots of the p53 gene, was cleaved with piperidine and Fpg treatments.	piperidine	123-133	P53	Homo sapiens	96-99
22901138-2	2012	METHODS: Stool DNA was isolated and tumor-associated high molecular weight DNA (1.476 kb fragment including exons 6-9 of the p53 gene) was amplified using PCR and visualized on ethidium bromide-stained agarose gels.	Sepharose	202-209	P53	Homo sapiens	125-128
22454691-6	2012	The expression of p53 protein was markedly upregulated, and the p21 level was also obviously elevated in zerumbone-treated PANC-1 cells.	zerumbone	105-114	P53	Homo sapiens	18-21
16964264-0	2006	iASPP preferentially binds p53 proline-rich region and modulates apoptotic function of codon 72-polymorphic p53.	Proline	31-38	P53	Homo sapiens	27-30
15025498-3	2004	Our studies of the effects of noncytotoxic concentrations of Cd2+ on the levels of p53 and p21 in (+/-)-anti-benzo[a]pyrene-7,8-diol-9,10-epoxide (BPDE)-treated human fibroblasts showed that Cd2+ decreased BPDE-induced p21 levels in a dose-dependent manner whereas p53 accumulation is attenuated only at higher noncytotoxic concentrations of cadmium.	pyrene-7,8-diol-9,10-epoxide	117-145	P53	Homo sapiens	83-86
16964264-2	2006	We show here that, in addition to the DNA-binding domain, the ASPP family members also bind to the proline-rich region of p53, which contains the most common p53 polymorphism at codon 72.	Proline	99-106	P53	Homo sapiens	122-125
22962562-4	2012	In this pilot study, changes in p53 and its transcriptional targets, p21/waf1 and MDM2 were analyzed by immunoblotting and densitometry in CLL cells from 10 patients immediately prior to the start of chemotherapy, and after culture for 24 hours (h) with fludarabine (n=7) or chlorambucil (n=3).	Chlorambucil	275-287	P53	Homo sapiens	32-35
16964264-2	2006	We show here that, in addition to the DNA-binding domain, the ASPP family members also bind to the proline-rich region of p53, which contains the most common p53 polymorphism at codon 72.	Proline	99-106	P53	Homo sapiens	158-161
22200421-0	2012	Indoxyl sulfate induces endothelial cell senescence by increasing reactive oxygen species production and p53 activity.	Indican	0-15	P53	Homo sapiens	105-108
16925398-1	2006	The most potent inhibitor of the p53-MDM2 interaction reported to date is an 8-mer p53 peptide analogue (Novartis peptide), which contains 6-chlorotryptophane (Cl-Trp) and phosphonomethylphenylalanine (Pmp) as key residues for the enhanced activity.	6-chlorotryptophane	139-158	P53	Homo sapiens	33-36
16925398-1	2006	The most potent inhibitor of the p53-MDM2 interaction reported to date is an 8-mer p53 peptide analogue (Novartis peptide), which contains 6-chlorotryptophane (Cl-Trp) and phosphonomethylphenylalanine (Pmp) as key residues for the enhanced activity.	6-chlorotryptophane	139-158	P53	Homo sapiens	83-86
18228447-5	2004	It has also been proposed that the presence of negatively charged poly(ADP-ribose) at the site of DNA damage may play several roles in regulation of base excision repair, p53 functions, and apoptosis.	Poly Adenosine Diphosphate Ribose	66-82	P53	Homo sapiens	171-174
14719118-11	2004	Incubating cells with a caspase-8-specific inhibitor Ac-IETD-CHO prior to Ad-p53 infection inhibited caspase-8 activity and apoptosis.	Ac-IETD-CHO	53-64	P53	Homo sapiens	77-80
22025681-6	2012	Furthermore, PNR significantly boosted actinomycin D-stimulated p53 acetylation.	Dactinomycin	39-52	P53	Homo sapiens	64-67
14711380-7	2004	Duplication time, plating efficiency, colony formation in agarose, and contact inhibition were also altered in the p53 mutated tumor cultures compared to those carrying wild-type p53.	Sepharose	58-65	P53	Homo sapiens	115-118
16835507-3	2006	We evaluated the linkage of the polymorphic variants (Arg/Pro) on TP53 codon 72 with nasopharyngeal cancer development in a case-control study with 392 individuals from a northern Portuguese population, including 107 patients with nasopharyngeal carcinoma and 285 healthy controls.	Proline	58-61	P53	Homo sapiens	66-70
22642109-11	2012	The 24-hour treatment of MOLT-4 leukemia cells with 2 mM VA results in radiosensitizing, increases apoptosis induction, H2AX phosphorylation, and also p53 and p21 activation.	Valproic Acid	57-59	P53	Homo sapiens	151-154
16620878-2	2006	Recent reports reveal the presence in p53 of non-CG methylation in CC and CCC sequences, complementary to sites of selective guanosine adduct formation (GG and GGG), and the association of genetic instability with methylation at repetitive sequences.	Guanosine	125-134	P53	Homo sapiens	38-41
14704126-10	2004	CONCLUSION: These results indicated that the wt p53 gene transfection not only induced suppression of cell growth, but also increased the sensitivity of Bel7402/5-FU cells to 5-FU, vincristine, and doxorubicin.	Vincristine	181-192	P53	Homo sapiens	48-51
15651660-2	2004	The functional oligonucleotide polymorphism of the p53 gene causes the substitution of arginine (Arg) for praline (Pro) in the codon 72.	Proline	115-118	P53	Homo sapiens	51-54
21964832-7	2012	To verify the regulatory mechanism of p53 protein expression, we investigated             the effects of proteasomal inhibitors (ALLN and MG132) or a lysosomal inhibitor             (chloroquine) on TPA-induced down-regulation of p53.	Chloroquine	183-194	P53	Homo sapiens	230-233
14634213-5	2003	Although wild-type p53 and several p53 mutants were sensitive to dicoumarol-induced degradation, the most frequent "hot-spot" p53 mutants in human cancer, R175H, R248H, and R273H, were resistant to dicoumarol-induced degradation, but remained sensitive to Mdm2-ubiquitin-mediated degradation.	Dicumarol	65-75	P53	Homo sapiens	35-38
14634213-7	2003	Further mutational analysis showed that arginines at positions 175 and 248 were essential for dicoumarol-induced p53 degradation.	Dicumarol	94-104	P53	Homo sapiens	113-116
14634213-9	2003	Compared with wild-type p53, the hot-spot p53 mutants showed increased binding to NQO1, which can explain their resistance to dicoumarol-induced degradation.	Dicumarol	126-136	P53	Homo sapiens	24-27
14634213-9	2003	Compared with wild-type p53, the hot-spot p53 mutants showed increased binding to NQO1, which can explain their resistance to dicoumarol-induced degradation.	Dicumarol	126-136	P53	Homo sapiens	42-45
16995472-6	2006	RESULTS: The p53 gene mutation has been shown in 16 (61.5%) of the PA patients (9 in exon 5 and 7 in exon 7) and in 2 (8.6%) of CP patients (1 in exon 5 and 1 in exon 8; p &lt; 0.001).	Protactinium	67-69	P53	Homo sapiens	13-16
16600594-0	2006	Enhanced pharmacokinetic properties of 1,4-benzodiazepine-2,5-dione antagonists of the HDM2-p53 protein-protein interaction through structure-based drug design.	Bz-423	39-67	P53	Homo sapiens	92-95
23071787-6	2012	The frequency of somatic TP53 inactivation was 25.4% in Arg/Arg, 20.9% in Arg/Pro, and 16.7% in Pro/Pro patients, which may reflect a higher selective pressure to mutate the Arg-allele.	Proline	78-81	P53	Homo sapiens	25-29
16462765-3	2006	A polymorphic site at codon 72 in exon 4 encodes either an arginine amino acid (Trp53(72R)) or a proline residue (Trp53(72P)).	Proline	97-104	P53	Homo sapiens	114-119
16627976-0	2006	Selenomethionine induces p53 mediated cell cycle arrest and apoptosis in human colon cancer cells.	Selenomethionine	0-16	P53	Homo sapiens	25-28
16627976-3	2006	More recently, it has been suggested that selenium may exert growth inhibitory effects by activating p53.	Selenium	42-50	P53	Homo sapiens	101-104
16627976-5	2006	In the present study we tested the hypothesis that selenomethionine might affect colon cancer cell growth by p53 mediated apoptosis and/or cell cycle regulation.	Selenomethionine	51-67	P53	Homo sapiens	109-112
14654788-6	2003	Infection of Ptx-resistant lines with a wild-type TP53-bearing adenovirus (AdWTp53) changed cell cycle distribution and increased the levels of p21(WAF1/Cip1), but caused no changes in stathmin levels.	ptx	13-16	P53	Homo sapiens	50-54
14513366-1	2003	PURPOSE: Resistance to chemotherapeutic drugs is a hallmark of many human cancers, which can occur independent of p53 gene status; however, the presence of wild-type p53 in chemorefractory tumors confers greater resistance to cisplatin, but such tumors do not display complete cross-resistance to the platinum analog (1R,2R-diaminocyclohexane)(trans-diacetato)(dichloro)platinumIV (DACH-Ac-Pt).	trans-diacetato)(dichloro)platinumiv	344-380	P53	Homo sapiens	166-169
14513366-5	2003	Although phosphorylation of p53 at Ser-392 was also observed in CDDP-treated sensitive and resistant cells, it was weak or absent in response to DACH-Ac-Pt.	1,2-cyclohexanediamine	145-149	P53	Homo sapiens	28-31
14612427-8	2003	Interference with ribosomal biogenesis by a low concentration of actinomycin D is associated with an increased L11-HDM2 interaction and subsequent p53 stabilization.	Dactinomycin	65-78	P53	Homo sapiens	147-150
16627976-12	2006	Cell cycle arrest and apoptosis observed in HCT116 and RKO cell lines were accompanied by a marked increase in p53 protein expression following selenium treatment.	Selenium	144-152	P53	Homo sapiens	111-114
16627976-13	2006	These results clearly suggest that selenomethionine exerts p53 dependent growth inhibitory effects in colon cancer cells by inducing G2/M cell cycle arrest as well as apoptosis.	Selenomethionine	35-51	P53	Homo sapiens	59-62
23071787-6	2012	The frequency of somatic TP53 inactivation was 25.4% in Arg/Arg, 20.9% in Arg/Pro, and 16.7% in Pro/Pro patients, which may reflect a higher selective pressure to mutate the Arg-allele.	Proline	96-99	P53	Homo sapiens	25-29
16518417-0	2006	Dicoumarol potentiates cisplatin-induced apoptosis mediated by c-Jun N-terminal kinase in p53 wild-type urogenital cancer cell lines.	Dicumarol	0-10	P53	Homo sapiens	90-93
14617104-0	2003	Effects of a melanogenic bicyclic monoterpene diol on cell cycle, p53, TNF-alpha, and PGE2 are distinct from those of UVB.	monoterpene diol	34-50	P53	Homo sapiens	66-69
23071787-6	2012	The frequency of somatic TP53 inactivation was 25.4% in Arg/Arg, 20.9% in Arg/Pro, and 16.7% in Pro/Pro patients, which may reflect a higher selective pressure to mutate the Arg-allele.	Proline	96-99	P53	Homo sapiens	25-29
14666730-2	2003	We have reported that hypoxic cytotoxins, such as TX-1102, tirapazamine (TPZ) and TX-402, selectively induced tumor cells to p53-independent apoptosis under hypoxic conditions and inhibited angiogenesis.	3-amino-2-quinoxalinecarbonitrile	82-88	P53	Homo sapiens	125-128
16518417-1	2006	3-3"-Methylene-bis [4-hydroxycoumarin] (dicoumarol), an inhibitor of NADPH:quinone oxidoreductase 1, has been reported to possess potential antineoplastic effects and the ability to abrogate p53 protein.	Dicumarol	0-38	P53	Homo sapiens	191-194
16518417-1	2006	3-3"-Methylene-bis [4-hydroxycoumarin] (dicoumarol), an inhibitor of NADPH:quinone oxidoreductase 1, has been reported to possess potential antineoplastic effects and the ability to abrogate p53 protein.	Dicumarol	40-50	P53	Homo sapiens	191-194
16518417-4	2006	On the other hand, pretreatment with dicoumarol enhanced cytotoxicity of CDDP in three cell lines with wild type of p53 (RT112, 253J and LNCap), but not in three other cell lines with mutant p53 or in RT112 stable transfectants with a dominant-negative mutant of p53.	Dicumarol	37-47	P53	Homo sapiens	116-119
23049825-3	2012	In this study we evaluate the association between a p53 variant functionally known to influence apoptosis (codon 72 Pro/Arg) and the subset of primary open angle glaucoma (POAG) patients with early loss of central visual field.	Proline	116-119	P53	Homo sapiens	52-55
16518417-4	2006	On the other hand, pretreatment with dicoumarol enhanced cytotoxicity of CDDP in three cell lines with wild type of p53 (RT112, 253J and LNCap), but not in three other cell lines with mutant p53 or in RT112 stable transfectants with a dominant-negative mutant of p53.	Dicumarol	37-47	P53	Homo sapiens	191-194
16426903-4	2006	Chloroquine treatment and other manipulations that produce chromatin defects in the absence of detectable double strand breaks also trigger ATM phosphorylation and the phosphorylation of p53 in primary human fibroblasts, while other downstream substrates of ATM that are involved in the repair of DNA double strand breaks remain unphosphorylated.	Chloroquine	0-11	P53	Homo sapiens	187-190
12925527-5	2003	This rapid induction of p21 was wild-type p53-dependent and resulted in cell cycle arrest along with a marked reduction of phosphorylated Rb in normally growing cells.	Rubidium	138-140	P53	Homo sapiens	42-45
22558087-0	2012	JKA97, a novel benzylidene analog of harmine, exerts anti-cancer effects by inducing G1 arrest, apoptosis, and p53-independent up-regulation of p21.	Harmine	37-44	P53	Homo sapiens	111-114
14581358-0	2003	Retention of the p53 codon 72 arginine allele is associated with a reduction of disease-free and overall survival in arginine/proline heterozygous breast cancer patients.	Proline	126-133	P53	Homo sapiens	17-20
14581358-5	2003	RESULTS: We found that the retention of the p53 codon 72 arginine allele in the tumor tissue of proline/arginine heterozygous breast cancer patients is associated with statistically significant reduced disease-free and overall survivals.	Proline	96-103	P53	Homo sapiens	44-47
14581358-6	2003	CONCLUSIONS: Our findings suggest that the genotyping for p53 codon 72 locus in both the tumor tissue and in the lymph node of breast cancer patients could contribute to identify a subset of arginine/proline heterozygous patients who have a reduced survival that is associated with the specific retention of the arginine allele in the tumor tissue.	Proline	200-207	P53	Homo sapiens	58-61
14581372-1	2003	In recent studies, we found that sulindac sulfide (SS), exisulind, CP248, and CP461 induce growth inhibition and apoptosis in a series of human prostate cancer cell lines, irrespective of cyclooxygenase expression, p53 mutations, or bcl-2 overexpression.	sulindac sulfide	33-49	P53	Homo sapiens	215-218
14581372-1	2003	In recent studies, we found that sulindac sulfide (SS), exisulind, CP248, and CP461 induce growth inhibition and apoptosis in a series of human prostate cancer cell lines, irrespective of cyclooxygenase expression, p53 mutations, or bcl-2 overexpression.	sulindac sulfide	51-53	P53	Homo sapiens	215-218
14583485-5	2003	In addition to its cytotoxic properties, we found that Bz-423 is also a potent antiproliferative agent that induces a G(1)-phase arrest independent of p53.	Bz-423	55-61	P53	Homo sapiens	151-154
16314399-6	2006	Furthermore, we found a significant gene-gene interaction between P53BP1 Gln1136Lys and p53 Arg72Pro variants in relation to breast cancer, and the OR of interaction for the presence of both P53BP1 1136Gln/Lys+Lys/Lys and p53 72Arg/Pro+Pro/Pro genotypes was 1.93 (95% CI 1.06-3.52) (P=0.031 for interaction).	Proline	97-100	P53	Homo sapiens	88-91
16314399-6	2006	Furthermore, we found a significant gene-gene interaction between P53BP1 Gln1136Lys and p53 Arg72Pro variants in relation to breast cancer, and the OR of interaction for the presence of both P53BP1 1136Gln/Lys+Lys/Lys and p53 72Arg/Pro+Pro/Pro genotypes was 1.93 (95% CI 1.06-3.52) (P=0.031 for interaction).	Proline	97-100	P53	Homo sapiens	222-225
16314399-6	2006	Furthermore, we found a significant gene-gene interaction between P53BP1 Gln1136Lys and p53 Arg72Pro variants in relation to breast cancer, and the OR of interaction for the presence of both P53BP1 1136Gln/Lys+Lys/Lys and p53 72Arg/Pro+Pro/Pro genotypes was 1.93 (95% CI 1.06-3.52) (P=0.031 for interaction).	Proline	232-235	P53	Homo sapiens	88-91
16318864-11	2006	There was also a higher incidence of, but without reaching a statistical significance, p53 mutation in patients with p53 overexpression (OR[95% CI]: 2.18 [0.52-9.6]) and codon 72 Arg/Arg genotype (OR [95% CI] of 0.8 [0.13-4.2], comparing genotypes of Pro/Pro and Arg/Pro with Arg/Arg).	Proline	251-254	P53	Homo sapiens	87-90
16318864-11	2006	There was also a higher incidence of, but without reaching a statistical significance, p53 mutation in patients with p53 overexpression (OR[95% CI]: 2.18 [0.52-9.6]) and codon 72 Arg/Arg genotype (OR [95% CI] of 0.8 [0.13-4.2], comparing genotypes of Pro/Pro and Arg/Pro with Arg/Arg).	Proline	255-258	P53	Homo sapiens	87-90
16318864-11	2006	There was also a higher incidence of, but without reaching a statistical significance, p53 mutation in patients with p53 overexpression (OR[95% CI]: 2.18 [0.52-9.6]) and codon 72 Arg/Arg genotype (OR [95% CI] of 0.8 [0.13-4.2], comparing genotypes of Pro/Pro and Arg/Pro with Arg/Arg).	Proline	255-258	P53	Homo sapiens	87-90
14705644-0	2003	Mechanisms of selenium-mediated protection from photocarcinogenesis and cell death are not solely p53-dependent.	Selenium	14-22	P53	Homo sapiens	98-101
22359668-6	2012	Expressions of p16(Ink4a), Rb, p53, and p21(Cip1), which have been associated with cellular senescence, were all reduced in human MSCs by the pharmacological inhibition of LPA signaling.	lysophosphatidic acid	172-175	P53	Homo sapiens	31-34
14705644-5	2003	USA ascribe a role for selenium, acting through wild type p53, in protecting skin cells in culture from ultraviolet radiation-induced death.	Selenium	23-31	P53	Homo sapiens	58-61
16380082-3	2006	We previously demonstrated that an N-terminal portion of NS3 formed a complex with the tumor suppressor p53 and suppressed actinomycin D-induced apoptosis.	Dactinomycin	123-136	P53	Homo sapiens	104-107
22242180-9	2012	Thus this study suggests that ROS/RNS contributed to change of p53 tertiary structure and that unfolded p53 can be considered as an early marker of oxidative imbalance in these patients.	Radon	34-37	P53	Homo sapiens	63-66
16521213-10	2006	When only the data from the 11 patients treated with anthraquinone drug, mitoxantrone, were analyzed, however, the number of patients who showed poor response to treatment was significantly higher among the p53-positive patients (P=0.012), irrespective of the survival outcome.	Mitoxantrone	73-85	P53	Homo sapiens	207-210
17113725-1	2006	BACKGROUND: A common Arg/Pro polymorphism at codon 72 of the TP53 gene has been investigated as a risk factor for cancer in different populations.	Proline	25-28	P53	Homo sapiens	61-65
12927789-5	2003	Pretreatment of the cells with 10nM morphine caused a transient, naloxone-reversible suppression of the appearance of activated p53 and the generation of DNA laddering.	Naloxone	65-73	P53	Homo sapiens	128-131
21685937-9	2011	Finally, we show that overexpression of SPARC renders cells more resistant to the p53-mediated cytotoxic effects of the DNA-damaging drug actinomycin-D.	Dactinomycin	138-149	P53	Homo sapiens	82-85
12944903-2	2003	Labeling with [(3)H] nucleosides resulted in growth inhibition by both p53-dependent and -independent mechanisms.	[(3)h] nucleosides	14-32	P53	Homo sapiens	71-74
16403018-0	2006	Recognition of DNA modified by trans-[PtClNH(4-hydroxymethylpyridine)] by tumor suppressor protein p53 and character of DNA adducts of this cytotoxic complex.	trans-[ptclnh	31-44	P53	Homo sapiens	99-102
21986580-0	2011	Crocetin induces cytotoxicity and enhances vincristine-induced cancer cell death via p53-dependent and -independent mechanisms.	Vincristine	43-54	P53	Homo sapiens	85-88
16314136-7	2006	Nevertheless, TQ is known to induce apoptosis by p53-dependent and p53-independent pathways in cancer cell lines.	thymoquinone	14-16	P53	Homo sapiens	49-52
16314136-7	2006	Nevertheless, TQ is known to induce apoptosis by p53-dependent and p53-independent pathways in cancer cell lines.	thymoquinone	14-16	P53	Homo sapiens	67-70
16896365-4	2006	P53 gene polymorphisms include codon11 Glu/Gln or Lys (GAG-&gt;CAG or AAG), codon 72 Arg/Pro (CGC-&gt;CCC), and codon 248 Arg/Thr (CGG-&gt;TCG).	TMG-chitotriomycin	139-142	P53	Homo sapiens	0-3
12700117-0	2003	Efficacy of adenoviral p53 delivery with SCH58500 in the intracranial 9l and RG2 models.	sch58500	41-49	P53	Homo sapiens	23-26
12702572-14	2003	Our results suggest that morphine, alone or in combination with Nx, may reduce the growth of certain tumors, apparently in part through activation of p53.	Naloxone	64-66	P53	Homo sapiens	150-153
12727806-4	2003	It has been reported that lung cancer from workers exposed to Cr(VI) has a high percentage of G to T transversion mutations in the non-transcribed strand of the p53 gene, a hallmark of PAH-induced mutation.	Chromium	62-64	P53	Homo sapiens	161-164
12727806-6	2003	These results raise the possibility that Cr(VI) may enhance PAH binding at the p53 gene in lung tissue.	Chromium	41-43	P53	Homo sapiens	79-82
22077725-3	2011	We have examined potential alterations in p53 in response to 2-ME(2), E(2) and the microtubule disruptor taxol in T47D breast cancer cells.	Mercaptoethanol	61-65	P53	Homo sapiens	42-45
12529318-1	2003	NAD(P)H:quinone oxidoreductase 1 (NQO1) has been proposed to stabilize p53 via a redox mechanism involving oxidation of NAD(P)H as a consequence of the catalytic activity of NQO1.	nad(p)h	0-7	P53	Homo sapiens	71-74
18528466-5	2006	These two p53-regulated proteins control microtubule dynamics, regulate the sensitivity to taxanes and vinca alkaloids by changing the polymerization dynamics of tubulin and affecting the binding of drugs to microtubules.	Vinca Alkaloids	103-118	P53	Homo sapiens	10-13
18528466-10	2006	We also discovered that p53 could regulate the expression of multidrug resistance protein-1 (MRP1), a member of the ABC family of transporters that mediates the sensitivity to vinca alkaloids and anthracyclines.	Vinca Alkaloids	176-191	P53	Homo sapiens	24-27
22077725-7	2011	Addition of 10 nM - 1 microM 2-ME(2) induced significant up-regulation in p53, and this response gradually diminished to levels comparable to the control upon treatment with higher concentrations (2.5 - 10 microM).	Mercaptoethanol	29-33	P53	Homo sapiens	74-77
16362795-2	2005	TP53 codon 72, which produces variant proteins with an arginine (Arg) or proline (Pro), has been reported to be associated with cancers of the lung, oesophagus, stomach and cervix.	Proline	73-80	P53	Homo sapiens	0-4
16362795-2	2005	TP53 codon 72, which produces variant proteins with an arginine (Arg) or proline (Pro), has been reported to be associated with cancers of the lung, oesophagus, stomach and cervix.	Proline	82-85	P53	Homo sapiens	0-4
12628849-2	2003	A common polymorphism at codon 72 of exon 4 encoding either arginine (Arg) or proline (Pro) has been shown to affect HPV-mediated degradation of p53 in vitro, and may represent a risk factor for HPV-induced carcinogenesis.	Proline	78-85	P53	Homo sapiens	145-148
12628849-2	2003	A common polymorphism at codon 72 of exon 4 encoding either arginine (Arg) or proline (Pro) has been shown to affect HPV-mediated degradation of p53 in vitro, and may represent a risk factor for HPV-induced carcinogenesis.	Proline	87-90	P53	Homo sapiens	145-148
12567188-1	2003	The gene TP53, encoding p53, has a common sequence polymorphism that results in either proline or arginine at amino-acid position 72.	Proline	87-94	P53	Homo sapiens	9-13
22077725-8	2011	The observed upregulation of p53 induced by 2-ME(2) is inhibited by concurrent treatment with 1 microM taxol.	Mercaptoethanol	44-48	P53	Homo sapiens	29-32
12567188-1	2003	The gene TP53, encoding p53, has a common sequence polymorphism that results in either proline or arginine at amino-acid position 72.	Proline	87-94	P53	Homo sapiens	24-27
12567188-2	2003	This polymorphism occurs in the proline-rich domain of p53, which is necessary for the protein to fully induce apoptosis.	Proline	32-39	P53	Homo sapiens	55-58
16373706-7	2005	With Western hybridization and real-time reverse transcription-PCR, we further showed that the antitumor activities of valproic acid correlated with induction of histone (H3 and H4) hyperacetylation, activation of p21, and suppression of TP53, CDK4, and CMYC expression.	Valproic Acid	119-132	P53	Homo sapiens	238-242
22077725-11	2011	In a concentration dependent manner, treatment with 2-ME(2) for 24 h differentially influenced cellular localization of p53.	Mercaptoethanol	52-56	P53	Homo sapiens	120-123
22057999-9	2011	Meta-analysis results  showed that the Pro allele and Pro carrier (Arg/Pro + Pro/Pro) of p53 codon 72  polymorphism were significantly related with endometrial cancer risk (OR =  1.25, 95%CI = 1.10-1.41, P = 0.0005; OR = 1.34, 95%CI = 1.12-1.59, P = 0.001,  respectively).	Proline	39-42	P53	Homo sapiens	89-92
15906362-9	2005	Overall, these results offer a potential mechanism for TQ-induced apoptosis in p53-null HL-60 cancer cells.	thymoquinone	55-57	P53	Homo sapiens	79-82
16123044-6	2005	In this regard, it has been recently observed that the prolyl isomerase Pin1 can interact with proteins phosphorylated on serine or threonine residues that precede prolines (pS/T-P), such as the transcription factors p53 and c-Jun, thereby controlling their activity by promoting the cis-trans isomerization of these pS/T-P bonds.	Proline	164-172	P53	Homo sapiens	217-220
12609712-7	2003	Oxoguanine modifications persisted in cells affected by ovulation in which synthesis of p53 was negated in culture by an antisense oligonucleotide.	oxoguanine	0-10	P53	Homo sapiens	88-91
12708345-1	2003	In codon 72 of the p53 antioncogene there are two alleles, arginine and proline; the arg/arg genotype has recently been identified as a risk factor for developing of cervicouterine cancer (CuCa) associated to human papillomavirus (HVP) infection.	Proline	72-79	P53	Homo sapiens	19-22
12708345-5	2003	From 102 analyzed samples, p53-arginine allele corresponded to 67.64% and p53-proline allele corresponded to 32.36%; 47 women (46.10%) were arg/arg homocygotes, 11 women (10.77%) were pro/pro homocygotes, 44 women (43.13%) were arg/pro heterocigotes; the genotype distribution was within the Hardy-Weinberg equilibrium.	Proline	78-85	P53	Homo sapiens	74-77
22057999-9	2011	Meta-analysis results  showed that the Pro allele and Pro carrier (Arg/Pro + Pro/Pro) of p53 codon 72  polymorphism were significantly related with endometrial cancer risk (OR =  1.25, 95%CI = 1.10-1.41, P = 0.0005; OR = 1.34, 95%CI = 1.12-1.59, P = 0.001,  respectively).	Proline	54-57	P53	Homo sapiens	89-92
22057999-9	2011	Meta-analysis results  showed that the Pro allele and Pro carrier (Arg/Pro + Pro/Pro) of p53 codon 72  polymorphism were significantly related with endometrial cancer risk (OR =  1.25, 95%CI = 1.10-1.41, P = 0.0005; OR = 1.34, 95%CI = 1.12-1.59, P = 0.001,  respectively).	Proline	54-57	P53	Homo sapiens	89-92
16243804-9	2005	CONCLUSION: Our study indicates that breast cancer patients with the Pro/Pro variant may be less sensitive to anthracycline-based treatment than those with the Pro/Arg or Arg/Arg variant and suggests that analysis of p53 codon 72 polymorphism may provide a simple predictive marker for selecting the right breast cancer patients to anthracycline-based neoadjuvant chemotherapy in clinical setting.	Proline	69-72	P53	Homo sapiens	217-220
22057999-11	2011	We  concluded that the Pro allele (Arg/Pro + Pro/Pro) of p53 codon 72 polymorphism  is a potential risk factor for endometrial cancer.	Proline	23-26	P53	Homo sapiens	57-60
22057999-11	2011	We  concluded that the Pro allele (Arg/Pro + Pro/Pro) of p53 codon 72 polymorphism  is a potential risk factor for endometrial cancer.	Proline	39-42	P53	Homo sapiens	57-60
12374798-2	2002	We investigated possible alterations of MUC2 gene expression by p53 and p21(Sdi1/Waf1/Cip1) in a human colon cancer cell line, DLD-1, establishing subclones in which a tetracycline-regulatable promoter controls exogenous p53 and p21 expression.	Tetracycline	168-180	P53	Homo sapiens	221-224
22057999-11	2011	We  concluded that the Pro allele (Arg/Pro + Pro/Pro) of p53 codon 72 polymorphism  is a potential risk factor for endometrial cancer.	Proline	39-42	P53	Homo sapiens	57-60
12374798-9	2002	In MCF7 breast cancer and A427 lung cancer cells, MUC2 expression was increased along with the endogenous p53 level by actinomycin D, UVC, and x-ray, but not in RERF-LC-MS lung cancer cells carrying a mutated p53.	Dactinomycin	119-132	P53	Homo sapiens	106-109
16203772-1	2005	PURPOSE: The Arg/Pro polymorphism in codon 72 of p53 was recently associated with age of onset of colorectal cancer in Lynch syndrome.	Proline	17-20	P53	Homo sapiens	49-52
21832879-4	2011	Mutant p53 melanoma were resistant to a comparable metabolic restriction, only showing PARP fragmentation when glucose depletion was accompanied by treatment with diphenylene iodonium (DPI), a NADPH oxidase inhibitor of superoxide (O2*-) generation.	diphenyleneiodonium	163-183	P53	Homo sapiens	7-10
16199549-1	2005	The polymorphic variants at codon 72 of the p53 gene were shown to be functionally distinct in vitro, whereby the arginine (arg) variant induces apoptosis more efficiently than the proline (pro) variant.	Proline	181-188	P53	Homo sapiens	44-47
12388558-2	2002	The increase in p53 stability depends critically on its phosphorylation on serine/threonine residues, including those preceding a proline (Ser(P)/Thr-Pro).	Proline	130-137	P53	Homo sapiens	16-19
12478472-3	2002	In spite of the ability of both compounds to up-regulate p53 at cytotoxic concentrations, exposure to BBR 3464 resulted in cell cycle arrest but only cisplatin was capable of inducing significant levels of apoptosis and phosphorylation at the Ser15 residue of p53.	bbr	102-105	P53	Homo sapiens	260-263
12478472-6	2002	The regulation of p21(WAF1) after cisplatin or BBR 3464 exposure required a p53 signal, as documented using stable transfectants expressing a dominant-negative form of p53 (175(his)).	bbr	47-50	P53	Homo sapiens	76-79
12478472-6	2002	The regulation of p21(WAF1) after cisplatin or BBR 3464 exposure required a p53 signal, as documented using stable transfectants expressing a dominant-negative form of p53 (175(his)).	bbr	47-50	P53	Homo sapiens	168-171
16172238-1	2005	Polymorphism at codon 72 of p53 results in either the arginine or proline form of p53, whose functional significance in carcinogenesis is controversial.	Proline	66-73	P53	Homo sapiens	28-31
21832879-4	2011	Mutant p53 melanoma were resistant to a comparable metabolic restriction, only showing PARP fragmentation when glucose depletion was accompanied by treatment with diphenylene iodonium (DPI), a NADPH oxidase inhibitor of superoxide (O2*-) generation.	diphenyleneiodonium	185-188	P53	Homo sapiens	7-10
16172238-1	2005	Polymorphism at codon 72 of p53 results in either the arginine or proline form of p53, whose functional significance in carcinogenesis is controversial.	Proline	66-73	P53	Homo sapiens	82-85
16172238-2	2005	We have investigated if the expression of these p53 polymorphs is selectively regulated, using mRNA from peripheral blood of healthy Asian (Chinese) and the Caucasian (Polish) arginine/proline (arg/pro) heterozygote subjects.	Proline	185-192	P53	Homo sapiens	48-51
16172238-2	2005	We have investigated if the expression of these p53 polymorphs is selectively regulated, using mRNA from peripheral blood of healthy Asian (Chinese) and the Caucasian (Polish) arginine/proline (arg/pro) heterozygote subjects.	Proline	185-188	P53	Homo sapiens	48-51
12402298-6	2002	With formamidopyrimidine-DNA glycosylase treatment, N-OH-AF induced cleavage at guanine residues, especially of the ACG sequence complementary to codon 273, a well-known hot spot of the p53 gene.	formamidopyrimidine	5-24	P53	Homo sapiens	186-189
21832879-5	2011	DPI-mediated apoptosis in mutant p53 cells was counteracted by 2.77 mM glucose or pyruvate, but not by lactate supplementation.	diphenyleneiodonium	0-3	P53	Homo sapiens	33-36
21832879-7	2011	Our results show for the first time that melanoma cells harbouring a p53 (R175H) mutation increase: a) survival under glucose depletion, counteracted by NADPH-oxidase modulators like DPI; b) resistance to DPI when supplemented with exogenous pyruvate.	diphenyleneiodonium	183-186	P53	Homo sapiens	69-72
16193384-0	2005	Inactivation of p53 sensitizes astrocytic glioma cells to BCNU and temozolomide, but not cisplatin.	Carmustine	58-62	P53	Homo sapiens	16-19
21832879-7	2011	Our results show for the first time that melanoma cells harbouring a p53 (R175H) mutation increase: a) survival under glucose depletion, counteracted by NADPH-oxidase modulators like DPI; b) resistance to DPI when supplemented with exogenous pyruvate.	diphenyleneiodonium	205-208	P53	Homo sapiens	69-72
16193384-1	2005	p53 inactivation sensitizes U87MG astrocytic glioma cells to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and temozolomide (TMZ), drugs used clinically to treat high-grade astrocytomas.	Carmustine	61-97	P53	Homo sapiens	0-3
16193384-1	2005	p53 inactivation sensitizes U87MG astrocytic glioma cells to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and temozolomide (TMZ), drugs used clinically to treat high-grade astrocytomas.	Carmustine	99-103	P53	Homo sapiens	0-3
12386819-8	2002	These results strongly suggested that p130 and its truncated form might substitute Rb in mediating p53-induced cell cycle arrest in Rb(-/-) Saos2 cells.	Rubidium	83-85	P53	Homo sapiens	99-102
21943426-8	2011	Further local structure analyses revealed that, guided by all-atom MD ensemble of fragments, the p53 N-terminal domain ensemble was biased to kinked structures in the AD1 region and biased to extended conformers in a proline-rich region and these biases contributed to improvement of the reproduction of the experiments.	Proline	217-224	P53	Homo sapiens	97-100
12234998-2	2002	We have measured the formation and nucleotide excision repair of covalent DNA adducts formed by the DNA-reactive metabolite of this compound in human fibroblasts, in which expression of the p53 tumor suppressor gene could be controlled by a tetracycline-inducible promoter.	Tetracycline	241-253	P53	Homo sapiens	190-193
11964141-10	2002	These results suggest that p53 is vulnerable to free radical-mediated oxidation at cysteine residues.	Free Radicals	48-60	P53	Homo sapiens	27-30
12144822-2	2002	A common polymorphism of p53 in exon 4 codon 72, resulting in either proline (Pro) or arginine (Arg), affects HPV16/18 E6-mediated degradation of p53 protein in vivo.	Proline	69-76	P53	Homo sapiens	25-28
16193384-3	2005	Compared to control cells with intact p53 function, derived lines in which p53 was inactivated displayed significantly reduced clonogenic survival after exposure to BCNU and TMZ.	Carmustine	165-169	P53	Homo sapiens	75-78
16193384-5	2005	These findings suggest that enhanced sensitivity to BCNU and TMZ is a general property of human astrocytic glioma cells in which p53 was disrupted.	Carmustine	52-56	P53	Homo sapiens	129-132
15998635-0	2005	Reactivation of mutant p53 and induction of apoptosis in human tumor cells by maleimide analogs.	maleimide	78-87	P53	Homo sapiens	23-26
15998635-2	2005	We demonstrate here that the maleimide-derived molecule MIRA-1 can reactivate DNA binding and preserve the active conformation of mutant p53 protein in vitro and restore transcriptional transactivation to mutant p53 in living cells.	maleimide	29-38	P53	Homo sapiens	137-140
15998635-2	2005	We demonstrate here that the maleimide-derived molecule MIRA-1 can reactivate DNA binding and preserve the active conformation of mutant p53 protein in vitro and restore transcriptional transactivation to mutant p53 in living cells.	maleimide	29-38	P53	Homo sapiens	212-215
15998635-3	2005	MIRA-1 induced mutant p53-dependent cell death in different human tumor cells carrying tetracycline-regulated mutant p53.	Tetracycline	87-99	P53	Homo sapiens	22-25
12144822-2	2002	A common polymorphism of p53 in exon 4 codon 72, resulting in either proline (Pro) or arginine (Arg), affects HPV16/18 E6-mediated degradation of p53 protein in vivo.	Proline	69-76	P53	Homo sapiens	146-149
12144822-2	2002	A common polymorphism of p53 in exon 4 codon 72, resulting in either proline (Pro) or arginine (Arg), affects HPV16/18 E6-mediated degradation of p53 protein in vivo.	Proline	78-81	P53	Homo sapiens	25-28
12144822-2	2002	A common polymorphism of p53 in exon 4 codon 72, resulting in either proline (Pro) or arginine (Arg), affects HPV16/18 E6-mediated degradation of p53 protein in vivo.	Proline	78-81	P53	Homo sapiens	146-149
15998635-3	2005	MIRA-1 induced mutant p53-dependent cell death in different human tumor cells carrying tetracycline-regulated mutant p53.	Tetracycline	87-99	P53	Homo sapiens	117-120
21855354-0	2011	Design, synthesis, and biological evaluation of imidazoline derivatives as p53-MDM2 binding inhibitors.	Imidazolines	48-59	P53	Homo sapiens	75-78
15800902-0	2005	Pharmaceutical-mediated inactivation of p53 sensitizes U87MG glioma cells to BCNU and temozolomide.	Carmustine	77-81	P53	Homo sapiens	40-43
16109171-1	2005	BACKGROUND: A common sequence polymorphism at codon 72 of the p53 gene encoding either arginine or proline was recently shown to be functionally relevant for apoptosis induction in vitro.	Proline	99-106	P53	Homo sapiens	62-65
12144822-7	2002	The frequency of distribution of the three genotypes of p53 codon 72 in a subgroup of the HPV16/18-positive cervical cancer patients was Pro/Pro 0.18 and Arg/Arg 0.26, with the heterozygous Pro/Arg 0.56, differing significantly from the genotype frequency in the normal healthy women (chi(2) = 6.928, df = 2, P &lt; 0.05).	Proline	137-140	P53	Homo sapiens	56-59
12144822-7	2002	The frequency of distribution of the three genotypes of p53 codon 72 in a subgroup of the HPV16/18-positive cervical cancer patients was Pro/Pro 0.18 and Arg/Arg 0.26, with the heterozygous Pro/Arg 0.56, differing significantly from the genotype frequency in the normal healthy women (chi(2) = 6.928, df = 2, P &lt; 0.05).	Proline	141-144	P53	Homo sapiens	56-59
15950406-2	2005	The protein and mRNA levels of p53 in L-02 cells were measured after in vitro cultured L-02 was exposed to sodium fluoride at different doses (40, 80, and 160 microg/ml) for 24 h. The results showed that the cell survival rate of L-02 cells in the high dose fluoride group was significantly lower than that of the control group.	Sodium Fluoride	107-122	P53	Homo sapiens	31-34
21855354-1	2011	Three series of novel imidazoline derivatives were designed, synthesized, and evaluated for their p53-MDM2 binding inhibitory activities, and anti-proliferation activities against PC3, A549, KB, and HCT116 cancer cell lines.	Imidazolines	22-33	P53	Homo sapiens	98-101
12127985-6	2002	MG132 or actinomycin D both led to a significant increase in p53, but the expressions of the p53 response proteins increased only in MG132 treated chondrocytes.	Dactinomycin	9-22	P53	Homo sapiens	61-64
21667044-5	2011	Specifically, we found naphthazarin inhibited the PI3K/Akt cell survival signalling pathway, measured by p53 and caspase-3 activation, and PARP cleavage.	naphthazarin	23-35	P53	Homo sapiens	105-108
12096336-6	2002	Using tetracycline-regulated retroviral vectors for conditional expression of p53 mutants, we found that transcription of the dUTPase gene is increased within 24 h after tetracycline withdrawal, and the cells acquire higher resistance to 5-FU.	Tetracycline	6-18	P53	Homo sapiens	78-81
12096336-6	2002	Using tetracycline-regulated retroviral vectors for conditional expression of p53 mutants, we found that transcription of the dUTPase gene is increased within 24 h after tetracycline withdrawal, and the cells acquire higher resistance to 5-FU.	Tetracycline	170-182	P53	Homo sapiens	78-81
12084746-8	2002	RESULTS: There were significant differences in the distribution of the polymorphism between the control subjects and the POAG patients (p = 0.00782) The proline form of p53 gene codon 72 appears to be a significant risk factor in the development of POAG (odds ratio 2.389, 95% confidence interval: 1.14 to 5.01).	Proline	153-160	P53	Homo sapiens	169-172
16061648-8	2005	Stabilization of p53 by FIP200 could be partially reversed by NQO1 inhibitor, dicoumarol.	Dicumarol	78-88	P53	Homo sapiens	17-20
16082197-3	2005	Studies on the tumor suppressor p53 have indeed demonstrated that poly-ubiquitination of p53 by different E3 ubiquin ligases targets p53 for degradation by the 26S proteasomes.	ubiquin	109-116	P53	Homo sapiens	32-35
21548882-0	2011	Metabolic oxidative stress elicited by the copper(II) complex [Cu(isaepy)2] triggers apoptosis in SH-SY5Y cells through the induction of the AMP-activated protein kinase/p38MAPK/p53 signalling axis: evidence for a combined use with 3-bromopyruvate in neuroblastoma treatment.	cupric ion	43-53	P53	Homo sapiens	178-181
16082197-3	2005	Studies on the tumor suppressor p53 have indeed demonstrated that poly-ubiquitination of p53 by different E3 ubiquin ligases targets p53 for degradation by the 26S proteasomes.	ubiquin	109-116	P53	Homo sapiens	89-92
16082197-3	2005	Studies on the tumor suppressor p53 have indeed demonstrated that poly-ubiquitination of p53 by different E3 ubiquin ligases targets p53 for degradation by the 26S proteasomes.	ubiquin	109-116	P53	Homo sapiens	89-92
12036943-4	2002	To test this hypothesis, the effect of exogenous mutant p53 protein expression on genomic instability in human p53-/- Saos-2 cells was measured by the frequency of formation of N-(phosphoacetyl)-L-aspartate (PALA)-resistant (PALA(R)) colonies, mediated by gene amplification.	(phosphoacetyl)-l-aspartate	179-206	P53	Homo sapiens	56-59
15999534-4	2005	The results also demonstrated that 3-hydroxycinnamic acid increased the expression of p53, caspase-3, Bax and cyclin B.	3-coumaric acid	35-57	P53	Homo sapiens	86-89
21548882-0	2011	Metabolic oxidative stress elicited by the copper(II) complex [Cu(isaepy)2] triggers apoptosis in SH-SY5Y cells through the induction of the AMP-activated protein kinase/p38MAPK/p53 signalling axis: evidence for a combined use with 3-bromopyruvate in neuroblastoma treatment.	bis((2-oxindol-3-ylimino)-2-(2-aminoethyl)pyridine-N,N')copper(II)	63-74	P53	Homo sapiens	178-181
15999534-5	2005	These results demonstrated that 3-hydroxycinnamic acid induced apoptosis through p53- and caspase-3-dependent pathways.	3-coumaric acid	32-54	P53	Homo sapiens	81-84
12060632-12	2002	The 64 DCC-positive patients with wild p53, N-ras, and FLT3 had statistically better CR attainment compared with the other 106 patients (P &lt; 0.0001).	Chromium	85-87	P53	Homo sapiens	39-42
21548882-1	2011	We have demonstrated previously that the complex bis[(2-oxindol-3-ylimino)-2-(2-aminoethyl)pyridine-N,N"]copper(II), named [Cu(isaepy)(2)], induces AMPK (AMP-activated protein kinase)-dependent/p53-mediated apoptosis in tumour cells by targeting mitochondria.	bis[(2-oxindol-3-ylimino)-2-(2-aminoethyl)pyridine-n,n"]copper	49-111	P53	Homo sapiens	194-197
22103129-4	2011	PDMS-based microfluidic chips with pillar structure were prepared for the detection of exon 7 of p53 gene by using QD-DNA probe attached to polystyrene micro beads.	Polystyrenes	140-151	P53	Homo sapiens	97-100
11947902-10	2002	Stabilisation of p53 was prevented by preincubation with the NO-donor GSNO or 8-br-cGMP, thus implying a downmodulatory effect of cGMP on pathways that upregulate the tumor suppressor p53.	8-bromoguanosino-3',5'-cyclic monophosphorothioate	78-87	P53	Homo sapiens	17-20
11947902-10	2002	Stabilisation of p53 was prevented by preincubation with the NO-donor GSNO or 8-br-cGMP, thus implying a downmodulatory effect of cGMP on pathways that upregulate the tumor suppressor p53.	8-bromoguanosino-3',5'-cyclic monophosphorothioate	78-87	P53	Homo sapiens	184-187
11894136-2	2002	CPT and homocamptothecin (hCPT), derivative with enhanced lactone stability, induced growth inhibition in HT29 cells via p53-independent apoptosis.	homocamptothecin	8-24	P53	Homo sapiens	121-124
15964795-5	2005	Proline 82 of p53 was identified to be essential for its interaction with the checkpoint kinase 2 (Chk2) and consequent phosphorylation of p53 on serine 20, following DNA damage.	Proline	0-7	P53	Homo sapiens	14-17
15964795-5	2005	Proline 82 of p53 was identified to be essential for its interaction with the checkpoint kinase 2 (Chk2) and consequent phosphorylation of p53 on serine 20, following DNA damage.	Proline	0-7	P53	Homo sapiens	139-142
21519790-0	2011	Histone deacetylase inhibitors, valproic acid and trichostatin-A induce apoptosis and affect acetylation status of p53 in ERG-positive prostate cancer cells.	Valproic Acid	32-45	P53	Homo sapiens	115-118
15865936-0	2005	Fenretinide: a p53-independent way to kill cancer cells.	Fenretinide	0-11	P53	Homo sapiens	15-18
15865936-4	2005	Increased evidence suggests that the apoptotic pathway activated by fenretinide is p53-independent and this may represent a novel way to treat tumors resistant to DNA-damaging chemotherapeutic agents.	Fenretinide	68-79	P53	Homo sapiens	83-86
11807792-3	2002	A common polymorphism of p53, encoding either proline (Pro) or arginine (Arg) at position 72, affects the susceptibility of p53 to E6 mediated degradation in vivo.	Proline	46-53	P53	Homo sapiens	25-28
11807792-3	2002	A common polymorphism of p53, encoding either proline (Pro) or arginine (Arg) at position 72, affects the susceptibility of p53 to E6 mediated degradation in vivo.	Proline	46-53	P53	Homo sapiens	124-127
11807792-3	2002	A common polymorphism of p53, encoding either proline (Pro) or arginine (Arg) at position 72, affects the susceptibility of p53 to E6 mediated degradation in vivo.	Proline	55-58	P53	Homo sapiens	25-28
11807792-3	2002	A common polymorphism of p53, encoding either proline (Pro) or arginine (Arg) at position 72, affects the susceptibility of p53 to E6 mediated degradation in vivo.	Proline	55-58	P53	Homo sapiens	124-127
15878356-0	2005	Isoliquiritigenin induces apoptosis and cell cycle arrest through p53-dependent pathway in Hep G2 cells.	isoliquiritigenin	0-17	P53	Homo sapiens	66-69
21519790-11	2011	We found that VPA and TSA induce apoptosis, upregulate p21/Waf1/CIP1, repress TMPRSS2-ERG expression and affect acetylation status of p53 in VCaP cells.	Valproic Acid	14-17	P53	Homo sapiens	134-137
21561866-5	2011	Knockdown of S27a significantly attenuates the p53 activation in cells in response to treatment with ribosomal stress-inducing agent actinomycin D or 5-fluorouracil.	Dactinomycin	133-146	P53	Homo sapiens	47-50
15746940-2	2005	While p53 is constitutively acetylated at Lys320 in LNCaP cells, treatment with CG-1521, stabilizes the acetylation of p53 at Lys373, elevating p21 (and inducing cell cycle arrest).	cysteinylglycine	80-82	P53	Homo sapiens	119-122
15809436-2	2005	NQO1 binds and stabilizes WT p53, whereas NQO1 inhibitors including dicoumarol and various other coumarins and flavones induce ubiquitin-independent proteasomal p53 degradation and thus inhibit p53-induced apoptosis.	Dicumarol	68-78	P53	Homo sapiens	161-164
15625077-8	2005	Thus, in HepG2 cells pravastatin and simvastatin pretreatment attenuated the p53 response to DNA damage induced by 5-fluorouracil and benzo(a)pyrene.	Pravastatin	21-32	P53	Homo sapiens	77-80
15625077-13	2005	We also show that the p53 response to a challenging dose of diethylnitrosamine was attenuated in hepatocytes in situ and in primary cultures of hepatocytes by pravastatin pretreatment.	Pravastatin	159-170	P53	Homo sapiens	22-25
11756188-3	2002	CDDO-Me decreased the viability of leukemic cell lines, including multidrug resistant (MDR)-1-overexpressing, p53(null) HL-60-Dox and of primary AML cells, and it was 3- to 5-fold more active than CDDO.	2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid	0-4	P53	Homo sapiens	110-113
11786482-0	2002	Sodium butyrate induces P53-independent, Fas-mediated apoptosis in MCF-7 human breast cancer cells.	Butyric Acid	0-15	P53	Homo sapiens	24-27
21269693-0	2011	Dimethyl sulfoxide activates tumor necrosis factoralpha-p53 mediated apoptosis and down regulates D-fructose-6-phosphate-2-kinase and lactate dehydrogenase-5 in Dalton"s lymphoma in vivo.	Dimethyl Sulfoxide	0-18	P53	Homo sapiens	56-59
11807952-4	2002	Western immunoblot analyses of MCF7 human mammary cancer cells exposed to actinomycin D (used as a positive control for G(1) cell-cycle arrest) or hydrocarbon carcinogens revealed that while all of these chemicals caused an increase in p53, only trace levels of p21(waf1/cip1) protein were observed in the hydrocarbon carcinogen-treated samples.	Dactinomycin	74-87	P53	Homo sapiens	236-239
11698345-0	2001	Mutational spectrum induced by acetaldehyde in the HPRT gene of human T lymphocytes resembles that in the p53 gene of esophageal cancers.	Acetaldehyde	31-43	P53	Homo sapiens	106-109
15932166-0	2005	p53 immunohistochemical expression in Barrett"s esophagus before and after endoscopic ablation by argon plasma coagulation.	Argon	98-103	P53	Homo sapiens	0-3
15720190-10	2005	Small molecules that have been reported to disrupt the p53-MDM2 binding, thereby enhancing p53 activity to elicit anticancer effects include the following: synthetic chalcones, norbornane derivatives, cis-imidazoline derivatives (Nutlins), a pyrazolidinedione sulfonamide and 1,4-benzodiazepine-2,5-diones, as well as tryptophan derivatives.	Bz-423	276-305	P53	Homo sapiens	55-58
15720190-10	2005	Small molecules that have been reported to disrupt the p53-MDM2 binding, thereby enhancing p53 activity to elicit anticancer effects include the following: synthetic chalcones, norbornane derivatives, cis-imidazoline derivatives (Nutlins), a pyrazolidinedione sulfonamide and 1,4-benzodiazepine-2,5-diones, as well as tryptophan derivatives.	Bz-423	276-305	P53	Homo sapiens	91-94
11710596-3	2001	STUDY DESIGN: Immunohistochemical staining for detecting VEGF protein, factor VIII-related antigen of endothelial cells, and p53 protein was performed by the labeled streptavidin-biotin method on the formalin-fixed and paraffin-embedded tumor tissue of 104 patients with endometrial (endometrioid) carcinoma, including 69 with well-differentiated, 25 with moderately differentiated, and ten with poorly differentiated adenocarcinoma.	Biotin	179-185	P53	Homo sapiens	125-128
21269693-3	2011	This article describes that DMSO, being non-toxic to the normal lymphocytes, up regulated TNFalpha and p53, declined Bcl-2/Bax ratio, activated caspase 9 and PARP-1 cleavage and produced apoptotic pattern of DNA ladder in Dalton"s lymphoma (DL) in vivo.	Dimethyl Sulfoxide	28-32	P53	Homo sapiens	103-106
15713892-0	2005	Silymarin induces apoptosis primarily through a p53-dependent pathway involving Bcl-2/Bax, cytochrome c release, and caspase activation.	Silymarin	0-9	P53	Homo sapiens	48-51
21269693-5	2011	The findings suggest induction of TNFalpha-p53-mitochondrial pathway of apoptosis by DMSO in a non-Hodgkin"s lymphoma and support evolving concept of glycolytic inhibition led apoptosis in a tumor cell in vivo.	Dimethyl Sulfoxide	85-89	P53	Homo sapiens	43-46
15713892-3	2005	Here, we report that treatment of JB6 C141 cells (preneoplastic epidermal keratinocytes) and p53+/+ fibroblasts with silymarin and silibinin (a major constituent of silymarin) resulted in a dose-dependent inhibition of cell viability and induction of apoptosis in an identical manner.	Silymarin	117-126	P53	Homo sapiens	93-96
15713892-5	2005	The silymarin-induced apoptosis was primarily p53 dependent because apoptosis occurred to a much greater extent in the cells expressing wild-type p53 (p53+/+, 9-61%) than in p53-deficient cells (p53-/-, 6-20%).	Silymarin	4-13	P53	Homo sapiens	46-49
11489880-2	2001	In the present study, we investigated this cell death pathway by stably transfecting the p53-null H358 cell line with a tetracycline-dependent wild type p53-expressing vector.	Tetracycline	120-132	P53	Homo sapiens	89-92
11489880-2	2001	In the present study, we investigated this cell death pathway by stably transfecting the p53-null H358 cell line with a tetracycline-dependent wild type p53-expressing vector.	Tetracycline	120-132	P53	Homo sapiens	153-156
11489880-3	2001	Restoration of p53 triggered a G(2)/M cell cycle arrest and enhanced BAX protein expression, without inducing apoptosis or potentiating the cytotoxic effect of etoposide, vincristine, and cis-platinum.	Vincristine	171-182	P53	Homo sapiens	15-18
15713892-5	2005	The silymarin-induced apoptosis was primarily p53 dependent because apoptosis occurred to a much greater extent in the cells expressing wild-type p53 (p53+/+, 9-61%) than in p53-deficient cells (p53-/-, 6-20%).	Silymarin	4-13	P53	Homo sapiens	146-149
21702904-4	2011	Low and high prevalence E6 variants displayed similar abilities in abrogation of growth arrest and inhibition of p53 elevation induced by actinomycin D.	Dactinomycin	138-151	P53	Homo sapiens	113-116
15713892-5	2005	The silymarin-induced apoptosis was primarily p53 dependent because apoptosis occurred to a much greater extent in the cells expressing wild-type p53 (p53+/+, 9-61%) than in p53-deficient cells (p53-/-, 6-20%).	Silymarin	4-13	P53	Homo sapiens	146-149
15713892-5	2005	The silymarin-induced apoptosis was primarily p53 dependent because apoptosis occurred to a much greater extent in the cells expressing wild-type p53 (p53+/+, 9-61%) than in p53-deficient cells (p53-/-, 6-20%).	Silymarin	4-13	P53	Homo sapiens	146-149
15713892-5	2005	The silymarin-induced apoptosis was primarily p53 dependent because apoptosis occurred to a much greater extent in the cells expressing wild-type p53 (p53+/+, 9-61%) than in p53-deficient cells (p53-/-, 6-20%).	Silymarin	4-13	P53	Homo sapiens	146-149
15713892-11	2005	These observations show that silymarin-induced apoptosis is primarily p53 dependent and mediated through the activation of caspase-3.	Silymarin	29-38	P53	Homo sapiens	70-73
15842803-2	2005	METHODS: Four different p53-GST (glutathione S-transferase) fusion proteins and GST were expressed in E. coli and purified through glutathione sepharose 4B beads.	Sepharose	143-152	P53	Homo sapiens	24-27
11536301-4	2001	METHODS: A conditional eukaryotic expression vector (under tetracycline regulation) expressing antisense p53 cDNA was constructed and either directly transfected into LNCaP cells or tranduced into these cells using recombinant retroviruses containing the vector.	Tetracycline	59-71	P53	Homo sapiens	105-108
21406194-6	2011	Using a modified biotin switch assay we demonstrated that NO-ASA S-nitrosylates the signaling proteins p53, beta-catenin, and NF-kappaB, in colon cancer cells in a time- and concentration-dependent manner.	Biotin	17-23	P53	Homo sapiens	103-106
11571642-0	2001	p53 binds the nuclear matrix in normal cells: binding involves the proline-rich domain of p53 and increases following genotoxic stress.	Proline	67-74	P53	Homo sapiens	0-3
11571642-0	2001	p53 binds the nuclear matrix in normal cells: binding involves the proline-rich domain of p53 and increases following genotoxic stress.	Proline	67-74	P53	Homo sapiens	90-93
11571642-7	2001	However, the proline-rich domain towards the N-terminus of p53 (residues 67 to 98) appeared important for binding to the nuclear matrix.	Proline	13-20	P53	Homo sapiens	59-62
11571642-9	2001	The proline-rich domain of p53 has potential for SH3 protein-protein interaction, and has a role in p53-mediated apoptosis and possibly base excision repair of DNA damage.	Proline	4-11	P53	Homo sapiens	27-30
11571642-9	2001	The proline-rich domain of p53 has potential for SH3 protein-protein interaction, and has a role in p53-mediated apoptosis and possibly base excision repair of DNA damage.	Proline	4-11	P53	Homo sapiens	100-103
16122882-1	2005	BACKGROUND: The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene has been implicated in increasing susceptibility of the cervix to human papillomavirus (HPV) infection and thus altering cancer risk.	Proline	44-47	P53	Homo sapiens	78-81
16122882-1	2005	BACKGROUND: The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene has been implicated in increasing susceptibility of the cervix to human papillomavirus (HPV) infection and thus altering cancer risk.	Proline	51-54	P53	Homo sapiens	78-81
16122882-1	2005	BACKGROUND: The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene has been implicated in increasing susceptibility of the cervix to human papillomavirus (HPV) infection and thus altering cancer risk.	Proline	51-54	P53	Homo sapiens	78-81
15732191-9	2005	Replacement of arginine (Arg) by proline (Pro) at position 72 of human p53 decreases its apoptotic potential [Dumont et al., 2003.	Proline	33-40	P53	Homo sapiens	71-74
15732191-9	2005	Replacement of arginine (Arg) by proline (Pro) at position 72 of human p53 decreases its apoptotic potential [Dumont et al., 2003.	Proline	42-45	P53	Homo sapiens	71-74
11399766-10	2001	Certain BLM mutants (C1055S or Delta133-237) that have a reduced ability to localize to the NBs when expressed in normal cells can impair the localization of wild type BLM to NBs and block p53-mediated apoptosis, suggesting a dominant-negative effect.	Bromosuccinimide	92-95	P53	Homo sapiens	189-192
11399766-11	2001	Taken together, our results indicate both a novel mechanism of p53 function by which p53 mediates nuclear trafficking of BLM to NBs and the cooperation of p53 and BLM to induce apoptosis.	Bromosuccinimide	128-131	P53	Homo sapiens	63-66
11399766-11	2001	Taken together, our results indicate both a novel mechanism of p53 function by which p53 mediates nuclear trafficking of BLM to NBs and the cooperation of p53 and BLM to induce apoptosis.	Bromosuccinimide	128-131	P53	Homo sapiens	85-88
21480648-8	2011	In addition, the distinct p53 activation profile of 1 compared with cisplatin provides an explanation for the activity of this ruthenium drug against cisplatin-resistant cells.	Ruthenium	127-136	P53	Homo sapiens	26-29
11399766-11	2001	Taken together, our results indicate both a novel mechanism of p53 function by which p53 mediates nuclear trafficking of BLM to NBs and the cooperation of p53 and BLM to induce apoptosis.	Bromosuccinimide	128-131	P53	Homo sapiens	85-88
11375983-3	2001	When ectopic wild-type p53 expression was induced to a physiologically relevant level in "tet-off" cultured cells in which p53 expression was tightly regulated by tetracycline, it was found that POLD1 steady-state mRNA was repressed by about 65%.	Tetracycline	163-175	P53	Homo sapiens	23-26
11375983-3	2001	When ectopic wild-type p53 expression was induced to a physiologically relevant level in "tet-off" cultured cells in which p53 expression was tightly regulated by tetracycline, it was found that POLD1 steady-state mRNA was repressed by about 65%.	Tetracycline	163-175	P53	Homo sapiens	123-126
15901131-5	2005	Intermediate expression of p53 was noted in cells with missense mutations or polymorphism to proline at codon 72 in exons 4-5, whereas there was slight or no visible expression in wild type cells and in cells with nonsense and frameshift mutations.	Proline	93-100	P53	Homo sapiens	27-30
15844595-1	2005	OBJECTIVE: To investigate the codon-72 polymorphism of the tumor suppressor gene p53, codon-72 encodes arginine (Arg) or proline (Pro) for a genetic predisposition,to keloid or hypertrophic scar.	Proline	130-133	P53	Homo sapiens	81-84
21463108-6	2011	Both dATP and CdATP cause an initial accumulation of DNA strand breaks in lymphocytes and this results in the activation of p53, the release of cytochrome c from mitochondria, and apoptosis.	cdatp	14-19	P53	Homo sapiens	124-127
11463759-8	2001	Moreover, upregulation of p53, a proapoptotic molecule, was observed in hypoxia, whereas treatment with probucol attenuated the expression of p53 accompanied by suppression of NF-kappaB activation.	Probucol	104-112	P53	Homo sapiens	142-145
15371422-5	2004	The integrity of the DNA-binding core domain, the N-terminal transactivation domain, and the C-terminal oligomerization domains of p53 was essential for hTERT promoter repression, whereas the proline-rich domain and the extreme C terminus were not required.	Proline	192-199	P53	Homo sapiens	131-134
21120637-6	2011	Remarkably, the synergistic effect of 8-Br-cAMP and VPA on cellular reprogramming may be due to the transient decrease of p53 protein during the early stages of reprogramming.	Valproic Acid	52-55	P53	Homo sapiens	122-125
21562496-2	2011	Here, we report that histone deacetylase inhibitors (HDACI), that is, MS-275, valproic acid or SAHA, provide a novel strategy for sensitization of medulloblastoma to DNA-damaging drugs such as Doxorubicin, VP16 and Cisplatin by promoting p53-dependent, mitochondrial apoptosis.	Valproic Acid	78-91	P53	Homo sapiens	238-241
15297371-10	2004	In conclusion, FTY720 is a novel anticancer agent that induces apoptosis of hepatoma cell lines both in vitro and in vivo through PI3-K-mediated Akt dephosphorylation in a p53-independent manner.	Fingolimod Hydrochloride	15-21	P53	Homo sapiens	172-175
11359905-0	2001	The corepressor mSin3a interacts with the proline-rich domain of p53 and protects p53 from proteasome-mediated degradation.	Proline	42-49	P53	Homo sapiens	65-68
11359905-4	2001	Stabilization of p53 by Sin3 requires the Sin3-binding domain, determined here to map to the proline-rich region of p53, from amino acids 61 to 75.	Proline	93-100	P53	Homo sapiens	17-20
11359905-4	2001	Stabilization of p53 by Sin3 requires the Sin3-binding domain, determined here to map to the proline-rich region of p53, from amino acids 61 to 75.	Proline	93-100	P53	Homo sapiens	116-119
21542687-1	2011	AIM: The objective of the present study is to prepare and characterize nutlin-3a loaded polymeric poly(lactide-co-glycolide) nanoparticles (NPs) surface functionalized with transferrin ligand, to deliver the encapsulated drug in a targeted manner to its site of action and to evaluate the efficacy of the nanoformulation in terms of its cellular uptake, cell cytotoxicity, cell cycle arrest, apoptosis and activation of p53 pathway at molecular level in MCF-7 breast cancer cell line.	Polyglactin 910	98-123	P53	Homo sapiens	420-423
11323395-0	2001	Mechanisms of Cr(VI)-induced p53 activation: the role of phosphorylation, mdm2 and ERK.	Chromium	14-16	P53	Homo sapiens	29-32
11323395-4	2001	The degradation of p53 was dramatically decreased upon stimulation by Cr(VI).	Chromium	70-72	P53	Homo sapiens	19-22
15365822-2	2004	A recent report suggests that a polymorphism of the p53 tumor suppressor gene that results in the substitution of a proline residue with an arginine residue at position 72 of the p53 protein might act as a risk factor in the malignant transformation of colorectal adenoma to cancer.	Proline	116-123	P53	Homo sapiens	52-55
15365822-2	2004	A recent report suggests that a polymorphism of the p53 tumor suppressor gene that results in the substitution of a proline residue with an arginine residue at position 72 of the p53 protein might act as a risk factor in the malignant transformation of colorectal adenoma to cancer.	Proline	116-123	P53	Homo sapiens	179-182
21530768-4	2011	The increased potency of bendamustine may be due to secondary mechanisms such as inhibition of mitotic checkpoints, inefficient DNA repair, and initiation of p53-dependent DNA-damage stress response, all of which lead to mitotic catastrophe and apoptosis.	Bendamustine Hydrochloride	25-37	P53	Homo sapiens	158-161
15610529-3	2004	Here, we show that the p53-related gene p73 is a target of tazarotene.	tazarotene	59-69	P53	Homo sapiens	23-26
11280728-0	2001	Proline oxidase, encoded by p53-induced gene-6, catalyzes the generation of proline-dependent reactive oxygen species.	Proline	76-83	P53	Homo sapiens	28-31
11280728-1	2001	The p53-dependent initiation of apoptosis is accompanied by the induction of proline oxidase (POX), a mitochondrial enzyme catalyzing the conversion of proline to pyrroline-5-carboxylate with the concomitant transfer of electrons to cytochrome c.	Proline	77-84	P53	Homo sapiens	4-7
21394211-3	2011	Here, we have analyzed the p53-regulated pathways induced by Actinomycin D and Etoposide treatment resulting in more growth arrested versus apoptotic cells respectively.	Dactinomycin	61-74	P53	Homo sapiens	27-30
11372187-17	2001	Functional mutations within the p53 gene were considered a possible reason for the absence of apoptosis induction by ALA-PDT.	5-amino levulinic acid	117-120	P53	Homo sapiens	32-35
15533911-1	2004	A polymorphism at codon 72 of the human tumor suppressor p53 determines translation into either arginine or proline.	Proline	108-115	P53	Homo sapiens	57-60
15540942-8	2004	BA-1,2-dihydrodiol induced a Fpg sensitive and piperidine labile G lesion at the 5"-ACG-3" sequence complementary to codon 273 of the human p53 tumor suppressor gene, which is known as a hotspot.	piperidine	47-57	P53	Homo sapiens	140-143
21123835-8	2011	We observed an association between TP53 alterations in the tumors and constitutive TP53 genotype (P &lt; 0.01), with alterations preferentially occurring on the proline allele.	Proline	161-168	P53	Homo sapiens	35-39
15258255-10	2004	In marked contrast, disruption of p53 and p21 was associated with increased sensitivity to C-1305.	C 1305	91-97	P53	Homo sapiens	34-37
15269203-10	2004	In addition, it was shown that NBS1, SMC1, and p53 were phosphorylated in an ATM-dependent manner, and p53 phosphorylation on serine 20 is dependent on CHK2 after irofulven treatment.	irofulven	163-172	P53	Homo sapiens	103-106
11168396-2	2001	Significant differences were observed; p53CD produced a relatively small and continuous retardation of scDNA, in contrast to the ladder of distinct bands formed by p53 in agarose gels.	Sepharose	171-178	P53	Homo sapiens	164-167
11669337-10	2001	A common polymorphism in p53 at codon 72 (arginine/proline) was found in 6/8 of the patients.	Proline	51-58	P53	Homo sapiens	25-28
21123835-8	2011	We observed an association between TP53 alterations in the tumors and constitutive TP53 genotype (P &lt; 0.01), with alterations preferentially occurring on the proline allele.	Proline	161-168	P53	Homo sapiens	83-87
20882314-2	2011	Our study proposes to rationally design a p53 antisense oligonucleotide (ASO) repository, which contains a series of ASOs containing single nucleotide differences to discriminate between each mutant and wild type (WT) p53.	Oligonucleotides, Antisense	73-76	P53	Homo sapiens	42-45
11174479-1	2001	OBJECTIVE: It has recently been suggested that white women who are homozygous for the allele of the gene for wild-type p53 protein (TP53) that encodes arginine at position 72 are more susceptible to human papillomavirus-associated cervical carcinoma than are women who are heterozygous for this polymorphism and women who are homozygous for the allele that encodes proline at that position.	Proline	365-372	P53	Homo sapiens	119-122
11174479-1	2001	OBJECTIVE: It has recently been suggested that white women who are homozygous for the allele of the gene for wild-type p53 protein (TP53) that encodes arginine at position 72 are more susceptible to human papillomavirus-associated cervical carcinoma than are women who are heterozygous for this polymorphism and women who are homozygous for the allele that encodes proline at that position.	Proline	365-372	P53	Homo sapiens	132-136
11374803-5	2001	The immunolocalization of P53 protein was performed using the Labelled Streptavidin Biotin (LSAB) method.	Biotin	84-90	P53	Homo sapiens	26-29
15131588-1	2004	A common arginine to proline polymorphism is harboured at codon 72 of the human p53 gene.	Proline	21-28	P53	Homo sapiens	80-83
15273281-3	2004	In this context, the proline form of TP53 codon 72 polymorphism has been recently associated with the risk of developing endometriosis.	Proline	21-28	P53	Homo sapiens	37-41
20882314-2	2011	Our study proposes to rationally design a p53 antisense oligonucleotide (ASO) repository, which contains a series of ASOs containing single nucleotide differences to discriminate between each mutant and wild type (WT) p53.	Oligonucleotides, Antisense	73-76	P53	Homo sapiens	218-221
20882314-3	2011	The Sfold software was used to predict target-accessibility and we designed an initial series of antisense oligonucleotides (ASO) that target the p53 mutants A161T, R175H and R249S.	Oligonucleotides, Antisense	125-128	P53	Homo sapiens	146-149
15548361-0	2004	Selective loss of codon 72 proline p53 and frequent mutational inactivation of the retained arginine allele in colorectal cancer.	Proline	27-34	P53	Homo sapiens	35-38
20882314-5	2011	In three cancer lines harboring each of the p53 mutations, mutant-specific ASO treatment led to a dose-dependent inhibition of cell growth, cell viability, colony formation and invasion, and expression of mutant p53-dependent survival proteins.	Oligonucleotides, Antisense	75-78	P53	Homo sapiens	44-47
15548361-1	2004	According to recent reports, some cancer types exhibit nonrandom allele loss at codon 72 in exon 4 of the p53 gene [coding for proline (72Pro) or arginine (72Arg)].	Proline	127-134	P53	Homo sapiens	106-109
11129289-8	2000	Only tumors injected with SCH58500 had detectable levels of exogenous p53 DNA and mRNA.	sch58500	26-34	P53	Homo sapiens	70-73
11129289-9	2000	After SCH58500 treatment, 3-11-fold elevations of p21 expression were observed in tumor xenografts containing nonfunctional p53 (MDA-MB-468, MDA-MB-231, MIAPaCa2, DU-145, and SK-OV-3), but no change in p21 mRNA in wild-type p53 PA-1 tumors.	sch58500	6-14	P53	Homo sapiens	124-127
15246561-3	2004	ELISA assay demonstrated that acacetin significantly increased the expression of p53 and p21/WAF1 protein, which caused cell cycle arrest.	acacetin	30-38	P53	Homo sapiens	81-84
20882314-5	2011	In three cancer lines harboring each of the p53 mutations, mutant-specific ASO treatment led to a dose-dependent inhibition of cell growth, cell viability, colony formation and invasion, and expression of mutant p53-dependent survival proteins.	Oligonucleotides, Antisense	75-78	P53	Homo sapiens	212-215
20658471-6	2011	The apoptosis induction with liquiritigenin is associated with the up-regulation of p53 and Bax, along with down-regulation of Bcl-2 and survivin.	liquiritigenin	29-43	P53	Homo sapiens	84-87
15073048-0	2004	beta-Carotene exacerbates DNA oxidative damage and modifies p53-related pathways of cell proliferation and apoptosis in cultured cells exposed to tobacco smoke condensate.	beta Carotene	0-13	P53	Homo sapiens	60-63
11027272-5	2000	Likewise, expression of a tetracycline-regulated wild-type p53 cDNA in p53-null fibroblasts caused a reduction in 53BP2 protein levels.	Tetracycline	26-38	P53	Homo sapiens	59-62
11027272-5	2000	Likewise, expression of a tetracycline-regulated wild-type p53 cDNA in p53-null fibroblasts caused a reduction in 53BP2 protein levels.	Tetracycline	26-38	P53	Homo sapiens	71-74
11027272-6	2000	However, 53BP2 levels were not reduced if the tetracycline-regulated p53 cDNA was expressed after UV damage in these cells.	Tetracycline	46-58	P53	Homo sapiens	69-72
15073048-8	2004	In contrast, fibroblasts treated with tar and beta-carotene, after an initial arrest of cell growth at 12 h, re-entered in cell cycle and were unable to undergo apoptosis at 36 h. Concomitantly, their p53 expression, after an increase at 12 h, progressively returned at basal levels at 36 h by a mechanism independent of Mdm2.	beta Carotene	46-59	P53	Homo sapiens	201-204
15253698-7	2004	Indeed, salvage of GTP with guanosine prevented the ischemia-induced increase in p53 protein.	Guanosine	28-37	P53	Homo sapiens	81-84
11032912-0	2000	Combination therapy with SCH58500 (p53 adenovirus) and cyclophosphamide in preclinical cancer models.	sch58500	25-33	P53	Homo sapiens	35-38
20658471-8	2011	Overall, the results indicate that liquiritigenin induces apoptosis in part via the mitochondrial pathway, which is associated with p53 up-regulation, release of cytochrome c and elevated activity of caspase-9 and -3 in HeLa cells.	liquiritigenin	35-49	P53	Homo sapiens	132-135
21264228-10	2011	These results suggest that (1) mitochondrial ROS and NIX are essential factors for MALM, (2) MIV is a novel mechanism for lysosomal degradation of mitochondria, and (3) the p53-Mieap pathway plays a pivotal role in MQC by repairing or eliminating unhealthy mitochondria via MALM or MIV generation, respectively.	Mycinamicin IV	93-96	P53	Homo sapiens	173-176
11032912-2	2000	In preclinical models, SCH58500 has therapeutic efficacy against a wide range of human tumor types containing nonfunctional p53 and it has enhanced activity in combination with many chemotherapeutic drugs.	sch58500	23-31	P53	Homo sapiens	124-127
15363324-11	2004	When treated with LY294002 or U0126 for 24 hours, the amount of wild p53 protein in MCF7-neu3 cells was 1.7 or 1.5 times higher than those in DMSO treated cells.	Dimethyl Sulfoxide	142-146	P53	Homo sapiens	69-72
15183530-0	2004	Proline homozygosity in codon 72 of p53 is a factor of susceptibility for thyroid cancer.	Proline	0-7	P53	Homo sapiens	36-39
15183530-1	2004	A common germline polymorphism of p53 gene produces an Arginine to Proline change at aminoacid position 72.	Proline	67-74	P53	Homo sapiens	34-37
11059778-13	2000	Overall, the data indicate that O6MeG induces apoptosis via secondary lesions that trigger Bcl-2 decline, cytochrome c release, and caspase-9 and caspase-3 activation independently of Fas/Fas ligand and p53, for which the cells are mutated.	O-(6)-methylguanine	32-37	P53	Homo sapiens	203-206
20818437-6	2011	Nuclear localization is a prerequisite for proper functioning of p53 and our results confirm that TPEN, and not Bapta-AM, could abrogate p53 nuclear localization and it interfered with p53 transcriptional activation.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	98-102	P53	Homo sapiens	65-68
11045785-13	2000	In conclusion, the codon 72 germ-line polymorphism (Arg/Pro) of the common tumor suppressor gene p53 contributes to heritable susceptibility for smoke-induced lung adenocarcinoma.	Proline	56-59	P53	Homo sapiens	97-100
15087457-8	2004	In addition, the dependence on p53 was confirmed using a second cell type operating a tetracycline-inducible system.	Tetracycline	86-98	P53	Homo sapiens	31-34
11107048-5	2000	MKN-28 well-differentiated adenocarcinoma cell line reveals mutations in p53 and APC tumor suppressor genes and silencing of CD44.	mkn-28	0-6	P53	Homo sapiens	73-76
20818437-6	2011	Nuclear localization is a prerequisite for proper functioning of p53 and our results confirm that TPEN, and not Bapta-AM, could abrogate p53 nuclear localization and it interfered with p53 transcriptional activation.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	98-102	P53	Homo sapiens	137-140
20818437-6	2011	Nuclear localization is a prerequisite for proper functioning of p53 and our results confirm that TPEN, and not Bapta-AM, could abrogate p53 nuclear localization and it interfered with p53 transcriptional activation.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	98-102	P53	Homo sapiens	137-140
20818437-7	2011	Addition of zinc suppressed the known p53 feedback MDM2 activation, which could be restored by TPEN.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	95-99	P53	Homo sapiens	38-41
20818437-8	2011	Co-immunoprecipitation studies verified that MI-219-mediated MDM2-p53 disruption could be suppressed by TPEN and restored by zinc.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	104-108	P53	Homo sapiens	66-69
11008209-10	2000	This result remained similar (OR 2.2, 95% CI 1.0-4.8 for p53 Pro/Pro vs. Arg/Arg), even after further adjustment for NAT2 and GSTP1 polymorphisms.	Proline	61-64	P53	Homo sapiens	57-60
11008209-10	2000	This result remained similar (OR 2.2, 95% CI 1.0-4.8 for p53 Pro/Pro vs. Arg/Arg), even after further adjustment for NAT2 and GSTP1 polymorphisms.	Proline	65-68	P53	Homo sapiens	57-60
15293391-2	2004	In this study, we prepared an inexpensive linear polyacrylamide (LPA), and successfully applied it to CE-SSCP analysis and tandem CE-SSCP/heteroduplex analysis (HA) of the P53 gene on an ABI capillary genetic analyzer.	lpa	65-68	P53	Homo sapiens	172-175
21790217-3	2011	The ERE-linked p53 gene with the proline variant at codon 72 showed lower transfection rates than the gene without ERE or with the arginine variant at codon 72.	Proline	33-40	P53	Homo sapiens	15-18
15163545-1	2004	It has been reported that the hexavalent chromium compound (Cr(VI)) can induce both p53-dependent and p53-independent apoptosis.	Chromium	41-49	P53	Homo sapiens	84-87
15163545-1	2004	It has been reported that the hexavalent chromium compound (Cr(VI)) can induce both p53-dependent and p53-independent apoptosis.	Chromium	41-49	P53	Homo sapiens	102-105
15163545-4	2004	When human lymphoma U937 cells, p53 mutated cells, were treated with 20 microM Cr(VI) for 24 h, nuclear morphological changes and DNA fragmentation were observed.	Chromium	79-81	P53	Homo sapiens	32-35
10942736-11	2000	Sodium formate and aspirin,.OH radical scavengers, also suppressed p53 activation.	.oh radical	27-38	P53	Homo sapiens	67-70
10942736-13	2000	NADPH, which accelerated the one-electron reduction of Cr(VI) to Cr(V) and increased.OH radical generation, dramatically enhanced p53 activation.	Chromium	55-57	P53	Homo sapiens	130-133
10942736-13	2000	NADPH, which accelerated the one-electron reduction of Cr(VI) to Cr(V) and increased.OH radical generation, dramatically enhanced p53 activation.	Chromium	65-67	P53	Homo sapiens	130-133
21790217-5	2011	We consider that the presence of an upstream ERE promotes the transcriptional effects of the exogenous p53 gene with the proline variant, which strengthens the expression of p21, and results in lower transfection rates through cell cycle inhibition.	Proline	121-128	P53	Homo sapiens	103-106
11042678-1	2000	Resveratrol (3,5,4"-trihydroxy-trans-stilbene), in the concentration range of 20 microM and above, induced arrest in the S-phase and apoptosis in the T cell-derived T-ALL lymphocytic leukemia cell line CEM-C7H2 which is deficient in functional p53 and p16.	3,5,4"-trihydroxy-trans-stilbene	13-45	P53	Homo sapiens	244-247
15105048-3	2004	The p53 gene displays a common genetic Arg/Pro polymorphism at codon 72 with functional significance, that has been investigated as risk factor in several cancer models.	Proline	43-46	P53	Homo sapiens	4-7
21631964-8	2011	It can be concluded that: 1) mitoxantrone- induced phosphorylation of p53 on serine 15 and serine 392 is ATM dependent and MEK1/2-ERK1/2 independent.	Mitoxantrone	29-41	P53	Homo sapiens	70-73
14990579-7	2004	Tetracycline-regulated IFI16 also induced apoptosis when coexpressed with p53 in p53-deficient EJ cells subjected to IR, suggesting that IFI16 is involved in p53-mediated transmission of apoptosis signaling.	Tetracycline	0-12	P53	Homo sapiens	74-77
14990579-7	2004	Tetracycline-regulated IFI16 also induced apoptosis when coexpressed with p53 in p53-deficient EJ cells subjected to IR, suggesting that IFI16 is involved in p53-mediated transmission of apoptosis signaling.	Tetracycline	0-12	P53	Homo sapiens	81-84
14990579-7	2004	Tetracycline-regulated IFI16 also induced apoptosis when coexpressed with p53 in p53-deficient EJ cells subjected to IR, suggesting that IFI16 is involved in p53-mediated transmission of apoptosis signaling.	Tetracycline	0-12	P53	Homo sapiens	81-84
11240705-1	2000	Recent analysis of the codon-72 polymorphism of the p53 gene, the allele encoding proline or arginine, suggested that the homozygous Arg/Arg genotype is a significant risk factor for cervical cancer associated with human papillomavirus (HPV).	Proline	82-89	P53	Homo sapiens	52-55
10900010-4	2000	Here we show that treatment with the small molecule nuclear export inhibitor, leptomycin B, and actinomycin D leads to the accumulation of transcriptionally active p53 in the nucleus of HeLa, CaSki, and SiHa cells.	Dactinomycin	96-109	P53	Homo sapiens	164-167
10854536-3	2000	p53 expression was examined by immunohistochemical staining using the streptavidin-biotin method.	Biotin	83-89	P53	Homo sapiens	0-3
21631964-9	2011	2) ATM inhibition by caffeine prevents G2 cell arrest and in p53-positive cells MOLT-4 delays the onset of mitoxantrone-induced cell death.	Mitoxantrone	107-119	P53	Homo sapiens	61-64
18969416-1	2004	In combination with abasic site (AP site)-containing oligodeoxynucleotides (ODNs), we demonstrate potential use of a hydrogen bond forming ligand, 2-amino-7-methyl-1,8-naphthyridine (AMND), for the fluorescence detection of the cytosine (C)/guanine (G) mutation sequence of the cancer repression gene p53.	2-amino-7-methyl-1,8-naphthyridine	147-181	P53	Homo sapiens	301-304
21778786-0	2011	P53 codon 72 (Arg72Pro) polymorphism and prostate cancer risk: association between disease onset and proline genotype.	Proline	101-108	P53	Homo sapiens	0-3
15111320-6	2004	The Ishikawa cell line, with stable or tetracycline-regulated expression of mutant beta-catenin, showed an increase in expression levels of cyclin D1, p14ARF, p53, and p21WAF1 but not PML, and activation of beta-catenin-TCF4-mediated transcription determined with TOP/FOP constructs.	Tetracycline	39-51	P53	Homo sapiens	159-162
12578696-4	2000	Compare with previously untreated AL, relapse/refractory AL patients had higher Bcl-2 and P53 protein level, lower marrow complete remission, and was easy to relapse.	Aluminum	57-59	P53	Homo sapiens	90-93
10815759-0	2000	Cell-cycle arrest and p53-independent induction of apoptosis in vitro by the new anticancer drugs 5-FdUrd-P-FdCydOct and dCydPam-P-FdUrd in DU-145 human prostate cancer cells.	5-fdurd-p-fdcydoct	98-116	P53	Homo sapiens	22-25
21695255-5	2011	Combining dysregulated beta-catenin with homozygous deletion of PTEN in the OSE resulted in development of significantly more aggressive tumors, which was correlated with inhibition of p53 expression and cellular senescence.	serine O-sulfate	76-79	P53	Homo sapiens	185-188
10909873-0	2000	Sequence-specific 1H, 15N, and 13C assignment of the N-terminal domain of the human oncoprotein MDM2 that binds to p53.	13c	31-34	P53	Homo sapiens	115-118
15163458-11	2004	CONCLUSIONS: This study provides evidence that redox-active (Fe2+), (Mn2+), (Cu2+), and (Zn2+) ion-induced apoptosis in PBL by (H2O2)/(.OH) generation, resulting in mitochondria depolarization, caspase-3 activation, and nuclear fragmentation independent of NF-kappaB and p53 transcription factors activation.	cupric ion	77-81	P53	Homo sapiens	271-274
15099969-2	2004	In this regard, genetic polymorphism at codon 72 (CCC/proline to CGC/arginine [Pro(72)Arg]) of the p53 gene is one of the most frequently studied subjects.	Proline	54-61	P53	Homo sapiens	99-102
21110861-8	2010	The Meq variants L-Meq and S-Meq, but not VS-Meq and  Meq, which were expressed in MD tumor cells and MDV-infected cells, exerted an inhibitory effect on p53 transcriptional activity.	6-METHOXY-N-ETHYLQUINOLINIUM IODIDE	4-7	P53	Homo sapiens	154-157
15087041-6	2004	METHOD: Serum analysis of p53 antibodies was performed by enzyme-linked immunosorbent assay (ELISA) in 38 patients with esophageal cancer preoperatively, then surgically resected specimens were analyzed for their chemosensitivity to cisdichlorodiammineplatinum (DDP),5-fluorouracil (5-FU), and Adriamycin (ADM) by in vitro drug response assay MTT colorimetry.	cisdichlorodiammineplatinum	233-260	P53	Homo sapiens	26-29
11042529-9	2000	In conclusion, As(2) O(3) might become a new therapeutic tool in the treatment of ATL as As(2) O(3) induces apoptosis by destruction of the bcl-2 protein and enhancement of the bak protein production proceeding to activate caspases, and also induces G(1) phase accumulation by enhancement of p53, Cip1/p21, Kip1/p27 and dephosphorylation of pRb to HTLV-I infected T-cell lines.	(2) o(3)	17-25	P53	Homo sapiens	292-295
21110861-8	2010	The Meq variants L-Meq and S-Meq, but not VS-Meq and  Meq, which were expressed in MD tumor cells and MDV-infected cells, exerted an inhibitory effect on p53 transcriptional activity.	6-METHOXY-N-ETHYLQUINOLINIUM IODIDE	19-22	P53	Homo sapiens	154-157
15144569-2	2004	Two p53-mutant lines, COH and CC-M2, derived from high-grade colon adenocarcinoma, showed signs of apoptosis after treatment with 250 IU/ml of HuIFN- beta in the culture medium.	huifn- beta	143-154	P53	Homo sapiens	4-7
20805583-4	2010	p53 protein was characterized by mass spectrometry and covalently immobilized through amide linkage to the (3-aminopropyl)trietoxysilane-modified glass surface.	(3-aminopropyl)trietoxysilane	107-136	P53	Homo sapiens	0-3
14713754-6	2004	Molecular data demonstrate that selenium prevents clonal expansion of nascent tumors by causing cell cycle arrest, promoting apoptosis, and modulating p53 dependent DNA repair mechanisms.	Selenium	32-40	P53	Homo sapiens	151-154
10794489-1	2000	A case-control study was performed to investigate the risk of cervical cancer associated with p53 polymorphism at codon 72, encoding either arginine or proline.	Proline	152-159	P53	Homo sapiens	94-97
10719037-0	2000	p53 mutations experimentally induced by 8-methoxypsoralen plus UVA (PUVA) differ from those found in human skin cancers in PUVA-treated patients.	uva	63-66	P53	Homo sapiens	0-3
21317459-0	2010	Evaluation of an Actinomycin D/VX-680 aurora kinase inhibitor combination in p53-based cyclotherapy.	Dactinomycin	17-30	P53	Homo sapiens	77-80
10660538-4	2000	Contrary to bax, another known pro-apoptotic p53-target gene, both mouse and human FAS p53REs are still activated by the discriminatory p53 mutants Pro-175 and Ala-143, a class of mutants unable to induce apoptosis.	Proline	148-151	P53	Homo sapiens	87-90
10660538-4	2000	Contrary to bax, another known pro-apoptotic p53-target gene, both mouse and human FAS p53REs are still activated by the discriminatory p53 mutants Pro-175 and Ala-143, a class of mutants unable to induce apoptosis.	Proline	148-151	P53	Homo sapiens	87-90
14744727-1	2004	The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene has been implicated as a risk marker in cervical neoplasia.	Proline	32-35	P53	Homo sapiens	66-69
14744727-1	2004	The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene has been implicated as a risk marker in cervical neoplasia.	Proline	39-42	P53	Homo sapiens	66-69
14744727-1	2004	The Arg/Arg genotype versus Arg/Pro or Pro/Pro at codon 72 of the p53 gene has been implicated as a risk marker in cervical neoplasia.	Proline	39-42	P53	Homo sapiens	66-69
21317459-3	2010	Here we sought to evaluate whether low doses of Actinomycin D (LDActD), a clinically-approved drug and potent p53 activator, could substitute Nutlin-3 in p53-based cyclotherapy.	Dactinomycin	48-61	P53	Homo sapiens	110-113
14971655-3	2004	Under certain conditions, some hexavalent chromium [Cr(VI)] compounds are toxic and carcinogenic in the human respiratory tract, and we have shown that they induce apoptosis and/or cell cycle arrest in a p53-dependent fashion.	Chromium	42-50	P53	Homo sapiens	204-207
15263792-7	2004	The proline form of p53 gene codon 72 was significantly higher than the arginine form, with an odds ratio of 2.606 (95% CI = 1.052-6.455).	Proline	4-11	P53	Homo sapiens	20-23
15263792-11	2004	The proline form of p53 gene codon 72 might be a more significant risk factor for the development of metastasis than the arginine form.	Proline	4-11	P53	Homo sapiens	20-23
11996107-1	2000	A polymorphism at codon 72 of gene p53 results in the presence of either arginine or proline at this position.	Proline	85-92	P53	Homo sapiens	35-38
21317459-3	2010	Here we sought to evaluate whether low doses of Actinomycin D (LDActD), a clinically-approved drug and potent p53 activator, could substitute Nutlin-3 in p53-based cyclotherapy.	Dactinomycin	48-61	P53	Homo sapiens	154-157
10601610-2	2000	In preclinical studies, SCH58500 has shown efficacy against many tumor-types with non-functional p53.	sch58500	24-32	P53	Homo sapiens	97-100
14695179-0	2003	Inactivation of wild-type p53 protein function by reactive oxygen and nitrogen species in malignant glioma cells.	reactive oxygen and nitrogen species	50-86	P53	Homo sapiens	26-29
20676140-3	2010	p53 inactivation led to formation of estrogen receptor-positive raloxifene-responsive mammary carcinomas with features of luminal subtype B. Rb deficiency was insufficient to initiate carcinogenesis but promoted genomic instability and growth rate of neoplasms associated with p53 inactivation.	Raloxifene Hydrochloride	64-74	P53	Homo sapiens	277-280
14695212-2	2003	We, in the present study, first confirmed that some substantial extent of apoptotic cell death was seen when p53-deficient cells (KATO-III) were transfected with wild-type p53 and treated with sodium butyrate (SB) or trichostatin A.	Butyric Acid	193-208	P53	Homo sapiens	109-112
14695212-2	2003	We, in the present study, first confirmed that some substantial extent of apoptotic cell death was seen when p53-deficient cells (KATO-III) were transfected with wild-type p53 and treated with sodium butyrate (SB) or trichostatin A.	Butyric Acid	193-208	P53	Homo sapiens	172-175
14695212-2	2003	We, in the present study, first confirmed that some substantial extent of apoptotic cell death was seen when p53-deficient cells (KATO-III) were transfected with wild-type p53 and treated with sodium butyrate (SB) or trichostatin A.	Butyric Acid	210-212	P53	Homo sapiens	109-112
14695212-2	2003	We, in the present study, first confirmed that some substantial extent of apoptotic cell death was seen when p53-deficient cells (KATO-III) were transfected with wild-type p53 and treated with sodium butyrate (SB) or trichostatin A.	Butyric Acid	210-212	P53	Homo sapiens	172-175
14695212-5	2003	Furthermore, reverse transcription-PCR demonstrated that among various p53-related proapoptotic genes, expression of PIG3 and NOXA were clearly enhanced by SB treatment in KATO-III/p53 cells but not in KATO-III/K320R or KATO-III/K373R cells.	Butyric Acid	156-158	P53	Homo sapiens	71-74
14695212-5	2003	Furthermore, reverse transcription-PCR demonstrated that among various p53-related proapoptotic genes, expression of PIG3 and NOXA were clearly enhanced by SB treatment in KATO-III/p53 cells but not in KATO-III/K320R or KATO-III/K373R cells.	Butyric Acid	156-158	P53	Homo sapiens	181-184
14695212-6	2003	Finally, we revealed that apoptosis could be evoked by SB even in cells where p53 mutations occur at residues other than 320 lysine or 373 lysine (TMK-1 and HSC-39 cells) and that this apoptosis was significantly, although not totally, suppressed by the anti-p53 antisense.	Butyric Acid	55-57	P53	Homo sapiens	78-81
10588737-2	1999	A modified tetracycline-inducible system was established to search for transcripts that were activated soon after p53 induction.	Tetracycline	11-23	P53	Homo sapiens	114-117
10602500-2	1999	Novel potential functions of Cdk2 have been uncovered by using two potent and specific inhibitors of its kinase activity, roscovitine and olomoucine, on human wt p53-expresser untransformed and tumor-derived cells.	olomoucine	138-148	P53	Homo sapiens	162-165
14695212-6	2003	Finally, we revealed that apoptosis could be evoked by SB even in cells where p53 mutations occur at residues other than 320 lysine or 373 lysine (TMK-1 and HSC-39 cells) and that this apoptosis was significantly, although not totally, suppressed by the anti-p53 antisense.	Butyric Acid	55-57	P53	Homo sapiens	259-262
20427142-1	2010	A common polymorphism at codon 72 of human TP53 gene determines a proline to arginine aminoacidic substitution within the proline-rich domain of p53 protein.	Proline	66-73	P53	Homo sapiens	43-47
21432092-8	2003	Previously, we demonstrated that HDAC inhibitors, such as sodium butyrate and trichostatin A (TSA), transcriptionally induce the cyclin-dependent kinase inhibitor p21(WAF1/Cip1), a downstream target gene of p53, in a p53-independent manner.	Butyric Acid	58-73	P53	Homo sapiens	207-210
21432092-8	2003	Previously, we demonstrated that HDAC inhibitors, such as sodium butyrate and trichostatin A (TSA), transcriptionally induce the cyclin-dependent kinase inhibitor p21(WAF1/Cip1), a downstream target gene of p53, in a p53-independent manner.	Butyric Acid	58-73	P53	Homo sapiens	217-220
14580323-10	2003	The possibility that oxidized p53 contained significant amounts of sulfenic (-SOH), sulfinic (-SO2H), or sulfonic acid (-SO3H) was ruled out.	Sulfonic Acids	105-118	P53	Homo sapiens	30-33
10554039-12	1999	When Y79 cells were exposed to combinations of sodium butyrate and MG132, the latter compound suppressed the decreasing effect induced by sodium butyrate on the levels of p53, N-myc, and IkappaBalpha and the increasing effect on the nuclear level of nuclear factor kappaB.	Butyric Acid	47-62	P53	Homo sapiens	171-174
10554039-12	1999	When Y79 cells were exposed to combinations of sodium butyrate and MG132, the latter compound suppressed the decreasing effect induced by sodium butyrate on the levels of p53, N-myc, and IkappaBalpha and the increasing effect on the nuclear level of nuclear factor kappaB.	Butyric Acid	138-153	P53	Homo sapiens	171-174
20427142-1	2010	A common polymorphism at codon 72 of human TP53 gene determines a proline to arginine aminoacidic substitution within the proline-rich domain of p53 protein.	Proline	66-73	P53	Homo sapiens	145-148
10531402-2	1999	When cells were grown in media containing normal concentrations (10%) of serum, induction of p53 by tetracycline withdrawal resulted in an 8-fold decrease in sensitivity to CP.	Tetracycline	100-112	P53	Homo sapiens	93-96
20427142-1	2010	A common polymorphism at codon 72 of human TP53 gene determines a proline to arginine aminoacidic substitution within the proline-rich domain of p53 protein.	Proline	122-129	P53	Homo sapiens	43-47
10469618-5	1999	It has recently been reported that the extent of p53 dysfunction caused by HPVs depends on the status of a polymorphism at codon 72 of p53, Pro or Arg.	Proline	140-143	P53	Homo sapiens	49-52
12919725-1	2003	The p53 gene has a polymorphism at codon 72 that presents the arginine or proline genotype, although this polymorphism has been associated with genetically determined susceptibility to lung cancers, the literature has not been consistent with this association.	Proline	74-81	P53	Homo sapiens	4-7
20427142-1	2010	A common polymorphism at codon 72 of human TP53 gene determines a proline to arginine aminoacidic substitution within the proline-rich domain of p53 protein.	Proline	122-129	P53	Homo sapiens	145-148
10425273-2	1999	A polymorphism at codon 72 of p53 results in translation to either arginine (p53Arg) or proline (p53Pro), and recent study showed that Caucasian women with arginine form of p53 are more susceptible to HPV-associated carcinoma of the cervix.	Proline	88-95	P53	Homo sapiens	30-33
12925221-5	2003	Lomefloxacin also triggered various stress responses: heme-oxygenase-1 expression in fibroblasts, changes in p53 status as shown by the accumulation of p53 and p21 proteins or the induction of MDM2 and GADD45 genes, and stimulation of melanogenesis by increasing the tyrosinase activity in melanocytes.	lomefloxacin	0-12	P53	Homo sapiens	109-112
12925221-5	2003	Lomefloxacin also triggered various stress responses: heme-oxygenase-1 expression in fibroblasts, changes in p53 status as shown by the accumulation of p53 and p21 proteins or the induction of MDM2 and GADD45 genes, and stimulation of melanogenesis by increasing the tyrosinase activity in melanocytes.	lomefloxacin	0-12	P53	Homo sapiens	152-155
20577877-1	2010	The TP53 tumor suppressor gene contains a well-studied polymorphism that encodes either proline (P) or arginine (R) at codon 72, and over half of the world"s population is homozygous for R at this codon.	Proline	88-95	P53	Homo sapiens	4-8
12794767-0	2003	In vitro and in vivo studies of the anticancer action of terbinafine in human cancer cell lines: G0/G1 p53-associated cell cycle arrest.	Terbinafine	57-68	P53	Homo sapiens	103-106
12794767-4	2003	The TB-induced cell cycle arrest in colon cancer cell line (COLO 205) occurred when the cyclin-dependent kinase (cdk) system was inhibited just as the levels of p53, p21/Cip1 and p27/Kip1 proteins were augmented.	Terbinafine	4-6	P53	Homo sapiens	161-164
12794767-5	2003	In the TB-treated COLO 205, the binding between p53 protein and p53 consensus binding site in p21/Cip1 promoter DNA probe was increased.	Terbinafine	7-9	P53	Homo sapiens	48-51
12794767-5	2003	In the TB-treated COLO 205, the binding between p53 protein and p53 consensus binding site in p21/Cip1 promoter DNA probe was increased.	Terbinafine	7-9	P53	Homo sapiens	64-67
12794767-6	2003	Pretreatment of COLO 205 with p53-specific antisense oligodeoxynucleotide decreased the TB-induced elevations of p53 and p21/Cip1 proteins, which in turn led to arrest in the cell cycle at the G0/G1 phase.	Terbinafine	88-90	P53	Homo sapiens	30-33
10582657-15	1999	Induction of p53 levels was observed in WHCO3 cells exposed to GLA, AA, PGA2, indomethacin and the combination of indomethacin and GLA or AA.	whco3	40-45	P53	Homo sapiens	13-16
10582657-15	1999	Induction of p53 levels was observed in WHCO3 cells exposed to GLA, AA, PGA2, indomethacin and the combination of indomethacin and GLA or AA.	Indomethacin	78-90	P53	Homo sapiens	13-16
10446979-0	1999	DNA damage increases sensitivity to vinca alkaloids and decreases sensitivity to taxanes through p53-dependent repression of microtubule-associated protein 4.	Vinca Alkaloids	36-51	P53	Homo sapiens	97-100
12794767-6	2003	Pretreatment of COLO 205 with p53-specific antisense oligodeoxynucleotide decreased the TB-induced elevations of p53 and p21/Cip1 proteins, which in turn led to arrest in the cell cycle at the G0/G1 phase.	Terbinafine	88-90	P53	Homo sapiens	113-116
12794767-7	2003	Moreover, in the p53 null cells, HL60, TB treatment did not induce cell cycle arrest.	Terbinafine	39-41	P53	Homo sapiens	17-20
20619728-7	2010	The mRNA and protein level of p53 was significantly higher in high fluoride+high selenium group than that in other two groups.	Selenium	81-89	P53	Homo sapiens	30-33
12794767-8	2003	Taken together, these results suggest an involvement of the p53-associated signaling pathway in the TB-induced antiproliferation in COLO 205.	Terbinafine	100-102	P53	Homo sapiens	60-63
10364153-5	1999	These data support the hypothesis that p53 can induce apoptosis through the modulation of specific DExH-containing DNA helicases and may have implications for the cancer predisposition observed in WS patients.	dexh	99-103	P53	Homo sapiens	39-42
20619728-8	2010	These results suggest that selenium may influence the protein and gene expression associated with p38 signal transduction pathway and up-regulate p53 expression in PBMCs from patients with coal-combustion-type fluorosis.	Selenium	27-35	P53	Homo sapiens	146-149
20827430-4	2010	However, we found that the p53 Arg72Pro was associated with an increased risk of esophageal cancer ((Pro/Arg +Pro/Pro) versus Arg/Arg: OR=1.20, 95%CI=1.06-1.36) without any between-study heterogeneity.	Proline	36-39	P53	Homo sapiens	27-30
10455409-1	1999	In this article, we investigated the effect induced by the reintroduction of wild-type p53 (wt-p53) protein on BCNU sensitivity in the ADF glioblastoma line.	Carmustine	111-115	P53	Homo sapiens	87-90
10455409-1	1999	In this article, we investigated the effect induced by the reintroduction of wild-type p53 (wt-p53) protein on BCNU sensitivity in the ADF glioblastoma line.	Carmustine	111-115	P53	Homo sapiens	95-98
10455409-2	1999	Using a wt-p53 recombinant adenovirus (Ad-p53), we demonstrated that exogenous wt-p53 expression was able to increase the sensitivity to BCNU in ADF cells.	Carmustine	137-141	P53	Homo sapiens	11-14
12763222-5	2003	Treatment with 10xIC(50) values of AG337 for 48 h resulted in S phase arrest in all Lovo and WiDr cells (up to 50% of cells being in S phase), irrespective of their p53 status.	nolatrexed	35-40	P53	Homo sapiens	165-168
12771391-11	2003	Workers with DPC above the median level had a significantly higher risk of having pantropic p53 &gt;150 pg/ml (adjusted OR 2.5, 95% CI 1.2 to 5.4).	dpc	13-16	P53	Homo sapiens	92-95
10455409-2	1999	Using a wt-p53 recombinant adenovirus (Ad-p53), we demonstrated that exogenous wt-p53 expression was able to increase the sensitivity to BCNU in ADF cells.	Carmustine	137-141	P53	Homo sapiens	42-45
20827430-4	2010	However, we found that the p53 Arg72Pro was associated with an increased risk of esophageal cancer ((Pro/Arg +Pro/Pro) versus Arg/Arg: OR=1.20, 95%CI=1.06-1.36) without any between-study heterogeneity.	Proline	101-104	P53	Homo sapiens	27-30
10455409-2	1999	Using a wt-p53 recombinant adenovirus (Ad-p53), we demonstrated that exogenous wt-p53 expression was able to increase the sensitivity to BCNU in ADF cells.	Carmustine	137-141	P53	Homo sapiens	42-45
10455409-7	1999	In contrast, BCNU--&gt;Ad-p53 sequence provoked G2-M arrest similar to that observed after treatment with BCNU alone, but prevented the later recovery of the cells through the cell cycle, by driving the cells to apoptotic death.	Carmustine	13-17	P53	Homo sapiens	26-29
12776195-6	2003	In contrast to hypoxia, 5-flourouracil (5-FU)-induced p53-dependent cell death correlated with enhanced Ser(392) phosphorylation of p53 and elevated p21(WAF1) protein levels.	5-flourouracil	24-38	P53	Homo sapiens	54-57
12776195-6	2003	In contrast to hypoxia, 5-flourouracil (5-FU)-induced p53-dependent cell death correlated with enhanced Ser(392) phosphorylation of p53 and elevated p21(WAF1) protein levels.	5-flourouracil	24-38	P53	Homo sapiens	132-135
10455409-10	1999	The data obtained confirm that the wt-p53 gene transfer enhances BCNU sensitivity in glioblastoma cells depending on the administration sequence.	Carmustine	65-69	P53	Homo sapiens	38-41
20827430-4	2010	However, we found that the p53 Arg72Pro was associated with an increased risk of esophageal cancer ((Pro/Arg +Pro/Pro) versus Arg/Arg: OR=1.20, 95%CI=1.06-1.36) without any between-study heterogeneity.	Proline	101-104	P53	Homo sapiens	27-30
20827430-5	2010	In the stratified analysis by ethnicity, we found that the increased esophageal cancer risk associated with p53 Arg72Pro polymorphism was more evident in Asian group ((Pro/Arg +Pro/Pro) versus Arg/Arg: OR=1.35, 95%CI=1.14-1.60, P=0.09 for heterogeneity test), although we still failed to find any significant association between GSTP1 Ile105Val polymorphism and esophageal cancer risk in different ethnicity.	Proline	117-120	P53	Homo sapiens	108-111
20827430-5	2010	In the stratified analysis by ethnicity, we found that the increased esophageal cancer risk associated with p53 Arg72Pro polymorphism was more evident in Asian group ((Pro/Arg +Pro/Pro) versus Arg/Arg: OR=1.35, 95%CI=1.14-1.60, P=0.09 for heterogeneity test), although we still failed to find any significant association between GSTP1 Ile105Val polymorphism and esophageal cancer risk in different ethnicity.	Proline	168-171	P53	Homo sapiens	108-111
10533721-6	1999	Agarose gel electrophoresis confirmed the AdCMV.p53-dependent cellular apoptosis.	Sepharose	0-7	P53	Homo sapiens	48-51
12759393-11	2003	Serum selenium levels in the upper three quartiles were associated with similar reductions in risk of 17p (p53) LOH (OR = 0.5, 95% CI = 0.2 to 0.9) and increased 4N fraction (OR = 0.6, 95% CI = 0.3 to 1.2).	Selenium	6-14	P53	Homo sapiens	107-110
12684648-2	2003	A sequence polymorphism at codon 72 of the p53 gene results in either a proline or an arginine and may induce different functional activities.	Proline	72-79	P53	Homo sapiens	43-46
20827430-5	2010	In the stratified analysis by ethnicity, we found that the increased esophageal cancer risk associated with p53 Arg72Pro polymorphism was more evident in Asian group ((Pro/Arg +Pro/Pro) versus Arg/Arg: OR=1.35, 95%CI=1.14-1.60, P=0.09 for heterogeneity test), although we still failed to find any significant association between GSTP1 Ile105Val polymorphism and esophageal cancer risk in different ethnicity.	Proline	168-171	P53	Homo sapiens	108-111
12702563-2	2003	We have used microPET and fluorescence imaging to detect interactions between p53 tumor suppressor and large T antigen (TAg) of SV40 virus in a tetracycline-inducible two-hybrid system.	Tetracycline	144-156	P53	Homo sapiens	78-81
20662736-7	2010	Anthracycline (topoisomerase II inhibitors such as mitoxantrone and ellipticine) and camptothecin (topoisomerase I inhibitor) derivatives including topotecan induce DNA double strand breaks, which activate the p53 pathway through the ataxia telangiectasia mutated-checkpoint kinase 2 (ATM-CHK2) DNA damage response pathway.	Mitoxantrone	51-63	P53	Homo sapiens	210-213
10368691-2	1999	In this study we examined cytotoxicity of MGI 114 against human tumor cell lines (MCF7, MDA.MB.468, EJ1, J82, SCaBER, KG-1, HL60, and IMR-90) with differing expression of p53 and/or p21 (WAF1) tumor suppressor genes.	irofulven	42-49	P53	Homo sapiens	171-174
20662736-8	2010	Although mitoxantrone, ellipticine, camptothecin, and topotecan all exhibited concentration-dependent disruption of the p53-hDM2 PPIB, they were much less potent than Nutlin-3.	Mitoxantrone	9-21	P53	Homo sapiens	120-123
20421238-6	2010	We identified a novel germ line variant of the 177 mutant (Pro to Arg; P177R) of p53 by genomic sequencing.	Proline	59-62	P53	Homo sapiens	81-84
10023783-2	1999	Most recently, p53 protein containing an arginine residue in codon 72 was shown to be more effectively degraded by the E6 oncoprotein of human papillomavirus (HPV) than the corresponding proline isoform in cervical carcinoma cells.	Proline	187-194	P53	Homo sapiens	15-18
9891044-1	1999	The wild-type p53 protein exhibits a common polymorphism at amino acid 72, resulting in either a proline residue (p53Pro) or an arginine residue (p53Arg) at this position.	Proline	97-104	P53	Homo sapiens	14-17
12648751-2	2003	We performed a case-control association study between sporadic AD and the common proline/arginine polymorphism at codon 72 in the pro-apoptotic gene p53, in 109 sporadic AD patients and in 111 controls.	Proline	81-88	P53	Homo sapiens	149-152
12726864-3	2003	A polymorphism encoding either arginine (72R) or proline (72P) at codon 72 of p53 influences inhibition of p73 by a range of p53 mutants identified in squamous cancers.	Proline	49-56	P53	Homo sapiens	78-81
12726864-3	2003	A polymorphism encoding either arginine (72R) or proline (72P) at codon 72 of p53 influences inhibition of p73 by a range of p53 mutants identified in squamous cancers.	Proline	49-56	P53	Homo sapiens	125-128
20596254-2	2010	BaP 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of benzo(a)pyrene (BaP), attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 gene mutations.	7,8-diol	4-12	P53	Homo sapiens	146-149
12527807-7	2003	Further experiments with p53-null (10)1 cells treated with these same drugs also demonstrate decreased NF-Y binding to the topo IIalpha ICBs.	icbs	136-140	P53	Homo sapiens	25-28
12527807-8	2003	The data presented points to the existence of both p53-dependent and -independent mechanisms for regulating NF-Y binding to ICBs in the topo IIalpha promoter and thus the modulation of topo IIalpha gene expression.	icbs	124-128	P53	Homo sapiens	51-54
10363568-2	1999	The aim of this work was to investigate the role of p53 in the apoptosis of colorectal cancer cells in vitro, induced by 5-fluorouracil (5-FU) and hydroxy-camptothecin (HCPT).	hydroxycamptothecinum	147-167	P53	Homo sapiens	52-55
10363568-2	1999	The aim of this work was to investigate the role of p53 in the apoptosis of colorectal cancer cells in vitro, induced by 5-fluorouracil (5-FU) and hydroxy-camptothecin (HCPT).	hydroxycamptothecinum	169-173	P53	Homo sapiens	52-55
10527073-7	1999	In an in vivo experiment, injection of VV or rVV-p53 after the C6 cells had been implanted in nude mice induced effective inhibition of tumor growth in comparison with control PBS groups.	Lead	176-179	P53	Homo sapiens	49-52
14513722-2	2003	(1998) implicated the proline/argine polymorphism of the codon 72 of the tumor-suppressor gene p53 in the development of cervical cancer (CC) with the observation that the p53 protein is more efficiently inactivated by the E6 oncoprotein of human papillomavirus in p53 arginine as compared with its proline isoform.	Proline	22-29	P53	Homo sapiens	95-98
9772303-5	1998	Tetracycline-inducible antisense expression of HPV18 E6 in human cervical carcinoma HeLa cells resulted in increased level of p53 but did not affect expression of MN/CA IX protein.	Tetracycline	0-12	P53	Homo sapiens	126-129
14513722-2	2003	(1998) implicated the proline/argine polymorphism of the codon 72 of the tumor-suppressor gene p53 in the development of cervical cancer (CC) with the observation that the p53 protein is more efficiently inactivated by the E6 oncoprotein of human papillomavirus in p53 arginine as compared with its proline isoform.	Proline	22-29	P53	Homo sapiens	172-175
20596254-2	2010	BaP 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of benzo(a)pyrene (BaP), attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 gene mutations.	9,10-epoxide	13-25	P53	Homo sapiens	146-149
14513722-2	2003	(1998) implicated the proline/argine polymorphism of the codon 72 of the tumor-suppressor gene p53 in the development of cervical cancer (CC) with the observation that the p53 protein is more efficiently inactivated by the E6 oncoprotein of human papillomavirus in p53 arginine as compared with its proline isoform.	Proline	22-29	P53	Homo sapiens	172-175
14513722-2	2003	(1998) implicated the proline/argine polymorphism of the codon 72 of the tumor-suppressor gene p53 in the development of cervical cancer (CC) with the observation that the p53 protein is more efficiently inactivated by the E6 oncoprotein of human papillomavirus in p53 arginine as compared with its proline isoform.	Proline	299-306	P53	Homo sapiens	95-98
20336762-7	2010	The results showed that DBDCT-mediated cell-cycle arrest might occur through the induction of p21 in a p53-dependent manner and that DBDCT induction of the mitochondrial apoptotic signaling pathway is perhaps mediated by increasing Bax/Bcl-2 ratios, which result in the loss of DeltaPsi(m), release of cytochrome c into the cytoplasm, activation of caspase-3 and -9, and increased reactive oxygen species (ROS) generation.	dbdct	24-29	P53	Homo sapiens	103-106
14513722-2	2003	(1998) implicated the proline/argine polymorphism of the codon 72 of the tumor-suppressor gene p53 in the development of cervical cancer (CC) with the observation that the p53 protein is more efficiently inactivated by the E6 oncoprotein of human papillomavirus in p53 arginine as compared with its proline isoform.	Proline	299-306	P53	Homo sapiens	172-175
14513722-2	2003	(1998) implicated the proline/argine polymorphism of the codon 72 of the tumor-suppressor gene p53 in the development of cervical cancer (CC) with the observation that the p53 protein is more efficiently inactivated by the E6 oncoprotein of human papillomavirus in p53 arginine as compared with its proline isoform.	Proline	299-306	P53	Homo sapiens	172-175
12572700-12	2003	The balance between cyclin-dependent kinases and their inhibitors regulates the level of Rb phosphorylation and its function at G1-S transition; P53 plays at least two functions (cell cycle and apoptosis control).	Rubidium	89-91	P53	Homo sapiens	145-148
12635827-4	2003	The genotype of p53 codon 72 (Arg/Arg, Arg/Pro, or Pro/Pro) was determined for all subjects by polymerase chain reaction-restricted fragment length polymorphism (PCR-RFLP).	Proline	43-46	P53	Homo sapiens	16-19
9808165-4	1998	Similarly, induction of p53 also required a higher dose of benzo[g]chrysene 11S, 12R-dihydrodiol 13R, 14S-epoxide.	benzo[g]chrysene 11s, 12r-dihydrodiol 13r, 14s-epoxide	59-113	P53	Homo sapiens	24-27
11245004-0	1998	[A study on the tumor suppressing effect of a specific point mutant p53 minigene in the expression regulated model with a tetracycline-transactivative response promoter].	Tetracycline	122-134	P53	Homo sapiens	68-71
11245004-1	1998	OBJECTIVE: To establish a tetracycline-regulated expression model and to determine and verify whether a specific point mutant type p53 minigene, containing an Arg--&gt;Leu substitution at amino acid 172, possesses a suppressing effect on human lung cancer.	Tetracycline	26-38	P53	Homo sapiens	131-134
11245004-3	1998	Then the specific p53 minigene was sub-cloned into a tetracycline-transactivative controlled expression vector pBPSTR1 by gene recombination methods.	Tetracycline	53-65	P53	Homo sapiens	18-21
11245004-6	1998	The tetracycline transactivative p53 minigene-regulated transgene model was successfully established.	Tetracycline	4-16	P53	Homo sapiens	33-36
20507639-1	2010	BACKGROUND: Our previous study showed that, in basal cell carcinoma cells, arecoline reduces levels of the tumor cell survival factor interleukin-6 (IL-6), increases levels of tumor suppressor factor p53, and elicits cell cycle arrest, followed by apoptosis.	Arecoline	75-84	P53	Homo sapiens	200-203
12616342-8	2003	Thus, CET and HHT were more active in cell lines without p53 mutation.	Homoharringtonine	6-9	P53	Homo sapiens	57-60
20212049-5	2010	We also found that activation domains 1-2 and the proline-rich domain are required for mutant p53 gain of function.	Proline	50-57	P53	Homo sapiens	94-97
12406566-0	2002	Proline homozygosity in codon 72 of p53: a risk genotype for human papillomavirus related cervical cancer in Indian women.	Proline	0-7	P53	Homo sapiens	36-39
12406566-7	2002	Thus, proline homozygosity at codon 72 of p53 and not arginine homozygosity, could be a risk factor for development of CaCx associated with high risk HPV among Indian women.	Proline	6-13	P53	Homo sapiens	42-45
12406566-7	2002	Thus, proline homozygosity at codon 72 of p53 and not arginine homozygosity, could be a risk factor for development of CaCx associated with high risk HPV among Indian women.	cacx	119-123	P53	Homo sapiens	42-45
20026309-3	2010	For this purpose, we analyzed the effects of a known anti-neoplastic drug, thymoquinone (TQ), on the p53-deficient acute lymphoblastic leukemia (ALL) Jurkat cell line.	thymoquinone	75-87	P53	Homo sapiens	101-104
12496062-1	2002	An Arg/Pro polymorphism in codon 72 of the TP53 gene was analyzed in blood samples from 390 breast and 162 colorectal cancer patients previously investigated for TP53 mutations in their tumors.	Proline	7-10	P53	Homo sapiens	43-47
20026309-3	2010	For this purpose, we analyzed the effects of a known anti-neoplastic drug, thymoquinone (TQ), on the p53-deficient acute lymphoblastic leukemia (ALL) Jurkat cell line.	thymoquinone	89-91	P53	Homo sapiens	101-104
12530090-2	2002	The human tumor suppressor gene TP53 contains single nucleotide polymorphism that encodes either arginin (Arg) or proline (Pro) at amino acid codon 72 of the p53 protein.	Proline	114-121	P53	Homo sapiens	32-36
12530090-2	2002	The human tumor suppressor gene TP53 contains single nucleotide polymorphism that encodes either arginin (Arg) or proline (Pro) at amino acid codon 72 of the p53 protein.	Proline	114-121	P53	Homo sapiens	158-161
20019240-0	2010	Differential levels of transcription of p53-regulated genes by the arginine/proline polymorphism: p53 with arginine at codon 72 favors apoptosis.	Proline	76-83	P53	Homo sapiens	40-43
12530090-2	2002	The human tumor suppressor gene TP53 contains single nucleotide polymorphism that encodes either arginin (Arg) or proline (Pro) at amino acid codon 72 of the p53 protein.	Proline	123-126	P53	Homo sapiens	32-36
12530090-2	2002	The human tumor suppressor gene TP53 contains single nucleotide polymorphism that encodes either arginin (Arg) or proline (Pro) at amino acid codon 72 of the p53 protein.	Proline	123-126	P53	Homo sapiens	158-161
12439598-8	2002	Treatment of cells with PD98059 or UO126 after cisplatin incubation or inhibition of signaling through ERK by tetracycline-regulated expression of dominant-inhibitory ERK enhanced resistance to cisplatin in p53-negative osteosarcoma cells and reduced cisplatin-induced apoptosis.	Tetracycline	110-122	P53	Homo sapiens	207-210
20019240-0	2010	Differential levels of transcription of p53-regulated genes by the arginine/proline polymorphism: p53 with arginine at codon 72 favors apoptosis.	Proline	76-83	P53	Homo sapiens	98-101
12370767-0	2002	Homozygous proline at codon 72 of p53 as a potential risk factor favoring the development of undifferentiated thyroid carcinoma.	Proline	11-18	P53	Homo sapiens	34-37
20019240-4	2010	The largest difference between p53-arginine and p53-proline was found with the PERP gene involved in cell-cell adhesion and apoptosis.	Proline	52-59	P53	Homo sapiens	48-51
12370767-13	2002	We conclude that homozygous proline is a potential risk factor favoring the development of an undifferentiated thyroid carcinoma, and that the homozygous phenotypes at codon 72 of p53 are associated with a poorer prognosis of thyroid carcinoma.	Proline	28-35	P53	Homo sapiens	180-183
20019240-6	2010	LIF, a cytokine that is required for optimal reproductive function, was produced at 2x higher levels by the p53-arginine than the p53-proline allele.	Proline	134-141	P53	Homo sapiens	130-133
12214265-1	2002	By inducing p53-dependent G2 arrest, the pretreatment with low concentrations of DNA damaging drugs (e.g., doxorubicin, DOX) can prevent cell death caused by microtubule-active drugs (e.g., paclitaxel, PTX), thus potentially permitting selective killing of p53-deficient cancer cells.	ptx	202-205	P53	Homo sapiens	12-15
20019240-7	2010	The genes that induced their mRNAs at the highest levels compared to the baseline tended to be synthesized better by the p53-arginine protein than the p53-proline protein.	Proline	155-162	P53	Homo sapiens	151-154
12214265-3	2002	The present work overcomes this obstacle by adding an abrogator of p53-independent checkpoint (e.g., UCN-01) to the DOX-PTX sequence.	ptx	120-123	P53	Homo sapiens	67-70
20175992-1	2010	Selective binding of the wild type tumor suppressor protein p53 to negatively and positively supercoiled (sc) DNA was studied using intercalative drugs chloroquine (CQ), ethidium bromide, acridine derivatives and doxorubicin as a modulators of the level of DNA supercoiling.	Chloroquine	152-163	P53	Homo sapiens	60-63
12214265-6	2002	Induction of G2 arrest with sequential abrogation of a p53-independent checkpoint allows pharmacological manipulation of Raf-1/Bcl-2 hyperphosphorylation, PARP and Rb cleavage and cell death caused by PTX in p53-deficient cells.	ptx	201-204	P53	Homo sapiens	55-58
12205043-10	2002	Findings indicate that CLA elicits mainly proapoptotic effects in human breast tumor cells through both p53-dependent and p53-independent pathways, according to cell type.	Linoleic Acids, Conjugated	23-26	P53	Homo sapiens	104-107
12205043-10	2002	Findings indicate that CLA elicits mainly proapoptotic effects in human breast tumor cells through both p53-dependent and p53-independent pathways, according to cell type.	Linoleic Acids, Conjugated	23-26	P53	Homo sapiens	122-125
20175992-1	2010	Selective binding of the wild type tumor suppressor protein p53 to negatively and positively supercoiled (sc) DNA was studied using intercalative drugs chloroquine (CQ), ethidium bromide, acridine derivatives and doxorubicin as a modulators of the level of DNA supercoiling.	Chloroquine	165-167	P53	Homo sapiens	60-63
20096117-8	2010	Finally, because TAF6delta regulates certain p53 target genes, we tested and demonstrated a physical and functional interaction between TAF6delta and p53.	taf6delta	17-26	P53	Homo sapiens	45-48
12164929-1	2002	Upregulation of p53 protein induces either growth arrest or apoptosis in response to cellular injury This is signaled from a highly conserved p53 domain between codons 64 and 92, where a functional polymorphism results in either a proline (p53-72P) or an arginine (p53-72R) at codon 72.	Proline	231-238	P53	Homo sapiens	16-19
20096117-8	2010	Finally, because TAF6delta regulates certain p53 target genes, we tested and demonstrated a physical and functional interaction between TAF6delta and p53.	taf6delta	17-26	P53	Homo sapiens	150-153
12164929-1	2002	Upregulation of p53 protein induces either growth arrest or apoptosis in response to cellular injury This is signaled from a highly conserved p53 domain between codons 64 and 92, where a functional polymorphism results in either a proline (p53-72P) or an arginine (p53-72R) at codon 72.	Proline	231-238	P53	Homo sapiens	142-145
12164929-1	2002	Upregulation of p53 protein induces either growth arrest or apoptosis in response to cellular injury This is signaled from a highly conserved p53 domain between codons 64 and 92, where a functional polymorphism results in either a proline (p53-72P) or an arginine (p53-72R) at codon 72.	Proline	231-238	P53	Homo sapiens	142-145
21338227-2	2010	In the tumour suppressor Trp53 gene, a codon 72 polymorphism is frequent in the form of a single nucleotide polymorphism that leads to substitution of an arginine for a proline.	Proline	169-176	P53	Homo sapiens	25-30
12164929-1	2002	Upregulation of p53 protein induces either growth arrest or apoptosis in response to cellular injury This is signaled from a highly conserved p53 domain between codons 64 and 92, where a functional polymorphism results in either a proline (p53-72P) or an arginine (p53-72R) at codon 72.	Proline	231-238	P53	Homo sapiens	142-145
12065694-7	2002	Treatment with the p53 inhibitor alpha-2-(2-imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone (PFT) before cisplatin exposure inhibited p53 nuclear expression at 4, 8, and 12 h and inhibited phosphatidylserine externalization and caspase 3 activation at 12 h. Neither DEVD-fmk nor ZVAD-fmk inhibited cisplatin-induced p53 nuclear expression.	bentiromide	106-109	P53	Homo sapiens	19-22
12082016-9	2002	Further exploration of antimalarial compounds identified the common medicinals chloroquine, quinacrine, and amodiaquine as Tp53-inducers.	Chloroquine	79-90	P53	Homo sapiens	123-127
19576684-5	2010	These results suggest that a proline in position 72 of p53 increases the risk of cervical carcinoma in Chinese population.	Proline	29-36	P53	Homo sapiens	55-58
12168882-5	2002	The amino acid residue at this position is either arginine (p53-Arg) or proline (p53-Pro).	Proline	72-79	P53	Homo sapiens	81-84
12006537-1	2002	PURPOSE: It is known that a common p53 polymorphism, encodingeither proline (Pro) or arginine (Arg) at residue 72, produces marked change in the structure of p53.	Proline	68-75	P53	Homo sapiens	35-38
12006537-1	2002	PURPOSE: It is known that a common p53 polymorphism, encodingeither proline (Pro) or arginine (Arg) at residue 72, produces marked change in the structure of p53.	Proline	68-75	P53	Homo sapiens	158-161
12006537-1	2002	PURPOSE: It is known that a common p53 polymorphism, encodingeither proline (Pro) or arginine (Arg) at residue 72, produces marked change in the structure of p53.	Proline	77-80	P53	Homo sapiens	35-38
20666726-8	2010	The cis-imidazolines were the first discovered potent and selective small-molecule inhibitors of the p53-MDM2 interaction and they continue to show therapeutic potential.	cis-imidazolines	4-20	P53	Homo sapiens	101-104
12006537-1	2002	PURPOSE: It is known that a common p53 polymorphism, encodingeither proline (Pro) or arginine (Arg) at residue 72, produces marked change in the structure of p53.	Proline	77-80	P53	Homo sapiens	158-161
12006537-7	2002	RESULTS: There was a bias to mutate and express the Arg allele in the p53 -mutated TCCs arising in individuals with heterozygosity (Pro/Arg).	Proline	132-135	P53	Homo sapiens	70-73
19557511-3	2010	Modulation of the aglycones of GD1 and GM1b was observed in wild-type p53-treated cells.	ganglioside M1b	39-43	P53	Homo sapiens	70-73
12133541-13	2002	Hispidus Hoo polysaccharides selectively inhibited the proliferation, the colony forming ability, and the viability and function of human gastric cancer cells through the low protein expression of c-myc, bcl-2 and the high protein expression of p53, fas, fas-L and the cell factor TGF beta(1).	hispidus hoo polysaccharides	0-28	P53	Homo sapiens	245-248
11986953-1	2002	The retinoid, N-(4-hydroxyphenyl)retinamide (4-HPR), mediates p53-independent cytotoxicity and can increase reactive oxygen species and ceramide in solid tumor cell lines.	Fenretinide	14-43	P53	Homo sapiens	62-65
20563922-6	2010	The TP53 polymorphism distribution in this population was 64 (21.1%) Arg/Arg, 55 (18.1%) Pro/Pro, and 185 (60.9%) Arg/Pro.	Proline	89-92	P53	Homo sapiens	4-8
11934438-4	2002	Our results show that MTZ increased proliferation in a dose response manner in all P53 functional cell lines without inducing changes on the levels of P53 nor MN.	mtz	22-25	P53	Homo sapiens	83-86
11934438-5	2002	However, MTZ hydroxy metabolite induced a dose response increase of P53 and MN, while cell proliferation was not increased.	mtz	9-12	P53	Homo sapiens	68-71
11912124-6	2002	We additionally demonstrate that TRAIL/Apo2L-induced death of p53(+/+)- or p53(-/-)- BAX-proficient but not BAX-deficient colorectal cancer cells is augmented by reducing nuclear factor-kappaB-dependent expression of Bcl-x(L) with either a peptide that disrupts the inhibitor of kappaB kinase complex or the nonsteroidal anti-inflammatory drug, sulindac sulfide.	sulindac sulfide	345-361	P53	Homo sapiens	62-65
19954513-0	2009	Identification of colorectal cancer patients with tumors carrying the TP53 mutation on the codon 72 proline allele that benefited most from 5-fluorouracil (5-FU) based postoperative chemotherapy.	Proline	100-107	P53	Homo sapiens	70-74
11861384-11	2002	The induction of apoptosis and the expression of phospho-Ser15 and phospho-Ser20 in these cells were also enhanced by the combination of Ad-p53 and other DNA-damaging agents such as cisplatin and bichloroethyl nitrosourea.	bichloroethyl nitrosourea	196-221	P53	Homo sapiens	140-143
20025549-0	2009	HDAC inhibitor, valproic acid, induces p53-dependent radiosensitization of colon cancer cells.	Valproic Acid	16-29	P53	Homo sapiens	39-42
11821962-5	2002	Mutant p53 stimulates recombination induced by the replication elongation inhibitors (aphidicolin, hydroxyurea and Ara-C) but is without effect on recombination induced by the initiation inhibitors (mimosine and ciclopirox olamine).	Ciclopirox	212-230	P53	Homo sapiens	7-10
11791172-0	2002	The proline-rich domain of p53 is required for cooperation with anti-neoplastic agents to promote apoptosis of tumor cells.	Proline	4-11	P53	Homo sapiens	27-30
11779589-0	2002	The proline form of p53 codon 72 polymorphism is associated with endometriosis.	Proline	4-11	P53	Homo sapiens	20-23
20025549-8	2009	Exposure to VPA resulted in enhancement of IR-induced mitochondrial localizations of Bax and Bcl-xL, mitochondrial membrane potential, and cytochrome c release only in wild-type p53 cell lines.	Valproic Acid	12-15	P53	Homo sapiens	178-181
19693773-1	2009	Previously, we demonstrated that the extracellular signal-regulated kinase (ERK)-mediated pathway contributes to the terbinafine (TB)-induced increases of p21 and p53 protein level as well as decrease of DNA synthesis in human umbilical venous endothelial cells (HUVEC).	Terbinafine	117-128	P53	Homo sapiens	163-166
12462448-5	2002	Observations that mutations in gene p53 appear under conditions of occupational and environmental exposures to chemical and physical carcinogens, such as vinyl chloride, radon, or aflatoxin B1, have proved to be of enormous importance for the occupational and environmental health.	Radon	170-175	P53	Homo sapiens	36-39
19693773-1	2009	Previously, we demonstrated that the extracellular signal-regulated kinase (ERK)-mediated pathway contributes to the terbinafine (TB)-induced increases of p21 and p53 protein level as well as decrease of DNA synthesis in human umbilical venous endothelial cells (HUVEC).	Terbinafine	130-132	P53	Homo sapiens	163-166
19693773-4	2009	Transfection of HUVEC with JNK1 dominant negative (DN-JNK1) prevented the TB-induced increases of p21 and p53 protein level and decrease of DNA synthesis, suggesting that JNK1/2 activation is involved in the TB-induced cell cycle arrest in HUVEC.	Terbinafine	74-76	P53	Homo sapiens	106-109
19009304-3	2009	For this reason, we established ponasterone A-inducible the wild-type p53 (wt-p53) protein-expressing clones by transfecting a ponasterone-inducible vector containing the wt-p53 gene into HSC-1 cells, which harbor the mutated p53 (m/w) at codon 173 (GTG --&gt; TTG in one allele).	ponasterone	32-43	P53	Homo sapiens	70-73
12588696-7	2002	Serum concentrations of beta-carotene and zeaxanthin + lutein were significantly associated with the risk of breast cancer in p53-positive and p53-negative cancers.	beta Carotene	24-37	P53	Homo sapiens	126-129
12588696-7	2002	Serum concentrations of beta-carotene and zeaxanthin + lutein were significantly associated with the risk of breast cancer in p53-positive and p53-negative cancers.	beta Carotene	24-37	P53	Homo sapiens	143-146
19009304-3	2009	For this reason, we established ponasterone A-inducible the wild-type p53 (wt-p53) protein-expressing clones by transfecting a ponasterone-inducible vector containing the wt-p53 gene into HSC-1 cells, which harbor the mutated p53 (m/w) at codon 173 (GTG --&gt; TTG in one allele).	ponasterone	32-43	P53	Homo sapiens	78-81
19009304-3	2009	For this reason, we established ponasterone A-inducible the wild-type p53 (wt-p53) protein-expressing clones by transfecting a ponasterone-inducible vector containing the wt-p53 gene into HSC-1 cells, which harbor the mutated p53 (m/w) at codon 173 (GTG --&gt; TTG in one allele).	ponasterone	32-43	P53	Homo sapiens	78-81
19009304-3	2009	For this reason, we established ponasterone A-inducible the wild-type p53 (wt-p53) protein-expressing clones by transfecting a ponasterone-inducible vector containing the wt-p53 gene into HSC-1 cells, which harbor the mutated p53 (m/w) at codon 173 (GTG --&gt; TTG in one allele).	ponasterone	32-43	P53	Homo sapiens	78-81
11892838-2	2001	We therefore used a p53-null human NSCLC cell line in which we reintroduced the wild-type p53 gene under control of a tetracycline-dependent promoter.	Tetracycline	118-130	P53	Homo sapiens	20-23
11892838-2	2001	We therefore used a p53-null human NSCLC cell line in which we reintroduced the wild-type p53 gene under control of a tetracycline-dependent promoter.	Tetracycline	118-130	P53	Homo sapiens	90-93
18930193-1	2009	OBJECTIVE: To determine whether the p53 codon 72 single nucleotide polymorphism, a change of the amino acid arginine (Arg) to proline (Pro) resulting from a single nucleotide mutation of guanine (G) to cytosine (C), has a clinically significant effect on implantation rate in fresh IVF cycles.	amino acid arginine	97-116	P53	Homo sapiens	36-39
18930193-1	2009	OBJECTIVE: To determine whether the p53 codon 72 single nucleotide polymorphism, a change of the amino acid arginine (Arg) to proline (Pro) resulting from a single nucleotide mutation of guanine (G) to cytosine (C), has a clinically significant effect on implantation rate in fresh IVF cycles.	Proline	126-133	P53	Homo sapiens	36-39
18930193-1	2009	OBJECTIVE: To determine whether the p53 codon 72 single nucleotide polymorphism, a change of the amino acid arginine (Arg) to proline (Pro) resulting from a single nucleotide mutation of guanine (G) to cytosine (C), has a clinically significant effect on implantation rate in fresh IVF cycles.	Proline	135-138	P53	Homo sapiens	36-39
11687965-7	2001	Interestingly, at the protein level, p53 tumor suppressor was substantially increased upon flurbiprofen treatment, yet the level of p21, a downstream target for p53 remained unchanged.	Flurbiprofen	91-103	P53	Homo sapiens	37-40
19452524-8	2009	This was especially true for TP53 transversion mutations and dietary antioxidants (OR for beta-carotene 0.51 95% CI 0.27, 0.97, p trend 0.03; alpha-tocopherol 0.41 95% CI 0.20, 0.84, p trend 0.02) Beta-carotene and ibuprofen significantly altered risk of KRAS2 tumors.	beta Carotene	90-103	P53	Homo sapiens	29-33
11687965-10	2001	These observations suggest that the interaction of COX-2 with p53 may cause p21-independent suppression of tumor cell growth upon flurbiprofen treatment.	Flurbiprofen	130-142	P53	Homo sapiens	62-65
19452524-8	2009	This was especially true for TP53 transversion mutations and dietary antioxidants (OR for beta-carotene 0.51 95% CI 0.27, 0.97, p trend 0.03; alpha-tocopherol 0.41 95% CI 0.20, 0.84, p trend 0.02) Beta-carotene and ibuprofen significantly altered risk of KRAS2 tumors.	beta Carotene	197-210	P53	Homo sapiens	29-33
11593403-3	2001	In contrast, agents that inhibit the elongation phase of transcription, such as UV light, camptothecin or actinomycin D, induced the accumulation of nuclear p53 proteins that were modified at both of these sites.	Dactinomycin	106-119	P53	Homo sapiens	157-160
19639960-4	2009	We used a clone of H358, stably transfected with a tetracycline-inducible wild-type p53-expressing vector.	Tetracycline	51-63	P53	Homo sapiens	84-87
11593387-3	2001	Here, we report that p63, like p53 and p73, induces replicative senescence when expressed in a tetracycline-regulated manner in EJ cells lacking a functional p53.	Tetracycline	95-107	P53	Homo sapiens	31-34
11593330-6	2001	The aerosol delivery of PEI-based formulations of p53 or synthetic p53 variant genes represents a promising new strategy for the treatment of established human osteosarcoma lung metastases.	pei	24-27	P53	Homo sapiens	50-53
11593330-6	2001	The aerosol delivery of PEI-based formulations of p53 or synthetic p53 variant genes represents a promising new strategy for the treatment of established human osteosarcoma lung metastases.	pei	24-27	P53	Homo sapiens	67-70
19890497-1	2009	Pin1 specifically catalyzes the cis/trans isomerization of phospho-Ser/Thr-Pro bonds and plays an important role in many cellular events through the effects of conformational change on the function of its biological substrates, including cell division cycle 25 C (Cdc25C), c-Jun and p53.	Proline	75-78	P53	Homo sapiens	283-286
11774736-7	2001	The combination treatment with a recombinant adenovirus carrying a wild-type p53 gene (AxCAp53) and CDDP significantly suppressed tumor growth of ovarian cancer cells with and without p53 gene, compared with a single treatment of either AxCAp53 or CDDP in ovarian cancer xenograft.	axcap53	87-94	P53	Homo sapiens	77-80
11466694-2	2001	To elucidate whether a novel antimicrotubule agent, TZT-1027, is influenced by the p53 status of tumors, the authors investigated the sensitivities of specimens obtained from patients with nonsmall cell lung carcinoma (NSCLC) and renal cell carcinoma (RCC) to various anticancer agents, including TZT-1027, and the status of the p53 gene in those specimens.	triazinate	52-55	P53	Homo sapiens	83-86
11522280-5	2001	p53 content of MCF-7 breast cancer cells (wild-type) was increased by caffeic acid, decreased by resveratrol, and showed a twofold increase with catechin, that reached borderline statistical significance; however, none of these effects were dose-responsive.	caffeic acid	70-82	P53	Homo sapiens	0-3
11358839-0	2001	Inactivation of p53 sensitizes U87MG glioma cells to 1,3-bis(2-chloroethyl)-1-nitrosourea.	Carmustine	53-89	P53	Homo sapiens	16-19
11358839-1	2001	We examined the effect of p53 inactivation on the response of U87MG glioma cells to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU).	Carmustine	84-120	P53	Homo sapiens	26-29
19052714-4	2009	RESULTS: The Arg/Pro and Pro/Pro genotypes of TP53 codon 72 were significantly correlated with a lower response rate to the combination chemotherapy when compared to the Arg/Arg genotype (35.7 vs. 66.7%, P-value 0.019) in a logistic regression analysis.	Proline	17-20	P53	Homo sapiens	46-50
11358839-3	2001	Here, we observed that p53 inactivation by transfection with pCMV-E6 sensitized U87MG cells to BCNU.	Carmustine	95-99	P53	Homo sapiens	23-26
19052714-4	2009	RESULTS: The Arg/Pro and Pro/Pro genotypes of TP53 codon 72 were significantly correlated with a lower response rate to the combination chemotherapy when compared to the Arg/Arg genotype (35.7 vs. 66.7%, P-value 0.019) in a logistic regression analysis.	Proline	25-28	P53	Homo sapiens	46-50
11368358-2	2001	A comparison of leukemic cell lines with different p53 gene status revealed a considerably higher sensitivity to HHT-induced apoptosis in the cells with a wt p53, and apoptotic events in wt p53 leukemia cells (MOLT-3 cell line) were studied in more detail.	Homoharringtonine	113-116	P53	Homo sapiens	51-54
19052714-4	2009	RESULTS: The Arg/Pro and Pro/Pro genotypes of TP53 codon 72 were significantly correlated with a lower response rate to the combination chemotherapy when compared to the Arg/Arg genotype (35.7 vs. 66.7%, P-value 0.019) in a logistic regression analysis.	Proline	25-28	P53	Homo sapiens	46-50
11368358-2	2001	A comparison of leukemic cell lines with different p53 gene status revealed a considerably higher sensitivity to HHT-induced apoptosis in the cells with a wt p53, and apoptotic events in wt p53 leukemia cells (MOLT-3 cell line) were studied in more detail.	Homoharringtonine	113-116	P53	Homo sapiens	158-161
11368358-2	2001	A comparison of leukemic cell lines with different p53 gene status revealed a considerably higher sensitivity to HHT-induced apoptosis in the cells with a wt p53, and apoptotic events in wt p53 leukemia cells (MOLT-3 cell line) were studied in more detail.	Homoharringtonine	113-116	P53	Homo sapiens	158-161
19052714-5	2009	A multivariate survival analysis also showed that the time to progression for the patients with the Arg/Pro and Pro/Pro genotypes of TP53 codon 72 was worse than for the patients with the Arg/Arg genotype (Hazard ratio = 3.056, P-value = 0.047), whereas the overall survival was not significantly different.	Proline	104-107	P53	Homo sapiens	133-137
19470478-3	2009	The p53 allele encoding proline at codon 72 (P72) was found to be significantly enriched over the allele encoding arginine (R72) among in vitro fertilization (IVF) patients.	Proline	24-31	P53	Homo sapiens	4-7
12577360-1	2001	OBJECTIVE: To investigate the common regulative effects of the Chinese drug Bailong and hexamethylen bisacetamide (HMBA) on expressions of oncogenes (c-H-ras and c-myc), and tumor suppressor genes (Rb, p53 and p21) of MGC80-3 in human cancer cell cycle.	hexamethylene bisacetamide	88-113	P53	Homo sapiens	202-205
12577360-1	2001	OBJECTIVE: To investigate the common regulative effects of the Chinese drug Bailong and hexamethylen bisacetamide (HMBA) on expressions of oncogenes (c-H-ras and c-myc), and tumor suppressor genes (Rb, p53 and p21) of MGC80-3 in human cancer cell cycle.	hexamethylene bisacetamide	115-119	P53	Homo sapiens	202-205
12577360-8	2001	But the effect of Bailong on the expression of p53 gene which was increased obviously by 125.0%-233.4% in majority phase of MGC80-3 cells is similar to HMBA.	hexamethylene bisacetamide	152-156	P53	Homo sapiens	47-50
19517019-3	2009	Fatty acid synthase (FASN), a key enzyme that synthesizes long-chain fatty acids and is involved in both embryogenesis and cancer, has been recently proposed as a direct target of p53 family members, including p63 and p73.	long-chain fatty acids	58-80	P53	Homo sapiens	180-183
11250899-2	2001	Here we demonstrate that, unlike phosphorylation, p53 invariably undergoes acetylation in cells exposed to a variety of stress-inducing agents including hypoxia, anti-metabolites, nuclear export inhibitor and actinomycin D treatment.	Dactinomycin	209-222	P53	Homo sapiens	50-53
11313880-3	2001	p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2",7"-dichlorofluorescin (DCFH) into 2",7"-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase.	2',7'-dichlorofluorescein	207-231	P53	Homo sapiens	0-3
19451596-7	2009	Subjects carrying the TP53 Arg72Pro polymorphism were found to have a significantly increased death risk (Pro/Pro versus Arg/Arg; hazard ratio, 2.90; 95% CI, 1.28-6.66).	Proline	32-35	P53	Homo sapiens	22-26
11313880-3	2001	p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2",7"-dichlorofluorescin (DCFH) into 2",7"-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase.	2',7'-dichlorofluorescein	244-269	P53	Homo sapiens	0-3
11313880-3	2001	p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2",7"-dichlorofluorescin (DCFH) into 2",7"-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase.	2',7'-dichlorofluorescein	233-236	P53	Homo sapiens	0-3
19451596-7	2009	Subjects carrying the TP53 Arg72Pro polymorphism were found to have a significantly increased death risk (Pro/Pro versus Arg/Arg; hazard ratio, 2.90; 95% CI, 1.28-6.66).	Proline	106-109	P53	Homo sapiens	22-26
11267976-1	2001	To elucidate the mechanism of action of sodium butyrate (NaB), we examined its effect on the expression of some cell cycle-related proteins (cyclins D1 and E, p16(ink4), p21(waf1), p27(kip1)) in 2 human non-small cell lung cancer cell lines (NCI-460 and NCI-H23) characterized by wild- type and mutant TP53, respectively.	Butyric Acid	40-55	P53	Homo sapiens	302-306
19451596-8	2009	In the subgroup of 130 high-grade osteosarcomas, the TP53 Arg72Pro was an independent marker of EFS (Pro/Pro versus Arg/Arg; hazard ratio, 2.67; 95% CI, 1.17-6.11).	Proline	63-66	P53	Homo sapiens	53-57
19451596-8	2009	In the subgroup of 130 high-grade osteosarcomas, the TP53 Arg72Pro was an independent marker of EFS (Pro/Pro versus Arg/Arg; hazard ratio, 2.67; 95% CI, 1.17-6.11).	Proline	101-104	P53	Homo sapiens	53-57
11783017-8	2001	Positive correlation was also found between p53 and Ki67 overexpressions.	ki67	52-56	P53	Homo sapiens	44-47
19383811-7	2009	p53 Pro/Pro was strongly associated with shorter survival in the entire cohort (MS of 11.8 versus 29.1 months, P &lt; 0.0001; adjusted hazard ratio for death, 2.05; 95% confidence interval, 1.30-3.24; P = 0.002 for Pro/Pro versus Arg/Arg).	Proline	4-7	P53	Homo sapiens	0-3
11314008-3	2001	Core sequence of the predicted clam p53 (Map53) and p73 (Map73) proteins is virtually identical and includes the following highly conserved regions: the transcriptional activation domain (TAD), MDM2 binding site, ATM phosphorylation site, proline rich domain, DNA binding domains (DBDs) II-V, nuclear import and export signals and the tetramerization domain.	Proline	239-246	P53	Homo sapiens	36-39
19383811-7	2009	p53 Pro/Pro was strongly associated with shorter survival in the entire cohort (MS of 11.8 versus 29.1 months, P &lt; 0.0001; adjusted hazard ratio for death, 2.05; 95% confidence interval, 1.30-3.24; P = 0.002 for Pro/Pro versus Arg/Arg).	Proline	8-11	P53	Homo sapiens	0-3
11820605-4	2001	The immunolocalization of p53 protein was performed using the Labelled Streptavidyn Biotin (LSAB) method.	Biotin	84-90	P53	Homo sapiens	26-29
19254688-8	2009	Collectively, our findings demonstrate that asparanin A induces cell cycle arrest and triggers apoptosis via a p53-independent manner in HepG2 cells.	asparanin A	44-55	P53	Homo sapiens	111-114
11106681-1	2000	BACKGROUND: We previously reported that N-(4-hydroxyphenyl)retinamide (4-HPR, fenretinide) treatment caused large increases of ceramide levels in neuroblastoma cell lines and induced cell death by a combination of apoptosis and necrosis through p53 (also known as TP53)-independent and caspase-independent pathways.	Fenretinide	40-69	P53	Homo sapiens	245-248
11106681-1	2000	BACKGROUND: We previously reported that N-(4-hydroxyphenyl)retinamide (4-HPR, fenretinide) treatment caused large increases of ceramide levels in neuroblastoma cell lines and induced cell death by a combination of apoptosis and necrosis through p53 (also known as TP53)-independent and caspase-independent pathways.	Fenretinide	40-69	P53	Homo sapiens	264-268
11106681-1	2000	BACKGROUND: We previously reported that N-(4-hydroxyphenyl)retinamide (4-HPR, fenretinide) treatment caused large increases of ceramide levels in neuroblastoma cell lines and induced cell death by a combination of apoptosis and necrosis through p53 (also known as TP53)-independent and caspase-independent pathways.	Fenretinide	78-89	P53	Homo sapiens	245-248
11106681-1	2000	BACKGROUND: We previously reported that N-(4-hydroxyphenyl)retinamide (4-HPR, fenretinide) treatment caused large increases of ceramide levels in neuroblastoma cell lines and induced cell death by a combination of apoptosis and necrosis through p53 (also known as TP53)-independent and caspase-independent pathways.	Fenretinide	78-89	P53	Homo sapiens	264-268
19064630-6	2009	To better understand the mechanism by which PUVA treatment induces p53, we exposed human skin fibroblasts with PUVA under conditions that differentially produce monoadducts and ICLs and found that psoralen-induced ICLs induced phosphorylation of the Ser-15 site of p53 and apoptosis much more effectively than psoralen-induced monoadducts.	ser-15	250-256	P53	Homo sapiens	67-70
11716435-8	2000	At an ASO concentration of 300 nM, p53 protein was induced 12.5-fold and p21 was induced 8-fold over background levels, 24 h after start of ASO treatment.	Oligonucleotides, Antisense	6-9	P53	Homo sapiens	35-38
19048622-2	2009	We have previously shown that complete responses to high doses epirubicin-cyclophosphamide were observed only in human tumors bearing a TP53 mutation.	epirubicin-cyclophosphamide	63-90	P53	Homo sapiens	136-140
11069295-6	2000	Proline oxidase, a mitochondrial enzyme involved in the proline/pyrroline-5-carboxylate redox cycle, was up-regulated by p53 in ECV but not in DECV cells.	Proline	56-63	P53	Homo sapiens	121-124
11069295-9	2000	The results directly implicate proline oxidase and the proline/P5C pathway in p53-induced growth suppression and apoptosis.	Proline	31-38	P53	Homo sapiens	78-81
11050162-6	2000	Therefore, we exposed a wild-type p53 TK-6 lymphoblastoid cell line to 4-hydroxynonenal, an unsaturated aldehyde involved in lipid peroxidation, and observed an increase in G to T transversions at p53 codon 249 (AGG to AGT).	unsaturated aldehyde	92-112	P53	Homo sapiens	34-37
11129289-9	2000	After SCH58500 treatment, 3-11-fold elevations of p21 expression were observed in tumor xenografts containing nonfunctional p53 (MDA-MB-468, MDA-MB-231, MIAPaCa2, DU-145, and SK-OV-3), but no change in p21 mRNA in wild-type p53 PA-1 tumors.	sch58500	6-14	P53	Homo sapiens	224-227
19048622-8	2009	Thus, in these in vivo models, epirubicin-cyclophosphamide treatment induces senescence-like features in TP53 wild-type tumor, likely accounting for cell cycle arrest and subsequent resistance to treatment.	epirubicin-cyclophosphamide	31-58	P53	Homo sapiens	105-109
11046142-8	2000	Those differences are also manifest in HeLa cells which express the human papillomavirus E6 protein, suggesting that p53 C-terminal lysine residues are also implicated in E6-AP-mediated ubiquitination.	e6-ap	171-176	P53	Homo sapiens	117-120
18801387-5	2009	The tetracycline inducible promoter, cloned in opposite orientation to the ROSA26 locus and separated from the rtTA element by a 5 kb human p53 intron, drives Cre recombinase expression.	Tetracycline	4-16	P53	Homo sapiens	140-143
11006574-5	2000	Treatment of Y79 cells with sodium butyrate alone lowered the levels of p53, E2F-1 and Bcl-2.	Butyric Acid	28-43	P53	Homo sapiens	72-75
10998350-6	2000	PDTC treatment prevented actinomycin D-mediated up-regulation of two p53 effector gene products, murine double minute clone 2 oncoprotein and p21(WAF1/CIP1) (where WAF1 corresponds to wild-type p53-activated fragment 1 and CIP1 corresponds to cyclin-dependent kinase-interacting protein 1).	Dactinomycin	25-38	P53	Homo sapiens	194-197
10998350-7	2000	Actinomycin D treatment led to accumulation of p53 protein in the nucleus.	Dactinomycin	0-13	P53	Homo sapiens	47-50
19139020-9	2009	Our results indicate that selenium is not inversely related to risk of bladder cancer overall; however, they raise the possibility that selenium may be preventive in certain molecular phenotypes of tumors (e.g., p53 positive) or within certain subsets of a population (e.g., women or moderate smokers).	Selenium	136-144	P53	Homo sapiens	212-215
10998350-8	2000	However, when cells were simultaneously treated with PDTC and actinomycin D, p53 accumulated in both the nucleus and the cytoplasm.	Dactinomycin	62-75	P53	Homo sapiens	77-80
11025661-2	2000	Treatment with vincristine or paclitaxel before DNA-damage or before leptomycin B treatment reduces nuclear accumulation of p53 and expression of mdm2 and p21.	Vincristine	15-26	P53	Homo sapiens	124-127
18937971-7	2009	As in our previously published analysis on platinum-cyclophosphamide-treated group, complete remission showed a borderline negative (paradoxic) association with high BAX expression in the whole group (p=0.058) and with BCL-2 expression in the TP53(-) group (p=0.058).	platinum-cyclophosphamide	43-68	P53	Homo sapiens	243-247
11191113-6	2000	In contrast, the co-treatment with the AhR antagonist, alpha-naphthoflavone (ANF), abrogated the deleterious effects of B[a]P on BRCA-1 expression, while preventing the accumulation of p53 and disruption of cell cycle profile.	alpha-naphthoflavone	55-75	P53	Homo sapiens	185-188
11191113-6	2000	In contrast, the co-treatment with the AhR antagonist, alpha-naphthoflavone (ANF), abrogated the deleterious effects of B[a]P on BRCA-1 expression, while preventing the accumulation of p53 and disruption of cell cycle profile.	alpha-naphthoflavone	77-80	P53	Homo sapiens	185-188
19107440-9	2009	Significant correlation between G:C --&gt; A:T transitions in the TP53 gene and promoter methylation of the O6 -methylguanine-DNA methyltransferase (MGMT) gene in glio-mas have been reported in several studies, suggesting the possible involvement of O6-methylguanine DNA adducts, which may be produced by exogenous or endogenous alkylating agents in the development of gliomas.	O-(6)-methylguanine	250-266	P53	Homo sapiens	66-70
10874024-0	2000	P53 expression, p53 and Ha-ras mutation and telomerase activation during nitrosamine-mediated hamster pouch carcinogenesis.	Nitrosamines	73-84	P53	Homo sapiens	0-3
10850407-2	2000	The arginine allele at codon 72 of p53 was found to be more susceptible to degradation by HPV E6 protein than is the proline allele in vivo, thus resulting in a high frequency of cervical SCC in individuals homozygous for arginine at the codon.	Proline	117-124	P53	Homo sapiens	35-38
19020764-0	2008	Differential role of diphenyleneiodonium, a flavoenzyme inhibitor, on p53-dependent and -independent cell cycle progression.	diphenyleneiodonium	21-40	P53	Homo sapiens	70-73
12725069-0	2000	[Mutation of p53 and Ki-ras gene in human fetal lung fibroblast cells in vitro by sterigmatocystin].	Sterigmatocystin	82-98	P53	Homo sapiens	13-16
12725069-1	2000	To explore the carcinogenic effects of sterigmatocystin(ST), one of the predominant contaminating mycotoxins in high risk areas of cancer in China, mutation of tumor suppressor gene p53 and oncogene Ki-ras in human fetal lung cells in vitro induced by ST was studied using cell culture and silver-staining PCR-SSCP methods.	Sterigmatocystin	39-55	P53	Homo sapiens	182-185
10813720-3	2000	RESULTS: Among these polymorphisms, the individuals carrying arginine/proline genotypes of p53 showed a 9.5-fold increase of cervical carcinoma risk (95% confidence interval [CI], 4.9-18.6) compared with those individuals carrying arginine/arginine genotypes.	Proline	70-77	P53	Homo sapiens	91-94
10813720-6	2000	The individuals carrying both the arginine/proline genotype of p53 and the null genotype of GSTT1 showed a 3.5-fold increase of cervical carcinoma risk (95% CI, 1.8-7.1) compared with those individuals carrying both the arginine/arginine genotype of p53 and the GSTT1 positive genotype.	Proline	43-50	P53	Homo sapiens	63-66
19020764-2	2008	DPI efficiently blocked the transition from G0/G1 to S phase by serum stimulation in quiescent HCT-116 (wild-type p53) and HL-60 (null p53) cells.	diphenyleneiodonium	0-3	P53	Homo sapiens	114-117
10813720-9	2000	CONCLUSIONS: The results of the current study suggested that the arginine/proline genotype of p53, independently or in conjunction with the GSTT1 null genotype, could affect the genetic susceptibility for cervical carcinoma, and HPV positive women carrying both null genotypes of GSTT1 and GSTM1 have an increased risk of cervical carcinoma developing before age 40 years.	Proline	74-81	P53	Homo sapiens	94-97
19020764-2	2008	DPI efficiently blocked the transition from G0/G1 to S phase by serum stimulation in quiescent HCT-116 (wild-type p53) and HL-60 (null p53) cells.	diphenyleneiodonium	0-3	P53	Homo sapiens	135-138
19020764-3	2008	Concomitant with G0/G1 arrest, HCT-116 cells treated with DPI resulted in strong and sustained upregulation of p53 and p21.	diphenyleneiodonium	58-61	P53	Homo sapiens	111-114
19020764-4	2008	p53- or p21-deficient HCT-116 cells using a small interfering RNA (siRNA) significantly increased the progression into S phase by stimulation of DPI, compared with DPI alone.	diphenyleneiodonium	145-148	P53	Homo sapiens	0-3
10775606-8	2000	The deletion analysis of the p53 protein shows that the RPA binding, proline-rich regulatory, DNA-binding, and oligomerization domains are necessary for p53 action in both replication systems.	Proline	69-76	P53	Homo sapiens	29-32
10775606-8	2000	The deletion analysis of the p53 protein shows that the RPA binding, proline-rich regulatory, DNA-binding, and oligomerization domains are necessary for p53 action in both replication systems.	Proline	69-76	P53	Homo sapiens	153-156
19020764-4	2008	p53- or p21-deficient HCT-116 cells using a small interfering RNA (siRNA) significantly increased the progression into S phase by stimulation of DPI, compared with DPI alone.	diphenyleneiodonium	164-167	P53	Homo sapiens	0-3
10719058-4	2000	It was revealed that the arginine form of p53 is more susceptible to degradation by the HPV E6 protein than the proline form and that patients with the arginine form have a higher risk of developing cancer than those with the proline form.	Proline	112-119	P53	Homo sapiens	42-45
19020764-5	2008	However, the silencing of p53 resulted in more efficient transition into S phase than the silencing of p21 siRNA and significantly inhibited p21 upregulation by DPI stimulation.	diphenyleneiodonium	161-164	P53	Homo sapiens	26-29
10719058-4	2000	It was revealed that the arginine form of p53 is more susceptible to degradation by the HPV E6 protein than the proline form and that patients with the arginine form have a higher risk of developing cancer than those with the proline form.	Proline	226-233	P53	Homo sapiens	42-45
19020764-7	2008	These results suggest that p53 upregulation sustains G0/G1 cell cycle arrest and p21 upregulation by DPI stimulation in HCT-116 cells.	diphenyleneiodonium	101-104	P53	Homo sapiens	27-30
19020764-8	2008	In HL-60 cells, DPI also induced p21 upregulation in a p53-independent manner and the increase of p21 expression seems to be regulated by DPI-mediated ERK activation.	diphenyleneiodonium	16-19	P53	Homo sapiens	55-58
19137883-9	2008	RESULTS: The genetic genotype of p53 gene codon 72 in keloids included Arg/Arg in 7 cases, Pro/Arg in 21 cases, Pro/ Pro in 7 cases.	Proline	91-94	P53	Homo sapiens	33-36
10777217-2	2000	A p53 protein lacking the proline-rich region (p53delta62-91) induces many p53-responsive genes but not PIG3.	Proline	26-33	P53	Homo sapiens	2-5
10777217-2	2000	A p53 protein lacking the proline-rich region (p53delta62-91) induces many p53-responsive genes but not PIG3.	Proline	26-33	P53	Homo sapiens	47-50
10777217-4	2000	We show here that the replacement of the N-terminal (amino acids 1-80) or C-terminal (amino acids 344-393) domains of p53 with heterologous domains does not interfere with transcription from the PIG3 promoter, but these chimeras still require the proline-rich region for PIG3 activation.	Proline	247-254	P53	Homo sapiens	118-121
10777217-10	2000	Our results suggest that the proline-rich domain of p53 affects the ability of the central domain to bind DNA.	Proline	29-36	P53	Homo sapiens	52-55
19137883-9	2008	RESULTS: The genetic genotype of p53 gene codon 72 in keloids included Arg/Arg in 7 cases, Pro/Arg in 21 cases, Pro/ Pro in 7 cases.	Proline	112-115	P53	Homo sapiens	33-36
10777217-11	2000	Moreover, some tumor-derived mutations within the central DNA binding domain of p53 mimic the loss of the proline-rich domain.	Proline	106-113	P53	Homo sapiens	80-83
19137883-9	2008	RESULTS: The genetic genotype of p53 gene codon 72 in keloids included Arg/Arg in 7 cases, Pro/Arg in 21 cases, Pro/ Pro in 7 cases.	Proline	112-115	P53	Homo sapiens	33-36
18787402-3	2008	In p53(+/+) cells, the combination of Ly + Te + Ca (10(-3) M of each) caused significant accumulation of cells in PreG(1) (64% at 48 hours); less preG(1) increase was observed in response to Ly + Te (25%) or Ly + Ca (14%).	te + ca	43-50	P53	Homo sapiens	3-6
10792785-2	2000	P53 protein was detected by the streptavidin-biotin method and point mutation of K-ras codon 12 was detected by polymerase chain reaction-restriction fragment length polymorphism analysis.	Biotin	45-51	P53	Homo sapiens	0-3
18836303-7	2008	After treatment with FLX, A549 and HT29 cells demonstrated concentration-dependent decrease in the expression of c-fos, c-jun, cyclin A, cyclin D1, and increased expression of p21(waf1) and p53 genes, which resulted in slowing of the cell cycle progression.	Fluoxetine	21-24	P53	Homo sapiens	190-193
10708967-4	2000	This manuscript reports on the mutagenic consequences of replication past anti-BaPDE-deoxyadenosine adducts located within a sequence context related to codon 157 in exon 5 of the p53 gene.	bapde	79-84	P53	Homo sapiens	180-183
18818514-6	2008	Assays using okadaic and cantharidic acid, two different PP2A inhibitors, showed an increase in microtubule-bound phospho-p53 and reduced sensitivity to chemotherapy.	okadaic	13-20	P53	Homo sapiens	122-125
10680816-2	2000	Sequencing of the p53 gene, exon 4, showed heterozygosity (Arg-Pro) at codon 72 in five of six PML patients.	Proline	63-66	P53	Homo sapiens	18-21
18662769-0	2008	The mycotoxin Zearalenone induces apoptosis in human hepatocytes (HepG2) via p53-dependent mitochondrial signaling pathway.	Zearalenone	14-25	P53	Homo sapiens	77-80
10719810-7	2000	Multivariate analysis revealed that p53 positive group was associated with less CR rate compared to the p53 negative group (p=0.046), whereas overall survival was correlated with stage (p=0.0320), not with p53 status.	Chromium	80-82	P53	Homo sapiens	36-39
10719810-8	2000	p53 expression was associated with less CR rate in patients with DLBL.	Chromium	40-42	P53	Homo sapiens	0-3
10719811-1	2000	A common polymorphism of the wild type p53 is known at codon 72 of exon 4, with 2 alleles encoding either arginine (CGC, p53Arg) or proline (CCC, p53Pro).	Proline	132-139	P53	Homo sapiens	39-42
18662769-14	2008	In summary, these data suggested that Zen induced apoptosis in a dose-dependent manner in HepG2 cells via a p53-dependent mitochondrial pathway.	Zearalenone	38-41	P53	Homo sapiens	108-111
18758421-2	2008	A common polymorphism at codon 72 of exon 4 of the p53 gene encoding either an arginine or proline has been shown to confer susceptibility to the development of different human malignancies.	Proline	91-98	P53	Homo sapiens	51-54
10673394-2	2000	Supershifting of p53-DNA complexes by MAbs in agarose gels was applied to studies of activation of p53 for sequence-specific binding within scDNA.	Sepharose	46-53	P53	Homo sapiens	17-20
10673394-2	2000	Supershifting of p53-DNA complexes by MAbs in agarose gels was applied to studies of activation of p53 for sequence-specific binding within scDNA.	Sepharose	46-53	P53	Homo sapiens	99-102
18782054-2	2008	A wide range of potential mechanisms have been proposed for the antitumorigenic effects of selenium and these include antiandrogen activity, growth inhibitory effects by regulation of p53 and antioxidant function, and through DNA damage.	Selenium	91-99	P53	Homo sapiens	184-187
10982614-6	2000	Investigation of K-ras mutation and overexpression of p53 protein was performed using an enriched polymerase chain reaction (PCR) and enzyme-linked mini-sequence assay (ELMA), and by the streptavidin-biotin (SAB) method, using DO-7 antibodies, respectively.	Biotin	200-206	P53	Homo sapiens	54-57
18632613-2	2008	To identify such apoptosis-associated p53 target genes, we used the pro-oxidant plant-derived drug thymoquinone and compared p53+/+ and p53-/- colon cancer cells HCT116.	thymoquinone	99-111	P53	Homo sapiens	38-41
10772725-0	2000	Excision of beta-L- and beta-D-nucleotide analogs from DNA by p53 protein.	beta-l- and beta-d-nucleotide	12-41	P53	Homo sapiens	62-65
18583938-5	2008	p53-like isoforms of p73 (TAp73) are upregulated early during the transformation process in response to RB pathway alterations and block progression to the fully transformed state.	Rubidium	104-106	P53	Homo sapiens	0-3
10606231-0	1999	Combination therapy with the farnesyl protein transferase inhibitor SCH66336 and SCH58500 (p53 adenovirus) in preclinical cancer models.	sch58500	81-89	P53	Homo sapiens	91-94
10606231-4	1999	In preclinical models, SCH58500 has therapeutic efficacy against a wide range of human tumor types containing nonfunctional p53 and enhanced activity in combination with many chemotherapeutic drugs.	sch58500	23-31	P53	Homo sapiens	124-127
18348141-1	2008	In vitro studies suggest that p53 codon 72 genotype alters the apoptotic capacity of p53 protein, with the 72 arginine (R) form of wild-type p53 harboring a greater apoptosis-inducing potential than the 72 proline (P) variant.	Proline	206-213	P53	Homo sapiens	30-33
18348141-1	2008	In vitro studies suggest that p53 codon 72 genotype alters the apoptotic capacity of p53 protein, with the 72 arginine (R) form of wild-type p53 harboring a greater apoptosis-inducing potential than the 72 proline (P) variant.	Proline	206-213	P53	Homo sapiens	85-88
18348141-1	2008	In vitro studies suggest that p53 codon 72 genotype alters the apoptotic capacity of p53 protein, with the 72 arginine (R) form of wild-type p53 harboring a greater apoptosis-inducing potential than the 72 proline (P) variant.	Proline	206-213	P53	Homo sapiens	85-88
18600519-4	2008	Raji cells treated with FdA (3 micro M, 24 hours), accumulate multiple phosphorylated forms of p53 in the nucleus that in turn degrade to phosphorylated forms of p40.	fda	24-27	P53	Homo sapiens	95-98
18483381-4	2008	RESULTS: In this report, we show that the HDIs trichostatin A, sodium butyrate, and low nanomolar doses of LAQ824 combined with the glycolysis inhibitor 2-deoxy-d-glucose induce strong apoptosis in cancer cell lines of brain, breast, and cervix in a p53-independent manner.	Butyric Acid	63-78	P53	Homo sapiens	250-253
18489080-7	2008	An RP-HPLC-ECD assay was used to detect the formation of 8-oxo-dGuo in p53 cDNA exposed to representative quinones, BP-7,8-dione, BA-3,4-dione, and DMBA-3,4-dione under redox cycling conditions.	bp-7,8-dione	116-128	P53	Homo sapiens	71-74
18296503-3	2008	The binding of hnRNPC1/C2 is strongly enhanced in response to the DNA-damaging drug cisplatin [cis-diamminedichloroplatinum(II)] and the cytostatic transcriptional inhibitor actinomycin D (dactinomycin), both known inducers of apoptosis and p53.	Dactinomycin	174-187	P53	Homo sapiens	241-244
18296503-3	2008	The binding of hnRNPC1/C2 is strongly enhanced in response to the DNA-damaging drug cisplatin [cis-diamminedichloroplatinum(II)] and the cytostatic transcriptional inhibitor actinomycin D (dactinomycin), both known inducers of apoptosis and p53.	Dactinomycin	189-201	P53	Homo sapiens	241-244
18215142-0	2008	The 7-amino-acid site in the proline-rich region of the N-terminal domain of p53 is involved in the interaction with FAK and is critical for p53 functioning.	Proline	29-36	P53	Homo sapiens	141-144
18215142-4	2008	In the present study, using phage display, sitedirected mutagenesis, pulldown and immunoprecipitation assays we localized the site of FAK binding to a 7-amino-acid region(amino acids 65-71) in the N-terminal proline-rich domain of human p53.	Proline	208-215	P53	Homo sapiens	237-240
17610029-0	2008	Selenium activates p53 and p38 pathways and induces caspase-independent cell death in cervical cancer cells.	Selenium	0-8	P53	Homo sapiens	19-22
18288414-2	2008	Several reports have focused on p53 polymorphisms as risk factors in lung cancer, in particular at codon 72 of exon 4, encoding either an arginine (Arg72R) or a proline (Pro72P) amino acid.	arg72r	148-154	P53	Homo sapiens	32-35
18288414-2	2008	Several reports have focused on p53 polymorphisms as risk factors in lung cancer, in particular at codon 72 of exon 4, encoding either an arginine (Arg72R) or a proline (Pro72P) amino acid.	Proline	161-168	P53	Homo sapiens	32-35
18235226-2	2008	In most cases, apoptosis in response to Rb inactivation involves the activation of p53 but the molecular details of the signaling pathway connecting Rb loss to p53 are poorly understood.	Rubidium	40-42	P53	Homo sapiens	83-86
18245478-3	2008	In vitro treatment with etoposide only and in vivo treatment with either etoposide or mitoxantrone induces DNA damage, elevates expression (600-fold) and promotes nuclear translocation of p53, and results in apoptosis of leukemic clam hemocytes.	Mitoxantrone	86-98	P53	Homo sapiens	188-191
18024214-2	2008	Chromium exposure resulted in a 500-1000 fold increase in apoptosis-induced cell death in p21-/- HCT116 cells compared to wild-type or p53-/- cells.	Chromium	0-8	P53	Homo sapiens	135-138
18202802-10	2008	Although further studies are needed to prove that an increased expression of Egr-1 by PTX-2 directly leads to NAG-1 induction and then apoptosis induction in p53-deficient Hep3B cells, the results of this study suggest that PTX-2 may be a good candidate for the development of a potential anti-tumorigenic agent in p53-deficient tumors.	ptx	86-89	P53	Homo sapiens	158-161
19065769-3	2008	TP53 codon 72 polymorphism results in either the arginine or proline form of the p53 protein; several studies have investigated whether codon 72 polymorphisms are risk and prognostic factors for cancer.	Proline	61-68	P53	Homo sapiens	0-4
19065769-3	2008	TP53 codon 72 polymorphism results in either the arginine or proline form of the p53 protein; several studies have investigated whether codon 72 polymorphisms are risk and prognostic factors for cancer.	Proline	61-68	P53	Homo sapiens	81-84
18097482-3	2008	Chloroquine-induced cell death in primary MEFs and human colorectal cancer cells was dependent upon p53, but not upon the p53 modulators Atm or Arf.	Chloroquine	0-11	P53	Homo sapiens	100-103
18670615-5	2008	Previous studies showed that proline oxidase is a p53-induced gene and its overexpression can initiate proline-dependent apoptosis by both intrinsic and extrinsic pathways.	Proline	29-36	P53	Homo sapiens	50-53
18089819-4	2007	Here we show that ACNU and BCNU induce apoptosis in U87MG [p53 wild-type (p53wt)] and U138MG [p53 mutant (p53mt)] glioma cells.	Carmustine	27-31	P53	Homo sapiens	59-62
18089819-4	2007	Here we show that ACNU and BCNU induce apoptosis in U87MG [p53 wild-type (p53wt)] and U138MG [p53 mutant (p53mt)] glioma cells.	Carmustine	27-31	P53	Homo sapiens	74-77
18089819-4	2007	Here we show that ACNU and BCNU induce apoptosis in U87MG [p53 wild-type (p53wt)] and U138MG [p53 mutant (p53mt)] glioma cells.	Carmustine	27-31	P53	Homo sapiens	74-77
17971768-6	2007	Combination treatment and PEG-IFN monotherapy also significantly elevated the p53 protein and mRNA levels in the tumour but only combination treatment increased the degree of p53 phosphorylation at serine46 and induced p53-regulated apoptosis-inducing protein 1 (p53AIP1) expression.	serine46	198-206	P53	Homo sapiens	175-178
17971768-7	2007	The antitumour effects of combination treatment is due in part to the elevation by PEG-IFN of p53 protein and mRNA expression and in part to the DNA damage that is generated by 5-FU, which induces p53 serine46 phosphorylation, which in turn upregulates p53AIP1 expression.	serine46	201-209	P53	Homo sapiens	197-200
17855051-3	2007	In this study, we show that Bax translocation, caspase-3 activation and cell death by UV irradiation are not affected by Z-IETD-fmk (caspase-8 inhibitor), but delayed by Pifithrin-alpha (p53 inhibitor), although Bid cleavage could be completely abolished by Z-IETD-fmk.	benzyloxycarbonyl-isoleucyl-glutamyl-threonyl-aspartic acid fluoromethyl ketone	258-268	P53	Homo sapiens	187-190
17929901-9	2007	Also, a decrease in the longer chain gangliosides, GD1 and GM1b, is observed in wild-type p53 (treated) cells.	ganglioside M1b	59-63	P53	Homo sapiens	90-93
17653713-3	2007	On the other hand, a common polymorphism of the tumour suppressor P53 gene results in either arginine (A) or proline (P) at amino-acid position 72.	Proline	109-116	P53	Homo sapiens	66-69
17954263-0	2007	Proline homozygosity in codon 72 of TP53 is a factor of susceptibility to nasopharyngeal carcinoma in Tunisia.	Proline	0-7	P53	Homo sapiens	36-40
17954263-1	2007	A common polymorphism at codon 72 of TP53, the gene encoding the tumor suppressor protein p53, encodes either arginine or proline.	Proline	122-129	P53	Homo sapiens	37-41
17954263-1	2007	A common polymorphism at codon 72 of TP53, the gene encoding the tumor suppressor protein p53, encodes either arginine or proline.	Proline	122-129	P53	Homo sapiens	90-93
17698841-5	2007	Ubiquitination of p53 in mock-infected LU cells was sensitive to inhibition by trans-4-iodo, 4"-boranyl-chalcone, consistent with HDM2-catalyzing ubiquitination of p53.	trans-4-iodo	79-91	P53	Homo sapiens	18-21
17698841-5	2007	Ubiquitination of p53 in mock-infected LU cells was sensitive to inhibition by trans-4-iodo, 4"-boranyl-chalcone, consistent with HDM2-catalyzing ubiquitination of p53.	trans-4-iodo	79-91	P53	Homo sapiens	164-167
17045269-7	2007	Furthermore, cyanidin also restored S-nitrosylation of caspase-3 and reduced the rise in expression and acetylation of tumor suppression gene p53.	cyanidin	13-21	P53	Homo sapiens	142-145
21603516-5	2007	EXPERIMENTAL DESIGN: The p53-null human erythroleukemia cell line, K-562, was stably transfected with a tetracycline-repressible p53 expression construct (p53/pUHD10-3).	Tetracycline	104-116	P53	Homo sapiens	25-28
21603516-5	2007	EXPERIMENTAL DESIGN: The p53-null human erythroleukemia cell line, K-562, was stably transfected with a tetracycline-repressible p53 expression construct (p53/pUHD10-3).	Tetracycline	104-116	P53	Homo sapiens	129-132
21603516-5	2007	EXPERIMENTAL DESIGN: The p53-null human erythroleukemia cell line, K-562, was stably transfected with a tetracycline-repressible p53 expression construct (p53/pUHD10-3).	Tetracycline	104-116	P53	Homo sapiens	129-132
21603516-6	2007	p53 protein in these cells is expressed in the absence of tetracycline but down-regulated upon tetracycline treatment.	Tetracycline	58-70	P53	Homo sapiens	0-3
21603516-6	2007	p53 protein in these cells is expressed in the absence of tetracycline but down-regulated upon tetracycline treatment.	Tetracycline	95-107	P53	Homo sapiens	0-3
16973168-4	2007	The high-arsenic exposure group with GSTP1 variant genotypes of Ile/Val and Val/Val, and with the p53 variant genotypes of Arg/Pro and Pro/Pro had 6.0- and 3.1-fold higher risks of carotid atherosclerosis, respectively.	Proline	127-130	P53	Homo sapiens	98-101
16973168-4	2007	The high-arsenic exposure group with GSTP1 variant genotypes of Ile/Val and Val/Val, and with the p53 variant genotypes of Arg/Pro and Pro/Pro had 6.0- and 3.1-fold higher risks of carotid atherosclerosis, respectively.	Proline	135-138	P53	Homo sapiens	98-101
16973168-4	2007	The high-arsenic exposure group with GSTP1 variant genotypes of Ile/Val and Val/Val, and with the p53 variant genotypes of Arg/Pro and Pro/Pro had 6.0- and 3.1-fold higher risks of carotid atherosclerosis, respectively.	Proline	135-138	P53	Homo sapiens	98-101
17671760-2	2007	The proapoptotic activity of p53 seems to be strictly related to proline-rich regions, homologous to the SH3 binding domain.	Proline	65-72	P53	Homo sapiens	29-32
17485089-5	2007	In addition, our immunoblot data revealed that DHMC treatment led to down-regulation of Bcl-xl, Bax, p21, Cox-2, p53 and upregulation of c-Myc.	7,8-dihydroxy-4-methylcoumarin	47-51	P53	Homo sapiens	113-116
17686239-9	2007	The CR rate of the p53 positive patients was 74%, higher than that of the p53 negative patients (44%, P = 0.065).	Chromium	4-6	P53	Homo sapiens	19-22
17208332-1	2007	The TP53 gene has a polymorphism in exon 4 at codon 72 that presents the arginine or proline genotype.	Proline	85-92	P53	Homo sapiens	4-8
17428192-6	2007	The effect of LIUS on the apoptotic event was further demonstrated by changes in the expression of apoptosis/viability related genes of p53, bax, bcl-2, and PCNA.	lius	14-18	P53	Homo sapiens	136-139
17118344-0	2007	Irofulven induces replication-dependent CHK2 activation related to p53 status.	irofulven	0-9	P53	Homo sapiens	67-70
17118344-9	2007	Overall, this study demonstrates that in response to irofulven-induced DNA damage, the activation of CHK2 is dependent on DNA replication and related to p53 status.	irofulven	53-62	P53	Homo sapiens	153-156
17223878-1	2007	BACKGROUND: p53 has a common polymorphism at amino acid 72, encoding either arginine or proline.	Proline	88-95	P53	Homo sapiens	12-15
17257432-6	2007	We also find that selenium induces expression of Ref-1 which, in turn, modifies the activity of p53 during the cell cycle.	Selenium	18-26	P53	Homo sapiens	96-99
17257432-7	2007	CONCLUSION: We can conclude from the results that the suppression of gene repair by introduction of selenomethionine occurs through a p53-associated pathway.	Selenomethionine	100-116	P53	Homo sapiens	134-137
17136495-0	2007	Increased ROS generation and p53 activation in alpha-lipoic acid-induced apoptosis of hepatoma cells.	Thioctic Acid	47-64	P53	Homo sapiens	29-32
17172818-6	2007	p21waf1/cip1 protein levels increased without a significant increase in wild-type p53, suggesting that sulindac sulfide induces a p53-independent pathway regulating p2lwafl/ciP1 protein levels in SCCHN.	sulindac sulfide	103-119	P53	Homo sapiens	130-133
17210690-2	2007	To identify novel regulators of p53, we have used a phenotype-based selection in which a total cDNA library in a retroviral vector has been introduced into TR9-7ER cells, which arrest when p53 is expressed from a tetracycline-regulated promoter.	Tetracycline	213-225	P53	Homo sapiens	189-192
17319790-11	2007	In the younger women group, the p53 BstUI polymorphism genotype frequencies were 6.2% for BstUIPro/Pro, 31.0% for BstUIArg/Pro and 62.8% for BstUIArg/Arg in controls and 11.11 %, 40.74% and 48.15% in cases respectively.	Proline	95-98	P53	Homo sapiens	32-35
17213797-3	2006	BaP 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of BaP, attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 mutations.	7,8-diol	4-12	P53	Homo sapiens	129-132
17213797-3	2006	BaP 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of BaP, attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 mutations.	9,10-epoxide	13-25	P53	Homo sapiens	129-132
17133272-1	2006	HIV-1 protease inhibitor (PI), nelfinavir (NFV) induced growth arrest and apoptosis of NCI-H460 and -H520, A549, EBC-1 and ABC-1 non-small-cell lung cancer (NSCLC) cells in association with upregulation of p21waf1, p27kip1 and p53, and downregulation of Bcl-2 and matrix metalloproteinase (MMP)-2 proteins.	Nelfinavir	31-41	P53	Homo sapiens	227-230
16971506-10	2006	p53 phosphorylation was induced by serum withdrawal and other chemotherapeutic reagents such as actinomycin D, doxorubicin, and etoposide.	Dactinomycin	96-109	P53	Homo sapiens	0-3
17172419-6	2006	Previously, we have shown that irofulven activates ATM and its targets, NBS1, SMC1, CHK2, and p53.	irofulven	31-40	P53	Homo sapiens	94-97
16798066-6	2006	o-PD and Cl-PD caused piperidine-labile and formamidopyrimidine-DNA glycosylase-sensitive lesions at cytosine and guanine residues respectively in the 5"-ACG-3" sequence, complementary to codon 273, a well-known hotspot of the human p53 tumor suppressor gene.	formamidopyrimidine	44-63	P53	Homo sapiens	233-236
17094395-1	2006	BACKGROUND: The oncoprotein E6 binds to and degrades the p53 tumor suppressor protein, with different efficacy depending on the p53 codon 72 (arg/pro) polymorphism.	Proline	20-23	P53	Homo sapiens	57-60
17094395-1	2006	BACKGROUND: The oncoprotein E6 binds to and degrades the p53 tumor suppressor protein, with different efficacy depending on the p53 codon 72 (arg/pro) polymorphism.	Proline	20-23	P53	Homo sapiens	128-131
16966095-2	2006	Using a model cell line in which p53 expression is regulated exogenously in a tetracycline-off system (TR9-7 cells) , our laboratory has shown that arsenite disrupts mitosis and that p53-deficient cells [p53(-)], in contrast to p53-expressing cells [p53(+)], display greater sensitivity to arsenite-induced mitotic arrest and apoptosis.	Tetracycline	78-90	P53	Homo sapiens	33-36
16923170-3	2006	Tauroursodeoxycholic acid (TUDCA) modulates exogenous Abeta-induced apoptosis by interfering with E2F-1/p53/Bax.	ursodoxicoltaurine	27-32	P53	Homo sapiens	104-107
16923170-9	2006	Overexpression of p53, but not mutant p53, in wild-type and mutant neuroblastoma cells was sufficient to induce apoptosis, which, in turn, was reduced by TUDCA.	ursodoxicoltaurine	154-159	P53	Homo sapiens	18-21
16923170-10	2006	In addition, inhibition of the phosphatidylinositide 3"-OH kinase pathway reduced TUDCA protection against p53-induced apoptosis.	ursodoxicoltaurine	82-87	P53	Homo sapiens	107-110
10600330-11	1999	We propose that leflunomide prevents the expansion of activated and autoimmune lymphocytes by interfering with the cell cycle progression due to inadequate production of rUMP and utilizing mechanisms involving p53.	Leflunomide	16-27	P53	Homo sapiens	210-213
16906043-4	2006	Whole blood (part 1+2) was stimulated (24 hr) with eight different concentrations of actinomycin-D (0-800 nM), an apoptosis inductor acting via p53-pathway.	Dactinomycin	85-98	P53	Homo sapiens	144-147
10570149-7	1999	Substitution of Ser-20 was sufficient to abrogate p53 stabilization in response to both IR and UV light.	ser-20	16-22	P53	Homo sapiens	50-53
10597242-6	1999	Inhibition of transcription by Actinomycin D blocks both KILLER/DR5 and p21 induction in cells undergoing p53-dependent apoptosis.	Dactinomycin	31-44	P53	Homo sapiens	106-109
16830228-0	2006	Apoptotic effect of ethyl-4-isothiocyanatobutanoate is associated with DNA damage, proteasomal activity and induction of p53 and p21cip1/waf1.	ethyl 4-isothiocyanatobutanoate	20-51	P53	Homo sapiens	121-124
10567774-0	1999	Cellular effects of olomoucine in human lymphoma cells differing in p53 function.	olomoucine	20-30	P53	Homo sapiens	68-71
10567774-2	1999	In this study we investigated the cellular effects of olomoucine in two human Burkitt"s lymphoma cell lines, WMN (containing wild-type p53) and CA46 (containing mutant p53), and found that in consistency with its ability to block the activity of cyclin E/Cdk2 and cyclin B1/Cdc2 kinases, olomoucine caused cell cycle arrest at both G1/S and G2/S boundaries.	olomoucine	54-64	P53	Homo sapiens	135-138
10567774-2	1999	In this study we investigated the cellular effects of olomoucine in two human Burkitt"s lymphoma cell lines, WMN (containing wild-type p53) and CA46 (containing mutant p53), and found that in consistency with its ability to block the activity of cyclin E/Cdk2 and cyclin B1/Cdc2 kinases, olomoucine caused cell cycle arrest at both G1/S and G2/S boundaries.	olomoucine	54-64	P53	Homo sapiens	168-171
10567774-4	1999	A similar p53-independent fashion was also observed in the cytotoxic potency and apoptosis induction of olomoucine, in contrast to ionizing radiation which caused more cytotoxic activity and apoptosis in the WMN cell line bearing wild-type p53 compared with CA46 cells bearing mutant p53.	olomoucine	104-114	P53	Homo sapiens	10-13
16624812-3	2006	To further understand how excess HDM2 regulates p53-mediated functions, we generated H1299 cell clones that constitutively express both ectopic HDM2 and tetracycline-regulated inducible p53.	Tetracycline	153-165	P53	Homo sapiens	48-51
10567774-5	1999	Such p53-independent cytotoxicity of olomoucine was also confirmed in other human Burkitt"s lymphoma and lymphoid cell lines containing wild-type and mutant p53.	olomoucine	37-47	P53	Homo sapiens	5-8
10567774-5	1999	Such p53-independent cytotoxicity of olomoucine was also confirmed in other human Burkitt"s lymphoma and lymphoid cell lines containing wild-type and mutant p53.	olomoucine	37-47	P53	Homo sapiens	157-160
10567774-6	1999	Therefore, our results give an impetus to continued research into olomoucine that might be a very useful chemotherapeutic strategy in the treatment of patients with mutant p53 tumors, at least in lymphoma patients.	olomoucine	66-76	P53	Homo sapiens	172-175
16624812-3	2006	To further understand how excess HDM2 regulates p53-mediated functions, we generated H1299 cell clones that constitutively express both ectopic HDM2 and tetracycline-regulated inducible p53.	Tetracycline	153-165	P53	Homo sapiens	186-189
10626356-0	1999	Role of p53 in the ability of 1,2-diaminocyclohexane-diacetato-dichloro-Pt(IV) to circumvent cisplatin resistance.	1,2-diaminocyclohexane-diacetato-dichloro-pt	30-74	P53	Homo sapiens	8-11
10545796-5	1999	Western analyses revealed that, though both actinomycin D and 5-MeCDE treatment stabilized p53, only trace levels of p21(waf1/cip1) were seen in the latter case.	Dactinomycin	44-57	P53	Homo sapiens	91-94
16981429-0	2006	The inhibitory action of long-chain fatty acids on the DNA binding activity of p53.	long-chain fatty acids	25-47	P53	Homo sapiens	79-82
10449610-1	1999	A polymorphism at codon 72 of the p53 gene, resulting in either an arginine or a proline residue in the protein, has been reported to affect the susceptibility of p53 to human papillomavirus (HPV) E6-mediated degradation in cultured cells.	Proline	81-88	P53	Homo sapiens	34-37
10449610-1	1999	A polymorphism at codon 72 of the p53 gene, resulting in either an arginine or a proline residue in the protein, has been reported to affect the susceptibility of p53 to human papillomavirus (HPV) E6-mediated degradation in cultured cells.	Proline	81-88	P53	Homo sapiens	163-166
9707426-6	1998	To explain this discrepancy, evidence is given for a proline-rich domain-mediated cellular activation of p53 DNA binding.	Proline	53-60	P53	Homo sapiens	105-108
16697770-9	2006	Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033].	Proline	51-54	P53	Homo sapiens	47-50
10473656-10	1999	The results in KS, as compared with K562, confirm that wild-type p53 can prevent further cycling of polyploid cells by blocking rereplication.	Potassium	15-17	P53	Homo sapiens	65-68
10582657-15	1999	Induction of p53 levels was observed in WHCO3 cells exposed to GLA, AA, PGA2, indomethacin and the combination of indomethacin and GLA or AA.	Indomethacin	114-126	P53	Homo sapiens	13-16
9658131-2	1998	Oligomerization, intact DNA-binding, replication protein A-binding, and proline-rich domains of the p53 protein were essential for efficient inhibition, while the N-terminal transcriptional activation and C-terminal regulatory domains were dispensable for the suppressor activity of the p53 protein.	Proline	72-79	P53	Homo sapiens	100-103
16697770-9	2006	Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033].	Proline	55-58	P53	Homo sapiens	47-50
10467417-5	1999	Using a series of point and deletion mutants of p53 under the control of tetracycline-regulated promoter we show that certain mutants, like the wild type, protect cells at low levels but lead to apoptosis when overexpressed.	Tetracycline	73-85	P53	Homo sapiens	48-51
9690520-3	1998	Here we report that exposure of macrophages to lipopolysaccharide/interferon-gamma or lipophilic cAMP analogs such as dibutyryl-cAMP or 8-bromo-cAMP for 15 h attenuated DNA fragmentation and accumulation of the tumor suppressor p53 in response to the chemotherapeutic agents cisplatin and etoposide, compared to cells that received chemotherapeutic agents only.	Bucladesine	118-132	P53	Homo sapiens	228-231
16697770-9	2006	Higher ORs for COPD were seen for persons with p53 Pro/Pro or Pro/Arg genotypes against Arg/Arg genotype [OR = 2.35, 95% CI 1.27-4.39, P = 0.008], or p21 Arg/Arg and Arg/Ser genotypes against Ser/Ser genotype [OR = 2.07, 95% CI 1.06-4.05, P = 0.033].	Proline	55-58	P53	Homo sapiens	47-50
10432310-1	1999	The ability to separate the isoforms of human tumour suppressor protein p53 expressed in insect cells using heparin-Sepharose correlates with differences in the isoelectric point of p53, demonstrating that p53 can be heterogeneously modified and providing support for the use of insect cells as a model system for identifying novel signalling pathways that target p53.	Sepharose	116-125	P53	Homo sapiens	72-75
16364678-5	2006	The Streptavidin-biotin method of immunohistochemistry was used for the staining with p53 and Ki67 in 22 cases of OLP and 27 cases diagnosed as OLL.	Biotin	17-23	P53	Homo sapiens	86-89
10403534-0	1999	Differential apoptosis by indomethacin in gastric epithelial cells through the constitutive expression of wild-type p53 and/or up-regulation of c-myc.	Indomethacin	26-38	P53	Homo sapiens	116-119
10682599-0	1998	[Mutation of p53 gene in human fetal gastric mucosal cells by sterigmatocystin in vitro].	Sterigmatocystin	62-78	P53	Homo sapiens	13-16
16518417-4	2006	On the other hand, pretreatment with dicoumarol enhanced cytotoxicity of CDDP in three cell lines with wild type of p53 (RT112, 253J and LNCap), but not in three other cell lines with mutant p53 or in RT112 stable transfectants with a dominant-negative mutant of p53.	Dicumarol	37-47	P53	Homo sapiens	191-194
16518417-5	2006	In RT112 and LNCap, CDDP induced p53 and p21 expression, while pretreatment of dicoumarol suppressed induction of p53/p21 and resulted in sequential activation of c-Jun N-terminal kinase (JNK) in a time-dependent manner.	Dicumarol	79-89	P53	Homo sapiens	114-117
9563901-1	1998	In the present study, we report our findings on the impact of p53 disruption on the sensitivity of human cell lines to the antimitotic agents Taxol and vincristine.	Vincristine	152-163	P53	Homo sapiens	62-65
10347180-4	1999	The yeast two-hybrid and in vitro binding analyses revealed that necdin bound to a narrow region (amino acids 35-62) located between the MDM2-binding site and the proline-rich region in the amino-terminal domain of p53.	Proline	163-170	P53	Homo sapiens	215-218
16518417-7	2006	These results suggested that dicoumarol could enhance cytotoxicity of CDDP in urogenital cancer cells with wild-type p53 through the p53/p21/JNK pathways.	Dicumarol	29-39	P53	Homo sapiens	117-120
10226945-3	1999	One tumor sample (case 23) showed a mis-sense point mutation at codon 177, changing CCC to CTC, which resulted in a substitution of proline to leucine in the p53 protein.	Proline	132-139	P53	Homo sapiens	158-161
9563901-5	1998	We also found that contrary to gamma-irradiation, Taxol and vincristine could induce apoptosis in lymphoma cell lines harboring p53 mutations.	Vincristine	60-71	P53	Homo sapiens	128-131
9506540-3	1998	When p53 was expressed at sublethal levels, it sensitized cells to the DNA-damaging drugs Adriamycin, mitomycin C, actinomycin D, etoposide (VP16), cisplatin and CPT11.	Dactinomycin	115-128	P53	Homo sapiens	5-8
16518417-7	2006	These results suggested that dicoumarol could enhance cytotoxicity of CDDP in urogenital cancer cells with wild-type p53 through the p53/p21/JNK pathways.	Dicumarol	29-39	P53	Homo sapiens	133-136
16426567-2	2006	Using a competition assay on agarose gels we found that the p53 consensus sequences in longer DNA fragments are better targets than the same sequences in shorter DNAs.	Sepharose	29-36	P53	Homo sapiens	60-63
9528853-5	1998	By 8 days after a brief exposure to DNA strand breaking agents, bleomycin or actinomycin D, p53 protein is at baseline levels, while the p53 transactivation level is only slightly above its baseline.	Dactinomycin	77-90	P53	Homo sapiens	92-95
10321740-2	1999	Several functional domains necessary for mediating cell cycle arrest and apoptosis in p53 have been mapped, e.g., the proline-rich domain.	Proline	118-125	P53	Homo sapiens	86-89
10321740-5	1999	We found that p53(delta62-91), which lacks all five PXXP motifs in human p53, is capable of inducing cell cycle arrest but not apoptosis, while p53(gln22-ser23/delta62-91), which contains a double point mutation in the activation domain as well as deletion of the proline-rich domain, completely loses its activity.	Proline	264-271	P53	Homo sapiens	14-17
10321740-10	1999	These results suggest that the proline-rich region may play a role in chromatin remodeling, which counteracts chromatin-mediated repression for some of the endogenous p53 target genes.	Proline	31-38	P53	Homo sapiens	167-170
10079089-4	1999	Ribozyme derivatives that combine a mutation which indirectly slows down the rate of the chemical cleavage step by weakening guanosine binding with additional mutations that weaken substrate binding have greatly enhanced specificity with short oligonucleotide substrates and an mRNA fragment derived from the p53 gene.	Guanosine	125-134	P53	Homo sapiens	309-312
9537652-4	1998	Removal of N,N,N",N"-tetrakis(2-pyridylmethyl)ethylenediamine from culture medium allowed p53 to refold into the immunologically wild-type form, followed by a transient increase in DNA binding, expression of the cyclin-dependent kinase inhibitor p21WAF1, and cell-cycle delay in the G1 phase.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	11-61	P53	Homo sapiens	90-93
9891062-7	1999	Induction of p53 in response to actinomycin D or hypoxic stress decreases AFP expression.	Dactinomycin	32-45	P53	Homo sapiens	13-16
16619485-1	2006	Selenium, in the form of seleno-L-methionine (SeMet), induced Redox-factor-1 (Ref1) and p53 proteins in normal human and mouse fibroblasts.	Selenium	0-8	P53	Homo sapiens	88-91
10626228-2	1999	A plasmid bearing cDNA containing the human p53 gene was reacted in vitro with CAA, then dehydrated for conversion of hydroxyethano into etheno adducts, and primer extension by T7 DNA polymerase in the presence of four dNTPs was performed.	hydroxyethano	118-131	P53	Homo sapiens	44-47
9464250-2	1998	We used doxorubicin (DOX) and sodium butyrate (NaB) to accumulate p53 protein.	Butyric Acid	30-45	P53	Homo sapiens	66-69
16251206-2	2006	Cr(VI) exposure-related lung cancer has a high mutation incidence in the p53 gene.	Chromium	0-2	P53	Homo sapiens	73-76
16531837-5	2006	Western blotting showed increased p53 protein expression in MOLT-4 cells, but not in BEAS-2B cells, after exposure to 0.5 and 3 muM hexavalent chromium for 12 hours and 4 hours, respectively.	Chromium	143-151	P53	Homo sapiens	34-37
9516963-6	1998	Data demonstrated p53-dependent sensitization (&gt; or = 4-fold) to bleomycin, actinomycin D, and 5-fluorouracil and considerably less p53-dependence (&lt; or = 2-fold) for doxorubicin, topotecan, etoposide, and cisplatin in Cl.#27 compared to an equivalent clone containing the pGRE5-EBV vector alone (VC#3).	Dactinomycin	79-92	P53	Homo sapiens	18-21
9516979-6	1998	The results suggest that MDM2-mediated resistance to p53 may be bypassed by p21 and that the Rb phosphorylation state may predict the effects on growth after Ad-p53 or Ad-p21 infection.	Rubidium	93-95	P53	Homo sapiens	161-164
10757447-0	1999	Sodium butyrate modulates p53 and Bcl-2 expression in human retinoblastoma cell lines.	Butyric Acid	0-15	P53	Homo sapiens	26-29
10757447-1	1999	Sodium butyrate (SB) is a potent biological modifier that can induce diverse effects including growth inhibition, differentiation, or apoptosis of many cell types including retinoblastoma (Rb), and modulation of genes such as c-fos and p53.	Butyric Acid	0-15	P53	Homo sapiens	236-239
10757447-1	1999	Sodium butyrate (SB) is a potent biological modifier that can induce diverse effects including growth inhibition, differentiation, or apoptosis of many cell types including retinoblastoma (Rb), and modulation of genes such as c-fos and p53.	Butyric Acid	17-19	P53	Homo sapiens	236-239
9450475-2	1997	While these cells, which express wild-type p53, were arrested in G1 after treatment with actinomycin D (a positive control), treatment with the mammary carcinogen did not cause G1 arrest but instead delayed the cells in the DNA synthesis phase.	Dactinomycin	89-102	P53	Homo sapiens	43-46
9450475-3	1997	In concert with the absence of a G1 arrest, it was found that though both chemical treatments led to increased levels of p53, only the p53 induced by actinomycin D was transcriptionally active and increased the levels of the cyclin dependent kinase inhibitor, p21(waf1/cip1).	Dactinomycin	150-163	P53	Homo sapiens	135-138
11835772-2	1999	METHODS: The expressions of P53 protein and proliferating cell nuclear antigen (PCNA) in 102 cases with malignant eyelid tumors were examined by labelled streptravidin biotin (LSAB) immunohistochemical technique.	Biotin	168-174	P53	Homo sapiens	28-31
16186801-8	2006	Taken together, these data suggest that loss of Rb creates strong selective pressure, via DSB accumulation, for inactivating p53 mutations and that E2F1 contributes to the genetic instability associated with transformation and tumorigenesis.	Rubidium	48-50	P53	Homo sapiens	125-128
14646475-8	1998	Two other agents known to induce apoptosis, vinblastine and actinomycin D, induced a similar pattern of acidic p53 species as that observed for 2-MeOE2.	Dactinomycin	60-73	P53	Homo sapiens	111-114
10023442-9	1998	We also provided wild-type p53 and p53 delta 326 with tetracycline-regulated promoters and stably introduced these constructs into Saos2 and SKBR3 cells.	Tetracycline	54-66	P53	Homo sapiens	35-38
9567617-9	1997	In the breast cancers the p53 is already utilized as chemoresistance marker, directing the therapy, if changed to alternative drugs (Taxolo) which have a p53-independent action.	taxolo	133-139	P53	Homo sapiens	26-29
9567617-9	1997	In the breast cancers the p53 is already utilized as chemoresistance marker, directing the therapy, if changed to alternative drugs (Taxolo) which have a p53-independent action.	taxolo	133-139	P53	Homo sapiens	154-157
9434849-8	1997	All nitro-PAHs tested induced C.G--&gt;A.T transversion, which is observed as the most frequent base-substitution mutation of p53 tumor suppressor gene in human lung cancer.	nitro-pahs	4-14	P53	Homo sapiens	126-129
9788606-2	1998	A common polymorphism of p53, encoding either proline or arginine at position 72, affects the susceptibility of p53 to E6-mediated degradation in vivo; Caucasian women homozygous for arginine 72 reportedly are about seven times more susceptible to HPV-associated carcinoma of the cervix than heterozygotes.	Proline	46-53	P53	Homo sapiens	25-28
9788606-2	1998	A common polymorphism of p53, encoding either proline or arginine at position 72, affects the susceptibility of p53 to E6-mediated degradation in vivo; Caucasian women homozygous for arginine 72 reportedly are about seven times more susceptible to HPV-associated carcinoma of the cervix than heterozygotes.	Proline	46-53	P53	Homo sapiens	112-115
16399623-5	2006	Silymarin pre-treatment reversed the effect of UV irradiation on the expression of phosphorylated Akt and phosphorylated p53 (regulated by Akt activation), followed by down-regulation of Bax and up-regulated expressions of Bcl-2 and Bcl-xL proteins in UV-irradiated A375-S2 cells.	Silymarin	0-9	P53	Homo sapiens	121-124
9893672-1	1998	A new recombinant adenovirus carrying a wild-type p53 gene (AxCAp53) was developed and the combination effect of p53 gene transfer and cis-diamminedichloroplatinum (II) (CDDP) was examined in an ovarian cancer cell line, SK-OV-3, with deletion of the p53 gene.	axcap53	60-67	P53	Homo sapiens	50-53
9764849-4	1998	Prior treatment of cells with cycloheximide or actinomycin D abolished the p53 increase and apoptosis induced by curcumin, suggesting that either de novo p53 protein synthesis or some proteins synthesis for stabilization of p53 is required for apoptosis.	Dactinomycin	47-60	P53	Homo sapiens	75-78
9395239-7	1997	Actinomycin D or cycloheximide prevented cell death, suggesting that, in this system, p53-induced apoptosis depends upon macromolecule biosynthesis.	Dactinomycin	0-13	P53	Homo sapiens	86-89
9315105-7	1997	The relationship between KET and the invertebrate p53 protein sheds light on the evolutionary origin of p53.	ket	25-28	P53	Homo sapiens	50-53
9315105-7	1997	The relationship between KET and the invertebrate p53 protein sheds light on the evolutionary origin of p53.	ket	25-28	P53	Homo sapiens	104-107
9764849-4	1998	Prior treatment of cells with cycloheximide or actinomycin D abolished the p53 increase and apoptosis induced by curcumin, suggesting that either de novo p53 protein synthesis or some proteins synthesis for stabilization of p53 is required for apoptosis.	Dactinomycin	47-60	P53	Homo sapiens	154-157
9764849-4	1998	Prior treatment of cells with cycloheximide or actinomycin D abolished the p53 increase and apoptosis induced by curcumin, suggesting that either de novo p53 protein synthesis or some proteins synthesis for stabilization of p53 is required for apoptosis.	Dactinomycin	47-60	P53	Homo sapiens	154-157
16418181-2	2006	The promoter of PIG3 contains a variable number of tandem repeats (VNTRs) of pentanucleotides (TGYCC)n (Y = C or T) and the number of VNTRs was reported to be correlated with the activation by TP53.	pentanucleotides	77-93	P53	Homo sapiens	193-197
9714716-1	1998	The ability of Cu(II) and Fe(III) to promote site-specific DNA damage in the presence of endogenous reductants was investigated by using 32P-5"-end-labeled DNA fragments obtained from the human p53 tumor suppressor gene and the c-Ha-ras-1 protooncogene.	ferric sulfate	26-33	P53	Homo sapiens	194-197
9719458-0	1998	p53 may mediate the mdr-1 expression via the WT1 gene in human vincristine-resistant leukemia/lymphoma cell lines.	Vincristine	63-74	P53	Homo sapiens	0-3
9223475-8	1997	Induction of DNA damage in normal, uninfected fibroblasts (FB) or FB expressing IE86 by actinomycin D (Act D) resulted in increased p53 levels, a predominance of the hypophosphorylated form of Rb, and increased expression of both p21(CIP1/WAF1) and mdm-2.	Dactinomycin	88-101	P53	Homo sapiens	132-135
16205645-0	2006	Enhanced selenium effect on growth arrest by BiP/GRP78 knockdown in p53-null human prostate cancer cells.	Selenium	9-17	P53	Homo sapiens	68-71
11596302-0	1997	[Wild-type p53 stimulates vincristine-induced apoptosis].	Vincristine	26-37	P53	Homo sapiens	11-14
11596302-4	1997	After treatment with Vincristine(VCR), the wild type p53-expression cells presented typical morphology characteristic of apoptosis analysed under electron and fluorescence microscopes.	Vincristine	21-32	P53	Homo sapiens	53-56
9661919-5	1998	We found that these cells are positive for Ki-67 even when they are arrested in G1/S or G2/M by using synchronizing inhibitors, by inducing p21(Waf1/Cip1) in a tetracycline-regulated expression system or by inducing wild type p53 and p21 after inflicting DNA damage.	Tetracycline	160-172	P53	Homo sapiens	226-229
16205645-8	2006	Under this condition, the selenium effect on wild-type p53-activated fragment p21 (p21(WAF)), cyclin-dependent kinase (CDK)1 and CDK2 was also magnified in a manner consistent with enhanced cell growth arrest.	Selenium	26-34	P53	Homo sapiens	55-58
17153599-8	2006	Altogether our results suggest that Tau-Cl is able to eliminate the cells with both functional (RA FLS) and mutated (Jurkat) p53 tumor suppressor.	tau-cl	36-42	P53	Homo sapiens	125-128
9681825-6	1998	Actinomycin D, a potent inhibitor of transcription, as well as a DNA damaging agent, abrogated the restraint apoptosis mediated by mutant p53.	Dactinomycin	0-13	P53	Homo sapiens	138-141
9652798-1	1998	The prognostic value of the mutation of the p53 tumor suppressor gene in non-small cell lung carcinomas (NSCLC) is controversial and a polymorphism of the p53 gene at codon 72 consisting of two alleles, arginine (Arg) and proline (Pro), has been reported to be associated with the incidence of smoking-related NSCLC.	Proline	222-229	P53	Homo sapiens	155-158
9253509-2	1997	Codon 72 of the p53 gene is highly polymorphic with a reported arginine/proline allelotype frequency of 0.65/0.35 for Caucasians and a reversal of this ratio in African-Americans.	Proline	72-79	P53	Homo sapiens	16-19
9053847-6	1997	Moreover, detection of ThaI polymorphism of codon 72 showed that MCF-7 cells predominantly express wild-type p53 with proline, while mutated p53 in MCF-7/Adr cells contains an arginine residue at codon 72.	Proline	118-125	P53	Homo sapiens	109-112
9652798-1	1998	The prognostic value of the mutation of the p53 tumor suppressor gene in non-small cell lung carcinomas (NSCLC) is controversial and a polymorphism of the p53 gene at codon 72 consisting of two alleles, arginine (Arg) and proline (Pro), has been reported to be associated with the incidence of smoking-related NSCLC.	Proline	231-234	P53	Homo sapiens	155-158
16699611-4	2006	AIM: To investigate the possible association between p53 arginine/72 proline polymorphism and susceptibility to colorectal cancer.	Proline	69-76	P53	Homo sapiens	53-56
9667752-4	1998	N-Methyl-N"-nitro-nitrosoguanidine and N-ethyl-N-nitrosourea, two direct-acting genotoxic (DNA-reactive) carcinogens, caused p53 induction as early as 2 h following treatment, with peak increases within 4-12 h. Aflatoxin B1 and 2-acetylaminofluorene, indirect-acting genotoxic carcinogens, caused a later induction of p53, with the peak increase appearing between 16 and 24 h following treatment.	n-methyl-n"-nitro-nitrosoguanidine	0-34	P53	Homo sapiens	125-128
9667752-4	1998	N-Methyl-N"-nitro-nitrosoguanidine and N-ethyl-N-nitrosourea, two direct-acting genotoxic (DNA-reactive) carcinogens, caused p53 induction as early as 2 h following treatment, with peak increases within 4-12 h. Aflatoxin B1 and 2-acetylaminofluorene, indirect-acting genotoxic carcinogens, caused a later induction of p53, with the peak increase appearing between 16 and 24 h following treatment.	n-methyl-n"-nitro-nitrosoguanidine	0-34	P53	Homo sapiens	318-321
9066726-0	1997	Induction of cyclin-dependent kinase inhibitor, p21WAF1, by treatment with 3,4-dihydro-6-[4-(3,4)-dimethoxybenzoyl)-1-piperazinyl]-2(1H)-quinoline (vesnarinone) in a human salivary cancer cell line with mutant p53 gene.	3,4-dihydro-6-[4-(3,4)-dimethoxybenzoyl)-1-piperazinyl]-2(1h)-quinoline	75-146	P53	Homo sapiens	210-213
16168468-3	2006	RESULTS: When p53 codon 72 genotype was classified into two subgroups of Arg/Arg and Arg/Pro + Pro/Pro, the Arg/Arg genotype was associated with an increased risk for the development of endometrial cancer (OR = 1.86, 95% CI = 1.06 to 3.26) compared with the Arg/Pro + Pro/Pro genotype (P = 0.0301).	Proline	89-92	P53	Homo sapiens	14-17
9600920-9	1998	Furthermore, synthetic peptides spanning this newly identified proline-rich negative regulatory region (residues 80-93) are able to activate p53 sequence-specific DNA binding in vitro.	Proline	63-70	P53	Homo sapiens	141-144
9607760-2	1998	A common polymorphism that occurs in the p53 amino-acid sequence results in the presence of either a proline or an arginine at position 72.	Proline	101-108	P53	Homo sapiens	41-44
8973593-3	1996	When SV40-immortalized cells were treated with 2.5% DMSO, dissociation of the complex was observed by immunoblotting of SV40 T antigen from immunoprecipitated p53 protein fraction.	Dimethyl Sulfoxide	52-56	P53	Homo sapiens	159-162
9607760-3	1998	The effect of this polymorphism on the susceptibility of p53 to E6-mediated degradation has been investigated and the arginine form of p53 was found to be significantly more susceptible than the proline form.	Proline	195-202	P53	Homo sapiens	57-60
16369916-4	2006	We demonstrate cyclic resveratrol-mediated expression of p53, mdm2, p21(cip/waf), Rb, and cyclin G at both the RNA and the protein level at &lt;8 h. However, ras was not differentially expressed at either the RNA or the protein level.	cyclic resveratrol	15-33	P53	Homo sapiens	57-60
9607760-3	1998	The effect of this polymorphism on the susceptibility of p53 to E6-mediated degradation has been investigated and the arginine form of p53 was found to be significantly more susceptible than the proline form.	Proline	195-202	P53	Homo sapiens	135-138
9565608-0	1998	Poly(ADP-ribose) binds to specific domains of p53 and alters its DNA binding functions.	Poly Adenosine Diphosphate Ribose	0-16	P53	Homo sapiens	46-49
9565608-8	1998	Additionally, poly(ADP-ribose) also interfered with the DNA single strand end binding of p53.	Poly Adenosine Diphosphate Ribose	14-30	P53	Homo sapiens	89-92
8863680-8	1996	Cell lines derived from nitrosamine-induced pancreatic tumors in the hamster contained K-ras and p53 alterations similar to those found in cell lines derived from human pancreatic carcinomas.	Nitrosamines	24-35	P53	Homo sapiens	97-100
15906362-0	2005	Thymoquinone induces apoptosis through activation of caspase-8 and mitochondrial events in p53-null myeloblastic leukemia HL-60 cells.	thymoquinone	0-12	P53	Homo sapiens	91-94
9031099-11	1996	The induction of apoptosis by CLB is paralleled by an increase in P53 and Mdm-2 but this increase in not observed in patients with p53 mutations indicating that with high drug concentrations CLB can produce cell death through P53 independent pathways.	Chlorambucil	30-33	P53	Homo sapiens	226-229
9031099-11	1996	The induction of apoptosis by CLB is paralleled by an increase in P53 and Mdm-2 but this increase in not observed in patients with p53 mutations indicating that with high drug concentrations CLB can produce cell death through P53 independent pathways.	Chlorambucil	191-194	P53	Homo sapiens	226-229
9031099-14	1996	Finally, whereas CLB and nucleoside analogs may produce cell death in CLL by a P53 dependent pathway other agents, such as dexamethasone or vincristine, may act through P53-independent pathways.	Chlorambucil	17-20	P53	Homo sapiens	79-82
9031099-14	1996	Finally, whereas CLB and nucleoside analogs may produce cell death in CLL by a P53 dependent pathway other agents, such as dexamethasone or vincristine, may act through P53-independent pathways.	Vincristine	140-151	P53	Homo sapiens	169-172
9563650-2	1998	When the p53 tumor suppressor gene was used, 4-nitro-2-aminophenol caused Cu(II)-dependent piperidine-labile sites at poly G sequences.	piperidine	91-101	P53	Homo sapiens	9-12
16054204-4	2005	RESULTS: The observed association of proline homozygosity at codon 72 of p53 with CaCx infection (Bhattacharya, P., Duttagupta, C., Sengupta, S. 2002.Proline homozygosity in codon 72 of p53: A risk genotype for Human Papillomavirus related cervical cancer in Indian women.	Proline	37-44	P53	Homo sapiens	73-76
9492043-3	1998	The p53-induced regulation of IGF-IR levels was studied in a tetracycline-regulated expression system.	Tetracycline	61-73	P53	Homo sapiens	4-7
9472095-1	1998	The polymorphism of p53 gene at codon 72 consisting of either arginine (Arg)- or proline (Pro)-encoded allele is suggested to be associated with the susceptibility of tobacco-related lung cancer.	Proline	81-88	P53	Homo sapiens	20-23
9472095-1	1998	The polymorphism of p53 gene at codon 72 consisting of either arginine (Arg)- or proline (Pro)-encoded allele is suggested to be associated with the susceptibility of tobacco-related lung cancer.	Proline	90-93	P53	Homo sapiens	20-23
8822937-6	1996	For p53 we observed an overexpression in the presence of chlorambucil or both theophylline-chlorambucil and a decrease after theophylline incubation.	Chlorambucil	57-69	P53	Homo sapiens	4-7
8822937-6	1996	For p53 we observed an overexpression in the presence of chlorambucil or both theophylline-chlorambucil and a decrease after theophylline incubation.	theophylline-chlorambucil	78-103	P53	Homo sapiens	4-7
16054204-4	2005	RESULTS: The observed association of proline homozygosity at codon 72 of p53 with CaCx infection (Bhattacharya, P., Duttagupta, C., Sengupta, S. 2002.Proline homozygosity in codon 72 of p53: A risk genotype for Human Papillomavirus related cervical cancer in Indian women.	Proline	37-44	P53	Homo sapiens	186-189
16054204-4	2005	RESULTS: The observed association of proline homozygosity at codon 72 of p53 with CaCx infection (Bhattacharya, P., Duttagupta, C., Sengupta, S. 2002.Proline homozygosity in codon 72 of p53: A risk genotype for Human Papillomavirus related cervical cancer in Indian women.	cacx	82-86	P53	Homo sapiens	73-76
8877102-2	1996	The mutant p53 proteins present in the KHOS-240, A 431, and T47-D tumor-derived cell lines enter very rapidly in the nucleus in early postmitotic cells before the chromosomes have fully decondensed; they continue accumulating in this location without any obvious cytoplasmic retention throughout the cell cycle until prophase.	khos	39-43	P53	Homo sapiens	11-14
9541643-3	1998	DNA damage by 2,5-DMHF and 4,5-DMHF was investigated by using DNA fragments obtained from the p53 tumor suppressor gene.	furaneol	14-22	P53	Homo sapiens	94-97
9541643-3	1998	DNA damage by 2,5-DMHF and 4,5-DMHF was investigated by using DNA fragments obtained from the p53 tumor suppressor gene.	4,5-dimethyl-3-hydroxy-2(5H)-furanone	27-35	P53	Homo sapiens	94-97
16054204-4	2005	RESULTS: The observed association of proline homozygosity at codon 72 of p53 with CaCx infection (Bhattacharya, P., Duttagupta, C., Sengupta, S. 2002.Proline homozygosity in codon 72 of p53: A risk genotype for Human Papillomavirus related cervical cancer in Indian women.	Proline	150-157	P53	Homo sapiens	73-76
8622872-5	1996	To further investigate the mechanisms underlying p53-independent regulation of p21, the transcription inhibitor, Actinomycin D (AMD), was used to block p21 expression.	Dactinomycin	113-126	P53	Homo sapiens	49-52
9508372-4	1998	After treatment with 100 nM of vincristine, on average 18% of the wild-type p53 melanoma cells survived compared with 55% of the mutant p53 cells (P = 0.04).	Vincristine	31-42	P53	Homo sapiens	76-79
16054204-4	2005	RESULTS: The observed association of proline homozygosity at codon 72 of p53 with CaCx infection (Bhattacharya, P., Duttagupta, C., Sengupta, S. 2002.Proline homozygosity in codon 72 of p53: A risk genotype for Human Papillomavirus related cervical cancer in Indian women.	Proline	150-157	P53	Homo sapiens	186-189
9508372-4	1998	After treatment with 100 nM of vincristine, on average 18% of the wild-type p53 melanoma cells survived compared with 55% of the mutant p53 cells (P = 0.04).	Vincristine	31-42	P53	Homo sapiens	136-139
9508372-8	1998	Cisplatin, camptothecin and vincristine all induced apoptosis in wild-type p53 melanoma cells, but not in mutant p53 cells.	Vincristine	28-39	P53	Homo sapiens	75-78
16054204-8	2005	The p21 arginine allele was significantly associated with CaCx in the p53 proline non-homozygous group of subjects (OR(age-adjusted) = 2.68; 95% CI: 1.21-5.91; P = 0.01), and specifically in the p53 heterozygous group (OR(age-adjusted) = 2.91; 95% CI = 1.12-7.56; P = 0.03).	cacx	58-62	P53	Homo sapiens	70-73
16054204-8	2005	The p21 arginine allele was significantly associated with CaCx in the p53 proline non-homozygous group of subjects (OR(age-adjusted) = 2.68; 95% CI: 1.21-5.91; P = 0.01), and specifically in the p53 heterozygous group (OR(age-adjusted) = 2.91; 95% CI = 1.12-7.56; P = 0.03).	Proline	74-81	P53	Homo sapiens	70-73
8611406-2	1996	Expression of P53 protein was detected by an immunohistochemical approach using the monoclonal antibody PAb1801 on paraffin-embedded sections of tumours obtained surgically from 102 stage II - IIIa patients with non-small-cell lung cancer (52 squamous cell carcinomas, 50 adenocarcinomas).	pab1801	104-111	P53	Homo sapiens	14-17
9467956-3	1998	Here, we show, using a tetracycline-regulated system, that expression of wild-type p21 in p53-deficient DLD1 human colon cancer cells inhibits DNA synthesis and causes G1 and G2 cell cycle arrest.	Tetracycline	23-35	P53	Homo sapiens	90-93
16054204-10	2005	However, the two risk factors, p53 proline homozygosity and p21 arginine allele, although part of a common causal pathway, appear to act in a mutually exclusive manner.	Proline	35-42	P53	Homo sapiens	31-34
15880444-10	2005	These studies indicate that physiological concentrations of CLA inhibit growth of colon cancer cells with either wild-type or mutant p53, and may have therapeutic benefits in vivo.	Linoleic Acids, Conjugated	60-63	P53	Homo sapiens	133-136
9406706-14	1997	Response in the Y-90-ChL6 treated HBT 3477 xenograft tumors was independent of p53 and occurred by apoptosis.	ChL6 monoclonal antibody	21-25	P53	Homo sapiens	79-82
8524298-8	1996	The possibility that c-FosER-induced apoptosis requires a p53 function was examined.	c-foser	21-28	P53	Homo sapiens	58-61
8570169-7	1995	In addition, cycloheximide and actinomycin D inhibited wt p53-induced apoptosis.	Dactinomycin	31-44	P53	Homo sapiens	58-61
20818013-5	2005	Specifically, we present an improved immobilization method that covalently anchors one end (5" end) of a dual labelled (5"-thiol, 3"-biotin) p53 DNA molecule onto a gold substrate via gold-thiol chemistry, whilst the biotinylated 3" end is available for "pick-up" using a streptavidin modified AFM tip.	5"-thiol	120-128	P53	Homo sapiens	141-144
8563884-1	1995	An immunohistochemical study using PAb1801, a monoclonal antibody specific to the human p53 protein (wild and mutant), was performed to detect over-expression of p53 protein in colorectal cancers and dysplasia complicating ulcerative colitis, compared with that in sporadic colorectal cancers and adenomas.	pab1801	35-42	P53	Homo sapiens	88-91
8563884-1	1995	An immunohistochemical study using PAb1801, a monoclonal antibody specific to the human p53 protein (wild and mutant), was performed to detect over-expression of p53 protein in colorectal cancers and dysplasia complicating ulcerative colitis, compared with that in sporadic colorectal cancers and adenomas.	pab1801	35-42	P53	Homo sapiens	162-165
9346961-9	1997	The specificity of the effect of wild-type p53 on nucleotide excision repair was demonstrated in a p53 homozygous mutant cell line containing a tetracycline-regulated wild-type p53 gene.	Tetracycline	144-156	P53	Homo sapiens	43-46
9346961-9	1997	The specificity of the effect of wild-type p53 on nucleotide excision repair was demonstrated in a p53 homozygous mutant cell line containing a tetracycline-regulated wild-type p53 gene.	Tetracycline	144-156	P53	Homo sapiens	99-102
9346961-9	1997	The specificity of the effect of wild-type p53 on nucleotide excision repair was demonstrated in a p53 homozygous mutant cell line containing a tetracycline-regulated wild-type p53 gene.	Tetracycline	144-156	P53	Homo sapiens	99-102
9346961-10	1997	Wild-type p53 expression and activity were suppressed in the presence of tetracycline, whereas withdrawal of tetracycline resulted in the induction of p53 expression, cell cycle checkpoint activation, and DNA damage-induced apoptosis.	Tetracycline	73-85	P53	Homo sapiens	10-13
9346961-10	1997	Wild-type p53 expression and activity were suppressed in the presence of tetracycline, whereas withdrawal of tetracycline resulted in the induction of p53 expression, cell cycle checkpoint activation, and DNA damage-induced apoptosis.	Tetracycline	109-121	P53	Homo sapiens	151-154
16082224-1	2005	A common polymorphism at codon 72 in p53 gene leads to an arginine to proline aminoacidic substitution which affects in an age-dependent manner the susceptibility of cells to undergo apoptosis after oxidative stress.	Proline	70-77	P53	Homo sapiens	37-40
9343109-3	1997	Thiolamine-induced apoptosis appeared to be a p53-independent process since it was induced by WR-1065 exposure in human HL60 cells.	thiolamine	0-10	P53	Homo sapiens	46-49
7571423-1	1995	The E6 oncoprotein of human papillomavirus type 16 (HPV 16) [151amino acids (AA) long] contains four metal-binding motifs, C-X-X-C, and is postulated to form two 29-AA finger-like structures in the N-terminal and C-terminal halves, which mediate degradation of p53 and binding to p53, respectively.	151amino acids	61-75	P53	Homo sapiens	261-264
7571423-1	1995	The E6 oncoprotein of human papillomavirus type 16 (HPV 16) [151amino acids (AA) long] contains four metal-binding motifs, C-X-X-C, and is postulated to form two 29-AA finger-like structures in the N-terminal and C-terminal halves, which mediate degradation of p53 and binding to p53, respectively.	151amino acids	61-75	P53	Homo sapiens	280-283
7783370-3	1995	The results of several fixation methods demonstrated that formalin and methanol, formalin and ethanol (1:9) and buffered formalin acetone gave good results for detecting p53 protein.	formalin acetone	121-137	P53	Homo sapiens	170-173
15800902-4	2005	This was of interest because E6 silencing of p53 sensitizes U87MG astrocytic glioma cells to BCNU and temozolomide (TMZ), cytotoxic drugs that are modestly helpful in the treatment of aggressive astrocytic gliomas.	Carmustine	93-97	P53	Homo sapiens	45-48
15902285-4	2005	Mutations were not detected solely at the time of transformation; in three patients, mutated TP53 arose in at least one antecedent FL sample (6 months, 2.5 years and 4 years prior to transformation).	fl sample	131-140	P53	Homo sapiens	93-97
7567152-2	1995	Two 20-base oligomers complementary to bases 872-891 of human p53 cDNA with a single nucleotide difference in the third position of codon 249 were end-labelled with biotin-conjugated dATP using terminal deoxynucleotidyltransferase (TdT).	Biotin	165-171	P53	Homo sapiens	62-65
7834638-4	1995	We show that p53-independent induction of WAF1/CIP1 occurs in human leukemia cells treated with 12-O-tetradecanoylphorbol-13-acetate, okadaic acid, or IFN-gamma but not with retinoic acid, vitamin D3, or DMSO.	Dimethyl Sulfoxide	204-208	P53	Homo sapiens	13-16
9393978-1	1997	Wild type human tumor suppressor protein p53 (expressed in insect cells) binds strongly to negatively supercoiled (sc) plasmid DNA at a native superhelix density, as evidenced by electrophoretic retardation of scDNA in agarose gels and imaging by scanning force microscopy (SFM).	Sepharose	219-226	P53	Homo sapiens	41-44
9446323-5	1997	The p53 Arg/Pro polymorphism study revealed the elevated frequency of Arg allele in lung and stomach cancer groups.	Proline	12-15	P53	Homo sapiens	4-7
16024796-3	2005	In this report, we demonstrate that the mitochondrial ribosomal protein L41 (MRPL41) enhances p53 stability and contributes to p53-induced apoptosis in response to growth-inhibitory conditions such as actinomycin D treatment and serum starvation.	Dactinomycin	201-214	P53	Homo sapiens	94-97
9261472-7	1997	One of the p53 positive AIDS-KS samples showed mobilized shifts in exon 6 suggestive of a mutation.	Potassium	29-31	P53	Homo sapiens	11-14
7715579-1	1995	DNA effects of oxygen free radicals exemplified by the NF kappa B transcription factor and the p53 tumor suppressor gene].	oxygen free radicals	15-35	P53	Homo sapiens	95-98
16024796-3	2005	In this report, we demonstrate that the mitochondrial ribosomal protein L41 (MRPL41) enhances p53 stability and contributes to p53-induced apoptosis in response to growth-inhibitory conditions such as actinomycin D treatment and serum starvation.	Dactinomycin	201-214	P53	Homo sapiens	127-130
9169452-3	1997	The invariant guanosines in the highly conserved C(A/T) (T/A)G parts of the consensus half-sites are critical to the p53DBD-DNA binding.	Guanosine	14-24	P53	Homo sapiens	117-120
15961301-0	2005	Bitter gourd seed fatty acid rich in 9c,11t,13t-conjugated linolenic acid induces apoptosis and up-regulates the GADD45, p53 and PPARgamma in human colon cancer Caco-2 cells.	seed fatty acid	13-28	P53	Homo sapiens	121-124
9219564-3	1997	We found that exposure of human lung adenocarcinoma A549 cells to sodium arsenite (0.08-2 microM) or sodium arsenate (30-300 microM), but not dimethylarsenic acid (2-2000 microM), produced significant dose-responsive hypermethylation within a 341-base pair fragment of the promoter of p53.	sodium arsenate	101-116	P53	Homo sapiens	285-288
7626788-6	1995	As its mouse and human counterparts, the ovine p53 contains a high proportion of proline residues, an acidic N-terminal domain and a basic C-terminal domain.	Proline	81-88	P53	Homo sapiens	47-50
7704245-1	1995	The expression of p53 protein was studied in formalin-fixed paraffin-embedded specimens of 41 well-differentiated adenocarcinomas of the gall-bladder, six cases of acute cholecystitis and 23 cases of chronic cholecystitis, using a monoclonal p53 (PAb 1801) antibody and streptavidin-biotin.	Biotin	283-289	P53	Homo sapiens	18-21
7938006-2	1994	Using a tetracycline-regulated p53 expression system and cDNA library subtraction procedure, we identified several p53-induced gene transcripts in human Saos-2 osteosarcoma cells that are novel on the basis of their size, regulation, and low abundance.	Tetracycline	8-20	P53	Homo sapiens	31-34
9169150-2	1997	We recently identified a novel gene, GML (glycosylphosphatidylinositol (GPI)-anchored molecule-like protein), whose expression is specifically induced by wildtype p53.	Glycosylphosphatidylinositols	42-70	P53	Homo sapiens	163-166
9169150-2	1997	We recently identified a novel gene, GML (glycosylphosphatidylinositol (GPI)-anchored molecule-like protein), whose expression is specifically induced by wildtype p53.	Glycosylphosphatidylinositols	72-75	P53	Homo sapiens	163-166
7938006-2	1994	Using a tetracycline-regulated p53 expression system and cDNA library subtraction procedure, we identified several p53-induced gene transcripts in human Saos-2 osteosarcoma cells that are novel on the basis of their size, regulation, and low abundance.	Tetracycline	8-20	P53	Homo sapiens	115-118
15961301-0	2005	Bitter gourd seed fatty acid rich in 9c,11t,13t-conjugated linolenic acid induces apoptosis and up-regulates the GADD45, p53 and PPARgamma in human colon cancer Caco-2 cells.	alpha-Linolenic Acid	59-73	P53	Homo sapiens	121-124
7937752-2	1994	A considerable number of environmentally induced, cancer-related p53 mutations in human tumors have been found in a highly conserved proline-rich sequence of the p53 protein encompassed by amino acid residues 147-158.	Proline	133-140	P53	Homo sapiens	65-68
7937752-2	1994	A considerable number of environmentally induced, cancer-related p53 mutations in human tumors have been found in a highly conserved proline-rich sequence of the p53 protein encompassed by amino acid residues 147-158.	Proline	133-140	P53	Homo sapiens	162-165
15870701-3	2005	Among these, pectenotoxin-2 (PTX-2), which was first identified as a cytotoxic entity in marine sponges, which depolymerizes actin filaments, was found to be highly effective and more potent to activate an intrinsic pathway of apoptosis in p53-deficient tumor cells compared to those with functional p53 both in vitro and in vivo.	ptx	29-32	P53	Homo sapiens	240-243
8028344-3	1994	We determined the extent to which p53 abnormality was associated with proliferation by measuring p53 immunohistochemically with a polyclonal antibody and monoclonal PAb1801 in invasive carcinomas of known S-phase fraction (SPF) assessed histologically by bromodeoxyuridine incorporation.	pab1801	165-172	P53	Homo sapiens	34-37
9174104-5	1997	The findings further imply that selenium compounds may be effective chemopreventive agents for human breast carcinogenesis, in which p53 mutations are frequent.	Selenium	32-40	P53	Homo sapiens	133-136
15870701-3	2005	Among these, pectenotoxin-2 (PTX-2), which was first identified as a cytotoxic entity in marine sponges, which depolymerizes actin filaments, was found to be highly effective and more potent to activate an intrinsic pathway of apoptosis in p53-deficient tumor cells compared to those with functional p53 both in vitro and in vivo.	ptx	29-32	P53	Homo sapiens	300-303
15964795-0	2005	Mutations in proline 82 of p53 impair its activation by Pin1 and Chk2 in response to DNA damage.	Proline	13-20	P53	Homo sapiens	27-30
9070653-3	1997	An E1A mutant incapable of physically interacting with Rb retained the capacity to inhibit transactivation by p53, whereas E1A mutants of the p300/CBP-interacting domain failed to inhibit p53.	Rubidium	55-57	P53	Homo sapiens	110-113
8014109-0	1994	p53 gene mutation in hepatocellular carcinoma induced by 2-amino-3-methylimidazo[4,5-f]quinoline in nonhuman primates.	2-amino-3-methylimidazo(4,5-f)quinoline	57-96	P53	Homo sapiens	0-3
15905035-4	2005	In the present study, we examined the effect of CoQ and its isoprenoid side chain length variants on the growth of cells having different p53 statuses.	coq	48-51	P53	Homo sapiens	138-141
15905035-10	2005	Overall, these results suggested that short tail CoQ induces ROS generation and further p53-dependent apoptosis.	coq	49-52	P53	Homo sapiens	88-91
15899386-2	2005	TP53 has two common polymorphic forms encoding either proline or arginine, at position 72, and the presence of homozygous arginine has been reported as a risk factor for cervical cancer in many populations.	Proline	54-61	P53	Homo sapiens	0-4
8105878-2	1993	Using PAb1801, an anti-p53 monoclonal antibody p53 immunoreactivity was detected in the nuclei of cancer cells in 113 cases (32%).	pab1801	6-13	P53	Homo sapiens	23-26
8105878-2	1993	Using PAb1801, an anti-p53 monoclonal antibody p53 immunoreactivity was detected in the nuclei of cancer cells in 113 cases (32%).	pab1801	6-13	P53	Homo sapiens	47-50
10374529-0	1997	[Detection of p53 and MDM2 gene expression in osteosarcoma with biotin-labelled in situ].	Biotin	64-70	P53	Homo sapiens	14-17
9098910-2	1997	The serum levels of pantropic p53 proteins were determined in workers with past exposure to hexavalent chromium compounds.	Chromium	103-111	P53	Homo sapiens	30-33
16004600-0	2005	RITA--a small-molecule anticancer drug that targets p53.	rita-	0-5	P53	Homo sapiens	52-55
9010220-5	1997	Expression of antisense GSEs led to decreased intracellular levels of p53 protein.	gses	24-28	P53	Homo sapiens	70-73
9010220-9	1997	We have identified short structural domains of p53 which are capable of independent functional interactions and highlighted the efficacy of this approach to discriminate biologically active GSEs from a random fragment library.	gses	190-194	P53	Homo sapiens	47-50
8476653-1	1993	p53 gene which is known as a tumor suppressor gene locates in chromosome 17p and has a polymorphism at codon 72 (Arginine CGC--&gt;Proline CCC).	Proline	131-138	P53	Homo sapiens	0-3
15966238-0	2005	Arginine and proline alleles of the p53 gene are associated with different locations of gastric cancer.	Proline	13-20	P53	Homo sapiens	36-39
1391801-2	1992	We found an alteration of the p53 gene in one of 5 AL patients.	Aluminum	51-53	P53	Homo sapiens	30-33
1279244-2	1992	We therefore investigated the immunohistochemical reactivity of the anti-p53 antibody, PAb1801, in specimens taken from 149 cases of primary gastric cancer and processed by acetone fixation, in order to elucidate the incidence and clinicopathological significance of p53 alterations in gastric cancer.	pab1801	87-94	P53	Homo sapiens	73-76
9107076-0	1997	Bcl-2 protein expression and p53 gene mutation in chronic lymphocytic leukemia: correlation with in vitro sensitivity to chlorambucil and purine analogs.	Chlorambucil	121-133	P53	Homo sapiens	29-32
9107076-2	1997	p53 gene mutations have also been suggested to account for the chlorambucil resistance in CLL.	Chlorambucil	63-75	P53	Homo sapiens	0-3
15966238-14	2005	CONCLUSIONS: The proline allele at p53 codon 72 is associated with adenocarcinoma of the gastric cardia, and the arginine allele is associated with cancer of the antral and corpus locations.	Proline	17-24	P53	Homo sapiens	35-38
16128105-6	2005	The p53 Pro/Pro genotype significantly increased the risk for developing keloid, compared to the combination of Pro/Arg and Arg/Arg genotypes,with the odds ratio (OR) of 2.400 (95%CI: 1.048-5.498).	Proline	8-11	P53	Homo sapiens	4-7
9038605-4	1996	In 4 cases, the mutations lead to distinct changes in the primary or secondary structure of the protein (cysteine--&gt;tyrosine, proline--&gt;leucine) and were associated with marked accumulation of p53 protein.	Proline	129-136	P53	Homo sapiens	199-202
9031099-10	1996	Loss of wild-type p53 by mutation or deletion occurs in 10 to 15% of CLL patients and appears to correlate strongly with poor clinical response to CLB.	Chlorambucil	147-150	P53	Homo sapiens	18-21
8706243-3	1996	Sublines that were resistant to melphalan, pyrazafurin, mitoxantrone, etoposide and PALA all retained expression of wild-type p53.	Mitoxantrone	56-68	P53	Homo sapiens	126-129
8780893-0	1996	Expression of memory, differentiation, and repression of c-myc and p53 genes in human RD/TE-671 cells induced by a ureido-derivative of pyridine (UDP-4).	2-(3-ethylureido)-6-methylpyridine	146-151	P53	Homo sapiens	67-70
1540970-1	1992	Immunohistochemical staining for the p53 protein was performed in 107 snap frozen primary endometrial adenocarcinomas and 15 benign uterine tissues using monoclonal antibody PAb1801.	pab1801	174-181	P53	Homo sapiens	37-40
1737852-7	1992	The other two nonhereditary p53 mutations included a T to G transversion at codon 270 (phenylalanine to cysteine) and a G to C transversion at codon 248 (arginine to proline).	Proline	166-173	P53	Homo sapiens	28-31
8605209-1	1996	Oxidative DNA damage by NAD(P)H in the presence of metal ions has been characterized by using 32P 5" end-labeled DNA fragments obtained from human p53 tumor suppressor gene and c-Ha-ras-1 protooncogene.	nad(p)h	24-31	P53	Homo sapiens	147-150
15727877-4	2005	3-(1-Piperazinyl)methyl and 3-(quinuclidin-3-yl)aminomethyl derivatives of 4,11-dihydroxynaphtho[2,3-f]indole-5,10-dione killed HCT116 colon carcinoma cells (carrying wild type p53) and their p53-null variant within the similar range of concentrations.	4,11-dihydroxynaphtho(2,3-f)indole-5,10-dione	75-120	P53	Homo sapiens	177-180
8937739-12	1996	Biophys: 13, 147 (1993)], perturbations that would enhance rates of populating G-C sites with enol-imine states could accelerate point mutation "activation" of "p53-type" genes that could be manifested as premature cancer in living populations or expressed as spontaneous abortion in unborn populations.	enol-imine	94-104	P53	Homo sapiens	161-164
1923535-2	1991	Immunohistochemical staining with new polyclonal (CM-1) and monoclonal antibodies (BP 53-12 and BP53-24) to p53 on methacarn-fixed paraffin sections showed positive staining in 161 (76%).	methacarn	115-124	P53	Homo sapiens	108-111
15727877-4	2005	3-(1-Piperazinyl)methyl and 3-(quinuclidin-3-yl)aminomethyl derivatives of 4,11-dihydroxynaphtho[2,3-f]indole-5,10-dione killed HCT116 colon carcinoma cells (carrying wild type p53) and their p53-null variant within the similar range of concentrations.	4,11-dihydroxynaphtho(2,3-f)indole-5,10-dione	75-120	P53	Homo sapiens	192-195
33799444-0	2021	6-Azauridine Induces Autophagy-Mediated Cell Death via a p53- and AMPK-Dependent Pathway.	Azauridine	0-12	P53	Homo sapiens	57-60
15715472-10	2005	The butyric acid and formaldehyde induced cell differentiation and increased p53 and p21 levels, suggesting that both affect cancer cells, the acid by inhibiting HDAC and the aldehyde by an as yet unknown mechanism.	Butyric Acid	4-16	P53	Homo sapiens	77-80
33799444-8	2021	In addition, we demonstrated that the cytotoxic effect of 6-AZA was dependent on AMPK and p53.	Azauridine	58-63	P53	Homo sapiens	90-93
8542574-5	1996	Wortmannin inhibited the induction of p53 DNA-binding activity by actinomycin D and radiation and blocked the transcriptional activation of a p53 CAT reporter gene by actinomycin D.	Dactinomycin	66-79	P53	Homo sapiens	38-41
15664854-0	2005	1,4-Benzodiazepine-2,5-diones as small molecule antagonists of the HDM2-p53 interaction: discovery and SAR.	Bz-423	0-29	P53	Homo sapiens	72-75
8542574-5	1996	Wortmannin inhibited the induction of p53 DNA-binding activity by actinomycin D and radiation and blocked the transcriptional activation of a p53 CAT reporter gene by actinomycin D.	Dactinomycin	167-180	P53	Homo sapiens	142-145
8542583-0	1996	p53 mutations in bladder tumors from arylamine-exposed workers.	aniline	37-46	P53	Homo sapiens	0-3
8542583-1	1996	In this study we compared the frequency and pattern of p53 mutations in 34 bladder tumors from people with high-level occupational exposure to arylamines to those in 30 bladder tumors from people without such exposure.	aniline	143-153	P53	Homo sapiens	55-58
34843865-1	2022	We report a novel topoisomerase IIalpha inhibitor, mercaptopyridine oxide (MPO), which induces G2/M arrest and senescence with distinctly different cell cycle regulators (p21 or p14ARF) in HCT116p 53WT and HCT116 p53-/- cells, respectively.	mercaptopyridine oxide	51-73	P53	Homo sapiens	213-216
34959424-10	2021	The results also indicated that treatment with THQ formula significantly increased caspase-3, Bax, Bcl-2, and p53 mRNA expression compared to plain formula and THQ.	thymoquinone	47-50	P53	Homo sapiens	110-113
7566979-5	1995	Induction of both terminal differentiation and reversible differentiation (MEZ treatment) results in a temporal decrease in DNA synthesis and the percentage of cells in S phase and a decrease in the expression of cell cycle and growth regulated genes, including cdc2, cyclin A, cyclin B, histone H1, histone H4, nm23-H1, p53 and c-myc.	mezerein	75-78	P53	Homo sapiens	321-324
15664854-1	2005	A library of 1,4-benzodiazepine-2,5-diones was screened for binding to the p53-binding domain of HDM2 using Thermofluor, a miniaturized thermal denaturation assay.	Bz-423	13-42	P53	Homo sapiens	75-78
8579493-1	1995	The ability of exogenous p53 tumor-suppressor and activated N-PAS oncogene to influence differentiation state of human colon carcinoma LIM 1215 cells and their derivatives with acquired resistance to actinomycin D or methotrexate was analysed Introduction of retroviral construct expressing human wild-type (wt) p53 into LIM 1215 cells induced electron microscopic manifestations of enterocytic differentiation, i.e. caused an increase in the numbers of cells with microvilli, desmosomes and glandular-like lumens.	Dactinomycin	200-213	P53	Homo sapiens	25-28
15633234-0	2005	Homozygosity for Pro of p53 Arg72Pro as a potential risk factor for hepatocellular carcinoma in Chinese population.	Proline	17-20	P53	Homo sapiens	24-27
8532700-6	1995	p53 was identified with PAb1801 antibody using a labeled avidin-biotin immunoperoxidase technique.	pab1801	24-31	P53	Homo sapiens	0-3
34880421-3	2021	We recently found that p53 binds via its proline-rich domain to peptidase D (PEPD) and is activated when the binding is disrupted.	Proline	41-48	P53	Homo sapiens	23-26
34085157-5	2021	Inhibition of collagen biosynthesis (proline utilizing process) by 2-methoxyestradiol (2ME) contributed to induction of apoptosis in MCF-7WT cells, as detected by increase in the expression of active caspase-3, -9 and p53.	Proline	37-44	P53	Homo sapiens	218-221
21552819-4	1995	Transient cob transfection of a urokinase-producing cell line with a wildtype p53 expression vector and a CAT reporter driven by the urokinase promoter led to a dramatic reduction in CAT activity.	COB protocol	10-13	P53	Homo sapiens	78-81
15633234-10	2005	CONCLUSION: Homozygosity for Pro of p53 Arg72Pro is potentially one of the genetic risk factors for HCC in Chinese population.	Proline	29-32	P53	Homo sapiens	36-39
15827887-7	2005	This strong immunoreactivity of proapototic proteins (p53 and BAX) in hippocampal cultures exposed to anoxia or/and TPEN correlated with previous ultrastructural evidences of anoxia- and TPEN-induced apoptosis, while the overexpression of anti-apoptotic protein (BCL-2 and BCL-X) in zinc-pretreated cultures evidenced the protective ability of this metal against apoptosis in model of anoxia in vitro.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	116-120	P53	Homo sapiens	54-57
7790313-3	1995	Immunostaining revealed nuclear accumulation of p53 within 6 h after various stresses [heat shock, osmotic shock, heavy metal (Cd), blockers of the cellular respiratory system (NaN3), amino acid analogues (azetidine and canavanine), an inhibitor of protein synthesis (puromycin), and oxygen free radicals (H2O2)].	Sodium Azide	177-181	P53	Homo sapiens	48-51
7790313-3	1995	Immunostaining revealed nuclear accumulation of p53 within 6 h after various stresses [heat shock, osmotic shock, heavy metal (Cd), blockers of the cellular respiratory system (NaN3), amino acid analogues (azetidine and canavanine), an inhibitor of protein synthesis (puromycin), and oxygen free radicals (H2O2)].	oxygen free radicals	284-304	P53	Homo sapiens	48-51
7726729-10	1995	CONCLUSIONS: Microwave pretreatment in conjunction with the use of either PAb1801 or DO7 is highly efficacious in the immunohistochemical detection of aberrant p53 expression in formalin-fixed, paraffin-embedded tissues.	pab1801	74-81	P53	Homo sapiens	160-163
16695986-2	1995	The monoclonal antibody pAb1801 was used to detect p53 nuclear protein overexpression.	pab1801	24-31	P53	Homo sapiens	51-54
7957681-3	1994	A recombinant human wild type p53 fused with glutathione S-transferase was immobilized on glutathione-agarose as a ligand for affinity column.	Sepharose	102-109	P53	Homo sapiens	30-33
15827887-7	2005	This strong immunoreactivity of proapototic proteins (p53 and BAX) in hippocampal cultures exposed to anoxia or/and TPEN correlated with previous ultrastructural evidences of anoxia- and TPEN-induced apoptosis, while the overexpression of anti-apoptotic protein (BCL-2 and BCL-X) in zinc-pretreated cultures evidenced the protective ability of this metal against apoptosis in model of anoxia in vitro.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	187-191	P53	Homo sapiens	54-57
16145866-9	2005	Only marginally statistically significant influence of p53 expression was found on patient survival between MPG and PPG.	ppg	116-119	P53	Homo sapiens	55-58
7531056-2	1994	Here, we tested the role of p53 in the angiogenic process by introducing a tetracycline-regulated wild type p53 gene into null glioblastoma cells.	Tetracycline	75-87	P53	Homo sapiens	28-31
7531056-2	1994	Here, we tested the role of p53 in the angiogenic process by introducing a tetracycline-regulated wild type p53 gene into null glioblastoma cells.	Tetracycline	75-87	P53	Homo sapiens	108-111
15844595-1	2005	OBJECTIVE: To investigate the codon-72 polymorphism of the tumor suppressor gene p53, codon-72 encodes arginine (Arg) or proline (Pro) for a genetic predisposition,to keloid or hypertrophic scar.	Proline	121-128	P53	Homo sapiens	81-84
15531296-9	2004	Western blotting showed that the synthesis of intracellular p53 and bax protein was gradually up-regulated in the virus-loading period of 72 h. Naloxone had an apparent additive rather than antagonistic effect on the morphine-associated enhancement of bax expression.	Naloxone	144-152	P53	Homo sapiens	60-63
8076368-0	1994	Hyperphosphorylation of p53 induced by benzene, toluene, and chloroform.	Chloroform	61-71	P53	Homo sapiens	24-27
8076368-6	1994	Hyperphosphorylation of p53 may be involved in tumor promotion by benzene, toluene and chloroform.	Chloroform	87-97	P53	Homo sapiens	24-27
15488639-8	2004	After 48 h of EEPP treatment, the apoptosis of Hep G2 cells was found to associate with an elevated p53, and CD95 and CD95L proteins expression.	eepp	14-18	P53	Homo sapiens	100-103
17180005-5	1994	In addition, staining with PAb1801 revealed a number of strongly fluorescent cell fragments in cultures transfected by wt p53.	pab1801	27-34	P53	Homo sapiens	122-125
8061893-5	1994	IHC assays revealed nuclear p53 immunostaining in 53% of cases (32 of 60) with PAb1801, 38% (23 of 60) with PAb421, and 32% (19 of 60) with PAb240.	pab1801	79-86	P53	Homo sapiens	28-31
15240512-5	2004	The p53 codon 72 proline allele carriers were found to be more susceptible to progress to GC than to IM (OR = 2.22, 95%CI = 1.05-4.70, P = 0.038).	Proline	17-24	P53	Homo sapiens	4-7
15337531-2	2004	We show here that a decrease in Ras in SW480 cells induced either by the Ras inhibitor farnesylthiosalicylic acid (FTS) or by K-Ras antisense oligonucleotides, resulted in a similar increase in p53 protein.	farnesylthiosalicylic acid	87-113	P53	Homo sapiens	194-197
8206402-1	1994	Epithelial ovarian tumors of varying malignancy as well as normal ovaries were examined for their expression of p53 with the monoclonal antibody PAb1801.	pab1801	145-152	P53	Homo sapiens	112-115
8238731-4	1993	Since immunoreactivity for p53 correlates closely with the presence of missense mutations in the p53 gene, we performed immunohistochemical staining with the monoclonal antibody PAb1801.	pab1801	178-185	P53	Homo sapiens	27-30
8238731-4	1993	Since immunoreactivity for p53 correlates closely with the presence of missense mutations in the p53 gene, we performed immunohistochemical staining with the monoclonal antibody PAb1801.	pab1801	178-185	P53	Homo sapiens	97-100
15337531-2	2004	We show here that a decrease in Ras in SW480 cells induced either by the Ras inhibitor farnesylthiosalicylic acid (FTS) or by K-Ras antisense oligonucleotides, resulted in a similar increase in p53 protein.	farnesylthiosalicylic acid	115-118	P53	Homo sapiens	194-197
15337531-4	2004	Consistent with the Ras/Raf/MEK/ERK-mediated control of Mdm2, treatment of SW480 cells with the Ras inhibitor FTS caused a marked (80%) decrease in Mdm2, which itself would account for the increase in p53.	farnesylthiosalicylic acid	110-113	P53	Homo sapiens	201-204
15337531-5	2004	However, FTS also caused a 1.6-fold increase in p53 mRNA, indicative of a Ras-dependent mechanism that regulates p53 transcription.	farnesylthiosalicylic acid	9-12	P53	Homo sapiens	48-51
15337531-5	2004	However, FTS also caused a 1.6-fold increase in p53 mRNA, indicative of a Ras-dependent mechanism that regulates p53 transcription.	farnesylthiosalicylic acid	9-12	P53	Homo sapiens	113-116
8378352-5	1993	Whereas the KS cells express wild-type p53, the protein is undetectable in the parental K562 cells.	Potassium	12-14	P53	Homo sapiens	39-42
15520174-0	2004	Overexpression of histone deacetylase 1 confers resistance to sodium butyrate-mediated apoptosis in melanoma cells through a p53-mediated pathway.	Butyric Acid	62-77	P53	Homo sapiens	125-128
15352034-3	2004	Here, we show that taurolidine treatment reduces endogenous levels of IkappaBalpha, p105, c-Jun, p53 and p27 in a dose-dependent manner in colon adenocarcinoma cells, which can be in part due to massive cell death.	taurolidine	19-30	P53	Homo sapiens	97-100
8220069-0	1993	Effect of sodium butyrate on the expression of retinoblastoma (RB1) and P53 gene and phosphorylation of retinoblastoma protein in human colon tumor cell line HT29.	Butyric Acid	10-25	P53	Homo sapiens	72-75
8220069-2	1993	In our present study we observed that sodium butyrate treatment caused a decrease in the level of expression of RB1 gene on day seven of butyrate treatment but a gradual six to sevenfold decrease in the level of expression of p53 gene.	Butyric Acid	38-53	P53	Homo sapiens	226-229
15352034-7	2004	In contrast, translation of c-Jun or p53 mRNA was completely inhibited by taurolidine.	taurolidine	74-85	P53	Homo sapiens	37-40
8389669-2	1993	The wild-type of p53 protein exists as at least two forms of variants among human populations, ascribed to amino acid replacement at codon 72 of Arg by Pro.	Proline	152-155	P53	Homo sapiens	17-20
15634502-13	2004	CONCLUSIONS: In northern Chinese women, p53 codon 72 Pro/Arg and p53 PIN3 gene polymorphisms are not associated with development of ovarian cancer.	Proline	53-56	P53	Homo sapiens	40-43
8389669-3	1993	In this study, we show that this germ line Arg-Pro polymorphism at codon 72 of the p53 gene is associated with genetically determined susceptibility to smoking-induced lung cancer; a susceptible genotype Pro/Pro has a 1.7-fold higher risk of this cancer compared with other genotypes.	Proline	47-50	P53	Homo sapiens	83-86
8485705-2	1993	Activation of p53-DNA binding was seen for treatment with radiation, hydrogen peroxide, actinomycin D, Adriamycin, etoposide, camptothecin, 5-fluorouracil, mitomycin C, and cisplatin.	Dactinomycin	88-101	P53	Homo sapiens	14-17
8387205-6	1993	We treated primary keratinocytes with the DNA-damaging agent actinomycin D and demonstrated inhibition of replicative DNA synthesis and a significant increase in p53 protein levels.	Dactinomycin	61-74	P53	Homo sapiens	162-165
15308643-8	2004	Actinomycin D-induced p53 was inhibited by small interference RNA against L5.	Dactinomycin	0-13	P53	Homo sapiens	22-25
15310756-3	2004	We found here that knock-down of Tip60 affects the p53-dependent response following actinomycin D treatment, most likely because it inhibits p21 (CDKN1A) accumulation.	Dactinomycin	84-97	P53	Homo sapiens	51-54
1486864-9	1992	The p53 gene is a tumor-suppressor gene that can encode either a proline or an arginine in the 72nd residue.	Proline	65-72	P53	Homo sapiens	4-7
15375533-0	2004	Thymoquinone extracted from black seed triggers apoptotic cell death in human colorectal cancer cells via a p53-dependent mechanism.	thymoquinone	0-12	P53	Homo sapiens	108-111
1468914-3	1992	We report here an analysis of p53 overexpression in fixed, embedded specimens from 81 prospectively collected head and neck tumors, both benign and malignant, including 55 squamous cell carcinomas, using monoclonal pAb1801.	pab1801	215-222	P53	Homo sapiens	30-33
15269203-10	2004	In addition, it was shown that NBS1, SMC1, and p53 were phosphorylated in an ATM-dependent manner, and p53 phosphorylation on serine 20 is dependent on CHK2 after irofulven treatment.	irofulven	163-172	P53	Homo sapiens	47-50
15381546-1	2004	OBJECTIVE: To quantitatively examine changes in p53 tumor suppressor gene immunostaining after carbon dioxide (CO(2)) laser resurfacing of photodamaged skin to assess the potential value of this treatment in reducing the risk of progression to cutaneous carcinoma.	Carbon Dioxide	111-116	P53	Homo sapiens	48-51
1394133-2	1992	The frequency of G-T transversions and the incidence of guanosine mutations in the nontranscribed strand of the p53 gene were found to be higher than expected, and we suggest, therefore, that exogenous carcinogens have an etiological role in sporadic breast cancers.	Guanosine	56-65	P53	Homo sapiens	112-115
15381546-10	2004	CONCLUSIONS: There was a consistent decrease in p53 immunostaining in the interfollicular epidermis lasting for at least 6 moths after CO(2) laser resurfacing of photodamaged skin.	Carbon Dioxide	135-140	P53	Homo sapiens	48-51
15314173-5	2004	The interaction of L23 with MDM2 was enhanced by treatment with actinomycin D but not by gamma-irradiation, leading to p53 activation.	Dactinomycin	64-77	P53	Homo sapiens	119-122
1450522-2	1992	The sequence -Thr-Pro-Ala-Pro-Lys-, as found in p53 protein, was also phosphorylated by this enzyme, but less efficiently than in the sequence described above.	Proline	18-21	P53	Homo sapiens	48-51
1450522-2	1992	The sequence -Thr-Pro-Ala-Pro-Lys-, as found in p53 protein, was also phosphorylated by this enzyme, but less efficiently than in the sequence described above.	Proline	26-29	P53	Homo sapiens	48-51
15265702-2	2004	We have previously demonstrated that an inhibitor of HDAC, sodium butyrate (NaB), induces apoptosis of breast cancer cells in a P53-independent and P21(waf1)-dependent manner.	Butyric Acid	59-74	P53	Homo sapiens	128-131
1906503-4	1991	The production of p53 became detectable 3 to 6 h after addition of phorbol, 12,13,-dibutyrate and ionomycin, and peaked at 30 to 42 h. To further delineate the relationship of the synthesis and metabolism of the proteins to cell cycle progression, we used three agents to arrest progression of activated T cells at various points in the cell cycle.	12,13,-dibutyrate	76-93	P53	Homo sapiens	18-21
15196141-4	2004	The streptavidin-biotin complex stain was used to detect the human DNA mismatch repair proteins hMSH2, hMLH1 and p53 protein.	Biotin	17-23	P53	Homo sapiens	113-116
2056391-1	1991	In a study of 90 breast cancer patients, tumour p53 protein expression was determined by immunohistochemistry using the monoclonal antibody PAb1801.	pab1801	140-147	P53	Homo sapiens	48-51
1999338-1	1991	We describe a simple method for characterizing a frequent polymorphism (that substitutes an arginine for a proline) in the coding sequence of the Tp53 gene in patients with colonic cancer and in a control population.	Proline	107-114	P53	Homo sapiens	146-150
15140542-5	2004	The mean percentage of p53 positive cells was 28% in RT and 38% in B with 81% CR between B and RT and 19% FP on B.	Chromium	78-80	P53	Homo sapiens	23-26
26640580-5	2015	The results revealed that LW6 was not toxic and decreased apoptosis and the levels of the pro-apoptotic tumor suppressor p53.	LW6	26-29	P53	Homo sapiens	121-124
25311433-4	2014	The aim of this study was to investigate whether a novel compound derived from diterpene triepoxide (Minnelide ) can reactivate wild-type p53 function in HPV-positive HNSCC.	diterpene triepoxide	79-99	P53	Homo sapiens	138-141
15274301-0	2004	Selenium compounds regulate p53 by common and distinctive mechanisms.	Selenium	0-8	P53	Homo sapiens	28-31
18802665-0	2009	p53-dependent antiproliferative and antitumor effect of novel alkyl series of diorganotin(IV) compounds.	diorganotin	78-89	P53	Homo sapiens	0-3
15274301-3	2004	The main dietary form is selenomethionine, which we showed modulated p53 activity by causing redox regulation of key p53 cysteine residues.	Selenomethionine	25-41	P53	Homo sapiens	69-72
15274301-3	2004	The main dietary form is selenomethionine, which we showed modulated p53 activity by causing redox regulation of key p53 cysteine residues.	Selenomethionine	25-41	P53	Homo sapiens	117-120
15274301-7	2004	In addition to the reduction of cysteine sulfhydryl groups, p53 phosphorylation was also affected in cells treated with selenium compounds.	Selenium	120-128	P53	Homo sapiens	60-63
16167361-11	2005	In multivariate analysis with logistic regression, TMBC was defined by the association of P-cadherin (R=2.29), MIB1 &gt; 50 (R=3.80), ERBB2 negativity (R=2.24) and p53 positivity (RR=1.45).	tmbc	51-55	P53	Homo sapiens	164-167
15274301-11	2004	Our data show that, although p53 modulation may be a common denominator of selenium compounds, specific mechanisms of p53 activation differ among selenium chemical forms.	Selenium	75-83	P53	Homo sapiens	29-32
15274301-11	2004	Our data show that, although p53 modulation may be a common denominator of selenium compounds, specific mechanisms of p53 activation differ among selenium chemical forms.	Selenium	146-154	P53	Homo sapiens	118-121
15274301-13	2004	Different selenium chemical forms may differentially modify p53 for DNA repair or apoptosis in conjunction with a given level of endogenous or exogenous DNA damage.	Selenium	10-18	P53	Homo sapiens	60-63
15216398-9	2004	The frequency of pro/pro, pro/arg, and arg/arg in p53 codon 72 in cases was 15% (15/99), 58% (57/99), and 27% (27/99) and in controls was 17% (34/193), 48% (92/193), and 35% (67/193), respectively, which was not significantly different.	Proline	17-20	P53	Homo sapiens	50-53
8070357-4	1994	Clofibric acid, a known peroxisome proliferator, suppressed JEG-3 cell growth in association with increases in the tumor suppressor p53 protein and its messenger RNA (mRNA).	Clofibric Acid	0-14	P53	Homo sapiens	132-135
15216398-9	2004	The frequency of pro/pro, pro/arg, and arg/arg in p53 codon 72 in cases was 15% (15/99), 58% (57/99), and 27% (27/99) and in controls was 17% (34/193), 48% (92/193), and 35% (67/193), respectively, which was not significantly different.	Proline	21-24	P53	Homo sapiens	50-53
15216398-9	2004	The frequency of pro/pro, pro/arg, and arg/arg in p53 codon 72 in cases was 15% (15/99), 58% (57/99), and 27% (27/99) and in controls was 17% (34/193), 48% (92/193), and 35% (67/193), respectively, which was not significantly different.	Proline	21-24	P53	Homo sapiens	50-53
15069555-2	2004	The p53 codon 72 Arg right curved arrow Pro polymorphism has been suggested to be associated with risk for different kind of cancers, but the data on gastric cancer (GC) is very limited.	Proline	40-43	P53	Homo sapiens	4-7
34585830-2	2022	To obtain residue level information on these mobile systems we introduce two 1 H alpha -detected, proline selective, real-time homodecoupled NMR experiments and analyze the proline abundant transactivation domain of p53.	Proline	173-180	P53	Homo sapiens	216-219
34886743-0	2022	Fludarabine nucleoside induces major changes in the p53 interactome in human B-lymphoid cancer cell lines.	fludarabine nucleoside	0-22	P53	Homo sapiens	52-55
34886743-2	2022	Results from our laboratory indicate that 2-FaraAMP (fludarabine) has multiple mechanisms of cytotoxicity that include accumulation of isoforms and phosphorylated derivatives of p53, and induction of the unfolded protein response (UPR).	fludarabine phosphate	42-51	P53	Homo sapiens	178-181
34886743-3	2022	Using protein pull-downs with Dynabeads coated with p53 antibody, we have found that 2-FaraA (fludarabine nucleoside) induces major changes in the p53 interactome in human Raji lymphoma and IM9 multiple myeloma cells.	fludarabine nucleoside	94-116	P53	Homo sapiens	52-55
34886743-3	2022	Using protein pull-downs with Dynabeads coated with p53 antibody, we have found that 2-FaraA (fludarabine nucleoside) induces major changes in the p53 interactome in human Raji lymphoma and IM9 multiple myeloma cells.	fludarabine nucleoside	94-116	P53	Homo sapiens	147-150
34845969-9	2021	Cisatracurium besilate also promoted the expression of p53 and PUMA in AGS cells.	cisatracurium	0-22	P53	Homo sapiens	55-58
34845969-12	2021	Therefore, the present study suggested that cisatracurium besilate enhanced the TRAIL-induced apoptosis of GC cells via p53 signaling, and the synergistic effects of cisatracurium besilate and TRAIL may achieve maximal therapeutic efficacy in GC management.	cisatracurium	44-66	P53	Homo sapiens	120-123
34794098-7	2021	The most balanced potent and safe derivatives; 5i and 5q were more active than 5-fluorouracil, exhibited low mumrange MDM2 binding (KD=1.32and 1.72 mum, respectively), induced apoptosis-dependent anticancer activities up to 50%, activated p53 by 47-63%, downregulated the BCL2 gene to 59.8%, and reduced its protein level (13.75%) in the treated cancer cells.	5i	47-49	P53	Homo sapiens	239-242
34794098-9	2021	Docking simulations displayed that the active MDM2 inhibitors resided well into the p53 binding sites of MDM2, and shared key interactions with the co-crystalized inhibitor posed by the indolinone scaffold (5i, 5p, and 5q), the halogen substituents (5r), or the installed spiro ring (5s).	Oxindoles	186-196	P53	Homo sapiens	84-87
34855076-1	2021	Incubation of primary culture of pulmonary fibroblasts with non-opiate analogue of leuenkephalin (NALE; Phe-D-Ala-Gly-Phe-Leu-Arg, 0.1 muM) reduced generation of superoxide anion-radical (by 20.7%) and decreased the number of p53+ cells (by 40.2%) induced by exposure to H2O2 (60 muM).	phe-d-ala-gly-phe-leu-arg	104-129	P53	Homo sapiens	226-229
14991574-7	2004	2-MeOE2 bis-sulfamate and 2-EtE2 sulfamate both induced BCL-2 phosphorylation, p53 protein expression and apoptosis in HUVECs.	2-meoe2 bis-sulfamate	0-21	P53	Homo sapiens	79-82
34783171-6	2021	Immunocytochemical analysis found p53-positive RRTCs in all the samples (68/68, 100%) with an average p53 positivity rate of RRTCs per sample at 47.7% (range, 3.8%-96.5%).	rrtcs	47-52	P53	Homo sapiens	34-37
34783171-6	2021	Immunocytochemical analysis found p53-positive RRTCs in all the samples (68/68, 100%) with an average p53 positivity rate of RRTCs per sample at 47.7% (range, 3.8%-96.5%).	rrtcs	125-130	P53	Homo sapiens	102-105
34974862-4	2021	The effect of miR-214 packaged with lipidosome nanoparticles on proliferation and apoptosis of intestinal cancer cells and p53 pathway in intestinal cancer cells was observed.	lipidosome	36-46	P53	Homo sapiens	123-126
15177039-0	2004	The isoflavonoids genistein and quercetin activate different stress signaling pathways as shown by analysis of site-specific phosphorylation of ATM, p53 and histone H2AX.	isoflavonoids	4-17	P53	Homo sapiens	149-152
34974862-11	2021	The antagonist of miR-214 packaged with lipidosome nanoparticles could target on p53 pathway.	lipidosome	40-50	P53	Homo sapiens	81-84
34783171-10	2021	CONCLUSION: To avoid false positives of p53 immunocytochemistry, cytologists must consider the fact that RRTCs from patients with glomerular disease are positive for p53.	rrtcs	105-110	P53	Homo sapiens	40-43
34783171-10	2021	CONCLUSION: To avoid false positives of p53 immunocytochemistry, cytologists must consider the fact that RRTCs from patients with glomerular disease are positive for p53.	rrtcs	105-110	P53	Homo sapiens	166-169
15104235-5	2004	Enzyme-linked immunosorbent assay showed that acacetin significantly increased the expression of p53 and p21/WAF1 protein, contributing to cell cycle arrest.	acacetin	46-54	P53	Homo sapiens	97-100
34747697-3	2021	These results suggest that DNA repair capacities, mutational susceptibility and p53m are crucial for MIBC development.	4-METHYL-2-PENTANOL	101-105	P53	Homo sapiens	80-83
34681730-0	2021	Transcriptome Analysis of Cells Exposed to Actinomycin D and Nutlin-3a Reveals New Candidate p53-Target Genes and Indicates That CHIR-98014 Is an Important Inhibitor of p53 Activity.	Dactinomycin	43-56	P53	Homo sapiens	93-96
34681730-0	2021	Transcriptome Analysis of Cells Exposed to Actinomycin D and Nutlin-3a Reveals New Candidate p53-Target Genes and Indicates That CHIR-98014 Is an Important Inhibitor of p53 Activity.	Dactinomycin	43-56	P53	Homo sapiens	169-172
34681730-1	2021	Co-treatment with actinomycin D and nutlin-3a (A + N) strongly activates p53.	Dactinomycin	18-31	P53	Homo sapiens	73-76
15104235-7	2004	Taken together, our study suggests that the induction of p53 and activity of the Fas/Fas ligand apoptotic system may participate in the antiproliferative activity of acacetin in Hep G2 cells.	acacetin	166-174	P53	Homo sapiens	57-60
14965371-0	2004	p53-independent anti-tumor effects of the nitrogen-containing bisphosphonate zoledronic acid.	Zoledronic Acid	77-92	P53	Homo sapiens	0-3
14965371-5	2004	Therefore, we investigated the dependence of ZOL-induced apoptosis on intact p53 by using wt-p53 HCT116 and a p53-degraded HCT116 subline, and observed no significant difference.	Zoledronic Acid	45-48	P53	Homo sapiens	77-80
34582772-3	2021	MCC1734 exerted cytotoxicity on cell lines expressing different mechanisms of drug resistance (P-glycoprotein, BCRP, ABCB5, EGFR, p53 knockout) to a different extent.	mcc1734	0-7	P53	Homo sapiens	130-133
34671620-7	2021	In this review, we summarize recent advances with Wee1 inhibitors, statins, and mevalonate pathway inhibitors in cancers with p53 mutations.	Mevalonic Acid	80-90	P53	Homo sapiens	126-129
14724564-0	2004	Apoptosis triggered by DNA damage O6-methylguanine in human lymphocytes requires DNA replication and is mediated by p53 and Fas/CD95/Apo-1.	O-(6)-methylguanine	34-50	P53	Homo sapiens	116-119
34660288-0	2021	Valproic Acid Enhanced Temozolomide-Induced Anticancer Activity in Human Glioma Through the p53-PUMA Apoptosis Pathway.	Valproic Acid	0-13	P53	Homo sapiens	92-95
34660288-5	2021	In this study, we analyzed the impact of VPA on GBM patient survival and its possible correlation with TMZ treatment and p53 gene mutation.	Valproic Acid	41-44	P53	Homo sapiens	121-124
34660288-7	2021	Our analysis of clinical data indicates that the survival benefit of a combined TMZ and VPA treatment in GBM patients is dependent on their p53 gene status.	Valproic Acid	88-91	P53	Homo sapiens	140-143
34660288-8	2021	In cellular experiments, our results show that VPA enhanced the antineoplastic effect of TMZ by enhancing p53 activation and promoting the expression of its downstream pro-apoptotic protein, PUMA.	Valproic Acid	47-50	P53	Homo sapiens	106-109
34324743-0	2021	A rohitukine derivative IIIM-290 induces p53 dependent mitochondrial apoptosis in acute lymphoblastic leukemia cells.	5,7-dihydroxy-2-methyl-8-(4-(3-hydroxy-1-methyl)-piperidinyl)-4H-1-benzopyran-4-one	2-12	P53	Homo sapiens	41-44
34425189-0	2021	3,3"-diselenodipropionic acid (DSePA) induces reductive stress in A549 cells triggering p53-independent apoptosis: A novel mechanism for diselenides.	3,3'-diselenodipropionic acid	0-29	P53	Homo sapiens	88-91
34425189-0	2021	3,3"-diselenodipropionic acid (DSePA) induces reductive stress in A549 cells triggering p53-independent apoptosis: A novel mechanism for diselenides.	3,3'-diselenodipropionic acid	31-36	P53	Homo sapiens	88-91
34425189-10	2021	In conclusion, above results suggest that DSePA induces apoptosis in a p53 independent manner by involving extrinsic and intrinsic pathways together with ER stress which can an interesting strategy for lung cancer therapy.	3,3'-diselenodipropionic acid	42-47	P53	Homo sapiens	71-74
34469060-10	2021	As4 S4 upregulated p53 expression and downregulated PD-L1 expression in A549/DDP cells.	as4	0-3	P53	Homo sapiens	19-22
34217709-2	2021	Previously we found that the novel selective RNA polymerase I inhibitor CX-5461 induced a robust response of p53 phosphorylation and activation in vascular smooth muscle cells.	CX 5461	72-79	P53	Homo sapiens	109-112
14971655-17	2004	These data suggest that both p53-dependent and -independent apoptotic and growth-inhibitory pathways are markedly affected by Cr(VI) exposure.	Chromium	126-128	P53	Homo sapiens	29-32
34217709-5	2021	The inhibitory effects of CX-5461 were primarily mediated by activation of the p53 pathway rather than limiting the rate of ribosome biogenesis.	CX 5461	26-33	P53	Homo sapiens	79-82
34703821-5	2021	During the differentiation process that induced manifestation of breast cancer stem-like cells, DS significantly inhibited mammosphere formation in a dose-dependent manner and increased the expression of p53 and p21 in breast cancer stem-like cells, reducing the expression of cdc2 and cyclin B1 in MDA-MB-231 cells and cyclin D, cyclin E, CDK4, and CDK2 in MCF-7 cells.	dioscin	96-98	P53	Homo sapiens	204-207
15456634-10	2004	Women who were estrogen positive (either premenopausal or recent users of HRT) were at a significantly increased risk of an acquired p53 mutation if they consumed a diet with a high sugar index (odds ratio = 2.94; 95% confidence interval = 1.47-5.89); similar increases in risk of p53 mutations were not observed for men or women who were estrogen negative.	Sugars	182-187	P53	Homo sapiens	133-136
34533079-3	2022	We observed that MEMA decreased cell viability and colony formation in both HCT116 p53+/+ cells and HCT116 p53-/- cells.	mema	17-21	P53	Homo sapiens	107-110
34146926-7	2021	Delta9-THC and Delta8-THC also downregulated cyclin D1, p53, NOXA, PUMAalpha, and DRAM expressions but increased p21 and H2AX expression.	Dronabinol	7-10	P53	Homo sapiens	56-59
34146926-7	2021	Delta9-THC and Delta8-THC also downregulated cyclin D1, p53, NOXA, PUMAalpha, and DRAM expressions but increased p21 and H2AX expression.	Dronabinol	22-25	P53	Homo sapiens	56-59
15456634-10	2004	Women who were estrogen positive (either premenopausal or recent users of HRT) were at a significantly increased risk of an acquired p53 mutation if they consumed a diet with a high sugar index (odds ratio = 2.94; 95% confidence interval = 1.47-5.89); similar increases in risk of p53 mutations were not observed for men or women who were estrogen negative.	Sugars	182-187	P53	Homo sapiens	281-284
14634213-3	2003	The NQO1 inhibitor dicoumarol induces ubiquitin-independent p53 degradation.	Dicumarol	19-29	P53	Homo sapiens	60-63
34298093-7	2021	Heme-iron induced lipid peroxidation and DNA oxidation by interacting with Nox4-independent mechanisms, promoting p53/p21 activity and cellular senescence.	Heme	0-4	P53	Homo sapiens	114-117
34577545-0	2021	Actinomycin D Arrests Cell Cycle of Hepatocellular Carcinoma Cell Lines and Induces p53-Dependent Cell Death: A Study of the Molecular Mechanism Involved in the Protective Effect of IRS-4.	Dactinomycin	0-13	P53	Homo sapiens	84-87
14634213-4	2003	We now show that, like dicoumarol, several other coumarin and flavone inhibitors of NQO1 activity, which compete with NAD(P)H for binding to NQO1, induced ubiquitin-independent p53 degradation and inhibited wild-type p53-mediated apoptosis.	Dicumarol	23-33	P53	Homo sapiens	177-180
34393505-5	2021	Results: The distribution of TP53 Pro72Arg differed in T2DM patients from the controls, with a moderately increased proportion of TP53 Arg72 variant carriers (Pro/Arg and Arg/Arg genotypes) (88.3% vs 81.2%, p=0.022; OR=1.089, 95% CI=1.018-1.164).	Proline	159-162	P53	Homo sapiens	29-33
34393505-5	2021	Results: The distribution of TP53 Pro72Arg differed in T2DM patients from the controls, with a moderately increased proportion of TP53 Arg72 variant carriers (Pro/Arg and Arg/Arg genotypes) (88.3% vs 81.2%, p=0.022; OR=1.089, 95% CI=1.018-1.164).	Proline	159-162	P53	Homo sapiens	130-134
14634213-4	2003	We now show that, like dicoumarol, several other coumarin and flavone inhibitors of NQO1 activity, which compete with NAD(P)H for binding to NQO1, induced ubiquitin-independent p53 degradation and inhibited wild-type p53-mediated apoptosis.	Dicumarol	23-33	P53	Homo sapiens	217-220
34490348-6	2021	Since downregulation of GSDME was of benefit to breast cancer cells, p53 inhibition blocked the elevation of GSDME induced by CDK7 inhibition and retrieved cells from the tumor suppressive effect of CDK7 inhibition.	gsdme	109-114	P53	Homo sapiens	69-72
34490348-7	2021	Therefore, CDK7 inhibition exerted a negative effect on breast cancer cell proliferation and colony formation in a p53-GSDME dependent manner.	gsdme	119-124	P53	Homo sapiens	115-118
14634213-4	2003	We now show that, like dicoumarol, several other coumarin and flavone inhibitors of NQO1 activity, which compete with NAD(P)H for binding to NQO1, induced ubiquitin-independent p53 degradation and inhibited wild-type p53-mediated apoptosis.	nad(p)h	118-125	P53	Homo sapiens	177-180
14634213-4	2003	We now show that, like dicoumarol, several other coumarin and flavone inhibitors of NQO1 activity, which compete with NAD(P)H for binding to NQO1, induced ubiquitin-independent p53 degradation and inhibited wild-type p53-mediated apoptosis.	nad(p)h	118-125	P53	Homo sapiens	217-220
14634213-5	2003	Although wild-type p53 and several p53 mutants were sensitive to dicoumarol-induced degradation, the most frequent "hot-spot" p53 mutants in human cancer, R175H, R248H, and R273H, were resistant to dicoumarol-induced degradation, but remained sensitive to Mdm2-ubiquitin-mediated degradation.	Dicumarol	65-75	P53	Homo sapiens	19-22
34306252-10	2021	The main compounds of XYS include Quercetin, Naringenin, Isorhamnetin, and Stigmasterol, which mainly regulate the targets such as TP53, Akt1, and MYC and PI3K/Akt, p53, and cell cycle signal pathways.	3-methylquercetin	57-69	P53	Homo sapiens	131-135
34306252-10	2021	The main compounds of XYS include Quercetin, Naringenin, Isorhamnetin, and Stigmasterol, which mainly regulate the targets such as TP53, Akt1, and MYC and PI3K/Akt, p53, and cell cycle signal pathways.	3-methylquercetin	57-69	P53	Homo sapiens	165-168
34306319-7	2021	Results: Rotenone upregulated LRRK2 phosphorylation and beta-gal levels through the activation of the p53-p21 signaling axis and downregulated Rb phosphorylation.	Rotenone	9-17	P53	Homo sapiens	102-105
14634213-5	2003	Although wild-type p53 and several p53 mutants were sensitive to dicoumarol-induced degradation, the most frequent "hot-spot" p53 mutants in human cancer, R175H, R248H, and R273H, were resistant to dicoumarol-induced degradation, but remained sensitive to Mdm2-ubiquitin-mediated degradation.	Dicumarol	65-75	P53	Homo sapiens	35-38
34063628-5	2021	Interestingly, pretreatment with jorunnamycin A at 0.5 muM for 24 h considerably sensitized lung CSCs to cisplatin-induced apoptosis, as evidenced by upregulated p53 and decreased Bcl-2 in jorunnamycin A-pretreated CSC-enriched spheroids.	jorunnamycin A	33-47	P53	Homo sapiens	162-165
14612423-0	2003	The proline repeat domain of p53 binds directly to the transcriptional coactivator p300 and allosterically controls DNA-dependent acetylation of p53.	Proline	4-11	P53	Homo sapiens	29-32
34386269-6	2021	Western blot analysis revealed that GA stimulated programmed OC cell death via a p53-dependent intrinsic signaling.	Gallic Acid	36-38	P53	Homo sapiens	81-84
34386269-7	2021	In addition, GA arrested cell cycle at the S or G2 phase via p53-p21-Cdc2-cyclin B pathway in the same cells.	Gallic Acid	13-15	P53	Homo sapiens	61-64
35331874-0	2022	Tanshinol suppresses osteosarcoma by specifically inducing apoptosis of U2-OS cells through p53-mediated mechanism.	tanshinol	0-9	P53	Homo sapiens	92-95
14612423-0	2003	The proline repeat domain of p53 binds directly to the transcriptional coactivator p300 and allosterically controls DNA-dependent acetylation of p53.	Proline	4-11	P53	Homo sapiens	145-148
34570571-5	2021	In the patients with a stable disease, strong significant negative correlations between Cho/Cr and Cho/NAA with p53 mutation (-0.945 and -0.812 respectively, p < 0.05) and between Cho/Cr and IDH1, 2 mutation (-0.796, p < 0.05) were found.	Chromium	92-94	P53	Homo sapiens	112-115
14612423-5	2003	p300 binds in vitro to PXXP-containing peptides derived from the proline repeat domain, and PXXP-containing peptides inhibit sequence-specific DNA-dependent acetylation of p53, indicating that p300 docking to both the LXXLL and contiguous PXXP motif in p53 is required for p53 acetylation.	Proline	65-72	P53	Homo sapiens	172-175
34570571-6	2021	In the patients with tumour progression, a significant positive correlation of NAA/Cr with 1p19q codeletion (0.486, p < 0.05) and of Cho/Cr and Cho/NAA values with p53 mutation (0.477 and 0.416, p < 0.05) were identified.	Chromium	137-139	P53	Homo sapiens	164-167
14612423-5	2003	p300 binds in vitro to PXXP-containing peptides derived from the proline repeat domain, and PXXP-containing peptides inhibit sequence-specific DNA-dependent acetylation of p53, indicating that p300 docking to both the LXXLL and contiguous PXXP motif in p53 is required for p53 acetylation.	Proline	65-72	P53	Homo sapiens	253-256
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	cupric ion	207-211	P53	Homo sapiens	160-163
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	cupric ion	207-211	P53	Homo sapiens	165-168
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	Carbon Dioxide	219-223	P53	Homo sapiens	160-163
35320348-2	2022	We show the nucleoside reverse transcriptase inhibitor 3TC targets activities of these repeat elements in CRC pre-clinical models with a preferential effect in P53 mutant cell lines linked with direct binding of P53 to repeat elements.	Lamivudine	55-58	P53	Homo sapiens	160-163
35320348-2	2022	We show the nucleoside reverse transcriptase inhibitor 3TC targets activities of these repeat elements in CRC pre-clinical models with a preferential effect in P53 mutant cell lines linked with direct binding of P53 to repeat elements.	Lamivudine	55-58	P53	Homo sapiens	212-215
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	Carbon Dioxide	219-223	P53	Homo sapiens	165-168
14612423-5	2003	p300 binds in vitro to PXXP-containing peptides derived from the proline repeat domain, and PXXP-containing peptides inhibit sequence-specific DNA-dependent acetylation of p53, indicating that p300 docking to both the LXXLL and contiguous PXXP motif in p53 is required for p53 acetylation.	Proline	65-72	P53	Homo sapiens	253-256
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	ferric sulfate	237-241	P53	Homo sapiens	160-163
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	ferric sulfate	237-241	P53	Homo sapiens	165-168
14612423-6	2003	Deletion of the proline repeat motif of p53 prevents DNA-dependent acetylation of p53 by occluding p300 from the p53-DNA complex.	Proline	16-23	P53	Homo sapiens	40-43
35366141-7	2022	The administration of Ki16425 triggered apoptosis by down-regulating the expression of Bcl2 and up-regulating p53, Bax, cleaved caspase-3, and Cyt c expression.	3-(4-(4-((1-(2-chlorophenyl)ethoxy)carbonyl amino)-3-methyl-5-isoxazolyl) benzylsulfanyl) propanoic acid	22-29	P53	Homo sapiens	110-113
14612423-6	2003	Deletion of the proline repeat motif of p53 prevents DNA-dependent acetylation of p53 by occluding p300 from the p53-DNA complex.	Proline	16-23	P53	Homo sapiens	82-85
14612423-6	2003	Deletion of the proline repeat motif of p53 prevents DNA-dependent acetylation of p53 by occluding p300 from the p53-DNA complex.	Proline	16-23	P53	Homo sapiens	82-85
14612423-7	2003	Sequence-specific DNA places an absolute requirement for the proline repeat domain to drive p53 acetylation in vivo.	Proline	61-68	P53	Homo sapiens	92-95
35610491-0	2022	Cerium oxide-doped PEDOT nanocomposite for label-free electrochemical immunosensing of anti-p53 autoantibodies.	ceric oxide	0-12	P53	Homo sapiens	92-95
35523729-4	2022	A combination of fluorine and sulfur substituents on an aromatic ring induces microdipoles that enhance cell uptake of 12-residue peptide inhibitors of p53-HDM2 interaction and of cell-penetrating cyclic peptides.	Sulfur	30-36	P53	Homo sapiens	152-155
14612423-8	2003	Chromatin immunoprecipitation was used to show that the proline repeat deletion mutant p53 is bound to the p21 promoter in vivo, but it is not acetylated, indicating that proline-directed acetylation of p53 is a post-DNA binding event.	Proline	56-63	P53	Homo sapiens	87-90
14612423-8	2003	Chromatin immunoprecipitation was used to show that the proline repeat deletion mutant p53 is bound to the p21 promoter in vivo, but it is not acetylated, indicating that proline-directed acetylation of p53 is a post-DNA binding event.	Proline	56-63	P53	Homo sapiens	203-206
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	mesoporous	174-184	P53	Homo sapiens	65-68
14612423-8	2003	Chromatin immunoprecipitation was used to show that the proline repeat deletion mutant p53 is bound to the p21 promoter in vivo, but it is not acetylated, indicating that proline-directed acetylation of p53 is a post-DNA binding event.	Proline	171-178	P53	Homo sapiens	87-90
35585048-7	2022	Mechanistically, tRF-Val directly bound to the chaperone molecule EEF1A1, mediated its transport into the nucleus and promoted its interaction with MDM2 (a specific p53 E3 ubiquitin ligase), thus inhibiting the downstream molecular pathway of p53 and promoting GC progression.	trf-val	17-24	P53	Homo sapiens	165-168
35585048-7	2022	Mechanistically, tRF-Val directly bound to the chaperone molecule EEF1A1, mediated its transport into the nucleus and promoted its interaction with MDM2 (a specific p53 E3 ubiquitin ligase), thus inhibiting the downstream molecular pathway of p53 and promoting GC progression.	trf-val	17-24	P53	Homo sapiens	243-246
35383292-0	2022	The genotypes and phenotypes of missense mutations in the proline domain of the p53 protein.	Proline	58-65	P53	Homo sapiens	80-83
14612423-8	2003	Chromatin immunoprecipitation was used to show that the proline repeat deletion mutant p53 is bound to the p21 promoter in vivo, but it is not acetylated, indicating that proline-directed acetylation of p53 is a post-DNA binding event.	Proline	171-178	P53	Homo sapiens	203-206
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	mesoporous	174-184	P53	Homo sapiens	101-104
14612423-9	2003	The PXXP repeat expands the basic interface of a p300-targeted transactivation domain, and proline-directed acetylation of p53 at promoters indicates that p300-mediated acetylation can be highly constrained by substrate conformation in vivo.	Proline	91-98	P53	Homo sapiens	123-126
14637245-0	2003	Formation of trans-4-hydroxy-2-nonenal- and other enal-derived cyclic DNA adducts from omega-3 and omega-6 polyunsaturated fatty acids and their roles in DNA repair and human p53 gene mutation.	omega-3	87-94	P53	Homo sapiens	175-178
35290795-7	2022	We conclude that interactions with NT* help to unblock translation of the proline-rich disordered region of p53.	Proline	74-81	P53	Homo sapiens	108-111
35541917-0	2022	Long noncoding RNA Linc01612 represses hepatocellular carcinoma progression by regulating miR-494/ATF3/p53 axis and promoting ubiquitination of YBX1.	linc01612	19-28	P53	Homo sapiens	103-106
35541917-5	2022	Mechanistically, in p53-expressing hepatoma cells, Linc01612 acts as a competitive endogenous RNA and promotes the expression of activation transcription factor 3 (ATF3) by sponging microRNA-494 (miR-494), which in turn inhibits MDM2-mediated ubiquitination of p53 and activates the p53 pathway.	linc01612	51-60	P53	Homo sapiens	20-23
35541917-5	2022	Mechanistically, in p53-expressing hepatoma cells, Linc01612 acts as a competitive endogenous RNA and promotes the expression of activation transcription factor 3 (ATF3) by sponging microRNA-494 (miR-494), which in turn inhibits MDM2-mediated ubiquitination of p53 and activates the p53 pathway.	linc01612	51-60	P53	Homo sapiens	261-264
35541917-5	2022	Mechanistically, in p53-expressing hepatoma cells, Linc01612 acts as a competitive endogenous RNA and promotes the expression of activation transcription factor 3 (ATF3) by sponging microRNA-494 (miR-494), which in turn inhibits MDM2-mediated ubiquitination of p53 and activates the p53 pathway.	linc01612	51-60	P53	Homo sapiens	283-286
14577584-0	2003	Polymorphism of the p53 codon 72 Arg/Pro and the risk of HPV type 16/18-associated cervical and oral cancer in India.	Proline	37-40	P53	Homo sapiens	20-23
35541917-6	2022	Furthermore, in p53-null hepatoma cells, Linc01612 exerts its biological functions by physically interacting with Y-box binding protein 1 protein (YBX1) and promoting the ubiquitin-mediated degradation of YBX1.	linc01612	41-50	P53	Homo sapiens	16-19
35541917-7	2022	Interestingly, the Linc01612-YBX1 signaling pathway is also present in p53-expressing hepatoma cells.	linc01612	19-28	P53	Homo sapiens	71-74
35558561-4	2022	In this study, we examined the effect of salts, including KCl and sugars, on the aggregation of p53C by monitoring two distinct aggregates: amorphous-like and amyloid-like.	Sugars	66-72	P53	Homo sapiens	96-99
14577584-3	2003	This degradation is controlled by a common polymorphism of the p53 gene encoding either a proline or an arginine at its codon 72 in exon 4.	Proline	90-97	P53	Homo sapiens	63-66
35370938-6	2022	Accordingly, enrichment analyses of GO terms and KEGG pathways showed that several pathways (e.g., lysosome pathway (hsa04142) and p53 signaling pathway (hsa04115)) may be involved in the response of HK-2 cells to oxamate.	Oxamic Acid	214-221	P53	Homo sapiens	131-134
14577584-4	2003	Recently, it has been demonstrated that the presence of homozygous arginine at codon 72 renders p53 about seven times more susceptible to E6-mediated proteolytic degradation as well as to cervical cancer than those with proline homozygotes or proline/arginine heterozygotes.	Proline	243-250	P53	Homo sapiens	96-99
12927789-4	2003	It was found that induction of apoptosis (characterized by DNA laddering) by actinomycin D was accompanied by a stimulation of the expression of active (phosphorylated) form of p53.	Dactinomycin	77-90	P53	Homo sapiens	177-180
35455441-0	2022	Synthetic Design and Biological Evaluation of New p53-MDM2 Interaction Inhibitors Based on Imidazoline Core.	Imidazolines	91-102	P53	Homo sapiens	50-53
35455441-2	2022	In this study, we have applied a simple approach of two-step synthesis of imidazoline-based alkoxyaryl compounds, which are able to efficiently inhibit p53-MDM2 protein-protein interactions, promote accumulation of p53 and p53-inducible proteins in various cancer cell lines.	Imidazolines	74-85	P53	Homo sapiens	152-155
35455441-2	2022	In this study, we have applied a simple approach of two-step synthesis of imidazoline-based alkoxyaryl compounds, which are able to efficiently inhibit p53-MDM2 protein-protein interactions, promote accumulation of p53 and p53-inducible proteins in various cancer cell lines.	Imidazolines	74-85	P53	Homo sapiens	215-218
35133203-7	2022	Naphtho (2,3-b) thiophen-4,9-quinone presents antiproliferative activity regardless TP53 status and may be a promising agent in the treatment of bladder cancer, as they have an oxidizing effect and interfere with cell cycle.	naphtho (2,3-b) thiophen-4,9-quinone	0-36	P53	Homo sapiens	84-88
12948823-3	2003	Procarbazine plus Cu(II) induced piperidine-labile and formamidopyrimidine-DNA glycosylase-sensitive lesions at the 5"-ACG-3" sequence, complementary to a hotspot of the p53 gene, and the 5"-TG-3" sequence.	formamidopyrimidine	55-74	P53	Homo sapiens	170-173
35163524-6	2022	Herein, we report that EP4 receptor agonists PgE1-OH and L-902688 have exhibited enhanced cytotoxicity when applied together with anti-CD20 MAbs rituximab, ofatumumab and obinutuzumab in vitro in Burkitt lymphoma cells Ramos, as well as in p53-deficient chronic lymphocytic leukemia (CLL) cells MEC-1.	L-902688	57-65	P53	Homo sapiens	240-243
35455441-2	2022	In this study, we have applied a simple approach of two-step synthesis of imidazoline-based alkoxyaryl compounds, which are able to efficiently inhibit p53-MDM2 protein-protein interactions, promote accumulation of p53 and p53-inducible proteins in various cancer cell lines.	Imidazolines	74-85	P53	Homo sapiens	223-226
12893432-2	2003	To address on the genetic risk factor for NPC, we investigated association between the p53 codon 72 polymorphism (Pro/Arg) and NPC susceptibility in the Thai.	Proline	114-117	P53	Homo sapiens	87-90
35251293-7	2022	Here, metformin bicarbonate (MetC) is synthesized to develop pH-responsive MetC-nanoparticles with a unique "bomb" for effective cytosolic delivery of POLR2A siRNA, which greatly facilitates its endo/lysosomal escape into the cytosol and augments its therapeutic efficacy of cancer harboring TP53 deficiency.	metc	29-33	P53	Homo sapiens	292-296
35265212-4	2022	Expectedly, oral DPAICP@ME played its predetermined role in vivo to restore p53 signaling pathway for cancer therapy in B16F10 homograft malignant melanoma model, LLC Lewis orthotopic transplantation model of lung cancer and patient-derived orthotopic xenograft (PDOX) mice model of colon cancer.	dpaicp@me	17-26	P53	Homo sapiens	76-79
35163037-0	2022	Sesquiterpene Lactones Potentiate Olaparib-Induced DNA Damage in p53 Wildtype Cancer Cells.	sesquiterpene lactones	0-22	P53	Homo sapiens	65-68
35163037-2	2022	In this work, we show that the two structurally-related sesquiterpene lactones, a 2-bromobenzyloxy derivative of dehydrosantonin (BdS) and alantolactone (ATL) sensitise p53 wildtype, homologous recombination-proficient cancer cells to low-dose treatment with the PARP inhibitor, olaparib.	sesquiterpene lactones	56-78	P53	Homo sapiens	169-172
12881708-1	2003	The N-terminal proline-rich domain of human p53 has been shown to be important for the induction of apoptosis.	Proline	15-22	P53	Homo sapiens	44-47
35053312-7	2022	HepG2 mitochondrial membrane potential (DeltaPsim) significantly declined and cytoplasmic localization of P53, caspase 3, and caspase 9 increased after TDCPP exposure.	tris(1,3-dichloro-2-propyl)phosphate	152-157	P53	Homo sapiens	106-109
35163553-9	2022	As the autophagy was suppressed through the autophagy inhibitor chloroquine, hinokitiol-induced senescence in U-2 OS cells was significantly enhanced accompanying more abundant p53 expression.	Chloroquine	64-75	P53	Homo sapiens	177-180
12821135-0	2003	Dephosphorylation of p53 during cell death by N-alpha-tosyl-L-phenylalanyl chloromethyl ketone.	n-alpha-tosyl-l-phenylalanyl chloromethyl ketone	46-94	P53	Homo sapiens	21-24
12853970-3	2003	Previously, we and others have shown that some functional domains in p53, such as the DNA-binding and tetramerization domains, are required for inducing both cell cycle arrest and apoptosis whereas others, such as the second activation domain, the proline-rich domain, and the C-terminal basic domain, are only required for inducing apoptosis.	Proline	248-255	P53	Homo sapiens	69-72
12855662-3	2003	We have also evaluated the influence of major resistance mechanisms, such as expression of multidrug resistance-associated drug efflux pumps, cisplatin resistance, loss of p53 function, and absence of mismatch repair on the cytotoxic activity of irofulven.	irofulven	246-255	P53	Homo sapiens	172-175
12883038-4	2003	Low adozelesin concentrations (e.g., 0.5 nM) induced a transient S-phase block and cell cycle arrest in G(2)-M, as well as increased induction of p53 and p21, whereas a high drug concentration (e.g., 2.5 nM) caused apoptosis but no p21 induction.	adozelesin	4-14	P53	Homo sapiens	146-149
12771997-2	2003	Mut-p53 cells were significantly resistant to the cytotoxicity of the microtubule-targeted drugs (vinca alkaloids and taxanes), as compared with wt-p53 cells.	Vinca Alkaloids	98-113	P53	Homo sapiens	4-7
12796380-8	2003	After adjustment for age and gender, a logistic regression analysis suggested that the risk for a p53 Arg homozygous patient to develop cardia cancer is 3.1 95% confidence interval, 1.4-7.3) times greater than for p53 Pro homozygous and p53 Arg/Pro heterozygous patients.	Proline	218-221	P53	Homo sapiens	98-101
12796380-8	2003	After adjustment for age and gender, a logistic regression analysis suggested that the risk for a p53 Arg homozygous patient to develop cardia cancer is 3.1 95% confidence interval, 1.4-7.3) times greater than for p53 Pro homozygous and p53 Arg/Pro heterozygous patients.	Proline	218-221	P53	Homo sapiens	214-217
12796380-8	2003	After adjustment for age and gender, a logistic regression analysis suggested that the risk for a p53 Arg homozygous patient to develop cardia cancer is 3.1 95% confidence interval, 1.4-7.3) times greater than for p53 Pro homozygous and p53 Arg/Pro heterozygous patients.	Proline	218-221	P53	Homo sapiens	214-217
12771935-3	2003	Following 8 h of exposure to taxol, the cell line DoHH2 (p53 wild type) exhibited mitotic arrest and engagement of apoptosis, whereas the cell line SU-DHL-4 (p53 mutant) breached cell-cycle arrest with progression to an abnormal cycle and a 24 h delay in the engagement of apoptosis.	su-dhl-4	148-156	P53	Homo sapiens	158-161
12609999-0	2003	The activation domains, the proline-rich domain, and the C-terminal basic domain in p53 are necessary for acetylation of histones on the proximal p21 promoter and interaction with p300/CREB-binding protein.	Proline	28-35	P53	Homo sapiens	84-87
12609999-1	2003	The p53 transcription factor contains two separate tandem activation domains (AD1 and AD2), a proline-rich domain (PRD), and a C-terminal basic domain (BD).	Proline	94-101	P53	Homo sapiens	4-7
12743601-6	2003	Tumor-associated p53 mutants however are attenuated for YB1 nuclear localization as are mutants mutated in the proline-rich domain of p53.	Proline	111-118	P53	Homo sapiens	17-20
12743601-6	2003	Tumor-associated p53 mutants however are attenuated for YB1 nuclear localization as are mutants mutated in the proline-rich domain of p53.	Proline	111-118	P53	Homo sapiens	134-137
12684687-4	2003	We report that Brca1-deficiency in p53-null cells was associated with increased sensitivity to the topoisomerase I poisons camptothecin and topotecan, the topoisomerase II poisons doxorubicin, mitoxantrone and etoposide, and to the platinum compounds carboplatin and oxaliplatin, but not to the antimetabolites 5-fluorouracil and gemcitabine and the taxanes docetaxel and paclitaxel.	Mitoxantrone	193-205	P53	Homo sapiens	35-38
12711114-1	2003	The p53 gene is frequently mutated in lung tumors, and mutations may be caused by both polycyclic aromatic hydrocarbons (PAHs) and nitrosamines found in tobacco smoke.	Nitrosamines	131-143	P53	Homo sapiens	4-7
12711114-12	2003	These results suggest that p53 mutations in both types of lung tumors may arise from adduction by both PAHs and nitrosamines.	Nitrosamines	112-124	P53	Homo sapiens	27-30
12694871-4	2003	Binding of active, latent, and in vitro-activated p53 protein to DNA fragments modified by antitumor cisplatin was studied using electrophoretic mobility shift assay in agarose gels and immunoblotting analysis.	Sepharose	169-176	P53	Homo sapiens	50-53
12644821-8	2003	Another novel finding is that CR was negatively influenced by high BAX expression in all patients group (P=0.047) and by BCL2 expression in the TP53(-) group (P=0.05).	Chromium	30-32	P53	Homo sapiens	144-148
12624953-3	2003	To study the effect of dominant-negative inhibitor GSE22 on the p53 activity, cultures coexpressing GSE22 and tetracycline-suppressible p53 were derived from p53-negative cell lines.	Tetracycline	110-122	P53	Homo sapiens	136-139
12624953-3	2003	To study the effect of dominant-negative inhibitor GSE22 on the p53 activity, cultures coexpressing GSE22 and tetracycline-suppressible p53 were derived from p53-negative cell lines.	Tetracycline	110-122	P53	Homo sapiens	136-139
12616342-6	2003	As the tumor suppressor p53 is another important factor of chemoresistance, we also analyzed the possibility that p53 affects the response of tumor cells to CET and HHT.	Homoharringtonine	157-160	P53	Homo sapiens	114-117
12492370-7	2003	The initiation of this TP53-dependent G1-phase arrest occurs despite the presence of substantial levels of cyclin D1/CDK4 and cyclin E/CDK2 kinase activities, hyperphosphoryated RB, and active E2F1.	Rubidium	178-180	P53	Homo sapiens	23-27
12459171-2	2002	In this report, we addressed the question whether the natural variability at p53 locus (the proline-arginine substitution at codon 72) affects the capacity of peripheral-blood mononuclear cells from healthy subjects to undergo in vitro apoptosis in response to the cytotoxic drug cytosine arabinoside.	Proline	92-99	P53	Homo sapiens	77-80
12479728-8	2002	All PAs were found negative for Ki-67 and p53.	Protactinium	4-7	P53	Homo sapiens	42-45
12397361-3	2002	Here we report that DNA damage specifically induces p53 phosphorylation on Ser/Thr-Pro motifs, which facilitates its interaction with Pin1, a member of peptidyl-prolyl isomerase.	Proline	83-86	P53	Homo sapiens	52-55
12481433-9	2002	When p53 expression was induced, cells became chemosensitive to actinomycin D in the presence or absence of MDM2 expression; this result suggests that MDM2 cannot inhibit p53-mediated chemosensitivity.	Dactinomycin	64-77	P53	Homo sapiens	5-8
12232053-3	2002	Inhibition of NQO1 activity by dicoumarol induces p53 and p73 proteasomal degradation.	Dicumarol	31-41	P53	Homo sapiens	50-53
12232053-4	2002	A mutant p53 (p53([22,23])), which is resistant to Mdm-2-mediated degradation, was susceptible to dicoumarol-induced degradation.	Dicumarol	98-108	P53	Homo sapiens	9-12
12232053-4	2002	A mutant p53 (p53([22,23])), which is resistant to Mdm-2-mediated degradation, was susceptible to dicoumarol-induced degradation.	Dicumarol	98-108	P53	Homo sapiens	14-17
12232053-6	2002	The tumor suppressor p14(ARF) and the viral oncogenes SV40 LT and adenovirus E1A that are known to stabilize p53 inhibited dicoumarol-induced p53 degradation.	Dicumarol	123-133	P53	Homo sapiens	109-112
12232053-6	2002	The tumor suppressor p14(ARF) and the viral oncogenes SV40 LT and adenovirus E1A that are known to stabilize p53 inhibited dicoumarol-induced p53 degradation.	Dicumarol	123-133	P53	Homo sapiens	142-145
12232053-8	2002	In vitro studies indicate that dicoumarol-induced p53 degradation was ubiquitin-independent and ATP-dependent.	Dicumarol	31-41	P53	Homo sapiens	50-53
12368717-4	2002	The proline residue at codon 72 of the p53 gene was significantly over represented in the POAG patients relative to healthy controls.	Proline	4-11	P53	Homo sapiens	39-42
12368717-12	2002	CONCLUSIONS: Association between the p53 gene encoding for proline at codon 72 and POAG presumably exists in some ethnic populations but cannot be used as a predictor for the role of the gene as a common regulator of cell death of retinal ganglions leading to POAG.	Proline	59-66	P53	Homo sapiens	37-40
12065086-3	2002	The p53 codon 72 Arg/Pro polymorphism has been suggested to be associated with susceptibility to tobacco-related cancers, but this association remains controversial.	Proline	21-24	P53	Homo sapiens	4-7
12160929-6	2002	Cotreatment of p53-WT H460 cells with free radical scavengers, such as D-mannitol, uric acid, and sodium selenite, significantly attenuated the TCE- or PERC-induced lipid peroxidation.	Free Radicals	38-50	P53	Homo sapiens	15-18
12067581-9	2002	Similarly, the disruption of correct p53 folding and DNA binding by Cd(II), Ni(II) and Co(II) has been shown by other authors.	cd(ii)	68-74	P53	Homo sapiens	37-40
12144822-7	2002	The frequency of distribution of the three genotypes of p53 codon 72 in a subgroup of the HPV16/18-positive cervical cancer patients was Pro/Pro 0.18 and Arg/Arg 0.26, with the heterozygous Pro/Arg 0.56, differing significantly from the genotype frequency in the normal healthy women (chi(2) = 6.928, df = 2, P &lt; 0.05).	Proline	141-144	P53	Homo sapiens	56-59
12130688-4	2002	Our recent investigations with electrophilic prostaglandins enabled us to devise a pharmacophore and mechanism of action hypothesis relevant to this problem: a cross-conjugated alpha,beta-unsaturated dienone with two sterically accessible electrophilic beta-carbons is a molecular determinant that confers activity among this class of ubiquitin isopeptidases inhibitors, and that inhibitors of ubiquitin isopeptidases cause cell death in vitro independently of p53.	alpha,beta-unsaturated dienone	177-207	P53	Homo sapiens	461-464
12115545-1	2002	p53 codon 72, which produces variant proteins with an arginine (Arg) or proline (Pro), has been reported to be associated with cancers of the lung, esophagus and cervix.	Proline	72-79	P53	Homo sapiens	0-3
12115545-1	2002	p53 codon 72, which produces variant proteins with an arginine (Arg) or proline (Pro), has been reported to be associated with cancers of the lung, esophagus and cervix.	Proline	81-84	P53	Homo sapiens	0-3
12221910-1	2002	A polymorphism at codon 72 in the p53 gen has been reported as a potential risk factor to cervical cancer (CC) because human papillomavirus (HPV) is more effective at degrading p53 Arg-72 than p53 Pro-72, making individuals homozygous for p53 Arg-72 seven times more likely to develop HPV-associated CC.	Proline	197-200	P53	Homo sapiens	34-37
12221910-1	2002	A polymorphism at codon 72 in the p53 gen has been reported as a potential risk factor to cervical cancer (CC) because human papillomavirus (HPV) is more effective at degrading p53 Arg-72 than p53 Pro-72, making individuals homozygous for p53 Arg-72 seven times more likely to develop HPV-associated CC.	Proline	197-200	P53	Homo sapiens	177-180
12221910-1	2002	A polymorphism at codon 72 in the p53 gen has been reported as a potential risk factor to cervical cancer (CC) because human papillomavirus (HPV) is more effective at degrading p53 Arg-72 than p53 Pro-72, making individuals homozygous for p53 Arg-72 seven times more likely to develop HPV-associated CC.	Proline	197-200	P53	Homo sapiens	177-180
12221910-1	2002	A polymorphism at codon 72 in the p53 gen has been reported as a potential risk factor to cervical cancer (CC) because human papillomavirus (HPV) is more effective at degrading p53 Arg-72 than p53 Pro-72, making individuals homozygous for p53 Arg-72 seven times more likely to develop HPV-associated CC.	Proline	197-200	P53	Homo sapiens	177-180
12221910-6	2002	Among cases with CC the proportions of the p53 genotypes at codon 72 were 0.05 to proline homozygous, 0.5 to heterozygous, and 0.45 to arginine-homozygous.	Proline	82-89	P53	Homo sapiens	43-46
12069238-5	2002	The combination of the optimized LPA matrix (6% LPA, Mw 600 kDa) and a hydrophilic, adsorbed polyDuramide wall coating was found to be essential for resolution of CAE-SSCP/HA peaks and yielded sensitive mutation detection in all 11 p53 samples initially studied.	poly-N-(2-hydroxyethyl)acrylamide	93-105	P53	Homo sapiens	232-235
12067251-8	2002	Treatment of p53 cDNA with micromolar concentrations of (+/-)-anti-7,8-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydro-benzo[a]pyrene, (anti-BPDE, an ultimate carcinogen) or sub-micromolar concentrations of BP-7,8-dione in the presence of redox-cycling conditions (NADPH and CuCl(2)) also caused p53 mutations in a dose-dependent manner.	10alpha-epoxy-7,8,9,10-tetrahydro-benzo[a]pyrene	88-136	P53	Homo sapiens	13-16
12067251-8	2002	Treatment of p53 cDNA with micromolar concentrations of (+/-)-anti-7,8-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydro-benzo[a]pyrene, (anti-BPDE, an ultimate carcinogen) or sub-micromolar concentrations of BP-7,8-dione in the presence of redox-cycling conditions (NADPH and CuCl(2)) also caused p53 mutations in a dose-dependent manner.	benzo(a)pyrene-7,8-dione	210-222	P53	Homo sapiens	13-16
12067251-10	2002	p53 mutagenesis by BP-7,8-dione was attenuated by ROS scavengers and completely abrogated by a combination of superoxide dismutase and catalase, indicating that both superoxide anion and hydroxyl radicals were the responsible mutagens.	benzo(a)pyrene-7,8-dione	19-31	P53	Homo sapiens	0-3
12032289-4	2002	An oligonucleotide microarray analysis demonstrated that, in addition to the heat shock-responsive and redox-responsive genes, the p53-responsive genes, such as gadd45, cyclin G1, and cathepsin D, were significantly up-regulated in the cells treated with 15d-PGJ(2).	-pgj(	258-263	P53	Homo sapiens	131-134
12007564-0	2002	Expression of p53-family members and associated target molecules in breast cancer cell lines in response to vincristine treatment.	Vincristine	108-119	P53	Homo sapiens	14-17
12007564-1	2002	As the antimitotic agent vincristine (VCR) has been reported to induce a weak p53 response in some studies, we hypothesised that p73 and p63, the recently described p53 homologues, may replace p53 in triggering apoptosis or cell cycle arrest effectors in VCR-treated cell lines.	Vincristine	25-36	P53	Homo sapiens	78-81
12007564-1	2002	As the antimitotic agent vincristine (VCR) has been reported to induce a weak p53 response in some studies, we hypothesised that p73 and p63, the recently described p53 homologues, may replace p53 in triggering apoptosis or cell cycle arrest effectors in VCR-treated cell lines.	Vincristine	25-36	P53	Homo sapiens	165-168
12007564-1	2002	As the antimitotic agent vincristine (VCR) has been reported to induce a weak p53 response in some studies, we hypothesised that p73 and p63, the recently described p53 homologues, may replace p53 in triggering apoptosis or cell cycle arrest effectors in VCR-treated cell lines.	Vincristine	25-36	P53	Homo sapiens	165-168
12575207-1	2002	OBJECTIVE: A polymorphism at codon 72 of the human tumor-suppressor gene, p53, results in translation to either arginine or proline.	Proline	124-131	P53	Homo sapiens	74-77
11867746-3	2002	We have reported previously that inhibition of NAD(P)H: quinone oxidoreductase 1 (NQO1) activity by dicoumarol induces degradation of p53, indicating that NQO1 plays a role in p53 stabilization.	Dicumarol	100-110	P53	Homo sapiens	134-137
11867746-3	2002	We have reported previously that inhibition of NAD(P)H: quinone oxidoreductase 1 (NQO1) activity by dicoumarol induces degradation of p53, indicating that NQO1 plays a role in p53 stabilization.	Dicumarol	100-110	P53	Homo sapiens	176-179
11867746-8	2002	Differences in the effectiveness of dicoumarol and hsp90 inhibitors to induce p53 degradation and suppress apoptosis in these cell types indicate that NQO1 and hsp90 stabilize p53 through different mechanisms.	Dicumarol	36-46	P53	Homo sapiens	78-81
11867746-8	2002	Differences in the effectiveness of dicoumarol and hsp90 inhibitors to induce p53 degradation and suppress apoptosis in these cell types indicate that NQO1 and hsp90 stabilize p53 through different mechanisms.	Dicumarol	36-46	P53	Homo sapiens	176-179
12014658-0	2002	Influence of p53 status on radiation and 5-flourouracil synergy in pancreatic cancer cells.	5-flourouracil	41-55	P53	Homo sapiens	13-16
11785968-4	2002	BP-7,8-dione strongly damaged the G and C of the ACG sequence complementary to codon 273 of the p53 gene.	benzo(a)pyrene-7,8-dione	0-12	P53	Homo sapiens	96-99
14577491-10	2002	P53 mutation was confirmed only in 1 patient with pTaG2 tumor in exon 5 (deletion of proline 128).	Proline	85-92	P53	Homo sapiens	0-3
11802048-0	2002	Prognostic significance of the proline form of p53 codon 72 polymorphism in nasopharyngeal carcinoma.	Proline	31-38	P53	Homo sapiens	47-50
11709051-10	2001	The antagonism between RB and c-Abl/p73 may modulate the function of p53 to direct the choice between growth arrest and apoptosis in DNA damaged cells.	Rubidium	23-25	P53	Homo sapiens	69-72
11564578-1	2001	The p53 codon 72 polymorphism, resulting in either an arginine or a proline residue has been proposed to affect the susceptibility of p53 protein to human papilloma virus (HPV) E6-mediated degradation in vitro.	Proline	68-75	P53	Homo sapiens	4-7
11564578-1	2001	The p53 codon 72 polymorphism, resulting in either an arginine or a proline residue has been proposed to affect the susceptibility of p53 protein to human papilloma virus (HPV) E6-mediated degradation in vitro.	Proline	68-75	P53	Homo sapiens	134-137
11554766-0	2001	Cell cycle regulation via p53 phosphorylation by a 5"-AMP activated protein kinase activator, 5-aminoimidazole- 4-carboxamide-1-beta-D-ribofuranoside, in a human hepatocellular carcinoma cell line.	acadesine	94-149	P53	Homo sapiens	26-29
11593402-1	2001	Two specific inhibitors of cyclin-dependent kinase 2 (Cdk2), roscovitine and olomoucine, have been shown recently to induce nuclear accumulation of wt p53 and nucleolar unravelling in interphase human untransformed IMR-90 and breast tumor-derived MCF-7 cells.	olomoucine	77-87	P53	Homo sapiens	151-154
11555596-8	2001	Competition analysis with monoclonal antibodies showed that Fab binding could be inhibited most effectively with DO11 and, to a lesser extent, Pab240, indicating an epitope within or adjacent to residues 181-190 of p53.	do11	113-117	P53	Homo sapiens	215-218
11493433-4	2001	These pathways are themselves influenced by a number of lipid products (diacylglycerol, sphingosine-1 phosphate, and glucosyl ceramide), reactive oxygen species, oncogenes (such as the tumor suppressor gene p53), protein kinases (protein kinase C and phosphoinositide-3 kinase), and external stimuli (hematopoietic growth factors and the extracellular matrix).	sphingosine 1-phosphate	88-111	P53	Homo sapiens	207-210
11429426-2	2001	A recent report suggests that a polymorphism of the p53 tumour suppressor gene that results in the substitution of a proline residue with an arginine residue at position 72 of the p53 protein might act as a risk factor in HPV associated malignancies.	Proline	117-124	P53	Homo sapiens	52-55
11429426-2	2001	A recent report suggests that a polymorphism of the p53 tumour suppressor gene that results in the substitution of a proline residue with an arginine residue at position 72 of the p53 protein might act as a risk factor in HPV associated malignancies.	Proline	117-124	P53	Homo sapiens	180-183
11429426-7	2001	RESULTS: The proportions of p53 codon 72 genotypes found were 78% arginine homozygous, 2% proline homozygous, and 20% heterozygous among patients with skin cancer and 79% arginine homozygous, 3.5% proline homozygous, and 17.5% heterozygous among the control population.	Proline	90-97	P53	Homo sapiens	28-31
11429426-7	2001	RESULTS: The proportions of p53 codon 72 genotypes found were 78% arginine homozygous, 2% proline homozygous, and 20% heterozygous among patients with skin cancer and 79% arginine homozygous, 3.5% proline homozygous, and 17.5% heterozygous among the control population.	Proline	197-204	P53	Homo sapiens	28-31
11434920-2	2001	We established osteosarcoma cell lines in which a tetracycline-regulatable promoter controls the induction of RB, p53 and p21.	Tetracycline	50-62	P53	Homo sapiens	114-117
11434920-5	2001	Similar changes occurred to p53 and p21 when RB is present.	Rubidium	45-47	P53	Homo sapiens	28-31
11434920-6	2001	However, in the absence of RB, some of the E2F-responsive genes decreased in response to p53 but not to p21.	Rubidium	27-29	P53	Homo sapiens	89-92
11407516-11	2001	The p53 mutation was noted in 16 patients: NR in 5 patients, PR in 9 patients, and CR in 2 patients (P = .638).	Chromium	83-85	P53	Homo sapiens	4-7
11384212-6	2001	However, lung H441 adenocarcinoma cells, with a mutation in exon 5, codon 158 of p53, exhibited partial G1 arrest after the diol epoxides as well as actinomycin D, and H2030 adenocarcinoma cells did not show G1 arrest after any of the chemicals despite a normal p53.	Dactinomycin	149-162	P53	Homo sapiens	81-84
11358839-4	2001	Compared with control U87MG-neo cells with intact p53 function, the clonogenic survival of U87MG-E6 cells exposed to BCNU was reduced significantly.	Carmustine	117-121	P53	Homo sapiens	50-53
11358839-6	2001	In contrast, resistance to BCNU in U87MG-neo cells was associated with up-regulation of p53, prolonged induction of p21(WAF1), sustained cell cycle arrest in S phase, and enhancement of DNA repair.	Carmustine	27-31	P53	Homo sapiens	88-91
11358839-7	2001	U87MG cells with disrupted p53 function were less able to repair BCNU-induced DNA damage and survive this chemotherapeutic insult.	Carmustine	65-69	P53	Homo sapiens	27-30
11497287-7	2001	After 24 hours of the N-1-sulfonylpyrimidine derivative application, the p53 oncoprotein expression could not be detected by immunocytochemical analysis.	N-1-sulfonylpyrimidine	22-44	P53	Homo sapiens	73-76
11373271-4	2001	We established tetracycline-regulated, stable hRAD50 expression systems in SaOS-2 cells, which retain mutated p53, and in HeLa cells.	Tetracycline	15-27	P53	Homo sapiens	110-113
11350911-2	2001	A p53-null, MGMT-proficient lung tumor cell line (H1299) was engineered to express wt p53 in a tetracycline-regulated system.	Tetracycline	95-107	P53	Homo sapiens	86-89
11350911-3	2001	High levels of p53 induction achieved by tetracycline withdrawal were accompanied by G(1) cell cycle arrest without significant apoptosis in this cell line.	Tetracycline	41-53	P53	Homo sapiens	15-18
11350911-9	2001	Induction of wt p53 in these models led to a 3- and 2-fold increase in sensitivity to 1,3-bis(2-chloroethyl)-1-nitrosourea and temozolomide, respectively, which generate the MGMT-repairable O(6)-alkyl adducts in DNA.	Carmustine	86-122	P53	Homo sapiens	16-19
11368358-0	2001	Apoptotic response to homoharringtonine in human wt p53 leukemic cells is independent of reactive oxygen species generation and implicates Bax translocation, mitochondrial cytochrome c release and caspase activation.	Homoharringtonine	22-39	P53	Homo sapiens	52-55
11258898-6	2001	Activated MAPK immunoprecipitates of nuclei from T(4)-treated cells accumulated p53 in a time-dependent manner; T(4) and T(4)-agarose were more effective than T(3).	Sepharose	126-133	P53	Homo sapiens	80-83
11280728-9	2001	We hypothesize that proline oxidation supports the generation of ROS by donating reducing potential to an electron transport chain altered either by p53-dependent mechanisms or by overexpression of POX.	Proline	20-27	P53	Homo sapiens	149-152
11158294-5	2001	We found that induction of p53 either by diverse stress signals or ectopically using a tetracycline-regulated promoter causes a marked reduction in CHK1 protein levels.	Tetracycline	87-99	P53	Homo sapiens	27-30
11158615-5	2001	The NQO1 inhibitor dicoumarol caused a reduction in the level of both endogenous and gamma-irradiation-induced p53 in HCT116 human colon carcinoma cells.	Dicumarol	19-29	P53	Homo sapiens	111-114
11158615-6	2001	This reduction was prevented by the proteasome inhibitors MG132 and lactacystin, suggesting enhanced p53 degradation in the presence of dicoumarol.	Dicumarol	136-146	P53	Homo sapiens	101-104
11158615-7	2001	Dicoumarol-induced degradation of p53 also was prevented in the presence of simian virus 40 large T antigen, which is known to bind and to stabilize p53.	Dicumarol	0-10	P53	Homo sapiens	34-37
11158615-7	2001	Dicoumarol-induced degradation of p53 also was prevented in the presence of simian virus 40 large T antigen, which is known to bind and to stabilize p53.	Dicumarol	0-10	P53	Homo sapiens	149-152
11158615-8	2001	Cells overexpressing NQO1 were resistant to dicoumarol, and this finding indicates the direct involvement of NQO1 in p53 stabilization.	Dicumarol	44-54	P53	Homo sapiens	117-120
11158615-10	2001	Dicoumarol also reduced the level of p53 in its mutant form in M1 cells.	Dicumarol	0-10	P53	Homo sapiens	37-40
11013253-4	2001	Furthermore, the levels of p202 also decrease after exposure of cells to ultra violet light, which correlate with increase in the levels of p53.	ultra violet	73-85	P53	Homo sapiens	140-143
11244509-6	2001	p53 phosphorylation also varied in a MTI-dependent manner, as Taxol and Vincristine induced more p53 phospho-forms than nocodazole.	Vincristine	72-83	P53	Homo sapiens	0-3
11244509-6	2001	p53 phosphorylation also varied in a MTI-dependent manner, as Taxol and Vincristine induced more p53 phospho-forms than nocodazole.	Vincristine	72-83	P53	Homo sapiens	97-100
11260862-8	2001	Indomethacin reduces the proliferation rate and induces apoptosis in CaCo-2 colon cancer cells through enhanced expression of c-myc, p53, and p27 proteins.	Indomethacin	0-12	P53	Homo sapiens	133-136
11108661-3	2000	When a tetracycline-regulatable dominant-negative c-jun (TAM67, having a truncated transactivation domain) was expressed in tumorigenic human keratinocytes, AP-1- and NFkappaB- but not p53-dependent reporter activity was inhibited by 40-60%.	Tetracycline	7-19	P53	Homo sapiens	185-188
11101222-0	2000	Assignment of 1H(N), 15N, 13C(alpha), 13CO and 13C(beta) resonances in a 67 kDa p53 dimer using 4D-TROSY NMR spectroscopy.	13c	26-29	P53	Homo sapiens	80-83
11101222-0	2000	Assignment of 1H(N), 15N, 13C(alpha), 13CO and 13C(beta) resonances in a 67 kDa p53 dimer using 4D-TROSY NMR spectroscopy.	13c	38-41	P53	Homo sapiens	80-83
11195849-0	2000	The phototumorigenic fluoroquinolone, lomefloxacin, photosensitises p53 accumulation and transcriptional activity in human skin cells.	lomefloxacin	38-50	P53	Homo sapiens	68-71
11195849-4	2000	Western blots revealed that lomefloxacin photosensitised the stabilisation of p53 protein in human fibroblasts.	lomefloxacin	28-40	P53	Homo sapiens	78-81
11195849-5	2000	Lomefloxacin also photosensitised p53 transcriptional activity in amelanotic melanoma cells expressing wild-type p53 and stably transfected with a construct containing a beta-galactosidase reporter gene downstream from a p53 consensus binding sequence.	lomefloxacin	0-12	P53	Homo sapiens	34-37
11195849-5	2000	Lomefloxacin also photosensitised p53 transcriptional activity in amelanotic melanoma cells expressing wild-type p53 and stably transfected with a construct containing a beta-galactosidase reporter gene downstream from a p53 consensus binding sequence.	lomefloxacin	0-12	P53	Homo sapiens	113-116
11195849-5	2000	Lomefloxacin also photosensitised p53 transcriptional activity in amelanotic melanoma cells expressing wild-type p53 and stably transfected with a construct containing a beta-galactosidase reporter gene downstream from a p53 consensus binding sequence.	lomefloxacin	0-12	P53	Homo sapiens	113-116
11195849-7	2000	Interestingly, p21CIP1/WAFI protein was upregulated by lomefloxacin in the dark by a p53-independent mechanism.	lomefloxacin	55-67	P53	Homo sapiens	85-88
11127705-0	2000	Distributions of p53 codon 72 polymorphism in bladder cancer--proline form is prominent in invasive tumor.	Proline	62-69	P53	Homo sapiens	17-20
11048643-0	2000	Effects of allyl sulfur compounds and garlic extract on the expression of Bcl-2, Bax, and p53 in non small cell lung cancer cell lines.	Sulfur	17-23	P53	Homo sapiens	90-93
11072671-2	2000	In invasive cervical cancer, the arginine form of the p53 gene is estimated to be more susceptible to degradation mediated by tumour-associated human papilloma viruses (HPV) than the proline form.	Proline	183-190	P53	Homo sapiens	54-57
10951577-8	2000	Rotenone, an inhibitor of mitochondrial complex I, and 4,4"-diisothiocyanato-stilbene-2,2"-disulfonate, a mitochondrial anion channel inhibitor, also abolished the increase in ROS signal and p53 levels during hypoxia.	Rotenone	0-8	P53	Homo sapiens	191-194
11100817-7	2000	Upon treatment with retinoic acid (RA) and dibutyryl cyclic AMP (dbcAMP), overall GSP staining were increased concomitant with suppression of nuclear m-p53.	Bucladesine	43-63	P53	Homo sapiens	152-155
11100817-7	2000	Upon treatment with retinoic acid (RA) and dibutyryl cyclic AMP (dbcAMP), overall GSP staining were increased concomitant with suppression of nuclear m-p53.	Bucladesine	65-71	P53	Homo sapiens	152-155
10900468-5	2000	In addition, by using western blotting, we found that p53 protein levels increased fourfold to sixfold after exposure to sodium chromate.	sodium chromate(VI)	121-136	P53	Homo sapiens	54-57
10900468-8	2000	The necessity of p53 for chromium-induced apoptosis was examined in two ways.	Chromium	25-33	P53	Homo sapiens	17-20
10900468-10	2000	These studies showed that chromium-induced apoptosis was p53 dependent.	Chromium	26-34	P53	Homo sapiens	57-60
10762623-0	2000	Induction of apoptosis by hexamethylene bisacetamide is p53-dependent associated with telomerase activity but not with terminal differentiation.	hexamethylene bisacetamide	26-52	P53	Homo sapiens	56-59
10762623-2	2000	We found that hexamethylene bisacetamide (HMBA) induced apoptosis in human colon carcinoma LoVo cells harbouring wild-type p53 but not in SW1116 cells harbouring mutant p53.	hexamethylene bisacetamide	14-40	P53	Homo sapiens	123-126
10762623-2	2000	We found that hexamethylene bisacetamide (HMBA) induced apoptosis in human colon carcinoma LoVo cells harbouring wild-type p53 but not in SW1116 cells harbouring mutant p53.	hexamethylene bisacetamide	42-46	P53	Homo sapiens	123-126
10762623-4	2000	Taken together, our results suggest that HMBA can induce apoptosis via a p53-dependent pathway, but apoptosis and terminal differentiation may be separately regulated in LoVo cells.	hexamethylene bisacetamide	41-45	P53	Homo sapiens	73-76
10757806-5	2000	Although normal cells and wild-type p53-expressing tumor cells showed similar responses to actinomycin D and camptothecin treatment, the transcriptional activity of stabilized p53 induced by deferoxamine mesylate, which mimics hypoxia, in normal cells was lost in all three tumor cell lines tested.	Dactinomycin	91-104	P53	Homo sapiens	36-39
10802655-3	2000	The binding of such mutants is influenced by whether TP53 (encoding p53) codon 72, by virtue of a common polymorphism in the human population, encodes Arg or Pro.	Proline	158-161	P53	Homo sapiens	53-57
10802655-3	2000	The binding of such mutants is influenced by whether TP53 (encoding p53) codon 72, by virtue of a common polymorphism in the human population, encodes Arg or Pro.	Proline	158-161	P53	Homo sapiens	68-71
10788560-7	2000	P53 levels increased 4- to 6-fold in chromium-treated cells.	Chromium	37-45	P53	Homo sapiens	0-3
10738214-4	2000	Phenol-chloroform-extracted DNA specimens were employed for the detection of HBV infection and p53 gene mutations.	Chloroform	7-17	P53	Homo sapiens	95-98
10777217-0	2000	Tumor-derived mutations within the DNA-binding domain of p53 that phenotypically resemble the deletion of the proline-rich domain.	Proline	110-117	P53	Homo sapiens	57-60
10717525-2	2000	The GML gene (glycosylphosphatidylinositol-anchored molecule-like protein gene) is a novel gene specifically induced by wild-type p53, which may participate in cell cycle control or the cell apoptotic pathway.	Glycosylphosphatidylinositols	14-42	P53	Homo sapiens	130-133
10682666-9	2000	Our study suggests that immunohistochemical expression of p53 and TS could assist the clinician in predicting response of colorectal cancer patients to modulated MTX-5-FU therapy.	mtx-5-fu	162-170	P53	Homo sapiens	58-61
10673501-0	2000	The human homologs of checkpoint kinases Chk1 and Cds1 (Chk2) phosphorylate p53 at multiple DNA damage-inducible sites.	cds1	50-54	P53	Homo sapiens	76-79
10673501-8	2000	The human homolog of the second S. pombe checkpoint kinase, Cds1 (CHK2/hCds1), phosphorylates tetrameric p53 but not monomeric p53 in vitro at sites similar to those phosphorylated by hCHK1 kinase, suggesting that both checkpoint kinases can play roles in regulating p53 after DNA damage.	cds1	60-64	P53	Homo sapiens	105-108
10673501-8	2000	The human homolog of the second S. pombe checkpoint kinase, Cds1 (CHK2/hCds1), phosphorylates tetrameric p53 but not monomeric p53 in vitro at sites similar to those phosphorylated by hCHK1 kinase, suggesting that both checkpoint kinases can play roles in regulating p53 after DNA damage.	cds1	60-64	P53	Homo sapiens	127-130
10673501-8	2000	The human homolog of the second S. pombe checkpoint kinase, Cds1 (CHK2/hCds1), phosphorylates tetrameric p53 but not monomeric p53 in vitro at sites similar to those phosphorylated by hCHK1 kinase, suggesting that both checkpoint kinases can play roles in regulating p53 after DNA damage.	cds1	60-64	P53	Homo sapiens	127-130
10754986-4	2000	ras and p53 oncoprotein expression was analyzed by an automated biotin-avidin immunoproxidase technique.	Biotin	64-70	P53	Homo sapiens	8-11
10801075-3	2000	The data obtained demonstrate that the growth factor activity of PAs is associated with: - a rapid transient activation of early response genes, c-fos, c-jun and c-myc; - the subsequent coordinated down-regulation of p53 and p21CIP1; - the constant expression of the MEK1 mRNA in every phase of the cell cycle.	Protactinium	65-68	P53	Homo sapiens	217-220
22607421-7	2000	Compared to the intrinsic zinc strongly bound to Cys 176, Cys 238, Cys 242 and His 179 in the p53 core domain, binding of additional Zn(2+) to p53 was much weaker as shown by an easy removal of the latter ions by low concentrations of EDTA.	Edetic Acid	235-239	P53	Homo sapiens	143-146
11173660-4	2000	Protein p53 accumulation was detected by the streptavidin-biotin method using DO-7 (Dako) antibody.	Biotin	58-64	P53	Homo sapiens	8-11
10602521-6	1999	In contrast, human p53 is not a substrate for recombinant MAP kinase nor are there any detectable levels of protein kinase activity in stimulated human cell extracts which phosphorylate the proline rich domain of human p53 in vitro.	Proline	190-197	P53	Homo sapiens	219-222
10574967-7	1999	Docking of the computed low energy conformations for the C-terminal peptide with those for a recently defined proline-rich regulatory region from the N-terminal domain of p53 suggests a unique low energy complex between the two peptide domains.	Proline	110-117	P53	Homo sapiens	171-174
10574974-6	1999	p53 is activated by Cr(VI), mostly by ROS-mediated free radical reactions.	Chromium	20-22	P53	Homo sapiens	0-3
10632350-2	1999	Overexpression of the p53 protein was present in 49% of the samples studied with CM1, 18% with PAb1801, 30% with DO7, and 44% with DO7.	pab1801	95-102	P53	Homo sapiens	22-25
10647890-2	1999	A common p53 polymorphism at codon-72 of exon 4 results in translation to either arginine or proline.	Proline	93-100	P53	Homo sapiens	9-12
10597302-6	1999	In contrast, conditional expression of wild-type p53 failed to modify SAHA actions, but markedly potentiated HMBA-induced apoptosis.	hexamethylene bisacetamide	109-113	P53	Homo sapiens	49-52
10523638-2	1999	We now show, for the first time, that the interaction of p53 with DNA can be stabilized by small molecules, such as ADP and dADP.	Dapsone	124-128	P53	Homo sapiens	57-60
10531375-4	1999	Cadmium at 10-30 microM impairs the p53 induction in response to DNA-damaging agents such as actinomycin D, methylmethane sulfonate, and hydrogen peroxide.	Dactinomycin	93-106	P53	Homo sapiens	36-39
10403534-11	1999	It can be concluded that wild-type p53 and/or up-regulation of c-myc is associated with indomethacin-mediated differential apoptosis in gastric epithelial cells.	Indomethacin	88-100	P53	Homo sapiens	35-38
10334204-0	1999	The level of DNA modification by (+)-syn-(11S,12R,13S,14R)- and (-)-anti-(11R,12S,13S,14R)-dihydrodiol epoxides of dibenzo[a,l]pyrene determined the effect on the proteins p53 and p21WAF1 in the human mammary carcinoma cell line MCF-7.	(+)-syn-(11s,12r,13s,14r)	33-58	P53	Homo sapiens	172-175
10218673-5	1999	P53 and Ki-67 immunoreactivity correlated significantly with the histopathologic stage of KS (r=0.63, p=0.0001; r=0.42, p=0.0084, respectively).	Potassium	90-92	P53	Homo sapiens	0-3
10218673-10	1999	The expression of p53 and Ki-67 was significantly lower in iatrogenic cases than in the classic cases (p=0.009, p=0.0014, respectively), although no statistical difference was found between the histopathologic stages in the two clinical forms of KS.	Potassium	246-248	P53	Homo sapiens	18-21
10405637-5	1999	Complete remission (CR) was observed in 9 of the 17 patients (53%) with mutated forms of p53 and 18 of the 35 patients (51%) with wild-type p53 genes.	Chromium	20-22	P53	Homo sapiens	89-92
10099829-3	1999	In contrast, UV light or actinomycin D induced a modest G1 arrest that was p53-dependent only at lower doses.	Dactinomycin	25-38	P53	Homo sapiens	75-78
10196666-6	1999	The 8-oxo-G gives rise predominantly to G to T transversions, the type of mutations found in ras or p53 gene from IR-induced tumors.	8-oxo-	4-10	P53	Homo sapiens	100-103
9891091-7	1999	Treatment of RKO cells with a tetracycline derivative, doxycycline, resulted in 15-fold-induced expression of TS protein and nearly complete suppression of p53 protein expression.	Tetracycline	30-42	P53	Homo sapiens	156-159
10078201-0	1999	RB regulates the stability and the apoptotic function of p53 via MDM2.	Rubidium	0-2	P53	Homo sapiens	57-60
10078201-1	1999	The binding of RB to MDM2 is shown to be essential for RB to overcome both the antiapoptotic function of MDM2 and the MDM2-dependent degradation of p53.	Rubidium	15-17	P53	Homo sapiens	148-151
10078201-1	1999	The binding of RB to MDM2 is shown to be essential for RB to overcome both the antiapoptotic function of MDM2 and the MDM2-dependent degradation of p53.	Rubidium	55-57	P53	Homo sapiens	148-151
9989808-3	1999	Here we report on the correlation between inhibition of mRNA synthesis and the induction of p53, p21WAF1 and apoptosis in diploid human fibroblasts treated with either UV light, cisplatin or the RNA synthesis inhibitors actinomycin D, DRB, H7 and alpha-amanitin.	Dactinomycin	220-233	P53	Homo sapiens	92-95
9927213-4	1999	This hybrid protein binds to p53 and can interact with a synthetic promoter containing tetracycline-operator sequences.	Tetracycline	87-99	P53	Homo sapiens	29-32
9888876-9	1999	ANP, NOR3, and 8-bromo-cGMP caused marked accumulations of the tumor suppressor gene product p53 but not of bcl-2, as determined by Western blot analysis.	FK 409	5-9	P53	Homo sapiens	93-96
10029405-2	1999	In this study, we showed that the p53 response to a chemotherapeutic drug, actinomycin D, was reversible in both normal and tumor cells, even when a substantial proportion of tumor cells were undergoing apoptosis.	Dactinomycin	75-88	P53	Homo sapiens	34-37
10029405-3	1999	Despite the clear reversibility of the p53-induced cell-cycle arrest after removal of actinomycin D, a substantial proportion of the cells arrested in G2 failed to resume normal cell-cycle progression and underwent another round of DNA synthesis.	Dactinomycin	86-99	P53	Homo sapiens	39-42
10757447-6	1999	Up to 12 h after 1 mM SB treatment, p53 and Bcl-2 expressions were similar to control levels, then gradually decreased to very low levels at 5 days.	Butyric Acid	22-24	P53	Homo sapiens	36-39
10757447-9	1999	SB-induced modulation of p53 and Bcl-2 expression may have implications for controlling Rb growth, particularly in combination with chemotherapy drugs, which are increasingly used in the treatment of Rb.	Butyric Acid	0-2	P53	Homo sapiens	25-28
9879988-7	1998	Moreover, 3AB but not its analog inhibited irradiation-induced activation of sequence-specific DNA binding of wtp53 as detected using 32P-labeled or biotin-labeled p53 consensus sequence (p53CON).	Biotin	149-155	P53	Homo sapiens	112-115
9879988-8	1998	However, immunoblotting with an anti-poly(ADP-ribose) antibody showed that p53 proteins of the p53CON-bound fraction did not contain poly(ADP-ribose) (PAR).	Poly Adenosine Diphosphate Ribose	37-53	P53	Homo sapiens	75-78
9879988-8	1998	However, immunoblotting with an anti-poly(ADP-ribose) antibody showed that p53 proteins of the p53CON-bound fraction did not contain poly(ADP-ribose) (PAR).	Poly Adenosine Diphosphate Ribose	37-53	P53	Homo sapiens	95-98
9769362-12	1998	Cr-induced DNA-DNA interstrand crosslinks (DDC), the tumor suppressor gene p53 and oxidative processes are some of the major factors that may play a significant role in determining the cellular outcome in response to Cr exposure.	Chromium	217-219	P53	Homo sapiens	75-78
9786962-4	1998	If FAK or the correct ECM is absent, cells enter apoptosis through a p53-dependent pathway activated by protein kinase C lambda/iota and cytosolic phospholipase A2.	iota	128-132	P53	Homo sapiens	69-72
9770348-13	1998	Although inhibitors of transcription, such as actinomycin D, also damage DNA, reduction of Mdm-2 or other putative "sensor" proteins may contribute to their p53-stabilizing activity.	Dactinomycin	46-59	P53	Homo sapiens	157-160
9766676-7	1998	Moreover, analysis of a tetracycline-regulated p53-inducible system in null-p53 cell lines showed that RTP/rit42 mRNA expression increased concomitantly with p53 expression and followed a similar time course.	Tetracycline	24-36	P53	Homo sapiens	47-50
9766676-7	1998	Moreover, analysis of a tetracycline-regulated p53-inducible system in null-p53 cell lines showed that RTP/rit42 mRNA expression increased concomitantly with p53 expression and followed a similar time course.	Tetracycline	24-36	P53	Homo sapiens	76-79
9766676-7	1998	Moreover, analysis of a tetracycline-regulated p53-inducible system in null-p53 cell lines showed that RTP/rit42 mRNA expression increased concomitantly with p53 expression and followed a similar time course.	Tetracycline	24-36	P53	Homo sapiens	76-79
30650922-3	1998	p53 expression was examined by im-munohistochemical staining using the streptavidin-biotin method.	Biotin	84-90	P53	Homo sapiens	0-3
9742979-1	1998	BACKGROUND: A polymorphism at codon 72 of the human tumour-suppressor gene, p53, results in translation to either arginine or proline.	Proline	126-133	P53	Homo sapiens	76-79
9707426-0	1998	The requirement for the p53 proline-rich functional domain for mediation of apoptosis is correlated with specific PIG3 gene transactivation and with transcriptional repression.	Proline	28-35	P53	Homo sapiens	24-27
9707426-2	1998	The human p53 proline-rich domain localized between amino acids 64 and 92 has been reported to be necessary for efficient growth suppression.	Proline	14-21	P53	Homo sapiens	10-13
9664074-5	1998	We found that treatment of Molt-4 cells with low concentrations of actinomycin D or gamma-irradiation, which activate p53-dependent apoptosis, induces apoptosis only in cells expressing normal levels of p53.	Dactinomycin	67-80	P53	Homo sapiens	118-121
9664074-5	1998	We found that treatment of Molt-4 cells with low concentrations of actinomycin D or gamma-irradiation, which activate p53-dependent apoptosis, induces apoptosis only in cells expressing normal levels of p53.	Dactinomycin	67-80	P53	Homo sapiens	203-206
11189516-4	1998	The expression rates of MDM2 and p53 gene proteins were 71.7% and 21.7% respectively in 46 AL patients.	Aluminum	91-93	P53	Homo sapiens	33-36
9635521-5	1998	Mutant p53 was immunohistochemically stained using the monoclonal antibody PAb1801.	pab1801	75-82	P53	Homo sapiens	7-10
9626359-8	1998	These results suggest that SB induces cellular differentiation and suppresses growth and tumorigenicity of HCC cells in vitro and in viva by a mechanism independent of p53 but possibly dependent on p21.	Butyric Acid	27-29	P53	Homo sapiens	168-171
9581865-5	1998	Not only murine but also human mutant p53 proteins carrying the mutational hot spot amino acid exchanges 175Arg--&gt;His, 273Arg--&gt;Pro, or 273Arg--&gt;His bound to the Xbal-IgE-MAR-DNA fragment.	Proline	134-137	P53	Homo sapiens	38-41
9575175-6	1998	Employing a stable cell line derived from p53-deficient human fibroblast that contains tetracycline-regulated transactivator and operator plasmids to control the expression of wild-type p53 (TR9-7 cells), we then show that the induction of p21(WAF1/Cip1), which occurs in response to the inhibition of PP5 expression, requires the p53 protein.	Tetracycline	87-99	P53	Homo sapiens	186-189
9575175-6	1998	Employing a stable cell line derived from p53-deficient human fibroblast that contains tetracycline-regulated transactivator and operator plasmids to control the expression of wild-type p53 (TR9-7 cells), we then show that the induction of p21(WAF1/Cip1), which occurs in response to the inhibition of PP5 expression, requires the p53 protein.	Tetracycline	87-99	P53	Homo sapiens	186-189
9677462-5	1998	Molecular analysis of the same specimen showed mutations of the p53 gene in 13.3% of OLs and 9, 6% of OSCCs.	osccs	102-107	P53	Homo sapiens	64-67
9610789-5	1998	The p53 mutation spectrum of these cyclophosphamide-associated bladder cancers differed significantly from patterns reported for sporadic (P = 0.020), smoking-related (0.043), and schistosomiasis-linked (P = 0.002) tumors but not arylamine-associated neoplasms (P = 0.860).	aniline	230-239	P53	Homo sapiens	4-7
9581676-6	1998	Sodium butyrate decreased p53 expression and increased p21WAF-1 expression in HCC-T and HCC-M cells having the wild-type p53 gene.	Butyric Acid	0-15	P53	Homo sapiens	26-29
9581676-6	1998	Sodium butyrate decreased p53 expression and increased p21WAF-1 expression in HCC-T and HCC-M cells having the wild-type p53 gene.	Butyric Acid	0-15	P53	Homo sapiens	121-124
9548807-7	1998	Wild type p53 induction by AZQ was suppressed when DT-diaphorase activity was inhibited by pretreating the cells with dicumarol.	Dicumarol	118-127	P53	Homo sapiens	10-13
9499413-0	1998	Metaphase fragility of the human RNU1 and RNU2 loci is induced by actinomycin D through a p53-dependent pathway.	Dactinomycin	66-79	P53	Homo sapiens	90-93
9499413-4	1998	Remarkably, we now find that very low doses of actinomycin D (5-50 ng/ml) can phenocopy Ad12 infection: metaphase fragility of the RNU1 and RNU2 loci is induced specifically in the absence of virus, and induction also requires U2 promoter elements and p53 function.	Dactinomycin	47-60	P53	Homo sapiens	252-255
9499413-6	1998	We propose that Ad12 infection, actinomycin D and araC all induce a similar or identical global damage arrest signal (perhaps a modification or altered conformation of p53) that preferentially interferes with metaphase condensation of the RNU1 and RNU2 loci.	Dactinomycin	32-45	P53	Homo sapiens	168-171
9568133-4	1998	p53 Protein expression was investigated immunocytochemically using the monoclonal antibody pAb1801.	pab1801	91-98	P53	Homo sapiens	0-3
9488478-6	1998	Immunofluorescence analysis showed that expression of the p53-inducible cyclin/kinase inhibitor p21sdi1/WAF1 was greatly diminished by targeting p53 with either PAb1801 or DO-1 but remained high and, moreover, still p53 dependent in cells expressing SV40 T antigen.	pab1801	161-168	P53	Homo sapiens	58-61
9488478-6	1998	Immunofluorescence analysis showed that expression of the p53-inducible cyclin/kinase inhibitor p21sdi1/WAF1 was greatly diminished by targeting p53 with either PAb1801 or DO-1 but remained high and, moreover, still p53 dependent in cells expressing SV40 T antigen.	pab1801	161-168	P53	Homo sapiens	145-148
9488478-6	1998	Immunofluorescence analysis showed that expression of the p53-inducible cyclin/kinase inhibitor p21sdi1/WAF1 was greatly diminished by targeting p53 with either PAb1801 or DO-1 but remained high and, moreover, still p53 dependent in cells expressing SV40 T antigen.	pab1801	161-168	P53	Homo sapiens	145-148
14646501-0	1998	Crocidolite asbestos causes an induction of p53 and apoptosis in cultured A-549 lung carcinoma cells.	Asbestos, Crocidolite	0-11	P53	Homo sapiens	44-47
14646501-4	1998	We have studied the p53 response to the exposure of crocidolite asbestos in A-549 lung carcinoma cells using three different methods, i.e., p53 immunohistochemistry, Western blotting and metabolic labelling followed by p53 immunoprecipitation.	Asbestos, Crocidolite	52-72	P53	Homo sapiens	20-23
14646501-5	1998	With these techniques we demonstrate a dose-dependent p53 nuclear response to crocidolite exposure.	Asbestos, Crocidolite	78-89	P53	Homo sapiens	54-57
14646501-8	1998	Our data support the idea that increased apoptotic activity, induced by crocidolite, is mediated by p53.	Asbestos, Crocidolite	72-83	P53	Homo sapiens	100-103
9398049-4	1997	Levels of p53 protein and mRNA were measured in adherent cells which had been incubated with growth-inhibitory concentrations of sodium butyrate (a by-product of dietary fibre fermentation) or sodium deoxycholate (a bile acid) for up to 48 hr.	Butyric Acid	129-144	P53	Homo sapiens	10-13
9570369-4	1997	In wt-p53 transfected cells, the expression of MDRI gene was significantly increased, accumulation of adriamycin (ADM) was decreased, and the sensitivity to vincristine (VCR), ADM and 5-fluorouracil (5-FU) was increased compared with the parent KBv200 cells.	Vincristine	157-168	P53	Homo sapiens	6-9
9315628-8	1997	In contrast, 1,10-orthophenanthroline, a cell-permeable chelator of Cu2+, promoted the redox activity of copper and up-regulated p53 DNA-binding activity through a DNA damage-dependent pathway.	cupric ion	68-72	P53	Homo sapiens	129-132
10374339-6	1997	The densities of cells positive for proliferating cell nuclear antigen and Ki-67 antigen staining in tumor groups were higher than that in CBT group and were elevated with the malignant degree and the level of p53 protein expression of the tumors.	N,N-BIS(4-CHLOROBENZYL)-1H-1,2,3,4-TETRAAZOL-5-AMINE	139-142	P53	Homo sapiens	210-213
10374339-7	1997	On the contrary, the density of apoptotic cell in tumor groups was lower than that in CBT group, reducing in accord with the increase of malignancy and the level of p53 protein expression of the tumors.	N,N-BIS(4-CHLOROBENZYL)-1H-1,2,3,4-TETRAAZOL-5-AMINE	86-89	P53	Homo sapiens	165-168
9192816-1	1997	The frequency of oxidative base damage along the human p53 and PGK1 genes was determined at nucleotide resolution by cleaving DNA at oxidized bases with endonuclease III and formamidopyrimidine DNA glycosylase and then using the ligation-mediated PCR technique to map induced break frequency.	formamidopyrimidine	174-193	P53	Homo sapiens	55-58
9150394-0	1997	Role of p21Waf1/Cip1/Sdi1 in cell death and DNA repair as studied using a tetracycline-inducible system in p53-deficient cells.	Tetracycline	74-86	P53	Homo sapiens	107-110
9136984-1	1997	Human p53 was expressed in E. coli, purified, labeled with fluorescein iodoacetamide (IAF) and characterized for sequence-specific DNA binding and epitope disposition.	5-iodoacetamidofluorescein	59-84	P53	Homo sapiens	6-9
9018125-0	1997	Induction of apoptosis in human lung cancer cells after wild-type p53 activation by methoxyestradiol.	Methoxyestradiol	84-100	P53	Homo sapiens	66-69
9307845-1	1997	We analyzed the survival of 89 surgically treated patients presenting non-small-cell lung cancer in regard to the accumulation of p53 protein as detected by indirect immunoperoxidase reactivity of PAb1801 anti-human p53 protein.	pab1801	197-204	P53	Homo sapiens	130-133
8954979-4	1996	We also observed that induction of p53 expression by actinomycin D treatment was weaker in the NS3DeltaC-expressing cells than in the control cells.	Dactinomycin	53-66	P53	Homo sapiens	35-38
8986812-4	1996	This region of the human p53 protein is localized between amino acids 61 and 94 (out of 393) and is noteworthy in that it contains five repeats of the sequence PXXP (where P represents proline and X any amino acid).	Proline	185-192	P53	Homo sapiens	25-28
3207512-3	1988	Moreover, we obtained some evidence that the processing of the HTLV-III precursor protein p53 to p24 is inhibited by Avarol in infected cells, suggesting that the compound interferes with the expression of the viral protease gene.	avarol	117-123	P53	Homo sapiens	90-93
8986812-6	1996	A p53 cDNA deletion mutant (delta pro AE), which lacks this entire proline-rich domain (deleted for amino acids 62-91), was created and characterized for a variety of p53 functions.	Proline	67-74	P53	Homo sapiens	2-5
8986812-12	1996	These data indicate that, in addition to the transcriptional activation domain, the p53 proline-rich domain plays a critical role in the transmission of antiproliferative signals down-stream of the p53 protein and may link p53 to a direct signal transduction pathway.	Proline	88-95	P53	Homo sapiens	84-87
33963002-0	2021	Clinical Outcomes in Patients with Multi-Hit TP53 Chronic Lymphocytic Leukemia Treated with Ibrutinib.	ibrutinib	92-101	P53	Homo sapiens	45-49
33845261-7	2021	Furthermore, the protein expression of P53, CASPASE 8 (Cleaved/Pro), CASPASE 9 (Cleaved/Pro) and CASPASE 3 (Cleaved/Pro) in granulosa cells of mice treated with spermidine were significantly upregulated, while BCL2 expression was significantly downregulated.	Spermidine	161-171	P53	Homo sapiens	39-42
33963002-10	2021	Conclusions: In this study, single-hit TP53 defines a distinct subgroup of patients with an excellent long-term response to single-agent ibrutinib, while multi-hit TP53 is independently associated with shorter PFS.	ibrutinib	137-146	P53	Homo sapiens	39-43
34035828-10	2021	The molecular docking results showed that quercetin, formononetin, kaempferol, isorhamnetin, beta-sitosterol had a good binding activity with VEGFA, IL6, TNF, AKT1, and TP53.	gamma-sitosterol	93-108	P53	Homo sapiens	169-173
8986812-12	1996	These data indicate that, in addition to the transcriptional activation domain, the p53 proline-rich domain plays a critical role in the transmission of antiproliferative signals down-stream of the p53 protein and may link p53 to a direct signal transduction pathway.	Proline	88-95	P53	Homo sapiens	198-201
34044759-0	2021	miR-29a sensitizes the response of glioma cells to temozolomide by modulating the P53/MDM2 feedback loop.	Temozolomide	51-63	P53	Homo sapiens	82-85
8986812-12	1996	These data indicate that, in addition to the transcriptional activation domain, the p53 proline-rich domain plays a critical role in the transmission of antiproliferative signals down-stream of the p53 protein and may link p53 to a direct signal transduction pathway.	Proline	88-95	P53	Homo sapiens	198-201
34044759-8	2021	Moreover, miR-29a regulating p53/MDM2 signaling sensitized the response of glioma cells to temozolomide treatment.	Temozolomide	91-103	P53	Homo sapiens	29-32
33996626-0	2021	Doxycycline Induces Apoptosis of Brucella Suis S2 Strain-Infected HMC3 Microglial Cells by Activating Calreticulin-Dependent JNK/p53 Signaling Pathway.	Doxycycline	0-11	P53	Homo sapiens	129-132
8900110-3	1996	Ara-C treatment of cells that express wild type or a dominant negative, kinase-inactive c-Abl(K-R) was associated with formation of c-Abl-p53 complexes and increased expression of the cyclin-dependent kinase (Cdk) inhibitor p21.	Krypton	94-97	P53	Homo sapiens	138-141
33996626-11	2021	Our results confirm that Dox induces JNK/p53-dependent apoptosis in B. suis S2-infected HMC3 cells through inhibition of CALR protein expression.	Doxycycline	25-28	P53	Homo sapiens	41-44
33618250-8	2021	In addition, the expression levels of p53 are dramatically changed by higenamine in an LSD1-dependent manner in MV4-11 cells.	higenamine	70-80	P53	Homo sapiens	38-41
34047071-0	2021	Targeting the S100A2-p53 interactions with a series of novel 3,5-bistrifluoromethylbenzene sulfonamides: Synthesis and cytotoxicity.	3,5-bistrifluoromethylbenzene sulfonamides	61-103	P53	Homo sapiens	21-24
8797888-5	1996	MKN-28 was an exception; it contained mutated p53, and expressed mRNAs for p21, CDK2 and G1 cyclins at high levels.	mkn-28	0-6	P53	Homo sapiens	46-49
34020277-6	2021	Western blot analysis of the levels of p-STAT3, p-ERK, PARP, p53 and cleaved caspase-3 revealed p-ERK1/2 and p-STA3 were drastically decreased in BT-20 cells under 25a incubation, suggesting the involvement of these two kinases in the mechanisms underlying 25a-induced cell cycle arrest, besides loss of proliferation and viability of the breast cancer cell.	CHEMBL414948	164-167	P53	Homo sapiens	61-64
33325610-9	2021	Co-administration of the ROS inhibitor NAC largely abolished the up-regulated p53 protein level, and rescued the suppressed viability and colony formation ability in butein-exposed U-2 OS cells.	nac	39-42	P53	Homo sapiens	78-81
33509905-6	2021	Several PI3K or AKT inhibitors were among the top drug combinations identified and subsequent work showed CPI0610 synergized with alpelisib or MK2206 by inducing p53-independent apoptosis.	CPI-0610	106-113	P53	Homo sapiens	162-165
33509905-6	2021	Several PI3K or AKT inhibitors were among the top drug combinations identified and subsequent work showed CPI0610 synergized with alpelisib or MK2206 by inducing p53-independent apoptosis.	MK 2206	143-149	P53	Homo sapiens	162-165
33952867-2	2021	We previously showed that non-naturally occurring, stable helical trimers of bicyclic beta-amino acids (Abh) with all-trans amide bonds can block the p53-MDM2/MDMX alpha-helix-helix interaction, which plays a role in regulating p53 function.	Amides	124-129	P53	Homo sapiens	150-153
8797205-1	1996	Evaluation of the p53 gene protein expression and proliferative potential with MIB-1 monoclonal antibody (MBL Co.), a new marker of cellular proliferation that binds Ki67 in paraffin sections, by immunohistochemical studies were made in 10 cases of the non-recurrent meningiomas and the 8 cases (17 samples) of the recurrent meningiomas.	ki67	166-170	P53	Homo sapiens	18-21
33733756-3	2021	Herein, we report irreversible inhibitors of the human double minute 2 (HDM2)/p53 PPI, which employ a reactive N-acyl-N-alkyl sulfonamide (NASA) group as a warhead.	nasa	139-143	P53	Homo sapiens	78-81
33071125-0	2021	Changes in miR-222 expression, DNA repair capacity, and MDM2-p53 axis in association with low-dose benzene genotoxicity and hematotoxicity.	Benzene	99-106	P53	Homo sapiens	61-64
33713860-4	2021	NC loaded with omega 3 polyunsaturated fatty acid (NC-EPA:DHA 6:1) were more effective than native EPA:DHA 6:1 to prevent Ang II-induced VCAM-1 and p53 upregulation, and SA-beta- galactosidase activity in coronary artery segments.	nc-epa	51-57	P53	Homo sapiens	148-151
8809405-2	1996	To assess the biological significance of p53 inactivation in the development of SCLC, tetracycline (Tc)-inducible p53 expression plasmids were introduced into a SCLC cell line, N417, in which the p53 gene as well as the RB gene was inactivated.	Tetracycline	86-98	P53	Homo sapiens	114-117
33071125-5	2021	Subsequently, the observed activities in lymphocytes were verified using human HL-60 (p53 null) and TK6 (p53 wild-type) cells via 1,4-benzoquinone (1,4-BQ) treatment and miR-222 interferences.	quinone	130-146	P53	Homo sapiens	86-89
33071125-5	2021	Subsequently, the observed activities in lymphocytes were verified using human HL-60 (p53 null) and TK6 (p53 wild-type) cells via 1,4-benzoquinone (1,4-BQ) treatment and miR-222 interferences.	quinone	130-146	P53	Homo sapiens	105-108
33071125-5	2021	Subsequently, the observed activities in lymphocytes were verified using human HL-60 (p53 null) and TK6 (p53 wild-type) cells via 1,4-benzoquinone (1,4-BQ) treatment and miR-222 interferences.	quinone	148-154	P53	Homo sapiens	105-108
33071125-12	2021	In conclusion, our in vivo observations were confirmed by in vitro studies showing that BZ/1,4-BQ exposures caused genotoxicity and high expression of miR-222 which obstructed expression of the MDM2-p53 axis that led to failed activation of p53, abnormal DRC and serious biological consequences.	Benzene	88-90	P53	Homo sapiens	199-202
33071125-12	2021	In conclusion, our in vivo observations were confirmed by in vitro studies showing that BZ/1,4-BQ exposures caused genotoxicity and high expression of miR-222 which obstructed expression of the MDM2-p53 axis that led to failed activation of p53, abnormal DRC and serious biological consequences.	Benzene	88-90	P53	Homo sapiens	241-244
33071125-12	2021	In conclusion, our in vivo observations were confirmed by in vitro studies showing that BZ/1,4-BQ exposures caused genotoxicity and high expression of miR-222 which obstructed expression of the MDM2-p53 axis that led to failed activation of p53, abnormal DRC and serious biological consequences.	quinone	91-97	P53	Homo sapiens	199-202
33071125-12	2021	In conclusion, our in vivo observations were confirmed by in vitro studies showing that BZ/1,4-BQ exposures caused genotoxicity and high expression of miR-222 which obstructed expression of the MDM2-p53 axis that led to failed activation of p53, abnormal DRC and serious biological consequences.	quinone	91-97	P53	Homo sapiens	241-244
33648535-12	2021	Consistently, an increased nuclear accumulation of p53 was seen in all selinexor-treated models.	selinexor	71-80	P53	Homo sapiens	51-54
33649538-11	2021	Mutation of the SIM inhibits beta-arr2 nuclear import, its ability to delocalize Mdm2 from the nucleus to the cytoplasm and enhanced p53 signaling in lung and breast tumor cell lines.	sim	16-19	P53	Homo sapiens	133-136
8809405-2	1996	To assess the biological significance of p53 inactivation in the development of SCLC, tetracycline (Tc)-inducible p53 expression plasmids were introduced into a SCLC cell line, N417, in which the p53 gene as well as the RB gene was inactivated.	Tetracycline	86-98	P53	Homo sapiens	114-117
33326188-4	2021	Therefore, a CD44-targeted delivery system is designed and constructed by self-assembly of tyrosine (Tyr)-hyaluronic acid (HA)-polyethyleneimine (PEI), which can radiolabel 131/125 I and load a p53 mutant restoring regent, Prima-1.	-polyethyleneimine	126-144	P53	Homo sapiens	194-197
8809405-2	1996	To assess the biological significance of p53 inactivation in the development of SCLC, tetracycline (Tc)-inducible p53 expression plasmids were introduced into a SCLC cell line, N417, in which the p53 gene as well as the RB gene was inactivated.	Tetracycline	100-102	P53	Homo sapiens	114-117
33710861-9	2021	Furthermore, Olmesartan potently reversed the increased K382 acetylation of p53 and the downregulation of SIRT1.	olmesartan	13-23	P53	Homo sapiens	76-79
8809405-2	1996	To assess the biological significance of p53 inactivation in the development of SCLC, tetracycline (Tc)-inducible p53 expression plasmids were introduced into a SCLC cell line, N417, in which the p53 gene as well as the RB gene was inactivated.	Tetracycline	100-102	P53	Homo sapiens	114-117
33710861-10	2021	Moreover, we show that the effect of Olmesartan against cell senescence and deacetylation of p53 was abolished by inhibition of SIRT1, either by using nicotinamide or by transfection with SIRT1 siRNA.	olmesartan	37-47	P53	Homo sapiens	93-96
33710861-11	2021	In conclusion, Olmesartan prevents oligomerized Abeta-induced cellular senescence in neuronal cells by downregulating p16 and p21 through a SIRT1 dependent deacetylation of p53; our finding indicates that Olmesartan has a protective effect in Abeta-induced neurotoxicity.	olmesartan	15-25	P53	Homo sapiens	173-176
8809405-5	1996	Thus, wild-type p53-inducible clones were further established by transfection in the presence (repressed) of Tc.	Tetracycline	109-111	P53	Homo sapiens	16-19
8635153-5	1996	The expression of p53 protein was determined with the avidin-biotin complex-peroxidase staining procedure and CM-1 antiserum.	Biotin	61-67	P53	Homo sapiens	18-21
33918387-0	2021	Distinct Classes of Flavonoids and Epigallocatechin Gallate, Polyphenol Affects an Oncogenic Mutant p53 Protein, Cell Growth and Invasion in a TNBC Breast Cancer Cell Line.	Polyphenols	61-71	P53	Homo sapiens	100-103
32971485-5	2021	After the sandwich-type immunoassay with the free p53 protein, with the release of probe DAP after the electrochemical signal amplificated by PEDOT:PSS and AuNPs, the ultra-sensitive and quantitative determination of p53 protein was realized with working range of 1-120 ng mL-1 and low detection limit of 0.09 ng mL-1.	dap	89-92	P53	Homo sapiens	217-220
33075425-0	2021	A Novel cytarabine analog evokes synthetic lethality by targeting MK2 in p53-deficient cancer cells.	Cytarabine	8-18	P53	Homo sapiens	73-76
8649776-2	1996	By using recombination PCR in vitro mutagenesis, we introduced point mutations into the codon 273 of wild-type (wt) p53 (pC53-SN3) from Arg to His (pC53-273H [273H]), Asp (273D), Pro (273P), Lys (273K), Leu (273L) or Thr (273T), and compared their biological and biochemical activities with wt p53 and cancer-derived 175H, 248W and 273H/309S.	Proline	179-182	P53	Homo sapiens	116-119
33075425-2	2021	However, 2"-fluoro-4"-seleno-ara-C (F-Se-Ara-C), a new generation of cytarabine (Ara-C) analogs, exhibited potent antitumor activity against the p53-deficient prostate cancer cell line PC-3.	Cytarabine	69-79	P53	Homo sapiens	145-148
33075425-2	2021	However, 2"-fluoro-4"-seleno-ara-C (F-Se-Ara-C), a new generation of cytarabine (Ara-C) analogs, exhibited potent antitumor activity against the p53-deficient prostate cancer cell line PC-3.	Cytarabine	41-46	P53	Homo sapiens	145-148
9162298-3	1996	A germline polymorphism of p53 with a single-base change at codon 72 that causes an amino acid replacement of arginine (Arg; CGC) by proline (PRO; CCC) has also been reported to be associated with cancer susceptibility in a Japanese population.	Proline	133-140	P53	Homo sapiens	27-30
33320772-0	2021	Influence of common dietary supplements (curcumin, andrographolide, and d-limonene) on the radiobiological responses of p53-competent colonic cancer epithelial cells.	andrographolide	51-66	P53	Homo sapiens	120-123
33320772-1	2021	PURPOSE: The main goal of the research was to determine whether commercially available common dietary phytochemical supplements (curcumin, andrographolide, and d-limonene) have radiomodulatory effects on p53-competent human colonic epithelial cells.	andrographolide	139-154	P53	Homo sapiens	204-207
33541735-5	2021	METHODS: TP53 mutational status was determined and correlated with progression-free survival (PFS) and overall survival (OS) on GOG-86P.	gog-86p	128-135	P53	Homo sapiens	9-13
9162298-3	1996	A germline polymorphism of p53 with a single-base change at codon 72 that causes an amino acid replacement of arginine (Arg; CGC) by proline (PRO; CCC) has also been reported to be associated with cancer susceptibility in a Japanese population.	Proline	142-145	P53	Homo sapiens	27-30
33638700-5	2021	The genotoxicity of GO and RGOs against ARPE-19 (a typical RPE cell line) cells was investigated using the alkaline comet assay, the expression level of phosphorylated p53 determined via Western blots, and the release level of reactive oxygen species (ROS).	graphene oxide	20-22	P53	Homo sapiens	168-171
8835823-1	1996	The expression of p53 protein was studied in odontogenic keratocysts (OKC, 11 solitary, 5 recurrent and 6 NBCCS cysts), radicular (RC, n = 5) and dentigerous (DC, n = 5) cysts, using a panel of antibodies to p53 (clone BP53-12, clone 1801 and polyclonal CM1) and a sensitive biotin-streptavidin method on paraffin embedded sections.	Biotin	275-281	P53	Homo sapiens	18-21
33668328-5	2021	Treatment of CaSki cells with some (lopinavir, ritonavir, nelfinavir, and saquinavir) but not other (indinavir and atazanavir) protease inhibitors reduced E6 and E7 protein levels, correlating with increased p53 protein levels and decreased cell viability.	Saquinavir	74-84	P53	Homo sapiens	208-211
33096451-6	2021	TC-treatment caused mitochondrial membrane damage and cell cycle G0/G1 phase arrest, increasing the presence of the p53 protein and decreasing beta-catenin, in addition, to inducing cell death by autophagy.	Technetium	0-2	P53	Homo sapiens	116-119
33096451-8	2021	CONCLUSION: In vitro TC activity in the human HCC HuH7.5 tumor cell line is shown to be a potential molecule to develop new therapies to repair the p53 pathway and prevent the overexpression of Wnt/beta-catenin tumor development inducing autophagy cell death and decreasing metastatic capacity of HuH7.5 cell line.	Technetium	21-23	P53	Homo sapiens	148-151
8835823-9	1996	When data for the NBCCS-related OKC group were excluded, there was a significant correlation (r = 0.55, P &lt; 0.01) between p53 and Ki67 labelling.	ki67	133-137	P53	Homo sapiens	125-128
8609696-10	1996	The CR rates overall and of primary tumors tended to be higher in the p53-positive than negative group, but the differences were not significant.	Chromium	4-6	P53	Homo sapiens	70-73
33297377-0	2020	p53 Enhances Artemisia annua L. Polyphenols-Induced Cell Death Through Upregulation of p53-Dependent Targets and Cleavage of PARP1 and Lamin A/C in HCT116 Colorectal Cancer Cells.	Polyphenols	32-43	P53	Homo sapiens	0-3
33297377-0	2020	p53 Enhances Artemisia annua L. Polyphenols-Induced Cell Death Through Upregulation of p53-Dependent Targets and Cleavage of PARP1 and Lamin A/C in HCT116 Colorectal Cancer Cells.	Polyphenols	32-43	P53	Homo sapiens	87-90
33297377-2	2020	The aim of this study was to investigate the role of p53 on the anticancer effect of polyphenols isolated from Korean Artemisia annua L. (pKAL) in HCT116 human colorectal cancer cells.	Polyphenols	85-96	P53	Homo sapiens	53-56
33188383-7	2020	Molecular analysis revealed that the enhanced anticancer potency was due to the synergic effect induced by the simultaneous activation of p53 by AS1411 and the inhibition of thymidylate synthase by FUdR, respectively, both of which were generated from the DNA nanoparticles.	AGRO 100	145-151	P53	Homo sapiens	138-141
33599867-7	2021	CONCLUSION: High expression of immunohistochemically detected p53 was strongly and significantly associated with decreased OS and BCSS than low p53 expression, suggesting that p53 may be a powerful prognostic factor in HR-positive, HER2-negative breast cancer patients receiving NAC.	nac	279-282	P53	Homo sapiens	62-65
33404935-7	2021	LIPUFU were more cytotoxic than LIP, LIFU, and LIPU in both LS174T (p53+/+, bax-/-) and HT-29 (p53-/0, bax+/+) cell lines.	lipu	0-4	P53	Homo sapiens	68-71
33404935-7	2021	LIPUFU were more cytotoxic than LIP, LIFU, and LIPU in both LS174T (p53+/+, bax-/-) and HT-29 (p53-/0, bax+/+) cell lines.	lipu	0-4	P53	Homo sapiens	95-98
33456714-0	2021	Correction: Cepharanthine hydrochloride reverses the mdr1 (P-glycoprotein)-mediated esophageal squamous cell carcinoma cell cisplatin resistance through JNK and p53 signals.	cepharanthine hydrochloride	12-39	P53	Homo sapiens	161-164
33201894-9	2020	Importantly, the addition of exogenous uridine, which reconstitutes the cellular pool of pyrimidine by the salvage pathway, to the culture media recovered the impaired rDNA transcription, nucleolar morphology, p53 levels, and proliferation of glioblastoma cells caused by the DHODH inhibitors.	Uridine	39-46	P53	Homo sapiens	210-213
8632915-6	1996	We propose that any intervention which prevents this intramolecular interaction, including addition of bulky residues such as sugar groups, can activate DNA binding by p53.	Sugars	126-131	P53	Homo sapiens	168-171
32631113-3	2021	The expression of p53 is regulated transcriptionally by promoter methylation and post-transcriptionally by N-6-methyladenosine (m6A) RNA methylation.	N-methyladenosine	107-126	P53	Homo sapiens	18-21
8625447-1	1996	The p53 tumor suppressor gene is often mutated in various human cancers and a common polymorphism is known at codon 72 of exon 4, with two alleles encoding either arginine (CGC) or proline (CCC).	Proline	181-188	P53	Homo sapiens	4-7
33148606-13	2020	Western blotting showed that celecoxib could partially reverse MIF-induced COX-2 upregulation and P53 downregulation.	Celecoxib	29-38	P53	Homo sapiens	98-101
7554063-5	1995	alpha-Naphthoflavone, an inhibitor of cytochrome P450 (CYP)1A1, decreased both the formation of diolepoxide metabolites and the p53 response.	alpha-naphthoflavone	0-20	P53	Homo sapiens	128-131
33148342-5	2020	The therapeutic effect of selinexor in HGBCL-DH cells was significantly enhanced when combined with a BET inhibitor INCB057643, overcoming the drug resistance in Mut-p53-expressing cells.	selinexor	26-35	P53	Homo sapiens	166-169
33248145-5	2021	In addition, western blotting assay revealed the increased expressions of the p53, Bax, caspase 3, and a reduction of Bcl-2 and CDK2, resulting in Se-TE-induced apoptosis.	se-te	147-152	P53	Homo sapiens	78-81
7667317-2	1995	To study the effects of p53 without the complication of DNA damage, we used tetracycline to regulate its expression in MDAH041 human fibroblasts that lack endogenous p53.	Tetracycline	76-88	P53	Homo sapiens	24-27
32785787-3	2020	We report a case of oligodendroglioma that acquired imbalanced 1p/19q codeletion and TP53 mutation at recurrence after temozolomide therapy.	Temozolomide	119-131	P53	Homo sapiens	85-89
32785787-6	2020	The copy-neutral loss of heterozygosity might have imbalanced the 1p/19q codeletion, while temozolomide therapy possibly caused the TP53 mutation.	Temozolomide	91-103	P53	Homo sapiens	132-136
32726721-2	2020	Adverse factors produced by environmental exposures, such as reactive oxygen species, inflammation, and cyclobutane pyrimidine dimers, mediate m6A modification, thereby regulating downstream gene and protein expression, and signaling pathways, such as FTO/m6A RNA/p53 axis, PI3K/AKT/mTOR pathway, and PARP/METTL3/m6A RNA/Pol kappa pathway.	cyclobutane pyrimidine	104-126	P53	Homo sapiens	264-267
33137095-0	2020	Docosahexaenoic acid inhibits the proliferation of Kras/TP53 double mutant pancreatic ductal adenocarcinoma cells through modulation of glutathione level and suppression of nucleotide synthesis.	Docosahexaenoic Acids	0-20	P53	Homo sapiens	56-60
7667317-6	1995	MDAH041 cells arrested by tetracycline-regulated p53 for as long as 20 days resumed growth when the p53 level was lowered, in striking contrast to the irreversible arrest mediated by DNA damage.	Tetracycline	26-38	P53	Homo sapiens	49-52
32524685-5	2020	PURPOSE: To investigate the feasibility of amide proton transfer MRI in assessing p53 and Ki-67 expression of rectal adenocarcinoma, and compare it with conventional diffusion-weighted imaging (DWI).	Amides	43-48	P53	Homo sapiens	82-85
7667317-6	1995	MDAH041 cells arrested by tetracycline-regulated p53 for as long as 20 days resumed growth when the p53 level was lowered, in striking contrast to the irreversible arrest mediated by DNA damage.	Tetracycline	26-38	P53	Homo sapiens	100-103
7559091-4	1995	The molecular weight of p53 protein in SAOS-MC43 was lower than that in SAOS-MC11, SAOS-MC11 and SAOS-MC43 were more sensitive and more resistant, respectively, to ionizing radiation than the parental SAOS-2.	mc43	44-48	P53	Homo sapiens	24-27
32557898-0	2020	Editorial for "Comparative Analysis of Amide Proton Transfer MRI and Diffusion-Weighted Imaging in Assessing p53 and Ki-67 Expression of Rectal Adenocarcinoma".	Amides	39-44	P53	Homo sapiens	109-112
32572277-4	2020	Using chemoproteomic platforms, we show that members of the manumycin family of polyketides, which bear multiple potentially reactive sites, target C374 of the putative E3 ligase UBR7 in breast cancer cells, and engage in molecular glue interactions with the neosubstrate tumor-suppressor TP53, leading to p53 transcriptional activation and cell death.	manumycin	60-69	P53	Homo sapiens	289-293
33038821-8	2020	Moreover, the protein expression of PP2A was remarkably inhibited, whereas the expression of p53, BAX, Caspase3 and Cleaved-caspase3 were prominently increased in the 60 muM MC-LR-exposed oocytes.	cyanoginosin LR	174-179	P53	Homo sapiens	93-96
7559095-2	1995	The wild-type p53 gene has a polymorphism at codon 72 that presents the arginine (CGC) or proline (CCC) genotype, which recently has been reported to be associated with genetically determined susceptibility to smoking-related lung cancers.	Proline	90-97	P53	Homo sapiens	14-17
32572277-4	2020	Using chemoproteomic platforms, we show that members of the manumycin family of polyketides, which bear multiple potentially reactive sites, target C374 of the putative E3 ligase UBR7 in breast cancer cells, and engage in molecular glue interactions with the neosubstrate tumor-suppressor TP53, leading to p53 transcriptional activation and cell death.	manumycin	60-69	P53	Homo sapiens	306-309
7982477-6	1994	The phosphorylation status of Rb was altered following DNA damage in p53 wild-type cell lines, but was not altered in p53 mutant cell lines, nor in cell lines where p53 function was abrogated by viral gene products.	Rubidium	30-32	P53	Homo sapiens	69-72
33193609-8	2020	Taken together, our findings revealed the essential significance of the MC-LR and ctHBx on the PP2A/MAPK/p53, cdc25C and cdc2 axis in the formation and development of HCC and identified MC-LR and ctHBx as potential causal cofactors of hepatocarcinogenesis.	cyanoginosin LR	72-77	P53	Homo sapiens	105-108
33238621-6	2020	The mutation profiles of CIMP-high tumors were significantly different from those of CIMP-low or CIMP-0 tumors (i.e., higher frequencies of BRAF, POLD1, MSH3, and SMAD4 mutations but lower frequencies of APC, TP53, and KRAS mutations).	Cyclic IMP	25-29	P53	Homo sapiens	209-213
33828376-9	2020	The mechanism includes cell cycle progression and protein expression, which was detected using specific antibody-conjugated fluorescent dye, p53-FITC, by flow cytometry.	Fluorescein-5-isothiocyanate	145-149	P53	Homo sapiens	141-144
21559675-0	1994	Effect of actinomycin-d on the cell-cycle progression and the expression of p53, waf1/cip1, gadd45, and mdm-2 genes in human oral keratinocytes - implication of human papillomavirus infection.	Dactinomycin	10-23	P53	Homo sapiens	76-79
32833105-1	2020	Ibrutinib-based therapy represents a recent success in managing high-risk CLL patients with 17p/TP53 deletion.	ibrutinib	0-9	P53	Homo sapiens	96-100
32833105-10	2020	In summary, the data presented establish an association between LPL deletion, resistance to ibrutinib-based therapy, and poorer overall survival in TP53-deleted CLL patients.	ibrutinib	92-101	P53	Homo sapiens	148-152
21559675-4	1994	Actinomycin D significantly increased the levels of intranuclear wild-type p53 and mdm-2 proteins and the transcripts of WAF1/CIP1, gadd45 and mdm-2 in normal cells, but it did not increase them in the HPV-immortalized cells.	Dactinomycin	0-13	P53	Homo sapiens	75-78
32988919-7	2020	CONCLUSION: Mutations in TP53 and PIK3CA hotspot at exon 9 may be potential negative predictors of ER+HER2+ BC treated with neoadjuvant letrozole and lapatinib, while MLL2 inactivating mutation might confer therapeutic benefit in these patients.	Letrozole	136-145	P53	Homo sapiens	25-29
33060632-11	2020	This signature, decreased by ICS/LABA treatment was enriched for genes associated with increased p53 mediated apoptosis was replicated in bronchial biopsies of COPD patients.	LABA	33-37	P53	Homo sapiens	97-100
32738659-5	2020	Meanwhile, the intracellular ROS-P53 crosstalk can be upregulated by diallyl disulfide (up to 8-fold increase of ROS) and valproate (up to 18-fold increase of P53) to enhance early apoptosis.	diallyl disulfide	69-86	P53	Homo sapiens	33-36
21559675-5	1994	These data indicate that actinomycin D-induced transient cell cycle arrest may be associated with enhanced level of wild-type p53 protein and the transcripts of WAF1/CIP1 and gadd45 in normal human oral keratinocytes.	Dactinomycin	25-38	P53	Homo sapiens	126-129
32738659-5	2020	Meanwhile, the intracellular ROS-P53 crosstalk can be upregulated by diallyl disulfide (up to 8-fold increase of ROS) and valproate (up to 18-fold increase of P53) to enhance early apoptosis.	diallyl disulfide	69-86	P53	Homo sapiens	159-162
7947202-11	1994	As p53 positivity was associated with the proliferation marker Ki67, the accumulation of p53 is possibly a response to an increased proliferation rate of the keratinocytes in these skin diseases, or alternatively it may be associated with apoptosis.	ki67	63-67	P53	Homo sapiens	3-6
32516515-10	2020	Likewise, the conditional expression (doxycycline-controlled) of HNF4alpha even in cells that retained short telomeres, accrued DNA damage, and exhibited p53 stabilization, successfully restored hepatocyte formation from hESCS.	Doxycycline	38-49	P53	Homo sapiens	154-157
33134795-5	2020	Objective: The role of miR-125b in the regulation of TP53 expression in endometriosis was tested with a bioinformatics approach.	mir-125b	23-31	P53	Homo sapiens	53-57
7947202-11	1994	As p53 positivity was associated with the proliferation marker Ki67, the accumulation of p53 is possibly a response to an increased proliferation rate of the keratinocytes in these skin diseases, or alternatively it may be associated with apoptosis.	ki67	63-67	P53	Homo sapiens	89-92
7955057-3	1994	Only one case of hydatidiform mole was found to have a missense point mutation (codon 295, CCT--&gt;CTT, i.e. proline to leucine) of the p53 gene.	Proline	110-117	P53	Homo sapiens	137-140
31965420-4	2020	The efficacy of ibrutinib, a B cell receptor inhibitor, for B-PLL with the TP53 abnormality as second-line therapy was recently demonstrated.	ibrutinib	16-25	P53	Homo sapiens	75-79
31965420-5	2020	We herein report that low-dose ibrutinib as upfront therapy induced a complete response in a B-PLL patient with the TP53 abnormality, whose condition has since remained stable with no recurrence for 12 months.	ibrutinib	31-40	P53	Homo sapiens	116-120
8062281-3	1994	Expression of the p53 protein was analyzed in 36 cases of carcinoma in adenoma in the colon by immunohistochemistry using an anti-human p53 monoclonal antibody (PAb1801).	pab1801	161-168	P53	Homo sapiens	18-21
32942546-4	2020	Results indicated a significant 130% excess of 8-oxodG at -TGC- position of p53 codon 176 in HCV-HCC cases as compared to controls, after correction for age and gender, whereas a not significant increment of 5-OHC at -TGC- position was found.	8-ohdg	47-54	P53	Homo sapiens	76-79
8057451-0	1994	The ability of human papillomavirus E6 proteins to target p53 for degradation in vivo correlates with their ability to abrogate actinomycin D-induced growth arrest.	Dactinomycin	128-141	P53	Homo sapiens	58-61
33205006-5	2020	We report herewith that globotriaosylceramide (Gb3) is associated with cSrc kinase in GEMs and plays a crucial role in modulating expression of p53 R273H mutant and drug resistance.	globotriaosylceramide	24-45	P53	Homo sapiens	144-147
33205006-7	2020	Inhibition of GCS with Genz-161 (GENZ 667161) resensitized cells to apoptosis in these p53 mutant-carrying cancer cells.	genz-161	23-31	P53	Homo sapiens	87-90
33205006-7	2020	Inhibition of GCS with Genz-161 (GENZ 667161) resensitized cells to apoptosis in these p53 mutant-carrying cancer cells.	genz 667161	33-44	P53	Homo sapiens	87-90
33205006-8	2020	Genz-161 effectively inhibited GCS activity, and substantially suppressed the elevated Gb3 levels seen in GEMs of p53-mutant cells exposed to doxorubicin.	genz-161	0-8	P53	Homo sapiens	114-117
8057451-5	1994	Expression of HPV-16 E6 or mutated E6 proteins that bound and targeted p53 for degradation in vitro sharply reduced the level of intracellular p53 induced by actinomycin D in human keratinocytes.	Dactinomycin	158-171	P53	Homo sapiens	71-74
8057451-5	1994	Expression of HPV-16 E6 or mutated E6 proteins that bound and targeted p53 for degradation in vitro sharply reduced the level of intracellular p53 induced by actinomycin D in human keratinocytes.	Dactinomycin	158-171	P53	Homo sapiens	143-146
8057451-6	1994	A perfect correlation between the ability of E6 proteins to reduce the level of intracellular p53 and their ability to block actinomycin D-induced cellular growth arrest was observed.	Dactinomycin	125-138	P53	Homo sapiens	94-97
8058314-4	1994	Mobility-shift assays showed that the oligomerization-defective mutant p53(1-326), from which the final 67 C-terminal amino acids were deleted, retained the wild-type p53"s ability to bind the p53CON element in the presence of anti-p53 monoclonal antibody PAb1801.	pab1801	256-263	P53	Homo sapiens	71-74
32588678-6	2020	Cells exposed to BaP showed prominent changes in the expression of mitochondrial microRNAs (miR-24, miR-34a, miR-150, and miR-155) and their respective gene targets (NF-kappabeta, MYC, and p53).	Benzo(a)pyrene	17-20	P53	Homo sapiens	189-192
8076381-3	1994	By using a monoclonal antibody, PAb1801, it was possible to detect the accumulation of an altered p53 protein in standard sections of colon-preserving histopathological criteria.	pab1801	32-39	P53	Homo sapiens	98-101
32679123-5	2020	The treatment of nifedipine dose-dependently suppressed H2O2-induced senescence by reducing Ca2+ entry, autophagy impairment and mTOR signaling, and this suppression was found to be related to senescence-associated beta-galactosidase (SA-beta-gal) activity and the expressions of senescence marker protein 30 (SMP30), p53, and p21.	Nifedipine	17-27	P53	Homo sapiens	318-321
32641480-3	2020	DFO and MLN-4924, but not FG-4592, induced accumulation of both lytic EBV proteins and phosphorylated p53 in cell lines that contain a wild-type p53 gene.	Deferoxamine	0-3	P53	Homo sapiens	102-105
32641480-3	2020	DFO and MLN-4924, but not FG-4592, induced accumulation of both lytic EBV proteins and phosphorylated p53 in cell lines that contain a wild-type p53 gene.	Deferoxamine	0-3	P53	Homo sapiens	145-148
32641480-7	2020	Importantly, DFO induced binding of p53 as well as HIF-1alpha to Zp in ChIP assays, but only when the HRE was present.	Deferoxamine	13-16	P53	Homo sapiens	36-39
32641480-9	2020	Conversely, KU-55933, a drug that inhibits ataxia telangiectasia mutated thereby preventing p53 phosphorylation, inhibited DFO-induced EBV reactivation.	Deferoxamine	123-126	P53	Homo sapiens	92-95
8118380-5	1994	We assessed p53 nuclear overexpression by the use of anti-p53 antibody PAb1801 and immunohistochemistry, and identified 45 of 109 patients (41%) displaying p53-positive phenotype.	pab1801	71-78	P53	Homo sapiens	12-15
32921957-12	2020	PLK1 inhibitors (volasertib and GSK461364) or a BIRC5 inhibitor (YM155) selectively targeted Huh7 cells with mutated p53, but not HepG2 cells with wild-type p53.	BI 6727	17-27	P53	Homo sapiens	117-120
7909153-4	1994	Because immunoreactivity for p53 correlates closely with the presence of mutation in the p53 gene, we performed immunohistochemical staining with the monoclonal antibody PAb1801.	pab1801	170-177	P53	Homo sapiens	29-32
32791549-7	2020	Patients with the high-risk parameters deletion 17p or TP53mutation are known to poorly respond to chemo(immuno)therapy and should receive either ibrutinib or venetoclax/obinutuzumab.Thus, a choice has to be made between a continuous monotherapy with ibrutinib or a time-limited combination with either venetoclax/obinutuzumab (12 months) or chemoimmunotherapy (usually 6 months).	ibrutinib	146-155	P53	Homo sapiens	55-59
32791549-7	2020	Patients with the high-risk parameters deletion 17p or TP53mutation are known to poorly respond to chemo(immuno)therapy and should receive either ibrutinib or venetoclax/obinutuzumab.Thus, a choice has to be made between a continuous monotherapy with ibrutinib or a time-limited combination with either venetoclax/obinutuzumab (12 months) or chemoimmunotherapy (usually 6 months).	ibrutinib	251-260	P53	Homo sapiens	55-59
7909153-4	1994	Because immunoreactivity for p53 correlates closely with the presence of mutation in the p53 gene, we performed immunohistochemical staining with the monoclonal antibody PAb1801.	pab1801	170-177	P53	Homo sapiens	89-92
7508232-3	1993	Using streptavidin-biotin complex method, p53 was identified in 33% of dysplastic squamous lesions, 50% of squamous cell carcinomas (SCCs) and 36% of basal cell carcinomas (BCCs) on frozen section, whereas 25% of dysplastic squamous lesions, 40% of SCCs, and 32% of BCCs showed p53 positivity on paraffin-embedded sections.	Biotin	19-25	P53	Homo sapiens	42-45
31432292-0	2020	Benzothiazole derivative bearing amide moiety induces p53-mediated apoptosis in HPV16 positive cervical cancer cells.	benzothiazole	0-13	P53	Homo sapiens	54-57
31432292-0	2020	Benzothiazole derivative bearing amide moiety induces p53-mediated apoptosis in HPV16 positive cervical cancer cells.	Amides	33-38	P53	Homo sapiens	54-57
8397167-0	1993	Sodium butyrate induces apoptosis in human colonic tumour cell lines in a p53-independent pathway: implications for the possible role of dietary fibre in the prevention of large-bowel cancer.	Butyric Acid	0-15	P53	Homo sapiens	74-77
32733026-6	2020	Pharmacological inhibitor of AKT, MK2206, rescues KLF6 expression and suppresses p53-R273H-induced cell migration.	MK 2206	34-40	P53	Homo sapiens	81-84
8352280-1	1993	A rare germ-line polymorphism in codon 47 of the p53 gene replaces the wild-type proline (CCG) with a serine (TCG).	Proline	81-88	P53	Homo sapiens	49-52
32726539-0	2020	Ibrutinib for Chronic Lymphocytic Leukemia with TP53 Alterations.	ibrutinib	0-9	P53	Homo sapiens	48-52
8352280-1	1993	A rare germ-line polymorphism in codon 47 of the p53 gene replaces the wild-type proline (CCG) with a serine (TCG).	TMG-chitotriomycin	110-113	P53	Homo sapiens	49-52
8502477-9	1993	In contrast, p53-Ala-15 was partially defective in blocking cell cycle progression.	ala-15	17-23	P53	Homo sapiens	13-16
8495305-1	1993	An immunohistochemical method using Pab1801, a monoclonal antibody specific to the human p53 protein, was applied to detect p53 expression in colorectal cancer and dysplasia complicating ulcerative colitis.	pab1801	36-43	P53	Homo sapiens	89-92
32519803-0	2020	Polysaccharides derived from Balanophora polyandra significantly suppressed the proliferation of ovarian cancer cells through P53-mediated pathway.	balanophora polyandra	29-50	P53	Homo sapiens	126-129
8495305-1	1993	An immunohistochemical method using Pab1801, a monoclonal antibody specific to the human p53 protein, was applied to detect p53 expression in colorectal cancer and dysplasia complicating ulcerative colitis.	pab1801	36-43	P53	Homo sapiens	124-127
32541631-9	2020	CONCLUSIONS: Serum anti-p53 antibody can serve as a surrogate marker for TP53 alterations and help predict the presence of HGD/INV in cases with IPMN, in combination with CEA and CA 19-9.	ipmn	145-149	P53	Homo sapiens	24-27
8517643-5	1993	Immunoreactive p53 was observed in the nuclei of the cancer cells in 15/33 (45%) by pAbDO-7, 11/26 (42%) by pAb1801, and 16/33 (48%) by pAbCM-1.	pab1801	108-115	P53	Homo sapiens	15-18
32238452-10	2020	SIGNIFICANCE STATEMENT: This study reported duloxetine markedly reduces neuropathic pain evoked by Paclitaxel (PTX), and related to PARP, p53 and the Bcl2 family.	Duloxetine Hydrochloride	44-54	P53	Homo sapiens	138-141
1620551-1	1992	Mouse 10T1/2 cells were transfected with combinations of T24 H-ras, human c-myc and the proline 193 mutant form of p53.	Proline	88-95	P53	Homo sapiens	115-118
32356241-11	2020	In conclusion, our findings provided a novel evidence that NTZ could be a dual potential IL6/JAK2/STAT3 signaling inhibitor and p53/caspases-dependent pathway activator in CRC cell line.	nitazoxanide	59-62	P53	Homo sapiens	128-131
1322917-4	1992	Immunoprecipitation of 35S-labelled cellular proteins with anti-p53 and anti-T antibodies revealed that the level of the cellular protein, p53, declined markedly in the presence of sodium butyrate.	Butyric Acid	181-196	P53	Homo sapiens	64-67
32347709-6	2020	We demonstrate that the loaded vancomycin was able to kill intracellular S. aureus efficiently in an in vitro model of S. aureus infected RAW-264.7 macrophage cells, and U87-MG (p53-wt) and LN229 (p53-mt) cancer cells, compared to free-vancomycin treatment (P<0.001).	Vancomycin	31-41	P53	Homo sapiens	197-200
1322917-4	1992	Immunoprecipitation of 35S-labelled cellular proteins with anti-p53 and anti-T antibodies revealed that the level of the cellular protein, p53, declined markedly in the presence of sodium butyrate.	Butyric Acid	181-196	P53	Homo sapiens	139-142
33939688-4	2021	Using a cell-based screen, we identified a small molecule, the phenylpyrazoleanilide Y-320, that potently enhances TP53, DMD, and COL17A1 PTC readthrough by G418.	phenylpyrazoleanilide	63-84	P53	Homo sapiens	115-119
31978617-9	2020	In addition, RSV reduced the levels of senescence-associated secretory phenotype (SASP), gene markers associated with senescence (P53, P16, and P21), intracellular ROS levels and increased gene expression of enzymes protecting cells from oxidative damage (HMOX1 and SOD3).	resveratrol	13-16	P53	Homo sapiens	130-133
32017928-9	2020	Our results indicate that PLSCR1 plays a critical role in p53-dependent regulation of autophagy and apoptosis in sodium selenite-treated leukemia cells.	Sodium Selenite	113-128	P53	Homo sapiens	58-61
33939688-4	2021	Using a cell-based screen, we identified a small molecule, the phenylpyrazoleanilide Y-320, that potently enhances TP53, DMD, and COL17A1 PTC readthrough by G418.	Y-320	85-90	P53	Homo sapiens	115-119
33591178-0	2021	p53 Is Potentially Regulated by Cyclophilin D in the Triple-Proline Loop of the DNA Binding Domain.	Proline	60-67	P53	Homo sapiens	0-3
32017928-10	2020	Manipulation of p53-PLSCR1 cascade might be beneficial to enhance the anti-tumor effects of sodium selenite.	Sodium Selenite	92-107	P53	Homo sapiens	16-19
33591178-6	2021	We have identified the specific cyclophilin D binding site on p53 that is located at proline 151 in the DNA binding domain.	Proline	85-92	P53	Homo sapiens	62-65
33591178-7	2021	As a peptidyl-prolyl isomerase, cyclophilin D binds p53 and catalyzes the cis-trans isomerization of the peptide bond preceding proline 151.	Proline	128-135	P53	Homo sapiens	52-55
32196468-9	2020	At certain parametric regions, there is a correlation between the outcomes of cell fate and endpoints of BE, suggesting that the intercellular coupling of p53 network may manifest itself as the form of observed BEs.	BES	211-214	P53	Homo sapiens	155-158
32600719-0	2020	Immunosensors containing solution blow spun fibers of poly(lactic acid) to detect p53 biomarker.	poly(lactide)	54-71	P53	Homo sapiens	82-85
33591178-8	2021	We have also characterized the effect of such an isomerization and found that the p53 domain in the cis state is overall more rigid than the trans state except for the local region around proline 151.	Proline	188-195	P53	Homo sapiens	82-85
32600719-1	2020	This paper reports on biosensors made with a matrix of polylactic acid (PLA) fibers, which are suitable for immobilization of the anti-p53 active layer for detection of p53 biomarker.	poly(lactide)	55-70	P53	Homo sapiens	135-138
32600719-1	2020	This paper reports on biosensors made with a matrix of polylactic acid (PLA) fibers, which are suitable for immobilization of the anti-p53 active layer for detection of p53 biomarker.	poly(lactide)	55-70	P53	Homo sapiens	169-172
26560363-2	2015	Here, we report that p53 regulates iron metabolism through the transcriptional regulation of ISCU (iron-sulfur cluster assembly enzyme), which encodes a scaffold protein that plays a critical role in Fe-S cluster biogenesis.	Sulfur	104-110	P53	Homo sapiens	21-24
31838664-6	2020	The direct measurement of the reactive oxygen species by 2,7-Dichlorodihydrofluorescein diacetate confirmed the antioxidant activity of P53 in the vasculature.	2',7'-dichlorodihydrofluorescein diacetate	57-97	P53	Homo sapiens	136-139
26560363-2	2015	Here, we report that p53 regulates iron metabolism through the transcriptional regulation of ISCU (iron-sulfur cluster assembly enzyme), which encodes a scaffold protein that plays a critical role in Fe-S cluster biogenesis.	Sulfur	94-95	P53	Homo sapiens	21-24
26628962-3	2015	To identify the detailed mechanism, we examined the functional importance of p21 and p53 in DPA-induced anticancer effect.	dpa	92-95	P53	Homo sapiens	85-88
32213959-0	2020	Induction of p53-Dependent Apoptosis by Prostaglandin A2.	prostaglandin A2	40-56	P53	Homo sapiens	13-16
32619887-6	2020	Compound 5q up-regulated the expression of both pro-apoptotic Bax and P53, while down-regulated anti-apoptotic Bcl-2 expression.	CHEMBL3739943	9-11	P53	Homo sapiens	70-73
32213959-2	2020	Although PGA2 has been reported to cause activation of apoptosis by altering the expression of apoptosis-related genes, the role of p53, one of the most critical pro-apoptotic genes, on PGA2-induced apoptosis has not been clarified yet.	prostaglandin A2	186-190	P53	Homo sapiens	132-135
26628962-6	2015	Additionally, Western blot showed that DPA treatment induced the p21, p53, and cyclin-E protein expressions in HCT-116 cells.	dpa	39-42	P53	Homo sapiens	70-73
32213959-6	2020	While PGA2 induced apoptosis in HCT116 cells, phosphorylation of p53 and transcriptional induction of p53-target genes such as p21WAF1, PUMA, BAX, NOXA, and DR5 occurred.	prostaglandin A2	6-10	P53	Homo sapiens	102-105
32213959-7	2020	Besides, pretreatment of pifithrin-alpha (PFT-alpha), a chemical inhibitor of p53"s transcriptional activity, interfered with the induction of apoptosis in PGA2-treated HCT116 cells.	prostaglandin A2	156-160	P53	Homo sapiens	78-81
32867831-0	2020	Boswellic acid sensitizes gastric cancer cells to Cisplatin-induced apoptosis via p53-mediated pathway.	boswellic acid	0-14	P53	Homo sapiens	82-85
26628962-8	2015	DPA decreased cell migration in HCT-116 and HCT-116 p53(-/-) but not in HCT-116 p21(-/-) cells.	dpa	0-3	P53	Homo sapiens	52-55
32213959-8	2020	Pretreatment of NU7441, a small molecule inhibitor of DNA-activated protein kinase (DNA-PK) suppressed PGA2-induced phosphorylation of p53 and apoptosis as well.	8-dibenzothiophen-4-yl-2-morpholin-4-yl-chromen-4-one	16-22	P53	Homo sapiens	135-138
32213959-8	2020	Pretreatment of NU7441, a small molecule inhibitor of DNA-activated protein kinase (DNA-PK) suppressed PGA2-induced phosphorylation of p53 and apoptosis as well.	prostaglandin A2	103-107	P53	Homo sapiens	135-138
12780718-9	2003	Collectively, this data suggests that selenium prevents UVR-induced cell death by inhibiting p53-independent cell death pathways.	Selenium	38-46	P53	Homo sapiens	93-96
32213959-9	2020	Moreover, among target genes of p53, knockdown of DR5 expression by RNA interference, suppressed PGA2-induced apoptosis.	prostaglandin A2	97-101	P53	Homo sapiens	32-35
32213959-10	2020	In the meanwhile, in HCT116 p53-/- cells, PGA2 induced apoptosis in delayed time points and with less potency.	prostaglandin A2	42-46	P53	Homo sapiens	28-31
32213959-11	2020	Delayed apoptosis by PGA2 in HCT116 p53-/- cells was also associated with phosphorylation of H2AX but was not inhibited by either PFT-  or NU7441.	prostaglandin A2	21-25	P53	Homo sapiens	36-39
31547774-0	2020	Sulfonamide phenylalanine (SPA) series of analogues as an antibacterial, antifungal, anticancer agents along with p53 tumor suppressor-DNA complex inhibitor - part 1.	Sulfonamides	0-25	P53	Homo sapiens	114-117
31547774-0	2020	Sulfonamide phenylalanine (SPA) series of analogues as an antibacterial, antifungal, anticancer agents along with p53 tumor suppressor-DNA complex inhibitor - part 1.	Sulfonamides	27-30	P53	Homo sapiens	114-117
34845969-0	2021	Cisatracurium besilate enhances the TRAIL-induced apoptosis of gastric cancer cells via p53 signaling.	cisatracurium	0-22	P53	Homo sapiens	88-91
32917321-9	2020	Western blot analysis further demonstrated that hinokitiol treatment increased the levels of p53 and p21, and concomitantly reduced the expression of cell cycle regulatory proteins, including cyclin D and cyclin E. SA-beta-gal assay showed that hinokitiol treatment significantly induced beta-galactosidase activity.	beta-thujaplicin	48-58	P53	Homo sapiens	93-96
32213959-13	2020	PGA2 may induce p53-dependent apoptosis in which DNA-PK activates p53, and DR5, a transcriptional target of p53, plays a pivotal role in HCT116 cells.	prostaglandin A2	0-4	P53	Homo sapiens	16-19
32213959-13	2020	PGA2 may induce p53-dependent apoptosis in which DNA-PK activates p53, and DR5, a transcriptional target of p53, plays a pivotal role in HCT116 cells.	prostaglandin A2	0-4	P53	Homo sapiens	66-69
32213959-13	2020	PGA2 may induce p53-dependent apoptosis in which DNA-PK activates p53, and DR5, a transcriptional target of p53, plays a pivotal role in HCT116 cells.	prostaglandin A2	0-4	P53	Homo sapiens	66-69
33944652-2	2021	Recent studies reported that cisatracurium could inhibit the progression of colon cancer by upregulating tumor suppressor gene p53.	cisatracurium	29-42	P53	Homo sapiens	127-130
32213959-14	2020	In contrast to apoptosis in HCT116 cells, PGA2 may induce apoptosis in a fashion of less potency, which is independent of p53 and DNA-PK in HCT116 p53-/- cells.	prostaglandin A2	42-46	P53	Homo sapiens	147-150
31831363-0	2020	Effects of DHA-enriched fish oil on gene expression levels of p53 and NF-kappaB and PPAR-gamma activity in PBMCs of patients with T2DM: A randomized, double-blind, clinical trial.	Docosahexaenoic Acids	11-14	P53	Homo sapiens	62-65
31831363-3	2020	The aim of our study was to investigate the effects of docosahexaenoic acid (DHA)-enriched fish oil supplement on PPAR-gamma activity and mRNA expression levels of p53 and NF-kappaB.	Docosahexaenoic Acids	55-75	P53	Homo sapiens	164-167
31831363-3	2020	The aim of our study was to investigate the effects of docosahexaenoic acid (DHA)-enriched fish oil supplement on PPAR-gamma activity and mRNA expression levels of p53 and NF-kappaB.	Docosahexaenoic Acids	77-80	P53	Homo sapiens	164-167
32842595-3	2020	Studies on HepG2 cells (human HCC) demonstrated C60 fullerene ability to inhibit cell growth (IC50 = 108.2 mumol), to induce apoptosis, to downregulate glucose-6-phosphate dehydrogenase, to upregulate vimentin and p53 expression and to alter HepG2 redox state.	Fullerenes	52-61	P53	Homo sapiens	214-217
32825184-4	2020	As a follow-up study of our previous findings, here we have identified that the pharmacological substances, leptomycin B and doxorubicin, can improve the sensitivity of cervical cancer cells to cisplatin inducing HP1gamma-mediated elevation of p53.	leptomycin B	108-120	P53	Homo sapiens	244-247
32825184-5	2020	Leptomycin B, which inhibits the nuclear export of HP1gamma, increased cisplatin-dependent apoptosis induction by promoting the activation of p53 signaling.	leptomycin B	0-12	P53	Homo sapiens	142-145
32782319-4	2020	Results showed that 47% of all p53 transcripts contained an uridine misincorporation opposite the lesion at 6 h post transfection, which was decreased to 18% at 24 h. TM at these levels reduced DNA binding activity of p53 to 21% and 80% compared to wild type p53, respectively.	Uridine	60-67	P53	Homo sapiens	31-34
32417172-0	2020	O-linked N-acetylgalactosamine modification is present on the tumor suppressor p53.	Acetylgalactosamine	9-30	P53	Homo sapiens	79-82
31641820-0	2020	Activation of death receptor, DR5 and mitochondria-mediated apoptosis by a 3,4,5-trimethoxybenzyloxy derivative in wild-type and p53 mutant colorectal cancer cell lines.	BW 1069C85	75-100	P53	Homo sapiens	129-132
33944652-9	2021	As a result, cisatracurium could increase the expressions of p53 and lincRNA-p21 of ovarian cancer cell line (OVCAR-3) in a dose-dependent manner.	cisatracurium	13-26	P53	Homo sapiens	61-64
33944652-13	2021	In conclusion, cisatracurium inhibited the progression of OVCAR-3 cells through upregulation of lincRNA-p21 expression activated by p53 inhibiting miR-181b expression.	cisatracurium	15-28	P53	Homo sapiens	132-135
34478957-7	2021	In addition, PA-C1b can deliver p53-eGFP plasmids into MCF-7 cancer cells, and the proliferation of cells was inhibited and even caused cell death.	pa-c1b	13-19	P53	Homo sapiens	32-35
32296580-12	2020	Our data confirmed that SNRPG suppression sensitizes GBM cells to TMZ by targeting Myc via the p53 signaling cascade.	Temozolomide	66-69	P53	Homo sapiens	95-98
32664789-3	2020	Data from The Genomics of Drug Sensitivity in Cancer database showed that three drugs: (5Z)-7-oxozeaenol, dabrafenib and nutlin-3a (-), have shown more resistance in patients with TP53 mutation.	dabrafenib	106-116	P53	Homo sapiens	180-184
34835028-12	2021	These results suggest that AdBcl-xL plays negative roles in GSIV-induced mitochondrial apoptosis and virus replication by binding to AdBak and inhibiting p53 activation.	gsiv	60-64	P53	Homo sapiens	154-157
32060401-2	2020	MEDI2228, more effectively than its anti-tubulin MMAF-ADC homolog, induces cytotoxicity against MM cells regardless of drug resistance, BCMA levels, p53 status, and the protection conferred by bone marrow stromal cells and IL-6.	medi2228	0-8	P53	Homo sapiens	149-152
32801647-0	2020	Nano-Graphene Oxide-supported APTES-Spermine, as Gene Delivery System, for Transfection of pEGFP-p53 into Breast Cancer Cell Lines.	nano	0-4	P53	Homo sapiens	97-100
32801647-0	2020	Nano-Graphene Oxide-supported APTES-Spermine, as Gene Delivery System, for Transfection of pEGFP-p53 into Breast Cancer Cell Lines.	graphene oxide	5-19	P53	Homo sapiens	97-100
31971801-0	2020	alpha-Helix-Mimicking Sulfono-gamma-AApeptide Inhibitors for p53-MDM2/MDMX Protein-Protein Interactions.	sulfoquinovosylacylglycerol	22-35	P53	Homo sapiens	61-64
31971801-4	2020	Using fluorescence polarization assays, circular dichroism (CD), NMR spectroscopy, and computational simulations we demonstrate that sulfono-gamma-AApeptides adopt helical structures resembling p53 and competitively inhibit the p53-MDM2 interaction by binding to the hydrophobic cleft of MDM2.	sulfoquinovosylacylglycerol	133-146	P53	Homo sapiens	194-197
31971801-4	2020	Using fluorescence polarization assays, circular dichroism (CD), NMR spectroscopy, and computational simulations we demonstrate that sulfono-gamma-AApeptides adopt helical structures resembling p53 and competitively inhibit the p53-MDM2 interaction by binding to the hydrophobic cleft of MDM2.	sulfoquinovosylacylglycerol	133-146	P53	Homo sapiens	228-231
34711005-7	2021	The PCR products of all the exons of TP53 (Exons 2 to 11) were electrophoresed on agarose gel, purified and sequenced by Sanger method.	Sepharose	82-89	P53	Homo sapiens	37-41
31894286-0	2020	BMP9 mediates the anticancer activity of evodiamine through HIF-1alpha/p53 in human colon cancer cells.	evodiamine	41-51	P53	Homo sapiens	71-74
34697748-7	2021	While andrographolide when used in combination with a p53 inhibitor (pifithrin-alpha) showed potent restriction over its response.	1-(2H-1,3-Benzodioxol-5-yl)propan-1-amine	79-84	P53	Homo sapiens	54-57
31974389-3	2020	We reported that both polyphenols show antioxidant and oto-protective activity in the cochlea by up-regulating Nrf-2/HO-1 pathway and downregulating p53 phosphorylation.	Polyphenols	22-33	P53	Homo sapiens	149-152
32705436-0	2021	HIF1alpha and p53 Regulated MED30, a Mediator Complex Subunit, is Involved in Regulation of Glioblastoma Pathogenesis and Temozolomide Resistance.	Temozolomide	122-134	P53	Homo sapiens	14-17
32681102-9	2020	A combination treatment with AZD5363 and FH535 enhanced p53 expression, by modulating MDM2 activation; however, AZD5363 treatment alone restricted p53 to the nucleus by inhibiting dynamin-related protein activation.	FH535	41-46	P53	Homo sapiens	56-59
34386081-7	2021	A higher frequency of CYP1A1*2C heterozygotes and TP53 rare homozygotes, which include the proline (Pro)/Pro genotype, was observed among children with ALL and control subjects, whereas no significant differences were observed for the CXCL12 SNP.	Proline	91-98	P53	Homo sapiens	50-54
32678213-8	2020	We found that dihydrotanshinone-I (DHTS-I), a plant-derived product which prevents HuR binding to specific RNAs, prevented HuR-mediated upregulation of TRIM21, while increasing the HuR-mediated upregulation of p53.	dhts-i	35-41	P53	Homo sapiens	210-213
32668972-0	2020	Cryptotanshinone-Induced p53-Dependent Sensitization of Colon Cancer Cells to Apoptotic Drive by Regulation of Calpain and Calcium Homeostasis.	cryptotanshinone	0-16	P53	Homo sapiens	25-28
34386081-7	2021	A higher frequency of CYP1A1*2C heterozygotes and TP53 rare homozygotes, which include the proline (Pro)/Pro genotype, was observed among children with ALL and control subjects, whereas no significant differences were observed for the CXCL12 SNP.	Proline	100-103	P53	Homo sapiens	50-54
32628053-3	2022	OBJECTIVES: To evaluate the effectiveness of daylight photodynamic therapy (PDT) with methyl amino levulinate (MAL) based on clinical evaluation, histological examination and immunohistochemical expression of p53 and Ki67.	mal	111-114	P53	Homo sapiens	209-212
32013837-7	2020	RESULTS: Here, we reported that pisosterol markedly induced G2/M arrest and apoptosis and decreased the cell viability and proliferation potential of glioma cells in a dose-dependent manner by increasing the expression of ATM, CASP3, CDK1, CDKN1A, CDKN2A, CDKN2B, CHEK1, p14ARF and TP53 and decreasing the expression of MYC, BCL2, BMI1 and MDM2.	pisosterol	32-42	P53	Homo sapiens	282-286
32013837-8	2020	Pisosterol also triggered both caspase-independent and caspase-dependent apoptotic pathways by regulating the expression of Bcl-2 and activating caspase-3 and p53.	pisosterol	0-10	P53	Homo sapiens	159-162
34203338-7	2021	Under pristane stimulation, alveolar epithelial cells had increased p53, lincRNA-p21 and downstream Bax levels with elevated apoptotic ratios.	pristane	6-14	P53	Homo sapiens	68-71
32044796-9	2020	The combination of C61-LNP and CDDP changed in alterations of the cell cycle regulatory proteins p53, p21, p27, cyclin D1 and cyclin E levels.	AT 61	19-22	P53	Homo sapiens	97-100
32208876-5	2020	Polyphyllin I dose-dependent increased the release of mitochondrial cytochrome c, and levels of Fas, p53, p21, and Bax/ Bcl-2 ratios, as well as the activation of cleaved caspase-3, -8, -9, and subsequent cleavage of the poly (ADP-ribose) polymerase (PARP).	polyphyllin I	0-13	P53	Homo sapiens	101-104
34203338-10	2021	Our findings demonstrate increased p53-dependent lncRNA expression with accelerated cell apoptosis in the lungs of SLE-associated DAH patients, and show the therapeutic potential of targeting intra-pulmonary lncRNA expression in a pristane-induced model of DAH.	pristane	231-239	P53	Homo sapiens	35-38
31004736-0	2020	Anti-cancer effects of polyphenols via targeting p53 signaling pathway: updates and future directions.	Polyphenols	23-34	P53	Homo sapiens	49-52
31004736-1	2020	The anticancer effects of polyphenols are ascribed to several signaling pathways including the tumor suppressor gene tumor protein 53 (p53).	Polyphenols	26-37	P53	Homo sapiens	117-133
32238452-0	2020	Duloxetine attenuates paclitaxel-induced peripheral nerve injury by inhibiting p53-related pathways.	Duloxetine Hydrochloride	0-10	P53	Homo sapiens	79-82
34207315-7	2021	The mechanism of pevonedistat cytotoxicity depended on p53 status.	pevonedistat	17-29	P53	Homo sapiens	55-58
32238452-8	2020	As a result, duloxetine acts by inhibiting PARP cleavage and p53 activation and regulating the Bcl2 family to reverse paclitaxel(PTX)-induced oxidative stress and apoptosis.	Duloxetine Hydrochloride	13-23	P53	Homo sapiens	61-64
32356241-8	2020	NTZ also modulated significantly the p53/caspases-dependent signaling pathways, leading to enhancement of apoptosis and an increase of DNA fragmentation.	nitazoxanide	0-3	P53	Homo sapiens	37-40
32428506-18	2020	The MLL-complex antagonists MI-2-2 (inhibitor of protein interaction) and OICR-9492 (inhibitor of activity) specifically inhibited proliferation of HCC cells that express TP53R249S at nanomolar concentrations.	oicr-9492	74-83	P53	Homo sapiens	171-175
31004736-1	2020	The anticancer effects of polyphenols are ascribed to several signaling pathways including the tumor suppressor gene tumor protein 53 (p53).	Polyphenols	26-37	P53	Homo sapiens	135-138
31004736-3	2020	A number of polyphenols from a wide variety of dietary sources could upregulate p53 expression in several cancer cell lines through distinct mechanisms of action.	Polyphenols	12-23	P53	Homo sapiens	80-83
31004736-4	2020	The aim of this review is to focus the significance of p53 signaling pathways and to provide molecular intuitions of dietary polyphenols in chemoprevention by monitoring p53 expression that have a prominent role in tumor suppression.	Polyphenols	125-136	P53	Homo sapiens	170-173
32065108-7	2020	In Sodium sulphite and boric acid treated cells, expression levels of p53 was up-regulated, while that of the Bcl2 was significantly down-regulated.	boric acid	23-33	P53	Homo sapiens	70-73
32534357-10	2020	The apoptosis induced by EPI in MKN-45 cells would be effectively inhibited with the treatment of p53 siRNA and p53 inhibitor PFT-alpha.	mkn-45	32-38	P53	Homo sapiens	98-101
34108527-0	2021	DNA-PK inhibitor peposertib enhances p53-dependent cytotoxicity of DNA double-strand break inducing therapy in acute leukemia.	nedisertib	17-27	P53	Homo sapiens	37-40
32534357-10	2020	The apoptosis induced by EPI in MKN-45 cells would be effectively inhibited with the treatment of p53 siRNA and p53 inhibitor PFT-alpha.	mkn-45	32-38	P53	Homo sapiens	112-115
33053575-0	2020	Metabolic Syndrome Instead of Aflatoxin-Related TP53 R249S Mutation as a Hepatocellular Carcinoma Risk Factor.	Aflatoxins	30-39	P53	Homo sapiens	48-52
32691668-7	2020	In addition, knockdown of protein phosphatase, Mg2+/Mn2+ dependent 1D enhanced the expressions of p-p38 and p53 in AML-193 cells and KG-1 cells.	Manganese(2+)	52-56	P53	Homo sapiens	108-111
32691668-8	2020	The above observation suggested that protein phosphatase, Mg2+/Mn2+ dependent 1D knockdown suppressed cell proliferation, promoted cell apoptosis, and activated p38 MAPK/p53 signaling pathway in acute myeloid leukemia cells.	Manganese(2+)	63-67	P53	Homo sapiens	170-173
31852795-6	2019	We also reveal that p53 restoration markedly improves the sensitivity of these tumor cells to everolimus, a mammalian target of rapamycin (mTOR) inhibitor that failed to show clinical benefits in advanced HCC and NSCLC.	Everolimus	94-104	P53	Homo sapiens	20-23
33053575-3	2020	OBJECTIVE: The objective of the study was to explore if HCCs carry the TP53 R249S mutation that has linked them to aflatoxin exposure and describe the associated risk factors.	Aflatoxins	115-124	P53	Homo sapiens	71-75
34108527-3	2021	By suppressing DNA-PK catalytic activity in the presence of DNA DSB, M3814 potentiates ATM/p53 signaling leading to enhanced p53-dependent antitumor activity in tumor cells.	nedisertib	69-74	P53	Homo sapiens	91-94
34108527-3	2021	By suppressing DNA-PK catalytic activity in the presence of DNA DSB, M3814 potentiates ATM/p53 signaling leading to enhanced p53-dependent antitumor activity in tumor cells.	nedisertib	69-74	P53	Homo sapiens	125-128
34108527-5	2021	We show that in the presence of IR or topoisomerase II inhibitors, M3814 boosts the ATM/p53 response in acute leukemia cells leading to the elevation of p53 protein levels as well as its transcriptional activity.	nedisertib	67-72	P53	Homo sapiens	88-91
34108527-5	2021	We show that in the presence of IR or topoisomerase II inhibitors, M3814 boosts the ATM/p53 response in acute leukemia cells leading to the elevation of p53 protein levels as well as its transcriptional activity.	nedisertib	67-72	P53	Homo sapiens	153-156
31944316-8	2020	Doxycycline was also found to activate p53-, ATF6-, NRF1/2-, and MTF1-mediated transcription and inhibit the transcription of histones, proteasomal genes, fibroblast growth factor, and other oncogenic factors.	Doxycycline	0-11	P53	Homo sapiens	39-42
34108527-8	2021	Further, combined with the fixed-ratio liposomal formulation of daunorubicin and cytarabine, CPX-351, M3814 enhanced the efficacy against leukemia cells in vitro and in vivo without increasing hematopoietic toxicity, suggesting that DNA-PK inhibition could offer a novel clinical strategy for harnessing the anticancer potential of p53 in AML therapy.	nedisertib	102-107	P53	Homo sapiens	332-335
31806011-7	2019	Additionally, inhibition of p53 by morpholino significantly reduced the mortality of eftud2-/- larvae.	Morpholinos	35-45	P53	Homo sapiens	28-31
34070493-5	2021	The application of 5-ALA led to a significant increase in apoptotic cells, enhancement of Bax and p53 expressions, reduction in Bcl-2 expression, and an increase in ROS generation.	5-amino levulinic acid	19-24	P53	Homo sapiens	98-101
31472244-6	2019	Furthermore, while Hcy induces the levels of senescence regulators PAI-1, p16, p53 and integrin beta3, and suppresses catalase expression, treatment with PAI-1 inhibitors blocks the Hcy-induced stimulation of senescence cadres, and reverses the Hcy-induced suppression of catalase, indicating that PAI-1 specific small molecule inhibitors are efficient to prevent Hcy-induced cellular senescence.	Homocysteine	19-22	P53	Homo sapiens	79-82
32187452-6	2020	On multivariable analyses, temporary ibrutinib interruption (hazard ratio [HR]: 2.37, P = .006) and TP53 disruption at ibrutinib initiation (HR: 1.81, P = .048) were associated with shorter EFS, whereas only TP53 disruption (HR: 2.38, P = .015) was associated with shorter OS.	ibrutinib	119-128	P53	Homo sapiens	100-104
31943524-8	2020	The mechanism of the regenerative and protective effects of CS may be related to the decreased reactive oxygen species generation, improved senescent state (SA-beta-gal expression decreased), upregulated expression of Smad2 and phosphorylated Smad2, and downregulated expression of p16, p21 and p53.	calcium silicate	60-62	P53	Homo sapiens	295-298
31560893-18	2019	The MLL-complex antagonists MI-2-2 (inhibitor of protein interaction) and OICR-9492 (inhibitor of activity) specifically inhibited proliferation of HCC cells that express TP53R249S at nanomolar concentrations.	oicr-9492	74-83	P53	Homo sapiens	171-175
35358657-5	2022	SI treatment also resulted in a p-53 dependent downregulation of SLC7A11.	sinapine	0-2	P53	Homo sapiens	32-36
31815044-0	2019	BRCA1 identified as a modulator of temozolomide resistance in P53 wild-type GBM using a high-throughput shRNA-based synthetic lethality screening.	temozolomide	35-47	P53	Homo sapiens	62-65
31815044-6	2019	BRCA1 knockdown resulted in antitumor activity with TMZ in P53 wild-type GSCs but not in P53 mutant GSCs.	temozolomide	52-55	P53	Homo sapiens	59-62
31815044-7	2019	TMZ treatment induced a DNA damage repair response; the activation of BRCA1 DNA repair pathway targets and knockdown of BRCA1, together with TMZ, led to increased DNA damage and cell death in P53 wild-type GSCs.	temozolomide	0-3	P53	Homo sapiens	192-195
32219291-4	2020	Our results demonstrate that oleacein is able to reduce the proliferation of the SH-SY5Y cells by blocking the cell cycle in the S phase and inducing apoptotic cell death through the increase in both Bax and p53 as well as a reduction in the Bcl-2 expression and STAT3 phosphorylation.	oleacein	29-37	P53	Homo sapiens	208-211
32300098-0	2020	Tomatidine Alleviates Osteoporosis by Downregulation of p53.	tomatidine	0-10	P53	Homo sapiens	56-59
31815044-7	2019	TMZ treatment induced a DNA damage repair response; the activation of BRCA1 DNA repair pathway targets and knockdown of BRCA1, together with TMZ, led to increased DNA damage and cell death in P53 wild-type GSCs.	temozolomide	141-144	P53	Homo sapiens	192-195
35217253-8	2022	Biotin-C3 peptide characterized luminal BC according to p53 status and to HER2 expression, being the biosensor a better strategy when compared to ELISA test.	biotin-c3	0-9	P53	Homo sapiens	56-59
31815044-8	2019	Our study identified BRCA1 as a potential target that sensitizes TMZ-induced cell death in P53 wild-type GBM, suggesting that the combined inhibition of BRCA1 and TMZ treatment will be a successful targeted therapy for GBM patients.	temozolomide	65-68	P53	Homo sapiens	91-94
31815044-8	2019	Our study identified BRCA1 as a potential target that sensitizes TMZ-induced cell death in P53 wild-type GBM, suggesting that the combined inhibition of BRCA1 and TMZ treatment will be a successful targeted therapy for GBM patients.	temozolomide	163-166	P53	Homo sapiens	91-94
32300098-16	2020	CONCLUSIONS Tomatidine can improve osteoporosis, and one of the mechanisms of its action is achieved by modulating p53.	tomatidine	12-22	P53	Homo sapiens	115-118
35635647-10	2022	Moreover, TPEN significantly increased the counts of cells positive for the oxidation of the stress sensor protein DJ-1, a sign of the formation of H2O2, and significantly increased the counts of cells positive for the pro-apoptotic proteins TP53, PUMA, and CASPASE-3 (CASP-3), indicative of apoptosis, in B-ALL cells.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	10-14	P53	Homo sapiens	242-246
32276424-7	2020	The major findings of this study are that (i) blockage of KPNB1 specifically enhanced the radiation-induced apoptosis and radiosensitivity of HNSCC cells; (ii) importazole elevated p53-upregulated modulator of apoptosis (PUMA) expression via blocking the nuclear import of SCC-specific oncogene DeltaNp63 in HNSCC cells; and (iii) blockage of KPNB1 attenuated the upregulation of cell surface PD-L1 expression on irradiated HNSCC cells.	importazole	160-171	P53	Homo sapiens	181-184
31357283-4	2019	Herein, a functional nanosystem for in situ and real-time monitoring levels of p53 and p21 mRNA was constructed using reduced graphene oxide nanosheet assisted fluorescence probes.	graphene oxide	126-140	P53	Homo sapiens	79-82
31289209-8	2020	BAY87-2243 also overcomes the constitutive fludarabine resistance of TP53dis leukemic cells and elicits a strongly synergistic cytotoxic effect in combination with ibrutinib, thus providing preclinical evidences for its further investigation as a potential new drug in chronic lymphocytic leukemia.	1-cyclopropyl-4-(4-((5-methyl-3-(3-(4-(trifluoromethoxy)phenyl)-1,2,4-oxadiazol-5-yl)-1H-pyrazol-1-yl)methyl)pyridin-2-yl)piperazine	0-10	P53	Homo sapiens	69-73
35546176-7	2022	UA significantly decreased the expression of senescence-associated p53 and p21, and increased the expression of mitophagy-related proteins, in H2O2-induced senescent cells and cochlear explants.	3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-one	0-2	P53	Homo sapiens	67-70
32048269-0	2020	Synergistic effects of tanshinone IIA and andrographolide on the apoptosis of cancer cells via crosstalk between p53 and reactive oxygen species pathways.	andrographolide	42-57	P53	Homo sapiens	113-116
32048269-11	2020	CONCLUSION: The combination of Tan IIA and Andro showed significant synergistic effects on cancer cell apoptosis by promoting crosstalk between ROS and p53, providing a novel and effective combination that has the potential to be applied in clinical anticancer therapy.	andrographolide	43-48	P53	Homo sapiens	152-155
31652456-13	2019	Co-transfection of P53 could partially reverse the promotive effects of miR-151a-3p on NPC cell progression.	mir-151a-3p	72-83	P53	Homo sapiens	19-22
31652456-14	2019	Our data indicated that blocking p53 expression and mediated signal pathways contribute to the positive effects of miR-151a-3p on NPC cell proliferation, migration and invasion.	mir-151a-3p	115-126	P53	Homo sapiens	33-36
31652659-6	2019	Furthermore, we found that the activation of nuclear factor-kappaB (NF-kappaB) and subsequent p53 induction were associated with the apoptotic effect of Ivalin.	ivalin	153-159	P53	Homo sapiens	94-97
35577753-6	2022	In the first case, a patient with CLL, complex karyotype, del 17p, and a mutation in TP53 experiences progression after ibrutinib, venetoclax, bendamustine, rituximab, and idelalisib.	Bendamustine Hydrochloride	143-155	P53	Homo sapiens	85-89
31597910-11	2019	Treatment of DLD-1 cells with imidazole suppressed Bcl-2 and promoted Bax, p53, and cytc expression.	imidazole	30-39	P53	Homo sapiens	75-78
32197606-7	2020	Moreover, limonin, a compound found in ER, reduced the viability of both serous-type (SKOV-3 and A2780) and mucinous-type (RMUG-S) ovarian cancer cells by inducing apoptosis via activation of the p53 signaling pathway.	limonin	10-17	P53	Homo sapiens	196-199
32197606-9	2020	CONCLUSION: Taken together, our findings suggest that limonin contributes to the anti-ovarian cancer effects of ER by inducing apoptosis via activation of the p53 signaling pathway.	limonin	54-61	P53	Homo sapiens	159-162
35577753-6	2022	In the first case, a patient with CLL, complex karyotype, del 17p, and a mutation in TP53 experiences progression after ibrutinib, venetoclax, bendamustine, rituximab, and idelalisib.	idelalisib	172-182	P53	Homo sapiens	85-89
32172299-4	2020	However, 17p-deleted, p53-mutated or IGHV-UM subgroups are generally resistant to FCR, and much better responses are seen with ibrutinib and venetoclax, frequently inducing MRD negativity that hopefully will be translated into durable remissions.	ibrutinib	127-136	P53	Homo sapiens	22-25
31132711-13	2019	Our results suggested that ALX4 was inactivated by DNA methylation and played a tumor suppressor function through the P53 pathway in MC-LR induced liver cancer.	cyanoginosin LR	133-138	P53	Homo sapiens	118-121
35083778-0	2022	TP53 mutations at codon 234 are associated with chlorambucil treatment in chronic lymphocytic leukemia.	Chlorambucil	48-60	P53	Homo sapiens	0-4
31063779-10	2019	LCCLs with inactivating mutations in TSC1 and TSC2 were sensitive to the mammalian target of rapamycin inhibitor rapamycin, and cells with inactivating mutations in TP53 were sensitive to the Aurora kinase A inhibitor alisertib.	MLN 8237	218-227	P53	Homo sapiens	165-169
32063101-6	2020	The anticancer effects of Pd/MgO nanoparticles were accentuated by the upregulation of Bax and p53 and downregulation of Bcl-2 protein expressions.	Magnesium	29-32	P53	Homo sapiens	95-98
32045477-1	2020	The selective inhibitor of nuclear export (SINE) compounds selinexor (KPT-330) and eltanexor (KPT-8602) are from a novel class of small molecules that target exportin-1 (XPO1 [CRM1]), an essential nucleo-cytoplasmic transport protein responsible for the nuclear export of major tumor suppressor proteins and growth regulators such as p53, p21, and p27.	selinexor	94-102	P53	Homo sapiens	334-337
35354152-13	2022	CONCLUSION: The present IBC-CP case is triple-negative breast cancer with TP53 mutation.	ibc-cp	24-30	P53	Homo sapiens	74-78
31404021-5	2019	RESULTS: TP53 mutation rates in D-PDC, C-PDC, and noninvasive IPMN were 67%, 66%, and 10%, respectively.	ipmn	62-66	P53	Homo sapiens	9-13
35391801-9	2022	This minireview covers the role of p53 in the mevalonate pathway and how bioactive phytochemicals target the mevalonate pathway and promote p53-dependent anticancer activities.	Mevalonic Acid	46-56	P53	Homo sapiens	35-38
31592435-0	2019	Synergetic Impact of Combined 5-Fluorouracil and Rutin on Apoptosis in PC3 Cancer Cells through the Modulation of P53 Gene Expression.	Rutin	49-54	P53	Homo sapiens	114-117
31592435-9	2019	Combination of 5-FU/rutin enhanced apoptosis and p53 gene expression in PC3 cells.	Rutin	20-25	P53	Homo sapiens	49-52
32172951-5	2020	Nervosine VII simultaneously induced autophagy and apoptosis by activated MAPKs signaling pathway including JNK, ERK1/2 and p38, suppressing the p53 signaling pathway.	nervosine vii	0-13	P53	Homo sapiens	145-148
31924585-2	2020	Although recently introduced small-molecule B-cell receptor signalling inhibitors have revolutionized CLL treatment, data for ibrutinib still point to impaired prognosis for TP53-affected patients.	ibrutinib	126-135	P53	Homo sapiens	174-178
31894286-12	2020	In HCT116 cells, Evo increased the phosphorylation of p53, which was enhanced by BMP9 but reduced by BMP9 silencing.	evodiamine	17-20	P53	Homo sapiens	54-57
31592435-11	2019	Conclusion: Synergistic effects of 5-FU/rutin combination on PC3 cells line enhanced apoptosis, p53 gene expression, and down-regulation of Bcl-2 protein, compared to control separate application.	Rutin	40-45	P53	Homo sapiens	96-99
35391801-9	2022	This minireview covers the role of p53 in the mevalonate pathway and how bioactive phytochemicals target the mevalonate pathway and promote p53-dependent anticancer activities.	Mevalonic Acid	109-119	P53	Homo sapiens	140-143
31894286-13	2020	Furthermore, the effect of Evo on p53 was potentiated by HIF-1alpha and reduced by HIF-1alpha silencing.	evodiamine	27-30	P53	Homo sapiens	34-37
31894286-14	2020	The present findings therefore strongly indicated that the anticancer activity of Evo may be partly mediated by BMP9 upregulation, which can activate p53 through upregulation of HIF-1alpha, at least in human colon cancer.	evodiamine	82-85	P53	Homo sapiens	150-153
35377359-6	2022	Total cellular Flag-tagged p53 protein was purified with anti-Flag antibody-conjugated agarose under nondenaturing conditions.	Sepharose	87-94	P53	Homo sapiens	27-30
31894839-7	2020	Furthermore, EPS1-1-mediated apoptosis is regulated by inactivation of mammalian target of rapamycin complex 1 (mTORC1) and activation of the jun-NH2 kinase (JNK)-p53 signaling axis dependent on AMPK activation.	Ammonia	146-149	P53	Homo sapiens	163-166
31974389-9	2020	Thanks to their biphasic activity of antioxidant in normal cells undergoing stressful conditions and pro-oxidant in cancer cells, these polyphenols probably engage an interplay among the key factors Nrf-2, NF-kappaB, STAT-3 and p53.	Polyphenols	136-147	P53	Homo sapiens	228-231
31173230-7	2019	Additionally, the methylation level of the TP53 promoter was identified to be associated with carotid intima-media thickness, the degree of carotid atherosclerosis and the circulating levels of homocysteine in peripheral blood.	Homocysteine	194-206	P53	Homo sapiens	43-47
31366902-0	2019	Ru(II)-thymine complex causes DNA damage and apoptotic cell death in human colon carcinoma HCT116 cells mediated by JNK/p38/ERK1/2 via a p53-independent signaling.	ru(ii)-thymine	0-14	P53	Homo sapiens	137-140
35178099-11	2022	The experimental results showed that baicalein and wogonin could inhibit proliferation and induce apoptosis of NPC cells and downregulate the expression of PI3K, AKT, and p53, the key proteins of the PI3K/AKT and p53 signaling pathway in CNE2 cells.	baicalein	37-46	P53	Homo sapiens	171-174
31363127-5	2019	Although the detailed molecular mechanisms are still to be defined, our work shows for the first time that in primary B cells, metabolic stressors enhance BTK signaling and suggest that metabolic rewiring to hyperglycemia affects ibrutinib resistance in TP53 deficient chronic lymphocytic leukemia (CLL) lymphocytes.	ibrutinib	230-239	P53	Homo sapiens	254-258
31603527-6	2020	Prolonged CPX treatment leads to p53-independent Caspase-3/7 activation and induction of apoptosis.	cpx	10-13	P53	Homo sapiens	33-36
35178099-11	2022	The experimental results showed that baicalein and wogonin could inhibit proliferation and induce apoptosis of NPC cells and downregulate the expression of PI3K, AKT, and p53, the key proteins of the PI3K/AKT and p53 signaling pathway in CNE2 cells.	baicalein	37-46	P53	Homo sapiens	213-216
35178099-12	2022	Conclusion: Baicalein and wogonin, the main active ingredients of S. barbata, inhibited the proliferation and induced apoptosis of NPC cells through the PI3K/AKT and p53 signaling pathways.	baicalein	12-21	P53	Homo sapiens	166-169
31733192-7	2020	Moreover, decreased phosphorylation of p53(Ser15) and NFkappaB(Ser536) was required for GV-induced cell death.	Gentian Violet	88-90	P53	Homo sapiens	39-42
35159039-2	2022	Here we report a p53-independent mechanism responsible for Growth Factor Independence-1 (GFI1) support of MM cell survival by its modulation of sphingolipid metabolism to increase the sphingosine-1-phosphate (S1P) level regardless of the p53 status.	sphingosine 1-phosphate	209-212	P53	Homo sapiens	17-20
32598859-4	2020	While its exact antitumor mechanisms await revelation, icaritin has been found to regulate several key molecules and pathways concerning cell fate, including CDK-dependent pathways, mitogen-activated protein kinases (MAPKs), the serine-threonine kinase AKT, signal transducer and activator of transcription 3 (STAT3), and p53.	icaritin	55-63	P53	Homo sapiens	322-325
31216622-14	2019	Overall, these three mutations showed a large deviation in total SASA in both p53 and ERalpha.	sasa	65-69	P53	Homo sapiens	78-81
30872077-5	2019	In fact, abrogation of p53 in cells with functional p53 blocks the radiosensitizing effect of Palbociclib.	palbociclib	94-105	P53	Homo sapiens	23-26
30872077-5	2019	In fact, abrogation of p53 in cells with functional p53 blocks the radiosensitizing effect of Palbociclib.	palbociclib	94-105	P53	Homo sapiens	52-55
30872077-6	2019	Moreover, no radiosensitizing effect is observed in cells with non-functional p53, but restoration of p53 function promotes radiosensitivity associated to Palbociclib.	palbociclib	155-166	P53	Homo sapiens	102-105
31180577-1	2020	The Bruton"s tyrosine kinase (BTK) inhibitor ibrutinib is inducing durable responses in chronic lymphocytic leukemia (CLL) patients with refractory/relapsed disease or with TP53 defect, with BTK and phospholipase C gamma 2 (PLCG2) mutations representing the predominant mechanisms conferring secondary ibrutinib resistance.	ibrutinib	45-54	P53	Homo sapiens	173-177
31223423-7	2019	We found that MHY2233 increased the expression of SIRT1, and its deacetylase activity thereby decreased expression of the cellular senescence biomarkers, p53, p16, and p21.	mhy2233	14-21	P53	Homo sapiens	154-157
35159039-2	2022	Here we report a p53-independent mechanism responsible for Growth Factor Independence-1 (GFI1) support of MM cell survival by its modulation of sphingolipid metabolism to increase the sphingosine-1-phosphate (S1P) level regardless of the p53 status.	sphingosine 1-phosphate	209-212	P53	Homo sapiens	238-241
35022897-10	2022	DUB-IN-1, an USP8 inhibitor, caused DNA damage, led to G2/M phase block by p53-p21 axis, and triggered apoptosis by regulating the p53 target proteins including Bax, Noxa, and Puma.	DUBs-IN-1	0-8	P53	Homo sapiens	75-78
31190889-9	2019	The results of computational analysis revealed the interplay between examined miRNAs and their targets involved in processes of glioblastoma chemosensitivity, including the genes relevant to temozolomide response (MGMT, PTEN, MDM2, TP53, BBC3A).	Temozolomide	191-203	P53	Homo sapiens	232-236
30742880-0	2019	Polychlorinated biphenyl quinone-induced signaling transition from autophagy to apoptosis is regulated by HMGB1 and p53 in human hepatoma HepG2 cells.	polychlorinated biphenyl quinone	0-32	P53	Homo sapiens	116-119
31810938-6	2019	RESULTS: We showed that HDAC6-selecitve inhibitors block activation of the EGFR and p53 pathways in TMZ-resistant GBM cells.	temozolomide	100-103	P53	Homo sapiens	84-87
31772153-9	2019	Chaetocin mediated apoptosis sensitization was achieved through ROS generation and consequent DNA damage induction that involved P53 activity.	chaetocin	0-9	P53	Homo sapiens	129-132
35022897-10	2022	DUB-IN-1, an USP8 inhibitor, caused DNA damage, led to G2/M phase block by p53-p21 axis, and triggered apoptosis by regulating the p53 target proteins including Bax, Noxa, and Puma.	DUBs-IN-1	0-8	P53	Homo sapiens	131-134
35022897-13	2022	USP8 inhibitor, DUB-IN-1, treatment could inhibit esophageal squamous cell carcinoma cell growth and induce G2/M cell cycle arrest, apoptosis, and autophagy by DNA damage-induced p53 activation.	DUBs-IN-1	16-24	P53	Homo sapiens	179-182
31207703-0	2019	[High-dose methylprednisolone with Rituximab and fresh frozen plasma in the treatment of six patients with B-cell lymphoproliferative disorders harboring TP53 abnormalities].	Methylprednisolone	11-29	P53	Homo sapiens	154-158
35022897-14	2022	DUB-IN-1 treatment led to G2/M cell cycle arrest by upregulating the protein level of p21 and triggered apoptosis by modulating the p53 target proteins including Bax, Noxa, and Puma.	DUBs-IN-1	0-8	P53	Homo sapiens	132-135
31519237-0	2019	Ratiometric fluorescence strategy for p53 gene assay by using nitrogen doped graphene quantum dots and berberine as fluorescence reporters.	Graphite	77-85	P53	Homo sapiens	38-41
31519237-2	2019	Nitrogen doped graphene quantum dots (NGQDs) were firstly bound with a single-stranded DNA (P1 DNA), which contains berberine aptamer sequence and p53 gene complementary sequence (Cp53 DNA).	Graphite	15-23	P53	Homo sapiens	147-150
35022897-15	2022	Meanwhile, DUB-IN-1 treatment stimulated protective autophagy through p53-dependent AMPK activation.	DUBs-IN-1	11-19	P53	Homo sapiens	70-73
35070453-6	2022	Aluminum poisoning has complex and multidimensional effects, such as disruption or inhibition of enzymes activities, changing protein synthesis, nucleic acid function, and cell membrane permeability, preventing DNA repair, altering the stability of DNA organization, inhibition of the protein phosphatase 2A (PP2A) activity, increasing reactive oxygen species (ROS) production, inducing oxidative stress, decreasing activity of antioxidant enzymes, altering cellular iron homeostasis, and changing NF-kB, p53, and JNK pathway leading to apoptosis.	Aluminum	0-8	P53	Homo sapiens	505-508
31481464-1	2019	Wildtype P53-induced phosphatase 1 (WIP1) is a member of the magnesium-dependent serine/threonine protein phosphatase (PPM) family and is induced by P53 in response to DNA damage.	Magnesium	61-70	P53	Homo sapiens	9-12
31481464-1	2019	Wildtype P53-induced phosphatase 1 (WIP1) is a member of the magnesium-dependent serine/threonine protein phosphatase (PPM) family and is induced by P53 in response to DNA damage.	Magnesium	61-70	P53	Homo sapiens	149-152
30859681-12	2019	Overall, the p53 wild-type cell lines were more sensitive to volasertib treatment, suggesting that p53 might be a predictive biomarker for Plk1 inhibition in NSCLC.	BI 6727	61-71	P53	Homo sapiens	13-16
30859681-12	2019	Overall, the p53 wild-type cell lines were more sensitive to volasertib treatment, suggesting that p53 might be a predictive biomarker for Plk1 inhibition in NSCLC.	BI 6727	61-71	P53	Homo sapiens	99-102
35072516-6	2022	The role of a gene variant in Tp53 that modifies proline to arginine was examined using nasal brushings from study participants in the Lovelace Smokers Cohort, primary human AECs, and mice with a modified Tp53 gene.	Proline	49-56	P53	Homo sapiens	30-34
30507085-0	2019	Amentoflavone Induces Autophagy and Modulates p53.	amentoflavone	0-13	P53	Homo sapiens	46-49
30507085-11	2019	In particular, the levels of p53 and p-p21 proteins were increased in the presence of amentoflavone.	amentoflavone	86-99	P53	Homo sapiens	29-32
31339188-5	2019	Furthermore, we found that palbociclib suppressed chemerin-induced apoptotic protein expression, reversing the Bcl-2/Bax ratio and inhibiting the p53/p21 waf pathway.	palbociclib	27-38	P53	Homo sapiens	146-149
30507085-12	2019	Furthermore, amentoflavone increased the level of SIRT1 deacetylating p53.	amentoflavone	13-26	P53	Homo sapiens	70-73
33934760-0	2021	Construction of a ternary nano-architecture based graphene oxide sheets, toward electrocatalytic determination of tumor-associated anti-p53 autoantibodies in human serum.	graphene oxide	50-64	P53	Homo sapiens	136-139
30507085-13	2019	Conclusion: Our results suggest that amentoflavone could play a positive role in the inhibition of various diseases associated with autophagy and the modulation of p53.	amentoflavone	37-50	P53	Homo sapiens	164-167
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	Glycolipids	13-23	P53	Homo sapiens	80-83
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	Glycolipids	13-23	P53	Homo sapiens	99-102
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	p-csso	38-44	P53	Homo sapiens	80-83
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	p-csso	38-44	P53	Homo sapiens	99-102
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	p-csso	92-98	P53	Homo sapiens	80-83
30554018-4	2019	PEG modified glycolipid-like polymer (P-CSSO) was electrostatic interacted with p53 to form P-CSSO/p53 complexes, which exhibited an enhanced redox sensitivity in that the disulfide bond was degraded and the rate the plasmid released from P-CSSO was 2.29-fold that of nonresponsive platform (P-CSO-SA) in 10 mM levels of glutathione (GSH).	p-csso	92-98	P53	Homo sapiens	99-102
30628674-0	2019	Bergapten induces G1 arrest of non-small cell lung cancer cells, associated with the p53-mediated cascade.	5-Methoxypsoralen	0-9	P53	Homo sapiens	85-88
30628674-11	2019	Overall, these results suggested that bergapten may inhibit cell viability and trigger G1 arrest and apoptosis in A549 and NCI-H460 cells, which may be attributed to the activation of p53-mediated cascades.	5-Methoxypsoralen	38-47	P53	Homo sapiens	184-187
30842655-0	2019	p53 regulation of ammonia metabolism through urea cycle controls polyamine biosynthesis.	Ammonia	18-25	P53	Homo sapiens	0-3
30598263-0	2019	AZD3759 induces apoptosis in hepatoma cells by activating a p53-SMAD4 positive feedback loop.	AZD3759	0-7	P53	Homo sapiens	60-63
30598263-3	2019	Furthermore, we found that the activation of p53-SMAD family member 4 (SMAD4) positive feedback loop was involved in the induction of bulks of apoptosis in HepG2 cells in response to AZD3759 treatment.	AZD3759	183-190	P53	Homo sapiens	45-69
30338509-0	2019	Unravelling the suboptimal response of TP53-mutated chronic lymphocytic leukaemia to ibrutinib.	ibrutinib	85-94	P53	Homo sapiens	39-43
30338509-1	2019	TP53-disrupted chronic lymphocytic leukaemia (CLL) patients show a suboptimal long-term response to ibrutinib.	ibrutinib	100-109	P53	Homo sapiens	0-4
30338509-2	2019	We hereby report that ibrutinib-induced in vitro apoptosis and proliferation inhibition were significantly lower in TP53-mutated (TP53-M) CLL cells compared to TP53 wild-type cells.	ibrutinib	22-31	P53	Homo sapiens	116-120
30338509-2	2019	We hereby report that ibrutinib-induced in vitro apoptosis and proliferation inhibition were significantly lower in TP53-mutated (TP53-M) CLL cells compared to TP53 wild-type cells.	ibrutinib	22-31	P53	Homo sapiens	130-134
30338509-2	2019	We hereby report that ibrutinib-induced in vitro apoptosis and proliferation inhibition were significantly lower in TP53-mutated (TP53-M) CLL cells compared to TP53 wild-type cells.	ibrutinib	22-31	P53	Homo sapiens	130-134
30431068-8	2019	Furthermore, western blot analysis and ROS measurements indicated that AMPK inhibition, using dorsomorphin dihydrochloride, accelerated necroptosis by increasing ROS generation in HCT116 p53-/- cells.	Dorsomorphin dihydrochloride	94-122	P53	Homo sapiens	187-190
31353662-0	2019	Protective effects of hawthorn (Crataegus pinnatifida) polyphenol extract against UVB-induced skin damage by modulating the p53 mitochondrial pathway in vitro and in vivo.	Polyphenols	55-65	P53	Homo sapiens	124-127
31353662-6	2019	Treatment with HPE or its polyphenol components inhibited the UVB-induced damage by removing an excess of reactive oxygen species (ROS), reducing DNA damage and p53 activation, regulating the protein expression of B-cell lymphoma 2 family members toward antiapoptotic ratios, and reducing caspase activation.	Polyphenols	26-36	P53	Homo sapiens	161-164
30697266-12	2019	Co-treatment with captopril and the AKT inhibitor MK-2206 reduced the H2O2-induced P53 and ICAM-1 protein expression (p &lt; 0.05).	MK 2206	50-57	P53	Homo sapiens	83-86
30183082-8	2019	WM patients with TP53 mutations show response to ibrutinib.	ibrutinib	49-58	P53	Homo sapiens	17-21
31495738-4	2019	Transfection with the p53 cDNA construct resulted in the accumulation of p53 and bax, in a reduced level of released PCNA and PGF, and in an increased PGE output.	Prostaglandins F	126-129	P53	Homo sapiens	22-25
31495738-6	2019	These observations are the first demonstration of the involvement of p53 in the control of healthy human ovarian cell functions, namely, in the downregulation of proliferation, in the upregulation of apoptosis, and in the alteration of PGF and PGE release, but not of P4, IGF-I, or OT.	Prostaglandins F	236-239	P53	Homo sapiens	69-72
31168028-6	2019	Interestingly, p53 was activated by PHMG-p treatment and p53 knockdown suppressed PHMG-p-induced apoptosis and cell cycle arrest.	polyhexamethyleneguanidine	36-42	P53	Homo sapiens	15-18
31168028-6	2019	Interestingly, p53 was activated by PHMG-p treatment and p53 knockdown suppressed PHMG-p-induced apoptosis and cell cycle arrest.	polyhexamethyleneguanidine	82-88	P53	Homo sapiens	15-18
31168028-6	2019	Interestingly, p53 was activated by PHMG-p treatment and p53 knockdown suppressed PHMG-p-induced apoptosis and cell cycle arrest.	polyhexamethyleneguanidine	82-88	P53	Homo sapiens	57-60
30613017-7	2018	Danu caused cell cycle arrest in G2/M phase in HepG2 cells and led to polyploidy accumulation via up-regulating the expressions of p53 and p21 and down-regulating the expressions of cyclin B1 and DC2.	danusertib	0-4	P53	Homo sapiens	131-134
28374118-1	2018	In the proposed work, we have explicated the mechanism of dibenzo[a,l]pyrene (DBP) and benzo[a]pyrene (BP) modulated cell proliferation by assessing the plausible binding with CASPASES, BAX, Bcl-2, MDM2, p53, p21, p16, CylinD1-CDK4 complex, CylinE1-CDK2 complex, H-Ras, K-Ras, BRCA1, and BRCA2 through exploiting the inherent potential of AutoDock Tools 4.0.	dibenzo(a,l)pyrene	58-76	P53	Homo sapiens	204-207
29644528-0	2018	A novel, semi-synthetic diterpenoid 16(R and S)-phenylamino-cleroda-3,13(14), Z-dien-15,16 olide (PGEA-AN) inhibits the growth and cell survival of human neuroblastoma cell line SH-SY5Y by modulating P53 pathway.	z-dien-15,16 olide	78-96	P53	Homo sapiens	200-203
30272369-4	2018	Annexin V/PI staining, a CCK-8 assay and western blot analysis demonstrated that JIB-04 induced apoptosis in MHCC97H and HepG2 cells, which was evidenced by the expression of proapoptotic and apoptotic proteins including p53, Bak, Bax, caspase-3 and caspase-9.	jib	81-84	P53	Homo sapiens	221-224
30149215-2	2018	In this work, a PEC biosensor based on [Ru(dcbpy)2dppz]2+/Rose Bengal dyes co-sensitized C60 NPs was constructed for ultrasensitive DNA (a fragment sequence of p53 gene) detection.	[ru(dcbpy)2dppz]2+/rose bengal	39-69	P53	Homo sapiens	160-163
30396956-8	2018	In transforming growth factor-beta-treated cells, evodiamine attenuated variations in morphology, growth and migration, and increased p21 and p53 protein levels, and decreased beta-catenin, N-cadherin, vimentin, phospho-AKT, matrix metalloproteinase-2 and matrix metalloproteinase-9 protein levels.	evodiamine	50-60	P53	Homo sapiens	142-145
30059864-0	2018	Label-free distinction between p53+/+ and p53 -/- colon cancer cells using a graphene based SERS platform.	Graphite	77-85	P53	Homo sapiens	31-34
30059864-0	2018	Label-free distinction between p53+/+ and p53 -/- colon cancer cells using a graphene based SERS platform.	Graphite	77-85	P53	Homo sapiens	42-45
30059864-0	2018	Label-free distinction between p53+/+ and p53 -/- colon cancer cells using a graphene based SERS platform.	sers	92-96	P53	Homo sapiens	31-34
30059864-1	2018	Surface-Enhanced Raman Scattering (SERS) is used to differentiate two colon cancer cell line HCT 116, that is, to distinguish a TP53 gene knockout cell line (p53 -/-) from a wild type (p53 +/+).	sers	35-39	P53	Homo sapiens	128-132
30059864-1	2018	Surface-Enhanced Raman Scattering (SERS) is used to differentiate two colon cancer cell line HCT 116, that is, to distinguish a TP53 gene knockout cell line (p53 -/-) from a wild type (p53 +/+).	sers	35-39	P53	Homo sapiens	158-161
30059864-1	2018	Surface-Enhanced Raman Scattering (SERS) is used to differentiate two colon cancer cell line HCT 116, that is, to distinguish a TP53 gene knockout cell line (p53 -/-) from a wild type (p53 +/+).	sers	35-39	P53	Homo sapiens	185-188
29933074-5	2018	Furthermore, increased intracellular reactive oxygen species, p-p53, and p21 (but not p38) levels were detected in MSCs from PGF patients.	Prostaglandins F	125-128	P53	Homo sapiens	64-67
30214587-5	2018	c-Jun N-terminal kinase/p38-mitogen-activated protein kinase-induced endoplasmic reticulum (ER) stress through serial exposure to celecoxib and bortezomib may have induced the intracellular Ca2+ release, leading to the generation of autophagosomes in p53-expressing HCT-116 cells.	Celecoxib	130-139	P53	Homo sapiens	251-254
30214587-7	2018	Although p53-/- HCT-116 cells were less sensitive to sequential treatment with celecoxib and bortezomib, co-localization of autophagosomes was detected in the absence of CCAAT-enhancer-binding protein homologous protein expression.	Celecoxib	79-88	P53	Homo sapiens	9-12
30142612-0	2018	Novel antitumor compound optimized from natural saponin Albiziabioside A induced caspase-dependent apoptosis and ferroptosis as a p53 activator through the mitochondrial pathway.	saponin albiziabioside a	48-72	P53	Homo sapiens	130-133
30106571-9	2018	p53-dependence of Ru-NO complexes [3]Cl2 and [4]Cl2 was studied and p53-independent mode of action was confirmed.	[4]cl2	45-51	P53	Homo sapiens	0-3
30115935-0	2018	Anti-tumor efficacy of Selinexor (KPT-330) in gastric cancer is dependent on nuclear accumulation of p53 tumor suppressor.	selinexor	23-32	P53	Homo sapiens	101-104
30115935-0	2018	Anti-tumor efficacy of Selinexor (KPT-330) in gastric cancer is dependent on nuclear accumulation of p53 tumor suppressor.	selinexor	34-41	P53	Homo sapiens	101-104
30115935-7	2018	XPO1 inhibition by selinexor resulted in nuclear accumulation of p53, causing cell cycle arrest and apoptosis.	selinexor	19-28	P53	Homo sapiens	65-68
29492964-7	2018	Both of lung CSGs and CDGs showed significant enrichment in pathways such as cell cycle and p53 signaling pathway.	cdgs	22-26	P53	Homo sapiens	92-95
29845212-0	2018	Andrographolide induces degradation of mutant p53 via activation of Hsp70.	andrographolide	0-15	P53	Homo sapiens	46-49
29845212-4	2018	In the current study, a small-molecule screen identified andrographlide (ANDRO) as a mutant p53 suppressor.	andrographolide	73-78	P53	Homo sapiens	92-95
29680675-4	2018	Thioketal-crosslinked polyethylenimine (TK-PEI) was synthesized to condense p53 gene to form nanocomplexes (NCs), and hyaluronic acid (HA) modified with pheophytin a (Pha) was coated onto NCs to enhance their colloidal stability and enable cancer cell targeting.	thioketal	0-9	P53	Homo sapiens	76-79
29681573-8	2018	Likewise, activation of p53 (a critical inducer of senescence) was markedly suppressed by treatment with amlodipine or the R+ enantiomer.	Amlodipine	105-115	P53	Homo sapiens	24-27
29691156-1	2018	Five lactam chemotypes amenable by the Castagnoli-Cushman reaction of imines and cyclic anhydrides have been investigated for their ability to activate p53 tumor suppressing transcription factor thus induce apoptosis in p53+ cancer cells.	cyclic anhydrides	81-98	P53	Homo sapiens	152-155
29756671-5	2018	Interestingly, 6-MSITC inhibited the cell proliferation in both types of cells with similar IC50 value although a light increase in the phosphorylation and accumulation of P53 protein was observed in HCT116 p53+/+ cells at 24 h after treatment.	6-(Methylsulfinyl)hexyl isothiocyanate	15-22	P53	Homo sapiens	172-175
29796170-8	2018	We observed that wild-type p53 can promote pladienolide B-induced death in tumour cells.	pladienolide B	43-57	P53	Homo sapiens	27-30
29796170-9	2018	However, p53 is commonly inactivated by mutation in cSCCs and p53 participates in killing normal skin cells at high concentrations of pladienolide B.	pladienolide B	134-148	P53	Homo sapiens	9-12
29796170-9	2018	However, p53 is commonly inactivated by mutation in cSCCs and p53 participates in killing normal skin cells at high concentrations of pladienolide B.	pladienolide B	134-148	P53	Homo sapiens	62-65
29054521-0	2018	Computational simulations and experimental validation of structure- physicochemical properties of pristine and functionalized graphene: Implications for adverse effects on p53 mediated DNA damage response.	Graphite	126-134	P53	Homo sapiens	172-175
29429877-7	2018	Furthermore, we provide evidence that haemanthamine and other Amaryllidaceae alkaloids also inhibit specifically ribosome biogenesis, triggering nucleolar stress response and leading to p53 stabilization in cancer cells.	Amaryllidaceae Alkaloids	62-86	P53	Homo sapiens	186-189
29158005-9	2018	In the 1,25(OH)2D3 + HDAC2 overexpression group, the expressions of p53, Bax, DR5 and caspase 8 were significantly lower but the expression of Bcl-2 was significantly higher than those of the 1,25(OH)2D3 treatment group (P &lt; 0.05).	25(oh)	9-15	P53	Homo sapiens	68-71
29248874-0	2018	Oxidative stress-mediated p53/p21WAF1/CIP1 pathway may be involved in microcystin-LR-induced cytotoxicity in HepG2 cells.	cyanoginosin LR	70-84	P53	Homo sapiens	26-29
29248874-2	2018	In the present study, we investigated whether oxidative stress-mediated p53/p21WAF1/CIP1 is involved in this process to further elucidate the mechanism of cytotoxicity induced by MC-LR.	cyanoginosin LR	179-184	P53	Homo sapiens	72-75
29248874-5	2018	The protein levels of p-p53 and p21 were markedly increased by MC-LR exposure in a concentration-dependent manner, suggesting that p53 and p21 may be involved in the process.	cyanoginosin LR	63-68	P53	Homo sapiens	24-27
29248874-5	2018	The protein levels of p-p53 and p21 were markedly increased by MC-LR exposure in a concentration-dependent manner, suggesting that p53 and p21 may be involved in the process.	cyanoginosin LR	63-68	P53	Homo sapiens	131-134
29175474-7	2018	The in vitro study revealed that H3K4me3 mark was enriched in the promoters of several DNA damage responsive (DDR) genes including CRY1, ERCC2, and TP53 in primary human lymphocytes treated with hydroquinone.	hydroquinone	195-207	P53	Homo sapiens	148-152
29484684-3	2018	Recently, ibrutinib was approved for patients with relapsed/refractory CLL or for untreated CLL patients with del 17p or TP53 mutation.	ibrutinib	10-19	P53	Homo sapiens	121-125
29445290-6	2018	We found that treatment using MEK inhibitor, CDK 4/6 inhibitor, and TP53 inhibitor may provide a new therapeutic direction for GCCL.	gccl	127-131	P53	Homo sapiens	68-72
29089331-0	2018	Prevalence of Aflatoxin-Associated TP53R249S Mutation in Hepatocellular Carcinoma in Hispanics in South Texas.	Aflatoxins	14-23	P53	Homo sapiens	35-39
29113888-0	2018	Ultrasensitive electrochemical immunosensing of tumor suppressor protein p53 in unprocessed human plasma and cell lysates using a novel nanocomposite based on poly-cysteine/graphene quantum dots/gold nanoparticle.	Graphite	173-181	P53	Homo sapiens	73-76
29113888-2	2018	In this work, p53-antibody was immobilized onto a green and biocompatible nanocomposite containing poly l-cysteine (P-Cys) as conductive matrix and graphene quantum dots (GQDs)/gold nanoparticles (GNPs) as dual amplification elements.	Graphite	148-156	P53	Homo sapiens	14-17
29391428-0	2018	beta-Sitosterol targets Trx/Trx1 reductase to induce apoptosis in A549 cells via ROS mediated mitochondrial dysregulation and p53 activation.	gamma-sitosterol	0-15	P53	Homo sapiens	126-129
29378575-6	2018	DHA, Omegaven  and oxaliplatin were associated with significant downregulation of VEGF and p53 protein, and upregulation of p21 protein.	fish oil triglycerides	5-13	P53	Homo sapiens	91-94
29515795-9	2018	In combination with Ad.p53-DC vaccine, the maximum-tolerated dose of indoximod was 1600 mg twice daily.	1-methyltryptophan	69-78	P53	Homo sapiens	23-26
29515795-16	2018	Conclusions: Indoximod 1600 mg twice daily with Ad.p53-DC was well tolerated.	1-methyltryptophan	13-22	P53	Homo sapiens	51-54
29541415-2	2018	We found that NSAIDs including celecoxib (CCB) and ibuprofen (IBU) significantly potentiated the cytotoxicity of Hsp90 inhibitors in human multidrug-resistant (MDR) cells expressing high levels of mutant p53 (mutp53) protein and P-glycoprotein (P-gp), and reversed Hsp90 inhibitor resistance caused by activation of heat shock factor 1 (HSF1) and by up-regulation of heat shock proteins (Hsps) and P-gp.	Celecoxib	31-40	P53	Homo sapiens	204-207
29541415-2	2018	We found that NSAIDs including celecoxib (CCB) and ibuprofen (IBU) significantly potentiated the cytotoxicity of Hsp90 inhibitors in human multidrug-resistant (MDR) cells expressing high levels of mutant p53 (mutp53) protein and P-glycoprotein (P-gp), and reversed Hsp90 inhibitor resistance caused by activation of heat shock factor 1 (HSF1) and by up-regulation of heat shock proteins (Hsps) and P-gp.	Celecoxib	42-45	P53	Homo sapiens	204-207
29308745-0	2018	Polyphyllin I Induces Cell Cycle Arrest and Cell Apoptosis in Human Retinoblastoma Y-79 Cells through Targeting p53.	polyphyllin I	0-13	P53	Homo sapiens	112-115
29308745-10	2018	RESULT: These results demonstrated that PPI exhibits anti-proliferation effect on human retinoblastoma Y-79 cells through modulating p53 expression, stabilization and activation.	polyphyllin I	40-43	P53	Homo sapiens	133-136
29866022-8	2018	Moreover, we observed that the inhibitory effect of BHP on cell proliferation and premature senescence in a p53-dependent manner.	bhp	52-55	P53	Homo sapiens	108-111
29793319-6	2018	The results indicated that oroxyloside significantly suppressed the proliferation of human glioma cells through inducing cell cycle arrest at G0/G1 phase through reducing Cyclin D1 and cyclin-dependent kinase 2 (CDK2) while enhancing p53 and p21 expressions.	oroxylin A-7-O-glucuronide	27-38	P53	Homo sapiens	234-237
29793319-9	2018	In vivo, oroxyloside administration significantly inhibited the glioma cell xenograft tumorigenesis through various signaling pathways, including suppression of Cyclin D1/CDK2 and ECM pathways, as well as potentiation of p53/p21 and Caspases pathways.	oroxylin A-7-O-glucuronide	9-20	P53	Homo sapiens	221-224
28949066-1	2018	In previous work, we presented experimental and theoretical evidence that D-3F or 4-N-(2-Amino-3-fluoropyridine)-4-deoxidation-4"-demethylepipofophyllotoxin induced G2 /M phase arrest and apoptosis, purportedly by increasing the expression of P53.	4-n-(2-amino-3-fluoropyridine)-4-deoxidation-4"-demethylepipofophyllotoxin	82-156	P53	Homo sapiens	243-246
29222275-7	2017	TP53 disruption by gene mutation and/or deletion associates with chemoimmunotherapy failure and mandates treatment with innovative drugs, including ibrutinib, idelalisib, or venetoclax.	ibrutinib	148-157	P53	Homo sapiens	0-4
28745318-8	2017	Our findings suggest a novel mechanism linking mucin-type core 3 O-glycan to the EMT-MET plasticity of CRC cells via MUC1/p53/miR-200c-dependent signaling cascade and shed light on therapeutic strategies to treat this malignancy.	3 o-glycan	63-73	P53	Homo sapiens	122-125
29234595-4	2017	Here we present a case of relapsed TP53 mutated CLL treated with ibrutinib as a bridge to alloHCT, discussing risks and benefits of different treatment options in a "real life" situation.	ibrutinib	65-74	P53	Homo sapiens	35-39
29061817-6	2017	CONCLUSION: The co-delivery of p53 plasmid DNA and bcl-2 AS ODN in PEI-CA complexes enhanced therapeutic activities of both p53 plasmid DNA and bcl-2 AS ODN.	pei-ca	67-73	P53	Homo sapiens	31-34
29061817-6	2017	CONCLUSION: The co-delivery of p53 plasmid DNA and bcl-2 AS ODN in PEI-CA complexes enhanced therapeutic activities of both p53 plasmid DNA and bcl-2 AS ODN.	pei-ca	67-73	P53	Homo sapiens	124-127
28608578-3	2017	Cantharidin has anticancer activity in vitro, since it is able of inducing p53-dependent apoptosis and double-strand breakage of DNA in cancer cells.	Cantharidin	0-11	P53	Homo sapiens	75-78
28691888-11	2017	The ability of gingipains to stimulate p53 and Bid expression was mimicked by PD-0325901 and MK-2206, the specific extracellular signal-regulated protein kinases (ERK) and protein kinase B (PKB) inhibitors, respectively.	MK 2206	93-100	P53	Homo sapiens	39-42
29072435-7	2017	These results showthe importance of 19-triisopropyl-andrographolide in its emerging selectivity to primary target on topoisomerase IIalphaenzyme, inducing DNA damage and apoptosis by p53- independent mechanism.	19-triisopropyl-andrographolide	36-67	P53	Homo sapiens	183-186
29022913-6	2017	Furthermore, anti-miR-301a-5p significantly blocked VAN-induced apoptosis and caspase activity in HK-2 cells, which was accompanied by downregulation of p53, and upregulation of MITF, HDGF and MDM-4 together.	Vancomycin	52-55	P53	Homo sapiens	153-156
29022913-11	2017	Together, these results show the novel MBD2/miR-301a-5p/MITF, HDGF and MDM-4/p53 pathway in VAN-induced AKI.	Vancomycin	92-95	P53	Homo sapiens	77-80
28765913-8	2017	Taken together, the results of the present study suggest that DSS inhibits the harmful effects of ALD on cardiomyocytes via interfering with the p53 signaling pathway.	3,4-dihydroxyphenyllactic acid	62-65	P53	Homo sapiens	145-148
28973705-3	2017	METHODS: Among individuals with multigene panel testing (inclusive of the TP53 gene) who were part of either the Inherited Cancer Registry or the Vanderbilt Hereditary Cancer Registry protocols and were confirmed to have a P/LP variant in TP53, pedigree was reviewed to characterize personal and family history, including original clinical context for genetic testing and whether they met clinical diagnostic criteria for TP53.	leucylproline	225-227	P53	Homo sapiens	239-243
28973705-3	2017	METHODS: Among individuals with multigene panel testing (inclusive of the TP53 gene) who were part of either the Inherited Cancer Registry or the Vanderbilt Hereditary Cancer Registry protocols and were confirmed to have a P/LP variant in TP53, pedigree was reviewed to characterize personal and family history, including original clinical context for genetic testing and whether they met clinical diagnostic criteria for TP53.	leucylproline	225-227	P53	Homo sapiens	239-243
28928376-5	2017	Subsequent administration of Oligo-Fucoidan to etoposide-treated cells promotes p53 accumulation, p21 expression and significant decreases in ataxia-telangiectasia-mutated (ATM), checkpoint kinase 1 (Chk1) and gamma-H2AX phosphorylation in p53+/+ cells compared with p53-/- cells.	oligo-fucoidan	29-43	P53	Homo sapiens	80-83
28928376-5	2017	Subsequent administration of Oligo-Fucoidan to etoposide-treated cells promotes p53 accumulation, p21 expression and significant decreases in ataxia-telangiectasia-mutated (ATM), checkpoint kinase 1 (Chk1) and gamma-H2AX phosphorylation in p53+/+ cells compared with p53-/- cells.	oligo-fucoidan	29-43	P53	Homo sapiens	240-243
28928376-5	2017	Subsequent administration of Oligo-Fucoidan to etoposide-treated cells promotes p53 accumulation, p21 expression and significant decreases in ataxia-telangiectasia-mutated (ATM), checkpoint kinase 1 (Chk1) and gamma-H2AX phosphorylation in p53+/+ cells compared with p53-/- cells.	oligo-fucoidan	29-43	P53	Homo sapiens	240-243
28444915-0	2017	Hydroquinone induces TK6 cell growth arrest and apoptosis through PARP-1/p53 regulatory pathway.	hydroquinone	0-12	P53	Homo sapiens	73-76
28714021-6	2017	These findings demonstrated that iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/t-BID/cytochrome c/caspase-3 signaling pathway.	Iodine-131	33-43	P53	Homo sapiens	104-107
28436014-3	2017	We assessed the extent to which the pharmacokinetic characteristics are a function of the staple for a peptide inhibiting the interaction of p53 with the human double minute 2 (Hdm2) protein and differ from those of the standard cationic cell-penetrating peptide nona-arginine.	nona-	263-268	P53	Homo sapiens	141-144
28453190-8	2017	The increased expression of genes involved in the NGFR-MAPK10-TP53-Bax/Bcl2 pathway during incubation with AZA plus everolimus was validated by western blotting in MZ-CRC-1 cells.	Everolimus	116-126	P53	Homo sapiens	62-66
28258023-4	2017	Additionally, excessive ROS caused by physapubescin B also induced p53-dependent apoptotic cell death.	physapubescin B	38-53	P53	Homo sapiens	67-70
28554861-4	2017	Abeta1-40-induced ROS production and p53 expression were increased as determined by DCF-derived fluorescence using flow cytometry and Western blotting and reduced in response to galantamine pretreatment.	Pentostatin	84-87	P53	Homo sapiens	37-40
28726196-2	2017	The mechanisms of tumor cell sensitivity to temozolomide are complex and are determined by not only the level of O6-methylguanine-DNA-methyltransferase (MGTM) expression, but also activity of oncosuppressor protein p53.	Temozolomide	44-56	P53	Homo sapiens	215-218
28415713-7	2017	Blocking FAK with its inhibitor can also enhance miR-135a expression through inducing p53.	mir-135a	49-57	P53	Homo sapiens	86-89
28454566-8	2017	RESULTS: AAE induced apoptosis via PTEN/p53/PDK1/Akt signal pathways through PTEN/p53-independent manner.	acetoacetic acid	9-12	P53	Homo sapiens	82-85
28454566-14	2017	In consequence, these results indicate that AAE induced apoptosis by means of a mitochondrial event through the regulation of proteins such as Bax, Bak and cytochrome c in PDK1/Akt signaling pathways via PTEM/p53-independent manner.	acetoacetic acid	44-47	P53	Homo sapiens	209-212
28427200-12	2017	P53 was involved in the resistance mechanism of temozolomide mediated by Nrf2 and NQO1.	Temozolomide	48-60	P53	Homo sapiens	0-3
28361959-6	2017	Gene knockdown experiments revealed that p53 downregulation only increased the threshold of dinaciclib induced apoptosis in iPS cells.	IPS	124-127	P53	Homo sapiens	41-44
28330470-12	2017	KEGG pathway analysis showed that DHA may induce the apoptosis of cancer cells preferentially through mediating P53, MAPK, TNF, PI3K/AKT, and NF-kappaB signaling pathways.	Docosahexaenoic Acids	34-37	P53	Homo sapiens	112-115
28330470-14	2017	The pro-apoptotic effect of DHA on DU145 cells may involve mediation various pathways, especially P53, MAPK, TNF, PI3K/AKT, and NF-kappaB signaling pathways.	Docosahexaenoic Acids	28-31	P53	Homo sapiens	98-101
28182987-8	2017	This Cu(II) complex induced neither the production of reactive oxygen species (ROS) nor the accumulation of p53 protein, suggesting the lack of DNA damage.	cu(ii)	5-11	P53	Homo sapiens	108-111
27535981-8	2017	A validation sample of 15 CLL carrying TP53 mutations, of which 13 carried both del17p and a TP53 mutation, confirmed substantially less sensitivity to ibrutinib-induced apoptosis.Conclusions: This study identifies that CLL harboring del17p/TP53-mutated cells are substantially less sensitive to ibrutinib-induced apoptosis than del17p/TP53 wild-type cells.	ibrutinib	152-161	P53	Homo sapiens	39-43
27535981-8	2017	A validation sample of 15 CLL carrying TP53 mutations, of which 13 carried both del17p and a TP53 mutation, confirmed substantially less sensitivity to ibrutinib-induced apoptosis.Conclusions: This study identifies that CLL harboring del17p/TP53-mutated cells are substantially less sensitive to ibrutinib-induced apoptosis than del17p/TP53 wild-type cells.	ibrutinib	152-161	P53	Homo sapiens	93-97
27535981-8	2017	A validation sample of 15 CLL carrying TP53 mutations, of which 13 carried both del17p and a TP53 mutation, confirmed substantially less sensitivity to ibrutinib-induced apoptosis.Conclusions: This study identifies that CLL harboring del17p/TP53-mutated cells are substantially less sensitive to ibrutinib-induced apoptosis than del17p/TP53 wild-type cells.	ibrutinib	152-161	P53	Homo sapiens	93-97
27535981-8	2017	A validation sample of 15 CLL carrying TP53 mutations, of which 13 carried both del17p and a TP53 mutation, confirmed substantially less sensitivity to ibrutinib-induced apoptosis.Conclusions: This study identifies that CLL harboring del17p/TP53-mutated cells are substantially less sensitive to ibrutinib-induced apoptosis than del17p/TP53 wild-type cells.	ibrutinib	152-161	P53	Homo sapiens	93-97
28035418-5	2017	Importantly, RTS inhibited the cellular antioxidant defense system leading to abundant ROS accumulation, and activated cell cycle arrest and mitochondrial pathway of apoptosis mediated by activating p53 due to cellular uncontrolled ROS.	rts	13-16	P53	Homo sapiens	199-202
27943171-0	2017	Spiro-oxindoles as a Promising Class of Small Molecule Inhibitors of p53-MDM2 Interaction Useful in Targeted Cancer Therapy.	spiro-oxindoles	0-15	P53	Homo sapiens	69-72
27943171-5	2017	In this review, we present a comprehensive account of the systematic development of and recent progress in diverse spiro-oxindole derivatives active as potent selective inhibitors of p53-MDM2 interaction with special emphasis on spiro-pyrrolidinyl oxindoles (the MI series), their mechanism of action, and structure-activity relationship.	2-methyl-4-isothiazolin-3-one	263-265	P53	Homo sapiens	183-186
27943171-6	2017	This review will help in understanding the molecular mechanism of p53 reactivation by spiro-oxindoles in tumor tissues and also facilitates the design and exploration of more potent analogues with high efficacy and low side effects for the treatment of cancer.	spiro-oxindoles	86-101	P53	Homo sapiens	66-69
27793694-8	2017	In addition, BI 6727 treatment caused a marked induction of p53 and p21 in vitro as well as in vivo.	BI 6727	13-20	P53	Homo sapiens	60-63
28185174-3	2017	Ibrutinib was proven as a primary choice for patients with the TP53 gene deletion/mutation, who otherwise have no active treatment available.	ibrutinib	0-9	P53	Homo sapiens	63-67
27813686-3	2017	Here, we find out whether the effect of sodium selenite and selenomethionine on telomerase activity in human umbilical cord-derived mesenchymal stem cells (hUCMSCs) is associated with different levels of c-Myc and p53 expression.	Sodium Selenite	40-55	P53	Homo sapiens	214-217
28232952-11	2017	To target the mutant p53- poly ADP-ribose polymerase-minichromosome maintenance axis we treated cells with the poly ADP-ribose polymerase inhibitor talazoparib and the alkylating agent temozolomide and detected synergistic activation of apoptosis only in the presence of mutant p53.	Temozolomide	185-197	P53	Homo sapiens	278-281
27880058-0	2017	Fish-Oil-Derived DHA-mediated Enhancement of Apoptosis in Acute Lymphoblastic Leukemia Cells is Associated with Accumulation of p53, Downregulation of Survivin, and Caspase-3 Activation.	Docosahexaenoic Acids	17-20	P53	Homo sapiens	128-131
27880058-4	2017	In this study, we investigated the alterations of the p53 and survivin expression and induction of apoptosis in DHA-treated Molt-4 cells that serve as a model for ALL cells.	Docosahexaenoic Acids	112-115	P53	Homo sapiens	54-57
27880058-7	2017	We also found that treatment for 48 h with 200 muM DHA resulted in 10.8- and 3.6-fold increase in p53 protein level and caspase-3 activation followed by 4.7-and 1.6-fold decrease in survivin mRNA and protein levels, respectively, compared to untreated cells.	Docosahexaenoic Acids	51-54	P53	Homo sapiens	98-101
27880058-8	2017	Treatment of cells with different concentrations of DHA dramatically increased the p53/survivin and caspase-3/survivin ratios by 2.8- to 16.9-fold and 3.3 to 5.6-fold increases, respectively, compared to untreated cells.	Docosahexaenoic Acids	52-55	P53	Homo sapiens	83-86
27880058-10	2017	In conclusion, p53 and survivin may provide promising targets of DHA in ALL cells and this compound with high proapoptotic capacity represents the possibility of its therapeutic application for ALL treatment.	Docosahexaenoic Acids	65-68	P53	Homo sapiens	15-18
28000777-0	2016	BACH1 Promotes Temozolomide Resistance in Glioblastoma through Antagonizing the Function of p53.	Temozolomide	15-27	P53	Homo sapiens	92-95
28000777-5	2016	Further investigation revealed that BACH1 activation significantly enhanced the expression of MGMT, and depletion of p53 disrupted the effects of BACH1 on MGMT and temozolomide resistance.	Temozolomide	164-176	P53	Homo sapiens	117-120
28000777-9	2016	Collectively, our findings identify a potential mechanism by which wild-type TP53 GBM cells develop resistance to temozolomide and suggest that targeting this pathway may be beneficial for overcoming resistance.	Temozolomide	114-126	P53	Homo sapiens	77-81
27941921-6	2016	In human renal tubular epithelial cell line (HK-2), VAN induced p53 accumulation and miR-192-5p expression.	Vancomycin	52-55	P53	Homo sapiens	64-67
27917009-1	2016	We established an experimental system that can induce p53-dependent apoptosis by doxycycline treatment to analyze characteristics of the apoptosis-resistant cancer cell subpopulation in the human breast cancer cell line HCC1937.	Doxycycline	81-92	P53	Homo sapiens	54-57
27592685-4	2016	On the other hand, the microRNA miR-125b is reported to repress p53 expression and stress-induced apoptosis.	mir-125b	32-40	P53	Homo sapiens	64-67
27644244-9	2016	In conclusion, these results demonstrated that PP-22 activated p38, inhibited cdc25B, increased p-cdc2 (Tyr15), and triggered S and G2/M phase arrest, as well as activated p53 through the p38-p53 pathway, inhibited the MAPK/ERK pathway, activated the caspase 8/caspase 3 pathway, and triggered the extrinsic apoptotic pathway in SCC-15 cells.	CHEMBL86597	47-52	P53	Homo sapiens	172-175
27644244-9	2016	In conclusion, these results demonstrated that PP-22 activated p38, inhibited cdc25B, increased p-cdc2 (Tyr15), and triggered S and G2/M phase arrest, as well as activated p53 through the p38-p53 pathway, inhibited the MAPK/ERK pathway, activated the caspase 8/caspase 3 pathway, and triggered the extrinsic apoptotic pathway in SCC-15 cells.	CHEMBL86597	47-52	P53	Homo sapiens	192-195
27780269-0	2016	Comparative Assessment of Vitamin-B12, Folic Acid and Homocysteine Levels in Relation to p53 Expression in Megaloblastic Anemia.	Homocysteine	54-66	P53	Homo sapiens	89-92
27698449-6	2016	By applying antioxidant Trolox, we also confirmed that ROS mediated p53 activation.	6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid	24-30	P53	Homo sapiens	68-71
27464528-5	2016	Indigocarpan induces p53-dependent p21 upregulation and apoptosis in LS174T cells, upregulates p53 and p21(WAF1) protein levels, enhances cleavage of caspase-3 and downregulates cyclin D1, cyclin B1 and PCNA protein levels, indicating its role in modulating cell cycle progression.	Indigocarpan	0-12	P53	Homo sapiens	21-24
27464528-5	2016	Indigocarpan induces p53-dependent p21 upregulation and apoptosis in LS174T cells, upregulates p53 and p21(WAF1) protein levels, enhances cleavage of caspase-3 and downregulates cyclin D1, cyclin B1 and PCNA protein levels, indicating its role in modulating cell cycle progression.	Indigocarpan	0-12	P53	Homo sapiens	95-98
27213669-6	2016	Adipose tissue HCB concentrations were associated positively with ER and PR expression (p-trends=0.044 and 0.005, respectively) and negatively with E-Cadherin and p53 expression (p-trends=0.012 and 0.027, respectively).	Hexachlorobenzene	15-18	P53	Homo sapiens	163-166
27515134-0	2016	Hydroquinone-induced malignant transformation of TK6 cells by facilitating SIRT1-mediated p53 degradation and up-regulating KRAS.	hydroquinone	0-12	P53	Homo sapiens	90-93
27729773-0	2016	Andrographolide promotes vincristine-induced SK-NEP-1 tumor cell death via PI3K-AKT-p53 signaling pathway.	andrographolide	0-15	P53	Homo sapiens	84-87
27656146-4	2016	Cyanidin-3-O-glucoside also decreased the UVB-augmented levels of the DNA damage indicators phospho-p53 and phospho-ATM/ATR.	cyanidin-3-o-glucoside	0-22	P53	Homo sapiens	100-103
30090463-0	2016	Hydroxylated-graphene quantum dots induce cells senescence in both p53-dependent and -independent manner.	Graphite	13-21	P53	Homo sapiens	67-70
27402273-0	2016	A novel alkaloid, evodiamine causes nuclear localization of cytochrome-c and induces apoptosis independent of p53 in human lung cancer cells.	evodiamine	18-28	P53	Homo sapiens	110-113
27402273-12	2016	Pifithrin-alpha, a p53 inhibitor, slightly inhibited growth of A549 cells and under p53 inhibitory condition evodiamine-induced apoptosis could not be reversed.	evodiamine	109-119	P53	Homo sapiens	84-87
27402273-13	2016	Together these findings suggest that evodiamine is a strong inducer of apoptosis in lung epithelial cancer cells independent of their p53 status and that could involve both intrinsic as well as extrinsic pathway of apoptosis.	evodiamine	37-47	P53	Homo sapiens	134-137
27586304-9	2016	We found that 198 out of 3177 Alu-exonized genes exhibit signatures of selection within Alu-miRNA sites, with 60 of them containing SNPs supported by multiple evidences (global-FST &gt; 0.3, pair-wise-FST &gt; 0.5, Fay-Wu"s H &lt; -20, iHS &gt; 2.0, high DeltaDAF) and implicated in p53 network.	METHYL HYDROGEN (S)-ACETYLPHOSPHONATE	30-33	P53	Homo sapiens	283-286
27431420-6	2016	The current study demonstrated that the rs78378222 polymorphism minor allele introduces a novel potential miR-125b binding site in the TP53 3"-UTR with a consecutive 8-bp perfect match, creating a "gain-of-function" variant and affecting the regulation of TP53 expression.	mir-125b	106-114	P53	Homo sapiens	135-139
27431420-6	2016	The current study demonstrated that the rs78378222 polymorphism minor allele introduces a novel potential miR-125b binding site in the TP53 3"-UTR with a consecutive 8-bp perfect match, creating a "gain-of-function" variant and affecting the regulation of TP53 expression.	mir-125b	106-114	P53	Homo sapiens	256-260
27431420-10	2016	Additionally, transfection with 50 nM miR-125b mimics markedly reduced the mRNA and protein expression levels of TP53 in the cultured lens epithelial cells, and miR-125b significantly induced apoptosis in the epithelial cells compared with negative control cells.	mir-125b	38-46	P53	Homo sapiens	113-117
27260513-0	2016	8-Oxo-7,8-dihydro-2"-deoxyguanosine and other lesions along the coding strand of the exon 5 of the tumour suppressor gene P53 in a breast cancer case-control study.	8-ohdg	0-35	P53	Homo sapiens	122-125
27260513-3	2016	We detected a significant "in vitro" generation of 8-oxodG between the codons 163 and 175, corresponding to a TP53 region with high mutation prevalence, after treatment with xanthine plus xanthine oxidase, a ROS-generating system.	8-ohdg	51-58	P53	Homo sapiens	110-114
27177208-0	2016	A novel all-trans retinoic acid derivative 4-amino-2-trifluoromethyl-phenyl retinate inhibits the proliferation of human hepatocellular carcinoma HepG2 cells by inducing G0/G1 cell cycle arrest and apoptosis via upregulation of p53 and ASPP1 and downregulation of iASPP.	4-amino-2-trifluoromethyl-phenyl retinate	43-84	P53	Homo sapiens	228-231
27298583-6	2016	Aspartame suppresses apoptosis process in cancer cells by down-regulation of mRNA expression of tumor suppressor gene p53, and pro-apoptotic gene bax.	Aspartame	0-9	P53	Homo sapiens	118-121
26477317-8	2016	A fine characterization of the DNA deformation caused by p53 binding is obtained, with "static" deformations always present and measured by the slide parameter in the central thymine-adenine base pairs; we also detect "dynamic" deformations switched on and off by particular p53 tetrameric conformations and measured by the roll and twist parameters in the same base pairs.	Thymine	175-182	P53	Homo sapiens	57-60
27284738-6	2016	We show that ibrutinib was effective in increasing survival, activating cellular programs outside the p53 pathway and did not place selective pressure on the remaining wild-type Trp53 allele.	ibrutinib	13-22	P53	Homo sapiens	102-105
27284738-7	2016	These data provide evidence that ibrutinib acts as an effective treatment for aggressive forms of CLL with TP53 mutations.	ibrutinib	33-42	P53	Homo sapiens	107-111
27084510-6	2016	This study reports on andrographolide induced apoptosis and its possible mechanism in highly proliferative, invasive breast cancer cells, MDA-MB-231 lacking a functional p53 and estrogen receptor (ER).	andrographolide	22-37	P53	Homo sapiens	170-173
27040702-5	2016	Patients with a del(17p) or TP53 mutation should be treated with the kinase inhibitors ibrutinib or a combination of idelalisib and rituximab.	ibrutinib	87-96	P53	Homo sapiens	28-32
26676373-7	2016	Furthermore, p53-deficient FA HSCs are more sensitive to 2-DG-mediated metabolic stress.	Deoxyglucose	57-61	P53	Homo sapiens	13-16
26597532-1	2016	We first demonstrated that cordycepin inhibited cell growth and triggered apoptosis in U87MG cells with wild-type p53, but not in T98G cells with mutant-type p53.	cordycepin	27-37	P53	Homo sapiens	114-117
26398108-8	2016	Selinexor induced p53, p21, and cleaved PARP in several solid tumor models.	selinexor	0-9	P53	Homo sapiens	18-21
26585673-7	2016	Furthermore, we observed that miR-125b inhibits p53 to induce fibroblast proliferation.	mir-125b	30-38	P53	Homo sapiens	48-51
27221835-2	2016	This study investigated the effect of celecoxib on cell cycle arrest in HeLa cervical cancer cells through p53 expression.	Celecoxib	38-47	P53	Homo sapiens	107-110
26599622-3	2016	At the physiological pH 7.4 in the bloodstream, PEG-PLL(DA) could extend the circulating time by shielding the positively charged FK/p53 complexes.	amsonic acid	56-58	P53	Homo sapiens	133-136
27075390-3	2016	METHODS: We used a Real-Time PCR test for measuring expression of p53 gene also flow cytometry assay for apoptotic and survival cell rate after treatment of MCF-7 cells with A1 receptor agonist CPA (N6-Cyclopentyladenosine) and A1 receptor antagonist DPCPX (1,3-dipropyl-8-cyclopentylxanthine) in 24,48 and 72 hours.	N(6)-cyclopentyladenosine	194-197	P53	Homo sapiens	66-69
27075390-6	2016	CPA treatment increased the survival cell rate and down-regulated this apoptosis-relevant gene P53 (p &gt; 0.05).	N(6)-cyclopentyladenosine	0-3	P53	Homo sapiens	95-98
27992315-0	2016	Inhibition of the p53 Y220C Mutant by 1-Hydroxy-2- Methylanthraquinone Derivatives: A Novel Strategy for Cancer Therapy.	1-hydroxy-2-methylanthraquinone	38-70	P53	Homo sapiens	18-21
27992315-4	2016	Docking of mutated p53 was performed to determine the drug of choice from the derivatives of 1-hydroxy-2- methylanthraquinone exhibiting anti-cancer properties.	1-hydroxy-2-methylanthraquinone	93-125	P53	Homo sapiens	19-22
26942868-5	2016	EPA/DHA significantly induced PPARgamma and p53 overexpression as observed in immunoblotting assay and the induction of p53 by EPA/DHA was abolished by GW9662.	Docosahexaenoic Acids	4-7	P53	Homo sapiens	44-47
26942868-5	2016	EPA/DHA significantly induced PPARgamma and p53 overexpression as observed in immunoblotting assay and the induction of p53 by EPA/DHA was abolished by GW9662.	Docosahexaenoic Acids	131-134	P53	Homo sapiens	120-123
26555243-0	2015	Novel beta-Carboline/Hydroxamic Acid Hybrids Targeting Both Histone Deacetylase and DNA Display High Anticancer Activity via Regulation of the p53 Signaling Pathway.	Hydroxamic Acids	21-36	P53	Homo sapiens	143-146
26428461-0	2015	A stapled peptide antagonist of MDM2 carried by polymeric micelles sensitizes glioblastoma to temozolomide treatment through p53 activation.	Temozolomide	94-106	P53	Homo sapiens	125-128
26451628-0	2015	Polychlorinated Biphenyl Quinone Metabolite Promotes p53-Dependent DNA Damage Checkpoint Activation, S-Phase Cycle Arrest and Extrinsic Apoptosis in Human Liver Hepatocellular Carcinoma HepG2 Cells.	polychlorinated biphenyl quinone	0-32	P53	Homo sapiens	53-56
26352194-2	2015	In the present study, cinnamaldehyde derivative-induced apoptosis and its signaling pathways were assessed in p53-wild (SGT) and p53-mutant (YD-10B) human head and neck cancer cells.	cinnamaldehyde	22-36	P53	Homo sapiens	110-113
26352194-2	2015	In the present study, cinnamaldehyde derivative-induced apoptosis and its signaling pathways were assessed in p53-wild (SGT) and p53-mutant (YD-10B) human head and neck cancer cells.	cinnamaldehyde	22-36	P53	Homo sapiens	129-132
26400171-0	2015	Base damage, local sequence context and TP53 mutation hotspots: a molecular dynamics study of benzo[a]pyrene induced DNA distortion and mutability.	Benzo(a)pyrene	94-108	P53	Homo sapiens	40-44
26400171-3	2015	Benzo[a]pyrene,diol epoxide (BPDE) is a potent cigarette smoke carcinogen that forms guanine adducts at TP53 CpG mutation hotspot sites including codons 157, 158, 245, 248 and 273.	Benzo(a)pyrene	0-14	P53	Homo sapiens	104-108
24798519-0	2015	Gallotannin is a DNA damaging compound that induces senescence independently of p53 and p21 in human colon cancer cells.	Hydrolyzable Tannins	0-11	P53	Homo sapiens	80-83
24798859-5	2015	Here, we report that the environmental carcinogen benzo[a]pyrene (BaP) upregulated the expression of seven p53-targeting miRNAs (miR-25, miR-15a, miR-16, miR-92, miR-125b, miR-141, and miR-200a), while 2,3,7,8-tetrachlorodibenzo-rho-dioxin (TCDD) upregulated two of them (miR-25 and miR-92) in MM cells.	Benzo(a)pyrene	50-64	P53	Homo sapiens	107-110
25388787-3	2015	Benzimidazole libraries were prepared using an efficient solution-phase approach and screened for inhibition of the MDM2-p53 and MDMX-p53 protein-protein interactions.	benzimidazole	0-13	P53	Homo sapiens	121-124
25388787-3	2015	Benzimidazole libraries were prepared using an efficient solution-phase approach and screened for inhibition of the MDM2-p53 and MDMX-p53 protein-protein interactions.	benzimidazole	0-13	P53	Homo sapiens	134-137
26189912-4	2015	SQDG selectively targets ALL MOLT-4 cells by inhibiting catalytic activity of topoisomerase I enzyme and inducing p53 dependent apoptotic pathway.	sulfoquinovosyl diglyceride	0-4	P53	Homo sapiens	114-117
26189912-6	2015	Down-regulation of topoisomerase I or p53 renders the cells less sensitive for SQDG, while ectopic expression of wild type p53 protein in p53 deficient K562 cells results in chemosensitization of the cells for SQDG.	sulfoquinovosyl diglyceride	79-83	P53	Homo sapiens	38-41
26189912-6	2015	Down-regulation of topoisomerase I or p53 renders the cells less sensitive for SQDG, while ectopic expression of wild type p53 protein in p53 deficient K562 cells results in chemosensitization of the cells for SQDG.	sulfoquinovosyl diglyceride	210-214	P53	Homo sapiens	123-126
26189912-6	2015	Down-regulation of topoisomerase I or p53 renders the cells less sensitive for SQDG, while ectopic expression of wild type p53 protein in p53 deficient K562 cells results in chemosensitization of the cells for SQDG.	sulfoquinovosyl diglyceride	210-214	P53	Homo sapiens	123-126
25756738-10	2015	SUD also induced apoptosis in MCF-7 and BGC-823 cell lines through the mitochondrial pathway in a p53-dependent manner.	4-diphosphocytidyl-2C methylerythritol 2-phosphate	0-3	P53	Homo sapiens	98-101
26110921-6	2015	Mechanistic studies suggested that As4S4 acted synergistically with As3+ to down-regulate Bcl-2 and nuclear factor-kappaB expression, up-regulate Bax and p53 expression, and induce activation of caspase-12 and caspase-3.	as3+	68-72	P53	Homo sapiens	154-157
25698149-5	2015	Results indicated that TNBC patients with a p53-positive tumor had a shorter relapse-free and overall survival than patients carrying a p53-negative TNBC, corroborating our hypothesis about the relationship between TNBC phenotype (basal-like versus normal-like) and p53 status as predictor of response to anthracycline/CMF-based chemotherapy.	CMF regimen	319-322	P53	Homo sapiens	44-47
25625235-0	2015	p53 upregulated modulator of apoptosis sensitizes drug-resistant U251 glioblastoma stem cells to temozolomide through enhanced apoptosis.	Temozolomide	97-109	P53	Homo sapiens	0-3
25625235-7	2015	TMZ achieves its cytotoxic effect by inducing DNA lesions and p53 upregulated modulator of apoptosis (PUMA) is an essential mediator of DNA damage-induced apoptosis independently of p53 status.	Temozolomide	0-3	P53	Homo sapiens	62-65
28962410-0	2015	Occupational health hazards of trichloroethylene among workers in relation to altered mRNA expression of cell cycle regulating genes (p53, p21, bax and bcl-2) and PPARA.	Trichloroethylene	31-48	P53	Homo sapiens	134-137
25851939-3	2015	The results suggest that chromane containing glitazones are apoptic agonist (activating p53 by intrinsic pathway leading to the apoptosis) and those which do not contain the chromane are devoid of this.	Chromans	25-33	P53	Homo sapiens	88-91
25851939-6	2015	Immunoblot analysis further confirm our hypothesis that troglitazone (chromane containing glitazone), but not rosiglitazone and pioglitazone (non-chromane containing glitazone) increased the levels of p53 in a time-dependent manner.	Chromans	70-78	P53	Homo sapiens	201-204
25681668-0	2015	The synergistic effect of combination temozolomide and chloroquine treatment is dependent on autophagy formation and p53 status in glioma cells.	Temozolomide	38-50	P53	Homo sapiens	117-120
25681668-4	2015	Combination treatment of U87 cell (wild type p53) with TMZ and CQ synergistically reduced cell proliferation and enhanced apoptosis, with increased sub-G1 hypodiploid cells and caspase activation.	Temozolomide	55-58	P53	Homo sapiens	45-48
25681668-12	2015	Our data support the beneficial effect of combination treatment with TMZ and CQ in glioma via differential autophagy-associated mechanisms, depending on p53 status.	Temozolomide	69-72	P53	Homo sapiens	153-156
25758253-4	2015	A secondary objective was to determine the role of the p53 family of transcriptional regulators, commonly mutated in TNBC, in determining the phenotypic response to the AurA inhibitor alisertib (MLN8237).	MLN 8237	184-193	P53	Homo sapiens	55-58
25758253-6	2015	The induction of apoptosis in response to alisertib exposure was dependent on p53 and p73 activity.	MLN 8237	42-51	P53	Homo sapiens	78-81
25758253-7	2015	In the absence of functional p53 or p73, there was a shift in the phenotypic response following alisertib exposure from apoptosis to cellular senescence.	MLN 8237	96-105	P53	Homo sapiens	29-32
25915649-9	2015	Furthermore, we demonstrated that the combination of DHM and NDP activated the p53/Bcl-2 signaling pathway, which resulted in mitochondrial dysfunction and induced cell death and growth inhibition in HCC cells.	nedaplatin	61-64	P53	Homo sapiens	79-82
25799988-2	2015	Here we show that p53 inhibits cystine uptake and sensitizes cells to ferroptosis, a non-apoptotic form of cell death, by repressing expression of SLC7A11, a key component of the cystine/glutamate antiporter.	Cystine	31-38	P53	Homo sapiens	18-21
25799988-2	2015	Here we show that p53 inhibits cystine uptake and sensitizes cells to ferroptosis, a non-apoptotic form of cell death, by repressing expression of SLC7A11, a key component of the cystine/glutamate antiporter.	Cystine	179-186	P53	Homo sapiens	18-21
25799988-6	2015	Our findings uncover a new mode of tumour suppression based on p53 regulation of cystine metabolism, ROS responses and ferroptosis.	Cystine	81-88	P53	Homo sapiens	63-66
25588103-7	2015	Their photoprotective effects also involved the enhanced repair of 8-hydroxy-2"-deoxyguanosine (8-OHdG) and cyclobutane pyrimidine dimers (CPDs) as mediated by the augment of p53 expression after UVA radiation.	cyclobutane pyrimidine	108-130	P53	Homo sapiens	175-178
25326397-7	2015	IOWA-1T harbors a homozygous R248Q mutation of the TP53 gene; in vitro invasion assay was comparable to BT-549 and greater than MCF-7.	benzothiazole	104-106	P53	Homo sapiens	51-55
25834606-8	2015	Multivariate analysis showed that only p53 expression was independently associated with pCR to NAC (odds ratio, 3.961; p=0.003).	nac	95-98	P53	Homo sapiens	39-42
25834606-11	2015	CONCLUSION: Expression of p53 was significantly associated with pCR after NAC in patients with TNBC, suggesting that this biomarker might be particularly valuable in identifying TNBC patients prone to have residual disease after NAC.	nac	74-77	P53	Homo sapiens	26-29
25834606-11	2015	CONCLUSION: Expression of p53 was significantly associated with pCR after NAC in patients with TNBC, suggesting that this biomarker might be particularly valuable in identifying TNBC patients prone to have residual disease after NAC.	nac	229-232	P53	Homo sapiens	26-29
25366143-4	2015	Treatment of a human tongue squamous cell carcinoma cell line, HSC-3, with alisertib to inhibition of Aurora-A kinases reduced proliferation and induced apoptosis, which was accompanied by activation of the ATM/Chk2/p53 pathway.	MLN 8237	75-84	P53	Homo sapiens	216-219
25611347-0	2015	Quinofuracins A-E, produced by the fungus Staphylotrichum boninense PF1444, show p53-dependent growth suppression.	quinofuracins a-e	0-17	P53	Homo sapiens	81-84
25611347-1	2015	Quinofuracins A-E, novel anthraquinone derivatives containing beta-D-galactofuranose that were isolated from the fungus Staphylotrichum boninense PF1444, induced p53-dependent cell death in human tumor cells.	quinofuracins a-e	0-17	P53	Homo sapiens	162-165
24469051-0	2015	Selective killing of lung cancer cells by miRNA-506 molecule through inhibiting NF-kappaB p65 to evoke reactive oxygen species generation and p53 activation.	mirna-506	42-51	P53	Homo sapiens	142-145
25667459-6	2015	Results from western blotting showed that cantharidin inhibited the expression of DNA-dependent serine/threonine protein kinase, poly-ADP ribose polymerase, phosphate-ataxia-telangiectasia and RAD3-related, O-6-methylguanine-DNA methyltransferase, breast cancer susceptibility protein 1, mediator of DNA damage checkpoint protein 1, phospho-histone H2A.X, but increased that of phosphorylated p53 following 6 and 24 h treatment.	Cantharidin	42-53	P53	Homo sapiens	393-396
25667459-7	2015	Confocal laser microscopy was used to examine the protein translocation; cantharidin suppressed the levels of p-H2A.X and MDC1 but increased the levels of p-p53 in TSGH8301 cells.	Cantharidin	73-84	P53	Homo sapiens	157-160
25444896-8	2015	Oxovanadium compounds may thus represent novel leads as p53-independent therapeutics for neuroblastoma.	Vanadium(II) oxide	0-11	P53	Homo sapiens	56-59
25510514-0	2015	Affinities of organophosphate flame retardants to tumor suppressor gene p53: an integrated in vitro and in silico study.	Organophosphates	14-29	P53	Homo sapiens	72-75
26553592-4	2015	Furthermore, following treatment with the autophagy inducer temozolomide (TMZ) and low glucose (LG), MIR517C degraded KPNA2 (karyopherin alpha 2 [RAG cohort 1, importin alpha 1]) and subsequently disturbed the nuclear translocation of TP53 in the GBM cell line U87 in vitro.	Temozolomide	60-72	P53	Homo sapiens	235-239
26553592-4	2015	Furthermore, following treatment with the autophagy inducer temozolomide (TMZ) and low glucose (LG), MIR517C degraded KPNA2 (karyopherin alpha 2 [RAG cohort 1, importin alpha 1]) and subsequently disturbed the nuclear translocation of TP53 in the GBM cell line U87 in vitro.	Temozolomide	74-77	P53	Homo sapiens	235-239
26785947-3	2015	Treatment of the Jurkat cells with the ATI5 compound for 48 hrs resulted in a strong G2/M cell cycle arrest and p53-independent apoptotic cell death accompanied by the induction of the active form of caspase-3 and poly(ADP-ribose) polymerase-1 (PARP-1) cleavage.	ati5	39-43	P53	Homo sapiens	112-115
25590866-0	2015	Cordycepin induces cell cycle arrest and apoptosis by inducing DNA damage and up-regulation of p53 in Leukemia cells.	cordycepin	0-10	P53	Homo sapiens	95-98
26199569-0	2015	Effect of beta-sitosterol on the expression of HPV E6 and p53 in cervical carcinoma cells.	gamma-sitosterol	10-25	P53	Homo sapiens	58-61
25092802-5	2015	Inhibition of astrocyte proliferation by ammonia was mediated by a l-methionine sulfoximine-, oxidative stress-, and p38(MAPK) -dependent activation of p53 associated with enhanced transcription of cell cycle inhibitory genes GADD45alpha and p21.	Ammonia	41-48	P53	Homo sapiens	152-155
25092802-5	2015	Inhibition of astrocyte proliferation by ammonia was mediated by a l-methionine sulfoximine-, oxidative stress-, and p38(MAPK) -dependent activation of p53 associated with enhanced transcription of cell cycle inhibitory genes GADD45alpha and p21.	L-Methionine sulfoximine	67-91	P53	Homo sapiens	152-155
26062943-6	2015	Fortunately, significant progress in the understanding of CLL biology has enabled the development of new molecular drugs targeting the B-cell receptor signaling pathway, such as ibrutinib and idelalisib, which have shown impressive results in patients with relapsed/refractory disease or with TP53 mutation/deletion.	ibrutinib	178-187	P53	Homo sapiens	293-297
25164962-4	2015	Sequential treatment of Taxol or cisplatin, followed by MK-2206, induced a synergistic inhibition of cell proliferation and effectively promoted cell death, either by inhibiting the phosphorylation of Akt and its downstream effectors 4E-BP1 and p70S6K in SKOV3 cells or by restoring p53 levels, which were downregulated after Taxol or cisplatin treatment, in ES2 cells.	MK 2206	56-63	P53	Homo sapiens	283-286
25751508-7	2015	In this article, we have shown for the first time that 2DG induced a transient expression of p21 and a continuous expression of p53 in colorectal cancer cells (SW620).	Deoxyglucose	55-58	P53	Homo sapiens	128-131
25751508-9	2015	The effects of 2DG on p21 and p53 protein levels were totally independent of its inhibitory effect on either hexokinase or ATP levels.	Deoxyglucose	15-18	P53	Homo sapiens	30-33
25876968-0	2015	[Inhibitors of DNA-dependent protein kinase promote p53-independent apoptosis induced by 1, 4-benzoquinone in HL60 cells].	quinone	89-106	P53	Homo sapiens	52-55
25876968-13	2015	CONCLUSION: Inhibitors of DNA-PK, NU7026 and Wortmannin, promote p53-independent apoptosis induced by 1, 4-benzoquinone in HL60 cells.	quinone	102-119	P53	Homo sapiens	65-68
25539912-0	2014	WNT activation by lithium abrogates TP53 mutation associated radiation resistance in medulloblastoma.	Lithium	18-25	P53	Homo sapiens	36-40
25539912-8	2014	Lithium, an activator of the WNT pathway, sensitized TP53 mutant medulloblastoma to radiation (SF2 of 43.5%+-1.5% in lithium treated cells vs. 56.6+-3% (p&lt;0.01)) accompanied by increased number of gammaH2AX foci.	Lithium	0-7	P53	Homo sapiens	53-57
25539912-11	2014	Since constitutive activation of the WNT pathway by lithium sensitizes TP53 mutant medulloblastoma cells and protect normal neural stem cells from radiation, this oral drug may represent an attractive novel therapy for high-risk medulloblastomas.	Lithium	52-59	P53	Homo sapiens	71-75
25040077-8	2014	Agents that target B-cell receptor signalling, BH3-mimetics and others induce apoptosis of the neoplastic B-cells in a TP53-independent manner.	BH 3	47-50	P53	Homo sapiens	119-123
25143260-1	2014	UNLABELLED: Human NAD(P)H: quinone oxidoreductase 1 (NQO1) is essential for the antioxidant defense system, stabilization of tumor suppressors (e.g. p53, p33, and p73), and activation of quinone-based chemotherapeutics.	quinone	27-34	P53	Homo sapiens	149-152
25175641-0	2014	Diallyl disulfide induces G2/M arrest and promotes apoptosis through the p53/p21 and MEK-ERK pathways in human esophageal squamous cell carcinoma.	diallyl disulfide	0-17	P53	Homo sapiens	73-76
25198897-0	2014	Design, synthesis and biological evaluation of sulfamide and triazole benzodiazepines as novel p53-MDM2 inhibitors.	fusarubin	47-56	P53	Homo sapiens	95-98
25181509-6	2014	When MI-63 was combined with the BH3 mimetic ABT-737, enhanced activity was seen in both wild-type and mutant p53 models.	BH 3	33-36	P53	Homo sapiens	110-113
24568186-4	2014	Treatment of MCF-7 cells with 15d-PGJ2 led to time-dependent increases in the expression of p53 as well as HO-1.	15-deoxy-delta(12,14)-prostaglandin J2	30-38	P53	Homo sapiens	92-95
24568186-5	2014	Upregulation of p53 expression by 15d-PGJ2 was abrogated by si-RNA knock-down of HO-1.	15-deoxy-delta(12,14)-prostaglandin J2	34-42	P53	Homo sapiens	16-19
24568186-8	2014	We speculated that iron, a by-product of HO-1-catalyzed reactions, could mediate 15d-PGJ2-induced p53 expression.	15-deoxy-delta(12,14)-prostaglandin J2	81-89	P53	Homo sapiens	98-101
24568186-9	2014	Upregulation of p53 expression by 15d-PGJ2 was abrogated by the iron chelator desferrioxamine in MCF-7 cells.	15-deoxy-delta(12,14)-prostaglandin J2	34-42	P53	Homo sapiens	16-19
24568186-9	2014	Upregulation of p53 expression by 15d-PGJ2 was abrogated by the iron chelator desferrioxamine in MCF-7 cells.	Deferoxamine	78-93	P53	Homo sapiens	16-19
24568186-11	2014	When MCF-7 cells were treated with the Fe(2+)-specific chelator phenanthroline, 15d-PGJ2-induced p53 expression was attenuated.	15-deoxy-delta(12,14)-prostaglandin J2	80-88	P53	Homo sapiens	97-100
25042256-0	2014	Optimization beyond AMG 232: discovery and SAR of sulfonamides on a piperidinone scaffold as potent inhibitors of the MDM2-p53 protein-protein interaction.	Sulfonamides	50-62	P53	Homo sapiens	123-126
25071014-8	2014	Our results show that the clinical candidate AKT inhibitor MK-2206 promotes ARF nucleolar localization, reduced p53(mut) stability and increased sensitivity to ionizing radiation in a xenograft model of pancreatic cancer.	MK 2206	59-66	P53	Homo sapiens	112-115
25111876-11	2014	Instead, from concentrations of 20 to 100 microg/mL, PHMB kills cells of all types in less than 3 h. The expression of genes involved in the mechanisms of cell death induced by PHMB, including p53, the pro apoptotic gene bax and others, the anti-apoptotic bcl-2 and caspase-3 has been evaluated by RT-PCR.	polihexanide	53-57	P53	Homo sapiens	193-196
25026173-9	2014	DADS induced apoptosis by activating a mitochondria-dependent pathway with the executor of caspase-3, increasing p53 level and Bax/Bcl-2 ratio, and downregulating the RAF/MEK/ERK pathway in ECA109 xenograft tumosr.	diallyl disulfide	0-4	P53	Homo sapiens	113-116
24675086-0	2014	Chromosome breakage induced by the genotoxic agents mitomycin C and cytosine arabinoside is concentration and p53 dependent.	Cytarabine	68-88	P53	Homo sapiens	110-113
24675086-8	2014	On the other hand, higher levels of micronucleus and p53 induction were shown in TK6 cells treated with araC and a G1/S arrest was observed after araC treatment.	Cytarabine	104-108	P53	Homo sapiens	53-56
24675086-9	2014	p53 deficient NH32 cells showed an increased sensitivity of micronucleus (MN) induction after araC treatment compared with TK6 cells and less of an active G1/S phase checkpoint.	Cytarabine	94-98	P53	Homo sapiens	0-3
25009787-5	2014	Later on, DMF stimulated p21 mRNA expression through a process dependent on p53 activity.	Dimethyl Fumarate	10-13	P53	Homo sapiens	76-79
25009787-10	2014	In conclusion, DMF prevented abnormal proliferation in VSMCs by G1 cell cycle arrest via p21 upregulation driven by Nrf2 and p53 activity, and had a beneficial effect on TNF-alpha-induced apoptosis and dysfunction in endothelial cells through Nrf2-NQO1 activity suggesting that DMF might be a therapeutic drug for patients with vascular disease.	Dimethyl Fumarate	15-18	P53	Homo sapiens	125-128
24647572-8	2014	Elacridar also markedly improved TMZ/ABT-888 combination treatment in the spontaneous p53;p16(Ink4a)/p19(Arf);K-Ras(v12);LucR glioblastoma model.	Temozolomide	33-36	P53	Homo sapiens	86-89
24657665-3	2014	The G to T transversion at the third position of codon 249 (AGG) of the TP53 gene, substituting arginine to serine, is the most common aflatoxin-induced mutation linked to HCC.	Aflatoxins	135-144	P53	Homo sapiens	72-76
24493299-7	2014	Moreover, in MDS unbalanced 5q translocations were associated with clonal evolution (109/188; 58.0% vs. 124/385; 32.2%; P &lt; 0.001), mutation of TP53 (64/67; 95.5% vs. 40/120; 40.0%; P &lt; 0.001), and shorter survival (15.3 months vs. not reached; P &lt; 0.001).	CHEMBL3739943	28-30	P53	Homo sapiens	147-151
24570003-7	2014	Furthermore, PI-1840 sensitizes human cancer cells to the mdm2/p53 disruptor, nutlin, and to the pan-Bcl-2 antagonist BH3-M6.	PI-1840	13-20	P53	Homo sapiens	63-66
24173372-6	2014	In the present study, we report that cryptotanshinone, a natural compound isolated from Salvia miltiorrhiza, robustly activated AMPK signaling pathway, including LKB1, p53, TSC2, thereby leading to suppression of mTORC1 in a number of LKB1-expressing cancer cells including HepG2 human hepatoma, but not in LKB1-deficient cancer cells.	cryptotanshinone	37-53	P53	Homo sapiens	168-171
24248532-0	2014	Gain of function of mutant TP53 in glioblastoma: prognosis and response to temozolomide.	Temozolomide	75-87	P53	Homo sapiens	27-31
24248532-1	2014	PURPOSE: Our aim was to investigate the relationship between mutant p53 and the prognosis of malignant glioma treated with temozolomide, and the regulation of mutant TP53 induced drug resistance, by molecular experimentation and a clinical trial.	Temozolomide	123-135	P53	Homo sapiens	68-71
24248532-10	2014	Knockdown of mutant TP53 led to a fivefold increase in chemosensitivity to temozolomide but not semustine.	Temozolomide	75-87	P53	Homo sapiens	20-24
24248532-13	2014	Also, TP53 mutation may decrease the chemosensitivity of glioblastoma to temozolomide by increasing MGMT expression.	Temozolomide	73-85	P53	Homo sapiens	6-10
24476133-7	2014	We observed that administration of MK-2206, an allosteric AKT inhibitor, increased levels of reactive oxygen species, up-regulated the microRNA miR-182 and several senescence-associated genes (including p16, p53, p21, and beta-galactosidase), and drove leiomyoma cells into stress-induced premature senescence (SIPS).	MK 2206	35-42	P53	Homo sapiens	208-211
24535435-5	2014	In this study, we examined the effect of GV on wild-type (wt) p53 activity in cancer cells.	Gentian Violet	41-43	P53	Homo sapiens	62-65
24535435-6	2014	We found that GV was able to overcome the inhibitory effect of the NADPH oxidase Nox1 on p53 transcriptional activity.	Gentian Violet	14-16	P53	Homo sapiens	89-92
24535435-7	2014	For the first time we show that GV was able to directly induce p53/DNA binding and transcriptional activity.	Gentian Violet	32-34	P53	Homo sapiens	63-66
31681507-2	2019	In this study, we analyzed the estrogen-like effects of BPA on the expression of estrogen receptor (ER)alpha and p53 with hormonal and antihormonal treatments in T-47D and MCF-7 cells.	Estrogens	31-39	P53	Homo sapiens	113-116
31306909-7	2019	(R)-4"-methylklavuzon inhibited CRM1 protein providing increased retention of p53 and RIOK2 protein in the nucleus.	(r)-4"-methylklavuzon	0-21	P53	Homo sapiens	78-81
31601054-0	2019	Actinomycin V Suppresses Human Non-Small-Cell Lung Carcinoma A549 Cells by Inducing G2/M Phase Arrest and Apoptosis via the p53-Dependent Pathway.	ACTINOMYCIN V	0-13	P53	Homo sapiens	124-127
31601054-2	2019	In this study, the involvement of p53 in the cell cycle arrest and pro-apoptotic action of actinomycin V was investigated in human non-small-cell lung carcinoma A549 cells.	ACTINOMYCIN V	91-104	P53	Homo sapiens	34-37
31601054-3	2019	Results from the 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide assay showed that cytotoxic activity of actinomycin V on A549 cells (with wild-type p53) was stronger than the NCI-H1299 cells (p53-deficient).	ACTINOMYCIN V	113-126	P53	Homo sapiens	157-160
31601054-3	2019	Results from the 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide assay showed that cytotoxic activity of actinomycin V on A549 cells (with wild-type p53) was stronger than the NCI-H1299 cells (p53-deficient).	ACTINOMYCIN V	113-126	P53	Homo sapiens	201-204
31601054-4	2019	Actinomycin V upregulated both of the protein and mRNA expression levels of p53, p21Waf1/Cip1 and Bax in A549 cells.	ACTINOMYCIN V	0-13	P53	Homo sapiens	76-79
31601054-6	2019	Furthermore, the effects of cell cycle arrest and apoptosis in A549 cells which were induced by actinomycin V could be reversed by the pifithrin-alpha, a specific inhibitor of p53 transcriptional activity.	ACTINOMYCIN V	96-109	P53	Homo sapiens	176-179
31601054-7	2019	Collectively, our results suggest that actinomycin V causes up-regulation of p53 by which the growth of A549 cells is suppressed for cell cycle arrest and apoptosis.	ACTINOMYCIN V	39-52	P53	Homo sapiens	77-80
30832755-5	2019	Increased p53 expression stimulated the induction of apoptosis by axitinib and promoted asymmetric cell division (ACD) of NSCLC CSCs.	Axitinib	66-74	P53	Homo sapiens	10-13
30832755-9	2019	TP53 stimulates the induction of apoptosis in NSCLC by axitinib and the ACD of lung CSCs through its regulatory effects on the p53/Akt/ GSK3beta pathways.	Axitinib	55-63	P53	Homo sapiens	0-4
31478534-0	2019	Organocatalytic diastereoselective [3+2] cyclization of MBH carbonates with dinucleophiles: synthesis of bicyclic imidazoline derivatives that inhibit MDM2-p53 interaction.	bicyclic	105-113	P53	Homo sapiens	156-159
31308060-10	2019	Combination of COTI-2 with cisplatin or radiation may be highly relevant in treating patients with HNSCC harboring TP53 mutations.	COTI-2	15-21	P53	Homo sapiens	115-119
31648477-1	2019	Objective: To improve the knowledge and experience of ibrutinib combined with CAR-T cells in the treatment of high-risk chronic lymphoblastic leukemia (CLL) patients or small lymphocytic lymphoma (SLL) with TP53 gene aberration.	ibrutinib	54-63	P53	Homo sapiens	207-211
31151060-0	2019	Epigenetic inactivation of LHX6 mediated microcystin-LR induced hepatocarcinogenesis via the Wnt/beta-catenin and P53 signaling pathways.	cyanoginosin LR	41-55	P53	Homo sapiens	114-117
31534224-8	2019	Enforcing the accumulation of alphaKG in p53-deficient PDAC cells through the inhibition of oxoglutarate dehydrogenase-an enzyme of the tricarboxylic acid cycle-specifically results in increased 5hmC, tumour-cell differentiation and decreased tumour-cell fitness.	Tricarboxylic Acids	136-154	P53	Homo sapiens	41-44
31534224-9	2019	Conversely, increasing the intracellular levels of succinate (a competitive inhibitor of alphaKG-dependent dioxygenases) blunts p53-driven tumour suppression.	Succinic Acid	51-60	P53	Homo sapiens	128-131
31555576-7	2019	The continuous administration of ibrutinib single agent has led to prolonged PFS and OS in relapsed/refractory and treatment naive CLL, including those with TP53 deletion/mutation or unmutated IGHV genes, though the clinical responses are rarely complete.	ibrutinib	33-42	P53	Homo sapiens	157-161
31470629-8	2019	The effects of FUS were more potent than those of AFU, with FUS up-regulating p21 expression in a p53-dependent manner, as detected by Western blot analyses, likely the consequence of decreased ERK phosphorylation and increased p38 expression (both of which increase p21 stability).	fusarubin	15-18	P53	Homo sapiens	98-101
31470629-8	2019	The effects of FUS were more potent than those of AFU, with FUS up-regulating p21 expression in a p53-dependent manner, as detected by Western blot analyses, likely the consequence of decreased ERK phosphorylation and increased p38 expression (both of which increase p21 stability).	fusarubin	60-63	P53	Homo sapiens	98-101
31534534-14	2019	Finally, MTBP silencing increased the sensitivity of TP53wt GSCs to radiation and TMZ treatment in vitro and in vivo.	Temozolomide	82-85	P53	Homo sapiens	53-57
31428569-10	2019	Apoptosis of A549 cells was decreased after transfected with p53 shRNA or treated with reactive oxygen species inhibitor NAC and p38MAPK inhibitor SB203580, suggesting that the p53/ROS/p38MAPK pathway appeared to mediate the LBP-induced apoptosis of A549 cells.	nac	121-124	P53	Homo sapiens	61-64
31428569-10	2019	Apoptosis of A549 cells was decreased after transfected with p53 shRNA or treated with reactive oxygen species inhibitor NAC and p38MAPK inhibitor SB203580, suggesting that the p53/ROS/p38MAPK pathway appeared to mediate the LBP-induced apoptosis of A549 cells.	nac	121-124	P53	Homo sapiens	177-180
31336690-0	2019	Flavopereirine Suppresses the Growth of Colorectal Cancer Cells through P53 Signaling Dependence.	flavopereirine	0-14	P53	Homo sapiens	72-75
31336690-9	2019	Moreover, flavopereirine enhanced P53 expression and phosphorylation in CRC cells.	flavopereirine	10-24	P53	Homo sapiens	34-37
31336690-10	2019	CRC cells with P53 knockout or loss-of-function mutation significantly diminished flavopereirine-mediated viability reduction, indicating that P53 activity plays a major role in flavopereirine-mediated CRC cell growth suppression.	flavopereirine	82-96	P53	Homo sapiens	15-18
31336690-10	2019	CRC cells with P53 knockout or loss-of-function mutation significantly diminished flavopereirine-mediated viability reduction, indicating that P53 activity plays a major role in flavopereirine-mediated CRC cell growth suppression.	flavopereirine	82-96	P53	Homo sapiens	143-146
31336690-10	2019	CRC cells with P53 knockout or loss-of-function mutation significantly diminished flavopereirine-mediated viability reduction, indicating that P53 activity plays a major role in flavopereirine-mediated CRC cell growth suppression.	flavopereirine	178-192	P53	Homo sapiens	15-18
31336690-10	2019	CRC cells with P53 knockout or loss-of-function mutation significantly diminished flavopereirine-mediated viability reduction, indicating that P53 activity plays a major role in flavopereirine-mediated CRC cell growth suppression.	flavopereirine	178-192	P53	Homo sapiens	143-146
31336690-11	2019	Flavopereirine also significantly repressed CRC cell xenograft growth in vivo by upregulating P53 and P21 and inducing apoptosis.	flavopereirine	0-14	P53	Homo sapiens	94-97
31336690-12	2019	In conclusion, flavopereirine-mediated growth suppression in CRC cells depended on the P53-P21, but not the JAKs-STATs-c-Myc signaling pathway.	flavopereirine	15-29	P53	Homo sapiens	87-90
31336690-13	2019	The present study suggests that flavopereirine may be efficacious in the clinical treatment of CRC harboring functional P53 signaling.	flavopereirine	32-46	P53	Homo sapiens	120-123
31372050-10	2019	Good response to NAC was associated with p53 expression.	nac	17-20	P53	Homo sapiens	41-44
30928633-0	2019	8-Acetonyldihydronitidine inhibits the proliferation of human colorectal cancer cells via activation of p53.	8-acetonyldihydronitidine	0-25	P53	Homo sapiens	104-107
30981936-10	2019	These results suggest that aryl-PFRs (e.g., BDP, MDPP, CDP) cause oxidative stress-mediated DNA damage and mitochondrial impairment, and p53-dependent pathway was involved in the aryl-PFRs-induced DNA damage and cell cycle arrest.	diphenylcresyl phosphate	55-58	P53	Homo sapiens	137-140
30981113-0	2019	Synthesis, and evaluation of in vitro and in vivo anticancer activity of 14-substituted oridonin analogs: A novel and potent cell cycle arrest and apoptosis inducer through the p53-MDM2 pathway.	14-substituted oridonin	73-96	P53	Homo sapiens	177-180
31026379-11	2019	Consistently, our findings demonstrate the inhibitory effect of vildagliptin on p53 acetylation, which is mediated by sirtuin 1 (SIRT1) as the inhibition of SIRT1 negated the inhibitory action of vildagliptin on p53 acetylation.	Vildagliptin	64-76	P53	Homo sapiens	212-215
31026379-11	2019	Consistently, our findings demonstrate the inhibitory effect of vildagliptin on p53 acetylation, which is mediated by sirtuin 1 (SIRT1) as the inhibition of SIRT1 negated the inhibitory action of vildagliptin on p53 acetylation.	Vildagliptin	196-208	P53	Homo sapiens	80-83
31026379-11	2019	Consistently, our findings demonstrate the inhibitory effect of vildagliptin on p53 acetylation, which is mediated by sirtuin 1 (SIRT1) as the inhibition of SIRT1 negated the inhibitory action of vildagliptin on p53 acetylation.	Vildagliptin	196-208	P53	Homo sapiens	212-215
31181622-9	2019	The results indicate the potential for repurposing the benzimidazole anthelmintics for the treatment of cancers overexpressing p53 negative regulators.	benzimidazole	55-68	P53	Homo sapiens	127-130
30872077-0	2019	P53 pathway is a major determinant in the radiosensitizing effect of Palbociclib: Implication in cancer therapy.	palbociclib	69-80	P53	Homo sapiens	0-3
30872077-4	2019	Our results indicate that the presence of a p53 wild type is strictly required for Palbociclib to exert its radiosensitizing effect, independently of the inhibitory effect exerted on CDK4/6.	palbociclib	83-94	P53	Homo sapiens	44-47
31089945-0	2019	Role of tea polyphenols in delaying hyperglycemia-induced senescence in human glomerular mesangial cells via miR-126/Akt-p53-p21 pathways.	Polyphenols	12-23	P53	Homo sapiens	121-124
30888162-0	2019	Avenanthramide A Induces Cellular Senescence via miR-129-3p/Pirh2/p53 Signaling Pathway To Suppress Colon Cancer Growth.	avenanthramide A	0-16	P53	Homo sapiens	66-69
30831390-6	2019	These results revealed that L-Ru exerted a strong inhibitory effect on the cells proliferation,G0/G1-arrest, accompanied with upregulation of p53, p21, p15, cleaved Poly (ADP-ribose) polymerase (PARP) protein and downregulation of cell cycle markers.	l-ru	28-32	P53	Homo sapiens	142-145
30796178-0	2019	The SIAH1-HIPK2-p53ser46 Damage Response Pathway is Involved in Temozolomide-Induced Glioblastoma Cell Death.	Temozolomide	64-76	P53	Homo sapiens	16-19
30796178-5	2019	Upon temozolomide treatment, p53 becomes phosphorylated whereby HIPK2kd had impact exclusively on ser46, but not ser15.	Temozolomide	5-17	P53	Homo sapiens	29-32
30796178-7	2019	Thus, the expression of FAS was attenuated following HIPK2kd, supporting the conclusion that HIPK2 regulates temozolomide-induced apoptosis via p-p53ser46-driven FAS expression.	Temozolomide	109-121	P53	Homo sapiens	146-149
30796178-10	2019	We further show that downregulation of the HIPK2 inactivator SIAH1 significantly ameliorates temozolomide-induced apoptosis, suggesting that the ATM/ATR target SIAH1 together with HIPK2 plays a proapoptotic role in glioma cells exhibiting p53wt status.	Temozolomide	93-105	P53	Homo sapiens	239-242
30796178-12	2019	IMPLICATIONS: The identification of a novel apoptotic pathway triggered by the temozolomide-induced DNA damage O6 -methylguanine supports the role of p53 in the decision between survival and death and suggests SIAH1 and HIPK2 as new therapeutic targets.	Temozolomide	79-91	P53	Homo sapiens	150-153
31086338-0	2019	Publisher Correction: p53 regulation of ammonia metabolism through urea cycle controls polyamine biosynthesis.	Ammonia	40-47	P53	Homo sapiens	22-25
30855964-3	2019	In this study, we investigated a fragment of the disordered p53 C-terminal domain (CTDf) that interacts with one of its partner molecules, S100B, as a representative IDR.	BRN 3178119	83-87	P53	Homo sapiens	60-63
30896891-3	2019	In the mechanistic study, NXQ was found to downregulate MDM2 expression by inducing its proteasomal degradation, and thus upregulated p53 expression, which was a substrate protein of MDM2.	2-[5-fluoranyl-2-[[3-[methyl(oxidanyl)-$l^{3}-sulfanyl]phenyl]methylcarbamoyl]phenoxy]ethanoic acid	26-29	P53	Homo sapiens	134-137
30896891-5	2019	These results demonstrated that NXQ displayed anti-SCLC activity by suppressing MDM2 expression, which suggested that anti-infective NXQ had potential for SCLC treatment by targeting the MDM2/p53 axis.	2-[5-fluoranyl-2-[[3-[methyl(oxidanyl)-$l^{3}-sulfanyl]phenyl]methylcarbamoyl]phenoxy]ethanoic acid	32-35	P53	Homo sapiens	192-195
30896891-5	2019	These results demonstrated that NXQ displayed anti-SCLC activity by suppressing MDM2 expression, which suggested that anti-infective NXQ had potential for SCLC treatment by targeting the MDM2/p53 axis.	2-[5-fluoranyl-2-[[3-[methyl(oxidanyl)-$l^{3}-sulfanyl]phenyl]methylcarbamoyl]phenoxy]ethanoic acid	133-136	P53	Homo sapiens	192-195
30804118-9	2019	The PTX+CPt combination exhibited the highest rate of apoptosis, a decrease in cell viability and significant caspase activation, as well as loss of mitochondrial membrane potential, release of cytochrome c, and increased p53 protein levels.	Pentoxifylline	4-7	P53	Homo sapiens	222-225
30664150-6	2019	The TMZ + acteoside combination treatment increased the cleavage of caspase-3 and levels of B-cell lymphoma 2 (Bcl-2)-associated X protein and phosphorylated p53, and decreased the level of Bcl-2.	Temozolomide	4-7	P53	Homo sapiens	158-161
30325501-6	2019	Furthermore, combined treatment with progesterone plus mifepristone (PG+MIFE) gave an enhanced anti-proliferative effect in comparison with hydrocortisone plus mifepristone (HC+MIFE) by significantly reducing markers of proliferation (BrdU+ and Ki67 expression) and tumor suppressors (PTEN, TP53), and increasing the percentage of pro-apoptotic cells.	mife	72-76	P53	Homo sapiens	291-295
30578766-5	2019	Furthermore, glycosphingolipids (particularly globotriaosylceramide) generated from serial ceramide glycosylation were seen to activate cSrc and beta-catenin signaling so as to upregulate METTL3 expression, in turn promoting expression of p53 R273H mutant protein, with consequent drug resistance.	globotriaosylceramide	46-67	P53	Homo sapiens	239-242
30388553-0	2019	CdS nanocrystals/graphene oxide-AuNPs based electrochemiluminescence immunosensor in sensitive quantification of a cancer biomarker: p53.	graphene oxide	17-31	P53	Homo sapiens	133-136
30177840-10	2019	In line with these findings, BRCA2-depleted and BRCA2-mutant human cell lines, or tumor cell lines derived from Brca2-/-;p53-/- mice showed increased sensitivity to the Aurora-A kinase inhibitor alisertib, with delayed mitotic progression and frequent mitotic failure.	MLN 8237	195-204	P53	Homo sapiens	121-124
30766866-4	2019	In this study, we made modifications in this scaffold by including combinations of different substituents in the pyrazoline ring in order to obtain novel small molecules that could modulate p53 activity and act as differentiation inducer agents.	pyrazoline	113-123	P53	Homo sapiens	190-193
30634697-6	2019	Furthermore, molecular mechanisms of cytotoxicity of [4-NH2-2-Me(Q)H][VO(bcma)(H2O)]2H2O (T1) were dependent on antiproliterative activity, increased ROS generation, cell cycle arrest in G2/M phase with simultaneous triggering of the p53/p21 pathway, binucleation, and induction of autophagy.	[4-nh2-2-me	53-64	P53	Homo sapiens	234-237
30634697-6	2019	Furthermore, molecular mechanisms of cytotoxicity of [4-NH2-2-Me(Q)H][VO(bcma)(H2O)]2H2O (T1) were dependent on antiproliterative activity, increased ROS generation, cell cycle arrest in G2/M phase with simultaneous triggering of the p53/p21 pathway, binucleation, and induction of autophagy.	(q)h][vo(	64-73	P53	Homo sapiens	234-237
30848216-8	2019	Anisosciadone elevated the expression and activity of Caspase 3 as well as p53 expression without affecting Caspase 9 in HepG2 cells.	anisosciadone	0-13	P53	Homo sapiens	75-78
30442421-1	2019	Methyltrioxorhenium mediated oxidative addition/elimination nucleophilic substitution yielded alkylamino and arylamino cambinol derivatives characterized by anti-proliferative activity against wild-type and p53 mutated MGH-U1 and RT112 bladder cancer cell lines.	alkylamino and arylamino cambinol	94-127	P53	Homo sapiens	207-210
30414976-10	2019	Overall, the work reveals that andrographolide through modulation of p53 and HNF4A, regulates miRNAs leading to upregulation of HO-1, glutathione and thioredoxin systems.	andrographolide	31-46	P53	Homo sapiens	69-72
30240018-7	2019	Cells lacking p53 activity were slightly more resistant to photoactivated DMMB, which was correlated with a smaller sub-G1 population, indicative of a lower level of apoptosis.	1,9-dimethylmethylene blue	74-78	P53	Homo sapiens	14-17
29991711-7	2018	Knockdown of Rictor or treatment with the Akt inhibitor MK-2206 attenuated senescence-associated beta-galactosidase (beta-gal) staining and expression of p53 and p21 proteins in the senescent endothelial cells, suggesting that mTORC2/Akt facilitates endothelial senescence.	MK 2206	56-63	P53	Homo sapiens	154-157
30526032-8	2018	Molecular docking studies illustrated the possible interaction of the target spiro-oxindoles with the p53 binding site on MDM2.	spiro-oxindoles	77-92	P53	Homo sapiens	102-105
30175400-12	2018	Demonstration of TP53 and NSD2 mutations in patients who developed blastoid transformation and ATM and TP53 mutations in patients who progressed, opens the door for future investigations in ibrutinib-refractory MCL.	ibrutinib	190-199	P53	Homo sapiens	17-21
30175400-12	2018	Demonstration of TP53 and NSD2 mutations in patients who developed blastoid transformation and ATM and TP53 mutations in patients who progressed, opens the door for future investigations in ibrutinib-refractory MCL.	ibrutinib	190-199	P53	Homo sapiens	103-107
30193876-7	2018	The effects of miR-125b on the expression of TP53INP1, p53 and release of proinflammatory cytokines were evaluated by synthetic miRs.	mir-125b	15-23	P53	Homo sapiens	55-58
30193876-12	2018	Treatment with miR-125b mimic markedly decreased the protein levels of TP53INP1, p53 and cytokines interleukin (IL)-1beta and tumour necrosis factor (TNF)-alpha, whereas miR-125b control or inhibitor did not have the above-mentioned effects.	mir-125b	15-23	P53	Homo sapiens	81-84
30193876-14	2018	Fluorescent staining and quantification further indicated that miR-125b mimic decreased the immunoreactivities of p53 and cleaved caspase 3 in neurons and simultaneously reduced the number of double-labelled cells with TP53INP1.	mir-125b	63-71	P53	Homo sapiens	114-117
30193876-15	2018	CONCLUSIONS: miR-125b mimic partially protected neurons against neuroinflammation and aberrant p53 network activation-induced apoptosis during IR injury through downregulation of TP53INP1.	mir-125b	13-21	P53	Homo sapiens	95-98
30395490-6	2018	However, little is known whether in vitro concentrations of DHA equal to the human plasma levels are able to modulate expression of survivin and sensitize mutant-p53 CRC cells to gamma-irradiation.	Docosahexaenoic Acids	60-63	P53	Homo sapiens	162-165
30395490-13	2018	Significant decreases in ED50 values at concentrations of DHA equal to human plasma levels, suggesting that DHA could be used as an attractive radiosensitizer agent in CRC patients with mutant-p53.	Docosahexaenoic Acids	108-111	P53	Homo sapiens	193-196
29941676-2	2018	We have detected a primate-specific adrenal androgen-mediated tumor suppression system in which circulating DHEAS is converted to DHEA specifically in cells in which TP53 has been inactivated DHEA is an uncompetitive inhibitor of glucose-6-phosphate dehydrogenase (G6PD), an enzyme indispensable for maintaining reactive oxygen species within limits survivable by the cell.	Dehydroepiandrosterone	108-112	P53	Homo sapiens	166-170
29941676-5	2018	In human somatic cells, loss of TP53 thus triggers activation of DHEAS transport proteins and steroid sulfatase, which converts circulating DHEAS into intracellular DHEA, and hexokinase which increases glucose-6-phosphate substrate concentration.	Dehydroepiandrosterone	65-69	P53	Homo sapiens	32-36
30081213-10	2018	Finally, this study showed that low and continuous exposure of H2S serves as a novel, selective and effective strategy in harnessing TNBC oncogenic profile through cGMP dependent and independent pathways where alterations of cell cycle regulatory proteins such as TP53 and c-Myc was observed.	Hydrogen Sulfide	63-66	P53	Homo sapiens	264-268
30217455-0	2018	4-Hydroxybenzoic acid (4-HBA) enhances the sensitivity of human breast cancer cells to adriamycin as a specific HDAC6 inhibitor by promoting HIPK2/p53 pathway.	4-hydroxybenzoic acid	0-21	P53	Homo sapiens	147-150
30217455-0	2018	4-Hydroxybenzoic acid (4-HBA) enhances the sensitivity of human breast cancer cells to adriamycin as a specific HDAC6 inhibitor by promoting HIPK2/p53 pathway.	4-hydroxybenzoic acid	23-28	P53	Homo sapiens	147-150
30217455-7	2018	4-HBA significantly promoted the anticancer effect of ADM on apoptosis induction, as evidenced by the increased expressions of Caspase-3 and PARP cleavage, which was associated with the promotion p53 and homeodomain interacting protein kinase-2 (HIPK2) expressions in ADM-resistant breast cancer cells.	4-hydroxybenzoic acid	0-5	P53	Homo sapiens	196-199
29334602-7	2018	The combination of TMZ and metformin enhanced AMPK phosphorylation and inhibited mammalian target of rapamycin phosphorylation, AKT phosphorylation, and p53 expression.	Temozolomide	19-22	P53	Homo sapiens	153-156
30282320-0	2018	Dimetallic Ru(II) arene complexes appended on bis-salicylaldimine induce cancer cell death and suppress invasion via p53-dependent signaling.	ru(ii) arene	11-23	P53	Homo sapiens	117-120
29749584-3	2018	The role of aflatoxin in HCC from a given population is commonly estimated through the prevalence of R249S mutation of TP53, a hallmark for previous exposure to the mycotoxin.	Aflatoxins	12-21	P53	Homo sapiens	119-123
29863754-3	2018	The mesocate isomer shows the reverse selectivity, with the achiral isomer being preferentially cytotoxic towards HCT116 p53+/+ .	mesocate	4-12	P53	Homo sapiens	121-124
29973205-13	2018	p53 was enriched in the nucleus following LMB treatments, but did not seem to be required for sensitization; additional experiments suggested that p53 opposed the apoptotic effects of LMB and TRAIL.	leptomycin B	42-45	P53	Homo sapiens	0-3
29973205-13	2018	p53 was enriched in the nucleus following LMB treatments, but did not seem to be required for sensitization; additional experiments suggested that p53 opposed the apoptotic effects of LMB and TRAIL.	leptomycin B	184-187	P53	Homo sapiens	0-3
29973205-13	2018	p53 was enriched in the nucleus following LMB treatments, but did not seem to be required for sensitization; additional experiments suggested that p53 opposed the apoptotic effects of LMB and TRAIL.	leptomycin B	184-187	P53	Homo sapiens	147-150
30050935-5	2018	As anticipated, TMZ caused DNA damage mediated by the ATM/p53/p21 signaling pathway and induced significant G2 delay.	Temozolomide	16-19	P53	Homo sapiens	58-61
30050935-7	2018	Mechanistic study showed that coadministration of caffeine and TMZ suppressed the phosphorylation of ATM and p53 and downregulated p21 expression, thus releasing DNA-damaged cells from G2 arrest into premature mitosis.	Temozolomide	63-66	P53	Homo sapiens	109-112
30050935-10	2018	In conclusion, our study demonstrated that caffeine enhanced the efficacy of TMZ through mitotic cell death by impeding ATM/p53/p21-mediated G2 arrest.	Temozolomide	77-80	P53	Homo sapiens	124-127
29625193-0	2018	Icaritin induces ovarian cancer cell apoptosis through activation of p53 and inhibition of Akt/mTOR pathway.	icaritin	0-8	P53	Homo sapiens	69-72
29625193-9	2018	The icaritin-induced OC cell apoptosis may be associated with the activation of p53 and the suppression of Akt/mTOR pathway.	icaritin	4-12	P53	Homo sapiens	80-83
29054521-2	2018	Here, we used computational technique to understand the interaction of both pristine (pG) or carboxyl functionalized graphene (fG) of different sizes (1, 6, and 10nm) with an important DNA repair protein p53.	Graphite	117-125	P53	Homo sapiens	204-207
29054521-6	2018	Thus, computational and experimental results revealed the structure-physicochemical property dependent adverse effects of graphene in DNA repair protein p53.	Graphite	122-130	P53	Homo sapiens	153-156
29681859-6	2018	All studied polyphenols evoked anti-proliferative activity, accompanied by increased PRODH/POX, P53, active caspases-3 and -9 expressions and decreased collagen biosynthesis, prolidase activity and proline concentration in CAL-27 cells.	Polyphenols	12-23	P53	Homo sapiens	96-125
29356571-10	2018	In addition, EO-PCL-PEG electrospun nanofibrous mats significantly upregulated the expression levels of cell cycle regulated genes (Cyclin D1, pRb, and P53) and stemness markers (Nanog, OCT-4, Rex-1, and Sox-2) than PCL-PEG nanofiber and tissue culture polystyrene in 7 and 14 days of cell culture.	pcl-peg	16-23	P53	Homo sapiens	152-155
29377550-4	2018	Indeed, our results delineate anti-neoplastic activity of Axitinib in medulloblastoma cell lines modelling the most aggressive c-myc-amplified Non-WNT/Non-SHH and SHH-TP53-mutated tumours.	Axitinib	58-66	P53	Homo sapiens	167-171
29471073-1	2018	Polycyclic aromatic hydrocarbons such as benzo[a]pyrene (BaP) can induce cytochrome P450 1A1 (CYP1A1) via a p53-dependent mechanism.	Benzo(a)pyrene	41-55	P53	Homo sapiens	108-111
29665895-5	2018	CONCLUSION: Down-regulation of miR-125b can inhibit K562 cell proliferation via down-regulating the expressions of BCL-2 and up-regulating the expression of BAK1, p53 and Puma.	mir-125b	31-39	P53	Homo sapiens	163-166
28549767-2	2018	Ibrutinib, an inhibitor of Bruton"s tyrosine kinase, has demonstrated impressive response rates in the relapsed/refractory setting, including in the setting of Del17p and/or TP53 mutations.	ibrutinib	0-9	P53	Homo sapiens	174-178
29393340-7	2018	In comparison to TP53 wt human neuroblastoma cells, Trp53 wt murine control and TH-MYCN cell lines were significantly less sensitive to growth inhibition mediated by MI-63 and RG7388.	2-methyl-4-isothiazolin-3-one	166-168	P53	Homo sapiens	52-57
29334216-8	2018	All the results above indicated that PTX-DODAB/p53-rHDL nanoparticles held broad prospects in combination of chemotherapeutics and gene therapeutic agents for cancer-targeted therapy.	ptx-dodab	37-46	P53	Homo sapiens	47-50
29600625-0	2018	[Effect of microRNA-34a/SIRT1/p53 signal pathway on notoginsenoside R1 delaying vascular endothelial cell senescence].	notoginsenoside	52-67	P53	Homo sapiens	30-33
29600625-1	2018	This study aimed to investigate the effect of notoginsenoside R1 in delaying H2O2-induced vascular endothelial cell senescence through microRNA-34a/SIRT1/p53 signal pathway.	notoginsenoside	46-61	P53	Homo sapiens	154-157
29378575-8	2018	CONCLUSION: DHA, Omegaven  and oxaliplatin were associated with downregulation of p53 and VEGF in both cells.	fish oil triglycerides	17-25	P53	Homo sapiens	82-85
30037299-4	2018	Two mechanistically distinct small molecules that act via p53 are the selective inhibitor of nuclear export, selinexor, and MDM2 inhibitor, nutlin-3a.	selinexor	109-118	P53	Homo sapiens	58-61
30037299-7	2018	Matched cell lines with and without p53 expression indicate that while loss-of-function results in altered cell cycle signatures to selinexor treatment, it does not diminish overall cell loss.	selinexor	132-141	P53	Homo sapiens	36-39
29416795-2	2018	Whether temozolomide (TMZ)-induced mutagenesis of the TP53 DNA-binding domain (DBD) can drive the pathogenesis of gliosarcoma is unclear.	Temozolomide	8-20	P53	Homo sapiens	54-58
29416795-2	2018	Whether temozolomide (TMZ)-induced mutagenesis of the TP53 DNA-binding domain (DBD) can drive the pathogenesis of gliosarcoma is unclear.	Temozolomide	22-25	P53	Homo sapiens	54-58
29416795-11	2018	Ex vivo treatment of the GBM spheres with TMZ generated numerous variants in cancer driver genes, including TP53 and CDH1, which were mutated in the post-treatment tumor.	Temozolomide	42-45	P53	Homo sapiens	108-112
29416795-12	2018	Conclusions: TMZ-induced TP53 gain-of-function mutations can have a driving role in secondary gliosarcoma pathogenesis.	Temozolomide	13-16	P53	Homo sapiens	25-29
29082795-7	2017	Because patients with a TP53 deletion/mutation are resistant to chemo-immunotherapy, treatment with the BTK inhibitor ibrutinib is recommended in this setting.	ibrutinib	118-127	P53	Homo sapiens	24-28
28946186-4	2017	Mechanistic study revealed that Cryptotanshinone suppressed the expression of p-STAT3, Bcl-2, CDK2, Snail and MMP2, and induced the expression of E-cadherin, P53, P21 and beta-catenin.	cryptotanshinone	32-48	P53	Homo sapiens	158-161
28425621-0	2017	p53-competent cells and p53-deficient cells display different susceptibility to oxygen functionalized graphene cytotoxicity and genotoxicity.	Graphite	102-110	P53	Homo sapiens	0-3
28425621-0	2017	p53-competent cells and p53-deficient cells display different susceptibility to oxygen functionalized graphene cytotoxicity and genotoxicity.	Graphite	102-110	P53	Homo sapiens	24-27
28425621-5	2017	Here, we show that p53 functional status correlates with oxygen functionalized graphene (f-G) cytotoxicity and genotoxicity in vitro.	Graphite	79-87	P53	Homo sapiens	19-22
28807874-10	2017	DHA induced the Bax/Bcl-2 ratio, mitochondrial accumulation of OSGIN1 and p53, and cytochrome c release; knockdown of OSGIN1 diminished these effects.	Docosahexaenoic Acids	0-3	P53	Homo sapiens	74-77
28836764-2	2017	In this work, we studied the changes in the structure and dynamics of wild type p53DBD in comparison with two of its "hot-spot" DNA-contact mutants, R248Q and R273H, by analysis of backbone amide chemical shift perturbations and 15N spin relaxation measurements.	Amides	190-195	P53	Homo sapiens	80-83
28910957-12	2017	Conclusion: These results indicated that the copy number variations of c-Myc, CCND1, p53, and p16 in patients were significant correlation with poor effect of NAC.	nac	159-162	P53	Homo sapiens	85-88
28782884-14	2017	Patients with a del(17p) or TP53 mutation can be treated with ibrutinib, venetoclax, or a combination of idelalisib and rituximab.	ibrutinib	62-71	P53	Homo sapiens	28-32
28714021-0	2017	Iodine-131 induces apoptosis in human cardiac muscle cells through the p53/Bax/caspase-3 and PIDD/caspase-2/ t-BID/cytochrome c/caspase-3 signaling pathway.	Iodine-131	0-10	P53	Homo sapiens	71-74
28882572-7	2017	Validation studies confirmed the role of p53 in reducing gamma-H2AX formation and DNA breaks measured by COMET assay after BaP and AFB1 exposure.	Benzo(a)pyrene	123-126	P53	Homo sapiens	41-44
28528452-10	2017	CONCLUSION: Our data for the first time highlight the role of p53 as a negative regulator of functional NIS expression in BC, where the latter is a potential targeted radioiodine therapy candidate.	Iodine-131	167-178	P53	Homo sapiens	62-65
28428144-5	2017	In 54 patients with gallbladder cancer, tumor tissue was examined for the R249S mutation in TP53, associated with aflatoxin exposure, through targeted sequencing.	Aflatoxins	114-123	P53	Homo sapiens	92-96
27780855-3	2017	DCR was 70% in TP53-mutated patients compared with 88% in TP53-wild type (wt) patients [relative risk, RR, of disease progression: 3.17 (95% CI, 1.21-8.48), P = 0.019].	dimethylamide-crotonin	0-3	P53	Homo sapiens	15-19
27797975-1	2017	Background: Ibrutinib is an active therapy with an acceptable safety profile for patients with chronic lymphocytic leukemia (CLL), including high-risk patients with del17p or with TP53 mutations.	ibrutinib	12-21	P53	Homo sapiens	180-184
28147244-11	2017	Protein microarray analyses showed that treatment with TMZ+GDC-0941+IR induced higher levels of p53 and glycogen synthase kinase 3-beta (GSK3-beta) expression in SHG44GBM cells than those induced by other treatments.	Temozolomide	55-58	P53	Homo sapiens	96-99
28092770-8	2017	RESULTS: Magnolin inhibited the proliferation and viability of the tumor cells by triggering cell cycle arrest via P53/P21 activation and inducing apoptosis in vitro and in vivo.	magnolin	9-17	P53	Homo sapiens	115-118
28012015-4	2017	Herein, we tried to decipher the underlying mechanism of the action of Mn-N-(2-hydroxyacetophenone) glycinate (MnNG) against differential p53 status bearing Hct116, MCF-7, and MDA-MB-468 cells on the backdrop of intracellular GSH level and reveal the role of p53 status in modulating GSH-dependant abrogation of MnNG-induced apoptosis in these cancer cells.	mn-n-(2-hydroxyacetophenone) glycinate	71-109	P53	Homo sapiens	138-141
28012015-4	2017	Herein, we tried to decipher the underlying mechanism of the action of Mn-N-(2-hydroxyacetophenone) glycinate (MnNG) against differential p53 status bearing Hct116, MCF-7, and MDA-MB-468 cells on the backdrop of intracellular GSH level and reveal the role of p53 status in modulating GSH-dependant abrogation of MnNG-induced apoptosis in these cancer cells.	mn-n-(2-hydroxyacetophenone) glycinate	71-109	P53	Homo sapiens	259-262
28182005-0	2017	Constitutive p53 heightens mitochondrial apoptotic priming and favors cell death induction by BH3 mimetic inhibitors of BCL-xL.	BH 3	94-97	P53	Homo sapiens	13-16
28143426-0	2017	The marine triterpene glycoside frondoside A induces p53-independent apoptosis and inhibits autophagy in urothelial carcinoma cells.	triterpene glycoside	11-31	P53	Homo sapiens	53-56
28143426-5	2017	The purpose of the current research is to investigate the anticancer effects and the mode of action of the marine triterpene glycoside frondoside A in p53-wild type and p53-deficient human urothelial carcinoma cells.	triterpene glycoside	114-134	P53	Homo sapiens	151-154
28143426-5	2017	The purpose of the current research is to investigate the anticancer effects and the mode of action of the marine triterpene glycoside frondoside A in p53-wild type and p53-deficient human urothelial carcinoma cells.	triterpene glycoside	114-134	P53	Homo sapiens	169-172
27177180-7	2017	Pharmacodynamic studies demonstrated that inhibition of cell growth following exposure to TMZ/nutlin3a correlated with: 1) activation of the p53 pathway, 2) downregulation of DNA repair proteins, 3) persistence of DNA damage, and 4) decreased invasion.	Temozolomide	90-93	P53	Homo sapiens	141-144
27177180-11	2017	CONCLUSIONS Modulation of MDM2/p53-associated signaling pathways is a novel approach for decreasing TMZ resistance in GBM.	Temozolomide	100-103	P53	Homo sapiens	31-34
28052008-0	2017	Targeting P-glycoprotein function, p53 and energy metabolism: Combination of metformin and 2-deoxyglucose reverses the multidrug resistance of MCF-7/Dox cells to doxorubicin.	Deoxyglucose	91-105	P53	Homo sapiens	35-38
28099584-2	2017	This study aimed to investigate the expression of p53 and BTG2 genes following 131I therapy in thyroid cancer cell line SW579 and the possible underlying mechanism.	Iodine-131	79-83	P53	Homo sapiens	50-53
29362667-5	2017	Moreover, pretreatment with a caspase-3 inhibitor (Z-DEVD-FMK), but not with a p53 inhibitor (cyclic pifithrin-alpha), reduced xylopine-induced apoptosis, indicating induction of caspase-mediated apoptosis by the p53-independent pathway.	benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone	51-61	P53	Homo sapiens	213-216
27651340-1	2017	AIM: To observe the correlation between 1p/19q codeletion, isocytrate dehydrogenase-1 (IDH1) mutation and p53 protein overexpression and their prognostic value in Turkish anaplastic oligodendroglioma patients who were treated with adjuvant radiotherapy and temozolomide chemotherapy.	Temozolomide	257-269	P53	Homo sapiens	106-109
27823629-0	2016	Javamide-I-O-methyl ester increases p53 acetylation and induces cell death via activating caspase 3/7 in monocytic THP-1 cells.	javamide-I-O-methyl ester	0-25	P53	Homo sapiens	36-39
27907160-0	2016	AS1411-Induced Growth Inhibition of Glioma Cells by Up-Regulation of p53 and Down-Regulation of Bcl-2 and Akt1 via Nucleolin.	AGRO 100	0-6	P53	Homo sapiens	69-72
27907160-3	2016	Here we report that AS1411 induces cell apoptosis and cycle arrest, and inhibits cell viability by up-regulation of p53 and down-regulation of Bcl-2 and Akt1 in human glioma cells.	AGRO 100	20-26	P53	Homo sapiens	116-119
27663262-9	2016	In contrast, alpha-naphthyl tropolone upregulated p53 expression and phosphorylation of Akt and mTOR in a manner that was not rescued by caspase inhibition.	alpha-naphthyl tropolone	13-37	P53	Homo sapiens	50-53
27556514-8	2016	The anti-apoptotic activity of Y-27632 correlated with a reduction in p53 serine 15 phosphorylation and the consequent reduction in the expression of downstream target genes p21 and DAPK1, two genes involved in the induction of cell death.	Y 27632	31-38	P53	Homo sapiens	70-73
27763329-6	2016	Moreover, while Ni(II) thiosemicarbazone compound significantly increased levels of p53 and cleaved caspase-3 proteins, it decreased level of Phospho-Akt1 protein in HL60 cells.	ni(ii) thiosemicarbazone	16-40	P53	Homo sapiens	84-87
27235580-0	2016	Regulation of proapoptotic proteins Bak1 and p53 by miR-125b in an experimental model of Alzheimer"s disease: Protective role of 17beta-estradiol.	mir-125b	52-60	P53	Homo sapiens	45-48
27527552-9	2016	Additionally, by241 inhibited mTOR, activated p53 and its downstream proteins, cleaved MDM2 and PI3K/AKT as well as NF-kappaB signaling pathway.	by241	14-19	P53	Homo sapiens	46-49
27118659-7	2016	Interestingly, the mutant p53-driven mTOR stimulation sensitized cancer cells to the treatment with the mTOR inhibitor everolimus.	Everolimus	119-129	P53	Homo sapiens	26-29
27483224-1	2016	We previously reported that prenylated chalcone 2 (PC2), the O-prenyl derivative (2) of 2"-hydroxy-3,4,4",5,6"-pentamethoxychalcone (1), induced cytotoxicity of tumor cells via disruption of p53-MDM2 interaction.	phytochelatin 2	51-54	P53	Homo sapiens	191-194
26914593-8	2016	In contrast, MK-2206, an inhibitor of pAKT, strongly blocked the expression of the differentiation markers and p53 and the activation of Notch1.	MK 2206	13-20	P53	Homo sapiens	111-114
27131434-14	2016	The cell cycle arrest in DCM-DS-treated MDA-MB-231 cells is possibly via p53-independent but p21-dependent pathway.	Methylene Chloride	25-28	P53	Homo sapiens	73-76
27035231-0	2016	Regulation of myo-inositol biosynthesis by p53-ISYNA1 pathway.	Inositol	14-26	P53	Homo sapiens	43-46
27035231-4	2016	Through a microarray screening, we found that five genes related with myo-inositol metabolism were induced by p53.	Inositol	70-82	P53	Homo sapiens	110-113
27035231-5	2016	DNA damage enhanced intracellular myo-inositol content in HCT116 p53+/+ cells, but not in HCT116 p53-/- cells.	Inositol	34-46	P53	Homo sapiens	65-68
27035231-6	2016	We also indicated that inositol 3-phosphate synthase (ISYNA1) which encodes an enzyme essential for myo-inositol biosynthesis as a direct target of p53.	Inositol	100-112	P53	Homo sapiens	148-151
27035231-11	2016	Our findings revealed a novel role of p53 in myo-inositol biosynthesis which could be a potential therapeutic target.	Inositol	45-57	P53	Homo sapiens	38-41
26402383-8	2016	Both Ki67 and p53 showed strong nuclear positivity in the basal/parabasal layers of DSIN.	dsin	84-88	P53	Homo sapiens	14-17
25789847-7	2016	Our results suggest that miR-34a is an essential component of the anti-proliferative activities of I3C, artemisinin, and artesunate and demonstrate that both wild-type p53 dependent and independent pathways are responsible for miR-34a induction.	Artesunate	121-131	P53	Homo sapiens	168-171
26996126-0	2016	Cisplatin-induced apoptosis in non-small-cell lung cancer cells is dependent on Bax- and Bak-induction pathway and synergistically activated by BH3-mimetic ABT-263 in p53 wild-type and mutant cells.	BH 3	144-147	P53	Homo sapiens	167-170
27123999-0	2016	Phosphatidylinositol 3-Kinase/AKT Pathway Inhibition by Doxazosin Promotes Glioblastoma Cells Death, Upregulation of p53 and Triggers Low Neurotoxicity.	Doxazosin	56-65	P53	Homo sapiens	117-120
25995008-2	2016	Previous findings have shown that p53 expression can influence DNA adduct formation of the environmental carcinogen benzo[a]pyrene (BaP) in human cells, indicating a role for p53 in the cytochrome P450 (CYP) 1A1-mediated biotransformation of BaP in vitro.	Benzo(a)pyrene	116-130	P53	Homo sapiens	34-37
25995008-2	2016	Previous findings have shown that p53 expression can influence DNA adduct formation of the environmental carcinogen benzo[a]pyrene (BaP) in human cells, indicating a role for p53 in the cytochrome P450 (CYP) 1A1-mediated biotransformation of BaP in vitro.	Benzo(a)pyrene	116-130	P53	Homo sapiens	175-178
26276565-9	2016	Up-regulation of messenger RNA (mRNA) expression of p53, bax, and caspase 3 were found in AgNP-treated HeLa cells.	agnp	90-94	P53	Homo sapiens	52-55
26704388-0	2016	Combination of galectin inhibitor GCS-100 and BH3 mimetics eliminates both p53 wild type and p53 null AML cells.	BH 3	46-49	P53	Homo sapiens	75-78
26704388-0	2016	Combination of galectin inhibitor GCS-100 and BH3 mimetics eliminates both p53 wild type and p53 null AML cells.	BH 3	46-49	P53	Homo sapiens	93-96
27642319-0	2016	Celecoxib Treatment Alters p53 and MDM2 Expression via COX-2 Crosstalk in A549 Cells.	Celecoxib	0-9	P53	Homo sapiens	27-30
27642319-7	2016	Western blot analysis demonstrated that Celecoxib could augment p53 expression within 24 h, independently of COX-2 inhibition.	Celecoxib	40-49	P53	Homo sapiens	64-67
27642319-8	2016	In contrast, Celecoxib treatment not only returned p53 to the control level, but also strikingly induced COX-2 expression within 48 h. Of further relevance, Celecoxib exposure could significantly result in MDM2 elevation at 48 h. These findings represent p53 as a molecular target being interconnected with COX-2 signaling axis upon Celecoxib treatment.	Celecoxib	13-22	P53	Homo sapiens	51-54
27461656-6	2016	RESULTS: Western blot analysis showed down-regulation of the cyclin D1, c-Myc, and p53 protein activities, and up-regulation of p27KIP1 activity after flavopiridol treatment.	alvocidib	151-163	P53	Homo sapiens	83-86
26801686-3	2016	Therefore, the present study aimed to elucidate the impact of 15-deoxy-Delta(12,14)-PGJ2 (15d-PGJ2, a stable PGD2 degradation product) on cell death/cell survival pathways in p53-deficient MG-63 OS cells.	15-deoxy-delta(12,14)-prostaglandin J2	62-88	P53	Homo sapiens	175-178
26794443-7	2016	In contrast, NADPH oxidase and p53 (especially acetylation-defective mutant p53) act as positive regulators of ferroptosis by promotion of ROS production and inhibition of expression of SLC7A11 (a specific light-chain subunit of the cystine/glutamate antiporter), respectively.	Cystine	233-240	P53	Homo sapiens	31-34
26794443-7	2016	In contrast, NADPH oxidase and p53 (especially acetylation-defective mutant p53) act as positive regulators of ferroptosis by promotion of ROS production and inhibition of expression of SLC7A11 (a specific light-chain subunit of the cystine/glutamate antiporter), respectively.	Cystine	233-240	P53	Homo sapiens	76-79
26443342-7	2016	The anatomical characteristic of DIO-S was correlated with differential expression of cellular proliferation (ALDH3A1 and MYC) and antioxidant and DNA protection (GSTM2, SIRT1), and tumor suppression (TP53, PTEN, TGFB1) genes.	dio-s	33-38	P53	Homo sapiens	201-205
26772154-9	2016	The closely positive correlations between MMA/DMA and MEG3/TUG1/HOTAIR/MALAT1 were found, but negative correlation between DMA/MALAT1 and the base modifications of exon 7 and 8 of p53 were found also (P &lt; 0.05).	N-myristoyl-alaninol	123-126	P53	Homo sapiens	180-183
26937175-5	2016	RESULTS AND CONCLUSION: We found that the MDM2 inhibitor MI-319 induced RCC cell apoptosis mainly dependent on p53 overexpression, while the mTOR antagonist rapamycin promoted RCC cell apoptosis primarily through upregulation of HIF1alpha expression.	2-methyl-4-isothiazolin-3-one	57-59	P53	Homo sapiens	111-114
26866273-10	2016	In LP MSCs treated with t-BHQ for ~7 days, the phosphorylation and nuclear localization of NRF2 improved and SIRT1 protein level increased, whereas p53 protein levels decreased.	leucylproline	3-5	P53	Homo sapiens	148-151
25398514-8	2016	CYP1A1 is inducible via the aryl hydrocarbon receptor (AHR), but we did not find that expression of AHR was dependent on p53; rather, we found that BaP-induced CYP1A1 expression was regulated through p53 binding to a p53 response element in the CYP1A1 promoter region, thereby enhancing its transcription.	Benzo(a)pyrene	148-151	P53	Homo sapiens	200-203
25398514-8	2016	CYP1A1 is inducible via the aryl hydrocarbon receptor (AHR), but we did not find that expression of AHR was dependent on p53; rather, we found that BaP-induced CYP1A1 expression was regulated through p53 binding to a p53 response element in the CYP1A1 promoter region, thereby enhancing its transcription.	Benzo(a)pyrene	148-151	P53	Homo sapiens	200-203
26586108-0	2016	Idaein chloride induced p53 dependent apoptosis in cervical cancer cells through inhibition of viral oncoproteins.	cyanidin 3-galactoside	0-15	P53	Homo sapiens	24-27
26586108-5	2016	In addition, the idaein chloride significantly inhibited the expression of E6 and E7 proteins, resulting in p53 re-expression and hence triggering of p53 dependent apoptosis.	cyanidin 3-galactoside	17-32	P53	Homo sapiens	108-111
26586108-5	2016	In addition, the idaein chloride significantly inhibited the expression of E6 and E7 proteins, resulting in p53 re-expression and hence triggering of p53 dependent apoptosis.	cyanidin 3-galactoside	17-32	P53	Homo sapiens	150-153
26713361-0	2016	Evodiamine selectively targets cancer stem-like cells through the p53-p21-Rb pathway.	evodiamine	0-10	P53	Homo sapiens	66-69
26713361-7	2016	Surprisingly, evodiamine selectively activated p53 and p21 and decreased inactive Rb, the master molecules in G1/S checkpoint.	evodiamine	14-24	P53	Homo sapiens	47-50
26795951-0	2016	Study of Arsenic Sulfide in Solid Tumor Cells Reveals Regulation of Nuclear Factors of Activated T-cells by PML and p53.	arsenic trisulfide	9-24	P53	Homo sapiens	116-119
26942868-7	2016	Our findings suggested that DHA may be more effective than EPA in growth suppression of TOV-21G cells and the biologic effects may be partly mediated by PPARgamma and p53 activation.	Docosahexaenoic Acids	28-31	P53	Homo sapiens	167-170
26498391-6	2016	Furthermore, we showed that resveratrol enhanced glioblastoma-initiating cells to temozolomide-induced apoptosis through DNA double-stranded breaks/pATM/pATR/p53 pathway activation, and promoted glioblastoma-initiating cell differentiation involving p-STAT3 inactivation.	Temozolomide	82-94	P53	Homo sapiens	158-161
30198696-4	2016	Simultaneous action ofNaBut and low concentration of AMD sharply reduced the clonogenic survival of transformed cells, in parallelwith increased apoptotic cell death.The study of the mechanisms of cell death induced by the combined actionof NaBut and low concentrations of AMD showed that the joint treatment resulted in activation of proapoptotictranscription factor p53 and the suppression of the activity of anti-apoptotic factor NF-kB.	nabut	22-27	P53	Homo sapiens	368-371
26788175-4	2015	The results revealed that low or negative expression of p53, Bcl-2 and COX-2, and high or positive expression of cleaved caspase-3 were significantly correlated with high sensitivity to NDP.	nedaplatin	186-189	P53	Homo sapiens	56-59
26343999-10	2015	Up-regulation of the endogenous p53 with benzo[alpha]pyrene--a well-known p53 activator--increased the expression of the p53 responsive positive control and the CYP2A6-5"-Luc construct containing the intact p53 binding site but not the mutated CYP2A6-5"-Luc construct.	Benzo[alpha]pyrene	41-59	P53	Homo sapiens	32-35
26343999-10	2015	Up-regulation of the endogenous p53 with benzo[alpha]pyrene--a well-known p53 activator--increased the expression of the p53 responsive positive control and the CYP2A6-5"-Luc construct containing the intact p53 binding site but not the mutated CYP2A6-5"-Luc construct.	Benzo[alpha]pyrene	41-59	P53	Homo sapiens	74-77
26343999-10	2015	Up-regulation of the endogenous p53 with benzo[alpha]pyrene--a well-known p53 activator--increased the expression of the p53 responsive positive control and the CYP2A6-5"-Luc construct containing the intact p53 binding site but not the mutated CYP2A6-5"-Luc construct.	Benzo[alpha]pyrene	41-59	P53	Homo sapiens	74-77
26343999-10	2015	Up-regulation of the endogenous p53 with benzo[alpha]pyrene--a well-known p53 activator--increased the expression of the p53 responsive positive control and the CYP2A6-5"-Luc construct containing the intact p53 binding site but not the mutated CYP2A6-5"-Luc construct.	Benzo[alpha]pyrene	41-59	P53	Homo sapiens	74-77
26343999-11	2015	Finally, inducibility of the native CYP2A6 gene by benzo[alpha]pyrene was demonstrated by dose-dependent increases in CYP2A6 mRNA and protein levels along with increased p53 levels in the nucleus.	Benzo[alpha]pyrene	51-69	P53	Homo sapiens	170-173
26627563-2	2015	In the present paper, we investigated how p53 dynamics are modulated by PDCD5 during the deoxyribose nucleic acid damage response using methods of bifurcation analysis and potential landscape.	Deoxyribose	89-100	P53	Homo sapiens	42-45
24664296-7	2014	Moreover, the level of activated p53 and PARP-1 were significantly induced by BaP, whereas this induction was markedly reduced after curcumin and VE co-treatment.	Benzo(a)pyrene	78-81	P53	Homo sapiens	33-36
24664296-10	2014	Taken together, BaP-induced cytotoxicity occurs through DNA damage, cell cycle arrest, ROS production, modulation of metabolizing enzymes, and the expression/activation of p53, PARP-1, survivin, and Bax/Bcl-2.	Benzo(a)pyrene	16-19	P53	Homo sapiens	172-175
24361490-8	2014	Interestingly, the p53 signaling pathway was activated by BaP, but not by TCDD, in BeWo cells and co-treatment by the p53 inhibitor pifithrin-alpha or siRNAs-mediated silencing of p53 prevented up-regulation of beta-hCG and syncytin-2 induced by BaP.	Benzo(a)pyrene	58-61	P53	Homo sapiens	19-22
24361490-8	2014	Interestingly, the p53 signaling pathway was activated by BaP, but not by TCDD, in BeWo cells and co-treatment by the p53 inhibitor pifithrin-alpha or siRNAs-mediated silencing of p53 prevented up-regulation of beta-hCG and syncytin-2 induced by BaP.	Benzo(a)pyrene	58-61	P53	Homo sapiens	118-121
24361490-8	2014	Interestingly, the p53 signaling pathway was activated by BaP, but not by TCDD, in BeWo cells and co-treatment by the p53 inhibitor pifithrin-alpha or siRNAs-mediated silencing of p53 prevented up-regulation of beta-hCG and syncytin-2 induced by BaP.	Benzo(a)pyrene	58-61	P53	Homo sapiens	118-121
24361490-8	2014	Interestingly, the p53 signaling pathway was activated by BaP, but not by TCDD, in BeWo cells and co-treatment by the p53 inhibitor pifithrin-alpha or siRNAs-mediated silencing of p53 prevented up-regulation of beta-hCG and syncytin-2 induced by BaP.	Benzo(a)pyrene	246-249	P53	Homo sapiens	19-22
24361490-8	2014	Interestingly, the p53 signaling pathway was activated by BaP, but not by TCDD, in BeWo cells and co-treatment by the p53 inhibitor pifithrin-alpha or siRNAs-mediated silencing of p53 prevented up-regulation of beta-hCG and syncytin-2 induced by BaP.	Benzo(a)pyrene	246-249	P53	Homo sapiens	118-121
24361490-8	2014	Interestingly, the p53 signaling pathway was activated by BaP, but not by TCDD, in BeWo cells and co-treatment by the p53 inhibitor pifithrin-alpha or siRNAs-mediated silencing of p53 prevented up-regulation of beta-hCG and syncytin-2 induced by BaP.	Benzo(a)pyrene	246-249	P53	Homo sapiens	118-121
24361490-9	2014	Taken together, these data demonstrate that BaP induces differentiation of placental trophoblastic BeWo cells in an AhR- and p53-dependent manner.	Benzo(a)pyrene	44-47	P53	Homo sapiens	125-128
24365999-0	2014	A novel oxiranylchromenone derivative, MHY336, induces apoptosis and cell cycle arrest via a p53- and p21-dependent pathway in HCT116 human colon cancer cells.	oxiranylchromenone	8-26	P53	Homo sapiens	93-96
24868967-0	2014	[Roles of p53 in the interaction of p21 and cell cycle proteins induced by benzo [a] pyrene].	Benzo(a)pyrene	75-91	P53	Homo sapiens	10-13
24868967-1	2014	OBJECTIVE: To investigate the roles of p53 in the interaction of p21, cyclin D1 and CDK4 in human embryonic lung fibroblasts (HELFs) induced by benzo (a) pyrene.	Benzo(a)pyrene	144-160	P53	Homo sapiens	39-42
24575839-0	2014	Phospho-aspirin (MDC-22) inhibits breast cancer in preclinical animal models: an effect mediated by EGFR inhibition, p53 acetylation and oxidative stress.	phosphoaspirin	0-15	P53	Homo sapiens	117-120
24406729-0	2014	Modulation of cyclins, p53 and mitogen-activated protein kinases signaling in breast cancer cell lines by 4-(3,4,5-trimethoxyphenoxy)benzoic acid.	4-(3,4,5-trimethoxyphenoxy)benzoic acid	106-145	P53	Homo sapiens	23-26
24406729-5	2014	Western blot analysis revealed the ability of TMPBA to target pathways mediated by mitogen-activated protein (MAP) kinases, 5" adenosine monophosphate-activated protein kinase (AMPK), and p53, of which the concerted action underlined its antitumor efficacy.	4-(3,4,5-trimethoxyphenoxy)benzoic acid	46-51	P53	Homo sapiens	188-191
24406729-7	2014	Taken together, the current study underscores evidence that TMPBA induces apoptosis in breast cancer cells via the modulation of cyclins and p53 expression as well as the modulation of AMPK and mitogen-activated protein kinases (MAPK) signaling.	4-(3,4,5-trimethoxyphenoxy)benzoic acid	60-65	P53	Homo sapiens	141-144
24621507-3	2014	Conversely, Tip60 activates p53 through direct association on target promoters as well as acetylation of p53 at lysine 120 (K120).	k120	124-128	P53	Homo sapiens	105-108
24240108-10	2014	Inhibition of AURKA using an investigational small-molecule specific inhibitor, alisertib, decreased the HDM2 protein level and induced P53 transcriptional activity.	MLN 8237	80-89	P53	Homo sapiens	136-139
24876817-0	2014	Comparison of 4-hydroxynonenal-induced p53-mediated apoptosis in prostate cancer cells LNCaP and DU145.	4-hydroxy-2-nonenal	14-30	P53	Homo sapiens	39-42
24876817-7	2014	CONCLUSIONS: These studies suggest that 4-HNE promotes prostate cancer cell apoptosis through the p53 signaling pathway; the differences of sensitivity to 4-HNE in LNCaP and DU145 cells may be related to the androgen sensitivity of prostate cancer cells; and the 4-HNE-induced p53-mediated apoptosis signal is regulated by GSTA-4.	4-hydroxy-2-nonenal	40-45	P53	Homo sapiens	98-101
24724504-3	2014	In addition, drug Gliotoxin (GTX) and targeting molecules (Lysozyme, p53 and Folic acid) have been incorporated into f-SWNT-COS. f-SWNTs-COS-GTX-p53, f-SWNTs-COS-GTX-lysozyme, f-SWNTs-COS-GTX-FA have been physiochemically characterized for DDS.	Gliotoxin	18-27	P53	Homo sapiens	145-148
24724504-3	2014	In addition, drug Gliotoxin (GTX) and targeting molecules (Lysozyme, p53 and Folic acid) have been incorporated into f-SWNT-COS. f-SWNTs-COS-GTX-p53, f-SWNTs-COS-GTX-lysozyme, f-SWNTs-COS-GTX-FA have been physiochemically characterized for DDS.	Gliotoxin	29-32	P53	Homo sapiens	145-148
24611509-0	2014	L-carvone induces p53, caspase 3 mediated apoptosis and inhibits the migration of breast cancer cell lines.	carvone	0-9	P53	Homo sapiens	18-21
24219989-5	2013	We find that acetylation of K120 in the DNA-binding domain of p53 augments its association with the Drosha microprocessor and promotes nuclear primary miRNA processing.	k120	28-32	P53	Homo sapiens	62-65
24219989-6	2013	Knockdown of human orthologue of Males absent On the First (hMOF), the acetyltransferase that targets K120 in p53, abolishes induction of miR-203 and cell death mediated by CPT.	k120	102-106	P53	Homo sapiens	110-113
24169356-0	2013	MiR-125b acts as an oncogene in glioblastoma cells and inhibits cell apoptosis through p53 and p38MAPK-independent pathways.	mir-125b	0-8	P53	Homo sapiens	87-90
24078627-0	2013	Azadirone, a limonoid tetranortriterpene, induces death receptors and sensitizes human cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) through a p53 protein-independent mechanism: evidence for the role of the ROS-ERK-CHOP-death receptor pathway.	azadirone	0-9	P53	Homo sapiens	177-180
24071451-10	2013	Silencing of p53 in Huh-7 and HepG2 cells abrogated the effects of the alpha-dicarbonyls on cell invasion.	alpha-dicarbonyls	71-88	P53	Homo sapiens	13-16
24071451-13	2013	The effects of both compounds on cell invasion are dependent on p53 and imply that alpha-dicarbonyls could be efficacious in the treatment of p53-expressing invasive liver tumors.	alpha-dicarbonyls	83-100	P53	Homo sapiens	64-67
24071451-13	2013	The effects of both compounds on cell invasion are dependent on p53 and imply that alpha-dicarbonyls could be efficacious in the treatment of p53-expressing invasive liver tumors.	alpha-dicarbonyls	83-100	P53	Homo sapiens	142-145
23943501-5	2013	Colony formation efficiency revealed that FP potentiated the cytotoxicity of TMZ in glioma cells in a p53-independent manner.	Temozolomide	77-80	P53	Homo sapiens	102-105
24136231-0	2013	USP7 inhibitor P22077 inhibits neuroblastoma growth via inducing p53-mediated apoptosis.	1-(5-((2,4-difluorophenyl)thio)-4-nitrothiophen-2-yl)ethanone	15-21	P53	Homo sapiens	65-68
26416444-8	2015	We therefore tested a chemotherapeutic agent (8-amino-adenosine) that induces p53-independent cell death for higher clinically relevant cytotoxicity.	8-aminoadenosine	46-63	P53	Homo sapiens	78-81
27551477-7	2015	Using a doxycycline-regulated inducible p53 expression system demonstrated that apoptosis induced by the ING1b fragment was p53 independent.	Doxycycline	8-19	P53	Homo sapiens	40-43
27551477-7	2015	Using a doxycycline-regulated inducible p53 expression system demonstrated that apoptosis induced by the ING1b fragment was p53 independent.	Doxycycline	8-19	P53	Homo sapiens	124-127
26255117-7	2015	Exposure to beta-glucans increased apoptosis, necrosis, oxidative stress, mRNA expression of p53, p27 and Bax; the activity of AMP-activated protein-kinase, Forkhead transcription factor FOXO3a, Bax and caspase-3; and decreased the activity of p70S6K in MCF-7 cells.	beta-Glucans	12-24	P53	Homo sapiens	93-96
24798859-5	2015	Here, we report that the environmental carcinogen benzo[a]pyrene (BaP) upregulated the expression of seven p53-targeting miRNAs (miR-25, miR-15a, miR-16, miR-92, miR-125b, miR-141, and miR-200a), while 2,3,7,8-tetrachlorodibenzo-rho-dioxin (TCDD) upregulated two of them (miR-25 and miR-92) in MM cells.	Benzo(a)pyrene	66-69	P53	Homo sapiens	107-110
33968195-1	2021	Wild-type (wt) p53-induced phosphatase 1 (Wip1), encoded by the protein phosphatase, Mg2+/Mn2+ dependent 1D (PPM1D) gene, is a serine/threonine phosphatase induced upon genotoxic stress in a p53-dependent manner.	Manganese(2+)	90-94	P53	Homo sapiens	15-18
26516353-9	2015	Leptomycin B (LMB), which was able to block UBXN2A nuclear export following Etoposide treatment, sustained p53-mot-2 interaction and had partially antagonistic effects with Etoposide on cell apoptosis.	leptomycin B	0-12	P53	Homo sapiens	107-110
26516353-9	2015	Leptomycin B (LMB), which was able to block UBXN2A nuclear export following Etoposide treatment, sustained p53-mot-2 interaction and had partially antagonistic effects with Etoposide on cell apoptosis.	leptomycin B	14-17	P53	Homo sapiens	107-110
26516353-11	2015	In addition, LMB-dependent suppression of UBXN2A"s translocation to the cytoplasm upon stress allows the presence of an active mot-2 oncoprotein in the cytoplasm, resulting in p53 sequestration as well as activation of other mot-2-dependent growth promoting pathways.	leptomycin B	13-16	P53	Homo sapiens	176-179
24639390-9	2015	Protein translocation of p-p53, p-H2A.X (S140), and MDC1 from cytoplasm to nucleus was induced by cantharidin in NCI-H460 cells.	Cantharidin	98-109	P53	Homo sapiens	27-30
23686743-7	2013	In conclusion, corilagin is a potential antitumour drug that is effective in retarding the growth of HCC, which is correlated with the activation of p-p53-p21(Cip1) -cdc2/cyclin B1.	corilagin	15-24	P53	Homo sapiens	151-154
23784084-11	2013	TA-induced apoptosis was ameliorated by the knockout of p65 and p53 and the point mutation of p65 at Ser276 residue.	tolfenamic acid	0-2	P53	Homo sapiens	64-67
23836507-5	2013	We have analyzed the associations between 19 SNPs spanning the TP53 locus and a single specific aflatoxin-induced TP53 mutation (R249S) in 85 in hepatocellular carcinoma cases and 132 controls from Thailand.	Aflatoxins	96-105	P53	Homo sapiens	63-67
34032749-0	2021	The important role of MDM2, RPL5, and TP53 in mycophenolic acid-induced cleft lip and palate.	Mycophenolic Acid	46-63	P53	Homo sapiens	38-42
23836507-5	2013	We have analyzed the associations between 19 SNPs spanning the TP53 locus and a single specific aflatoxin-induced TP53 mutation (R249S) in 85 in hepatocellular carcinoma cases and 132 controls from Thailand.	Aflatoxins	96-105	P53	Homo sapiens	114-118
27314071-2	2016	We have uncovered a novel function of p53 that contributes to tumor suppression through regulation of cystine metabolism, reactive oxygen species responses, and ferroptosis.	Cystine	102-109	P53	Homo sapiens	38-41
23652278-12	2013	An inhibitor of p53, pifithrin-alpha, attenuated the anticancer effects of OSU-03012 and downregulated the expression of Bax and cleaved caspase-9.	OSU 03012	75-84	P53	Homo sapiens	16-19
34032749-7	2021	The genes most relevant to MPA-induced CLP included ABCB1, COL1A1, Rac1, TGFbeta1, EDN1, and TP53, as well as the TP53-associated genes MDM2 and RPL5.	Mycophenolic Acid	27-30	P53	Homo sapiens	93-97
25808868-8	2015	Mechanistically, DcR1 attenuates temozolomide efficacy by blunting activation of the Fas receptor pathway in p53(+/+) glioma cells.	Temozolomide	33-45	P53	Homo sapiens	109-112
23652278-13	2013	Altogether, our results show that OSU-03012 could induce apoptosis in human esophageal carcinoma cells through a p53/Bax/cytochrome c/caspase-9-dependent pathway.	OSU 03012	34-43	P53	Homo sapiens	113-116
34035828-9	2021	Further analysis showed that the HGD activity of quercetin, formononetin, kaempferol, isorhamnetin, and beta-sitosterol ingredients is possible through VEGFA, IL6, TNF, AKT1, and TP53 targets involved in TNF, toll-like receptors, and MAPK-related pathways, which have anti-inflammatory, antiapoptosis, antioxidation, and autophagy effects, relieve renal fibrosis and renal cortex injury, and improve renal function, thus delaying the development of DN.	gamma-sitosterol	104-119	P53	Homo sapiens	179-183
25908509-14	2015	Patients with a del(17p) or TP53 mutation can be treated with ibrutinib or a combination of idelalisib and rituximab.	ibrutinib	62-71	P53	Homo sapiens	28-32
33691199-0	2021	Knockdown of TRIM32 inhibits tumor growth and increases the therapeutic sensitivity to temozolomide in glioma in a p53-dependent and -independent manner.	Temozolomide	87-99	P53	Homo sapiens	115-118
25521189-4	2015	Dexrazoxane induced DNA damage responses, shown by enhanced levels of gamma-H2AX/53BP1 foci, ATM (ataxia telangiectasia mutated), ATR (ATM and Rad3-related), Chk1 and Chk2 phosphorylation, and by p53 accumulation.	Dexrazoxane	0-11	P53	Homo sapiens	196-199
25521189-7	2015	Knockdown of ATF3 gene expression by siRNA triggered apoptosis in control cells and diminished the p53 protein level in both control and dexrazoxane -treated cells.	Dexrazoxane	137-148	P53	Homo sapiens	99-102
23702662-8	2013	In telmisartan-treated ECs, phosphorylation and activation of Akt, as well as MDM2, were reduced, leading to accumulation of p53 in the nucleus, where it represses the transcription of cell cycle-promoting genes.	Telmisartan	3-14	P53	Homo sapiens	125-128
23545415-4	2013	In MDA-MB-231 and HCT116 cells, expressing mutant or wild type p53, respectively, autophagy occurred following exposure to PRIMA-1, as shown by acridine orange staining, anti-LC3 immunofluorescence and immunoblots, as well as by electron microscopy.	Acridine Orange	144-159	P53	Homo sapiens	63-66
25521189-11	2015	The DNA damage-triggered ATF3 controlled p53 accumulation and generation of double-strand breaks and is proposed to serve as a switch between DNA damage and cell death following dexrazoxane treatment.	Dexrazoxane	178-189	P53	Homo sapiens	41-44
33691199-5	2021	Conversely, knockdown of TRIM32 inhibited glioma cells proliferation in vitro and in vivo and sensitized glioma cells to the treatment of TMZ in a p53-dependent and -independent manner.	Temozolomide	138-141	P53	Homo sapiens	147-150
33735664-9	2021	Ibrutinib/BTKi showed potential benefit in relapsed/refractory patients and patients without CXCR4NS/MS including those with TP53 mutations.	ibrutinib	0-9	P53	Homo sapiens	125-129
25802231-2	2015	Oral ibrutinib is indicated for the treatment of patients with relapsed/refractory mantle cell lymphoma (MCL) or chronic lymphocytic leukaemia (CLL) and for the treatment of patients with CLL and a chromosome 17 deletion (del 17p) or TP53 mutation.	ibrutinib	5-14	P53	Homo sapiens	234-238
25802231-7	2015	Given its efficacy and tolerability, once-daily, oral ibrutinib is an emerging treatment option for patients with relapsed/refractory MCL or CLL and CLL patients with del 17p or TP53 mutation.	ibrutinib	54-63	P53	Homo sapiens	178-182
23649769-0	2013	Hepatocellular carcinoma and liver cirrhosis TP53 mutation analysis reflects a moderate dietary exposure to aflatoxins in Espirito Santo State, Brazil.	Aflatoxins	108-118	P53	Homo sapiens	45-49
23649769-1	2013	The close relationship between aflatoxins and 249ser TP53 gene mutation (AGG to AGT, Arg to Ser) in hepatocellular carcinoma (HCC) makes this mutation an indirect indicator of dietary contamination with this toxin.	Aflatoxins	31-41	P53	Homo sapiens	53-57
23649769-9	2013	TP53 exon 7 mutations, which are related to aflatoxins exposure, were found at 14.6% (249ser), 7.3% (250leu) and 2.4% (250ser) in 41 cases of HCC and 1.4% in 74 liver cirrhosis (without HCC) cases, suggesting a moderate dietary exposure to aflatoxins in the Espirito Santo State, Brazil.	Aflatoxins	44-54	P53	Homo sapiens	0-4
23649769-9	2013	TP53 exon 7 mutations, which are related to aflatoxins exposure, were found at 14.6% (249ser), 7.3% (250leu) and 2.4% (250ser) in 41 cases of HCC and 1.4% in 74 liver cirrhosis (without HCC) cases, suggesting a moderate dietary exposure to aflatoxins in the Espirito Santo State, Brazil.	Aflatoxins	240-250	P53	Homo sapiens	0-4
33627789-2	2021	We recently showed that impairing cellular antioxidant systems via inhibition of SLC7A11, a component of the system xc- cystine-glutamate antiporter, enhances sensitivity to mutant-p53 targeted therapy, APR-246.	Cystine	120-127	P53	Homo sapiens	181-184
23481022-8	2013	Among the analogs tested, SC144 exhibited the highest cytotoxicity in a panel of colon cancer cell lines in a p53-independent manner, accompanied by cell cycle arrest in G0/G1 with downregulation of Cyclin D1 levels, and apoptosis induction with upregulation of cell surface-bound Fas/CD95.	SC 144	26-31	P53	Homo sapiens	110-113
23640975-0	2013	PI3K/mTOR inhibitor PF-04691502 antitumor activity is enhanced with induction of wild-type TP53 in human xenograft and murine knockout models of head and neck cancer.	2-amino-8-(4-(2-hydroxyethoxy)cyclohexyl)-6-(6-methoxypyridin-3-yl)-4-methylpyrido(2,3-d)pyrimidin-7(8H)-one	20-31	P53	Homo sapiens	91-95
25377899-0	2015	Identification of antipsychotic drug fluspirilene as a potential p53-MDM2 inhibitor: a combined computational and experimental study.	Fluspirilene	37-49	P53	Homo sapiens	65-68
25377899-7	2015	The molecular dynamics simulations suggested stable binding of fluspirilene to the p53-binding pocket on MDM2 protein.	Fluspirilene	63-75	P53	Homo sapiens	83-86
25377899-8	2015	The experimental testing of fluspirilene showed significant growth inhibition of human colon tumor cells in a p53-dependent manner.	Fluspirilene	28-40	P53	Homo sapiens	110-113
25377899-10	2015	Taken together, these computational and experimental data suggest a potentially novel role of fluspirilene in inhibiting the p53-MDM2 interaction.	Fluspirilene	94-106	P53	Homo sapiens	125-128
25377899-12	2015	Furthermore, fluspirilene could also serve as a structurally-novel lead molecule for the development of more potent, small-molecule p53-MDM2 inhibitors against several types of cancer.	Fluspirilene	13-25	P53	Homo sapiens	132-135
25092068-8	2015	Delivered cisplatin cooperated with piroxicam in modulating cell cycle regulators as caspase-3, p53 and p21.	Piroxicam	36-45	P53	Homo sapiens	96-99
23238567-4	2013	Here, we show that Sestrin2 (Sesn2), also known as Hi95, a p53 target gene that protects cells against oxidative and genotoxic stresses, participates in the protective role of Akt in response to an energetic stress induced by 2-deoxyglucose (2-DG).	Deoxyglucose	226-240	P53	Homo sapiens	59-62
23238567-4	2013	Here, we show that Sestrin2 (Sesn2), also known as Hi95, a p53 target gene that protects cells against oxidative and genotoxic stresses, participates in the protective role of Akt in response to an energetic stress induced by 2-deoxyglucose (2-DG).	Deoxyglucose	242-246	P53	Homo sapiens	59-62
23161404-3	2013	In this study, we demonstrated that lithium and SB216763, which are pharmacological inhibitors of GSK3, attenuated p53 accumulation and caspase-3 activation, as shown by PARP cleavage induced by the DNA-damaging agents doxorubicin, etoposide and camptothecin.	Lithium	36-43	P53	Homo sapiens	115-118
33573023-2	2021	The purpose of this study was to elucidate the role of JNK on the anticancer effects of the Korean plant Artemisia annua L. (pKAL) polyphenols in p53 wild-type HCT116 human colorectal cancer cells.	Polyphenols	131-142	P53	Homo sapiens	146-149
27481281-0	2013	Molecular Dynamics Investigation on the Inhibition of MDM2-p53 Interaction by Polyphenols.	Polyphenols	78-89	P53	Homo sapiens	59-62
25448278-3	2015	PFT significantly abrogated DHA-induced cytotoxicity in wild-type HepG2 cells (normal expression of p53) and after p53-knockdown by siRNA, as well as in Hep3B (p53 null) and Huh7 (p53 mutant) cells.	Docosahexaenoic Acids	28-31	P53	Homo sapiens	100-103
33509226-0	2021	The miR-1185-2-3p-GOLPH3L pathway promotes glucose metabolism in breast cancer by stabilizing p53-induced SERPINE1.	mir-1185-2-3p	4-17	P53	Homo sapiens	94-97
25359865-4	2015	APPROACH AND RESULTS: When compared with primary human umbilical vein endothelial cells grown under standard conditions, ECs with chronic homocysteine treatment showed accelerated upregulation of p16, p21, and p53, markers of cellular senescence, during 6 to 10 passages.	Homocysteine	138-150	P53	Homo sapiens	210-213
23065571-3	2013	Incubation of NCI-H460 cells with the combination of 2DG and FA for 24 h before irradiation upregulated the expression of proapoptotic proteins p53 and Bax.	Deoxyglucose	53-56	P53	Homo sapiens	144-147
23065571-8	2013	Taken together, the results of our study clearly suggested that the cell death induced by the combination of 2DG and FA along with irradiation would involve alteration in expression of p53, p21, NF-kappaB, Bax, and caspase-3, indicating oxidative mechanism in NCI-H460 cells.	Deoxyglucose	109-112	P53	Homo sapiens	185-188
33680372-10	2021	AgNP treatments also induced the p53 expression in HT-29 cells.	agnp	0-4	P53	Homo sapiens	33-36
23334421-5	2013	We show that p53 represses the expression of the tricarboxylic-acid-cycle-associated malic enzymes ME1 and ME2 in human and mouse cells.	Tricarboxylic Acids	49-67	P53	Homo sapiens	13-16
25921120-0	2015	Betaine Effects on Morphology, Proliferation, and p53-induced Apoptosis of HeLa Cervical Carcinoma Cells in Vitro.	Betaine	0-7	P53	Homo sapiens	50-53
26558272-4	2015	2DG significantly inhibited the viability of MCF-7/MDR cells and enhanced DOX-induced apoptosis by upregulating protein expression of AMPKalpha, P53, and caspase-3.	Deoxyglucose	0-3	P53	Homo sapiens	145-148
23268733-0	2013	Siladenoserinols A-L: new sulfonated serinol derivatives from a tunicate as inhibitors of p53-Hdm2 interaction.	siladenoserinols a-l	0-20	P53	Homo sapiens	90-93
33131904-8	2021	The mechanism of mebendazole was associated with p53-independent induction of p21 and tubule depolymerization.	Mebendazole	17-28	P53	Homo sapiens	49-52
23268733-1	2013	Siladenoserinols A-L were isolated from a tunicate as inhibitors of p53-Hdm2 interaction, a promising target for cancer chemotherapy.	siladenoserinols a-l	0-20	P53	Homo sapiens	68-71
23841076-3	2013	Results show that, in addition to apoptosis, DHA increased the expression levels of lipidated form LC3B and potently stimulated the autophagic flux, suggesting that DHA induces both autophagy and apoptosis in cancer cells expressing mutant p53.	Docosahexaenoic Acids	45-48	P53	Homo sapiens	240-243
23841076-3	2013	Results show that, in addition to apoptosis, DHA increased the expression levels of lipidated form LC3B and potently stimulated the autophagic flux, suggesting that DHA induces both autophagy and apoptosis in cancer cells expressing mutant p53.	Docosahexaenoic Acids	165-168	P53	Homo sapiens	240-243
23841076-5	2013	Similarly, pretreatment with the antioxidant N-acetyl-cysteine (NAC) markedly inhibited both the autophagy and the apoptosis triggered by DHA, indicating that mitochondrial ROS mediate the cytotoxicity of DHA in mutant p53 cells.	Docosahexaenoic Acids	138-141	P53	Homo sapiens	219-222
23841076-7	2013	Collectively, these findings present a novel mechanism of ROS-regulated apoptosis and autophagy that involves Akt-mTOR signaling in prostate cancer cells with mutant p53 exposed to DHA.	Docosahexaenoic Acids	181-184	P53	Homo sapiens	166-169
26218928-3	2015	We recently discovered a novel mechanism whereby p53 inhibits cystine uptake through repression of the SLC7A11 gene to mediate ferroptosis.	Cystine	62-69	P53	Homo sapiens	49-52
26637744-5	2015	New B-cell receptor inhibitors, such as ibrutinib and idelalisib, may have a role in the management of B-PLL, especially for the patients harboring abnormalities of TP53.	ibrutinib	40-49	P53	Homo sapiens	165-169
26637745-6	2015	Ibrutinib and idelalisib are currently approved for the treatment of relapsed or refractory CLL or frontline treatment of 17p-/TP53mut CLL regardless of fitness.	ibrutinib	0-9	P53	Homo sapiens	127-131
33381593-5	2020	Further research found ellagic acid and corilagin induced G2 phase cell cycle arrest by upregulating levels of P53, Bcl-2, caspase 3, and caspase 9, while the Bax was reduced.	corilagin	40-49	P53	Homo sapiens	111-114
25446094-3	2014	Moreover, HMA upregulated p21 and p27, while it downregulated p53 and Akt.	herbimycin	10-13	P53	Homo sapiens	62-65
25446094-4	2014	In HMA-treated condition, knockdown of E-cadherin and overexpression of p53 increased N-cadherin and vimentin, and mitigated the inhibitory effects of HMA on cell growth and migration.	herbimycin	3-6	P53	Homo sapiens	72-75
25446094-4	2014	In HMA-treated condition, knockdown of E-cadherin and overexpression of p53 increased N-cadherin and vimentin, and mitigated the inhibitory effects of HMA on cell growth and migration.	herbimycin	151-154	P53	Homo sapiens	72-75
25446094-7	2014	Therefore, we propose that HMA suppresses cell growth, and reverses EMT in conjunction with the activation of E-cadherin, p21 and p27 and the inactivation of p53 and PI3K/Akt signaling in ATC cells.	herbimycin	27-30	P53	Homo sapiens	158-161
22995069-0	2013	Riccardin D-26, a synthesized macrocyclic bisbibenzyl compound, inhibits human hepatocellular carcinoma growth through induction of apoptosis in p53-dependent way.	Riccardin D-26	0-14	P53	Homo sapiens	145-148
22995069-7	2013	Overall, Riccardin D-26 may inhibit hepatocellular carcinoma growth through induction of apoptosis in p53-dependent pathway.	Riccardin D-26	9-23	P53	Homo sapiens	102-105
23164604-9	2013	Stimulation also induced activation of E2F1 and downregulation of p53, indicating that SQS induces cell cycle arrest and apoptosis via a p53-independent pathway; p53-independent apoptosis may be mediated by E2F1 activation.	22-O-angeloylcamelliagenin C-3-O-(glucopyranosyl-1-2)(glucopyranosyl-1-2-O-arabinopyranosyl-1-3-)glucopyranosiduronic acid	87-90	P53	Homo sapiens	66-69
23164604-9	2013	Stimulation also induced activation of E2F1 and downregulation of p53, indicating that SQS induces cell cycle arrest and apoptosis via a p53-independent pathway; p53-independent apoptosis may be mediated by E2F1 activation.	22-O-angeloylcamelliagenin C-3-O-(glucopyranosyl-1-2)(glucopyranosyl-1-2-O-arabinopyranosyl-1-3-)glucopyranosiduronic acid	87-90	P53	Homo sapiens	137-140
23164604-9	2013	Stimulation also induced activation of E2F1 and downregulation of p53, indicating that SQS induces cell cycle arrest and apoptosis via a p53-independent pathway; p53-independent apoptosis may be mediated by E2F1 activation.	22-O-angeloylcamelliagenin C-3-O-(glucopyranosyl-1-2)(glucopyranosyl-1-2-O-arabinopyranosyl-1-3-)glucopyranosiduronic acid	87-90	P53	Homo sapiens	137-140
25456271-11	2014	These effects are suggested to be to be linked to AOH-induced DSB (via a reported effect on topoisomerase activity), resulting in an activation of p53 and the Sestrin2-AMPK-mTOR-S6K signaling pathway.	alternariol	50-53	P53	Homo sapiens	147-150
32886933-0	2020	Induction of Cell Cycle Arrest in MKN45 Cells after Schiff Base Oxovanadium Complex Treatment Using Changes in Gene Expression of CdC25 and P53.	Vanadium(II) oxide	64-75	P53	Homo sapiens	140-143
25392275-7	2014	In 2014, several new compounds were approved for patients with ultrahigh risk genetic factors (17p-, TP53mut) and for relapsed/refractory CLL: both idelalisib and ibrutinib are orally bioavailable kinase inhibitors that block key regulators of central pathways.	ibrutinib	163-172	P53	Homo sapiens	101-105
23349842-4	2013	Our results demonstrated that homocysteine inhibited hepatocyte proliferation by up-regulating protein levels of p53 as well as mRNA and protein levels of p21(Cip1) in primary cultured hepatocytes.	Homocysteine	30-42	P53	Homo sapiens	113-116
23349842-6	2013	A p53 inhibitor pifithrin-alpha inhibited the expression of p21(Cip1) and attenuated homocysteine-induced cell growth arrest.	Homocysteine	85-97	P53	Homo sapiens	2-5
33209128-2	2020	In the present study, the small molecule 2-[1-(4-(benzyloxy)phenyl)-3-oxoisoindolin-2-yl)-2-(4-methoxyphenyl)] acetic acid (CDS-3078) significantly increased p53 mRNA expression levels in a dose-dependent manner.	cds-3078	124-132	P53	Homo sapiens	158-161
23341789-5	2012	The role of p53 protein in the sensitivity of c-Met TKI (SU11274) was examined by Western blot analysis and immunohistochemistry.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	57-64	P53	Homo sapiens	12-15
23341789-6	2012	RESULTS: SU11274 significantly induced apoptosis in A549 cells with wild-type p53, compared with that in Calu-1 cells with null-type p53.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	9-16	P53	Homo sapiens	78-81
23341789-7	2012	SU11274 increased p53 protein by enhancing the stability of p53 protein.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	0-7	P53	Homo sapiens	18-21
23341789-7	2012	SU11274 increased p53 protein by enhancing the stability of p53 protein.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	0-7	P53	Homo sapiens	60-63
25411799-8	2014	Modest differences with respect to passage number and response to DCVC exposure were observed in expression of three key proteins (Hsp27, GADD153, p53) involved in stress response.	S-(1,2-dichlorovinyl)cysteine	66-70	P53	Homo sapiens	147-150
28962324-9	2014	A strong transcriptional down-regulation of the proapoptotic gene p53 occurred at 0.05 and 0.5 mg/ml SiO2-NP.	sio2-np	101-108	P53	Homo sapiens	66-69
23341789-8	2012	Increased p53 protein by SU11274 induced up-regulation of Bax and PUMA expression and down-regulation of Bcl-2 expression, subsequently activating caspase 3.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	25-32	P53	Homo sapiens	10-13
33209128-3	2020	Treatment with CDS-3078 increased p53 expression levels and p53-mediated activation of its downstream target genes in HeLa cells.	cds-3078	15-23	P53	Homo sapiens	34-37
23341789-9	2012	In p53 knock-out and knock-in systems, we confirmed that SU11274 caused apoptosis through the p53-mediated apoptotic pathway.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	57-64	P53	Homo sapiens	3-6
23341789-9	2012	In p53 knock-out and knock-in systems, we confirmed that SU11274 caused apoptosis through the p53-mediated apoptotic pathway.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	57-64	P53	Homo sapiens	94-97
25216351-13	2014	Flavopiridol induced growth inhibition and apoptosis at the IC(50) dose (500 nM), resulting in a significant increase in immunofluorescence staining of caspase-3, caspase-8 and p53.	alvocidib	0-12	P53	Homo sapiens	177-180
23341789-10	2012	Likewise, in the A549 xenograft model, SU11274 effectively shrank tumor volume and induced apoptosis via increased p53 protein expression.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	39-46	P53	Homo sapiens	115-118
33209128-3	2020	Treatment with CDS-3078 increased p53 expression levels and p53-mediated activation of its downstream target genes in HeLa cells.	cds-3078	15-23	P53	Homo sapiens	60-63
23341789-12	2012	CONCLUSION: Our finding suggested that p53 plays an important role in SU11274-induced apoptosis, and p53 status seems to be related to the sensitivity to SU11274 in lung cancer.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	70-77	P53	Homo sapiens	39-42
23341789-12	2012	CONCLUSION: Our finding suggested that p53 plays an important role in SU11274-induced apoptosis, and p53 status seems to be related to the sensitivity to SU11274 in lung cancer.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	154-161	P53	Homo sapiens	101-104
33209128-4	2020	Additionally, p53+/+ HeLa cells treated with CDS-3078 presented with dysfunctional mitochondria, as indicated by the decrease in Bcl-2 levels, the increase in Bcl-2 homologous antagonist killer and the increase in cytochrome c release from the mitochondria to the cytoplasm.	cds-3078	45-53	P53	Homo sapiens	14-17
33209128-6	2020	Therefore, CDS-3078 administration induced apoptosis via p53-mediated cell cycle arrest, causing mitochondrial dysfunction and resulting in apoptotic cell death in cervical cancer cells.	cds-3078	11-19	P53	Homo sapiens	57-60
23072738-5	2012	Moreover, these indazoles were able to trigger apoptosis through the upregulation of the typical apoptosis markers p53 and bax.	Indazoles	16-25	P53	Homo sapiens	115-118
25688502-12	2014	After irradiation with carbon ions and temozolomide, cell survival rates depended on p53 status, with a decreased survival rate in wildtype cells.	Temozolomide	39-51	P53	Homo sapiens	85-88
33376724-6	2020	Among the most shared significant pathways between ODs and CDs, we found pathways in cancer, p53 signaling, mismatch repair, mTOR signaling, B cell receptor signaling, and apoptosis pathways.	cds	59-62	P53	Homo sapiens	93-96
25019692-4	2014	Abyssinones promoted apoptosis by up regulation of p53 and Bax, along with down regulation of Bcl-2.	abyssinones	0-11	P53	Homo sapiens	51-54
24944268-3	2014	Magnesium deficiency significantly increased cisplatin-associated weight loss and markers of renal damage (plasma blood urea nitrogen and creatinine), histological changes, inflammation, and renal cell apoptosis and modulated signaling pathways (e.g., ERK1/2, p53, and STAT3).	Magnesium	0-9	P53	Homo sapiens	260-263
22689670-12	2012	miR-125b blocks myeloid differentiation in part by targeting CBFB, blocks apoptosis through down-regulation of multiple genes involved in the p53 pathway, and confers a proliferative advantage to human and mouse myeloid cell lines in part by targeting ABTB1.	mir-125b	0-8	P53	Homo sapiens	142-145
23086311-7	2012	The in vitro cell growth inhibition effect of CaCO(3)-KALA-p53-DOX nanoparticles was evaluated by MTT assay.	Calcium Carbonate	46-53	P53	Homo sapiens	59-62
33211826-5	2020	The impact of TP53mut VAF on clinical outcomes was driven by patients treated with a cytarabine-based regimen (median OS, 4.7 vs 7.3 months for VAF >40% vs <=40%; P = .006), whereas VAF did not significantly affect OS in patients treated with HMA.	Cytarabine	85-95	P53	Homo sapiens	14-21
23086311-8	2012	Compared with CaCO(3)-p53-DOX nanoparticles, CaCO(3)-KALA-p53-DOX nanoparticles exhibited enhanced delivery efficiency, which led to a stronger inhibition effect on HeLa cells.	Calcium Carbonate	45-52	P53	Homo sapiens	58-61
22664907-6	2012	Downregulation of miR-125b upregulates p53 cascade in both human and mouse embryos.	mir-125b	18-26	P53	Homo sapiens	39-42
25100434-5	2014	By RT-PCR and western blot assays, Kuding tea polyphenol significantly induced apoptosis in BcaCD885 cancer cells (p &lt; 0.05) by upregulating caspase-3, caspase-8, caspase-9, Fas/FasL, Bax, p53, p21, E2F1, p73 and downregulating Bcl-2, Bcl-xL, HIAP-1, and HIAP-2 mRNA and protein expressions.	Polyphenols	46-56	P53	Homo sapiens	192-195
24939757-0	2014	Xylarianaphthol-1, a novel dinaphthofuran derivative, activates p21 promoter in a p53-independent manner.	dinaphthofuran	27-41	P53	Homo sapiens	82-85
33211826-8	2020	The best long-term outcomes were observed in those with 1 TP53 mutation with VAF <=40% who received a frontline cytarabine-based regimen (2-year OS, 38% vs 6% for all others; P < .001).	Cytarabine	112-122	P53	Homo sapiens	58-62
32035228-6	2020	We highlight recent research that the biological functions of beta-cryptoxanthin and lycopene are mediated, partially via their oxidative metabolites, through their effects on key molecular targeting events, such as NF-kappaB signaling pathway, RAR/PPARs signaling, SIRT1 signaling pathway, and p53 tumor suppressor pathways.	Cryptoxanthins	62-80	P53	Homo sapiens	295-298
24839007-0	2014	Role of Bax/Bcl-2 family members in green tea polyphenol induced necroptosis of p53-deficient Hep3B cells.	Polyphenols	46-56	P53	Homo sapiens	80-83
24839007-1	2014	Green tea polyphenol (GTP) is one of the most promising chemopreventive agent for cancer; it can inhibit cancer cell proliferation and induce apoptosis through p53-dependent cell signaling pathways.	Polyphenols	10-20	P53	Homo sapiens	160-163
22593008-0	2012	E2F1-dependent pathways are involved in amonafide analogue 7-d-induced DNA damage, G2/M arrest, and apoptosis in p53-deficient K562 cells.	amonafide	40-49	P53	Homo sapiens	113-116
22593008-3	2012	For this purpose, a amonafide analogue, 7-d (2-(3-(2-(Dimethylamino)ethylamino)propyl)-6-(dodecylamino)-1H-benzo[de]isoquinoline-1,3(2H)-dione) was screened, which exhibited high antitumor activity against p53-deficient human Chronic Myelogenous Leukemia (CML) K562 cells.	amonafide	20-29	P53	Homo sapiens	206-209
32035228-6	2020	We highlight recent research that the biological functions of beta-cryptoxanthin and lycopene are mediated, partially via their oxidative metabolites, through their effects on key molecular targeting events, such as NF-kappaB signaling pathway, RAR/PPARs signaling, SIRT1 signaling pathway, and p53 tumor suppressor pathways.	lycopene	85-93	P53	Homo sapiens	295-298
24832164-9	2014	Our series of IC-PBL and PT-PBL cases revealed differential expression of CD10 (0% vs. 42%, respectively), CD56 (22% vs. 42%, respectively), TP53 (67% vs. 8%, respectively), and BCL2 (88% vs. 25%, respectively).	ic-pbl	14-20	P53	Homo sapiens	141-145
32457483-0	2020	BH3 mimetics selectively eliminate chemotherapy-induced senescent cells and improve response in TP53 wild-type breast cancer.	BH 3	0-3	P53	Homo sapiens	96-100
24832557-4	2014	Human gene copy number alteration data, microarray expression data, and TMA analysis indicate that TP53 haploinsufficiency and increased EGFR expression co-occur in human MPNST samples.	4,4-dimethylcholesta-8,14-dien-3-ol	72-75	P53	Homo sapiens	99-103
24793593-5	2014	In fact, the hexamethylbenzene-ruthenium complexes activated caspase activity, with consequent DNA fragmentation, accumulation of pro-apoptotic proteins (p27, p53, p89 PARP fragments), and the concomitant down-regulation of antiapoptotic protein Bcl-2.	hexamethylbenzene	13-30	P53	Homo sapiens	159-162
24787013-7	2014	Exogenous activation of p38 and JNK pathways by dihydrosphingosine reverted resistance of TP53-mutated BL cells to spindle poisons.	safingol	48-66	P53	Homo sapiens	90-94
23323463-5	2012	CIMP negative cases have a high rate of p53 mutations and lower rates of MSI or mutations of BRAF or KRAS.	Cyclic IMP	0-4	P53	Homo sapiens	40-43
33053351-0	2020	Rucaparib Treatment Alters p53 Oscillations in Single Cells to Enhance DNA-Double-Strand-Break-Induced Cell Cycle Arrest.	rucaparib	0-9	P53	Homo sapiens	27-30
22829200-3	2012	We previously showed that SDHx variants result in elevated reactive oxygen species (ROS), disruption of nicotinamide adenine dinucleotide (NAD) equilibrium, and destabilization of p53 hence apoptosis resistance in CS/CSL patient-derived lymphoblastoid cells.	sdhx	26-30	P53	Homo sapiens	180-183
24787013-8	2014	Dihydrosphingosine treatment of TP53-deficient Jurkat and K562 cell lines was also able to induce cell death.	safingol	0-18	P53	Homo sapiens	32-36
33053351-4	2020	The small-molecule rucaparib, an inhibitor of the alternative end-joining-associated protein poly (ADP-ribose) polymerase (PARP), increased p53 pulse duration, altering the temporal expression of multiple p53 target genes.	rucaparib	19-28	P53	Homo sapiens	140-143
24727577-0	2014	Nuclear NF-kappaB contributes to chlorpyrifos-induced apoptosis through p53 signaling in human neural precursor cells.	Chlorpyrifos	33-45	P53	Homo sapiens	72-75
22705644-11	2012	CIL-102-treatment induced apoptosis in MCF-7 cells in association with increased nuclear accumulation of p53 and p21 suggesting that apoptosis is triggered through a p53-p21 dependent pathway.	1-(4-(furo(2,3-b)quinolin-4-ylamino)phenyl)ethanone	0-7	P53	Homo sapiens	105-108
33053351-4	2020	The small-molecule rucaparib, an inhibitor of the alternative end-joining-associated protein poly (ADP-ribose) polymerase (PARP), increased p53 pulse duration, altering the temporal expression of multiple p53 target genes.	rucaparib	19-28	P53	Homo sapiens	205-208
22705644-11	2012	CIL-102-treatment induced apoptosis in MCF-7 cells in association with increased nuclear accumulation of p53 and p21 suggesting that apoptosis is triggered through a p53-p21 dependent pathway.	1-(4-(furo(2,3-b)quinolin-4-ylamino)phenyl)ethanone	0-7	P53	Homo sapiens	166-169
22542754-5	2012	AOH-induced apoptosis was mediated through a mitochondria-dependent pathway, characterized by a p53 activation, an opening of the mitochondrial permeability transition pore (PTP), a loss of mitochondrial transmembrane potential (DeltaPsim), a downstream generation of O(2)(*-) and caspase 9 and 3 activation.	alternariol	0-3	P53	Homo sapiens	96-99
24762088-9	2014	A stable overexpression of miR-125b in human melanoma cell line Mel-Juso resulted in a G0/G1 cell cycle block and emergence of large cells expressing senescence markers: senescence-associated beta-galactosidase, p21, p27 and p53.	mir-125b	27-35	P53	Homo sapiens	225-228
32666844-6	2020	Results showed that the effect of Temozolomide (TMZ) with SMF and FMF together increased the cytotoxicity, free radical production, and p53 followed by p53 protein expression in the human glioblastoma cell line (A172).	Temozolomide	34-46	P53	Homo sapiens	136-139
22519734-0	2012	Expression of the polyalanine expansion mutant of nuclear poly(A)-binding protein induces apoptosis via the p53 pathway.	polyalanine	18-29	P53	Homo sapiens	108-111
22519734-11	2012	Our findings suggest a key role of p53-mediated apoptosis in death of cells expressing the polyalanine expansion mutant of PABPN1.	polyalanine	91-102	P53	Homo sapiens	35-38
32666844-6	2020	Results showed that the effect of Temozolomide (TMZ) with SMF and FMF together increased the cytotoxicity, free radical production, and p53 followed by p53 protein expression in the human glioblastoma cell line (A172).	Temozolomide	34-46	P53	Homo sapiens	152-155
24631733-5	2014	All compounds containing a quinone moiety were able to inhibit p53-dependant transcriptional activity and exerted moderate inhibitory effects on HeLa cell colony formation.	quinone	27-34	P53	Homo sapiens	63-66
32666844-6	2020	Results showed that the effect of Temozolomide (TMZ) with SMF and FMF together increased the cytotoxicity, free radical production, and p53 followed by p53 protein expression in the human glioblastoma cell line (A172).	Temozolomide	48-51	P53	Homo sapiens	136-139
23368763-0	2014	Evaluation of naproxen and cromolyn activities against cancer cells viability, proliferation, apoptosis, p53 and gene expression of survivin and caspase-3.	Cromolyn Sodium	27-35	P53	Homo sapiens	105-108
22494262-9	2012	Our analyses indicate that the R282W mutation of p53 destabilizes the L1 loop and loosens the H2 helix conformation, but the loosened L1 loop can be rescued by residue H115, preventing the R282W mutation from completely destabilizing the protein or abolishing activity.	h115	168-172	P53	Homo sapiens	49-52
32666844-6	2020	Results showed that the effect of Temozolomide (TMZ) with SMF and FMF together increased the cytotoxicity, free radical production, and p53 followed by p53 protein expression in the human glioblastoma cell line (A172).	Temozolomide	48-51	P53	Homo sapiens	152-155
32994268-2	2020	Ibrutinib, a tyrosine kinase inhibitor, is the treatment of choice on relapse or p53-dysfunction.	ibrutinib	0-9	P53	Homo sapiens	81-84
22491426-9	2012	Taken together, DON-induced rRNA cleavage is likely to be closely linked to apoptosis activation and appears to involve the sequential activation of PKR/Hck  p38 p53 caspase 8/9 caspase 3.	deoxynivalenol	16-19	P53	Homo sapiens	162-165
22035418-9	2012	Ara-C causes neuronal cell death by introduction of apoptosis with reactive oxygen species, causing oxidative DNA damage and initiating the p53-dependent apoptotic program.	Cytarabine	0-5	P53	Homo sapiens	140-143
24453002-6	2014	Cell death was p53-independent but caspase-dependent and enhanced with temozolomide, a chemotherapeutic agent used as a present standard of care.	Temozolomide	71-83	P53	Homo sapiens	15-18
32987854-5	2020	Next-generation-sequencing analysis showed that WHO 2015 LNENs classes, could be characterized also by specific molecular alterations: frequently mutated genes involving chromatin remodeling and generally characterized by low mutational burden (MB) are frequently detected in both TC and AC; otherwise, TP53 and RB1 tumor suppressor genes alterations and high MB are usually detected in LCNEC and SCLC.	Technetium	281-283	P53	Homo sapiens	303-307
24362009-0	2014	Cell cycle changes mediated by the p53/miR-34c axis are involved in the malignant transformation of human bronchial epithelial cells by benzo[a]pyrene.	Benzo(a)pyrene	136-150	P53	Homo sapiens	35-38
24362009-2	2014	In this investigation, we evaluated changes in p53 function and its downstream target miRNAs in benzo[a]pyrene (BaP)-induced transformation of human bronchial epithelial (HBE) cells.	Benzo(a)pyrene	96-110	P53	Homo sapiens	47-50
24362009-2	2014	In this investigation, we evaluated changes in p53 function and its downstream target miRNAs in benzo[a]pyrene (BaP)-induced transformation of human bronchial epithelial (HBE) cells.	Benzo(a)pyrene	112-115	P53	Homo sapiens	47-50
24362009-3	2014	Chronic exposure to BaP induced malignant transformation of cells, in which there were increased levels of mutant p53 (mt-p53) and reduced expression of wild-type p53 (wt-p53) and phosphorylated p53 (p-p53).	Benzo(a)pyrene	20-23	P53	Homo sapiens	114-117
24362009-3	2014	Chronic exposure to BaP induced malignant transformation of cells, in which there were increased levels of mutant p53 (mt-p53) and reduced expression of wild-type p53 (wt-p53) and phosphorylated p53 (p-p53).	Benzo(a)pyrene	20-23	P53	Homo sapiens	122-125
22421154-4	2012	ssRNAs containing an adenosine and uridine-rich (ARE) element are permissive targets for p53-mediated degradation.	Uridine	35-42	P53	Homo sapiens	89-92
32987854-5	2020	Next-generation-sequencing analysis showed that WHO 2015 LNENs classes, could be characterized also by specific molecular alterations: frequently mutated genes involving chromatin remodeling and generally characterized by low mutational burden (MB) are frequently detected in both TC and AC; otherwise, TP53 and RB1 tumor suppressor genes alterations and high MB are usually detected in LCNEC and SCLC.	Charcoal	288-290	P53	Homo sapiens	303-307
24362009-3	2014	Chronic exposure to BaP induced malignant transformation of cells, in which there were increased levels of mutant p53 (mt-p53) and reduced expression of wild-type p53 (wt-p53) and phosphorylated p53 (p-p53).	Benzo(a)pyrene	20-23	P53	Homo sapiens	122-125
24362009-3	2014	Chronic exposure to BaP induced malignant transformation of cells, in which there were increased levels of mutant p53 (mt-p53) and reduced expression of wild-type p53 (wt-p53) and phosphorylated p53 (p-p53).	Benzo(a)pyrene	20-23	P53	Homo sapiens	122-125
20978925-0	2012	Novel histone deacetylase inhibitor CG200745 induces clonogenic cell death by modulating acetylation of p53 in cancer cells.	N1-(3-(dimethylamino)propyl)-N8-hydroxy-2-((naphthalene-1-loxy)methyl)oct-2-enediamide	36-44	P53	Homo sapiens	104-107
24362009-3	2014	Chronic exposure to BaP induced malignant transformation of cells, in which there were increased levels of mutant p53 (mt-p53) and reduced expression of wild-type p53 (wt-p53) and phosphorylated p53 (p-p53).	Benzo(a)pyrene	20-23	P53	Homo sapiens	122-125
32878802-5	2020	TMZ+AZD increased the expression of phospho-p53 (p-p53), p-p38 mitogen-activated protein kinase, and phosphatase and tensin homolog; and decreased the expression of p-extracellular signal-regulated kinase 1/2 and p-signal transducer and activator of transcription 3 in glioma cells.	Temozolomide	0-3	P53	Homo sapiens	44-47
24362009-3	2014	Chronic exposure to BaP induced malignant transformation of cells, in which there were increased levels of mutant p53 (mt-p53) and reduced expression of wild-type p53 (wt-p53) and phosphorylated p53 (p-p53).	Benzo(a)pyrene	20-23	P53	Homo sapiens	122-125
24362009-4	2014	With acute (12h) exposure to BaP, p-p53 was increased, and with increasing time of exposure (24h), the increase in p-p53 at a concentration of 1muM BaP was followed by a decline with increasing concentrations; wt-p53 and mt-p53 did not change.	Benzo(a)pyrene	29-32	P53	Homo sapiens	36-39
24362009-4	2014	With acute (12h) exposure to BaP, p-p53 was increased, and with increasing time of exposure (24h), the increase in p-p53 at a concentration of 1muM BaP was followed by a decline with increasing concentrations; wt-p53 and mt-p53 did not change.	Benzo(a)pyrene	29-32	P53	Homo sapiens	117-120
24362009-4	2014	With acute (12h) exposure to BaP, p-p53 was increased, and with increasing time of exposure (24h), the increase in p-p53 at a concentration of 1muM BaP was followed by a decline with increasing concentrations; wt-p53 and mt-p53 did not change.	Benzo(a)pyrene	29-32	P53	Homo sapiens	117-120
24362009-4	2014	With acute (12h) exposure to BaP, p-p53 was increased, and with increasing time of exposure (24h), the increase in p-p53 at a concentration of 1muM BaP was followed by a decline with increasing concentrations; wt-p53 and mt-p53 did not change.	Benzo(a)pyrene	29-32	P53	Homo sapiens	117-120
24362009-4	2014	With acute (12h) exposure to BaP, p-p53 was increased, and with increasing time of exposure (24h), the increase in p-p53 at a concentration of 1muM BaP was followed by a decline with increasing concentrations; wt-p53 and mt-p53 did not change.	Benzo(a)pyrene	148-151	P53	Homo sapiens	117-120
24362009-4	2014	With acute (12h) exposure to BaP, p-p53 was increased, and with increasing time of exposure (24h), the increase in p-p53 at a concentration of 1muM BaP was followed by a decline with increasing concentrations; wt-p53 and mt-p53 did not change.	Benzo(a)pyrene	148-151	P53	Homo sapiens	117-120
20978925-8	2012	CG200745 increased acetylation of p53 lysine residues K320, K373, and K382.	N1-(3-(dimethylamino)propyl)-N8-hydroxy-2-((naphthalene-1-loxy)methyl)oct-2-enediamide	0-8	P53	Homo sapiens	34-37
20978925-8	2012	CG200745 increased acetylation of p53 lysine residues K320, K373, and K382.	chromic phosphate	60-64	P53	Homo sapiens	34-37
20862736-1	2012	p53 can mediate DNA damage-induced apoptosis in various cell lines treated with Benzo(a)pyrene (BaP).	Benzo(a)pyrene	96-99	P53	Homo sapiens	0-3
20862736-2	2012	However, the potential role of p73, one of the p53 family members, in BaP-induced apoptotic cell death remains to be determined.	Benzo(a)pyrene	70-73	P53	Homo sapiens	47-50
24362009-4	2014	With acute (12h) exposure to BaP, p-p53 was increased, and with increasing time of exposure (24h), the increase in p-p53 at a concentration of 1muM BaP was followed by a decline with increasing concentrations; wt-p53 and mt-p53 did not change.	Benzo(a)pyrene	148-151	P53	Homo sapiens	117-120
24362009-8	2014	Thus, changes in the cell cycle mediated by the p53/miR-34c axis are involved in the transformation cells induced by BaP.	Benzo(a)pyrene	117-120	P53	Homo sapiens	48-51
32878802-5	2020	TMZ+AZD increased the expression of phospho-p53 (p-p53), p-p38 mitogen-activated protein kinase, and phosphatase and tensin homolog; and decreased the expression of p-extracellular signal-regulated kinase 1/2 and p-signal transducer and activator of transcription 3 in glioma cells.	Temozolomide	0-3	P53	Homo sapiens	51-54
32461254-7	2020	Using CEBIT-based high-throughput screening assays, we identified known inhibitors of the p53/MDM2 (MDM2) interaction and of the histone methyltransferase, suppressor of variegation 3-9 homolog 1 (SUV39H1), from a compound library.	cebit	6-11	P53	Homo sapiens	90-93
24743130-5	2014	Nitrooxide defficiency in gingival mucosal cells is characterized by decreased protein P-53 expression and terminal differentiation disorder of the cells.	nitrooxide	0-10	P53	Homo sapiens	87-91
21827374-2	2012	Cenersen, an oligonucleotide targeting TP53, has been shown to abrogate the activity of TP53 gain-of-function mutants and to increase sensitivity of lymphoma cells to cytotoxic chemotherapy in vitro.	cenersen	0-8	P53	Homo sapiens	39-43
21827374-2	2012	Cenersen, an oligonucleotide targeting TP53, has been shown to abrogate the activity of TP53 gain-of-function mutants and to increase sensitivity of lymphoma cells to cytotoxic chemotherapy in vitro.	cenersen	0-8	P53	Homo sapiens	88-92
21717444-0	2012	Phase 2 randomized study of p53 antisense oligonucleotide (cenersen) plus idarubicin with or without cytarabine in refractory and relapsed acute myeloid leukemia.	cenersen	59-67	P53	Homo sapiens	28-31
32784977-8	2020	Furthermore, the anthraquinone-rich dichloromethane fraction displayed the highest anticancer activity when evaluated in a human hepatoma cancer cell line (HepG2), in which it induced increased apoptosis mediated by p53 and caspase activation.	Methylene Chloride	36-51	P53	Homo sapiens	216-219
21765464-7	2012	Our approaches involving gene manipulation and pharmacological interference finally highlight that celecoxib alters pro- and anti-p53 networks, not in isolation but in concert, to rejuvenate p53-dependent apoptotic program in HPV-infected cervical cancer cells.	Celecoxib	99-108	P53	Homo sapiens	130-133
21765464-7	2012	Our approaches involving gene manipulation and pharmacological interference finally highlight that celecoxib alters pro- and anti-p53 networks, not in isolation but in concert, to rejuvenate p53-dependent apoptotic program in HPV-infected cervical cancer cells.	Celecoxib	99-108	P53	Homo sapiens	191-194
22715313-9	2012	Here, we have identified three drug-like compounds that are ZINC01019934, ZINC00624418 and ZINC00664532 adequate to interrupt stability of p53-mortalin complex that warrant for anticancer agent.	zinc00624418	74-86	P53	Homo sapiens	139-142
24246761-2	2014	We previously showed that the PAH prototype, benzo[a]pyrene (B[a]P), triggers apoptosis via DNA damage-induced p53 activation (genotoxic pathway) and via remodeling of the membrane cholesterol-rich microdomains called lipid rafts, leading to changes in pH homeostasis (non-genotoxic pathway).	Benzo(a)pyrene	45-59	P53	Homo sapiens	111-114
32472321-0	2020	Novel Mannich base 3FB3FA8H induces apoptosis by upregulating P53 pathway in neuroblastoma cells.	mannich base 3fb3fa8h	6-27	P53	Homo sapiens	62-65
24269226-8	2014	Ingenuity pathway analysis by IPA put the following factors in a central position of the hypothetical networks: myc and p53 for aaptamine; tumor necrosis factor (TNF) for demethyloxyaaptamine; and all three, myc, p53, and TNF for isoaaptamine.	aaptamine	128-137	P53	Homo sapiens	120-123
24275138-4	2014	p53 Silencing decreased survival of glucose-starved C8161 melanoma with pyruvate supplementation under hypoxia (&lt;=1% oxygen), but increased resistance to glycolytic inhibitors oxamate and 2-deoxyglucose in 5mM glucose, preferentially under normoxia.	Deoxyglucose	191-205	P53	Homo sapiens	0-3
22202062-2	2012	Regulation of anti-tumor p53 functions by dietary plant polyphenols particularly black tea and its active component theaflavins has gained immense recognition from the point of view of both efficacy and safety.	Polyphenols	56-67	P53	Homo sapiens	25-28
22912688-0	2012	Aciculatin induces p53-dependent apoptosis via MDM2 depletion in human cancer cells in vitro and in vivo.	aciculatin	0-10	P53	Homo sapiens	19-22
32261335-7	2013	Furthermore, Se@Trolox effectively blocked the cisplatin-induced reactive oxygen species (ROS) accumulation, activation of AKT and MAPK signaling and DNA damage-mediated p53 phosphorylation in HK-2 cells.	6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid	16-22	P53	Homo sapiens	170-173
32472321-10	2020	Series of experiments provide the evidence that Mannich base 3FB3FA8H leads to P53-mediated apoptosis.	mannich base 3fb3fa8h	48-69	P53	Homo sapiens	79-82
23703817-1	2013	Benzo(a)pyrene (BaP), a typical environmental carcinogen, can induce cell death both by protein 53 or tumor protein 53 (p53)-independent and -dependent pathways.	Benzo(a)pyrene	0-14	P53	Homo sapiens	88-98
22912688-4	2012	We demonstrated that p53 allele-null (-/-) (p53-KO) HCT116 cells were more resistant to aciculatin than cells with wild-type p53 (+/+).	aciculatin	88-98	P53	Homo sapiens	21-24
22912688-4	2012	We demonstrated that p53 allele-null (-/-) (p53-KO) HCT116 cells were more resistant to aciculatin than cells with wild-type p53 (+/+).	aciculatin	88-98	P53	Homo sapiens	44-47
22912688-4	2012	We demonstrated that p53 allele-null (-/-) (p53-KO) HCT116 cells were more resistant to aciculatin than cells with wild-type p53 (+/+).	aciculatin	88-98	P53	Homo sapiens	44-47
22912688-5	2012	The same result was achieved by knocking down p53 with siRNA in p53 wild-type cells, indicating that p53 plays a crucial role in aciculatin-induced apoptosis.	aciculatin	129-139	P53	Homo sapiens	46-49
22912688-5	2012	The same result was achieved by knocking down p53 with siRNA in p53 wild-type cells, indicating that p53 plays a crucial role in aciculatin-induced apoptosis.	aciculatin	129-139	P53	Homo sapiens	64-67
22912688-5	2012	The same result was achieved by knocking down p53 with siRNA in p53 wild-type cells, indicating that p53 plays a crucial role in aciculatin-induced apoptosis.	aciculatin	129-139	P53	Homo sapiens	64-67
23703817-1	2013	Benzo(a)pyrene (BaP), a typical environmental carcinogen, can induce cell death both by protein 53 or tumor protein 53 (p53)-independent and -dependent pathways.	Benzo(a)pyrene	0-14	P53	Homo sapiens	102-118
23703817-1	2013	Benzo(a)pyrene (BaP), a typical environmental carcinogen, can induce cell death both by protein 53 or tumor protein 53 (p53)-independent and -dependent pathways.	Benzo(a)pyrene	0-14	P53	Homo sapiens	120-123
22912688-7	2012	Interestingly, the aciculatin-induced downregulation of MDM2, an important negative regulator of p53, contributed to p53 accumulation.	aciculatin	19-29	P53	Homo sapiens	97-100
32683571-12	2020	Graphical abstract Schematic representation of the electrochemiluminescence sensor based on a Zn-MOF/GO nanocomposite, which can be applied to the determination of p53 antibody.	graphene oxide	101-103	P53	Homo sapiens	164-167
22912688-7	2012	Interestingly, the aciculatin-induced downregulation of MDM2, an important negative regulator of p53, contributed to p53 accumulation.	aciculatin	19-29	P53	Homo sapiens	117-120
22912688-9	2012	Collectively, these results indicate that aciculatin treatment induces cell cycle arrest and apoptosis via inhibition of MDM2 expression, thereby inducing p53 accumulation without significant DNA damage and genome toxicity.	aciculatin	42-52	P53	Homo sapiens	155-158
21887816-6	2013	Pretreatment with cytochrome P450 inhibitor alpha-naphthoflavone or p53 inhibitor pifithrin-alpha inhibited the benzo-[a]-pyrene-induced p21 expression.	Benzo(a)pyrene	112-128	P53	Homo sapiens	68-71
24038521-7	2013	Using combinations of doxycycline-inducible K-ras(G12D) and p53 loss, we show that tumors induced by the cooperative actions of these genes remain dependent on active K-ras expression, as deinduction of K-ras(G12D) leads to complete tumor regression despite absence of p53.	Doxycycline	22-33	P53	Homo sapiens	269-272
32449599-6	2020	The expression of p53, Bax, bcl-2, caspase-3 and GRP78 in Eca109 cells after xylogranatin C treatment was examined by western blot assay.	xylogranatin C	77-91	P53	Homo sapiens	18-21
23561593-0	2013	MGMT repletion after treatment of glioblastoma cells with temozolomide and O6-benzylguanine implicates NFkappaB and mutant p53.	Temozolomide	58-70	P53	Homo sapiens	123-126
22768182-11	2012	TMZ induced in monocytes the DNA damage response pathways ATM-Chk2 and ATR-Chk1 resulting in p53 activation.	Temozolomide	0-3	P53	Homo sapiens	93-96
22412944-2	2012	Our previous study has shown leptomycin B (LMB) significantly inhibited proliferation of lung cancer cells; however, p53 wild type lung cancer cells were resistant to LMB.	leptomycin B	167-170	P53	Homo sapiens	117-120
32348937-6	2020	In addition, miR-1468-3p promotes cellular senescence with increased senescence-associated beta-galactosidase activity and increased expression of p53 and p16.	mir-1468-3p	13-24	P53	Homo sapiens	147-150
22412944-9	2012	In conclusion, our results suggest that drug-resistant lung cancer cells with p53 wild type could be sensitized to cell death by scheduled combination treatment of DOX and LMB through activating and restoring p53 as well as potentially other signaling pathway(s) involving sequestosome 1.	leptomycin B	172-175	P53	Homo sapiens	78-81
22412944-9	2012	In conclusion, our results suggest that drug-resistant lung cancer cells with p53 wild type could be sensitized to cell death by scheduled combination treatment of DOX and LMB through activating and restoring p53 as well as potentially other signaling pathway(s) involving sequestosome 1.	leptomycin B	172-175	P53	Homo sapiens	209-212
22319594-0	2012	Benzo[a]pyrene, aflatoxine B1 and acetaldehyde mutational patterns in TP53 gene using a functional assay: relevance to human cancer aetiology.	Benzo(a)pyrene	0-14	P53	Homo sapiens	70-74
22319594-6	2012	By using a functional assay, the Functional Analysis of Separated Alleles in Yeast (FASAY), the present study depicts the mutational pattern of TP53 in normal human fibroblasts after in vitro exposure to well-known carcinogens: benzo[a]pyrene, aflatoxin B(1) and acetaldehyde.	Benzo(a)pyrene	228-242	P53	Homo sapiens	144-148
21431842-6	2011	RESULTS: Surgical specimens from COX-2 positive endometrial cancer patients treated with etodolac had significantly reduced expression levels of COX-2, Ki-67, p53, p21, p27, and cyclin D1 as determined by immunohistochemistry, while AI was not affected.	Etodolac	89-97	P53	Homo sapiens	159-162
24052075-0	2013	The sodium/iodide symporter NIS is a transcriptional target of the p53-family members in liver cancer cells.	Sodium Iodide	4-17	P53	Homo sapiens	67-70
23848581-6	2013	The resulting cyclotide MCo-PMI was able to bind with low nanomolar affinity to both Hdm2 and HdmX, showed high stability in human serum, and was cytotoxic to wild-type p53 cancer cell lines by activating the p53 tumor suppressor pathway both in vitro and in vivo.	mco-pmi	24-31	P53	Homo sapiens	169-172
23848581-6	2013	The resulting cyclotide MCo-PMI was able to bind with low nanomolar affinity to both Hdm2 and HdmX, showed high stability in human serum, and was cytotoxic to wild-type p53 cancer cell lines by activating the p53 tumor suppressor pathway both in vitro and in vivo.	mco-pmi	24-31	P53	Homo sapiens	209-212
32492431-3	2020	Here, we show that the original version of catalytically dead Cas12a (dCas12a)-conjugated BEs induce a basal level of DNA breaks and minimally activate DDR proteins, including H2AX, ATM, ATR, and p53.	BES	90-93	P53	Homo sapiens	196-199
23689617-9	2013	Furthermore, transcriptomic analyses revealed CIMP-specific gene expression signatures, indicating the impact of genetic status (IDH mutation, 1p/19q codeletion, TP53 mutation) on gene expression, and pointing to candidate biomarkers.	Cyclic IMP	46-50	P53	Homo sapiens	162-166
23652278-0	2013	OSU-03012, a non-Cox inhibiting celecoxib derivative, induces apoptosis of human esophageal carcinoma cells through a p53/Bax/cytochrome c/caspase-9-dependent pathway.	OSU 03012	0-9	P53	Homo sapiens	118-121
23986050-9	2013	Subsequently, she was treated with five courses of BR therapy, because bendamustine had been reported to be effective for p53 gene-deficient B cell neoplasms.	Bromine	51-53	P53	Homo sapiens	122-125
21957016-0	2011	MEK-ERK signaling dictates DNA-repair gene MGMT expression and temozolomide resistance of stem-like glioblastoma cells via the MDM2-p53 axis.	Temozolomide	63-75	P53	Homo sapiens	132-135
32382660-0	2020	Analysis of TP53 aflatoxin signature mutation in hepatocellular carcinomas from Guatemala: A cross-sectional study (2016-2017).	Aflatoxins	17-26	P53	Homo sapiens	12-16
21911080-3	2011	This study focused on mitochondria-mediated cell death and the occurrence of p73 protein accumulation in BaP-treated human hepatoma Hep3B (p53-null) cells.	Benzo(a)pyrene	105-108	P53	Homo sapiens	139-142
21855885-6	2011	As predicted, use of poly-SUS allowed separation of the His-tagged tumor suppressor protein, p53, at sample buffer concentrations as low as 0.08% w/v (2.9 mM), which is 24 times lower than required for SDS in the standard reducing PAGE protocol.	poly(N-undecanoylsulfuric acid)	21-29	P53	Homo sapiens	93-96
23224642-0	2013	Mutant TP53 enhances the resistance of glioblastoma cells to temozolomide by up-regulating O(6)-methylguanine DNA-methyltransferase.	Temozolomide	61-73	P53	Homo sapiens	7-11
23224642-2	2013	This study aimed to investigate the possible mechanism of mutant TP53 inducing temozolomide resistance in glioblastoma cells.	Temozolomide	79-91	P53	Homo sapiens	65-69
31201607-0	2020	Anti-tumor activity of the MDM2-TP53 inhibitor BI-907828 in dedifferentiated liposarcoma patient-derived xenograft models harboring MDM2 amplification.	bi-907828	47-56	P53	Homo sapiens	32-36
23224642-12	2013	Knockdown of mutant TP53 in T98G and U138 cells led to a fivefold increase in chemosensitivity to temozolomide, but not semustine.	Temozolomide	98-110	P53	Homo sapiens	20-24
23224642-15	2013	TP53 mutation decreases the chemosensitivity of malignant gliomas to temozolomide.	Temozolomide	69-81	P53	Homo sapiens	0-4
23840442-8	2013	Further studies identified p53 as a downstream effector of the GSK-3beta-mediated repression of let-7 biosynthesis.	let-7	96-101	P53	Homo sapiens	27-30
22067657-4	2011	We have developed a derivative of p53-suppressed human cells with constitutive depletion of Topo IIbeta and doxycycline-regulated conditional depletion of Topo IIalpha.	Doxycycline	108-119	P53	Homo sapiens	34-37
31201607-3	2020	We tested the in vivo efficacy of BI-907828, a small molecule inhibitor of the MDM2-TP53 interaction, in two DDLPS patient-derived xenografts (PDX).	bi-907828	34-43	P53	Homo sapiens	84-88
31931413-0	2020	N6-methyladenosine mediates arsenite-induced human keratinocyte transformation by suppressing p53 activation.	N-methyladenosine	0-18	P53	Homo sapiens	94-97
21355850-6	2011	DHEA (dehydroepiandrosterone) is an abundant steroid that is produced at high levels in the adrenal cells, and withdrawal of DHEA increases the levels of p53 in the epithelial and stromal cells, resulting in increased levels of apoptotic cells; meanwhile, DHEA decreases cellular apoptosis.	Dehydroepiandrosterone	0-4	P53	Homo sapiens	154-157
21355850-6	2011	DHEA (dehydroepiandrosterone) is an abundant steroid that is produced at high levels in the adrenal cells, and withdrawal of DHEA increases the levels of p53 in the epithelial and stromal cells, resulting in increased levels of apoptotic cells; meanwhile, DHEA decreases cellular apoptosis.	Dehydroepiandrosterone	6-28	P53	Homo sapiens	154-157
23650627-0	2013	Simultaneous evaluation of p53 and p21 expression level for early cancer diagnosis using SERS technique.	sers	89-93	P53	Homo sapiens	27-30
21355850-6	2011	DHEA (dehydroepiandrosterone) is an abundant steroid that is produced at high levels in the adrenal cells, and withdrawal of DHEA increases the levels of p53 in the epithelial and stromal cells, resulting in increased levels of apoptotic cells; meanwhile, DHEA decreases cellular apoptosis.	Dehydroepiandrosterone	125-129	P53	Homo sapiens	154-157
23650627-1	2013	Simultaneous detection of tumor suppressor p53 and cyclin-dependent kinase inhibitor p21 has been achieved for the first time with a high sensitivity using surface enhanced Raman scattering (SERS) technique.	sers	191-195	P53	Homo sapiens	43-46
32017928-0	2020	p53 controls the switch between autophagy and apoptosis through regulation of PLSCR1 in sodium selenite-treated leukemia cells.	Sodium Selenite	88-103	P53	Homo sapiens	0-3
23650627-3	2013	Qualitative and quantitative analysis of p53 and p21 were achieved by characterizing SERS signals of two different Raman reporters (4MBA and DTNB), which were labeled on the corresponding optical probes.	sers	85-89	P53	Homo sapiens	41-44
23650627-7	2013	Since the combined evaluation of p53 and p21 expression level acts as an indicator for early cancer prediction, our demonstrated immunoassay will potentially promote the application of SERS technique to practical clinical diagnoses.	sers	185-189	P53	Homo sapiens	33-36
21355850-6	2011	DHEA (dehydroepiandrosterone) is an abundant steroid that is produced at high levels in the adrenal cells, and withdrawal of DHEA increases the levels of p53 in the epithelial and stromal cells, resulting in increased levels of apoptotic cells; meanwhile, DHEA decreases cellular apoptosis.	Dehydroepiandrosterone	125-129	P53	Homo sapiens	154-157
21355850-7	2011	DHEA could improve the efficacy of reprogramming yield due to a decrease in apoptosis via the p53 pathway and an increase in cell viability.	Dehydroepiandrosterone	0-4	P53	Homo sapiens	94-97
32017928-4	2020	In this study, we showed that sodium selenite switched protective autophagy to apoptosis in p53-wild type NB4 cells without obvious caspase-8/apoptosis-inducing factor (AIF) axis activation, while induced autophagy-dependent caspase-8/AIF axis activation in p53-mutant Jurkat cells.	Sodium Selenite	30-45	P53	Homo sapiens	92-95
21810437-1	2011	The objective was to investigate the upstream apoptotic mechanisms that were triggered by a styrylpyrone derivative, goniothalamin (GTN), in tumor protein p53 (TP53)-positive and -negative hepatocellular carcinoma (HCC)-derived cells.	styrylpyrone	92-104	P53	Homo sapiens	155-158
32017928-4	2020	In this study, we showed that sodium selenite switched protective autophagy to apoptosis in p53-wild type NB4 cells without obvious caspase-8/apoptosis-inducing factor (AIF) axis activation, while induced autophagy-dependent caspase-8/AIF axis activation in p53-mutant Jurkat cells.	Sodium Selenite	30-45	P53	Homo sapiens	258-261
21810437-1	2011	The objective was to investigate the upstream apoptotic mechanisms that were triggered by a styrylpyrone derivative, goniothalamin (GTN), in tumor protein p53 (TP53)-positive and -negative hepatocellular carcinoma (HCC)-derived cells.	styrylpyrone	92-104	P53	Homo sapiens	160-164
23363223-6	2013	Addition of pentoxifylline at the peak of radiation-induced G2/M blocks resulted in a p53-independent reduction in cell survival in all cell lines.	Pentoxifylline	12-26	P53	Homo sapiens	86-89
23363223-9	2013	CONCLUSIONS: These results are at variance with the view that pentoxifylline preferentially sensitizes p53 mutant cells, and that sensitization occurs only when cells are irradiated in the presence of the drug.	Pentoxifylline	62-76	P53	Homo sapiens	103-106
32017928-6	2020	p53-dependent up-regulation of PLSCR1 accounted for the differential regulation of autophagy and apoptosis induced by sodium selenite.	Sodium Selenite	118-133	P53	Homo sapiens	0-3
23519841-10	2013	The combination of TMZ and lomeguatrib in primary GBM cell cultures and glioma cell lines decreased MGMT expression, increased p53 expression, and did not change MGMT methylation.	Temozolomide	19-22	P53	Homo sapiens	127-130
21929745-8	2011	In responsive cell lines, the MI-319/sorafenib combination induced the disappearance of p53 from the nucleus, the down modulation of Bcl-2 and Bcl-xL, the translocation of p53 to the mitochondria and that of AIF to the nuclei.	2-methyl-4-isothiazolin-3-one	30-32	P53	Homo sapiens	88-91
21929745-8	2011	In responsive cell lines, the MI-319/sorafenib combination induced the disappearance of p53 from the nucleus, the down modulation of Bcl-2 and Bcl-xL, the translocation of p53 to the mitochondria and that of AIF to the nuclei.	2-methyl-4-isothiazolin-3-one	30-32	P53	Homo sapiens	172-175
31732977-1	2020	A major revolution in the treatment of chronic lymphocytic leukemia (CLL) began with the approval of ibrutinib, a first-in-class oral inhibitor of Bruton tyrosine kinase (BTK), for the treatment of relapsed/refractory (R/R) and/or TP53 mutated patients with CLL.	ibrutinib	101-110	P53	Homo sapiens	231-235
21907923-1	2011	Inactivation of the TCA cycle enzyme, fumarate hydratase (FH), drives a metabolic shift to aerobic glycolysis in FH-deficient kidney tumors and cell lines from patients with hereditary leiomyomatosis renal cell cancer (HLRCC), resulting in decreased levels of AMP-activated kinase (AMPK) and p53 tumor suppressor, and activation of the anabolic factors, acetyl-CoA carboxylase and ribosomal protein S6.	Trichloroacetic Acid	20-23	P53	Homo sapiens	292-295
21457773-2	2011	The activation of benzo(a)pyrene (BP), a model compound of polycyclic aromatic hydrocarbons, to its genotoxic BP-diolepoxide (BPDE) and p53 response and cell viability after BP exposure, and the p53 status in these cell lines were analyzed.	Benzo(a)pyrene	18-32	P53	Homo sapiens	136-139
21457773-2	2011	The activation of benzo(a)pyrene (BP), a model compound of polycyclic aromatic hydrocarbons, to its genotoxic BP-diolepoxide (BPDE) and p53 response and cell viability after BP exposure, and the p53 status in these cell lines were analyzed.	Benzo(a)pyrene	18-32	P53	Homo sapiens	195-198
21457773-2	2011	The activation of benzo(a)pyrene (BP), a model compound of polycyclic aromatic hydrocarbons, to its genotoxic BP-diolepoxide (BPDE) and p53 response and cell viability after BP exposure, and the p53 status in these cell lines were analyzed.	Benzo(a)pyrene	34-36	P53	Homo sapiens	136-139
21457773-2	2011	The activation of benzo(a)pyrene (BP), a model compound of polycyclic aromatic hydrocarbons, to its genotoxic BP-diolepoxide (BPDE) and p53 response and cell viability after BP exposure, and the p53 status in these cell lines were analyzed.	Benzo(a)pyrene	34-36	P53	Homo sapiens	195-198
21457773-5	2011	After BP-treatment the strongest p53 protein induction and phosphorylation at serine 392 was found in ZR-75-1 cells with a wt TP53 gene.	Benzo(a)pyrene	6-8	P53	Homo sapiens	33-36
21457773-5	2011	After BP-treatment the strongest p53 protein induction and phosphorylation at serine 392 was found in ZR-75-1 cells with a wt TP53 gene.	Benzo(a)pyrene	6-8	P53	Homo sapiens	126-130
21796156-0	2011	Treatment with a BH3 mimetic overcomes the resistance of latency III EBV (+) cells to p53-mediated apoptosis.	BH 3	17-20	P53	Homo sapiens	86-89
21730979-8	2011	In A2780 cells sensitisation to cisplatin was greatest in cells with functional p53 and mismatch repair (MMR) and sensitisation to temozolomide was greatest in p53 mutant cells with functional MMR.	Temozolomide	131-143	P53	Homo sapiens	160-163
21701130-10	2011	The mRNA and protein expression levels of p53 and bax were increased in Sertoli cells treated with MC-LR at 10 microg/ml compared with the control group (P &lt; 0.05), while the bcl-2 protein levels were decreased in cells treated with MC-LR at 10 microg/ml (P &lt; 0.05).	cyanoginosin LR	99-104	P53	Homo sapiens	42-45
21339736-14	2011	Although p53-pathway-dependent apoptotic agents could upregulate endogenous hOTAG-12b and p53 in UCI-101/107 OC cells, hOTAG-12b could also induce apoptosis in p53-null and platinum-resistant SKOV3 OC cells and Doxycycline-induced hOTAG-12b did not alter p53.	Doxycycline	211-222	P53	Homo sapiens	9-12
20803015-0	2011	p53-Dependent anticancer effects of leptomycin B on lung adenocarcinoma.	leptomycin B	36-48	P53	Homo sapiens	0-3
20803015-1	2011	PURPOSE: Leptomycin B (LMB) and/or its derivatives are considered a novel class of cancer therapeutics through blocking chromosome maintenance region 1, which mediates p53 nuclear export.	leptomycin B	9-21	P53	Homo sapiens	168-171
20803015-1	2011	PURPOSE: Leptomycin B (LMB) and/or its derivatives are considered a novel class of cancer therapeutics through blocking chromosome maintenance region 1, which mediates p53 nuclear export.	leptomycin B	23-26	P53	Homo sapiens	168-171
20803015-3	2011	METHODS: Cells were treated with 0.01-100 nM LMB or 0.1% ethanol (vehicle control) for 4-72 h. Gene expression analyses using gene array for 84 genes involved in p53-mediated signaling pathways were performed in A549 and NCI-H358 after treatment with 20 nM LMB or vehicle control for 24 h. RESULTS: Cytotoxic results from MTS assays revealed a significant dose- and time-dependent effect of LMB on all cell lines.	leptomycin B	45-48	P53	Homo sapiens	162-165
21764706-0	2011	[Inhibitory effect of somatostatin analogue octreotide on the expression of p53 and Ras in human gastric cancer].	Octreotide	44-54	P53	Homo sapiens	76-79
21764706-5	2011	RESULTS: Compared with the control group, gastric cancer tissue in octreotide group showed significantly increased necrosis (P&lt;0.05) and enhanced proliferation of fibrous tissues (P&lt;0.05) with lowered expressions of p53 and Ras protein (P&lt;0.05).	Octreotide	67-77	P53	Homo sapiens	222-225
21764706-6	2011	CONCLUSION: Octreotide can inhibit the expressions of p53 and Ras and suppress the growth of the human gastric cancer.	Octreotide	12-22	P53	Homo sapiens	54-57
21382167-0	2011	Aflatoxin genotoxicity is associated with a defective DNA damage response bypassing p53 activation.	Aflatoxins	0-9	P53	Homo sapiens	84-87
21382167-2	2011	Aflatoxins, which may play a causative role in 5-28% of HCCs worldwide, are activated in liver cells and induce principally G T mutations, including the TP53 codon 249(G T) hotspot mutation.	Aflatoxins	0-10	P53	Homo sapiens	153-157
21106301-6	2011	Both 4-OHE(1) and 4-OHE(2) are mutagenic and carcinogenic and may exert their biological effects by inducing DNA adducts in cancer-related genes, including the tumor suppressor gene p53 and the proto-oncogene K-ras.	4-ohe	5-10	P53	Homo sapiens	182-185
21106301-6	2011	Both 4-OHE(1) and 4-OHE(2) are mutagenic and carcinogenic and may exert their biological effects by inducing DNA adducts in cancer-related genes, including the tumor suppressor gene p53 and the proto-oncogene K-ras.	4-ohe	18-23	P53	Homo sapiens	182-185
21106301-9	2011	More specifically, cigarette smoke stimulates metabolism of E(2) into the genotoxic metabolites, 4-OHE(1) and 4-OHE(2,) which interact with DNA in cancer-related genes, including the tumor suppressor gene, p53, and the proto-oncogene K-ras, two genes frequently mutated in patients with lung cancer.	4-ohe	97-102	P53	Homo sapiens	206-209
21106301-9	2011	More specifically, cigarette smoke stimulates metabolism of E(2) into the genotoxic metabolites, 4-OHE(1) and 4-OHE(2,) which interact with DNA in cancer-related genes, including the tumor suppressor gene, p53, and the proto-oncogene K-ras, two genes frequently mutated in patients with lung cancer.	4-ohe	110-115	P53	Homo sapiens	206-209
21163271-0	2011	Solamargine induces apoptosis associated with p53 transcription-dependent and transcription-independent pathways in human osteosarcoma U2OS cells.	beta-solamarine	0-11	P53	Homo sapiens	46-49
21163271-2	2011	In this study, the involvement of p53 in the pro-apoptotic action of solamargine was investigated in human osteosarcoma U2OS cells.	beta-solamarine	69-80	P53	Homo sapiens	34-37
21163271-9	2011	In this connection, solamargine increased the mRNA and protein expressions of p53 and Bax (a pro-apoptotic protein downstream to p53).	beta-solamarine	20-31	P53	Homo sapiens	78-81
21163271-9	2011	In this connection, solamargine increased the mRNA and protein expressions of p53 and Bax (a pro-apoptotic protein downstream to p53).	beta-solamarine	20-31	P53	Homo sapiens	129-132
21163271-11	2011	Furthermore, solamargine induced mitochondrial translocation of p53, loss of mitochondrial membrane potential, cytochrome c release and activation of caspase-9 and -3.	beta-solamarine	13-24	P53	Homo sapiens	64-67
21163271-12	2011	p53-specific transcriptional inhibitor pifithrin-alpha or mitochondrial translocation inhibitor pifithrin-mu partially reversed solamargine-induced apoptosis.	beta-solamarine	128-139	P53	Homo sapiens	0-3
21163271-13	2011	SIGNIFICANCE: Solamargine activates the mitochondria-mediated apoptotic pathway in U2OS cells via both p53 transcription-dependent and -independent mechanisms.	beta-solamarine	14-25	P53	Homo sapiens	103-106
21541041-9	2011	Based on the collective results, we have proposed a model for the PDT-triggered inactivation of the survival signal and apoptotic signaling cascade with Rose Bengal (RB), which sequentially involves singlet oxygen, Ca(2+), NO, p53, caspase-9, caspase-3, PAK2, and JNK.	Rose Bengal	153-164	P53	Homo sapiens	227-230
21541041-9	2011	Based on the collective results, we have proposed a model for the PDT-triggered inactivation of the survival signal and apoptotic signaling cascade with Rose Bengal (RB), which sequentially involves singlet oxygen, Ca(2+), NO, p53, caspase-9, caspase-3, PAK2, and JNK.	Rose Bengal	166-168	P53	Homo sapiens	227-230
22174603-6	2011	Since K562 is p53 negative, aaptamine was demonstrated to be a p53-independent p21 inducer in CML cells.	aaptamine	28-37	P53	Homo sapiens	63-66
22174613-8	2011	Findings in our preclinical animal studies have indicated that feeding with CLN resulted in inhibition of colorectal tumorigenesis through modulation of apoptosis and expression of PPARgamma and p53.	colostrinine	76-79	P53	Homo sapiens	195-198
21897876-0	2011	The combination of BH3-mimetic ABT-737 with the alkylating agent temozolomide induces strong synergistic killing of melanoma cells independent of p53.	Temozolomide	65-77	P53	Homo sapiens	146-149
21897876-7	2011	We found that TMZ treatment elevated p53 levels, and that the pro-apoptotic protein Noxa was elevated in TMZ/ABT-737 treated cells.	Temozolomide	14-17	P53	Homo sapiens	37-40
20880848-0	2010	Activation of AMP-activated protein kinase by temozolomide contributes to apoptosis in glioblastoma cells via p53 activation and mTORC1 inhibition.	Temozolomide	46-58	P53	Homo sapiens	110-113
20880848-9	2010	In further studies, we found that activation of AMPK is involved in TMZ-induced p53 activation and subsequent p21, Noxa, and Bax up-regulation.	Temozolomide	68-71	P53	Homo sapiens	80-83
20577783-4	2010	We also demonstrate that the levels of survivin and bcl-2 protein expression in HepG2 cells decreased concurrently, and the levels of p53 protein increased significantly after treatment with quercetin nickel (II) complex by immunocytochemistry analysis.	quercetin nickel (ii)	191-212	P53	Homo sapiens	134-137
21042727-3	2010	The current study shows that a glycolytic inhibitor, 2-deoxy-D-glucose (2DG), exhibits the cytotoxic effect on non-small cell lung cancer in a p53-dependent manner.	Deoxyglucose	53-70	P53	Homo sapiens	143-146
21042727-3	2010	The current study shows that a glycolytic inhibitor, 2-deoxy-D-glucose (2DG), exhibits the cytotoxic effect on non-small cell lung cancer in a p53-dependent manner.	Deoxyglucose	72-75	P53	Homo sapiens	143-146
21042727-4	2010	2DG significantly inhibits ATP production in p53-deficient lung cancer cells (H358) but not in p53-wt cells (A549).	Deoxyglucose	0-3	P53	Homo sapiens	45-48
21042727-7	2010	Importantly, 2DG selectively induces the expression of the antioxidant enzymes manganese superoxide dismutase (MnSOD) and glutathione peroxidase 1 (GPx1) in a p53-dependent manner.	Deoxyglucose	13-16	P53	Homo sapiens	159-162
21159612-3	2010	The combination of vorinostat and flavopiridol was synergistic and significantly more cytotoxic (P &lt; 0.001) in cell lines with p53-LOF and in the clones stably transfected with dominant-negative p53 plasmids.	alvocidib	34-46	P53	Homo sapiens	130-133
21159612-3	2010	The combination of vorinostat and flavopiridol was synergistic and significantly more cytotoxic (P &lt; 0.001) in cell lines with p53-LOF and in the clones stably transfected with dominant-negative p53 plasmids.	alvocidib	34-46	P53	Homo sapiens	198-201
21159612-9	2010	The combination of HDAC inhibitor and flavopiridol may be a unique approach to treating neuroblastomas with p53 LOF, one that evokes induction of mitotic failure.	alvocidib	38-50	P53	Homo sapiens	108-111
20840854-7	2010	A dioxin-like PCB (DL-PCB 126) was used as reference and gave results that were predictable from previous studies, i.e. it attenuated BP-induced p53 response and apoptosis.	Benzo(a)pyrene	134-136	P53	Homo sapiens	145-148
20840854-10	2010	This phosphorylation promotes a cytoplasmic translocation of FoxO3a and p53 and our data suggest that NDL-PCBs may inhibit BP-induced apoptosis by preventing a FoxO3a-dependent translocation of p53 to the cytoplasm.	ndl-pcbs	102-110	P53	Homo sapiens	72-75
20840854-10	2010	This phosphorylation promotes a cytoplasmic translocation of FoxO3a and p53 and our data suggest that NDL-PCBs may inhibit BP-induced apoptosis by preventing a FoxO3a-dependent translocation of p53 to the cytoplasm.	ndl-pcbs	102-110	P53	Homo sapiens	194-197
20840854-10	2010	This phosphorylation promotes a cytoplasmic translocation of FoxO3a and p53 and our data suggest that NDL-PCBs may inhibit BP-induced apoptosis by preventing a FoxO3a-dependent translocation of p53 to the cytoplasm.	Benzo(a)pyrene	123-125	P53	Homo sapiens	72-75
20840854-10	2010	This phosphorylation promotes a cytoplasmic translocation of FoxO3a and p53 and our data suggest that NDL-PCBs may inhibit BP-induced apoptosis by preventing a FoxO3a-dependent translocation of p53 to the cytoplasm.	Benzo(a)pyrene	123-125	P53	Homo sapiens	194-197
20878071-7	2010	Cantharidin-induced G0/G1 arrest was associated with a marked decrease in the protein expressions of cyclin E and Cdc25c but promoted the levels of p21 and p-p53.	Cantharidin	0-11	P53	Homo sapiens	158-161
21472335-5	2010	The HRM and sequencing analysis demonstrated that the positive rates of p53 mutation were 0.0, 12.7 and 21.6% in UDH, ADH and DCIS, respectively.	6-AMINOHEXYL-URIDINE-C1,5'-DIPHOSPHATE	113-116	P53	Homo sapiens	72-75
20976220-7	2010	Following irradiation, iPS cells activate checkpoint signaling, evidenced by phosphorylation of ATM, NBS1, CHEK2, and TP53, localization of ATM to the double strand breaks (DSB), and localization of TP53 to the nucleus of NANOG-positive cells.	IPS	23-26	P53	Homo sapiens	118-122
20976220-7	2010	Following irradiation, iPS cells activate checkpoint signaling, evidenced by phosphorylation of ATM, NBS1, CHEK2, and TP53, localization of ATM to the double strand breaks (DSB), and localization of TP53 to the nucleus of NANOG-positive cells.	IPS	23-26	P53	Homo sapiens	199-203
21059509-7	2010	Furthermore, amongst those treated with temozolomide (TMZ) based CRT, the presence of EGFR amplification, maintenance of PTEN and wild-type p53 and p16 were each associated with trends towards improved survival.	Temozolomide	40-52	P53	Homo sapiens	140-143
21059509-7	2010	Furthermore, amongst those treated with temozolomide (TMZ) based CRT, the presence of EGFR amplification, maintenance of PTEN and wild-type p53 and p16 were each associated with trends towards improved survival.	Temozolomide	54-57	P53	Homo sapiens	140-143
20476886-13	2010	CONCLUSION: We conclude that H(2)S can induce apoptosis in human keratinocyte stem cells, a key component of the epithelial barrier, following DNA damage and p53 activation.	Hydrogen Sulfide	29-34	P53	Homo sapiens	158-161
20730604-6	2010	Reduced cancer cell growth and increased expression of caspase-3 and p53 were seen in T47D and MCF-7 cells treated with CAN.	Rapeseed Oil	120-123	P53	Homo sapiens	69-72
23428467-8	2013	Overall, in this work, a novel small-molecule inhibitor of p53-MDM2 interaction with a xanthone scaffold was identified for the first time.	xanthone	87-95	P53	Homo sapiens	59-62
23483119-4	2013	In the present study, we show that, in addition to these well-studied molecular mechanisms, the treatment of wild-type TP53 MCF-7 and mutant TP53 MDA-MB-231 human breast cancer cells with desferrioxamine (DFO), a model iron chelator, causes significant epigenetic alterations at the global and gene-specific levels.	Deferoxamine	188-203	P53	Homo sapiens	119-123
23483119-4	2013	In the present study, we show that, in addition to these well-studied molecular mechanisms, the treatment of wild-type TP53 MCF-7 and mutant TP53 MDA-MB-231 human breast cancer cells with desferrioxamine (DFO), a model iron chelator, causes significant epigenetic alterations at the global and gene-specific levels.	Deferoxamine	188-203	P53	Homo sapiens	141-145
23483119-4	2013	In the present study, we show that, in addition to these well-studied molecular mechanisms, the treatment of wild-type TP53 MCF-7 and mutant TP53 MDA-MB-231 human breast cancer cells with desferrioxamine (DFO), a model iron chelator, causes significant epigenetic alterations at the global and gene-specific levels.	Deferoxamine	205-208	P53	Homo sapiens	119-123
23483119-4	2013	In the present study, we show that, in addition to these well-studied molecular mechanisms, the treatment of wild-type TP53 MCF-7 and mutant TP53 MDA-MB-231 human breast cancer cells with desferrioxamine (DFO), a model iron chelator, causes significant epigenetic alterations at the global and gene-specific levels.	Deferoxamine	205-208	P53	Homo sapiens	141-145
23585871-0	2013	Oncomir miR-125b suppresses p14(ARF) to modulate p53-dependent and p53-independent apoptosis in prostate cancer.	mir-125b	8-16	P53	Homo sapiens	49-52
23585871-0	2013	Oncomir miR-125b suppresses p14(ARF) to modulate p53-dependent and p53-independent apoptosis in prostate cancer.	mir-125b	8-16	P53	Homo sapiens	67-70
23585871-3	2013	In this study, we further extend our studies by showing that miR-125b represses the protein product of the ink4a/ARF locus, p14(ARF), in two prostate cancer cell lines, LNCaP (wild type-p53) and 22Rv1 (both wild type and mutant p53), as well as in the PC-346C prostate cancer xenograft model that lentivirally overexpressed miR-125b.	mir-125b	61-69	P53	Homo sapiens	186-189
23585871-3	2013	In this study, we further extend our studies by showing that miR-125b represses the protein product of the ink4a/ARF locus, p14(ARF), in two prostate cancer cell lines, LNCaP (wild type-p53) and 22Rv1 (both wild type and mutant p53), as well as in the PC-346C prostate cancer xenograft model that lentivirally overexpressed miR-125b.	mir-125b	61-69	P53	Homo sapiens	228-231
23585871-4	2013	Our results highlight that miR-125b modulates the p53 network by hindering the down-regulation of Mdm2, thereby affecting p53 and its target genes p21 and Puma to a degree sufficient to inhibit apoptosis.	mir-125b	27-35	P53	Homo sapiens	50-53
23585871-4	2013	Our results highlight that miR-125b modulates the p53 network by hindering the down-regulation of Mdm2, thereby affecting p53 and its target genes p21 and Puma to a degree sufficient to inhibit apoptosis.	mir-125b	27-35	P53	Homo sapiens	122-125
23585871-6	2013	In addition, overexpression of miR-125b in p53-deficient PC3 cells induced down-regulation of p14(ARF), which leads to increased cell proliferation through a p53-independent manner.	mir-125b	31-39	P53	Homo sapiens	43-46
23585871-6	2013	In addition, overexpression of miR-125b in p53-deficient PC3 cells induced down-regulation of p14(ARF), which leads to increased cell proliferation through a p53-independent manner.	mir-125b	31-39	P53	Homo sapiens	158-161
23585871-7	2013	Thus, we conclude that miR-125b acts as an oncogene which regulates p14(ARF)/Mdm2 signaling, stimulating proliferation of prostate cancer cells through a p53-dependent or p53-independent function.	mir-125b	23-31	P53	Homo sapiens	154-157
23585871-7	2013	Thus, we conclude that miR-125b acts as an oncogene which regulates p14(ARF)/Mdm2 signaling, stimulating proliferation of prostate cancer cells through a p53-dependent or p53-independent function.	mir-125b	23-31	P53	Homo sapiens	171-174
23468244-3	2013	The NQO1 was shown to act as a p53 stabilizer and was suggested to play an important role in the protection against carcinogenic catechol estrogens.	catechol	129-137	P53	Homo sapiens	31-34
23459853-1	2013	Tumor suppressor p53 are frequently mutated in glioblastomas (GBMs) and appears to contribute, in part, to resistance to temozolomide (TMZ) and therapeutic drugs.	Temozolomide	121-133	P53	Homo sapiens	17-20
23459853-1	2013	Tumor suppressor p53 are frequently mutated in glioblastomas (GBMs) and appears to contribute, in part, to resistance to temozolomide (TMZ) and therapeutic drugs.	Temozolomide	135-138	P53	Homo sapiens	17-20
23459853-7	2013	We propose that triggering WWOX activation by therapeutic drugs under p53 functional deficiency is needed to overcome TMZ resistance and induce GBM cell death.	Temozolomide	118-121	P53	Homo sapiens	70-73
23497288-10	2013	CONCLUSIONS: Our findings suggest that miR-125b may play a role in the development of chemoresistance in EWS by suppressing the expression of the apoptotic mediators, such as p53 and Bak.	mir-125b	39-47	P53	Homo sapiens	175-178
23392172-6	2013	The role of unfolded p53 in cell death resistance and lack of GAP-43 transcription was demonstrated by ZnCl(2) treatment.	zncl	103-107	P53	Homo sapiens	21-24
22410783-7	2013	In comparison, SHD cells immortalized by the powerful polycyclic hydrocarbon carcinogen benzo(a)pyrene display transversion point mutations in the DNA-binding domain of p53 coupled with INK4 alterations such as loss of expression of p15.	Benzo(a)pyrene	88-102	P53	Homo sapiens	169-172
23841076-0	2013	The omega-3 polyunsaturated fatty acid DHA induces simultaneous apoptosis and autophagy via mitochondrial ROS-mediated Akt-mTOR signaling in prostate cancer cells expressing mutant p53.	Docosahexaenoic Acids	39-42	P53	Homo sapiens	181-184
23841076-1	2013	Docosahexaenoic acid (DHA) induces autophagy-associated apoptotic cell death in wild-type p53 cancer cells via regulation of p53.	Docosahexaenoic Acids	0-20	P53	Homo sapiens	90-93
23841076-1	2013	Docosahexaenoic acid (DHA) induces autophagy-associated apoptotic cell death in wild-type p53 cancer cells via regulation of p53.	Docosahexaenoic Acids	0-20	P53	Homo sapiens	125-128
23841076-1	2013	Docosahexaenoic acid (DHA) induces autophagy-associated apoptotic cell death in wild-type p53 cancer cells via regulation of p53.	Docosahexaenoic Acids	22-25	P53	Homo sapiens	90-93
23841076-1	2013	Docosahexaenoic acid (DHA) induces autophagy-associated apoptotic cell death in wild-type p53 cancer cells via regulation of p53.	Docosahexaenoic Acids	22-25	P53	Homo sapiens	125-128
24335178-2	2013	In this study, we sought to examine the hypothesis that neoadjuvant chemotherapy (NAC) is a better approach with improved prognosis and outcomes after laparoscopical radical hysterectomy (LRH) on patients with cervical cancer and to elucidate the potential roles of the p53:miR-34a:E2F1 and the p53:miR-605:Mdm2 signaling pathways in this therapy.	nac	82-85	P53	Homo sapiens	270-273
24335178-2	2013	In this study, we sought to examine the hypothesis that neoadjuvant chemotherapy (NAC) is a better approach with improved prognosis and outcomes after laparoscopical radical hysterectomy (LRH) on patients with cervical cancer and to elucidate the potential roles of the p53:miR-34a:E2F1 and the p53:miR-605:Mdm2 signaling pathways in this therapy.	nac	82-85	P53	Homo sapiens	295-298
24335178-10	2013	Furthermore, molecular biology analyses revealed that the protein and mRNA levels of p53 were both markedly increased in patients who received NAC than those who did not, and oppositely, the levels of E2F1 and Mdm2 were significantly lower in the NAC+LRH patients than in the LRH patients.	nac	143-146	P53	Homo sapiens	85-88
24335178-10	2013	Furthermore, molecular biology analyses revealed that the protein and mRNA levels of p53 were both markedly increased in patients who received NAC than those who did not, and oppositely, the levels of E2F1 and Mdm2 were significantly lower in the NAC+LRH patients than in the LRH patients.	nac	247-250	P53	Homo sapiens	85-88
24335178-14	2013	CONCLUSION: These findings not only indicate NAC as a rational approach for better treatment of cervical cancer with improved therapeutic outcomes, due partly to the ability of cisplatin to promote the p53:miR-34a:E2F1 positive feed-forward loop and the p53:miR-605:Mdm2 positive feedback loop.	nac	45-48	P53	Homo sapiens	202-205
24335178-14	2013	CONCLUSION: These findings not only indicate NAC as a rational approach for better treatment of cervical cancer with improved therapeutic outcomes, due partly to the ability of cisplatin to promote the p53:miR-34a:E2F1 positive feed-forward loop and the p53:miR-605:Mdm2 positive feedback loop.	nac	45-48	P53	Homo sapiens	254-257
24112172-8	2013	CONCLUSION: The soluble divalent iron and, to a greater degree trivalent iron, inhibited HASMC proliferation in a dosedependent manner, which may be attributed to reduction of PCNA expression and increase of p53 expression.	hasmc	89-94	P53	Homo sapiens	208-211
22674530-8	2013	Remarkably, Pi/doxorubicin combination-induced cytotoxicity was accompanied by an increase of p53 protein levels and of p53 target genes mdm2, p21 and Bax, and was significantly reduced by the p53 inhibitor pifithrine-alpha.	pifithrine	207-217	P53	Homo sapiens	94-97
22674530-8	2013	Remarkably, Pi/doxorubicin combination-induced cytotoxicity was accompanied by an increase of p53 protein levels and of p53 target genes mdm2, p21 and Bax, and was significantly reduced by the p53 inhibitor pifithrine-alpha.	pifithrine	207-217	P53	Homo sapiens	120-123
22674530-8	2013	Remarkably, Pi/doxorubicin combination-induced cytotoxicity was accompanied by an increase of p53 protein levels and of p53 target genes mdm2, p21 and Bax, and was significantly reduced by the p53 inhibitor pifithrine-alpha.	pifithrine	207-217	P53	Homo sapiens	120-123
24082817-14	2013	TMA analysis showed p53 overexpression in 25.7% of SA and 0% RAA, high Ki-67 in 35.3% of SA and 44.4% RAA, and hTERT expression in 100% of SA and RAA.	4,4-dimethylcholesta-8,14-dien-3-ol	0-3	P53	Homo sapiens	20-23
24082817-14	2013	TMA analysis showed p53 overexpression in 25.7% of SA and 0% RAA, high Ki-67 in 35.3% of SA and 44.4% RAA, and hTERT expression in 100% of SA and RAA.	sa	51-53	P53	Homo sapiens	20-23
24082817-15	2013	TP53 mutations were detected in 13.5% of SA and 11.1% RAA.	sa	41-43	P53	Homo sapiens	0-4
22576985-4	2012	Treatment of cells with lithium resulted in a dose-dependent induction of p53, retinoblastoma (Rb) and bax expression which was accompanied by concomitant inhibition of bcl-2 expression as demonstrated using immunohistochemical microscopy.	Lithium	24-31	P53	Homo sapiens	74-98
22973058-0	2012	8-Amino-adenosine activates p53-independent cell death of metastatic breast cancers.	8-aminoadenosine	0-17	P53	Homo sapiens	28-31
22948151-6	2012	Induction of p53 can be achieved by several means, such as UV radiation and treatment with anti-cancer agents (including doxorubicin, etoposide, roscovitine, flavopiridol, and nutlin-3).	alvocidib	158-170	P53	Homo sapiens	13-16
22595758-2	2012	PIDD has been implicated in p53-mediated cell death in response to DNA damage but also in DNA repair and nuclear factor kappa-light-chain enhancer (NF-kappaB) activation upon genotoxic stress, together with RIP-1 kinase and Nemo/IKKgamma.	pidd	0-4	P53	Homo sapiens	28-31
22940704-0	2012	Structure-activity relationship and antitumor activity of thio-benzodiazepines as p53-MDM2 protein-protein interaction inhibitors.	thio-benzodiazepines	58-78	P53	Homo sapiens	82-85
21912889-6	2012	RESULTS: Screening of analogues for potentiation of radiation-induced G(1)-phase cell cycle arrest using NZOV11, an ovarian tumour cell line containing a p53(R248Q) mutation, demonstrated that the (2-benzofuranyl)-quinazoline derivative 5 was among the most active of the analogues.	(2-benzofuranyl)-quinazoline	197-225	P53	Homo sapiens	154-157
22993307-0	2012	A new chalcone derivative (E)-3-(4-methoxyphenyl)-2-methyl-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-one suppresses prostate cancer involving p53-mediated cell cycle arrests and apoptosis.	(e)-3-(4-methoxyphenyl)-2-methyl-1-(3,4,5-trimethoxyphenyl)prop-2-en-1-one	26-100	P53	Homo sapiens	138-141
22529011-0	2012	Calcium carbonate microparticles used as a gene vector for delivering p53 gene into cancer cells.	Calcium Carbonate	0-17	P53	Homo sapiens	70-73
22529011-1	2012	Calcium carbonate (CaCO(3) ) microparticles were for the first time used for efficient delivery of p53 gene to transfect human cancer cells HeLa.	Calcium Carbonate	0-17	P53	Homo sapiens	99-102
22529011-1	2012	Calcium carbonate (CaCO(3) ) microparticles were for the first time used for efficient delivery of p53 gene to transfect human cancer cells HeLa.	Calcium Carbonate	19-26	P53	Homo sapiens	99-102
22638860-6	2012	We demonstrated that co-infusion of 6-OHDA with adenovirus expressing siRNA of iNOS blocked the activation of microglia, iNOS transcription, and p53-Bax-CC3 apoptotic cascade as well as significantly blocking 6-OHDA-induced decreases in DA, DOPAC, HVA, and TH levels and effectively decreased rotation number.	amsonic acid	40-42	P53	Homo sapiens	145-148
22763759-6	2012	However, the growth-inhibitory activity of vincristine, doxorubicin, carboplatin, etoposide, and temozolomide was significantly impaired by silencing of TP53.	Temozolomide	97-109	P53	Homo sapiens	153-157
22847428-8	2012	Our work provides in vivo evidence that expanded CAG RNAs trigger nucleolar stress and induce apoptosis via p53 and describes a polyQ pathogenic mechanism that involves the nucleolus.	polyglutamine	128-133	P53	Homo sapiens	108-111
21633925-3	2012	In the present study, we show that retinoic acid enhances the cytostatic and apoptogenic properties of the novel adamantyl retinoid ST1926 in a panel of neuroblastoma cells with different p53 status and caspase 8 expression, resulting in synergistic effects as assessed by Combination Index and Isobologram analysis.	adamantyl	113-122	P53	Homo sapiens	188-191
22593187-0	2012	Integrin alpha5beta1 plays a critical role in resistance to temozolomide by interfering with the p53 pathway in high-grade glioma.	Temozolomide	60-72	P53	Homo sapiens	97-100
22593187-2	2012	In this study, we show that high expression of the alpha5 integrin subunit compromises temozolomide-induced tumor suppressor p53 activity in human glioblastoma cells.	Temozolomide	87-99	P53	Homo sapiens	125-128
22593187-5	2012	In a functional p53 background, nutlin-3a downregulated the alpha5 integrin subunit, thereby increasing the cytotoxic effect of temozolomide.	Temozolomide	128-140	P53	Homo sapiens	16-19
22593187-7	2012	Taken together, our findings indicate that negative cross-talk between alpha5beta1 integrin and p53 supports glioma resistance to temozolomide, providing preclinical proof-of-concept that alpha5beta1 integrin represents a therapeutic target for high-grade brain tumors.	Temozolomide	130-142	P53	Homo sapiens	96-99
22198862-7	2012	TMA studies showed overexpression of KI67, P53, SURVIVIN and APOLLON protein and failure of expression of P27, BCL2, BAX, CHROMOGRANIN-A, SYNAPTOPHYSIN, CYCLIND1, FLIP, TRAIL, CK8, CK18, CK19 in parathyroid carcinoma was detected.	4,4-dimethylcholesta-8,14-dien-3-ol	0-3	P53	Homo sapiens	43-46
22481618-0	2012	The Rho kinase inhibitor fasudil is involved in p53-mediated apoptosis in human hepatocellular carcinoma cells.	fasudil	25-32	P53	Homo sapiens	48-51
22426690-8	2012	Irbesartan also significantly altered p53, PCNA and cyclin D1 expression, which was also influenced by activated AT1R in AT1R(+)-MCF-7 cells.	Irbesartan	0-10	P53	Homo sapiens	38-41
22118713-6	2012	Our data demonstrate that 4-HNE induces neuronal cell death through abnormal expression of apoptotic markers (p53, Bax and caspase-3).	4-hydroxy-2-nonenal	26-31	P53	Homo sapiens	110-113
22331826-8	2012	Mechanistic studies demonstrated that miR-125b protected against anoikis by increasing ERK phosphorylation and by suppressing p53.	mir-125b	38-46	P53	Homo sapiens	126-129
21604265-3	2012	High salt and sorbitol were found to activate similar molecular pathways, including the p38 MAPK and the p53-p21(WAF1)-pRb axis, that were not stimulated by high urea.	Sorbitol	14-22	P53	Homo sapiens	105-108
21604265-5	2012	Furthermore, salt- and sorbitol-treated cells were able to phosphorylate histone H2A.X on Ser139, in contrast to cells exposed to urea, indicating a common mechanism for DNA repair, which was achieved by a p53-dependent activation of the G1 checkpoint by both solutes.	Sorbitol	23-31	P53	Homo sapiens	206-209
22227536-8	2012	Our results demonstrated that BaP could induce the malignant transformation of 16HBE cells, and p53 and p-Akt (Ser473) might play crucial roles in BaP-induced carcinogenesis.	Benzo(a)pyrene	147-150	P53	Homo sapiens	96-99
21914463-0	2012	Transcriptional analysis of the Aurora inhibitor Danusertib leading to biomarker identification in TP53 wild type cells.	danusertib	49-59	P53	Homo sapiens	99-103
21914463-3	2012	To characterize the effects of Danusertib at the transcriptional level we carried out gene expression profiling of wt and TP53 mutant tumor cells showing differential cell cycle response upon drug treatment.	danusertib	31-41	P53	Homo sapiens	122-126
21914463-4	2012	We found that treatment with Danusertib induces a strong transcriptional response only in TP53 wt cells, with an overlapping pattern of expression of TP53-dependent genes among the three cell lines tested, while a prevalent signature could not be identified in the two TP53 mutant cells, suggesting that TP53 status is a key determinant for the observed transcriptional effects.	danusertib	29-39	P53	Homo sapiens	90-94
21914463-4	2012	We found that treatment with Danusertib induces a strong transcriptional response only in TP53 wt cells, with an overlapping pattern of expression of TP53-dependent genes among the three cell lines tested, while a prevalent signature could not be identified in the two TP53 mutant cells, suggesting that TP53 status is a key determinant for the observed transcriptional effects.	danusertib	29-39	P53	Homo sapiens	150-154
21914463-4	2012	We found that treatment with Danusertib induces a strong transcriptional response only in TP53 wt cells, with an overlapping pattern of expression of TP53-dependent genes among the three cell lines tested, while a prevalent signature could not be identified in the two TP53 mutant cells, suggesting that TP53 status is a key determinant for the observed transcriptional effects.	danusertib	29-39	P53	Homo sapiens	150-154
21914463-4	2012	We found that treatment with Danusertib induces a strong transcriptional response only in TP53 wt cells, with an overlapping pattern of expression of TP53-dependent genes among the three cell lines tested, while a prevalent signature could not be identified in the two TP53 mutant cells, suggesting that TP53 status is a key determinant for the observed transcriptional effects.	danusertib	29-39	P53	Homo sapiens	150-154
21914463-6	2012	One of these is GDF15, a secreted protein belonging to the TGF-beta superfamily, for which we found a potential role in resistance to Danusertib, and which could represent a potential biomarker for Danusertib treatment in TP53 WT tumors and in surrogate tissues such as blood or skin.	danusertib	198-208	P53	Homo sapiens	222-226
21981310-4	2012	iPS containing an extra copy of the p53 or Ink4a/ARF locus show normal pluripotency, as determined by in vitro and in vivo differentiation assays.	IPS	0-3	P53	Homo sapiens	36-39
21827374-0	2012	Phase II study of cenersen, an antisense inhibitor of p53, in combination with fludarabine, cyclophosphamide and rituximab for high-risk chronic lymphocytic leukemia.	cenersen	18-26	P53	Homo sapiens	54-57
22957303-7	2012	In addition, two compounds inhibiting Hdmx function or expression, SAH-p53-8 and XI-011, also elicited a growth inhibitory effect in a partly p53-independent manner.	(10-methyl-9-anthryl)methyl imidothiocarbamate	81-87	P53	Homo sapiens	142-145
23317197-7	2012	Overexpression of p53 and PCNA were higher in LSCC (62.7%, 57.8%) than in LP (38%, 33.3%) (P&lt;0.005, and P&lt;0.005, respectively).	leucylproline	74-76	P53	Homo sapiens	18-21
22112837-5	2012	At the molecular level, AQ and AZ formed DNA adducts, generated free radicals, and upregulated pro-apoptotic signaling molecules (p53, caspases, PARP, death effectors).	alizarin	31-33	P53	Homo sapiens	130-133
22200421-11	2012	Thus, both IS and ADMA induced endothelial senescence through ROS and p53.	N,N-dimethylarginine	18-22	P53	Homo sapiens	70-73
23285096-0	2012	Green tea polyphenols induce p53-dependent and p53-independent apoptosis in prostate cancer cells through two distinct mechanisms.	Polyphenols	10-21	P53	Homo sapiens	29-32
23285096-0	2012	Green tea polyphenols induce p53-dependent and p53-independent apoptosis in prostate cancer cells through two distinct mechanisms.	Polyphenols	10-21	P53	Homo sapiens	47-50
21982800-5	2011	RCC patients with the p53Arg/Arg genotype had a signicantly low percentage of inorganic arsenic, a low percentage of monomethylarsonic acid (MMA), and a high percentage of dimethylarsinic acid (DMA), which indicates efcient arsenic methylation capacity.	monomethylarsonic acid	117-139	P53	Homo sapiens	22-25
21982800-5	2011	RCC patients with the p53Arg/Arg genotype had a signicantly low percentage of inorganic arsenic, a low percentage of monomethylarsonic acid (MMA), and a high percentage of dimethylarsinic acid (DMA), which indicates efcient arsenic methylation capacity.	monomethylarsonic acid	141-144	P53	Homo sapiens	22-25
21196432-5	2011	Both strategies could use tyrosinase-mediated activation of quercetin, a dietary polyphenol that induces the expression of p53 and modulates reactive oxygen species.	Polyphenols	81-91	P53	Homo sapiens	123-126
21741467-0	2011	para-Phenylenediamine-induced autophagy in human uroepithelial cell line mediated mutant p53 and activation of ERK signaling pathway.	4-phenylenediamine	0-21	P53	Homo sapiens	89-92
21811093-0	2011	Docosahexaenoic acid induces autophagy through p53/AMPK/mTOR signaling and promotes apoptosis in human cancer cells harboring wild-type p53.	Docosahexaenoic Acids	0-20	P53	Homo sapiens	47-50
21811093-0	2011	Docosahexaenoic acid induces autophagy through p53/AMPK/mTOR signaling and promotes apoptosis in human cancer cells harboring wild-type p53.	Docosahexaenoic Acids	0-20	P53	Homo sapiens	136-139
21811093-4	2011	We also observed that DHA-induced autophagy was accompanied by p53 loss.	Docosahexaenoic Acids	22-25	P53	Homo sapiens	63-66
21811093-5	2011	Inhibition of p53 increased DHA-induced autophagy and prevention of p53 degradation significantly led to the attenuation of DHA-induced autophagy, suggesting that DHA-induced autophagy is mediated by p53.	Docosahexaenoic Acids	28-31	P53	Homo sapiens	14-17
21811093-5	2011	Inhibition of p53 increased DHA-induced autophagy and prevention of p53 degradation significantly led to the attenuation of DHA-induced autophagy, suggesting that DHA-induced autophagy is mediated by p53.	Docosahexaenoic Acids	124-127	P53	Homo sapiens	14-17
21811093-5	2011	Inhibition of p53 increased DHA-induced autophagy and prevention of p53 degradation significantly led to the attenuation of DHA-induced autophagy, suggesting that DHA-induced autophagy is mediated by p53.	Docosahexaenoic Acids	124-127	P53	Homo sapiens	68-71
21811093-5	2011	Inhibition of p53 increased DHA-induced autophagy and prevention of p53 degradation significantly led to the attenuation of DHA-induced autophagy, suggesting that DHA-induced autophagy is mediated by p53.	Docosahexaenoic Acids	124-127	P53	Homo sapiens	68-71
21811093-5	2011	Inhibition of p53 increased DHA-induced autophagy and prevention of p53 degradation significantly led to the attenuation of DHA-induced autophagy, suggesting that DHA-induced autophagy is mediated by p53.	Docosahexaenoic Acids	124-127	P53	Homo sapiens	14-17
21811093-5	2011	Inhibition of p53 increased DHA-induced autophagy and prevention of p53 degradation significantly led to the attenuation of DHA-induced autophagy, suggesting that DHA-induced autophagy is mediated by p53.	Docosahexaenoic Acids	124-127	P53	Homo sapiens	68-71
21811093-5	2011	Inhibition of p53 increased DHA-induced autophagy and prevention of p53 degradation significantly led to the attenuation of DHA-induced autophagy, suggesting that DHA-induced autophagy is mediated by p53.	Docosahexaenoic Acids	124-127	P53	Homo sapiens	68-71
21811093-6	2011	Further experiments showed that the mechanism of DHA-induced autophagy associated with p53 attenuation involved an increase in the active form of AMP-activated protein kinase and a decrease in the activity of mammalian target of rapamycin.	Docosahexaenoic Acids	49-52	P53	Homo sapiens	87-90
21811093-8	2011	Overall, our results demonstrate that autophagy contributes to the cytotoxicity of DHA in cancer cells harboring wild-type p53.	Docosahexaenoic Acids	83-86	P53	Homo sapiens	123-126
21996465-0	2011	Synthesis and biological evaluation of thio-benzodiazepines as novel small molecule inhibitors of the p53-MDM2 protein-protein interaction.	thio-benzodiazepines	39-59	P53	Homo sapiens	102-105
21996465-6	2011	The thio-benzodiazepines represent a promising class of non-peptide inhibitors of the p53-MDM2 interaction.	thio-benzodiazepines	4-24	P53	Homo sapiens	86-89
22277391-5	2011	Previously, we demonstrated that Interferon-beta (IFN-beta) markedly enhanced chemosensitivity to TMZ in an in vitro study of human glioma cells; this finding suggested that one of the major mechanisms by which IFN-beta enhances chemosensitivity is the downregulation of MGMT transcription via p53 induction.	Temozolomide	98-101	P53	Homo sapiens	294-297
21872580-6	2011	Furthermore, the MDQ-induced G(0)/G(1) arrest was correlated with an increase in p27 and a decrease in cyclin D1 and p53.	mdq	17-20	P53	Homo sapiens	117-120
21804388-7	2011	STIC and p53 signature as precursor lesions of pelvic serous cancer were seen in macroscopically inconspicuous contralateral fallopian tubes in unilateral TC, in patients with elective bilateral salpingo-oophorectomy, and in patients affected by PPC.	Technetium	155-157	P53	Homo sapiens	9-12
21327711-1	2011	Our previous study demonstrated that interferon-beta markedly enhanced chemosensitivity to temozolomide; one of the major mechanisms is downregulation of O(6)-methylguanine DNA-methyltransferase transcription via p53 induction.	Temozolomide	91-103	P53	Homo sapiens	213-216
21508685-5	2011	Unexpectedly, we found that two distinct BH3 mimetics, ABT737 and HA14-1, also stimulate other pro-autophagic pathways and hence activate the nutrient sensors Sirtuin 1 and AMPK, inhibit mTOR, deplete cytoplasmic p53 and trigger the IKK kinase.	BH 3	41-44	P53	Homo sapiens	213-216
21340650-0	2011	Dimethylfumarate inhibits MIF-induced proliferation of keratinocytes by inhibiting MSK1 and RSK1 activation and by inducing nuclear p-c-Jun (S63) and p-p53 (S15) expression.	Dimethyl Fumarate	0-16	P53	Homo sapiens	152-155
21340650-9	2011	CONCLUSION: Our results indicate that the specific inhibitory effects of DMF on RSK1 and MSK1 activation together with the induction of p-c-Jun (S63) and p-p53 (S15) lead to the inhibition of keratinocyte proliferation, partly explaining the anti-psoriatic effect of DMF.	Dimethyl Fumarate	73-76	P53	Homo sapiens	156-159
21340650-9	2011	CONCLUSION: Our results indicate that the specific inhibitory effects of DMF on RSK1 and MSK1 activation together with the induction of p-c-Jun (S63) and p-p53 (S15) lead to the inhibition of keratinocyte proliferation, partly explaining the anti-psoriatic effect of DMF.	Dimethyl Fumarate	267-270	P53	Homo sapiens	156-159
21663495-4	2011	The cyclins and tumor suppressors were modulated by amentoflavone in SiHa and CaSki human cervical cancer cells: cyclin and hyperphosphorylated retinoblastoma (p-pRb) were down-regulated, whereas cyclin-dependent kinase inhibitors and p53 were enhanced.	amentoflavone	52-65	P53	Homo sapiens	235-238
21250978-6	2011	KEY RESULTS: 2,5-diaziridinyl-3-(hydroxymethyl)-6-methyl-1,4-benzoquinone induced apoptosis and clonogenic death, dependent on NQO1 and p53.	2,5-diaziridinyl-3-(hydroxymethyl)-6-methyl-1,4-benzoquinone	13-73	P53	Homo sapiens	136-139
21411502-4	2011	Drug transport studies revealed that p53 inhibited both basal and PKCalpha-stimulated transport of glutathione conjugates of 4HNE (GSHNE) and doxorubicin.	4-hydroxy-2-nonenal	125-129	P53	Homo sapiens	37-40
21389894-13	2011	This case suggests that preserving MSH6 function is essential for responsiveness to TMZ treatment in MGMT-negative and p53-mutated atypical pituitary adenoma or pituitary carcinoma.	Temozolomide	84-87	P53	Homo sapiens	119-122
21269821-7	2011	NBDHEX provoked a higher level of p53 phosphorylation with respect to TMZ and the drug combination caused a more than additive increase of p53 activation.	Temozolomide	70-73	P53	Homo sapiens	34-37
21510869-16	2011	Cellular pools of PPARgamma and phospho-p53 were increased by CCM+DHA relative to either compound alone.	Docosahexaenoic Acids	66-69	P53	Homo sapiens	40-43
21462329-3	2011	METHODS AND RESULTS: Annexin V/PI co-staining assay demonstrated that 5HHMF and 5HTMF significantly induced apoptosis in HCT116 (p53(+/+) ) cells but not in HCT116 (p53(-/-) ) cells.	5-hydroxy-3,6,7,8,3',4'-hexamethoxyflavone	70-75	P53	Homo sapiens	129-132
21462329-3	2011	METHODS AND RESULTS: Annexin V/PI co-staining assay demonstrated that 5HHMF and 5HTMF significantly induced apoptosis in HCT116 (p53(+/+) ) cells but not in HCT116 (p53(-/-) ) cells.	5-hydroxy-3,6,7,8,3',4'-hexamethoxyflavone	70-75	P53	Homo sapiens	165-168
21462329-7	2011	CONCLUSION: Our results demonstrated that 5OH-PMFs, especially 5HHMF and 5HTMF, induce apoptosis and cell-cycle arrest by p53-, Bax- and p21-dependent mechanism.	5-hydroxy-3,6,7,8,3',4'-hexamethoxyflavone	63-68	P53	Homo sapiens	122-125
21445240-11	2011	Both tetramers and hexamers bind the target peptide from p53 with retained stoichiometry of one peptide per S100B monomer, and with high affinity (lgK = 7.3+-0.2 and 7.2+-0.2, respectively in 10 mM BisTris, 5 mM CaCl(2), pH 7.0), which is less than one order of magnitude reduced compared to dimer under the same buffer conditions.	cacl	212-216	P53	Homo sapiens	57-60
21359924-7	2011	Immunocytochemistry indicated that the expression of Bcl-2 protein decreased, while the expression of p53 and Bax proteins increased in A549 cells treated with Inotodiol, compared with the control cells (P&lt;0.05).	inotodiol	160-169	P53	Homo sapiens	102-105
21359924-8	2011	CONCLUSION: Inotodiol can inhibit proliferation and induce the apoptosis of A549 cells, and its molecular mechanism may be associated with the up-regulating expression of p53 and bax proteins and down-regulating expression of Bcl-2 protein, which arrested A549 cells in S phase.	inotodiol	12-21	P53	Homo sapiens	171-174
22977494-9	2011	p53 overexpression may be a key predictor of a favorable response to NAC.	nac	69-72	P53	Homo sapiens	0-3
20593219-0	2011	Effect of aberrant p53 function on temozolomide sensitivity of glioma cell lines and brain tumor initiating cells from glioblastoma.	Temozolomide	35-47	P53	Homo sapiens	19-22
20593219-6	2011	The effect of p53 status on response to TMZ was explored in traditional glioma cell lines (U87MG, U251MG, U343MG, U373MG, SF767, LN443 and LNZ308) and brain tumor initiating cells (BTICs--BT012, BT025, BT042, BT048, BT060 and BT069) in two ways: (1) inhibition of p53 by RNAi and (2) sensitivity in relation to intrinsic p53 status, either wild-type or mutant.	Temozolomide	40-43	P53	Homo sapiens	14-17
20593219-8	2011	Altered p53 expression or function had only minor effects on TMZ sensitivity in BTICs and tended to decrease sensitivity to TMZ.	Temozolomide	61-64	P53	Homo sapiens	8-11
20593219-8	2011	Altered p53 expression or function had only minor effects on TMZ sensitivity in BTICs and tended to decrease sensitivity to TMZ.	Temozolomide	124-127	P53	Homo sapiens	8-11
20593219-11	2011	P53 status may influence response to TMZ in differentiated cells in a GBM with a negligible affect on its initiating cells.	Temozolomide	37-40	P53	Homo sapiens	0-3
21262846-1	2011	The inositol pyrophosphate, diphosphoinositol pentakisphosphate, regulates p53 and protein kinase Akt signaling, and its aberrant increase in cells has been implicated in apoptosis and insulin resistance.	1-diphosphoinositol pentakisphosphate	28-63	P53	Homo sapiens	75-78
21210663-0	2011	Functionalized graphene oxide as a nanocarrier in a multienzyme labeling amplification strategy for ultrasensitive electrochemical immunoassay of phosphorylated p53 (S392).	graphene oxide	15-29	P53	Homo sapiens	161-164
21210663-2	2011	We report a new electrochemical immunosensor for ultrasensitive detection of phosphorylated p53 at Ser392 (phospho-p53(392)) based on graphene oxide (GO) as a nanocarrier in a multienzyme amplification strategy.	graphene oxide	134-148	P53	Homo sapiens	92-95
21210663-2	2011	We report a new electrochemical immunosensor for ultrasensitive detection of phosphorylated p53 at Ser392 (phospho-p53(392)) based on graphene oxide (GO) as a nanocarrier in a multienzyme amplification strategy.	graphene oxide	134-148	P53	Homo sapiens	115-118
21210663-2	2011	We report a new electrochemical immunosensor for ultrasensitive detection of phosphorylated p53 at Ser392 (phospho-p53(392)) based on graphene oxide (GO) as a nanocarrier in a multienzyme amplification strategy.	graphene oxide	150-152	P53	Homo sapiens	92-95
21210663-2	2011	We report a new electrochemical immunosensor for ultrasensitive detection of phosphorylated p53 at Ser392 (phospho-p53(392)) based on graphene oxide (GO) as a nanocarrier in a multienzyme amplification strategy.	graphene oxide	150-152	P53	Homo sapiens	115-118
21112369-4	2011	PG activated caspases 3, 8, and 9 and increased the levels of p53, Bax, Fas, and Fas ligand.	Propyl Gallate	0-2	P53	Homo sapiens	62-65
21359449-6	2011	p53 positivity was observed in 93.3% of PMD, in 63.3% of OSCC and in 80% of OEH.	oscc	57-61	P53	Homo sapiens	0-3
22312557-11	2011	Inhibition of Chk2 pathway with a Chk2 inhibitor (C3742) increased cisplatin efficacy, especially those with defective p53.	c3742	50-55	P53	Homo sapiens	119-122
22708054-0	2011	Catalytic, Enantioselective Synthesis of Stilbene cis-Diamines: A Concise Preparation of (-)-Nutlin-3, a Potent p53/MDM2 Inhibitor.	stilbene cis-diamines	41-62	P53	Homo sapiens	112-115
20038571-7	2011	Further studies on apoptotic mechanisms of Cin showed that it downregulated the expression of Bcl-(XL), upregulated CD95 (APO-1), p53 and Bax proteins, as well as cleaving the poly (ADP-ribose) polymerase (PARP) in a time-dependent pattern.	cinnamaldehyde	43-46	P53	Homo sapiens	130-133
20038571-10	2011	This study indicates that Cin was the most potent antiproliferative constituent of C. cassia, and its apoptotic mechanism in Hep G2 cells could be mediated through the p53 induction and CD95 (APO-1) signaling pathways.	cinnamaldehyde	26-29	P53	Homo sapiens	168-171
21760996-4	2011	TP53 and CTNNB1 mutations were not mutually exclusive, and most of TP53 mutations were R249S, suggesting a significant impact of aflatoxin-induced mutagenesis in HCC development.	Aflatoxins	129-138	P53	Homo sapiens	0-4
21760996-4	2011	TP53 and CTNNB1 mutations were not mutually exclusive, and most of TP53 mutations were R249S, suggesting a significant impact of aflatoxin-induced mutagenesis in HCC development.	Aflatoxins	129-138	P53	Homo sapiens	67-71
21720516-3	2011	Standard ethidium bromide and acridine orange assays were used to detect apoptotic cells and indicated that a significantly larger percentage of the cells (approx 40%) were dead after 72 hours of exposure to f-SWCNTs-p53 as compared to the control cells, which were exposed to only p53 or f-SWCNTs, respectively.	Acridine Orange	30-45	P53	Homo sapiens	217-220
21221951-6	2010	An exopolysaccharide purified from the acidophilic strain was added to cultured U937 cells, resulting in significantly increased transcription levels of p53 and p21 genes.	exopolysaccharide	3-20	P53	Homo sapiens	153-156
21092078-6	2010	Furthermore, the role of p53 in flavopiridol- and 4OH-Tam-mediated induction of cell cycle arrest and apoptosis was characterized using RNA interference (siRNA) analysis.	alvocidib	32-44	P53	Homo sapiens	25-28
21092078-7	2010	The effect of p53 on flavopiridol-mediated induction of caspases 2, 3, 8 and 9 was also determined.	alvocidib	21-33	P53	Homo sapiens	14-17
21092078-9	2010	Low nanomolar concentrations of flavopiridol induced G2 arrest, which was correlated to down-modulation of cyclin B1 and up-regulation of p53.	alvocidib	32-44	P53	Homo sapiens	138-141
21092078-11	2010	Abrogation of p53 by siRNA abolished flavopiridol-induced G2 arrest, but enhanced flavopiridol- (but not 4OH-Tam-) mediated apoptosis, by enhancing caspase 2 and 3 activities.	alvocidib	37-49	P53	Homo sapiens	14-17
21092078-11	2010	Abrogation of p53 by siRNA abolished flavopiridol-induced G2 arrest, but enhanced flavopiridol- (but not 4OH-Tam-) mediated apoptosis, by enhancing caspase 2 and 3 activities.	alvocidib	82-94	P53	Homo sapiens	14-17
21092078-13	2010	The potency of flavopiridol was enhanced by abrogation of p53.	alvocidib	15-27	P53	Homo sapiens	58-61
20155316-4	2010	Sildenafil enhanced sensitivity to adriamycin markedly in the p53 mutant MDA-MB231 and p53 null MCF-7/E6 cells and moderately in the MCF-7/caspase 3 and 4T1 cell lines.	Sildenafil Citrate	0-10	P53	Homo sapiens	62-65
20155316-4	2010	Sildenafil enhanced sensitivity to adriamycin markedly in the p53 mutant MDA-MB231 and p53 null MCF-7/E6 cells and moderately in the MCF-7/caspase 3 and 4T1 cell lines.	Sildenafil Citrate	0-10	P53	Homo sapiens	87-90
20548097-8	2010	In both MK classes, AZD1152-HQPA induced p53 activation and retinoblastoma hypophosphorylation.	AZD 1152-HQPA	20-32	P53	Homo sapiens	41-44
20445579-6	2010	In this study, as a simple preclinical model, we constructed a doxycycline-regulated bidirectional vector harboring a reporter gene encoding red fluorescence protein and p53.	Doxycycline	63-74	P53	Homo sapiens	170-173
20017137-2	2010	Convincing epidemiological and experimental evidence also links HCC to aflatoxin, a naturally occurring mycotoxin that produces a signature p53-249(ser) mutation.	Aflatoxins	71-80	P53	Homo sapiens	140-143
20306157-7	2010	In conclusion, although codon 249 mutation of p53 gene has been found very rare but it exists showing the effect of aflatoxins in HCC patients in Turkey.	Aflatoxins	116-126	P53	Homo sapiens	46-49
20660730-7	2010	When encapsulated in liposomes decorated with an integrin-targeting cyclic-RGD peptide, however, (D)PMI-alpha exerted potent p53-dependent growth inhibitory activity against human glioblastoma in cell cultures and nude mouse xenograft models.	pmi-alpha	100-109	P53	Homo sapiens	125-128
20558185-7	2010	While the benzofurylquinazolines increased the expression level of the pro-inflammatory gene IL1-alpha as well as p21 and p53 in the PC3 cell line, a phenylpyrrolocarbazole had the converse effect on p53 expression.	benzofurylquinazolines	10-32	P53	Homo sapiens	122-125
20565132-2	2010	Here, we demonstrate that 4-HNE induces signaling for apoptosis via both the Fas-mediated extrinsic and the p53-mediated intrinsic pathways in HepG2 cells.	4-hydroxy-2-nonenal	26-31	P53	Homo sapiens	108-111
20700368-1	2010	PURPOSE: Benzo[a]pyrene 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of benzo[a]pyrene, attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 mutations.	Benzo(a)pyrene	9-23	P53	Homo sapiens	160-163
20700368-1	2010	PURPOSE: Benzo[a]pyrene 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of benzo[a]pyrene, attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 mutations.	Benzo(a)pyrene	80-94	P53	Homo sapiens	160-163
19862502-0	2010	Benzene-induced mutational pattern in the tumour suppressor gene TP53 analysed by use of a functional assay, the functional analysis of separated alleles in yeast, in human lung cells.	Benzene	0-7	P53	Homo sapiens	65-69
19862502-3	2010	Since mutations in the tumour suppressor gene TP53 are the most common genetic alterations involved in human cancer, our objective was to establish the first mutational pattern induced by benzene on the TP53 gene in human type II-like alveolar epithelial A549 cells by using the Functional Analysis of Separated Alleles in Yeast (FASAY).	Benzene	188-195	P53	Homo sapiens	46-50
19862502-3	2010	Since mutations in the tumour suppressor gene TP53 are the most common genetic alterations involved in human cancer, our objective was to establish the first mutational pattern induced by benzene on the TP53 gene in human type II-like alveolar epithelial A549 cells by using the Functional Analysis of Separated Alleles in Yeast (FASAY).	Benzene	188-195	P53	Homo sapiens	203-207
19862502-7	2010	Data arising from this benzene-induced mutational pattern affecting TP53, a critical target gene in human carcinogenesis, have been compared with those reported in human acute myeloid leukaemia, the aetiology of which is clearly linked to benzene exposure, and in experimental benzene-induced carcinoma.	Benzene	23-30	P53	Homo sapiens	68-72
20043141-6	2010	The p21Cip1 is a downstream target of p53 that may be affected by the activation of p53 by 4"-chloroflavanone.	4'-chloroflavanone	91-109	P53	Homo sapiens	38-41
20043141-6	2010	The p21Cip1 is a downstream target of p53 that may be affected by the activation of p53 by 4"-chloroflavanone.	4'-chloroflavanone	91-109	P53	Homo sapiens	84-87
20043141-7	2010	These results indicate that activation of p53 played some role in 4"-chloroflavanone-induced cell cycle arrest of human breast cancer cells.	4'-chloroflavanone	66-84	P53	Homo sapiens	42-45
19918798-5	2010	PTX/LPC combination acted by favoring p53 stabilization through a lowering in p-Akt levels and in ps166-MDM2, the phosphorylated-MDM2 form that enters the nucleus and induces p53 export and degradation.	beta-lapachone	4-7	P53	Homo sapiens	38-41
19918798-5	2010	PTX/LPC combination acted by favoring p53 stabilization through a lowering in p-Akt levels and in ps166-MDM2, the phosphorylated-MDM2 form that enters the nucleus and induces p53 export and degradation.	beta-lapachone	4-7	P53	Homo sapiens	175-178
19918798-8	2010	PTX/LPC treatment induced a weakness of Akt-MDM2-p53 complex and increased nuclear p53 levels.	beta-lapachone	4-7	P53	Homo sapiens	49-52
19918798-8	2010	PTX/LPC treatment induced a weakness of Akt-MDM2-p53 complex and increased nuclear p53 levels.	beta-lapachone	4-7	P53	Homo sapiens	83-86
20126473-4	2010	The p53 C-terminal domain is clustered with potential nuclear leading sequences and showed strong electrostatic ion-ion interactions with cardiolipin, phosphatidylglycerol and phosphatidic acid in vitro.	Cardiolipins	138-149	P53	Homo sapiens	4-7
20126473-4	2010	The p53 C-terminal domain is clustered with potential nuclear leading sequences and showed strong electrostatic ion-ion interactions with cardiolipin, phosphatidylglycerol and phosphatidic acid in vitro.	Phosphatidylglycerols	151-171	P53	Homo sapiens	4-7
19933157-6	2010	Binding of the probe bis-ANS (bis-8-anilinonaphthalene-1-sulfonate) indicates that there is an increase in the exposure of hydrophobic pockets for both wt and mutant p53C at low pH.	5,5'-bis(8-(phenylamino)-1-naphthalenesulfonate)	21-28	P53	Homo sapiens	166-169
20008633-1	2010	PURPOSE: Flavopiridol downmodulates antiapoptotic proteins associated with resistance to fludarabine and rituximab and is effective against p53-mutated chronic lymphocytic leukemia (CLL).	alvocidib	9-21	P53	Homo sapiens	140-143
20013323-3	2010	MV4-11 TP53 R248W cells were relatively resistant to AZD1152-HQPA-mediated growth arrest, as measured by MTT and clonogenic assays.	AZD 1152-HQPA	53-65	P53	Homo sapiens	7-11
20013323-4	2010	AZD1152-HQPA (10-100 nM, 48 h) strikingly induced apoptosis of MV4-11 cells, as assessed by Annexin V binding, loss of mitochondrial outer membrane potential, and activation of caspase cascade, in parallel with up-regulation of p53 and its target molecules Bax and Noxa.	AZD 1152-HQPA	0-12	P53	Homo sapiens	228-231
20013323-5	2010	Notably, AZD1152-HQPA (10-100 nM, 48 h) induced polyploidy rather than apoptosis in MV4-11 TP53 R248W cells.	AZD 1152-HQPA	9-21	P53	Homo sapiens	91-95
31732977-5	2020	A possible strategy to overcome some of these obstacles is to combine ibrutinib with other targeted agents especially in high-risk disease, such as previously treated refractory patients or those with TP53 aberrations or complex karyotypes, in whom rapid eradication of disease is most desirable.	ibrutinib	70-79	P53	Homo sapiens	201-205
19946262-0	2010	Selective FLT3 inhibitor FI-700 neutralizes Mcl-1 and enhances p53-mediated apoptosis in AML cells with activating mutations of FLT3 through Mcl-1/Noxa axis.	FI-700	25-31	P53	Homo sapiens	63-66
19946262-5	2010	We found that FI-700 immediately reduced antiapoptotic Mcl-1 levels and enhanced Nutlin-induced p53-mediated mitochondrial apoptosis in FLT3/internal tandem duplication cells through the Mcl-1/Noxa axis.	FI-700	14-20	P53	Homo sapiens	96-99
32218822-7	2020	In regard to TP53 mutation, the rate of TP53 mutation in the NAC-resistant cases was significantly higher compared with NAC-sensitive cases.	nac	61-64	P53	Homo sapiens	13-17
32218822-7	2020	In regard to TP53 mutation, the rate of TP53 mutation in the NAC-resistant cases was significantly higher compared with NAC-sensitive cases.	nac	61-64	P53	Homo sapiens	40-44
32218822-7	2020	In regard to TP53 mutation, the rate of TP53 mutation in the NAC-resistant cases was significantly higher compared with NAC-sensitive cases.	nac	120-123	P53	Homo sapiens	13-17
32218822-7	2020	In regard to TP53 mutation, the rate of TP53 mutation in the NAC-resistant cases was significantly higher compared with NAC-sensitive cases.	nac	120-123	P53	Homo sapiens	40-44
21290342-6	2010	MDM2 - associated APC fluorescence and p53 - associated FITC fluorescence were measured by the laser scanning cytometer.	Fluorescein-5-isothiocyanate	56-60	P53	Homo sapiens	39-42
32218822-9	2020	These results indicated that gene mutation can be profiled and monitored using liquid biopsy-based CAPP-Seq in patients with advanced ovarian cancer with NAC treatment, and TP53 mutation in the ctDNA and bTMB may be novel biomarkers that can be used for patient monitoring during NAC treatment.	nac	280-283	P53	Homo sapiens	173-177
20023923-2	2009	Azide, a singlet oxygen quencher, greatly reduced the p53 photocrosslinking, consistent with the idea that singlet oxygen is the reactive oxygen species involved in p53 photocrosslinking.	Azides	0-5	P53	Homo sapiens	54-57
20023923-2	2009	Azide, a singlet oxygen quencher, greatly reduced the p53 photocrosslinking, consistent with the idea that singlet oxygen is the reactive oxygen species involved in p53 photocrosslinking.	Azides	0-5	P53	Homo sapiens	165-168
31990147-9	2020	We further found that the effect of Lobetyolin on HCT-116 was related to the expressions of p21 and bax, and transportation of p53 to nucleus.	lobetyolin	36-46	P53	Homo sapiens	127-130
19679195-7	2009	Finally, 4,4"-dihydroxy-trans-stilbene increased p21(CDKN1A) and p53 protein levels, whereas resveratrol led to phosphorylation of the S-phase checkpoint protein Chk1.	4,4'-dihydroxystilbene	9-38	P53	Homo sapiens	65-68
31990147-10	2020	The inhibition of p53 by Pifithrin-alpha promoted the inhibitory effect of Lobetyolin on ASCT2-mediated apoptosis.	lobetyolin	75-85	P53	Homo sapiens	18-21
20201230-0	2009	P53 detection by fluorescence lifetime on a hybrid fluorescein isothiocyanate gold nanosensor.	Fluorescein-5-isothiocyanate	51-77	P53	Homo sapiens	0-3
31628428-4	2020	Ibrutinib benefit was also consistent in patients with high prognostic risk (TP53 mutation, 11q deletion, and/or unmutated IGHV) (PFS: HR [95% CI]: 0.083 [0.047-0.145]; OS: HR [95% CI]: 0.366 [0.181-0.736]).	ibrutinib	0-9	P53	Homo sapiens	77-81
19994847-7	2009	Additionally, the Bcl-2 antiapoptotic protein is predicted to bind pargyline, and the antiapoptic p53 interacting protein MDM2 is suggested to bind clofazimine.	Clofazimine	148-159	P53	Homo sapiens	98-101
19703338-0	2010	Prognostic and predictive value of p53 in low MGMT expressing glioblastoma treated with surgery, radiation and adjuvant temozolomide chemotherapy.	Temozolomide	120-132	P53	Homo sapiens	35-38
20639499-5	2010	The HCS campaign yielded 3 structurally related methylbenzo-naphthyridin-5-amine (MBNA) hits with IC(50)s between 30 and 50 microM in the p53-hDM2 PPIB.	Homocysteine	4-7	P53	Homo sapiens	138-141
20639499-5	2010	The HCS campaign yielded 3 structurally related methylbenzo-naphthyridin-5-amine (MBNA) hits with IC(50)s between 30 and 50 microM in the p53-hDM2 PPIB.	nitrosomethyl-N-butylamine	82-86	P53	Homo sapiens	138-141
31464976-8	2020	Inhibition of ROS generation by NAC or p38 MAPK signaling by SB203580 attenuated the p53-mediated cell cycle arrest and apoptosis induced by LY.	nac	32-35	P53	Homo sapiens	85-88
20118823-7	2010	In wtp53 cells, losartan increased p53 transcription and activated caspase-3 in both cell lines.	Losartan	16-24	P53	Homo sapiens	5-8
19770592-4	2009	The present study demonstrates that cisplatin induces the PIDD (p53 induced protein with a death domain) dependent activation of caspase-2.	pidd	58-62	P53	Homo sapiens	64-67
19397966-1	2009	Benzo(a)pyrene (BP) forms benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE)-DNA adducts in human breast adenocarcinoma MCF-7 cells, leading to p53 protein induction and phosphorylation.	Benzo(a)pyrene	0-14	P53	Homo sapiens	144-147
19397966-1	2009	Benzo(a)pyrene (BP) forms benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE)-DNA adducts in human breast adenocarcinoma MCF-7 cells, leading to p53 protein induction and phosphorylation.	Benzo(a)pyrene	16-18	P53	Homo sapiens	144-147
19397966-3	2009	Here we have analyzed the effects of BP on p53 related apoptotic proteins, cell cycle and cell death in MCF-7 cells.	Benzo(a)pyrene	37-39	P53	Homo sapiens	43-46
31936679-11	2020	To further substantiate the mechanism of cell death mediated by endoplasmic reticulum stress (ERS), we determined the expression of the inositol-requiring enzyme (IRE1), (PKR-like ER kinase) PERK, activating transcription factor 6 (ATF6), and activating transcription factor 4 ATF4, the apoptotic markers p53, Bax, and caspase 3, and the anti-apoptotic marker Bcl-2.	Inositol	136-144	P53	Homo sapiens	305-308
19397966-4	2009	PUMA-protein (p53 up-regulated modulator of apoptosis) levels were changed after BP exposure so that PUMA-alpha protein was statistically significantly increased whereas PUMA-beta protein was statistically significantly decreased.	Benzo(a)pyrene	81-83	P53	Homo sapiens	14-17
19397966-9	2009	Our results suggest that PUMA-alpha protein is involved in BP-induced cell death most likely through a p53 dependent apoptotic pathway.	Benzo(a)pyrene	59-61	P53	Homo sapiens	103-106
19723051-6	2009	DHA increased the protein levels of p53, cytochrome c, and Bax in gastric cancer cells.	Docosahexaenoic Acids	0-3	P53	Homo sapiens	36-39
19723051-7	2009	DHA-induced DNA fragmentation and protein levels of p53, cytochrome c, and Bax were inhibited in the cells transfected with c-jun dominant-negative mutant (TAM67).	Docosahexaenoic Acids	0-3	P53	Homo sapiens	52-55
19723057-8	2009	Moreover, isolated MCF-7 nuclear extracts directly treated with 15d-PGJ(2) exhibite diminished DNA-binding ability of p53, while the same concentration of PGA(2) or 2-cyclopenten-1-one was much less inhibitory.	-pgj	67-71	P53	Homo sapiens	118-121
19723057-9	2009	Thus, the electrophilic carbon center located in the alpha,beta-unsaturated carbonyl moiety of the cyclopentenone ring might be critical for the control of DNA-binding activity as well as cellular levels of p53 by 15d-PGJ(2).	cyclopentenone	99-113	P53	Homo sapiens	207-210
20371965-6	2010	Moreover, it was shown that cotreatment with MDA-LDL and BaP markedly induced the expression of human cytochrome P4501A1 (hCYP1A1) messenger ribonucleic acid (mRNA) and significantly induced the expressions of p53 and p21 mRNAs.	Benzo(a)pyrene	57-60	P53	Homo sapiens	210-213
20054683-6	2010	RESULTS: Within 2-4 hr, lidocaine and procaine (&gt; or = 1 mM) induced massive cell vacuolization, a response abated by the V-ATPase inhibitor, bafilomycin A1, and activated macroautophagic signalling (LC3 II formation) but not other stress signalling (p38, ERK1/2, p53, no influence on serum-controlled Akt phosphorylation).	Procaine	38-46	P53	Homo sapiens	267-270
19723085-7	2009	DHA and ALA inhibited DNA fragmentation, inhibited the decrease in cell viability, and inhibited the expression of apoptotic genes (p53, Bax, apoptosis-inducing factor) induced by hydrogen peroxide in pancreatic acinar cells.	Docosahexaenoic Acids	0-3	P53	Homo sapiens	132-135
31744518-0	2019	TPP-related mitochondrial targeting copper (II) complex induces p53-dependent apoptosis in hepatoma cells through ROS-mediated activation of Drp1.	Phosphines	0-3	P53	Homo sapiens	64-67
19297420-0	2009	Influence of magnesium ion on the binding of p53 DNA-binding domain to DNA-response elements.	Magnesium	13-22	P53	Homo sapiens	45-48
20067417-0	2010	Effect of date seed oil on p53 expression in normal human skin.	seed oil	15-23	P53	Homo sapiens	27-30
19853978-0	2010	The role of p53 in the cellular toxicity by active trans-platinum complexes containing isopropylamine and hydroxymethylpyridine.	trans-platinum	51-65	P53	Homo sapiens	12-15
19853978-2	2010	Based on the proposed mechanism of action for the trans-platinum compounds, they might form DNA adducts initiating a DNA-damage response and ultimately ending in the activation of the p53 protein.	trans-platinum	50-64	P53	Homo sapiens	184-187
31446323-0	2019	Loading of some quinoxaline derivatives in poly (l-lactic) acid/Pluronic  F-127 nanofibers enhances their anticancer efficiency and induces a p53 and p21 apoptotic-signaling pathway.	poly(lactide)	43-63	P53	Homo sapiens	142-145
19890398-6	2009	We show that oncogenic RAS synergizes with cytotoxic agents such as cytarabine in activation of DNA damage checkpoints, resulting in a p53-dependent genetic program that reduces clonogenicity and increases myeloid differentiation.	Cytarabine	68-78	P53	Homo sapiens	135-138
19890398-7	2009	Our data can explain the beneficial effects observed for AML patients with oncogenic RAS treated with higher dosages of cytarabine and suggest that induction of p53-dependent differentiation, e.g. by interfering with Mdm2-mediated degradation, may be a rational approach to increase cure rate in response to chemotherapy.	Cytarabine	120-130	P53	Homo sapiens	161-164
19146838-5	2009	Moreover, ASDO treatment up-regulated the expression levels of total p53 and its target gene p21Waf1.	asdo	10-14	P53	Homo sapiens	69-72
19146838-8	2009	Taken together, we conclude that ASDO induces MCF-7 cell apoptosis through a p53-dependent and mitochondria-mediated pathway.	asdo	33-37	P53	Homo sapiens	77-80
31450059-2	2019	Chitosan-grafted poly-(N-3-carbobenzyloxy-lysine) (CCL) decorated with human immunodeficiency virus-1 transactivator of transcription (TAT) can co-deliver p53 and doxorubicin into the nucleus simultaneously, such that their antitumor functions are exerted.	poly-(n-3-carbobenzyloxy-lysine)	17-49	P53	Homo sapiens	155-158
19505915-0	2009	Association of genetic polymorphisms, mRNA expression of p53 and p21 with chronic benzene poisoning in a chinese occupational population.	Benzene	82-89	P53	Homo sapiens	57-60
19796171-5	2009	Here, we report that the tumor suppressor p53 is colocalized with FE65 in the nuclear patches and is stabilized by FE65 in sorbitol-treated cells.	Sorbitol	123-131	P53	Homo sapiens	42-45
19796171-6	2009	In FE65 knockdown cells, protein levels of p53 targeted to the nuclear matrix were rapidly decreased through the proteasome degradation pathway after sorbitol treatment, as compared with control cells.	Sorbitol	150-158	P53	Homo sapiens	43-46
31450059-2	2019	Chitosan-grafted poly-(N-3-carbobenzyloxy-lysine) (CCL) decorated with human immunodeficiency virus-1 transactivator of transcription (TAT) can co-deliver p53 and doxorubicin into the nucleus simultaneously, such that their antitumor functions are exerted.	Cefaclor	51-54	P53	Homo sapiens	155-158
31612051-9	2019	When assessing the underlying molecular mechanism, it was revealed that PPI and PPVII enhanced DDP-induced apoptosis in A549/DDP cells via p53 upregulation and the caspase-dependent pathway.	polyphyllin I	72-75	P53	Homo sapiens	139-142
19996705-11	2009	Moreover, both CS and PS induced expression of the p53 tumor suppressor gene and the Cdk inhibitor p21.	ps	22-24	P53	Homo sapiens	51-54
19097688-0	2009	Andrographolide enhances 5-fluorouracil-induced apoptosis via caspase-8-dependent mitochondrial pathway involving p53 participation in hepatocellular carcinoma (SMMC-7721) cells.	andrographolide	0-15	P53	Homo sapiens	114-117
19097688-8	2009	Surprisingly, the addition of ANDRO to 5-FU induces synergistic apoptosis, which could be corroborated to the increased caspase-8, p53 activity and the significant changes of Bax conformation in these cells, resulting in increased losses of mitochondrial membrane potential, increased release of cytochrome c, and activation of caspase-9 and caspase-3.	andrographolide	30-35	P53	Homo sapiens	131-134
31612051-11	2019	Overall, the results from the present study demonstrated that PPI and PPVII may function as chemosensitizers by enhancing apoptosis via the p53 pathway, reversing EMT and suppressing the CIP2A/AKT/mTOR signaling axis, and the combination with DDP may be a promising strategy for the development of new therapeutic agents.	polyphyllin I	62-65	P53	Homo sapiens	140-143
31647033-7	2019	AURKA inhibition using 100 nM MLN8237 for 48 h decreases cell growth in a partially P53-dependent manner, and the survival rates of H460, HCC2429, and H1299 cells were 56, 50, and 77%, respectively.	MLN 8237	30-37	P53	Homo sapiens	84-87
19265549-5	2009	RESULTS: Significant differential modulation of 151 genes were found at 4 h after start of induction therapy with cytarabine and anthracycline, including significant overexpression of 31 genes associated with p53 regulation.	Cytarabine	114-124	P53	Homo sapiens	209-212
19265549-7	2009	FLT3 mutations indicated that non-responders (5/7 patients, 8 versus 49 months survival) are characterized by a unique gene response profile before and at 4 h. At 18-24 h after chemotherapy, the gene expression of p53 target genes was attenuated, while genes involved in chemoresistance, cytarabine detoxification, chemokine networks and T cell receptor were prominent.	Cytarabine	288-298	P53	Homo sapiens	214-217
19733546-3	2009	Cordycepin treatment, at a dose of 200 microM (IC(50)) during cell-cycle progression resulted in significant and dose-dependent growth inhibition, which was largely due to G2/M-phase arrest, and resulted in an up-regulation of p21WAF1 expression, independent of the p53 pathway.	cordycepin	0-10	P53	Homo sapiens	266-269
19789321-7	2009	RESULTS: The SET8 CC and TP53 GG genotypes were independently associated with an earlier age of breast cancer onset in an allele-dose-dependent manner (for SET8, 52.2 years for TT, 51.4 for TC, and 49.5 for CC; and for TP53, 53.1 years for CC, 51.5 for GC, 50.7 for GG).	Technetium	190-192	P53	Homo sapiens	25-29
19305157-0	2009	Diversity of DNA damage response of astrocytes and glioblastoma cell lines with various p53 status to treatment with etoposide and temozolomide.	Temozolomide	131-143	P53	Homo sapiens	88-91
31647033-11	2019	Modulation of P53 function could provide a new option for reversing cell resistance to the AURKA inhibitor MLN8237, which deserves further investigation.	MLN 8237	107-114	P53	Homo sapiens	14-17
31637188-10	2019	Obtusifolin reduced the expression of Cyclin D1 and proliferating cell nuclear antigen (PCNA) in the hypoxic environment and increased the expression of p53 and p21.	obtusifolin	0-11	P53	Homo sapiens	153-156
19220630-8	2009	"This relationship may be accounted for by the facts that smoking and use of BQ may induce an alteration to p53 that, in turn, may lead to the development and progression of SCC".	bulaquine	77-79	P53	Homo sapiens	108-111
19367569-4	2009	Furthermore, it is shown that the codons at which LF/LFL germline missense mutations occur, correlate with CpG-containing ESEs (r = 0.181, P = 0.014) which are all methylated in p53.	eses	122-126	P53	Homo sapiens	178-181
31703757-0	2019	Inhibitory effects of polyphyllins I and VII on human cisplatin-resistant NSCLC via p53 upregulation and CIP2A/AKT/mTOR signaling axis inhibition.	polyphyllin I	22-36	P53	Homo sapiens	84-87
19596022-1	2009	Benzene reactive metabolites can lead to DNA damage and trigger the p53-dependent defense responses to maintain genomic stability.	Benzene	0-7	P53	Homo sapiens	68-71
19596022-2	2009	We hypothesized that the p53-dependent genes may play a role in the development of chronic benzene poisoning (CBP).	Benzene	91-98	P53	Homo sapiens	25-28
19059205-7	2009	The cell adhesion strength in the presence of SPBE, beta-sitosterol and cholesterol and the observation was that the increase in p53 expression triggered an increase in the intracellular force generation.	gamma-sitosterol	52-67	P53	Homo sapiens	129-132
31703757-8	2019	Further examination of the mechanism revealed that the PPI and PPVII significantly upregulated the p53, induced caspase-dependent apoptosis and suppressed the CIP2A/AKT/mTOR pathway.	polyphyllin I	55-58	P53	Homo sapiens	99-102
19037090-4	2009	Aza also reduced the global methylation levels in glioblastoma cells and activated the pathway of p53 tumor suppressor.	Azathioprine	0-3	P53	Homo sapiens	98-101
19037090-5	2009	Methylation-specific polymerase chain reaction revealed that Aza treatment of tumor cells reduced the methylation of p53 promoter, which was accompanied by increased expression of p53 gene and protein.	Azathioprine	61-64	P53	Homo sapiens	117-120
19634013-3	2009	N-methyl-N-nitrosourea (MNU), a model S(N)1 methylating agent, induced cell death through a distinct mechanism in two human NSCLC cell lines studied, A549(p53(wt)) and H157(p53(null)).	Methylnitrosourea	0-22	P53	Homo sapiens	155-158
19634013-3	2009	N-methyl-N-nitrosourea (MNU), a model S(N)1 methylating agent, induced cell death through a distinct mechanism in two human NSCLC cell lines studied, A549(p53(wt)) and H157(p53(null)).	Methylnitrosourea	0-22	P53	Homo sapiens	173-176
19634013-3	2009	N-methyl-N-nitrosourea (MNU), a model S(N)1 methylating agent, induced cell death through a distinct mechanism in two human NSCLC cell lines studied, A549(p53(wt)) and H157(p53(null)).	Methylnitrosourea	24-27	P53	Homo sapiens	155-158
19037090-5	2009	Methylation-specific polymerase chain reaction revealed that Aza treatment of tumor cells reduced the methylation of p53 promoter, which was accompanied by increased expression of p53 gene and protein.	Azathioprine	61-64	P53	Homo sapiens	180-183
31102418-5	2019	1-HMP treatment resulted in significantly (~40-fold) higher DNA adduct levels in TP53(+/+) cells than in the other cell lines.	1-hydroxymethylpyrene	0-5	P53	Homo sapiens	81-85
19037090-7	2009	Furthermore, Aza treatment or overexpression of the wild-type p53 in glioblastoma cells increased the binding of p53 to FPR promoter region shown by chromatin immunoprecipitation.	Azathioprine	13-16	P53	Homo sapiens	113-116
19208740-1	2009	The p53 protein is a key regulator of cell responses to DNA damage, and it has been shown that it sensitizes glioma cells to the alkylating agent temozolomide by up-regulating the extrinsic apoptotic pathway, whereas it increases the resistance to chloroethylating agents, such as ACNU and BCNU, probably by enhancing the efficiency of DNA repair.	Temozolomide	146-158	P53	Homo sapiens	4-7
19208740-7	2009	Collectively, the data indicate that unrepaired DNA lesions induce apoptosis in p53 mutant gliomas despite the resistance of these gliomas to temozolomide, suggesting that efficiency of treatment of p53 mutant gliomas might be higher with agents that induce the formation of DNA lesions whose global genomic repair is dependent on p53.	Temozolomide	142-154	P53	Homo sapiens	199-202
19208740-7	2009	Collectively, the data indicate that unrepaired DNA lesions induce apoptosis in p53 mutant gliomas despite the resistance of these gliomas to temozolomide, suggesting that efficiency of treatment of p53 mutant gliomas might be higher with agents that induce the formation of DNA lesions whose global genomic repair is dependent on p53.	Temozolomide	142-154	P53	Homo sapiens	199-202
19127257-0	2009	Temozolomide- and fotemustine-induced apoptosis in human malignant melanoma cells: response related to MGMT, MMR, DSBs, and p53.	Temozolomide	0-12	P53	Homo sapiens	124-127
19634013-3	2009	N-methyl-N-nitrosourea (MNU), a model S(N)1 methylating agent, induced cell death through a distinct mechanism in two human NSCLC cell lines studied, A549(p53(wt)) and H157(p53(null)).	Methylnitrosourea	24-27	P53	Homo sapiens	173-176
19634013-4	2009	In A549(p53(wt)), MNU induced G2/M arrest, accompanied by cdc25A degradation, hnRNP B1 induction, hnRNP C1/C2 downregulation.	Methylnitrosourea	18-21	P53	Homo sapiens	8-11
19634013-6	2009	In H157(p53(null)), MNU induced apoptotic cell death, confirmed by cytofluorometry of DNA content and immunodetection of apoptotic markers, accompanied by overexpression of hnRNP B1 and C1/C2.	Methylnitrosourea	20-23	P53	Homo sapiens	8-11
19639181-0	2009	p53 is an important factor for the radiosensitization effect of 2-deoxy-D-glucose.	Deoxyglucose	64-81	P53	Homo sapiens	0-3
19639181-3	2009	In this study which uses lung cancer as the model, we demonstrate that the improvement of radiotherapy by 2-deoxy-D-glucose (2DG) is p53-dependent.	Deoxyglucose	106-123	P53	Homo sapiens	133-136
19639181-3	2009	In this study which uses lung cancer as the model, we demonstrate that the improvement of radiotherapy by 2-deoxy-D-glucose (2DG) is p53-dependent.	Deoxyglucose	125-128	P53	Homo sapiens	133-136
19639181-4	2009	Based on clonogenic survival data, we show that p53-deficient lung cancer cells (H358) are more sensitive to 2DG treatment when compared to p53 wild-type lung cancer cells (A549).	Deoxyglucose	109-112	P53	Homo sapiens	48-51
19639181-7	2009	Treatment with 2DG increases radiation-induced p53 protein levels in A549 cells.	Deoxyglucose	15-18	P53	Homo sapiens	47-50
19639181-8	2009	siRNA inhibition of p53 in A549 cells reduces the radiosensitization effect of 2DG.	Deoxyglucose	79-82	P53	Homo sapiens	20-23
18930016-0	2008	4-Hydroxynonenal induces p53-mediated apoptosis in retinal pigment epithelial cells.	4-hydroxy-2-nonenal	0-16	P53	Homo sapiens	25-28
19639181-9	2009	Furthermore, ectopic expression of wild-type p53 in H358 cells significantly enhances the radiosensitization effect of 2DG as determined by colony formation assay.	Deoxyglucose	119-122	P53	Homo sapiens	45-48
18930016-3	2008	Our results show that 4-HNE causes induction, phosphorylation, and nuclear accumulation of p53 which is accompanied with down regulation of MDM2, activation of the pro-apoptotic p53 target genes viz.	4-hydroxy-2-nonenal	22-27	P53	Homo sapiens	91-94
31102418-6	2019	Higher levels of 1-HMP-induced DNA adducts in TP53(+/+) cells correlated with higher basal expression of SULT1A1/3 in this cell line, but 1-HMP treatment showed no effect on the expression of this protein.	1-hydroxymethylpyrene	17-22	P53	Homo sapiens	46-50
18930016-3	2008	Our results show that 4-HNE causes induction, phosphorylation, and nuclear accumulation of p53 which is accompanied with down regulation of MDM2, activation of the pro-apoptotic p53 target genes viz.	4-hydroxy-2-nonenal	22-27	P53	Homo sapiens	178-181
31607305-6	2019	RESULTS: Compared with patients without P53 expression, the patients with P53 expression had higher LDH level, higher NCCN-IPI scores, lower response to chemotherapy,poorer overall survival(OS) and a higher rate of death(P<0.05).	diprotin A	123-126	P53	Homo sapiens	74-77
18798266-3	2008	TE/E6 cell lines exhibiting low levels of p53 and undetectable levels of p21(WAF1/CIP1) were sensitized to the growth inhibiting and apoptotic effects of OSU03012.	OSU 03012	154-162	P53	Homo sapiens	42-45
18798266-5	2008	OSU03012 reduced the number of cells in the S phase of the TE/E7 and TE/V cell lines with intact p53-p21(WAF1/CIP1) checkpoint, but not in the checkpoint defective TE/E6 cell lines.	OSU 03012	0-8	P53	Homo sapiens	97-100
19668191-7	2009	Furthermore, in the p53-null background, iPS cells were generated from terminally differentiated T lymphocytes.	IPS	41-44	P53	Homo sapiens	20-23
19706164-0	2009	Enhanced sensitivity of celecoxib in human glioblastoma cells: Induction of DNA damage leading to p53-dependent G1 cell cycle arrest and autophagy.	Celecoxib	24-33	P53	Homo sapiens	98-101
30879173-6	2019	The cytotoxicity of RH1 was inhibited in A549 cells treated with the p53-inhibitor pifithrin-alpha or transfected p53 siRNA and in human colon cancer HCT116 isogenic (p53-/-) cells.	2,5-diaziridinyl-3-(hydroxymethyl)-6-methyl-1,4-benzoquinone	20-23	P53	Homo sapiens	69-72
19706164-6	2009	We investigated whether the anti-glioblastoma responses of celecoxib were p53-dependent, and whether celecoxib induced DNA damage leading to p53-dependent G1 cell cycle arrest, followed by autophagy or apoptosis.	Celecoxib	101-110	P53	Homo sapiens	141-144
19706164-8	2009	Inhibition of functional p53 in glioblastoma cells significantly reduced the anti-proliferative effect of celecoxib.	Celecoxib	106-115	P53	Homo sapiens	25-28
19706164-9	2009	In U87MG cells, celecoxib (8 and 30 muM) significantly induced DNA damage and inhibited DNA synthesis, corresponding with p53 activation.	Celecoxib	16-25	P53	Homo sapiens	122-125
19706164-16	2009	CONCLUSION: Our findings reveal that p53 increases human glioblastoma sensitivity to celecoxib.	Celecoxib	85-94	P53	Homo sapiens	37-40
19706164-17	2009	Celecoxib inhibits glioblastoma cell viability by induction of DNA damage, leading to p53-dependent G1 cell cycle arrest and p53-dependent autophagy, but not apoptosis.	Celecoxib	0-9	P53	Homo sapiens	86-89
19706164-17	2009	Celecoxib inhibits glioblastoma cell viability by induction of DNA damage, leading to p53-dependent G1 cell cycle arrest and p53-dependent autophagy, but not apoptosis.	Celecoxib	0-9	P53	Homo sapiens	125-128
30879173-6	2019	The cytotoxicity of RH1 was inhibited in A549 cells treated with the p53-inhibitor pifithrin-alpha or transfected p53 siRNA and in human colon cancer HCT116 isogenic (p53-/-) cells.	2,5-diaziridinyl-3-(hydroxymethyl)-6-methyl-1,4-benzoquinone	20-23	P53	Homo sapiens	114-117
31632492-7	2019	Rsv enhanced the sensitivity of K562/RA cells to ATO and reduced the required dose of ATO as well as associated adverse reactions by promoting the proliferation inhibitory and apoptosis-inducing effects of ATO, which may be associated with reduced expression of the drug resistance genes mdr1/P-gp, mrp1/MRP1 and bcrp/BCRP, as well as the apoptotic inhibitory genes bcl-2, NF-kappaB and P53, and conversely, activation of caspase-3.	resveratrol	0-3	P53	Homo sapiens	387-390
19473450-10	2009	One TP53-mutated OLP patient developed OSCC in a different site.	oscc	39-43	P53	Homo sapiens	4-8
31497354-5	2019	GSI sensitivity exhibited remarkable selectivity among wild-type TP53 (wt-p53) GSCs.	2-(5-Chlorothiophen-2-Yl)-N-[(3s)-1-(4-{2-[(Dimethylamino)methyl]-1h-Imidazol-1-Yl}-2-Fluorophenyl)-2-Oxopyrrolidin-3-Yl]ethanesulfonamide	0-3	P53	Homo sapiens	65-69
19428812-0	2009	Ammonia-induced activation of p53 in cultured astrocytes: role in cell swelling and glutamate uptake.	Ammonia	0-7	P53	Homo sapiens	30-33
19428812-3	2009	As p53, a tumor suppressor protein and transcription factor, is a downstream target of ONS and MAPKs, we examined its potential role in the mechanism of ammonia-induced astrocyte swelling.	Ammonia	153-160	P53	Homo sapiens	3-6
19428812-8	2009	We therefore examined the potential role of p53 in the ammonia-induced inhibition of glutamate uptake and found that PFT also reversed the ammonia-induced inhibition of glutamate uptake.	Ammonia	55-62	P53	Homo sapiens	44-47
19428812-9	2009	Our results indicate that a potentially important downstream target of ammonia neurotoxicity is p53, whose activation contributes to astrocyte swelling and glutamate uptake inhibition, processes likely a consequence of ONS derived from the mPT and activation of NF-kappaB.	Ammonia	71-78	P53	Homo sapiens	96-99
31497354-5	2019	GSI sensitivity exhibited remarkable selectivity among wild-type TP53 (wt-p53) GSCs.	2-(5-Chlorothiophen-2-Yl)-N-[(3s)-1-(4-{2-[(Dimethylamino)methyl]-1h-Imidazol-1-Yl}-2-Fluorophenyl)-2-Oxopyrrolidin-3-Yl]ethanesulfonamide	0-3	P53	Homo sapiens	74-77
31497354-10	2019	Taken together, we identified wt-p53 as a potential marker for GSI sensitivity in GSCs.	2-(5-Chlorothiophen-2-Yl)-N-[(3s)-1-(4-{2-[(Dimethylamino)methyl]-1h-Imidazol-1-Yl}-2-Fluorophenyl)-2-Oxopyrrolidin-3-Yl]ethanesulfonamide	63-66	P53	Homo sapiens	33-36
30601067-0	2019	Anticancer activity of polyphyllin I in nasopharyngeal carcinoma by modulation of lncRNA ROR and P53 signalling.	polyphyllin I	23-36	P53	Homo sapiens	97-100
19407340-7	2009	However, down-regulation of p53, a target of lithium in EC, dampens both basal and lithium-induced MMP-1 expression, which further links MMP-1 up-regulation with the establishment of cell senescence.	Lithium	45-52	P53	Homo sapiens	28-31
19407340-7	2009	However, down-regulation of p53, a target of lithium in EC, dampens both basal and lithium-induced MMP-1 expression, which further links MMP-1 up-regulation with the establishment of cell senescence.	Lithium	83-90	P53	Homo sapiens	28-31
19558663-1	2009	BACKGROUND: Ser-249 TP53 mutation (249(Ser)) is a molecular evidence for aflatoxin-related carcinogenesis in Hepatocellular Carcinoma (HCC) and it is frequent in some African and Asian regions, but it is unusual in Western countries.	Aflatoxins	73-82	P53	Homo sapiens	20-24
19267931-6	2009	Moderate hypoxia decreased p21 synthesis without affecting p53 synthesis, whereas severe hypoxia and DFX increased synthesis of both p21 and p53.	Deferoxamine	101-104	P53	Homo sapiens	141-144
19267931-9	2009	p21 and p53 gene silencing lessened the decrease in DNA synthesis due to severe hypoxia or DFX exposure.	Deferoxamine	91-94	P53	Homo sapiens	8-11
30601067-6	2019	LncRNA ROR/P53 signalling was essential for PP I-suppressed NPC progression.	polyphyllin I	44-48	P53	Homo sapiens	11-14
30601067-7	2019	These data indicated that PP I suppressed tumour growth and induced apoptosis of NPC in vitro and in vivo through down-regulation of lncRNA-ROR, subsequently upregulating of P53 signalling.	polyphyllin I	26-30	P53	Homo sapiens	174-177
31134974-4	2019	The p53-MDM2 complex was captured in one fluidic channel covered with consensus double-stranded (ds)-DNA, while the other channel was pre-immobilized with caspase-3-specific biotinylated DEVD-containing peptides.	Peptides	203-211	P53	Homo sapiens	4-7
19250610-5	2009	The apoptotic effect of ar-turmerone was associated with the induction of Bax and p53 proteins, rather than Bcl-2 and p21.	ar-turmerone	24-36	P53	Homo sapiens	82-85
19137017-8	2009	In the Mapo1-defective mutant cells treated with MNU, the mitochondrial membrane depolarization and caspase-3 activation were severely suppressed, although phosphorylation of p53, CHK1 and histone H2AX was observed.	Methylnitrosourea	49-52	P53	Homo sapiens	175-178
30928633-5	2019	Mechanistically, 8-AHN induced p53 expression and enhanced transcriptional activity, subsequently elevating the expression of p53 target genes, including p21, FAS, and BAX, and then increased the level of activated caspase-3 and decreased the level of cyclin B and cyclin A.	8-acetonyldihydronitidine	17-22	P53	Homo sapiens	31-34
19059205-3	2009	In this work, DU-145 cells were used to demonstrate that SPBE and its sterol components, beta-sitosterol and stigmasterol, inhibit prostate cancer growth by increasing p53 protein expression and also inhibit carcinoma development by decreasing p21 and p27 protein expression.	gamma-sitosterol	89-104	P53	Homo sapiens	168-171
30928633-5	2019	Mechanistically, 8-AHN induced p53 expression and enhanced transcriptional activity, subsequently elevating the expression of p53 target genes, including p21, FAS, and BAX, and then increased the level of activated caspase-3 and decreased the level of cyclin B and cyclin A.	8-acetonyldihydronitidine	17-22	P53	Homo sapiens	126-129
19116135-4	2009	Pieper, p53 effects both the duration of G2/M arrest and the fate of temozolomide-treated human glioblastoma cells, Cancer Res.	Temozolomide	69-81	P53	Homo sapiens	8-11
30928633-6	2019	Moreover, pifithrin-alpha, the p53 inhibitor, markedly reversed the above responses induced by 8-AHN, and small interfering RNA-mediated knockdown of TP53 also significantly decreased 8-AHN-induced cell apoptosis.	8-acetonyldihydronitidine	95-100	P53	Homo sapiens	31-34
30928633-6	2019	Moreover, pifithrin-alpha, the p53 inhibitor, markedly reversed the above responses induced by 8-AHN, and small interfering RNA-mediated knockdown of TP53 also significantly decreased 8-AHN-induced cell apoptosis.	8-acetonyldihydronitidine	184-189	P53	Homo sapiens	150-154
30928633-8	2019	In summary, 8-AHN displays an antitumor effect through cell cycle arrest and apoptosis in colorectal cells via activating p53, which suggests that 8-AHN, exerted a therapeutic potential against colorectal cancer cells, and may be regarded as an effective lead compound.	8-acetonyldihydronitidine	12-17	P53	Homo sapiens	122-125
19027820-0	2009	Cyclin A is essential for the p53-modulated inhibition from benzo(a)pyrene toxicity in A549 cells.	Benzo(a)pyrene	60-74	P53	Homo sapiens	30-33
30928633-8	2019	In summary, 8-AHN displays an antitumor effect through cell cycle arrest and apoptosis in colorectal cells via activating p53, which suggests that 8-AHN, exerted a therapeutic potential against colorectal cancer cells, and may be regarded as an effective lead compound.	8-acetonyldihydronitidine	147-152	P53	Homo sapiens	122-125
19027820-8	2009	These results indicated that cyclin A is regulated by p53, not by B(a)P, and it is essential in the p53-modulated inhibition from benzo(a)pyrene toxicity in A549 cells, cyclin E and p21 also as downstream genes of p53 involved it, which is p27-independent.	Benzo(a)pyrene	130-144	P53	Homo sapiens	100-103
19027820-8	2009	These results indicated that cyclin A is regulated by p53, not by B(a)P, and it is essential in the p53-modulated inhibition from benzo(a)pyrene toxicity in A549 cells, cyclin E and p21 also as downstream genes of p53 involved it, which is p27-independent.	Benzo(a)pyrene	130-144	P53	Homo sapiens	100-103
31945889-5	2019	As results, we found a significant correlation of purine metabolism and p53 signaling pathway role in colorectal cancer progression.	Purines	50-56	P53	Homo sapiens	72-75
19280465-6	2009	The cell line LN229 was more sensitive to TMZ treatment than the U87MG cell line expressing wild-type p53 only.	Temozolomide	42-45	P53	Homo sapiens	102-105
18938143-6	2009	GSK-3 inhibitors also stabilized p53 and the down-regulation of p53 by RNA interference abolished the sensitizing effect of lithium on caspase-3 activation.	Lithium	124-131	P53	Homo sapiens	64-67
31026379-9	2019	Moreover, vildagliptin suppresses the three major TNF-alpha-induced chondrocyte senescence proteins including p53, p21, and plasminogen activator inhibitor-1 (PAI-1).	Vildagliptin	10-22	P53	Homo sapiens	110-113
31026379-10	2019	Vildagliptin also suppresses TNF-alpha-induced p53 acetylation at K382.	Vildagliptin	0-12	P53	Homo sapiens	47-50
31026379-11	2019	Consistently, our findings demonstrate the inhibitory effect of vildagliptin on p53 acetylation, which is mediated by sirtuin 1 (SIRT1) as the inhibition of SIRT1 negated the inhibitory action of vildagliptin on p53 acetylation.	Vildagliptin	64-76	P53	Homo sapiens	80-83
31128995-0	2019	Inotodiol inhibits cells migration and invasion and induces apoptosis via p53-dependent pathway in HeLa cells.	inotodiol	0-9	P53	Homo sapiens	74-77
19117505-5	2008	Possible CIMP tumors were identified by comparing the methylation profile with microsatellite instability (MSI), BRAF-, KRAS-, and TP53 mutation status.	Cyclic IMP	9-13	P53	Homo sapiens	131-135
31128995-3	2019	PURPOSE: The aim of the present study was to investigate the effect of Inotodiol on HeLa cell migration, invasion and apoptosis through p53-dependent pathway.	inotodiol	71-80	P53	Homo sapiens	136-139
19031317-2	2008	Previous treatment of H4 cells with DHEA for 18 h reduced the gamma-ray-induced phosphorylation of Akt, activated p21(waf1) synthesis and up-regulated phosphorylation of Rb independent of p53.	Dehydroepiandrosterone	36-40	P53	Homo sapiens	188-191
31128995-10	2019	Finally, the anti-tumor activity of Inotodiol was attenuated by silencing p53 tumor suppressor, the result revealed that pre-treatment with p53-specific small interfering RNA (si-p53) markedly inhibited Intodiol-indeuced HeLa cell apoptosis and decreased the caspase-3 activity.	inotodiol	36-45	P53	Homo sapiens	74-77
31128995-10	2019	Finally, the anti-tumor activity of Inotodiol was attenuated by silencing p53 tumor suppressor, the result revealed that pre-treatment with p53-specific small interfering RNA (si-p53) markedly inhibited Intodiol-indeuced HeLa cell apoptosis and decreased the caspase-3 activity.	inotodiol	36-45	P53	Homo sapiens	140-143
18718914-0	2008	15-deoxy-Delta(12,14)-prostaglandin J2 induces vascular endothelial cell apoptosis through the sequential activation of MAPKS and p53.	15-deoxy-delta(12,14)-prostaglandin J2	0-38	P53	Homo sapiens	130-133
18718914-3	2008	Both 15d-PGJ(2)-induced apoptosis and the induction of p21(Waf1) and Bax can be abolished by p53 small interfering RNA but not by peroxisome proliferator-activated receptor gamma inhibitors.	-pgj	8-12	P53	Homo sapiens	93-96
31128995-10	2019	Finally, the anti-tumor activity of Inotodiol was attenuated by silencing p53 tumor suppressor, the result revealed that pre-treatment with p53-specific small interfering RNA (si-p53) markedly inhibited Intodiol-indeuced HeLa cell apoptosis and decreased the caspase-3 activity.	inotodiol	36-45	P53	Homo sapiens	140-143
31128995-11	2019	What is more, the inhibitory effect of Inotodiol on tumor migration and invasion was blocked under p53 knockdown.	inotodiol	39-48	P53	Homo sapiens	99-102
30536898-3	2019	This is the first study to evaluate the in vivo efficacy of the intravenous idasanutlin prodrug, RO6839921 (RG7775), both alone and in combination with temozolomide in TP53 wt orthotopic neuroblastoma models.	ro6839921	97-106	P53	Homo sapiens	168-172
18760266-0	2008	Celecoxib induces p53-PUMA pathway for apoptosis in human colorectal cancer cells.	Celecoxib	0-9	P53	Homo sapiens	18-21
18760266-2	2008	The existence of functional p53 but not securin in colorectal cancer cells was higher on the induction of cytotoxicity than the p53-mutational colorectal cancer cells following celecoxib treatment.	Celecoxib	177-186	P53	Homo sapiens	28-31
18760266-2	2008	The existence of functional p53 but not securin in colorectal cancer cells was higher on the induction of cytotoxicity than the p53-mutational colorectal cancer cells following celecoxib treatment.	Celecoxib	177-186	P53	Homo sapiens	128-131
30536898-3	2019	This is the first study to evaluate the in vivo efficacy of the intravenous idasanutlin prodrug, RO6839921 (RG7775), both alone and in combination with temozolomide in TP53 wt orthotopic neuroblastoma models.	rg7775	108-114	P53	Homo sapiens	168-172
30536898-3	2019	This is the first study to evaluate the in vivo efficacy of the intravenous idasanutlin prodrug, RO6839921 (RG7775), both alone and in combination with temozolomide in TP53 wt orthotopic neuroblastoma models.	Temozolomide	152-164	P53	Homo sapiens	168-172
18811869-5	2008	TL01 therapy induced a threefold increase in the number of p53-positive epidermal cells, a 12-fold increase in sunburn cells and a twofold decrease in Langerhans cells.	tl01	0-4	P53	Homo sapiens	59-62
30755439-7	2019	Alisertib caused spindle defects, G2-M arrest and inhibitory CDK1 phosphorylation, and cytostasis in TP53 mutant HNSCC FaDu and UNC7 cells.	MLN 8237	0-9	P53	Homo sapiens	101-105
18811869-6	2008	The increase in epidermal p53 expression and apoptosis of keratinocytes together with the depletion of Langerhans cells in the non-lesional skin of psoriasis patients are likely to contribute to the effectiveness of TL01 phototherapy.	tl01	216-220	P53	Homo sapiens	26-29
18494939-6	2008	By immunoprecipitation assay, we also investigated whether 4-hydroxy-2-transnonenal (HNE), an aldehydic product of lipid peroxidation, was bound in excess to p53 in IPL from subjects with MCI and AD compared to control.	4-hydroxy-2-nonenal	59-83	P53	Homo sapiens	158-161
18400537-5	2008	In both Molt-4 LXSN leukemia cells exposed to gamma-irradiation and in EB-1 colon cancer cells treated with ZnCl(2), p53 up-regulation led to de novo ceramide synthesis with predominance of N-palmitoylsphingosine (C16-ceramide) synthesis.	zncl	108-112	P53	Homo sapiens	117-120
31081046-0	2019	Targeted therapy based on p53 reactivation reduces both glioblastoma cell growth and resistance to temozolomide.	Temozolomide	99-111	P53	Homo sapiens	26-29
18440733-0	2008	Benzo(a)pyrene increases phosphorylation of p53 at serine 392 in relation to p53 induction and cell death in MCF-7 cells.	Benzo(a)pyrene	0-14	P53	Homo sapiens	44-47
18440733-0	2008	Benzo(a)pyrene increases phosphorylation of p53 at serine 392 in relation to p53 induction and cell death in MCF-7 cells.	Benzo(a)pyrene	0-14	P53	Homo sapiens	77-80
31081046-3	2019	Considering that alterations of the p53 tumor suppressor pathway have a key role in both GB development and resistance to TMZ treatment, the re-activation of p53 could be an effective therapeutic approach against GB.	Temozolomide	122-125	P53	Homo sapiens	36-39
18440733-10	2008	These results suggest that serine 392 phosphorylation is the first stabilizing event of p53 associated with BP exposure and subsequent cell death in MCF-7 cells.	Benzo(a)pyrene	108-110	P53	Homo sapiens	88-91
31081046-3	2019	Considering that alterations of the p53 tumor suppressor pathway have a key role in both GB development and resistance to TMZ treatment, the re-activation of p53 could be an effective therapeutic approach against GB.	Temozolomide	122-125	P53	Homo sapiens	158-161
18084327-3	2008	When p53(wt) HCT116 and A549 cells were pretreated with AZD1152-HQPA prior to IR, additive effects were observed.	AZD 1152-HQPA	56-68	P53	Homo sapiens	5-8
31121972-2	2019	The xanthone 5 was used as a starting point for the construction of a library of 3,4-dioxygenated xanthones bearing chemical moieties of described MDM2-p53 inhibitors.	xanthone	4-12	P53	Homo sapiens	152-155
18215142-0	2008	The 7-amino-acid site in the proline-rich region of the N-terminal domain of p53 is involved in the interaction with FAK and is critical for p53 functioning.	7-amino-acid	4-16	P53	Homo sapiens	77-80
18215142-0	2008	The 7-amino-acid site in the proline-rich region of the N-terminal domain of p53 is involved in the interaction with FAK and is critical for p53 functioning.	7-amino-acid	4-16	P53	Homo sapiens	141-144
19056673-10	2008	Using either MGMT small interfering RNA, p53 small interfering RNA, or a p53 dominant-negative mutant to block MGMT protein expression resulted in increased sensitization to temozolomide.	Temozolomide	174-186	P53	Homo sapiens	41-44
19056673-10	2008	Using either MGMT small interfering RNA, p53 small interfering RNA, or a p53 dominant-negative mutant to block MGMT protein expression resulted in increased sensitization to temozolomide.	Temozolomide	174-186	P53	Homo sapiens	73-76
31121972-4	2019	With this approach, xanthone 37 was identified as a putative p53-activating agent through inhibition of interaction with MDM2.	xanthone	20-28	P53	Homo sapiens	61-64
18760266-3	2008	The p53-wild type HCT116 cells were more susceptible to increase approximately 25% cell death than the p53-null HCT116 cells after treatment with 100 microM celecoxib for 24 h. Transfection with a small interfering RNA of p53 reduced the celecoxib-induced cytotoxicity in the RKO (p53-wild type) colorectal cancer cells.	Celecoxib	157-166	P53	Homo sapiens	4-7
18760266-3	2008	The p53-wild type HCT116 cells were more susceptible to increase approximately 25% cell death than the p53-null HCT116 cells after treatment with 100 microM celecoxib for 24 h. Transfection with a small interfering RNA of p53 reduced the celecoxib-induced cytotoxicity in the RKO (p53-wild type) colorectal cancer cells.	Celecoxib	157-166	P53	Homo sapiens	103-106
18381438-0	2008	The cyclin-dependent kinase inhibitor flavopiridol potentiates the effects of topoisomerase I poisons by suppressing Rad51 expression in a p53-dependent manner.	alvocidib	38-50	P53	Homo sapiens	139-142
31121972-5	2019	Xanthone 37 inhibited the growth of human colon adenocarcinoma HCT116 cell lines in a p53-dependent manner.	xanthone	0-8	P53	Homo sapiens	86-89
18760266-3	2008	The p53-wild type HCT116 cells were more susceptible to increase approximately 25% cell death than the p53-null HCT116 cells after treatment with 100 microM celecoxib for 24 h. Transfection with a small interfering RNA of p53 reduced the celecoxib-induced cytotoxicity in the RKO (p53-wild type) colorectal cancer cells.	Celecoxib	157-166	P53	Homo sapiens	103-106
18760266-3	2008	The p53-wild type HCT116 cells were more susceptible to increase approximately 25% cell death than the p53-null HCT116 cells after treatment with 100 microM celecoxib for 24 h. Transfection with a small interfering RNA of p53 reduced the celecoxib-induced cytotoxicity in the RKO (p53-wild type) colorectal cancer cells.	Celecoxib	157-166	P53	Homo sapiens	103-106
31121972-6	2019	The growth inhibitory effect of xanthone 37 was associated with the induction of G1-phase cell cycle arrest and increased protein expression levels of p53 transcriptional targets.	xanthone	32-40	P53	Homo sapiens	151-154
18760266-3	2008	The p53-wild type HCT116 cells were more susceptible to increase approximately 25% cell death than the p53-null HCT116 cells after treatment with 100 microM celecoxib for 24 h. Transfection with a small interfering RNA of p53 reduced the celecoxib-induced cytotoxicity in the RKO (p53-wild type) colorectal cancer cells.	Celecoxib	238-247	P53	Homo sapiens	4-7
18760266-4	2008	Celecoxib (80-100 microM for 24 h) significantly increased total p53 proteins and the phosphorylated p53 proteins at serine-15, -20, -46, and -392 in RKO cells.	Celecoxib	0-9	P53	Homo sapiens	65-68
17932951-0	2008	Anti-diol epoxide of benzo[a]pyrene induces transient Mdm2 and p53 Ser15 phosphorylation, while anti-diol epoxide of dibenzo[a,l]pyrene induces a nontransient p53 Ser15 phosphorylation.	Benzo(a)pyrene	21-35	P53	Homo sapiens	63-66
17932951-0	2008	Anti-diol epoxide of benzo[a]pyrene induces transient Mdm2 and p53 Ser15 phosphorylation, while anti-diol epoxide of dibenzo[a,l]pyrene induces a nontransient p53 Ser15 phosphorylation.	dibenzo(a,l)pyrene	117-135	P53	Homo sapiens	159-162
18760266-4	2008	Celecoxib (80-100 microM for 24 h) significantly increased total p53 proteins and the phosphorylated p53 proteins at serine-15, -20, -46, and -392 in RKO cells.	Celecoxib	0-9	P53	Homo sapiens	101-104
31121972-7	2019	These results demonstrated the potential usefulness of coupling amine-containing structural motifs of known MDM2-p53 disruptors into a 3,4-dioxygenated xanthone scaffold in the design of novel and potent p53 activators with antitumor activity and favorable drug-like properties.	xanthone	152-160	P53	Homo sapiens	204-207
18760266-6	2008	Interestingly, the p53 up-regulated modulator of apoptosis (PUMA) protein, which located on the mitochondria, was induced by celecoxib in the p53-functional colorectal cancer cells but not in the p53-mutational cells.	Celecoxib	125-134	P53	Homo sapiens	19-22
18760266-6	2008	Interestingly, the p53 up-regulated modulator of apoptosis (PUMA) protein, which located on the mitochondria, was induced by celecoxib in the p53-functional colorectal cancer cells but not in the p53-mutational cells.	Celecoxib	125-134	P53	Homo sapiens	142-145
30940658-0	2019	Temozolomide Treatment Induces lncRNA MALAT1 in an NF-kappaB and p53 Codependent Manner in Glioblastoma.	Temozolomide	0-12	P53	Homo sapiens	65-68
18760266-6	2008	Interestingly, the p53 up-regulated modulator of apoptosis (PUMA) protein, which located on the mitochondria, was induced by celecoxib in the p53-functional colorectal cancer cells but not in the p53-mutational cells.	Celecoxib	125-134	P53	Homo sapiens	142-145
18760266-7	2008	Together, this study provides the first time that celecoxib induces the various phosphorylated sites of p53 and activates p53-PUMA pathway, which potentiates the apoptosis induction in human colorectal cancer cells.	Celecoxib	50-59	P53	Homo sapiens	104-107
18760266-7	2008	Together, this study provides the first time that celecoxib induces the various phosphorylated sites of p53 and activates p53-PUMA pathway, which potentiates the apoptosis induction in human colorectal cancer cells.	Celecoxib	50-59	P53	Homo sapiens	122-125
18096571-7	2008	The more mutagenic dibenzo[a,l]pyrene as well as higher BP concentrations instead induced gammaH2AX and p53 Ser15 association with chromatin.	dibenzo(a,l)pyrene	19-37	P53	Homo sapiens	104-107
18096571-7	2008	The more mutagenic dibenzo[a,l]pyrene as well as higher BP concentrations instead induced gammaH2AX and p53 Ser15 association with chromatin.	Benzo(a)pyrene	56-58	P53	Homo sapiens	104-107
18096571-8	2008	Acrolein potentiated the effect of BP on p53 stabilization and chromatin binding.	Benzo(a)pyrene	35-37	P53	Homo sapiens	41-44
18838865-3	2008	Here, we show by epistatic analysis that p53 inhibition results in a maximum level of autophagy that cannot be further enhanced by a variety of different autophagy inducers including lithium, tunicamycin-induced stress of the endoplasmic reticulum (ER) or inhibition of Bcl-2 and Bcl-X(L) with the BH3 mimetic ABT737.	Lithium	183-190	P53	Homo sapiens	41-44
30940658-5	2019	Temozolomide treatment inhibited p50 recruitment to its cognate element as a function of Ser329 phosphorylation while concomitantly increasing p53 recruitment.	Temozolomide	0-12	P53	Homo sapiens	143-146
18838865-3	2008	Here, we show by epistatic analysis that p53 inhibition results in a maximum level of autophagy that cannot be further enhanced by a variety of different autophagy inducers including lithium, tunicamycin-induced stress of the endoplasmic reticulum (ER) or inhibition of Bcl-2 and Bcl-X(L) with the BH3 mimetic ABT737.	BH 3	298-301	P53	Homo sapiens	41-44
18838865-4	2008	Chemical inducers of autophagy (including rapamycin, lithium, tunicamycin and ABT737) induced rapid depletion of the p53 protein.	Lithium	53-60	P53	Homo sapiens	117-120
18724895-0	2008	[mRNA expression levels of p53 and DNA damage and repair genes in peripheral blood lymphocytes of benzene-exposed workers].	Benzene	98-105	P53	Homo sapiens	27-30
18724895-1	2008	OBJECTIVE: To investigate the relationship between the mRNA expression levels of p53-mediating DNA damage and repair genes in the peripheral blood lymphocytes of workers and their exposures to benzene in their working environment.	Benzene	193-200	P53	Homo sapiens	81-84
18724895-10	2008	CONCLUSION: The mRNA expression levels of some p53-mediating DNA damage and repair genes are downregulated in the workers chronically exposed to low benzene concentration.	Benzene	149-156	P53	Homo sapiens	47-50
30940658-6	2019	Moreover, luciferase reporter studies demonstrated that both kappaB and p53 cis-elements were required for efficient transactivation in response to temozolomide.	Temozolomide	148-160	P53	Homo sapiens	72-75
18547833-7	2008	The secondary objective was to investigate the association between clinical examination using acetic acid and expression of the tumor marker, p53.	Acetic Acid	94-105	P53	Homo sapiens	142-145
18547833-12	2008	There was a statistically significant association between clinical examination using acetic acid and expression of p53 protein (P = .000).	Acetic Acid	85-96	P53	Homo sapiens	115-118
30842083-6	2019	The PFS benefit with ibrutinib was independent of baseline risk factors, although patients with >=2 prior therapies had shorter PFS than those with <2 prior therapies, and the presence of TP53 or SF3B1 mutations showed a trend toward shorter PFS vs without these factors.	ibrutinib	21-30	P53	Homo sapiens	188-192
18604159-6	2008	Several distinct autophagy inducers (e.g., starvation, rapamycin, lithium, tunicamycin and thapsigargin) stimulate the rapid degradation of p53.	Lithium	66-73	P53	Homo sapiens	140-143
18221455-4	2008	The carcinomas, and the UVB signature mutations that they carry in their p53 genes, can be linked most specifically to the induction of cyclobutane pyrimidine dimers (CPDs).	cyclobutane pyrimidine	136-158	P53	Homo sapiens	73-76
18042465-4	2008	In addition, the blockage of HO activity with the iron chelator DFO or with HO-1 siRNA inhibited the CoPP-induced expression of p53.	Deferoxamine	64-67	P53	Homo sapiens	128-131
30730256-5	2019	Signaling data revealed that the activation of ERK1/2, rather than p53, is recruited for 6-MSITC-induced apoptosis.	6-(Methylsulfinyl)hexyl isothiocyanate	89-96	P53	Homo sapiens	67-70
17942461-0	2008	Identification through microarray gene expression analysis of cellular responses to benzo(a)pyrene and its diol-epoxide that are dependent or independent of p53.	Benzo(a)pyrene	84-98	P53	Homo sapiens	157-160
18097607-0	2008	Diallyl disulfide induces reversible G2/M phase arrest on a p53-independent mechanism in human colon cancer HCT-116 cells.	diallyl disulfide	0-17	P53	Homo sapiens	60-63
18640498-0	2008	Flavopiridol potentiates the cytotoxic effects of radiation in radioresistant tumor cells in which p53 is mutated or Bcl-2 is overexpressed.	alvocidib	0-12	P53	Homo sapiens	99-102
18640498-3	2008	The purpose of the present study is to clarify whether flavopiridol enhances the cytotoxic effects of radiation in tumor cells that contain dysfunction p53 or that overexpress Bcl-2.	alvocidib	55-67	P53	Homo sapiens	152-155
18640498-10	2008	CONCLUSIONS: Flavopiridol enhanced the cytotoxic effect of radiation in radioresistant tumor cells that harbor p53 dysfunction or Bcl-2 overexpression.	alvocidib	13-25	P53	Homo sapiens	111-114
18640498-11	2008	A combination treatment of flavopiridol with radiation has the potential to conquer the radioresistance of malignant tumors induced by the genetic alteration of p53 or bcl-2.	alvocidib	27-39	P53	Homo sapiens	161-164
18097607-6	2008	DADS also significantly induced the expression of p53, which contributes to cell cycle arrest in cancer cells, at a late time-point of 24 h. In addition, knockdown of p53 by siRNA did not affect cell cycle arrest, its reversibility, or the expression of cyclin B1 in the G2/M phase induced by DADS.	diallyl disulfide	0-4	P53	Homo sapiens	50-53
30942456-1	2019	The Na+/K+-ATPase inhibitor cinobufagin exhibits numerous anticancer effects on hepatocellular carcinoma (HCC) cells expressing wild-type p53 via inhibition of aurora kinase A (AURKA) and activation of p53 signaling.	cinobufagin	28-39	P53	Homo sapiens	138-141
17717041-0	2007	Synergy between docosahexaenoic acid and butyrate elicits p53-independent apoptosis via mitochondrial Ca(2+) accumulation in colonocytes.	Docosahexaenoic Acids	16-36	P53	Homo sapiens	58-61
18632630-3	2008	Treatment of cells that express the mutated receptor variants with the Met inhibitor SU11274 leads, in a mutant-dependent manner, to a reduction of tyrosine phosphorylated levels of Abl and Rad51, impairs radiation-induced nuclear translocation of Rad51, and acts as a radiosensitizer together with the p53 inhibitor pifithrin-alpha by increasing cellular double-strand DNA break levels following exposure to ionizing radiation.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	85-92	P53	Homo sapiens	303-306
17717041-11	2007	On the basis of these data, we propose that the combination of DHA and butyrate compared with butyrate alone further enhances colonocyte apoptosis by inducing a p53-independent, oxidation-sensitive, mitochondrial Ca(2+) -dependent (intrinsic) pathway.	Docosahexaenoic Acids	63-66	P53	Homo sapiens	161-164
30942456-1	2019	The Na+/K+-ATPase inhibitor cinobufagin exhibits numerous anticancer effects on hepatocellular carcinoma (HCC) cells expressing wild-type p53 via inhibition of aurora kinase A (AURKA) and activation of p53 signaling.	cinobufagin	28-39	P53	Homo sapiens	202-205
18428185-2	2008	Herein we report the design and characterisation of a new class of isoquinolinone inhibitors of the MDM2-p53 interaction.	1-Hydroxyisoquinoline	67-81	P53	Homo sapiens	105-108
30942456-8	2019	These results indicated that cinobufagin may induce anticancer effects on Huh-7 cells via the inhibition of AURKA and p53 signaling, and via the activation of p73 signaling, in an AURKA-dependent manner.	cinobufagin	29-40	P53	Homo sapiens	118-121
30817944-5	2019	The sensitizing effect of AC to TRAIL was well correlated with inhibition of death receptor 5 (DR5) CHOP, and p53 expression.	auriculasin	26-28	P53	Homo sapiens	110-113
18223691-9	2008	Inhibition of p53 transactivation by pifithrin-alpha or the kinase activity of ATM by either the specific ATM inhibitor KU-5593 or caffeine abrogated p21(WAF1/CIP1) upregulation, indicating that DAC upregulation of p21(WAF1/CIP1) was p53- and ATM-dependent in leukemia cells.	ku-5593	120-127	P53	Homo sapiens	14-17
17978477-5	2007	The expression of Bid, Bax, or p53 proteins have been shown to increase correlated with the acquisition of Ara-C resistance.	Cytarabine	107-112	P53	Homo sapiens	31-34
17678638-7	2007	Further studies using 1,2-dihydroxy-1,2-dihydro-6-hydroxylaminochrysene (1,2-DHD-6-NHOH-C), the putative ultimate genotoxic metabolite of 6-NC, was conducted and showed a significant induction of p53 (p&lt;0.05) in MCF-7 cells; however, this effect was not evident in MCF-10A cells, indicating the varied DNA damage responses between the two cell lines.	1,2-dihydroxy-1,2-dihydro-6-hydroxylaminochrysene	22-71	P53	Homo sapiens	196-199
17678638-8	2007	By contrast to numerous DNA damaging agents such as BaP which is known to stimulate p53 expression, the lack of p53 response by 6-NC imply the lack of protective functions mediated by p53 (e.g. DNA repair machinery) after exposure to 6-NC and this may, in part, account for its remarkable carcinogenicity in the mammary tissue.	Benzo(a)pyrene	52-55	P53	Homo sapiens	84-87
18446845-6	2008	ESS-mediated G2/M arrest was found to be associated with up-regulation of cyclin A, Cdc2, tumor suppressor p53 and cyclin dependent kinase (Cdk) inhibitor p21(WAF1/CIP1), whereas the expressions of other G2/M regulatory proteins, including cyclin B1 and Cdk2, were down-regulated compared with the control.	ESS	0-3	P53	Homo sapiens	107-110
17681284-2	2007	The tumour suppressor, p53, has been reported to play a crucial role in apoptosis induced by oxidants, therefore we assessed the ability of a ONOO(-) donor, GEA 3162, to activate caspases and induce mitochondrial permeability in a p53-deficient murine bone marrow cell line, Jaws II.	onoo	142-146	P53	Homo sapiens	23-26
30988561-1	2019	Ibrutinib is the only approved novel agent that is available for the treatment of relapsed-refractory and treatment-naive chronic lymphocytic leukemia patients with deletion 17p or TP53 mutation in India.	ibrutinib	0-9	P53	Homo sapiens	181-185
17891139-3	2007	Here, we identify the major poly(ADP-ribosyl)ated sites of p53 by PARP-1 and find that PARP-1-mediated poly(ADP-ribosyl)ation blocks the interaction between p53 and the nuclear export receptor Crm1, resulting in nuclear accumulation of p53.	poly(adp	28-36	P53	Homo sapiens	59-62
17891139-3	2007	Here, we identify the major poly(ADP-ribosyl)ated sites of p53 by PARP-1 and find that PARP-1-mediated poly(ADP-ribosyl)ation blocks the interaction between p53 and the nuclear export receptor Crm1, resulting in nuclear accumulation of p53.	poly(adp	28-36	P53	Homo sapiens	157-160
17891139-3	2007	Here, we identify the major poly(ADP-ribosyl)ated sites of p53 by PARP-1 and find that PARP-1-mediated poly(ADP-ribosyl)ation blocks the interaction between p53 and the nuclear export receptor Crm1, resulting in nuclear accumulation of p53.	poly(adp	28-36	P53	Homo sapiens	157-160
17632137-12	2007	CONCLUSIONS: 4-Hydroxy-2-nonenal impairs the proliferation of germ cells through the up-regulation of p53 protein, especially in testes with varicocele.	2-nonenal	22-32	P53	Homo sapiens	102-105
17632137-13	2007	Modification by 4-hydroxy-2-nonenal might alter normal function and stabilization of p53 protein.	4-hydroxy-2-nonenal	16-35	P53	Homo sapiens	85-88
17559811-9	2007	Persistent sensitivity to oxaliplatin of the p53-mutated V9P cell line was associated with oxalipatin-induced apoptosis but TAp73 was not the responsible alternative pathway.	oxalipatin	91-101	P53	Homo sapiens	45-48
17469128-9	2007	Temozolomide reverses this pattern at the onset, but this effect is often brief in patients whose tumors overexpress p53 and do not harbor the 1p-19q codeletion, suggesting acquired chemoresistance.	Temozolomide	0-12	P53	Homo sapiens	117-120
17472673-0	2007	Apoptosis, P53 and Bcl-2 expression in response to topical calcipotriol therapy for psoriasis.	calcipotriene	59-71	P53	Homo sapiens	11-14
17472673-6	2007	RESULTS: After topical calcipotriol therapy, keratinocytes of psoriatic skin showed significant decrease of P53 (P = 0.002) and increase of Bcl-2 (P = 0.01) expression.	calcipotriene	23-35	P53	Homo sapiens	108-111
17472673-9	2007	CONCLUSIONS: The results of the study suggested that one of the actions of calcipotriol in psoriasis might be exerted through induction of apoptosis, especially of keratinocytes, through a P53-independent pathway.	calcipotriene	75-87	P53	Homo sapiens	189-192
17270239-6	2007	After stratification by sex, location, tumor differentiation, RUNX3 status, KRAS/BRAF status, or p53 status, CIMP-high was persistently correlated with TGFBR2 mutation.	Cyclic IMP	109-113	P53	Homo sapiens	97-100
17449938-7	2007	In addition, minoxidil plus ATRA elevated phosphorylated Erk, phosphorylated Akt and the ratio of Bcl-2/Bax, but decreased the expressions of P53 and P21 more effectively than by minoxidil alone.	Minoxidil	13-22	P53	Homo sapiens	142-145
17449938-8	2007	Our results suggest that minoxidil plus ATRA would additively enhance hair growth by mediating dual functions: 1) the prolongation of cell survival by activating the Erk and Akt signaling pathways, and 2) the prevention of apoptosis of DPCs and epithelial cells by increasing the ratio of Bcl-2/Bax and downregulating the expressions of P53 and P21.	Minoxidil	25-34	P53	Homo sapiens	337-340
17216584-6	2007	Conversely, Noxa transcription in response to the chemotherapeutic agents cisplatin or temozolomide was inhibited by p53 knockdown.	Temozolomide	87-99	P53	Homo sapiens	117-120
17216584-7	2007	Apoptosis in response to cisplatin or temozolomide was also inhibited by abrogation of p53 expression yet apoptosis in response to fenretinide or thapsigargin was unaffected.	Temozolomide	38-50	P53	Homo sapiens	87-90
17298100-7	2007	We demonstrated that SERS-encoded beads could be used for multiplex detection with a model using streptavidin and p53.	sers	21-25	P53	Homo sapiens	114-117
17191126-0	2007	Different levels of p53 induced either apoptosis or cell cycle arrest in a doxycycline-regulated hepatocellular carcinoma cell line in vitro.	Doxycycline	75-86	P53	Homo sapiens	20-23
17147976-0	2007	Desferrioxamine (DFX) has genotoxic effects on cultured human lymphocytes and induces the p53-mediated damage response.	Deferoxamine	0-15	P53	Homo sapiens	90-93
17147976-0	2007	Desferrioxamine (DFX) has genotoxic effects on cultured human lymphocytes and induces the p53-mediated damage response.	Deferoxamine	17-20	P53	Homo sapiens	90-93
17147976-6	2007	Western blot analysis using antibodies to proteins involved in the p53-mediated response to DNA damage revealed that p53 was accumulated and DNA damage checkpoint kinases were activated in lymphocytes treated with DFX.	Deferoxamine	214-217	P53	Homo sapiens	67-70
17147976-6	2007	Western blot analysis using antibodies to proteins involved in the p53-mediated response to DNA damage revealed that p53 was accumulated and DNA damage checkpoint kinases were activated in lymphocytes treated with DFX.	Deferoxamine	214-217	P53	Homo sapiens	117-120
17147976-12	2007	Taken together, these results indicate that DFX activates p53-mediated checkpoint signals and induces apoptosis via mitochondrial damage in human peripheral blood lymphocytes.	Deferoxamine	44-47	P53	Homo sapiens	58-61
17116745-8	2007	We propose that the genotoxic action of H2S propels the cell toward apoptotic death triggered initially by stabilization of p53 and subsequently involving a cascade of downstream products.	Hydrogen Sulfide	40-43	P53	Homo sapiens	124-127
17145881-0	2006	A novel BH3 mimetic reveals a mitogen-activated protein kinase-dependent mechanism of melanoma cell death controlled by p53 and reactive oxygen species.	BH 3	8-11	P53	Homo sapiens	120-123
17123452-6	2006	When evaluated by several pathway and biological process analysis programs, these proteins are demonstrated to be involved with a high degree of confidence (p values &lt; 2.0 E-05) in glycolysis, propanoate metabolism, pyruvate metabolism, urea cycle and arginine/proline metabolism, as well as in the non-metabolic p53 and FAS pathways.	Propionates	196-206	P53	Homo sapiens	316-319
17079445-7	2006	Nutlin-3 pretreatment also conferred protection of p53-proficient cells against cytosine arabinoside but not against doxorubicin or cisplatin.	Cytarabine	80-100	P53	Homo sapiens	51-54
16926039-7	2006	Furthermore, BaP increased p53 levels in both p53 positive cell lines, as well as p21 levels in MCF-7 cells, an effect that was prevented by the p53-specific inhibitor pifithrin-alpha.	Benzo(a)pyrene	13-16	P53	Homo sapiens	27-30
16926039-7	2006	Furthermore, BaP increased p53 levels in both p53 positive cell lines, as well as p21 levels in MCF-7 cells, an effect that was prevented by the p53-specific inhibitor pifithrin-alpha.	Benzo(a)pyrene	13-16	P53	Homo sapiens	46-49
16926039-7	2006	Furthermore, BaP increased p53 levels in both p53 positive cell lines, as well as p21 levels in MCF-7 cells, an effect that was prevented by the p53-specific inhibitor pifithrin-alpha.	Benzo(a)pyrene	13-16	P53	Homo sapiens	46-49
17050687-3	2006	In addition to its role in activating the G(1) and G(2) checkpoints, p53 also helps to protect cells in S phase when they are starved for DNA precursors by treatment with the specific aspartate transcarbamylase inhibitor N-phosphonacetyl-l-aspartate (PALA), which blocks the synthesis of pyrimidine nucleotides.	Pyrimidine Nucleotides	288-310	P53	Homo sapiens	69-72
17093398-0	2006	Oxidative stress in pterygium: relationship between p53 and 8-hydroxydeoxyguanosine.	8-ohdg	60-83	P53	Homo sapiens	52-55
17093398-7	2006	To verify a possible significant association between p53 and 8-OHdG, we examined a series of 31 Ecuadorian pterygia for the expression of the two markers.	8-ohdg	61-67	P53	Homo sapiens	53-56
17093398-16	2006	All samples positive for p53 (11/31, 35.48%) were also positive for 8-OHdG immunostaining, and all specimens negative for 8-OHdG (10/31, 32.26%) were also negative for p53.	8-ohdg	68-74	P53	Homo sapiens	25-28
17093398-17	2006	When analyzed by Fisher"s exact test, 8-OHdG expression was significantly associated with p53 positivity (p=0.0049).	8-ohdg	38-44	P53	Homo sapiens	90-93
17093398-20	2006	CONCLUSIONS: Although pterygium is a lesion with limited local invasion and an inability to metastasize, the concomitant presence of altered p53 in 8-OHdG-immunoreactive cells could provide evidence of apparent genetic instability, which is in contrast to its benign clinical course.	8-ohdg	148-154	P53	Homo sapiens	141-144
16738694-0	2006	Alemtuzumab in combination with high-dose methylprednisolone is a logical, feasible and highly active therapeutic regimen in chronic lymphocytic leukaemia patients with p53 defects.	Methylprednisolone	42-60	P53	Homo sapiens	169-172
16759640-4	2006	Suppression of HASMC proliferation by resveratrol was accompanied by a dose-dependent increase in the expression of tumor suppressor gene p53 and heat shock protein HSP27.	hasmc	15-20	P53	Homo sapiens	138-141
16760658-8	2006	Given that glucose deprivation leads to p53 activation and 2-DG led to activation of p53 response genes in our present study (e.g., PMAIP1 and GADD45A), we examined the impact of transient p53 knockdown and observed that induction of PMAIP1 and GADD45A appear to be via p53-independent mechanisms.	Deoxyglucose	59-63	P53	Homo sapiens	85-88
16760658-8	2006	Given that glucose deprivation leads to p53 activation and 2-DG led to activation of p53 response genes in our present study (e.g., PMAIP1 and GADD45A), we examined the impact of transient p53 knockdown and observed that induction of PMAIP1 and GADD45A appear to be via p53-independent mechanisms.	Deoxyglucose	59-63	P53	Homo sapiens	85-88
16760658-8	2006	Given that glucose deprivation leads to p53 activation and 2-DG led to activation of p53 response genes in our present study (e.g., PMAIP1 and GADD45A), we examined the impact of transient p53 knockdown and observed that induction of PMAIP1 and GADD45A appear to be via p53-independent mechanisms.	Deoxyglucose	59-63	P53	Homo sapiens	85-88
16684279-9	2006	Following calcipotriol and MPA treatments, there was a significant reduction in p53 and ki-67 positivity accompanied by an increase in bcl-2 positivity (P &lt; 0.05 each).	calcipotriene	10-22	P53	Homo sapiens	80-83
16625087-9	2006	Compared with adjacent nonatypical and nondysplastic (metaplastic) BE, areas of BCDA showed a significantly elevated prevalence rate of p53 positivity (60% vs. 13%, P&lt;0.02) and a significantly elevated total crypt and basal crypt MIB-1 proliferation rate (P&lt;0.001).	5-Bromo-4-chloro-3-indolyl acetate	80-84	P53	Homo sapiens	136-139
16625087-11	2006	Patients with BCDA showed a significantly increased rate of 17p(TP53) LOH (P = 0.016), aneuploidy (P = 0.004), and a trend in increased 9p(p16) LOH (P = 0.08), compared with control patients without BCDA.	5-Bromo-4-chloro-3-indolyl acetate	14-18	P53	Homo sapiens	64-68
16504179-2	2006	To determine whether this effect is due only to high level expression or the mutant nature of the protein, we have used a doxycycline-inducible lung carcinoma cell line capable of expressing wild-type p53.	Doxycycline	122-133	P53	Homo sapiens	201-204
16538381-5	2006	Quinaprilat reduced Bax and p53.	quinaprilat	0-11	P53	Homo sapiens	28-31
16503551-1	2006	Flavopiridol downregulates anti-apoptotic regulators including Mcl-1, upregulates p53, globally attenuates transcription through inhibition of P-TEFb, binds to DNA, and inhibits angiogenesis.	alvocidib	0-12	P53	Homo sapiens	82-85
16302260-3	2006	We recently identified a synthetic thiazolidin compound, 5-(2,4-dihydroxybenzylidene)-2-(phenylimino)-1,3-thiazolidione (DBPT), that induces apoptosis in human colon cancer cells, independent of p53 and P-glycoprotein status.	dbpt	121-125	P53	Homo sapiens	195-198
16414131-0	2006	Monochloramine inhibits ultraviolet B-induced p53 activation and DNA repair response in human fibroblasts.	chloramine	0-14	P53	Homo sapiens	46-49
16414131-5	2006	Consequently, UVB-induced increase in the downstream effectors of p53, namely p21Cip1 and Gadd45a, were almost completely inhibited by NH2Cl.	chloramine	135-140	P53	Homo sapiens	66-69
16414131-9	2006	As UVB-induced DNA damage is repaired by nucleotide excision repair (NER) in human cells, these findings indicated that NH2Cl inhibited NER through the inhibition of p53 phosphorylation and accumulation, and NH2Cl probably impaired DNA damage recognition and/or ATR activation.	chloramine	120-125	P53	Homo sapiens	166-169
16405512-11	2006	Conversely, p53 mimetic agents designed to stabilize the wild-type conformation of p53 sensitize glioma cells for TMZ cytotoxicity.	Temozolomide	114-117	P53	Homo sapiens	12-15
16405512-11	2006	Conversely, p53 mimetic agents designed to stabilize the wild-type conformation of p53 sensitize glioma cells for TMZ cytotoxicity.	Temozolomide	114-117	P53	Homo sapiens	83-86
16405512-12	2006	Collectively, these results suggest that the determination of MGMT expression and p53 status will help to identify glioma patients who will or will not respond to TMZ.	Temozolomide	163-166	P53	Homo sapiens	82-85
17310826-3	2006	Comparison of the ability of the PIs indinavir, ritonavir, amprenavir, lopinavir, atazanavir, nelfinavir and saquinavir to inhibit E6-mediated proteasomal degradation of mutant p53 in E6-transfected C33A cells showed that 15 microM lopinavir, 1 mM indinavir or 125 microM ritonavir treatment for 24 h produced a stable increase in the level of nuclear p53 in these cells with minimal cell death.	Saquinavir	109-119	P53	Homo sapiens	177-180
17310826-3	2006	Comparison of the ability of the PIs indinavir, ritonavir, amprenavir, lopinavir, atazanavir, nelfinavir and saquinavir to inhibit E6-mediated proteasomal degradation of mutant p53 in E6-transfected C33A cells showed that 15 microM lopinavir, 1 mM indinavir or 125 microM ritonavir treatment for 24 h produced a stable increase in the level of nuclear p53 in these cells with minimal cell death.	Saquinavir	109-119	P53	Homo sapiens	352-355
16298346-6	2005	AT514 induced p53 accumulation in wild-type p53 cells but cell death was observed in both deficient and wild-type p53 cells.	at514	0-5	P53	Homo sapiens	14-17
16298346-6	2005	AT514 induced p53 accumulation in wild-type p53 cells but cell death was observed in both deficient and wild-type p53 cells.	at514	0-5	P53	Homo sapiens	44-47
16298346-6	2005	AT514 induced p53 accumulation in wild-type p53 cells but cell death was observed in both deficient and wild-type p53 cells.	at514	0-5	P53	Homo sapiens	44-47
16298346-7	2005	Our results indicate that AT514 induces cell cycle arrest and apoptosis in breast cancer cells irrespectively of p53 status, suggesting that it might represent a potential new chemotherapeutic agent.	at514	26-31	P53	Homo sapiens	113-116
16322335-5	2005	Moreover, TAp63alpha antagonizes the effect of p53 on target genes, cell viability and foci formation, and p63 gene silencing by small interfering (si) RNA results in improved p53 activity.	tap63alpha	10-20	P53	Homo sapiens	47-50
16225996-6	2005	Regarding radiosensitization of tumors, a large body of evidence suggests that Ptx improves tumor oxygenation and sensitizes p53 mutant tumors.	Pentoxifylline	79-82	P53	Homo sapiens	125-128
16232203-0	2005	Cisplatin-controlled p53 gene therapy for human non-small cell lung cancer xenografts in athymic nude mice via the CArG elements.	carg	115-119	P53	Homo sapiens	21-24
16227412-0	2005	WMC-79, a potent agent against colon cancers, induces apoptosis through a p53-dependent pathway.	WMC-79	0-6	P53	Homo sapiens	74-77
16227412-5	2005	We hypothesized that WMC-79 binding to DNA is recognized as an unrepairable damage in the tumor cells, which results in p53 activation.	WMC-79	21-27	P53	Homo sapiens	120-123
16227412-10	2005	However, whereas this pathway is important in wild-type p53 colon tumors, other pathways are also in operation because colon cancer cell lines in which the p53 gene is mutated are also affected by higher concentrations of WMC-79.	WMC-79	222-228	P53	Homo sapiens	156-159
16143123-9	2005	However, CIMP-high unstable tumors were significantly more likely than their stable counterparts to be KRAS2 wild type, TP53 wild type, poorly differentiated, proximally located, occur at lower stages, and have the BRAF V600E mutation (64.1% vs 17.6%).	Cyclic IMP	9-13	P53	Homo sapiens	120-124
15976193-4	2005	DON readily induced the phosphorylation and activity of p53 and this was inhibitable by SB203580.	deoxynivalenol	0-3	P53	Homo sapiens	56-59
15976193-6	2005	The p53 inhibitor PFTalpha reduced both DON-induced phosphorylation of p53 and p53 binding activity.	deoxynivalenol	40-43	P53	Homo sapiens	4-7
15976193-6	2005	The p53 inhibitor PFTalpha reduced both DON-induced phosphorylation of p53 and p53 binding activity.	deoxynivalenol	40-43	P53	Homo sapiens	71-74
15976193-6	2005	The p53 inhibitor PFTalpha reduced both DON-induced phosphorylation of p53 and p53 binding activity.	deoxynivalenol	40-43	P53	Homo sapiens	71-74
15976193-7	2005	Moreover, both PFTalpha and p53 siRNA transfection suppressed DON-induced caspase-3 activity and subsequent DNA fragmentation.	deoxynivalenol	62-65	P53	Homo sapiens	28-31
15976193-9	2005	Taken together, the results indicate that DON initiates competing apoptotic (p38/p53/Bax/Mitochondria/Caspase-3) and survival (ERK/AKT/p90Rsk/Bad) pathways in the macrophage.	deoxynivalenol	42-45	P53	Homo sapiens	81-84
16177561-4	2005	We also found that several randomly chosen acridine derivatives, including 9-aminoacridine, amsacrine, quinacrine and acridine orange, induced p53 transcriptional activity.	Acridine Orange	118-133	P53	Homo sapiens	143-146
16103461-0	2005	Absence of TP53 codon 249 mutations in young Guinean children with high aflatoxin exposure.	Aflatoxins	72-81	P53	Homo sapiens	11-15
16103461-3	2005	A mutation in the TP53 tumor suppressor gene at codon 249 (TP53 Ser249 mutation) has been reported previously for hepatocellular carcinoma tumors and matched plasma DNA samples in individuals from areas with high aflatoxin exposure.	Aflatoxins	213-222	P53	Homo sapiens	18-22
16103461-3	2005	A mutation in the TP53 tumor suppressor gene at codon 249 (TP53 Ser249 mutation) has been reported previously for hepatocellular carcinoma tumors and matched plasma DNA samples in individuals from areas with high aflatoxin exposure.	Aflatoxins	213-222	P53	Homo sapiens	59-63
16098148-5	2005	Doxycycline-induced expression of SEI proteins results in activation of the p21 gene and inhibition of cell growth, but the growth arrest was not suppressed by the siRNA-mediated knockdown of the endogenous p53 protein.	Doxycycline	0-11	P53	Homo sapiens	207-210
16048565-1	2005	BACKGROUND AND AIMS: A specific mutation at codon 249 of the p53 tumor suppressor gene (guanine to thymine; arginine to serine [249(serine)p53]) is present in the cell-free plasma of 30-47% of patients with hepatocellular carcinoma (HCC) in regions with uniformly high levels of dietary exposure to the fungal toxin, aflatoxin B(1).	Thymine	99-106	P53	Homo sapiens	61-64
16048565-1	2005	BACKGROUND AND AIMS: A specific mutation at codon 249 of the p53 tumor suppressor gene (guanine to thymine; arginine to serine [249(serine)p53]) is present in the cell-free plasma of 30-47% of patients with hepatocellular carcinoma (HCC) in regions with uniformly high levels of dietary exposure to the fungal toxin, aflatoxin B(1).	Thymine	99-106	P53	Homo sapiens	139-142
15993273-8	2005	Three families (4.4%) had a diagnosis of Li-Fraumeni syndrome and germline mutations in TP53 (Lys292Ile, Pro278Ser and Pro278Thr).	pro278thr	119-128	P53	Homo sapiens	88-92
15897584-1	2005	PURPOSE: Flavopiridol potently enhances the effect of irinotecan with cures in colorectal cancer xenografts, and is associated with modulation of several molecular targets, including p21, Differentiation-related gene 1 (Drg1), and p53.	alvocidib	9-21	P53	Homo sapiens	231-234
15809736-11	2005	Etodolac-induced cell-cycle arrest might be caused by increases in p53 and P21WAF1 protein expression.	Etodolac	0-8	P53	Homo sapiens	67-70
15671037-3	2005	We previously showed that RelA-NF-kappaB functioned as a proapoptotic factor by activating the p53-signaling pathway in response to doxycycline-induced superoxide.	Doxycycline	132-143	P53	Homo sapiens	95-98
15837761-1	2005	beta-Lapachone, an o-naphthoquinone, induces a novel caspase- and p53-independent apoptotic pathway dependent on NAD(P)H:quinone oxidoreductase 1 (NQO1).	beta-lapachone	0-14	P53	Homo sapiens	66-69
15805253-5	2005	With the Hupki assay we examined here whether benzo(a)pyrene (BaP), a major tobacco smoke carcinogen could elicit p53 mutation patterns characterizing the human lung tumor p53 mutation spectrum.	Benzo(a)pyrene	46-60	P53	Homo sapiens	114-117
15805253-5	2005	With the Hupki assay we examined here whether benzo(a)pyrene (BaP), a major tobacco smoke carcinogen could elicit p53 mutation patterns characterizing the human lung tumor p53 mutation spectrum.	Benzo(a)pyrene	46-60	P53	Homo sapiens	172-175
15784129-3	2005	A hereditary p53 mutation (pro309ser) supported the Li-Fraumeni syndrome diagnosis in this family.	pro309ser	27-36	P53	Homo sapiens	13-16
15837074-0	2005	Benzo[a]pyrene, but not 2,3,7,8-TCDD, induces G2/M cell cycle arrest, p21CIP1 and p53 phosphorylation in human choriocarcinoma JEG-3 cells: a distinct signaling pathway.	Benzo(a)pyrene	0-14	P53	Homo sapiens	82-85
15797377-2	2005	Here we show that RAD001 (everolimus), a rapamycin derivative, dramatically enhances cisplatin-induced apoptosis in wild-type p53, but not mutant p53 tumor cells.	Everolimus	26-36	P53	Homo sapiens	126-129
15752352-0	2005	Dehydroepiandrosterone inhibits the proliferation of human umbilical vein endothelial cells by enhancing the expression of p53 and p21, restricting the phosphorylation of retinoblastoma protein, and is androgen- and estrogen-receptor independent.	Dehydroepiandrosterone	0-22	P53	Homo sapiens	123-126
15752352-5	2005	DHEA diminished the levels of phosphorylated retinoblastoma protein and increased the expression of p53 and p21 mRNAs.	Dehydroepiandrosterone	0-4	P53	Homo sapiens	100-103
19035040-1	2008	OBJECTIVE: To investigate the roles of p53 in cell cycle changes on human embryo lung fibroblasts (HELF) induced by benzo(a) pyrene[ B(a) P], and relationships between p53 and p21, E2F-1.	Benzo(a)pyrene	116-131	P53	Homo sapiens	39-42
18305114-0	2008	Mycophenolic acid activation of p53 requires ribosomal proteins L5 and L11.	Mycophenolic Acid	0-17	P53	Homo sapiens	32-35
18489080-0	2008	The pattern of p53 mutations caused by PAH o-quinones is driven by 8-oxo-dGuo formation while the spectrum of mutations is determined by biological selection for dominance.	8-ohdg	67-77	P53	Homo sapiens	15-18
18717335-0	2008	[Hydroxysafflor yellow A up-regulates HIF-1alpha via inhibition of VHL and p53 in Eahy 926 cell line exposed to hypoxia].	hydroxysafflor yellow A	1-24	P53	Homo sapiens	75-78
17998932-6	2008	In cell lines ensuing from benzo(a)pyrene-treated cultures the combined p53 mutation pattern from experiments with the 3 codon 72 genotypes showed a predominance of strand-biased G to T transversions (18 of 36 mutations), and mutations recurring at smokers" lung tumour hotspot codons 157 and 273, supporting involvement of tobacco carcinogens in shaping the mutation signature in lung cancers of smokers.	Benzo(a)pyrene	27-41	P53	Homo sapiens	72-75
17564708-2	2008	In our previous experiments, we observed that IFN-beta sensitized TMZ-resistant glioma cells with the unmethylated MGMT promoter and that the mechanism of action was possibly due to attenuation of MGMT expression via induction of TP53.	Temozolomide	66-69	P53	Homo sapiens	230-234
18314014-6	2008	Both DNA repair proteins, containing Fe-S clusters, and the transcription factor, p53, which is regulated through thiol-disulfide switches, can be oxidized from a distance through DNA-mediated CT.	thiol-disulfide	114-129	P53	Homo sapiens	82-85
18324703-2	2008	Using analysis of proteins related to cell cycle and apoptotic pathways, we confirmed an elevated level of p53 accompanying p21 Waf1/Cip1 protein in genistein-treated or genistin-treated A549 and WI-38 cells, but not in HeLa cells.	genistin	170-178	P53	Homo sapiens	107-110
18510179-13	2008	The p53 Ab-negative patients may predict a high clinical OR rate in anthracycline-based NAC.	nac	88-91	P53	Homo sapiens	4-7
18284706-5	2008	Wild type full-length p53 protein was produced in fusion with biotin carboxyl carrier peptide (BCCP) or hexahistidine [(His)6] using pAK400 and pET15b(+) vectors, respectively.	His-His-His-His-His-His	104-117	P53	Homo sapiens	22-25
18006205-5	2008	Gene expression of p21 was also induced by DON treatment in a dose-dependent manner with no increase in p53 protein levels, suggesting p53-independent p21 induction.	deoxynivalenol	43-46	P53	Homo sapiens	135-138
17942461-7	2008	Interestingly, DNA adduct formation after BaP, but not BPDE, exposure was p53 dependent with 10-fold lower levels detected in p53-null cells.	Benzo(a)pyrene	42-45	P53	Homo sapiens	74-77
17942461-7	2008	Interestingly, DNA adduct formation after BaP, but not BPDE, exposure was p53 dependent with 10-fold lower levels detected in p53-null cells.	Benzo(a)pyrene	42-45	P53	Homo sapiens	126-129
17942461-8	2008	Other cell lines were investigated for BaP-DNA adduct formation and in these the effect of p53 knockdown was also to reduce adduct formation.	Benzo(a)pyrene	39-42	P53	Homo sapiens	91-94
17942461-9	2008	Taken together, these results give further insight into the role of p53 in the response of human cells to BaP and BPDE and suggest that loss of this tumour suppressor can influence the metabolic activation of BaP.	Benzo(a)pyrene	106-109	P53	Homo sapiens	68-71
17942461-9	2008	Taken together, these results give further insight into the role of p53 in the response of human cells to BaP and BPDE and suggest that loss of this tumour suppressor can influence the metabolic activation of BaP.	Benzo(a)pyrene	209-212	P53	Homo sapiens	68-71
17981542-3	2008	Consistent with these observations, doxycyclin-induced NBS1 caused accumulation of p21WAF1 and increased phosphorylation of p53 Ser37, leading to cell cycle arrest in G1 phase.	Doxycycline	36-46	P53	Homo sapiens	124-127
18784437-4	2008	In this study, we assessed whether LMB augments the transduced p53 gene effect.	leptomycin B	35-38	P53	Homo sapiens	63-66
18784437-8	2008	RESULTS: LMB induced cell death in a dose-dependent manner and p53 drastically accumulated in the nucleus after LMB treatment.	leptomycin B	112-115	P53	Homo sapiens	63-66
17804695-7	2007	Molecular studies indicate the prevalent activities of DMAPT include induction of oxidative stress responses, inhibition of NF-kappaB, and activation of p53.	LC-1 compound	55-60	P53	Homo sapiens	153-156
17958425-7	2007	Finally, we show that treatment of adhered LNCaP or T-47D cells with (+)-avrainvillamide leads to an increase in cellular p53 concentrations, and that siRNA-promoted depletion of nucleophosmin in a population of HeLa S3 cells leads to increased sensitivity of that population toward apoptotic death upon treatment with (+)-avrainvillamide.	avrainvillamide	69-88	P53	Homo sapiens	122-125
17968428-3	2007	In the present study, we show that sensitivity of melanoma cells to TMZ was dependent on their p53 status and levels of MGMT.	Temozolomide	68-71	P53	Homo sapiens	95-98
17968428-9	2007	These results are consistent with the view that TMZ is relatively ineffective against melanoma due to defective apoptotic signalling resulting from activation of p53.	Temozolomide	48-51	P53	Homo sapiens	162-165
17631051-5	2007	CD8(+) T cell precursors responsive to wt p53 epitopes were detected in the circulation of most subjects with early disease, and an elevated blood Tc(1)/Tc(2) ratio distinguished wt p53 peptide responders from non-responders.	tc(2)	153-158	P53	Homo sapiens	182-185
17938270-7	2007	Moreover, epothilone B and D increased the expressions of NF-kappaB-dependent apoptotic cell death regulatory genes, i.e., Bax, p53, and the active form of caspase-3, but reduced Bcl-2 expression, and these actions were partially reversed by salicylic acid.	epothilone B	10-22	P53	Homo sapiens	128-131
17636258-8	2007	We hypothesize that targeted necrosis by p53p-Ant is dependent on mutant p53, is mediated by O(2)(.)	o(2)	93-97	P53	Homo sapiens	41-45
17636258-8	2007	We hypothesize that targeted necrosis by p53p-Ant is dependent on mutant p53, is mediated by O(2)(.)	o(2)	93-97	P53	Homo sapiens	41-44
17517898-2	2007	To develop a Chk1-specific cell-based assay, stable clones were established in which Chk1 kinase domain fused at its N-terminus with p53 through 4 tandem repeats of Gly-Gly-Gly-Gly-Ser was expressed in an inducible manner.	glycyl-glycyl-glycyl-glycine	165-180	P53	Homo sapiens	133-136
17638905-5	2007	beta-Lapachone (beta-lap; also known as ARQ 501), currently in phase II clinical trials for the treatment of pancreatic cancer, causes a novel caspase- and p53-independent cell death in cancer cells overexpressing NAD(P)H:quinone oxidoreductase-1 (NQO1).	beta-lapachone	0-14	P53	Homo sapiens	156-159
17638905-5	2007	beta-Lapachone (beta-lap; also known as ARQ 501), currently in phase II clinical trials for the treatment of pancreatic cancer, causes a novel caspase- and p53-independent cell death in cancer cells overexpressing NAD(P)H:quinone oxidoreductase-1 (NQO1).	beta-lapachone	16-24	P53	Homo sapiens	156-159
17609380-8	2007	Kinetically, beta-lapachone-induced cell death was characterized by the following: (i) dramatic reactive oxygen species (ROS) formation, eliciting extensive DNA damage; (ii) hyperactivation of poly(ADP-ribose)polymerase-1 (PARP-1); (iii) depletion of NAD+/ATP levels; and (iv) proteolytic cleavage of p53/PARP-1, indicating mu-calpain activation and apoptosis.	beta-lapachone	13-27	P53	Homo sapiens	301-304
17610718-7	2007	Oxidative stress response genes diminish the activity of cantharidin by inducing DNA strand breaks which may be subject to base excision repair and induce apoptosis in a p53- and Bcl2-dependent manner.	Cantharidin	57-68	P53	Homo sapiens	170-173
17695552-6	2007	Celecoxib had no effects on expression of MAPKs, Bax, or p21; however, it increased expression of p53 and 14-3-4sigma, and reduced expression of Bcl-2.	Celecoxib	0-9	P53	Homo sapiens	98-101
17695552-9	2007	CONCLUSION: The results suggest that celecoxib induced cytotoxicity and apoptosis in this line of glioma cells and that such effects might be related to activation of p53 and 14-3-3sigma, reduced Bcl-2 and Bcl-2/Bax ratio, and increased caspace-3 activity.	Celecoxib	37-46	P53	Homo sapiens	167-186
17599036-5	2007	GLA decreased the anti-oxidant content of tumor cells, expression of oncogenes ras, and Bcl-2, enhanced the activity of p53, protected normal cells and tissues from the toxic actions of radiation and anti-cancer drugs, enhanced the cytotoxic action of anti-cancer drugs and reversed tumor cell drug resistance.	gamma-Linolenic Acid	0-3	P53	Homo sapiens	120-123
17408702-1	2007	We analyzed the effect of exposure to carcinogenic polycyclic aromatic hydrocarbons (c-PAHs) in ambient air on the plasma levels of p53 and p21(WAF1) proteins among city policemen, bus drivers and controls in three European cities: Prague (Czech Republic), Kosice (Slovakia) and Sofia (Bulgaria).	c-pahs	85-91	P53	Homo sapiens	132-135
17408702-11	2007	Among all subjects p53 plasma levels were positively correlated with p21(WAF1) levels, exposure to B[a]P, c-PAHs and levels of total DNA adducts; for p21(WAF1) levels we observed the positive correlation with cotinine, c-PAHs exposure, total and B[a]P-like DNA adduct levels.	c-pahs	106-112	P53	Homo sapiens	19-22
17408702-11	2007	Among all subjects p53 plasma levels were positively correlated with p21(WAF1) levels, exposure to B[a]P, c-PAHs and levels of total DNA adducts; for p21(WAF1) levels we observed the positive correlation with cotinine, c-PAHs exposure, total and B[a]P-like DNA adduct levels.	c-pahs	219-225	P53	Homo sapiens	19-22
17408702-12	2007	In conclusion our results suggest that p53 and p21(WAF1) proteins plasma levels may be useful biomarkers of c-PAHs environmental exposure.	c-pahs	108-114	P53	Homo sapiens	39-42
17563398-6	2007	Additionally, DFO treatment also led to the activation of Chk1, p53, and Akt, where DFO-induced activation of p53, Chk1, and Akt occurred in both PKCdelta-dependent and -independent manners.	Deferoxamine	14-17	P53	Homo sapiens	64-67
17563398-6	2007	Additionally, DFO treatment also led to the activation of Chk1, p53, and Akt, where DFO-induced activation of p53, Chk1, and Akt occurred in both PKCdelta-dependent and -independent manners.	Deferoxamine	14-17	P53	Homo sapiens	110-113
17563398-6	2007	Additionally, DFO treatment also led to the activation of Chk1, p53, and Akt, where DFO-induced activation of p53, Chk1, and Akt occurred in both PKCdelta-dependent and -independent manners.	Deferoxamine	84-87	P53	Homo sapiens	64-67
17563398-6	2007	Additionally, DFO treatment also led to the activation of Chk1, p53, and Akt, where DFO-induced activation of p53, Chk1, and Akt occurred in both PKCdelta-dependent and -independent manners.	Deferoxamine	84-87	P53	Homo sapiens	110-113
17439265-0	2007	Theoretical prediction of the p53 gene mutagenic mechanism induced by trans-4-hydroxy-2-nonenal.	4-hydroxy-2-nonenal	70-95	P53	Homo sapiens	30-33
17499812-3	2007	In the present study, we report that black tea polyphenol, Theaflavins (TF)-induced apoptosis in human prostate carcinoma, LNCaP cells is mediated via modulation of two related pathways: up-regulation of p53 and down-regulation of NF-kappa B activity, causing a change in the ratio of pro-and antiapoptotic proteins leading to apoptosis.	Polyphenols	47-57	P53	Homo sapiens	204-207
17239930-12	2007	In conclusion, cytoplasmic p27 expression is inversely associated with MSI-H and CIMP-high, particularly in p53-negative tumors, suggesting interplay of functional losses of p27 and p53 in the development of various molecular subtypes of colorectal cancer.	Cyclic IMP	81-85	P53	Homo sapiens	182-185
17300232-2	2007	OBJECTIVES: To investigate the role of CDKN2A and p53 in the pathogenesis of EGCs and their precursor lesions vulval intraepithelial neoplasia (VIN3), penile intraepithelial neoplasia and lichen sclerosus (LS).	gallocatechol	77-81	P53	Homo sapiens	50-53
17300232-6	2007	CDKN2A or p53 mutations were observed more frequently in LS-derived EGCs than in human papillomavirus-derived EGCs (P = 0.053).	gallocatechol	68-72	P53	Homo sapiens	10-13
17300232-6	2007	CDKN2A or p53 mutations were observed more frequently in LS-derived EGCs than in human papillomavirus-derived EGCs (P = 0.053).	gallocatechol	110-114	P53	Homo sapiens	10-13
17159900-2	2007	PIDD (p53-induced protein with a death domain) is constitutively processed giving rise to a 48-kDa N-terminal fragment containing the leucine-rich repeats (LRRs, PIDD-N) and a 51-kDa C-terminal fragment containing the death domain (DD, PIDD-C).	pidd	0-4	P53	Homo sapiens	6-9
17245118-0	2007	CYFIP2, a direct p53 target, is leptomycin-B sensitive.	leptomycin B	32-44	P53	Homo sapiens	17-20
17200364-4	2007	This enhancement of temozolomide-induced cytotoxicity is not dependent on p53 status as we transfected an ovarian cancer cell line with a dominant-negative p53-expressing plasmid (IGROV-1mp53) and obtained similar results.	Temozolomide	20-32	P53	Homo sapiens	156-159
17189186-6	2006	Thus, our study demonstrates that Tip60-dependent acetylation of p53 at K120 modulates the decision between cell-cycle arrest and apoptosis, and it reveals that the DNA-binding core domain is an important target for p53 regulation by posttranslational modifications.	k120	72-76	P53	Homo sapiens	65-68
17189187-4	2006	Mutation of K120 to arginine, as occurs in human cancer, debilitates K120 acetylation and diminishes p53-mediated apoptosis without affecting cell-cycle arrest.	k120	12-16	P53	Homo sapiens	101-104
17189187-8	2006	These data suggest that K120 acetylation may help distinguish the cell-cycle arrest and apoptotic functions of p53.	k120	24-28	P53	Homo sapiens	111-114
16826403-9	2006	Treatment with AN-7 or doxorubicin increased p53 acetylation that was further potentiated by their combination.	an-7	15-19	P53	Homo sapiens	45-48
16840563-10	2006	U-NTA was also genotoxic in LT97 cells and primary colon cells, where it additionally increased migration of TP53 into the comet tail.	u-nta	0-5	P53	Homo sapiens	109-113
16840563-11	2006	In LT97 cells, 0.5-2mM U-NTA increased chromosomal aberrations in chromosomes 5, 12, and 17, which harbor the tumor-related genes APC, KRAS, and TP53.	u-nta	23-28	P53	Homo sapiens	145-149
16797759-3	2006	By Western blot, the expression of 14-3-3sigma, p53 and p21 was coordinately upregulated in astrocytes following exposure to hydrogen peroxide, 4-hydroxy-2-nonenal (4-HNE) or etoposide, a topoisomerase II inhibitor.	4-hydroxy-2-nonenal	144-163	P53	Homo sapiens	48-51
16797759-3	2006	By Western blot, the expression of 14-3-3sigma, p53 and p21 was coordinately upregulated in astrocytes following exposure to hydrogen peroxide, 4-hydroxy-2-nonenal (4-HNE) or etoposide, a topoisomerase II inhibitor.	4-hydroxy-2-nonenal	165-170	P53	Homo sapiens	48-51
16925398-1	2006	The most potent inhibitor of the p53-MDM2 interaction reported to date is an 8-mer p53 peptide analogue (Novartis peptide), which contains 6-chlorotryptophane (Cl-Trp) and phosphonomethylphenylalanine (Pmp) as key residues for the enhanced activity.	pmp	202-205	P53	Homo sapiens	33-36
16925398-1	2006	The most potent inhibitor of the p53-MDM2 interaction reported to date is an 8-mer p53 peptide analogue (Novartis peptide), which contains 6-chlorotryptophane (Cl-Trp) and phosphonomethylphenylalanine (Pmp) as key residues for the enhanced activity.	pmp	202-205	P53	Homo sapiens	83-86
16632641-9	2006	SP600125 (anthra [1,9-cd]pyrazol-6(2H)-one-1,9-pyrazoloanthrone), a specific inhibitor of JNK, significantly decreased apoptosis by inhibiting the phosphorylation of p53 (serine 15) and subsequently increased the interaction of p53 and MDM2.	anthra [1,9-cd]pyrazol-6(2h)-one-1,9-pyrazoloanthrone	10-63	P53	Homo sapiens	166-169
16632641-9	2006	SP600125 (anthra [1,9-cd]pyrazol-6(2H)-one-1,9-pyrazoloanthrone), a specific inhibitor of JNK, significantly decreased apoptosis by inhibiting the phosphorylation of p53 (serine 15) and subsequently increased the interaction of p53 and MDM2.	anthra [1,9-cd]pyrazol-6(2h)-one-1,9-pyrazoloanthrone	10-63	P53	Homo sapiens	228-231
16814113-9	2006	The effects of RSVL on ERKs and on p53 phosphorylation were abrogated by either the MAPK inhibitor PD98059 or the p53 inhibitor pifithrine-alpha.	pifithrine	128-138	P53	Homo sapiens	35-38
16814113-9	2006	The effects of RSVL on ERKs and on p53 phosphorylation were abrogated by either the MAPK inhibitor PD98059 or the p53 inhibitor pifithrine-alpha.	pifithrine	128-138	P53	Homo sapiens	114-117
16759082-0	2006	Structure-based design of spiro-oxindoles as potent, specific small-molecule inhibitors of the MDM2-p53 interaction.	spiro-oxindoles	26-41	P53	Homo sapiens	100-103
16820091-4	2006	CIMP-high tumors were much less frequent in COX-2+/p53+ tumors (4.6%) than in COX-2+/p53- tumors (19%; P &lt; .0001), COX-2-/p53+ tumors (17%; P = .04), and COX-2-/p53- tumors (28%; P &lt; .0001).	Cyclic IMP	0-4	P53	Homo sapiens	51-54
16820091-4	2006	CIMP-high tumors were much less frequent in COX-2+/p53+ tumors (4.6%) than in COX-2+/p53- tumors (19%; P &lt; .0001), COX-2-/p53+ tumors (17%; P = .04), and COX-2-/p53- tumors (28%; P &lt; .0001).	Cyclic IMP	0-4	P53	Homo sapiens	85-88
16820091-4	2006	CIMP-high tumors were much less frequent in COX-2+/p53+ tumors (4.6%) than in COX-2+/p53- tumors (19%; P &lt; .0001), COX-2-/p53+ tumors (17%; P = .04), and COX-2-/p53- tumors (28%; P &lt; .0001).	Cyclic IMP	0-4	P53	Homo sapiens	85-88
16820091-4	2006	CIMP-high tumors were much less frequent in COX-2+/p53+ tumors (4.6%) than in COX-2+/p53- tumors (19%; P &lt; .0001), COX-2-/p53+ tumors (17%; P = .04), and COX-2-/p53- tumors (28%; P &lt; .0001).	Cyclic IMP	0-4	P53	Homo sapiens	85-88
16820091-6	2006	In conclusion, COX-2 and p53 alterations were synergistically inversely correlated with both MSI-H and CIMP-high.	Cyclic IMP	103-107	P53	Homo sapiens	25-28
16546733-2	2006	METHODS: MTT assay was performed to evaluate the cytotoxicity of PTX on p53-defective human hepatocellular carcinoma cell line Hep3b and clonogenic assay employed to observe its effects on the radiosensitivity of the cells quantified by calculating the sensitive enhancement ratio (SER).	Pentoxifylline	65-68	P53	Homo sapiens	72-75
16546733-6	2006	Clonogenic survival assays up to 12 Gy demonstrated that p53-defective Hep3b cells (SER of 2.68+/-0.24) were sensitized by PTX (2 mmol/L).	Pentoxifylline	123-126	P53	Homo sapiens	57-60
16271357-0	2006	Erybraedin C and bitucarpin A, two structurally related pterocarpans purified from Bituminaria bituminosa, induced apoptosis in human colon adenocarcinoma cell lines MMR- and p53-proficient and -deficient in a dose-, time-, and structure-dependent fashion.	bitucarpin A	17-29	P53	Homo sapiens	175-178
16413759-2	2006	In order to identify new p53 downstream genes, we established a new system of p53 gene inducible expression, U251-pTet-p53 cell line, with the Tet-On Gene Expression System, in which exogenous p53 gene could overexpress in doxycycline (Dox) medium but not in the medium without Dox.	Doxycycline	223-234	P53	Homo sapiens	25-28
16413759-2	2006	In order to identify new p53 downstream genes, we established a new system of p53 gene inducible expression, U251-pTet-p53 cell line, with the Tet-On Gene Expression System, in which exogenous p53 gene could overexpress in doxycycline (Dox) medium but not in the medium without Dox.	Doxycycline	223-234	P53	Homo sapiens	78-81
16413759-2	2006	In order to identify new p53 downstream genes, we established a new system of p53 gene inducible expression, U251-pTet-p53 cell line, with the Tet-On Gene Expression System, in which exogenous p53 gene could overexpress in doxycycline (Dox) medium but not in the medium without Dox.	Doxycycline	223-234	P53	Homo sapiens	78-81
16413759-2	2006	In order to identify new p53 downstream genes, we established a new system of p53 gene inducible expression, U251-pTet-p53 cell line, with the Tet-On Gene Expression System, in which exogenous p53 gene could overexpress in doxycycline (Dox) medium but not in the medium without Dox.	Doxycycline	223-234	P53	Homo sapiens	78-81
16413759-2	2006	In order to identify new p53 downstream genes, we established a new system of p53 gene inducible expression, U251-pTet-p53 cell line, with the Tet-On Gene Expression System, in which exogenous p53 gene could overexpress in doxycycline (Dox) medium but not in the medium without Dox.	Doxycycline	236-239	P53	Homo sapiens	25-28
16413759-2	2006	In order to identify new p53 downstream genes, we established a new system of p53 gene inducible expression, U251-pTet-p53 cell line, with the Tet-On Gene Expression System, in which exogenous p53 gene could overexpress in doxycycline (Dox) medium but not in the medium without Dox.	Doxycycline	236-239	P53	Homo sapiens	78-81
16413759-2	2006	In order to identify new p53 downstream genes, we established a new system of p53 gene inducible expression, U251-pTet-p53 cell line, with the Tet-On Gene Expression System, in which exogenous p53 gene could overexpress in doxycycline (Dox) medium but not in the medium without Dox.	Doxycycline	236-239	P53	Homo sapiens	78-81
16413759-2	2006	In order to identify new p53 downstream genes, we established a new system of p53 gene inducible expression, U251-pTet-p53 cell line, with the Tet-On Gene Expression System, in which exogenous p53 gene could overexpress in doxycycline (Dox) medium but not in the medium without Dox.	Doxycycline	236-239	P53	Homo sapiens	78-81
16413759-2	2006	In order to identify new p53 downstream genes, we established a new system of p53 gene inducible expression, U251-pTet-p53 cell line, with the Tet-On Gene Expression System, in which exogenous p53 gene could overexpress in doxycycline (Dox) medium but not in the medium without Dox.	Doxycycline	278-281	P53	Homo sapiens	25-28
16413759-2	2006	In order to identify new p53 downstream genes, we established a new system of p53 gene inducible expression, U251-pTet-p53 cell line, with the Tet-On Gene Expression System, in which exogenous p53 gene could overexpress in doxycycline (Dox) medium but not in the medium without Dox.	Doxycycline	278-281	P53	Homo sapiens	78-81
16413759-2	2006	In order to identify new p53 downstream genes, we established a new system of p53 gene inducible expression, U251-pTet-p53 cell line, with the Tet-On Gene Expression System, in which exogenous p53 gene could overexpress in doxycycline (Dox) medium but not in the medium without Dox.	Doxycycline	278-281	P53	Homo sapiens	78-81
16413759-2	2006	In order to identify new p53 downstream genes, we established a new system of p53 gene inducible expression, U251-pTet-p53 cell line, with the Tet-On Gene Expression System, in which exogenous p53 gene could overexpress in doxycycline (Dox) medium but not in the medium without Dox.	Doxycycline	278-281	P53	Homo sapiens	78-81
16467109-8	2006	In contrast, the radiosensitization by TSA of cells expressing low levels of p53 was enhanced by transfection of wild-type p53-expressing vector or pretreatment with leptomycin B, an inhibitor of nuclear export that increased intracellular levels of p53.	leptomycin B	166-178	P53	Homo sapiens	77-80
17113242-0	2006	Novel adenine adducts, N7-guanine-AFB1 adducts, and p53 mutations in patients with schistosomiasis and aflatoxin exposure.	Aflatoxins	103-112	P53	Homo sapiens	52-55
16297369-0	2005	p38 MAP kinase regulates benzo(a)pyrene-induced apoptosis through the regulation of p53 activation.	Benzo(a)pyrene	25-39	P53	Homo sapiens	84-87
16297369-5	2005	Also, pharmacological inhibition of p38 markedly inhibited the phosphorylation, accumulated expression, and transactivation activity of p53 in BaP-treated cells.	Benzo(a)pyrene	143-146	P53	Homo sapiens	136-139
16297369-7	2005	Furthermore, p53 mediated apoptotic activity in BaP-treated cells was inhibited by p38 kinase inhibitor.	Benzo(a)pyrene	48-51	P53	Homo sapiens	13-16
16271069-8	2005	However, BQ chewers exhibited significantly higher incidence of p53 gene mutations than non-chewers (67.6% vs 32.4%, P = 0.007).	bulaquine	9-11	P53	Homo sapiens	64-67
15993080-3	2005	The introduced N at position 8 of the purine ring generally lowered CDK2 inhibitory activity of new 8-azapurines (1,2,3-triazolo[4,5-d]pyrimidines) in comparison to the model trisubstituted purines, whereas the antiproliferative potential of some derivatives remained very high, reflecting their ability to activate p53 tumor suppressor.	Purines	105-112	P53	Homo sapiens	316-319
16061257-3	2005	Nonetheless, we previously showed that the model p53-mutated human adenocarcinoma strain SW480 is proficient in the removal of UV-induced cyclobutane pyrimidine dimers (CPD) via NER.	cyclobutane pyrimidine	138-160	P53	Homo sapiens	49-52
16193384-0	2005	Inactivation of p53 sensitizes astrocytic glioma cells to BCNU and temozolomide, but not cisplatin.	Temozolomide	67-79	P53	Homo sapiens	16-19
16193384-1	2005	p53 inactivation sensitizes U87MG astrocytic glioma cells to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and temozolomide (TMZ), drugs used clinically to treat high-grade astrocytomas.	Temozolomide	109-121	P53	Homo sapiens	0-3
16193384-1	2005	p53 inactivation sensitizes U87MG astrocytic glioma cells to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and temozolomide (TMZ), drugs used clinically to treat high-grade astrocytomas.	Temozolomide	123-126	P53	Homo sapiens	0-3
16193384-3	2005	Compared to control cells with intact p53 function, derived lines in which p53 was inactivated displayed significantly reduced clonogenic survival after exposure to BCNU and TMZ.	Temozolomide	174-177	P53	Homo sapiens	75-78
16193384-5	2005	These findings suggest that enhanced sensitivity to BCNU and TMZ is a general property of human astrocytic glioma cells in which p53 was disrupted.	Temozolomide	61-64	P53	Homo sapiens	129-132
15833387-5	2005	A NO inhibitor, carboxy-PTIO inhibited the p53 expression induced by liriodenine.	1,3-dihydroxy-4,4,5,5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole	16-28	P53	Homo sapiens	43-46
15994771-6	2005	Mutation of the C-terminal nuclear export signal (NES) of p53 or treatment with leptomycin B inhibited the 18E6-mediated nuclear export of p53.	leptomycin B	80-92	P53	Homo sapiens	139-142
15955105-10	2005	Topical application of calcipotriol to lesional psoriatic skin for 4 d resulted in increased NF-kappaB binding to the p53 kappaB site and decreased NF-kappaB binding to the IL-8 kappaB site.	calcipotriene	23-35	P53	Homo sapiens	118-121
15802278-0	2005	Worse survival for TP53 (p53)-mutated breast cancer patients receiving adjuvant CMF.	CMF regimen	80-83	P53	Homo sapiens	19-23
15802278-0	2005	Worse survival for TP53 (p53)-mutated breast cancer patients receiving adjuvant CMF.	CMF regimen	80-83	P53	Homo sapiens	25-28
15802278-7	2005	Univariate analyses showed TP53 to be a significant prognostic factor with regard to RFS, BCCS and OS in patients who received adjuvant CMF.	CMF regimen	136-139	P53	Homo sapiens	27-31
15688362-10	2005	Increased nuclear localization of both p53 and p21(cip1) was observed in BDO2-treated cells, suggesting that the cell cycle arrest was p21(cip1)-mediated.	bdo2	73-77	P53	Homo sapiens	39-42
15735718-8	2005	Attenuated p53 expression and p21 induction also eliminates DAP-induced G(1)-phase arrest and inhibition of Cdk4 and Cdk2 activities.	dap	60-63	P53	Homo sapiens	11-14
15735718-9	2005	Together, these findings establish that activation of the p53-p21 pathway is responsible for the DAP-induced G(1)-phase checkpoint response and provide the first solid evidence that p21 induction by p53 during a DNA damage-induced G(1)-phase checkpoint response inhibits both Cdk4 and Cdk2 activities.	dap	97-100	P53	Homo sapiens	58-61
15735718-9	2005	Together, these findings establish that activation of the p53-p21 pathway is responsible for the DAP-induced G(1)-phase checkpoint response and provide the first solid evidence that p21 induction by p53 during a DNA damage-induced G(1)-phase checkpoint response inhibits both Cdk4 and Cdk2 activities.	dap	97-100	P53	Homo sapiens	199-202
15757539-7	2005	Rank correlation analysis showed that protein expression of 8-OH-dG positively correlated with those of k-ras (RS=0.643, P &lt; 0.01), and p53 (RS=0.827, P &lt; 0.01)u protein expression of k-ras positively correlated with that of p53 (RS=0.897, P &lt; 0.01).	8-ohdg	60-67	P53	Homo sapiens	139-142
15757539-7	2005	Rank correlation analysis showed that protein expression of 8-OH-dG positively correlated with those of k-ras (RS=0.643, P &lt; 0.01), and p53 (RS=0.827, P &lt; 0.01)u protein expression of k-ras positively correlated with that of p53 (RS=0.897, P &lt; 0.01).	8-ohdg	60-67	P53	Homo sapiens	231-234
15710358-4	2005	In leukemia cells, cantharidin induces apoptosis by a p53-dependent mechanism.	Cantharidin	19-30	P53	Homo sapiens	54-57
15710358-8	2005	These data suggest that cantharidin treatment causes oxidative stress that provokes DNA damage and p53-dependent apoptosis.	Cantharidin	24-35	P53	Homo sapiens	99-102
15756021-2	2005	Avicins induce apoptosis in Jurkat T leukemia cells by targeting mitochondria and release of cytochrome c that occurs in a p53-independent manner.	avicins	0-7	P53	Homo sapiens	123-126
15625077-8	2005	Thus, in HepG2 cells pravastatin and simvastatin pretreatment attenuated the p53 response to DNA damage induced by 5-fluorouracil and benzo(a)pyrene.	Benzo(a)pyrene	134-148	P53	Homo sapiens	77-80
15625077-9	2005	Similar attenuation was induced when p53 stabilization was induced by the inhibitor of nuclear export, leptomycin B.	leptomycin B	103-115	P53	Homo sapiens	37-40
15561702-0	2005	Nitric oxide inhibition of homocysteine-induced human endothelial cell apoptosis by down-regulation of p53-dependent Noxa expression through the formation of S-nitrosohomocysteine.	Homocysteine	27-39	P53	Homo sapiens	103-106
15705463-2	2005	Research published in 1996 by Denissenko and colleagues demonstrated patterned in-vitro mutagenic effects on p53 of benzo[a]pyrene, a carcinogen present in tobacco smoke.	Benzo(a)pyrene	116-130	P53	Homo sapiens	109-112
15878303-5	2005	Artesunate triggers apoptosis both by p53-dependent and -independent pathways.	Artesunate	0-10	P53	Homo sapiens	38-41
15595848-1	2004	Codon 273 ((5)(")CGT) of the human P53 gene is a mutational hot spot for the environmental carcinogen benzo[a]pyrene.	Benzo(a)pyrene	102-116	P53	Homo sapiens	35-38
15379854-6	2004	Lithium treatment reduced the senescence-associated accumulation of p53 and caused cells to enter a reversible quiescent state.	Lithium	0-7	P53	Homo sapiens	68-71
15473930-6	2004	In addition,the expression of Ki76 had a positive correlation with the expressions of p53, and C-erbB-2 (P&lt; 0.05), but not with the expression of VEGF (P &gt;0.05).	ki76	30-34	P53	Homo sapiens	86-89
15475437-9	2004	Budesonide treatment resulted in a modest decrease in p53 and BclII protein expression in bronchial biopsies and a slightly higher rate of resolution of computed tomography-detected lung nodules.	Budesonide	0-10	P53	Homo sapiens	54-57
15561702-10	2005	These results suggest that up-regulation of p53-dependent Noxa expression may play an important role in the pathogenesis of atherosclerosis induced by HCy and that an increase in vascular NO production may prevent HCy-induced endothelial dysfunction by S-nitrosylation.	Homocysteine	151-154	P53	Homo sapiens	44-47
15546879-4	2005	Our results showed that simultaneous 5-FU and DENSPM, a spermine analogue, synergistically increased transcript levels of the polyamine catabolism enzyme spermidine/spermine N1-acetyltransferase, depleted spermine and spermidine, increased acetylated spermidine, and produced synergistic tumor cell apoptosis in both p53 wild-type and p53-null variants.	Spermidine	154-164	P53	Homo sapiens	317-320
15546879-4	2005	Our results showed that simultaneous 5-FU and DENSPM, a spermine analogue, synergistically increased transcript levels of the polyamine catabolism enzyme spermidine/spermine N1-acetyltransferase, depleted spermine and spermidine, increased acetylated spermidine, and produced synergistic tumor cell apoptosis in both p53 wild-type and p53-null variants.	Spermidine	154-164	P53	Homo sapiens	335-338
15607904-0	2005	4-Hydroxynonenal modulation of p53 family gene expression in the SK-N-BE neuroblastoma cell line.	4-hydroxy-2-nonenal	0-16	P53	Homo sapiens	31-34
15482940-0	2004	Identification and structure-activity relationship studies of 3-methylene-2-norbornanone as potent anti-proliferative agents presumably working through p53 mediated apoptosis.	3-methylene-2-norbornanone	62-88	P53	Homo sapiens	152-155
15482940-2	2004	The lead molecule, 3-methylene-2-norbornanone (3) showed potent activity (LC(50)=3-8 microM) against mutant p53 cell types and many fold selectivity (&gt;13-29) over wild-type p53 cells.	3-methylene-2-norbornanone	19-45	P53	Homo sapiens	108-111
15482940-2	2004	The lead molecule, 3-methylene-2-norbornanone (3) showed potent activity (LC(50)=3-8 microM) against mutant p53 cell types and many fold selectivity (&gt;13-29) over wild-type p53 cells.	3-methylene-2-norbornanone	19-45	P53	Homo sapiens	176-179
15475000-6	2004	Lithium acted through deregulation of GSK-3beta signaling since (1) it provoked a rapid and sustained phosphorylation of GSK-3beta on the inhibitory serine 9 residue; (2) the GSK-3beta inhibitor SB-415286 mimicked lithium effects by repressing drug-induced apoptosis and CD95 membrane expression; and (3) lithium promoted the disruption of nuclear GSK-3beta/p53 complexes.	Lithium	0-7	P53	Homo sapiens	358-361
15308759-7	2004	Levels of p53 were quantified by sensitive fluorogenic enzyme-linked immunosorbent assay at intervals up to 24 h after exposure of cells to various concentrations of melphalan and monohydroxymelphalan.	monohydroxymelphalan	180-200	P53	Homo sapiens	10-13
15485790-0	2004	[Apoptosis and regulation of expressions of apoptosis-related gene Bcl-2 and p53 induced by selenium dioxide in three leukemia cell lines].	Selenium Oxides	92-108	P53	Homo sapiens	77-80
15485790-1	2004	OBJECTIVE: To investigate the mechanisms underlying the effect of selenium dioxide (SeO(2)) on the proliferation, apoptosis, and apoptosis-related gene expressions of Bcl-2 and p53 in 3 leukemia cell lines NB4, K562 and HL-60.	Selenium Oxides	66-82	P53	Homo sapiens	177-180
15262986-4	2004	MDA, including epothilone B analogue (BMS-247550) and vinblastine, induced apoptosis of Bax-positive HCT116 cells in a p53-dependent manner; p53 was required for MDA-induced Bax conformational change.	epothilone B	15-27	P53	Homo sapiens	119-122
15262986-4	2004	MDA, including epothilone B analogue (BMS-247550) and vinblastine, induced apoptosis of Bax-positive HCT116 cells in a p53-dependent manner; p53 was required for MDA-induced Bax conformational change.	epothilone B	15-27	P53	Homo sapiens	141-144
15247902-6	2004	Along the same line, HCT116 derivatives with increased basal p53 levels, and glioblastoma cells with a doxycycline-inducible p53, also revealed proportionate mitochondrial p53 levels, and even unstressed HCT116 cells had some p53 located at the mitochondria.	Doxycycline	103-114	P53	Homo sapiens	125-128
15247902-6	2004	Along the same line, HCT116 derivatives with increased basal p53 levels, and glioblastoma cells with a doxycycline-inducible p53, also revealed proportionate mitochondrial p53 levels, and even unstressed HCT116 cells had some p53 located at the mitochondria.	Doxycycline	103-114	P53	Homo sapiens	125-128
15247902-6	2004	Along the same line, HCT116 derivatives with increased basal p53 levels, and glioblastoma cells with a doxycycline-inducible p53, also revealed proportionate mitochondrial p53 levels, and even unstressed HCT116 cells had some p53 located at the mitochondria.	Doxycycline	103-114	P53	Homo sapiens	125-128
15293988-0	2004	A nonpeptidic sulfonamide inhibits the p53-mdm2 interaction and activates p53-dependent transcription in mdm2-overexpressing cells.	Sulfonamides	14-25	P53	Homo sapiens	39-42
15293988-0	2004	A nonpeptidic sulfonamide inhibits the p53-mdm2 interaction and activates p53-dependent transcription in mdm2-overexpressing cells.	Sulfonamides	14-25	P53	Homo sapiens	74-77
15293988-1	2004	The evaluation of a sulfonamide inhibitor of the p53-mdm2 interaction is presented.	Sulfonamides	20-31	P53	Homo sapiens	49-52
15319038-4	2004	Coinfection of Ad vectors containing the siRNA expression system under the control of the Dox-inducible H1 promoter and Ad vectors expressing a tetracycline repressor inhibited the expression levels of p53 and c-Myc in a dose-dependent manner with both Dox and viral dose.	Doxycycline	90-93	P53	Homo sapiens	202-205
15319038-4	2004	Coinfection of Ad vectors containing the siRNA expression system under the control of the Dox-inducible H1 promoter and Ad vectors expressing a tetracycline repressor inhibited the expression levels of p53 and c-Myc in a dose-dependent manner with both Dox and viral dose.	Doxycycline	253-256	P53	Homo sapiens	202-205
15193998-2	2004	Though it was previously reported that LMB induces cell cycle arrest and p53-mediated apoptosis in certain cancer cells, however, the mechanism by which LMB induces apoptosis remains poorly understood.	leptomycin B	39-42	P53	Homo sapiens	73-76
15107830-7	2004	Most cells exhibited elevated levels of p53 in response to hypoxia mimetics such as deferoxamine mesylate and CoCl(2), regardless of their HIF-alpha protein expression profile.	Deferoxamine	84-105	P53	Homo sapiens	40-43
15095302-2	2004	A selective mutation in TP53 (AGG--&gt;AGT at codon 249, Arg--&gt;Ser) has been identified as a hotspot in HCCs from such areas, reflecting DNA damage caused by aflatoxin metabolites.	Aflatoxins	161-170	P53	Homo sapiens	24-28
15494865-5	2004	Significant correlations were also found between Ki-67 (p &lt; 0.0005) and p53 (p &lt; 0.0005) LIs and histologic subtypes.	lis	95-98	P53	Homo sapiens	75-78
15376261-3	2004	The present study investigated the frequency and nature of p53 expression and mutation in 11 biphasic and three monophasic MCBs by immunohistochemistry and either needle-assisted or laser-capture microdissection, followed by PCR and direct sequencing.	mcbs	123-127	P53	Homo sapiens	59-62
15370252-15	2004	Therefore, the association of IPI with cellular factors, such as p53 mutation, can be very helpful in deciding when we should indicate more aggressive therapies in patients with DLBCL, to somehow increase the chance of cure in these patients.	diprotin A	30-33	P53	Homo sapiens	65-68
30925722-3	2019	In p53 wild-type cells, TMZ activates p-p53ser15 and p-p53ser46, which have opposing dual functions regulating survival and death, respectively.	Temozolomide	24-27	P53	Homo sapiens	3-6
15302096-3	2004	NALM-6, which had a high expression level of p53, a tumor suppressor gene, was most susceptible to Ara-C.	Cytarabine	99-104	P53	Homo sapiens	45-48
15302096-7	2004	Pifithrin-alpha, a chemical inhibitor of wild-type p53, ameliorated the cytotoxicity of Ara-C in NALM-6 and MOLT-4, but not Jurkat, U937 or HL-60.	Cytarabine	88-93	P53	Homo sapiens	51-54
15302096-8	2004	Our data suggest that the mechanism of Ara-C-induced cell death is a common one, involving an increase in the production of ROS and p53-dependent cell death.	Cytarabine	39-44	P53	Homo sapiens	132-135
30418550-8	2019	Overall, the p53 status turned out to be an important determinant for the potential benefit of dietary ellagitannins in cancer chemoprevention or use in adjuvant therapy.	Hydrolyzable Tannins	103-116	P53	Homo sapiens	13-16
15342409-4	2004	Using synthetic DNA containing 8-oxo-7,8-dihydro-2"-deoxyguanosine (8-oxoG), we showed that p53 was pulled down together with two BER proteins, human 8-oxoguanine glycosylase (hOGG1) and AP endonuclease (APE).	8-ohdg	31-66	P53	Homo sapiens	92-95
15342409-4	2004	Using synthetic DNA containing 8-oxo-7,8-dihydro-2"-deoxyguanosine (8-oxoG), we showed that p53 was pulled down together with two BER proteins, human 8-oxoguanine glycosylase (hOGG1) and AP endonuclease (APE).	8-ohdg	68-74	P53	Homo sapiens	92-95
30765875-6	2019	RESULTS: Using a proteomic approach, we have shown that Notch3 is strongly involved in brivanib resistance through a p53-dependent regulation of enzymes of the tricarboxylic acid (TCA), both in vitro and in vivo.	Tricarboxylic Acids	160-178	P53	Homo sapiens	117-120
15231731-3	2004	Based on cDNA microarrays and protein analysis, we found that FUS at the intermediate peak pressure of 1.5 MPa induced a complex signaling cascade with upregulation of proapoptotic genes [e.g., p53, p21, Thy1 (CD 90)].	fusarubin	62-65	P53	Homo sapiens	194-197
30765875-6	2019	RESULTS: Using a proteomic approach, we have shown that Notch3 is strongly involved in brivanib resistance through a p53-dependent regulation of enzymes of the tricarboxylic acid (TCA), both in vitro and in vivo.	Tricarboxylic Acids	180-183	P53	Homo sapiens	117-120
30842655-4	2019	Here we report that the tumour suppressor p53, the most frequently mutated gene in human tumours, regulates ammonia metabolism by repressing the urea cycle.	Ammonia	108-115	P53	Homo sapiens	42-45
30842655-5	2019	Through transcriptional downregulation of CPS1, OTC and ARG1, p53 suppresses ureagenesis and elimination of ammonia in vitro and in vivo, leading to the inhibition of tumour growth.	Ammonia	108-115	P53	Homo sapiens	62-65
15212949-2	2004	We demonstrate here that exposing A549 human alveolar type 2 adenocarcinoma cells to hyperoxia (95% O(2)) for 0.5-24 h time-dependently increases phospho-ERK, phospho-p53(Ser15), p53, and p21(CIP1) protein levels.	o(2)	100-104	P53	Homo sapiens	167-170
15212949-2	2004	We demonstrate here that exposing A549 human alveolar type 2 adenocarcinoma cells to hyperoxia (95% O(2)) for 0.5-24 h time-dependently increases phospho-ERK, phospho-p53(Ser15), p53, and p21(CIP1) protein levels.	o(2)	100-104	P53	Homo sapiens	179-182
30550954-5	2019	Early results from our group indicated that 4-nerolidylcatechol (4-NC), a catechol compound extracted from Pothomorphe umbellata, induces DNA damage, ROS production, increased p53 expression culminating in apoptosis in melanoma but with no data regarding the 4-NC effects in cells resistant to BRAFi or MEKi.	catechol	55-63	P53	Homo sapiens	176-179
15102862-3	2004	In this report, we show that doxycycline increased superoxide generation and subsequently activated NF-kappaB, which in turn up-regulated p53 expression and increased the stability and DNA binding activity of p53.	Doxycycline	29-40	P53	Homo sapiens	138-141
15102862-3	2004	In this report, we show that doxycycline increased superoxide generation and subsequently activated NF-kappaB, which in turn up-regulated p53 expression and increased the stability and DNA binding activity of p53.	Doxycycline	29-40	P53	Homo sapiens	209-212
30591552-7	2019	SIGNIFICANCE: Disruption of the Rbm38-eIF4E complex via synthetic peptides induces wild-type p53 expression, suppresses tumor growth and progression, and may serve as a novel cancer therapeutic strategy.	Peptides	66-74	P53	Homo sapiens	93-96
15149862-3	2004	Loss of WRN or TP53 function resulted in induction of apoptosis and lesser proliferative survival in response to AraC and bleomycin.	Cytarabine	113-117	P53	Homo sapiens	15-19
15064747-3	2004	In contrast, in these cells, IPTG-dependent induction of p14ARF, which sequesters MDM2 away from p53, does not lead to detectable phosphorylation of any of the five N-terminal serine residues tested (6, 9, 15, 20, 37).	Isopropyl Thiogalactoside	29-33	P53	Homo sapiens	97-100
30754632-0	2019	Nanoformulation of a Novel Pyrano[2,3-c] Pyrazole Heterocyclic Compound AMDPC Exhibits Anti-Cancer Activity via Blocking the Cell Cycle through a P53-Independent Pathway.	pyrano[2,3-c] pyrazole	27-49	P53	Homo sapiens	146-149
15081398-3	2004	BP-treatment was found to dramatically alter their functional capacities and to trigger a caspase- and mitochondrion-related apoptosis, associated with down-regulation of the survival factors c-FLIP(L) and Bcl-X(L) and up-regulation of the pro-apoptotic factor p53.	Benzo(a)pyrene	0-2	P53	Homo sapiens	261-264
30578766-0	2019	An N6-methyladenosine at the transited codon 273 of p53 pre-mRNA promotes the expression of R273H mutant protein and drug resistance of cancer cells.	N-methyladenosine	3-21	P53	Homo sapiens	52-55
15163458-11	2004	CONCLUSIONS: This study provides evidence that redox-active (Fe2+), (Mn2+), (Cu2+), and (Zn2+) ion-induced apoptosis in PBL by (H2O2)/(.OH) generation, resulting in mitochondria depolarization, caspase-3 activation, and nuclear fragmentation independent of NF-kappaB and p53 transcription factors activation.	Manganese(2+)	69-73	P53	Homo sapiens	271-274
30578766-3	2019	Herein, we report that an N6-methyladenosine (m6A) at the point-mutated codon 273 (G &gt; A) of p53 pre-mRNA determines the mutant protein expression.	N-methyladenosine	26-44	P53	Homo sapiens	96-99
14980218-1	2004	Using high-density oligonucleotide arrays representing essentially all nonrepetitive sequences on human chromosomes 21 and 22, we map the binding sites in vivo for three DNA binding transcription factors, Sp1, cMyc, and p53, in an unbiased manner.	density oligonucleotide	11-34	P53	Homo sapiens	220-223
30578766-3	2019	Herein, we report that an N6-methyladenosine (m6A) at the point-mutated codon 273 (G &gt; A) of p53 pre-mRNA determines the mutant protein expression.	N-methyladenosine	46-49	P53	Homo sapiens	96-99
30559058-0	2019	Aggressive Leukemic Non-Nodal Mantle Cell Lymphoma With P53 Gene Rearrangement/Mutation is Highly Responsive to Rituximab/Ibrutinib Combination Therapy.	ibrutinib	122-131	P53	Homo sapiens	56-59
14960327-9	2004	Furthermore, the interaction of p53 with Bcl-x(L) is blocked by the binding of a 25-residue peptide derived from the BH3 region of the pro-apoptotic protein referred to as Bad.	BH 3	117-120	P53	Homo sapiens	32-35
30400061-2	2019	This tumor suppression system is based upon the kill switch being triggered in cells in which p53 has been inactivated; such kill switch consisting of a rapid, catastrophic increase in ROS caused by the induction of irreversible uncompetitive inhibition of glucose-6- phosphate dehydrogenase (G6PD), which requires high concentrations of both inhibitor (DHEA) and G6P substrate.	Dehydroepiandrosterone	354-358	P53	Homo sapiens	94-97
14712090-0	2004	Tocotrienol-rich fraction of palm oil activates p53, modulates Bax/Bcl2 ratio and induces apoptosis independent of cell cycle association.	Tocotrienols	0-11	P53	Homo sapiens	48-51
31459462-5	2019	Dialkyne 3 was successfully employed for "peptide stapling" of a p53-based diazido peptide, whereby two azides are bridged to give a product with a stabilized conformation.	Azides	104-110	P53	Homo sapiens	65-68
14737105-8	2004	Further, GGTIs suppress survivin expression and induce programmed cell death in both wild-type p53 and p53-deficient ovarian cancer cell lines.	ggtis	9-14	P53	Homo sapiens	95-98
30745855-0	2019	Andrographolide Enhances TRAIL-Induced Apoptosis via p53-Mediated Death Receptors Up-Regulation and Suppression of the NF-kB Pathway in Bladder Cancer Cells.	andrographolide	0-15	P53	Homo sapiens	53-56
14657672-2	2004	Two distinct synthetic CDK1/2 inhibitors, Roscovitine and NU2058, are pharmacologically distinct in their ability to modify p53-dependent transcription and perturb cell cycle progression.	NU2058	58-64	P53	Homo sapiens	124-127
14702110-7	2004	Avicins inhibited epidermal hyperplasia, reduced p53 mutation, enhanced apoptosis, decreased generation of 8-hydroxy-2"-deoxyguanosine, and enhanced expression of NADPH:quinone oxidoreductase 1 and heme oxygenase-1.	avicins	0-7	P53	Homo sapiens	49-52
30362193-0	2019	beta-Ketoiminato Iridium(III) Organometallic Complexes: Selective Cytotoxicity towards Colorectal Cancer Cells HCT116 p53-/.	Iridium	17-24	P53	Homo sapiens	118-121
14662026-0	2003	Leptomycin B enhances CDDP-sensitivity via nuclear accumulation of p53 protein in HPV-positive cells.	leptomycin B	0-12	P53	Homo sapiens	67-70
30362193-4	2019	This work provides a preliminary understanding of the cytotoxicity of iridium compounds in the absence of p53 and has potential applications in treatment of cancers for which the p53 gene is absent or mutant.	Iridium	70-77	P53	Homo sapiens	179-182
14662026-7	2003	After exposure to LMB or CDDP alone, we observed weak p53 staining in HeLa, SiHa and Yumoto cells.	leptomycin B	18-21	P53	Homo sapiens	54-57
14662026-8	2003	Nuclear p53 staining was significantly increased by combined treatment with CDDP and LMB in HeLa and SiHa cells, but not in Yumoto cells.	leptomycin B	85-88	P53	Homo sapiens	8-11
14662026-10	2003	The present study demonstrated that LMB enhanced CDDP-sensitivity via nuclear accumulation of p53 protein in HPV-positive cells.	leptomycin B	36-39	P53	Homo sapiens	94-97
30361254-5	2019	Temozolomide-induced senescence required functional p53 and was dependent on sustained p21 induction.	Temozolomide	0-12	P53	Homo sapiens	52-55
14612973-5	2003	The induction of apoptosis by manumycin involved the upregulation of p53 and p21WAF1, the activation of caspases, and the inhibition of nuclear factor-kappaB (NF-kappaB) pathway.	manumycin	30-39	P53	Homo sapiens	69-72
30145226-6	2019	Treatment with pifithrin-alpha-HBr (PFTalpha), a specific blocker of p53-responsive gene transactivation, reduced the P4-increased p27 promoter activity and p27 protein expression.	pifithrin-alpha-hbr	15-34	P53	Homo sapiens	69-72
14612935-8	2003	The addition of ubiquitin carboxyl terminal hydrolase (UCH-L1) inhibitor (NaBH4) inhibited up-regulation of p53 and p53 related molecules by XK469 and reduced the loss of viability.	sodium borohydride	74-79	P53	Homo sapiens	108-111
31168028-9	2019	Taken together, our results demonstrate that PHMG-p triggered G1/S arrest and apoptosis through the ROS/ATM/p53 pathway in lung epithelial cells.	polyhexamethyleneguanidine	45-51	P53	Homo sapiens	108-111
14612935-8	2003	The addition of ubiquitin carboxyl terminal hydrolase (UCH-L1) inhibitor (NaBH4) inhibited up-regulation of p53 and p53 related molecules by XK469 and reduced the loss of viability.	sodium borohydride	74-79	P53	Homo sapiens	116-119
14713572-9	2003	Moreover, in the G2/M-phase, an increase in p53 and a decrease in survivin occurred that were X-ray and Ara-C dose dependent.	Cytarabine	104-109	P53	Homo sapiens	44-47
30199712-4	2018	Anti-p53 antibodies were captured on the modified ITO electrode through the cross-linking of chitosan and glutaraldehyde.	Glutaral	106-120	P53	Homo sapiens	5-8
15130758-4	2004	Therefore, we investigated the roles of the mitogen-activated protein kinases (MAPKs) and the tumor suppressor gene, p53, during cantharidin-induced apoptosis in U937 human leukemic cells.	Cantharidin	129-140	P53	Homo sapiens	117-120
30296496-0	2018	Mutant p53 prevents GAPDH nuclear translocation in pancreatic cancer cells favoring glycolysis and 2-deoxyglucose sensitivity.	Deoxyglucose	99-113	P53	Homo sapiens	7-10
15130758-9	2004	Cantharidin alone induced the apoptosis by phosphorylation of p53, up-regulation of downstream target genes, MDM2 and p21 and also cleaved caspase-3, whereas SB202190 and SP600125 caused the down-regulation of p53, MDM-2, p21 and cleaved caspase-3 after a co-treatment with cantharidin.	Cantharidin	0-11	P53	Homo sapiens	62-65
15130758-9	2004	Cantharidin alone induced the apoptosis by phosphorylation of p53, up-regulation of downstream target genes, MDM2 and p21 and also cleaved caspase-3, whereas SB202190 and SP600125 caused the down-regulation of p53, MDM-2, p21 and cleaved caspase-3 after a co-treatment with cantharidin.	Cantharidin	0-11	P53	Homo sapiens	210-213
15130758-11	2004	Taken together, these results suggest that cantharidin can induce apoptosis by activation of p38 and JNK MAP kinase pathways associated with p53 and caspase-3.	Cantharidin	43-54	P53	Homo sapiens	141-144
12934079-7	2003	p53-deficient neurons demonstrated decreased sensitivity to ara-C, but neither p53 nor multiple p53-regulated genes were induced.	Cytarabine	60-65	P53	Homo sapiens	0-3
12969763-7	2003	In addition, UVA-induced enhanced expression of p53, a hallmark of UV-induced DNA damage and cell death, was also significantly inhibited by pretreatment with asiatic acid or ursolic acid.	asiatic acid	159-171	P53	Homo sapiens	48-51
15150125-0	2004	Flavopiridol induces p53 via initial inhibition of Mdm2 and p21 and, independently of p53, sensitizes apoptosis-reluctant cells to tumor necrosis factor.	alvocidib	0-12	P53	Homo sapiens	21-24
30296496-7	2018	Finally, our data suggest that mutp53-dependent enhanced glycolysis permits cancer cells to acquire sensitivity to anti-glycolytic drugs, such as 2-deoxyglucose, suggesting a potential personalized therapeutic approach in human cancers carrying mutant TP53 gene.	Deoxyglucose	146-160	P53	Homo sapiens	252-256
28374118-1	2018	In the proposed work, we have explicated the mechanism of dibenzo[a,l]pyrene (DBP) and benzo[a]pyrene (BP) modulated cell proliferation by assessing the plausible binding with CASPASES, BAX, Bcl-2, MDM2, p53, p21, p16, CylinD1-CDK4 complex, CylinE1-CDK2 complex, H-Ras, K-Ras, BRCA1, and BRCA2 through exploiting the inherent potential of AutoDock Tools 4.0.	Benzo(a)pyrene	87-101	P53	Homo sapiens	204-207
15072824-8	2004	The high formation of BPDE-N(2)-dG adducts in bronchial epithelial cells and investigations showing that the profile of mutations induced by BPDE in these cells is similar to that seen in the p53 gene isolated from human lung tumors implicates benzo[a]pyrene as important carcinogen in tobacco-induced lung cancer in human beings.	benzo(a)pyrene 7,8-diol-9,10-epoxide-N2-deoxyguanosine	22-34	P53	Homo sapiens	192-195
15072824-8	2004	The high formation of BPDE-N(2)-dG adducts in bronchial epithelial cells and investigations showing that the profile of mutations induced by BPDE in these cells is similar to that seen in the p53 gene isolated from human lung tumors implicates benzo[a]pyrene as important carcinogen in tobacco-induced lung cancer in human beings.	Benzo(a)pyrene	244-258	P53	Homo sapiens	192-195
12807757-3	2003	The current study examines the ability of acrolein to modulate the effect of benzo[a]pyrene (B[a]P), a major carcinogen found in smoke, on p53.	Benzo(a)pyrene	77-91	P53	Homo sapiens	139-142
28374118-1	2018	In the proposed work, we have explicated the mechanism of dibenzo[a,l]pyrene (DBP) and benzo[a]pyrene (BP) modulated cell proliferation by assessing the plausible binding with CASPASES, BAX, Bcl-2, MDM2, p53, p21, p16, CylinD1-CDK4 complex, CylinE1-CDK2 complex, H-Ras, K-Ras, BRCA1, and BRCA2 through exploiting the inherent potential of AutoDock Tools 4.0.	Benzo(a)pyrene	79-81	P53	Homo sapiens	204-207
12807744-3	2003	Interestingly, the methylxanthine caffeine can abrogate the p53 accumulation induced by certain DNA-damaging agents by an unknown mechanism.	methylxanthine	19-33	P53	Homo sapiens	60-63
12807744-5	2003	Caffeine inhibited the accumulation of p53 induced by leptomycin B (LMB), an inhibitor of CRM1, but not N-acetyl-leu-leu-norleucinal, a proteasome inhibitor.	leptomycin B	54-66	P53	Homo sapiens	39-42
28374118-4	2018	Diol-epoxides of DBP and BP were found to bind to p53 with tighter interaction than MDM2 and p53-MDM2 complex.	Benzo(a)pyrene	18-20	P53	Homo sapiens	50-53
12807744-5	2003	Caffeine inhibited the accumulation of p53 induced by leptomycin B (LMB), an inhibitor of CRM1, but not N-acetyl-leu-leu-norleucinal, a proteasome inhibitor.	leptomycin B	68-71	P53	Homo sapiens	39-42
15087416-0	2004	Correspondence re: M. V. Swamy et al., Inhibition of COX-2 in colon cancer cell lines by celecoxib increases the nuclear localization of active p53.	Celecoxib	89-98	P53	Homo sapiens	144-147
28374118-4	2018	Diol-epoxides of DBP and BP were found to bind to p53 with tighter interaction than MDM2 and p53-MDM2 complex.	Benzo(a)pyrene	18-20	P53	Homo sapiens	93-96
30384473-8	2018	We found that Evo significantly induced cell cycle arrest at the G2/M phase, upregulated P53 and Bcl-2 associated X proteins (Bax) proteins, and downregulated B-cell lymphoma-2 (Bcl-2), cyclinB1, and cdc2 proteins in HCC cells.	evodiamine	14-17	P53	Homo sapiens	89-92
14660655-4	2004	When p53-mutated cancer cell lines (MDA-MB-231 breast cancer cell and SW620 colon cancer cell) were treated with 10 microM HCA or BCA, it induced growth arrest and apoptosis of tumor cells.	hca	123-126	P53	Homo sapiens	5-8
14766355-8	2004	These results support the conclusion that doxycycline induces p53-dependent apoptosis in MM7P.	Doxycycline	42-53	P53	Homo sapiens	62-65
14513366-1	2003	PURPOSE: Resistance to chemotherapeutic drugs is a hallmark of many human cancers, which can occur independent of p53 gene status; however, the presence of wild-type p53 in chemorefractory tumors confers greater resistance to cisplatin, but such tumors do not display complete cross-resistance to the platinum analog (1R,2R-diaminocyclohexane)(trans-diacetato)(dichloro)platinumIV (DACH-Ac-Pt).	(diaminocyclohexane)(diacetato)(dichloro)platinum	382-392	P53	Homo sapiens	166-169
14513366-4	2003	RESULTS: In response to CDDP and DACH-Ac-Pt, both CDDP-sensitive and CDDP-resistant models demonstrated time- and dose-dependent inductions of total p53 protein and an increase in Ser-15 phosphorylation, which was more pronounced with CDDP.	(diaminocyclohexane)(diacetato)(dichloro)platinum	33-43	P53	Homo sapiens	149-152
14617104-0	2003	Effects of a melanogenic bicyclic monoterpene diol on cell cycle, p53, TNF-alpha, and PGE2 are distinct from those of UVB.	bicyclic	25-33	P53	Homo sapiens	66-69
12787880-0	2003	Enforced expression of the tumor suppressor p53 renders human leukemia cells (U937) more sensitive to 1-[beta-D-arabinofuranosyl]cytosine (ara-C)-induced apoptosis.	Cytarabine	102-137	P53	Homo sapiens	44-47
12787880-0	2003	Enforced expression of the tumor suppressor p53 renders human leukemia cells (U937) more sensitive to 1-[beta-D-arabinofuranosyl]cytosine (ara-C)-induced apoptosis.	Cytarabine	139-144	P53	Homo sapiens	44-47
12787880-7	2003	Significantly, ptsp53 cells synchronized in S phase were markedly more sensitive to ara-C-mediated mitochondrial injury and apoptosis at 32 degrees, indicating that wild-type p53 specifically enhances the susceptibility of this subpopulation to ara-C lethality.	Cytarabine	84-89	P53	Homo sapiens	18-21
12787880-8	2003	Consistent with these results, transient transfection of human wild-type p53 cDNA rendered parental U937 cells more sensitive to ara-C-mediated cell death.	Cytarabine	129-134	P53	Homo sapiens	73-76
12787880-9	2003	Collectively, these findings indicate that p53 expression renders S-phase U937 cells more susceptible to ara-C-mediated mitochondrial dysfunction, cytochrome c release, apoptosis, and loss of clonogenic survival without enhancing ara-C metabolism.	Cytarabine	105-110	P53	Homo sapiens	43-46
12781215-7	2003	Ara-C increased the level of p53 in both CV1-P and SH-SY5Y cells compared to control.	Cytarabine	0-5	P53	Homo sapiens	29-32
12781215-10	2003	Our results prove that Ara-C- induced apoptosis in CV1-P cells is associated with an increase of p53 and activation of caspase-3.	Cytarabine	23-28	P53	Homo sapiens	97-100
12642583-5	2003	1,5-Dihydroxyisoquinoline treatment prior to ionizing radiation delayed and attenuated the induction of two p53-responsive genes, p21 and mdm-2, and led to suppression of the p53-mediated G1-arrest response in MCF-7 and BJ/TERT cells.	1,5-dihydroxyisoquinoline	0-25	P53	Homo sapiens	108-111
12642583-5	2003	1,5-Dihydroxyisoquinoline treatment prior to ionizing radiation delayed and attenuated the induction of two p53-responsive genes, p21 and mdm-2, and led to suppression of the p53-mediated G1-arrest response in MCF-7 and BJ/TERT cells.	1,5-dihydroxyisoquinoline	0-25	P53	Homo sapiens	175-178
14633737-9	2003	Treatment with Let, Tam, or E2W resulted in a dose- and time-dependent increase in active caspase-7 and up-regulation of p53 and p21 protein.	Letrozole	15-18	P53	Homo sapiens	121-124
29883905-13	2018	Also, the decrease in p53 gene expression, even at low exposure levels, reinforces the carcinogenicity effect of benzene in this pathway.	Benzene	113-120	P53	Homo sapiens	22-25
14644313-10	2003	Thus, for benzo(a)pyrene (at 10-50 adducts per 10(8) nucleotides) repair was essentially complete within 1 day in p53(+/+) human fibroblasts while no repair was detected within 3 days in p53(-/-) cells.	Benzo(a)pyrene	10-24	P53	Homo sapiens	114-117
14644313-10	2003	Thus, for benzo(a)pyrene (at 10-50 adducts per 10(8) nucleotides) repair was essentially complete within 1 day in p53(+/+) human fibroblasts while no repair was detected within 3 days in p53(-/-) cells.	Benzo(a)pyrene	10-24	P53	Homo sapiens	187-190
14644313-11	2003	The levels of all four DNA adducts formed by benzo(g)chrysene, also exhibited p53-dependent control in human fibroblasts.	benzo(g)chrysene	45-61	P53	Homo sapiens	78-81
12713809-5	2003	The in situ repair kinetics revealed that p53-WT normal fibroblasts are proficient for the repair of both CPD and 6-4PP, whereas, p53-Null Li-Fraumeni syndrome (LFS) fibroblasts fail to efficiently repair CPD but not 6-4PP.	6-4pp	114-119	P53	Homo sapiens	42-45
12713809-5	2003	The in situ repair kinetics revealed that p53-WT normal fibroblasts are proficient for the repair of both CPD and 6-4PP, whereas, p53-Null Li-Fraumeni syndrome (LFS) fibroblasts fail to efficiently repair CPD but not 6-4PP.	6-4pp	217-222	P53	Homo sapiens	42-45
12713809-5	2003	The in situ repair kinetics revealed that p53-WT normal fibroblasts are proficient for the repair of both CPD and 6-4PP, whereas, p53-Null Li-Fraumeni syndrome (LFS) fibroblasts fail to efficiently repair CPD but not 6-4PP.	6-4pp	217-222	P53	Homo sapiens	130-133
12702563-4	2003	In HeLa cells stably transfected with the reporter gene and interacting (p53-TAg) or noninteracting (p53 and polyoma virus coat protein) pairs of proteins, treatment with doxycycline produced time- and dose-dependent increases in expression of hybrid proteins.	Doxycycline	171-182	P53	Homo sapiens	73-76
12702563-4	2003	In HeLa cells stably transfected with the reporter gene and interacting (p53-TAg) or noninteracting (p53 and polyoma virus coat protein) pairs of proteins, treatment with doxycycline produced time- and dose-dependent increases in expression of hybrid proteins.	Doxycycline	171-182	P53	Homo sapiens	101-104
14500353-14	2003	Inhibition of COX-2 by celecoxib appears to alleviate this effect on p53 by reducing electrophilic PG synthesis.	Celecoxib	23-32	P53	Homo sapiens	69-72
29883905-14	2018	Therefore, our results suggest that the promotion of immune evasion together with a decrease in p53 gene expression may play an important role in the benzene toxicity mechanism.	Benzene	150-157	P53	Homo sapiens	96-99
30197678-8	2018	In conclusion, TGCG induced cell cycle arrest at the G0/G1 and G2/M phases and induced apoptosis in HT-29 cells through the c-Myc- and p53-mediated signaling pathways, possibly in response to DNA damage.	tgcg	15-19	P53	Homo sapiens	135-138
12820894-2	2003	It has been reported that 4-HNE treatment in human cells induces a high frequency of G.C to T.A mutations at the third base of codon 249 (AGG*) of the p53 gene, a mutational hot spot in human cancers, particularly in hepatocellular carcinoma.	4-hydroxy-2-nonenal	26-31	P53	Homo sapiens	151-154
12679912-1	2003	AIM: One of the characteristics of hepatocellular carcinoma (HCC) in Qidong area is the selective mutation resulting in a serine substitution at codon 249 of the p53 gene (1, 20), and it has been identified as a "hotspot" mutation in heptocellular carcinomas occurring in populations exposed to aflatoxin and with high prevalence of hepatitis B virus carriers (2,3,9, 10,16,24).	Aflatoxins	295-304	P53	Homo sapiens	162-165
12424231-0	2003	Electrophilic prostaglandins and lipid aldehydes repress redox-sensitive transcription factors p53 and hypoxia-inducible factor by impairing the selenoprotein thioredoxin reductase.	lipid aldehydes	33-48	P53	Homo sapiens	95-98
12712406-9	2003	Re-introduction of wild type p53 into PC-3 and DU145 completely suppressed these inhibitory effects.	du145	47-52	P53	Homo sapiens	29-32
29908302-0	2018	Inhibitory effect of PXR on ammonia-induced hepatocyte autophagy via P53.	Ammonia	28-35	P53	Homo sapiens	69-72
12714181-1	2003	G--&gt;T transversions in the TP53 gene are more common in lung cancers from smokers than in any other cancer except for hepatocellular carcinomas linked to aflatoxin.	Aflatoxins	157-166	P53	Homo sapiens	30-34
12538356-4	2003	Ultraviolet (UV) light from the sun and polycyclic aromatic hydrocarbons, such as benzo[a]pyrene, are strongly implicated in the spectrum of p53 mutations found in human non-melanoma skin cancers and smoking-associated lung cancers, respectively.	Benzo(a)pyrene	82-96	P53	Homo sapiens	141-144
12183079-0	2002	Asiatic acid, a triterpene, induces apoptosis through intracellular Ca2+ release and enhanced expression of p53 in HepG2 human hepatoma cells.	asiatic acid	0-12	P53	Homo sapiens	108-111
12628256-2	2003	The recent design of a backbone cyclized protein catenane based on the p53tet domain suggested that topological cross-linking provided increased stability against thermal and chemical denaturation.	catenane	49-57	P53	Homo sapiens	71-74
12435813-6	2002	We further investigated p53/p56 Lyn activation in PKCzeta-overexpressing U937 cells treated with ara-C or DNR.	Cytarabine	97-102	P53	Homo sapiens	24-27
29908302-7	2018	These findings indicate that PXR is a factor interfering the formation of ammonia-induced hepatocyte autophagy, and its inhibitory effect is achieved when P53 downregulates the expression and activity of AMPKbeta1.	Ammonia	74-81	P53	Homo sapiens	155-158
12641444-7	2003	Of this group, arsenic trioxide was the strongest inducer of cellular p53, while dimethylarsinic acid, iododimethylarsine, and sodium arsenite also caused p53 induction in a dose- and time-dependent manner.	Iododimethylarsine	103-121	P53	Homo sapiens	155-158
30246777-6	2018	We also found that the protein and mRNA levels of Bax, p53, and Fas dose-dependently increased in DFO-treated K562 cells, while the level of Bcl-2 markedly decreased in a dose-dependent manner.	Deferoxamine	98-101	P53	Homo sapiens	55-58
12650433-5	2003	In MGMT-depleted cells, TMZ exposure led to DNA single-strand breaks and phosphorylation of cdc2, followed by G2-M arrest, induction of p53/p21, and DNA double-strand breaks.	Temozolomide	24-27	P53	Homo sapiens	136-139
12390361-8	2002	p53 protein was more often positive in stromal cells of HCP (67%) than in LCP (50%).	hcp	56-59	P53	Homo sapiens	0-3
29752478-6	2018	Furthermore, bafilomycin C1 decreased the expression of Bcl-2; increased the expression of Bax, p53, and P-p53; and increased cleavage of caspase-9 and caspase-3, thereby inducing the intrinsic caspase-dependent apoptotic pathway.	bafilomycin C1	13-27	P53	Homo sapiens	96-99
12395332-7	2002	A similar relative risk was found using 249ser-p53 mutation as a marker for aflatoxin exposure.	Aflatoxins	76-85	P53	Homo sapiens	47-50
12435844-3	2002	The improvements in exposure assessment and their application in prospective epidemiological studies and the demonstration of a specific mutation in the TP53 gene in hepatocellular carcinomas from areas of high aflatoxin exposure have contributed significantly to the classification of aflatoxins as human carcinogens.	Aflatoxins	211-220	P53	Homo sapiens	153-157
12435844-3	2002	The improvements in exposure assessment and their application in prospective epidemiological studies and the demonstration of a specific mutation in the TP53 gene in hepatocellular carcinomas from areas of high aflatoxin exposure have contributed significantly to the classification of aflatoxins as human carcinogens.	Aflatoxins	286-296	P53	Homo sapiens	153-157
29752478-6	2018	Furthermore, bafilomycin C1 decreased the expression of Bcl-2; increased the expression of Bax, p53, and P-p53; and increased cleavage of caspase-9 and caspase-3, thereby inducing the intrinsic caspase-dependent apoptotic pathway.	bafilomycin C1	13-27	P53	Homo sapiens	107-110
30302047-6	2018	Ammonia-induced senescence in astrocytes involves glutamine synthesis-dependent formation of reactive oxygen species (ROS), p53 activation and upregulation of cell cycle inhibitory factors p21 and GADD45alpha.	Ammonia	0-7	P53	Homo sapiens	124-127
12376521-2	2002	A specific missense mutation resulting from a guanine to thymine transversion at the third position of codon 249 in the p53 tumor suppressor gene has been reported in 10-70% of HCCs from areas of high dietary exposure to aflatoxin B(1.)	Thymine	57-64	P53	Homo sapiens	120-123
11945174-9	2002	Finally, DFO-induced senescence-like arrest was found to be independent of p53, since cell-cycle arrest was still observed with two p53-negative cell lines, Huh7 and Hep3B cells.	dfo	9-12	P53	Homo sapiens	132-135
29749471-9	2018	Furthermore, blockade of temozolomide (TMZ)-induced autophagy by 3-methyladenine (3-MA) resulted in enhanced activation of apoptotic markers, as well as tumor suppresor protein p53 (p53) expression in U87MG cells.	Temozolomide	25-37	P53	Homo sapiens	177-180
12175902-1	2002	Wild-type p53 protein is known to regulate the global genomic repair (GGR), removing bulky chemical DNA adducts as well as cyclobutane pyrimidine dimers from the genome overall and from non-transcribed strands (NTS) in DNA.	cyclobutane pyrimidine	123-145	P53	Homo sapiens	10-13
29749471-9	2018	Furthermore, blockade of temozolomide (TMZ)-induced autophagy by 3-methyladenine (3-MA) resulted in enhanced activation of apoptotic markers, as well as tumor suppresor protein p53 (p53) expression in U87MG cells.	Temozolomide	25-37	P53	Homo sapiens	182-185
12160929-8	2002	The levels of p53 and Bax proteins were elevated, while Bcl-2 protein was downregulated in TCE- or PERC-treated p53-WT H460 cells.	Trichloroethylene	91-94	P53	Homo sapiens	112-115
29749471-9	2018	Furthermore, blockade of temozolomide (TMZ)-induced autophagy by 3-methyladenine (3-MA) resulted in enhanced activation of apoptotic markers, as well as tumor suppresor protein p53 (p53) expression in U87MG cells.	Temozolomide	39-42	P53	Homo sapiens	177-180
12160929-10	2002	These data suggest that, in human lung cancer cells, GSH plays a vital role in the protection of TCE- and PERC-induced oxidative stress and apoptosis, which may be mediated through a p53-dependent pathway.	Trichloroethylene	97-100	P53	Homo sapiens	183-186
29749471-9	2018	Furthermore, blockade of temozolomide (TMZ)-induced autophagy by 3-methyladenine (3-MA) resulted in enhanced activation of apoptotic markers, as well as tumor suppresor protein p53 (p53) expression in U87MG cells.	Temozolomide	39-42	P53	Homo sapiens	182-185
29853637-5	2018	We also found that they bind the fluorescent dye 4,4"-dianilino-1,1"-binaphthyl-5,5"-disulfonic acid (bis-ANS) and have a native-like tertiary structure that occludes the single Trp residue in p53.	4,4"-dianilino-1,1"-binaphthyl-5,5"-disulfonic acid	49-100	P53	Homo sapiens	193-196
12118329-3	2002	We created a doxycycline-inducible p53 model from the p53-negative PC-3 prostate cancer cell line.	Doxycycline	13-24	P53	Homo sapiens	35-38
12118329-3	2002	We created a doxycycline-inducible p53 model from the p53-negative PC-3 prostate cancer cell line.	Doxycycline	13-24	P53	Homo sapiens	54-57
12118329-4	2002	Doxycycline treatment increased both p53 and IGFBP-3 levels.	Doxycycline	0-11	P53	Homo sapiens	37-40
29853637-5	2018	We also found that they bind the fluorescent dye 4,4"-dianilino-1,1"-binaphthyl-5,5"-disulfonic acid (bis-ANS) and have a native-like tertiary structure that occludes the single Trp residue in p53.	5,5'-bis(8-(phenylamino)-1-naphthalenesulfonate)	102-109	P53	Homo sapiens	193-196
29508061-4	2018	In the presence of elevated levels of H2S and thiosulfate, the sulfhydryl groups of p53 protein as well as Bcl-2 protein could be modified via HBITC-induced S-sulfuration or by oxidative stress.	Hydrogen Sulfide	38-41	P53	Homo sapiens	84-87
12432259-7	2002	In LNCaP, a prostate cancer cell line which is highly sensitive to p21-induced growth arrest (p21-sensitive), low concentrations of FL (50 nM) induced p21 (without induction of p53) and caused G1 and G2 arrest.	alvocidib	132-134	P53	Homo sapiens	177-180
12065694-7	2002	Treatment with the p53 inhibitor alpha-2-(2-imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone (PFT) before cisplatin exposure inhibited p53 nuclear expression at 4, 8, and 12 h and inhibited phosphatidylserine externalization and caspase 3 activation at 12 h. Neither DEVD-fmk nor ZVAD-fmk inhibited cisplatin-induced p53 nuclear expression.	alpha-2-(2-imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p	33-90	P53	Homo sapiens	19-22
12065694-7	2002	Treatment with the p53 inhibitor alpha-2-(2-imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone (PFT) before cisplatin exposure inhibited p53 nuclear expression at 4, 8, and 12 h and inhibited phosphatidylserine externalization and caspase 3 activation at 12 h. Neither DEVD-fmk nor ZVAD-fmk inhibited cisplatin-induced p53 nuclear expression.	alpha-2-(2-imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p	33-90	P53	Homo sapiens	147-150
12065694-7	2002	Treatment with the p53 inhibitor alpha-2-(2-imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone (PFT) before cisplatin exposure inhibited p53 nuclear expression at 4, 8, and 12 h and inhibited phosphatidylserine externalization and caspase 3 activation at 12 h. Neither DEVD-fmk nor ZVAD-fmk inhibited cisplatin-induced p53 nuclear expression.	alpha-2-(2-imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p	33-90	P53	Homo sapiens	147-150
29756671-5	2018	Interestingly, 6-MSITC inhibited the cell proliferation in both types of cells with similar IC50 value although a light increase in the phosphorylation and accumulation of P53 protein was observed in HCT116 p53+/+ cells at 24 h after treatment.	6-(Methylsulfinyl)hexyl isothiocyanate	15-22	P53	Homo sapiens	207-210
12049655-0	2002	Doxorubicin and octreotide induce a 40 kDa breakdown product of p53 in human hepatoma and tumoral colon cell lines.	Octreotide	16-26	P53	Homo sapiens	64-67
12049655-1	2002	The chemotherapeutic drug doxorubicin and the anti-proliferative long-acting somatostatin analogue octreotide, both used in cancer treatment, have been shown to increase the expression of the p53 tumour suppressor protein.	Octreotide	99-109	P53	Homo sapiens	192-195
29756671-6	2018	In addition, 6-MSITC increased the ratio of proapoptotic cells in both types of cells with the same fashion in a p53-independent manner.	6-(Methylsulfinyl)hexyl isothiocyanate	13-20	P53	Homo sapiens	113-116
12049655-10	2002	These results also suggest that octreotide, a molecule with different signalling pathways, was able as doxorubicin to generate a p53 breakdown product.	Octreotide	32-42	P53	Homo sapiens	129-132
29756671-9	2018	These findings suggest that 6-MSITC might be a potential agent for colon cancer chemoprevention although with p53 mutation.	6-(Methylsulfinyl)hexyl isothiocyanate	28-35	P53	Homo sapiens	110-113
12082016-8	2002	Tp53 was also strongly induced by an N-oxide of quinoline and by dabequine, an experimental antimalarial evaluated in humans; dabequine was reported to be negative in other screens of mutagenicity and clastogenicity but carcinogenic in animal studies.	dabequin	65-74	P53	Homo sapiens	0-4
29805751-4	2018	Our results show that flavopiridol can drastically decrease survival in these osteosarcoma cell lines at nanomolar concentrations and induce mitotic catastrophe in p53-null osteosarcomas.	alvocidib	22-34	P53	Homo sapiens	164-167
12082016-8	2002	Tp53 was also strongly induced by an N-oxide of quinoline and by dabequine, an experimental antimalarial evaluated in humans; dabequine was reported to be negative in other screens of mutagenicity and clastogenicity but carcinogenic in animal studies.	dabequin	126-135	P53	Homo sapiens	0-4
12082016-11	2002	A reported clinical association of Tp53 immunopositive colorectal cancers with use of the antihypertensive agents was extended by the demonstration of hydralazine and nifedipine as Tp53-inducers.	Nifedipine	167-177	P53	Homo sapiens	35-39
12082016-11	2002	A reported clinical association of Tp53 immunopositive colorectal cancers with use of the antihypertensive agents was extended by the demonstration of hydralazine and nifedipine as Tp53-inducers.	Nifedipine	167-177	P53	Homo sapiens	181-185
29436583-9	2018	PD0332991 also inhibited CDK6-specific phosphorylation of retinoblastoma on Ser780, reduced the expression of cyclin D1, and induced expression of p53 and p27.	palbociclib	0-9	P53	Homo sapiens	147-150
11839765-12	2002	However, there was an increase in p53 protein level concomitant with Y-27632-induced cell death.	Y 27632	69-76	P53	Homo sapiens	34-37
11896587-4	2002	In a mouse JB6 epidermal cell line, dominant negative JNK1 abrogated UVB-induced phosphorylation of p53 at serine 20, whereas dominant negative p38 kinase or its inhibitor, SB202190, partially attenuated the phosphorylation.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	173-181	P53	Homo sapiens	100-103
29480432-3	2018	RECENT FINDINGS: Ibrutinib was FDA-approved for the upfront treatment of CLL in 2016 after being studied in older patients and those with 17p deletions or TP53 mutations.	ibrutinib	17-26	P53	Homo sapiens	155-159
11856177-8	2002	When pentoxifylline is added 12-24 h post-irradiation when the cell cycle blocks have reached their maximum the appearance of cells with phosphorylated H3 increases 3-5-fold in the p53 mutant cell lines MeWo and 4451.	Pentoxifylline	5-19	P53	Homo sapiens	181-184
11821962-5	2002	Mutant p53 stimulates recombination induced by the replication elongation inhibitors (aphidicolin, hydroxyurea and Ara-C) but is without effect on recombination induced by the initiation inhibitors (mimosine and ciclopirox olamine).	Cytarabine	115-120	P53	Homo sapiens	7-10
29565268-11	2018	These observations indicate that hinokitiol inhibited the migration of lung cancer A549 cells through several mechanisms, including the activation of caspases-9 and -3, induction of p53/Bax and antioxidant CAT and SOD, and reduction of MMP-2 and -9 activities.	beta-thujaplicin	33-43	P53	Homo sapiens	182-185
11698292-9	2001	In contrast, in vitro treatment with cytarabine and etoposide induced p53 protein, CD95 receptor expression, CD95 sensitivity, and CD95 receptor-ligand interaction in stimulated cycling lymphocytes, but no such induction was seen in resting cells.	Cytarabine	37-47	P53	Homo sapiens	70-73
11593383-8	2001	Depletion of the dephosphorylated HIF-1alpha, by using the Hsp90 inhibitor geldanamycin A that had little effect on the phosphorylated HIF-1alpha expression, suppressed p53 induction and subsequent apoptosis.	geldanamycin a	75-89	P53	Homo sapiens	169-172
29563788-1	2018	Introduction: The nucleobase 2-amino-6-chloropurine-modified polyamidoamine (AP-PAMAM) was used as a carrier for p53 gene delivery to achieve the antitumor effects.	amino-6-chloropurine	31-51	P53	Homo sapiens	113-116
28751770-4	2018	We show that venetoclax synergizes with cytarabine and idarubicin to increase antileukemic efficacy in a TP53-dependent manner.	Cytarabine	40-50	P53	Homo sapiens	105-109
11522624-13	2001	These data are consistent with the hypothesis that chemical carcinogens such as BP in cigarette smoke cause G:C to T:A transversions at p53 codons 157, 248, and 249 and that nontumorous lung tissues from smokers with lung cancer carry a high p53 mutational load at these codons.	Benzo(a)pyrene	80-82	P53	Homo sapiens	136-139
11522624-13	2001	These data are consistent with the hypothesis that chemical carcinogens such as BP in cigarette smoke cause G:C to T:A transversions at p53 codons 157, 248, and 249 and that nontumorous lung tissues from smokers with lung cancer carry a high p53 mutational load at these codons.	Benzo(a)pyrene	80-82	P53	Homo sapiens	242-245
11390388-2	2001	Like the prostaglandins of the A series, prostaglandins of the J series have a structural determinant (endocyclic cyclopentenone) that confers the ability to impair the conformation, the phosphorylation, and the transcriptional activity of the p53 tumor suppressor with equivalent potency and efficacy.	cyclopentenone	114-128	P53	Homo sapiens	244-247
28751770-4	2018	We show that venetoclax synergizes with cytarabine and idarubicin to increase antileukemic efficacy in a TP53-dependent manner.	Idarubicin	55-65	P53	Homo sapiens	105-109
11554448-8	2001	In this network, p53 can control the timely production of reactive oxygen intermediates (e.g., to initiate apoptosis), but this activity is itself under the control of changes in metal levels and in cellular redox status.	reactive oxygen intermediates	58-87	P53	Homo sapiens	17-20
29600625-9	2018	Moreover, notoginsenoside R1 decreased the mRNA expressions of miRNA-34a and p53 and the protein expression of p53, p21 and p16.At the same time, notoginsenoside R1 increased the protein and mRNA expressions of SIRT1.	notoginsenoside	10-25	P53	Homo sapiens	77-80
11522280-0	2001	Do wine polyphenols modulate p53 gene expression in human cancer cell lines?	Polyphenols	8-19	P53	Homo sapiens	29-32
11522280-8	2001	CONCLUSIONS: The observed p53 concentration changes upon stimulation by polyphenols are relatively small, do not follow a uniform pattern in the four cell lines tested, and do not exhibit a dose-response effect.	Polyphenols	72-83	P53	Homo sapiens	26-29
29600625-9	2018	Moreover, notoginsenoside R1 decreased the mRNA expressions of miRNA-34a and p53 and the protein expression of p53, p21 and p16.At the same time, notoginsenoside R1 increased the protein and mRNA expressions of SIRT1.	notoginsenoside	10-25	P53	Homo sapiens	111-114
29600625-9	2018	Moreover, notoginsenoside R1 decreased the mRNA expressions of miRNA-34a and p53 and the protein expression of p53, p21 and p16.At the same time, notoginsenoside R1 increased the protein and mRNA expressions of SIRT1.	notoginsenoside	146-161	P53	Homo sapiens	111-114
29600625-14	2018	The possible mechanism is that notoginsenoside R1 can delay the senescence process of vascular endothelial cells induced by H2O2 by regulating microRNA-34a/SIRT1/p53 signal pathway.	notoginsenoside	31-46	P53	Homo sapiens	162-165
30179144-10	2018	Results demonstrated that the gene expression of P53 genes was altered up to fourteen-fold levels in SK-BR-3 cell lines whereas it reached 2.5-fold in the MCF-12A cell line after treatment with VA.	vulpinic acid	194-196	P53	Homo sapiens	49-52
11461962-7	2001	These data support a model in which AraC induces neuronal apoptosis by provoking the generation of reactive oxygen species, causing oxidative DNA damage and initiating the p53-dependent apoptotic program.	Cytarabine	36-40	P53	Homo sapiens	172-175
11699407-5	2001	In cells treated with OL(1) p53 and Idarubicin, truncated p53 message of a predicted 201 base pair length based on RNAase H cleavage of the OL(1) p53-p53 mRNA heteroduplex was detected after 7 hours of incubation.	Idarubicin	36-46	P53	Homo sapiens	58-61
11699407-5	2001	In cells treated with OL(1) p53 and Idarubicin, truncated p53 message of a predicted 201 base pair length based on RNAase H cleavage of the OL(1) p53-p53 mRNA heteroduplex was detected after 7 hours of incubation.	Idarubicin	36-46	P53	Homo sapiens	58-61
11699407-5	2001	In cells treated with OL(1) p53 and Idarubicin, truncated p53 message of a predicted 201 base pair length based on RNAase H cleavage of the OL(1) p53-p53 mRNA heteroduplex was detected after 7 hours of incubation.	Idarubicin	36-46	P53	Homo sapiens	58-61
29054408-3	2017	Here, we show HDAC6 negatively regulates pro-apoptotic acetylation of p53 at lysine residue 120 (K120) in mesenchymal stem cells (MSCs).	k120	97-101	P53	Homo sapiens	70-73
11699407-9	2001	Therefore, synergistic cytotoxicity of Idarubicin for lymphoma cells treated with an oligonucleotide targeting p53 message was demonstrated at oligonucleotide and Idarubicin concentrations which were minimally toxic to hematopoietic progenitor cells.	Idarubicin	39-49	P53	Homo sapiens	111-114
11699407-9	2001	Therefore, synergistic cytotoxicity of Idarubicin for lymphoma cells treated with an oligonucleotide targeting p53 message was demonstrated at oligonucleotide and Idarubicin concentrations which were minimally toxic to hematopoietic progenitor cells.	Idarubicin	163-173	P53	Homo sapiens	111-114
11325852-6	2001	Nonetheless, the ligation-mediated PCR technology was used here to demonstrate, at nucleotide resolution, that p53-/-p21+/+ DLD1 excises UVB-induced cyclobutane pyrimidine dimers from the c-jun proto-oncogene at a significantly lower rate than the isogenic p53-/-p21-/- derivative.	cyclobutane pyrimidine	149-171	P53	Homo sapiens	111-114
29054408-4	2017	The loss of HDAC6 expression in MSCs increases K120 acetylation of p53, which is successfully reversed by the wild-type but not by catalytically dead HDAC6.	k120	47-51	P53	Homo sapiens	67-70
11325852-6	2001	Nonetheless, the ligation-mediated PCR technology was used here to demonstrate, at nucleotide resolution, that p53-/-p21+/+ DLD1 excises UVB-induced cyclobutane pyrimidine dimers from the c-jun proto-oncogene at a significantly lower rate than the isogenic p53-/-p21-/- derivative.	cyclobutane pyrimidine	149-171	P53	Homo sapiens	257-260
29250930-7	2017	In the relapsed or refractory setting, patients with del(17p) or TP53 aberrations should be offered treatment with a novel agent, such as ibrutinib, idelalisib-rituximab or venetoclax.	ibrutinib	138-147	P53	Homo sapiens	65-69
11423906-3	2001	In the present study we demonstrated that infection with p53 expressing adenovirus (Ad-p53), enhances chemosensitivity of MR-deficient tumor cell lines to the methylating agent temozolomide (TZM), either used as single agent or, more efficiently, when combined with PARP inhibitor.	Temozolomide	177-189	P53	Homo sapiens	57-60
28691888-0	2017	Signal-Regulated Protein Kinases/Protein Kinase B-p53-BH3-Interacting Domain Death Agonist Pathway Regulates Gingipain-Induced Apoptosis in Osteoblasts.	BH 3	54-57	P53	Homo sapiens	50-53
11423906-3	2001	In the present study we demonstrated that infection with p53 expressing adenovirus (Ad-p53), enhances chemosensitivity of MR-deficient tumor cell lines to the methylating agent temozolomide (TZM), either used as single agent or, more efficiently, when combined with PARP inhibitor.	Temozolomide	177-189	P53	Homo sapiens	87-90
28691888-11	2017	The ability of gingipains to stimulate p53 and Bid expression was mimicked by PD-0325901 and MK-2206, the specific extracellular signal-regulated protein kinases (ERK) and protein kinase B (PKB) inhibitors, respectively.	mirdametinib	78-88	P53	Homo sapiens	39-42
11423906-3	2001	In the present study we demonstrated that infection with p53 expressing adenovirus (Ad-p53), enhances chemosensitivity of MR-deficient tumor cell lines to the methylating agent temozolomide (TZM), either used as single agent or, more efficiently, when combined with PARP inhibitor.	Temozolomide	191-194	P53	Homo sapiens	57-60
28819011-6	2017	In conclusion, we show that TP53 mutations identify a phenotypically distinct and highly aggressive form of MCL with poor or no response to regimens including cytarabine, rituximab, and autologous stem-cell transplant (ASCT).	Cytarabine	159-169	P53	Homo sapiens	28-32
11423906-3	2001	In the present study we demonstrated that infection with p53 expressing adenovirus (Ad-p53), enhances chemosensitivity of MR-deficient tumor cell lines to the methylating agent temozolomide (TZM), either used as single agent or, more efficiently, when combined with PARP inhibitor.	Temozolomide	191-194	P53	Homo sapiens	87-90
11423906-5	2001	Cells, growth arrested by p53 transduction, and then subsequently exposed to the drugs, were still highly susceptible to cytotoxicity induced by TZM and PARP inhibitor.	Temozolomide	145-148	P53	Homo sapiens	26-29
11423906-7	2001	It is conceivable to envisage future possible strategies to enhance cytostatic or cytotoxic effects induced by Ad-p53, based on the use of TZM, alone or combined with PARP inhibitor for the therapy of resistant tumors.	Temozolomide	139-142	P53	Homo sapiens	114-117
11313880-3	2001	p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2",7"-dichlorofluorescin (DCFH) into 2",7"-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase.	hydroethidium	115-128	P53	Homo sapiens	0-3
11280752-6	2001	p53-proficient U87 MG cells underwent a prolonged, p53- and p21(Waf1/Cip1)-associated G2-M arrest beginning 2 days after TMZ treatment.	Temozolomide	121-124	P53	Homo sapiens	0-3
11280752-8	2001	p53-deficient (E6-transfected U87 and LN-Z308) cells similarly underwent G2-M arrest in response to TMZ, but this arrest was accompanied by only minor changes in p53 or p21(Waf1/Cip1) and was reversed within 7 days of TMZ treatment in association with the appearance of cells with either 8n or subG1 DNA content.	Temozolomide	100-103	P53	Homo sapiens	0-3
11280752-8	2001	p53-deficient (E6-transfected U87 and LN-Z308) cells similarly underwent G2-M arrest in response to TMZ, but this arrest was accompanied by only minor changes in p53 or p21(Waf1/Cip1) and was reversed within 7 days of TMZ treatment in association with the appearance of cells with either 8n or subG1 DNA content.	Temozolomide	218-221	P53	Homo sapiens	0-3
11280752-10	2001	p53 is not necessary for this G2-M arrest to occur but is important in the duration of G2-M arrest and in the ultimate fate of TMZ-treated cells.	Temozolomide	127-130	P53	Homo sapiens	0-3
11182788-4	2001	Likewise, accumulation of these proteins was observed in the wild-type TP53 cells after exposure to conditioned medium from irradiated mutant TP53 cells, and the accumulation was abolished by the addition of a specific nitric oxide scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide, to the medium.	1,3-dihydroxy-4,4,5,5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole	243-309	P53	Homo sapiens	71-75
12592381-1	2003	The nuclear export inhibitor leptomycin B (LMB) prevents the export of proteins from the nucleus to the cytoplasm, protects p53 from Mdm2-mediated degradation and is a very potent inducer of the p53 transcriptional activity.	leptomycin B	29-41	P53	Homo sapiens	124-127
12592381-1	2003	The nuclear export inhibitor leptomycin B (LMB) prevents the export of proteins from the nucleus to the cytoplasm, protects p53 from Mdm2-mediated degradation and is a very potent inducer of the p53 transcriptional activity.	leptomycin B	29-41	P53	Homo sapiens	195-198
12592381-1	2003	The nuclear export inhibitor leptomycin B (LMB) prevents the export of proteins from the nucleus to the cytoplasm, protects p53 from Mdm2-mediated degradation and is a very potent inducer of the p53 transcriptional activity.	leptomycin B	43-46	P53	Homo sapiens	124-127
12592381-1	2003	The nuclear export inhibitor leptomycin B (LMB) prevents the export of proteins from the nucleus to the cytoplasm, protects p53 from Mdm2-mediated degradation and is a very potent inducer of the p53 transcriptional activity.	leptomycin B	43-46	P53	Homo sapiens	195-198
12600942-6	2003	Specifically, loss of one p53 allele dramatically facilitates the progression of mammary tumors to a Wnt1-independent state both by impairing the regression of primary tumors following doxycycline withdrawal and by promoting the recurrence of fully regressed tumors in the absence of doxycycline.	Doxycycline	185-196	P53	Homo sapiens	26-29
12600942-6	2003	Specifically, loss of one p53 allele dramatically facilitates the progression of mammary tumors to a Wnt1-independent state both by impairing the regression of primary tumors following doxycycline withdrawal and by promoting the recurrence of fully regressed tumors in the absence of doxycycline.	Doxycycline	284-295	P53	Homo sapiens	26-29
11182788-4	2001	Likewise, accumulation of these proteins was observed in the wild-type TP53 cells after exposure to conditioned medium from irradiated mutant TP53 cells, and the accumulation was abolished by the addition of a specific nitric oxide scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide, to the medium.	1,3-dihydroxy-4,4,5,5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole	243-309	P53	Homo sapiens	142-146
28910957-10	2017	Among them, the effect of NAC in patients with two or more genes copy number variations of c-Myc, CCND1, p53, p16 were poorer than that in patients with one or not gene copy number variations (P=0.000).	nac	26-29	P53	Homo sapiens	105-108
11273007-5	2001	IPTG induction of AD7c-NTP gene expression resulted in increased cell death mediated by apoptosis, impaired mitochondrial function, and increased cellular levels of the p53 and CD95 pro-apoptosis gene products as occur in AD.	Isopropyl Thiogalactoside	0-4	P53	Homo sapiens	169-172
12507920-8	2002	These results are also consistent with the hypothesis that BP (PAH) induce G:C to T:A transversion mutations in the hotspot codons of the p53 tumor suppressor gene and are thus involved in malignant transformation of the lung tissue of smokers.	Benzo(a)pyrene	59-61	P53	Homo sapiens	138-141
12402298-6	2002	With formamidopyrimidine-DNA glycosylase treatment, N-OH-AF induced cleavage at guanine residues, especially of the ACG sequence complementary to codon 273, a well-known hot spot of the p53 gene.	n-oh-af	52-59	P53	Homo sapiens	186-189
28821714-9	2017	In MGMT-deficient/TMZ-sensitive cells (U87 and U373), GADD45Akd decreased TMZ-induced TP53 expression.	Temozolomide	18-21	P53	Homo sapiens	86-90
12419825-0	2002	The major lipid peroxidation product, trans-4-hydroxy-2-nonenal, preferentially forms DNA adducts at codon 249 of human p53 gene, a unique mutational hotspot in hepatocellular carcinoma.	4-hydroxy-2-nonenal	38-63	P53	Homo sapiens	120-123
11104898-3	2000	Very recent studies clarified that P53 independent expression of p21 and gadd 45, activation of PPARgamma are involved in antitumor mechanism of these PGs.	Phosphatidylglycerols	151-154	P53	Homo sapiens	35-38
28821714-9	2017	In MGMT-deficient/TMZ-sensitive cells (U87 and U373), GADD45Akd decreased TMZ-induced TP53 expression.	Temozolomide	74-77	P53	Homo sapiens	86-90
11090076-8	2000	These findings indicate that treatment with etoposide, Ara-C, or doxorubicin up-regulates DR5 levels in a p53-independent manner and sensitizes human acute leukemia cells to Apo-2L-induced apoptosis.	Cytarabine	55-60	P53	Homo sapiens	106-109
28821714-10	2017	Thus, in this study, we investigated the genes influenced by TMZ that were important in GBM therapy, and revealed that GADD45A plays a protective role against TMZ treatment which may through TP53-dependent and MGMT-dependent pathway in TMZ-sensitive and TMZ-resistant GBM, respectively.	Temozolomide	61-64	P53	Homo sapiens	191-195
12373335-13	2002	Whereas the p53-positive endothelial cells underwent programmed cell death as demonstrated by M30, ISEL and Hoechst 33342, some fibroblasts seemed to accumulate the p53 antibody, but this did not induce apoptotic cascades.	bisbenzimide ethoxide trihydrochloride	108-121	P53	Homo sapiens	12-15
28797070-4	2017	We find that methyl pyruvate protects irinotecan-treated normal lung fibroblast cell line (MRC-5) probably by turning off the p53/p21 axis of the apoptotic pathways.	methyl pyruvate	13-28	P53	Homo sapiens	126-129
12205035-5	2002	p53 activation was largely attenuated if SMCs were pretreated with SB202190, a specific p38MAPK inhibitor, or were stably transfected with dominant negative rac, an upstream signal transducer of p38MAPK pathways.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	67-75	P53	Homo sapiens	0-3
11964141-7	2002	Bathocuproinedisulphonic acid as well as the hydroxyl radical scavenger d-mannitol inhibited the PDTC-dependent increase in p53 protein and oxidation.	Mannitol	72-82	P53	Homo sapiens	124-127
12194756-0	2002	Preferential radiosensitization in p53-mutated human tumour cell lines by pentoxifylline-mediated disruption of the G2/M checkpoint control.	Pentoxifylline	74-88	P53	Homo sapiens	35-38
11351862-5	2000	The Northern blot analysis revealed marked up-regulation of p53, p16(MTS1), p21 (WAF1) gene expressions in PAMC82 cells treated with lanthanum chloride and cerium chloride, as compared to control PAMC82 cells.	lanthanum chloride	133-151	P53	Homo sapiens	60-63
11050162-6	2000	Therefore, we exposed a wild-type p53 TK-6 lymphoblastoid cell line to 4-hydroxynonenal, an unsaturated aldehyde involved in lipid peroxidation, and observed an increase in G to T transversions at p53 codon 249 (AGG to AGT).	4-hydroxy-2-nonenal	71-87	P53	Homo sapiens	34-37
11050162-6	2000	Therefore, we exposed a wild-type p53 TK-6 lymphoblastoid cell line to 4-hydroxynonenal, an unsaturated aldehyde involved in lipid peroxidation, and observed an increase in G to T transversions at p53 codon 249 (AGG to AGT).	4-hydroxy-2-nonenal	71-87	P53	Homo sapiens	197-200
10998350-2	2000	Methoxy-polyethylene glycol-maleimide MW 2000 (MAL-PEG) was used to covalently tag p53 protein that was oxidized at cysteine residues in cultured cells.	methoxy-polyethylene glycol-maleimide	0-37	P53	Homo sapiens	83-86
11025661-2	2000	Treatment with vincristine or paclitaxel before DNA-damage or before leptomycin B treatment reduces nuclear accumulation of p53 and expression of mdm2 and p21.	leptomycin B	69-81	P53	Homo sapiens	124-127
12194756-2	2002	We studied the radiosensitizing potential of pentoxifylline (PTX) and the PTX-mediated modulation of cell-cycle progression dependent on the p53 status of various human tumour cell lines.	Pentoxifylline	74-77	P53	Homo sapiens	141-144
28527359-7	2017	Further, indium oxide nanocubes induced a mitochondrial membrane potential loss and altered the mRNA expression levels of apoptotic genes (p53, bax, bcl-2, CASP3 &amp; CASP9).	indium oxide	9-21	P53	Homo sapiens	139-142
12058275-0	2002	The farnesyltransferase inhibitor, FTI-2153, inhibits bipolar spindle formation during mitosis independently of transformation and Ras and p53 mutation status.	FTI-2153	35-43	P53	Homo sapiens	139-142
12432259-0	2002	Flavopiridol inversely affects p21(WAF1/CIP1) and p53 and protects p21-sensitive cells from paclitaxel.	alvocidib	0-12	P53	Homo sapiens	50-53
10993631-2	2000	MATERIALS AND METHODS: The influence of pentoxifylline on radiotoxicity was assessed by colony assay in TP53 wild-type Bell and mutant MeWo melanoma, and in TP53 wild-type 4197 and mutant 4451 squamous cell carcinoma (SCC) cell lines.	Pentoxifylline	40-54	P53	Homo sapiens	104-108
10993631-6	2000	RESULTS: Pentoxifylline, when combined with irradiation, significantly increased radiotoxicity in the TP53 mutant MeWo and 4451 cell lines by radiotoxicity enhancement factors of 3 and 14.5 respectively.	Pentoxifylline	9-23	P53	Homo sapiens	102-106
12432259-5	2002	High concentrations of FL (500 nM) decreased levels of p21 and Mdm-2 but dramatically induced p53.	alvocidib	23-25	P53	Homo sapiens	94-97
28676915-14	2017	We describe, for the first time, the characterization of a new human PUS TP53-null cell line called mfh-val2.	PUS	69-72	P53	Homo sapiens	73-77
12089228-9	2002	p53-positive phenotype was associated with worse local control with LP (LCLP; 49% v 23%, P =.053) and inferior overall survival (OS; 51% v 29%, P =.017) at 5 years.	leucylproline	68-70	P53	Homo sapiens	0-3
11020243-1	2000	The p53 tumor-suppressor gene has been implicated in the inducible activation of excision repair of ultraviolet (UV)-induced cyclobutane pyrimidine dimers (CPDs) in human cells.	cyclobutane pyrimidine	125-147	P53	Homo sapiens	4-7
11191113-0	2000	Disruption of cell cycle kinetics by benzo[a]pyrene: inverse expression patterns of BRCA-1 and p53 in MCF-7 cells arrested in S and G2.	Benzo(a)pyrene	37-51	P53	Homo sapiens	95-98
28611469-4	2017	The capacity of sulfonamides to impair MDM2-p53 complex formation was detected by an enzyme-linked immunosorbent assay method.	Sulfonamides	16-28	P53	Homo sapiens	44-47
10910962-0	2000	Multicolour FISH detection of radioactive iodine-induced 17cen-p53 chromosomal breakage in buccal cells from therapeutically exposed patients.	radioactive iodine	30-48	P53	Homo sapiens	63-66
10884347-5	2000	An alanine mutation at any one of four key positions abrogates the efficacy of a synthetic peptide containing this motif as an inhibitor of cyclin A-cdk2 phosphorylation of p53 protein.	Peptides	91-98	P53	Homo sapiens	173-176
12065679-7	2002	In these studies using mitogen-activated protein kinase inhibitors, infection-induced increases in the p53 level were partially blocked by PD98059, a synthetic inhibitor of MEK1 that is the immediate upstream kinase of extracellular signal-regulated kinases 1/2 (ERK1/2), but not by SB202190, a potent p38 kinase inhibitor.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	283-291	P53	Homo sapiens	103-106
12432277-1	2002	Previous studies have demonstrated the irradiation-induced phosphorylation of p53 at Thrl8 and Ser20, residues integral within an a-helical segment of the transactivation domain.	thrl8	85-90	P53	Homo sapiens	78-81
28656213-0	2017	BMH-21 inhibits viability and induces apoptosis by p53-dependent nucleolar stress responses in SKOV3 ovarian cancer cells.	BMH-21	0-6	P53	Homo sapiens	51-54
10777712-6	2000	The GSH analogue, gamma-glutamylcysteinyl-ethyl ester, down-regulated Bax/p53 abundance but restored that of Bcl-2, thereby increasing Bcl-2/Bax.	N-gamma-glutamylcysteine ethyl ester	18-53	P53	Homo sapiens	74-77
11925476-0	2002	Diallyl disulfide (DADS) induces the antitumorigenic NSAID-activated gene (NAG-1) by a p53-dependent mechanism in human colorectal HCT 116 cells.	diallyl disulfide	0-17	P53	Homo sapiens	87-90
28656213-7	2017	Taken together, these data provide the first reported evidence that induction of p53-dependent nucleolar stress by BMH-21 induces apoptosis in ovarian cancer.	BMH-21	115-121	P53	Homo sapiens	81-84
11925476-0	2002	Diallyl disulfide (DADS) induces the antitumorigenic NSAID-activated gene (NAG-1) by a p53-dependent mechanism in human colorectal HCT 116 cells.	diallyl disulfide	19-23	P53	Homo sapiens	87-90
11925476-7	2002	In HCT-116 cells, DADS induced p53 and NAG-1 in a dose-dependent manner and the induction of p53 preceded that of NAG-1.	diallyl disulfide	18-22	P53	Homo sapiens	31-34
28754018-0	2017	Investigating the Influence of Magnesium Ions on p53-DNA Binding Using Atomic Force Microscopy.	Magnesium	31-40	P53	Homo sapiens	49-52
11925476-7	2002	In HCT-116 cells, DADS induced p53 and NAG-1 in a dose-dependent manner and the induction of p53 preceded that of NAG-1.	diallyl disulfide	18-22	P53	Homo sapiens	93-96
11925476-12	2002	Thus, DADS-induced apoptosis and NAG-1 protein expression appear to occur via p53.	diallyl disulfide	6-10	P53	Homo sapiens	78-81
11960384-7	2002	Furthermore, MDM2, a negative regulator of p53 expression was upregulated 3 days after Adv/p16 infection, and MDM2 was subsequently cleaved by caspase-3; MDM2 cleavage was inhibited by Ac-DEVD-CHO treatment.	acetyl-aspartyl-glutamyl-valyl-aspartal	185-196	P53	Homo sapiens	43-46
10753968-0	2000	Decreased DNA repair efficiency by loss or disruption of p53 function preferentially affects removal of cyclobutane pyrimidine dimers from non-transcribed strand and slow repair sites in transcribed strand.	cyclobutane pyrimidine	104-126	P53	Homo sapiens	57-60
28754018-2	2017	Metal ions, such as magnesium and zinc ions, have important influences on p53-DNA interactions for stabilizing the structure of the protein and enhancing its affinity to DNA.	Magnesium	20-29	P53	Homo sapiens	74-77
10725664-0	2000	p53-degradation by HPV-16 E6 preferentially affects the removal of cyclobutane pyrimidine dimers from non-transcribed strand and sensitizes mammary epithelial cells to UV-irradiation.	cyclobutane pyrimidine	67-89	P53	Homo sapiens	0-3
28754018-6	2017	The influence of magnesium ions on p53-DNA binding was studied by AFM at various ion strengths through visualization.	Magnesium	17-26	P53	Homo sapiens	35-38
10741727-11	2000	The relationship between p53 and response to temozolomide was also examined.	Temozolomide	45-57	P53	Homo sapiens	25-28
11914144-10	2002	To elucidate the mechanisms of ALA induced apoptosis, we examined its effect on p53 expression.	Aminolevulinic Acid	31-34	P53	Homo sapiens	80-83
28754018-8	2017	Furthermore, the high concentrations of magnesium ions can promote p53 aggregation and even lead to the formation of self-assembly networks of DNA and p53 proteins.	Magnesium	40-49	P53	Homo sapiens	67-70
28754018-8	2017	Furthermore, the high concentrations of magnesium ions can promote p53 aggregation and even lead to the formation of self-assembly networks of DNA and p53 proteins.	Magnesium	40-49	P53	Homo sapiens	151-154
10708967-0	2000	Mutagenicity of benzo[a]pyrene-deoxyadenosine adducts in a sequence context derived from the p53 gene.	Benzo(a)pyrene	16-30	P53	Homo sapiens	93-96
10708967-2	2000	Recent research has shown that tobacco-associated cancer in the human lung is related to mutation of the p53 gene mediated by the carcinogen benzo[a]pyrene (BaP), and the mutations are targeted to DNA "hot spots" at specific codons.	Benzo(a)pyrene	141-155	P53	Homo sapiens	105-108
28247504-3	2017	Co-treatment with 5 microM BaP and 20 microM EGCG in BEAS-2B promoted a significant reduction in cell viability and greater G2/M cell cycle arrest, induction of ROS, and reductions in BaP-induced CYP1A1/CYP1B1/COMT, EGFR, p-Akt (Ser473), p-p53 (Thr55), and survivin mRNA/protein expression, as well as an increase in p-p53 (Ser15).	Benzo(a)pyrene	27-30	P53	Homo sapiens	240-243
10708967-2	2000	Recent research has shown that tobacco-associated cancer in the human lung is related to mutation of the p53 gene mediated by the carcinogen benzo[a]pyrene (BaP), and the mutations are targeted to DNA "hot spots" at specific codons.	Benzo(a)pyrene	157-160	P53	Homo sapiens	105-108
11977632-3	2002	The expressions of p53, p16 and cyclin D1 were stained by indirect immunofluorescence of fluorescein isothiocyanate(FTTC), which were detected by flow cytometry (FCM).	Fluorescein-5-isothiocyanate	89-115	P53	Homo sapiens	19-22
10732766-16	2000	Taken together, these observations indicate that MSI and p53 alterations could be associated with different CPT-11 sensitivities; MSI phenotype moderately influences the CPT-11 sensitivity, MSI+ being more sensitive than MSI(-)CRC freshly obtained from patients, mutp53 status being associated with a poor response to CPT-11.	cpt	108-111	P53	Homo sapiens	57-60
28247504-3	2017	Co-treatment with 5 microM BaP and 20 microM EGCG in BEAS-2B promoted a significant reduction in cell viability and greater G2/M cell cycle arrest, induction of ROS, and reductions in BaP-induced CYP1A1/CYP1B1/COMT, EGFR, p-Akt (Ser473), p-p53 (Thr55), and survivin mRNA/protein expression, as well as an increase in p-p53 (Ser15).	Benzo(a)pyrene	27-30	P53	Homo sapiens	319-322
11731425-10	2001	Immunohistochemistry of the resected specimen demonstrated that FUS homogeneously induced lethal and sublethal tumor damage with consecutive up-regulation of p53 and loss of proliferative activity.	fusarubin	64-67	P53	Homo sapiens	158-161
29057306-2	2017	We found that mutant p53 impairs the function of nuclear factor (erythroid-derived 2)-like 2 (NFE2L2, commonly known as NRF2), suppresses solute carrier family 7 member 11 (SLC7A11) expression, and diminishes cellular glutamate/cystine exchange.	Cystine	228-235	P53	Homo sapiens	21-24
11536301-7	2001	RESULTS: LNCaP/Asp53 cells showed reduced expression of p53 protein when cultured in a medium containing doxycycline and tested sublines were able to efficiently form tumors in castrated male nude mice only when the mice were treated with doxycycline.	Doxycycline	105-116	P53	Homo sapiens	17-20
11536301-7	2001	RESULTS: LNCaP/Asp53 cells showed reduced expression of p53 protein when cultured in a medium containing doxycycline and tested sublines were able to efficiently form tumors in castrated male nude mice only when the mice were treated with doxycycline.	Doxycycline	239-250	P53	Homo sapiens	17-20
10645001-6	2000	Inhibition of nuclear export by leptomycin B also results in retention of nascent p53 in the nucleus, suggesting that cytoplasmic distribution of p53 results from efficient export of nuclear p53 in combination with MDM2-mediated degradation.	leptomycin B	32-44	P53	Homo sapiens	82-85
10602494-0	1999	Effects on normal fibroblasts and neuroblastoma cells of the activation of the p53 response by the nuclear export inhibitor leptomycin B.	leptomycin B	124-136	P53	Homo sapiens	79-82
10602494-1	1999	p53 tumour suppressor protein levels and p53-dependent transcriptional activity have been recently shown to increase in cells treated with leptomycin B (LMB), an inhibitor of nuclear export.	leptomycin B	139-151	P53	Homo sapiens	0-3
10602494-1	1999	p53 tumour suppressor protein levels and p53-dependent transcriptional activity have been recently shown to increase in cells treated with leptomycin B (LMB), an inhibitor of nuclear export.	leptomycin B	139-151	P53	Homo sapiens	41-44
11532872-12	2001	Determination of the role of safrole and other carcinogens present in BQ on the pattern of p53 gene mutation in OSCC will require further study.	Safrole	29-36	P53	Homo sapiens	91-94
10602494-1	1999	p53 tumour suppressor protein levels and p53-dependent transcriptional activity have been recently shown to increase in cells treated with leptomycin B (LMB), an inhibitor of nuclear export.	leptomycin B	153-156	P53	Homo sapiens	0-3
28918747-0	2017	Omega-3 Polyunsaturated Fatty Acids Eicosapentaenoic Acid and Docosahexaenoic Acid Enhance Dexamethasone Sensitivity in Multiple Myeloma Cells by the p53/miR-34a/Bcl-2 Axis.	Docosahexaenoic Acids	62-82	P53	Homo sapiens	150-153
10602494-1	1999	p53 tumour suppressor protein levels and p53-dependent transcriptional activity have been recently shown to increase in cells treated with leptomycin B (LMB), an inhibitor of nuclear export.	leptomycin B	153-156	P53	Homo sapiens	41-44
10656873-3	1999	beta-Lapachone, a novel topoisomerase inhibitor, has been shown to induce cell death in human promyelocytic leukemia and prostate cancer cells through a p53-independent pathway.	beta-lapachone	0-14	P53	Homo sapiens	153-156
10656873-13	1999	Furthermore, down-regulation of mutant p53 and induction of p27 in SW480 cells, and induction of pro-apoptotic protein Bax in DLD1 cells may be pertinent to the anti-proliferative and apoptotic effects of beta-lapachone on these cells.	beta-lapachone	205-219	P53	Homo sapiens	39-42
11561778-0	2001	Reversal of cytosine arabinoside (ara-C) resistance by the synergistic combination of 6-thioguanine plus ara-C plus PEG-asparaginase (TGAP) in human leukemia lines lacking or expressing p53 protein.	Cytarabine	34-39	P53	Homo sapiens	186-189
11457508-4	2001	Here we demonstrate increased expression and co-localization of p53 and Mdm2 in the nuclei of degenerating neurons following treatment with either the excitotoxin, kainic acid, or the topoisomerase I inhibitor, camptothecin.	Kainic Acid	164-175	P53	Homo sapiens	64-67
10656873-14	1999	CONCLUSIONS: beta-Lapachone induced cell cycle arrest and apoptosis in human colon cancer cells through a p53-independent pathway.	beta-lapachone	13-27	P53	Homo sapiens	106-109
28092678-4	2017	Depletion of PFKFB4 from p53-deficient cancer cells increased levels of the allosteric regulator fructose-2,6-bisphosphate, leading to increased glycolytic activity but decreased routing of metabolites through the oxidative arm of the pentose-phosphate pathway.	fructose 2,6-diphosphate	97-122	P53	Homo sapiens	25-28
10656873-15	1999	For human colon cancers, which often contain p53 mutations, beta-lapachone may prove to be a promising anticancer agent that can target cancer cells, especially those with mutant p53.	beta-lapachone	60-74	P53	Homo sapiens	45-48
10656873-15	1999	For human colon cancers, which often contain p53 mutations, beta-lapachone may prove to be a promising anticancer agent that can target cancer cells, especially those with mutant p53.	beta-lapachone	60-74	P53	Homo sapiens	179-182
11375905-7	2001	Both lactacystin, a specific inhibitor of the 26S proteasome, and leptomycin B, a specific inhibitor of the nuclear export protein CRM1, could block the effect that DCA had on p53 protein levels, suggesting that DCA suppressed p53 by stimulating the process of proteasome-mediated degradation of p53.	leptomycin B	66-78	P53	Homo sapiens	176-179
11375905-7	2001	Both lactacystin, a specific inhibitor of the 26S proteasome, and leptomycin B, a specific inhibitor of the nuclear export protein CRM1, could block the effect that DCA had on p53 protein levels, suggesting that DCA suppressed p53 by stimulating the process of proteasome-mediated degradation of p53.	leptomycin B	66-78	P53	Homo sapiens	227-230
11375905-7	2001	Both lactacystin, a specific inhibitor of the 26S proteasome, and leptomycin B, a specific inhibitor of the nuclear export protein CRM1, could block the effect that DCA had on p53 protein levels, suggesting that DCA suppressed p53 by stimulating the process of proteasome-mediated degradation of p53.	leptomycin B	66-78	P53	Homo sapiens	227-230
11401911-3	2001	A G to T transversion at codon 249 of the p53 gene (249(ser)) is commonly found in HCCs from patients in regions with dietary aflatoxin exposure.	Aflatoxins	126-135	P53	Homo sapiens	42-45
28482147-0	2017	1,4,5-Trisubstituted Imidazole-Based p53-MDM2/MDMX Antagonists with Aliphatic Linkers for Conjugation with Biological Carriers.	1,4,5-trisubstituted imidazole	0-30	P53	Homo sapiens	37-40
11401911-9	2001	Second, we present a meta-analysis, using our results along with those from 48 published studies, that examines the interrelationships among aflatoxin exposure, HBV infection, and p53 mutations in HCCs.	Aflatoxins	141-150	P53	Homo sapiens	180-183
11482875-0	2001	Flavopiridol induces apoptosis and caspase-3 activation of a newly characterized Burkitt"s lymphoma cell line containing mutant p53 genes.	alvocidib	0-12	P53	Homo sapiens	128-131
28482147-3	2017	Here we present the syntheses, activities, and crystal structures of the p53-MDM2/MDMX inhibitors based on the 1,4,5-trisubstituted imidazole scaffold which are appended with aliphatic linkers that enable coupling to bioactive carriers.	1,4,5-trisubstituted imidazole	111-141	P53	Homo sapiens	73-76
27340212-5	2017	In particular, a careful analysis of the Amide I Raman band, which is highly sensitive to protein secondary structure elements such as alpha-helices, beta-sheets and random coils, has revealed the presence of extended random coils in p53 and predominant beta-sheet regions in its DBD.	Amides	41-46	P53	Homo sapiens	234-237
11106643-3	2001	Treatment of K562(pTet-on/p53) cells with doxycycline resulted in a dose-dependent expression of p53 protein and transcripts, increased p21 protein, decreased dihydrofolate reductase, and G(1) arrest with decreased numbers of cells in S-phase.	Doxycycline	42-53	P53	Homo sapiens	26-29
11106643-3	2001	Treatment of K562(pTet-on/p53) cells with doxycycline resulted in a dose-dependent expression of p53 protein and transcripts, increased p21 protein, decreased dihydrofolate reductase, and G(1) arrest with decreased numbers of cells in S-phase.	Doxycycline	42-53	P53	Homo sapiens	97-100
11106643-6	2001	When the hRFC-B promoter was expressed as full-length and basal promoter-luciferase reporter constructs in K562(pTet-on/p53) cells, induction of p53 with doxycycline resulted in a 3-fold loss of promoter activity, which was reversed by cotransfection with a trans-dominant-negative p53.	Doxycycline	154-165	P53	Homo sapiens	145-148
11106643-6	2001	When the hRFC-B promoter was expressed as full-length and basal promoter-luciferase reporter constructs in K562(pTet-on/p53) cells, induction of p53 with doxycycline resulted in a 3-fold loss of promoter activity, which was reversed by cotransfection with a trans-dominant-negative p53.	Doxycycline	154-165	P53	Homo sapiens	145-148
28513299-0	2017	Anti-tumor effect of cisplatin in human oral squamous cell carcinoma was enhanced by andrographolide via upregulation of phospho-p53 in vitro and in vivo.	andrographolide	85-100	P53	Homo sapiens	129-132
14510167-1	2001	Mutations of p53 tumour suppressor gene often occur in hepatocellular carcinoma and, in particular, codon 249 hot-spot mutation is displayed by hepatocellular carcinomas occurring in hepatitis B virus-endemic areas with high dietary aflatoxin intake.	Aflatoxins	233-242	P53	Homo sapiens	13-16
10502284-2	1999	By using cultured cerebellar granule cells, two types of apoptosis can be induced, one by adding cytosine arabinoside (Ara-c; p53-dependent apoptosis) and one by lowering the K(+) concentrations of the medium (p53-independent apoptosis).	Cytarabine	97-117	P53	Homo sapiens	126-129
28454566-4	2017	In this study, we suggested that AAE may exert cancer cell apoptosis through PTEN/PDK1/Akt/p53signal pathway and mitochondria-mediated apoptotic proteins.	acetoacetic acid	33-36	P53	Homo sapiens	91-94
11245472-5	2001	Stable expression of a dominant negative mutant of ERK2 or p38 kinase or their respective inhibitor, PD98059 or SB202190, repressed the phosphorylation of p53 at serine 15.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	112-120	P53	Homo sapiens	155-158
28454566-8	2017	RESULTS: AAE induced apoptosis via PTEN/p53/PDK1/Akt signal pathways through PTEN/p53-independent manner.	acetoacetic acid	9-12	P53	Homo sapiens	40-43
28395470-6	2017	Results: After treatment with TCE for 24 h in L-02 cells, the 36 TCE related histone methylation sites in 28 peptide segments were identified by MS. After treatment with TCE in concentrations of 0 and 8.0 mmol/L in L-02 cells for 24 h, the relative expression level of histone H3K79 me3 were 1.00+-0.06, 0.70+-0.09 (t=15.01, P=0.015); the relative expression level of histone H3K79 me2 were 1.00+-0.05, 0.74+-0.07 (t=16.69, P=0.018); the Olive Tail Moment about DNA damage were 1.46+-0.28, 3.12+- 0.68 (t=15.22, P=0.018); the relative expression levels of p53 were 1.00+-0.04, 1.24+-0.04 (t=18.71, P= 0.012); and the relative expression levels of  H2AX were 1.00 +- 0.03, 1.56 +- 0.11 (t=8.32, P=0 045).	Trichloroethylene	30-33	P53	Homo sapiens	556-559
11118634-5	2000	Subtoxic concentrations (&lt;TD50)added after irradiation at maximum expression of the G2/M block show that pentoxifylline and A802710 effectively abrogate the G2/M block, whereas A802715 and propentofylline prolong the G2/M block or remain ineffective depending on the p53 status of the cell line.	Pentoxifylline	108-122	P53	Homo sapiens	270-273
10470825-11	1999	In contrast, the lines that had mutant, nonfunctional P53 did not undergo spontaneous apoptosis, but they were rendered more sensitive to the apoptosis-inducing effect of ara-C.	Cytarabine	171-176	P53	Homo sapiens	54-57
10582657-15	1999	Induction of p53 levels was observed in WHCO3 cells exposed to GLA, AA, PGA2, indomethacin and the combination of indomethacin and GLA or AA.	gamma-Linolenic Acid	131-134	P53	Homo sapiens	13-16
11133809-1	2000	In human fibroblasts, N:-phosphoacetyl-L-aspartate (PALA) and gamma-radiation induce reversible and irreversible p53-mediated G(1) cell cycle arrest, respectively.	-phosphoacetyl-l-aspartate	24-50	P53	Homo sapiens	113-116
11127820-4	2000	In the current study, MDM2-mediated degradation of p53 was partially inhibited in cells treated with leptomycin B (LMB), a specific inhibitor of nuclear export.	leptomycin B	101-113	P53	Homo sapiens	51-54
10475376-11	1999	These studies also demonstrated that calphostin C induced apoptosis by a mechanism independent of p53 and pRb status and the presence or absence of 9p21 deletions.	calphostin C	37-49	P53	Homo sapiens	98-101
11127820-4	2000	In the current study, MDM2-mediated degradation of p53 was partially inhibited in cells treated with leptomycin B (LMB), a specific inhibitor of nuclear export.	leptomycin B	115-118	P53	Homo sapiens	51-54
27903750-4	2017	Further analysis indicated that tumor suppressor p53 was one of the proteins exported from nuclei upon proteasome inhibition, and in the presence of CRM1 inhibitor KPT330, nuclear p53, and expression of its target genes were increased markedly.	selinexor	164-170	P53	Homo sapiens	49-52
10397746-8	1999	Further studies examined the effect of 311 and DFO on the expression of p53-transactivated genes that are crucial for cell cycle control and DNA repair, namely WAF1, GADD45, and mdm-2.	Deferoxamine	47-50	P53	Homo sapiens	72-75
27903750-5	2017	Moreover, knockdown of p53 significantly reduced the synergistic cytotoxic action of bortezomib and KPT330 on p53+/+ HCT116 cells.	selinexor	100-106	P53	Homo sapiens	23-26
10397512-0	1999	Expression of p53 protein and Ki-67 antigen in gingival hyperplasia induced by nifedipine and phenytoin.	Nifedipine	79-89	P53	Homo sapiens	14-17
11045730-9	2000	In addition, exposure of XPA and XPG fibroblasts to UV (5, 10 or 20 J/m2) followed by incubation without araC resulted in a strong upregulation of p53.	Cytarabine	105-109	P53	Homo sapiens	147-150
27903750-5	2017	Moreover, knockdown of p53 significantly reduced the synergistic cytotoxic action of bortezomib and KPT330 on p53+/+ HCT116 cells.	selinexor	100-106	P53	Homo sapiens	110-113
10397512-3	1999	METHODS: We immunohistochemically examined the expression of tumor-related markers such as p53 protein and Ki-67 antigen in 11 hyperplastic gingival tissues induced by nifedipine and phenytoin, as well as 5 control tissues using an avidin-biotin-peroxidase complex method.	Nifedipine	168-178	P53	Homo sapiens	91-94
10397512-4	1999	RESULTS: Two specimens out of 4 nifedipine-induced and 4 out of 7 phenytoin-induced hyperplastic gingival tissues revealed the expression of p53 protein in the nuclei of epithelial cells, while no expression of p53 protein was observed in the epithelia of the 5 non-hyperplastic control tissues.	Nifedipine	32-42	P53	Homo sapiens	141-144
10942736-12	2000	Deferoxamine, a metal chelator, inhibited p53 activation by chelating Cr(V) to make it incapable of generating radicals from H(2)O(2).	Deferoxamine	0-12	P53	Homo sapiens	42-45
27903750-6	2017	In mice, KPT330 markedly augmented the antitumor action of bortezomib against HCT116 xenografts as well as patient-derived xenografts that harbored functional p53.	selinexor	9-15	P53	Homo sapiens	159-162
27903750-7	2017	These results indicate that nuclear p53 is a major mediator in the synergistic antitumor effect of bortezomib and KPT330, and provides a rationale for the use of proteasome inhibitor together with nuclear export blocker in the treatment of colorectal cancer.	selinexor	114-120	P53	Homo sapiens	36-39
28356713-0	2017	Artonin E induces p53-independent G1 cell cycle arrest and apoptosis through ROS-mediated mitochondrial pathway and livin suppression in MCF-7 cells.	artonin E	0-9	P53	Homo sapiens	18-21
10958934-13	2000	TP53 mutational analysis showed that both HKCI-1 and the primary tumor had the aflatoxin-associated mutation in codon 249 and an additional TP53 polymorphism in codon 72.	Aflatoxins	79-88	P53	Homo sapiens	0-4
10900010-4	2000	Here we show that treatment with the small molecule nuclear export inhibitor, leptomycin B, and actinomycin D leads to the accumulation of transcriptionally active p53 in the nucleus of HeLa, CaSki, and SiHa cells.	leptomycin B	78-90	P53	Homo sapiens	164-167
10340385-9	1999	In concordance with these observations we have found that expression of ras oncogene caused in p53-defective cells further mitigation of ethyl-metansulphonate-induced G1 and G2 cell cycle arrest, but did not abrogate G1 and G2 cell cycle checkpoints in cells with normal p53 function.	ethyl-metansulphonate	137-158	P53	Homo sapiens	95-98
10340385-9	1999	In concordance with these observations we have found that expression of ras oncogene caused in p53-defective cells further mitigation of ethyl-metansulphonate-induced G1 and G2 cell cycle arrest, but did not abrogate G1 and G2 cell cycle checkpoints in cells with normal p53 function.	ethyl-metansulphonate	137-158	P53	Homo sapiens	271-274
28386336-8	2017	A combination of celecoxib and irradiation treatment induced much more gamma-H2AX foci formation, higher levels of radiation injury-related proteins phosphorylation, G2/M arrest, apoptosis, and p53 and p21 expression, and lower levels of Cyclin B1 in HCT116 cells than those in cells treated with irradiation alone.	Celecoxib	17-26	P53	Homo sapiens	194-197
10360653-7	1999	p21 expression is induced by boswellic acids via a p53-independent pathway.	boswellic acid	29-44	P53	Homo sapiens	51-54
10360653-8	1999	Ectopic expression of wild-type p53 also induces p21, and facilitates boswellic acid-induced apoptosis.	boswellic acid	70-84	P53	Homo sapiens	32-35
11229523-6	2000	Genes that encode proteins important for cellular defenses against oxidative stress, such as the cysteine-rich metallothioneins (MTs), are also activated by hemopexin, as are proteins that regulate cell cycle control including p21WAF1 and the tumor suppressor p53.	cysteine-rich metallothioneins	97-127	P53	Homo sapiens	260-263
28386336-11	2017	Celecoxib affects the functions of p53 and inhibits the recovery from the irradiation-induced injury by up-regulating the expression of BCCIP, and subsequently regulates the expressions of genes such as p21 and Cyclin B1 to enhance the radiosensitivity of HCT116 cells in a COX-2 independent manner.	Celecoxib	0-9	P53	Homo sapiens	35-38
10212189-5	1999	UVC-induced phosphorylation of p53 at serine 389 was markedly impaired by either pretreatment of cells with p38 kinase inhibitor, SB202190, or stable expression of a dominant negative mutant of p38 kinase.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	130-138	P53	Homo sapiens	31-34
28130034-0	2017	NICE guidance on ibrutinib for previously treated chronic lymphocytic leukaemia and untreated chronic lymphocytic leukaemia in the presence of 17p deletion or TP53 mutation.	ibrutinib	17-26	P53	Homo sapiens	159-163
10212189-9	1999	Furthermore, pretreatment of cells with SB202190 blocked the p53 DNA binding activity and p53-dependent transcription.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	40-48	P53	Homo sapiens	61-64
10212189-9	1999	Furthermore, pretreatment of cells with SB202190 blocked the p53 DNA binding activity and p53-dependent transcription.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	40-48	P53	Homo sapiens	90-93
10837373-3	2000	In the present study, the induction of p53 target gene expression after the treatment with either benzo(a)pyrene (B[a]P) or 1-nitropyrene (1-NP) was investigated.	Benzo(a)pyrene	98-112	P53	Homo sapiens	39-42
28031409-3	2017	The current study demonstrates that, unlike cisplatin, platinum analogues oxaliplatin and DACH-diacetato-dichloro-Pt(IV) (DAP) strongly stabilize and activate p53v172F in resistant cells, as indicated by prolonged p53 half-life and transactivation of targets p21 (CDKN1A) and MDM2.	dap	122-125	P53	Homo sapiens	159-162
10811119-3	2000	Consistent with this possibility, treatment of A549 human lung cancer cells with clinically achievable concentrations of flavopiridol resulted in rapid elevations of the DNA damage-responsive protein p53.	alvocidib	121-133	P53	Homo sapiens	200-203
10811129-0	2000	Microsatellite instability at selected tetranucleotide repeats is associated with p53 mutations in non-small cell lung cancer.	tetranucleotide	39-54	P53	Homo sapiens	82-85
10811129-11	2000	Primary lung cancers with microsatellite alterations at selected tetranucleotide repeats have a high frequency of p53 mutations and do not display a phenotype consistent with defects in mismatch repair.	tetranucleotide	65-80	P53	Homo sapiens	114-117
10216216-7	1999	Mutations in p53 exons 6 and 7 have been reported in the childhood papillary thyroid carcinomas in Belarus presumably as a result of radioiodine fall-out.	Iodine-131	133-144	P53	Homo sapiens	13-16
10075936-5	1999	This report also demonstrates that the cytoplasmic localization of p53 in neuroblastoma cells is due to its hyperactive nuclear export: p53 in these cells can be trapped in the nucleus by the export-inhibiting drug leptomycin B or by binding a p53-tetramerization domain peptide that masks the NES.	leptomycin B	215-227	P53	Homo sapiens	67-70
10075936-5	1999	This report also demonstrates that the cytoplasmic localization of p53 in neuroblastoma cells is due to its hyperactive nuclear export: p53 in these cells can be trapped in the nucleus by the export-inhibiting drug leptomycin B or by binding a p53-tetramerization domain peptide that masks the NES.	leptomycin B	215-227	P53	Homo sapiens	136-139
10075936-5	1999	This report also demonstrates that the cytoplasmic localization of p53 in neuroblastoma cells is due to its hyperactive nuclear export: p53 in these cells can be trapped in the nucleus by the export-inhibiting drug leptomycin B or by binding a p53-tetramerization domain peptide that masks the NES.	leptomycin B	215-227	P53	Homo sapiens	136-139
10937051-8	2000	Boric acid was used for antigen retrieval on sections stored for 12 weeks at 20 degrees C. For both p53 protein and MIB1 antigen, this resulted in an extent and intensity of immunostaining equal to or higher than (MIB1) that obtained in freshly cut sections, using citrate buffer.	boric acid	0-10	P53	Homo sapiens	100-103
28031409-3	2017	The current study demonstrates that, unlike cisplatin, platinum analogues oxaliplatin and DACH-diacetato-dichloro-Pt(IV) (DAP) strongly stabilize and activate p53v172F in resistant cells, as indicated by prolonged p53 half-life and transactivation of targets p21 (CDKN1A) and MDM2.	dap	122-125	P53	Homo sapiens	214-217
28231799-5	2017	METHODS: We aimed to compare the cytotoxic effects of cisplatin and a trans-sulfonamide-platinum-complex (TSPC), in two human melanoma cell lines that differ in their TP53 status: SK-MEL-5, TP53 wild type, and SK-MEL-28, TP53 mutated.	trans-sulfonamide-platinum	70-96	P53	Homo sapiens	167-171
10671668-4	2000	In tumors treated with nedaplatin, they also increased, but the incidences of p53 protein-positive cells and apoptosis induced by 32 mg/kg nedaplatin, 1/2 LD50, were lower than those induced by 1 Gy irradiation.	nedaplatin	23-33	P53	Homo sapiens	78-81
10064859-13	1999	More strikingly, the relationship between aflatoxin exposure and development of human hepatocellular carcinoma (HHC) was demonstrated by the studies on the p53 tumor suppressor gene.	Aflatoxins	42-51	P53	Homo sapiens	156-159
10064859-14	1999	High frequency of p53 mutations (G--&gt;T transversion at codon 249) was found to occur in HHC collected from populations exposed to high levels of dietary aflatoxin in China and Southern Africa.	Aflatoxins	156-165	P53	Homo sapiens	18-21
10751606-2	2000	To further characterize p53-mediated DNA repair, we studied the effect of p53 status on the ability of the DNA repair inhibitor 1-ss-D-arabinofuranosylcytosine (AraC) to sensitize MEF to bleomycin-induced chromatid aberrations.	Cytarabine	161-165	P53	Homo sapiens	24-27
10751606-2	2000	To further characterize p53-mediated DNA repair, we studied the effect of p53 status on the ability of the DNA repair inhibitor 1-ss-D-arabinofuranosylcytosine (AraC) to sensitize MEF to bleomycin-induced chromatid aberrations.	Cytarabine	161-165	P53	Homo sapiens	74-77
28231799-5	2017	METHODS: We aimed to compare the cytotoxic effects of cisplatin and a trans-sulfonamide-platinum-complex (TSPC), in two human melanoma cell lines that differ in their TP53 status: SK-MEL-5, TP53 wild type, and SK-MEL-28, TP53 mutated.	trans-sulfonamide-platinum	70-96	P53	Homo sapiens	190-194
28231799-5	2017	METHODS: We aimed to compare the cytotoxic effects of cisplatin and a trans-sulfonamide-platinum-complex (TSPC), in two human melanoma cell lines that differ in their TP53 status: SK-MEL-5, TP53 wild type, and SK-MEL-28, TP53 mutated.	trans-sulfonamide-platinum	70-96	P53	Homo sapiens	190-194
10037682-0	1999	Long term lithium treatment suppresses p53 and Bax expression but increases Bcl-2 expression.	Lithium	10-17	P53	Homo sapiens	39-42
27550999-3	2017	Here, we evaluated the antitumor effect of a novel small-molecule inhibitor of the MDM2-p53 interaction (MI-773) combined with cisplatin in patient-derived xenograft (PDX) ACC tumors.Experimental Design: Therapeutic strategies with MI-773 and/or cisplatin were evaluated in SCID mice harboring PDX ACC tumors (UM-PDX-HACC-5) and in low passage primary human ACC cells (UM-HACC-2A, -2B, -5, -6) in vitro The effect of therapy on the fraction of cancer stem cells (CSC) was determined by flow cytometry for ALDH activity and CD44 expression.Results: Combined therapy with MI-773 with cisplatin caused p53 activation, induction of apoptosis, and regression of ACC PDX tumors.	2-methyl-4-isothiazolin-3-one	105-107	P53	Homo sapiens	88-91
10769646-10	2000	All of the cell lines studied, CEM/0 (wt) and the ara-C resistant clones, showed functional p53 protein.	Cytarabine	50-55	P53	Homo sapiens	92-95
10769646-11	2000	The cell treatment with 0.1, 1 and 10 microM ara-C for 48 hours showed increased p53 protein expression in most of these lines.	Cytarabine	45-50	P53	Homo sapiens	81-84
27894814-7	2017	Building upon LASAGNA-search and kinetics binding assay, p53 was found to be a potential transcription factor for PTPN11.	lasagna	14-21	P53	Homo sapiens	57-60
10585590-4	2000	Moreover, expression of wt-p53 in MCF7/Adr cells induced the production of reactive oxygen intermediates (ROIs) and caused glutathione (GSH) depletion, indicating disturbances in the cellular redox state.	reactive oxygen intermediates	75-104	P53	Homo sapiens	27-30
10082308-3	1999	METHODS: We report here a parallel flow cytometric method for semiquantitative detection of p53 protein and apoptosis (percent of apoptotic cells) in a pre-B leukemic cell line (NALM-6) exposed to various antitumor agents (2.35 microg/ml etoposide; 0.175 microg/ml FCE296; 0.4 microg/ml FCE624; and 1.5 microg/ml L-PAM).	fce296	265-271	P53	Homo sapiens	92-95
9927185-3	1999	When treated with N-(phosphonacetyl)-L-aspartate (PALA), which inhibits pyrimidine nucleotide synthesis, leading to synthesis of damaged DNA from highly unbalanced dNTP pools, p53-null cells enter mitosis after they have completed DNA replication, but cells with wild-type p53 do not, revealing that p53 also mediates a checkpoint that monitors the quality of newly replicated DNA.	Pyrimidine Nucleotides	72-93	P53	Homo sapiens	176-179
27637603-10	2017	CONCLUSIONS: The presence of serum p53 antibody can be used as a novel, noninvasive predictor of the pathological tumor response to NAC with DCF in ESCC patients.	nac	132-135	P53	Homo sapiens	35-38
9819415-4	1998	It is predicted that LMB should inhibit nuclear-cytoplasmic shuttling by MDM2 and subsequently stabilize p53.	leptomycin B	21-24	P53	Homo sapiens	105-108
9819415-10	1998	In addition, LMB reduced E6"s ability to degrade p53 in the absence of MDM2, demonstrating that complete degradation of p53 by E6 requires nuclear export and therefore likely occurs in cytoplasmic proteasomes.	leptomycin B	13-16	P53	Homo sapiens	49-52
9819415-10	1998	In addition, LMB reduced E6"s ability to degrade p53 in the absence of MDM2, demonstrating that complete degradation of p53 by E6 requires nuclear export and therefore likely occurs in cytoplasmic proteasomes.	leptomycin B	13-16	P53	Homo sapiens	120-123
10611334-3	1999	Here, the highly sensitive ligation-mediated PCR was employed to quantify, at nucleotide resolution, the repair of UVB-induced cyclobutane pyrimidine dimers (CPDs) in genetically p53-deficient Li-Fraumeni skin fibroblasts, as well as in human lung fibroblasts expressing the human papillomavirus (HPV) E6 oncoprotein that functionally inactivates p53.	cyclobutane pyrimidine	127-149	P53	Homo sapiens	179-182
10575010-0	1999	Benzo[a]pyrene activates the human p53 gene through induction of nuclear factor kappaB activity.	Benzo(a)pyrene	0-14	P53	Homo sapiens	35-38
10575010-2	1999	In the present study, the effect of a potent lung cancer carcinogen, benzo[a]pyrene (B[a]P) on p53 expression was investigated.	Benzo(a)pyrene	69-83	P53	Homo sapiens	95-98
10543945-1	1999	In human skin cancers, more than 30 % of all mutations in the p53 gene are transitions at dipyrimidines within the sequence context CpG, i.e. 5"-TCG and 5"-CCG, found at several mutational hotspots.	5"-ccg	153-159	P53	Homo sapiens	62-65
9753464-0	1998	Phosphorylation of the C-terminal sites of human p53 reduces non-sequence-specific DNA binding as modeled with synthetic peptides.	Peptides	121-129	P53	Homo sapiens	49-52
10582657-15	1999	Induction of p53 levels was observed in WHCO3 cells exposed to GLA, AA, PGA2, indomethacin and the combination of indomethacin and GLA or AA.	gamma-Linolenic Acid	63-66	P53	Homo sapiens	13-16
27888811-3	2017	Overexpression of mutated p53 with reduced or abolished function is often connected to resistance to standard medications, including cisplatin, alkylating agents (temozolomide), anthracyclines, (doxorubicin), antimetabolites (gemcitabine), antiestrogenes (tamoxifen) and EGFR-inhibitors (cetuximab).	Temozolomide	163-175	P53	Homo sapiens	26-29
10582657-15	1999	Induction of p53 levels was observed in WHCO3 cells exposed to GLA, AA, PGA2, indomethacin and the combination of indomethacin and GLA or AA.	prostaglandin A2	72-76	P53	Homo sapiens	13-16
14634277-3	1999	Four-day treatment with L-745,337 caused a concentration-dependent inhibition of cell growth (IC50: 0.9 mM) associated with the induction of p21WAF-1/cip1 and an increase in the proportion of apoptotic nuclei (EC50: 0.1 and 0.34 mM, respectively) while reducing the levels of m273-p53 (IC50: 0.2 mM).	l-745	24-29	P53	Homo sapiens	281-284
9748583-13	1998	Parry, Enhanced restriction site mutation (RSM) analysis of 1, 2-dimethylhydrazine-induced mutations, using endogenous p53 intron sequences, Mutagenesis 12 (1997) pp.	1,2-Dimethylhydrazine	60-82	P53	Homo sapiens	119-122
9658074-9	1998	Using biotinylated peptides, we show that phosphorylation of Ser15 alone inhibits p53-TFIID interaction.	Peptides	19-27	P53	Homo sapiens	82-85
14634277-6	1999	We conclude that high concentrations of L-745,337 and sodium salicylate inhibit colon cancer cell growth by a mechanism unrelated to cyclooxygenase inhibition that may involve p53-independent induction of the tumor suppressor p21WAF-1/cip1.	l-745	40-45	P53	Homo sapiens	176-179
28052008-8	2017	Taken together, combination of metformin and 2-deoxyglucose reverses MDR of MCF-7/Dox cells by recovering p53 function and increasing doxorubicin accumulation.	Deoxyglucose	45-59	P53	Homo sapiens	106-109
9714716-1	1998	The ability of Cu(II) and Fe(III) to promote site-specific DNA damage in the presence of endogenous reductants was investigated by using 32P-5"-end-labeled DNA fragments obtained from the human p53 tumor suppressor gene and the c-Ha-ras-1 protooncogene.	cu(ii)	15-21	P53	Homo sapiens	194-197
28116660-8	2017	Moreover, 10 and 20 mug/mL Sal B reduced the expression levels of p53, increased the Bcl-2/Bax ratio and inhibited the caspase-3 activity in ox-LDL-treated HUVECs (P&lt;0.05).	sal	27-30	P53	Homo sapiens	66-69
9667752-6	1998	Phenol, diethylstilbestrol and ethylacrylate also induced increases in cellular p53.	ethyl acrylate	31-44	P53	Homo sapiens	80-83
9610719-6	1998	Elevated c-myc and p53 expression appears to be responsible for the time-dependent accumulation of apoptotic cells after prolonged 2-DG treatment.	Deoxyglucose	131-135	P53	Homo sapiens	19-22
10389978-5	1999	All seven HCCs with a p53 mutation from Qidong and three of five from Shanghai had the aflatoxin-associated point mutation with a G to T transversion at codon 249, position 3.	Aflatoxins	87-96	P53	Homo sapiens	22-25
10037682-9	1999	These results strongly suggest that lithium-induced Bcl-2 up-regulation and p53 and Bax down-regulation play a prominent role in neuroprotection against excitotoxicity.	Lithium	36-43	P53	Homo sapiens	76-79
28957796-10	2017	In 8505c cells transfected with wild-type p53, treatment with radioiodine resulted in increased radioiodine uptake and increased apoptotic cell death compared with 8505c cells harboring the p53 mutation.	Iodine-131	62-73	P53	Homo sapiens	42-45
10100719-13	1999	In particular, the greater activity of DACH-acetato-Pt in cisplatin-resistant wild-type p53 ovarian tumor models can be ascribed to its ability to more efficiently induce p53 protein and activate p53 functions.	(diaminocyclohexane)(diacetato)(dichloro)platinum	39-54	P53	Homo sapiens	88-91
10100719-13	1999	In particular, the greater activity of DACH-acetato-Pt in cisplatin-resistant wild-type p53 ovarian tumor models can be ascribed to its ability to more efficiently induce p53 protein and activate p53 functions.	(diaminocyclohexane)(diacetato)(dichloro)platinum	39-54	P53	Homo sapiens	171-174
10100719-13	1999	In particular, the greater activity of DACH-acetato-Pt in cisplatin-resistant wild-type p53 ovarian tumor models can be ascribed to its ability to more efficiently induce p53 protein and activate p53 functions.	(diaminocyclohexane)(diacetato)(dichloro)platinum	39-54	P53	Homo sapiens	171-174
9605744-3	1998	Using a UvrABC incision method, we have found that cytosine methylation greatly enhances guanine alkylation at all CpG sites in the p53 gene by a variety of carcinogens, including benzo(a)pyrene diol epoxide, benzo(g)chrysene diol epoxide, aflatoxin B1 8,9-epoxide, and N-acetoxy-2-acetylaminofluorene.	Acetoxyacetylaminofluorene	270-301	P53	Homo sapiens	132-135
9580640-0	1998	Role of wild-type p53 on the antineoplastic activity of temozolomide alone or combined with inhibitors of poly(ADP-ribose) polymerase.	Temozolomide	56-68	P53	Homo sapiens	18-21
9580640-6	1998	Treatment with TZM concentrations not toxic for the cells transduced with the control vector (p53-cells), induced apoptosis in p53+ cells.	Temozolomide	15-18	P53	Homo sapiens	94-97
9580640-6	1998	Treatment with TZM concentrations not toxic for the cells transduced with the control vector (p53-cells), induced apoptosis in p53+ cells.	Temozolomide	15-18	P53	Homo sapiens	127-130
28957796-10	2017	In 8505c cells transfected with wild-type p53, treatment with radioiodine resulted in increased radioiodine uptake and increased apoptotic cell death compared with 8505c cells harboring the p53 mutation.	Iodine-131	62-73	P53	Homo sapiens	190-193
9499413-6	1998	We propose that Ad12 infection, actinomycin D and araC all induce a similar or identical global damage arrest signal (perhaps a modification or altered conformation of p53) that preferentially interferes with metaphase condensation of the RNU1 and RNU2 loci.	Cytarabine	50-54	P53	Homo sapiens	168-171
10202240-7	1999	The presence of peripheral stem cell (PSC) products was found to decrease the effect of Adv-p53 on TC clonogenic growth, suggesting that PSC products could compete with TC for infection by recombinant Adv.	Technetium	99-101	P53	Homo sapiens	92-95
10202240-9	1999	We conclude that a 4-hour incubation of stem cell products (2 x 10(8)/ml) with 4 x 10(11) Adv-p53 particles is sufficient to completely purge TC with no effect on hematopoietic cell function.	Technetium	142-144	P53	Homo sapiens	94-97
9468547-14	1998	Thus, BP-induced aberrant proliferation is inhibited by the natural phytochemicals in part due to regulation of cell cycle progression and induction of p53 dependent apoptosis.	Benzo(a)pyrene	6-8	P53	Homo sapiens	152-155
28957796-10	2017	In 8505c cells transfected with wild-type p53, treatment with radioiodine resulted in increased radioiodine uptake and increased apoptotic cell death compared with 8505c cells harboring the p53 mutation.	Iodine-131	96-107	P53	Homo sapiens	42-45
9468185-5	1998	p53 gene transfer reduced thymidine incorporation of VSMCs stimulated by platelet-derived growth factor-BB (P&lt;.001).	vsmcs	53-58	P53	Homo sapiens	0-3
9864421-0	1999	Penclomedine-induced DNA fragmentation and p53 accumulation correlate with reproductive cell death in colorectal carcinoma cells with altered p53 status.	penclomedine	0-12	P53	Homo sapiens	142-145
9864421-3	1999	We previously reported that telomerase positive colorectal carcinoma (RKO) cells with abrogated p53 function were more sensitive to penclomedine than were telomerase positive cells with wild-type p53.	penclomedine	132-144	P53	Homo sapiens	96-99
28957796-11	2017	CONCLUSION: In summary, transfection with wild-type p53 can increase the therapeutic effect of radioiodine by regulating the expression of the NIS.	Iodine-131	95-106	P53	Homo sapiens	52-55
9864421-4	1999	The present study demonstrates that significant differences in DNA fragmentation in response to penclomedine were observed in RKO cells lacking functional p53 compared with RKO cells with normal p53 function.	penclomedine	96-108	P53	Homo sapiens	155-158
9864421-4	1999	The present study demonstrates that significant differences in DNA fragmentation in response to penclomedine were observed in RKO cells lacking functional p53 compared with RKO cells with normal p53 function.	penclomedine	96-108	P53	Homo sapiens	195-198
9864421-6	1999	RKO cells with functional p53 respond to penclomedine treatment with a dose-dependent increase in p53 protein levels.	penclomedine	41-53	P53	Homo sapiens	26-29
9864421-6	1999	RKO cells with functional p53 respond to penclomedine treatment with a dose-dependent increase in p53 protein levels.	penclomedine	41-53	P53	Homo sapiens	98-101
9346961-1	1997	We have shown previously that Li-Fraumeni syndrome fibroblasts homozygous for p53 mutations are deficient in the removal of UV-induced cyclobutane pyrimidine dimers from genomic DNA, but still proficient in the transcription-coupled repair pathway (Ford, J. M., and Hanawalt, P. C. (1995) Proc.	cyclobutane pyrimidine	135-157	P53	Homo sapiens	78-81
9346961-8	1997	Cells homozygous for p53 mutations were deficient in the repair of both photoproducts, whereas cells heterozygous for mutant p53 exhibited normal repair of 6-4 photoproducts, but decreased initial rates of removal of cyclobutane pyrimidine dimers, compared with normal cells.	cyclobutane pyrimidine	217-239	P53	Homo sapiens	125-128
9864421-9	1999	These studies suggest that penclomedine may have a therapeutic advantage in killing cells that have abrogated p53 function.	penclomedine	27-39	P53	Homo sapiens	110-113
29130967-4	2017	RESULTS: Mutant p53 cells exhibited increased expression of the C/EBP homologous protein (CHOP), glucose-regulated protein 78 (GRP78), and inositol-requiring enzyme-1alpha (IRE1alpha).	Inositol	139-147	P53	Homo sapiens	16-19
9865721-4	1998	The iron chelator deferoxamine induced both HIF-1alpha and p53, but p53 up-regulation could still be detected in HIF-1alpha-deficient cells, suggesting that mechanisms other than HIF-1alpha activation contribute to oxygen-regulated p53 induction.	Deferoxamine	18-30	P53	Homo sapiens	59-62
9346961-11	1997	The regulated expression of wild-type p53 resulted in the recovery of normal levels of repair of both cyclobutane pyrimidine dimers and 6-4 photoproducts in genomic DNA, but did not alter the transcription-coupled repair of cyclobutane pyrimidine dimers.	cyclobutane pyrimidine	102-124	P53	Homo sapiens	38-41
9346961-11	1997	The regulated expression of wild-type p53 resulted in the recovery of normal levels of repair of both cyclobutane pyrimidine dimers and 6-4 photoproducts in genomic DNA, but did not alter the transcription-coupled repair of cyclobutane pyrimidine dimers.	cyclobutane pyrimidine	224-246	P53	Homo sapiens	38-41
9282168-3	1997	Western blot analysis demonstrated the expression of wt p53 in H-358 cells following infection with rAAVp53.	raavp53	100-107	P53	Homo sapiens	56-59
28193070-4	2016	After magnetic capture of the modified MBs onto screen-printed carbon working electrodes, the amperometric signal using the system hydroquinone/H2O2 was related to the levels of p53-autoantibodies in the sample.	hydroquinone	131-143	P53	Homo sapiens	178-181
21590120-2	1997	Pentoxifylline has recently been shown to sensitize breast cancer cells in which the wild-type p53 function was abrogated to cisplatin-induced apoptosis.	Pentoxifylline	0-14	P53	Homo sapiens	95-98
21590120-7	1997	Pentoxifylline increased the amount of radiation-induced DNA fragmentation and apoptosis in p53-defective U251 and LN-Z308 cells.	Pentoxifylline	0-14	P53	Homo sapiens	92-95
9843965-0	1998	A p53-dependent S-phase checkpoint helps to protect cells from DNA damage in response to starvation for pyrimidine nucleotides.	Pyrimidine Nucleotides	104-126	P53	Homo sapiens	2-5
27989139-10	2016	The modulation of RAD51 is correlated with p53 level, which suggests p53 has a role in TCBQ-induced RAD51 clearance.	tetrachlorobenzoquinone	87-91	P53	Homo sapiens	43-46
9808524-7	1998	Of 216 pieces near or adjacent to p53- tumors, p53+ frequencies were 25% of BCH, 25% of DYS and 0% of CIS.	bis(cyclohexylammonium)sulfate	76-79	P53	Homo sapiens	47-50
9808574-9	1998	These data demonstrate that flavopiridol has significant in vitro activity against human CLL cells through activation of caspase-3, which appears to occur independently of bcl-2 modulation, the presence of IL-4, or p53 status.	alvocidib	28-40	P53	Homo sapiens	215-218
9176489-1	1997	We demonstrate here that synthetic 22-mer peptide 46, corresponding to the carboxy-terminal amino acid residues 361-382 of p53, can activate specific DNA binding of wild-type p53 in vitro and can restore the transcriptional transactivating function of at least some mutant p53 proteins in living cells.	Peptides	42-49	P53	Homo sapiens	123-126
9176489-1	1997	We demonstrate here that synthetic 22-mer peptide 46, corresponding to the carboxy-terminal amino acid residues 361-382 of p53, can activate specific DNA binding of wild-type p53 in vitro and can restore the transcriptional transactivating function of at least some mutant p53 proteins in living cells.	Peptides	42-49	P53	Homo sapiens	175-178
27989139-10	2016	The modulation of RAD51 is correlated with p53 level, which suggests p53 has a role in TCBQ-induced RAD51 clearance.	tetrachlorobenzoquinone	87-91	P53	Homo sapiens	69-72
9176489-1	1997	We demonstrate here that synthetic 22-mer peptide 46, corresponding to the carboxy-terminal amino acid residues 361-382 of p53, can activate specific DNA binding of wild-type p53 in vitro and can restore the transcriptional transactivating function of at least some mutant p53 proteins in living cells.	Peptides	42-49	P53	Homo sapiens	175-178
27934110-6	2016	Next we evaluated the performance of the biosensor in HepG2 cells by treatment with ginkgolic acid, a drug that reduces p53 sumoylation, as well as trichostatin A, a potential inducer of p53 sumoylation by enhancement of its nuclear export.	ginkgolic acid	84-98	P53	Homo sapiens	120-123
9065745-0	1997	Effect of penclomedine (NSC-338720) on telomere fusions, chromatin blebbing, and cell viability with and without telomerase activity and abrogated p53 function.	penclomedine	10-22	P53	Homo sapiens	147-150
9065745-8	1997	In addition, telomerase positive colorectal carcinoma cells with abrogated p53 (RC-10.3 cells) were more sensitive to penclomedine than were telomerase positive cells with wild-type p53 (RKO cells).	penclomedine	118-130	P53	Homo sapiens	75-78
9065745-9	1997	These studies suggest that penclomedine may have a therapeutic advantage in killing tumor cells that are positive for telomerase activity and defective in p53 function.	penclomedine	27-39	P53	Homo sapiens	155-158
9739169-1	1998	We previously reported that deferoxamine, an iron chelating agent, induced p53 and cell accumulation in the G1 phase of ML-1 cells in the same way as the DNA damaging agent, etoposide.	Deferoxamine	28-40	P53	Homo sapiens	75-78
9726816-5	1998	In contrast, PDTC, DDTC, and ammonium dithiocarbamate (ADTC) did not induce apoptosis; rather they led to the induction of p53 and p21 followed by G1/S arrest.	adtc	55-59	P53	Homo sapiens	123-126
9703875-0	1998	Increased p21/WAF-1 and p53 protein levels following sequential three drug combination regimen of fludarabine, cytarabine and docetaxel induces apoptosis in human leukemia cells.	Cytarabine	111-121	P53	Homo sapiens	24-27
9698467-2	1998	The possibility that such an agent could be directed specifically against p53-defective tumor cells led us to study the new methylxanthine, Lisofylline, for its ability to sensitize ovary cancer cells to cis-diamminedichloroplatinum(II) (CDDP).	methylxanthine	124-138	P53	Homo sapiens	74-77
27913471-7	2016	These recently approved drugs (ibrutinib, idelalisib, and venetoclax) are reporting excellent outcomes, including patients with high-risk disease such as 17p deletion (17p-) or TP53 mutations (TP53mut).	ibrutinib	31-40	P53	Homo sapiens	177-181
8952546-11	1996	Immunohistochemistry of FLS cultured in chamber slides localized the p53 to the cytoplasm of most resting FLS, with nuclear staining in only 10.7 +/- 2.4%.	CHEMBL1232769	24-27	P53	Homo sapiens	69-72
27198718-2	2016	Ibrutinib, a Bruton"s tyrosine kinase inhibitor is approved for relapsed/refractory and del(17p)/TP53 mutated chronic lymphocytic leukemia.	ibrutinib	0-9	P53	Homo sapiens	97-101
8957493-6	1996	RESULTS: p53 mutations occurred in 11 (61%) patients with TCV compared with two (11%) in control group (p = 0.05).	Trichloroethylene	58-61	P53	Homo sapiens	9-12
8957493-10	1996	CONCLUSIONS: TCV was associated with a significantly higher rate of p53 positivity than common papillary carcinoma.	Trichloroethylene	13-16	P53	Homo sapiens	68-71
9704902-2	1998	As a tumor promoter, heptachlor induces human myeloblastic leukemia cells to differentiate, and also down-regulates the tumor suppressor gene p53 in human immune cells.	Heptachlor	21-31	P53	Homo sapiens	142-145
9735599-6	1998	The induction of wild type p53 protein by addition of IPTG did not significantly increased radiosensitivity.	Isopropyl Thiogalactoside	54-58	P53	Homo sapiens	27-30
9610719-3	1998	Moreover, 2-DG appears to restore the normal half-life of the tumor suppressor gene product p53, because the protein is strongly up-regulated after HPV 18 E6/E7 suppression.	Deoxyglucose	10-14	P53	Homo sapiens	92-95
8900110-7	1996	Cells lacking the c-abl gene also responded to ara-C and MMS with increases in p53 levels and induction of p21.	Cytarabine	47-52	P53	Homo sapiens	79-82
27075340-10	2016	Furthermore, AgNP-induced apoptosis was found dependent on the overproduction of reactive oxygen species (ROS) and affecting of MAPKs and AKT signaling and DNA damage-mediated p53 phosphorylation to advance HePG-2 cells apoptosis.	agnp	13-17	P53	Homo sapiens	176-179
8832894-0	1996	Preferential formation of benzo[a]pyrene adducts at lung cancer mutational hotspots in P53.	Benzo(a)pyrene	26-40	P53	Homo sapiens	87-90
9563650-2	1998	When the p53 tumor suppressor gene was used, 4-nitro-2-aminophenol caused Cu(II)-dependent piperidine-labile sites at poly G sequences.	cu(ii)	74-80	P53	Homo sapiens	9-12
9548807-0	1998	Induction of p53 by the concerted actions of aziridine and quinone moieties of diaziquone.	quinone	59-66	P53	Homo sapiens	13-16
9548807-6	1998	Diaziquone (AZQ), an anticancer agent, and its derivatives, diaziridinequinone (DZQ) and methyldiaziridinequinone (MeDZQ), induced p53 in a dose- and time-dependent manner as measured by the electrophoretic mobility shift assay.	diaziridinequinone	60-78	P53	Homo sapiens	131-134
27907160-7	2016	Further, AS1411 induced cell apoptosis, which was prevented by silencing of p53 and overexpression of Bcl-2.	AGRO 100	9-15	P53	Homo sapiens	76-79
27777210-8	2016	Both RITA and TMZ, especially the latter, significantly increased the expressions of p53, p21, puma, and other apoptosis-associated genes to accelerate apoptosis and inhibit the growth and colony formation of U87 cells, and the effect was more obvious with a combined treatment.	Temozolomide	14-17	P53	Homo sapiens	85-88
9525497-9	1998	The results demonstrate that human colon and cervical cancer cells characterized by a mutated or disrupted p53 (i.e. not transfected) are radiosensitized by PTX, which alleviates the postirradiation G2/M-phase block.	Pentoxifylline	157-160	P53	Homo sapiens	107-110
8921985-5	1996	The most significant finding is that more than 50% of HCC patients from high aflatoxin exposure areas such as southern Africa and Qidong, China harboured a codon 249 G to T transversion in the p53 tumor suppressor gene, which is found to be consistent with the mutagenic specificity of AFB1 observed in vitro.	Aflatoxins	77-86	P53	Homo sapiens	193-196
8706243-3	1996	Sublines that were resistant to melphalan, pyrazafurin, mitoxantrone, etoposide and PALA all retained expression of wild-type p53.	pyrazafurin	43-54	P53	Homo sapiens	126-129
7586197-6	1995	Treatment of PBLs with 2.5 microM of (+/-)-anti-BPDE and 1 mM of 3-aminobenzamide, an inhibitor of the DNA strand break-dependent enzyme poly(ADP-ribose) polymerase, resulted in increased p53 levels, in comparison to cells treated with (+/-)-anti-BPDE alone.	(+/-)-anti-	37-48	P53	Homo sapiens	188-191
9414172-4	1997	The recently developed individual biochemical and molecular markers of aflatoxin exposure, i.e., aflatoxin-albumin adducts in blood and a specific GC to TA transversion mutation in codon 249 of the p53 gene (249ser p53 mutation) in hepatocellular carcinomas, permit a better quantitative estimation of aflatoxin exposure in different populations of the world.	Aflatoxins	71-80	P53	Homo sapiens	198-201
27580721-6	2016	P53 inhibitors can block the apoptosis induced by both ZIKVC and ZIKVM in hNPCs, with higher potency against ZIKVC-induced apoptosis.	zikvc	55-60	P53	Homo sapiens	0-3
9433478-6	1997	Our results indicate that p53 accumulation followed by transcriptional activation of genes implicated in growth arrest is triggered in TTD/XP-D cells by the persistence of cyclobutane pyrimidine dimers, which are known to block transcription, on the transcribed strands of active genes.	cyclobutane pyrimidine	172-194	P53	Homo sapiens	26-29
7641180-0	1995	Beta-lapachone-mediated apoptosis in human promyelocytic leukemia (HL-60) and human prostate cancer cells: a p53-independent response.	beta-lapachone	0-14	P53	Homo sapiens	109-112
7641180-9	1995	These events are p53 independent, since PC-3 and HL-60 cells are null cells, LNCaP are wild-type, and DU-145 contain mutant p53, yet all undergo apoptosis after beta-lapachone treatment.	beta-lapachone	161-175	P53	Homo sapiens	17-20
7641180-10	1995	Interestingly, beta-lapachone treatment of p53 wild type-containing prostate cancer cells (i.e., LNCaP) did not result in the induction of nuclear levels of p53 protein, as did camptothecin-treated cells.	beta-lapachone	15-29	P53	Homo sapiens	43-46
7641180-11	1995	Like other Topo I inhibitors, beta-lapachone may induce apoptosis by locking Topo I onto DNA, blocking replication fork movement, and inducing apoptosis in a p53-independent fashion.	beta-lapachone	30-44	P53	Homo sapiens	158-161
9661701-0	1997	Induction of fragility at the human RNU2 locus by cytosine arabinoside is dependent upon a transcriptionally competent U2 small nuclear RNA gene and the expression of p53.	Cytarabine	50-70	P53	Homo sapiens	167-170
7605578-0	1995	Characterization of a murine p53ser246 mutant equivalent to the human p53ser249 associated with hepatocellular carcinoma and aflatoxin exposure.	Aflatoxins	125-134	P53	Homo sapiens	70-73
27580721-6	2016	P53 inhibitors can block the apoptosis induced by both ZIKVC and ZIKVM in hNPCs, with higher potency against ZIKVC-induced apoptosis.	zikvc	109-114	P53	Homo sapiens	0-3
7605578-1	1995	A mutation in the tumor suppressor p53 gene resulting in an Arg--&gt;Ser substitution in position 249 is found frequently in human hepatocellular carcinomas associated with hepatitis B infection and with aflatoxin exposure.	Aflatoxins	204-213	P53	Homo sapiens	35-38
27468725-0	2016	Dimethylfumarate inhibits melanoma cell proliferation via p21 and p53 induction and bcl-2 and cyclin B1 downregulation.	Dimethyl Fumarate	0-16	P53	Homo sapiens	66-69
7664937-0	1995	Recent aflatoxin exposure and mutation at codon 249 of the human p53 gene: lack of association.	Aflatoxins	7-16	P53	Homo sapiens	65-68
9278485-3	1997	Here we analyse spontaneously arising mutations at the tetranucleotide CCGG ( Msp I recognition site), at positions 14 067-14 070 of the p53 gene sequence, in three colon cancer cell lines, two with microsatellite instability and one without this characteristic.	tetranucleotide	55-70	P53	Homo sapiens	137-140
9268054-7	1997	Results of this investigation show that the mechanism of G1 accumulation induced by DFO involves a p53-independent pathway and that expression of p21 protein may be regulated posttranscriptionally.	Deferoxamine	84-87	P53	Homo sapiens	99-102
7664937-1	1995	Experiments were done to show whether a G to T mis-sense mutation at the third base of codon 249 of the p53 tumour suppressor gene is a "hot spot" of aflatoxin attack as suggested by the results of epidemiological studies.	Aflatoxins	150-159	P53	Homo sapiens	104-107
27468725-11	2016	Interestingly, DMF induced p53 and p21 yet inhibited cyclin B1 expression in a concentration-dependent manner.	Dimethyl Fumarate	15-18	P53	Homo sapiens	27-30
27468725-13	2016	The knockdown of DMF induced p53 via siRNA led to significantly reduced apoptosis but had no influence on cell cycle arrest.	Dimethyl Fumarate	17-20	P53	Homo sapiens	29-32
9815799-11	1997	These results indicate that p53 overexpression in TBB specimens predicts poor prognosis and chemoresistance in advanced stage NSCLC.	2-ethylhexyl 2,3,4,5-tetrabromobenzoate	50-53	P53	Homo sapiens	28-31
27468725-15	2016	These data provide evidence that DMF inhibits melanoma proliferation by reinduction of important cell cycle inhibitors leading to a concentration-dependent G0/G1 or G2/M cell cycle arrest and induction of apoptosis via downregulation of bcl-2 and induction of p53 and PARP-1 cleavage.	Dimethyl Fumarate	33-36	P53	Homo sapiens	260-263
9772449-4	1997	The TC, TG and CE contents in vascular AS tissues in p53 gene mutation group were higher than those in non-mutations group (ANOV: F = 4.56-9.97, P &lt; 0.05-0.01, no differences in PL contents).	Technetium	4-6	P53	Homo sapiens	53-56
7712469-0	1995	Disruption of p53 function sensitizes breast cancer MCF-7 cells to cisplatin and pentoxifylline.	Pentoxifylline	81-95	P53	Homo sapiens	14-17
27609895-3	2016	Kras activation and Trp53 deletion in the pancreas or the lung result in pancreatic ductal adenocarinoma (PDAC) or non-small cell lung carcinoma (NSCLC), respectively, but despite the same initiating events, these tumors use branched-chain amino acids (BCAAs) differently.	Amino Acids, Branched-Chain	225-251	P53	Homo sapiens	20-25
7712469-12	1995	Our results show that a combination of CDDP and pentoxifylline is capable of synergistic and preferential killing of p53-defective tumor cells that do not readily undergo apoptosis.	Pentoxifylline	48-62	P53	Homo sapiens	117-120
8867673-9	1995	In addition, Mn2+ strongly promoted activation of p58c-fgr and p53/56lyn without additional stimuli.	Manganese(2+)	13-17	P53	Homo sapiens	63-66
9812584-3	1997	Lanthanum chloride, cerium chloride and mixed rare-earth chloride at levels of 0.5 to 1.5 mmol/L could inhibit obviously growth of cancer cells and change cell morphology and microtubule structure of PAMC82, similar to that of normal cells, their colony-forming ability lowered in soft agar, and expression of tumor suppressor gene p53, p16 and p21 increased and that of gene nm23 lowered.	lanthanum chloride	0-18	P53	Homo sapiens	332-335
9163674-9	1997	It appears that, in contrast to the frequently reported G--&gt;T transversions in codon 249 of the p53 gene in primary hepatomas in aflatoxin-exposed humans, the failure to detect Ha-ras mutations in these tumours is not due to an inability of aflatoxin B1 to activate this proto-oncogene.	Aflatoxins	132-141	P53	Homo sapiens	99-102
27609895-3	2016	Kras activation and Trp53 deletion in the pancreas or the lung result in pancreatic ductal adenocarinoma (PDAC) or non-small cell lung carcinoma (NSCLC), respectively, but despite the same initiating events, these tumors use branched-chain amino acids (BCAAs) differently.	Amino Acids, Branched-Chain	253-258	P53	Homo sapiens	20-25
27321910-7	2016	The stabilization of p53 by nutlin-3a abolished butaprost-mediated cell death protection.	butaprost	48-57	P53	Homo sapiens	21-24
9102461-7	1997	The annealing activity of p53 is almost abolished in the presence of magnesium indicating that it can be sharply regulated in vitro and, in principle, could also be regulated in vivo.	Magnesium	69-78	P53	Homo sapiens	26-29
25765771-4	2016	METHODS: The RDP-p53 fusion proteins are expressed in Escherichia coli, and they are labeled with FITC and rhodamine B by chemical modification.	Fluorescein-5-isothiocyanate	98-102	P53	Homo sapiens	17-20
9006107-2	1996	A high rate of mutations in the p53 tumor suppressor gene in hepatocellular carcinomas of predominantly hepatitis B virus (HBV) carrier patients has been recently related to dietary aflatoxin.	Aflatoxins	182-191	P53	Homo sapiens	32-35
9006107-9	1996	Overall, our findings indicate that in woodchucks and in ground squirrels exposure to aflatoxin may affect the development of p53 mutations less than in humans.	Aflatoxins	86-95	P53	Homo sapiens	126-129
7923176-2	1994	Recently, a broad range of mutations in the p53 tumor suppressor gene has been reported in human HCCs, predominantly from hepatitis B virus carriers in areas with either high or low levels of exposure to dietary aflatoxin.	Aflatoxins	212-221	P53	Homo sapiens	44-47
7923176-12	1994	In view of the considerably lower apparent rate of mutations in comparison to human HCCs, we suggest a less important role for aflatoxin in the induction of p53 mutations in HCCs of ground squirrels.	Aflatoxins	127-136	P53	Homo sapiens	157-160
27576884-11	2016	However, only p53 overexpression was associated with predicting CSS independently of tumor stage.&amp;nbsp.	nbsp	102-106	P53	Homo sapiens	14-17
7930673-9	1994	Dithranol (1 microgram/microliter, n = 8), sodium dodecylsulphate (5%, n = 4), and retinoic acid (0.5%, n = 4), applied for 48 h, caused erythema, significantly increased p53 protein levels (p &lt; 0.05), and also increased p53 mRNA.	Anthralin	0-9	P53	Homo sapiens	171-174
7930673-9	1994	Dithranol (1 microgram/microliter, n = 8), sodium dodecylsulphate (5%, n = 4), and retinoic acid (0.5%, n = 4), applied for 48 h, caused erythema, significantly increased p53 protein levels (p &lt; 0.05), and also increased p53 mRNA.	Anthralin	0-9	P53	Homo sapiens	224-227
8076368-0	1994	Hyperphosphorylation of p53 induced by benzene, toluene, and chloroform.	Benzene	39-46	P53	Homo sapiens	24-27
9118908-0	1996	Carcinogenic potential of benzene and toluene when evaluated using cyclin-dependent kinase activation and p53-DNA binding.	Benzene	26-33	P53	Homo sapiens	106-109
9118908-4	1996	Kinase activation and subsequent hyperphosphorylation of pRb105 and p53 by benzene or toluene may be responsible for their growth promotional effects, but it does not account for increased potential of benzene to induce cancer.	Benzene	75-82	P53	Homo sapiens	68-71
9118908-6	1996	Benzene increased p53-DNA site-specific DNA binding in RLE cells compared to control levels or the effects of toluene.	Benzene	0-7	P53	Homo sapiens	18-21
9118908-7	1996	Increased p53-DNA site-specific binding by benzene may be caused by damage to cellular DNA.	Benzene	43-50	P53	Homo sapiens	10-13
8967975-1	1996	With the use of clonogenic survival assays, we show that wild-type p53-expressing A2780 human ovarian cell lines transfected with a dominant negative mutant p53 gene (codon 143, valine to alanine) acquired cross-resistance to ionizing radiation, cisplatin, doxorubicin, and 1-beta-D-arabinofuranosylcytosine.	Cytarabine	274-307	P53	Homo sapiens	67-70
8967975-1	1996	With the use of clonogenic survival assays, we show that wild-type p53-expressing A2780 human ovarian cell lines transfected with a dominant negative mutant p53 gene (codon 143, valine to alanine) acquired cross-resistance to ionizing radiation, cisplatin, doxorubicin, and 1-beta-D-arabinofuranosylcytosine.	Cytarabine	274-307	P53	Homo sapiens	157-160
8076368-6	1994	Hyperphosphorylation of p53 may be involved in tumor promotion by benzene, toluene and chloroform.	Benzene	66-73	P53	Homo sapiens	24-27
7923066-3	1994	This led us to screen for p53 germ-line mutations in a group of seven patients affected with SMN, but characterized by an older age of onset than in the previous reports.	(S)-(+)-Mandelic acid	93-96	P53	Homo sapiens	26-29
27389299-0	2016	Photodynamic therapy with 5-aminolaevulinic acid and DNA damage: unravelling roles of p53 and ABCG2.	Aminolevulinic Acid	26-48	P53	Homo sapiens	86-89
8036011-3	1994	We have studied the capacity of hydrogen peroxide plus ferric chloride (FeCl3) to induce base pair changes in the hotspot codons 248 and 249 of the p53 tumor suppressor gene in human fibroblasts.	ferric chloride	55-70	P53	Homo sapiens	148-151
8036011-3	1994	We have studied the capacity of hydrogen peroxide plus ferric chloride (FeCl3) to induce base pair changes in the hotspot codons 248 and 249 of the p53 tumor suppressor gene in human fibroblasts.	ferric chloride	72-77	P53	Homo sapiens	148-151
8036011-7	1994	It is evident that H2O2/FeCl3 possesses essentially the same mutagenic specificity for codons 249 and 250 of p53 as bulky carcinogens such as aflatoxin B1, benzo(a)pyrene or heterocyclic amines.	ferric chloride	24-29	P53	Homo sapiens	109-112
8036011-7	1994	It is evident that H2O2/FeCl3 possesses essentially the same mutagenic specificity for codons 249 and 250 of p53 as bulky carcinogens such as aflatoxin B1, benzo(a)pyrene or heterocyclic amines.	Benzo(a)pyrene	156-170	P53	Homo sapiens	109-112
8956076-4	1996	The C-terminal segment p53(361-393) (3) and its derivative phosphorylated at serine 392 (3P392) were synthesized as partially protected peptides in the solid phase using Fmoc chemistry.	Peptides	136-144	P53	Homo sapiens	23-26
8956076-5	1996	Phosphoamino acid was incorporated into the N-terminal segment (1P315) at the residue corresponding to p53 serine 315 as Boc-Ser(PO3(Bzl)2)-OH during synthesis.	boc	121-124	P53	Homo sapiens	103-106
8764129-8	1996	We also found that a DNA fragment that contains the p53 promoters is nearly twice as sensitive to cyclobutane pyrimidine dimer induction by UV irradiation than are the surrounding fragments, which have the expected sensitivity.	cyclobutane pyrimidine	98-120	P53	Homo sapiens	52-55
27389299-1	2016	OBJECTIVES: In spite of high sensitivity of A549 cells (p53(+/+) ) to lethal effects of photodynamic therapy with 5-aminolaevulinic acid (5-ALA/PDT), DNA damage was observed only in H1299 cells (p53(-/-) ), suggesting that p53 may exert a protective effect.	Aminolevulinic Acid	114-136	P53	Homo sapiens	56-59
27389299-1	2016	OBJECTIVES: In spite of high sensitivity of A549 cells (p53(+/+) ) to lethal effects of photodynamic therapy with 5-aminolaevulinic acid (5-ALA/PDT), DNA damage was observed only in H1299 cells (p53(-/-) ), suggesting that p53 may exert a protective effect.	Aminolevulinic Acid	114-136	P53	Homo sapiens	195-198
8622677-9	1996	Our results highlight the chemotherapeutic potential of PGA2, particularly for suppressing growth of tumors lacking p53 function.	prostaglandin A2	56-60	P53	Homo sapiens	116-119
8033110-10	1994	Positive staining with PAb240 or DO7 antibodies against human p53 or with an antibody generated in our laboratory against the hamster p53 fusion protein was observed only in the solid form of well-differentiated ductal adenocarcinoma and in rare cells scattered in 4 of 28 MNU-induced tumors analyzed.	Methylnitrosourea	273-276	P53	Homo sapiens	134-137
27389299-1	2016	OBJECTIVES: In spite of high sensitivity of A549 cells (p53(+/+) ) to lethal effects of photodynamic therapy with 5-aminolaevulinic acid (5-ALA/PDT), DNA damage was observed only in H1299 cells (p53(-/-) ), suggesting that p53 may exert a protective effect.	Aminolevulinic Acid	114-136	P53	Homo sapiens	195-198
27235693-4	2016	Moreover, we also found that p53 and Bax might play an important role in MC-LR-induced apoptosis in HepG2 cells in which PUMA and survivin were involved.	cyanoginosin LR	73-78	P53	Homo sapiens	29-32
8033311-1	1994	Dietary aflatoxin and hepatitis B virus infection may play a role in generating the p53 tumor suppressor gene codon 249 hotspot mutation found in human hepatocellular carcinomas (HCCs) from Qidong (China) and southern Africa.	Aflatoxins	8-17	P53	Homo sapiens	84-87
8128225-3	1994	Ligation-mediated polymerase chain reaction was used to analyze at nucleotide resolution the repair of cyclobutane pyrimidine dimers along the p53 gene in ultraviolet-irradiated human fibroblasts.	cyclobutane pyrimidine	103-125	P53	Homo sapiens	143-146
8114714-9	1994	Exposure of normal cells and excision repair-deficient xeroderma pigmentosum cells to low doses of UV light, under conditions in which thymine dimers appear but DNA replication-associated strand breaks were prevented, resulted in p53 induction attributable to DNA strand breaks associated with excision repair.	Thymine	135-142	P53	Homo sapiens	230-233
8615594-8	1996	A 24-bp oligonucleotide corresponding to the putative p53 binding site was used for this assay.	24-bp oligonucleotide	2-23	P53	Homo sapiens	54-57
27259808-2	2016	We synthesized several indolo-pyrido-isoquinolin based alkaloids to activate p53 function and examined their therapeutic efficacy using NCI-60 screening.	indolo-pyrido-isoquinolin based alkaloids	23-64	P53	Homo sapiens	77-80
8854073-4	1996	The immunoreactivity of p53 significantly correlated with that of PCNA, while a dissociation of the positive correlation between p53 immunoreactivity and PCNA expression was noted in the TCCs with high 2cDI value (&gt; or = 2.0) and/or high 5cER (&gt; or = 10%).	2cdi	202-206	P53	Homo sapiens	129-132
27330773-10	2016	The p53 LIs were 24.5+-19.9, 25.7+-16.9 and 19.8+-13.8 in the CR, PR and SD/PD groups, respectively (P&gt;0.05).	lis	8-11	P53	Homo sapiens	4-7
7499360-4	1995	When cells were grown for 4-5 days in culture medium containing charcoal-treated fetal calf serum, p53 levels declined to 10% of the level seen in the control (no charcoal treatment) group.	Charcoal	64-72	P53	Homo sapiens	99-102
7499360-5	1995	Supplementation of culture medium containing charcoal-treated calf serum with 0.1-1 nM 17 beta-estradiol restored p53 to its normal levels.	Charcoal	45-53	P53	Homo sapiens	114-117
8790556-5	1994	Aflatoxins have been shown to induce specific mutations of the p53 tumour suppressor gene thus providing a clue to how an environmental factor may contribute to tumour development at the molecular level.	Aflatoxins	0-10	P53	Homo sapiens	63-66
26827144-0	2016	Highly sensitive electrochemiluminescence detection of p53 protein using functionalized Ru-silica nanoporous@gold nanocomposite.	ru-silica	88-97	P53	Homo sapiens	55-58
8238731-1	1993	In areas of the world where hepatitis B and aflatoxin ingestion are common, alterations of the p53 tumor suppressor gene have frequently been reported in hepatocellular carcinoma (HCC).	Aflatoxins	44-53	P53	Homo sapiens	95-98
8221675-1	1993	We have measured the gene-specific and strand-specific DNA repair of UV-induced cyclobutane pyrimidine dimers in the p53 tumor suppressor gene in a normal, repair-proficient human fibroblast strain and in fibroblasts from a patient with the repair deficient disorder xeroderma pigmentosum, complementation xeroderma pigmentosum group C (XP-C).	cyclobutane pyrimidine	80-102	P53	Homo sapiens	117-120
8093978-2	1993	Recently, there have been reports that p53 mutations are found to occur at high frequency (50%) in aflatoxin-related human primary hepatocellular carcinomas (HCC) (Hsu et al., 1991 Nature, vol 350, p. 427; Bressac et al., 1991 Nature, vol 350, p. 429).	Aflatoxins	99-108	P53	Homo sapiens	39-42
7568035-3	1995	DNA repair analysis revealed reduced removal of cyclobutane pyrimidine dimers from overall genomic DNA in vivo in p53 mut cells compared with p53 wt/mut or normal cells.	cyclobutane pyrimidine	48-70	P53	Homo sapiens	114-117
7554056-5	1995	The genotypic mutation assay, which has a sensitivity of 1 x 10(-6), showed that 4 mM ENU induces detectable numbers of G --&gt; A transitions in codon 248 of p53 while 5-methylcytosine deamination was not detected in either iNOS-transfected cells or cells exposed to 4 mM DEA/NO.	dea	273-276	P53	Homo sapiens	159-162
26480024-5	2016	The activation of ERK1/2 and STAT3 pathways and the expression and/or activation of molecules involved in cell cycle regulation such as p21(Waf1/Cip1) and p53, are very differently regulated by DHA treatments in each cell model.	Docosahexaenoic Acids	194-197	P53	Homo sapiens	155-158
7656242-0	1995	Preferential promutagenic lesions at exons 7-8 of human p53 genomic DNA induced by the direct-acting hepatocarcinogens N-nitroso-2-acetylaminofluorene and N-acetoxy-2-acetylaminofluorene.	Acetoxyacetylaminofluorene	155-186	P53	Homo sapiens	56-59
21556622-6	1995	Like GADD45, the WAF1/CIP1 induction by IR can be enhanced by the radiosensitizer iododeoxyuridine, and provides further evidence that DNA strand breaks can act as a signal for activation of the p53 pathway.	Idoxuridine	82-98	P53	Homo sapiens	195-198
1330867-6	1992	Our results showed that p53-positive hepatocellular carcinoma is a rare finding in patients exposed to a low dietary aflatoxin intake and that p53 mutation seems to occur at a late stage of the tumoral process and could contribute to an aggressive tumoral phenotype.	Aflatoxins	117-126	P53	Homo sapiens	24-27
26480024-6	2016	DHA selectively: (i) arrests non tumoral MCF-10A breast cells in G0 /G1 cycle phase, activating p21(Waf1/Cip1) , and p53, (ii) induces to death highly transformed breast cells SK-BR-3, reducing ERK1/2 and STAT3 phosphorylation and (iii) only slightly affects each analyzed process in MCF-7 breast cell line with transformation degree lower than SK-BR-3 cells.	Docosahexaenoic Acids	0-3	P53	Homo sapiens	117-120
27032906-0	2016	Trichosanthin-induced autophagy in gastric cancer cell MKN-45 is dependent on reactive oxygen species (ROS) and NF-kappaB/p53 pathway.	mkn-45	55-61	P53	Homo sapiens	122-125
1394191-11	1992	The finding of transition mutations exclusively at GG sites may be of predictive value in attempts to link dietary aflatoxin exposure to cancers associated with specific mutations in the c-ras oncogene and the p53 tumor suppressor gene.	Aflatoxins	115-124	P53	Homo sapiens	210-213
7766306-6	1995	The other two benzo[a]pyrene-induced base-pair changes in codon 248, namely the C-to-A transversion in the first position and G-to-T transversion in the third position, do not lead to a change in the amino-acid composition of the p53 protein.	Benzo(a)pyrene	14-28	P53	Homo sapiens	230-233
7766306-8	1995	It follows that benzo[a]pyrene-induced mutability on the DNA level in p53 codons 247-250 correlates well with the type of mutation found in tumors of the lung.	Benzo(a)pyrene	16-30	P53	Homo sapiens	70-73
1310637-7	1992	The occurrence of mutation in codon 249 of the p53 gene in selective samples of human hepatocellular cancers may indicate involvement of environmental carcinogens other than aflatoxin B1 or that hepatitis B virus-related hepatitis is a prerequisite for aflatoxin B1 induction of G to T transversion in codon 249.	Aflatoxins	174-183	P53	Homo sapiens	47-50
27172057-8	2016	Expression of the stress response gene TP53 showed significantly higher expression in COCs graded as low quality by LB staining.	green 5	116-118	P53	Homo sapiens	39-43
1682737-0	1991	p53 mutation in hepatocellular carcinoma after aflatoxin exposure.	Aflatoxins	47-56	P53	Homo sapiens	0-3
7530044-5	1995	Coimmunoprecipitations with anti-p34cdc2 support binding of this protein to the Src-like p56/p53lyn tyrosine kinase in ara-C-treated, but not untreated, cells.	Cytarabine	119-124	P53	Homo sapiens	93-96
8031463-4	1994	We measured the induction and repair of ultraviolet light-induced cyclobutane pyrimidine dimers (CPD) in each strand of the human p53 gene in a normal human lung fibroblast cell line using quantitative Southern hybridization.	cyclobutane pyrimidine	66-88	P53	Homo sapiens	130-133
1682737-9	1991	A codon 249 mutation of the p53 gene identifies an endemic form of HCC strongly associated with dietary aflatoxin intake.	Aflatoxins	104-113	P53	Homo sapiens	28-31
27094403-9	2016	The pretreatments with monohydroxy-DMC and monohydroxy-BDMC reduced c-jun and c-fos mRNA expression and p53 tumor suppressor protein expression and increased HO-1 protein expression and glutathione peroxidase (GPx) activity, respectively, compared to cells with direct hydrogen peroxide treatments.	monohydroxy-bdmc	43-59	P53	Homo sapiens	104-107
8290606-6	1994	Mozambican-type of hepatocellular carcinomas are characterized by a high incidence of p53 mutations related to aflatoxins.	Aflatoxins	111-121	P53	Homo sapiens	86-89
27132887-4	2016	We report here that a compound cocktail containing cyclic pifithrin-a (a P53 inhibitor), A-83-01, CHIR99021, thiazovivin, NaB, and PD0325901 significantly improves the reprogramming efficiency (170-fold more) for hUCs.	mirdametinib	131-140	P53	Homo sapiens	73-76
2175605-2	1990	We found a novel mutation of the p53 gene in a small cell lung carcinoma cell line, Lu-143.	lu-143	84-90	P53	Homo sapiens	33-36
27035337-9	2016	Co-transfection of AMO-21 and AMO-221 resulted in a marked reduction in Akt phosphorylation and enhanced expression of PTEN and p53 were observed; consequently, leading to an amplification of the transcription of 6 pro-apoptotic miRNAs.	amo-21	19-25	P53	Homo sapiens	128-131
33771647-0	2021	PARP-1 via regulation of p53 and p16, is involved in the hydroquinone-induced malignant transformation of TK6 cells by decelerating the cell cycle.	hydroquinone	57-69	P53	Homo sapiens	25-28
8307460-1	1994	p53 mutations are a common genetic finding in hepatocellular carcinoma from areas of high aflatoxin exposure.	Aflatoxins	90-99	P53	Homo sapiens	0-3
8307460-6	1994	This study shows that p53 mutations are a rare event in hepatocarcinogenesis in Great Britain, an area of low aflatoxin exposure, and supports the concept of geographical variations in the cause and pathogenesis of hepatocellular carcinoma.	Aflatoxins	110-119	P53	Homo sapiens	22-25
27035337-9	2016	Co-transfection of AMO-21 and AMO-221 resulted in a marked reduction in Akt phosphorylation and enhanced expression of PTEN and p53 were observed; consequently, leading to an amplification of the transcription of 6 pro-apoptotic miRNAs.	amo-221	30-37	P53	Homo sapiens	128-131
26986084-5	2016	Cantharidin treatment in the HCSCs for 48 h increased expression of histone H2AX, Myt1, cyclin A2, cyclin B1, p53 and cdc2 (Tyr15) phosphorylation significantly compared to the parental cells.	Cantharidin	0-11	P53	Homo sapiens	110-113
8100480-1	1993	BACKGROUND: p53 gene mutations at codon 249 have been reported in hepatocellular carcinoma (HCC) from China and South Africa, a phenomenon shown to be closely associated with food contamination by aflatoxin.	Aflatoxins	197-206	P53	Homo sapiens	12-15
1406679-3	1992	Serines 15 and 37 in the amino-terminal transactivation domain of human p53, and serines 7 and 18 of mouse p53, were phosphorylated by DNA-PK in the context of synthetic peptides.	Peptides	170-178	P53	Homo sapiens	72-75
33824975-10	2021	In addition, our findings caution against use of sub-lethal BH3-mimetic drug regimens, which may enhance the risk of disease progression driven by emergent TP53 mutant clones.	BH 3	60-63	P53	Homo sapiens	156-160
34791836-12	2022	While nonresponder-associated genes included well-known TP53 and CARD11, genetic classifiers developed using nonresponder-associated genes included ATP6AP1, EP400, ARID1A, SOCS1, and TBL1XR1, suggesting resistance to ibrutinib may be related to broad biological functions connected to epigenetic modification, telomere maintenance, and cancer-associated signaling pathways (mTOR, JAK/STAT, NF-kappaB).	ibrutinib	217-226	P53	Homo sapiens	56-60
26883409-0	2016	Au nanoparticle decorated graphene nanosheets for electrochemical immunosensing of p53 antibodies for cancer prognosis.	Graphite	26-34	P53	Homo sapiens	83-86
1347900-0	1992	p53 codon 249ser mutations in hepatocellular carcinoma patients with low aflatoxin exposure.	Aflatoxins	73-82	P53	Homo sapiens	0-3
26883409-2	2016	We report a novel and sensitive label-free immunosensor based on gold nanoparticles (Au NPs) self-assembled onto electrochemically reduced graphene oxide (ERGO) for the detection of p53 antibodies.	graphene oxide	139-153	P53	Homo sapiens	182-185
1506270-5	1992	Addition of a potent protein-tyrosine kinase inhibitor, herbimycin A, to the anchorage-provided cells caused an elevated level of p53, and inhibitions of cell proliferation and p53 phosphorylation, without interfering with the cell adhesion to the substratum.	herbimycin	56-68	P53	Homo sapiens	130-133
1506270-5	1992	Addition of a potent protein-tyrosine kinase inhibitor, herbimycin A, to the anchorage-provided cells caused an elevated level of p53, and inhibitions of cell proliferation and p53 phosphorylation, without interfering with the cell adhesion to the substratum.	herbimycin	56-68	P53	Homo sapiens	177-180
34920321-15	2022	Brazilin, by activating p38 MAPK and elevating p53 levels within the exposed cells.	brazilin	0-8	P53	Homo sapiens	47-50
25995008-2	2016	Previous findings have shown that p53 expression can influence DNA adduct formation of the environmental carcinogen benzo[a]pyrene (BaP) in human cells, indicating a role for p53 in the cytochrome P450 (CYP) 1A1-mediated biotransformation of BaP in vitro.	Benzo(a)pyrene	132-135	P53	Homo sapiens	34-37
34854682-4	2021	In this study, we used immunofluorescence staining of Saos-2 cells harboring doxycycline-inducible p53R175H (Saos-2 (p53R175H) cells) to search for compounds from natural sources that can target mut p53 and found an extract of Colletotrichum sp.	Doxycycline	77-88	P53	Homo sapiens	199-202
1506270-6	1992	These results demonstrated that the growth inhibition by anchorage-deficiency or by herbimycin A is associated with an elevated p53 level and reduced p53 phosphorylation at tyrosine.	herbimycin	84-96	P53	Homo sapiens	128-131
1506270-6	1992	These results demonstrated that the growth inhibition by anchorage-deficiency or by herbimycin A is associated with an elevated p53 level and reduced p53 phosphorylation at tyrosine.	herbimycin	84-96	P53	Homo sapiens	150-153
25995008-2	2016	Previous findings have shown that p53 expression can influence DNA adduct formation of the environmental carcinogen benzo[a]pyrene (BaP) in human cells, indicating a role for p53 in the cytochrome P450 (CYP) 1A1-mediated biotransformation of BaP in vitro.	Benzo(a)pyrene	132-135	P53	Homo sapiens	175-178
25995008-2	2016	Previous findings have shown that p53 expression can influence DNA adduct formation of the environmental carcinogen benzo[a]pyrene (BaP) in human cells, indicating a role for p53 in the cytochrome P450 (CYP) 1A1-mediated biotransformation of BaP in vitro.	Benzo(a)pyrene	242-245	P53	Homo sapiens	34-37
1332185-3	1992	Recent reports of a guanine to thymine mutation of the third base of codon 249 of the tumour suppressor gene, p53, in 50% of patients with hepatocellular carcinoma in regions of high aflatoxin exposure, and mutagenic experiments showing that aflatoxin B1 binds particularly to guanine residues in G-C-rich domains and that codon 249 is a preferred target have suggested a mechanism whereby aflatoxin might induce malignant transformation.	Aflatoxins	183-192	P53	Homo sapiens	110-113
27642319-8	2016	In contrast, Celecoxib treatment not only returned p53 to the control level, but also strikingly induced COX-2 expression within 48 h. Of further relevance, Celecoxib exposure could significantly result in MDM2 elevation at 48 h. These findings represent p53 as a molecular target being interconnected with COX-2 signaling axis upon Celecoxib treatment.	Celecoxib	13-22	P53	Homo sapiens	255-258
1332185-3	1992	Recent reports of a guanine to thymine mutation of the third base of codon 249 of the tumour suppressor gene, p53, in 50% of patients with hepatocellular carcinoma in regions of high aflatoxin exposure, and mutagenic experiments showing that aflatoxin B1 binds particularly to guanine residues in G-C-rich domains and that codon 249 is a preferred target have suggested a mechanism whereby aflatoxin might induce malignant transformation.	Aflatoxins	242-251	P53	Homo sapiens	110-113
34937948-0	2022	Correction: Lithium enhances the antitumour effect of temozolomide against TP53 wild-type glioblastoma cells via NFAT1/FasL signaling.	Lithium	12-19	P53	Homo sapiens	75-79
34937948-0	2022	Correction: Lithium enhances the antitumour effect of temozolomide against TP53 wild-type glioblastoma cells via NFAT1/FasL signaling.	Temozolomide	54-66	P53	Homo sapiens	75-79
27642319-8	2016	In contrast, Celecoxib treatment not only returned p53 to the control level, but also strikingly induced COX-2 expression within 48 h. Of further relevance, Celecoxib exposure could significantly result in MDM2 elevation at 48 h. These findings represent p53 as a molecular target being interconnected with COX-2 signaling axis upon Celecoxib treatment.	Celecoxib	157-166	P53	Homo sapiens	51-54
27642319-8	2016	In contrast, Celecoxib treatment not only returned p53 to the control level, but also strikingly induced COX-2 expression within 48 h. Of further relevance, Celecoxib exposure could significantly result in MDM2 elevation at 48 h. These findings represent p53 as a molecular target being interconnected with COX-2 signaling axis upon Celecoxib treatment.	Celecoxib	157-166	P53	Homo sapiens	255-258
27642319-8	2016	In contrast, Celecoxib treatment not only returned p53 to the control level, but also strikingly induced COX-2 expression within 48 h. Of further relevance, Celecoxib exposure could significantly result in MDM2 elevation at 48 h. These findings represent p53 as a molecular target being interconnected with COX-2 signaling axis upon Celecoxib treatment.	Celecoxib	157-166	P53	Homo sapiens	51-54
34919323-6	2022	And then it was attested that cells had a lower level of p53 but SIRT1 expression was upregulated on RSV-AA-P(CL-DLLA), which might be related with resveratrol release from RSV-AA-P(CL-DLLA).	rsv-aa-p	173-181	P53	Homo sapiens	57-60
1933877-4	1991	Thirteen of 14 nucleotide residues of the p53 gene which underwent G:C to T:A mutations in lung cancers were targeted by benzo(a)pyrene.	Benzo(a)pyrene	121-135	P53	Homo sapiens	42-45
27642319-8	2016	In contrast, Celecoxib treatment not only returned p53 to the control level, but also strikingly induced COX-2 expression within 48 h. Of further relevance, Celecoxib exposure could significantly result in MDM2 elevation at 48 h. These findings represent p53 as a molecular target being interconnected with COX-2 signaling axis upon Celecoxib treatment.	Celecoxib	157-166	P53	Homo sapiens	255-258
33824975-0	2021	Intact TP53 function is essential for sustaining durable responses to BH3-mimetic drugs in leukemias.	BH 3	70-73	P53	Homo sapiens	7-11
33824975-7	2021	Our study reveals the key role of TP53 in shaping long-term responses to BH3-mimetic drugs and reconciles the disparate pattern of initial clinical response to venetoclax, followed by subsequent treatment failure among patients with TP53-mutant chronic lymphocytic leukemia (CLL) or acute myeloid leukemia (AML).	BH 3	73-76	P53	Homo sapiens	34-38
27108384-8	2016	CONCLUSION: MDM2 inhibition with MI-219 results in p53-dependent sensitization of prostate cancer cells to radiation, antiandrogen therapy, and the combination.	2-methyl-4-isothiazolin-3-one	33-35	P53	Homo sapiens	51-54
33804175-0	2021	Semi-Synthesis of Small Molecules of Aminocarbazoles: Tumor Growth Inhibition and Potential Impact on p53.	aminocarbazoles	37-52	P53	Homo sapiens	102-105
34521099-0	2021	Ibrutinib induces durable remissions in treatment-naive patients with CLL and 17p deletion/TP53 mutations.	ibrutinib	0-9	P53	Homo sapiens	91-95
34521099-3	2021	Here, we report the long-term outcome of 27 patients with CLL treatment naive with 17p deletion and/or TP53 mutation treated with ibrutinib alone or in combination with rituximab on a Phase-2 clinical study.	ibrutinib	130-139	P53	Homo sapiens	103-107
34521099-5	2021	These data corroborate that ibrutinib therapy, induces durable remissions in patients with 17p deletion and/or TP53 mutations, and suggest that BTK inhibitor therapy should be a preferred treatment for these patients outside of clinical trials.	ibrutinib	28-37	P53	Homo sapiens	111-115
34959709-3	2021	We previously revealed that apoptosis was mediated in p53-negative Hep3B cells, and mulberry leaf polyphenol extract (MLPE) induced autophagy in p53-transfected Hep3B cells.	mlpe	118-122	P53	Homo sapiens	145-148
34959709-13	2021	Moreover, this work provides insight into the mechanism of p53 action in MLPE-induced cytotoxicity in hepatocellular carcinoma.	mlpe	73-77	P53	Homo sapiens	59-62
26891889-5	2016	Sublytic concentrations of hydrogen peroxide (H2O2) plus NO donor S-nitroso-N-acetyl-D, L-penicillamine (SNAP) enabled to induce a toxic oxidative/nitrosative stress through activating both p38 MAPK and p53 cascades, and cause DNA damage and protein tyrosine nitration in primary neuronal cultures.	s-nitroso-n-acetyl-d, l-penicillamine	66-103	P53	Homo sapiens	203-206
34886886-0	2021	Roles of reactive oxygen species, mitochondrial membrane potential, and p53 in evodiamine-induced apoptosis and G2/M arrest of human anaplastic thyroid carcinoma cells.	evodiamine	79-89	P53	Homo sapiens	72-75
34886886-8	2021	Mechanistic studies showed that increased p53 and its downstream proteins, and disrupted MMP with increased intracellular peroxide production participated in EVO-induced apoptosis and G2/M arrest of SW1736 cells.	evodiamine	158-161	P53	Homo sapiens	42-45
34886886-11	2021	CONCLUSION: Evidence indicated that the endogenous p53 status affected the sensitivity of ATC cells to EVO-induced apoptosis and G2/M arrest, revealing the potential role of p53 related to increased ROS production and disrupted MMP in the anticancer actions of EVO, and alkylation at position 14 of EVO is a critical substitution for apoptosis of ATC cells.	evodiamine	103-106	P53	Homo sapiens	51-54
34886886-11	2021	CONCLUSION: Evidence indicated that the endogenous p53 status affected the sensitivity of ATC cells to EVO-induced apoptosis and G2/M arrest, revealing the potential role of p53 related to increased ROS production and disrupted MMP in the anticancer actions of EVO, and alkylation at position 14 of EVO is a critical substitution for apoptosis of ATC cells.	evodiamine	103-106	P53	Homo sapiens	174-177
34886886-11	2021	CONCLUSION: Evidence indicated that the endogenous p53 status affected the sensitivity of ATC cells to EVO-induced apoptosis and G2/M arrest, revealing the potential role of p53 related to increased ROS production and disrupted MMP in the anticancer actions of EVO, and alkylation at position 14 of EVO is a critical substitution for apoptosis of ATC cells.	evodiamine	261-264	P53	Homo sapiens	51-54
33032195-8	2020	A sandwich-type immunoreaction was achieved via the Fc-specific FITC@SiO2-NH2-anti-IgG binding to the captured anti-p53aAbs.	Fluorescein-5-isothiocyanate	64-68	P53	Homo sapiens	116-119
27073518-5	2016	Furthermore, western blot analysis indicated that NDP decreased the protein expression of P-glycoprotein, tumor protein p53 and B-cell lymphoma 2, and increased the expression of Bcl-2-associated X protein, all of which could possibly improve the NDP intracellular drug concentration and promote cell apoptosis.	nedaplatin	50-53	P53	Homo sapiens	120-123
26319559-9	2016	Associated with these subcellular changes, the apoptosis of hypoxic oligodendrocytes was evident with an increase in p53 and caspase-3 expression, which was attenuated when these cells were treated with deferoxamine.	Deferoxamine	203-215	P53	Homo sapiens	117-120
34886886-11	2021	CONCLUSION: Evidence indicated that the endogenous p53 status affected the sensitivity of ATC cells to EVO-induced apoptosis and G2/M arrest, revealing the potential role of p53 related to increased ROS production and disrupted MMP in the anticancer actions of EVO, and alkylation at position 14 of EVO is a critical substitution for apoptosis of ATC cells.	evodiamine	261-264	P53	Homo sapiens	174-177
34886886-11	2021	CONCLUSION: Evidence indicated that the endogenous p53 status affected the sensitivity of ATC cells to EVO-induced apoptosis and G2/M arrest, revealing the potential role of p53 related to increased ROS production and disrupted MMP in the anticancer actions of EVO, and alkylation at position 14 of EVO is a critical substitution for apoptosis of ATC cells.	evodiamine	299-302	P53	Homo sapiens	51-54
26986569-13	2016	In the same cells, the amide also increased the acetylation of lysine (K382) in p53, but not (K305).	Amides	23-28	P53	Homo sapiens	80-83
21570152-5	2011	RESULTS: DFSP-FS was associated with tumor history longer than 5 years (P = .009), tumor size greater than 4 cm (P = .001), more stages of modified Mohs micrographic surgery (P = .005), expansive subcutaneous infiltration (P = .005), muscular invasion (P = .0001), absence of CD34 staining (P = .018), p53 positivity (P = .006), and increased proliferative activity (P = .004) compared with DFSP.	dfsp-fs	9-16	P53	Homo sapiens	302-305
26974436-12	2016	Treatment with DMDP-1 &amp; -2 also showed up-regulation of total and phosphorylated p53 levels in a time dependent manner.	dmdp-1	15-21	P53	Homo sapiens	85-88
34964241-7	2022	In further studies, it was found that the expression of PINK1 and mitophagy flux downstream was downregulated in GBM cells, which were secondary to the upregulation of TP53 in tumour cells under TMZ treatment.	Temozolomide	195-198	P53	Homo sapiens	168-172
34959709-0	2021	Mulberry Leaf Polyphenol Extract and Rutin Induces Autophagy Regulated by p53 in Human Hepatoma HepG2 Cells.	Polyphenols	14-24	P53	Homo sapiens	74-77
34959709-0	2021	Mulberry Leaf Polyphenol Extract and Rutin Induces Autophagy Regulated by p53 in Human Hepatoma HepG2 Cells.	Rutin	37-42	P53	Homo sapiens	74-77
34959709-3	2021	We previously revealed that apoptosis was mediated in p53-negative Hep3B cells, and mulberry leaf polyphenol extract (MLPE) induced autophagy in p53-transfected Hep3B cells.	Polyphenols	98-108	P53	Homo sapiens	145-148
26816656-0	2016	Polyethyleneimine-modified calcium carbonate nanoparticles for p53 gene delivery.	Calcium Carbonate	27-44	P53	Homo sapiens	63-66
34865212-0	2022	Long-term efficacy of first-line ibrutinib treatment for chronic lymphocytic leukaemia in patients with TP53 aberrations: a pooled analysis from four clinical trials.	ibrutinib	33-42	P53	Homo sapiens	104-108
34865212-3	2022	The pooled analysis included 89 patients with TP53 aberrations receiving first-line treatment with single-agent ibrutinib (n = 45) or ibrutinib in combination with an anti-CD20 antibody (n = 44).	ibrutinib	112-121	P53	Homo sapiens	46-50
34794098-7	2021	The most balanced potent and safe derivatives; 5i and 5q were more active than 5-fluorouracil, exhibited low mumrange MDM2 binding (KD=1.32and 1.72 mum, respectively), induced apoptosis-dependent anticancer activities up to 50%, activated p53 by 47-63%, downregulated the BCL2 gene to 59.8%, and reduced its protein level (13.75%) in the treated cancer cells.	CHEMBL3739943	54-56	P53	Homo sapiens	239-242
34959348-4	2021	In this study, we generated gold nanoparticles (AuNPs) chemically modified with low molecular branched polyethylenimine (bPEI) for the efficient delivery of gapmers targeting p53 mutant protein.	low molecular branched polyethylenimine	80-119	P53	Homo sapiens	175-178
34895043-9	2021	Lastly, the expression level of p21 and p53 was greatly elevated in chondrocytes by stimulation with TNF-alpha which was then pronouncedly repressed by treatment with Celecoxib.	Celecoxib	167-176	P53	Homo sapiens	40-43
26816656-4	2016	After modified with polyethyleneimine (PEI), the ability of PEI-CaCO3 nanoparticles to carry GFP-marked p53 gene (pEGFP-C1-p53) into cancer cells to express P53 protein were studied.	Calcium Carbonate	64-69	P53	Homo sapiens	104-107
34690024-8	2021	BaP-conditioned medium significantly increased DNA damage, p53 stabilization, AhR activation and POMC secretion in keratinocytes.	Benzo(a)pyrene	0-3	P53	Homo sapiens	59-62
26816656-4	2016	After modified with polyethyleneimine (PEI), the ability of PEI-CaCO3 nanoparticles to carry GFP-marked p53 gene (pEGFP-C1-p53) into cancer cells to express P53 protein were studied.	Calcium Carbonate	64-69	P53	Homo sapiens	123-126
26816656-4	2016	After modified with polyethyleneimine (PEI), the ability of PEI-CaCO3 nanoparticles to carry GFP-marked p53 gene (pEGFP-C1-p53) into cancer cells to express P53 protein were studied.	Calcium Carbonate	64-69	P53	Homo sapiens	157-160
34537545-0	2021	The important role of RPS14, RPL5 and MDM2 in TP53-associated ribosome stress in mycophenolic acid-induced microtia.	Mycophenolic Acid	81-98	P53	Homo sapiens	46-50
26816656-8	2016	And with the expression of GFP-P53 fusion protein, pEGFP-C1-p53-gene-loaded PEI-CaCO3 particles significantly reduced the proliferation of cancer cells.	Calcium Carbonate	80-85	P53	Homo sapiens	31-34
26816656-8	2016	And with the expression of GFP-P53 fusion protein, pEGFP-C1-p53-gene-loaded PEI-CaCO3 particles significantly reduced the proliferation of cancer cells.	Calcium Carbonate	80-85	P53	Homo sapiens	60-63
34707773-7	2021	More importantly, STAT3 overexpression, SLC7A11 overexpression, and pretreatment with pifithrin-alpha (P53 inhibitor) rescued OS cell ferroptosis induced by bavachin.	bavachin	157-165	P53	Homo sapiens	103-106
26440706-2	2016	Our recent animal studies showed that low dose arsenic (LDA)-induced transient p53 inhibition selectively protected normal tissues from chemotherapy-induced toxicity.	lda	56-59	P53	Homo sapiens	79-82
34217708-0	2021	Iso-suillin-induced DNA damage leading to cell cycle arrest and apoptosis arised from p53 phosphorylation in A549 cells.	iso-suillin	0-11	P53	Homo sapiens	86-89
34217708-5	2021	Phosphorylation of p53 at serines 15 and 20 may be one of the pivotal factors for cell cycle arrest and apoptosis after treatment of iso-suillin in A549 cells.	iso-suillin	133-144	P53	Homo sapiens	19-22
34733363-6	2021	TMZ enhanced the autophagic response and senescence, which was mediated via the p53 and p21 pathways.	Temozolomide	0-3	P53	Homo sapiens	80-83
26407653-6	2015	Celecoxib-induced apoptosis of SGC-7901/DDP cells led to increased p53 expression, decreased Bcl-2/Bax ratio and up-regulated caspase-3 level.	Celecoxib	0-9	P53	Homo sapiens	67-70
34765011-8	2021	Fluorescence real-time quantitative PCR and western blot analysis showed that episamarcandin increased the expression of PTEN, p53, and Bax and decreased the expression of P-Akt, Akt, mTOR, Bcl-xl, and Bcl-2.	Nevskin	78-92	P53	Homo sapiens	127-130
34610339-0	2021	Malignant transformation of human bronchial epithelial cells induced by benzo (a) pyrene suggests a negative feedback of TP53 to PPP1R13L via binding a possible enhancer element.	Benzo(a)pyrene	72-88	P53	Homo sapiens	121-125
34217708-8	2021	The in vitro and in vivo anti-tumor effects implied that iso-suillin may act as a tumor growth inhibitor, and its induction of p53 phosphorylation is pivotal for cell cycle arrest and apoptosis in A549 cells.	iso-suillin	57-68	P53	Homo sapiens	127-130
34496888-16	2021	hnRNPA2B1 bound to N6-methyladenosine sites on the 3" untranslated region of p53 pre-mRNA and maintained its stability.	N-methyladenosine	19-37	P53	Homo sapiens	77-80
34571936-7	2021	Pathways of necroptosis, ferroptosis, p53, NRF2, ATF4, WNT, MAPK, NF-kappaB, EGFR, and ERK may be connected to the tumor suppressive effect caused by pretreatment of DHA/EPA prior to bortezomib.	Docosahexaenoic Acids	166-169	P53	Homo sapiens	38-41
26400160-7	2015	More importantly, we found that miR-125b-loaded miRISC contributes to the specific recruitment of PARN to TP53 mRNA, and that can be reverted by the ARE-binding protein HuR.	mir-125b	32-40	P53	Homo sapiens	106-110
34539842-8	2021	TMZ treatment induced apoptosis in GBM cells by activating the p53 pathway, whilst simultaneously downregulating mitophagy and enhancing mitochondrial fusion.	Temozolomide	0-3	P53	Homo sapiens	63-66
26335100-11	2015	Interestingly, we found that miR-125b, a negative regulator of p53, exhibited an inverse expression relationship with CT-Cx43 in the breast cancer samples tested.	mir-125b	29-37	P53	Homo sapiens	63-66
34778250-4	2021	Furthermore, the effects of TP53 on esophageal squamous cell carcinoma (ESCC) cell migration and proliferation were examined using the Transwell assay, scratch test, and crystal violet assay.	Gentian Violet	170-184	P53	Homo sapiens	28-32
34127506-0	2021	TP53 disruption in chronic lymphocytic leukemia under ibrutinib: more is worse?	ibrutinib	54-63	P53	Homo sapiens	0-4
34127506-1	2021	Chronic lymphocytic leukemia patients carrying a single TP53 hit (chromosome 17p deletion or single TP53 mutation) demonstrate excellent progression-free and overall survival on ibrutinib compared to cases harboring multiple TP53 hits.	ibrutinib	178-187	P53	Homo sapiens	56-60
34127506-1	2021	Chronic lymphocytic leukemia patients carrying a single TP53 hit (chromosome 17p deletion or single TP53 mutation) demonstrate excellent progression-free and overall survival on ibrutinib compared to cases harboring multiple TP53 hits.	ibrutinib	178-187	P53	Homo sapiens	100-104
34707773-6	2021	Further investigation showed that bavachin upregulated the expression of transferrin receptor, divalent metal transporter-1, and P53, along with downregulating the expression of ferritin light chain, ferritin heavy chain, p-STAT3 (705), SLC7A11, and glutathione peroxidase-4 in OS cells.	bavachin	34-42	P53	Homo sapiens	129-132
26904387-2	2015	Herein we propose a model of tumor growth inhibition integrating a tumor"s genetic characteristics (p53 mutation and 1p/19q codeletion) that successfully describes the time course of tumor size in patients with low-grade gliomas treated with first-line temozolomide chemotherapy.	Temozolomide	253-265	P53	Homo sapiens	100-103
34676046-4	2021	Using human cytotoxic T-cell line TALL-104 injected intraperitoneally into immunodeficient NCRU-nude athymic mice bearing mismatch repair-deficient (MMR-d) human colon carcinoma HCT116 p53-null (but not wild-type p53) tumor xenograft, we observed accelerated tumor growth after PD-1 blockade with pembrolizumab administration.	tall-104	34-42	P53	Homo sapiens	185-188
34440533-7	2021	We were able to detect p53 asymmetric-dimethylarginine signals in breast cancer cells and breast cancer tissues from patients, and the signals could be significantly weakened by silencing of PRMT1 with shRNA, or inhibiting PRMT1 activity with a specific inhibitor.	dimethylarginine	38-54	P53	Homo sapiens	23-26
34109118-10	2021	Another CDK7 inhibitor, LDC4297, also potently interfered with the expression of mutated p53.	LDC4297	24-31	P53	Homo sapiens	89-92
26628631-7	2015	Ibrutinib and idelalisib are active in patients with high-risk features, achieving superior disease control in difficult-to-treat patients than prior best therapy, making them the preferred agents for chronic lymphocytic leukemia with TP53 aberrations and for patients resistant to chemoimmunotherapy.	ibrutinib	0-9	P53	Homo sapiens	235-239
34086162-0	2021	Dichloromethane fraction of Moringa oleifera leaf methanolic extract selectively inhibits breast cancer cells (MCF7) by induction of apoptosis via upregulation of Bax, p53 and caspase 8 expressions.	Methylene Chloride	0-15	P53	Homo sapiens	168-171
34255251-7	2021	Real-time RT-PCR indicated that the co-administration of Schiff base oxovanadium complex 40 microg/ml and arsenic trioxide 0.001 microM could increase the expression of P53 and P21 genes by 3.76 +- 0.19 and 6.57 +- 1.29 fold change, respectively to the control sample.	schiff base oxovanadium complex	57-88	P53	Homo sapiens	169-172
34660288-0	2021	Valproic Acid Enhanced Temozolomide-Induced Anticancer Activity in Human Glioma Through the p53-PUMA Apoptosis Pathway.	Temozolomide	23-35	P53	Homo sapiens	92-95
34660288-7	2021	Our analysis of clinical data indicates that the survival benefit of a combined TMZ and VPA treatment in GBM patients is dependent on their p53 gene status.	Temozolomide	80-83	P53	Homo sapiens	140-143
26580615-9	2015	Taken together, our results suggest that EVO modulates the activity of the p53 signaling pathway to induce apoptosis and downregulate MMP3 expression by inactivating the JAK2/STAT3 pathway through the downregulation of PGI to inhibit migration of HCT-116 human colorectal cancer cells.	evodiamine	41-44	P53	Homo sapiens	75-78
34660288-8	2021	In cellular experiments, our results show that VPA enhanced the antineoplastic effect of TMZ by enhancing p53 activation and promoting the expression of its downstream pro-apoptotic protein, PUMA.	Temozolomide	89-92	P53	Homo sapiens	106-109
35563493-0	2022	Suppression of the Proliferation of Huh7 Hepatoma Cells Involving the Downregulation of Mutant p53 Protein and Inactivation of the STAT 3 Pathway with Ailanthoidol.	ailanthoidol	151-163	P53	Homo sapiens	95-98
34253592-12	2021	Despite a linear increase in the O6MeG adduct level, DSBs and p53 activation, the low curative effect of TMZ results presumably from the low rate of apoptosis compared to senescence.	Temozolomide	105-108	P53	Homo sapiens	62-65
26231140-4	2015	In the resting neutrophils resveratrol and to lesser extent other polyphenols increased DNA damage and increased the level of p53.	Polyphenols	66-77	P53	Homo sapiens	126-129
35398141-0	2022	Graphene oxide leads to mitochondrial-dependent apoptosis by activating ROS-p53-mPTP pathway in intestinal cells.	graphene oxide	0-14	P53	Homo sapiens	76-79
26171006-5	2015	DP significantly inhibited the growth of SK-MES-1 cells by inducing apoptosis and G1/G0 cell cycle arrest in a dose-dependent manner via activation of p53 (P&lt;0.05).	sk-mes	41-47	P53	Homo sapiens	151-154
35051466-0	2022	Organophosphate flame retardants induce oxidative stress and Chop/Caspase 3-related apoptosis via Sod1/p53/Map3k6/Fkbp5 in NCI-1975 cells.	Organophosphates	0-15	P53	Homo sapiens	103-106
34252861-10	2021	Cell cycle distribution analysis showed that hyrtiosone A arrested the S and G2/M phase of cell cycle and upregulate the gene expression of p53 and p27 in hepatocellular carcinoma HepG2 cells.	hyrtiosone a	45-57	P53	Homo sapiens	140-143
34443300-6	2021	Treatment with 8.5-11.8 muM TrxFTL reduced proliferation of all cancer cells to half in 48 h. This anti-proliferative effect encompasses the p53 pathway since it was significantly reduced in p53-null colon cancer cells (HCT116 p53-/-; GI50 of 25.0 +- 3.0 muM), when compared to the isogenic p53-positive cells (HCT116 p53+/+; GI50 of 8.7 +- 1.8 muM; p < 0.002).	trxftl	28-34	P53	Homo sapiens	141-144
25818601-0	2015	Polychlorinated biphenyl quinone induces oxidative DNA damage and repair responses: The activations of NHEJ, BER and NER via ATM-p53 signaling axis.	polychlorinated biphenyl quinone	0-32	P53	Homo sapiens	129-132
34443300-6	2021	Treatment with 8.5-11.8 muM TrxFTL reduced proliferation of all cancer cells to half in 48 h. This anti-proliferative effect encompasses the p53 pathway since it was significantly reduced in p53-null colon cancer cells (HCT116 p53-/-; GI50 of 25.0 +- 3.0 muM), when compared to the isogenic p53-positive cells (HCT116 p53+/+; GI50 of 8.7 +- 1.8 muM; p < 0.002).	trxftl	28-34	P53	Homo sapiens	191-194
34443300-6	2021	Treatment with 8.5-11.8 muM TrxFTL reduced proliferation of all cancer cells to half in 48 h. This anti-proliferative effect encompasses the p53 pathway since it was significantly reduced in p53-null colon cancer cells (HCT116 p53-/-; GI50 of 25.0 +- 3.0 muM), when compared to the isogenic p53-positive cells (HCT116 p53+/+; GI50 of 8.7 +- 1.8 muM; p < 0.002).	trxftl	28-34	P53	Homo sapiens	227-230
35033575-0	2022	Selinexor improves the anti-cancer effect of tucidinostat on TP53 wild-type breast cancer.	selinexor	0-9	P53	Homo sapiens	61-65
35033575-9	2022	Taken together, we believe that tucidinostat and selinexor are potentially effective drug combinations for the treatment of wt-TP53 BC, and the molecular mechanism may be through enhancing the activity of p53 in the nucleus of BC cells to suppress proliferation and invasion and promote apoptosis.	HBI-8000	32-44	P53	Homo sapiens	127-131
34361036-0	2021	Hinokitiol Exhibits Antitumor Properties through Induction of ROS-Mediated Apoptosis and p53-Driven Cell-Cycle Arrest in Endometrial Cancer Cell Lines (Ishikawa, HEC-1A, KLE).	beta-thujaplicin	0-10	P53	Homo sapiens	89-92
26118882-2	2015	Ibrutinib has been approved in USA in February 2014 and in France in October 2014 for the treatment of patients with relapsed/refractory mantle cell lymphoma (MCL) or chronic lymphocytic leukaemia (CLL) and for the treatment of patients with CLL and a chromosome 17 deletion (del 17p) or TP53 mutation.	ibrutinib	0-9	P53	Homo sapiens	288-292
34361036-5	2021	Hinokitiol significantly suppressed cell proliferation through the inhibition of the expression of cell-cycle mediators, such as cyclin D1 and cyclin-dependent kinase 4 (CDK4), as well as the induction of the tumor suppressor protein p53.	beta-thujaplicin	0-10	P53	Homo sapiens	234-237
35217309-0	2022	Combining selinexor with alisertib to target the p53 pathway in neuroblastoma.	selinexor	10-19	P53	Homo sapiens	49-52
35217309-0	2022	Combining selinexor with alisertib to target the p53 pathway in neuroblastoma.	MLN 8237	25-34	P53	Homo sapiens	49-52
35217309-5	2022	We found that selinexor induced its cytotoxic effects in neuroblastoma through the predominantly nuclear accumulation of p53 and global activation of apoptosis pathways.	selinexor	14-23	P53	Homo sapiens	121-124
35217309-6	2022	Selinexor also induced p53 phosphorylation at site S315, which is one initiating step for p53 degradation.	selinexor	0-9	P53	Homo sapiens	23-26
35217309-6	2022	Selinexor also induced p53 phosphorylation at site S315, which is one initiating step for p53 degradation.	selinexor	0-9	P53	Homo sapiens	90-93
34196654-8	2021	Cell experiments further confirmed that H2 could reverse MNU damage to CECs by decreasing oxidative stress injury, interfering with the NF-kappaB/NLRP3 pathway and the FOXO3a/p53/p21 pathway.	Methylnitrosourea	57-60	P53	Homo sapiens	175-178
34257824-5	2021	Dietary intake of flavonoids, a C15 group of polyphenols, is known to inhibit cancer progression and assist DNA repair through p53-mediated mechanisms in human cells via their antioxidant activities.	Polyphenols	45-56	P53	Homo sapiens	127-130
34257824-7	2021	Other polyphenols such as resveratrol upregulate p53 expression in several cancer cell lines by promoting p53 stability, which in colon cancer cells results in the activation of p53-mediated apoptosis.	Polyphenols	6-17	P53	Homo sapiens	49-52
34257824-7	2021	Other polyphenols such as resveratrol upregulate p53 expression in several cancer cell lines by promoting p53 stability, which in colon cancer cells results in the activation of p53-mediated apoptosis.	Polyphenols	6-17	P53	Homo sapiens	106-109
34257824-7	2021	Other polyphenols such as resveratrol upregulate p53 expression in several cancer cell lines by promoting p53 stability, which in colon cancer cells results in the activation of p53-mediated apoptosis.	Polyphenols	6-17	P53	Homo sapiens	178-181
35260928-12	2022	1O2 was generated during HMME-PDT, and inhibition of 1O2 production could reverse the regulation of HMME-PDT on P53, miR-21, and its target proteins, thus restoring cell viability.	CHEBI:63768	53-56	P53	Homo sapiens	112-115
25962755-0	2015	Cantharidin inhibits cell proliferation and promotes apoptosis in tongue squamous cell carcinoma through suppression of miR-214 and regulation of p53 and Bcl-2/Bax.	Cantharidin	0-11	P53	Homo sapiens	146-149
35204103-5	2022	The two oxyquinoline inhibitors exerted the same activation of HIF-triggered glycolytic pathways but opposite effects on signaling pathways linked to alternative substrates of HIF PHD 1 and 3, such as p53, NF-kappaB, and ATF4.	Oxyquinoline	8-20	P53	Homo sapiens	201-204
34202736-0	2021	Proteomics Analysis of Andrographolide-Induced Apoptosis via the Regulation of Tumor Suppressor p53 Proteolysis in Cervical Cancer-Derived Human Papillomavirus 16-Positive Cell Lines.	andrographolide	23-38	P53	Homo sapiens	96-99
34202736-5	2021	This study aimed to determine the activities of andrographolide (Androg) on the disturbance of E6-mediated p53 degradation in cervical cancer cell lines using a proteomic approach.	andrographolide	48-63	P53	Homo sapiens	107-110
34202736-5	2021	This study aimed to determine the activities of andrographolide (Androg) on the disturbance of E6-mediated p53 degradation in cervical cancer cell lines using a proteomic approach.	andrographolide	65-71	P53	Homo sapiens	107-110
34202736-6	2021	These results demonstrated that Androg could restore the intracellular p53 level, leading to apoptosis-induced cell death in HPV16-positive cervical cancer cell lines, SiHa and CaSki.	andrographolide	32-38	P53	Homo sapiens	71-74
35163037-2	2022	In this work, we show that the two structurally-related sesquiterpene lactones, a 2-bromobenzyloxy derivative of dehydrosantonin (BdS) and alantolactone (ATL) sensitise p53 wildtype, homologous recombination-proficient cancer cells to low-dose treatment with the PARP inhibitor, olaparib.	dehydrosantonin	113-128	P53	Homo sapiens	169-172
34202736-9	2021	Collectively, the restoration of p53 in HPV16-positive cervical cancer cells might be achieved by disruption of E3 ubiquitin ligase activity by Androg, which could be an alternative treatment for HPV-associated epithelial lesions.	andrographolide	144-150	P53	Homo sapiens	33-36
25962755-10	2015	Cantharidin markedly weakened miR-214 expression level, activated p53 protein expression, and suppressed the Bcl-2/Bax signaling pathway in Tca8113 cells.	Cantharidin	0-11	P53	Homo sapiens	66-69
25962755-12	2015	However, the overexpression of miR-214 reduced the anticancer effect of cantharidin on the proliferation and apoptosis of TSCC Tca8113 cells, inhibited p53 protein expression, and increased the Bcl-2/Bax signaling pathway.	Cantharidin	72-83	P53	Homo sapiens	152-155
25746954-0	2015	Novel structurally similar chromene derivatives with opposing effects on p53 and apoptosis mechanisms in colorectal HCT116 cancer cells.	Benzopyrans	27-35	P53	Homo sapiens	73-76
34207699-7	2021	The molecular mechanism causing the anti-proliferative effect between EO-L and 2-DG is potentially through pronounced up-regulation of P53 (4.40-fold), HIF1alpha (1.92-fold), HK2 (2.88-fold) and down-regulation of CYP3A5 (0.11-fold), as supported by quantitative mRNA expression analysis.	Deoxyglucose	79-83	P53	Homo sapiens	135-138
34072831-6	2021	BMX and TMZ cotreatment also upregulated WT-p53 mediated MGMT inhibition, thereby triggering the activation of caspase-3 and eventually leading to apoptosis in GBM-R cells.	Temozolomide	8-11	P53	Homo sapiens	44-47
35053532-9	2022	We also demonstrated that reactivating p53 by MDM2 inhibitors concomitantly with the inhibition of this integrin in recurrent cells may overcome the TMZ resistance.	Temozolomide	149-152	P53	Homo sapiens	39-42
25746954-6	2015	Chromene derivative 2a at concentrations higher than its GI50 remarkably induced caspases-dependent apoptosis in a p53-independent manner.	Benzopyrans	0-8	P53	Homo sapiens	115-118
25746954-9	2015	In conclusion, two novel and structurally similar chromene derivatives showed cytotoxicity to HCT16 cells through opposing effects on p53 levels and apoptosis mechanisms, which may be relevant for further development of drugs acting on distinct molecular targets useful in the treatment of cancers with different genetic profiles and for personalized medicine.	Benzopyrans	50-58	P53	Homo sapiens	134-137
25981919-13	2015	CONCLUSION: The current findings strongly indicate that both CTS and DTS could inhibit the growth of apoptosis-resistant colon cancer cells through induction of autophagic cell death and p53-independent cytotoxicity.	cryptotanshinone	61-64	P53	Homo sapiens	187-190
34173113-7	2021	The established features of immune regulation (hyperproduction of IgG to benzene, imbalance of apoptosis markers (CD127-, CD3+CD95+, p53, and TNFR) against the background of altered polymorphism of candidate genes (FOXP3, SOD2) form a complex of genetic and immunological markers of autonomic regulation disorders in men living under conditions of aerogenic exposure to benzene.	Benzene	370-377	P53	Homo sapiens	133-136
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	Manganese(2+)	231-235	P53	Homo sapiens	160-163
35487360-7	2022	Therefore, a quantitative structure-activity relationship (QSAR) model was constructed to characterize the binding constants (Ka) between DNA binding domain of p53 (p53 DBD) and nine metal ions (Mg2+, Ca2+, Cu2+, Zn2+, Co2+, Ni2+, Mn2+, Fe3+ and Ba2+).	Manganese(2+)	231-235	P53	Homo sapiens	165-168
25818142-2	2015	This approach was developed by designing a single-stranded probe (P1) that carries a binding region to facilitate the interaction with GO, which induces fluorescence quenching of the labeled fluorophore (FAM, 6-carboxyfluorescein), and a sensing region, which contains a hemi-methylated site of 5"-CmCGG-3", to specifically recognize the target (T1, a 32-mer DNA from the promoter region of p53 gene) and hybridize with it to form a P1/T1 duplex.	graphene oxide	135-137	P53	Homo sapiens	391-394
35306047-6	2022	Finally, we examine the utility of p53 potentiators to boost leukemia cell killing by cytarabine in the context of mutant DNMT3A.	Cytarabine	86-96	P53	Homo sapiens	35-38
25886382-6	2015	A mutation of TP53 at codon 249 (R249S), specific for exposure to aflatoxin, was detected in cell-free DNA extracted from plasma.	Aflatoxins	66-75	P53	Homo sapiens	14-18
35619328-2	2022	Here, it is demonstrated that the WEE1 inhibitor AZD1775 induces endoplasmic reticulum stress and activates the protein kinase RNA-like ER kinase (PERK) and inositol-required enzyme 1alpha (IRE1alpha) branches of the unfolded protein response (UPR) in TP53 mutant (mtTP53) ovarian cancer models.	Inositol	157-165	P53	Homo sapiens	252-256
25886382-14	2015	About 1/3 of carriers have moderate to severe liver fibrosis and 60% have detectable aflatoxin-related TP53 R249S mutation.	Aflatoxins	85-94	P53	Homo sapiens	103-107
35614936-7	2022	The comprehensive results showed that patients in the IPI-high subgroup were exhibited characters as metabolism-related signaling pathways activation, lower TP53 and TTN mutation rate, more infiltrations of CD8 T cells, dendritic cells and macrophages M1, especially earned more benefit from ICB treatment.	diprotin A	54-57	P53	Homo sapiens	157-161
35614936-8	2022	In contrast, patients in the IPI-low subgroup were exhibited characters as p53 signaling pathways activation, higher TP53 and TTN mutation rate, more infiltrations of resting memory CD4 T cells, macrophages M2, immune-suppressive response and less benefit from ICB treatment.	diprotin A	29-32	P53	Homo sapiens	75-78
25515142-0	2015	Iodine-131 induces apoptosis in HTori-3 human thyrocyte cell line and G2/M phase arrest in a p53-independent pathway.	Iodine-131	0-10	P53	Homo sapiens	93-96
35614936-8	2022	In contrast, patients in the IPI-low subgroup were exhibited characters as p53 signaling pathways activation, higher TP53 and TTN mutation rate, more infiltrations of resting memory CD4 T cells, macrophages M2, immune-suppressive response and less benefit from ICB treatment.	diprotin A	29-32	P53	Homo sapiens	117-121
25548100-7	2015	Concurrent Bcl-xL antagonism by the BH3 mimetic ABT-263 combined with carfilzomib synergistically enhanced apoptosis that was dependent on Bax or p53, and was attenuated by Noxa or Bik shRNA.	BH 3	36-39	P53	Homo sapiens	146-149
35571124-0	2022	Corrigendum: Diplatin, a Novel and Low-Toxicity Anti-Lung Cancer Platinum Complex, Activation of Cell Death in Tumors via a ROS/JNK/p53-Dependent Pathway, and a Low Rate of Acquired Treatment Resistance.	diplatin	13-21	P53	Homo sapiens	132-135
35033575-9	2022	Taken together, we believe that tucidinostat and selinexor are potentially effective drug combinations for the treatment of wt-TP53 BC, and the molecular mechanism may be through enhancing the activity of p53 in the nucleus of BC cells to suppress proliferation and invasion and promote apoptosis.	HBI-8000	32-44	P53	Homo sapiens	205-208
35033575-9	2022	Taken together, we believe that tucidinostat and selinexor are potentially effective drug combinations for the treatment of wt-TP53 BC, and the molecular mechanism may be through enhancing the activity of p53 in the nucleus of BC cells to suppress proliferation and invasion and promote apoptosis.	selinexor	49-58	P53	Homo sapiens	127-131
35033575-9	2022	Taken together, we believe that tucidinostat and selinexor are potentially effective drug combinations for the treatment of wt-TP53 BC, and the molecular mechanism may be through enhancing the activity of p53 in the nucleus of BC cells to suppress proliferation and invasion and promote apoptosis.	selinexor	49-58	P53	Homo sapiens	205-208
25767399-2	2015	METHODS: The expression level of p53 protein was detected by immunohistochemistry in primary early-stage ER-positive breast tumor specimens from 293 postmenopausal breast cancer patients who received first-line AI treatment (letrozole, anastrozole, or exemestane) until relapse, and analysis was performed to determine whether expression of p53 protein affected the response to endocrine therapy.	Letrozole	225-234	P53	Homo sapiens	33-36
35007916-16	2022	The protein levels of P53 and Caspase 3 increased with BA, NaB and SPT treatment for 72 h. CONCLUSIONS: BA, NaB and SPT show anti-cancer activity in the DMS-114 cell line without damaging MRC-5 cells, and some of the molecular mechanisms are involved in apoptosis and cell cycle arrest.	boric acid	55-57	P53	Homo sapiens	22-25
25761368-6	2015	Chemical inhibition of Mcl-1 and the related proteins Bcl-2 and Bcl-xL by a BH3 mimetic enhances the mitotic DDR, promotes p53 activation and inhibits subsequent cell cycle progression.	BH 3	76-79	P53	Homo sapiens	123-126
35007916-16	2022	The protein levels of P53 and Caspase 3 increased with BA, NaB and SPT treatment for 72 h. CONCLUSIONS: BA, NaB and SPT show anti-cancer activity in the DMS-114 cell line without damaging MRC-5 cells, and some of the molecular mechanisms are involved in apoptosis and cell cycle arrest.	boric acid	104-106	P53	Homo sapiens	22-25
25597471-0	2015	Dual functional graphene derivative-based electrochemical platforms for detection of the TP53 gene with single nucleotide polymorphism selectivity in biological samples.	Graphite	16-24	P53	Homo sapiens	89-93
35001521-8	2022	Taken together, these results confirmed that ATPR inhibited the expression of E2A/c-Myc, which led to the activation of the P53 pathway, and induced cell differentiation and cycle arrest in AML.	4-amino-2-trifluoromethyl-phenyl retinate	45-49	P53	Homo sapiens	124-127
35163553-6	2022	In U-2 OS cells with wild-type tumor suppressor p53, we found that hinokitiol exposure induced p53 expression and cellular senescence, and knockdown of p53 suppressed the senescence.	beta-thujaplicin	67-77	P53	Homo sapiens	48-51
35163553-6	2022	In U-2 OS cells with wild-type tumor suppressor p53, we found that hinokitiol exposure induced p53 expression and cellular senescence, and knockdown of p53 suppressed the senescence.	beta-thujaplicin	67-77	P53	Homo sapiens	95-98
35163553-7	2022	However, in MG-63 cells with mutated p53, a high percentage of cells underwent apoptosis with cleaved-PARP expression and Annexin V staining after hinokitiol treatment.	beta-thujaplicin	147-157	P53	Homo sapiens	37-40
35163553-9	2022	As the autophagy was suppressed through the autophagy inhibitor chloroquine, hinokitiol-induced senescence in U-2 OS cells was significantly enhanced accompanying more abundant p53 expression.	beta-thujaplicin	77-87	P53	Homo sapiens	177-180
25733818-5	2015	Danu significantly decreased the expression of B-cell lymphoma-extra-large (Bcl-xl) and B-cell lymphoma 2 (Bcl-2), but increased the expression of Bcl-2-associated X protein (Bax) and p53-upregulated modulator of apoptosis (PUMA), and promoted the cleavage of caspases 3 and 9.	danusertib	0-4	P53	Homo sapiens	184-187
35121394-0	2022	Andrographolide, a diterpene lactone from the Traditional Chinese Medicine Andrographis paniculate, induces senescence in human lung adenocarcinoma via p53/p21 and Skp2/p27.	andrographolide	0-15	P53	Homo sapiens	152-155
25555420-0	2015	Ibrutinib for previously untreated and relapsed or refractory chronic lymphocytic leukaemia with TP53 aberrations: a phase 2, single-arm trial.	ibrutinib	0-9	P53	Homo sapiens	97-101
35047402-0	2021	Dihydroartemisinin-Transferrin Adducts Enhance TRAIL-Induced Apoptosis in Triple-Negative Breast Cancer in a P53-Independent and ROS-Dependent Manner.	dihydroartemisinin-transferrin	0-30	P53	Homo sapiens	109-112
25555420-2	2015	We investigated the safety and activity of ibrutinib in previously untreated and relapsed or refractory CLL with TP53 aberrations.	ibrutinib	43-52	P53	Homo sapiens	113-117
25555420-17	2015	INTERPRETATION: The activity and safety profile of single-agent ibrutinib in CLL with TP53 aberrations is encouraging and supports its consideration as a novel treatment option for patients with this high-risk disease in both first-line and second-line settings.	ibrutinib	64-73	P53	Homo sapiens	86-90
25240597-2	2015	It was previously demonstrated that delivery of exogenous wild-type tumor suppressor gene p53 via a tumor-targeted nanocomplex (SGT-53) which crosses the blood-brain barrier could sensitize highly TMZ-resistant GBM tumors to TMZ.	Temozolomide	197-200	P53	Homo sapiens	90-93
35144430-9	2022	This report describes the use of concurrent apatinib and dose-dense TMZ in a clinically inoperable patient who had a refractory brainstem glioblastoma with a TP53 germline mutation.	Temozolomide	68-71	P53	Homo sapiens	158-162
25240597-2	2015	It was previously demonstrated that delivery of exogenous wild-type tumor suppressor gene p53 via a tumor-targeted nanocomplex (SGT-53) which crosses the blood-brain barrier could sensitize highly TMZ-resistant GBM tumors to TMZ.	Temozolomide	225-228	P53	Homo sapiens	90-93
25240597-8	2015	FROM THE CLINICAL EDITOR: Using human glioblastoma multiforma cell lines, this research team demonstrated that the delivery of exogenous wild-type tumor suppressor gene p53 via a tumor-targeted nanocomplex limited the development of temozolomide resistance and prolonged its anti-tumor effect, which may enable future human application of this or similar techniques.	Temozolomide	233-245	P53	Homo sapiens	169-172
26745097-4	2015	DOX and 2DG treatments resulted in altered radiation-induced expression levels of p53 and PTEN genes in T47D as well as SKBR3 cells.	Deoxyglucose	8-11	P53	Homo sapiens	82-85
26785947-6	2015	More importantly, findings showing that ATI5 treatment induced p53-independent apoptosis are of great importance from a therapeutic point of view since p53 mutations are common genetic alterations in human neoplasms.	ati5	40-44	P53	Homo sapiens	63-66
26785947-6	2015	More importantly, findings showing that ATI5 treatment induced p53-independent apoptosis are of great importance from a therapeutic point of view since p53 mutations are common genetic alterations in human neoplasms.	ati5	40-44	P53	Homo sapiens	152-155
25411358-6	2015	Early DNA damage checkpoint response, mediated through p53/p21, led to G1 arrest in TPA-exposed cells.	terephthalic acid	84-87	P53	Homo sapiens	55-58
25705818-3	2015	We proved that the colon cancer cell line HCT116 responded to Liofenol  treatment by reducing their proliferation, in association with an increase of p53 and p21 cell cycle gate keepers.	liofenol	62-70	P53	Homo sapiens	150-153
25482724-5	2014	TP53 was the most frequently mutated gene in TETs (n = 13; 17%), especially in TCs (26%), and was associated with a poorer overall survival (p &lt; 0.0001).	Technetium	79-82	P53	Homo sapiens	0-4
25464339-5	2014	p,p"-DDT treatment elevated the level of reactive oxygen species (ROS) generation, induced mitochondrial membrane potential, and released cytochrome c into the cytosol, with subsequent elevations of Bax and p53, along with suppression of Bcl-2.	p,p"-ddt	0-8	P53	Homo sapiens	207-210
26579413-0	2014	ETME, a novel beta-elemene derivative, synergizes with arsenic trioxide in inducing apoptosis and cell cycle arrest in hepatocarcinoma cells via a p53-dependent pathway.	N-(beta-elemene-13-yl)tryptophan methyl ester	0-4	P53	Homo sapiens	147-150
25312242-7	2014	In addition,an inverse relationship between miR-125b and p53 expression was seen in age-related cataract tissue.	mir-125b	44-52	P53	Homo sapiens	57-60
25404244-8	2014	Furthermore, the accumulations of carcinogens such as aflatoxin were shown to yield an oncogenic mutated p53 protein.	Aflatoxins	54-63	P53	Homo sapiens	105-108
25375376-10	2014	We conclude that a downregulation of mitochondrial ETC generally induces adaptive pro-survival responses, which are specifically abrogated by the suicidal p53 response triggered by the genetic risks of the pyrimidine nucleotide deficiency.	Pyrimidine Nucleotides	206-227	P53	Homo sapiens	155-158
25078313-5	2014	Data revealed that the andrographolide derivative-mediated cell death in cancer cells was p53 dependent.	andrographolide	23-38	P53	Homo sapiens	90-93
23625588-6	2014	The anti-proliferation effect of budesonide in TP53 wild type A549 cells was abolished in SK-MES-1 cells that do not have wild type TP53 protein.	Budesonide	33-43	P53	Homo sapiens	47-51
23625588-6	2014	The anti-proliferation effect of budesonide in TP53 wild type A549 cells was abolished in SK-MES-1 cells that do not have wild type TP53 protein.	Budesonide	33-43	P53	Homo sapiens	132-136
23625588-7	2014	An additive effect against cell proliferation by budesonide and fenofibrate combination was observed only in TP53 wild type A549 cancer cells.	Budesonide	49-59	P53	Homo sapiens	109-113
24954032-0	2014	PCB153, TCDD and estradiol compromise the benzo[a]pyrene-induced p53-response via FoxO3a.	Benzo(a)pyrene	42-56	P53	Homo sapiens	65-68
24954032-4	2014	We show that all three compounds amplified the accumulation of nuclear p53, elicited by benzo[a]pyrene (BaP) or dibenzo[al]pyrene (DBP).	Benzo(a)pyrene	88-102	P53	Homo sapiens	71-74
24954032-4	2014	We show that all three compounds amplified the accumulation of nuclear p53, elicited by benzo[a]pyrene (BaP) or dibenzo[al]pyrene (DBP).	Benzo(a)pyrene	104-107	P53	Homo sapiens	71-74
24954032-4	2014	We show that all three compounds amplified the accumulation of nuclear p53, elicited by benzo[a]pyrene (BaP) or dibenzo[al]pyrene (DBP).	dibenzo[al]pyrene	112-129	P53	Homo sapiens	71-74
24954032-4	2014	We show that all three compounds amplified the accumulation of nuclear p53, elicited by benzo[a]pyrene (BaP) or dibenzo[al]pyrene (DBP).	dbp	131-134	P53	Homo sapiens	71-74
24954032-7	2014	We found that inhibition of PP2A phosphatase restored levels of phosphorylated FoxO3a, led to cytosolic translocation of p53, and activated BaP-induced p53-mediated apoptosis.	Benzo(a)pyrene	140-143	P53	Homo sapiens	152-155
24954032-8	2014	These results were confirmed by silencing FoxO3a with siRNA or by inhibiting 14-3-3 protein; also these treatments trapped BaP-induced p53 in the nucleus.	Benzo(a)pyrene	123-126	P53	Homo sapiens	135-138
24954032-9	2014	Our data indicate interplay between p53, FoxO3a and 14-3-3 leading to an attenuated BaP induced apoptosis in cells co-exposed to TCDD, PCB 153 or estradiol.	Benzo(a)pyrene	84-87	P53	Homo sapiens	36-39
25002230-4	2014	We report herein on the radioprotective activity of 8-hydroxyquinoline (8HQ) derivatives that were initially designed so as to interact with the Zn(2+) in p53.	Oxyquinoline	52-70	P53	Homo sapiens	155-158
25002230-4	2014	We report herein on the radioprotective activity of 8-hydroxyquinoline (8HQ) derivatives that were initially designed so as to interact with the Zn(2+) in p53.	Oxyquinoline	72-75	P53	Homo sapiens	155-158
24939851-2	2014	In this report, we demonstrate that the stress response gene ATF3 is required for endoplasmic reticulum stress-mediated DR5 induction upon zerumbone (ZER) and celecoxib (CCB) in human p53-deficient colorectal cancer cells.	Celecoxib	159-168	P53	Homo sapiens	184-187
24939851-2	2014	In this report, we demonstrate that the stress response gene ATF3 is required for endoplasmic reticulum stress-mediated DR5 induction upon zerumbone (ZER) and celecoxib (CCB) in human p53-deficient colorectal cancer cells.	Celecoxib	170-173	P53	Homo sapiens	184-187
24867323-5	2014	Cell response to homocysteine-induced DNA damage involved the up-regulation of Bax and, at a greater extent, Bcl-2, but not caspase-3, in association with a p53-independent increase of p21 levels; concomitantly, also p16 levels were increased.	Homocysteine	17-29	P53	Homo sapiens	157-160
24500794-9	2014	Furthermore, for p-HTMI,a LCO functionalized with methylated imidazole moieties, the staining was dependent on the p53 status of the cells, indicating that the molecular target for the dye is a cellular component regulated by p53.	imidazole	61-70	P53	Homo sapiens	115-118
24500794-9	2014	Furthermore, for p-HTMI,a LCO functionalized with methylated imidazole moieties, the staining was dependent on the p53 status of the cells, indicating that the molecular target for the dye is a cellular component regulated by p53.	imidazole	61-70	P53	Homo sapiens	226-229
24736433-11	2014	Using p53 heterozygous mutant epithelial cells from patients with Li-Fraumeni syndrome, we show that monoallelic mutation of p53 was associated with elevated levels of CYP1A1 and CYP1B1 under both basal conditions and following treatment with benzo[a]pyrene.	Benzo(a)pyrene	243-257	P53	Homo sapiens	125-128
24736433-12	2014	Treatment with CP-31398, a p53 rescue compound, suppressed benzo[a]pyrene-mediated induction of CYP1A1 and CYP1B1 and the formation of DNA adducts.	Benzo(a)pyrene	59-73	P53	Homo sapiens	27-30
24662134-1	2014	BACKGROUND: The aim of this study was to evaluate association of expression of survivin and p53 with the effects of neoadjuvant chemotherapy (NAC) in patients with advanced ovarian cancer (AOC).	nac	142-145	P53	Homo sapiens	92-95
24604579-5	2014	Furthermore, miR-125b was observed to mediate DNR resistance in leukemia cell lines through decreasing expression of G protein-coupled receptor kinase 2 and p53-upregulated modulator of apoptosis, which were shown to be direct targets of miR-125b using a dual-luciferase reporter.	mir-125b	13-21	P53	Homo sapiens	157-160
24604579-5	2014	Furthermore, miR-125b was observed to mediate DNR resistance in leukemia cell lines through decreasing expression of G protein-coupled receptor kinase 2 and p53-upregulated modulator of apoptosis, which were shown to be direct targets of miR-125b using a dual-luciferase reporter.	mir-125b	238-246	P53	Homo sapiens	157-160
25337568-0	2014	Polyphenols Isolated from Allium cepa L. Induces Apoptosis by Induction of p53 and Suppression of Bcl-2 through Inhibiting PI3K/Akt Signaling Pathway in AGS Human Cancer Cells.	Polyphenols	0-11	P53	Homo sapiens	75-78
25028149-5	2014	The in silico docking study has provided an insight and evidence for the antineoplastic activity of monocrotaline against p53, HGF and TREM1 proteins which play a threatening role in causing hepatocellular carcinoma.	Monocrotaline	100-113	P53	Homo sapiens	122-125
24385693-5	2013	Propafenone could elevate the protein level of P53 effectively (P&lt;0.01).	Propafenone	0-11	P53	Homo sapiens	47-50
24223226-10	2013	Interestingly, the protein levels of p21, a p53 target and well-known gene essential for the execution of cellular senescence, were upregulated in the presence of BCAAs.	Amino Acids, Branched-Chain	163-168	P53	Homo sapiens	44-47
24518718-0	2013	Differential cytotoxicity of the glycolytic inhibitor 2-deoxy-D-glucose in isogenic cell lines varying in their p53 status.	Deoxyglucose	54-71	P53	Homo sapiens	112-115
24518718-1	2013	CONTEXT: Earlier studies have shown that cytotoxicity of glycolic inhibitor 2-deoxy-D-glucose is heterogeneous among different tumor cell lines due to a number of reasons including difference in p53 status.	Deoxyglucose	76-93	P53	Homo sapiens	195-198
24518718-9	2013	CONCLUSIONS: 2-DG could be considered as a potential therapeutic agent that induces cell death (which could be linked to induced oxidative stress) selectively in tumors with p53 mutations (particularly in the proline rich region).	Deoxyglucose	13-17	P53	Homo sapiens	174-177
24043769-2	2013	We investigated whether cenersen, a clinically active 20-mer antisense oligonucleotide complementary to TP53 exon10, could suppress p53 expression and restore erythropoiesis in del(5q) MDS.	cenersen	24-32	P53	Homo sapiens	104-108
24043769-2	2013	We investigated whether cenersen, a clinically active 20-mer antisense oligonucleotide complementary to TP53 exon10, could suppress p53 expression and restore erythropoiesis in del(5q) MDS.	cenersen	24-32	P53	Homo sapiens	132-135
24043769-3	2013	Cenersen treatment of ribosomal protein S-14-deficient erythroblasts significantly reduced cellular p53 and p53-up-regulated modulator of apoptosis expression compared with controls, accompanied by a significant reduction in apoptosis and increased cell proliferation.	cenersen	0-8	P53	Homo sapiens	100-103
24043769-3	2013	Cenersen treatment of ribosomal protein S-14-deficient erythroblasts significantly reduced cellular p53 and p53-up-regulated modulator of apoptosis expression compared with controls, accompanied by a significant reduction in apoptosis and increased cell proliferation.	cenersen	0-8	P53	Homo sapiens	108-111
24043769-4	2013	In a two-stage erythroid differentiation assay, cenersen significantly suppressed nuclear p53 in bone marrow CD34+ cells isolated from patients with del(5q) MDS, whereas erythroid burst recovery increased proportionally to the magnitude of p53 suppression without evidence of del(5q) clonal suppression (r = -0.6; P = 0.005).	cenersen	48-56	P53	Homo sapiens	90-93
24043769-4	2013	In a two-stage erythroid differentiation assay, cenersen significantly suppressed nuclear p53 in bone marrow CD34+ cells isolated from patients with del(5q) MDS, whereas erythroid burst recovery increased proportionally to the magnitude of p53 suppression without evidence of del(5q) clonal suppression (r = -0.6; P = 0.005).	cenersen	48-56	P53	Homo sapiens	240-243
23856033-2	2013	Within this scope, several nanosphere and nanocapsule formulations of a new inhibitor of p53-MDM2 interaction (xanthone 1) were developed and their physicochemical properties analyzed.	xanthone	111-119	P53	Homo sapiens	89-92
23895620-0	2013	Synthesis and quantitative structure-activity relationship of imidazotetrazine prodrugs with activity independent of O6-methylguanine-DNA-methyltransferase, DNA mismatch repair, and p53.	imidazotetrazine	62-78	P53	Homo sapiens	182-185
23514434-4	2013	AgNP exposure increased apoptosis, as demonstrated by an increase in 4 ,6-diamidino-2-phenylindole-stained apoptotic nuclei, BAX/BCL-XL ratio, cleaved poly(ADP-ribose) polymerase, p53, p21 and caspases 3, 8 and 9, and by a decrease in the levels of AKT and NF-kappaB.	agnp	0-4	P53	Homo sapiens	180-183
23887718-8	2013	Treatment of A549 cells with PA resulted in a strong inhibition of NF-kappaB activation, which was consistent with a decrease in nuclear levels of NF-kappaB/p65 and NF-kappaB/p50 and the elevation of p53 and p21.	panduratin A	29-31	P53	Homo sapiens	200-203
23759586-10	2013	In summary, dexamethasone-induced miR-125b induces cell death resistance mechanisms in MM cells via the p53/miR-34a/SIRT1 signaling network and provides these cells with an enhanced level of resistance to cytotoxic chemotherapeutics.	mir-125b	34-42	P53	Homo sapiens	104-107
23874066-5	2013	Notably, tolfenamic acid increased apoptosis-related proteins, such as p53 and p21, within 48 h. Furthermore, in vivo experiments showed that tolfenamic acid treatment resulted in a significant reduction in tumor volume over 5 weeks.	tolfenamic acid	9-24	P53	Homo sapiens	71-74
23874066-5	2013	Notably, tolfenamic acid increased apoptosis-related proteins, such as p53 and p21, within 48 h. Furthermore, in vivo experiments showed that tolfenamic acid treatment resulted in a significant reduction in tumor volume over 5 weeks.	tolfenamic acid	142-157	P53	Homo sapiens	71-74
23030661-0	2013	p53-Pathway activity and apoptosis in hydrogen sulfide-exposed stem cells separated from human gingival epithelium.	Hydrogen Sulfide	38-54	P53	Homo sapiens	0-3
23030661-7	2013	The main objective of the present study was to explore the implications of the p53 pathway in OKSCs following exposure to H2S.	Hydrogen Sulfide	122-125	P53	Homo sapiens	79-82
23642081-5	2013	MAP kinase, WNT signaling and p53 pathways were found to be activated in DMA-treated cells.	N-myristoyl-alaninol	73-76	P53	Homo sapiens	30-33
23200676-0	2013	Association between HBX status, aflatoxin-induced R249S TP53 mutation and risk of hepatocellular carcinoma in a case-control study from Thailand.	Aflatoxins	32-41	P53	Homo sapiens	56-60
23200676-1	2013	Hepatocellular carcinoma (HCC) is associated with hepatitis B virus (HBV) chronicity and dietary exposure to aflatoxin, a mutagen targeting codon 249 of tumor suppressor TP53 (R249S mutation).	Aflatoxins	109-118	P53	Homo sapiens	170-174
23450436-2	2013	The combination of bendamustine and cytarabine has demonstrated distinct and synergistic mechanisms of action in preclinical studies on cell lines and primary tumor cells of several B-cell lymphomas, including 17p deleted or TP53 mutated CLL.	Cytarabine	36-46	P53	Homo sapiens	225-229
22833338-5	2013	Concomitantly, however, treatments at both concentration ranges resulted in a marked increase in K373-acetylated p53 and lysine-acetylated FOXO3a.	chromic phosphate	97-101	P53	Homo sapiens	113-116
23076534-9	2013	Pretreatment of periostin-overexpressing cells with an Akt inhibitor, MK-2206, partially rescued periostin-mediated inhibition of p53 expression and drug resistance.	MK 2206	70-77	P53	Homo sapiens	130-133
23804139-5	2013	In a comparison between the 9 (5%) sensitive patients and 30 (16%) insensitive patients, overexpression of p53 but not overexpression of either HER2 or EGFR was associated with a good response to NAC.	nac	196-199	P53	Homo sapiens	107-110
23804139-6	2013	p53 (p=0.045) and histological grade 3 (p=0.011) were important and significant predictors of the response to NAC.	nac	110-113	P53	Homo sapiens	0-3
23804139-10	2013	We conclude that the level of p53 expression in the CNB was an effective and reliable predictor of treatment response to NAC.	nac	121-124	P53	Homo sapiens	30-33
24460352-0	2013	Prevalence of aflatoxin induced p53 mutation at codon 249 (R249s) in hepatocellular carcinoma patients with and without hepatitis B surface antigen (HBsAg).	Aflatoxins	14-23	P53	Homo sapiens	32-35
24460352-14	2013	CONCLUSIONS: Our study shows moderate prevalence of aflatoxin B1-related p53 mutation (R249S) in HCC with or without HBsAg.	Aflatoxins	52-61	P53	Homo sapiens	73-76
23167625-4	2013	We studied the relation between sensitivity to celecoxib and the phenotypic p53 status of PCa cells lines, LNCaP (wild type p53), PC3 (null p53) and DU145 (mutated p53).	Celecoxib	47-56	P53	Homo sapiens	76-79
23167625-8	2013	The effects of celecoxib on cellular growth and its association with p53 were assessed after down-regulation of p53 using synthetic interfering RNAs (siRNA) in LNCaP cells.	Celecoxib	15-24	P53	Homo sapiens	69-72
23167625-10	2013	We found that celecoxib inhibited cellular growth and proliferation in a dose-dependent manner in all three cell lines; LNCaP cells with a native p53 were the most sensitive to celecoxib.	Celecoxib	14-23	P53	Homo sapiens	146-149
23167625-11	2013	We observed a down- regulation effect on p53 in LNCaP cells exposed to &gt;= 30 muM celecoxib for 72 h, but found no significant changes in the p53 levels of DU145 cells, which have a mutated p53.	Celecoxib	84-93	P53	Homo sapiens	41-44
23167625-12	2013	Reduced COX-2 expression was found with decreased p53 in LNCaP and PC-3 cells that were exposed to &gt;= 20 muM of celecoxib for 72 h, but COX-2 expression was increased in DU145 cells.	Celecoxib	115-124	P53	Homo sapiens	50-53
23167625-14	2013	When p53 expression was inhibited using siRNA in LNCaP cells, the inhibitory effects on cellular growth usually exerted by celecoxib were not changed significantly.	Celecoxib	123-132	P53	Homo sapiens	5-8
25198662-0	2013	Activation of p53 by sodium selenite switched human leukemia NB4 cells from autophagy to apoptosis.	Sodium Selenite	21-36	P53	Homo sapiens	14-17
23038644-8	2013	Positive expression of p53 was associated with distally located SIACs (jejunum or ileum; p = 0.006).	siacs	64-69	P53	Homo sapiens	23-26
23308284-6	2013	Because miRNA-16 is a putative tumor suppressor miRNA, and others have found that miRNA-16 suppresses proliferation, we hypothesized that the p53-dependent G1 arrest associated with PAD inhibition was, in turn, dependent on miRNA-16 expression.	mirna-16	8-16	P53	Homo sapiens	142-145
23308284-6	2013	Because miRNA-16 is a putative tumor suppressor miRNA, and others have found that miRNA-16 suppresses proliferation, we hypothesized that the p53-dependent G1 arrest associated with PAD inhibition was, in turn, dependent on miRNA-16 expression.	mirna-16	82-90	P53	Homo sapiens	142-145
22750268-3	2012	In the present work, we focused on reviewing the current knowledge about the dysregulation of the proteins/enzymes involved in the key regulatory steps of glucose transport, glycolysis, TCA cycle and glutaminolysis by several oncogenes including c-Myc and hypoxia inducible factor-1 (HIF-1) and tumor suppressor, p53, in cancer cells.	Tricarboxylic Acids	186-189	P53	Homo sapiens	313-316
22944355-4	2012	Based on this rationale, Cenersen, a phosphorothioate oligonucleotide antisense to p53-mRNA was synthesized and tested in clinical trials for patients with acute myeloid leukemia (AML).	cenersen	25-33	P53	Homo sapiens	83-86
22828135-7	2012	In addition, a reduction in the number of cells in S-phase, characterized by a concomitant increase in the levels of p21 and p53 proteins, together with a strong inhibition of pRb protein phosphorylation, was observed in DHS-treated cells.	4,4'-dihydroxystilbene	221-224	P53	Homo sapiens	125-128
23120745-0	2012	Integrins and p53 pathways in glioblastoma resistance to temozolomide.	Temozolomide	57-69	P53	Homo sapiens	14-17
23120745-9	2012	Although the p53 pathway appears often altered in glioblastoma, conflicting results can be found in the literature about the clinically relevant impact of the p53 status in the resistance to TMZ.	Temozolomide	191-194	P53	Homo sapiens	159-162
22982226-9	2012	In conclusion, our finding demonstrates that H(2)S/CSE pathway plays a radioprotection role by inhibiting radiation-induced ROS production, P53 phosphorylation, NF-kappaB activation and decrease of Bcl-2/Bax, indicating that modulation of H(2)S may be a novel protection strategy for liver radiation injury in radiotherapy.	Hydrogen Sulfide	45-50	P53	Homo sapiens	140-143
22120717-8	2012	Supplementation with methyl-pyruvate, a mitochondrial substrate, rescued p53 wild-type but not p53 mutant cells from hypoxic cell death, demonstrating a p53-mediated selective aptitude to metabolize mitochondrial substrates.	methyl pyruvate	21-36	P53	Homo sapiens	73-76
22673765-4	2012	Western blot analysis also showed that CTC and TYL affected the activation of DNA damage responsive proteins, as well as cell cycle regulatory proteins, such as p53, p21(Waf1/Cip1) and Rb protein, which are crucial in the G1-S transition.	Tylosin	47-50	P53	Homo sapiens	161-164
22676643-0	2012	Mulberry leaf polyphenol extract induced apoptosis involving regulation of adenosine monophosphate-activated protein kinase/fatty acid synthase in a p53-negative hepatocellular carcinoma cell.	Polyphenols	14-24	P53	Homo sapiens	149-152
22676643-3	2012	In this study, we aimed to detect the effect of the mulberry leaf polyphenol extract (MLPE) on inducing cell death in p53-negative (Hep3B) and p53-positive (Hep3B with transfected p53) hepatocellular carcinoma cells and also to clarify the role of p53 in MLPE-treated cells.	Polyphenols	66-76	P53	Homo sapiens	118-121
22676643-3	2012	In this study, we aimed to detect the effect of the mulberry leaf polyphenol extract (MLPE) on inducing cell death in p53-negative (Hep3B) and p53-positive (Hep3B with transfected p53) hepatocellular carcinoma cells and also to clarify the role of p53 in MLPE-treated cells.	Polyphenols	66-76	P53	Homo sapiens	143-146
22676643-3	2012	In this study, we aimed to detect the effect of the mulberry leaf polyphenol extract (MLPE) on inducing cell death in p53-negative (Hep3B) and p53-positive (Hep3B with transfected p53) hepatocellular carcinoma cells and also to clarify the role of p53 in MLPE-treated cells.	Polyphenols	66-76	P53	Homo sapiens	143-146
22676643-3	2012	In this study, we aimed to detect the effect of the mulberry leaf polyphenol extract (MLPE) on inducing cell death in p53-negative (Hep3B) and p53-positive (Hep3B with transfected p53) hepatocellular carcinoma cells and also to clarify the role of p53 in MLPE-treated cells.	Polyphenols	66-76	P53	Homo sapiens	143-146
22676643-6	2012	We demonstrated that acridine orange staining and protein expressions of LC-3 and beclin-1 were increased in p53-transfected cells.	Acridine Orange	21-36	P53	Homo sapiens	109-112
22552582-0	2012	Green tea polyphenols increase p53 transcriptional activity and acetylation by suppressing class I histone deacetylases.	Polyphenols	10-21	P53	Homo sapiens	31-34
22552582-3	2012	In this study, we demonstrate that green tea polyphenols (GTPs) and their major constituent, (-) epigallocatechin-3-gallate (EGCG), activate p53 through acetylation at the Lys373 and Lys382 residues by inhibiting class I HDACs in LNCaP human prostate cancer cells.	Polyphenols	45-56	P53	Homo sapiens	141-144
22382783-5	2012	Aurora B inhibition with AZD1152-HQPA blocked cell division in four different p53-mutant glioma cell lines (U251, T98G, U373, and U118).	AZD 1152-HQPA	25-37	P53	Homo sapiens	78-81
22517433-7	2012	In contrast, pre-incubation of p53-mutant cells with tenovin-6 or leptomycin B reduces the efficacy of vinca alkaloids, suggesting that these p53 activators could be effective as chemoprotectants if combined with S- but not M-phase poisons.	leptomycin B	66-78	P53	Homo sapiens	31-34
22517433-7	2012	In contrast, pre-incubation of p53-mutant cells with tenovin-6 or leptomycin B reduces the efficacy of vinca alkaloids, suggesting that these p53 activators could be effective as chemoprotectants if combined with S- but not M-phase poisons.	leptomycin B	66-78	P53	Homo sapiens	142-145
22252650-6	2012	In addition, we demonstrated that CPT induced apoptosis in cancer cells by miR-125b-mediated mitochondrial pathways via targeting to the 3"-untranslated (UTR) regions of Bak1, Mcl1, and p53.	mir-125b	75-83	P53	Homo sapiens	186-189
22273545-0	2012	Design, synthesis and CoMFA studies of N1-amino acid substituted 2,4,5-triphenyl imidazoline derivatives as p53-MDM2 binding inhibitors.	n1-amino acid	39-52	P53	Homo sapiens	108-111
21659424-8	2012	One non-CIMP subgroup is distinguished by a significantly higher frequency of TP53 mutations and frequent occurrence in the distal colon, while the tumors that belong to the fourth group exhibit a low frequency of both cancer-specific DNA hypermethylation and gene mutations and are significantly enriched for rectal tumors.	Cyclic IMP	8-12	P53	Homo sapiens	78-82
21979946-0	2012	Germline SDHx variants modify breast and thyroid cancer risks in Cowden and Cowden-like syndrome via FAD/NAD-dependant destabilization of p53.	sdhx	9-13	P53	Homo sapiens	138-141
21760828-6	2012	Notably, terpinen-4-ol was able to increase p53 levels in A549 and CL1-0 cells.	terpinenol-4	9-22	P53	Homo sapiens	44-47
21760828-7	2012	Diminution of p53 by RNA interference induced necrosis instead of apoptosis in A549 cells following terpinen-4-ol treatment, indicating that terpinen-4-ol-elicited apoptosis is p53-dependent.	terpinenol-4	100-113	P53	Homo sapiens	14-17
21760828-7	2012	Diminution of p53 by RNA interference induced necrosis instead of apoptosis in A549 cells following terpinen-4-ol treatment, indicating that terpinen-4-ol-elicited apoptosis is p53-dependent.	terpinenol-4	141-154	P53	Homo sapiens	14-17
21760828-7	2012	Diminution of p53 by RNA interference induced necrosis instead of apoptosis in A549 cells following terpinen-4-ol treatment, indicating that terpinen-4-ol-elicited apoptosis is p53-dependent.	terpinenol-4	141-154	P53	Homo sapiens	177-180
22466960-0	2012	Activation of ERK-p53 and ERK-mediated phosphorylation of Bcl-2 are involved in autophagic cell death induced by the c-Met inhibitor SU11274 in human lung cancer A549 cells.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	133-140	P53	Homo sapiens	18-21
22466960-7	2012	Further study showed that ERK and p53 were activated after SU11274 treatment.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	59-66	P53	Homo sapiens	34-37
22466960-8	2012	Interruption of ERK and p53 activities decreased SU11274-induced autophagy, and blocking of ERK by the specific inhibitor PD98059 suppressed SU11274-induced p53 activation.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	49-56	P53	Homo sapiens	24-27
22466960-8	2012	Interruption of ERK and p53 activities decreased SU11274-induced autophagy, and blocking of ERK by the specific inhibitor PD98059 suppressed SU11274-induced p53 activation.	((3Z)-N-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-N-methyl-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide)	141-148	P53	Homo sapiens	157-160
22200421-7	2012	N-acetylcysteine, an antioxidant, and pifithrin alpha p-nitro, a p53 inhibitor, were used to determine the role of reactive oxygen species (ROS) and p53 in the induction of cell senescence.	pifithrin alpha p-nitro	38-61	P53	Homo sapiens	65-68
22905155-6	2012	In the present study, we analyzed p53 oligomerization status using glutaraldehyde cross-linking.	Glutaral	67-81	P53	Homo sapiens	34-37
22911819-5	2012	We further demonstrated that, in a dose- and time-dependent manner, 25-OCH(3)-PPD inhibited MDM2 expression at both transcriptional and post-translational levels in human breast cancer cells with various p53 statuses (wild type and mutant).	25-methoxylprotopanaxadiol	68-81	P53	Homo sapiens	204-207
22675488-0	2012	Aflatoxin-induced TP53 R249S mutation in hepatocellular carcinoma in Thailand: association with tumors developing in the absence of liver cirrhosis.	Aflatoxins	0-9	P53	Homo sapiens	18-22
22675488-3	2012	Most HCC are associated with chronic infection by Hepatitis B Virus while a G   T mutation at codon 249 of the TP53 gene, R249S, specific for exposure to aflatoxin, is detected in tumors for up to 30% of cases.	Aflatoxins	154-163	P53	Homo sapiens	111-115
22044530-5	2011	TCDD suppressed 1-NP- but not BaP-induced p53 activity, and in contrast, pifithrin-alpha (PFT-alpha), a p53 inhibitor, suppressed both 1-NP- and BaP-induced p53 activity.	Benzo(a)pyrene	145-148	P53	Homo sapiens	104-107
22044530-5	2011	TCDD suppressed 1-NP- but not BaP-induced p53 activity, and in contrast, pifithrin-alpha (PFT-alpha), a p53 inhibitor, suppressed both 1-NP- and BaP-induced p53 activity.	Benzo(a)pyrene	145-148	P53	Homo sapiens	104-107
22044530-9	2011	beta-Naphthoflavon (beta-NF), an aryl hydrocarbon receptor (AHR) agonist, mimicked TCDD"s action and abolished 1-NP-induced p53 expression.	beta-Naphthoflavone	20-27	P53	Homo sapiens	124-127
21903092-0	2011	Silencing of the SNARE protein NAPA sensitizes cancer cells to cisplatin by inducing ERK1/2 signaling, synoviolin ubiquitination and p53 accumulation.	Acecainide	31-35	P53	Homo sapiens	133-136
21903092-1	2011	We found earlier that NAPA represents an anti-apoptotic protein that promotes resistance to cisplatin in cancer cells by inducing the degradation of the tumor suppressor p53.	Acecainide	22-26	P53	Homo sapiens	170-173
21903092-2	2011	In the present study, we investigated the cellular mechanism underlying the degradation of p53 by NAPA.	Acecainide	98-102	P53	Homo sapiens	91-94
21903092-3	2011	Knockdown of NAPA using short-hairpin RNA was shown to induce p53 accumulation and to sensitize HEK293 cells to cisplatin.	Acecainide	13-17	P53	Homo sapiens	62-65
21903092-5	2011	Expression of exogenous p53 in H1299 cells was increased following knockdown of NAPA and these cells showed increased sensitivity to cisplatin-induced apoptosis.	Acecainide	80-84	P53	Homo sapiens	24-27
21903092-6	2011	Notably, knockdown of NAPA induced the ubiquitination and degradation of the E3 ubiquitin ligase synoviolin and the accumulation of p53 in unstressed HEK293 cells.	Acecainide	22-26	P53	Homo sapiens	132-135
21903092-7	2011	Conversely, NAPA overexpression decreased the ubiquitination and degradation of synoviolin, and reduced p53 protein level.	Acecainide	12-16	P53	Homo sapiens	104-107
21903092-8	2011	Knockdown of NAPA disrupted the interaction between synoviolin and proteins that form the endoplasmic reticulum-associated degradation (ERAD) complex and in turn decreased the ability of this complex to ubiquitinate p53.	Acecainide	13-17	P53	Homo sapiens	216-219
21903092-9	2011	In addition, knockdown of NAPA induced the activation of the MAPK kinases ERK, JNK and p38, but only inhibition of ERK reduced synoviolin ubiquitination and p53 accumulation.	Acecainide	26-30	P53	Homo sapiens	157-160
21903092-10	2011	These results indicate that NAPA promotes resistance to cisplatin through synoviolin and the ERAD complex which together induce the degradation of p53 and thus prevent apoptosis.	Acecainide	28-32	P53	Homo sapiens	147-150
21903092-11	2011	Based on these findings, we propose that the combination of cisplatin and knockdown of NAPA represents a novel and attractive strategy to eradicate p53-sensitive cancer cells.	Acecainide	87-91	P53	Homo sapiens	148-151
22248668-5	2011	p53 negatively regulates glycolysis through activation of TIGAR (an inhibitor of the fructose-2,6-bisphosphate).	fructose 2,6-diphosphate	85-110	P53	Homo sapiens	0-3
21660463-1	2011	In this study, in order to investigate the p53-independent function of p14ARF, we established p14ARF-inducible clones in the p53-deficient HCT cell line using the doxycycline-inducible expression system.	Doxycycline	163-174	P53	Homo sapiens	125-128
21660463-2	2011	A strong cell growth inhibition and G1/S arrest were observed after doxycycline induction in p53-/-HCT cells, and the cells also exhibited an obvious decrease of DNA synthesis.	Doxycycline	68-79	P53	Homo sapiens	93-96
22035408-0	2011	Effect of Benzothiazole based conjugates in causing apoptosis by Regulating p53, PTEN and MAP Kinase proteins affecting miR-195a and miR-101-1.	benzothiazole	10-23	P53	Homo sapiens	76-79
21815631-5	2011	We further characterized the DNA damage, generation of highly reactive oxygen species (hROS), and expression of proteins p21 and p53 in cells after exposure to iAs(III), DMA(III), and DMMTA(V).	N-myristoyl-alaninol	170-173	P53	Homo sapiens	129-132
21925390-7	2011	These results provide insights into the differential effects on p53 and Mdmx by Mdm2 in vivo and reveal a critical role for noncoding 5S rRNA in modulating the p53-Mdmx axis.	CHEMBL3739852	134-136	P53	Homo sapiens	160-163
21418191-0	2011	Fangchinoline induces autophagic cell death via p53/sestrin2/AMPK signalling in human hepatocellular carcinoma cells.	fangchinoline	0-13	P53	Homo sapiens	48-51
21418191-6	2011	Nuclear translocation of p53 was involved in induction of autophagy by fangchinoline, followed by selective transactivation of the autophagy-related gene sestrin2 and initiation of the autophagic process.	fangchinoline	71-84	P53	Homo sapiens	25-28
21418191-8	2011	siRNA for Atg 5 or pharmacological block of p53 abolished fangchinoline-induced autophagy and inhibition of autophagy switched cell death to apoptosis in these cells, suggesting that cell death is irreversible once autophagy is induced by fangchinoline.	fangchinoline	58-71	P53	Homo sapiens	44-47
21441950-8	2011	Instead, a natural antisense transcript of TP53, WRAP53, was strongly augmented by idarubicin and etoposide, but only less so by the other anthracyclines under study.	Idarubicin	83-93	P53	Homo sapiens	43-47
21750655-5	2011	However, the mechanism(s) by which XI-011 activates p53 and the effects of XI-011 on growth of breast cancer cells are currently unknown.	(10-methyl-9-anthryl)methyl imidothiocarbamate	35-41	P53	Homo sapiens	52-55
21701130-10	2011	The mRNA and protein expression levels of p53 and bax were increased in Sertoli cells treated with MC-LR at 10 microg/ml compared with the control group (P &lt; 0.05), while the bcl-2 protein levels were decreased in cells treated with MC-LR at 10 microg/ml (P &lt; 0.05).	cyanoginosin LR	236-241	P53	Homo sapiens	42-45
21399871-9	2011	Our analysis of miR-125b focused on the miR-125b/p53 pathway.	mir-125b	16-24	P53	Homo sapiens	49-52
21399871-10	2011	In vitro assays revealed that overexpression of miR-125b repressed the endogenous level of p53 protein in human colorectal cancer cells.	mir-125b	48-56	P53	Homo sapiens	91-94
21390062-4	2011	We show that DFO treatment induces phosphorylation of SMC1 at Ser966, NBS1 at Ser343, Chk1 at Ser317, Chk2 at Thr68, and p53 at Ser15.	Deferoxamine	13-16	P53	Homo sapiens	121-124
20966961-1	2011	In response to DNA damage, p53-induced protein with a death domain (PIDD) forms a complex called the PIDDosome, which either consists of PIDD, RIP-associated protein with a death domain and caspase-2, forming a platform for the activation of caspase-2, or contains PIDD, RIP1 and NEMO, important for NF-kappaB activation.	pidd	68-72	P53	Homo sapiens	27-30
20966961-1	2011	In response to DNA damage, p53-induced protein with a death domain (PIDD) forms a complex called the PIDDosome, which either consists of PIDD, RIP-associated protein with a death domain and caspase-2, forming a platform for the activation of caspase-2, or contains PIDD, RIP1 and NEMO, important for NF-kappaB activation.	pidd	101-105	P53	Homo sapiens	27-30
21468560-10	2011	The AngII + losartan group displayed longer telomere lengths, further reduced beta-galactosidase staining and decreased P53 and P21 expression compared to the AngII group.	Losartan	12-20	P53	Homo sapiens	120-123
21071400-6	2011	p53DBD binds to sites containing CAAG and CTAG with measurable affinity only when imbedded in two contiguous p53 half-sites and only as tetramers (with very high cooperativity).	caag	33-37	P53	Homo sapiens	0-3
21335238-1	2011	TAp63alpha, a homolog of the p53 tumor suppressor, is a quality control factor in the female germline.	tap63alpha	0-10	P53	Homo sapiens	29-32
20818437-4	2011	ZnCl(2) enhanced MI-219 activity (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), apoptosis and colony formation), and chelation of zinc not only blocked the activity of MI-219, but also suppressed reactivation of the p53 and its downstream effector molecules p21(WAF1) and Bax.	zncl	0-4	P53	Homo sapiens	238-241
21208455-0	2011	Impact of Alu repeats on the evolution of human p53 binding sites.	METHYL HYDROGEN (S)-ACETYLPHOSPHONATE	10-13	P53	Homo sapiens	48-51
21208455-11	2011	The binding affinity of p53 to the Alu-residing sites generally correlates with the age of Alu subfamilies, so that the strongest sites are embedded in the "relatively young" Alu repeats.	METHYL HYDROGEN (S)-ACETYLPHOSPHONATE	35-38	P53	Homo sapiens	24-27
21809637-1	2011	People exposed to chronic influence of hydrogen sulphide gas demonstrate accelerated aging, increase of proinflammatory cytokine interleukin-8 level and the marker of apoptosis protein p53.	Hydrogen Sulfide	39-56	P53	Homo sapiens	185-188
21938919-1	2011	The authors revealed increase in ageing pace, higher level of pro-inflammatory cytokine Interleukin-8 and apoptosis marker (p53 protein) in individuals with chronic exposure to gas containing hydrogen sulfide.	Hydrogen Sulfide	192-208	P53	Homo sapiens	124-127
21695227-11	2011	Exposure to 9NC-LP led to increased expression of p53, p21, p27, Bax, caspase-3, caspase-8, caspase-9 and apoptosis-inducing factor, mitochondrion-associated 1 and decreased expression of Bcl-2, cyclin E, cyclin A, Cdk2 and cyclin D1.	9nc-lp	12-18	P53	Homo sapiens	50-53
20886531-0	2010	Exposure to benzene induces oxidative stress, alters the immune response and expression of p53 in gasoline filling workers.	Benzene	12-19	P53	Homo sapiens	91-94
20886531-10	2010	CONCLUSION: Occupational exposure to benzene causes oxidative stress, immune suppression and increases the expression of tumor-suppressing gene p53 in gasoline filling workers.	Benzene	37-44	P53	Homo sapiens	144-147
21159612-0	2010	Combination of vorinostat and flavopiridol is selectively cytotoxic to multidrug-resistant neuroblastoma cell lines with mutant TP53.	alvocidib	30-42	P53	Homo sapiens	128-132
20840854-3	2010	We have evaluated the effects of some highly purified NDL-PCBs and benzo[a]pyrene (BP) on BP-induced Raf, Erk, Mdm2, p53 signaling and on BP-induced apoptosis and cell cycle arrest.	ndl-pcbs	54-62	P53	Homo sapiens	117-120
20840854-3	2010	We have evaluated the effects of some highly purified NDL-PCBs and benzo[a]pyrene (BP) on BP-induced Raf, Erk, Mdm2, p53 signaling and on BP-induced apoptosis and cell cycle arrest.	Benzo(a)pyrene	83-85	P53	Homo sapiens	117-120
20961098-4	2010	Both the p53 TAD and NCBD are intrinsically disordered and fold synergistically upon binding, as evidenced by the observed increase in helicity and increased level of dispersion of the amide proton resonances.	Amides	185-190	P53	Homo sapiens	9-12
20856941-2	2010	We find that a well known BH3 family inhibitor can potently inhibit the p53/hDM2 interaction.	BH 3	26-29	P53	Homo sapiens	72-75
20805583-4	2010	p53 protein was characterized by mass spectrometry and covalently immobilized through amide linkage to the (3-aminopropyl)trietoxysilane-modified glass surface.	Amides	86-91	P53	Homo sapiens	0-3
21280514-6	2010	The PTTs and TCs stained negative and few basal cells for p53 and Ki-67, respectively.	Technetium	13-16	P53	Homo sapiens	58-61
20658636-0	2010	Acute lymphoblastic leukemia after temozolomide treatment for anaplastic astrocytoma in a child with a germline TP53 mutation.	Temozolomide	35-47	P53	Homo sapiens	112-116
20658636-1	2010	We present a case of a 12-year-old female with a germline TP53 mutation who presented with anaplastic astrocytoma and subsequent acute lymphoblastic leukemia (ALL) 13 months after starting treatment with temozolomide (TMZ).	Temozolomide	204-216	P53	Homo sapiens	58-62
20658636-1	2010	We present a case of a 12-year-old female with a germline TP53 mutation who presented with anaplastic astrocytoma and subsequent acute lymphoblastic leukemia (ALL) 13 months after starting treatment with temozolomide (TMZ).	Temozolomide	218-221	P53	Homo sapiens	58-62
20658636-4	2010	We demonstrate a rare case of TMZ-related ALL in a child with glioma possibly associated with a germline TP53 mutation.	Temozolomide	30-33	P53	Homo sapiens	105-109
25961194-3	2010	The cells grown in charcoal-treated serum were treated with 1 nM E2 or different concentrations of LY117018 for 24 h. E2 or LY117018 treatments caused a 2- to 3-fold increase in the level of p53 and hyperphosphorylation of pRb.	Charcoal	19-27	P53	Homo sapiens	191-194
25961194-7	2010	Importantly, LY11708 inhibits estrogen-induced cell proliferation while mimicking E2 actions on p53 induction and pRb phosphorylation.	ly11708	13-20	P53	Homo sapiens	96-99
20480226-7	2010	Patients that responded to everolimus treatment with significant reductions in proliferation (fall in % Ki67 positive cells) also had significant decreases in the expression of genes involved in cell cycle (P = 8.70E-09) and p53 signalling (P = 0.01) pathways.	Everolimus	27-37	P53	Homo sapiens	225-228
20171194-5	2010	Inhibition of p38 using SB202190 or SB203580 inhibited BEL-induced increases in P-p53 (ser15), p53 and p21, and altered the number of cells in G1 in LNCaP cells, and S-phase in PC-3 cells.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	24-32	P53	Homo sapiens	82-85
20540768-8	2010	RESULTS: After treatment with TMZ, DB-1 cells demonstrated increased phosphorylation of ataxia telangiectasia mutated (ATM) and p53.	Temozolomide	30-33	P53	Homo sapiens	128-131
20596254-2	2010	BaP 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of benzo(a)pyrene (BaP), attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 gene mutations.	Benzo(a)pyrene	0-3	P53	Homo sapiens	146-149
20596254-2	2010	BaP 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of benzo(a)pyrene (BaP), attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 gene mutations.	Benzo(a)pyrene	60-74	P53	Homo sapiens	146-149
20596254-2	2010	BaP 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of benzo(a)pyrene (BaP), attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 gene mutations.	Benzo(a)pyrene	76-79	P53	Homo sapiens	146-149
20423286-3	2010	Cell lines naturally devoid of p53 or expressing shRNA targeting p53 are refractory to apoptosis induction by MI-63, indicating that the effects of MI-63 require p53 expression.	2-methyl-4-isothiazolin-3-one	148-150	P53	Homo sapiens	65-68
20423286-3	2010	Cell lines naturally devoid of p53 or expressing shRNA targeting p53 are refractory to apoptosis induction by MI-63, indicating that the effects of MI-63 require p53 expression.	2-methyl-4-isothiazolin-3-one	148-150	P53	Homo sapiens	65-68
20423286-7	2010	Interestingly, treatment with MI-63 also led to a reduction in levels of MDM4 protein, a repressor of p53 mediated transcription, in AML cells.	2-methyl-4-isothiazolin-3-one	30-32	P53	Homo sapiens	102-105
20215500-0	2010	Targeting cancer cell metabolism: the combination of metformin and 2-deoxyglucose induces p53-dependent apoptosis in prostate cancer cells.	Deoxyglucose	67-81	P53	Homo sapiens	90-93
20215500-6	2010	At the cellular level, the combination of metformin and 2DG induced p53-dependent apoptosis via the energy sensor pathway AMP kinase, and the reexpression of a functional p53 in p53-deficient prostate cancer cells restored caspase-3 activity.	Deoxyglucose	56-59	P53	Homo sapiens	68-71
20215500-6	2010	At the cellular level, the combination of metformin and 2DG induced p53-dependent apoptosis via the energy sensor pathway AMP kinase, and the reexpression of a functional p53 in p53-deficient prostate cancer cells restored caspase-3 activity.	Deoxyglucose	56-59	P53	Homo sapiens	171-174
20215500-7	2010	In addition to apoptosis, the combination of metformin and 2DG arrested prostate cancer cells in G(2)-M. This G(2)-M arrest was independent of p53 and correlated with a stronger decrease in cell viability than obtained with either drug.	Deoxyglucose	59-62	P53	Homo sapiens	143-146
19638426-2	2010	CRCs with CIMP show a specific pattern of genetic alterations, including a high frequency of BRAF mutations and a low frequency of p53 mutations.	Cyclic IMP	10-14	P53	Homo sapiens	131-134
20067818-6	2010	Treatment of cells with the p38 inhibitor SB202190, but not the ERK1/2 inhibitor PD98059, partially reversed BrO(3)(-)-induced G2/M arrest and decreased BrO(3)(-)-induced p-p53, p21 and cyclin B1 expression.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	42-50	P53	Homo sapiens	173-176
20067818-8	2010	The antioxidant ascorbic acid inhibited BrO(3)(-)-induced p38 activation, G2/M arrest, p-p53, p21 and cyclin B1 expression; however, ascorbic acid had no effect on BrO(3)(-)-induced formation of 8-OHdG, a marker of DNA oxidative damage, whose increases preceded cell death by 24h.	bro(3)(-)	40-49	P53	Homo sapiens	89-92
20070102-0	2010	Polyphenol-rich extract from mulberry leaf inhibits vascular smooth muscle cell proliferation involving upregulation of p53 and inhibition of cyclin-dependent kinase.	Polyphenols	0-10	P53	Homo sapiens	120-123
20043073-8	2010	We also found that mild heat shock increased HSP27 and p53 protein levels dependent on PI3K and suppressed the GD-induced increase in RIPA-insoluble HSP27 and p53 protein levels dependent on PI3K and ERK1/2.	Gadolinium	111-113	P53	Homo sapiens	55-58
20043073-8	2010	We also found that mild heat shock increased HSP27 and p53 protein levels dependent on PI3K and suppressed the GD-induced increase in RIPA-insoluble HSP27 and p53 protein levels dependent on PI3K and ERK1/2.	Gadolinium	111-113	P53	Homo sapiens	159-162
20043073-9	2010	In conclusion, these results indicate that PI3K-dependent HSP27 and p53 induction and PI3K- and ERK1/2-dependent inhibition of the GD-induced increase in RIPA-insoluble HSP27 and p53 protein levels by heat play a key role(s) in heat shock-mediated switch of GD-induced necrosis to apoptosis.	Gadolinium	131-133	P53	Homo sapiens	179-182
20043073-9	2010	In conclusion, these results indicate that PI3K-dependent HSP27 and p53 induction and PI3K- and ERK1/2-dependent inhibition of the GD-induced increase in RIPA-insoluble HSP27 and p53 protein levels by heat play a key role(s) in heat shock-mediated switch of GD-induced necrosis to apoptosis.	Gadolinium	258-260	P53	Homo sapiens	179-182
19760628-7	2010	RESULTS: Inhibition of CK2 by TBB led to a decrease in cell viability and apoptosis in two cell lines which express wild-type p53 whereas two other cell lines expressing mutant or no p53 failed to show signs of apoptosis.	2-ethylhexyl 2,3,4,5-tetrabromobenzoate	30-33	P53	Homo sapiens	126-129
20165695-6	2010	In vitro, NPI-0052 showed a dose-dependent toxicity, and its combination with temozolomide resulted in radiosensitization of only the cell lines with a mutated p53.	Temozolomide	78-90	P53	Homo sapiens	160-163
19557511-0	2010	Polar lipid remodeling and increased sulfatide expression are associated with the glioma therapeutic candidates, wild type p53 elevation and the topoisomerase-1 inhibitor, irinotecan.	Sulfoglycosphingolipids	37-46	P53	Homo sapiens	123-126
19557511-2	2010	Sulfatides (sulfonated glycolipids) were most highly modulated by wild-type p53 treatment; however, no changes were observed in expression levels of mRNA for genes involved in sulfatide metabolism, indicating post-transcriptional control of sulfatide synthesis.	Sulfoglycosphingolipids	0-10	P53	Homo sapiens	76-79
19557511-2	2010	Sulfatides (sulfonated glycolipids) were most highly modulated by wild-type p53 treatment; however, no changes were observed in expression levels of mRNA for genes involved in sulfatide metabolism, indicating post-transcriptional control of sulfatide synthesis.	Glycolipids	23-34	P53	Homo sapiens	76-79
19557511-5	2010	These dramatic changes in the composition of cellular glycolipids in response to p53 gene expression and cytotoxic chemotherapy treatment indicate the large role that they play in cell signaling.	Glycolipids	54-65	P53	Homo sapiens	81-84
20980775-0	2010	Influence of cell cycle checkpoints and p53 function on the toxicity of temozolomide in human pancreatic cancer cells.	Temozolomide	72-84	P53	Homo sapiens	40-43
20980775-3	2010	RESULTS: The wt-p53 human pancreatic tumor cell line Capan-2 and p53-efficient mouse embryonic fibroblasts (MEFs) were more responsive to treatment with TMZ + BG than mutant p53 Capan-1 and p53-null MEFs.	Temozolomide	153-156	P53	Homo sapiens	16-19
20980775-3	2010	RESULTS: The wt-p53 human pancreatic tumor cell line Capan-2 and p53-efficient mouse embryonic fibroblasts (MEFs) were more responsive to treatment with TMZ + BG than mutant p53 Capan-1 and p53-null MEFs.	Temozolomide	153-156	P53	Homo sapiens	65-68
20980775-6	2010	The effect of p53 on BG + TMZ toxicity was supported by a marked change in apoptosis when p53 function was restored/inactivated.	Temozolomide	26-29	P53	Homo sapiens	14-17
20980775-6	2010	The effect of p53 on BG + TMZ toxicity was supported by a marked change in apoptosis when p53 function was restored/inactivated.	Temozolomide	26-29	P53	Homo sapiens	90-93
20699632-5	2010	RESULTS: the oxamic and tartronic acids inhibited aerobic glycolysis, impaired the growth of both cell lines and also induced an increased expression of p53-upregulated modulator of apoptosis, a signal of cell death.	tartronic acid	24-39	P53	Homo sapiens	153-156
20349730-8	2010	Western blot showed cryptotanshinone decreased expressions of HPV E6 and increased expressions of p53 and p21 proteins.	cryptotanshinone	20-36	P53	Homo sapiens	98-101
20211059-10	2010	NT4-p53(N15)-Ant and its potential mechanism was detected by light microscopy, electron microscopy, MTT, LDH-release assay and annexin V-PI double staining.	annexin v-pi	127-139	P53	Homo sapiens	4-7
19751709-8	2009	This effect correlated with lowered basal levels of p53, as well as with an attenuated p53 response induced by etoposide and leptomycin B.	leptomycin B	125-137	P53	Homo sapiens	87-90
19345001-3	2009	Aflatoxin B1, the most commonly occurring and potent of the aflatoxins is associated with a specific AGG to AGT transversion mutation at codon 249 of the p53 gene in human HCC, providing mechanistic support to a causal link between exposure and disease.	Aflatoxins	60-70	P53	Homo sapiens	154-157
19376640-0	2009	The aflatoxin-induced TP53 mutation at codon 249 (R249S): biomarker of exposure, early detection and target for therapy.	Aflatoxins	4-13	P53	Homo sapiens	22-26
19641144-7	2009	We demonstrate by EMSA that nitration of p53 by ONOO(-) (300 x 10(-6) M) abrogates DNA binding, while H(2)O(2)-oxidized p53 (10(-3) M) enhances DNA binding capacity and prevents ONOO(-)-induced abrogation of DNA binding.	onoo	48-52	P53	Homo sapiens	41-44
19641144-7	2009	We demonstrate by EMSA that nitration of p53 by ONOO(-) (300 x 10(-6) M) abrogates DNA binding, while H(2)O(2)-oxidized p53 (10(-3) M) enhances DNA binding capacity and prevents ONOO(-)-induced abrogation of DNA binding.	onoo	178-182	P53	Homo sapiens	41-44
19526460-9	2009	Yet, PD0325901, but not U0126, was able to inhibit a cell line lacking Ras proteins that owed its proliferative properties to loss of p53.	mirdametinib	5-14	P53	Homo sapiens	134-137
19846942-5	2009	Doxycycline consistently activated transcription of p53, p21 and Fas/FasL-cascade-related genes, while reducing the expression of Bcl-xL and Mcl-1.	Doxycycline	0-11	P53	Homo sapiens	52-55
19659469-0	2009	Altered p53 and Bcl-2 expression in keratinocytes of vulvar lichen sclerosus during pimecrolimus treatment.	pimecrolimus	84-96	P53	Homo sapiens	8-11
19328784-7	2009	Induction of apoptosis by TMPyP4 was associated with increased expression of phosphorylated DNA damage response factor H2AX (Ser139), phosphorylated p53 (Ser46) protein and activation of mitogen-activated protein kinases in Y79 and WERI-Rb1 cells.	tetra(4-N-methylpyridyl)porphine	26-32	P53	Homo sapiens	149-152
19346293-2	2009	In our recent study, magnesium can also bind to the p53DBD and enhance its DNA-binding activity.	Magnesium	21-30	P53	Homo sapiens	52-55
19406223-0	2009	Identification of epigallocatechin-3-gallate in green tea polyphenols as a potent inducer of p53-dependent apoptosis in the human lung cancer cell line A549.	Polyphenols	58-69	P53	Homo sapiens	93-96
19567395-0	2009	Early modification of c-myc, Ha-ras and p53 expressions by chemical carcinogens (DMBA, MNU).	Methylnitrosourea	87-90	P53	Homo sapiens	40-43
19567395-4	2009	In the liver, DMBA induced strong onco/suppressor gene expression as early as 6 hours after the treatment, but MNU increased the p53 gene expression 12 hours after the treatment.	Methylnitrosourea	111-114	P53	Homo sapiens	129-132
19548636-4	2009	Arrays of amides were synthesized with improved hydrophilicity and retainment and/or improvement of p53/mdm2 inhibitory activity.	Amides	10-16	P53	Homo sapiens	100-103
19505915-2	2009	Using a case-control study that included 307 benzene-poisoned patients and 299 workers occupationally exposed to benzene in south China, we aimed to investigate the association between genetic polymorphisms of p53 and p21 and the odds of CBP.	Benzene	45-52	P53	Homo sapiens	210-213
19505915-2	2009	Using a case-control study that included 307 benzene-poisoned patients and 299 workers occupationally exposed to benzene in south China, we aimed to investigate the association between genetic polymorphisms of p53 and p21 and the odds of CBP.	Benzene	113-120	P53	Homo sapiens	210-213
19505915-3	2009	To investigate whether benzene exposure may influence mRNA expression of p53 and p21 in benzene-exposed workers, we also chose 39 CBP workers, 38 occupationally benzene-exposure workers, and 37 nonexposure workers in the same region of China.	Benzene	23-30	P53	Homo sapiens	73-76
19505915-3	2009	To investigate whether benzene exposure may influence mRNA expression of p53 and p21 in benzene-exposed workers, we also chose 39 CBP workers, 38 occupationally benzene-exposure workers, and 37 nonexposure workers in the same region of China.	Benzene	88-95	P53	Homo sapiens	73-76
19505915-3	2009	To investigate whether benzene exposure may influence mRNA expression of p53 and p21 in benzene-exposed workers, we also chose 39 CBP workers, 38 occupationally benzene-exposure workers, and 37 nonexposure workers in the same region of China.	Benzene	88-95	P53	Homo sapiens	73-76
19505915-7	2009	In addition, p53 mRNA expression of CBP workers or benzene-exposure workers was significantly lower than that of nonexposure workers.	Benzene	51-58	P53	Homo sapiens	13-16
19366907-2	2009	A single base substitution at the third nucleotide of codon 249 of TP53 (R249S) is common in HCC in these regions and has been associated with aflatoxin-DNA adducts.	Aflatoxins	143-152	P53	Homo sapiens	67-71
19123473-4	2009	Cantharidin and norcantharidin, a derivative with reduced toxicity, decreased HLF protein levels and induced apoptosis in the AML cell line MV4-11 by modulating the expression of several molecules that govern survival pathway, including HLF, SLUG, NFIL3 and c-myc, thereby inducing p53 and the mitochondrial caspase cascade.	Cantharidin	0-11	P53	Homo sapiens	282-285
19386914-6	2009	p53 inhibition-induced axonal growth cone collapse was significantly reduced by the Rho kinase (ROCK) inhibitor, Y27632 [(R)-(+)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide].	Y 27632	113-119	P53	Homo sapiens	0-3
19386914-6	2009	p53 inhibition-induced axonal growth cone collapse was significantly reduced by the Rho kinase (ROCK) inhibitor, Y27632 [(R)-(+)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide].	Y 27632	121-188	P53	Homo sapiens	0-3
19127257-16	2009	Melanoma lines expressing p53 wild-type were more resistant to TMZ and fotemustine than p53 mutant melanoma lines, which is in marked contrast to previous data reported for glioma cells treated with TMZ.	Temozolomide	63-66	P53	Homo sapiens	26-29
19127257-16	2009	Melanoma lines expressing p53 wild-type were more resistant to TMZ and fotemustine than p53 mutant melanoma lines, which is in marked contrast to previous data reported for glioma cells treated with TMZ.	Temozolomide	199-202	P53	Homo sapiens	26-29
18996371-3	2009	In this study we established a lentiviral-based system for doxycyclin (Dox)-induced conditional interference of HIPK2 expression to evaluate the molecular mechanisms involved in p53 deregulation.	Doxycycline	59-69	P53	Homo sapiens	178-181
18996371-3	2009	In this study we established a lentiviral-based system for doxycyclin (Dox)-induced conditional interference of HIPK2 expression to evaluate the molecular mechanisms involved in p53 deregulation.	Doxycycline	71-74	P53	Homo sapiens	178-181
19202565-3	2009	In the present study, p53-independent cell cycle arrest at G2/M phase was observed with DADS treatment, along with time-dependent increase of cyclin B1.	diallyl disulfide	88-92	P53	Homo sapiens	22-25
19202565-6	2009	Scavenging of DADS-induced ROS by N-acetyl cysteine or reduced glutathione inhibited cell cycle arrest, apoptosis and p53 activation by DADS.	diallyl disulfide	14-18	P53	Homo sapiens	118-121
19202565-6	2009	Scavenging of DADS-induced ROS by N-acetyl cysteine or reduced glutathione inhibited cell cycle arrest, apoptosis and p53 activation by DADS.	diallyl disulfide	136-140	P53	Homo sapiens	118-121
19202565-7	2009	These results suggest that ROS trigger the DADS-induced cell cycle arrest and apoptosis and that ROS are involved in stress-induced signaling upstream of p53 activation.	diallyl disulfide	43-47	P53	Homo sapiens	154-157
19202565-9	2009	Moreover, DADS-induced apoptosis was also prevented by treatment with oligomycin, which is known to prevent p53-dependent apoptosis by reducing ROS levels in mitochondria.	diallyl disulfide	10-14	P53	Homo sapiens	108-111
19202565-10	2009	These results suggest that mitochondrial ROS may serve as second messengers in DADS-induced apoptosis, which requires activation of p53.	diallyl disulfide	79-83	P53	Homo sapiens	132-135
18506760-8	2009	Celecoxib also inhibited p(473Ser)Akt, raf and p53 expression, and induced apoptosis by release of cytochrome c and activation of caspase 9, 3, and 6, which were more remarkably in HBx positive cells than in control cells.	Celecoxib	0-9	P53	Homo sapiens	47-50
18819919-3	2008	Following the induction of p53 in H1299 lung cancer cells containing a doxycycline-inducible p53, an increase in both H and L subunits of ferritin protein was observed.	Doxycycline	71-82	P53	Homo sapiens	27-30
18819919-3	2008	Following the induction of p53 in H1299 lung cancer cells containing a doxycycline-inducible p53, an increase in both H and L subunits of ferritin protein was observed.	Doxycycline	71-82	P53	Homo sapiens	93-96
18671758-0	2008	Nuclear accumulation and up-regulation of p53 and its associated proteins after H2S treatment in human lung fibroblasts.	Hydrogen Sulfide	80-83	P53	Homo sapiens	42-45
19181008-0	2008	Early modification of c-myc, Ha-ras and p53 expressions by N-methyl-N-nitrosourea.	Methylnitrosourea	59-81	P53	Homo sapiens	40-43
3025664-2	1986	Two p53 proteins, separable by polyacrylamide gel electrophoresis, are expressed by the human transformed cell line SV-80.	polyacrylamide	31-45	P53	Homo sapiens	4-7
19181008-9	2008	Our findings suggest that MNU has an impact on the expression of c-myc, Ha-ras and p53 genes in 12 hours, especially in bone marrow.	Methylnitrosourea	26-29	P53	Homo sapiens	83-86
18788085-1	2008	Benzo[a]pyrene diol epoxide (B[a]PDE), the ultimate carcinogenic metabolite of benzo[a] pyrene, has been implicated in the mutagenesis of the p53 gene involved in smoking-associated lung cancer.	Benzo(a)pyrene	79-94	P53	Homo sapiens	142-145
18703674-7	2008	Over-expression of p53 resulted in reduced accumulation of a marker of proliferation (cyclin B1), P(4), and PGF secretion and increased OT and PGE secretion.	Prostaglandins F	108-111	P53	Homo sapiens	19-22
3161558-2	1985	53 kilodalton) with electrophoretic mobility identical to that of protein detected in leukocytes of patients with Down"s syndrome and of protein p53 obtained from mouse ascites carcinoma was demonstrated by polyacrylamide gel electrophoresis in healthy donors" leukocytes cultured with PHA and in peripheral blood of patients with chronic myeloleukemia.	polyacrylamide	207-221	P53	Homo sapiens	145-148
18818514-6	2008	Assays using okadaic and cantharidic acid, two different PP2A inhibitors, showed an increase in microtubule-bound phospho-p53 and reduced sensitivity to chemotherapy.	cantharidic acid	25-41	P53	Homo sapiens	122-125
18818522-2	2008	Moreover, autophagy-inducing stimuli such as nutrient depletion, rapamycin or lithium cause the depletion of cytoplasmic p53, which in turn is required for the induction of autophagy.	Lithium	78-85	P53	Homo sapiens	121-124
6088530-2	1984	Analysis of the immunocomplexes on sodium dodecyl sulfate-polyacrylamide gell electrophoresis revealed that p53, p28, and p19 of adult T-cell leukemia-associated antigens were phosphorylated in vivo.	polyacrylamide	58-72	P53	Homo sapiens	108-111
18806741-5	2008	RESULTS: A clinically achievable concentration of epothilone B induced a cytotoxic response in p53 mutant glioblastoma cells, as a consequence of survivin down-regulation and tubulin redistribution, while a cytostatic response was observed in p53 null glioblastoma cells with a modest increase in survivin expression post-epothilone B treatment.	epothilone B	50-62	P53	Homo sapiens	95-98
33652124-6	2021	Our results have shown that glibenclamide and glimepiride decrease 1.2B4 cells viability with accompanied increase in intracellular Ca2+ concentration and increased expression of apoptosis-related CASP-3 and TP53.	glimepiride	46-57	P53	Homo sapiens	208-212
18806741-5	2008	RESULTS: A clinically achievable concentration of epothilone B induced a cytotoxic response in p53 mutant glioblastoma cells, as a consequence of survivin down-regulation and tubulin redistribution, while a cytostatic response was observed in p53 null glioblastoma cells with a modest increase in survivin expression post-epothilone B treatment.	epothilone B	50-62	P53	Homo sapiens	243-246
33983670-4	2021	Further, BBT activates tumor-suppressing bim and p53-puma axes to inhibit cancer survival.	bbt	9-12	P53	Homo sapiens	49-52
33662352-5	2021	The use of 5-FU and L-OHP, either alone or in combination, strongly suppressed Akt activation, Survivin, Bcl-2, and Bcl-xL expression, and enhanced Puma, phospho-p53, and p53 expression in Caco-2 cells than in DLD-1 cells.	Oxaliplatin	20-25	P53	Homo sapiens	162-165
33662352-5	2021	The use of 5-FU and L-OHP, either alone or in combination, strongly suppressed Akt activation, Survivin, Bcl-2, and Bcl-xL expression, and enhanced Puma, phospho-p53, and p53 expression in Caco-2 cells than in DLD-1 cells.	Oxaliplatin	20-25	P53	Homo sapiens	171-174
18806741-7	2008	CONCLUSION: Epothilone B, induced positive differential responses in glioblastoma cells with abnormal p53 status, but not in p53 wild-type cells.	epothilone B	12-24	P53	Homo sapiens	102-105
18806741-8	2008	This suggests that epothilone B is a potential alternative to classic microtubule inhibiting agents (ie vincristine, paclitaxel) used to treat clinical glioblastomas with p53 mutations.	epothilone B	19-31	P53	Homo sapiens	171-174
18645021-4	2008	Mechanistic studies showed that induction of p21 in both RKO (p53 wild-type) and HT-29 (p53 mutant) cells by 5,5"-dibromoDIM was Kruppel-like factor 4 (KLF4) dependent, and induction of p53 in RKO cells was also KLF4 dependent.	5,5'-dibromo-1,1-bis(3'-indolyl)methane	109-124	P53	Homo sapiens	62-65
33555513-10	2021	Moreover, regulation of MAP kinases and activation of p53 was also observed upon DCME treatment.	dcme	81-85	P53	Homo sapiens	54-57
18645021-4	2008	Mechanistic studies showed that induction of p21 in both RKO (p53 wild-type) and HT-29 (p53 mutant) cells by 5,5"-dibromoDIM was Kruppel-like factor 4 (KLF4) dependent, and induction of p53 in RKO cells was also KLF4 dependent.	5,5'-dibromo-1,1-bis(3'-indolyl)methane	109-124	P53	Homo sapiens	88-91
18645021-4	2008	Mechanistic studies showed that induction of p21 in both RKO (p53 wild-type) and HT-29 (p53 mutant) cells by 5,5"-dibromoDIM was Kruppel-like factor 4 (KLF4) dependent, and induction of p53 in RKO cells was also KLF4 dependent.	5,5'-dibromo-1,1-bis(3'-indolyl)methane	109-124	P53	Homo sapiens	88-91
18645026-0	2008	Andrographolide sensitizes cancer cells to TRAIL-induced apoptosis via p53-mediated death receptor 4 up-regulation.	andrographolide	0-15	P53	Homo sapiens	71-74
33928980-1	2021	In this paper, a novel photoelectrochemical (PEC) "signal-on" biosensor based on a Bi2Sn2O7/Bi2S3 heterojunctioncoupled with target-switchable DNA hydrogels is reported for the ultrasensitive detection of P53 gene DNA.	Bismuth sulfide (Bi2S3)	92-97	P53	Homo sapiens	205-208
18647495-0	2008	Impact of p53 status to response of temozolomide in low MGMT expression glioblastomas: preliminary results.	Temozolomide	36-48	P53	Homo sapiens	10-13
33922007-0	2021	Oxaliplatin-Induced Senescence in Colorectal Cancer Cells Depends on p14ARF-Mediated Sustained p53 Activation.	Oxaliplatin	0-11	P53	Homo sapiens	95-98
18647495-1	2008	OBJECTIVE: This study was designed to assess the clinical outcomes of MGMT low expression glioblastomas with different p53 statuses to the treatment of temozolomide capsule chemotherapy.	Temozolomide	152-164	P53	Homo sapiens	119-122
18647495-8	2008	CONCLUSION: p53 in addition to MGMT plays a role in chemotherapy resistance to temozolomide.	Temozolomide	79-91	P53	Homo sapiens	12-15
18486125-11	2008	These findings suggest that MC-4 and MR-4 may share a common mechanism whereby the perinucear mitochondrial clustering, rather than p53, p21, or microtubule depolymerization, is critical for their pro-apoptotic action.	MC-4	28-32	P53	Homo sapiens	132-135
18448277-0	2008	Benzo(a)pyrene-caused increased G1-S transition requires the activation of c-Jun through p53-dependent PI-3K/Akt/ERK pathway in human embryo lung fibroblasts.	Benzo(a)pyrene	0-14	P53	Homo sapiens	89-92
33346776-5	2021	By 12 hours, maslinic acid regulates the majority of genes involved in the cell cycle, p53 and NF-kappaB signaling pathways.	maslinic acid	13-26	P53	Homo sapiens	87-90
18406507-0	2008	MAPK regulate p53-dependent cell death induced by benzo[a]pyrene: involvement of p53 phosphorylation and acetylation.	Benzo(a)pyrene	50-64	P53	Homo sapiens	14-17
33850227-0	2021	Methylglyoxal induces p53 activation and inhibits mTORC1 in human umbilical vein endothelial cells.	Pyruvaldehyde	0-13	P53	Homo sapiens	22-25
33850227-2	2021	We have previously reported that MGO induces transcriptional changes compatible with p53 activation in cultured human endothelial cells.	Pyruvaldehyde	33-36	P53	Homo sapiens	85-88
33850227-3	2021	To further substantiate this finding and to explore the underlying mechanisms and possible consequences of p53 activation, we aimed (1) to provide direct evidence for p53 activation in MGO-treated human umbilical vein endothelial cells (HUVECs), (2) to assess putative mechanisms by which this occurs, (3) to analyze down-stream effects on mTOR and autophagy pathways, and (4) to assess the potential benefit of carnosine herein.	Pyruvaldehyde	185-188	P53	Homo sapiens	107-110
33850227-3	2021	To further substantiate this finding and to explore the underlying mechanisms and possible consequences of p53 activation, we aimed (1) to provide direct evidence for p53 activation in MGO-treated human umbilical vein endothelial cells (HUVECs), (2) to assess putative mechanisms by which this occurs, (3) to analyze down-stream effects on mTOR and autophagy pathways, and (4) to assess the potential benefit of carnosine herein.	Pyruvaldehyde	185-188	P53	Homo sapiens	167-170
18406507-0	2008	MAPK regulate p53-dependent cell death induced by benzo[a]pyrene: involvement of p53 phosphorylation and acetylation.	Benzo(a)pyrene	50-64	P53	Homo sapiens	81-84
33850227-4	2021	Exposure of HUVECs to 800 microM of MGO for 5 h induced p53 phosphorylation.	Pyruvaldehyde	36-39	P53	Homo sapiens	56-59
18483381-4	2008	RESULTS: In this report, we show that the HDIs trichostatin A, sodium butyrate, and low nanomolar doses of LAQ824 combined with the glycolysis inhibitor 2-deoxy-d-glucose induce strong apoptosis in cancer cell lines of brain, breast, and cervix in a p53-independent manner.	Deoxyglucose	153-170	P53	Homo sapiens	250-253
33850227-6	2021	Compatible with p53 activation, MGO treatment resulted in cell cycle arrest, inhibition of mTORC1 and induction of autophagy.	Pyruvaldehyde	32-35	P53	Homo sapiens	16-19
33850227-8	2021	In conclusion, our results demonstrate that MGO elicits DNA damage and p53 activation in HUVECs, resulting in modulation of downstream pathways, e.g. mTORC1.	Pyruvaldehyde	44-47	P53	Homo sapiens	71-74
2834865-9	1988	A 46K fragment, spanning residues 131-517, was immunoprecipitated with the anti-p53 monoclonal PAb122 and therefore is likely to contain the p53 binding site.	pab122	95-101	P53	Homo sapiens	80-83
33868388-3	2021	A major natural thiamine derivative, thiamine diphosphate (ThDP), is a coenzyme of central metabolism, also known to affect transcriptional activity of the master metabolic regulator and genome guardian p53.	Thiamine	16-24	P53	Homo sapiens	203-206
18451217-2	2008	Epigenetic alterations affect genetic events: Loss of MGMT via hypermethylation reportedly predisposes to guanine-to-adenine or cytosine-to-thymine (G:C--&gt;A:T) transition mutations in KRAS and P53, and silencing of hMLH1 leads to high levels of microsatellite instability (MSI-H)/mutator phenotype, suggesting that epigenetic-genetic subtypes exist.	Thymine	140-147	P53	Homo sapiens	196-199
33868388-10	2021	Correlation analysis of the p53 expression and enzymatic activities upon variations in cellular thiamine/ThDP levels indicates that p21 knockdown substitutes positive correlation of the p53 expression with the activity of 2-oxoglutarate dehydrogenase complex (OGDHC) for that with the activity of glutamate dehydrogenase (GDH).	Thiamine	96-104	P53	Homo sapiens	28-31
33868388-10	2021	Correlation analysis of the p53 expression and enzymatic activities upon variations in cellular thiamine/ThDP levels indicates that p21 knockdown substitutes positive correlation of the p53 expression with the activity of 2-oxoglutarate dehydrogenase complex (OGDHC) for that with the activity of glutamate dehydrogenase (GDH).	Thiamine	96-104	P53	Homo sapiens	186-189
33757400-0	2022	Luteolin Induces Apoptosis and Autophagy in HCT116 Colon Cancer Cells via p53-Dependent Pathway.	Luteolin	0-8	P53	Homo sapiens	74-77
33757400-5	2022	Luteolin at 10 - 20 muM induced cytotoxicity in p53 wild-type HCT116 colon cancer cells but not in p53 mutant HT-29 cells and normal colon cells.	Luteolin	0-8	P53	Homo sapiens	48-51
2834865-9	1988	A 46K fragment, spanning residues 131-517, was immunoprecipitated with the anti-p53 monoclonal PAb122 and therefore is likely to contain the p53 binding site.	pab122	95-101	P53	Homo sapiens	141-144
6318442-4	1983	Human p53 proteins of at least five different apparent molecular-weight classes in SDS-polyacrylamide gels have been detected.	polyacrylamide	87-101	P53	Homo sapiens	6-9
33757400-7	2022	We identified that luteolin can induce autophagy in p53 wild-type cells but not in p53 mutant cells, suggesting that luteolin-induced autophagy is p53-dependent; however, chloroquine-mediated inhibition of autophagy did not alter cytotoxicity and apoptosis of cells treated with luteolin.	Luteolin	19-27	P53	Homo sapiens	52-55
18489080-7	2008	An RP-HPLC-ECD assay was used to detect the formation of 8-oxo-dGuo in p53 cDNA exposed to representative quinones, BP-7,8-dione, BA-3,4-dione, and DMBA-3,4-dione under redox cycling conditions.	8-ohdg	57-67	P53	Homo sapiens	71-74
33938965-2	2021	AA-I forms the 7-(2"-deoxyadenosin-N6-yl)aristolactam I (dA-AL-I) adduct, which induces multiple A:T-to-T:A transversion mutations in TP53 of AA-I exposed UTUC patients.	7-(2'-Deoxyadenosin-N6-yl)aristolactam I	15-55	P53	Homo sapiens	134-138
18489080-10	2008	By contrast, micromolar concentrations of (+/-)- anti-BPDE generated (+)- trans- anti-BPDE-N (2)-dGuo adducts (detected by stable-isotope dilution LC/MS methodology) in p53 cDNA that correlated in a linear fashion with mutagenic frequency, but no 8-oxo-dGuo was detected.	8-ohdg	247-257	P53	Homo sapiens	169-172
33310890-7	2021	In subcutaneous tumor models, combination of ixazomib and alectinib prominently induced tumor regression and apoptosis even though the tumors were generated from ALK-rearranged NSCLC cells with non-functional p53.	alectinib	58-67	P53	Homo sapiens	209-212
18646516-0	2008	[Overexpression and higher phosphorylation of p53 induced by benzo(a) pyrene through activated protein 1 independent pathway].	Benzo(a)pyrene	61-76	P53	Homo sapiens	46-49
33310890-8	2021	Conclusions:These clinical and preclinical results indicate concomitant TP53 mutations reduce the efficacy of alectinib for ALK-rearranged NSCLC and the combined use of a proteasome inhibitor with alectinib is a promising therapy for ALK-rearranged/TP53-mutated NSCLC.	alectinib	110-119	P53	Homo sapiens	72-76
33310890-8	2021	Conclusions:These clinical and preclinical results indicate concomitant TP53 mutations reduce the efficacy of alectinib for ALK-rearranged NSCLC and the combined use of a proteasome inhibitor with alectinib is a promising therapy for ALK-rearranged/TP53-mutated NSCLC.	alectinib	110-119	P53	Homo sapiens	249-253
33542522-0	2021	ATO stabilizes structural p53 mutants.	ato	0-3	P53	Homo sapiens	26-29
33230830-7	2021	Moreover, DAPP inhibited the Vero cells apoptosis induced by EV71 via P53 signalling pathway.	1-(diethylaminopropyl)-4-phenylpiperazine	10-14	P53	Homo sapiens	70-73
34047450-1	2021	In silico approaches identified 1, N-(6-((4-bromo- benzyl)amino)hexyl)-3,5-bis(trifluoromethyl)benzene sulfonamide, as a potential inhibitor of S100A2-p53 protein-protein interaction, a validated pancreatic cancer drug target.	1, n-(6-((4-bromo- benzyl)amino)hexyl)-3,5-bis(trifluoromethyl)benzene sulfonamide	32-114	P53	Homo sapiens	151-154
18646516-1	2008	OBJECTIVE: To investigate changes of p53 expression, p53 phosphorylation, and their subcellular localizations and activated protein 1 (AP-1) activity on human embryo lung fibroblasts (HELF) induced by benzo(a)pyrene (B(a)P), and relationships between p53 and AP-1.	Benzo(a)pyrene	201-215	P53	Homo sapiens	37-40
18434539-3	2008	p53 is activated in normal cells starved for pyrimidine nucleotides by treatment with N-(phosphonacetyl)-l-aspartate (PALA).	Pyrimidine Nucleotides	45-67	P53	Homo sapiens	0-3
34028092-0	2021	The p53/p21/p16 and PI3K/Akt signaling pathways are involved in the ameliorative effects of maltol on D-galactose-induced liver and kidney aging and injury.	maltol	92-98	P53	Homo sapiens	4-7
34028092-3	2021	Interestingly, 4-weeks maltol treatment at 50 and 100 mg/kg activated aging-associated proteins including p53, p21, and p16 followed by inhibiting malondialdehyde (MDA)"s over-production and increasing the levels of antioxidant enzymes.	maltol	23-29	P53	Homo sapiens	106-109
33578781-4	2021	We found that FK866 markedly inhibited the senescent characteristics of hDPCs after exposure to H2O2, as revealed by an increase in the number of senescence-associated beta-galactosidase (SA-beta-gal)-positive hDPCs and the upregulation of the p21 and p53 proteins, which acts as molecular indicators of cellular senescence.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	14-19	P53	Homo sapiens	252-255
33546743-0	2021	Transcriptomic and metabolomic profiling reveal the p53-dependent benzeneacetic acid attenuation of silica-induced epithelial-mesenchymal transition in human bronchial epithelial cells.	Phenylacetates	66-84	P53	Homo sapiens	52-55
33075425-2	2021	However, 2"-fluoro-4"-seleno-ara-C (F-Se-Ara-C), a new generation of cytarabine (Ara-C) analogs, exhibited potent antitumor activity against the p53-deficient prostate cancer cell line PC-3.	f-se-ara-c	36-46	P53	Homo sapiens	145-148
33075425-3	2021	The distinct activity of F-Se-Ara-C was achieved by targeting the synthetic lethal interaction between p53 and mitogen-activated protein kinase-activated protein kinase-2 (MK2).	f-se-ara-c	25-35	P53	Homo sapiens	103-106
18381438-3	2008	With the combination therapy of SN-38 (the active metabolite of CPT-11) followed by flavopiridol, the induction of apoptosis was 5-fold greater in the p53+/+ cells compared with the p53-/- cells.	alvocidib	84-96	P53	Homo sapiens	151-154
33075425-6	2021	F-Se-Ara-C effectively induced anti-prostate cancer activity in vitro and in vivo by inhibition of MK2 activation in p53-deficient prostate cancer cells.	f-se-ara-c	0-10	P53	Homo sapiens	117-120
33075425-7	2021	Moreover, combining F-Se-Ara-C with cabozantinib, an anticancer drug currently in clinical use, induced synergistic antitumor activity in p53-deficient prostate cancer cells.	f-se-ara-c	20-30	P53	Homo sapiens	138-141
33987937-0	2021	Lovastatin reduces PEL cell survival by phosphorylating ERK1/2 that blocks the autophagic flux and engages a cross-talk with p53 to activate p21.	Lovastatin	0-10	P53	Homo sapiens	125-128
33075425-8	2021	Taken together, these data show that F-Se-Ara-C may become great anticancer drug candidate with its unique mechanism of action for overcoming the apoptotic resistance of p53-deficient cells by targeting the synthetic lethal interaction.	f-se-ara-c	37-47	P53	Homo sapiens	170-173
18381438-3	2008	With the combination therapy of SN-38 (the active metabolite of CPT-11) followed by flavopiridol, the induction of apoptosis was 5-fold greater in the p53+/+ cells compared with the p53-/- cells.	alvocidib	84-96	P53	Homo sapiens	182-185
33987937-4	2021	At molecular level, Lovastatin by dephosphorylating STAT3, induced ERK1/2 activation that inhibited autophagy and phosphorylated p53ser15 that in turn maintained ERK1/2 activated and up-regulated p21.	Lovastatin	20-30	P53	Homo sapiens	129-132
33869031-10	2021	In PDX models with mutated p53 status, there was significant tumor growth inhibition from the combination of AZD1775 with irinotecan or capecitabine (P <= 0.03), while PDX models with wild type p53 did not show anti-tumor synergy from the same combinations (P >= 0.08).	adavosertib	109-116	P53	Homo sapiens	27-30
33575281-0	2021	Case Report: Long-Term Chemotherapy With Hydroxyurea and Prednisolone in a Cat With a Meningioma: Correlation of FDG Uptake and Tumor Grade Assessed by Histopathology and Expression of Ki-67 and p53.	Fluorodeoxyglucose F18	113-116	P53	Homo sapiens	195-198
18381438-5	2008	Rad51 bound to p53-Ser(15) within the first 5 hours of combination therapy, and then was transcriptionally suppressed at 24 hours by flavopiridol only in p53+/+ cells.	alvocidib	133-145	P53	Homo sapiens	154-157
33446200-0	2021	Verteporfin disrupts multiple steps of autophagy and regulates p53 to sensitize osteosarcoma cells.	Verteporfin	0-11	P53	Homo sapiens	63-66
33869031-10	2021	In PDX models with mutated p53 status, there was significant tumor growth inhibition from the combination of AZD1775 with irinotecan or capecitabine (P <= 0.03), while PDX models with wild type p53 did not show anti-tumor synergy from the same combinations (P >= 0.08).	Capecitabine	136-148	P53	Homo sapiens	27-30
18381438-9	2008	Because flavopiridol inhibits Cdk9, we found that inhibition of Cdk9 by DRB or by siRNA could recapitulate the flavopiridol effects, with suppression of Rad51 and induction of apoptosis only in p53+/+ cells.	alvocidib	8-20	P53	Homo sapiens	194-197
33446200-11	2021	Interestingly, VP treated protein lysates showed a ROS-dependent high molecular weight (HMW) band when probed for P62 and P53 protein.	Verteporfin	15-17	P53	Homo sapiens	122-125
18381438-10	2008	In conclusion, after DNA damage by Topo I poisons, flavopiridol targets homologous recombination through a p53-dependent down-regulation of Rad51, resulting in enhancement of apoptosis.	alvocidib	51-63	P53	Homo sapiens	107-110
18093815-0	2008	Differentially expressed pro- and anti-apoptogenic genes in response to benzene exposure: Immunohistochemical localization of p53, Bag, Bad, Bax, Bcl-2, and Bcl-w in lung epithelia.	Benzene	72-79	P53	Homo sapiens	126-129
32748741-8	2021	These result of verification suggested that SP exerted therapeutic effects against COAD via a PPI network involving TP53, MYC, MAPK8 and CASP3.	sp	44-46	P53	Homo sapiens	116-120
33317146-9	2020	IPNB showing mutation of TP53, SMAD4 and PIK3CA might reflect complicated and other features characterizing type 2.	ipnb	0-4	P53	Homo sapiens	25-29
18155176-1	2008	Overexpression of the tumor suppressor gene, wild-type p53 (wtp53), using adenoviral vectors (Adp53) has been suggested to kill cancer cells by hydroperoxide-mediated oxidative stress [1,2] and nutrient distress induced by the glucose analog, 2-deoxyglucose (2DG), has been suggested to enhance tumor cell killing by agents that induce oxidative stress via disrupting hydroperoxide metabolism [3,4].	Deoxyglucose	243-257	P53	Homo sapiens	55-58
33166398-4	2020	Mutation of residues S315 and D48/D49, which abrogate p53 interactions with the DNA repair and replication proteins topoisomerase I and RPA, respectively, and residues L22/W23, which disrupt formation of p53-POLiota complexes, all prevent this DDT pathway.	DDT	244-247	P53	Homo sapiens	204-207
18155176-1	2008	Overexpression of the tumor suppressor gene, wild-type p53 (wtp53), using adenoviral vectors (Adp53) has been suggested to kill cancer cells by hydroperoxide-mediated oxidative stress [1,2] and nutrient distress induced by the glucose analog, 2-deoxyglucose (2DG), has been suggested to enhance tumor cell killing by agents that induce oxidative stress via disrupting hydroperoxide metabolism [3,4].	Deoxyglucose	259-262	P53	Homo sapiens	55-58
17628743-5	2008	We conclude that PARP inhibitor INO-1001 has high potential for enhancing the anti-tumor effects of chemotherapy agents such as Doxorubicin against p53 deficient breast cancer.	INO 1001	32-40	P53	Homo sapiens	148-151
33254717-8	2020	ASD children had significantly higher serum levels of 15 elements, among which arsenic, silicon, strontium, and vanadium were positively associated with both Hipk2 and p53.	Strontium	97-106	P53	Homo sapiens	168-171
17977830-3	2008	In this study, the relationship between p53 activation and its posttranslational modifications was investigated in the human cancer cell lines A549 and HCT116 in response to 5-aza-2"-deoxycytidine (5-aza-CdR) or cytarabine treatment.	Cytarabine	212-222	P53	Homo sapiens	40-43
33080341-0	2020	PBA2, a novel compound, enhances radiosensitivity in various carcinoma cells by activating the p53 pathway in vitro and in vivo.	pba2	0-4	P53	Homo sapiens	95-98
18202802-10	2008	Although further studies are needed to prove that an increased expression of Egr-1 by PTX-2 directly leads to NAG-1 induction and then apoptosis induction in p53-deficient Hep3B cells, the results of this study suggest that PTX-2 may be a good candidate for the development of a potential anti-tumorigenic agent in p53-deficient tumors.	pectenotoxin 2	86-91	P53	Homo sapiens	158-161
17984111-0	2008	Impaired repair of cyclobutane pyrimidine dimers in human keratinocytes deficient in p53 and p63.	cyclobutane pyrimidine	19-41	P53	Homo sapiens	85-88
32781854-5	2020	KM6 retained the sensitivity of LCC2 through upregulation of key enzymes of apoptosis and proteins of cell death including caspases 3, 8, 9, P53, BAX/BCL-2 ratio and LDH in media.	km6	0-3	P53	Homo sapiens	141-144
18028886-7	2007	Moreover, the lithium-induced neuroprotection was accompanied by down-regulation of pro-apoptotic p53 in the CA1 but up-regulation of anti-apoptotic Bcl-2 and heat shock protein 70 (HSP70) in the ischemic brain.	Lithium	14-21	P53	Homo sapiens	98-101
33160274-0	2020	p53 coordinates glucose and choline metabolism during the mesendoderm differentiation of human embryonic stem cells.	Choline	28-35	P53	Homo sapiens	0-3
17853924-5	2007	The cellular growth inhibition and apoptosis of HPhA-mediated p53 transfection were assessed by XTT (sodium 3"-[1-(phenylaminocarbonyl)-3,4-tetrazolium]-bis(4-methoxy-6-nitro)benzene sulfonic acid hydrate) assay and annexin V-FITC (fluorescein isothiocyanate) staining, respectively.	Fluorescein-5-isothiocyanate	232-258	P53	Homo sapiens	62-65
17673346-5	2007	Cin down-regulated the expression of Bcl-(XL), up-regulated mutant p53 and Bax proteins and promoted caspase-3 to active forms, as well as cleaving poly (ADP-ribose) polymerase (PARP) in a time-dependent pattern.	cinnamaldehyde	0-3	P53	Homo sapiens	67-70
32814173-0	2020	Ilimaquinone inhibits neovascular age-related macular degeneration through modulation of Wnt/beta-catenin and p53 pathways.	ilimaquinone	0-12	P53	Homo sapiens	110-113
17673346-10	2007	These results suggest that p53 induction and MAPK signaling pathways are required for Cin-mediated apoptosis in PLC/PRF/5 cells.	cinnamaldehyde	86-89	P53	Homo sapiens	27-30
18003927-9	2007	CIMP-negative cases have a high rate of p53 mutations (71%) and lower rates of MSI (12%) or mutations of BRAF (2%) or KRAS (33%).	Cyclic IMP	0-4	P53	Homo sapiens	40-43
33081324-0	2020	Deferasirox-Dependent Iron Chelation Enhances Mitochondrial Dysfunction and Restores p53 Signaling by Stabilization of p53 Family Members in Leukemic Cells.	Deferasirox	0-11	P53	Homo sapiens	85-88
33081324-0	2020	Deferasirox-Dependent Iron Chelation Enhances Mitochondrial Dysfunction and Restores p53 Signaling by Stabilization of p53 Family Members in Leukemic Cells.	Deferasirox	0-11	P53	Homo sapiens	119-122
33081324-6	2020	The aim of this study has been to investigate the potential anti-leukemic effect of DFX, by functionally and molecularly analyzing its effects in three different leukemia cell lines, harboring or not p53 mutations, and in human primary cells derived from 15 MDS/AML patients.	Deferasirox	84-87	P53	Homo sapiens	200-203
17929901-0	2007	Method for lipidomic analysis: p53 expression modulation of sulfatide, ganglioside, and phospholipid composition of U87 MG glioblastoma cells.	Sulfoglycosphingolipids	60-69	P53	Homo sapiens	31-34
33251049-3	2020	In this study, we report that the LINC00460-miR-149-5p/miR-150-5p-mutant p53 feedback loop is responsible for oxaliplatin resistance in CRC.	Oxaliplatin	110-121	P53	Homo sapiens	73-76
17929901-6	2007	Sulfatides are most highly modulated by wild-type p53 treatment.	Sulfoglycosphingolipids	0-10	P53	Homo sapiens	50-53
33251049-6	2020	LINC00460 functions as a competing endogenous RNA (ceRNA) to promote oxaliplatin resistance through sequestering miR-149-5p/miR-150-5p and upregulating the expression of the microRNA (miRNA) target p53.	Oxaliplatin	69-80	P53	Homo sapiens	198-201
33251049-7	2020	Knockdown of LINC00460 sensitized SW480/OxR cells to oxaliplatin by modulating p53 in vitro and in vivo.	Oxaliplatin	53-64	P53	Homo sapiens	79-82
17906315-0	2007	Arsenic salt-induced DNA damage and expression of mutant p53 and COX-2 proteins in SV-40 immortalized human uroepithelial cells.	arsenic salt	0-12	P53	Homo sapiens	57-60
33251049-10	2020	Our findings uncover a mechanism for the LINC00460-miR-149-5p/miR-150-5p-mutant p53 feedback loop in oxaliplatin resistance of CRC, and they provide potential therapeutic targets for tumor chemoresistance.	Oxaliplatin	101-112	P53	Homo sapiens	80-83
17690113-6	2007	Next, doxycycline-regulated p53-inducible H1299 cell lines were established by applying a retrovirus-mediated gene transfer system to a p53-null human H1299 cell line.	Doxycycline	6-17	P53	Homo sapiens	28-31
33149857-9	2020	Generally, metabolic memory increased p53 and acetyl-P53 and decreased SIRT1 proteins in HUVECs, which were reversed by alpha-mangostin and metformin.	mangostin	120-135	P53	Homo sapiens	38-41
33149857-9	2020	Generally, metabolic memory increased p53 and acetyl-P53 and decreased SIRT1 proteins in HUVECs, which were reversed by alpha-mangostin and metformin.	mangostin	120-135	P53	Homo sapiens	53-56
17690113-6	2007	Next, doxycycline-regulated p53-inducible H1299 cell lines were established by applying a retrovirus-mediated gene transfer system to a p53-null human H1299 cell line.	Doxycycline	6-17	P53	Homo sapiens	136-139
17509529-1	2007	Using high-throughput screening with small-molecule libraries, we identified a compound, KCG165 [(2-(3-(2-(pyrrolidin-1-yl)ethoxy)-1,10b-dihydro-[1,2,4]triazolo[1,5-c]quinazolin-5(6H)-one)], which strongly activated p53-mediated transcriptional activity.	3-(2-(pyrrolidin-1-yl)ethoxy)-1,10b-dihydro-(1,2,4)triazolo(1,5-c)quinazolin-5(6H)-one	89-95	P53	Homo sapiens	216-219
32873579-7	2020	A deeper understanding of the molecular basis for DNE may drive development of drugs that release WT p53 and allow tumor suppression.	dne	50-53	P53	Homo sapiens	101-104
17509529-2	2007	KCG165-induced phosphorylations of p53 at Ser(6), Ser(15), and Ser(20)(,) which are all key residues involved in the activation and stabilization of p53.	3-(2-(pyrrolidin-1-yl)ethoxy)-1,10b-dihydro-(1,2,4)triazolo(1,5-c)quinazolin-5(6H)-one	0-6	P53	Homo sapiens	35-38
17509529-2	2007	KCG165-induced phosphorylations of p53 at Ser(6), Ser(15), and Ser(20)(,) which are all key residues involved in the activation and stabilization of p53.	3-(2-(pyrrolidin-1-yl)ethoxy)-1,10b-dihydro-(1,2,4)triazolo(1,5-c)quinazolin-5(6H)-one	0-6	P53	Homo sapiens	149-152
32851091-0	2020	AURKA Increase the Chemosensitivity of Colon Cancer Cells to Oxaliplatin by Inhibiting the TP53-Mediated DNA Damage Response Genes.	Oxaliplatin	61-72	P53	Homo sapiens	91-95
17509529-4	2007	Notably, KCG165-induced p53-dependent apoptosis in cancer cells.	3-(2-(pyrrolidin-1-yl)ethoxy)-1,10b-dihydro-(1,2,4)triazolo(1,5-c)quinazolin-5(6H)-one	9-15	P53	Homo sapiens	24-27
17695552-3	2007	Western blot analysis was used to study celecoxib effects on the expression of mitogen-activated protein kinases (MAPKs), p53, p21, 14-3-4sigma, Bcl-2 and Bax.	Celecoxib	40-49	P53	Homo sapiens	122-125
17567683-8	2007	Inhibition of p53 resulted in excessive oxidation of DNA; control SiHa cells exhibited a more rapid removal of 8-oxo-7,8-dihydro-2"-deoxyguanosine from DNA compared with p53-deficient SiHa cells exposed to the same level of H2O2 challenge.	8-ohdg	111-146	P53	Homo sapiens	14-17
17570035-8	2007	Accordingly, our results suggested that Aurora-B dysfunction increases in the appearance of multinucleated cells in p53 gene deficient cells, and TMZ treatment in combination with the inhibition of Aurora-B function may become a potential therapy against p53 gene deficient and chemotherapeutic-resistant human gliomas.	Temozolomide	146-149	P53	Homo sapiens	255-258
17418817-7	2007	The trans-platinum compounds tested show induction of p53 as well as time dependent gammaH2AX induction, consistent with the promotion of DNA lesions.	trans-platinum	4-18	P53	Homo sapiens	54-57
17290384-4	2007	The nuclear export protein inhibitor leptomycin B (LMB) has been shown to cause the nuclear sequestration of p53 in cervical carcinoma cells.	leptomycin B	37-49	P53	Homo sapiens	109-112
17290384-4	2007	The nuclear export protein inhibitor leptomycin B (LMB) has been shown to cause the nuclear sequestration of p53 in cervical carcinoma cells.	leptomycin B	51-54	P53	Homo sapiens	109-112
17374986-4	2007	We showed in colorectal cancer cell lines that the expression of MV-H/F, but also of RSV-F, as well as VSV-G can synergistically enhance p53-independent clinically relevant chemotherapy (FOLFOX) over most of the cytotoxic dose range.	rsv-f	85-90	P53	Homo sapiens	137-140
17409429-6	2007	The critical role of p53 localization in cells with increased p53 levels was supported by enhanced apoptosis induction in cells cotreated with Nutlin-3a and the nuclear export inhibitor leptomycin B.	leptomycin B	186-198	P53	Homo sapiens	21-24
17409429-6	2007	The critical role of p53 localization in cells with increased p53 levels was supported by enhanced apoptosis induction in cells cotreated with Nutlin-3a and the nuclear export inhibitor leptomycin B.	leptomycin B	186-198	P53	Homo sapiens	62-65
17454128-2	2007	We demonstrated that UVA-irradiated NADH induced damage to (32)P-labeled DNA fragments obtained from the p53 gene in the presence of Cu(II).	cu(ii)	133-139	P53	Homo sapiens	105-108
17276397-3	2007	In this study, we have identified a novel p53 mutant lacking its COOH-terminal region in neuroblastoma SK-N-AS cells.	sk-n-as	103-110	P53	Homo sapiens	42-45
17192950-6	2007	Likewise, a thymine to cytosine substitution occurred in TTT, codon 270 of exon 8 in p53 gene, to TCT in tumor sample of Case 2.	Thymine	12-19	P53	Homo sapiens	85-88
17471156-3	2007	In addition, the improved effectiveness of guanine cytosine (GC)-clamped DHPLC for TP53 screening is detailed.	gallocatechol	61-63	P53	Homo sapiens	83-87
33824865-0	2021	TRIM29 Reverses Oxaliplatin Resistance of P53 Mutant Colon Cancer Cell.	Oxaliplatin	16-27	P53	Homo sapiens	42-45
17244262-5	2007	Paclitaxel treatment combined with apoptin expression significantly inhibited the survival of p53-positive human osteosarcoma U2OS and non-small lung carcinoma A549 cells, p53-negative human osteosarcoma Saos-2 cells and p53-mutant human prostate cancer Du145 cells, already at low doses of the chemotherapeutic agent.	apoptin	35-42	P53	Homo sapiens	94-97
33824865-3	2021	In our experiments, we aim to elucidate the associations among TRIM29 protein, mutant P53, and the resistance of colon cancer cells to oxaliplatin.	Oxaliplatin	135-146	P53	Homo sapiens	86-89
33824865-10	2021	TRIM29 significantly increased the sensitivity of P53 mutant colon cancer cell HT29 to oxaliplatin.	Oxaliplatin	87-98	P53	Homo sapiens	50-53
33824865-11	2021	The oxaliplatin-resistant model of P53 mutant colon cancer cell HT29 was successfully constructed.	Oxaliplatin	4-15	P53	Homo sapiens	35-38
33824865-14	2021	Conclusion: In mutant P53 colon cancer cell HT29, TRIM29 greatly increased the sensitivity of HT29 to oxaliplatin and reverse oxaliplatin resistance.	Oxaliplatin	102-113	P53	Homo sapiens	22-25
33824865-14	2021	Conclusion: In mutant P53 colon cancer cell HT29, TRIM29 greatly increased the sensitivity of HT29 to oxaliplatin and reverse oxaliplatin resistance.	Oxaliplatin	126-137	P53	Homo sapiens	22-25
33824865-15	2021	The underlying mechanism is TRIM29 may increase the sensitivity of HT29 to oxaliplatin by blocking the transcriptional function of mutant P53, which inhibits the transcription function of its downstream gene such as MDR1.	Oxaliplatin	75-86	P53	Homo sapiens	138-141
33732640-6	2021	In conclusion, mEHT monotherapy of melanoma xenograft tumors induced irreversible heat and cell stress leading to caspase dependent apoptosis to be driven by p53.	meht	15-19	P53	Homo sapiens	158-161
17244262-5	2007	Paclitaxel treatment combined with apoptin expression significantly inhibited the survival of p53-positive human osteosarcoma U2OS and non-small lung carcinoma A549 cells, p53-negative human osteosarcoma Saos-2 cells and p53-mutant human prostate cancer Du145 cells, already at low doses of the chemotherapeutic agent.	apoptin	35-42	P53	Homo sapiens	172-175
17244262-5	2007	Paclitaxel treatment combined with apoptin expression significantly inhibited the survival of p53-positive human osteosarcoma U2OS and non-small lung carcinoma A549 cells, p53-negative human osteosarcoma Saos-2 cells and p53-mutant human prostate cancer Du145 cells, already at low doses of the chemotherapeutic agent.	apoptin	35-42	P53	Homo sapiens	172-175
17234766-3	2007	p53 is of interest because, in addition to often being mutated in glioblastoma, inactivation sensitizes some astrocytoma cell lines to temozolomide.	Temozolomide	135-147	P53	Homo sapiens	0-3
33672646-7	2021	AZD-1775, a Wee1 inhibitor, was predicted to have preferential activity in TNBC (p < 2.2 x 10-16) and its efficacy was highly associated with TP53 mutations (p = 1.2 x 10-46).	adavosertib	0-8	P53	Homo sapiens	142-146
17404014-0	2007	Apoptotic effect of celecoxib dependent upon p53 status in human ovarian cancer cells.	Celecoxib	20-29	P53	Homo sapiens	45-48
33314700-2	2021	The compound APR-246 (PRIMA-1Met/Eprenetapopt) is converted to methylene quinuclidinone (MQ) that targets mutant p53 protein and perturbs cellular antioxidant balance.	SCHEMBL4738034	63-87	P53	Homo sapiens	113-116
33253914-0	2021	Dysregulation of lysophospholipid signaling by p53 in malignant cells and the tumor microenvironment.	Lysophospholipids	17-33	P53	Homo sapiens	47-50
33253914-4	2021	In particular, intermediates of the sphingolipid and lysophospholipid pathways regulate many cellular responses common to p53 such as cell survival, migration, DNA damage repair and apoptosis.	Sphingolipids	36-48	P53	Homo sapiens	122-125
33253914-4	2021	In particular, intermediates of the sphingolipid and lysophospholipid pathways regulate many cellular responses common to p53 such as cell survival, migration, DNA damage repair and apoptosis.	Lysophospholipids	53-69	P53	Homo sapiens	122-125
17404014-4	2007	To explore the importance of functional status of p53 in apoptosis by celecoxib in ovarian cancer cells, the cellular response to celecoxib was determined in SK-OV3 ovarian cancer cells with null type p53 and PA-1 with wild-type p53.	Celecoxib	70-79	P53	Homo sapiens	50-53
17404014-9	2007	These results suggest that death receptor and mitochondria-mediated apoptotic pathways may be involved in celecoxib-induced apoptosis dependent upon the functional status of p53.	Celecoxib	106-115	P53	Homo sapiens	174-177
17404014-10	2007	Our article demonstrated that the celecoxib effectively inhibited cell growth and induced apoptosis in human ovarian cancer cells with wild-type p53.	Celecoxib	34-43	P53	Homo sapiens	145-148
17404014-11	2007	Thus, apoptotic effect by celecoxib seemed to be different dependent upon the functional status of p53.	Celecoxib	26-35	P53	Homo sapiens	99-102
32792599-8	2021	TP53 mutations occurred in 73% (22/30) VSCC, 85% (11/13) dVIN, 70% (7/10) ?dVIN and no VC (0/8), DE-VIL (0/6) nor VAAD (0/2).	dvin	57-61	P53	Homo sapiens	0-4
17143546-0	2007	Structure-activity relationship of a glycolipid, sulfoquinovosyl diacylglycerol, with the DNA binding activity of p53.	Glycolipids	37-47	P53	Homo sapiens	114-117
33259807-9	2021	AMG900 bound to the p53 binding site of TCTP with a free binding energy of -9.63 +- 0.01 kcal/mol.	N-(4-((3-(2-amino-4-pyrimidinyl)-2-pyridinyl)oxy)phenyl)-4-(4-methyl-2-thienyl)-1-phthalazinamine	0-6	P53	Homo sapiens	20-23
17143546-0	2007	Structure-activity relationship of a glycolipid, sulfoquinovosyl diacylglycerol, with the DNA binding activity of p53.	[(2~{S},3~{S},4~{S},5~{R},6~{S})-6-[(2~{S})-3-butanoyloxy-2-heptanoyloxy-propoxy]-3,4,5-tris(oxidanyl)oxan-2-yl]methanesulfonic acid	49-79	P53	Homo sapiens	114-117
17143546-2	2007	We isolated the glycolipid fraction from spinach (Spinacia oleracea L.) and found that the fraction inhibited the double-stranded DNA (dsDNA) binding activity of p53 DBD.	Glycolipids	16-26	P53	Homo sapiens	162-165
33259807-13	2021	Moreover, AMG900 disturbed TCTP-p53 complexation as shown by co-immunoprecipitation and increased expression of free p53.	N-(4-((3-(2-amino-4-pyrimidinyl)-2-pyridinyl)oxy)phenyl)-4-(4-methyl-2-thienyl)-1-phthalazinamine	10-16	P53	Homo sapiens	32-35
17143546-7	2007	The inhibitory activity of SQDG was weakened by the R248A mutant of p53 DBD, suggesting that R248 in the dsDNA binding site of p53 must be important for the inhibitory activity of SQDG.	sulfoquinovosyl diglyceride	27-31	P53	Homo sapiens	68-71
33259807-13	2021	Moreover, AMG900 disturbed TCTP-p53 complexation as shown by co-immunoprecipitation and increased expression of free p53.	N-(4-((3-(2-amino-4-pyrimidinyl)-2-pyridinyl)oxy)phenyl)-4-(4-methyl-2-thienyl)-1-phthalazinamine	10-16	P53	Homo sapiens	117-120
17143546-7	2007	The inhibitory activity of SQDG was weakened by the R248A mutant of p53 DBD, suggesting that R248 in the dsDNA binding site of p53 must be important for the inhibitory activity of SQDG.	sulfoquinovosyl diglyceride	27-31	P53	Homo sapiens	127-130
33039869-11	2021	These results indicated that Cr(VI)-induced apoptosis of Hep3B cells (p53-null) was closely associated with calcium overload, and was accompanied by the activation of Ca2+/CaM/CaMKII signaling pathway.	chromium hexavalent ion	29-35	P53	Homo sapiens	70-73
33039869-13	2021	These results provide additional experimental evidence of the molecular mechanisms involved in Cr(VI)-induced p53-independent apoptosis.	chromium hexavalent ion	95-101	P53	Homo sapiens	110-113
17143546-7	2007	The inhibitory activity of SQDG was weakened by the R248A mutant of p53 DBD, suggesting that R248 in the dsDNA binding site of p53 must be important for the inhibitory activity of SQDG.	sulfoquinovosyl diglyceride	180-184	P53	Homo sapiens	68-71
17143546-7	2007	The inhibitory activity of SQDG was weakened by the R248A mutant of p53 DBD, suggesting that R248 in the dsDNA binding site of p53 must be important for the inhibitory activity of SQDG.	sulfoquinovosyl diglyceride	180-184	P53	Homo sapiens	127-130
17143546-8	2007	SQDG binding to p53 DBD could be reversed with a non-ionic detergent, Nonidet P-40.	sulfoquinovosyl diglyceride	0-4	P53	Homo sapiens	16-19
17143546-9	2007	This is the first study of a glycolipid, SQDG, acting as a dsDNA binding inhibitor of p53, and it could be considered that a SQDG-containing thylakoid membrane in plant chloroplasts might regulate the activity of p53 for cell division, cell cycle checkpoint and tumor suppression.	Glycolipids	29-39	P53	Homo sapiens	86-89
33159515-3	2020	The first mechanism is the inhibition of co-expressed wild-type p53 (WTp53) activity, dubbed the dominant-negative effect (DNE).	dne	123-126	P53	Homo sapiens	64-67
32950498-0	2020	Tetrandrine enhances antitumor effects of the histone deacetylase inhibitor MS-275 in human cancer in a Bax- and p53-dependent manner.	entinostat	76-82	P53	Homo sapiens	113-116
32950498-10	2020	Based on our findings, tetrandrine enhanced the antitumor effects of MS-275 in a Bax- and p53-dependent manner.	entinostat	69-75	P53	Homo sapiens	90-93
17143546-9	2007	This is the first study of a glycolipid, SQDG, acting as a dsDNA binding inhibitor of p53, and it could be considered that a SQDG-containing thylakoid membrane in plant chloroplasts might regulate the activity of p53 for cell division, cell cycle checkpoint and tumor suppression.	Glycolipids	29-39	P53	Homo sapiens	213-216
17143546-9	2007	This is the first study of a glycolipid, SQDG, acting as a dsDNA binding inhibitor of p53, and it could be considered that a SQDG-containing thylakoid membrane in plant chloroplasts might regulate the activity of p53 for cell division, cell cycle checkpoint and tumor suppression.	sulfoquinovosyl diglyceride	41-45	P53	Homo sapiens	86-89
17143546-9	2007	This is the first study of a glycolipid, SQDG, acting as a dsDNA binding inhibitor of p53, and it could be considered that a SQDG-containing thylakoid membrane in plant chloroplasts might regulate the activity of p53 for cell division, cell cycle checkpoint and tumor suppression.	sulfoquinovosyl diglyceride	41-45	P53	Homo sapiens	213-216
17143546-9	2007	This is the first study of a glycolipid, SQDG, acting as a dsDNA binding inhibitor of p53, and it could be considered that a SQDG-containing thylakoid membrane in plant chloroplasts might regulate the activity of p53 for cell division, cell cycle checkpoint and tumor suppression.	sulfoquinovosyl diglyceride	125-129	P53	Homo sapiens	86-89
32958825-5	2020	RESULTS: CB11 causes cell death via ROS-mediated ATM-p53-GADD45alpha signalling in human NSCLC cells, and diphenyleneiodonium (DPI), an NADPH oxidase inhibitor, decreases cell death by inhibiting CB11-mediated ATM signalling.	cb11	9-13	P53	Homo sapiens	53-56
17143546-9	2007	This is the first study of a glycolipid, SQDG, acting as a dsDNA binding inhibitor of p53, and it could be considered that a SQDG-containing thylakoid membrane in plant chloroplasts might regulate the activity of p53 for cell division, cell cycle checkpoint and tumor suppression.	sulfoquinovosyl diglyceride	125-129	P53	Homo sapiens	213-216
16777982-9	2006	Endogenous lipid electrophiles have been our primary focus; however, metabolic activation of hormones can generate endogenous mutagens, and we demonstrate that estrone-quinone attenuates p53 function in human MCF7 cells.	estrone-quinone	160-175	P53	Homo sapiens	187-190
33096424-9	2020	TP53/CTNNB1-altered patient groups laso showed different prognostic outcomes and tumor infiltration levels.	laso	35-39	P53	Homo sapiens	0-4
16633716-0	2006	MDDD, a 4,9-diazapyrenium derivative, is selectively toxic to glioma cells by inducing growth arrest at G0/G1 independently of p53.	4-methyl-2,7-diamino-5,10-diphenyl-4,9-diaz-apyrenium chloride	0-4	P53	Homo sapiens	127-130
32629056-0	2020	Characterization of a polysaccharide from Sanghuangporus vaninii and its antitumor regulation via activation of the p53 signaling pathway in breast cancer MCF-7 cells.	Polysaccharides	22-36	P53	Homo sapiens	116-119
16633716-5	2006	MDDD treatment also triggers induction of p53 and p21 at the protein levels, suggesting the activation of DNA damage response.	4-methyl-2,7-diamino-5,10-diphenyl-4,9-diaz-apyrenium chloride	0-4	P53	Homo sapiens	42-45
33140956-4	2020	Circular dichroism spectra, 2D-NMR spectroscopy, and the computational simulations suggested that these helical sulfono-gamma-AA peptides could mimic the critical side chains of p53 and disrupt p53/MDM2 PPI effectively.	sulfono-gamma-aa peptides	112-137	P53	Homo sapiens	178-181
16633716-6	2006	However, MDDD mediated growth inhibition does not require the p53 pathway since p53+/- isogenic cell pairs display the same sensitivity.	4-methyl-2,7-diamino-5,10-diphenyl-4,9-diaz-apyrenium chloride	9-13	P53	Homo sapiens	80-83
33140956-4	2020	Circular dichroism spectra, 2D-NMR spectroscopy, and the computational simulations suggested that these helical sulfono-gamma-AA peptides could mimic the critical side chains of p53 and disrupt p53/MDM2 PPI effectively.	sulfono-gamma-aa peptides	112-137	P53	Homo sapiens	194-197
17029827-4	2006	The response of phosphorylated p53 may be more sensitive towards benzo[a]pyrene exposure than normal p53.	Benzo(a)pyrene	65-79	P53	Homo sapiens	31-34
33177647-6	2020	The activation of p53 through the cooperative effects of these unidentified component(s), caffeine, and tamoxifen appeared to be due to the suppression of the ERK and Akt pathways.	Caffeine	90-98	P53	Homo sapiens	18-21
17029827-5	2006	Following DNA damage, the activation of p53 acts as a transcriptional regulator of several target genes, including, p21 protein; a gene that encodes the Cdk inhibitor and is induced by exposure to benzo[a]pyrene.	Benzo(a)pyrene	197-211	P53	Homo sapiens	40-43
32901866-4	2020	Co-treatment with the TOPK inhibitor, OTS514, in combination with H2O2 increased p53 acetylation and its expression, whereas it decreased Sirtuin 1 (SIRT1) expression, contributing to the promotion of apoptosis.	OTS514	38-44	P53	Homo sapiens	81-84
17029827-6	2006	The p53 mRNA level was increased after the treatment of cells with benzo[a]pyrene, as well as following the induction of p53 protein, suggesting the benzo[a]pyrene-stimulated p53 accumulation may also be transcriptionally induced.	Benzo(a)pyrene	67-81	P53	Homo sapiens	4-7
32901866-6	2020	Furthermore, the p53 inhibitor, Pifithrin-mu, diminished the augmentation in poly(ADP-ribose) polymerase (PARP) cleavage induced by OTS514 plus H2O2, while the Mdm2 antagonist, Nutlin 3, increased PARP cleavage.	OTS514	132-138	P53	Homo sapiens	17-20
17029827-6	2006	The p53 mRNA level was increased after the treatment of cells with benzo[a]pyrene, as well as following the induction of p53 protein, suggesting the benzo[a]pyrene-stimulated p53 accumulation may also be transcriptionally induced.	Benzo(a)pyrene	149-163	P53	Homo sapiens	4-7
33001126-6	2020	The PCL-ss-P(PEGMA-co-GHA) amphiphilic copolymer could self-assemble into nanoparticles, which could be used to encapsulate anticancer drug doxorubicin (DOX) and compress the p53 gene to form the DOX-loaded PCL-ss-P(PEGMA-co-GHA)/p53 complex (abbreviated as DPGHAP/p53).	pegma-co-gha	13-25	P53	Homo sapiens	175-178
33001126-6	2020	The PCL-ss-P(PEGMA-co-GHA) amphiphilic copolymer could self-assemble into nanoparticles, which could be used to encapsulate anticancer drug doxorubicin (DOX) and compress the p53 gene to form the DOX-loaded PCL-ss-P(PEGMA-co-GHA)/p53 complex (abbreviated as DPGHAP/p53).	pegma-co-gha	13-25	P53	Homo sapiens	230-233
17029827-6	2006	The p53 mRNA level was increased after the treatment of cells with benzo[a]pyrene, as well as following the induction of p53 protein, suggesting the benzo[a]pyrene-stimulated p53 accumulation may also be transcriptionally induced.	Benzo(a)pyrene	149-163	P53	Homo sapiens	121-124
33001126-6	2020	The PCL-ss-P(PEGMA-co-GHA) amphiphilic copolymer could self-assemble into nanoparticles, which could be used to encapsulate anticancer drug doxorubicin (DOX) and compress the p53 gene to form the DOX-loaded PCL-ss-P(PEGMA-co-GHA)/p53 complex (abbreviated as DPGHAP/p53).	pegma-co-gha	13-25	P53	Homo sapiens	258-269
17029827-6	2006	The p53 mRNA level was increased after the treatment of cells with benzo[a]pyrene, as well as following the induction of p53 protein, suggesting the benzo[a]pyrene-stimulated p53 accumulation may also be transcriptionally induced.	Benzo(a)pyrene	149-163	P53	Homo sapiens	121-124
17029827-7	2006	The overall results suggest that benzo[a]pyrene leads to serious DNA damage, which leads to the transcription of the p53 gene; that the subsequent p53 protein accumulation up-regulates the cellular p21 protein.	Benzo(a)pyrene	33-47	P53	Homo sapiens	117-120
33497945-6	2020	Combined treatment with Cd and Z-YVAD-FMK remarkably elevated Bcl-2 mRNA and protein levels, inhibited p53, Bax, Bak-1, Cyt C, Caspase-9 and Caspase-3 mRNA levels and p53, Bax, Bak-1, Caspase-9/cleaved Caspase-9 and Caspase-3/cleaved Caspase-3 protein levels, increased mitochondrial membrane potential (MMP), decreased apoptosis ratio and cell damage compared to treatment with Cd alone.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	31-41	P53	Homo sapiens	103-106
33497945-6	2020	Combined treatment with Cd and Z-YVAD-FMK remarkably elevated Bcl-2 mRNA and protein levels, inhibited p53, Bax, Bak-1, Cyt C, Caspase-9 and Caspase-3 mRNA levels and p53, Bax, Bak-1, Caspase-9/cleaved Caspase-9 and Caspase-3/cleaved Caspase-3 protein levels, increased mitochondrial membrane potential (MMP), decreased apoptosis ratio and cell damage compared to treatment with Cd alone.	benzyloxycarbonyltyrosyl-valyl-alanyl-aspartic acid fluoromethyl ketone	31-41	P53	Homo sapiens	167-170
17029827-7	2006	The overall results suggest that benzo[a]pyrene leads to serious DNA damage, which leads to the transcription of the p53 gene; that the subsequent p53 protein accumulation up-regulates the cellular p21 protein.	Benzo(a)pyrene	33-47	P53	Homo sapiens	147-150
17029827-8	2006	Oxidative DNA damage and p53 accumulation seem to be related to benzo[a]pyrene toxicity; however, their potential as biomarkers in environmental monitoring and risk assessment needs to be validated in the context of their specificity and sensitivity.	Benzo(a)pyrene	64-78	P53	Homo sapiens	25-28
17026772-11	2006	The clinical behavior, the high recurrence rate and the even higher malignant transformation occurrence, as well as the presence of carcinogenetic indicators (K-ras mutation, overexpression of p53, MUC and Tn antigens) strongly support that BP is a low-grade neoplasm with high malignant potential.	Benzo(a)pyrene	241-243	P53	Homo sapiens	193-196
33110364-9	2020	Furthermore, CAPE treatment increased the Serine 15 (Ser15) and Serine 46 (Ser46) phosphorylation of p53, while decreased the survivin expression.	caffeic acid phenethyl ester	13-17	P53	Homo sapiens	101-104
33110364-10	2020	The results suggested that CAPE induced apoptosis by regulating p53 phosphorylation, leading to inhibition of the survivin expression.	caffeic acid phenethyl ester	27-31	P53	Homo sapiens	64-67
16728435-12	2006	These results suggest that genetic polymorphisms in WRN, TP53 and BRCA2 that maintain genomic stability impact benzene-induced hematotoxicity.	Benzene	111-118	P53	Homo sapiens	57-61
32712543-12	2020	The FUC and DOX combination increased the levels and activity of caspases (CASP3, CASP8) and p53, while decreased the levels and activity of CYP3A4, GST, and PXR in resistant cancer cells.	fucoxanthin	4-7	P53	Homo sapiens	93-96
16673127-6	2006	Bcl-2(+)/p53(+) group was found to be associated with advanced stage (p=0.008) and higher IPI (p=0.001), compared with the other groups.	diprotin A	90-93	P53	Homo sapiens	9-12
32900227-11	2021	In conclusion, downregulations of protein expression of mutant p53, cyclin D1, mTOR, and beta-catenin were increased after both cell lines had been treated with pterostilbene.	pterostilbene	161-174	P53	Homo sapiens	63-66
33072537-0	2020	Restoring of miR-193a-5p Sensitizes Breast Cancer Cells to Paclitaxel through P53 Pathway.	mir-193a-5p	13-24	P53	Homo sapiens	78-81
33072537-4	2020	Therefore, the aim of this study was to evaluate the potential function of miR-193a-5p and paclitaxel in the apoptosis induction by targeting P53 in BC cells.	mir-193a-5p	75-86	P53	Homo sapiens	142-145
16966095-4	2006	METHODS: p53(+) and p53(-) cells were synchronized in G2 phase using Hoechst 33342 and released from synchrony in the presence or absence of 5 microM sodium arsenite.	bisbenzimide ethoxide trihydrochloride	69-82	P53	Homo sapiens	9-12
16966095-4	2006	METHODS: p53(+) and p53(-) cells were synchronized in G2 phase using Hoechst 33342 and released from synchrony in the presence or absence of 5 microM sodium arsenite.	bisbenzimide ethoxide trihydrochloride	69-82	P53	Homo sapiens	20-23
33015038-7	2020	Mechanistically, caffeine bound to SIRT3 with high affinity (K D = 6.858 x 10-7 M); the binding affinity between SIRT3 and its substrate acetylated p53 was also 9.03 (without NAD+) or 6.87 (with NAD+) times higher in the presence of caffeine.	Caffeine	17-25	P53	Homo sapiens	148-151
16720374-7	2006	Dox-induced apoptosis included decrease in Bcl-2 expression, increase in Bak expression and caspase-3 and -9 activation but appeared to be p53- and Bax-independent.	Doxycycline	0-3	P53	Homo sapiens	139-142
32641480-9	2020	Conversely, KU-55933, a drug that inhibits ataxia telangiectasia mutated thereby preventing p53 phosphorylation, inhibited DFO-induced EBV reactivation.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	12-20	P53	Homo sapiens	92-95
16714289-6	2006	Overexpression of a MKK3 construct, but not MKK1, stimulated SB202190-sensitive p53 Ser(15) phosphorylation.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	61-69	P53	Homo sapiens	80-83
32984059-0	2020	Dysregulated Phosphorylation of p53, Autophagy and Stemness Attributes the Mutant p53 Harboring Colon Cancer Cells Impaired Sensitivity to Oxaliplatin.	Oxaliplatin	139-150	P53	Homo sapiens	32-35
32984059-0	2020	Dysregulated Phosphorylation of p53, Autophagy and Stemness Attributes the Mutant p53 Harboring Colon Cancer Cells Impaired Sensitivity to Oxaliplatin.	Oxaliplatin	139-150	P53	Homo sapiens	82-85
32984059-3	2020	The current study was aimed to investigate the response of wild-type TP53 harboring HCT 116 and mutant TP53 harboring HT 29 colon cancer cells to chemotherapeutic drug oxaliplatin (OX) and to elucidate the underlying molecular mechanisms of sensitivity/resistance in correlation to their p53 status.	Oxaliplatin	168-179	P53	Homo sapiens	69-73
32984059-3	2020	The current study was aimed to investigate the response of wild-type TP53 harboring HCT 116 and mutant TP53 harboring HT 29 colon cancer cells to chemotherapeutic drug oxaliplatin (OX) and to elucidate the underlying molecular mechanisms of sensitivity/resistance in correlation to their p53 status.	Oxaliplatin	168-179	P53	Homo sapiens	103-107
16891474-0	2006	Inorganic selenium sensitizes prostate cancer cells to TRAIL-induced apoptosis through superoxide/p53/Bax-mediated activation of mitochondrial pathway.	inorganic selenium	0-18	P53	Homo sapiens	98-101
16510557-1	2006	We investigated p53-dependent and -independent molecular events associated with cell cycle alteration and cell death in human lung adenocarcinoma A549 cells using cryptolepine, a DNA-damaging agent.	cryptolepine	163-175	P53	Homo sapiens	16-19
32847053-8	2020	In summary, this pilot study suggested a link between del(17p)/TP53 alteration and high SUVmax on 18F-FDG PET/CT in RRMM patients.	Fluorodeoxyglucose F18	98-105	P53	Homo sapiens	63-67
16510557-2	2006	After a 24-h treatment, cryptolepine caused an accumulation of p53 at concentrations of 1.25-10 microM and induction of p21(Cip1/WAF1) but only at concentrations up to 5muM.	cryptolepine	24-36	P53	Homo sapiens	63-66
32002592-1	2020	PURPOSE: This study aimed to determine if major gene mutations including in KRAS, SMAD4, TP53, and CDKN2A were related to imaging phenotype using 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET)-based radiomics in patients with pancreatic ductal adenocarcinoma (PDAC).	Fluorodeoxyglucose F18	146-168	P53	Homo sapiens	89-93
32002592-1	2020	PURPOSE: This study aimed to determine if major gene mutations including in KRAS, SMAD4, TP53, and CDKN2A were related to imaging phenotype using 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET)-based radiomics in patients with pancreatic ductal adenocarcinoma (PDAC).	Fluorodeoxyglucose F18	170-173	P53	Homo sapiens	89-93
16510557-3	2006	p21(Cip1/WAF1) was also strongly induced by cryptolepine (2.5-5 microM) in cells with p53 largely ablated via small interfering RNA-mediated gene silencing.	cryptolepine	44-56	P53	Homo sapiens	86-89
32723300-1	2020	BACKGROUND: Wogonin, a natural flavonoid-like chemical compound, exhibits anti-inflammatory, antitumor, antiviral, neuroprotective, and anxiolytic effects by modulating a variety of cellular signaling pathways including PI3K-Akt, p53, nuclear factor kappaB (NF-kappaB), mitogen-activated protein kinase (MAPK) pathways.	wogonin	12-19	P53	Homo sapiens	230-233
16510557-7	2006	The addition of wortmannin partially prevented cryptolepine-induced expression of p53 and p21(Cip1/WAF1) together with the S-phase block and sensitized cells to induction of cell death.	cryptolepine	47-59	P53	Homo sapiens	82-85
16480688-0	2006	Aaptamine, a spongean alkaloid, activates p21 promoter in a p53-independent manner.	aaptamine	0-9	P53	Homo sapiens	60-63
32661168-5	2020	Enhanced apoptosis was also observed when entinostat was combined with clinically relevant, p53-activating chemotherapy in vitro, and this translated into enhanced in vivo efficacy.	entinostat	42-52	P53	Homo sapiens	92-95
33040724-0	2020	Regulation of Thiamine (Vitamin B1)-Dependent Metabolism in Mammals by p53.	Thiamine	14-22	P53	Homo sapiens	71-74
16480688-0	2006	Aaptamine, a spongean alkaloid, activates p21 promoter in a p53-independent manner.	spongean alkaloid	13-30	P53	Homo sapiens	60-63
33040724-0	2020	Regulation of Thiamine (Vitamin B1)-Dependent Metabolism in Mammals by p53.	Thiamine	24-34	P53	Homo sapiens	71-74
33040724-3	2020	Thiamine diphosphate (ThDP), which is a major thiamine derivative, affects p53 binding to DNA.	Thiamine	46-54	P53	Homo sapiens	75-78
16480688-6	2006	The activation of p21 promoter by aaptamine was led through acting Sp1 sites between -82 and -50bp in a p53-independent manner.	aaptamine	34-43	P53	Homo sapiens	104-107
16405512-0	2006	O6-methylguanine DNA methyltransferase and p53 status predict temozolomide sensitivity in human malignant glioma cells.	Temozolomide	62-74	P53	Homo sapiens	43-46
32519803-0	2020	Polysaccharides derived from Balanophora polyandra significantly suppressed the proliferation of ovarian cancer cells through P53-mediated pathway.	Polysaccharides	0-15	P53	Homo sapiens	126-129
16405512-3	2006	Using a panel of 12 human glioma cell lines, we here defined the sensitivity to TMZ in acute cytotoxicity and clonogenic survival assays in relation to MGMT, mismatch repair and p53 status and its modulation by dexamethasone, irradiation and BCL-X(L).	Temozolomide	80-83	P53	Homo sapiens	178-181
17115080-1	2006	In the present work, we have reviewed data showing that triiodothyronine and its nuclear receptors modify expression of different genes/proteins involved in cell cycle control beginning from growth factors (such as EGF and TGF-beta), to cell surface receptors (EGFR), as well as proteins acting at the cell membrane (Ras), various transcription factors (c-Fos, c-Myc, E2F1), cyclins, Cip/Kip family of cdk2 inhibitors, and p53 inhibitor Mdm2 (Table 1).	Triiodothyronine	56-72	P53	Homo sapiens	423-426
32382022-7	2020	The administration of regular used in vitro dose (10 microM) in 3D and 2D cultures, as well as the dose-response analysis in 2D cultures showed Sorafenib and Regorafenib were increasingly effective in reducing cell proliferation, and inducing apoptosis in well-differentiated and expressing wild-type p53 in HCC cells.	regorafenib	158-169	P53	Homo sapiens	301-304
16351810-7	2005	In the subgroup of P53-negative patients, TC group had similar CR rate and PFS to PC group.	Technetium	42-44	P53	Homo sapiens	19-22
32163218-4	2020	First, we confirmed that the presence of KRAS/TP53 mutations significantly increased the IC50 of oxaliplatin (L-OHP) and NF-kappaB activity in HCT116 cells in vitro.	Oxaliplatin	97-108	P53	Homo sapiens	46-50
32163218-4	2020	First, we confirmed that the presence of KRAS/TP53 mutations significantly increased the IC50 of oxaliplatin (L-OHP) and NF-kappaB activity in HCT116 cells in vitro.	Oxaliplatin	110-115	P53	Homo sapiens	46-50
16357511-0	2005	Cooperation between BRCA1 and p53 in repair of cyclobutane pyrimidine dimers.	cyclobutane pyrimidine	47-69	P53	Homo sapiens	30-33
32421130-6	2020	The effect of SWZ-4-H was further confirmed by analyzing the expression of p53, p21, p16, and Rb (p-RB); SWZ-4-H significantly increased the expression of p53, p21, and p16 and decreased phosphorylated Rb (p-RB) in a dose-dependent manner.	swz-4-h	14-21	P53	Homo sapiens	75-78
32421130-6	2020	The effect of SWZ-4-H was further confirmed by analyzing the expression of p53, p21, p16, and Rb (p-RB); SWZ-4-H significantly increased the expression of p53, p21, and p16 and decreased phosphorylated Rb (p-RB) in a dose-dependent manner.	swz-4-h	14-21	P53	Homo sapiens	155-158
16225614-0	2005	Differential effects of 5-aminolaevulinic acid photodynamic therapy and psoralen + ultraviolet A therapy on p53 phosphorylation in normal human skin in vivo.	Aminolevulinic Acid	24-46	P53	Homo sapiens	108-111
32509062-5	2020	Many of these differentially expressed genes in AGS cells are involved in Nrf2-mediated oxidative stress response, p53 signaling, and integrin signaling, which suggested the mechanism of Crocin functions in therapy of gastric cancer.	crocin	187-193	P53	Homo sapiens	115-118
16507397-0	2005	Study of COX-2, Ki67, and p53 expression to predict effectiveness of 5-flurouracil, epirubicin and cyclophosphamide with celecoxib treatment in breast cancer patients.	Celecoxib	121-130	P53	Homo sapiens	26-29
31894477-10	2020	Mechanistic studies showed that PFTalpha could attenuate the upregulation of P53, MKK3, and cleaved caspase 3 expression that was induced by PTK7 knockdown in CSC-like cells.	QB 102	32-40	P53	Homo sapiens	77-80
16006125-1	2005	15-Deoxy-delta(12,14)-prostaglandin J2 (15d-PGJ2), a dehydration product of prostaglandin D2, is an important pharmacological molecule, which with the virtue of its electrophilicity, has been reported to covalently modify some cellular proteins (such as nuclear factor-kappa B (NF-kappaB), AP-1, p53, and thioredoxin) and elicit its physiological effects.	15-deoxy-delta(12,14)-prostaglandin J2	0-38	P53	Homo sapiens	296-299
32198346-5	2020	In Calu-6 cancer cells, in which TP53 gene has a UGA nonsense mutation, DAP treatment increases p53 level.	2,6-diaminopurine	72-75	P53	Homo sapiens	33-37
32198346-5	2020	In Calu-6 cancer cells, in which TP53 gene has a UGA nonsense mutation, DAP treatment increases p53 level.	2,6-diaminopurine	72-75	P53	Homo sapiens	96-99
16006125-1	2005	15-Deoxy-delta(12,14)-prostaglandin J2 (15d-PGJ2), a dehydration product of prostaglandin D2, is an important pharmacological molecule, which with the virtue of its electrophilicity, has been reported to covalently modify some cellular proteins (such as nuclear factor-kappa B (NF-kappaB), AP-1, p53, and thioredoxin) and elicit its physiological effects.	15-deoxy-delta(12,14)-prostaglandin J2	40-48	P53	Homo sapiens	296-299
32391422-2	2020	Here, PBRM1 (polybromo-1) is identified as a reader for acetylated lysine382 on p53 through its bromodomain 4 (BD4).	lysine382	67-76	P53	Homo sapiens	80-83
16006125-3	2005	Another aim is to characterize whether p53 is a direct target for covalent modification by 15d-PGJ2.	15-deoxy-delta(12,14)-prostaglandin J2	91-99	P53	Homo sapiens	39-42
16006125-7	2005	Further, comparative results indicate that p53 protein may also be a target for direct modification by 15d-PGJ2.	15-deoxy-delta(12,14)-prostaglandin J2	103-111	P53	Homo sapiens	43-46
15795939-13	2005	Taken together, DHA induces apoptosis in proliferating, but not in resting HUVEC, potentially via the phosphorylation of p53, resulting in decreased p53 DNA binding.	Docosahexaenoic Acids	16-19	P53	Homo sapiens	121-124
32021192-12	2020	Compared with the other groups, the level of apoptosis-related protein (P53, cleaved caspase-9, Bax and cleaved caspase-3) were upregulated in DNR-CdTe-CD123 group (P<0.05).	dnr-cdte	143-151	P53	Homo sapiens	72-75
31979361-0	2020	The Antiproliferative Activity of Oxypeucedanin via Induction of G2/M Phase Cell Cycle Arrest and p53-Dependent MDM2/p21 Expression in Human Hepatoma Cells.	oxypeucadanin	34-47	P53	Homo sapiens	98-101
15795939-13	2005	Taken together, DHA induces apoptosis in proliferating, but not in resting HUVEC, potentially via the phosphorylation of p53, resulting in decreased p53 DNA binding.	Docosahexaenoic Acids	16-19	P53	Homo sapiens	149-152
15800902-0	2005	Pharmaceutical-mediated inactivation of p53 sensitizes U87MG glioma cells to BCNU and temozolomide.	Temozolomide	86-98	P53	Homo sapiens	40-43
31897241-7	2020	Additionally, genipin induced p53 expression in AGS, MKN45, and MKN28 cells.	genipin	14-21	P53	Homo sapiens	30-33
15800902-4	2005	This was of interest because E6 silencing of p53 sensitizes U87MG astrocytic glioma cells to BCNU and temozolomide (TMZ), cytotoxic drugs that are modestly helpful in the treatment of aggressive astrocytic gliomas.	Temozolomide	102-114	P53	Homo sapiens	45-48
31897241-10	2020	In summary, we showed that genipin increases the oxaliplatin-induced cell death via p53-DRAM autophagy.	genipin	27-34	P53	Homo sapiens	84-87
15800902-4	2005	This was of interest because E6 silencing of p53 sensitizes U87MG astrocytic glioma cells to BCNU and temozolomide (TMZ), cytotoxic drugs that are modestly helpful in the treatment of aggressive astrocytic gliomas.	Temozolomide	116-119	P53	Homo sapiens	45-48
15800902-5	2005	We observed that exposure of U87MG cells to PFTalpha before cytotoxic chemotherapy attenuated p53-mediated induction of p21WAF1 protein levels, sensitizing U87MG cells to BCNU and TMZ.	Temozolomide	180-183	P53	Homo sapiens	94-97
16115936-13	2005	Flavopiridol induced increased p53 and pSTAT3 levels in patient PBMCs but had no effects on cyclin D1, phosphoRNA polymerase II, or Mcl-1.	alvocidib	0-12	P53	Homo sapiens	31-34
31821701-0	2020	Lovastatin-mediated MCF-7 cancer cell death involves LKB1-AMPK-p38MAPK-p53-survivin signalling cascade.	Lovastatin	0-10	P53	Homo sapiens	71-74
31821701-6	2020	Lovastatin also increased p53 phosphorylation, acetylation and its reporter activities.	Lovastatin	0-10	P53	Homo sapiens	26-29
31821701-7	2020	Results from chromatin immunoprecipitation analysis showed that p53 binding to the survivin promoter region was increased, while Sp1 binding to the region was decreased, in MCF-7 cells after lovastatin exposure.	Lovastatin	191-201	P53	Homo sapiens	64-67
31821701-9	2020	Lovastatin"s enhancing effects on p53 activation, p21 elevation and survivin reduction were significantly reduced in the presence of p38MAPK signalling inhibitor.	Lovastatin	0-10	P53	Homo sapiens	34-37
31821701-10	2020	Furthermore, LKB1-AMPK signalling blockade abrogated lovastatin-induced p38MAPK and p53 phosphorylation.	Lovastatin	53-63	P53	Homo sapiens	84-87
31821701-11	2020	Together these results suggest that lovastatin may activate LKB1-AMPK-p38MAPK-p53-survivin cascade to cause MCF-7 cell death.	Lovastatin	36-46	P53	Homo sapiens	78-81
16009942-9	2005	Additionally, dose-dependent formation of oxidized and ring-opened purines and abasic sites was established in the p53 gene in only UVA1-irradiated cells.	Purines	67-74	P53	Homo sapiens	115-118
31659693-11	2020	The results exposed the novel mechanistic pathway of neuroprotection by 5-LOX inhibition is likely to be mediated by DNA DSB repair through p53 isoforms and PI3K/Akt pathway.	5-lox	72-77	P53	Homo sapiens	140-143
15870701-3	2005	Among these, pectenotoxin-2 (PTX-2), which was first identified as a cytotoxic entity in marine sponges, which depolymerizes actin filaments, was found to be highly effective and more potent to activate an intrinsic pathway of apoptosis in p53-deficient tumor cells compared to those with functional p53 both in vitro and in vivo.	pectenotoxin 2	13-27	P53	Homo sapiens	240-243
15870701-3	2005	Among these, pectenotoxin-2 (PTX-2), which was first identified as a cytotoxic entity in marine sponges, which depolymerizes actin filaments, was found to be highly effective and more potent to activate an intrinsic pathway of apoptosis in p53-deficient tumor cells compared to those with functional p53 both in vitro and in vivo.	pectenotoxin 2	13-27	P53	Homo sapiens	300-303
15870701-5	2005	In p53-deficient cells, PTX-2 triggers apoptosis through mitochondrial dysfunction, and this is followed by the release of proapoptotic factors and caspase activation.	pectenotoxin 2	24-29	P53	Homo sapiens	3-6
15870701-6	2005	Furthermore, we observed Bax activation and Bim induction only in p53-deficient cells after PTX-2 treatment.	pectenotoxin 2	92-97	P53	Homo sapiens	66-69
31927560-0	2019	Naringin Protects Against Interleukin 1beta (IL-1beta)-Induced Human Nucleus Pulposus Cells Degeneration via Downregulation Nuclear Factor kappa B (NF-kappaB) Pathway and p53 Expression.	naringin	0-8	P53	Homo sapiens	171-174
16263657-11	2005	In contrast, K562 cells treated with radiation and HMA had an accelerated cell death and induced a p53-independent apoptosis.	herbimycin	51-54	P53	Homo sapiens	99-102
31891063-5	2019	Chlorido drugs showed similar behavior to cisplatin; they both required p53 to induce apoptosis but only cis-ipa showed DNA damage requirement for apoptosis induction.	chlorido(cyclohexyldiphenylphosphine)gold(I)	0-8	P53	Homo sapiens	72-75
15735718-5	2005	Here we demonstrate that DAP treatment of human cancer cells activates the p53-p21 pathway without activating other known mechanisms that inhibit Cdk4 and Cdk2 activities.	dap	25-28	P53	Homo sapiens	75-78
15821341-2	2005	After treatment with evodiamine for the indicated time periods, anti-apoptotic protein SIRT1 expression was decreased; p53 expression and its phosphorylation were both enhanced, whereas transient induction of downstream p21 was not enough to promote cell cycle arrest.	evodiamine	21-31	P53	Homo sapiens	119-122
31677863-0	2019	Corrigendum to "Selective anti-tumor activity of wogonin targeting the Warburg effect through stablizing p53" [Pharmacol.	wogonin	49-56	P53	Homo sapiens	105-108
15821341-4	2005	In addition, p53 activation in response to evodiamine administration was correlated with the activation of the PI3-K/PKC pro-apoptotic pathway, but did not require ERK participation.	evodiamine	43-53	P53	Homo sapiens	13-16
15748635-3	2005	In human skin cancers, about 35% of all mutations in the p53 gene are transitions at dipyrimidines within the sequence 5"-TCG and 5"-CCG, and these are localized at several mutational hotspots.	5"-ccg	130-136	P53	Homo sapiens	57-60
15757539-2	2005	8-hydoxy-2deoxy-guanosine (8-OH-dG), a biomarker of oxidative DNA damage, plays important roles in initiation, progression, and prognosis of lung cancer, and closely relates with mutations of k-ras and p53 genes in carcinogenesis of lung tissue.	8-hydoxy-2deoxy-guanosine	0-25	P53	Homo sapiens	202-205
31386885-9	2019	The marked apoptosis induction in the XN-treated RPMI8226 cells was related to initiation of mitochondrial and extrinsic pathways, as indicated by the altered p53, Bax, and Bcl-2 protein expression, cleavage of procaspase 8 and 9, and elevated caspase-3 activity.	xanthohumol	38-40	P53	Homo sapiens	159-162
15757539-2	2005	8-hydoxy-2deoxy-guanosine (8-OH-dG), a biomarker of oxidative DNA damage, plays important roles in initiation, progression, and prognosis of lung cancer, and closely relates with mutations of k-ras and p53 genes in carcinogenesis of lung tissue.	8-ohdg	27-34	P53	Homo sapiens	202-205
15746064-4	2005	Here we have investigated the effect of combined treatment with ionizing radiation and patupilone or paclitaxel in the P-glycoprotein-overexpressing, p53-mutated human colon adenocarcinoma cell line SW480 and in murine, genetically defined E1A/ras-transformed paclitaxel-sensitive embryo fibroblasts.	epothilone B	87-97	P53	Homo sapiens	150-153
31383362-9	2019	Also, luteolin induced oxidative stress and ER stress in p53-null Hep3B cells.	Luteolin	6-14	P53	Homo sapiens	57-60
31425749-0	2019	An oral 2-hydroxypropyl-beta-cyclodextrin-loaded spirooxindole-pyrrolizidine derivative restores p53 activity via targeting MDM2 and JNK1/2 in hepatocellular carcinoma.	Spirooxindole	49-62	P53	Homo sapiens	97-100
15365767-3	2005	In the work reported here we investigated the ability of docosahexaenoic acid (DHA) to potentiate the antineoplastic activity of 5-fluorouracil (5-FU) in p53-wildtype (LS-174 and Colo 320) and p53-mutant (HT-29 and Colo 205) human colon cancer cells.	Docosahexaenoic Acids	57-77	P53	Homo sapiens	154-157
31390185-6	2019	In the current study, we were interested in examining the cell selectivity of cHLH-p53-R, its cellular internalization, and ability to reactivate the p53 pathway.	chlh	78-82	P53	Homo sapiens	83-86
31390185-8	2019	Our studies show that cHLH is an excellent scaffold to stabilize and constrain p53-mimetic peptides with helical conformation, and reveal that anticancer properties of cHLH-p53-R are mediated by its ability to selectively target, cross, and disrupt cancer cell membranes, and not by activation of the p53 pathway.	chlh	22-26	P53	Homo sapiens	79-82
31390185-8	2019	Our studies show that cHLH is an excellent scaffold to stabilize and constrain p53-mimetic peptides with helical conformation, and reveal that anticancer properties of cHLH-p53-R are mediated by its ability to selectively target, cross, and disrupt cancer cell membranes, and not by activation of the p53 pathway.	chlh	22-26	P53	Homo sapiens	173-176
31390185-8	2019	Our studies show that cHLH is an excellent scaffold to stabilize and constrain p53-mimetic peptides with helical conformation, and reveal that anticancer properties of cHLH-p53-R are mediated by its ability to selectively target, cross, and disrupt cancer cell membranes, and not by activation of the p53 pathway.	chlh	22-26	P53	Homo sapiens	173-176
15365767-3	2005	In the work reported here we investigated the ability of docosahexaenoic acid (DHA) to potentiate the antineoplastic activity of 5-fluorouracil (5-FU) in p53-wildtype (LS-174 and Colo 320) and p53-mutant (HT-29 and Colo 205) human colon cancer cells.	Docosahexaenoic Acids	79-82	P53	Homo sapiens	154-157
15671536-0	2005	Visualization of endogenous p53-mediated transcription in vivo using sodium iodide symporter.	Sodium Iodide	69-82	P53	Homo sapiens	28-31
31059712-8	2019	In addition, DS preferentially inhibited the cell growth of p53 wild-type NSCLC cell lines than the mutant p53 models.	lyoniside	13-15	P53	Homo sapiens	60-63
16145866-9	2005	Only marginally statistically significant influence of p53 expression was found on patient survival between MPG and PPG.	(9H-purin-6-yl)thiomethyl glutamate	108-111	P53	Homo sapiens	55-58
15492260-4	2004	In two melanomas with wild-type p53 but with differential expression of APAF-1, treatment with camptothecin, celecoxib, or an nitric oxide synthase inhibitor (1400W) significantly modulated expression of 36 of 96 genes in an apoptosis-specific cDNA macroarray, but APAF-1 mRNA levels were not induced (in APAF-1(-) cells) nor up-regulated (in APAF-1(+) cells), a finding confirmed at the protein level.	Celecoxib	109-118	P53	Homo sapiens	32-35
31074217-8	2019	The expression of both p53 and p16 senescence regulators was significantly increased by Ang II (p53: 1.39+-0.17, p16: 1.19+-0.10-fold vs. the control), and inhibited by fimasartan.	fimasartan	169-179	P53	Homo sapiens	23-26
15450416-6	2004	Using several statistical tests, we found that missense mutations in TP53 are strongly colocalized with ESEs, and that only a small fraction of ESE sites contributes to the association.	eses	104-108	P53	Homo sapiens	69-73
30923017-4	2019	We showed that PRI-2191 induces the CDKN1A (gene encoding p21Waf1/Cip1) expression directly through vitamin D receptor (VDR) in a p53-independent manner and thus decreases the thymidylate synthase expression both at the mRNA and protein level.	1 alpha,24-dihydroxyvitamin D3	15-23	P53	Homo sapiens	130-133
15450428-2	2004	For example expression of HBx in cultured cells has been shown to inhibit global nucleotide excision repair, a p53-dependent subpathway of nucleotide excision repair (NER) which eliminates helix-distorting DNA adducts, e.g., UV-induced cyclobutane pyrimidine dimers (CPDs), from the genome overall.	cyclobutane pyrimidine	236-258	P53	Homo sapiens	111-114
15297405-16	2004	The changes in p53 and phospho-Rb in buccal mucosa suggest that a biological effect with flavopiridol was achieved.	alvocidib	89-101	P53	Homo sapiens	15-18
30935902-6	2019	The inhibitory effect of curcumin, piperine and vitamin E on cell proliferation involves different markers, and in particular inhibits beta-catenin, cyclinD1 and p53, making them candidates for a possible use in alternative therapies although further studies are needed.	piperine	35-43	P53	Homo sapiens	162-165
15149862-0	2004	Distinct functions for WRN and TP53 in a shared pathway of cellular response to 1-beta-D-arabinofuranosylcytosine and bleomycin.	Cytarabine	80-113	P53	Homo sapiens	31-35
31092272-2	2019	We have previously shown that fusing p53 (or its DNA binding domain, DBD, alone) to the mitochondrial targeting signal (MTS) from Bak or Bax can target p53 to the mitochondria and induce apoptosis in gynecological cancer cell lines including cervical cancer cells (HeLa; wt p53), ovarian cancer cells (SKOV-3; p53 267del non-expressing), and breast cancer cells (T47D; L194F p53 mutation).	bakuchiol	130-133	P53	Homo sapiens	152-155
31092272-2	2019	We have previously shown that fusing p53 (or its DNA binding domain, DBD, alone) to the mitochondrial targeting signal (MTS) from Bak or Bax can target p53 to the mitochondria and induce apoptosis in gynecological cancer cell lines including cervical cancer cells (HeLa; wt p53), ovarian cancer cells (SKOV-3; p53 267del non-expressing), and breast cancer cells (T47D; L194F p53 mutation).	bakuchiol	130-133	P53	Homo sapiens	152-155
15274301-9	2004	By contrast sodium selenite caused phosphorylation of p53 serines 20, 37 and 46 known to mediate apoptosis.	Sodium Selenite	12-27	P53	Homo sapiens	54-57
31092272-2	2019	We have previously shown that fusing p53 (or its DNA binding domain, DBD, alone) to the mitochondrial targeting signal (MTS) from Bak or Bax can target p53 to the mitochondria and induce apoptosis in gynecological cancer cell lines including cervical cancer cells (HeLa; wt p53), ovarian cancer cells (SKOV-3; p53 267del non-expressing), and breast cancer cells (T47D; L194F p53 mutation).	bakuchiol	130-133	P53	Homo sapiens	152-155
15081873-3	2004	Based on Western blot analysis and immunocytochemistry, pergolide was found to prevent H(2)O(2)-induced apoptosis by inhibiting NF-kappaB nuclear translocation and activation of p53 signalling pathway.	Pergolide	56-65	P53	Homo sapiens	178-181
31092272-3	2019	However, p53 with Bak or Bax MTSs have not been previously tested in cancers with strong dominant negative (DN) mutant p53 which are capable of inactivating wt p53 by homo-oligomerization.	bakuchiol	18-21	P53	Homo sapiens	9-12
14976336-8	2004	In addition, the p21 mRNA level was elevated in 1,4-BQ-treated cells, suggesting that human CD34(+) cells utilize the p53 pathway in response to 1,4-BQ-induced DNA damage.	quinone	48-54	P53	Homo sapiens	118-121
30596962-5	2019	We further confirmed that co-treatment with OPCs sensitized the chemoresistant cells to 5FU and oxaliplatin, as observed by improvement in cell cycle arrest, double-strand breaks and p53 accumulation in these cells.	Oxaliplatin	96-107	P53	Homo sapiens	183-186
31002510-5	2019	Compound 14 arrested the cell cycle at S and G2 phases and up-regulated thymidylate synthase and p53, consistent with the results of the combination, suggesting 14 adopted a collaborative mode of 5-FU and oxaliplatin to kill cancer cells.	Oxaliplatin	205-216	P53	Homo sapiens	97-100
14976336-8	2004	In addition, the p21 mRNA level was elevated in 1,4-BQ-treated cells, suggesting that human CD34(+) cells utilize the p53 pathway in response to 1,4-BQ-induced DNA damage.	quinone	145-151	P53	Homo sapiens	118-121
30679201-2	2019	Previously, we determined that p53 deficiency sensitizes head and neck cancer cells to AZD1775, a WEE1 kinase inhibitor, and translated our findings into a phase I clinical trial.	adavosertib	87-94	P53	Homo sapiens	31-34
14976336-11	2004	These results show that human CD34(+) cells are sensitive targets for 1,4-BQ toxicity that use the p53 DNA damage response pathway in response to genotoxic stress.	quinone	70-76	P53	Homo sapiens	99-102
30679201-3	2019	Here, we investigate how p53 affects cellular responses to AZD1775 at the molecular level.	adavosertib	59-66	P53	Homo sapiens	25-28
30679201-10	2019	IMPLICATIONS: The data encourage the use of AZD1775 in combination with genotoxic modalities against p53-deficient head and neck squamous cell carcinoma.	adavosertib	44-51	P53	Homo sapiens	101-104
15052690-13	2004	After being treated with octreotide, the expressions of both mutant-type p53 and bcl-2 decreased considering the percentage of positive cells (P&lt;0.05).	Octreotide	25-35	P53	Homo sapiens	73-76
31097990-3	2019	Library screening in assays that measure readthrough at a PTC in the TP53 gene in human HDQ-P1 cells identified six novel 2-aminothiazole-4-carboxamide derivatives that potentiate the PTC readthrough (PTCR) efficiency of G418 when used in combination.	antibiotic G 418	221-225	P53	Homo sapiens	69-73
15052690-15	2004	The reduction of mutant-type p53 and bcl-2 expressions may be associated with the apoptosis induced by octreotide.	Octreotide	103-113	P53	Homo sapiens	29-32
15177039-3	2004	We previously showed that genistein, a naturally occurring isoflavonoid, induced increased ATM protein kinase activity, ATM-dependent phosphorylation of p53 on serine 15 and activation of the DNA-binding properties of p53.	isoflavonoid	59-71	P53	Homo sapiens	218-221
14712481-6	2004	These results suggest that in neuroblastoma cell lines clinically attainable concentrations of mycophenolic acid deplete guanine nucleotide pools triggering G(1) arrest and apoptosis through p53-mediated pathways, indicating a potential role of its morpholinoethyl ester pro-drug in the management of patients with neuroectodermal tumors.	Mycophenolic Acid	95-112	P53	Homo sapiens	191-194
30939155-5	2019	Our data showed that the statins-fluvastatin and lovastatin-induced p21 expression as general histone deacetylase inhibitors in a p53-independent manner, which is mediated through various pathways, such as apoptosis, autophagy, cell cycle progression, and DNA damage, to be involved in the function of p21 in HeLa cells.	Lovastatin	49-59	P53	Homo sapiens	130-133
14757188-5	2004	Furthermore, the nuclear export inhibitor leptomycin B showed a similar synergy with IR as did DRB regarding ser15 phosphorylation of p53 and p21 induction.	leptomycin B	42-54	P53	Homo sapiens	134-137
31019655-13	2019	Meanwhile, ROS scavenger NAC, JNK inhibitor SP600125, and p53 inhibitor PFTalpha were used to verify that autophagy-mediated upregulation of DR5 was regulated by the SNX-2112-stimulated activation of the ROS-JNK-p53 signaling pathway.	SNX 2112	166-174	P53	Homo sapiens	58-61
31019655-13	2019	Meanwhile, ROS scavenger NAC, JNK inhibitor SP600125, and p53 inhibitor PFTalpha were used to verify that autophagy-mediated upregulation of DR5 was regulated by the SNX-2112-stimulated activation of the ROS-JNK-p53 signaling pathway.	SNX 2112	166-174	P53	Homo sapiens	212-215
14741120-19	2004	Elucidation of parts of the apoptin-induced apoptotic pathway revealed unique characteristics: apoptin-induced apoptosis is independent of the tumor suppressor p53.	apoptin	28-35	P53	Homo sapiens	160-163
30391516-0	2019	25-hydroxycholesterol down-regulates oxysterol binding protein like 2 (OSBPL2) via the p53/SREBF2/NFYA signaling pathway.	25-hydroxycholesterol	0-21	P53	Homo sapiens	87-90
30842655-0	2019	p53 regulation of ammonia metabolism through urea cycle controls polyamine biosynthesis.	Polyamines	65-74	P53	Homo sapiens	0-3
15143984-6	2004	Median values and ranges of p53 protein expression were as follows: 0.0% (range, 0.0-1.8%) in NS, 0.0% (range, 0.0-6.5%) in PS, 9.2% (range, 0.0-24.0%) in KA, 19.3% (range, 0.0-48.1%) in BCC and 30.1% (range, 0.0-68.1%) in SCC.	ps	124-126	P53	Homo sapiens	28-31
14647446-5	2003	Moreover, calicheamicin triggers apoptosis in a p53-independent manner as shown by the use of p53 knockout cells.	calicheamicin T	10-23	P53	Homo sapiens	48-51
30873235-0	2019	Design of indole- and MCR-based macrocycles as p53-MDM2 antagonists.	indole	10-16	P53	Homo sapiens	47-50
14647446-5	2003	Moreover, calicheamicin triggers apoptosis in a p53-independent manner as shown by the use of p53 knockout cells.	calicheamicin T	10-23	P53	Homo sapiens	94-97
14551737-0	2003	High dose methylprednisolone can induce remissions in CLL patients with p53 abnormalities.	Methylprednisolone	10-28	P53	Homo sapiens	72-75
30431128-13	2019	The experimental results demonstrated that cIAP2 regulated the expression of p53 and thus was likely to be a potential mechanism for PFDA-induced growth promotion.	perfluorodecanoic acid	133-137	P53	Homo sapiens	77-80
30431128-14	2019	Overall, the results revealed that PFDA may suppress cellular senescence induced by p53 through the regulation of cIAP2 protein expression.	perfluorodecanoic acid	35-39	P53	Homo sapiens	84-87
32630719-3	2020	Our laboratory has demonstrated that the thyroid hormone deaminated analogue, tetrac, activates p53 and induces antiproliferation in colorectal cancer.	tetraiodothyroacetic acid	78-84	P53	Homo sapiens	96-99
33040724-4	2020	In order to elucidate the mechanism of regulation of thiamine-dependent metabolism by p53, we assessed putative p53-binding sites near transcription starting points in genes coding for transporters and enzymes, whose function is associated with thiamine and/or its derivatives.	Thiamine	53-61	P53	Homo sapiens	86-89
33040724-4	2020	In order to elucidate the mechanism of regulation of thiamine-dependent metabolism by p53, we assessed putative p53-binding sites near transcription starting points in genes coding for transporters and enzymes, whose function is associated with thiamine and/or its derivatives.	Thiamine	53-61	P53	Homo sapiens	112-115
14551737-2	2003	We have used high dose methylprednisolone (HDMP) to treat 25 patients with advanced refractory CLL of whom 45% had p53 abnormalities shown by one or more methods: flow cytometry, fluorescent in situ hybridisation and direct DNA sequencing.	Methylprednisolone	23-41	P53	Homo sapiens	115-118
30792807-0	2019	Anticancer response to disulfiram may be enhanced by co-treatment with MEK inhibitor or oxaliplatin: modulation by tetrathiomolybdate, KRAS/BRAF mutations and c-MYC/p53 status.	Oxaliplatin	88-99	P53	Homo sapiens	165-168
14599774-3	2003	Pentoxifylline and the related drug Caffeine are known radiosensitizers especially in p53 mutant cells.	Pentoxifylline	0-14	P53	Homo sapiens	86-89
30723502-7	2019	We observed that the proteasomal inhibitor, peptide aldehyde N-acetyl-leu-leu-norleucinal (commonly termed as ALLN), caused an activation of cellular homeostatic machinery, autophagy in R273H-P53 cells.	Aldehydes	52-60	P53	Homo sapiens	192-195
30370860-12	2019	We also observed that both compounds up-regulated the p53 expression where Emodin causes nuclear p53 localization, which leads to down-regulation in mTOR expression and induces autophagy while Chrysophanol inhibits p53 translocation into nucleus, up-regulates mTOR expression and inhibits autophagy.	Emodin	75-81	P53	Homo sapiens	54-57
30370860-12	2019	We also observed that both compounds up-regulated the p53 expression where Emodin causes nuclear p53 localization, which leads to down-regulation in mTOR expression and induces autophagy while Chrysophanol inhibits p53 translocation into nucleus, up-regulates mTOR expression and inhibits autophagy.	Emodin	75-81	P53	Homo sapiens	97-100
30370860-12	2019	We also observed that both compounds up-regulated the p53 expression where Emodin causes nuclear p53 localization, which leads to down-regulation in mTOR expression and induces autophagy while Chrysophanol inhibits p53 translocation into nucleus, up-regulates mTOR expression and inhibits autophagy.	Emodin	75-81	P53	Homo sapiens	97-100
32530958-0	2020	Dietary flavonoid fisetin binds human SUMO1 and blocks sumoylation of p53.	flavonoid fisetin	8-25	P53	Homo sapiens	70-73
32642409-0	2020	20(S)-Protopanaxatriol promotes the binding of P53 and DNA to regulate the antitumor network via multiomic analysis.	protopanaxadiol	0-22	P53	Homo sapiens	47-50
14637245-0	2003	Formation of trans-4-hydroxy-2-nonenal- and other enal-derived cyclic DNA adducts from omega-3 and omega-6 polyunsaturated fatty acids and their roles in DNA repair and human p53 gene mutation.	4-hydroxy-2-nonenal	13-38	P53	Homo sapiens	175-178
32468080-8	2020	This correlated with differential upregulation of p53/p21 pathway, with S and G2/M arrests by cisplatin and satraplatin in contrast to G1 arrest by oxaliplatin and DAP.	Oxaliplatin	148-159	P53	Homo sapiens	50-53
32468080-11	2020	CONCLUSIONS: Oxaliplatin and DAP robustly activate p53 and p21, which downregulate HR proteins to enhance drug activity.	Oxaliplatin	13-24	P53	Homo sapiens	51-54
30799796-6	2019	RESULTS: The antiproliferative activity of derivative 6 could be attributed to its unique capability of formation of free radicals such as phenoxide radicals which arrested the cell cycle through enhancing the expression of p53 and induced apoptosis by induction of both caspases 9 and 3.	phenoxide radicals	139-157	P53	Homo sapiens	224-227
32483145-6	2020	miR-130b-3p suppressed MB tumorigenesis by targeting a previously unknown target, serine/threonine-protein kinase 1 (SIK1), through the p53 signaling pathways.	mir-130b-3p	0-11	P53	Homo sapiens	136-139
14500353-0	2003	Inhibition of COX-2 in colon cancer cell lines by celecoxib increases the nuclear localization of active p53.	Celecoxib	50-59	P53	Homo sapiens	105-108
14500353-4	2003	We determined the localization and expression of p53 in the presence of PGA(1) and celecoxib, a selective COX-2 inhibitor in human colon cell lines HCT-116 (wild-type p53) and HT-29 (mutant p53).	Celecoxib	83-92	P53	Homo sapiens	49-52
31089357-12	2019	The combined use of cAgNPs and cisplatin resulted in upregulated expression of p53 gene and downregulated expression of MPP-9 gene.	cagnps	20-26	P53	Homo sapiens	79-82
14500353-11	2003	However, in the presence of 100 micro M celecoxib, p53 levels increased in the nucleus.	Celecoxib	40-49	P53	Homo sapiens	51-54
32004752-11	2020	We also show that ionising radiation at 5 Gy results in phosphorylation of p53 at serine 15, a key phosphorylation site for p53-mediated apoptosis, and that hypoxia attenuates this phosphorylation.	cholecystokinin C-terminal flanking peptide	82-88	P53	Homo sapiens	75-78
12958168-7	2003	Despite nuclear export blockade by leptomycin B and HTLV1-Rex protein, two potent CRM1 inhibitors, nuclear degradation of endogenous wild-type p53 and HDM2 occurs during down-regulation of the p53 response.	leptomycin B	35-47	P53	Homo sapiens	143-146
32004752-11	2020	We also show that ionising radiation at 5 Gy results in phosphorylation of p53 at serine 15, a key phosphorylation site for p53-mediated apoptosis, and that hypoxia attenuates this phosphorylation.	cholecystokinin C-terminal flanking peptide	82-88	P53	Homo sapiens	124-127
31811920-10	2020	Moreover, microbiota analysis revealed that nitrate could partially decrease the enriched metabolic pathways (p53 signaling pathway and colorectal cancer pathway) compared with that in the DSS and DSS + NaCl groups.	Nitrates	44-51	P53	Homo sapiens	110-113
30347260-10	2019	Treatment with phenyl benzoxime markedly increased the expression of Bax, caspase-3 and p53 and decreased Bcl-2 mRNA.	phenyl benzoxime	15-31	P53	Homo sapiens	88-91
30783055-5	2019	Thus, we investigated crocetin"s effects on the PI3K/AKT, MAPK, and p53/p21 pathways in esophageal squamous carcinoma cell line KYSE-150 cells.	crocetin	22-30	P53	Homo sapiens	68-71
32421130-6	2020	The effect of SWZ-4-H was further confirmed by analyzing the expression of p53, p21, p16, and Rb (p-RB); SWZ-4-H significantly increased the expression of p53, p21, and p16 and decreased phosphorylated Rb (p-RB) in a dose-dependent manner.	swz-4-h	105-112	P53	Homo sapiens	75-78
30783055-11	2019	Furthermore, we have found that crocetin not only inhibited the activation of PI3K/AKT, extracellular signal-regulated kinase-1/2 (ERK1/2), and p38 but also upregulated the p53/p21 level.	crocetin	32-40	P53	Homo sapiens	173-176
14646222-2	2003	The increase in the p53 expression and SAPK/JNK activation after X irradiation was also inhibited by a Trolox treatment, but the expression of BCL-2 and BAX, which would occur downstream from p53, was not changed.	6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid	103-109	P53	Homo sapiens	20-23
30354111-0	2018	Induction of Apoptosis and Cell-Cycle Arrest in Human Colon-Cancer Cells by Whole-Grain Alkylresorcinols via Activation of the p53 Pathway.	alkylresorcinols	88-104	P53	Homo sapiens	127-130
32421130-6	2020	The effect of SWZ-4-H was further confirmed by analyzing the expression of p53, p21, p16, and Rb (p-RB); SWZ-4-H significantly increased the expression of p53, p21, and p16 and decreased phosphorylated Rb (p-RB) in a dose-dependent manner.	swz-4-h	105-112	P53	Homo sapiens	155-158
32421130-8	2020	To sum up, our data indicated that SWZ-4-H could induce lung cancer senescence by regulating p53, p21, p16, and p-Rb, thus providing a novel perspective on anti-cancer mechanisms of SWZ-4-H in human lung cancer A549 cells.	swz-4-h	35-42	P53	Homo sapiens	93-96
32035620-0	2020	Crotonylation at serine 46 impairs p53 activity.	cholecystokinin C-terminal flanking peptide	17-23	P53	Homo sapiens	35-38
12944903-0	2003	Metabolic labeling of human cells with tritiated nucleosides results in activation of the ATM-dependent p53 signaling pathway and acceleration of DNA repair.	tritiated nucleosides	39-60	P53	Homo sapiens	104-107
32035620-3	2020	Crotonic acid (CA) treatment induces p53 crotonylation, but surprisingly reduces its protein, but not mRNA level, leading to inhibition of p53 activity in a dose dependent fashion.	crotonic acid	0-13	P53	Homo sapiens	37-40
32035620-3	2020	Crotonic acid (CA) treatment induces p53 crotonylation, but surprisingly reduces its protein, but not mRNA level, leading to inhibition of p53 activity in a dose dependent fashion.	crotonic acid	0-13	P53	Homo sapiens	139-142
32035620-4	2020	Surprisingly this crotonylation targets serine 46, instead of any predicted lysine residues, of p53, as detected in TCEP-probe labeled crotonylation and anti-crotonylated peptide antibody reaction assays.	cholecystokinin C-terminal flanking peptide	40-46	P53	Homo sapiens	96-99
30207732-0	2018	Synergetic and Antagonistic Molecular Effects Mediated by the Feedback Loop of p53 and JNK between Saikosaponin D and SP600125 on Lung Cancer A549 Cells.	saikosaponin D	99-113	P53	Homo sapiens	79-82
32035620-7	2020	Since serine 46 is only found in human p53, our studies unveil an unconventional PTM unique for human p53, impairing its activity in response to CA.	cholecystokinin C-terminal flanking peptide	6-12	P53	Homo sapiens	39-42
12948823-3	2003	Procarbazine plus Cu(II) induced piperidine-labile and formamidopyrimidine-DNA glycosylase-sensitive lesions at the 5"-ACG-3" sequence, complementary to a hotspot of the p53 gene, and the 5"-TG-3" sequence.	cu(ii)	18-24	P53	Homo sapiens	170-173
32035620-7	2020	Since serine 46 is only found in human p53, our studies unveil an unconventional PTM unique for human p53, impairing its activity in response to CA.	cholecystokinin C-terminal flanking peptide	6-12	P53	Homo sapiens	102-105
32062581-3	2020	Caffeine exposure also induced a strong DDR along with subsequent activation of wildtype p53 protein.	Caffeine	0-8	P53	Homo sapiens	89-92
12807757-0	2003	Modulation of benzo[a]pyrene-induced p53 DNA activity by acrolein.	Benzo(a)pyrene	14-28	P53	Homo sapiens	37-40
32062581-10	2020	Thus, prolonged caffeine exposure stalls the cell cycle, induces a p53-mediated apoptotic response and a down-regulation of critical HR proteins, and for reasons discussed, stimulates early steps of HR, but not the formation of complete recombination products.	Caffeine	16-24	P53	Homo sapiens	67-70
12860918-10	2003	Through the mediation of p21WAF1/CIP1 and Bax, the induced p53 protein negatively regulates the growth of dividing VSMCs, thereby minimizing the inappropriate accumulation of VSMCs.	vsmcs	115-120	P53	Homo sapiens	59-62
32163135-0	2020	Involvement of p53-dependent apoptosis signal in antitumor effect of Colchicine on human papilloma virus (HPV)-positive human cervical cancer cells.	Colchicine	69-79	P53	Homo sapiens	15-18
32163135-3	2020	Moreover, reduced expression of E6 and E7 induced by Colchicine resulted in the up-regulation of tumor suppressor proteins, p53 and Rb, as well as down-regulation of phospho Rb (pRb) protein.	Colchicine	53-63	P53	Homo sapiens	124-127
12798071-4	2003	Our results showed that direct exposure to cpTi and ZrO(2) particles compromises cell viability through the induction of apoptosis, eliciting increased levels of the tumor suppressor proteins p53 and p73, in a manner dependent on material composition, particle dosage, and time.	cpti	43-47	P53	Homo sapiens	192-195
32041924-6	2020	Functional studies demonstrated that ectopic miR-1203 overexpression in endometrial cells alleviated OGDR-induced programmed necrosis, inhibiting mitochondrial CypD-p53-adenine nucleotide translocator 1 association, mitochondrial depolarization, reactive oxygen species production, and medium lactate dehydrogenase release.	Adenine Nucleotides	169-187	P53	Homo sapiens	165-168
30856053-14	2020	Abbreviations SA Saccharin SSA Sodium Saccharin Pp53g promoter of human p53 gene MD Molecular dynamics RMSD Root-mean-square deviation RMSF Root-mean-square fluctuation Rg Radius of Gyration SASA Solvent-Accessible Surface Area ADI Acceptable daily intake MM/PBSA Molecular Mechanics/Poisson-Boltzmann Surface Area Communicated by Ramaswamy H. Sarma.	poly(tetramethylene succinate-co-tetramethylene adipate)	259-263	P53	Homo sapiens	49-52
31974410-0	2020	p53 functional states are associated with distinct aldehyde dehydrogenase transcriptomic signatures.	Aldehydes	51-59	P53	Homo sapiens	0-3
12802279-4	2003	We were interested in examining the effect of 2-AP on p53 phosphorylation and its possible consequences on checkpoint control in cells subjected to various forms of DNA damage.	2-Aminopurine	46-50	P53	Homo sapiens	54-57
31715134-11	2020	Collectively, these results for the first time demonstrated the selective apoptotic effect of usnic acid (10-25 muM) through ROS generation and DNA damage on human gastric cancer cells accompanied with upregulation of gammaH2A.X (Ser139) phosphorylation, DNA-PKcs and p53.	usnic acid	94-104	P53	Homo sapiens	268-271
12802279-5	2003	Here, we show that 2-AP suppresses p53 phosphorylation in response to gamma radiation, adriamycin, or ultraviolet treatment.	2-Aminopurine	19-23	P53	Homo sapiens	35-38
12802279-7	2003	However, 2-AP is also capable of inhibiting p53 phosphorylation in cells deficient in ATM, DNA-PK, or ATR suggesting the existence of multiple pathways by which this kinase inhibitor modulates p53 activation.	2-Aminopurine	9-13	P53	Homo sapiens	44-47
32405344-8	2020	Crocin can induce apoptosis through activation of caspase 8, up-regulation of p53 expression, Bax/Bcl-2 ratio, and down-regulation expression of Bcl-2, survivin, and cyclin D1.	crocin	0-6	P53	Homo sapiens	78-81
12802279-7	2003	However, 2-AP is also capable of inhibiting p53 phosphorylation in cells deficient in ATM, DNA-PK, or ATR suggesting the existence of multiple pathways by which this kinase inhibitor modulates p53 activation.	2-Aminopurine	9-13	P53	Homo sapiens	193-196
12802279-8	2003	Biologically, the 2-AP-mediated inhibition of p53 stabilization enables wild-type p53-containing cells to bypass adriamycin-induced G(2)/M arrest.	2-Aminopurine	18-22	P53	Homo sapiens	46-49
12802279-8	2003	Biologically, the 2-AP-mediated inhibition of p53 stabilization enables wild-type p53-containing cells to bypass adriamycin-induced G(2)/M arrest.	2-Aminopurine	18-22	P53	Homo sapiens	82-85
12704785-11	2003	Inhibition of nuclear export by leptomycin B prevented accelerated degradation of p53 in PARP-1 KO cells and led to accumulation of p53 protein.	leptomycin B	32-44	P53	Homo sapiens	82-85
31897170-5	2020	The results demonstrated that TP53 mRNA level in patients with ALL was higher compared with that in the ITP donors (P=0.019).	Inosine Triphosphate	104-107	P53	Homo sapiens	30-34
31786318-0	2020	Dulcitol suppresses proliferation and migration of hepatocellular carcinoma via regulating SIRT1/p53 pathway.	Galactitol	0-8	P53	Homo sapiens	97-100
12704785-11	2003	Inhibition of nuclear export by leptomycin B prevented accelerated degradation of p53 in PARP-1 KO cells and led to accumulation of p53 protein.	leptomycin B	32-44	P53	Homo sapiens	132-135
31786318-10	2020	RESULTS: The results showed that Dulcitol inhibited HepG2 cells proliferation by down-regulating the protein expression of SIRT1, Bcl-2, along with up-regulating p53, acetylated-p53 (K382), cleaved-caspase9, cleaved-caspase3, Bax, and cytochrome c in a dose-dependent manner.	Galactitol	33-41	P53	Homo sapiens	162-165
12653667-8	2003	Here we describe the effect of a potent activator of the p53 response, the nuclear export inhibitor leptomycin B, on Mdm2 degradation and we provide evidence for the oligomerization of the p14ARF tumour suppressor and Mdm2 inhibitor in response to oxidative stress.	leptomycin B	100-112	P53	Homo sapiens	57-60
31786318-10	2020	RESULTS: The results showed that Dulcitol inhibited HepG2 cells proliferation by down-regulating the protein expression of SIRT1, Bcl-2, along with up-regulating p53, acetylated-p53 (K382), cleaved-caspase9, cleaved-caspase3, Bax, and cytochrome c in a dose-dependent manner.	Galactitol	33-41	P53	Homo sapiens	178-181
31786318-12	2020	In vivo, Dulcitol distinctly inhibited the growth of HepG2 cancer xenograft tumors via inhibiting SIRT1/p53 pathway.	Galactitol	9-17	P53	Homo sapiens	104-107
31786318-13	2020	CONCLUSIONS: Our findings suggested that Dulcitol acted as a SIRT1 inhibitor, inducing apoptosis and inhibiting proliferation, migration and invasion of HepG2 cells and its modulatory mechanism seemed to be associated with regulation of MMPs, SIRT1/p53 pathways.	Galactitol	41-49	P53	Homo sapiens	249-252
12539224-0	2003	Leptomycin B stabilizes and activates p53 in primary prostatic epithelial cells and induces apoptosis in the LNCaP cell line.	leptomycin B	0-12	P53	Homo sapiens	38-41
31725331-6	2019	SNAP acted principally through post-translational modification of p53, phosphorylated N-myc downstream regulated gene 1, and MGMT protein stability in TMZ-R GBM cells.	S-Nitroso-N-Acetylpenicillamine	0-4	P53	Homo sapiens	66-69
31617338-0	2019	Dephosphorylation of p53 Ser 392 Enhances Trimethylation of Histone H3 Lys 9 via SUV39h1 Stabilization in CK2 Downregulation-Mediated Senescence.	pentalysine	71-74	P53	Homo sapiens	21-24
12539224-3	2003	Leptomycin B (LMB) has recently been found to increase the protein level and transcriptional activity of p53 by interfering with nucleocytoplasmic export and subsequent degradation by the proteasome.	leptomycin B	0-12	P53	Homo sapiens	105-108
31799200-2	2019	TIGAR (TP53-induced glycolysis and apoptosis regulator) is a fructose-2,6-bisphosphatase that is regulated by p53.	Fructose	61-88	P53	Homo sapiens	110-113
12539224-3	2003	Leptomycin B (LMB) has recently been found to increase the protein level and transcriptional activity of p53 by interfering with nucleocytoplasmic export and subsequent degradation by the proteasome.	leptomycin B	14-17	P53	Homo sapiens	105-108
12539224-10	2003	CONCLUSIONS: p53 in primary cultures of normal and malignant prostate cells, although dysfunctional in that it is not responsive to DNA damage, is activated by LMB.	leptomycin B	160-163	P53	Homo sapiens	13-16
12570745-12	2003	O(6)-alkylguanine in DNA leads to very high rates of G:C deltaA:T transitions in p53 gene.	(6)-alkylguanine	1-17	P53	Homo sapiens	81-84
31732686-0	2019	Expression of Concern: Tumor suppressor SMAR1 activates and stabilizes p53 through its arginine-serine-rich motif.	arginine-serine polymer	87-102	P53	Homo sapiens	71-74
12688354-7	2003	These results show for the first time that flavopiridol modulates specific cellular signal transduction pathways in B-CLL cells thereby altering the balance between survival and cell death signals and providing a rationale for the p53-independent nature of flavopiridol-induced apoptosis.	alvocidib	43-55	P53	Homo sapiens	231-234
31323387-10	2019	LACs carrying KEAP1/NFE2L2 mutations were characterized by elevated expression of phosphorylated ataxia telangiectasia mutated protein and phosphorylated ataxia telangiectasia mutated protein in association with a pattern of mutual exclusivity with TP53 alterations.	Lactose	0-4	P53	Homo sapiens	249-253
12701214-22	2003	This lithium protection was correlated with up-regulation of cytoprotective Bcl-2 and down-regulation of apoptotic proteins p53 and Bax, and neurons showing DNA damage and caspase-3 activation.	Lithium	5-12	P53	Homo sapiens	124-127
31762593-3	2019	The TP53 or p53 gene plays a prominent role in regulating various metabolic activities such as glycolysis, lipolysis, and glycogen synthesis.	Glycogen	122-130	P53	Homo sapiens	4-8
31762593-3	2019	The TP53 or p53 gene plays a prominent role in regulating various metabolic activities such as glycolysis, lipolysis, and glycogen synthesis.	Glycogen	122-130	P53	Homo sapiens	12-15
31498987-7	2019	More interestingly, the developed Li-Al LDH efficiently induces GFP-p53 mediated apoptosis in HeLa cells exclusively sparing the normal tissue cells like NIH-3T3.	li-al	34-39	P53	Homo sapiens	68-71
27025925-5	2019	Psoralidin also increases the expression of pro-apoptosis genes Bax, Bid and p53 while decreases the expression of pro-survival genes Bcl-2 and Bcl-xL, both in a concentration dependent manner between 4 and 64 mumol/L (P<0.05 at 16 and 64 mumol/L).	psoralidin	0-10	P53	Homo sapiens	77-80
27025925-6	2019	Caspase-3 inhibitor (Ac-DEVD-CHO at concentrations between 10 to 20 mumol/L), p53 inhibitor (pifithrin-alpha at 5 mumol/L) and cyclosporin A can attenuate the apoptotic effect of psoralidin.	psoralidin	179-189	P53	Homo sapiens	78-81
31480728-0	2019	C2-Ceramide-Induced Rb-Dominant Senescence-Like Phenotype Leads to Human Breast Cancer MCF-7 Escape from p53-Dependent Cell Death.	N-acetylsphingosine	0-11	P53	Homo sapiens	105-108
31480728-4	2019	The growth assessment showed that C2-ceramide caused significant growth inhibition and apoptosis in MDA-MB-231 cells through down-regulating the expression of mutant p53 whereas up-regulating the expression of pro-apoptotic Bad, and the proteolytic activation of caspase-3.	N-acetylsphingosine	34-45	P53	Homo sapiens	166-169
31607444-5	2019	In contrast, P53 induction by Nutlin and Hsp90 inhibitor AUY922 enhanced the BBB function.	nutlin	30-36	P53	Homo sapiens	13-16
31439619-1	2019	2-phenylacetylenesulfonamide (PAS) induces p53-independent apoptotic killing of B-chronic lymphocytic leukemia (CLL) cells.	2-phenylacetylenesulfonamide	0-28	P53	Homo sapiens	43-46
31439619-1	2019	2-phenylacetylenesulfonamide (PAS) induces p53-independent apoptotic killing of B-chronic lymphocytic leukemia (CLL) cells.	2-phenylacetylenesulfonamide	30-33	P53	Homo sapiens	43-46
31395785-5	2019	Comprehensive mutational scanning of p53 single-amino acid variants demonstrated that missense variants in the DNA-binding domain exert a dominant-negative effect (DNE).	dne	164-167	P53	Homo sapiens	37-40
31388677-7	2019	Even when more abundantly present than after exposure to the radiomimetic bleomycin, Cr(VI)-stabilized p53 showed a much more limited activation of its target genes in two types of primary human cells.	chromium hexavalent ion	85-91	P53	Homo sapiens	103-106
31388677-9	2019	A weak transcription activity of Cr(VI)-upregulated p53 was associated with its low lysine acetylation in the regulatory C-terminal domain, resulting from the inability of Cr(VI) to activate ATM in ascorbate-restored cells.	chromium hexavalent ion	33-39	P53	Homo sapiens	52-55
31067004-0	2019	Association of p38MAPK-p53-Fas aggregation in S-allyl cysteine mediated regulation of hepatocarcinoma.	S-allylcysteine	46-62	P53	Homo sapiens	23-26
31268155-3	2019	The aim of the present study was to examine the possible association of the gene expression of VHL, HIF1A, HIF2A, VEGFA and tumor protein P53 (P53) in cancer tissue with the outcome of ccRCC patients who were treated with sunitinib as first-line therapy following nephrectomy.	Sunitinib	222-231	P53	Homo sapiens	138-141
31268155-3	2019	The aim of the present study was to examine the possible association of the gene expression of VHL, HIF1A, HIF2A, VEGFA and tumor protein P53 (P53) in cancer tissue with the outcome of ccRCC patients who were treated with sunitinib as first-line therapy following nephrectomy.	Sunitinib	222-231	P53	Homo sapiens	143-146
30912145-0	2019	Activation of alpha7-nAChRs protects SH-SY5Y cells from 1-methyl-4-phenylpyridinium-induced apoptotic cell death via ERK/p53 signaling pathway.	1-Methyl-4-phenylpyridinium	56-83	P53	Homo sapiens	121-124
31307507-0	2019	p53 mutant-type in human prostate cancer cells determines the sensitivity to phenethyl isothiocyanate induced growth inhibition.	phenethyl isothiocyanate	77-101	P53	Homo sapiens	0-3
31307507-9	2019	RESULTS: We demonstrated that PEITC inhibits the growth of prostate cancer cells with different "hotspot" p53 mutations (structural and contact), however, preferentially towards structural mutants.	phenethyl isothiocyanate	30-35	P53	Homo sapiens	106-109
31307507-12	2019	The mutant p53 restored by PEITC induces apoptosis in DU145 cells by activating canonical p53 targets, delaying cells in G1 phase and phosphorylating ATM.	phenethyl isothiocyanate	27-32	P53	Homo sapiens	11-14
31307507-12	2019	The mutant p53 restored by PEITC induces apoptosis in DU145 cells by activating canonical p53 targets, delaying cells in G1 phase and phosphorylating ATM.	phenethyl isothiocyanate	27-32	P53	Homo sapiens	90-93
31307525-15	2019	When combined with ATO, HHT further upregulated P53, whereas HHT-induced NF-kappaB pathway activation was significantly suppressed.	ato	19-22	P53	Homo sapiens	48-51
31064869-8	2019	AZD6738 exerted a strong synergistic cytotoxic effect in combination with both AZD7762 and AZD1775 in the 2 lymphoma subtypes regardless of their TP53, MYC, and ATM mutational status.	ceralasertib	0-7	P53	Homo sapiens	146-150
31181622-0	2019	Benzimidazoles Downregulate Mdm2 and MdmX and Activate p53 in MdmX Overexpressing Tumor Cells.	Benzimidazoles	0-14	P53	Homo sapiens	55-58
31181622-7	2019	In summary, we established a new tool for testing the impact of small molecule compounds on the activity of p53 and used it to identify the action of benzimidazoles in melanoma cells.	Benzimidazoles	150-164	P53	Homo sapiens	108-111
31239671-0	2019	In vitro cytotoxicity and transfection efficiency of pDNA encoded p53 gene-loaded chitosan-sodium deoxycholate nanoparticles.	Deoxycholic Acid	91-110	P53	Homo sapiens	66-69
31039479-0	2019	Protective effects of novel derivatives of vitamin D3 and lumisterol against UVB-induced damage in human keratinocytes involve activation of Nrf2 and p53 defense mechanisms.	Cholecalciferol	43-53	P53	Homo sapiens	150-153
31039479-12	2019	In conclusion, pretreatment of keratinocytes with 1,25(OH)2D3 or CYP11A1-derived vitamin D3- or lumisterol hydroxy-derivatives, protected them against UVB-induced damage via activation of the Nrf2-dependent antioxidant response and p53-phosphorylation, as well as by the induction of the DNA repair system.	Calcitriol	50-61	P53	Homo sapiens	232-235
31039479-12	2019	In conclusion, pretreatment of keratinocytes with 1,25(OH)2D3 or CYP11A1-derived vitamin D3- or lumisterol hydroxy-derivatives, protected them against UVB-induced damage via activation of the Nrf2-dependent antioxidant response and p53-phosphorylation, as well as by the induction of the DNA repair system.	Cholecalciferol	81-91	P53	Homo sapiens	232-235
31039479-12	2019	In conclusion, pretreatment of keratinocytes with 1,25(OH)2D3 or CYP11A1-derived vitamin D3- or lumisterol hydroxy-derivatives, protected them against UVB-induced damage via activation of the Nrf2-dependent antioxidant response and p53-phosphorylation, as well as by the induction of the DNA repair system.	lumisterol hydroxy-	96-115	P53	Homo sapiens	232-235
30898612-6	2019	Interestingly, co-treatment with nutlin-3a and certain chemotherapeutic drug such as irinotecan and oxaliplatin resulted in antagonistic effects in cells both lacking and containing WT-TP53 activity.	Oxaliplatin	100-111	P53	Homo sapiens	185-189
30802707-5	2019	Molecular modeling revealed that the compound 4d binds through hydrophobic-hydrophobic interactions with the essential amino acids (LEU: 57, GLY: 58, ILE: 61, and HIS: 96) in the p53-binding cleft, as a standard p53-MDM2 inhibitor (6SJ).	Isoleucine	150-153	P53	Homo sapiens	179-182
30842129-3	2019	Acrolein is a major cigarette-related carcinogen that preferentially causes p53 mutations and inhibits DNA repair function in lung cancer.	Acrolein	0-8	P53	Homo sapiens	76-79
30831390-0	2019	Anticancer activity and mechanism of bis-pyrimidine based dimetallic Ru(II)(eta6-p-cymene) complex in human non-small cell lung cancer via p53-dependent pathway.	ru(ii)	69-75	P53	Homo sapiens	139-142
31086338-0	2019	Publisher Correction: p53 regulation of ammonia metabolism through urea cycle controls polyamine biosynthesis.	Polyamines	87-96	P53	Homo sapiens	22-25
30988205-7	2019	In vitro and in vivo DNA binding analyses showed that the NT reduced p53 DNA binding affinity but improved the ability of p53 to distinguish between specific and nonspecific sequences.	nt	58-60	P53	Homo sapiens	69-72
30988205-7	2019	In vitro and in vivo DNA binding analyses showed that the NT reduced p53 DNA binding affinity but improved the ability of p53 to distinguish between specific and nonspecific sequences.	nt	58-60	P53	Homo sapiens	122-125
30894685-0	2019	p53 expression status is associated with cancer-specific survival in stage III and high-risk stage II colorectal cancer patients treated with oxaliplatin-based adjuvant chemotherapy.	Oxaliplatin	142-153	P53	Homo sapiens	0-3
30894685-1	2019	BACKGROUND: We attempted to elucidate whether p53 expression or TP53 mutation status was associated with cancer-specific survival in adjuvant FOLFOX-treated patients with stage III or high-risk stage II colorectal cancer (CRC).	Folfox protocol	142-148	P53	Homo sapiens	46-49
30894685-1	2019	BACKGROUND: We attempted to elucidate whether p53 expression or TP53 mutation status was associated with cancer-specific survival in adjuvant FOLFOX-treated patients with stage III or high-risk stage II colorectal cancer (CRC).	Folfox protocol	142-148	P53	Homo sapiens	64-68
30894685-7	2019	CONCLUSIONS: p53-mild expression status was found to be an independent prognostic marker in adjuvant FOLFOX-treated patients with stage III and high-risk stage II CRC.	Folfox protocol	101-107	P53	Homo sapiens	13-16
30943845-2	2019	Here, we show that the p53 target and CDK inhibitor p21 protects against MK1775-induced DNA damage during S-phase.	adavosertib	73-79	P53	Homo sapiens	23-26
30403169-8	2018	These findings suggested that this patient"s cancer might be sensitive to AZD1775 (a TP53-targeted drug) or targeted drugs such as FGF19, CCND1 and FGFR2, and should be sensitive to imatinib.	adavosertib	74-81	P53	Homo sapiens	85-89
30250533-10	2018	Western blotting demonstrated that the expression of NF-kappaB, Akt and GADD45B increased over time in lung cells treated with benzopyrene, whereas the expression levels of cyclin B and P53 decreased.	Benzopyrenes	127-138	P53	Homo sapiens	186-189
30513211-15	2018	On the other hand, O-EGCG induced HCT116 cells apoptosis mainly by increasing the expression of p53 and cleaved caspase-3, which might be the underlying reason why O-EGCG had stronger inhibitory effect on HCT116 cells line than EGCG.	o-egcg	19-25	P53	Homo sapiens	96-99
30513211-15	2018	On the other hand, O-EGCG induced HCT116 cells apoptosis mainly by increasing the expression of p53 and cleaved caspase-3, which might be the underlying reason why O-EGCG had stronger inhibitory effect on HCT116 cells line than EGCG.	o-egcg	164-170	P53	Homo sapiens	96-99
29980405-5	2018	Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisplatin, irinotecan, oxaliplatin, and paclitaxel increased significantly.	Oxaliplatin	215-226	P53	Homo sapiens	28-32
29845212-4	2018	In the current study, a small-molecule screen identified andrographlide (ANDRO) as a mutant p53 suppressor.	andrographlide	57-71	P53	Homo sapiens	92-95
29668110-0	2018	Phenylbutyl isoselenocyanate induces reactive oxygen species to inhibit androgen receptor and to initiate p53-mediated apoptosis in LNCaP prostate cancer cells.	ISC-4 compound	0-28	P53	Homo sapiens	106-109
29859204-6	2018	Zolpidem prevented death of P19 neurons exposed to glutamate, and abolished the glutamate-induced increase in ROS production, p53 and Bax expression, and caspase-3/7 activity.	Zolpidem	0-8	P53	Homo sapiens	126-129
30093863-7	2018	Moreover, triptolide dose-dependently increased the protein expression levels of Fas, Bax, p53, p21, cyclin E, cleaved caspase-3, 8, and 9; and subsequent cleavage of poly (ADP-ribose) polymerase (PARP).	triptolide	10-20	P53	Homo sapiens	91-94
30029680-13	2018	CONCLUSION: Our results show that oxaliplatin mediates differential cellular responses in colon cancer cells depending on their p53 status, and demonstrate that the ROS-p53 axis is important for regulating POU3F2 and its downstream target, tNOX.	Oxaliplatin	34-45	P53	Homo sapiens	128-131
30029680-13	2018	CONCLUSION: Our results show that oxaliplatin mediates differential cellular responses in colon cancer cells depending on their p53 status, and demonstrate that the ROS-p53 axis is important for regulating POU3F2 and its downstream target, tNOX.	Oxaliplatin	34-45	P53	Homo sapiens	169-172
30029680-14	2018	Notably, the depletion of tNOX sensitizes p53-null cells to both spontaneous and oxaliplatin-induced apoptosis.	Oxaliplatin	81-92	P53	Homo sapiens	42-45
29923573-0	2018	Sensory acceptable equivalent doses of beta-phenylethyl isothiocyanate (PEITC) induce cell cycle arrest and retard the growth of p53 mutated oral cancer in vitro and in vivo.	phenethyl isothiocyanate	39-70	P53	Homo sapiens	129-132
29923573-0	2018	Sensory acceptable equivalent doses of beta-phenylethyl isothiocyanate (PEITC) induce cell cycle arrest and retard the growth of p53 mutated oral cancer in vitro and in vivo.	phenethyl isothiocyanate	72-77	P53	Homo sapiens	129-132
29923573-5	2018	Mechanistically, PEITC induced ROS accumulation, nuclear translocation of p53 and p21 and G1/S cell cycle arrest in vitro; increased p53 and 8-oxo-dG levels; and decreased Ki-67 intense/mild staining ratios without TUNEL changes in vivo.	phenethyl isothiocyanate	17-22	P53	Homo sapiens	74-77
29923573-5	2018	Mechanistically, PEITC induced ROS accumulation, nuclear translocation of p53 and p21 and G1/S cell cycle arrest in vitro; increased p53 and 8-oxo-dG levels; and decreased Ki-67 intense/mild staining ratios without TUNEL changes in vivo.	phenethyl isothiocyanate	17-22	P53	Homo sapiens	133-136
29571073-14	2018	Conversely, treatment with DAPT alone only increased expression of BAX and P53 (P &lt; .05), suggesting that the reduction of Bcl-2 expression may play an important role in the synergetic antitumor and proapoptosis effects of the combined treatment.	dapt	27-31	P53	Homo sapiens	75-78
29876013-5	2018	Even aggressive models of cancer, such as p53-/- or TET2-/- cells, responded to MC2884, suggesting MC2884 therapeutic potential also for the therapy of TP53 or TET2-deficient human cancers.	mc2884	99-105	P53	Homo sapiens	42-45
29876013-5	2018	Even aggressive models of cancer, such as p53-/- or TET2-/- cells, responded to MC2884, suggesting MC2884 therapeutic potential also for the therapy of TP53 or TET2-deficient human cancers.	mc2884	99-105	P53	Homo sapiens	152-156
29896290-4	2018	This study outlines the regulatory effects of oxaliplatin on miRNAs expression in colon cancer cells and correlates it with the changing microRNA expression with p53 and p73 expression status in cells.	Oxaliplatin	46-57	P53	Homo sapiens	162-165
29896290-10	2018	A selective set of miRNAs were either up-regulated or down-regulated in response to the oxaliplatin treatment with a presumable role of p53 and p73 proteins.	Oxaliplatin	88-99	P53	Homo sapiens	136-139
29896290-11	2018	The miRNAs expression is known to influence the pharmacodynamic mechanisms of oxaliplatin and these effects have been observed to be regulated by p53 and p73.	Oxaliplatin	78-89	P53	Homo sapiens	146-149
29483209-11	2018	Serial ctDNA evaluation in an illustrative patient treated with capecitabine demonstrated emergence of a new TP53 alteration after progression.	Capecitabine	64-76	P53	Homo sapiens	109-113
29054521-2	2018	Here, we used computational technique to understand the interaction of both pristine (pG) or carboxyl functionalized graphene (fG) of different sizes (1, 6, and 10nm) with an important DNA repair protein p53.	pg	86-88	P53	Homo sapiens	204-207
28653608-13	2018	In addition, decreased SOX4 expression could increase the level of miR-138 via upregulation of p53.	mir-138	67-74	P53	Homo sapiens	95-98
28653608-14	2018	Introduction of miR-138 dramatically inhibited growth, invasion, and EMT of NSCLC cells through a SOX4/p53 feedback loop.	mir-138	16-23	P53	Homo sapiens	103-106
29316508-0	2018	Synthesis and biological evaluation of naphthalimide-polyamine conjugates modified by alkylation as anticancer agents through p53 pathway.	Naphthalimides	39-52	P53	Homo sapiens	126-129
29316508-0	2018	Synthesis and biological evaluation of naphthalimide-polyamine conjugates modified by alkylation as anticancer agents through p53 pathway.	Polyamines	53-62	P53	Homo sapiens	126-129
29382728-5	2018	Here, we report on the effects of a curcumin analog, HO-3867, on p53 activity in cancer cells from different origins.	Holmium	53-55	P53	Homo sapiens	65-68
29382728-7	2018	In conclusion, HO-3867 is a p53 mutant-reactivating drug with high clinical anticancer potential.	Holmium	15-17	P53	Homo sapiens	28-31
29158005-9	2018	In the 1,25(OH)2D3 + HDAC2 overexpression group, the expressions of p53, Bax, DR5 and caspase 8 were significantly lower but the expression of Bcl-2 was significantly higher than those of the 1,25(OH)2D3 treatment group (P &lt; 0.05).	Calcitriol	7-18	P53	Homo sapiens	68-71
29355754-7	2018	We went on to study the effect of blocking protein aggregation by emodin (1,3,8-trihydroxy-6-methyl-anthraquinone) and figured that inhibiting p53 protein aggregation can elevate the level of autophagy in A549 lung cancer cell line while there is no significant effect on autophagy in normal non-cancerous HaCaT cells.	Emodin	74-113	P53	Homo sapiens	143-146
29485619-9	2018	Resveratrol and to a greater extent pterostilbene downregulates the HPV oncoprotein E6, induces caspase-3 activation, and upregulates p53 protein levels.	pterostilbene	36-49	P53	Homo sapiens	134-137
29485619-10	2018	Results point to a mechanism that may involve the downregulation of the HPV E6 oncoprotein, activation of apoptotic pathways, and re-establishment of functional p53 protein, with pterostilbene showing greater efficacy than resveratrol.	pterostilbene	179-192	P53	Homo sapiens	161-164
29483845-12	2018	A rescue in the expression of both MLL genes was observed in KCL22S, a CML cell line sensitive to IM, after treatment with dasatinib or nilotinib which was associated with a higher rate of apoptosis, an enhanced expression of p21 (CDKN1A) and a concomitant decrease in the expression of CDK2, CDK4 and Cyclin B1 (CCNB1) in comparison to untreated KCL22S control or IM resistant KCL22R cell line, which suggests involvement of p53 regulated pathway.	nilotinib	136-145	P53	Homo sapiens	426-429
29326019-0	2018	Isolation of a peptide containing d-amino acid residues that inhibits the alpha-helix-mediated p53-MDM2 interaction from a one-bead one-compound library.	d-amino acid	34-46	P53	Homo sapiens	95-98
30664150-6	2019	The TMZ + acteoside combination treatment increased the cleavage of caspase-3 and levels of B-cell lymphoma 2 (Bcl-2)-associated X protein and phosphorylated p53, and decreased the level of Bcl-2.	acteoside	10-19	P53	Homo sapiens	158-161
30325501-6	2019	Furthermore, combined treatment with progesterone plus mifepristone (PG+MIFE) gave an enhanced anti-proliferative effect in comparison with hydrocortisone plus mifepristone (HC+MIFE) by significantly reducing markers of proliferation (BrdU+ and Ki67 expression) and tumor suppressors (PTEN, TP53), and increasing the percentage of pro-apoptotic cells.	pg	69-71	P53	Homo sapiens	291-295
30543781-7	2019	TCCP treatment caused endogenous ROS generation, increase in intracellular calcium and phosphorylation of p53 in a concentration-dependent manner, which was reverted upon pre-treatment with pifithrin-mu.	Triclosan	0-4	P53	Homo sapiens	106-109
30543781-12	2019	Overall, TCCP was shown to be efficient in inducing ROS and mitochondrial-mediated apoptosis by restoring p53 activity in MDA-MB-231 cells and also induced EAT cell death in vivo thereby inhibiting tumor proliferation.	Triclosan	9-13	P53	Homo sapiens	106-109
30584071-9	2019	The newly identified HBx/GYS2/p53 axis is responsible for the deregulation of glycogen metabolism and represents a promising therapeutic target for the clinical management of HCC.	Glycogen	78-86	P53	Homo sapiens	30-33
30584071-10	2019	SIGNIFICANCE: We elucidated the clinical significance, biological function, and regulation of the HBx/GYS2/p53 axis, which supplement the understanding of tumor glycogen metabolism and provide potential prognostic and therapeutic targets for HCC treatment.Graphical Abstract: http://cancerres.aacrjournals.org/content/canres/79/3/534/F1.large.jpg.	Glycogen	161-169	P53	Homo sapiens	107-110
29207138-0	2018	Anticancer pyridines induce G2/M arrest and apoptosis via p53 and JNK upregulation in liver and breast cancer cells.	Pyridines	11-20	P53	Homo sapiens	58-61
12459171-0	2002	p53 codon 72 genotype affects apoptosis by cytosine arabinoside in blood leukocytes.	Cytarabine	43-63	P53	Homo sapiens	0-3
29378575-6	2018	DHA, Omegaven  and oxaliplatin were associated with significant downregulation of VEGF and p53 protein, and upregulation of p21 protein.	Oxaliplatin	19-30	P53	Homo sapiens	91-94
30336239-0	2019	A polysaccharide from Enterobacter cloacae induces apoptosis of human osteosarcoma cells through the activation of p53 and mitochondrial intrinsic pathway.	Polysaccharides	2-16	P53	Homo sapiens	115-118
30592172-9	2019	RNA-seq and bioinformatics analysis showed that apoptosis, death receptor signaling pathway, TNF signaling pathway, and TP53 regulated transcription of cell death genes pathway were closely associated with paclitaxel in the treatment of GCTB.	gctb	237-241	P53	Homo sapiens	120-124
29370077-0	2018	p53 Gene (NY-CO-13) Levels in Patients with Chronic Myeloid Leukemia: The Role of Imatinib and Nilotinib.	nilotinib	95-104	P53	Homo sapiens	0-3
29370077-5	2018	The purpose of the present study was to evaluate the differential effect of imatinib and nilotinib on p53 gene serum levels in patients with CML.	nilotinib	89-98	P53	Homo sapiens	102-105
29370077-11	2018	CONCLUSIONS: Nilotinib is more effective than imatinib in raising p53 serum levels in patients with chronic myeloid leukemia.	nilotinib	13-22	P53	Homo sapiens	66-69
12459171-2	2002	In this report, we addressed the question whether the natural variability at p53 locus (the proline-arginine substitution at codon 72) affects the capacity of peripheral-blood mononuclear cells from healthy subjects to undergo in vitro apoptosis in response to the cytotoxic drug cytosine arabinoside.	Cytarabine	280-300	P53	Homo sapiens	77-80
29323295-6	2018	Moreover, deletion of p53 completely rescues the survival of aldehyde-stressed and mutated haematopoietic stem cells, but does not change the pattern or the intensity of genome instability within individual stem cells.	Aldehydes	61-69	P53	Homo sapiens	22-25
30820346-0	2019	Activation of TAp73 and inhibition of TrxR by Verteporfin for improved cancer therapy in TP53 mutant pancreatic tumors.	Verteporfin	46-57	P53	Homo sapiens	89-93
12429980-0	2002	Phosphorylation of p53, induction of Bax and activation of caspases during beta-lapachone-mediated apoptosis in human prostate epithelial cells.	beta-lapachone	75-89	P53	Homo sapiens	19-22
29911263-0	2019	Novel Competitive Chemiluminescence DNA Assay Based on Fe3O4@SiO2@Au-Functionalized Magnetic Nanoparticles for Sensitive Detection of p53 Tumor Suppressor Gene.	Gold	66-68	P53	Homo sapiens	134-137
29911263-1	2019	A simple, rapid response time and ultrahigh sensitive chemiluminescence (CL) DNA assay based on Fe3O4@SiO2@Au-functionalized magnetic nanoparticles (Au-MNPs) was developed for detection of p53 tumor suppressor gene.	Gold	107-109	P53	Homo sapiens	189-192
29323295-8	2018	Furthermore, we identify how the choice of DNA-repair pathway and a stringent p53 response limit the transmission of aldehyde-induced mutations in stem cells.	Aldehydes	117-125	P53	Homo sapiens	78-81
30636605-2	2018	In our previous studies, we demonstrated that p53 directly regulates Bak in mouse JB6 cells and that p53-Bak signaling axis plays an important role in mediating EGCG-induced apoptosis.	bakuchiol	105-108	P53	Homo sapiens	101-104
31091472-1	2019	NAD(P)H quinone oxidoreductase 1 (NQO1) is a multi-functional protein that catalyses the reduction of quinones (and other molecules), thus playing roles in xenobiotic detoxification and redox balance, and also has roles in stabilising apoptosis regulators such as p53.	Quinones	102-110	P53	Homo sapiens	264-267
12429980-4	2002	The apoptotic effects of beta-lapachone were associated with marked induction of p53 phosphorylation and Bax protein without altering the expression of p53 and Bcl-2 protein.	beta-lapachone	25-39	P53	Homo sapiens	81-84
12429980-7	2002	The present results suggest that apoptotic signals evoked by beta-lapachone in human prostate epithelial cells may converge caspases activation through up-regulation of phosphorylation of p53 and Bax rather than down-regulation of c-IAPs family.	beta-lapachone	61-75	P53	Homo sapiens	188-191
12399131-4	2002	Aberrant p53 expression was less frequent in carcinoma with EB (29.0%) than in carcinoma without EB (47.9%, P = 0.043).	Eriochrome Blue SE	60-62	P53	Homo sapiens	9-12
29842822-0	2019	Biosynthesized composites of Au-Ag nanoparticles using Trapa peel extract induced ROS-mediated p53 independent apoptosis in cancer cells.	Gold	29-31	P53	Homo sapiens	95-98
28922542-8	2018	On the other hand, DPDS 6, the compound with the highest selectivity index for cancer cells, resulted in G2 /M cell cycle arrest and caspase-independent cell death in p53 deficient HTB-54 lung cancer cells.	dpds 6	19-25	P53	Homo sapiens	167-170
12399131-4	2002	Aberrant p53 expression was less frequent in carcinoma with EB (29.0%) than in carcinoma without EB (47.9%, P = 0.043).	Eriochrome Blue SE	97-99	P53	Homo sapiens	9-12
29115606-3	2018	However, its regulation of chemosensitivity to gemcitabine (GEM) and oxaliplatin (OXA) in p53-deficient PDAC remains unclear.	Oxaliplatin	69-80	P53	Homo sapiens	90-93
30651826-0	2019	Saikosaponin D inhibits proliferation of human osteosarcoma cells via the p53 signaling pathway.	saikosaponin D	0-14	P53	Homo sapiens	74-77
29115606-3	2018	However, its regulation of chemosensitivity to gemcitabine (GEM) and oxaliplatin (OXA) in p53-deficient PDAC remains unclear.	Oxaliplatin	82-85	P53	Homo sapiens	90-93
12481430-13	2002	UCN-01 potently enhanced the activity of 1-beta-D-arabinofuranosylcytosine in both p53 wild-type and mutant cells, whereas ICP-1 was inactive in this combination.	Cytarabine	41-74	P53	Homo sapiens	83-86
12160929-0	2002	Possible involvement of glutathione and p53 in trichloroethylene- and perchloroethylene-induced lipid peroxidation and apoptosis in human lung cancer cells.	Trichloroethylene	47-64	P53	Homo sapiens	40-43
12160929-2	2002	The aim of this study was to elucidate the role of glutathione (GSH) and p53 in TCE- and PERC-induced lung toxicity.	Trichloroethylene	80-83	P53	Homo sapiens	73-76
29311933-5	2017	As a measure of anti-proliferative activity, DEAE-Dextran exhibited reduced ki67, p53, and PCNA levels.	DEAE-Dextran	45-57	P53	Homo sapiens	82-85
30647850-0	2018	The molecular mechanism of action of methylene quinuclidinone and its effects on the structure of p53 mutants.	SCHEMBL4738034	37-61	P53	Homo sapiens	98-101
12160929-4	2002	The results showed that exposure to vapor TCE and PERC produced a dose-dependent and more pronounced accumulation of H(2)O(2) in p53-WT H460 than p53-null H1299 cells.	Trichloroethylene	42-45	P53	Homo sapiens	129-132
12160929-4	2002	The results showed that exposure to vapor TCE and PERC produced a dose-dependent and more pronounced accumulation of H(2)O(2) in p53-WT H460 than p53-null H1299 cells.	Trichloroethylene	42-45	P53	Homo sapiens	146-149
12160929-6	2002	Cotreatment of p53-WT H460 cells with free radical scavengers, such as D-mannitol, uric acid, and sodium selenite, significantly attenuated the TCE- or PERC-induced lipid peroxidation.	Mannitol	71-81	P53	Homo sapiens	15-18
12160929-6	2002	Cotreatment of p53-WT H460 cells with free radical scavengers, such as D-mannitol, uric acid, and sodium selenite, significantly attenuated the TCE- or PERC-induced lipid peroxidation.	Sodium Selenite	98-113	P53	Homo sapiens	15-18
30448921-8	2018	Determination of the MM/PBSA free energy indicated that the binding of DHP-8 to SIRT1 significantly increased the binding affinity of SIRT1 to its substrate p53-W as well as to NAD+.	poly(tetramethylene succinate-co-tetramethylene adipate)	24-28	P53	Homo sapiens	157-160
29212503-5	2017	RESULTS: Combined treatment with equipotent doses of VPA and 5"-DFUR resulted in synergistic effects in CRC lines expressing p53 (wild-type or mutant).	doxifluridine	61-68	P53	Homo sapiens	125-128
12160929-6	2002	Cotreatment of p53-WT H460 cells with free radical scavengers, such as D-mannitol, uric acid, and sodium selenite, significantly attenuated the TCE- or PERC-induced lipid peroxidation.	Trichloroethylene	144-147	P53	Homo sapiens	15-18
29089230-0	2017	Proapoptotic modification of substituted isoindolinones as MDM2-p53 inhibitors.	phthalimidine	41-55	P53	Homo sapiens	64-67
12160929-7	2002	In contrast, depletion of GSH in p53-null H1299 cells enhanced TCE- or PERC-induced lipid peroxidation.	Trichloroethylene	63-66	P53	Homo sapiens	33-36
28745318-0	2017	Core 3 mucin-type O-glycan restoration in colorectal cancer cells promotes MUC1/p53/miR-200c-dependent epithelial identity.	o-glycan	18-26	P53	Homo sapiens	80-83
30442142-5	2018	We later clarified the effect of metformin on p53 protein stability using transient transfection and cycloheximide chase analyses.	Cycloheximide	101-114	P53	Homo sapiens	46-49
12171906-3	2002	Resistance to TMZ varied most notably with the p53 status of the tumor.	Temozolomide	14-17	P53	Homo sapiens	47-50
30226785-4	2018	This interaction displaces pro-apoptotic Bak and subsequently leads to intrinsic apoptosis via mimicking a p53 transcription-independent pathway.	bakuchiol	41-44	P53	Homo sapiens	107-110
28970011-10	2017	Crocetin induced G1 arrest, reduced PCNA protein expression and increased the p21 and p53 accumulation in ARPE-19 cells.	crocetin	0-8	P53	Homo sapiens	86-89
12171906-5	2002	The p21-related cell cycle arrest was intimately linked to TMZ toxicity because tumors with wt p53 but lacking a robust increase in p21 protein level (D-54) were resistant to TMZ.	Temozolomide	59-62	P53	Homo sapiens	95-98
29133879-7	2017	Importantly, the system is sensitive enough to specifically target TP53 loss-of-function cells with the HSV-TK pro-drug Ganciclovir both in vitro and in vivo.	Ganciclovir	120-131	P53	Homo sapiens	67-71
30121400-9	2018	In addition, the p53-independent apoptotic pathways induced by vanadyl complexes may provide new insights for future discovery of new anticancer drugs overcoming the chemo-resistance due to p53 mutation.	Vanadates	63-70	P53	Homo sapiens	17-20
30121400-9	2018	In addition, the p53-independent apoptotic pathways induced by vanadyl complexes may provide new insights for future discovery of new anticancer drugs overcoming the chemo-resistance due to p53 mutation.	Vanadates	63-70	P53	Homo sapiens	190-193
12171906-8	2002	CONCLUSIONS: By testing a limited number of glial tumors in cell culture and also as xenografts, we have shown that mobilization of the p53 in response to TMZ damage is likely to induce a cell cycle arrest and apoptosis in glial tumors.	Temozolomide	155-158	P53	Homo sapiens	136-139
12171906-9	2002	Additional pathways linking cell cycle arrest and apoptosis contribute to the efficacy of TMZ against p53 mutated glial tumors.	Temozolomide	90-93	P53	Homo sapiens	102-105
12171907-8	2002	Exposure of WSU-CLL cells to 4 and 5 nM CA4P was associated with overproduction of total p53 and no dramatic change in MDM2, 14-3-3sigma, GADD45, the cyclin-dependent kinase cdc2, its inhibitory phosphorylation, the cdc2-inhibitory kinase (wee1), chk1, or cdc25 hyperphosphorylation.	CA4P	40-44	P53	Homo sapiens	89-92
29113182-4	2017	Additionally, western blot analysis, Hoechst 33342 staining and cytometry analysis revealed that PAG not only inhibited the viability of HCT116 cells by suppressing the dishevelled segment polarity protein 2/glycogen synthase kinase 3 beta/beta-catenin pathway, but also induced the apoptosis of HCT116 cells by downregulating nuclear factor-kappaB p65 activity, stimulating p53 expression and promoting the generation of intracellular reactive oxygen species.	pag	97-100	P53	Homo sapiens	375-378
12171907-10	2002	Our findings suggest that CA4P induces mitotic catastrophe and arrest of WSU-CLL cells mostly in the M phase independent of p53 and independent of chk1 and cdc2 phosphorylation pathways.	CA4P	26-30	P53	Homo sapiens	124-127
30713659-9	2019	Furthermore, TCS activated p53 mediated apoptosis in HepG2 cells in a caspase-independent manner, while MTCS induced apoptosis was dependent on caspase.	Triclosan	13-16	P53	Homo sapiens	27-30
12194756-5	2002	RESULTS: Clonogenic survival assays up to 8 Gy demonstrated that p53-defective HT-29 cells (sensitizer enhancement ratio [SER]=1.54) were sensitized by PTX (2 mM) to a significantly higher degree than p53 wild-type MCF-7 (SER=1.14) cells.	Pentoxifylline	152-155	P53	Homo sapiens	65-68
12194756-5	2002	RESULTS: Clonogenic survival assays up to 8 Gy demonstrated that p53-defective HT-29 cells (sensitizer enhancement ratio [SER]=1.54) were sensitized by PTX (2 mM) to a significantly higher degree than p53 wild-type MCF-7 (SER=1.14) cells.	Pentoxifylline	152-155	P53	Homo sapiens	201-204
30059758-4	2018	Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-).	Oxaliplatin	89-100	P53	Homo sapiens	43-46
30059758-4	2018	Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-).	Oxaliplatin	89-100	P53	Homo sapiens	261-264
29093644-15	2017	Conclusions: We concluded that crocetin combined with cisplatin exerts a synergistic anticancer effect by up-regulating the p53/p21 pathway.	crocetin	31-39	P53	Homo sapiens	124-127
30059758-4	2018	Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-).	Oxaliplatin	89-100	P53	Homo sapiens	261-264
12194756-6	2002	Exposure of irradiated (6 Gy) cells to PTX (2 mM) resulted in abrogation of the radiation-induced G2/M arrest in the p53-defective HT-29 and WiDr cells, whereas the p53 wild-type-expressing MCF-7 and HPR600 cells showed less significant impairment of the G2/M checkpoint.	Pentoxifylline	39-42	P53	Homo sapiens	117-120
30059758-7	2018	Stable knockdown of CerS5 expression using CerS5-targeting shRNA led to an increased sensitivity of HCT-116 p53wt cells, but not of p53-/- cells, to oxaliplatin and 5-FU.	Oxaliplatin	149-160	P53	Homo sapiens	108-111
30059758-10	2018	In conclusion, in p53wt colon cancer cells chemosensitivity against oxaliplatin or 5-FU could be enhanced by downregulation of CerS5 expression leading to reduced autophagy and mitochondrial respiration.	Oxaliplatin	68-79	P53	Homo sapiens	18-21
12194756-6	2002	Exposure of irradiated (6 Gy) cells to PTX (2 mM) resulted in abrogation of the radiation-induced G2/M arrest in the p53-defective HT-29 and WiDr cells, whereas the p53 wild-type-expressing MCF-7 and HPR600 cells showed less significant impairment of the G2/M checkpoint.	Pentoxifylline	39-42	P53	Homo sapiens	165-168
28637689-4	2017	Among 164 cases with rising CA125 detected with the UKCTOCS risk of ovarian cancer algorithm (ROCA), 20.7% had elevated TP53 autoantibody.	roca	94-98	P53	Homo sapiens	120-124
12194756-9	2002	CONCLUSIONS: Since PTX was less effective in cells expressing intact p53, the application of PTX suggests a promising strategy of pharmacological disruption of the G2/M checkpoint control by which preferentially radiation-resistant tumours with defective p53 function might be rendered more sensitive to ionizing radiation.	Pentoxifylline	93-96	P53	Homo sapiens	69-72
28637689-5	2017	In cases missed by the ROCA, 16% of cases had elevated TP53 autoantibody.	roca	23-27	P53	Homo sapiens	55-59
12194756-9	2002	CONCLUSIONS: Since PTX was less effective in cells expressing intact p53, the application of PTX suggests a promising strategy of pharmacological disruption of the G2/M checkpoint control by which preferentially radiation-resistant tumours with defective p53 function might be rendered more sensitive to ionizing radiation.	Pentoxifylline	93-96	P53	Homo sapiens	255-258
28637689-6	2017	Of the 34 ovarian cancer cases detected with the ROCA, TP53 autoantibody titers were elevated 11.0 months before CA125.	roca	49-53	P53	Homo sapiens	55-59
28637689-7	2017	In the 9 cases missed by the ROCA, TP53 autoantibody was elevated 22.9 months before cancer diagnosis.	roca	29-33	P53	Homo sapiens	35-39
28637689-8	2017	Similar sensitivity was obtained using assays with specific mutant and wild-type TP53.Conclusions: TP53 autoantibody levels provide a biomarker with clinically significant lead time over elevation of CA125 or an elevated ROCA value.	roca	221-225	P53	Homo sapiens	99-103
30056083-3	2018	Compared to 5-FU alone, MH synergistically enhanced the chemotherapeutic effects of 5-FU, by reducing cell proliferation through the suppression of EGFR, HER2, p-Akt and p-mTOR expression, and promoting apoptosis by the modulation pro-apoptotic (p53, Bax, Cyto c, FasL caspase-3, -8, -9 and cleave-PARP) and anti-apoptotic (Bcl-2) markers.	mh	24-26	P53	Homo sapiens	246-249
12190289-3	2002	RESULTS: p53 was detected more frequently in CIN and invasive carcinoma (100% of CIN I, 74.2% CIN II + III and 70.1% invasive carcinoma) compared with benign cervices (P&lt; 0.001); however, only three squamous cell carcinomas, 11 adenocarcinomas and two adenosquamous carcinomas exhibited p53 expression in &gt;75% of tumour nuclei.	cin i	81-86	P53	Homo sapiens	9-12
29885407-8	2018	The percentage of tumor cells with strong p53 staining was positively correlated with TP53 mutation VAF (R2 = 0.95, P &lt; .001).	vaf	100-103	P53	Homo sapiens	42-45
29885407-8	2018	The percentage of tumor cells with strong p53 staining was positively correlated with TP53 mutation VAF (R2 = 0.95, P &lt; .001).	vaf	100-103	P53	Homo sapiens	86-90
28902369-0	2017	Synergistic inhibitory effects on hepatocellular carcinoma with recombinant human adenovirus Aspp2 and oxaliplatin via p53-independent pathway in vitro and in vivo.	Oxaliplatin	103-114	P53	Homo sapiens	119-122
28902369-1	2017	The present study was designed to investigate the synergistic inhibitory effects on hepatocellular carcinoma with recombinant human adenovirus Aspp2 (Aspp2-ad) and oxaliplatin via p53-independent pathway in vitro and in vivo.	Oxaliplatin	164-175	P53	Homo sapiens	180-183
12190289-5	2002	p53 immunoreactive cells were randomly distributed in invasive carcinoma, confined to the lower third of the epithelium in CIN I, reached the middle third in 20% of CIN II and upper third in 16.6% of CIN III.	cin i	123-128	P53	Homo sapiens	0-3
29058293-10	2017	After 24-h exposure to CE-SS, the expression of cleaved-caspase-9, cleaved-caspase-8 and cleaved-caspase-3 protein was activated, the expression of p53 protein increased while the ratio of Bax/Bcl-2 also increased.	ce-ss	23-28	P53	Homo sapiens	148-151
30085332-11	2018	In addition, the expression of Ser216p-Cdc25C was also increased in the combined group, indicating that irinotecan likely radiosensitized the p53-mutant HT29 and SW620 cells through the ATM/Chk/Cdc25C/Cdc2 pathway.	ser216p	31-38	P53	Homo sapiens	142-145
30282320-13	2018	Taken together, we demonstrated that bis-salicylaldimine based dimetallic Ru-(p-cymene) complexes exerts anticancer effects by p53 pathway, suggesting the promising chemotherapeutic potentials of these Ru(II) complexes for the treatment of cancer.	ru-(p-cymene	74-86	P53	Homo sapiens	127-130
12006592-1	2002	Insulin receptor substrate p53/p58 (IRSp53) is involved in cytoskeletal dynamics and is a candidate disease sensor in polyglutamine expansion neurodegeneration.	polyglutamine	118-131	P53	Homo sapiens	27-30
30282320-13	2018	Taken together, we demonstrated that bis-salicylaldimine based dimetallic Ru-(p-cymene) complexes exerts anticancer effects by p53 pathway, suggesting the promising chemotherapeutic potentials of these Ru(II) complexes for the treatment of cancer.	ru(ii)	202-208	P53	Homo sapiens	127-130
28791403-10	2017	Among DLBCL cases, the TP53 mutations shortened both OS and PFS of patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) and decreased both OS and PFS of patients with secondary DLBCL disease.	Prednisone	155-165	P53	Homo sapiens	23-27
28870911-5	2017	Apoptotic death induced by sunitinib in MCF7 cells was mediated by activation of caspase-3 and p53 mRNA and protein expression and an increase in the percentage of apoptotic cells (40%) as determined by flow cytometry.	Sunitinib	27-36	P53	Homo sapiens	95-98
28870911-7	2017	Mechanistically, blocking of de novo RNA synthesis by actinomycin D significantly inhibited sunitinib-induced expression of p53 mRNA, but not that of caspase-3, indicating involvement of a transcriptional mechanism.	Sunitinib	92-101	P53	Homo sapiens	124-127
30041135-4	2018	The obtained results led to the identification of a hit compound, prenylchalcone 2e, which behaved as potential inhibitor of the MDM2-p53 interaction in yeast, and showed improved cytotoxicity against human tumor cells expressing wild-type p53, including liver hepatocellular carcinoma HepG2, breast adenocarcinoma MCF-7, and malignant melanoma A375 cells.	prenylchalcone	66-80	P53	Homo sapiens	134-137
30041135-4	2018	The obtained results led to the identification of a hit compound, prenylchalcone 2e, which behaved as potential inhibitor of the MDM2-p53 interaction in yeast, and showed improved cytotoxicity against human tumor cells expressing wild-type p53, including liver hepatocellular carcinoma HepG2, breast adenocarcinoma MCF-7, and malignant melanoma A375 cells.	prenylchalcone	66-80	P53	Homo sapiens	240-243
12120703-7	2002	Moderate to strong TP53 protein staining was seen in 56% of OSCC, 32% of OLP but only in 13% of HK.	oscc	60-64	P53	Homo sapiens	19-23
30041135-5	2018	In colon cancer cells, it was also shown that the growth inhibitory effect of prenylchalcone 2e was associated with the induction of cell cycle arrest, apoptosis, and increased protein expression levels of p53 transcriptional targets.	prenylchalcone	78-92	P53	Homo sapiens	206-209
30029680-0	2018	Regulation of tNOX expression through the ROS-p53-POU3F2 axis contributes to cellular responses against oxaliplatin in human colon cancer cells.	Oxaliplatin	104-115	P53	Homo sapiens	46-49
30029680-3	2018	We recently established that oxaliplatin also exert its anti-cancer activity in gastric cancer cell lines by targeting tumor-associated NADH oxidase (tNOX), attenuate NAD+ generation and reduce NAD+-dependent sirtuin 1 (SIRT1) deacetylase activity, which in turn enhances p53 acetylation and apoptosis.	Oxaliplatin	29-40	P53	Homo sapiens	272-275
30029680-4	2018	METHODS: In this study, differential cellular outcomes in response to oxaliplatin exposure of p53-wild-type versus p53-null HCT116 human colon cancer cells were examined.	Oxaliplatin	70-81	P53	Homo sapiens	94-97
30029680-4	2018	METHODS: In this study, differential cellular outcomes in response to oxaliplatin exposure of p53-wild-type versus p53-null HCT116 human colon cancer cells were examined.	Oxaliplatin	70-81	P53	Homo sapiens	115-118
30029680-8	2018	RESULTS: In p53-wild-type cells, we found that oxaliplatin inhibited cell growth by inducing apoptosis and concurrently down-regulating tNOX at both the transcriptional and translational levels.	Oxaliplatin	47-58	P53	Homo sapiens	12-15
30029680-9	2018	In p53-null cells, in contrast, oxaliplatin moderately up-regulated tNOX expression and yielded no apoptosis and much less cytotoxicity.	Oxaliplatin	32-43	P53	Homo sapiens	3-6
28677789-0	2017	miRNA-504 inhibits p53-dependent vascular smooth muscle cell apoptosis and may prevent aneurysm formation.	mirna-504	0-9	P53	Homo sapiens	19-22
28796247-0	2017	P53-dependent downregulation of hTERT protein expression and telomerase activity induces senescence in lung cancer cells as a result of pterostilbene treatment.	pterostilbene	136-149	P53	Homo sapiens	0-3
30029680-10	2018	Further experiments revealed that in p53-wild-type cells, oxaliplatin enhanced ROS generation and p53 transcriptional activation, leading to down-regulation of the transcriptional factor, POU3F2, which enhances the expression of tNOX.	Oxaliplatin	58-69	P53	Homo sapiens	37-40
30029680-10	2018	Further experiments revealed that in p53-wild-type cells, oxaliplatin enhanced ROS generation and p53 transcriptional activation, leading to down-regulation of the transcriptional factor, POU3F2, which enhances the expression of tNOX.	Oxaliplatin	58-69	P53	Homo sapiens	98-101
30029680-11	2018	Moreover, the addition of a ROS scavenger reversed the p53 activation, POU3F2 down-regulation, and apoptosis induced by oxaliplatin in p53-wild-type cells.	Oxaliplatin	120-131	P53	Homo sapiens	55-58
30029680-11	2018	Moreover, the addition of a ROS scavenger reversed the p53 activation, POU3F2 down-regulation, and apoptosis induced by oxaliplatin in p53-wild-type cells.	Oxaliplatin	120-131	P53	Homo sapiens	135-138
30029680-12	2018	In the p53-null line, on the other hand, oxaliplatin treatment triggered less ROS generation and no p53 protein, such that POU3F2 and tNOX were not down-regulated and oxaliplatin-mediated cytotoxicity was attenuated.	Oxaliplatin	41-52	P53	Homo sapiens	7-10
28796247-7	2017	A more detailed mechanistic study revealed that PT-induced senescence partially occurred via a p53-dependent mechanism, triggering inhibition of telomerase activity and protein expression, and leading to the DDR, S phase arrest and, finally, cellular senescence.	pterostilbene	48-50	P53	Homo sapiens	95-98
28790461-9	2017	In conclusion, para-nitro may enhance the anticancer effect of CAPE by inhibiting colon cancer cell viability, inducing apoptosis and cell cycle arrest via the P53 pathway and inhibiting tumour growth and reducing tumour invasion by decreasing the expression of VEGF; additionally, metabolites of CAPE-pNO2 showed differences in cells and organs.	para-nitro	15-25	P53	Homo sapiens	160-163
30029680-12	2018	In the p53-null line, on the other hand, oxaliplatin treatment triggered less ROS generation and no p53 protein, such that POU3F2 and tNOX were not down-regulated and oxaliplatin-mediated cytotoxicity was attenuated.	Oxaliplatin	41-52	P53	Homo sapiens	100-103
28790461-9	2017	In conclusion, para-nitro may enhance the anticancer effect of CAPE by inhibiting colon cancer cell viability, inducing apoptosis and cell cycle arrest via the P53 pathway and inhibiting tumour growth and reducing tumour invasion by decreasing the expression of VEGF; additionally, metabolites of CAPE-pNO2 showed differences in cells and organs.	caffeic acid phenethyl ester	63-67	P53	Homo sapiens	160-163
30029680-12	2018	In the p53-null line, on the other hand, oxaliplatin treatment triggered less ROS generation and no p53 protein, such that POU3F2 and tNOX were not down-regulated and oxaliplatin-mediated cytotoxicity was attenuated.	Oxaliplatin	167-178	P53	Homo sapiens	7-10
11850804-7	2002	Presence of T(3) in the medium caused a gradual increase in the level of p53 in a concentration-dependent manner.	Triiodothyronine	12-16	P53	Homo sapiens	73-76
30050935-7	2018	Mechanistic study showed that coadministration of caffeine and TMZ suppressed the phosphorylation of ATM and p53 and downregulated p21 expression, thus releasing DNA-damaged cells from G2 arrest into premature mitosis.	Caffeine	50-58	P53	Homo sapiens	109-112
30050935-10	2018	In conclusion, our study demonstrated that caffeine enhanced the efficacy of TMZ through mitotic cell death by impeding ATM/p53/p21-mediated G2 arrest.	Caffeine	43-51	P53	Homo sapiens	124-127
11730842-0	2002	Detection of anti-p53 antibodies by ELISA using p53 synthetic or phage-displayed peptides.	Peptides	81-89	P53	Homo sapiens	18-21
29950991-7	2018	The activity of caspase-8, caspase-9 and the expression of p53 were significantly increased after treatment with HJB.	3-[7,7-bis(oxidanyl)-8-oxa-7-boranuidabicyclo[4.3.0]nona-1(6),2,4-trien-5-yl]propanoic acid	113-116	P53	Homo sapiens	59-62
28925469-0	2017	1,25-Dihydroxyvitamin D3 regulates T lymphocyte proliferation through activation of P53 and inhibition of ERK1/2 signaling pathway in children with Kawasaki disease.	Calcitriol	0-24	P53	Homo sapiens	84-87
28925469-10	2017	After the intervention with 1,25(OH)2D3 in vitro, STAT3 and NF-kappaB P65 had no significant changes, the activation of ERK1/2 signaling pathway was inhibited and the P53 protein was activated.	Calcitriol	28-39	P53	Homo sapiens	167-170
28465245-0	2017	1,25-Dihydroxyvitamin D3 suppresses gastric cancer cell growth through VDR- and mutant p53-mediated induction of p21.	Calcitriol	0-24	P53	Homo sapiens	87-90
11878895-10	2001	A partially purified fraction that elutes at 0.6 M KCl from phosphocellulose contains the activity that degrades p53 in a 3C(Pro)-dependent manner.	phosphocellulose	60-76	P53	Homo sapiens	113-116
28465245-5	2017	We demonstrated the important role of vitamin D receptor (VDR) and mutant p53 (mutp53) in mediating the antitumor action of 1,25(OH)2D3 by using siRNA, western-blot, immunofluorescent staining and immunoprecipitation assays.	Calcitriol	124-135	P53	Homo sapiens	74-77
11677656-8	2001	Interestingly, caffeine and other methyl xanthines preferentially radiosensitize cells that lack normal p53 function.	methylxanthine	34-50	P53	Homo sapiens	104-107
28400072-8	2017	Compared with the control group, the mRNA abundances of HES1, MYC, BAX, BCL2 and CYP19A1 in DAPT-treated groups was lower (P&lt;0.05), respectively; whereas, the expression of CCND2, CDKN1A and TP53 mRNA showed no remarkable difference compared with control group.	dapt	92-96	P53	Homo sapiens	194-198
28415713-6	2017	Bioinformatics analysis and molecular experiments further prove that miR-135a is a novel downstream gene of tumor suppressor p53.	135a	73-77	P53	Homo sapiens	125-128
29783721-0	2018	AZD1775 Increases Sensitivity to Olaparib and Gemcitabine in Cancer Cells with p53 Mutations.	adavosertib	0-7	P53	Homo sapiens	79-82
29783721-6	2018	We show that AZD1775 alone is effective as a therapeutic agent against some p53 mutated cell models.	adavosertib	13-20	P53	Homo sapiens	76-79
29783721-7	2018	Moreover, the combination of AZD1775 with olaparib or gemcitabine is synergistic in cells with mutant p53 and constitutes a new approach that should be considered in the treatment of advanced and recurrent gynecologic cancer.	adavosertib	29-36	P53	Homo sapiens	102-105
11685745-5	2001	Exposure to aflatoxin is associated with a specific mutation in the tumor-suppressor gene p53.	Aflatoxins	12-21	P53	Homo sapiens	90-93
29499407-0	2018	Physalin B induces cell cycle arrest and triggers apoptosis in breast cancer cells through modulating p53-dependent apoptotic pathway.	physalin B	0-10	P53	Homo sapiens	102-105
28292017-6	2017	We found that (-)-curine induced G1 arrest and cell death in HepG2 cells with wild-type p53 as well as Huh-7 cells with mutant p53.	curine	14-24	P53	Homo sapiens	88-91
28292017-6	2017	We found that (-)-curine induced G1 arrest and cell death in HepG2 cells with wild-type p53 as well as Huh-7 cells with mutant p53.	curine	14-24	P53	Homo sapiens	127-130
29499407-6	2018	Further studies showed that PB induced breast cancer cells apoptosis in a p53-dependent manner in MCF-7 cells.	physalin B	28-30	P53	Homo sapiens	74-77
11448536-3	2001	In order to investigate the influence of the mutant protein extracted from adrenocortical tumors on normal adrenal cells, we first cloned p53 cDNA from the human primary aldosteronism and constituted it with isopropyl thiogalactoside (IPTG) inducible expression vector as recombinant plasmid.	Isopropyl Thiogalactoside	208-233	P53	Homo sapiens	138-141
29670092-5	2018	APR-246 is converted to the reactive electrophile methylene quinuclidinone (MQ), which binds covalently to p53 core domain.	SCHEMBL4738034	50-74	P53	Homo sapiens	107-110
28292017-8	2017	Taken together, our data demonstrate that (-)-curine can inhibit viability of hepatocellular carcinoma cells in regardless of p53 status.	curine	42-52	P53	Homo sapiens	126-129
29034069-0	2017	Scaffold hopping via ANCHOR.QUERY: beta-lactams as potent p53-MDM2 antagonists .	beta-Lactams	35-47	P53	Homo sapiens	58-61
29034069-1	2017	Using the pharmacophore-based virtual screening platform ANCHOR.QUERY, we morphed our recently described Ugi-4CR scaffold towards a beta-lactam scaffold with potent p53-MDM2 antagonizing activities.	beta-Lactams	132-143	P53	Homo sapiens	165-168
29596799-0	2018	p53 mediated transcriptional regulation of long non-coding RNA by 1-hydroxy-1-norresistomycin triggers intrinsic apoptosis in adenocarcinoma lung cancer.	1-hydroxy-1-norresistomycin	66-93	P53	Homo sapiens	0-3
29596799-4	2018	In the present study, marine actinomycetes derived 1-hydroxy-1-norresistomycin (HNM) was used to enhance the expression of lncRNAs through p53 transcriptional regulation and induced intrinsic apoptosis in non-small cell lung cancer cells.	1-hydroxy-1-norresistomycin	51-78	P53	Homo sapiens	139-142
28240971-1	2017	Purpose To evaluate MK-8242 in patients with wild-type TP53 advanced solid tumors.	mk-8242	20-27	P53	Homo sapiens	55-59
11448536-7	2001	On the other hand, cell morphological changes and cell proliferation rate increase were observed when we used IPTG to induce the expression of the p53 protein, which mutated at codon 249, in adrenocortical cells.	Isopropyl Thiogalactoside	110-114	P53	Homo sapiens	147-150
28240971-12	2017	Conclusion At the RP2D of 400 mg twice a day, MK-8242 activated the p53 pathway with an acceptable safety and tolerability profile.	mk-8242	46-53	P53	Homo sapiens	68-71
11522624-3	2001	In the present study, we have used a highly sensitive mutation assay to determine the p53 mutation load in nontumorous human lung and to study the mutability of p53 codons 157, 248, 249, and 250 to benzo(a)pyrene-diol-epoxide (BPDE), an active metabolite of BP in human bronchial epithelial BEAS-2B cells.	Benzo(a)pyrene	227-229	P53	Homo sapiens	161-164
29314176-6	2018	Addition of p53 IHC decreased the mean proportion of IND diagnoses from 10 of 60 to eight of 60 (P = 0.071).	indole	53-56	P53	Homo sapiens	12-15
11494312-2	2001	Irradiation with ultraviolet (UV) resulted in nuclear accumulation of p53 in normal human fibroblast cells, and this accumulation was suppressed by treatment with HuIFN-beta.	huifn-beta	163-173	P53	Homo sapiens	70-73
29512724-9	2018	Results of western blot analysis demonstrated that phosphorylation of JNK and expression of p53, caspase-9 and caspase-3 were upregulated in the polysaccharide-treated MCF-7 cells.	Polysaccharides	145-159	P53	Homo sapiens	92-95
28108275-0	2017	Benzofuran-2-acetic ester derivatives induce apoptosis in breast cancer cells by upregulating p21Cip/WAF1 gene expression in p53-independent manner.	benzofuran-2-acetic ester	0-25	P53	Homo sapiens	125-128
29054521-3	2018	The molecular docking study revealed strong interaction between pG and DNA binding domains (DBD) of p53 with binding free energies (BE) varying from -12.0 (1nm) to -34 (6nm)kcal/mol, while fG showed relatively less interaction with BE varying from -6.7 (1nm) to -11.1 (6nm)kcal/mol.	pg	64-66	P53	Homo sapiens	100-103
11479224-0	2001	Abrogation of the Chk1-mediated G(2) checkpoint pathway potentiates temozolomide-induced toxicity in a p53-independent manner in human glioblastoma cells.	Temozolomide	68-80	P53	Homo sapiens	103-106
29731965-10	2018	In this study, the presence of both TP53 mutation and 17p/TP53 deletion, but not the individual variants, was associated with poor prognosis in DLBCL patients after treatment with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) or similar regimens.	Prednisone	238-248	P53	Homo sapiens	36-40
29731965-10	2018	In this study, the presence of both TP53 mutation and 17p/TP53 deletion, but not the individual variants, was associated with poor prognosis in DLBCL patients after treatment with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) or similar regimens.	Prednisone	238-248	P53	Homo sapiens	58-62
28148293-8	2017	HE staining and the quantification of DNA content indicated a significantly higher proportion of polyploidy and aneuploidy cells in the TP53 mutant group than in the wild-type group (p &lt; 0.05).	Helium	0-2	P53	Homo sapiens	136-140
28272690-0	2017	Licorice and its active compound glycyrrhizic acid ameliorates cisplatin-induced nephrotoxicity through inactivation of p53 by scavenging ROS and overexpression of p21 in human renal proximal tubular epithelial cells.	Glycyrrhizic Acid	33-50	P53	Homo sapiens	120-123
29330202-6	2018	pN+ENE+ patients had the highest proportion of high-risk TP53 mutations.	pn+ene	0-6	P53	Homo sapiens	57-61
11479224-2	2001	We found previously that in p53-proficient human glioma cells, TMZ-induced futile DNA MMR resulted not in apoptosis but rather in prolonged, p53- and p21-associated G(2)-M arrest and senescence.	Temozolomide	63-66	P53	Homo sapiens	28-31
11479224-2	2001	We found previously that in p53-proficient human glioma cells, TMZ-induced futile DNA MMR resulted not in apoptosis but rather in prolonged, p53- and p21-associated G(2)-M arrest and senescence.	Temozolomide	63-66	P53	Homo sapiens	141-144
27254419-3	2017	Fisetin (25-100 muM) caused significant decrease in the levels of G1 phase cyclins and CDKs, and increased the levels of p53 and its S15 phosphorylation in gastric cancer cells.	fisetin	0-7	P53	Homo sapiens	121-124
11479224-9	2001	In addition to enhancing TMZ-induced cytotoxicity in p53-proficient cells, UCN-01 also blocked TMZ-induced Chk1 activation and transient G(2)-M arrest in p53-deficient U87MG-E6 cells and similarly enhanced TMZ-induced mitotic catastrophe and cell death.	Temozolomide	25-28	P53	Homo sapiens	53-56
11479224-9	2001	In addition to enhancing TMZ-induced cytotoxicity in p53-proficient cells, UCN-01 also blocked TMZ-induced Chk1 activation and transient G(2)-M arrest in p53-deficient U87MG-E6 cells and similarly enhanced TMZ-induced mitotic catastrophe and cell death.	Temozolomide	95-98	P53	Homo sapiens	154-157
27254419-7	2017	Fisetin-induced apoptosis was observed to be independent of p53.	fisetin	0-7	P53	Homo sapiens	60-63
29523159-7	2018	RESULTS: Triptolide inhibited cell proliferation and induced marked apoptosis in multiple HCC cell lines with different p53 status.	triptolide	9-19	P53	Homo sapiens	120-123
11479224-9	2001	In addition to enhancing TMZ-induced cytotoxicity in p53-proficient cells, UCN-01 also blocked TMZ-induced Chk1 activation and transient G(2)-M arrest in p53-deficient U87MG-E6 cells and similarly enhanced TMZ-induced mitotic catastrophe and cell death.	Temozolomide	95-98	P53	Homo sapiens	154-157
29185024-5	2018	Here we assessed SIRT1 function on fluoride-induced Ac-p53 formation using CRISPR/Cas9-mediated Sirt1 knockout (LS8Sirt/KO) cells or CRISPR/dCas9/SAM-mediated Sirt1 overexpressing (LS8Sirt1/over) cells.	Actinium	52-54	P53	Homo sapiens	55-58
11479224-11	2001	Furthermore, inhibition of the cytoprotective G(2) arrest pathway sensitizes cells to TMZ-induced cytotoxicity and may represent a novel, mechanism-based means of increasing TMZ efficacy in both p53 wild-type and p53 mutant glioma cells.	Temozolomide	86-89	P53	Homo sapiens	195-198
11479224-11	2001	Furthermore, inhibition of the cytoprotective G(2) arrest pathway sensitizes cells to TMZ-induced cytotoxicity and may represent a novel, mechanism-based means of increasing TMZ efficacy in both p53 wild-type and p53 mutant glioma cells.	Temozolomide	86-89	P53	Homo sapiens	213-216
27370399-3	2017	One such clinical-stage drug candidate, CBL0137, is a curaxin, small molecules which simultaneously downregulate nuclear factor-kappaB (NF-kB) and activate p53 by inactivating the chromatin remodeling complex, Facilitates Chromatin Transcription (FACT).	CBLC137	40-47	P53	Homo sapiens	156-159
11479224-11	2001	Furthermore, inhibition of the cytoprotective G(2) arrest pathway sensitizes cells to TMZ-induced cytotoxicity and may represent a novel, mechanism-based means of increasing TMZ efficacy in both p53 wild-type and p53 mutant glioma cells.	Temozolomide	174-177	P53	Homo sapiens	195-198
27370399-8	2017	CBL0137 induced loss of chromatin-unbound FACT, activated p53, inhibited NF-kB-dependent transcription, and was toxic to GBM cells.	CBLC137	0-7	P53	Homo sapiens	58-61
28081035-10	2017	p53, by preferential removal of purine over pyrimidine ribonucleotides, may affect the ribonucleotide mutation spectra produced by HIV-1 reverse transcriptase.	pyrimidine ribonucleotides	44-70	P53	Homo sapiens	0-3
29435010-5	2018	The inhibition of autophagy by CQ enhanced sunitinib-induced apoptosis, which was characterized by the activation of caspase-3, caspase-9, Bcl-2 and p53.	Sunitinib	43-52	P53	Homo sapiens	149-152
11479224-11	2001	Furthermore, inhibition of the cytoprotective G(2) arrest pathway sensitizes cells to TMZ-induced cytotoxicity and may represent a novel, mechanism-based means of increasing TMZ efficacy in both p53 wild-type and p53 mutant glioma cells.	Temozolomide	174-177	P53	Homo sapiens	213-216
28993998-8	2018	Also, an increase in pro-apoptotic p53 protein expression and a decrease in anti-apoptotic Bcl-2 protein expression were observed after LCA treatment of MCF-7 cells.	Lithocholic Acid	136-139	P53	Homo sapiens	35-38
27833016-0	2017	The small molecule 2-phenylethynesulfonamide induces covalent modification of p53.	2-phenylacetylenesulfonamide	19-44	P53	Homo sapiens	78-81
11445854-2	2001	Apoptotic inductions in MKN-45 and MKN-74 were stronger than those in MKN-28 and KATO-III, suggesting that wild-type p53 may contribute to the induction of apoptosis.	mkn-45	24-30	P53	Homo sapiens	117-120
27833016-2	2017	The small molecule 2-phenylethynesulfonamide (PES) was originally identified as the inhibitor of p53 effects on the mitochondrial death pathway.	2-phenylacetylenesulfonamide	19-44	P53	Homo sapiens	97-100
27833016-2	2017	The small molecule 2-phenylethynesulfonamide (PES) was originally identified as the inhibitor of p53 effects on the mitochondrial death pathway.	2-phenylacetylenesulfonamide	46-49	P53	Homo sapiens	97-100
27833016-3	2017	In this report we demonstrate that p53 protein from PES-treated cells was detected in reduced mobility bands between molecular weights 95-220 kDa.	2-phenylacetylenesulfonamide	52-55	P53	Homo sapiens	35-38
28578487-0	2018	Gambogic Acid Induces Cell Apoptosis and Inhibits MAPK Pathway in PTEN-/-/p53-/- Prostate Cancer Cells In Vitro and Ex Vivo.	gambogic acid	0-13	P53	Homo sapiens	74-77
28578487-16	2018	CONCLUSION: GA was a potent anti-tumor compound as for PTEN-/-/p53-/- PC, which contributed to cell apoptosis via inhibition of the MAPK pathway and c-fos.	gambogic acid	12-14	P53	Homo sapiens	63-66
11501666-7	2001	The level of thymine dimers decreased over time and was followed by a p53 response in the same cells.	Thymine	13-20	P53	Homo sapiens	70-73
29285650-10	2018	Furthermore, gemigliptin augments the inhibitory effect of metformin on proliferation and migration through involvement of matrix metalloproteinase-2, matrix metalloproteinase-9, p53, p21, VCAM-1, and ERK in thyroid carcinoma cells.	LC15-0444	13-24	P53	Homo sapiens	179-182
29378575-8	2018	CONCLUSION: DHA, Omegaven  and oxaliplatin were associated with downregulation of p53 and VEGF in both cells.	Oxaliplatin	31-42	P53	Homo sapiens	82-85
29259993-7	2017	Exposure to 3-O-L-AO caused upregulation of Bax and p53 and downregulation of survivin in NCI-H292 cells.	3-o-l-ao	12-20	P53	Homo sapiens	52-55
11350911-9	2001	Induction of wt p53 in these models led to a 3- and 2-fold increase in sensitivity to 1,3-bis(2-chloroethyl)-1-nitrosourea and temozolomide, respectively, which generate the MGMT-repairable O(6)-alkyl adducts in DNA.	Temozolomide	127-139	P53	Homo sapiens	16-19
28848088-6	2017	In the present paper we aim to characterize the combined effects of 64CuCl2 and SI113 on human GBM cell lines with variable p53 expression.	64cucl2	68-75	P53	Homo sapiens	124-127
21044462-9	2001	The different biological effect between 172Leu and 172His shows that some p53 variants such as 172 Arg-&gt;Leu may act as wild-type p53.	172his	51-57	P53	Homo sapiens	74-77
29174981-7	2018	Excitingly, Lys-104 (K104), a previously identified lysine acetylation site of TIP60 with unknown function, was observed to be indispensable for inducing p53-mediated apoptosis under low glucose condition.	DL-ETHIONINE	21-25	P53	Homo sapiens	154-157
21044462-9	2001	The different biological effect between 172Leu and 172His shows that some p53 variants such as 172 Arg-&gt;Leu may act as wild-type p53.	172his	51-57	P53	Homo sapiens	132-135
27698118-0	2016	Activation of SAT1 engages polyamine metabolism with p53-mediated ferroptotic responses.	Polyamines	27-36	P53	Homo sapiens	53-56
11280752-0	2001	p53 effects both the duration of G2/M arrest and the fate of temozolomide-treated human glioblastoma cells.	Temozolomide	61-73	P53	Homo sapiens	0-3
27698118-8	2016	Thus, our findings uncover a metabolic target of p53 involved in ferroptotic cell death and provide insight into the regulation of polyamine metabolism and ferroptosis-mediated tumor suppression.	Polyamines	131-140	P53	Homo sapiens	49-52
29515779-0	2018	Reversible LSD1 inhibition with HCI-2509 induces the p53 gene expression signature and disrupts the MYCN signature in high-risk neuroblastoma cells.	SP2509	32-40	P53	Homo sapiens	53-56
29515779-5	2018	HCI-2509 results in increased histone methyl marks and p53 levels along with cell cycle arrest in the G2/M phase and inhibition of colony formation of NGP cells.	SP2509	0-8	P53	Homo sapiens	55-58
29515779-6	2018	Our findings indicate that LSD1 inhibition with HCI-2509 has a multi-target effect in neuroblastoma cell lines, mediated in part via p53.	SP2509	48-56	P53	Homo sapiens	133-136
11139340-4	2001	beta-Lapachone, a topoisomerase inhibitor, increased KILLER/DR5 mRNA in colon cancer cell lines with wild-type p53 but not with mutant p53.	beta-lapachone	0-14	P53	Homo sapiens	111-114
30060809-8	2018	This complex relationship is based on several molecular mechanisms including the p53-dependent transcriptional regulation of enzymes in sphingolipid pathways, the activation of mutant p53 through ceramide-mediated alternative splicing, as well as modulation of the p53 function through direct and indirect effects on p53 coregulators and downstream targets.	Sphingolipids	136-148	P53	Homo sapiens	81-84
27554639-6	2016	Vitamin D3 can also inhibit cell proliferation by promoting p53 expression in ICC cells.	Cholecalciferol	0-10	P53	Homo sapiens	60-63
30108691-6	2017	At the molecular level, the pharmacological effect of DLC-carboranes is exerted through activation of the p53/p21 axis.	carboranes	58-68	P53	Homo sapiens	106-109
11139340-4	2001	beta-Lapachone, a topoisomerase inhibitor, increased KILLER/DR5 mRNA in colon cancer cell lines with wild-type p53 but not with mutant p53.	beta-lapachone	0-14	P53	Homo sapiens	135-138
27698449-9	2016	The results suggest that Cr(VI) has a role in premature senescence by promoting ROS-dependent p53 activation in L-02 hepatocytes.	chromium hexavalent ion	25-31	P53	Homo sapiens	94-97
11196182-2	2001	A specific missense mutation resulting from a guanine to thymine transversion at the third position of codon 249 in the p53 tumor suppressor gene has been reported in 10-70% of HCCs from areas of high dietary exposure to aflatoxin B1.	Thymine	57-64	P53	Homo sapiens	120-123
27569455-4	2016	Theanine and DTBrC completely suppressed HGF- and EGF+HGF-induced migration with a reduction of p53 tumor suppressor level and enhanced the p53 protein expression in HHC cells.	dtbrc	13-18	P53	Homo sapiens	96-99
27569455-4	2016	Theanine and DTBrC completely suppressed HGF- and EGF+HGF-induced migration with a reduction of p53 tumor suppressor level and enhanced the p53 protein expression in HHC cells.	dtbrc	13-18	P53	Homo sapiens	140-143
27622714-0	2016	Crocetin exploits p53-induced death domain (PIDD) and FAS-associated death domain (FADD) proteins to induce apoptosis in colorectal cancer.	crocetin	0-8	P53	Homo sapiens	18-21
30205729-0	2018	HMGB1 represses the anti-cancer activity of sunitinib by governing TP53 autophagic degradation via its nucleus-to-cytoplasm transport.	Sunitinib	44-53	P53	Homo sapiens	67-71
30205729-3	2018	Here we report that resistance to sunitinib therapy was driven by autophagic degradation of TP53/p53.	Sunitinib	34-43	P53	Homo sapiens	92-96
30205729-3	2018	Here we report that resistance to sunitinib therapy was driven by autophagic degradation of TP53/p53.	Sunitinib	34-43	P53	Homo sapiens	97-100
30205729-5	2018	Mechanistically, the transport of TP53 from the nucleus to the cytoplasm was essential for the sunitinib-induced autophagic degradation of TP53 and did not require TP53 nuclear export signals (NESs).	Sunitinib	95-104	P53	Homo sapiens	34-38
30205729-5	2018	Mechanistically, the transport of TP53 from the nucleus to the cytoplasm was essential for the sunitinib-induced autophagic degradation of TP53 and did not require TP53 nuclear export signals (NESs).	Sunitinib	95-104	P53	Homo sapiens	139-143
30205729-5	2018	Mechanistically, the transport of TP53 from the nucleus to the cytoplasm was essential for the sunitinib-induced autophagic degradation of TP53 and did not require TP53 nuclear export signals (NESs).	Sunitinib	95-104	P53	Homo sapiens	139-143
30205729-8	2018	Importantly, sunitinib induced the degradation of all TP53 proteins, except for TP53 proteins with mutations in the interaction domain of TP53 with HMGB1 (amino acids 313 to 352).	Sunitinib	13-22	P53	Homo sapiens	54-58
30205729-9	2018	In conclusion, our data identify an alternative HMGB1-mediated TP53 protein turnover mechanism that participates in the resistance of sunitinib and suggest HMGB1 as a potential therapeutic target for improving clinical outcomes of sunitinib.	Sunitinib	134-143	P53	Homo sapiens	63-67
30205729-9	2018	In conclusion, our data identify an alternative HMGB1-mediated TP53 protein turnover mechanism that participates in the resistance of sunitinib and suggest HMGB1 as a potential therapeutic target for improving clinical outcomes of sunitinib.	Sunitinib	231-240	P53	Homo sapiens	63-67
30207285-7	2018	Using this combined approach, we could identify 7 AAb-positive patients that were negative for CA-125 (concentrations below 35 IU/mL); this represents 26% of the p53 positive patients in the total population.	4-Aminoazobenzene	50-53	P53	Homo sapiens	162-165
27622714-4	2016	Here we have shown the effectiveness of crocetin, a dietary component, in inducing apoptosis of colon cancer cells with varying p53 status.	crocetin	40-48	P53	Homo sapiens	128-131
27551077-0	2016	2-Sulfonylpyrimidines: Mild alkylating agents with anticancer activity toward p53-compromised cells.	2-sulfonylpyrimidines	0-21	P53	Homo sapiens	78-81
27551077-3	2016	We found certain 2-sulfonylpyrimidines, including one named PK11007, to be mild thiol alkylators with anticancer activity in several cell lines, especially those with mutationally compromised p53.	2-sulfonylpyrimidines	17-38	P53	Homo sapiens	192-195
11220661-9	2001	Aflatoxin-related mutations at codon 249 of the p53 gene in plasma may be more relevant in this regard but their application requires further understanding of the temporal appearance of this biomarker in relation to the natural history of the disease.	Aflatoxins	0-9	P53	Homo sapiens	48-51
27461934-4	2016	In addition, by using caspase-3, caspase-8 and caspase-9 activity assays and western blot analysis, the anticancer effects of triptolide against osteosarcoma growth were found to involve activation of the DR-5/p53/Bax/caspase-9/ caspase-3 signaling pathway and the DR-5/FADD/caspase-8/lysosomal/cathepsin B/caspase-3 signaling pathway in the MG-63 cells.	triptolide	126-136	P53	Homo sapiens	210-213
29138869-3	2018	Mutated p53 in CRC was reported to be associated with resistance to commonly used chemotherapeutic agents including, 5-fluorouracil, oxaliplatin and irinotecan.	Oxaliplatin	133-144	P53	Homo sapiens	8-11
11384868-3	2001	The expression of p53 in T47D cells grown for 4-5 days in culture medium containing charcoal-treated (stripped) fetal bovine serum declined gradually to 10% of the level seen in control (whole serum, non charcoal-treated) groups.	Charcoal	84-92	P53	Homo sapiens	18-21
29151915-8	2017	Additionally, phloretin exhibited potent anticancer activity in vitro, as evidenced by the downregulation of the anti-apoptosis-associated molecule B-cell lymphoma 2 (bcl-2) and an increase in the levels of the apoptosis-associated molecules bcl-2-like protein 4 and tumor protein p53.	Phloretin	14-23	P53	Homo sapiens	281-284
27698914-3	2016	cDNA array performed on the control and CAPE-treated breast cancer cells revealed activation of DNA damage signaling involving upregulation of GADD45alpha and p53 tumor suppressor proteins.	caffeic acid phenethyl ester	40-44	P53	Homo sapiens	159-162
27698914-4	2016	Molecular docking analysis revealed that CAPE is capable of disrupting mortalin-p53 complexes.	caffeic acid phenethyl ester	41-45	P53	Homo sapiens	80-83
27698914-5	2016	We provide experimental evidence and demonstrate that CAPE induced disruption of mortalin-p53 complexes led to nuclear translocation and activation of p53 resulting in growth arrest in cancer cells.	caffeic acid phenethyl ester	54-58	P53	Homo sapiens	90-93
27698914-5	2016	We provide experimental evidence and demonstrate that CAPE induced disruption of mortalin-p53 complexes led to nuclear translocation and activation of p53 resulting in growth arrest in cancer cells.	caffeic acid phenethyl ester	54-58	P53	Homo sapiens	151-154
11128725-0	2000	Anaplastic changes associated with p53 gene mutation in differentiated thyroid carcinoma after insufficient radioactive iodine (131I) therapy.	radioactive iodine	108-126	P53	Homo sapiens	35-38
26794389-12	2016	The worst CSS was seen in pN+ patients with double negative p16 and p53 expression (8 vs. 34 months; P = .01).	thiocysteine	10-13	P53	Homo sapiens	68-71
28891579-2	2017	Here, we developed a highly sensitive and selective p53 gene assay based on the coupling of a triple-helix magnetic probe (THMP) to a fluorescent liposome hybridization assembly, a process initiated by rolling circle amplification (RCA).	tissue polypeptide specific antigen	123-127	P53	Homo sapiens	52-55
28891579-3	2017	In the presence of p53, the THMP unfolds and activates an enzymatic cleavage reaction, thus releasing the RCA primer and initiating the RCA product-assisted fluorescent liposome hybridization assembly.	tissue polypeptide specific antigen	28-32	P53	Homo sapiens	19-22
11128725-0	2000	Anaplastic changes associated with p53 gene mutation in differentiated thyroid carcinoma after insufficient radioactive iodine (131I) therapy.	Iodine-131	128-132	P53	Homo sapiens	35-38
28891579-5	2017	In the absence of p53, the THMP remains intact and blocks the trigger release and fluorescent liposome assembly, thus resulting in a low background signal.	tissue polypeptide specific antigen	27-31	P53	Homo sapiens	18-21
28891579-9	2017	The excellent capacity of the THMP to specifically detect the involved targets and the precise site-specific endonuclease cleavage ensured remarkable selectivity for p53 against single-base mismatches.	tissue polypeptide specific antigen	30-34	P53	Homo sapiens	166-169
27483224-1	2016	We previously reported that prenylated chalcone 2 (PC2), the O-prenyl derivative (2) of 2"-hydroxy-3,4,4",5,6"-pentamethoxychalcone (1), induced cytotoxicity of tumor cells via disruption of p53-MDM2 interaction.	4-Hydroxychalcone	39-49	P53	Homo sapiens	191-194
11128725-8	2000	Our results suggest that 131I therapy may be useful for patients with distant metastases, with or without p53 gene mutations, which show accumulation of 131I from tracer and therapeutic doses.	Iodine-131	25-29	P53	Homo sapiens	106-109
27465066-7	2016	The 120-day survival rate of rNDV-P53-treated mice was 75 %, survival rate of rNDV-treated mice was 12.5 %.	rndv	29-33	P53	Homo sapiens	34-37
29042910-0	2017	Tumoricidal activities of pterostilbene depend upon destabilizing the MTA1-NuRD complex and enhancing P53 acetylation in hepatocellular carcinoma.	pterostilbene	26-39	P53	Homo sapiens	102-105
11128725-8	2000	Our results suggest that 131I therapy may be useful for patients with distant metastases, with or without p53 gene mutations, which show accumulation of 131I from tracer and therapeutic doses.	Iodine-131	153-157	P53	Homo sapiens	106-109
11128725-9	2000	In contrast, 131I therapy is apparently not effective in patients who do not show sufficient accumulation of 131I, but rather, may cause early anaplastic changes with a p53 gene mutation.	Iodine-131	13-17	P53	Homo sapiens	169-172
27109893-9	2016	The oxidative stress generated in both PG and PGT conditions stabilised p53 by localising it in the nuclei of HeLa cells, which would have otherwise undergone HPV-mediated inactivation.	pg	39-41	P53	Homo sapiens	72-75
11061552-8	2000	Furthermore, 15deltaPGJ2, but not troglitazone, up-regulates p53 expression and promotes trophoblast apoptosis.	15-deoxy-delta(12,14)-prostaglandin J2	13-24	P53	Homo sapiens	61-64
27101738-9	2016	D5D knockdown along with DGLA treatment also enhanced the cytotoxicities of various chemotherapeutic drugs, including 5-fluorouracil, regorafenib, and irinotecan, potentially through the activation of pro-apoptotic proteins, e.g. p53 and caspase 9.	8,11,14-Eicosatrienoic Acid	25-29	P53	Homo sapiens	230-233
28843398-5	2017	Compared to the E6/E7 SP alone, E6/E7 SP with cisplatin treatment effectively restored TP53 and RB/E2F signaling and contributes to differences in cell fate, such as apoptosis or cell cycle arrest.	sp	38-40	P53	Homo sapiens	87-91
28765903-9	2017	Furthermore, the alterations in FN and p53 expression in response to TPA were prevented by a specific MEK inhibitor, UO126.	U 0126	117-122	P53	Homo sapiens	39-42
11048643-5	2000	The level of p53 protein in H460 cell was increased following DADS treatment.	diallyl disulfide	62-66	P53	Homo sapiens	13-16
29200721-10	2017	SUMMARY: Helichrysetin induced DNA damage in Ca Ski cellsDNA damage caused JNK-mediated phosphorylation of p53 resulting in p53-mediated apoptosisHelichrysetin is a potential DNA damage inducing agent through JNK activation to kill human cervical carcinoma cells.	helichrysetin	9-22	P53	Homo sapiens	107-110
29200721-10	2017	SUMMARY: Helichrysetin induced DNA damage in Ca Ski cellsDNA damage caused JNK-mediated phosphorylation of p53 resulting in p53-mediated apoptosisHelichrysetin is a potential DNA damage inducing agent through JNK activation to kill human cervical carcinoma cells.	helichrysetin	9-22	P53	Homo sapiens	124-127
27005777-11	2016	The expression level of TP53 increased when the Cr(VI)concentration above 5muM.	chromium hexavalent ion	48-54	P53	Homo sapiens	24-28
10911911-11	2000	By contrast, CIMP- cases evolve along a more classic genetic instability pathway, with a high rate of p53 mutations and chromosomal changes.	Cyclic IMP	13-17	P53	Homo sapiens	102-105
27004407-15	2016	Our study helps to elucidate the p53-independent regulatory function of MDM2 in Akt signaling, offering a novel view of the mechanism by which triptolide functions as an anticancer agent.	triptolide	143-153	P53	Homo sapiens	33-36
28878842-8	2017	GSK-343-treated cells displayed moderate expressional changes, with CCND1 increased in HPV-positive cell lines and decreased TP53 in HPV-negative SCC-1.	gsk	0-3	P53	Homo sapiens	125-129
10757806-5	2000	Although normal cells and wild-type p53-expressing tumor cells showed similar responses to actinomycin D and camptothecin treatment, the transcriptional activity of stabilized p53 induced by deferoxamine mesylate, which mimics hypoxia, in normal cells was lost in all three tumor cell lines tested.	Deferoxamine	191-212	P53	Homo sapiens	36-39
28743509-9	2017	We further evaluated p53 levels in the presence of cycloheximide (CHX) and the results showed that the p53 stabilization was regulated at post-translational level through blockage of its degradation.	Cycloheximide	51-64	P53	Homo sapiens	21-24
28743509-9	2017	We further evaluated p53 levels in the presence of cycloheximide (CHX) and the results showed that the p53 stabilization was regulated at post-translational level through blockage of its degradation.	Cycloheximide	51-64	P53	Homo sapiens	103-106
10757806-5	2000	Although normal cells and wild-type p53-expressing tumor cells showed similar responses to actinomycin D and camptothecin treatment, the transcriptional activity of stabilized p53 induced by deferoxamine mesylate, which mimics hypoxia, in normal cells was lost in all three tumor cell lines tested.	Deferoxamine	191-212	P53	Homo sapiens	176-179
28743509-9	2017	We further evaluated p53 levels in the presence of cycloheximide (CHX) and the results showed that the p53 stabilization was regulated at post-translational level through blockage of its degradation.	Cycloheximide	66-69	P53	Homo sapiens	21-24
28743509-9	2017	We further evaluated p53 levels in the presence of cycloheximide (CHX) and the results showed that the p53 stabilization was regulated at post-translational level through blockage of its degradation.	Cycloheximide	66-69	P53	Homo sapiens	103-106
26846469-7	2016	The results indicated that Dp treatment significantly inhibited cell proliferation in a dose- and time-dependent manner, and blocked cell cycle progression at the G1/S phase in the U87MG and T98G cells via the upregulation of p53 and p21 protein expression, and simultaneous downregulation of Cdc25A, Cdc2 and P-Cdc2 protein expression.	dracorhodin	27-29	P53	Homo sapiens	226-229
10639144-5	2000	By contrast, p53 mutations were found in 24% (10/41) of CIMP(+) CRCs vs. 60% (30/46) of CIMP(-) cases (P = 0.002).	Cyclic IMP	56-60	P53	Homo sapiens	13-16
26967735-3	2016	We demonstrate that Rb and p53 cooperate to metabolize the xenobiotic 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC).	3,5-diethoxycarbonyl-1,4-dihydrocollidine	70-111	P53	Homo sapiens	27-30
26967735-3	2016	We demonstrate that Rb and p53 cooperate to metabolize the xenobiotic 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC).	3,5-diethoxycarbonyl-1,4-dihydrocollidine	113-116	P53	Homo sapiens	27-30
27644130-9	2017	Our results suggest that in FAD lymphocytes, the p53-mediated increase in p21 transcription, together with a shift in the nucleocytoplasmic localization of p21, confers a survival advantage against 2dRib-induced apoptosis.	2drib	198-203	P53	Homo sapiens	49-52
10639144-5	2000	By contrast, p53 mutations were found in 24% (10/41) of CIMP(+) CRCs vs. 60% (30/46) of CIMP(-) cases (P = 0.002).	Cyclic IMP	88-92	P53	Homo sapiens	13-16
28656293-7	2017	Increased expression of apoptosis-related proteins (caspase-3, -8 and -9) and the changed levels of cell cycle checkpoint proteins (p27, p53 and cyclin A) further convinced of the anti-viability effect of barbaloin in A549 cells.	barbaloin	205-214	P53	Homo sapiens	137-140
26967735-7	2016	These findings provide strong evidence that synergistic functions of Rb and p53 are essential for metabolism of DDC.	3,5-diethoxycarbonyl-1,4-dihydrocollidine	112-115	P53	Homo sapiens	76-79
26967735-11	2016	Furthermore our results indicate that Rb and p53 not only function as tumor suppressors in response to carcinogenic injury, but also in response to non-carcinogenic injury such as DDC.	3,5-diethoxycarbonyl-1,4-dihydrocollidine	180-183	P53	Homo sapiens	45-48
10634809-8	2000	The antiapoptotic effect of agLDL was abrogated by a specific proteasome inhibitor, which also increased the half-life of p53 in monocytes.	agldl	28-33	P53	Homo sapiens	122-125
26850851-0	2016	Fenofibrate inhibited pancreatic cancer cells proliferation via activation of p53 mediated by upregulation of LncRNA MEG3.	Fenofibrate	0-11	P53	Homo sapiens	78-81
26850851-7	2016	Fenofibrate significantly inhibited proliferation of pancreatic cancer cells, increased MEG3 expression and p53 levels.	Fenofibrate	0-11	P53	Homo sapiens	108-111
26850851-10	2016	Our results indicated fenofibrate inhibited pancreatic cancer cells proliferation via activation of p53 mediated by upregulation of MEG3.	Fenofibrate	22-33	P53	Homo sapiens	100-103
28536076-6	2017	Here in this study we focus on the inhibitory effects of polyarginine and its analogues polyornithine, canavanine, and citrulline on the inhibition of p53 mutant peptide aggregation, and p53 mutant cancer cell proliferation inhibition in vitro.	Citrulline	119-129	P53	Homo sapiens	151-154
28536076-6	2017	Here in this study we focus on the inhibitory effects of polyarginine and its analogues polyornithine, canavanine, and citrulline on the inhibition of p53 mutant peptide aggregation, and p53 mutant cancer cell proliferation inhibition in vitro.	Citrulline	119-129	P53	Homo sapiens	187-190
28351773-6	2017	Glyphosate at 0.25 mM and 0.5 mM increased p53 promoter methylation, while it did not induce statistically significant changes in methylation of p16 promoter.	glyphosate	0-10	P53	Homo sapiens	43-46
10960967-6	2000	Finally, aflatoxins have been shown to induce specific mutations of the p53 tumor suppressor gene, thus pointing to the contribution of environmental factors to tumor development at the molecular level.	Aflatoxins	9-19	P53	Homo sapiens	72-75
28111262-0	2017	Dihydroartemisin inhibits glioma invasiveness via a ROS to P53 to beta-catenin signaling.	dihydroartemisin	0-16	P53	Homo sapiens	59-62
26833700-2	2016	We describe the first cellular synthesis of protein catenanes through the use of the p53 dimerization domain to guide the intertwining of two protein chains and SpyTag-SpyCatcher chemistry for efficient cyclization.	Catenanes	52-61	P53	Homo sapiens	85-88
10609655-9	1999	More significantly, intravenous administration of LipT-p53 markedly sensitized established SCCHN nude mouse xenograft tumors to radiotherapy.	lipt	50-54	P53	Homo sapiens	55-58
26563132-6	2016	In TP53- or ATM-defective CLL cells, inhibition of ATR signaling by AZD6738 led to an accumulation of unrepaired DNA damage, which was carried through into mitosis because of defective cell cycle checkpoints, resulting in cell death by mitotic catastrophe.	ceralasertib	68-75	P53	Homo sapiens	3-7
26563132-7	2016	Consequently, AZD6738 was selectively cytotoxic to both TP53- and ATM-defective CLL cell lines and primary cells.	ceralasertib	14-21	P53	Homo sapiens	56-60
26563132-8	2016	This was confirmed in vivo using primary xenograft models of TP53- or ATM-defective CLL, where treatment with AZD6738 resulted in decreased tumor load and reduction in the proportion of CLL cells with such defects.	ceralasertib	110-117	P53	Homo sapiens	61-65
26563132-9	2016	Moreover, AZD6738 sensitized TP53- or ATM-defective primary CLL cells to chemotherapy and ibrutinib.	ceralasertib	10-17	P53	Homo sapiens	29-33
28098861-0	2017	Triptolide inhibits viability and induces apoptosis in liver cancer cells through activation of the tumor suppressor gene p53.	triptolide	0-10	P53	Homo sapiens	122-125
28098861-4	2017	Western blot assay showed that treatment of HepG2 cells with 50 microM concentration of triptolide significantly induced phosphorylation of p53 in a 2 h-treatment.	triptolide	88-98	P53	Homo sapiens	140-143
28098861-6	2017	The level of nuclear p53 in a 6 h-treatment with 0, 10, 20, 30, 40 and 50 microM concentration of triptolide was found to be 15.3, 19.6, 28.5, 43.7, 63.8 and 91.5%, respectively.	triptolide	98-108	P53	Homo sapiens	21-24
28098861-7	2017	Treatment of HepG2 cells with triptolide at 50 microM concentration caused a significant increase in the binding potential of p53 to DNA.	triptolide	30-40	P53	Homo sapiens	126-129
28098861-10	2017	Treatment of HepG2 cells with p53 inhibitor, pifithrin-alpha prior to incubation with triptolide significantly prevented induction of cell apoptosis.	triptolide	86-96	P53	Homo sapiens	30-33
28098861-12	2017	In conclusion, triptolide inhibits viability and induces apoptosis in liver cancer cells through activation of the tumor suppressor gene p53.	triptolide	15-25	P53	Homo sapiens	137-140
10544021-6	1999	Although MDM2 protein was rapidly cleaved and degraded after anticancer drug treatment, cotreatment with caspase inhibitor Z-VAD blocked degradation, while wt p53 remained activated, suggesting MDM2 degradation not to be essential for the activation of p53.	z-vad	123-128	P53	Homo sapiens	253-256
26870698-7	2016	One of these molecules, APR-246, is a prodrug that is converted to the Michael acceptor methylene quinuclidinone (MQ) that binds covalently to cysteines in p53, leading to refolding and restoration of wild type p53 function.	SCHEMBL4738034	88-112	P53	Homo sapiens	156-159
26870698-7	2016	One of these molecules, APR-246, is a prodrug that is converted to the Michael acceptor methylene quinuclidinone (MQ) that binds covalently to cysteines in p53, leading to refolding and restoration of wild type p53 function.	SCHEMBL4738034	88-112	P53	Homo sapiens	211-214
28122359-5	2017	In AGS cells, we found that the oxaliplatin-inhibited tNOX effectively attenuated the NAD+/NADH ratio and reduced the deacetylase activity of an NAD+-dependent sirtuin 1, thereby enhancing p53 acetylation and apoptosis.	Oxaliplatin	32-43	P53	Homo sapiens	189-192
10535931-3	1999	Furthermore, treatment of human cells with the S(N)1 DNA methylators N-methyl-N-nitrosourea or N-methyl-N"-nitro-N-nitrosoguanidine results in p53 phosphorylation on serine residues 15 and 392, and these phosphorylation events depend on the presence of functional hMutSalpha and hMutLalpha.	Methylnitrosourea	69-91	P53	Homo sapiens	143-146
28119023-4	2017	Further study showed that khasuanine A was able to induce the apoptosis of PC3 cells by activation of caspase 3 and p53, and by inhibition of Bcl-2.	khasuanine A	26-38	P53	Homo sapiens	116-119
26735173-0	2016	Reactivation of wild-type and mutant p53 by tryptophanolderived oxazoloisoindolinone SLMP53-1, a novel anticancer small-molecule.	tryptophanolderived	44-63	P53	Homo sapiens	37-40
10537362-0	1999	Flavopiridol induces cell cycle arrest and p53-independent apoptosis in non-small cell lung cancer cell lines.	alvocidib	0-12	P53	Homo sapiens	43-46
26784898-1	2016	BACKGROUND/AIMS: Human SIRT1 is reported to be involved in tumorgenesis, mainly due to its modulating effect on p53 by deacetylation on lysine382.	lysine382	136-145	P53	Homo sapiens	112-115
27073720-9	2016	Interestingly, while knockdown of YAP had no effect on the ability of Verteporfin to induce 14-3-3sigma, p53 is required for this effect of Verteporfin.	Verteporfin	140-151	P53	Homo sapiens	105-108
27899303-0	2017	Gambogic acid counteracts mutant p53 stability by inducing autophagy.	gambogic acid	0-13	P53	Homo sapiens	33-36
27899303-6	2017	We demonstrated that GA may induce mutp53 degradation through autophagy in cancer cells expressing the p53-R280K (MDA-MB-231) and the p53-S241F (DLD1) proteins.	gambogic acid	21-23	P53	Homo sapiens	38-41
10537362-8	1999	Although flavopiridol resulted in the accumulation of p53 in A549 cells, flavopiridol-mediated apoptosis was p53 independent because it occurred to the same degree in A549 cells in which p53 was targeted for degradation by HPV16E6 expression.	alvocidib	9-21	P53	Homo sapiens	54-57
27899303-6	2017	We demonstrated that GA may induce mutp53 degradation through autophagy in cancer cells expressing the p53-R280K (MDA-MB-231) and the p53-S241F (DLD1) proteins.	gambogic acid	21-23	P53	Homo sapiens	103-106
26437226-4	2015	V158411 potentiated the cytotoxicity of gemcitabine, cisplatin, SN38 and camptothecin in a variety of p53 deficient human tumor cell lines in vitro, p53 proficient cells were unaffected.	V158411	0-7	P53	Homo sapiens	102-105
26437226-4	2015	V158411 potentiated the cytotoxicity of gemcitabine, cisplatin, SN38 and camptothecin in a variety of p53 deficient human tumor cell lines in vitro, p53 proficient cells were unaffected.	V158411	0-7	P53	Homo sapiens	149-152
28143426-0	2017	The marine triterpene glycoside frondoside A induces p53-independent apoptosis and inhibits autophagy in urothelial carcinoma cells.	frondoside A	32-44	P53	Homo sapiens	53-56
28143426-5	2017	The purpose of the current research is to investigate the anticancer effects and the mode of action of the marine triterpene glycoside frondoside A in p53-wild type and p53-deficient human urothelial carcinoma cells.	frondoside A	135-147	P53	Homo sapiens	151-154
28143426-5	2017	The purpose of the current research is to investigate the anticancer effects and the mode of action of the marine triterpene glycoside frondoside A in p53-wild type and p53-deficient human urothelial carcinoma cells.	frondoside A	135-147	P53	Homo sapiens	169-172
10537362-8	1999	Although flavopiridol resulted in the accumulation of p53 in A549 cells, flavopiridol-mediated apoptosis was p53 independent because it occurred to the same degree in A549 cells in which p53 was targeted for degradation by HPV16E6 expression.	alvocidib	73-85	P53	Homo sapiens	109-112
26520390-17	2015	Sarkar et al review summarized multifunctional roles of ASPP (apoptosis stimulating proteins of p53) family in cancer.	aspp	56-60	P53	Homo sapiens	96-99
10537362-8	1999	Although flavopiridol resulted in the accumulation of p53 in A549 cells, flavopiridol-mediated apoptosis was p53 independent because it occurred to the same degree in A549 cells in which p53 was targeted for degradation by HPV16E6 expression.	alvocidib	73-85	P53	Homo sapiens	109-112
10486243-4	1999	An in vitro study was carried out to determine whether p53 could be mutated at position 277 so that it binds preferentially to a sequence containing thymine or cytidine.	Thymine	149-156	P53	Homo sapiens	55-58
26490659-4	2015	This study aimed to evaluate the predictive significance of the serum p53 antibody status in metastatic colorectal cancer (mCRC) patients treated with fluoropyrimidine, oxaliplatin, plus bevacizumab as first-line chemotherapy.	Oxaliplatin	169-180	P53	Homo sapiens	70-73
28296564-1	2017	AZD1775 is a small molecule WEE1 inhibitor used in combination with DNA-damaging agents to cause premature mitosis and cell death in p53-mutated cancer cells.	adavosertib	0-7	P53	Homo sapiens	133-136
28296564-3	2017	AZD1775 significantly improved the cytotoxicity of 5-FU in a p53-mutated colorectal cancer cell line (HT29 cells), decreasing the IC50 from 9.3 muM to 3.5 muM.	adavosertib	0-7	P53	Homo sapiens	61-64
28296564-7	2017	In conclusion, AZD1775 enhances 5-FU cytotoxicity through increased DS-DNA breaks, not premature mitosis, in p53-mutated colorectal cancer cells.	adavosertib	15-22	P53	Homo sapiens	109-112
11104412-0	1999	Aflatoxin, Tobacco, Ammonia and the p53 Tumor-Suppressor Gene: Cancer"s Missing Link?	Aflatoxins	0-9	P53	Homo sapiens	36-39
26494474-6	2017	Also As2 O3 plus DTT upregulated Bax and Bak, downregulated Bcl-2 and p53, caused a loss of mitochondria membrane potential in oral cancer cells.	Dithiothreitol	17-20	P53	Homo sapiens	70-73
26356821-12	2015	In conclusion, this study demonstrated that DA induced autophagy in human oral cancer cells by modulating p53 expression, activating JNK1/2, and inhibiting Akt and p38.	dehydroandrographolide	44-46	P53	Homo sapiens	106-109
11104412-4	1999	Tobacco-related cancers, including those associated with ETS, often show the same p53 mutations associated with aflatoxin exposure.	Aflatoxins	112-121	P53	Homo sapiens	82-85
10341297-6	1999	Western blot analysis showed that auristatin-PE up-regulated the expression of wt-p53, p21WAF1 and Bax, and down-regulated Bcl-2 and cyclin B in HPAC cells, while only up-regulation of p21WAF1 and Bax was observed in PANC-1 cells.	auristatin	34-44	P53	Homo sapiens	82-85
27615555-0	2017	Targeting acute myeloid leukemia with TP53-independent vosaroxin.	vosaroxin	55-64	P53	Homo sapiens	38-42
27615555-1	2017	Vosaroxin is a quinolone compound that intercalates DNA and induces TP53-independent apoptosis, demonstrating activity against acute myeloid leukemia (AML) in Phase I-III trials.	vosaroxin	0-9	P53	Homo sapiens	68-72
26225749-3	2015	Data from the present study demonstrated that p53 knockdown or mutation has a negative effect on metformin or phenformin-induced growth inhibition, senescence and apoptosis in breast cancer cells.	Phenformin	110-120	P53	Homo sapiens	46-49
10334192-6	1999	Repair analysis of specific genomic sequences, at a single nucleotide resolution, revealed that the removal of cyclobutane pyrimidine dimers in a non-transcribed strand was significantly slower in p53-Mut and p53-Null cell lines compared with the normal p53-WT cells.	cyclobutane pyrimidine	111-133	P53	Homo sapiens	197-200
28117010-3	2017	Here in this study we focus on the inhibitory effects of cationic osmolyte molecules acetylcholine chloride, and choline on an aggregation prone 10 amino acid p53 mutant peptide WRPILTIITL, and the corresponding wildtype peptide RRPILTIITL in vitro.	Choline	91-98	P53	Homo sapiens	159-162
10334192-6	1999	Repair analysis of specific genomic sequences, at a single nucleotide resolution, revealed that the removal of cyclobutane pyrimidine dimers in a non-transcribed strand was significantly slower in p53-Mut and p53-Null cell lines compared with the normal p53-WT cells.	cyclobutane pyrimidine	111-133	P53	Homo sapiens	209-212
10334192-6	1999	Repair analysis of specific genomic sequences, at a single nucleotide resolution, revealed that the removal of cyclobutane pyrimidine dimers in a non-transcribed strand was significantly slower in p53-Mut and p53-Null cell lines compared with the normal p53-WT cells.	cyclobutane pyrimidine	111-133	P53	Homo sapiens	209-212
26238015-10	2015	S1PR1 positivity was correlated with shorter CSS in p53-positive T1HG carcinoma (P=0.003) in contrast to p53-negative T1HG carcinoma (P=0.205).	thiocysteine	45-48	P53	Homo sapiens	52-55
27998224-10	2016	Conclusion To our knowledge, this is the first report providing clinical proof that AZD1775 enhances carboplatin efficacy in TP53-mutated tumors.	adavosertib	84-91	P53	Homo sapiens	125-129
10334204-0	1999	The level of DNA modification by (+)-syn-(11S,12R,13S,14R)- and (-)-anti-(11R,12S,13S,14R)-dihydrodiol epoxides of dibenzo[a,l]pyrene determined the effect on the proteins p53 and p21WAF1 in the human mammary carcinoma cell line MCF-7.	dibenzo(a,l)pyrene	115-133	P53	Homo sapiens	172-175
25388787-1	2015	Two libraries of substituted benzimidazoles were designed using a "scaffold-hopping" approach based on reported MDM2-p53 inhibitors.	Benzimidazoles	29-43	P53	Homo sapiens	117-120
10334204-5	1999	(-)-anti-DB[a,l]PDE exhibited a higher binding efficiency that correlated with a significantly stronger p53 response at low concentrations of the dihydrodiol epoxides.	dihydrodiol epoxides	146-166	P53	Homo sapiens	104-107
10222137-2	1999	We show that addition of leptomycin B to human primary fibroblasts increased the levels of the p53 tumor suppressor protein.	leptomycin B	25-37	P53	Homo sapiens	95-98
25820822-3	2015	AFB1 can induce the mutations of genes such as tumor suppressor p53 through its metabolite AFB1-8,9-exo-epoxide, which acts as a mutagen to react with DNA.	afb1-8,9-exo-epoxide	91-111	P53	Homo sapiens	64-67
27941214-6	2016	Particularly, loading with BAPTA attenuated phosphorylation of the main DNA damage response members, including ATM, 53BP1 and H2A.X and reduced activation of the p53/p21/Rb pathway in H2O2-stimulated cells.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	27-32	P53	Homo sapiens	162-165
28105237-6	2016	Furthermore, xanthohumol treatment (40 microM) induced SCC4 cell apoptosis, as indicated by the significant increase in activity and expression of caspase-3, caspase-8, caspase-9, PARP, p53 and AIF.	xanthohumol	13-24	P53	Homo sapiens	186-189
28105237-8	2016	Taken together, the results of the present study indicated that xanthohumol mediates growth suppression and apoptosis induction, which was mediated via the suppression of Bcl-2 and Mcl-1 and activation of PARP, p53 and AIF signaling pathways.	xanthohumol	64-75	P53	Homo sapiens	211-214
27535334-4	2016	In a cohort of 93 breast cancer metastatic patients, cmDetect identified ctDNA mutations in 54% of the patients and recovered somatic mutations in cancer genes EGFR, PIK3CA, and TP53 We further showed that cmDetect detected ctDNA in 89% of patients with confirmed mutated cell-free tumor DNA by plasma analyses (n = 9) within 46 pan-cancer patients.	cmdetect	53-61	P53	Homo sapiens	178-182
27535334-4	2016	In a cohort of 93 breast cancer metastatic patients, cmDetect identified ctDNA mutations in 54% of the patients and recovered somatic mutations in cancer genes EGFR, PIK3CA, and TP53 We further showed that cmDetect detected ctDNA in 89% of patients with confirmed mutated cell-free tumor DNA by plasma analyses (n = 9) within 46 pan-cancer patients.	cmdetect	206-214	P53	Homo sapiens	178-182
26018087-4	2015	As a consequence of disturbed iron metabolism, archazolid caused S-phase arrest, double-stranded DNA breaks, and p53 stabilization, leading to apoptosis.	archazolid	47-57	P53	Homo sapiens	113-116
10222137-4	1999	Leptomycin B induced the accumulation of p53 and HDM2 in the nucleus and the appearance of discrete nuclear aggregates containing both proteins.	leptomycin B	0-12	P53	Homo sapiens	41-44
26184141-4	2015	In fact, CAPE is well documented as inducing cell death by inhibiting NFkappaB and by inducing pro-apoptotic pathways (i.e., p53).	caffeic acid phenethyl ester	9-13	P53	Homo sapiens	125-128
10222137-7	1999	Since HDM2 has recently been shown to contain a functional NES of the REV type, the most likely explanation for our results is that the effect of leptomycin B on HDM2 and p53 is due to the inhibition of nuclear export.	leptomycin B	146-158	P53	Homo sapiens	171-174
26184141-9	2015	Similarly to CAPE, analog compounds elicited p53 activation.	caffeic acid phenethyl ester	13-17	P53	Homo sapiens	45-48
26184141-11	2015	These results suggest that our new CAPE analog compounds may display the capacity to induce breast cancer apoptosis in a p53-dependent and/or independent manner.	caffeic acid phenethyl ester	35-39	P53	Homo sapiens	121-124
26184141-12	2015	These CAPE analogs could thus provide new therapeutic approaches for patients with varying genotypic signatures (such as p53 mutations) in a more specific and targeted fashion.	caffeic acid phenethyl ester	6-10	P53	Homo sapiens	121-124
27568863-0	2016	Subcellular mechanisms involved in apoptosis induced by aminoglycoside antibiotics: Insights on p53, proteasome and endoplasmic reticulum.	Aminoglycosides	56-70	P53	Homo sapiens	96-99
10321495-0	1999	Lithium attenuates p53 levels in human neuroblastoma SH-SY5Y cells.	Lithium	0-7	P53	Homo sapiens	19-22
10321495-2	1999	Because the tumor suppressor p53 is linked to cell death, we tested whether lithium administration to human neuroblastoma SH-SY5Y cells modulated the activation of p53.	Lithium	76-83	P53	Homo sapiens	164-167
27564099-9	2016	Moreover, pretreatment with U0126 suppressed curcumin and cisplatin-induced upregulation of p53, p21, and p-STAT3 and downregulation of survival proteins in both cells.	U 0126	28-33	P53	Homo sapiens	92-95
26146058-1	2015	OBJECTIVE: To investigate the role of apoptosis stimulating p53 binding protein 2 (ASPP2)-induced p53-dependent and p53-independent autophagy inhibition in apoptosis-promoting function of oxaliplatin (OXA).	Oxaliplatin	188-199	P53	Homo sapiens	60-63
10321495-5	1999	Pretreatment with 2 mM lithium for 1 or 14 days reduced the 25 microM H7-induced elevations of nuclear p53 by 40 and 70%, respectively, and even a 14-day pretreatment with 1 mM lithium caused a significant 16% reduction.	Lithium	23-30	P53	Homo sapiens	103-106
26146058-1	2015	OBJECTIVE: To investigate the role of apoptosis stimulating p53 binding protein 2 (ASPP2)-induced p53-dependent and p53-independent autophagy inhibition in apoptosis-promoting function of oxaliplatin (OXA).	Oxaliplatin	201-204	P53	Homo sapiens	60-63
10321495-6	1999	Since increased nuclear p53 is a critical intermediate step in many signaling processes that culminate in cell death, attenuation of p53 activation by lithium reveals a mechanism by which lithium may support neuronal survival.	Lithium	151-158	P53	Homo sapiens	133-136
27612029-0	2016	ATM/CHK/p53 Pathway Dependent Chemopreventive and Therapeutic Activity on Lung Cancer by Pterostilbene.	pterostilbene	89-102	P53	Homo sapiens	8-11
27612029-4	2016	Given that ATM/CHK signaling requires p53 for its biological effects, we hypothesized that p53 is required for the anticancer effect of pterostilbene.	pterostilbene	136-149	P53	Homo sapiens	38-41
10321495-6	1999	Since increased nuclear p53 is a critical intermediate step in many signaling processes that culminate in cell death, attenuation of p53 activation by lithium reveals a mechanism by which lithium may support neuronal survival.	Lithium	188-195	P53	Homo sapiens	133-136
27612029-4	2016	Given that ATM/CHK signaling requires p53 for its biological effects, we hypothesized that p53 is required for the anticancer effect of pterostilbene.	pterostilbene	136-149	P53	Homo sapiens	91-94
27612029-7	2016	Pterostilbene also activated ATM and CHK1/2, which are upstream of p53, in both cell lines, though pterostilbene-induced senescence was dependent on the presence of p53.	pterostilbene	0-13	P53	Homo sapiens	67-70
26158294-0	2015	p53 directly activates cystatin D/CST5 to mediate mesenchymal-epithelial transition: a possible link to tumor suppression by vitamin D3.	Cholecalciferol	125-135	P53	Homo sapiens	0-3
10374839-2	1999	An association has been detected between human exposure to aflatoxins, and mutations in the third base of codon 249 of the p53 gene in hepatomas.	Aflatoxins	59-69	P53	Homo sapiens	123-126
27612029-7	2016	Pterostilbene also activated ATM and CHK1/2, which are upstream of p53, in both cell lines, though pterostilbene-induced senescence was dependent on the presence of p53.	pterostilbene	99-112	P53	Homo sapiens	67-70
27612029-7	2016	Pterostilbene also activated ATM and CHK1/2, which are upstream of p53, in both cell lines, though pterostilbene-induced senescence was dependent on the presence of p53.	pterostilbene	99-112	P53	Homo sapiens	165-168
27612029-8	2016	Finally, pterostilbene more effectively inhibited p53-dependent cell proliferation compared to the other three stilbenoids.	pterostilbene	9-22	P53	Homo sapiens	50-53
27612029-9	2016	These results strongly support the potential chemopreventive effect of pterostilbene on p53-positive cells during early carcinogenesis.	pterostilbene	71-84	P53	Homo sapiens	88-91
10211969-9	1999	Quantification of the DNA content by Hoechst staining and computer-assisted image analysis showed that a fraction of the p53-positive blasts had a DNA content higher than 2N, indicating entry into the S/G2 phases.	hoechst	37-44	P53	Homo sapiens	121-124
27220476-7	2016	In GM, we report somatic mutations in KIT and TP53.	gm	3-5	P53	Homo sapiens	46-50
25283841-1	2015	AZD1775 targets the cell cycle checkpoint kinase Wee1 and potentiates genotoxic agent cytotoxicity through p53-dependent or -independent mechanisms.	adavosertib	0-7	P53	Homo sapiens	107-110
25283841-2	2015	Here, we report that AZD1775 interacted synergistically with histone deacetylase inhibitors (HDACIs, for example, Vorinostat), which interrupt the DNA damage response, to kill p53-wild type (wt) or -deficient as well as FLT3-ITD leukemia cells in association with pronounced Wee1 inhibition and diminished cdc2/Cdk1 Y15 phosphorylation.	adavosertib	21-28	P53	Homo sapiens	176-179
25434397-0	2015	Deoxycholic acid inhibits the growth of BGC-823 gastric carcinoma cells via a p53-mediated pathway.	Deoxycholic Acid	0-16	P53	Homo sapiens	78-81
10100719-4	1999	In contrast, DACH-acetato-Pt was considerably more active in wild-type p53 models (IC50, 0.17-1.5 microM) than it was in mutant or null models (IC50, 2.7-11.3 microM).	(diaminocyclohexane)(diacetato)(dichloro)platinum	13-28	P53	Homo sapiens	71-74
25434397-7	2015	In addition, the expression of p53, cyclin D1 and CDK2 was altered following DCA treatment.	Deoxycholic Acid	77-80	P53	Homo sapiens	31-34
25434397-8	2015	These results suggest that DCA induces apoptosis in gastric carcinoma cells through activation of an intrinsic mitochondrial-dependent pathway, in which p53 is involved.	Deoxycholic Acid	27-30	P53	Homo sapiens	153-156
27374783-5	2016	In addition, the good antitumor effects of CHO-PGEA and PI-PGEA were confirmed with suppressor tumor gene p53 systems in vitro and in vivo.	pgea	47-51	P53	Homo sapiens	106-109
10100719-5	1999	Inactivation of wild-type p53 function in OVCA-429 cells by the human papillomavirus type 16 (HPV 16) E6 plasmid increased resistance to DACH-acetato-Pt by 3-5-fold, which confirmed the drug"s dependence on wild-type p53 for its high cytotoxic potency.	(diaminocyclohexane)(diacetato)(dichloro)platinum	137-152	P53	Homo sapiens	26-29
10100719-6	1999	Differences between the two platinum agents were also evident in cell cycle studies: cisplatin arrested both wild-type and mutant p53 cells in G2-M, whereas DACH-acetato-Pt arrested wild-type p53 cells in G1 and mutant p53 cells in G2-M.	(diaminocyclohexane)(diacetato)(dichloro)platinum	157-172	P53	Homo sapiens	192-195
27537898-4	2016	In this study, we observed that the selected marine life-derived compounds (Chromomycin A2, Psammaplin A, and Ilimaquinone) induce expression of several autophagic signaling intermediates in human squamous cell carcinoma, glioblastoma, and colorectal carcinoma cells in vitro through a transcriptional regulation by tumor protein (TP)-p53 family members.	ilimaquinone	110-122	P53	Homo sapiens	335-338
10100719-6	1999	Differences between the two platinum agents were also evident in cell cycle studies: cisplatin arrested both wild-type and mutant p53 cells in G2-M, whereas DACH-acetato-Pt arrested wild-type p53 cells in G1 and mutant p53 cells in G2-M.	(diaminocyclohexane)(diacetato)(dichloro)platinum	157-172	P53	Homo sapiens	192-195
25789029-5	2015	The expression of p53 protein in the MM RPMI 8226 cells following treatment with curcumin was detected by western blotting and ELISA.	rpmi	40-44	P53	Homo sapiens	18-21
10100719-8	1999	In agreement with effects on cell cycle progression, a 2-h pulse exposure to low concentrations (&lt; or =25 microM) of DACH-acetato-Pt induced marked increases in p53 and p21Waf1/Cip1 expression in OVCA-429 cells.	(diaminocyclohexane)(diacetato)(dichloro)platinum	120-135	P53	Homo sapiens	164-167
25789029-7	2015	In the MM RPMI 8226 cells treated with curcumin, the expression of the p53 and Bax genes was upregulated, while the expression of the MDM2 gene was downregulated.	rpmi	10-14	P53	Homo sapiens	71-74
25789029-10	2015	In the MM RPMI 8226 cells treated with curcumin, p53 protein levels were upregulated, which suggested that curcumin may promote the apoptosis of MM cells by upregulating p53 protein expression.	rpmi	10-14	P53	Homo sapiens	49-52
27501149-0	2016	Minnelide/Triptolide Impairs Mitochondrial Function by Regulating SIRT3 in P53-Dependent Manner in Non-Small Cell Lung Cancer.	triptolide	10-20	P53	Homo sapiens	75-78
9891091-7	1999	Treatment of RKO cells with a tetracycline derivative, doxycycline, resulted in 15-fold-induced expression of TS protein and nearly complete suppression of p53 protein expression.	Doxycycline	55-66	P53	Homo sapiens	156-159
25789029-10	2015	In the MM RPMI 8226 cells treated with curcumin, p53 protein levels were upregulated, which suggested that curcumin may promote the apoptosis of MM cells by upregulating p53 protein expression.	rpmi	10-14	P53	Homo sapiens	170-173
9920731-4	1999	The topical application of 50 microg/cm2 BaP to EpiDerm resulted in the accumulation of BaP-DNA adducts and c-fos and p53 proteins as evidenced by immunohistochemical localization.	Benzo(a)pyrene	41-44	P53	Homo sapiens	118-121
25504633-2	2015	We found that cisplatin treatment of HNSCC cells with mutant TP53 leads to arrest of cells in the G2 phase of the cell cycle, leading us to hypothesize that the wee-1 kinase inhibitor MK-1775 would abrogate the cisplatin-induced G2 block and thereby sensitize isogenic HNSCC cells with mutant TP53 or lacking p53 expression to cisplatin.	adavosertib	184-191	P53	Homo sapiens	61-65
25504633-2	2015	We found that cisplatin treatment of HNSCC cells with mutant TP53 leads to arrest of cells in the G2 phase of the cell cycle, leading us to hypothesize that the wee-1 kinase inhibitor MK-1775 would abrogate the cisplatin-induced G2 block and thereby sensitize isogenic HNSCC cells with mutant TP53 or lacking p53 expression to cisplatin.	adavosertib	184-191	P53	Homo sapiens	293-297
25504633-2	2015	We found that cisplatin treatment of HNSCC cells with mutant TP53 leads to arrest of cells in the G2 phase of the cell cycle, leading us to hypothesize that the wee-1 kinase inhibitor MK-1775 would abrogate the cisplatin-induced G2 block and thereby sensitize isogenic HNSCC cells with mutant TP53 or lacking p53 expression to cisplatin.	adavosertib	184-191	P53	Homo sapiens	309-312
25504633-5	2015	Clonogenic survival analyses indicate that nanomolar concentration of MK-1775 sensitizes HNSCC cells with high-risk mutant p53 to cisplatin.	adavosertib	70-77	P53	Homo sapiens	123-126
25504633-6	2015	Consistent with its ability to chemosensitize, MK-1775 abrogated the cisplatin-induced G2 block in p53-defective cells leading to mitotic arrest associated with a senescence-like phenotype.	adavosertib	47-54	P53	Homo sapiens	99-102
27302066-1	2016	Our previous study suggested that ceramide synthase 6 (CerS6), an enzyme in sphingolipid biosynthesis, is regulated by p53: CerS6 was elevated in several cell lines in response to transient expression of p53 or in response to folate stress, which is known to activate p53.	Sphingolipids	76-88	P53	Homo sapiens	119-122
27302066-1	2016	Our previous study suggested that ceramide synthase 6 (CerS6), an enzyme in sphingolipid biosynthesis, is regulated by p53: CerS6 was elevated in several cell lines in response to transient expression of p53 or in response to folate stress, which is known to activate p53.	Sphingolipids	76-88	P53	Homo sapiens	204-207
27302066-1	2016	Our previous study suggested that ceramide synthase 6 (CerS6), an enzyme in sphingolipid biosynthesis, is regulated by p53: CerS6 was elevated in several cell lines in response to transient expression of p53 or in response to folate stress, which is known to activate p53.	Sphingolipids	76-88	P53	Homo sapiens	204-207
26733174-9	2016	The meta-analysis revealed a significantly statistical association of P53, ki67, and b-catenin with an increased risk of LNM in EGC patients (P53, OR = 1.81, p = 0.017; ki67, OR = 2.53, p = 0.0003; b-catenin, OR = 0.53, p = 0.01).	(-)-Epigallocatechin	128-131	P53	Homo sapiens	70-73
26733174-9	2016	The meta-analysis revealed a significantly statistical association of P53, ki67, and b-catenin with an increased risk of LNM in EGC patients (P53, OR = 1.81, p = 0.017; ki67, OR = 2.53, p = 0.0003; b-catenin, OR = 0.53, p = 0.01).	(-)-Epigallocatechin	128-131	P53	Homo sapiens	142-145
26733174-10	2016	Tumor size (&gt;=20 mm), the depth of invasion (submucosa), and P53 overexpression may be helpful predictors of LNM in EGC patients.	(-)-Epigallocatechin	119-122	P53	Homo sapiens	64-67
25504633-7	2015	Furthermore, MK-1775 enhanced the efficacy of cisplatin in vivo in tumors harboring TP53 mutations.	adavosertib	13-20	P53	Homo sapiens	84-88
25504633-8	2015	These results indicate that HNSCC cells expressing high-risk p53 mutations are significantly sensitized to cisplatin therapy by the selective wee-1 kinase inhibitor, supporting the clinical evaluation of MK-1775 in combination with cisplatin for the treatment of patients with TP53 mutant HNSCC.	adavosertib	204-211	P53	Homo sapiens	61-64
25504633-8	2015	These results indicate that HNSCC cells expressing high-risk p53 mutations are significantly sensitized to cisplatin therapy by the selective wee-1 kinase inhibitor, supporting the clinical evaluation of MK-1775 in combination with cisplatin for the treatment of patients with TP53 mutant HNSCC.	adavosertib	204-211	P53	Homo sapiens	277-281
27420968-0	2016	Effect of SNX-2112 on proliferation of esophageal cancer cells via regulation of excision repair cross-complementing 1, epidermal growth factor receptor, and p53 expression.	SNX 2112	10-18	P53	Homo sapiens	158-161
27420968-7	2016	We also observed a significant increase in ERCC1 expression, and decrease in p53 and EGFR expression, in EC-9706 cells treated with SNX-2112 (P &lt; 0.05), indicating the regulation of EC by SNX-2112.	SNX 2112	132-140	P53	Homo sapiens	77-80
27420968-9	2016	In summary, SNX-2112 inhibits the proliferation of EC cells by regulating the expression of ERCC1, EGFR, and p53.	SNX 2112	12-20	P53	Homo sapiens	109-112
25342596-6	2015	The Western blot analysis showed that the expression of Bcl-2 was noticeably decreased in response to britannin treatment, while the expression of Bax protein was increased, which were positively correlated with elevated expression of p53.	britannin	102-111	P53	Homo sapiens	235-238
9808574-5	1998	Exposure of CLL cells to 0.18 micromol/L of flavopiridol resulted in both decreased expression of p53 protein and cleavage of the caspase-3 zymogen 32-kD protein with the appearance of its 20-kD subunit.	alvocidib	44-56	P53	Homo sapiens	98-101
25510514-2	2015	In this study, the effects of two typical OPFRs (TCPP and TPhP) on p53 gene expression in human embryo liver L02 cells were determined by quantitative real-time PCR.	tetracarboxyphenylporphine	49-53	P53	Homo sapiens	67-70
27314292-10	2016	CONCLUSION: HER2 and P53 were identified as independent predictors for the response to mFOLFOX7 NACT in AGC.	mfolfox7 nact	87-100	P53	Homo sapiens	21-24
9813083-3	1998	The appearance of CTX-A-K63 in the Golgi induces a marked dispersion of Erd2p and p53 but not of the Golgi marker giantin.	ctx-a	18-23	P53	Homo sapiens	82-85
27183959-2	2016	In this paper, we found that miR-138 showed a pronounced increase after p53 activation in human non-small cell lung cancer (NSCLC) cells, which is mediated by p53 binding sites in the promoter region of its host gene, but this did not happen with rat and mouse cells.	mir-138	29-36	P53	Homo sapiens	72-75
27183959-2	2016	In this paper, we found that miR-138 showed a pronounced increase after p53 activation in human non-small cell lung cancer (NSCLC) cells, which is mediated by p53 binding sites in the promoter region of its host gene, but this did not happen with rat and mouse cells.	mir-138	29-36	P53	Homo sapiens	159-162
26996126-5	2016	Moreover, in wild-type p53-expressing cells, cisplatin mainly used the Bak-dependent apoptotic pathway, but this apoptotic pathway shifted to the Bax-dependent pathway by loss-of-function of p53.	bakuchiol	71-74	P53	Homo sapiens	23-26
25603347-0	2015	Activation of p53 with ilimaquinone and ethylsmenoquinone, marine sponge metabolites, induces apoptosis and autophagy in colon cancer cells.	ilimaquinone	23-35	P53	Homo sapiens	14-17
25603347-2	2015	Here, we used a cell-based reporter system for the detection of p53 response transcription to identify the marine sponge metabolites, ilimaquinone and ethylsmenoquinone, as activators of the p53 pathway.	ilimaquinone	134-146	P53	Homo sapiens	64-67
25603347-2	2015	Here, we used a cell-based reporter system for the detection of p53 response transcription to identify the marine sponge metabolites, ilimaquinone and ethylsmenoquinone, as activators of the p53 pathway.	ilimaquinone	134-146	P53	Homo sapiens	191-194
25603347-3	2015	We demonstrated that ilimaquinone and ethylsmenoquinone efficiently stabilize the p53 protein through promotion of p53 phosphorylation at Ser15 in both HCT116 and RKO colon cancer cells.	ilimaquinone	21-33	P53	Homo sapiens	82-85
25603347-3	2015	We demonstrated that ilimaquinone and ethylsmenoquinone efficiently stabilize the p53 protein through promotion of p53 phosphorylation at Ser15 in both HCT116 and RKO colon cancer cells.	ilimaquinone	21-33	P53	Homo sapiens	115-118
25603347-7	2015	Our findings suggest that ilimaquinone and ethylsmenoquinone exert their anti-cancer activity by activation of the p53 pathway and may have significant potential as chemo-preventive and therapeutic agents for human colon cancer.	ilimaquinone	26-38	P53	Homo sapiens	115-118
25446071-8	2015	DTT was able to reverse cadmium inhibition only for p53 and p73.	Dithiothreitol	0-3	P53	Homo sapiens	52-55
27004407-4	2016	We observed that triptolide inhibits MDM2 expression in human breast cancer cells with either wild-type or mutant p53.	triptolide	17-27	P53	Homo sapiens	114-117
9855010-9	1998	There was also a significant correlation between serum p53 protein levels and the cumulated benzo[a]pyrene exposure dose.	Benzo(a)pyrene	92-106	P53	Homo sapiens	55-58
26801686-3	2016	Therefore, the present study aimed to elucidate the impact of 15-deoxy-Delta(12,14)-PGJ2 (15d-PGJ2, a stable PGD2 degradation product) on cell death/cell survival pathways in p53-deficient MG-63 OS cells.	9-deoxy-delta-9-prostaglandin D2	83-88	P53	Homo sapiens	175-178
27085860-11	2016	CONCLUSIONS: Taken together, our results reveal that cationic LSN-mediated p53 gene delivery may have potential application as a non-viral vector-mediated breast cancer gene therapy due to its effective induction of apoptosis and tumor growth inhibition.	lsn	62-65	P53	Homo sapiens	75-78
25987034-11	2015	In the study, we report Cis-imidazoline derivative compound; Pubcid: 68870345 to have highest inhibitory potential in blocking MDM2-p53 interactions hitherto discovered.	cis-imidazoline	24-39	P53	Homo sapiens	132-135
26357513-8	2015	Bax/Bcl-2 expression ratio and expression of p53 were significantly lower in cells cocultured with alpha-mangostin and MPP(+).	mangostin	99-114	P53	Homo sapiens	45-48
25398514-6	2016	Bypass of the need for metabolic activation by treating cells with the corresponding reactive PAH-diol-epoxide metabolites resulted in similar adduct levels in all cell lines, which confirms that the influence of p53 is on the metabolism of the parent PAHs.	Epoxy Compounds	103-110	P53	Homo sapiens	213-216
10022218-7	1998	The immunoexpression of p53 protein (60%) and rate of K-ras point mutation (84%) were also higher in the PTAH-positive group.	Phenyltrimethylammonium hydroxide	105-109	P53	Homo sapiens	24-27
27109156-10	2016	Some of the polysaccharides may also influence tumorigenic pathways, such as Wnt and p53 to play their anti-tumor roles.	Polysaccharides	12-27	P53	Homo sapiens	85-88
25527123-11	2014	The activation of p53-p21 pathway by SC-III3 was also reversed by Ku55933 treatment.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	66-73	P53	Homo sapiens	18-21
9766444-6	1998	The differentiation response to transfected p53 with or without INF-gamma was inhibited by cyclic adenosine monophosphate (cAMP)-inducing agents (dibutyryl cyclic adenosine 3":5"-monophosphate, forskolin, and 3-isobutyl-1-methylxanthine) in a dose-dependent manner.	dibutyryl cyclic adenosine 3"	146-175	P53	Homo sapiens	44-47
10200513-0	1998	Differential p53 phosphorylation and activation of apoptosis-promoting genes Bax and Fas/APO-1 by irradiation and ara-C treatment.	Cytarabine	114-119	P53	Homo sapiens	13-16
25472472-6	2014	Rigosertib could markedly inhibit the activation of the Akt-PI3K and Wnt pathways, whereas it activated the SAPK/JNK and P53 pathways in high-grade MDS.	ON 01910	0-10	P53	Homo sapiens	121-124
26722046-6	2016	RESULTS: MCS-C3 induced appreciable caspase-dependent apoptosis associated with the significant up-regulation of p53-dependent p21(CIP1) in LNCaP cells.	mcs-c3	9-15	P53	Homo sapiens	113-116
26722046-9	2016	CONCLUSION: We identified that induction of intrinsic apoptosis in LNCaP cells by 6 muM MCS-C3 is associated not only with p53 activation but also with mediation of AR.	mcs-c3	88-94	P53	Homo sapiens	123-126
26722046-10	2016	In the present study, we identified the cellular functions and underlying molecular mechanisms of p53-dependent and AR-associated p21(CIP1) on apoptotic induction via direct binding to BCL2 in LNCaP cells treated with 6 muM MCS-C3.	mcs-c3	224-230	P53	Homo sapiens	98-101
26696550-7	2016	CONCLUSIONS: TP53 codon 72 polymorphisms was effective in predicting the response to chemotherapy and correlate with PFS and OS in patients with advanced gastric cancer treated with paclitaxel and capecitabine chemotherapy.	Capecitabine	197-209	P53	Homo sapiens	13-17
25330770-5	2014	Kinome screens identified eukaryotic elongation factor-2 kinase (eEF2K) inhibitors as more potent than PI3K/AKT/mTOR inhibitors on both mouse and human Pten/p53-deficient TNBC cells.	tnbc	171-175	P53	Homo sapiens	157-160
10200513-3	1998	Both irradiation and ara-C treatment resulted in apoptosis and induction of p53 proteins within hours.	Cytarabine	21-26	P53	Homo sapiens	76-79
10200513-10	1998	Using two-dimensional gel electrophoresis, we found that the p53 proteins in irradiated and ara-C-treated BV173 cells have different isoelectric points; they converged to a single isoelectric point after in vitro treatment with phosphatase.	Cytarabine	92-97	P53	Homo sapiens	61-64
26636375-3	2016	In the present study by using the specific inhibitors Ku55933 and Pifithrin-alpha, we confirmed implication of both ATM and p53 in H(2)O(2)-induced senescence of hMESCs.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	54-61	P53	Homo sapiens	124-127
9576849-10	1998	The induction of p53 by H2O2 was abolished by the iron chelator deferoxamine and the protein synthesis inhibitor cycloheximide.	Deferoxamine	64-76	P53	Homo sapiens	17-20
25282590-0	2014	Verbascoside promotes apoptosis by regulating HIPK2-p53 signaling in human colorectal cancer.	acteoside	0-12	P53	Homo sapiens	52-55
9607592-4	1998	Cells treated with the thymidylate synthase inhibitor 5-fluoro-2"-deoxyuridine (FdUrd) were used to study changes in various p53-associated gene expressions.	5-fluoro-2'-deoxyuridine	54-78	P53	Homo sapiens	125-128
25217394-8	2014	The therapeutic mechanism of the HSV-tk/GCV suicide gene system on human breast cancer cell line MCF-7 is probably by upregulating the expression of p21 through a p53-dependent DNA damage signalling pathway, leading the decrease of protein expression of PCNA, cyclin B, CDK1 in MCF-7 cells and promoting the cell cycle arrest at G1/S phase.	Ganciclovir	40-43	P53	Homo sapiens	163-166
24568186-3	2014	In the present work, we investigated the effects of HO-1 on the expression of p53 induced by 15-deoxy-Delta(12,14)-prostaglandin J2 (15d-PGJ2) in human breast cancer (MCF-7) cells.	9-deoxy-delta-9-prostaglandin D2	115-131	P53	Homo sapiens	78-81
26573436-9	2016	Furthermore, LJ12 induced tumor cell apoptosis and the protein expression of B cell lymphoma-2-associated X protein, caspase-3 and p53.	lj12	13-17	P53	Homo sapiens	131-134
26641105-2	2015	Site-specific synthesis of the C8-dG-ABA adduct in the oligodeoxynucleotide 5"-d(GTGCXTGTTTGT)-3":5"-d(ACAAACACGCAC)-3"; X = C8-dG-ABA adduct, including codons 272-275 of the p53 gene, has allowed for investigation into the structural and thermodynamic properties of this adduct.	c8-dg-aba	31-40	P53	Homo sapiens	175-178
9607592-4	1998	Cells treated with the thymidylate synthase inhibitor 5-fluoro-2"-deoxyuridine (FdUrd) were used to study changes in various p53-associated gene expressions.	5-fluoro-2'-deoxyuridine	80-85	P53	Homo sapiens	125-128
9548807-10	1998	Thiotepa, a non-quinone aziridine-containing agent, and 1,4-benzoquinone (p-BQ), a redox cycling quinone, increased p53 levels.	quinone	56-72	P53	Homo sapiens	116-119
26465677-0	2015	A Novel Platinum-Maurocalcine Conjugate Induces Apoptosis of Human Glioblastoma Cells by Acting through the ROS-ERK/AKT-p53 Pathway.	platinum-maurocalcine	8-29	P53	Homo sapiens	120-123
25135691-12	2014	Knock down study revealed that p53 is essential for loss of ZR751 cell viability induced by PE extract.	naphtha	92-94	P53	Homo sapiens	31-34
9548807-10	1998	Thiotepa, a non-quinone aziridine-containing agent, and 1,4-benzoquinone (p-BQ), a redox cycling quinone, increased p53 levels.	quinone	65-72	P53	Homo sapiens	116-119
9548807-13	1998	Moreover, the induction of p53 by AZQ requires both the quinone and the aziridine moieties of the AZQ molecule.	quinone	56-63	P53	Homo sapiens	27-30
9537326-6	1998	HIF-1alpha is found in p53 immunoprecipitates from MCF7 cells that express wild-type p53 and are either hypoxic or have been exposed to desferrioxamine.	Deferoxamine	136-151	P53	Homo sapiens	23-26
24862437-5	2014	The present work explores for the first time a new matrix of l-methionine-agarose to efficiently purify the supercoiled p53-encoding plasmid.	l-methionine-agarose	61-81	P53	Homo sapiens	120-123
26349782-5	2015	EMMQ caused transient elevation of p53 that assists in cytochrome c release, cleavage of downstream PARP and procaspase-3 and mitochondria-related apoptosis.	3-((7-ethyl-1H-indol-3-yl)-methyl)-2-methylquinoline	0-4	P53	Homo sapiens	35-38
26349782-10	2015	Given its small molecular weight acting as an effective p53 regulator in NSCLC cells, EMMQ could be an addition to the current list of lung cancer treatment.	3-((7-ethyl-1H-indol-3-yl)-methyl)-2-methylquinoline	86-90	P53	Homo sapiens	56-59
9544696-0	1998	The effect of heptachlor, a chlorinated hydrocarbon insecticide, on p53 tumor suppressor in human lymphocytes.	Heptachlor	14-24	P53	Homo sapiens	68-71
26287402-5	2015	A double-stranded synthetic miR-1285 mimic promoted SC viability, increased levels of ATP, and phosphorylated mammalian target of rapamycin (mTOR) and Skp2 mRNA and protein, whereas p53 and p27 expression decreased, and 17beta-estradiol-mediated effects on SCs were significantly attenuated.	mir-1285	28-36	P53	Homo sapiens	182-185
26518890-2	2015	Moreover, another molecule regulating wild-ype p53 function is ASPP (apoptosis stimulating proteins of p53) family.	aspp	63-67	P53	Homo sapiens	47-50
24974868-1	2014	For the first time, a new platform based on electrochemical growth of Au nanoparticles on aligned multi-walled carbon nanotubes (A-MWCNT) was developed for sensitive lable-free DNA detection of the TP53 gene mutation, one of the most popular genes in cancer research.	Gold	70-72	P53	Homo sapiens	198-202
24954315-6	2014	Moreover, KR22332 significantly reduced the protein expression levels of ataxia telangiectasia mutated protein, p53, and tumor necrosis factor (TNF)-alpha compared to significant increases observed after radiation treatment.	3-amino-3-(4-fluorophenyl)-1H-quinoline-2,4-dione	10-17	P53	Homo sapiens	112-115
26518890-2	2015	Moreover, another molecule regulating wild-ype p53 function is ASPP (apoptosis stimulating proteins of p53) family.	aspp	63-67	P53	Homo sapiens	103-106
9544696-3	1998	The ability of tumor promoters to suppress apoptosis prompted us to address the question of whether heptachlor is capable of effecting the expression of genes involved in lymphocyte apoptosis, in particular, the p53 tumor suppressor gene.	Heptachlor	100-110	P53	Homo sapiens	212-215
14646501-1	1998	A number of genotoxic chemicals and agents, such as benzo(a)pyrene and ultraviolet light, are able to induce nuclear accumulation of p53 protein.	Benzo(a)pyrene	52-66	P53	Homo sapiens	133-136
24814347-1	2014	Under conditions of genotoxic stress, human p53 activates the apoptotic effectors BAX or BAK to result in mitochondrial outer-membrane permeabilization and apoptosis.	bakuchiol	89-92	P53	Homo sapiens	44-47
23821376-10	2014	Patients with KRAS/NRAS, BRAF and TP53 wild-type tumours could derive the maximal benefits from treatment with cetuximab, oxaliplatin and UFT.	Oxaliplatin	122-133	P53	Homo sapiens	34-38
26297991-7	2015	The mechanisms involved in these effects of XN were associated with cell growth inhibition by induction of cell cycle arrest in the G1 phase, increased p53 and p21/WAF1 expression levels, downregulation of cyclin D1 and Bcl-2, and activation of caspases-9, -8, and -3.	xanthohumol	44-46	P53	Homo sapiens	152-155
24798859-5	2015	Here, we report that the environmental carcinogen benzo[a]pyrene (BaP) upregulated the expression of seven p53-targeting miRNAs (miR-25, miR-15a, miR-16, miR-92, miR-125b, miR-141, and miR-200a), while 2,3,7,8-tetrachlorodibenzo-rho-dioxin (TCDD) upregulated two of them (miR-25 and miR-92) in MM cells.	tetrachlorodibenzo-rho-dioxin	210-239	P53	Homo sapiens	107-110
24798859-8	2015	We found that (-)-epigallocatechin-3-gallate (EGCG), a constituent of green tea and a major component of the botanical drug Polyphenon  E, reduced the expression of four p53-targeting miRNAs, including miR-25, miR-92, miR-141, and miR-200a.	polyphenon E	124-137	P53	Homo sapiens	170-173
9472715-4	1998	Immunohistochemical detection of p53 protein showed positive cells in human skin after UV-irradiation, in mouse skin after benzo[a]pyrene treatment and in mouse spleen, thymus and bone after gamma-irradiation.	Benzo(a)pyrene	123-137	P53	Homo sapiens	33-36
26208523-6	2015	Oxaliplatin induced early p53 accumulation, upregulation of primary miR-34a transcript expression, and subsequent downregulation of E2F3 and E2F1.	Oxaliplatin	0-11	P53	Homo sapiens	26-29
26208523-9	2015	In addition to DUT-N, oxaliplatin repressed, in a p53-dependent manner, the expression of genes encoding enzymes involved in thymidylate biosynthesis.	Oxaliplatin	22-33	P53	Homo sapiens	50-53
26208523-10	2015	Consequently, oxaliplatin significantly decreased the level of dTTP in the dNTP pool in a p53-dependent manner.	Oxaliplatin	14-25	P53	Homo sapiens	90-93
26208523-11	2015	These data indicate that the DACH carrier ligand in oxaliplatin triggers signaling via the p53-miR-34a-E2F axis, leading to transcriptional regulation that ultimately results in accumulation of dUTP and reduced dTTP biosynthesis, potentially enhancing 5-FU cytotoxicity.	Oxaliplatin	52-63	P53	Homo sapiens	91-94
24444450-7	2014	The ACR-induced increases in the levels of p53 and pp53 in primary astrocytes could be attenuated by caffeine.	Caffeine	101-109	P53	Homo sapiens	43-46
9488246-9	1998	In some cancers, direct physical evidence exists identifying the p53 gene as a target of known environmental carcinogens such as UV light and benzolalpyrene in cancers of the skin and lung.	benzolalpyrene	142-156	P53	Homo sapiens	65-68
25241782-0	2014	[Phosphorylation status of ASPP2 modulates p53 apoptotic function in oxaliplatin-induced apoptosis of colorectal cancer HCT116 cells].	Oxaliplatin	69-80	P53	Homo sapiens	43-46
25241782-10	2014	These results indicate that phosphorylated ASPP2 promoted the oxaliplatin-induced apoptosis of HCT116 cells through a p53-dependent pathway.	Oxaliplatin	62-73	P53	Homo sapiens	118-121
25241782-12	2014	CONCLUSION: Phosphorylation status of ASPP2 modulates p53 apoptotic function in oxaliplatin-induced apoptosis of colorectal cancer HCT116 cells.	Oxaliplatin	80-91	P53	Homo sapiens	54-57
26363315-6	2015	Induction of p53 acetylation at lysine382 was involved in CPZ-mediated tumor apoptosis, and this induction was attenuated by sirtuin 1 (SIRT1), a class III histone deacetylase.	lysine382	32-41	P53	Homo sapiens	13-16
9383997-0	1997	UVB-induced cyclobutane pyrimidine dimer frequency correlates with skin cancer mutational hotspots in p53.	cyclobutane pyrimidine	12-34	P53	Homo sapiens	102-105
26141769-0	2015	Discovery of dihydroisoquinolinone derivatives as novel inhibitors of the p53-MDM2 interaction with a distinct binding mode.	CHEMBL1824269	13-34	P53	Homo sapiens	74-77
24885082-3	2014	In this study we aimed to investigate the functional role of this p53 acetylation in nutlin-sensitivity, and further to explore if nutlin-induced protein acetylation in general could indicate novel targets for the enhancement of nutlin-based therapy.	nutlin	85-91	P53	Homo sapiens	66-69
9315663-7	1997	Notably, the lack of pRB in these U937-derived clones renders these p53-null cells highly resistant to apoptosis induced by serum withdrawal, calphostin C, and ceramide.	calphostin C	142-154	P53	Homo sapiens	68-71
24615755-6	2014	In addition, DHR upregulated the cell cycle repressors p21 and p53.	1',2'-dihydrorotenone	13-16	P53	Homo sapiens	63-66
24615755-7	2014	DHR also increased the phosphorylation level of p53, suggesting the upregulated transactivation function of p53, which was confirmed by the induction of p21, a substrate of activated p53.	1',2'-dihydrorotenone	0-3	P53	Homo sapiens	48-51
24615755-7	2014	DHR also increased the phosphorylation level of p53, suggesting the upregulated transactivation function of p53, which was confirmed by the induction of p21, a substrate of activated p53.	1',2'-dihydrorotenone	0-3	P53	Homo sapiens	108-111
26177745-0	2015	Concentration-dependent differential effects of an epothilone analog on cell cycle and p53 signaling.	Epothilones	51-61	P53	Homo sapiens	87-90
26177745-4	2015	In the present study, we demonstrated that UTD1, a genetically engineered epothilone analog and a new microtubule inhibitor, activated p53 as a transcription factor at low concentrations demonstrated by its enhanced transcriptional activity and accumulation of p21, which led to cell cycle arrest.	Epothilones	74-84	P53	Homo sapiens	135-138
26177745-6	2015	These observations indicate that the epothilone analog has differential effects on intracellular signaling and implies that p53 plays different roles in cells exposed to different concentrations of the anticancer agent.	Epothilones	37-47	P53	Homo sapiens	124-127
24615755-7	2014	DHR also increased the phosphorylation level of p53, suggesting the upregulated transactivation function of p53, which was confirmed by the induction of p21, a substrate of activated p53.	1',2'-dihydrorotenone	0-3	P53	Homo sapiens	108-111
9171939-7	1997	Reverse transcriptase polymerase chain reaction analysis showed that AO induced a 2-fold increase in the levels of c-fos and p53 transcripts in comparison to RO which had no significant effect.	Acridine Orange	69-71	P53	Homo sapiens	125-128
26181851-0	2015	Discovery of a Dihydroisoquinolinone Derivative (NVP-CGM097): A Highly Potent and Selective MDM2 Inhibitor Undergoing Phase 1 Clinical Trials in p53wt Tumors.	CHEMBL1824269	15-36	P53	Homo sapiens	145-148
9111202-3	1997	Here we examine whether wild-type (wt) p53 protein suppresses X-ray-induced mutations using an isopropyl-beta-D-thiogalactopyranoside (IPTG)-regulated p53 expression system in human osteosarcoma Saos-2 cells.	Isopropyl Thiogalactoside	95-133	P53	Homo sapiens	151-154
26302043-8	2015	Early cellular effects activated by SB225002 included the up-regulation of GLIPR1, a p53-target gene shown to have pro-apoptotic activities in prostate and bladder cancer.	SB 225002	36-44	P53	Homo sapiens	85-88
26302043-13	2015	Inhibition of tubulin function with concurrent activation of the p53 pathway, in particular, its downstream target GLIPR1, seems to underlie the anti-leukemic effect of SB225002.	SB 225002	169-177	P53	Homo sapiens	65-68
24634414-6	2014	We show for the first time that OXA and 5-FU induce higher levels of intracellular labile zinc, as measured using the fluorescent probe FLUOZIN-3, and that such zinc contributes to the activation of p53 and repression of NF-kappaB.	Oxaliplatin	32-35	P53	Homo sapiens	199-202
24626782-7	2014	PL increased the phosphorylated p53 protein levels (active form) in whole-cell lysates and the nuclei of the cells.	Pyridoxal	0-2	P53	Homo sapiens	32-35
26171006-5	2015	DP significantly inhibited the growth of SK-MES-1 cells by inducing apoptosis and G1/G0 cell cycle arrest in a dose-dependent manner via activation of p53 (P&lt;0.05).	dracorhodin	0-2	P53	Homo sapiens	151-154
9111202-3	1997	Here we examine whether wild-type (wt) p53 protein suppresses X-ray-induced mutations using an isopropyl-beta-D-thiogalactopyranoside (IPTG)-regulated p53 expression system in human osteosarcoma Saos-2 cells.	Isopropyl Thiogalactoside	135-139	P53	Homo sapiens	151-154
24380881-5	2014	The inhibition of HO-1 activity obtained by Zinc (II) protoprophyrin IX (ZnPPIX) was able to significantly increase the pro-apoptotic effect of BTZ in a p53- and p21-independent way.	zinc (ii) protoprophyrin ix	44-71	P53	Homo sapiens	153-156
9111202-5	1997	Furthermore, arrest at the G/S boundary was induced by X-ray irradiation when p53 protein was expressed by treatment with IPTG.	Isopropyl Thiogalactoside	122-126	P53	Homo sapiens	78-81
26835380-8	2015	Moreover, polyamine depletion regimens exert potent anti-tumor activity in pre-clinical models of established neuroblastoma as well, in combination with numerous chemotherapeutic agents and even in tumors with unfavorable genetic features such as MYCN, ALK or TP53 mutation.	Polyamines	10-19	P53	Homo sapiens	260-264
9189703-0	1997	Hepatocellular carcinoma p53 G &gt; T transversions at codon 249: the fingerprint of aflatoxin exposure?	Aflatoxins	85-94	P53	Homo sapiens	25-28
26041883-5	2015	Tetraiodothyroacetic acid (tetrac) is a T4 derivative that, in a model of resveratrol-induced p53-dependent apoptosis in glioma cells, blocks the anti-apoptotic action of thyroid hormone, permitting specific serine phosphorylation of p53 and apoptosis to proceed.	tetraiodothyroacetic acid	0-25	P53	Homo sapiens	94-97
9189703-7	1997	Patients from areas with high aflatoxin levels were more likely to have p53 mutations than were patients from areas with low aflatoxin levels.	Aflatoxins	30-39	P53	Homo sapiens	72-75
26041883-5	2015	Tetraiodothyroacetic acid (tetrac) is a T4 derivative that, in a model of resveratrol-induced p53-dependent apoptosis in glioma cells, blocks the anti-apoptotic action of thyroid hormone, permitting specific serine phosphorylation of p53 and apoptosis to proceed.	tetraiodothyroacetic acid	0-25	P53	Homo sapiens	234-237
26041883-5	2015	Tetraiodothyroacetic acid (tetrac) is a T4 derivative that, in a model of resveratrol-induced p53-dependent apoptosis in glioma cells, blocks the anti-apoptotic action of thyroid hormone, permitting specific serine phosphorylation of p53 and apoptosis to proceed.	tetraiodothyroacetic acid	27-33	P53	Homo sapiens	94-97
26041883-5	2015	Tetraiodothyroacetic acid (tetrac) is a T4 derivative that, in a model of resveratrol-induced p53-dependent apoptosis in glioma cells, blocks the anti-apoptotic action of thyroid hormone, permitting specific serine phosphorylation of p53 and apoptosis to proceed.	tetraiodothyroacetic acid	27-33	P53	Homo sapiens	234-237
9189703-8	1997	In the group with p53 mutations, patients from areas with high aflatoxin levels had higher proportions of mutations with codon 249 G &gt; T transversions.	Aflatoxins	63-72	P53	Homo sapiens	18-21
9189703-10	1997	Aflatoxin may increase the proportion of p53 mutations by causing a single mutation, the codon 249 G &gt; T transversion, thus explaining some of the excess liver cancer associated with aflatoxin exposure.	Aflatoxins	0-9	P53	Homo sapiens	41-44
9189703-10	1997	Aflatoxin may increase the proportion of p53 mutations by causing a single mutation, the codon 249 G &gt; T transversion, thus explaining some of the excess liver cancer associated with aflatoxin exposure.	Aflatoxins	186-195	P53	Homo sapiens	41-44
18726304-1	1997	Human mutant-type (mt) p53 cDNA was synthesized and cloned from human lung cancer cell line GL containing mt-p53 gene by using polymerase chain reaction (PCR).	glycylleucine	92-94	P53	Homo sapiens	23-26
25650067-0	2015	Resistance exercise with low glycogen increases p53 phosphorylation and PGC-1alpha mRNA in skeletal muscle.	Glycogen	29-37	P53	Homo sapiens	48-51
25650067-11	2015	CONCLUSION: Undertaking resistance exercise with low glycogen availability may enhance mitochondrial-related adaptations through p53 and PGC-1alpha-mediated signalling.	Glycogen	53-61	P53	Homo sapiens	129-132
18726304-1	1997	Human mutant-type (mt) p53 cDNA was synthesized and cloned from human lung cancer cell line GL containing mt-p53 gene by using polymerase chain reaction (PCR).	glycylleucine	92-94	P53	Homo sapiens	109-112
9032539-6	1997	Although there was a wide scatter of 2cDI and 5cER values between p53 positive and negative RCCs, the RCC with positive p53 exhibited significantly higher values in 2cDI as well as 5cER, as compared to that with negative p53 (p &lt; 0.02 and p &lt; 0.005, respectively).	2cdi	165-169	P53	Homo sapiens	120-123
25358520-7	2015	TP53 P1 promoter was found to be in an open chromatin state, with a relatively high enrichment of H4Ac and similar TP53 transcription levels in all 21 T cell lines.	h4ac	98-102	P53	Homo sapiens	0-4
25359126-5	2015	PD-AgNP-mediated apoptosis in CRCs is a p53 dependent process involving ROS and JNK cascade.	pd-agnp	0-7	P53	Homo sapiens	40-43
9032539-6	1997	Although there was a wide scatter of 2cDI and 5cER values between p53 positive and negative RCCs, the RCC with positive p53 exhibited significantly higher values in 2cDI as well as 5cER, as compared to that with negative p53 (p &lt; 0.02 and p &lt; 0.005, respectively).	2cdi	165-169	P53	Homo sapiens	120-123
8900110-2	1996	The present studies demonstrate that the antimetabolite 1-beta-D-arabinofuranosylcytosine (ara-C) induces binding of c-Abl and p53.	Cytarabine	91-96	P53	Homo sapiens	127-130
25788262-0	2015	Caffeic acid phenethyl ester induced cell cycle arrest and growth inhibition in androgen-independent prostate cancer cells via regulation of Skp2, p53, p21Cip1 and p27Kip1.	caffeic acid phenethyl ester	0-28	P53	Homo sapiens	147-150
8900110-3	1996	Ara-C treatment of cells that express wild type or a dominant negative, kinase-inactive c-Abl(K-R) was associated with formation of c-Abl-p53 complexes and increased expression of the cyclin-dependent kinase (Cdk) inhibitor p21.	Cytarabine	0-5	P53	Homo sapiens	138-141
25788262-6	2015	Overexpression of Skp2, or siRNA knockdown of p21Cip1, p27Kip1, or p53 blocked suppressive effect of CAPE treatment.	caffeic acid phenethyl ester	101-105	P53	Homo sapiens	67-70
8895489-1	1996	Human lung cancer exhibits a high frequency of transversion mutations at G:C base pairs of the p53 gene, possibly the result of DNA damage by cigarette smoke constituents, most notably benzo[a]pyrene.	Benzo(a)pyrene	185-199	P53	Homo sapiens	95-98
25788262-8	2015	Our finding suggested that CAPE treatment induced cell cycle arrest and growth inhibition in CRPC cells via regulation of Skp2, p53, p21Cip1, and p27Kip1.	caffeic acid phenethyl ester	27-31	P53	Homo sapiens	128-131
8676917-0	1996	p53 accumulates in micronuclei after treatment with a DNA breaking chemical, methylnitrosourea, and with the spindle poison, vinblastine.	Methylnitrosourea	77-94	P53	Homo sapiens	0-3
25184957-8	2015	Finally, the GLO1 regulation of SCC-13 cells might be relevant to methylglyoxal-induced p53 translocation.	Pyruvaldehyde	66-79	P53	Homo sapiens	88-91
8640905-0	1996	An aflatoxin-associated mutational hotspot at codon 249 in the p53 tumor suppressor gene occurs in hepatocellular carcinomas from Mexico.	Aflatoxins	3-12	P53	Homo sapiens	63-66
25647416-4	2015	While contribution from the p53CON to the stability of the p53-DNA complexes was detected between 100 and 170 mM KCl, p53 complexes with circular DNAs (but not linear) exhibited considerable resistance towards salt treatment for KCl concentrations as high as 2 M provided that the p53 basic C-terminal DNA binding site (CTDBS) was available for DNA binding.	Potassium Chloride	113-116	P53	Homo sapiens	28-31
25647416-4	2015	While contribution from the p53CON to the stability of the p53-DNA complexes was detected between 100 and 170 mM KCl, p53 complexes with circular DNAs (but not linear) exhibited considerable resistance towards salt treatment for KCl concentrations as high as 2 M provided that the p53 basic C-terminal DNA binding site (CTDBS) was available for DNA binding.	Potassium Chloride	113-116	P53	Homo sapiens	59-62
25647416-4	2015	While contribution from the p53CON to the stability of the p53-DNA complexes was detected between 100 and 170 mM KCl, p53 complexes with circular DNAs (but not linear) exhibited considerable resistance towards salt treatment for KCl concentrations as high as 2 M provided that the p53 basic C-terminal DNA binding site (CTDBS) was available for DNA binding.	Potassium Chloride	113-116	P53	Homo sapiens	59-62
25647416-4	2015	While contribution from the p53CON to the stability of the p53-DNA complexes was detected between 100 and 170 mM KCl, p53 complexes with circular DNAs (but not linear) exhibited considerable resistance towards salt treatment for KCl concentrations as high as 2 M provided that the p53 basic C-terminal DNA binding site (CTDBS) was available for DNA binding.	Potassium Chloride	113-116	P53	Homo sapiens	59-62
25647416-5	2015	On the contrary, when the CTDBS was blocked by antibody used for immunoprecipitation, all p53-DNA complexes were completely dissociated from the p53 protein in KCl concentrations&gt;=200 mM under the same conditions.	Potassium Chloride	160-163	P53	Homo sapiens	90-93
25647416-5	2015	On the contrary, when the CTDBS was blocked by antibody used for immunoprecipitation, all p53-DNA complexes were completely dissociated from the p53 protein in KCl concentrations&gt;=200 mM under the same conditions.	Potassium Chloride	160-163	P53	Homo sapiens	145-148
25584615-1	2015	Crocin, a bioactive molecule of saffron, inhibited proliferation of both HCT116 wild-type and HCT116 p53(-/-) cell lines at a concentration of 10 mM.	crocin	0-6	P53	Homo sapiens	101-104
8590632-1	1995	Deferoxamine (DFO)-induced iron deprivation caused an increase in p53 expression in ML-1 and Raji cells.	Deferoxamine	0-12	P53	Homo sapiens	66-69
8590632-1	1995	Deferoxamine (DFO)-induced iron deprivation caused an increase in p53 expression in ML-1 and Raji cells.	Deferoxamine	14-17	P53	Homo sapiens	66-69
26189254-7	2015	Significant pathways were determined to be p53 signaling pathway, amino sugar, and nucleotide sugar metabolism.	Amino Sugars	66-77	P53	Homo sapiens	43-46
8590632-2	1995	In ML-1 cells, with express wild type p53, p53 protein levels were transiently increased 6 h after addition of 10(-4)M DFO.	Deferoxamine	119-122	P53	Homo sapiens	38-41
8590632-2	1995	In ML-1 cells, with express wild type p53, p53 protein levels were transiently increased 6 h after addition of 10(-4)M DFO.	Deferoxamine	119-122	P53	Homo sapiens	43-46
8590632-3	1995	In Raji cells, which carry a mutant p53 allele, p53 increased 6 h after addition of 10(-4)M DFO and remained elevated for 24 h. Growth inhibition was observed in both cell types 6 h after addition of 10(-4)M DFO.	Deferoxamine	92-95	P53	Homo sapiens	36-39
8590632-3	1995	In Raji cells, which carry a mutant p53 allele, p53 increased 6 h after addition of 10(-4)M DFO and remained elevated for 24 h. Growth inhibition was observed in both cell types 6 h after addition of 10(-4)M DFO.	Deferoxamine	92-95	P53	Homo sapiens	48-51
8590632-3	1995	In Raji cells, which carry a mutant p53 allele, p53 increased 6 h after addition of 10(-4)M DFO and remained elevated for 24 h. Growth inhibition was observed in both cell types 6 h after addition of 10(-4)M DFO.	Deferoxamine	208-211	P53	Homo sapiens	36-39
8590632-3	1995	In Raji cells, which carry a mutant p53 allele, p53 increased 6 h after addition of 10(-4)M DFO and remained elevated for 24 h. Growth inhibition was observed in both cell types 6 h after addition of 10(-4)M DFO.	Deferoxamine	208-211	P53	Homo sapiens	48-51
25949267-8	2015	Taken together, these findings indicate that xanthohumol-induced cell death might involve intrinsic and extrinsic apoptotic pathways, as well as downregulation of XIAP, upregulation of p53 proteins, and S phase cell cycle arrest in Ca Ski cervical cancer cells.	xanthohumol	45-56	P53	Homo sapiens	185-188
8541111-4	1995	The detection of p53 in a relatively high percentage of the HCC cases in Hungary, a country in which aflatoxin contamination of the diet is rare, suggests that factors other than aflatoxin led to the accumulation or overexpression of p53 in these patients.	Aflatoxins	101-110	P53	Homo sapiens	17-20
25505253-15	2015	Cell lines established from recurrent, AZD1208-resistant tumors again revealed downregulation of the p53 pathway.	AZD1208	39-46	P53	Homo sapiens	101-104
25505253-16	2015	Irradiated AZD1208-treated tumors robustly upregulated p53, providing a possible mechanistic explanation for the effectiveness of combination therapy.	AZD1208	11-18	P53	Homo sapiens	55-58
7557882-1	1995	The p53 gene is frequently mutated in human tumors; in hepatocellular carcinomas, there is a high frequency of a specific mutation at codon 249 in regions with significant aflatoxin exposure.	Aflatoxins	172-181	P53	Homo sapiens	4-7
7554063-0	1995	p53 protein expression is correlated with benzo[a]pyrene-DNA adducts in carcinoma cell lines.	Benzo(a)pyrene	42-56	P53	Homo sapiens	0-3
25260383-6	2014	Our results demonstrated that deoxyelephantopin-induced G2/M phase arrest was associated with a marked increase in the levels of p53 and p21 and a decrease in phospho-signal transducer and activator of transcription 3 (pSTAT3-Tyr705), cyclin-dependent kinase 1 (cdc2), and cyclin B1.	deoxyelephantopin	30-47	P53	Homo sapiens	129-132
7554063-2	1995	We have measured benzo[a]pyrene (BP)-induced DNA damage in association with p53 expression.	Benzo(a)pyrene	17-31	P53	Homo sapiens	76-79
25260383-9	2014	Our findings provided the first evidence that STAT3/p53/p21 signaling, MAPK pathway, PI3k/Akt/mTOR pathway, caspase cascades, and ROS play critical roles in deoxyelephantopin-induced G2/M phase arrest and apoptosis of SiHa cells.	deoxyelephantopin	157-174	P53	Homo sapiens	52-55
7554063-2	1995	We have measured benzo[a]pyrene (BP)-induced DNA damage in association with p53 expression.	Benzo(a)pyrene	33-35	P53	Homo sapiens	76-79
7554063-4	1995	Activation of BP in A-549 lung carcinoma and MCF-7 breast adenocarcinoma cell lines containing wild-type p53 was followed by an increase in p53 protein expression.	Benzo(a)pyrene	14-16	P53	Homo sapiens	105-108
7554063-4	1995	Activation of BP in A-549 lung carcinoma and MCF-7 breast adenocarcinoma cell lines containing wild-type p53 was followed by an increase in p53 protein expression.	Benzo(a)pyrene	14-16	P53	Homo sapiens	140-143
25474278-1	2014	PURPOSE: The aim of this study was to evaluate the prognostic value of MSI-H and p53 overexpression in metastatic colorectal cancer (mCRC) treated with oxaliplatin and fluoropyrimidine-based first line chemotherapy.	Oxaliplatin	152-163	P53	Homo sapiens	81-84
7554063-8	1995	These findings indicate that p53 protein is part of the response of the cells to BP-induced DNA damage.	Benzo(a)pyrene	81-83	P53	Homo sapiens	29-32
7656818-2	1995	In order to demonstrate the mechanism at molecular level, Multiple tumor suppressor genes Rb, p53, APC and MCC in human fetus esophageal epithelium treated with NMBzA (in vitro) for 24 hours or three weeks and esophageal carcinoma induced by NMBzA were analyzed with PCR amplification and direct sequencing.	nitrosobenzylmethylamine	161-166	P53	Homo sapiens	94-97
25474278-11	2014	mCRC patients with p53 overexpression undergoing an irinotecan containing second- or third-line chemotherapy after oxaliplatin failure have a significantly longer post-progression survival compared to patients without p53 overexpression.	Oxaliplatin	115-126	P53	Homo sapiens	19-22
25350970-3	2014	In this study, we report an antitumor molecule that bears a pyrrolo[3,4-c]pyrazole scaffold and functions as an enantiomeric inhibitor against both the p53-MDM2 interaction and the NF-kappaB activation.	pyrrolo[3,4-c]pyrazole	60-82	P53	Homo sapiens	152-155
25268766-12	2014	Our results indicate that hispolon inhibits the cell viability, induces G0/G1 cell cycle arrest and apoptosis in lung cancer cells and p53 plays a critical role in hispolon-mediated antitumor activity.	hispolon	164-172	P53	Homo sapiens	135-138
7656818-5	1995	PCR direct sequencing analysis revealed mutation of p53, Rb and MCC genes in human fetal esophageal epithelium treated with NMBzA for three weeks.	nitrosobenzylmethylamine	124-129	P53	Homo sapiens	52-55
7757303-5	1995	Sequence analysis of p53 cDNA revealed a homozygous double mutation at codon 249 (commonly mutated in aflatoxin-associated hepatocellular carcinoma) and codon 250.	Aflatoxins	102-111	P53	Homo sapiens	21-24
25286005-11	2014	This suggests that FKA"s anti-cancer activity is dependent on the p53 status.	BENZYL-CARBAMIC ACID [8-DEETHYL-ASCOMYCIN-8-YL]ETHYL ESTER	19-22	P53	Homo sapiens	66-69
7955067-8	1994	To demonstrate the program, the mutational spectra of single base substitutions in the p53 gene are compared in (i) bladder cancers from smokers and non-smokers, (ii) small-cell lung cancers, non-small-cell lung cancers and colon cancers and (iii) hepatocellular carcinomas from high- and low-aflatoxin exposure groups.	Aflatoxins	293-302	P53	Homo sapiens	87-90
25115399-5	2014	We also showed that Bcl-XL and Bak can substitute for Bcl-w and Bax, respectively, regulating complex-I activity and supporting the cytoplasmic function of p53; nuclear p53 also suppresses complex-I activity by inducing Bax expression.	bakuchiol	31-34	P53	Homo sapiens	156-159
8058315-0	1994	Immunochemical analysis of the interaction of p53 with MDM2;--fine mapping of the MDM2 binding site on p53 using synthetic peptides.	Peptides	123-131	P53	Homo sapiens	103-106
8146274-0	1994	High levels of stable p53 protein and the expression of c-myc in cultured human epithelial tissue after cobalt-60 irradiation.	Cobalt-60	104-113	P53	Homo sapiens	22-25
25056872-0	2014	Electrochemical detection of DNA binding by tumor suppressor p53 protein using osmium-labeled oligonucleotide probes and catalytic hydrogen evolution at the mercury electrode.	Mercury	157-164	P53	Homo sapiens	61-64
25056872-4	2014	To detect the p53-bound osmium-labeled probes, we took advantage of a catalytic peak yielded by Os,bipy-modified DNA at the mercury-based electrodes, allowing facile determination of subnanogram quantities of the labeled oligonucleotides.	Mercury	124-131	P53	Homo sapiens	14-17
25217394-6	2014	Western blotting detected the protein expression of p21 and p53 increased and PCNA, CDK1, cyclin B decreased in GCV+rAAV+Dox group.	raav	116-120	P53	Homo sapiens	60-63
24480042-4	2014	alpha-Mangostin also activated caspases-8, -9, and -7; increased the protein levels of Bax, p53, and cytosolic cytochrome c; and induced PARP cleavage while reducing Bid and Bcl-2 protein expression.	mangostin	0-15	P53	Homo sapiens	92-95
8390289-1	1993	In hepatocellular carcinoma, mutation within the p53 gene occurs mainly at codon 249 and its frequency has been associated with exposure to aflatoxin.	Aflatoxins	140-149	P53	Homo sapiens	49-52
24413339-1	2014	Recently, it has been reported that anti-viral drugs, such as indinavir and lopinavir (originally targeted for HIV), also inhibit E6-mediated proteasomal degradation of mutant p53 in E6-transfected C33A cells.	Lopinavir	76-85	P53	Homo sapiens	176-179
24411335-5	2014	The results of an inverted fluorescence microscopy, flow cytometry (FCM) and western blotting methods demonstrated that PC-3 prostate cancer cells treated with EGFP-p53/PEI/PAH-Cit/AuNP-CS expressed higher levels of GFP than cells treated with EGFP-p53/PEI.	aunp	181-185	P53	Homo sapiens	249-252
24952138-0	2014	Phenethyl isothiocyanate induces DNA damage-associated G2/M arrest and subsequent apoptosis in oral cancer cells with varying p53 mutations.	phenethyl isothiocyanate	0-24	P53	Homo sapiens	126-129
24952138-4	2014	PEITC inhibited the growth of OC2, SCC4, and SCC25 cells (functional p53 mutants) in a dose-dependent manner with low toxicity to normal cells.	phenethyl isothiocyanate	0-5	P53	Homo sapiens	69-72
24952138-10	2014	These results provide new insights into the critical roles of both GSH redox stress and p53 in the regulation of PEITC-induced G2/M cell cycle arrest and apoptosis in OSCCs.	phenethyl isothiocyanate	113-118	P53	Homo sapiens	88-91
8390289-2	1993	As Senegal is a country where liver cancer incidence is one of the highest in the world and where people are highly exposed to aflatoxin, we screened 15 liver cancer samples from this country for mutation at codon 249 of the p53 gene.	Aflatoxins	127-136	P53	Homo sapiens	225-228
23474763-9	2014	A novel small-molecule CH1 inhibitor, CH1iB, reactivates p53 and potentiates the anticancer activity of cis-platinum in HPV-positive HNSCC cells.	ch1ib	38-43	P53	Homo sapiens	57-60
25395712-5	2014	Western-blotting was applied to detect P53 and PTEN protein expression in the cells treated with cactus polysaccharides.	cactus polysaccharides	97-119	P53	Homo sapiens	39-42
8393124-6	1993	These results suggest a role for other environmental factors, such as aflatoxin, in the etiology of p53 mutation in hepatocellular carcinoma in Oriental patients.	Aflatoxins	70-79	P53	Homo sapiens	100-103
25395712-8	2014	Furthermore, cactus polysaccharides induced growth arrest and apoptosis may be due to the increase of P53 and phosphatase and tension homolog deleted on chromosome ten (PTEN) protein.	Polysaccharides	20-35	P53	Homo sapiens	102-105
24905957-7	2014	VIP effects could be blocked by cell incubation with a specific p53 inhibitor, cyclin pifithrin-alpha hydrobromide (CPFT-alphaH).	cpft-alphah	116-127	P53	Homo sapiens	64-67
24333670-2	2014	The detailed mechanisms of caffeine in tumor suppression via tumor suppressor protein p53 remain unclear.	Caffeine	27-35	P53	Homo sapiens	86-89
7583984-5	1993	In addition, the tumor suppressor gene p53 is frequently mutated in aflatoxin-induced hepatoma.	Aflatoxins	68-77	P53	Homo sapiens	39-42
24333670-4	2014	In this study, we investigated how caffeine modulated cell cycle arrest and apoptosis via the expression of various alternatively spliced p53 isoforms.	Caffeine	35-43	P53	Homo sapiens	138-141
24333670-5	2014	Caffeine reduced p53alpha expression and induced the expression of p53beta, which contains an alternatively spliced p53 C-terminus.	Caffeine	0-8	P53	Homo sapiens	17-20
24333670-5	2014	Caffeine reduced p53alpha expression and induced the expression of p53beta, which contains an alternatively spliced p53 C-terminus.	Caffeine	0-8	P53	Homo sapiens	67-70
24333670-7	2014	Serine/arginine-rich splicing factor 3 was a promising candidate for the serine/arginine-rich splicing factors responsible for the alternative splicing of p53 in response to caffeine treatment.	Caffeine	174-182	P53	Homo sapiens	155-158
25036040-10	2014	Trichostatin A and MS-275 (both HDAC inhibitors) inhibited the downstream pathway of HDAC1 and caused cell growth arrest via activation of p53 and p21; the effects of digoxigenin were totally opposite.	entinostat	19-25	P53	Homo sapiens	139-142
1332921-7	1992	They support the suggestion of a possible link between dietary exposure to aflatoxin and selective G to T mutations at codon 249 of the p53 gene.	Aflatoxins	75-84	P53	Homo sapiens	136-139
24880464-0	2014	Selective tumor cell killing by triptolide in p53 wild-type and p53 mutant ovarian carcinomas.	triptolide	32-42	P53	Homo sapiens	46-49
24880464-0	2014	Selective tumor cell killing by triptolide in p53 wild-type and p53 mutant ovarian carcinomas.	triptolide	32-42	P53	Homo sapiens	64-67
24880464-10	2014	This study shows that triptolide selectively kills ovarian cancer cells with different p53 status predominantly through regulating the coordinate and dynamic cellular processes of proliferation and apoptosis, thereby making it a promising chemotherapeutic agent against a broad spectrum of ovarian carcinomas.	triptolide	22-32	P53	Homo sapiens	87-90
24968304-10	2014	These results suggested that nilotinib can inhibit MDM2 and induce a p53-independent apoptosis pathway by downregulating XIAP; thus, nilotinib can treat not only Ph+, but also Ph- ALL patients whose cancer cells overexpress MDM2.	nilotinib	29-38	P53	Homo sapiens	69-72
23821376-0	2014	Lack of KRAS, NRAS, BRAF and TP53 mutations improves outcome of elderly metastatic colorectal cancer patients treated with cetuximab, oxaliplatin and UFT.	Oxaliplatin	134-145	P53	Homo sapiens	29-33
24333670-8	2014	In addition to p53-dependent functions, multiple target genes of serine/arginine-rich splicing factor 3 suggest that caffeine can regulate epithelial-mesenchymal-transition and hypoxic conditions to inhibit the survival of tumor cells.	Caffeine	117-125	P53	Homo sapiens	15-18
24239715-10	2014	There were significant decreases in the expression levels of p53, p21, cyclin D1 and PCNA in AA SFs treated with rhEndostatin, and a significant increase in CDK4 expression.	rhendostatin	113-125	P53	Homo sapiens	61-64
24239715-12	2014	This is partly due to the inhibitory effect of rhEndostatin on cyclin D1 and PCNA by a p53-p21-CDK4-independent mechanism.	rhendostatin	47-59	P53	Homo sapiens	87-90
1279184-0	1992	Mutations of p53 gene in hepatocellular carcinoma: roles of hepatitis B virus and aflatoxin contamination in the diet.	Aflatoxins	82-91	P53	Homo sapiens	13-16
25379568-11	2014	Moreover, LY29002, a PI-3K inhibitor, restored promotion of HRS by VorinostatSAHA in the p53 mutant U118 cells to levels similar to the p53 wild type cells.	ly29002	10-17	P53	Homo sapiens	89-92
24584189-7	2014	Overexpression of PIAS3 in the A549 wt p53-expressing cell line was found to significantly increase the half-life of p53 in the presence of cycloheximide, an inhibitor of protein synthesis.	Cycloheximide	140-153	P53	Homo sapiens	39-42
24584189-7	2014	Overexpression of PIAS3 in the A549 wt p53-expressing cell line was found to significantly increase the half-life of p53 in the presence of cycloheximide, an inhibitor of protein synthesis.	Cycloheximide	140-153	P53	Homo sapiens	117-120
1279184-2	1992	These reports suggested an association of p53 mutations with high levels of aflatoxin in the diet.	Aflatoxins	76-85	P53	Homo sapiens	42-45
1279184-5	1992	PURPOSE: The purpose of this study was to evaluate the relationship of p53 gene mutation to high or low levels of aflatoxin in the diet and to HBV infection.	Aflatoxins	114-123	P53	Homo sapiens	71-74
1279184-11	1992	CONCLUSION: Mutations of the tumor suppressor gene p53 in hepatocellular carcinomas are not limited to patients from geographic regions where the ingestion of aflatoxin is high.	Aflatoxins	159-168	P53	Homo sapiens	51-54
24493576-6	2014	Fenofibrate exhibited dose-dependent p53-independent anti-proliferative effects on HGG starting at 25 muM and pro-apoptotic effects starting at 50 muM, suggesting that the anti-proliferative actions are present only at 25 muM.	Fenofibrate	0-11	P53	Homo sapiens	37-40
24270669-1	2014	The effect of 2-phenylethynesulfonamide (PES), which is a p53 and HSP70 inhibitor in mammalian cells, was studied on the rainbow trout (Oncorhynchus mykiss) gill epithelial cell line, RTgill-W1, in order to evaluate PES as a tool for understanding the cellular survival pathways operating in fish.	2-phenylacetylenesulfonamide	14-39	P53	Homo sapiens	58-61
1525830-3	1992	Normal and LFS cells containing wild-type p53 arrested in G1 when challenged with the uridine biosynthesis inhibitor PALA and did not undergo PALA-selected gene amplification.	Uridine	86-93	P53	Homo sapiens	42-45
24270669-1	2014	The effect of 2-phenylethynesulfonamide (PES), which is a p53 and HSP70 inhibitor in mammalian cells, was studied on the rainbow trout (Oncorhynchus mykiss) gill epithelial cell line, RTgill-W1, in order to evaluate PES as a tool for understanding the cellular survival pathways operating in fish.	2-phenylacetylenesulfonamide	41-44	P53	Homo sapiens	58-61
24761875-8	2014	p53 PIN3 genotype was determined using electrophoresis of PCR products on 8% non-denaturing polyacrylamide gels and silver staining.	polyacrylamide	92-106	P53	Homo sapiens	0-3
24573532-8	2014	In addition, PFT-alpha (a p53 inhibitor) reduced the apoptotic rates and the expression of p53, p21, caspase-3 and caspase-9 induced by tangeretin, indicating that tangeretin-induced apoptosis was p53-dependent.	tangeretin	136-146	P53	Homo sapiens	26-29
24573532-8	2014	In addition, PFT-alpha (a p53 inhibitor) reduced the apoptotic rates and the expression of p53, p21, caspase-3 and caspase-9 induced by tangeretin, indicating that tangeretin-induced apoptosis was p53-dependent.	tangeretin	136-146	P53	Homo sapiens	91-94
24573532-8	2014	In addition, PFT-alpha (a p53 inhibitor) reduced the apoptotic rates and the expression of p53, p21, caspase-3 and caspase-9 induced by tangeretin, indicating that tangeretin-induced apoptosis was p53-dependent.	tangeretin	136-146	P53	Homo sapiens	91-94
21584516-6	1992	The data indicate that NMF treatment induces a reduction in the growth fraction of HT29 colon carcinoma cells accompanied by a reduction in c-myc, H3 histone, p53, and beta-actin gene expression, and that prolonged exposure to NMF induces elevated expresssion of alpha6/beta4 integrin receptor, These data suggest that NMF-induced reduction of the proliferative capacity supports a different "maturation status" of colon carcinoma cells which is defined by an elevated expression of the alpha6/beta4 integrin.	methylformamide	23-26	P53	Homo sapiens	159-162
25114837-6	2014	Our study shows that the exclusive DGLA s free radical derivatives from C-8 oxygenation lead to cell growth inhibition, cell cycle arrest and apoptosis in the human colon cancer cell line HCA-7 colony 29, probably by up-regulating the cancer suppressor p53 and the cell cycle inhibitor p27.	8,11,14-Eicosatrienoic Acid	35-39	P53	Homo sapiens	253-256
25700359-5	2014	TEA treatment also caused significant increases in mRNA and protein levels of tumor-suppressor proteins p53 and p21, and the upregulation was attenuated by pretreatment of NAC.	Tetraethylammonium	0-3	P53	Homo sapiens	104-107
2140591-3	1990	Simultaneous differential staining of p53 (identified by a FITC-labeled monoclonal antibody) versus DNA (stained with propidium iodide, PI), followed by bivariate analysis with flow cytometry (FCM) made it possible to evaluate p53 expression with respect to cell position during the cell cycle.	Fluorescein-5-isothiocyanate	59-63	P53	Homo sapiens	38-41
24324808-8	2013	Among glycan traits with low heritability probe cg08392591 maps to a CpG island 5" from the ANKRD11 gene, a p53 activator on chromosome 16.	Polysaccharides	6-12	P53	Homo sapiens	108-111
24595168-4	2014	METHODOLOGY/PRINCIPAL FINDINGS: We have shown here that caffeine up-regulates the tumor suppressor proteins p16, p21, p53 and Cav-1, and reduces the expression/secretion of various cytokines (IL-6, TGF-beta, SDF-1 and MMP-2), and down-regulates alpha-SMA.	Caffeine	56-64	P53	Homo sapiens	118-121
24366007-11	2014	Collectively, these results suggest that nutlin-3 induces HO-1 expression via the activation of both JNK which is dependent on ROS generated by p53 translocated to the mitochondria and p38 MAPK which appears to be stimulated by a ROS-independent mechanism, and this HO-1 induction may inhibit nutlin-3-induced apoptosis, constituting a negative feedback loop of p53-induced apoptosis.	nutlin	41-47	P53	Homo sapiens	144-147
24366007-11	2014	Collectively, these results suggest that nutlin-3 induces HO-1 expression via the activation of both JNK which is dependent on ROS generated by p53 translocated to the mitochondria and p38 MAPK which appears to be stimulated by a ROS-independent mechanism, and this HO-1 induction may inhibit nutlin-3-induced apoptosis, constituting a negative feedback loop of p53-induced apoptosis.	nutlin	41-47	P53	Homo sapiens	362-365
24016853-8	2013	Further, the use of 4-MU (a hyaluronan synthase inhibitor) on HepR21 cells reduces the HA level and downregulates the expression of growth promoting factors like pAKT and PKC; while upregulating the expression of the tumor suppressor p53.	Hymecromone	20-24	P53	Homo sapiens	234-237
33236129-8	2021	Furthermore, the proliferation inhibitory effect of CECU was due to the inactivation of AKT and ERK signaling, upregulation of p53 and p21, and downregulation of cyclin B1 and cyclin D1, but not reactive oxygen species (ROS) generation.	cecu	52-56	P53	Homo sapiens	127-130
24498496-11	2013	Combination of CTB and Salermide in 72 h through decreasing expression of Sirtuin1 and P300 genes induced acetylation of P53 protein and consequently showed the most apoptosis in MCF-7 cells, but it could be well-tolerated in MRC-5.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	23-32	P53	Homo sapiens	121-124
24486204-3	2014	In this report we prepared various peptide-MCAs (4-methylcoumaryl-7-amides) related to histone tail and protein-substrates such as p53 and estrogen receptor-alpha.	4-methyl-coumaryl-7-amide	49-74	P53	Homo sapiens	131-134
34776240-0	2022	Corrigendum to "Oxidative stress-mediated p53/p21WAF1/CIP1 pathway may be involved in microcystin-LR-induced cytotoxicity in HepG2 cells" (Chemosphere 194 (2018) 773-783).	cyanoginosin LR	86-100	P53	Homo sapiens	42-45
24694607-5	2014	We also found that cordycepol C induced the expression of Bax protein, followed by its translocation from the cytosol to mitochondria in both wild type and p53 knockdown HepG2 cells.	cordycepol C	19-31	P53	Homo sapiens	156-159
24244715-0	2013	Triptolide induces growth inhibition and apoptosis of human laryngocarcinoma cells by enhancing p53 activities and suppressing E6-mediated p53 degradation.	triptolide	0-10	P53	Homo sapiens	96-99
24244715-0	2013	Triptolide induces growth inhibition and apoptosis of human laryngocarcinoma cells by enhancing p53 activities and suppressing E6-mediated p53 degradation.	triptolide	0-10	P53	Homo sapiens	139-142
24244715-5	2013	Moreover, triptolide enhances p53 expression by increasing its stability via down-regulation of E6 and E6AP.	triptolide	10-20	P53	Homo sapiens	30-33
34919898-0	2022	Amperometric detection of tumor suppressor protein p53 via pencil graphite electrode for fast cancer diagnosis.	Graphite	66-74	P53	Homo sapiens	51-54
24244715-7	2013	In addition, we found that short time treatment with triptolide induced DNA damage, which was consistent with the increase in p53.	triptolide	53-63	P53	Homo sapiens	126-129
24244715-8	2013	Furthermore, the cytotoxicity of triptolide is decreased by p53 knockdown or use of caspases inhibitor.	triptolide	33-43	P53	Homo sapiens	60-63
24244715-9	2013	In conclusion, our results demonstrated that triptolide inhibits cell proliferation and induces apoptosis in laryngocarcinoma cells by enhancing p53 expression and activating p53 functions through induction of DNA damage and suppression of E6 mediated p53 degradation.	triptolide	45-55	P53	Homo sapiens	145-148
24244715-9	2013	In conclusion, our results demonstrated that triptolide inhibits cell proliferation and induces apoptosis in laryngocarcinoma cells by enhancing p53 expression and activating p53 functions through induction of DNA damage and suppression of E6 mediated p53 degradation.	triptolide	45-55	P53	Homo sapiens	175-178
25215281-7	2014	Nuclear factors AP-1, NF-kappaB, and p53 are involved in the cellular response to high and nontoxic concentrations of aaptamine alkaloids 1-3.	aaptamine alkaloids	118-137	P53	Homo sapiens	37-40
34919898-4	2022	The immunosensor was fabricated by immobilizing anti-p53 antibodies onto the pencil graphite electrode (PGE).	Graphite	84-92	P53	Homo sapiens	53-56
34948081-5	2021	The optimized ETO loaded NE was then investigated for its anticancer potential employing A549 lung cancer cell line via cytotoxicity, apoptotic activity, mitochondrial membrane potential activity, cell migration assay, cell cycle analysis, Caspase-3, 9, and p53 activity by ELISA and molecular biomarker analysis through RT-PCR test.	Etoricoxib	14-17	P53	Homo sapiens	258-261
24345738-7	2014	Interestingly, we identified a previously undetected point mutation of p53 (p.Arg249Ser) in IST-MES 2, and showed that RITA is also able to reactivate this p53 mutant protein and its apoptotic function.	2-(N-morpholino)ethanesulfonic acid	96-99	P53	Homo sapiens	71-74
25268087-10	2014	On the molecular level, our results showed that saikosaponin-d treatment increased the expression of p53 and bax, and decreased the expression of Bcl-2.	saikosaponin D	48-62	P53	Homo sapiens	101-104
23974517-9	2013	Moreover, fucoxanthin dose-dependently decreased the levels of phosphorylated Akt and its downstream proteins p53, p70S6K, and mTOR, and increases the expression of PTEN in HeLa cells.	fucoxanthin	10-21	P53	Homo sapiens	110-113
34647981-0	2021	Preexisting TP53-Variant Clonal Hematopoiesis and Risk of Secondary Myeloid Neoplasms in Patients With High-grade Ovarian Cancer Treated With Rucaparib.	rucaparib	142-151	P53	Homo sapiens	12-16
23959424-0	2013	Upregulation of sestrin-2 expression via P53 protects against 1-methyl-4-phenylpyridinium (MPP+) neurotoxicity.	1-Methyl-4-phenylpyridinium	62-89	P53	Homo sapiens	41-44
24018803-5	2013	In contrast, the expression of acetylated-P53 predicted favourable OS, RFS, and CSS.	thiocysteine	80-83	P53	Homo sapiens	42-45
24118195-8	2013	While oxaliplatin induced p53- and p21-dependent G2 -phase arrest associated with downregulation of cyclin B1 and Cdk1, LA-12 allowed cells to enter M-phase of the cell cycle regardless of p53/p21 status.	Oxaliplatin	6-17	P53	Homo sapiens	26-29
24245874-4	2013	However, the relationship between the ASPP family members and p53, as well as the dissemination and expression pattern of ASPP family members in p53+ BC, has not been elucidated.	aspp	122-126	P53	Homo sapiens	145-148
34647981-15	2021	Conclusions and Relevance: The findings of this genetic association study suggest that preexisting TP53 CHIP variants may be associated with t-MNs after rucaparib treatment.	rucaparib	153-162	P53	Homo sapiens	99-103
24244715-9	2013	In conclusion, our results demonstrated that triptolide inhibits cell proliferation and induces apoptosis in laryngocarcinoma cells by enhancing p53 expression and activating p53 functions through induction of DNA damage and suppression of E6 mediated p53 degradation.	triptolide	45-55	P53	Homo sapiens	175-178
34744708-5	2021	We describe the protein modifications induced by these polyphenols and their effect on the central elements of several signaling pathways including PI3K, Akt, mTOR, RAS, and MAPK and particularly those affecting the tumor suppressor p53 protein.	Polyphenols	55-66	P53	Homo sapiens	233-236
24100270-11	2013	Cd induced p53-dependent apoptosis through cooperation between Bak upregulation without changing the Bcl-2 and Bax expression.	bakuchiol	63-66	P53	Homo sapiens	11-14
23953587-6	2013	The results demonstrate that choline substitution leads to: (i) an improved preservation of oocytes and follicular cells; (ii) the recovery of a higher percentage of grade-1 follicles negative for p53, p21 and Apaf-1 apoptotic markers; (iii) a reduced mitochondrial damage as observed at an ultrastructural level; and (iv) a better preservation of ovarian tissue stroma.	Choline	29-36	P53	Homo sapiens	197-200
34744708-6	2021	Modifications of p53 induced by these polyphenols regulate p53 gene expression and protein levels and posttranslational modifications such as phosphorylation, acetylation, and ubiquitination that influence stability, subcellular location, activation of new transcriptional targets, and the role of p53 in response to DNA damage, apoptosis control, cell- cycle regulation, senescence, and cell fate.	Polyphenols	38-49	P53	Homo sapiens	17-20
23578198-0	2013	Sunitinib induces cellular senescence via p53/Dec1 activation in renal cell carcinoma cells.	Sunitinib	0-9	P53	Homo sapiens	42-45
23578198-4	2013	Mechanistic investigations indicated that therapy-induced senescence (TIS) following sunitinib treatment mainly attributed to p53/Dec1 signaling activation mediated by Raf-1/NF-kappaB inhibition in vitro.	Sunitinib	85-94	P53	Homo sapiens	126-129
23578198-7	2013	Taken together, our findings suggested that sunitinib treatment performance could be attributable to TIS, depending on p53/Dec1 activation via inhibited Raf-1/nuclear factor (NF)-kappaB activity.	Sunitinib	44-53	P53	Homo sapiens	119-122
24094550-5	2013	SA-beta-gal activity and cytoplasm size in senescent hCPC(c-kit+) were significantly reduced, with reduced TP53 and cMdm2 expression after treatment with a specific ERK inhibitor (U0126).	U 0126	180-185	P53	Homo sapiens	107-111
34744708-6	2021	Modifications of p53 induced by these polyphenols regulate p53 gene expression and protein levels and posttranslational modifications such as phosphorylation, acetylation, and ubiquitination that influence stability, subcellular location, activation of new transcriptional targets, and the role of p53 in response to DNA damage, apoptosis control, cell- cycle regulation, senescence, and cell fate.	Polyphenols	38-49	P53	Homo sapiens	59-62
34697748-0	2021	Andrographolide Induces Apoptosis in Gastric Cancer Cells through Reactivation of p53 and Inhibition of Mdm-2.	andrographolide	0-15	P53	Homo sapiens	82-85
24004950-5	2013	We have previously shown that p63, a member of the p53 family of nuclear proteins, is expressed in proliferative cytotrophoblast (CTB), precursors to terminally differentiated syncytiotrophoblast (STB) in chorionic villi and extravillous trophoblast (EVT) at the implantation site.	EVT	251-254	P53	Homo sapiens	51-54
23504997-11	2013	Finally, actopaxin down-regulation enhanced the chemosensitivity of HCC cells towards oxaliplatin treatment by way of a collective result of suppression of survivin protein, beta-catenin, and mammalian target of rapamycin pathways and up-regulation of p53.	Oxaliplatin	86-97	P53	Homo sapiens	252-255
34697748-6	2021	Effect of andrographolide on p53 activity was ascertained by using a p53 activator (RITA) which showed synergistic inhibition of cell proliferation.	andrographolide	10-25	P53	Homo sapiens	29-32
34697748-7	2021	While andrographolide when used in combination with a p53 inhibitor (pifithrin-alpha) showed potent restriction over its response.	andrographolide	6-21	P53	Homo sapiens	54-57
23756562-13	2013	Notably, the increased expression of phosphorylated p53 in HBE/TOB1 cells after IR was sufficiently blocked by U0126, a specific inhibitor of MEK1/2.	U 0126	111-116	P53	Homo sapiens	52-55
34697748-9	2021	Andrographolide activated the expression of p53 protein and gene and downregulated the levels of Mdm-2 (negative regulator of p53).	andrographolide	0-15	P53	Homo sapiens	44-47
34697748-9	2021	Andrographolide activated the expression of p53 protein and gene and downregulated the levels of Mdm-2 (negative regulator of p53).	andrographolide	0-15	P53	Homo sapiens	126-129
34697748-10	2021	Andrographolide inhibited the colony formation abilities in SGC7901 in a p53-dependent manner followed by induction of mitochondrial intrinsic apoptosis through activation of caspases-9 and -3, cleavage of PARP, and inhibition of pro-apoptotic Bcl-2.	andrographolide	0-15	P53	Homo sapiens	73-76
34697748-11	2021	Andrographolide induced p53 mediated apoptosis in gastric carcinoma cells which adds to a novel approach in anticancer therapies.	andrographolide	0-15	P53	Homo sapiens	24-27
23887629-11	2013	The use of a p53 shRNA rescued apoptosis, and only partially the defect in PPT formation.	4,4',4''-(4-propyl-((1)H)-pyrazole-1,3,5-triyl) tris-phenol	75-78	P53	Homo sapiens	13-16
34209894-4	2021	eGFP lifetime-photoconversion was used to follow redistribution dynamics of NPMmut and p53 in Selinexor-treated cells.	selinexor	94-103	P53	Homo sapiens	87-90
23802716-3	2013	Derivative 5-bromo-3"-(cyclohexane carbonyl)-1-methyl-2-oxospiro[indoline-3,2"-thiazolidine] (4n) emerged as the most potent compound of this series, inhibiting in vitro 30% of p53-MDM2 interaction at 5 muM and the cell growth of different human tumor cells at nanomolar concentrations.	5-bromo-3"-(cyclohexane carbonyl)-1-methyl-2-oxospiro[indoline-3,2"-thiazolidine	11-91	P53	Homo sapiens	177-180
34109976-5	2021	This research addresses the growth inhibitory efficacy of rutin against E6 and E7 oncoprotein in HeLa cells, which is known to inactivate several tumor suppressor protein such as p53 and pRB.	Rutin	58-63	P53	Homo sapiens	179-182
23462281-5	2013	Multiple studies have evaluated the connection between thiamine and PD pathology, and candidate pathways involve the transcription factor Sp1, p53, Bcl-2, caspase-3, tyrosine hydroxylase, glycogen synthase kinase-3beta, vascular endothelial growth factor, advanced glycation end products, nuclear factor kappa B, mitogen-activated protein kinase, and the reduced form of nicotinamide adenine dinucleotide phosphate.	Thiamine	55-63	P53	Homo sapiens	143-146
34109976-7	2021	Additionally rutin treatment has also led to downregulation of E6 and E7 expression associated with an increased expression of p53 and pRB levels.	Rutin	13-18	P53	Homo sapiens	127-130
34108527-8	2021	Further, combined with the fixed-ratio liposomal formulation of daunorubicin and cytarabine, CPX-351, M3814 enhanced the efficacy against leukemia cells in vitro and in vivo without increasing hematopoietic toxicity, suggesting that DNA-PK inhibition could offer a novel clinical strategy for harnessing the anticancer potential of p53 in AML therapy.	Cytarabine	81-91	P53	Homo sapiens	332-335
23608671-7	2013	Besides, the binding abilities of amino-PAHs to p53 DNA seemed stronger than that for C-myc DNA.	amino-pahs	34-44	P53	Homo sapiens	48-51
34149863-13	2021	SCDP key active ingredients are mainly quercetin, wogonin, baicalein, acacetin, oroxylin A, and beta-sitosterol, which function mainly by regulating targets, such as PTGS2, CASP3, TP53, IL-6, TNF, and AKT1, and are associated with multiple signaling pathways as pathways in cancer, PI3K-Akt signaling pathway, apoptosis, IL-17 signaling pathways.	gamma-sitosterol	96-111	P53	Homo sapiens	180-184
23376190-0	2013	Lactose binding to human galectin-7 (p53-induced gene 1) induces long-range effects through the protein resulting in increased dimer stability and evidence for positive cooperativity.	Lactose	0-7	P53	Homo sapiens	37-40
34072831-8	2021	In conclusion, BMX overcomes TMZ resistance by enhancing TMZ-mediated cytotoxic effect by downregulating the beta-catenin/c-Myc/SOX2 signaling pathway and upregulating WT-p53 mediated MGMT inhibition.	Temozolomide	29-32	P53	Homo sapiens	171-174
34072831-8	2021	In conclusion, BMX overcomes TMZ resistance by enhancing TMZ-mediated cytotoxic effect by downregulating the beta-catenin/c-Myc/SOX2 signaling pathway and upregulating WT-p53 mediated MGMT inhibition.	Temozolomide	57-60	P53	Homo sapiens	171-174
23426995-1	2013	The anticancer activities of gambogic acid (GA) on two hepatocellular carcinoma cells with either p53 deletion (Hep3B) or p53 mutation (Huh7) were investigated in the present study.	gambogic acid	29-42	P53	Homo sapiens	98-101
23426995-1	2013	The anticancer activities of gambogic acid (GA) on two hepatocellular carcinoma cells with either p53 deletion (Hep3B) or p53 mutation (Huh7) were investigated in the present study.	gambogic acid	29-42	P53	Homo sapiens	122-125
34072831-9	2021	These findings indicate a promising drug combination for precision personal treating of TMZ-resistant WT-p53 GBM cells.	Temozolomide	88-91	P53	Homo sapiens	105-108
34221338-5	2021	We synthesized a set of chemically homogeneous full-length p53 carrying one (Ser20ph and Ser15ph) or two (Ser15,20ph) naturally occurring, damage-associated phosphoryl marks.	ser20ph	77-84	P53	Homo sapiens	59-62
23540934-0	2013	Alpha-mangostin and gambogic acid as potential inhibitors of the p53-MDM2 interaction revealed by a yeast approach.	mangostin	0-15	P53	Homo sapiens	65-68
23540934-0	2013	Alpha-mangostin and gambogic acid as potential inhibitors of the p53-MDM2 interaction revealed by a yeast approach.	gambogic acid	20-33	P53	Homo sapiens	65-68
35568224-6	2022	Expressions of genes responses to DNA damage, ATM, ATR, p53, p21, Bax, H2AX, and GADD45A were disturbed by NIT treatment.	nitenpyram	107-110	P53	Homo sapiens	56-59
23492773-10	2013	Pretreatment with PUMA and Bak siRNAs abolished miR-128-induced apoptosis in HCT116 p53+/+ and HCT116 p53-/- cells.	bakuchiol	27-30	P53	Homo sapiens	84-87
23492773-10	2013	Pretreatment with PUMA and Bak siRNAs abolished miR-128-induced apoptosis in HCT116 p53+/+ and HCT116 p53-/- cells.	bakuchiol	27-30	P53	Homo sapiens	102-105
35510223-13	2022	The molecular docking results showed that there was a certain affinity between the main compounds (kaempferol, quercetin, beta-sitosterol, naringenin) and core target genes (PTGS2, CASP3, MAPK1, MAPK3, TP53).	gamma-sitosterol	122-137	P53	Homo sapiens	202-206
23096768-12	2013	CONCLUSIONS: Specific polymorphisms in XRCC1, XPD, and TP53 were associated with increased toxicity to NT in patients with rectal cancer.	nt	103-105	P53	Homo sapiens	55-59
35114328-0	2022	Chemically synthesized cinobufagin suppresses nasopharyngeal carcinoma metastasis by inducing ENKUR to stabilize p53 expression.	cinobufagin	23-34	P53	Homo sapiens	113-116
23165797-7	2013	Interestingly, there was a trend toward longer time to progression after chemotherapy for tumors with the apoptosis-prone p53 variant R72 (P = .07), which was strongest with doxorubicin/ifosfamide-based regimens (P = .01).	Ifosfamide	186-196	P53	Homo sapiens	122-125
22815158-0	2013	Involvement of p53 in the cytotoxic activity of the NAMPT inhibitor FK866 in myeloid leukemic cells.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	68-73	P53	Homo sapiens	15-18
22815158-6	2013	Activation of p53 by FK866 involved increased acetylation of p53 at lysine 382 with subsequent increase in the expression of p21 and BAX.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	21-26	P53	Homo sapiens	14-17
35517429-8	2022	This effect could be weakened in the presence of dimethyloxalylglycine (DMOG), suggesting that EGLN1 down-regulated p53 based on its hydroxylase activity.	oxalylglycine	49-70	P53	Homo sapiens	116-119
22815158-6	2013	Activation of p53 by FK866 involved increased acetylation of p53 at lysine 382 with subsequent increase in the expression of p21 and BAX.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	21-26	P53	Homo sapiens	61-64
22815158-7	2013	Further, knockdown of p53 attenuated the effects of FK866 on apoptosis and cell cycle arrest, which was partly associated with decreased expression of p21 and BAX.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	52-57	P53	Homo sapiens	22-25
22815158-8	2013	Our results suggest the role of p53 acetylation pathway in the anti-leukemic effect of FK866.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	87-92	P53	Homo sapiens	32-35
35517429-8	2022	This effect could be weakened in the presence of dimethyloxalylglycine (DMOG), suggesting that EGLN1 down-regulated p53 based on its hydroxylase activity.	oxalylglycine	72-76	P53	Homo sapiens	116-119
23088536-2	2013	Human ASPPs (apoptosis-stimulating proteins of p53) comprise three family members: ASPP1, ASPP2 and iASPP (inhibitory ASPP), which is uniquely overexpressed in many cancers.	aspp	6-10	P53	Homo sapiens	47-50
35204825-8	2022	The p53 complexes with SIRT2, MUL1, USP7, TXN, PIN1 and PPIF control regulation of p53 function through post-translational modifications, such as lysine acetylation or ubiquitination, cysteine/cystine redox transformation and peptidyl-prolyl cis-trans isomerization.	Cystine	193-200	P53	Homo sapiens	4-7
35204825-8	2022	The p53 complexes with SIRT2, MUL1, USP7, TXN, PIN1 and PPIF control regulation of p53 function through post-translational modifications, such as lysine acetylation or ubiquitination, cysteine/cystine redox transformation and peptidyl-prolyl cis-trans isomerization.	Cystine	193-200	P53	Homo sapiens	83-86
35205710-2	2022	Here, we demonstrate that miR-101-3p regulates the RPL11-MDM2-p53 pathway by targeting ubiquitin-specific peptidase 47 (USP47), consequently inhibiting cancer cell proliferation.	mir-101-3p	26-36	P53	Homo sapiens	62-65
22565822-6	2013	Furthermore, emodin increased the protein level of p53 and decreased the protein level of NF-kappaB/p65 in HepG2 cells, which indicated these two regulators might play a role in emodin-induced apoptosis.	Emodin	13-19	P53	Homo sapiens	51-54
23281693-9	2013	CONCLUSION: The present study suggests that one of the actions of PUVA therapy in psoriasis might be exerted through induction of apoptosis especially of lymphocytes by suppression of Bcl-2 expression and of keratinocytes through P53 and Fas pathways leading to healing of psoriasis.	puva	66-70	P53	Homo sapiens	230-233
35205710-4	2022	In addition, the overexpression of miR-101-3p suppresses cell proliferation in a p53-dependent manner.	mir-101-3p	35-45	P53	Homo sapiens	81-84
35205710-5	2022	MiR-101-3p promotes interaction between RPL11 and MDM2 by inducing the translocation of RPL11 from the nucleolus to the nucleoplasm, thus preventing the MDM2-mediated proteasomal degradation of p53.	mir-101-3p	0-10	P53	Homo sapiens	194-197
35045602-5	2022	Moreover, SA significantly enhanced the antitumor immunity relative to free HK, and the mechanism has notable selectivity to the p53 pathway.	sa	10-12	P53	Homo sapiens	129-132
35090313-8	2022	MP treatment alleviated the H2O2-induced increases in ROS levels, inhibited apoptosis, relieved cell cycle arrest, and downregulated cleaved caspase 3 and P53 protein expression.	6-trimethylsilylthio-9-trimethylsilylpurine	0-2	P53	Homo sapiens	155-158
23085367-6	2013	Xanthohumol, beside the induction of GSTs and HO-1, significantly elevated NQO1 expression in concert with p53 level in normal hepatocytes.	xanthohumol	0-11	P53	Homo sapiens	107-110
23942225-2	2013	Although it is supported by a large body of literatures that p53 and caspase-3 played key roles in Cr(VI)-induced cytotoxicity, it is clear that Cr(VI) could induce apoptosis either without activating caspase, or in a p53- independent manner.	chromium hexavalent ion	99-105	P53	Homo sapiens	61-64
3291921-2	1988	Twenty-three (51.1%), 26 (57.8%) and 27 (60%) of 45 ER-ICA -ve cancers were respectively p53 +ve, VIM +ve and EGF-R +ve; whereas of 151 ER-ICA +ve tumours 8 (5.3%) were p53 +ve (P less than 0.0001), 23 (15.2%) VIM +ve (P less than 0.001) and 40 (26.5%) EGF-R +ve P less than 0.001).	isocyanic acid	55-58	P53	Homo sapiens	89-92
23062949-3	2013	This study investigated the role of p53 in the cellular response to the Auger-emitting radionuclide indium-111.	Radioisotopes	87-99	P53	Homo sapiens	36-39
23530648-4	2013	The objective of the present study was to determine the effect of natural isothiocyanate (phenethyl isothiocyanate; PEITC) on different HSPs (27, 70, and 90) and HSF1 in 2 breast cancer cell lines, namely breast adenocarcinoma MCF-7 (with wild type p53) and highly metastatic breast cancer cell MDA-MB-231 (with mutated p53).	phenethyl isothiocyanate	90-114	P53	Homo sapiens	249-252
23530648-4	2013	The objective of the present study was to determine the effect of natural isothiocyanate (phenethyl isothiocyanate; PEITC) on different HSPs (27, 70, and 90) and HSF1 in 2 breast cancer cell lines, namely breast adenocarcinoma MCF-7 (with wild type p53) and highly metastatic breast cancer cell MDA-MB-231 (with mutated p53).	phenethyl isothiocyanate	90-114	P53	Homo sapiens	320-323
23530648-4	2013	The objective of the present study was to determine the effect of natural isothiocyanate (phenethyl isothiocyanate; PEITC) on different HSPs (27, 70, and 90) and HSF1 in 2 breast cancer cell lines, namely breast adenocarcinoma MCF-7 (with wild type p53) and highly metastatic breast cancer cell MDA-MB-231 (with mutated p53).	phenethyl isothiocyanate	116-121	P53	Homo sapiens	249-252
23530648-4	2013	The objective of the present study was to determine the effect of natural isothiocyanate (phenethyl isothiocyanate; PEITC) on different HSPs (27, 70, and 90) and HSF1 in 2 breast cancer cell lines, namely breast adenocarcinoma MCF-7 (with wild type p53) and highly metastatic breast cancer cell MDA-MB-231 (with mutated p53).	phenethyl isothiocyanate	116-121	P53	Homo sapiens	320-323
23469203-6	2013	We demonstrated that pterostilbene (PTER), found in blueberries, had greater increase in MTA1-mediated p53 acetylation, confirming superior potency over resveratrol as dietary epigenetic agent.	pterostilbene	21-34	P53	Homo sapiens	103-106
23469203-6	2013	We demonstrated that pterostilbene (PTER), found in blueberries, had greater increase in MTA1-mediated p53 acetylation, confirming superior potency over resveratrol as dietary epigenetic agent.	pterostilbene	36-40	P53	Homo sapiens	103-106
23520471-8	2013	Additionally, MK1775 significantly enhances the cytotoxic effect of gemcitabine in sarcoma cells lines with different p53 mutational status.	adavosertib	14-20	P53	Homo sapiens	118-121
23451065-7	2013	On the other hand, higher concentrations of OME (450 and 600 microg/mL) triggered a massive apoptosis through the extrinsic pathway, including the activation of tumor necrosis factor-alpha (TNF-alpha), caspase 8, caspase 3, and cleavage of PARP, downregulation of survivin as well as depletion of the mutant p53 in MDA-MB-231 cells.	ome	44-47	P53	Homo sapiens	308-311
23066038-2	2012	We investigated the ability of various common chemotherapeutic drugs to induce p21 expression in p53-negative cancer cells and showed that the induction of p21 expression by oxaliplatin is caused by the derepression of a previously unrecognized negative regulatory element with a Sp1/Sp3 palindrome sequence core at -216 to -236 of the p21 proximal promoter.	Oxaliplatin	174-185	P53	Homo sapiens	97-100
22886373-8	2012	ROS-mediated p53 activation was found to involve in Cr(VI)-induced cell cycle arrest, and p53 inhibitor Pifithrin-alpha (PFT-alpha) rescued Cr(VI)-induced reduction of check point proteins Mrc1 and BubR1, thus inhibiting cell cycle arrest.	chromium hexavalent ion	52-58	P53	Homo sapiens	13-16
22886373-8	2012	ROS-mediated p53 activation was found to involve in Cr(VI)-induced cell cycle arrest, and p53 inhibitor Pifithrin-alpha (PFT-alpha) rescued Cr(VI)-induced reduction of check point proteins Mrc1 and BubR1, thus inhibiting cell cycle arrest.	chromium hexavalent ion	140-146	P53	Homo sapiens	13-16
23192191-2	2012	In this work, the interactions of two selected pyrene derivatives (1-OHP and 1-PBO) and human tumor-related DNA (p53 DNA and C-myc DNA) are investigated by spectroscopic and non-native polyacrylamide gel electrophoresis (PAGE) methods.	Oxaliplatin	67-72	P53	Homo sapiens	113-116
23192191-5	2012	The binding constants of 1-OHP are 1.16 x 10(6) L x mol(-1) and 4.04 x 10(5) L x mol(-1) for p53 DNA and C-myc DNA, respectively, while that of 1-PBO are only 2.04 x 10(3) L x mol(-1) and 1.39 x 10(3) L x mol(-1) for p53 DNA and C-myc DNA, respectively.	Oxaliplatin	25-30	P53	Homo sapiens	93-96
23192191-5	2012	The binding constants of 1-OHP are 1.16 x 10(6) L x mol(-1) and 4.04 x 10(5) L x mol(-1) for p53 DNA and C-myc DNA, respectively, while that of 1-PBO are only 2.04 x 10(3) L x mol(-1) and 1.39 x 10(3) L x mol(-1) for p53 DNA and C-myc DNA, respectively.	Oxaliplatin	25-30	P53	Homo sapiens	217-220
23127292-5	2012	Expression of p53 defined as &gt;10% positive nuclei was analyzed together with prior immunohistochemical assays of ER performed at central pathological review of whole tumor sections.	Aminoglutethimide	26-32	P53	Homo sapiens	14-17
22407755-3	2012	XN induced a higher rate of apoptosis in glioblastoma cells than in normal astrocytes, which was associated with activation of p53 and an elevated Bax/Bcl-2 ratio in glioblastoma cells, indicating an intrinsic caspase-dependent apoptotic pathway.	xanthohumol	0-2	P53	Homo sapiens	127-130
23035244-5	2012	We found from in silico screening and confirmed by experiment that lithocholic acid (LCA) binds to the p53 binding sites of both MDM2 and MDM4 with a fivefold preference for MDM4.	Lithocholic Acid	67-83	P53	Homo sapiens	103-106
22692362-8	2012	Caffeic acid phenethyl ester, an antioxidant, prevented the As-induced decreases in SOD1, p53, and ferritin mRNA and protein levels.	caffeic acid phenethyl ester	0-28	P53	Homo sapiens	90-93
22847136-3	2012	Cell viability tests (MTT assay, xCELLigence system) showed that PEITC exhibits lower cytotoxicity to A549 cells containing wild-type p53.	phenethyl isothiocyanate	65-70	P53	Homo sapiens	134-137
22859066-5	2012	Furthermore, the low concentration of DHT induced lower mRNA levels in the p53 and p21 genes in HNTEP cells.	Dihydrotestosterone	38-41	P53	Homo sapiens	75-78
22859066-6	2012	In turn, high DHT concentrations induced a significant increase in the expression of the p53 and p21 genes.	Dihydrotestosterone	14-17	P53	Homo sapiens	89-92
22213398-8	2012	Finally, we isolated ursolic and oleanolic acids as the bioactive compounds able to upregulate p53 expression and inhibit breast cancer cell growth.	ursolic	21-28	P53	Homo sapiens	95-98
23017148-1	2012	BACKGROUND: Nucleoside analogs used in the chemotherapy of solid tumors, such as the capecitabine catabolite 5"-deoxy-5-fluorouridine (5"-DFUR) trigger a transcriptomic response that involves the aquaglyceroporin aquaporin 3 along with other p53-dependent genes.	doxifluridine	109-133	P53	Homo sapiens	242-245
23017148-1	2012	BACKGROUND: Nucleoside analogs used in the chemotherapy of solid tumors, such as the capecitabine catabolite 5"-deoxy-5-fluorouridine (5"-DFUR) trigger a transcriptomic response that involves the aquaglyceroporin aquaporin 3 along with other p53-dependent genes.	doxifluridine	135-142	P53	Homo sapiens	242-245
22989009-0	2012	HDM2 antagonist MI-219 (spiro-oxindole), but not Nutlin-3 (cis-imidazoline), regulates p53 through enhanced HDM2 autoubiquitination and degradation in human malignant B-cell lymphomas.	MI-219	16-22	P53	Homo sapiens	87-90
22627294-7	2012	The phosphorylation of p53 was inhibited by KU-55933, an inhibitor of ataxia-telangiectasia mutated kinase (ATM), but not by NU7026, an inhibitor of DNA-dependent protein kinase (DNA-PK).	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	44-52	P53	Homo sapiens	23-26
22707197-0	2012	Triptolide sensitizes TRAIL-induced apoptosis in prostate cancer cells via p53-mediated DR5 up-regulation.	triptolide	0-10	P53	Homo sapiens	75-78
22707197-4	2012	Triptolide treatment can suppress Akt/Hdm2 signaling pathway, and lead to p53 accumulation, thereby up-regulating DR5 expression.	triptolide	0-10	P53	Homo sapiens	74-77
22766503-1	2012	iASPP was an inhibitory member of ASPP family and could specifically inhibit the apoptotic function of p53.	aspp	1-5	P53	Homo sapiens	103-106
24750915-3	2012	The results demonstrated that C. kwangsiensis polysaccharides can significantly inhibit the proliferation of CNE-2 cells, which was possibly through the induction of apoptosis mediated by attenuating Bcl-2 expression and promoting p53 expression.	Polysaccharides	46-61	P53	Homo sapiens	231-234
22349266-7	2012	When inhibition of UGCG and treatment with mitomycin C were combined, p53-deficient, but not p53-expressing cells, showed a significant increase in cell death, suggesting that the regulation of sphingolipid metabolism could be used to sensitize cells to chemotherapeutic drugs.	Sphingolipids	194-206	P53	Homo sapiens	70-73
22340582-5	2012	In vivo, the emulsion, with better dispersion than the polypolex and more specific tumour-target than lipiodol, mediated specific 4% p53 expression and antitumoural nanoparticle retention in the target tumour site, also significantly reduced tumour growth and prolonged the animal survival times more than the lipiodol (P &lt; 0.05).	Ethiodized Oil	102-110	P53	Homo sapiens	133-136
22764405-3	2012	Thermally crosslinked SPIONs (TCL-SPIONs) were conjugated with branched polyethylenimine (PEI 1800 Da) by EDC-NHS chemistry for p53 plasmid DNA delivery.	Triclosan	30-33	P53	Homo sapiens	128-131
22542944-7	2012	The expression levels of p53 and p21 were also induced by SKLB70326 treatment.	3-amino-6-(3-methoxyphenyl)thieno(2.3-b)pyridine-2-carboxamide	58-67	P53	Homo sapiens	25-28
22314934-9	2012	RESULTS: Sunitinib has the potential to moderately inhibit proliferation in the Huh7.5 cell line, induce p53 in the p53-wild-type cell line SK-hep-1, and to increase the S-phase and the sub-G1 component of the cell cycle in the Hep3B cell line.	Sunitinib	9-18	P53	Homo sapiens	105-108
22314934-9	2012	RESULTS: Sunitinib has the potential to moderately inhibit proliferation in the Huh7.5 cell line, induce p53 in the p53-wild-type cell line SK-hep-1, and to increase the S-phase and the sub-G1 component of the cell cycle in the Hep3B cell line.	Sunitinib	9-18	P53	Homo sapiens	116-119
23408470-10	2012	Moreover, in the presence of lithium chloride there were increased levels of p53 in cytoplasm and nucleus (p&lt;0.05).	Lithium Chloride	29-45	P53	Homo sapiens	77-80
22285236-8	2012	Based on the detection of protein expression (PARP, p53, Bcl-2/Bcl-xL, Bax, p38, pp38) we found that usnic acid and atranorin are activators of programmed cell death in A2780 and HT-29, probably through the mitochondrial pathway.	usnic acid	101-111	P53	Homo sapiens	52-55
22450683-6	2012	Xathatin also increased total p53 protein levels, decreased Bcl-2/Bax ratio and expression of the downstream factors procaspase-9 and procaspase-3, which triggered the intrinsic apoptosis pathway.	xathatin	0-8	P53	Homo sapiens	30-33
22306306-4	2012	Both DBC and the sarcomagen N-MeDBC induced significant levels of DNA strand-breaks, micronuclei, and DNA adducts followed by the phosphorylation of the p53 protein and histone H2AX in HaCaT cells.	N-methyl-7H-dibenzo(c,g)carbazole	28-35	P53	Homo sapiens	153-156
22135025-10	2012	Five-year CSS was 84% in p53-negative and 51% in p53-positive PC patients (p=0.003).	thiocysteine	10-13	P53	Homo sapiens	25-28
22135025-10	2012	Five-year CSS was 84% in p53-negative and 51% in p53-positive PC patients (p=0.003).	thiocysteine	10-13	P53	Homo sapiens	49-52
22135025-11	2012	Multivariable analysis showed p53 (HR=3.20; p=0.041) and pT-stage (HR=4.29; p&lt;0.001) as independent significant prognostic factors for CSS.	thiocysteine	138-141	P53	Homo sapiens	30-33
22109882-10	2012	An apoptosis protein array showed that the 1,25-D3 and lenalidomide combination increased pro-apoptotic proteins (phosphorylated p53) and decreased BCL-2 expression.	Calcitriol	43-50	P53	Homo sapiens	129-132
22020547-7	2012	Our results showed that the TPA-induced up-regulation             of p21 and down-regulation of p53 was reversed by UO126 (a MEK1/2 inhibitor),             but not by SP600125 (a JNK inhibitor) or SB203580 (a p38 inhibitor), although             TPA increased the phosphorylation of ERK and JNK in MCF-7 cells.	U 0126	116-121	P53	Homo sapiens	96-99
22053912-9	2012	In addition, both anti-BPDE and B[a]P-7,8-trans-dihydrodiol induced p53 expression ~6 h post-treatment at concentrations as low as 1 muM consistent with extensive DNA damage.	7,8-trans-dihydrodiol	38-59	P53	Homo sapiens	68-71
22223345-5	2012	PA inhibited cell proliferation and induced sub-G(1) arrest, elevating the mRNA levels of the apoptotic genes p53 and p21.	pomolic acid	0-2	P53	Homo sapiens	110-113
21964066-6	2012	The pharmacologic inhibitor (caffeine) of ataxia telangiectasia mutated (ATM) and ataxia telangiectasia and Rad3 related (ATR) protein kinases abolished activation of the p53-p21(WAF1) pathway upon FOXF1 knockdown, suggesting that suppression of FOXF1 function triggered the ATM/ATR-mediated DNA damage response.	Caffeine	29-37	P53	Homo sapiens	171-174
22919418-7	2012	PEITC induced G(0)/G(1) phase arrest through the effects of associated protein such as p53, p21, p17, CDK2 and cyclin E, and it triggered apoptosis through promotion of Bax and Bid expression and reduction of Bcl-2, leading to decrease the levels of mitochondrial membrane potential (DeltaPsi(m)), and followed the releases of cytochrome c, AIF and Endo G then for causing apoptosis in HSC-3 cells.	phenethyl isothiocyanate	0-5	P53	Homo sapiens	87-90
22577295-7	2012	In conclusion, alpha-mangostin may be useful as a therapeutic agent for breast cancer carrying a p53 mutation and having HER2- and hormone receptor-negative subtypes.	mangostin	15-30	P53	Homo sapiens	97-100
23216635-0	2012	Reactive oxygen species mediate Cr(VI)-induced S phase arrest through p53 in human colon cancer cells.	chromium hexavalent ion	32-38	P53	Homo sapiens	70-73
21607682-8	2011	Although no changes in the expression of the P53 tumor-suppressor gene were found, CYN up-regulated the expression of the P53 downstream-regulated genes CDKN1A, GADD45alpha, and MDM2.	cylindrospermopsin	83-86	P53	Homo sapiens	122-125
21225623-8	2011	Further, stilbene-elicited signaling cascade leading to p53 activation was examined in MCF-7 cells and results showed that resveratrol and triacetyl-resveratrol induced both ERK and p38 phosphorylation, whereas only marginal changes in state of phosphorylation in these two kinases were observed in trimethoxy-resveratrol-treated cells.	triacetylresveratrol	139-160	P53	Homo sapiens	56-59
21864635-13	2011	In contrast, BCAA, but not NaClO(2), increased BrO(3)(-)-induced phosphorylation of p53.	bro(3)(	47-54	P53	Homo sapiens	84-87
22009531-6	2011	Exposure to DMBA and TPA activated p53 and decreased MnSOD expression via p53-mediated suppression of Sp1 binding to the MnSOD promoter in normal-appearing skin and benign papillomas.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	12-16	P53	Homo sapiens	35-38
22009531-6	2011	Exposure to DMBA and TPA activated p53 and decreased MnSOD expression via p53-mediated suppression of Sp1 binding to the MnSOD promoter in normal-appearing skin and benign papillomas.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	12-16	P53	Homo sapiens	74-77
22030623-7	2011	The nuclear transfer of p53, but not of p73, was abrogated by protein kinase C inhibitor Go6976.	Go 6976	89-95	P53	Homo sapiens	24-27
21875801-0	2011	MDM2-p53 protein-protein interaction inhibitors: a-ring substituted isoindolinones.	phthalimidine	68-82	P53	Homo sapiens	5-8
22014055-5	2011	There were differences between the groups in expression of p53, p16 and Ki67, which were seen more consistently and earlier in proliferation in DIPNECH.	dipnech	144-151	P53	Homo sapiens	59-62
21897369-1	2011	iASPP, an inhibitory member of the ASPP (apoptosis stimulating protein of p53) family, is an evolutionarily conserved inhibitor of p53 which is frequently upregulated in human cancers.	aspp	1-5	P53	Homo sapiens	74-77
21897369-1	2011	iASPP, an inhibitory member of the ASPP (apoptosis stimulating protein of p53) family, is an evolutionarily conserved inhibitor of p53 which is frequently upregulated in human cancers.	aspp	1-5	P53	Homo sapiens	131-134
21251937-6	2011	Nilotinib induced apoptosis of HSCs, which was correlated with reduced bcl-2 expression, increased p53 expression, cleavage of PARP, as well as increased expression of PPARgamma and TRAIL-R. Nilotinib also induced cell cycle arrest, accompanied by increased expression of p27 and downregulation of cyclin D1.	nilotinib	0-9	P53	Homo sapiens	99-102
21425328-0	2011	Novel quinazoline HMJ-30 induces U-2 OS human osteogenic sarcoma cell apoptosis through induction of oxidative stress and up-regulation of ATM/p53 signaling pathway.	6-fluoro-2-(3-fluorophenyl)-4-(cyanoanilino)quinazoline	18-24	P53	Homo sapiens	143-146
21425328-9	2011	HMJ-30 induced early phosphorylation of p53(Ser18) was through the activation of ataxia telangiectasia mutated (ATM) in U-2 OS cells.	6-fluoro-2-(3-fluorophenyl)-4-(cyanoanilino)quinazoline	0-6	P53	Homo sapiens	40-43
20179988-0	2011	B1, a novel naphthalimide-based DNA intercalator, induces cell cycle arrest and apoptosis in HeLa cells via p53 activation.	Naphthalimides	12-25	P53	Homo sapiens	108-111
21802012-0	2011	Cholesterol secosterol aldehydes induce amyloidogenesis and dysfunction of wild-type tumor protein p53.	secosterol aldehydes	12-32	P53	Homo sapiens	99-102
21550660-5	2011	Interestingly, inhibition of caspase 3 by the pan-caspase inhibitor attenuated the combination of 5-AzadC and MS-275-mediated apoptosis and down-regulation of Mcl-1 in MV4-11 TP53 R248W cells.	entinostat	110-116	P53	Homo sapiens	175-179
21550660-8	2011	Combination of 5-AzadC and MS-275 may be a promising treatment strategy for individuals with leukemia in which TP53 is inactivated.	entinostat	27-33	P53	Homo sapiens	111-115
21668955-1	2011	BACKGROUND: Heterozygosity of TP53 missense mutations is related to the phenomenon of the dominant-negative effect (DNE).	dne	116-119	P53	Homo sapiens	30-34
20734047-11	2011	The data suggest that the loss of p53 can increase oxaliplatin resistance but not satraplatin resistance.	Oxaliplatin	51-62	P53	Homo sapiens	34-37
21636709-6	2011	We have examined inhibitors of the PI3K/Akt/mTOR signaling pathway and find that PI-103 and TCN show particular promise for inhibiting growth in Nf1 and Trp53 mutant astrocytoma cells.	PI103	81-87	P53	Homo sapiens	153-158
21617228-0	2011	Phenethyl isothiocyanate (PEITC) promotes G2/M phase arrest via p53 expression and induces apoptosis through caspase- and mitochondria-dependent signaling pathways in human prostate cancer DU 145 cells.	phenethyl isothiocyanate	0-24	P53	Homo sapiens	64-67
21106189-5	2011	RESULTS: Alpha-mangostin showed excellent apoptotic effects on HNSCC cell lines, which induced the down-regulation of bcl-2, but up-regulation of bax and p53 in HN-22, HN-30 and HN-31.	mangostin	9-24	P53	Homo sapiens	154-157
21106189-6	2011	CONCLUSION: The present study suggests that the induction of apoptosis by alpha-mangostin seemed to be modulated by bcl-2, bax and p53 level in HNSCC cell lines.	mangostin	74-89	P53	Homo sapiens	131-134
21350558-7	2011	We conclude that HDM-2 inhibition with MI-219 effectively induces p53-dependent apoptosis in most blast crisis CML cells, with or without BCR-ABL mutation(s).	MI-219	39-45	P53	Homo sapiens	66-69
21623005-9	2011	Individually silencing central nodes in these five hubsinterfered with MI-219-oxaliplatin activity confirming their critical role in aiding p53 mediated apoptotic response.	Oxaliplatin	78-89	P53	Homo sapiens	140-143
21559393-0	2011	Molecular mode of action and role of TP53 in the sensitivity to the novel epothilone sagopilone (ZK-EPO) in A549 non-small cell lung cancer cells.	Epothilones	74-84	P53	Homo sapiens	37-41
21508389-2	2011	Preclinical work has shown that the Kirsten ras (KRAS) oncogene sensitizes colorectal tumour cells to oxaliplatin and capecitabine in a wild-type tumour suppressor p53 (TP53)-dependent manner.	Oxaliplatin	102-113	P53	Homo sapiens	169-173
21508389-2	2011	Preclinical work has shown that the Kirsten ras (KRAS) oncogene sensitizes colorectal tumour cells to oxaliplatin and capecitabine in a wild-type tumour suppressor p53 (TP53)-dependent manner.	Capecitabine	118-130	P53	Homo sapiens	164-167
21508389-2	2011	Preclinical work has shown that the Kirsten ras (KRAS) oncogene sensitizes colorectal tumour cells to oxaliplatin and capecitabine in a wild-type tumour suppressor p53 (TP53)-dependent manner.	Capecitabine	118-130	P53	Homo sapiens	169-173
21134979-11	2011	Furthermore, voreloxin was active in the p53-null K562 cell line suggesting that the action of voreloxin is not affected by p53 status.	vosaroxin	13-22	P53	Homo sapiens	41-44
21500551-11	2011	KU55993, an inhibitor of ATM, significantly reduced the levels of gamma-H2AX, phosphorylated P53 protein, and positive rate of senescence-associated beta-galactosidase staining.	ku55993	0-7	P53	Homo sapiens	93-96
21241062-5	2011	Furthermore, we show that cells with p53 mutations are more sensitive to cytotoxicity induced by phenethyl isothiocyanate (PEITC) than those with the wild-type protein.	phenethyl isothiocyanate	97-121	P53	Homo sapiens	37-40
21241062-5	2011	Furthermore, we show that cells with p53 mutations are more sensitive to cytotoxicity induced by phenethyl isothiocyanate (PEITC) than those with the wild-type protein.	phenethyl isothiocyanate	123-128	P53	Homo sapiens	37-40
21229611-4	2011	We show that disruption of microtubule polymerization using colchicine suppresses nuclear localization of p53 but not of SV40TAg.	Colchicine	60-70	P53	Homo sapiens	106-109
20980803-8	2011	On the other hand, EGFR siRNA induced contradictory effects, decreasing PEA3 and MMP7 expression in control and oxaliplatin-treated RHCT116 p53-/- cells but increasing basal- and oxaliplatin-induced PEA3 and MMP7 in the HT29 and RHT29 cells.	Oxaliplatin	112-123	P53	Homo sapiens	140-143
21045015-8	2011	Exposure to resveratrol or triacetyl-resveratrol activated p53, increased p21 and p53R2 and decreased PSA expression in LNCaP cells.	triacetylresveratrol	27-48	P53	Homo sapiens	59-62
21045015-12	2011	CWR22Rv1 cells exposed to resveratrol and triacetyl-resveratrol showed a G1S block, concomitant with increased p53 and p21 expression; however, identically treated PC-3 cells showed attenuated progression through the SG2M phases.	triacetylresveratrol	42-63	P53	Homo sapiens	111-114
21467739-0	2011	Cycloheximide suppresses radiation-induced apoptosis in MOLT-4 cells with Arg72 variant of p53 through translational inhibition of p53 accumulation.	Cycloheximide	0-13	P53	Homo sapiens	91-94
21467739-0	2011	Cycloheximide suppresses radiation-induced apoptosis in MOLT-4 cells with Arg72 variant of p53 through translational inhibition of p53 accumulation.	Cycloheximide	0-13	P53	Homo sapiens	131-134
22174876-8	2011	Finally, transduction of target cells with an adenovirus vector encoding the thymidine kinase gene under transcriptional control of the Rad51 core promoter resulted in efficient killing of p53 defective cancer cells, but not of normal cells, upon addition of ganciclovir.	Ganciclovir	259-270	P53	Homo sapiens	189-192
21858223-9	2011	However, the down-regulation of FOXM1 by either thiostrepton or U0126 required the presence of p53 in ovarian cancer cells.	U 0126	64-69	P53	Homo sapiens	95-98
20708607-10	2010	In addition, oxaliplatin increased the levels of phospho-p53 (Ser-15) and total p53 proteins.	Oxaliplatin	13-24	P53	Homo sapiens	57-60
20708607-10	2010	In addition, oxaliplatin increased the levels of phospho-p53 (Ser-15) and total p53 proteins.	Oxaliplatin	13-24	P53	Homo sapiens	80-83
20708607-11	2010	Inhibition of p53 expression by a specific p53 inhibitor pifithrin-alpha reduced the phosphorylated p38 MAP kinase and active caspase-3 proteins in the oxaliplatin-exposed RKO cells.	Oxaliplatin	152-163	P53	Homo sapiens	14-17
20708607-11	2010	Inhibition of p53 expression by a specific p53 inhibitor pifithrin-alpha reduced the phosphorylated p38 MAP kinase and active caspase-3 proteins in the oxaliplatin-exposed RKO cells.	Oxaliplatin	152-163	P53	Homo sapiens	43-46
20683666-3	2010	Here, we report a new diarylsulfonylurea derivative, LB2A, that upregulates RhoB, thereby inducing potent apoptosis in HCT-116 human colon cancer cells independently of p53 status.	diarylsulfonylurea	22-40	P53	Homo sapiens	169-172
21042714-5	2010	Moreover, we discovered that a representative HQNBA derivative (JLK1486) induces strong but transient senescence in U87 cells in a P53-independent manner.	hqnba	46-51	P53	Homo sapiens	131-134
20413215-0	2010	Gambogic acid triggers DNA damage signaling that induces p53/p21(Waf1/CIP1) activation through the ATR-Chk1 pathway.	gambogic acid	0-13	P53	Homo sapiens	57-60
20413215-3	2010	However, GA-induced p53 activation could be partially reversed by caffeine, a PI3k inhibitor.	gambogic acid	9-11	P53	Homo sapiens	20-23
20413215-3	2010	However, GA-induced p53 activation could be partially reversed by caffeine, a PI3k inhibitor.	Caffeine	66-74	P53	Homo sapiens	20-23
20413215-4	2010	Therefore, questions of whether GA induces post-translational modifications of p53 and subsequent activation of p53; and if that is the case, which upstream signaling pathway(s) is (are) responsible for that are proposed.	gambogic acid	32-34	P53	Homo sapiens	79-82
20413215-4	2010	Therefore, questions of whether GA induces post-translational modifications of p53 and subsequent activation of p53; and if that is the case, which upstream signaling pathway(s) is (are) responsible for that are proposed.	gambogic acid	32-34	P53	Homo sapiens	112-115
20413215-5	2010	Here, the relationship between p53 activation and its post-translational modifications was investigated in the human cancer cell lines HepG2 and A549 in response to GA or adriamycin treatment.	gambogic acid	165-167	P53	Homo sapiens	31-34
20413215-6	2010	GA induces p53 phosphorylation at sites Ser15 and Ser20 in a concentration- or time-dependent way, which was a direct result of DNA damage, as gamma-HA2X foci and "comet" DNA fragments were detected.	gambogic acid	0-2	P53	Homo sapiens	11-14
20413215-7	2010	GA induces p53 phosphorylation through activation of an ATM- and Rad3-related pathway, and GA-induced phosphorylation of Chk1 is also involved.	gambogic acid	0-2	P53	Homo sapiens	11-14
20413215-8	2010	Upon treatment with GA, ATR activation is clearly associated with p53 phosphorylation, as well as activation of its target gene p21(Waf/CIP1).	gambogic acid	20-22	P53	Homo sapiens	66-69
20637980-0	2010	Enhancement of p53-mutant human colorectal cancer cells radiosensitivity by flavonoid fisetin.	flavonoid fisetin	76-93	P53	Homo sapiens	15-18
20637980-5	2010	RESULTS: Fisetin pretreatment enhanced the radiosensitivity of p53-mutant HT-29 human colorectal cancer cells but not human keratocyte HaCaT cells; it also prolonged radiation-induced G(2)/M arrest, enhanced radiation-induced cell growth arrest in HT-29 cells, and suppressed radiation-induced phospho-H2AX (Ser-139) and phospho-Chk2 (Thr-68) in p53-mutant HT-29 cells.	fisetin	9-16	P53	Homo sapiens	63-66
20637980-5	2010	RESULTS: Fisetin pretreatment enhanced the radiosensitivity of p53-mutant HT-29 human colorectal cancer cells but not human keratocyte HaCaT cells; it also prolonged radiation-induced G(2)/M arrest, enhanced radiation-induced cell growth arrest in HT-29 cells, and suppressed radiation-induced phospho-H2AX (Ser-139) and phospho-Chk2 (Thr-68) in p53-mutant HT-29 cells.	fisetin	9-16	P53	Homo sapiens	346-349
20432447-6	2010	Tyr/Phe, Gln and Met restriction increase phosphorylation of GSK3beta-Ser(9), phosphorylation of p53-Ser(15) and reduce the mitochondrial localization of PDH.	Phenylalanine	4-7	P53	Homo sapiens	97-100
20432447-8	2010	In p53-null PC3 cells, Tyr/Phe, Gln and Met restriction decreases glucose consumption, reduces phosphorylation of Akt-Ser(473), and increases phosphorylation of GSK3beta-Ser(9).	Phenylalanine	27-30	P53	Homo sapiens	3-6
20092938-2	2010	We now report that a lower dose of edaravone enhanced X-ray-induced apoptosis of some cell lines harboring p53 wild-type status, such as MOLT-4, Nalm-6, and HepG2.	Edaravone	35-44	P53	Homo sapiens	107-110
20092938-3	2010	The knock-down of p53 using siRNA in MOLT-4 cells abolished the radiosensitizing effect of edaravone.	Edaravone	91-100	P53	Homo sapiens	18-21
20092938-4	2010	Enhanced phosphorylations of p53 at Ser 15 and Ser 20 and up-regulation of PUMA, a p53 target protein, were observed after X-irradiation in the presence of edaravone.	Edaravone	156-165	P53	Homo sapiens	29-32
20092938-4	2010	Enhanced phosphorylations of p53 at Ser 15 and Ser 20 and up-regulation of PUMA, a p53 target protein, were observed after X-irradiation in the presence of edaravone.	Edaravone	156-165	P53	Homo sapiens	83-86
20092938-5	2010	We conclude that the low dose of edaravone sensitized cells to X-irradiation by promoting the p53-dependent apoptotic signaling pathway.	Edaravone	33-42	P53	Homo sapiens	94-97
19845468-4	2010	Lipofectaminemediated transfection of siRNAs directed against Trp53 and Pten resulted in decreased expression levels as determined by quantitative RT-PCR and immunoblotting.	lipofectaminemediated	0-21	P53	Homo sapiens	62-67
20499882-5	2010	Low concentrations of the NO donor, DETA NONOate (&lt;200 microM), exclusively nitrate Tyr327 within the tetramerization domain promoting p53 oligomerization, nuclear accumulation, and increased DNA-binding activity without p53 Ser15 phosphorylation.	Nitrates	79-86	P53	Homo sapiens	138-141
20530685-6	2010	LMW-E induces additional mitotic defects in cooperation with p53 loss in both normal and tumor cells.	lmw-e	0-5	P53	Homo sapiens	61-64
20493293-1	2010	In this paper we extend the application area of the label-free structure-sensitive electrochemical DNA sensing with mercury-based electrodes which is for the first time used, in combination with immunoprecipitation at magnetic beads (MB), for the probing of DNA interactions with tumor suppressor protein p53.	Mercury	116-123	P53	Homo sapiens	305-308
20354524-7	2010	RESULTS: Oncogenic KRAS sensitised colorectal tumour cells to oxaliplatin and 5-FU in a p53-dependent manner and promoted p53 phosphorylation at Ser37 and Ser392, without affecting p53 stabilisation, p21 induction, or cell-cycle arrest.	Oxaliplatin	62-73	P53	Homo sapiens	88-91
20354524-11	2010	CONCLUSION: Oncogenic KRAS determines the cellular response to p53 activation by oxaliplatin or 5-FU, by facilitating apoptosis induction through Noxa.	Oxaliplatin	81-92	P53	Homo sapiens	63-66
20107315-7	2010	Enhancement by MK-1775 was specific for p53-deficient cells since this compound did not sensitize p53-wild type human colon cancer cells to 5-FU in vitro.	adavosertib	15-22	P53	Homo sapiens	40-43
20371709-7	2010	Consistently, Sirtinol and Salermide, but not EX527, treatment resulted in the in vivo acetylation of the SIRT1/2 target p53 and SIRT2 target tubulin in MCF-7 cells, suggesting that EX527 is ineffective in inhibiting SIRT2 and that p53 mediates the cytotoxic function of Sirtinol and Salermide.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	27-36	P53	Homo sapiens	121-124
20371709-7	2010	Consistently, Sirtinol and Salermide, but not EX527, treatment resulted in the in vivo acetylation of the SIRT1/2 target p53 and SIRT2 target tubulin in MCF-7 cells, suggesting that EX527 is ineffective in inhibiting SIRT2 and that p53 mediates the cytotoxic function of Sirtinol and Salermide.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	27-36	P53	Homo sapiens	232-235
20371712-3	2010	Previous studies have reported that Nutlin promotes growth arrest and/or apoptosis in cancer cells that express wild-type p53.	nutlin	36-42	P53	Homo sapiens	122-125
20371712-9	2010	Taken together, these findings reveal that Nutlin treatment can inhibit the migration and invasion capacity of p53 wild-type cells, adding to the potential therapeutic benefit of Nutlin and other small molecule MDM2 inhibitors.	nutlin	43-49	P53	Homo sapiens	111-114
20298590-7	2010	RESULTS: We demonstrate that lovastatin induces apoptosis of ovarian cancer cells in a p53-independent manner and synergizes with doxorubicin, a chemotherapeutic agent used to treat recurrent cases of ovarian cancer.	Lovastatin	29-39	P53	Homo sapiens	87-90
19515076-4	2010	RESULTS: All lesions showed positive immunostaining of p53, affecting to the lower two thirds of the epidermis in BD and bAK, and only the basal layer in non-bAK.	bakuchiol	121-124	P53	Homo sapiens	55-58
20103602-9	2010	The p53 independency was also confirmed by a significant caffeine-mediated radiosensitization of the glioma cell lines T98G and U373MG that are deficient for both PTEN and p53.	Caffeine	57-65	P53	Homo sapiens	4-7
20103602-9	2010	The p53 independency was also confirmed by a significant caffeine-mediated radiosensitization of the glioma cell lines T98G and U373MG that are deficient for both PTEN and p53.	Caffeine	57-65	P53	Homo sapiens	172-175
19853978-0	2010	The role of p53 in the cellular toxicity by active trans-platinum complexes containing isopropylamine and hydroxymethylpyridine.	2-PYRIDINEMETHANOL	106-127	P53	Homo sapiens	12-15
19853978-3	2010	In the present work, we have studied the biochemical properties of the trans-[PtCl2(isopropylamine)(L)] complexes (where L is 3- or 4-(hydroxymethyl)-pyridine) against several cell lines and the relationship between cytotoxicity and the protein p53.	trans-[ptcl2(isopropylamine)(l)]	71-103	P53	Homo sapiens	245-248
19608275-7	2010	The enhanced cytotoxicity of ATO+bortezomib was associated with augmented STAT3 inhibition and JNK activation, up-regulation of Bim, p21, p27, p53 as well as down-regulation of Bcl-2.	ato	29-32	P53	Homo sapiens	143-146
20003329-0	2009	Role of p53 mutation in the effect of boron neutron capture therapy on oral squamous cell carcinoma.	Boron	38-43	P53	Homo sapiens	8-11
19935879-7	2009	Collectively, our data suggested that wogonin induced G1 phase arrest in HeLa cells by modulating several key G1 regulatory proteins, such as Cdk4 and cyclin D1, as well as up-regulation of a p53-mediated p21Cip1 expression.	wogonin	38-45	P53	Homo sapiens	192-195
19934289-2	2009	The cis-imidazoline nutlin-3 can disrupt the p53-Hdm2 interaction and activate p53, inducing apoptosis in vitro in many malignancies, including multiple myeloma (MM).	cis-imidazoline	4-19	P53	Homo sapiens	45-48
19934289-2	2009	The cis-imidazoline nutlin-3 can disrupt the p53-Hdm2 interaction and activate p53, inducing apoptosis in vitro in many malignancies, including multiple myeloma (MM).	cis-imidazoline	4-19	P53	Homo sapiens	79-82
19582475-1	2009	PURPOSE: In this study, we investigated the correlation between p53 and bcl-2 in gambogic acid (GA)-induced apoptosis.	gambogic acid	81-94	P53	Homo sapiens	64-67
19582475-1	2009	PURPOSE: In this study, we investigated the correlation between p53 and bcl-2 in gambogic acid (GA)-induced apoptosis.	gambogic acid	96-98	P53	Homo sapiens	64-67
19582475-12	2009	CONCLUSIONS: Gambogic acid induced human breast cancer cells MCF-7 apoptosis by reducing bcl-2 expression via p53.	gambogic acid	13-26	P53	Homo sapiens	110-113
19885592-0	2009	Triptolide induces apoptosis in human anaplastic thyroid carcinoma cells by a p53-independent but NF-kappaB-related mechanism.	triptolide	0-10	P53	Homo sapiens	78-81
19885592-5	2009	Our studies suggest that triptolide functions as an effective apoptotic inducer in a p53-independent, but NF-kappaB-dependent mechanism, thus providing a promising agent for tumor types with p53 mutation/deletion.	triptolide	25-35	P53	Homo sapiens	85-88
19885592-5	2009	Our studies suggest that triptolide functions as an effective apoptotic inducer in a p53-independent, but NF-kappaB-dependent mechanism, thus providing a promising agent for tumor types with p53 mutation/deletion.	triptolide	25-35	P53	Homo sapiens	191-194
19524422-0	2009	Effects of triptolide from Tripterygium wilfordii on ERalpha and p53 expression in two human breast cancer cell lines.	triptolide	11-21	P53	Homo sapiens	65-68
19524422-2	2009	Considering that MCF-7 cells express functional Estrogen receptor alpha (ERalpha) and wild-type p53, whereas MDA-MB-231 cells which are ERalpha-negative express mutant p53, the anti-proliferation effect of triptolide on MCF-7 and MDA-MB-231 cells were examined, the apoptotic effect and cell cycle arrest caused by triptolide were investigated, ERalpha and p53 expression were also observed in this paper.	triptolide	206-216	P53	Homo sapiens	96-99
19524422-2	2009	Considering that MCF-7 cells express functional Estrogen receptor alpha (ERalpha) and wild-type p53, whereas MDA-MB-231 cells which are ERalpha-negative express mutant p53, the anti-proliferation effect of triptolide on MCF-7 and MDA-MB-231 cells were examined, the apoptotic effect and cell cycle arrest caused by triptolide were investigated, ERalpha and p53 expression were also observed in this paper.	triptolide	206-216	P53	Homo sapiens	168-171
19524422-2	2009	Considering that MCF-7 cells express functional Estrogen receptor alpha (ERalpha) and wild-type p53, whereas MDA-MB-231 cells which are ERalpha-negative express mutant p53, the anti-proliferation effect of triptolide on MCF-7 and MDA-MB-231 cells were examined, the apoptotic effect and cell cycle arrest caused by triptolide were investigated, ERalpha and p53 expression were also observed in this paper.	triptolide	206-216	P53	Homo sapiens	168-171
19866438-5	2009	Among the 40 samples, 23, 11, and 10 showed p53, Rad50, and cyclin-E expression, respectively, in moderately differentiated adenocarcinomas, demonstrating the prevalence and invasiveness of this disease in the methyl isocyanate-exposed population (P = 0.0009).	methyl isocyanate	210-227	P53	Homo sapiens	44-47
19866438-7	2009	We conclude that there was altered expression of p53, Rad50, and cyclin-E in the malignant transformation of gallbladder carcinoma in this methyl isocyanate gas-exposed cohort.	methyl isocyanate	139-156	P53	Homo sapiens	49-52
19805223-0	2009	The p53 target Wig-1 regulates p53 mRNA stability through an AU-rich element.	Gold	61-63	P53	Homo sapiens	4-7
19805223-0	2009	The p53 target Wig-1 regulates p53 mRNA stability through an AU-rich element.	Gold	61-63	P53	Homo sapiens	31-34
19299014-1	2009	Oncoprotein inhibitory member of the ASPP family (iASPP) is a key inhibitor of tumor suppressor p53.	aspp	37-41	P53	Homo sapiens	96-99
19723892-2	2009	A clear p53-dependent expression pattern of PDF was shown in a panel of colorectal cancer cell lines following acute exposure to oxaliplatin, 5-fluorouracil, and SN38.	Oxaliplatin	129-140	P53	Homo sapiens	8-11
19564019-4	2009	The following factors increased accuracy of D&amp;C: depth of uterus cavity &gt; or = 9 cm (P = .043), deep (&gt; 50%) myometrial invasion (P = .03), P53 positivity (P = .023), grade 2 (P = .01), and grade 3 (P = .048).	Benzoic acid, 2-[[4-[bis(2-hydroxyethyl)amino]phenyl]azo]-	44-49	P53	Homo sapiens	150-153
19468031-12	2009	Positive p53 status was related to poorer OS and CSS.	thiocysteine	49-52	P53	Homo sapiens	9-12
19723092-0	2009	Phloretin induces apoptosis in H-Ras MCF10A human breast tumor cells through the activation of p53 via JNK and p38 mitogen-activated protein kinase signaling.	Phloretin	0-9	P53	Homo sapiens	95-98
19723092-4	2009	Prominent upregulation of p53 and Bax and cleavage of poly (ADP)-ribose polymerase were also detected in the phloretin-treated cells.	Phloretin	109-118	P53	Homo sapiens	26-29
19351655-1	2009	We hypothesized that NRH:quinone oxidoreductase 2 (NQO2) is a candidate susceptibility gene for breast cancer because of its known enzymatic activity on estrogen-derived quinones and its ability to stabilize p53.	Quinones	170-178	P53	Homo sapiens	208-211
19536869-6	2009	The specific ATM inhibitor caffeine significantly decreased ISL-mediated G2/M arrest by inhibiting the phosphorylation of p53 (Serine15) and Chk2.	Caffeine	27-35	P53	Homo sapiens	122-125
19328230-6	2009	Conversely, oxaliplatin-induced translocation of p53 was prevented by cotreatment with an exogenous NO donor.	Oxaliplatin	12-23	P53	Homo sapiens	49-52
19508737-0	2009	Eurycomanone induce apoptosis in HepG2 cells via up-regulation of p53.	eurycomanone	0-12	P53	Homo sapiens	66-69
19508737-9	2009	This study also found that apoptotic process triggered by eurycomanone involved the up-regulation of p53 tumor suppressor protein.	eurycomanone	58-70	P53	Homo sapiens	101-104
19508737-12	2009	CONCLUSION: The data suggest that eurycomanone was cytotoxic on HepG2 cells by inducing apoptosis through the up-regulation of p53 and Bax, and down-regulation of Bcl-2.	eurycomanone	34-46	P53	Homo sapiens	127-130
19270508-0	2009	Modulation of thymidilate synthase and p53 expression by HDAC inhibitor vorinostat resulted in synergistic antitumor effect in combination with 5FU or raltitrexed.	raltitrexed	151-162	P53	Homo sapiens	39-42
19351839-4	2009	Pretreatment of several melanoma lines just before gamma-irradiation with the inhibitor of ATM kinase KU-55933 suppressed p53 and nuclear factor-kappaB (NF-kappaB) activation but notably increased radiation-induced DR5 surface expression, down-regulated cFLIP (caspase-8 inhibitor) levels, and substantially enhanced exogenous TRAIL-induced apoptosis.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	102-110	P53	Homo sapiens	122-151
20126301-7	2009	We also suggest the potential for two p53 target genes, START domain-containing protein 4 (StARD4) and oxysterol-binding protein (OSBP), with the concomitant synthesis of the signaling molecule oxysterol, to participate in adipogenesis.	Oxysterols	103-112	P53	Homo sapiens	38-41
19202066-0	2009	Loss of p53 enhances catalytic activity of IKKbeta through O-linked beta-N-acetyl glucosamine modification.	o-linked beta-n-acetyl glucosamine	59-93	P53	Homo sapiens	8-11
20157519-8	2009	However, p53 acetylation (K382Ac) was barely detectable.	k382ac	26-32	P53	Homo sapiens	9-12
19165821-0	2009	Cytoprotective effects of the lipoidic-liquiform pro-vitamin C tetra-isopalmitoyl-ascorbate (VC-IP) against ultraviolet-A ray-induced injuries in human skin cells together with collagen retention, MMP inhibition and p53 gene repression.	vc-ip	93-98	P53	Homo sapiens	216-219
19137016-0	2009	9-Aminoacridine-based anticancer drugs target the PI3K/AKT/mTOR, NF-kappaB and p53 pathways.	Aminacrine	0-15	P53	Homo sapiens	79-82
19137016-3	2009	The small molecule 9-aminoacridine (9AA) and its derivative, the antimalaria drug quinacrine, have selective toxicity for tumor cells and can simultaneously suppress nuclear factor-kappaB (NF-kappaB) and activate p53 signaling.	Aminacrine	19-34	P53	Homo sapiens	213-216
19137016-3	2009	The small molecule 9-aminoacridine (9AA) and its derivative, the antimalaria drug quinacrine, have selective toxicity for tumor cells and can simultaneously suppress nuclear factor-kappaB (NF-kappaB) and activate p53 signaling.	Aminacrine	36-39	P53	Homo sapiens	213-216
19154901-14	2009	CONCLUSION: FDG-PET maximal standardized uptake values correlate with an increased expression of glucose transporter 1 and p53 in lung adenocarcinoma, but not squamous cell cancer.	Fluorodeoxyglucose F18	12-15	P53	Homo sapiens	123-126
19015155-0	2009	Regulation of human dUTPase gene expression and p53-mediated transcriptional repression in response to oxaliplatin-induced DNA damage.	Oxaliplatin	103-114	P53	Homo sapiens	48-51
19047160-6	2008	Up-regulated expression of p53/56 Lyn kinase, both at the mRNA and protein level, was found in one of the resistant cell lines and Lyn silencing by small interfering RNA restored sensitivity to nilotinib.	nilotinib	194-203	P53	Homo sapiens	27-30
19127115-7	2008	Direct sequencing of TP53 gene exons 5, 6, 8, 9, and 11 revealed a ermline missense mutation, resulting in an amino acid change from an arginine to a histidine (g.13203G&gt;A, p.R175H).	ermline	67-74	P53	Homo sapiens	21-25
18959403-0	2008	Analysis of chemical shift changes reveals the binding modes of isoindolinone inhibitors of the MDM2-p53 interaction.	phthalimidine	64-77	P53	Homo sapiens	101-104
18959403-1	2008	In this study we present a method for defining the binding modes of a set of structurally related isoindolinone inhibitors of the MDM2-p53 interaction.	phthalimidine	98-111	P53	Homo sapiens	135-138
18959403-2	2008	This approach derives the location and orientation of isoindolinone binding, based on an analysis of the patterns of magnitude and direction of chemical shift perturbations for a series of inhibitors of the MDM2-p53 interaction.	phthalimidine	54-67	P53	Homo sapiens	212-215
18787402-2	2008	Here we show that combining the three sage bioactive compounds, Linalyl acetate (Ly), Terpeniol (Te) and Camphor (Ca), caused synergistic inhibition of the growth of two isogenic human colon cancer cell lines HCT-116 (p53(+/+) and p53(-/-)) and had no effect on growth of FHs74Int normal human intestinal cell line.	linalyl acetate	64-79	P53	Homo sapiens	218-221
18787402-2	2008	Here we show that combining the three sage bioactive compounds, Linalyl acetate (Ly), Terpeniol (Te) and Camphor (Ca), caused synergistic inhibition of the growth of two isogenic human colon cancer cell lines HCT-116 (p53(+/+) and p53(-/-)) and had no effect on growth of FHs74Int normal human intestinal cell line.	linalyl acetate	64-79	P53	Homo sapiens	231-234
18787402-2	2008	Here we show that combining the three sage bioactive compounds, Linalyl acetate (Ly), Terpeniol (Te) and Camphor (Ca), caused synergistic inhibition of the growth of two isogenic human colon cancer cell lines HCT-116 (p53(+/+) and p53(-/-)) and had no effect on growth of FHs74Int normal human intestinal cell line.	linalyl acetate	81-83	P53	Homo sapiens	218-221
18787402-2	2008	Here we show that combining the three sage bioactive compounds, Linalyl acetate (Ly), Terpeniol (Te) and Camphor (Ca), caused synergistic inhibition of the growth of two isogenic human colon cancer cell lines HCT-116 (p53(+/+) and p53(-/-)) and had no effect on growth of FHs74Int normal human intestinal cell line.	linalyl acetate	81-83	P53	Homo sapiens	231-234
18707164-2	2008	The result of the calculation, based on structures from nanosecond molecular dynamics simulation, revealed that (19)Phe, (22)Leu, and (23)Trp of p53 have the strongest binding interaction with MDM2 followed by (26)Leu and (27)Pro.	Phenylalanine	116-119	P53	Homo sapiens	145-148
19035306-3	2008	MATERIALS AND METHODS: The effect of the synthetic sulfonate ester, p-methoxyphenyl p-toluenesulfonate on growth inhibitory activity depending upon the estrogen-receptor (ER), p53, bcl-2 and caspase-3 status of cells was investigated by comparing its effects on three distinct human breast cancer cell lines (MCF-7, MDA-MB-231 and MDA-MB-453) and on one normal human mammary epithelial cell line (MCF-10A).	sulfonate ester	51-66	P53	Homo sapiens	176-179
18850641-2	2008	Three 9-fluorenylmethoxycarbonyl (Fmoc)-labeled peptide substrates derived from the amino acid sequence of p53, i.e. Fmoc-KK(Ac)-NH(2), Fmoc-KK(Ac)L-NH(2) and Fmoc-RHKK(Ac)-NH(2), were synthesized and evaluated as substrates of the human isoenzyme SIRT1.	9-fluorenylmethoxycarbonyl	6-32	P53	Homo sapiens	107-110
18550670-3	2008	Given these attributes, we were interested in the activity of small-molecule inhibitor 9-aminoacridine (9AA), an anticancer drug that targets two important stress response pathways, NF-kappaB and p53.	Aminacrine	87-102	P53	Homo sapiens	196-199
18550670-3	2008	Given these attributes, we were interested in the activity of small-molecule inhibitor 9-aminoacridine (9AA), an anticancer drug that targets two important stress response pathways, NF-kappaB and p53.	Aminacrine	104-107	P53	Homo sapiens	196-199
18550670-10	2008	These results suggest that Tax-repressed p53 function in HTLV-1-transformed cells is "druggable" and can be restored by treatment with 9AA.	Aminacrine	135-138	P53	Homo sapiens	41-44
18550670-11	2008	The fact that 9AA induces p53 and inhibits NF-kappaB suggests a promising strategy for the treatment of HTLV-1-transformed cells.	Aminacrine	14-17	P53	Homo sapiens	26-29
18391982-0	2008	Cancer-specific enhancement of cisplatin-induced cytotoxicity with triptolide through an interaction of inactivated glycogen synthase kinase-3beta with p53.	triptolide	67-77	P53	Homo sapiens	152-155
18391982-3	2008	Our results showed that a combined CDDP/triptolide therapy induced apoptosis in urothelial cancer cell lines with wild-type p53, but not in those with mutant-type p53 or normal human urothelium.	triptolide	40-50	P53	Homo sapiens	124-127
18391982-4	2008	As the mechanism, triptolide suppressed CDDP-induced p53 transcriptional activity, leading to p21 attenuation, which promoted apoptosis via the activation of c-Jun N-terminal kinase (JNK) and Bax.	triptolide	18-28	P53	Homo sapiens	53-56
18391982-5	2008	We further demonstrated that the functional regulation of p53 by triptolide was mediated by an intranuclear association of p53 with glycogen synthase kinase-3beta (GSK3beta), which was inactivated by protein kinase C (PKC).	triptolide	65-75	P53	Homo sapiens	58-61
18391982-5	2008	We further demonstrated that the functional regulation of p53 by triptolide was mediated by an intranuclear association of p53 with glycogen synthase kinase-3beta (GSK3beta), which was inactivated by protein kinase C (PKC).	triptolide	65-75	P53	Homo sapiens	123-126
18340116-4	2008	MI-43 induced the accumulation of p53 and its downstream target genes, Mdm2, p21, Noxa and Puma only in wt p53-containing cells, indicating that disruption of Mdm2-p53 binding increases p53, which is transcriptionally active.	mi-43	0-5	P53	Homo sapiens	34-37
18340116-4	2008	MI-43 induced the accumulation of p53 and its downstream target genes, Mdm2, p21, Noxa and Puma only in wt p53-containing cells, indicating that disruption of Mdm2-p53 binding increases p53, which is transcriptionally active.	mi-43	0-5	P53	Homo sapiens	107-110
18340116-4	2008	MI-43 induced the accumulation of p53 and its downstream target genes, Mdm2, p21, Noxa and Puma only in wt p53-containing cells, indicating that disruption of Mdm2-p53 binding increases p53, which is transcriptionally active.	mi-43	0-5	P53	Homo sapiens	107-110
18340116-4	2008	MI-43 induced the accumulation of p53 and its downstream target genes, Mdm2, p21, Noxa and Puma only in wt p53-containing cells, indicating that disruption of Mdm2-p53 binding increases p53, which is transcriptionally active.	mi-43	0-5	P53	Homo sapiens	107-110
18340116-5	2008	MI-43 preferentially inhibited the growth of wt p53-containing cells in a p53 dependent manner, but was much less effective in p53-null cells.	mi-43	0-5	P53	Homo sapiens	48-51
18340116-5	2008	MI-43 preferentially inhibited the growth of wt p53-containing cells in a p53 dependent manner, but was much less effective in p53-null cells.	mi-43	0-5	P53	Homo sapiens	74-77
18340116-5	2008	MI-43 preferentially inhibited the growth of wt p53-containing cells in a p53 dependent manner, but was much less effective in p53-null cells.	mi-43	0-5	P53	Homo sapiens	74-77
18340116-9	2008	Thus, MI-43 or its analogues could be further developed as a novel class of anticancer drug for lung cancer cells harboring wt p53 as a single agent or in combination with chemo-drugs.	mi-43	6-11	P53	Homo sapiens	127-130
18400537-8	2008	The SPT inhibitor ISP-1 or the ceramide synthase inhibitor fumonisin B1 led to substantial inhibition of ceramide accumulation in response to p53 up-regulation.	fumonisin B1	59-71	P53	Homo sapiens	142-145
18377871-8	2008	Further characterization of the transcriptional response to wogonin in HCT116 human colon cancer cells demonstrated that PUMA induction was p53-dependent; deficiency in either p53 or PUMA significantly protected HCT116 cells against wogonin-induced apoptosis.	wogonin	60-67	P53	Homo sapiens	176-179
18395372-0	2008	Verminoside- and verbascoside-induced genotoxicity on human lymphocytes: involvement of PARP-1 and p53 proteins.	acteoside	17-29	P53	Homo sapiens	99-102
18243662-6	2008	On the other hand, LiCl, having no effect on caspase-3 activation, significantly increased p53 phosphorylation and apoptotic death of the normal MRC5CV1 cells while IR, activating both caspase-3 and p53, profoundly affected AT5BIVA cell death.	Lithium Chloride	19-23	P53	Homo sapiens	91-94
18243662-6	2008	On the other hand, LiCl, having no effect on caspase-3 activation, significantly increased p53 phosphorylation and apoptotic death of the normal MRC5CV1 cells while IR, activating both caspase-3 and p53, profoundly affected AT5BIVA cell death.	Lithium Chloride	19-23	P53	Homo sapiens	199-202
18096571-8	2008	Acrolein potentiated the effect of BP on p53 stabilization and chromatin binding.	Acrolein	0-8	P53	Homo sapiens	41-44
18348731-7	2008	In this current study, we show that a small chemical molecule, 9-aminoacridine (9AA) at low concentrations, could efficiently reactivate p53 pathway and thereby restoring the p21/waf1 function.	Aminacrine	63-78	P53	Homo sapiens	137-140
18348731-7	2008	In this current study, we show that a small chemical molecule, 9-aminoacridine (9AA) at low concentrations, could efficiently reactivate p53 pathway and thereby restoring the p21/waf1 function.	Aminacrine	80-83	P53	Homo sapiens	137-140
18288380-9	2008	Studies on the regulation of apoptosis showed that apicidin induces the up-regulation of p53 and the downstream activation of ERK in MCF10A-ras cells.	apicidin	51-59	P53	Homo sapiens	89-92
18315954-3	2008	We found that the NO donor S-nitroso-N-acetylpenicillamine (SNAP) increased apoptotic cell death in p53-deficient VSMCs compared with wild-type cells.	S-Nitroso-N-Acetylpenicillamine	27-58	P53	Homo sapiens	100-103
18048073-0	2008	Central role of mitochondria and p53 in PUVA-induced apoptosis in human keratinocytes cell line NCTC-2544.	puva	40-44	P53	Homo sapiens	33-36
18179182-5	2008	The cysteine residues on the exterior of the p53 molecule were derivatized for the attachment of gold nanoparticle/streptavidin conjugates capped with multiple ferrocene (Fc) groups.	ferrocene	160-169	P53	Homo sapiens	45-48
18179182-5	2008	The cysteine residues on the exterior of the p53 molecule were derivatized for the attachment of gold nanoparticle/streptavidin conjugates capped with multiple ferrocene (Fc) groups.	ferrocene	171-173	P53	Homo sapiens	45-48
18299254-5	2008	The results showed that the high levels of integrin beta4, p53 and ROS induced by the deprivation of serum and FGF-2 could be inhibited by the treatment of 40 microM ISO-9.	iso-9	166-171	P53	Homo sapiens	59-62
18154926-6	2008	Blocking ERK1/2 activation with the upstream inhibitor U0126 inhibited NMDA-mediated p53 expression, suggesting that ERK1/2 signals drive the cells to apoptosis under these conditions.	U 0126	55-60	P53	Homo sapiens	85-88
18042465-2	2008	Here, we investigated the effects of HO activity on the expression of p53 in the human retinal pigment epithelium (RPE) cell line ARPE-19.	Holmium	37-39	P53	Homo sapiens	70-73
18042465-3	2008	Cobalt protoporphyrin (CoPP) induced the expression of both HO-1 and p53 without significant toxicity to the cells.	cobaltiprotoporphyrin	0-21	P53	Homo sapiens	69-72
18042465-3	2008	Cobalt protoporphyrin (CoPP) induced the expression of both HO-1 and p53 without significant toxicity to the cells.	cobaltiprotoporphyrin	23-27	P53	Homo sapiens	69-72
18042465-4	2008	In addition, the blockage of HO activity with the iron chelator DFO or with HO-1 siRNA inhibited the CoPP-induced expression of p53.	cobaltiprotoporphyrin	101-105	P53	Homo sapiens	128-131
18042465-6	2008	Also, CoPP-induced p53 expression was not affected by the formation of reactive oxygen species (ROS).	cobaltiprotoporphyrin	6-10	P53	Homo sapiens	19-22
18042465-7	2008	Based on these results, we conclude that HO activity is involved in the regulation of p53 expression in a ROS-independent mechanism, and also suggest that the expression of p53 in ARPE-19 cells is associated with heme metabolites such as biliverdin/bilirubin, carbon monoxide, and iron produced by the activity of HO.	Biliverdine	238-248	P53	Homo sapiens	173-176
18540844-5	2008	This article also covers the relationship between Cr(VI)-induced oxidative stress and activation of transcription factors NF-kappaB, AP-1, p53, and hypoxia-inducible factor 1, regulation of cell cycle, and induction of apoptosis.	chromium hexavalent ion	50-56	P53	Homo sapiens	139-142
17717041-3	2007	In this study, we further examined the mechanism of DHA-butyrate synergism in 1) human colon tumor (HCT-116 isogenic p53+/+ vs. p53-/-) cells and 2) primary cultures of rat colonic crypts.	dha-butyrate	52-64	P53	Homo sapiens	117-120
17270229-4	2007	There are certain "hot-spots" in the p53 gene where mutations are commonly found that result in a mutated dipyrimidine site.	dipyrimidine	106-118	P53	Homo sapiens	37-40
17487454-0	2007	Involvement of PPAR-gamma and p53 in DHA-induced apoptosis in Reh cells.	Dihydroalprenolol	37-40	P53	Homo sapiens	30-33
17487454-6	2007	Interestingly, DHA was found to induce the expression of p53 protein in Reh cells in a PPAR-gamma-dependent manner.	Dihydroalprenolol	15-18	P53	Homo sapiens	57-60
17487454-7	2007	The up-regulation of p53 protein by DHA kinetically correlated with the activation of caspase 9, caspase 3, and induction of apoptosis, suggesting a role for p53 in DHA-mediated apoptosis in Reh cells.	Dihydroalprenolol	36-39	P53	Homo sapiens	21-24
17487454-7	2007	The up-regulation of p53 protein by DHA kinetically correlated with the activation of caspase 9, caspase 3, and induction of apoptosis, suggesting a role for p53 in DHA-mediated apoptosis in Reh cells.	Dihydroalprenolol	165-168	P53	Homo sapiens	21-24
17487454-8	2007	Taken together, these findings suggest a new signaling pathway, DHA-PPAR-gamma-p53, in mediating the apoptotic effect of DHA in Reh cells.	Dihydroalprenolol	64-67	P53	Homo sapiens	79-82
17671694-11	2007	Therefore, pGSK-3beta-ser-9 may confer the cisplatin resistance of ovarian carcinomas through the stabilization of p53 expression.	pgsk-3beta	11-21	P53	Homo sapiens	115-118
17559811-5	2007	Exposure to oxaliplatin resulted in G0/G1 arrest in p53 wild-type cell lines, and in S phase in p53-mutated cell lines.	Oxaliplatin	12-23	P53	Homo sapiens	52-55
17559811-5	2007	Exposure to oxaliplatin resulted in G0/G1 arrest in p53 wild-type cell lines, and in S phase in p53-mutated cell lines.	Oxaliplatin	12-23	P53	Homo sapiens	96-99
17559811-7	2007	The major role of the p53-p21 pathway in oxaliplatin sensitivity was confirmed in the p53 wild-type HCT116 cell line, using siRNA duplex, and knockdown of the TAp73 protein also enhanced resistance to oxaliplatin in this cell line.	Oxaliplatin	41-52	P53	Homo sapiens	22-25
17559811-7	2007	The major role of the p53-p21 pathway in oxaliplatin sensitivity was confirmed in the p53 wild-type HCT116 cell line, using siRNA duplex, and knockdown of the TAp73 protein also enhanced resistance to oxaliplatin in this cell line.	Oxaliplatin	41-52	P53	Homo sapiens	86-89
17559811-9	2007	Persistent sensitivity to oxaliplatin of the p53-mutated V9P cell line was associated with oxalipatin-induced apoptosis but TAp73 was not the responsible alternative pathway.	Oxaliplatin	26-37	P53	Homo sapiens	45-48
17442733-0	2007	p53-dependent NDRG1 expression induces inhibition of intestinal epithelial cell proliferation but not apoptosis after polyamine depletion.	Polyamines	118-127	P53	Homo sapiens	0-3
17442733-2	2007	Our previous studies have shown that polyamine depletion stabilizes p53, resulting in inhibition of intestinal epithelial cell (IEC) proliferation, but the exact downstream targets of induced p53 are still unclear.	Polyamines	37-46	P53	Homo sapiens	68-71
17442733-4	2007	The current study tests the hypothesis that induced p53 inhibits IEC proliferation by upregulating NDRG1 expression following polyamine depletion.	Polyamines	126-135	P53	Homo sapiens	52-55
17442733-5	2007	Depletion of cellular polyamines by inhibiting ornithine decarboxylase (ODC) with alpha-difluoromethylornithine not only induced p53 but also increased NDRG1 transcription as indicated by induction of the NDRG1 promoter activity and increased levels of NDRG1 mRNA and protein, all of which were prevented by using specific p53 siRNA and in cells with a targeted deletion of p53.	Polyamines	22-32	P53	Homo sapiens	129-132
17442733-5	2007	Depletion of cellular polyamines by inhibiting ornithine decarboxylase (ODC) with alpha-difluoromethylornithine not only induced p53 but also increased NDRG1 transcription as indicated by induction of the NDRG1 promoter activity and increased levels of NDRG1 mRNA and protein, all of which were prevented by using specific p53 siRNA and in cells with a targeted deletion of p53.	Polyamines	22-32	P53	Homo sapiens	323-326
17442733-5	2007	Depletion of cellular polyamines by inhibiting ornithine decarboxylase (ODC) with alpha-difluoromethylornithine not only induced p53 but also increased NDRG1 transcription as indicated by induction of the NDRG1 promoter activity and increased levels of NDRG1 mRNA and protein, all of which were prevented by using specific p53 siRNA and in cells with a targeted deletion of p53.	Polyamines	22-32	P53	Homo sapiens	323-326
17442733-6	2007	In contrast, increased levels of cellular polyamines by ectopic expression of the ODC gene decreased p53 and repressed expression of NDRG1.	Polyamines	42-52	P53	Homo sapiens	101-104
17442733-7	2007	Consistently, polyamine depletion-induced activation of the NDRG1-promoter was decreased when p53-binding sites within the NDRG1 proximal promoter region were deleted.	Polyamines	14-23	P53	Homo sapiens	94-97
17311302-7	2007	Furthermore, 80% of the most common mutants show a capacity to exert dominant-negative effect (DNE) over wild-type p53, compared to only 45% of the less frequent mutants studied, suggesting that DNE may play a role in shaping mutation patterns.	dne	195-198	P53	Homo sapiens	115-118
17391696-1	2007	iASPP is an inhibitory member of ASPP (apoptosis stimulating protein of p53, or Ankyrin repeats, SH3 domain and proline-rich region contain Protein) family.	aspp	1-5	P53	Homo sapiens	72-75
17390022-2	2007	cEPA inhibited the cell growth of two human leukemia cell lines, NALM-6, which is a p53-wild type, and HL-60, which is a p53-null mutant, with LD50 values of 37.5 and 12.5 microM, respectively.	ethephon	0-4	P53	Homo sapiens	84-87
17390022-2	2007	cEPA inhibited the cell growth of two human leukemia cell lines, NALM-6, which is a p53-wild type, and HL-60, which is a p53-null mutant, with LD50 values of 37.5 and 12.5 microM, respectively.	ethephon	0-4	P53	Homo sapiens	121-124
17292432-9	2007	Transcriptional activation of p53 and DNA fragmentation in A549 cells treated with NaVO(3) were suppressed only slightly by S15A mutation, suggesting that Ser15 phosphorylation is not essential for these responses.	Vanadates	83-90	P53	Homo sapiens	30-33
17292432-10	2007	The present results showed that vanadate induces the phosphorylation of p53 at Ser15 depending on ATM, one of the members of PIKK family, in this human pulmonary epithelial cell line.	Vanadates	32-40	P53	Homo sapiens	72-75
17121856-3	2007	This study investigates the action of two HDAC inhibitors, CG-1521 and trichostatin A, which stabilize Ac-Lys-373 p53 and Ac-Lys-382 p53, respectively, in LNCaP prostate cancer cells.	Actinium	103-105	P53	Homo sapiens	114-117
17234782-5	2007	We found that coexpression of FUS1 and p53 by N-[1-(2,3-dioleoyloxyl)propyl]-NNN-trimethylammoniummethyl sulfate:cholesterol nanoparticle-mediated gene transfer significantly and synergistically inhibited NSCLC cell growth and induced apoptosis in vitro.	n-[1-(2,3-dioleoyloxyl)propyl]-nnn-trimethylammoniummethyl sulfate	46-112	P53	Homo sapiens	39-42
17245120-7	2007	We also analyzed the antiproliferative effects of the bile pigments in an in vitro system where bilirubin/biliverdin caused p53 dependent cell cycle arrest by hypophosphorylation of the retinoblastoma tumor suppressor protein in growth factor stimulated VSMCs.	Biliverdine	106-116	P53	Homo sapiens	124-127
17237273-7	2007	Western blot analyses showed that SSAT protein expression was dramatically enhanced when DENSpm was combined with oxaliplatin or 5-FU in HCT116 p53(+/+) cells.	Oxaliplatin	114-125	P53	Homo sapiens	144-147
17088865-7	2006	Lovastatin attenuated the doxorubicin-induced increase in p53 as well as activation of checkpoint kinase (Chk-1) and stress-activated protein kinase/c-Jun-N-terminal kinase (SAPK/JNK).	Lovastatin	0-10	P53	Homo sapiens	58-61
16905769-2	2006	This is supported by the potent activation of P53 in tumor cells by Nutlin, a cis-imidazoline that inhibits the Hdm2-P53 interaction.	cis-imidazoline	78-93	P53	Homo sapiens	46-49
17034127-0	2006	Small-molecule inhibitors of the MDM2-p53 protein-protein interaction based on an isoindolinone scaffold.	phthalimidine	82-95	P53	Homo sapiens	38-41
16865280-3	2006	Here, we show that ionizing radiation can promote FOXO3a (FKHRL1) transcriptional activity and protein expression level, and induce nuclear translocation of FOXO3a in Saos2, a p53-null osteosarcoma cell line.	saos2	167-172	P53	Homo sapiens	176-179
16624827-5	2006	Lauryl gallate increased p53 expression only in MCF7, and upregulated p21(Cip1) and reduced cyclin D1 levels in all three cell lines.	lauryl gallate	0-14	P53	Homo sapiens	25-28
16624827-9	2006	These findings suggest a potential use of lauryl gallate against tumors harboring p53 mutations and drug-resistant phenotypes.	lauryl gallate	42-56	P53	Homo sapiens	82-85
16690610-0	2006	Polyamine depletion increases cytoplasmic levels of RNA-binding protein HuR leading to stabilization of nucleophosmin and p53 mRNAs.	Polyamines	0-9	P53	Homo sapiens	122-125
16690610-1	2006	Polyamines are essential for maintaining normal intestinal epithelial integrity, an effect that relies, at least in part, on their ability to keep low levels of nucleophosmin (NPM) and p53 mRNAs.	Polyamines	0-10	P53	Homo sapiens	185-188
16690610-6	2006	HuR silencing rendered the NPM and p53 mRNAs unstable and prevented increases in NPM and p53 mRNA and protein in polyamine-deficient cells.	Polyamines	113-122	P53	Homo sapiens	89-92
16690610-7	2006	These results indicate that polyamines modulate cytoplasmic HuR levels in intestinal epithelial cells, in turn controlling the stability of the NPM and p53 mRNAs and influencing NPM and p53 protein levels.	Polyamines	28-38	P53	Homo sapiens	152-155
16690610-7	2006	These results indicate that polyamines modulate cytoplasmic HuR levels in intestinal epithelial cells, in turn controlling the stability of the NPM and p53 mRNAs and influencing NPM and p53 protein levels.	Polyamines	28-38	P53	Homo sapiens	186-189
16510697-1	2006	In this study, a cationic water-soluble ceramide analog L-threo-C6-pyridinium-ceramide-bromide (L-t-C6-Pyr-Cer), which exhibits high solubility and bioavailability, inhibited the growth of various human head and neck squamous cell carcinoma (HNSCC) cell lines at low IC50 concentrations, independent of their p53 status.	l-t-c6-pyr-cer	96-110	P53	Homo sapiens	309-312
16700548-8	2006	On the basis of the comparison of the NQO1 structure in complex with different NQO1 inhibitors and our previous analysis of NQO1 mutants, we propose that the specific conformation of Tyr 128 and Phe 232 is important for NQO1 interaction with p53 and other client proteins.	Phenylalanine	195-198	P53	Homo sapiens	242-245
16585172-9	2006	Mitochondrial extracts from p53+/+ cells more efficiently stimulated (32)P-dCTP incorporation into a uracil-oligonucleotide.	uracil-oligonucleotide	101-123	P53	Homo sapiens	28-31
16533058-2	2006	However, we previously showed that cells lacking ATM robustly activate p53 in response to DNA strand breaks induced by the radiomimetic enediyne C-1027.	Enediynes	136-144	P53	Homo sapiens	71-74
16302260-3	2006	We recently identified a synthetic thiazolidin compound, 5-(2,4-dihydroxybenzylidene)-2-(phenylimino)-1,3-thiazolidione (DBPT), that induces apoptosis in human colon cancer cells, independent of p53 and P-glycoprotein status.	Timonacic	35-46	P53	Homo sapiens	195-198
16251187-3	2006	To identify an oxidized lipid that induces p53 phosphorylation, we conducted a screening of lipid peroxidation products in human neuroblastoma SH-SY5Y cells and identified 4-oxo-2-nonenal (ONE), a recently identified aldehyde originating from the peroxidation of omega6 polyunsaturated fatty acids, as a potential inducer of the p53 phosphorylation.	Aldehydes	217-225	P53	Homo sapiens	43-46
17310826-4	2006	After 4 h exposure of HPV16+ve SiHa cells to 15 microM lopinavir, a transient increase in wild-type p53 expression was observed associated with a 7% reduction in the chymotryptic activity of the 205 proteasome and apoptosis after 24h.	Lopinavir	55-64	P53	Homo sapiens	100-103
17310826-6	2006	In conclusion, these data show that specific HIV PIs such as lopinavir and possibly indinavir, can induce selective toxicity of HPV-transformed cervical carcinoma cells expressing wild-type p53 and may form the basis of a topically applied alternative to surgery for the treatment of HPV-related premalignant lesions of the cervix.	Lopinavir	61-70	P53	Homo sapiens	190-193
16267831-7	2006	Inhibition of MAPK kinase (MEK), an upstream kinase, by U0126, blocked TPA-induced activation of ERK1/2 in wild-type p53 cells and in mutant p53 cells.	U 0126	56-61	P53	Homo sapiens	117-120
16267831-7	2006	Inhibition of MAPK kinase (MEK), an upstream kinase, by U0126, blocked TPA-induced activation of ERK1/2 in wild-type p53 cells and in mutant p53 cells.	U 0126	56-61	P53	Homo sapiens	141-144
16838851-3	2006	In addition to the GCV-induced cytotoxicity, apoptosis via caspase-7/8, cleavage of poly(ADP-ribose) polymerase, and accumulation of p53 and p21 were induced by GCV treatment.	Ganciclovir	19-22	P53	Homo sapiens	133-136
16838851-3	2006	In addition to the GCV-induced cytotoxicity, apoptosis via caspase-7/8, cleavage of poly(ADP-ribose) polymerase, and accumulation of p53 and p21 were induced by GCV treatment.	Ganciclovir	161-164	P53	Homo sapiens	133-136
16179969-1	2005	We recently identified two thiazolidin compounds, 5-[(4-methylphenyl)methylene]-2-(phenylamino)-4(5H)-thiazolone (MMPT) and 5-(2,4-dihydroxybenzylidene)-2-(phenylimino)-1,3-thiazolidin (DBPT), that inhibit the growth of human non-small-cell lung and colon cancer cells independent of P-glycoprotein and p53 status.	5-((4-methylphenyl)methylene)-2-(phenylamino)-4(5H)-thiazolone	50-112	P53	Homo sapiens	303-306
16179969-1	2005	We recently identified two thiazolidin compounds, 5-[(4-methylphenyl)methylene]-2-(phenylamino)-4(5H)-thiazolone (MMPT) and 5-(2,4-dihydroxybenzylidene)-2-(phenylimino)-1,3-thiazolidin (DBPT), that inhibit the growth of human non-small-cell lung and colon cancer cells independent of P-glycoprotein and p53 status.	5-((4-methylphenyl)methylene)-2-(phenylamino)-4(5H)-thiazolone	114-118	P53	Homo sapiens	303-306
16227409-5	2005	Oxaliplatin caused strong p21waf1/cip1 induction and G0-G1 arrest in p53 wild-type cells, whereas cisplatin did not induce G0-G1 arrest.	Oxaliplatin	0-11	P53	Homo sapiens	69-72
16227409-8	2005	In p53 mutant cells, on the other hand, oxaliplatin caused an abrupt transition from G1 to S phase and eventually resulted in G2-M arrest.	Oxaliplatin	40-51	P53	Homo sapiens	3-6
16227409-10	2005	These findings suggest that p21waf1/cip1 plays a role in oxaliplatin-mediated cell cycle and growth control in p53-dependent and -independent pathways.	Oxaliplatin	57-68	P53	Homo sapiens	111-114
16127747-1	2005	AIM: p53-inducible ribonucleotide reductase small subunit 2 (p53R2) encodes a 351-amino-acid peptide, which catalyzes conversion of ribonucleoside diphosphates to the corresponding deoxyribonucleotides required for DNA replication and repair.	ribonucleoside diphosphates	132-159	P53	Homo sapiens	5-8
15983031-4	2005	Pancaspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone or p53 inhibitor pifithrin-alpha markedly prevented mitochondrial release of AIF, suggesting that caspases and p53 are involved in this release.	Caspase Inhibitor VI	21-69	P53	Homo sapiens	181-184
23900402-6	2013	Toxoflavin treatment in A549 cells increased the acetylated form of p53, which is a substrate of SIRT1.	toxoflavin	0-10	P53	Homo sapiens	68-71
23977270-4	2013	We report that a new small-molecule inhibitor of MDM2 with a spirooxoindolepyrrolidine core structure, named ISA27, effectively reactivated p53 function and inhibited human GBM cell growth in vitro by inducing cell cycle arrest and apoptosis.	spirooxoindolepyrrolidine	61-86	P53	Homo sapiens	140-143
23652278-10	2013	Ser-15 of p53 was phosphorylated after 24 h of treatment of the cancer cells with OSU-03012.	osu	82-85	P53	Homo sapiens	10-13
23754252-6	2013	In combination with cerulenin and oxaliplatin, activation of the p53-p21 pathway and p38 occurred in a smaller concentration and finally induced caspase-3 cleavage in a smaller concentration of cerulenin and oxaliplatin.	Oxaliplatin	208-219	P53	Homo sapiens	65-68
23754252-5	2013	Oxaliplatin induced activation of the p53-p21 pathway and p38.	Oxaliplatin	0-11	P53	Homo sapiens	38-41
23754252-6	2013	In combination with cerulenin and oxaliplatin, activation of the p53-p21 pathway and p38 occurred in a smaller concentration and finally induced caspase-3 cleavage in a smaller concentration of cerulenin and oxaliplatin.	Oxaliplatin	34-45	P53	Homo sapiens	65-68
23877442-6	2013	Using ligation-mediated PCR, we quantified the CPD formation at 952 dipyrimidine sites among the PGK1 (phosphoglycerate kinase 1), JUN, HRAS, KRAS, NRAS and TP53 genes.	dipyrimidine	68-80	P53	Homo sapiens	157-161
23877442-10	2013	Also, most of the frequently damaged dipyrimidine sites in cellulo that are not frequently damaged in vitro are found on TP53 and NRAS.	dipyrimidine	37-49	P53	Homo sapiens	121-125
23856246-5	2013	Furthermore, we identify pharmacogenomic correlations between specific variants in genes such as TP53, BRAF, ERBBs, and ATAD5 and anticancer agents such as nutlin, vemurafenib, erlotinib, and bleomycin showing one of many ways the data could be used to validate and generate novel hypotheses for further investigation.	nutlin	156-162	P53	Homo sapiens	97-101
23611835-2	2013	The present study presented an evidence for the cell cycle-targeting activity of SB in a panel of p53-mutant human cancer cell lines of different origin, and investigated the underlying molecular mechanisms.	SB 225002	81-83	P53	Homo sapiens	98-101
23393228-6	2013	Irrespective of the tested in vitro model, the most uniformly expressed pathways following GTX exposure are the p53 and those that are subsequently induced.	hexylglutathione	91-94	P53	Homo sapiens	112-115
23599430-3	2013	Considering that MES is a form of physiological stress, we hypothesized that it can activate the tumor suppressor p53, which is a key modulator of the cell cycle and apoptosis in response to cell stresses.	2-(N-morpholino)ethanesulfonic acid	17-20	P53	Homo sapiens	114-117
23599430-6	2013	MES-induced p53 phosphorylation was inhibited by pretreatment with a p38 MAPK inhibitor and transfection of dominant-negative mutants of p38, MKK3b, and MKK6b, implying the involvement of the p38 MAPK signaling pathway.	2-(N-morpholino)ethanesulfonic acid	0-3	P53	Homo sapiens	12-15
23599430-7	2013	Furthermore, MES treatment enhanced p53 transcriptional function and increased the expression of p53 target genes p21, BAX, PUMA, NOXA, and IRF9.	2-(N-morpholino)ethanesulfonic acid	13-16	P53	Homo sapiens	36-39
23599430-7	2013	Furthermore, MES treatment enhanced p53 transcriptional function and increased the expression of p53 target genes p21, BAX, PUMA, NOXA, and IRF9.	2-(N-morpholino)ethanesulfonic acid	13-16	P53	Homo sapiens	97-100
23599430-10	2013	These findings identify some molecular targets of electrical stimulation and incorporate the p38-p53 signaling pathway among the transduction pathways that MES affects.	2-(N-morpholino)ethanesulfonic acid	156-159	P53	Homo sapiens	97-100
23420450-1	2013	iASPP (inhibitory member of the ASPP family), the conserved key inhibitor of p53, is overexpressed and plays an important oncogenetic role in many human cancers.	aspp	1-5	P53	Homo sapiens	77-80
23494867-10	2013	Altholactone also caused a decrease in bcl-2 and an increase in p53 expression.	altholactone	0-12	P53	Homo sapiens	64-67
22809997-0	2013	Ruthenium oligonucleotides, targeting HPV16 E6 oncogene, inhibit the growth of cervical cancer cells under illumination by a mechanism involving p53.	ruthenium oligonucleotides	0-26	P53	Homo sapiens	145-148
23128353-6	2013	Glucosamine at 50 mM was demonstrated to elevate both the mRNA and protein expression of p53 and heme oxygenase-1 (HO-1), but also caused a reduction in p21 protein expression.	Glucosamine	0-11	P53	Homo sapiens	89-92
23128353-8	2013	Altogether, our results suggest that a high dose of glucosamine may inhibit cell proliferation through apoptosis and disturb cell cycle progression with a halt at G(0)/G(1) phase, and that this occurs, at least in part, by a reduction in Rb phosphorylation together with modulation of p21, p53 and HO-1 expression, and nuclear p21 accumulation.	Glucosamine	52-63	P53	Homo sapiens	290-293
24019817-10	2013	Salermide, by decreasing the expression of sirtuin1 gene, can induce acetylation of P53 protein and consequently induce significant cell death in MCF-7 that was well tolerated in MRC-5.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	0-9	P53	Homo sapiens	84-87
23497256-4	2013	RESULTS: Sunitinib treatment increased p53 levels in RCC xenografts and transiently induced the expression of p21(waf1), Noxa, and HDM2, the levels of which subsequently declined to baseline (or undetectable) with the emergence of sunitinib resistance.	Sunitinib	9-18	P53	Homo sapiens	39-42
23271636-7	2013	The reduced expression of VEGF and p53 as determined by enzyme-linked immunosorbent assay and PCR suggests the suitability of the use of Lovastatin in adjunct to WJMSC-derived chondrocytes for the treatment of osteoarthritis.	Lovastatin	137-147	P53	Homo sapiens	35-38
23345169-5	2013	In addition, 5-geranyloxy-7-methoxycoumarin arrested cells at the G0/G1 phase, and induction of apoptosis was demonstrated through the activation of tumour suppressor gene p53, caspase8/3, regulation of Bcl2, and inhibition of p38 MAPK phosphorylation.	5-geranyloxy-7-methoxycoumarin	13-43	P53	Homo sapiens	172-175
23233170-5	2013	The real-time PCR technique was used to examine DNA damage and repair gene expression (mRNA) and results indicated that triptolide led to a decrease in the ataxia telangiectasia mutated (ATM), ataxia-telangiectasia and Rad3-related (ATR), breast cancer 1, early onset (BRCA-1), p53, DNA-dependent serine/threonine protein kinase (DNA-PK) and O6-methylguanine-DNA methyltransferase (MGMT) mRNA expression.	triptolide	120-130	P53	Homo sapiens	278-281
23267009-3	2013	Here, we demonstrate direct binding of both ssDNA and the transactivation domain 2 of p53 (p53TAD2) to DBD-F, as well as DBD-F-directed dsDNA strand separation by RPA, all of which are inhibited by fumaropimaric acid (FPA).	fumaropimaric acid	198-216	P53	Homo sapiens	86-89
23267009-3	2013	Here, we demonstrate direct binding of both ssDNA and the transactivation domain 2 of p53 (p53TAD2) to DBD-F, as well as DBD-F-directed dsDNA strand separation by RPA, all of which are inhibited by fumaropimaric acid (FPA).	fumaropimaric acid	218-221	P53	Homo sapiens	86-89
22847135-8	2013	In addition, administration of naringin increased the expression of caspases, p53 and Bax, Fas death receptor and its adaptor protein FADD.	naringin	31-39	P53	Homo sapiens	78-81
23360998-6	2013	Ensemble-based virtual screening against this newly revealed pocket selects stictic acid as a potential p53 reactivation compound.	stictic acid	76-88	P53	Homo sapiens	104-107
23859040-0	2013	Epicatechin gallate induces cell death via p53 activation and stimulation of p38 and JNK in human colon cancer SW480 cells.	epicatechin gallate	0-19	P53	Homo sapiens	43-46
23859040-2	2013	In this study, the in vitro anticancer effects of ECG on SW480 colon cancer cell line was investigated by analyzing the cell cycle, apoptosis, key proteins involved in cellular survival/proliferation, namely AKT/phosphatidylinositol-3-kinase (PI3K) and mitogen-activated protein kinases (MAPKs), and the role of p53 in these processes.	epicatechin gallate	50-53	P53	Homo sapiens	312-315
23859040-3	2013	ECG induced cell cycle arrest at the G0/G1-S phase border associated with the stimulation of p21, p-p53, and p53 and the suppression of cyclins D1 and B1.	epicatechin gallate	0-3	P53	Homo sapiens	100-103
23859040-3	2013	ECG induced cell cycle arrest at the G0/G1-S phase border associated with the stimulation of p21, p-p53, and p53 and the suppression of cyclins D1 and B1.	epicatechin gallate	0-3	P53	Homo sapiens	109-112
23859040-5	2013	The presence of pifithrin, an inhibitor of p53 function, blocked ECG-induced apoptosis as was manifested by restored cell viability and caspase-3 activity to control values and reestablished the balance among Bcl-2 anti- and proapoptotic protein levels.	epicatechin gallate	65-68	P53	Homo sapiens	43-46
23859040-8	2013	The results suggest that the activation of the p53-p38/JNK cascade is required for ECG-induced cell death in SW480 cells.	epicatechin gallate	83-86	P53	Homo sapiens	47-50
23359652-8	2013	In cells expressing wild-type p53 (OV2008 and C13*), SB225002 increased total and phospho-Ser p53 levels, and p53 knock-down decreased SB225002-induced apoptosis, without affecting premature mitosis.	SB 225002	53-61	P53	Homo sapiens	30-33
23359652-8	2013	In cells expressing wild-type p53 (OV2008 and C13*), SB225002 increased total and phospho-Ser p53 levels, and p53 knock-down decreased SB225002-induced apoptosis, without affecting premature mitosis.	SB 225002	53-61	P53	Homo sapiens	94-97
23359652-8	2013	In cells expressing wild-type p53 (OV2008 and C13*), SB225002 increased total and phospho-Ser p53 levels, and p53 knock-down decreased SB225002-induced apoptosis, without affecting premature mitosis.	SB 225002	53-61	P53	Homo sapiens	94-97
23359652-8	2013	In cells expressing wild-type p53 (OV2008 and C13*), SB225002 increased total and phospho-Ser p53 levels, and p53 knock-down decreased SB225002-induced apoptosis, without affecting premature mitosis.	SB 225002	135-143	P53	Homo sapiens	30-33
23359652-9	2013	These results suggest that SB225002 induces p53-dependent apoptosis, and provokes mitotic catastrophe in p53-independent manner in p53 wild-type cells.	SB 225002	27-35	P53	Homo sapiens	44-47
23359652-9	2013	These results suggest that SB225002 induces p53-dependent apoptosis, and provokes mitotic catastrophe in p53-independent manner in p53 wild-type cells.	SB 225002	27-35	P53	Homo sapiens	105-108
23359652-9	2013	These results suggest that SB225002 induces p53-dependent apoptosis, and provokes mitotic catastrophe in p53-independent manner in p53 wild-type cells.	SB 225002	27-35	P53	Homo sapiens	105-108
23359652-10	2013	Reconstitution with wild-type P53 in P53-null SKOV3 cell attenuated SB225002-induced mitotic catastrophe, suggesting p53 prevented mitotic catastrophe induced by SB225002 in p53-deficient OVCA cells.	SB 225002	68-76	P53	Homo sapiens	30-33
23359652-10	2013	Reconstitution with wild-type P53 in P53-null SKOV3 cell attenuated SB225002-induced mitotic catastrophe, suggesting p53 prevented mitotic catastrophe induced by SB225002 in p53-deficient OVCA cells.	SB 225002	68-76	P53	Homo sapiens	37-40
23359652-10	2013	Reconstitution with wild-type P53 in P53-null SKOV3 cell attenuated SB225002-induced mitotic catastrophe, suggesting p53 prevented mitotic catastrophe induced by SB225002 in p53-deficient OVCA cells.	SB 225002	68-76	P53	Homo sapiens	174-177
23359652-10	2013	Reconstitution with wild-type P53 in P53-null SKOV3 cell attenuated SB225002-induced mitotic catastrophe, suggesting p53 prevented mitotic catastrophe induced by SB225002 in p53-deficient OVCA cells.	SB 225002	162-170	P53	Homo sapiens	30-33
23359652-10	2013	Reconstitution with wild-type P53 in P53-null SKOV3 cell attenuated SB225002-induced mitotic catastrophe, suggesting p53 prevented mitotic catastrophe induced by SB225002 in p53-deficient OVCA cells.	SB 225002	162-170	P53	Homo sapiens	37-40
23359652-10	2013	Reconstitution with wild-type P53 in P53-null SKOV3 cell attenuated SB225002-induced mitotic catastrophe, suggesting p53 prevented mitotic catastrophe induced by SB225002 in p53-deficient OVCA cells.	SB 225002	162-170	P53	Homo sapiens	117-120
23359652-10	2013	Reconstitution with wild-type P53 in P53-null SKOV3 cell attenuated SB225002-induced mitotic catastrophe, suggesting p53 prevented mitotic catastrophe induced by SB225002 in p53-deficient OVCA cells.	SB 225002	162-170	P53	Homo sapiens	174-177
23359652-12	2013	The present studies demonstrate for the first time that SB225002 has dual actions in OVCA cells, inducing classic apoptosis through p53 activation and provoking mitotic catastrophe in both p53 wild-type and deficient cells by Chk1 inhibition and Cdk activation.	SB 225002	56-64	P53	Homo sapiens	132-135
23359652-12	2013	The present studies demonstrate for the first time that SB225002 has dual actions in OVCA cells, inducing classic apoptosis through p53 activation and provoking mitotic catastrophe in both p53 wild-type and deficient cells by Chk1 inhibition and Cdk activation.	SB 225002	56-64	P53	Homo sapiens	189-192
23177934-6	2012	PYGL depletion and the consequent glycogen accumulation led to increased reactive oxygen species (ROS) levels that contributed to a p53-dependent induction of senescence and markedly impaired tumorigenesis in vivo.	Glycogen	34-42	P53	Homo sapiens	132-135
22985798-9	2012	Subsequent p53 nuclear translocation and induction of wild-type and phosphorylated p53 are early steps in oxysterol-induced lysosomal-mitochondrial pathways involved in cell death.	Oxysterols	106-115	P53	Homo sapiens	11-14
22985798-9	2012	Subsequent p53 nuclear translocation and induction of wild-type and phosphorylated p53 are early steps in oxysterol-induced lysosomal-mitochondrial pathways involved in cell death.	Oxysterols	106-115	P53	Homo sapiens	83-86
22886373-8	2012	ROS-mediated p53 activation was found to involve in Cr(VI)-induced cell cycle arrest, and p53 inhibitor Pifithrin-alpha (PFT-alpha) rescued Cr(VI)-induced reduction of check point proteins Mrc1 and BubR1, thus inhibiting cell cycle arrest.	chromium hexavalent ion	140-146	P53	Homo sapiens	90-93
23046248-0	2012	Discovery, synthesis, and biological evaluation of orally active pyrrolidone derivatives as novel inhibitors of p53-MDM2 protein-protein interaction.	Pyrrolidinones	65-76	P53	Homo sapiens	112-115
23046248-2	2012	Novel p53-MDM2 inhibitors bearing pyrrolidone scaffolds were successfully identified by structure-based design.	Pyrrolidinones	34-45	P53	Homo sapiens	6-9
23046248-4	2012	Further hit optimization led to the discovery of a number of highly potent pyrrolidone derivatives with improved p53-MDM2 inhibitory activity and in vitro antiproliferative potency.	Pyrrolidinones	75-86	P53	Homo sapiens	113-116
23046248-8	2012	The novel pyrrolidone p53-MDM2 inhibitors represent promising lead structures for the development of novel antitumor agents.	Pyrrolidinones	10-21	P53	Homo sapiens	22-25
22955915-1	2012	TP53 mutation is an independent marker of poor prognosis in patients with diffuse large B-cell lymphoma (DLBCL) treated with cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone (CHOP) therapy.	Prednisone	181-191	P53	Homo sapiens	0-4
23058634-7	2012	Pretreatment of resting T cells with KU 55933 blocked phosphorylation of ATM, H2AX and p53, which, in turn, prevented PUMA expression, caspase activation and apoptosis.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	37-45	P53	Homo sapiens	87-90
22865487-5	2012	Radicicol and geldanamycin induced a decrease in Bid, Bcl-2, Bcl-xL and survivin protein levels, an increase in Bax levels, the mitochondrial transmembrane potential loss, cytochrome c release, activation of caspases (-8, -9, and -3), cleavage of PARP-1, and an increase in the tumor suppressor p53 levels.	monorden	0-9	P53	Homo sapiens	295-298
22791815-9	2012	We propose that these Cr(VI)-induced BDA and ODD contribute to mutagenesis of the p53 gene that leads to lung carcinogenesis.	chromium hexavalent ion	22-28	P53	Homo sapiens	82-85
21883038-0	2012	Anti-cancer characteristics of mevinolin against three different solid tumor cell lines was not solely p53-dependent.	Lovastatin	31-40	P53	Homo sapiens	103-106
21883038-6	2012	In addition, the MVN-induced cytotoxicity was inferred to be multi-factorial and not solely dependent on p53 expression.	Lovastatin	17-20	P53	Homo sapiens	105-108
22993875-5	2004	Among the different glucose transporters, GLUT2 and GLUT4 can also transport GlcN, and both of these isoforms are transcriptionally repressed by the p53 protein, a tumor suppressor protein that regulates the cell cycle and promotes apoptosis (3).	Glucosamine	77-81	P53	Homo sapiens	149-152
22993301-2	2012	Caffeine affects tumour cells through various pathways, including phosphatase and tensin homolog deleted on chromosome 10 (PTEN), AKT, Bcl-2-associated X protein (BAX), caspase-3 and p53, and has therefore been indicated as being useful for the treatment of malignant tumours.	Caffeine	0-8	P53	Homo sapiens	183-186
22578852-11	2012	From these results, we concluded that nutlin-3 has an antitumor effect on feline lymphoma cell lines harboring the wt-p53 gene through accumulation and activation of P53 leading to cell cycle arrest and apoptosis.	nutlin	38-44	P53	Homo sapiens	118-121
22578852-11	2012	From these results, we concluded that nutlin-3 has an antitumor effect on feline lymphoma cell lines harboring the wt-p53 gene through accumulation and activation of P53 leading to cell cycle arrest and apoptosis.	nutlin	38-44	P53	Homo sapiens	166-169
22670709-8	2012	In p53 positive LNCaP cells, pterostilbene blocked the progression of cell cycle at G1 phase by inducing p53 expression and further up-regulating p21 expression.	pterostilbene	29-42	P53	Homo sapiens	105-108
22670709-9	2012	However, pterostilbene induced apoptosis in p53 negative PC3 cells.	pterostilbene	9-22	P53	Homo sapiens	44-47
21494837-0	2012	A novel synthetic C-1 analogue of 7-deoxypancratistatin induces apoptosis in p53 positive and negative human colorectal cancer cells by targeting the mitochondria: enhancement of activity by tamoxifen.	7-deoxypancratistatin	34-55	P53	Homo sapiens	77-80
21494837-5	2012	We found that a C-1 acetoxymethyl derivative of 7-deoxypancratistatin, JC-TH-acetate-4 (JCTH-4), was effective in inducing apoptosis in both p53 positive (HCT 116) and p53 negative (HT-29) human CRC cell lines, demonstrating similar efficacy to that of natural PST.	7-deoxypancratistatin	48-69	P53	Homo sapiens	141-144
21494837-5	2012	We found that a C-1 acetoxymethyl derivative of 7-deoxypancratistatin, JC-TH-acetate-4 (JCTH-4), was effective in inducing apoptosis in both p53 positive (HCT 116) and p53 negative (HT-29) human CRC cell lines, demonstrating similar efficacy to that of natural PST.	7-deoxypancratistatin	48-69	P53	Homo sapiens	168-171
22233482-0	2012	QSAR models for isoindolinone-based p53-MDM2 interaction inhibitors using linear and non-linear statistical methods.	phthalimidine	16-29	P53	Homo sapiens	36-39
22233482-2	2012	Systematical 2D-QSAR studies on 98 isoindolinone-based p53-MDM2 interaction inhibitors were carried out using linear and the non-linear mathematical methods.	phthalimidine	35-48	P53	Homo sapiens	55-58
22504299-4	2012	The IFN-gamma-dependent poly(ADP-ribosyl)ation of DNA-PKcs (which activates its kinase function) and concomitant activation of the tumor suppressor p53 were specifically prevented by Trp-SA, an analog of Trp-AMP that disrupted the TrpRS-DNA-PKcs-PARP-1 complex.	trp-sa	183-189	P53	Homo sapiens	148-151
21544805-1	2012	The small molecule Quinacrine (QC, a derivative of 9-aminoacridine), an anti-malaria drug, displays activity against cancer cell lines and can simultaneously suppress nuclear factor-kappaB (NF-kappaB) and activate p53 signaling.	Aminacrine	51-66	P53	Homo sapiens	214-217
22103929-0	2012	The chemoadjuvant potential of grape seed procyanidins on p53-related cell death in oral cancer cells.	Proanthocyanidins	42-54	P53	Homo sapiens	58-61
22211565-4	2012	CR2408 leads to fragmentation of cells and induces an accumulation in the subG1 phase accompanied with moderately decreased levels of cyclin D1 and cdk4 and strongly decreased levels of cdc25a, pRb and p53.	CR2408	0-6	P53	Homo sapiens	202-205
22350004-13	2012	p53 might play a role in the malignant transformation of GCTB.	gctb	57-61	P53	Homo sapiens	0-3
22056410-5	2012	The Raman reporter bifunctional linker 4-aminothiophenol (4-ATP) first assembled onto 50 nm gold nanoparticles (Nps) has then been azotated to bind low concentration wild-type and two mutated forms of p53 proteins.	4-aminothiophenol	39-56	P53	Homo sapiens	201-204
22056410-5	2012	The Raman reporter bifunctional linker 4-aminothiophenol (4-ATP) first assembled onto 50 nm gold nanoparticles (Nps) has then been azotated to bind low concentration wild-type and two mutated forms of p53 proteins.	4-aminothiophenol	58-63	P53	Homo sapiens	201-204
22182776-5	2012	Wogonin-induced apoptosis was accompanied by a significant decrease of the Bcl-2 and survivin and increase of Bax and p53.	wogonin	0-7	P53	Homo sapiens	118-121
22270919-4	2012	These data demonstrate that generation of PA downstream of DGK-alpha is essential to connect expression of mutant p53s or inhibition of alphavbeta3 to RCP and for this Rab11 effector to drive the trafficking of alpha5beta1 that is required for tumor cell invasion through three-dimensional matrices.	Phosphatidic Acids	42-44	P53	Homo sapiens	114-117
21852684-7	2012	Furthermore, we show that TM5275 induced apoptosis in both myofibroblasts (TGF-beta1-treated) and naive (TGF-beta1-untreated) human lung fibroblasts, and this apoptosis was associated with the activation of caspase-3/7, the induction of p53, and the inhibition of alpha-smooth muscle actin, fibronectin, and PAI-1 expression.	5-chloro-2-(((2-(4-(diphenylmethyl)piperazin-1-yl)-2-oxoethoxy)acetyl)amino)benzoate	26-32	P53	Homo sapiens	237-240
22901112-0	2012	Recent candidate molecular markers: vitamin D signaling and apoptosis specific regulator of p53 (ASPP) in breast cancer.	aspp	97-101	P53	Homo sapiens	92-95
23098467-0	2012	Crocetin induces cytotoxicity in colon cancer cells via p53-independent mechanisms.	crocetin	0-8	P53	Homo sapiens	56-59
23098467-7	2012	Crocetin (0.8 mmol/L) significantly induced cell cycle arrest through p53-independent mechanisms accompanied by P21 induction.	crocetin	0-8	P53	Homo sapiens	70-73
22368399-3	2012	AIM: This in silico study aimed to predict the main mechanism of fucoxanthin; whether with its binding to p53 gene, CDK2, or tubulin.	fucoxanthin	65-76	P53	Homo sapiens	106-109
22368399-5	2012	The mechanisms being analyzed by comparison of fucoxanthin and native ligands binding energies in p53 gene (1RV1), CDK2 (1AQ1), and three binding sites of tubulin (1JFF-paclitaxel, 1SA0-colchicine, and 1Z2B-vinblastine site).	fucoxanthin	47-58	P53	Homo sapiens	98-101
22662219-7	2012	P53 reactivation substantially improved the apoptotic response after effective KIT inhibition with sunitinib and 17-AAG in IM-resistant cell lines.	Sunitinib	99-108	P53	Homo sapiens	0-3
21937706-7	2011	The cytoplasmic THOC5-dependent mRNAs were recovered by treatment with ATM kinase-specific or p53-specific siRNA, as well as by treatment with ATM kinase inhibitor, KU55933, under DNA damage conditions, suggesting that the ATM-kinase-p53 pathway is involved in this response to the DNA damage.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	165-172	P53	Homo sapiens	234-237
21796794-4	2011	Our results show that bromo- and chloropurine-conjugated benzoxathiepines containing a propylenoxy linker are able to inhibit PI3 kinase (PI3K) phosphorylation in MCF-7 breast cancer cells, indicating that the activation of eIF2alpha, together with inhibition of the PI3K pathway, is the mechanism of action by which these compounds effect their antitumor activity in the MCF-7 cell line; apoptosis was induced in a p53-independent manner.	2-chloro-9H-purine	33-45	P53	Homo sapiens	416-419
21796794-4	2011	Our results show that bromo- and chloropurine-conjugated benzoxathiepines containing a propylenoxy linker are able to inhibit PI3 kinase (PI3K) phosphorylation in MCF-7 breast cancer cells, indicating that the activation of eIF2alpha, together with inhibition of the PI3K pathway, is the mechanism of action by which these compounds effect their antitumor activity in the MCF-7 cell line; apoptosis was induced in a p53-independent manner.	benzoxathiepines	57-73	P53	Homo sapiens	416-419
21821060-5	2011	We report here that p53 contributes to Bcl-2 down-regulation induced by B1, a novel naphthalimide-based DNA intercalating agent.	Naphthalimides	84-97	P53	Homo sapiens	20-23
21821060-10	2011	Our study strengthens the links between p53 and Bcl-2 at a transcriptional level, upon naphthalimide-based DNA intercalator treatment.	Naphthalimides	87-100	P53	Homo sapiens	40-43
21799033-0	2011	MK-1775, a novel Wee1 kinase inhibitor, radiosensitizes p53-defective human tumor cells.	adavosertib	0-7	P53	Homo sapiens	56-59
21799033-8	2011	RESULTS: Clonogenic survival analyses indicated that nanomolar concentrations of MK-1775 radiosensitized p53-defective human lung, breast, and prostate cancer cells but not similar lines with wild-type p53.	adavosertib	81-88	P53	Homo sapiens	105-108
21799033-8	2011	RESULTS: Clonogenic survival analyses indicated that nanomolar concentrations of MK-1775 radiosensitized p53-defective human lung, breast, and prostate cancer cells but not similar lines with wild-type p53.	adavosertib	81-88	P53	Homo sapiens	202-205
21799033-9	2011	Consistent with its ability to radiosensitize, MK-1775 abrogated the radiation-induced G2 block in p53-defective cells but not in p53 wild-type lines.	adavosertib	47-54	P53	Homo sapiens	99-102
21799033-10	2011	MK-1775 also significantly enhanced the antitumor efficacy of radiation in vivo as shown in tumor growth delay studies, again for p53-defective tumors.	adavosertib	0-7	P53	Homo sapiens	130-133
21799033-11	2011	CONCLUSIONS: These results indicate that p53-defective human tumor cells are significantly radiosensitized by the potent and selective wee1 kinase inhibitor, MK-1775, in both the in vitro and in vivo settings.	adavosertib	158-165	P53	Homo sapiens	41-44
30780881-9	2011	This study found that cells harboring p53 mutations were more resistant to the cytotoxic effects of 4-hydroxytamoxifen than their p53 wild-type counterparts.	hydroxytamoxifen	100-118	P53	Homo sapiens	38-41
30780881-10	2011	Furthermore, mutant p53 cells were actually stimulated by low concentrations of 4-hydroxytamoxifen, with evidence that this may be mediated through enhanced growth factor signaling.	hydroxytamoxifen	80-98	P53	Homo sapiens	20-23
21374707-3	2011	BITC and PEITC induced cell cycle arrest at G2/M phase at 48 h treatment and inhibited the levels of cell cycle regulatory proteins such as cyclin A and B1 in U-2 OS cells but promoted the level of Chk1 and p53 that led to G2/M arrest.	phenethyl isothiocyanate	9-14	P53	Homo sapiens	207-210
21671598-3	2011	The results indicate that 3 induces apoptosis through a p53-bak pathway, a finding that could serve as a new strategy to reduce the resistance of cancer cells to p53-induced apoptosis.	bakuchiol	60-63	P53	Homo sapiens	56-59
21671598-3	2011	The results indicate that 3 induces apoptosis through a p53-bak pathway, a finding that could serve as a new strategy to reduce the resistance of cancer cells to p53-induced apoptosis.	bakuchiol	60-63	P53	Homo sapiens	162-165
21696969-0	2011	18beta-Glycyrrhetinic acid derivatives induced mitochondrial-mediated apoptosis through reactive oxygen species-mediated p53 activation in NTUB1 cells.	18alpha-glycyrrhetinic acid	0-26	P53	Homo sapiens	121-124
21280026-4	2011	In this study, substitution of F5Phe or Cha for three Phe residues at positions 328, 338, and 341 in the tetramerization domain of the tumor suppressor protein p53 was performed.	Phenylalanine	33-36	P53	Homo sapiens	160-163
21333732-7	2011	Obacunone upregulated expression of tumor suppressor protein p53, pro-apoptotic protein Bax and downregulated anti-apoptotic protein Bcl2.	obacunone	0-9	P53	Homo sapiens	61-64
21549095-3	2011	We found that TopIn (7-phenyl-6H-[1,2,5]oxadiazolo[3,4-e]indole 3-oxide) efficiently activated p53-mediated transcriptional activity and induced phosphorylation of p53 at Ser15, thereby stabilizing the p53 protein.	7-phenyl-6H-(1,2,5)oxadiazolo(3,4-e)indole 3-oxide	21-71	P53	Homo sapiens	95-98
21549095-3	2011	We found that TopIn (7-phenyl-6H-[1,2,5]oxadiazolo[3,4-e]indole 3-oxide) efficiently activated p53-mediated transcriptional activity and induced phosphorylation of p53 at Ser15, thereby stabilizing the p53 protein.	7-phenyl-6H-(1,2,5)oxadiazolo(3,4-e)indole 3-oxide	21-71	P53	Homo sapiens	164-167
21549095-3	2011	We found that TopIn (7-phenyl-6H-[1,2,5]oxadiazolo[3,4-e]indole 3-oxide) efficiently activated p53-mediated transcriptional activity and induced phosphorylation of p53 at Ser15, thereby stabilizing the p53 protein.	7-phenyl-6H-(1,2,5)oxadiazolo(3,4-e)indole 3-oxide	21-71	P53	Homo sapiens	164-167
21609428-2	2011	LiCl is a well-established inhibitor of Glycogen synthase kinase-3, a kinase that controls several cellular processes, among which is the degradation of the tumour suppressor protein p53.	Lithium Chloride	0-4	P53	Homo sapiens	183-186
21609428-3	2011	We therefore wondered whether LiCl induces p53-dependent cell death in cancer cell lines and experimental tumours.	Lithium Chloride	30-34	P53	Homo sapiens	43-46
21562496-8	2011	Thus, HDACI such as MS-275 present a promising approach for chemosensitization of medulloblastoma by enhancing mitochondrial apoptosis in a p53-dependent manner.	entinostat	20-26	P53	Homo sapiens	140-143
21623005-0	2011	Network modeling of MDM2 inhibitor-oxaliplatin combination reveals biological synergy in wt-p53 solid tumors.	Oxaliplatin	35-46	P53	Homo sapiens	92-95
21167122-8	2011	To further decipher the mechanism of p53 stabilization, we investigated half-life of p53 in cells treated with cycloheximide to block de novo protein synthesis.	Cycloheximide	111-124	P53	Homo sapiens	85-88
21462329-0	2011	The p53-, Bax- and p21-dependent inhibition of colon cancer cell growth by 5-hydroxy polymethoxyflavones.	5-hydroxy polymethoxyflavones	75-104	P53	Homo sapiens	4-7
21445240-11	2011	Both tetramers and hexamers bind the target peptide from p53 with retained stoichiometry of one peptide per S100B monomer, and with high affinity (lgK = 7.3+-0.2 and 7.2+-0.2, respectively in 10 mM BisTris, 5 mM CaCl(2), pH 7.0), which is less than one order of magnitude reduced compared to dimer under the same buffer conditions.	Bistris	198-205	P53	Homo sapiens	57-60
21278235-9	2011	Inhibition of ceramide synthase with fumonisin B1 prevented p53 reactivation induced by GCS silencing, whereas addition of exogenous C6-ceramide reactivated p53 function in p53-mutant cells.	fumonisin B1	37-49	P53	Homo sapiens	60-63
20593219-8	2011	Altered p53 expression or function had only minor effects on TMZ sensitivity in BTICs and tended to decrease sensitivity to TMZ.	btics	80-85	P53	Homo sapiens	8-11
21054790-0	2011	Fisetin, a dietary flavonoid, induces cell cycle arrest and apoptosis through activation of p53 and inhibition of NF-kappa B pathways in bladder cancer cells.	fisetin	0-7	P53	Homo sapiens	92-95
21054790-2	2011	In the present study, we report that fisetin-induced apoptosis in human bladder cancer is mediated via modulation of two related pathways: up-regulation of p53 and down-regulation of NF-kappa B activity, causing a change in the ratio of pro- and anti-apoptotic proteins.	fisetin	37-44	P53	Homo sapiens	156-159
21054790-6	2011	Our study suggests that the activation of p53 and inhibition of the NF-kappa B system may play important roles in the fisetin-induced apoptosis in bladder cancer cells.	fisetin	118-125	P53	Homo sapiens	42-45
21081844-2	2011	All known mechanisms of apoptosis induced by caffeine act through cell cycle modulation or p53 induction.	Caffeine	45-53	P53	Homo sapiens	91-94
21268072-0	2011	Gambogic acid-induced degradation of mutant p53 is mediated by proteasome and related to CHIP.	gambogic acid	0-13	P53	Homo sapiens	44-47
21268072-3	2011	In the present study, we demonstrate that mutant p53 protein stability is regulated by gambogic acid (GA).	gambogic acid	87-100	P53	Homo sapiens	49-52
21268072-3	2011	In the present study, we demonstrate that mutant p53 protein stability is regulated by gambogic acid (GA).	gambogic acid	102-104	P53	Homo sapiens	49-52
21268072-4	2011	Following GA exposure, protein levels of mutant p53 decreased while the mRNA levels were not affected in MDA-MB-435 cells, which indicate that GA down-regulates mutant p53 at post-transcription level.	gambogic acid	10-12	P53	Homo sapiens	48-51
21268072-4	2011	Following GA exposure, protein levels of mutant p53 decreased while the mRNA levels were not affected in MDA-MB-435 cells, which indicate that GA down-regulates mutant p53 at post-transcription level.	gambogic acid	10-12	P53	Homo sapiens	168-171
21268072-5	2011	Co-treatment with GA and cycloheximide, a protein synthesis inhibitor, induced a decrease of half-life of mutant p53 protein.	gambogic acid	18-20	P53	Homo sapiens	113-116
21268072-5	2011	Co-treatment with GA and cycloheximide, a protein synthesis inhibitor, induced a decrease of half-life of mutant p53 protein.	Cycloheximide	25-38	P53	Homo sapiens	113-116
21268072-6	2011	These findings indicated that the reduction of mutant p53 by GA was due to the destabilization and degradation of the protein.	gambogic acid	61-63	P53	Homo sapiens	54-57
21268072-7	2011	Furthermore, inhibition of proteasome activity by MG132 blocked GA-induced down-regulation of mutant p53, causing mutant p53 accumulation in detergent-insoluble cellular fractions.	gambogic acid	64-66	P53	Homo sapiens	101-104
21268072-7	2011	Furthermore, inhibition of proteasome activity by MG132 blocked GA-induced down-regulation of mutant p53, causing mutant p53 accumulation in detergent-insoluble cellular fractions.	gambogic acid	64-66	P53	Homo sapiens	121-124
21268072-9	2011	In addition, GA prevented Hsp90/mutant p53 complex formation and enhanced interaction of mutant p53 with Hsp70.	gambogic acid	13-15	P53	Homo sapiens	39-42
21268072-9	2011	In addition, GA prevented Hsp90/mutant p53 complex formation and enhanced interaction of mutant p53 with Hsp70.	gambogic acid	13-15	P53	Homo sapiens	96-99
21229159-7	2011	Additionally, increased nuclear localization of p53 and caspase-3 expression was observed in cells exposed to the charged Au NPs, while the neutral Au NPs caused an increase in both nuclear and cytoplasmic p53 expression.	Gold	122-124	P53	Homo sapiens	48-51
21229159-7	2011	Additionally, increased nuclear localization of p53 and caspase-3 expression was observed in cells exposed to the charged Au NPs, while the neutral Au NPs caused an increase in both nuclear and cytoplasmic p53 expression.	Gold	148-150	P53	Homo sapiens	206-209
20871630-8	2011	p21 was found to mediate nutlin-induced p53-dependent downregulation of another antiapoptotic protein, survivin, without significantly affecting the apoptotic outcome.	nutlin	25-31	P53	Homo sapiens	40-43
20980256-4	2011	Here we show that the genotoxic stress induced by oxaliplatin elicits an ATM-, CHK2-, and p53-dependent splicing switch that favors the production of the proapoptotic Bcl-x(S) variant.	Oxaliplatin	50-61	P53	Homo sapiens	90-93
20980256-6	2011	Interestingly, the ATM/CHK2/p53/tyrosine phosphatases pathway activated by oxaliplatin regulates Bcl-x splicing through the same regulatory sequence element (SB1) that receives signals from the PKC pathway.	Oxaliplatin	75-86	P53	Homo sapiens	28-31
22708054-3	2011	This method then became the lynchpin for an enantioselective synthesis of (-)-Nutlin-3 (Hoffmann-LaRoche), a potent cis-imidazoline small molecule inhibitor of p53-MDM2 used extensively as a probe of cell biology and currently in drug development.	cis-imidazoline	116-131	P53	Homo sapiens	160-163
21275261-0	2011	Triazoloacridone C-1305 abrogates the restriction checkpoint in cells lacking functional p53 and promotes their accumulation in the G2/M phase of the cell cycle.	triazoloacridone c-1305	0-23	P53	Homo sapiens	89-92
21391736-1	2011	The oncoprotein inhibitory member of the ASPP family (iASPP) is a key inhibitor of the p53 tumor suppressor and is upregulated in patients with acute leukemia and breast carcinoma.	aspp	41-45	P53	Homo sapiens	87-90
20688913-3	2010	Here, we elucidate the role of the adenine nucleotide in the Hsp90 chaperone cycle, by taking advantage of a unique in vitro assay measuring Hsp90-dependent p53 binding to the promoter sequence.	Adenine Nucleotides	35-53	P53	Homo sapiens	157-160
21713362-0	2010	Implication of NF-kappaB and p53 in the expression of TRAIL-death receptors and apoptosis by apple procyanidins in human metastatic SW620 cells.	Proanthocyanidins	99-111	P53	Homo sapiens	29-32
22216443-3	2010	As substrate for the assay, we used a 9-fluorenylmethoxycarbonyl (Fmoc)-labeled tetrapeptide derived from the amino acid sequence of p53, a known substrate of hSIRT1.	9-fluorenylmethoxycarbonyl	38-64	P53	Homo sapiens	133-136
22216443-3	2010	As substrate for the assay, we used a 9-fluorenylmethoxycarbonyl (Fmoc)-labeled tetrapeptide derived from the amino acid sequence of p53, a known substrate of hSIRT1.	9-fluorenylmethoxycarbonyl	66-70	P53	Homo sapiens	133-136
20599920-6	2010	Subsequently, S phase arrest, caspase 9/3 activaton, p53 and Bax up-regulation, as well as Bcl-2 down-regulation were observed in bakuchiol-treated A549 cells.	bakuchiol	130-139	P53	Homo sapiens	53-56
20720205-9	2010	Furthermore, DMBA-3,4-dihydrodiol-1,2-epoxide, a DNA-reactive metabolite of DMBA, was sufficient to upregulate p53, induce caspase-9 cleavage, and initiate B cell apoptosis in the absence of stromal cells, suggesting that production of this metabolite by the stromal cells and transfer to the B cells are proximal events in triggering apoptosis.	9,10-Dimethyl-1,2-benzanthracene	13-17	P53	Homo sapiens	111-114
20449638-0	2010	Induction of apoptosis in hepatocellular carcinoma Smmc-7721 cells by vitamin K(2) is associated with p53 and independent of the intrinsic apoptotic pathway.	Vitamin K	70-79	P53	Homo sapiens	102-105
20435884-3	2010	Losses of TP53 and CDKN2A, observed in 8% and 35% of patients, respectively, were significantly associated with a shorter survival after rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) treatment, independently of the International Prognostic Index and of the cell of origin.	Prednisone	196-206	P53	Homo sapiens	10-14
20660093-7	2010	These changes were normalized to those observed in ZN by treating ZS cells with Pifitherin, an inhibitor of p53 transactivation activity.	pifitherin	80-90	P53	Homo sapiens	108-111
20227286-15	2010	The p53 mutations are a predictor of significantly reduced postoperative survival following surgical resection of EADC, and would appear to be a clinically useful molecular prognostic biomarker.	AlEtCl2	114-118	P53	Homo sapiens	4-7
20417621-6	2010	Ectopic expression of miR-1285 inhibits expression of p53 mRNA and protein.	mir-1285	22-30	P53	Homo sapiens	54-57
20417621-7	2010	In contrast, silencing of miR-1285 increases p53 expression.	mir-1285	26-34	P53	Homo sapiens	45-48
20417621-8	2010	Furthermore, miR-1285 inhibits the transcription of p21, a master gene downstream of p53.	mir-1285	13-21	P53	Homo sapiens	85-88
20417621-9	2010	In conclusion, our findings provide the first evidence that miR-1285 directly regulates the expression of p53 by directly targeting its 3" UTR.	mir-1285	60-68	P53	Homo sapiens	106-109
20406950-0	2010	1,25-dihydroxyvitamin D3 enhances the apoptotic activity of MDM2 antagonist nutlin-3a in acute myeloid leukemia cells expressing wild-type p53.	Calcitriol	0-24	P53	Homo sapiens	139-142
20700368-1	2010	PURPOSE: Benzo[a]pyrene 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of benzo[a]pyrene, attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 mutations.	bpde-n2-dg	129-139	P53	Homo sapiens	160-163
20182344-17	2010	One case showed p53 over-expression aznd none showed DPC4/Smad4 loss.	aznd	36-40	P53	Homo sapiens	16-19
19833818-5	2010	RESULTS: In univariate analyses, addition of oxaliplatin significantly improved DFS provided that tumour overexpressed p53 [hazard ratio (HR) 0.39; 95% confidence interval (CI) 0.19-0.82; P = 0.01] or displayed MSI phenotype (HR 0.17; 95% CI 0.04-0.68; P = 0.01).	Oxaliplatin	45-56	P53	Homo sapiens	119-122
19833818-6	2010	In multivariate analyses, p53 was confirmed as an independent factor predictive of benefit from FOLFOX (P = 0.03), while the interaction of MSI with chemotherapy could not be determined in the absence of relapse in the MSI group treated with FOLFOX.	Folfox protocol	96-102	P53	Homo sapiens	26-29
19833818-7	2010	CONCLUSION: Our observations indicate that MSI status and p53 expression may influence the impact of oxaliplatin on adjuvant treatment of stage III colon cancer patients.	Oxaliplatin	101-112	P53	Homo sapiens	58-61
20199127-11	2010	This discrepancy could be attributed to the different mechanisms of TK/ganciclovir-induced apoptosis in tumor protein p53 (TP53)-expressing (HCT116) and -deficient (SW480) cells.	Ganciclovir	71-82	P53	Homo sapiens	118-121
20199127-11	2010	This discrepancy could be attributed to the different mechanisms of TK/ganciclovir-induced apoptosis in tumor protein p53 (TP53)-expressing (HCT116) and -deficient (SW480) cells.	Ganciclovir	71-82	P53	Homo sapiens	123-127
20107315-5	2010	MK-1775 enhanced the cytotoxic effects of 5-FU in p53-deficient human colon cancer cells.	adavosertib	0-7	P53	Homo sapiens	50-53
20227041-0	2010	Modulation of the vitamin D3 response by cancer-associated mutant p53.	Cholecalciferol	18-28	P53	Homo sapiens	66-69
20128802-6	2010	KEY RESULTS: In oxaliplatin-treated CHK2 KO cells, accelerated apoptosis was accompanied by attenuated p53 stabilization and p21(WAF-1) up-regulation correlating with increased Bax expression, cytochrome c release and elevated caspase activity.	Oxaliplatin	16-27	P53	Homo sapiens	103-106
20128802-8	2010	This "uncoupling" of p53 stabilization and Bax up-regulation in CHK2 KO cells suggested oxaliplatin-induced apoptosis was due to a p53-independent response.	Oxaliplatin	88-99	P53	Homo sapiens	21-24
20128802-8	2010	This "uncoupling" of p53 stabilization and Bax up-regulation in CHK2 KO cells suggested oxaliplatin-induced apoptosis was due to a p53-independent response.	Oxaliplatin	88-99	P53	Homo sapiens	131-134
22993551-4	2010	Treatment with thymoquinone-4-alpha-linolenoylhydrazone (TQ-H-10) or thymoquinone-4-palmitoylhydrazone (TQ-H-11) induced a cytostatic effect, particularly in p53-competent HCT116 cells, mediated by an up-regulation of p21(cip1/waf1) and a down-regulation of cyclin E, and associated with an S/G(2) arrest of the cell cycle.	tq-h-11	104-111	P53	Homo sapiens	158-161
20187803-8	2010	This discrepancy may stem from differences in the mechanisms of TK/GCV-induced apoptosis in p53-proficient (HCT116) and -deficient (SW480) cells.	Ganciclovir	67-70	P53	Homo sapiens	92-95
19922491-10	2010	In addition, 2HBZ caused a marked increase in p21, p53 and Bax protein expressions and these effects were associated with an increase in G1 and G2 arrest of the cell cycle and a reduction in S-phase.	2hbz	13-17	P53	Homo sapiens	51-54
20126473-4	2010	The p53 C-terminal domain is clustered with potential nuclear leading sequences and showed strong electrostatic ion-ion interactions with cardiolipin, phosphatidylglycerol and phosphatidic acid in vitro.	Phosphatidic Acids	176-193	P53	Homo sapiens	4-7
20686229-0	2010	Genipin induced apoptosis associated with activation of the c-Jun NH2-terminal kinase and p53 protein in HeLa cells.	genipin	0-7	P53	Homo sapiens	90-93
20686229-8	2010	Western blot analysis revealed that the phosphorylated c-Jun NH(2)-terminal kinase (JNK) protein, phospho-Jun protein, p53 protein and bax protein significantly increased in a dose-dependent manner after treatment of genipin for 24 h, and to our knowledge, the activation of JNK maybe result in the increase of the p53 protein level, and the increase of the p53 protein led to the accumulation of bax protein, bax protein further induced cell apoptotic death eventually.	genipin	217-224	P53	Homo sapiens	119-122
20686229-8	2010	Western blot analysis revealed that the phosphorylated c-Jun NH(2)-terminal kinase (JNK) protein, phospho-Jun protein, p53 protein and bax protein significantly increased in a dose-dependent manner after treatment of genipin for 24 h, and to our knowledge, the activation of JNK maybe result in the increase of the p53 protein level, and the increase of the p53 protein led to the accumulation of bax protein, bax protein further induced cell apoptotic death eventually.	genipin	217-224	P53	Homo sapiens	315-318
20686229-8	2010	Western blot analysis revealed that the phosphorylated c-Jun NH(2)-terminal kinase (JNK) protein, phospho-Jun protein, p53 protein and bax protein significantly increased in a dose-dependent manner after treatment of genipin for 24 h, and to our knowledge, the activation of JNK maybe result in the increase of the p53 protein level, and the increase of the p53 protein led to the accumulation of bax protein, bax protein further induced cell apoptotic death eventually.	genipin	217-224	P53	Homo sapiens	315-318
20048077-1	2010	Sodium orthovanadate (vanadate) inhibits the DNA-binding activity of p53, but its precise effects on p53 function have not been examined.	Vanadates	12-20	P53	Homo sapiens	69-72
20048077-4	2010	Vanadate suppressed p53-associated apoptotic events at the mitochondria, including the loss of mitochondrial membrane potential, the conformational change of Bax and Bak, the mitochondrial translocation of p53, and the interaction of p53 with Bcl-2.	Vanadates	0-8	P53	Homo sapiens	20-23
20048077-4	2010	Vanadate suppressed p53-associated apoptotic events at the mitochondria, including the loss of mitochondrial membrane potential, the conformational change of Bax and Bak, the mitochondrial translocation of p53, and the interaction of p53 with Bcl-2.	Vanadates	0-8	P53	Homo sapiens	206-209
20048077-4	2010	Vanadate suppressed p53-associated apoptotic events at the mitochondria, including the loss of mitochondrial membrane potential, the conformational change of Bax and Bak, the mitochondrial translocation of p53, and the interaction of p53 with Bcl-2.	Vanadates	0-8	P53	Homo sapiens	206-209
20048077-5	2010	Similarly, vanadate suppressed the apoptosis-inducing activity of a mitochondrially targeted temperature-sensitive p53 in stable transfectants of SaOS-2 cells.	Vanadates	11-19	P53	Homo sapiens	115-118
20048077-7	2010	Together, our findings indicated that vanadate effectively suppresses p53-mediated apoptosis by both transcription-dependent and transcription-independent pathways, and suggested that both pathways must be inhibited to completely block p53-mediated apoptosis.	Vanadates	38-46	P53	Homo sapiens	70-73
20048077-7	2010	Together, our findings indicated that vanadate effectively suppresses p53-mediated apoptosis by both transcription-dependent and transcription-independent pathways, and suggested that both pathways must be inhibited to completely block p53-mediated apoptosis.	Vanadates	38-46	P53	Homo sapiens	236-239
20013323-7	2010	Taken together, p53 plays an important role in AZD1152-HQPA-induced growth arrest and early onset of apoptosis in AML cells.	hqpa	55-59	P53	Homo sapiens	16-19
19895660-8	2010	Lithium chloride (5 mM), which can modulate p53-mediated pathways, also reduced p53 expression and reduced microglial apoptosis suggesting glycogen synthase kinase-3 plays a role.	Lithium Chloride	0-16	P53	Homo sapiens	44-47
19895660-8	2010	Lithium chloride (5 mM), which can modulate p53-mediated pathways, also reduced p53 expression and reduced microglial apoptosis suggesting glycogen synthase kinase-3 plays a role.	Lithium Chloride	0-16	P53	Homo sapiens	80-83
21290342-0	2010	Simultaneous assessment of p53 and MDM2 expression in leukemic cells in response to initial prednisone therapy in children with acute lymphoblastic leukemia.	Prednisone	92-102	P53	Homo sapiens	27-30
21290342-2	2010	p53 plays a crucial role in triggering apoptosis of ALL in response to prednisone treatment.	Prednisone	71-81	P53	Homo sapiens	0-3
21290342-4	2010	This study is aimed to evaluate changes in MDM2 and p53 expression in peripheral blood mononuclear cells collected from children with ALL prior to and after 6 and 12 h of prednisone administration in relation to early treatment response.	Prednisone	171-181	P53	Homo sapiens	52-55
19735649-0	2009	Oxaliplatin-induced gamma-H2AX activation via both p53-dependent and -independent pathways but is not associated with cell cycle arrest in human colorectal cancer cells.	Oxaliplatin	0-11	P53	Homo sapiens	51-54
19735649-4	2009	In this study, we investigated the roles of p53 and gamma-H2AX following oxaliplatin treatment, as they are important effector proteins for apoptosis and DSB repair, respectively.	Oxaliplatin	73-84	P53	Homo sapiens	44-47
19735649-5	2009	Both phosphorylated-p53 (Ser-15) and gamma-H2AX were up-regulated and accumulated in the nuclei of p53-wild type human colorectal cancer HCT116 cells after exposure to oxaliplatin.	Oxaliplatin	168-179	P53	Homo sapiens	20-23
19735649-5	2009	Both phosphorylated-p53 (Ser-15) and gamma-H2AX were up-regulated and accumulated in the nuclei of p53-wild type human colorectal cancer HCT116 cells after exposure to oxaliplatin.	Oxaliplatin	168-179	P53	Homo sapiens	99-102
19735649-7	2009	Release of G2/M arrest by caffeine was accompanied by a decrease in the levels of p53/p21; however, gamma-H2AX levels were unchanged.	Caffeine	26-34	P53	Homo sapiens	82-85
19735649-8	2009	Furthermore, inhibition of p53 phosphorylation by pifithrin-alpha was sufficient to reduce the oxaliplatin-induced up-regulation of gamma-H2AX and apoptosis.	Oxaliplatin	95-106	P53	Homo sapiens	27-30
19735649-9	2009	Oxaliplatin-induced gamma-H2AX via a p53-independent pathway but did not cause caspase-3 activation in p53-null HCT116 cells.	Oxaliplatin	0-11	P53	Homo sapiens	37-40
19735649-11	2009	Taken together, these data indicate that a molecular pathway involving p53, gamma-H2AX and cell cycle arrest plays a pivotal role in the cellular response to oxaliplatin.	Oxaliplatin	158-169	P53	Homo sapiens	71-74
20071291-5	2009	we found that GA uptake into SPC-A1 cells was higher than into SK-MES-1 cells; apoptosis-related proteins Caspase 2, Caspase 9, Caspase 10, Bax and p53 were involved in GA-induced apoptosis.	gambogic acid	14-16	P53	Homo sapiens	148-151
20071291-5	2009	we found that GA uptake into SPC-A1 cells was higher than into SK-MES-1 cells; apoptosis-related proteins Caspase 2, Caspase 9, Caspase 10, Bax and p53 were involved in GA-induced apoptosis.	gambogic acid	169-171	P53	Homo sapiens	148-151
19524422-9	2009	The results showed that triptolide is much more sensitive to ERalpha-positive MCF-7 cells than to ERalpha-negative MDA-MB-231 cells, and the sensitivity is significantly associated with the ERalpha and p53 status.	triptolide	24-34	P53	Homo sapiens	202-205
19428175-2	2009	Although it was proved that GA enhances p53 protein level through inhibition of MDM2 in p53 wild-type cancer cells, the mechanisms of MDM2 inhibition especially with the absence of p53 are not fully understood.	gambogic acid	28-30	P53	Homo sapiens	40-43
19428175-2	2009	Although it was proved that GA enhances p53 protein level through inhibition of MDM2 in p53 wild-type cancer cells, the mechanisms of MDM2 inhibition especially with the absence of p53 are not fully understood.	gambogic acid	28-30	P53	Homo sapiens	88-91
19631264-5	2009	Piceatannol treatment strongly induced the expression of p21WAF1 via independence of p27KIP and p53 expression.	3,3',4,5'-tetrahydroxystilbene	0-11	P53	Homo sapiens	96-99
19705844-6	2009	The specific ATM inhibitor caffeine significantly decreased tricetin-mediated G2/M arrest by inhibiting the phosphorylation of p53 (serine 15) and Chk2.	Caffeine	27-35	P53	Homo sapiens	127-130
19268405-7	2009	Compound 7 and other synthesized 5-benzylidene hydantoin derivatives increased p53 levels, suggesting that the dual mechanism of action was a common feature shared by compound 7 and other member of the series.	5-Benzylidenehydantoin	33-56	P53	Homo sapiens	79-82
19584241-0	2009	Inhibition of S-adenosylmethionine decarboxylase by inhibitor SAM486A connects polyamine metabolism with p53-Mdm2-Akt/protein kinase B regulation and apoptosis in neuroblastoma.	Polyamines	79-88	P53	Homo sapiens	105-108
19509161-12	2009	A combination of vincristine or actinomycin D with nutlin-3 enhanced the antitumor activity in RMS cell lines with wild-type p53.	nutlin	51-57	P53	Homo sapiens	125-128
19414261-0	2009	Stereochemical studies of hexylitaconic acid, an inhibitor of p53-HDM2 interaction.	2-methylene-3-hexylbutanedioic acid	26-44	P53	Homo sapiens	62-65
19411846-10	2009	Surprisingly, blocking the transcriptional arm of p53, either via alpha-Amanitin or the p53-specific transcriptional inhibitor Pifithrin alpha, not only fails to inhibit, but greatly potentiates Nutlin-induced apoptosis.	nutlin	195-201	P53	Homo sapiens	50-53
19411846-10	2009	Surprisingly, blocking the transcriptional arm of p53, either via alpha-Amanitin or the p53-specific transcriptional inhibitor Pifithrin alpha, not only fails to inhibit, but greatly potentiates Nutlin-induced apoptosis.	nutlin	195-201	P53	Homo sapiens	88-91
19264955-0	2009	Induction of p53 contributes to apoptosis of HCT-116 human colon cancer cells induced by the dietary compound fisetin.	fisetin	110-117	P53	Homo sapiens	13-16
19264955-12	2009	The induction of p53 results in the translocation of Bax to the mitochondria, which contributes to fisetin-induced apoptosis in HCT-116 cells.	fisetin	99-106	P53	Homo sapiens	17-20
19091460-7	2009	The hexachlorophene modulation of Siah-1 and beta-catenin is independent of p53 and results in reduced expression of cyclin-D1 and c-Myc (target genes of beta-catenin), leading to the growth arrest of B lymphoma cells.	Hexachlorophene	4-19	P53	Homo sapiens	76-79
19397439-1	2009	We have shown that parthenolide, a sesquiterpene lactone, is a radiation sensitizer for human CGL1 hybrid cells that have constitutively activated NF-kappaB and wild-type p53.	sesquiterpene lactone	35-56	P53	Homo sapiens	171-174
19203291-3	2009	Three of the calothrixins (1-3) were tested for their cytotoxicity toward cultured (p53 proficient) CEM leukemia cells and found to exhibit IC(50) values ranging from 0.20 to 5.13 muM.	calothrixins	13-25	P53	Homo sapiens	84-87
19086036-9	2009	Lithocholic acid (LCA) treatment of primary human hepatocytes and HuH-7 cells induced a similar switch from Mnt to Myc and increased p53 and cyclin D1 promoter activity and endogenous p53 and cyclin D1 expression and apoptosis.	Lithocholic Acid	0-16	P53	Homo sapiens	133-136
19086036-9	2009	Lithocholic acid (LCA) treatment of primary human hepatocytes and HuH-7 cells induced a similar switch from Mnt to Myc and increased p53 and cyclin D1 promoter activity and endogenous p53 and cyclin D1 expression and apoptosis.	Lithocholic Acid	0-16	P53	Homo sapiens	184-187
19086036-9	2009	Lithocholic acid (LCA) treatment of primary human hepatocytes and HuH-7 cells induced a similar switch from Mnt to Myc and increased p53 and cyclin D1 promoter activity and endogenous p53 and cyclin D1 expression and apoptosis.	Lithocholic Acid	18-21	P53	Homo sapiens	133-136
19086036-9	2009	Lithocholic acid (LCA) treatment of primary human hepatocytes and HuH-7 cells induced a similar switch from Mnt to Myc and increased p53 and cyclin D1 promoter activity and endogenous p53 and cyclin D1 expression and apoptosis.	Lithocholic Acid	18-21	P53	Homo sapiens	184-187
19086036-10	2009	Blocking c-Myc induction in HuH-7 cells prevented the LCA-mediated increase in p53 and cyclin D1 expression and reduced apoptosis.	Lithocholic Acid	54-57	P53	Homo sapiens	79-82
19086036-11	2009	Lowering Mnt expression further enhanced LCA"s inductive effect on p53 and cyclin D1.	Lithocholic Acid	41-44	P53	Homo sapiens	67-70
19086036-13	2009	CONCLUSION: The switch from Mnt to Myc during bile duct ligation and in hepatocytes treated with LCA is responsible for the induction in p53 and cyclin D1 expression and contributes to apoptosis.	Lithocholic Acid	97-100	P53	Homo sapiens	137-140
19208740-1	2009	The p53 protein is a key regulator of cell responses to DNA damage, and it has been shown that it sensitizes glioma cells to the alkylating agent temozolomide by up-regulating the extrinsic apoptotic pathway, whereas it increases the resistance to chloroethylating agents, such as ACNU and BCNU, probably by enhancing the efficiency of DNA repair.	Nimustine	281-285	P53	Homo sapiens	4-7
18845789-4	2009	By contrast, treatment of cells with C2-ceramide (a potent PP2A activator) or expression of the PP2A catalytic subunit (PP2A/C) inhibits Bcl2 phosphorylation, leading to increased p53/Bcl2 binding and apoptotic cell death.	N-acetylsphingosine	37-48	P53	Homo sapiens	180-183
19015155-6	2009	Treatment of HCT116 p53(+/+) cells with the DNA-damaging agent oxaliplatin induced a p53-dependent transcriptional downregulation of dUTPase not observed in the isogenic null cell line.	Oxaliplatin	63-74	P53	Homo sapiens	20-23
19015155-6	2009	Treatment of HCT116 p53(+/+) cells with the DNA-damaging agent oxaliplatin induced a p53-dependent transcriptional downregulation of dUTPase not observed in the isogenic null cell line.	Oxaliplatin	63-74	P53	Homo sapiens	85-88
19015155-7	2009	Oxaliplatin treatment induced enrichment of p53 at the dUTPase promoter with a concomitant reduction in Sp1.	Oxaliplatin	0-11	P53	Homo sapiens	44-47
19266094-7	2009	MMP7 was also upregulated by oxaliplatin in both HT29 (p53 mutant) and RHCT116 p53(-/-) but not in the RHCT116 p53(+/+).	Oxaliplatin	29-40	P53	Homo sapiens	55-58
19266094-7	2009	MMP7 was also upregulated by oxaliplatin in both HT29 (p53 mutant) and RHCT116 p53(-/-) but not in the RHCT116 p53(+/+).	Oxaliplatin	29-40	P53	Homo sapiens	79-82
19266094-7	2009	MMP7 was also upregulated by oxaliplatin in both HT29 (p53 mutant) and RHCT116 p53(-/-) but not in the RHCT116 p53(+/+).	Oxaliplatin	29-40	P53	Homo sapiens	79-82
19266094-8	2009	Inhibition of MMP by 1,10-phenantroline monohydrate or siRNA of MMP7 restores cell sensitivity to oxaliplatin-induced apoptosis in both HT29 and RHCT116 p53(-/-) but not in the RHCT116 p53(+/+).	Oxaliplatin	98-109	P53	Homo sapiens	153-156
19266094-8	2009	Inhibition of MMP by 1,10-phenantroline monohydrate or siRNA of MMP7 restores cell sensitivity to oxaliplatin-induced apoptosis in both HT29 and RHCT116 p53(-/-) but not in the RHCT116 p53(+/+).	Oxaliplatin	98-109	P53	Homo sapiens	185-188
18847491-11	2008	Pretreatment of cells with pifithrin-alpha or U0126, specific inhibitors of p53 or MEK-1/2, significantly attenuated Triphala-induced apoptosis.	U 0126	46-51	P53	Homo sapiens	76-79
18847491-12	2008	Moreover, NAC or U0126 pretreatment significantly attenuated Triphala-induced p53 transcriptional activity.	U 0126	17-22	P53	Homo sapiens	78-81
18548093-0	2008	The dual PI3 kinase/mTOR inhibitor PI-103 prevents p53 induction by Mdm2 inhibition but enhances p53-mediated mitochondrial apoptosis in p53 wild-type AML.	PI103	35-41	P53	Homo sapiens	51-54
18548093-0	2008	The dual PI3 kinase/mTOR inhibitor PI-103 prevents p53 induction by Mdm2 inhibition but enhances p53-mediated mitochondrial apoptosis in p53 wild-type AML.	PI103	35-41	P53	Homo sapiens	97-100
18548093-0	2008	The dual PI3 kinase/mTOR inhibitor PI-103 prevents p53 induction by Mdm2 inhibition but enhances p53-mediated mitochondrial apoptosis in p53 wild-type AML.	PI103	35-41	P53	Homo sapiens	97-100
18790751-4	2008	Xanthohumol inhibition of K562 cell viability was associated with induction of apoptosis, increased p21 and p53 expression, and decreased survivin levels.	xanthohumol	0-11	P53	Homo sapiens	108-111
18524447-4	2008	Our data indicate that (-)-anonaine up-regulated the expression of Bax and p53 proteins in HeLa cancer cells.	anonaine	23-35	P53	Homo sapiens	75-78
18561895-8	2008	Cucurbitacins induced the expression of p53 and p21 predominantly in HCT116 cells that harbor mutant Ras.	Cucurbitacins	0-13	P53	Homo sapiens	40-43
18561895-9	2008	Using HCT116 cells with targeted deletion of p53 or p21 we confirmed that p53 and p21 protect cells from apoptosis induced by cucurbitacins.	Cucurbitacins	126-139	P53	Homo sapiens	45-48
18561895-9	2008	Using HCT116 cells with targeted deletion of p53 or p21 we confirmed that p53 and p21 protect cells from apoptosis induced by cucurbitacins.	Cucurbitacins	126-139	P53	Homo sapiens	74-77
18561895-10	2008	These results demonstrated that sensitivity of human colon cancer cell lines to cucurbitacins depends on the kRas and p53/p21 status, and established that cucurbitacins can exert antitumorigenic activity in the absence of activated STAT3.	Cucurbitacins	80-93	P53	Homo sapiens	118-121
18486125-0	2008	Trans- and cis-stilbene polyphenols induced rapid perinuclear mitochondrial clustering and p53-independent apoptosis in cancer cells but not normal cells.	trans- and cis-stilbene polyphenols	0-35	P53	Homo sapiens	91-94
18223691-9	2008	Inhibition of p53 transactivation by pifithrin-alpha or the kinase activity of ATM by either the specific ATM inhibitor KU-5593 or caffeine abrogated p21(WAF1/CIP1) upregulation, indicating that DAC upregulation of p21(WAF1/CIP1) was p53- and ATM-dependent in leukemia cells.	Caffeine	131-139	P53	Homo sapiens	14-17
18223691-9	2008	Inhibition of p53 transactivation by pifithrin-alpha or the kinase activity of ATM by either the specific ATM inhibitor KU-5593 or caffeine abrogated p21(WAF1/CIP1) upregulation, indicating that DAC upregulation of p21(WAF1/CIP1) was p53- and ATM-dependent in leukemia cells.	Caffeine	131-139	P53	Homo sapiens	234-237
18506185-5	2008	The NO donor S-nitroso-N-acetylpenicillamine (SNAP) increased p53 protein levels and induced apoptosis in both cell types, and enhanced cisplatin-induced apoptosis in C13(*) cells in a p53-dependent manner (i.e., enhancement blocked by p53 siRNA).	S-Nitroso-N-Acetylpenicillamine	13-44	P53	Homo sapiens	62-65
18506185-5	2008	The NO donor S-nitroso-N-acetylpenicillamine (SNAP) increased p53 protein levels and induced apoptosis in both cell types, and enhanced cisplatin-induced apoptosis in C13(*) cells in a p53-dependent manner (i.e., enhancement blocked by p53 siRNA).	S-Nitroso-N-Acetylpenicillamine	13-44	P53	Homo sapiens	185-188
18506185-5	2008	The NO donor S-nitroso-N-acetylpenicillamine (SNAP) increased p53 protein levels and induced apoptosis in both cell types, and enhanced cisplatin-induced apoptosis in C13(*) cells in a p53-dependent manner (i.e., enhancement blocked by p53 siRNA).	S-Nitroso-N-Acetylpenicillamine	13-44	P53	Homo sapiens	185-188
18506185-5	2008	The NO donor S-nitroso-N-acetylpenicillamine (SNAP) increased p53 protein levels and induced apoptosis in both cell types, and enhanced cisplatin-induced apoptosis in C13(*) cells in a p53-dependent manner (i.e., enhancement blocked by p53 siRNA).	S-Nitroso-N-Acetylpenicillamine	46-50	P53	Homo sapiens	62-65
18506185-5	2008	The NO donor S-nitroso-N-acetylpenicillamine (SNAP) increased p53 protein levels and induced apoptosis in both cell types, and enhanced cisplatin-induced apoptosis in C13(*) cells in a p53-dependent manner (i.e., enhancement blocked by p53 siRNA).	S-Nitroso-N-Acetylpenicillamine	46-50	P53	Homo sapiens	185-188
18506185-5	2008	The NO donor S-nitroso-N-acetylpenicillamine (SNAP) increased p53 protein levels and induced apoptosis in both cell types, and enhanced cisplatin-induced apoptosis in C13(*) cells in a p53-dependent manner (i.e., enhancement blocked by p53 siRNA).	S-Nitroso-N-Acetylpenicillamine	46-50	P53	Homo sapiens	185-188
18315559-7	2008	The protein synthesis inhibitor cycloheximide blocked apoptosis that was induced by over-expressed shTIF-IA or active form of p53.	Cycloheximide	32-45	P53	Homo sapiens	126-129
18379047-8	2008	Triptolide-induced apoptosis was accompanied by loss of mitochondrial membrane potential and release of cytochrome c (cyt-c) from the mitochondria to the cytosol and down-regulation of anti-apoptotic protein Bcl-2 levels with concurrent up-regulation in pro-apoptotic protein Bax levels and tumor suppressor protein p53 levels.	triptolide	0-10	P53	Homo sapiens	316-319
17724473-2	2008	P-TEFb (positive transcription elongation factor b) inhibitors such as flavopiridol or 4-amino-6-hydrazino-7-b-d-ribofuranosyl-7H-pyrrolo[2,3-d]-pyrimidine-5-carboxamide (ARC) upregulate p53 protein levels, but inhibit the expression of its targets p21 and hdm2.	4-amino-6-hydrazino-7-b-d-ribofuranosyl-7h-pyrrolo[2,3-d]-pyrimidine-5-carboxamide	87-169	P53	Homo sapiens	187-190
18284706-5	2008	Wild type full-length p53 protein was produced in fusion with biotin carboxyl carrier peptide (BCCP) or hexahistidine [(His)6] using pAK400 and pET15b(+) vectors, respectively.	Bccp	95-99	P53	Homo sapiens	22-25
17390215-1	2008	The aim of this study was to evaluate the in vitro and in vivo effects of the new chemotherapy agent Casiopeina III-ia [(4,4"-dimethyl-2,2"-bipiridine)(acetylacetonate) Copper (II) nitrate] on HCT-15 (p53-/-) colon cellular line.	(4,4"-dimethyl-2,2"-bipiridine)	120-151	P53	Homo sapiens	201-204
18024214-3	2008	p53 shRNA (or transient p53 siRNA) into p21-/- HCT116 cells reduced Cr(VI) sensitivity, suggesting the enhanced apoptosis in p21-/- cells is p53-dependent.	chromium hexavalent ion	68-74	P53	Homo sapiens	24-27
17621272-7	2008	Furthermore, the DMBA-induced transformation was accompanied by a complete loss of DNA damage-induced p53 response and activation of the MAPK pathway in MAD2DeltaC cells.	9,10-Dimethyl-1,2-benzanthracene	17-21	P53	Homo sapiens	102-105
18348463-3	2008	There are certain "hot-spots" in the p53 gene where mutations are commonly found that result in a mutated dipyrimidine site.	dipyrimidine	106-118	P53	Homo sapiens	37-40
18034278-8	2008	Lovastatin induces apoptosis and necrosis in lung cancer cell lines by causing alterations in the cell cycle, reducing glutathione, and activating p53, Bax protein, and caspases while increasing cytochrome c in apoptosis pathways.	Lovastatin	0-10	P53	Homo sapiens	147-150
17764803-9	2007	NtBHA pre-treated cells showed significant inhibition of apoptotic features such as activation of caspase-3, up-regulation of Bax and p53, and down-regulation of Bcl-2 compared to control cells upon exposure to ionizing radiation.	N-tert-butylhydroxylamine	0-5	P53	Homo sapiens	134-137
18088187-5	2007	The G2 arrest in p53+/+ cells was abrogated by caffeine, but not by staurosporine and UCN-01, whereas the G2 arrest in p53-/- cells was sensitive to all three inhibitors.	Caffeine	47-55	P53	Homo sapiens	17-20
17434925-8	2007	We predict that the observed p53 mutation spectrum will be dominated by AT --&gt; TA transversion mutations as has already been demonstrated in the human p53 gene of immortalized cells after exposure to AAI and urothelial tumours from BEN patients in Croatia.	aai	203-206	P53	Homo sapiens	29-32
17434925-8	2007	We predict that the observed p53 mutation spectrum will be dominated by AT --&gt; TA transversion mutations as has already been demonstrated in the human p53 gene of immortalized cells after exposure to AAI and urothelial tumours from BEN patients in Croatia.	aai	203-206	P53	Homo sapiens	154-157
17727682-8	2007	Caffeine, an inhibitor of ataxia-telangiectasia mutated protein kinase, alleviated the genistein-induced p53 and CHK2 phosphorylation, suggesting the involvement of DNA damage at 30 microM.	Caffeine	0-8	P53	Homo sapiens	105-108
16131835-0	2005	Role of p53/p21(Waf1/Cip1) in the regulation of polyamine analogue-induced growth inhibition and cell death in human breast cancer cells.	Polyamines	48-57	P53	Homo sapiens	8-11
16131835-7	2005	Stable transfection of small interfering RNA (siRNA) targeting p53 blocked the expression of p21 induced by the polyamine analogues and significantly reduced polyamine analogue-induced growth inhibition and apoptosis, suggesting that polyamine analogue-induced p21 expression occurs through p53-dependent mechanisms.	Polyamines	112-121	P53	Homo sapiens	63-66
16131835-7	2005	Stable transfection of small interfering RNA (siRNA) targeting p53 blocked the expression of p21 induced by the polyamine analogues and significantly reduced polyamine analogue-induced growth inhibition and apoptosis, suggesting that polyamine analogue-induced p21 expression occurs through p53-dependent mechanisms.	Polyamines	158-167	P53	Homo sapiens	63-66
16131835-7	2005	Stable transfection of small interfering RNA (siRNA) targeting p53 blocked the expression of p21 induced by the polyamine analogues and significantly reduced polyamine analogue-induced growth inhibition and apoptosis, suggesting that polyamine analogue-induced p21 expression occurs through p53-dependent mechanisms.	Polyamines	158-167	P53	Homo sapiens	63-66
16131835-9	2005	Expression of p53 siRNA reversed only BENSpm-modulated the cell cycle arrest, suggesting that regulation of cell cycle arrest by p53/p21 induced by polyamine analogues occurs through agent-specific mechanisms.	Polyamines	148-157	P53	Homo sapiens	14-17
16131835-9	2005	Expression of p53 siRNA reversed only BENSpm-modulated the cell cycle arrest, suggesting that regulation of cell cycle arrest by p53/p21 induced by polyamine analogues occurs through agent-specific mechanisms.	Polyamines	148-157	P53	Homo sapiens	129-132
16131835-10	2005	Understanding the mechanism of p53-mediated cellular responses to polyamine analogue may help to improve the therapeutic efficacy of polyamine analogues in human breast cancer.	Polyamines	66-75	P53	Homo sapiens	31-34
16131835-10	2005	Understanding the mechanism of p53-mediated cellular responses to polyamine analogue may help to improve the therapeutic efficacy of polyamine analogues in human breast cancer.	Polyamines	133-142	P53	Homo sapiens	31-34
16140939-2	2005	We show that roscovitine, R-roscovitine, and CGP74514A (collectively referred to as CKIs) induce the apoptosis of LNCaP and LNCaP-Rf cells, both of which express wild-type p53.	N(2)-(2-aminocyclohexyl)-N(6)-(3-chlorophenyl)-9-ethyl-9H-purine-2,6-diamine	45-54	P53	Homo sapiens	172-175
16177561-4	2005	We also found that several randomly chosen acridine derivatives, including 9-aminoacridine, amsacrine, quinacrine and acridine orange, induced p53 transcriptional activity.	Aminacrine	75-90	P53	Homo sapiens	143-146
16177561-4	2005	We also found that several randomly chosen acridine derivatives, including 9-aminoacridine, amsacrine, quinacrine and acridine orange, induced p53 transcriptional activity.	Amsacrine	92-101	P53	Homo sapiens	143-146
16177561-8	2005	In addition, in vivo delivery of quinacrine and amsacrine induced p53 transcriptional activity in tumor xenografts.	Amsacrine	48-57	P53	Homo sapiens	66-69
15963507-0	2005	The p53 pathway is synergized by p38 MAPK signaling to mediate 11,11"-dideoxyverticillin-induced G2/M arrest.	11,11"-dideoxyverticillin	63-88	P53	Homo sapiens	4-7
15963507-3	2005	A concentration- and time-dependent cell cycle blockade at G2/M phase was observed in human colon cancer cells (HCT-116) following 11,11"-dideoxyverticillin treatment and was associated with marked increases in levels of p53, phospho-p53(ser20) and phospho-Chk2(Thr 68).	11,11"-dideoxyverticillin	131-156	P53	Homo sapiens	234-237
15963507-4	2005	When wild type p53 expression was specifically inhibited by RNA interference, HCT-116 cells treated with 11,11"-dideoxyverticillin failed to arrest in G2/M and did not show increased phospho-Chk2(Thr 68).	11,11"-dideoxyverticillin	105-130	P53	Homo sapiens	15-18
15963507-8	2005	Together, these findings indicate that p53-mediated phosphorylation of Chk2 maybe plays a vital role in 11,11"-dideoxyverticillin-induced G2/M arrest, and that p38 MAPK might accelerate this progression.	11,11"-dideoxyverticillin	104-129	P53	Homo sapiens	39-42
15622519-2	2005	About 5% and 3% of the PTTs and 4.5% and 6.8% of BBTs showed alterations in HER2 and p53 expression, respectively.	N-tert-Butyl-2-benzothiazolesulfenamide	49-53	P53	Homo sapiens	85-88
15846119-6	2005	Although treatment with the patellazoles resulted in an increased amount of p53, the p53 null cells were still strongly affected by treatment.	patellazoles	28-40	P53	Homo sapiens	76-79
15837761-1	2005	beta-Lapachone, an o-naphthoquinone, induces a novel caspase- and p53-independent apoptotic pathway dependent on NAD(P)H:quinone oxidoreductase 1 (NQO1).	1,2-naphthoquinone	19-35	P53	Homo sapiens	66-69
15691587-8	2005	Targeting HIF-1alpha and p53 by reactive nitrogen intermediates (RNI) may help to understand a sphere of NO-evoked transcriptional regulation ranging from cellular adaptation to death, i.e. apoptosis with important implications for medicine.	reactive nitrogen	32-49	P53	Homo sapiens	25-28
15591050-3	2005	Close register of Trp(143) and Trp(53) was demonstrated by ACh-mediated quenching of intrinsic Trp fluorescence, elimination of quenching by mutation of one or both Trps to Phe, and decreased lifetime of Trp fluorescence by bound ACh.	Phenylalanine	173-176	P53	Homo sapiens	31-37
15713419-0	2005	Isoindolinone-based inhibitors of the MDM2-p53 protein-protein interaction.	phthalimidine	0-13	P53	Homo sapiens	43-46
15592511-4	2005	In wild-type p53-expressing U87 cells, exposure to GCV and 5-FC resulted in a weak p53 response, although apoptosis was efficiently induced.	Ganciclovir	51-54	P53	Homo sapiens	13-16
15592511-4	2005	In wild-type p53-expressing U87 cells, exposure to GCV and 5-FC resulted in a weak p53 response, although apoptosis was efficiently induced.	Ganciclovir	51-54	P53	Homo sapiens	83-86
15592511-9	2005	These data suggest that TK/GCV- and CD/5-FC-induced apoptosis does neither require p53 nor death receptors, but converges at a mitochondrial pathway triggered by different mechanisms of modulation of Bcl-2 proteins.	Ganciclovir	27-30	P53	Homo sapiens	83-86
15546879-4	2005	Our results showed that simultaneous 5-FU and DENSPM, a spermine analogue, synergistically increased transcript levels of the polyamine catabolism enzyme spermidine/spermine N1-acetyltransferase, depleted spermine and spermidine, increased acetylated spermidine, and produced synergistic tumor cell apoptosis in both p53 wild-type and p53-null variants.	Polyamines	126-135	P53	Homo sapiens	317-320
15546879-4	2005	Our results showed that simultaneous 5-FU and DENSPM, a spermine analogue, synergistically increased transcript levels of the polyamine catabolism enzyme spermidine/spermine N1-acetyltransferase, depleted spermine and spermidine, increased acetylated spermidine, and produced synergistic tumor cell apoptosis in both p53 wild-type and p53-null variants.	Polyamines	126-135	P53	Homo sapiens	335-338
15650224-4	2005	HHV-6B infection induced Ser20 and Ser15 phosphorylation on p53, and the latter was inhibited by caffeine, an ataxia telangiectasia mutated kinase inhibitor.	Caffeine	97-105	P53	Homo sapiens	60-63
15582354-0	2005	Pyrrolizidine alkaloid clivorine induces apoptosis in human normal liver L-02 cells and reduces the expression of p53 protein.	clivorine	23-32	P53	Homo sapiens	114-117
15582354-4	2005	In this paper we show here that clivorine can induce apoptosis in L-02 cells, reduce the expression of p53 protein but has no effect on the expression of Bcl-2 protein, and clivorine also induces the cleavage of the poly(ADP-ribose) polymerase in L-02 cells.	clivorine	32-41	P53	Homo sapiens	103-106
15257984-12	2005	It is concluded that p53 plays a role in CGRP-induced inhibition of cell proliferation and cAMP/PKA appears to mediate this effect in ASMC and PASMC, whereas cGMP appears to be involved in PASMC proliferation.	asmc	134-138	P53	Homo sapiens	21-24
15642166-0	2005	The p53-dependent apoptotic pathway of breast cancer cells (BC-M1) induced by the bis-type bioreductive compound aziridinylnaphthoquinone.	aziridinylnaphthoquinone	113-137	P53	Homo sapiens	4-7
15916863-0	2005	The suppressed proliferation and premature senescence by ganciclovir in p53-mutated human non-small-lung cancer cells acquiring herpes simplex virus-thymidine kinase cDNA.	Ganciclovir	57-68	P53	Homo sapiens	72-75
15916863-2	2005	Here we show that the highly invasive, tumorigenic human non-small-cell-lung cancer (NSCLC) cells carrying mutated p53 alleles were transfected with herpes simplex virus-thymidine kinase (HSV-tk) cDNA and the selected clone was susceptible to exogenous ganciclovir (GCV).	Ganciclovir	253-264	P53	Homo sapiens	115-118
15916863-2	2005	Here we show that the highly invasive, tumorigenic human non-small-cell-lung cancer (NSCLC) cells carrying mutated p53 alleles were transfected with herpes simplex virus-thymidine kinase (HSV-tk) cDNA and the selected clone was susceptible to exogenous ganciclovir (GCV).	Ganciclovir	266-269	P53	Homo sapiens	115-118
15916863-5	2005	These data showed that the GCV-suppressed tumor cell proliferation can be coordinated by cell cycle arrest and cellular senescence in HSV-tk transfectant lacking wild-type p53.	Ganciclovir	27-30	P53	Homo sapiens	172-175
15653994-5	2005	PATIENTS AND METHODS: We examined by immunohistochemistry the expression of p53, p21, bax, bcl-2, and caspase-3 in association with DNA strand breaks detected by terminal deoxynucleotide transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling (TUNEL) in bronchial and alveolar epithelial cells in lung specimens taken by biopsy in 12 IPF patients and 10 control subjects.	deoxyuridine triphosphate-biotin	208-240	P53	Homo sapiens	76-79
16050136-0	2005	Influence of p53 status on the HSV-Tk/GCV-induced bystander effect in a panel of human ovarian carcinoma cell lines.	Ganciclovir	38-41	P53	Homo sapiens	13-16
16050136-2	2005	We investigated if p53 mutations influence the herpes simplex virus thymidine kinase (HSV-tk)/ganciclovir (GCV)-induced bystander effect (BE).	Ganciclovir	94-105	P53	Homo sapiens	19-22
16050136-2	2005	We investigated if p53 mutations influence the herpes simplex virus thymidine kinase (HSV-tk)/ganciclovir (GCV)-induced bystander effect (BE).	Ganciclovir	107-110	P53	Homo sapiens	19-22
16050136-13	2005	In conclusion, HSV-tk/GCV-induced BE is influenced by p53 mutations.	Ganciclovir	22-25	P53	Homo sapiens	54-57
15545975-6	2004	Targeted inactivation of Bax or p53 in HCT116 cells resulted in significantly increased resistance to oxaliplatin.	Oxaliplatin	102-113	P53	Homo sapiens	32-35
15525938-7	2004	The crystal structure of a ternary complex of Set9 with a p53 peptide and the cofactor product S-adenosyl-l-homocysteine (AdoHcy) provides the molecular basis for recognition of p53 by this lysine methyltransferase.	S-Adenosylhomocysteine	97-120	P53	Homo sapiens	58-61
15525938-7	2004	The crystal structure of a ternary complex of Set9 with a p53 peptide and the cofactor product S-adenosyl-l-homocysteine (AdoHcy) provides the molecular basis for recognition of p53 by this lysine methyltransferase.	S-Adenosylhomocysteine	97-120	P53	Homo sapiens	178-181
15525938-7	2004	The crystal structure of a ternary complex of Set9 with a p53 peptide and the cofactor product S-adenosyl-l-homocysteine (AdoHcy) provides the molecular basis for recognition of p53 by this lysine methyltransferase.	S-Adenosylhomocysteine	122-128	P53	Homo sapiens	58-61
15525938-7	2004	The crystal structure of a ternary complex of Set9 with a p53 peptide and the cofactor product S-adenosyl-l-homocysteine (AdoHcy) provides the molecular basis for recognition of p53 by this lysine methyltransferase.	S-Adenosylhomocysteine	122-128	P53	Homo sapiens	178-181
15292706-6	2004	Our data show that in all cell lines tested Naph-DNB was able to form ISCLs, to upregulate p53 oncosuppressor-protein and to induce apoptosis.	naph	44-48	P53	Homo sapiens	91-94
15509798-9	2004	These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity.	Thiamine	179-187	P53	Homo sapiens	61-64
15509798-9	2004	These effects are likely due to a direct effect of NAD(+) on p53, as a molecule structurally related to part of NAD(+), TDP, also inhibits p53 DNA binding, and the TDP precursor, thiamine (vitamin B(1)), inhibits intracellular p53 activity.	Thiamine	189-201	P53	Homo sapiens	61-64
15509798-10	2004	Niacinamide and thiamine affect two p53-regulated cellular responses to ionizing radiation: rereplication and apoptosis.	Thiamine	16-24	P53	Homo sapiens	36-39
15509798-11	2004	Thus, niacinamide and thiamine form a novel basis for the development of small molecules that affect p53 function in vivo, and these results suggest that changes in cellular energy metabolism may regulate p53.	Thiamine	22-30	P53	Homo sapiens	101-104
15173313-4	2004	Treatment of HeLa cells with TPT-CuCl(2) rescues the accumulation of p53 from the suppression of human papilloma virus E6, resulting in a dramatic up-regulation of Bax and Bak and down-regulation of the antiapoptotic factor Survivin.	bakuchiol	172-175	P53	Homo sapiens	69-72
15802048-0	2004	Loss of p53 function in colon cancer cells results in increased phosphocholine and total choline.	Choline	71-78	P53	Homo sapiens	8-11
15802048-5	2004	Here we have used (1)H MRS to characterize the choline phospholipid metabolite levels of p53(+/ +) and p53(-/-) cells, and demonstrated that loss of p53 function results in increased phosphocholine and total choline.	Choline	47-54	P53	Homo sapiens	89-92
15802048-5	2004	Here we have used (1)H MRS to characterize the choline phospholipid metabolite levels of p53(+/ +) and p53(-/-) cells, and demonstrated that loss of p53 function results in increased phosphocholine and total choline.	Choline	47-54	P53	Homo sapiens	103-106
15802048-5	2004	Here we have used (1)H MRS to characterize the choline phospholipid metabolite levels of p53(+/ +) and p53(-/-) cells, and demonstrated that loss of p53 function results in increased phosphocholine and total choline.	Choline	47-54	P53	Homo sapiens	103-106
15802048-5	2004	Here we have used (1)H MRS to characterize the choline phospholipid metabolite levels of p53(+/ +) and p53(-/-) cells, and demonstrated that loss of p53 function results in increased phosphocholine and total choline.	Choline	190-197	P53	Homo sapiens	89-92
15802048-6	2004	These data suggest that the increased malignancy of cancer cells resulting from loss of p53 may be mediated, in part, through the choline phospholipid pathway.	Choline	130-137	P53	Homo sapiens	88-91
15334062-4	2004	In addition, we observed that p53 only contributed marginally to oxaliplatin-induced cytotoxicity and was not involved in oxaliplatin resistance.	Oxaliplatin	65-76	P53	Homo sapiens	30-33
15371552-0	2004	Down-regulation of MDM2 and activation of p53 in human cancer cells by antisense 9-aminoacridine-PNA (peptide nucleic acid) conjugates.	9-aminoacridine-pna	81-100	P53	Homo sapiens	42-45
15371552-4	2004	Using such lipofectamine-delivered Acr-PNA conjugates, one PNA targeting a cryptic AUG initiation site was identified that at a concentration of 2 microM caused a reduction of MDM2 levels to approximately 20% (but no reduction in mdm2 mRNA levels) and a 3-fold increase in p53 levels, whereas a 2-base mismatch control had no such effects.	acr-pna	35-42	P53	Homo sapiens	273-276
34051014-6	2021	This enhanced cell death was dependent on wild-type-p53 status and autophagosome forming ability because TP53 knockout (KO) and ATG5-KO cells attenuated AZM-enhanced cytotoxicity.	Azithromycin	153-156	P53	Homo sapiens	105-109
15273730-4	2004	Selective blockage of caspase-9 activities by Z-LEHD-FMK completely attenuated DAC-induced enhancement of apoptosis mediated by Ad-p53 infection, and ectopic overexpression of procaspase-9 sensitized cells to Ad-p53-induced apoptosis in p53-null cells.	benzyloxycarbonyl-leucyl-glutamyl-histidyl-aspartic acid fluoromethyl ketone	46-56	P53	Homo sapiens	131-134
33986248-2	2021	In this study, lncRNA P53 inHibiting LncRNA (PiHL) was shown to be highly induced in oxaliplatin-resistant CRC cells and tumor tissues.	Oxaliplatin	85-96	P53	Homo sapiens	22-25
15260130-4	2004	However, pre-treatment with FK506 and V10367 significantly prevented any increase in this ratio or p53 mRNA expression.	V 10367	38-44	P53	Homo sapiens	99-102
33957011-7	2021	We found that 4-NP, in a range of concentration from 50 to 100 muM, significantly reduced cell viability; it caused a partial block of proliferation and induced apoptosis with activation of caspase-3 and overexpression of p53.	4-nonylphenol	14-18	P53	Homo sapiens	222-225
15094782-3	2004	We have previously found that the kinase and mRNA synthesis inhibitor DRB (5,6-dichloro-1-b-D-ribofuranosylbenzimidazole) induces the nuclear accumulation of p53 without concomitant phosphorylation of the ser15 site of p53, which is thought to be a modification important for the attenuation of p53-MDM2 interaction.	5,6-dichloro-1-b-d-ribofuranosylbenzimidazole	75-120	P53	Homo sapiens	158-161
15240786-6	2004	RESULTS: Acrylamide and glycidamide formed DNA adducts at similar specific locations within TP53 and cII, and DNA adduct formation was more pronounced after glycidamide treatment than after acrylamide treatment at all doses tested.	Acrylamide	9-19	P53	Homo sapiens	92-96
33382531-0	2021	6,8-Diprenylorobol induces apoptosis in human colon cancer cells via activation of intracellular reactive oxygen species and p53.	6,8-Diprenylorobol	0-18	P53	Homo sapiens	125-128
15169897-4	2004	The increase in p53 expression and the G(1) phase arrest could be blocked by caffeine, an inhibitor of ATR.	Caffeine	77-85	P53	Homo sapiens	16-19
33382531-7	2021	Mechanistically, 6,8-diprenylorobol activated p53 and its phosphorylated form (Ser15, Ser20, and Ser46) expression but suppressed Akt and mitogen-activated protein kinases (MAPKs) phosphorylation in LoVo and HCT15 cells.	6,8-Diprenylorobol	17-35	P53	Homo sapiens	46-49
15141015-6	2004	DNA damage checkpoint proteins including p53, chk1, and chk2 were differentially activated by hedamycin depending on the concentration and duration of treatment.	hedamycin	94-103	P53	Homo sapiens	41-44
33382531-11	2021	Taken together, these results indicate that 6,8-diprenylorobol has the potential antiproliferative effect against LoVo and HCT15 colon cancer cells through activation of p53 and generation of ROS.	6,8-Diprenylorobol	44-62	P53	Homo sapiens	170-173
33922007-3	2021	Oxaliplatin treatment resulted in the G2-phase arrest in all CRC lines tested (HCT116p53+/+, HCT116p53-/-, LoVo, SW48 and SW480).	Oxaliplatin	0-11	P53	Homo sapiens	85-88
15180186-0	2004	Polyamine biosynthesis in relation to K-ras and p-53 mutations in colorectal carcinoma.	Polyamines	0-9	P53	Homo sapiens	48-52
15180186-10	2004	Polyamine biosynthesis was significantly higher in cancers showing K-ras mutation, either with or without p53 mutation [K-ras(+)/p53(-) and K-ras(+)/p53(+)], compared to samples with K-ras wild type [K-ras(-)/p53(-) and K-ras(-)/p53(+)].	Polyamines	0-9	P53	Homo sapiens	106-109
15180186-10	2004	Polyamine biosynthesis was significantly higher in cancers showing K-ras mutation, either with or without p53 mutation [K-ras(+)/p53(-) and K-ras(+)/p53(+)], compared to samples with K-ras wild type [K-ras(-)/p53(-) and K-ras(-)/p53(+)].	Polyamines	0-9	P53	Homo sapiens	129-132
33922007-4	2021	Immunoblot analysis showed that within the p53-competent lines p53 and p21CIP1 are activated at early times upon oxaliplatin treatment.	Oxaliplatin	113-124	P53	Homo sapiens	43-46
15180186-10	2004	Polyamine biosynthesis was significantly higher in cancers showing K-ras mutation, either with or without p53 mutation [K-ras(+)/p53(-) and K-ras(+)/p53(+)], compared to samples with K-ras wild type [K-ras(-)/p53(-) and K-ras(-)/p53(+)].	Polyamines	0-9	P53	Homo sapiens	129-132
33922007-4	2021	Immunoblot analysis showed that within the p53-competent lines p53 and p21CIP1 are activated at early times upon oxaliplatin treatment.	Oxaliplatin	113-124	P53	Homo sapiens	63-66
33922007-9	2021	Our data show that oxaliplatin-induced senescence in CRC cells is dependent on p53 proficiency; however, a significant induction can only be observed upon p14ARF-mediated p53 stabilization.	Oxaliplatin	19-30	P53	Homo sapiens	79-82
33922007-9	2021	Our data show that oxaliplatin-induced senescence in CRC cells is dependent on p53 proficiency; however, a significant induction can only be observed upon p14ARF-mediated p53 stabilization.	Oxaliplatin	19-30	P53	Homo sapiens	171-174
33963708-10	2021	OBJECTIVE: EPS and Oxa can synergistically inhibit the proliferation of HCT116 cells possibly through the PI3K-Akt, MAPK, VEGF, and p53 signaling pathways.	Oxaliplatin	19-22	P53	Homo sapiens	132-135
15041737-0	2004	Characterization of p53 wild-type and null isogenic colorectal cancer cell lines resistant to 5-fluorouracil, oxaliplatin, and irinotecan.	Oxaliplatin	110-121	P53	Homo sapiens	20-23
15041737-5	2004	In addition, we found that resistance to 5-FU and oxaliplatin was higher in parental p53(-/-) cells compared with parental p53(+/+) cells, with an approximately 5-fold increase in IC(50 (72 h)) for each drug.	Oxaliplatin	50-61	P53	Homo sapiens	85-88
15041737-5	2004	In addition, we found that resistance to 5-FU and oxaliplatin was higher in parental p53(-/-) cells compared with parental p53(+/+) cells, with an approximately 5-fold increase in IC(50 (72 h)) for each drug.	Oxaliplatin	50-61	P53	Homo sapiens	123-126
15041737-7	2004	Furthermore, apoptosis after treatment with 5-FU and oxaliplatin, but not CPT-11, was significantly reduced in parental p53(-/-) cells compared with parental p53(+/+) cells.	Oxaliplatin	53-64	P53	Homo sapiens	120-123
15041737-7	2004	Furthermore, apoptosis after treatment with 5-FU and oxaliplatin, but not CPT-11, was significantly reduced in parental p53(-/-) cells compared with parental p53(+/+) cells.	Oxaliplatin	53-64	P53	Homo sapiens	158-161
14660655-4	2004	When p53-mutated cancer cell lines (MDA-MB-231 breast cancer cell and SW620 colon cancer cell) were treated with 10 microM HCA or BCA, it induced growth arrest and apoptosis of tumor cells.	2'-benzoyloxycinnamaldehyde	130-133	P53	Homo sapiens	5-8
33852836-3	2021	We show that CBL0137 displays profound cytotoxic activity against a panel of patient-derived DIPG cultures by restoring tumor suppressor TP53 and Rb activity.	CBLC137	13-20	P53	Homo sapiens	137-141
17638302-0	2007	Neuroprotective effects of caffeine against complex I inhibition-induced apoptosis are mediated by inhibition of the Atm/p53/E2F-1 path in cerebellar granule neurons.	Caffeine	27-35	P53	Homo sapiens	121-124
17638302-4	2007	Our data indicate that the neuroprotective effects of caffeine in the MPP+ model of apoptosis are mediated through activation of the ATM/p53 pathway.	Caffeine	54-62	P53	Homo sapiens	137-140
33852837-3	2021	Here, we disclose the p53-activating anticancer drug (3S)-6,7-bis(hydroxymethyl)-5-methyl-3-phenyl-1H,3H-pyrrolo[1,2-c]thiazole (MANIO).	(3s)-6,7-bis(hydroxymethyl)-5-methyl-3-phenyl-1h,3h-pyrrolo[1,2-c]thiazole	53-127	P53	Homo sapiens	22-25
14625298-4	2004	CAPE activated Fas by a Fas ligand (Fas-L)-independent mechanism, induced p53-regulated Bax protein, and activated caspases.	caffeic acid phenethyl ester	0-4	P53	Homo sapiens	74-77
14625298-6	2004	SB203580, a specific inhibitor of p38 MAPK, partially suppressed CAPE-induced p53 activation, Bax expression, and apoptosis, consistent with a mechanism by which CAPE leads to Bax activation, known to be regulated by p38 and p53.	caffeic acid phenethyl ester	65-69	P53	Homo sapiens	78-81
18025273-3	2007	Moreover, in vitro studies suggested that blocking Hsp90 could overcome p53-mediated resistance of cancer cells to oxaliplatin.	Oxaliplatin	115-126	P53	Homo sapiens	72-75
14625298-6	2004	SB203580, a specific inhibitor of p38 MAPK, partially suppressed CAPE-induced p53 activation, Bax expression, and apoptosis, consistent with a mechanism by which CAPE leads to Bax activation, known to be regulated by p38 and p53.	caffeic acid phenethyl ester	65-69	P53	Homo sapiens	225-228
18025273-11	2007	Importantly, combining oxaliplatin with 17-DMAG in vivo significantly improved growth inhibitory and proapoptotic effects on p53-deficient cells, compared with either substance alone.	Oxaliplatin	23-34	P53	Homo sapiens	125-128
33156559-7	2021	RESULTS: Our results revealed that DMBA treated hamsters exhibited 100% oral tumor cell formation with high-tumor incidence (TI), tumor number (TN), tumor volume (TV), decreased levels of antioxidants, increased status of lipid peroxidation (LPO), and modulated the activities of liver marker agents as well as NF-kB, cell proliferation (PCNA), and p53 proteins.	9,10-Dimethyl-1,2-benzanthracene	35-39	P53	Homo sapiens	349-352
17510082-8	2007	Aspirin induced the phosphorylation of p53 at residue Ser15 within 8 h in a caffeine-dependent manner, and also caused the activation of checkpoint kinase 2 and the cleavage of caspase 7.	Caffeine	76-84	P53	Homo sapiens	39-42
14625298-6	2004	SB203580, a specific inhibitor of p38 MAPK, partially suppressed CAPE-induced p53 activation, Bax expression, and apoptosis, consistent with a mechanism by which CAPE leads to Bax activation, known to be regulated by p38 and p53.	caffeic acid phenethyl ester	162-166	P53	Homo sapiens	225-228
17564309-4	2004	Moreover, the detection of p53 in immune complexes is complicated by the presence of comigrating immunoglobulin chains in SDS-polyacrylamide gels.	polyacrylamide	126-140	P53	Homo sapiens	27-30
33868388-12	2021	Thus, a p53/p21-dependent change in partitioning of the glutamate conversion to 2-oxoglutarate through GOT2 or GDH, linked to NAD(P)-dependent metabolism of 2-oxoglutarate in affiliated pathways, adapts A549 cells to thiamine deficiency or cisplatin treatment.	Thiamine	217-225	P53	Homo sapiens	8-11
17763087-3	2007	After 6 h of exposure to CYN, concentration-dependent increases in mRNA levels were observed for the p53 target genes CDKN1A, GADD45alpha, BAX, and MDM2, indicating an early activation of p53.	cylindrospermopsin	25-28	P53	Homo sapiens	101-104
17763087-3	2007	After 6 h of exposure to CYN, concentration-dependent increases in mRNA levels were observed for the p53 target genes CDKN1A, GADD45alpha, BAX, and MDM2, indicating an early activation of p53.	cylindrospermopsin	25-28	P53	Homo sapiens	188-191
14635187-9	2003	Additionally, PEITC-induced upregulation of GADD153 mRNA expression did not appear to require p53, based on the observation that PEITC also increased GADD153 mRNA expression in HCT-15 colonocytes, which are known to express mutant p53.	phenethyl isothiocyanate	14-19	P53	Homo sapiens	231-234
14712316-5	2003	Following transduction with rAAV-p53, cell growth of all NSCLC cell lines was significantly reduced in a dose-dependent manner between 44 and 71.7% in comparison with rAAV-GFP transduced cells.	raav	28-32	P53	Homo sapiens	33-36
33868388-13	2021	Cellular thiamine deficiency may interfere with antiproliferative action of cisplatin due to their common modulation of the p53/p21-dependent metabolic switch between the glutamate oxidation and transamination.	Thiamine	9-17	P53	Homo sapiens	124-127
17704360-9	2007	TP53-mutated glioma cell lines demonstrated a very prominent dose-responsive G2 checkpoint and were sensitized to radiation by caffeine, which inhibits G2/S phase checkpoint activation.	Caffeine	127-135	P53	Homo sapiens	0-4
33745946-6	2021	Administration of KPT-8602, an XPO1 inhibitor, followed by AZD-6738, an ATR inhibitor, resulted in dramatic antitumor effects and prolonged survival in TP53-mutant models of CRC.	ceralasertib	59-67	P53	Homo sapiens	152-156
17559811-0	2007	p53 dependent and independent sensitivity to oxaliplatin of colon cancer cells.	Oxaliplatin	45-56	P53	Homo sapiens	0-3
17559811-3	2007	Sensitivity to oxaliplatin was a characteristic of p53 wild-type colon cancer cells.	Oxaliplatin	15-26	P53	Homo sapiens	51-54
17559811-4	2007	In contrast, all p53-mutated cell lines had a high IC50 to oxaliplatin, with the exception of the V9P cell line.	Oxaliplatin	59-70	P53	Homo sapiens	17-20
14506229-2	2003	The present study showed that 1,25-dihydroxyvitamin D3 causes cell cycle arrest at the G2/M transition through p53-independent induction of GADD45 in ovarian cancer cells.	Calcitriol	30-54	P53	Homo sapiens	111-114
14761612-3	2003	In the presence of G418, HL-60-pN53cG and K562 pN53cG clones expressing p53 protein were selected.	antibiotic G 418	19-23	P53	Homo sapiens	72-75
33310890-8	2021	Conclusions:These clinical and preclinical results indicate concomitant TP53 mutations reduce the efficacy of alectinib for ALK-rearranged NSCLC and the combined use of a proteasome inhibitor with alectinib is a promising therapy for ALK-rearranged/TP53-mutated NSCLC.	alectinib	197-206	P53	Homo sapiens	249-253
14581372-1	2003	In recent studies, we found that sulindac sulfide (SS), exisulind, CP248, and CP461 induce growth inhibition and apoptosis in a series of human prostate cancer cell lines, irrespective of cyclooxygenase expression, p53 mutations, or bcl-2 overexpression.	(5-fluoro-2-methyl-1-(4-pyridyl)methylene-3-(N-benzyl)-indene)-acetamide hydrochloride	78-83	P53	Homo sapiens	215-218
17070097-6	2007	In addition, cotreatment with the AHR antagonist, 3"-methoxy-4"-nitroflavone (MNF) blocked the effects of TCDD and CSC on p53 and CYP1A1 expression.	3'-methoxy-4'-nitroflavone	50-76	P53	Homo sapiens	122-125
33538587-7	2021	We conclude that the benzothiazoyl, benzoxazoyl, and benzimidazoyl hydrazones can function as ZMCs to reactivate mutant p53 in vitro and in vivo.	benzimidazoyl hydrazones	53-77	P53	Homo sapiens	120-123
17442733-10	2007	These results indicate that NDRG1 is one of the direct mediators of induced p53 following polyamine depletion and that p53-dependent NDRG1 expression plays a critical role in the negative control of IEC proliferation.	Polyamines	90-99	P53	Homo sapiens	76-79
17697526-5	2007	Since U87MG has a wildtype p53 gene while U251MG harbours a mutated p53 gene, these results indicate that triptolide induces apoptosis in GBM cells via a p53-independent pathway.	triptolide	106-116	P53	Homo sapiens	68-71
12890678-5	2003	We found that H2O2 induced phosphorylation of the PDGF beta receptor and increased ATM kinase activity, two events integral to p53 activation as either AG1433 (a PDGF beta receptor inhibitor) or caffeine (an ATM kinase inhibitor) inhibited Ser-15 phosphorylation.	Tyrphostin AG 1433	152-158	P53	Homo sapiens	127-130
17697526-5	2007	Since U87MG has a wildtype p53 gene while U251MG harbours a mutated p53 gene, these results indicate that triptolide induces apoptosis in GBM cells via a p53-independent pathway.	triptolide	106-116	P53	Homo sapiens	68-71
33626352-6	2021	With KrasG12D, p53, or p16 mutations or both, Fgf10-induced IPNB shows stepwise carcinogenesis, causing associated invasive carcinoma.	ipnb	60-64	P53	Homo sapiens	15-18
17343830-5	2007	Consistent with these, an HCT116 p53(-/-) line, lacking p21, showed resistance to oxaliplatin, failure to enter apoptosis, and an accumulation of cells in S-phase.	Oxaliplatin	82-93	P53	Homo sapiens	33-36
12891704-10	2003	Renaturation of temperature sensitive A135V mutant p53 (ts-p53) was found to alter the sensitivity of p53 mRNA translation, but not bulk mRNA translation, to the translocation-specific elongation inhibitor, cycloheximide (Cx).	Cycloheximide	207-220	P53	Homo sapiens	51-54
12891704-10	2003	Renaturation of temperature sensitive A135V mutant p53 (ts-p53) was found to alter the sensitivity of p53 mRNA translation, but not bulk mRNA translation, to the translocation-specific elongation inhibitor, cycloheximide (Cx).	Cycloheximide	207-220	P53	Homo sapiens	59-62
12891704-10	2003	Renaturation of temperature sensitive A135V mutant p53 (ts-p53) was found to alter the sensitivity of p53 mRNA translation, but not bulk mRNA translation, to the translocation-specific elongation inhibitor, cycloheximide (Cx).	Cycloheximide	207-220	P53	Homo sapiens	59-62
12891704-10	2003	Renaturation of temperature sensitive A135V mutant p53 (ts-p53) was found to alter the sensitivity of p53 mRNA translation, but not bulk mRNA translation, to the translocation-specific elongation inhibitor, cycloheximide (Cx).	Cycloheximide	222-224	P53	Homo sapiens	51-54
12891704-10	2003	Renaturation of temperature sensitive A135V mutant p53 (ts-p53) was found to alter the sensitivity of p53 mRNA translation, but not bulk mRNA translation, to the translocation-specific elongation inhibitor, cycloheximide (Cx).	Cycloheximide	222-224	P53	Homo sapiens	59-62
12891704-10	2003	Renaturation of temperature sensitive A135V mutant p53 (ts-p53) was found to alter the sensitivity of p53 mRNA translation, but not bulk mRNA translation, to the translocation-specific elongation inhibitor, cycloheximide (Cx).	Cycloheximide	222-224	P53	Homo sapiens	59-62
17343830-8	2007	We conclude that in colon cancer cells with impaired p53 function, interventions directed to cycle arrest in G1 may potentiate oxaliplatin activity.	Oxaliplatin	127-138	P53	Homo sapiens	53-56
33546743-7	2021	Through integrated data analysis, we obtained five significant p53-dependent metabolic pathways including phenylalanine, glyoxylate, dicarboxylate, and linoleic acid metabolism, and the citrate cycle.	Phenylalanine	106-119	P53	Homo sapiens	63-66
33546743-8	2021	Through metabolite screening, we further identified that benzeneacetic acid, a key regulation metabolite in the phenylalanine metabolic pathway, attenuated the silica-induced EMT in HBE cells in a p53-dependent manner.	Phenylacetates	57-75	P53	Homo sapiens	197-200
17521297-2	2007	This report argues in favour of pro-apoptotic and cell cycle blockage activities of Z-ajoene on various cell lines involving activation of the p53-family gene products, p53, p63 and p73, at indicated doses.	(Z)-Ajoene	84-92	P53	Homo sapiens	143-153
17521297-2	2007	This report argues in favour of pro-apoptotic and cell cycle blockage activities of Z-ajoene on various cell lines involving activation of the p53-family gene products, p53, p63 and p73, at indicated doses.	(Z)-Ajoene	84-92	P53	Homo sapiens	143-146
14555704-3	2003	We have shown previously that triptolide (PG490), an oxygenated diterpene derived from a Chinese medicinal plant, induces apoptosis in cultured tumor cells and sensitizes tumor cells to topoisomerase inhibitors by blocking p53-mediated induction of p21.	triptolide	30-40	P53	Homo sapiens	223-226
14555704-3	2003	We have shown previously that triptolide (PG490), an oxygenated diterpene derived from a Chinese medicinal plant, induces apoptosis in cultured tumor cells and sensitizes tumor cells to topoisomerase inhibitors by blocking p53-mediated induction of p21.	triptolide	42-47	P53	Homo sapiens	223-226
33546743-8	2021	Through metabolite screening, we further identified that benzeneacetic acid, a key regulation metabolite in the phenylalanine metabolic pathway, attenuated the silica-induced EMT in HBE cells in a p53-dependent manner.	Phenylalanine	112-125	P53	Homo sapiens	197-200
17440101-0	2007	p53 and p21 determine the sensitivity of noscapine-induced apoptosis in colon cancer cells.	Noscapine	41-50	P53	Homo sapiens	0-3
33092912-0	2021	Corrigendum to "FLLL12 induces apoptosis in lung cancer cells through a p53/p73-independent but death receptor 5-dependent pathway" [Canc.	flll12	16-22	P53	Homo sapiens	72-75
17292432-0	2007	Phosphorylation of p53 at serine 15 in A549 pulmonary epithelial cells exposed to vanadate: involvement of ATM pathway.	Vanadates	82-90	P53	Homo sapiens	19-22
17292432-1	2007	When A549 cells were exposed to sodium metavanadate (NaVO(3)), the pentavalent species of vanadium (vanadate), phosphorylation of p53 protein at Ser15 was found in a time (8-48 h)- and dose (10-200 microM)-dependent manner.	Vanadates	32-51	P53	Homo sapiens	130-133
17292432-1	2007	When A549 cells were exposed to sodium metavanadate (NaVO(3)), the pentavalent species of vanadium (vanadate), phosphorylation of p53 protein at Ser15 was found in a time (8-48 h)- and dose (10-200 microM)-dependent manner.	Vanadates	53-60	P53	Homo sapiens	130-133
17292432-1	2007	When A549 cells were exposed to sodium metavanadate (NaVO(3)), the pentavalent species of vanadium (vanadate), phosphorylation of p53 protein at Ser15 was found in a time (8-48 h)- and dose (10-200 microM)-dependent manner.	Vanadates	43-51	P53	Homo sapiens	130-133
17292432-2	2007	After the incubation with 50 or 100 microM NaVO(3) for 48 h, accumulation of p53 protein was accompanied with Ser15 phosphorylation.	Vanadates	43-50	P53	Homo sapiens	77-80
17292432-3	2007	Among serines in p53 protein immunoprecipitated from A549 cells treated with 100 microM NaVO(3) for 48 h, only Ser15 was markedly phosphorylated.	Vanadates	88-95	P53	Homo sapiens	17-20
17292432-4	2007	Treatment with other vanadate compounds, sodium orthovanadate (Na(3)VO(4)) and ammonium metavanadate (NH(4)VO(3)), also induced Ser15 phosphorylation and accumulation of p53 protein.	Vanadates	21-29	P53	Homo sapiens	170-173
12902982-6	2003	Treatment with the ATM/ATR kinase inhibitor caffeine prevented p53 accumulation upon activation of Myc or E2F1.	Caffeine	44-52	P53	Homo sapiens	63-66
12921975-8	2003	After aldehydes exposition a decreased expression of p53 and c-myc mRNA, genes involved in cell death regulation, was also demonstrated by RT-PCR.	Aldehydes	6-15	P53	Homo sapiens	53-56
12811820-0	2003	Caffeine induces G2/M arrest and apoptosis via a novel p53-dependent pathway in NB4 promyelocytic leukemia cells.	Caffeine	0-8	P53	Homo sapiens	55-58
12811820-1	2003	Methylxantine derivative, caffeine, is known to prevent the p53-dependent apoptosis pathway via inhibition of ATM (ataxia telangiectasia mutated) kinase, which activates p53 by phosphorylation of the Ser-15 residue.	Caffeine	26-34	P53	Homo sapiens	60-63
17292432-4	2007	Treatment with other vanadate compounds, sodium orthovanadate (Na(3)VO(4)) and ammonium metavanadate (NH(4)VO(3)), also induced Ser15 phosphorylation and accumulation of p53 protein.	nh(4)vo	102-109	P53	Homo sapiens	170-173
12811820-1	2003	Methylxantine derivative, caffeine, is known to prevent the p53-dependent apoptosis pathway via inhibition of ATM (ataxia telangiectasia mutated) kinase, which activates p53 by phosphorylation of the Ser-15 residue.	Caffeine	26-34	P53	Homo sapiens	170-173
17292432-6	2007	On the other hand, treatment with wortmannin or caffeine, the inhibitors to phosphatidylinositol 3-kinase related kinases (PIKKs), suppressed both NaVO(3)-induced Ser15 phosphorylation and accumulation of p53 protein.	Caffeine	48-56	P53	Homo sapiens	205-208
33275947-0	2021	Up-regulation of miRNA-151-3p enhanced the neuroprotective effect of dexmedetomidine against beta-amyloid by targeting DAPK-1 and TP53.	mirna-151-3p	17-29	P53	Homo sapiens	130-134
17292432-6	2007	On the other hand, treatment with wortmannin or caffeine, the inhibitors to phosphatidylinositol 3-kinase related kinases (PIKKs), suppressed both NaVO(3)-induced Ser15 phosphorylation and accumulation of p53 protein.	Vanadates	147-154	P53	Homo sapiens	205-208
12811820-2	2003	In contrast, it has been reported that caffeine induces p53-mediated apoptosis through Bax protein in non-small-cell lung cancer cells.	Caffeine	39-47	P53	Homo sapiens	56-59
12811820-6	2003	Caffeine induced G(2)/M phase cell cycle arrest in NB4 cells in association with the induction of phosphorylation at the Ser-15 residue of p53 and induction of tyrosine phosphorylation of cdc2.	Caffeine	0-8	P53	Homo sapiens	139-142
12811820-8	2003	Interestingly, the antisense oligonucleotides for p53 significantly reduced p53 expression and caffeine-induced G(2)/M phase cell cycle arrest in NB4 cells.	Caffeine	95-103	P53	Homo sapiens	50-53
12811820-9	2003	These results suggest that caffeine induces cell cycle arrest and apoptosis in association with activation of p53 by a novel pathway to phosphorylate the Ser-15 residue and induction of phosphorylation of cdc 2 in leukemic cells with normal p53.	Caffeine	27-35	P53	Homo sapiens	110-113
12811820-9	2003	These results suggest that caffeine induces cell cycle arrest and apoptosis in association with activation of p53 by a novel pathway to phosphorylate the Ser-15 residue and induction of phosphorylation of cdc 2 in leukemic cells with normal p53.	Caffeine	27-35	P53	Homo sapiens	241-244
33275947-13	2021	miRNA-151-3p enhanced the neuroprotective effect of Dex against Abeta by targeting DAPK-1 and TP53.	mirna-151-3p	0-12	P53	Homo sapiens	94-98
17105820-3	2007	We demonstrate that wild-type p53 protein is expressed in primary leukemic blasts from patients with de novo AML using 2-dimensional polyacrylamide gel electrophoresis (2D-PAGE) and phospho-specific flow cytometry.	polyacrylamide	133-147	P53	Homo sapiens	30-33
12802789-5	2003	However, TS induction abrogated p53, p21, Fas, and Bak induction in response to TDX, but not 5-FU.	raltitrexed	80-83	P53	Homo sapiens	32-35
33421460-6	2021	The results showed that polysaccharides treatment inhibited the expression of Cyclin E, Cyclin A and CDK2 and up regulated the expression of P53.	Polysaccharides	24-39	P53	Homo sapiens	141-144
12646262-4	2003	Administration of caffeine to G2-arrested cells induced a drastic change in cell phenotype, the nature of which depended on the status of p53.	Caffeine	18-26	P53	Homo sapiens	138-141
12646262-5	2003	Flow cytometric and microscopic observations revealed that cells that either contained or lacked p53 resumed their cell cycles and entered mitosis upon caffeine treatment.	Caffeine	152-160	P53	Homo sapiens	97-100
17300232-1	2007	BACKGROUND: p53 has been extensively studied in external genital carcinoma (EGC), and is frequently inactivated, but little is known about the role of the CDKN2A tumour suppressor gene in the oncogenesis of EGC.	(-)-Epigallocatechin	76-79	P53	Homo sapiens	12-15
17300232-9	2007	CONCLUSIONS: Our study shows a high prevalence of co-inactivating mutations of p53 and/or CDKN2A genes in EGC, that seem to occur preferentially in LS-derived tumours and late in oncogenesis.	(-)-Epigallocatechin	106-109	P53	Homo sapiens	79-82
32737944-2	2021	Structural optimization of the hit compound SLMP53-1 led to the identification of a ( R )-tryptophanol-derived isoindolinone 6-fold more active and with increased selectivity for colon cancer HCT116 cells with p53 and with low toxicity in normal cells.	phthalimidine	111-124	P53	Homo sapiens	210-213
17096346-5	2007	The BITC-induced p53 phosphorylation was counteracted by caffeine treatment, implying the involvement of an ATM/ataxia telangiectasia and Rad3-related kinase signaling pathway.	Caffeine	57-65	P53	Homo sapiens	17-20
16905748-2	2007	We show here that the secondary bile acid, deoxycholic acid (DCA), is the only one of the commonly refluxed bile acids tested here, to show genotoxicity, in terms of chromosome damage and mutation induction in the human p53 gene.	Deoxycholic Acid	43-59	P53	Homo sapiens	220-223
16905748-2	2007	We show here that the secondary bile acid, deoxycholic acid (DCA), is the only one of the commonly refluxed bile acids tested here, to show genotoxicity, in terms of chromosome damage and mutation induction in the human p53 gene.	Deoxycholic Acid	61-64	P53	Homo sapiens	220-223
12719724-6	2003	An ATR-kinase dead mutant or caffeine, which blocks the kinase activity of ATR, effectively abolishes the ability of NO to cause p53 nuclear retention, concomitant with its inhibition of p53 serine 15 phosphorylation.	Caffeine	29-37	P53	Homo sapiens	129-132
12719724-6	2003	An ATR-kinase dead mutant or caffeine, which blocks the kinase activity of ATR, effectively abolishes the ability of NO to cause p53 nuclear retention, concomitant with its inhibition of p53 serine 15 phosphorylation.	Caffeine	29-37	P53	Homo sapiens	187-190
32451414-7	2021	RNA-sequencing analyses revealed that avasimibe suppressed the expression of CDK2, cyclin E1, CDK4, cyclin D, CDK1, cyclin B1, Aurora A, and PLK1, while induced the expression of p53, p21, p27, and GADD45A, which was validated by Western blot analysis.	avasimibe	38-47	P53	Homo sapiens	179-182
12663497-5	2003	Data presented shows that, when treated with a dose of NaBt that induced significant apoptosis (4 mM for 48 h), there was an upregulation of IGFBP-3 protein in both wildtype and mutant p53 expressing cell lines.	NABT	55-59	P53	Homo sapiens	185-188
12570658-7	2003	Indeed, the effect of oxaliplatin could be reduced in tumor cells expressing mutant p53.	Oxaliplatin	22-33	P53	Homo sapiens	84-87
16620158-1	2007	Mutations detected in the p53 gene in human nonmelanoma skin cancers show a highly UV-specific mutation pattern, a dominance of C --&gt; T base substitutions at dipyrimidine sites plus frequent CC --&gt; TT tandem substitutions, indicating a major involvement of solar UV in the skin carcinogenesis.	dipyrimidine	161-173	P53	Homo sapiens	26-29
17045763-6	2006	The p53-functional RKO cells were higher on the cytotoxicity and cell cycle arrest at the G1 and G2/M phases than the p53-mutational SW480 cells after treatment with oxaliplatin.	Oxaliplatin	166-177	P53	Homo sapiens	4-7
32451414-8	2021	These results demonstrated that avasimibe induced mitochondria-dependent apoptosis in glioblastoma cells, which was associated with arresting the cell cycle at G0/G1 phase and G2/M phase by regulating the p53/p21 pathway, p53/GADD45A and Aurora A/PLK1 signaling pathways.	avasimibe	32-41	P53	Homo sapiens	205-208
17045763-6	2006	The p53-functional RKO cells were higher on the cytotoxicity and cell cycle arrest at the G1 and G2/M phases than the p53-mutational SW480 cells after treatment with oxaliplatin.	Oxaliplatin	166-177	P53	Homo sapiens	118-121
17045763-7	2006	Oxaliplatin inhibited the securin protein expression in the p53-functional cells but not in the p53-mutational cells.	Oxaliplatin	0-11	P53	Homo sapiens	60-63
32451414-8	2021	These results demonstrated that avasimibe induced mitochondria-dependent apoptosis in glioblastoma cells, which was associated with arresting the cell cycle at G0/G1 phase and G2/M phase by regulating the p53/p21 pathway, p53/GADD45A and Aurora A/PLK1 signaling pathways.	avasimibe	32-41	P53	Homo sapiens	222-225
17045763-9	2006	Nevertheless, oxaliplatin elevated the activation of p53 in both securin-wild type and securin-null cells.	Oxaliplatin	14-25	P53	Homo sapiens	53-56
32638380-7	2021	For targeting mutant KRAS and reactivating mutant p53, trials have progressed to a phase III stage, i.e., the mutant-p53 reactivating drug, APR-246 is currently being investigated in patients with myelodysplastic syndrome (MDS) and the RAS inhibitor, rigosertib is also undergoing evaluation in patients with MDS.	ON 01910	251-261	P53	Homo sapiens	117-120
17045763-10	2006	As a whole, it is the first time to demonstrate that oxaliplatin inhibits the securin protein expression via a p53-dependent pathway, and p53 and securin may modulate the oxaliplatin-induced cytotoxicity in human colorectal cancer cells.	Oxaliplatin	53-64	P53	Homo sapiens	111-114
17045763-10	2006	As a whole, it is the first time to demonstrate that oxaliplatin inhibits the securin protein expression via a p53-dependent pathway, and p53 and securin may modulate the oxaliplatin-induced cytotoxicity in human colorectal cancer cells.	Oxaliplatin	171-182	P53	Homo sapiens	138-141
17072987-1	2006	AIM: To investigate the role of the polymorphism of p53 codon 72 in early gastric cancer (EGC) and advanced gastric cancer (AGC) in Korean patients.	(-)-Epigallocatechin	90-93	P53	Homo sapiens	52-55
17030796-0	2006	Acrolein is a major cigarette-related lung cancer agent: Preferential binding at p53 mutational hotspots and inhibition of DNA repair.	Acrolein	0-8	P53	Homo sapiens	81-84
12517773-5	2003	However, Go6976 potently abrogated S and G(2) arrest and enhanced the cytotoxicity of the topoisomerase I inhibitor SN38 only in p53-defective cells.	Go 6976	9-15	P53	Homo sapiens	129-132
14622914-2	2003	In this study, we examined the role of p53 in neuronal death induced by the sodium channel modulator veratridine.	Veratridine	101-112	P53	Homo sapiens	39-42
14622914-5	2003	p53-Like immunoreactivity, undetectable in neurons under control conditions, was observed in about 25% of neurons, 7 h after veratridine exposure.	Veratridine	125-136	P53	Homo sapiens	0-3
14622914-8	2003	Treatments of neuronal cultures with the permeability transitory pore blockers cyclosporin A and bongkrekic acid prevented veratridine-induced p53 immunoreactivity and neuronal death, placing mitochondria upstream of veratridine-induced p53 immunoreactivity.	Veratridine	123-134	P53	Homo sapiens	143-146
14622914-8	2003	Treatments of neuronal cultures with the permeability transitory pore blockers cyclosporin A and bongkrekic acid prevented veratridine-induced p53 immunoreactivity and neuronal death, placing mitochondria upstream of veratridine-induced p53 immunoreactivity.	Veratridine	123-134	P53	Homo sapiens	237-240
14622914-10	2003	Antisense knockdown of p53 resulted in a significant increase in neuronal survival after veratridine treatment.	Veratridine	89-100	P53	Homo sapiens	23-26
14622914-12	2003	These results together suggest that p53-expression is involved in veratridine-induced neuronal death and that p53 might be a link between toxic stimuli of different types and neuronal death.	Veratridine	66-77	P53	Homo sapiens	36-39
16964247-0	2006	Modification of p53 with O-linked N-acetylglucosamine regulates p53 activity and stability.	o-linked n-acetylglucosamine	25-53	P53	Homo sapiens	16-19
16964247-0	2006	Modification of p53 with O-linked N-acetylglucosamine regulates p53 activity and stability.	o-linked n-acetylglucosamine	25-53	P53	Homo sapiens	64-67
33383653-8	2020	Furthermore, cycloheximide treatment increased HO-1 abundance in p53 KO cells suggesting that p53 modulates HO-1 protein stability.	Cycloheximide	13-26	P53	Homo sapiens	65-68
16964247-1	2006	Post-translational addition of O-linked N-acetylglucosamine (O-GlcNAc) to p53 is known to occur, but the site of O-GlcNAcylation and its effects on p53 are not understood.	o-linked n-acetylglucosamine	31-59	P53	Homo sapiens	74-77
16500682-6	2006	Treatment with sulforaphane (15 microM), PEITC (10 microM), indole-3-carbinol (10 microM) and 3,3"-diindolylmethane (10 microM) induced PARP cleavage after 24 and 48 h in both 40-16 and the 379.2 cell lines, suggestive of a p53-independent mechanism of apoptosis induction.	phenethyl isothiocyanate	41-46	P53	Homo sapiens	224-227
12171915-2	2002	We found that phenylethyl isothiocyanate (PEITC) was capable of inducing JNK activation and apoptosis in prostate cancer cell lines with distinct p53 statuses.	phenethyl isothiocyanate	14-40	P53	Homo sapiens	146-149
12171915-2	2002	We found that phenylethyl isothiocyanate (PEITC) was capable of inducing JNK activation and apoptosis in prostate cancer cell lines with distinct p53 statuses.	phenethyl isothiocyanate	42-47	P53	Homo sapiens	146-149
12176904-6	2002	Fludarabine and FCM induce p53 stabilization, but do not seem to be essential in inducing Bax and Bak conformational changes, as they are also observed in dexamethasone-treated CLL cells.	Fosfomycin	16-19	P53	Homo sapiens	27-30
11925449-6	2002	Furthermore, mutation of the conserved Phe(270) within the S10 beta-sheet resulted in a mutant p53, which binds more stably to RNA.MDM2 complexes in vitro and which is strikingly hyper-ubiquitinated in vivo.	Phenylalanine	39-42	P53	Homo sapiens	95-98
16434201-3	2006	Furthermore, bis-chalcone 8 exhibited a more potent inhibition of colon cancer cells expressing wild-type p53 than of an isogenic cell line that was p53-null.	bis-chalcone	13-25	P53	Homo sapiens	106-109
16434201-3	2006	Furthermore, bis-chalcone 8 exhibited a more potent inhibition of colon cancer cells expressing wild-type p53 than of an isogenic cell line that was p53-null.	bis-chalcone	13-25	P53	Homo sapiens	149-152
33383653-8	2020	Furthermore, cycloheximide treatment increased HO-1 abundance in p53 KO cells suggesting that p53 modulates HO-1 protein stability.	Cycloheximide	13-26	P53	Homo sapiens	94-97
33288579-7	2020	Furthermore, maslinic acid elevated the levels of p-ATMSer1981, p-ATRSer428, p53, p-p53Ser151, p-H2A.XSer139, BRCA1 and PARP at 30-40 muM.	maslinic acid	13-26	P53	Homo sapiens	77-80
19771269-9	2006	NaBT treatment in combination with PI3K inhibitors showed the increased expression of the CDK inhibitors p21(Cip1/Waf1) and p27(Kip1), in a p53 dependent manner, and also the increased dephosphorylation of Rb whereas there was a reduction in the expression levels of cyclin A, cyclin D1 and cyclin B1.	NABT	0-4	P53	Homo sapiens	140-143
12097262-0	2002	Phenethyl isothiocyanate-induced apoptosis in p53-deficient PC-3 human prostate cancer cell line is mediated by extracellular signal-regulated kinases.	phenethyl isothiocyanate	0-24	P53	Homo sapiens	46-49
12097262-1	2002	Previous studies have suggested that p53 is required for apoptosis induction by phenethyl isothiocyanate (PEITC), which is a highly promising cancer chemopreventive agent.	phenethyl isothiocyanate	80-104	P53	Homo sapiens	37-40
12097262-1	2002	Previous studies have suggested that p53 is required for apoptosis induction by phenethyl isothiocyanate (PEITC), which is a highly promising cancer chemopreventive agent.	phenethyl isothiocyanate	106-111	P53	Homo sapiens	37-40
11947902-11	2002	CONCLUSIONS: OxLDL induces cytochrome c release and apoptosis in human macrophages in close association with p53 accumulation.	oxldl	13-18	P53	Homo sapiens	109-112
11947902-12	2002	NO attenuates OxLDL-induced cytochrome c release and p53 accumulation via activation of sGC and cGMP formation.	oxldl	14-19	P53	Homo sapiens	53-56
16443602-3	2006	One important mechanism by which p53 achieves OMMP is by forming an inhibitory complex with the anti-apoptotic BclXL protein.	ommp	46-50	P53	Homo sapiens	33-36
33288579-7	2020	Furthermore, maslinic acid elevated the levels of p-ATMSer1981, p-ATRSer428, p53, p-p53Ser151, p-H2A.XSer139, BRCA1 and PARP at 30-40 muM.	maslinic acid	13-26	P53	Homo sapiens	84-87
32886187-0	2020	Mutagenicity of acrylamide and glycidamide in human TP53 knock-in (Hupki) mouse embryo fibroblasts.	Acrylamide	16-26	P53	Homo sapiens	52-56
32886187-7	2020	Mutations induced by glycidamide occurred at specific TP53 codons that have also been found to be mutated in human tumours (i.e., breast, ovary, colorectal, and lung) previously associated with acrylamide exposure.	Acrylamide	194-204	P53	Homo sapiens	54-58
16411021-2	2006	In the study of the molecular mechanism of this phenomenon, it was found that GnTV-AS reduced the expressions of anti-apoptotic proteins, such as phosphorylated protein kinase B and phosphorylated Bad as well as Bcl-2 and Bcl-X (L), and elevated those of pro-apoptotic proteins, including Bax, full length caspase-3 and its activated fragments as well as anti-oncoprotein p53.	gntv	78-82	P53	Homo sapiens	372-375
12027749-0	2002	Isolation of streptonigrin and its novel derivative from Micromonospora as inducing agents of p53-dependent cell apoptosis.	Streptonigrin	13-26	P53	Homo sapiens	94-97
33091670-0	2020	Novel 1,2,4-triazole derivatives as apoptotic inducers targeting p53: Synthesis and antiproliferative activity.	1,2,4-triazole	6-20	P53	Homo sapiens	65-68
16467108-10	2006	Lovastatin affected various IR-induced stress responses in HUVEC: It attenuated the increase in p53/p21 protein level and impaired the activation of nuclear factor-kappaB, Chk-1, and Akt kinase but did not inhibit extracellular signal-regulated kinase activation.	Lovastatin	0-10	P53	Homo sapiens	96-99
16287968-3	2005	Among the compounds isolated were derivatives of 9-aminoacridine (9AA), including the antimalaria drug quinacrine, which strongly induced p53 function in RCC and other types of cancer cells.	Aminacrine	49-64	P53	Homo sapiens	138-141
16287968-3	2005	Among the compounds isolated were derivatives of 9-aminoacridine (9AA), including the antimalaria drug quinacrine, which strongly induced p53 function in RCC and other types of cancer cells.	Aminacrine	66-69	P53	Homo sapiens	138-141
12006651-2	2002	Herein, we show that human Cdc6 is rapidly destroyed by a p53-independent, proteasome-, and ubiquitin-dependent pathway during early stages of programmed cell death induced by the DNA-damaging drug adozelesin, or by a separate caspase-dependent pathway in cells undergoing apoptosis through an extrinsic pathway induced by tumor necrosis factor-alpha and cycloheximide.	Cycloheximide	355-368	P53	Homo sapiens	58-61
33091670-6	2020	The docking study of the new compounds 3a-n revealed high binding scores for the new compounds toward p53 binding domain in MDM2.	3a-n	39-43	P53	Homo sapiens	102-105
16159876-6	2005	Upon mdm2 binding this motif becomes a well defined full helix turn whose hydrophobic face formed by the side chains of Ile-50, Trp-53, and Phe-54 inserts deeply into the helix binding pocket.	Isoleucine	120-123	P53	Homo sapiens	128-134
11835680-0	2002	Caffeine induces TP53-independent G(1)-phase arrest and apoptosis in human lung tumor cells in a dose-dependent manner.	Caffeine	0-8	P53	Homo sapiens	17-21
32958825-8	2020	However, PPARgamma deficiency inhibited cell death by blocking the ATM-p53 axis in radiation/CB11-induced radiation-resistant human NSCLC cells.	cb11	93-97	P53	Homo sapiens	71-74
11835680-3	2002	Surprisingly, at a concentration of 5 mM, caffeine not only induced apoptosis by itself and acted synergistically to enhance radiation-induced apoptosis, but also induced a TP53-independent G(1)-phase arrest.	Caffeine	42-50	P53	Homo sapiens	173-177
33160274-3	2020	More intriguingly, the disruption of p53 in hESCs leads to dramatic upregulation of phosphatidylcholine and decrease of total choline in both pluripotent and differentiated state of hESCs, suggesting abnormal choline metabolism in the absence of p53.	Choline	96-103	P53	Homo sapiens	37-40
16308485-9	2005	The transduction of redox signals into zinc signals and vice versa affects mitochondrial functions and signaling pathways (NF-kappaB, p53, AP-1) where zinc and the zinc donor/acceptor pair metallothionein/thionein are critically involved in life and death decisions of the cell.	Lys-Cys-Thr-Cys-Cys-Ala	196-204	P53	Homo sapiens	134-137
16204068-10	2005	We conclude that CPT-11 and tomudex may be more effective than 5-FU and oxaliplatin in the treatment of p53 mutant colorectal cancer tumors by sensitizing them to Fas-mediated apoptosis in a STAT1-dependent manner.	Oxaliplatin	72-83	P53	Homo sapiens	104-107
16179969-1	2005	We recently identified two thiazolidin compounds, 5-[(4-methylphenyl)methylene]-2-(phenylamino)-4(5H)-thiazolone (MMPT) and 5-(2,4-dihydroxybenzylidene)-2-(phenylimino)-1,3-thiazolidin (DBPT), that inhibit the growth of human non-small-cell lung and colon cancer cells independent of P-glycoprotein and p53 status.	Timonacic	27-38	P53	Homo sapiens	303-306
12509296-10	2002	Since HPV16 (E6/E7) transformed XPV cells were highly UV sensitive and not further sensitized by caffeine, it appears likely that caffeine sensitization proceeds through a p53 pathway.	Caffeine	130-138	P53	Homo sapiens	172-175
33160274-3	2020	More intriguingly, the disruption of p53 in hESCs leads to dramatic upregulation of phosphatidylcholine and decrease of total choline in both pluripotent and differentiated state of hESCs, suggesting abnormal choline metabolism in the absence of p53.	Choline	126-133	P53	Homo sapiens	37-40
33216890-2	2020	There is concern, however, that nutlin therapy might stimulate the emergence or expansion of TP53-mutated subclones.	nutlin	32-38	P53	Homo sapiens	93-97
11753684-0	2001	Functional p53 is required for triptolide-induced apoptosis and AP-1 and nuclear factor-kappaB activation in gastric cancer cells.	triptolide	31-41	P53	Homo sapiens	11-14
11753684-4	2001	We showed that triptolide inhibited cell growth, induced apoptosis and suppressed NK-kappaB and AP-1 transactivation in AGS cells with wild-type p53.	triptolide	15-25	P53	Homo sapiens	145-148
11753684-5	2001	Triptolide induced apoptosis by stimulating the expressions of p53, p21(waf1/cip1), bax protein, and increased the activity of caspases.	triptolide	0-10	P53	Homo sapiens	63-66
16024610-8	2005	NO treatment also induced the phosphorylation of p53 at Ser15; pretreatment with phosphoinositide-3 kinase (PI3K) family inhibitors, wortmannin, LY294002, and caffeine, blocked such phosphorylation, but the p38 mitogen-activated protein kinase inhibitor, SB203580, did not.	Caffeine	159-167	P53	Homo sapiens	49-52
11753684-7	2001	To examine the role of p53 in these functions, we showed that suppression of p53 level with antisense oligonucleotide abrogated triptolide-induced apoptosis and over-expression of dominant negative p53 abolished the inhibitory effect on NF-kappaB activation.	triptolide	128-138	P53	Homo sapiens	23-26
32950500-0	2020	Targeting DNA and mutant p53 by a naphthalimide derivative, NA20, exhibits selective inhibition in gastric tumorigenesis by blocking mutant p53-EGFR signaling pathway.	Naphthalimides	34-47	P53	Homo sapiens	25-28
11753684-7	2001	To examine the role of p53 in these functions, we showed that suppression of p53 level with antisense oligonucleotide abrogated triptolide-induced apoptosis and over-expression of dominant negative p53 abolished the inhibitory effect on NF-kappaB activation.	triptolide	128-138	P53	Homo sapiens	77-80
11753684-7	2001	To examine the role of p53 in these functions, we showed that suppression of p53 level with antisense oligonucleotide abrogated triptolide-induced apoptosis and over-expression of dominant negative p53 abolished the inhibitory effect on NF-kappaB activation.	triptolide	128-138	P53	Homo sapiens	77-80
11753684-8	2001	Furthermore, we demonstrated that triptolide had differential effects on gastric cancer cells with different p53 status.	triptolide	34-44	P53	Homo sapiens	109-112
16019469-2	2005	In this review we will focus on downstream events in ATO-induced intrinsic and extrinsic apoptotic pathways with an emphasis on the role of pro-apoptotic and anti-apoptotic proteins and the role of p53 in ATO-induced apoptosis including its effect on cell cycle, its anti-mitotic effect and the role of apoptosis inducing factors (AIF) in ATO-induced apoptosis, chromatin condensation and nuclear fragmentation in myeloma cells as a model.	ato	53-56	P53	Homo sapiens	198-201
16019469-2	2005	In this review we will focus on downstream events in ATO-induced intrinsic and extrinsic apoptotic pathways with an emphasis on the role of pro-apoptotic and anti-apoptotic proteins and the role of p53 in ATO-induced apoptosis including its effect on cell cycle, its anti-mitotic effect and the role of apoptosis inducing factors (AIF) in ATO-induced apoptosis, chromatin condensation and nuclear fragmentation in myeloma cells as a model.	ato	205-208	P53	Homo sapiens	198-201
11753684-9	2001	We showed that triptolide also inhibited cell growth and induced apoptosis in MKN-45 with wild-type p53, whereas it had no significant growth-inhibition and apoptosis induction effects on the MKN-28 and SGC-7901 cells with mutant p53.	triptolide	15-25	P53	Homo sapiens	100-103
32950500-0	2020	Targeting DNA and mutant p53 by a naphthalimide derivative, NA20, exhibits selective inhibition in gastric tumorigenesis by blocking mutant p53-EGFR signaling pathway.	Naphthalimides	34-47	P53	Homo sapiens	140-143
16019469-2	2005	In this review we will focus on downstream events in ATO-induced intrinsic and extrinsic apoptotic pathways with an emphasis on the role of pro-apoptotic and anti-apoptotic proteins and the role of p53 in ATO-induced apoptosis including its effect on cell cycle, its anti-mitotic effect and the role of apoptosis inducing factors (AIF) in ATO-induced apoptosis, chromatin condensation and nuclear fragmentation in myeloma cells as a model.	ato	205-208	P53	Homo sapiens	198-201
32950500-3	2020	We show here that gain-of-function p53 mutation in gastric cancer cells promotes tumorigenesis by enhancing p53-EGFR (epidermal growth factor receptor) signaling pathway, and such process can be blocked by small molecule NA20, a naphthalimide derivative that exhibited selective inhibition in p53 mutant gastric cancer cell lines.	Naphthalimides	229-242	P53	Homo sapiens	35-38
32950500-3	2020	We show here that gain-of-function p53 mutation in gastric cancer cells promotes tumorigenesis by enhancing p53-EGFR (epidermal growth factor receptor) signaling pathway, and such process can be blocked by small molecule NA20, a naphthalimide derivative that exhibited selective inhibition in p53 mutant gastric cancer cell lines.	Naphthalimides	229-242	P53	Homo sapiens	108-111
32950500-3	2020	We show here that gain-of-function p53 mutation in gastric cancer cells promotes tumorigenesis by enhancing p53-EGFR (epidermal growth factor receptor) signaling pathway, and such process can be blocked by small molecule NA20, a naphthalimide derivative that exhibited selective inhibition in p53 mutant gastric cancer cell lines.	Naphthalimides	229-242	P53	Homo sapiens	108-111
11720884-1	2001	OBJECTIVE: The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, lovastatin, induces apoptosis in the thyroid cell line TAD-2 and in proliferating normal human thyroid cells in culture, through a p53-independent mechanism involving caspase-3-like proteases.	Lovastatin	74-84	P53	Homo sapiens	205-208
32860803-7	2020	The p38-p53 axis was also further activated by the combination of AOAA or PAG with DIM.	pag	74-77	P53	Homo sapiens	8-11
11489880-0	2001	Caffeine sensitizes human H358 cell line to p53-mediated apoptosis by inducing mitochondrial translocation and conformational change of BAX protein.	Caffeine	0-8	P53	Homo sapiens	44-47
11489880-8	2001	All together, caffeine synergizes with p53 for inducing cell death through a cell cycle-independent mechanism, involving mitochondrial translocation and conformational change of BAX protein.	Caffeine	14-22	P53	Homo sapiens	39-42
15816444-6	2005	p53 nuclear staining was positive only in 3 of 7 invasive IPMCs (43%) and 9 of 21 DCs (43%).	ipmcs	58-63	P53	Homo sapiens	0-3
15765147-0	2005	Glycyrrhizic acid alters Kaposi sarcoma-associated herpesvirus latency, triggering p53-mediated apoptosis in transformed B lymphocytes.	Glycyrrhizic Acid	0-17	P53	Homo sapiens	83-86
15456408-1	2005	p53 deficiency confers resistance to doxo (doxorubicin), a clinically active and widely used antitumour anthracycline antibiotic.	Desoxycorticosterone Acetate	37-41	P53	Homo sapiens	0-3
15456408-2	2005	The purpose of the present study was to investigate the reversal mechanism of doxo resistance by the potent PARP [poly(ADP-ribose) polymerase] inhibitor ANI (4-amino-1,8-naphthalimide) in the p53-deficient breast cancer cell lines EVSA-T and MDA-MB-231.	Desoxycorticosterone Acetate	78-82	P53	Homo sapiens	192-195
11589834-4	2001	The initial purified recombinant adenovirus containing the p53 tumor suppressor gene was produced from 293 cells grown on microcarriers and purified by passage through DEAE-Fractogel and gel-filtration chromatography.	2-diethylaminoethanol	168-172	P53	Homo sapiens	59-62
11526536-5	2001	In contrast, HSV-tk/GCV-induced apoptosis was reduced in p53-negative Hep3B cells as compared with p53-positive HepG2 cells.	Ganciclovir	20-23	P53	Homo sapiens	57-60
11526536-5	2001	In contrast, HSV-tk/GCV-induced apoptosis was reduced in p53-negative Hep3B cells as compared with p53-positive HepG2 cells.	Ganciclovir	20-23	P53	Homo sapiens	99-102
15456408-2	2005	The purpose of the present study was to investigate the reversal mechanism of doxo resistance by the potent PARP [poly(ADP-ribose) polymerase] inhibitor ANI (4-amino-1,8-naphthalimide) in the p53-deficient breast cancer cell lines EVSA-T and MDA-MB-231.	evsa-t	231-237	P53	Homo sapiens	192-195
11526536-6	2001	HSV-tk/GCV, but not PNP/fludarabine, caused up-regulation of Fas in p53-positive HepG2 cells and of Fas ligand (FasL) in both HCC cell lines.	Ganciclovir	7-10	P53	Homo sapiens	68-71
32860803-9	2020	Taken together, AOAA or PAG inhibited the expression of endogenous H2S biosynthesis enzymes and effectively enhanced susceptibility of gastric cancer to DIM through activating p38-p53 axis.	pag	24-27	P53	Homo sapiens	180-183
15720190-10	2005	Small molecules that have been reported to disrupt the p53-MDM2 binding, thereby enhancing p53 activity to elicit anticancer effects include the following: synthetic chalcones, norbornane derivatives, cis-imidazoline derivatives (Nutlins), a pyrazolidinedione sulfonamide and 1,4-benzodiazepine-2,5-diones, as well as tryptophan derivatives.	cis-imidazoline	201-216	P53	Homo sapiens	91-94
32485257-4	2020	In total, 66 types of polysaccharides from 58 kinds of plant have shown hepatoprotective effect through the pathological process of inflammation, apoptosis and oxidative stress by regulating NF-kappaB, JAK/STAT, TGF-beta, PI3K/AKT, MAPK, caspase cascade, p53 and Nrf2-Keap1 pathways, lipid metabolism as well as cytochrome P450 enzymes.	Polysaccharides	22-37	P53	Homo sapiens	255-258
15720190-10	2005	Small molecules that have been reported to disrupt the p53-MDM2 binding, thereby enhancing p53 activity to elicit anticancer effects include the following: synthetic chalcones, norbornane derivatives, cis-imidazoline derivatives (Nutlins), a pyrazolidinedione sulfonamide and 1,4-benzodiazepine-2,5-diones, as well as tryptophan derivatives.	pyrazolidinedione sulfonamide	242-271	P53	Homo sapiens	55-58
15720190-10	2005	Small molecules that have been reported to disrupt the p53-MDM2 binding, thereby enhancing p53 activity to elicit anticancer effects include the following: synthetic chalcones, norbornane derivatives, cis-imidazoline derivatives (Nutlins), a pyrazolidinedione sulfonamide and 1,4-benzodiazepine-2,5-diones, as well as tryptophan derivatives.	pyrazolidinedione sulfonamide	242-271	P53	Homo sapiens	91-94
15804027-6	2005	However, when wt-p53 gene combined with HSV-tk/GCV system, the killing effects was significantly stronger (P &lt; 0.05) and the cell survival rate decreased to 20%.	Ganciclovir	47-50	P53	Homo sapiens	17-20
11724337-0	2001	9-Hydroxyellipticine alters the conformation and DNA binding characteristics of mutated p53 protein.	9-hydroxyellipticine	0-20	P53	Homo sapiens	88-91
11724337-3	2001	We examined whether 9-hydroxyellipticine (9HE), a cytotoxic agent, affected the tertiary structure of mutant p53 and DNA binding characteristics.	9-hydroxyellipticine	20-40	P53	Homo sapiens	109-112
11724337-3	2001	We examined whether 9-hydroxyellipticine (9HE), a cytotoxic agent, affected the tertiary structure of mutant p53 and DNA binding characteristics.	9-hydroxyellipticine	42-45	P53	Homo sapiens	109-112
33251049-0	2020	LINC00460-miR-149-5p/miR-150-5p-Mutant p53 Feedback Loop Promotes Oxaliplatin Resistance in Colorectal Cancer.	Oxaliplatin	66-77	P53	Homo sapiens	39-42
11448931-5	2001	In contrast, in the two pairs of related human tumor cell lines (HCT-116 and HCT-116/N7 and A2780 and A2780/CP70) cells with functional p53 were more sensitive to Alimta- and raltitrexed-induced growth inhibition (P = 0.002).	raltitrexed	175-186	P53	Homo sapiens	136-139
15595848-2	2004	We incorporated a single (+)- or (-)-trans-anti-benzo[a]pyrene diol epoxide (BPDE) DNA adduct at the second position of codon 273 of the human P53 gene and explored the mutagenic potential of this lesion in mammalian cells.	ORALIT	25-32	P53	Homo sapiens	143-146
15610526-6	2004	The characteristic PUVA-induced mutations predominate in the p53 mutational spectrum in controlled in vivo test systems or in high-dose PUVA-treated patients, and also are easily recognizable in the overall PUVA-treated patients.	puva	19-23	P53	Homo sapiens	61-64
15610526-6	2004	The characteristic PUVA-induced mutations predominate in the p53 mutational spectrum in controlled in vivo test systems or in high-dose PUVA-treated patients, and also are easily recognizable in the overall PUVA-treated patients.	puva	136-140	P53	Homo sapiens	61-64
32993568-13	2020	CONCLUSIONS: Acteoside exerts an antitumor effect possibly through its up-regulation of p53 levels as well as inhibition of KLK expression and angiogenesis.	acteoside	13-22	P53	Homo sapiens	88-91
15610526-6	2004	The characteristic PUVA-induced mutations predominate in the p53 mutational spectrum in controlled in vivo test systems or in high-dose PUVA-treated patients, and also are easily recognizable in the overall PUVA-treated patients.	puva	136-140	P53	Homo sapiens	61-64
15610526-8	2004	The signature mutations of PUVA are discernible in the p53 mutational spectrum in PUVA-treated patients but complex exposure to other therapeutic/environmental carcinogens also leads to the frequent occurrence of other types of mutations in this population.	puva	27-31	P53	Homo sapiens	55-58
15540942-8	2004	BA-1,2-dihydrodiol induced a Fpg sensitive and piperidine labile G lesion at the 5"-ACG-3" sequence complementary to codon 273 of the human p53 tumor suppressor gene, which is known as a hotspot.	ba-1,2-dihydrodiol	0-18	P53	Homo sapiens	140-143
11375905-4	2001	We found that exposure of the cells to elevated concentrations of DCA suppressed accumulation of p53 protein as well as p53 transactivation and impaired the p53 response of the cells to DNA damaging agents, such as ionizing radiation.	Deoxycholic Acid	66-69	P53	Homo sapiens	97-100
11375905-4	2001	We found that exposure of the cells to elevated concentrations of DCA suppressed accumulation of p53 protein as well as p53 transactivation and impaired the p53 response of the cells to DNA damaging agents, such as ionizing radiation.	Deoxycholic Acid	66-69	P53	Homo sapiens	120-123
11375905-4	2001	We found that exposure of the cells to elevated concentrations of DCA suppressed accumulation of p53 protein as well as p53 transactivation and impaired the p53 response of the cells to DNA damaging agents, such as ionizing radiation.	Deoxycholic Acid	66-69	P53	Homo sapiens	120-123
11375905-6	2001	Further examination revealed that instead of inhibition, DCA induced p53 mRNA in a dose-dependent manner, indicating that the inhibitory effect of DCA on p53 protein is mediated by a post-transcriptional mechanism.	Deoxycholic Acid	57-60	P53	Homo sapiens	69-72
11375905-6	2001	Further examination revealed that instead of inhibition, DCA induced p53 mRNA in a dose-dependent manner, indicating that the inhibitory effect of DCA on p53 protein is mediated by a post-transcriptional mechanism.	Deoxycholic Acid	57-60	P53	Homo sapiens	154-157
11375905-6	2001	Further examination revealed that instead of inhibition, DCA induced p53 mRNA in a dose-dependent manner, indicating that the inhibitory effect of DCA on p53 protein is mediated by a post-transcriptional mechanism.	Deoxycholic Acid	147-150	P53	Homo sapiens	69-72
11375905-6	2001	Further examination revealed that instead of inhibition, DCA induced p53 mRNA in a dose-dependent manner, indicating that the inhibitory effect of DCA on p53 protein is mediated by a post-transcriptional mechanism.	Deoxycholic Acid	147-150	P53	Homo sapiens	154-157
11375905-7	2001	Both lactacystin, a specific inhibitor of the 26S proteasome, and leptomycin B, a specific inhibitor of the nuclear export protein CRM1, could block the effect that DCA had on p53 protein levels, suggesting that DCA suppressed p53 by stimulating the process of proteasome-mediated degradation of p53.	Deoxycholic Acid	165-168	P53	Homo sapiens	176-179
11375905-7	2001	Both lactacystin, a specific inhibitor of the 26S proteasome, and leptomycin B, a specific inhibitor of the nuclear export protein CRM1, could block the effect that DCA had on p53 protein levels, suggesting that DCA suppressed p53 by stimulating the process of proteasome-mediated degradation of p53.	Deoxycholic Acid	165-168	P53	Homo sapiens	227-230
11375905-7	2001	Both lactacystin, a specific inhibitor of the 26S proteasome, and leptomycin B, a specific inhibitor of the nuclear export protein CRM1, could block the effect that DCA had on p53 protein levels, suggesting that DCA suppressed p53 by stimulating the process of proteasome-mediated degradation of p53.	Deoxycholic Acid	165-168	P53	Homo sapiens	227-230
11375905-7	2001	Both lactacystin, a specific inhibitor of the 26S proteasome, and leptomycin B, a specific inhibitor of the nuclear export protein CRM1, could block the effect that DCA had on p53 protein levels, suggesting that DCA suppressed p53 by stimulating the process of proteasome-mediated degradation of p53.	Deoxycholic Acid	212-215	P53	Homo sapiens	176-179
11375905-7	2001	Both lactacystin, a specific inhibitor of the 26S proteasome, and leptomycin B, a specific inhibitor of the nuclear export protein CRM1, could block the effect that DCA had on p53 protein levels, suggesting that DCA suppressed p53 by stimulating the process of proteasome-mediated degradation of p53.	Deoxycholic Acid	212-215	P53	Homo sapiens	227-230
11375905-7	2001	Both lactacystin, a specific inhibitor of the 26S proteasome, and leptomycin B, a specific inhibitor of the nuclear export protein CRM1, could block the effect that DCA had on p53 protein levels, suggesting that DCA suppressed p53 by stimulating the process of proteasome-mediated degradation of p53.	Deoxycholic Acid	212-215	P53	Homo sapiens	227-230
15579021-9	2004	Considering HIF-1alpha and p53 as targets of reactive nitrogen intermediates (RNI) may provide insights into basic chemical reactions, biochemical signal transduction pathways with broad implications for medicine.	reactive nitrogen	45-62	P53	Homo sapiens	27-30
15531428-10	2004	Risk associated with mono-ortho PCBs was slightly higher for tumors with mutations in the p53 gene but was not modified by mutations in K-ras.	Polychlorinated Biphenyls	32-36	P53	Homo sapiens	90-93
11375905-8	2001	Significantly, blocking extracellular signal-regulated kinase (ERK) signaling, but not protein kinase C (PKC), blunted suppression by DCA of p53 protein levels and transactivation activity, suggesting that DCA suppressed p53, in part, by stimulating the ERK signaling pathway.	Deoxycholic Acid	134-137	P53	Homo sapiens	141-144
32611648-0	2020	A biomarker-enriched, randomized Phase II trial of adavosertib (AZD1775) plus paclitaxel and carboplatin for women with platinum-sensitive TP53-mutant ovarian cancer.	adavosertib	51-62	P53	Homo sapiens	139-143
11375905-8	2001	Significantly, blocking extracellular signal-regulated kinase (ERK) signaling, but not protein kinase C (PKC), blunted suppression by DCA of p53 protein levels and transactivation activity, suggesting that DCA suppressed p53, in part, by stimulating the ERK signaling pathway.	Deoxycholic Acid	134-137	P53	Homo sapiens	221-224
11375905-8	2001	Significantly, blocking extracellular signal-regulated kinase (ERK) signaling, but not protein kinase C (PKC), blunted suppression by DCA of p53 protein levels and transactivation activity, suggesting that DCA suppressed p53, in part, by stimulating the ERK signaling pathway.	Deoxycholic Acid	206-209	P53	Homo sapiens	141-144
11375905-8	2001	Significantly, blocking extracellular signal-regulated kinase (ERK) signaling, but not protein kinase C (PKC), blunted suppression by DCA of p53 protein levels and transactivation activity, suggesting that DCA suppressed p53, in part, by stimulating the ERK signaling pathway.	Deoxycholic Acid	206-209	P53	Homo sapiens	221-224
15361841-1	2004	A mutant version of p53 (p53-121F), in which phenylalanine replaces the 121st serine residue, can induce apoptosis more effectively than wild-type p53 (wt-p53).	Phenylalanine	45-58	P53	Homo sapiens	20-23
15361841-1	2004	A mutant version of p53 (p53-121F), in which phenylalanine replaces the 121st serine residue, can induce apoptosis more effectively than wild-type p53 (wt-p53).	Phenylalanine	45-58	P53	Homo sapiens	25-28
15361841-1	2004	A mutant version of p53 (p53-121F), in which phenylalanine replaces the 121st serine residue, can induce apoptosis more effectively than wild-type p53 (wt-p53).	Phenylalanine	45-58	P53	Homo sapiens	25-28
15361841-1	2004	A mutant version of p53 (p53-121F), in which phenylalanine replaces the 121st serine residue, can induce apoptosis more effectively than wild-type p53 (wt-p53).	Phenylalanine	45-58	P53	Homo sapiens	25-28
15258255-9	2004	Disruption of p53 and p21 had minor influence on the cytotoxicity of doxorubicin, whereas p53 but not p21 disruption was associated with increased resistance to amsacrine.	Amsacrine	161-170	P53	Homo sapiens	90-93
11422444-7	2001	The c2-ceramide treatment also increases levels of c-jun, c-fos and p53 mRNA in primary cortical neuron cultures, but this is independent of p38 activation.	N-acetylsphingosine	4-15	P53	Homo sapiens	68-71
32611648-1	2020	PURPOSE: Preclinical studies show that adavosertib, a WEE1 kinase inhibitor, sensitizes TP53-mutant cells to chemotherapy.	adavosertib	39-50	P53	Homo sapiens	88-92
11422444-8	2001	Our study further elucidates the time-courses of MAPK cascade modulation, and of c-jun, c-fos and p53 activation during c2-ceramide-induced neuronal apoptosis.	N-acetylsphingosine	120-131	P53	Homo sapiens	98-101
32611648-2	2020	We hypothesized that adavosertib, plus chemotherapy, would enhance efficacy versus placebo in TP53-mutated ovarian cancer.	adavosertib	21-32	P53	Homo sapiens	94-98
32742376-5	2020	In HCT116 cells expressing wild-type (wt) TP53, SIRT inhibitors were found to act antagonistically with multiple chemotherapeutic agents (cisplatin, 5-fluorouracil, oxaliplatin, gefitinib, LY294002 and metformin), and decreased the anti-tumor effects of these agents.	Oxaliplatin	165-176	P53	Homo sapiens	42-46
11429785-5	2001	Although CAPE treatment of two p53 mutant tumor cell lines, NCI-H358 and SK-OV-3, and p53-deficient (p53(-/-)) cells caused the cleavage of caspase-3 as well as DNA fragmentation, caspase-3 cleavage was seen early (at 6 h) only in cells expressing wild-type p53 (p53(+/+)) and Cl 41 cells.	caffeic acid phenethyl ester	9-13	P53	Homo sapiens	31-34
11323395-6	2001	In response to Cr(VI) treatment, p53 protein became phosphorylated and acetylated at Ser15 and Lys382, respectively.	chromium hexavalent ion	15-21	P53	Homo sapiens	33-36
15327837-0	2004	Involvement of p53, nuclear factor kappaB and Fas/Fas ligand in induction of apoptosis and cell cycle arrest by saikosaponin d in human hepatoma cell lines.	saikosaponin D	112-126	P53	Homo sapiens	15-18
15327837-3	2004	In Hep G2, saikosaponin d blocked the progression of cell cycle at G1 phase by inducing p53 expression and further up-regulating p21/WAF1 expression.	saikosaponin D	11-23	P53	Homo sapiens	88-91
15327837-5	2004	Saikosaponin d therefore decreased the cell proliferation and inducted apoptosis both in p53-positive Hep G2 and p53-negative Hep 3B cells.	saikosaponin D	0-14	P53	Homo sapiens	89-92
15327837-5	2004	Saikosaponin d therefore decreased the cell proliferation and inducted apoptosis both in p53-positive Hep G2 and p53-negative Hep 3B cells.	saikosaponin D	0-14	P53	Homo sapiens	113-116
15371598-0	2004	Guanidine alkaloid analogs as inhibitors of HIV-1 Nef interactions with p53, actin, and p56lck.	Guanidine	0-9	P53	Homo sapiens	72-75
11291094-10	2001	Results of Western hybridization reveal a p53-independent mechanism of radiosensitization caused by caffeine.	Caffeine	100-108	P53	Homo sapiens	42-45
32472321-5	2020	In this study, we have targeted the P53 pathway by novel Mannich base (3FB3FA8H) which can be a future prospect to cure neuroblastoma.	3fb3fa8h	71-79	P53	Homo sapiens	36-39
15325273-3	2004	In a panel of colorectal cancer cell lines that carry Ras mutations and have constitutively active MEK/MAPK, we found that inhibition of the MAPK upstream kinase MEK by the small molecular MEK inhibitor U0126 induced cell death only in p53 wild-type cells.	U 0126	203-208	P53	Homo sapiens	236-239
15325273-5	2004	Using isogenic colon cancer cell lines and RNA interference, we show that loss of p53 significantly reduces MAPK phosphorylation and renders cells resistant to U0126 treatment.	U 0126	160-165	P53	Homo sapiens	82-85
32472321-6	2020	3FB3FA8H has shown modulation of P53 pathway leading to apoptosis of neuroblastoma cells.	3fb3fa8h	0-8	P53	Homo sapiens	33-36
32472321-7	2020	Mitochondrial membrane permeability is also increased by 3FB3FA8H which may be a consequence of P53 pathway modulation.	3fb3fa8h	57-65	P53	Homo sapiens	96-99
11331958-0	2001	Transcriptional activation of p21 by vitamin D(3) or vitamin K(2) leads to differentiation of p53-deficient MG-63 osteosarcoma cells.	Vitamin K	53-62	P53	Homo sapiens	94-97
32622356-6	2020	After biopsy confirmation, patient was initially started on gemcitabine and oxaliplatin combination followed by gene sequencing, which showed Tp53 (exon 7-c.713 G > A and exon 5-c.376-2A > G) and EGFR (exon 20-T790M) mutation, and erlotinib was added to chemotherapy, after 6 cycles of chemotherapy patient showed a 90% partial radiological response as per RECIST criteria.	Oxaliplatin	76-87	P53	Homo sapiens	142-146
11331958-6	2001	The transcriptional activation of p21 by vitamin D(3) or vitamin K(2) in p53-deficient osteosarcoma cells demonstrated the p53-independent role of p21 in human osseous differentiation.	Vitamin K	57-66	P53	Homo sapiens	73-76
11307620-5	2001	Wild-type p53 gene transfer promotes lovastatin-induced apoptosis in p53 wild-type LN-229 cells but not in p53 mutant T98G cells.	Lovastatin	37-47	P53	Homo sapiens	10-13
15178678-7	2004	Furthermore, p53 binds regions of the S100B promoter, one of which matches the 20-nucleotide p53-binding consensus DNA sequence perfectly.	20-nucleotide	79-92	P53	Homo sapiens	13-16
15178678-7	2004	Furthermore, p53 binds regions of the S100B promoter, one of which matches the 20-nucleotide p53-binding consensus DNA sequence perfectly.	20-nucleotide	79-92	P53	Homo sapiens	93-96
15363324-11	2004	When treated with LY294002 or U0126 for 24 hours, the amount of wild p53 protein in MCF7-neu3 cells was 1.7 or 1.5 times higher than those in DMSO treated cells.	U 0126	30-35	P53	Homo sapiens	69-72
15363324-12	2004	There were 4.7 or 5.3 times increase in the p53 protein when MCF7-neu3 cells were treated with LY294002 or U0126 for 48 hours (P &lt; 0.01).	U 0126	107-112	P53	Homo sapiens	44-47
11307620-5	2001	Wild-type p53 gene transfer promotes lovastatin-induced apoptosis in p53 wild-type LN-229 cells but not in p53 mutant T98G cells.	Lovastatin	37-47	P53	Homo sapiens	69-72
31898356-8	2020	The relative mRNA abundance of BAK, BAX, CASP3, CASP8, and TP53 and protein abundance of Bak, cleaved caspase-3, caspase-8, and P53 was activated by U73122 or inhibited by m-3M3FBS, while the relative mRNA and protein level of BCL6 showed the opposite trend.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	149-155	P53	Homo sapiens	59-63
11307620-5	2001	Wild-type p53 gene transfer promotes lovastatin-induced apoptosis in p53 wild-type LN-229 cells but not in p53 mutant T98G cells.	Lovastatin	37-47	P53	Homo sapiens	69-72
11280728-1	2001	The p53-dependent initiation of apoptosis is accompanied by the induction of proline oxidase (POX), a mitochondrial enzyme catalyzing the conversion of proline to pyrroline-5-carboxylate with the concomitant transfer of electrons to cytochrome c.	delta-1-pyrroline-5-carboxylate	163-186	P53	Homo sapiens	4-7
11313826-3	2001	Here, we report that adenoviral (Ad)-TK/GCV-induced death is p53-independent and does not involve altered CD95 or CD95L expression.	Ganciclovir	40-43	P53	Homo sapiens	61-64
15219811-4	2004	ELISA assay showed that Saikosaponin D significantly increased the expression of p53 and p21/WAF1 protein, contributing to cell cycle arrest.	saikosaponin D	24-38	P53	Homo sapiens	81-84
31898356-8	2020	The relative mRNA abundance of BAK, BAX, CASP3, CASP8, and TP53 and protein abundance of Bak, cleaved caspase-3, caspase-8, and P53 was activated by U73122 or inhibited by m-3M3FBS, while the relative mRNA and protein level of BCL6 showed the opposite trend.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	149-155	P53	Homo sapiens	60-63
15219811-6	2004	Taken together, our study suggests that the induction of p53 and activity of the Fas/FasL apoptotic system may participate in the antiproliferative activity of Saikosaponin D in A549 cells.	saikosaponin D	160-174	P53	Homo sapiens	57-60
32605658-0	2020	A ruthenium(II)-curcumin compound modulates NRF2 expression balancing the cancer cell death/survival outcome according to p53 status.	Ruthenium(II)	2-15	P53	Homo sapiens	122-125
15212949-3	2004	Decreasing phospho-ERK with the pharmacological inhibitors, PD98059 and U0126, markedly suppresses hyperoxia-stimulated phospho-p53(Ser15), p53, and p21(CIP1), and also restores the hyperoxia-reduced kinase activities of cyclin D1/E1-Cdks.	U 0126	72-77	P53	Homo sapiens	128-131
15212949-3	2004	Decreasing phospho-ERK with the pharmacological inhibitors, PD98059 and U0126, markedly suppresses hyperoxia-stimulated phospho-p53(Ser15), p53, and p21(CIP1), and also restores the hyperoxia-reduced kinase activities of cyclin D1/E1-Cdks.	U 0126	72-77	P53	Homo sapiens	140-143
15293391-2	2004	In this study, we prepared an inexpensive linear polyacrylamide (LPA), and successfully applied it to CE-SSCP analysis and tandem CE-SSCP/heteroduplex analysis (HA) of the P53 gene on an ABI capillary genetic analyzer.	polyacrylamide	49-63	P53	Homo sapiens	172-175
11240376-11	2001	These data suggest that deoxycholate caused DNA damage in colon epithelial cells that was sufficient to trigger apoptosis in a p53-independent manner.	Deoxycholic Acid	24-36	P53	Homo sapiens	127-130
32642717-4	2020	Methods: Using a well-established Sleeping Beauty (SB) transposon strategy, we injected human HGF and MET cDNA together with a short hairpin siRNA against Trp53 (SB-hHgf.Met.ShP53) into the lateral ventricle of neonatal mice to induce spontaneous glioma initiation and characterized the tumors with H&E and immunohistochemistry analysis.	Helium	299-302	P53	Homo sapiens	155-160
10922372-8	2000	Furthermore, vanadate-induced apoptosis occurred in cells expressing wild-type p53 (p53+/+) but was very weak in p53-deficient (p53-/-) cells.	Vanadates	13-21	P53	Homo sapiens	84-87
10922372-8	2000	Furthermore, vanadate-induced apoptosis occurred in cells expressing wild-type p53 (p53+/+) but was very weak in p53-deficient (p53-/-) cells.	Vanadates	13-21	P53	Homo sapiens	84-87
10922372-9	2000	These results demonstrate that vanadate induces p53 activation mainly through H(2)O(2) generation, and this activation is required for vanadate-induced apoptosis.	Vanadates	31-39	P53	Homo sapiens	48-51
10942736-0	2000	The role of hydroxyl radical as a messenger in Cr(VI)-induced p53 activation.	chromium hexavalent ion	47-53	P53	Homo sapiens	62-65
10942736-13	2000	NADPH, which accelerated the one-electron reduction of Cr(VI) to Cr(V) and increased.OH radical generation, dramatically enhanced p53 activation.	oh radical	85-95	P53	Homo sapiens	130-133
10942736-14	2000	Thus.OH radical generated from Cr(VI) reduction in A549 cells is responsible for Cr(VI)-induced p53 activation.	oh radical	5-15	P53	Homo sapiens	96-99
10942736-14	2000	Thus.OH radical generated from Cr(VI) reduction in A549 cells is responsible for Cr(VI)-induced p53 activation.	chromium hexavalent ion	31-37	P53	Homo sapiens	96-99
10942736-14	2000	Thus.OH radical generated from Cr(VI) reduction in A549 cells is responsible for Cr(VI)-induced p53 activation.	chromium hexavalent ion	81-87	P53	Homo sapiens	96-99
15130282-5	2004	Indeed, in addition to transition-type mutations at dipyrimidine sites, G:C to T:A transversions, which may be induced by the presence of 8-oxoguanine during DNA replication, are frequently observed in the ras oncogene and p53 tumor suppressor gene in human skin cancers of sun-exposed areas and in UV-induced mouse skin cancers.	dipyrimidine	52-64	P53	Homo sapiens	223-226
15004035-7	2004	By using a temperature-sensitive mutant of p53 where cytoplasmic-nuclear movement occurs by shift to permissive temperature, we show that p53 movement is impeded when p53 binding to hsp90 is inhibited by the hsp90 inhibitor radicicol.	monorden	224-233	P53	Homo sapiens	43-46
15004035-7	2004	By using a temperature-sensitive mutant of p53 where cytoplasmic-nuclear movement occurs by shift to permissive temperature, we show that p53 movement is impeded when p53 binding to hsp90 is inhibited by the hsp90 inhibitor radicicol.	monorden	224-233	P53	Homo sapiens	138-141
15004035-7	2004	By using a temperature-sensitive mutant of p53 where cytoplasmic-nuclear movement occurs by shift to permissive temperature, we show that p53 movement is impeded when p53 binding to hsp90 is inhibited by the hsp90 inhibitor radicicol.	monorden	224-233	P53	Homo sapiens	138-141
32382022-10	2020	Conclusions: Sorafenib and Regorafenib were especially active in well-differentiated cells, with wild-type p53 and increased mitochondrial respiration.	regorafenib	27-38	P53	Homo sapiens	107-110
15064743-6	2004	In contrast, abrogation of p53 function by the expression of HPV16 E6 in K1 and K2 cells either at the same time as DNhTERT or just prior to the onset of senescence allowed cells to continue growing until "crisis".	dnhtert	116-123	P53	Homo sapiens	27-30
10825467-1	2000	The dietary isothiocyanates and cancer chemopreventive agents phenethyl isothiocyanate and allyl isothiocyanate and their cysteine conjugates inhibited the growth and induced apoptosis of human leukaemia HL60 (p53-) and human myeloblastic leukaemia-1 cells (p53+) in vitro.	phenethyl isothiocyanate	62-86	P53	Homo sapiens	210-213
10825467-1	2000	The dietary isothiocyanates and cancer chemopreventive agents phenethyl isothiocyanate and allyl isothiocyanate and their cysteine conjugates inhibited the growth and induced apoptosis of human leukaemia HL60 (p53-) and human myeloblastic leukaemia-1 cells (p53+) in vitro.	phenethyl isothiocyanate	62-86	P53	Homo sapiens	258-261
32202904-10	2020	Results showed that the expression of p-p53, p53, Bax and PUMA was upregulated after CBL0137 administration.	CBLC137	85-92	P53	Homo sapiens	40-43
10867037-7	2000	Nuclear p53 protein levels were &gt;100% higher in the ZD Opti-MEM cells than in ZA cells.	opti-mem	58-66	P53	Homo sapiens	8-11
15183084-13	2004	An immunologic prozone effect was observed above 1000 ng p53 antibodies per milliliter of serum.	prozone	15-22	P53	Homo sapiens	57-60
14987952-7	2004	Taken together, emodin displays effective inhibitory effects on the growth of various human hepatoma cell lines and stimulates the expression of p53 and p21 that resulted in the cell cycle arrest of HepG2/C3A cells at G(2)/M phase.	Emodin	16-22	P53	Homo sapiens	145-148
32202904-10	2020	Results showed that the expression of p-p53, p53, Bax and PUMA was upregulated after CBL0137 administration.	CBLC137	85-92	P53	Homo sapiens	45-48
10914555-6	2000	Treatment of cells with protein tyrosine phosphatase inhibitor vanadate blocked the p53-induced differentiation, but not that of cell death or growth arrest.	Vanadates	63-71	P53	Homo sapiens	84-87
32321992-6	2020	Significant decrease of clonogenic capacity and higher apoptosis rates were also observed after ATO exposure, being cell death more pronounced (>70%) for the SHH-MB TP53-mutated.	ato	96-99	P53	Homo sapiens	165-169
10809772-6	2000	In contrast, caffeine abolishes the accumulation of p53 caused by all the compounds.	Caffeine	13-21	P53	Homo sapiens	52-55
14757171-7	2004	Caffeine, an ATM kinase inhibitor, inhibited these effects of genistein on Chk2, p53, and p21waf1/cip1.	Caffeine	0-8	P53	Homo sapiens	81-84
15075671-2	2004	MEN15658 induces p53 accumulation, and activation of gadd-45, p21, c-fos and bcl-2 family genes in human ovarian carcinoma A2780 cell line.	2-((1,10)phenanthrolin-2-ylhydrazono)-3,4-dihydro-2H-naphthalen-1-one	0-8	P53	Homo sapiens	17-20
32321992-9	2020	Herein, we showed ATO cytotoxicity in pediatric SHH cell lines, with marked radiosensitizing effect for the MB-SHH TP53-mutated cells.	ato	18-21	P53	Homo sapiens	115-119
10737899-0	2000	p53/56(lyn) antisense shifts the 1,25-dihydroxyvitamin D3-induced G1/S block in HL60 cells to S phase.	Calcitriol	33-57	P53	Homo sapiens	0-3
32325827-0	2020	Tumor-Targeted Delivery of the p53-Activating Peptide VIP116 with PEG-Stabilized Lipodisks.	vip116	54-60	P53	Homo sapiens	31-34
10737899-2	2000	In this study, we demonstrate the participation of p53/56(lyn) in 1,25-dihydroxyvitamin D(3) (1, 25D(3))-induced growth arrest in HL60 cells.	Calcitriol	66-92	P53	Homo sapiens	51-54
10815759-2	2000	Therefore, we investigated the utility of new heterodinucleoside phosphate dimers of 5-fluorodeoxyuridine (5-FdUrd) in p53-mutated and androgen-independent DU-145 human prostate tumour cells.	heterodinucleoside phosphate	46-74	P53	Homo sapiens	119-122
10738214-4	2000	Phenol-chloroform-extracted DNA specimens were employed for the detection of HBV infection and p53 gene mutations.	Phenol	0-6	P53	Homo sapiens	95-98
15055483-6	2004	The reduction of Cr (VI) to Cr (III) results in the formation of reactive intermediates that together with oxidative stress and oxidative tissue damage, and a cascade of cellular events including modulation of apoptosis regulatory gene p53 contribute to the cytotoxicity, genotoxicity and carcinogenicity of Cr(VI)-containing compounds.	chromium hexavalent ion	17-24	P53	Homo sapiens	236-239
15055483-6	2004	The reduction of Cr (VI) to Cr (III) results in the formation of reactive intermediates that together with oxidative stress and oxidative tissue damage, and a cascade of cellular events including modulation of apoptosis regulatory gene p53 contribute to the cytotoxicity, genotoxicity and carcinogenicity of Cr(VI)-containing compounds.	chromium hexavalent ion	308-314	P53	Homo sapiens	236-239
31278615-6	2020	Our study presents two preliminary findings: (a) in HaVSMCs, FOLFIRI treatment significantly induces oxidative damage to both DNA and protein, leading to a dramatic increase in caspase-dependent apoptotic death through P53-mediated Caspase3-dependent mitochondrial apoptosis, and results in TNF-alpha/Caspase8-mediated necrotic death, and (b) flavonoids not only regulate the expression of genes encoding antioxidant enzymes and increase DNA damage but also limit programmed and necrotic cell death processes in HaVSMCs.	FOLFIRI regimen	61-68	P53	Homo sapiens	219-222
14704122-3	2004	RESULTS: The 15d-PGJ2 induced apoptosis in ECV304 endothelial cells in a dose-dependent manner (the percentage of apoptosis was enhanced from 10.0 %+/-1.3 % to 32.8 %+/-1.6 %), which was accompanied by inhibition of NF-?B and AP-1 DNA binding activity, down-regulation of c-myc, upregulation of Gadd45 and p53, and activation of p38 kinase.	9-deoxy-delta-9-prostaglandin D2	17-21	P53	Homo sapiens	306-309
14971655-3	2004	Under certain conditions, some hexavalent chromium [Cr(VI)] compounds are toxic and carcinogenic in the human respiratory tract, and we have shown that they induce apoptosis and/or cell cycle arrest in a p53-dependent fashion.	chromium hexavalent ion	52-58	P53	Homo sapiens	204-207
14564515-8	2003	CONCLUSIONS: These results suggest that DCA induced up-regulation of EphA2 in colon cancer cells is due to activation of erk1/2 cascade, and is p53-independent.	Deoxycholic Acid	40-43	P53	Homo sapiens	144-147
10702305-5	2000	The addition of the broad-spectrum caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethyl ketone (zVAD-fmk) directly after transduction almost completely prevented p53-induced apoptotic cell death but did not inhibit mitochondrial cytochrome c release.	Caspase Inhibitor VI	53-102	P53	Homo sapiens	170-173
10937051-8	2000	Boric acid was used for antigen retrieval on sections stored for 12 weeks at 20 degrees C. For both p53 protein and MIB1 antigen, this resulted in an extent and intensity of immunostaining equal to or higher than (MIB1) that obtained in freshly cut sections, using citrate buffer.	Citric Acid	265-272	P53	Homo sapiens	100-103
10719037-0	2000	p53 mutations experimentally induced by 8-methoxypsoralen plus UVA (PUVA) differ from those found in human skin cancers in PUVA-treated patients.	puva	68-72	P53	Homo sapiens	0-3
10719037-9	2000	Through a rigorous statistical test, the PUVA-induced p53 mutation spectrum appears to differ significantly (P &lt; 0.0002) from that observed in SCC in PUVA-treated patients.	puva	41-45	P53	Homo sapiens	54-57
10719037-9	2000	Through a rigorous statistical test, the PUVA-induced p53 mutation spectrum appears to differ significantly (P &lt; 0.0002) from that observed in SCC in PUVA-treated patients.	puva	153-157	P53	Homo sapiens	54-57
10738085-3	2000	RESULTS: The radiosensitizing effect of caffeine (2 mM) expressed itself as a significant decrease in surviving fraction at 2 Gy and a significant increase in alpha-values in RT112 and TE671, both with non-functional p53.	Caffeine	40-48	P53	Homo sapiens	217-220
14643431-4	2003	Incubation in caffeine did not increase the percentage of cells entering the S phase 6-8h after irradiation; ATM-dependent phosphorylation of p53 and transactivation of p21(Cip1/Waf1) post-IR were resistant to caffeine.	Caffeine	14-22	P53	Homo sapiens	142-145
10738085-9	2000	CONCLUSION: The data presented confirm that p53 status can be a significant determinant of the efficacy of caffeine as radiosensitizer in these tumour cell lines, and document the importance of the G2 checkpoint in this effect.	Caffeine	107-115	P53	Homo sapiens	44-47
31751608-7	2020	Glyphosate decreased expression of P16 and TP53 as well as an increase in the expression of BCl2, CCND1 and P21.	glyphosate	0-10	P53	Homo sapiens	43-47
10713709-8	2000	These data indicate that WR1065, a polyamine analog with thiol anti-oxidant properties, activates a cell cycle check-point involving p53.	Polyamines	35-44	P53	Homo sapiens	133-136
14981925-7	2003	Apoptosis induced by CAPE or CAO is associated with increased expression of p53, p21 and c-Jun.	caffeic acid phenethyl ester	21-25	P53	Homo sapiens	76-79
14580323-3	2003	Recombinant p53, purified in the presence of the reducing agent dithiothreitol (DTT), contains five free thiol groups on the surface of the protein.	Dithiothreitol	64-78	P53	Homo sapiens	12-15
14580323-3	2003	Recombinant p53, purified in the presence of the reducing agent dithiothreitol (DTT), contains five free thiol groups on the surface of the protein.	Dithiothreitol	80-83	P53	Homo sapiens	12-15
32027268-6	2020	Western blot analysis showed that sorafenib combined with decitabine significantly up-regulated the levels of Bax/Bcl-2, P53, C-Caspase3 and C-PARP and activated apoptosis by inhibiting PI3K-AKT pathway.	decitabine	58-68	P53	Homo sapiens	121-124
14580323-9	2003	Electromobility shift assays showed that binding of oxidized p53 to DNA was enhanced upon addition of DTT, indicating that oxidation is reversible.	Dithiothreitol	102-105	P53	Homo sapiens	61-64
14580323-10	2003	The possibility that oxidized p53 contained significant amounts of sulfenic (-SOH), sulfinic (-SO2H), or sulfonic acid (-SO3H) was ruled out.	-so2h	94-99	P53	Homo sapiens	30-33
10690553-7	2000	This change resulted in a Val to Phe substitution and was associated with a constitutive production of high levels of p53, which was inactive as a transcriptional activator of bax and p21.	Phenylalanine	33-36	P53	Homo sapiens	118-121
32027268-7	2020	CONCLUSION: Sorafenib combined with decitabine induces the apoptosis of diffuse large B-cell lymphoma cell line OCI-LY1 by inhibiting PI3K-AKT pathway and activating P53.	decitabine	36-46	P53	Homo sapiens	166-169
10611293-2	1999	Here, a combination of biochemical and nuclear magnetic resonance experiments demonstrates that the activation domain of the tumor suppressor p53 has an FXXPhiPhi motif (F, Phe; X, any amino acids; Phi, hydrophobic residues) that folds into an alpha-helix upon binding to one of its targets, hTAF(II)31 (a human TFIID TATA box-binding protein-associated factor).	Phenylalanine	173-176	P53	Homo sapiens	142-145
14607978-2	2003	Treatment of HeLa cells with TPT-benzimidazolethiol arrests the cell cycle at G0/G1 phase and transcriptionally downregulates HPV-encoded E6, restoring p53 expression from E6 suppression.	triphenyl tin benzimidazolethiol	29-51	P53	Homo sapiens	152-155
31900123-0	2020	Rapid response of stage IV colorectal cancer with APC/TP53/KRAS mutations to FOLFIRI and Bevacizumab combination chemotherapy: a case report of use of liquid biopsy.	FOLFIRI regimen	77-84	P53	Homo sapiens	54-58
10588903-5	1999	According to quantitative analysis with folded Gaussian distributions, the bending induced by p53 varied from approximately 40 degrees to 48 degrees upon decreasing of the KCl concentration from 50 mM to approximately 1 mM in the mounting buffer used for adsorption of the complexes to the carbon film surface.	Potassium Chloride	172-175	P53	Homo sapiens	94-97
10574974-9	1999	These results suggest that ROS generated through Cr(VI) reduction is responsible to the early stage of apoptosis, whereas p53 contributes to the late stage of apoptosis and is responsible for the enhancement of Cr(VI)-induced apoptosis at this stage.	chromium hexavalent ion	211-217	P53	Homo sapiens	122-125
31900123-3	2020	Retrospective cell free DNA testing showed that the APC/TP53/KRAS major clone responded quickly after 3 cycles of FOLFIRI + Bevacizumab.	FOLFIRI regimen	114-121	P53	Homo sapiens	56-60
14527683-7	2003	When the DCI values were analyzed by regression analysis, a significant positive relationship between IkappaBalpha superrepressor and dominant-negative IKKbeta and an inverse relationship between p53 and Mdm2 were consistent with previous reports.	dci	9-12	P53	Homo sapiens	196-199
32067620-12	2020	CONCLUSION: The results suggested that podophyllum derivatives containing fluorine atom in the 3-position of 2-aminopyridine could inhibit the growth of HCC harboring p53-R249S by restoring the activity of p53 with decreasing the level of c-Myc.	alpha-aminopyridine	109-124	P53	Homo sapiens	167-170
12807757-3	2003	The current study examines the ability of acrolein to modulate the effect of benzo[a]pyrene (B[a]P), a major carcinogen found in smoke, on p53.	Acrolein	42-50	P53	Homo sapiens	139-142
12807757-7	2003	However, acrolein treatments profoundly inhibited the DNA binding of p53 under both basal and B[a]P-induced conditions.	Acrolein	9-17	P53	Homo sapiens	69-72
12807757-8	2003	Depleting glutathione with buthionine sulfoximine in B[a]P-treated cells to levels similar to those obtained with acrolein decreased p53 DNA binding substantially less than with acrolein.	Acrolein	114-122	P53	Homo sapiens	133-136
12807757-9	2003	Using a p53 dual luciferase reporter assay, acrolein caused an 83% decrease in the p53 activity induced by B[a]P (1 mM for 24 h post-transfection).	Acrolein	44-52	P53	Homo sapiens	8-11
12807757-9	2003	Using a p53 dual luciferase reporter assay, acrolein caused an 83% decrease in the p53 activity induced by B[a]P (1 mM for 24 h post-transfection).	Acrolein	44-52	P53	Homo sapiens	83-86
10571245-2	1999	Caffeine has been shown to abrogate the S and G2 arrest in p53-defective cells and to enhance cytotoxicity, but at concentrations too toxic to administer to humans.	Caffeine	0-8	P53	Homo sapiens	59-62
10590231-3	1999	This study investigated whether the mutational hot spots of the Apc and p53 genes for human colorectal cancer are mutated in dimethylhydrazine-induced colorectal neoplasms and whether dietary folate can modulate mutations in these regions.	Dimethylhydrazines	125-142	P53	Homo sapiens	72-75
12807757-10	2003	The p53 protein that was immunoprecipitated after acrolein treatment was reactive with an anti-acrolein antibody indicating covalent modification.	Acrolein	50-58	P53	Homo sapiens	4-7
32067620-12	2020	CONCLUSION: The results suggested that podophyllum derivatives containing fluorine atom in the 3-position of 2-aminopyridine could inhibit the growth of HCC harboring p53-R249S by restoring the activity of p53 with decreasing the level of c-Myc.	alpha-aminopyridine	109-124	P53	Homo sapiens	206-209
12807757-11	2003	Results from this study suggest that acrolein can inhibit p53 DNA binding and activity by direct covalent modification as well as alteration of intracellular redox status.	Acrolein	37-45	P53	Homo sapiens	58-61
10590231-12	1999	These data suggest that in the dimethylhydrazine rat model of colorectal cancer, the Apc gene is mutated in early stages, albeit to a lesser degree than observed in human colorectal cancer, whereas the mutational hot spot of the p53 gene for human colorectal cancer is not commonly mutated.	Dimethylhydrazines	31-48	P53	Homo sapiens	229-232
32749126-6	2020	The effect of EGb761 on the p53 signaling pathway was further confirmed by adding pifithrin (PFT)-alpha, an inhibitor of p53.	-alpha	97-103	P53	Homo sapiens	28-31
10543945-1	1999	In human skin cancers, more than 30 % of all mutations in the p53 gene are transitions at dipyrimidines within the sequence context CpG, i.e. 5"-TCG and 5"-CCG, found at several mutational hotspots.	5"-tcg	142-148	P53	Homo sapiens	62-65
32749126-6	2020	The effect of EGb761 on the p53 signaling pathway was further confirmed by adding pifithrin (PFT)-alpha, an inhibitor of p53.	-alpha	97-103	P53	Homo sapiens	121-124
31680191-6	2020	Specifically, lysine 370/372/373 and 381/382/386 mutations decreased p53 stability, and lysine 305 mutation reduced p53 phosphorylation level at serine 15, while lysine 120 and 164 mutations decreased p53 acetylation level at lysine 382.	cholecystokinin C-terminal flanking peptide	145-151	P53	Homo sapiens	116-119
31680191-6	2020	Specifically, lysine 370/372/373 and 381/382/386 mutations decreased p53 stability, and lysine 305 mutation reduced p53 phosphorylation level at serine 15, while lysine 120 and 164 mutations decreased p53 acetylation level at lysine 382.	cholecystokinin C-terminal flanking peptide	145-151	P53	Homo sapiens	116-119
12869633-7	2003	In p53-deficient cells, little K2-5F is expressed, and thus HSV-TK is expressed, allowing the cells to be killed by ganciclovir (GCV).	Ganciclovir	116-127	P53	Homo sapiens	3-6
31856867-5	2019	METHODS: We implemented a screening of a chemical library for compounds with potential to abrogate cancer cell specific mortalin-p53 interactions, and identified a new compound (named it as Mortaparib) that caused nuclear enrichment of p53 and shift in mortalin from perinuclear (typical of cancer cells) to pancytoplasmic (typical of normal cells).	mortaparib	190-200	P53	Homo sapiens	129-132
12869633-7	2003	In p53-deficient cells, little K2-5F is expressed, and thus HSV-TK is expressed, allowing the cells to be killed by ganciclovir (GCV).	Ganciclovir	129-132	P53	Homo sapiens	3-6
12869633-8	2003	K2-5F induced by exogenous p53 dramatically reduced the expression of HSV-TK in human embryonic kidney 293 cells, and it subsequently increased cell survival in response to GCV.	Ganciclovir	173-176	P53	Homo sapiens	27-30
12869633-10	2003	Stable expression of moderate levels of p53 in Saos-2 cells was able to induce the expression of K2-5F and reduce HSV-TK expression and resulted in a modest but distinct protection from GCV toxicity.	Ganciclovir	186-189	P53	Homo sapiens	40-43
12874009-3	2003	In HT1080 cells expressing a dominant-negative form of p53, treatment with etoposide still caused G(2) arrest, but the arrest could be overcome by additional treatment with caffeine, which inhibits the damage-responsive kinases ataxia telangiectasia mutated (ATM) and atm and rad3-related (ATR).	Caffeine	173-181	P53	Homo sapiens	55-58
10479688-5	1999	Adenovirus-mediated delivery of p53 to cerebellar granule neurons resulted in caspase-3 (CPP32) activation followed by terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL) staining and loss of viability as determined by an MTT survival assay.	Uridine Triphosphate	179-182	P53	Homo sapiens	32-35
10485486-6	1999	Similar concentrations of caffeine also inhibit gamma- and UV radiation-induced phosphorylation of p53 on Ser15, a modification that may be directly mediated by the ATM and ATR kinases.	Caffeine	26-34	P53	Homo sapiens	99-102
12807744-3	2003	Interestingly, the methylxanthine caffeine can abrogate the p53 accumulation induced by certain DNA-damaging agents by an unknown mechanism.	Caffeine	34-42	P53	Homo sapiens	60-63
31856867-5	2019	METHODS: We implemented a screening of a chemical library for compounds with potential to abrogate cancer cell specific mortalin-p53 interactions, and identified a new compound (named it as Mortaparib) that caused nuclear enrichment of p53 and shift in mortalin from perinuclear (typical of cancer cells) to pancytoplasmic (typical of normal cells).	mortaparib	190-200	P53	Homo sapiens	236-239
12807744-5	2003	Caffeine inhibited the accumulation of p53 induced by leptomycin B (LMB), an inhibitor of CRM1, but not N-acetyl-leu-leu-norleucinal, a proteasome inhibitor.	Caffeine	0-8	P53	Homo sapiens	39-42
12807744-6	2003	Furthermore, caffeine also inhibited the accumulation of p53 by a variety of stress-inducing agents in vivo, such as 5-fluorouracil, doxorubicin, mitomycin C, camptothecin and roscovitine.	Caffeine	13-21	P53	Homo sapiens	57-60
10652599-0	1999	Mutant p53 mediated induction of cell cycle arrest and apoptosis at G1 phase by 9-hydroxyellipticine.	9-hydroxyellipticine	80-100	P53	Homo sapiens	7-10
31856867-6	2019	Biochemical and molecular assays were used to demonstrate the effect of Mortaparib on mortalin, p53 and PARP1 activities.	mortaparib	72-82	P53	Homo sapiens	96-99
10652599-2	1999	Although in many cancer cells p53 is frequently mutated and loses its functions, we have proposed that mutant p53 may be involved in the anticancer mechanism of 9-hydroxy ellipticine (9HE).	9-hydroxyellipticine	161-182	P53	Homo sapiens	30-33
10652599-2	1999	Although in many cancer cells p53 is frequently mutated and loses its functions, we have proposed that mutant p53 may be involved in the anticancer mechanism of 9-hydroxy ellipticine (9HE).	9-hydroxyellipticine	161-182	P53	Homo sapiens	110-113
10652599-2	1999	Although in many cancer cells p53 is frequently mutated and loses its functions, we have proposed that mutant p53 may be involved in the anticancer mechanism of 9-hydroxy ellipticine (9HE).	9-hydroxyellipticine	184-187	P53	Homo sapiens	30-33
10652599-2	1999	Although in many cancer cells p53 is frequently mutated and loses its functions, we have proposed that mutant p53 may be involved in the anticancer mechanism of 9-hydroxy ellipticine (9HE).	9-hydroxyellipticine	184-187	P53	Homo sapiens	110-113
12963547-4	2003	Following treatment with DHT, in vivo binding of p53 to its response elements was strongly inhibited.	Dihydrotestosterone	25-28	P53	Homo sapiens	49-52
31856867-8	2019	Bioinformatics analysis revealed that although Mortaparib could interact with mortalin, its binding with p53 interaction site was not stable.	mortaparib	47-57	P53	Homo sapiens	105-108
31711520-9	2019	The effects of decitabine on P15INK4B and TP53 in MDS cells after inhibiting HO-1 were detected by Western blotting.	decitabine	15-25	P53	Homo sapiens	42-46
12782109-9	2003	Also, t-BuOOH treatment caused an elevation in the levels of the pro-apoptotic proteins p53 and p21/WAF-1 and a reduction in the levels of the anti-apoptotic protein bcl-2 compared to their levels in control HCN1-A cells, while pretreatment with nicotinamide reduced p53 and p21/WAF-1 levels even in the presence of t-BuOOH.	di-tert-butyl peroxide	6-13	P53	Homo sapiens	88-91
12782109-9	2003	Also, t-BuOOH treatment caused an elevation in the levels of the pro-apoptotic proteins p53 and p21/WAF-1 and a reduction in the levels of the anti-apoptotic protein bcl-2 compared to their levels in control HCN1-A cells, while pretreatment with nicotinamide reduced p53 and p21/WAF-1 levels even in the presence of t-BuOOH.	di-tert-butyl peroxide	6-13	P53	Homo sapiens	267-270
12802789-7	2003	Our results indicate that inducible TS expression in M7TS90 cells modulates p53 and p53 target gene expression in response to TDX, but not 5-FU.	raltitrexed	126-129	P53	Homo sapiens	76-79
12802789-7	2003	Our results indicate that inducible TS expression in M7TS90 cells modulates p53 and p53 target gene expression in response to TDX, but not 5-FU.	raltitrexed	126-129	P53	Homo sapiens	84-87
10336811-1	1999	AIMS: To determine the incidence and prognostic value of p53 immunopositivity in resectable distal bile duct carcinoma (DBDC).	dibenzyldithiocarbamate	120-124	P53	Homo sapiens	57-60
10336811-8	1999	CONCLUSIONS: This study indicates that low (0-30%) p53 expression is a favourable prognostic factor in patients with resected DBDC.	dibenzyldithiocarbamate	126-130	P53	Homo sapiens	51-54
10361685-4	1999	During the induction of apoptosis by phloretin, the expression of Bax protein in B16 cells increased and the levels of p53, Bcl-2, and Bcl-XL proteins did not change.	Phloretin	37-46	P53	Homo sapiens	119-122
31436301-7	2019	Silencing of DHRS2 in HCT116/Oxa cells effectively restored Oxa-sensitivity by suppressing the expression of excision repair cross-complementing group 1 protein via a p53-dependent pathway, and reversed the EMT phenotype.	Oxaliplatin	29-32	P53	Homo sapiens	167-170
10082548-6	1999	Following microinjection of HaeIII into lactacystin-treated normal fibroblasts, lactacystin-induced p53 protein is phosphorylated at serine 15 and stabilized even in the presence of cycloheximide.	Cycloheximide	182-195	P53	Homo sapiens	100-103
10037682-3	1999	Long term, but not acute, treatment of cultured cerebellar granule cells with LiCl induces a concentration-dependent decrease in mRNA and protein levels of proapoptotic p53 and Bax; conversely, mRNA and protein levels of cytoprotective Bcl-2 are remarkably increased.	Lithium Chloride	78-82	P53	Homo sapiens	169-172
10037682-6	1999	Pretreatment with LiCl for 7 days prevents glutamate-induced increase in p53 and Bax expression and maintains Bcl-2 in an elevated state.	Lithium Chloride	18-22	P53	Homo sapiens	73-76
12894503-3	2003	Caffeine, a nonspecific inhibitor of ATR, enhanced the cytotoxic effect of cisplatin, modestly decreased the p53 and p21WAF-1 response to cisplatin, and affected the cdc2-p34/cyclin B1 complex by decreasing both cyclin B1 protein accumulation and cdc2-p34 tyrosine 15 phosphorylation.	Caffeine	0-8	P53	Homo sapiens	109-112
31111543-10	2019	CONCLUSIONS: The presence of aneuploidy, p53 positivity and development of HGD or adenocarcinoma on follow-up indicate that CCA likely represents a dysplastic lesion (at least LGD) and is a histological marker of neoplastic progression.	1-methylcyclohexanecarboxylic acid	124-127	P53	Homo sapiens	41-44
12648234-1	2003	Squamous cell carcinomas in psoralen-plus-ultraviolet A (PUVA) treated patients frequently exhibit p53 tumor suppressor genes and Ha-ras protooncogenes that are mutated at dipyrimidine sites and carry the ultraviolet fingerprint (i.e., C-to-T or CC-to-TT transitions).	dipyrimidine	172-184	P53	Homo sapiens	99-102
12628923-9	2003	CK2 phosphoryl ates Thr155, which targets p53 to degradation by the Ub system.	ates	15-19	P53	Homo sapiens	42-45
10195885-6	1999	Treating MCF-7 cells with AdHSV-tk/GCV led to the predicted increase in endogenous p53 and p21WAF1/CIP1 protein levels, and apoptosis was observed in a significant proportion of the target cell population.	Ganciclovir	35-38	P53	Homo sapiens	83-86
10195885-8	1999	This latter result suggested that HSV-tk/GCV treatment can activate a strong p53-independent apoptotic response in tumor cells that lack functional p53.	Ganciclovir	41-44	P53	Homo sapiens	77-80
10195885-8	1999	This latter result suggested that HSV-tk/GCV treatment can activate a strong p53-independent apoptotic response in tumor cells that lack functional p53.	Ganciclovir	41-44	P53	Homo sapiens	148-151
12527938-10	2003	This type of mutated-p53 in TYS cells prevents cell death from DNA damage, and probably accumulates genetic alterations and accelerates the malignant progression of the cells by DNA damaging therapy.	TYS	28-31	P53	Homo sapiens	21-24
31540454-6	2019	Apoptosis and cell cycle arrest were induced by fludioxonil (10-7-10-5 M) in the Jurkat T cells at 24 and 48 h and Ramos B cells at 48 h. Moreover, the protein levels of pro-apoptotic proteins, such as p53, BAX, and cleaved caspase 3, were increased and anti-apoptotic protein Bcl-2 was decreased by fludioxonil.	fludioxonil	48-59	P53	Homo sapiens	202-205
12538356-7	2003	As expected, BPDE produced predominantly G to T transversions and simulated sunlight produced mostly C to T transitions at dipyrimidine sites in the p53 coding sequence.	dipyrimidine	123-135	P53	Homo sapiens	149-152
12488329-0	2003	p53 Is required for 1,25-dihydroxyvitamin D3-induced G0 arrest but is not required for G1 accumulation or apoptosis of LNCaP prostate cancer cells.	Calcitriol	20-44	P53	Homo sapiens	0-3
12183079-4	2002	In addition, AA profoundly increased protein level of p53, which was also inhibited by BAPTA/AM, an intracellular Ca(2+) chelator, TMB-8 and dantrolene.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	87-92	P53	Homo sapiens	54-57
10026322-8	1999	In vivo studies showed that the growth of subcutaneous tumours of p53 mutant MKN1 cells was significantly inhibited by direct injection of AdCAp53, but no significant growth inhibition was detected in the growth of p53 wild type MKN45 tumours.	adcap53	139-146	P53	Homo sapiens	66-69
9886259-0	1999	Thymidine dinucleotide mimics the effect of solar simulated irradiation on p53 and p53-regulated proteins.	thymidine dinucleotide	0-22	P53	Homo sapiens	75-78
9886259-0	1999	Thymidine dinucleotide mimics the effect of solar simulated irradiation on p53 and p53-regulated proteins.	thymidine dinucleotide	0-22	P53	Homo sapiens	83-86
9886259-2	1999	We have previously reported that the thymidine dinucleotide (pTpT), a common target for DNA photoproduct formation by UV light, mimics many effects of UV irradiation in cultured skin-derived cells, at least in part through the activation of p53.	thymidine dinucleotide	37-59	P53	Homo sapiens	241-244
9865726-5	1998	In combination with gamma-irradiation, isogranulatimide selectively kills MCF-7 cells lacking p53 function.	isogranulatimide	39-55	P53	Homo sapiens	94-97
12439598-8	2002	Treatment of cells with PD98059 or UO126 after cisplatin incubation or inhibition of signaling through ERK by tetracycline-regulated expression of dominant-inhibitory ERK enhanced resistance to cisplatin in p53-negative osteosarcoma cells and reduced cisplatin-induced apoptosis.	U 0126	35-40	P53	Homo sapiens	207-210
31183995-10	2019	CONCLUSION: In C26 colorectal adenocarcinoma mEHT-induced irreversible cell stress can activate both caspase-dependent apoptosis and p21waf1 mediated growth arrest pathways, likely to be driven by the upregulated nuclear p53 protein.	meht	45-49	P53	Homo sapiens	221-224
12376477-7	2002	Tangeretin also increased the content of the Cdk inhibitor p21 protein and this effect correlated with the elevation in p53 levels.	tangeretin	0-10	P53	Homo sapiens	120-123
9808165-0	1998	DNA adduct levels associated with p53 induction and delay of MCF-7 cells in S phase after exposure to benzo[g]chrysene dihydrodiol epoxide enantiomers.	benzo[g]chrysene dihydrodiol epoxide	102-138	P53	Homo sapiens	34-37
11245004-2	1998	METHODS: The tumor suppressing effects of inducing apoptosis and inhibition of the formation of G418 resistant colonies of the specific point mutated p53 minigene in a structural expression vector on a human cancer cell line PG with preexisting dominant negative p53 were preliminarily verified.	antibiotic G 418	96-100	P53	Homo sapiens	150-153
11245004-2	1998	METHODS: The tumor suppressing effects of inducing apoptosis and inhibition of the formation of G418 resistant colonies of the specific point mutated p53 minigene in a structural expression vector on a human cancer cell line PG with preexisting dominant negative p53 were preliminarily verified.	antibiotic G 418	96-100	P53	Homo sapiens	263-266
12371145-5	2002	In view of its upregulation in many tumors and transcriptional inactivation function of p53, its potential use in biotechnology and biomedicine is discussed.	biomedicine	132-143	P53	Homo sapiens	88-91
31059712-0	2019	Daucosterol disturbs redox homeostasis and elicits oxidative-stress mediated apoptosis in A549 cells via targeting thioredoxin reductase by a p53 dependent mechanism.	lyoniside	0-11	P53	Homo sapiens	142-145
9743293-7	1998	All four compounds can induce apoptosis in A2780, which is reduced in mutant p53 transfectants, as measured using the terminal DNA transferase-mediated b-d UTP nick end labelling (TUNEL) assay.	Uridine Triphosphate	156-159	P53	Homo sapiens	77-80
31379992-10	2019	Also, the analysis correlated with induced cell death elucidated that concurrent treatment of polysaccharide plus paclitaxel had a further anti-cancer effect against A2780cp cells mainly through restoration of p53 and mitochondrial apoptosis cell death induction.	Polysaccharides	94-108	P53	Homo sapiens	210-213
9713990-1	1998	We established a colon cancer cell line SW480-LOWTP53-1 carrying a wild-type TP53 transgene that is inducible under control of the lactose operon.	Lactose	131-138	P53	Homo sapiens	49-53
12208600-3	2002	The reduction of Cr(VI) to Cr(III) results in the formation of reactive intermediates that together with oxidative stress oxidative tissue damage and a cascade of cellular events including modulation of apoptosis regulatory gene p53, contribute to the cytotoxicity, genotoxicity and carcinogenicity of Cr(VI)-containing compounds.	chromium hexavalent ion	17-23	P53	Homo sapiens	229-232
12208600-3	2002	The reduction of Cr(VI) to Cr(III) results in the formation of reactive intermediates that together with oxidative stress oxidative tissue damage and a cascade of cellular events including modulation of apoptosis regulatory gene p53, contribute to the cytotoxicity, genotoxicity and carcinogenicity of Cr(VI)-containing compounds.	chromium hexavalent ion	302-308	P53	Homo sapiens	229-232
9696808-9	1998	Thus, although E4orf6 may play some role, these results suggested that E4orf4 may be the major E4 product responsible for induction of p53-independent apoptosis.	e4orf4	71-77	P53	Homo sapiens	135-138
31239671-1	2019	Purpose: The objective of this work was to formulate a delivery system of pDNA encoded p53 gene-loaded chitosan-sodium deoxycholate (CS-DS) nanoparticles, and to evaluate their influence on in vitro cytotoxicity and transfection efficiency of p53 gene.	Deoxycholic Acid	112-131	P53	Homo sapiens	87-90
9726816-5	1998	In contrast, PDTC, DDTC, and ammonium dithiocarbamate (ADTC) did not induce apoptosis; rather they led to the induction of p53 and p21 followed by G1/S arrest.	prolinedithiocarbamate	13-17	P53	Homo sapiens	123-126
12124477-0	2002	Fluorodeoxyglucose positron emission tomography and somatostatin receptor scintigraphy for diagnosing and staging carcinoid tumours: correlations with the pathological indexes p53 and Ki-67.	Fluorodeoxyglucose F18	0-18	P53	Homo sapiens	176-179
31059076-0	2019	Pressure suppresses hepatocellular glycogen synthesis through activating the p53/Pten pathway.	Glycogen	35-43	P53	Homo sapiens	77-80
12072912-0	2002	Clinically relevant aminoglycosides can suppress disease-associated premature stop mutations in the IDUA and P53 cDNAs in a mammalian translation system.	Aminoglycosides	20-35	P53	Homo sapiens	109-112
12072912-9	2002	Experiments with mammalian cDNAs confirmed these results and demonstrated that these aminoglycosides can also suppress disease-associated premature stop mutations previously identified in the IDUA gene (responsible for the lysosomal storage disease mucopolysaccharidosis I) and the P53 gene (associated with many forms of cancer).	Aminoglycosides	85-100	P53	Homo sapiens	282-285
9714336-0	1998	p53-independent induction of WAF1/Cip1 is correlated with osteoblastic differentiation by vitamin D3.	Cholecalciferol	90-100	P53	Homo sapiens	0-3
9714336-3	1998	Here we show that in a p53-null human osteoblastic osteosarcoma MG-63 cell line, 10 nM of 1,25(OH)2D3 completely inhibits cell growth and increases alkaline phosphatase activity, which suggests the induction of osteoblastic differentiation.	1,25(oh)2d3	90-101	P53	Homo sapiens	23-26
9714336-6	1998	Our results suggest that the p53-independent WAF1/Cip1 induction by 1,25(OH)2D3 is important for osteoblastic differentiation of MG-63 cells.	1,25(oh)2d3	68-79	P53	Homo sapiens	29-32
31059076-5	2019	RNA-seq analysis revealed that mechanical pressure suppressed glycogen synthesis by activating the p53/phosphatase and tensin homolog pathway, further suppressing glycogen synthase activity.	Glycogen	62-70	P53	Homo sapiens	99-102
9649119-10	1998	In agreement with this finding, p53 accumulated rapidly in drug-treated A2780 cells, indicative of a role for titanocene dichloride as a DNA-damaging agent.	titanocene dichloride	110-131	P53	Homo sapiens	32-35
31120902-0	2019	The antimalarial drug mefloquine enhances TP53 premature termination codon readthrough by aminoglycoside G418.	Aminoglycosides	90-104	P53	Homo sapiens	42-46
11864976-4	2002	The activation of p53 by etoposide resulted in the up-regulation of the pro-apoptotic protein Bax, a result that was prevented by the protein synthesis inhibitor cycloheximide.	Cycloheximide	162-175	P53	Homo sapiens	18-21
11980662-6	2002	Inactivation of p53 significantly increased resistance to 5-FU and the antifolates with IC-50(72 h) doses for 5-FU and TDX of &gt;100 and &gt;10 microM, respectively, in the M7TS90-E6 cell line.	raltitrexed	119-122	P53	Homo sapiens	16-19
12094375-8	2002	Nuclear p53 immunostaining was detected in 30% of IPN-L as a whole and increased in tandem with the progression of IPN-L (P &lt; 0.01).	ipn-l	50-55	P53	Homo sapiens	8-11
9672245-7	1998	Finally, radicicol depletes SKBR3 cells of p185erbB2, Raf-1 and mutant p53, similar to geldanamycin.	monorden	9-18	P53	Homo sapiens	71-74
31120902-0	2019	The antimalarial drug mefloquine enhances TP53 premature termination codon readthrough by aminoglycoside G418.	antibiotic G 418	105-109	P53	Homo sapiens	42-46
31120902-3	2019	The aminoglycoside G418 can induce TP53 premature termination codon readthrough and thus increase cellular levels of full-length protein.	Aminoglycosides	4-18	P53	Homo sapiens	35-39
9535218-3	1998	Treatment of cells with p53 or MnSOD antisense oligonucleotides prior to stimulation with oxLDL, C2-ceramide, TNF-alpha, or H2O2 caused an inhibition of the expression of the respective protein together with a marked reduction of apoptosis.	N-acetylsphingosine	97-108	P53	Homo sapiens	24-27
31120902-3	2019	The aminoglycoside G418 can induce TP53 premature termination codon readthrough and thus increase cellular levels of full-length protein.	antibiotic G 418	19-23	P53	Homo sapiens	35-39
9535218-4	1998	Exposure to N-acetylcysteine before treatment with oxLDL, C2-ceramide, TNF-alpha, or H2O2 reversed a decrease in cellular glutathione concentrations as well as the enhanced production of p53 and MnSOD mRNA and protein.	N-acetylsphingosine	58-69	P53	Homo sapiens	187-190
11884587-0	2002	Stat1-dependent, p53-independent expression of p21(waf1) modulates oxysterol-induced apoptosis.	Oxysterols	67-76	P53	Homo sapiens	17-20
31120902-8	2019	Exposure to G418 and mefloquine increased p53 phosphorylation at Ser15 and P21 transcript levels following DNA damage, indicating p53 produced via readthrough was functional.	antibiotic G 418	12-16	P53	Homo sapiens	42-45
11948395-10	2002	This was prevented by cycloheximide, suggesting that any stabilizing action of CP-31398 would have to be on newly synthesized p53.	Cycloheximide	22-35	P53	Homo sapiens	126-129
31120902-8	2019	Exposure to G418 and mefloquine increased p53 phosphorylation at Ser15 and P21 transcript levels following DNA damage, indicating p53 produced via readthrough was functional.	antibiotic G 418	12-16	P53	Homo sapiens	130-133
9773296-8	1998	The most suitable fixatives for immunohistochemical detection of p53 are 70% ethanol and Carnoy solution.	carnoy solution	89-104	P53	Homo sapiens	65-68
11791172-5	2002	Many agents also effectively increase cell death when a transcriptionally-defective p53, p53([gln22ser23]), is induced, although a dramatic exception is treatment with 5-FU, which strongly cooperates with wild-type but not p53([gln22ser23]).	gln22ser23	94-104	P53	Homo sapiens	84-87
31210846-10	2019	Taken together, decreased ribosome biogenesis in ASMCs resulting in p53-dependent proliferative inhibition, oxidative stress, and apoptosis is one of the underlying mechanisms of AD.	asmcs	49-54	P53	Homo sapiens	68-71
11791172-5	2002	Many agents also effectively increase cell death when a transcriptionally-defective p53, p53([gln22ser23]), is induced, although a dramatic exception is treatment with 5-FU, which strongly cooperates with wild-type but not p53([gln22ser23]).	gln22ser23	94-104	P53	Homo sapiens	89-92
11791172-5	2002	Many agents also effectively increase cell death when a transcriptionally-defective p53, p53([gln22ser23]), is induced, although a dramatic exception is treatment with 5-FU, which strongly cooperates with wild-type but not p53([gln22ser23]).	gln22ser23	94-104	P53	Homo sapiens	89-92
11791172-5	2002	Many agents also effectively increase cell death when a transcriptionally-defective p53, p53([gln22ser23]), is induced, although a dramatic exception is treatment with 5-FU, which strongly cooperates with wild-type but not p53([gln22ser23]).	gln22ser23	228-238	P53	Homo sapiens	84-87
9395239-7	1997	Actinomycin D or cycloheximide prevented cell death, suggesting that, in this system, p53-induced apoptosis depends upon macromolecule biosynthesis.	Cycloheximide	17-30	P53	Homo sapiens	86-89
9815821-6	1997	This p53-defective cell line was also radiosensitized by CAF, whereas the vector control (AA/PCMV/D), which retained wt p53 activity, was not.	Caffeine	57-60	P53	Homo sapiens	5-8
11786354-3	2002	We propose a method for the determination of traces of GST in the p53 C-terminus based on the constant current chronopotentiometric stripping analysis (CPSA) with hanging mercury drop electrode (HMDE).	Mercury	171-178	P53	Homo sapiens	66-69
30724469-7	2019	In pancreatic cancer cells, SRPK2 downregulation or overexpression led to modulation of Numb and wild-type p53 protein expression in response to oxaliplatin treatment.	Oxaliplatin	145-156	P53	Homo sapiens	107-110
9175647-2	1997	We used human osteosarcoma Saos-LP12 cells, in which wild type (wt) p53 protein was induced by treatment with isopopyl-beta-D-thiogalactopyranoside.	isopopyl-beta-d-thiogalactopyranoside	110-147	P53	Homo sapiens	68-71
9175647-5	1997	In addition, we found that frequency of G : C to A : T transition mutations which occurred at the 3" base pair of dipyrimidine sites were significantly lower in the cells with induced wt p53 protein than in the uninduced cells.	dipyrimidine	114-126	P53	Homo sapiens	187-190
11719445-2	2001	The p53 tumor suppressor gene is usually mutated in these tumors, and the mutations are "UV signature" single or tandem transitions at dipyrimidine sequences in the DNA-binding domain (DBD).	dipyrimidine	135-147	P53	Homo sapiens	4-7
30724469-11	2019	Conversely, SRPK2 silencing decreased cell invasion and migration and increased chemosensitivity; these effects were reversed by silencing p53 in oxaliplatin-treated pancreatic cancer cells.	Oxaliplatin	146-157	P53	Homo sapiens	139-142
30987009-5	2019	Intriguingly, 25 muM luteolin reduced cell viability through apoptotic induction, which was intensified in p53-expressing cells while 1 muM oxaliplatin caused cell cycle arrest at G0/G1-phase via the p53/p21-dependent mechanism.	Oxaliplatin	140-151	P53	Homo sapiens	200-203
11585742-3	2001	p53 codons containing methylated CpG sequences are preferential targets for formation of adducts by (+/-) anti-7beta,8alpha-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE).	7beta	111-116	P53	Homo sapiens	0-3
11684014-4	2001	Inhibition of endogenous ASPP function suppresses the apoptotic function of endogenous p53 in response to apoptotic stimuli.	aspp	25-29	P53	Homo sapiens	87-90
11684014-5	2001	ASPP enhance the DNA binding and transactivation function of p53 on the promoters of proapoptotic genes in vivo.	aspp	0-4	P53	Homo sapiens	61-64
11684014-6	2001	Two tumor-derived p53 mutants with reduced apoptotic function were defective in cooperating with ASPP in apoptosis induction.	aspp	97-101	P53	Homo sapiens	18-21
11684014-7	2001	The expression of ASPP is frequently downregulated in human breast carcinomas expressing wild-type p53 but not mutant p53.	aspp	18-22	P53	Homo sapiens	99-102
11684014-8	2001	Therefore, ASPP regulate the tumor suppression function of p53 in vivo.	aspp	11-15	P53	Homo sapiens	59-62
11390388-1	2001	Electrophilic eicosanoids of the J series, with their distinctive cross-conjugated alpha,beta-unsaturated ketone, inactivate genetically wild type tumor suppressor p53 in a manner analogous to prostaglandins of the A series.	alpha,beta-unsaturated ketone	83-112	P53	Homo sapiens	164-167
11477204-8	2001	Furthermore, thromboxane A(2) enhanced trophoblast apoptosis, determined using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining, cell morphology, and a concentration-dependent increase in p53 expression.	thromboxane a	13-26	P53	Homo sapiens	218-221
11406660-8	2001	p53 mutations were detected in AFX (4/6; 67%) and S-MFH (1/4; 25%), but not in BFH (0/5; 0%) using polymerase chain reaction-single-strand conformation polymorphism, and all of the mutations in AFX were either C-T transitions or at dipyrimidine sites.	dipyrimidine	232-244	P53	Homo sapiens	0-3
11313183-10	2001	Our data indicate that BBR3464 may be a promising agent in the treatment of tumours unresponsive to cisplatin and with a non-functional p53.	BBR 3464	23-30	P53	Homo sapiens	136-139
11181455-0	2001	Resveratrol analog, 3,4,5,4"-tetrahydroxystilbene, differentially induces pro-apoptotic p53/Bax gene expression and inhibits the growth of transformed cells but not their normal counterparts.	3,4,5,4'-tetrahydroxystilbene	20-49	P53	Homo sapiens	88-91
11159753-0	2001	Role of TP53 in repair of N-(deoxyguanosin-8-yl)-4-aminobiphenyl adducts in human transitional cell carcinoma of the urinary bladder.	N-(deoxyguanosin-8-yl)-4-aminobiphenyl	26-64	P53	Homo sapiens	8-12
11106264-11	2000	Therefore, in colon carcinomas that express wtp53, the approach to sensitize tumors to Fas-mediated apoptosis may be further enhanced from the effect of FUra-LV in elevating Fas expression in a p53-dependent manner.	fura-lv	153-160	P53	Homo sapiens	46-49
11033415-1	2000	The antiproliferative effect of Tempol, a stable nitroxide free radical, was investigated on the p53-negative human leukemia cell line HL60.	tempol	32-38	P53	Homo sapiens	97-100
10969787-7	2000	Moreover, AdRSVpHyde induced apoptosis and stimulated p53 expression.	adrsvphyde	10-20	P53	Homo sapiens	54-57
10867037-5	2000	p53 mRNA abundance was 187% higher in ZD Opti-MEM cells and &gt;100% higher in ZD Chelex cells compared with their respective controls.	opti-mem	41-49	P53	Homo sapiens	0-3
10842192-1	2000	We have previously shown that bladder urothelium of people living in the cesium-137 ((137)Cs)-contaminated areas of Ukraine demonstrates accumulation of stable p53 and p53 mutational inactivation, preferentially through G:C to A:T transition mutations at CpG dinucleotides, with a codon 245 hot spot.	Cesium-137	73-83	P53	Homo sapiens	160-163
10842192-1	2000	We have previously shown that bladder urothelium of people living in the cesium-137 ((137)Cs)-contaminated areas of Ukraine demonstrates accumulation of stable p53 and p53 mutational inactivation, preferentially through G:C to A:T transition mutations at CpG dinucleotides, with a codon 245 hot spot.	Cesium-137	73-83	P53	Homo sapiens	168-171
10785598-0	2000	Molecular downstream events and induction of thymidylate synthase in mutant and wild-type p53 colon cancer cell lines after treatment with 5-fluorouracil and the thymidylate synthase inhibitor raltitrexed.	raltitrexed	193-204	P53	Homo sapiens	90-93
10785598-6	2000	TS induction was highest after ZD1694 exposure in the mt p53 cells HT29 and WiDr/F (6-10-fold).	raltitrexed	31-37	P53	Homo sapiens	57-60
10777712-5	2000	Pretreatment of fATII cells with l-buthionine-(S,R)-sulfoximine, an irreversible inhibitor of gamma-glutamylcysteine synthetase, the rate-limiting enzyme in the biosynthesis of glutathione (GSH), enhanced Bax and p53 expression over Bcl-2.	l-buthionine sulfoximine	33-63	P53	Homo sapiens	213-216
10811471-4	2000	Ad-p53 and DNA-damaging agents (cis-diamminedichloroplatinum(II), etoposide, and 7-ethyl-10-hydrocycamptothecin) showed synergistic effects in six of seven cell lines but additive effects against a p53-mutated cell line.	7-ethyl-10-hydrocycamptothecin	81-111	P53	Homo sapiens	3-6
10811471-4	2000	Ad-p53 and DNA-damaging agents (cis-diamminedichloroplatinum(II), etoposide, and 7-ethyl-10-hydrocycamptothecin) showed synergistic effects in six of seven cell lines but additive effects against a p53-mutated cell line.	7-ethyl-10-hydrocycamptothecin	81-111	P53	Homo sapiens	198-201
10676641-9	2000	These findings suggest that nt -450 may constitute a critical site for initiation of de novo methylation and processive spreading of methylation associated with transcriptional inactivation of the p53 gene.	nt -450	28-35	P53	Homo sapiens	197-200
10631110-0	2000	Nitric oxide nitrates tyrosine residues of tumor-suppressor p53 protein in MCF-7 cells.	Nitrates	13-21	P53	Homo sapiens	60-63
10631110-2	2000	As nitration of tyrosine residues in various proteins has been shown to inhibit their functions, we examined whether NO nitrates tyrosine residues in p53 protein.	Nitrates	120-128	P53	Homo sapiens	150-153
10769661-1	2000	The present study was performed to investigate whether the introduction of a wild-type p53 gene into human osteosarcoma cells could alter the growth rate and enhance the cytocidal effect of cisplatin (CDDP) and the synergistic antitumor effect of caffeine.	Caffeine	247-255	P53	Homo sapiens	87-90
10769661-5	2000	Caffeine significantly potentiated the cytocidal effect of CDDP in the Saos2/p53 cells.	Caffeine	0-8	P53	Homo sapiens	77-80
10769661-6	2000	Furthermore, the TUNEL assay revealed that following treatment both with CDDP alone and with CDDP combined with caffeine, a higher percentage of the Saos2/p53 cells underwent apoptosis than did the parental Saos2 cells.	Caffeine	112-120	P53	Homo sapiens	155-158
10769661-7	2000	Therefore the cytocidal effect of CDDP and the synergistic antitumor effect of caffeine are enhanced by the introduction of a wild-type p53 gene into a human osteosarcoma cell line null for p53.	Caffeine	79-87	P53	Homo sapiens	136-139
10772337-5	2000	The altered gene expression of c-myc and p53 suggested that a novel apoptosis pathway, other than that suppressed by IL-6, might be triggered by a complex of DM650 and IL-6.	dm650	158-163	P53	Homo sapiens	41-44
10536167-4	1999	The initial transient cell arrest at the G1 checkpoint seen at 8-16 h of treatment with 0.15 microM CPT was accompanied by the rapid accumulation of p53 (preventable by cycloheximide) in the nucleus; the rise (&gt;20-fold) in p53 was maximal for S phase cells.	Cycloheximide	169-182	P53	Homo sapiens	149-152
10545796-3	1999	In this study, we demonstrate that the tumor suppressor protein p53 is stabilized in response to DNA damage by 5-MeCDE but fails to induce the cells" protective mechanism of G1 arrest in the human breast carcinoma cell line, MCF-7.	1,2-dihydroxy-epoxy-1,2,3,4-tetrahydro-5-methylchrysene	111-118	P53	Homo sapiens	64-67
10545796-5	1999	Western analyses revealed that, though both actinomycin D and 5-MeCDE treatment stabilized p53, only trace levels of p21(waf1/cip1) were seen in the latter case.	1,2-dihydroxy-epoxy-1,2,3,4-tetrahydro-5-methylchrysene	62-69	P53	Homo sapiens	91-94
10545796-6	1999	This lack of p21(waf1/cip1) expression in 5-MeCDE-treated cells is attributed to a stealth characteristic of this environmental carcinogen that allows it to damage DNA and still escape the p53-mediated cellular defense mechanism of G1 arrest.	1,2-dihydroxy-epoxy-1,2,3,4-tetrahydro-5-methylchrysene	42-49	P53	Homo sapiens	189-192
10628368-6	1999	The status of the p53 gene of tumor cells thereby may influence the efficacy of the HSV-TK/GCV system.	Ganciclovir	91-94	P53	Homo sapiens	18-21
10411938-2	1999	Here we show that TK/GCV treatment induces p53 accumulation and increases cell surface expression of CD95 and tumor necrosis factor receptor, which is likely to involve p53-mediated translocation of CD95 to the cell surface.	Ganciclovir	21-24	P53	Homo sapiens	43-46
10411938-2	1999	Here we show that TK/GCV treatment induces p53 accumulation and increases cell surface expression of CD95 and tumor necrosis factor receptor, which is likely to involve p53-mediated translocation of CD95 to the cell surface.	Ganciclovir	21-24	P53	Homo sapiens	169-172
10380883-8	1999	We also show that relatively low concentrations of dithiothreitol but not of 2-mercaptoethanol decrease the concentration of free zinc ions, thereby preventing their inhibitory effect on binding of p53 to DNA.	Dithiothreitol	51-65	P53	Homo sapiens	198-201
9106619-7	1997	It was also shown that vanadate blocked differentiation of IW32 cells induced by sodium butyrate, VM-26, and p53.	Vanadates	23-31	P53	Homo sapiens	109-112
9066726-1	1997	It has been found by PCR-SSCP analysis and direct DNA sequencing that a human salivary adenosquamous carcinoma-forming cell line, TYS, has a mutant p53 gene at codon 281Asp--&gt;His.	TYS	130-133	P53	Homo sapiens	148-151
9118908-0	1996	Carcinogenic potential of benzene and toluene when evaluated using cyclin-dependent kinase activation and p53-DNA binding.	Toluene	38-45	P53	Homo sapiens	106-109
9118908-4	1996	Kinase activation and subsequent hyperphosphorylation of pRb105 and p53 by benzene or toluene may be responsible for their growth promotional effects, but it does not account for increased potential of benzene to induce cancer.	Toluene	86-93	P53	Homo sapiens	68-71
8946936-4	1996	However, a cell-cycle arrest in G0/G1 phase was observed in Raji cells after the treatment with C2-ceramide, which was accompanied by the dephosphorylation of retinoblastoma (RB) gene products and decreased expression of p53 proteins.	N-acetylsphingosine	96-107	P53	Homo sapiens	221-224
8840989-2	1996	With a single exposure at a concentration of 1 microM for 2 h, ZD1694 completely inhibits thymidylate synthase over 72 h and causes a sustained growth for at least 120 h, DNA damage, and p53 induction in human carcinoma cells.	raltitrexed	63-69	P53	Homo sapiens	187-190
8870682-8	1996	Expression of the inducible NO synthase in response to lipopolysaccharide and interferon-gamma caused apoptosis in RAW 264.7 macrophages and neomycin-vector controls within 24 h. In contrast, p53 antisense RNA-expressing clones appeared highly resistant towards endogenous NO, although inducible NO synthase induction with concomitant nitrite production remained unchanged.	Nitrites	335-342	P53	Homo sapiens	192-195
8837615-0	1996	Selective radiosensitization of p53-deficient cells by caffeine-mediated activation of p34cdc2 kinase.	Caffeine	55-63	P53	Homo sapiens	32-35
8837615-6	1996	We demonstrate that abrogation of G2 arrest by caffeine-mediated activation of p34cdc2 kinase results in the selective sensitization of p53-deficient primary and tumor cells to irradiation-induced apoptosis.	Caffeine	47-55	P53	Homo sapiens	136-139
8831577-11	1996	Treatment with DX or AMSA caused similar effects, suggesting that p53-induced changes in cyclin, cdk, and cdk inhibitors after DNA damage are not responsible for the marked reduction in the cytotoxicity of DX we observed in wt p53-expressing cells.	Amsacrine	21-25	P53	Homo sapiens	66-69
8603415-5	1996	Cycloheximide treatment of the cells showed that the low level of p53 mRNA in non-BL lymphoid cells can not be attributed to posttranscriptional regulation by a labile protein.	Cycloheximide	0-13	P53	Homo sapiens	66-69
8570169-7	1995	In addition, cycloheximide and actinomycin D inhibited wt p53-induced apoptosis.	Cycloheximide	13-26	P53	Homo sapiens	58-61
7478511-2	1995	Exogenous wild-type p53 transcripts were detected at various expression levels in 8 of 117 G418-resistant clones.	antibiotic G 418	91-95	P53	Homo sapiens	20-23
7591958-0	1995	Inhibition of p53 protein phosphorylation by 9-hydroxyellipticine: a possible anticancer mechanism.	9-hydroxyellipticine	45-65	P53	Homo sapiens	14-17
7591958-2	1995	We found that ellipticine and 9-hydroxyellipticine (9HE), antitumor alkaloids, caused selective inhibition of p53 protein phosphorylation in Lewis lung carcinoma and SW480 (human colon cancer cell line) in a concentration-dependent manner from 0.1 to 100 microM.	9-hydroxyellipticine	30-50	P53	Homo sapiens	110-113
7591958-2	1995	We found that ellipticine and 9-hydroxyellipticine (9HE), antitumor alkaloids, caused selective inhibition of p53 protein phosphorylation in Lewis lung carcinoma and SW480 (human colon cancer cell line) in a concentration-dependent manner from 0.1 to 100 microM.	9-hydroxyellipticine	52-55	P53	Homo sapiens	110-113
7656242-2	1995	Two "hot regions" at codons 223-250 and 257-283 of the p53 gene were easily attacked by nitroso-2-acetylaminofluorene or acetoxy-2-acetylaminofluorene.	nitroso-2-acetylaminofluorene	88-117	P53	Homo sapiens	55-58
7753562-3	1995	Here we report the effect of calcium phosphate-mediated transfection, a technique commonly used in studies of transient gene expression in mammalian cells, on fibroblasts containing wild-type p53.	calcium phosphate	29-46	P53	Homo sapiens	192-195
7897229-10	1995	Third, p53-56lyn was probably activated after cell stimulation with zymosan, because the phosphorylation levels of a synthetic copolymer of glutamine-tyrosine were increased in Triton X-100-insoluble fraction.	Zymosan	68-75	P53	Homo sapiens	7-10
7897229-14	1995	Because zymosan interacts with human monocytes via beta 2 integrins, which are known to be cytoskeleton-associated, we suggest that p53-56lyn provides the molecular link between zymosan receptors and cytoskeleton, and directs the cytoskeletal reorganization in the periphagosomal area.	Zymosan	8-15	P53	Homo sapiens	132-135
7705936-1	1995	We introduced the mutant p53 gene (codon 273Arg-His) into human fibroblasts (SUSM-I cells) previously immortalized with 4-nitroquinoline I-oxide (4NQO) and obtained 2 clonal cell lines (SUSM-i/p53-1 and SUSM-1/p53-6) expressing the mutant p53.	4-Nitroquinoline	120-136	P53	Homo sapiens	25-28
7883998-4	1995	Induced differentiation of the p53-deficient promyelocytic HL-60 cells along the monocytic lineage by phorbol ester or 1a,25 dihydroxyvitamin D3 resulted in a marked increase of both p21WAF1/CIP1/SDI1 mRNA and protein expression due to enhanced mRNA stability.	Calcitriol	119-144	P53	Homo sapiens	31-34
7854771-6	1995	The expression of p53 was reduced to 60% for the first 4 h after the addition of cycloheximide, and showed no significant changes at least for 20 h. Treatment with Triton X-100 increased p53 immunoreactivity throughout the cell cycle.	Cycloheximide	81-94	P53	Homo sapiens	18-21
7845676-2	1995	Freshly isolated PBMCs, which are in the Go phase of the cell cycle, were shown to express low levels of p53 mRNA that was rapidly degraded with a half life of 1 h. The rapid decay of p53 mRNA in quiescent PBMCs was dependent on global protein synthesis as treatment with cycloheximide resulted in stabilization of the p53 message.	Cycloheximide	272-285	P53	Homo sapiens	105-108
7834638-4	1995	We show that p53-independent induction of WAF1/CIP1 occurs in human leukemia cells treated with 12-O-tetradecanoylphorbol-13-acetate, okadaic acid, or IFN-gamma but not with retinoic acid, vitamin D3, or DMSO.	Cholecalciferol	189-199	P53	Homo sapiens	13-16
7860045-1	1995	Several studies of benign breast lesions using methacran-fixed, paraffin-embedded tissues and cytological preparations have suggested that p53 accumulation in these lesions as detected by immunohistochemical (IHC) staining is rare to absent.	methacran	47-56	P53	Homo sapiens	139-142
7527943-5	1994	Altogether, microwave boiling of the tissue sections in citrate buffer clearly improved the immunoreactivity for cytokeratin 18, oestrogen receptor, Ki-67 protein, PCNA, p53 protein, retinoblastoma gene protein and c-erbB-2 protein.	Citric Acid	56-63	P53	Homo sapiens	170-173
8033087-4	1994	The frequency of tumors with mutations in p53, often multiple, accompanied by the appearance of multiple altered-length alleles suggest that DNA replication or repair defects may presage genomic instability in cases with FHBC.	fhbc	221-225	P53	Homo sapiens	42-45
7926727-6	1994	In addition, hydrophobic residues Leu-14 and Phe-19 are crucial for the interactions between p53 and human mdm-2 (hdm-2).	Phenylalanine	45-48	P53	Homo sapiens	93-96
7510864-6	1994	It was found that addition of sodium vanadate to the lysis buffer converted part of p53 molecules into a mutant conformation that is recognized by the PAb 240 monoclonal antibodies.	Vanadates	30-45	P53	Homo sapiens	84-87
7510864-7	1994	The effect of vanadate on p53 conformation was prominent even if it was added to the cell lysates after 15 min of pre-incubation at 37 degrees C. This further excluded its possible role as phosphatase inhibitor in the system and suggested a direct interaction with the p53 protein itself.	Vanadates	14-22	P53	Homo sapiens	26-29
7510864-7	1994	The effect of vanadate on p53 conformation was prominent even if it was added to the cell lysates after 15 min of pre-incubation at 37 degrees C. This further excluded its possible role as phosphatase inhibitor in the system and suggested a direct interaction with the p53 protein itself.	Vanadates	14-22	P53	Homo sapiens	269-272
7510864-8	1994	Based on these data we recommend to avoid using sodium vanadate as a phosphatase inhibitor in experiments where in vivo conformational changes of wild type p53 are studied.	Vanadates	48-63	P53	Homo sapiens	156-159
8278402-4	1994	Mutant p53 fusion proteins carrying amino acid substitutions Glu-213, Ile-237, or Tyr-238, derived from mutant p53 genes of Burkitt lymphomas, failed to catalyze these reactions.	Isoleucine	70-73	P53	Homo sapiens	7-10
7807177-5	1994	Of several G418-resistant clones obtained from each transfection, a few expressed the s-Myc or wt-p53 proteins.	antibiotic G 418	11-15	P53	Homo sapiens	98-101
8496597-0	1993	Differential action of cycloheximide and activation stimuli on transcription of tumor necrosis factor-alpha, IL-1 beta, IL-8, and P53 genes in human monocytes.	Cycloheximide	23-36	P53	Homo sapiens	130-133
8455934-3	1993	Both wild-type and mutant forms of p53 stimulated the number of G418-resistant colonies between 5- and 36-fold.	antibiotic G 418	64-68	P53	Homo sapiens	35-38
8455934-5	1993	Nonetheless, we suggest that an initial slowing of cell growth caused by expression of the unintegrated p53 plasmids renders the transfectants resistant to selection with G418, thus causing a higher frequency of G418-resistant colonies.	antibiotic G 418	171-175	P53	Homo sapiens	104-107
10422567-3	1999	(2) Only one cell line, ED-S, which was the most sensitive to ADM carried non-functional mutated-type p53.	Einsteinium	24-28	P53	Homo sapiens	102-105
10331854-4	1999	RESULTS: Both BL-13 and BL-28 cells (each expressing p53 with a wild-type sequence) fail to arrest at the G2 checkpoint after radiation, but nevertheless caffeine did induce radiosensitization.	Caffeine	154-162	P53	Homo sapiens	53-56
10331854-5	1999	In contrast, in BL-17/2 cells (expressing p53 with a point mutation in codon 280), caffeine treatment abrogated the radiation-induced G2 arrest but was not accompanied by radiosensitization.	Caffeine	83-91	P53	Homo sapiens	42-45
10096560-0	1999	Polyamine analogue induction of the p53-p21WAF1/CIP1-Rb pathway and G1 arrest in human melanoma cells.	Polyamines	0-9	P53	Homo sapiens	36-39
10096560-9	1999	Rather, these cells rapidly underwent programmed cell death within 48 h. Overall, these findings provide the first indication of the cell cycle regulatory pathways by which polyamine antagonists such as analogues might inhibit growth in cells containing wild-type p53 and further suggest a mechanistic basis for differential cellular responses to these agents.	Polyamines	173-182	P53	Homo sapiens	264-267
10082308-3	1999	METHODS: We report here a parallel flow cytometric method for semiquantitative detection of p53 protein and apoptosis (percent of apoptotic cells) in a pre-B leukemic cell line (NALM-6) exposed to various antitumor agents (2.35 microg/ml etoposide; 0.175 microg/ml FCE296; 0.4 microg/ml FCE624; and 1.5 microg/ml L-PAM).	fce624	287-293	P53	Homo sapiens	92-95
10030268-2	1999	This study tests the hypothesis that the response of cell lines derived from GM to fractionated radiotherapy depends on the function of wild-type p53 (wt p53), a tumor suppressor gene frequently mutated in GM tumors.	gm	77-79	P53	Homo sapiens	146-149
1280773-4	1992	Sodium dodecyl sulfate-polyacrylamide gel electrophoretic analysis demonstrated unequivocal heterogeneity of migration rate in p53 bands.	polyacrylamide	23-37	P53	Homo sapiens	127-130
21584507-1	1992	The nuclear phosphoprotein p53, named according to its apparent molecular weight on SDS-polyacrylamide gels is expressed, albeit at low levels, in a variety of cell types.	polyacrylamide	88-102	P53	Homo sapiens	27-30
10030268-2	1999	This study tests the hypothesis that the response of cell lines derived from GM to fractionated radiotherapy depends on the function of wild-type p53 (wt p53), a tumor suppressor gene frequently mutated in GM tumors.	gm	77-79	P53	Homo sapiens	154-157
30987009-6	2019	Moreover, luteolin treatment was found to reduce oxaliplatin-treated p53-null cell viability and colony counts further, thereby demonstrating an additional effect of luteolin in the killing of human colorectal tumor HCT116 cells not expressing functional p53 protein.	Oxaliplatin	49-60	P53	Homo sapiens	69-72
10030268-11	1999	CONCLUSIONS: The effect of fractionated radiotherapy in GM may depend on the function of the tumor suppressor gene p53.	gm	56-58	P53	Homo sapiens	115-118
1737852-7	1992	The other two nonhereditary p53 mutations included a T to G transversion at codon 270 (phenylalanine to cysteine) and a G to C transversion at codon 248 (arginine to proline).	Phenylalanine	87-100	P53	Homo sapiens	28-31
30987009-7	2019	The findings suggest that luteolin can induce p53-mediated apoptosis regardless of oxaliplatin treatment and may eliminate oxaliplatin-resistant p53-null colorectal cells.	Oxaliplatin	123-134	P53	Homo sapiens	145-148
30715803-0	2019	A fluorinated indole-based MDM2 antagonist selectively inhibits the growth of p53wt osteosarcoma cells.	indole	14-20	P53	Homo sapiens	78-81
1933891-5	1991	Caffeine treatment blocks both the G1 arrest and the induction of p53 protein after gamma-irradiation, thus suggesting that blocking the induction of p53 protein may contribute to the previously observed effects of caffeine on cell cycle changes after DNA damage.	Caffeine	0-8	P53	Homo sapiens	66-69
1933891-5	1991	Caffeine treatment blocks both the G1 arrest and the induction of p53 protein after gamma-irradiation, thus suggesting that blocking the induction of p53 protein may contribute to the previously observed effects of caffeine on cell cycle changes after DNA damage.	Caffeine	0-8	P53	Homo sapiens	150-153
1933891-5	1991	Caffeine treatment blocks both the G1 arrest and the induction of p53 protein after gamma-irradiation, thus suggesting that blocking the induction of p53 protein may contribute to the previously observed effects of caffeine on cell cycle changes after DNA damage.	Caffeine	215-223	P53	Homo sapiens	66-69
1933891-5	1991	Caffeine treatment blocks both the G1 arrest and the induction of p53 protein after gamma-irradiation, thus suggesting that blocking the induction of p53 protein may contribute to the previously observed effects of caffeine on cell cycle changes after DNA damage.	Caffeine	215-223	P53	Homo sapiens	150-153
10049063-0	1999	DNA damage-associated cell cycle and cell death control is differentially modulated by caffeine in clones with p53 mutations.	Caffeine	87-95	P53	Homo sapiens	111-114
10049063-1	1999	Caffeine is known to potentiate the cytotoxic effects of DNA damaging agents and increases the sensitivity of p53-deficient cells to X-irradiation (X-IR).	Caffeine	0-8	P53	Homo sapiens	110-113
10049063-7	1999	These results suggest that the cytocidal effect of caffeine may need to be verified independently of its cell cycle regulatory activities at least in some cases with p53 mutation.	Caffeine	51-59	P53	Homo sapiens	166-169
30542116-5	2019	Treatment of neuroblastoma cells with quarfloxin or CX-5461, two small molecule inhibitors of RNA polymerase I, suppressed MycN expression, induced DNA damage, and activated p53 followed by cell cycle arrest or apoptosis.	CX 3543	38-48	P53	Homo sapiens	174-177
9929158-8	1998	These results suggest that vesnarinone possesses activity to induce p21 protein by stabilizing its mRNA with induction of differentiation of squamous cell carcinoma cells in a p53-independent manner.	vesnarinone	27-38	P53	Homo sapiens	176-179
10047792-0	1998	Polyamine analogue-mediated cell cycle responses in human melanoma cells involves the p53, p21, Rb regulatory pathway.	Polyamines	0-9	P53	Homo sapiens	86-89
1946467-6	1991	The p53-mediated repression of c-fos gene expression occurred even in the presence of cycloheximide.	Cycloheximide	86-99	P53	Homo sapiens	4-7
24909504-6	2014	Similarily, TP53 mutations were associated with a shorter OS (22 vs. 80 months, p = 0.03) and a tendency to shorter RFS (17 vs. 33 months, p = 0.06) in patients treated with FUMI.	FuMi protocol	174-178	P53	Homo sapiens	12-16
24909504-11	2014	CONCLUSION: TP53 inactivating mutations are associated with an inferior long-term prognosis in patients with LABC treated with conventional chemotherapy.	labc	109-113	P53	Homo sapiens	12-16
9792828-0	1998	p53-Independent activation of the gadd45 promoter by Delta12-prostaglandin J2.	9-deoxy-delta-9-prostaglandin D2	61-77	P53	Homo sapiens	0-3
31019655-0	2019	Hsp90 Inhibitor SNX-2112 Enhances TRAIL-Induced Apoptosis of Human Cervical Cancer Cells via the ROS-Mediated JNK-p53-Autophagy-DR5 Pathway.	SNX 2112	16-24	P53	Homo sapiens	114-117
18096695-8	2008	Instead, SuperArray analysis showed that PXR-mediated deoxycholic acid resistance was associated with up-regulation of multiple antiapoptotic genes, including BAG3, BIRC2, and MCL-1, and down-regulation of proapoptotic genes, such as BAK1 and TP53/p53.	Deoxycholic Acid	54-70	P53	Homo sapiens	243-247
31019655-8	2019	ROS scavenger NAC rescued SNX-2112/TRAIL-induced apoptosis and suppressed SNX-2112-induced p-JNK and p53.	SNX 2112	74-82	P53	Homo sapiens	101-104
18096695-8	2008	Instead, SuperArray analysis showed that PXR-mediated deoxycholic acid resistance was associated with up-regulation of multiple antiapoptotic genes, including BAG3, BIRC2, and MCL-1, and down-regulation of proapoptotic genes, such as BAK1 and TP53/p53.	Deoxycholic Acid	54-70	P53	Homo sapiens	248-251
9818284-0	1998	Association between [18F]fluorodeoxyglucose uptake and postoperative histopathology, hormone receptor status, thymidine labelling index and p53 in primary breast cancer: a preliminary observation.	Fluorodeoxyglucose F18	20-43	P53	Homo sapiens	140-143
30418550-6	2019	P53 was dispensable for the G2/M arrest in HCT116 cells but required for induction of a senescence-like phenotype upon long-term exposure and for the observed synergism with oxaliplatin.	Oxaliplatin	174-185	P53	Homo sapiens	0-3
9818284-5	1998	Our data demonstrate that FDG uptake, expressed as SUV, is associated with certain prognostic factors in breast cancer, such as histopathological grading and p53 expression, which can be assessed only by means of postoperative in vitro examinations.	Fluorodeoxyglucose F18	26-29	P53	Homo sapiens	158-161
9764849-4	1998	Prior treatment of cells with cycloheximide or actinomycin D abolished the p53 increase and apoptosis induced by curcumin, suggesting that either de novo p53 protein synthesis or some proteins synthesis for stabilization of p53 is required for apoptosis.	Cycloheximide	30-43	P53	Homo sapiens	75-78
30639360-5	2019	Mechanistically, our findings showed that OMA activated p53-mediated apoptosis through ROS-dependent ATM-Chk2 signaling and reduced the expression of vascular endothelial growth factor through ROS-dependent E2F1-mediated hypoxia inducible factor-1alpha degradation.	oxalomalic acid	42-45	P53	Homo sapiens	56-59
9764849-4	1998	Prior treatment of cells with cycloheximide or actinomycin D abolished the p53 increase and apoptosis induced by curcumin, suggesting that either de novo p53 protein synthesis or some proteins synthesis for stabilization of p53 is required for apoptosis.	Cycloheximide	30-43	P53	Homo sapiens	154-157
9764849-4	1998	Prior treatment of cells with cycloheximide or actinomycin D abolished the p53 increase and apoptosis induced by curcumin, suggesting that either de novo p53 protein synthesis or some proteins synthesis for stabilization of p53 is required for apoptosis.	Cycloheximide	30-43	P53	Homo sapiens	154-157
9667752-6	1998	Phenol, diethylstilbestrol and ethylacrylate also induced increases in cellular p53.	Phenol	0-6	P53	Homo sapiens	80-83
9605744-3	1998	Using a UvrABC incision method, we have found that cytosine methylation greatly enhances guanine alkylation at all CpG sites in the p53 gene by a variety of carcinogens, including benzo(a)pyrene diol epoxide, benzo(g)chrysene diol epoxide, aflatoxin B1 8,9-epoxide, and N-acetoxy-2-acetylaminofluorene.	benzo(g)chrysene diol epoxide	209-238	P53	Homo sapiens	132-135
34562520-0	2022	Choline-induced SLC5A7 impairs colorectal cancer growth by stabilizing p53 protein.	Choline	0-7	P53	Homo sapiens	71-74
30690027-9	2019	In this study, we observed an enhanced DNA damage and cellular apoptosis via the ATM/CHK2/P53 pathway(s) in HeLa and SiHa cells treated with cisplatin combined with DAPT of Notch1 inhibitor.	dapt	165-169	P53	Homo sapiens	90-93
34433903-6	2022	Benzimidazoles treatment also dose-dependently induced the GBM cell cycle arrest at the G2/M phase via the P53/P21/cyclin B1 pathway.	Benzimidazoles	0-14	P53	Homo sapiens	107-114
34687773-7	2021	Taken together, CYN may induce ROS overproduction, leading to increased p53 expression and ultimately promoting VSMC apoptosis.	cylindrospermopsin	16-19	P53	Homo sapiens	72-75
9619826-6	1998	Inhibition of CD protease with Pepstatin A suppressed p53-dependent apoptosis in lymphoid cells, suggesting a possible role for CD in p53-dependent cell death.	pepstatin	31-42	P53	Homo sapiens	54-57
9619826-6	1998	Inhibition of CD protease with Pepstatin A suppressed p53-dependent apoptosis in lymphoid cells, suggesting a possible role for CD in p53-dependent cell death.	pepstatin	31-42	P53	Homo sapiens	134-137
30867754-4	2019	KRAS, PIK3CA and TP53 mutations were associated with carbohydrate antigen 19-9 expression, invasive growth, vacuolar signs and margin lobulation on chest CT.	carbohydrate antigen	53-73	P53	Homo sapiens	17-21
9586815-5	1998	These findings suggest that quinones may lead to a p53-independent and pRb-preventable G2/M arrest and apoptosis, which correlate with p21 induction.	Quinones	28-36	P53	Homo sapiens	51-54
9537648-0	1998	p53-independent WAF1 induction by ACNU in human glioblastoma cells.	Nimustine hydrochloride	34-38	P53	Homo sapiens	0-3
34862374-0	2021	Structural basis of reactivation of oncogenic p53 mutants by a small molecule: methylene quinuclidinone (MQ).	SCHEMBL4738034	79-103	P53	Homo sapiens	46-49
34862374-3	2021	PRIMA-1 and eprenetapopt (APR-246/PRIMA-1MET) are small molecules that are converted into the biologically active compound, methylene quinuclidinone (MQ), shown to reactivate mutant p53 by binding covalently to cysteine residues.	SCHEMBL4738034	124-148	P53	Homo sapiens	182-185
30767202-9	2019	While p53 was induced by FIR, no epithelial-mesenchymal transition could be found.	fir	25-28	P53	Homo sapiens	6-9
34719205-13	2021	Besides, overexpression of MAP17 accelerated cycloheximide (CHX, a protein synthesis inhibitor)-induced p53 degradation, while low expression of MAP17 slowed down CHX-induced p53 degradation, suggesting that MAP17 can regulate p53 stability.	Cycloheximide	45-58	P53	Homo sapiens	104-107
9484835-6	1998	were slow requiring at least 1 h and slowly increasing thereafter with full activation observed at 6 h. Treatment of cells with cycloheximide (CHX) prevented the activation of p53 in all phases of the cell cycle and its accumulation in G1/S and S. However, removing CHX-block allowed full activation and accumulation of p53 with fast kinetics even if 4 h had lapsed since the initial U.V.C.	Cycloheximide	128-141	P53	Homo sapiens	176-179
9484835-6	1998	were slow requiring at least 1 h and slowly increasing thereafter with full activation observed at 6 h. Treatment of cells with cycloheximide (CHX) prevented the activation of p53 in all phases of the cell cycle and its accumulation in G1/S and S. However, removing CHX-block allowed full activation and accumulation of p53 with fast kinetics even if 4 h had lapsed since the initial U.V.C.	Cycloheximide	128-141	P53	Homo sapiens	320-323
9484835-6	1998	were slow requiring at least 1 h and slowly increasing thereafter with full activation observed at 6 h. Treatment of cells with cycloheximide (CHX) prevented the activation of p53 in all phases of the cell cycle and its accumulation in G1/S and S. However, removing CHX-block allowed full activation and accumulation of p53 with fast kinetics even if 4 h had lapsed since the initial U.V.C.	Cycloheximide	143-146	P53	Homo sapiens	176-179
9484835-6	1998	were slow requiring at least 1 h and slowly increasing thereafter with full activation observed at 6 h. Treatment of cells with cycloheximide (CHX) prevented the activation of p53 in all phases of the cell cycle and its accumulation in G1/S and S. However, removing CHX-block allowed full activation and accumulation of p53 with fast kinetics even if 4 h had lapsed since the initial U.V.C.	Cycloheximide	143-146	P53	Homo sapiens	320-323
9460707-1	1998	In human neuroblastoma SH-SY5Y cells, S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide (NO)-donor, caused cell death accompanying p53 expression, nucleosomal DNA fragmentation and cell death.	S-Nitroso-N-Acetylpenicillamine	38-69	P53	Homo sapiens	136-139
9460707-1	1998	In human neuroblastoma SH-SY5Y cells, S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide (NO)-donor, caused cell death accompanying p53 expression, nucleosomal DNA fragmentation and cell death.	S-Nitroso-N-Acetylpenicillamine	71-75	P53	Homo sapiens	136-139
34099490-6	2021	Inhibition of VCP either by genetic depletion or the pharmacological inhibitor CB-5083 increased ubiquitination and degradation of p53-R273H, leading to cell death.	CB-5083	79-86	P53	Homo sapiens	131-134
9417863-8	1997	hsp90 does not bind p53 in a spatial-specific manner because it remains bound to p53 when induced to translocate to the nucleus by the protein synthesis inhibitor cycloheximide (CHX).	Cycloheximide	163-176	P53	Homo sapiens	81-84
30362193-0	2019	beta-Ketoiminato Iridium(III) Organometallic Complexes: Selective Cytotoxicity towards Colorectal Cancer Cells HCT116 p53-/.	beta-ketoiminato	0-16	P53	Homo sapiens	118-121
9417863-8	1997	hsp90 does not bind p53 in a spatial-specific manner because it remains bound to p53 when induced to translocate to the nucleus by the protein synthesis inhibitor cycloheximide (CHX).	Cycloheximide	178-181	P53	Homo sapiens	81-84
34238736-0	2021	(Dibenzyl trisulfide inhibits proliferation and induces apoptosis of HN30 cells via Akt/ p53 signaling pathway).	dibenzyl trisulfide	1-20	P53	Homo sapiens	89-92
31582633-6	2019	In this study, we show that bicyclic beta-proline oligomer derivatives inhibit p53-MDM2 and p53-MDMX protein-protein interactions, exhibiting MDM2-antagonistic and MDMX-antagonistic activities.	isoleucyl-prolyl-proline	37-49	P53	Homo sapiens	79-82
34238736-6	2021	The phosphorylation levels of Akt and p53 in HN30 cells were detected using Western blotting after treatment with 10 mumol/L DTS for 0.5, 1, 2, 4, 8, or 16 h. OBJECTIVE: DTS at 1 mumol/L significantly inhibited the proliferation of HN30, HN12 and SCC25 cells as shown by colony formation assay.	dibenzyl trisulfide	125-128	P53	Homo sapiens	38-41
34238736-6	2021	The phosphorylation levels of Akt and p53 in HN30 cells were detected using Western blotting after treatment with 10 mumol/L DTS for 0.5, 1, 2, 4, 8, or 16 h. OBJECTIVE: DTS at 1 mumol/L significantly inhibited the proliferation of HN30, HN12 and SCC25 cells as shown by colony formation assay.	dibenzyl trisulfide	170-173	P53	Homo sapiens	38-41
34238736-9	2021	Treatment with 10 mumol/L DTS for 16 h significantly inhibited Akt phosphorylation (P < 0.001) and enhanced p53 phosphorylation (P < 0.01) in HN30 cells.	dibenzyl trisulfide	26-29	P53	Homo sapiens	108-111
34238736-10	2021	OBJECTIVE: DTS inhibits proliferation and induces apoptosis of HN30 cells possibly through mechanisms involving the inhibition of Akt and the activation of p53.	dibenzyl trisulfide	11-14	P53	Homo sapiens	156-159
9356500-0	1997	Enhancement of DNA repair in human skin cells by thymidine dinucleotides: evidence for a p53-mediated mammalian SOS response.	thymidine dinucleotides	49-72	P53	Homo sapiens	89-92
31582633-6	2019	In this study, we show that bicyclic beta-proline oligomer derivatives inhibit p53-MDM2 and p53-MDMX protein-protein interactions, exhibiting MDM2-antagonistic and MDMX-antagonistic activities.	isoleucyl-prolyl-proline	37-49	P53	Homo sapiens	92-95
31168028-8	2019	The antioxidant N-acetylcysteine reduced the expression of phosphorylated ATM and H2AX, and the ATM inhibitor, caffeine, inhibited p53 activation.	Caffeine	111-119	P53	Homo sapiens	131-134
9369245-1	1997	Cycloheximide in sublethal doses caused apoptosis in liver cells in vivo, inducing c-myc, c-fos, c-jun and p53 genes and accumulation of sphingosine, a toxic product of the sphingomyelin cycle.	Cycloheximide	0-13	P53	Homo sapiens	107-110
34155600-14	2021	This study suggests that SPPA inhibits H2O2-induced human KGN cell apoptosis through antioxidation, and the SIRT1/p53 signal pathway mediates the antioxidation.	sppa	25-29	P53	Homo sapiens	114-117
30463244-6	2018	Mass spectrometry analysis revealed that streptonigrin binds to the N-terminus of TGase 2 (amino acids 95-116), which is associated with inhibition of TGase 2 activity in vitro and with p53 stabilization in RCC.	Streptonigrin	41-54	P53	Homo sapiens	186-189
34094678-6	2021	Further studies revealed that exposure to Triptolide increased the levels of p53 and pRb.	triptolide	42-52	P53	Homo sapiens	77-80
9389932-8	1997	Both m-AMCA and amsacrine induced p53 protein expression in proliferating but not in non-proliferating H460 cells, and induced p21WAF1 regardless of proliferation status.	Amsacrine	16-25	P53	Homo sapiens	34-37
9338145-4	1997	We transfected a mutant p53 gene (mp53: codon 273Arg-His) into normal human fibroblasts and obtained two G418-resistant mp53-containing clones.	antibiotic G 418	105-109	P53	Homo sapiens	24-27
35395477-5	2022	In addition, TH287 allies with ROS to eliminate the mutated p53 protein in tumor cells, thus reducing the self-protective capacity of tumor cells.	TH287	13-18	P53	Homo sapiens	60-63
30463244-8	2018	In addition, a single dose of streptonigrin (0.2 mg/kg) showed marked anti-tumor effects in a preclinical RCC model by stabilizing p53.	Streptonigrin	30-43	P53	Homo sapiens	131-134
9108075-2	1997	We have previously mapped the distribution of (+/-) anti-7beta,8alpha-dihydroxy-9alpha,10alpha-epoxy -7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE) adducts along the human P53 gene [Denissenko, M. F., Pao, A., Tang, M.-s. &amp; Pfeifer, G. P. (1996) Science 274, 430-432].	7beta	57-62	P53	Homo sapiens	167-170
35619328-0	2022	Inhibiting the IRE1alpha Axis of the Unfolded Protein Response Enhances the Antitumor Effect of AZD1775 in TP53 Mutant Ovarian Cancer.	adavosertib	96-103	P53	Homo sapiens	107-111
30463244-9	2018	Inhibition of TGase 2 using streptonigrin increased p53 stability, which resulted in p53-mediated apoptosis of RCC.	Streptonigrin	28-41	P53	Homo sapiens	52-55
35619328-2	2022	Here, it is demonstrated that the WEE1 inhibitor AZD1775 induces endoplasmic reticulum stress and activates the protein kinase RNA-like ER kinase (PERK) and inositol-required enzyme 1alpha (IRE1alpha) branches of the unfolded protein response (UPR) in TP53 mutant (mtTP53) ovarian cancer models.	adavosertib	49-56	P53	Homo sapiens	252-256
9108075-2	1997	We have previously mapped the distribution of (+/-) anti-7beta,8alpha-dihydroxy-9alpha,10alpha-epoxy -7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE) adducts along the human P53 gene [Denissenko, M. F., Pao, A., Tang, M.-s. &amp; Pfeifer, G. P. (1996) Science 274, 430-432].	10alpha-epoxy -7,8,9,10-tetrahydrobenzo[a]	87-129	P53	Homo sapiens	167-170
30463244-9	2018	Inhibition of TGase 2 using streptonigrin increased p53 stability, which resulted in p53-mediated apoptosis of RCC.	Streptonigrin	28-41	P53	Homo sapiens	85-88
9072541-3	1997	DNA of the critical p53 exons 5-8 were amplified and run on horizontal polyacrylamide gels under defined temperature conditions (TGGE) to yield specific gel shifts and sets of homo- and heteroduplexes in case of mutation.	polyacrylamide	71-85	P53	Homo sapiens	20-23
35323988-0	2022	TP53 loss-of-function mutations reduce sensitivity of acute leukaemia to the curaxin CBL0137.	CBLC137	85-92	P53	Homo sapiens	0-4
30221846-4	2018	AMG900 inhibited proliferation of A172, U-87MG, and U-118MG glioblastoma cells by upregulating p53 and p21 and subsequently inducing cell cycle arrest and senescence.	N-(4-((3-(2-amino-4-pyrimidinyl)-2-pyridinyl)oxy)phenyl)-4-(4-methyl-2-thienyl)-1-phthalazinamine	0-6	P53	Homo sapiens	95-98
35429966-0	2022	Therapeutic synergy of Triptolide and MDM2 inhibitor against acute myeloid leukemia through modulation of p53-dependent and -independent pathways.	triptolide	23-33	P53	Homo sapiens	106-109
35429966-3	2022	In this study, we reported that Triptolide synergized with MDM2 inhibitor Nutlin-3a to suppress cell proliferation and induce mitochondrial-mediated apoptosis in p53 wt AML in vitro and ex vivo.	triptolide	32-42	P53	Homo sapiens	162-165
9249905-7	1997	Immunoreactivity for p53 protein, indicative of a defective p53 function, predicted shorter CSS in univariate (52 vs 123 months, p &lt; 0.0001), but not in multivariate analysis.	thiocysteine	92-95	P53	Homo sapiens	21-24
30366906-3	2018	RNA sequencing revealed that the mutant TRP53 DNE does not globally repress wild-type TRP53 function but disproportionately impacts a subset of wild-type TRP53 target genes.	dne	46-49	P53	Homo sapiens	40-45
8968086-4	1996	However, the introduction of 2 mM caffeine led to a sensitization enhancement ratio (at 10% survival) of 1.8 in p53(-/-) cells, but only 1.3 in wild-type (p53+/+) cells.	Caffeine	34-42	P53	Homo sapiens	112-115
8968086-4	1996	However, the introduction of 2 mM caffeine led to a sensitization enhancement ratio (at 10% survival) of 1.8 in p53(-/-) cells, but only 1.3 in wild-type (p53+/+) cells.	Caffeine	34-42	P53	Homo sapiens	155-158
8968086-6	1996	The differential sensitivity of p53(-/-) cells to X-rays and caffeine was thought to be due to override of the G2-M block to cell cycle progression.	Caffeine	61-69	P53	Homo sapiens	32-35
8968086-9	1996	However, for p53(-/-) cells, a greater proportion were in S phase after treatment with caffeine, and a complete loss of S-phase delay was observed after UV irradiation.	Caffeine	87-95	P53	Homo sapiens	13-16
35429966-5	2022	In addition, we observed that Triptolide and Nutlin-3a were also cooperative in part of p53 deficient cases.	triptolide	30-40	P53	Homo sapiens	88-91
35429966-6	2022	Mechanistically, Nutlin-3a upregulated the transcriptional expressions of the p53 downstream targets PUMA and p21, while Triptolide declined the mRNA levels of two anti-apoptotic factors, XIAP and Mcl-1, in p53 wt cells.	triptolide	121-131	P53	Homo sapiens	78-81
35429966-6	2022	Mechanistically, Nutlin-3a upregulated the transcriptional expressions of the p53 downstream targets PUMA and p21, while Triptolide declined the mRNA levels of two anti-apoptotic factors, XIAP and Mcl-1, in p53 wt cells.	triptolide	121-131	P53	Homo sapiens	207-210
35429966-8	2022	Our results revealed that Triptolide monotherapy exerted its antileukemia effect via both p53-dependent and independent ways, with the latter through perturbation of the MYC-ATF4 axis-mediated ER stress.	triptolide	26-36	P53	Homo sapiens	90-93
8968086-11	1996	Greater sensitization of p53(-/-) cells to caffeine could be mediated via override of S-phase delay.	Caffeine	43-51	P53	Homo sapiens	25-28
30366906-5	2018	This reveals that, in our studies of lymphomagenesis, mutant TRP53 drives tumorigenesis primarily through the DNE, which modulates wild-type TRP53 function in a manner advantageous for neoplastic transformation.	dne	110-113	P53	Homo sapiens	61-66
35417717-3	2022	This rational screening identified antiparasitic drug potassium antimony tartrate (PAT) as an agent that can thermostabilize the representative TS mutant p53-V272M via noncovalent binding.	Antimony Potassium Tartrate	54-81	P53	Homo sapiens	154-157
9042236-0	1996	Effects of microtubule inhibitors-taxol, vinblastine and estramustine on the growth and p53 gene expression in the hormone independent human prostatic JCA-1 cells.	Estramustine	57-69	P53	Homo sapiens	88-91
35417717-3	2022	This rational screening identified antiparasitic drug potassium antimony tartrate (PAT) as an agent that can thermostabilize the representative TS mutant p53-V272M via noncovalent binding.	Antimony Potassium Tartrate	83-86	P53	Homo sapiens	154-157
30366906-5	2018	This reveals that, in our studies of lymphomagenesis, mutant TRP53 drives tumorigenesis primarily through the DNE, which modulates wild-type TRP53 function in a manner advantageous for neoplastic transformation.	dne	110-113	P53	Homo sapiens	141-146
30057300-5	2018	Further experimental testing demonstrated that Michael acceptors, aldehydes, imines, and primary alcohols can promote thermodynamic stabilization of mutant p53.	Aldehydes	66-75	P53	Homo sapiens	156-159
35456673-6	2022	Furthermore, the biopsy specimen from TFBPC-treated xenografts revealed decreased expressions of P53, Ki-67 and PD-L1 coupled with higher expression of cleaved caspase 3, suggesting TFBPC treatment was effective and resulted in good prognostic indications.	tfbpc	38-43	P53	Homo sapiens	97-100
35456673-6	2022	Furthermore, the biopsy specimen from TFBPC-treated xenografts revealed decreased expressions of P53, Ki-67 and PD-L1 coupled with higher expression of cleaved caspase 3, suggesting TFBPC treatment was effective and resulted in good prognostic indications.	tfbpc	182-187	P53	Homo sapiens	97-100
8964480-4	1996	Treatment of cells with caffeine decreased the p53wt content and increased the proportion of metaphases with chromosome breaks; however, it did not induce hyperdiploidy in the majority of cell lines.	Caffeine	24-32	P53	Homo sapiens	47-50
30057300-6	2018	Moreover, mild thiol reactivity, often coupled with combined chemical functional groups, such as in imines, aldehydes, and primary alcohols, can stimulate mutant p53 refolding.	Aldehydes	108-117	P53	Homo sapiens	162-165
29932882-9	2018	After treatment with Nutlin, increased nuclear localization of p53 (4.05%-80.56%) was observed in pterygium cells along with increasing Nutlin dosages (from 0 to 50 muM, p &lt; 0.001).	nutlin	21-27	P53	Homo sapiens	63-66
8707401-7	1996	A search of our database of p53 mutations revealed that out of 8 p53 mutations reported by others, 4 are C:G--&gt;T:A transitions at dipyrimidine sites, and one is a tandem CC--&gt;TT mutation.	dipyrimidine	133-145	P53	Homo sapiens	28-31
35399143-5	2022	RESULTS: Carbohydrate antigen 19-9 (CA19-9) had the best ability to classify patients with short-term recurrence and long-term survivors (odds ratio 21.04, 95% confidence interval (CI) 4.612-96.019), followed by SMAD4 and TP53 mutation scoring (odds ratio 41.322, 95% CI 3.156-541.035).	carbohydrate antigen	9-29	P53	Homo sapiens	222-226
29665004-5	2018	Combined treatment of thiostrepton and cycloheximide/chloroquine prevented the degradation of mutant p53 protein, reinforcing autophagy as the means of mutant p53 destabilization.	Cycloheximide	39-52	P53	Homo sapiens	101-104
35259468-7	2022	Xanthohumol activated mitochondrial apoptosis through upregulation of (p53-upregulated modulator of apoptosis) PUMA expression.	xanthohumol	0-11	P53	Homo sapiens	71-74
8626797-6	1996	Furthermore, we found that amino acids 100-150 of p53 can function as an independent domain to induce Trypanosoma brucei ODC, a stable protein, to be degraded in vivo or, by cooperating with an antizyme binding domain of ODC, to confer polyamine-dependent regulation.	Polyamines	236-245	P53	Homo sapiens	50-53
8597035-14	1995	The induction of skin carcinoma by ultraviolet light is indicated by the occurrence of p53 mutations at dipyrimidine sites including CC to TT double base changes.	dipyrimidine	104-116	P53	Homo sapiens	87-90
35220221-2	2022	Here, we report the anticancer effects of AZOX on the p53-negative human myelogenous leukemia cell line HL-60RG and the p53 positive human T-cell leukemia cell line MOLT-4F.	azoxystrobin	42-46	P53	Homo sapiens	54-57
35220221-7	2022	CONCLUSION: AZOX has p53-independent anticancer effects in leukemia cells, but the mechanisms underlying the damage differ between cell lines.	azoxystrobin	12-16	P53	Homo sapiens	21-24
29665004-5	2018	Combined treatment of thiostrepton and cycloheximide/chloroquine prevented the degradation of mutant p53 protein, reinforcing autophagy as the means of mutant p53 destabilization.	Cycloheximide	39-52	P53	Homo sapiens	159-162
30235848-8	2018	This study aimed to examine the inhibitory effects of two 4"-aminochalcones on the migration/invasion of the U2OS (p53+/+) and SAOS-2 (p53-/-) OS cell lines as well as the underlying molecular mechanisms.	4"-aminochalcones	58-75	P53	Homo sapiens	115-118
34995485-5	2022	When CAPE was combined with cisplatin in nine cell lines representative of various histotypes a synergistic effect was observed in TOV112D cells and in the cisplatin-resistant IGROV-1/Pt1 variant, both of endometrioid type and carrying mutant TP53.	caffeic acid phenethyl ester	5-9	P53	Homo sapiens	243-247
7628635-3	1995	Western analysis using anti-p53 or anti-WAF1 monoclonal antibodies demonstrated that these two protein levels were increased 3 h after delta 12-PGJ2 treatment, and accumulated for up to 12 h. The induction of p53 protein seemed to be dependent on the increase of p53 mRNA level, which was inhibited by CHX treatment.	Cycloheximide	302-305	P53	Homo sapiens	209-212
7628635-3	1995	Western analysis using anti-p53 or anti-WAF1 monoclonal antibodies demonstrated that these two protein levels were increased 3 h after delta 12-PGJ2 treatment, and accumulated for up to 12 h. The induction of p53 protein seemed to be dependent on the increase of p53 mRNA level, which was inhibited by CHX treatment.	Cycloheximide	302-305	P53	Homo sapiens	209-212
7726729-4	1995	With the formalin-fixed tissues, we compared pepsin predigestion with microwave irradiation in citrate buffer as means of enhancing the sensitivity of p53 detection.	Citric Acid	95-102	P53	Homo sapiens	151-154
35051709-4	2022	Mechanistic studies showed that FY-56 moderately inhibited the proliferation and clone formation of leukemia cells, induced H3K4me1/2 accumulation and p53 activation as well as reduced the mRNA levels of the transcription factors HOXA9 and MEIS1.	fy-56	32-37	P53	Homo sapiens	151-154
30235848-11	2018	The two 4"-aminochalcones showed low capacity to inhibit the viability of OS cells independent of p53 status, but preferentially suppressed the migration of U2OS cells and of a SAOS-2 cell line expressing p53.	4"-aminochalcones	8-25	P53	Homo sapiens	98-101
30235848-11	2018	The two 4"-aminochalcones showed low capacity to inhibit the viability of OS cells independent of p53 status, but preferentially suppressed the migration of U2OS cells and of a SAOS-2 cell line expressing p53.	4"-aminochalcones	8-25	P53	Homo sapiens	205-208
30280787-13	2018	Verteporfin, an inhibitor of TLR4, increased the level of P53 and aging of RPMI8226 cells.	Verteporfin	0-11	P53	Homo sapiens	58-61
35192728-4	2022	Together with extended tumor exposure to therapeutically effective drug levels via reversible conjugation to Pluronic F-108 (PF108), these features translated into rapid tumor regression and long-term survival in models of both ABCG2-overexpressing and p53-mutant high-risk neuroblastomas, in contrast to a marginal effect of the clinically used camptothecin derivative, irinotecan.	FS-108	118-123	P53	Homo sapiens	253-256
7816803-0	1995	Expression of the wild-type p53 antioncogene induces guanine nucleotide-dependent stem cell division kinetics.	Guanine Nucleotides	53-71	P53	Homo sapiens	28-31
7816803-5	1995	We show that through a guanine nucleotide-dependent mechanism, the p53 antioncogene can induce exponentially dividing cells to switch to an asymmetric stem cell growth pattern.	Guanine Nucleotides	23-41	P53	Homo sapiens	67-70
7930674-3	1994	Six of eight aberrations of p53 gene were determined to be single nucleotide substitutions, and five of these were located at a dipyrimidine site.	dipyrimidine	128-140	P53	Homo sapiens	28-31
30127884-7	2018	Further investigation of genipin-treated HCT116 cells revealed that the expression of p53, Bax and cleaved caspase-3 in genipin-treated cells was increased compared with the vehicle control, whereas B-cell lymphoma-2 expression appeared to be lower in genipin-treated cells.	genipin	25-32	P53	Homo sapiens	86-89
8076368-0	1994	Hyperphosphorylation of p53 induced by benzene, toluene, and chloroform.	Toluene	48-55	P53	Homo sapiens	24-27
8076368-6	1994	Hyperphosphorylation of p53 may be involved in tumor promotion by benzene, toluene and chloroform.	Toluene	75-82	P53	Homo sapiens	24-27
17180005-4	1994	The wt protein was expressed essentially in the nucleus, while mutant p53 showed both nuclear and cytoplasmic expression, as determined by immunofluorescence staining with PAb122.	pab122	172-178	P53	Homo sapiens	70-73
7510864-0	1994	p53 undergoes epitopic changes in vitro by sodium-vanadate.	Vanadates	43-58	P53	Homo sapiens	0-3
35042152-13	2022	Detection of mutant TP53 in baseline plasma resulted in numerically shorter PFS with alectinib (hazard ratio 1.88, 95% confidence interval 0.9-3.93).	alectinib	85-94	P53	Homo sapiens	20-24
35042152-15	2022	Alectinib prolonged PFS versus chemotherapy in patients with wild-type or mutant TP53; however, alectinib activity was considerably decreased in patients with mutant TP53.	alectinib	0-9	P53	Homo sapiens	81-85
35042152-15	2022	Alectinib prolonged PFS versus chemotherapy in patients with wild-type or mutant TP53; however, alectinib activity was considerably decreased in patients with mutant TP53.	alectinib	96-105	P53	Homo sapiens	166-170
30127884-7	2018	Further investigation of genipin-treated HCT116 cells revealed that the expression of p53, Bax and cleaved caspase-3 in genipin-treated cells was increased compared with the vehicle control, whereas B-cell lymphoma-2 expression appeared to be lower in genipin-treated cells.	genipin	120-127	P53	Homo sapiens	86-89
35164239-3	2022	PDA-66, a structural analogue of the inhibitor of serine-threonine kinase glycogen synthase kinase 3beta SB216763, has shown preclinical antitumour effects in various cell lines, with the key pathways of its anticancer activity being cell cycle modulation, DNA replication and p53 signalling.	PDA-66	0-6	P53	Homo sapiens	277-280
30127884-7	2018	Further investigation of genipin-treated HCT116 cells revealed that the expression of p53, Bax and cleaved caspase-3 in genipin-treated cells was increased compared with the vehicle control, whereas B-cell lymphoma-2 expression appeared to be lower in genipin-treated cells.	genipin	120-127	P53	Homo sapiens	86-89
30128010-6	2018	Triptolide treatment suppressed the expression of phosphorylated (p)-protein kinase B (Akt), p-mechanistic target of rapamycin (mTOR), and p-p70S6K, activated the expression of p-p38, mitogen-activated protein kinase (MAPK) and p53 and inhibited the expression of p-forkhead box O3 (Foxo3a) in SiHa cells.	triptolide	0-10	P53	Homo sapiens	228-231
35121390-10	2022	RESULTS: Pachymic acid, shionone, peiminine and astragaloside A was verified as therapeutic agents for improving the condition of COPD by acting on the EGFR, ERK1, PAI-1 and p53 target, respectively.	pachymic acid	9-22	P53	Homo sapiens	174-177
8018562-2	1994	When treated with lovastatin, the cells were blocked in G1 and appeared to express increased levels of wild-type p53 when examined by immunostaining.	Lovastatin	18-28	P53	Homo sapiens	113-116
8018565-9	1994	The protein synthesis inhibitor cycloheximide completely abolished the PMA-induced down-modulation of the p53 mRNA, suggesting that a short-lived protein was involved in the down-modulation.	Cycloheximide	32-45	P53	Homo sapiens	106-109
8106638-13	1994	As p53 protein is a regulator of guanine nucleotide synthesis, the loss of normal inhibitory regulation by the p53 mutation would serve to increase the availability of GTP for the transduction of signals essential for increased cell growth and hormone expression in the adrenal tumors.	Guanine Nucleotides	33-51	P53	Homo sapiens	3-6
8106638-13	1994	As p53 protein is a regulator of guanine nucleotide synthesis, the loss of normal inhibitory regulation by the p53 mutation would serve to increase the availability of GTP for the transduction of signals essential for increased cell growth and hormone expression in the adrenal tumors.	Guanine Nucleotides	33-51	P53	Homo sapiens	111-114
30128010-7	2018	These results suggested that triptolide induces protective autophagy, suppresses cell viability and promotes apoptosis in human cervical cancer cells by inducing the autophagy-targeting phosphoinositide 3-kinase/Akt/mTOR, p38, MAPK, p53 and Foxo3a pathways.	triptolide	29-39	P53	Homo sapiens	233-236
30197757-8	2018	Cross-talk between Zac1, IL-11, p53, and suppressor of cytokine signaling 3 was differentially affected by copper sulfate, digoxin, and caffeine.	Caffeine	136-144	P53	Homo sapiens	32-35
7997128-6	1994	The results showed that cab enhanced the immunoreactivity of the following antigens: estrogen receptors (AMAC), progesterone receptors (Novocastra), HMB45, vimentin, leukocyte common antigen, PCNA, p53, MIB-1 (Ki-67) and prostatic specific antigen.	cabotegravir	24-27	P53	Homo sapiens	198-201
29574239-4	2018	Considering the antitumor activity of benzothiazolic derivatives, this study aimed to demonstrate the action of benzothiazolic (E)-2-((2-(benzo[d]thiazol-2-yl)hydrazono)methyl)-4-nitrophenol (AFN01) against three established human melanoma cell lines that recapitulate the molecular landscape of the disease in terms of its genetic alterations and mutations, such as the TP53, NRAS and B-RAF genes.	(E)-2-((2-(benzo(d)thiazol-2-yl)hydrazono)methyl)-4-nitrophenol	127-190	P53	Homo sapiens	371-375
8485705-4	1993	The protein synthesis inhibitor cycloheximide blocks the increase in p53 following DNA damage.	Cycloheximide	32-45	P53	Homo sapiens	69-72
29853637-3	2018	Here, perturbation of the p53 core domain (p53C) with subdenaturing concentrations of guanidine hydrochloride and high hydrostatic pressure revealed native-like molten globule (MG) states, a subset of which were highly prone to amyloidogenic aggregation.	Guanidine	86-109	P53	Homo sapiens	26-29
1466808-3	1992	Using conformational energy analysis based on ECEPP (Empirical Conformational Energies for Polypeptides Program), we have determined the preferred three dimensional structures for this tridecapeptide sequence for the human wild-type p53 protein and four cancer-related mutant p53 proteins (Ala 245, Ile 246, Trp 248, Ser 249).	Isoleucine	299-302	P53	Homo sapiens	233-236
1466808-3	1992	Using conformational energy analysis based on ECEPP (Empirical Conformational Energies for Polypeptides Program), we have determined the preferred three dimensional structures for this tridecapeptide sequence for the human wild-type p53 protein and four cancer-related mutant p53 proteins (Ala 245, Ile 246, Trp 248, Ser 249).	Isoleucine	299-302	P53	Homo sapiens	276-279
30123351-5	2018	Moreover, phosphor mutants of CAP1 at the S307/S309 regulatory site had compromised rescue effects for both the invasiveness and the proliferation in CAP1-knockdown cells and GSK3beta kinase inhibitor LiCl inhibited cell phosphorylation site S307/S309 by up-regulating the expression of p53, BAK, BAD and cleaved PARP induced ROS production, decreased lung cancer cell viability, adhesion, proliferation, migration and invasion, and induction of apoptosis.	Lithium Chloride	201-205	P53	Homo sapiens	287-290
1639275-1	1992	A common polymorphism at codon 72 of the p53 gene in patients with acute myelogenous leukemia (AML) was analyzed by single-strand conformation polymorphism assay and sodium dodecyl sulfate polyacrylamide-gel electrophoresis of immunoprecipitated 35S-labeled P53 protein.	polyacrylamide	189-203	P53	Homo sapiens	41-44
29963241-5	2018	Compared to CPT-11, L-OHP is a stronger inducer of caspases and p53-dependent apoptosis.	Oxaliplatin	20-25	P53	Homo sapiens	64-67
1640738-4	1992	Direct sequencing of p53 cDNA revealed a missense point mutation in KYO-1 and a single base pair deletion consistent with a coding frame shift in KCL-22.	Potassium Chloride	146-149	P53	Homo sapiens	21-24
29963241-7	2018	We additionally show that L-OHP suppresses survivin through p53 and its downstream target p21, which stalls cell cycle progression as a cyclin-dependent kinase inhibitor (CDKi).	Oxaliplatin	26-31	P53	Homo sapiens	60-63
33824292-0	2021	Taraxasterol acetate targets RNF31 to inhibit RNF31/p53 axis-driven cell proliferation in colorectal cancer.	taraxasteryl acetate	0-20	P53	Homo sapiens	52-55
29030986-3	2018	Using a cell-based screening method with a p53-responsive luciferase-reporter assay system involving benzoxazole derivatives, we found that AU14022 administration significantly increased p53 transcriptional activity in a concentration-dependent manner.	Benzoxazoles	101-112	P53	Homo sapiens	187-190
25311433-11	2014	CONCLUSION: Triptolide and Minnelide caused cell death in vitro and in vivo in HPV-positive HNSCC by reactivating wild-type p53 and thus inducing apoptosis.	triptolide	12-22	P53	Homo sapiens	124-127
29653431-7	2018	After combining etoposide and FK866 treatment SIRTUIN2 was further decreased and accumulation and acetylation of the downstream target p53 was further enhanced in MOLT4 cells.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	30-35	P53	Homo sapiens	135-138
34785775-0	2022	Inhibition of cathepsin K sensitizes oxaliplatin-induced apoptotic cell death by Bax upregulation through OTUB1-mediated p53 stabilization in vitro and in vivo.	Oxaliplatin	37-48	P53	Homo sapiens	121-124
34785775-11	2022	Our results demonstrate that cathepsin K inhibition enhances oxaliplatin-induced apoptosis by increasing OTUB1 phosphorylation via CK2 activation, thereby promoting p53 stabilization, and hence upregulating Bax.	Oxaliplatin	61-72	P53	Homo sapiens	165-168
29876013-5	2018	Even aggressive models of cancer, such as p53-/- or TET2-/- cells, responded to MC2884, suggesting MC2884 therapeutic potential also for the therapy of TP53 or TET2-deficient human cancers.	mc2884	80-86	P53	Homo sapiens	42-45
34542202-4	2022	It is now obvious that urolithins can involve several cellular mechanisms including inhibition of MDM2-p53 interaction, modulation of mitogen-activated protein kinase pathway, and suppressing nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) activity.	urolithins	23-33	P53	Homo sapiens	103-106
29508534-5	2018	Biological evaluation showed that the sulfamate is essential for biological activity, and modification of the acyl group on the bicycloketal can improve the inhibitory activity against the p53-Hdm2 interaction.	bicycloketal	128-140	P53	Homo sapiens	189-192
34958576-4	2022	Hoping to create a novel class of membrane-permeable PPI inhibitors, the phenylalanine, tryptophan, and leucine residues that play a critical role in inhibiting the p53-HDM2 interaction were grafted into the framework of CADY2 a cell-penetrating peptide (CPP) having a helical propensity.	Phenylalanine	73-86	P53	Homo sapiens	165-168
29158005-14	2018	In conclusion, 1,25(OH)2D3 inhibited the proliferation of HCC cells and induced their apoptosis by down-regulating the expression of HDAC2, up-regulating p53, and regulating its downstream mitochondria-mediated pathway and the exogenous DR-mediated pathway.	Calcitriol	15-26	P53	Homo sapiens	154-157
34348580-12	2021	Additionally, triptolide targets were found to be significantly enriched in CXCR4-related chemokine and cancer-related p53 signaling pathways.	triptolide	14-24	P53	Homo sapiens	119-122
29285847-0	2018	2-anilino-4-amino-5-aroylthiazole-type compound AS7128 inhibits lung cancer growth through decreased iASPP and p53 interaction.	AS7128	48-54	P53	Homo sapiens	111-114
34827693-0	2021	p53-Mediated Radiosensitization of 177Lu-DOTATATE in Neuroblastoma Tumor Spheroids.	lutetium Lu 177 dotatate	35-49	P53	Homo sapiens	0-3
29285847-5	2018	In addition, we also found that iASPP, an oncogenic protein that functionally inhibits p53, might be associated with AS7128 through mass identification.	AS7128	117-123	P53	Homo sapiens	87-90
34827693-3	2021	The aim of this study was to investigate the novel p53-stabilizing peptide VIP116 in neuroblastoma, both as monotherapy and together with 177Lu-DOTATATE.	vip116	75-81	P53	Homo sapiens	51-54
34827693-3	2021	The aim of this study was to investigate the novel p53-stabilizing peptide VIP116 in neuroblastoma, both as monotherapy and together with 177Lu-DOTATATE.	lutetium Lu 177 dotatate	138-152	P53	Homo sapiens	51-54
29285847-6	2018	Further exploration indicated that AS7128 treatment could restore the transactivation ability of p53 and, thus, increase the expressions of its downstream target genes, which are related to cell cycle arrest and apoptosis.	AS7128	35-41	P53	Homo sapiens	97-100
34827693-10	2021	VIP116 and combination treatment increased p53 levels with subsequent induction of p21, Bax and cleaved caspase 3.	vip116	0-6	P53	Homo sapiens	43-46
29285847-8	2018	Taken together, AS7128 could bind to iASPP, disrupt the interaction between iASPP and p53, and result in cell cycle arrest and apoptosis.	AS7128	16-22	P53	Homo sapiens	86-89
29745082-13	2018	Cho/NAA and Cho/Cr in the tumor were positively correlated with p53 in the tumor, but negatively correlated with PTEN in the tumor.	Choline	0-3	P53	Homo sapiens	64-67
34771652-6	2021	We showed that pharmacologically blocking KDM1A activity in neuroblastoma cells with the small molecule inhibitor, SP-2509, increased FAS cell-surface expression in a strictly TP53-dependent manner.	SP2509	115-122	P53	Homo sapiens	176-180
29745082-13	2018	Cho/NAA and Cho/Cr in the tumor were positively correlated with p53 in the tumor, but negatively correlated with PTEN in the tumor.	Choline	12-15	P53	Homo sapiens	64-67
34769049-6	2021	Altogether, our findings demonstrate piceatannol"s effectiveness in counteracting senescence by targeting its associated pathways and detecting and affecting P53-dependent and P53-independent senescence.	3,3',4,5'-tetrahydroxystilbene	37-48	P53	Homo sapiens	158-161
34769049-6	2021	Altogether, our findings demonstrate piceatannol"s effectiveness in counteracting senescence by targeting its associated pathways and detecting and affecting P53-dependent and P53-independent senescence.	3,3',4,5'-tetrahydroxystilbene	37-48	P53	Homo sapiens	176-179
29581845-0	2018	TP53 mutations and number of alterations correlate with maximum standardized uptake value (SUVmax) determined by positron emission tomography/computed tomography (PET/CT) [18F] fluorodeoxyglucose (18F-FDG PET).	Fluorodeoxyglucose F18	172-195	P53	Homo sapiens	0-4
34645785-9	2021	Co-expression of each alternative p53-isoform together with p53alpha exacerbated the DDT pathway defects, unveiling impaired POLiota recruitment and replication deceleration already under unperturbed conditions.	DDT	85-88	P53	Homo sapiens	34-37
29581845-0	2018	TP53 mutations and number of alterations correlate with maximum standardized uptake value (SUVmax) determined by positron emission tomography/computed tomography (PET/CT) [18F] fluorodeoxyglucose (18F-FDG PET).	Fluorodeoxyglucose F18	201-204	P53	Homo sapiens	0-4
29472838-10	2018	PARP-1 and p53 mRNA levels were elevated in Ca&amp;AD lymphocytes compared with controls.	ca&amp	44-50	P53	Homo sapiens	11-14
34426149-0	2021	Design, synthesis and biological evaluation of novel pyrrolidone-based derivatives as potent p53-MDM2 inhibitors.	Pyrrolidinones	53-64	P53	Homo sapiens	93-96
34496888-14	2021	CircMYH9 promoted serine/glycine metabolism, the NAD + /NADH ratio, and glutathione recycling and inhibited reactive oxygen species (ROS) in a p53-dependent manner, impacting tumour growth.	circmyh9	0-8	P53	Homo sapiens	143-146
29302672-0	2018	Synthesis of spiro-tetrahydrothiopyran-oxindoles by Michael-aldol cascade reactions: discovery of potential P53-MDM2 inhibitors with good antitumor activity.	spiro-tetrahydrothiopyran-oxindoles	13-48	P53	Homo sapiens	108-111
34175723-0	2021	3-Arylamino-quinoxaline-2-carboxamides inhibit the PI3K/Akt/mTOR signaling pathways to activate P53 and induce apoptosis.	3-arylamino-quinoxaline-2-carboxamides	0-38	P53	Homo sapiens	96-99
34212455-7	2021	In UMUC3 cell xenografts and two patient-derived xenograft lines with MDM2 overexpression, in which the p53/cell cycle pathway was inactivated, AZD-1775 combined with CDDP suppressed tumor growth inducing both M-phase entry and apoptosis, whereas AZD-1775 alone was as effective as the combination in RT4 cell xenografts.	adavosertib	144-152	P53	Homo sapiens	104-107
29346757-5	2018	This delay requires the p53 transcriptional target CDKN1A (encoding p21) and is associated with both slower depletion of intracellular glutathione and a reduced accumulation of toxic lipid-reactive oxygen species (ROS).	lipid-reactive oxygen species	183-212	P53	Homo sapiens	24-27
29354595-0	2017	Synergistic Rescue of Nonsense Mutant Tumor Suppressor p53 by Combination Treatment with Aminoglycosides and Mdm2 Inhibitors.	Aminoglycosides	89-104	P53	Homo sapiens	55-58
29354595-3	2017	Aminoglycosides G418 (geneticin) and gentamicin have been shown to induce translational readthrough and expression of full-length p53.	Aminoglycosides	0-15	P53	Homo sapiens	130-133
29354595-3	2017	Aminoglycosides G418 (geneticin) and gentamicin have been shown to induce translational readthrough and expression of full-length p53.	antibiotic G 418	16-20	P53	Homo sapiens	130-133
29354595-5	2017	Here, we show that combination treatment with a proteasome inhibitor or compounds that disrupt p53-Mdm2 binding can synergistically enhance levels of full-length p53 upon aminoglycoside-induced readthrough of R213X nonsense mutant p53.	Aminoglycosides	171-185	P53	Homo sapiens	95-98
29354595-5	2017	Here, we show that combination treatment with a proteasome inhibitor or compounds that disrupt p53-Mdm2 binding can synergistically enhance levels of full-length p53 upon aminoglycoside-induced readthrough of R213X nonsense mutant p53.	Aminoglycosides	171-185	P53	Homo sapiens	162-165
29354595-5	2017	Here, we show that combination treatment with a proteasome inhibitor or compounds that disrupt p53-Mdm2 binding can synergistically enhance levels of full-length p53 upon aminoglycoside-induced readthrough of R213X nonsense mutant p53.	Aminoglycosides	171-185	P53	Homo sapiens	162-165
29354595-7	2017	Thus, our results demonstrate that combination treatment with aminoglycosides and compounds that inhibit p53 degradation is synergistic and can provide significantly improved efficacy of readthrough when compared with aminoglycosides alone.	Aminoglycosides	62-77	P53	Homo sapiens	105-108
29354595-7	2017	Thus, our results demonstrate that combination treatment with aminoglycosides and compounds that inhibit p53 degradation is synergistic and can provide significantly improved efficacy of readthrough when compared with aminoglycosides alone.	Aminoglycosides	218-233	P53	Homo sapiens	105-108
28832998-9	2017	Pifithrin-mu, a selective inhibitor of p53 mitochondrial translocation, prevented the mitochondrial translocation of the p53 probe in a concentration-dependent manner.	2-phenylacetylenesulfonamide	0-12	P53	Homo sapiens	39-42
28832998-9	2017	Pifithrin-mu, a selective inhibitor of p53 mitochondrial translocation, prevented the mitochondrial translocation of the p53 probe in a concentration-dependent manner.	2-phenylacetylenesulfonamide	0-12	P53	Homo sapiens	121-124
28929344-8	2017	Although the apoptosis inducing effect of GluIIbeta inhibition appeared to be p53-dependent, we found that a combined treatment with lysosomal inhibitors to block autophagy enhanced the apoptotic effect of GluIIbeta inhibition in both wild-type p53 and p53-null cells.	gluiibeta	42-51	P53	Homo sapiens	78-81
28790110-0	2017	Replication Stress Leading to Apoptosis within the S-phase Contributes to Synergism between Vorinostat and AZD1775 in HNSCC Harboring High-Risk TP53 Mutation.	adavosertib	107-114	P53	Homo sapiens	144-148
29093644-0	2017	Synergistic anticancer effect of combined crocetin and cisplatin on KYSE-150 cells via p53/p21 pathway.	crocetin	42-50	P53	Homo sapiens	87-90
29093644-14	2017	The wild-type p53 inhibitor, PFT-alpha suppressed the overexpression of p53/p21 and the synergistic effect induced by the combination of crocetin and cisplatin.	crocetin	137-145	P53	Homo sapiens	14-17
29093644-14	2017	The wild-type p53 inhibitor, PFT-alpha suppressed the overexpression of p53/p21 and the synergistic effect induced by the combination of crocetin and cisplatin.	crocetin	137-145	P53	Homo sapiens	72-75
28673807-0	2017	Walsuronoid B induces mitochondrial and lysosomal dysfunction leading to apoptotic rather than autophagic cell death via ROS/p53 signaling pathways in liver cancer.	walsuronoid B	0-13	P53	Homo sapiens	125-128
28673807-8	2017	In addition, ROS induced by walsuronoid B upregulated p53 levels; conversely, p53 stimulated ROS.	walsuronoid B	28-41	P53	Homo sapiens	54-57
28673807-12	2017	In summary, our findings demonstrated that walsuronoid B caused G2/M phase arrest and induced mitochondrial and lysosomal apoptosis through the ROS/p53 signaling pathway in human liver cancer cells in vitro and in vivo.	walsuronoid B	43-56	P53	Homo sapiens	148-151
28753773-11	2017	Mutations in BAP1 (q=0.004) and TP53 (q=0.001) were associated with decreased CSS in a multivariable model; only TP53 (q=0.005) remained significant when SSIGN score was included.	thiocysteine	78-81	P53	Homo sapiens	32-36
28753773-11	2017	Mutations in BAP1 (q=0.004) and TP53 (q=0.001) were associated with decreased CSS in a multivariable model; only TP53 (q=0.005) remained significant when SSIGN score was included.	thiocysteine	78-81	P53	Homo sapiens	113-117
28753773-15	2017	After adjustment for clinical confounders, mutations of TP53 and SETD2 were associated with decreased CSS and RFS, respectively.	thiocysteine	102-105	P53	Homo sapiens	56-60
28878400-0	2017	Thiamine antagonists trigger p53-dependent apoptosis in differentiated SH-SY5Y cells.	Thiamine	0-8	P53	Homo sapiens	29-32
28878400-1	2017	Accumulating evidences suggest that p53 is a key coordinator of cellular events triggered by oxidative stress often associated with the impairment in thiamine metabolism and its functions.	Thiamine	150-158	P53	Homo sapiens	36-39
28618133-11	2017	Our results indicate that hispolon inhibits the cell viability, induces G2/M cell cycle arrest and apoptosis in glioblastoma U87MG cells, and p53 should play a role in hispolon-mediated antitumor activity.	hispolon	168-176	P53	Homo sapiens	142-145
28012196-3	2017	Oncoprotein inhibitory member of the ASPP family (iASPP), a key inhibitor of tumor suppressor p53, has been reported to play oncogenic role in cancers.	aspp	37-41	P53	Homo sapiens	94-97
28927115-9	2017	Results from the cell cycle analysis and western blotting indicated that MK1775 abrogated the G2/M checkpoint through inhibiting the phosphorylation of CDK1 and inducing the apoptosis of ovarian cancer cells that lacked mutations in p53 and breast cancer 1 (BRCA1).	adavosertib	73-79	P53	Homo sapiens	233-236
29100379-4	2017	We screened eleven traditional Chinese medicines against a panel of androgen-independent Pten/Tp53 null PrCa-derived cell lines and identified gambogic acid (GA) as a highly potent growth inhibitor.	gambogic acid	143-156	P53	Homo sapiens	94-98
28767099-0	2017	Fisetin Induces Apoptosis Through p53-Mediated Up-Regulation of DR5 Expression in Human Renal Carcinoma Caki Cells.	fisetin	0-7	P53	Homo sapiens	34-37
28767099-6	2017	Furthermore, fisetin induced p53 protein expression through up-regulation of protein stability, whereas down-regulation of p53 by siRNA markedly inhibited fisetin-induced DR5 expression.	fisetin	13-20	P53	Homo sapiens	29-32
28769054-6	2017	We have previously reported p53-mediated activation of miR-138 in human non-small-cell lung cancer (NSCLC) cells.	mir-138	55-62	P53	Homo sapiens	28-31
28769054-9	2017	Our results suggested that p53 could alternatively upregulate GADD45A in human NSCLC cells through a post-transcriptional pathway in which miR-138 is involved.	mir-138	139-146	P53	Homo sapiens	27-30
28214706-10	2017	Results suggest that the long-term culturing of human hepatoma cells at a low, more physiological pO2 induces antioxidant adaptations that could be mediated by p53, and may alter the cellular response to a subsequent oxidant challenge.	PO-2	98-101	P53	Homo sapiens	160-163
28092678-4	2017	Depletion of PFKFB4 from p53-deficient cancer cells increased levels of the allosteric regulator fructose-2,6-bisphosphate, leading to increased glycolytic activity but decreased routing of metabolites through the oxidative arm of the pentose-phosphate pathway.	Pentoses	235-242	P53	Homo sapiens	25-28
28558682-9	2017	Meanwhile, the expression of several regulators that contribute to G1/S phased transition, such as Cyclin D1, CDK4 and CDK6, were significantly down-regulated with the up-regulation of cell cycle inhibitors, p21 and p53, after treatment with glucosamine.	Glucosamine	242-253	P53	Homo sapiens	216-219
34348712-6	2021	Further studies revealed that circFAM13B, a sponge of miR-212, is involved in the regulation of E2F5 gene expression by competitively binding to miR-212, inhibits the activation of the P53 signalling pathway, and promotes the proliferation of HCC cells.	circfam13b	30-40	P53	Homo sapiens	185-188
34149899-6	2021	Compared with the PBS control group, the A549, A549/DDP and A549/Taxol cells treated with NaI131, GA or a combination of the drugs exhibited G2/M arrest and increased percentages of total apoptotic cells, as well as significantly decreased protein levels of CDK1, cyclin B, mtp53, HSP90, Bcl-2 and P-gp, increased protein levels of Bax and decreased mRNA levels of p53 and HSP90.	gambogic acid	98-100	P53	Homo sapiens	365-368
28444994-7	2017	As representative compounds, PCB 20 and 22 induced micronuclei in relatively high concentrations in HepG2 cells (p53-proficient), though they did not induce Hprt gene mutations in V79-Mz cells.	Polychlorinated Biphenyls	29-32	P53	Homo sapiens	113-116
34350116-7	2021	The connection between UBD and p53 was analyzed using Western blotting, immunoprecipitation, proteasome inhibition assay and Cycloheximide (CHX) chase assay.	Cycloheximide	125-138	P53	Homo sapiens	31-34
34350116-7	2021	The connection between UBD and p53 was analyzed using Western blotting, immunoprecipitation, proteasome inhibition assay and Cycloheximide (CHX) chase assay.	Cycloheximide	140-143	P53	Homo sapiens	31-34
28343940-6	2017	We show that LCA derivatives may be considered as future therapeutics for the treatment of cyclin D1-addicted p53-expressing and p53-defective cancer types.	Lithocholic Acid	13-16	P53	Homo sapiens	110-113
34335799-20	2021	Tangeretin inhibits metastasis in breast cancer cells by targeting TP53, PTGS2, MMP9, and PIK3CA and regulating the PI3K/Akt signaling pathway.	tangeretin	0-10	P53	Homo sapiens	67-71
28343940-6	2017	We show that LCA derivatives may be considered as future therapeutics for the treatment of cyclin D1-addicted p53-expressing and p53-defective cancer types.	Lithocholic Acid	13-16	P53	Homo sapiens	129-132
34126912-2	2022	Among similar compounds, monastrol being the most prominent due to cell-permeant inhibitor of mitosis therefore, we investigated the new Pyrimidine-5-carbonitrile as a cytotoxic agent for p53 pathway.	monastrol	25-34	P53	Homo sapiens	188-191
28284059-0	2017	Reactivating p53 and Inducing Tumor Apoptosis (RITA) Enhances the Response of RITA-Sensitive Colorectal Cancer Cells to Chemotherapeutic Agents 5-Fluorouracil and Oxaliplatin.	Oxaliplatin	163-174	P53	Homo sapiens	13-16
34183962-10	2021	Piperine (20 muM) and cisplatin (5 muM) for 24 h induce apoptosis strongly through reduction of Bcl-2 and increase of caspase 3, p53, caspase 9, and Bax.	piperine	0-8	P53	Homo sapiens	129-132
34183962-11	2021	Conclusion: Piperine in combination with cisplatin could trigger p53-mediated apoptosis more effective than cisplatin alone in MCF-7 breast cancer cells, reducing the toxic dose of cisplatin used in cancer chemotherapy.	piperine	12-20	P53	Homo sapiens	65-68
28443465-9	2017	Furthermore, bauerenol-mediated S-phase arrest was associated with downregulation of cell cycle-rate-limiting factor (cyclin D1) and upregulation of cyclin-dependent kinase inhibitor p21 and tumor suppressor p53.	bauerenol	13-22	P53	Homo sapiens	208-211
35584569-1	2022	Cathepsin K inhibitor (odanacatib; ODN) and cathepsin K knockdown (siRNA) enhance oxaliplatin-induced apoptosis through p53-dependent Bax upregulation.	Oxaliplatin	82-93	P53	Homo sapiens	120-123
28212554-0	2017	AFB1 hepatocarcinogenesis is via lipid peroxidation that inhibits DNA repair, sensitizes mutation susceptibility and induces aldehyde-DNA adducts at p53 mutational hotspot codon 249.	Aldehydes	125-133	P53	Homo sapiens	149-152
35500691-7	2022	Both LCA conjugated micelles decreased lipogenic activity and increased expressions of Bax (1.3 fold) and p53 (1.2 fold) apoptotic genes.	Lithocholic Acid	5-8	P53	Homo sapiens	106-109
28435526-6	2017	Evaluating the impact of 7h on proteins targeted by RITA (p53, c-Myc, and Mcl-1) indicated that it acts via a different mechanism of action to that of RITA.	7,8-diacetoxy-3-(4-nitrophenyl)coumarin	25-27	P53	Homo sapiens	58-61
35579989-13	2022	In addition, we found that "crizotinib pretreatment", "liver metastasis", and "TP53 co-mutation" were individually associated with shorter PFS in alectinib treatment.	alectinib	146-155	P53	Homo sapiens	79-83
28382091-11	2017	RESULTS: FK866 treatment was able to increase p53 levels and acetylation, upregulate BAX and p21 expression, and induce apoptosis in MCF-7 cells.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	9-14	P53	Homo sapiens	46-49
35600955-8	2022	Results: The network pharmacology analysis showed that quercetin, luteolin, and kaempferol are the most significant active components in BHHD; STAT3, Jun, AKT1, MAPK3, MAPK1, and TP53 are the most critical drug targets; regulating hormones, reversing insulin (INS) resistance, exerting anti-inflammatory effects, and improving fertility might be the most important mechanisms of BHHD in the treatment of PCOS.	Luteolin	66-74	P53	Homo sapiens	179-183
28031409-3	2017	The current study demonstrates that, unlike cisplatin, platinum analogues oxaliplatin and DACH-diacetato-dichloro-Pt(IV) (DAP) strongly stabilize and activate p53v172F in resistant cells, as indicated by prolonged p53 half-life and transactivation of targets p21 (CDKN1A) and MDM2.	Oxaliplatin	74-85	P53	Homo sapiens	159-162
28031409-3	2017	The current study demonstrates that, unlike cisplatin, platinum analogues oxaliplatin and DACH-diacetato-dichloro-Pt(IV) (DAP) strongly stabilize and activate p53v172F in resistant cells, as indicated by prolonged p53 half-life and transactivation of targets p21 (CDKN1A) and MDM2.	Oxaliplatin	74-85	P53	Homo sapiens	214-217
35594815-5	2022	TP53 interacts with the majority of lung disease-related genes and regulates important and commonly occurring biological functions and pathways, including gland development, aging, reactive oxygen species metabolic process, the response to oxygen levels, and fluid shear stress, among others.	oxygen species	190-204	P53	Homo sapiens	0-4
27387714-0	2017	Polyvinyl pyrrolidone-coated silver nanoparticles in a human lung cancer cells: time- and dose-dependent influence over p53 and caspase-3 protein expression and epigenetic effects.	Povidone	0-21	P53	Homo sapiens	120-123
35511749-7	2022	One of the combinations, MK-1775 with Doxorubicin, significantly reduced tumor growth in a sporadic PDOX model (MPNST-SP-01) (sevenfold) and in an NF1-PDOX model (MPNST-NF1-09) (fourfold) and presented greater effects in TP53 mutated MPNST cell lines.	adavosertib	25-32	P53	Homo sapiens	221-225
35323988-2	2022	The curaxin CBL0137 has demonstrated promising antitumour activities in multiple cancers such as glioblastoma, acting through p53 activation, NF-kappaB inhibition and chromatin remodelling.	CBLC137	12-19	P53	Homo sapiens	126-129
35323988-3	2022	In the present study, it was revealed using Annexin-V/7-AAD apoptosis assays that CBL0137 has efficacy across several human acute leukaemia cell lines with wild-type TP53, but sensitivity is reduced in TP53-mutated subtypes.	CBLC137	82-89	P53	Homo sapiens	166-170
35323988-3	2022	In the present study, it was revealed using Annexin-V/7-AAD apoptosis assays that CBL0137 has efficacy across several human acute leukaemia cell lines with wild-type TP53, but sensitivity is reduced in TP53-mutated subtypes.	CBLC137	82-89	P53	Homo sapiens	202-206
27637603-0	2017	The Presence of Serum p53 Antibody Predicts the Pathological Tumor Response to Neoadjuvant Chemotherapy with Docetaxel, Cisplatin and Fluorouracil (DCF) in Esophageal Squamous Cell Carcinoma.	dcf	148-151	P53	Homo sapiens	22-25
35323988-4	2022	A heterozygous TP53 loss-of-function mutation in the KMT2A-AFF1 human RS4;11 cell line was generated, and it was demonstrated that heterozygous TP53 loss-of-function is sufficient to cause a significant reduction in CBL0137 sensitivity.	CBLC137	216-223	P53	Homo sapiens	144-148
35323988-5	2022	To the best of our knowledge, this is the first evidence to suggest a clinically significant role for functional p53 in the efficacy of CBL0137 in acute leukaemia.	CBLC137	136-143	P53	Homo sapiens	113-116
27637603-10	2017	CONCLUSIONS: The presence of serum p53 antibody can be used as a novel, noninvasive predictor of the pathological tumor response to NAC with DCF in ESCC patients.	dcf	141-144	P53	Homo sapiens	35-38
35323988-6	2022	Future CBL0137 clinical trials should include TP53 mutation screening, to establish the clinical relevance of TP53 mutations in CBL0137 efficacy.	CBLC137	128-135	P53	Homo sapiens	110-114
27871965-4	2017	In this review, we analytically summarize recent findings, which indicate that gain-of-function (GOF) mutant p53 proteins counteract the autophagic machinery by various molecular mechanisms including the regulation of AMPK and Akt/mTOR pathways, autophagy-related genes (ATGs), HIF-1alpha target genes, and the mitochondrial citrate carrier CIC.	Citric Acid	325-332	P53	Homo sapiens	109-112
35191521-8	2022	The present results suggested that AZD6738 enhanced the effect of 5-FU in p53-mutated colorectal cancer.	ceralasertib	35-42	P53	Homo sapiens	74-77
28954989-5	2017	Significant correlation of serum appearance of p53Abs with negative expression of ER (P = 0.011), the proportion of TNBC (P = 0.013), NG (P = 0.017), and TGS (P = 0.0005).	tnbc	116-120	P53	Homo sapiens	47-50
35388306-4	2022	The experiment found that Rg1 plays an antiaging role in reversing the SA-beta-gal staining associated with LiCl-induced hematopoietic stem cell senescence, the increase in p53 and p21 proteins, and sustained DNA damage.	Lithium Chloride	108-112	P53	Homo sapiens	173-176
35165262-0	2022	DNAJB8 in small extracellular vesicles promotes Oxaliplatin resistance through TP53/MDR1 pathway in colon cancer.	Oxaliplatin	48-59	P53	Homo sapiens	79-83
35165262-5	2022	On the mechanism, we demonstrated that DNAJB8 could interact with TP53 and inhibit the ubiquitination degradation of TP53, leading to MDR1 upregulation which promotes colon cancer L-OHP resistance.	Oxaliplatin	180-185	P53	Homo sapiens	66-70
35165262-5	2022	On the mechanism, we demonstrated that DNAJB8 could interact with TP53 and inhibit the ubiquitination degradation of TP53, leading to MDR1 upregulation which promotes colon cancer L-OHP resistance.	Oxaliplatin	180-185	P53	Homo sapiens	117-121
28194257-4	2017	p53 has been found to regulate multiple biochemical processes such as glycolysis, oxidative phosphorylation, lipolysis, lipogenesis, beta-oxidation, gluconeogenesis, and glycogen synthesis.	Glycogen	170-178	P53	Homo sapiens	0-3
35056723-8	2022	The molecular mechanism of action of low-dose 7HF in TNBC cells primarily involved G2/M-phase arrest through upregulation of the expression of Bub3, cyclin B1, phosphorylated Cdk1 (Tyr 15) and p53-independent p21.	7alpha-hydroxyfrullanolide	46-49	P53	Homo sapiens	193-196
35053438-0	2022	The Antitumor Effect of Caffeic Acid Phenethyl Ester by Downregulating Mucosa-Associated Lymphoid Tissue 1 via AR/p53/NF-kappaB Signaling in Prostate Carcinoma Cells.	caffeic acid phenethyl ester	24-52	P53	Homo sapiens	114-117
35053438-4	2022	In p53- and androgen receptor (AR)-positive prostate carcinoma cells, CAPE downregulated AR and MALT1 expression but enhanced that of p53, thus decreasing androgen-induced activation of MALT1 and prostate-specific antigen expressions.	caffeic acid phenethyl ester	70-74	P53	Homo sapiens	3-6
35053438-4	2022	In p53- and androgen receptor (AR)-positive prostate carcinoma cells, CAPE downregulated AR and MALT1 expression but enhanced that of p53, thus decreasing androgen-induced activation of MALT1 and prostate-specific antigen expressions.	caffeic acid phenethyl ester	70-74	P53	Homo sapiens	134-137
35053438-6	2022	CAPE downregulated MALT1 expression and thus inhibited NF-kappaB activity in p53- and AR-negative prostate carcinoma PC-3 cells, eventually reducing cell proliferation, invasion, and tumor growth in vitro and in vivo.	caffeic acid phenethyl ester	0-4	P53	Homo sapiens	77-80
28144352-0	2016	Synthesis of spiro[isoindole-1,5"-isoxazolidin]-3(2H)-ones as potential inhibitors of the MDM2-p53 interaction.	spiro[isoindole-1,5"-isoxazolidin]-3(2h)-ones	13-58	P53	Homo sapiens	95-98
35053438-8	2022	Our findings verify that CAPE is an effective antitumor agent for human androgen-dependent and -independent prostate carcinoma cells in vitro and in vivo through the inhibition of MALT1 expression via the AR/p53/NF-kappaB signaling pathways.	caffeic acid phenethyl ester	25-29	P53	Homo sapiens	208-211
27825136-9	2016	Importantly, these results on Trp53-null and our prior studies on DMBA-induced mammary tumorigenesis demonstrate a pubertal window of susceptibility to the promotional effects of HFD, indicating the potential of early life dietary intervention to reduce breast cancer risk.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	66-70	P53	Homo sapiens	30-35
27693049-6	2016	Based on in vivo studies, the growth of breast tumor and expression of CD31, Bcl-2 and nonfunctional p53 were inhibited more effectively by ES-R than by ES-Zn.	es-zn	153-158	P53	Homo sapiens	101-104
27748837-6	2016	This study demonstrated that EMMQ induced DNA damage by activating p53 and gamma-H2AX and cell arrest by suppressing cyclin D1 and CDK2.	3-((7-ethyl-1H-indol-3-yl)-methyl)-2-methylquinoline	29-33	P53	Homo sapiens	67-70
27748837-10	2016	In brief, the study demonstrates that the effectiveness of EMMQ accentuated apoptosis of hepatocarcinoma cells by activating p53.	3-((7-ethyl-1H-indol-3-yl)-methyl)-2-methylquinoline	59-63	P53	Homo sapiens	125-128
27693124-10	2016	There were significant decreases in the expression levels of p53, p27, CDK4, cyclinD1 and PCNA in HSFs treated with rhEndostatin.	rhendostatin	116-128	P53	Homo sapiens	61-64
27122200-2	2016	In this work, p53/BPEI-beta-CD/AD-dox complex was fabricated and employed to investigate the interaction manner between p53 and doxorubicin (Dox).	ad-dox	31-37	P53	Homo sapiens	14-17
27122200-2	2016	In this work, p53/BPEI-beta-CD/AD-dox complex was fabricated and employed to investigate the interaction manner between p53 and doxorubicin (Dox).	ad-dox	31-37	P53	Homo sapiens	120-123
27434219-4	2016	Knockdown of DDT and MIF in PANC-1 cells cooperatively inhibited ERK1/2 and AKT phosphorylation, increased p53 expression, and reduced cell proliferation, invasion and tumor formation.	DDT	13-16	P53	Homo sapiens	107-110
27791175-0	2016	Ironing out how p53 regulates ferroptosis.	ironing	0-7	P53	Homo sapiens	16-19
27751972-7	2016	The serum anti-p53 Ab level was low in healthy volunteers while it was higher in both lung cancer patients and NAPN patients (p&lt;0.05).	napn	111-115	P53	Homo sapiens	15-18
27258787-0	2016	Reactivation of mutant p53 by a dietary-related compound phenethyl isothiocyanate inhibits tumor growth.	phenethyl isothiocyanate	57-81	P53	Homo sapiens	23-26
27258787-6	2016	In this study, we show that cruciferous-vegetable-derived phenethyl isothiocyanate (PEITC) can reactivate p53 mutant under in vitro and in vivo conditions, revealing a new mechanism of action for a dietary-related compound.	phenethyl isothiocyanate	58-82	P53	Homo sapiens	106-109
27258787-6	2016	In this study, we show that cruciferous-vegetable-derived phenethyl isothiocyanate (PEITC) can reactivate p53 mutant under in vitro and in vivo conditions, revealing a new mechanism of action for a dietary-related compound.	phenethyl isothiocyanate	84-89	P53	Homo sapiens	106-109
27258787-8	2016	Mechanistic studies revealed that PEITC induces apoptosis in a p53(R175) mutant-dependent manner by restoring p53 WT conformation and transactivation functions.	phenethyl isothiocyanate	34-39	P53	Homo sapiens	63-66
27258787-8	2016	Mechanistic studies revealed that PEITC induces apoptosis in a p53(R175) mutant-dependent manner by restoring p53 WT conformation and transactivation functions.	phenethyl isothiocyanate	34-39	P53	Homo sapiens	110-113
27258787-9	2016	Accordingly, in PEITC-treated cells the reactivated p53(R175) mutant induces apoptosis by activating canonical WT p53 targets, inducing a delay in S and G2/M phase, and by phosphorylating ATM/CHK2.	phenethyl isothiocyanate	16-21	P53	Homo sapiens	52-55
27258787-9	2016	Accordingly, in PEITC-treated cells the reactivated p53(R175) mutant induces apoptosis by activating canonical WT p53 targets, inducing a delay in S and G2/M phase, and by phosphorylating ATM/CHK2.	phenethyl isothiocyanate	16-21	P53	Homo sapiens	114-117
27258787-12	2016	PEITC-induced reactivation of p53(R175) and its subsequent sensitivity to the degradation pathways likely contribute to its anticancer activities.	phenethyl isothiocyanate	0-5	P53	Homo sapiens	30-33
27633119-5	2016	Furthermore, we observed that the generation of reactive oxygen species (ROS) and the phosphorylation of Jun N-terminal kinase (JNK), p53, caspase-9 and -3 were induced in the polysaccharide-treated MKN45 cells.	Polysaccharides	176-190	P53	Homo sapiens	134-137
27633119-7	2016	Finally, we found that pretreatment with NAC prevented the JNK, p53, caspase-9 and -3 protein phosphorylation induced by the polysaccharide, however, pretreatment with SP600125 did not affect the generation of ROS, suggesting that ROS is upstream of JNK.	Polysaccharides	125-139	P53	Homo sapiens	64-67
27238606-1	2016	BACKGROUND: MK-8242 is an inhibitor of MDM2 that stabilizes the tumor suppressor TP53 and induces growth arrest or apoptosis downstream of TP53 induction.	mk-8242	12-19	P53	Homo sapiens	81-85
27238606-1	2016	BACKGROUND: MK-8242 is an inhibitor of MDM2 that stabilizes the tumor suppressor TP53 and induces growth arrest or apoptosis downstream of TP53 induction.	mk-8242	12-19	P53	Homo sapiens	139-143
27238606-3	2016	RESULTS: The median IC50 for MK-8242 was 0.07 muM for TP53 wild-type cell lines versus &gt;10 muM for TP53 mutant cell lines.	mk-8242	29-36	P53	Homo sapiens	54-58
27238606-4	2016	MK-8242 induced a twofold or greater delay in time to event in 10 of 17 (59%) of TP53 wild-type solid tumor xenografts, excluding osteosarcoma xenografts that have very low TP53 expression.	mk-8242	0-7	P53	Homo sapiens	81-85
27238606-4	2016	MK-8242 induced a twofold or greater delay in time to event in 10 of 17 (59%) of TP53 wild-type solid tumor xenografts, excluding osteosarcoma xenografts that have very low TP53 expression.	mk-8242	0-7	P53	Homo sapiens	173-177
27238606-8	2016	The expected pharmacodynamic responses to TP53 activation were observed in TP53 wild-type models treated with MK-8242.	mk-8242	110-117	P53	Homo sapiens	42-46
27238606-8	2016	The expected pharmacodynamic responses to TP53 activation were observed in TP53 wild-type models treated with MK-8242.	mk-8242	110-117	P53	Homo sapiens	75-79
27609465-0	2016	Upregulation of CYP2S1 by oxaliplatin is associated with p53 status in colorectal cancer cell lines.	Oxaliplatin	26-37	P53	Homo sapiens	57-60
27609465-3	2016	In the present study, oxaliplatin was found to strongly inhibit the growth of HCT116 cells harboring wild-type p53 but to only weakly inhibit SW480 cells, HT29 cells or p53-/- HCT116 cells, which all lack p53 expression.	Oxaliplatin	22-33	P53	Homo sapiens	111-114
27609465-3	2016	In the present study, oxaliplatin was found to strongly inhibit the growth of HCT116 cells harboring wild-type p53 but to only weakly inhibit SW480 cells, HT29 cells or p53-/- HCT116 cells, which all lack p53 expression.	Oxaliplatin	22-33	P53	Homo sapiens	169-172
27609465-3	2016	In the present study, oxaliplatin was found to strongly inhibit the growth of HCT116 cells harboring wild-type p53 but to only weakly inhibit SW480 cells, HT29 cells or p53-/- HCT116 cells, which all lack p53 expression.	Oxaliplatin	22-33	P53	Homo sapiens	169-172
27609465-4	2016	Administration of oxaliplatin significantly induced p53 accumulation and enhanced expression of CYP2S1 in HCT116 cells with wild-type p53.	Oxaliplatin	18-29	P53	Homo sapiens	52-55
27609465-4	2016	Administration of oxaliplatin significantly induced p53 accumulation and enhanced expression of CYP2S1 in HCT116 cells with wild-type p53.	Oxaliplatin	18-29	P53	Homo sapiens	134-137
27609465-6	2016	Interestingly, enzyme immunoassays, TOPFlash/FOPFlash reporter activity assays and western blotting analysis demonstrated oxaliplatin-mediated downregulation of PGE2 and Wnt/beta-catenin signaling in a manner dependent on p53.	Oxaliplatin	122-133	P53	Homo sapiens	222-225
27609465-8	2016	These results suggest that oxaliplatin exerts its inhibitory effects in human CRC cells via upregulation of CYP2S1 expression in a p53-dependent manner.	Oxaliplatin	27-38	P53	Homo sapiens	131-134
25268149-9	2016	The level of the tumor suppressor protein p53 in HeLa cells increased significantly upon treatment with free epirubicin, but remained relatively unchanged when cells were treated with equivalent dose of nanoparticle-loaded drug, suggesting a possible shift from p53-dependent DNA/RNA intercalation-based induction of cytotoxicity by free epirubicin to a caspase 3-induced cell death by the epirubicin-loaded PBCA formulation.	Enbucrilate	408-412	P53	Homo sapiens	42-45
27288242-11	2016	Besides, sunitinib boosted cortical and hippocampal p53 and executioner caspase-3 and decreased nuclear factor kappa B and Bcl-2 levels promoting apoptotic cell death.	Sunitinib	9-18	P53	Homo sapiens	52-55
27485825-9	2016	Further analysis indicated that co-expression of VHL and P53 inhibited cell proliferation by completely inhibiting the cell cycle at the G0/G1 phase, and promoted apoptosis following treatment with ADM or sunitinib.	Sunitinib	205-214	P53	Homo sapiens	57-60
27576884-8	2016	However, the p53 overexpression was significantly associated with decreased CSS (P = .028).	thiocysteine	76-79	P53	Homo sapiens	13-16
27576884-11	2016	However, only p53 overexpression was associated with predicting CSS independently of tumor stage.&amp;nbsp.	thiocysteine	64-67	P53	Homo sapiens	14-17
27374783-5	2016	In addition, the good antitumor effects of CHO-PGEA and PI-PGEA were confirmed with suppressor tumor gene p53 systems in vitro and in vivo.	pgea	59-63	P53	Homo sapiens	106-109
27368132-5	2016	Furthermore, it was shown that a combination of D5D knockdown along with DGLA treatment could also significantly sensitize BxPC-3 cells to various chemotherapy drugs, likely via a p53-independent pathway through downregulating of anti-apoptotic proteins (e.g., Bcl-2) and activating pro-apoptotic proteins (e.g., caspase 3, -9).	8,11,14-Eicosatrienoic Acid	73-77	P53	Homo sapiens	180-183
27278810-3	2016	PG inhibited the growth of HPF cells with an IC50 of ~50-100 microM at 24 h. PG induced a G1 phase arrest of the cell cycle and also triggered cell death accompanied by the loss of mitochondrial membrane potential (MMP;  psim), Bcl-2 decrease, p53 increase and the activation of caspase-3.	Pyrogallol	0-2	P53	Homo sapiens	244-247
27278810-3	2016	PG inhibited the growth of HPF cells with an IC50 of ~50-100 microM at 24 h. PG induced a G1 phase arrest of the cell cycle and also triggered cell death accompanied by the loss of mitochondrial membrane potential (MMP;  psim), Bcl-2 decrease, p53 increase and the activation of caspase-3.	Pyrogallol	77-79	P53	Homo sapiens	244-247
27464624-13	2016	However, BF + GCV only induced apoptosis via Fas/FasL signal pathway accompanied with increased P53 expression.	Ganciclovir	14-17	P53	Homo sapiens	96-99
27317433-8	2016	In addition a novel finding is represented by the demonstration that pre-treatment with vitamin D3 is also able to significantly counteract tumoral biomarkers activation, such as p53, pan-Ras, Ki67 and c-Myc, and consequently the catalytic iron-induced cellular injury.	Cholecalciferol	88-98	P53	Homo sapiens	179-182
26975930-0	2016	Wee1 Kinase Inhibitor AZD1775 Radiosensitizes Hepatocellular Carcinoma Regardless of TP53 Mutational Status Through Induction of Replication Stress.	adavosertib	22-29	P53	Homo sapiens	85-89
27017265-10	2016	Therefore, this class of benzimidazole-2-subsituted phenyl or pyridine propyl ketene derivatives represents a promising lead structure for the development of possible p53-MDM2 inhibitors as new antitumour agents.	benzimidazole 2	25-40	P53	Homo sapiens	167-170
27017265-10	2016	Therefore, this class of benzimidazole-2-subsituted phenyl or pyridine propyl ketene derivatives represents a promising lead structure for the development of possible p53-MDM2 inhibitors as new antitumour agents.	phenyl or pyridine propyl ketene	52-84	P53	Homo sapiens	167-170
27132887-4	2016	We report here that a compound cocktail containing cyclic pifithrin-a (a P53 inhibitor), A-83-01, CHIR99021, thiazovivin, NaB, and PD0325901 significantly improves the reprogramming efficiency (170-fold more) for hUCs.	QB 102	51-69	P53	Homo sapiens	73-76
26965143-5	2016	Specifically, either inhibition of ATM with caffeine or mutation of p53 (serine 15 to alanine) restored MDM2-dependent polyubiquitination of otherwise monoubiquitinated mutant p53.	Caffeine	44-52	P53	Homo sapiens	176-179
26965143-6	2016	Caffeine treatment rescued MDM2-dependent proteasome degradation of mutant p53 in cells exhibiting active DNA damage signaling, and ATM knockdown phenocopied the caffeine effect.	Caffeine	0-8	P53	Homo sapiens	75-78
26883409-0	2016	Au nanoparticle decorated graphene nanosheets for electrochemical immunosensing of p53 antibodies for cancer prognosis.	Gold	0-2	P53	Homo sapiens	83-86
26883409-4	2016	The Au NP/ERGO hybrid interface provides a large surface area for the effective immobilization of p53 antigens, as well as it ascertains the bioactivity and stability of immobilized p53 antigens.	Gold	4-6	P53	Homo sapiens	98-101
26883409-4	2016	The Au NP/ERGO hybrid interface provides a large surface area for the effective immobilization of p53 antigens, as well as it ascertains the bioactivity and stability of immobilized p53 antigens.	Gold	4-6	P53	Homo sapiens	182-185
27077811-6	2016	We have found that a treatment with a low dose (75 nM) of MK-1775, a recently described specific chemical inhibitor of Wee1, decreases CDDP-induced H2AX phosphorylation in p53-negative cells and enhances the Wip1-sensitization of p53-negative tumors.	adavosertib	58-65	P53	Homo sapiens	172-175
27077811-6	2016	We have found that a treatment with a low dose (75 nM) of MK-1775, a recently described specific chemical inhibitor of Wee1, decreases CDDP-induced H2AX phosphorylation in p53-negative cells and enhances the Wip1-sensitization of p53-negative tumors.	adavosertib	58-65	P53	Homo sapiens	230-233
26934443-0	2016	Exogenous p53 and ASPP2 expression enhances rAdV-TK/ GCV-induced death in hepatocellular carcinoma cells lacking functional p53.	Ganciclovir	53-56	P53	Homo sapiens	10-13
26934443-2	2016	We hypothesize that the efficacy of HSV-TK/GCV therapy is at least partially dependent on p53 status in hepatocellular carcinoma (HCC) patients.	Ganciclovir	43-46	P53	Homo sapiens	90-93
26934443-6	2016	Similarly, ASPP2 reduced survival in rAdV-TK/GCV-treated primary HCC cells expressing p53 wild-type but not a p53 R249S mutant.	Ganciclovir	45-48	P53	Homo sapiens	86-89
26934443-7	2016	Mutated p53 was unable to bind to ASPP2, suggesting that the increase in rAdV-TK/GCV-induced cell death resulting from ASPP2 overexpression was dependent on its interaction with p53.	Ganciclovir	81-84	P53	Homo sapiens	8-11
26934443-7	2016	Mutated p53 was unable to bind to ASPP2, suggesting that the increase in rAdV-TK/GCV-induced cell death resulting from ASPP2 overexpression was dependent on its interaction with p53.	Ganciclovir	81-84	P53	Homo sapiens	178-181
25840959-9	2016	CONCLUSIONS: Lectin microarrays can be used to very accurately quantify the reaction of glycans with tumor tissues, and such profiles may represent the specific phenotypes, including N+ status, histological type, or p53 mutation of AGC.	Polysaccharides	88-95	P53	Homo sapiens	216-219
27108384-4	2016	RESULTS: MDM2 inhibition by MI-219 resulted in dose- and time-dependent p53 activation and decreased clonogenic cell survival after radiation in a p53-dependent manner.	MI-219	28-34	P53	Homo sapiens	72-75
27108384-4	2016	RESULTS: MDM2 inhibition by MI-219 resulted in dose- and time-dependent p53 activation and decreased clonogenic cell survival after radiation in a p53-dependent manner.	MI-219	28-34	P53	Homo sapiens	147-150
27108384-6	2016	Similarly, treatment with MI-219 enhanced response to antiandrogen therapy via a p53-dependent increase in apoptotic cell death.	MI-219	26-32	P53	Homo sapiens	81-84
26883108-7	2016	In addition, combined treatment with GSK2830371 and doxorubicin or nutlin-3 potentiated cell death through a strong induction of p53 pathway and activation of caspase 9.	nutlin	67-73	P53	Homo sapiens	129-132
26965928-12	2016	Moreover, deferasirox induced G1 arrest; upregulated p21, p27, and p53 expression; and downregulated cyclin D1, cyclin B, and CDK4 expression.	Deferasirox	10-21	P53	Homo sapiens	67-70
26775629-4	2016	METHODS: The expression, phosphorylation and subcellular localization of p53 were detected by real-time PCR, luciferase reporter assay, cycloheximide chase analysis, immunoblotting and immunocytochemistry.	Cycloheximide	136-149	P53	Homo sapiens	73-76
26668309-0	2016	A Novel Naphthalimide Compound Restores p53 Function in Non-small Cell Lung Cancer by Reorganizing the Bak Bcl-xl Complex and Triggering Transcriptional Regulation.	Naphthalimides	8-21	P53	Homo sapiens	40-43
26668309-8	2016	This work provided new insights into the molecular interactions and anticancer mechanisms of phospho-p53-dependent naphthalimide compounds.	Naphthalimides	115-128	P53	Homo sapiens	101-104
26338274-5	2016	Here we demonstrate that the pan-PI3K/mammalian target of rapamycin inhibitor SAR245409 (voxtalisib/XL765) was more pro-apoptotic to CLL cells--irrespective of their ATM/p53 status--than PI3Kalpha or PI3Kdelta isoform selective inhibitors.	XL765	78-87	P53	Homo sapiens	170-173
26718026-0	2016	Anticancer effect of xanthohumol induces growth inhibition and apoptosis of human liver cancer through NF-kappaB/p53-apoptosis signaling pathway.	xanthohumol	21-32	P53	Homo sapiens	113-116
26718026-2	2016	We investigate whether the anticancer effect of xanthohumol induces growth inhibition and apoptosis of human liver cancer through NF-kappaB/p53-apoptosis signaling pathway.	xanthohumol	48-59	P53	Homo sapiens	140-143
26718026-5	2016	In addition, 48-h treatment with xanthohumol suppressed NF-kappaB expression and promoted p53, cleaved PARP, AIF and cytochrome c expression and downregulated XIAP and Bcl-2/Bax expression in human liver cancer HepG2 cells.	xanthohumol	33-44	P53	Homo sapiens	90-93
26718026-6	2016	Therefore, the anticancer effect of xanthohumol induces growth inhibition and apoptosis of human liver cancer through the NF-kappaB/p53-apoptosis signaling pathway.	xanthohumol	36-47	P53	Homo sapiens	132-135
26696550-0	2016	TP53 Codon 72 Polymorphism Predicts Efficacy of Paclitaxel Plus Capecitabine Chemotherapy in Advanced Gastric Cancer Patients.	Capecitabine	64-76	P53	Homo sapiens	0-4
26696550-1	2016	BACKGROUND AND AIMS: The present study analyzed the relationship between TP53 codon 72 polymorphisms and the clinical outcome of advanced gastric cancer patients receiving capecitabine plus paclitaxel chemotherapy.	Capecitabine	172-184	P53	Homo sapiens	73-77
26696550-5	2016	RESULTS: The Pro/Pro genotypes of TP53 codon 72 were significantly correlated with a lower response rate to capecitabine plus paclitaxel chemotherapy in patients with gastric cancer when compared to the Arg/Arg genotype (30.6 vs. 63.2%, p value 0.000).	Capecitabine	108-120	P53	Homo sapiens	34-38
26471831-3	2016	METHODS: Potentiation of mTOR inhibitor cytotoxicity by the Chk1 inhibitor V158411 was determined in p53 mutant colon cancer cells.	V158411	75-82	P53	Homo sapiens	101-104
26471831-5	2016	RESULTS: mTOR inhibitors AZD8055, RAD-001, rapamycin and BEZ235 induced synergistic cytotoxicity with the Chk1 inhibitor V158411 in p53 mutant colon cancer cells.	V158411	121-128	P53	Homo sapiens	132-135
27098147-10	2016	The observed elevated expression of p53 and p16 by RTX may contribute to the reduction of cyclin A/CDK2.	raltitrexed	51-54	P53	Homo sapiens	36-39
26330291-7	2015	We found that FK866 induced cell senescence and diminished cellular NAD(+) levels and SIRT1 activity (detected by acetylation of p53), and these effects were dramatically antagonized by co-treatment with nicotinic acid, nicotinamide, or NAD(+).	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	14-19	P53	Homo sapiens	129-132
26475964-11	2015	Prenylchalcone 2 represents a starting basis for the design of new p53-MDM2 interaction inhibitors with improved antitumor properties.	prenylchalcone	0-14	P53	Homo sapiens	67-70
26521794-0	2015	Caffeine Suppresses Apoptosis of Bladder Cancer RT4 Cells in Response to Ionizing Radiation by Inhibiting Ataxia Telangiectasia Mutated-Chk2-p53 Axis.	Caffeine	0-8	P53	Homo sapiens	141-144
26521794-11	2015	RT-PCR indicated caffeine also attenuated transactivation of p53 and p53-inducible genes.	Caffeine	17-25	P53	Homo sapiens	61-64
26521794-11	2015	RT-PCR indicated caffeine also attenuated transactivation of p53 and p53-inducible genes.	Caffeine	17-25	P53	Homo sapiens	69-72
26521794-13	2015	CONCLUSION: Caffeine may inhibit IR-related apoptosis of bladder cancer RT4 cells by suppressing activation of the ATM-Chk2-p53-Puma axis.	Caffeine	12-20	P53	Homo sapiens	124-127
26456774-6	2015	DHT inhibited resveratrol-stimulated phosphorylation of Ser-15 of p53 in a concentration-dependent manner.	Dihydrotestosterone	0-3	P53	Homo sapiens	66-69
26456774-8	2015	DHT inhibited resveratrol-induced nuclear complex of p53-COX-2 formation which is required p53-dependent apoptosis.	Dihydrotestosterone	0-3	P53	Homo sapiens	53-56
26456774-8	2015	DHT inhibited resveratrol-induced nuclear complex of p53-COX-2 formation which is required p53-dependent apoptosis.	Dihydrotestosterone	0-3	P53	Homo sapiens	91-94
26456774-9	2015	ChIP studies of COX-2/p53 binding to DNA and expression of p53-responsive genes indicated that DHT inhibited resveratrol-induced p53-directed transcriptional activity.	Dihydrotestosterone	95-98	P53	Homo sapiens	22-25
26456774-9	2015	ChIP studies of COX-2/p53 binding to DNA and expression of p53-responsive genes indicated that DHT inhibited resveratrol-induced p53-directed transcriptional activity.	Dihydrotestosterone	95-98	P53	Homo sapiens	59-62
26456774-9	2015	ChIP studies of COX-2/p53 binding to DNA and expression of p53-responsive genes indicated that DHT inhibited resveratrol-induced p53-directed transcriptional activity.	Dihydrotestosterone	95-98	P53	Homo sapiens	59-62
26456774-10	2015	In addition, DHT did inhibit resveratrol-induced COX-2/p53-dependent gene expression.	Dihydrotestosterone	13-16	P53	Homo sapiens	55-58
26456774-11	2015	These results suggest that DHT inhibits p53-dependent apoptosis in breast cancer cells by interfering with nuclear COX-2 accumulation which is essential for stimulation of apoptotic pathways.	Dihydrotestosterone	27-30	P53	Homo sapiens	40-43
25944179-1	2015	ZMC1 {azetidinecarbothioic acid, [1-(2-pyridinyl) ethylidene] hydrazide} is a lead compound being developed as one of the first mutant p53 targeted anti-cancer drugs.	azetidinecarbothioic acid	6-31	P53	Homo sapiens	135-138
26386653-7	2015	We also found that under serum deprivation condition, leptin decreases p53 levels and the inhibitory leptin effect is lost when cells were pretreated with 50 muM PD98059 or 10 muM LY29004; or were transfected with dominant negative mutants of intermediates of these pathways, suggesting that MAPK and PI3K signaling pathways are necessaries for leptin action.	ly29004	180-187	P53	Homo sapiens	71-74
25716429-4	2015	Among them, compound 4 (quercetagetin 3,4"-dimethyl ether) showed inhibitory activity against cellular senescence, which was confirmed by senescence-associated beta-galactosidase (SA-beta-gal) activity, p53 and p21 protein levels, and intracellular ROS levels.	quercetagetin 3,4'-dimethyl ether	24-57	P53	Homo sapiens	203-206
26208523-0	2015	The 1,2-Diaminocyclohexane Carrier Ligand in Oxaliplatin Induces p53-Dependent Transcriptional Repression of Factors Involved in Thymidylate Biosynthesis.	Oxaliplatin	45-56	P53	Homo sapiens	65-68
26208523-3	2015	In the p53-proficient colorectal cancer cell line HCT116, oxaliplatin represses the expression of deoxyuridine triphosphatase (dUTPase), a ubiquitous pyrophosphatase that catalyzes the hydrolysis of dUTP to dUMP and inhibits dUTP-mediated cytotoxicity.	Oxaliplatin	58-69	P53	Homo sapiens	7-10
26091798-7	2015	The results show that short-term exposure of BEAS-2B cells to arsenic or Cr(VI) was able to activate both p53 and p21.	chromium hexavalent ion	73-79	P53	Homo sapiens	106-109
26225749-5	2015	Treatment of MCF-7 cells with metformin or phenformin induced increase in p53 protein levels and the transcription of its downstream target genes, Bax and p21, in a dose-dependent manner.	Phenformin	43-53	P53	Homo sapiens	74-77
26225749-7	2015	The present study showed that p53 is required for metformin or phenformin-induced growth inhibition, senescence and apoptosis in breast cancer cells.	Phenformin	63-73	P53	Homo sapiens	30-33
26194899-4	2015	In further experiments, p53 protein expression was increased, and H2AX phosphorylation and p21 protein expression were induced after treatment with 3EZ, 20Ac-ingenol.	20ac-ingenol	153-165	P53	Homo sapiens	24-27
25407396-9	2015	The comparison of the different ligands demonstrates that stictic acid has a great potential as a p53 activator in terms of less adverse effects although it has poorer pharmacokinetic properties.	stictic acid	58-70	P53	Homo sapiens	98-101
25917567-0	2015	FLLL12 induces apoptosis in lung cancer cells through a p53/p73-independent but death receptor 5-dependent pathway.	flll12	0-6	P53	Homo sapiens	56-59
26086967-4	2015	APR-246 is a prodrug that is converted to the active compound methylene quinuclidinone (MQ), a Michael acceptor that binds to cysteine residues in mutant p53 and restores its wild-type conformation.	SCHEMBL4738034	62-86	P53	Homo sapiens	154-157
25651236-0	2015	Apoptosis of Bel-7402 human hepatoma cells induced by a ruthenium(II) complex coordinated by cordycepin through the p53 pathway.	Ruthenium(II)	56-69	P53	Homo sapiens	116-119
25981919-13	2015	CONCLUSION: The current findings strongly indicate that both CTS and DTS could inhibit the growth of apoptosis-resistant colon cancer cells through induction of autophagic cell death and p53-independent cytotoxicity.	dibenzyl trisulfide	69-72	P53	Homo sapiens	187-190
26222594-2	2015	The obtained xPolyR8-KLA(TPP) could not only initiate tumor cell apoptosis by C-KLA(TPP) with improved cell penetrating ability, but was also capable of loading and delivering the tumor cell suppressing p53 gene.	xpolyr8-kla	13-24	P53	Homo sapiens	203-206
26222594-4	2015	By regulating both the intrinsic and extrinsic apoptotic pathways, the xPolyR8-KLA(TPP)/p53 complex performed as a synergetic system and lead to a more efficient cancer cell death.	xpolyr8-kla	71-82	P53	Homo sapiens	88-91
25875797-0	2015	Primary and liver metastasis-derived cell lines from KrasG12D; Trp53R172H; Pdx-1 Cre animals undergo apoptosis in response to triptolide.	triptolide	126-136	P53	Homo sapiens	63-68
25914461-8	2015	Alternol activated caspase 3, upregulated p53 and p21 expression, and downregulated Bcl-2 expression in a dose-dependent manner.	Alternol	0-8	P53	Homo sapiens	42-45
25534115-0	2015	ASPP2 enhances oxaliplatin (L-OHP)-induced colorectal cancer cell apoptosis in a p53-independent manner by inhibiting cell autophagy.	Oxaliplatin	28-33	P53	Homo sapiens	81-84
25534115-4	2015	In this study, ASPP2 was found to enhance L-OHP-induced apoptosis in HCT116 p53(-/-) cells in a p53-independent manner.	Oxaliplatin	42-47	P53	Homo sapiens	76-79
25922718-5	2015	RESULTS: We found that CK could significantly enhance cisplatin-induced p53 expression and activity in two lung cancer cell lines, H460 and A549.	ginsenoside M1	23-25	P53	Homo sapiens	72-75
26312880-8	2015	FINDINGS: AZD6738 provided potent and specific inhibition of ATR signalling with compensatory activation of ATM/p53 pathway in cycling CLL cells in the presence of genotoxic stress.	ceralasertib	10-17	P53	Homo sapiens	112-115
26312880-9	2015	In p53 or ATM defective cells, AZD6738 treatment resulted in replication fork stalls and accumulation of unrepaired DNA damage, as evidenced by gammaH2AX and 53BP1 foci formation, which was carried through into mitosis, resulting in cell death by mitotic catastrophe.	ceralasertib	31-38	P53	Homo sapiens	3-6
26312880-10	2015	AZD6738 displayed selective cytotoxicity towards ATM or p53 deficient CLL cells, and was highly synergistic in combination with cytotoxic chemotherapy.	ceralasertib	0-7	P53	Homo sapiens	56-59
26312880-11	2015	This finding was confirmed in primary xenograft models of DDR-defective CLL, where treatment with AZD6738 resulted in decreased tumour load and selective reduction of CLL subclones with ATM or TP53 alterations.	ceralasertib	98-105	P53	Homo sapiens	193-197
25932127-9	2015	On the molecular level, tanshinone IIA administration altered the expression of apoptosis-related proteins such as p53, Bax, Bcl-2 and cyto C. In addition, MGO treatment remarkably increased the phosphorylation of MAPK family including p38, JNK and ERK.	Pyruvaldehyde	156-159	P53	Homo sapiens	115-118
25619394-8	2015	Addition of the p53 inhibitor cyclic PFT-alpha (5, 25 mumol/L) in HepG2 cells dose-dependently enhanced the metabolism of DEM and TEST, whereas addition of the p53 activator NSC 66811 (3, 10, 25 mumol/L) dose-dependently inhibited the metabolism.	QB 102	30-46	P53	Homo sapiens	16-19
25311224-7	2015	The resistant profile caused by p53 defect also caused a cell type-specific response to PA pool depletion and SSAT overexpression.	Polyamines	88-90	P53	Homo sapiens	32-35
25550548-0	2015	Influence of p53 status on the effects of boron neutron capture therapy in glioblastoma.	Boron	42-47	P53	Homo sapiens	13-16
25550548-2	2015	We studied the relationship between the p53 gene and the biological effects of boron neutron capture therapy (BNCT).	Boron	79-84	P53	Homo sapiens	40-43
25603814-0	2015	Growth suppression and cell death by pyridoxal is dependent on p53 in the human breast cancer cell line MCF-7.	Pyridoxal	37-46	P53	Homo sapiens	63-66
25603814-7	2015	The cell growth suppression by 0.5 mM PL did not occur when p53 expression was knocked down using siRNA.	Pyridoxal	38-40	P53	Homo sapiens	60-63
25603814-8	2015	Together, these data suggest that PL accumulate p53 and PL-induced cell growth suppression is dependent on p53 in MCF-7 breast cancer cells.	Pyridoxal	34-36	P53	Homo sapiens	48-51
25603814-8	2015	Together, these data suggest that PL accumulate p53 and PL-induced cell growth suppression is dependent on p53 in MCF-7 breast cancer cells.	Pyridoxal	34-36	P53	Homo sapiens	107-110
25603814-8	2015	Together, these data suggest that PL accumulate p53 and PL-induced cell growth suppression is dependent on p53 in MCF-7 breast cancer cells.	Pyridoxal	56-58	P53	Homo sapiens	107-110
25821561-7	2015	Treatment of A375 and Hs294t cells with GTPs resulted in a decrease in the levels of cyclins and cyclin dependent kinases of G1 phase of cell cycle whereas upregulated the levels of tumor suppressor proteins (Cip1/WAF1/p21, p16 and p53).	gtps	40-44	P53	Homo sapiens	232-235
25179905-5	2014	Following 2-MeO-E2 treatment, only HCT116 (p53(+/+)) cells exhibited an enhancement in the levels of p53, p-p53 (Ser-15), p21(WAF1/CIP1), and Bax; however, the Bak level remained relatively constant in both cell types, and the Bcl-2 level decreased only in HCT116 (p53(+/+)) cells.	2-meo	10-15	P53	Homo sapiens	43-46
25179905-5	2014	Following 2-MeO-E2 treatment, only HCT116 (p53(+/+)) cells exhibited an enhancement in the levels of p53, p-p53 (Ser-15), p21(WAF1/CIP1), and Bax; however, the Bak level remained relatively constant in both cell types, and the Bcl-2 level decreased only in HCT116 (p53(+/+)) cells.	2-meo	10-15	P53	Homo sapiens	101-104
25179905-5	2014	Following 2-MeO-E2 treatment, only HCT116 (p53(+/+)) cells exhibited an enhancement in the levels of p53, p-p53 (Ser-15), p21(WAF1/CIP1), and Bax; however, the Bak level remained relatively constant in both cell types, and the Bcl-2 level decreased only in HCT116 (p53(+/+)) cells.	2-meo	10-15	P53	Homo sapiens	101-104
25179905-5	2014	Following 2-MeO-E2 treatment, only HCT116 (p53(+/+)) cells exhibited an enhancement in the levels of p53, p-p53 (Ser-15), p21(WAF1/CIP1), and Bax; however, the Bak level remained relatively constant in both cell types, and the Bcl-2 level decreased only in HCT116 (p53(+/+)) cells.	2-meo	10-15	P53	Homo sapiens	101-104
25521755-8	2014	Moreover, suppression of HDAC3 by either siRNA or a potent HDAC3 inhibitor (MS-275) inhibited cell proliferation, increased p53 acetylation and transcription activity.	entinostat	76-82	P53	Homo sapiens	124-127
25242357-5	2014	Moreover, in the presence of cycloheximide, KLF9 significantly increased p53 stability in HCC cells.	Cycloheximide	29-42	P53	Homo sapiens	73-76
25375376-6	2014	The suppression was dependent on the p53 response, which is triggered by the impairment of the complex III-dependent de novo biosynthesis of pyrimidines by mitochondrial dihydroorotate dehydrogenase.	Pyrimidines	141-152	P53	Homo sapiens	37-40
25139326-0	2014	2-Phenylethynesulfonamide (PES) uncovers a necrotic process regulated by oxidative stress and p53.	2-phenylacetylenesulfonamide	0-25	P53	Homo sapiens	94-97
25139326-0	2014	2-Phenylethynesulfonamide (PES) uncovers a necrotic process regulated by oxidative stress and p53.	2-phenylacetylenesulfonamide	27-30	P53	Homo sapiens	94-97
25139326-7	2014	Genetically modified p53-null or p53 knocked-down cells show resistance to PES-driven necrosis.	2-phenylacetylenesulfonamide	75-78	P53	Homo sapiens	21-24
25139326-7	2014	Genetically modified p53-null or p53 knocked-down cells show resistance to PES-driven necrosis.	2-phenylacetylenesulfonamide	75-78	P53	Homo sapiens	33-36
25139326-9	2014	On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES.	2-phenylacetylenesulfonamide	138-141	P53	Homo sapiens	63-66
25139326-9	2014	On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES.	2-phenylacetylenesulfonamide	138-141	P53	Homo sapiens	111-114
25139326-9	2014	On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES.	2-phenylacetylenesulfonamide	138-141	P53	Homo sapiens	111-114
25139326-9	2014	On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES.	2-phenylacetylenesulfonamide	220-223	P53	Homo sapiens	63-66
25139326-9	2014	On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES.	2-phenylacetylenesulfonamide	220-223	P53	Homo sapiens	111-114
25139326-9	2014	On the other hand, we report an augmented production of ROS in p53-positive cells that, added to the increased p53 content in response to PES-elicited ROS, suggests that p53 and ROS are mutually regulated in response to PES.	2-phenylacetylenesulfonamide	220-223	P53	Homo sapiens	111-114
24747221-6	2014	RESULTS: We found that acrolein induced cellular senescence by increasing both p53 and p21.	Acrolein	23-31	P53	Homo sapiens	79-82
24747221-9	2014	Acrolein-induced down-regulation of WRN protein was rescued by p53 knockdown or proteasome inhibition.	Acrolein	0-8	P53	Homo sapiens	63-66
24747221-11	2014	CONCLUSIONS: These results suggest that acrolein induces p53-mediated cellular senescence accompanied by enhanced telomere attrition and WRN protein down-regulation.	Acrolein	40-48	P53	Homo sapiens	57-60
23625588-5	2014	Fenofibrate inhibited cell proliferation in both TP53 wild type and deficient lung cancer cells.	Fenofibrate	0-11	P53	Homo sapiens	49-53
23625588-7	2014	An additive effect against cell proliferation by budesonide and fenofibrate combination was observed only in TP53 wild type A549 cancer cells.	Fenofibrate	64-75	P53	Homo sapiens	109-113
24633417-0	2014	Delivery of a monomeric p53 subdomain with mitochondrial targeting signals from pro-apoptotic Bak or Bax.	bakuchiol	94-97	P53	Homo sapiens	24-27
24633417-9	2014	The apoptotic mechanism of p53-BakMTS and DBD-BakMTS was Bak dependent.	bakuchiol	31-34	P53	Homo sapiens	27-30
25023790-8	2014	RESULTS: beta-OH-S infusion prior to reperfusion reduced coronary and cardiac oxidative DNA-damage, diminished neutrophil infiltration at the site of ischemia, preserved mitochondrial membrane potential and reduced apoptosis in the ischemic myocardium (lower mRNA levels of Fas, casp8, p53, and casp3 and mitochondrial-p-Bcl2; and reduced TUNEL and active caspase-3; p&lt;0.05 vs. vehicle/control).	beta-oh-s	9-18	P53	Homo sapiens	286-289
24960055-5	2014	Moreover, HBCD and PCBs could induce the transcriptional activity of NF-kappab and suppress the p53 expression in HepG2 and MHCC97H cells.	Polychlorinated Biphenyls	19-23	P53	Homo sapiens	96-99
24960055-6	2014	In MHCC97L cells, however, opposite changes for NF-kappaB protein expression, NF-kappaB transcriptional activity, and p53/Mdm4 expression were observed after HBCD and PCBs exposure.	Polychlorinated Biphenyls	167-171	P53	Homo sapiens	118-121
24960055-9	2014	Taken together, HBCD and PCBs at low concentrations could increase the resistance of HCC cells to cisplatin through modulation on NF-kappaB pathway activation and p53 function, which is associated with the activity of PI3K/Akt pathway.	Polychlorinated Biphenyls	25-29	P53	Homo sapiens	163-166
24970803-5	2014	Clonogenic survival analyses indicated that micromolar concentrations of niraparib radiosensitized tumor cell lines derived from lung, breast, and prostate cancers independently of their p53 status but not cell lines derived from normal tissues.	niraparib	73-82	P53	Homo sapiens	187-190
24997497-2	2014	Previously, our laboratory demonstrated the in vitro and in vivo bioactivity of CAPE and addressed the role of p53 and the p38 mitogen-activated protein kinase (MAPK) pathway in regulating CAPE-induced apoptosis in C6 glioma cells.	caffeic acid phenethyl ester	189-193	P53	Homo sapiens	111-114
24968304-10	2014	These results suggested that nilotinib can inhibit MDM2 and induce a p53-independent apoptosis pathway by downregulating XIAP; thus, nilotinib can treat not only Ph+, but also Ph- ALL patients whose cancer cells overexpress MDM2.	nilotinib	133-142	P53	Homo sapiens	69-72
24885658-6	2014	For example, combining p53 tumor expression data with mutational status could guide selection of tumors for therapeutic studies of agents where p53 status purportedly affects efficacy (e.g., MK-1775).	adavosertib	191-198	P53	Homo sapiens	23-26
24885658-6	2014	For example, combining p53 tumor expression data with mutational status could guide selection of tumors for therapeutic studies of agents where p53 status purportedly affects efficacy (e.g., MK-1775).	adavosertib	191-198	P53	Homo sapiens	144-147
24480460-5	2014	Treatment of cells overexpressing Aurora-A and ATM/Chk2 with the ATM specific inhibitor KU-55933 increased the cell sensitivity to cisplatin and irradiation through increasing the phosphorylation of p53 at Ser15 and inhibiting the expression of Chk2, gammaH2AX (Ser319), and RAD51.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	88-96	P53	Homo sapiens	199-202
24584843-4	2014	Farnesol increased the expression of p53, p-c-Jun N-terminal kinase, cleaved-caspase-3, Bax, and cleaved-caspase-9, but decreased the expression of p-phosphatidylinositol-3-kinase (PI3K), p-Akt, p-p38, Bcl-2, and p-extracellular signal-regulated protein kinase, in a dose-dependent manner.	Farnesol	0-8	P53	Homo sapiens	37-40
24272201-0	2014	Piperine induces apoptosis of lung cancer A549 cells via p53-dependent mitochondrial signaling pathway.	piperine	0-8	P53	Homo sapiens	57-60
24272201-6	2014	In addition, piperine treatment decreased Bcl-2 protein expression, but increased Bax protein expression in A549 cells, which were positively correlated with an elevated expression of p53 compared to control.	piperine	13-21	P53	Homo sapiens	184-187
24272201-7	2014	Taken together, these results suggested that piperine could induce p53-mediated cell cycle arrest and apoptosis via activation of caspase-3 and caspase-9 cascades, as well as increasing the Bax/Bcl-2 ratio.	piperine	45-53	P53	Homo sapiens	67-70
24424889-12	2014	Taken together, these findings suggest that MHY-449 induces apoptosis via downregulation of the Akt/FoxO1 and activation of ERK in androgen-independent, p53-null and PTEN-negative PC3 human prostate cancer cells.	MHY-449	44-51	P53	Homo sapiens	153-156
24428757-5	2014	A series of pyrrolo[3,4-c]pyrazole derivatives were rationally designed and synthesized as the first-in-class inhibitors of p53-MDM2 interaction and NF-kappaB pathway.	pyrrolo[3,4-c]pyrazole	12-34	P53	Homo sapiens	124-127
25482947-6	2014	We found that inhibitors of the mTOR pathway including rapamycin, wortmannin, and caffeine blunted the p53 response to nucleolar stress induced by actinomycin D.	Caffeine	82-90	P53	Homo sapiens	103-106
24213358-0	2014	Triptolide induces apoptosis in endometrial cancer via a p53-independent mitochondrial pathway.	triptolide	0-10	P53	Homo sapiens	57-60
24241349-0	2013	Hsp90 inhibitor BIIB021 enhances triptolide-induced apoptosis of human T-cell acute lymphoblastic leukemia cells in vitro mainly by disrupting p53-MDM2 balance.	triptolide	33-43	P53	Homo sapiens	143-146
24280450-2	2013	In this paper, we report that vanadate has a unique activity for inducing the denaturation of p53 relative to other known radioprotective p53 inhibitors, pifithrin-alpha (PFTalpha) and pifithrin-micro (PFTmicro).	Vanadates	30-38	P53	Homo sapiens	94-97
24280450-2	2013	In this paper, we report that vanadate has a unique activity for inducing the denaturation of p53 relative to other known radioprotective p53 inhibitors, pifithrin-alpha (PFTalpha) and pifithrin-micro (PFTmicro).	Vanadates	30-38	P53	Homo sapiens	138-141
23973282-0	2013	Antitumour activity on extrinsic apoptotic targets of the triterpenoid maslinic acid in p53-deficient Caco-2 adenocarcinoma cells.	maslinic acid	71-84	P53	Homo sapiens	88-91
24000115-6	2013	Real-time PCR analyses showed that berberine, NAX012 and NAX014 compounds increased the expression of some cell-cycle checkpoint molecules involved in cell senescence such as p53, p21(WAF1) , p16(INK4a) , and PAI-1, already after 24 h of 50 microM treatments.	13-(4-chlorophenylethyl)berberine	57-63	P53	Homo sapiens	175-178
24032713-6	2013	Enhancer of zeste homologue 2 (EZH2), an important histone-modifying enzyme, is able to trimethylate histone 3 on lysine 27 (H3K27Me3), consequently leading to gene silencing, especially silencing of tumor suppressor genes such as p53.	trimethylate	88-100	P53	Homo sapiens	231-234
23939933-1	2013	Bioorthogonal covalent cross-linking of DNA-binding proteins (p53) to DNA was achieved through novel DNA probes bearing a reactive vinylsulfonamide (VS) group.	vinyl sulfonamide	131-147	P53	Homo sapiens	62-65
23939933-1	2013	Bioorthogonal covalent cross-linking of DNA-binding proteins (p53) to DNA was achieved through novel DNA probes bearing a reactive vinylsulfonamide (VS) group.	vinyl sulfonamide	149-151	P53	Homo sapiens	62-65
23845085-5	2013	RESULTS: Cathinone, cathine and norephedrine generally reduced post-translational modifications of intracellular signal transducers in T-lymphocytes, B-lymphocytes, natural killer cells and monocytes, most prominently affecting c-Cbl (pTyr700), ERK1/2 (p-Thr202/p-Tyr204), p38 MAPK (p-Thr180/p-Tyr182) and p53 (both total p53 protein and p-Ser15).	Phenylpropanolamine	32-44	P53	Homo sapiens	306-309
23845085-5	2013	RESULTS: Cathinone, cathine and norephedrine generally reduced post-translational modifications of intracellular signal transducers in T-lymphocytes, B-lymphocytes, natural killer cells and monocytes, most prominently affecting c-Cbl (pTyr700), ERK1/2 (p-Thr202/p-Tyr204), p38 MAPK (p-Thr180/p-Tyr182) and p53 (both total p53 protein and p-Ser15).	Phenylpropanolamine	32-44	P53	Homo sapiens	322-325
23845085-10	2013	Cathinone, cathine and norephedrine reduced phosphorylation of c-Cbl, ERK1/2, p38 MAPK and p53(Ser15), and norephedrine induced T-lymphocyte proliferation.	Phenylpropanolamine	23-35	P53	Homo sapiens	91-94
23525071-9	2013	hnRNP A2/B1 siRNA combined with gemcitabine, 5-FU and oxaliplatin significantly increased (P&lt;0.01) apoptosis of pancreatic cancer cell lines SW1990 and BxPC-3, increased the expression level of Bax mRNA, decreased Bcl-2 mRNA and MDR1 mRNA expression (P&lt;0.01), and induced no change in p53, TRAIL, and Survivin mRNA expression in SW1990.	Oxaliplatin	54-65	P53	Homo sapiens	291-294
24022933-6	2013	L-OHP induced S cell cycle arrest in HepG2 cell; down-regulated the levels of CDK4, cyclinD1 and up-regulated the levels of p21, p53.	Oxaliplatin	0-5	P53	Homo sapiens	129-132
23523585-0	2013	Newly synthesized quinazolinone HMJ-38 suppresses angiogenetic responses and triggers human umbilical vein endothelial cell apoptosis through p53-modulated Fas/death receptor signaling.	2-(3'-methoxyphenyl)-6-pyrrolidinyl-4-quinazolinone	32-38	P53	Homo sapiens	142-145
23523585-7	2013	HMJ-38-influenced HUVECs were performed by determining the oxidative stress (ROS production) and ATM/p53-modulated Fas and DR4/DR5 signals that were examined by flow cytometry, Western blotting, siRNA and real-time RT-PCR analyses, respectively.	2-(3'-methoxyphenyl)-6-pyrrolidinyl-4-quinazolinone	0-6	P53	Homo sapiens	101-104
23523585-8	2013	Our findings demonstrate that p53-regulated extrinsic pathway might fully contribute to HMJ-38-provoked apoptotic death in HUVECs.	2-(3'-methoxyphenyl)-6-pyrrolidinyl-4-quinazolinone	88-94	P53	Homo sapiens	30-33
23455057-0	2013	Microwave-assisted synthesis of arene ruthenium(II) complexes that induce S-phase arrest in cancer cells by DNA damage-mediated p53 phosphorylation.	Ruthenium(II)	38-51	P53	Homo sapiens	128-131
23455057-6	2013	In conclusion, the synthetic arene Ru(II) complexes could serve as novel p53 activator with potential application in cancer chemotherapy.	ru(ii)	35-41	P53	Homo sapiens	73-76
23262037-0	2013	Negative regulation of transcription factor FoxM1 by p53 enhances oxaliplatin-induced senescence in hepatocellular carcinoma.	Oxaliplatin	66-77	P53	Homo sapiens	53-56
23262037-3	2013	Our data indicated that due to the repression by p53, FoxM1 played a critical role in oxaliplatin-induced senescence via regulating cycle-related proteins p21, p27, cyclins B1 and D1.	Oxaliplatin	86-97	P53	Homo sapiens	49-52
23492773-0	2013	miR-128 exerts pro-apoptotic effect in a p53 transcription-dependent and -independent manner via PUMA-Bak axis.	bakuchiol	102-105	P53	Homo sapiens	41-44
2834865-4	1988	The p53 sedimented at about 8-10 S in sucrose gradients, possibly corresponding to a tetramer.	Sucrose	38-45	P53	Homo sapiens	4-7
23184057-4	2013	Furthermore, hSSB1 also associates with the acetyltransferase p300 and is required for efficient transcriptional activation of the p53 target gene p21 by affecting the acetylation of p53 at lysine382.	lysine382	190-199	P53	Homo sapiens	131-134
34047450-0	2021	Novel cytotoxic 1,2,3-triazoles as potential new leads targeting the S100A2-p53complex.	1,2,3-triazoles	16-31	P53	Homo sapiens	76-79
23184057-4	2013	Furthermore, hSSB1 also associates with the acetyltransferase p300 and is required for efficient transcriptional activation of the p53 target gene p21 by affecting the acetylation of p53 at lysine382.	lysine382	190-199	P53	Homo sapiens	183-186
22749133-0	2013	The flavonoids diosmetin and luteolin exert synergistic cytostatic effects in human hepatoma HepG2 cells via CYP1A-catalyzed metabolism, activation of JNK and ERK and P53/P21 up-regulation.	Luteolin	29-37	P53	Homo sapiens	167-174
34037269-10	2021	Studies in cultured cancer cells confirmed that the Ola-mediated inhibition of the ph-S6-p53-PARP1-ALCD axis inhibits proliferation of cancer cells.	ola	52-55	P53	Homo sapiens	89-92
23085367-7	2013	The activation of Nrf2 pathway and subsequently phase II enzymes in concert with p53 induction in normal hepatocytes may account for the molecular mechanism of the chemopreventive activity of xanthohumol.	xanthohumol	192-203	P53	Homo sapiens	81-84
34002651-8	2021	Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	P53	Homo sapiens	211-214
24289617-8	2013	The rate of p53 mutation was 44.3% in TN tumors versus 28.2% in the NTN group (p&lt;0.001).	ISONICOTINAMIDINE	68-71	P53	Homo sapiens	12-15
34002651-8	2021	Our results showed that MG132 downregulated the expression of antiapoptotic proteins, including CDK2, CDK4, Bcl-xL, and Bcl-2, whereas it upregulated the expression of proapoptotic proteins, including p21, p27, p53, p-p53 (ser15, ser20, and ser46), cleaved forms of caspase-3, caspase-7, caspase-9, and PARP, and FOXO3 in U2OS cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	24-29	P53	Homo sapiens	218-221
33325610-0	2021	Butein induces cellular senescence through reactive oxygen species-mediated p53 activation in osteosarcoma U-2 OS cells.	butein	0-6	P53	Homo sapiens	76-79
33325610-7	2021	Knockdown of p53 suppressed the senescence and rescued the viability in butein-treated U-2 OS cells.	butein	72-78	P53	Homo sapiens	13-16
33325610-10	2021	Taken together, our data proposed the increased ROS by butein exposure activated p53, and the activated p53 was involved in the anti-proliferative effect of butein via inducing senescence in U-2 OS cells.	butein	55-61	P53	Homo sapiens	81-84
33325610-10	2021	Taken together, our data proposed the increased ROS by butein exposure activated p53, and the activated p53 was involved in the anti-proliferative effect of butein via inducing senescence in U-2 OS cells.	butein	157-163	P53	Homo sapiens	104-107
22767080-4	2013	The potential induction of p53 expression and activation by GSM-900 was investigated after in vitro exposure of human amniotic cells for 24 h to average specific absorption rates (SARs) of 0.25, 1, 2, and 4 W/kg in the temperature range of 36.3-39.7  C. The exposures were carried out using a wire-patch cell (WPC) under strictly controlled conditions of temperature.	gsm-900	60-67	P53	Homo sapiens	27-30
22846543-0	2012	Wogonin induces apoptosis by activating the AMPK and p53 signaling pathways in human glioblastoma cells.	wogonin	0-7	P53	Homo sapiens	53-56
32943750-8	2021	The benefit of lomustine in nonadverse chromosomal aberrations was restricted to patients with RUNX1, ASXL1, TP53, and FLT3-ITDhigh/NPM1WT mutations in contrast to the intermediate and favorable ELN2017 patients.	Lomustine	15-24	P53	Homo sapiens	109-113
22945757-0	2012	IPH-926 lobular breast cancer cells harbor a p53 mutant with temperature-sensitive functional activity and allow for profiling of p53-responsive genes.	Phenol	0-3	P53	Homo sapiens	45-48
33968744-4	2021	Gene expression profiles induced by Ad-p53 treatment were evaluated using the Nanostring IO 360 panel.	io 360	89-95	P53	Homo sapiens	39-42
33710861-10	2021	Moreover, we show that the effect of Olmesartan against cell senescence and deacetylation of p53 was abolished by inhibition of SIRT1, either by using nicotinamide or by transfection with SIRT1 siRNA.	Niacinamide	151-163	P53	Homo sapiens	93-96
22945757-0	2012	IPH-926 lobular breast cancer cells harbor a p53 mutant with temperature-sensitive functional activity and allow for profiling of p53-responsive genes.	Phenol	0-3	P53	Homo sapiens	130-133
22945757-2	2012	We report on the utilization of IPH-926 human lobular breast cancer cells for the profiling of p53-responsive genes using a novel approach without such modifications.	Phenol	32-35	P53	Homo sapiens	95-98
33668835-5	2021	Idasanutlin induced a robust p53-dependent transcriptional signature in macrophages, including several pro-apoptotic genes.	RG7388	0-11	P53	Homo sapiens	29-32
22945757-3	2012	We discovered that IPH-926 cells harbor a homozygous TP53 missense mutation encoding for a rare p53 mutant (E285K) with temperature-sensitive (ts) loss of function characteristics.	Phenol	19-22	P53	Homo sapiens	53-57
22945757-3	2012	We discovered that IPH-926 cells harbor a homozygous TP53 missense mutation encoding for a rare p53 mutant (E285K) with temperature-sensitive (ts) loss of function characteristics.	Phenol	19-22	P53	Homo sapiens	96-99
33595161-3	2021	NAM, a water-soluble form of vitamin B3, interferes with skin carcinogenesis as it regulates immunosuppressor genes such as p53 and sirtuins and restores intracellular level of NAD+, a co-enzyme essential for energy production.	Niacinamide	29-39	P53	Homo sapiens	124-127
22945757-5	2012	In vitro temperature shifts reconstituted endogenous wild-type p53 activity in IPH-926, as evidenced by induction of p21(Waf1).	Phenol	79-82	P53	Homo sapiens	63-66
22945757-11	2012	From a molecular point of view, IPH-926 thus provides a new tool to study transcriptional programs controlled by p53.	Phenol	32-35	P53	Homo sapiens	113-116
22945757-12	2012	From a tumor pathology perspective, IPH-926 also provides the first direct evidence of a p53-related clonal evolutionary pathway in lobular breast cancer progression.	Phenol	36-39	P53	Homo sapiens	89-92
23035244-5	2012	We found from in silico screening and confirmed by experiment that lithocholic acid (LCA) binds to the p53 binding sites of both MDM2 and MDM4 with a fivefold preference for MDM4.	Lithocholic Acid	85-88	P53	Homo sapiens	103-106
33561393-0	2021	Arsenic and an Old Place: Rescuing p53 Mutants in Cancer.	Arsenic	0-7	P53	Homo sapiens	35-38
33561393-4	2021	The arsenic atom binds in a conserved, cryptic site and reactivates multiple p53 mutants.	Arsenic	4-11	P53	Homo sapiens	77-80
23035244-7	2012	The comparison of LCA effects on apoptosis in HCT116 p53(+/+) vs. p53(-/-) cells shows a predominantly p53-mediated induction of caspase-3/7.	Lithocholic Acid	18-21	P53	Homo sapiens	53-56
22711363-0	2012	Dracorhodin perchlorate inhibits PI3K/Akt and NF-kappaB activation, up-regulates the expression of p53, and enhances apoptosis.	dracorhodin	0-23	P53	Homo sapiens	99-102
33880358-0	2021	Bioinformatics and In Vitro Studies Reveal the Importance of p53, PPARG and Notch Signaling Pathway in Inhibition of Breast Cancer Stem Cells by Hesperetin.	hesperetin	145-155	P53	Homo sapiens	61-64
33880358-7	2021	Results: Using a bioinformatics approach, we identified P53, PPARG, and Notch signaling as potential targets of hesperetin in inhibition of BCSCs.	hesperetin	112-122	P53	Homo sapiens	56-59
33880358-10	2021	Moreover, hesperetin treatment modulates the expression of p53, PPARG, and NOTCH1.	hesperetin	10-20	P53	Homo sapiens	59-62
33880358-11	2021	Conclusion: Taken together, hesperetin has potential for the treatment of BCSC by targeting p53, PPARG and Notch signaling.	hesperetin	28-38	P53	Homo sapiens	92-95
22711363-6	2012	Dracorhodin perchlorate-induced apoptosis is mediated via upregulation of p53, inhibiting the activation of PI3K/Akt, and NF-kappaB, thereby decreasing the expression of the anti-apoptotic proteins, Bcl-2 and Bcl-XL.	dracorhodin	0-23	P53	Homo sapiens	74-77
22711363-8	2012	Dracorhodin perchlorate induced up-regulation of p53, thereby resulting in the activation of its downstream targets p21 and Bax following the dissipation of mitochondrial membrane potential and activation of caspase-3 and its substrate, PARP.	dracorhodin	0-23	P53	Homo sapiens	49-52
22711363-10	2012	These results reveal functional interplay among the PI3K/Akt, p53 and NF-kappaB pathways that are frequently deregulated in cancer and suggest that their simultaneous targeting by Dracorhodin perchlorate could result in efficacious and selective killing of cancer cells.	dracorhodin	180-203	P53	Homo sapiens	62-65
22728882-0	2012	Inhibition of NAMPT pathway by FK866 activates the function of p53 in HEK293T cells.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	31-36	P53	Homo sapiens	63-66
33468997-5	2021	After treatment with DEN, while the induction of gammaH2AX and p53 were comparable in the G9aDeltaHep and wild-type livers, more apoptotic hepatocytes were detected in the G9aDeltaHep liver.	Diethylnitrosamine	21-24	P53	Homo sapiens	63-66
22728882-3	2012	Using the 293T cell line (HEK293 cells transformed with large T antigen) as a model, we provide evidence that p53 is one of the critical downstream targets involved in FK866-mediated killing of 293T cells.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	168-173	P53	Homo sapiens	110-113
33367935-3	2021	Mechanistically, isatin inhibited lysine-specific histone demethylase (LSD)1 and reversed the blockade on p53, thereby activating the apoptotic pathway.	Isatin	17-23	P53	Homo sapiens	106-109
22728882-6	2012	Additionally, knockdown of p53 attenuated the effect of FK866 on cell proliferation, apoptosis, and cell cycle arrest.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	56-61	P53	Homo sapiens	27-30
22728882-7	2012	The data presented here shed light on two important facts: (1) that p53 in 293T cells is active in the presence of FK866, an inhibitor of NAMPT pathway; (2) the apoptosis induced by FK866 in 293T cells is associated with increased acetylation of p53 at Lys382, which is required for the functional activity of p53.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	115-120	P53	Homo sapiens	68-71
22728882-7	2012	The data presented here shed light on two important facts: (1) that p53 in 293T cells is active in the presence of FK866, an inhibitor of NAMPT pathway; (2) the apoptosis induced by FK866 in 293T cells is associated with increased acetylation of p53 at Lys382, which is required for the functional activity of p53.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	115-120	P53	Homo sapiens	246-249
33425404-0	2020	Efficacy of Venetoclax and Dexamethasone in Refractory IgM Primary Plasma Cell Leukemia with t(11;14) and TP53 Mutation: A Case Report and Literature Review.	venetoclax	12-22	P53	Homo sapiens	106-110
22728882-7	2012	The data presented here shed light on two important facts: (1) that p53 in 293T cells is active in the presence of FK866, an inhibitor of NAMPT pathway; (2) the apoptosis induced by FK866 in 293T cells is associated with increased acetylation of p53 at Lys382, which is required for the functional activity of p53.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	115-120	P53	Homo sapiens	246-249
22728882-7	2012	The data presented here shed light on two important facts: (1) that p53 in 293T cells is active in the presence of FK866, an inhibitor of NAMPT pathway; (2) the apoptosis induced by FK866 in 293T cells is associated with increased acetylation of p53 at Lys382, which is required for the functional activity of p53.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	182-187	P53	Homo sapiens	68-71
22728882-7	2012	The data presented here shed light on two important facts: (1) that p53 in 293T cells is active in the presence of FK866, an inhibitor of NAMPT pathway; (2) the apoptosis induced by FK866 in 293T cells is associated with increased acetylation of p53 at Lys382, which is required for the functional activity of p53.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	182-187	P53	Homo sapiens	246-249
22728882-7	2012	The data presented here shed light on two important facts: (1) that p53 in 293T cells is active in the presence of FK866, an inhibitor of NAMPT pathway; (2) the apoptosis induced by FK866 in 293T cells is associated with increased acetylation of p53 at Lys382, which is required for the functional activity of p53.	N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide	182-187	P53	Homo sapiens	246-249
33338300-6	2021	Additionally, AZD5363 is capable of inducing FOXO1 and p53 nuclear localization and reduces BAD phosphorylation, which is generally increased by cisplatin and doxorubicin.	capivasertib	14-21	P53	Homo sapiens	55-58
22696098-0	2012	MiR-138 promotes induced pluripotent stem cell generation through the regulation of the p53 signaling.	mir-138	0-7	P53	Homo sapiens	88-91
33736280-7	2020	Consequently, the novel curcuminoid macromolecule showed significant feasibility in triggering the high expression of apoptotic caspases caspase 3, caspase 8, P53, and Bax (P < 0.01 to P < 0.001) after 48 h of chemotherapy.	Diarylheptanoids	24-35	P53	Homo sapiens	159-162
22696098-4	2012	Exploration of the mechanism showed that miR-138 directly targeted the 3" untranslated region (UTR) of p53, significantly decreasing the expression of p53 and its downstream genes.	mir-138	41-48	P53	Homo sapiens	103-106
32767230-8	2020	In irradiation-induced, p53-dependent pathways of apoptosis, the pro-apoptotic Noxa represents one of several, yet to be identified, pathways simultaneously triggered by p53 to produce mitochondrial ceramide accumulation and apoptosis.	Ceramides	199-207	P53	Homo sapiens	24-27
22696098-4	2012	Exploration of the mechanism showed that miR-138 directly targeted the 3" untranslated region (UTR) of p53, significantly decreasing the expression of p53 and its downstream genes.	mir-138	41-48	P53	Homo sapiens	151-154
32767230-8	2020	In irradiation-induced, p53-dependent pathways of apoptosis, the pro-apoptotic Noxa represents one of several, yet to be identified, pathways simultaneously triggered by p53 to produce mitochondrial ceramide accumulation and apoptosis.	Ceramides	199-207	P53	Homo sapiens	170-173
22696098-5	2012	Furthermore, the ectopic expression of p53 having a mutant 3"-UTR, which cannot be bound by miR-138, seriously impaired the effect of miR-138 on p53 signaling and OSKM-initiated somatic cell reprogramming.	mir-138	92-99	P53	Homo sapiens	39-42
32767230-10	2020	Altogether, these results indicate that members of the Bcl-2 family differentially regulate ceramide accumulation and reveal the existence of crosstalk between Bcl-2 family members and ceramide in mediating p53-dependent apoptosis in Molt-4 human T-cell leukemia.	Ceramides	92-100	P53	Homo sapiens	207-210
32767230-10	2020	Altogether, these results indicate that members of the Bcl-2 family differentially regulate ceramide accumulation and reveal the existence of crosstalk between Bcl-2 family members and ceramide in mediating p53-dependent apoptosis in Molt-4 human T-cell leukemia.	Ceramides	185-193	P53	Homo sapiens	207-210
22696098-5	2012	Furthermore, the ectopic expression of p53 having a mutant 3"-UTR, which cannot be bound by miR-138, seriously impaired the effect of miR-138 on p53 signaling and OSKM-initiated somatic cell reprogramming.	mir-138	134-141	P53	Homo sapiens	39-42
22696098-5	2012	Furthermore, the ectopic expression of p53 having a mutant 3"-UTR, which cannot be bound by miR-138, seriously impaired the effect of miR-138 on p53 signaling and OSKM-initiated somatic cell reprogramming.	mir-138	134-141	P53	Homo sapiens	145-148
22696098-6	2012	Combined with the fact that miR-138 is endogenously expressed in fibroblasts, iPS cells, and embryonic stem cells, our study demonstrated that regulation of the p53 signaling pathway and promotion of iPS cell generation represent an unrevealed important function of miR-138.	mir-138	28-35	P53	Homo sapiens	161-164
22696098-6	2012	Combined with the fact that miR-138 is endogenously expressed in fibroblasts, iPS cells, and embryonic stem cells, our study demonstrated that regulation of the p53 signaling pathway and promotion of iPS cell generation represent an unrevealed important function of miR-138.	mir-138	266-273	P53	Homo sapiens	161-164
33141854-14	2020	These data indicate that TP53 suppression leads to 5hmC reduction in part through A3B induction.	5-hydroxymethylcytosine	51-55	P53	Homo sapiens	25-29
22395446-0	2012	3-Nitro-naphthalimide and nitrogen mustard conjugate NNM-25 induces hepatocellular carcinoma apoptosis via PARP-1/p53 pathway.	Mechlorethamine	26-42	P53	Homo sapiens	114-117
32943478-8	2020	P53 appears to be involved in mediating these palliative effects, since selepressin strongly induced its expression levels, suppressed the inflammatory RhoA/MLC2 pathway and triggered the barrier protective effects of the GTPase Rac1.	SELEPRESSIN	72-83	P53	Homo sapiens	0-3
33001126-4	2020	We found that the transfection efficiency of the PGHA/p53 complex was higher than those of the other three polymer/gene complexes through MTT assay and laser scanning confocal microscopy.	monooxyethylene trimethylolpropane tristearate	138-141	P53	Homo sapiens	54-57
22534478-4	2012	RESULTS: p53 expression were associated with the significantly shorter disease-free survival (DFS) (p&lt;0.001) and overall survival (OS) (p=0.012) in the curatively resected advanced gastric cancer patients receiving capecitabine plus paclitaxel.	Capecitabine	218-230	P53	Homo sapiens	9-12
33001126-8	2020	MTT assay showed that the DPGHAP/p53 complex had a significant antitumor effect on A549 cells and H1299 cells compared with free DOX or/and p53 gene therapy alone.	monooxyethylene trimethylolpropane tristearate	0-3	P53	Homo sapiens	33-36
22534478-6	2012	CONCLUSIONS: p53 expression positive might predict prognosis in gastric cancer patients who underwent curative surgery followed by adjuvant capecitabine plus paclitaxel chemotherapy.	Capecitabine	140-152	P53	Homo sapiens	13-16
33113997-0	2020	Targeting P53 as a Future Strategy to Overcome Gemcitabine Resistance in Biliary Tract Cancers.	gemcitabine	47-58	P53	Homo sapiens	10-13
22670709-0	2012	Activation of AMPK by pterostilbene suppresses lipogenesis and cell-cycle progression in p53 positive and negative human prostate cancer cells.	pterostilbene	22-35	P53	Homo sapiens	89-92
33113997-4	2020	Preclinical studies have demonstrated that p53 mutations in BTCs are associated with enhanced gemcitabine resistance, therefore targeting p53 may be a novel therapeutic strategy for treatment of BTCs.	gemcitabine	94-105	P53	Homo sapiens	43-46
33113997-4	2020	Preclinical studies have demonstrated that p53 mutations in BTCs are associated with enhanced gemcitabine resistance, therefore targeting p53 may be a novel therapeutic strategy for treatment of BTCs.	gemcitabine	94-105	P53	Homo sapiens	138-141
22670709-4	2012	Using the p53 wild type LNCaP and p53 null PC3 cells, we found that treatment with pterostilbene resulted in dose-dependent inhibition of cellular proliferation, which suggested that the interaction of pterostilbene with the p53 might not fully explain its inhibitory effect on proliferation.	pterostilbene	83-96	P53	Homo sapiens	10-13
22670709-4	2012	Using the p53 wild type LNCaP and p53 null PC3 cells, we found that treatment with pterostilbene resulted in dose-dependent inhibition of cellular proliferation, which suggested that the interaction of pterostilbene with the p53 might not fully explain its inhibitory effect on proliferation.	pterostilbene	83-96	P53	Homo sapiens	34-37
22670709-4	2012	Using the p53 wild type LNCaP and p53 null PC3 cells, we found that treatment with pterostilbene resulted in dose-dependent inhibition of cellular proliferation, which suggested that the interaction of pterostilbene with the p53 might not fully explain its inhibitory effect on proliferation.	pterostilbene	83-96	P53	Homo sapiens	34-37
22670709-4	2012	Using the p53 wild type LNCaP and p53 null PC3 cells, we found that treatment with pterostilbene resulted in dose-dependent inhibition of cellular proliferation, which suggested that the interaction of pterostilbene with the p53 might not fully explain its inhibitory effect on proliferation.	pterostilbene	202-215	P53	Homo sapiens	10-13
33083850-1	2020	A disposable electrochemical immunosensors is presented suitable to detect cancer biomarker p53 using screen-printed carbon electrodes modified with a layer-by-layer (LbL) matrix of carboxylated NiFe2O4 nanoparticles and polyethyleneimine, onto which anti-p53 antibodies were adsorbed.	aziridine	221-238	P53	Homo sapiens	92-95
33083850-4	2020	The immunosensor performance is among the best reported in the literature for determination of p53, with the additional advantage of being disposable and operating with low-volume solutions.Graphical abstract Schematic representation of immunosensor fabrication depicting the immobilization of specific antibodies against p53 protein onto the surfaces of disposable printed electrodes modified with films of polyethyleneimine and different concentrations of carboxylated magnetic nanoparticles.	aziridine	408-425	P53	Homo sapiens	95-98
22670709-4	2012	Using the p53 wild type LNCaP and p53 null PC3 cells, we found that treatment with pterostilbene resulted in dose-dependent inhibition of cellular proliferation, which suggested that the interaction of pterostilbene with the p53 might not fully explain its inhibitory effect on proliferation.	pterostilbene	202-215	P53	Homo sapiens	34-37
33078453-0	2021	Fructose-1,6-bisphosphate induces generation of reactive oxygen species and activation of p53-dependent cell death in human endometrial cancer cells.	fructose-1,6-diphosphate	0-25	P53	Homo sapiens	90-93
22670709-4	2012	Using the p53 wild type LNCaP and p53 null PC3 cells, we found that treatment with pterostilbene resulted in dose-dependent inhibition of cellular proliferation, which suggested that the interaction of pterostilbene with the p53 might not fully explain its inhibitory effect on proliferation.	pterostilbene	202-215	P53	Homo sapiens	34-37
22670709-5	2012	In this study, we found that pterostilbene activated AMPK in both p53 positive and negative human prostate cancer cells.	pterostilbene	29-42	P53	Homo sapiens	66-69
22670709-8	2012	In p53 positive LNCaP cells, pterostilbene blocked the progression of cell cycle at G1 phase by inducing p53 expression and further up-regulating p21 expression.	pterostilbene	29-42	P53	Homo sapiens	3-6
33086722-0	2020	Low Dose Astaxanthin Treatments Trigger the Hormesis of Human Astroglioma Cells by Up-Regulating the Cyclin-Dependent Kinase and Down-Regulated the Tumor Suppressor Protein P53.	astaxanthine	9-20	P53	Homo sapiens	173-176
33086722-8	2020	Western blot analysis showed that treatment with a low concentration of AXT upregulated cyclin-dependent kinase (Cdk) 2 and p-Cdk2/3 levels and downregulated the expression of tumor protein p53.	astaxanthine	72-75	P53	Homo sapiens	190-193
22677378-3	2012	Here, we proposed an integrated model of the p53 network to characterize how the cellular response is regulated by key cofactors of p53, Hzf and ASPP.	aspp	145-149	P53	Homo sapiens	45-48
21373875-0	2012	TP53 genomics predict higher clinical and pathologic tumor response in operable early-stage breast cancer treated with docetaxel-capecitabine +- trastuzumab.	Capecitabine	129-141	P53	Homo sapiens	0-4
32866467-0	2020	Novel pyrrolopyrimidine derivatives induce p53-independent apoptosis via the mitochondrial pathway in colon cancer cells.	pyrrolopyrimidine	6-23	P53	Homo sapiens	43-46
22329423-1	2012	The synthesis of neopeltolide analogues that contain variations in the oxazole-containing side chain and in the macrolide core are reported along with the GI(50) values for these compounds against MCF-7, HCT-116, and p53 knockout HCT-116 cell lines.	neopeltolide	17-29	P53	Homo sapiens	217-220
32920746-13	2020	Therefore, effects of TACN at the nucleus, produced a p53 response to initiate DNA repair and did not culminate in cell death.	triazacyclononane	22-26	P53	Homo sapiens	54-57
22329423-3	2012	Neopeltolide and several of the more potent analogues were significantly less potent against p53 knockout cells, suggesting that p53 plays an auxiliary role in the activity of these compounds.	neopeltolide	0-12	P53	Homo sapiens	93-96
22329423-3	2012	Neopeltolide and several of the more potent analogues were significantly less potent against p53 knockout cells, suggesting that p53 plays an auxiliary role in the activity of these compounds.	neopeltolide	0-12	P53	Homo sapiens	129-132
32938995-0	2020	SHOC2 scaffold protein modulates daunorubicin-induced cell death through p53 modulation in lymphoid leukemia cells.	Daunorubicin	33-45	P53	Homo sapiens	73-76
22142888-4	2012	We previously showed that the anti-malarial Chloroquine, a 4-alkylamino substituted quinoline, is a p53 activator and reduced the incidence of breast tumors in animal models.	4-alkylamino substituted quinoline	59-93	P53	Homo sapiens	100-103
32942546-0	2020	Ligation-Mediated Polymerase Chain Reaction Detection of 8-Oxo-7,8-Dihydro-2"-Deoxyguanosine and 5-Hydroxycytosine at the Codon 176 of the p53 Gene of Hepatitis C-Associated Hepatocellular Carcinoma Patients.	5-hydroxycytosine	97-114	P53	Homo sapiens	139-142
22901112-8	2012	This review describes the landscape of different molecular markers with particular spotlight on vitamin D signaling pathway and apoptotic specific protein of p53 (ASPP) family members in breast cancer.	aspp	163-167	P53	Homo sapiens	158-161
22678405-3	2012	METHODS: Following our published data from S-adenosylmethionine (SAMe), oxaliplatin and sorafenib were further used to stimulate GADD45beta expression in cultured HepG2 (p53 wild type) and Hep3B (p53 null) hepatoma cells in vitro.	Oxaliplatin	72-83	P53	Homo sapiens	170-173
32973966-0	2020	Small ceramide tames big p53 mutant beast.	Ceramides	6-14	P53	Homo sapiens	25-28
33205006-3	2020	Previous studies showed that ceramide glycosylation correlates with upregulated expression of p53 hotspot mutant R273H and cancer drug resistance.	Ceramides	29-37	P53	Homo sapiens	94-97
22678405-3	2012	METHODS: Following our published data from S-adenosylmethionine (SAMe), oxaliplatin and sorafenib were further used to stimulate GADD45beta expression in cultured HepG2 (p53 wild type) and Hep3B (p53 null) hepatoma cells in vitro.	Oxaliplatin	72-83	P53	Homo sapiens	196-199
32878786-5	2020	In contrast, CDKN1A gene expression was significantly increased by both SBHA and SAHA treatment of TP53-mutated RPMI8226 cells.	Vorinostat	72-76	P53	Homo sapiens	99-103
22084170-8	2012	The cytotoxic effect of Wee1 inhibition on sarcoma cells seems to be independent of p53 status as all sarcoma cell lines with different p53 mutation were highly sensitive to MK1775 treatment.	adavosertib	174-180	P53	Homo sapiens	136-139
32099034-0	2020	Reinstated p53 response and high anti-T-cell leukemia activity by the novel alkylating deacetylase inhibitor tinostamustine.	tinostamustine	109-123	P53	Homo sapiens	11-14
23112878-2	2012	AFB1-8,9-exo-epoxide, one of AFB1 metabolites, acts as a mutagen to react with DNA and induce gene mutations, including the tumor suppressor p53.	afb1-8,9-exo-epoxide	0-20	P53	Homo sapiens	141-144
32922194-0	2020	Sesamin inhibits cervical cancer cell proliferation by promoting p53/PTEN-mediated apoptosis.	sesamin	0-7	P53	Homo sapiens	65-68
32922194-2	2020	Here, we explored whether sesamin activates p53, which is widely inhibited in cervical cancer cells, thereby inducing p53-mediated apoptosis.	sesamin	26-33	P53	Homo sapiens	44-47
22848370-0	2012	Noscapine induced apoptosis via downregulation of survivin in human neuroblastoma cells having wild type or null p53.	Noscapine	0-9	P53	Homo sapiens	113-116
32922194-2	2020	Here, we explored whether sesamin activates p53, which is widely inhibited in cervical cancer cells, thereby inducing p53-mediated apoptosis.	sesamin	26-33	P53	Homo sapiens	118-121
32922194-9	2020	Furthermore, sesamin induced p53 phosphorylation at serine-46 and serine-15 and upregulated the levels of PUMA, Bax, and PTEN, while inhibiting AKT phosphorylation at serine-473.	sesamin	13-20	P53	Homo sapiens	29-32
22848370-6	2012	The Noscapine treatment increased levels of total and Ser(15)-phosphorylated p53 protein in SK-SY5Y cells, but the proapoptotic response to this agent was maintained even after knockdown of the p53 protein level.	Noscapine	4-13	P53	Homo sapiens	77-80
22848370-6	2012	The Noscapine treatment increased levels of total and Ser(15)-phosphorylated p53 protein in SK-SY5Y cells, but the proapoptotic response to this agent was maintained even after knockdown of the p53 protein level.	Noscapine	4-13	P53	Homo sapiens	194-197
32540572-6	2020	CP55940 increased dichlorofluorescein fluorescence (DCF) intensity, increased DJ-1 Cys106- sulfonate, a marker of intracellular stress, induced the up-regulation of p53 and phosphorylation of transcription factor c-JUN.	3-(2-hydroxy-4-(1,1-dimethylheptyl)phenyl)-4-(3-hydroxypropyl)cyclohexanol	0-7	P53	Homo sapiens	165-168
21986580-0	2011	Crocetin induces cytotoxicity and enhances vincristine-induced cancer cell death via p53-dependent and -independent mechanisms.	crocetin	0-8	P53	Homo sapiens	85-88
32234756-12	2020	The sensitivity of TP53mut PDAC to gemcitabine in CONKO-001 provides a lead for further mechanistic investigations.	pdac	27-31	P53	Homo sapiens	19-23
32234756-12	2020	The sensitivity of TP53mut PDAC to gemcitabine in CONKO-001 provides a lead for further mechanistic investigations.	gemcitabine	35-46	P53	Homo sapiens	19-23
21986580-9	2011	Crocetin (240 mumol/L) significantly induced cell cycle arrest through p53-dependent and -independent mechanisms accompanied with p21(WAF1/Cip1) induction.	crocetin	0-8	P53	Homo sapiens	71-74
21867723-7	2011	CYN induced changes in the mRNA expression of P53 and its downstream regulated DNA damage responsive genes MDM2, GADD45alpha and apoptosis genes, BCL-2 and BAX, as well as oxidative stress responsive genes (GPX1, SOD1, GSR, GCLC), while no changes in the expression of genes CDKN1A and CAT were observed.	cylindrospermopsin	0-3	P53	Homo sapiens	46-49
32456796-0	2020	CD147 promotes DNA damage response and gemcitabine resistance via targeting ATM/ATR/p53 and affects prognosis in pancreatic cancer.	gemcitabine	39-50	P53	Homo sapiens	84-87
32456796-5	2020	CD147 knockdown or monoclonal antibodies improved the killing effects of gemcitabine in gemcitabine resistant cells, exhibiting reduced activation of ATM/p53.	gemcitabine	73-84	P53	Homo sapiens	154-157
32456796-5	2020	CD147 knockdown or monoclonal antibodies improved the killing effects of gemcitabine in gemcitabine resistant cells, exhibiting reduced activation of ATM/p53.	gemcitabine	88-99	P53	Homo sapiens	154-157
32456796-6	2020	Moreover, we found the interaction of CD147 with ATM, ATR and p53, which was augmented in gemcitabine resistant cells.	gemcitabine	90-101	P53	Homo sapiens	62-65
21741966-8	2011	In the MDA-MB-231 cells, Frondoside A effectively increased the sub-G1 (apoptotic) cell fraction through the activation of p53, and subsequently the caspases 9 and 3/7 cell death pathways.	frondoside A	25-37	P53	Homo sapiens	123-126
21887591-2	2011	The current studies indicate that the combination of 1,25-dihydroxyvitamin D3 with radiation appears to kill p53 wild-type, estrogen receptor-positive ZR-75-1 breast tumor cells through autophagy.	Calcitriol	53-77	P53	Homo sapiens	109-112
32247830-8	2020	Meanwhile, KEGG enrichment analysis showed that the DEGs were mainly mapped on the immune pathways like "TNF signal pathway", "p53 signal pathway" and "JAK-STAT signal pathway", suggesting that these signal pathways may be responsible for the delayed peak of CyHV-2 infection in gibel carp after poly I:C treatment.	Poly I-C	296-304	P53	Homo sapiens	127-130
21815631-5	2011	We further characterized the DNA damage, generation of highly reactive oxygen species (hROS), and expression of proteins p21 and p53 in cells after exposure to iAs(III), DMA(III), and DMMTA(V).	dmmta	184-189	P53	Homo sapiens	129-132
32638521-8	2020	Increased DSBs were associated with enhanced expression and activation of pro-apoptotic p53 and significant apoptosis in oxLDL-treated BRCA2-silenced ECs.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	10-14	P53	Homo sapiens	88-91
21815631-6	2011	Cellular exposure to DMMTA(V) resulted in reduced protein expression of p53 and p21, increased DNA damage, and increased intracellular hROS (hydroxyl radical).	dmmta	21-26	P53	Homo sapiens	72-75
21892948-9	2011	Direct sequencing of p53 identified a G:C A:T mutation at a dipyrimidine site.	dipyrimidine	60-72	P53	Homo sapiens	21-24
32583791-6	2020	As main findings, phenolic compounds, saponins and alkaloids interfere with cancer progression by stimulating p53 expression, which can cause pro-apoptotic onset and restrict the anti-apoptotic activity, in addition to preventing telomerase enzyme activity.	Saponins	38-46	P53	Homo sapiens	110-113
21666438-5	2011	As a monotherapy, triphendiol-inhibited cell proliferation-induced p53-independent G2/M cell cycle arrest and activation of the intrinsic (mitochondrial) apoptosis pathway.	triphendiol	18-29	P53	Homo sapiens	67-70
32030889-9	2020	In 34 patients who received treatment with decitabine, 25 with TP53 mutations had higher overall response rate than those with wild-type TP53 (60% vs 22.2%, P = .03).	Decitabine	43-53	P53	Homo sapiens	63-67
32030889-9	2020	In 34 patients who received treatment with decitabine, 25 with TP53 mutations had higher overall response rate than those with wild-type TP53 (60% vs 22.2%, P = .03).	Decitabine	43-53	P53	Homo sapiens	137-141
21671008-0	2011	Insulin receptor signaling activated by penta-O-galloyl-alpha-D: -glucopyranose induces p53 and apoptosis in cancer cells.	penta-o-galloyl-alpha-d	40-63	P53	Homo sapiens	88-91
32186773-0	2020	Growth inhibitory role of the p53 activator SCH 529074 in non-small cell lung cancer cells expressing mutant p53.	SCH 529074	44-54	P53	Homo sapiens	30-33
21946198-3	2011	RESULTS: Compared with other control groups, the comet assay showed that MCF-7 cells with HSV-TK/GCV treatment had obvious comet tails, and the expression level of DNA damage response active genes and proteins changed obviously in the HSV-TK/GCV treatment group,such as ATM, p53 and p27,but CyclinE and CDK2 did not change.	Ganciclovir	97-100	P53	Homo sapiens	275-278
32186773-0	2020	Growth inhibitory role of the p53 activator SCH 529074 in non-small cell lung cancer cells expressing mutant p53.	SCH 529074	44-54	P53	Homo sapiens	109-112
32186773-3	2020	Recently, several p53 mutant reactivating compounds were discovered including SCH 529074.	SCH 529074	78-88	P53	Homo sapiens	18-21
32186773-8	2020	The results demonstrated that SCH 529074 treatment caused significant reduction in cell viability and colony formation activity in p53 mutant, p53 WT and p53-deficient cells.	SCH 529074	30-40	P53	Homo sapiens	131-134
32186773-8	2020	The results demonstrated that SCH 529074 treatment caused significant reduction in cell viability and colony formation activity in p53 mutant, p53 WT and p53-deficient cells.	SCH 529074	30-40	P53	Homo sapiens	143-146
32186773-8	2020	The results demonstrated that SCH 529074 treatment caused significant reduction in cell viability and colony formation activity in p53 mutant, p53 WT and p53-deficient cells.	SCH 529074	30-40	P53	Homo sapiens	143-146
32186773-9	2020	The treatment of NSCLC cells with SCH 529074 resulted in a dose-dependent induction of apoptosis and G0/G1 cell cycle arrest, which was associated with the activation of caspases (3 and 7), p53-independent upregulation of p21 and PUMA as well as increased LC3II, a biomarker of autophagy.	SCH 529074	34-44	P53	Homo sapiens	190-193
32186773-11	2020	The data indicated that SCH 529074 may exert its growth inhibitory function in a p53-independent manner in NSCLC cells.	SCH 529074	24-34	P53	Homo sapiens	81-84
21946198-4	2011	CONCLUSION: DNA damage on MCF-7 cells is resulted from HSV-TK/GCV in suicide gene therapy system through a p53-dependent signal pathway, causing cell cycle arrest and cell death.	Ganciclovir	62-65	P53	Homo sapiens	107-110
20839263-2	2011	Oxaliplatin-resistant HCT116 p53wt and p53(-/-) cell lines were generated, and the effects of oxaliplatin in combination with curcumin on resistance- and proliferation-associated proteins investigated.	Oxaliplatin	0-11	P53	Homo sapiens	29-32
31112603-6	2020	We provide in silico, molecular dynamics and experimental data to support that CucWi-N (i) possesses high capability to target mortalin-p53 interaction and hnRNP-K proteins, (ii) triggers replicative senescence and inhibits metastatic potential of the cancer cells, and (iii) inhibits tumor progression and metastasis in vivo.	cucwi	79-84	P53	Homo sapiens	136-139
20839263-5	2011	Curcumin in combination with oxaliplatin was able to decrease proliferative capacity of oxaliplatin-resistant p53 wildtype and p53(-/-) cell lines more effectively than oxaliplatin alone.	Oxaliplatin	29-40	P53	Homo sapiens	110-113
32167393-2	2020	Idasanutlin is a small-molecule inhibitor of MDM2, a negative regulator of tumor suppressor p53.	RG7388	0-11	P53	Homo sapiens	92-95
32167393-3	2020	By preventing the p53-MDM2 interaction, idasanutlin allows for p53 activation, particularly in patients with TP53 wild-type (WT) status.	RG7388	40-51	P53	Homo sapiens	18-21
20839263-5	2011	Curcumin in combination with oxaliplatin was able to decrease proliferative capacity of oxaliplatin-resistant p53 wildtype and p53(-/-) cell lines more effectively than oxaliplatin alone.	Oxaliplatin	29-40	P53	Homo sapiens	127-130
32167393-3	2020	By preventing the p53-MDM2 interaction, idasanutlin allows for p53 activation, particularly in patients with TP53 wild-type (WT) status.	RG7388	40-51	P53	Homo sapiens	63-66
32167393-3	2020	By preventing the p53-MDM2 interaction, idasanutlin allows for p53 activation, particularly in patients with TP53 wild-type (WT) status.	RG7388	40-51	P53	Homo sapiens	109-113
20839263-5	2011	Curcumin in combination with oxaliplatin was able to decrease proliferative capacity of oxaliplatin-resistant p53 wildtype and p53(-/-) cell lines more effectively than oxaliplatin alone.	Oxaliplatin	88-99	P53	Homo sapiens	110-113
20839263-5	2011	Curcumin in combination with oxaliplatin was able to decrease proliferative capacity of oxaliplatin-resistant p53 wildtype and p53(-/-) cell lines more effectively than oxaliplatin alone.	Oxaliplatin	88-99	P53	Homo sapiens	110-113
21486687-5	2011	It has been suggested that triptolide activates the p53 pathway to trigger apoptosis in these cells.	triptolide	27-37	P53	Homo sapiens	52-55
32323826-10	2020	Western blot analysis and RT-qPCR revealed that p53 activation and the expression of p21 were increased in glioma cells treated with lenalidomide.	Lenalidomide	133-145	P53	Homo sapiens	48-51
32216337-6	2020	Unexpectedly, this prodrug presents strikingly enhanced tumor penetration ability and utilizes a distinct action mode to overcome drug resistance, i.e., coumaplatin but not oxaliplatin induces cell senescence, p53-independent cell death, and immunogenic cell death along with T cell activation.	coumaplatin	153-164	P53	Homo sapiens	210-213
21628572-5	2011	As a consequence, when tumors arising from oncogenic Ras-transformed p53(-/-) and p53(-/-)Cry1(-/-)Cry2(-/-) cells are treated with the anticancer drug oxaliplatin, p53(-/-) tumors continue to grow whereas p53(-/-)Cry1(-/-)Cry2(-/-) tumors exhibit extensive apoptosis and stop growing.	Oxaliplatin	152-163	P53	Homo sapiens	82-85
31954175-7	2020	SKi also enhanced the stimulatory effect of the proteasome inhibitor, MG132 on the expression of the pro-survival protein XBP-1s and this was reduced by siRNA knockdown of SK2 and increased by knockdown of p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	70-75	P53	Homo sapiens	206-209
21628572-5	2011	As a consequence, when tumors arising from oncogenic Ras-transformed p53(-/-) and p53(-/-)Cry1(-/-)Cry2(-/-) cells are treated with the anticancer drug oxaliplatin, p53(-/-) tumors continue to grow whereas p53(-/-)Cry1(-/-)Cry2(-/-) tumors exhibit extensive apoptosis and stop growing.	Oxaliplatin	152-163	P53	Homo sapiens	82-85
32196468-2	2020	Since p53 network gives oscillatory response to DSBs, such interaction among cells could be modelled as an excitatory coupling of p53 network oscillators.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	48-52	P53	Homo sapiens	6-9
21628572-5	2011	As a consequence, when tumors arising from oncogenic Ras-transformed p53(-/-) and p53(-/-)Cry1(-/-)Cry2(-/-) cells are treated with the anticancer drug oxaliplatin, p53(-/-) tumors continue to grow whereas p53(-/-)Cry1(-/-)Cry2(-/-) tumors exhibit extensive apoptosis and stop growing.	Oxaliplatin	152-163	P53	Homo sapiens	82-85
32196468-2	2020	Since p53 network gives oscillatory response to DSBs, such interaction among cells could be modelled as an excitatory coupling of p53 network oscillators.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	48-52	P53	Homo sapiens	130-133
21454715-7	2011	A citrulline-mimicking Arg-NLS-Gln ING4 mutant, which has all Arg residues in the NLS mutated to Gln, loses its affinity for p53, can no longer promote p53 acetylation, and results in repression of downstream p21 expression.	Citrulline	2-12	P53	Homo sapiens	125-128
31638087-7	2020	H2S exerts its antioxidant effect by limiting free radical reactions through the activation of antioxidant enzymes, including superoxide dismutase, catalase, and glutathione peroxidase, which protect against the effects of aging by regulating apoptosis-related genes, including p53, Bax, and Bcl-2.	hydrogen sulfite	0-3	P53	Homo sapiens	278-281
21454715-7	2011	A citrulline-mimicking Arg-NLS-Gln ING4 mutant, which has all Arg residues in the NLS mutated to Gln, loses its affinity for p53, can no longer promote p53 acetylation, and results in repression of downstream p21 expression.	Citrulline	2-12	P53	Homo sapiens	152-155
31831363-0	2020	Effects of DHA-enriched fish oil on gene expression levels of p53 and NF-kappaB and PPAR-gamma activity in PBMCs of patients with T2DM: A randomized, double-blind, clinical trial.	Fish Oils	24-32	P53	Homo sapiens	62-65
31831363-3	2020	The aim of our study was to investigate the effects of docosahexaenoic acid (DHA)-enriched fish oil supplement on PPAR-gamma activity and mRNA expression levels of p53 and NF-kappaB.	Fish Oils	91-99	P53	Homo sapiens	164-167
21562496-2	2011	Here, we report that histone deacetylase inhibitors (HDACI), that is, MS-275, valproic acid or SAHA, provide a novel strategy for sensitization of medulloblastoma to DNA-damaging drugs such as Doxorubicin, VP16 and Cisplatin by promoting p53-dependent, mitochondrial apoptosis.	entinostat	70-76	P53	Homo sapiens	238-241
21562496-4	2011	Combined treatment with MS-275 and Doxorubicin or VP16 cooperates to promote binding of p53 to Bax and p53-dependent Bax activation, resulting in enhanced loss of mitochondrial membrane potential, cytochrome c release and caspase-dependent apoptosis.	entinostat	24-30	P53	Homo sapiens	88-91
21562496-4	2011	Combined treatment with MS-275 and Doxorubicin or VP16 cooperates to promote binding of p53 to Bax and p53-dependent Bax activation, resulting in enhanced loss of mitochondrial membrane potential, cytochrome c release and caspase-dependent apoptosis.	entinostat	24-30	P53	Homo sapiens	103-106
21617228-0	2011	Phenethyl isothiocyanate (PEITC) promotes G2/M phase arrest via p53 expression and induces apoptosis through caspase- and mitochondria-dependent signaling pathways in human prostate cancer DU 145 cells.	phenethyl isothiocyanate	26-31	P53	Homo sapiens	64-67
32080210-0	2020	Phase I studies of vorinostat with ixazomib or pazopanib imply a role of antiangiogenesis-based therapy for TP53 mutant malignancies.	Vorinostat	19-29	P53	Homo sapiens	108-112
32080210-1	2020	We performed two phase I trials of the histone deacetylase inhibitor vorinostat combined with either the vascular endothelial growth factor inhibitor pazopanib (NCT01339871) or the proteasome inhibitor ixazomib (NCT02042989) in patients with metastatic TP53 mutant solid tumors.	Vorinostat	69-79	P53	Homo sapiens	253-257
21524306-0	2011	The natural triterpene maslinic acid induces apoptosis in HT29 colon cancer cells by a JNK-p53-dependent mechanism.	maslinic acid	23-36	P53	Homo sapiens	91-94
31645443-7	2020	Intriguingly, Cer-RUB nanomicelle treatments restored p53-dependent tumor suppression and sensitivity to cisplatin in OVCAR-3 ovarian cancer cells and xenograft tumors carrying p53 R248Q mutation.	Ceramides	14-17	P53	Homo sapiens	54-57
31645443-7	2020	Intriguingly, Cer-RUB nanomicelle treatments restored p53-dependent tumor suppression and sensitivity to cisplatin in OVCAR-3 ovarian cancer cells and xenograft tumors carrying p53 R248Q mutation.	Ceramides	14-17	P53	Homo sapiens	177-180
21524306-11	2011	We show here that the anti-tumoral activity of maslinic acid might proceed via p53-mediated apoptosis by acting upon the main signaling components that lead to an increase in p53 activity and the induction of the rest of the factors that participate in the apoptotic pathway.	maslinic acid	47-60	P53	Homo sapiens	79-82
32016852-10	2020	For all compounds, a stronger effect on the level of the p53 protein was observed than for the reference compound-ellipticine.	ellipticine	114-125	P53	Homo sapiens	57-60
21524306-11	2011	We show here that the anti-tumoral activity of maslinic acid might proceed via p53-mediated apoptosis by acting upon the main signaling components that lead to an increase in p53 activity and the induction of the rest of the factors that participate in the apoptotic pathway.	maslinic acid	47-60	P53	Homo sapiens	175-178
21524306-12	2011	We found that in HT29 cells maslinic acid activated the expression of c-Jun NH2-terminal kinase (JNK), thus inducing p53.	maslinic acid	28-41	P53	Homo sapiens	117-120
21524306-15	2011	CONCLUSION: All these results suggest that maslinic acid induces apoptosis in human HT29 colon-cancer cells through the JNK-Bid-mediated mitochondrial apoptotic pathway via the activation of p53.	maslinic acid	43-56	P53	Homo sapiens	191-194
32731241-5	2020	Intestinal-type adenocarcinoma carrying a functional p53 protein may be treated with preoperative cisplatin, 5-fluorouracil, and leucovorin.	Leucovorin	129-139	P53	Homo sapiens	53-56
21412069-12	2011	All IPNB-M were negative for p53, and the frequency of positive p53 protein in IPNB-NM was at the middle level of that in IPNB-M and nonpapillary cholangiocarcinoma.	ipnb	79-83	P53	Homo sapiens	64-67
33163985-2	2020	Methods: From our predictive synthetic lethality model used in SL-BioDP, we inferred TP53 mutation lead to potential synergistic drug combination of Bortezomib and Vorinostat.	Vorinostat	164-174	P53	Homo sapiens	85-89
21412069-12	2011	All IPNB-M were negative for p53, and the frequency of positive p53 protein in IPNB-NM was at the middle level of that in IPNB-M and nonpapillary cholangiocarcinoma.	ipnb	79-83	P53	Homo sapiens	64-67
33163985-6	2020	Using drug screening data in cancer cell line, the sensitivity of the HDAC inhibitor drug Vorinostat was found to be increased in TP53 mutated cells where the proteasome pathway was downregulated.	Vorinostat	90-100	P53	Homo sapiens	130-134
21411309-8	2011	DUBs also control the level or subcellular compartmentalization of selective transcription factors, including the tumour suppressor p53.	dubs	0-4	P53	Homo sapiens	132-135
32463309-9	2020	Exposure of MCF7 cells with isopicrinine affected the expression of various genes involved in p53 signaling pathway.	isopicrinine	28-40	P53	Homo sapiens	94-97
21149266-0	2011	Rescue of non-sense mutated p53 tumor suppressor gene by aminoglycosides.	Aminoglycosides	57-72	P53	Homo sapiens	28-31
31871844-8	2019	Three drugs, mitomycin-C, doxorubicin and gemcitabine, were especially more sensitive to bladder cancer with the TP53 mutation.	gemcitabine	42-53	P53	Homo sapiens	113-117
2416545-4	1986	Our data demonstrated 3 major effects of halothane on the SEP: (a) a small but significant decrease in the average amplitude of the first two components (N25 and P30), (b) a significant increase in the average latency of the late positive component (P53) of the wave form, and (c) occasional obliteration of components N25, N40, P53, and N71, but never of P30.	Halothane	41-50	P53	Homo sapiens	250-253
2416545-4	1986	Our data demonstrated 3 major effects of halothane on the SEP: (a) a small but significant decrease in the average amplitude of the first two components (N25 and P30), (b) a significant increase in the average latency of the late positive component (P53) of the wave form, and (c) occasional obliteration of components N25, N40, P53, and N71, but never of P30.	Halothane	41-50	P53	Homo sapiens	329-332
21149266-4	2011	In this study, we explored the possibility of using aminoglycoside antibiotics to induce the production of a full-length functional p53 protein from a gene carrying a PTC.	Aminoglycosides	52-66	P53	Homo sapiens	132-135
31888155-7	2019	At the molecular level, ITR NPs were more effective than ITR solution in inducing pro-apoptotic Bax and p53 while reducing anti-apoptotic Bcl2 protein expression.	Itraconazole	24-27	P53	Homo sapiens	104-107
31888155-7	2019	At the molecular level, ITR NPs were more effective than ITR solution in inducing pro-apoptotic Bax and p53 while reducing anti-apoptotic Bcl2 protein expression.	Itraconazole	57-60	P53	Homo sapiens	104-107
21149266-6	2011	Using these cells, we demonstrated that aminoglycoside treatment stabilized the mutant mRNA, which would otherwise have been degraded by non-sense-mediated decay, resulting in the production of a functional full-length p53 protein.	Aminoglycosides	40-54	P53	Homo sapiens	219-222
21149266-7	2011	Finally, we showed that aminoglycoside treatment decreased the viability of cancer cells specifically in the presence of nonsense-mutated p53 gene.	Aminoglycosides	24-38	P53	Homo sapiens	138-141
33960434-6	2021	SP600125 also inhibited mRNA levels for all the aforementioned proteins, while SB203580 only affected p53 mRNA.	SB 203580	79-87	P53	Homo sapiens	102-105
21035490-3	2011	Further studies focusing on sphingolipid metabolizing enzymes have revealed that they function similarly both upstream and downstream of p53 activation.	Sphingolipids	28-40	P53	Homo sapiens	137-140
31578205-8	2019	Specifically, TP53 (p=0.01) and splicing factor (SF, SF3B1, ZRSR2, SRSF2; p&amp;lt;0.001), but not TET2 mutations were associated with reduced TFS which was not mitigated by RUX treatment.	ruxolitinib	174-177	P53	Homo sapiens	14-18
31004033-5	2019	In this study we tested the second-generation MDM2 inhibitor, RG7388, in patient-derived CLL cells and normal cells, examining its effect on the induction of p53-transcriptional targets.	RG7388	62-68	P53	Homo sapiens	158-161
21035490-5	2011	Thus, we propose that regulation of bioactive sphingolipid signaling molecules could be of therapeutic benefit in the treatment of p53-dependent cancers.	Sphingolipids	46-58	P53	Homo sapiens	131-134
31004033-6	2019	RG7388 potently decreased viability in p53-functional CLL cells, whereas p53-non-functional samples were more resistant to the drug.	RG7388	0-6	P53	Homo sapiens	39-42
33954816-0	2022	Venetoclax and decitabine in refractory TP53-mutated early T-cell precursor acute lymphoblastic leukemia.	venetoclax	0-10	P53	Homo sapiens	40-44
33954816-0	2022	Venetoclax and decitabine in refractory TP53-mutated early T-cell precursor acute lymphoblastic leukemia.	Decitabine	15-25	P53	Homo sapiens	40-44
31004033-7	2019	RG7388 induced a pro-apoptotic gene expression signature with upregulation of p53-target genes involved in the intrinsic (PUMA, BAX) and extrinsic (TNFRSF10B, FAS) pathways of apoptosis, as well as MDM2 Only a slight induction of CDKN1A was observed and upregulation of pro-apoptotic genes dominated, indicating that CLL cells are primed for p53-dependent apoptosis.	RG7388	0-6	P53	Homo sapiens	78-81
20974518-3	2011	Fisetin-induced apoptosis in HCT116 cells as indicated by TUNEL assay, Annexin V-FITC/PI double staining, Ser15-phosphorylation of p53, and cleavages of procaspase-3 and PARP.	fisetin	0-7	P53	Homo sapiens	131-134
31004033-7	2019	RG7388 induced a pro-apoptotic gene expression signature with upregulation of p53-target genes involved in the intrinsic (PUMA, BAX) and extrinsic (TNFRSF10B, FAS) pathways of apoptosis, as well as MDM2 Only a slight induction of CDKN1A was observed and upregulation of pro-apoptotic genes dominated, indicating that CLL cells are primed for p53-dependent apoptosis.	RG7388	0-6	P53	Homo sapiens	342-345
32346712-9	2019	No homozygous deletion of TP53(7) was found in three groups.Homozygous deletion of TP53 (8) was found in group A2(7/42), group A3(10/30) and group A3(10/60).The 1-year and 3-year DFS rates were 75.00% and 70.83% in group A1, 70.59% and 58.82% in group A2, 46.67% and 40.00% in group A3, with significant difference(P<0.05).	dfs	179-182	P53	Homo sapiens	83-87
33932107-4	2021	Prophylactic use of decitabine followed by DLI was planned in patients with TP53 or epigenetic modifier gene mutations.	Decitabine	20-30	P53	Homo sapiens	76-80
20974518-6	2011	Knockdown of securin in HCT116 p53-null cells potentiated fisetin-induced cytotoxicity by induction of apoptosis.	fisetin	58-65	P53	Homo sapiens	31-34
33879127-13	2021	These differences could be attributed to the lack of functional p53 in coordinating the cells response following cytotoxic treatment with daunorubicin, which appears to delay apoptosis and utilises alternative signalling mechanisms that need to be further explored.	Daunorubicin	138-150	P53	Homo sapiens	64-67
21976978-4	2011	p53 molecules were anchored to gold nanoparticles by means of the bifunctional linker 4-aminothiophenol (4-ATP).	4-aminothiophenol	86-103	P53	Homo sapiens	0-3
33876223-5	2021	The evolution pattern towards t-MN is then a complex process, shaped by the type of cancer therapy, the aging process, and the individual exposures, that favor additional hits, such as the acquisition of TP53 mutations and unfavorable karyotype abnormalities.	t-mn	30-34	P53	Homo sapiens	204-208
31819692-6	2019	Methylation-specific polymerase chain reaction (MS-PCR) technique was used to define the methylation status of the TP53 gene promoter that encompasses DNA extraction, bisulfite conversion, conventional PCR amplification, running on agarose gel and documentation.	hydrogen sulfite	167-176	P53	Homo sapiens	115-119
21976978-4	2011	p53 molecules were anchored to gold nanoparticles by means of the bifunctional linker 4-aminothiophenol (4-ATP).	4-aminothiophenol	105-110	P53	Homo sapiens	0-3
31683960-7	2019	Treatment of MDA-MB-231 cells with fruit ethyl acetate fraction (RSF EtOAc) increased expression 11of P53, Bax and activation of caspase 3/7.	SDZ 33-243	65-74	P53	Homo sapiens	102-105
33620775-2	2021	In bladder cancer, a unique distribution of mutations amongst several codons of TP53 has been hypothesised to be caused by environmental carcinogens including 4-aminobiphenyl (4-ABP).	4-biphenylamine	159-174	P53	Homo sapiens	80-84
33620775-2	2021	In bladder cancer, a unique distribution of mutations amongst several codons of TP53 has been hypothesised to be caused by environmental carcinogens including 4-aminobiphenyl (4-ABP).	4-biphenylamine	176-181	P53	Homo sapiens	80-84
21976978-6	2011	The Raman signal enhancement achieved by 4-ATP-mediated crosslinking of p53 to 50 nm gold nanoparticles enabled detect of this protein at a concentration down to 5 x 10-13 M.	4-aminothiophenol	41-46	P53	Homo sapiens	72-75
33620775-12	2021	In conclusion, the observed difference in the N-OH-4-ABP-induced TP53 mutation spectrum to that observed in human bladder tumours do not support a role of 4-ABP in human bladder cancer development.	4-biphenylamine	51-56	P53	Homo sapiens	65-69
21277993-15	2011	In addition, CYN increased the expression of p53 regulated genes involved in cell cycle arrest, DNA damage repair, and apoptosis.	cylindrospermopsin	13-16	P53	Homo sapiens	45-48
33733756-3	2021	Herein, we report irreversible inhibitors of the human double minute 2 (HDM2)/p53 PPI, which employ a reactive N-acyl-N-alkyl sulfonamide (NASA) group as a warhead.	n-acyl-n-alkyl sulfonamide	111-137	P53	Homo sapiens	78-81
33257842-6	2021	RT-PCR shows that TriCurin activates p53 and suppresses HPV16 mRNAs E1, E2, E4, E6 and E7 at 24 h in W12 cells.	tricurin	18-26	P53	Homo sapiens	37-40
31502598-7	2019	The feasibility of the method for the screening of the DNA-PK inhibitor and the inhibitor of p53-MDM2 interaction has been demonstrated and the half-maximal inhibitory concentration (IC50) values of wortmannin and Nutlin-3 (21 nM and 83 nM, respectively) were highly comparable with those obtained by other methods.	Wortmannin	199-209	P53	Homo sapiens	93-96
32184861-7	2019	The result showed that Baneh gum (100 microg/mL) significantly induced cell damage, activated caspase3, and increased P53 protein level.	baneh gum	23-32	P53	Homo sapiens	118-121
21399233-4	2011	Resistance to discodermolide is mediated via resistance to accelerated cell senescence, and is associated with reduced expression of the mTORC1 substrate, 4E-BP1 and increased expression of p53 [1].	discodermolide	14-28	P53	Homo sapiens	190-193
31288004-7	2019	beta-Cryptoxanthin treatment induced G0/G1 arrest, and reduced the expression of Cyclin E, Cyclin D1, cyclin-dependent kinases (CDK) of CDK4 and CDK6, and increased the expression of p53 and p21 in the two GC cells.	Beta-Cryptoxanthin	0-18	P53	Homo sapiens	183-186
33172976-4	2021	Here, we show that BGB324 (bemcentinib), a selective small-molecule AXL inhibitor, caused DNA damage and induced replication stress, indicated by ATR/CHK1 phosphorylation, more significantly in TP53-deficient NSCLC cell lines.	bemcentinib	19-25	P53	Homo sapiens	194-198
33172976-4	2021	Here, we show that BGB324 (bemcentinib), a selective small-molecule AXL inhibitor, caused DNA damage and induced replication stress, indicated by ATR/CHK1 phosphorylation, more significantly in TP53-deficient NSCLC cell lines.	bemcentinib	27-38	P53	Homo sapiens	194-198
20607649-3	2011	To further elucidate it, the effects of mitogen activated protein kinases (MAPKs) on the activity of triptolide towards prostate cancer cell lines were investigated in the present study using both LNCaP (p53 positive and androgen-dependent) and PC-3 (p53 deficient and androgen-independent) cells.	triptolide	101-111	P53	Homo sapiens	204-207
33511794-8	2021	Both in vitro and in vivo therapeutic results have exhibited high tumor inhibition efficiency (greater than 90%) of FA-N-GQDs as sonosensitizers while the oxidative stress response of tumor cells is activated through the PEX pathway and induced apoptosis via the p53 pathway.	fa-n-gqds	116-125	P53	Homo sapiens	263-266
31500399-5	2019	Depending on the GnRH isoform and the presence of 4Lys(Bu), the conjugates could regulate the expression of several apoptosis-related genes, especially tumor necrosis factor (TNF), tumor protein p53 (TP53) and the members of growth-factor signaling.	4lys	50-54	P53	Homo sapiens	195-198
31500399-5	2019	Depending on the GnRH isoform and the presence of 4Lys(Bu), the conjugates could regulate the expression of several apoptosis-related genes, especially tumor necrosis factor (TNF), tumor protein p53 (TP53) and the members of growth-factor signaling.	4lys	50-54	P53	Homo sapiens	200-204
31500399-6	2019	The stronger cytotoxicity of GnRH-I and GnRH-III conjugates containing 4Lys(Bu) was associated with a stronger inhibitory effect on the expression of growth-factor signaling elements in comparison with their 4Ser counterparts, in which the upregulation of TP53 and caspases (e.g., CASP9) seemed to play a more important role.	4lys	71-75	P53	Homo sapiens	256-260
20607649-3	2011	To further elucidate it, the effects of mitogen activated protein kinases (MAPKs) on the activity of triptolide towards prostate cancer cell lines were investigated in the present study using both LNCaP (p53 positive and androgen-dependent) and PC-3 (p53 deficient and androgen-independent) cells.	triptolide	101-111	P53	Homo sapiens	251-254
21058726-0	2010	Identification of the spiro(oxindole-3,3"-thiazolidine)-based derivatives as potential p53 activity modulators.	spiro(oxindole-3,3"-thiazolidine)	22-55	P53	Homo sapiens	87-90
31322224-10	2019	Furthermore, knockdown of MCM2 together with carboplatin treatment or UV irradiation increased the protein expression level of gamma-H2A histone family member X and p53 compared with control cells.	Carboplatin	45-56	P53	Homo sapiens	165-168
31322224-11	2019	The present data suggested that the increased sensitivity to carboplatin may occur via the p53-dependent apoptotic response.	Carboplatin	61-72	P53	Homo sapiens	91-94
30792212-0	2019	TP53 immunohistochemistry correlates with TP53 mutation status and clearance in decitabine-treated patients with myeloid malignancies.	Decitabine	80-90	P53	Homo sapiens	0-4
30792212-0	2019	TP53 immunohistochemistry correlates with TP53 mutation status and clearance in decitabine-treated patients with myeloid malignancies.	Decitabine	80-90	P53	Homo sapiens	42-46
33673439-6	2021	Our data further emphasize the impact of p53 status on the decay of gammaH2AX foci and the associated efficacy of the DSB repair in NSCLC cells survived after MFR.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	118-121	P53	Homo sapiens	41-44
33671256-6	2021	By four rounds of visual assays for mortalin and p53, we identified a novel synthetic small-molecule triazole derivative (4-[(1E)-2-(2-phenylindol-3-yl)-1-azavinyl]-1,2,4-triazole, henceforth named MortaparibPlus).	mortaparibplus	198-212	P53	Homo sapiens	49-52
21058726-1	2010	Here, we report the design of new analogues of spirooxoindolepyrrolidine nucleus as modulators of p53 activity.	spirooxoindolepyrrolidine	47-72	P53	Homo sapiens	98-101
33528589-11	2021	In 10-6 M SB-269970 treated PC-3 cells, there was significant increase in the expression of CAS-3 (4-fold), CAS-9 (2.5-fold), BAX (1.9-fold), and Tp-53 (4.8-fold) gene mRNA levels when compared to non-treated control group.	SB 269970	10-19	P53	Homo sapiens	146-151
20840854-0	2010	Non-dioxin-like PCBs interact with benzo[a]pyrene-induced p53-responses and inhibit apoptosis.	Polychlorinated Biphenyls	16-20	P53	Homo sapiens	58-61
21045142-6	2010	WP1130-mediated inhibition of tumor-activated DUBs results in downregulation of antiapoptotic and upregulation of proapoptotic proteins, such as MCL-1 and p53.	dubs	46-50	P53	Homo sapiens	155-158
33002289-0	2021	Gallic acid potentiates the apoptotic effect of paclitaxel and carboplatin via overexpression of Bax and P53 on the MCF-7 human breast cancer cell line.	Carboplatin	63-74	P53	Homo sapiens	105-108
31418371-4	2019	The expression of P53 mRNA increased in KMS-18 cells after treatment of decitabine (P&lt;0.05).	Decitabine	72-82	P53	Homo sapiens	18-21
31418371-5	2019	The methylation status of the P53 gene promoter in KMS-18 cells could be partially reversed by decitabine.	Decitabine	95-105	P53	Homo sapiens	30-33
31418371-6	2019	CONCLUSION: Decitabine can inhibit the proliferation of KMS-18 cells and induce their apoptosis, its mechanism ralates with partially reversing the methylation of P53 gene promoter in KMS-18 cells.	Decitabine	12-22	P53	Homo sapiens	163-166
31367258-10	2019	CF129 directly binds to p53 and E3 ligase MKRN1, and such an interaction leading to p53 protein ubiquitination and degradation.	cf129	0-5	P53	Homo sapiens	24-27
33557658-0	2021	Suberoylanilide hydroxamic acid enhances the radiosensitivity of lung cancer cells through acetylated wild-type and mutant p53-dependent modulation of mitochondrial apoptosis.	Vorinostat	0-31	P53	Homo sapiens	123-126
20380827-4	2010	Specifically, we focus on the role of asbestos in augmenting AEC apoptosis by the mitochondria- and p53-regulated death pathways that result from the production of iron-derived reactive oxygen species (ROS) and DNA damage.	iron-derived reactive oxygen species	164-200	P53	Homo sapiens	100-103
33557658-7	2021	RESULTS: Our results showed that SAHA induced radiosensitization in H1299 cells expressing wild-type p53, p53R175H or p53P223L, but this enhanced clonogenic cell death was not observed in parental H1299 (p53-null) cells or H1299 cells expressing p53 with K120R, A161T and V274R mutations.	Vorinostat	33-37	P53	Homo sapiens	101-104
33557658-7	2021	RESULTS: Our results showed that SAHA induced radiosensitization in H1299 cells expressing wild-type p53, p53R175H or p53P223L, but this enhanced clonogenic cell death was not observed in parental H1299 (p53-null) cells or H1299 cells expressing p53 with K120R, A161T and V274R mutations.	Vorinostat	33-37	P53	Homo sapiens	106-109
33557658-7	2021	RESULTS: Our results showed that SAHA induced radiosensitization in H1299 cells expressing wild-type p53, p53R175H or p53P223L, but this enhanced clonogenic cell death was not observed in parental H1299 (p53-null) cells or H1299 cells expressing p53 with K120R, A161T and V274R mutations.	Vorinostat	33-37	P53	Homo sapiens	106-109
33557658-10	2021	CONCLUSIONS: The results of this study suggest that wild-type and specific mutant forms of p53 mediate SAHA-induced radiosensitization by regulating mitochondrial apoptosis, and the stabilization of K120 acetylation by SAHA is the molecular basis contributing to radiosensitization in lung cancer cells.	Vorinostat	103-107	P53	Homo sapiens	91-94
33557658-10	2021	CONCLUSIONS: The results of this study suggest that wild-type and specific mutant forms of p53 mediate SAHA-induced radiosensitization by regulating mitochondrial apoptosis, and the stabilization of K120 acetylation by SAHA is the molecular basis contributing to radiosensitization in lung cancer cells.	Vorinostat	219-223	P53	Homo sapiens	91-94
31367258-10	2019	CF129 directly binds to p53 and E3 ligase MKRN1, and such an interaction leading to p53 protein ubiquitination and degradation.	cf129	0-5	P53	Homo sapiens	84-87
31367258-14	2019	Conclusions: Our study suggests that CF129 inhibits pancreatic cell proliferation and invasion by suppression of FOXC2 transcription, which depends on MKRN1-mediated ubiquitin-dependent p53 degradation.	cf129	37-42	P53	Homo sapiens	186-189
31062077-1	2019	PURPOSE: Idasanutlin, a selective small-molecule MDM2 antagonist in phase 3 testing for refractory/relapsed AML, is a non-genotoxic p53 activator with oral administration.	RG7388	9-20	P53	Homo sapiens	132-135
20945139-8	2010	Importantly, the synergistic effect of CsA or SFA with cisplatin was shown even in p53 defective Hep3B cells.	sanglifehrin A	46-49	P53	Homo sapiens	83-86
31231607-0	2019	p53-Dependent Anti-Proliferative and Pro-Apoptotic Effects of a Gold(I) N-Heterocyclic Carbene (NHC) Complex in Colorectal Cancer Cells.	carbene	87-94	P53	Homo sapiens	0-3
33321328-6	2021	E7 expression was restored by 5-Aza-2 deoxycytidine in p53 KO lines, suggesting a role of DNA methylation in this process.	Decitabine	30-51	P53	Homo sapiens	55-58
20945139-10	2010	In conclusion, CsA or SFA synergistically enhances cisplatin-induced apoptosis in HCC cells including the p53-defective Hep3B.	sanglifehrin A	22-25	P53	Homo sapiens	106-109
33501840-0	2021	Role of inhibiting Chk1-p53 pathway in hepatotoxicity caused by chronic arsenic exposure from coal-burning.	Arsenic	72-79	P53	Homo sapiens	24-27
30935902-6	2019	The inhibitory effect of curcumin, piperine and vitamin E on cell proliferation involves different markers, and in particular inhibits beta-catenin, cyclinD1 and p53, making them candidates for a possible use in alternative therapies although further studies are needed.	Vitamin E	48-57	P53	Homo sapiens	162-165
20637980-9	2010	CONCLUSIONS: To our knowledge, this study is the first to provide evidence that fisetin exerts a radiosensitizing effect in p53-mutant HT-29 cells.	fisetin	80-87	P53	Homo sapiens	124-127
33501840-5	2021	The results showed that arsenic induced liver damage, increased hepatocyte apoptosis and elevated the expression level of Chk1 and the ratios of p-p53/p53 and Bax/Bcl-2 in liver tissues, which were significantly attenuated by GBE.	Arsenic	24-31	P53	Homo sapiens	147-150
33501840-5	2021	The results showed that arsenic induced liver damage, increased hepatocyte apoptosis and elevated the expression level of Chk1 and the ratios of p-p53/p53 and Bax/Bcl-2 in liver tissues, which were significantly attenuated by GBE.	Arsenic	24-31	P53	Homo sapiens	151-154
33575281-0	2021	Case Report: Long-Term Chemotherapy With Hydroxyurea and Prednisolone in a Cat With a Meningioma: Correlation of FDG Uptake and Tumor Grade Assessed by Histopathology and Expression of Ki-67 and p53.	Prednisolone	57-69	P53	Homo sapiens	195-198
31011161-0	2019	Design and synthesis of anticancer 1-hydroxynaphthalene-2-carboxanilides with a p53 independent mechanism of action.	1-hydroxynaphthalene-2-carboxanilides	35-72	P53	Homo sapiens	80-83
20432447-2	2010	This study shows that restriction of tyrosine and phenylalanine (Tyr/Phe), glutamine (Gln), or methionine (Met) differentially modulates glucose metabolism, glycogen synthase kinase 3beta (GSK3beta), p53, and pyruvate dehydrogenase (PDH) in these two cell lines.	Phenylalanine	50-63	P53	Homo sapiens	200-203
30524021-0	2019	Targeted polyethylenimine/(p53 plasmid) nanocomplexes for potential antitumor applications.	Polyethyleneimine	9-25	P53	Homo sapiens	27-30
33399480-0	2021	Decitabine treatment in 311 patients with acute myeloid leukemia: outcome and impact of TP53 mutations - a registry based analysis.	Decitabine	0-10	P53	Homo sapiens	88-92
20566882-5	2010	The p53 response is triggered by the deficiency in pyrimidines that is developed due to a suppression of the functionally coupled mitochondrial pyrimidine biosynthesis enzyme dihydroorotate dehydrogenase (DHODH).	Pyrimidines	51-62	P53	Homo sapiens	4-7
32816178-13	2021	Besides, in the presence of arsenic, both of HOTAIR and LincRNA-p21 were upregulated significantly when P53 was knocked down.	Arsenic	28-35	P53	Homo sapiens	104-107
20596254-2	2010	BaP 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of benzo(a)pyrene (BaP), attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 gene mutations.	bpde-n2-dg	115-125	P53	Homo sapiens	146-149
30909652-5	2019	Here, we investigated three selected 4,11-diaminoanthra[2,3-b]furan-5,10-dione derivatives (compounds 1-3) for their cytotoxicity and the underlying molecular mechanisms in wild-type or p53-deficient HCC cells.	4,11-diaminoanthra[2,3-b]furan-5,10-dione	37-78	P53	Homo sapiens	186-189
20482847-0	2010	Griseofulvin stabilizes microtubule dynamics, activates p53 and inhibits the proliferation of MCF-7 cells synergistically with vinblastine.	Griseofulvin	0-12	P53	Homo sapiens	56-59
30721669-9	2019	The anti-proliferation effects of bepridil and azelastine on the cell lines with mutated and deleted p53 implied some p53-independent anti-proliferation effects.	Bepridil	34-42	P53	Homo sapiens	101-104
30721669-9	2019	The anti-proliferation effects of bepridil and azelastine on the cell lines with mutated and deleted p53 implied some p53-independent anti-proliferation effects.	Bepridil	34-42	P53	Homo sapiens	118-121
30837643-5	2019	Moreover, CHK1 knockdown or addition of a CHK1 inhibitor such as MK-8776, rabusertib or prexasertib enhances CPX-351-induced apoptosis in multiple TP53-null and TP53-wildtype AML cell lines.	CPX-351	109-116	P53	Homo sapiens	147-151
30837643-5	2019	Moreover, CHK1 knockdown or addition of a CHK1 inhibitor such as MK-8776, rabusertib or prexasertib enhances CPX-351-induced apoptosis in multiple TP53-null and TP53-wildtype AML cell lines.	CPX-351	109-116	P53	Homo sapiens	161-165
33097839-0	2021	Corrections: Reinstated p53 response and high anti-T-cell leukemia activity by the novel alkylating deacetylase inhibitor tinostamustine.	tinostamustine	122-136	P53	Homo sapiens	24-27
20424123-10	2010	In contrast, doxorubicin or nutlin-3 treatment-both leading to p53-p21 activation-or CDK2 inhibition had no effect on SKP2 regulation in MYCN-amplified cells.	nutlin	28-34	P53	Homo sapiens	63-66
33352689-7	2020	To gain further insight into the mode of action of ginsenoside M1, we demonstrated that ginsenoside M1 increased the expression levels of Bak, Bad, and p53 and induced apoptotic DNA breaks, G1 phase arrest, PI/Annexin V double-positive staining, and caspase-3/9 activation.	Ginsenosides	88-99	P53	Homo sapiens	152-155
33254717-6	2020	In animals, we found that arsenic exposures caused difficulties of social interaction and increased stereotypic behaviors in a dose-dependent manner, accompanied by increased neuronal apoptosis and upregulation of Hipk2-p53 pathway in the frontal cortex.	Arsenic	26-33	P53	Homo sapiens	220-223
33254717-8	2020	ASD children had significantly higher serum levels of 15 elements, among which arsenic, silicon, strontium, and vanadium were positively associated with both Hipk2 and p53.	Arsenic	79-86	P53	Homo sapiens	168-171
33254717-8	2020	ASD children had significantly higher serum levels of 15 elements, among which arsenic, silicon, strontium, and vanadium were positively associated with both Hipk2 and p53.	Silicon	88-95	P53	Homo sapiens	168-171
33254717-9	2020	Results from both the rat arsenic exposure and human case-control studies suggest a likely role of Hipk2-p53 pathway in ASD development induced by exposures to environmental pollutants such as arsenic.	Arsenic	26-33	P53	Homo sapiens	105-108
33254717-9	2020	Results from both the rat arsenic exposure and human case-control studies suggest a likely role of Hipk2-p53 pathway in ASD development induced by exposures to environmental pollutants such as arsenic.	Arsenic	193-200	P53	Homo sapiens	105-108
30667081-4	2019	A CRISPR-Cas9 system and a TP53 inhibitor, NSC59984, were also used to specifically knock-out and inhibit mutant TP53 in the human osteosarcoma cell lines, KHOS, and KHOSR2.	1-(4-methylpiperazin-1-yl)-3-(5-nitrofuran-2-yl)prop-2-en-1-one	43-51	P53	Homo sapiens	113-117
32767230-0	2020	Crosstalk between Noxa, Bcl-2, and ceramide in mediating p53-dependent apoptosis in Molt-4 human T-cell leukemia.	Ceramides	35-43	P53	Homo sapiens	57-60
19728331-0	2010	Ursodeoxycholic acid switches oxaliplatin-induced necrosis to apoptosis by inhibiting reactive oxygen species production and activating p53-caspase 8 pathway in HepG2 hepatocellular carcinoma.	Oxaliplatin	30-41	P53	Homo sapiens	136-139
32767230-2	2020	The tumor suppressor p53 stimulates various downstream targets that presumably trigger, individually or in concert, de novo ceramide synthesis and intrinsic apoptosis via mitochondrial outer membrane permeabilization (MOMP).	Ceramides	124-132	P53	Homo sapiens	21-24
32767230-3	2020	Among these targets, BH3-only protein Noxa was found to be promptly activated by p53 prior to ceramide accumulation and apoptosis in response to irradiation.	Ceramides	94-102	P53	Homo sapiens	81-84
30499118-6	2019	Vorinostat sensitized DU145 cells to PARPi/IR and decreased mutant p53.	Vorinostat	0-10	P53	Homo sapiens	67-70
20393600-0	2010	Acrolein induces apoptosis through the death receptor pathway in A549 lung cells: role of p53.	Acrolein	0-8	P53	Homo sapiens	90-93
30554333-3	2019	In this study, we aimed to further clarify the mechanism of inactivation of TP53 in GAED in the light of promoter methylation of TP53, and expression of methylation-associated proteins such as Ten-eleven translocation (TET) 1 and 5-hydroxymethylcytosine (5-hmc) in addition to ATM mutations.	5-hydroxymethylcytosine	230-253	P53	Homo sapiens	76-80
33253182-4	2020	Using this system and quantitative omics analyses, we demonstrate that acetyl-CoA depletion alters the integrity of the nucleolus, impairing ribosomal RNA synthesis and evoking the ribosomal protein-dependent activation of p53.	Acetyl Coenzyme A	71-81	P53	Homo sapiens	223-226
20393600-9	2010	Activation of p53 and increased expression of p53-upregulated modulator of apoptosis (PUMA) occurred in response to acrolein.	Acrolein	116-124	P53	Homo sapiens	14-17
30813936-12	2019	CONCLUSIONS: The delay in DSB repair and lower sensitivity to daunorubicin seen in the B lymphocyte derived SUP-B15 cells could be due to loss of function of p53 that may be correlated to increased expression of SOD2 and lower ROS production.	Daunorubicin	62-74	P53	Homo sapiens	158-161
30838093-3	2019	Wild type (WT) p53 contains a proline at amino acid 47, but approximately 1% of African-Americans express a p53 allele with a serine at amino acid 47 (Pro47Ser, hereafter S47).	pro47ser	151-159	P53	Homo sapiens	108-111
32911193-7	2020	Acyl-lysine peptide competition, pharmacological inhibition, and inhibitory post-translational modification of Sirt1 resulted in the loss of p53 ABP labeling both in vitro and in HEK293T cell lysates, consistent with the ABP measuring decreased Sirt1 activity.	acyl-lysine peptide	0-19	P53	Homo sapiens	141-144
32524685-18	2020	APT SImean exhibited a positive correlation with p53 labeling index and Ki-67 labeling index (r = 0.3741, P = 0.0135; r = 0.7048; P < 0.001, respectively).	apt simean	0-10	P53	Homo sapiens	49-52
20393600-9	2010	Activation of p53 and increased expression of p53-upregulated modulator of apoptosis (PUMA) occurred in response to acrolein.	Acrolein	116-124	P53	Homo sapiens	46-49
20140875-3	2010	RESULTS: The frequency of p53 deletion in the 38 patients with CCA (44.74%) was significantly higher than that in the 24 cases without CCA (4.16%) (P&lt;0.01).	1-methylcyclohexanecarboxylic acid	63-66	P53	Homo sapiens	26-29
32905825-4	2020	In addition, we found that miR-513a-5p-induced by 4-ABP could suppress p53 expression and HR repair activity.	4-biphenylamine	50-55	P53	Homo sapiens	71-74
32905825-5	2020	On the other hand, the levels of p53, miR-513a-5p, and gammaH2AX were attenuated by 5 mM N-acetyl-l-cysteine (NAC) pretreatment, indicating that the reactive oxygen species (ROS)-dependent p53-miR-513a-5p was involved in DSB repair in 4-ABP-treated cells.	4-biphenylamine	235-240	P53	Homo sapiens	33-36
32905825-6	2020	These findings indicated that the ROS/p53/miR-513a-5p/p53 loop axis plays a relevant role in regulating HR repair which may facilitate our understanding of molecular mechanisms regarding how miR-513a-5p impacts DSB repair in 4-ABP-treated cells.	4-biphenylamine	225-230	P53	Homo sapiens	38-41
32905825-6	2020	These findings indicated that the ROS/p53/miR-513a-5p/p53 loop axis plays a relevant role in regulating HR repair which may facilitate our understanding of molecular mechanisms regarding how miR-513a-5p impacts DSB repair in 4-ABP-treated cells.	4-biphenylamine	225-230	P53	Homo sapiens	54-57
29769744-7	2019	Taken together, NADPH abrogated MPTP-induced p38MAPK phosphorylation, TP53 nuclear translocation, and Bax induction, and finally, MPTP/MPP+-induced apoptosis of DA neurons.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	32-36	P53	Homo sapiens	70-74
19913028-13	2010	Disrupting the nonnative DBD-DBD interaction or transiently inhibiting tetramerization and allowing p53 to fold as a monomer may be potential strategies for pharmacological intervention in cancer.	dbd-dbd	25-32	P53	Homo sapiens	100-103
30139768-4	2019	We found that anlotinib inhibits the cell viability of papillary thyroid cancer and ATC cell lines, likely due to abnormal spindle assembly, G2/M arrest, and activation of TP53 upon anlotinib treatment.	anlotinib	14-23	P53	Homo sapiens	172-176
30139768-4	2019	We found that anlotinib inhibits the cell viability of papillary thyroid cancer and ATC cell lines, likely due to abnormal spindle assembly, G2/M arrest, and activation of TP53 upon anlotinib treatment.	anlotinib	182-191	P53	Homo sapiens	172-176
30258223-3	2019	Herein, we performed an in vitro biology test and found that 4,4"-SAD stimulated the apoptosis of tumor cells in the human hepatocellular carcinoma cell lines PLC/PRF/5 and HuH-7 by activating caspase-3, caspase-8, caspase-9, PARP, p53, and cyclin B1, as well as by regulating the Bax/Bcl-2 ratio.	4,4"-sad	61-69	P53	Homo sapiens	232-235
33194542-0	2020	Efficacy of ruxolitinib in a patient with myelodysplastic/myeloproliferative neoplasm unclassifiable and co-mutated JAK2, SF3B1 and TP53.	ruxolitinib	12-23	P53	Homo sapiens	132-136
33149608-8	2020	Conversely, RNF126 overexpression downregulated p53 and p21 but promoted pRb expression, which was reversed by a classic proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	P53	Homo sapiens	48-51
33193609-8	2020	Taken together, our findings revealed the essential significance of the MC-LR and ctHBx on the PP2A/MAPK/p53, cdc25C and cdc2 axis in the formation and development of HCC and identified MC-LR and ctHBx as potential causal cofactors of hepatocarcinogenesis.	cthbx	82-87	P53	Homo sapiens	105-108
19751709-0	2009	Non-dioxin-like-PCBs phosphorylate Mdm2 at Ser166 and attenuate the p53 response in HepG2 cells.	Polychlorinated Biphenyls	15-20	P53	Homo sapiens	68-71
19880322-0	2009	N-acylpolyamine inhibitors of HDM2 and HDMX binding to p53.	n-acylpolyamine	0-15	P53	Homo sapiens	55-58
32881246-0	2020	Pioglitazone alleviates cisplatin nephrotoxicity by suppressing mitochondria-mediated apoptosis via SIRT1/p53 signalling.	Pioglitazone	0-12	P53	Homo sapiens	106-109
32881246-6	2020	Pioglitazone treatment significantly increased cell viability, promoted SIRT1-p53 interaction, upregulated Bcl-2 expression, activated SIRT1 and elevated mitochondrial ATP synthesis after cisplatin treatment.	Pioglitazone	0-12	P53	Homo sapiens	78-81
29968167-7	2019	These results were further corroborated by studies that demonstrate biacacetin to regulate several key markers of apoptosis like Caspase 3, p53, Bax, and poly-ADP-ribose polymerase-1.	biacacetin	68-78	P53	Homo sapiens	140-143
30475060-3	2019	Butyrate differentiates HT-29 cells by relaxing the perturbation, caused by mutations of Adenomatous polyposis coli (APC) and TP53 genes, the most frequent mutations observed in CRC.	Butyrates	0-8	P53	Homo sapiens	126-130
33042406-6	2020	In vitro PDA treatment could dose-dependently induce the expression of the transcription factor FOXM1 (forkhead box M1) and several proapoptotic genes, such as PUMA (p53-upregulated modulator of apoptosis), BAX (B-cell/lymphoma 2-associated X) and APAF1 (apoptotic peptidase activating factor 1), thereby causing apoptosis.	pentadecanoic acid	9-12	P53	Homo sapiens	166-169
30475060-4	2019	We constructed protein-protein interaction network (PPIN) with the differentially expressed genes after butyrate treatment and extracted the hub genes from the PPIN, which also participated in the APC-TP53 network.	Butyrates	104-112	P53	Homo sapiens	201-205
19582475-0	2009	Gambogic acid reduced bcl-2 expression via p53 in human breast MCF-7 cancer cells.	gambogic acid	0-13	P53	Homo sapiens	43-46
19858236-6	2009	The results indicated that gene expressions concerning antioxidant system, i.e., thioredoxin family, 24-dehydrocholesterol reductase (DHCR24), and tumor suppressor protein p53, were altered by PBDEs exposure in HUVECs.	Halogenated Diphenyl Ethers	193-198	P53	Homo sapiens	172-175
30577494-0	2018	ATM Dependent DUSP6 Modulation of p53 Involved in Synergistic Targeting of MAPK and p53 Pathways with Trametinib and MDM2 Inhibitors in Cutaneous Melanoma.	trametinib	102-112	P53	Homo sapiens	34-37
30577494-0	2018	ATM Dependent DUSP6 Modulation of p53 Involved in Synergistic Targeting of MAPK and p53 Pathways with Trametinib and MDM2 Inhibitors in Cutaneous Melanoma.	trametinib	102-112	P53	Homo sapiens	84-87
30577494-3	2018	The combination treatments induced higher levels of p53 target gene transcripts and protein products, resulting in increased cell cycle arrest and apoptosis compared with MDM2 inhibitors alone, suggesting trametinib synergized with MDM2 inhibitors via upregulation of p53-dependent pathways.	trametinib	205-215	P53	Homo sapiens	52-55
30577494-3	2018	The combination treatments induced higher levels of p53 target gene transcripts and protein products, resulting in increased cell cycle arrest and apoptosis compared with MDM2 inhibitors alone, suggesting trametinib synergized with MDM2 inhibitors via upregulation of p53-dependent pathways.	trametinib	205-215	P53	Homo sapiens	268-271
29644528-0	2018	A novel, semi-synthetic diterpenoid 16(R and S)-phenylamino-cleroda-3,13(14), Z-dien-15,16 olide (PGEA-AN) inhibits the growth and cell survival of human neuroblastoma cell line SH-SY5Y by modulating P53 pathway.	Diterpenes	24-35	P53	Homo sapiens	200-203
30501707-10	2018	Among 87 patients received decitabine treatment, the TP53 gene mutation occured in 11 (12.6%) patients.	Decitabine	27-37	P53	Homo sapiens	53-57
32934219-5	2020	Small-molecule drugs targeting the CDK9 kinase, dinaciclib, flavopiridol, roscovitine, AT-7519, SNS-032, and DRB, diminished MDM4 levels and activated p53 in A375 melanoma and MCF7 breast carcinoma cells with only a limited effect on MDM2.	dinaciclib	48-58	P53	Homo sapiens	151-154
33205006-10	2020	Suppression of ceramide glycosylation significantly decreased Gb3-cSrc in GEMs, beta-catenin, and methyltransferase-like 3 for m6A RNA methylation, thus altering pre-mRNA splicing, resulting in upregulated expression of wild-type p53 protein, but not mutants, in cells carrying p53 R273H.	Ceramides	15-23	P53	Homo sapiens	230-233
33205006-10	2020	Suppression of ceramide glycosylation significantly decreased Gb3-cSrc in GEMs, beta-catenin, and methyltransferase-like 3 for m6A RNA methylation, thus altering pre-mRNA splicing, resulting in upregulated expression of wild-type p53 protein, but not mutants, in cells carrying p53 R273H.	Ceramides	15-23	P53	Homo sapiens	278-281
30501707-12	2018	Multivariate logistic regression model showed that the complex karyotype, Plt count doubling after 1 course treatment, TP53 mulation and high expression of hENT1 mRNA were the independent prognostic factors for predicting the CR after decitabine treatment.	Decitabine	235-245	P53	Homo sapiens	119-123
32705198-8	2020	Moreover, the expression levels of p53, Bax, apoptotic peptidase activating factor 1, cytochrome C, cleaved caspase-3/9 and cleaved poly (ADP-ribose) polymerase were upregulated, and the expression levels of Bcl-2, Bcl-xl and phosphorylated ATM serine/threonine kinase were downregulated by aconitine.	Aconitine	291-300	P53	Homo sapiens	35-38
19642109-1	2009	The tumor suppressor p53 interacts with the redox copper protein Azurin (AZ) forming a complex which is of some relevance in biomedicine and cancer therapy.	biomedicine	125-136	P53	Homo sapiens	21-24
32417172-0	2020	O-linked N-acetylgalactosamine modification is present on the tumor suppressor p53.	o-linked	0-8	P53	Homo sapiens	79-82
32417172-8	2020	RESULTS: The p53 was O-GalNAc glycosylated in cells.	N-acetylgalactosaminuronic acid	23-29	P53	Homo sapiens	13-16
30483050-7	2018	We found that treatment of 400 muM GM elicited the formation of ROS, which, in turn, led to PINK1 degradation, parkin recruitment, autophagy formation, an increase of p53 and cleaved-caspase 3 in HEI-OC1 cells and murine HCs.	Gentamicins	35-37	P53	Homo sapiens	167-170
30483050-9	2018	Moreover, PINK1 interference contributed to a decrease of autophagy but an increase of p53 level in HEI-OC1 cells in response to GM stimulus.	Gentamicins	129-131	P53	Homo sapiens	87-90
30483050-10	2018	Findings from this work indicate that PINK1 alleviates the GM-elicited ototoxicity via induction of autophagy and resistance the increase of p53 in HCs.	Gentamicins	59-61	P53	Homo sapiens	141-144
19887545-0	2009	Small-molecule inhibition of Wee1 kinase by MK-1775 selectively sensitizes p53-deficient tumor cells to DNA-damaging agents.	adavosertib	44-51	P53	Homo sapiens	75-78
30253242-0	2018	The development of piperidinones as potent MDM2-P53 protein-protein interaction inhibitors for cancer therapy.	2-piperidone	19-32	P53	Homo sapiens	48-51
32428595-0	2020	Corrigendum to "Sesamin suppresses NSCLC cell proliferation through cyclin D1 inhibition-dependent cell cycle arrest via Akt/p53 pathway" [Toxicology and applied pharmacology, 387 (2020) 114848].	sesamin	16-23	P53	Homo sapiens	125-128
32727075-10	2020	In addition, Rapha Myr  suppresses the expression of the oncogenic p53 mutant protein.	rapha myr	13-22	P53	Homo sapiens	67-70
30253242-4	2018	This review is focused on the discovery and development of piperidinone-based MDM2-p53 inhibitors for cancer therapy, including the identification of hit compounds, hit-to-lead optimizations, binding models of ligands in the active site of MDM2, metabolic studies, and preclinical data of advanced piperidinone-based MDM2-p53 inhibitors.	2-piperidone	59-71	P53	Homo sapiens	83-86
19887545-6	2009	MK-1775 abrogates G(2) DNA damage checkpoint, leading to apoptosis in combination with DNA-damaging chemotherapeutic agents such as gemcitabine, carboplatin, and cisplatin selectively in p53-deficient cells.	adavosertib	0-7	P53	Homo sapiens	187-190
30253242-4	2018	This review is focused on the discovery and development of piperidinone-based MDM2-p53 inhibitors for cancer therapy, including the identification of hit compounds, hit-to-lead optimizations, binding models of ligands in the active site of MDM2, metabolic studies, and preclinical data of advanced piperidinone-based MDM2-p53 inhibitors.	2-piperidone	59-71	P53	Homo sapiens	322-325
30253242-4	2018	This review is focused on the discovery and development of piperidinone-based MDM2-p53 inhibitors for cancer therapy, including the identification of hit compounds, hit-to-lead optimizations, binding models of ligands in the active site of MDM2, metabolic studies, and preclinical data of advanced piperidinone-based MDM2-p53 inhibitors.	2-piperidone	298-310	P53	Homo sapiens	83-86
32681102-9	2020	A combination treatment with AZD5363 and FH535 enhanced p53 expression, by modulating MDM2 activation; however, AZD5363 treatment alone restricted p53 to the nucleus by inhibiting dynamin-related protein activation.	capivasertib	29-36	P53	Homo sapiens	56-59
32681102-9	2020	A combination treatment with AZD5363 and FH535 enhanced p53 expression, by modulating MDM2 activation; however, AZD5363 treatment alone restricted p53 to the nucleus by inhibiting dynamin-related protein activation.	capivasertib	112-119	P53	Homo sapiens	147-150
21160963-4	2009	In both the BilIN and IPNB series, the expression of p21, p53, and cyclin D1 was upregulated with histological progression.	ipnb	22-26	P53	Homo sapiens	58-61
32404543-4	2020	Latifolin reversed the senescence-like phenotypes of the oxidant-challenged model, including senescence-associated beta-galactosidase (SA-beta-gal) staining, cell proliferation, and the expression of senescence-related proteins, such as caveolin-1, ac-p53, p21Cip1/WAF1, p16Ink4alpha, pRb, and cyclinD1.	latifolin	0-9	P53	Homo sapiens	252-255
32373892-7	2020	Moreover, linc-ROR siRNA also down-regulated the PI3K/AKT pathway in arsenite-transformed HaCaT cells, and treatment with AKT inhibitor wortmannin restored P53 activity, implying that linc-ROR inhibits P53 activity by activating the PI3K/AKT pathway.	Wortmannin	136-146	P53	Homo sapiens	156-159
30352966-0	2018	Prolonged Idasanutlin (RG7388) Treatment Leads to the Generation of p53-Mutated Cells.	RG7388	10-21	P53	Homo sapiens	68-71
30352966-6	2018	In the present study, we show that secondary resistance occurs also after treatment of p53wt cells with idasanutlin (RG7388, RO5503781), which is the only MDM2 antagonist that has passed phase II and entered phase III clinical trials, so far.	RG7388	104-115	P53	Homo sapiens	87-90
32373892-7	2020	Moreover, linc-ROR siRNA also down-regulated the PI3K/AKT pathway in arsenite-transformed HaCaT cells, and treatment with AKT inhibitor wortmannin restored P53 activity, implying that linc-ROR inhibits P53 activity by activating the PI3K/AKT pathway.	Wortmannin	136-146	P53	Homo sapiens	202-205
30352966-7	2018	Idasanutlin strongly activates p53, as evidenced by the induction of p21 expression and potent cell cycle arrest in all the three cell lines tested, i.e., MCF-7, U-2 OS, and SJSA-1.	RG7388	0-11	P53	Homo sapiens	31-34
30352966-12	2018	Thus, although idasanutlin presents much improved activities compared to its precursor, it displays the similar weaknesses, which are limited elimination of cancer cells and the generation of p53-mutated drug-resistant subpopulations.	RG7388	15-26	P53	Homo sapiens	192-195
30297838-5	2018	Ceramide binding stabilizes p53 and disrupts its complex with E3 ligase MDM2 leading to the p53 accumulation, nuclear translocation and activation of the downstream targets.	Ceramides	0-8	P53	Homo sapiens	28-31
30297838-5	2018	Ceramide binding stabilizes p53 and disrupts its complex with E3 ligase MDM2 leading to the p53 accumulation, nuclear translocation and activation of the downstream targets.	Ceramides	0-8	P53	Homo sapiens	92-95
32642409-3	2020	Transcriptome and proteome profiling revealed that the antitumor activity of ginsenosides is closely associated with P53 protein.	Ginsenosides	77-89	P53	Homo sapiens	117-120
32642409-5	2020	The results of integrative multiomics analysis revealed P53 protein as a potential key target that influences the anti-tumor activity of ginsenosides.	Ginsenosides	137-149	P53	Homo sapiens	56-59
32642409-6	2020	Furthermore, by applying affinity mass spectrometry (MS) screening and surface plasmon resonance fragment library screening, we confirmed that 20(S)-protopanaxatriol directly targeted adjacent regions of the P53 DNA-binding pocket and promoted the stability of P53-DNA interactions, which further induced a series of omics changes.	protopanaxatriol	145-165	P53	Homo sapiens	208-211
32642409-6	2020	Furthermore, by applying affinity mass spectrometry (MS) screening and surface plasmon resonance fragment library screening, we confirmed that 20(S)-protopanaxatriol directly targeted adjacent regions of the P53 DNA-binding pocket and promoted the stability of P53-DNA interactions, which further induced a series of omics changes.	protopanaxatriol	145-165	P53	Homo sapiens	261-264
19428175-2	2009	Although it was proved that GA enhances p53 protein level through inhibition of MDM2 in p53 wild-type cancer cells, the mechanisms of MDM2 inhibition especially with the absence of p53 are not fully understood.	gambogic acid	28-30	P53	Homo sapiens	88-91
19428175-8	2009	Additionally, GA increased p21(Waf1/CIP1) expression in p53 null cancer cells, which was associated with GA-mediated impairing of the interaction between MDM2 and p21(Waf1/CIP1).	gambogic acid	14-16	P53	Homo sapiens	56-59
32217375-0	2020	Bromocoumarinplatin, targeting simultaneously mitochondria and nuclei with p53 apoptosis pathway to overcome cisplatin resistance.	bromocoumarinplatin	0-19	P53	Homo sapiens	75-78
29945994-3	2018	Well-known mutations of TP53, APC, RNF43, and RPL22 were recurrently detected in synchronous GA/GC pairs.	Gallium	93-95	P53	Homo sapiens	24-28
19428175-9	2009	Furthermore, the apoptosis, cytotoxicity and G2/M cell cycle arrest induced by GA were detected in both p53 wild-type and p53 null cancer cells.	gambogic acid	79-81	P53	Homo sapiens	104-107
32172299-4	2020	However, 17p-deleted, p53-mutated or IGHV-UM subgroups are generally resistant to FCR, and much better responses are seen with ibrutinib and venetoclax, frequently inducing MRD negativity that hopefully will be translated into durable remissions.	venetoclax	141-151	P53	Homo sapiens	22-25
19428175-9	2009	Furthermore, the apoptosis, cytotoxicity and G2/M cell cycle arrest induced by GA were detected in both p53 wild-type and p53 null cancer cells.	gambogic acid	79-81	P53	Homo sapiens	122-125
19428175-11	2009	It is concluded that GA down-regulates the MDM2 oncogene and exerts the anti-tumor activity independent of p53, and therefore provide more evidences for its therapeutic application.	gambogic acid	21-23	P53	Homo sapiens	107-110
30097406-2	2018	Lenalidomide resistance, including primary resistance, occurs by clonal evolution, which is frequently attributable to the presence of somatic mutations in the DNA-binding domain of the TP53 gene.	Lenalidomide	0-12	P53	Homo sapiens	186-190
19247656-0	2009	Polymorphisms in p53, GSTP1 and XRCC1 predict relapse and survival of gastric cancer patients treated with oxaliplatin-based adjuvant chemotherapy.	Oxaliplatin	107-118	P53	Homo sapiens	17-20
30274821-0	2018	Synergistic effect of Nutlin-3 combined with MG-132 on schwannoma cells through restoration of merlin and p53 tumour suppressors.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	45-51	P53	Homo sapiens	106-109
30274821-11	2018	Nutlin-3 combined with MG-132 narrowed this between-group difference and triggered stronger inhibitory effects on the growth of schwannomas through coordinated reactivation of p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	23-29	P53	Homo sapiens	176-179
32042057-13	2020	GLS2 expression and nuclear accrual notably increased by treatment of SH-SY5Y cells with PMA and it correlated with cell cycle arrest at G2/M, upregulation of tumor suppressor p53 and p21 protein.	20-oxo-20-deoxy-12-myristate 13-acetate	89-92	P53	Homo sapiens	176-179
19247656-6	2009	CONCLUSION: Testing for p53 Arg72Pro, GSTP1 Ile105Val, and XRCC1 Arg399Gln polymorphisms may allow identification of gastric cancer patients who will benefit from oxaliplatin-based adjuvant chemotherapy.	Oxaliplatin	163-174	P53	Homo sapiens	24-27
31937750-9	2020	In CRC cells, carboplatin upregulated the expression of BORG and BORG negatively regulated p53.	Carboplatin	14-25	P53	Homo sapiens	91-94
19581934-0	2009	Impaired p53 binding to importin: a novel mechanism of cytoplasmic sequestration identified in oxaliplatin-resistant cells.	Oxaliplatin	95-106	P53	Homo sapiens	9-12
30233720-8	2018	In addition, propofol treatment significantly increased the levels of forkhead box (FOX)O1, FOXO3, Bim, pro-caspase-3, active caspase-3, p53 and p21.	Propofol	13-21	P53	Homo sapiens	137-140
31883611-7	2020	Moreover, MWE reduced the serum ALT and AST, HCC marker, cleavage caspases, Ser-15-p53 and Ser46-p53 induced by DEN.	Diethylnitrosamine	112-115	P53	Homo sapiens	83-86
19581934-2	2009	Drug-resistant KB cells selected with cisplatin or oxaliplatin were found to have increased p53 levels and in oxaliplatin-selected cells, a larger p53 predominantly in the cytoplasm.	Oxaliplatin	51-62	P53	Homo sapiens	92-95
31883611-7	2020	Moreover, MWE reduced the serum ALT and AST, HCC marker, cleavage caspases, Ser-15-p53 and Ser46-p53 induced by DEN.	Diethylnitrosamine	112-115	P53	Homo sapiens	97-100
29498006-7	2018	Furthermore, nimesulide with MPTP increased apoptotic protein cleaved caspase-3 and also induced expression of p53 gene.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	29-33	P53	Homo sapiens	111-114
19581934-2	2009	Drug-resistant KB cells selected with cisplatin or oxaliplatin were found to have increased p53 levels and in oxaliplatin-selected cells, a larger p53 predominantly in the cytoplasm.	Oxaliplatin	51-62	P53	Homo sapiens	147-150
19581934-2	2009	Drug-resistant KB cells selected with cisplatin or oxaliplatin were found to have increased p53 levels and in oxaliplatin-selected cells, a larger p53 predominantly in the cytoplasm.	Oxaliplatin	110-121	P53	Homo sapiens	147-150
19581934-3	2009	In oxaliplatin-selected cells a single nucleotide deletion in the sequence-encoding amino acid 382, part of NLSIII, resulted in a frame shift and a 420 amino acid protein (p53(420)).	Oxaliplatin	3-14	P53	Homo sapiens	172-175
31563647-5	2019	Notably, administration of proteasome inhibitor MG132 significantly inhibited the expression of cullin7 and up-regulated the expression of p53 in pulmonary arteries concomitantly with improvement of hypoxia-induced pulmonary vascular remodeling.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	48-53	P53	Homo sapiens	139-142
19531487-2	2009	In the present study, a mass spectrometry-based approach was used to analyze the effects of cytosine methylation on the kinetics of AGT repair of O(6)-methyldeoxyguanosine (O(6)-Me-dG) adducts placed within frequently mutated 5"-CG-3" dinucleotides of the p53 tumor suppressor gene.	O(6)-methyl-2'-deoxyguanosine	146-171	P53	Homo sapiens	256-259
31621389-8	2019	In addition, p53 overexpression attenuated the effects of EPEL overexpression on cancer cell viability under carboplatin treatment.	Carboplatin	109-120	P53	Homo sapiens	13-16
28027118-0	2018	Gain of TP53 Mutation in Imatinib-treated SDH-Deficient Gastrointestinal Stromal Tumor and Clinical Utilization of Targeted Next-generation Sequencing Panel for Therapeutic Decision Support.	Imatinib Mesylate	25-33	P53	Homo sapiens	8-12
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	Vorinostat	0-4	P53	Homo sapiens	72-75
30091530-5	2018	SAHA and MG132 treatment increased the expression levels of ING5, PTEN, p53, Caspase-3, Bax, p21, and p27 but decreased the expression levels of 14-3-3, MMP-2, MMP-9, ADFP, Nanog, c-myc, CyclinD1, CyclinB1, and Cdc25c concentration dependently, similar to ING5.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	9-14	P53	Homo sapiens	72-75
31234033-8	2019	However, laptinib reduced the EGFR protein expression and EGFR signals, it raised the apoptotic cells and TP53 gene signals, which triggered extensive DNA damage.	laptinib	9-17	P53	Homo sapiens	106-110
19531487-2	2009	In the present study, a mass spectrometry-based approach was used to analyze the effects of cytosine methylation on the kinetics of AGT repair of O(6)-methyldeoxyguanosine (O(6)-Me-dG) adducts placed within frequently mutated 5"-CG-3" dinucleotides of the p53 tumor suppressor gene.	O(6)-methyl-2'-deoxyguanosine	173-183	P53	Homo sapiens	256-259
29800662-3	2018	Spectroscopic experiments and molecular simulation suggested that alisol A, alisol B and their mixture interact with p53DNA in by partial insertion and the strength of binding affinity was consistent with the MTT assay.	monooxyethylene trimethylolpropane tristearate	209-212	P53	Homo sapiens	117-120
19531487-6	2009	AGT repair of O(6)-Me-dG adducts placed within 5"-CG-3" dinucleotides of p53 codons 245 and 248 was hindered when (Me)C was present in both DNA strands.	O(6)-methyl-2'-deoxyguanosine	14-24	P53	Homo sapiens	73-76
19531487-7	2009	In contrast, cytosine methylation within p53 codon 158 slightly increased the rate of O(6)-Me-dG repair by AGT.	O(6)-methyl-2'-deoxyguanosine	86-96	P53	Homo sapiens	41-44
19502594-6	2009	Moreover, we observed that CPS activates ATM kinase that is involved in Ser15, Ser20 and Ser392 p53 phosphorylation as shown by the use of the specific inhibitor KU55933.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	162-169	P53	Homo sapiens	96-99
29984871-4	2018	We observed that DMF induced cell apoptosis through mitochondrial-dependent and p53 pathway.	Dimethylformamide	17-20	P53	Homo sapiens	80-83
31542870-5	2019	Hence, with its novel mechanism of action and convenient oral once-daily regimen, venetoclax monotherapy or fixed 24-month combination therapy with rituximab represents an important option for treating RR CLL, including in patients with del(17p) or TP53 mutation and those failing a B cell receptor (BCR) inhibitor and/or chemotherapy.	venetoclax	82-92	P53	Homo sapiens	249-253
31481667-9	2019	In conclusion, we demonstrate that p53 DBD Nbs positively affect protein stability whilst adversely affecting protein function, attesting to their ability to modulate protein properties in a very subtle manner.	dbd nbs	39-46	P53	Homo sapiens	35-38
31480728-3	2019	In this study, we observed that exogenous ceramide induced two distinct morphologies of cell fate following C2-ceramide treatment between the two breast cancer cell lines MCF-7 (wild type p53) and MDA-MB-231 (mutant p53) cells.	Ceramides	42-50	P53	Homo sapiens	188-191
31480728-3	2019	In this study, we observed that exogenous ceramide induced two distinct morphologies of cell fate following C2-ceramide treatment between the two breast cancer cell lines MCF-7 (wild type p53) and MDA-MB-231 (mutant p53) cells.	Ceramides	42-50	P53	Homo sapiens	216-219
29504068-0	2018	Histone deacetylase inhibitor chidamide induces growth inhibition and apoptosis in NK/T lymphoma cells through ATM-Chk2-p53-p21 signalling pathway.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	30-39	P53	Homo sapiens	120-123
29504068-6	2018	In addition, we found that chidamide suppressed the phosphorylation levels of proteins in the AKT/mTOR and MAPK signalling pathways and activated the DDR cell cycle checkpoint pathway, that is, the ATM-Chk2-p53-p21 pathway.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	27-36	P53	Homo sapiens	207-210
29504068-9	2018	Our results provide evidence that chidamide shows antitumour effects by inhibiting the AKT/mTOR and MAPK signalling pathways and activating the ATM-Chk2-p53-p21 signalling pathway in vitro.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	34-43	P53	Homo sapiens	153-156
19346293-9	2009	Analysis of acrylamide quenching experiments revealed that the binding of metal ions to p53DBD induced a structural modification of the protein and this change provided significant protection against acrylamide quenching.	Acrylamide	12-22	P53	Homo sapiens	88-91
29680675-4	2018	Thioketal-crosslinked polyethylenimine (TK-PEI) was synthesized to condense p53 gene to form nanocomplexes (NCs), and hyaluronic acid (HA) modified with pheophytin a (Pha) was coated onto NCs to enhance their colloidal stability and enable cancer cell targeting.	Polyethyleneimine	22-38	P53	Homo sapiens	76-79
31534224-7	2019	Increased levels of the alphaKG-dependent chromatin modification 5-hydroxymethylcytosine (5hmC) accompany the tumour-cell differentiation that is triggered by p53, whereas decreased 5hmC characterizes the transition from premalignant to de-differentiated malignant lesions that is associated with mutations in Trp53.	5-hydroxymethylcytosine	65-88	P53	Homo sapiens	159-162
31534224-7	2019	Increased levels of the alphaKG-dependent chromatin modification 5-hydroxymethylcytosine (5hmC) accompany the tumour-cell differentiation that is triggered by p53, whereas decreased 5hmC characterizes the transition from premalignant to de-differentiated malignant lesions that is associated with mutations in Trp53.	5-hydroxymethylcytosine	90-94	P53	Homo sapiens	159-162
19346293-9	2009	Analysis of acrylamide quenching experiments revealed that the binding of metal ions to p53DBD induced a structural modification of the protein and this change provided significant protection against acrylamide quenching.	Acrylamide	200-210	P53	Homo sapiens	88-91
19567395-0	2009	Early modification of c-myc, Ha-ras and p53 expressions by chemical carcinogens (DMBA, MNU).	9,10-Dimethyl-1,2-benzanthracene	81-85	P53	Homo sapiens	40-43
19513541-6	2009	Furthermore, p53, the tumor suppressor which transcriptionally regulates p21, was also upregulated with PI-103 treatment.	PI103	104-110	P53	Homo sapiens	13-16
31452796-9	2019	In summary, shikonin can sensitize esophageal cancer cells to paclitaxel-treatment by promoting cell mitotic arrest and reinforcing the susceptibility of esophageal cancer cells to apoptosis induced by paclitaxel, which is potentially associated with altered levels of Bcl-2 and p53.	shikonin	12-20	P53	Homo sapiens	279-282
31067004-5	2019	Distinctive p38MAPK-p53 axis dependent Fas-FasL-FADD mediated caspase activities along with perturbed cell cycling became normalized with continuation of SAC treatment for another month to diethylnitrosamine induced liver carcinoma.	Diethylnitrosamine	189-207	P53	Homo sapiens	20-23
31067004-6	2019	Co-treatment with SB203580, the p38MAPK inhibitor, prevented pro-apoptotic effect of SAC by altering p53 phosphorylation and death inducing signaling complex conformation in HepG2 and induced HCC.	SB 203580	18-26	P53	Homo sapiens	101-104
31428569-10	2019	Apoptosis of A549 cells was decreased after transfected with p53 shRNA or treated with reactive oxygen species inhibitor NAC and p38MAPK inhibitor SB203580, suggesting that the p53/ROS/p38MAPK pathway appeared to mediate the LBP-induced apoptosis of A549 cells.	SB 203580	147-155	P53	Homo sapiens	61-64
31428569-10	2019	Apoptosis of A549 cells was decreased after transfected with p53 shRNA or treated with reactive oxygen species inhibitor NAC and p38MAPK inhibitor SB203580, suggesting that the p53/ROS/p38MAPK pathway appeared to mediate the LBP-induced apoptosis of A549 cells.	SB 203580	147-155	P53	Homo sapiens	177-180
29530932-3	2018	Erlotinib resistance due to acquired MTOR mutation was functionally evaluated by in vivo and in vitro studies.Results: In 200 EGFR-mutant pretreatment samples, the most frequent concurrent alterations were mutations in TP53, PIK3CA, CTNNB1, and RB1 and focal amplifications in EGFR, TTF1, MDM2, CDK4, and FOXA1 Shorter time to progression on EGFR TKI was associated with amplification of ERBB2 (HR = 2.4, P = 0.015) or MET (HR = 3.7, P = 0.019), or mutation in TP53 (HR = 1.7, P = 0.006).	Erlotinib Hydrochloride	0-9	P53	Homo sapiens	219-223
29530932-3	2018	Erlotinib resistance due to acquired MTOR mutation was functionally evaluated by in vivo and in vitro studies.Results: In 200 EGFR-mutant pretreatment samples, the most frequent concurrent alterations were mutations in TP53, PIK3CA, CTNNB1, and RB1 and focal amplifications in EGFR, TTF1, MDM2, CDK4, and FOXA1 Shorter time to progression on EGFR TKI was associated with amplification of ERBB2 (HR = 2.4, P = 0.015) or MET (HR = 3.7, P = 0.019), or mutation in TP53 (HR = 1.7, P = 0.006).	Erlotinib Hydrochloride	0-9	P53	Homo sapiens	461-465
29843463-3	2018	We are currently developing a new class of mutant p53 reactivators called zinc metallochaperones (ZMCs) and, here, we review our current understanding of them.	zmcs	98-102	P53	Homo sapiens	50-53
29843463-6	2018	ZMCs reactivate mutant p53 using a novel two-part mechanism that involves restoring the wild-type structure by reestablishing zinc binding and activating p53 through post-translational modifications induced by cellular reactive oxygen species (ROS).	zmcs	0-4	P53	Homo sapiens	23-26
29843463-6	2018	ZMCs reactivate mutant p53 using a novel two-part mechanism that involves restoring the wild-type structure by reestablishing zinc binding and activating p53 through post-translational modifications induced by cellular reactive oxygen species (ROS).	zmcs	0-4	P53	Homo sapiens	154-157
29843463-8	2018	ZMCs are small molecule metal ion chelators that bind zinc and other divalent metal ions strong enough to remove zinc from serum albumin, but weak enough to donate it to mutant p53.	zmcs	0-4	P53	Homo sapiens	177-180
29691156-1	2018	Five lactam chemotypes amenable by the Castagnoli-Cushman reaction of imines and cyclic anhydrides have been investigated for their ability to activate p53 tumor suppressing transcription factor thus induce apoptosis in p53+ cancer cells.	Imines	70-76	P53	Homo sapiens	152-155
31215421-13	2019	Meanwhile, treatment with elemene significantly up-regulates the protein expression of P53, while down-regulate the protein expression of Bcl-2 in the tumor tissues, respectively.	elemene	26-33	P53	Homo sapiens	87-90
31215421-14	2019	Furthermore, the western blot result showed that treatment with elemene increased the expression of P53 and decreased the expression of Bcl-2, compared with the control group, which is similar to the results of immunohistochemical staining.	elemene	64-71	P53	Homo sapiens	100-103
31215421-15	2019	CONCLUSIONS: This study suggests that elemene has a potential anti pancreatic cancer effect, down-regulation the protein expression of Bcl-2 and up-regulation the protein expression of P53 in a dose dependent manner may be is the anti-tumor mechanism.	elemene	38-45	P53	Homo sapiens	185-188
19584241-8	2009	The results presented in this study highlight the importance of PA homeostasis and provide a direct link between PA metabolism and apoptotic cell signaling pathways in p53 wild-type NB cells.	Polyamines	113-115	P53	Homo sapiens	168-171
29445054-8	2018	Finally, toxicogenomics analysis of HepG2 and HepaRG cells after exposure to AFB1 and CPA revealed that numerous p53-related genes were upregulated- and the expression of these genes was greater in HepaRG than in HepG2 cells.	Cyclophosphamide	86-89	P53	Homo sapiens	113-116
19320642-7	2009	GalphasQL also augmented cisplatin-induced apoptosis of H1299 human lung cancer cells that lack functional p53.	galphasql	0-9	P53	Homo sapiens	107-110
29229990-6	2018	A moderate upregulation of ACER2 inhibited cell cycle arrest and cellular senescence in response to low-level expression of p53 or low-dose IR by elevating S1P, a pro-proliferative and pro-survival bioactive lipid, and/or decreasing ceramides whereas its robust upregulation mediated PCD in response to high-level expression of p53 or high-dose IR likely by accumulating cellular sphingosine, a pro-death bioactive lipid.	Ceramides	233-242	P53	Homo sapiens	124-127
29229990-6	2018	A moderate upregulation of ACER2 inhibited cell cycle arrest and cellular senescence in response to low-level expression of p53 or low-dose IR by elevating S1P, a pro-proliferative and pro-survival bioactive lipid, and/or decreasing ceramides whereas its robust upregulation mediated PCD in response to high-level expression of p53 or high-dose IR likely by accumulating cellular sphingosine, a pro-death bioactive lipid.	Sphingosine	380-391	P53	Homo sapiens	124-127
30924378-10	2019	Apoptotic markers such as caspases 3 and 9, cytochrome c, Apaf-1, Bax, and p53 gene expressions were significantly increased upon SA treatment indicating the possibility of apoptosis induction in HepG2 cells.	syringic acid	130-132	P53	Homo sapiens	75-78
30548678-6	2019	SIRT1 inhibitor (nicotinamide) decreased SIRT1, reduced the effects of miRNA-141 on nerve cell apoptosis in vitro model of epilepsy through SIRT1/p53.	Niacinamide	17-29	P53	Homo sapiens	146-149
19246451-4	2009	Although the general interaction regions are known, details of the interfaces for each p53-ASPP complex have not been evaluated.	aspp	91-95	P53	Homo sapiens	87-90
31041982-3	2019	In addition, compounds 14d-f, 14h and 14k are able to increase the p53 expression levels, activating also the apoptotic pathway.	14d-	23-27	P53	Homo sapiens	67-70
29561706-4	2018	Among these new drugs, venetoclax, an orally bioavailable BCL2 inhibitor, has shown high efficacy also in relapsed/refractory CLL with TP53 disruption.	venetoclax	23-33	P53	Homo sapiens	135-139
29561706-9	2018	Venetoclax has achieved responses also in patients with TP53 disruption.	venetoclax	0-10	P53	Homo sapiens	56-60
19246451-8	2009	Our detailed structural analyses of the ASPP-p53 interactions provide insight into the structural basis of the differential behavior of pro- and antiapoptotic ASPP family members.	aspp	40-44	P53	Homo sapiens	45-48
30608891-8	2019	However, the potential synergistic anti-neoplastic effects of lenalidomide in combination with other biological agents, i.e. ibrutinib and venetoclax, especially in the management of p53-mutated cases, still remain an open issue.	Lenalidomide	62-74	P53	Homo sapiens	183-186
30608891-8	2019	However, the potential synergistic anti-neoplastic effects of lenalidomide in combination with other biological agents, i.e. ibrutinib and venetoclax, especially in the management of p53-mutated cases, still remain an open issue.	venetoclax	139-149	P53	Homo sapiens	183-186
29854627-4	2018	Thalidomide and carboplatin induced up-regulation of the expression of p53, tumor necrosis factor-alpha and interleukin-6 in brain and kidney.	Carboplatin	16-27	P53	Homo sapiens	71-74
19246451-8	2009	Our detailed structural analyses of the ASPP-p53 interactions provide insight into the structural basis of the differential behavior of pro- and antiapoptotic ASPP family members.	aspp	159-163	P53	Homo sapiens	45-48
29854314-0	2018	Foretinib (GSK1363089) induces p53-dependent apoptosis in endometrial cancer.	GSK 1363089	0-9	P53	Homo sapiens	31-34
29854314-0	2018	Foretinib (GSK1363089) induces p53-dependent apoptosis in endometrial cancer.	GSK 1363089	11-21	P53	Homo sapiens	31-34
30501014-0	2019	Butyrate inhibits HBV replication and HBV-induced hepatoma cell proliferation via modulating SIRT-1/Ac-p53 regulatory axis.	Butyrates	0-8	P53	Homo sapiens	103-106
30501014-7	2019	Inhibition of SIRT-1 by butyrate or SIRT-1 siRNA increased the levels of Ac-p53.	Butyrates	24-32	P53	Homo sapiens	76-79
19190243-4	2009	Of note, Nutlin-3 up-regulated Notch1 expression also in primary TP53(wild-type) B-chronic lymphocytic leukemia (B-CLL) cells and the combined use of Nutlin-3 plus pharmacological gamma-secretase inhibitors of the Notch signaling showed a synergistic cytotoxicity in both TP53(wild-type) leukemic cell lines and primary B-CLL cells.	nutlin	9-15	P53	Homo sapiens	65-69
29854314-3	2018	Inhibiting the HGF/Met signaling with foretinib induced p53-dependent apoptosis in endometrial cancer cell lines in vitro.	GSK 1363089	38-47	P53	Homo sapiens	56-59
29854314-7	2018	Foretinib induces an anti-cancer effect through the anti-phosphorylation of Met, which results in the induction of p53-dependent apoptosis; foretinib was found to exert greater anti-cancer activity in endometrial cancer specimens with wild-type p53 than in specimens with p53 mutations.	GSK 1363089	0-9	P53	Homo sapiens	115-118
29854314-7	2018	Foretinib induces an anti-cancer effect through the anti-phosphorylation of Met, which results in the induction of p53-dependent apoptosis; foretinib was found to exert greater anti-cancer activity in endometrial cancer specimens with wild-type p53 than in specimens with p53 mutations.	GSK 1363089	0-9	P53	Homo sapiens	245-248
29854314-7	2018	Foretinib induces an anti-cancer effect through the anti-phosphorylation of Met, which results in the induction of p53-dependent apoptosis; foretinib was found to exert greater anti-cancer activity in endometrial cancer specimens with wild-type p53 than in specimens with p53 mutations.	GSK 1363089	0-9	P53	Homo sapiens	245-248
29854314-7	2018	Foretinib induces an anti-cancer effect through the anti-phosphorylation of Met, which results in the induction of p53-dependent apoptosis; foretinib was found to exert greater anti-cancer activity in endometrial cancer specimens with wild-type p53 than in specimens with p53 mutations.	GSK 1363089	140-149	P53	Homo sapiens	245-248
29854314-7	2018	Foretinib induces an anti-cancer effect through the anti-phosphorylation of Met, which results in the induction of p53-dependent apoptosis; foretinib was found to exert greater anti-cancer activity in endometrial cancer specimens with wild-type p53 than in specimens with p53 mutations.	GSK 1363089	140-149	P53	Homo sapiens	245-248
29854314-8	2018	Our immunochemical analysis revealed that foretinib-induced p53-dependent apoptosis can be expected to have therapeutic potential in approximately 90% of endometrial cancer patients.	GSK 1363089	42-51	P53	Homo sapiens	60-63
30720086-5	2019	In addition, oxfendazole induced cell cycle arrest at the G0/G1 phase, and downregulated the protein levels of Cyclin-dependent kinase (CDK)-4, CDK6, retinoblastoma protein and E2 transcription factor 1, and upregulated the expression levels of p53 and p21 in NSCLC cells.	oxfendazole	13-24	P53	Homo sapiens	245-248
19190243-4	2009	Of note, Nutlin-3 up-regulated Notch1 expression also in primary TP53(wild-type) B-chronic lymphocytic leukemia (B-CLL) cells and the combined use of Nutlin-3 plus pharmacological gamma-secretase inhibitors of the Notch signaling showed a synergistic cytotoxicity in both TP53(wild-type) leukemic cell lines and primary B-CLL cells.	nutlin	9-15	P53	Homo sapiens	272-276
29386219-1	2018	Purpose: We aimed to investigate the therapeutic efficacy of single agent and the combination of quinacrine and suberoylanilide hydroxamic acid (SAHA) in wt- and mut-p53 upper gastrointestinal cancer (UGC) cell models.Experimental Design: ATP-Glo, clonogenic cell survival, Annexin V, comet, DNA double-strand breaks (DSBs), qPCR, and Western blot analysis assays were utilized.Results: Using clonogenic cell survival, ATP-Glo cell viability, Annexin V, and sub-G0 population analysis, we demonstrated that a combination of quinacrine and SAHA significantly decreased colony formation and increased cancer cell death (range, 4-20 fold) in six UGC cell models, as compared with single-agent treatments, irrespective of the p53 status (P < 0.01).	Vorinostat	112-143	P53	Homo sapiens	166-169
19265193-2	2009	Here we demonstrate that p53 acetylation at Lys-320/Lys-373/Lys-382 is also required for its transcription-independent functions in BAX activation, reactive oxygen species production, and apoptosis in response to the histone deacetylase inhibitors (HDACi) suberoylanilide hydroxamic acid and LAQ824.	LAQ824	292-298	P53	Homo sapiens	25-28
30935019-5	2019	ZNF143 knockdown affected the stability of p53, which showed a dependence on MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	77-82	P53	Homo sapiens	43-46
19153082-2	2009	The p53 residues Leu(26), Trp(23), and Phe(19) are crucial to mediate these interactions.	Phenylalanine	39-42	P53	Homo sapiens	4-7
30871527-6	2019	The methylation status of the TP53 promoter was analyzed using by methylation-specific PCR on bisulfite-converted DNA.	hydrogen sulfite	94-103	P53	Homo sapiens	30-34
29636527-4	2018	ViscumTT treatment induced G1 arrest in TP53 wild-type and null-mutant cells, but S arrest in TP53 mutant cells.	viscumtt	0-8	P53	Homo sapiens	40-44
29269520-0	2018	Emergence and evolution of TP53 mutations are key features of disease progression in myelodysplastic patients with lower-risk del(5q) treated with lenalidomide.	Lenalidomide	147-159	P53	Homo sapiens	27-31
19046801-12	2009	Mutations of p53 determined in NHL cases (30%) were of Arg-176 (1/20: 5%), Phe-238 (1/20: 5%), Ser-249 (2/20; 10%), Lys-249 (1/20: 5%) and Phe-250 (1/20: 5%).	Phenylalanine	75-78	P53	Homo sapiens	13-16
29319823-0	2018	Differentially Expressed mRNA Targets of Differentially Expressed miRNAs Predict Changes in the TP53 Axis and Carcinogenesis-Related Pathways in Human Keratinocytes Chronically Exposed to Arsenic.	Arsenic	188-195	P53	Homo sapiens	96-100
30606076-0	2019	Progressive diffuse large B-cell lymphoma with TP53 gene mutation treated with chidamide-based chemotherapy.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	79-88	P53	Homo sapiens	47-51
30606076-2	2019	Herein, we report the case of a patient with DLBCL having TP53 mutation who showed progression following four cycles of rituximab-based immunochemotherapy but achieved sustained partial remission following chidamide-based chemotherapy.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	206-215	P53	Homo sapiens	58-62
30606076-4	2019	Moreover, chidamide can reduce the mRNA and protein expression levels of mutant TP53 and upregulate the surface expression of the CD20 antigen in lymphoma cells.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	10-19	P53	Homo sapiens	80-84
30863051-1	2019	Background: An amphiphilic cationic copolymer cholesterol-g-poly(amine-co-ester), namely Chol-g-PMSC-PPDL synthesized in a chemoenzymatic route has been utilized as a carrier for p53 gene delivery to check its antitumor efficacy, using human prostate cancer cell line PC-3 (p53 null) as a model.	chol-g-pmsc	89-100	P53	Homo sapiens	179-182
29471073-0	2018	The impact of chemotherapeutic drugs on the CYP1A1-catalysed metabolism of the environmental carcinogen benzo[a]pyrene: Effects in human colorectal HCT116 TP53(+/+), TP53(+/-) and TP53(-/-) cells.	benzo	104-109	P53	Homo sapiens	155-159
29400463-0	2018	Peloruside A-Induced Cell Death in Hypoxia Is p53 Dependent in HCT116 Colorectal Cancer Cells.	peloruside A	0-12	P53	Homo sapiens	46-49
30863051-1	2019	Background: An amphiphilic cationic copolymer cholesterol-g-poly(amine-co-ester), namely Chol-g-PMSC-PPDL synthesized in a chemoenzymatic route has been utilized as a carrier for p53 gene delivery to check its antitumor efficacy, using human prostate cancer cell line PC-3 (p53 null) as a model.	chol-g-pmsc	89-100	P53	Homo sapiens	274-277
30578766-5	2019	Furthermore, glycosphingolipids (particularly globotriaosylceramide) generated from serial ceramide glycosylation were seen to activate cSrc and beta-catenin signaling so as to upregulate METTL3 expression, in turn promoting expression of p53 R273H mutant protein, with consequent drug resistance.	Ceramides	59-67	P53	Homo sapiens	239-242
30578766-7	2019	Concordantly, suppression of ceramide glycosylation repressed METTL3 expression and m6A formation in p53 pre-mRNA, thus sensitizing cells carrying R273H to anticancer drugs.	Ceramides	29-37	P53	Homo sapiens	101-104
19046801-12	2009	Mutations of p53 determined in NHL cases (30%) were of Arg-176 (1/20: 5%), Phe-238 (1/20: 5%), Ser-249 (2/20; 10%), Lys-249 (1/20: 5%) and Phe-250 (1/20: 5%).	Phenylalanine	139-142	P53	Homo sapiens	13-16
30578766-9	2019	Suppressing both RNA methylation and ceramide glycosylation might constitute an efficacious and specific approach for targeting TP53 missense mutations coding for a G &gt; A transition, thereby improving cancer treatments.	Ceramides	37-45	P53	Homo sapiens	128-132
19064630-6	2009	To better understand the mechanism by which PUVA treatment induces p53, we exposed human skin fibroblasts with PUVA under conditions that differentially produce monoadducts and ICLs and found that psoralen-induced ICLs induced phosphorylation of the Ser-15 site of p53 and apoptosis much more effectively than psoralen-induced monoadducts.	puva	44-48	P53	Homo sapiens	67-70
30766866-3	2019	Spiropyrazoline oxindoles have previously been shown to induce apoptosis and cell cycle arrest, as well as upregulate p53 steady-state levels, while decreasing its main inhibitor MDM2 in the HCT116 human colorectal carcinoma cell line.	spiropyrazoline oxindoles	0-25	P53	Homo sapiens	118-121
30598450-12	2019	Combining MDM2 inhibitors with lenalidomide targeting CK1alpha or an MDM4 inhibitor caused synergistic activation of p53, leading to an apoptotic response in MCV-positive MCC cells and MCC-derived xenografts in mice.	Lenalidomide	31-43	P53	Homo sapiens	117-120
29368050-1	2018	PURPOSE: Idasanutlin, a selective small-molecule MDM2 antagonist in phase 3 testing for refractory/relapsed AML, is a non-genotoxic oral p53 activator.	RG7388	9-20	P53	Homo sapiens	137-140
29392451-1	2018	PURPOSE: Idasanutlin, a selective small-molecule MDM2 antagonist in phase 3 testing for refractory/relapsed AML, is a non-genotoxic oral p53 activator.	RG7388	9-20	P53	Homo sapiens	137-140
19064630-6	2009	To better understand the mechanism by which PUVA treatment induces p53, we exposed human skin fibroblasts with PUVA under conditions that differentially produce monoadducts and ICLs and found that psoralen-induced ICLs induced phosphorylation of the Ser-15 site of p53 and apoptosis much more effectively than psoralen-induced monoadducts.	puva	44-48	P53	Homo sapiens	265-268
29483845-12	2018	A rescue in the expression of both MLL genes was observed in KCL22S, a CML cell line sensitive to IM, after treatment with dasatinib or nilotinib which was associated with a higher rate of apoptosis, an enhanced expression of p21 (CDKN1A) and a concomitant decrease in the expression of CDK2, CDK4 and Cyclin B1 (CCNB1) in comparison to untreated KCL22S control or IM resistant KCL22R cell line, which suggests involvement of p53 regulated pathway.	kcl22s	61-67	P53	Homo sapiens	426-429
19064630-6	2009	To better understand the mechanism by which PUVA treatment induces p53, we exposed human skin fibroblasts with PUVA under conditions that differentially produce monoadducts and ICLs and found that psoralen-induced ICLs induced phosphorylation of the Ser-15 site of p53 and apoptosis much more effectively than psoralen-induced monoadducts.	puva	111-115	P53	Homo sapiens	67-70
30622244-3	2019	In this study, we found that EPO suppresses p53-dependent apoptosis induced by genotoxic (daunorubicin, doxorubicin, and gamma-radiation) and non-genotoxic (nutlin-3a) agents and induces a senescence-like state in myeloid leukemia cells.	Daunorubicin	90-102	P53	Homo sapiens	44-47
19060927-8	2009	Although p53 has been reported to be a target of Sirt1, genetic p53 knockdowns showed that the Sirt1-dependent proapoptotic effect of Salermide is p53-independent.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	134-143	P53	Homo sapiens	9-12
31468429-7	2019	In conclusion, taurine may play an anti-tumor role by activating tumor suppressor PTEN and p53.	Taurine	15-22	P53	Homo sapiens	91-94
29451912-12	2018	In summary, mutation analysis in TP53 plays a minor role in the subgroup of high-risk GIST before adjuvant treatment with imatinib.	Imatinib Mesylate	122-130	P53	Homo sapiens	33-37
19060927-8	2009	Although p53 has been reported to be a target of Sirt1, genetic p53 knockdowns showed that the Sirt1-dependent proapoptotic effect of Salermide is p53-independent.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	134-143	P53	Homo sapiens	64-67
28833404-3	2018	Ascochlorin promoted the G1 arrest, upregulated p53 and p21WAF1/CIP1 , and downregulated c-Myc in HCT116 cells.	ascochlorin	0-11	P53	Homo sapiens	48-51
28833404-4	2018	In p53-deficient cells, ascochlorin enhanced the expression of G1 arrest-related genes except p53.	ascochlorin	24-35	P53	Homo sapiens	3-6
19060927-8	2009	Although p53 has been reported to be a target of Sirt1, genetic p53 knockdowns showed that the Sirt1-dependent proapoptotic effect of Salermide is p53-independent.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	134-143	P53	Homo sapiens	64-67
30339780-0	2019	A redox ruthenium compound directly targets PHD2 and inhibits the HIF1 pathway to reduce tumor angiogenesis independently of p53.	Ruthenium Compounds	8-26	P53	Homo sapiens	125-128
19202565-9	2009	Moreover, DADS-induced apoptosis was also prevented by treatment with oligomycin, which is known to prevent p53-dependent apoptosis by reducing ROS levels in mitochondria.	Oligomycins	70-80	P53	Homo sapiens	108-111
18787402-2	2008	Here we show that combining the three sage bioactive compounds, Linalyl acetate (Ly), Terpeniol (Te) and Camphor (Ca), caused synergistic inhibition of the growth of two isogenic human colon cancer cell lines HCT-116 (p53(+/+) and p53(-/-)) and had no effect on growth of FHs74Int normal human intestinal cell line.	Camphor	105-112	P53	Homo sapiens	218-221
30301863-7	2019	Corroborating the basis of sensitivity, transcriptional profiling of platinum-resistant ARID1A-mutated HT1197 cells treated with panobinostat reveals negative enrichment for both cyto-proliferative (MYC and E2F targets) and DNA repair gene sets, and positive enrichment for TP53 and inflammatory gene sets.	Panobinostat	129-141	P53	Homo sapiens	274-278
29429512-12	2018	RESULTS: The saline-treated HCC group (with prior 15 week DEN exposure) showed higher levels of wnt4 and p53 gene expression (1.59 and 1.36 fold, respectively) and increased percentage in OV6+ progenitor cells (+4.9% in absolute terms) compared to saline-treated controls (p &lt; 0.01, ANOVA).	Diethylnitrosamine	58-61	P53	Homo sapiens	105-108
18787402-2	2008	Here we show that combining the three sage bioactive compounds, Linalyl acetate (Ly), Terpeniol (Te) and Camphor (Ca), caused synergistic inhibition of the growth of two isogenic human colon cancer cell lines HCT-116 (p53(+/+) and p53(-/-)) and had no effect on growth of FHs74Int normal human intestinal cell line.	Camphor	105-112	P53	Homo sapiens	231-234
29568362-6	2018	The antitumor activity was partly due to NO-cGMP dependent pathway, contributing to reduced cell number and apoptosis, and partly to the salicylaldehyde moiety and reactive oxygen species (ROS) activated ERK1/2 signaling converging on p53 dependent caspase-3 cleavage.	salicylaldehyde	137-152	P53	Homo sapiens	235-238
29370077-0	2018	p53 Gene (NY-CO-13) Levels in Patients with Chronic Myeloid Leukemia: The Role of Imatinib and Nilotinib.	Imatinib Mesylate	82-90	P53	Homo sapiens	0-3
30577494-6	2018	Trametinib synergizes with MDM2 inhibitors through a novel DUSP6 mechanism in BRAFV600E and p53WT melanoma cells, in which DUSP6 regulation of p53 phosphorylation is mediated by ATM.	trametinib	0-10	P53	Homo sapiens	92-95
30577494-6	2018	Trametinib synergizes with MDM2 inhibitors through a novel DUSP6 mechanism in BRAFV600E and p53WT melanoma cells, in which DUSP6 regulation of p53 phosphorylation is mediated by ATM.	trametinib	0-10	P53	Homo sapiens	143-146
29370077-5	2018	The purpose of the present study was to evaluate the differential effect of imatinib and nilotinib on p53 gene serum levels in patients with CML.	Imatinib Mesylate	76-84	P53	Homo sapiens	102-105
18787402-3	2008	In p53(+/+) cells, the combination of Ly + Te + Ca (10(-3) M of each) caused significant accumulation of cells in PreG(1) (64% at 48 hours); less preG(1) increase was observed in response to Ly + Te (25%) or Ly + Ca (14%).	linalyl acetate	38-42	P53	Homo sapiens	3-6
29370077-10	2018	Patients with CML that were treated with either imatinib or nilotinib showed insignificant differences in most of the hematological profile (p &gt; 0.05) whereas, p53 serum levels were high (3.22 +- 1.99 ng/mL) in nilotinib-treated patients and relatively low (1.18 +- 0.19 ng/mL) in imatinib-treated patients (p = 0.0001).	Imatinib Mesylate	48-56	P53	Homo sapiens	163-166
29370077-11	2018	CONCLUSIONS: Nilotinib is more effective than imatinib in raising p53 serum levels in patients with chronic myeloid leukemia.	Imatinib Mesylate	46-54	P53	Homo sapiens	66-69
30225664-12	2018	In addition, taurine increased the levels of PTEN (phosphatase and tensin homolog deleted on chromosome 10) and p53, and reduced phosphorylated Akt (protein kinase B).	Taurine	13-20	P53	Homo sapiens	112-115
19181008-4	2008	Previously, an animal model was developed by our research group to investigate the expression of three genes c-myc, Ha-ras and p53 as early molecular epidemiological biomarkers of carcinogenic exposure or carcinogenesis caused by DMBA (dimethylbenz[alpha]anthracene).	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	230-234	P53	Homo sapiens	127-130
18296682-4	2008	In addition, naringin treatment strongly induced p21WAF1 expression, independent of the p53 pathway, and downregulated expression of cyclins and cyclin dependent kinases (CDKs).	naringin	13-21	P53	Homo sapiens	88-91
30466751-3	2018	Decitabine is emerging as an alternative treatment option for patients with TP53 mutated AML, although the agent has not been associated with deep molecular remissions and requires additional consolidation.	Decitabine	0-10	P53	Homo sapiens	76-80
29277758-3	2018	The goal of this study was to investigate the chemotherapeutic effects of sphingosine on PAX3-FOXO1-positive ARMS cells [tumor protein p53 (TP53)-mutated RH30 and TP53 wild-type RH18 cells].	Sphingosine	74-85	P53	Homo sapiens	135-138
18548093-6	2008	We suggest that PI-103 actively enhances downstream p53 signaling and that a combination strategy aimed at inhibiting PI3K/Akt/mTOR signaling and activating p53 signaling is potentially effective in AML, where TP53 mutations are rare and downstream p53 signaling is intact.	PI103	16-22	P53	Homo sapiens	52-55
29368980-5	2018	SK1-I, an analog of sphingosine and isozyme-specific SPHK1 inhibitor, suppressed cancer cell growth and clonogenic survival in a TP53-dependent manner.	Sphingosine	20-31	P53	Homo sapiens	129-133
29115606-3	2018	However, its regulation of chemosensitivity to gemcitabine (GEM) and oxaliplatin (OXA) in p53-deficient PDAC remains unclear.	gemcitabine	47-58	P53	Homo sapiens	90-93
30484863-8	2018	Taken together, we propose that LBH589 inhibits ESCC cell proliferation mainly through inducing cell cycle arrest by increasing p21 and decreasing cyclin D1 in a p53-independent manner.	Panobinostat	32-38	P53	Homo sapiens	162-165
29115606-3	2018	However, its regulation of chemosensitivity to gemcitabine (GEM) and oxaliplatin (OXA) in p53-deficient PDAC remains unclear.	gemcitabine	60-63	P53	Homo sapiens	90-93
18345033-0	2008	P53-mediated upregulation of DcR1 impairs oxaliplatin/TRAIL-induced synergistic anti-tumour potential in colon cancer cells.	Oxaliplatin	42-53	P53	Homo sapiens	0-3
29115606-3	2018	However, its regulation of chemosensitivity to gemcitabine (GEM) and oxaliplatin (OXA) in p53-deficient PDAC remains unclear.	pdac	104-108	P53	Homo sapiens	90-93
29115632-8	2018	Furthermore, combination treatment with SAHA and 5-Aza-CdR significantly increased expression of TP53 and P16.	Vorinostat	40-44	P53	Homo sapiens	97-101
30086334-5	2018	TP53 alterations were more common in patients with PCs in BM (45.4% versus 18.7%; P = .0049), as was a complex karyotype (26.4% versus 9%; P = .019).	pcs	51-54	P53	Homo sapiens	0-4
29333130-3	2017	Here, curcumin, flavokawain B, and alpinetin were docked against the crystal structure of R273H mutant p53 in silico.	flavokawain B	16-29	P53	Homo sapiens	103-106
18345033-1	2008	Oxaliplatin has emerged as a major chemotherapeutic drug in the treatment of advanced colorectal cancer, yet like most conventional cancer therapeutics, its efficacy is often compromised due to p53 mutations.	Oxaliplatin	0-11	P53	Homo sapiens	194-197
29333130-4	2017	Consequently, all the compounds bind to the cavity of R273H mutant p53 with a dissociation constant estimated to have 36.57, 70.77, and 75.11 microM for curcumin, flavokawain B, and alpinetin, respectively.	flavokawain B	163-176	P53	Homo sapiens	67-70
30546426-11	2018	Markedly decreased Akt phosphorylation and cyclin D1 levels and increased p53 levels were detected when cells were transfected with miR-128 mimics.	mir-128	132-139	P53	Homo sapiens	74-77
18345033-5	2008	Impaired TRAIL-induced cell death resulted from a strong p53 dependent, oxaliplatin-mediated, DcR1 receptor expression increase.	Oxaliplatin	72-83	P53	Homo sapiens	57-60
30546426-14	2018	In conclusion, the results suggested that miR-128 was a specific negative regulator of RPN2, which regulated colorectal cancer cell proliferation and migration by affecting the Akt-p53-cyclin pathway.	mir-128	42-49	P53	Homo sapiens	181-184
29089230-1	2017	A series of novel amino acid ester derivatives of 2,3-substituted isoindolinones was synthesized and evaluated for p53-mediated apoptotic activity.	amino acid ester	18-34	P53	Homo sapiens	115-118
18345033-6	2008	According to our finding, downregulation of DcR1 using siRNA, in p53 wild-type colon cancer cells, restored oxaliplatin/TRAIL synergistic apoptotic activity.	Oxaliplatin	108-119	P53	Homo sapiens	65-68
18345033-8	2008	Altogether we demonstrate for the first time that p53 negatively regulates oxaliplatin-mediated TRAIL-induced apoptotic activity through DcR1 upregulation.	Oxaliplatin	75-86	P53	Homo sapiens	50-53
29143344-4	2017	5-Aza-dC inhibited E6 and E7 expression and up-regulated p53, p21, and Rb expression.	Decitabine	0-8	P53	Homo sapiens	57-60
18345033-9	2008	Our findings could have important implications for future therapeutic strategies, and suggest that the association oxaliplatin/TRAIL should be restricted to patients harbouring a non-functional p53 protein.	Oxaliplatin	115-126	P53	Homo sapiens	194-197
30454541-14	2018	Furthermore, Western blot analysis showed that microwave hyperthermia combined with gemcitabine could up-regulate the p53, Caspase-3, Cleaved-Caspase-3, Cleaved-PARP and Bax protein expression.	gemcitabine	84-95	P53	Homo sapiens	118-121
30068711-6	2018	Trametinib and radiotherapy both induced senescence in a p53-dependent manner, but in WT LKB1 cells, the combination also activated the AMPK-autophagy pathway to rescue damaged cells from senescence.	trametinib	0-10	P53	Homo sapiens	57-60
28733702-8	2017	Finally, we tested the ability of CXCR4 and FAK inhibitors (WZ811 and PF-573228, respectively) to suppress the migratory and invasive potential of p53/PTEN deficient NSCLC cells, in vitro and in vivo using metastatic models of human NSCLC.	N,N'-di-2-pyridinyl-1,4-benzenedimethanamine	60-65	P53	Homo sapiens	147-150
18508032-9	2008	Cell cycle distribution after exposure to oxaliplatin showed arrest in G2/M (A2780) or in S-phase (LoVo-92) for wt-p53 cells.	Oxaliplatin	42-53	P53	Homo sapiens	115-118
29061817-0	2017	Synergistic Inhibition of Human Carcinoma Cell Growth via Co-Delivery of p53 Plasmid DNA and bcl-2 Antisense Oligodeoxyribonucleotide by Cholic Acid-modified Polyethylenimine.	Cholic Acid	137-148	P53	Homo sapiens	73-76
29061817-0	2017	Synergistic Inhibition of Human Carcinoma Cell Growth via Co-Delivery of p53 Plasmid DNA and bcl-2 Antisense Oligodeoxyribonucleotide by Cholic Acid-modified Polyethylenimine.	Polyethyleneimine	158-174	P53	Homo sapiens	73-76
30462771-13	2018	Knockdown of p53 or employing the caspase inhibitor, Boc-D-FMK, reversed the effect of oridonin on cell viability and apoptosis-related protein expression.	Boc-D-FMK	53-62	P53	Homo sapiens	13-16
28618116-1	2017	Mutations in the tumor suppressor p53 are highly prevalent in cancers and are known to influence the sensitivity of cells to various chemotherapeutics including the anti-cancer candidates 1,25-dihydrovitamin D3 [1,25D3] and metformin.	1,25-dihydrovitamin d3	188-210	P53	Homo sapiens	34-37
18511169-6	2008	Specific ATM inhibitor, caffeine, significantly decreased KTA-mediated G2/M arrest by inhibiting the phosphorylation of p53 (Serine15) and Chk2.	Caffeine	24-32	P53	Homo sapiens	120-123
30405800-8	2018	Notably, the combination of dinaciclib and DOX inhibited cell growth and promoted senescence by transforming the suppressive effects of the ATM/Chk2/p53/p21 signaling pathway and enhancing the p16 signaling pathway.	dinaciclib	28-38	P53	Homo sapiens	149-152
29035366-4	2017	Consequently, targeting of EGFR-driven glucose metabolism in combination with pharmacological stabilization of p53 with the brain-penetrant small molecule idasanutlin resulted in synthetic lethality in orthotopic glioblastoma xenograft models.	RG7388	155-166	P53	Homo sapiens	111-114
18645022-0	2008	Differential antiproliferative mechanisms of novel derivative of benzimidazo[1,2-alpha]quinoline in colon cancer cells depending on their p53 status.	benzimidazo[1,2-alpha]quinoline	65-96	P53	Homo sapiens	138-141
18440285-5	2008	Caffeine increased apoptosis levels and inhibited p53 activation in proliferating cells, suggesting a protective role for p53.	Caffeine	0-8	P53	Homo sapiens	50-53
29051574-7	2017	Furthermore, FLO also induces G0/G1 cell cycle arrest via increase of p21 levels through activating ROS/p53/p21 pathway.	florfenicol	13-16	P53	Homo sapiens	104-107
29051574-9	2017	In addition, FLO-induced upregulation of cytosolic p53 may contribute to mitophagy deficiency via regulation of Parkin recruitment.	florfenicol	13-16	P53	Homo sapiens	51-54
30283098-2	2018	ROS and RNS can influence tumor cell malignancy via the redox-regulated transcription factor NF-kappaB, whose activation is further regulated by the mutation status of p53.	Reactive Nitrogen Species	8-11	P53	Homo sapiens	168-171
30283098-5	2018	Nanoparticle activity was related to the decreased level of intracellular ROS and RNS, which downregulated NF-kappaB signaling depending on the p53 status of the cell line.	Reactive Nitrogen Species	82-85	P53	Homo sapiens	144-147
18440285-5	2008	Caffeine increased apoptosis levels and inhibited p53 activation in proliferating cells, suggesting a protective role for p53.	Caffeine	0-8	P53	Homo sapiens	122-125
30059758-4	2018	Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-).	Ceramides	156-164	P53	Homo sapiens	43-46
18483381-4	2008	RESULTS: In this report, we show that the HDIs trichostatin A, sodium butyrate, and low nanomolar doses of LAQ824 combined with the glycolysis inhibitor 2-deoxy-d-glucose induce strong apoptosis in cancer cell lines of brain, breast, and cervix in a p53-independent manner.	LAQ824	107-113	P53	Homo sapiens	250-253
30059758-4	2018	Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-).	Ceramides	156-164	P53	Homo sapiens	261-264
30059758-4	2018	Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-).	Ceramides	156-164	P53	Homo sapiens	261-264
30059758-6	2018	By contrast, in the p53-deficient cells CerS2 expression and CerS2-related C24:0- and C24:1-ceramide levels were elevated which is possibly related to enhanced polyadenylation of the CerS2 transcript in these cells.	Ceramides	92-100	P53	Homo sapiens	20-23
28802167-11	2017	Bioinformatics analyses predicted that 5-Aza-dC functions as a p53 inducer, radiosensitizer, and inhibitor of some enzymes.	Decitabine	39-47	P53	Homo sapiens	63-66
18489080-7	2008	An RP-HPLC-ECD assay was used to detect the formation of 8-oxo-dGuo in p53 cDNA exposed to representative quinones, BP-7,8-dione, BA-3,4-dione, and DMBA-3,4-dione under redox cycling conditions.	Quinones	106-114	P53	Homo sapiens	71-74
28802167-13	2017	In this study, we provide experimental evidence showing HDM2 is one of the targets of 5-AZA-dC leading to activation of p53 pathway and growth arrest of cells.	Decitabine	86-94	P53	Homo sapiens	120-123
18489080-7	2008	An RP-HPLC-ECD assay was used to detect the formation of 8-oxo-dGuo in p53 cDNA exposed to representative quinones, BP-7,8-dione, BA-3,4-dione, and DMBA-3,4-dione under redox cycling conditions.	benz(a)anthracene-3,4-dione	130-142	P53	Homo sapiens	71-74
28791403-10	2017	Among DLBCL cases, the TP53 mutations shortened both OS and PFS of patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) and decreased both OS and PFS of patients with secondary DLBCL disease.	Cyclophosphamide	108-124	P53	Homo sapiens	23-27
30237540-2	2018	Here, we report that p53 physically interacts with histone deacetylase SIRT6 in vitro and in vivo, and this interaction increases following palmitic acid (PA) treatment.	Palmitic Acid	140-153	P53	Homo sapiens	21-24
30237540-2	2018	Here, we report that p53 physically interacts with histone deacetylase SIRT6 in vitro and in vivo, and this interaction increases following palmitic acid (PA) treatment.	Palmitic Acid	155-157	P53	Homo sapiens	21-24
18187663-0	2008	Triptolide sensitizes AML cells to TRAIL-induced apoptosis via decrease of XIAP and p53-mediated increase of DR5.	triptolide	0-10	P53	Homo sapiens	84-87
30237540-3	2018	In response to PA, p53 and SIRT6 localize to chromatin in a p53-dependent manner.	Palmitic Acid	15-17	P53	Homo sapiens	19-22
30237540-3	2018	In response to PA, p53 and SIRT6 localize to chromatin in a p53-dependent manner.	Palmitic Acid	15-17	P53	Homo sapiens	60-63
30103756-3	2018	Our study has finally revealed 9 genes (DBP, NR3C1, TCF12, TP53, ZNF12, SOCS6, ZFP36, ACYP1, and DRD1) involved in imatinib-resistant GIST-T1 cells.	Imatinib Mesylate	115-123	P53	Homo sapiens	59-63
30103756-4	2018	TP53 and SOCS6 may be the most promising candidate genes for imatinib-resistance due to the possible signaling pathway, such as apoptosis pathway and Wnt signaling pathway, JAK-STAT signaling pathway.	Imatinib Mesylate	61-69	P53	Homo sapiens	0-4
28919752-7	2017	ZnO NP-treated cells showed upregulation of p53 and LC3, indicating that ZnO NPs are able to upregulate apoptosis and autophagy.	zno np	0-6	P53	Homo sapiens	44-47
27432539-7	2017	TP53 and/or SMAD4 mutations were commonly detected in juice samples from patients with PDAC and were not detected in controls (p&lt;0.0001); mutant TP53/SMAD4 concentrations could distinguish PDAC from IPMN cases with 32.4% sensitivity, 100% specificity (area under the curve, AUC 0.73, p=0.0002) and controls (AUC 0.82, p&lt;0.0001).	pdac	87-91	P53	Homo sapiens	0-4
27432539-7	2017	TP53 and/or SMAD4 mutations were commonly detected in juice samples from patients with PDAC and were not detected in controls (p&lt;0.0001); mutant TP53/SMAD4 concentrations could distinguish PDAC from IPMN cases with 32.4% sensitivity, 100% specificity (area under the curve, AUC 0.73, p=0.0002) and controls (AUC 0.82, p&lt;0.0001).	pdac	87-91	P53	Homo sapiens	148-152
29879296-2	2018	Overexpression of CtBP occurs in many human cancers where they promote the epithelial-to-mesenchymal transition, stem cell-like features, and cell survival, while knockdown of CtBP in tumor cells results in p53-independent apoptosis.	ctbp	176-180	P53	Homo sapiens	207-210
27432539-7	2017	TP53 and/or SMAD4 mutations were commonly detected in juice samples from patients with PDAC and were not detected in controls (p&lt;0.0001); mutant TP53/SMAD4 concentrations could distinguish PDAC from IPMN cases with 32.4% sensitivity, 100% specificity (area under the curve, AUC 0.73, p=0.0002) and controls (AUC 0.82, p&lt;0.0001).	pdac	192-196	P53	Homo sapiens	148-152
18507003-8	2008	CONCLUSION: These findings provide new insights into the molecular mechanisms of the synergistic effect of caffeine related to p53 gene status in osteosarcoma, providing candidates for an assay of responsiveness to caffeine-potentiated chemotherapy for osteosarcoma.	Caffeine	107-115	P53	Homo sapiens	127-130
29750295-5	2018	Here, we report the discovery of a canine mammary gland tumor cell line CTB-m2, which contains the Leu332Gln (L332Q) mutation corresponding to Leu344 in the tetramerization domain of human p53.	leu332gln	99-108	P53	Homo sapiens	189-192
18248856-11	2008	Furthermore, persistent inhibition of foci growth of phosphorylated ATM by an ATM inhibitor, KU55933, completely abrogated p53 phosphorylation.	2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one	93-100	P53	Homo sapiens	123-126
29950865-8	2018	Conclusion: In particular, luciferase assay showed that SPL-A inhibited Bcl-2 promoter activity, and p53 inhibitor PFT-alpha could reverse the effect of SPL-A on Bcl-2 expression.	spindlactone A	153-158	P53	Homo sapiens	101-104
28813679-3	2017	Here, we show that TP53 limits erastin-induced ferroptosis by blocking dipeptidyl-peptidase-4 (DPP4) activity in a transcription-independent manner.	erastin	31-38	P53	Homo sapiens	19-23
18024214-3	2008	p53 shRNA (or transient p53 siRNA) into p21-/- HCT116 cells reduced Cr(VI) sensitivity, suggesting the enhanced apoptosis in p21-/- cells is p53-dependent.	chromium hexavalent ion	68-74	P53	Homo sapiens	0-3
28601699-0	2017	Apoptotic induction mediated p53 mechanism and Caspase-3 activity by novel promising cyanoacrylamide derivatives in breast carcinoma.	cyanoacrylamide	85-100	P53	Homo sapiens	29-32
29575058-1	2018	The absolute configurations of the diastereomers of novel amino acid ester derivatives of 2,3-substituted isoindolinones, which are known as apoptosis activators due to their ability to inhibit the MDM2-p53 PPI, were assigned using NMR and computational methods.	amino acid ester	58-74	P53	Homo sapiens	203-206
18024214-3	2008	p53 shRNA (or transient p53 siRNA) into p21-/- HCT116 cells reduced Cr(VI) sensitivity, suggesting the enhanced apoptosis in p21-/- cells is p53-dependent.	chromium hexavalent ion	68-74	P53	Homo sapiens	24-27
17919121-1	2008	Polyamines are required for maintenance of intestinal epithelial integrity, and a decrease in cellular polyamines increases the cytoplasmic levels of RNA-binding protein HuR stabilizing p53 and nucleophosmin mRNAs, thus inhibiting IEC (intestinal epithelial cell) proliferation.	Polyamines	103-113	P53	Homo sapiens	186-189
29587241-5	2018	Results demonstrate that milimolar concentrations of butyrate has an anti-proliferative effect in all three colon cancer cell lines under study, leading to a decrease on cell viability, expression of P21, P53 and beta-catenin, being able to modulate P-glycoprotein activity and to induce apoptosis by modulation of BAX/BCL-2 ratio.	Butyrates	53-61	P53	Homo sapiens	205-208
28393288-15	2017	In addition, it was determined that both p38 MAPK inhibitors caused significant increases on the Ser15 phosphorylation of mutant p53 in MDA-MB-231 under these experimental conditions; while SB202190 was more potent than SB203580.	SB 203580	220-228	P53	Homo sapiens	129-132
18089819-4	2007	Here we show that ACNU and BCNU induce apoptosis in U87MG [p53 wild-type (p53wt)] and U138MG [p53 mutant (p53mt)] glioma cells.	Nimustine	18-22	P53	Homo sapiens	59-62
27967292-5	2017	P53 antagonism by lenalidomide or other therapeutics such as antisense oligonucleotides, repopulates erythroid precursors and enhances effective erythropoiesis.	Lenalidomide	18-30	P53	Homo sapiens	0-3
32254384-5	2018	After that, the prodrug and the gene vector copolymers were mixed in an aqueous solution in order to self-assemble into hybrid micelles, which could then condense the p53 gene and finally form DOX prodrug/p53 co-loaded nanoparticles.	copolymers	44-54	P53	Homo sapiens	167-170
18089819-4	2007	Here we show that ACNU and BCNU induce apoptosis in U87MG [p53 wild-type (p53wt)] and U138MG [p53 mutant (p53mt)] glioma cells.	Nimustine	18-22	P53	Homo sapiens	74-77
32254384-5	2018	After that, the prodrug and the gene vector copolymers were mixed in an aqueous solution in order to self-assemble into hybrid micelles, which could then condense the p53 gene and finally form DOX prodrug/p53 co-loaded nanoparticles.	copolymers	44-54	P53	Homo sapiens	205-208
28453190-8	2017	The increased expression of genes involved in the NGFR-MAPK10-TP53-Bax/Bcl2 pathway during incubation with AZA plus everolimus was validated by western blotting in MZ-CRC-1 cells.	Decitabine	107-110	P53	Homo sapiens	62-66
18089819-4	2007	Here we show that ACNU and BCNU induce apoptosis in U87MG [p53 wild-type (p53wt)] and U138MG [p53 mutant (p53mt)] glioma cells.	Nimustine	18-22	P53	Homo sapiens	74-77
18089819-11	2007	ACNU-induced apoptosis in p53wt glioma cells is executed via both the extrinsic and intrinsic apoptotic pathway, whereas in p53mt glioma cells, the mitochondrial pathway becomes activated.	Nimustine	0-4	P53	Homo sapiens	26-29
28446729-7	2017	The administration of MG132, a proteasome inhibitor, or knockdown of ubiquitin-specific peptidase 9, X-linked (USP9X) both eliminated the effect of WP1130 in decreasing p53 expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	22-27	P53	Homo sapiens	169-172
18089819-11	2007	ACNU-induced apoptosis in p53wt glioma cells is executed via both the extrinsic and intrinsic apoptotic pathway, whereas in p53mt glioma cells, the mitochondrial pathway becomes activated.	Nimustine	0-4	P53	Homo sapiens	124-127
29899847-7	2018	HSP90 inhibitors suppressed ubiquitination processes which were involved in p53 degradation, but a proteasome inhibitor, MG-132, prevented the HSP90 inhibitors-induced p53 down-regulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-127	P53	Homo sapiens	168-171
18088187-8	2007	In the presence of caffeine Chk1 phosphorylation was inhibited regardless of p53 status.	Caffeine	19-27	P53	Homo sapiens	77-80
29783721-0	2018	AZD1775 Increases Sensitivity to Olaparib and Gemcitabine in Cancer Cells with p53 Mutations.	gemcitabine	46-57	P53	Homo sapiens	79-82
29783721-7	2018	Moreover, the combination of AZD1775 with olaparib or gemcitabine is synergistic in cells with mutant p53 and constitutes a new approach that should be considered in the treatment of advanced and recurrent gynecologic cancer.	gemcitabine	54-65	P53	Homo sapiens	102-105
28196872-9	2017	Also, MUC16 overexpression induced cisplatin and gemcitabine resistance by downregulation of p53.Conclusions: Our findings indicate a significant role of MUC16 in tumorigenesis and metastasis of lung cancer cells possibly via regulation of TSPYL5 through the JAK2/STAT3/GR axis.	gemcitabine	49-60	P53	Homo sapiens	93-96
17965547-0	2007	Free radical scavenger edaravone suppresses x-ray-induced apoptosis through p53 inhibition in MOLT-4 cells.	Edaravone	23-32	P53	Homo sapiens	76-79
28671946-0	2017	Depletion of runt-related transcription factor 2 (RUNX2) enhances SAHA sensitivity of p53-mutated pancreatic cancer cells through the regulation of mutant p53 and TAp63.	Vorinostat	66-70	P53	Homo sapiens	86-89
28671946-3	2017	In this study, we have found for the first time that RUNX2/mutant p53/TAp63-regulatory axis has a pivotal role in the determination of SAHA sensitivity of p53-mutated pancreatic cancer MiaPaCa-2 cells.	Vorinostat	135-139	P53	Homo sapiens	66-69
28671946-3	2017	In this study, we have found for the first time that RUNX2/mutant p53/TAp63-regulatory axis has a pivotal role in the determination of SAHA sensitivity of p53-mutated pancreatic cancer MiaPaCa-2 cells.	Vorinostat	135-139	P53	Homo sapiens	155-158
28671946-5	2017	Forced depletion of mutant p53 stimulated SAHA-mediated cell death of MiaPaCa-2 cells, which was accomapanied by a further accumulation of gammaH2AX and cleaved PARP.	Vorinostat	42-46	P53	Homo sapiens	27-30
29788155-14	2018	Among patients treated with GDC-0575 and gemcitabine, there were four confirmed partial responses, three occurring in patients with tumors harboring TP53 mutation.	gemcitabine	41-52	P53	Homo sapiens	149-153
29229990-0	2018	Tumor suppressor p53 links ceramide metabolism to DNA damage response through alkaline ceramidase 2.	Ceramides	27-35	P53	Homo sapiens	17-20
17965547-7	2007	The accumulation and phosphorylation of p53 and the expression of p21(WAF1), a target protein of p53, which were induced by X-irradiation, were also suppressed by adding edaravone.	Edaravone	170-179	P53	Homo sapiens	40-43
29624044-2	2018	Herein, a dual-color ECL strategy is proposed by transferring ECL to two PMTs in a waveband-resolved way via dichroic mirror, simultaneously detecting wild-type p53 (WTp53) in near-infrared wavebands with CdTe (lambdamax = 782 nm) nanocrystals as tag and mutant p53 (MUp53) in eye-visible wavebands with CdSe (lambdamax = 554 nm) nanocrystals as tag.	pyridinium 3-methoxyestra-1,3,5(10)-trien-6-yl sulfate	73-77	P53	Homo sapiens	161-164
29624044-2	2018	Herein, a dual-color ECL strategy is proposed by transferring ECL to two PMTs in a waveband-resolved way via dichroic mirror, simultaneously detecting wild-type p53 (WTp53) in near-infrared wavebands with CdTe (lambdamax = 782 nm) nanocrystals as tag and mutant p53 (MUp53) in eye-visible wavebands with CdSe (lambdamax = 554 nm) nanocrystals as tag.	pyridinium 3-methoxyestra-1,3,5(10)-trien-6-yl sulfate	73-77	P53	Homo sapiens	168-171
17965547-7	2007	The accumulation and phosphorylation of p53 and the expression of p21(WAF1), a target protein of p53, which were induced by X-irradiation, were also suppressed by adding edaravone.	Edaravone	170-179	P53	Homo sapiens	97-100
29624044-2	2018	Herein, a dual-color ECL strategy is proposed by transferring ECL to two PMTs in a waveband-resolved way via dichroic mirror, simultaneously detecting wild-type p53 (WTp53) in near-infrared wavebands with CdTe (lambdamax = 782 nm) nanocrystals as tag and mutant p53 (MUp53) in eye-visible wavebands with CdSe (lambdamax = 554 nm) nanocrystals as tag.	cdse	304-308	P53	Homo sapiens	161-164
28505595-8	2017	Functional mapping of transcripts uniquely regulated by the azacitidine-panobinostat combination in MV4;11 cells identified p53 as an upstream regulator.	Panobinostat	72-84	P53	Homo sapiens	124-127
28505595-9	2017	A comparison of the uniquely modulated transcripts by azacitidine-panobinostat combination in MV4;11 cells versus AML-193 and THP-1 cells, bearing mutated p53, also revealed p53 as the topmost upstream regulator.	Panobinostat	66-78	P53	Homo sapiens	174-177
29731965-10	2018	In this study, the presence of both TP53 mutation and 17p/TP53 deletion, but not the individual variants, was associated with poor prognosis in DLBCL patients after treatment with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) or similar regimens.	Cyclophosphamide	191-207	P53	Homo sapiens	36-40
28505595-10	2017	Finally, expression of mutant p53 in MV4;11 cells reduced sensitivity to azacitidine-panobinostat combination, suggesting that p53 may be a predictor of response to epigenetic therapy in pediatric AML.	Panobinostat	85-97	P53	Homo sapiens	30-33
17965547-8	2007	We conclude that the free radical scavenger edaravone suppresses X-ray-induced apoptosis in MOLT-4 cells by inhibiting p53.	Edaravone	44-53	P53	Homo sapiens	119-122
28505595-10	2017	Finally, expression of mutant p53 in MV4;11 cells reduced sensitivity to azacitidine-panobinostat combination, suggesting that p53 may be a predictor of response to epigenetic therapy in pediatric AML.	Panobinostat	85-97	P53	Homo sapiens	127-130
29731965-10	2018	In this study, the presence of both TP53 mutation and 17p/TP53 deletion, but not the individual variants, was associated with poor prognosis in DLBCL patients after treatment with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) or similar regimens.	Cyclophosphamide	191-207	P53	Homo sapiens	58-62
17804813-2	2007	Recently, polyamines were shown to regulate the subcellular localization of the RNA-binding protein HuR, which stabilizes its target transcripts such as nucleophosmin and p53 mRNAs.	Polyamines	10-20	P53	Homo sapiens	171-174
29670376-0	2018	Butein activates p53 in hepatocellular carcinoma cells via blocking MDM2-mediated ubiquitination.	butein	0-6	P53	Homo sapiens	17-20
29670376-1	2018	Introduction: In this study, we aimed to investigate the effect of butein on p53 in hepatocellular carcinoma (HCC) cells and the related molecular mechanisms by which p53 was activated.	butein	67-73	P53	Homo sapiens	77-80
29670376-1	2018	Introduction: In this study, we aimed to investigate the effect of butein on p53 in hepatocellular carcinoma (HCC) cells and the related molecular mechanisms by which p53 was activated.	butein	67-73	P53	Homo sapiens	167-170
29670376-9	2018	Mechanism studies demonstrated that the interaction between MDM2 and p53 was blocked by butein and MDM2-mediated p53 ubiquitination was substantially decreased.	butein	88-94	P53	Homo sapiens	69-72
28661474-9	2017	Moreover, we show that mutant p53 forms cytoplasmic complexes with c-Abl, thereby dictating the subcellular localization of c-Abl and the sensitivity of MDA-MB-231 cells to Imatinib.	Imatinib Mesylate	173-181	P53	Homo sapiens	30-33
17624594-8	2007	Western blot analyses showed that while pretreatment of TEA and Tet produced an increase in expressions of p53, p21, and Bax, pretreatment of these two agents led to a decrease in expressions of heat shock protein (hsp)90alpha, hsp90beta, and hsp70.	Tetraethylammonium	56-59	P53	Homo sapiens	107-110
28644127-5	2017	These phenotypes are caused by induction of p53 and accumulation of the glycolytic intermediate fructose 6-phosphate, leading to engagement of the hexosamine biosynthetic pathway (HBP), increased O-GlcNAcylation, and p53 stabilization.	fructose-6-phosphate	96-116	P53	Homo sapiens	217-220
28903382-12	2017	Taken together, our findings demonstrated that miR-16 suppressed glioma cell proliferation and invasion, promoted apoptosis and inhibited cell cycle by targeting Wip1-ATM-p53 signaling pathway.	mir-16	47-53	P53	Homo sapiens	171-174
29670376-9	2018	Mechanism studies demonstrated that the interaction between MDM2 and p53 was blocked by butein and MDM2-mediated p53 ubiquitination was substantially decreased.	butein	88-94	P53	Homo sapiens	113-116
29670376-10	2018	Short-hairpin RNA experiment results showed that the sensitivity of HCC cells to butein was substantially impaired after p53 was knocked down and butein-induced apoptosis was dramatically decreased.	butein	81-87	P53	Homo sapiens	121-124
29670376-11	2018	In vivo experiments validated substantial antitumor efficacy of butein against HepG2 xenograft growth, and the expression of p53 in butein-treated tumor tissue was significantly increased.	butein	132-138	P53	Homo sapiens	125-128
29670376-12	2018	Conclusion: Butein demonstrated potent antitumor activities in HCC by activating p53, and butein or its analogs had therapeutic potential for HCC management.	butein	12-18	P53	Homo sapiens	81-84
29360968-10	2018	Pretreatment with p38 MAPK inhibitor (SB203580) suppressed PPV-induced p53 accumulation and translocation, SLCs apoptosis, and progesterone production reduction.	SB 203580	38-46	P53	Homo sapiens	71-74
17696482-10	2007	Pterostilbene increased the p53, p21, p27, and p16 proteins and decreased levels of cyclin A, cyclin E, cyclin-dependent kinase 2 (Cdk2), Cdk4, and Cdk6, but the expression of cyclin D1 was not affected.	pterostilbene	0-13	P53	Homo sapiens	28-31
29471006-5	2018	Astilbin significantly decreased reactive oxygen species (ROS) accumulation and alleviated ROS-induced activation of p53, MAPKs and AKT signaling cascades, which in turn attenuated cisplatin-induced HEK-293 cell apoptosis.	astilbin	0-8	P53	Homo sapiens	117-120
28410239-0	2017	Homoharringtonine suppresses imatinib resistance via the Bcl-6/p53 pathway in chronic myeloid leukemia cell lines.	Imatinib Mesylate	29-37	P53	Homo sapiens	63-66
29393409-4	2018	Overexpression of miR-24 induced p53 expression and p53 was verified as a direct target of miR-24.	mir-24	18-24	P53	Homo sapiens	33-36
17627614-0	2007	CR229, a novel derivative of beta-carbolin-1-one, induces cell cycle arrest and apoptosis in HeLa cells via p53 activation.	beta-carbolinone	29-48	P53	Homo sapiens	108-111
29393409-4	2018	Overexpression of miR-24 induced p53 expression and p53 was verified as a direct target of miR-24.	mir-24	91-97	P53	Homo sapiens	52-55
29393409-5	2018	Overexpression of miR-24 enhanced LEC death by directly targeting p53.	mir-24	18-24	P53	Homo sapiens	66-69
29393409-7	2018	These results suggest that the miR-24-p53 signaling pathway is involved in a novel mechanism of age-associated cataractogenesis and miR-24 may be a useful therapeutic target for age-associated cataracts.	mir-24	31-37	P53	Homo sapiens	38-41
29393409-7	2018	These results suggest that the miR-24-p53 signaling pathway is involved in a novel mechanism of age-associated cataractogenesis and miR-24 may be a useful therapeutic target for age-associated cataracts.	mir-24	132-138	P53	Homo sapiens	38-41
29955707-8	2017	Tumor suppressor p53 (p53), mitochondrial transcription factor A (TFAM), and cytochrome c oxidase subunit IV (COXIV) expression was greater for CON than for CHO+EAA treatments (drink main effect, P &lt; 0.05).	Excitatory Amino Acids	161-164	P53	Homo sapiens	17-20
28415717-0	2017	The imidazoacridinone C-1311 induces p53-dependent senescence or p53-independent apoptosis and sensitizes cancer cells to radiation.	imidazoacridinone c-1311	4-28	P53	Homo sapiens	37-40
28415717-0	2017	The imidazoacridinone C-1311 induces p53-dependent senescence or p53-independent apoptosis and sensitizes cancer cells to radiation.	imidazoacridinone c-1311	4-28	P53	Homo sapiens	65-68
17900403-7	2007	Since U87MG has the wild-type p53 gene whereas U251MG harbours a mutated p53 gene, our results indicate that triptolide induces apoptosis in GBM cells via a p53-independent pathway.	triptolide	109-119	P53	Homo sapiens	73-76
28459194-6	2017	Therapy-induced senescence by 3-deazaneplanocin A was mediated through p53-p21 pathway and triggered by enhanced ataxia-telangiectasia mutated activation related to chromatin changes.	3-deazaneplanocin	30-49	P53	Homo sapiens	71-74
28442631-6	2017	In many of the tested cell lines, we found that p53 abundance oscillated in response to ionizing radiation or the DNA-damaging chemotherapeutic neocarzinostatin and that the periodicity of the oscillations was fixed.	Zinostatin	144-160	P53	Homo sapiens	48-51
28577130-0	2018	Gemcitabine/Cisplatin Treatment Induces Concomitant SERTAD1, CDKN2B and GADD45A Modulation and Cellular Changes in Bladder Cancer Cells Regardless of the Site of TP53 Mutation.	gemcitabine	0-11	P53	Homo sapiens	162-166
29471073-4	2018	We found that etoposide and ellipticine induced CYP1A1 in TP53(+/+) cells but not in TP53(-/-) cells, demonstrating that the mechanism of CYP1A1 induction is p53-dependent; cisplatin had no such effect.	ellipticine	28-39	P53	Homo sapiens	58-62
29471073-4	2018	We found that etoposide and ellipticine induced CYP1A1 in TP53(+/+) cells but not in TP53(-/-) cells, demonstrating that the mechanism of CYP1A1 induction is p53-dependent; cisplatin had no such effect.	ellipticine	28-39	P53	Homo sapiens	158-161
17900403-7	2007	Since U87MG has the wild-type p53 gene whereas U251MG harbours a mutated p53 gene, our results indicate that triptolide induces apoptosis in GBM cells via a p53-independent pathway.	triptolide	109-119	P53	Homo sapiens	73-76
29301826-0	2018	p53-Reactive T Cells Are Associated with Clinical Benefit in Patients with Platinum-Resistant Epithelial Ovarian Cancer After Treatment with a p53 Vaccine and Gemcitabine Chemotherapy.	gemcitabine	159-170	P53	Homo sapiens	0-3
17616157-4	2007	Using these modified SP microarrays, enhancement factors of 229 and 126 were obtained for prostate-specific antigen (PSA) and p53 oligonucleotide detection, respectively.	sp	21-23	P53	Homo sapiens	126-129
28152473-0	2017	Combination of arabinogalactan and curcumin induces apoptosis in breast cancer cells in vitro and inhibits tumor growth via overexpression of p53 level in vivo.	arabinogalactan	15-30	P53	Homo sapiens	142-145
28099249-10	2017	CONCLUSIONS: The classification tree using p53, S100P, and claudin 4 seems to successfully distinguish PDAC from the accompanying BE.	pdac	103-107	P53	Homo sapiens	43-46
17433031-8	2007	Survival analysis showed that the expression of p53 was an independent prognostic factor for CSS.	thiocysteine	93-96	P53	Homo sapiens	48-51
28068628-0	2017	Epoxy clerodane diterpene inhibits MCF-7 human breast cancer cell growth by regulating the expression of the functional apoptotic genes Cdkn2A, Rb1, mdm2 and p53.	Diterpenes	16-25	P53	Homo sapiens	158-161
29371630-6	2018	We moreover demonstrated that although the CDH1 locus in the p53-independent cells, but not in fibroblasts, becomes high-H3K27ac by butyrate and allows p53-biniding, their CDH1 expression does not become dependent on p53.	Butyrates	132-140	P53	Homo sapiens	61-64
29268127-0	2018	Design, synthesis and biological evaluation of 1, 4-dihydro indeno[1,2-c] pyrazole linked oxindole analogues as potential anticancer agents targeting tubulin and inducing p53 dependent apoptosis.	1, 4-dihydro indeno[1,2-c] pyrazole	47-82	P53	Homo sapiens	171-174
17433031-11	2007	The expression of p53 is an independent predictor of CSS in Chinese patients with penile cancer.	thiocysteine	53-56	P53	Homo sapiens	18-21
30060809-1	2018	Ceramides, important players in signal transduction, interact with multiple cellular pathways, including p53 pathways.	Ceramides	0-9	P53	Homo sapiens	105-108
17310348-5	2007	(2) A significant difference in the incidence of p53, c-erbB-2, EGFR overexpression was observed only between malignant component of Ca-ex-PA and benign component of Ca-ex-PA.	ca-ex-pa	133-141	P53	Homo sapiens	49-52
30060809-2	2018	However, the relationship between ceramide and p53 is very complex, and mechanisms underlying their coregulation are diverse and not fully characterized.	Ceramides	34-42	P53	Homo sapiens	47-50
30060809-7	2018	We discuss the recent studies, which underscore the function of p53 in the regulation of ceramide pathways and the reciprocal regulation of p53 by ceramide.	Ceramides	89-97	P53	Homo sapiens	64-67
30060809-7	2018	We discuss the recent studies, which underscore the function of p53 in the regulation of ceramide pathways and the reciprocal regulation of p53 by ceramide.	Ceramides	147-155	P53	Homo sapiens	140-143
28225682-0	2017	Decitabine in TP53-Mutated AML.	Decitabine	0-10	P53	Homo sapiens	14-18
17310348-5	2007	(2) A significant difference in the incidence of p53, c-erbB-2, EGFR overexpression was observed only between malignant component of Ca-ex-PA and benign component of Ca-ex-PA.	ca-ex-pa	166-174	P53	Homo sapiens	49-52
29749241-6	2018	In conclusion, our results suggested that miRNA-489 may be considered as a biomarker in cervical cancer and had suppressed the cell proliferation and stimulated cell apoptosis via PI3K/AKT/P53 signaling pathway (Fig.	mirna-489	42-51	P53	Homo sapiens	189-192
17310348-6	2007	(3) The incidence of PCNA, Ki67, p53, c-erbB-2 overexpression in malignant component of Ca-ex-PA showed the highest data among the four groups.	ca-ex-pa	88-96	P53	Homo sapiens	33-36
17258428-6	2007	A screening study on 31 metal compounds, showed that the classified human carcinogens (NaAsO2, CdSO4 .8H2O, Na2CrO4 .4H2O, MnCl2, (NH4)2PtCl6) significantly increased cytotoxicity in p53-expressing cells compared to non-expressing cells, suggesting that their cytotoxicity was p53-mediated.	na2cro4 .4h2o	108-121	P53	Homo sapiens	183-186
30109812-0	2018	Novel isatin-derived molecules activate p53 via interference with Mdm2 to promote apoptosis.	Isatin	6-12	P53	Homo sapiens	40-43
30109812-5	2018	In this study we characterize the biological effects of a novel class of non-genotoxic isatin Schiff and Mannich base derivatives (ISMBDs) that stabilize p53 on the protein level.	Mannich Bases	105-117	P53	Homo sapiens	154-157
17258428-6	2007	A screening study on 31 metal compounds, showed that the classified human carcinogens (NaAsO2, CdSO4 .8H2O, Na2CrO4 .4H2O, MnCl2, (NH4)2PtCl6) significantly increased cytotoxicity in p53-expressing cells compared to non-expressing cells, suggesting that their cytotoxicity was p53-mediated.	na2cro4 .4h2o	108-121	P53	Homo sapiens	277-280
17258428-6	2007	A screening study on 31 metal compounds, showed that the classified human carcinogens (NaAsO2, CdSO4 .8H2O, Na2CrO4 .4H2O, MnCl2, (NH4)2PtCl6) significantly increased cytotoxicity in p53-expressing cells compared to non-expressing cells, suggesting that their cytotoxicity was p53-mediated.	(nh4)2ptcl6	130-141	P53	Homo sapiens	183-186
17258428-6	2007	A screening study on 31 metal compounds, showed that the classified human carcinogens (NaAsO2, CdSO4 .8H2O, Na2CrO4 .4H2O, MnCl2, (NH4)2PtCl6) significantly increased cytotoxicity in p53-expressing cells compared to non-expressing cells, suggesting that their cytotoxicity was p53-mediated.	(nh4)2ptcl6	130-141	P53	Homo sapiens	277-280
30257238-14	2018	Besides, miR-374a affected propofol-treated HepG2 cells by targeting TP53.	Propofol	27-35	P53	Homo sapiens	69-73
17483435-4	2007	p53 treatment resulted in complete and durable remission of the injected lesion by fluorodeoxyglucose-positron emission tomography scans with improvement of tumor-related symptoms.	Fluorodeoxyglucose F18	83-101	P53	Homo sapiens	0-3
29115375-0	2018	Persistent STAT5-mediated ROS production and involvement of aberrant p53 apoptotic signaling in the resistance of chronic myeloid leukemia to imatinib.	Imatinib Mesylate	142-150	P53	Homo sapiens	69-72
17440101-4	2007	Using these isogenic variants, we investigated the roles of p53, BAX, and p21 in the cellular response to treatment with noscapine.	Noscapine	121-130	P53	Homo sapiens	60-63
29115375-10	2018	Taken together, these findings suggest that the resistance of CML to the tyrosine kinase inhibitor, imatinib, may be associated with persistent STAT5-mediated ROS production, and the abnormality of the p53 pathway.	Imatinib Mesylate	100-108	P53	Homo sapiens	202-205
17440101-5	2007	Our results show that noscapine treatment increases the expression of p53 over time in cells with wild-type p53 status.	Noscapine	22-31	P53	Homo sapiens	70-73
17440101-5	2007	Our results show that noscapine treatment increases the expression of p53 over time in cells with wild-type p53 status.	Noscapine	22-31	P53	Homo sapiens	108-111
17440101-7	2007	Conversely, loss of p53 and p21 alleles had a counter effect on both BAX and Bcl-2 expression and the p53-null and p21-null cells were significantly resistant to the antiproliferative and apoptotic effects of noscapine.	Noscapine	209-218	P53	Homo sapiens	20-23
29272311-12	2017	One or more of these altered genes may be involved in p53-dependent ceramide accumulation.	Ceramides	68-76	P53	Homo sapiens	54-57
17440101-7	2007	Conversely, loss of p53 and p21 alleles had a counter effect on both BAX and Bcl-2 expression and the p53-null and p21-null cells were significantly resistant to the antiproliferative and apoptotic effects of noscapine.	Noscapine	209-218	P53	Homo sapiens	102-105
17440101-8	2007	All but the p53-null cells displayed p53 protein accumulation in a time-dependent manner on noscapine treatment.	Noscapine	92-101	P53	Homo sapiens	12-15
17440101-8	2007	All but the p53-null cells displayed p53 protein accumulation in a time-dependent manner on noscapine treatment.	Noscapine	92-101	P53	Homo sapiens	37-40
29046392-5	2017	Here, we reported that nutlin-3 plus tanshinone IIA significantly potentiated the cytotoxic and apoptotic induction effects of imatinib by downregulation of the AKT/mTOR pathway and reactivating p53 pathway deeply in Ph+ acute lymphoblastic leukemia cell line.	Imatinib Mesylate	127-135	P53	Homo sapiens	195-198
17204746-0	2007	Bifunctional alkylating agent-induced p53 and nonclassical nuclear factor kappaB responses and cell death are altered by caffeic acid phenethyl ester: a potential role for antioxidant/electrophilic response-element signaling.	caffeic acid phenethyl ester	121-149	P53	Homo sapiens	38-41
28821555-3	2017	Moreover, p53 reactivation via RG7388, a second-generation MDM2 inhibitor, strongly enhances the in vivo antitumor activity of temsirolimus.	RG7388	31-37	P53	Homo sapiens	10-13
17204746-7	2007	CAPE disrupted BFA-induced phosphorylation of p53 and p90 ribosomal S6 kinase (p90RSK) in both cell lines.	caffeic acid phenethyl ester	0-4	P53	Homo sapiens	46-49
28800961-0	2017	Functional consequences of inducible genetic elements from the p53 SOS response in a mammalian organ system.	sulfur monoxide	67-70	P53	Homo sapiens	63-66
17471156-3	2007	In addition, the improved effectiveness of guanine cytosine (GC)-clamped DHPLC for TP53 screening is detailed.	guanine-cytosine	43-59	P53	Homo sapiens	83-87
28765903-12	2017	Under the same condition, p53 protein expression, but not mRNA expression, was reversed by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	P53	Homo sapiens	26-29
17297654-6	2007	The expression profiles of smad 4, cyclin D1 and p53 in the DMBA-induced tumors were similar to those of human pancreatic cancer, suggesting that this would be a useful mouse model for studying the morphological and molecular mechanisms involved in pancreatic carcinogenesis.	9,10-Dimethyl-1,2-benzanthracene	60-64	P53	Homo sapiens	49-52
28782884-14	2017	Patients with a del(17p) or TP53 mutation can be treated with ibrutinib, venetoclax, or a combination of idelalisib and rituximab.	venetoclax	73-83	P53	Homo sapiens	28-32
17211478-3	2007	So far, the best-known function of the ASPP family members is their ability to regulate the apoptotic function of p53 and its family members, p63 and p73.	aspp	39-43	P53	Homo sapiens	114-117
28628491-0	2017	Calcein-acetoxymethy ester enhances the antitumor effects of doxorubicin in nonsmall cell lung cancer by regulating the TopBP1/p53RR pathway.	calcein-acetoxymethy ester	0-26	P53	Homo sapiens	127-130
17196878-3	2007	In this study, we examined CEPA-induced gene expression in DLD-1 colorectal adenocarcinoma human cells carrying a mutant p53, in order to understand the details of CEPA-induced apoptosis via lipid peroxidation.	ethephon	27-31	P53	Homo sapiens	121-124
28700975-6	2017	Detailed study shows that astilbin leads to S phase arrest of the cell cycle by induction of p53 and p21 and activated-AMPK.	astilbin	26-34	P53	Homo sapiens	93-96
28927122-10	2017	The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group.	Silicon	10-12	P53	Homo sapiens	18-21
17196878-6	2007	In addition, activation of the mutant p53 was also induced by CEPA, and these effects showed lipid-peroxidation dependency.	ethephon	62-66	P53	Homo sapiens	38-41
28927122-10	2017	The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group.	Silicon	10-12	P53	Homo sapiens	46-49
28927122-10	2017	The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group.	Silicon	10-12	P53	Homo sapiens	46-49
17508933-6	2007	Several clusters of the Trp/Met/Phe residues are involved in the p53 protein-protein interactions.	Phenylalanine	32-35	P53	Homo sapiens	65-68
28927122-10	2017	The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group.	Silicon	43-45	P53	Homo sapiens	18-21
28927122-10	2017	The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group.	Silicon	43-45	P53	Homo sapiens	46-49
28927122-10	2017	The expression of P53 in the EGCG-combined si-P53 group was higher than that of the si-P53 group, but lower than the EGCG group.	Silicon	43-45	P53	Homo sapiens	46-49
28927122-11	2017	The Bcl-2 expression level in the EGCG-combined si-P53 group was lower than that of the si-P53 group and higher than that of the EGCG group.	Silicon	16-18	P53	Homo sapiens	51-54
17213797-3	2006	BaP 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of BaP, attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 mutations.	bpde-n2-dg	98-108	P53	Homo sapiens	129-132
28927122-11	2017	The Bcl-2 expression level in the EGCG-combined si-P53 group was lower than that of the si-P53 group and higher than that of the EGCG group.	Silicon	16-18	P53	Homo sapiens	91-94
28927122-11	2017	The Bcl-2 expression level in the EGCG-combined si-P53 group was lower than that of the si-P53 group and higher than that of the EGCG group.	Silicon	48-50	P53	Homo sapiens	51-54
16971506-0	2006	Cycloheximide protects HepG2 cells from serum withdrawal-induced apoptosis by decreasing p53 and phosphorylated p53 levels.	Cycloheximide	0-13	P53	Homo sapiens	89-92
16971506-0	2006	Cycloheximide protects HepG2 cells from serum withdrawal-induced apoptosis by decreasing p53 and phosphorylated p53 levels.	Cycloheximide	0-13	P53	Homo sapiens	112-115
16971506-12	2006	These results suggest the possibility that kinases that phosphorylate p53 might be affected by CHX administration.	Cycloheximide	95-98	P53	Homo sapiens	70-73
30563957-7	2017	To elucidate this issue, we recently initiated a study clarifying different modes of SAHA-induced cell death in two human uterine sarcoma cell lines which led to the conclusion that the tumor suppressor protein p53 could act as a molecular switch between SAHA-triggered autophagic or apoptotic cell death.	Vorinostat	85-89	P53	Homo sapiens	211-214
17045763-0	2006	Opposing securin and p53 protein expression in the oxaliplatin-induced cytotoxicity of human colorectal cancer cells.	Oxaliplatin	51-62	P53	Homo sapiens	21-24
30563957-7	2017	To elucidate this issue, we recently initiated a study clarifying different modes of SAHA-induced cell death in two human uterine sarcoma cell lines which led to the conclusion that the tumor suppressor protein p53 could act as a molecular switch between SAHA-triggered autophagic or apoptotic cell death.	Vorinostat	255-259	P53	Homo sapiens	211-214
17045763-5	2006	The phospho-p53 (Ser-15), total p53, and p21 proteins were elevated by oxaliplatin in RKO cells; conversely, oxaliplatin decreased the securin protein expression.	Oxaliplatin	71-82	P53	Homo sapiens	12-15
17045763-5	2006	The phospho-p53 (Ser-15), total p53, and p21 proteins were elevated by oxaliplatin in RKO cells; conversely, oxaliplatin decreased the securin protein expression.	Oxaliplatin	71-82	P53	Homo sapiens	32-35
16316721-0	2006	Triptolide induces Bcl-2 cleavage and mitochondria dependent apoptosis in p53-deficient HL-60 cells.	triptolide	0-10	P53	Homo sapiens	74-77
28854261-13	2017	Gemcitabine-induced uPA promoted invasion, sphere formation and colony formation and attenuated apoptosis induced by gemcitabine in panc-1 CSCs, depending on interaction with mutant p53-R273H.	gemcitabine	0-11	P53	Homo sapiens	182-185
28854261-13	2017	Gemcitabine-induced uPA promoted invasion, sphere formation and colony formation and attenuated apoptosis induced by gemcitabine in panc-1 CSCs, depending on interaction with mutant p53-R273H.	gemcitabine	117-128	P53	Homo sapiens	182-185
28854261-15	2017	CONCLUSION: Gemcitabine treatment induced ER stress and promoted mutant p53-R273H stabilization via transcriptionally activated uPA which may contribute to chemoresistance to gemcitabine.	gemcitabine	12-23	P53	Homo sapiens	72-75
28854261-15	2017	CONCLUSION: Gemcitabine treatment induced ER stress and promoted mutant p53-R273H stabilization via transcriptionally activated uPA which may contribute to chemoresistance to gemcitabine.	gemcitabine	175-186	P53	Homo sapiens	72-75
28854261-16	2017	Notably, upregulation of uPA by gemcitabine treatment may lead to the failure of CP-31398; thus, a novel strategy for modulating mutant p53 function needs to be developed.	gemcitabine	32-43	P53	Homo sapiens	136-139
16316721-1	2006	Triptolide, a bioactive component of the Chinese medicinal herb Tripterygium wilfordii Hook F., induces p53-mediated apoptosis in cancer cells.	triptolide	0-10	P53	Homo sapiens	104-107
16316721-2	2006	This study demonstrated that triptolide activated an alternative p53-independent apoptotic pathway in HL-60 cells.	triptolide	29-39	P53	Homo sapiens	65-68
16316721-6	2006	In the MCF-7 cells that possessed the wild type p53 but lacked caspases 3, triptolide induced cell death with an increase in p53 but Bcl-2 remained unaltered.	triptolide	75-85	P53	Homo sapiens	48-51
28714514-0	2017	Nuclear expression of Y box binding-1 is important for resistance to chemotherapy including gemcitabine in TP53-mutated bladder cancer.	gemcitabine	92-103	P53	Homo sapiens	107-111
28714514-10	2017	Nuclear expression of YB-1 is important for resistance to chemotherapy including gemcitabine in TP53-mutated bladder cancer.	gemcitabine	81-92	P53	Homo sapiens	96-100
16316721-6	2006	In the MCF-7 cells that possessed the wild type p53 but lacked caspases 3, triptolide induced cell death with an increase in p53 but Bcl-2 remained unaltered.	triptolide	75-85	P53	Homo sapiens	125-128
16831876-10	2006	Given that methylglyoxal is frequently generated under both physiological and pathological conditions, we postulate that GLX2 serves as a pro-survival factor of the p53 family and plays a critical role in the normal development and in the pathogenesis of various human diseases, including cancer, diabetes, and neurodegenerative diseases.	Pyruvaldehyde	11-24	P53	Homo sapiens	165-168
28536076-6	2017	Here in this study we focus on the inhibitory effects of polyarginine and its analogues polyornithine, canavanine, and citrulline on the inhibition of p53 mutant peptide aggregation, and p53 mutant cancer cell proliferation inhibition in vitro.	polyornithine	88-101	P53	Homo sapiens	151-154
28536076-6	2017	Here in this study we focus on the inhibitory effects of polyarginine and its analogues polyornithine, canavanine, and citrulline on the inhibition of p53 mutant peptide aggregation, and p53 mutant cancer cell proliferation inhibition in vitro.	polyornithine	88-101	P53	Homo sapiens	187-190
28536076-8	2017	The results show that polyarginine, and polyornithine, in micromolar concentrations, significantly inhibits p53 conserved peptide aggregation, and the cell proliferation of p53 mutant cancer cells.	polyornithine	40-53	P53	Homo sapiens	108-111
28536076-8	2017	The results show that polyarginine, and polyornithine, in micromolar concentrations, significantly inhibits p53 conserved peptide aggregation, and the cell proliferation of p53 mutant cancer cells.	polyornithine	40-53	P53	Homo sapiens	173-176
28333845-4	2017	METHODS: The expression of highly sulfated chondroitin sulfate (CS-E), a characteristic glycosaminoglycan of the cancer-associated ECM, was assessed by immunohistochemistry in a large cohort of precursor lesions of the full spectrum of HGSC development, including 97 serous tubal intraepithelial carcinomas (STICs), 27 serous tubal intraepithelial lesions, and 24 p53 signatures.	Chondroitin Sulfates	43-62	P53	Homo sapiens	364-367
28333845-4	2017	METHODS: The expression of highly sulfated chondroitin sulfate (CS-E), a characteristic glycosaminoglycan of the cancer-associated ECM, was assessed by immunohistochemistry in a large cohort of precursor lesions of the full spectrum of HGSC development, including 97 serous tubal intraepithelial carcinomas (STICs), 27 serous tubal intraepithelial lesions, and 24 p53 signatures.	Chondroitin Sulfates	64-68	P53	Homo sapiens	364-367
28320780-2	2017	We previously discovered that small-molecule zinc chelators called zinc metallochaperones (ZMCs) reactivate mutant p53 by restoring zinc binding to zinc-deficient p53 mutants.	zmcs	91-95	P53	Homo sapiens	115-118
16798066-6	2006	o-PD and Cl-PD caused piperidine-labile and formamidopyrimidine-DNA glycosylase-sensitive lesions at cytosine and guanine residues respectively in the 5"-ACG-3" sequence, complementary to codon 273, a well-known hotspot of the human p53 tumor suppressor gene.	4-chloro-1,2-diaminobenzene	9-14	P53	Homo sapiens	233-236
28320780-2	2017	We previously discovered that small-molecule zinc chelators called zinc metallochaperones (ZMCs) reactivate mutant p53 by restoring zinc binding to zinc-deficient p53 mutants.	zmcs	91-95	P53	Homo sapiens	163-166
28187856-0	2017	Corrigendum to "PCB153, TCDD and estradiol compromise the benzo[a]pyrene-induced p53-response via FoxO3a" [Chem.	2,4,5,2',4',5'-hexachlorobiphenyl	16-22	P53	Homo sapiens	81-84
16325375-3	2006	Here, we report that overexpression of CKIP-1 in SK-BR-3 breast cancer cells prevents p53 degradation induced by cycloheximide treatment through increase of p53 N-terminal Ser-15 phosphorylation level.	Cycloheximide	113-126	P53	Homo sapiens	86-89
28187856-0	2017	Corrigendum to "PCB153, TCDD and estradiol compromise the benzo[a]pyrene-induced p53-response via FoxO3a" [Chem.	benzo[a]	58-66	P53	Homo sapiens	81-84
16325375-3	2006	Here, we report that overexpression of CKIP-1 in SK-BR-3 breast cancer cells prevents p53 degradation induced by cycloheximide treatment through increase of p53 N-terminal Ser-15 phosphorylation level.	Cycloheximide	113-126	P53	Homo sapiens	157-160
16720642-5	2006	Cytoplasmic p53 was still observed after the translation activities were blocked by cycloheximide.	Cycloheximide	84-97	P53	Homo sapiens	12-15
28220348-7	2017	The resulted showed that MG132 induced significant apoptosis, and caused the accumulation of p53 protein in both p53 wild-type and mutant-type thyroid cancer cell lines, whereas the proapoptotic targets of p53 were transcriptionally upregulated only in the p53 wild-type cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	P53	Homo sapiens	93-96
28220348-7	2017	The resulted showed that MG132 induced significant apoptosis, and caused the accumulation of p53 protein in both p53 wild-type and mutant-type thyroid cancer cell lines, whereas the proapoptotic targets of p53 were transcriptionally upregulated only in the p53 wild-type cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	P53	Homo sapiens	113-116
28220348-7	2017	The resulted showed that MG132 induced significant apoptosis, and caused the accumulation of p53 protein in both p53 wild-type and mutant-type thyroid cancer cell lines, whereas the proapoptotic targets of p53 were transcriptionally upregulated only in the p53 wild-type cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	P53	Homo sapiens	113-116
28220348-7	2017	The resulted showed that MG132 induced significant apoptosis, and caused the accumulation of p53 protein in both p53 wild-type and mutant-type thyroid cancer cell lines, whereas the proapoptotic targets of p53 were transcriptionally upregulated only in the p53 wild-type cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	P53	Homo sapiens	113-116
28977833-4	2017	This combination, named as TriCurin, rapidly down regulated HPV18 E6 and NF-kB expression while concomitantly inducing the tumor suppressor protein p53 in HeLa cells.	tricurin	27-35	P53	Homo sapiens	148-151
28270613-7	2017	Intron retention was concomitant with a strong induction of the p53 pathway and DNA damage response, manifesting as gamma-H2A.X positivity in neurons of the spinal cord and brain.	gamma-h2a	116-125	P53	Homo sapiens	64-67
28611319-12	2017	Also, increase in intake of Vitamin E might help in reducing the risk of recurrence in KCOT by reducing the dysregulation of Cyclin D1 and Down-Regulation of mutant p53.	Vitamin E	28-37	P53	Homo sapiens	165-168
28229579-0	2017	Decitabine in TP53-Mutated AML.	Decitabine	0-10	P53	Homo sapiens	14-18
28337271-12	2017	Long term low- or high-dose arsenic induces epithelial-mesenchymal transition, likely via downregulation of E-cadherin, activates p53, and differently affects cell proliferation/growth.	Arsenic	28-35	P53	Homo sapiens	130-133
27984642-0	2017	TP53 mutations predict decitabine-induced complete responses in patients with myelodysplastic syndromes.	Decitabine	23-33	P53	Homo sapiens	0-4
27984642-9	2017	In summary, TP53 mutations might predict decitabine-induced complete responses in patients with MDS.	Decitabine	41-51	P53	Homo sapiens	12-16
27907876-0	2017	Rational design and synthesis of 1,5-disubstituted tetrazoles as potent inhibitors of the MDM2-p53 interaction.	1,5-disubstituted tetrazoles	33-61	P53	Homo sapiens	95-98
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-229	P53	Homo sapiens	92-95
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-229	P53	Homo sapiens	92-95
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-229	P53	Homo sapiens	26-29
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-229	P53	Homo sapiens	92-95
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-229	P53	Homo sapiens	92-95
29049989-0	2017	The USP7 Inhibitor P5091 Induces Cell Death in Ovarian Cancers with Different P53 Status.	P5091	19-24	P53	Homo sapiens	78-81
27029827-6	2017	The combination of Aza+SAHA significantly increased p53 protein binding to DNA in pax5 promoter region (p&lt;0.01).	Vorinostat	23-27	P53	Homo sapiens	52-55
27029827-7	2017	More efficient binding of the transcription factor p53 to pax5 promoter region is likely because SAHA increased accessibility of the chromatin conformation and Aza-demethylated DNA was more permissive, allowing transcription factors to bind.	Vorinostat	97-101	P53	Homo sapiens	51-54
27029827-8	2017	CONCLUSION: Our study not only explained an underlying mechanism, that pax5 re-expression was induced by Aza+SAHA combination in H460 cells via p53, but also demonstrated a pattern showing that the combination of demethylating agent and HDAC inhibitor can re-activate tumor suppressor gene (TSG) which is associated with the enhancement of transcription factors binding to the promoter region of the TSG.	Vorinostat	109-113	P53	Homo sapiens	144-147
28031111-0	2017	[Cucurbitacin I (JSI-124)-induced apoptosis of HepG2 cells via p53 signaling pathway].	cucurbitacin I	1-15	P53	Homo sapiens	63-66
28031111-0	2017	[Cucurbitacin I (JSI-124)-induced apoptosis of HepG2 cells via p53 signaling pathway].	cucurbitacin I	17-24	P53	Homo sapiens	63-66
27965580-0	2016	OSU-2S/Sorafenib Synergistic Antitumor Combination against Hepatocellular Carcinoma: The Role of PKCdelta/p53.	OSU-2S	0-6	P53	Homo sapiens	106-109
27965580-7	2016	The knockdown/over-expression of p53 was used to explain the differential sensitivity of HCC cell lines to sorafenib and/or OSU-2S.	OSU-2S	124-130	P53	Homo sapiens	33-36
27965580-13	2016	The p53 status in HCC cells predicts their sensitivity toward both sorafenib and OSU-2S.	OSU-2S	81-87	P53	Homo sapiens	4-7
27959731-10	2016	CONCLUSIONS: Patients with AML and MDS who had cytogenetic abnormalities associated with unfavorable risk, TP53 mutations, or both had favorable clinical responses and robust (but incomplete) mutation clearance after receiving serial 10-day courses of decitabine.	Decitabine	252-262	P53	Homo sapiens	107-111
27678524-4	2016	ABT-751 also induced early autophagy via upregulation of nuclear TP53 and downregulation of the AKT serine/threonine kinase (AKT)/mechanistic target of rapamycin (MTOR) pathway.	ABT751	0-7	P53	Homo sapiens	65-69
27473386-6	2016	Apigenin attenuated the proteasome inhibitors (MG132 and MG115)-induced decrease in the levels of Bid and Bcl-2, increase in the levels of Bax and p53, loss of the mitochondrial transmembrane potential, release of cytochrome c, activation of caspases (-8, -9 and -3), cleavage of PARP-1 and cell death in both cell lines.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	47-52	P53	Homo sapiens	147-150
27611952-3	2016	TP53 status was correlated to response to neoadjuvant anthracycline/taxane-based chemotherapy with or without carboplatin and trastuzumab/lapatinib in HER2-positive and bevacizumab in TNBC.	Carboplatin	110-121	P53	Homo sapiens	0-4
27568863-4	2016	In order to better understand the multiple interconnected pathways of gentamicin-induced apoptosis and ensuing renal cell toxicity, we investigated the effect of gentamicin on p53 and p21 levels.	Gentamicins	162-172	P53	Homo sapiens	176-179
27165055-8	2016	Keratinocytes treated with erlotinib in vitro showed a significant down-modulation of hyaluronan synthases (HAS2 and HAS3), whereas senescence-associated genes (p21, p53, IL-6, maspin) were upregulated, along with a G1 cell cycle arrest and stronger SA beta-Gal activity.	Erlotinib Hydrochloride	27-36	P53	Homo sapiens	166-169
27601937-0	2016	Molecular mechanism leading to SAHA-induced autophagy in tumor cells: evidence for a p53-dependent pathway.	Vorinostat	31-35	P53	Homo sapiens	85-88
27706682-9	2016	Ginsenoside Rg1 can inhibit VSMC senescence, and the mechanisms may be related to its partial inhibition of the p16INK4a/Rb and p53-p21Cip1/Waf1 signaling pathways during the cell cycle.	Ginsenosides	0-11	P53	Homo sapiens	128-131
27655732-8	2016	In p53-deficient cells, diminished localization of 53BP1 is accompanied by a reciprocal increase in BRCA1 recruitment to DSBs.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	121-125	P53	Homo sapiens	3-6
26640145-8	2016	Alternatively, in CTCL cells lacking functional p53, miR-16 induced compensatory apoptosis.	mir-16	53-59	P53	Homo sapiens	48-51
26640145-10	2016	Furthermore, we found that the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) restored the expression of miR-16 and its essential targets, induced senescence in CTCL cells expressing wild-type p53 and promoted apoptosis in cells with nonfunctional p53.	Vorinostat	61-92	P53	Homo sapiens	215-218
26640145-10	2016	Furthermore, we found that the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) restored the expression of miR-16 and its essential targets, induced senescence in CTCL cells expressing wild-type p53 and promoted apoptosis in cells with nonfunctional p53.	Vorinostat	61-92	P53	Homo sapiens	270-273
26640145-10	2016	Furthermore, we found that the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) restored the expression of miR-16 and its essential targets, induced senescence in CTCL cells expressing wild-type p53 and promoted apoptosis in cells with nonfunctional p53.	Vorinostat	94-98	P53	Homo sapiens	215-218
26640145-10	2016	Furthermore, we found that the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) restored the expression of miR-16 and its essential targets, induced senescence in CTCL cells expressing wild-type p53 and promoted apoptosis in cells with nonfunctional p53.	Vorinostat	94-98	P53	Homo sapiens	270-273
26640145-10	2016	Furthermore, we found that the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) restored the expression of miR-16 and its essential targets, induced senescence in CTCL cells expressing wild-type p53 and promoted apoptosis in cells with nonfunctional p53.	mir-16	127-133	P53	Homo sapiens	270-273
27069256-0	2016	The BCL2 selective inhibitor venetoclax induces rapid onset apoptosis of CLL cells in patients via a TP53-independent mechanism.	venetoclax	29-39	P53	Homo sapiens	101-105
27223263-5	2016	At the molecular level, aphidicolin enhanced purine analog-induced phosphorylation of p53 and accumulation of gammaH2AX, consistent with increase in DNA damage.	Aphidicolin	24-35	P53	Homo sapiens	86-89
26984670-0	2016	5-Caffeoylquinic acid inhibits invasion of non-small cell lung cancer cells through the inactivation of p70S6K and Akt activity: Involvement of p53 in differential regulation of signaling pathways.	5'-O-caffeoylquinic acid	0-21	P53	Homo sapiens	144-147
26984670-1	2016	In the present study, we investigated the effects and molecular mechanism of 5-caffeoylquinic acid (5-CQA), a natural phenolic compound isolated from Ligularia fischeri, on cell invasion, proliferation and adhesion in p53 wild-type A549 and p53-deficient H1299 non-small cell lung cancer (NSCLC) cells.	5'-O-caffeoylquinic acid	77-98	P53	Homo sapiens	218-221
26967561-3	2016	Here we show that miR-24, which has been demonstrated to target genes involved in the DNA repair process, targets p38, p53, PML and H2AX simultaneously.	mir-24	18-24	P53	Homo sapiens	119-122
26704388-0	2016	Combination of galectin inhibitor GCS-100 and BH3 mimetics eliminates both p53 wild type and p53 null AML cells.	GCS-100	34-41	P53	Homo sapiens	75-78
26704388-0	2016	Combination of galectin inhibitor GCS-100 and BH3 mimetics eliminates both p53 wild type and p53 null AML cells.	GCS-100	34-41	P53	Homo sapiens	93-96
27044842-0	2016	The novel anthraquinone derivative IMP1338 induces death of human cancer cells by p53-independent S and G2/M cell cycle arrest.	IMP1338	35-42	P53	Homo sapiens	82-85
28345329-0	2017	Lycopene Extracts from Different Tomato-Based Food Products Induce Apoptosis in Cultured Human Primary Prostate Cancer Cells and Regulate TP53, Bax and Bcl-2 Transcript Expression Carotenoids are the main tomato components, especially lycopene.	Lycopene	0-8	P53	Homo sapiens	138-142
28345329-5	2017	Using real time PCR assay, we found that lycopene promotedan upregulation of TP53 and Bax transcript expression and also downregulation of Bcl-2 expression in PCa cells.	Lycopene	41-49	P53	Homo sapiens	77-81
27380217-5	2017	The top two compounds, DTOM (ZINC 28639308) and TTOM (ZINC 38143676) with Glide score of -12.27 and -12.16, respectively, were identified with the potential to abrogate mortalin-p53 interaction.	zinc 28639308	29-42	P53	Homo sapiens	178-181
27380217-5	2017	The top two compounds, DTOM (ZINC 28639308) and TTOM (ZINC 38143676) with Glide score of -12.27 and -12.16, respectively, were identified with the potential to abrogate mortalin-p53 interaction.	ttom	48-52	P53	Homo sapiens	178-181
27995947-0	2017	Haematological cancer: TP53 mutations sensitize to decitabine.	Decitabine	51-61	P53	Homo sapiens	23-27
28035403-0	2017	Propofol induces proliferation partially via downregulation of p53 protein and promotes migration via activation of the Nrf2 pathway in human breast cancer cell line MDA-MB-231.	Propofol	0-8	P53	Homo sapiens	63-66
28035403-3	2017	Thus, we aimed to investigate the function of p53 and Nrf2 in the human breast cancer cell line MDA-MB-231 following treatment with propofol.	Propofol	132-140	P53	Homo sapiens	46-49
27888811-3	2017	Overexpression of mutated p53 with reduced or abolished function is often connected to resistance to standard medications, including cisplatin, alkylating agents (temozolomide), anthracyclines, (doxorubicin), antimetabolites (gemcitabine), antiestrogenes (tamoxifen) and EGFR-inhibitors (cetuximab).	gemcitabine	226-237	P53	Homo sapiens	26-29
28129641-4	2017	AML cells with p53 mutations in humans treated with decitabine are killed by differentiation or senescense, but then relapse at a high rate becoming drug resistant.	Decitabine	52-62	P53	Homo sapiens	15-18
28031536-8	2017	Molecular analysis revealed that propranolol treatment of the SK-BR-3 breast cancer line, which showed high sensitivity to beta blockade, led to a reduction in Ki67 protein expression, decreased phosphorylation of the mitogenic signaling regulators p44/42 MAPK, p38 MAPK, JNK, and CREB, increased phosphorylation of the cell survival/apoptosis regulators AKT, p53, and GSK3beta.	Propranolol	33-44	P53	Homo sapiens	360-363
27926517-6	2017	Moreover, cell cycle real-time PCR array and proteome profiler antibody array confirmed that Leptin and SAHA treatment significantly changed the expressions of factors associated with cell cycle regulation and apoptosis including p53 and p21WAF1/CIP1.In DNA-ChIP analysis, we found that acetylation levels binding with p21WAF1/CIP1 promoters are regulated in a manner specific to histone type, lysine residue and selective promoter regions.	Vorinostat	104-108	P53	Homo sapiens	230-233
27766434-0	2017	MG132 plus apoptosis antigen-1 (APO-1) antibody cooperate to restore p53 activity inducing autophagy and p53-dependent apoptosis in HPV16 E6-expressing keratinocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	P53	Homo sapiens	69-72
27766434-0	2017	MG132 plus apoptosis antigen-1 (APO-1) antibody cooperate to restore p53 activity inducing autophagy and p53-dependent apoptosis in HPV16 E6-expressing keratinocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	P53	Homo sapiens	105-108
27766434-3	2017	We investigated whether in HPV16 E6-expressing keratinocytes (KE6 cells), the restoration of p53 levels mediated by MG132 and/or activation of the CD95 pathway through apoptosis antigen-1 (APO-1) antibody are responsible for the induction of apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	P53	Homo sapiens	93-96
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	P53	Homo sapiens	26-29
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	P53	Homo sapiens	92-95
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	P53	Homo sapiens	92-95
27766434-7	2017	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in the elevation of p53 protein levels and its phosphorylation in Ser46 and Ser20; the p53 protein was localized mainly at nucleus after treatment with MG132 or APO-1 plus MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	224-229	P53	Homo sapiens	26-29
28484169-8	2017	In the case of TP53 mutations, prognosis is poor for both hematopoietic stem cell transplantation and AZA treatment, although, patients with TP53 mutations have been shown to respond favorably to decitabine administration for 10 days.	Decitabine	196-206	P53	Homo sapiens	15-19
28484169-8	2017	In the case of TP53 mutations, prognosis is poor for both hematopoietic stem cell transplantation and AZA treatment, although, patients with TP53 mutations have been shown to respond favorably to decitabine administration for 10 days.	Decitabine	196-206	P53	Homo sapiens	141-145
30460048-2	2017	In this study, we explored the cellular and molecular mechanisms induced on exposure to different concentrations of cadmium chloride (CdCl2), on three different human cell lines with wild type p53, viz., A549, HEK293 and HCT116.	Cadmium Chloride	116-132	P53	Homo sapiens	193-196
27693638-0	2016	DNA-PKcs, a novel functional target of acriflavine, mediates acriflavine"s p53-dependent synergistic anti-tumor efficiency with melphalan.	Acriflavine	39-50	P53	Homo sapiens	75-78
27693638-0	2016	DNA-PKcs, a novel functional target of acriflavine, mediates acriflavine"s p53-dependent synergistic anti-tumor efficiency with melphalan.	Acriflavine	61-72	P53	Homo sapiens	75-78
27863490-7	2016	Interestingly, we found that a lower dose of SAHA (1 muM and 2.5 muM) inhibited GSCs via cell cycle arrest and induced premature senescence through p53 up-regulation and p38 activation.	Vorinostat	45-49	P53	Homo sapiens	148-151
27863490-8	2016	CONCLUSION: SAHA induces apoptosis and functions as a potent modulator of senescence via the p38-p53 pathway in GSCs.	Vorinostat	12-16	P53	Homo sapiens	97-100
27904708-6	2016	We found that abnormal expression of CPA4 was positively associated with Ki67 (P=0.002) and reversely correlated with p53 (P=0.035) in GC.	cpa4	37-41	P53	Homo sapiens	118-121
26993060-8	2016	CONCLUSIONS: Obinutuzumab plus idasanutlin enhanced cell death of p53 wild-type tumour cells vs. rituximab plus idasanutlin without affecting obinutuzumab-mediated ADCC or B-cell depletion and showed robust antitumour efficacy in xenograft models, strongly supporting the investigation of this combination in clinical trials.	RG7388	31-42	P53	Homo sapiens	66-69
27644244-8	2016	Furthermore, the p38/mitogen-activated protein kinase (MAPK) inhibitor SB203580 reversed the increase of the expression level of p38, p-cdc2 (Tyr15), cleaved caspase 3, cleaved PARP, p-p53, and p53 and reversed the decrease in cdc25B expression.	SB 203580	71-79	P53	Homo sapiens	185-188
27644244-8	2016	Furthermore, the p38/mitogen-activated protein kinase (MAPK) inhibitor SB203580 reversed the increase of the expression level of p38, p-cdc2 (Tyr15), cleaved caspase 3, cleaved PARP, p-p53, and p53 and reversed the decrease in cdc25B expression.	SB 203580	71-79	P53	Homo sapiens	194-197
27601937-7	2016	Upon re-introduction of wild-type TP53, SAHA-treated ESS-1 cells underwent immediate apoptotic cell death as supported by upregulation of PUMA and caspase-9 as well as by activation of caspases-3 and -7 and PARP-1 cleavage.	Vorinostat	40-44	P53	Homo sapiens	34-38
27601937-11	2016	Using MES-SA cells with RNAi-silenced p53 expression and several p53-deficient tumor cell lines undergoing SAHA-induced autophagy, we could generally validate our finding suggesting an inhibitory role for p53 in the autophagic pathway in response to SAHA treatment.	Vorinostat	107-111	P53	Homo sapiens	65-68
27601937-11	2016	Using MES-SA cells with RNAi-silenced p53 expression and several p53-deficient tumor cell lines undergoing SAHA-induced autophagy, we could generally validate our finding suggesting an inhibitory role for p53 in the autophagic pathway in response to SAHA treatment.	Vorinostat	107-111	P53	Homo sapiens	65-68
27601937-12	2016	CONCLUSIONS: Conclusively, these results could identify cytoplasmic p53 protein as a molecular switch that directly mediates the cytotoxic response of SAHA and thus open new therapeutic avenues.	Vorinostat	151-155	P53	Homo sapiens	68-71
26258493-5	2016	DNA demethylation with 5-aza-2"-deoxycytidine restored GLS2 mRNA and protein content in human GB cell lines with both mutated (T98G) and wild-type (U87MG) p53 and reduced the methylation of CpG1 (promoter region island), and CpG2 (first intron island) in both cell lines.	Decitabine	23-45	P53	Homo sapiens	155-158
27425828-0	2016	Low doses of arsenic, via perturbing p53, promotes tumorigenesis.	Arsenic	13-20	P53	Homo sapiens	37-40
27425828-3	2016	In this study, we demonstrate that low doses of arsenic exposure mitigate or mask p53 function and further perturb intracellular redox state, which triggers persistent endoplasmic reticulum (ER) stress and activates UPR (unfolded protein response), leading to transformation or tumorigenesis.	Arsenic	48-55	P53	Homo sapiens	82-85
27425828-4	2016	Thus, the results suggest that low doses of arsenic exposure, through attenuating p53-regulated tumor suppressive function, change the state of intracellular redox and create a microenvironment for tumorigenesis.	Arsenic	44-51	P53	Homo sapiens	82-85
27302066-8	2016	This study has shown that by direct transcriptional activation of CerS6, p53 can regulate specific ceramide biosynthesis, which contributes to the pro-apoptotic cellular response.	Ceramides	99-107	P53	Homo sapiens	73-76
27461834-0	2016	P53 overexpression and Ki67-index are associated with outcome in ductal pancreatic adenocarcinoma with adjuvant gemcitabine treatment.	gemcitabine	112-123	P53	Homo sapiens	0-3
27461834-6	2016	However, stratified analysis according to treatment arm revealed that the effect of deregulated p53 expression and high Ki67 expression was restricted to the disease free survival of patients treated with adjuvant gemcitabine.	gemcitabine	214-225	P53	Homo sapiens	96-99
26640144-7	2016	Importantly, LBH589 treatment in combination with castration prevents mCRPC development and significantly prolongs survival following castration by enhancing p53 and androgen receptor acetylation and in turn sensitizing castration-resistant mesenchymal-like tumor cells to androgen deprivation therapy.	Panobinostat	13-19	P53	Homo sapiens	158-161
27432897-1	2016	In normal human cells, centrosome loss induced by centrinone-a specific centrosome duplication inhibitor-leads to irreversible, p53-dependent G1 arrest by an unknown mechanism.	centrinone	50-60	P53	Homo sapiens	128-131
27432897-2	2016	A genome-wide CRISPR/Cas9 screen for centrinone resistance identified genes encoding the p53-binding protein 53BP1, the deubiquitinase USP28, and the ubiquitin ligase TRIM37.	centrinone	37-47	P53	Homo sapiens	89-92
27432897-7	2016	Thus, analysis of centrinone resistance identified a 53BP1-USP28 module as critical for communicating mitotic challenges to the p53 circuit and TRIM37 as an enforcer of the singularity of centrosome assembly.	centrinone	18-28	P53	Homo sapiens	128-131
27154500-0	2016	Synthesis of intracellular reduction-sensitive amphiphilic polyethyleneimine and poly(epsilon-caprolactone) graft copolymer for on-demand release of doxorubicin and p53 plasmid DNA.	aziridine	59-76	P53	Homo sapiens	165-168
27174050-5	2016	In the present study, we identified 9 Ru (II)-Arene Schiff-base (RAS) complexes able to induce p53-independent cytotoxicity and discuss structural features that are required for their p53-independent activity.	Radium	65-68	P53	Homo sapiens	95-98
27174050-5	2016	In the present study, we identified 9 Ru (II)-Arene Schiff-base (RAS) complexes able to induce p53-independent cytotoxicity and discuss structural features that are required for their p53-independent activity.	Radium	65-68	P53	Homo sapiens	184-187
27174050-8	2016	This was despite significant differences in their physicochemical properties, suggesting that the iminoquinoline ligand, a common structural feature for all the complexes, is required for the p53-independent activity.	iminoquinoline	98-112	P53	Homo sapiens	192-195
27235710-14	2016	Furthermore, the results of qRT-PCR showed that lupeol pre-treatment significantly (p&lt;0.05) decreased mancozeb-induced expression of DNA damage (p53, MDM2, COX-2, GADD45alpha and p21) and increased expression of DNA repair responsive genes (hOGG1 and XRCC1) in CHLs.	mancozeb	105-113	P53	Homo sapiens	148-151
26987571-6	2016	Moreover, the tumors treated with MG132/m showed higher levels of tumor suppressing proteins, hScrib and p53, as well as apoptotic degree, than tumors treated with free MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	34-39	P53	Homo sapiens	105-108
26876786-3	2016	Further, SAHA and NaB decrease the phosphorylation, protein and mRNA levels of mutant p53 (mtp53) in TNBC cells.	Vorinostat	9-13	P53	Homo sapiens	86-89
26876786-7	2016	The luciferase assay and ChIP analysis reveal that both SAHA and NaB can reduce the binding of transcription factor Yin Yang 1 (YY1) with the -102 to -96 position of human p53 promoter.	Vorinostat	56-60	P53	Homo sapiens	172-175
26876786-9	2016	Further, SAHA and NaB can inhibit the association of HDAC8 and YY1, increase acetylation of residues 170-200 of YY1, then decrease its transcription activities, and finally suppress YY1 induced p53 transcription.	Vorinostat	9-13	P53	Homo sapiens	194-197
26939786-11	2016	Thus, for the first time, these data highlighted the potential use of the diterpene in the sensitization of GBM cells to chemotherapy through a direct re-activation of p53 pathway.	Diterpenes	74-83	P53	Homo sapiens	168-171
26987028-10	2016	The results showed that both GA and cisplatin changed the morphology, inhibited the growth and induced apoptosis in the H446 cells by inducing generation of ROS, disruption of MMP, downregulation of XIAP expression, and upregulation of Bax, Apaf-1, DIABLO and p53 expression.	Gallium	29-31	P53	Homo sapiens	260-263
27044842-3	2016	The MTT cell viability assay showed that treatment with IMP1338 selectively inhibited HCT116, HCT116 p53(-/-), HT29, and A549 cancer cell proliferation compared to that of Beas2B normal epithelial cells.	IMP1338	56-63	P53	Homo sapiens	101-104
27044842-7	2016	In addition, IMP1338 markedly induced the phosphorylation of histone H2AX and Chk1 in both cell lines while the combination of 5-fluorouracil (5-FU) and radiation inhibited the viability of HCT116, HCT116 p53(-/-), and HT29 cells compared to 5-FU or radiation alone.	IMP1338	13-20	P53	Homo sapiens	205-208
26882972-6	2016	Moringin showed to be effective in inducing apoptosis through p53 and Bax activation and Bcl-2 inhibition.	moringin	0-8	P53	Homo sapiens	62-65
26967821-7	2016	This analysis indicates that lenalidomide is active in patients with relapsed/refractory CLL with unfavorable genetic profiles, including TP53 inactivation or unmutated IGHV.	Lenalidomide	29-41	P53	Homo sapiens	138-142
26775629-12	2016	CONCLUSION: IMQ induced ROS production to stimulate ATM/ATR pathways and contributed to p53-dependent apoptosis in a skin basal cell carcinoma cell line BCC/KMC1.	Imiquimod	12-15	P53	Homo sapiens	88-91
26928575-7	2016	Our analysis provides an explanation why cancer cell lines known to have vastly diverse expression levels of Wip1 and PTEN exhibit a broad spectrum of responses to DNA damage: from a fast transition to a high level of p53 killer (a p53 phosphoform which promotes commitment to apoptosis) in cells characterized by high PTEN and low Wip1 levels to long-lasting p53 level oscillations in cells having PTEN promoter methylated (as in, e.g., MCF-7 cell line).	phosphoform	236-247	P53	Homo sapiens	218-221
26928575-7	2016	Our analysis provides an explanation why cancer cell lines known to have vastly diverse expression levels of Wip1 and PTEN exhibit a broad spectrum of responses to DNA damage: from a fast transition to a high level of p53 killer (a p53 phosphoform which promotes commitment to apoptosis) in cells characterized by high PTEN and low Wip1 levels to long-lasting p53 level oscillations in cells having PTEN promoter methylated (as in, e.g., MCF-7 cell line).	phosphoform	236-247	P53	Homo sapiens	232-235
26928575-7	2016	Our analysis provides an explanation why cancer cell lines known to have vastly diverse expression levels of Wip1 and PTEN exhibit a broad spectrum of responses to DNA damage: from a fast transition to a high level of p53 killer (a p53 phosphoform which promotes commitment to apoptosis) in cells characterized by high PTEN and low Wip1 levels to long-lasting p53 level oscillations in cells having PTEN promoter methylated (as in, e.g., MCF-7 cell line).	phosphoform	236-247	P53	Homo sapiens	232-235
26772154-0	2016	LincRNAs and base modifications of p53 induced by arsenic methylation in workers.	Arsenic	50-57	P53	Homo sapiens	35-38
26772154-1	2016	Arsenic (As) metabolites could induce methylation changes of DNA and base modifications of p53, which play role in the toxicity of As.	Arsenic	0-7	P53	Homo sapiens	91-94
26772154-1	2016	Arsenic (As) metabolites could induce methylation changes of DNA and base modifications of p53, which play role in the toxicity of As.	Arsenic	9-11	P53	Homo sapiens	91-94
26772154-1	2016	Arsenic (As) metabolites could induce methylation changes of DNA and base modifications of p53, which play role in the toxicity of As.	Arsenic	131-133	P53	Homo sapiens	91-94
26772154-11	2016	These findings suggest potentially widespread roles of p53 and relative RNAs in arsenic workers, which may be caused by As metabolism.	Arsenic	80-87	P53	Homo sapiens	55-58
27013776-7	2016	Furthermore, supplementation of 5-methyltetrahydrofolate to the dihydrofolate reductase knockdown cells could weaken the inhibitory effect of dihydrofolate reductase knockdown on cell proliferation, simultaneously, inducing the expression of p53 and p21(waf/cip1) falling back moderately.	5-methyltetrahydrofolate	32-56	P53	Homo sapiens	242-245
26953705-5	2016	A slight increase in promoter methylation of p53 in cord blood lymphocytes which correlated with arsenic accumulation in nails was observed in these exposed newborns.	Arsenic	97-104	P53	Homo sapiens	45-48
16651407-9	2006	In addition, p53 induced VDR target genes in a vitamin D3-dependent manner.	Cholecalciferol	47-57	P53	Homo sapiens	13-16
26756315-7	2016	On the other hand, mutant p53 RPMI7951 cell death occurred by PBD-GA-mediated mitochondria- and caspase-dependent pathways via lysosomal membrane permeabilization (LMP), but not through p53 signaling.	Gallium	66-68	P53	Homo sapiens	26-29
26756315-7	2016	On the other hand, mutant p53 RPMI7951 cell death occurred by PBD-GA-mediated mitochondria- and caspase-dependent pathways via lysosomal membrane permeabilization (LMP), but not through p53 signaling.	Gallium	66-68	P53	Homo sapiens	186-189
26771712-1	2016	We found that inhibitors of mitochondrial respiratory chain complexes III (myxothiazol) and I (piericidin A) in some epithelial carcinoma cell lines induce transcription of the p53-responsive SESN2 gene that plays an important role in stress response and homeostatic regulation.	myxothiazol	75-86	P53	Homo sapiens	177-180
26464433-8	2016	Analysis of DTIE in the tumor suppressor p53 confirmed a similar function.	Dacarbazine	12-16	P53	Homo sapiens	41-44
26866273-10	2016	In LP MSCs treated with t-BHQ for ~7 days, the phosphorylation and nuclear localization of NRF2 improved and SIRT1 protein level increased, whereas p53 protein levels decreased.	2-tert-butylhydroquinone	24-29	P53	Homo sapiens	148-151
26712469-4	2016	Combination of nicotinamide (sirtuin inhibitor) with berberine potentiated sirtuins inhibition and increased the expression of FoxO1/3a and phosphorylation of p53 tumor suppressor protein.	Niacinamide	15-27	P53	Homo sapiens	159-162
26771712-1	2016	We found that inhibitors of mitochondrial respiratory chain complexes III (myxothiazol) and I (piericidin A) in some epithelial carcinoma cell lines induce transcription of the p53-responsive SESN2 gene that plays an important role in stress response and homeostatic regulation.	piericidin A	95-107	P53	Homo sapiens	177-180
16580498-0	2006	Enhanced radiosensitization of p53 mutant cells by oleamide.	oleylamide	51-59	P53	Homo sapiens	31-34
26517689-1	2016	This study identifies BNIP3L as the key regulator of p53-dependent cell death mechanism in colon cancer cells targeted by the novel gallium based anticancer drug, KP46.	Gallium	132-139	P53	Homo sapiens	53-56
16580498-9	2006	In p53 wild-type cells, both oleamide and radiation induced Bax translocation to mitochondria.	oleylamide	29-37	P53	Homo sapiens	3-6
26586723-10	2016	DPBQ activates p53 and triggers apoptosis in a polyploid-specific manner, but does not inhibit topoisomerase or bind DNA.	DPBQ	0-4	P53	Homo sapiens	15-18
26497683-1	2015	We previously described diaryl trifluorothiazoline compound 1a (hereafter referred to as fluorizoline) as a first-in-class small molecule that induces p53-independent apoptosis in a wide range of tumor cell lines.	diaryl trifluorothiazoline	24-50	P53	Homo sapiens	151-154
26497683-1	2015	We previously described diaryl trifluorothiazoline compound 1a (hereafter referred to as fluorizoline) as a first-in-class small molecule that induces p53-independent apoptosis in a wide range of tumor cell lines.	Fluorizoline	89-101	P53	Homo sapiens	151-154
16580498-10	2006	On the other hand, in p53 mutant cells, radiation alone slightly induced Bax translocation to mitochondria, whereas oleamide induced a larger translocation.	oleylamide	116-124	P53	Homo sapiens	22-25
16580498-11	2006	CONCLUSIONS: Oleamide may exhibit synergistic radiosensitization in p53 mutant cells through p53-independent Bax translocation to mitochondria.	oleylamide	13-21	P53	Homo sapiens	68-71
16580498-11	2006	CONCLUSIONS: Oleamide may exhibit synergistic radiosensitization in p53 mutant cells through p53-independent Bax translocation to mitochondria.	oleylamide	13-21	P53	Homo sapiens	93-96
26404525-6	2015	Interestingly, inhibition of p53 or knockdown of p21, abolished LMP-induced caspase-3 activity and cell death.	(2~{s},3~{r},4~{s})-2-[(2~{s},3~{r})-1,3-Bis(Oxidanyl)-1-Oxidanylidene-Butan-2-Yl]-4-[(3~{s},5~{s})-5-(Dimethylcarbamoyl)pyrrolidin-3-Yl]sulfanyl-3-Methyl-3,4-Dihydro-2~{h}-Pyrrole-5-Carboxylic Acid	64-67	P53	Homo sapiens	29-32
26545632-6	2016	Inactivation of mitogen-activated protein kinase cascades, reduced p53 phosphorylation, and down-regulation of p53-upregulated modulator of apoptosis on K560 treatment were also observed.	PHTHALIDE	153-157	P53	Homo sapiens	111-114
16180010-0	2006	Involvement of the extracellular signal-regulated protein kinase pathway in phosphorylation of p53 protein and exerting cytotoxicity in human neuroblastoma cells (SH-SY5Y) exposed to acrylamide.	Acrylamide	183-193	P53	Homo sapiens	95-98
25975351-5	2015	Our data show that BI 2536 and GSK461364 increased the population of cells in the G2/M phase compared with controls, while treatment with poloxin and thymoquinone increased cell population in the S phase as well as in G2/M, in a p53-independent manner.	Bismuth	19-21	P53	Homo sapiens	229-232
26717387-8	2015	Cooccurrence of TP53 and BCL2 aberrations ameliorated the poor prognostic impact of single TP53+ or BCL2+ in MYC positive patients.This pilot study generates evidence for the complex interplay between the alterations of genetic pathways in DLBCL, which goes beyond the concept of DHL.	Cysteamine	280-283	P53	Homo sapiens	16-20
26717387-8	2015	Cooccurrence of TP53 and BCL2 aberrations ameliorated the poor prognostic impact of single TP53+ or BCL2+ in MYC positive patients.This pilot study generates evidence for the complex interplay between the alterations of genetic pathways in DLBCL, which goes beyond the concept of DHL.	Cysteamine	280-283	P53	Homo sapiens	91-95
16180010-1	2006	Using human neuroblastoma SH-SY5Y cells, effects of acrylamide on p53 protein and intracellular signal transducting pathways were examined.	Acrylamide	52-62	P53	Homo sapiens	66-69
26488797-5	2015	p53 signaling was identified as an important pathway modulated by both arene ruthenium compounds.	Ruthenium Compounds	77-96	P53	Homo sapiens	0-3
26463240-10	2015	Our data bring new insight to consider the betanin/isobetanin mix as therapeutic anticancer compound, alone or in combination with classical chemotherapeutic drugs, especially in functional p53 tumors.	betanin	43-50	P53	Homo sapiens	190-193
16180010-2	2006	Acrylamide increased p53, phosphorylated p53, and p53-associated protein murine double minute 2 (MDM2).	Acrylamide	0-10	P53	Homo sapiens	41-44
26463240-10	2015	Our data bring new insight to consider the betanin/isobetanin mix as therapeutic anticancer compound, alone or in combination with classical chemotherapeutic drugs, especially in functional p53 tumors.	betanin	51-61	P53	Homo sapiens	190-193
16180010-6	2006	In contrast, a specific inhibitor of ERK kinase (U0126 or PD98059) could abolish the accumulation as well as the phosphorylation of p53 at Ser15.	U 0126	49-54	P53	Homo sapiens	132-135
25199682-9	2015	A tumor protein p53 (TP53) subnetwork was identified, showing the interactions of TP53 with other genes affected by arsenic.	Arsenic	116-123	P53	Homo sapiens	16-19
16180010-9	2006	Hence, acrylamide increases p53 protein and its phosphorylation at Ser15 through ERK and/or PIKK pathways.	Acrylamide	7-17	P53	Homo sapiens	28-31
25199682-9	2015	A tumor protein p53 (TP53) subnetwork was identified, showing the interactions of TP53 with other genes affected by arsenic.	Arsenic	116-123	P53	Homo sapiens	21-25
26553132-5	2015	It promoted the association of p53 to the promoter region of miR-128, and enhanced the transcriptional activation of p53 on miR-128 expression.	mir-128	61-68	P53	Homo sapiens	31-34
16138109-3	2006	Further investigations revealed that vanadate suppressed upstream of apoptotic events, such as the loss of mitochondrial membrane potential, the conformational change of Bax, and p53 transactivation, although the accumulation, total phosphorylation, and phosphorylation of six individual sites of p53 were not affected.	Vanadates	37-45	P53	Homo sapiens	179-182
26384351-2	2015	Cytotoxic effect was increased by decitabine through activation of p53 and inhibition of c-Myc, Survivin and Bcl-2.	Decitabine	34-44	P53	Homo sapiens	67-70
25199682-9	2015	A tumor protein p53 (TP53) subnetwork was identified, showing the interactions of TP53 with other genes affected by arsenic.	Arsenic	116-123	P53	Homo sapiens	82-86
26377961-0	2015	Erratum to: The collective nuclear migration of p53 and phosphorylated S473 of Akt during ellipticine-mediated apoptosis in human lung epithelial cancer cells.	ellipticine	90-101	P53	Homo sapiens	48-51
16138109-3	2006	Further investigations revealed that vanadate suppressed upstream of apoptotic events, such as the loss of mitochondrial membrane potential, the conformational change of Bax, and p53 transactivation, although the accumulation, total phosphorylation, and phosphorylation of six individual sites of p53 were not affected.	Vanadates	37-45	P53	Homo sapiens	297-300
16138109-4	2006	Importantly, vanadate suppressed p53-dependent apoptosis, but not p53-independent apoptosis.	Vanadates	13-21	P53	Homo sapiens	33-36
16138109-5	2006	Finally, gel-shift and chromatin immunoprecipitation assays conclusively demonstrated that vanadate inhibits the DNA-binding activity of p53.	Vanadates	91-99	P53	Homo sapiens	137-140
26163092-12	2015	A larger population of senescence-activated beta-galactosidase-positive cells was seen in the trametinib pretreated group, and this correlated with activation of two of the major mediators of induced senescence, p53 and pRb.	trametinib	94-104	P53	Homo sapiens	212-215
26427042-5	2015	Gemcitabine was found to be a lytic inducer via activation of the ataxia telangiectasia-mutated (ATM)/p53 genotoxic stress pathway in EBVaGC.	gemcitabine	0-11	P53	Homo sapiens	102-105
16138109-6	2006	Vanadate is conventionally used as an inhibitor of protein tyrosine phosphatases (PTPs); however, we recommend that the influence of vanadate not only on PTPs but also on p53 be considered before using it.	Vanadates	0-8	P53	Homo sapiens	171-174
16138109-6	2006	Vanadate is conventionally used as an inhibitor of protein tyrosine phosphatases (PTPs); however, we recommend that the influence of vanadate not only on PTPs but also on p53 be considered before using it.	Vanadates	133-141	P53	Homo sapiens	171-174
16152620-3	2006	This report shows that U0126 inhibits early response (ERK) kinase activation and cyclin A expression in wt p53 C8161 melanoma exposed to either UV radiation or betulinic acid.	U 0126	23-28	P53	Homo sapiens	107-110
26100227-10	2015	The transcription factors TP53, MYC, NFkappaB and NUPR1 were predicted to be activated upon PA treatment.	Pyrrolizidine Alkaloids	92-94	P53	Homo sapiens	26-30
26363315-4	2015	CPZ effectively inhibited tumor growth and induced apoptosis in CRC cells in a p53-dependent manner.	Chlorpromazine	0-3	P53	Homo sapiens	79-82
26363315-5	2015	Activation of c-jun N-terminal kinase (JNK) was crucial for CPZ-induced p53 expression and the subsequent induction of tumor apoptosis.	Chlorpromazine	60-63	P53	Homo sapiens	72-75
26363315-6	2015	Induction of p53 acetylation at lysine382 was involved in CPZ-mediated tumor apoptosis, and this induction was attenuated by sirtuin 1 (SIRT1), a class III histone deacetylase.	Chlorpromazine	58-61	P53	Homo sapiens	13-16
26881646-5	2015	Deletion of the TP53 gene may be a major contributing factor in the development of resistance to imatinib and blast crisis.	Imatinib Mesylate	97-105	P53	Homo sapiens	16-20
16152620-5	2006	Protection from the latter drug by joint treatment with U0126 was also evident in wt p53 MelJuso melanoma and mutant p53 WM164 melanoma.	U 0126	56-61	P53	Homo sapiens	85-88
16152620-5	2006	Protection from the latter drug by joint treatment with U0126 was also evident in wt p53 MelJuso melanoma and mutant p53 WM164 melanoma.	U 0126	56-61	P53	Homo sapiens	117-120
26410576-6	2015	Furthermore, vorinostat-NPs have similar effectiveness in the suppression or expression of histone deacetylase, mutant type p53, p21, and PARP/cleaved caspase-3.	Vorinostat	13-23	P53	Homo sapiens	124-127
27005182-0	2015	A polyethylenimine derivative-based nanocarrier for the highly efficient delivery of p53 gene to inhibit the proliferation of cancer cells.	Polyethyleneimine	2-18	P53	Homo sapiens	85-88
25605253-2	2015	Interestingly, suberoylanilide hydroxamic acid (SAHA) or knockdown of HDAC2 induced downregulation of Mdm2, a negative regulator of p53, at the protein level.	Vorinostat	15-46	P53	Homo sapiens	132-135
26116623-0	2015	C6 ceramide dramatically increases vincristine sensitivity both in vivo and in vitro, involving AMP-activated protein kinase-p53 signaling.	Ceramides	3-11	P53	Homo sapiens	125-128
16531837-2	2006	In vitro experiments show Cr (VI) induces cell death by apoptosis by activating p53 protein.	chromium hexavalent ion	26-33	P53	Homo sapiens	80-83
26244686-4	2015	Sesamin potently inhibited cyclin D1 and CDK4 expression, pRb phosphorylation, and expression of the proliferating cell nuclear antigen (PCNA); and upregulated p27(KIP1), p21(CIP1), and p53.	sesamin	0-7	P53	Homo sapiens	186-189
26244686-5	2015	The results thus indicate that the antiproliferative effect of sesamin on PDGF-stimulated VSMCs is attributable to arrest of the cell cycle in G0/G1 caused, in turn, by upregulation of p27(KIP1), p21(CIP1), and p53, and inhibition of cyclin E-CDK2 and cyclin D1-CDK4 expression.	sesamin	63-70	P53	Homo sapiens	211-214
26119034-6	2015	Drp1-associated genes, such as Bcl-2-associated X protein, cytochrome c, tumour suppressor gene p53 and p53-up-regulated modulator of apoptosis, were highly up-regulated in the astaxanthin group compared with those in the sham group.	astaxanthine	177-188	P53	Homo sapiens	96-99
26119034-6	2015	Drp1-associated genes, such as Bcl-2-associated X protein, cytochrome c, tumour suppressor gene p53 and p53-up-regulated modulator of apoptosis, were highly up-regulated in the astaxanthin group compared with those in the sham group.	astaxanthine	177-188	P53	Homo sapiens	104-107
16489026-7	2006	Moreover, p53 was still stabilized in ataxia telangiectasia cells or in cells treated with caffeine, suggesting that ATM was not a critical determinant.	Caffeine	91-99	P53	Homo sapiens	10-13
25944617-0	2015	The predictive value of ERCC1 and p53 for the effect of panobinostat and cisplatin combination treatment in NSCLC.	Panobinostat	56-68	P53	Homo sapiens	34-37
26309132-0	2015	Phytometabolite Dehydroleucodine Induces Cell Cycle Arrest, Apoptosis, and DNA Damage in Human Astrocytoma Cells through p73/p53 Regulation.	dehydroleucodine	16-32	P53	Homo sapiens	125-128
16461916-6	2006	We mutated one such buried pair, Tyr-236 and Thr-253 to Phe-236 and Ile-253 (as found in the paralogs p63 and p73), and stabilized p53 by 1.6 kcal/mol.	Isoleucine	68-71	P53	Homo sapiens	131-134
26309132-6	2015	A marked induction of the levels of total TP73 and phosphorylated TP53, TP73, and gamma-H2AX proteins was observed in D384 cells exposed to DhL, but no increase in total TP53 levels was detected.	dehydroleucodine	140-143	P53	Homo sapiens	66-70
26309132-7	2015	Overall these studies demonstrated the marked effect of DhL on the diminished survival of human astrocytoma cells through the induced expression of TP73 and phosphorylation of TP73 and TP53, suggesting their key roles in the tumor cell response to DhL treatment.	dehydroleucodine	56-59	P53	Homo sapiens	185-189
26426889-0	2015	Synthesis of androstanopyridine and pyrimidine compounds as novel activators of the tumor suppressor protein p53.	androstanopyridine	13-31	P53	Homo sapiens	109-112
16465307-7	2006	In addition to transition-type mutations at dipyrimidine sites, mutations which may be induced by the presence of oxidative DNA damage, are frequently observed in the ras oncogene and p53 tumor suppressor gene in human skin cancers of sun-exposed area and in UV-induced mouse skin cancers.	dipyrimidine	44-56	P53	Homo sapiens	184-187
25797839-3	2015	The aim of this study is to monitor the effects of NO donor PAPANONOate on ceramide trafficking in human glioma cell lines, CCF-STTG1 (PTEN-mutated, p53-wt) and T98G (PTEN-harboring, p53-mutated), together with the assessment of their differential molecular signature by 2D-DIGE and MALDI mass spectrometry.	Ceramides	75-83	P53	Homo sapiens	183-186
25994202-4	2015	RESULTS: TH-302 cytotoxicity is greatly enhanced by Chk1 inhibition in p53-deficient but not in p53-proficient human cancer cell lines.	Thorium	9-11	P53	Homo sapiens	71-74
26112218-6	2015	Knocking-down of PKM2 significantly enhanced gemcitabine-induced cell apoptosis through the activation of caspase 3/7 and PARP cleavage, and this inhibitory activity was associated with p38-mediated activation of p53 phosphorylation at serine 46.	gemcitabine	45-56	P53	Homo sapiens	213-216
26178881-7	2015	RESULTS: Here, we show that the combination of HIT and SAHA induced a significant delay of tumor growth through increased rate of apoptosis, increased expression of p53 and p21(Waf1/Cip1), inhibition of proliferation and angiogenesis compared to tumors treated with HIT only.	Vorinostat	55-59	P53	Homo sapiens	165-168
16397265-3	2006	Based on clonogenic survival, the three single agents (IR, IUdR, and caffeine) as well as IUdR or caffeine combined with IR are less or equally effective in p53-deficient human tumor cells compared with p53-proficient tumor cells.	Caffeine	69-77	P53	Homo sapiens	157-160
26029997-5	2015	Here we describe effects of the small molecule MJ25 (2-{[2-(1,3-benzothiazol-2-ylsulfonyl)ethyl]thio}-1,3-benzoxazole), which increased the level of p53-dependent transactivation both as a single agent and in combination with nutlin-3.	MJ25 compound	53-117	P53	Homo sapiens	149-152
26075044-9	2015	Recurrent TP53 mutations have been associated with an increased risk of disease evolution and with decreased response to the drug lenalidomide in del(5q) MDS patients.	Lenalidomide	130-142	P53	Homo sapiens	10-14
16397265-3	2006	Based on clonogenic survival, the three single agents (IR, IUdR, and caffeine) as well as IUdR or caffeine combined with IR are less or equally effective in p53-deficient human tumor cells compared with p53-proficient tumor cells.	Caffeine	98-106	P53	Homo sapiens	157-160
16397265-9	2006	Cell cycle analyses also showed a greater abrogation of IR-induced S- and G2-phase arrests by caffeine in p53-deficient cells, particularly when combined with IUdR.	Caffeine	94-102	P53	Homo sapiens	106-109
25430047-1	2015	This study aimed to clarify the association between the TP53 rs1625895 polymorphism and the efficiency of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) therapy in 106 patients with diffuse large B cell lymphoma (DLBCL).	Cyclophosphamide	125-141	P53	Homo sapiens	56-60
25430047-1	2015	This study aimed to clarify the association between the TP53 rs1625895 polymorphism and the efficiency of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) therapy in 106 patients with diffuse large B cell lymphoma (DLBCL).	Prednisolone	169-181	P53	Homo sapiens	56-60
25283841-2	2015	Here, we report that AZD1775 interacted synergistically with histone deacetylase inhibitors (HDACIs, for example, Vorinostat), which interrupt the DNA damage response, to kill p53-wild type (wt) or -deficient as well as FLT3-ITD leukemia cells in association with pronounced Wee1 inhibition and diminished cdc2/Cdk1 Y15 phosphorylation.	Vorinostat	114-124	P53	Homo sapiens	176-179
25996383-8	2015	FALHE administration induced apoptosis in breast tumor cells, and this was confirmed by high expression levels of Bax, p53 and caspase 3.	falhe	0-5	P53	Homo sapiens	119-122
25795251-6	2015	Both NBDHEX and MC3181 induced marked antiproliferative and apoptotic effects in A375-VR8 cells and, at equitoxic concentrations, caused a strong phosphorylation of JNK, p38, and of the downstream mediators of apoptosis ATF2 and p53.	MC3181	16-22	P53	Homo sapiens	229-232
16397265-11	2006	This differential dual mode of radiosensitization by combining IUdR and caffeine-like drugs (e.g., UCN-01) in p53-deficient human tumors may lead to a greater therapeutic gain.	Caffeine	72-80	P53	Homo sapiens	110-113
25621498-4	2015	Preclinical studies suggest that noncytotoxic concentrations of the DNA methyltransferase 1 (DNMT1) inhibitor decitabine produce p53-independent cell-cycle exits by reversing aberrant epigenetic repression of proliferation-terminating (MYC-antagonizing) differentiation genes in cancer cells.	Decitabine	110-120	P53	Homo sapiens	129-132
16166740-7	2005	In these cells, Cr(VI)-induced apoptosis is mediated by p53 upregulation of p53-upregulated modulator of apoptosis (PUMA), BAX translocation to mitochondria, cytochrome c release, and caspase-3 activation.	chromium hexavalent ion	16-22	P53	Homo sapiens	56-59
25611347-5	2015	These quinofuracins induced p53-dependent growth suppression in human glioblastoma LNZTA3 cells.	quinofuracins	6-19	P53	Homo sapiens	28-31
25674170-2	2015	Immunohistochemical analysis of p53 and Ki67 proteins is a simple and inexpensive method widely used in non-dysplastic OLs to reveal lesions predicted to develop oral cancer.	N-biotin-C-Co4(mu3-O)4(Py)4(H2O)4-beta-alanine	119-122	P53	Homo sapiens	32-35
25674170-5	2015	OLs were considered at high risk in the presence of either high p53 expression (&gt;20%), or low/normal p53 expression associated with high Ki67 expression (Ki67/p53 ratio &gt;3).	N-biotin-C-Co4(mu3-O)4(Py)4(H2O)4-beta-alanine	0-3	P53	Homo sapiens	64-67
25652455-4	2015	RESULTS: TP53 and RUNX1 mutations are strongly associated with the presence of SNP-A-based aCNA/cnLOH, while FLT3 and NPM1 mutations are strongly associated with the absence of aCNA/cnLOH.	snp-a	79-84	P53	Homo sapiens	9-13
25812484-5	2015	Furthermore, ATM/ATR inhibitor caffeine, p53- or ATM/ATR-specific siRNA significantly attenuated 8-ADEQ-induced G2/M arrest.	(E)-8-acetoxy-2-(2-(3,4-diacetoxyphenyl)ethenyl)quinazoline	97-103	P53	Homo sapiens	41-44
25812484-7	2015	8-ADEQ-induced G2/M arrest is mediated by the activation of both Chk1/2-Cdc25 and p53-p21CIP1/WAF1 via ATM/ATR pathway, and indicates that 8-ADEQ appears to have potential in the treatment of cervical cancer.	(E)-8-acetoxy-2-(2-(3,4-diacetoxyphenyl)ethenyl)quinazoline	0-6	P53	Homo sapiens	82-85
25674170-5	2015	OLs were considered at high risk in the presence of either high p53 expression (&gt;20%), or low/normal p53 expression associated with high Ki67 expression (Ki67/p53 ratio &gt;3).	N-biotin-C-Co4(mu3-O)4(Py)4(H2O)4-beta-alanine	0-3	P53	Homo sapiens	104-107
16166740-7	2005	In these cells, Cr(VI)-induced apoptosis is mediated by p53 upregulation of p53-upregulated modulator of apoptosis (PUMA), BAX translocation to mitochondria, cytochrome c release, and caspase-3 activation.	chromium hexavalent ion	16-22	P53	Homo sapiens	76-79
25674170-5	2015	OLs were considered at high risk in the presence of either high p53 expression (&gt;20%), or low/normal p53 expression associated with high Ki67 expression (Ki67/p53 ratio &gt;3).	N-biotin-C-Co4(mu3-O)4(Py)4(H2O)4-beta-alanine	0-3	P53	Homo sapiens	104-107
16166740-9	2005	This result establishes p53 as the "necessary" player in Cr(VI)-induced apoptosis.	chromium hexavalent ion	57-63	P53	Homo sapiens	24-27
16225614-5	2005	RESULTS: We found that p53 activation was induced selectively by PUVA treatment, while 8-oxo-7,8-dihydroguanine DNA damage was induced selectively by 5-aminolaevulinic acid (ALA)-PDT treatment.	puva	65-69	P53	Homo sapiens	23-26
25744307-9	2015	We show that 10(-8)M levels of CdCl2 activate ERK1/2 (Tyr 204) and the p53 specific ubiquitin ligase Mdm2 (Ser 166) via Raf and MEK by acting through the epidermal growth factor receptor (EGFR).	Cadmium Chloride	31-36	P53	Homo sapiens	71-74
16204068-2	2005	We found that 5-fluorouracil (5-FU) and oxaliplatin only sensitized p53 wild-type (WT) colorectal cancer cell lines to Fas-mediated apoptosis.	Oxaliplatin	40-51	P53	Homo sapiens	68-71
25408290-3	2015	In this paper we describe preliminary studies on the use of a multivalent N-alkylated aromatic oligoamide helix mimetic for inhibition of p53/hDM2 and establish that protein dimerisation is promoted, rather than enhanced binding resulting from a higher effective concentration of the ligand.	n-alkylated aromatic oligoamide	74-105	P53	Homo sapiens	138-141
16204068-3	2005	In contrast, irinotecan (CPT-11) and tomudex sensitized p53 WT, mutant, and null cells to Fas-mediated cell death.	raltitrexed	37-44	P53	Homo sapiens	56-59
25987034-11	2015	In the study, we report Cis-imidazoline derivative compound; Pubcid: 68870345 to have highest inhibitory potential in blocking MDM2-p53 interactions hitherto discovered.	pubcid	61-67	P53	Homo sapiens	132-135
25987037-6	2015	Furthermore, sesamin increased the expression of apoptotic markers of Bax, caspase-3, and cell cycle control proteins, p53 and checkpoint kinase 2.	sesamin	13-20	P53	Homo sapiens	119-122
26131172-10	2015	Interestingly, in the subgroup analysis regarding P53 codon 72 polymorphism, increased HCC risk could be observed in the Pro/Pro+Pro/Arg subgroup under a recessive model (OR=1.78; 95% CI=1.29-2.44).	pro/pro+pro	121-132	P53	Homo sapiens	50-53
16204068-4	2005	Furthermore, CPT-11 and tomudex, but not 5-FU or oxaliplatin, up-regulated Fas cell surface expression in a p53-independent manner.	raltitrexed	24-31	P53	Homo sapiens	108-111
16204068-5	2005	In addition, increased Fas cell surface expression in p53 mutant and null cell lines in response to CPT-11 and tomudex was accompanied by only a slight increase in total Fas mRNA and protein expression, suggesting that these agents trigger p53-independent trafficking of Fas to the plasma membrane.	raltitrexed	111-118	P53	Homo sapiens	54-57
16204068-5	2005	In addition, increased Fas cell surface expression in p53 mutant and null cell lines in response to CPT-11 and tomudex was accompanied by only a slight increase in total Fas mRNA and protein expression, suggesting that these agents trigger p53-independent trafficking of Fas to the plasma membrane.	raltitrexed	111-118	P53	Homo sapiens	240-243
25751281-5	2015	In temozolomide-resistant GBM cells, decitabine can potentiate the cytotoxic DNA alkylation by counteracting cytosine methylation and reactivating tumor suppressor genes, such as p53 and p21.	Decitabine	37-47	P53	Homo sapiens	179-182
25311384-6	2015	Despite the adverse activation of mutant p53 by gemcitabine, simultaneous treatment of PDAC cells with gemcitabine and p53-reactivating molecules (CP-31398 and RITA) reduced growth rate and induced apoptosis.	gemcitabine	103-114	P53	Homo sapiens	41-44
16204068-6	2005	Treatment with CPT-11 or tomudex induced STAT1 phosphorylation (Ser727) in the p53-null HCT116 cell line but not the p53 WT cell line.	raltitrexed	25-32	P53	Homo sapiens	79-82
25311384-10	2015	Together, our results show that gemcitabine aberrantly stimulates mutant p53 activity in PDAC cells identifying key processes with potential for therapeutic targeting.	gemcitabine	32-43	P53	Homo sapiens	73-76
16204068-10	2005	We conclude that CPT-11 and tomudex may be more effective than 5-FU and oxaliplatin in the treatment of p53 mutant colorectal cancer tumors by sensitizing them to Fas-mediated apoptosis in a STAT1-dependent manner.	raltitrexed	28-35	P53	Homo sapiens	104-107
16181779-6	2005	Although variolins induced an increase in the levels of p53 with an increase in p21, their cytotoxicities did not appear to be dependent on p53 status as their potency was comparable in cells with wild-type p53, or in sub-lines with inactivated p53.	variolins	9-18	P53	Homo sapiens	56-59
25482928-7	2015	We found that cotreatment with cucurbitacin-I significantly increased Bcl(-)2/Bcl(-)xL family member antagonist ABT-737-induced cell death regardless of EGFR/PTEN/p53 status of malignant human glioma cell lines.	cucurbitacin I	31-45	P53	Homo sapiens	163-166
26642705-10	2015	Treatment with AdCMVE2F-1 plus gemcitabine enhanced endogenous p53 expression in LoVo cells, which contain wild-type p53; however, the finding that the synergistic effect can also be observed in mutant p53-expressing SW620 and DLD-1 cells suggests that wild-type p53 function may not be necessary for the therapeutic effects of this drug combination.	gemcitabine	31-42	P53	Homo sapiens	63-66
26642705-10	2015	Treatment with AdCMVE2F-1 plus gemcitabine enhanced endogenous p53 expression in LoVo cells, which contain wild-type p53; however, the finding that the synergistic effect can also be observed in mutant p53-expressing SW620 and DLD-1 cells suggests that wild-type p53 function may not be necessary for the therapeutic effects of this drug combination.	gemcitabine	31-42	P53	Homo sapiens	117-120
26642705-10	2015	Treatment with AdCMVE2F-1 plus gemcitabine enhanced endogenous p53 expression in LoVo cells, which contain wild-type p53; however, the finding that the synergistic effect can also be observed in mutant p53-expressing SW620 and DLD-1 cells suggests that wild-type p53 function may not be necessary for the therapeutic effects of this drug combination.	gemcitabine	31-42	P53	Homo sapiens	117-120
26642705-10	2015	Treatment with AdCMVE2F-1 plus gemcitabine enhanced endogenous p53 expression in LoVo cells, which contain wild-type p53; however, the finding that the synergistic effect can also be observed in mutant p53-expressing SW620 and DLD-1 cells suggests that wild-type p53 function may not be necessary for the therapeutic effects of this drug combination.	gemcitabine	31-42	P53	Homo sapiens	117-120
24898668-3	2015	Here we analyzed the activity and mechanism of a p53 reactivator, ellipticine, in a cellular model of cutaneous T-cell lymphoma (CTCL), a disease that is progressive, chemoresistant and refractory to treatment.	ellipticine	66-77	P53	Homo sapiens	49-52
24898668-5	2015	Ellipticine caused apoptosis in MyLa2000 and SeAx and restored the transcriptional activity of (G245S)p53 in SeAx.	ellipticine	0-11	P53	Homo sapiens	102-105
25775024-6	2015	It has displayed increased binding affinity and a longer dissociation time when compared to rituximab resulting in improved complement dependent cellular cytotoxicity (CDCC); a mechanism with the potential to overcome apoptosis-resistance in TP53 disruption.	cdcc	168-172	P53	Homo sapiens	242-246
16181779-13	2005	In conclusion, these variolins are a new class of CDK inhibitors that activate apoptosis in a p53-independent fashion and thus they may be effective against tumours with p53 mutations or deletions.	variolins	21-30	P53	Homo sapiens	94-97
16181779-13	2005	In conclusion, these variolins are a new class of CDK inhibitors that activate apoptosis in a p53-independent fashion and thus they may be effective against tumours with p53 mutations or deletions.	variolins	21-30	P53	Homo sapiens	170-173
16039116-5	2005	Combined with previously reported lower nitrite levels with 1,25(OH)(2)D(3), this increased p53 expression may favor DNA repair over apoptosis.	Nitrites	40-47	P53	Homo sapiens	92-95
25658463-9	2015	Treatment of wild-type TP53 neuroblastoma cell lines with both GSK2830371 and either doxorubicin or carboplatin resulted in enhanced cell death, mediated through caspase 3/7 induction, as compared to either agent alone.	Carboplatin	100-111	P53	Homo sapiens	23-27
25242579-8	2015	Deguelin induced differentiation of OCI-AML3 cells at a nontoxic concentration which was associated with a decrease in expression of activated caspase-8, p53, p21, and the 30-kD form of CCAAT/enhancer binding protein alpha (C/EBPalpha), whereas no effects were found in OCIM2 cells expressing NPM-wt.	deguelin	0-8	P53	Homo sapiens	154-157
26089937-9	2015	Our findings demonstrated the beneficial effects of RT saponins in enhancing neuroprotective effects by deducing iNOS activity, normalizing SOD level, and inhibiting p-p38 and p53 expression, hence offering significant therapeutic implications for SAH.	Saponins	55-63	P53	Homo sapiens	176-179
25821312-7	2015	Bleomycin A5 could significantly increase the expression of p53, with concentration dependence.	bleomycetin	0-12	P53	Homo sapiens	60-63
20818013-5	2005	Specifically, we present an improved immobilization method that covalently anchors one end (5" end) of a dual labelled (5"-thiol, 3"-biotin) p53 DNA molecule onto a gold substrate via gold-thiol chemistry, whilst the biotinylated 3" end is available for "pick-up" using a streptavidin modified AFM tip.	5-[(3aR,4R,6aS)-2-oxo-1,3,3a,4,6,6a-hexahydrothieno[3,4-d]imidazol-4-yl]pentanoic acid	130-139	P53	Homo sapiens	141-144
25624096-3	2015	MB-NSi-p53-CS ternary complexes displayed nanosized diameter, effective p53 condensation ability, efficient p53 protection profile, and superior bovine serum albumin stability in vitro.	Chondroitin Sulfates	11-13	P53	Homo sapiens	7-10
25624096-3	2015	MB-NSi-p53-CS ternary complexes displayed nanosized diameter, effective p53 condensation ability, efficient p53 protection profile, and superior bovine serum albumin stability in vitro.	Chondroitin Sulfates	11-13	P53	Homo sapiens	72-75
25624096-3	2015	MB-NSi-p53-CS ternary complexes displayed nanosized diameter, effective p53 condensation ability, efficient p53 protection profile, and superior bovine serum albumin stability in vitro.	Chondroitin Sulfates	11-13	P53	Homo sapiens	72-75
25490861-9	2015	This was associated with larger necrotic areas, a lobular tumor structure and increased p53 and p16 expression of the carboplatin-treated shGDF15-A2780cis tumors.	Carboplatin	118-129	P53	Homo sapiens	88-91
25384678-8	2015	MG132, a specific inhibitor of the 26S proteasome, could block the effect of p53 on 14-3-3gamma protein levels, suggesting that p53 suppressed 14-3-3gamma by stimulating the process of proteasome-mediated degradation of 14-3-3gamma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	P53	Homo sapiens	77-80
16006125-1	2005	15-Deoxy-delta(12,14)-prostaglandin J2 (15d-PGJ2), a dehydration product of prostaglandin D2, is an important pharmacological molecule, which with the virtue of its electrophilicity, has been reported to covalently modify some cellular proteins (such as nuclear factor-kappa B (NF-kappaB), AP-1, p53, and thioredoxin) and elicit its physiological effects.	Prostaglandin D2	76-92	P53	Homo sapiens	296-299
25384678-8	2015	MG132, a specific inhibitor of the 26S proteasome, could block the effect of p53 on 14-3-3gamma protein levels, suggesting that p53 suppressed 14-3-3gamma by stimulating the process of proteasome-mediated degradation of 14-3-3gamma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	P53	Homo sapiens	128-131
25404486-0	2015	Selective ROS-dependent p53-associated anticancer effects of the hypoxoside derivative rooperol on human teratocarcinomal cancer stem-like cells.	hypoxoside	65-75	P53	Homo sapiens	24-27
25349305-4	2015	We hypothesized that combined CDKN1A-TP53 loss would make bladder cancer sensitive to combined treatment with gemcitabine and Chk1 inhibitor.	gemcitabine	110-121	P53	Homo sapiens	37-41
16096427-3	2005	Usnic acid, a normal component of lichens, showed activity against the wild-type p53 breast cancer cell line MCF7 as well as the non-functional p53 breast cancer cell line MDA-MB-231 and the lung cancer cell line H1299 (null for p53).	usnic acid	0-10	P53	Homo sapiens	81-84
25349305-5	2015	Here, we show that TP53-CDKN1A double-mutant bladder cancer cell lines, 647V and RT-112, have a remarkable increase in p-Chk1 levels and G2-M arrest in response to gemcitabine treatment, with a heightened sensitivity to combination treatment with gemcitabine and either Chk1 inhibitor PF477736 or AZD7762, in comparison with other bladder cancer cell lines (either TP53 or p21 deficient).	gemcitabine	164-175	P53	Homo sapiens	19-23
25349305-5	2015	Here, we show that TP53-CDKN1A double-mutant bladder cancer cell lines, 647V and RT-112, have a remarkable increase in p-Chk1 levels and G2-M arrest in response to gemcitabine treatment, with a heightened sensitivity to combination treatment with gemcitabine and either Chk1 inhibitor PF477736 or AZD7762, in comparison with other bladder cancer cell lines (either TP53 or p21 deficient).	gemcitabine	164-175	P53	Homo sapiens	365-369
25349305-5	2015	Here, we show that TP53-CDKN1A double-mutant bladder cancer cell lines, 647V and RT-112, have a remarkable increase in p-Chk1 levels and G2-M arrest in response to gemcitabine treatment, with a heightened sensitivity to combination treatment with gemcitabine and either Chk1 inhibitor PF477736 or AZD7762, in comparison with other bladder cancer cell lines (either TP53 or p21 deficient).	gemcitabine	247-258	P53	Homo sapiens	19-23
25349305-5	2015	Here, we show that TP53-CDKN1A double-mutant bladder cancer cell lines, 647V and RT-112, have a remarkable increase in p-Chk1 levels and G2-M arrest in response to gemcitabine treatment, with a heightened sensitivity to combination treatment with gemcitabine and either Chk1 inhibitor PF477736 or AZD7762, in comparison with other bladder cancer cell lines (either TP53 or p21 deficient).	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	297-304	P53	Homo sapiens	19-23
25118313-7	2015	Inhibitors of BH4 activity or synthesis also inhibited NF-kappaB activation and, similar to MTX, increased JNK, p53, p21 and JUN activity.	sapropterin	14-17	P53	Homo sapiens	112-115
25261582-5	2015	In this article, we analyse the binding of the p53 proline-rich region with a pool of selected polyproline binding domains (i.e. SH3 and WW), and we present the first demonstration that the purified SH3 domains of the CD2AP/Cin85 protein family are able to directly bind the p53 protein, and to discriminate between the two polymorphic variants P72R.	polyproline	95-106	P53	Homo sapiens	47-50
25311384-0	2015	Mutant p53 stimulates chemoresistance of pancreatic adenocarcinoma cells to gemcitabine.	gemcitabine	76-87	P53	Homo sapiens	7-10
25311384-3	2015	The purpose of this study was to assess the relevance of the p53 status on the PDAC cells response to the standard drug gemcitabine.	gemcitabine	120-131	P53	Homo sapiens	61-64
25311384-5	2015	We showed that gemcitabine stabilized mutant p53 protein in the nuclei and induced chemoresistance, concurrent with the mutant p53-dependent expression of Cdk1 and CCNB1 genes, resulting in a hyperproliferation effect.	gemcitabine	15-26	P53	Homo sapiens	45-48
25311384-5	2015	We showed that gemcitabine stabilized mutant p53 protein in the nuclei and induced chemoresistance, concurrent with the mutant p53-dependent expression of Cdk1 and CCNB1 genes, resulting in a hyperproliferation effect.	gemcitabine	15-26	P53	Homo sapiens	127-130
25311384-6	2015	Despite the adverse activation of mutant p53 by gemcitabine, simultaneous treatment of PDAC cells with gemcitabine and p53-reactivating molecules (CP-31398 and RITA) reduced growth rate and induced apoptosis.	gemcitabine	48-59	P53	Homo sapiens	41-44
25714397-5	2015	In this study, we examine the ability of 2 tumor suppressor miRNAs, let-7b and miR-34a to sensitize KRAS;TP53 mutant non-small cell lung cancer cells to the action of erlotinib.	Erlotinib Hydrochloride	167-176	P53	Homo sapiens	105-109
26177380-7	2015	Functionally, loss of p53 drives spermatogonia out of the undifferentiated state and causes a consistent expansion of early differentiating spermatogonia until the stage of preleptotene (premeiotic) spermatocyte.	preleptotene	173-185	P53	Homo sapiens	22-25
25876968-13	2015	CONCLUSION: Inhibitors of DNA-PK, NU7026 and Wortmannin, promote p53-independent apoptosis induced by 1, 4-benzoquinone in HL60 cells.	2-(morpholin-4-yl)benzo(h)chromen-4-one	34-40	P53	Homo sapiens	65-68
25876968-13	2015	CONCLUSION: Inhibitors of DNA-PK, NU7026 and Wortmannin, promote p53-independent apoptosis induced by 1, 4-benzoquinone in HL60 cells.	Wortmannin	45-55	P53	Homo sapiens	65-68
16096427-3	2005	Usnic acid, a normal component of lichens, showed activity against the wild-type p53 breast cancer cell line MCF7 as well as the non-functional p53 breast cancer cell line MDA-MB-231 and the lung cancer cell line H1299 (null for p53).	usnic acid	0-10	P53	Homo sapiens	144-147
25821312-11	2015	CONCLUSION: Bleomycin A5 can increase caspase-3 and p53 levels and inhibit telomerase activity to induce ECV304 apoptosis.	bleomycetin	12-24	P53	Homo sapiens	52-55
16096427-3	2005	Usnic acid, a normal component of lichens, showed activity against the wild-type p53 breast cancer cell line MCF7 as well as the non-functional p53 breast cancer cell line MDA-MB-231 and the lung cancer cell line H1299 (null for p53).	usnic acid	0-10	P53	Homo sapiens	144-147
25384157-1	2014	Structure-based rational design and extensive structure-activity relationship studies led to the discovery of AMG 232 (1), a potent piperidinone inhibitor of the MDM2-p53 association, which is currently being evaluated in human clinical trials for the treatment of cancer.	2-piperidone	132-144	P53	Homo sapiens	167-170
16096427-4	2005	In MCF7 cells treated with usnic acid, although there was an accumulation of p53 and p21 proteins, the transcriptional activity of p53 remained unaffected.	usnic acid	27-37	P53	Homo sapiens	77-80
16096427-4	2005	In MCF7 cells treated with usnic acid, although there was an accumulation of p53 and p21 proteins, the transcriptional activity of p53 remained unaffected.	usnic acid	27-37	P53	Homo sapiens	131-134
25641429-0	2015	Flavokawain B inhibits the growth of acute lymphoblastic leukemia cells via p53 and caspase-dependent mechanisms.	flavokawain B	0-13	P53	Homo sapiens	76-79
16096427-6	2005	The property of usnic acid as a non-genotoxic anti-cancer agent that works in a p53-independent manner makes it a potential candidate for novel cancer therapy.	usnic acid	16-26	P53	Homo sapiens	80-83
25641429-5	2015	Furthermore, the enhancement of p53-dependent apoptosis by flavokawain B could be rescued by pifithrin-alpha, a pharmacological inhibitor of p53 transcriptional activity.	flavokawain B	59-72	P53	Homo sapiens	32-35
25641429-5	2015	Furthermore, the enhancement of p53-dependent apoptosis by flavokawain B could be rescued by pifithrin-alpha, a pharmacological inhibitor of p53 transcriptional activity.	flavokawain B	59-72	P53	Homo sapiens	141-144
25501220-0	2014	Gene expression of the p16(INK4a)-Rb and p19(Arf)-p53-p21(Cip/Waf1) signaling pathways in the regulation of hematopoietic stem cell aging by ginsenoside Rg1.	Ginsenosides	141-152	P53	Homo sapiens	50-53
15844214-8	2005	DMBA induced MDM2 expression in a dose- and time-dependent fashion in the MCF-7 cells, and this activation appeared to be p53 dependent.	6,11-dimethylbenzo(b)naphtho(2,3-d)thiophene	0-4	P53	Homo sapiens	122-125
23818300-1	2014	The genetic or functional inactivation of the p53 pathway plays an important role with regards to disease progression from the chronic phase (CP) to blast phase (BP) and imatinib treatment response in chronic myeloid leukemia (CML).	Imatinib Mesylate	170-178	P53	Homo sapiens	46-49
23818300-2	2014	Two functional single nucleotide polymorphisms (SNPs), p53 R72P and MDM2 SNP309, are associated with alternation of p53 activity, however the association regarding CML susceptibility and BP transformation under imatinib treatment is unclear.	Imatinib Mesylate	211-219	P53	Homo sapiens	55-58
25685256-0	2015	Naphthoquinone derivative PPE8 induces endoplasmic reticulum stress in p53 null H1299 cells.	ppe8	26-30	P53	Homo sapiens	71-74
25685256-12	2015	Such results did not arise in A549 cells, but p53 knockdown by siRNA restored PPE8-induced GRP78 expression and JNK phosphorylation.	ppe8	78-82	P53	Homo sapiens	46-49
25189993-3	2014	Exposure of tumor cells to JQ-101 significantly enhanced acetylation of p53 and histone H4K16 at known sites of SIRT1 deacetylation, validating SIRT1 as its cellular target.	jq-101	27-33	P53	Homo sapiens	72-75
26021170-4	2015	NaBu activated the TP53 protein via hyper acetylation at lysine residue K382, without significant changes in the level of protein expression.	C12H10N6O3S	72-76	P53	Homo sapiens	19-23
15705792-4	2005	Using genome-wide gene expression analysis, stress-induced up-regulation of the p53 transcriptional targets and their specific inhibition by oligomycin has been demonstrated.	Oligomycins	141-151	P53	Homo sapiens	80-83
23818300-2	2014	Two functional single nucleotide polymorphisms (SNPs), p53 R72P and MDM2 SNP309, are associated with alternation of p53 activity, however the association regarding CML susceptibility and BP transformation under imatinib treatment is unclear.	Imatinib Mesylate	211-219	P53	Homo sapiens	116-119
25623760-8	2014	RESULTS: The MTT assay showed a stronger inhibitory effect of gefitinib on MDA-MB-468 cells infected with Ad-p53 than on the control cells.	monooxyethylene trimethylolpropane tristearate	13-16	P53	Homo sapiens	109-112
24853077-10	2014	Concomitant with its enhancement of ploidy, NIC strongly enhanced the activity of three TFs with known involvement in terminal MK maturation: FLI-1, NF-E2, and p53.	Niacinamide	44-47	P53	Homo sapiens	160-163
16204849-0	2005	The contribution of the Trp/Met/Phe residues to physical interactions of p53 with cellular proteins.	Phenylalanine	32-35	P53	Homo sapiens	73-76
24913304-7	2014	Furthermore, p53(mut_c) cells exhibited a pronounced side population that could be suppressed by RNAi knockdown of ABCG2 as well as treatment with the ATP-binding-cassette transporter inhibitors imatinib, MK571 and tariquidar.	Imatinib Mesylate	195-203	P53	Homo sapiens	13-16
25195822-0	2014	Ceramide modulates pre-mRNA splicing to restore the expression of wild-type tumor suppressor p53 in deletion-mutant cancer cells.	Ceramides	0-8	P53	Homo sapiens	93-96
25195822-3	2014	Being different from these, we report that ceramide can restore the expression of wild-type p53 and induce p53-dependent apoptosis in deletion-mutant cancer cells.	Ceramides	43-51	P53	Homo sapiens	92-95
25195822-3	2014	Being different from these, we report that ceramide can restore the expression of wild-type p53 and induce p53-dependent apoptosis in deletion-mutant cancer cells.	Ceramides	43-51	P53	Homo sapiens	107-110
24839208-2	2014	Reactive oxygen species (ROS) and reactive nitrogen species generations have been proposed to be an important mechanism of DOX-induced cardiotoxicity and cardiomyocyte apoptosis, which may be mediated by p53 protein.	Reactive Nitrogen Species	34-59	P53	Homo sapiens	204-207
16204849-8	2005	Several clusters of the Trp/Met/Phe residues are involved in the p53 protein-protein interactions.	Phenylalanine	32-35	P53	Homo sapiens	65-68
25688502-13	2014	CONCLUSIONS: Irinotecan and paclitaxel are an effective treatment for HCT 116 wt cells, whereas HCT 116 cells with p53 deficiency can be treated successfully with paclitaxel and gemcitabine.	gemcitabine	178-189	P53	Homo sapiens	115-118
15748635-3	2005	In human skin cancers, about 35% of all mutations in the p53 gene are transitions at dipyrimidines within the sequence 5"-TCG and 5"-CCG, and these are localized at several mutational hotspots.	5"-tcg	119-125	P53	Homo sapiens	57-60
25166596-5	2014	Here, we report that the FDA-approved HDACi Vorinostat/SAHA inhibits HIF-1alpha expression in liver cancer-derived cell lines, by a new mechanism independent of p53, prolyl-hydroxylases, autophagy and proteasome degradation.	Vorinostat	44-54	P53	Homo sapiens	161-164
15854413-1	2005	OBJECTIVE: To study the role of mutant p53 gene induced by anti-7,8-dihydrodiol-9,10-epoxide benzo(a)pyrene (BPDE) in the development of lung cancer and the effects of wild-type p53 substitution on malignant phenotype and resistance to drugs.	7,8-dihydrodiol-9,10-epoxide benzo(a)pyrene	64-107	P53	Homo sapiens	39-42
25042256-0	2014	Optimization beyond AMG 232: discovery and SAR of sulfonamides on a piperidinone scaffold as potent inhibitors of the MDM2-p53 protein-protein interaction.	2-piperidone	68-80	P53	Homo sapiens	123-126
25042256-1	2014	We recently reported on the discovery of AMG 232, a potent and selective piperidinone inhibitor of the MDM2-p53 interaction.	2-piperidone	73-85	P53	Homo sapiens	108-111
25261655-10	2014	RT-PCR assay confirmed that SAHA could upregulate the mRNA expressions of p53 and bax genes.	Vorinostat	28-32	P53	Homo sapiens	74-77
25261655-13	2014	CONCLUSION: SAHA inhibited cell proliferation and promoted human hepatoma Bel-7402 cell apoptosis by affecting caspase-3 protein activity and mRNA expressions of p53, bcl-2 and bax genes.	Vorinostat	12-16	P53	Homo sapiens	162-165
25336953-11	2014	CuONP also induced decreases in p53 and p-p53 levels in both cell types.	cuonp	0-5	P53	Homo sapiens	32-35
25336953-11	2014	CuONP also induced decreases in p53 and p-p53 levels in both cell types.	cuonp	0-5	P53	Homo sapiens	42-45
25336953-15	2014	These data demonstrate that the activation of Erk and p53 plays an important role in CuONP-induced cytotoxicity, and agents that preserve Erk or p53 activation may prevent CuONP-induced cytotoxicity.	cuonp	85-90	P53	Homo sapiens	54-57
25336953-15	2014	These data demonstrate that the activation of Erk and p53 plays an important role in CuONP-induced cytotoxicity, and agents that preserve Erk or p53 activation may prevent CuONP-induced cytotoxicity.	cuonp	172-177	P53	Homo sapiens	145-148
15715472-10	2005	The butyric acid and formaldehyde induced cell differentiation and increased p53 and p21 levels, suggesting that both affect cancer cells, the acid by inhibiting HDAC and the aldehyde by an as yet unknown mechanism.	Aldehydes	25-33	P53	Homo sapiens	77-80
25227113-7	2014	Furthermore, poly(I:C) transfection increased the levels of phosphorylated p53, NOXA, and tBid.	Poly I-C	13-21	P53	Homo sapiens	75-78
24852275-1	2014	A novel class of small-molecule inhibitors of MDM2-p53 interaction with a (E)-3-benzylideneindolin-2-one scaffold was identified using an integrated virtual screening strategy that combined both pharmacophore- and structure-based approaches.	(e)-3-benzylideneindolin-2-one	74-104	P53	Homo sapiens	51-54
24967612-1	2014	We recently reported the discovery of AMG 232 (1), a potent and selective piperidinone inhibitor of the MDM2-p53 protein-protein interaction.	2-piperidone	74-86	P53	Homo sapiens	109-112
15684474-0	2005	Dracorhodin perchlorate induces A375-S2 cell apoptosis via accumulation of p53 and activation of caspases.	dracorhodin	0-23	P53	Homo sapiens	75-78
24789513-0	2014	Pingyangmycin stimulates apoptosis in human hemangioma-derived endothelial cells through activation of the p53 pathway.	bleomycetin	0-13	P53	Homo sapiens	107-110
24789513-10	2014	The data demonstrated that the pro-apoptotic activity of pingyangmycin against infantile hemangiomas involves p53 pathway activation.	bleomycetin	57-70	P53	Homo sapiens	110-113
24682512-3	2014	In this study, bone marrow biopsies from 85 patients treated with lenalidomide in the MDS-004 clinical trial were retrospectively assessed for p53 expression by immunohistochemistry in association with outcome.	Lenalidomide	66-78	P53	Homo sapiens	143-146
24929515-9	2014	Methylation-specific PCR (MSP) showed that the amount of unmethylated p53 increased, indicating that the anthocyanins can down-regulate the methylation of p53.	Anthocyanins	105-117	P53	Homo sapiens	70-73
24929515-9	2014	Methylation-specific PCR (MSP) showed that the amount of unmethylated p53 increased, indicating that the anthocyanins can down-regulate the methylation of p53.	Anthocyanins	105-117	P53	Homo sapiens	155-158
15684474-4	2005	Dracorhodin perchlorate upregulated the expression ratio of Bax/Bcl-2 and significantly increased the expression of p53 and p21(WAF1) proteins.	dracorhodin	0-23	P53	Homo sapiens	116-119
24682388-5	2014	In addition, ALO induced cell cycle arrest at the G2/M phase with a concomitant increase in p21 and p53 and a decrease in cyclin D1 and B1.	aloperine	13-16	P53	Homo sapiens	100-103
15684474-8	2005	Taken together, dracorhodin perchlorate induces apoptosis in A375-S2 cells via accumulation of p53, alters the Bax/Bcl-2 ratio, and activates caspases and p38/JNK MAPKs.	dracorhodin	16-39	P53	Homo sapiens	95-98
24792472-6	2014	In addition, PDT led to an appreciable accumulation of pSer15-p53/COX-2 complexes, and this association of complexes was partially inhibited by SB203580, an inhibitor of p38.	SB 203580	144-152	P53	Homo sapiens	62-65
15474986-0	2005	p53 protein activates the transcription of human proliferating cell nuclear antigen in response to 4-nitroquinoline N-oxide treatment.	4-Nitroquinoline	99-115	P53	Homo sapiens	0-3
17977211-4	2005	P53 levels were also determined in supernatants of MCs isolated from synovial fluid (SFMCs) of RA and OA patients.	mcs	51-54	P53	Homo sapiens	0-3
24627193-11	2014	TP53 mutations are important predictors of AML progression and possible resistance to lenalidomide.	Lenalidomide	86-98	P53	Homo sapiens	0-4
24486139-7	2014	Conversely, the inhibition of necroptosis and p53 signaling accelerated the changes in the cell cycle triggered by PA exposure.	Palmitic Acid	115-117	P53	Homo sapiens	46-49
15720815-0	2005	Grape seed proanthocyanidins induce apoptosis through p53, Bax, and caspase 3 pathways.	Proanthocyanidins	11-28	P53	Homo sapiens	54-57
24494589-4	2014	Using the well characterized p53-Mdm2 interaction as a model system, we designed a 9-(2-carboxy-2-cyanovinyl) julolidine-based p53 peptide reporter, JP1-R, which fluoresces conditionally only upon Mdm2 binding.	9-(2-carboxy-2-cyanovinyl)julolidine	83-120	P53	Homo sapiens	29-32
15358769-2	2004	We show that geldanamycin or radicicol, specific inhibitors of Hsp90, diminish specific wild-type p53 binding to the p21 promoter sequence.	monorden	29-38	P53	Homo sapiens	98-101
24494589-4	2014	Using the well characterized p53-Mdm2 interaction as a model system, we designed a 9-(2-carboxy-2-cyanovinyl) julolidine-based p53 peptide reporter, JP1-R, which fluoresces conditionally only upon Mdm2 binding.	9-(2-carboxy-2-cyanovinyl)julolidine	83-120	P53	Homo sapiens	127-130
24810255-9	2014	Obviously, p53 protects cells from the cytotoxicity of Enzastaurin in combination with SBE13.	enzastaurin	55-66	P53	Homo sapiens	11-14
15736417-0	2004	Analysis of central regulatory pathways in p53-deficient primary cultures of malignant fibrous histiocytoma exposed to ifosfamide.	Ifosfamide	119-129	P53	Homo sapiens	43-46
24380881-5	2014	The inhibition of HO-1 activity obtained by Zinc (II) protoprophyrin IX (ZnPPIX) was able to significantly increase the pro-apoptotic effect of BTZ in a p53- and p21-independent way.	zinc protoporphyrin	73-79	P53	Homo sapiens	153-156
15486204-0	2004	Differential recognition by the tumor suppressor protein p53 of DNA modified by the novel antitumor trinuclear platinum drug BBR3464 and cisplatin.	BBR 3464	125-132	P53	Homo sapiens	57-60
24333234-11	2014	Fetal kidney cells exposed to carboplatin showed a concentration-dependent increased expression of apoptosis-inducing factor and p53 apoptosis proteins and a time-dependent increase in expression Bax apoptosis protein expression.	Carboplatin	30-41	P53	Homo sapiens	129-132
24411335-7	2014	Propidium iodide (PI) flow cytometric assays were conducted to demonstrate that EGFP-p53/PEI/PAH-Cit/AuNP-CS elevated the level of apoptosis in PC-3 cells.	Propidium	0-16	P53	Homo sapiens	85-88
15486204-2	2004	BBR3464 retains significant activity in human tumor cell lines and xenografts that are refractory or poorly responsive to cisplatin, and displays a high activity in human tumor cell lines that are characterized by both wild-type and mutant p53 gene.	BBR 3464	0-7	P53	Homo sapiens	240-243
24514456-0	2014	A dual-targeting, p53-independent, apoptosis-inducing platinum(II) anticancer complex, [Pt(BDI(QQ))]Cl.	[pt(bdi(qq))]cl	87-102	P53	Homo sapiens	18-21
15486204-6	2004	This study, using gel-mobility-shift assays, was undertaken to examine the interactions of active and latent p53 protein with DNA fragments and oligodeoxyribonucleotide duplexes modified by BBR3464 in a cell free medium and to compare these results with those describing the interactions of these proteins with DNA modified by cisplatin.	BBR 3464	190-197	P53	Homo sapiens	109-112
15486204-7	2004	The results indicate that structurally different DNA adducts of BBR3464 and cisplatin exhibit a different efficiency to affect the binding affinity of the modified DNA to p53 protein.	BBR 3464	64-71	P53	Homo sapiens	171-174
24514456-10	2014	In p53-null cells, [Pt(BDI(QQ))]Cl induces cell death through mitochondrial dysfunction.	[pt(bdi(qq))]cl	19-34	P53	Homo sapiens	3-6
15486204-8	2004	It has been suggested that different structural perturbations induced in DNA by the adducts of BBR3464 and cisplatin produce a differential response to p53 protein activation and recognition and that a "molecular approach" to control of downstream effects such as protein recognition and pathways of apoptosis induction may consist in design of structurally unique DNA adducts as cell signals.	BBR 3464	95-102	P53	Homo sapiens	152-155
24575839-0	2014	Phospho-aspirin (MDC-22) inhibits breast cancer in preclinical animal models: an effect mediated by EGFR inhibition, p53 acetylation and oxidative stress.	mdc-22	17-23	P53	Homo sapiens	117-120
15298872-2	2004	Here we report an intermediate structure of the core domain of the tumor suppressor protein p53 (p53C) during equilibrium and kinetic folding/unfolding transitions induced by guanidinium chloride.	Guanidine	175-195	P53	Homo sapiens	92-95
23474763-4	2014	In this study, we determined if targeting the E6-p300 interaction is an effective approach to reactivate p53 in HPV-positive HNSCC.	e6-p300	46-53	P53	Homo sapiens	105-108
15466201-5	2004	Sensitization to IR-induced apoptosis by caffeine or UCN-01 was abrogated neither by cycloheximide nor by pifithrin-alpha, an inhibitor of the transcriptional activity of p53.	Caffeine	41-49	P53	Homo sapiens	171-174
24525822-0	2014	Transactivation of bad by vorinostat-induced acetylated p53 enhances doxorubicin-induced cytotoxicity in cervical cancer cells.	Vorinostat	26-36	P53	Homo sapiens	56-59
15326376-4	2004	We here show that inhibition of Chk1 but not of Chk2 in p21(-/-) and p53(-/-) cells caused a greater abrogation of G(2) block induced by ionizing radiation and cis-diamine-dichloroplatinum treatments and a greater sensitization to the same treatments than in the parental cell line with p53 and p21 wild type proteins.	Platinum(II) chloride	172-188	P53	Homo sapiens	69-72
24281001-5	2014	RESULTS: Vorinostat was equally effective in p53 wild-type and null cells, whereas entinostat was less effective in p53 null cells.	Vorinostat	9-19	P53	Homo sapiens	45-48
24281001-9	2014	CONCLUSION: These results demonstrate that vorinostat activates p53, but does not require p53 for inducing its anticancer action.	Vorinostat	43-53	P53	Homo sapiens	64-67
24177958-7	2014	When these cells were simultaneously treated with a c-ABL kinase inhibitor, STI571, or a c-ABL-specific siRNA along with adriamycin, the p53-dependent p21 induction was dramatically diminished, even though p53 is substantially induced.	Imatinib Mesylate	76-82	P53	Homo sapiens	137-140
15016620-3	2004	Both S-nitroso-N-acetyl penicillamine and diethylenetriaminelNONOate dose-dependently suppressed [3H]-thymidine incorporation in cultured HPASMC, and induced the expression of p53 and p21 protein.	S-Nitroso-N-Acetylpenicillamine	5-37	P53	Homo sapiens	176-179
24078446-5	2014	Furthermore, we revealed that artemisinin treatment led to an increased expression of p53.	artemisinin	30-41	P53	Homo sapiens	86-89
24275138-1	2014	We demonstrated that exogenous pyruvate promotes survival under glucose depletion in aerobic mutant p53 (R175H) human melanoma cells.	Pyruvic Acid	31-39	P53	Homo sapiens	100-103
25276123-0	2014	Comparative Evaluation of Cytotoxic and Apoptogenic Effects of Several Coumarins on Human Cancer Cell Lines: Osthole Induces Apoptosis in p53-Deficient H1299 Cells.	osthol	109-116	P53	Homo sapiens	138-141
25276123-12	2014	The effects of osthole on H1299 cells are important because the loss of p53 has been associated with poor clinical prognosis in cancer treatment.	osthol	15-22	P53	Homo sapiens	72-75
15016620-3	2004	Both S-nitroso-N-acetyl penicillamine and diethylenetriaminelNONOate dose-dependently suppressed [3H]-thymidine incorporation in cultured HPASMC, and induced the expression of p53 and p21 protein.	diethylenetriaminelnonoate	42-68	P53	Homo sapiens	176-179
15297424-6	2004	In cell lines with wild-type p53, treatment with the protein synthesis inhibitor cycloheximide (CHX) together with anti-CD95 overcame the resistance, suggesting the presence of a labile inhibiting protein.	Cycloheximide	81-94	P53	Homo sapiens	29-32
24870784-0	2014	Rice bran phytic acid induced apoptosis through regulation of Bcl-2/Bax and p53 genes in HepG2 human hepatocellular carcinoma cells.	Phytic Acid	10-21	P53	Homo sapiens	76-79
24870784-9	2014	PA treated HepG2 cells showed up-regulation of p53, Bax, Caspase-3 and -9, and down- regulation of Bcl-2 gene (p &lt;= 0.01).	Phytic Acid	0-2	P53	Homo sapiens	47-50
24870784-10	2014	At the IC50 (2.49 mM) of PA, the p53, Bax, Caspase-3 and-9 genes were up- regulated by 6.03, 7.37, 19.7 and 14.5 fold respectively.	Phytic Acid	25-27	P53	Homo sapiens	33-36
15297424-6	2004	In cell lines with wild-type p53, treatment with the protein synthesis inhibitor cycloheximide (CHX) together with anti-CD95 overcame the resistance, suggesting the presence of a labile inhibiting protein.	Cycloheximide	96-99	P53	Homo sapiens	29-32
15276867-9	2004	DCQ treatment also induced an upregulation of p53 and p21 protein levels, key mediators of cell cycle arrest and apoptosis.	2-benzoyl-3-phenyl-6,7-dichloroquinoxaline-1,4-dioxide	0-3	P53	Homo sapiens	46-49
25371703-6	2014	Our analyses indicated that SAHA selectively disrupted the DNA damage response, cell cycle, p53 expression, and mitochondrial integrity of tumor samples to induce selective tumor cell apoptosis.	Vorinostat	28-32	P53	Homo sapiens	92-95
24247204-11	2014	Tumors of patients with response to FOLFIRINOX showed a higher expression level of p53 and Ki67 as well as higher serum levels of CA19.9 compared to non-responders, which was statistically not significant.	folfirinox	36-46	P53	Homo sapiens	83-86
15276867-11	2004	These findings indicate that DCQ inhibits the growth of ATL cell lines, at least in part, by inducing apoptosis mediated by the modulation of TGF expression, the upregulation in p53 and p21 proteins and downregulation in Bcl-2alpha expression.	2-benzoyl-3-phenyl-6,7-dichloroquinoxaline-1,4-dioxide	29-32	P53	Homo sapiens	178-181
15194001-0	2004	A novel bis-benzylidenecyclopentanone derivative, BPR0Y007, inducing a rapid caspase activation involving upregulation of Fas (CD95/APO-1) and wild-type p53 in human oral epidermoid carcinoma cells.	bis-benzylidenecyclopentanone	8-37	P53	Homo sapiens	153-156
25140197-5	2014	Therefore, combination of ATRA with DAC and SAHA represents promising tool for therapy of leukemic disease with nonfunctional p53 signalization.	Vorinostat	44-48	P53	Homo sapiens	126-129
15180186-10	2004	Polyamine biosynthesis was significantly higher in cancers showing K-ras mutation, either with or without p53 mutation [K-ras(+)/p53(-) and K-ras(+)/p53(+)], compared to samples with K-ras wild type [K-ras(-)/p53(-) and K-ras(-)/p53(+)].	Polyamines	0-9	P53	Homo sapiens	129-132
15180186-10	2004	Polyamine biosynthesis was significantly higher in cancers showing K-ras mutation, either with or without p53 mutation [K-ras(+)/p53(-) and K-ras(+)/p53(+)], compared to samples with K-ras wild type [K-ras(-)/p53(-) and K-ras(-)/p53(+)].	Polyamines	0-9	P53	Homo sapiens	129-132
24464562-0	2013	Polymorphisms in the p53 pathway genes and micronucleus occurrence in Chinese vinyl chloride-exposed workers.	Vinyl Chloride	78-92	P53	Homo sapiens	21-24
15180186-12	2004	CONCLUSIONS: The present study provides evidence of a close relationship between K-ras mutation and polyamine biosynthesis in human colorectal carcinoma in a way that is largely p53 independent.	Polyamines	100-109	P53	Homo sapiens	178-181
24464562-1	2013	OBJECTIVES: To investigate the association between polymorphisms in the p53 pathway genes and chromosomal damage in vinyl chloride (VC)-exposed workers.	Vinyl Chloride	116-130	P53	Homo sapiens	72-75
15116093-4	2004	Pretreatment of MCF7 cells with an ERK2 chemical inhibitor, PD98059 or U0126, blocked doxorubicin-induced p53 activation and suppressed phosphorylation of p53Thr55.	U 0126	71-76	P53	Homo sapiens	106-109
24464562-1	2013	OBJECTIVES: To investigate the association between polymorphisms in the p53 pathway genes and chromosomal damage in vinyl chloride (VC)-exposed workers.	Vinyl Chloride	132-134	P53	Homo sapiens	72-75
24236158-6	2013	In contrast, SAHA increased expression of Caspase-3, p21 and p53 mRNA, and upregulated acetyl-Histones H3 and H4, Caspase-8, and p53 proteins.	Vorinostat	13-17	P53	Homo sapiens	61-64
24236158-6	2013	In contrast, SAHA increased expression of Caspase-3, p21 and p53 mRNA, and upregulated acetyl-Histones H3 and H4, Caspase-8, and p53 proteins.	Vorinostat	13-17	P53	Homo sapiens	129-132
15116093-4	2004	Pretreatment of MCF7 cells with an ERK2 chemical inhibitor, PD98059 or U0126, blocked doxorubicin-induced p53 activation and suppressed phosphorylation of p53Thr55.	U 0126	71-76	P53	Homo sapiens	155-158
14991574-7	2004	2-MeOE2 bis-sulfamate and 2-EtE2 sulfamate both induced BCL-2 phosphorylation, p53 protein expression and apoptosis in HUVECs.	2-ete2 sulfamate	26-42	P53	Homo sapiens	79-82
24269881-6	2013	Ceramide treatment also upregulated (p&lt;0.05) p53 and p21 protein expression, that was reversed by either pifithrin-alpha or shRNA for p53.	Ceramides	0-8	P53	Homo sapiens	48-51
24269881-6	2013	Ceramide treatment also upregulated (p&lt;0.05) p53 and p21 protein expression, that was reversed by either pifithrin-alpha or shRNA for p53.	Ceramides	0-8	P53	Homo sapiens	137-140
15041737-8	2004	These data suggest that p53 may be an important determinant of sensitivity to 5-FU and oxaliplatin but not CPT-11.	Oxaliplatin	87-98	P53	Homo sapiens	24-27
14757188-1	2004	It has been recently shown that ionizing radiation (IR) and the mRNA synthesis inhibitor 5,6-dichloro-1-b-D-ribofuranosylbenzimidazole (DRB) act in synergy to induce p53-mediated transactivation of reporter plasmids in human cells [Oncogene 19 (2000) 3829].	5,6-dichloro-1-b-d-ribofuranosylbenzimidazole	89-134	P53	Homo sapiens	166-169
24074410-2	2013	We sought to investigate the role of the p53-p21(waf1/cip1) pathway in relation to EZH2-mediated inhibition of PDAC.	pdac	111-115	P53	Homo sapiens	41-44
14751246-1	2004	Caffeine has been widely described as a chemo/radiosensitizing agent, presumably by inhibiting DNA repair, and affecting preferentially cells with an altered p53 status.	Caffeine	0-8	P53	Homo sapiens	158-161
14743382-6	2004	When their DNA is damaged, p53-defective tumor cells preferentially arrest in S or G2 phase where they are susceptible to checkpoint inhibitors such as caffeine and UCN-01.	Caffeine	152-160	P53	Homo sapiens	27-30
23913470-6	2013	Conversely, acetylation of p53 is activating when class III deacetylases (DACs), or sirtuins, are inhibited by niacinamide.	Niacinamide	111-122	P53	Homo sapiens	27-30
24512488-7	2014	Conversely, TP53 mutant-type cells were resistant to DZNep.	3-deazaneplanocin	53-58	P53	Homo sapiens	12-16
24512488-8	2014	Strikingly, the combination of DZNep with PRIMA-1 restored the sensitivity of TP53 mutant-type cells to DZNep.	3-deazaneplanocin	31-36	P53	Homo sapiens	78-82
24512488-8	2014	Strikingly, the combination of DZNep with PRIMA-1 restored the sensitivity of TP53 mutant-type cells to DZNep.	3-deazaneplanocin	104-109	P53	Homo sapiens	78-82
24512488-10	2014	CONCLUSION: Our data demonstrated that DZNep responsiveness was strongly associated with TP53 genomic status in thyroid cancer cells.	3-deazaneplanocin	39-44	P53	Homo sapiens	89-93
14985457-0	2004	Enhanced oxaliplatin-induced apoptosis following antisense Bcl-xl down-regulation is p53 and Bax dependent: Genetic evidence for specificity of the antisense effect.	Oxaliplatin	9-20	P53	Homo sapiens	85-88
24646317-4	2014	These effects were counterbalanced by pifithrin-beta, a small molecule interfering with the p53 functions.	pifithrin-beta	38-52	P53	Homo sapiens	92-95
24646317-8	2014	In particular, 2-(4-methoxyphenyl)-7-methyl-7H-pyrazolo[4,3-e][1,2,4]triazolo[1,5-c]pyrimidine resulted in a promising lead compound for further development of anti-AD agents in terms of neuroprotection, reducing the rate of NAC-induced cell death with an activity higher than that of pifithrin-beta, as a result of a more effective functional inhibition of p53 target gene transcription.	pifithrin-beta	285-299	P53	Homo sapiens	358-361
23810988-6	2013	With ER-alpha positive cells AZA increased the abundance of the tumour suppressor gene, p53 and induced demethylation of the IGFBP-3 promoter, whereas with ER negative cells, AZA epigenetically increased the transcription factor AP2-alpha, which when silenced prevented the increase in IGFBP-3.	Decitabine	29-32	P53	Homo sapiens	88-91
24236568-9	2014	The increase of apoptosis induced by osthole was correlated with down-regulation expression of anti-apoptotic Bcl-2 protein and up-regulation expression of pro-apoptotic Bax and p53 proteins.	osthol	37-44	P53	Homo sapiens	178-181
14985457-6	2004	RESULTS: At clinically relevant concentrations, oxaliplatin induced p53 and p53-dependent Bax, Bcl-xl, and p21/WAF1 protein accumulation.	Oxaliplatin	48-59	P53	Homo sapiens	68-71
23773853-8	2013	Our results demonstrate that Pho-s induces a cell cycle arrest in the G1 phase through an inhibition of cyclin D1 and stimulates p53.	phosphorylethanolamine	29-34	P53	Homo sapiens	129-132
24114124-10	2014	Consistent with abrogation of the Chk1 and p53-dependent G2/M checkpoint, mutant TP53 HT-29 colon cancer cells were more sensitive to gemcitabine when also treated with LY2603618, while wild-type TP53 HCT116 cells were not sensitized by LY2603618 to gemcitabine.	gemcitabine	250-261	P53	Homo sapiens	81-85
14985457-6	2004	RESULTS: At clinically relevant concentrations, oxaliplatin induced p53 and p53-dependent Bax, Bcl-xl, and p21/WAF1 protein accumulation.	Oxaliplatin	48-59	P53	Homo sapiens	76-79
24114124-11	2014	Treatment of Calu-6 human mutant TP53 lung cancer cell xenografts with gemcitabine resulted in a stimulation of Chk1 kinase activity that was inhibited by co-administration of LY2603618.	gemcitabine	71-82	P53	Homo sapiens	33-37
14690663-1	2004	The purpose of this study was to investigate the relationship between epithelial dysplasia unstained with iodine and the expression of proliferating cell nuclear antigen (PCNA) and/or tumour suppressor gene (p53) and the existence of glycogen.	Glycogen	234-242	P53	Homo sapiens	208-211
24548297-1	2014	We previously reported the discovery of AMG 232, a highly potent and selective piperidinone inhibitor of the MDM2-p53 interaction.	2-piperidone	79-91	P53	Homo sapiens	114-117
14637186-0	2003	Involvement of tumor suppressor protein p53 and p38 MAPK in caffeic acid phenethyl ester-induced apoptosis of C6 glioma cells.	caffeic acid phenethyl ester	60-88	P53	Homo sapiens	40-43
24486524-8	2014	CONCLUSIONS: (a) ERalpha(+) breast cancer cells dysfunctional for TP53 which proliferate irrespective of low estrogen and chemical MEK inhibition are likely to increase metabolic consumption becoming increasingly susceptible to 3-BrPA; (b) targeting the pyruvate pathway may improve response to endocrine therapy in ERalpha(+) breast cancer with p53 dysfunction.	Pyruvic Acid	254-262	P53	Homo sapiens	66-70
14637186-7	2003	CAPE application also enhanced the expression of p53, Bax, and Bak.	caffeic acid phenethyl ester	0-4	P53	Homo sapiens	49-52
14637186-10	2003	More importantly, p38 kinase formed a complex with p53 after the treatment of CAPE for 0.5 hr.	caffeic acid phenethyl ester	78-82	P53	Homo sapiens	51-54
23524579-0	2014	Low-dose arsenic induces chemotherapy protection via p53/NF-kappaB-mediated metabolic regulation.	Arsenic	9-16	P53	Homo sapiens	53-56
14637186-12	2003	The resultant data suggest that p38 MAPK mediated the CAPE-induced p53-dependent apoptosis in C6 glioma cells.	caffeic acid phenethyl ester	54-58	P53	Homo sapiens	67-70
23524579-3	2014	Pretreatment of untransformed cells with low doses of arsenic induced concerted p53 suppression and NF-kappaB activation, which elicited a marked induction of glycolysis.	Arsenic	54-61	P53	Homo sapiens	80-83
14643411-8	2003	Cr(VI) exposure elicits a classical DNA damage response within cells including activation of the p53 signaling pathway and cell cycle arrest or apoptosis.	chromium hexavalent ion	0-6	P53	Homo sapiens	97-100
23524579-5	2014	Using both in vitro and in vivo models, we demonstrated an absolute requirement of functional p53 in arsenic-mediated protection.	Arsenic	101-108	P53	Homo sapiens	94-97
14636064-3	2003	In the study presented here, we investigated the molecular mechanisms involved in the 15d-PGJ(2)-induced accumulation of p53.	9-deoxy-delta-9-prostaglandin D2	90-96	P53	Homo sapiens	121-124
24242917-8	2014	However, in colon carcinoma (Caco-2) cells with mutant p53, treatment with either AZD5438 or NU6140 blocked proliferation, albeit more robustly with AZD5438.	AZD5438	82-89	P53	Homo sapiens	55-58
14599774-3	2003	Pentoxifylline and the related drug Caffeine are known radiosensitizers especially in p53 mutant cells.	Caffeine	36-44	P53	Homo sapiens	86-89
14672267-10	2003	4) Following lovastatin treatment, increased p53 protein is detected only in D341 Med, and bax protein is unchanged in all cell lines.	Lovastatin	13-23	P53	Homo sapiens	45-48
24491565-2	2014	Here, we report that in CdCl2-exposed human bronchial epithelial cells (BEAS-2B), the level of p53 is dramatically decreased in a time- and dose-dependent manner, suggesting that the observed Cd-induced cytotoxicity is not likely due to the pro-apoptotic function of p53.	Cadmium Chloride	24-29	P53	Homo sapiens	95-98
24491565-2	2014	Here, we report that in CdCl2-exposed human bronchial epithelial cells (BEAS-2B), the level of p53 is dramatically decreased in a time- and dose-dependent manner, suggesting that the observed Cd-induced cytotoxicity is not likely due to the pro-apoptotic function of p53.	Cadmium Chloride	24-29	P53	Homo sapiens	267-270
14672267-12	2003	Lovastatin-induced apoptosis in medulloblastoma is probably p53 independent, but p53 and p21WAF1 gene expression may also mediate anti-proliferative effects of lovastatin on specific medulloblastoma cell lines.	Lovastatin	0-10	P53	Homo sapiens	60-63
24456472-1	2014	We recently reported the discovery of AM-8553 (1), a potent and selective piperidinone inhibitor of the MDM2-p53 interaction.	2-piperidone	74-86	P53	Homo sapiens	109-112
14672267-12	2003	Lovastatin-induced apoptosis in medulloblastoma is probably p53 independent, but p53 and p21WAF1 gene expression may also mediate anti-proliferative effects of lovastatin on specific medulloblastoma cell lines.	Lovastatin	160-170	P53	Homo sapiens	81-84
14637245-0	2003	Formation of trans-4-hydroxy-2-nonenal- and other enal-derived cyclic DNA adducts from omega-3 and omega-6 polyunsaturated fatty acids and their roles in DNA repair and human p53 gene mutation.	omega-6 polyunsaturated fatty acids	99-134	P53	Homo sapiens	175-178
24391088-0	2014	A low-dose arsenic-induced p53 protein-mediated metabolic mechanism of radiotherapy protection.	Arsenic	11-18	P53	Homo sapiens	27-30
24391088-4	2014	Of importance is that low-dose arsenic-induced HIF-1alpha requires functional p53, limiting the glycolytic shift to normal cells.	Arsenic	31-38	P53	Homo sapiens	78-81
14529628-5	2003	Nuclear magnetic resonance (1H15N-NMR) data showed that the alternative p53C conformation resembled that of the hot-spot oncogenic mutant R248Q.	1h15n	28-33	P53	Homo sapiens	72-75
24507760-3	2014	METHOD: We have developed a redox-responsive thiolated gelatin based nanoparticle system that efficiently delivers its payload in the presence of glutathione-mediated reducing intra-cellular environment and could be successfully used for site-specific wt-p53 expressing plasmid DNA as well as gemcitabine delivery by targeting epidermal growth factor receptor (EGFR).	gemcitabine	293-304	P53	Homo sapiens	255-258
12907610-11	2003	These data show that a low concentration of caffeine can induce p53-dependent apoptosis in JB6 cells through the Bax and caspase 3 pathways.	Caffeine	44-52	P53	Homo sapiens	64-67
24640606-5	2014	Further studies indicated that kirenol treatment triggered the arrest of cell cycle S period which might resulted from the up-regulation of phosphorylation of p53 (Ser 6 and Ser 37) and expression of p21 protein.	kirenol	31-38	P53	Homo sapiens	159-162
24452144-2	2014	Recently, we have shown that Roslin 2 or R2 (1-benzyl-15,3,5,7-tetraazatricyclo[3.3.1.1~3,7~]decane) compound disrupts FAK and p53 proteins, activates p53 transcriptional activity, and blocks tumor growth.	decane	93-99	P53	Homo sapiens	127-130
12798071-4	2003	Our results showed that direct exposure to cpTi and ZrO(2) particles compromises cell viability through the induction of apoptosis, eliciting increased levels of the tumor suppressor proteins p53 and p73, in a manner dependent on material composition, particle dosage, and time.	zro(2)	52-58	P53	Homo sapiens	192-195
24452144-2	2014	Recently, we have shown that Roslin 2 or R2 (1-benzyl-15,3,5,7-tetraazatricyclo[3.3.1.1~3,7~]decane) compound disrupts FAK and p53 proteins, activates p53 transcriptional activity, and blocks tumor growth.	decane	93-99	P53	Homo sapiens	151-154
24275138-4	2014	p53 Silencing decreased survival of glucose-starved C8161 melanoma with pyruvate supplementation under hypoxia (&lt;=1% oxygen), but increased resistance to glycolytic inhibitors oxamate and 2-deoxyglucose in 5mM glucose, preferentially under normoxia.	Pyruvic Acid	72-80	P53	Homo sapiens	0-3
12637545-8	2003	We also show that physiological targets of ATM, p53 Ser-15 and Chk2 Thr-68, were phosphorylated by Cr(VI) exposure in an ATM-dependent fashion.	chromium hexavalent ion	99-105	P53	Homo sapiens	48-51
25013761-0	2014	p53 is a key regulator for osthole-triggered cancer pathogenesis.	osthol	27-34	P53	Homo sapiens	0-3
12684687-4	2003	We report that Brca1-deficiency in p53-null cells was associated with increased sensitivity to the topoisomerase I poisons camptothecin and topotecan, the topoisomerase II poisons doxorubicin, mitoxantrone and etoposide, and to the platinum compounds carboplatin and oxaliplatin, but not to the antimetabolites 5-fluorouracil and gemcitabine and the taxanes docetaxel and paclitaxel.	Oxaliplatin	267-278	P53	Homo sapiens	35-38
25013761-6	2014	This study also provides evidence supporting the potential of osthole in p53 activation.	osthol	62-69	P53	Homo sapiens	73-76
25013761-7	2014	Expression of p53, an apoptotic protein, was remarkably upregulated in cells treated with osthole.	osthol	90-97	P53	Homo sapiens	14-17
12446453-0	2003	The vitamin D3 analog EB1089 induces apoptosis via a p53-independent mechanism involving p38 MAP kinase activation and suppression of ERK activity in B-cell chronic lymphocytic leukemia cells in vitro.	Cholecalciferol	4-14	P53	Homo sapiens	53-56
25013761-8	2014	Importantly, the levels of phosphorylation of p53 on Ser15 (p-p53) and acetylation of p53 on Lys379 (acetyl-p53) were increased under osthole treatment.	osthol	134-141	P53	Homo sapiens	46-49
25013761-8	2014	Importantly, the levels of phosphorylation of p53 on Ser15 (p-p53) and acetylation of p53 on Lys379 (acetyl-p53) were increased under osthole treatment.	osthol	134-141	P53	Homo sapiens	62-65
25013761-8	2014	Importantly, the levels of phosphorylation of p53 on Ser15 (p-p53) and acetylation of p53 on Lys379 (acetyl-p53) were increased under osthole treatment.	osthol	134-141	P53	Homo sapiens	62-65
25013761-8	2014	Importantly, the levels of phosphorylation of p53 on Ser15 (p-p53) and acetylation of p53 on Lys379 (acetyl-p53) were increased under osthole treatment.	osthol	134-141	P53	Homo sapiens	62-65
25013761-10	2014	Our study provides novel insights of p53-mediated responses under osthole treatment.	osthol	66-73	P53	Homo sapiens	37-40
24345738-7	2014	Interestingly, we identified a previously undetected point mutation of p53 (p.Arg249Ser) in IST-MES 2, and showed that RITA is also able to reactivate this p53 mutant protein and its apoptotic function.	ist	92-95	P53	Homo sapiens	71-74
12615712-12	2003	In response to UV irradiation, p53R2 and hRRM2 dissociate from p53 and p53R2, and hRRM2 and hRRM1 transfer to the nucleus and form an active RR complex to provide dNDPs for DNA repair.	dndps	163-168	P53	Homo sapiens	31-34
24059226-2	2014	Cell death induced by ellipticine has been shown to engage a p53-dependent pathway, cell cycle arrest, interaction with several kinases and induction of the mitochondrial pathway of apoptotic cell death.	ellipticine	22-33	P53	Homo sapiens	61-64
25140197-0	2014	Decitabine and SAHA-induced apoptosis is accompanied by survivin downregulation and potentiated by ATRA in p53-deficient cells.	Decitabine	0-10	P53	Homo sapiens	107-110
12570841-1	2003	The hydroxy group in 9-hydroxyellipticines increases the apparent affinity for DNA, stabilisation of toposiomerase II-DNA cleavable complex, oxidation to reactive quinone-imine intermediates, phosphorylation of p53 suppressor proteins and cytotoxicity relative to the parent ellipticines.	9-hydroxyellipticine	21-42	P53	Homo sapiens	211-214
25140197-0	2014	Decitabine and SAHA-induced apoptosis is accompanied by survivin downregulation and potentiated by ATRA in p53-deficient cells.	Vorinostat	15-19	P53	Homo sapiens	107-110
25140197-1	2014	While p53-dependent apoptosis is triggered by combination of methyltransferase inhibitor decitabine (DAC) and histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) in leukemic cell line CML-T1, reactive oxygen species (ROS) generation as well as survivin and Bcl-2 deregulation participated in DAC + SAHA-induced apoptosis in p53-deficient HL-60 cell line.	Vorinostat	140-171	P53	Homo sapiens	6-9
25140197-1	2014	While p53-dependent apoptosis is triggered by combination of methyltransferase inhibitor decitabine (DAC) and histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) in leukemic cell line CML-T1, reactive oxygen species (ROS) generation as well as survivin and Bcl-2 deregulation participated in DAC + SAHA-induced apoptosis in p53-deficient HL-60 cell line.	Vorinostat	173-177	P53	Homo sapiens	6-9
25140197-1	2014	While p53-dependent apoptosis is triggered by combination of methyltransferase inhibitor decitabine (DAC) and histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) in leukemic cell line CML-T1, reactive oxygen species (ROS) generation as well as survivin and Bcl-2 deregulation participated in DAC + SAHA-induced apoptosis in p53-deficient HL-60 cell line.	Vorinostat	173-177	P53	Homo sapiens	341-344
25140197-1	2014	While p53-dependent apoptosis is triggered by combination of methyltransferase inhibitor decitabine (DAC) and histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) in leukemic cell line CML-T1, reactive oxygen species (ROS) generation as well as survivin and Bcl-2 deregulation participated in DAC + SAHA-induced apoptosis in p53-deficient HL-60 cell line.	Vorinostat	315-319	P53	Homo sapiens	6-9
12570841-1	2003	The hydroxy group in 9-hydroxyellipticines increases the apparent affinity for DNA, stabilisation of toposiomerase II-DNA cleavable complex, oxidation to reactive quinone-imine intermediates, phosphorylation of p53 suppressor proteins and cytotoxicity relative to the parent ellipticines.	Ellipticines	30-42	P53	Homo sapiens	211-214
12839645-3	2003	The recombinant plasmid pcDNA-p53/p21 was constructed by inserting the p53/p21 fusion gene into eukaryotic expression vector pcDNA3.1 and subsequently transfected into human oral squamous cell carcinoma cell line (Tca8113) with lipofectamine.	tca8113	214-221	P53	Homo sapiens	30-33
24309939-0	2013	Wentilactone A as a novel potential antitumor agent induces apoptosis and G2/M arrest of human lung carcinoma cells, and is mediated by HRas-GTP accumulation to excessively activate the Ras/Raf/ERK/p53-p21 pathway.	wentilactone	0-12	P53	Homo sapiens	198-201
23926120-6	2013	Moreover, 5DT dose-dependently upregulated p53 and p21(Cip1/Waf1), and downregulated Cdc-2 (Cdk-1) and cyclin B1.	gardenin B	10-13	P53	Homo sapiens	43-46
12547280-4	2003	Using the alkaline comet assay, we showed that amsacrine at concentrations from the range 0.01 to 10 microM induced DNA damage in normal human lymphocytes, human promyelocytic leukemia HL-60 cells lacking the p53 gene and murine pro-B lymphoid cells BaF3 expressing BCR/ABL oncogene measured as the increase in percentage tail DNA.	Amsacrine	47-56	P53	Homo sapiens	209-212
24107137-5	2013	Furthermore, the stearyl-rMel/p53 plasmid complex exhibited higher p53 expression and antitumor activity than stearyl-Mel, confirming the fact that stearyl-rMel displayed higher transfection efficiency.	stearyl-rmel	17-29	P53	Homo sapiens	30-33
24107137-5	2013	Furthermore, the stearyl-rMel/p53 plasmid complex exhibited higher p53 expression and antitumor activity than stearyl-Mel, confirming the fact that stearyl-rMel displayed higher transfection efficiency.	stearyl-rmel	17-29	P53	Homo sapiens	67-70
12524540-1	2003	We have previously shown that ASPP1 and ASPP2 are specific activators of p53; one mechanism by which wild-type p53 is tolerated in human breast carcinomas is through loss of ASPP activity.	aspp	30-34	P53	Homo sapiens	73-76
23928048-7	2013	For hairpins containing CTG repeats, the extent of p53 binding was proportional to the size of the repeat.	ctg	24-27	P53	Homo sapiens	51-54
12524540-1	2003	We have previously shown that ASPP1 and ASPP2 are specific activators of p53; one mechanism by which wild-type p53 is tolerated in human breast carcinomas is through loss of ASPP activity.	aspp	30-34	P53	Homo sapiens	111-114
12524540-4	2003	Hence, an inhibitory form of ASPP resembling 53BP2 could allow cells to bypass the tumor-suppressor functions of p53 and the ASPP proteins.	aspp	29-33	P53	Homo sapiens	113-116
23881403-8	2013	Meanwhile, Numb knockdown increased chemoresistance but decreased activated p53 and cleaved-caspase-3 protein expression in gemcitabine-treated Capan-2 cells.	gemcitabine	124-135	P53	Homo sapiens	76-79
12524540-9	2003	iASPP expression is upregulated in human breast carcinomas expressing wild-type p53 and normal levels of ASPP.	aspp	1-5	P53	Homo sapiens	80-83
12499281-5	2002	Carboplatin and oxaliplatin treatment led also to stabilization of p53, whereas none of the platinums changed p73 levels.	Oxaliplatin	16-27	P53	Homo sapiens	67-70
24255851-3	2013	We had earlier demonstrated the hypermethylation of promoter region of p53 and p16 genes in persons exposed to different doses of arsenic.	Arsenic	130-137	P53	Homo sapiens	71-74
12499281-8	2002	Clonogenic survival was enhanced by expressing a dominant negative p53 or ectopic HPV16 E6 in SiHa and HeLa cells treated with IR, carboplatin, or oxaliplatin or with a combination of IR + carboplatin or oxaliplatin.	Oxaliplatin	147-158	P53	Homo sapiens	67-70
23620409-9	2013	Importantly, we show that glioma with mutant p53 is much more sensitive to KU-60019 radiosensitization than genetically matched wild-type glioma.	2-(2,6-dimethylmorpholin-4-yl)-N-(5-(6-morpholin-4-yl-4-oxo-4H-pyran-2-yl)-9H-thioxanthen-2-yl)acetamide	75-83	P53	Homo sapiens	45-48
12473608-9	2002	Up-regulation of p53, bax, and p21 expression was induced in wild-type p53-expressing LNCaP cells only after cryptophycin 52 exposure.	cryptophycin	109-121	P53	Homo sapiens	17-20
23750283-7	2013	Additionally, tumor angiogenesis was inhibited, and p53 protein levels were augmented, by intratumoral injection of the ubiquitin-proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	151-156	P53	Homo sapiens	52-55
24283803-12	2013	CK2 negative regulation of the protein levels of tumor suppressor p53 and activation of the STAT3 anti-apoptotic pathway might antagonize apoptosis and could be involved in acute myeloid leukemia cell resistance to daunorubicin.	Daunorubicin	215-227	P53	Homo sapiens	66-69
12473608-9	2002	Up-regulation of p53, bax, and p21 expression was induced in wild-type p53-expressing LNCaP cells only after cryptophycin 52 exposure.	cryptophycin	109-121	P53	Homo sapiens	71-74
23769318-10	2013	Erlotinib treatment at clinically relevant concentrations induced autophagy (increased LC3II expression, Atg-5/Atg12 conjugation, formation of AVO and p62 degradation) in sensitive NSCLC cell lines, via p53 nuclear translocation, AMPK activation and mTOR suppression.	Erlotinib Hydrochloride	0-9	P53	Homo sapiens	203-206
12480914-13	2002	In practice, p53 and hMLH1 immunohistochemistry discriminated Ca-NIN from L-NIN and H-NIN tumors.	ca-nin	62-68	P53	Homo sapiens	13-16
23839309-6	2013	Treatment of p53-deficient HNSCC cells with the Chk inhibitor AZD7762 sensitizes them to cisplatin through induction of mitotic cell death.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	62-69	P53	Homo sapiens	13-16
23582784-0	2013	Decitabine, a DNA methyltransferases inhibitor, induces cell cycle arrest at G2/M phase through p53-independent pathway in human cancer cells.	Decitabine	0-10	P53	Homo sapiens	96-99
23582784-5	2013	DNA flow cytometric analyses indicated that decitabine induced a G2/M arrest in AGS gastric and A549 lung carcinoma cell lines, which have wild type p53.	Decitabine	44-54	P53	Homo sapiens	149-152
23582784-7	2013	However, similar results were found using the A549 cell line, where decitabine induced a dramatic up-regulation of both p53 and p21 expression, and the increased levels of p21 were associated with increased binding of p21 with Cdks, cyclin A, and cyclin B1.	Decitabine	68-78	P53	Homo sapiens	120-123
23582784-8	2013	Knockdown of p53 by small interfering RNA (siRNA) markedly abolished p53 induction by decitabine in AGS cells, yet p53 siRNA had no attenuating effect on p21 induction.	Decitabine	86-96	P53	Homo sapiens	13-16
23582784-8	2013	Knockdown of p53 by small interfering RNA (siRNA) markedly abolished p53 induction by decitabine in AGS cells, yet p53 siRNA had no attenuating effect on p21 induction.	Decitabine	86-96	P53	Homo sapiens	69-72
23582784-8	2013	Knockdown of p53 by small interfering RNA (siRNA) markedly abolished p53 induction by decitabine in AGS cells, yet p53 siRNA had no attenuating effect on p21 induction.	Decitabine	86-96	P53	Homo sapiens	69-72
24244905-3	2013	In particular, we found that cyclophosphamide stimulates anticancer immune responses upon the perception by the immune system of inflammatory danger signals associated with the death of leukocytes, via p53 and type I interferon-related mechanisms.	Cyclophosphamide	29-45	P53	Homo sapiens	202-205
23582784-10	2013	We also observed that decitabine strongly induced G2/M arrest associated with p21 induction in both p53 allele-null (-/-) HCT116 and wild type p53 (+/+) HCT116 cell lines.	Decitabine	22-32	P53	Homo sapiens	100-103
23582784-10	2013	We also observed that decitabine strongly induced G2/M arrest associated with p21 induction in both p53 allele-null (-/-) HCT116 and wild type p53 (+/+) HCT116 cell lines.	Decitabine	22-32	P53	Homo sapiens	143-146
23648290-7	2013	Exposure of MM cells to [Gem+Clo] also decreased the level of ribosomal RNA (rRNA), which might have resulted in nucleolar stress, as reported previously, and caused a p53-dependent cell death.	gemcitabine	25-28	P53	Homo sapiens	168-171
23376231-6	2013	Using 3D organotypic culture and other assays, we report that the stroma containing p53-deficient fibroblasts could induce the nontumorigenic epithelial cells of oral and ovarian tissue origins to become invasive through reactive nitrogen species (RNS)-mediated release of the cytokine ICAM1.	Reactive Nitrogen Species	221-246	P53	Homo sapiens	84-87
23648290-8	2013	A reduction by approximately 50% in the cytotoxicity of Gem and Clo was observed in the presence of pifithrin alpha, a p53 inhibitor.	gemcitabine	56-59	P53	Homo sapiens	119-122
12457968-9	2002	p21/Waf1, RNase L and p53 are known to have the PEST (proline-glutamic acid-serine-threonine) motif with relatively high scores in their sequences and considered to be sensitive to intracellular degradation.	proline-glutamic acid-serine-threonine	54-92	P53	Homo sapiens	22-25
23998584-2	2013	Apoptosis of HL-60 cells was detected by flow cytometry, the expression of P21, P27 and P53 proteins in HL-60 cells treated with MG132 was assayed by Western blot.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	129-134	P53	Homo sapiens	88-91
23856246-5	2013	Furthermore, we identify pharmacogenomic correlations between specific variants in genes such as TP53, BRAF, ERBBs, and ATAD5 and anticancer agents such as nutlin, vemurafenib, erlotinib, and bleomycin showing one of many ways the data could be used to validate and generate novel hypotheses for further investigation.	Erlotinib Hydrochloride	177-186	P53	Homo sapiens	97-101
23376231-6	2013	Using 3D organotypic culture and other assays, we report that the stroma containing p53-deficient fibroblasts could induce the nontumorigenic epithelial cells of oral and ovarian tissue origins to become invasive through reactive nitrogen species (RNS)-mediated release of the cytokine ICAM1.	Reactive Nitrogen Species	248-251	P53	Homo sapiens	84-87
23376231-7	2013	The p53-deficient fibroblasts have increased RNS production and accumulation of oxidative DNA-damage products associated with specific upregulation of endothelial nitric oxide synthase (eNOS).	Reactive Nitrogen Species	45-48	P53	Homo sapiens	4-7
23376231-9	2013	Our study uncovers the novel mechanism by which redox alteration associated with loss of p53 in stromal fibroblasts functions as a key inducer of epithelial transformation and invasion via RNS-mediated ICAM1 signaling.	Reactive Nitrogen Species	189-192	P53	Homo sapiens	89-92
23540934-3	2013	In this work, using yeast-based assays, it was shown that both xanthones are potential inhibitors of the p53-MDM2 interaction.	Xanthones	63-72	P53	Homo sapiens	105-108
23869206-10	2013	Finally, as an example of a novel design application, we describe the automated design of an oligooxopiperazine that inhibits the p53-MDM2 protein-protein interaction.	oligooxopiperazine	93-111	P53	Homo sapiens	130-133
12221076-4	2002	With the loss of the p53 gene, the levels of phosphorylation of Ser-63 of c-Jun and Thr-183/Tyr-185 of JNK1/2 in p53-/- cells did not increase as markedly as in p53+/+ cells in response to a 1-h treatment with nocodazole or other microtubule-disrupting drugs such as vinblastine and colchicine.	Colchicine	283-293	P53	Homo sapiens	21-24
12221076-4	2002	With the loss of the p53 gene, the levels of phosphorylation of Ser-63 of c-Jun and Thr-183/Tyr-185 of JNK1/2 in p53-/- cells did not increase as markedly as in p53+/+ cells in response to a 1-h treatment with nocodazole or other microtubule-disrupting drugs such as vinblastine and colchicine.	Colchicine	283-293	P53	Homo sapiens	113-116
23593342-5	2013	In the absence of CSK, fulvestrant-induced proteasomal degradation of ERalpha protein was suppressed in both MCF-7 and T47D estrogen-dependent breast cancer cells whereas the TP53-mutated T47D cells were resistant to the cytocidal action of fulvestrant in the presence or absence of CSK.	Fulvestrant	23-34	P53	Homo sapiens	175-179
12221076-4	2002	With the loss of the p53 gene, the levels of phosphorylation of Ser-63 of c-Jun and Thr-183/Tyr-185 of JNK1/2 in p53-/- cells did not increase as markedly as in p53+/+ cells in response to a 1-h treatment with nocodazole or other microtubule-disrupting drugs such as vinblastine and colchicine.	Colchicine	283-293	P53	Homo sapiens	113-116
23579097-8	2013	Taken together, our results provide evidence that BLU can effectively regulate the pro-apoptotic and anti-angiogenic activity of gemcitabine through the direct interaction with vascular endothelial growth factor receptor-2, as well as the up-regulation of p21 and p53 expression.	gemcitabine	129-140	P53	Homo sapiens	264-267
12171899-3	2002	Recently it was reported that triptolide (PG490), a purified compound from Tripterygium, possessed antitumor properties and induced apoptosis by p53-independent mechanisms in a variety of malignant cell lines.	triptolide	30-40	P53	Homo sapiens	145-148
23373735-0	2013	Regulation of carboxylesterase-2 expression by p53 family proteins and enhanced anti-cancer activities among 5-fluorouracil, irinotecan and doxazolidine prodrug.	doxazolidine	140-152	P53	Homo sapiens	47-50
12171899-3	2002	Recently it was reported that triptolide (PG490), a purified compound from Tripterygium, possessed antitumor properties and induced apoptosis by p53-independent mechanisms in a variety of malignant cell lines.	triptolide	42-47	P53	Homo sapiens	145-148
23364678-0	2013	Poly(beta-amino ester) nanoparticle delivery of TP53 has activity against small cell lung cancer in vitro and in vivo.	poly(beta-amino ester)	0-22	P53	Homo sapiens	48-52
23500768-5	2013	Compared with the control group, the astaxanthin-treated groups exhibited downregulated protein expressions of alpha-smooth muscle actin, vimentin, hydroxyproline, and B cell lymphoma/leukemia-2 as well as upregulated protein expressions of E-cadherin and p53 in vitro and in vivo.	astaxanthine	37-48	P53	Homo sapiens	256-259
12171899-9	2002	Higher concentrations of triptolide induced apoptosis that was unexpectedly associated with nuclear accumulation of p53.	triptolide	25-35	P53	Homo sapiens	116-119
12171899-11	2002	Our preclinical studies suggest that triptolide might be an effective preventive as well as therapeutic agent against prostate cancer and that triptolide may activate a functional p53 pathway in prostate cells.	triptolide	143-153	P53	Homo sapiens	180-183
12716463-4	2002	To analyze the mechanism of p53 accumulation by E2, the stability of p53, ERalpha and MDM2 proteins was analyzed in the presence of cycloheximide under an E2-supplemented or -depleted condition.	Cycloheximide	132-145	P53	Homo sapiens	69-72
23635777-7	2013	The addition of SAHA to Btz treatment was synergistic, as SAHA induced early acetylation of p53 and reduced interaction with its negative regulator MDM2, augmenting the effects of Btz.	Vorinostat	16-20	P53	Homo sapiens	92-95
23635777-7	2013	The addition of SAHA to Btz treatment was synergistic, as SAHA induced early acetylation of p53 and reduced interaction with its negative regulator MDM2, augmenting the effects of Btz.	Vorinostat	58-62	P53	Homo sapiens	92-95
23446751-11	2013	Immunohistochemical analysis showed p53 to be expressed significantly more frequently in IES (29 %) than in BilIN-3 (8 %).	Yttrium	89-92	P53	Homo sapiens	36-39
23492773-10	2013	Pretreatment with PUMA and Bak siRNAs abolished miR-128-induced apoptosis in HCT116 p53+/+ and HCT116 p53-/- cells.	mir-128	48-55	P53	Homo sapiens	84-87
23492773-10	2013	Pretreatment with PUMA and Bak siRNAs abolished miR-128-induced apoptosis in HCT116 p53+/+ and HCT116 p53-/- cells.	mir-128	48-55	P53	Homo sapiens	102-105
23492773-11	2013	Taken together, we present the first evidence of miR-128 to be a new component joining the p53 network.	mir-128	49-56	P53	Homo sapiens	91-94
23492773-12	2013	This study emphasizes that miR-128 is a novel mitochondria-targeted miRNA that can be further evaluated as a chemotherapeutic agent for human cancers as it induces apoptosis irrespective of p53 status.	mir-128	27-34	P53	Homo sapiens	190-193
25337543-9	2013	Urushiol induced cytostatic cell growth inhibition via upregulation of the cyclin-dependent kinase inhibitors, p21 (WAF1/CIP1) and p27 (KIP1) proteins and down-regulation of cyclin-dependent kinase 2 and 4 proteins in a p53-independent manner.	urushiol	0-8	P53	Homo sapiens	220-223
12492119-6	2002	PKC activator phorbol 12, 13-dibutyrate attenuated constitutive p53 levels in both HeLa and HeLa/CP cells.	Phorbol 12,13-Dibutyrate	14-39	P53	Homo sapiens	64-67
23536721-2	2013	MK-8776 synergistically potentiated vorinostat-mediated apoptosis in various p53-wt or -deficient leukemia cell lines, whereas p53 knockdown by short hairpin RNA (shRNA) sensitized p53-wt cells to lethality of this regimen.	Vorinostat	36-46	P53	Homo sapiens	77-80
23433851-0	2013	Arginine homozygosity in codon 72 of p53 correlates with failure to imatinib response in chronic myeloid leukemia.	Imatinib Mesylate	68-76	P53	Homo sapiens	37-40
23433851-1	2013	PURPOSE: In this study, the role of the polymorphism at codon 72 of tumor protein p53 gene (TP53) was investigated regarding the response to treatment with imatinib in chronic myeloid leukemia (CML).	Imatinib Mesylate	156-164	P53	Homo sapiens	82-85
12107653-11	2002	Increase of p53 protein was associated with wogonin- and fisetin-induced apoptosis; however, a p53-controlled gene, p21(Waf/Cip-1), was only induced in wogonin- (not fisetin-) treated SK-HEP-1 cells.	fisetin	57-64	P53	Homo sapiens	12-15
23433851-1	2013	PURPOSE: In this study, the role of the polymorphism at codon 72 of tumor protein p53 gene (TP53) was investigated regarding the response to treatment with imatinib in chronic myeloid leukemia (CML).	Imatinib Mesylate	156-164	P53	Homo sapiens	92-96
23433851-10	2013	CONCLUSION: The findings suggest that in CML patients, TP53 codon 72 polymorphism may contribute to a high Sokal score and failure to imatinib treatment.	Imatinib Mesylate	134-142	P53	Homo sapiens	55-59
23455468-2	2013	Some genotoxic stresses are able to induce p53-dependent ceramide accumulation leading to cell death.	Ceramides	57-65	P53	Homo sapiens	43-46
22665057-4	2013	Centriole overduplication assays in aphidicolin-arrested p53-deficient U2OS cells, in which the cell and the centrosome cycles are uncoupled, revealed that the effects of RhoD and its mutants on centrosome duplication and cell cycle are independent.	Aphidicolin	36-47	P53	Homo sapiens	57-60
23471649-4	2013	Because Rb inactivation primes cells for apoptosis by p53-independent induction of procaspases, we postulated that alphaB-crystallin, an inhibitor of procaspase-3 activation, would suppress caspase activation in cells with combined Rb and p53 inactivation.	alphab-crystallin	115-132	P53	Homo sapiens	54-57
23471649-4	2013	Because Rb inactivation primes cells for apoptosis by p53-independent induction of procaspases, we postulated that alphaB-crystallin, an inhibitor of procaspase-3 activation, would suppress caspase activation in cells with combined Rb and p53 inactivation.	alphab-crystallin	115-132	P53	Homo sapiens	239-242
23471649-10	2013	Our results indicate that alphaB-crystallin inhibits caspase activation in cells primed for apoptosis by Rb inactivation and plays a novel oncogenic role in the context of combined Rb and p53 inactivation.	alphab-crystallin	26-43	P53	Homo sapiens	188-191
23455468-6	2013	Furthermore, after highlighting the role and mechanism of action of p53 in apoptosis, we review the association of ceramide and p53 with respect to apoptosis.	Ceramides	115-123	P53	Homo sapiens	128-131
23455468-7	2013	Strikingly, the hypothesis for a direct interaction between ceramide and p53 is less favored.	Ceramides	60-68	P53	Homo sapiens	73-76
12067251-8	2002	Treatment of p53 cDNA with micromolar concentrations of (+/-)-anti-7,8-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydro-benzo[a]pyrene, (anti-BPDE, an ultimate carcinogen) or sub-micromolar concentrations of BP-7,8-dione in the presence of redox-cycling conditions (NADPH and CuCl(2)) also caused p53 mutations in a dose-dependent manner.	cupric chloride	278-285	P53	Homo sapiens	13-16
23455468-8	2013	Recent data suggest that ceramide can act either upstream or downstream of p53 protein through posttranscriptional regulation or through many potential mediators, respectively.	Ceramides	25-33	P53	Homo sapiens	75-78
23450781-9	2013	In contrast, sulphacetamide treatment lowered expression of p53/DRAM pathway in parallel with upregulation of Akt/mTOR pathway promoting cytoprotective autophagy.	Sulfacetamide	13-27	P53	Homo sapiens	60-63
11867746-7	2002	Inhibitors of heat shock protein 90 (hsp90), radicicol and geldanamycin, induced degradation of p53 and suppressed p53-induced apoptosis in normal thymocytes and myeloid leukemic cells.	monorden	45-54	P53	Homo sapiens	96-99
11867746-7	2002	Inhibitors of heat shock protein 90 (hsp90), radicicol and geldanamycin, induced degradation of p53 and suppressed p53-induced apoptosis in normal thymocytes and myeloid leukemic cells.	monorden	45-54	P53	Homo sapiens	115-118
23544166-5	2013	RESULTS: AZD7762 inhibited clonal proliferation in a panel of GBM cell lines and increased radiosensitivity in p53-mutated GBM cell lines to a greater extent compared to p53 wild-type cells.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	9-16	P53	Homo sapiens	111-114
22525275-0	2013	Lenalidomide promotes p53 degradation by inhibiting MDM2 auto-ubiquitination in myelodysplastic syndrome with chromosome 5q deletion.	Lenalidomide	0-12	P53	Homo sapiens	22-25
11859874-10	2002	A non-significant increased risk of breast cancer was observed in the highest exposure level of dieldrin and polychlorinated biphenyls among women who developed a tumor with mutant p53 (odds ratio (OR) = 3.53, 95% confidence interval (CI) = 0.79-15.79 and OR = 3.00, 95% CI = 0.66-13.62).	Polychlorinated Biphenyls	109-134	P53	Homo sapiens	181-184
22525275-4	2013	More importantly, we show that lenalidomide (Len) acts to stabilize MDM2, thereby accelerating p53 degradation.	Lenalidomide	31-43	P53	Homo sapiens	95-98
22525275-4	2013	More importantly, we show that lenalidomide (Len) acts to stabilize MDM2, thereby accelerating p53 degradation.	Lenalidomide	45-48	P53	Homo sapiens	95-98
23079745-10	2013	Furthermore, treatment of HCC cells with 5-aza-2"-deoxycytidine or ectopic expression of wildtype but not mutated p53 restored miR-125a-5p and miR-125b expression and inhibited tumor cell growth, suggesting their regulation by promoter methylation and p53 activity.	Decitabine	41-63	P53	Homo sapiens	252-255
11871818-7	2002	This cotransfection led to selective growth inhibition in the cotransfected p53-mutated cells mediated by ganciclovir, whereas a single transfection of pCALtkL caused nonselective growth inhibition in both cell lines following ganciclovir treatment.	Ganciclovir	106-117	P53	Homo sapiens	76-79
23549458-11	2013	Likewise, the expressions of activating transcription factor NF-kappaB and p53 genes in the arsenic-treated HaCaT cells were significantly higher than that in non-treated cells.	Arsenic	92-99	P53	Homo sapiens	75-78
11878895-10	2001	A partially purified fraction that elutes at 0.6 M KCl from phosphocellulose contains the activity that degrades p53 in a 3C(Pro)-dependent manner.	Potassium Chloride	51-54	P53	Homo sapiens	113-116
23174854-11	2013	Finally, in arsenic-treated HaCaT cells and in BD, a significant increase of dysfunctional p53 was found, and this event correlated with the increase in expression of Aurora-A.	Arsenic	12-19	P53	Homo sapiens	91-94
23201008-0	2013	Cytotoxicity of 5-Aza-2"-deoxycytidine against gastric cancer involves DNA damage in an ATM-P53 dependent signaling pathway and demethylation of P16(INK4A).	Decitabine	16-38	P53	Homo sapiens	92-95
23290777-7	2013	Mechanistic studies indicate that uncoupling ceramide glycosylation can modulate gene expression, decreasing MDR1 through the cSrc/beta-catenin pathway and restoring p53 expression via RNA splicing.	Ceramides	45-53	P53	Homo sapiens	166-169
11557753-0	2001	Inhibition of cell cycle progression by the novel cyclophilin ligand sanglifehrin A is mediated through the NFkappa B-dependent activation of p53.	sanglifehrin A	69-83	P53	Homo sapiens	142-145
24319226-2	2013	For example, 5-azacytidine and decitabine produce remissions and better overall survival in MDS with high-risk chromosome abnormalities at a surprisingly high rate, consistent with experimental observations that noncytotoxic DNA methyltransferase depletion by 5-azacytidine/decitabine can trigger cell cycle exit independently of p53, thus circumventing a basis for resistance to apoptosis-based DNA-damaging therapy.	Decitabine	31-41	P53	Homo sapiens	330-333
23520471-8	2013	Additionally, MK1775 significantly enhances the cytotoxic effect of gemcitabine in sarcoma cells lines with different p53 mutational status.	gemcitabine	68-79	P53	Homo sapiens	118-121
22672779-8	2013	DensNU was strongly correlated to the percentage of p53-marked nuclei in the epidermis, and DensPSB with the HSCORE.	densnu	0-6	P53	Homo sapiens	52-55
11557753-6	2001	We report that sanglifehrin A is capable of activating the tumor suppressor gene p53 at the transcription level, leading to up-regulation of p21 that then binds and inhibits the cylcinE-Cdk2 complex.	sanglifehrin A	15-29	P53	Homo sapiens	81-84
23739596-5	2013	At the same time, GN, but not gamma-Sch, inhibited the phosphorylation of checkpoint proteins such as p53, structural maintenance of chromosomes 1, and checkpoint kinase 1 in UV-irradiated cells.	schizandrin B	18-20	P53	Homo sapiens	102-105
22933333-9	2012	Our findings also suggest that sequencing of the TP53 gene should be included in the study of patients with del(5q) as a single abnormality or in complex karyotype before lenalidomide treatment.	Lenalidomide	171-183	P53	Homo sapiens	49-53
11557753-7	2001	Further analysis of different elements in the p53 promoter showed that sanglifehrin A activates p53 transcription primarily through the activation of the transcription factor NFkappaB by activating IkappaB kinase in a manner that is similar to several genotoxic agents.	sanglifehrin A	71-85	P53	Homo sapiens	46-49
11557753-7	2001	Further analysis of different elements in the p53 promoter showed that sanglifehrin A activates p53 transcription primarily through the activation of the transcription factor NFkappaB by activating IkappaB kinase in a manner that is similar to several genotoxic agents.	sanglifehrin A	71-85	P53	Homo sapiens	96-99
11745415-2	2001	This process was supposed to involve the tumor suppressor gene p53 as it was described that p53 negative cells were more sensitive to checkpoint inhibition by caffeine than the wildtype phenotype.	Caffeine	159-167	P53	Homo sapiens	63-66
23153533-2	2012	We found that the glycolytic enzyme phosphoglycerate mutase 1 (PGAM1), commonly upregulated in human cancers due to loss of TP53, contributes to biosynthesis regulation in part by controlling intracellular levels of its substrate, 3-phosphoglycerate (3-PG), and product, 2-phosphoglycerate (2-PG).	3-phosphoglycerate	231-249	P53	Homo sapiens	124-128
22955915-1	2012	TP53 mutation is an independent marker of poor prognosis in patients with diffuse large B-cell lymphoma (DLBCL) treated with cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone (CHOP) therapy.	Cyclophosphamide	125-141	P53	Homo sapiens	0-4
23127292-0	2012	Prognostic interaction between expression of p53 and estrogen receptor in patients with node-negative breast cancer: results from IBCSG Trials VIII and IX.	ibcsg	130-135	P53	Homo sapiens	45-48
23131146-4	2012	In contrast, while TP53 mutations have shown to predict response to cyclophosphamide high dose therapy, mutations in general have been associated with anthracycline resistance in human breast cancers.	Cyclophosphamide	68-84	P53	Homo sapiens	19-23
23527225-0	2013	The anti-melanoma activity of dinaciclib, a cyclin-dependent kinase inhibitor, is dependent on p53 signaling.	dinaciclib	30-40	P53	Homo sapiens	95-98
23527225-6	2013	Further mechanistic studies revealed that dinaciclib induces p53 expression whilst simultaneously downregulating the expression of the anti-apoptotic factors Mcl-1 and XIAP.	dinaciclib	42-52	P53	Homo sapiens	61-64
23527225-8	2013	Knockdown of p53 completely abolished the induction of apoptosis seen following dinaciclib treatment as shown by a lack of annexin-V staining and caspase-3 cleavage.	dinaciclib	80-90	P53	Homo sapiens	13-16
23527225-9	2013	Altogether, these data show that dinaciclib induces apoptosis in a large panel of melanoma cell lines through a mechanism requiring p53 expression.	dinaciclib	33-43	P53	Homo sapiens	132-135
23010984-1	2012	An efficient electrochemical approach is developed for ultrasensitive profiling of the methylation status of the p53 tumor suppressor gene based on a label-free biosensor in combination with bisulfite conversion.	hydrogen sulfite	191-200	P53	Homo sapiens	113-116
22973058-3	2012	Regardless of the breast cancer subtype tested or the p53 status of the cells, 8-NH(2)-Ado was more cytotoxic than either gemcitabine or etoposide.	8-nh(2)-ado	79-90	P53	Homo sapiens	54-57
11745415-2	2001	This process was supposed to involve the tumor suppressor gene p53 as it was described that p53 negative cells were more sensitive to checkpoint inhibition by caffeine than the wildtype phenotype.	Caffeine	159-167	P53	Homo sapiens	92-95
11745415-11	2001	In addition, caffeine restored a G1 delay after irradiation in the cell lines with abrogated p53 functions.	Caffeine	13-21	P53	Homo sapiens	93-96
11576999-9	2001	p53 null human lung cancer H1299 cells transfected with an ecdysone-inducible p53 exhibited equivalent sensitivity to tachpyridine in the presence and absence of p53, demonstrating the lack of requirement for p53 in an isogenic cell system.	Ecdysone	59-67	P53	Homo sapiens	0-3
22991965-5	2012	The ordering of the N-terminus upon binding of the piperidinones extends the current model of MDM2-p53 interaction and provides a new route to rational design of superior inhibitors.	2-piperidone	51-64	P53	Homo sapiens	99-102
22575263-8	2012	These data point to wood dust exposure as the causal factor in the mutagenesis of TP53, possibly caused by reactive nitrogen species generated through a chronic inflammatory process.	Reactive Nitrogen Species	107-132	P53	Homo sapiens	82-86
23086311-7	2012	The in vitro cell growth inhibition effect of CaCO(3)-KALA-p53-DOX nanoparticles was evaluated by MTT assay.	monooxyethylene trimethylolpropane tristearate	98-101	P53	Homo sapiens	59-62
11576999-9	2001	p53 null human lung cancer H1299 cells transfected with an ecdysone-inducible p53 exhibited equivalent sensitivity to tachpyridine in the presence and absence of p53, demonstrating the lack of requirement for p53 in an isogenic cell system.	Ecdysone	59-67	P53	Homo sapiens	78-81
11576999-9	2001	p53 null human lung cancer H1299 cells transfected with an ecdysone-inducible p53 exhibited equivalent sensitivity to tachpyridine in the presence and absence of p53, demonstrating the lack of requirement for p53 in an isogenic cell system.	Ecdysone	59-67	P53	Homo sapiens	78-81
22843330-4	2012	Focused gene expression array analysis followed by immunoblot detection revealed that DP rapidly activates the cytotoxic unfolded protein response (UPR; involving phospho-PERK, phospho-eIF2alpha, Grp78, CHOP, and Hsp70) and the mitochondrial pathway of apoptosis with p53 upregulation and modulation of Bcl-2 family members (involving Noxa, Mcl-1, and Bcl-2).	dp	86-88	P53	Homo sapiens	268-271
22825736-0	2012	The Chk1 inhibitor AZD7762 sensitises p53 mutant breast cancer cells to radiation in vitro and in vivo.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	19-26	P53	Homo sapiens	38-41
22903553-12	2012	Taken together, these results provide evidence that sMEK1 can effectively regulate the pro-apoptotic activity of gemcitabine through the up-regulation of p53 expression.	gemcitabine	113-124	P53	Homo sapiens	154-157
11576999-9	2001	p53 null human lung cancer H1299 cells transfected with an ecdysone-inducible p53 exhibited equivalent sensitivity to tachpyridine in the presence and absence of p53, demonstrating the lack of requirement for p53 in an isogenic cell system.	Ecdysone	59-67	P53	Homo sapiens	78-81
22678742-4	2012	Here, we found that PQ significantly decreases cell viability, increases sub-G1 hypodiploids DNA contents and caspase 3/7 activity in lung alveolar epithelial cell-derived L2 cells, which also caused mitochondrial dysfunction, and decreased the mRNA expression of Bcl-2 and increased that of Bax, Bak, and p53.	Primaquine	20-22	P53	Homo sapiens	306-309
22678742-10	2012	Cells transfected with Nrf-2 siRNA significantly reversed the PQ-induced toxicity, including depolarization of MMP, increased the Bax, Bak, p53 mRNAs expression, decreased the Bcl-2 mRNA expression, increased the caspase 3/7 activity,  Grp78, CHOP, and caspase-12 mRNAs and protein expression, and decreased that of pro-caspase-3.	Primaquine	62-64	P53	Homo sapiens	140-143
22825736-3	2012	In the present study, we aimed to demonstrate for the first time, that AZD7762 not only promotes radiation-induced apoptosis and mitotic catastrophe of p53 mutant T47D breast cancer cells in vitro, but also delays their xenograft growth in response to radiation in vivo.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	71-78	P53	Homo sapiens	152-155
22825736-5	2012	These results suggest that AZD7762 may effectively abrogate radiation-induced G2/M arrest and inhibit radiation damage repair in conferring radiosensitivity on p53 mutant T47D breast cancer cells, by promoting radiation-induced apoptosis and mitotic catastrophe.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	27-34	P53	Homo sapiens	160-163
11677656-8	2001	Interestingly, caffeine and other methyl xanthines preferentially radiosensitize cells that lack normal p53 function.	Caffeine	15-23	P53	Homo sapiens	104-107
22829200-9	2012	Interestingly, alpha-tocopherol (vitamin E) treatment, but not other antioxidants, rescued SDH(var+) cells from apoptosis resistance and protected SDH(var+) cells from oxidative damage such as decreased lipid peroxidation as well as partially recovered p53 expression and NAD/NADH levels.	Vitamin E	33-42	P53	Homo sapiens	253-256
11447225-3	2001	Induction of phosphorylation of p53 on multiple serine residues by H(2)O(2) was caffeine-sensitive and blocked in ATM(-/-) cells.	Caffeine	80-88	P53	Homo sapiens	32-35
22696202-7	2012	We found that BCR-ABL expression increases K317 acetylation of p53 and is able to prevent a drop in acetylation observed upon DNA damage, followed by translocation of p53 to the cytoplasm and by Bax activation.	1,2-cyclohexanedione	43-47	P53	Homo sapiens	63-66
22139992-0	2012	Potentiation of a p53-SLP vaccine by cyclophosphamide in ovarian cancer: a single-arm phase II study.	Cyclophosphamide	37-53	P53	Homo sapiens	18-21
22139992-1	2012	The purpose of the current phase II single-arm clinical trial was to evaluate whether pretreatment with low-dose cyclophosphamide improves immunogenicity of a p53-synthetic long peptide (SLP) vaccine in patients with recurrent ovarian cancer.	Cyclophosphamide	113-129	P53	Homo sapiens	159-162
22139992-10	2012	The outcome of this phase II trial warrants new studies on the use of low-dose cyclophosphamide to potentiate the immunogenicity of the p53-SLP vaccine or other antitumor vaccines.	Cyclophosphamide	79-95	P53	Homo sapiens	136-139
11559571-3	2001	In contrast, cells without p53 or cells expressing a DNA-binding mutant of p53 retain the provirus and become susceptible to killing by ganciclovir.	Ganciclovir	136-147	P53	Homo sapiens	75-78
22710877-7	2012	Tumors from nude mice injected with BxPC-3 PaCa cells and treated with a combination of oridonin and gemcitabine showed a significant upregulation in p38 and p53 activation (P&lt;0.05 vs. control, P&lt;0.05 vs. gemcitabine or oridonin alone).	gemcitabine	101-112	P53	Homo sapiens	158-161
22710877-8	2012	Taken together, our results demonstrate that oridonin can potentiate the effects of gemcitabine in PaCa through the mitogen-activated protein kinase (MAPK)-p38 signaling pathway, which is dependent on p53 activation.	gemcitabine	84-95	P53	Homo sapiens	201-204
22763759-6	2012	However, the growth-inhibitory activity of vincristine, doxorubicin, carboplatin, etoposide, and temozolomide was significantly impaired by silencing of TP53.	Carboplatin	69-80	P53	Homo sapiens	153-157
23139965-1	2012	OBJECTIVE: To investigate and compare the prognostic value of P53 and Ki67 markers in patients with breast cancer in Sabzevar, north east of Iran.	sabzevar	117-125	P53	Homo sapiens	62-65
11494027-6	2001	Twenty-two of 24 (92%) sero-positive patients had mutations in their p53 gene while only 22 of 64 (34%) sero-negative patients had p53 mutations (p&lt;0.01).	sero	23-27	P53	Homo sapiens	69-72
11494027-10	2001	Most of the p53 deletions in sero-negative patients were however located outside conserved regions (seven of eight deletions).	sero	29-33	P53	Homo sapiens	12-15
22687606-6	2012	In SKOV-3 cells DMU-212 caused up-regulation of pro-apoptotic Bax, Apaf-1 and p53 genes, specific to intrinsic pathway of apoptosis, and a decrease in Bcl-2 and Bcl 2110 mRNA expressions.	dmu	16-19	P53	Homo sapiens	78-81
23141446-14	2012	There might be antagonistic effect between p53 and 5-aza-dC.	Decitabine	51-59	P53	Homo sapiens	43-46
11494027-13	2001	Cellular protein binding to p53 or individual differences of major histocompatibility complex based presentation of p53 protein sequences by immune cells is therefore the most likely explanation between sero-negative and sero-positive patients.	sero	203-207	P53	Homo sapiens	28-31
22349266-2	2012	However, absence of a p53-mediated response does not necessarily abrogate programmed cell death, due to the existence of p53-independent apoptotic pathways, such as those mediated by the pro-apoptotic molecule ceramide.	Ceramides	210-218	P53	Homo sapiens	22-25
22349266-2	2012	However, absence of a p53-mediated response does not necessarily abrogate programmed cell death, due to the existence of p53-independent apoptotic pathways, such as those mediated by the pro-apoptotic molecule ceramide.	Ceramides	210-218	P53	Homo sapiens	121-124
11494027-13	2001	Cellular protein binding to p53 or individual differences of major histocompatibility complex based presentation of p53 protein sequences by immune cells is therefore the most likely explanation between sero-negative and sero-positive patients.	sero	203-207	P53	Homo sapiens	116-119
22349266-4	2012	When treated with mitomycin C, p53-deficient cells, but not p53-expressing cells, showed a marked increase in ceramide levels.	Ceramides	110-118	P53	Homo sapiens	31-34
22675170-13	2012	Clinical trials evaluating EZH2-targeting agents such as DZNep should consider stratifying patients with gastric cancer by their TP53 genomic status.	3-deazaneplanocin	57-62	P53	Homo sapiens	129-133
11494027-13	2001	Cellular protein binding to p53 or individual differences of major histocompatibility complex based presentation of p53 protein sequences by immune cells is therefore the most likely explanation between sero-negative and sero-positive patients.	sero	221-225	P53	Homo sapiens	28-31
22547059-0	2012	RNA processing and modification protein, carbon catabolite repression 4 (Ccr4), arrests the cell cycle through p21-dependent and p53-independent pathway.	carbon catabolite	41-58	P53	Homo sapiens	129-132
22564437-6	2012	Of the screened compounds, acriflavine (ACF) significantly increased p53-Luc activity in a concentration-dependent manner without causing toxicity.	Acriflavine	27-38	P53	Homo sapiens	69-72
11494027-13	2001	Cellular protein binding to p53 or individual differences of major histocompatibility complex based presentation of p53 protein sequences by immune cells is therefore the most likely explanation between sero-negative and sero-positive patients.	sero	221-225	P53	Homo sapiens	116-119
22564437-6	2012	Of the screened compounds, acriflavine (ACF) significantly increased p53-Luc activity in a concentration-dependent manner without causing toxicity.	Acriflavine	40-43	P53	Homo sapiens	69-72
11375905-0	2001	Deoxycholic acid suppresses p53 by stimulating proteasome-mediated p53 protein degradation.	Deoxycholic Acid	0-16	P53	Homo sapiens	28-31
22397410-1	2012	In the present study, we observed that the Golgi-SNARE (soluble N-ethylmaleimide-sensitive fusion protein-attachment protein receptor) GS28 forms a complex with p53 in HEK (human embryonic kidney)-293 cells.	Ethylmaleimide	64-80	P53	Homo sapiens	161-164
11375905-0	2001	Deoxycholic acid suppresses p53 by stimulating proteasome-mediated p53 protein degradation.	Deoxycholic Acid	0-16	P53	Homo sapiens	67-70
11697035-1	2001	The mechanism of metal-mediated DNA damage by carcinogenic danthron (1,8-dihydroxyanthraquinone) and anthraquinone was investigated by the DNA sequencing technique using 32P-labeled human DNA fragments obtained from the human c-Ha-ras-1 protooncogene and the p53 tumor suppressor gene.	danthron	59-67	P53	Homo sapiens	259-262
23359768-9	2012	Zinc-citrate compound increased the expression of P21(waf1) and P53, and reduced the expression of Bcl-2 and Bcl-xL proteins but induced the expression of Bax protein.	Zinc citrate	0-12	P53	Homo sapiens	64-67
22764405-3	2012	Thermally crosslinked SPIONs (TCL-SPIONs) were conjugated with branched polyethylenimine (PEI 1800 Da) by EDC-NHS chemistry for p53 plasmid DNA delivery.	Polyethyleneimine	72-88	P53	Homo sapiens	128-131
21968939-6	2012	Apoptosis in lenalidomide/docetaxel-treated cells was increased by 2.2-fold over single agent docetaxel and a corresponding increase in p53, p38, and BAD activation was observed in Western blots (P &lt; 0.001).	Lenalidomide	13-25	P53	Homo sapiens	136-139
22474335-6	2012	The ladders of polyubiquitinated p53 were not detectable in the presence of the proteasome inhibitor MG132 and were less sensitive to proteasome-mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	101-106	P53	Homo sapiens	33-36
11336476-6	2001	Transient co-transfection data indicate the possibility that DeltaNp73L can inhibit p53-, and more preferentially, p51-mediated transactivation.	deltanp73l	61-71	P53	Homo sapiens	84-87
22509835-0	2012	Quercetin enhancement of arsenic-induced apoptosis via stimulating ROS-dependent p53 protein ubiquitination in human HaCaT keratinocytes.	Arsenic	25-32	P53	Homo sapiens	81-84
22509835-5	2012	The decrease in the p53 protein by QUE/As(+3) was reversed by adding the proteasome inhibitor, MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	95-100	P53	Homo sapiens	20-23
22509835-8	2012	QUE plus As(+3) stimulation of apoptosis in human HaCaT keratinocytes via activating ROS-dependent p53 protein ubiquitination may offer a rationale for the use of QUE to improve the clinical efficacy of arsenics in treating psoriasis.	Arsenic	203-211	P53	Homo sapiens	99-102
22493413-12	2012	CONCLUSION: Alemtuzumab plus methypredisolone is the most effective induction regimen hitherto reported in TP53-deleted CLL.	methypredisolone	29-45	P53	Homo sapiens	107-111
22074401-0	2012	Gallium compound GaQ(3) -induced Ca(2+)  signalling triggers p53-dependent and -independent apoptosis in cancer cells.	Gallium	0-7	P53	Homo sapiens	61-64
11345135-7	2001	These data suggest that pancreatic cancer cells possess a p53-independent mechanism of CD95R and CD95L surface upregulation and that surface expression of CD95R is not predictive of apoptotic function.	cd95r	87-92	P53	Homo sapiens	58-61
21706156-0	2012	MDM2 SNP309 and TP53 R72P associated with severe and febrile neutropenia in breast cancer patients treated with 5-FU/epirubicin/cyclophosphamide.	Cyclophosphamide	128-144	P53	Homo sapiens	16-20
20978925-8	2012	CG200745 increased acetylation of p53 lysine residues K320, K373, and K382.	C12H10N6O3S	70-74	P53	Homo sapiens	34-37
22353361-0	2012	Involvement of p53 in gemcitabine mediated cytotoxicity and radiosensitivity in breast cancer cell lines.	gemcitabine	22-33	P53	Homo sapiens	15-18
22353361-9	2012	dFdCyd combined with radiation reduces the efficacy of chemo-radiotherapy in p53 mutated cells.	gemcitabine	0-6	P53	Homo sapiens	77-80
22353361-10	2012	Therefore, p53-mutated cancer could be a counter-indication for radiation-gemcitabine combined treatment.	gemcitabine	74-85	P53	Homo sapiens	11-14
11783085-5	2001	Induction of p53 expression could be blocked by phosphorothiate analogs of antisense oligonucleotides to NF-kappa B p65 and LMP1, but not by NF-kappa B p50.	phosphorothiate	48-63	P53	Homo sapiens	13-16
22723163-2	2012	METHODS: Recombinant plasmid of mutant p53 gene-targeting siRNA was transfected into gastric cancer SGC7901 cells by Lipofectamine(TM)2000.	Lipofectamine	117-130	P53	Homo sapiens	39-42
22227409-7	2012	In addition, treatment with MG132 blocked MDM2-mediated p53 ubiquitination and degradation, and led to accumulation of p53 in Gli3 siRNA-overexpressing cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	P53	Homo sapiens	56-59
22227409-7	2012	In addition, treatment with MG132 blocked MDM2-mediated p53 ubiquitination and degradation, and led to accumulation of p53 in Gli3 siRNA-overexpressing cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	P53	Homo sapiens	119-122
11302731-5	2001	On the other hand, treatment with wortmannin or caffeine suppressed CdCl(2)-induced Ser 15 phosphorylation and accumulation of p53 protein.	Caffeine	48-56	P53	Homo sapiens	127-130
22134754-7	2012	Belinostat induced the expression of p21 and             p27, acetylation of p53 and G2/M arrest associated with Bcl2 and Bcl-Xl downmodulation             and significant reduction of survivin, IAPs and Akt/pAkt and increased caspase-8             and -9 expression/activity.	belinostat	0-10	P53	Homo sapiens	77-80
22369882-8	2012	Human granulosa cells also showed dose-dependent morphological changes and reduced p53 expression levels after exposure to mancozeb.	mancozeb	123-131	P53	Homo sapiens	83-86
11258898-7	2001	T(4)-induced nuclear complexing of p53 and MAPK was inhibited by PD 98059 (PD) and U0126, two MAPK kinase (MEK) inhibitors, and was absent in cells treated with MEK antisense oligonucleotide and in dominant negative Ras cells.	U 0126	83-88	P53	Homo sapiens	35-38
21455989-0	2012	The DNA methyltransferase inhibitors zebularine and decitabine induce mitochondria-mediated apoptosis and DNA damage in p53 mutant leukemic T cells.	Decitabine	52-62	P53	Homo sapiens	120-123
21455989-11	2012	Our results suggest that the mitochondrial apoptotic pathway activated by decitabine and zebularine in p53 mutant leukemic T cells depends mainly on the induction of DNA damage.	Decitabine	74-84	P53	Homo sapiens	103-106
22159450-4	2012	qPCR of cell cycle regulatory             and apoptotic genes shows that CG-1521 and SAHA modulate similar cohorts of p53-responsive             genes, however, the levels of induction and the timing of the induction differs             significantly between the 2 inhibitors.	Vorinostat	85-89	P53	Homo sapiens	118-121
22340598-0	2012	Activation of p53 by SIRT1 inhibition enhances elimination of CML leukemia stem cells in combination with imatinib.	Imatinib Mesylate	106-114	P53	Homo sapiens	14-17
22109882-10	2012	An apoptosis protein array showed that the 1,25-D3 and lenalidomide combination increased pro-apoptotic proteins (phosphorylated p53) and decreased BCL-2 expression.	Lenalidomide	55-67	P53	Homo sapiens	129-132
22041920-11	2012	Among these changes, RT-PCR and Western blotting showed that expression of tumor protein 53-induced nuclear protein 1, a gene regulating cell death and DNA repair, was increased by gemcitabine treatment and substantially decreased by GSK3beta inhibition.	gemcitabine	181-192	P53	Homo sapiens	75-91
11240376-0	2001	Deoxycholate induces DNA damage and apoptosis in human colon epithelial cells expressing either mutant or wild-type p53.	Deoxycholic Acid	0-12	P53	Homo sapiens	116-119
20680659-4	2012	We found that nutlin-3 and HDACi cooperated to induce cell death in the p53 wild-type cell lines A549 and A2780, but not in the p53 null cell line PC-3, as assessed by Alamar Blue assay and flow cytometric analyses of propidium iodide uptake and mitochondrial depolarization.	Propidium	218-234	P53	Homo sapiens	72-75
20680659-8	2012	We observed vorinostat to induce p53 hyperacetylation, to reduce the constitutive gene expression of MDM2 and MDM4, and to counteract the nutlin-3-induced upregulation of MDM2 gene expression.	Vorinostat	12-22	P53	Homo sapiens	33-36
24319543-0	2012	C-6 Ceramide Induces p53 Dependent Apoptosis in Human Astrocytoma Grade4 (Glioblastoma Multiforme) Cells.	Ceramides	4-12	P53	Homo sapiens	21-24
11544835-4	2001	The present investigation deals with feasibility of gluthoxim-induced apoptosis in tumor cell cultures, including human myeloleukema cells HL60 which lack protein p53 gene, so crucial for apoptosis.	gluthoxim	52-61	P53	Homo sapiens	163-166
22056254-9	2012	CONCLUSION: Based on these in vitro data, the agonist (64)Cu-CB-TE2A-Y3-TATE demonstrates the most promise as an agent for targeted radiotherapy in p53 positive, SSTr2-positive tumors.	diflorasone	72-76	P53	Homo sapiens	148-151
22662219-8	2012	The commonly used imatinib-sensitive cell lines GIST882 and GIST-T1 were shown to harbor defective p53 and therefore failed to respond to nutlin-3 treatment.	Imatinib Mesylate	18-26	P53	Homo sapiens	99-102
21982800-0	2011	The polymorphisms of P53 codon 72 and MDM2 SNP309 and renal cell carcinoma risk in a low arsenic exposure area.	Arsenic	89-96	P53	Homo sapiens	21-24
21982800-5	2011	RCC patients with the p53Arg/Arg genotype had a signicantly low percentage of inorganic arsenic, a low percentage of monomethylarsonic acid (MMA), and a high percentage of dimethylarsinic acid (DMA), which indicates efcient arsenic methylation capacity.	Arsenic	88-95	P53	Homo sapiens	22-25
11544835-7	2001	Gluthoxim induction of cell death was demonstrated in both cell lines; however, apoptosis in cells C8 (with intact gene p53) was much more pronounced than in cells A4 without this gene.	gluthoxim	0-9	P53	Homo sapiens	120-123
11090099-0	2000	Effect of saikosaponin, a triterpene saponin, on apoptosis in lymphocytes: association with c-myc, p53, and bcl-2 mRNA.	saikosaponin D	10-22	P53	Homo sapiens	99-102
20499132-7	2011	Moreover, this effect was not restricted to cell lines as LQB-118 produced significant apoptosis rate in cells from CML patients exhibiting multifactorial drug resistance phenotype such as P-glycoprotein, MRP1 and p53 overexpression.	LQB 118	58-65	P53	Homo sapiens	214-217
22130357-4	2012	Further, taurine promoted endothelial cell cycle progression to the S and G2/M phases by up-regulating the positive cell cycle proteins, particularly cyclins D1 and B, as well as down-regulating the negative cell cycle proteins, p53 and p21(WAF1/CIP1), resulting in Rb phosphorylation.	Taurine	9-16	P53	Homo sapiens	229-232
11090099-21	2000	It is suggested that the apoptotic effect of saikosaponin-d may be partly mediated by increases in c-myc and p53 mRNA levels accompanied by a decrease in bcl-2 mRNA level.	saikosaponin D	45-59	P53	Homo sapiens	109-112
21907236-0	2011	Fluazinam-induced apoptosis of SH-SY5Y cells is mediated by p53 and Bcl-2 family proteins.	fluazinam	0-9	P53	Homo sapiens	60-63
23101268-4	2012	Pre-treatment with NU7026 resulted into decreased activation of checkpoint kinase-2 (Thr68), p53 (Ser15 and Ser392), and histone H2A.X (Ser139) 2 hours after irradiation.	2-(morpholin-4-yl)benzo(h)chromen-4-one	19-25	P53	Homo sapiens	93-96
11080661-0	2000	The effect of dibenzo[a,1]pyrene and benzo[a]pyrene on human diploid lung fibroblasts: the induction of DNA adducts, expression of p53 and p21(WAF1) proteins and cell cycle distribution.	dibenzo[a,1]pyrene	14-32	P53	Homo sapiens	131-134
10922372-0	2000	Vanadate induces p53 transactivation through hydrogen peroxide and causes apoptosis.	Vanadates	0-8	P53	Homo sapiens	17-20
22393286-7	2012	Both the mRNA and protein levels of tumor suppressor gene p53 and apoptotic gene bax were upregulated while the antiapoptotic gene bcl-2 was downregulated in ZnO NP-treated HepG2 cells.	zno np	158-164	P53	Homo sapiens	58-61
21880715-7	2011	In addition, a unique EDEE motif between the loop of anti-parallel beta7 and beta8 sheets of the SET core not only interacts with p53 substrate but also forms a hydrogen bond network with residues from CTD.	edee	22-26	P53	Homo sapiens	130-133
21880715-8	2011	These observations suggest that the tetratricopeptide repeat and EDEE motif may play an important role in determining p53 substrate binding specificity.	edee	65-69	P53	Homo sapiens	118-121
10922372-3	2000	The present study investigated the vanadate-induced p53 activation and involvement of reactive oxygen species (ROS) in p53 activation as well as the role of p53 in apoptosis induction by vanadate.	Vanadates	35-43	P53	Homo sapiens	52-55
21946324-8	2011	Pretreatment with the specific P38MAPK inhibitor SB203580 (5 mumol/L) significantly reduced CrTX-induced apoptosis and cleaved caspase-3 level, but G(1) arrest remained unchanged and highly expressed p53 sustained.	SB 203580	49-57	P53	Homo sapiens	200-203
22429346-4	2012	Hypermethylation of the promoters of the p53-BAX mitochondrial apoptosis genes cyclin-dependent kinase inhibitor 2A (CDKN2A), death-associated protein kinase 1 (DAPK1) and PYD and CARD domain containing (PYCARD) was detected by methylation-specific polymerase chain reaction, with and without DAC treatment.	Decitabine	293-296	P53	Homo sapiens	41-44
22429346-8	2012	CONCLUSIONS: DAC induces apoptosis of QBC939 cells by reactivation of hypermethylated p53-BAX mitchondrial apoptosis genes in cholangiocarcinoma cells.	Decitabine	13-16	P53	Homo sapiens	86-89
10922372-4	2000	Exposure of mouse epidermal JB6 cells to vanadate led to transactivation of p53 activity in a time- and dose-dependent manner.	Vanadates	41-49	P53	Homo sapiens	76-79
10922372-6	2000	Scavenging of vanadate-induced H(2)O(2) by N-acetyl-l-cysteine (a general antioxidant) or catalase (a specific H(2)O(2) inhibitor), or the chelation of vanadate by deferoxamine, resulted in inhibition of p53 activation and cell mitochondrial damage.	Vanadates	14-22	P53	Homo sapiens	204-207
10922372-8	2000	Furthermore, vanadate-induced apoptosis occurred in cells expressing wild-type p53 (p53+/+) but was very weak in p53-deficient (p53-/-) cells.	Vanadates	13-21	P53	Homo sapiens	79-82
21993662-0	2012	Plumbagin induces apoptosis via the p53 pathway and generation of reactive             oxygen species in human osteosarcoma cells.	plumbagin	0-9	P53	Homo sapiens	36-39
21868512-10	2011	The p53 pathway was involved in the synergism of RAD001 and carboplatin on breast cancer cell proliferation and apoptosis, since the synergistic effect was demonstrated in all tested breast cancer cell lines with wild-type p53 and the use of p53 inhibitor partially antagonized the effect of RAD001 and carboplatin on p53 and p21 expression, as well as their inhibitory effect on cell proliferation.	Carboplatin	60-71	P53	Homo sapiens	4-7
21868512-10	2011	The p53 pathway was involved in the synergism of RAD001 and carboplatin on breast cancer cell proliferation and apoptosis, since the synergistic effect was demonstrated in all tested breast cancer cell lines with wild-type p53 and the use of p53 inhibitor partially antagonized the effect of RAD001 and carboplatin on p53 and p21 expression, as well as their inhibitory effect on cell proliferation.	Carboplatin	60-71	P53	Homo sapiens	223-226
21868512-10	2011	The p53 pathway was involved in the synergism of RAD001 and carboplatin on breast cancer cell proliferation and apoptosis, since the synergistic effect was demonstrated in all tested breast cancer cell lines with wild-type p53 and the use of p53 inhibitor partially antagonized the effect of RAD001 and carboplatin on p53 and p21 expression, as well as their inhibitory effect on cell proliferation.	Carboplatin	60-71	P53	Homo sapiens	223-226
21868512-10	2011	The p53 pathway was involved in the synergism of RAD001 and carboplatin on breast cancer cell proliferation and apoptosis, since the synergistic effect was demonstrated in all tested breast cancer cell lines with wild-type p53 and the use of p53 inhibitor partially antagonized the effect of RAD001 and carboplatin on p53 and p21 expression, as well as their inhibitory effect on cell proliferation.	Carboplatin	60-71	P53	Homo sapiens	223-226
21868512-10	2011	The p53 pathway was involved in the synergism of RAD001 and carboplatin on breast cancer cell proliferation and apoptosis, since the synergistic effect was demonstrated in all tested breast cancer cell lines with wild-type p53 and the use of p53 inhibitor partially antagonized the effect of RAD001 and carboplatin on p53 and p21 expression, as well as their inhibitory effect on cell proliferation.	Carboplatin	303-314	P53	Homo sapiens	4-7
21993662-6	2012	PL up-regulated the expression of p53 in U2OS cells and p21 in the two osteosarcoma cell lines causing cell cycle arrest by decreasing the expression of murine double minute 2 (MDM2)/cyclin B1 and cyclin D1.	plumbagin	0-2	P53	Homo sapiens	34-37
10922372-8	2000	Furthermore, vanadate-induced apoptosis occurred in cells expressing wild-type p53 (p53+/+) but was very weak in p53-deficient (p53-/-) cells.	Vanadates	13-21	P53	Homo sapiens	84-87
11052474-7	2000	In flat-type carcinoma terminal deoxynucleotide transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling index in the p53 protein overexpression group was significantly smaller than that in the p53 protein-negative group (P &lt; 0.05).	deoxyuridine triphosphate-biotin	69-101	P53	Homo sapiens	133-136
22550391-8	2012	Western blot and quantitative analysis showed that both p53 and caspase-8 increased after cell exposure to cadmium chloride.	Cadmium Chloride	107-123	P53	Homo sapiens	56-59
22550391-10	2012	CONCLUSIONS: Cadmium chloride induced cytotoxicity and apoptosis in human lens epithelial cells and the mechanism of apoptosis involve an increased expression of p53 and caspase-8.	Cadmium Chloride	13-29	P53	Homo sapiens	162-165
21620827-0	2011	The labdane diterpene sclareol (labd-14-ene-8, 13-diol) induces apoptosis in human tumor cell lines and suppression of tumor growth in vivo via a p53-independent mechanism of action.	Diterpenes	12-21	P53	Homo sapiens	146-149
21620827-0	2011	The labdane diterpene sclareol (labd-14-ene-8, 13-diol) induces apoptosis in human tumor cell lines and suppression of tumor growth in vivo via a p53-independent mechanism of action.	sclareol	22-30	P53	Homo sapiens	146-149
21620827-0	2011	The labdane diterpene sclareol (labd-14-ene-8, 13-diol) induces apoptosis in human tumor cell lines and suppression of tumor growth in vivo via a p53-independent mechanism of action.	sclareol	32-54	P53	Homo sapiens	146-149
21620827-8	2011	In conclusion, we demonstrate herein that sclareol kills human tumor cells by inducing arrest at the G(1)-phase of the cell cycle followed by apoptosis that involves activation of caspases-8, -9 and -3 via a p53-independent mechanism.	sclareol	42-50	P53	Homo sapiens	208-211
21620827-9	2011	These findings suggest that liposome-encapsulated sclareol possesses chemotherapeutic potential for the treatment of colorectal and other types of human cancer regardless of the p53-status.	sclareol	50-58	P53	Homo sapiens	178-181
21708134-3	2011	Treatment with the cell cycle inhibitors, aphidicolin or nocodazole also revealed increased NDRG1 phosphorylation in p53-deficient cells.	Aphidicolin	42-53	P53	Homo sapiens	117-120
21554949-8	2011	The carcinogenic potential of arsenic may be attributed to activation of redox-sensitive transcription factors and other signaling pathways involving nuclear factor kappaB, activator protein-1, and p53.	Arsenic	30-37	P53	Homo sapiens	198-201
21649891-12	2011	4- The decrease of butyrate, a histone deacetylase inhibitor, elicits epigenic changes (PETEN, P53, IGFBP decrease; hexokinase, fetal-genes-M2, increase).	Butyrates	19-27	P53	Homo sapiens	95-98
21411502-2	2011	Our studies on the drug-resistant p53-mutant as compared with drug-resistant p53 wild-type neuroblastoma revealed a novel mechanism for resistance to apoptosis: a direct role of p53 in regulating the cellular concentration of proapoptotic alkenals by functioning as a specific and saturable allosteric inhibitor of the alkenal-glutathione conjugate transporter, RLIP76.	alkenals	239-247	P53	Homo sapiens	34-37
21411502-2	2011	Our studies on the drug-resistant p53-mutant as compared with drug-resistant p53 wild-type neuroblastoma revealed a novel mechanism for resistance to apoptosis: a direct role of p53 in regulating the cellular concentration of proapoptotic alkenals by functioning as a specific and saturable allosteric inhibitor of the alkenal-glutathione conjugate transporter, RLIP76.	alkenals	239-247	P53	Homo sapiens	77-80
21411502-2	2011	Our studies on the drug-resistant p53-mutant as compared with drug-resistant p53 wild-type neuroblastoma revealed a novel mechanism for resistance to apoptosis: a direct role of p53 in regulating the cellular concentration of proapoptotic alkenals by functioning as a specific and saturable allosteric inhibitor of the alkenal-glutathione conjugate transporter, RLIP76.	alkenals	239-247	P53	Homo sapiens	77-80
21619452-10	2011	Inhibition of proteosome function with MG-132 reversed the inhibitory effect of cAMP on p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-45	P53	Homo sapiens	88-91
21262221-4	2011	Moreover, inducing p53 accumulation with MG132 reduced autophagic ratio, and repressed the expression and activation of NF-kappaB expression.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	P53	Homo sapiens	19-22
21428456-1	2011	DNA damage from (+/-)-anti-benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE) at a hotspot TP53 gene sequence was electrochemically detected.	[a]pyrene-7,8-dihydrodiol-9,10-epoxide	32-70	P53	Homo sapiens	91-95
22087162-0	2011	The effect of desacetyluvaricin on the expression of TLR4 and P53 protein in Hepg 2.2.15.	desacetyluvaricin	14-31	P53	Homo sapiens	62-65
22087162-4	2011	OBJECTIVES: To investigate the effect of Des on the expression of Toll-like receptor 4 (TLR4) and P53 protein in HCC.	desacetyluvaricin	41-44	P53	Homo sapiens	98-101
21780454-0	2011	Identification of p53 gene by using CdSe/ZnS conjugation and hybridization.	cdse	36-40	P53	Homo sapiens	18-21
21167122-6	2011	Treatment of 8B20 cells with the UPP inhibitors, MG132 and clasto-lactacystin-beta-lactone, led to an increase in levels of p53 while treatment with non-proteasomal inhibitors did not alter p53 levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	49-54	P53	Homo sapiens	124-127
21167122-9	2011	Treatment of 8B20 cells with MG132 led to an increase in the half-life of p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	29-34	P53	Homo sapiens	74-77
21167122-11	2011	In vivo studies showed that MG132 induced p53 overexpression and reduced tumor growth, suggesting an important role of p53 stabilization in controlling melanoma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	P53	Homo sapiens	42-45
21167122-11	2011	In vivo studies showed that MG132 induced p53 overexpression and reduced tumor growth, suggesting an important role of p53 stabilization in controlling melanoma.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	28-33	P53	Homo sapiens	119-122
21489314-16	2011	The inverse effect was observed in the TP53 mutated T24 cell line where TFAP2alpha silencing augmented cisplatin and gemcitabine sensitivity and did not stimulate proliferation.	gemcitabine	117-128	P53	Homo sapiens	39-43
21278235-10	2011	Our findings indicate that restoring active ceramide to cells can resuscitate wild-type p53 function in p53-mutant cells, offering preclinical support for a novel type of mechanism-based therapy in the many human cancers harboring p53 mutations.	Ceramides	44-52	P53	Homo sapiens	88-91
21278235-10	2011	Our findings indicate that restoring active ceramide to cells can resuscitate wild-type p53 function in p53-mutant cells, offering preclinical support for a novel type of mechanism-based therapy in the many human cancers harboring p53 mutations.	Ceramides	44-52	P53	Homo sapiens	104-107
21278235-10	2011	Our findings indicate that restoring active ceramide to cells can resuscitate wild-type p53 function in p53-mutant cells, offering preclinical support for a novel type of mechanism-based therapy in the many human cancers harboring p53 mutations.	Ceramides	44-52	P53	Homo sapiens	104-107
21107702-0	2011	Mutant p53 exhibits trivial effects on mitochondrial functions which can be reactivated by ellipticine in lymphoma cells.	ellipticine	91-102	P53	Homo sapiens	7-10
21268072-7	2011	Furthermore, inhibition of proteasome activity by MG132 blocked GA-induced down-regulation of mutant p53, causing mutant p53 accumulation in detergent-insoluble cellular fractions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	P53	Homo sapiens	101-104
21268072-7	2011	Furthermore, inhibition of proteasome activity by MG132 blocked GA-induced down-regulation of mutant p53, causing mutant p53 accumulation in detergent-insoluble cellular fractions.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	P53	Homo sapiens	121-124
21212516-4	2011	Catalase (scavenger of H(2)O(2)), superoxide dismutase (SOD) (scavenger of O(2)( -)), and SB203580 (inhibitor of p38) attenuated upregulation of p53 expression, suggesting that p53 might be partially regulated by ROS-p38 pathway.	SB 203580	90-98	P53	Homo sapiens	145-148
21212516-4	2011	Catalase (scavenger of H(2)O(2)), superoxide dismutase (SOD) (scavenger of O(2)( -)), and SB203580 (inhibitor of p38) attenuated upregulation of p53 expression, suggesting that p53 might be partially regulated by ROS-p38 pathway.	SB 203580	90-98	P53	Homo sapiens	177-180
20931131-6	2011	Further, overexpression of the acetyltransferase p300 via BacMam increased the acetylation of GFP-p53 at Lys382.	bacmam	58-64	P53	Homo sapiens	98-101
21109480-8	2011	In combination therapy, p53RA small molecules enhanced the anti-tumor activity of cisplatin, 5-fluorouracil, paclitaxel, and erlotinib against HNSCC cells.	Erlotinib Hydrochloride	125-134	P53	Homo sapiens	24-27
21931726-5	2011	Vorinostat increased IGF-IR phosphorylation, produced acetylation of histone H3, up-regulated pTEN and p21 expression, and reduced p53 and cyclin D1 levels in Ishikawa cells.	Vorinostat	0-10	P53	Homo sapiens	131-134
21104938-3	2010	FNQ-induced G(2)/M arrest was correlated with a marked decrease in the expression levels of cyclin A and cyclin B, and their activating partner cyclin-dependent kinases (Cdk) 1 and 2 with concomitant induction of p53, p21, and p27.	furano-1,2-naphthoquinone	0-3	P53	Homo sapiens	213-216
21104938-6	2010	The combined treatment of FNQ with AG1478 (a specific EGFR inhibitor) significantly enhanced the G(2)/M arrest and apoptosis, and also led to up-regulation in Bax, p53, p21, p27, release of mitochondrial cytochrome c, and down-regulation of Bcl-2, XIAP, survivin, cyclin A, cyclin B, Cdk1, and Cdk2 in A549 cells.	furano-1,2-naphthoquinone	26-29	P53	Homo sapiens	164-167
20840860-7	2010	Treatment of the cells with the proteasome inhibitor MG-132 resulted in the accumulation of both p53 and PPP1R13L proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-59	P53	Homo sapiens	97-100
20655369-7	2010	While cyclophosphamide showed an elevation of activated P53 in the presence of S9, 7,12-dimethylbenz[a]anthracene and aflatoxin B(1) responded without the MAS.	Cyclophosphamide	6-22	P53	Homo sapiens	56-59
20655369-7	2010	While cyclophosphamide showed an elevation of activated P53 in the presence of S9, 7,12-dimethylbenz[a]anthracene and aflatoxin B(1) responded without the MAS.	anthracene	103-113	P53	Homo sapiens	56-59
20638924-4	2010	CONCLUSION: We introduced new data related to the contribution of p53 codon 72 to toxicity due to 5-fluorouracil and cyclophosphamide-based neoadjuvant chemotherapy in patients with breast cancer.	Cyclophosphamide	117-133	P53	Homo sapiens	66-69
20811720-5	2010	In this study, we investigated the effect of trichostatin A or TSA (an HDAC inhibitor), and epoxomycin (a proteasome inhibitor) on MYCN and p53 expression in MYCN-amplified neuroblastoma cells.	epoxomicin	92-102	P53	Homo sapiens	140-143
20811720-9	2010	Furthermore, Epoxomycin as a single agent and its combination with TSA enhance p53 expression in the MYCN-amplified neuroblastoma cell lines.	epoxomicin	13-23	P53	Homo sapiens	79-82
20505745-0	2010	Alterations in the p53 pathway and p16INK4a expression predict overall survival in metastatic melanoma patients treated with dacarbazine.	Dacarbazine	125-136	P53	Homo sapiens	19-22
20846458-6	2010	Immunocytochemistry analysis revealed that SAHA-resistant cells were positive for cyclin A (85%), ki-67 (100%), p53 (100%), survivin (100%), and p21 (90%) expression.	Vorinostat	43-47	P53	Homo sapiens	112-115
20590525-0	2010	p38(MAPK)/p53 signalling axis mediates neuronal apoptosis in response to tetrahydrobiopterin-induced oxidative stress and glucose uptake inhibition: implication for neurodegeneration.	sapropterin	73-92	P53	Homo sapiens	10-13
20590525-3	2010	We identified in p38(MAPK)/p53 a BH4-responsive pro-apoptotic signalling axis, as demonstrated by the recovery of neuronal viability achieved by gene silencing or pharmacological inhibition of both p38(MAPK) and p53.	sapropterin	33-36	P53	Homo sapiens	27-30
22489690-8	2012	Expression of phospho-Akt and p53 showed no detectable change during the first 48 h. Pretreatment with the NF-kappaB inhibitor MG132 before exposure to isorhamnetin blocked the nuclear accumulation of p50 and p65, thereby inhibiting cell proliferation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	127-132	P53	Homo sapiens	30-33
23300844-0	2012	Acute hypersensitivity of pluripotent testicular cancer-derived embryonal carcinoma to low-dose 5-aza deoxycytidine is associated with global DNA Damage-associated p53 activation, anti-pluripotency and DNA demethylation.	Decitabine	96-115	P53	Homo sapiens	164-167
22761954-3	2012	METHODOLOGY/PRINCIPAL FINDINGS: Using flow cytometric analysis of cells labeled with cyclin A, annexin V and propidium iodide, we describe a time and dose-dependent arrest of the cell cycle in G0/G1 phase of the cell cycle and apoptosis following extract treatment in MCF-7 (WT-p53) and MDA-MB-231 (mutant-p53) human breast cancer cell lines with a markedly reduced effect on primary human mammary epithelial cells.	Propidium	109-125	P53	Homo sapiens	278-281
22761954-3	2012	METHODOLOGY/PRINCIPAL FINDINGS: Using flow cytometric analysis of cells labeled with cyclin A, annexin V and propidium iodide, we describe a time and dose-dependent arrest of the cell cycle in G0/G1 phase of the cell cycle and apoptosis following extract treatment in MCF-7 (WT-p53) and MDA-MB-231 (mutant-p53) human breast cancer cell lines with a markedly reduced effect on primary human mammary epithelial cells.	Propidium	109-125	P53	Homo sapiens	306-309
22666341-11	2012	Additionally, using IPA together with ectopic expression of p53, we show p53 as an upstream regulator of Bcl-2 in Cr(VI)-transformed cells.	ipa	20-23	P53	Homo sapiens	73-76
22134241-6	2011	We found that the combination of AZD7762 and olaparib produced significant radiosensitization in p53 mutant pancreatic cancer cells and in all of the isogenic cancer cell lines.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	33-40	P53	Homo sapiens	97-100
22134241-7	2011	The magnitude of radiosensitization by AZD7762 and olaparib was greater in p53 mutant cells compared with p53 wild type cells.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	39-46	P53	Homo sapiens	75-78
22134241-7	2011	The magnitude of radiosensitization by AZD7762 and olaparib was greater in p53 mutant cells compared with p53 wild type cells.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	39-46	P53	Homo sapiens	106-109
21598070-6	2011	Vorinostat treatment resulted in increased p21 levels in all glioma cells tested in a p53 independent manner.	Vorinostat	0-10	P53	Homo sapiens	86-89
20590525-3	2010	We identified in p38(MAPK)/p53 a BH4-responsive pro-apoptotic signalling axis, as demonstrated by the recovery of neuronal viability achieved by gene silencing or pharmacological inhibition of both p38(MAPK) and p53.	sapropterin	33-36	P53	Homo sapiens	212-215
20836976-7	2010	Study of signal molecules through mRNA expressions revealed that NHMC caused down-regulation of cyclin-D1, proliferating cell nuclear antigen (PCNA), survivin and Stat-3, and up-regulation of p53 and caspase-3, that in turn induced a greater number of apoptosis vis-a-vis unencapsulated HMC.	nhmc	65-69	P53	Homo sapiens	192-195
11052474-8	2000	The Ki-67 labeling index/terminal deoxynucleotide transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling index ratio in the p53 protein overexpression group was significantly higher than that in the p53 protein-negative group (P &lt; 0.05).	deoxyuridine triphosphate-biotin	71-103	P53	Homo sapiens	141-144
20435884-3	2010	Losses of TP53 and CDKN2A, observed in 8% and 35% of patients, respectively, were significantly associated with a shorter survival after rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) treatment, independently of the International Prognostic Index and of the cell of origin.	Cyclophosphamide	148-164	P53	Homo sapiens	10-14
11101222-0	2000	Assignment of 1H(N), 15N, 13C(alpha), 13CO and 13C(beta) resonances in a 67 kDa p53 dimer using 4D-TROSY NMR spectroscopy.	13co	38-42	P53	Homo sapiens	80-83
21701495-3	2011	In vitro and in vivo regimens of the deoxycytidine analogue decitabine that deplete the chromatin-modifying enzyme DNA methyl-transferase 1 without phosphorylating p53 or inducing early apoptosis were determined.	Decitabine	60-70	P53	Homo sapiens	164-167
11027537-6	2000	Cycloheximide prevented the OxLDL-induced augmentation in both p53 binding activity and intracellular level.	Cycloheximide	0-13	P53	Homo sapiens	63-66
21701495-4	2011	These decitabine regimens but not equimolar DNA-damaging cytarabine upregulated the key late differentiation factors CCAAT enhancer-binding protein e and p27/cyclin dependent kinase inhibitor 1B (CDKN1B), induced cellular differentiation and terminated AML cell cycle, even in cytarabine-resistant p53- and p16/CDKN2A-null AML cells.	Decitabine	6-16	P53	Homo sapiens	298-301
22260024-9	2011	Further experiments confirmed that resveratrol-induced p53 activation was reduced by SB203580 whereas the activation of p38 was not affected by pifithrin-alpha.	SB 203580	85-93	P53	Homo sapiens	55-58
20422343-12	2010	Our data provide evidence that p73 might compensate for p53 function in gemcitabine-induced apoptosis of HuCCT1 cells.	gemcitabine	72-83	P53	Homo sapiens	56-59
20676223-0	2010	Design and Synthesis of Functionalized Trisaccharides as p53-Peptide Mimics.	Trisaccharides	39-53	P53	Homo sapiens	57-60
10866313-3	2000	Here, we report that mitochondria amplify TK/GCV-induced apoptosis by regulating p53 accumulation and the effector phase of apoptosis.	Ganciclovir	45-48	P53	Homo sapiens	81-84
20676223-2	2010	We report here the design and synthesis of functionalized trisaccharides modeled after an alpha-helical 15-mer peptide region of p53 which binds to its cellular regulator MDM2.	Trisaccharides	58-72	P53	Homo sapiens	129-132
21972148-0	2011	Resuscitating wild-type p53 expression by disrupting ceramide glycosylation: a novel approach to target mutant p53 tumors.	Ceramides	53-61	P53	Homo sapiens	24-27
21972148-0	2011	Resuscitating wild-type p53 expression by disrupting ceramide glycosylation: a novel approach to target mutant p53 tumors.	Ceramides	53-61	P53	Homo sapiens	111-114
21972148-3	2011	Recent evidence indicates that disrupting ceramide glycosylation can resuscitate wild-type p53 expression and p53-dependent apoptosis in mutant p53 tumors.	Ceramides	42-50	P53	Homo sapiens	91-94
20346922-0	2010	alpha-Bisabolol induces dose- and time-dependent apoptosis in HepG2 cells via a Fas- and mitochondrial-related pathway, involves p53 and NFkappaB.	alpha-Bisabolol	0-15	P53	Homo sapiens	129-132
21972148-3	2011	Recent evidence indicates that disrupting ceramide glycosylation can resuscitate wild-type p53 expression and p53-dependent apoptosis in mutant p53 tumors.	Ceramides	42-50	P53	Homo sapiens	110-113
10866313-7	2000	Perturbation of mitochondrial function mediated accumulation of wild-type p53 protein, since Bcl-2 overexpression, bongkrekic acid, or inhibition of mitochondrial protein synthesis with chloramphenicol strongly reduced TK/GCV-induced accumulation of wild-type p53 protein.	Ganciclovir	222-225	P53	Homo sapiens	74-77
21972148-3	2011	Recent evidence indicates that disrupting ceramide glycosylation can resuscitate wild-type p53 expression and p53-dependent apoptosis in mutant p53 tumors.	Ceramides	42-50	P53	Homo sapiens	110-113
20346922-6	2010	Detection of accumulation of nuclear wild-type p53 and up-regulated expression of NFkappaB indicated these two key regulator with transcriptional decision-making function in various signaling pathways might also play a role in alpha-bisabolol-induced apoptosis in HepG2 cells.	alpha-Bisabolol	227-242	P53	Homo sapiens	47-50
10866313-7	2000	Perturbation of mitochondrial function mediated accumulation of wild-type p53 protein, since Bcl-2 overexpression, bongkrekic acid, or inhibition of mitochondrial protein synthesis with chloramphenicol strongly reduced TK/GCV-induced accumulation of wild-type p53 protein.	Ganciclovir	222-225	P53	Homo sapiens	260-263
10842159-6	2000	A similar reduction in cellular proliferation and upregulation of p21 expression were achieved with iNOS gene transfer as well as treatment with the NO-donor S-nitroso-N-acetylpenicillamine (SNAP), demonstrating the p53-independent nature of these NO-mediated pathways.	S-Nitroso-N-Acetylpenicillamine	158-189	P53	Homo sapiens	216-219
20367642-4	2010	We thus hypothesized that various anticancer drugs such as p53-activating reagents and IFNs may potentiate poly I:C-induced tumor cell death through the up-regulation of TLR3 expression.	Poly I-C	107-115	P53	Homo sapiens	59-62
20367642-6	2010	We found that the DNA-damaging reagent 5-fluorouracil (5-FU) increased TLR3 mRNA expression and potentiated poly I:C-induced apoptosis in HCT116 p53(+/+) cells but had only minimal effect in p53(-/-) cells, indicating a p53-dependent pathway.	Poly I-C	108-116	P53	Homo sapiens	145-148
20367642-8	2010	Furthermore, the combination of poly I:C, 5-FU and IFN-alpha induced the highest apoptosis in HCT116 p53(+/+) and p53(-/-) cells.	Poly I-C	32-40	P53	Homo sapiens	101-104
20367642-8	2010	Furthermore, the combination of poly I:C, 5-FU and IFN-alpha induced the highest apoptosis in HCT116 p53(+/+) and p53(-/-) cells.	Poly I-C	32-40	P53	Homo sapiens	114-117
20367642-9	2010	Taken together, these data suggest that the anticancer drugs increased TLR3 expression and subsequently potentiated poly I:C-induced apoptosis likely via p53-dependent and -independent pathways.	Poly I-C	116-124	P53	Homo sapiens	154-157
22031102-4	2011	Blockage of apoptosis by MG132 correlates with p53 stabilization and upregulation of p21/WAF1, a p53 transcriptional target.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	P53	Homo sapiens	47-50
22031102-4	2011	Blockage of apoptosis by MG132 correlates with p53 stabilization and upregulation of p21/WAF1, a p53 transcriptional target.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	P53	Homo sapiens	97-100
22033280-7	2011	Authentic nuclear proteins such as PCNA, p53 and LAP2a were found both in the light and the heavy sucrose fractions together with lamin A.	Sucrose	98-105	P53	Homo sapiens	41-44
10762633-1	2000	Caffeine inhibits the G2 checkpoint activated by DNA damage and enhances the toxicity of DNA-damaging agents towards p53-defective cancer cells.	Caffeine	0-8	P53	Homo sapiens	117-120
20601342-3	2010	This variant show high frequency of p53 gene mutation and p53 over expression in comparison to the usual CCSK.	ccsk	105-109	P53	Homo sapiens	36-39
10737712-0	2000	Diverse effects of 9-hydroxyellipticine on the chemosensitivity of human pancreatic cancer cells harboring p53 mutations.	9-hydroxyellipticine	19-39	P53	Homo sapiens	107-110
20601342-3	2010	This variant show high frequency of p53 gene mutation and p53 over expression in comparison to the usual CCSK.	ccsk	105-109	P53	Homo sapiens	58-61
21514041-0	2011	Gene expression signature of TP53 but not its mutation status predicts response to sequential paclitaxel and 5-FU/epirubicin/cyclophosphamide in human breast cancer.	Cyclophosphamide	125-141	P53	Homo sapiens	29-33
10737712-1	2000	Recently, it has been shown that 9-hydroxyellipticine (9-HE), an antitumor alkaloid has a unique property of restoring functional wild-type (wt) p53 activity via inhibition of mutant (mt) p53 protein phosphorylation.	9-hydroxyellipticine	33-53	P53	Homo sapiens	145-148
21693655-3	2011	PATIENTS AND METHODS: Epithelial p53 expression was evaluated using two immunohistochemical antibodies (DO7 and 1801) in formalin-fixed, paraffin-embedded tissue from patients with node-positive breast cancer who were randomized to four cycles of cyclophosphamide and one of three doses of doxorubicin (60, 75, or 90 mg/m(2); AC) and to receive four subsequent cycles of paclitaxel (T) or not.	Cyclophosphamide	247-263	P53	Homo sapiens	33-36
19757179-0	2010	beta-Ionone-induced apoptosis in human osteosarcoma (U2os) cells occurs via a p53-dependent signaling pathway.	beta-ionone	0-11	P53	Homo sapiens	78-81
10737712-1	2000	Recently, it has been shown that 9-hydroxyellipticine (9-HE), an antitumor alkaloid has a unique property of restoring functional wild-type (wt) p53 activity via inhibition of mutant (mt) p53 protein phosphorylation.	9-hydroxyellipticine	33-53	P53	Homo sapiens	188-191
19757179-6	2010	Furthermore, Expression of the p53 protein increased in a concentration-dependent and time-dependent manner according to immunocytochemistry and immunoblotting after beta-ionone treatment.	beta-ionone	166-177	P53	Homo sapiens	31-34
19757179-8	2010	In summary, these data suggested that beta-ionone induced apoptosis in a concentration-dependent manner in U2os cells via a p53-dependent mitochondrial pathway.	beta-ionone	38-49	P53	Homo sapiens	124-127
10737712-1	2000	Recently, it has been shown that 9-hydroxyellipticine (9-HE), an antitumor alkaloid has a unique property of restoring functional wild-type (wt) p53 activity via inhibition of mutant (mt) p53 protein phosphorylation.	9-hydroxyellipticine	55-59	P53	Homo sapiens	145-148
21725200-3	2011	We report that the primary molecular mechanism of decitabine-depletion of DNA methyltransferase-1 following its "suicide" inactivation-is not absolutely associated with cell cycle progression in HCT 116 colon cancer cells, but is associated with their p53 genotype.	Decitabine	50-60	P53	Homo sapiens	252-255
21725200-5	2011	Secondary changes in CpG methylation occurred only in growing cells ~24-48 h after decitabine treatment; these epigenetic changes coincided with p53 accumulation, an index of DNA damage.	Decitabine	83-93	P53	Homo sapiens	145-148
10737712-1	2000	Recently, it has been shown that 9-hydroxyellipticine (9-HE), an antitumor alkaloid has a unique property of restoring functional wild-type (wt) p53 activity via inhibition of mutant (mt) p53 protein phosphorylation.	9-hydroxyellipticine	55-59	P53	Homo sapiens	188-191
10737712-3	2000	Exposure of cells to 9-HE at a relatively low concentration of 1 microM induced almost no cell death but was sufficient to restore wt p53 activity, as evidenced by an induction of endogenous p21WAF1/CIP1 concomitant with G1 and G2/M arrests in cell-cycle progression.	9-hydroxyellipticine	21-25	P53	Homo sapiens	134-137
20587660-0	2010	p53-independent induction of G1 arrest and p21WAF1/CIP1 expression by ascofuranone, an isoprenoid antibiotic, through downregulation of c-Myc.	ascofuranone	70-82	P53	Homo sapiens	0-3
10737712-6	2000	These effects of 9-HE were specific for several cell lines containing mt p53 and were not observed in p53-negative or wt p53 expressing cells.	9-hydroxyellipticine	17-21	P53	Homo sapiens	73-76
20587660-2	2010	Here, we study the effects of ascofuranone on cell cycle progression in human cancer cells and find that ascofuranone induces G(1) arrest without cytoxicity with upregulation of p53 and p21(WAF1/CIP1) while downregulating c-Myc and G(1) cyclins.	ascofuranone	105-117	P53	Homo sapiens	178-181
21565980-0	2011	Nicotinamide blocks proliferation and induces apoptosis of chronic lymphocytic leukemia cells through activation of the p53/miR-34a/SIRT1 tumor suppressor network.	Niacinamide	0-12	P53	Homo sapiens	120-123
20587660-3	2010	Chromatin immunoprecipitation assay and RNA interference studies with cells deficient in p53 and p21 show that ascofuranone induces p21(WAF1/CIP1) expression and subsequent G(1) arrest through the release of p21(WAF1/CIP1) promoter from c-Myc-mediated transcriptional repression, independent of p53.	ascofuranone	111-123	P53	Homo sapiens	89-92
10634797-6	2000	The increased expression of p21 mRNA or p53 activation during late G(1) or S phase was also caused by addition of 8-bromo-cGMP and effectively blocked by a specific inhibitor of the soluble guanylate cyclase.	8-bromocyclic GMP	114-126	P53	Homo sapiens	40-43
20587660-3	2010	Chromatin immunoprecipitation assay and RNA interference studies with cells deficient in p53 and p21 show that ascofuranone induces p21(WAF1/CIP1) expression and subsequent G(1) arrest through the release of p21(WAF1/CIP1) promoter from c-Myc-mediated transcriptional repression, independent of p53.	ascofuranone	111-123	P53	Homo sapiens	295-298
21565980-6	2011	Nicotinamide modulates the p53-dependent genes p21, NOXA, BAX, and Mcl-1, indicating an activation of the p53 pathway and of caspase-3.	Niacinamide	0-12	P53	Homo sapiens	27-30
21565980-6	2011	Nicotinamide modulates the p53-dependent genes p21, NOXA, BAX, and Mcl-1, indicating an activation of the p53 pathway and of caspase-3.	Niacinamide	0-12	P53	Homo sapiens	106-109
21565980-11	2011	We therefore concluded that nicotinamide has the dual property of inhibiting SIRT1 through a noncompetitive enzymatic block (p53 independent) and at the same time through miR-34a induction (p53 dependent).	Niacinamide	28-40	P53	Homo sapiens	125-128
21565980-11	2011	We therefore concluded that nicotinamide has the dual property of inhibiting SIRT1 through a noncompetitive enzymatic block (p53 independent) and at the same time through miR-34a induction (p53 dependent).	Niacinamide	28-40	P53	Homo sapiens	190-193
21565980-12	2011	These observations suggested the therapeutic potential of nicotinamide, a novel, safe, and inexpensive drug, to be used in addition to chemotherapy for CLL patients with wt p53.	Niacinamide	58-70	P53	Homo sapiens	173-176
21550660-3	2011	Another class of anti-epigenetic agent histone deacetylase inhibitor (HDACI) inhibited the proliferation of both MV4-11 and MV4-11 TP53 R248W cells.	mv4-11	124-130	P53	Homo sapiens	131-135
21550660-4	2011	Notably, when 5-AzadC was combined with HDACI MS-275, apoptosis in MV4-11 TP53 R248W cells was significantly enhanced in parallel with activation of the caspase cascade, up-regulation of p21waf1 and gamma-H2AX, and down-regulation of Mcl-1.	Decitabine	14-21	P53	Homo sapiens	74-78
21550660-5	2011	Interestingly, inhibition of caspase 3 by the pan-caspase inhibitor attenuated the combination of 5-AzadC and MS-275-mediated apoptosis and down-regulation of Mcl-1 in MV4-11 TP53 R248W cells.	Decitabine	98-105	P53	Homo sapiens	175-179
20133503-3	2010	By using pairs of isogenic colon cancer cell lines that differ only in p53 expression (RKO and HCT116), securinine was found to exhibit these properties.	securinine	104-114	P53	Homo sapiens	71-74
20133503-4	2010	Securinine (30 microM) induces apoptosis in 73% of p53-null HCT116 cells (LD(50) 17.5 microM) as opposed to 17.6% of HCT116 parental cells (LD(50) 50 microM) at 72 h after treatment.	securinine	0-10	P53	Homo sapiens	51-54
20133503-5	2010	The mechanism of securinine-mediated death in p53-deficient cells involves the induction of the p53 family member, p73.	securinine	17-27	P53	Homo sapiens	46-49
20133503-5	2010	The mechanism of securinine-mediated death in p53-deficient cells involves the induction of the p53 family member, p73.	securinine	17-27	P53	Homo sapiens	96-99
21550660-8	2011	Combination of 5-AzadC and MS-275 may be a promising treatment strategy for individuals with leukemia in which TP53 is inactivated.	Decitabine	15-22	P53	Homo sapiens	111-115
11322510-4	2000	We also report on the permissive effects of Vitamin D3 and the Vitamin D3 analog EB 1089 in the promotion of apoptosis in p53-wild-type cells.	Cholecalciferol	44-54	P53	Homo sapiens	122-125
21550362-0	2011	Metabolites of arsenic and increased DNA damage of p53 gene in arsenic plant workers.	Arsenic	63-70	P53	Homo sapiens	51-54
21550362-6	2011	Those findings suggested that DNA damage of exon 5 and 8 of p53 gene existed in the population occupationally exposed to arsenic.	Arsenic	121-128	P53	Homo sapiens	60-63
20480521-13	2010	However, gemcitabine and dicoumarol combination induced increased p53 and decreased Bcl-(XL) levels in KKU-100, but not in KKU-M214 cells.	gemcitabine	9-20	P53	Homo sapiens	66-69
20171273-5	2010	By the use of either small interfering RNAs to target SIRT1 or the SIRT1 inhibitor nicotinamide we found that Nox1-dependent inhibition of p53 transcriptional activity was SIRT1-dependent.	Niacinamide	83-95	P53	Homo sapiens	139-142
11322510-4	2000	We also report on the permissive effects of Vitamin D3 and the Vitamin D3 analog EB 1089 in the promotion of apoptosis in p53-wild-type cells.	Cholecalciferol	63-73	P53	Homo sapiens	122-125
21502403-7	2011	The p53 tumor suppressor was stabilized by an increased acetylation in response to vorinostat and a reduced Ser315 phosphorylation in response to aurora kinase A.	Vorinostat	83-93	P53	Homo sapiens	4-7
10534768-1	1999	We applied the differential mRNA display method to isolate genes regulated by wild-type TP53 in cells of a colon-cancer line (SW480) in which we had established an inducible TP53 expression system under the control of the lactose operon.	Lactose	222-229	P53	Homo sapiens	88-92
21377279-0	2011	Retention of the in vitro radiosensitizing potential of gemcitabine under anoxic conditions, in p53 wild-type and p53-deficient non-small-cell lung carcinoma cells.	gemcitabine	56-67	P53	Homo sapiens	96-99
21377279-9	2011	Although radiosensitization was observed in both p53 wild-type and p53-deficient cells, p53 status might influence induction of apoptosis after gemcitabine/radiation treatment, whereas no effect on cell cycle progression was noticed.	gemcitabine	144-155	P53	Homo sapiens	67-70
20096282-4	2010	Carboplatin and Akt inhibitor induced nuclear damage, decreased Bid and Bcl-2 protein levels, induced cytochrome c release, activated caspase-3 and increased tumor suppressor p53 levels.	Carboplatin	0-11	P53	Homo sapiens	175-178
21377279-9	2011	Although radiosensitization was observed in both p53 wild-type and p53-deficient cells, p53 status might influence induction of apoptosis after gemcitabine/radiation treatment, whereas no effect on cell cycle progression was noticed.	gemcitabine	144-155	P53	Homo sapiens	67-70
20332106-5	2010	When cells were treated with the proteasome inhibitor MG132, the size and frequency of p53-containing nucleolar cavities increased, and the protein partially colocalized with inactivated proteasomes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	P53	Homo sapiens	87-90
10534768-1	1999	We applied the differential mRNA display method to isolate genes regulated by wild-type TP53 in cells of a colon-cancer line (SW480) in which we had established an inducible TP53 expression system under the control of the lactose operon.	Lactose	222-229	P53	Homo sapiens	174-178
20700368-1	2010	PURPOSE: Benzo[a]pyrene 7,8-diol 9,10-epoxide (BPDE), an ultimate metabolite of benzo[a]pyrene, attacks deoxyguanosine to form a BPDE-N2-dG adduct resulting in p53 mutations.	7,8-diol 9,10-epoxide	24-45	P53	Homo sapiens	160-163
10526272-6	1999	RESULTS: Overexpression of p53 in the AGC group was significantly more frequent compared with that in the EGC group (P = 0.0386).	(-)-Epigallocatechin	106-109	P53	Homo sapiens	27-30
21454520-0	2011	Mutant p53 protein is targeted by arsenic for degradation and plays a role in arsenic-mediated growth suppression.	Arsenic	34-41	P53	Homo sapiens	7-10
21454520-0	2011	Mutant p53 protein is targeted by arsenic for degradation and plays a role in arsenic-mediated growth suppression.	Arsenic	78-85	P53	Homo sapiens	7-10
21454520-4	2011	Interestingly, wild type p53 is accumulated in cells treated with arsenic compounds, presumably due to arsenic-induced oxidative stresses.	Arsenic	66-73	P53	Homo sapiens	25-28
21454520-4	2011	Interestingly, wild type p53 is accumulated in cells treated with arsenic compounds, presumably due to arsenic-induced oxidative stresses.	Arsenic	103-110	P53	Homo sapiens	25-28
21454520-6	2011	In contrast, we found that arsenic compounds degrade both endogenous and ectopically expressed mutant p53 in time- and dose-dependent manners.	Arsenic	27-34	P53	Homo sapiens	102-105
21454520-7	2011	We also found that arsenic trioxide decreases the stability of mutant p53 protein through a proteasomal pathway, and blockage of mutant p53 nuclear export can alleviate the arsenic-induced mutant p53 degradation.	Arsenic	19-26	P53	Homo sapiens	70-73
20233881-6	2010	RESULTS: AZD7762 treatment enhanced the radiosensitivity of p53-mutated tumor cell lines (DMFs ranging from 1.6-1.7) to a greater extent than for p53 wild-type tumor lines (DMFs ranging from 1.1-1.2).	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	9-16	P53	Homo sapiens	60-63
20233881-10	2010	CONCLUSIONS: AZD7762 effectively enhanced the radiosensitivity of mutated p53 tumor cell lines and HT29 xenografts and was without untoward toxicity when administered alone or in combination with radiation.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	13-20	P53	Homo sapiens	74-77
21454520-9	2011	Taken together, we found that mutant p53 is a target of arsenic compounds, which provides an insight into exploring arsenic compound-based therapy for tumors harboring a mutant p53.	Arsenic	56-63	P53	Homo sapiens	37-40
21454520-9	2011	Taken together, we found that mutant p53 is a target of arsenic compounds, which provides an insight into exploring arsenic compound-based therapy for tumors harboring a mutant p53.	Arsenic	56-63	P53	Homo sapiens	177-180
21454520-9	2011	Taken together, we found that mutant p53 is a target of arsenic compounds, which provides an insight into exploring arsenic compound-based therapy for tumors harboring a mutant p53.	Arsenic	116-123	P53	Homo sapiens	37-40
21454520-9	2011	Taken together, we found that mutant p53 is a target of arsenic compounds, which provides an insight into exploring arsenic compound-based therapy for tumors harboring a mutant p53.	Arsenic	116-123	P53	Homo sapiens	177-180
20123963-3	2010	To elucidate the direct phosphorylation of p53 at Ser46 by ATM, an ATM mutant (ATM-AS) sensitive to ATP analogues was engineered.	Arsenic	83-85	P53	Homo sapiens	43-46
10397271-7	1999	In addition, the accumulation of hsp72 and p53 in the wtp53 cells was induced by the administration of an nitric oxide-generating agent, S-nitroso-N-acetylpenicillamine, to the medium.	S-Nitroso-N-Acetylpenicillamine	137-168	P53	Homo sapiens	43-46
21123063-0	2011	Improvement of the synthesis and pharmacokinetic properties of chromenotriazolopyrimidine MDM2-p53 protein-protein inhibitors.	chromenotriazolopyrimidine	63-89	P53	Homo sapiens	95-98
20334641-3	2010	However, amifostine has also been described as a potent hypoxia-mimetic compound and as a strong p53 inducer; both effects are known to potently modulate vascular endothelial growth factor (VEGF-A) expression.	Amifostine	9-19	P53	Homo sapiens	97-100
21123063-2	2011	We report several optimizations to the synthesis of the chromenotriazolopyrimidine series of MDM2-p53 protein-protein interaction inhibitors.	chromenotriazolopyrimidine	56-82	P53	Homo sapiens	98-101
10384915-6	1999	Exposure to PUVA induced an increase in p53 expression in non-lesional skin in 14/19 patients, putatively as a response to DNA damage caused by PUVA.	puva	12-16	P53	Homo sapiens	40-43
21472523-3	2011	Using a combination of top-down and middle-down FTICR mass spectrometry, we show that of the 10 Cys residues in the core domain of wild-type p53, Cys182 and Cys277 exhibit a remarkable preference for modification by the alkylating reagent N-ethylmaleimide.	Ethylmaleimide	239-255	P53	Homo sapiens	141-144
21241062-6	2011	2,2-Diphenylethyl ITC, a synthetic ITC, is one of the most potent depletors of mutant p53 studies and induces apoptosis to the greatest extent in mutant p53 breast cancer cells.	2,2-diphenylethyl itc	0-21	P53	Homo sapiens	86-89
21241062-6	2011	2,2-Diphenylethyl ITC, a synthetic ITC, is one of the most potent depletors of mutant p53 studies and induces apoptosis to the greatest extent in mutant p53 breast cancer cells.	2,2-diphenylethyl itc	0-21	P53	Homo sapiens	153-156
20036271-0	2010	Arsenite induced poly(ADP-ribosyl)ation of tumor suppressor P53 in human skin keratinocytes as a possible mechanism for carcinogenesis associated with arsenic exposure.	Arsenic	151-158	P53	Homo sapiens	60-63
20025073-2	2010	The aim of this study was to explore the effect of dietary folate and vitamin B(6) intake on p53 in the molecular pathogenesis of esophageal adenocarcinoma (EADC).	Niacinamide	70-79	P53	Homo sapiens	93-96
10384915-6	1999	Exposure to PUVA induced an increase in p53 expression in non-lesional skin in 14/19 patients, putatively as a response to DNA damage caused by PUVA.	puva	144-148	P53	Homo sapiens	40-43
21194611-2	2011	Previous studies have demonstrated that arsenic and chromium complexes are able to activate p53, but there is a dearth of data investigating whether uranium complexes exhibit similar effects.	Arsenic	40-47	P53	Homo sapiens	92-95
10360645-6	1999	Similarly, cell proliferation was abolished by C2-ceramide (5-20 microM) only in wild-type p53 cells.	N-acetylsphingosine	47-58	P53	Homo sapiens	91-94
21224072-4	2011	We found that well-known proteasome inhibitors such as MG132 and bortezomib, as well as the recently discovered proteasome inhibitor thiostrepton, induced p53-independent apoptosis in human cancer cell lines that correlated with p53-independent induction of proapoptotic Noxa but not Puma protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	P53	Homo sapiens	155-158
20081368-7	2010	Detailed sequence analysis shows the exceptional retention of key features of both proteins from man to Placazoan implying that the p53-Mdm2 interaction and its regulation have been conserved from a basal eumetazoan since the pre-cambrian era over 1 billion years ago.	eumetazoan	205-215	P53	Homo sapiens	132-135
20013323-3	2010	MV4-11 TP53 R248W cells were relatively resistant to AZD1152-HQPA-mediated growth arrest, as measured by MTT and clonogenic assays.	monooxyethylene trimethylolpropane tristearate	105-108	P53	Homo sapiens	7-11
10360645-7	1999	FACS-analysis revealed that C2-ceramide induced massive p53-dependent apoptosis (40-50% after 12-24 h) and cell cycle analysis showed a transient G1 arrest in p53-deficient tumour cells 12-24 h after C2-ceramide exposure.	N-acetylsphingosine	28-39	P53	Homo sapiens	56-59
21224072-4	2011	We found that well-known proteasome inhibitors such as MG132 and bortezomib, as well as the recently discovered proteasome inhibitor thiostrepton, induced p53-independent apoptosis in human cancer cell lines that correlated with p53-independent induction of proapoptotic Noxa but not Puma protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	55-60	P53	Homo sapiens	229-232
10100719-0	1999	Expression of p53 in cisplatin-resistant ovarian cancer cell lines: modulation with the novel platinum analogue (1R, 2R-diaminocyclohexane)(trans-diacetato)(dichloro)-platinum(IV).	dichloro)-platinum	157-175	P53	Homo sapiens	14-17
19857530-6	2010	CBB-detectable ubiquitinated p53 was easily purified from the insect cell-free protein synthesis system, allowing analysis of the Ub-conjugated proteins by mass spectrometry (MS).	coomassie Brilliant Blue	0-3	P53	Homo sapiens	29-32
9888876-9	1999	ANP, NOR3, and 8-bromo-cGMP caused marked accumulations of the tumor suppressor gene product p53 but not of bcl-2, as determined by Western blot analysis.	8-bromocyclic GMP	15-27	P53	Homo sapiens	93-96
19998502-7	2009	MTT assay showed that the growth of HepG2 cells was mucj more significantly inhibited by LV-NT4(Si)-p53(N15)-Ant than by LV-EGFP.	monooxyethylene trimethylolpropane tristearate	0-3	P53	Homo sapiens	100-103
19998502-11	2009	LDH release from HepG2 cells was analyzed at 24, 48, 72 and 96 h after infection with LV-NT4(Si)-p53(N15)-Ant and LV-EGFP, which showed that LDH release was significantly higher in LV-NT4(Si)-p53(N15)-Ant treatment group (682 IU/L) than in control group (45 IU/L, P &lt; 0.01).	Leucovorin	86-88	P53	Homo sapiens	97-100
22178888-7	2011	In the EMSA using a (32)P-labeled DNA probe to detect binding to the putative GATA-2 biding site on the p53 gene promoter, adenosine produced (32)P-positive signals in nuclear extracts from HepG2 cells.	Phosphorus-32	20-25	P53	Homo sapiens	104-107
22178888-7	2011	In the EMSA using a (32)P-labeled DNA probe to detect binding to the putative GATA-2 biding site on the p53 gene promoter, adenosine produced (32)P-positive signals in nuclear extracts from HepG2 cells.	Phosphorus-32	142-147	P53	Homo sapiens	104-107
21454974-0	2011	3,5-Dimethyl-H-furo[3,2-g]chromen-7-one as a potential anticancer drug by inducing p53-dependent apoptosis in human hepatoma HepG2 cells.	3,5-dimethyl-h-furo[3,2-g]chromen-7-one	0-39	P53	Homo sapiens	83-86
9883907-2	1998	We hypothesized that 9-hydroxyellipticine (9-HE), an antitumor alkaloid, would inhibit telomerase activity because the drug has a unique mechanism of inhibiting phosphorylation of mutant p53 protein via inhibition of protein kinases, thereby restoring wild-type p53 function.	9-hydroxyellipticine	21-41	P53	Homo sapiens	187-190
22279419-5	2011	We report for the first time C-PAC-induced modulation of five miRNAs in three EAC cell lines resulting in 26 validated gene targets and identification of key signaling pathways including p53, angiogenesis, T-cell activation and apoptosis.	c-pac	29-34	P53	Homo sapiens	187-190
20931131-5	2011	First, BacMam-mediated overexpression of SIRT1 resulted in dose-dependent deacetylation of GFP-p53 following etoposide treatment of U-2 OS cells, confirming that GFP-p53 serves as a SIRT1 substrate in this assay format.	bacmam	7-13	P53	Homo sapiens	95-98
20931131-5	2011	First, BacMam-mediated overexpression of SIRT1 resulted in dose-dependent deacetylation of GFP-p53 following etoposide treatment of U-2 OS cells, confirming that GFP-p53 serves as a SIRT1 substrate in this assay format.	bacmam	7-13	P53	Homo sapiens	166-169
9883907-2	1998	We hypothesized that 9-hydroxyellipticine (9-HE), an antitumor alkaloid, would inhibit telomerase activity because the drug has a unique mechanism of inhibiting phosphorylation of mutant p53 protein via inhibition of protein kinases, thereby restoring wild-type p53 function.	9-hydroxyellipticine	21-41	P53	Homo sapiens	262-265
21765936-8	2011	The effects of GRIM-19-dependent p53 accumulation on cell proliferation, cell cycle, apoptosis were explored by MTT, flow cytometry and transmission electron microscopy respectively.	monooxyethylene trimethylolpropane tristearate	112-115	P53	Homo sapiens	33-36
9883907-2	1998	We hypothesized that 9-hydroxyellipticine (9-HE), an antitumor alkaloid, would inhibit telomerase activity because the drug has a unique mechanism of inhibiting phosphorylation of mutant p53 protein via inhibition of protein kinases, thereby restoring wild-type p53 function.	9-hydroxyellipticine	43-47	P53	Homo sapiens	187-190
9883907-2	1998	We hypothesized that 9-hydroxyellipticine (9-HE), an antitumor alkaloid, would inhibit telomerase activity because the drug has a unique mechanism of inhibiting phosphorylation of mutant p53 protein via inhibition of protein kinases, thereby restoring wild-type p53 function.	9-hydroxyellipticine	43-47	P53	Homo sapiens	262-265
9883907-5	1998	We conclude that 9-HE may exert a strong inhibitory effect on telomerase activity possibly through inhibition of protein kinases rather than through restoration of functional wild-type p53.	9-hydroxyellipticine	17-21	P53	Homo sapiens	185-188
9811471-6	1998	Lastly, we show that lovastatin treatment of 76N-E6 breast cell line with an altered p53 pathway also results in G1 arrest and similar redistribution of CKIs from CDK4 to CDK2 as observed in other breast cell lines examined.	Lovastatin	21-31	P53	Homo sapiens	85-88
20923768-7	2010	We report that endocannabinoids stabilize lysosomes by preventing the Abeta-induced up-regulation of the tumor suppressor protein, p53, and its interaction with the lysosomal membrane.	Endocannabinoids	15-31	P53	Homo sapiens	131-134
21159612-3	2010	The combination of vorinostat and flavopiridol was synergistic and significantly more cytotoxic (P &lt; 0.001) in cell lines with p53-LOF and in the clones stably transfected with dominant-negative p53 plasmids.	Vorinostat	19-29	P53	Homo sapiens	130-133
21159612-3	2010	The combination of vorinostat and flavopiridol was synergistic and significantly more cytotoxic (P &lt; 0.001) in cell lines with p53-LOF and in the clones stably transfected with dominant-negative p53 plasmids.	Vorinostat	19-29	P53	Homo sapiens	198-201
9811471-7	1998	These observations suggest that lovastatin induced G1 arrest of breast cell lines is through a p53 independent pathway and is mediated by decreased CDK2 activity through redistribution of CKIs from CDK4 to CDK2.	Lovastatin	32-42	P53	Homo sapiens	95-98
20840854-7	2010	A dioxin-like PCB (DL-PCB 126) was used as reference and gave results that were predictable from previous studies, i.e. it attenuated BP-induced p53 response and apoptosis.	Dioxins	2-8	P53	Homo sapiens	145-148
9788435-1	1998	The p53-null human lung cancer cell line H1299 was used in order to generate clones with ecdysone-inducible p53 as well as ecdysone-inducible p21waf1.	Ecdysone	89-97	P53	Homo sapiens	4-7
20878066-0	2010	Amifostine enhancement of the anti-cancer effects of paclitaxel in endometrial cancer is TP53-dependent.	Amifostine	0-10	P53	Homo sapiens	89-93
20878066-5	2010	In this report, using a cell line with knock-down p53 expression through siRNA, we found that amifostine enhancement of paclitaxel"s anticancer effect is p53 status-dependent.	Amifostine	94-104	P53	Homo sapiens	50-53
20878066-5	2010	In this report, using a cell line with knock-down p53 expression through siRNA, we found that amifostine enhancement of paclitaxel"s anticancer effect is p53 status-dependent.	Amifostine	94-104	P53	Homo sapiens	154-157
9788435-1	1998	The p53-null human lung cancer cell line H1299 was used in order to generate clones with ecdysone-inducible p53 as well as ecdysone-inducible p21waf1.	Ecdysone	89-97	P53	Homo sapiens	108-111
20878066-6	2010	Amifostine promotes entry into the G2-M phase through regulation of cyclin-dependent kinase-1 activity in cells with dysfunctional p53, thereby enhancing cancer cell sensitivity to paclitaxel.	Amifostine	0-10	P53	Homo sapiens	131-134
9788435-1	1998	The p53-null human lung cancer cell line H1299 was used in order to generate clones with ecdysone-inducible p53 as well as ecdysone-inducible p21waf1.	Ecdysone	123-131	P53	Homo sapiens	4-7
20878066-8	2010	Sensitivity to the therapeutic effect of paclitaxel in combination with amifostine was dependent upon the status of p53.	Amifostine	72-82	P53	Homo sapiens	116-119
20878066-9	2010	A tumor with a nonsense TP53 mutation showed increased therapeutic response to paclitaxel and amifostine as measured by tumor weight compared to a tumor with wild- type TP53.	Amifostine	94-104	P53	Homo sapiens	24-28
9766444-7	1998	In contrast, the differentiation response of p53-negative U-937 cells to 1,25-dihydroxychole-calciferol or all-trans retinoic acid was enhanced by cAMP-inducing agents at optimal concentrations and inhibited at higher concentrations.	Calcitriol	73-103	P53	Homo sapiens	45-48
20878066-10	2010	Our study provides a rationale for a clinical trial of combined paclitaxel and amifostine in endometrial cancer patients whose tumors harbor TP53 mutations.	Amifostine	79-89	P53	Homo sapiens	141-145
9751619-0	1998	Essential role of p53 in phenethyl isothiocyanate-induced apoptosis.	phenethyl isothiocyanate	25-49	P53	Homo sapiens	18-21
20661218-6	2010	Whereas RO-3306, a selective inhibitor of cyclin-dependent kinase 1 (Cdk1), suppresses this phosphorylation at Ser315 of p53, ZM447439, targeting Aurora A/B kinases, shows no effect.	RO 3306	8-15	P53	Homo sapiens	121-124
9751619-5	1998	This was demonstrated not only by results that PEITC induction of p53 protein expression and p53-dependent transactivation but also by PEITC-induced apoptosis in p53 +/+ cells but not in p53 -/- cells.	phenethyl isothiocyanate	47-52	P53	Homo sapiens	66-69
20558835-0	2010	Cell cycle arrest and apoptosis in TP53 subtypes of bladder carcinoma cell lines treated with cisplatin and gemcitabine.	gemcitabine	108-119	P53	Homo sapiens	35-39
9751619-5	1998	This was demonstrated not only by results that PEITC induction of p53 protein expression and p53-dependent transactivation but also by PEITC-induced apoptosis in p53 +/+ cells but not in p53 -/- cells.	phenethyl isothiocyanate	47-52	P53	Homo sapiens	93-96
20558835-8	2010	TP53-wild type cells (RT4) were more sensitive to apoptosis than were mutated TP53 cells when treated with cisplatin or gemcitabine.	gemcitabine	120-131	P53	Homo sapiens	0-4
20558835-8	2010	TP53-wild type cells (RT4) were more sensitive to apoptosis than were mutated TP53 cells when treated with cisplatin or gemcitabine.	gemcitabine	120-131	P53	Homo sapiens	78-82
9751619-5	1998	This was demonstrated not only by results that PEITC induction of p53 protein expression and p53-dependent transactivation but also by PEITC-induced apoptosis in p53 +/+ cells but not in p53 -/- cells.	phenethyl isothiocyanate	47-52	P53	Homo sapiens	93-96
20499882-5	2010	Low concentrations of the NO donor, DETA NONOate (&lt;200 microM), exclusively nitrate Tyr327 within the tetramerization domain promoting p53 oligomerization, nuclear accumulation, and increased DNA-binding activity without p53 Ser15 phosphorylation.	2,2'-(hydroxynitrosohydrazono)bis-ethanamine	36-48	P53	Homo sapiens	138-141
20587334-0	2010	Synergistic efficacy of LBH and alphaB-crystallin through inhibiting transcriptional activities of p53 and p21.	alphab-crystallin	32-49	P53	Homo sapiens	99-102
9751619-5	1998	This was demonstrated not only by results that PEITC induction of p53 protein expression and p53-dependent transactivation but also by PEITC-induced apoptosis in p53 +/+ cells but not in p53 -/- cells.	phenethyl isothiocyanate	47-52	P53	Homo sapiens	93-96
20587334-6	2010	Transient transfection assays indicated that overexpression of LBH or alphaB-crystallin reduced the transcriptional activities of p53 and p21, respectively, Overexpression of both alphaB-crystallin and LBH together resulted in a stronger repression of the transcriptional activities of p21 and p53.	alphab-crystallin	70-87	P53	Homo sapiens	130-133
9751619-7	1998	Our results demonstrate for the first time that p53 elevation is required for PEITC-induced apoptosis, which may be involved in its cancer chemopreventive activity.	phenethyl isothiocyanate	78-83	P53	Homo sapiens	48-51
9576849-10	1998	The induction of p53 by H2O2 was abolished by the iron chelator deferoxamine and the protein synthesis inhibitor cycloheximide.	Cycloheximide	113-126	P53	Homo sapiens	17-20
20094798-4	2010	Moreover, nutlin-3 drastically enhanced imatinib-induced apoptosis in a p53-dependent manner in various BCR/ABL-expressing cells, which included primary leukemic cells from patients with CML blast crisis or Ph+ ALL and cells expressing the imatinib-resistant E255K BCR/ABL mutant.	Imatinib Mesylate	40-48	P53	Homo sapiens	72-75
9515788-0	1998	Frequent p53 mutations at dipyrimidine sites in patients with pyothorax-associated lymphoma.	dipyrimidine	26-38	P53	Homo sapiens	9-12
20094798-8	2010	The present study indicates that combined treatment with nutlin-3 and imatinib activates p53 without inducing p21 and synergistically activates Bax-mediated intrinsic mitochondrial pathway to induce apoptosis in BCR/ABL-expressing cells.	Imatinib Mesylate	70-78	P53	Homo sapiens	89-92
20180806-7	2010	In addition, it was observed that inhibition of heat-induced p53/HSF1 diminishes Hsp70 levels, thereby restoring the sensitivity of heat-stressed HepG2 cells to carboplatin-triggered cell death.	Carboplatin	161-172	P53	Homo sapiens	61-64
9488455-0	1998	p53-dependent elevation of p21Waf1 expression by UV light is mediated through mRNA stabilization and involves a vanadate-sensitive regulatory system.	Vanadates	112-120	P53	Homo sapiens	0-3
20208557-0	2010	15-Deoxy-Delta(12,14)-prostaglandin J(2) stabilizes, but functionally inactivates p53 by binding to the cysteine 277 residue.	15-deoxy-delta(12,14)-prostaglandin j	0-37	P53	Homo sapiens	82-85
9488455-7	1998	Treatment of the p53-/- MEFs with the protein tyrosine phosphatase inhibitor vanadate reversed the UVC-induced block on p21Waf1 induction and resulted in their enhanced survival following irradiation.	Vanadates	77-85	P53	Homo sapiens	17-20
20124408-7	2010	Binding of SCH529074 to the p53 DBD is specifically displaced by an oligonucleotide with a sequence derived from the p53-response element.	SCH 529074	11-20	P53	Homo sapiens	28-31
9803007-5	1998	DNA of the critical Tp53 exons 5-8 was amplified and run on horizontal polyacrylamide gels under defined temperature conditions (TGGE) to yield specific gel shifts and sets of homo- and heteroduplexes in case of mutation.	polyacrylamide	71-85	P53	Homo sapiens	20-24
20124408-7	2010	Binding of SCH529074 to the p53 DBD is specifically displaced by an oligonucleotide with a sequence derived from the p53-response element.	SCH 529074	11-20	P53	Homo sapiens	117-120
20124408-8	2010	In addition to reactivating mutant p53, SCH529074 binding inhibits ubiquitination of p53 by HDM2.	SCH 529074	40-49	P53	Homo sapiens	85-88
20124408-9	2010	We have also developed a novel variant of p53 by changing a single amino acid in the core domain of p53 (N268R), which abolishes binding of SCH529074.	SCH 529074	140-149	P53	Homo sapiens	42-45
20124408-9	2010	We have also developed a novel variant of p53 by changing a single amino acid in the core domain of p53 (N268R), which abolishes binding of SCH529074.	SCH 529074	140-149	P53	Homo sapiens	100-103
20124408-11	2010	Our novel findings indicate that through its interaction with p53 DBD, SCH529074 restores DNA binding activity to mutant p53 and inhibits HDM2-mediated ubiquitination.	SCH 529074	71-80	P53	Homo sapiens	62-65
20124408-11	2010	Our novel findings indicate that through its interaction with p53 DBD, SCH529074 restores DNA binding activity to mutant p53 and inhibits HDM2-mediated ubiquitination.	SCH 529074	71-80	P53	Homo sapiens	121-124
9436988-1	1998	We have proposed that reduced activity of inosine-5"-monophosphate dehydrogenase (IMPD; IMP:NAD oxidoreductase, EC 1.2.1.14), the rate-limiting enzyme for guanine nucleotide biosynthesis, in response to wild-type p53 expression, is essential for p53-dependent growth suppression.	Guanine Nucleotides	155-173	P53	Homo sapiens	213-216
20371965-6	2010	Moreover, it was shown that cotreatment with MDA-LDL and BaP markedly induced the expression of human cytochrome P4501A1 (hCYP1A1) messenger ribonucleic acid (mRNA) and significantly induced the expressions of p53 and p21 mRNAs.	mda-ldl	45-52	P53	Homo sapiens	210-213
20127688-6	2010	Knockdown of DJ-1 and MTA2, a core component of the NuRD complex, had a similar and pro-apoptotic effect on the transcriptional- and p53-dependent cell death induced by daunorubicin.	Daunorubicin	169-181	P53	Homo sapiens	133-136
9436988-1	1998	We have proposed that reduced activity of inosine-5"-monophosphate dehydrogenase (IMPD; IMP:NAD oxidoreductase, EC 1.2.1.14), the rate-limiting enzyme for guanine nucleotide biosynthesis, in response to wild-type p53 expression, is essential for p53-dependent growth suppression.	Guanine Nucleotides	155-173	P53	Homo sapiens	246-249
9436988-6	1998	Because of the role of IMPD in the production and balance of GTP and ATP, essential nucleotides for signal transduction, these results suggest that p53 controls cell division signals by regulating purine ribonucleotide metabolism.	purine ribonucleotide	197-218	P53	Homo sapiens	148-151
9393772-0	1997	Correspondence re: J. S. DeFrank et al., p53-null cells are more sensitive to ultraviolet light only in the presence of caffeine.	Caffeine	120-128	P53	Homo sapiens	41-44
20060030-0	2010	Indole-3-carbinol induces apoptosis through p53 and activation of caspase-8 pathway in lung cancer A549 cells.	indole-3-carbinol	0-17	P53	Homo sapiens	44-47
20060030-7	2010	Treatment with wortmannin significantly suppressed both I3C-induced Ser15 phosphorylation and accumulation of p53 protein.	Wortmannin	15-25	P53	Homo sapiens	110-113
19731376-5	2010	Conversion of the acetylated K382 to nonacetylated form with free energy perturbation (FEP) simulations of the p53 CBP complex and the free peptide showed that the relative contribution of the acetyl group to binding is 4.8 kcal/mol.	C12H10N6O3S	29-33	P53	Homo sapiens	111-114
9398049-0	1997	Modulation of p53 expression in cultured colonic adenoma cell lines by the naturally occurring lumenal factors butyrate and deoxycholate.	Deoxycholic Acid	124-136	P53	Homo sapiens	14-17
20018721-6	2010	This progression is consistent with failed growth arrest and/or senescence of premalignant lesions, since a mutant of p53, p53(R172P), which can still induce p21 and cell cycle arrest, is resistant to PDAC formation.	pdac	201-205	P53	Homo sapiens	118-121
20018721-6	2010	This progression is consistent with failed growth arrest and/or senescence of premalignant lesions, since a mutant of p53, p53(R172P), which can still induce p21 and cell cycle arrest, is resistant to PDAC formation.	pdac	201-205	P53	Homo sapiens	123-126
20018721-10	2010	In summary, by using "knock-in" mutations of Trp53 we have identified two critical acquired functions of a stably expressed mutant form of p53 that drive PDAC; first, an escape from Kras(G12D)-induced senescence/growth arrest and second, the promotion of metastasis.	pdac	154-158	P53	Homo sapiens	45-50
20018721-10	2010	In summary, by using "knock-in" mutations of Trp53 we have identified two critical acquired functions of a stably expressed mutant form of p53 that drive PDAC; first, an escape from Kras(G12D)-induced senescence/growth arrest and second, the promotion of metastasis.	pdac	154-158	P53	Homo sapiens	47-50
9398049-4	1997	Levels of p53 protein and mRNA were measured in adherent cells which had been incubated with growth-inhibitory concentrations of sodium butyrate (a by-product of dietary fibre fermentation) or sodium deoxycholate (a bile acid) for up to 48 hr.	Deoxycholic Acid	193-212	P53	Homo sapiens	10-13
9398049-5	1997	We report that both butyrate and deoxycholate can down-regulate the expression of wild-type and mutant p53.	Deoxycholic Acid	33-45	P53	Homo sapiens	103-106
19157829-6	2010	Lycopene prevented the arrest in G0/G1 phase of cell cycle induced by the oxysterol and counteracted the increased expression of p53 and p21.	Lycopene	0-8	P53	Homo sapiens	129-132
9350037-12	1997	We propose that the inhibition of T47D cell proliferation by phenanthroline, Rifampicin and ATA results from a number of cellular changes that include regulation of p53 and PR.	Rifampin	77-87	P53	Homo sapiens	165-168
20041160-0	2009	MiR-24 tumor suppressor activity is regulated independent of p53 and through a target site polymorphism.	mir-24	0-6	P53	Homo sapiens	61-64
20041160-5	2009	MiR-24 over expression in cells with wt-p53 upregulated TP53 and p21 protein; however, in p53-null cells miR-24 still induced cell cycle arrest without the involvement of p21.	mir-24	0-6	P53	Homo sapiens	40-43
20041160-5	2009	MiR-24 over expression in cells with wt-p53 upregulated TP53 and p21 protein; however, in p53-null cells miR-24 still induced cell cycle arrest without the involvement of p21.	mir-24	0-6	P53	Homo sapiens	56-60
20041160-9	2009	A novel function for miR-24 as a p53-independent cell cycle inhibitory miRNA is proposed.	mir-24	21-27	P53	Homo sapiens	33-36
9350037-12	1997	We propose that the inhibition of T47D cell proliferation by phenanthroline, Rifampicin and ATA results from a number of cellular changes that include regulation of p53 and PR.	Aurintricarboxylic Acid	92-95	P53	Homo sapiens	165-168
9815821-8	1997	This suggests that radiosensitization by CAF and increased cell death is dependent on loss of wt p53 function.	Caffeine	41-44	P53	Homo sapiens	97-100
19934315-0	2009	Imatinib mesylate induces cisplatin hypersensitivity in Bcr-Abl+ cells by differential modulation of p53 transcriptional and proapoptotic activity.	Imatinib Mesylate	0-17	P53	Homo sapiens	101-104
19934315-9	2009	Furthermore, p53 accumulated predominantly in the cytoplasm in Bcr-Abl(+) cells treated with imatinib and cisplatin.	Imatinib Mesylate	93-101	P53	Homo sapiens	13-16
9815821-10	1997	These results demonstrate that G2 checkpoint inhibition with CAF leads to preferential IR cell killing in cell lines in which wt p53 is inactivated and that this increased cell killing is not necessarily dependent on increased IR-induced apoptosis.	Caffeine	61-64	P53	Homo sapiens	129-132
19934315-10	2009	Silencing of p53 significantly reduced sensitivity to cisplatin in imatinib-treated Bcr-Abl(+) cells, indicating that p53 retains its proapoptotic activity.	Imatinib Mesylate	67-75	P53	Homo sapiens	13-16
19934315-10	2009	Silencing of p53 significantly reduced sensitivity to cisplatin in imatinib-treated Bcr-Abl(+) cells, indicating that p53 retains its proapoptotic activity.	Imatinib Mesylate	67-75	P53	Homo sapiens	118-121
9130140-4	1997	4-Aminopyridine (4-AP) inhibition of proliferation was dose dependent, and assessment using a TUNEL in situ assay revealed that apoptosis occurred in U87 cells with wild-type p53 but not in A172 cells with mutant p53 (24-hr incubation with mM 4-AP).	4-Aminopyridine	0-15	P53	Homo sapiens	175-178
19934315-12	2009	We conclude that imatinib sensitizes Bcr-Abl(+) cells to cisplatin by simultaneous inhibition of p53 transactivation, induction of p53 accumulation predominantly in the cytoplasm, and reduction of Bcl-x(L).	Imatinib Mesylate	17-25	P53	Homo sapiens	97-100
19934315-12	2009	We conclude that imatinib sensitizes Bcr-Abl(+) cells to cisplatin by simultaneous inhibition of p53 transactivation, induction of p53 accumulation predominantly in the cytoplasm, and reduction of Bcl-x(L).	Imatinib Mesylate	17-25	P53	Homo sapiens	131-134
19804594-11	2009	RESULTS: Nicotinamide cooperated with ssUV to increase enzymes involved in cellular energy metabolism and p53, and significantly protected against immunosuppression caused by UVB, longwave UVA and single and repeated ssUV exposures.	Niacinamide	9-21	P53	Homo sapiens	106-109
9106628-0	1997	p53 and WAF1 are induced and Rb protein is hypophosphorylated during cell growth inhibition by the thymidylate synthase inhibitor ZD1694 (Tomudex).	raltitrexed	130-136	P53	Homo sapiens	0-3
9106628-0	1997	p53 and WAF1 are induced and Rb protein is hypophosphorylated during cell growth inhibition by the thymidylate synthase inhibitor ZD1694 (Tomudex).	raltitrexed	138-145	P53	Homo sapiens	0-3
9100856-5	1997	The repair rate of cyclopyrimidine dimers is quite variable from nucleotide position to nucleotide position and we show that this variation along the p53 gene drives the C--&gt;T transition frequency of non-melanocytic skin tumors.	cyclopyrimidine	19-34	P53	Homo sapiens	150-153
19923910-2	2009	We previously demonstrated the feasibility of p53 pathway restoration in p53-deficient tumor cell populations using small molecules including ellipticine or its derivatives.	ellipticine	142-153	P53	Homo sapiens	46-49
8968086-0	1996	p53-null cells are more sensitive to ultraviolet light only in the presence of caffeine.	Caffeine	79-87	P53	Homo sapiens	0-3
8968086-1	1996	We have shown previously that p53(-/-) fibroblasts show greater sensitization by caffeine to the lethal effects of ionizing radiation compared with p53(+/+) cells.	Caffeine	81-89	P53	Homo sapiens	30-33
19729440-8	2009	In summary, our data lend support for a restrictive role for p53 activity in UB outgrowth from the WD.	BM	77-79	P53	Homo sapiens	61-64
19915967-11	2009	Similarly, lycopene significantly diminished the apoptosis ratio of oxidative injured cells, and also downregulated the expressions of p53 and caspase-3 mRNA induced by H(2)O(2).	Lycopene	11-19	P53	Homo sapiens	135-138
8878553-5	1996	Inhibition of protein synthesis by cycloheximide demonstrated increased p21 protein half-life in the presence of LC in mutant p53 containing cells.	Cycloheximide	35-48	P53	Homo sapiens	126-129
19915967-13	2009	CONCLUSIONS: Lycopene can decrease the oxidative injury of endothelial cells induced by H(2)O(2), can attenuate the expression of p53 and caspase-3 mRNA in injured cells, and can diminish the apoptosis of injured cells.	Lycopene	13-21	P53	Homo sapiens	130-133
19699254-5	2009	The proteasome inhibitor MG132 completely blocked capsaicin-induced p53 degradation and enhanced apoptotic cell death.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	P53	Homo sapiens	68-71
19797731-0	2009	Clonal heterogeneity in the 5q- syndrome: p53 expressing progenitors prevail during lenalidomide treatment and expand at disease progression.	Lenalidomide	84-96	P53	Homo sapiens	42-45
19681600-6	2009	To test the idea that dithio-disulfide exchange reactions between p53 and thioredoxin were responsible for p53 inhibition in mutant yeast, each p53 cysteine was changed to serine, and the effect of the substitution on p53 activity in TRR1 and Deltatrr1 yeast was determined.	dithio-disulfide	22-38	P53	Homo sapiens	66-69
19731257-3	2009	The dependence of p53-mediated chemosensitivity on pRb status was first investigated in a prospective study on the prognostic relevance of p53 in breast cancer patients treated with adjuvant chemotherapy (5-fluorouracil, methotrexate and cyclophosphamide).	Cyclophosphamide	238-254	P53	Homo sapiens	18-21
8816895-9	1996	p53 immunoperoxidase staining using citrate buffer/microwave antigen retrieval was performed.	Citric Acid	36-43	P53	Homo sapiens	0-3
19846904-7	2009	Taken together, these results suggest that sequestration of Sp1 could be one of the mechanisms by which p53 negatively regulates MGMT expression, thus enhancing sensitivity of tumor cells to O(6)-alkylguanine generating drugs.	o(6)-alkylguanine	191-208	P53	Homo sapiens	104-107
20719194-3	2009	METHODS: Cellulose-bound overlapping peptides (12 mers) derived from p53 wild type protein were synthesized using SOPTs synthesis technique by an AutoSpot robot -ASP SL (Intavis, Germany).	Cellulose	9-18	P53	Homo sapiens	69-72
20719194-6	2009	RESULTS: We synthesized on cellulose membranes twelve-amino-acid overlapping peptides which included all of the sequences of the polypeptide chain of p53.	Cellulose	27-36	P53	Homo sapiens	150-153
19387079-6	2009	Vorinostat increased p53 expression and activated caspases -8, -9 and -3, whereas caspase inhibition abrogated vorinostat-induced apoptosis.	Vorinostat	0-10	P53	Homo sapiens	21-24
8707401-7	1996	A search of our database of p53 mutations revealed that out of 8 p53 mutations reported by others, 4 are C:G--&gt;T:A transitions at dipyrimidine sites, and one is a tandem CC--&gt;TT mutation.	dipyrimidine	133-145	P53	Homo sapiens	65-68
8692199-7	1996	Modification of endogenous and exogenous p53 expression by caffeine, which interferes with normal induction of p53 in response to DNA damage, showed no correlation between the induction of chromosome breaks and heteroploidy.	Caffeine	59-67	P53	Homo sapiens	41-44
19625493-9	2009	The extent of UV-induced phosphorylation of p53 and Chk1 was markedly reduced by SchB in ATM-deficient but not siATR-treated cells.	schizandrin B	81-85	P53	Homo sapiens	44-47
18681908-8	2009	Activation of SIRT1 negatively regulates UV- and H(2)O(2)-induced p53 acetylation, because nicotinamide and sirtinol as well as SIRT1 siRNA enhance UV- and H(2)O(2)-induced p53 acetylation, whereas SIRT1 activator resveratrol inhibits it.	Niacinamide	91-103	P53	Homo sapiens	66-69
18681908-8	2009	Activation of SIRT1 negatively regulates UV- and H(2)O(2)-induced p53 acetylation, because nicotinamide and sirtinol as well as SIRT1 siRNA enhance UV- and H(2)O(2)-induced p53 acetylation, whereas SIRT1 activator resveratrol inhibits it.	Niacinamide	91-103	P53	Homo sapiens	173-176
19723072-5	2009	Chromatin immunoprecipitation analysis has revealed phenyl butyrate and its combinations with RA and vitamin B3 cause histone H4 acetylation in the p21 promoter regions corresponding to p53 and/or Sp1 sites.	Niacinamide	101-111	P53	Homo sapiens	186-189
8692199-7	1996	Modification of endogenous and exogenous p53 expression by caffeine, which interferes with normal induction of p53 in response to DNA damage, showed no correlation between the induction of chromosome breaks and heteroploidy.	Caffeine	59-67	P53	Homo sapiens	111-114
8692199-8	1996	We conclude that the caffeine- or mutant p53-induced increase in the frequency of chromosomal breaks in dividing LIM1215 cells is assonated with inactivation of wt-p53 function(s) responsible for control of G1 checkpoint and/or DNA repair, while numerical chromosome changes in these cells may be a result of elimination or modification of a separate p53 function, or due to gain-of-function activities of p53 mutants.	Caffeine	21-29	P53	Homo sapiens	41-44
19567674-6	2009	These data, by revealing that beta(4) expression is transcriptionally repressed in tumors by HIPK2 and p53 to impair beta(4)-dependent tumor progression, suggest that loss of p53 function favors the formation of coactivator complex with the TA members of the p53 family to allow beta(4) transcription.	beta(4)	30-37	P53	Homo sapiens	103-106
8692199-8	1996	We conclude that the caffeine- or mutant p53-induced increase in the frequency of chromosomal breaks in dividing LIM1215 cells is assonated with inactivation of wt-p53 function(s) responsible for control of G1 checkpoint and/or DNA repair, while numerical chromosome changes in these cells may be a result of elimination or modification of a separate p53 function, or due to gain-of-function activities of p53 mutants.	Caffeine	21-29	P53	Homo sapiens	164-167
19567674-6	2009	These data, by revealing that beta(4) expression is transcriptionally repressed in tumors by HIPK2 and p53 to impair beta(4)-dependent tumor progression, suggest that loss of p53 function favors the formation of coactivator complex with the TA members of the p53 family to allow beta(4) transcription.	beta(4)	30-37	P53	Homo sapiens	175-178
19567674-6	2009	These data, by revealing that beta(4) expression is transcriptionally repressed in tumors by HIPK2 and p53 to impair beta(4)-dependent tumor progression, suggest that loss of p53 function favors the formation of coactivator complex with the TA members of the p53 family to allow beta(4) transcription.	beta(4)	30-37	P53	Homo sapiens	175-178
19602465-5	2009	This prompted us to test the methylation of the TP53 gene promoter in a set of 14 families suggestive of LFS using bisulphite sequencing of three DNA fragments from the 5" region of the gene.	hydrogen sulfite	115-125	P53	Homo sapiens	48-52
8692199-8	1996	We conclude that the caffeine- or mutant p53-induced increase in the frequency of chromosomal breaks in dividing LIM1215 cells is assonated with inactivation of wt-p53 function(s) responsible for control of G1 checkpoint and/or DNA repair, while numerical chromosome changes in these cells may be a result of elimination or modification of a separate p53 function, or due to gain-of-function activities of p53 mutants.	Caffeine	21-29	P53	Homo sapiens	164-167
19584241-0	2009	Inhibition of S-adenosylmethionine decarboxylase by inhibitor SAM486A connects polyamine metabolism with p53-Mdm2-Akt/protein kinase B regulation and apoptosis in neuroblastoma.	4-amidinoindan-1-one 2'-amidinohydrazone	62-69	P53	Homo sapiens	105-108
8692199-8	1996	We conclude that the caffeine- or mutant p53-induced increase in the frequency of chromosomal breaks in dividing LIM1215 cells is assonated with inactivation of wt-p53 function(s) responsible for control of G1 checkpoint and/or DNA repair, while numerical chromosome changes in these cells may be a result of elimination or modification of a separate p53 function, or due to gain-of-function activities of p53 mutants.	Caffeine	21-29	P53	Homo sapiens	164-167
8700554-0	1996	Ganciclovir-induced ablation non-proliferating thyrocytes expressing herpesvirus thymidine kinase occurs by p53-independent apoptosis.	Ganciclovir	0-11	P53	Homo sapiens	108-111
19253369-0	2009	Ascochlorin activates p53 in a manner distinct from DNA damaging agents.	ascochlorin	0-11	P53	Homo sapiens	22-25
19253369-1	2009	Ascochlorin, a prenylphenol antitumor antibiotic, profoundly increases the expression of endogenous p53 by increasing protein stability in the human osteosarcoma cells and human colon cancer cells.	ascochlorin	0-11	P53	Homo sapiens	100-103
19253369-2	2009	Ascochlorin also increases DNA binding activity to the p53 consensus sequence in nuclear extract and enhances transcription of p53 downstream targets.	ascochlorin	0-11	P53	Homo sapiens	55-58
19253369-2	2009	Ascochlorin also increases DNA binding activity to the p53 consensus sequence in nuclear extract and enhances transcription of p53 downstream targets.	ascochlorin	0-11	P53	Homo sapiens	127-130
19253369-3	2009	Ascochlorin specifically induces p53 phosphorylation at ser 392 without affecting ser 15 or 20, whereas DNA damaging agents typically phosphorylate these serines.	ascochlorin	0-11	P53	Homo sapiens	33-36
19253369-5	2009	The structure-activity relationship suggests that p53 activation by ascochlorin is related to inhibition of mitochondrial respiration, which is further supported by the observation that respiratory inhibitors activate p53 in a manner similar to ascochlorin.	ascochlorin	68-79	P53	Homo sapiens	50-53
19291793-0	2009	Pml and TAp73 interacting at nuclear body mediate imatinib-induced p53-independent apoptosis of chronic myeloid leukemia cells.	Imatinib Mesylate	50-58	P53	Homo sapiens	67-70
19291793-4	2009	As reported previously, p53(wild) CML was more resistant to imatinib than that lacking p53.	Imatinib Mesylate	60-68	P53	Homo sapiens	24-27
19291793-5	2009	Here, we searched for an imatinib-induced p53 independent proapoptotic mechanism.	Imatinib Mesylate	25-33	P53	Homo sapiens	42-45
19291793-6	2009	We found imatinib up-regulated phosphorylation of p38 mitogen-activated protein kinase (MAPK), checkpoint kinase 2 (chk2) and transactivation-competent (TA) p73; expression of pml and bax; formation of PML-nuclear body (NB); and co-localization of TAp73/PML-NB in p53-nonfunctioning K562 and p53(mutant) Meg-01 CML cells, but not in BCR-ABL(-) HL60 cells.	Imatinib Mesylate	9-17	P53	Homo sapiens	264-267
19291793-6	2009	We found imatinib up-regulated phosphorylation of p38 mitogen-activated protein kinase (MAPK), checkpoint kinase 2 (chk2) and transactivation-competent (TA) p73; expression of pml and bax; formation of PML-nuclear body (NB); and co-localization of TAp73/PML-NB in p53-nonfunctioning K562 and p53(mutant) Meg-01 CML cells, but not in BCR-ABL(-) HL60 cells.	Imatinib Mesylate	9-17	P53	Homo sapiens	292-295
19291793-12	2009	The imatinib-induced co-localization was also found in primary CML cells from 3 of 6 patients, including 2 with p53(mutant) and one with p53(wild).	Imatinib Mesylate	4-12	P53	Homo sapiens	112-115
19291793-12	2009	The imatinib-induced co-localization was also found in primary CML cells from 3 of 6 patients, including 2 with p53(mutant) and one with p53(wild).	Imatinib Mesylate	4-12	P53	Homo sapiens	137-140
19291793-13	2009	A novel p53-independent proapoptotic mechanism using p38 MAPK /pml/TAp73 axis with a step processing at PML-NB and probably with chk2 and bax being involved is hereby evident in some imatinib-treated CML cells.	Imatinib Mesylate	183-191	P53	Homo sapiens	8-11
19253369-6	2009	These results suggest that ascochlorin, through the inhibition of mitochondrial respiration, activates p53 through a mechanism distinct from genotoxins.	ascochlorin	27-38	P53	Homo sapiens	103-106
19372630-8	2009	Additional analyses indicated the significant up-regulation (P = 0.001) of tumor suppressor p53 and p53-regulated pro-apoptotic Bax and Fas in MCF-7 cells following CPA treatment in combination with RES, which may contribute to the enhancement of the antitumor effect of CPA.	Cyclophosphamide	165-168	P53	Homo sapiens	92-95
19372630-8	2009	Additional analyses indicated the significant up-regulation (P = 0.001) of tumor suppressor p53 and p53-regulated pro-apoptotic Bax and Fas in MCF-7 cells following CPA treatment in combination with RES, which may contribute to the enhancement of the antitumor effect of CPA.	Cyclophosphamide	165-168	P53	Homo sapiens	100-103
19372630-8	2009	Additional analyses indicated the significant up-regulation (P = 0.001) of tumor suppressor p53 and p53-regulated pro-apoptotic Bax and Fas in MCF-7 cells following CPA treatment in combination with RES, which may contribute to the enhancement of the antitumor effect of CPA.	Cyclophosphamide	271-274	P53	Homo sapiens	92-95
8700554-6	1996	The fact that Ganciclovir phosphate can kill cells by a p53-independent apoptotic pathway is encouraging in relation to tumour ablation by methods based on transfection with HSV1-tk genes and administration of Ganciclovir.	ganciclovir phosphate	14-35	P53	Homo sapiens	56-59
19372630-8	2009	Additional analyses indicated the significant up-regulation (P = 0.001) of tumor suppressor p53 and p53-regulated pro-apoptotic Bax and Fas in MCF-7 cells following CPA treatment in combination with RES, which may contribute to the enhancement of the antitumor effect of CPA.	Cyclophosphamide	271-274	P53	Homo sapiens	100-103
19781349-16	2009	SB203580 significantly increased the cellular phosphorylated p53 protein level, but decreased the p-glycoprotein level in MCF-7/Adr cells.	SB 203580	0-8	P53	Homo sapiens	61-64
8700554-6	1996	The fact that Ganciclovir phosphate can kill cells by a p53-independent apoptotic pathway is encouraging in relation to tumour ablation by methods based on transfection with HSV1-tk genes and administration of Ganciclovir.	Ganciclovir	14-25	P53	Homo sapiens	56-59
8819013-3	1996	These mutations result in an Arg--&gt;Trp amino acid substitution at residue 249 and an Ile--&gt;Phe amino acid substitution at residue 255 in a highly conserved region in the DNA-binding core domain of the p53 protein.	Isoleucine	88-91	P53	Homo sapiens	207-210
19363521-6	2009	Our data indicates that demethylation of the survivin promoter by decitabine results in p53-dependent survivin repression and that p53 binding can be inhibited by DNA methylation.	Decitabine	66-76	P53	Homo sapiens	88-91
19220000-6	2009	In the context of the full-length p53 TAD, AD1 and AD2 bind synergistically to KIX.	kix	79-82	P53	Homo sapiens	34-37
8819013-3	1996	These mutations result in an Arg--&gt;Trp amino acid substitution at residue 249 and an Ile--&gt;Phe amino acid substitution at residue 255 in a highly conserved region in the DNA-binding core domain of the p53 protein.	Phenylalanine	97-100	P53	Homo sapiens	207-210
18619705-9	2009	Furthermore, ellipticine induced nucleus translocalization of p53 and Akt and recruitment of autophagosomes.	ellipticine	13-24	P53	Homo sapiens	62-65
8819013-4	1996	To determine the effects of these substitutions on the three-dimensional structure of the p53 protein, we have performed molecular dynamics calculations on this core domain of the wild-type and the Trp-249 and Phe-255 mutants to compute the average structures of each of the three forms.	Phenylalanine	210-213	P53	Homo sapiens	90-93
19274602-4	2009	The results demonstrated a statistically significant allele dosage effect of the XRCC1 399 variant on the production of the vinyl chloride-induced mutant p53 biomarker, even after controlling for confounders including cumulative vinyl chloride exposure (p = 0.03), with a potentially supramultiplicative gene-environment interaction.	Vinyl Chloride	124-138	P53	Homo sapiens	154-157
8829621-2	1996	Treatment of cells with vanadate, an inhibitor of protein tyrosine phosphatase, likewise led to a dramatic reduction in the level of p53 transcript.	Vanadates	24-32	P53	Homo sapiens	133-136
19274602-4	2009	The results demonstrated a statistically significant allele dosage effect of the XRCC1 399 variant on the production of the vinyl chloride-induced mutant p53 biomarker, even after controlling for confounders including cumulative vinyl chloride exposure (p = 0.03), with a potentially supramultiplicative gene-environment interaction.	Vinyl Chloride	229-243	P53	Homo sapiens	154-157
19270508-0	2009	Modulation of thymidilate synthase and p53 expression by HDAC inhibitor vorinostat resulted in synergistic antitumor effect in combination with 5FU or raltitrexed.	Vorinostat	72-82	P53	Homo sapiens	39-42
19270508-2	2009	In this study we demonstrated that the HDAC inhibitor vorinostat exerted potent antiproliferative effect in a panel of mut- and wt-p53 human CRC cell lines.	Vorinostat	54-64	P53	Homo sapiens	131-134
19270508-7	2009	Furthermore, p53, whose wild-type expression is critical for sensitivity to 5FU and RTX, was upregulated by vorinostat in wt- and downregulated in mut-p53 cells, suggesting an additional mechanism of the antiproliferative synergistic interactions observed.	Vorinostat	108-118	P53	Homo sapiens	13-16
19136317-3	2009	p53 expression was measured using Western blotting, NER using host cell reactivation (HCR) of a UV-damaged reporter gene and cell sensitivity using the MTT assay.	monooxyethylene trimethylolpropane tristearate	152-155	P53	Homo sapiens	0-3
18977148-7	2008	Lissoclinidine B inhibited ubiquitylation and degradation of p53, and selectively killed transformed cells harboring wild-type p53, suggesting this compound could be used to develop new treatments.	Lissoclinidine B	0-16	P53	Homo sapiens	61-64
18977148-7	2008	Lissoclinidine B inhibited ubiquitylation and degradation of p53, and selectively killed transformed cells harboring wild-type p53, suggesting this compound could be used to develop new treatments.	Lissoclinidine B	0-16	P53	Homo sapiens	127-130
19010883-0	2008	Induction of cytoplasmic accumulation of p53: a mechanism for low levels of arsenic exposure to predispose cells for malignant transformation.	Arsenic	76-83	P53	Homo sapiens	41-44
8814703-3	1996	The number of G418-resistant colonies from wild-type TP53-transfected cells was approximately half that from plasmid controls.	antibiotic G 418	14-18	P53	Homo sapiens	53-57
18949386-9	2008	SB203580, a chemical inhibitor of p38 kinase, was found to consistently inhibit p53-induced senescence.	SB 203580	0-8	P53	Homo sapiens	80-83
18779317-8	2008	Furthermore, the poly(I-C)-induced phosphorylation of IkappaB-alpha, nuclear translocation of NF-kappaB, and phosphorylation of interferon regulatory transcription factor 3, were drastically reduced in HCT116 p53(-/-) cells, indicating a dysregulation of the two signaling pathways governed by TLR3.	Poly I-C	17-26	P53	Homo sapiens	209-212
19150257-10	2009	Consistently, HCT116p53(-/-) cells are more resistant to imatinib than parental cells, suggesting that imatinib activity is partly dependent on p53 in colon cancer cells.	Imatinib Mesylate	57-65	P53	Homo sapiens	20-23
19150257-10	2009	Consistently, HCT116p53(-/-) cells are more resistant to imatinib than parental cells, suggesting that imatinib activity is partly dependent on p53 in colon cancer cells.	Imatinib Mesylate	103-111	P53	Homo sapiens	20-23
18779317-9	2008	Consequently, induction of interleukin-8 and beta interferon after poly(I-C) stimulation was impaired in HCT116 p53(-/-) cells.	Poly I-C	67-76	P53	Homo sapiens	112-115
8814703-4	1996	Exogenous wild-type TP53 transcripts were identified in four of the 20 G418-resistant clones analysed by reverse transcription PCR.	antibiotic G 418	71-75	P53	Homo sapiens	20-24
19159630-0	2009	Possible involvement of activation of P53/P21 and demethylation of RUNX 3 in the cytotoxicity against Lovo cells induced by 5-Aza-2"-deoxycytidine.	Decitabine	124-146	P53	Homo sapiens	38-45
8562931-0	1996	Expression of the p53 tumor suppressor gene induces differentiation and promotes induction of differentiation by 1,25-dihydroxycholecalciferol in leukemic U-937 cells.	Calcitriol	113-142	P53	Homo sapiens	18-21
19059205-3	2009	In this work, DU-145 cells were used to demonstrate that SPBE and its sterol components, beta-sitosterol and stigmasterol, inhibit prostate cancer growth by increasing p53 protein expression and also inhibit carcinoma development by decreasing p21 and p27 protein expression.	Stigmasterol	109-121	P53	Homo sapiens	168-171
18718914-5	2008	JNK inhibitor (SP600125) or p38 MAPK inhibitor (SB203580) pretreatment attenuated 15d-PGJ(2)-mediated apoptosis and suppressed the p21(Waf1) and Bax expressions without affecting p53 protein accumulation.	SB 203580	48-56	P53	Homo sapiens	179-182
8562931-3	1996	Moreover, wild-type p53-expressing cells were more sensitive than p53-negative control cells to induction of differentiation by 1,25-dihydroxycholecalciferol; a twofold to fourfold increase of the fraction of cells showing signs of terminal maturation was observed when wild-type p53-expressing cells were incubated with 1,25-dihydroxycholecalciferol at concentrations that only slightly affected control cells.	Calcitriol	128-157	P53	Homo sapiens	20-23
8562931-3	1996	Moreover, wild-type p53-expressing cells were more sensitive than p53-negative control cells to induction of differentiation by 1,25-dihydroxycholecalciferol; a twofold to fourfold increase of the fraction of cells showing signs of terminal maturation was observed when wild-type p53-expressing cells were incubated with 1,25-dihydroxycholecalciferol at concentrations that only slightly affected control cells.	Calcitriol	128-157	P53	Homo sapiens	66-69
18585854-4	2008	NS, genistein and IR increased phosphorylation of p53 and p21 CIP1 at serine 15 (phos-p53).	phosphorylethanolamine	31-35	P53	Homo sapiens	50-53
19176374-8	2009	Together, these results provide evidence, for the first time, of the critical role of p21 and p27 in mediating the anticancer efficacy of IP6, and suggest their redundant role in the antiproliferative and proapoptotic effects of IP6 in p53-lacking human PCa cells, both in vitro and in vivo.	Phytic Acid	138-141	P53	Homo sapiens	236-239
19176374-8	2009	Together, these results provide evidence, for the first time, of the critical role of p21 and p27 in mediating the anticancer efficacy of IP6, and suggest their redundant role in the antiproliferative and proapoptotic effects of IP6 in p53-lacking human PCa cells, both in vitro and in vivo.	Phytic Acid	229-232	P53	Homo sapiens	236-239
18585854-4	2008	NS, genistein and IR increased phosphorylation of p53 and p21 CIP1 at serine 15 (phos-p53).	phosphorylethanolamine	31-35	P53	Homo sapiens	86-89
8562931-3	1996	Moreover, wild-type p53-expressing cells were more sensitive than p53-negative control cells to induction of differentiation by 1,25-dihydroxycholecalciferol; a twofold to fourfold increase of the fraction of cells showing signs of terminal maturation was observed when wild-type p53-expressing cells were incubated with 1,25-dihydroxycholecalciferol at concentrations that only slightly affected control cells.	Calcitriol	128-157	P53	Homo sapiens	66-69
18619705-13	2009	Being a topoisomerase II inhibitor, ellipticine proved a regulator in autophagy-related cell death through corporation of p53 and Akt.	ellipticine	36-47	P53	Homo sapiens	122-125
8562931-3	1996	Moreover, wild-type p53-expressing cells were more sensitive than p53-negative control cells to induction of differentiation by 1,25-dihydroxycholecalciferol; a twofold to fourfold increase of the fraction of cells showing signs of terminal maturation was observed when wild-type p53-expressing cells were incubated with 1,25-dihydroxycholecalciferol at concentrations that only slightly affected control cells.	Calcitriol	321-350	P53	Homo sapiens	20-23
8562931-5	1996	The p53-induced cell death could be inhibited by incubation with 1,25-dihydroxy-cholecalciferol, but not all-trans retinoic acid.	Calcitriol	65-95	P53	Homo sapiens	4-7
8562931-6	1996	Thus, 1,25-dihydroxycholecalciferol, seemed to increase the survival of wild-type p53-expressing cells and to cooperate with wild-type p53 to induce differentiation.	Calcitriol	6-35	P53	Homo sapiens	82-85
20067883-15	2009	beta-carotene, lycopene and all-trans retinoic acid alone and in combination with docetaxel were found to influence the expression of bcl-2 and p53 antigen in the cells examined.	Lycopene	15-23	P53	Homo sapiens	144-147
18842998-1	2008	This study explores the relationship between genetic polymorphisms of p53, p21, and CCND1, and the susceptibility of chromosomal damage induced by vinyl chloride monomer (CH(2)=CHCl, VCM).	Vinyl Chloride	147-161	P53	Homo sapiens	70-73
8562931-6	1996	Thus, 1,25-dihydroxycholecalciferol, seemed to increase the survival of wild-type p53-expressing cells and to cooperate with wild-type p53 to induce differentiation.	Calcitriol	6-35	P53	Homo sapiens	135-138
18712872-1	2008	Chlorofusin is a recently isolated, naturally occurring inhibitor of p53-MDM2 complex formation whose structure is composed of a densely functionalized azaphilone-derived chromophore linked through the terminal amine of ornithine to a nine residue cyclic peptide.	Ornithine	220-229	P53	Homo sapiens	69-72
19033390-3	2008	We recently showed that p53 localizes to the nucleolus after proteasome inhibition with MG132 and this localization requires sequences within its carboxyl terminus.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	88-93	P53	Homo sapiens	24-27
19033390-4	2008	In the present study, we found that after treatment with MG132, p53 associates with a discrete sub-nucleolar component, the fibrillar center (FC), a region mainly enriched with RNA polymerase I.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	P53	Homo sapiens	64-67
7563172-0	1995	Accumulation of p53 protein as a possible predictor of response to adjuvant combination chemotherapy with cyclophosphamide, methotrexate, fluorouracil, and prednisone for breast cancer.	Prednisone	156-166	P53	Homo sapiens	16-19
19106635-0	2008	Non-genotoxic anti-neoplastic effects of ellipticine derivative NSC176327 in p53-deficient human colon carcinoma cells involve stimulation of p73.	ellipticine	41-52	P53	Homo sapiens	77-80
19106635-2	2008	Here we further examined the anti-tumor effects of selected compounds in vitro and showed that NSC176327, a derivative of the cytotoxic plant alkaloid ellipticine, exhibited strong anti-neoplastic effect sin wild-type p53, p53-mutant or p53-deficient human colon cancer cells.	ellipticine	151-162	P53	Homo sapiens	218-221
19106635-2	2008	Here we further examined the anti-tumor effects of selected compounds in vitro and showed that NSC176327, a derivative of the cytotoxic plant alkaloid ellipticine, exhibited strong anti-neoplastic effect sin wild-type p53, p53-mutant or p53-deficient human colon cancer cells.	ellipticine	151-162	P53	Homo sapiens	223-226
19106635-2	2008	Here we further examined the anti-tumor effects of selected compounds in vitro and showed that NSC176327, a derivative of the cytotoxic plant alkaloid ellipticine, exhibited strong anti-neoplastic effect sin wild-type p53, p53-mutant or p53-deficient human colon cancer cells.	ellipticine	151-162	P53	Homo sapiens	223-226
19106635-7	2008	These results demonstrate an important role of p73 in the anti-tumor effects of NSC176327,and suggest that a close analogue of ellipticine may act by a non-genotoxic mechanism targeting the p53/p73 pathway as compared to the original parent compound that targets the same pathway.	ellipticine	127-138	P53	Homo sapiens	190-193
18619459-8	2008	Similarly, high vitamin B(6) intake conferred a protective effect on p53-overexpressing cancers (top versus bottom quintile: RR, 0.57; 95% CI, 0.35-0.94; P(heterogeneity) = .01) but had no effect on p53 wild-type tumors.	Niacinamide	16-25	P53	Homo sapiens	199-202
18608210-0	2008	5-Aza-2"-deoxycytidine restores proapoptotic function of p53 in cancer cells resistant to p53-induced apoptosis.	Decitabine	0-22	P53	Homo sapiens	57-60
18608210-0	2008	5-Aza-2"-deoxycytidine restores proapoptotic function of p53 in cancer cells resistant to p53-induced apoptosis.	Decitabine	0-22	P53	Homo sapiens	90-93
7587895-8	1995	The relationship between p53 gene mutation and the metastatic potential of PG cells needs further exploration.	pg	75-77	P53	Homo sapiens	25-28
18608210-2	2008	The lack of p53 inducibility of Noxa was restored by treatment with the DNA methyltransferase inhibitor 5-Aza-2"-deoxycytidine (5-aza-CdR).	Decitabine	104-126	P53	Homo sapiens	12-15
19054132-7	2008	Accordingly, we demonstrated that reactive oxygen species (ROS) are highly produced in p53 yeast induced cell death as shown by dihydrorhodamine 123 staining.	dihydrorhodamine 123	128-144	P53	Homo sapiens	87-90
7537340-5	1995	Finally, we employed all three libraries to reveal the distinct mechanisms by which PAb421 and PAb122, two monoclonal antibodies that allosterically activate sequence-specific DNA binding by p53, react specifically with the same positively-charged C-terminal segment.	pab122	95-101	P53	Homo sapiens	191-194
19020741-5	2008	We also observed that curcumin induces p53 phosphorylation (Ser 15) and both compound C and SB203580 pretreatment inhibit p53 phosphorylation.	SB 203580	92-100	P53	Homo sapiens	122-125
19020042-6	2008	Treatment with p38 inhibitor, SB239063 protected primary dopaminergic neurons derived from human progenitor cells from MPP(+) mediated cell death and prevented the downstream phosphorylation of p53 and its translocation to the nucleus in vivo, in the ventral midbrain.	SB 239063	30-38	P53	Homo sapiens	194-197
18690840-11	2008	This retrospective study indicates that FHIT-/p53+ status might be a biological variable influencing the efficacy of carboplatin/gemcitabine treatment in NSCLC.	Carboplatin	117-128	P53	Homo sapiens	46-49
18690840-11	2008	This retrospective study indicates that FHIT-/p53+ status might be a biological variable influencing the efficacy of carboplatin/gemcitabine treatment in NSCLC.	gemcitabine	129-140	P53	Homo sapiens	46-49
7867767-5	1994	Both adrenalectomy-induced p53 expression and granule cell degeneration were prevented by daily administration of corticosterone.	Corticosterone	114-128	P53	Homo sapiens	27-30
18332866-4	2008	Conditional overexpression of p21 in p53-deficient cells revealed that hyperoxia also stimulates wortmannin-sensitive degradation of p21.	Wortmannin	97-107	P53	Homo sapiens	37-40
18511169-0	2008	Kotomolide A arrests cell cycle progression and induces apoptosis through the induction of ATM/p53 and the initiation of mitochondrial system in human non-small cell lung cancer A549 cells.	kotomolide A	0-12	P53	Homo sapiens	95-98
18085531-0	2008	Attenuation of DNA damage-induced p53 expression by arsenic: a possible mechanism for arsenic co-carcinogenesis.	Arsenic	52-59	P53	Homo sapiens	34-37
18085531-0	2008	Attenuation of DNA damage-induced p53 expression by arsenic: a possible mechanism for arsenic co-carcinogenesis.	Arsenic	86-93	P53	Homo sapiens	34-37
18085531-10	2008	Because p53 is required for proficient global NER, our data suggest that arsenic inhibits NER through suppressing p53 induction in response to DNA damage in cells with normal p53 gene expression.	Arsenic	73-80	P53	Homo sapiens	8-11
19010883-6	2008	Together, our data suggests that arsenic compounds predispose cells to malignant transformation by up-regulation of Hdm2 and subsequent p53 inactivation.	Arsenic	33-40	P53	Homo sapiens	136-139
18680765-4	2008	In addition to PML itself, numerous further tumour suppressors including transcriptional regulator p53, acetyl transferase CBP (CREB binding protein) and protein kinase HIPK2 (homeodomain interacting protein kinase 2) are recruited to PML NBs in response to genotoxic stress or oncogenic transformation and drive the senescence and apoptosis response by regulating p53 activity.	Niobium	239-242	P53	Homo sapiens	99-102
18680765-4	2008	In addition to PML itself, numerous further tumour suppressors including transcriptional regulator p53, acetyl transferase CBP (CREB binding protein) and protein kinase HIPK2 (homeodomain interacting protein kinase 2) are recruited to PML NBs in response to genotoxic stress or oncogenic transformation and drive the senescence and apoptosis response by regulating p53 activity.	Niobium	239-242	P53	Homo sapiens	365-368
18085531-10	2008	Because p53 is required for proficient global NER, our data suggest that arsenic inhibits NER through suppressing p53 induction in response to DNA damage in cells with normal p53 gene expression.	Arsenic	73-80	P53	Homo sapiens	114-117
18085531-10	2008	Because p53 is required for proficient global NER, our data suggest that arsenic inhibits NER through suppressing p53 induction in response to DNA damage in cells with normal p53 gene expression.	Arsenic	73-80	P53	Homo sapiens	114-117
18931711-5	2008	The CTL response triggered by p53 pulsed dendritic cells was assayed by MTT method.	monooxyethylene trimethylolpropane tristearate	72-75	P53	Homo sapiens	30-33
18619459-8	2008	Similarly, high vitamin B(6) intake conferred a protective effect on p53-overexpressing cancers (top versus bottom quintile: RR, 0.57; 95% CI, 0.35-0.94; P(heterogeneity) = .01) but had no effect on p53 wild-type tumors.	Niacinamide	16-25	P53	Homo sapiens	69-72
18619459-9	2008	CONCLUSIONS: We found that low folate and vitamin B(6) intake was associated with an increased risk of p53-overexpressing colon cancers but not wild-type tumors.	Niacinamide	42-51	P53	Homo sapiens	103-106
7954409-1	1994	The present study assessed the role of the p53 tumor suppressor gene in cell cycle arrest and apoptosis following treatment of Burkitt"s lymphoma and lymphoblastoid cell lines with gamma-rays, etoposide, nitrogen mustard, and cisplatin.	Mechlorethamine	204-220	P53	Homo sapiens	43-46
18621066-0	2008	Increased damage of exon 5 of p53 gene in workers from an arsenic plant.	Arsenic	58-65	P53	Homo sapiens	30-33
18249029-6	2008	Previously we have reported that the p53 codon 72 arginine (Arg) homozygous genotype is associated with the development of arsenic-induced keratosis.	Arsenic	123-130	P53	Homo sapiens	37-40
18249029-13	2008	This study suggests that individuals with keratosis are more susceptible to arsenic-induced health effects and genetic damage and that the arginine variant of p53 can further influence the repair capacity of arsenic-exposed individuals, leading to increased accumulation of chromosomal aberrations.	Arsenic	208-215	P53	Homo sapiens	159-162
18621066-11	2008	These results imply that base modification in exon 5 of p53 gene can be induced by arsenic.	Arsenic	83-90	P53	Homo sapiens	56-59
19062713-8	2008	PI3K activity and the expression of pAkt-S473 increased in a time-dependent manner, pmdm2-S166, p53 were also increased wortmannin inhibited phosphorylation of mdm2 and improved the p53 expression.	Wortmannin	120-130	P53	Homo sapiens	96-99
7954409-5	1994	The degree of G1 arrest observed with these agents correlated with the rate of p53 and p21Waf1/Cip1 protein accumulation: gamma-rays and etoposide induced rapid accumulation of both p53 and p21Waf1/Cip1; nitrogen mustard and cisplatin induced slow accumulation of p53 and no major accumulation of the p21Waf1/Cip1 protein.	Mechlorethamine	204-220	P53	Homo sapiens	79-82
19062713-8	2008	PI3K activity and the expression of pAkt-S473 increased in a time-dependent manner, pmdm2-S166, p53 were also increased wortmannin inhibited phosphorylation of mdm2 and improved the p53 expression.	Wortmannin	120-130	P53	Homo sapiens	182-185
7957582-7	1994	Radiation-induced apoptosis in TcR-alpha/beta+ T cells and B cells was efficiently inhibited by cycloheximide, indicating the requirement of de novo protein synthesis, including p53 protein, for radiation-induced apoptosis in both subpopulations.	Cycloheximide	96-109	P53	Homo sapiens	178-181
18430410-4	2008	Moreover, Elongator deficiency causes increased basal and daunomycin-induced expression of the pro-survival serum- and glucocorticoid-induced protein kinase (SGK) gene through a p53-dependent pathway.	Daunorubicin	58-68	P53	Homo sapiens	178-181
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	SB 203580	287-295	P53	Homo sapiens	85-88
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	SB 203580	287-295	P53	Homo sapiens	260-263
18719315-3	2008	Moreover, the ROS activated the p38 kinase, which in turn promoted the activation of p53, as verified by evidence showing that the ROS scavenger N-acetyl-cysteine (NAC) not only blocked the phosphorylation of p38 but also partially inhibited the activation of p53, and the p38 inhibitor SB203580 reduced the activation of p53 as well.	SB 203580	287-295	P53	Homo sapiens	260-263
8168107-3	1994	This p53-dependent response of GADD45 was further investigated in human cells with halogenated pyrimidines, which act as radiosensitizers when incorporated into cellular DNA.	Pyrimidines	95-106	P53	Homo sapiens	5-8
18541673-7	2008	The effect of butyrate is mediated through a release of NF-Y from the proximal CCAAT box and an enhancement of p53 binding.	Butyrates	14-22	P53	Homo sapiens	111-114
18541673-8	2008	The interaction of p53 with the promoter is dependent on p38 MAPK activity either in the absence or in the presence of butyrate.	Butyrates	119-127	P53	Homo sapiens	19-22
18266926-4	2008	We recently reported that PQ induces neuronal apoptosis through Bak activation, in contrast to MPP(+), the toxic metabolite of MPTP, which relies on Bax and p53.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	127-131	P53	Homo sapiens	157-160
8074464-2	1994	After infection with the retroviral vector Lhp53RNL expressing both the neomycin phosphotransferase gene and the wt p53 gene, the ability of infected cells to form colonies in G418 selective medium was markedly reduced and their morphology demonstrated changes toward a flattened and enlarged phenotype.	antibiotic G 418	176-180	P53	Homo sapiens	45-48
18492823-7	2008	Moreover, oxidized LDL increased luciferase activity of p53 in endothelial cells transfected with a p53 promoter construct, the increase of which was strikingly downregulated by EGCG and hesperetin.	hesperetin	187-197	P53	Homo sapiens	56-59
18492823-7	2008	Moreover, oxidized LDL increased luciferase activity of p53 in endothelial cells transfected with a p53 promoter construct, the increase of which was strikingly downregulated by EGCG and hesperetin.	hesperetin	187-197	P53	Homo sapiens	100-103
18406507-10	2008	SB203580 and PD98059, specific inhibitors of p38 MAPK and ERK, respectively, suppressed phosphorylation of p53 at Ser15, but the accumulation of p53 was only moderately reduced.	SB 203580	0-8	P53	Homo sapiens	107-110
18406507-10	2008	SB203580 and PD98059, specific inhibitors of p38 MAPK and ERK, respectively, suppressed phosphorylation of p53 at Ser15, but the accumulation of p53 was only moderately reduced.	SB 203580	0-8	P53	Homo sapiens	145-148
18406507-14	2008	Wortmannin, selective inhibitor of DNA-PK and ATM/ATR, abolished p53 phosphorylation, indicating an involvement of multiple pathways of p53 phosphorylation upon exposure to BaP.	Wortmannin	0-10	P53	Homo sapiens	65-68
18406507-14	2008	Wortmannin, selective inhibitor of DNA-PK and ATM/ATR, abolished p53 phosphorylation, indicating an involvement of multiple pathways of p53 phosphorylation upon exposure to BaP.	Wortmannin	0-10	P53	Homo sapiens	136-139
18523266-7	2008	The protein stability, Ser(392) phosphorylation and Lys(373)/Lys(382) acetylation of p53 were enhanced by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	106-111	P53	Homo sapiens	85-88
18523266-10	2008	Intracellular reactive oxygen species (ROS) generation after MG132 treatment contributed to p53, but not p65 nuclear translocation and DNA-binding activity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	61-66	P53	Homo sapiens	92-95
18400537-0	2008	De novo N-palmitoylsphingosine synthesis is the major biochemical mechanism of ceramide accumulation following p53 up-regulation.	Ceramides	79-87	P53	Homo sapiens	111-114
18400537-2	2008	Previously we had shown that, in a p53-dependent model of cell death, ceramide accumulated in a p53-dependent manner [Dbaibo GS, Pushkareva MY, Rachid RA, Alter N, Smyth MJ, Obeid LM, Hannun YA.	Ceramides	70-78	P53	Homo sapiens	35-38
18400537-2	2008	Previously we had shown that, in a p53-dependent model of cell death, ceramide accumulated in a p53-dependent manner [Dbaibo GS, Pushkareva MY, Rachid RA, Alter N, Smyth MJ, Obeid LM, Hannun YA.	Ceramides	70-78	P53	Homo sapiens	96-99
18400537-4	2008	In the current study, we investigated the biochemical pathways by which ceramide accumulated following p53 up-regulation.	Ceramides	72-80	P53	Homo sapiens	103-106
18400537-5	2008	In both Molt-4 LXSN leukemia cells exposed to gamma-irradiation and in EB-1 colon cancer cells treated with ZnCl(2), p53 up-regulation led to de novo ceramide synthesis with predominance of N-palmitoylsphingosine (C16-ceramide) synthesis.	Ceramides	150-158	P53	Homo sapiens	117-120
18400537-8	2008	The SPT inhibitor ISP-1 or the ceramide synthase inhibitor fumonisin B1 led to substantial inhibition of ceramide accumulation in response to p53 up-regulation.	Ceramides	31-39	P53	Homo sapiens	142-145
18289623-0	2008	Apoptotic death induced by the cyclophosphamide analogue mafosfamide in human lymphoblastoid cells: contribution of DNA replication, transcription inhibition and Chk/p53 signaling.	mafosfamide	57-68	P53	Homo sapiens	166-169
18289623-3	2008	Using the cyclophosphamide analogue mafosfamide, which does not need metabolic activation, we show that mafosfamide induces apoptosis dose and time dependently in lymphoblastoid cells, with clearly more apoptosis in p53(wt) cells.	mafosfamide	104-115	P53	Homo sapiens	216-219
18289623-9	2008	Mafosfamide caused p53 stabilization by phosphorylation of Ser15, 20 and 37, and activation of ATM/ATR and Chk1/Chk2.	mafosfamide	0-11	P53	Homo sapiens	19-22
7734145-2	1994	By immunoprecipitation with the PAb122 antibody, we show that serum stimulation of previously serum-deprived cells causes a dephosphorylation of the wild type P53 protein, which is accentuated by the TGF-beta 1 treatment.	pab122	32-38	P53	Homo sapiens	159-162
18474303-0	2008	Imatinib resistance in a novel translocation der(17)t(1;17)(q25;p13) with loss of TP53 but without BCR/ABL kinase domain mutation in chronic myelogenous leukemia.	Imatinib Mesylate	0-8	P53	Homo sapiens	82-86
18230337-0	2008	p53-, SIRT1-, and PARP-1-independent downregulation of p21WAF1 expression in nicotinamide-treated cells.	Niacinamide	77-89	P53	Homo sapiens	0-3
18230337-3	2008	In our study, the treatment of 10mM nicotinamide downregulated p21WAF1 expression in various human cells including p53-negative or SIRT1-knockdown cells indicating gene regulation not mediated by p53 or SIRT1.	Niacinamide	36-48	P53	Homo sapiens	115-118
18230337-3	2008	In our study, the treatment of 10mM nicotinamide downregulated p21WAF1 expression in various human cells including p53-negative or SIRT1-knockdown cells indicating gene regulation not mediated by p53 or SIRT1.	Niacinamide	36-48	P53	Homo sapiens	196-199
8221663-2	1993	Mutations of the p53 gene were found in six of seven ES cell lines: a missense mutation of TGC (Cys)--&gt;TAC (Try) at codon 141 in one, a missense mutation of CGT (Arg)--&gt;TGT (Cys) at codon 273 in one, a missense mutation of TGC (Cys)--&gt;TTC (Phe) at codon 176 in three, and one base deletion of CGC--&gt;CG at codon 283 in one.	Phenylalanine	249-252	P53	Homo sapiens	17-20
18058069-10	2008	Furthermore, we have shown that vincristine and lomustine up-regulated p21 protein level in a p53-independent manner.	Lomustine	48-57	P53	Homo sapiens	94-97
18413724-1	2008	BCR/ABL kinase-positive chronic myelogenous leukemia (CML) cells display genomic instability leading to point mutations in various genes including bcr/abl and p53, eventually causing resistance to imatinib and malignant progression of the disease.	Imatinib Mesylate	197-205	P53	Homo sapiens	159-162
8300928-6	1993	Most patients with lesions showing positive p53 immunoreactivity had, however, been exposed to additional risk factors before receiving PUVA therapy.	puva	136-140	P53	Homo sapiens	44-47
18249187-5	2008	Treatment of cells with nicotinamide, an inhibitor of Sirtuins, relieves the inhibition of p53 by Sirt2 and 14-3-3 beta/gamma.	Niacinamide	24-36	P53	Homo sapiens	91-94
18315954-8	2008	Moreover, pretreatment with FeSO4 and the carbon monoxide donor CORM-2, but not biliverdin, significantly protected p53-deficient cells from SNAP-induced cell death compared with normal cells.	Carbon Monoxide	42-57	P53	Homo sapiens	116-119
17724467-7	2008	The most of the p53 mutations (10/13) reactivated by amifostine were located in the part of the p53 gene coding for hydrophobic beta-sandwich structure of the DNA-binding domain.	Amifostine	53-63	P53	Homo sapiens	16-19
18027850-10	2008	Belinostat also increased the expression of p21 and decreased the expression of potentially oncogenic proteins (mutant p53 and ERG).	belinostat	0-10	P53	Homo sapiens	119-122
17724467-7	2008	The most of the p53 mutations (10/13) reactivated by amifostine were located in the part of the p53 gene coding for hydrophobic beta-sandwich structure of the DNA-binding domain.	Amifostine	53-63	P53	Homo sapiens	96-99
8300928-7	1993	p53 gene sequencing of PUVA-associated non-melanoma skin cancer (NMSC) may clarify whether p53 mutation contributes to the development of these tumors and whether this relates to PUVA therapy or prior carcinogen exposure.	puva	23-27	P53	Homo sapiens	0-3
18243168-0	2008	Sanguinarine causes DNA damage and p53-independent cell death in human colon cancer cell lines.	sanguinarine	0-12	P53	Homo sapiens	35-38
8300928-7	1993	p53 gene sequencing of PUVA-associated non-melanoma skin cancer (NMSC) may clarify whether p53 mutation contributes to the development of these tumors and whether this relates to PUVA therapy or prior carcinogen exposure.	puva	23-27	P53	Homo sapiens	91-94
18048073-8	2008	Simultaneous to p53 activation, psoralens induced mitochondrial depolarization, cytochrome c release, mitochondrial production of reactive oxygen species, as well as caspase-3 and -9 activation.	Furocoumarins	32-41	P53	Homo sapiens	16-19
8325885-5	1993	The functional DNA target for transcriptional modulation of the IL-6 promoter by p53 species included the multiple cytokine- and second messenger-response element (-173 to -145); point mutations in the transcription factor C/EBP beta-binding site within the second messenger-response element largely blocked the ability of p53 mutants Val-135 and Phe-132 to up-regulate this promoter.	Phenylalanine	347-350	P53	Homo sapiens	81-84
18179182-4	2008	In this work, double-stranded (ds-) oligonucleotides (ODNs) containing the consensus site are immobilized onto gold electrodes to capture wild-type p53.	double-stranded (ds-) oligonucleotides	14-52	P53	Homo sapiens	148-151
18283158-4	2008	RESULTS: In cells that express E6, proteasome inhibition with MG132 restored p53 protein levels and decreased proliferation in a dose-dependent fashion that was significantly more pronounced compared with controls.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	62-67	P53	Homo sapiens	77-80
17981542-4	2008	Wortmannin treatment was found to decrease p53 Ser37 phosphorylation in NBS-induced cells.	Wortmannin	0-10	P53	Homo sapiens	43-46
8517643-5	1993	Immunoreactive p53 was observed in the nuclei of the cancer cells in 15/33 (45%) by pAbDO-7, 11/26 (42%) by pAb1801, and 16/33 (48%) by pAbCM-1.	pabcm-1	136-143	P53	Homo sapiens	15-18
18154926-4	2008	Early p53 expression was also found after NMDA treatment but diminished later.	N-Methylaspartate	42-46	P53	Homo sapiens	6-9
18154926-6	2008	Blocking ERK1/2 activation with the upstream inhibitor U0126 inhibited NMDA-mediated p53 expression, suggesting that ERK1/2 signals drive the cells to apoptosis under these conditions.	N-Methylaspartate	71-75	P53	Homo sapiens	85-88
18154926-11	2008	We conclude that NMDA induces an early effect that involves activation of p53, ERK, PAK1, p21 and c-jun.	N-Methylaspartate	17-21	P53	Homo sapiens	74-77
18042465-5	2008	Similarly, zinc protoporphyrin (ZnPP), an inhibitor of HO, suppressed p53 expression in ARPE-19 cells, although ZnPP increased the level of HO-1 protein while inhibiting HO activity.	zinc protoporphyrin	11-30	P53	Homo sapiens	70-73
18042465-5	2008	Similarly, zinc protoporphyrin (ZnPP), an inhibitor of HO, suppressed p53 expression in ARPE-19 cells, although ZnPP increased the level of HO-1 protein while inhibiting HO activity.	zinc protoporphyrin	32-36	P53	Homo sapiens	70-73
18042465-7	2008	Based on these results, we conclude that HO activity is involved in the regulation of p53 expression in a ROS-independent mechanism, and also suggest that the expression of p53 in ARPE-19 cells is associated with heme metabolites such as biliverdin/bilirubin, carbon monoxide, and iron produced by the activity of HO.	Carbon Monoxide	260-275	P53	Homo sapiens	173-176
18669159-10	2008	Cidofovir inhibits the growth of strongly vascularized tumors via inhibition of the growth factor FGF2, and by increasing the expression of the tumor suppressor p53, leading to apoptosis.	Cidofovir	0-9	P53	Homo sapiens	161-164
8352892-4	1993	Serum-induced translocation of the p53 protein from the nucleus to the cytoplasm, as well as DNA and protein synthesis, were inhibited by cycloheximide.	Cycloheximide	138-151	P53	Homo sapiens	35-38
17945324-0	2007	Arsenic promotes centrosome abnormalities and cell colony formation in p53 compromised human lung cells.	Arsenic	0-7	P53	Homo sapiens	71-74
17945324-11	2007	Our present investigation demonstrated that arsenic would act specifically on p53 compromised cells (either with p53 dysfunction or inhibited) to induce centrosomal abnormality and colony formation.	Arsenic	44-51	P53	Homo sapiens	78-81
17945324-11	2007	Our present investigation demonstrated that arsenic would act specifically on p53 compromised cells (either with p53 dysfunction or inhibited) to induce centrosomal abnormality and colony formation.	Arsenic	44-51	P53	Homo sapiens	113-116
17945324-12	2007	These findings provided strong evidence on the carcinogenic promotional role of arsenic, especially under the condition of p53 dysfunction.	Arsenic	80-87	P53	Homo sapiens	123-126
18327303-6	2008	Incubation of tumor cells with pioglitazone resulted in increased levels of p53 and p27 and decreased levels of cyclin D1.	Pioglitazone	31-43	P53	Homo sapiens	76-79
1406686-2	1992	After treatment with proteinase K, the sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) band of p53 yields a single, discrete 157-nucleotide RNA, which was cloned, sequenced, and identified as 5.8S rRNA.	polyacrylamide	62-76	P53	Homo sapiens	116-119
19013355-6	2008	Generation of reactive oxygen species, accumulation of Ca(2+), upregulation of caspase-3, down regulation of bcl-2, and deficiency of p-53 lead to arsenic-induced apoptosis.	Arsenic	147-154	P53	Homo sapiens	134-138
17984062-4	2007	Mutation of the IP6-binding sites impair oligomerization, reduce interaction with Mdm2, and inhibit p53-dependent antiproliferative effects of beta-arr2, whereas the competence for receptor regulation and signaling is maintained.	Phytic Acid	16-19	P53	Homo sapiens	100-103
1501881-1	1992	The cellular p53 protein is so called because of its molecular weight as determined by SDS-polyacrylamide gel electrophoresis.	polyacrylamide	91-105	P53	Homo sapiens	13-16
17876337-1	2007	In advanced breast cancers, TP53 mutation is highly predictive of complete response to high-dose epirubicin/cyclophosphamide chemotherapy.	Cyclophosphamide	108-124	P53	Homo sapiens	28-32
23605632-5	2008	Sabarubicin exhibits a superior antitumor efficacy, presumably related to theactivation of p53-independent apoptosis.	sabarubicin	0-11	P53	Homo sapiens	91-94
2155427-6	1990	p53 synthesized by Mahlavu cells showed a slower migration on SDS/polyacrylamide gels suggesting it was an abnormal protein.	polyacrylamide	66-80	P53	Homo sapiens	0-3
17707793-0	2007	Isokotomolide A, a new butanolide extracted from the leaves of Cinnamomum kotoense, arrests cell cycle progression and induces apoptosis through the induction of p53/p21 and the initiation of mitochondrial system in human non-small cell lung cancer A549 cells.	kotomolide A	0-15	P53	Homo sapiens	162-165
17717041-0	2007	Synergy between docosahexaenoic acid and butyrate elicits p53-independent apoptosis via mitochondrial Ca(2+) accumulation in colonocytes.	Butyrates	41-49	P53	Homo sapiens	58-61
17912033-3	2007	We found that following knock-down of Plk2 in wild-type p53 expressing H460 human non-small cell lung cancer cells there was a significant increase in cell death observed in aphidicolin-treated cells and a further increase after release from aphidicolin-block.	Aphidicolin	174-185	P53	Homo sapiens	56-59
17912033-3	2007	We found that following knock-down of Plk2 in wild-type p53 expressing H460 human non-small cell lung cancer cells there was a significant increase in cell death observed in aphidicolin-treated cells and a further increase after release from aphidicolin-block.	Aphidicolin	242-253	P53	Homo sapiens	56-59
17704360-6	2007	We found that the glioma cell lines repaired DSBs more slowly and less effectively than did NHAs in the clinically relevant dose range, as assessed by induction and resolution of H2AX phosphorylation, and this was most marked in the three TP53-mutated cell lines (T98G, A7, and U373).	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	45-49	P53	Homo sapiens	239-243
17717041-11	2007	On the basis of these data, we propose that the combination of DHA and butyrate compared with butyrate alone further enhances colonocyte apoptosis by inducing a p53-independent, oxidation-sensitive, mitochondrial Ca(2+) -dependent (intrinsic) pathway.	Butyrates	71-79	P53	Homo sapiens	161-164
11931974-0	2002	Vanadate-induced cell growth arrest is p53-dependent through activation of p21 in C141 cells.	Vanadates	0-8	P53	Homo sapiens	39-42
17974987-10	2007	Inhibiting Aur-A by VX-680 induced expression of p53 and potently sensitized cells to radiotherapy, leading to significant cell death.	VX680	20-26	P53	Homo sapiens	49-52
17569822-3	2007	Importantly, the imatinib resistance mechanism in these variants also included aberrant acetylation of nonhistone proteins such as p53, Ku70, and Hsp90 that was due to upregulation of histone deacetylases (HDACs) and down-regulation of histone acetyltransferase (HAT).	Imatinib Mesylate	17-25	P53	Homo sapiens	131-134
17569822-4	2007	In comparison with K562 cells, the imatinib-resistant variants showed up-regulation of HDAC1, -2, and -3 (class I HDACs) and class III SIRT1 and down-regulation of CBP/p300 and PCAF with HAT activity, and thereby p53 and cytoplasmic Ku70 were aberrantly acetylated.	Imatinib Mesylate	35-43	P53	Homo sapiens	213-216
17569822-7	2007	These results indicate that alteration of the normal balance of HATs and HDACs leads to deregulated acetylation of Hsp90, p53, and Ku70 and thereby leads to imatinib resistance, suggesting the importance of the acetylation status of apoptosis-related nonhistone proteins in Bcr-Abl-independent imatinib resistance.	Imatinib Mesylate	157-165	P53	Homo sapiens	122-125
11931974-5	2002	The present study investigated the regulation of p53 on vanadate-induced cell growth arrest using both p53 wild type C141 cells and p53 deficient embryo fibroblasts (p53 -/-).	Vanadates	56-64	P53	Homo sapiens	49-52
17578896-0	2007	Low-dose BBR3610 toxicity in colon cancer cells is p53-independent and enhanced by inhibition of epidermal growth factor receptor (ERBB1)-phosphatidyl inositol 3 kinase signaling.	BBR3610	9-16	P53	Homo sapiens	51-54
18226366-1	2007	OBJECTIVE: To explore the relationship between genetic polymorphism of P53, P21, CCND1 and susceptibility of chromosomal damage induced by vinyl chloride monomer (VCM).	Vinyl Chloride	139-153	P53	Homo sapiens	71-74
17671697-7	2007	In addition, the gemcitabine pretreatment up-regulated DR-5 and p53 protein expression in a time-dependent manner, which suggests the possible involvement of the p53 protein as a transcriptional factor for DR-5 up-regulation.	gemcitabine	17-28	P53	Homo sapiens	64-67
17224908-6	2007	Proteasome inhibition by MG132 increases the occupancy of p53 protein at p53-responsive p21(waf1) promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	P53	Homo sapiens	58-61
17671697-7	2007	In addition, the gemcitabine pretreatment up-regulated DR-5 and p53 protein expression in a time-dependent manner, which suggests the possible involvement of the p53 protein as a transcriptional factor for DR-5 up-regulation.	gemcitabine	17-28	P53	Homo sapiens	162-165
11931974-8	2002	Luciferase assay showed that vanadate induced p53 activation in a dose- and time-dependent manner in p53 wild type C141 cells.	Vanadates	29-37	P53	Homo sapiens	46-49
17224908-6	2007	Proteasome inhibition by MG132 increases the occupancy of p53 protein at p53-responsive p21(waf1) promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	P53	Homo sapiens	73-76
11931974-8	2002	Luciferase assay showed that vanadate induced p53 activation in a dose- and time-dependent manner in p53 wild type C141 cells.	Vanadates	29-37	P53	Homo sapiens	101-104
11931974-12	2002	The results obtained from the present study suggest that vanadate is able to induce S phase arrest through p53- and p21-dependent pathway.	Vanadates	57-65	P53	Homo sapiens	107-110
17567589-0	2007	p53 response to arsenic exposure in epithelial cells: protein kinase B/Akt involvement.	Arsenic	16-23	P53	Homo sapiens	0-3
17567589-6	2007	Although in both cell systems arsenic leads to an increase in p53 and its binding to DNA, the final outcome is different.	Arsenic	30-37	P53	Homo sapiens	62-65
34708431-0	2022	Dieckol induces cell cycle arrest by down-regulating CDK2/cyclin E in response to p21/p53 activation in human tracheal fibroblasts.	dieckol	0-7	P53	Homo sapiens	86-89
17567589-8	2007	In sharp contrast, in C33-A cells, arsenic leads to a transient increase in p53 followed by a drastic reduction in its nuclear levels and an increase in cell proliferation.	Arsenic	35-42	P53	Homo sapiens	76-79
17567589-9	2007	These findings favor the notion that p53-stage and transcriptional abilities are important to understand modifications in the proliferation-differentiation balance, an equilibrium that is severely impaired by arsenic.	Arsenic	209-216	P53	Homo sapiens	37-40
17408702-11	2007	Among all subjects p53 plasma levels were positively correlated with p21(WAF1) levels, exposure to B[a]P, c-PAHs and levels of total DNA adducts; for p21(WAF1) levels we observed the positive correlation with cotinine, c-PAHs exposure, total and B[a]P-like DNA adduct levels.	Cotinine	209-217	P53	Homo sapiens	19-22
17005319-6	2007	Further, sanguinarine-treatment to AsPC-1 and BxPC-3 cells resulted in a dose dependent (i) increase in pro-apoptotic Bax, Bid and Bak proteins; (ii) decrease in anti-apoptotic Bcl-2 and Bcl-X(L) proteins; and (iii) decrease in p53 with an increase in its phosphorylation.	sanguinarine	9-21	P53	Homo sapiens	228-231
34708431-5	2022	The results showed that dieckol had significant anti-proliferative activity against Hs680.Tr human tracheal fibroblastsWestern blotting analysis also found that dieckol dose-dependently induced the cell cycle arrest of Hs680.Tr fibroblasts in the G0/G1 phase, accompanied by the downregulation of CDK2 and cyclin E and the upregulation of p21 and p53.	dieckol	24-31	P53	Homo sapiens	347-350
17397394-7	2007	Intriguingly, histone deacetylase inhibitor (nicotinamide) treatment strongly inhibited the oxidative stress-induced nuclear translocation of p53 as well as the p53-dependent apoptosis in Huh6 cells.	Niacinamide	45-57	P53	Homo sapiens	142-145
34708431-5	2022	The results showed that dieckol had significant anti-proliferative activity against Hs680.Tr human tracheal fibroblastsWestern blotting analysis also found that dieckol dose-dependently induced the cell cycle arrest of Hs680.Tr fibroblasts in the G0/G1 phase, accompanied by the downregulation of CDK2 and cyclin E and the upregulation of p21 and p53.	dieckol	161-168	P53	Homo sapiens	347-350
17397394-7	2007	Intriguingly, histone deacetylase inhibitor (nicotinamide) treatment strongly inhibited the oxidative stress-induced nuclear translocation of p53 as well as the p53-dependent apoptosis in Huh6 cells.	Niacinamide	45-57	P53	Homo sapiens	161-164
17725105-11	2007	The superiority of 5-FU-CPT-11 sequence was proven for p53 mutant colon cancer, SW480.	5-fu-cpt-11	19-30	P53	Homo sapiens	55-58
34708431-7	2022	These findings suggest that dieckol from E. cava inhibits the cell proliferation of Hs680.Tr, potentially through p21- and p53-mediated G0/G1 cell cycle arrest.	dieckol	28-35	P53	Homo sapiens	123-126
34970530-0	2021	Design, Synthesis, Chemical and Biochemical Insights Into Novel Hybrid Spirooxindole-Based p53-MDM2 Inhibitors With Potential Bcl2 Signaling Attenuation.	Spirooxindole	71-84	P53	Homo sapiens	91-94
17276690-8	2007	Thus, our novel naphthoindole based derivative of tryptamine gained new activities important for anticancer therapy, namely, suppression of topoisomerase I and the ability to overcome resistance mediated by P-glycoprotein expression and p53 dysfunction.	tryptamine	50-60	P53	Homo sapiens	237-240
17292432-6	2007	On the other hand, treatment with wortmannin or caffeine, the inhibitors to phosphatidylinositol 3-kinase related kinases (PIKKs), suppressed both NaVO(3)-induced Ser15 phosphorylation and accumulation of p53 protein.	Wortmannin	34-44	P53	Homo sapiens	205-208
17063488-3	2007	We report that Carb or 5-FU upregulate Gadd45alpha and p53 in both these cells.	Carboplatin	15-19	P53	Homo sapiens	55-58
17150195-0	2007	Mitochondria-mediated and p53-associated apoptosis induced in human cancer cells by a novel selenophene derivative, D-501036.	Selenophene	92-103	P53	Homo sapiens	26-29
34970530-3	2021	In this study, we utilized a rapid synthetic route to synthesize two novel hybrid spirooxindole-based p53-MDM2 inhibitors endowed with Bcl2 signaling attenuation.	Spirooxindole	82-95	P53	Homo sapiens	102-105
16990847-7	2007	Thus, activation of p53 results in the inhibition of distinct rapamycin- and wortmannin-sensitive pathways that target eIF4GI, and rapamycin-sensitive and -insensitive pathways that target 4E-BP1.	Wortmannin	77-87	P53	Homo sapiens	20-23
34926700-10	2021	Six candidate protein targets were identified in both triptolide target network and DCM-associated network: STAT3, VEGFA, FOS, TNF, TP53, and TGFB1.	triptolide	54-64	P53	Homo sapiens	132-136
17226097-6	2007	Our immunohistochemical study showed that pitavastatin prevented the alterations of NF-kappaB and p53 in the hippocampal CA1 sector 5 days after transient ischemia.	pitavastatin	42-54	P53	Homo sapiens	98-101
17388661-0	2007	Exquisite sensitivity of TP53 mutant and basal breast cancers to a dose-dense epirubicin-cyclophosphamide regimen.	Cyclophosphamide	89-105	P53	Homo sapiens	25-29
17388661-16	2007	CONCLUSIONS: This study demonstrates that, in noninflammatory breast cancers, TP53 status is a key predictive factor for response to this dose-dense epirubicin-cyclophosphamide regimen and further suggests that the basal subtype is exquisitely sensitive to this association.	Cyclophosphamide	160-176	P53	Homo sapiens	78-82
34794098-0	2021	Molecular hybridization design and synthesis of novel spirooxindole-based MDM2 inhibitors endowed with BCL2 signaling attenuation; a step towards the next generation p53 activators.	Spirooxindole	54-67	P53	Homo sapiens	166-169
17534123-8	2007	Phosphatidylinositol 3-kinase (PI3K) inhibitors, wortmannin and LY294002 abolished the effect of RSVL on p53 activation.	Wortmannin	49-59	P53	Homo sapiens	105-108
34258881-0	2021	Mechanistic insights into p53-regulated cytotoxicity of combined entinostat and irinotecan against colorectal cancer cells.	entinostat	65-75	P53	Homo sapiens	26-29
16528528-10	2006	FDXR gene expression, which is regulated at least in part by p53, is associated with both response and survival when metastatic colorectal cancer is treated with 5-FU plus LV.	Leucovorin	172-174	P53	Homo sapiens	61-64
16690105-7	2006	In the gemcitabine plus cisplatin treatment arm compared to either alone, there was also downregulation of MSH2, p53, and ERCC1 expression.	gemcitabine	7-18	P53	Homo sapiens	113-116
17263498-0	2007	6-shogaol (alkanone from ginger) induces apoptotic cell death of human hepatoma p53 mutant Mahlavu subline via an oxidative stress-mediated caspase-dependent mechanism.	mahlavu	91-98	P53	Homo sapiens	80-83
17278190-8	2007	CPE and MTT assay indicated that CNHK500-p53 selectively replicated in and killed HCC cells while leaving normal cells unaffected.	monooxyethylene trimethylolpropane tristearate	8-11	P53	Homo sapiens	41-44
17135248-8	2007	Importantly, we found that inhibition of Plk3 by wortmannin lead to a decrease in phosphorylation of p53 on serine 20 induced by DNA damage, demonstrating the effect of wortmannin on a downstream Plk3 target.	Wortmannin	49-59	P53	Homo sapiens	101-104
34850229-8	2022	MON 52276 and glyphosate altered the expression of genes in liver reflecting TP53 activation by DNA damage and circadian rhythm regulation.	glyphosate	14-24	P53	Homo sapiens	77-81
17135248-8	2007	Importantly, we found that inhibition of Plk3 by wortmannin lead to a decrease in phosphorylation of p53 on serine 20 induced by DNA damage, demonstrating the effect of wortmannin on a downstream Plk3 target.	Wortmannin	169-179	P53	Homo sapiens	101-104
17208232-0	2007	p53 regulates ERK activation in carboplatin induced apoptosis in cervical carcinoma: a novel target of p53 in apoptosis.	Carboplatin	32-43	P53	Homo sapiens	0-3
17208232-0	2007	p53 regulates ERK activation in carboplatin induced apoptosis in cervical carcinoma: a novel target of p53 in apoptosis.	Carboplatin	32-43	P53	Homo sapiens	103-106
16708390-0	2006	Adenovirus-mediated tBid overexpression results in therapeutic effects on p53-resistant hepatocellular carcinoma.	tBID	20-24	P53	Homo sapiens	74-77
34806333-4	2022	Moreover, WY-5 significantly up-regulate the protein level of p53 in SK-Hep-1 cells harboring wild-type p53.	wy-5	10-14	P53	Homo sapiens	62-65
17007547-11	2006	This study showed that the combination of cidofovir with ionizing radiation has an antiangiogenic effect associated with VEGF inhibition subsequent to E6 inhibition and TP53 restoration.	Cidofovir	42-51	P53	Homo sapiens	169-173
16459017-0	2006	Prognostic significance of p53 mutation in suboptimally resected advanced ovarian carcinoma treated with the combination chemotherapy of paclitaxel and carboplatin.	Carboplatin	152-163	P53	Homo sapiens	27-30
17208232-13	2007	Under similar treatment conditions p53 was also involved in Carb induced apoptosis in these cells.	Carboplatin	60-64	P53	Homo sapiens	35-38
17208232-14	2007	Therefore, we investigated the relation between p53 and ERK in Carb induced apoptosis in these cells.	Carboplatin	63-67	P53	Homo sapiens	48-51
17208232-15	2007	Abrogation of p53 transactivation activity by pifithrin alpha or dominant-negative mutant of p53 resulted in decrease in activation of ERK in Carb treated cells.	Carboplatin	142-146	P53	Homo sapiens	14-17
17208232-15	2007	Abrogation of p53 transactivation activity by pifithrin alpha or dominant-negative mutant of p53 resulted in decrease in activation of ERK in Carb treated cells.	Carboplatin	142-146	P53	Homo sapiens	93-96
17208232-16	2007	The present study for the first time proposes that p53 may act as one of the upstream regulators of ERK activation for the induction of apoptosis in Carb treated cervical cancer cells.	Carboplatin	149-153	P53	Homo sapiens	51-54
17679024-6	2007	Frequencies of p53 overexpression of carcinomas with MC were significantly lower compared to those without MC (21-27% vs. 55%).	Methylcholanthrene	53-55	P53	Homo sapiens	15-18
34806333-4	2022	Moreover, WY-5 significantly up-regulate the protein level of p53 in SK-Hep-1 cells harboring wild-type p53.	wy-5	10-14	P53	Homo sapiens	104-107
34583877-0	2021	Corrigendum to "Dihydroartemisin inhibits glioma invasiveness via a ROS to P53 to beta-catenin signaling" (Pharmacol.	dihydroartemisin	16-32	P53	Homo sapiens	75-78
16970927-0	2006	Indole-3-carbinol mediated cell cycle arrest of LNCaP human prostate cancer cells requires the induced production of activated p53 tumor suppressor protein.	indole-3-carbinol	0-17	P53	Homo sapiens	127-130
16880619-7	2006	The phoshatidylinositol 3-kinase (PI3-K) family inhibitor wortmanin and the MEK inhibitor (PD98059) rescued the viability loss induced by uncarinic acid E through the expression of p53.	Wortmannin	58-67	P53	Homo sapiens	181-184
16820892-7	2006	Gemcitabine and paclitaxel are highly efficient in the induction of apoptosis in ovarian cancer cells, which express a particular subset of the growth suppressor protein p53.	gemcitabine	0-11	P53	Homo sapiens	170-173
16632641-0	2006	Plumbagin (5-hydroxy-2-methyl-1,4-naphthoquinone) induces apoptosis and cell cycle arrest in A549 cells through p53 accumulation via c-Jun NH2-terminal kinase-mediated phosphorylation at serine 15 in vitro and in vivo.	plumbagin	0-9	P53	Homo sapiens	112-115
16632641-0	2006	Plumbagin (5-hydroxy-2-methyl-1,4-naphthoquinone) induces apoptosis and cell cycle arrest in A549 cells through p53 accumulation via c-Jun NH2-terminal kinase-mediated phosphorylation at serine 15 in vitro and in vivo.	plumbagin	11-48	P53	Homo sapiens	112-115
16872707-2	2006	It plays a crucial role in p53-dependent cellular response to DNA damage and oxidative stress by providing deoxyribonucleotides (dNTPs) to the DNA repair machinery and by scavenging reactive oxygen species (ROS).	Deoxyribonucleotides	107-127	P53	Homo sapiens	27-30
34729013-10	2021	Following Alectinib treatment, the allele frequency of ALK rearrangement and RB1 and TP53 mutations in plasma circulating tumor DNA decreased with the reduction in tumor size.	alectinib	10-19	P53	Homo sapiens	85-89
16741250-6	2006	However, inhibition of c-Abl with imatinib suppressed CD154-induced expression of p73, p73-induced expression of Bid and CD95, and blocked the sensitization of p53-deficient CLL cells to CD95-mediated or F-ara-A-induced apoptosis.	Imatinib Mesylate	34-42	P53	Homo sapiens	160-163
17079445-5	2006	In contrast, isogenic cells lacking functional p53 continued to enter S phase regardless of nutlin-3 pretreatment and remained highly susceptible to gemcitabine-mediated cytotoxicity.	gemcitabine	149-160	P53	Homo sapiens	47-50
16500682-6	2006	Treatment with sulforaphane (15 microM), PEITC (10 microM), indole-3-carbinol (10 microM) and 3,3"-diindolylmethane (10 microM) induced PARP cleavage after 24 and 48 h in both 40-16 and the 379.2 cell lines, suggestive of a p53-independent mechanism of apoptosis induction.	indole-3-carbinol	60-77	P53	Homo sapiens	224-227
16730688-10	2006	A 24 h treatment with 4-OHEN significantly induced p53 and p21WAF1 protein expression at 10 and 20 microM, as well as significantly induced the transactivation of a p53-luciferase reporter gene at 20 microM.	4-ohen	22-28	P53	Homo sapiens	51-54
17079445-6	2006	The sequential treatment with nutlin-3 alone, followed by transient exposure to nutlin-3 plus gemcitabine, efficiently compromised the clonogenicity of tumor cells with deletions or mutations of p53 but largely spared the proliferation of nontransformed human keratinocytes.	gemcitabine	94-105	P53	Homo sapiens	195-198
16730688-10	2006	A 24 h treatment with 4-OHEN significantly induced p53 and p21WAF1 protein expression at 10 and 20 microM, as well as significantly induced the transactivation of a p53-luciferase reporter gene at 20 microM.	4-ohen	22-28	P53	Homo sapiens	165-168
16510697-1	2006	In this study, a cationic water-soluble ceramide analog L-threo-C6-pyridinium-ceramide-bromide (L-t-C6-Pyr-Cer), which exhibits high solubility and bioavailability, inhibited the growth of various human head and neck squamous cell carcinoma (HNSCC) cell lines at low IC50 concentrations, independent of their p53 status.	Ceramides	40-48	P53	Homo sapiens	309-312
17034127-1	2006	From a set of weakly potent lead compounds, using in silico screening and small library synthesis, a series of 2-alkyl-3-aryl-3-alkoxyisoindolinones has been identified as inhibitors of the MDM2-p53 interaction.	2-alkyl-3-aryl-3-alkoxyisoindolinones	111-148	P53	Homo sapiens	195-198
17007547-0	2006	Cidofovir administered with radiation displays an antiangiogenic effect mediated by E6 inhibition and subsequent TP53-dependent VEGF repression in HPV18+ cell lines.	Cidofovir	0-9	P53	Homo sapiens	113-117
16611991-7	2006	Following our previous study on the contribution of residues 25 and 26 to p53-dependent hypoxia-induced apoptosis, we found that residues 25-26 and 53-54 and the polyproline- and DNA-binding regions are also required for both gene repression and the induction of apoptosis by p53 during hypoxia.	polyproline	162-173	P53	Homo sapiens	74-77
34770781-9	2021	RT-qPCR results indicated MPMC stimulated apoptosis as revealed by the upregulation of the pro-apoptosis gene markers Casepase-3, p53, Bax.	Xylylcarb	26-30	P53	Homo sapiens	130-133
16611991-7	2006	Following our previous study on the contribution of residues 25 and 26 to p53-dependent hypoxia-induced apoptosis, we found that residues 25-26 and 53-54 and the polyproline- and DNA-binding regions are also required for both gene repression and the induction of apoptosis by p53 during hypoxia.	polyproline	162-173	P53	Homo sapiens	276-279
16152627-0	2006	Indole-3-carbinol activates the ATM signaling pathway independent of DNA damage to stabilize p53 and induce G1 arrest of human mammary epithelial cells.	indole-3-carbinol	0-17	P53	Homo sapiens	93-96
16918599-10	2006	Similar to the primary tumour, the cell line showed p53 overexpression and had p53 mutation at codon 132: AAG (lys)--&gt;AAT (asp).	Adenosine Diphosphate Glucose	106-109	P53	Homo sapiens	79-82
16628227-9	2006	This enhancement of apoptosis by amifostine was associated with activation of p53 and dephosphorylation of Cdc2 proteins.	Amifostine	33-43	P53	Homo sapiens	78-81
16152627-9	2006	The p53-MDM2 interaction and absence of p21 production were restored in cells treated with I3C and the ATM inhibitor wortmannin.	Wortmannin	117-127	P53	Homo sapiens	4-7
34475048-0	2021	P53 Is Involved in Sunitinib Resistance and Poor Progression-free Survival After Sunitinib Treatment of Renal Cell Carcinoma.	Sunitinib	19-28	P53	Homo sapiens	0-3
16505115-1	2006	Nucleoside anticancer drugs like gemcitabine (2"-deoxy-2",2"-difluorocytidine) are potent inducers of p53, and ectopic expression of wild-type p53 sensitizes cells to these agents.	gemcitabine	33-44	P53	Homo sapiens	102-105
16505115-1	2006	Nucleoside anticancer drugs like gemcitabine (2"-deoxy-2",2"-difluorocytidine) are potent inducers of p53, and ectopic expression of wild-type p53 sensitizes cells to these agents.	gemcitabine	33-44	P53	Homo sapiens	143-146
16505115-1	2006	Nucleoside anticancer drugs like gemcitabine (2"-deoxy-2",2"-difluorocytidine) are potent inducers of p53, and ectopic expression of wild-type p53 sensitizes cells to these agents.	gemcitabine	46-77	P53	Homo sapiens	102-105
16885368-0	2006	The Aurora kinase inhibitor VX-680 induces endoreduplication and apoptosis preferentially in cells with compromised p53-dependent postmitotic checkpoint function.	VX680	28-34	P53	Homo sapiens	116-119
16885368-2	2006	Here, we define the role of p53 and p21(Waf1/Cip1) in cell cycle perturbations following exposure to VX-680.	VX680	101-107	P53	Homo sapiens	28-31
16885368-6	2006	In A549 cells, VX-680 induces the expression of p53 and p21(Waf1/Cip1) within 24 hours, with consequent inhibition of cyclin E-cdk2, and reduction of retinoblastoma protein phosphorylation, limiting endoreduplication.	VX680	15-21	P53	Homo sapiens	48-51
16505115-1	2006	Nucleoside anticancer drugs like gemcitabine (2"-deoxy-2",2"-difluorocytidine) are potent inducers of p53, and ectopic expression of wild-type p53 sensitizes cells to these agents.	gemcitabine	46-77	P53	Homo sapiens	143-146
34475048-0	2021	P53 Is Involved in Sunitinib Resistance and Poor Progression-free Survival After Sunitinib Treatment of Renal Cell Carcinoma.	Sunitinib	81-90	P53	Homo sapiens	0-3
16505115-3	2006	To clarify this issue, we examined the effects of gemcitabine and 4"-thio-beta-d-arabinofuranosylcytosine (T-ara-C) on p73, a structural and functional homologue of p53, whose activation could also account for nucleoside-induced apoptosis because no functionally significant mutations of p73 have been reported in cancers.	4'-thio-arabinofuranosylcytosine	66-105	P53	Homo sapiens	165-168
16505115-3	2006	To clarify this issue, we examined the effects of gemcitabine and 4"-thio-beta-d-arabinofuranosylcytosine (T-ara-C) on p73, a structural and functional homologue of p53, whose activation could also account for nucleoside-induced apoptosis because no functionally significant mutations of p73 have been reported in cancers.	4'-thio-arabinofuranosylcytosine	107-114	P53	Homo sapiens	165-168
34475048-3	2021	MATERIALS AND METHODS: We analysed the effects of p53 knockout on sunitinib resistance.	Sunitinib	66-75	P53	Homo sapiens	50-53
16505115-5	2006	T-ara-C and gemcitabine markedly induced p53 accumulation as well as increased levels of phospho-p53 (Ser15/Ser20/Ser46) and induced its binding to a consensus p53 response element.	4'-thio-arabinofuranosylcytosine	0-7	P53	Homo sapiens	41-44
16505115-5	2006	T-ara-C and gemcitabine markedly induced p53 accumulation as well as increased levels of phospho-p53 (Ser15/Ser20/Ser46) and induced its binding to a consensus p53 response element.	4'-thio-arabinofuranosylcytosine	0-7	P53	Homo sapiens	97-100
16527552-10	2006	Both Wortmannin and PD98059 elevated the level of p53 expression strikingly, however, only PD98059 suppressed the up-regulation trend of c-Myc expression induced by etoposide.	Wortmannin	5-15	P53	Homo sapiens	50-53
34475048-4	2021	p53 expression in 53 mRCC patients receiving first-line sunitinib was determined immunohistochemically.	Sunitinib	56-65	P53	Homo sapiens	0-3
16684279-2	2006	In the present study, we compared the effects of calcipotriol and methylprednisolone aseponate (MPA) treatments on bcl-2, p53 and ki-67 expressions in psoriatic patients in order to define a relationship between regulation of apoptosis and healing process in psoriasis.	methylprednisolone aseponate	66-94	P53	Homo sapiens	122-125
16505115-5	2006	T-ara-C and gemcitabine markedly induced p53 accumulation as well as increased levels of phospho-p53 (Ser15/Ser20/Ser46) and induced its binding to a consensus p53 response element.	4'-thio-arabinofuranosylcytosine	0-7	P53	Homo sapiens	97-100
16505115-5	2006	T-ara-C and gemcitabine markedly induced p53 accumulation as well as increased levels of phospho-p53 (Ser15/Ser20/Ser46) and induced its binding to a consensus p53 response element.	gemcitabine	12-23	P53	Homo sapiens	41-44
16505115-5	2006	T-ara-C and gemcitabine markedly induced p53 accumulation as well as increased levels of phospho-p53 (Ser15/Ser20/Ser46) and induced its binding to a consensus p53 response element.	gemcitabine	12-23	P53	Homo sapiens	97-100
34475048-6	2021	RESULTS: WST-1 assays showed that p53 knockout decreased sensitivity to sunitinib.	Sunitinib	72-81	P53	Homo sapiens	34-37
16505115-5	2006	T-ara-C and gemcitabine markedly induced p53 accumulation as well as increased levels of phospho-p53 (Ser15/Ser20/Ser46) and induced its binding to a consensus p53 response element.	gemcitabine	12-23	P53	Homo sapiens	97-100
34475048-9	2021	Kaplan-Meier analysis showed that p53-positive cases tended to be associated with poor progression-free survival (PFS) after first-line sunitinib treatment.	Sunitinib	136-145	P53	Homo sapiens	34-37
16505115-6	2006	Despite robust activation of p53 by T-ara-C and gemcitabine, we found that wild-type and p53-/- HCT 116 cells exhibited almost equivalent sensitivity towards these nucleosides.	4'-thio-arabinofuranosylcytosine	36-43	P53	Homo sapiens	29-32
16505115-6	2006	Despite robust activation of p53 by T-ara-C and gemcitabine, we found that wild-type and p53-/- HCT 116 cells exhibited almost equivalent sensitivity towards these nucleosides.	gemcitabine	48-59	P53	Homo sapiens	29-32
16505115-7	2006	Examination of p73 revealed that T-ara-C and gemcitabine markedly increased p73 protein levels and p73 DNA-binding activities in both p53-/- and wild-type cells.	4'-thio-arabinofuranosylcytosine	33-40	P53	Homo sapiens	134-137
16505115-7	2006	Examination of p73 revealed that T-ara-C and gemcitabine markedly increased p73 protein levels and p73 DNA-binding activities in both p53-/- and wild-type cells.	gemcitabine	45-56	P53	Homo sapiens	134-137
16505115-10	2006	HCT 116 lines, wherein the downstream p53/p73 targets Bax and PUMA (p53 up-regulated modulator of apoptosis) were deleted, were less sensitive to T-ara-C and gemcitabine.	4'-thio-arabinofuranosylcytosine	146-153	P53	Homo sapiens	38-41
16527443-4	2006	Flow cytometry analysis of the cell cycle indicated that sclareol was able to inhibit DNA synthesis induce arrest at the G(0/1) phase of the cycle apoptosis independent of p53.	sclareol	57-65	P53	Homo sapiens	172-175
16410370-7	2006	Aflatoxin B1, hepatitis B virus, hepatitis C virus, and vinyl chloride all caused TP53 mutations in human liver tumors, but the mutation spectrum for each agent differed.	Vinyl Chloride	56-70	P53	Homo sapiens	82-86
16505115-10	2006	HCT 116 lines, wherein the downstream p53/p73 targets Bax and PUMA (p53 up-regulated modulator of apoptosis) were deleted, were less sensitive to T-ara-C and gemcitabine.	4'-thio-arabinofuranosylcytosine	146-153	P53	Homo sapiens	68-71
16206288-6	2006	In vitro treatment with butyrate or propionic acid, but not succinic acid, elicited a positive response in the p53-p53R2 system.	Butyrates	24-32	P53	Homo sapiens	111-114
16505115-10	2006	HCT 116 lines, wherein the downstream p53/p73 targets Bax and PUMA (p53 up-regulated modulator of apoptosis) were deleted, were less sensitive to T-ara-C and gemcitabine.	gemcitabine	158-169	P53	Homo sapiens	38-41
34475048-10	2021	In the JAVELIN 101 study, TP53 mutation was significantly associated with poor PFS after sunitinib treatment.	Sunitinib	89-98	P53	Homo sapiens	26-30
16505115-10	2006	HCT 116 lines, wherein the downstream p53/p73 targets Bax and PUMA (p53 up-regulated modulator of apoptosis) were deleted, were less sensitive to T-ara-C and gemcitabine.	gemcitabine	158-169	P53	Homo sapiens	68-71
16206288-9	2006	Since failure of the p53-G(1) checkpoint may cause dysfunction of repair under the influence of butyrate, gene alterations may increase and spread through the genome, leading to tumorigenesis.	Butyrates	96-104	P53	Homo sapiens	21-24
34475048-11	2021	CONCLUSION: p53 may be involved in sunitinib resistance and represent a valuable marker for sunitinib treatment in mRCC.	Sunitinib	35-44	P53	Homo sapiens	12-15
16505115-0	2006	c-Abl-independent p73 stabilization during gemcitabine- or 4"-thio-beta-D-arabinofuranosylcytosine-induced apoptosis in wild-type and p53-null colorectal cancer cells.	4'-thio-arabinofuranosylcytosine	59-98	P53	Homo sapiens	134-137
34475048-11	2021	CONCLUSION: p53 may be involved in sunitinib resistance and represent a valuable marker for sunitinib treatment in mRCC.	Sunitinib	92-101	P53	Homo sapiens	12-15
16733561-0	2006	Quantitative analysis of the level of p53 and p21(WAF1) mRNA in human colon cancer HT-29 cells treated with inositol hexaphosphate.	Phytic Acid	108-130	P53	Homo sapiens	38-41
34212455-5	2021	MK-1775 synergized with CDDP to block proliferation, inducing apoptosis and mitotic catastrophe in TP53-mutant UC cells but not in TP53-wild-type cells.	adavosertib	0-7	P53	Homo sapiens	99-103
16251483-0	2006	DNA hypermethylation of promoter of gene p53 and p16 in arsenic-exposed people with and without malignancy.	Arsenic	56-63	P53	Homo sapiens	41-44
16170329-4	2005	Jasmonic acid and methyl jasmonate (0.25-3 mM) were each equally cytotoxic to both clones, whereas mutant p53-expressing cells were resistant to treatment with the radiomimetic agent neocarzinostatin and the chemotherapeutic agent bleomycin.	Zinostatin	183-199	P53	Homo sapiens	106-109
34212455-6	2021	Knocking down TP53 in TP53-wild-type cells induced synergism of MK-1775 and CDDP.	adavosertib	64-71	P53	Homo sapiens	14-18
16170329-5	2005	Neocarzinostatin and bleomycin induced an elevation in the p53 levels in wt p53-expressing cells, whereas methyl jasmonate did not.	Zinostatin	0-16	P53	Homo sapiens	59-62
34212455-6	2021	Knocking down TP53 in TP53-wild-type cells induced synergism of MK-1775 and CDDP.	adavosertib	64-71	P53	Homo sapiens	22-26
16170329-5	2005	Neocarzinostatin and bleomycin induced an elevation in the p53 levels in wt p53-expressing cells, whereas methyl jasmonate did not.	Zinostatin	0-16	P53	Homo sapiens	76-79
16297852-6	2006	However, mutant p53(143ala) increased the sensitivity of MRC-5 to C(2)-ceramide-induced apoptosis by markedly downregulating Bcl-2, pointing to a role for p53.	Ceramides	71-79	P53	Homo sapiens	16-19
16193384-6	2005	In contrast, p53 inactivation rendered D54 and U87MG cells significantly more resistant to cis-dichlorodiamminoplatinum (CDDP), another chemotherapeutic to which high-grade astrocytomas sometimes respond.	cis-dichlorodiamminoplatinum	91-119	P53	Homo sapiens	13-16
34484411-14	2021	Molecular docking results showed that daucosterol, delusive, dioxin, and panthogenin-B had the highest affinity for TP53, RPS27A, and UBC.	lyoniside	38-49	P53	Homo sapiens	116-120
15908516-6	2005	When treatment with E6 siRNA was coupled with chemotherapy, the p53 activity after treatment with carboplatin and paclitaxel was additively increased, whereas the p53 activation induced by the rest of the drugs was synergistically increased.	Carboplatin	98-109	P53	Homo sapiens	64-67
16297852-8	2006	Moreover, the ceramide-activated apoptotic pathway may be regulated by p53.	Ceramides	14-22	P53	Homo sapiens	71-74
16298757-2	2006	To clarify the mechanism of carcinogenesis, we investigated DNA damage by 4-hydrazinobenzoic acid using (32)P-labeled DNA fragments obtained from the human p53 and p16 tumor suppressor genes.	Phosphorus-32	104-109	P53	Homo sapiens	156-159
16024610-8	2005	NO treatment also induced the phosphorylation of p53 at Ser15; pretreatment with phosphoinositide-3 kinase (PI3K) family inhibitors, wortmannin, LY294002, and caffeine, blocked such phosphorylation, but the p38 mitogen-activated protein kinase inhibitor, SB203580, did not.	Wortmannin	133-143	P53	Homo sapiens	49-52
34484411-14	2021	Molecular docking results showed that daucosterol, delusive, dioxin, and panthogenin-B had the highest affinity for TP53, RPS27A, and UBC.	Boron	84-86	P53	Homo sapiens	116-120
16024610-8	2005	NO treatment also induced the phosphorylation of p53 at Ser15; pretreatment with phosphoinositide-3 kinase (PI3K) family inhibitors, wortmannin, LY294002, and caffeine, blocked such phosphorylation, but the p38 mitogen-activated protein kinase inhibitor, SB203580, did not.	SB 203580	255-263	P53	Homo sapiens	49-52
16432174-3	2006	Several groups have shown that treatment with cidofovir suppresses levels of E6 and E7, restoring cellular p53 and pRb levels, in turn slowing cell replication and increasing the susceptibility of the cancer cells to radiation and apoptosis.	Cidofovir	46-55	P53	Homo sapiens	107-110
34353269-12	2022	CONCLUSION: The novel imidazo(1,2-a)pyridine compound, La23, was synthesized and suppressed cell growth by inducing cell apoptosis via the p53/Bax mitochondrial apoptotic pathway.	la23	55-59	P53	Homo sapiens	139-142
16230356-0	2005	tumor suppressor p53 binds with high affinity to CTG.CAG trinucleotide repeats and induces topological alterations in mismatched duplexes.	ctg	49-52	P53	Homo sapiens	17-20
16230356-5	2005	We demonstrate for the first time that conformationally flexible CTG.CAG trinucleotide repeats comprise a novel class of p53-binding sites targeted by p53 in a DNA structure-dependent mode in vitro and in vivo.	ctg	65-68	P53	Homo sapiens	121-124
16230356-5	2005	We demonstrate for the first time that conformationally flexible CTG.CAG trinucleotide repeats comprise a novel class of p53-binding sites targeted by p53 in a DNA structure-dependent mode in vitro and in vivo.	ctg	65-68	P53	Homo sapiens	151-154
16230356-6	2005	Our major finding is that p53 binds to CTG.CAG tracts by different modes depending on the conformation of DNA.	ctg	39-42	P53	Homo sapiens	26-29
16230356-7	2005	Although p53 binds preferentially to hairpins formed by either CTG or CAG strands, it can also bind to linear forms of CTG.CAG tracts such as canonic B DNA or mismatched duplex.	ctg	63-66	P53	Homo sapiens	9-12
16230356-7	2005	Although p53 binds preferentially to hairpins formed by either CTG or CAG strands, it can also bind to linear forms of CTG.CAG tracts such as canonic B DNA or mismatched duplex.	ctg	119-122	P53	Homo sapiens	9-12
15958581-12	2005	Aminoflavone also induced RPA2 and p53 phosphorylation, and induced p21(Waf1/Cip1) and MDM2, demonstrating S-phase checkpoint activation.	aminoflavone	0-12	P53	Homo sapiens	35-38
15922892-4	2005	In 10 ACCs and five normal adrenal tissue specimens, methylation of the 16 CpG sites within the TP53 promoter was examined using bisulphite methylation sequencing.	hydrogen sulfite	129-139	P53	Homo sapiens	96-100
34413896-4	2021	Four compounds also showed antiproliferative activity, and compound AO-022/43452814 was the most potent hit with IC50 values of 19.35, 26.73, 12.63, and 24.14 muM against MCF7 (p53 +/+), MCF7 (p53 -/-), HCT116 (p53 +/+), and HCT116 (p53 -/-) cell lines, respectively.	ao-022	68-74	P53	Homo sapiens	177-180
15913393-7	2005	In addition, the acute onset of apoptosis correlates with transactivation of a standard wild-type TP53-responsive reporter (pG13-CAT) in CGL1 cells after radiation exposure.	pg13-cat	124-132	P53	Homo sapiens	98-102
16275167-4	2005	Cilostazol decreases the activity of phosphodiesterase type 3, leading to the accumulation of cyclic adenosine monophosphate, which initiates a cascade of events including upregulation of anti-oncogenes p53 and p21 and upregulation of hepatocyte growth factor (HGF).	Cilostazol	0-10	P53	Homo sapiens	203-206
34413896-4	2021	Four compounds also showed antiproliferative activity, and compound AO-022/43452814 was the most potent hit with IC50 values of 19.35, 26.73, 12.63, and 24.14 muM against MCF7 (p53 +/+), MCF7 (p53 -/-), HCT116 (p53 +/+), and HCT116 (p53 -/-) cell lines, respectively.	ao-022	68-74	P53	Homo sapiens	193-196
15981203-7	2005	The higher expression of p53 and p21/WAF1 in skin after single topical application of AO or isolated sanguinarine further confirms the tumorigenic response.	sanguinarine	101-113	P53	Homo sapiens	25-28
34413896-4	2021	Four compounds also showed antiproliferative activity, and compound AO-022/43452814 was the most potent hit with IC50 values of 19.35, 26.73, 12.63, and 24.14 muM against MCF7 (p53 +/+), MCF7 (p53 -/-), HCT116 (p53 +/+), and HCT116 (p53 -/-) cell lines, respectively.	ao-022	68-74	P53	Homo sapiens	211-214
16170329-7	2005	In contrast, neocarzinostatin and bleomycin induced death only in wt p53-expressing cells, in an apoptotic mode.	Zinostatin	13-29	P53	Homo sapiens	69-72
15882069-3	2005	In this study, Tb(3+) was used as a probe to examine how binding of a 22-residue peptide derived from the C-terminal regulatory domain of p53 affects the rate of Ca(2+) ion dissociation.	Terbium(3+)	15-21	P53	Homo sapiens	138-141
34413896-4	2021	Four compounds also showed antiproliferative activity, and compound AO-022/43452814 was the most potent hit with IC50 values of 19.35, 26.73, 12.63, and 24.14 muM against MCF7 (p53 +/+), MCF7 (p53 -/-), HCT116 (p53 +/+), and HCT116 (p53 -/-) cell lines, respectively.	ao-022	68-74	P53	Homo sapiens	233-236
34340691-14	2021	La3+, Ce3+, and F- are probably the main toxic substances in WSPM, and may be regulate the A549 cell cycle by affecting the expression of genes, such as MDM2, RB1, ATM, TP53, E2F1, CDK2 and CDK4.	ce3+	6-10	P53	Homo sapiens	169-173
15735711-2	2005	HMEC immortalized by a variety of agents (the chemical carcinogen benzo(a)pyrene, oncogenes c-myc and ZNF217, and/or dominant negative p53 genetic suppressor element GSE22) displayed marked upregulation (10-15 fold) of the telomere-binding protein, TRF2.	gse22	166-171	P53	Homo sapiens	135-138
16238441-3	2005	In the present study, we investigated the role of TP53 in the radiosensitizing effect of gemcitabine.	gemcitabine	89-100	P53	Homo sapiens	50-54
34321915-12	2021	Conclusion: The metabolic and volumetric parameters of 18F-FDG PET/CT were related to a variety of factors such as NSE, CFYRA21-1, SCC-ag, P53 and TNM stage, and have a predictive value in prognosis of NSCLC.	Fluorodeoxyglucose F18	55-62	P53	Homo sapiens	139-142
16196516-6	2005	On immunohistochemistry, only p53 reactivity was statistically different between MC and non-MC components in IMC cases.	Methylcholanthrene	81-83	P53	Homo sapiens	30-33
16196516-6	2005	On immunohistochemistry, only p53 reactivity was statistically different between MC and non-MC components in IMC cases.	Methylcholanthrene	92-94	P53	Homo sapiens	30-33
16127747-1	2005	AIM: p53-inducible ribonucleotide reductase small subunit 2 (p53R2) encodes a 351-amino-acid peptide, which catalyzes conversion of ribonucleoside diphosphates to the corresponding deoxyribonucleotides required for DNA replication and repair.	amino-acid peptide	82-100	P53	Homo sapiens	5-8
16127747-1	2005	AIM: p53-inducible ribonucleotide reductase small subunit 2 (p53R2) encodes a 351-amino-acid peptide, which catalyzes conversion of ribonucleoside diphosphates to the corresponding deoxyribonucleotides required for DNA replication and repair.	Deoxyribonucleotides	181-201	P53	Homo sapiens	5-8
15899123-10	2005	CONCLUSION: Shikonin induces HeLa cell apoptosis through the ERK, p53 and caspase pathways.	shikonin	12-20	P53	Homo sapiens	66-69
15727877-4	2005	3-(1-Piperazinyl)methyl and 3-(quinuclidin-3-yl)aminomethyl derivatives of 4,11-dihydroxynaphtho[2,3-f]indole-5,10-dione killed HCT116 colon carcinoma cells (carrying wild type p53) and their p53-null variant within the similar range of concentrations.	3-(1-piperazinyl)methyl	0-23	P53	Homo sapiens	177-180
15670751-0	2005	Indole-3-carbinol and 3,3"-diindolylmethane induce expression of NAG-1 in a p53-independent manner.	indole-3-carbinol	0-17	P53	Homo sapiens	76-79
15976193-4	2005	DON readily induced the phosphorylation and activity of p53 and this was inhibitable by SB203580.	SB 203580	88-96	P53	Homo sapiens	56-59
34298835-0	2021	D-Propranolol Impairs EGFR Trafficking and Destabilizes Mutant p53 Counteracting AKT Signaling and Tumor Malignancy.	DEXPROPRANOLOL	0-13	P53	Homo sapiens	63-66
16248462-3	2005	RESULT: The expression of p53 protein was 9.5% in chronic inflammation of nasopharyngeal epithelium(CINE), which was significantly lower than it in NPCs with 76.3% (P &lt; 0.01).	nicotinuric acid	100-104	P53	Homo sapiens	26-29
15688011-4	2005	While hypoxia induced p53 accumulation without expression of its responsive genes (bax and p21), daunomycin treatment restored p53 transactivation activity and cell cycle progression.	Daunorubicin	97-107	P53	Homo sapiens	127-130
15625077-13	2005	We also show that the p53 response to a challenging dose of diethylnitrosamine was attenuated in hepatocytes in situ and in primary cultures of hepatocytes by pravastatin pretreatment.	Diethylnitrosamine	60-78	P53	Homo sapiens	22-25
15561702-0	2005	Nitric oxide inhibition of homocysteine-induced human endothelial cell apoptosis by down-regulation of p53-dependent Noxa expression through the formation of S-nitrosohomocysteine.	S-nitrosohomocysteine	158-179	P53	Homo sapiens	103-106
15456408-2	2005	The purpose of the present study was to investigate the reversal mechanism of doxo resistance by the potent PARP [poly(ADP-ribose) polymerase] inhibitor ANI (4-amino-1,8-naphthalimide) in the p53-deficient breast cancer cell lines EVSA-T and MDA-MB-231.	4-amino-1,8-naphthalimide	153-156	P53	Homo sapiens	192-195
15456408-2	2005	The purpose of the present study was to investigate the reversal mechanism of doxo resistance by the potent PARP [poly(ADP-ribose) polymerase] inhibitor ANI (4-amino-1,8-naphthalimide) in the p53-deficient breast cancer cell lines EVSA-T and MDA-MB-231.	4-amino-1,8-naphthalimide	158-183	P53	Homo sapiens	192-195
15748509-8	2005	And in the group 3 of exposed intensity index, the positive rate of mutant p53 protein in the strata of Papanicolau grade III was higher than that in the strata of Papanicolau grade I significantly.	papanicolau	104-115	P53	Homo sapiens	75-78
15748509-8	2005	And in the group 3 of exposed intensity index, the positive rate of mutant p53 protein in the strata of Papanicolau grade III was higher than that in the strata of Papanicolau grade I significantly.	papanicolau	164-175	P53	Homo sapiens	75-78
15748509-11	2005	There was tight correlation between Papanicolau grade of exfoliated urothelial cells and the positive rate or the quantity of mutant p53 protein for the higher benzidine exposure intensity.	papanicolau	36-47	P53	Homo sapiens	133-136
15896464-8	2005	Taken together, we have concluded that the molecular mechanisms during ellipticine-mediated growth inhibition and induction of apoptosis in MCF-7 cells were due to (1) cell cycle arrest and induction of apoptosis, (2) induction of p53 and KIP1/p27 expression, (3) triggering of Fas/Fas ligand pathway, (4) disruption of mitochondrial function, and (5) the apoptotic signaling was amplified by cross-talk between Fas death receptor and mitochondrial apoptotic pathway.	ellipticine	71-82	P53	Homo sapiens	231-234
34253820-4	2021	This defect rendered accumulation of DNA damage in p53 mutant cells upon treatment with deoxyuridine analogues.	Deoxyuridine	88-100	P53	Homo sapiens	51-54
16158823-10	2005	We found overexpression of the p53 protein in lymphoid cells and a point missense mutation in codon 280 at exon 8 that changed AGA (Arg) to AGT (Ser).	polyethylene glycol-glutaminase-asparaginase	127-130	P53	Homo sapiens	31-34
16158962-10	2005	In our opinion, confirmed by the literature data, p53 immunostaining helps to biologically characterize CIN (in particular LCIN) when each case is evaluated separately considering HPV testing/typing.	lcin	123-127	P53	Homo sapiens	50-53
16227678-0	2005	Tyrosine kinase inhibitor STI571 (Imatinib) cooperates with wild-type p53 on K562 cell line to enhance its proapoptotic effects.	Imatinib Mesylate	26-32	P53	Homo sapiens	70-73
16227678-0	2005	Tyrosine kinase inhibitor STI571 (Imatinib) cooperates with wild-type p53 on K562 cell line to enhance its proapoptotic effects.	Imatinib Mesylate	34-42	P53	Homo sapiens	70-73
16227678-1	2005	In order to ascertain whether p53 has a role in chronic myeloid leukemia hematopoietic progenitor response to the innovative tyrosine kinase inhibitor STI571 (Imatinib), we overexpressed a wild type (wt) p53 construct in the K562 cell line, generated from a human blast crisis and lacking endogenous p53.	Imatinib Mesylate	159-167	P53	Homo sapiens	30-33
34447561-6	2021	To demonstrate its capability, we focussed on three PPIs between the eukaryotic regulatory protein 14-3-3sigma and its binding partners estrogen receptor ERalpha, the tumour suppressor p53, and the kinase LRRK2, whose interactions upon the addition of a small molecule, fusicoccin A, are differentially stabilised.	fusicoccin	270-282	P53	Homo sapiens	185-188
16097394-1	2005	The authors have recently demonstrated a significant gene-environment interaction between vinyl chloride exposure and polymorphisms in the DNA repair protein XRCC1 on the occurrence of mutant p53 biomarkers of vinyl chloride-induced genetic damage.	Vinyl Chloride	90-104	P53	Homo sapiens	192-195
16097394-1	2005	The authors have recently demonstrated a significant gene-environment interaction between vinyl chloride exposure and polymorphisms in the DNA repair protein XRCC1 on the occurrence of mutant p53 biomarkers of vinyl chloride-induced genetic damage.	Vinyl Chloride	210-224	P53	Homo sapiens	192-195
15609309-0	2005	5-Aza-2"-deoxycytidine induces p21WAF expression by demethylation of p73 leading to p53-independent apoptosis in myeloid leukemia.	Decitabine	0-22	P53	Homo sapiens	84-87
15738655-6	2005	However, PC3, an androgen-insensitive prostate cancer cell line with deletion of p53 showed an appreciable post-transcriptional induction of p21 expression after treatment with pioglitazone.	Pioglitazone	177-189	P53	Homo sapiens	81-84
34093774-9	2021	Notably, the latter was the only PDTC case exhibiting positivity for p53 and a cellular microenvironment similar to ATC.	prolinedithiocarbamate	33-37	P53	Homo sapiens	69-72
15837074-9	2005	The presence of Wortmannin, an inhibitor of PI-3 kinases, decreased BaP-induced p53 ser-15phos, as did the presence of the antioxidant vitamin E.	Wortmannin	16-26	P53	Homo sapiens	80-83
15837074-9	2005	The presence of Wortmannin, an inhibitor of PI-3 kinases, decreased BaP-induced p53 ser-15phos, as did the presence of the antioxidant vitamin E.	Vitamin E	135-144	P53	Homo sapiens	80-83
15582354-0	2005	Pyrrolizidine alkaloid clivorine induces apoptosis in human normal liver L-02 cells and reduces the expression of p53 protein.	Pyrrolizidine Alkaloids	0-22	P53	Homo sapiens	114-117
15533642-19	2005	Phenylacetate activates p53 and p21 through inhibition of methyltransferase and farnesylation of the RAS protein.	phenylacetate	0-13	P53	Homo sapiens	24-27
34172723-3	2021	Screening an oligopyridylamide library, previously shown to inhibit amyloid formation associated with Alzheimer"s disease and type II diabetes, identified a tripyridylamide, ADH-6, that abrogates self-assembly of the aggregation-nucleating subdomain of mutant p53 DBD.	oligopyridylamide	13-30	P53	Homo sapiens	260-263
16006755-0	2005	Enhancement of gemcitabine-induced apoptosis by restoration of p53 function in human pancreatic tumors.	gemcitabine	15-26	P53	Homo sapiens	63-66
16006755-7	2005	Moreover, the chemosensitization observed in tumors treated with the combination gemcitabine-p53 correlated with differential histological features such as important increases in intratumoral fibrosis and apoptotic levels, when compared with unimodal treatments.	gemcitabine	81-92	P53	Homo sapiens	93-96
16006755-8	2005	Taken together, our data indicate that reintroduction of p53 function in human pancreatic tumors in vivo allows to restore molecular pathways improving the response to gemcitabine.	gemcitabine	168-179	P53	Homo sapiens	57-60
15567145-5	2005	The ubiquitination and destabilization of p53 is observed in cells treated with the protease inhibitor MG132, implying that the HECT domain of hUREB1 suppresses the transcriptional activity of p53 through a ubiquitin-dependent degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	P53	Homo sapiens	42-45
15567145-5	2005	The ubiquitination and destabilization of p53 is observed in cells treated with the protease inhibitor MG132, implying that the HECT domain of hUREB1 suppresses the transcriptional activity of p53 through a ubiquitin-dependent degradation pathway.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	103-108	P53	Homo sapiens	193-196
34149863-13	2021	SCDP key active ingredients are mainly quercetin, wogonin, baicalein, acacetin, oroxylin A, and beta-sitosterol, which function mainly by regulating targets, such as PTGS2, CASP3, TP53, IL-6, TNF, and AKT1, and are associated with multiple signaling pathways as pathways in cancer, PI3K-Akt signaling pathway, apoptosis, IL-17 signaling pathways.	scdp	0-4	P53	Homo sapiens	180-184
15661398-8	2005	SAHA downregulated cyclin D1 and D2, and upregulated p53, p21, and p27.	Vorinostat	0-4	P53	Homo sapiens	53-56
15601469-5	2004	METHODS: The relationship between p53 and p21 protein levels and the cytotoxic effect of DOX was investigated, by MTT assay and western blot analysis, in HCT116 (p53-positive) and HT29 (p53-negative) colon cancer cells.	monooxyethylene trimethylolpropane tristearate	114-117	P53	Homo sapiens	34-37
34199777-5	2021	Carbon monoxide (CO) activated the ECE-1/endothelin-1 (ET-1) pathway, which could account for the protumoral effects of HO-1 in p53 wild-type cells, as demonstrated after treatment with bosentan (an antagonist of both ETRA and ETRB endothelin-1 receptors).	Bosentan	186-194	P53	Homo sapiens	128-131
15464845-7	2004	The over-expressed B1R protein induces the degradation of p53 in a concentration-dependent manner and is lost when Ser15 and Th18 are changed to alanine or when the B1R kinase is inactivated by introducing the K149Q substitution.	th18	125-129	P53	Homo sapiens	58-61
15611505-0	2004	Prediction of TP53 status for primary cisplatin, fluorouracil, and leucovorin chemotherapy in ethmoid sinus intestinal-type adenocarcinoma.	Leucovorin	67-77	P53	Homo sapiens	14-18
15509798-8	2004	Niacinamide (vitamin B(3)) increases the rate of intracellular NAD(+) synthesis, alters radiation-induced p53 DNA binding specificity, and modulates activation of a subset of p53 transcriptional targets.	Niacinamide	0-11	P53	Homo sapiens	106-109
15509798-8	2004	Niacinamide (vitamin B(3)) increases the rate of intracellular NAD(+) synthesis, alters radiation-induced p53 DNA binding specificity, and modulates activation of a subset of p53 transcriptional targets.	Niacinamide	0-11	P53	Homo sapiens	175-178
15509798-8	2004	Niacinamide (vitamin B(3)) increases the rate of intracellular NAD(+) synthesis, alters radiation-induced p53 DNA binding specificity, and modulates activation of a subset of p53 transcriptional targets.	Niacinamide	13-22	P53	Homo sapiens	106-109
15509798-8	2004	Niacinamide (vitamin B(3)) increases the rate of intracellular NAD(+) synthesis, alters radiation-induced p53 DNA binding specificity, and modulates activation of a subset of p53 transcriptional targets.	Niacinamide	13-22	P53	Homo sapiens	175-178
15492467-5	2004	The activation of p53 by oridonin was also blocked by wortmannin.	Wortmannin	54-64	P53	Homo sapiens	18-21
34199777-6	2021	Surprisingly, in cells with a non-active p53 or a mutated p53 with gain-of-function, ECE-1-produced ET-1 acted as a protective molecule, since treatment with bosentan led to increased efficiency for spheres formation and percentage of cancer stem cells (CSCs) markers.	Bosentan	158-166	P53	Homo sapiens	58-61
15509798-10	2004	Niacinamide and thiamine affect two p53-regulated cellular responses to ionizing radiation: rereplication and apoptosis.	Niacinamide	0-11	P53	Homo sapiens	36-39
15509798-11	2004	Thus, niacinamide and thiamine form a novel basis for the development of small molecules that affect p53 function in vivo, and these results suggest that changes in cellular energy metabolism may regulate p53.	Niacinamide	6-17	P53	Homo sapiens	101-104
34316707-5	2021	Notably, GPS167 impairs the growth of CRC cell lines and organoids, inhibits anchorage-independent colony formation, cell migration, and promotes cytoxicity in a manner that requires SRSF10 and p53.	gps167	9-15	P53	Homo sapiens	194-197
15509798-11	2004	Thus, niacinamide and thiamine form a novel basis for the development of small molecules that affect p53 function in vivo, and these results suggest that changes in cellular energy metabolism may regulate p53.	Niacinamide	6-17	P53	Homo sapiens	205-208
15371552-4	2004	Using such lipofectamine-delivered Acr-PNA conjugates, one PNA targeting a cryptic AUG initiation site was identified that at a concentration of 2 microM caused a reduction of MDM2 levels to approximately 20% (but no reduction in mdm2 mRNA levels) and a 3-fold increase in p53 levels, whereas a 2-base mismatch control had no such effects.	Lipofectamine	11-24	P53	Homo sapiens	273-276
15273730-0	2004	5-aza-2"-deoxycytidine upregulates caspase-9 expression cooperating with p53-induced apoptosis in human lung cancer cells.	Decitabine	0-22	P53	Homo sapiens	73-76
15273730-2	2004	However, when cells were treated with DAC and infected with a low dose of a recombinant wild-type p53 adenovirus vector (Ad-p53), a synergistic growth inhibitory effect was observed.	Decitabine	38-41	P53	Homo sapiens	98-101
15273730-2	2004	However, when cells were treated with DAC and infected with a low dose of a recombinant wild-type p53 adenovirus vector (Ad-p53), a synergistic growth inhibitory effect was observed.	Decitabine	38-41	P53	Homo sapiens	124-127
15273730-4	2004	Selective blockage of caspase-9 activities by Z-LEHD-FMK completely attenuated DAC-induced enhancement of apoptosis mediated by Ad-p53 infection, and ectopic overexpression of procaspase-9 sensitized cells to Ad-p53-induced apoptosis in p53-null cells.	Decitabine	79-82	P53	Homo sapiens	131-134
15131591-0	2004	Molecular mechanisms of TNF-alpha-induced ceramide formation in human glioma cells: P53-mediated oxidant stress-dependent and -independent pathways.	Ceramides	42-50	P53	Homo sapiens	84-87
15131591-2	2004	In cells possessing wild-type p53, TNF-alpha stimulated ceramide formation via the activation of both neutral and acid sphingomyelinases (SMases), accompanied by superoxide anion (O2-*) production, and induced mitochondrial depolarization and cytochrome c release, whereas p53-deficient cells were partially resistant to TNF-alpha and lacked O2-* generation and neutral SMase activation.	Ceramides	56-64	P53	Homo sapiens	30-33
15131591-2	2004	In cells possessing wild-type p53, TNF-alpha stimulated ceramide formation via the activation of both neutral and acid sphingomyelinases (SMases), accompanied by superoxide anion (O2-*) production, and induced mitochondrial depolarization and cytochrome c release, whereas p53-deficient cells were partially resistant to TNF-alpha and lacked O2-* generation and neutral SMase activation.	Ceramides	56-64	P53	Homo sapiens	273-276
15131591-6	2004	Two separate signaling cascades, p53-mediated ROS-dependent and -independent pathways, both of which are initiated by caspase-8 activation, thus contribute to ceramide formation in TNF-alpha-induced apoptosis of human glioma cells.	Ceramides	159-167	P53	Homo sapiens	33-36
15273730-4	2004	Selective blockage of caspase-9 activities by Z-LEHD-FMK completely attenuated DAC-induced enhancement of apoptosis mediated by Ad-p53 infection, and ectopic overexpression of procaspase-9 sensitized cells to Ad-p53-induced apoptosis in p53-null cells.	Decitabine	79-82	P53	Homo sapiens	212-215
15273730-4	2004	Selective blockage of caspase-9 activities by Z-LEHD-FMK completely attenuated DAC-induced enhancement of apoptosis mediated by Ad-p53 infection, and ectopic overexpression of procaspase-9 sensitized cells to Ad-p53-induced apoptosis in p53-null cells.	Decitabine	79-82	P53	Homo sapiens	212-215
15467443-0	2004	Treatment of chronic myeloid leukemia cells with imatinib (STI571) impairs p53 accumulation in response to DNA damage.	Imatinib Mesylate	49-57	P53	Homo sapiens	75-78
35562278-9	2022	RNA-seq of phenylalanine-treated organoids revealed that gene sets related to apoptosis, p53 signaling pathway, and TNF signaling pathway via NF-kB were enriched in upregulated genes, while those related to cell cycle and amino acid metabolism were enriched in downregulated genes.	Phenylalanine	11-24	P53	Homo sapiens	89-92
15467443-0	2004	Treatment of chronic myeloid leukemia cells with imatinib (STI571) impairs p53 accumulation in response to DNA damage.	Imatinib Mesylate	59-65	P53	Homo sapiens	75-78
15467443-4	2004	Here, we investigated the effect of STI571 treatment of CML cells on p53 regulation.	Imatinib Mesylate	36-42	P53	Homo sapiens	69-72
15467443-9	2004	CML cells expressing wild-type p53 are more resistant to treatment with STI571, but moderately more sensitive to DNA damage, than CML cells lacking p53.	Imatinib Mesylate	72-78	P53	Homo sapiens	31-34
15088070-0	2004	p53-Independent ceramide formation in human glioma cells during gamma-radiation-induced apoptosis.	Ceramides	16-24	P53	Homo sapiens	0-3
15088070-4	2004	The formation of ceramide by acid sphingomyelinase (A-SMase), but not by neutral sphingomyelinase, was associated with p53-independent apoptosis.	Ceramides	17-25	P53	Homo sapiens	119-122
15088070-9	2004	Moreover, cells with functional p53 could be sensitized to gamma-radiation by N-oleoylethanolamine, which suppressed radiation-induced acid ceramidase expression and then enhanced ceramide formation.	N-oleoylethanolamine	78-98	P53	Homo sapiens	32-35
15088070-9	2004	Moreover, cells with functional p53 could be sensitized to gamma-radiation by N-oleoylethanolamine, which suppressed radiation-induced acid ceramidase expression and then enhanced ceramide formation.	Ceramides	180-188	P53	Homo sapiens	32-35
15269146-0	2004	5" cytosine-phospho-guanine island methylation is responsible for p14ARF inactivation and inversely correlates with p53 overexpression in resected non-small cell lung cancer.	5" cytosine-phospho-guanine	0-27	P53	Homo sapiens	116-119
15764300-2	2004	A preliminary case-control study was conducted to explore the association between genetic polymorphisms of GSTT1, p53 codon 72 and bladder cancer in southern Taiwan, a former high arsenic exposure area.	Arsenic	180-187	P53	Homo sapiens	114-117
15088070-11	2004	These results indicate that ceramide may function as a mediator of p53-independent apoptosis in human glioma cells in response to gamma-radiation, and suggest that p53-dependent expression of acid ceramidase and blockage of A-SMase activation play pivotal roles in protection from gamma-radiation of cells with endogenous functional p53.	Ceramides	28-36	P53	Homo sapiens	67-70
35635656-4	2022	Furthermore, proteomics after p53 immunoprecipitation (RIME) uncovered the nuclear interactome under prolonged starvation, where we confirmed the novel p53 interactors SORBS1 (insulin receptor signaling) and UGP2 (glycogen synthesis).	Glycogen	214-222	P53	Homo sapiens	152-155
15088070-11	2004	These results indicate that ceramide may function as a mediator of p53-independent apoptosis in human glioma cells in response to gamma-radiation, and suggest that p53-dependent expression of acid ceramidase and blockage of A-SMase activation play pivotal roles in protection from gamma-radiation of cells with endogenous functional p53.	Ceramides	28-36	P53	Homo sapiens	164-167
15088070-11	2004	These results indicate that ceramide may function as a mediator of p53-independent apoptosis in human glioma cells in response to gamma-radiation, and suggest that p53-dependent expression of acid ceramidase and blockage of A-SMase activation play pivotal roles in protection from gamma-radiation of cells with endogenous functional p53.	Ceramides	28-36	P53	Homo sapiens	164-167
15293347-3	2004	METHODS: p53 nonviral-mediated gene transfer was achieved using glucosylated polyethylenimine (PEI) in conjunction with photochemical internalisation (PCI).	Polyethyleneimine	77-93	P53	Homo sapiens	9-12
15293347-3	2004	METHODS: p53 nonviral-mediated gene transfer was achieved using glucosylated polyethylenimine (PEI) in conjunction with photochemical internalisation (PCI).	Polyethyleneimine	95-98	P53	Homo sapiens	9-12
15111621-0	2004	Dioxin-induced immortalization of normal human keratinocytes and silencing of p53 and p16INK4a.	Dioxins	0-6	P53	Homo sapiens	78-81
15111621-3	2004	We have previously shown that in primary human keratinocytes, dioxin attenuates senescence while retaining the proliferative capacity and represses expression of the tumor suppressors, p16(INK4a) and p53.	Dioxins	62-68	P53	Homo sapiens	200-203
15111621-4	2004	Here, we show that repression of p16(INK4a) and p53 transcriptional activity by dioxin absolutely requires the AHR and is accompanied by promoter methylation.	Dioxins	80-86	P53	Homo sapiens	48-51
35536497-7	2022	The biological effects of the extracted polysaccharides from Ganoderma lucidum and Lentinula edodes on the MCF-7 cell line were investigated using an MTT assay and then its effects on the expression of the P53 cancer regulatory gene and HER-3 gene were investigated.	Polysaccharides	40-55	P53	Homo sapiens	206-209
15013522-6	2004	Combinations of 4-HPR and modulators of ceramide action and/or metabolism demonstrated increased anti-tumor activity in pre-clinical models with minimal toxicity for non-malignant cells, and were effective in a p53-independent manner against tumor cell lines resistant to standard cytotoxic agents.	Ceramides	40-48	P53	Homo sapiens	211-214
15010833-6	2004	MG132 treated HCT116 (wild-type) had a similar cell cycle distribution as the MG132 treated HCT116 (p53-/-) and HCT116 (p21-/-) cells, suggesting that p53 and p21 may not be essential for MG132-induced G2/M phase arrest.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	P53	Homo sapiens	151-154
15215325-7	2004	Amplification with Texas red- and fluorescein-tagged antibodies led, in the case of p53 in human cells, to red and green signals located in the comet tail (as well as in the head), indicating the presence of breaks in the vicinity of the gene.	Fluorescein	34-45	P53	Homo sapiens	84-87
35536497-9	2022	Polysaccharides of these two fungi increased the expression of the P53 gene and decreased the expression of the HER-3 gene in a dose and time-dependent manner.	Polysaccharides	0-15	P53	Homo sapiens	67-70
15201971-0	2004	Ceramide triggers caspase activation during gamma-radiation-induced apoptosis of human glioma cells lacking functional p53.	Ceramides	0-8	P53	Homo sapiens	119-122
15010833-6	2004	MG132 treated HCT116 (wild-type) had a similar cell cycle distribution as the MG132 treated HCT116 (p53-/-) and HCT116 (p21-/-) cells, suggesting that p53 and p21 may not be essential for MG132-induced G2/M phase arrest.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	P53	Homo sapiens	100-103
15010833-6	2004	MG132 treated HCT116 (wild-type) had a similar cell cycle distribution as the MG132 treated HCT116 (p53-/-) and HCT116 (p21-/-) cells, suggesting that p53 and p21 may not be essential for MG132-induced G2/M phase arrest.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	78-83	P53	Homo sapiens	100-103
15201971-1	2004	We have previously shown that treatment of human glioma U87-MG cells expressing wild-type p53 with a DNA topoisomerase II inhibitor, etoposide resulted in ceramide-dependent apoptotic cell death.	Ceramides	155-163	P53	Homo sapiens	90-93
15201971-6	2004	Activation of caspase-3, and formation of ceramide by acid sphingomyelinase, but not by neutral sphingomyelinase, were associated with p53-independent apoptosis.	Ceramides	42-50	P53	Homo sapiens	135-138
15010835-4	2004	The photosensitizer accumulation was similar in both cell lines, and survival measurements using MTT test and clonogenic assays demonstrated that wt p53 transfected cells (HT29A4) were significantly more sensitive to chlorin e6-mediated PDT.	monooxyethylene trimethylolpropane tristearate	97-100	P53	Homo sapiens	149-152
35499387-6	2022	In vitro profiling of luxeptinib against 186 AML fresh patient samples demonstrated greater potency relative to other FLT3 inhibitors, including cases with mutations in FLT3, IDH1/2, ASXL1, NPM1, SRSF2, TP53 or RAS, and activity was documented in a xenograft AML model.	Luxeptinib	22-32	P53	Homo sapiens	203-207
14737002-0	2004	2,2",4,6,6"-Pentachlorobiphenyl induces mitotic arrest and p53 activation.	2,2',4,6,6'-pentachlorobiphenyl	0-31	P53	Homo sapiens	59-62
14737002-3	2004	Among several congeners examined, 2,2",4,6,6"-pentachlorobiphenyl (PeCB) specifically activated p53-dependent transcription.	2,2',4,6,6'-pentachlorobiphenyl	34-65	P53	Homo sapiens	96-99
14737002-3	2004	Among several congeners examined, 2,2",4,6,6"-pentachlorobiphenyl (PeCB) specifically activated p53-dependent transcription.	2,2',4,6,6'-pentachlorobiphenyl	67-71	P53	Homo sapiens	96-99
14991746-1	2004	Wortmannin (WM) is a potent inhibitor of the catalytic sub-unit of DNA-PK, which is involved in one pathway of DNA double-strand break (DSB) rejoining, and of ATM, which functions upstream in the p53 signaling pathway.	Wortmannin	0-10	P53	Homo sapiens	196-199
14991746-1	2004	Wortmannin (WM) is a potent inhibitor of the catalytic sub-unit of DNA-PK, which is involved in one pathway of DNA double-strand break (DSB) rejoining, and of ATM, which functions upstream in the p53 signaling pathway.	Wortmannin	12-14	P53	Homo sapiens	196-199
14625298-6	2004	SB203580, a specific inhibitor of p38 MAPK, partially suppressed CAPE-induced p53 activation, Bax expression, and apoptosis, consistent with a mechanism by which CAPE leads to Bax activation, known to be regulated by p38 and p53.	SB 203580	0-8	P53	Homo sapiens	78-81
14625298-6	2004	SB203580, a specific inhibitor of p38 MAPK, partially suppressed CAPE-induced p53 activation, Bax expression, and apoptosis, consistent with a mechanism by which CAPE leads to Bax activation, known to be regulated by p38 and p53.	SB 203580	0-8	P53	Homo sapiens	225-228
15201971-10	2004	These results indicate that glioma cells with functional p53 were relatively resistant to gamma-radiation, and that ceramide may play an important role in caspase activation during gamma-radiation-induced apoptosis of glioma cells lacking functional p53.	Ceramides	116-124	P53	Homo sapiens	250-253
15182437-9	2004	In the p53 wild-type group, we found a positive correlation for the following drugs: ADM (P &lt; 0.02), ACNU (P &lt; 0.007), CPA (P &lt; 0.011), UFT (P &lt; 0.012), and FT-207 (P &lt; 0.02).	Cyclophosphamide	125-128	P53	Homo sapiens	7-10
15182437-10	2004	In the p53 mutant group, only CPA (P &lt; 0.003) showed a positive correlation.	Cyclophosphamide	30-33	P53	Homo sapiens	7-10
15184253-3	2004	Inactivation of the MGMT gene in association with promoter hypermethylation results in persistence of O(6)-alkylguanine in DNA, leading to G:C to A:T transition mutation and these G:C to A:T transition mutations can inactivate p53 tumor suppressor gene or activate ras proto-oncogene.	o(6)-alkylguanine	102-119	P53	Homo sapiens	227-230
15161352-1	2004	The accumulation of the cell cycle regulators TP53 and CDKN1A (p21/CIP1/WAF1) was investigated after exposure to X rays and carbon ions (170 keV microm(-1)) and xenon, bismuth and uranium ions (8900-15,000 keV microm(-1)) in normal human fibroblasts.	Xenon	161-166	P53	Homo sapiens	46-50
35348191-0	2022	Ricolinostat enhances adavosertib-induced mitotic catastrophe in TP53-mutated head and neck squamous cell carcinoma cells.	ricolinostat	0-12	P53	Homo sapiens	65-69
15161352-1	2004	The accumulation of the cell cycle regulators TP53 and CDKN1A (p21/CIP1/WAF1) was investigated after exposure to X rays and carbon ions (170 keV microm(-1)) and xenon, bismuth and uranium ions (8900-15,000 keV microm(-1)) in normal human fibroblasts.	Bismuth	168-175	P53	Homo sapiens	46-50
15081121-0	2004	Thirtyfold multiplex genotyping of the p53 gene using solid phase capturable dideoxynucleotides and mass spectrometry.	Dideoxynucleotides	77-95	P53	Homo sapiens	39-42
14979918-1	2004	INTRODUCTION: The aim of the present study was to identify the relationships between the uptake of radiotracers - namely pentavalent dimercaptosuccinic acid [(V)DMSA] and sestamibi (MIBI) - and the following parameters in primary breast cancer: steroid receptor concentrations (i.e. estrogen receptor [ER] and progesterone receptor [PR]), Ki-67 expression, tumor size, tumor grade, age, and levels of expression of p53 and c-erbB-2.	2-methoxyisobutylisonitrile	182-186	P53	Homo sapiens	415-418
14679006-7	2003	CT-32615-induced apoptosis was associated with phosphorylation of p53 and c-Jun NH(2)-terminal kinase (JNK); conversely, JNK inhibitor SP600125 and dominant-negative JNK inhibited CT-32615-induced apoptosis.	UNII-3SI12BK34I	0-8	P53	Homo sapiens	66-69
35348191-0	2022	Ricolinostat enhances adavosertib-induced mitotic catastrophe in TP53-mutated head and neck squamous cell carcinoma cells.	adavosertib	22-33	P53	Homo sapiens	65-69
14513366-1	2003	PURPOSE: Resistance to chemotherapeutic drugs is a hallmark of many human cancers, which can occur independent of p53 gene status; however, the presence of wild-type p53 in chemorefractory tumors confers greater resistance to cisplatin, but such tumors do not display complete cross-resistance to the platinum analog (1R,2R-diaminocyclohexane)(trans-diacetato)(dichloro)platinumIV (DACH-Ac-Pt).	1R,2R-diaminocyclohexane	318-342	P53	Homo sapiens	166-169
35467269-8	2022	Molecular docking showed that l- menthol targeted E6, E6AP and E7 onco-proteins of HPV that interact and inactivate TP53 and Rb1 in cervical cancer, respectively.	Menthol	30-40	P53	Homo sapiens	116-120
12891704-6	2003	p53 and eEF2 sedimented in sucrose gradients in both polyribosomal and subribosomal fractions.	Sucrose	27-34	P53	Homo sapiens	0-3
15099969-3	2004	An association between endometrial cancer and the polymorphism at codon 31 (AGC/serine to AGA/arginine [Ser(31)Arg]) of the p21 gene, which is known to be a downstream mediator of p53, has also been reported.	polyethylene glycol-glutaminase-asparaginase	90-93	P53	Homo sapiens	180-183
15981924-8	2004	Cells transfected with wt-p53 DNA-loaded nanoparticles demonstrated a sustained and significantly greater antiproliferative effect than those with naked wt-p53 DNA or wt-p53 DNA complexed with a commercially available transfecting agent (Lipofectamine).	Lipofectamine	238-251	P53	Homo sapiens	26-29
15981924-9	2004	Cells transfected with wt-p53 DNA-loaded nanoparticles demonstrated sustained p53 mRNA levels compared to cells which were transfected with naked wt-p53 DNA or the wt-p53 DNA-Lipofectamine complex, thus explaining the sustained antiproliferative activity of nanoparticles.	Lipofectamine	175-188	P53	Homo sapiens	26-29
35467269-11	2022	In vitro analysis confirmed that l-menthol was cytotoxic towards cervical cancer CaSki cells and altered expression of TP53, Rb1, CDKN1A, E2F1, NFKB1, Akt-1, caspase-3, CDH1 and MMP-2 genes identified through network pharmacology approach.	Menthol	33-42	P53	Homo sapiens	119-123
12912934-2	2003	This phenotype (CIMP+) is more frequently observed in tumors with proximal location, microsatellite instability, and normal p53.	cimp+	16-21	P53	Homo sapiens	124-127
35410346-8	2022	The connection between p53, MDM2 and RPL5/11 affected by RPL15 was analyzed using immunoprecipitation and Cycloheximide (CHX) chase assay.	Cycloheximide	106-119	P53	Homo sapiens	23-26
12871058-10	2003	Therapeutic responses have been obtained in several animal lung tumor models when PEI-based formulations of p53 and other antitumor genes were delivered by aerosol.	Polyethyleneimine	82-85	P53	Homo sapiens	108-111
14764594-10	2004	Consistently, a chemical inhibitor of p38 kinase, SB203580, was found to inhibit p53-induced senescence, but only when treated before the cellular commitment to senescence, implying that p38 kinase is necessary for senescence induction.	SB 203580	50-58	P53	Homo sapiens	81-84
15087041-6	2004	METHOD: Serum analysis of p53 antibodies was performed by enzyme-linked immunosorbent assay (ELISA) in 38 patients with esophageal cancer preoperatively, then surgically resected specimens were analyzed for their chemosensitivity to cisdichlorodiammineplatinum (DDP),5-fluorouracil (5-FU), and Adriamycin (ADM) by in vitro drug response assay MTT colorimetry.	ddp	262-265	P53	Homo sapiens	26-29
15087041-6	2004	METHOD: Serum analysis of p53 antibodies was performed by enzyme-linked immunosorbent assay (ELISA) in 38 patients with esophageal cancer preoperatively, then surgically resected specimens were analyzed for their chemosensitivity to cisdichlorodiammineplatinum (DDP),5-fluorouracil (5-FU), and Adriamycin (ADM) by in vitro drug response assay MTT colorimetry.	monooxyethylene trimethylolpropane tristearate	343-346	P53	Homo sapiens	26-29
15087041-12	2004	The chemosensitivity to DDP, 5-FU, and ADM (11.1%,16.1%,and 16.1%, respectively) of the patients with positive serum p53-Ab was significantly lower than that of the patients with negative p53-Ab (60%, 45%, and 35%; P&lt; 0.01,P&lt; 0.05, and P&lt; 0.05, respectively).	ddp	24-27	P53	Homo sapiens	117-120
15010833-5	2004	MG132 arrested HCT116 cells at G2/M phase, which was associated with drug-induced blockade of p53 degradation and/or induction of p53-related gene expression along with the accumulation of cyclin B, cyclin A and p21.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	P53	Homo sapiens	94-97
15010833-5	2004	MG132 arrested HCT116 cells at G2/M phase, which was associated with drug-induced blockade of p53 degradation and/or induction of p53-related gene expression along with the accumulation of cyclin B, cyclin A and p21.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	P53	Homo sapiens	130-133
12893186-7	2003	The cellular growth inhibition and apoptosis of DDC-mediated p53 transfection were assessed by trypan blue exclusion assay and annexin-V staining, respectively.	Trypan Blue	95-106	P53	Homo sapiens	61-64
12531799-4	2003	SAHA induced apoptosis in all tumor cells tested, with increased p21 and p53 protein levels and dephosphorylation of Rb.	Vorinostat	0-4	P53	Homo sapiens	73-76
35410346-8	2022	The connection between p53, MDM2 and RPL5/11 affected by RPL15 was analyzed using immunoprecipitation and Cycloheximide (CHX) chase assay.	Cycloheximide	121-124	P53	Homo sapiens	23-26
35331214-8	2022	Elevated plasma sphingolipids were associated with AR, TP53, RB1 and PI3K aberrations (p < 0.05).	Sphingolipids	16-29	P53	Homo sapiens	55-59
12556448-0	2003	Role of caspases, Bid, and p53 in the apoptotic response triggered by histone deacetylase inhibitors trichostatin-A (TSA) and suberoylanilide hydroxamic acid (SAHA).	Vorinostat	126-157	P53	Homo sapiens	27-30
12556448-9	2003	We also demonstrate that the susceptibility to TSA- and SAHA-induced cell death is regulated by p53.	Vorinostat	56-60	P53	Homo sapiens	96-99
14871987-6	2004	Deguelin treatment did not affect Bcl-2 protein levels but increased expression levels of the proapoptotic protein p53 and the cyclin-dependent kinase inhibitors p21 and p27 in the squamous HBE cells.	deguelin	0-8	P53	Homo sapiens	115-118
15055483-6	2004	The reduction of Cr (VI) to Cr (III) results in the formation of reactive intermediates that together with oxidative stress and oxidative tissue damage, and a cascade of cellular events including modulation of apoptosis regulatory gene p53 contribute to the cytotoxicity, genotoxicity and carcinogenicity of Cr(VI)-containing compounds.	cr (iii)	28-36	P53	Homo sapiens	236-239
35331214-11	2022	Furthermore, aggressive-variant prostate cancer (AVPC), defined as 2 or more aberrations in TP53, RB1 and/or PTEN, was associated with elevated sphingolipids.	Sphingolipids	144-157	P53	Homo sapiens	92-96
35331214-14	2022	CONCLUSIONS: Elevated circulating sphingolipids were associated with AR, TP53, RB1, PI3K and AVPC aberrations in mCRPC, and the combination of lipid and genetic abnormalities conferred a worse prognosis.	Sphingolipids	34-47	P53	Homo sapiens	73-77
14578369-1	2004	We recently reported that pyruvate inhibited translocation and activation of p53 caused by DNA damage due to oxidant injury (Lee YJ, Kang IJ, Bunger R, and Kang YH.	Pyruvic Acid	26-34	P53	Homo sapiens	77-80
12618886-5	2003	Compared with p53-deficient cells, p53-proficient cells exhibited low-level resistance to amifostine-induced apoptosis.	Amifostine	90-100	P53	Homo sapiens	14-17
12618886-5	2003	Compared with p53-deficient cells, p53-proficient cells exhibited low-level resistance to amifostine-induced apoptosis.	Amifostine	90-100	P53	Homo sapiens	35-38
35408798-9	2022	Indeed, EAPB0503 selectively downregulates HDM2 expression and activates the p53 pathway in NPM1c expressing cells, resulting in apoptosis.	EAPB0503	8-16	P53	Homo sapiens	77-80
12618886-6	2003	Amifostine induced the expression of p53 protein in p53-proficient cells and the expression of p21 protein in both p53-proficient and -deficient cells.	Amifostine	0-10	P53	Homo sapiens	37-40
12618886-6	2003	Amifostine induced the expression of p53 protein in p53-proficient cells and the expression of p21 protein in both p53-proficient and -deficient cells.	Amifostine	0-10	P53	Homo sapiens	52-55
12618886-6	2003	Amifostine induced the expression of p53 protein in p53-proficient cells and the expression of p21 protein in both p53-proficient and -deficient cells.	Amifostine	0-10	P53	Homo sapiens	52-55
12618886-7	2003	These findings indicate that amifostine-induced G1 arrest and cytoprotection are mediated via a pathway that is dependent on p53 protein and that amifostine-induced expression of p21 protein is not sufficient to sustain a G1 arrest or to mediate cytoprotection.	Amifostine	29-39	P53	Homo sapiens	125-128
12618886-8	2003	In addition, these findings identify p53 protein as a mechanism of resistance to amifostine-induced apoptosis.British	Amifostine	81-91	P53	Homo sapiens	37-40
15048068-3	2004	Here, we demonstrated that STI571 also induces growth arrest by activating the Chk2-Cdc25A-Cdk2 axis, a pathway complementary to p53 in the activation of G(1)/S cell cycle checkpoint.	Imatinib Mesylate	27-33	P53	Homo sapiens	129-132
14971643-0	2004	p53 expression in circulating lymphocytes of non-melanoma skin cancer patients from an arsenic contaminated region in Mexico.	Arsenic	87-94	P53	Homo sapiens	0-3
35178443-0	2022	Aldehyde Dehydrogenase 2 Family Member (ALDH2) Is a Therapeutic Index for Oxaliplatin Response on Colorectal Cancer Therapy with Dysfunction p53.	Oxaliplatin	74-85	P53	Homo sapiens	141-144
14525955-7	2004	Inactivation of trkA, but not of p75NTR, and wortmannin prevented NGF-induced p53 nuclear translocation.	Wortmannin	45-55	P53	Homo sapiens	78-81
12967322-0	2003	Ceramide and glutathione define two independently regulated pathways of cell death initiated by p53 in Molt-4 leukaemia cells.	Ceramides	0-8	P53	Homo sapiens	96-99
12967322-4	2003	In a model of irradiation-induced cell death of Molt-4 leukaemia cells, it was found that ceramide accumulation and glutathione depletion were dependent on p53 up-regulation.	Ceramides	90-98	P53	Homo sapiens	156-159
12641444-0	2003	Inorganic and dimethylated arsenic species induce cellular p53.	Arsenic	27-34	P53	Homo sapiens	59-62
35178443-1	2022	Oxaliplatin resistance is a major issue in the treatment of p53 mutant colorectal cancer (CRC).	Oxaliplatin	0-11	P53	Homo sapiens	60-63
12619106-6	2003	Chronic active hepatitis B and C (HCV) infection, and further inflammatory and oxyradical disorders including Wilson disease (WD) or hemochromatosis, generate reactive oxygen/nitrogen species that can damage DNA and mutate the p53 gene.	reactive oxygen/nitrogen species	159-191	P53	Homo sapiens	227-230
14695179-4	2003	Peroxynitrite (ONOO(-)) is a highly reactive molecule produced by excess NO and that can posttranslationally modify and inactivate proteins, especially zinc finger transcription factors such as p53.	Peroxynitrous Acid	0-13	P53	Homo sapiens	194-197
35178443-3	2022	In order to figure out the biomarker for CRC patients with mutant p53 access oxaliplatin, a Gene Expression Omnibus dataset (GSE42387) was used to determine differentially expressed genes (DEGs).	Oxaliplatin	77-88	P53	Homo sapiens	66-69
14695179-5	2003	We demonstrated previously that GBMs have evidence of tyrosine nitration, the "footprint" of peroxynitrite-mediated protein modification in vivo, and that peroxynitrite could inhibit the specific DNA binding ability of wild-type p53 protein in glioma cells in vitro.	Peroxynitrous Acid	93-106	P53	Homo sapiens	229-232
14695179-5	2003	We demonstrated previously that GBMs have evidence of tyrosine nitration, the "footprint" of peroxynitrite-mediated protein modification in vivo, and that peroxynitrite could inhibit the specific DNA binding ability of wild-type p53 protein in glioma cells in vitro.	Peroxynitrous Acid	155-168	P53	Homo sapiens	229-232
14695179-6	2003	Here we show that both authentic peroxynitrite and SIN-1 (3-morpholinosydnonimine hydrochloride), a molecule that decomposes into NO and to form peroxynitrite, can inhibit wild-type p53 function in malignant glioma cells.	Peroxynitrous Acid	33-46	P53	Homo sapiens	182-185
14695179-6	2003	Here we show that both authentic peroxynitrite and SIN-1 (3-morpholinosydnonimine hydrochloride), a molecule that decomposes into NO and to form peroxynitrite, can inhibit wild-type p53 function in malignant glioma cells.	Peroxynitrous Acid	145-158	P53	Homo sapiens	182-185
14695179-7	2003	Concentrations of peroxynitrite associated with a tumor inflammatory environment caused dysregulation of wild-type p53 transcriptional activity and downstream p21(WAF1) expression.	Peroxynitrous Acid	18-31	P53	Homo sapiens	115-118
12619896-0	2003	Nicotinamide- and caspase-mediated inhibition of poly(ADP-ribose) polymerase are associated with p53-independent cell cycle (G2) arrest and apoptosis.	Niacinamide	0-12	P53	Homo sapiens	97-100
12402298-2	2002	We investigated oxidative DNA damage by N-OH-AF, using (32)P-labeled human DNA fragments from the human p53 and p16 tumor-suppressor genes and the c-Ha-ras-1 protooncogene.	Phosphorus-32	55-60	P53	Homo sapiens	104-107
35178443-10	2022	Finally, we found that combined treatment with ALDH2 inhibitor and oxaliplatin will reduce the sensitivity to oxaliplatin in p53 mutant HT29 cells.	Oxaliplatin	67-78	P53	Homo sapiens	125-128
12151394-4	2002	We observed that in MNNG-treated normal human fibroblasts, up-regulation and phosphorylation of p53 was sensitive to the ATM kinase inhibitor wortmannin.	Wortmannin	142-152	P53	Homo sapiens	96-99
35178443-10	2022	Finally, we found that combined treatment with ALDH2 inhibitor and oxaliplatin will reduce the sensitivity to oxaliplatin in p53 mutant HT29 cells.	Oxaliplatin	110-121	P53	Homo sapiens	125-128
35178099-11	2022	The experimental results showed that baicalein and wogonin could inhibit proliferation and induce apoptosis of NPC cells and downregulate the expression of PI3K, AKT, and p53, the key proteins of the PI3K/AKT and p53 signaling pathway in CNE2 cells.	wogonin	51-58	P53	Homo sapiens	171-174
12358742-0	2002	A novel in vivo post-translational modification of p53 by PARP-1 in MPTP-induced parkinsonism.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	68-72	P53	Homo sapiens	51-54
12919957-0	2003	P53 alterations in bladder tumors from arsenic and tobacco exposed patients.	Arsenic	39-46	P53	Homo sapiens	0-3
12919957-2	2003	A case-case study was conducted to compare p53 mutations in 147 bladder tumors from South American patients by tobacco and arsenic exposure.	Arsenic	123-130	P53	Homo sapiens	43-46
35178099-11	2022	The experimental results showed that baicalein and wogonin could inhibit proliferation and induce apoptosis of NPC cells and downregulate the expression of PI3K, AKT, and p53, the key proteins of the PI3K/AKT and p53 signaling pathway in CNE2 cells.	wogonin	51-58	P53	Homo sapiens	213-216
12919957-4	2003	The prevalence of p53 mutations and protein expression was examined in relation to tumor stage, grade, patient age, gender, tobacco and arsenic exposure.	Arsenic	136-143	P53	Homo sapiens	18-21
12358742-5	2002	p53 is a target of the nuclear enzyme Poly(ADP-ribose)polymerase (PARP), and PARP is activated following DNA damage that occurs following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	138-182	P53	Homo sapiens	0-3
12358742-5	2002	p53 is a target of the nuclear enzyme Poly(ADP-ribose)polymerase (PARP), and PARP is activated following DNA damage that occurs following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	184-188	P53	Homo sapiens	0-3
12358742-8	2002	We find that p53 is heavily poly(ADP-ribosyl)ated by PARP-1 following MPTP intoxication.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	70-74	P53	Homo sapiens	13-16
35178099-12	2022	Conclusion: Baicalein and wogonin, the main active ingredients of S. barbata, inhibited the proliferation and induced apoptosis of NPC cells through the PI3K/AKT and p53 signaling pathways.	wogonin	26-33	P53	Homo sapiens	166-169
12358742-10	2002	These influences of PARP-1 on p53 may underlie the mechanisms of MPTP-induced parkinsonism and other models of neuronal death.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	65-69	P53	Homo sapiens	30-33
14577614-0	2003	Effects of 2-amino-4,6-dinitrotoluene on p53 tumor suppressor gene expression.	2-amino-4,6-dinitrotoluene	11-37	P53	Homo sapiens	41-44
35159039-2	2022	Here we report a p53-independent mechanism responsible for Growth Factor Independence-1 (GFI1) support of MM cell survival by its modulation of sphingolipid metabolism to increase the sphingosine-1-phosphate (S1P) level regardless of the p53 status.	Sphingolipids	144-156	P53	Homo sapiens	17-20
12205035-8	2002	Treatment with the antioxidant U-74389G abrogated p53 activation.	U 74389F	31-38	P53	Homo sapiens	50-53
35163511-4	2022	Treatment with MHY2245 decreased SIRT1 activity and caused DNA damage, leading to the upregulation of p53 acetylation, and increased levels of p53, phosphorylation of H2A histone family member X, ataxia telangiectasia and Rad3-related kinase, checkpoint kinase 1 (Chk1), and Chk2.	mhy2245	15-22	P53	Homo sapiens	102-105
11964141-7	2002	Bathocuproinedisulphonic acid as well as the hydroxyl radical scavenger d-mannitol inhibited the PDTC-dependent increase in p53 protein and oxidation.	bathocuproine sulfonate	0-29	P53	Homo sapiens	124-127
12928501-7	2003	Sensitivity to the Abl inhibitor STI571 suggests differential utilization of the p53 and c-Abl/p73 pathways by different tumor cell lines.	Imatinib Mesylate	33-39	P53	Homo sapiens	81-84
35163511-4	2022	Treatment with MHY2245 decreased SIRT1 activity and caused DNA damage, leading to the upregulation of p53 acetylation, and increased levels of p53, phosphorylation of H2A histone family member X, ataxia telangiectasia and Rad3-related kinase, checkpoint kinase 1 (Chk1), and Chk2.	mhy2245	15-22	P53	Homo sapiens	143-146
12142390-3	2002	METHODS: Using a series of overlapping fluorescein-labeled oligonucleotides complementary to a wild-type p53 sequence, we detected somatic mutations in colorectal cancers by aberrant probe:target melting temperatures (T(m)).	Fluorescein	39-50	P53	Homo sapiens	105-108
35053444-0	2022	Repositioning Fenofibrate to Reactivate p53 and Reprogram the Tumor-Immune Microenvironment in HPV+ Head and Neck Squamous Cell Carcinoma.	Fenofibrate	14-25	P53	Homo sapiens	40-43
12127985-6	2002	MG132 or actinomycin D both led to a significant increase in p53, but the expressions of the p53 response proteins increased only in MG132 treated chondrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	P53	Homo sapiens	61-64
12127985-6	2002	MG132 or actinomycin D both led to a significant increase in p53, but the expressions of the p53 response proteins increased only in MG132 treated chondrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	133-138	P53	Homo sapiens	93-96
12051701-2	2002	Fibroblasts treated with pyruvate undergo a rapid growth arrest accompanied by elevated levels of the cell-cycle regulatory molecules p53, p21, and p16.	Pyruvic Acid	25-33	P53	Homo sapiens	134-137
12065773-12	2002	Our result indicates that p53 alterations are infrequent in CCSK and do not seem to be primary genetic events in the pathogenesis of CCSK.	ccsk	60-64	P53	Homo sapiens	26-29
12076704-3	2002	Mutational screening of the coding region of TP53 revealed an A>T transversion in codon 144 of exon 5 (CAG>CTG, Gln>Leu) in the germline of one of the three affected members, with loss of heterozygosity (LOH) in the tumour tissue.	ctg	107-110	P53	Homo sapiens	45-49
12034325-0	2002	Acrylonitrile exposure: the effect on p53 and p21(WAF1) protein levels in the blood plasma of occupationally exposed workers and in vitro in human diploid lung fibroblasts.	Acrylonitrile	0-13	P53	Homo sapiens	38-41
12034325-3	2002	The aim of the present study was to assess the effect of ACN exposure on the expression of p53 and p21(WAF1) proteins in vitro as well as in vivo.	Acrylonitrile	57-60	P53	Homo sapiens	91-94
12034325-4	2002	In vitro ACN exposure of human lung fibroblasts resulted in the induction of both p53 and p21(WAF1) proteins.	Acrylonitrile	9-12	P53	Homo sapiens	82-85
12007018-4	2002	We examined the status of p53 in CMN and CCSK in comparison to AWT by immunohistochemistry and mRNA analysis of p53, the downstream effector p21(WAF-1/CIP-1) ( p21), the multidrug resistance gene MDR-1, a putative target of p53, and the p53-antagonist Mdm-2.	ccsk	41-45	P53	Homo sapiens	26-29
11948417-0	2002	Antiviral agent Cidofovir restores p53 function and enhances the radiosensitivity in HPV-associated cancers.	Cidofovir	16-25	P53	Homo sapiens	35-38
11948417-5	2002	Cidofovir induced the accumulation of active p53 and pRb associated to induction of cyclin dependent kinase inhibitor p21(WAF1/CIP1) in Me180 and HEP2 cells.	Cidofovir	0-9	P53	Homo sapiens	45-48
11822871-5	2002	Moreover, expression of functional p53 protein using a temperature-sensitive human p53val(138) induced ceramide generation by activation of neutral SMase but not acid SMase through ROS formation.	Ceramides	103-111	P53	Homo sapiens	35-38
11822871-5	2002	Moreover, expression of functional p53 protein using a temperature-sensitive human p53val(138) induced ceramide generation by activation of neutral SMase but not acid SMase through ROS formation.	Ceramides	103-111	P53	Homo sapiens	83-86
11802204-0	2002	Expression of a non-functional p53 affects the sensitivity of cancer cells to gemcitabine.	gemcitabine	78-89	P53	Homo sapiens	31-34
11802204-3	2002	The present study was performed to gain insight into the role of p53 status on the cytotoxicity of gemcitabine on cancer cells.	gemcitabine	99-110	P53	Homo sapiens	65-68
11706017-8	2002	MC induced p38 MAPK activation in p53 expressing cells but not in p53-deficient cells, indicating that the p38 MAPK activation was dependent on early p53 activation.	Methylcholanthrene	0-2	P53	Homo sapiens	34-37
11706017-9	2002	The current study shows that both p53 and p38 MAPK activation are required for MC-induced apoptosis and provides a novel model of a functional regulation between p53 and p38 MAPK in chemical stress-induced apoptosis.	Methylcholanthrene	79-81	P53	Homo sapiens	34-37
11706017-9	2002	The current study shows that both p53 and p38 MAPK activation are required for MC-induced apoptosis and provides a novel model of a functional regulation between p53 and p38 MAPK in chemical stress-induced apoptosis.	Methylcholanthrene	79-81	P53	Homo sapiens	162-165
11803460-8	2002	CD95-resistant HPV-positive cells underwent apoptosis within 3-5 h upon co-incubation with MG132 and agonistic antibodies or CD95 ligand, which was preceded by a strong re-expression of p53 and c-Myc, but not of other half-life controlled proteins such as Bax or IkappaBalpha.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	P53	Homo sapiens	186-189
12373514-1	2002	Previous work from our laboratory has suggested the functional contribution of p53 to the cascade of events triggered by excitatory amino acids and leading to cell death in primary neurons.	Excitatory Amino Acids	121-143	P53	Homo sapiens	79-82
12373514-3	2002	We found that exposure of the cells to either 300 microM or 2 mM NMDA induced an enhancement of p53 protein levels which was already significant at 60 min after the lesion, while very low staining of the protein was observed in untreated cells.	N-Methylaspartate	65-69	P53	Homo sapiens	96-99
12373514-4	2002	The effect was time- and concentration-dependent, reaching the maximal induction at 3 h. NMDA treatment also resulted in an increase of gadd45 protein levels which was evident in both treatment at 3 h, the time when p53 was maximally induced.	N-Methylaspartate	89-93	P53	Homo sapiens	216-219
11786482-16	2002	These results demonstrate that butyrate inhibited the growth of breast cancer cells in a P53-independent manner.	Butyrates	31-39	P53	Homo sapiens	89-92
11751391-3	2001	Here, we report that the DNA-dependent protein kinase (DNA-PK) and p53 are able to form a protein complex that interacts with the gemcitabine-containing DNA and plays a role in signaling to apoptotic pathways.	gemcitabine	130-141	P53	Homo sapiens	67-70
11751391-4	2001	DNA-PK/Ku and p53 were copurified in a protein fraction that binds to gemcitabine-containing DNA in preference to normal DNA.	gemcitabine	70-81	P53	Homo sapiens	14-17
11751391-6	2001	Treatment with gemcitabine resulted in an increase of DNA-PK and p53 protein and an increase in the phosphorylation of p53 at Ser15.	gemcitabine	15-26	P53	Homo sapiens	65-68
11751391-6	2001	Treatment with gemcitabine resulted in an increase of DNA-PK and p53 protein and an increase in the phosphorylation of p53 at Ser15.	gemcitabine	15-26	P53	Homo sapiens	119-122
11751391-7	2001	Furthermore, confocal microscopy demonstrated a colocalization of DNA-PK and p53 to the nucleus in cells treated with gemcitabine.	gemcitabine	118-129	P53	Homo sapiens	77-80
11751391-9	2001	Although the wild-type p53 present in the protein complex exhibited 3"-5" exonuclease activity, it was incapable of excising the incorporated gemcitabine from DNA.	gemcitabine	142-153	P53	Homo sapiens	23-26
11583595-0	2001	Critical roles for the serine 20, but not the serine 15, phosphorylation site and for the polyproline domain in regulating p53 turnover.	polyproline	90-101	P53	Homo sapiens	123-126
11583595-7	2001	We also show that the polyproline region of p53, a domain that has a key role in p53-induced apoptosis, exerts a critical influence over the Mdm2-mediated turnover of p53.	polyproline	22-33	P53	Homo sapiens	44-47
11583595-7	2001	We also show that the polyproline region of p53, a domain that has a key role in p53-induced apoptosis, exerts a critical influence over the Mdm2-mediated turnover of p53.	polyproline	22-33	P53	Homo sapiens	81-84
11583595-7	2001	We also show that the polyproline region of p53, a domain that has a key role in p53-induced apoptosis, exerts a critical influence over the Mdm2-mediated turnover of p53.	polyproline	22-33	P53	Homo sapiens	81-84
11589834-4	2001	The initial purified recombinant adenovirus containing the p53 tumor suppressor gene was produced from 293 cells grown on microcarriers and purified by passage through DEAE-Fractogel and gel-filtration chromatography.	fractogel	173-182	P53	Homo sapiens	59-62
11585734-2	2001	Here we show that E2F1 in combination with the most clinically efficient drug, gemcitabine, resulted in a strong induction of apoptosis independent of functional p53, whereas the effect of either therapy alone varied between different cell lines.	gemcitabine	79-90	P53	Homo sapiens	162-165
12541691-3	2001	RESULT: The expression of p53, bcl-2 proteins and EBV were found respectively in 1(7.7%), 3(23.1%) and 1(7.7%) of 13 CINEs, which were significantly lower than those in 54 NPCs with respectively 41(75.9%), 48(88.9%) and 47(87%) (P &lt; 0.01).	nicotinuric acid	117-122	P53	Homo sapiens	26-29
11568365-5	2001	Hyperoxia (95% O2, 5% CO2) increased p53 abundance, phosphorylation of p53 on serine 15, and p21 mRNA and protein in parental HCT116 cells that ceased proliferation.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	22-25	P53	Homo sapiens	37-40
11568365-5	2001	Hyperoxia (95% O2, 5% CO2) increased p53 abundance, phosphorylation of p53 on serine 15, and p21 mRNA and protein in parental HCT116 cells that ceased proliferation.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	22-25	P53	Homo sapiens	71-74
11507245-10	2001	In contrast, in AT cells in which ATM is absent or mutated activation of P53 and its target genes is abrogated, allowing cells to replicate with damage in the presence of As, with cell death ensuing by a pathway different from P53.	Arsenic	171-173	P53	Homo sapiens	73-76
11489842-0	2001	Radiosensitization by gemcitabine in p53 wild-type and mutant MCF-7 breast carcinoma cell lines.	gemcitabine	22-33	P53	Homo sapiens	37-40
11489842-9	2001	These results demonstrate that a wild-type p53 cell line can be radiosensitized by dFdCyd, presumably because it was able to deplete dATP levels and progress through the cell cycle for at least 24 h after drug and radiation treatment.	gemcitabine	83-89	P53	Homo sapiens	43-46
11458051-0	2001	Functional p53 mutation as a molecular determinant of paclitaxel and gemcitabine susceptibility in human bladder cancer.	gemcitabine	69-80	P53	Homo sapiens	11-14
11458051-4	2001	Susceptibility of these inducible p53 TCC cells to paclitaxel and gemcitabine induced cytotoxicity was evaluated and kill significance determined between sub-lethal and lethal doses.	gemcitabine	66-77	P53	Homo sapiens	34-37
11505223-4	2001	In cultured lymphocytes treated with 2.5 microM BPDE for 18 h, increased levels of p53 were found, which were positively related to BPDE-DNA adduct levels assessed by ICC (rs = 0.66, P &lt; 0.001) and 32P-postlabelling (rs = 0.56, P &lt; 0.001) and appeared to be higher in GSTM1(-/-) than in GSTM1(+) subjects (P = 0.003).	Phosphorus-32	201-204	P53	Homo sapiens	83-86
11464279-0	2001	CCNU-dependent potentiation of TRAIL/Apo2L-induced apoptosis in human glioma cells is p53-independent but may involve enhanced cytochrome c release.	Lomustine	0-4	P53	Homo sapiens	86-89
12811511-10	2003	There was a significant upregulation of p53, p21(waf1), and p27 in MCF7 and MCF-10A cells treated with the combination of gemcitabine and BRYO compared to gemcitabine-treated cells.	gemcitabine	122-133	P53	Homo sapiens	40-43
12935767-8	2003	The induction and nuclear translocation of p53 by H2O2 was blocked by pyruvate and appeared to be somewhat enhanced by L-lactate or aminooxyacetate in association with oxidant generation.	Pyruvic Acid	70-78	P53	Homo sapiens	43-46
12935767-8	2003	The induction and nuclear translocation of p53 by H2O2 was blocked by pyruvate and appeared to be somewhat enhanced by L-lactate or aminooxyacetate in association with oxidant generation.	Aminooxyacetic Acid	132-147	P53	Homo sapiens	43-46
12935767-10	2003	The pyruvate-related redox manipulation inhibited the H2O2-induced p53 activation, restored the downregulated bcl-2 and the upregulated bax, and hence enhanced the bcl-2/bax expression ratio.	Pyruvic Acid	4-12	P53	Homo sapiens	67-70
12750435-0	2003	Neocarzinostatin induces an effective p53-dependent response in human papillomavirus-positive cervical cancer cells.	Zinostatin	0-16	P53	Homo sapiens	38-41
12874000-5	2003	Strikingly, administration of just 6 micro g of the polyethyleneimine/DNA-p53 vector every 3 days for 3 weeks indicated restoration of normal cell cycle regulation and apoptotic mechanisms as demonstrated by efficient p53 expression, increased apoptosis, and a 70% reduction in tumor size in an orthotopic bladder cancer model.	Polyethyleneimine	52-69	P53	Homo sapiens	74-77
12874000-5	2003	Strikingly, administration of just 6 micro g of the polyethyleneimine/DNA-p53 vector every 3 days for 3 weeks indicated restoration of normal cell cycle regulation and apoptotic mechanisms as demonstrated by efficient p53 expression, increased apoptosis, and a 70% reduction in tumor size in an orthotopic bladder cancer model.	Polyethyleneimine	52-69	P53	Homo sapiens	218-221
12782031-5	2003	At the same time a chemical agent polyethylenimine that is also used for transient transfection of cells causes neither upregulation of p53 nor cellular response.	Polyethyleneimine	34-50	P53	Homo sapiens	136-139
14979067-0	2003	[Anti-p53 antibodies as markers of carcinogenesis in exposures to vinyl chloride].	Vinyl Chloride	66-80	P53	Homo sapiens	6-9
14979067-2	2003	The study carried on 167 male subject exposed to vinyl chloride (CV) (cumulative concentration ranged from 4 to 2823 ppm) tested anti-p53 positive in 5 cases (3.9%), all distributed in the high exposure group (&gt; 1000 ppm); No subject in the control group tested positive.	Vinyl Chloride	49-63	P53	Homo sapiens	134-137
12840224-15	2003	Overall, ZBP-89 is a butyrate-regulated coactivator of p53 and is able to induce p21(Waf1) gene expression through both p53-dependent and -independent mechanisms to inhibit cell growth.	Butyrates	21-29	P53	Homo sapiens	55-58
12823590-4	2003	To explain the p53-independent regulation of p21 by Core, we identified a Core-responsive element between positions -74 and -83 of the p21 promoter, exactly overlapped with a tumour growth factor beta (TGF-beta)/butyrate responsive element.	Butyrates	212-220	P53	Homo sapiens	15-18
12736687-5	2003	We have recently shown that Sir2 and its closest human homologue SIRT1, a p53 deacetylase, are strongly inhibited by the vitamin B3 precursor nicotinamide.	Niacinamide	121-131	P53	Homo sapiens	74-77
12736687-5	2003	We have recently shown that Sir2 and its closest human homologue SIRT1, a p53 deacetylase, are strongly inhibited by the vitamin B3 precursor nicotinamide.	Niacinamide	142-154	P53	Homo sapiens	74-77
12679488-8	2003	Taken together, these results suggest that selective suppression of c-ABL activity by STI571 may represent a potential anticancer strategy for p53-mutated undifferentiated thyroid carcinomas.	Imatinib Mesylate	86-92	P53	Homo sapiens	143-146
12612087-1	2003	CP-31398, a styrylquinazoline, emerged from a high throughput screen for therapeutic agents that restore a wild-type-associated epitope (monoclonal antibody 1620) on the DNA-binding domain of the p53 protein.	styrylquinazoline	12-29	P53	Homo sapiens	196-199
12597983-0	2003	Preclinical evaluation of a radiosensitizing effect of gemcitabine in p53 mutant and p53 wild type bladder cancer cells.	gemcitabine	55-66	P53	Homo sapiens	70-73
12432549-1	2002	The new disaccharide anthracycline MEN 10755 induces activation of both NF-kappaB and p53 transcription factors in A2780 cells.	Disaccharides	8-20	P53	Homo sapiens	86-89
12709297-8	2002	Moreover, our studies indicate that nicotinamide is able to prevent the up-regulation of the pro-apoptotic proteins p53 and p21/WAF-1, and the down-regulation of the anti-apoptotic protein bcl-2 that is induced by t-BuOOH in HCN2 cells.	Niacinamide	36-48	P53	Homo sapiens	116-119
12426127-15	2002	Taken together with previous findings that p53 mutations are involved in approximately 50% of all human cancers and nearly all chemotherapeutic agents kill cancer cells mainly by apoptotic induction, we suggest that arsenic may be a useful agent for the treatment of cancers with p53 mutations.	Arsenic	216-223	P53	Homo sapiens	43-46
12426127-15	2002	Taken together with previous findings that p53 mutations are involved in approximately 50% of all human cancers and nearly all chemotherapeutic agents kill cancer cells mainly by apoptotic induction, we suggest that arsenic may be a useful agent for the treatment of cancers with p53 mutations.	Arsenic	216-223	P53	Homo sapiens	280-283
12359055-6	2002	p53 overexpression also induced apoptosis and cell cycle arrest, as determined by annexin V and propidium iodide staining.	Propidium	96-112	P53	Homo sapiens	0-3
12160929-8	2002	The levels of p53 and Bax proteins were elevated, while Bcl-2 protein was downregulated in TCE- or PERC-treated p53-WT H460 cells.	Tetrachloroethylene	99-103	P53	Homo sapiens	112-115
12160929-10	2002	These data suggest that, in human lung cancer cells, GSH plays a vital role in the protection of TCE- and PERC-induced oxidative stress and apoptosis, which may be mediated through a p53-dependent pathway.	Tetrachloroethylene	106-110	P53	Homo sapiens	183-186
12171874-1	2002	Potentiation of 5-fluorouracil/leucovorin (FUra/LV) cytotoxicity by IFN-gamma in colon carcinoma cells is dependent on FUra-induced DNA damage, the Fas death receptor, and independent of p53 and RNA-mediated FUra toxicity, which occurs in normal gastrointestinal tissues.	Leucovorin	31-41	P53	Homo sapiens	187-190
12171874-1	2002	Potentiation of 5-fluorouracil/leucovorin (FUra/LV) cytotoxicity by IFN-gamma in colon carcinoma cells is dependent on FUra-induced DNA damage, the Fas death receptor, and independent of p53 and RNA-mediated FUra toxicity, which occurs in normal gastrointestinal tissues.	Leucovorin	48-50	P53	Homo sapiens	187-190
12065694-7	2002	Treatment with the p53 inhibitor alpha-2-(2-imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone (PFT) before cisplatin exposure inhibited p53 nuclear expression at 4, 8, and 12 h and inhibited phosphatidylserine externalization and caspase 3 activation at 12 h. Neither DEVD-fmk nor ZVAD-fmk inhibited cisplatin-induced p53 nuclear expression.	tolylethanone	91-104	P53	Homo sapiens	19-22
12065694-7	2002	Treatment with the p53 inhibitor alpha-2-(2-imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone (PFT) before cisplatin exposure inhibited p53 nuclear expression at 4, 8, and 12 h and inhibited phosphatidylserine externalization and caspase 3 activation at 12 h. Neither DEVD-fmk nor ZVAD-fmk inhibited cisplatin-induced p53 nuclear expression.	devd-fmk	279-287	P53	Homo sapiens	19-22
12066222-0	2002	Low dose of wortmannin reduces radiosensitivity of human glioblastoma cells through the p53 pathway.	Wortmannin	12-22	P53	Homo sapiens	88-91
12066222-7	2002	This result indicates that the PI3-kinase, or another wortmannin-sensitive enzyme, may affect the signal transduction of p53.	Wortmannin	54-64	P53	Homo sapiens	121-124
12180192-6	2002	We have investigated sequence specificity of DNA damage induced by carbamoyl radicals using 32P-labeled DNA fragments obtained from the human c-Ha-ras-1 and p53 genes.	Phosphorus-32	92-95	P53	Homo sapiens	157-160
12065773-2	2002	However, there are very few studies of p53 alterations in the other two rare and highly malignant renal tumors in childhood, in other words, clear cell sarcoma of the kidney (CCSK) and malignant rhabdoid tumor of the kidney (MRTK).	ccsk	175-179	P53	Homo sapiens	39-42
11864976-3	2002	Etoposide caused the phosphorylation of p53 within 6 h, an effect prevented by wortmannin, an inhibitor of DNA-dependent protein kinase (DNA-PK).	Wortmannin	79-89	P53	Homo sapiens	40-43
11923065-6	2002	Research data strongly suggest that arsenic influences distinct signaling pathways involved in mediating proliferation or apoptosis, including mitogen-activated protein kinases, p53, activator protein-1 or nuclear factor kappa B.	Arsenic	36-43	P53	Homo sapiens	178-181
12168940-0	2002	Correlation of clinical outcome with p53 and p21 status in patients with advanced transitional-cell carcinoma treated with paclitaxel and carboplatin.	Carboplatin	138-149	P53	Homo sapiens	37-40
12168940-1	2002	BACKGROUND: The purpose of the present study was to correlate the nuclear expression of p53 and p21 with response to paclitaxel and carboplatin, progression-free survival (PFS) as well as overall survival (OS), in patients with urothelial metastatic transitional-cell carcinoma (TCC).	Carboplatin	132-143	P53	Homo sapiens	88-91
11911839-0	2002	p53-Independent induction of Fas and apoptosis in leukemic cells by an adenosine derivative, Cl-IB-MECA.	2-chloro-N(6)-(3-iodobenzyl)adenosine-5'-N-methyluronamide	93-103	P53	Homo sapiens	0-3
11911839-13	2002	Therefore, Cl-IB-MECA induced apoptosis via a novel, p53-independent up-regulation of Fas.	2-chloro-N(6)-(3-iodobenzyl)adenosine-5'-N-methyluronamide	11-21	P53	Homo sapiens	53-56
11857452-12	2002	Wortmannin at 10 microM inhibited p53 activation for up to 2 h after heat shock suggesting the involvement of wortmannin-sensitive kinases, such as DNA-PK and ATM.	Wortmannin	0-10	P53	Homo sapiens	34-37
11935300-6	2002	RESULTS: Ex vivo chemosensitivity testing showed that tumors with p53 mutations were significantly more resistant to the cyclophosphamide/etoposide/epirubicin regimen than with normal p53 gene ( P = 0.012).	Cyclophosphamide	121-137	P53	Homo sapiens	66-69
11915341-0	2002	[Involvement of p53 in ceramide signaling cascade].	Ceramides	23-31	P53	Homo sapiens	16-19
11821962-4	2002	We show that expression of the mutant (His175)p53 strongly stimulates recombination induced by aphidicolin, in a late step (kinetically related to the RAD51 step).	Aphidicolin	95-106	P53	Homo sapiens	46-49
11821962-5	2002	Mutant p53 stimulates recombination induced by the replication elongation inhibitors (aphidicolin, hydroxyurea and Ara-C) but is without effect on recombination induced by the initiation inhibitors (mimosine and ciclopirox olamine).	Aphidicolin	86-97	P53	Homo sapiens	7-10
12462448-5	2002	Observations that mutations in gene p53 appear under conditions of occupational and environmental exposures to chemical and physical carcinogens, such as vinyl chloride, radon, or aflatoxin B1, have proved to be of enormous importance for the occupational and environmental health.	Vinyl Chloride	154-168	P53	Homo sapiens	36-39
11820739-0	2001	Distinct apoptotic phenotypes induced by radiation and ceramide in both p53-wild-type and p53-mutated lymphoblastoid cells.	Ceramides	55-63	P53	Homo sapiens	72-75
11820739-0	2001	Distinct apoptotic phenotypes induced by radiation and ceramide in both p53-wild-type and p53-mutated lymphoblastoid cells.	Ceramides	55-63	P53	Homo sapiens	90-93
11820739-6	2001	Radiation-induced apoptosis is p53-dependent and ceramide-induced apoptosis is p53-independent.	Ceramides	49-57	P53	Homo sapiens	79-82
11820739-8	2001	Since p53 is very often dysfunctional in tumour cells, modifying the ceramide pathway is a promising strategy to increase tumour sensitivity to radiation and other anticancer agents.	Ceramides	69-77	P53	Homo sapiens	6-9
11453316-5	2001	Thirty-three per cent of the DMPMs were positive for p53, 35% for p21 and 52% for metallothionein.	dmpms	29-34	P53	Homo sapiens	53-56
11429700-0	2001	Amifostine (WR2721) restores transcriptional activity of specific p53 mutant proteins in a yeast functional assay.	Amifostine	0-10	P53	Homo sapiens	66-69
11429700-4	2001	We have recently reported that the radio- and chemoprotector Amifostine (WR2721, Ethyol) activates wild-type p53 in cultured mammalian cells.	Amifostine	61-71	P53	Homo sapiens	109-112
11429700-4	2001	We have recently reported that the radio- and chemoprotector Amifostine (WR2721, Ethyol) activates wild-type p53 in cultured mammalian cells.	Amifostine	81-87	P53	Homo sapiens	109-112
11678599-11	2001	Treatment of genomic DNA with Cr (III) resulted in a marked inhibition of the amplification of a 1.6 kb target fragment of the p53 gene by Taq polymerase.	cr (iii)	30-38	P53	Homo sapiens	127-130
11484509-6	2001	An association was found between p53 expression and mdm2 overexpression in the WD group (comprising WDLS and WD components of DDLS) and in the DD group, significantly so in the WD group.	dd	126-128	P53	Homo sapiens	33-36
11106643-2	2001	Activation of p53 in REH cells by treatment with daunorubicin was accompanied by decreased ( approximately 5-fold) levels of hRFC transcripts and methotrexate transport.	Daunorubicin	49-61	P53	Homo sapiens	14-17
11307620-6	2001	Phenylacetate-induced apoptosis is attenuated by wild-type p53 gene transfer in both cell lines.	phenylacetic acid	0-13	P53	Homo sapiens	59-62
11718557-2	2001	The divalent cation Mg(2+) was used to loosely attach both DNA and p53 to a mica surface so they could be imaged by the AFM while interacting with each other.	mica	76-80	P53	Homo sapiens	67-70
35053444-7	2022	Systemic fenofibrate treatment induced p53 protein accumulation, and surprisingly, re-programmed the tumor-immune microenvironment to drive immune cell infiltration.	Fenofibrate	9-20	P53	Homo sapiens	39-42
33635505-8	2021	Significant induction of p53 also was observed after treatment with (+)-usnic acid.	usnic	72-77	P53	Homo sapiens	25-28
11672522-3	2001	Nicotinamide (Vitamin B3) inhibits an NAD-dependent p53 deacetylation induced by Sir2alpha, and also enhances the p53 acetylation levels in vivo.	Niacinamide	0-12	P53	Homo sapiens	52-55
11672522-3	2001	Nicotinamide (Vitamin B3) inhibits an NAD-dependent p53 deacetylation induced by Sir2alpha, and also enhances the p53 acetylation levels in vivo.	Niacinamide	0-12	P53	Homo sapiens	114-117
11672522-3	2001	Nicotinamide (Vitamin B3) inhibits an NAD-dependent p53 deacetylation induced by Sir2alpha, and also enhances the p53 acetylation levels in vivo.	Niacinamide	14-24	P53	Homo sapiens	52-55
11672522-3	2001	Nicotinamide (Vitamin B3) inhibits an NAD-dependent p53 deacetylation induced by Sir2alpha, and also enhances the p53 acetylation levels in vivo.	Niacinamide	14-24	P53	Homo sapiens	114-117
11606405-5	2001	Apoptotic cell death induced by STI571 is partially dependent on p53.	Imatinib Mesylate	32-38	P53	Homo sapiens	65-68
11745255-10	2001	CONCLUSIONS: Thus, deregulation of the cell cycle by p53 and p21 in this study was shown to play an important role in progression of Pen-A type early gastric carcinoma.	pen-a	133-138	P53	Homo sapiens	53-56
11585742-3	2001	p53 codons containing methylated CpG sequences are preferential targets for formation of adducts by (+/-) anti-7beta,8alpha-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE).	10alpha-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene	141-188	P53	Homo sapiens	0-3
11595686-8	2001	Resistance to adjuvant cisplatin or carboplatin chemotherapy was significantly more frequent in patients with p53 overexpression (P = 0.001) or p53 missense mutations (P = 0.008) than patients with normal p53.	Carboplatin	36-47	P53	Homo sapiens	110-113
11595686-8	2001	Resistance to adjuvant cisplatin or carboplatin chemotherapy was significantly more frequent in patients with p53 overexpression (P = 0.001) or p53 missense mutations (P = 0.008) than patients with normal p53.	Carboplatin	36-47	P53	Homo sapiens	144-147
11595686-8	2001	Resistance to adjuvant cisplatin or carboplatin chemotherapy was significantly more frequent in patients with p53 overexpression (P = 0.001) or p53 missense mutations (P = 0.008) than patients with normal p53.	Carboplatin	36-47	P53	Homo sapiens	144-147
11550287-7	2001	YSK-21 cells, expressing aberrant AML1-MTG8, TP53, and TP73 protein molecules, may be useful for elucidating the pathophysiology of these aberrant proteins and for studying the der(1)t(1;17)(p36;q21) chromosomal translocation.	tyrosylseryllysine	0-3	P53	Homo sapiens	45-49
11507071-9	2001	Loss of p53 function was selectively achieved by transduction of human papillomavirus 16 E6 (which degrades p53) into two drug-sensitive neuroblastoma cell lines with intact p53, causing high-level drug resistance to L-PAM, carboplatin, and etoposide.	Carboplatin	224-235	P53	Homo sapiens	8-11
11477551-4	2001	Gastric cancer cell lines AGS (p53 wild-type) and MKN-28 (p53 mutant) were treated with proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	P53	Homo sapiens	58-61
11509137-3	2001	The cytotoxicities of Ad-p53 to cells were measured by MTT assay.	monooxyethylene trimethylolpropane tristearate	55-58	P53	Homo sapiens	25-28
11423989-2	2001	Here we investigated the effects of n-butyrate, a cancer-preventive short-chain fatty acid produced by anaerobic bacteria in the gastrointestinal tract, on the human wild-type p53 and p21 expressing HCT116 colon carcinoma cell line and on HCT116 cells with either p53 or p21 alleles inactivated by homologous recombination.	Butyrates	36-46	P53	Homo sapiens	176-179
11409938-8	2001	Experiments with 32P-labeled DNA fragments obtained from the human p53 tumor suppressor gene and the c-Ha-ras-1 protooncogene suggested that KBrO3 induced 8-oxodG formation at 5"-site guanine of GG and GGG sequences of double-stranded DNA in the presence of GSH and that treatment of formamidopyrimidine-DNA glycosylase led to chain cleavages at the guanine residues.	Phosphorus-32	17-20	P53	Homo sapiens	67-70
11380242-5	2001	RESULTS: The percentage of cells that had died, as measured by trypan blue staining, among U251 cells infected with the Adv for p53 (Adv-p53) and treated with hyperthermia, was significantly higher than the percentage of cells that had died among U251 cells infected with Adv-p53 and not treated with hyperthermia, or those infected with the control Adv for dE (Adv-dE) and treated with hyperthermia.	Trypan Blue	63-74	P53	Homo sapiens	128-131
11306450-6	2001	Treatment with the demethylating agent 5-aza-2"-deoxycytidine was able to reinternalize MDM2 to the nucleus, and p53 expression was restored.	Decitabine	39-61	P53	Homo sapiens	113-116
11313880-0	2001	p53 regulates ceramide formation by neutral sphingomyelinase through reactive oxygen species in human glioma cells.	Ceramides	14-22	P53	Homo sapiens	0-3
11313880-1	2001	The present study was designed to elucidate the relationship between p53 and ceramide, both of which are involved in apoptotic signaling.	Ceramides	77-85	P53	Homo sapiens	69-72
11313880-3	2001	p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2",7"-dichlorofluorescin (DCFH) into 2",7"-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase.	Ceramides	304-312	P53	Homo sapiens	0-3
11332152-2	2001	The in situ bioactivation of cyclophosphamide by cytochrome p450-2B1 and subsequent p53 delivery were examined.	Cyclophosphamide	29-45	P53	Homo sapiens	84-87
11332991-0	2001	Improvement of nonviral p53 gene transfer in human carcinoma cells using glucosylated polyethylenimine derivatives.	Polyethyleneimine	86-102	P53	Homo sapiens	24-27
11172602-7	2001	Trypan blue cell viability assays and flow cytometric cell-cycle analysis demonstrated that the transfer of both p53 and E2F-2 induced cell death in D-54 MG, a p53-resistant glioma cell line.	Trypan Blue	0-11	P53	Homo sapiens	113-116
11161273-12	2001	EBNA-5 also enhanced the nucleolar translocation of a mutant p53 in a colon cancer line, SW480, treated with MG132.	ebna-5	0-6	P53	Homo sapiens	61-64
11161273-12	2001	EBNA-5 also enhanced the nucleolar translocation of a mutant p53 in a colon cancer line, SW480, treated with MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	109-114	P53	Homo sapiens	61-64
11161273-13	2001	The coordinated changes in EBNA-5 and Hsp70 localization and the effect of EBNA-5 on mutant p53 distribution upon MG132 treatment might reflect the involvement of EBNA-5 in the regulation of intracellular protein trafficking associated with the proteasome-mediated degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	114-119	P53	Homo sapiens	92-95
11212244-8	2001	p53 expression was significantly elevated in the cells treated with CV787 and taxane.	cv787	68-73	P53	Homo sapiens	0-3
11090962-0	2000	Wortmannin sensitizes human glioblastoma cell lines carrying mutant and wild type TP53 gene to radiation.	Wortmannin	0-10	P53	Homo sapiens	82-86
11090962-1	2000	The purpose of this paper is to investigate the effect of wortmannin, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K), on TP53 (formerly known as p53) signal transduction initiated by ionizing radiation and radiosensitization in isogenic derivatives of human glioblastoma cells differing in TP53 status.	Wortmannin	58-68	P53	Homo sapiens	135-139
11090962-1	2000	The purpose of this paper is to investigate the effect of wortmannin, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K), on TP53 (formerly known as p53) signal transduction initiated by ionizing radiation and radiosensitization in isogenic derivatives of human glioblastoma cells differing in TP53 status.	Wortmannin	58-68	P53	Homo sapiens	159-162
11090962-1	2000	The purpose of this paper is to investigate the effect of wortmannin, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K), on TP53 (formerly known as p53) signal transduction initiated by ionizing radiation and radiosensitization in isogenic derivatives of human glioblastoma cells differing in TP53 status.	Wortmannin	58-68	P53	Homo sapiens	304-308
11090962-2	2000	Wortmannin inhibited the accumulation of TP53 and CDKN1A (formerly known as WAF1) after 6 Gy irradiation in A-172/neo cells bearing wild-type TP53.	Wortmannin	0-10	P53	Homo sapiens	41-45
11090962-2	2000	Wortmannin inhibited the accumulation of TP53 and CDKN1A (formerly known as WAF1) after 6 Gy irradiation in A-172/neo cells bearing wild-type TP53.	Wortmannin	0-10	P53	Homo sapiens	142-146
11090962-6	2000	These studies indicate that wortmannin inhibits TP53 upregulation, but this suppression does not account for the radiosensitization by this drug.	Wortmannin	28-38	P53	Homo sapiens	48-52
11096420-0	2000	Abrogation of G(2)/M-phase block enhances the cytotoxicity of daunorubicin, melphalan and cisplatin in TP53 mutant human tumor cells.	Daunorubicin	62-74	P53	Homo sapiens	103-107
11096420-3	2000	In the TP53-mutated cell lines MeWo and 4451, the survival ratio at 7 Gy measured by colony formation was 2.3-2.8, 8.6-85 and 52-74 for daunorubicin, melphalan and cisplatin, respectively.	Daunorubicin	136-148	P53	Homo sapiens	7-11
11126357-0	2000	Activation of the p21WAF1/CIP1 promoter independent of p53 by the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) through the Sp1 sites.	Vorinostat	96-127	P53	Homo sapiens	55-58
11126357-0	2000	Activation of the p21WAF1/CIP1 promoter independent of p53 by the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) through the Sp1 sites.	Vorinostat	129-133	P53	Homo sapiens	55-58
11126357-2	2000	We have recently demonstrated that SAHA induces cell cycle arrest and apoptosis in human breast cancer cells, accompanied by up-regulation of the cyclin-dependent kinase inhibitor, p21WAF1/CIP1, via a p53-independent mechanism.	Vorinostat	35-39	P53	Homo sapiens	201-204
11032416-5	2000	Fluorescence anisotropy was employed to measure directly the binding of hdm2(1-126) to a p53 N-terminal peptide labeled with Oregon Green (an analogue of fluorescein).	Fluorescein	154-165	P53	Homo sapiens	89-92
11055588-7	2000	RESULTS: We demonstrate that FTS treatment alters the morphology and blocks the growth of SW480 and HT-29 colon cancer cells by both reducing the total amount of Ras and up-regulating the tumor suppressor p53.	fts	29-32	P53	Homo sapiens	205-208
11055588-9	2000	p53 antisense oligonucleotides not only reduced the level of p53 proteins but correspondingly also blocked the expression of p21(waf1/cip1) in FTS-treated colon cancer cells.	fts	143-146	P53	Homo sapiens	0-3
11055588-9	2000	p53 antisense oligonucleotides not only reduced the level of p53 proteins but correspondingly also blocked the expression of p21(waf1/cip1) in FTS-treated colon cancer cells.	fts	143-146	P53	Homo sapiens	61-64
10896848-11	2000	Compared with adriamycin, a known inducer of p53, MCTP-treated HPAEC expressed p53 only at high concentrations and p53 expression was not coordinated with G2 arrest or polyploidy.	monocrotaline pyrrole	50-54	P53	Homo sapiens	45-48
10896848-11	2000	Compared with adriamycin, a known inducer of p53, MCTP-treated HPAEC expressed p53 only at high concentrations and p53 expression was not coordinated with G2 arrest or polyploidy.	monocrotaline pyrrole	50-54	P53	Homo sapiens	79-82
10896848-11	2000	Compared with adriamycin, a known inducer of p53, MCTP-treated HPAEC expressed p53 only at high concentrations and p53 expression was not coordinated with G2 arrest or polyploidy.	monocrotaline pyrrole	50-54	P53	Homo sapiens	79-82
10896848-12	2000	We conclude that HPAEC treated with low concentrations of MCTP develop G2 arrest in association with persistent cyclin B1 expression, failure to completely activate cdc2, and continued DNA synthesis through a pathway that is unrelated to altered expression of p53.	monocrotaline pyrrole	58-62	P53	Homo sapiens	260-263
10891461-8	2000	In contrast, p53 was stabilized by MG132 or LLnL in malignant and normal cells undergoing apoptosis, indicating that in normal lymphocytes p53 is regulated mainly by calpains and not by the ubiquitin-proteasome system.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-40	P53	Homo sapiens	13-16
10814675-5	2000	METHODS: Here we have mapped the distribution of adducts induced by diol epoxides of additional PAHs: chrysene (CDE), 5-methylchrysene (5-MCDE), 6-methylchrysene (6-MCDE), benzo[c]phenanthrene (B[c]PDE), and benzo[g]chrysene (B[g]CDE) within exons 5, 7, and 8 of the p53 gene in human bronchial epithelial cells.	diol epoxides	68-81	P53	Homo sapiens	267-270
10775450-0	2000	Initiation of rapid, P53-dependent growth arrest in cultured human skin fibroblasts by reactive chlorine species.	reactive chlorine species	87-112	P53	Homo sapiens	21-24
10811472-5	2000	Although wt-p53 transduction before drug treatment induced chemoresistance, p53 transduction in cells treated previously with gemcitabine increased cytotoxicity.	gemcitabine	126-137	P53	Homo sapiens	76-79
10767618-9	2000	With the advent of new techniques of molecular biology, mutations were investigated in the ras and p53 genes of tumors induced by vinyl chloride and urethane.	Vinyl Chloride	130-144	P53	Homo sapiens	99-102
11324420-11	2000	The Western blot assay from cell extracts showed that the levels of protein p53 were decreased after ceramide treatment.	Ceramides	101-109	P53	Homo sapiens	76-79
10745271-8	2000	Ceramide-induced cell death was associated with increased c-myc, p53, Bax and p27kip1 levels; in contrast, cells transfected with Nur77 (A20Nur77), resistant to ceramide-induced apoptosis, showed a marked downregulation of p53 after ceramide treatment, with neither Bax nor p27kip1 induction.	Ceramides	0-8	P53	Homo sapiens	65-68
10745271-8	2000	Ceramide-induced cell death was associated with increased c-myc, p53, Bax and p27kip1 levels; in contrast, cells transfected with Nur77 (A20Nur77), resistant to ceramide-induced apoptosis, showed a marked downregulation of p53 after ceramide treatment, with neither Bax nor p27kip1 induction.	Ceramides	0-8	P53	Homo sapiens	223-226
10688665-4	2000	hDM2 can prevent p53(-/-) cells from entering E2F-dependent apoptosis, an outcome that is dependent upon the presence of the DP subunit.	dp	125-127	P53	Homo sapiens	17-20
10708967-0	2000	Mutagenicity of benzo[a]pyrene-deoxyadenosine adducts in a sequence context derived from the p53 gene.	2'-deoxyadenosine	31-45	P53	Homo sapiens	93-96
10708967-4	2000	This manuscript reports on the mutagenic consequences of replication past anti-BaPDE-deoxyadenosine adducts located within a sequence context related to codon 157 in exon 5 of the p53 gene.	2'-deoxyadenosine	85-99	P53	Homo sapiens	180-183
10677095-0	2000	Expression of p53 in arsenic-related and sporadic basal cell carcinoma.	Arsenic	21-28	P53	Homo sapiens	14-17
10677095-3	2000	Arsenic treatment has been shown to cause hypermethylation of the TP53 gene in lung carcinoma cell lines, but it is not known if this occurs in vivo in arsenic-related BCCs.	Arsenic	0-7	P53	Homo sapiens	66-70
10677095-9	2000	RESULTS: Arsenic-related BCCs express p53 less often and at a lower intensity than sporadic BCCs (P = .001; 2-tailed test).	Arsenic	9-16	P53	Homo sapiens	38-41
10677095-10	2000	The BCCs from sun-exposed sites, whether arsenic related or sporadic, more frequently showed overexpression of p53 than those from less-exposed areas (P = .004; 2-tailed test).	Arsenic	41-48	P53	Homo sapiens	111-114
10677095-12	2000	CONCLUSIONS: These results are consistent with the hypothesis that the TP53 gene is down-regulated by methylation in arsenic-related BCC, particularly those from less-exposed sites.	Arsenic	117-124	P53	Homo sapiens	71-75
10682666-1	2000	The purpose of this work was to analyse the ability of p53 and thymidilate synthase (TS) primary tumour expression to retrospectively predict clinical response to chemotherapy and long-term prognosis in patients with advanced colorectal cancers homogeneously treated by methotrexate (MTX)-modulated-5-fluorouracil (5-FU-FA).	5-fu-fa	315-322	P53	Homo sapiens	55-58
11498362-2	2000	Arsenic may be effective in counteracting drug resistance because it appears to induce apoptosis in tumor cells independently of p53 activation, thereby allowing it to be directed against p53-defective cancers.	Arsenic	0-7	P53	Homo sapiens	129-132
11498362-2	2000	Arsenic may be effective in counteracting drug resistance because it appears to induce apoptosis in tumor cells independently of p53 activation, thereby allowing it to be directed against p53-defective cancers.	Arsenic	0-7	P53	Homo sapiens	188-191
10935502-0	1999	p53-independent inhibition of proliferation and p21(WAF1/Cip1)-modulated induction of cell death by the antioxidants N-acetylcysteine and vitamin E.	Vitamin E	138-147	P53	Homo sapiens	0-3
10935502-5	1999	The antioxidants, N-acetylcysteine (NAC) and vitamin E either inhibited proliferation in a p53-independent manner without affecting cell viability or induced cell death.	Vitamin E	45-54	P53	Homo sapiens	91-94
10592324-6	1999	The genotoxic action of AFB1 was completely different from that of the alkylating agent ethyl-methane-sulfonate, where 28/30 induced mutations were linked to the TP53 target gene.	Ethyl Methanesulfonate	88-111	P53	Homo sapiens	162-166
10597243-2	1999	Here, we identify a cis-acting 66-nucleotide U-rich sequence in the human p53 mRNA 3" untranslated region that mediates translational repression.	66-nucleotide	31-44	P53	Homo sapiens	74-77
10536167-7	1999	Inhibition of DNA replication by aphidicolin prevented the accumulation of p53 in S and G2/M but had no effect on its induction in G1 cells.	Aphidicolin	33-44	P53	Homo sapiens	75-78
10536167-9	1999	Thus, the changes observed in S phase cells (nuclear accumulation of p53 preventable by aphidicolin, induction of Bax, apoptosis), triggered by the collisions of DNA replication forks with the CPT-induced lesions, were distinct from the changes in G1 (nuclear p53 accumulation unaffected by aphidicolin, induction of p21WAF1) presumably triggered by collisions of RNA polymerase with the CPT-lesions.	Aphidicolin	88-99	P53	Homo sapiens	69-72
10491313-0	1999	Arsenic disrupts cellular levels of p53 and mdm2: a potential mechanism of carcinogenesis.	Arsenic	0-7	P53	Homo sapiens	36-39
10491313-5	1999	We propose the disruption of the p53-mdm2 loop regulating cell cycle arrest as a model for arsenic-related skin carcinogenesis and it may be important in tumors with elevated mdm2 levels.	Arsenic	91-98	P53	Homo sapiens	33-36
10423403-7	1999	In the four specimens with abnormal PCR-SSCP bands, p53 gene mutation was identified by direct sequencing and revealed the same point mutation at codon 248 (CGG-to-CTG transversion) of exon 7 in all four specimens.	ctg	164-167	P53	Homo sapiens	52-55
10471039-9	1999	In addition, in contrast to cisplatin, the triplatinum complex was very effective as an inducer of apoptosis in a lung carcinoma cell line carrying mutant p53.	triplatinum	43-54	P53	Homo sapiens	155-158
10652612-8	1999	The experiments indicated that indole-3-carbinol suppressed MCF-7 cell growth in part by induction of apoptosis which was independent of p53 and bax expression and that the effect caused by indole-3-carbinol was partially due to its conversion to a more potent compound, 3,3"-diindolylmethane, in vitro.	indole-3-carbinol	31-48	P53	Homo sapiens	137-140
10407675-3	1999	The TP53 exon 8 sequence was amplified from genomic DNA samples under conditions of high polymerase fidelity using a fluorescein-labeled primer.	Fluorescein	117-128	P53	Homo sapiens	4-8
10397243-0	1999	Arsenic induces apoptosis through a c-Jun NH2-terminal kinase-dependent, p53-independent pathway.	Arsenic	0-7	P53	Homo sapiens	73-76
10397243-7	1999	Taken together with previous findings that p53 mutations are involved in approximately 50% of all human cancers and nearly all chemotherapeutic agents kill cancer cells mainly by apoptotic induction, we suggest that arsenic may be a useful agent for the treatment of cancers with p53 mutation.	Arsenic	216-223	P53	Homo sapiens	43-46
10397243-7	1999	Taken together with previous findings that p53 mutations are involved in approximately 50% of all human cancers and nearly all chemotherapeutic agents kill cancer cells mainly by apoptotic induction, we suggest that arsenic may be a useful agent for the treatment of cancers with p53 mutation.	Arsenic	216-223	P53	Homo sapiens	280-283
10340385-8	1999	Inactivation in these cells of p53 function by transduction of dominant-negative C-terminal p53 fragment (genetic suppressor element #22, GSE22) or mutant p53s significantly increased the frequency of both spontaneous and ras-induced karyotypic changes.	gse22	138-143	P53	Homo sapiens	31-34
10340385-8	1999	Inactivation in these cells of p53 function by transduction of dominant-negative C-terminal p53 fragment (genetic suppressor element #22, GSE22) or mutant p53s significantly increased the frequency of both spontaneous and ras-induced karyotypic changes.	gse22	138-143	P53	Homo sapiens	92-95
10340385-8	1999	Inactivation in these cells of p53 function by transduction of dominant-negative C-terminal p53 fragment (genetic suppressor element #22, GSE22) or mutant p53s significantly increased the frequency of both spontaneous and ras-induced karyotypic changes.	gse22	138-143	P53	Homo sapiens	92-95
10224095-3	1999	Specifically, CLDC-based intravenous delivery of the p53 and GM-CSF genes were each as effective as the potent antiangiogenic gene, angiostatin, in reducing both tumor metastasis and tumor angiogenesis.	cldc	14-18	P53	Homo sapiens	53-56
10224095-5	1999	CLDC-based intravenous delivery of the human wild type p53 gene transfected up to 80% of tumor cells metastatic to lung.	cldc	0-4	P53	Homo sapiens	55-58
9973219-3	1999	CENU-lex sequence specificity for DNA alkylation was determined using 32P-end-labeled restriction fragments of the p53 cDNA.	Phosphorus-32	70-73	P53	Homo sapiens	115-118
9927186-6	1999	Furthermore, Bcl-2 protein was shown to specifically suppress the p53-mediated transactivation of p21CIP1/WAF1 and PG13-CAT, which is a typical p53-binding-site reporter construct.	pg13-cat	115-123	P53	Homo sapiens	66-69
9927186-6	1999	Furthermore, Bcl-2 protein was shown to specifically suppress the p53-mediated transactivation of p21CIP1/WAF1 and PG13-CAT, which is a typical p53-binding-site reporter construct.	pg13-cat	115-123	P53	Homo sapiens	144-147
10048758-9	1999	These results suggest that members of the organochlorine class are able to downregulate Rb expression at the post-transcriptional level, an effect similar to that on p53 tumor suppressor previously reported by our laboratory.	Hydrocarbons, Chlorinated	42-56	P53	Homo sapiens	166-169
10228869-10	1999	The percentage of p53 overexpression with positive DO7 staining was 20.0% (6 out of 30).	[(2S,3S,4S,5R,6S)-6-methoxy-3,4,5-tris(oxidanyl)oxan-2-yl]methanesulfonic acid	51-54	P53	Homo sapiens	18-21
10626228-10	1999	The pattern of modification followed the pattern of p53 mutations found in vinyl chloride-associated liver angiosarcomas in humans and rats, but only in regions that showed 100% homology with the human sequence.	Vinyl Chloride	75-89	P53	Homo sapiens	52-55
11601009-2	1999	METHODS: By LipofectaMINE and electraporation methods, this mutant p53 gene which lacked of exon 1 and intron 1 expression vector driven by CMV promoter was co-transfected with PCMVneo into PG cell in which dominant negative p53 pre-exists.	Lipofectamine	12-25	P53	Homo sapiens	67-70
9886568-0	1998	Oltipraz, a novel inhibitor of hepatitis B virus transcription through elevation of p53 protein.	oltipraz	0-8	P53	Homo sapiens	84-87
9886568-8	1998	In addition, oltipraz induces endogenous wild-type p53 protein in a dose- and time-course-dependent manner.	oltipraz	13-21	P53	Homo sapiens	51-54
9886568-9	1998	Taken together, we speculate that the effects of oltipraz against replication of HBV and specific blocking of HBV transcription may be through the induction of p53-mediated pathway in 2.2.15 cells.	oltipraz	49-57	P53	Homo sapiens	160-163
9719464-6	1998	These findings suggest that ceramide-induced apoptosis is associated with the upregulation of p21 mRNA and protein in a p53-independent pathway.	Ceramides	28-36	P53	Homo sapiens	120-123
9695075-5	1998	These findings suggest that butyrate arrests the growth of WiDr by activating the WAF1 promoter through specific Sp1 sites in a p53-independent fashion.	Butyrates	28-36	P53	Homo sapiens	128-131
9695075-9	1998	Therefore the p53-independent activation of WAF1 by butyrate could be applied to the prevention of cancer when p53 is mutated.	Butyrates	52-60	P53	Homo sapiens	14-17
9695075-9	1998	Therefore the p53-independent activation of WAF1 by butyrate could be applied to the prevention of cancer when p53 is mutated.	Butyrates	52-60	P53	Homo sapiens	111-114
9605744-3	1998	Using a UvrABC incision method, we have found that cytosine methylation greatly enhances guanine alkylation at all CpG sites in the p53 gene by a variety of carcinogens, including benzo(a)pyrene diol epoxide, benzo(g)chrysene diol epoxide, aflatoxin B1 8,9-epoxide, and N-acetoxy-2-acetylaminofluorene.	aflatoxin B1-2,3-oxide	240-264	P53	Homo sapiens	132-135
9565608-9	1998	The results suggest that ADP-ribose polymers could play a role in regulating the DNA binding properties of p53.	adp-ribose polymers	25-44	P53	Homo sapiens	107-110
9499438-8	1998	The elevation of p53 protein levels in MCF-7 cells treated with CPT was significantly inhibited by preincubation with DNA breaks inhibitor aphidicolin, while the elevation of p21WAF1/CIP1 protein levels was not inhibited.	Aphidicolin	139-150	P53	Homo sapiens	17-20
10328543-0	1998	Accumulation of class I mutant p53 and apoptosis induced by carboplatin in a human glioma cell line.	Carboplatin	60-71	P53	Homo sapiens	31-34
9671178-2	1998	All 11 exons of the p53 gene were amplified along with a control sequence in four multiplex PCR reactions in the presence of fluorescein-labeled primers.	Fluorescein	125-136	P53	Homo sapiens	20-23
9356500-0	1997	Enhancement of DNA repair in human skin cells by thymidine dinucleotides: evidence for a p53-mediated mammalian SOS response.	sulfur monoxide	112-115	P53	Homo sapiens	89-92
9268365-0	1997	Butyrate activates the WAF1/Cip1 gene promoter through Sp1 sites in a p53-negative human colon cancer cell line.	Butyrates	0-8	P53	Homo sapiens	70-73
9268365-2	1997	We examined the effect of butyrate on the expression of WAF1/Cip1, a potent inhibitor of cyclin-dependent kinases, and its relation to growth arrest in a p53-mutated human colon cancer cell line WiDr.	Butyrates	26-34	P53	Homo sapiens	154-157
9268365-7	1997	These findings suggest that butyrate arrests the growth of WiDr by activating the WAF1/Cip1 promoter through specific Sp1 sites in a p53-independent fashion.	Butyrates	28-36	P53	Homo sapiens	133-136
9291435-6	1997	Our results suggest that mdm-2, which is known to disrupt p53 function, sensitizes ovarian-cancer cells to cisplatin/cyclophosphamide, possibly by inhibition of p53-mediated G1 cell-cycle arrest and p53-stimulated nucleotide-excision repair.	Cyclophosphamide	117-133	P53	Homo sapiens	58-61
9291435-6	1997	Our results suggest that mdm-2, which is known to disrupt p53 function, sensitizes ovarian-cancer cells to cisplatin/cyclophosphamide, possibly by inhibition of p53-mediated G1 cell-cycle arrest and p53-stimulated nucleotide-excision repair.	Cyclophosphamide	117-133	P53	Homo sapiens	161-164
9291435-6	1997	Our results suggest that mdm-2, which is known to disrupt p53 function, sensitizes ovarian-cancer cells to cisplatin/cyclophosphamide, possibly by inhibition of p53-mediated G1 cell-cycle arrest and p53-stimulated nucleotide-excision repair.	Cyclophosphamide	117-133	P53	Homo sapiens	161-164
9266962-0	1997	Transcriptional squelching by ectopic expression of E2F-1 and p53 is alleviated by proteasome inhibitors MG-132 and lactacystin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	105-111	P53	Homo sapiens	62-65
9266962-3	1997	Although the proteasome inhibitors MG-132 and lactacystin markedly increased the level of expression of E2F-1 and p53, these inhibitors completely alleviated squelching by both proteins.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	35-41	P53	Homo sapiens	114-117
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-36	P53	Homo sapiens	112-115
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-36	P53	Homo sapiens	169-172
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-36	P53	Homo sapiens	169-172
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-36	P53	Homo sapiens	169-172
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	30-36	P53	Homo sapiens	169-172
9219564-0	1997	Arsenic alters cytosine methylation patterns of the promoter of the tumor suppressor gene p53 in human lung cells: a model for a mechanism of carcinogenesis.	Arsenic	0-7	P53	Homo sapiens	90-93
9184111-5	1997	The extent of regional alterations in p53 expression and DNA fragmentation correlated with drug-related toxicity (i.e., NMDA &gt; KA).	N-Methylaspartate	120-124	P53	Homo sapiens	38-41
9066701-6	1997	p53 protein alterations were also associated with all grades of cell microenvironment heterogeneity in the observed OSs.	OSS	116-119	P53	Homo sapiens	0-3
8875926-3	1996	The crystal structure of the p53 core domain bound to the 53BP2 protein, which contains an SH3 (Src homology 3) domain and four ankyrin repeats, revealed that (i) the SH3 domain binds the L3 loop of p53 in a manner distinct from that of previously characterized SH3-polyproline peptide complexes, and (ii) an ankyrin repeat, which forms an L-shaped structure consisting of a beta hairpin and two alpha helices, binds the L2 loop of p53.	polyproline	266-277	P53	Homo sapiens	29-32
8875926-3	1996	The crystal structure of the p53 core domain bound to the 53BP2 protein, which contains an SH3 (Src homology 3) domain and four ankyrin repeats, revealed that (i) the SH3 domain binds the L3 loop of p53 in a manner distinct from that of previously characterized SH3-polyproline peptide complexes, and (ii) an ankyrin repeat, which forms an L-shaped structure consisting of a beta hairpin and two alpha helices, binds the L2 loop of p53.	polyproline	266-277	P53	Homo sapiens	199-202
8875926-3	1996	The crystal structure of the p53 core domain bound to the 53BP2 protein, which contains an SH3 (Src homology 3) domain and four ankyrin repeats, revealed that (i) the SH3 domain binds the L3 loop of p53 in a manner distinct from that of previously characterized SH3-polyproline peptide complexes, and (ii) an ankyrin repeat, which forms an L-shaped structure consisting of a beta hairpin and two alpha helices, binds the L2 loop of p53.	polyproline	266-277	P53	Homo sapiens	199-202
8666362-6	1996	Three (50%) BPB and WDFA stained for p53 and five (83%) for MDM2.	wdfa	20-24	P53	Homo sapiens	37-40
8542574-0	1996	The phosphatidylinositol 3-kinase inhibitor wortmannin sensitizes murine fibroblasts and human tumor cells to radiation and blocks induction of p53 following DNA damage.	Wortmannin	44-54	P53	Homo sapiens	144-147
8542574-5	1996	Wortmannin inhibited the induction of p53 DNA-binding activity by actinomycin D and radiation and blocked the transcriptional activation of a p53 CAT reporter gene by actinomycin D.	Wortmannin	0-10	P53	Homo sapiens	38-41
8542574-5	1996	Wortmannin inhibited the induction of p53 DNA-binding activity by actinomycin D and radiation and blocked the transcriptional activation of a p53 CAT reporter gene by actinomycin D.	Wortmannin	0-10	P53	Homo sapiens	142-145
8542574-6	1996	Wortmannin radiosensitized both wild-type (NIH-3T3 and MCF-7) and mutant (SW480 and HeLa) p53 cells, indicating that p53 induction was not required for radiosensitization by wortmannin.	Wortmannin	0-10	P53	Homo sapiens	90-93
7563172-0	1995	Accumulation of p53 protein as a possible predictor of response to adjuvant combination chemotherapy with cyclophosphamide, methotrexate, fluorouracil, and prednisone for breast cancer.	Cyclophosphamide	106-122	P53	Homo sapiens	16-19
7628635-0	1995	Induction of p53 and apoptosis by delta 12-PGJ2 in human hepatocarcinoma SK-HEP-1 cells.	delta 12-pgj2	34-47	P53	Homo sapiens	13-16
7628635-3	1995	Western analysis using anti-p53 or anti-WAF1 monoclonal antibodies demonstrated that these two protein levels were increased 3 h after delta 12-PGJ2 treatment, and accumulated for up to 12 h. The induction of p53 protein seemed to be dependent on the increase of p53 mRNA level, which was inhibited by CHX treatment.	delta 12-pgj2	135-148	P53	Homo sapiens	28-31
7628635-3	1995	Western analysis using anti-p53 or anti-WAF1 monoclonal antibodies demonstrated that these two protein levels were increased 3 h after delta 12-PGJ2 treatment, and accumulated for up to 12 h. The induction of p53 protein seemed to be dependent on the increase of p53 mRNA level, which was inhibited by CHX treatment.	delta 12-pgj2	135-148	P53	Homo sapiens	209-212
7628635-3	1995	Western analysis using anti-p53 or anti-WAF1 monoclonal antibodies demonstrated that these two protein levels were increased 3 h after delta 12-PGJ2 treatment, and accumulated for up to 12 h. The induction of p53 protein seemed to be dependent on the increase of p53 mRNA level, which was inhibited by CHX treatment.	delta 12-pgj2	135-148	P53	Homo sapiens	209-212
7628635-5	1995	Therefore, our results suggest that the initial events caused by delta 12-PGJ2, leading ultimately to SK-HEP-1 cell death, involve a certain process required for p53 induction.	delta 12-pgj2	65-78	P53	Homo sapiens	162-165
7726729-10	1995	CONCLUSIONS: Microwave pretreatment in conjunction with the use of either PAb1801 or DO7 is highly efficacious in the immunohistochemical detection of aberrant p53 expression in formalin-fixed, paraffin-embedded tissues.	[(2S,3S,4S,5R,6S)-6-methoxy-3,4,5-tris(oxidanyl)oxan-2-yl]methanesulfonic acid	85-88	P53	Homo sapiens	160-163
16695986-5	1995	All three patients whose tumours overexpressed p53 died and in a relatively short time compared with the patients who did not overexpress p53 (mean 3.7 months compared with a mean of 38.7 months in the p53 negative group).Conclusion-Overexpression of p53 in ETs is an uncommon event.	ets	258-261	P53	Homo sapiens	47-50
8720437-9	1995	When fibroblasts were extracted with saponin, p53 was still associated with the actin filaments, as well as mitochondrial membranes and granular structures of the nuclear matrix.	Saponins	37-44	P53	Homo sapiens	46-49
8035799-8	1994	USA 90:3319-3323, 1993) have reported that human p53 behaves as a larger molecule during gel filtration than it does during sucrose gradient sedimentation.	Sucrose	124-131	P53	Homo sapiens	49-52
8037710-6	1994	Nevertheless nuclear p53 accumulation is at much higher extent, whereas 32P-orthophosphate labelling, followed by immunoprecipitation, demonstrates a decrease of phosphorylation of both cytoplasmic and nuclear p53.	Phosphorus-32	72-75	P53	Homo sapiens	210-213
8013454-6	1994	Although 143Ala"s binding to p53 DNA recognition elements and its activation of reporter gene transcription at 32.5 degrees C is markedly higher than that of the wild-type p53, 143Ala inhibited proliferation less robustly than wild-type p53 and it did not increase inhibition of ras-induced focus formation.	143ala	9-15	P53	Homo sapiens	172-175
8013454-6	1994	Although 143Ala"s binding to p53 DNA recognition elements and its activation of reporter gene transcription at 32.5 degrees C is markedly higher than that of the wild-type p53, 143Ala inhibited proliferation less robustly than wild-type p53 and it did not increase inhibition of ras-induced focus formation.	143ala	9-15	P53	Homo sapiens	172-175
8013454-8	1994	143Ala therefore will be of use in dissecting the relationship between the structure of p53 and its different cellular functions.	143ala	0-6	P53	Homo sapiens	88-91
8168507-5	1994	From ultracentrifugation studies, pure p53 exhibited significant oligomerisation, and sedimented broadly within the 7-12-S region of sucrose gradients.	Sucrose	133-140	P53	Homo sapiens	39-42
8293534-0	1994	p53 mutations at A:T base pairs in angiosarcomas of vinyl chloride-exposed factory workers.	Vinyl Chloride	52-66	P53	Homo sapiens	0-3
8293534-5	1994	We examined tumors from five vinyl chloride-exposed patients, four with ASL and one with hepatocellular carcinoma (HCC), for evidence of MDM2 proto-oncogene amplification or p53 mutation in exons 5-8.	Vinyl Chloride	29-43	P53	Homo sapiens	174-177
8293534-7	1994	p53 sequence analysis of vinyl chloride associated cancers may provide valuable information on the relationship between carcinogen exposure and DNA damage in cancer-related genes.	Vinyl Chloride	25-39	P53	Homo sapiens	0-3
8302593-9	1994	The first detected electromobility shift of 32P-labelled DNA and was carried out in the presence of PAb421, which stabilises and supershifts p53-DNA complexes.	Phosphorus-32	44-47	P53	Homo sapiens	141-144
8055156-8	1994	Our results may reflect the presence of mutated p53 proteins due to the mutagenic effect of ultra-violet (UV), or wild-type p53 protein accumulation in response to UV-induced DNA damage, or may be produced by the interaction with HPV-encoded E6 proteins.	ultra-violet	92-104	P53	Homo sapiens	48-51
8221671-5	1993	The DNA-binding activity of wild-type p53 hybrid protein was inhibited by the metal chelator 1,10-phenanthroline.	1,10-phenanthroline	93-112	P53	Homo sapiens	38-41
8376401-4	1993	In the present work we demonstrate that the rapid decrease in the level of c-myc RNA, upon treatment of SW837 cells with 2 mM butyrate, is followed by a slower decrease in the level of p53 RNA and an increase in the RNA levels for fibronectin and a placental type alkaline phosphatase.	Butyrates	126-134	P53	Homo sapiens	185-188
8220069-2	1993	In our present study we observed that sodium butyrate treatment caused a decrease in the level of expression of RB1 gene on day seven of butyrate treatment but a gradual six to sevenfold decrease in the level of expression of p53 gene.	Butyrates	45-53	P53	Homo sapiens	226-229
1906503-4	1991	The production of p53 became detectable 3 to 6 h after addition of phorbol, 12,13,-dibutyrate and ionomycin, and peaked at 30 to 42 h. To further delineate the relationship of the synthesis and metabolism of the proteins to cell cycle progression, we used three agents to arrest progression of activated T cells at various points in the cell cycle.	phorbol	67-74	P53	Homo sapiens	18-21
1906503-7	1991	In the presence of aphidicolin, Rb phosphorylation and p53 production proceeded normally whereas cyclosporin A inhibited both events.	Aphidicolin	19-30	P53	Homo sapiens	55-58
33804175-6	2021	Naturally-occurring carbazoles 1-3 showed the most potent growth inhibitory effects on wild-type p53-expressing cells, being heptaphylline (1) the most promising in all the investigated cell lines.	heptaphylline	125-138	P53	Homo sapiens	97-100
33804175-9	2021	The yeast assay showed a potential reactivation of mutant p53 by heptaphylline derivatives, including compound 1d.	heptaphylline	65-78	P53	Homo sapiens	58-61
16287099-8	2006	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in elevated levels of active p53 as demonstrated by p53 small interfering RNA (siRNA) sensitive p21 upregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	P53	Homo sapiens	26-29
16287099-8	2006	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in elevated levels of active p53 as demonstrated by p53 small interfering RNA (siRNA) sensitive p21 upregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	P53	Homo sapiens	101-104
16287099-8	2006	Inhibition of E6-mediated p53 proteasomal degradation by MG132 resulted in elevated levels of active p53 as demonstrated by p53 small interfering RNA (siRNA) sensitive p21 upregulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	57-62	P53	Homo sapiens	101-104
16287099-9	2006	Although p53 siRNA partially inhibited MG132-induced DR5 upregulation in HeLa and SiHa, no effect on rhTRAIL-induced apoptosis was observed.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	P53	Homo sapiens	9-12
34665271-10	2022	While HDACi induce p21, AC220 suppresses the expression of p53 and p21.	quizartinib	24-29	P53	Homo sapiens	59-62
34728235-3	2022	AZD2461/UCN-01 combination activated p53/p21 and downregulated c-Myc in these cells, leading to a reduced expression level of RAD51, molecule involved in DNA repair.	AZD2461	0-7	P53	Homo sapiens	37-40
34728235-4	2022	The effect of AZD2461/UCN-01 on c-Myc and p53/p21 was inter-dependent and, besides impairing cell proliferation, contributed to the activation of the replicative cycle of KSHV, carried in a latent state in PEL cells.	AZD2461	14-21	P53	Homo sapiens	42-45
34959015-7	2021	Besides, arsenic-treatment obviously increased the levels of mitophagy (PINK1, Parkin, LC3, P62) and pro-apoptotic (Caspase-3, Caspase-9, Cleaved Caspase-3, Cytc, Bax, P53) indexes, and simultaneously resulted in reductions in anti-apoptosis index (Bcl-2).	Arsenic	9-16	P53	Homo sapiens	168-171
34756929-10	2021	The result from gene expression studies indicates that securinine induced apoptosis in MCF-7 cells through p53 dependent pathway.	securinine	55-65	P53	Homo sapiens	107-110
34970530-4	2021	The adducts mimic the thematic features of the chemically stable potent spiro (3H-indole-3,2"-pyrrolidin)-2(1H)-ones p53-MDM2 inhibitors, while installing a pyrrole ring via a carbonyl spacer inspired by the natural marine or synthetic products that efficiently inhibit Bcl2 family functions.	(3h-indole-3,2"-pyrrolidin)-2(1h)-ones	78-116	P53	Homo sapiens	117-120
34959348-0	2021	Modified Gold Nanoparticles to Overcome the Chemoresistance to Gemcitabine in Mutant p53 Cancer Cells.	gemcitabine	63-74	P53	Homo sapiens	85-88
34959348-4	2021	In this study, we generated gold nanoparticles (AuNPs) chemically modified with low molecular branched polyethylenimine (bPEI) for the efficient delivery of gapmers targeting p53 mutant protein.	bpei	121-125	P53	Homo sapiens	175-178
34959348-7	2021	The nanostructures generated here provide a non-toxic and powerful system for the delivery of gapmers in cancer cells, which significantly downregulated mutant p53 proteins and altered molecular markers related to cell growth and apoptosis, thus overcoming chemoresistance to gemcitabine.	gemcitabine	276-287	P53	Homo sapiens	160-163
34855076-2	2021	The cytoprotective effect of NALE was potentiated by NO synthase inhibitor L-NAME (1 mM): the number of p53+ cells decreased by 65.3% and morphometric parameters of the cell nuclei and nucleoli were improved.	NG-Nitroarginine Methyl Ester	75-81	P53	Homo sapiens	104-107
34651662-10	2021	GM-induced ototoxicity may be closely related to the upregulation of p53 expression and the activation of endogenous mitochondrial apoptosis pathways, and PU could protect cochlear hair cells from GM-mediated damage by reducing the production of ROS and inhibiting the mitochondria-dependent apoptosis pathway.	Gentamicins	0-2	P53	Homo sapiens	69-72
34917611-12	2021	KEGG and GSEA enrichment results suggested that the IL-17 signaling pathway and antigen processing and presentation pathways were significantly enriched in the TP53-mutant group.	kegg	0-4	P53	Homo sapiens	160-164
34867391-0	2021	Up-Regulation of p53/miR-628-3p Pathway, a Novel Mechanism of Shikonin on Inhibiting Proliferation and Inducing Apoptosis of A549 and PC-9 Non-Small Cell Lung Cancer Cell Lines.	shikonin	62-70	P53	Homo sapiens	17-20
34653407-0	2021	Anticancer effect of AZD2461 PARP inhibitor against colon cancer cells carrying wt or dysfunctional p53.	AZD2461	21-28	P53	Homo sapiens	100-103
34653407-6	2021	We found that AZD2461 reduced cell proliferation in wtp53 and p53-/- cancer cells by increasing ROS and DNA damage, while R273H mutant (mut) p53 counteracted these effects.	AZD2461	14-21	P53	Homo sapiens	62-65
34653407-8	2021	AZD2461 did not affect cell proliferation of mutp53 colon cancer cells also in combination with low dose radiation, suggesting that only wt p53 or p53 null colon cancer cells could benefit AZD2461 treatment.	AZD2461	189-196	P53	Homo sapiens	140-143
34653407-8	2021	AZD2461 did not affect cell proliferation of mutp53 colon cancer cells also in combination with low dose radiation, suggesting that only wt p53 or p53 null colon cancer cells could benefit AZD2461 treatment.	AZD2461	189-196	P53	Homo sapiens	147-150
34759291-7	2021	We observed that a combination of AZD5363 and AZD8055 treatment synergizes antiproliferative activity on p53 mutated or wild-type HCC cell lines and induces apoptotic cell death.	capivasertib	34-41	P53	Homo sapiens	105-108
34759291-8	2021	Mechanistic insights indicate that a combination of AZD5363 and AZD8055 activated FOXO3a to induce Bim-associated apoptosis in p53 mutated HCC cells, whereas cells retaining functional p53 enhanced Bax.	capivasertib	52-59	P53	Homo sapiens	127-130
34419958-0	2021	VALD-3 inhibits proliferation and induces apoptosis of colorectal cancer cells via upregulating tumor suppressor activity of p53 to inhibit Wnt/beta-catenin signal pathway.	vald-3	0-6	P53	Homo sapiens	125-128
34419958-17	2021	These results suggested that VALD-3 represses cell proliferation and induces apoptosis associated with upregulating tumor suppressor activity of p53 to inhibit Wnt/beta-catenin signal pathway, and it is a potential anticancer agent for colorectal cancer.	vald-	29-34	P53	Homo sapiens	145-148
34776862-14	2021	GSVA identified a series of cancer-related pathways related to GSRS, such as P13K-AKT and P53 pathways.	gsva	0-4	P53	Homo sapiens	90-93
34776862-14	2021	GSVA identified a series of cancer-related pathways related to GSRS, such as P13K-AKT and P53 pathways.	gsrs	63-67	P53	Homo sapiens	90-93
34255353-0	2021	Outcomes of TP53-mutant acute myeloid leukemia with decitabine and venetoclax.	venetoclax	67-77	P53	Homo sapiens	12-16
34502536-0	2021	Fe-N Co-Doped Titanium Dioxide Nanoparticles Induce Cell Death in Human Lung Fibroblasts in a p53-Independent Manner.	fe-n	0-4	P53	Homo sapiens	94-97
34422118-0	2021	Circulating TP53 mutations are associated with early tumor progression and poor survival in pancreatic cancer patients treated with FOLFIRINOX.	folfirinox	132-142	P53	Homo sapiens	12-16
34422118-6	2021	Results: Detection of a TP53 ctDNA mutation before start of FOLFIRINOX (odds ratio (OR) 10.51, 95% confidence interval (CI) 1.40-79.14) and the presence of a homozygous TP53 Pro72Arg germline variant (OR 6.98, 95% CI 1.31-37.30) were predictors of early tumor progression during FOLFIRINOX in multivariable analysis.	folfirinox	60-70	P53	Homo sapiens	24-28
34422118-6	2021	Results: Detection of a TP53 ctDNA mutation before start of FOLFIRINOX (odds ratio (OR) 10.51, 95% confidence interval (CI) 1.40-79.14) and the presence of a homozygous TP53 Pro72Arg germline variant (OR 6.98, 95% CI 1.31-37.30) were predictors of early tumor progression during FOLFIRINOX in multivariable analysis.	folfirinox	279-289	P53	Homo sapiens	24-28
34422118-10	2021	Conclusion: The combination of a TP53 ctDNA mutation before start of FOLFIRINOX and a homozygous TP53 Pro72Arg variant is a promising biomarker, associated with early tumor progression during FOLFIRINOX and poor OS.	folfirinox	69-79	P53	Homo sapiens	33-37
34422118-10	2021	Conclusion: The combination of a TP53 ctDNA mutation before start of FOLFIRINOX and a homozygous TP53 Pro72Arg variant is a promising biomarker, associated with early tumor progression during FOLFIRINOX and poor OS.	folfirinox	69-79	P53	Homo sapiens	97-101
34422118-10	2021	Conclusion: The combination of a TP53 ctDNA mutation before start of FOLFIRINOX and a homozygous TP53 Pro72Arg variant is a promising biomarker, associated with early tumor progression during FOLFIRINOX and poor OS.	folfirinox	192-202	P53	Homo sapiens	33-37
34422118-10	2021	Conclusion: The combination of a TP53 ctDNA mutation before start of FOLFIRINOX and a homozygous TP53 Pro72Arg variant is a promising biomarker, associated with early tumor progression during FOLFIRINOX and poor OS.	folfirinox	192-202	P53	Homo sapiens	97-101
34452218-3	2021	This innovative approach explored the great capacity of both polyamidoamine (PAMAM)-paclitaxel (PTX) conjugate and polyethylenimine (PEI) polymers to complex a p53-encoding plasmid DNA (pDNA), highlighting the utility of considering two compacting agents.	Poly(amidoamine)	61-75	P53	Homo sapiens	160-163
34452218-3	2021	This innovative approach explored the great capacity of both polyamidoamine (PAMAM)-paclitaxel (PTX) conjugate and polyethylenimine (PEI) polymers to complex a p53-encoding plasmid DNA (pDNA), highlighting the utility of considering two compacting agents.	Poly(amidoamine)	77-82	P53	Homo sapiens	160-163
34452218-3	2021	This innovative approach explored the great capacity of both polyamidoamine (PAMAM)-paclitaxel (PTX) conjugate and polyethylenimine (PEI) polymers to complex a p53-encoding plasmid DNA (pDNA), highlighting the utility of considering two compacting agents.	Polyethyleneimine	115-131	P53	Homo sapiens	160-163
34452218-3	2021	This innovative approach explored the great capacity of both polyamidoamine (PAMAM)-paclitaxel (PTX) conjugate and polyethylenimine (PEI) polymers to complex a p53-encoding plasmid DNA (pDNA), highlighting the utility of considering two compacting agents.	Polyethyleneimine	133-136	P53	Homo sapiens	160-163
34374263-7	2021	Results: In vitro experiments, shikonin could inhibit the proliferation of SMMC-7721 cells and induce their apoptosis(P<0.01), up-regulate the expression of p53 gene, down-regulate the phosphorylation levels of AKT and PI3K protein.	shikonin	31-39	P53	Homo sapiens	157-160
34103468-0	2021	A carbazole compound, 9-ethyl-9H-carbazole-3-carbaldehyde, plays an antitumor function through reactivation of the p53 pathway in human melanoma cells.	9-Ethyl-9H-carbazole-3-carbaldehyde	22-57	P53	Homo sapiens	115-118
34103388-10	2021	Abnormal p53 staining was noted in 48.0% of basal, 80.2% GU and 38.1% Uro cases.	3-(1H-imidazol-4-yl)propanoic acid	70-73	P53	Homo sapiens	9-12
34073459-4	2021	Results demonstrated that the cytotoxic effect of the Pt(II)-thiocarbohydrazone complexes against Caov-3 and HT-29 cells was highly significant, and this effect triggered the activation of the p53 and caspase-8 pathways.	pt(ii)	54-60	P53	Homo sapiens	193-196
34066975-2	2021	One of the most popular histone deacetylases inhibitors (HDACIs), suberoylanilide hydroxamic acid (SAHA), also known as Vorinostat, can directly activate p21WAF1/CIP1 gene transcription through hyperacetylation of histones by a p53 independent mechanism.	Vorinostat	66-97	P53	Homo sapiens	228-231
34066975-2	2021	One of the most popular histone deacetylases inhibitors (HDACIs), suberoylanilide hydroxamic acid (SAHA), also known as Vorinostat, can directly activate p21WAF1/CIP1 gene transcription through hyperacetylation of histones by a p53 independent mechanism.	Vorinostat	120-130	P53	Homo sapiens	228-231
34163734-11	2021	By mixing the Fl- and Rh 6G-loaded hairpin-functionalized UiO NMOFs, the multiplexed CRET detection of miRNA-155, miRNA-21 and the p53 and BRCA1 genes is demonstrated.	Fluorescein	14-16	P53	Homo sapiens	131-134
34163734-11	2021	By mixing the Fl- and Rh 6G-loaded hairpin-functionalized UiO NMOFs, the multiplexed CRET detection of miRNA-155, miRNA-21 and the p53 and BRCA1 genes is demonstrated.	Rhodium	22-24	P53	Homo sapiens	131-134
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	Poly(amidoamine)	140-155	P53	Homo sapiens	65-68
35513212-3	2022	Here, we constructed a self-assembled metal-organic nanomedicine p53/Ce6@ZF-T, which was composed of p53 plasmid-complexed chlorin e6 (Ce6)-poly(amidoamine), Fe2+-containing mesoporous zeolitic imidazolate framework-8 and naturally derived tannic acid (TA).	Poly(amidoamine)	140-155	P53	Homo sapiens	101-104
35528524-8	2022	According to bioinformatics analysis, the mechanisms of KTC treatment for PCOS could be linked to IL-17 signaling route, p53 signaling pathway, HIF-1 signaling pathway, etc.	5-ethyl-4-methoxy-2-phenylquinoline	56-59	P53	Homo sapiens	121-124
34980594-3	2022	Irradiated cancer cells devoid of p53 activity are especially sensitive to the DNA-PK inhibitor, as they lose a key cell cycle checkpoint circuit and enter mitosis with unrepaired DSBs, leading to catastrophic consequences.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	180-184	P53	Homo sapiens	34-37
34992144-0	2022	Small-molecule NSC59984 induces mutant p53 degradation through a ROS-ERK2-MDM2 axis in cancer cells.	1-(4-methylpiperazin-1-yl)-3-(5-nitrofuran-2-yl)prop-2-en-1-one	15-23	P53	Homo sapiens	39-42
34992144-7	2022	NSC59984 enhances phosphorylated-MDM2 binding to mutant p53, which leads to mutant p53 ubiquitination and degradation.	1-(4-methylpiperazin-1-yl)-3-(5-nitrofuran-2-yl)prop-2-en-1-one	0-8	P53	Homo sapiens	56-59
34992144-7	2022	NSC59984 enhances phosphorylated-MDM2 binding to mutant p53, which leads to mutant p53 ubiquitination and degradation.	1-(4-methylpiperazin-1-yl)-3-(5-nitrofuran-2-yl)prop-2-en-1-one	0-8	P53	Homo sapiens	83-86
34992144-8	2022	High cellular ROS increases the efficacy of NSC59984 targeting mutant p53 degradation and anti-tumor effects.	1-(4-methylpiperazin-1-yl)-3-(5-nitrofuran-2-yl)prop-2-en-1-one	44-52	P53	Homo sapiens	70-73
35419287-8	2022	The ferroptosis-related p53-SLC7A11-GPX4 pathway was also altered under different treatment propofol, doxorubicin, or paclitaxel regimens.	Propofol	92-100	P53	Homo sapiens	24-27
35273907-10	2021	Lastly, patients with EGFR and TP53 co-alterations showed similar responses to Gefitinib and Icotinib, and the co-occurring TP53 mutation was most likely to be a poor prognostic factor for patients receiving Gefitinib, indicating that the distributions and types of TP53 mutations may contribute to the efficacy and prognosis of molecular targeted therapy.	icotinib	93-101	P53	Homo sapiens	31-35
35273907-10	2021	Lastly, patients with EGFR and TP53 co-alterations showed similar responses to Gefitinib and Icotinib, and the co-occurring TP53 mutation was most likely to be a poor prognostic factor for patients receiving Gefitinib, indicating that the distributions and types of TP53 mutations may contribute to the efficacy and prognosis of molecular targeted therapy.	icotinib	93-101	P53	Homo sapiens	266-270
35204825-9	2022	Redox sensitivity of p53 functions is supported by (i) thioredoxin-dependent reduction of p53 disulfides, (ii) inhibition of the thioredoxin-dependent deoxyribonucleotide synthesis by p53 binding to RRM2B and (iii) changed intracellular distribution of p53 through its oxidation by CHCHD4 in the mitochondrial intermembrane space.	Deoxyribonucleotides	151-170	P53	Homo sapiens	21-24
35204825-9	2022	Redox sensitivity of p53 functions is supported by (i) thioredoxin-dependent reduction of p53 disulfides, (ii) inhibition of the thioredoxin-dependent deoxyribonucleotide synthesis by p53 binding to RRM2B and (iii) changed intracellular distribution of p53 through its oxidation by CHCHD4 in the mitochondrial intermembrane space.	Deoxyribonucleotides	151-170	P53	Homo sapiens	184-187
35204825-9	2022	Redox sensitivity of p53 functions is supported by (i) thioredoxin-dependent reduction of p53 disulfides, (ii) inhibition of the thioredoxin-dependent deoxyribonucleotide synthesis by p53 binding to RRM2B and (iii) changed intracellular distribution of p53 through its oxidation by CHCHD4 in the mitochondrial intermembrane space.	Deoxyribonucleotides	151-170	P53	Homo sapiens	253-256
35215593-2	2022	In this work, polyethylenimine (PEI) has been used to complex p53 encoded plasmid DNA (pDNA), and the anticancer drug methotrexate (MTX) has also been loaded into the vectors.	Polyethyleneimine	14-30	P53	Homo sapiens	62-65
35215593-2	2022	In this work, polyethylenimine (PEI) has been used to complex p53 encoded plasmid DNA (pDNA), and the anticancer drug methotrexate (MTX) has also been loaded into the vectors.	Polyethyleneimine	32-35	P53	Homo sapiens	62-65
35173828-7	2022	In contrast, several tumor suppressor proteins (p21 and p53) have been reported to be downregulated by miR-24.	mir-24	103-109	P53	Homo sapiens	56-59
35099326-13	2022	CONCLUSION: High concentration of ZnO NP caused toxicity to HGF-1 cells and inhibited cell proliferation by regulating MDM2 and p53 expression.	zno np	34-40	P53	Homo sapiens	128-131
11160753-5	2001	DNA-PKcs that was bound to EBNA-LP phosphorylated p53 or EBNA-LP in vitro, and the phosphorylation of EBNA-LP was inhibited by Wortmannin, a specific in vitro inhibitor of DNA-PKcs.	Wortmannin	127-137	P53	Homo sapiens	50-53
11992381-0	2001	O-phospho-L-tyrosine protects TP53 wild-type cells against ionizing radiation.	O-phospho-L-tyrosine	0-20	P53	Homo sapiens	30-34
11992381-3	2001	It could be demonstrated for the first time that P-Tyr at microM concentrations protects TP53 wild-type cells against ionizing radiation (SF4 minus BBI = 0.28, SF4 plus BBI = 0.45).	O-phospho-L-tyrosine	49-54	P53	Homo sapiens	89-93
11992381-5	2001	Treatment of wild-type TP53 cells with P-Tyr induced stabilization of TP53 within 3 and 16 hours and a subsequent increase in CDKN1A expression after treatment.	O-phospho-L-tyrosine	39-44	P53	Homo sapiens	23-27
11992381-5	2001	Treatment of wild-type TP53 cells with P-Tyr induced stabilization of TP53 within 3 and 16 hours and a subsequent increase in CDKN1A expression after treatment.	O-phospho-L-tyrosine	39-44	P53	Homo sapiens	70-74
11992381-8	2001	Thus, the present data suggest that P-Tyr-mediated radioprotection is dependent on preirradiation stabilization of TP53.	O-phospho-L-tyrosine	36-41	P53	Homo sapiens	115-119
11992381-9	2001	The results indicate that P-Tyr is a radioprotective agent that can potentially be very useful and easy to deliver for radiation protection in general and especially in radiation therapy of TP53-mutated tumors.	O-phospho-L-tyrosine	26-31	P53	Homo sapiens	190-194
11436421-8	2001	Induction of apoptosis in HPV-positive cells by CDV was associated with accumulation of the tumor suppressor proteins p53 and pRb and the cyclin-dependent kinase inhibitor p21/WAF-1.	Cidofovir	48-51	P53	Homo sapiens	118-121
11102893-8	2000	SDNA was greater in p53-positive and bcl-2-negative cases; SDNP was greater in p53-positive cases; SHF was lower in p53- and c-myc-positive cases.	sdna	0-4	P53	Homo sapiens	20-23
11103796-8	2000	Wortmannin, an inhibitor of phosphatidylinositol 3-kinases, inhibited arsenite- or X-ray irradiation-induced p53 accumulation but did not alter UV irradiation- or N-acetyl-Leu-Leu-norleucinal-induced p53 accumulation.	Wortmannin	0-10	P53	Homo sapiens	109-112
11103796-8	2000	Wortmannin, an inhibitor of phosphatidylinositol 3-kinases, inhibited arsenite- or X-ray irradiation-induced p53 accumulation but did not alter UV irradiation- or N-acetyl-Leu-Leu-norleucinal-induced p53 accumulation.	Wortmannin	0-10	P53	Homo sapiens	200-203
11085531-12	2000	After a 24 h incubation with dFdCyd alone or in combination with ionizing radiation, U251 cells readily accumulated in S-phase, which remained elevated for at least 72 h, consistent with previous results in other mutant p53 cell lines.	gemcitabine	29-35	P53	Homo sapiens	220-223
11085531-16	2000	These results suggest that the G1 block in D54 cells resulting from wild-type p53 induction prevented radiosensitization by dFdCyd.	gemcitabine	124-130	P53	Homo sapiens	78-81
11092975-6	2000	The silent TP53 could be reactivated by treatment with the demethylating agent 5-azadeoxycytidine.	Decitabine	79-97	P53	Homo sapiens	11-15
11042698-8	2000	The activity of p53 on pro-apoptotic genes expression in response to DNA damage induced by (-irradiation, was affected in the vinblastine (VLB) resistant cell line but not in CCRF-CEM sensitive cell line resulting in a much reduced apoptotic cell death of the multi-drug resistant cells.	2-chloroethyl methyl sulfide	180-183	P53	Homo sapiens	16-19
11042688-3	2000	By pulse-chase experiments, we found that the half-lives of mutant p53 protein were approximately 12, 17, and &gt;30 h in CEM, CEM/VM-1, and CEM/VM-1-5 cells, respectively.	2-chloroethyl methyl sulfide	122-125	P53	Homo sapiens	67-70
11073163-5	2000	Induction of apoptosis by lactacystin or ZLLLal was accompanied by cell cycle arrest at G2/M phase and by accumulation and stabilization of cyclin-dependent kinase inhibitor p21WAF1/Cip and tumor suppressor protein p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-47	P53	Homo sapiens	215-218
11006407-6	2000	Wortmannin significantly increased the BLM-induced aberration frequencies in all but the ATM-/- cells, elevating the sensitivity of p53-/- cells to ATM-/- levels and that of wild-type cells to intermediate levels.	Wortmannin	0-10	P53	Homo sapiens	132-135
11038045-1	2000	BACKGROUND: We assessed the hypothesis that a compromised p53 function could account for the non response of colon cancer patients with low thymidylate synthase (TS) expression receiving a bolus 5-fluorouracil (5-FU) leucovorin (LV) combination.	Leucovorin	217-227	P53	Homo sapiens	58-61
11038045-1	2000	BACKGROUND: We assessed the hypothesis that a compromised p53 function could account for the non response of colon cancer patients with low thymidylate synthase (TS) expression receiving a bolus 5-fluorouracil (5-FU) leucovorin (LV) combination.	Leucovorin	229-231	P53	Homo sapiens	58-61
10825467-1	2000	The dietary isothiocyanates and cancer chemopreventive agents phenethyl isothiocyanate and allyl isothiocyanate and their cysteine conjugates inhibited the growth and induced apoptosis of human leukaemia HL60 (p53-) and human myeloblastic leukaemia-1 cells (p53+) in vitro.	allyl isothiocyanate	91-111	P53	Homo sapiens	210-213
10825467-1	2000	The dietary isothiocyanates and cancer chemopreventive agents phenethyl isothiocyanate and allyl isothiocyanate and their cysteine conjugates inhibited the growth and induced apoptosis of human leukaemia HL60 (p53-) and human myeloblastic leukaemia-1 cells (p53+) in vitro.	allyl isothiocyanate	91-111	P53	Homo sapiens	258-261
10918588-5	2000	The processivity of nucleotide excision is decreased in the presence of 50 mM potassium phosphate and eliminated when full-length p53 is replaced with the core domain, comprised of amino acids 82-292.	potassium phosphate	78-97	P53	Homo sapiens	130-133
10867037-8	2000	Interestingly, the ZDA Opti-MEM cells had significantly lower levels of nuclear p53 protein than both the ZA and ZD cells.	zda opti-mem	19-31	P53	Homo sapiens	80-83
10848610-4	2000	Although coactivator competition is an emerging theme in transcriptional regulation, we have made the fortuitous observation that protein kinase A-phosphorylated CREB strongly enhances p53 association with KIX.	kix	206-209	P53	Homo sapiens	185-188
10837373-1	2000	Polycyclic aromatic hydrocarbon carcinogens (PAHs) and their metabolites have been found to result in a rapid accumulation of p53 gene product in human and mouse cells.	pahs	45-49	P53	Homo sapiens	126-129
10837373-8	2000	With the addition of MG-132, a proteasome inhibitor, to B[a]P or 1-NP treatments, both p21 and p53 protein levels were increased; however, the increase in p21 protein levels was significantly larger than the increase in p53 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	P53	Homo sapiens	95-98
10837373-8	2000	With the addition of MG-132, a proteasome inhibitor, to B[a]P or 1-NP treatments, both p21 and p53 protein levels were increased; however, the increase in p21 protein levels was significantly larger than the increase in p53 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-27	P53	Homo sapiens	220-223
10837373-11	2000	We conclude that PAHs-induced p53 protein is transcriptionally active.	pahs	17-21	P53	Homo sapiens	30-33
10928145-3	2000	The aim of this study was to determine the correlation between technetium-99m sestamibi (Tc-99m MIBI) breast imaging results and expression of the drug resistance proteins (p-glycoprotein (Pgp), Ki-67 and mutant p53) in human breast cancer tissues.	2-methoxyisobutylisonitrile	78-87	P53	Homo sapiens	212-215
10777712-8	2000	Sulfasalazine, a potent and specific inhibitor of NF-kappaB, induced Bax at the expense of Bcl-2, in a p53-dependent manner.	Sulfasalazine	0-13	P53	Homo sapiens	103-106
10771089-7	2000	Wortmannin or LY294002 pretreatment reduces p53 expression after gamma-irradiation to a lesser degree than that of p21.	Wortmannin	0-10	P53	Homo sapiens	44-47
10760090-12	2000	Positive staining for both iNOS and p53 proteins was observed in all cell lines incubated with CsA that were inhibited by CHX; L-NAME inhibited only p53 staining.	NG-Nitroarginine Methyl Ester	127-133	P53	Homo sapiens	149-152
10690553-0	2000	Mismatch repair and p53 independently affect sensitivity to N-(2-chloroethyl)-N"-cyclohexyl-N-nitrosourea.	Lomustine	60-105	P53	Homo sapiens	20-23
10690553-1	2000	The contributions of defective mismatch repair (MMR) and the p53-response to cell killing by N-(2-chloroethyl)-N"-cyclohexyl-N-nitrosourea (CCNU) were evaluated.	Lomustine	93-138	P53	Homo sapiens	61-64
10690553-1	2000	The contributions of defective mismatch repair (MMR) and the p53-response to cell killing by N-(2-chloroethyl)-N"-cyclohexyl-N-nitrosourea (CCNU) were evaluated.	Lomustine	140-144	P53	Homo sapiens	61-64
10690553-8	2000	The hMLH1/p53 defective variants displayed a less prominent cell cycle arrest and reduced apoptosis after CCNU treatment.	Lomustine	106-110	P53	Homo sapiens	10-13
11237205-7	2000	Analysis of the action mechanism of these natural carotenoids is now in progress, and some interesting results have already obtained; for example, beta-cryptoxanthin was suggested to stimulate the expression of RB gene, an anti-oncogene, and p73 gene, which is known as one of the p53-related genes.	Beta-Cryptoxanthin	147-165	P53	Homo sapiens	281-284
10803919-0	2000	The role of p53 in gemcitabine-mediated cytotoxicity and radiosensitization.	gemcitabine	19-30	P53	Homo sapiens	12-15
10803919-1	2000	PURPOSE: We compared the cytotoxic and radiosensitizing effects of gemcitabine (2",2"-difluoro-2"-deoxycytidine, dFdCyd), a clinically valuable radiosensitizer, in colon cancer RKO cells which differed in their p53 status.	gemcitabine	67-78	P53	Homo sapiens	211-214
10803919-5	2000	The cytotoxic effect of dFdCyd in RKO-P cells was accompanied by induction of the proapoptotic protein Bax at the time when p53 was induced.	gemcitabine	24-30	P53	Homo sapiens	124-127
10803919-6	2000	In contrast, similar treatment of RKO-E6 cells with dFdCyd resulted in only limited expression of Bax, suggesting that the cytotoxic effect of dFdCyd was mediated, in part, by a p53-dependent apoptosis pathway.	gemcitabine	52-58	P53	Homo sapiens	178-181
10803919-6	2000	In contrast, similar treatment of RKO-E6 cells with dFdCyd resulted in only limited expression of Bax, suggesting that the cytotoxic effect of dFdCyd was mediated, in part, by a p53-dependent apoptosis pathway.	gemcitabine	143-149	P53	Homo sapiens	178-181
10803919-11	2000	CONCLUSION: These results suggest that p53 status may influence dFdCyd-mediated apoptosis, cytotoxicity, and cell cycle progression but do not support an important role for p53 in radiosensitization.	gemcitabine	64-70	P53	Homo sapiens	39-42
10642304-5	2000	The protein of p53 was potentiated by cilostazol as well as forskolin and 8-bromo-cAMP, whereas PDGF decreased p53 expression.	Cilostazol	38-48	P53	Homo sapiens	15-18
10642304-6	2000	Upregulation of p53 protein by cAMP was further confirmed by the observation that the decrease in p21, a p53-inducible protein, by PDGF was significantly attenuated by cilostazol in a dose-dependent manner (P&lt;0.01).	Cilostazol	168-178	P53	Homo sapiens	16-19
10642304-6	2000	Upregulation of p53 protein by cAMP was further confirmed by the observation that the decrease in p21, a p53-inducible protein, by PDGF was significantly attenuated by cilostazol in a dose-dependent manner (P&lt;0.01).	Cilostazol	168-178	P53	Homo sapiens	105-108
10554039-12	1999	When Y79 cells were exposed to combinations of sodium butyrate and MG132, the latter compound suppressed the decreasing effect induced by sodium butyrate on the levels of p53, N-myc, and IkappaBalpha and the increasing effect on the nuclear level of nuclear factor kappaB.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	67-72	P53	Homo sapiens	171-174
10479688-5	1999	Adenovirus-mediated delivery of p53 to cerebellar granule neurons resulted in caspase-3 (CPP32) activation followed by terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL) staining and loss of viability as determined by an MTT survival assay.	monooxyethylene trimethylolpropane tristearate	260-263	P53	Homo sapiens	32-35
10377423-1	1999	The p53 gene was sequenced in 100 primary human lung cancers by using direct dideoxynucleotide cycle sequencing and compared with sequence analysis by using the p53 GeneChip assay.	Dideoxynucleotides	77-94	P53	Homo sapiens	4-7
10377423-4	1999	Dideoxynucleotide sequencing of the conserved regions of the p53 gene (exons 5-9) detected 76% of the mutations within this region of the gene.	Dideoxynucleotides	0-17	P53	Homo sapiens	61-64
10362120-1	1999	To understand the role of p53 tumour suppressor gene in the carcinogenesis of arsenic-related skin cancers from the blackfoot disease endemic area of Taiwan, we collected tumour samples from 23 patients with Bowen"s disease, seven patients with basal cell carcinomas (BCC) and nine patients with squamous cell carcinomas (SCC).	Arsenic	78-85	P53	Homo sapiens	26-29
10362120-8	1999	These findings showed that p53 gene mutation rate in arsenic-related skin cancers from the blackfoot disease endemic area of Taiwan is high and that the mutation types are different from those in UV-induced skin cancers.	Arsenic	53-60	P53	Homo sapiens	27-30
10328215-6	1999	A slight increase in risk observed for intake of saturated fat was largely due to an increased risk in cases without p53 over-expression (OR per 16.1 g/day, 1.46; 95% CI, 1.08-1.97), and no association in cases with p53 over-expression (OR, 1.07, 95% CI, 0.78-1.47).	saturated	49-58	P53	Homo sapiens	117-120
10328215-6	1999	A slight increase in risk observed for intake of saturated fat was largely due to an increased risk in cases without p53 over-expression (OR per 16.1 g/day, 1.46; 95% CI, 1.08-1.97), and no association in cases with p53 over-expression (OR, 1.07, 95% CI, 0.78-1.47).	saturated	49-58	P53	Homo sapiens	216-219
10222039-7	1999	Aminoacetone caused damage to 32P-5"-end-labeled DNA fragments, obtained from the human c-Ha-ras-1 and p53 genes, at cytosine and thymine residues in the presence of <protein-id="847">Cu(II).	aminoacetone	0-12	P53	Homo sapiens	103-106
10449043-0	1999	Common conformational effects in the p53 protein of vinyl chloride-induced mutations.	Vinyl Chloride	52-66	P53	Homo sapiens	37-40
10449043-2	1999	Vinyl chloride, a known human carcinogen, has been associated with specific A --&gt; T transversions at codons 179, 249, and 255 of the p53 gene.	Vinyl Chloride	0-14	P53	Homo sapiens	136-139
10408175-5	1999	Wortmannin was the most potent inhibitor of p53 accumulation.	Wortmannin	0-10	P53	Homo sapiens	44-47
10331640-2	1999	We show that nicotinamide and the resulting cellular NAD concentration modulate expression of the tumor suppressor protein, p53, in human breast, skin, and lung cells.	Niacinamide	13-25	P53	Homo sapiens	124-127
10226587-0	1999	Ginsenoside-Rs3, a new diol-type ginseng saponin, selectively elevates protein levels of p53 and p21WAF1 leading to induction of apoptosis in SK-HEP-1 cells.	Ginsenoside Rs3	0-15	P53	Homo sapiens	89-92
9811465-3	1998	We found that compared to the parental cell line, cells overexpressing mutant p53 (either 246val or 135ser) exhibited decreased apoptosis in response to gamma-radiation or cisplatin as measured by: propidium iodide (PI) staining of the cellular DNA (cell cycle analysis) and decrease in PARP (poly ADP-ribose polymerase) cleavage as detected by Western blotting.	Propidium	198-214	P53	Homo sapiens	78-81
9891449-12	1998	Further, IP6 treatment caused a decreased expression of mutant p53 protein in HepG2 cells, with no significant change in the expression of wild-type p53.	Phytic Acid	9-12	P53	Homo sapiens	63-66
9772293-7	1998	The accumulated p53 was biochemically active, as measured in a transient transfection assay upon treatment with gemcitabine, cisplatin, etoposide, and Taxol.	gemcitabine	112-123	P53	Homo sapiens	16-19
9821074-5	1998	The constant expression of bcl-2 i early dysplastic cells of BD and the earliest expression of P53 in the basal cells of perilesional normal skin indicate that the initial step of arsenic-induced carcinogenesis is from the basal germinative cells.	Arsenic	180-187	P53	Homo sapiens	95-98
9683793-9	1998	Terminal cell death was enhanced only in normal ECE cells as evidenced by increased envelope formation and was paralleled by an increase in the level of p53 following 3MC treatment.	Methylcholanthrene	167-170	P53	Homo sapiens	153-156
9664115-3	1998	Treatment with cisplatin and carboplatin also provoked an increase in the level of p53 and p21, and a lowering in Bcl-2.	Carboplatin	29-40	P53	Homo sapiens	83-86
9661904-2	1998	Here, we dissect the relationships among mitochondrial function, growth arrest, and apoptosis, reporting that initiation and maintenance of butyrate-mediated p53-independent p21WAF1/Cip1 induction and subsequent G0/G1 arrest require an intact mitochondrial membrane potential (delta psi(mt)) and that the process of dissipation of the delta psi(mt) is then essential for initiation of a butyrate-induced apoptotic cascade.	Butyrates	140-148	P53	Homo sapiens	158-161
9661904-2	1998	Here, we dissect the relationships among mitochondrial function, growth arrest, and apoptosis, reporting that initiation and maintenance of butyrate-mediated p53-independent p21WAF1/Cip1 induction and subsequent G0/G1 arrest require an intact mitochondrial membrane potential (delta psi(mt)) and that the process of dissipation of the delta psi(mt) is then essential for initiation of a butyrate-induced apoptotic cascade.	Butyrates	387-395	P53	Homo sapiens	158-161
9698467-0	1998	Lisofylline sensitizes p53 mutant human ovarian carcinoma cells to the cytotoxic effects of cis-diamminedichloroplatinum (II).	lisofylline	0-11	P53	Homo sapiens	23-26
9698467-2	1998	The possibility that such an agent could be directed specifically against p53-defective tumor cells led us to study the new methylxanthine, Lisofylline, for its ability to sensitize ovary cancer cells to cis-diamminedichloroplatinum(II) (CDDP).	lisofylline	140-151	P53	Homo sapiens	74-77
9698467-3	1998	In cell lines lacking functional p53 (SKOV3, SKOV3 CDDP-resistant, OVCAR3, and OVCAR432) Lisofylline (20-100 microM) enhanced the cytotoxicity of CDDP by approximately 50% as measured by the Alamar blue vital dye indicator assay.	lisofylline	89-100	P53	Homo sapiens	33-36
9698467-5	1998	Restoration of wild-type p53 phenotype by transfection of SKOV3 cells with a p53 cDNA expression vector showed reversal of sensitization by Lisofylline to CDDP cytotoxicity.	lisofylline	140-151	P53	Homo sapiens	25-28
9698467-5	1998	Restoration of wild-type p53 phenotype by transfection of SKOV3 cells with a p53 cDNA expression vector showed reversal of sensitization by Lisofylline to CDDP cytotoxicity.	lisofylline	140-151	P53	Homo sapiens	77-80
9698467-8	1998	Our results show that the combination of CDDP and Lisofylline preferentially sensitizes p53-defective cancer cells to the cytotoxic effect of CDDP by a yet undetermined mechanism.	lisofylline	50-61	P53	Homo sapiens	88-91
9695075-1	1998	We examined the effect of butyrate on the expression of WAF1, a potent inhibitor of cyclin-dependent kinases, and its relation to growth arrest in a p53-mutated human colon cancer cell line WiDr.	Butyrates	26-34	P53	Homo sapiens	149-152
9673359-0	1998	Up-regulation of the tumor suppressor gene p53 and WAF1 gene expression by IP6 in HT-29 human colon carcinoma cell line.	Phytic Acid	75-78	P53	Homo sapiens	43-46
9673359-3	1998	We hypothesize that the tumor suppressor genes such as p53 and WAF1/CIP1 may be involved in mediating the anti-neoplastic action of IP6 p53 acts as a molecular policeman prevention of genetically damaged cells; it causes the cells to arrest in the G1 phase of cell cycle, and regulates the level of p21waf1/cip1 which acts as a growth inhibitor.	Phytic Acid	132-135	P53	Homo sapiens	55-58
9673359-3	1998	We hypothesize that the tumor suppressor genes such as p53 and WAF1/CIP1 may be involved in mediating the anti-neoplastic action of IP6 p53 acts as a molecular policeman prevention of genetically damaged cells; it causes the cells to arrest in the G1 phase of cell cycle, and regulates the level of p21waf1/cip1 which acts as a growth inhibitor.	Phytic Acid	132-135	P53	Homo sapiens	136-139
9673359-4	1998	We therefore investigated the effects of IP6 on the expression of p53 and WAF1/p21 in HT-29 human colon carcinoma by immunocytochemistry and quantitative ELISA.	Phytic Acid	41-44	P53	Homo sapiens	66-69
9673359-5	1998	Our immunocytochemical studies with anti p53 antibodies (wild type-PAb246 and PAb1620) and anti p21waf1/cip1 (EA10) antibodies demonstrated an increased level of p53 and p21waf1/cip1 after 3 and 6 days of treatment with 3.3 and 5 mM IP6.	Phytic Acid	233-236	P53	Homo sapiens	162-165
9673359-6	1998	Quantitative assay for p53 and p21waf1/cip1 by ELISA did not show detectable levels in untreated control cells, while strong expression of p53 and p21waf1/cip1 protein by 3.3 and 5 mM IP6 was seen on day 3 and day 6 of treatment.	Phytic Acid	184-187	P53	Homo sapiens	139-142
9673359-8	1998	These data demonstrate that IP6 up-regulates the expression of the tumor suppressor gene p53 and p21WAF1/CIP1 gene and their modulation may be one of the mechanisms of the anti-neoplastic action of IP6.	Phytic Acid	28-31	P53	Homo sapiens	89-92
9673359-8	1998	These data demonstrate that IP6 up-regulates the expression of the tumor suppressor gene p53 and p21WAF1/CIP1 gene and their modulation may be one of the mechanisms of the anti-neoplastic action of IP6.	Phytic Acid	198-201	P53	Homo sapiens	89-92
9673359-9	1998	Since loss of p53 function enhances cancer cells" resistance to chemotherapeutic agents, the stimulating function of IP6 on p53 makes it an attractive adjuvant chemotherapeutic agent as well.	Phytic Acid	117-120	P53	Homo sapiens	124-127
9548807-0	1998	Induction of p53 by the concerted actions of aziridine and quinone moieties of diaziquone.	aziridine	45-54	P53	Homo sapiens	13-16
9515799-12	1998	In stage III, adjuvant therapy with 5FU plus levamisole improved 7-year survival in patients with wild-type Ki-ras (76 versus 44%; HR, 0.4; 95% CI, 0.2-0.8) and in those without p53 overexpression (64 versus 26%; HR, 0.3; 95% CI, 0.1-0.7).	Levamisole	45-55	P53	Homo sapiens	178-181
9528861-0	1998	Nuclear factor - kappaB-dependent regulation of p53 gene expression induced by daunomycin genotoxic drug.	Daunorubicin	79-89	P53	Homo sapiens	48-51
9528861-2	1998	In the HCT116 colon carcinoma cell line, which retains a wild-type inducible p53 gene, we show that the anthracycline daunomycin is a potent inducer of p53 and NF-kappaB transcription factors.	Daunorubicin	118-128	P53	Homo sapiens	77-80
9528861-2	1998	In the HCT116 colon carcinoma cell line, which retains a wild-type inducible p53 gene, we show that the anthracycline daunomycin is a potent inducer of p53 and NF-kappaB transcription factors.	Daunorubicin	118-128	P53	Homo sapiens	152-155
9528861-4	1998	In addition, daunomycin induced the p53 promoter through the binding of p50/p65 NF-kappaB heterodimers to the kappaB site in the p53 promoter.	Daunorubicin	13-23	P53	Homo sapiens	36-39
9528861-4	1998	In addition, daunomycin induced the p53 promoter through the binding of p50/p65 NF-kappaB heterodimers to the kappaB site in the p53 promoter.	Daunorubicin	13-23	P53	Homo sapiens	129-132
9528861-6	1998	Overexpression of a stable unresponsive IkappaBalpha mutant in HCT116 cells resulted in a complete inhibition of the NF-kappaB activation but only a partial impairment of the p53 protein accumulation induced by daunomycin.	Daunorubicin	211-221	P53	Homo sapiens	175-178
9528861-7	1998	We conclude that the p53-activating signal generated by daunomycin is partially regulated by NF-kappaB.	Daunorubicin	56-66	P53	Homo sapiens	21-24
9526736-8	1998	Similar results were obtained in the evaluation of p53 PI (P &lt; 0.05), suggesting that PCNA and p53 are useful biomarkers for predicting the efficacy of TPP chemotherapy.	tpp	155-158	P53	Homo sapiens	98-101
9463482-0	1998	Mining the National Cancer Institute Anticancer Drug Discovery Database: cluster analysis of ellipticine analogs with p53-inverse and central nervous system-selective patterns of activity.	ellipticine	93-104	P53	Homo sapiens	118-121
9467941-3	1998	The LD motifs of paxillin that bind BE6 share homology with the E6 binding site of E6-AP, a ubiquitin ligase that together with 16E6 targets the degradation of the p53 tumor suppressor.	(2R,3R,4R,5R)-2,5-BIS[(2,5-DIFLUOROBENZYL)OXY]-3,4-DIHYDROXY-N,N'-BIS[(1S,2R)-2-HYDROXY-2,3-DIHYDRO-1H-INDEN-1-YL]HEXANEDIAMIDE	36-39	P53	Homo sapiens	164-167
9438391-2	1998	Using the proteasome-specific inhibitors, MG132 (N-acetyl-L-leucinyl-L-leucinal-L-leucinal) and lactacystin, here we show that the p53-response proteins, bax and mdm2 as well as p21, are degraded by the ubiquitin-proteasome pathway in HeLa cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	P53	Homo sapiens	131-134
9438391-3	1998	MG132 also increased expression of the three proteins in cells that lack p53, showing that stabilization of the p53 response proteins is not due to increased levels of p53 itself.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	P53	Homo sapiens	73-76
9438391-3	1998	MG132 also increased expression of the three proteins in cells that lack p53, showing that stabilization of the p53 response proteins is not due to increased levels of p53 itself.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	P53	Homo sapiens	112-115
9438391-3	1998	MG132 also increased expression of the three proteins in cells that lack p53, showing that stabilization of the p53 response proteins is not due to increased levels of p53 itself.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	P53	Homo sapiens	112-115
9434882-7	1997	In addition, we transfected Jurkat cells and human lymphocytes with wild-type and mutated p53 genes; lymphocytes and Jurkat cells that received the mutated p53 showed increased sensitivity to arsenic cytotoxicity.	Arsenic	192-199	P53	Homo sapiens	90-93
9434882-7	1997	In addition, we transfected Jurkat cells and human lymphocytes with wild-type and mutated p53 genes; lymphocytes and Jurkat cells that received the mutated p53 showed increased sensitivity to arsenic cytotoxicity.	Arsenic	192-199	P53	Homo sapiens	156-159
9434882-8	1997	Data obtained indicate that arsenic induces p53 expression and that cells with a functional p53 contend better with damage induced by this metalloid.	Arsenic	28-35	P53	Homo sapiens	44-47
9434882-8	1997	Data obtained indicate that arsenic induces p53 expression and that cells with a functional p53 contend better with damage induced by this metalloid.	Arsenic	28-35	P53	Homo sapiens	92-95
9224745-0	1997	p53 expression and proliferative activity in Bowen"s disease with or without chronic arsenic exposure.	Arsenic	85-92	P53	Homo sapiens	0-3
9772449-2	1997	METHODS: p53 gene mutations were detected by a-32P-dCTP labelled radiative PCR-SSCP and the biochemical analyses of lipids in serum and AS tissues.	Phosphorus-32	47-50	P53	Homo sapiens	9-12
9209954-9	1997	K-ras mutation was determined by single-strand conformation polymorphism (SSCP) and slot-blot allele-specific oligonucleotide (ASO) hybridization of PCR-amplified DNA product p53 expression was scored on the basis of percent nuclear staining with the MAb DO7.	1,5-anhydroglucitol	127-130	P53	Homo sapiens	175-178
9092641-7	1997	In view of the in vitro evidence that redox state influences the sequence-specific DNA-binding of p53, we have examined the effect of oxidative stress on the in vivo ability of p53 to bind to and transactivate PG13-CAT, a reporter construct containing multiple copies of the p53 consensus binding site linked to the chloramphenicol acetyltransferase gene.	pg13-cat	210-218	P53	Homo sapiens	177-180
9092641-7	1997	In view of the in vitro evidence that redox state influences the sequence-specific DNA-binding of p53, we have examined the effect of oxidative stress on the in vivo ability of p53 to bind to and transactivate PG13-CAT, a reporter construct containing multiple copies of the p53 consensus binding site linked to the chloramphenicol acetyltransferase gene.	pg13-cat	210-218	P53	Homo sapiens	177-180
21541641-4	1996	Increased p53 protein levels have previously been shown to correlate with disease progression in a series of colorectal carcinoma patients treated with 5-FU/folinic acid biomodulated chemotherapy.	Leucovorin	157-169	P53	Homo sapiens	10-13
8956076-5	1996	Phosphoamino acid was incorporated into the N-terminal segment (1P315) at the residue corresponding to p53 serine 315 as Boc-Ser(PO3(Bzl)2)-OH during synthesis.	ser(po3(bzl)2	125-138	P53	Homo sapiens	103-106
8683384-0	1996	Detection of p53 in Hodgkin"s disease using the monoclonal antibody PAb248.	pab248	68-74	P53	Homo sapiens	13-16
8683384-1	1996	The recent demonstration that the murine anti-p53 monoclonal antibody PAb248 can identify human p53 in a variety of normal tissues proves that immunohistochemical detection does not necessarily indicate the presence of mutations.	pab248	70-76	P53	Homo sapiens	46-49
8683384-1	1996	The recent demonstration that the murine anti-p53 monoclonal antibody PAb248 can identify human p53 in a variety of normal tissues proves that immunohistochemical detection does not necessarily indicate the presence of mutations.	pab248	70-76	P53	Homo sapiens	96-99
8683384-2	1996	PAb248 can detect p53 protein in a cytoplasmic-perinuclear localization, not previously described.	pab248	0-6	P53	Homo sapiens	18-21
7586214-10	1995	Both features support the evidence linking vinyl chloride exposure to hepatic angiosarcomas containing an increased frequency of p53 mutations with a mutational spectrum (i.e. A:T --&gt; T:A transversions) characteristic of chloroethylene oxide, a carcinogenic metabolite of vinyl chloride.	Vinyl Chloride	43-57	P53	Homo sapiens	129-132
7586214-10	1995	Both features support the evidence linking vinyl chloride exposure to hepatic angiosarcomas containing an increased frequency of p53 mutations with a mutational spectrum (i.e. A:T --&gt; T:A transversions) characteristic of chloroethylene oxide, a carcinogenic metabolite of vinyl chloride.	Vinyl Chloride	275-289	P53	Homo sapiens	129-132
7591958-2	1995	We found that ellipticine and 9-hydroxyellipticine (9HE), antitumor alkaloids, caused selective inhibition of p53 protein phosphorylation in Lewis lung carcinoma and SW480 (human colon cancer cell line) in a concentration-dependent manner from 0.1 to 100 microM.	ellipticine	14-25	P53	Homo sapiens	110-113
7653176-9	1995	In the follow-up biopsies of 16 BP patients, treated with CO2 laser, recurrence of atypia was seen exclusively in lesions initially positive for both HPV DNA and p53 protein.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	58-61	P53	Homo sapiens	162-165
7705936-1	1995	We introduced the mutant p53 gene (codon 273Arg-His) into human fibroblasts (SUSM-I cells) previously immortalized with 4-nitroquinoline I-oxide (4NQO) and obtained 2 clonal cell lines (SUSM-i/p53-1 and SUSM-1/p53-6) expressing the mutant p53.	i-oxide	137-144	P53	Homo sapiens	25-28
7841034-4	1995	In the present study, we have used the chelator 1, 10-phenanthroline (OP) to probe the effect of temperature on the conformational stability of p53 translated in vitro.	1,10-phenanthroline	48-68	P53	Homo sapiens	144-147
7730147-6	1995	All-trans retinoic acid (all-trans RA) at 1 nM or granulocyte macrophage colony-stimulating factor (GM-CSF) at 35 pM inhibited the wt-p53-induced apoptosis over a 42-h treatment.	Radium	35-37	P53	Homo sapiens	134-137
8089212-1	1994	AIMS: To establish whether PAb248 recognises human p53 as well as murine p53 and if so, to determine its distribution in normal tissues.	pab248	27-33	P53	Homo sapiens	51-54
8089212-2	1994	METHODS: The ability of PAb248 to recognise human p53 was established by analysis of the human osteosarcoma derived Saos-2 cell line, which lacks the p53 gene, before and after transfection with p53 cDNA, using western blotting and immunoprecipitation.	pab248	24-30	P53	Homo sapiens	50-53
8089212-2	1994	METHODS: The ability of PAb248 to recognise human p53 was established by analysis of the human osteosarcoma derived Saos-2 cell line, which lacks the p53 gene, before and after transfection with p53 cDNA, using western blotting and immunoprecipitation.	pab248	24-30	P53	Homo sapiens	150-153
8089212-2	1994	METHODS: The ability of PAb248 to recognise human p53 was established by analysis of the human osteosarcoma derived Saos-2 cell line, which lacks the p53 gene, before and after transfection with p53 cDNA, using western blotting and immunoprecipitation.	pab248	24-30	P53	Homo sapiens	150-153
8089212-5	1994	RESULTS: The anti-p53 PAb248 monoclonal antibody stained the Saos-2 cell line after, but not before, transfection with p53 cDNA.	pab248	22-28	P53	Homo sapiens	18-21
8089212-5	1994	RESULTS: The anti-p53 PAb248 monoclonal antibody stained the Saos-2 cell line after, but not before, transfection with p53 cDNA.	pab248	22-28	P53	Homo sapiens	119-122
8089212-10	1994	CONCLUSIONS: Immunostaining of wild type p53 is demonstrable not only in its nuclear form using antibody PAb240 but also in it common cytoplasmic-perinuclear localisation in normal tissues using the PAb248 monoclonal antibody.	pab248	199-205	P53	Homo sapiens	41-44
8013454-6	1994	Although 143Ala"s binding to p53 DNA recognition elements and its activation of reporter gene transcription at 32.5 degrees C is markedly higher than that of the wild-type p53, 143Ala inhibited proliferation less robustly than wild-type p53 and it did not increase inhibition of ras-induced focus formation.	143ala	9-15	P53	Homo sapiens	29-32
8183576-0	1994	Human p53 directs DNA strand reassociation and is photolabelled by 8-azido ATP.	8-azidoadenosine 5'-triphosphate	67-78	P53	Homo sapiens	6-9
7957118-4	1994	SSCP analysis of exons 5 to 9 of p53 was performed using fragments from PCR end-labeled with 32P followed by autoradiography using an electrophoresis system with temperature control.	Phosphorus-32	93-96	P53	Homo sapiens	33-36
8239512-3	1993	Sequencing p53 cDNA for these cancer cells showed point mutations: In the FaDu cell line, a mutation of CGG to CTG occurred at codon 248; and in the SCC-4 cell line, a mutation of CCC to TCC occurred at codon 151.	ctg	111-114	P53	Homo sapiens	11-14
8467489-2	1993	Here we show that exposure to the metal chelator 1,10-phenanthroline induces wild-type p53 to adopt the mutant conformation and that this process is reversible.	1,10-phenanthroline	49-68	P53	Homo sapiens	87-90
2141685-9	1990	All subclasses of immunopurified p53 separable by sucrose density gradients or by sequential immunoprecipitation exhibited a protein kinase activity and served as substrates for this protein kinase.	Sucrose	50-57	P53	Homo sapiens	33-36
33939887-10	2021	Breast tissue-occurring metabolites" antiproliferation was mainly exerted in p53-wild-type MCF-7 cells by curcuminoids through cell cycle arrest, senescence, and apoptosis induction via p53/p21 induction, while isoflavone-derived metabolites exerted estrogenic-like activity.	Diarylheptanoids	106-118	P53	Homo sapiens	77-80
33824292-10	2021	The results of the CHX-chase experiment showed that depletion of RNF31 alleviated p53 degradation, which was inhibited by MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	122-127	P53	Homo sapiens	82-85
33032195-8	2020	A sandwich-type immunoreaction was achieved via the Fc-specific FITC@SiO2-NH2-anti-IgG binding to the captured anti-p53aAbs.	sio2-nh2	69-77	P53	Homo sapiens	116-119
33233699-0	2020	Astaxanthin Reduces Stemness Markers in BT20 and T47D Breast Cancer Stem Cells by Inhibiting Expression of Pontin and Mutant p53.	astaxanthine	0-11	P53	Homo sapiens	125-128
34843865-1	2022	We report a novel topoisomerase IIalpha inhibitor, mercaptopyridine oxide (MPO), which induces G2/M arrest and senescence with distinctly different cell cycle regulators (p21 or p14ARF) in HCT116p 53WT and HCT116 p53-/- cells, respectively.	mpo	75-78	P53	Homo sapiens	213-216
34820006-6	2022	The present study revealed that tanshinone IIA markedly potentiated the cytotoxic and apoptotic induction effects of imatinib by regulating the AKT-MDM2-P53 signaling pathway and inhibiting the anti-apoptotic proteins BCL2 and MCL1 apoptosis regulator, BCL2 family member in Ph+ ALL cell lines.	Imatinib Mesylate	117-125	P53	Homo sapiens	153-156
34798143-0	2022	Up-regulation of PUMA caused the activation of p53 phosphorylation and acetylation, enhancing the interaction between PUMA and Bcl-X and mediating arsenic-induced apoptosis.	Arsenic	147-154	P53	Homo sapiens	47-50
34937801-1	2022	Idasanutlin is a potent inhibitor of the p53-MDM2 interaction that enables re-activation of the p53 pathway which induces cell cycle arrest and/or apoptosis in tumor cells expressing functional p53.	RG7388	0-11	P53	Homo sapiens	41-44
34937801-1	2022	Idasanutlin is a potent inhibitor of the p53-MDM2 interaction that enables re-activation of the p53 pathway which induces cell cycle arrest and/or apoptosis in tumor cells expressing functional p53.	RG7388	0-11	P53	Homo sapiens	96-99
34937801-1	2022	Idasanutlin is a potent inhibitor of the p53-MDM2 interaction that enables re-activation of the p53 pathway which induces cell cycle arrest and/or apoptosis in tumor cells expressing functional p53.	RG7388	0-11	P53	Homo sapiens	194-197
34970579-9	2021	Syringic acid selectively developed apoptosis in a dose-dependent manner via enhanced regulation of caspase-3, caspase-9 and Poly ADP-ribose Polymerase (PARP) whereas decreasing the expression levels of p53 and BCL-2.	syringic acid	0-13	P53	Homo sapiens	203-206
34976720-4	2022	We present an unusual case of de novo TP53 mutated MDS/MPN overlap with bladder MS. Due to the high-risk nature of the disease, the patient was induced with decitabine and venetoclax combination therapy, resulting in complete remission.	venetoclax	172-182	P53	Homo sapiens	38-42
34876074-9	2021	The p53 signaling pathway was closely correlated with a decline in forced vital capacity and carbon monoxide diffusion capacity and with the activation of cellular senescence.	Carbon Monoxide	93-108	P53	Homo sapiens	4-7
34842019-3	2022	DHL with concomitant TP53 mutation appears to be associated with a very poor prognosis.	Cysteamine	0-3	P53	Homo sapiens	21-25
34732238-7	2021	RG7388 selectively inhibited the proliferation of the TP53 wild-type/PPM1D mutant DIPG cell lines in a dose- and time-dependent manner.	RG7388	0-6	P53	Homo sapiens	54-58
34732238-9	2021	RNA-Seq data showed that differential gene expression induced by RG7388 treatment was enriched in the p53 pathways.	RG7388	65-71	P53	Homo sapiens	102-105
34732238-10	2021	RG7388 reactivated the p53 pathway and induced apoptosis as well as G1 arrest.	RG7388	0-6	P53	Homo sapiens	23-26
34841700-0	2021	Decitabine activates type I interferon signaling to inhibit p53-deficient myeloid malignant cells.	Decitabine	0-10	P53	Homo sapiens	60-63
34681617-13	2021	Opposingly, the ANTH treatment led to increased TP53 and APC expression and decreased KRAS expression, suggesting an anti-carcinogenic effect.	anthracene	16-20	P53	Homo sapiens	48-52
34326482-3	2021	These quinofuracins induced tumor suppressor protein p53-dependent cell death in human glioblastoma LNZTA3 cells.	quinofuracins	6-19	P53	Homo sapiens	53-56
34417460-6	2021	Glucagon, adrenaline and glucocorticoids augment protein levels of p53, and administration of these hormones to p53 deficient human hepatocytes and to liver-specific p53 deficient mice fails to increase glucose levels.	Epinephrine	10-20	P53	Homo sapiens	67-70
34452194-8	2021	As peroxynitrite is known to be a potent inducer of S-nitrosylation, we further found that the nanosheets mediated the S-nitrosylation of p53 at C182, resulting in higher protein-protein complex stability, and this was likely to induce the surrounding residues, located in the interface region, to bind more strongly to each other.	Peroxynitrous Acid	3-16	P53	Homo sapiens	138-141
34373320-3	2021	Common TP53 mutations can be correctly modeled in human adult stem cell-derived colonic organoids with efficiencies up to 25% and up to 97% in hepatocyte organoids.	hepatocyte organoids	143-163	P53	Homo sapiens	7-11
34324416-0	2021	A subset of CB002 xanthine analogs bypass p53-signaling to restore a p53 transcriptome and target an S-phase cell cycle checkpoint in tumors with mutated-p53.	cb002 xanthine	12-26	P53	Homo sapiens	42-45
34324416-0	2021	A subset of CB002 xanthine analogs bypass p53-signaling to restore a p53 transcriptome and target an S-phase cell cycle checkpoint in tumors with mutated-p53.	cb002 xanthine	12-26	P53	Homo sapiens	69-72
34324416-0	2021	A subset of CB002 xanthine analogs bypass p53-signaling to restore a p53 transcriptome and target an S-phase cell cycle checkpoint in tumors with mutated-p53.	cb002 xanthine	12-26	P53	Homo sapiens	154-157
34306252-10	2021	The main compounds of XYS include Quercetin, Naringenin, Isorhamnetin, and Stigmasterol, which mainly regulate the targets such as TP53, Akt1, and MYC and PI3K/Akt, p53, and cell cycle signal pathways.	Stigmasterol	75-87	P53	Homo sapiens	131-135
34306252-10	2021	The main compounds of XYS include Quercetin, Naringenin, Isorhamnetin, and Stigmasterol, which mainly regulate the targets such as TP53, Akt1, and MYC and PI3K/Akt, p53, and cell cycle signal pathways.	Stigmasterol	75-87	P53	Homo sapiens	165-168
34066270-12	2021	This finding suggests that p53 plays a role in the protective effect of EMF-LTE against DNA DSBs.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	92-96	P53	Homo sapiens	27-30
34570571-5	2021	In the patients with a stable disease, strong significant negative correlations between Cho/Cr and Cho/NAA with p53 mutation (-0.945 and -0.812 respectively, p < 0.05) and between Cho/Cr and IDH1, 2 mutation (-0.796, p < 0.05) were found.	1-naphthaleneacetic acid	103-106	P53	Homo sapiens	112-115
34570571-6	2021	In the patients with tumour progression, a significant positive correlation of NAA/Cr with 1p19q codeletion (0.486, p < 0.05) and of Cho/Cr and Cho/NAA values with p53 mutation (0.477 and 0.416, p < 0.05) were identified.	1-naphthaleneacetic acid	148-151	P53	Homo sapiens	164-167
35487445-6	2022	Phthalates changed methylation pattern of the tested genes, decreased expression of P16 and TP53 genes and increased the expression of BCL2 and CCND1.	phthalic acid	0-10	P53	Homo sapiens	92-96
35189247-4	2022	Out of these, the most prominent genetic alterations (PRKAR-1A, CTNNB1, ZNRF3, TP53, CCNE1 and TERF2 genes) are linked with a glycolytic enzyme pyruvate kinase M2 (PKM2), which converts phosphoenolpyruvate (PEP) to pyruvate in the glycolytic pathway.	Pyruvic Acid	215-223	P53	Homo sapiens	79-83
35571131-0	2022	Corrigendum: Propofol Protects Myocardium From Ischemia/Reperfusion Injury by Inhibiting Ferroptosis Through the AKT/p53 Signaling Pathway.	Propofol	13-21	P53	Homo sapiens	117-120
35420431-3	2022	In three MDM4-overexpressing cancer cell lines harboring wild-type p53, 31 shows improved cell growth inhibition activities compared to RG7388, an MDM2-selective inhibitor in late-stage clinical trials.	RG7388	136-142	P53	Homo sapiens	67-70
35625571-7	2022	Hinokiflavone demonstrated p53-dependent and -independent tumor-suppressive activity.	hinokiflavone	0-13	P53	Homo sapiens	27-30
35236053-0	2022	Decitabine salvage for Tumor Protein P53-mutated, relapsed/refractory acute myeloid leukemia after cytotoxic induction therapy.	Decitabine	0-10	P53	Homo sapiens	37-40
35007916-16	2022	The protein levels of P53 and Caspase 3 increased with BA, NaB and SPT treatment for 72 h. CONCLUSIONS: BA, NaB and SPT show anti-cancer activity in the DMS-114 cell line without damaging MRC-5 cells, and some of the molecular mechanisms are involved in apoptosis and cell cycle arrest.	dms-114	153-160	P53	Homo sapiens	22-25
35188613-0	2022	Arsenic concentration in topsoil of central Chile is associated with aberrant methylation of P53 gene in human blood cells: a cross-sectional study.	Arsenic	0-7	P53	Homo sapiens	93-96
35222383-8	2022	Furthermore, GSEA and GSVA revealed significant enrichment of p53 pathway and mismatch repair pathways in high risk-score subgroups.	gsva	22-26	P53	Homo sapiens	62-65
35237000-0	2022	Chidamide and Decitabine in Combination with a HAG Priming Regimen for Acute Myeloid Leukemia with TP53 Mutation.	Decitabine	14-24	P53	Homo sapiens	99-103
35177982-11	2021	Treatment with the CXCR4 inhibitor AMD3100 or transduction of the AIP4 plasmid abrogated the pro-bone metastasis effects of TP53 deletion.	plerixafor	35-42	P53	Homo sapiens	124-128
35190375-1	2022	BACKGROUND: The efficacy of atezolizumab (A) and/or bevacizumab (B) with carboplatin/paclitaxel (CP) chemotherapy was explored in the phase III, randomized IMpower150 study in patients with non-squamous non-small cell lung cancer (NSCLC) according to KRAS mutations (mKRAS) and co-occurring STK11, KEAP1, or TP53 mutations.	Carboplatin	73-84	P53	Homo sapiens	308-312
35074928-5	2022	Mechanistically, stabilization of wild-type p53 and induction of the p53 target gene CDKN1A (p21) leads to decreased expression of the ribonucleotide reductase (RNR) subunits RRM1 and RRM2 RNR is the rate-limiting enzyme of de novo nucleotide synthesis that reduces ribonucleotides to deoxyribonucleotides in a glutathione-dependent manner.	Deoxyribonucleotides	285-305	P53	Homo sapiens	44-47
35074928-5	2022	Mechanistically, stabilization of wild-type p53 and induction of the p53 target gene CDKN1A (p21) leads to decreased expression of the ribonucleotide reductase (RNR) subunits RRM1 and RRM2 RNR is the rate-limiting enzyme of de novo nucleotide synthesis that reduces ribonucleotides to deoxyribonucleotides in a glutathione-dependent manner.	Deoxyribonucleotides	285-305	P53	Homo sapiens	69-72
34047175-6	2021	Such PML induction drives P53 activation, favoring blasts response to chemotherapy or arsenic in vivo.	Arsenic	86-93	P53	Homo sapiens	26-29
33676681-4	2021	The Fe3O4@SiO2-NH2-Au@Pd0.30NPs-protG exhibited a high binding affinity for the captured anti-p53aAbs and high catalytic performance towards the oxidation of 3,3",5,5"-tetramethylbenzidine (TMB).	sio2-nh2-au	10-21	P53	Homo sapiens	94-97
33676681-4	2021	The Fe3O4@SiO2-NH2-Au@Pd0.30NPs-protG exhibited a high binding affinity for the captured anti-p53aAbs and high catalytic performance towards the oxidation of 3,3",5,5"-tetramethylbenzidine (TMB).	3,3',5,5'-tetramethylbenzidine	158-188	P53	Homo sapiens	94-97
33676681-4	2021	The Fe3O4@SiO2-NH2-Au@Pd0.30NPs-protG exhibited a high binding affinity for the captured anti-p53aAbs and high catalytic performance towards the oxidation of 3,3",5,5"-tetramethylbenzidine (TMB).	3,3',5,5'-tetramethylbenzidine	190-193	P53	Homo sapiens	94-97
33676681-7	2021	The apparent binding affinity (KD) between the p53aAbs and Fe3O4@SiO2-NH2-Au@Pd0.30NPs-protG was 35.2 ng mL-1.	sio2-nh2-au	65-76	P53	Homo sapiens	47-50
33907694-0	2021	Rapidly Progressing Urothelial Carcinoma Due to a Rare TP53 (p.Arg110Pro) Mutation: A Case Report and Review of the Literature.	arg110pro	63-72	P53	Homo sapiens	55-59
33907694-3	2021	Molecular pathologic data obtained on the initial, non-muscle invasive tumor and the final cystectomy specimen, revealed the same TP53 mutation (p.Arg110Pro) in both specimens with a variant allele frequency of 44%.	arg110pro	147-156	P53	Homo sapiens	130-134
33655698-11	2021	Furthermore, in patients with NSCLC who underwent ICI treatment, patients with TP53/KMT2C co-mutations had significantly longer PFS and greater durable clinical benefit (HR: 0.48, 95% CI: 0.24-0.94, p = 0.033).	2-I-ICI-H	50-53	P53	Homo sapiens	79-83
33655698-14	2021	TP53/KMT2C co-mutation might serve as a predictive biomarker for ICI responses in NSCLC.	2-I-ICI-H	65-68	P53	Homo sapiens	0-4
33738256-0	2021	Chidamide Combined With Doxorubicin Induced p53-Driven Cell Cycle Arrest and Cell Apoptosis Reverse Multidrug Resistance of Breast Cancer.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	0-9	P53	Homo sapiens	44-47
33073684-3	2021	Our results showed that GMSC-EVs robustly abrogated oxidative stress-induced upregulation in the expression of cellular senescence-related genes, such as beta-galactosidase, p21, p53, and gammaH2AX, and mTOR/pS6 signaling pathway, in human umbilical vein endothelial cells (HUVECs) and skin fibroblasts.	gmsc-evs	24-32	P53	Homo sapiens	179-182
33538587-1	2021	We identified a set of thiosemicarbazone (TSC) metal ion chelators that reactivate specific zinc-deficient p53 mutants using a mechanism called zinc metallochaperones (ZMCs) that restore zinc binding by shuttling zinc into cells.	zmcs	168-172	P53	Homo sapiens	107-110
33538587-7	2021	We conclude that the benzothiazoyl, benzoxazoyl, and benzimidazoyl hydrazones can function as ZMCs to reactivate mutant p53 in vitro and in vivo.	benzothiazoyl	21-34	P53	Homo sapiens	120-123
33627797-0	2021	Decitabine may improve CAR-T efficacy in refractory/relapsed acute leukemia patients carrying TP53 alterations.	Decitabine	0-10	P53	Homo sapiens	94-98
33357454-4	2021	Crystal structures of arsenic-bound p53 mutants reveal a cryptic allosteric site involving three arsenic-coordinating cysteines within the DNA-binding domain, distal to the zinc-binding site.	Arsenic	22-29	P53	Homo sapiens	36-39
33357454-4	2021	Crystal structures of arsenic-bound p53 mutants reveal a cryptic allosteric site involving three arsenic-coordinating cysteines within the DNA-binding domain, distal to the zinc-binding site.	Arsenic	97-104	P53	Homo sapiens	36-39
33357454-5	2021	Arsenic binding stabilizes the DNA-binding loop-sheet-helix motif alongside the overall beta-sandwich fold, endowing p53 mutants with thermostability and transcriptional activity.	Arsenic	0-7	P53	Homo sapiens	117-120
32648994-1	2021	Fluorizoline is a new synthetic molecule that induces p53-independent apoptosis, in several tumor cell lines and in primary leukemia cells, by selectively targeting prohibitins (PHBs).	Fluorizoline	0-12	P53	Homo sapiens	54-57
33484475-4	2021	Previously, serine deprivation has been connected to the action of the tumor suppressor p53, and we have previously published on a role for p53 regulating sphingosine kinase 1 (SK1), an enzyme that phosphorylates sphingosine to form sphingosine-1-phosphate (S1P).	Sphingosine	155-166	P53	Homo sapiens	140-143
33466812-5	2021	The cytotoxicity of HI 5 was found to be intrinsically mediated apoptosis, which in turn, is associated with low Bcl-2 expression and high activation of caspase 3 and p53.	hi 5	20-24	P53	Homo sapiens	167-170
33469287-1	2021	Methods: In this study, we used MTT assays to demonstrate that a combination of SPIO-Serum and wild-type p53 overexpression can reduce ovarian cancer cell viability in vitro.	monooxyethylene trimethylolpropane tristearate	32-35	P53	Homo sapiens	105-108
33190064-6	2021	In our panel of ten cell lines with a spectrum of aberrations in the p53 and pRb pathway, idasanutlin and abemaciclib were the most potent MDM2 and CDK4/6 inhibitors, respectively.	RG7388	90-101	P53	Homo sapiens	69-72
32900849-3	2020	In this study we present two additional mechanisms by which tenovins are able to activate p53 and kill tumor cells in culture.	tenovins	60-68	P53	Homo sapiens	90-93
33323826-0	2020	Efficacy and safety of decitabine combined with low-dose cytarabine, aclarubicin, and granulocyte colony-stimulating factor compared with standard therapy in acute myeloid leukemia patients with TP53 mutation: a single-center analysis.	Decitabine	23-33	P53	Homo sapiens	195-199
31897925-10	2020	Neoadjuvant chemotherapy with cisplatin, 5-fluorouracil and leucovorin may offer high response rates and long-term control in a subgroup of patients affected by intestinal-type adenocarcinoma, and in particular in those whose tumors harbor a functional p53 protein.	Leucovorin	60-70	P53	Homo sapiens	253-256
31886905-0	2020	Mode of action of carboplatin via activating p53/miR-145 axis in head and neck cancers.	Carboplatin	18-29	P53	Homo sapiens	45-48
31886905-5	2020	Western blot was used to measure the levels of p53 and its acetylated versions in cells treated with carboplatin and/or pifithrin-alpha.	Carboplatin	101-112	P53	Homo sapiens	47-50
31886905-7	2020	In addition, we showed that inhibition of p53 by pifithrin-alpha in carboplatin-treated cells reduced miR-145 expression and reversed the suppression of miR-145 direct targets.	Carboplatin	68-79	P53	Homo sapiens	42-45
31886905-8	2020	CONCLUSIONS: Considering all these findings together, one of the proposed mechanisms of carboplatin to kill cells might be the induction of miR-145 and deregulation of its targets in parallel, via p53 activation, which happens through carboplatin"s DNA-damaging property.	Carboplatin	88-99	P53	Homo sapiens	197-200
31886905-8	2020	CONCLUSIONS: Considering all these findings together, one of the proposed mechanisms of carboplatin to kill cells might be the induction of miR-145 and deregulation of its targets in parallel, via p53 activation, which happens through carboplatin"s DNA-damaging property.	Carboplatin	235-246	P53	Homo sapiens	197-200
33245113-8	2020	Licochalcone A exhibited cytotoxicity towards human MCF-7 breast cancer cells, but not MCF-10A human breast epithelial cells, by upregulating p53 expression and blocking cell cycle progression at G2/M, followed by apoptosis.	licochalcone A	0-14	P53	Homo sapiens	142-145
33216890-0	2020	Transient expansion of TP53 mutated clones in polycythemia vera patients treated with idasanutlin.	RG7388	86-97	P53	Homo sapiens	23-27
33216890-4	2020	Here, we present data indicating that idasanutlin therapy is associated with expansion of TP53 mutant subclones.	RG7388	38-49	P53	Homo sapiens	90-94
33216890-7	2020	Follow-up samples were obtained from 4 of 5 patients in this cohort, and we observed that after cessation of idasanutlin, the variant allele frequency (VAF) of 8 of 9 TP53 mutations decreased.	RG7388	109-120	P53	Homo sapiens	167-171
33216890-9	2020	These data suggest that idasanutlin treatment may promote transient TP53 mutant clonal expansion.	RG7388	24-35	P53	Homo sapiens	68-72
32634060-9	2020	From the transcription factor-screening array, it was observed that TYKRIL knockdown increased the p53 activity, a known repressor of PDGFRbeta.	tykril	68-74	P53	Homo sapiens	99-102
32634060-10	2020	RNA immunoprecipitation using various p53 mutants demonstrated that TYKRIL binds to the N-terminal of p53 (an important region for p300 interaction with p53).	tykril	68-74	P53	Homo sapiens	38-41
32634060-10	2020	RNA immunoprecipitation using various p53 mutants demonstrated that TYKRIL binds to the N-terminal of p53 (an important region for p300 interaction with p53).	tykril	68-74	P53	Homo sapiens	102-105
32634060-10	2020	RNA immunoprecipitation using various p53 mutants demonstrated that TYKRIL binds to the N-terminal of p53 (an important region for p300 interaction with p53).	tykril	68-74	P53	Homo sapiens	102-105
32634060-11	2020	The proximity ligation assay revealed that TYKRIL interferes with the p53-p300 interaction (n = 3) and regulates p53 nuclear translocation.Conclusions: TYKRIL plays an important role in PAH by regulating the p53/PDGFRbeta axis.	tykril	43-49	P53	Homo sapiens	70-73
32634060-11	2020	The proximity ligation assay revealed that TYKRIL interferes with the p53-p300 interaction (n = 3) and regulates p53 nuclear translocation.Conclusions: TYKRIL plays an important role in PAH by regulating the p53/PDGFRbeta axis.	tykril	43-49	P53	Homo sapiens	113-116
32634060-11	2020	The proximity ligation assay revealed that TYKRIL interferes with the p53-p300 interaction (n = 3) and regulates p53 nuclear translocation.Conclusions: TYKRIL plays an important role in PAH by regulating the p53/PDGFRbeta axis.	tykril	43-49	P53	Homo sapiens	113-116
32634060-11	2020	The proximity ligation assay revealed that TYKRIL interferes with the p53-p300 interaction (n = 3) and regulates p53 nuclear translocation.Conclusions: TYKRIL plays an important role in PAH by regulating the p53/PDGFRbeta axis.	tykril	152-158	P53	Homo sapiens	113-116
32634060-11	2020	The proximity ligation assay revealed that TYKRIL interferes with the p53-p300 interaction (n = 3) and regulates p53 nuclear translocation.Conclusions: TYKRIL plays an important role in PAH by regulating the p53/PDGFRbeta axis.	tykril	152-158	P53	Homo sapiens	113-116
32860803-9	2020	Taken together, AOAA or PAG inhibited the expression of endogenous H2S biosynthesis enzymes and effectively enhanced susceptibility of gastric cancer to DIM through activating p38-p53 axis.	Aminooxyacetic Acid	16-20	P53	Homo sapiens	180-183
32877208-9	2020	LASSO regression showed that the CBFuniformity of the enhancing tumour and ETCM were predictive features for p53 mutation.	alachlor	0-5	P53	Homo sapiens	109-112
32881246-8	2020	Pioglitazone also reduced the activation of caspase-3 and caspase-9, lowered the ratio of Bax/Bcl-2, attenuated kidney pathological damage and dysfunction, down-regulated the expression of Acetyl-p53, PUMA-alpha and Bax and abated cell apoptosis after cisplatin treatment.	Pioglitazone	0-12	P53	Homo sapiens	196-199
33001991-2	2020	Recently, TP53 gene mutations have been described as a potential predictive biomarker of better outcome in patients treated with a ten-day decitabine regimen., However, functional characteristics of TP53 mutant are heterogeneous, as reflected in multiple functional TP53 classifications and their impact in patients treated with azacitidine is less clear.	Decitabine	139-149	P53	Homo sapiens	10-14
33001991-2	2020	Recently, TP53 gene mutations have been described as a potential predictive biomarker of better outcome in patients treated with a ten-day decitabine regimen., However, functional characteristics of TP53 mutant are heterogeneous, as reflected in multiple functional TP53 classifications and their impact in patients treated with azacitidine is less clear.	Decitabine	139-149	P53	Homo sapiens	199-203
33001991-2	2020	Recently, TP53 gene mutations have been described as a potential predictive biomarker of better outcome in patients treated with a ten-day decitabine regimen., However, functional characteristics of TP53 mutant are heterogeneous, as reflected in multiple functional TP53 classifications and their impact in patients treated with azacitidine is less clear.	Decitabine	139-149	P53	Homo sapiens	199-203
32922194-10	2020	Inhibition of p53 by pifithrin-alpha significantly reduced the levels of PUMA, Bax, and PTEN but restored AKT phosphorylation in SiHa cells exposed to sesamin.	sesamin	151-158	P53	Homo sapiens	14-17
32922194-12	2020	Conclusions: These findings indicate that sesamin inhibits cervical cancer cell proliferation, and its mechanism may be attributed to the induction of p53/PTEN-mediated apoptosis.	sesamin	42-49	P53	Homo sapiens	151-154
32472321-5	2020	In this study, we have targeted the P53 pathway by novel Mannich base (3FB3FA8H) which can be a future prospect to cure neuroblastoma.	Mannich Bases	57-69	P53	Homo sapiens	36-39
32741700-6	2022	Currently, multiple p53-MDM2/MDM4 antagonists are undergoing clinical trials, the most advanced being idasanutlin which is currently undergoing testing in a phase III clinical trial in patients with relapsed or refractory acute myeloid leukemia.	RG7388	102-113	P53	Homo sapiens	20-23
32234756-0	2020	TP53 mutations predict sensitivity to adjuvant gemcitabine in patients with pancreatic ductal adenocarcinoma: next-generation sequencing results from the CONKO-001 trial.	gemcitabine	47-58	P53	Homo sapiens	0-4
32234756-8	2020	In Gem treated patients, TP53 mutations were a positive predictive factor for gemcitabine efficacy (TP53mut: HR for DFS Gem vs Obs: 0.235 (0.130 - 0.423; p<0.001); TP53wt: HR for DFS Gem vs Obs: 0.794 (0.417 - 1.513; p = 0.483) with a significant test for interaction (p=0.003).	gemcitabine	78-89	P53	Homo sapiens	25-29
32234756-8	2020	In Gem treated patients, TP53 mutations were a positive predictive factor for gemcitabine efficacy (TP53mut: HR for DFS Gem vs Obs: 0.235 (0.130 - 0.423; p<0.001); TP53wt: HR for DFS Gem vs Obs: 0.794 (0.417 - 1.513; p = 0.483) with a significant test for interaction (p=0.003).	gemcitabine	78-89	P53	Homo sapiens	100-104
32234756-8	2020	In Gem treated patients, TP53 mutations were a positive predictive factor for gemcitabine efficacy (TP53mut: HR for DFS Gem vs Obs: 0.235 (0.130 - 0.423; p<0.001); TP53wt: HR for DFS Gem vs Obs: 0.794 (0.417 - 1.513; p = 0.483) with a significant test for interaction (p=0.003).	gemcitabine	78-89	P53	Homo sapiens	100-104
32234756-10	2020	CONCLUSION: In CONKO-001, the benefit from adjuvant gemcitabine was confined to the TP53mut patient group.	gemcitabine	52-63	P53	Homo sapiens	84-88
32753898-0	2020	Association of TP53 Mutations with Response to Anlotinib Treatment in Advanced Non-Small Cell Lung Cancer.	anlotinib	47-56	P53	Homo sapiens	15-19
32753898-4	2020	Herein, we report three pre-treated cases of advanced NSCLC with TP53 mutations, wherein these patients showed partial response to anlotinib.	anlotinib	131-140	P53	Homo sapiens	65-69
32753898-7	2020	In conclusion, TP53 mutations may represent a biomarker for predicting salutary effects of anlotinib.	anlotinib	91-100	P53	Homo sapiens	15-19
32622356-6	2020	After biopsy confirmation, patient was initially started on gemcitabine and oxaliplatin combination followed by gene sequencing, which showed Tp53 (exon 7-c.713 G > A and exon 5-c.376-2A > G) and EGFR (exon 20-T790M) mutation, and erlotinib was added to chemotherapy, after 6 cycles of chemotherapy patient showed a 90% partial radiological response as per RECIST criteria.	Erlotinib Hydrochloride	231-240	P53	Homo sapiens	142-146
32504186-0	2020	Monosomal karyotype and chromosome 17p loss or TP53 mutations in decitabine-treated patients with acute myeloid leukemia.	Decitabine	65-75	P53	Homo sapiens	47-51
32504186-1	2020	TP53 aberrations reportedly predict favorable responses to decitabine (DAC) in acute myeloid leukemia (AML).	Decitabine	59-69	P53	Homo sapiens	0-4
32504186-1	2020	TP53 aberrations reportedly predict favorable responses to decitabine (DAC) in acute myeloid leukemia (AML).	Decitabine	71-74	P53	Homo sapiens	0-4
32315827-9	2020	Our findings suggest that PEDF protects endothelial cells from arsenic-induced VED by increasing NO release and inhibiting apoptosis, where P53 and p38MAPK are its main targets.	Arsenic	63-70	P53	Homo sapiens	140-143
32386222-8	2020	The CPO-A treatment attenuated or restored (P < 0.05) these changes and inhibited (P < 0.05) the MPTP-induced activation of P38 mitogen-activated protein kinase (P38MAPK) and P53, along with the downstream expression of BCL-2 associated X protein (BAX) in the SN.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	97-101	P53	Homo sapiens	175-178
32077107-3	2020	Since MAPK signaling pathways regulate p53 expression and activation, here we determined bucillamine effect on UVB-mediated MAPK activation in vitro using human skin kerotinocyte cell line HaCaT and in vivo using SKH-1 hairless mouse skin.	bucillamine	89-100	P53	Homo sapiens	39-42
32583791-4	2020	Some bioactive compounds, in particular phenolic compounds, saponins and alkaloids have revealed good abilities to affect p53 expression and indirectly control the telomere length.	Saponins	60-68	P53	Homo sapiens	122-125
32446382-6	2020	Interestingly, kuanoniamine C-induced cell death and downregulation of GRP78 expression was regulated by p53 signaling.	Kuanoniamine C	15-29	P53	Homo sapiens	105-108
32446382-8	2020	These results suggest that co-treatment with bortezomib and kuanoniamine C is a novel therapeutic strategy for the treatment of osteosarcoma that enhances bortezomib-dependent cell death by the downregulation of GRP78, and this combination selectively targets the major cell population of osteosarcoma, which expresses wild-type p53.	Kuanoniamine C	60-74	P53	Homo sapiens	329-332
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	Imatinib Mesylate	55-63	P53	Homo sapiens	169-172
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	Imatinib Mesylate	121-129	P53	Homo sapiens	169-172
32655803-17	2020	CONCLUSION: We proposed a novel molecular mechanism of imatinib resistance in CML in which the high expression of Lyn in imatinib-resistant cells inhibited Ac-Foxo1 and p53 expression through the BCR-ABL/SIRT1/Foxo1 signaling pathway, thus reducing apoptosis and mediating imatinib resistance.	Imatinib Mesylate	121-129	P53	Homo sapiens	169-172
32072678-9	2020	Specifically, the combination of ART and CBP at a lower concentration suppressed cell clone numbers, promoted cell cycle arrest at the G2 /M phase, and induced the expression of the cell cycle and apoptosis related proteins BAX, p21, p53, and Caspae-3, while decreasing Bcl-2 and CyclinB1 expression.	Carboplatin	41-44	P53	Homo sapiens	234-237
32606052-7	2020	RESULTS: A GMS risk model consisting of eight genes (TP53, KRAS, STK11, EGFR, PTPRD, KMT2C, SMAD4, and HGF) was generated to classify patients into high and low GMS groups in the training cohort.	gms	11-14	P53	Homo sapiens	53-57
32427989-7	2020	However, depleting Mdm4 sensitized p53-/- cells to the nucleoside analog gemcitabine, raising the future perspective of using Mdm4 inhibitors as chemosensitizers.	gemcitabine	73-84	P53	Homo sapiens	35-38
32509176-5	2020	In MCA-SVHUC-AR cells, CpdA significantly reduced the expression levels of oncogenes (c-Fos/c-Jun/c-Myc) and induced those of tumor suppressors (UGT1A/p21/p27/p53/PTEN).	CPDA	23-27	P53	Homo sapiens	159-162
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	Imatinib Mesylate	283-291	P53	Homo sapiens	15-18
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	Imatinib Mesylate	283-291	P53	Homo sapiens	148-151
32084420-6	2020	Interestingly, p53 expression was elevated by the SN-38 mono-treatment, and was not further increased after the co-treatment; besides, knockdown of p53 could only reduce the expression of cleaved-PARP partially, and weaken the enhanced proliferation inhibition induced by SN-38 plus imatinib, indicating that there might be other factors involved in the synergistic effects besides p53.	Imatinib Mesylate	283-291	P53	Homo sapiens	148-151
31875995-9	2020	DNA repair proteins (OGG1, Ape-1, and MyH) involved in the base excision repair pathway, as well as p53 protein levels were down-regulated in all of the bisphenol-exposed groups.	bis(4-hydroxyphenyl)sulfone	153-162	P53	Homo sapiens	100-103
32251398-3	2020	TP53 mutations are detected in ~20% of LEN-resistant patients3.	Lenalidomide	39-42	P53	Homo sapiens	0-4
32088783-6	2020	METHODS/RESULTS: In this study, the results of the MTT and flow cytometry-based assays showed that Aloperine-Adbic (adenoviral vector expressing p14ARF/p53) combined treatment on NSCLC cells synergistically produced anti-proliferative effects, induced apoptosis, and arrested cell cycle at the G1 phase.	monooxyethylene trimethylolpropane tristearate	51-54	P53	Homo sapiens	152-155
32088783-6	2020	METHODS/RESULTS: In this study, the results of the MTT and flow cytometry-based assays showed that Aloperine-Adbic (adenoviral vector expressing p14ARF/p53) combined treatment on NSCLC cells synergistically produced anti-proliferative effects, induced apoptosis, and arrested cell cycle at the G1 phase.	aloperine	99-108	P53	Homo sapiens	152-155
32218822-9	2020	These results indicated that gene mutation can be profiled and monitored using liquid biopsy-based CAPP-Seq in patients with advanced ovarian cancer with NAC treatment, and TP53 mutation in the ctDNA and bTMB may be novel biomarkers that can be used for patient monitoring during NAC treatment.	3,5-Bis(trimethylsilyl)benzoic acid	204-208	P53	Homo sapiens	173-177
32154226-11	2020	Silencing CCNA2 could suppress cell proliferation, migration and invasion, as well as activate p53 pathway, even was seen to reverse the inhibitory effect of PFTbeta on p53.	pifithrin-beta	158-165	P53	Homo sapiens	169-172
32062612-10	2020	CONCLUSIONS: miR-24-3p/PIM-2/XIAP signaling contributes to BBR-mediated leukemia mitigation in p53-defect ALL, which should be further developed as a treatment strategy in ALL patients with p53 deficiency.	mir-24	13-19	P53	Homo sapiens	95-98
32062612-10	2020	CONCLUSIONS: miR-24-3p/PIM-2/XIAP signaling contributes to BBR-mediated leukemia mitigation in p53-defect ALL, which should be further developed as a treatment strategy in ALL patients with p53 deficiency.	mir-24	13-19	P53	Homo sapiens	190-193
32116712-0	2020	Clonal Selection of a Novel Deleterious TP53 Somatic Mutation Discovered in ctDNA of a KIT/PDGFRA Wild-Type Gastrointestinal Stromal Tumor Resistant to Imatinib.	Imatinib Mesylate	152-160	P53	Homo sapiens	40-44
32116712-10	2020	The de novo TP53 (c.560-7_560-2delCTCTTAinsT) mutation was in silico predicted to be associated with an aberrant RNA splicing and with an aggressive phenotype which might have contributed to a rapid disease spread despite the administration of an increased imatinib dosage.	Imatinib Mesylate	257-265	P53	Homo sapiens	12-16
31855686-5	2020	Moreover, the transfection with UCNPs(BTZ)@mSiO2-H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO2/p53.	Silicon	44-48	P53	Homo sapiens	53-56
31855686-5	2020	Moreover, the transfection with UCNPs(BTZ)@mSiO2-H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO2/p53.	Silicon	44-48	P53	Homo sapiens	60-63
31855686-5	2020	Moreover, the transfection with UCNPs(BTZ)@mSiO2-H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO2/p53.	Silicon	44-48	P53	Homo sapiens	60-63
31855686-5	2020	Moreover, the transfection with UCNPs(BTZ)@mSiO2-H2A/p53 in p53-deficient non-small cell lung cancer cells changed the status of p53 and substantially enhanced the p53-mediated sensitivity of encapsulated BTZ inside the UCNPs(BTZ)@mSiO2/p53.	Silicon	44-48	P53	Homo sapiens	60-63
31464976-8	2020	Inhibition of ROS generation by NAC or p38 MAPK signaling by SB203580 attenuated the p53-mediated cell cycle arrest and apoptosis induced by LY.	SB 203580	61-69	P53	Homo sapiens	85-88
31119730-4	2020	TP53 mutation carriers were significantly more likely to have early onset cancer (p < 0.001) and bilateral breast cancer (p = 0.03), they and were significantly more likely to respond to carboplatin-based neoadjuvant chemotherapy compared to anthracycline- or taxane-based regimen in terms of pathologic complete response (50% vs. 0%, p = 0.006).	Carboplatin	187-198	P53	Homo sapiens	0-4
31119730-6	2020	Our study suggested that TP53 germline mutations occur more frequently in very early onset unselected breast cancer patients; and TP53 germline mutation carriers have a very poor survival and may benefit from carboplatin-based neoadjuvant chemotherapy in unselected breast cancer patients.	Carboplatin	209-220	P53	Homo sapiens	25-29
31119730-6	2020	Our study suggested that TP53 germline mutations occur more frequently in very early onset unselected breast cancer patients; and TP53 germline mutation carriers have a very poor survival and may benefit from carboplatin-based neoadjuvant chemotherapy in unselected breast cancer patients.	Carboplatin	209-220	P53	Homo sapiens	130-134
31809756-10	2020	In addition, sesamin inhibited Akt activity and upregulated p53 expression both in vivo and in vitro.	sesamin	13-20	P53	Homo sapiens	60-63
31809756-14	2020	Taken together, this study demonstrates that sesamin suppresses NSCLC cell proliferation by induction of G1 phase cell cycle arrest and apoptosis via Akt/p53 pathway.	sesamin	45-52	P53	Homo sapiens	154-157
31948013-8	2020	Treatment with iPSC-CENVs significantly reduced the activity of senescence-associated-beta-galactosidase (SA-beta-Gal) in senescent HDFs, as well as suppressing the elevated expression of p53 and p21, key factors involved in cell cycle arrest, apoptosis, and cellular senescence signaling pathways.	ipsc-cenvs	15-25	P53	Homo sapiens	188-191
31568878-3	2019	PAMSPF was able to condense DNA and encapsulate RG7388 to form spherical nanoparticles (PAMSPF/p53/RG) with particle sizes of around 200 nm, and remain stable in the presence of heparin and nuclease.	RG7388	48-54	P53	Homo sapiens	95-98
31568878-4	2019	The drug loading capacity and encapsulation efficiency of RG7388 in PAMSPF/p53/RG were 0.5% and 92.5%, respectively.	RG7388	58-64	P53	Homo sapiens	75-78
31568878-8	2019	And the biological activities described above of PAMSPF/p53/RG were significantly higher than those of PAMSPF/53 and PAMSPF/RG, exhibiting the synergistic actions of p53 plasmid and RG7388.	RG7388	182-188	P53	Homo sapiens	56-59
31568878-11	2019	Collectively, PAMSPF/p53/RG is an excellent system for gene and drug co-delivery, and the combined treatment of p53 plasmid and RG7388 possesses a synergistic antitumor activity both in vitro and in vivo.	RG7388	128-134	P53	Homo sapiens	21-24
31571495-10	2019	Additionally, Belinostat activated PKC pathway by upgrading PKCdelta and P53 expressions.	belinostat	14-24	P53	Homo sapiens	73-76
31358486-0	2019	Bisphenol A exposure under metabolic stress induces accelerated cellular senescence in vivo in a p53 independent manner.	bis(4-hydroxyphenyl)sulfone	0-9	P53	Homo sapiens	97-100
31652983-7	2019	Finally, as oxidative stress-related signaling pathways can modulate the cell cycle through p53, we analyzed the expression of the p53 target gene p21 in BM cells, finding that it was significantly upregulated in patients with MDS and was significantly downregulated after DFX treatment.	deferasirox	273-276	P53	Homo sapiens	131-134
31632027-11	2019	Rh2HAZnO induced apoptotic process through p53-mediated pathway by upregulating p53 and BAX and downregulating BCL2.	Rhodium	0-8	P53	Homo sapiens	43-46
31632027-11	2019	Rh2HAZnO induced apoptotic process through p53-mediated pathway by upregulating p53 and BAX and downregulating BCL2.	Rhodium	0-8	P53	Homo sapiens	80-83
29064206-0	2019	Correlation of changes in HIF-1alpha and p53 expressions with vitamin B3 deficiency in skin cancer patients.	Niacinamide	62-72	P53	Homo sapiens	41-44
29064206-1	2019	BACKGROUND: To investigate the correlation of changes in hypoxia-inducible factor-1alpha (HIF-1alpha) and p53 expressions with vitamin B3 deficiency in skin cancer patients.	Niacinamide	127-137	P53	Homo sapiens	106-109
29064206-6	2019	The protein and mRNA expression levels of HIF-1alpha and p53 in tissues of skin cancer patients were significantly decreased at 1 week after the oral administration of vitamin B3 compared with those before the oral administration of vitamin B3 (P<0.05), but the protein and mRNA expression levels of HIF-1alpha and p53 in tissues of skin cancer patients in placebo group had no significant changes (P>0.05).	Niacinamide	168-178	P53	Homo sapiens	57-60
29064206-6	2019	The protein and mRNA expression levels of HIF-1alpha and p53 in tissues of skin cancer patients were significantly decreased at 1 week after the oral administration of vitamin B3 compared with those before the oral administration of vitamin B3 (P<0.05), but the protein and mRNA expression levels of HIF-1alpha and p53 in tissues of skin cancer patients in placebo group had no significant changes (P>0.05).	Niacinamide	168-178	P53	Homo sapiens	315-318
29064206-6	2019	The protein and mRNA expression levels of HIF-1alpha and p53 in tissues of skin cancer patients were significantly decreased at 1 week after the oral administration of vitamin B3 compared with those before the oral administration of vitamin B3 (P<0.05), but the protein and mRNA expression levels of HIF-1alpha and p53 in tissues of skin cancer patients in placebo group had no significant changes (P>0.05).	Niacinamide	233-243	P53	Homo sapiens	57-60
29064206-7	2019	The vitamin B3 deficiency in skin cancer patients was positively correlated with the expressions of HIF-1alpha and p53.	Niacinamide	4-14	P53	Homo sapiens	115-118
29064206-8	2019	CONCLUSIONS: The expression levels of HIF-1alpha and p53 in tissues of skin cancer patients are significantly increased compared with those in skin tissues of healthy people, and the changes in their expressions are positively correlated with the vitamin B3 deficiency.	Niacinamide	247-257	P53	Homo sapiens	53-56
31163195-0	2019	p53-dependent upregulation of miR-16-2 by sanguinarine induces cell cycle arrest and apoptosis in hepatocellular carcinoma.	sanguinarine	42-54	P53	Homo sapiens	0-3
31163195-4	2019	One compound, sanguinarine (SG), was capable of activating miR-16 in HCC cells with wildtype or mutated p53 expression but not in p53-deleted HCC cells.	sanguinarine	14-26	P53	Homo sapiens	104-107
31287365-1	2019	Purpose: To evaluate the effect of NU7026, a specific inhibitor of DNA-PKcs, on DNA-double strand break (DSB) repair in a cell cycle specific manner, on the G2/M checkpoint, mitotic progression, apoptosis and clonogenic survival in non-small-cell lung carcinoma (NSCLC) cell lines with different p53 status.	2-(morpholin-4-yl)benzo(h)chromen-4-one	35-41	P53	Homo sapiens	296-299
31998813-0	2019	Novel Isatin-based activator of p53 transcriptional functions in tumor cells.	Isatin	6-12	P53	Homo sapiens	32-35
31998813-4	2019	Here, we report novel data on p53 activating Isatin-based Cu(II) complex exhibiting cytotoxic properties towards HCT116 and MCF7 tumor cell lines, as confirmed by cell viability assay and flow cytometry analysis of apoptosis.	Isatin	45-51	P53	Homo sapiens	30-33
31029785-3	2019	The anticancer effect of ziyuglycoside II was examined in HCT116 (as p53 normal cells) and SW480 (as p53 mutant cells) colon cancer cells.	ziyuglycoside II	25-41	P53	Homo sapiens	69-72
31029785-6	2019	Apoptosis caused by p53 phosphorylation following ziyuglycoside II treatment in HCT116 cells involved activation of caspases, increased expression of BAX, mitochondrial cytochrome c and apoptosis inducing factor (AIF) release, while BCL-2 became down-regulated.	ziyuglycoside II	50-66	P53	Homo sapiens	20-23
31220582-7	2019	Mechanistic study revealed that ATF3 interacted with the p53 protein and upregulated its expression under ZnO NP treatment.	zno np	106-112	P53	Homo sapiens	57-60
31048321-11	2019	Targeting CLPB synergizes with venetoclax and the venetoclax/azacitidine combination in AML in a p53-independent manner.See related commentary by Savona and Rathmell, p. 831.This article is highlighted in the In This Issue feature, p. 813.	venetoclax	31-41	P53	Homo sapiens	97-100
31048321-11	2019	Targeting CLPB synergizes with venetoclax and the venetoclax/azacitidine combination in AML in a p53-independent manner.See related commentary by Savona and Rathmell, p. 831.This article is highlighted in the In This Issue feature, p. 813.	venetoclax	50-60	P53	Homo sapiens	97-100
31293428-11	2019	DT-010 restored Dox-mediated apoptosis and p53 induction in MCF-7/ADR cells.	DT-010	0-6	P53	Homo sapiens	43-46
30536898-3	2019	This is the first study to evaluate the in vivo efficacy of the intravenous idasanutlin prodrug, RO6839921 (RG7775), both alone and in combination with temozolomide in TP53 wt orthotopic neuroblastoma models.	RG7388	76-87	P53	Homo sapiens	168-172
30536898-4	2019	Detection of active idasanutlin using liquid chromatography-mass spectrometry and p53 pathway activation by ELISA assays and Western analysis showed peak plasma levels 1 h post-treatment with maximal p53 pathway activation 3-6 h post-treatment.	RG7388	20-31	P53	Homo sapiens	200-203
31466709-5	2019	RESULTS: Neoadjuvant propranolol decreased expression of the pro-proliferative Ki-67 and pro-survival Bcl-2 markers, and increased pro-apoptotic p53 expression in a patient with stage III breast cancer.	Propranolol	21-32	P53	Homo sapiens	145-148
31466709-7	2019	Furthermore, propranolol treatment of breast cancer cells increased p53 levels, enhanced caspase cleavage, and induced apoptosis.	Propranolol	13-24	P53	Homo sapiens	68-71
31128451-3	2019	One of the most remarkable among small molecules for the rescue of specific mutant p53, Y220C is PhiKan083 (1-(9-ethyl-9H-carbazole-3-yl)-N-methylmethanamine) that have been demonstrated effective in advanced pre-clinical trials.	1-(9-ethyl-9h-carbazole-3-yl)-n-methylmethanamine	108-157	P53	Homo sapiens	83-86
30367486-0	2019	Inhibition of the formation of autophagosome but not autolysosome augments ABT-751-induced apoptosis in TP53-deficient Hep-3B cells.	ABT751	75-82	P53	Homo sapiens	104-108
31002353-8	2019	When ovarian cells were treated with ginsenoside Rg3, cell apoptosis was observed to be promoted, while cell metastasis and invasion were inhibited at 48 h. The results of the present study revealed that in the promoter regions of p53, p16 and hMLH1, the methylation levels decreased, while the mRNA and protein levels significantly increased.	Ginsenosides	37-48	P53	Homo sapiens	231-234
31121972-0	2019	Synthesis, Biological Evaluation, and In Silico Studies of Novel Aminated Xanthones as Potential p53-Activating Agents.	Xanthones	74-83	P53	Homo sapiens	97-100
31121972-2	2019	The xanthone 5 was used as a starting point for the construction of a library of 3,4-dioxygenated xanthones bearing chemical moieties of described MDM2-p53 inhibitors.	Xanthones	98-107	P53	Homo sapiens	152-155
31121972-3	2019	Eleven aminated xanthones were successfully synthesized and initially screened for their ability to disrupt the MDM2-p53 interaction using a yeast cell-based assay.	Xanthones	16-25	P53	Homo sapiens	117-120
29523220-10	2019	Probenecid inhibits SLC2A9-mediated uric acid transport, which promotes cell proliferation, inhibits cell apoptosis, induces intracellular ROS, and decreases the expression of p53 in HCC cells.	Probenecid	0-10	P53	Homo sapiens	176-179
30834688-8	2019	This study establishes that GRA16 is a HAUSP inhibitor that targets the nuclear localization of PTEN and induces the anticancer effect in a p53-dependent manner.	gra16	28-33	P53	Homo sapiens	140-143
30993195-6	2019	Zinc metallochaperones (ZMCs) are a new class of anti-cancer drugs that specifically reactivate zinc-deficient mutant p53 by restoring zinc binding.	zmcs	24-28	P53	Homo sapiens	118-121
30780127-0	2019	Quinaldic acid induces changes in the expression of p53 tumor suppressor both on protein and gene level in colon cancer LS180 cells.	quinaldic acid	0-14	P53	Homo sapiens	52-55
30780127-9	2019	Concomitantly, the nuclear and cytoplasmic localization of phospho-p53 protein upon QA treatment is also presented.	quinaldic acid	84-86	P53	Homo sapiens	67-70
31015849-5	2019	Moreover, licochalcone A, alisol B, and hederagenin inhibited cell viability (p &lt; 0.05), induced cell apoptosis (p &lt; 0.01), reduced p-Akt levels, and increased cleaved-CASP3 (p &lt; 0.05) and p53 expression levels in HepG2 cells.	licochalcone A	10-24	P53	Homo sapiens	198-201
30899200-6	2019	However, apoptotic responses to trametinib and vemurafenib were greater in WM35 than WM35-R, evidenced by FACS analysis and caspase 3/7 activity, indicating that these MAPK inhibitors acted on the cells partially through p53-regulated pathways.	trametinib	32-42	P53	Homo sapiens	221-224
30899200-7	2019	SiRNA mediated p53 knockdown in WM35 replicated the same pattern of response to trametinib and vemurafenib as seen in WM35-R, confirming that p53 plays a role in trametinib and vemurafenib induced apoptosis.	trametinib	80-90	P53	Homo sapiens	15-18
30899200-7	2019	SiRNA mediated p53 knockdown in WM35 replicated the same pattern of response to trametinib and vemurafenib as seen in WM35-R, confirming that p53 plays a role in trametinib and vemurafenib induced apoptosis.	trametinib	80-90	P53	Homo sapiens	142-145
30899200-7	2019	SiRNA mediated p53 knockdown in WM35 replicated the same pattern of response to trametinib and vemurafenib as seen in WM35-R, confirming that p53 plays a role in trametinib and vemurafenib induced apoptosis.	trametinib	162-172	P53	Homo sapiens	15-18
30899200-7	2019	SiRNA mediated p53 knockdown in WM35 replicated the same pattern of response to trametinib and vemurafenib as seen in WM35-R, confirming that p53 plays a role in trametinib and vemurafenib induced apoptosis.	trametinib	162-172	P53	Homo sapiens	142-145
30578766-2	2019	Previously, we reported that suppression of ceramide glycosylation restored wild-type p53 protein and tumor suppressing function in cancer cells heterozygously carrying p53 R273H, a hot-spot missense mutation; however, the mechanisms underlying the control of mutant protein expression remain elusive.	Ceramides	44-52	P53	Homo sapiens	86-89
30578766-2	2019	Previously, we reported that suppression of ceramide glycosylation restored wild-type p53 protein and tumor suppressing function in cancer cells heterozygously carrying p53 R273H, a hot-spot missense mutation; however, the mechanisms underlying the control of mutant protein expression remain elusive.	Ceramides	44-52	P53	Homo sapiens	169-172
31459462-5	2019	Dialkyne 3 was successfully employed for "peptide stapling" of a p53-based diazido peptide, whereby two azides are bridged to give a product with a stabilized conformation.	diazido peptide	75-90	P53	Homo sapiens	65-68
30729133-8	2019	Levels of tumor suppressor proteins p53 and cav-1 were downregulated while those of the oncogenic protein as c-Myc were upregulated under high glucose and insulin supplementation in HBlEpC cotreated with pioglitazone and metformin.	Pioglitazone	204-216	P53	Homo sapiens	36-39
31468429-6	2019	Both PTEN and p53 activation were detected in a dose-dependent manner after taurine treatment in NPC cells.	Taurine	76-83	P53	Homo sapiens	14-17
30242876-5	2019	The apoptosis-related proteins p53, p21, Bax, and Bcl-2 in BGC-823 cells and mouse xenotransplant models treated with curcumin L6H4 were determined by Western blot analysis.	curcumin l6h4	118-131	P53	Homo sapiens	31-34
30242876-6	2019	Curcumin L6H4 can significantly inhibit the proliferation and induce the apoptosis of BGC-823 cells, thus enhancing the expression levels of p53, p21, Bax, and Bcl-2 noticeably in vivo and in vitro.	curcumin l6h4	0-13	P53	Homo sapiens	141-144
30535690-5	2019	Using these protocols, we recently detected a metabolic alteration that occurs during aging by the monitoring the lactate/pyruvate ratio in a long-lived mutant of the mammalian tumor suppressor p53 ortholog CEP-1 in C. elegans.	Pyruvic Acid	122-130	P53	Homo sapiens	194-197
30230059-4	2018	A series of compounds has been designed that contain iodinated phenols aimed for interaction and stabilization of the p53-Y220C surface cavity, and Zn-binding fragments for metallochaperone activity.	Phenols	63-70	P53	Homo sapiens	118-121
32123827-7	2019	The proteasome inhibitor MG132 stabilized p53(DeltaCp44), particularly in mock-infected cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	25-30	P53	Homo sapiens	42-45
30296375-6	2018	The synergistic effect between erlotinib-targeted therapy and photodynamic therapy significantly up-regulates cancer suppressor p53 and inhibits Survivin, which results in more apoptosis and cell cycle arrest.	Erlotinib Hydrochloride	31-40	P53	Homo sapiens	128-131
30080692-0	2018	VX-680 induces p53-mediated apoptosis in human cholangiocarcinoma cells.	VX680	0-6	P53	Homo sapiens	15-18
30080692-8	2018	We further found that pifithrin-alpha, a p53 inhibitor, attenuated the anticancer effects of VX-680 and downregulated the expression of apotosis-related proteins (Bax and caspase-9).	VX680	93-99	P53	Homo sapiens	41-44
30362332-2	2018	This studyexplored the cytotoxicity of (1,2-epoxy-3(3-(3,4-dimethoxyphenyl)-4H-1-benzopyran-4-on) propane (EPI) synthesizedfrom clove leaves oil on HeLa cells, its combination with doxorubicin (DOX) and cisplatin (CIS), and also their influenceon p53, TIMP-3, and miR-34a as therapeutic targets.	(1,2-epoxy-3(3-(3,4-dimethoxyphenyl)-4h-1-benzopyran-4-on) propane	39-105	P53	Homo sapiens	247-250
30057298-4	2018	However, the Az-triphenylphosphonium conjugate, Az-TPP-O3, localizes mainly to mitochondria of cancer cells where it inhibits the mortalin-p53 interaction and induces mitochondrial outer membrane permeabilization, consequently leading to mitochondria-mediated apoptosis.	az-triphenylphosphonium	13-36	P53	Homo sapiens	139-142
30057300-5	2018	Further experimental testing demonstrated that Michael acceptors, aldehydes, imines, and primary alcohols can promote thermodynamic stabilization of mutant p53.	Imines	77-83	P53	Homo sapiens	156-159
30057300-6	2018	Moreover, mild thiol reactivity, often coupled with combined chemical functional groups, such as in imines, aldehydes, and primary alcohols, can stimulate mutant p53 refolding.	Imines	100-106	P53	Homo sapiens	162-165
30533262-10	2018	However, RA treatment decreased the levels of p-ATM, p-p53, GADD45alpha, p21, MMP-3, -9, and -13 and increased the level of COL1A1 in a concentration-dependent manner.	Radium	9-11	P53	Homo sapiens	55-58
30115697-3	2018	Approximately 6% of Africans and 1% of African Americans express a p53 allele with a serine instead of proline at position 47 (Pro47Ser).	pro47ser	127-135	P53	Homo sapiens	67-70
29524123-4	2018	We confirmed that BCI significantly inhibited the viability of p53(-) NCI-H1299 cells as compared to NCI-H460 and A549 cells, which express wild-type p53.	2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one	18-21	P53	Homo sapiens	63-66
29524123-4	2018	We confirmed that BCI significantly inhibited the viability of p53(-) NCI-H1299 cells as compared to NCI-H460 and A549 cells, which express wild-type p53.	2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one	18-21	P53	Homo sapiens	150-153
30242200-1	2018	It has been reported that the ATM kinase inhibitor KU60019 preferentially radiosensitizes orthotopic high grade gliomas (HGG) driven by established U87 and U1242 cell lines bearing specific TP53 mutations.	2-(2,6-dimethylmorpholin-4-yl)-N-(5-(6-morpholin-4-yl-4-oxo-4H-pyran-2-yl)-9H-thioxanthen-2-yl)acetamide	51-58	P53	Homo sapiens	190-194
30249893-8	2018	Conclusions: Survivin may be implicated in the bcl-2 and p53 pathways and therefore in the biology of PDAC.	pdac	102-106	P53	Homo sapiens	57-60
30181808-5	2018	Plasmid pEGFP-TRAIL and pEGFP-p53 were selected and propagated in Escherichia coli grown in LB broth, in order to obtain the necessary amount.	lb broth	92-100	P53	Homo sapiens	30-33
29980405-5	2018	Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisplatin, irinotecan, oxaliplatin, and paclitaxel increased significantly.	gemcitabine	159-170	P53	Homo sapiens	28-32
30024623-2	2018	Previous researches have reported that propofol can inhibit extracellular signal-regulated kinase (ERK) 1/2 phosphorylation or activate p53-upregulated modulator of apoptosis (PUMA) signaling, resulting in apoptosis.	Propofol	39-47	P53	Homo sapiens	136-139
28537448-0	2018	Hesperetin induces an apoptosis-triggered extrinsic pathway and a p53- independent pathway in human lung cancer H522 cells.	hesperetin	0-10	P53	Homo sapiens	66-69
28537448-4	2018	This study shows that hesperetin induces apoptosis in H522 cells via a pathway independentof p53 and Bax but triggers the death-receptor Fas-initiated FADD/ caspase-8-dependent apoptotic pathway.	hesperetin	22-32	P53	Homo sapiens	93-96
29620279-0	2018	Impact of RUNX2 gene silencing on the gemcitabine sensitivity of p53-mutated pancreatic cancer MiaPaCa-2 spheres.	gemcitabine	38-49	P53	Homo sapiens	65-68
29620279-2	2018	In the present study, we have demonstrated that, similar to the conventional 2D monolayer culture systems which often lack in vivo physiological insights, RUNX2 gene silencing increases the gemcitabine (GEM) sensitivity of the 3D spheres generated from p53-mutated pancreatic cancer MiaPaCa-2 cells.	gemcitabine	190-201	P53	Homo sapiens	253-256
29620279-2	2018	In the present study, we have demonstrated that, similar to the conventional 2D monolayer culture systems which often lack in vivo physiological insights, RUNX2 gene silencing increases the gemcitabine (GEM) sensitivity of the 3D spheres generated from p53-mutated pancreatic cancer MiaPaCa-2 cells.	gemcitabine	203-206	P53	Homo sapiens	253-256
29735783-8	2018	CONCLUSION: We were able to demonstrate Wnt/ beta-catenin pathway modulation through E-cadherin up-regulation induced by 5aza-dC and TSA treatments, under an activation-pathway background, like CTNNB1 and TP53 mutations.	Decitabine	121-128	P53	Homo sapiens	205-209
29854627-8	2018	GSPE co-treatment with thalidomide and carboplatin reduced their brain and renal damage, oxidative stress, diminished cytokines, p53, neurotransmitters and biochemical parameters, and inhibited brain and renal cell apoptosis.	Carboplatin	39-50	P53	Homo sapiens	129-132
29409053-9	2018	Moreover, we observed a synergistic or additive effect of GDC-0575 together with gemcitabine in vitro and in vivo in TP53-proficient but not TP53-deficient sarcoma models.	gemcitabine	81-92	P53	Homo sapiens	117-121
29471073-7	2018	Our results indicate that the underlying mechanisms whereby etoposide and ellipticine regulate CYP1A1 expression must be different and may not be linked to p53 activation alone.	ellipticine	74-85	P53	Homo sapiens	156-159
29563788-0	2018	Inhibition of cell proliferation and migration through nucleobase-modified polyamidoamine-mediated p53 delivery.	Poly(amidoamine)	75-89	P53	Homo sapiens	99-102
29563788-1	2018	Introduction: The nucleobase 2-amino-6-chloropurine-modified polyamidoamine (AP-PAMAM) was used as a carrier for p53 gene delivery to achieve the antitumor effects.	Poly(amidoamine)	61-75	P53	Homo sapiens	113-116
29563788-6	2018	AP-PAMAM-mediated p53 delivery could achieve stronger antiproliferative effect than PAMAM/p53.	Poly(amidoamine)	3-8	P53	Homo sapiens	18-21
29563788-10	2018	Conclusion: The PAMAM derivative-mediated p53 delivery could be a promising strategy for achieving tumor gene therapy.	Poly(amidoamine)	16-21	P53	Homo sapiens	42-45
29466981-11	2018	Also, this pentasaccharide showed potentialities to up-regulate the expression of IKbalpha, P53 and TGF genes.	pentasaccharide	11-26	P53	Homo sapiens	92-95
29354595-3	2017	Aminoglycosides G418 (geneticin) and gentamicin have been shown to induce translational readthrough and expression of full-length p53.	Gentamicins	37-47	P53	Homo sapiens	130-133
29379285-4	2018	The formation of a single p53-COP1 bimolecular complex was visualized by atomic force microscopy imaging on a mica substrate.	mica	110-114	P53	Homo sapiens	26-29
30060809-8	2018	This complex relationship is based on several molecular mechanisms including the p53-dependent transcriptional regulation of enzymes in sphingolipid pathways, the activation of mutant p53 through ceramide-mediated alternative splicing, as well as modulation of the p53 function through direct and indirect effects on p53 coregulators and downstream targets.	Ceramides	196-204	P53	Homo sapiens	184-187
30060809-8	2018	This complex relationship is based on several molecular mechanisms including the p53-dependent transcriptional regulation of enzymes in sphingolipid pathways, the activation of mutant p53 through ceramide-mediated alternative splicing, as well as modulation of the p53 function through direct and indirect effects on p53 coregulators and downstream targets.	Ceramides	196-204	P53	Homo sapiens	184-187
30060809-8	2018	This complex relationship is based on several molecular mechanisms including the p53-dependent transcriptional regulation of enzymes in sphingolipid pathways, the activation of mutant p53 through ceramide-mediated alternative splicing, as well as modulation of the p53 function through direct and indirect effects on p53 coregulators and downstream targets.	Ceramides	196-204	P53	Homo sapiens	184-187
28749203-8	2018	R175H p53 expression was rescued by addition of proteasome inhibitor MG132 to CB002, suggesting a role for ubiquitin-mediated degradation of the mutant protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	69-74	P53	Homo sapiens	6-9
29877251-9	2018	Recently, increasing attention has been paid to a report, according to which, majority of the patients with TP53 mutations showed good response to a higher dose of decitabine.	Decitabine	164-174	P53	Homo sapiens	108-112
28804952-6	2017	In GBM 8401 cells, propofol induced G2/M phase cell arrest, which affected the CDK1, cyclin B1, p53, and p21 protein expression levels.	Propofol	19-27	P53	Homo sapiens	96-99
29250930-7	2017	In the relapsed or refractory setting, patients with del(17p) or TP53 aberrations should be offered treatment with a novel agent, such as ibrutinib, idelalisib-rituximab or venetoclax.	venetoclax	173-183	P53	Homo sapiens	65-69
28270077-0	2017	Combined Treatment with CCI779 and SB203580 Induces Cellular Senescence in Renal Cell Carcinoma Cell Line via p53 Pathway.	SB 203580	35-43	P53	Homo sapiens	110-113
28790110-0	2017	Replication Stress Leading to Apoptosis within the S-phase Contributes to Synergism between Vorinostat and AZD1775 in HNSCC Harboring High-Risk TP53 Mutation.	Vorinostat	92-102	P53	Homo sapiens	144-148
29416738-4	2018	p53-Reactivation and Induction of Massive Apoptosis-1 (PRIMA-1) and its methylated analogue PRIMA-1Met (also known as APR-246) are quinuclidine compounds that rescue the DNA-binding activity of mutant p53 (mut-p53) and restore the potential of wild-type p53.	Quinuclidines	131-143	P53	Homo sapiens	0-3
29416738-4	2018	p53-Reactivation and Induction of Massive Apoptosis-1 (PRIMA-1) and its methylated analogue PRIMA-1Met (also known as APR-246) are quinuclidine compounds that rescue the DNA-binding activity of mutant p53 (mut-p53) and restore the potential of wild-type p53.	Quinuclidines	131-143	P53	Homo sapiens	201-204
29416738-4	2018	p53-Reactivation and Induction of Massive Apoptosis-1 (PRIMA-1) and its methylated analogue PRIMA-1Met (also known as APR-246) are quinuclidine compounds that rescue the DNA-binding activity of mutant p53 (mut-p53) and restore the potential of wild-type p53.	Quinuclidines	131-143	P53	Homo sapiens	201-204
29416738-4	2018	p53-Reactivation and Induction of Massive Apoptosis-1 (PRIMA-1) and its methylated analogue PRIMA-1Met (also known as APR-246) are quinuclidine compounds that rescue the DNA-binding activity of mutant p53 (mut-p53) and restore the potential of wild-type p53.	Quinuclidines	131-143	P53	Homo sapiens	201-204
28927457-3	2017	Tetracyclines and macrolides via inhibiting p450 enzymes attenuate ATRA degradation, thereby increase p53.	Tetracyclines	0-13	P53	Homo sapiens	102-105
28841361-1	2017	p53R2 is a p53-inducible ribonucleotide reductase subunit involved in deoxyribonucleotide biosynthesis and DNA repair.	Deoxyribonucleotides	70-89	P53	Homo sapiens	0-3
28711224-7	2017	RESULTS: In vitro pTyr pre-treatment showed no radioprotection on Y79 cells, but led to p53 stabilisation in unirradiated Y79 cells and to a facilitation of radiation-induced p21 up-regulation, confirming a modulation of p53 activity by pTyr.	Phosphotyrosine	18-22	P53	Homo sapiens	88-91
28711224-7	2017	RESULTS: In vitro pTyr pre-treatment showed no radioprotection on Y79 cells, but led to p53 stabilisation in unirradiated Y79 cells and to a facilitation of radiation-induced p21 up-regulation, confirming a modulation of p53 activity by pTyr.	Phosphotyrosine	18-22	P53	Homo sapiens	221-224
28710496-5	2017	The target of pitavastatin, hydroxymethylglutarate coenzyme-A reductase (HMGCR), was found to be over-expressed in all ovarian cancer cell lines examined and upregulated by mutated TP53, a gene commonly altered in ovarian cancer.	pitavastatin	14-26	P53	Homo sapiens	181-185
28704484-0	2017	Apoptosis by [Pt(O,O"-acac)(gamma-acac)(DMS)] requires PKC-delta mediated p53 activation in malignant pleural mesothelioma.	gamma-acac)	28-39	P53	Homo sapiens	74-77
28671946-10	2017	Intriguingly, knockdown of mutant p53 or RUNX2 potentiated SAHA-induced up-regulation of TAp63.	Vorinostat	59-63	P53	Homo sapiens	34-37
28671946-12	2017	Collectively, our present observations strongly suggest that RUNX2/mutant p53/TAp63-regulatory axis is one of the key determinants of SAHA sensitivity of p53-mutated pancreatic cancer cells.	Vorinostat	134-138	P53	Homo sapiens	74-77
28671946-12	2017	Collectively, our present observations strongly suggest that RUNX2/mutant p53/TAp63-regulatory axis is one of the key determinants of SAHA sensitivity of p53-mutated pancreatic cancer cells.	Vorinostat	134-138	P53	Homo sapiens	154-157
28421382-0	2017	Relationship Between the Expression of O6-Methylguanine-DNA Methyltransferase (MGMT) and p53, and the Clinical Response in Metastatic Pancreatic Adenocarcinoma Treated with FOLFIRINOX.	folfirinox	173-183	P53	Homo sapiens	89-92
28421382-3	2017	OBJECTIVE: The aim of our study was to assess the prevalence of MGMT and p53 in patients with metastatic pancreatic adenocarcinoma treated with FOLFIRINOX as a first-line treatment and to investigate their association with therapeutic response and survival.	folfirinox	144-154	P53	Homo sapiens	73-76
29296763-1	2017	A man with cytopenias, dysplasia, excess blasts, P53 and RUNX1 mutations, and ring chromosome 7 recovered after stopping lenalidomide.	Lenalidomide	121-133	P53	Homo sapiens	49-52
28407181-11	2017	Moreover, lycopene could also upregulate the expression of p53 and Bax mRNAs in MCF-7 cells.	Lycopene	10-18	P53	Homo sapiens	59-62
28407181-12	2017	In conclusion, lycopene inhibits proliferation and facilitates apoptosis of MCF-7 cells in vitro, possibly by regulating the expression of p53 and Bax.	Lycopene	15-23	P53	Homo sapiens	139-142
28260016-6	2017	It was additionally revealed that treatment with 20(S)-ginsenoside Rg3 reduced global genomic DNA methylation, altered cystosine methylation of the promoter regions of P53, B cell lymphoma 2 and vascular endothelial growth factor, and downregulated the expression of DNA methyltransferase (DNMT) 3a and DNMT3b more than treatment with 20(R)-ginsenoside Rg3 in HepG2 cells.	Ginsenoside Rh2	49-66	P53	Homo sapiens	168-229
27993609-8	2017	The downregulation of p53 levels induced by CPF was partially blocked when cells were exposed to CPF in the presence of the proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	145-150	P53	Homo sapiens	22-25
28278226-0	2017	Correction: Phytometabolite Dehydroleucodine Induces Cell Cycle Arrest, Apoptosis, and DNA Damage in Human Astrocytoma Cells through p73/p53 Regulation.	dehydroleucodine	28-44	P53	Homo sapiens	137-140
27884971-6	2017	TP53 mutations were found in seven of nine patients who developed acute leukemia, and were documented to be present in the earliest sample (n=1) and acquired during lenalidomide treatment (n=6).	Lenalidomide	165-177	P53	Homo sapiens	0-4
28044473-0	2017	Synthesis, characterization, and in vitro evaluation of targeted gold nanoshelled poly(d,l-lactide-co-glycolide) nanoparticles carrying anti p53 antibody as a theranostic agent for ultrasound contrast imaging and photothermal therapy.	Polylactic Acid-Polyglycolic Acid Copolymer	82-112	P53	Homo sapiens	141-144
28228262-4	2017	Combination treatment with the AR signaling inhibitor enzalutamide (ENZ) and the Chk1/2 inhibitor AZD7762 demonstrates synergy with regard to inhibition of AR-CDC6-ATR-Chk1 signaling, ATM phosphorylation induction, and apoptosis in VCaP (mutant p53) and LNCaP-C4-2b (wild-type p53) cells.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	98-105	P53	Homo sapiens	245-248
28228262-4	2017	Combination treatment with the AR signaling inhibitor enzalutamide (ENZ) and the Chk1/2 inhibitor AZD7762 demonstrates synergy with regard to inhibition of AR-CDC6-ATR-Chk1 signaling, ATM phosphorylation induction, and apoptosis in VCaP (mutant p53) and LNCaP-C4-2b (wild-type p53) cells.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	98-105	P53	Homo sapiens	277-280
28035403-8	2017	After treatment with propofol for 12 h, the Nrf2 protein expression was increased, while the percentage of apoptotic cells, caspase-3 activity, and expression of p53 were significantly decreased.	Propofol	21-29	P53	Homo sapiens	162-165
28035403-10	2017	In conclusion, propofol increased the proliferation of human breast cancer MDA-MB-231 cells, which was at least partially associated with the inhibition of the expression of p53, and induced cell migration, which was involved in the activation of the Nrf2 pathway.	Propofol	15-23	P53	Homo sapiens	174-177
28103302-12	2017	Initial results from in vitro studies have shown the ability of the bioactive compounds of flavokawain B and alpinetin to target UCK2 enzyme specifically, inducing cell cycle arrest and subsequently leading to cancer cell death, possibly through interfering the MDM2-p53 signalling pathway.	flavokawain B	91-104	P53	Homo sapiens	267-270
28054709-5	2017	RA binds to the RING-finger region of MDM2 and stabilizes p53.	Radium	0-2	P53	Homo sapiens	58-61
29081884-6	2017	Further study suggests that overexpression of SIRT1 partly suppressed an NMDA-induced increase in p53 acetylation.	N-Methylaspartate	73-77	P53	Homo sapiens	98-101
29081884-7	2017	These results indicate that SIRT1 activation by either RSV or overexpression of SIRT1 can exert neuroprotective effects partly by inhibiting p53 acetylation in NMDA-induced neurotoxicity.	N-Methylaspartate	160-164	P53	Homo sapiens	141-144
27851896-0	2017	Corrigendum to "Low doses of arsenic, via perturbing p53, promotes tumorigenesis" [Toxicol.	Arsenic	29-36	P53	Homo sapiens	53-56
27998224-10	2016	Conclusion To our knowledge, this is the first report providing clinical proof that AZD1775 enhances carboplatin efficacy in TP53-mutated tumors.	Carboplatin	101-112	P53	Homo sapiens	125-129
27913471-7	2016	These recently approved drugs (ibrutinib, idelalisib, and venetoclax) are reporting excellent outcomes, including patients with high-risk disease such as 17p deletion (17p-) or TP53 mutations (TP53mut).	venetoclax	58-68	P53	Homo sapiens	177-181
27611480-11	2016	The proteasomal inhibitor MG-132 caused p53 protein to increase, but it had no effect on cyclin E2 protein levels.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-32	P53	Homo sapiens	40-43
27613187-8	2016	RESULTS: Our results clearly demonstrated that CDDP and VC treatment exhibited ameliorative effect on induction of cell death by p53 overexpression and generation of hydrogen peroxide in SiHa cells, thereby reducing the dosage of CDDP required to induce cell death in cancer cells.	Vinyl Chloride	56-58	P53	Homo sapiens	129-132
26756900-6	2016	Nutlin-3alpha or MG132 abolished the suppressive effect of a COX-2 inhibitor on DOX-induced p53 increase.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	P53	Homo sapiens	92-95
27907175-6	2016	We demonstrate that the interaction of p53 with intermolecular T.A.T triplex is comparable to the recognition of CTG-hairpin non-B DNA structure.	ctg	113-116	P53	Homo sapiens	39-42
27736841-5	2016	METHODS: Interactions of FAK-p53 or NF2-FAK were evaluated by phosphotyrosine-p53 immunoaffinity purification and tandem mass spectrometry, and p53, FAK, and NF2 immunoprecipitations.	Phosphotyrosine	62-77	P53	Homo sapiens	29-32
27736841-5	2016	METHODS: Interactions of FAK-p53 or NF2-FAK were evaluated by phosphotyrosine-p53 immunoaffinity purification and tandem mass spectrometry, and p53, FAK, and NF2 immunoprecipitations.	Phosphotyrosine	62-77	P53	Homo sapiens	78-81
27736841-5	2016	METHODS: Interactions of FAK-p53 or NF2-FAK were evaluated by phosphotyrosine-p53 immunoaffinity purification and tandem mass spectrometry, and p53, FAK, and NF2 immunoprecipitations.	Phosphotyrosine	62-77	P53	Homo sapiens	78-81
27122200-0	2016	Investigation of the Sequential Actions of Doxorubicin and p53 on Tumor Cell Growth Via Branched Polyethylenimine-beta-cyclodextrin Conjugates.	Polyethyleneimine	97-113	P53	Homo sapiens	59-62
27122200-2	2016	In this work, p53/BPEI-beta-CD/AD-dox complex was fabricated and employed to investigate the interaction manner between p53 and doxorubicin (Dox).	bpei	18-22	P53	Homo sapiens	14-17
27122200-2	2016	In this work, p53/BPEI-beta-CD/AD-dox complex was fabricated and employed to investigate the interaction manner between p53 and doxorubicin (Dox).	bpei	18-22	P53	Homo sapiens	120-123
27122200-3	2016	Briefly, branched polyethylenimine (BPEI) was conjugated with beta-cyclodextrin hydrate (beta-CD) to form BPEI-beta-CD backbone, and p53 plasmid was condensed by positively charged BPEI via electrostatic interaction, while Dox was first conjugated with adamantine (AD) and then assembled with BPEI-beta-CD backbone via the host-guest interaction.	Polyethyleneimine	18-34	P53	Homo sapiens	133-136
27122200-3	2016	Briefly, branched polyethylenimine (BPEI) was conjugated with beta-cyclodextrin hydrate (beta-CD) to form BPEI-beta-CD backbone, and p53 plasmid was condensed by positively charged BPEI via electrostatic interaction, while Dox was first conjugated with adamantine (AD) and then assembled with BPEI-beta-CD backbone via the host-guest interaction.	bpei	36-40	P53	Homo sapiens	133-136
27122200-5	2016	Moreover, p53/BPEI-beta-CD/AD-dox complex released Dox and enabled the expression of p53 gene in a sequential manner, and the released Dox and expressed p53 gene showed successive inhibition of the growth of HeLa cells in vitro.	bpei	14-18	P53	Homo sapiens	10-13
27122200-5	2016	Moreover, p53/BPEI-beta-CD/AD-dox complex released Dox and enabled the expression of p53 gene in a sequential manner, and the released Dox and expressed p53 gene showed successive inhibition of the growth of HeLa cells in vitro.	bpei	14-18	P53	Homo sapiens	85-88
27122200-5	2016	Moreover, p53/BPEI-beta-CD/AD-dox complex released Dox and enabled the expression of p53 gene in a sequential manner, and the released Dox and expressed p53 gene showed successive inhibition of the growth of HeLa cells in vitro.	bpei	14-18	P53	Homo sapiens	85-88
27713122-0	2016	Depletion of pro-oncogenic RUNX2 enhances gemcitabine (GEM) sensitivity of p53-mutated pancreatic cancer Panc-1 cells through the induction of pro-apoptotic TAp63.	gemcitabine	42-53	P53	Homo sapiens	75-78
27713122-0	2016	Depletion of pro-oncogenic RUNX2 enhances gemcitabine (GEM) sensitivity of p53-mutated pancreatic cancer Panc-1 cells through the induction of pro-apoptotic TAp63.	gemcitabine	55-58	P53	Homo sapiens	75-78
27713122-1	2016	Recently, we have described that siRNA-mediated silencing of runt-related transcription factor 2 (RUNX2) improves anti-cancer drug gemcitabine (GEM) sensitivity of p53-deficient human pancreatic cancer AsPC-1 cells through the augmentation of p53 family TAp63-dependent cell death pathway.	gemcitabine	131-142	P53	Homo sapiens	164-167
27713122-1	2016	Recently, we have described that siRNA-mediated silencing of runt-related transcription factor 2 (RUNX2) improves anti-cancer drug gemcitabine (GEM) sensitivity of p53-deficient human pancreatic cancer AsPC-1 cells through the augmentation of p53 family TAp63-dependent cell death pathway.	gemcitabine	144-147	P53	Homo sapiens	164-167
27713122-9	2016	Taken together, our current observations strongly suggest that depletion of RUNX2 enhances the cytotoxic effect of GEM on p53-mutated Panc-1 cells through the stimulation of TAp63-dependent cell death pathway even in the presence of a large amount of pro-oncogenic mutant p53, and might provide an attractive strategy to treat pancreatic cancer patients with p53 mutations.	gemcitabine	115-118	P53	Homo sapiens	122-125
27713122-9	2016	Taken together, our current observations strongly suggest that depletion of RUNX2 enhances the cytotoxic effect of GEM on p53-mutated Panc-1 cells through the stimulation of TAp63-dependent cell death pathway even in the presence of a large amount of pro-oncogenic mutant p53, and might provide an attractive strategy to treat pancreatic cancer patients with p53 mutations.	gemcitabine	115-118	P53	Homo sapiens	272-275
27713122-9	2016	Taken together, our current observations strongly suggest that depletion of RUNX2 enhances the cytotoxic effect of GEM on p53-mutated Panc-1 cells through the stimulation of TAp63-dependent cell death pathway even in the presence of a large amount of pro-oncogenic mutant p53, and might provide an attractive strategy to treat pancreatic cancer patients with p53 mutations.	gemcitabine	115-118	P53	Homo sapiens	272-275
27765925-7	2016	RA-GC status correlated with older age (P &lt; 0.001), differentiated histology (P = 0.001), intestinal or mixed type by Lauren classification (P &lt; 0.001), lymphovascular invasion (P = 0.026), and mutant-pattern of p53 (P &lt; 0.001).	Radium	0-2	P53	Homo sapiens	218-221
27789962-13	2016	Therefore, 18F-fludrodeoxyglucose PET/CT could be a new way of predicting p53 or ERCC1-related chemotherapy effect in NSCLC patients with more convenience.	18f-fludrodeoxyglucose	11-33	P53	Homo sapiens	74-77
27229883-6	2016	Furthermore, we showed that the inhibition of p38 mitogen-activated protein kinase (p38(MAPK))-dependent p53 promoter activity contributed to the protection of SH-SY5Y cells from apoptosis, which was validated by the use of SB203580 or p38beta dominant negative (DN) mutants.	SB 203580	224-232	P53	Homo sapiens	105-108
27517620-10	2016	Our results further indicate that restoration of p53 through inhibition of ceramide glycosylation might be an effective treatment approach for targeting cancers heterozygously harboring TP53 missense mutations.	Ceramides	75-83	P53	Homo sapiens	49-52
27517620-10	2016	Our results further indicate that restoration of p53 through inhibition of ceramide glycosylation might be an effective treatment approach for targeting cancers heterozygously harboring TP53 missense mutations.	Ceramides	75-83	P53	Homo sapiens	186-190
27257011-0	2016	Shikonin Induces Apoptotic Cell Death via Regulation of p53 and Nrf2 in AGS Human Stomach Carcinoma Cells.	shikonin	0-8	P53	Homo sapiens	56-59
25765771-6	2016	The inhibitory effect of RDP-p53 on SH-SY5Y and human glioma cells (U251) was evaluated by MTT assay.	monooxyethylene trimethylolpropane tristearate	91-94	P53	Homo sapiens	29-32
27133825-0	2016	Prevalence, clonal dynamics and clinical impact of TP53 mutations in patients with myelodysplastic syndrome with isolated deletion (5q) treated with lenalidomide: results from a prospective multicenter study of the german MDS study group (GMDS).	Lenalidomide	149-161	P53	Homo sapiens	51-55
27608947-1	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in converting nicotinamide to NAD(+), essential for a number of enzymes and regulatory proteins involved in a variety of cellular processes, including deacetylation enzyme SIRT1 which modulates several tumor suppressors such as p53 and FOXO.	Niacinamide	0-12	P53	Homo sapiens	314-317
27608947-1	2016	Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the first rate-limiting step in converting nicotinamide to NAD(+), essential for a number of enzymes and regulatory proteins involved in a variety of cellular processes, including deacetylation enzyme SIRT1 which modulates several tumor suppressors such as p53 and FOXO.	Niacinamide	100-112	P53	Homo sapiens	314-317
26586447-2	2016	Idasanutlin (RG7388) is a potent p53-MDM2 antagonist currently in clinical development for treatment of cancer.	RG7388	0-11	P53	Homo sapiens	33-36
26586447-2	2016	Idasanutlin (RG7388) is a potent p53-MDM2 antagonist currently in clinical development for treatment of cancer.	RG7388	13-19	P53	Homo sapiens	33-36
27462151-13	2016	Moreover, Se@PEI@siRNA exhibited enhanced cytotoxic effects on cancer cells and triggered intracellular reactive oxygen species, and the signaling pathways of p53 and AKT were activated to advance cell apoptosis.	se@pei	10-16	P53	Homo sapiens	159-162
27390612-6	2016	Using MTT assay, we demonstrated that M3-p53-R12 inhibited the growth of K562, Jurkat as well as HL-60 leukemia cells carrying mutant p53 genes.	monooxyethylene trimethylolpropane tristearate	6-9	P53	Homo sapiens	41-44
27281222-4	2016	Here we show--using proteomics, transcriptomics and network analyses--that in human LSCs, aberrantly expressed proteins, in both imatinib-responder and non-responder patients, are modulated in concert with p53 (also known as TP53) and c-MYC regulation.	Imatinib Mesylate	129-137	P53	Homo sapiens	206-209
27281222-4	2016	Here we show--using proteomics, transcriptomics and network analyses--that in human LSCs, aberrantly expressed proteins, in both imatinib-responder and non-responder patients, are modulated in concert with p53 (also known as TP53) and c-MYC regulation.	Imatinib Mesylate	129-137	P53	Homo sapiens	225-229
27294865-0	2016	Improvement of gemcitabine sensitivity of p53-mutated pancreatic cancer MiaPaCa-2 cells by RUNX2 depletion-mediated augmentation of TAp73-dependent cell death.	gemcitabine	15-26	P53	Homo sapiens	42-45
32263321-4	2016	In this system, Doxorubicin-loaded aptamer duplex and plasmid DNA (p53) can be bound by PEI by electronic interactions to form stable complexes which effectively protect the aptamer and p53 from DNase degradation.	Polyethyleneimine	88-91	P53	Homo sapiens	67-70
32263321-4	2016	In this system, Doxorubicin-loaded aptamer duplex and plasmid DNA (p53) can be bound by PEI by electronic interactions to form stable complexes which effectively protect the aptamer and p53 from DNase degradation.	Polyethyleneimine	88-91	P53	Homo sapiens	186-189
32263321-8	2016	RT-PCR and Western blot analysis confirmed that p53 could be effectively delivered and expressed in HeLa cells by PEI/ARAD/p53 complexes.	Polyethyleneimine	114-117	P53	Homo sapiens	48-51
32263321-9	2016	Moreover, the apoptosis percentage of HeLa cells treated with PEI/ARAD/Dox/p53 complex increased to 40.8%, compared to 24.7% for PEI/ARAD/Dox complex and 11.5% for PEI/ARAD/p53, respectively.	Polyethyleneimine	62-65	P53	Homo sapiens	75-78
32263321-9	2016	Moreover, the apoptosis percentage of HeLa cells treated with PEI/ARAD/Dox/p53 complex increased to 40.8%, compared to 24.7% for PEI/ARAD/Dox complex and 11.5% for PEI/ARAD/p53, respectively.	Polyethyleneimine	62-65	P53	Homo sapiens	173-176
32263321-9	2016	Moreover, the apoptosis percentage of HeLa cells treated with PEI/ARAD/Dox/p53 complex increased to 40.8%, compared to 24.7% for PEI/ARAD/Dox complex and 11.5% for PEI/ARAD/p53, respectively.	Polyethyleneimine	129-132	P53	Homo sapiens	75-78
32263321-9	2016	Moreover, the apoptosis percentage of HeLa cells treated with PEI/ARAD/Dox/p53 complex increased to 40.8%, compared to 24.7% for PEI/ARAD/Dox complex and 11.5% for PEI/ARAD/p53, respectively.	Polyethyleneimine	129-132	P53	Homo sapiens	75-78
27383327-0	2016	Vitamin E promotes breast cancer cell proliferation by reducing ROS production and p53 expression.	Vitamin E	0-9	P53	Homo sapiens	83-86
27383327-10	2016	CONCLUSIONS: Vitamin E accelerated breast cancer growth by reducing ROS production and p53 expression.	Vitamin E	13-22	P53	Homo sapiens	87-90
27144436-7	2016	Both NR4A1 knockdown and treatment with DIM-C-pPhOH and DIM-C-pPhCO2Me also induced ROS which activated stress genes and induced sestrin 2 which activated AMPK and inhibited mTOR in the mutant p53 RMS cells.	1,1-bis(3'-indolyl)-1-(4-hydroxyphenyl)methane	40-51	P53	Homo sapiens	193-196
26067140-1	2016	The AT-rich interactive domain 1A (ARID1A) gene encodes a member of the switch/sucrose nonfermentable (SWI-SNF) chromatin remodeling complex, and is considered to work as a tumor suppressor in concert with p53.	Sucrose	79-86	P53	Homo sapiens	206-209
26210997-7	2016	The activity of SA-beta-galactosidase and the expression of senescence proteins p53 and p16 were reduced in RG108-treated ALS-MSCs.	RG108	108-113	P53	Homo sapiens	80-83
26839308-5	2016	Our results showed that SAHA and cisplatin compromise distinct DNA damage repair pathways, and treatment with SAHA enhanced synergistic radiosensitization effects of cisplatin in established NSCLC cell lines in a p53-independent manner, and decreased the DNA damage repair capability in cisplatin-treated primary NSCLC tumor tissues in response to IR.	Vorinostat	110-114	P53	Homo sapiens	213-216
27069137-7	2016	Degradation of p53 protein by silencing PANDA was prevented by treatment of MG132, a proteasome inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-81	P53	Homo sapiens	15-18
26851285-4	2016	We found that histone deacetylase (HDAC) inhibitors, including butyrate, augment Lys-120 acetylation of p53 and thus Apaf-1 expression by inhibiting HDAC1.	Butyrates	63-71	P53	Homo sapiens	104-107
26851285-5	2016	In p53-null cells, transfection of wild-type but not K120R mutant p53 can restore the p53-dependent sensitivity to butyrate.	Butyrates	115-123	P53	Homo sapiens	3-6
26851285-5	2016	In p53-null cells, transfection of wild-type but not K120R mutant p53 can restore the p53-dependent sensitivity to butyrate.	Butyrates	115-123	P53	Homo sapiens	66-69
26851285-5	2016	In p53-null cells, transfection of wild-type but not K120R mutant p53 can restore the p53-dependent sensitivity to butyrate.	Butyrates	115-123	P53	Homo sapiens	66-69
25409339-4	2016	Simultaneous treatment of donor cells with TSA (50nM) and 5azadC (7.5nM) resulted in higher in vitro development to the blastocyst stage, reduction of the apoptotic index and the global level of H3K27 me3 and altered expression levels of HDAC1, P53, CASPASE3, CASPASE9 and DNMT3a in cloned blastocysts.	Decitabine	58-64	P53	Homo sapiens	245-248
26986569-13	2016	In the same cells, the amide also increased the acetylation of lysine (K382) in p53, but not (K305).	C12H10N6O3S	71-75	P53	Homo sapiens	80-83
26775629-6	2016	The role of p53 in IMQ-induced apoptosis and autophagy was assessed by genetically silencing p53 and evaluated by a DNA content assay, immunoblotting, LC3 puncta detection and acridine orange staining.	Imiquimod	19-22	P53	Homo sapiens	12-15
26775629-6	2016	The role of p53 in IMQ-induced apoptosis and autophagy was assessed by genetically silencing p53 and evaluated by a DNA content assay, immunoblotting, LC3 puncta detection and acridine orange staining.	Imiquimod	19-22	P53	Homo sapiens	93-96
26775629-7	2016	RESULTS: IMQ induced p53 mRNA expression and protein accumulation, increased Ser15 phosphorylation, promoted nuclear translocation and up-regulated its target genes in skin cancer cells in a TLR7/8-independent manner.	Imiquimod	9-12	P53	Homo sapiens	21-24
26775629-8	2016	In BCC/KMC1 cells, the induction of p53 by IMQ was achieved through increased ROS production to stimulate the ATM/ATR-Chk1/Chk2 axis but was not mediated by inducing DNA damage.	Imiquimod	43-46	P53	Homo sapiens	36-39
26775629-9	2016	The pharmacological inhibition of ATM/ATR significantly suppressed IMQ-induced p53 activation and apoptosis.	Imiquimod	67-70	P53	Homo sapiens	79-82
26775629-10	2016	Silencing of p53 significantly decreased the IMQ-induced caspase cascade activation and apoptosis but enhanced autophagy.	Imiquimod	45-48	P53	Homo sapiens	13-16
26775629-11	2016	Mutant p53 skin cancer cell lines were more resistant to IMQ-induced apoptosis than wildtype p53 skin cancer cell lines.	Imiquimod	57-60	P53	Homo sapiens	7-10
26816656-0	2016	Polyethyleneimine-modified calcium carbonate nanoparticles for p53 gene delivery.	Polyethyleneimine	0-17	P53	Homo sapiens	63-66
26816656-4	2016	After modified with polyethyleneimine (PEI), the ability of PEI-CaCO3 nanoparticles to carry GFP-marked p53 gene (pEGFP-C1-p53) into cancer cells to express P53 protein were studied.	Polyethyleneimine	20-37	P53	Homo sapiens	104-107
26816656-4	2016	After modified with polyethyleneimine (PEI), the ability of PEI-CaCO3 nanoparticles to carry GFP-marked p53 gene (pEGFP-C1-p53) into cancer cells to express P53 protein were studied.	Polyethyleneimine	60-63	P53	Homo sapiens	104-107
26816656-4	2016	After modified with polyethyleneimine (PEI), the ability of PEI-CaCO3 nanoparticles to carry GFP-marked p53 gene (pEGFP-C1-p53) into cancer cells to express P53 protein were studied.	Polyethyleneimine	60-63	P53	Homo sapiens	123-126
26816656-4	2016	After modified with polyethyleneimine (PEI), the ability of PEI-CaCO3 nanoparticles to carry GFP-marked p53 gene (pEGFP-C1-p53) into cancer cells to express P53 protein were studied.	Polyethyleneimine	60-63	P53	Homo sapiens	157-160
26890145-4	2016	Notably, Cu-I significantly decreases intracellular GSH/GSSG ratio by inhibiting NRF2 pathway to break cellular redox homeostasis, and subsequently induces the expression of GADD45alpha in a p53-independent manner, and activates JNK/p38 MAPK signaling.	cucurbitacin I	9-13	P53	Homo sapiens	191-194
26676515-4	2016	The present study demonstrated that butein-induced apoptosis was mediated by p53.	butein	36-42	P53	Homo sapiens	77-80
26676515-5	2016	KBM5 chronic myeloid leukemia (CML) cells expressing wild-type p53 were more sensitive to butein compared with p53-null K562 CML cells in terms of apoptotic cell death.	butein	90-96	P53	Homo sapiens	63-66
26676515-8	2016	Therefore, the present study suggested that p53 causes the butein-mediated apoptosis of leukemic cells.	butein	59-65	P53	Homo sapiens	44-47
26400731-8	2016	At the same time, phosphotyrosine at the focal adhesion sites detected by immunofluorescence assay obviously increased in Hela cells incubated with 2.0 mM FA for 2 h. The results suggested that paxillin and p53 genes expression may be involved in FA-related adverse effects and the mechanism may be involved in paxillin-tyrosine phosphorylation.	Phosphotyrosine	18-33	P53	Homo sapiens	207-210
25867061-0	2016	MiRNA-621 sensitizes breast cancer to chemotherapy by suppressing FBXO11 and enhancing p53 activity.	mirna-621	0-9	P53	Homo sapiens	87-90
26985323-0	2016	Discovery of Novel 3,3-Disubstituted Piperidines as Orally Bioavailable, Potent, and Efficacious HDM2-p53 Inhibitors.	3,3-disubstituted piperidines	19-48	P53	Homo sapiens	102-105
26238069-0	2016	TP53 mutations are associated with higher rates of pathologic complete response to anthracycline/cyclophosphamide-based neoadjuvant chemotherapy in operable primary breast cancer.	Cyclophosphamide	97-113	P53	Homo sapiens	0-4
26238069-7	2016	Our results suggested that patients with TP53 mutations are more likely to respond to anthracycline/ cyclophosphamide-based neoadjuvant chemotherapy and have a favorable survival.	Cyclophosphamide	101-117	P53	Homo sapiens	41-45
26440706-2	2016	Our recent animal studies showed that low dose arsenic (LDA)-induced transient p53 inhibition selectively protected normal tissues from chemotherapy-induced toxicity.	Arsenic	47-54	P53	Homo sapiens	79-82
26774139-8	2016	In addition, chidamide alone or in combination with 5-Fu increased the p53, phosphorylated-p53 (p-p53), p21 and gammaH2AX levels, but suppressed cyclin dependent kinase 4 (CDK4) expression in tumor cells.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	13-22	P53	Homo sapiens	71-74
26774139-8	2016	In addition, chidamide alone or in combination with 5-Fu increased the p53, phosphorylated-p53 (p-p53), p21 and gammaH2AX levels, but suppressed cyclin dependent kinase 4 (CDK4) expression in tumor cells.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	13-22	P53	Homo sapiens	91-94
26774139-8	2016	In addition, chidamide alone or in combination with 5-Fu increased the p53, phosphorylated-p53 (p-p53), p21 and gammaH2AX levels, but suppressed cyclin dependent kinase 4 (CDK4) expression in tumor cells.	N-(2-amino-5-fluorobenzyl)-4-(N-(pyridine-3-acrylyl)aminomethyl)benzamide	13-22	P53	Homo sapiens	91-94
26497680-5	2015	The MTT assay indicated that an increase in Nrf2 expression by mutant p53 is responsible for cisplatin resistance.	monooxyethylene trimethylolpropane tristearate	4-7	P53	Homo sapiens	70-73
25791792-0	2015	Prognostic Relevance of p53 Overexpression in Gastrointestinal Stromal Tumors of the Small Intestine: Potential Implication for Adjuvant Treatment with Imatinib.	Imatinib Mesylate	152-160	P53	Homo sapiens	24-27
26330291-7	2015	We found that FK866 induced cell senescence and diminished cellular NAD(+) levels and SIRT1 activity (detected by acetylation of p53), and these effects were dramatically antagonized by co-treatment with nicotinic acid, nicotinamide, or NAD(+).	Niacinamide	220-232	P53	Homo sapiens	129-132
26350565-0	2015	The cholesterol metabolite 27-hydroxycholesterol regulates p53 activity and increases cell proliferation via MDM2 in breast cancer cells.	27-hydroxycholesterol	27-48	P53	Homo sapiens	59-62
26350565-9	2015	Furthermore, 27-OHC-induced proliferation was attenuated using either the p53 activator Tenovin-1 or the MDM2 inhibitor Nutlin-3 and Mdm2 siRNA.	27-hydroxycholesterol	13-19	P53	Homo sapiens	74-77
26446704-6	2015	Additionally, a ceramide signal was needed for PKR activation to be triggered by glucolipotoxicity and TNFalpha stimulation, and stabilization of P53 required endogenous ceramide accumulation.	Ceramides	170-178	P53	Homo sapiens	146-149
26446704-7	2015	Glucolipotoxicity and pro-inflammatory cytokines therefore promote the sumoylation-dependent stability of P53 via the ceramide/PKR/Ubc9 signalling pathway that is involved in pancreatic beta-cell proliferation inhibition in the development of type 2 diabetes.	Ceramides	118-126	P53	Homo sapiens	106-109
27122327-0	2015	[Changes in mRNA expression of p53 and related downstream genes in peripheral blood lymphocytes in workers occupationally exposed to arsenic].	Arsenic	133-140	P53	Homo sapiens	31-34
27122327-1	2015	OBJECTIVE: To investigate the changes in mRNA expression of p53 and related downstream genes in peripheral blood lymphocytes in workers occupationally exposed to arsenic as well as its influencing factors, and to analyze the mechanism of genetic toxicity of arsenic.	Arsenic	162-169	P53	Homo sapiens	60-63
27122327-1	2015	OBJECTIVE: To investigate the changes in mRNA expression of p53 and related downstream genes in peripheral blood lymphocytes in workers occupationally exposed to arsenic as well as its influencing factors, and to analyze the mechanism of genetic toxicity of arsenic.	Arsenic	258-265	P53	Homo sapiens	60-63
27122327-6	2015	CONCLUSION: The changes in mRNA expression of p53 and related downstream genes are closely related to the metabolic transformation of inorganic arsenic in workers occupationally exposed to arsenic, and it also plays an important role in genetic toxicity and carcinogenic effect in people exposed to arsenic.	Arsenic	144-151	P53	Homo sapiens	46-49
27122327-6	2015	CONCLUSION: The changes in mRNA expression of p53 and related downstream genes are closely related to the metabolic transformation of inorganic arsenic in workers occupationally exposed to arsenic, and it also plays an important role in genetic toxicity and carcinogenic effect in people exposed to arsenic.	Arsenic	189-196	P53	Homo sapiens	46-49
27122327-6	2015	CONCLUSION: The changes in mRNA expression of p53 and related downstream genes are closely related to the metabolic transformation of inorganic arsenic in workers occupationally exposed to arsenic, and it also plays an important role in genetic toxicity and carcinogenic effect in people exposed to arsenic.	Arsenic	189-196	P53	Homo sapiens	46-49
26606261-0	2015	MicroRNA Profiling Implies New Markers of Gemcitabine Chemoresistance in Mutant p53 Pancreatic Ductal Adenocarcinoma.	gemcitabine	42-53	P53	Homo sapiens	80-83
26606261-4	2015	METHODS: Gemcitabine-resistant variants of two mutant p53 human PDAC cell lines were established.	gemcitabine	9-20	P53	Homo sapiens	54-57
26606261-12	2015	CONCLUSION: Consistent miR expression profiles, in part regulated by mutant TP53 gene, were identified in gemcitabine-resistant PDAC with significant MRP-1 and Bcl-2 overexpression.	gemcitabine	106-117	P53	Homo sapiens	76-80
26571493-6	2015	When ST is administered before or concomitantly with vorinostat there is activation of STAT3, MAPK and the p53 pathway.	Vorinostat	53-63	P53	Homo sapiens	107-110
26363031-7	2015	When p53 and Rb were turned down, the FF-exposed secretory cells overcame apoptosis and expanded the population carrying ROS and DSB.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	129-132	P53	Homo sapiens	5-8
26322477-0	2015	Induction of apoptosis in cancer cells through N-acetyl-l-leucine-modified polyethylenimine-mediated p53 gene delivery.	Polyethyleneimine	75-91	P53	Homo sapiens	101-104
26322477-1	2015	Herein, N-acetyl-L-leucine-modified polyethylenimine was successfully constructed through the EDC/NHS-mediated coupling reaction and employed as vectors to accomplish p53 gene delivery using HeLa (p53wt) and PC-3 cells (p53null) as models.	Polyethyleneimine	36-52	P53	Homo sapiens	167-170
26322477-4	2015	Flow cytometric analysis showed that the derivative-mediated p53 delivery could induce stronger early apoptosis than PEI25K and Lipofectamine(2000).	Lipofectamine	128-141	P53	Homo sapiens	61-64
26606645-5	2015	Several evidences have shown that mitochondrial disruption, caspase activation, MAPK signaling and p53 are the pathways for arsenic induced apoptosis.	Arsenic	124-131	P53	Homo sapiens	99-102
26365581-7	2015	Comparable cytotoxicity was observed towards p53 negative MCF-7 cells, implying that CSA is effective independent of the p53 status.	3-hydroxy-4-prenyl-5-methoxystilbene-2-carboxylic acid	85-88	P53	Homo sapiens	45-48
26365581-12	2015	CSA affected pathways related to p53, cancer and cell proliferation.	3-hydroxy-4-prenyl-5-methoxystilbene-2-carboxylic acid	0-3	P53	Homo sapiens	33-36
26722257-11	2015	Intra-arterial chemotherapy with 5-fluorourcil and carboplatin potentially exerts a therapeutic effect by reducing the expression of mutant p53.	5-fluorourcil	33-46	P53	Homo sapiens	140-143
26722257-11	2015	Intra-arterial chemotherapy with 5-fluorourcil and carboplatin potentially exerts a therapeutic effect by reducing the expression of mutant p53.	Carboplatin	51-62	P53	Homo sapiens	140-143
26091798-7	2015	The results show that short-term exposure of BEAS-2B cells to arsenic or Cr(VI) was able to activate both p53 and p21.	Arsenic	62-69	P53	Homo sapiens	106-109
26091798-9	2015	In arsenic-transformed BEAS-2B cells reductions in p53 promoter activity, mRNA expression, and phosphorylation of p53 at Ser392 were observed, while the total p53 protein level remained the same compared to those in passage-matched parent ones.	Arsenic	3-10	P53	Homo sapiens	51-54
26091798-9	2015	In arsenic-transformed BEAS-2B cells reductions in p53 promoter activity, mRNA expression, and phosphorylation of p53 at Ser392 were observed, while the total p53 protein level remained the same compared to those in passage-matched parent ones.	Arsenic	3-10	P53	Homo sapiens	114-117
26091798-9	2015	In arsenic-transformed BEAS-2B cells reductions in p53 promoter activity, mRNA expression, and phosphorylation of p53 at Ser392 were observed, while the total p53 protein level remained the same compared to those in passage-matched parent ones.	Arsenic	3-10	P53	Homo sapiens	114-117
26091798-13	2015	These results demonstrate that p53 is able to respond to exposure of arsenic or Cr(VI), suggesting that BEAS-2B cells are an appropriate in vitro model to investigate arsenic or Cr(VI) induced lung cancer.	Arsenic	69-76	P53	Homo sapiens	31-34
26091798-13	2015	These results demonstrate that p53 is able to respond to exposure of arsenic or Cr(VI), suggesting that BEAS-2B cells are an appropriate in vitro model to investigate arsenic or Cr(VI) induced lung cancer.	Arsenic	167-174	P53	Homo sapiens	31-34
25755006-9	2015	Increased expression of p53 with concomitant decrease in expression of the p53 inhibitor Mdm2 further supported that artemisinin-induced apoptosis was p53-dependent.	artemisinin	117-128	P53	Homo sapiens	24-27
25755006-9	2015	Increased expression of p53 with concomitant decrease in expression of the p53 inhibitor Mdm2 further supported that artemisinin-induced apoptosis was p53-dependent.	artemisinin	117-128	P53	Homo sapiens	75-78
25755006-9	2015	Increased expression of p53 with concomitant decrease in expression of the p53 inhibitor Mdm2 further supported that artemisinin-induced apoptosis was p53-dependent.	artemisinin	117-128	P53	Homo sapiens	75-78
24665044-9	2015	A significantly higher number of senescent cells, over-expression of p53 and p21 were observed in the As-exposed individuals when compared to unexposed.	Arsenic	102-104	P53	Homo sapiens	69-72
26014912-0	2015	The collective nuclear migration of p53 and phosphorylated S473 of Akt during ellipticine-mediated apoptosis in human lung epithelial cancer cells.	ellipticine	78-89	P53	Homo sapiens	36-39
26014912-4	2015	In addition, ellipticine induced cytotoxicity in p53-null H1299 cells with stable expression of ectopic p53.	ellipticine	13-24	P53	Homo sapiens	49-52
26014912-4	2015	In addition, ellipticine induced cytotoxicity in p53-null H1299 cells with stable expression of ectopic p53.	ellipticine	13-24	P53	Homo sapiens	104-107
26014912-5	2015	In this work, we further demonstrated that dominant-negative Akt (S473A) or p53 shRNA inhibited ellipticine-mediated translocalization of p53 and Akt and attenuated apoptotic cell death in A549 cells.	ellipticine	96-107	P53	Homo sapiens	76-79
26014912-5	2015	In this work, we further demonstrated that dominant-negative Akt (S473A) or p53 shRNA inhibited ellipticine-mediated translocalization of p53 and Akt and attenuated apoptotic cell death in A549 cells.	ellipticine	96-107	P53	Homo sapiens	138-141
26014912-6	2015	The presence of p53 predates ellipticine-mediated apoptotic cell death, assists in nucleus translocation of phosphorylated Akt and activation of autophagy pathway.	ellipticine	29-40	P53	Homo sapiens	16-19
26148435-0	2015	Arsenic-induced S phase cell cycle lengthening is associated with ROS generation, p53 signaling and CDC25A expression.	Arsenic	0-7	P53	Homo sapiens	82-85
26148435-1	2015	Cellular response to arsenic is strongly dependent on p53 functional status.	Arsenic	21-28	P53	Homo sapiens	54-57
26148435-2	2015	Primarily arresting the cell cycle in G1 or G2/M phases, arsenic treatment also induces an increase in the S-phase time in wild-type p53 cells.	Arsenic	57-64	P53	Homo sapiens	133-136
26148435-3	2015	In contrast, cells with a non-functional p53 display only a subtle increase in the S phase, indicating arsenic differentially affects the cell cycle depending on p53 status.	Arsenic	103-110	P53	Homo sapiens	41-44
26148435-3	2015	In contrast, cells with a non-functional p53 display only a subtle increase in the S phase, indicating arsenic differentially affects the cell cycle depending on p53 status.	Arsenic	103-110	P53	Homo sapiens	162-165
26148435-4	2015	Importantly, it has been reported that arsenic induces reactive oxygen species (ROS), a process counteracted by p53.	Arsenic	39-46	P53	Homo sapiens	112-115
26148435-5	2015	To evaluate the participation of p53 in the lengthening of the S phase and the connection between the transient cell cycle arrest and oxidative stress, we evaluated the cell response to arsenic in MCF-7 and H1299 cells, and analyzed p53"s role as a transcription factor in regulating genes involved in ROS reduction and S phase transition.	Arsenic	186-193	P53	Homo sapiens	33-36
26148435-6	2015	Herein, we discovered that arsenic induced an increase in the population of S phase cells that was dependent on the presence and transcriptional activity of p53.	Arsenic	27-34	P53	Homo sapiens	157-160
26148435-7	2015	Furthermore, for the first time, we demonstrate that arsenic activates p53-dependent transcription of ROS detoxification genes, such as SESN1, and by an indirect mechanism involving ATF3, genes that could be responsible for the S phase cell cycle arrest, such as CDC25A.	Arsenic	53-60	P53	Homo sapiens	71-74
26230955-2	2015	In this study, TP53 mutations were identified in 7% of 500 patients with de novo AML and 58.8% of patients with CK.	cyanogen chloride	112-114	P53	Homo sapiens	15-19
26288684-0	2015	Discovery of Novel Isatin-Based p53 Inducers.	Isatin	19-25	P53	Homo sapiens	32-35
25697053-7	2015	Our data provide evidence that 7-ketocholesterol and 5,6-secosterol are efficient instigators of apoptosis, which for 5,6-secosterol is associated to PKC and p53 up-regulation.	7-ketocholesterol	31-48	P53	Homo sapiens	158-161
25533804-5	2015	Genomic studies of ALCL-11 showed the TP53 loss and the in vivo subclonal expansion of lymphoma cells, lacking PRDM1/Blimp1 and carrying c-MYC gene amplification.	alcl-11	19-26	P53	Homo sapiens	38-42
25669829-0	2015	Phase I study of pazopanib and vorinostat: a therapeutic approach for inhibiting mutant p53-mediated angiogenesis and facilitating mutant p53 degradation.	Vorinostat	31-41	P53	Homo sapiens	88-91
25669829-0	2015	Phase I study of pazopanib and vorinostat: a therapeutic approach for inhibiting mutant p53-mediated angiogenesis and facilitating mutant p53 degradation.	Vorinostat	31-41	P53	Homo sapiens	138-141
26222594-2	2015	The obtained xPolyR8-KLA(TPP) could not only initiate tumor cell apoptosis by C-KLA(TPP) with improved cell penetrating ability, but was also capable of loading and delivering the tumor cell suppressing p53 gene.	c-kla	78-83	P53	Homo sapiens	203-206
26222594-3	2015	It was found that, after internalization by cancer cells, the xPolyR8-KLA(TPP)/p53 complex released the C-KLA(TPP) moiety and the p53 gene in the cytoplasm due to its reducible disulfide bonds.	c-kla	104-109	P53	Homo sapiens	79-82
26222594-3	2015	It was found that, after internalization by cancer cells, the xPolyR8-KLA(TPP)/p53 complex released the C-KLA(TPP) moiety and the p53 gene in the cytoplasm due to its reducible disulfide bonds.	c-kla	104-109	P53	Homo sapiens	130-133
25829127-0	2015	N-Isopropylacrylamide-modified polyethylenimine-mediated p53 gene delivery to prevent the proliferation of cancer cells.	Polyethyleneimine	31-47	P53	Homo sapiens	57-60
25829127-1	2015	In this paper, N-isopropylacrylamide-modified polyethylenimine (PEN) was constructed through Michael addition and employed as a carrier to achieve the p53 gene delivery, using HeLa (p53wt) and PC-3 cells (p53null) as models.	Polyethyleneimine	64-67	P53	Homo sapiens	151-154
25829127-1	2015	In this paper, N-isopropylacrylamide-modified polyethylenimine (PEN) was constructed through Michael addition and employed as a carrier to achieve the p53 gene delivery, using HeLa (p53wt) and PC-3 cells (p53null) as models.	Polyethyleneimine	64-67	P53	Homo sapiens	182-185
25829127-2	2015	After PEN-mediated p53 transfection, expression level of p53 in HeLa and PC3 cells was up-regulated at both mRNA and protein levels.	Polyethyleneimine	6-9	P53	Homo sapiens	19-22
25829127-2	2015	After PEN-mediated p53 transfection, expression level of p53 in HeLa and PC3 cells was up-regulated at both mRNA and protein levels.	Polyethyleneimine	6-9	P53	Homo sapiens	57-60
25829127-3	2015	Due to the exogenous p53 expression, the inhibition of cell proliferation was observed through MTT analysis, attributing to the activation of apoptosis and cell cycle arrest.	monooxyethylene trimethylolpropane tristearate	95-98	P53	Homo sapiens	21-24
25829127-4	2015	Using flow cytometric analysis, early apoptotic ratios of 54.95% and 27.06% after PEN-mediated p53 transfection were detected in PC-3 and HeLa cells, respectively, indicating that PC-3 cells were more sensitive to the exogenous p53 transfection than HeLa cells.	Polyethyleneimine	82-85	P53	Homo sapiens	95-98
25829127-4	2015	Using flow cytometric analysis, early apoptotic ratios of 54.95% and 27.06% after PEN-mediated p53 transfection were detected in PC-3 and HeLa cells, respectively, indicating that PC-3 cells were more sensitive to the exogenous p53 transfection than HeLa cells.	Polyethyleneimine	82-85	P53	Homo sapiens	228-231
25829127-6	2015	Through Western blotting, activity analysis of caspase-3, caspase-8 and caspase-9 and mitochondrial membrane potential measurement, the apoptosis induced by PEN-mediated p53 transfection was conducted in a mitochondria-dependent apoptosis pathway.	Polyethyleneimine	157-160	P53	Homo sapiens	170-173
25829127-7	2015	These results demonstrated that PEN could successfully mediate the p53 gene delivery and up-regulate the cellular p53 expression level, triggering a significant p53-dependent anti-proliferative effect on tumor cells.	Polyethyleneimine	32-35	P53	Homo sapiens	67-70
25829127-7	2015	These results demonstrated that PEN could successfully mediate the p53 gene delivery and up-regulate the cellular p53 expression level, triggering a significant p53-dependent anti-proliferative effect on tumor cells.	Polyethyleneimine	32-35	P53	Homo sapiens	114-117
25829127-7	2015	These results demonstrated that PEN could successfully mediate the p53 gene delivery and up-regulate the cellular p53 expression level, triggering a significant p53-dependent anti-proliferative effect on tumor cells.	Polyethyleneimine	32-35	P53	Homo sapiens	114-117
25814188-3	2015	Herein, we report the identification of a dual inhibitor of the p53 interaction with MDM2 and MDMX, the (S)-tryptophanol derivative OXAZ-1, from the screening of a small library of enantiopure tryptophanol-derived oxazolopiperidone lactams, using a yeast-based assay.	oxazolopiperidone lactams	214-239	P53	Homo sapiens	64-67
25589462-0	2015	Indole-3-carbinol suppresses NF-kappaB activity and stimulates the p53 pathway in pre-B acute lymphoblastic leukemia cells.	indole-3-carbinol	0-17	P53	Homo sapiens	67-70
25823924-10	2015	Thus, the p53-Snail binding inhibitor such as GN25 is a drug candidate for MPM.	GN25	46-50	P53	Homo sapiens	10-13
25744307-10	2015	Furthermore, our results suggest that the CdCl2-induced activation of ERK1/2 and Mdm2 may interfere with the p53 response to genotoxic compounds in cancer cell lines.	Cadmium Chloride	42-47	P53	Homo sapiens	109-112
24858040-7	2015	Oxidative stress induced SLC2A9 expression in a p53-dependent manner, and inhibition of SLC2A9 by small interfering RNA (siRNA) or anti-gout drugs such as probenecid significantly increased ROS levels in an uric acid-dependent manner and greatly sensitized cancer cells to chemotherapeutic drugs.	Probenecid	155-165	P53	Homo sapiens	48-51
25649747-5	2015	In addition, alpha-PA up-regulated nuclear p53 and down-regulated cytoplasmic p53 expression in J5 cells.	alpha phellandrene	13-21	P53	Homo sapiens	43-46
25649747-5	2015	In addition, alpha-PA up-regulated nuclear p53 and down-regulated cytoplasmic p53 expression in J5 cells.	alpha phellandrene	13-21	P53	Homo sapiens	78-81
25649747-7	2015	These results suggest that alpha-PA can induce J5 cell autophagy by regulating mTOR and LC-3II expression, p53 signaling, and NF-kappaB activation in J5 cells.	alpha phellandrene	27-35	P53	Homo sapiens	107-110
26028101-5	2015	Meanwhile, it could also significantly decrease gemcitabine-induced increase of transcellular and paracellular leak, ROS level, PARP-1 activity, Act-MMP9 level, mRNA expressions of p53 and Rac-1, expression of PARP-1 and apoptosis rate (p&lt;0.01).	gemcitabine	48-59	P53	Homo sapiens	181-184
26292025-4	2015	It was recently shown that low-dose arsenic leads to a metabolic shift from mitochondrial respiration to aerobic glycolysis via inactivation of tumor suppressor p53 and activation of NF-kappaB.	Arsenic	36-43	P53	Homo sapiens	161-164
26292025-5	2015	However, how inactivation of p53, activation of NF-kappaB, and metabolic change are coordinated in response to low-dose arsenic exposure is still not completely understood.	Arsenic	120-127	P53	Homo sapiens	29-32
28970873-5	2015	The transformation of the azidophenyl label to nitrophenyltriazole was used for electrochemical detection of DNA-protein interactions (p53 protein) since only those azidophenyl groups in the parts of the DNA not shielded by the bound p53 protein were transformed to nitrophenyltriazoles, whereas those covered by the protein were not.	4-nitro-5-phenyl-2H-1,2,3-triazole	47-66	P53	Homo sapiens	135-138
28970873-5	2015	The transformation of the azidophenyl label to nitrophenyltriazole was used for electrochemical detection of DNA-protein interactions (p53 protein) since only those azidophenyl groups in the parts of the DNA not shielded by the bound p53 protein were transformed to nitrophenyltriazoles, whereas those covered by the protein were not.	4-nitro-5-phenyl-2H-1,2,3-triazole	47-66	P53	Homo sapiens	234-237
25942059-9	2015	Interestingly, all hemiesters of 2,2-difluorodihydrobetulonic acid had higher activity against p53 knock-out p53-/- cancer cell line than against the non-mutated analog.	2,2-difluorodihydrobetulonic acid	33-66	P53	Homo sapiens	95-98
25942059-9	2015	Interestingly, all hemiesters of 2,2-difluorodihydrobetulonic acid had higher activity against p53 knock-out p53-/- cancer cell line than against the non-mutated analog.	2,2-difluorodihydrobetulonic acid	33-66	P53	Homo sapiens	109-112
25737737-0	2015	Shikonin Induces Apoptosis, Necrosis, and Premature Senescence of Human A549 Lung Cancer Cells through Upregulation of p53 Expression.	shikonin	0-8	P53	Homo sapiens	119-122
24679006-6	2015	Our findings indicate a significant difference between these two types of DHL at a molecular level with pathogenetic implications, as arguably, TP53 mutations inhibiting p53 mediated promotion of apoptosis pose a synergistic advantage in clonal evolution of cells with malignantly enforced overexpression of BCL2.	Cysteamine	74-77	P53	Homo sapiens	144-148
24679006-6	2015	Our findings indicate a significant difference between these two types of DHL at a molecular level with pathogenetic implications, as arguably, TP53 mutations inhibiting p53 mediated promotion of apoptosis pose a synergistic advantage in clonal evolution of cells with malignantly enforced overexpression of BCL2.	Cysteamine	74-77	P53	Homo sapiens	170-173
25521755-0	2014	Ginsenoside Rg3 inhibits melanoma cell proliferation through down-regulation of histone deacetylase 3 (HDAC3) and increase of p53 acetylation.	Ginsenosides	0-11	P53	Homo sapiens	126-129
25449279-0	2014	COH-203, a novel microtubule inhibitor, exhibits potent anti-tumor activity via p53-dependent senescence in hepatocellular carcinoma.	5-(3-hydroxy-4-methoxyphenyl)-4-(3,4,5-trimethoxyphenyl)-3H-1,2-dithiol-3-one	0-7	P53	Homo sapiens	80-83
25449279-7	2014	Furthermore, suppression of p53 via pifithrin-alpha (p53 inhibitor) and p53-siRNA attenuated COH-203-induced senescence in BEL-7402 cells, suggesting that COH-203 induced senescence p53-dependently.	5-(3-hydroxy-4-methoxyphenyl)-4-(3,4,5-trimethoxyphenyl)-3H-1,2-dithiol-3-one	93-100	P53	Homo sapiens	28-31
25449279-8	2014	In conclusion, we report for the first time that COH-203, one compound in the combretastatin family, promotes anti-proliferative activity through the induction of p-53 dependent senescence.	5-(3-hydroxy-4-methoxyphenyl)-4-(3,4,5-trimethoxyphenyl)-3H-1,2-dithiol-3-one	49-56	P53	Homo sapiens	163-167
25426548-0	2014	Targeting of mutant p53-induced FoxM1 with thiostrepton induces cytotoxicity and enhances carboplatin sensitivity in cancer cells.	Carboplatin	90-101	P53	Homo sapiens	20-23
25195822-6	2014	Furthermore, we elucidate that ceramide activates protein phosphatase-1, and then the dephosphorylated serine/arginine-rich splicing-factor 1 (SRSF1) is translocated to the nucleus, thus promoting pre-mRNA splicing preferentially to wild-type p53 expression.	Ceramides	31-39	P53	Homo sapiens	243-246
25195822-8	2014	Ceramide through SRSF1 restores wild-type p53 expression versus deletion-mutant and leads cancer cells to apoptosis.	Ceramides	0-8	P53	Homo sapiens	42-45
25412667-7	2014	Treatment with 200 mumol/L H2O2tended to up-regulate p53 and to down-regulate SIRT1 and AMPKalpha1, but had no effect on AMPKalpha2 and 14-3-3 sigma expression.	h2o2tended	27-37	P53	Homo sapiens	53-56
25295231-11	2014	Through its inhibitory effect on PP2A, lenalidomide stabilizes MDM2 to restore p53 degradation in erythroid precursors, with subsequent arrest in G2/M.	Lenalidomide	39-51	P53	Homo sapiens	79-82
25018059-0	2014	Taurine protects HK-2 cells from oxidized LDL-induced cytotoxicity via the ROS-mediated mitochondrial and p53-related apoptotic pathways.	Taurine	0-7	P53	Homo sapiens	106-109
25018059-12	2014	The inhibition of oxLDL-induced epithelial apoptosis by taurine was at least partially due to its anti-oxidant activity and its ability to modulate the ERK and p53 apoptotic pathways.	Taurine	56-63	P53	Homo sapiens	160-163
24990888-3	2014	Treatment with lenalidomide significantly inhibited CLL-cell proliferation, an effect that was associated with the p53-independent upregulation of the cyclin-dependent kinase inhibitor, p21(WAF1/Cip1) (p21).	Lenalidomide	15-27	P53	Homo sapiens	115-118
24990888-7	2014	These results indicate that lenalidomide can directly inhibit proliferation of CLL cells in a cereblon/p21-dependent but p53-independent manner, at concentrations achievable in vivo, potentially contributing to the capacity of this drug to inhibit disease-progression in patients with CLL.	Lenalidomide	28-40	P53	Homo sapiens	121-124
25164437-10	2014	CONCLUSION: pERK expression may have an impact on OS in erlotinib-treated patients with advanced pancreatic cancer; p53 should be further investigated for its potential role as a predictive marker for PFS and skin rash.	Erlotinib Hydrochloride	56-65	P53	Homo sapiens	116-119
25118938-5	2014	Inhibition of p53 activity with pifithrin-alpha or inhibition of PI3K with LY294002 suppressed CdCl2-induced cellular damage and elevation of Notch1-NICD.	Cadmium Chloride	95-100	P53	Homo sapiens	14-17
24954032-0	2014	PCB153, TCDD and estradiol compromise the benzo[a]pyrene-induced p53-response via FoxO3a.	2,4,5,2',4',5'-hexachlorobiphenyl	0-6	P53	Homo sapiens	65-68
24954032-3	2014	We have studied the effect of TCDD, PCB153 and estradiol on p53 signaling induced by PAHs.	2,4,5,2',4',5'-hexachlorobiphenyl	36-42	P53	Homo sapiens	60-63
24286323-4	2014	According to the results, Stigmasterol has up-regulated the expression of pro-apoptotic gene expressions (Bax, p53) while down-regulating the anti-apoptotic genes (Bcl-2).	Stigmasterol	26-38	P53	Homo sapiens	111-114
24996846-8	2014	Induction of gammaH2AX levels was chemotherapeutic dependent and correlated closely with potentiation of gemcitabine and camptothecin in p53 mutant colon cancer cells.	gemcitabine	105-116	P53	Homo sapiens	137-140
24880989-12	2014	HeLa cells transfected with PSMT/p53 plasmid nanoparticles showed cellular damage and apoptosis, which was confirmed through propidium iodide staining.	Propidium	125-141	P53	Homo sapiens	33-36
24804820-8	2014	Furthermore, as shown by our results, the inhibition of gemcitabine-induced autophagy by chloroquine shifts the expression of the p53 protein, Bcl-2 family proteins and the relative Bax/Bcl-xL ratio in favor of promoting apoptosis.	gemcitabine	56-67	P53	Homo sapiens	130-133
24144307-5	2014	[Flu + Clo + Bu + SAHA] resulted in synergistic cytotoxicity, which can be attributed to (1) activated DNA-damage response and cell cycle checkpoint activation through the ATM-CHK2-P53 (or P73) pathway or ATM-CHK2-cdc25-cdc2 pathway, (2) histone modifications and (3) activated apoptosis pathway.	Vorinostat	18-22	P53	Homo sapiens	181-184
24918290-4	2014	The results revealed that EPA attenuated PA-induced cell death and activation of apoptosis-related proteins, such as caspase-3, p53 and Bax.	Palmitic Acid	27-29	P53	Homo sapiens	128-131
24512488-0	2014	PRIMA-1, a mutant p53 reactivator, restores the sensitivity of TP53 mutant-type thyroid cancer cells to the histone methylation inhibitor 3-Deazaneplanocin A.	3-deazaneplanocin	138-157	P53	Homo sapiens	18-21
24512488-0	2014	PRIMA-1, a mutant p53 reactivator, restores the sensitivity of TP53 mutant-type thyroid cancer cells to the histone methylation inhibitor 3-Deazaneplanocin A.	3-deazaneplanocin	138-157	P53	Homo sapiens	63-67
24512488-5	2014	RESULTS: DZNep induced enhancer of zeste homolog 2 depletion and trimethylated lysine 27 in H3 histone (H3K27me3) mark reduction in all thyroid cancer cells; however, only TP53 wild-type cells exhibited growth inhibition with DZNep treatment.	3-deazaneplanocin	9-14	P53	Homo sapiens	172-176
24691740-9	2014	P-gp and NF-kappaB significantly decreased; however, p53 increased in FaDu/T + MG132 cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	P53	Homo sapiens	53-56
24691740-11	2014	MG132 was also able to inhibit the nuclear translocation of NF-kappaB and increase the expression of p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	P53	Homo sapiens	101-104
24676336-12	2014	For the TSA+DAC group, higher levels of p53, p21, cyclin B1 and Chk1 were detected, concomitant with lower levels of CDK1, when compared to the control group.	Decitabine	12-15	P53	Homo sapiens	40-43
24656661-1	2014	The discovery of 3,3-disubstituted piperidine 1 as novel p53-HDM2 inhibitors prompted us to implement subsequent SAR follow up directed towards piperidine core modifications.	3,3-disubstituted piperidine	17-45	P53	Homo sapiens	57-60
24601644-1	2014	We previously reported the discovery of potent and selective morpholinone and piperidinone inhibitors of the MDM2-p53 interaction.	2-piperidone	78-90	P53	Homo sapiens	114-117
24114124-10	2014	Consistent with abrogation of the Chk1 and p53-dependent G2/M checkpoint, mutant TP53 HT-29 colon cancer cells were more sensitive to gemcitabine when also treated with LY2603618, while wild-type TP53 HCT116 cells were not sensitized by LY2603618 to gemcitabine.	gemcitabine	134-145	P53	Homo sapiens	81-85
25512709-0	2014	Bioinformatic Dissecting of TP53 Regulation Pathway Underlying Butyrate-induced Histone Modification in Epigenetic Regulation.	Butyrates	63-71	P53	Homo sapiens	28-32
25512709-5	2014	TP53 pathway and their involvement in cellular functions modified by butyrate treatment were scrutinized in this report by data mining the RNA-sequencing data using IPA (Ingenuity System( )).	Butyrates	69-77	P53	Homo sapiens	0-4
25512709-7	2014	Downstream analysis predicted the activation of the TP53 pathway after butyrate treatment.	Butyrates	71-79	P53	Homo sapiens	52-56
24297112-8	2014	Furthermore, the activation of the p38 kinase promoted the activation of p53 and its downstream target p21, and further caused caspase-9 and -3 activation, as demonstrated by evidence showing that the p38 inhibitor SB203580 not only blocked the phosphorylation of p38 but also reduced the activation of p53, p21 and caspase-9 and -3.	SB 203580	215-223	P53	Homo sapiens	73-76
24297112-8	2014	Furthermore, the activation of the p38 kinase promoted the activation of p53 and its downstream target p21, and further caused caspase-9 and -3 activation, as demonstrated by evidence showing that the p38 inhibitor SB203580 not only blocked the phosphorylation of p38 but also reduced the activation of p53, p21 and caspase-9 and -3.	SB 203580	215-223	P53	Homo sapiens	303-306
24078446-0	2014	Artemisinin inhibits gastric cancer cell proliferation through upregulation of p53.	artemisinin	0-11	P53	Homo sapiens	79-82
25482947-6	2014	We found that inhibitors of the mTOR pathway including rapamycin, wortmannin, and caffeine blunted the p53 response to nucleolar stress induced by actinomycin D.	Wortmannin	66-76	P53	Homo sapiens	103-106
25482947-7	2014	Synthetic inhibitors of mTOR (temsirolimus, LY294.002 and PP242) also impaired actinomycin D triggered p53 stabilization and induction of p21.	ly294	44-49	P53	Homo sapiens	103-106
24180280-0	2014	Stimulation of DDX3 expression by ginsenoside Rg3 through the Akt/p53 pathway activates the innate immune response via TBK1/IKKepsilon/IRF3 signalling.	Ginsenosides	34-45	P53	Homo sapiens	66-69
24012657-0	2014	Acetyl-L-carnitine rescues scopolamine-induced memory deficits by restoring insulin-like growth factor II via decreasing p53 oxidation.	Scopolamine	27-38	P53	Homo sapiens	121-124
24161784-6	2013	Cell viability assays and cytometric analysis of p53 and p21 null cells indicated that BBR3610-DACH-induced cell cycle arrest was p21-dependent and partially p53-dependent.	BBR3610	87-94	P53	Homo sapiens	49-52
24161784-6	2013	Cell viability assays and cytometric analysis of p53 and p21 null cells indicated that BBR3610-DACH-induced cell cycle arrest was p21-dependent and partially p53-dependent.	BBR3610	87-94	P53	Homo sapiens	158-161
24163369-11	2013	These results identify NEK2 as a novel p53-repressed gene, illustrate that its repression by 5aza-dC is specific and associated with nucleosome reorganization, and provide evidence that identification of partially methylated regions can reveal novel p53 target genes.	Decitabine	93-100	P53	Homo sapiens	39-42
24163369-11	2013	These results identify NEK2 as a novel p53-repressed gene, illustrate that its repression by 5aza-dC is specific and associated with nucleosome reorganization, and provide evidence that identification of partially methylated regions can reveal novel p53 target genes.	Decitabine	93-100	P53	Homo sapiens	250-253
23982184-10	2013	According to the inhibition rate of si-P53, we choose the optimized volume of si-P53.	Silicon	36-38	P53	Homo sapiens	39-42
23982184-10	2013	According to the inhibition rate of si-P53, we choose the optimized volume of si-P53.	Silicon	36-38	P53	Homo sapiens	81-84
23982184-10	2013	According to the inhibition rate of si-P53, we choose the optimized volume of si-P53.	Silicon	78-80	P53	Homo sapiens	39-42
23982184-10	2013	According to the inhibition rate of si-P53, we choose the optimized volume of si-P53.	Silicon	78-80	P53	Homo sapiens	81-84
24280450-8	2013	Moreover, Bispicen, similar to vanadate, induces the denaturation of p53 as well as the blocking of both transcription-dependent and -independent apoptotic pathways.	N,N'-bis(pyridin-2-ylmethyl)ethane-1,2-diamine	10-18	P53	Homo sapiens	69-72
23994832-4	2013	When cells were treated with a proteasome inhibitor (MG132) or an MDM2 antagonist (Nutlin-3), p53 expression was not reduced in N protein-overexpressed cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	P53	Homo sapiens	94-97
24043769-0	2013	TP53 suppression promotes erythropoiesis in del(5q) MDS, suggesting a targeted therapeutic strategy in lenalidomide-resistant patients.	Lenalidomide	103-115	P53	Homo sapiens	0-4
24043769-7	2013	We conclude that targeted suppression of p53 could support effective erythropoiesis in lenalidomide-resistant del(5q) MDS.	Lenalidomide	87-99	P53	Homo sapiens	41-44
24041220-11	2013	The hexane extract showed highest toxicity against p53-deficient HL-60 cells (IC50 1.5 mg dry roots equivalent/ml medium) after 72 h and interestingly, inhibition of cell proliferation was preceded by the upregulation of the proto-oncogenes Cdc25A and cyclin D1 within 24 h. The hexane extract induced 18% apoptosis after 48 h of treatment.	Hexanes	4-10	P53	Homo sapiens	51-54
24076776-9	2013	Our results suggest that dysregulation of EGFR and p53 may play an important role in the development of DIPGs.	dipgs	104-109	P53	Homo sapiens	51-54
24074787-8	2013	We reported that TP53 mutated non inflammatory locally advanced breast carcinomas had a high rate of complete pathological response to dose-dense doxorubicin-cyclophosphamide chemotherapy, while TP53 wild-type (WT) tumors never achieved complete response.	Cyclophosphamide	158-174	P53	Homo sapiens	17-21
23759676-7	2013	CONCLUSIONS: Altogether, these data identify the cyclophosphamide-induced immunomodulatory factors in humans and indicate that preconditioning chemotherapy may stimulate immunity as a consequence of danger perception associated with blood cell death, through p53 and IFN-I-related mechanisms.	Cyclophosphamide	49-65	P53	Homo sapiens	259-262
22436021-0	2013	Myrtenal ameliorates diethylnitrosamine-induced hepatocarcinogenesis through the activation of tumor suppressor protein p53 and regulation of lysosomal and mitochondrial enzymes.	Diethylnitrosamine	21-39	P53	Homo sapiens	120-123
23495037-3	2013	Exposure to ceramide activates extracellular-signal-regulated kinases (ERK)1/2- and p38 kinase-dependent apoptosis in human ovarian cancer OVCAR-3 cells, concomitant with an increase in the expression of COX-2 and p53 phosphorylation.	Ceramides	12-20	P53	Homo sapiens	214-217
23495037-4	2013	Blockade of cyclooxygenase-2 (COX-2) activity by siRNA or NS398 correspondingly inhibited ceramide-induced p53 Ser-15 phosphorylation and apoptosis; thus COX-2 appears at the apex of the p38 kinase-mediated signaling cascade induced by ceramide.	Ceramides	90-98	P53	Homo sapiens	107-110
23495037-4	2013	Blockade of cyclooxygenase-2 (COX-2) activity by siRNA or NS398 correspondingly inhibited ceramide-induced p53 Ser-15 phosphorylation and apoptosis; thus COX-2 appears at the apex of the p38 kinase-mediated signaling cascade induced by ceramide.	Ceramides	236-244	P53	Homo sapiens	107-110
23495037-8	2013	In summary, resveratrol and ceramide converge on an endocytosis-requiring, ERK1/2-dependent signal transduction pathway and induction of COX-expression as an essential molecular antecedent for subsequent p53-dependent apoptosis.	Ceramides	28-36	P53	Homo sapiens	204-207
23614682-10	2013	This study reveals the importance of a low baseline platelet count, karyotypic complexity and TP53 mutational status for response to lenalidomide treatment.	Lenalidomide	133-145	P53	Homo sapiens	94-98
23614682-11	2013	It supports the molecular study of TP53 in MDS patients treated with lenalidomide.	Lenalidomide	69-81	P53	Homo sapiens	35-39
23759592-5	2013	Conversely, suppression of p38 MAPK with SB239063 inhibits IR-induced p53 phosphorylation at Ser15 and miR-34a expression in a dose-dependent manner.	SB 239063	41-49	P53	Homo sapiens	70-73
22999639-4	2013	In U937 cells, 7beta-hydroxycholesterol and 7-ketocholesterol induced production of reactive oxygen species (ROS), transient up-regulation of Egr1 followed by late induction of p53 and apoptosis.	7-ketocholesterol	44-61	P53	Homo sapiens	177-180
23579097-6	2013	The combined treatment with BLU and gemcitabine further activated p53 and p21 expression, whereas the productions of Bcl-2, Bcl-xL, and nuclear factor-kappa B proteins were decreased, with BLU possibly being more effective in the treatment of ovarian cancer when given in combination with gemcitabine, rather than as a single agent.	gemcitabine	36-47	P53	Homo sapiens	66-69
24195362-6	2013	MTT assay showed that the cell growth inhibition by CPPs-P53 was more efficient than P53, and the rate of cell growth inhibition is dose-dependent.	monooxyethylene trimethylolpropane tristearate	0-3	P53	Homo sapiens	57-60
24195362-6	2013	MTT assay showed that the cell growth inhibition by CPPs-P53 was more efficient than P53, and the rate of cell growth inhibition is dose-dependent.	monooxyethylene trimethylolpropane tristearate	0-3	P53	Homo sapiens	85-88
23470959-8	2013	In MCF-7 cells, depletion of DDX3 reduced by more than 50% camptothecin-induced p53 accumulation, and this effect was blocked by inhibition of the proteasome with MG132, indicating that DDX3 regulates p53 not at expression level but rather its stabilization after DNA damage.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	163-168	P53	Homo sapiens	201-204
25337543-0	2013	Urushiol Induces Apoptosis via a p53-dependent Pathway in Human Gastric Cancer Cells.	urushiol	0-8	P53	Homo sapiens	33-36
25337543-3	2013	METHODS: The cytotoxicity of urushiols was assessed by MTT assays on the two gastric adenocarcinoma cell lines, MKN-45 (wild type of p53) and MKN-28 (mutant type of p53).	urushiol	29-38	P53	Homo sapiens	133-136
25337543-3	2013	METHODS: The cytotoxicity of urushiols was assessed by MTT assays on the two gastric adenocarcinoma cell lines, MKN-45 (wild type of p53) and MKN-28 (mutant type of p53).	urushiol	29-38	P53	Homo sapiens	165-168
23416168-9	2013	Treatment of NRCM with proteasome inhibitor MG132 increased p53 and miR-34a levels and reduced BLC2/BAX ratio.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	44-49	P53	Homo sapiens	60-63
23645732-1	2013	BACKGROUND/AIM: The indole-3-carbinol cyclic tetrameric derivative (CTet) inhibits breast cancer cell proliferation by endoplasmic reticulum stress and autophagy-related cell death induction, AKT/PKB (protein kinase B) activity inhibition and p53-independent overexpression of cyclin-dependent kinase inhibitor-1A (p21/CDKN1A).	indole-3-carbinol	20-37	P53	Homo sapiens	243-246
23645732-1	2013	BACKGROUND/AIM: The indole-3-carbinol cyclic tetrameric derivative (CTet) inhibits breast cancer cell proliferation by endoplasmic reticulum stress and autophagy-related cell death induction, AKT/PKB (protein kinase B) activity inhibition and p53-independent overexpression of cyclin-dependent kinase inhibitor-1A (p21/CDKN1A).	ctet	68-72	P53	Homo sapiens	243-246
23530619-0	2013	p53-independent early and late apoptosis is mediated by ceramide after exposure of tumor cells to photon or carbon ion irradiation.	Ceramides	56-64	P53	Homo sapiens	0-3
23530619-1	2013	BACKGROUND: To determine whether ceramide is responsible for the induction of p53-independent early or late apoptosis in response to high- and low-Linear-Energy-Transfer (LET) irradiation.	Ceramides	33-41	P53	Homo sapiens	78-81
23530619-7	2013	CONCLUSIONS: Ceramide is a determining factor in the onset of early and late apoptosis after low and high-LET irradiation and is the mediator of the p53-independent-apoptotic pathway.	Ceramides	13-21	P53	Homo sapiens	149-152
23492773-0	2013	miR-128 exerts pro-apoptotic effect in a p53 transcription-dependent and -independent manner via PUMA-Bak axis.	mir-128	0-7	P53	Homo sapiens	41-44
23492773-4	2013	We herein demonstrate that miR-128 positively regulates p53 activity.	mir-128	27-34	P53	Homo sapiens	56-59
23492773-6	2013	miR-128 inhibition of SIRT1 led to an increase in acetylated p53 and its transcriptional targets.	mir-128	0-7	P53	Homo sapiens	61-64
23492773-8	2013	We further demonstrated that miR-128 augments the antitumor effect of compounds that target the p53 pathway.	mir-128	29-36	P53	Homo sapiens	96-99
23492773-9	2013	Furthermore, miR-128 induces apoptosis in wild (WT) p53 as well as in mutant p53-expressing cells in a p53-dependent and -independent manner via induction of PUMA.	mir-128	13-20	P53	Homo sapiens	52-55
23492773-9	2013	Furthermore, miR-128 induces apoptosis in wild (WT) p53 as well as in mutant p53-expressing cells in a p53-dependent and -independent manner via induction of PUMA.	mir-128	13-20	P53	Homo sapiens	77-80
23492773-9	2013	Furthermore, miR-128 induces apoptosis in wild (WT) p53 as well as in mutant p53-expressing cells in a p53-dependent and -independent manner via induction of PUMA.	mir-128	13-20	P53	Homo sapiens	77-80
23450231-11	2013	The inhibition of p38 MAPK activation by SB203580 or siRNA reduced Eag protein level but increased p53 protein level.	SB 203580	41-49	P53	Homo sapiens	99-102
24088253-4	2013	Furthermore, sesamin suppressed the constitutive and interleukin (IL)-6-induced signal transducer and activator of transcription 3 (STAT3) signalling pathway in HepG2 cells, leading to regulate the downstream genes, including p53, p21, cyclin proteins and the Bcl-2 protein family.	sesamin	13-20	P53	Homo sapiens	226-229
24601052-6	2013	p53 positive expression and Ki67 high expression were associated with high PTX (p = 0.01 and p &lt; 0.01, respectively) and CBDCA (p = 0.03 and p &lt; 0.01, respectively) sensitivity.	Carboplatin	124-129	P53	Homo sapiens	0-3
23535401-0	2013	Crotonaldehyde induces apoptosis in alveolar macrophages through intracellular calcium, mitochondria and p53 signaling pathways.	2-butenal	0-14	P53	Homo sapiens	105-108
23535401-7	2013	Crotonaldehyde-induced apoptosis was characterized by ROS generation, GSH depletion, loss of mitochondrial membrane potential (DeltaPsim), the release of cytochrome c from mitochondria, caspase-3/7 and caspase-9 activation, elevation of intracellular Ca(2+) concentration and the increase of p53 expression.	2-butenal	0-14	P53	Homo sapiens	292-295
23535401-8	2013	Furthermore, pretreatment with either p53 inhibitor pifithrin-alpha or calcium chelator BAPTA-AM effectively attenuated apoptosis induced by crotonaldehyde.	2-butenal	141-155	P53	Homo sapiens	38-41
23535401-9	2013	Taken together, our results showed that crotonaldehyde induce apoptosis in alveolar macrophages through intracellular calcium, mitochondria and p53 signaling pathways.	2-butenal	40-54	P53	Homo sapiens	144-147
22782330-4	2013	Deletions of p16 and p53 were detected in 50 % and 65.7 % of PDAC, respectively.	pdac	61-65	P53	Homo sapiens	21-24
22752636-10	2012	After prednisolone withdrawal, there was overexpression of H2AX, CC3, and p53 in the latter group.	Prednisolone	6-18	P53	Homo sapiens	74-77
23053941-0	2012	Toxicogenomic activity of gemcitabine in two TP53-mutated bladder cancer cell lines: special focus on cell cycle-related genes.	gemcitabine	26-37	P53	Homo sapiens	45-49
23053941-7	2012	Gemcitabine had distinct toxicogenomic effects in the bladder transitional carcinoma cell lines with two different TP53 mutations.	gemcitabine	0-11	P53	Homo sapiens	115-119
22973058-10	2012	Importantly 8-NH(2)-Ado was highly cytotoxic to triple-negative breast cancer cells and worked through a pathway that did not require wild-type p53 for cytoxicity.	8-nh(2)-ado	12-23	P53	Homo sapiens	144-147
22903553-10	2012	The p53 and p21 promoter luciferase activities were promoted by either sMEK1 or gemcitabine, and sMEK1 and gemcitabine combined additively activated the promoter further.	gemcitabine	80-91	P53	Homo sapiens	4-7
22903553-10	2012	The p53 and p21 promoter luciferase activities were promoted by either sMEK1 or gemcitabine, and sMEK1 and gemcitabine combined additively activated the promoter further.	gemcitabine	107-118	P53	Homo sapiens	4-7
22796259-0	2012	Mycoepoxydiene, a fungal polyketide inhibits MCF-7 cells through simultaneously targeting p53 and NF-kappaB pathways.	mycoepoxydiene	0-14	P53	Homo sapiens	90-93
23092836-5	2012	In response to propranolol, DeltaNp63alpha decreased, whereas TAp73beta and downstream proapoptotic p53 family target genes increased.	Propranolol	15-26	P53	Homo sapiens	100-103
22446899-8	2012	RESULTS: Shikonin induces the generation of ROS, depletion of GSH, disruption of mitochondrial transmembrane potential, upregulation of p53, and cleavage of PARP [poly(ADP-ribose) polymerase] in U87MG glioma cells.	shikonin	9-17	P53	Homo sapiens	136-139
22675170-0	2012	TP53 genomic status regulates sensitivity of gastric cancer cells to the histone methylation inhibitor 3-deazaneplanocin A (DZNep).	3-deazaneplanocin	103-122	P53	Homo sapiens	0-4
22675170-0	2012	TP53 genomic status regulates sensitivity of gastric cancer cells to the histone methylation inhibitor 3-deazaneplanocin A (DZNep).	3-deazaneplanocin	124-129	P53	Homo sapiens	0-4
22675170-9	2012	In TP53-WT lines, DZNep stabilized p53 by reducing ubiquitin conjugation through USP10 upregulation, resulting in activation of canonical p53 target genes.	3-deazaneplanocin	18-23	P53	Homo sapiens	3-7
22675170-9	2012	In TP53-WT lines, DZNep stabilized p53 by reducing ubiquitin conjugation through USP10 upregulation, resulting in activation of canonical p53 target genes.	3-deazaneplanocin	18-23	P53	Homo sapiens	35-38
22675170-9	2012	In TP53-WT lines, DZNep stabilized p53 by reducing ubiquitin conjugation through USP10 upregulation, resulting in activation of canonical p53 target genes.	3-deazaneplanocin	18-23	P53	Homo sapiens	138-141
22653969-0	2012	The checkpoint kinase inhibitor AZD7762 potentiates chemotherapy-induced apoptosis of p53-mutated multiple myeloma cells.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	32-39	P53	Homo sapiens	86-89
22653969-5	2012	The Chk1/2 inhibitor AZD7762 potentiated the antiproliferative effects of bendamustine, melphalan, and doxorubicin but not bortezomib in multiple myeloma cell lines that were p53-deficient.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	21-28	P53	Homo sapiens	175-178
22653969-8	2012	In summary, the cytotoxic effects of bendamustine, melphalan and doxorubicin on p53-deficient multiple myeloma cell lines were enhanced by the coadministration of AZD7762.	3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamide	163-170	P53	Homo sapiens	80-83
22551203-10	2012	RESULTS: Results showed that arsenic-exposed newborns had significantly higher levels of arsenic in cord blood, fingernails, toenails and hair than those of the unexposed subjects and a slight increase in promoter methylation of p53 in cord blood lymphocytes which significantly correlated with arsenic accumulation in nails (p &lt; 0.05) was observed, while LINE-1 methylation was unchanged.	Arsenic	29-36	P53	Homo sapiens	229-232
22551203-13	2012	CONCLUSIONS: This study provides an important finding that in utero arsenic exposure affects DNA methylation, particularly at the p53 promoter region, which may be linked to the mechanism of arsenic carcinogenesis and the observed increased incidence of cancer later in life.	Arsenic	68-75	P53	Homo sapiens	130-133
22170404-7	2012	Inhibition of AMPK, p53, or DAPK attenuated SB203580-induced autophagy.	SB 203580	44-52	P53	Homo sapiens	20-23
21543203-7	2012	We also observed that flavokawain B caused the G2/M phase arrest that was mediated through reductions in the levels of cyclin A, cyclin B1, Cdc2 and Cdc25C and increases in p21/WAF1, Wee1 and p53 levels.	flavokawain B	22-35	P53	Homo sapiens	192-195
23556117-4	2012	Other recent advances include a better understanding of the pathogenesis of disease including haplodeficiency of several candidate genes, and elucidation of the lenalidomide-specific effect on two phosphatases ultimately leading to p53 degradation in the erythroid progenitors and cell cycle arrest in earlier myeloid progenitors.	Lenalidomide	161-173	P53	Homo sapiens	232-235
22370485-6	2012	KU-60019 inhibited the phosphorylation of the major DNA damage effectors p53, H2AX and KAP1 as well as AKT.	2-(2,6-dimethylmorpholin-4-yl)-N-(5-(6-morpholin-4-yl-4-oxo-4H-pyran-2-yl)-9H-thioxanthen-2-yl)acetamide	0-8	P53	Homo sapiens	73-76
22120587-0	2012	Fluoranthene enhances p53 expression and decreases mutagenesis induced by benzo[a]pyrene.	fluoranthene	0-12	P53	Homo sapiens	22-25
22261445-0	2012	p53 nuclear expression correlates with hemizygous TP53 deletion and predicts an adverse outcome for patients with relapsed/refractory multiple myeloma treated with lenalidomide.	Lenalidomide	164-176	P53	Homo sapiens	0-3
22261445-1	2012	del(17p13)(TP53) seems to be an independent poor prognostic factor in patients with relapsed/refractory multiple myeloma (MM) receiving lenalidomide.	Lenalidomide	136-148	P53	Homo sapiens	11-15
22261445-2	2012	However, whether aberrant p53 nuclear expression detected by immunohistochemical analysis can be used as a surrogate marker for del(17p13)(TP53) in prognostic evaluation of lenalidomide-treated relapsed/refractory MM remains unclear.	Lenalidomide	173-185	P53	Homo sapiens	26-29
22261445-7	2012	Our results suggest that p53 nuclear expression is associated with adverse outcome in patients with relapsed/refractory MM receiving lenalidomide-based therapy and that p53 immunohistochemical analysis may serve as a simple, rapid method to predict del(17p13)(TP53) in this patient subgroup.	Lenalidomide	133-145	P53	Homo sapiens	25-28
22056254-2	2012	Here we determine the effect of the tumor suppressor protein, p53, on trafficking (64)Cu to tumor cell nuclei from DOTA vs. CB-TE2A-conjugated agonist Y3-TATE and the antagonist (64)Cu-CB-TE2A-sst2-ANT in cell lines that are positive or negative for p53.	diflorasone	154-158	P53	Homo sapiens	62-65
26316897-0	2012	Development of in vitro gene delivery system using ORMOSIL nanoparticle: Analysis of p53 gene expression in cultured breast cancer cell (MCF-7).	ormosil	51-58	P53	Homo sapiens	85-88
26316897-3	2012	In this context, ORMOSIL nanoparticles had been synthesized and incubated along with pCMV-Myc (3.8 kb) plasmid vector construct carrying p53gene, and transfected into the breast cancer cell line MCF-7 cells.	ormosil	17-24	P53	Homo sapiens	137-140
21964832-8	2012	We observed that TPA-induced             down-regulation of p53 protein was prevented by ALLN and MG132, but not by chloroquine.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	98-103	P53	Homo sapiens	60-63
23050037-10	2012	Since the treatment of senescent cells with phosphoinositide 3-kinase inhibitor, wortmannin, suppressed p53 phosphorylation, it is suggested that amplification of DNA damage signaling sustains persistent activation of ATM-p53 pathway, which is essential for replicative senescence.	Wortmannin	81-91	P53	Homo sapiens	104-107
23050037-10	2012	Since the treatment of senescent cells with phosphoinositide 3-kinase inhibitor, wortmannin, suppressed p53 phosphorylation, it is suggested that amplification of DNA damage signaling sustains persistent activation of ATM-p53 pathway, which is essential for replicative senescence.	Wortmannin	81-91	P53	Homo sapiens	222-225
22448262-7	2012	The cell lines exhibited different sensitivity to cadmium, and 24-hour exposure to different CdCl(2) concentrations induced dose- and cell type-dependent apoptotic response and inhibition of cell proliferation that correlated with accumulation of functional p53 and overexpression of p21 in wild type p53-expressing cell lines.	Cadmium Chloride	93-100	P53	Homo sapiens	258-261
22448262-7	2012	The cell lines exhibited different sensitivity to cadmium, and 24-hour exposure to different CdCl(2) concentrations induced dose- and cell type-dependent apoptotic response and inhibition of cell proliferation that correlated with accumulation of functional p53 and overexpression of p21 in wild type p53-expressing cell lines.	Cadmium Chloride	93-100	P53	Homo sapiens	301-304
23139858-6	2012	This phenotypic change was completely reversed by p53 reactivation via treatment with proteasome inhibitor MG132 or co-knockdown of E3 ligase HDM2 and partially suppressed by ATP treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	107-112	P53	Homo sapiens	50-53
21982800-7	2011	Taken together, this is the first study to show that a variant genotype of p53 Arg(72)Pro or MDM2 SNP309 may modify the arsenic-related RCC risk even in a non-obvious arsenic exposure area.	Arsenic	120-127	P53	Homo sapiens	75-78
21982800-7	2011	Taken together, this is the first study to show that a variant genotype of p53 Arg(72)Pro or MDM2 SNP309 may modify the arsenic-related RCC risk even in a non-obvious arsenic exposure area.	Arsenic	167-174	P53	Homo sapiens	75-78
22120628-10	2011	Both Velcade and MG132 increased the protein levels of DR5, a TRAIL receptor known to be up-regulated by p53, in U373MG cells where p53 is mutated.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	P53	Homo sapiens	105-108
22120628-10	2011	Both Velcade and MG132 increased the protein levels of DR5, a TRAIL receptor known to be up-regulated by p53, in U373MG cells where p53 is mutated.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	17-22	P53	Homo sapiens	132-135
22254155-6	2011	In this study, we found that 15-deoxy-Delta(12,14)-prostaglandin J(2) induced p53 expression and that endothelial apoptosis was reduced under the L-flow condition.	15-deoxy-delta(12,14)-prostaglandin j(	29-67	P53	Homo sapiens	78-81
21637290-0	2011	SAHA shows preferential cytotoxicity in mutant p53 cancer cells by destabilizing mutant p53 through inhibition of the HDAC6-Hsp90 chaperone axis.	Vorinostat	0-4	P53	Homo sapiens	47-50
21637290-0	2011	SAHA shows preferential cytotoxicity in mutant p53 cancer cells by destabilizing mutant p53 through inhibition of the HDAC6-Hsp90 chaperone axis.	Vorinostat	0-4	P53	Homo sapiens	88-91
21637290-7	2011	We show that SAHA exhibits preferential cytotoxicity for mutant, rather than wild-type and null p53 human cancer cells.	Vorinostat	13-17	P53	Homo sapiens	96-99
22076037-1	2011	OBJECTIVE: To evaluate the expressions of p53, p21, and CCND1 in the peripheral blood lymphocytes of vinyl chloride monomer (VCM)-exposed workers and potential relationships with their exposures, polymorphisms, and chromosomal aberrations.	Vinyl Chloride	101-115	P53	Homo sapiens	42-45
21880715-10	2011	Meanwhile, mutation of EDEE residues impairs both the binding and the enzymatic activity of SMYD2 to p53 Lys-370.	edee	23-27	P53	Homo sapiens	101-104
21832879-0	2011	Metabolic utilization of exogenous pyruvate by mutant p53 (R175H) human melanoma cells promotes survival under glucose depletion.	Pyruvic Acid	35-43	P53	Homo sapiens	54-57
21832879-6	2011	Metabolic utilization and survival under glucose depletion was increased by pyruvate in mutant p53 (R175H) cells.	Pyruvic Acid	76-84	P53	Homo sapiens	95-98
21832879-7	2011	Our results show for the first time that melanoma cells harbouring a p53 (R175H) mutation increase: a) survival under glucose depletion, counteracted by NADPH-oxidase modulators like DPI; b) resistance to DPI when supplemented with exogenous pyruvate.	Pyruvic Acid	242-250	P53	Homo sapiens	69-72
21933400-13	2011	Changes in the repair kinetics of DSB p53-independent apoptosis with p21 involvement may be part of the underlying mechanisms for radio-sensitization by SAHA.	Vorinostat	153-157	P53	Homo sapiens	38-41
21327578-6	2011	BTG2/p53 were expressed early after DEN treatment, peaked at 5 weeks and decreased gradually thereafter.	Diethylnitrosamine	36-39	P53	Homo sapiens	5-8
21674128-6	2011	TP53-depleted HCT116 cultures also had DSBs after high-dose 5-FU treatment but experienced a (transient) G1/S cell cycle arrest that protected them from apoptosis.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	39-43	P53	Homo sapiens	0-4
21878502-3	2011	We demonstrate here a crucial role of the gammaH2AX-ATM-p53 pathway in the regulation of the apoptotic outcome of MC resulting from cells entering mitosis with damaged DNA.	Methylcholanthrene	114-116	P53	Homo sapiens	56-59
21914522-11	2011	The results of the study in West Bengal suggest that deficiency in DNA repair capacity, perturbation of methylation of promoter region of p53 and p16 genes, and genomic methylation alteration may be involved in arsenic-induced disease manifestation in humans.	Arsenic	211-218	P53	Homo sapiens	138-141
21914522-12	2011	P53 polymorphism has been found to be associated with increased occurrence of arsenic-induced keratosis.	Arsenic	78-85	P53	Homo sapiens	0-3
21441950-4	2011	We show here that the anthracyclines doxorubicin, daunorubicin and epirubicin further increase the amounts of mutant p53 mRNA and protein in cancer cells.	Daunorubicin	50-62	P53	Homo sapiens	117-120
21482024-10	2011	The ERCC1 and p53 genes may play an integral role in the synergism between Ki23057 and chemotherapeutic agents in drug-resistant cell lines.	Ki23057	75-82	P53	Homo sapiens	14-17
21656826-11	2011	Treatment with p38-specific inhibitor SB203580 or knocking down p38 by siRNA significantly impaired the upregulation of p53 and p21 by docetaxel.	SB 203580	38-46	P53	Homo sapiens	120-123
21398407-4	2011	Moreover, these synergistic effects of vorinostat/ABT-737 were blunted in cells with an inactive p53 pathway or in cells lacking expression of the p53 target gene, noxa.	Vorinostat	39-49	P53	Homo sapiens	97-100
21398407-4	2011	Moreover, these synergistic effects of vorinostat/ABT-737 were blunted in cells with an inactive p53 pathway or in cells lacking expression of the p53 target gene, noxa.	Vorinostat	39-49	P53	Homo sapiens	147-150
21756780-1	2011	OBJECTIVE: To explore the influence of arsenic pollution caused by coal-burning on methylation (promoter and exon 5) and mutation (exon 5) of human p53 gene, and to analyze the relationship between methylation, mutation and arsenism.	Arsenic	39-46	P53	Homo sapiens	148-151
21756780-14	2011	CONCLUSION: Arsenic pollution caused by coal-burning can cause the hypermethylation of p53 gene in promoter region, hypomethylation and mutation of p53 gene (exon 5), and the changes of methylation of p53 gene are related with its mutation and might be one of the important etiological factors of arsenic pathogenicity or carcinogenesis.	Arsenic	12-19	P53	Homo sapiens	87-90
21756780-14	2011	CONCLUSION: Arsenic pollution caused by coal-burning can cause the hypermethylation of p53 gene in promoter region, hypomethylation and mutation of p53 gene (exon 5), and the changes of methylation of p53 gene are related with its mutation and might be one of the important etiological factors of arsenic pathogenicity or carcinogenesis.	Arsenic	12-19	P53	Homo sapiens	148-151
21756780-14	2011	CONCLUSION: Arsenic pollution caused by coal-burning can cause the hypermethylation of p53 gene in promoter region, hypomethylation and mutation of p53 gene (exon 5), and the changes of methylation of p53 gene are related with its mutation and might be one of the important etiological factors of arsenic pathogenicity or carcinogenesis.	Arsenic	12-19	P53	Homo sapiens	148-151
21321360-6	2011	Importantly, lenalidomide decreased the percentage and clonogenicity of SP cells, and also induced phosphorylation changes in Akt, GSK-3alpha/beta, MEK1, c-Jun, p53, and p70S6K in SP cells.	Lenalidomide	13-25	P53	Homo sapiens	161-164
21435243-9	2011	The inhibition of Akt activity and p53-independent p21/CDKN1A and GADD45A overexpression were identified as the main molecular events responsible for CTet activity in MCF-7 and p53-mutant MDA-MB-231 cells.	ctet	150-154	P53	Homo sapiens	35-38
21435243-9	2011	The inhibition of Akt activity and p53-independent p21/CDKN1A and GADD45A overexpression were identified as the main molecular events responsible for CTet activity in MCF-7 and p53-mutant MDA-MB-231 cells.	ctet	150-154	P53	Homo sapiens	177-180
21107702-10	2011	To reactivate mutant p53 and reverse chemoresistance, ellipticine (5,11-dimethyl-6H-pyrido[4,3-b]carbazole) was used to treat mutant p53 cells.	ellipticine	54-65	P53	Homo sapiens	21-24
21107702-10	2011	To reactivate mutant p53 and reverse chemoresistance, ellipticine (5,11-dimethyl-6H-pyrido[4,3-b]carbazole) was used to treat mutant p53 cells.	ellipticine	54-65	P53	Homo sapiens	133-136
21107702-10	2011	To reactivate mutant p53 and reverse chemoresistance, ellipticine (5,11-dimethyl-6H-pyrido[4,3-b]carbazole) was used to treat mutant p53 cells.	ellipticine	67-106	P53	Homo sapiens	21-24
21107702-10	2011	To reactivate mutant p53 and reverse chemoresistance, ellipticine (5,11-dimethyl-6H-pyrido[4,3-b]carbazole) was used to treat mutant p53 cells.	ellipticine	67-106	P53	Homo sapiens	133-136
21107702-11	2011	Ellipticine enhanced p53 mitochondrial translocation, decreased Complex I activity, and sensitized p53 mutant cells to doxorubicin-induced apoptosis.	ellipticine	0-11	P53	Homo sapiens	21-24
21107702-11	2011	Ellipticine enhanced p53 mitochondrial translocation, decreased Complex I activity, and sensitized p53 mutant cells to doxorubicin-induced apoptosis.	ellipticine	0-11	P53	Homo sapiens	99-102
21107702-13	2011	Therefore, restoring mutant p53 by ellipticine may sensitize these cells to chemotherapy.	ellipticine	35-46	P53	Homo sapiens	28-31
21324703-0	2011	Synthesis and biological evaluation of imidazolo[2,1-b]benzothiazole derivatives, as potential p53 inhibitors.	imidazolo[2,1-b]benzothiazole	39-68	P53	Homo sapiens	95-98
21324703-3	2011	The biochemical and biological evaluations supported that compounds of the tetrahydrobenzothiazole series were inhibitors of the p53 transcriptional activity and were effective in enhancing paclitaxel-induced apoptosis.	tetrahydrobenzothiazole	75-98	P53	Homo sapiens	129-132
20473904-3	2011	The EBNA-5 binding to MDM2 counteracted destabilizing effect of the latter on the p53.	ebna-5	4-10	P53	Homo sapiens	82-85
21270522-2	2011	However, it is still unclear whether the p53 status of the target cell might influence the sensitivity to Saq-NO.	saquinavir-NO	106-112	P53	Homo sapiens	41-44
21270522-3	2011	In this study we evaluated the in vitro and in vivo activity of Saq-NO on the p53-deficient hormone resistant prostate cancer PC-3 cells.	saquinavir-NO	64-70	P53	Homo sapiens	78-81
21035490-2	2011	Whereas some investigations have suggested that ceramide and more complex sphingolipids function upstream of p53 or in a p53-independent manner, other studies propose that p53-dependent alterations in these sphingolipids can also contribute to apoptosis.	Ceramides	48-56	P53	Homo sapiens	109-112
21035490-4	2011	However, whereas various components of the sphingolipid and p53 pathways may simultaneously function to elicit apoptosis and/or growth inhibition, SMase and SK1 may undergo explicit regulation by p53 that could contribute to ceramide-induced senescence in cells.	Ceramides	225-233	P53	Homo sapiens	196-199
21273598-4	2011	RESULTS: Renieramycin M treatment caused p53 activation, which subsequently down-regulated anti-apoptotic MCL-1 and BCL-2 proteins, while the level of pro-apoptotic BAX protein was not altered.	renieramycin M	9-23	P53	Homo sapiens	41-44
21273598-7	2011	CONCLUSION: These results reveal that renieramycin M induced lung cancer cells apoptosis through p53-dependent pathway and the compound may inhibit progression and metastasis of lung cancer cells.	renieramycin M	38-52	P53	Homo sapiens	97-100
22041910-0	2011	High dose of pyridoxine induces IGFBP-3 mRNA expression in MCF-7 cells and its induction is inhibited by the p53-specific inhibitor pifithrin-alpha.	Pyridoxine	13-23	P53	Homo sapiens	109-112
22041910-7	2011	The induction of IGFBP-3 by PN was inhibited by a p53-specific inhibitor, pifithrin-alpha, in a dose-dependent manner, but was not affected by PD169316 (MAPK inhibitor), AS601245 (c-Jun N-terminal kinase inhibitor) or SL327 (MEK1/2 inhibitor).	Pyridoxine	28-30	P53	Homo sapiens	50-53
21077998-9	2010	Treatment with OA and (-)-sesamin induced p53-independent DNA damage responses in NSCLC cells, including G(1) /S checkpoint activation and apoptosis, as evidenced by phosphorylation of checkpoint proteins (H2AX, Nbs1, and Chk2), caspase-3 cleavage, and sub-G(1) accumulation.	sesamin	22-33	P53	Homo sapiens	42-45
21159612-0	2010	Combination of vorinostat and flavopiridol is selectively cytotoxic to multidrug-resistant neuroblastoma cell lines with mutant TP53.	Vorinostat	15-25	P53	Homo sapiens	128-132
20840854-0	2010	Non-dioxin-like PCBs interact with benzo[a]pyrene-induced p53-responses and inhibit apoptosis.	Dioxins	4-10	P53	Homo sapiens	58-61
20840854-0	2010	Non-dioxin-like PCBs interact with benzo[a]pyrene-induced p53-responses and inhibit apoptosis.	benzo[a]	35-43	P53	Homo sapiens	58-61
21187919-8	2010	Furthermore, the combination of MNP-Fe3O4 with adriamycin or daunorubicin increased p53 protein levels and decreased NF-kappaB protein levels more than adriamycin or daunorubicin alone, indicating that MNP-Fe3O4 could enhance the effect of chemotherapeutic drugs on p53 and NF-kappaB.	Daunorubicin	61-73	P53	Homo sapiens	84-87
21187919-8	2010	Furthermore, the combination of MNP-Fe3O4 with adriamycin or daunorubicin increased p53 protein levels and decreased NF-kappaB protein levels more than adriamycin or daunorubicin alone, indicating that MNP-Fe3O4 could enhance the effect of chemotherapeutic drugs on p53 and NF-kappaB.	Daunorubicin	61-73	P53	Homo sapiens	266-269
20655369-8	2010	Inhibition of cellular CYP3A4 or CYP1A/1B suppressed the aflatoxin B(1)- and dimethylbenz[a]anthracene-mediated P53 response, respectively, indicating that HepG2 cells are capable of metabolizing these compounds in a CYP1A/B/3A4-dependent manner.	anthracene	92-102	P53	Homo sapiens	112-115
20976259-7	2010	Cell lines with truncation, deletion, and null status of p53 were resistant to gemcitabine without apparent relationship to RRM1 levels.	gemcitabine	79-90	P53	Homo sapiens	57-60
20976259-9	2010	The impact of p53 mutations in patients treated with gemcitabine should be studied in prospective clinical trials to develop a model with improved precision of predicting drug efficacy.	gemcitabine	53-64	P53	Homo sapiens	14-17
20421190-9	2010	Although Akt signaling was activated, the accumulation of p53 led cells to apoptosis after treatment with 50 nM microcystin-LR for 24 hr.	Lawrencium	124-126	P53	Homo sapiens	58-61
20662736-7	2010	Anthracycline (topoisomerase II inhibitors such as mitoxantrone and ellipticine) and camptothecin (topoisomerase I inhibitor) derivatives including topotecan induce DNA double strand breaks, which activate the p53 pathway through the ataxia telangiectasia mutated-checkpoint kinase 2 (ATM-CHK2) DNA damage response pathway.	ellipticine	68-79	P53	Homo sapiens	210-213
20662736-8	2010	Although mitoxantrone, ellipticine, camptothecin, and topotecan all exhibited concentration-dependent disruption of the p53-hDM2 PPIB, they were much less potent than Nutlin-3.	ellipticine	23-34	P53	Homo sapiens	120-123
19859801-5	2010	We also found that treating MCF7 cells with DAC restored induction of DFNA5 by p53, as well as by two other p53 family genes, p63gamma and p73beta.	Decitabine	44-47	P53	Homo sapiens	79-82
19859801-5	2010	We also found that treating MCF7 cells with DAC restored induction of DFNA5 by p53, as well as by two other p53 family genes, p63gamma and p73beta.	Decitabine	44-47	P53	Homo sapiens	108-111
20226587-3	2010	Co-treatment of etoposide and KG-135 markedly elevated the expression and phosphorylation at the serine 15 residue of p53 as well as the cellular levels of Bax and p21(Waf1/Cip1).	kg-135	30-36	P53	Homo sapiens	118-121
20226587-4	2010	The increased accumulation and phosphorylation of p53 (Ser15) were attenuated by treatment of cells with wortmannin, a pan-phosphatidylinositol-3 kinase inhibitor.	Wortmannin	105-115	P53	Homo sapiens	50-53
20226587-6	2010	Our results indicate that etoposide-induced apoptosis in HeLa cells can be potentiated in the presence of KG-135 through a mechanism that involves the stabilization of p53 and the stimulation of Bax- and p21-mediated apoptotic signaling pathways.	kg-135	106-112	P53	Homo sapiens	168-171
20554748-0	2010	PTEN and p53 cross-regulation induced by soy isoflavone genistein promotes mammary epithelial cell cycle arrest and lobuloalveolar differentiation.	isoflavone genistein	45-65	P53	Homo sapiens	9-12
20558137-0	2010	Ascochlorin, an isoprenoid antibiotic, induces G1 arrest via downregulation of c-Myc in a p53-independent manner.	ascochlorin	0-11	P53	Homo sapiens	90-93
20558137-5	2010	Furthermore, we used a chromatin immunoprecipitation assay, RNA interference, and p53-deficient cells to verify that p21(WAF1/CIP1) induction by ascochlorin is related to transcriptional repression of c-Myc.	ascochlorin	145-156	P53	Homo sapiens	82-85
20558137-7	2010	These results suggest that ascochlorin induces G1 arrest via the p53-independent suppression of c-Myc.	ascochlorin	27-38	P53	Homo sapiens	65-68
20514393-0	2010	Inhibition of p53 sensitizes MCF-7 cells to ceramide treatment.	Ceramides	44-52	P53	Homo sapiens	14-17
20514393-3	2010	Ceramide induced a selective arrest of MCF-7 cells in the G1-phase, which was associated with a decreased expression of cyclins D and E and increased expression of p53 and p21.	Ceramides	0-8	P53	Homo sapiens	164-167
20514393-4	2010	Interestingly, inhibition of p53 using pifithrin alpha or RNAi sensitized MCF-7 cells to ceramide-induced cell death.	Ceramides	89-97	P53	Homo sapiens	29-32
20514393-6	2010	The increased sensitivity to ceramide, in the context of p53 inhibition, may be due to decreased expression of p21, as siRNA targeted to p21 also sensitized MCF-7 cells to ceramide-induced death.	Ceramides	29-37	P53	Homo sapiens	57-60
20514393-7	2010	These data demonstrate that in tumors with inactivating mutations of p53, ceramide-based therapies might provide a novel and effective treatment option.	Ceramides	74-82	P53	Homo sapiens	69-72
20587660-5	2010	These results suggest that ascofuranone upregulates p21(WAF1/CIP1) through p53-independent suppression of c-Myc expression, leading to cytostatic G(1) arrest.	ascofuranone	27-39	P53	Homo sapiens	75-78
20587660-6	2010	Thus, ascofuranone represents a unique natural antitumor compound that targets c-Myc independent of p53.	ascofuranone	6-18	P53	Homo sapiens	100-103
20171194-5	2010	Inhibition of p38 using SB202190 or SB203580 inhibited BEL-induced increases in P-p53 (ser15), p53 and p21, and altered the number of cells in G1 in LNCaP cells, and S-phase in PC-3 cells.	SB 203580	36-44	P53	Homo sapiens	82-85
20171194-5	2010	Inhibition of p38 using SB202190 or SB203580 inhibited BEL-induced increases in P-p53 (ser15), p53 and p21, and altered the number of cells in G1 in LNCaP cells, and S-phase in PC-3 cells.	SB 203580	36-44	P53	Homo sapiens	95-98
20587334-6	2010	Transient transfection assays indicated that overexpression of LBH or alphaB-crystallin reduced the transcriptional activities of p53 and p21, respectively, Overexpression of both alphaB-crystallin and LBH together resulted in a stronger repression of the transcriptional activities of p21 and p53.	alphab-crystallin	70-87	P53	Homo sapiens	294-297
20587334-6	2010	Transient transfection assays indicated that overexpression of LBH or alphaB-crystallin reduced the transcriptional activities of p53 and p21, respectively, Overexpression of both alphaB-crystallin and LBH together resulted in a stronger repression of the transcriptional activities of p21 and p53.	alphab-crystallin	180-197	P53	Homo sapiens	130-133
20587334-6	2010	Transient transfection assays indicated that overexpression of LBH or alphaB-crystallin reduced the transcriptional activities of p53 and p21, respectively, Overexpression of both alphaB-crystallin and LBH together resulted in a stronger repression of the transcriptional activities of p21 and p53.	alphab-crystallin	180-197	P53	Homo sapiens	294-297
20587334-7	2010	These results showed that the interaction of LBH and alphaB-crystallin may inhibit synergistically the transcriptional regulation of p53 and p21.	alphab-crystallin	53-70	P53	Homo sapiens	133-136
20124408-0	2010	SCH529074, a small molecule activator of mutant p53, which binds p53 DNA binding domain (DBD), restores growth-suppressive function to mutant p53 and interrupts HDM2-mediated ubiquitination of wild type p53.	SCH 529074	0-9	P53	Homo sapiens	48-51
20124408-0	2010	SCH529074, a small molecule activator of mutant p53, which binds p53 DNA binding domain (DBD), restores growth-suppressive function to mutant p53 and interrupts HDM2-mediated ubiquitination of wild type p53.	SCH 529074	0-9	P53	Homo sapiens	65-68
20124408-0	2010	SCH529074, a small molecule activator of mutant p53, which binds p53 DNA binding domain (DBD), restores growth-suppressive function to mutant p53 and interrupts HDM2-mediated ubiquitination of wild type p53.	SCH 529074	0-9	P53	Homo sapiens	65-68
20124408-0	2010	SCH529074, a small molecule activator of mutant p53, which binds p53 DNA binding domain (DBD), restores growth-suppressive function to mutant p53 and interrupts HDM2-mediated ubiquitination of wild type p53.	SCH 529074	0-9	P53	Homo sapiens	65-68
20124408-4	2010	Here, we report a small molecule, SCH529074, that binds specifically to the p53 DBD in a saturable manner with an affinity of 1-2 microm.	SCH 529074	34-43	P53	Homo sapiens	76-79
19874801-5	2010	In wild-type p53 expressing CML cells MK-0457 sensitivity was modulation by alterations in p53 levels through HDM-2 inhibition and gene silencing.	VX680	38-45	P53	Homo sapiens	13-16
19874801-5	2010	In wild-type p53 expressing CML cells MK-0457 sensitivity was modulation by alterations in p53 levels through HDM-2 inhibition and gene silencing.	VX680	38-45	P53	Homo sapiens	91-94
19638426-7	2010	Treating methylated CRC cell lines with 5-aza-2"-deoxycytidine restored p53-induced IGFBP7 expression.	Decitabine	40-62	P53	Homo sapiens	72-75
19889954-10	2010	Interestingly, in HCT116 colon cancer cells, SAHA suppressed cisplatin-induced p53 activation, but enhanced apoptosis.	Vorinostat	45-49	P53	Homo sapiens	79-82
20465648-12	2010	The role of ultra-violet induced p53 mutation in skin carcinogenesis reinforces retinoids chemoprevention.	ultra-violet	12-24	P53	Homo sapiens	33-36
20208142-3	2010	HepG2 (p53wt) and Hep3B (p53null) responded to panobinostat treatment with a reduction of cell proliferation and a significant increase in apoptotic cell death at low micromolar concentrations.	Panobinostat	47-59	P53	Homo sapiens	7-10
20208142-3	2010	HepG2 (p53wt) and Hep3B (p53null) responded to panobinostat treatment with a reduction of cell proliferation and a significant increase in apoptotic cell death at low micromolar concentrations.	Panobinostat	47-59	P53	Homo sapiens	25-28
20557688-9	2010	In conclusion, the release of ROS by PU- or PTFE-treated THP-1 cells may induce iNOS expression and cause apoptosis in HUVECs via the p53, Bax and Bcl-2 proteins.	Polytetrafluoroethylene	44-48	P53	Homo sapiens	134-137
20053762-7	2010	This compound abrogates an etoposide-induced G(2) arrest with an IC(50) of 55 nmol/L in HT29 cells, and significantly enhances the cell killing of gemcitabine and SN38 by 3.0- to 29-fold in several colon tumor lines in vitro and in a p53-dependent fashion.	gemcitabine	147-158	P53	Homo sapiens	234-237
20228131-0	2010	Cyclophosphamide dose intensification may circumvent anthracycline resistance of p53 mutant breast cancers.	Cyclophosphamide	0-16	P53	Homo sapiens	81-84
20228131-7	2010	A sharp statistical interaction was detected between p53 status and cyclophosphamide dose intensity.	Cyclophosphamide	68-84	P53	Homo sapiens	53-56
20228131-10	2010	Thus, our data strongly suggest that cyclophosphamide dose intensification in ER(-) p53-mutated breast cancer patients could significantly improve their response.	Cyclophosphamide	37-53	P53	Homo sapiens	84-87
20364585-5	2010	RESULTS: Phytic acid treatment significantly inhibited the growth of human gastric cancer cell SGC-7901 and markedly caused their apoptosis following downregulation of P53 protein expression.	Phytic Acid	9-20	P53	Homo sapiens	168-171
20364585-6	2010	CONCLUSION: The downregulation of apoptosis relative protein P53 expression was the possible mechanism of phytic acid induced growth inhibition and apoptosis in SGC-7901 cells.	Phytic Acid	106-117	P53	Homo sapiens	61-64
20211059-8	2010	NT4-p53(N15)-Ant on HepG2 cells was measured by a colorimetric 3-[4,5-dimethyl thiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay.	monooxyethylene trimethylolpropane tristearate	126-129	P53	Homo sapiens	4-7
20211059-10	2010	NT4-p53(N15)-Ant and its potential mechanism was detected by light microscopy, electron microscopy, MTT, LDH-release assay and annexin V-PI double staining.	monooxyethylene trimethylolpropane tristearate	100-103	P53	Homo sapiens	4-7
19751709-0	2009	Non-dioxin-like-PCBs phosphorylate Mdm2 at Ser166 and attenuate the p53 response in HepG2 cells.	Dioxins	4-10	P53	Homo sapiens	68-71
19903850-7	2009	Pursuing these findings, we have determined that imatinib-induced DNA damage is responsible for the increased activity of p53, identifying a novel off-target activity for this drug.	Imatinib Mesylate	49-57	P53	Homo sapiens	122-125
19915967-2	2009	In this study, we investigated the effects of lycopene on the oxidative injury and apoptosis of endothelial cells induced by H(2)O(2), and the effects of lycopene on the expression of p53, caspase-3 mRNA in injured cells.	Lycopene	154-162	P53	Homo sapiens	184-187
19682442-6	2009	Furthermore, [Ru(terpy)(bpy)Cl]Cl was able to activate the P53-dependent and independent pathways, and induced human hepatoma cells to undergo apoptosis.	[ru(terpy)(bpy)cl]cl	13-33	P53	Homo sapiens	59-62
19923910-6	2009	We further show that p53-reporter activity is induced in DLD1 putative cancer stem cell side-populations analyzed by their Hoechst dye efflux properties following treatment with the p53 pathway restoring drug ellipticine.	ellipticine	209-220	P53	Homo sapiens	21-24
19923910-6	2009	We further show that p53-reporter activity is induced in DLD1 putative cancer stem cell side-populations analyzed by their Hoechst dye efflux properties following treatment with the p53 pathway restoring drug ellipticine.	ellipticine	209-220	P53	Homo sapiens	182-185
19729440-3	2009	We observed ectopic UB outgrowth from the Wolffian duct (WD) in one third of p53(-/-) embryos.	BM	20-22	P53	Homo sapiens	77-80
19729440-5	2009	Transgenic expression of dominant negative p53 or conditional inactivation of p53 in the UB but not in the metanephric mesenchyme lineage recapitulated the duplex phenotype.	BM	89-91	P53	Homo sapiens	78-81
19729440-6	2009	Mechanistically, p53 inactivation in the WD associated with enhanced sensitivity to glial cell line-derived neurotrophic factor (GDNF)-induced ectopic budding and potentiated phosphatidylinositol-3 kinase activation by GDNF in UB cells.	BM	227-229	P53	Homo sapiens	17-20
19233506-7	2009	Interestingly, both strategies substantially decrease cell survival of MPM cells but the antitumor activity of Decitabine, differently from DNMT1 silencing, is mediated, at least in part, by a p53-independent p21 upregulation, and is characterized by the arrest of MPM cells at the G2/M phase of the cell cycle.	Decitabine	111-121	P53	Homo sapiens	193-196
19887545-6	2009	MK-1775 abrogates G(2) DNA damage checkpoint, leading to apoptosis in combination with DNA-damaging chemotherapeutic agents such as gemcitabine, carboplatin, and cisplatin selectively in p53-deficient cells.	gemcitabine	132-143	P53	Homo sapiens	187-190
19887545-6	2009	MK-1775 abrogates G(2) DNA damage checkpoint, leading to apoptosis in combination with DNA-damaging chemotherapeutic agents such as gemcitabine, carboplatin, and cisplatin selectively in p53-deficient cells.	Carboplatin	145-156	P53	Homo sapiens	187-190
19452524-7	2009	Ibuprofen-type drugs, IL6 polymorphisms (rs1800796) and dietary alpha-tocopherol and lycopene significantly altered likelihood of having a TP53 mutation.	Lycopene	85-93	P53	Homo sapiens	139-143
19737941-8	2009	Furthermore, subtoxic concentrations of suberoylanilide hydroxamic acid sensitize two TRAIL resistant human oral cancer cells, SAS and Ca9-22, to exogenous recombinant TRAIL-induced apoptosis in a p53-independent manner.	Vorinostat	40-71	P53	Homo sapiens	197-200
19157955-5	2009	Western blot analyses demonstrated that the expression of p21 protein was remarkably augmented and hyperacetylation of p53 was induced after SAHA treatment.	Vorinostat	141-145	P53	Homo sapiens	119-122
19533719-1	2009	Flexibility required: We designed intramolecular bipartite tetracysteine sites in loops of p53 and the beta-sheets of EmGFP.	tetracysteine	59-72	P53	Homo sapiens	91-94
19584241-4	2009	Here, we show that p53 wild-type NB cells are highly sensitive to SAM486A treatment.	4-amidinoindan-1-one 2'-amidinohydrazone	66-73	P53	Homo sapiens	19-22
19584241-5	2009	Most notably, SAM486A treatment resulted in the rapid accumulation of proapoptotic proteins p53 and Mdm2.	4-amidinoindan-1-one 2'-amidinohydrazone	14-21	P53	Homo sapiens	92-95
19513507-5	2009	Further, tumor suppressor p53 was overexpressed in two arsenic-resistant cell lines, but the levels of p53 mediators MDM2 and gankyrin, which regulate the ubiquitination of p53, increased simultaneously.	Arsenic	55-62	P53	Homo sapiens	26-29
19513507-5	2009	Further, tumor suppressor p53 was overexpressed in two arsenic-resistant cell lines, but the levels of p53 mediators MDM2 and gankyrin, which regulate the ubiquitination of p53, increased simultaneously.	Arsenic	55-62	P53	Homo sapiens	103-106
19513507-5	2009	Further, tumor suppressor p53 was overexpressed in two arsenic-resistant cell lines, but the levels of p53 mediators MDM2 and gankyrin, which regulate the ubiquitination of p53, increased simultaneously.	Arsenic	55-62	P53	Homo sapiens	103-106
19347028-8	2009	Using the property of p53, we can deliver the chemical (propidium iodine) into K-Ras mutated cells selectively.	Propidium	56-72	P53	Homo sapiens	22-25
18836721-0	2009	Cytotoxic diarylheptanoid induces cell cycle arrest and apoptosis via increasing ATF3 and stabilizing p53 in SH-SY5Y cells.	Diarylheptanoids	10-25	P53	Homo sapiens	102-105
19179467-0	2009	Myc sensitizes p53-deficient cancer cells to the DNA-damaging effects of the DNA methyltransferase inhibitor decitabine.	Decitabine	109-119	P53	Homo sapiens	15-18
19265193-2	2009	Here we demonstrate that p53 acetylation at Lys-320/Lys-373/Lys-382 is also required for its transcription-independent functions in BAX activation, reactive oxygen species production, and apoptosis in response to the histone deacetylase inhibitors (HDACi) suberoylanilide hydroxamic acid and LAQ824.	Vorinostat	256-287	P53	Homo sapiens	25-28
18951928-5	2009	We show that Zn/PDTC induces p53 proteasomal degradation and that the proteasome inhibitor MG132 further increases fibroblast growth inhibition by Zn/PDTC, suggesting that p53 degradation plays an important role in fibroblast resistance to Zn/PDTC.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	91-96	P53	Homo sapiens	172-175
19176374-1	2009	Inositol hexaphosphate (IP6) causes G(1) arrest and increases cyclin-dependent kinase inhibitors p21/Cip1 and p27/Kip1 protein levels in human prostate cancer (PCa) DU145 cells lacking functional p53.	Phytic Acid	0-22	P53	Homo sapiens	196-199
19176374-1	2009	Inositol hexaphosphate (IP6) causes G(1) arrest and increases cyclin-dependent kinase inhibitors p21/Cip1 and p27/Kip1 protein levels in human prostate cancer (PCa) DU145 cells lacking functional p53.	Phytic Acid	24-27	P53	Homo sapiens	196-199
19010910-1	2008	While the therapeutic activity of the deoxycytidine analogue decitabine is thought to reflect its ability to reactivate methylation-silenced genes, this agent is also known to trigger p53-dependent DNA damage responses.	Decitabine	61-71	P53	Homo sapiens	184-187
19010910-2	2008	Here, we report that p53-inducible ribonucleotide reductase (p53R2/RRM2B) is a robust transcriptional target of decitabine.	Decitabine	112-122	P53	Homo sapiens	21-24
19010910-3	2008	In cancer cells, decitabine treatment induces p53R2 mRNA expression, protein expression, and promoter activity in a p53-dependent manner.	Decitabine	17-27	P53	Homo sapiens	46-49
18819005-4	2008	The peroxynitrite generator SIN-1 promoted apoptosis in monocytes based on oligonucleosomal DNA fragmentation, caspase-3 and -9 activation, Bcl-2 depletion and accumulation of Bax and p53 proteins.	Peroxynitrous Acid	4-17	P53	Homo sapiens	184-187
18951438-7	2008	In this article we discuss how LSDBs can accomplish these goals, using existing databases for BRCA1, BRCA2, MSH2, MLH1, TP53, and CDKN2A to illustrate the progress and remaining challenges in this field.	lsdbs	31-36	P53	Homo sapiens	120-124
19181008-4	2008	Previously, an animal model was developed by our research group to investigate the expression of three genes c-myc, Ha-ras and p53 as early molecular epidemiological biomarkers of carcinogenic exposure or carcinogenesis caused by DMBA (dimethylbenz[alpha]anthracene).	dimethylbenz[alpha]anthracene	236-265	P53	Homo sapiens	127-130
21479491-4	2008	Two representative chemotherapeutic agents for pancreatic cancer, 5-fluorouracil and gemcitabine, promoted cell death in a p53-dependent manner; however, 1% hypoxia caused chemoresistance to these drugs.	gemcitabine	85-96	P53	Homo sapiens	123-126
18640142-1	2008	INTRODUCTION: Polymorphisms in p53, p21 and CCND1 could regulate the progression of the cell cycle and might increase the susceptibility to inorganic arsenic-related cancer risk.	Arsenic	150-157	P53	Homo sapiens	31-34
18633130-4	2008	We found that MK-0457, which itself activates p53 signaling, acts synergistically with Nutlin-3 to induce apoptosis in wild-type p53 AML cell lines OCI-AML-3 and MOLM-13 but not in p53-null HL-60 cells.	VX680	14-21	P53	Homo sapiens	46-49
18633130-4	2008	We found that MK-0457, which itself activates p53 signaling, acts synergistically with Nutlin-3 to induce apoptosis in wild-type p53 AML cell lines OCI-AML-3 and MOLM-13 but not in p53-null HL-60 cells.	VX680	14-21	P53	Homo sapiens	129-132
18633130-4	2008	We found that MK-0457, which itself activates p53 signaling, acts synergistically with Nutlin-3 to induce apoptosis in wild-type p53 AML cell lines OCI-AML-3 and MOLM-13 but not in p53-null HL-60 cells.	VX680	14-21	P53	Homo sapiens	129-132
18633130-5	2008	MK-0457 and Nutlin-3 showed synergism in inducing p53, conformational change of Bax and Deltapsi(m) loss, suggesting an involvement of p53-mediated mitochondrial apoptosis.	VX680	0-7	P53	Homo sapiens	50-53
18633130-5	2008	MK-0457 and Nutlin-3 showed synergism in inducing p53, conformational change of Bax and Deltapsi(m) loss, suggesting an involvement of p53-mediated mitochondrial apoptosis.	VX680	0-7	P53	Homo sapiens	135-138
18708766-4	2008	DP, TSA and SAHA inhibited Aurora A, Aurora B and survivin expression with kinetics that were remarkably similar within individual cell lines, and appeared to coincide with p53 expression status.	dp	0-2	P53	Homo sapiens	173-176
18458532-3	2008	Cells with differing p53 genotype showed susceptibility to FNQ.	napabucasin	59-62	P53	Homo sapiens	21-24
18458532-4	2008	However, this response was attenuated in those overexpressing mutant p53, although a brief p53 induction was early seen in FNQ-treated wt p53 cells.	napabucasin	123-126	P53	Homo sapiens	91-94
18458532-4	2008	However, this response was attenuated in those overexpressing mutant p53, although a brief p53 induction was early seen in FNQ-treated wt p53 cells.	napabucasin	123-126	P53	Homo sapiens	91-94
18704310-11	2008	SB203580 significantly increased the level of cellular phosphorylated p53 protein, but decreased the p-gp protein level and MDR1 mRNA level in A2780/Taxol cells.	SB 203580	0-8	P53	Homo sapiens	70-73
18723490-4	2008	We previously identified a family of small molecules (HLI98s, 7-nitro-10-aryl-5-deazaflavins) that inhibit the E3 activity of Hdm2, increase cellular p53, and selectively kill transformed cells expressing wild-type p53.	7-nitro-10-aryl-5-deazaflavins	62-92	P53	Homo sapiens	150-153
18723490-4	2008	We previously identified a family of small molecules (HLI98s, 7-nitro-10-aryl-5-deazaflavins) that inhibit the E3 activity of Hdm2, increase cellular p53, and selectively kill transformed cells expressing wild-type p53.	7-nitro-10-aryl-5-deazaflavins	62-92	P53	Homo sapiens	215-218
18325917-2	2008	We analysed the efficacy of a preoperative combination between 5-fluorouracil, anthracyclines and cyclophosphamide according to both p53 status and molecular classification.	Cyclophosphamide	98-114	P53	Homo sapiens	133-136
21783897-0	2008	Suppression of zinc-induced p53 phosphorylation and p21 expression by wortmannin in A549 human pulmonary epithelial cells.	Wortmannin	70-80	P53	Homo sapiens	28-31
21783897-2	2008	Treatment with wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI3K)-related kinases, suppressed ZnSO(4)-induced phosphorylation and accumulation of p53 protein.	Wortmannin	15-25	P53	Homo sapiens	160-163
21783897-3	2008	Expression of cyclin-dependent kinase inhibitor p21, one of the genes regulated by p53, was up-regulated following exposure to ZnSO(4), and suppressed by preincubation with wortmannin.	Wortmannin	173-183	P53	Homo sapiens	83-86
21783897-4	2008	These results suggest that zinc might induce the phosphorylation of p53 at Ser15 through wortmannin-sensitive pathway(s) at least in part, and result in the transactivation of the p21 gene in this human pulmonary epithelial cell line.	Wortmannin	89-99	P53	Homo sapiens	68-71
18511169-6	2008	Specific ATM inhibitor, caffeine, significantly decreased KTA-mediated G2/M arrest by inhibiting the phosphorylation of p53 (Serine15) and Chk2.	kotomolide A	58-61	P53	Homo sapiens	120-123
18511169-8	2008	Taken together, these results suggest a critical role for ATM and p53 in KTA-induced G2/M arrest and apoptosis of human non-small cell lung cancer cells.	kotomolide A	73-76	P53	Homo sapiens	66-69
18400537-10	2008	These studies indicate that p53 specifically drives de novo ceramide synthesis by activation of a ceramide synthase that favors the synthesis of N-palmitoylsphingosine.	Ceramides	60-68	P53	Homo sapiens	28-31
18289623-10	2008	Inhibition of ATM/ATR, PI3-kinase and Chk1/Chk2 by CGK733, wortmannin and DBH, respectively, attenuated the apoptotic response in p53(wt) but not p53(mt) cells.	Wortmannin	59-69	P53	Homo sapiens	130-133
18263706-1	2008	Treatment of cancer patients with anthracyclin-based chemotherapeutic drugs induces congestive heart failure by a mechanism involving p53.	anthracyclin	34-46	P53	Homo sapiens	134-137
19145821-6	2008	The use of erbisol and glutargin in multimodality therapy normalizes the plasma concentration of TNF-alpha and diminishes the blood content of protein P53 by 33% and sTRAIL - by 42% which, nevertheless remains higher than the control value by 58% and 36% respectively.	arginine glutamate	23-32	P53	Homo sapiens	151-154
18181020-0	2008	A high-content chemical screen identifies ellipticine as a modulator of p53 nuclear localization.	ellipticine	42-53	P53	Homo sapiens	72-75
18181020-5	2008	With this image-based assay, we identified ellipticine that increased the nuclear localization of GFP-mutant p53 protein but not GFP alone in Saos-2 osteosarcoma cells.	ellipticine	43-54	P53	Homo sapiens	109-112
18181020-6	2008	In addition, ellipticine increased the nuclear localization of endogenous p53 in HCT116 colon cancer cells with a resultant increase in the transactivation of the p21 promoter.	ellipticine	13-24	P53	Homo sapiens	74-77
18181020-7	2008	Increased nuclear p53 after ellipticine treatment was not associated with an increase in DNA double stranded breaks, indicating that ellipticine shifts p53 to the nucleus through a mechanism independent of DNA damage.	ellipticine	28-39	P53	Homo sapiens	18-21
18181020-7	2008	Increased nuclear p53 after ellipticine treatment was not associated with an increase in DNA double stranded breaks, indicating that ellipticine shifts p53 to the nucleus through a mechanism independent of DNA damage.	ellipticine	28-39	P53	Homo sapiens	152-155
18181020-7	2008	Increased nuclear p53 after ellipticine treatment was not associated with an increase in DNA double stranded breaks, indicating that ellipticine shifts p53 to the nucleus through a mechanism independent of DNA damage.	ellipticine	133-144	P53	Homo sapiens	18-21
18181020-7	2008	Increased nuclear p53 after ellipticine treatment was not associated with an increase in DNA double stranded breaks, indicating that ellipticine shifts p53 to the nucleus through a mechanism independent of DNA damage.	ellipticine	133-144	P53	Homo sapiens	152-155
18204081-9	2008	We propose that oncogenic stress induced by ras causes ceramide accumulation, therefore, increasing PPP1CA activity, pRb dephosphorylation and onset of the p53-induced arrest, contributing to tumor suppression.	Ceramides	55-63	P53	Homo sapiens	156-159
18037521-2	2008	METHODS: Molecular effects of P-Tyr at the level of EGFR responses were investigated in vitro with TP53-wildtype bronchial carcinoma cell line A549, which is radio-protected by P-Tyr treatment.	O-phospho-L-tyrosine	30-35	P53	Homo sapiens	99-103
18037521-2	2008	METHODS: Molecular effects of P-Tyr at the level of EGFR responses were investigated in vitro with TP53-wildtype bronchial carcinoma cell line A549, which is radio-protected by P-Tyr treatment.	O-phospho-L-tyrosine	177-182	P53	Homo sapiens	99-103
17724467-0	2008	Analysis of transactivation capability and conformation of p53 temperature-dependent mutants and their reactivation by amifostine in yeast.	Amifostine	119-129	P53	Homo sapiens	59-62
17724467-6	2008	Amifostine-induced p53 reactivation occurred only in 13 of 23 td mutants, and this effect was temperature dependent and responsive element specific.	Amifostine	0-10	P53	Homo sapiens	19-22
18347429-4	2008	After VX2 rabbit hepatocarcinoma model was established, the transferrin-p53-LipofectAMINE complex was delivered into the hepatic artery via interventional techniques to analyze the therapeutic p53 gene transfer efficiency in vivo by Western blot, immunohistochemical/immunofluorescence staining analysis and survival time.	Lipofectamine	76-89	P53	Homo sapiens	72-75
17977830-0	2008	An ATM- and Rad3-related (ATR) signaling pathway and a phosphorylation-acetylation cascade are involved in activation of p53/p21Waf1/Cip1 in response to 5-aza-2"-deoxycytidine treatment.	Decitabine	153-175	P53	Homo sapiens	121-124
17977830-3	2008	In this study, the relationship between p53 activation and its posttranslational modifications was investigated in the human cancer cell lines A549 and HCT116 in response to 5-aza-2"-deoxycytidine (5-aza-CdR) or cytarabine treatment.	Decitabine	174-196	P53	Homo sapiens	40-43
18193822-5	2008	ROS and RNS escape results in the activation of cytosolic stress pathways, DNA damage, and the upregulation of JNK, p38, and p53.	Reactive Nitrogen Species	8-11	P53	Homo sapiens	125-128
18043262-7	2008	Subsequently, PRIMA-1 and ellipticine were found to be able to induce mutant p53-dependent cell death.	ellipticine	26-37	P53	Homo sapiens	77-80
18097557-2	2008	Trichostatin A (TSA), ITF2357 and suberoylanilide hydroxamic acid (SAHA), which were very effective agents, caused apoptotic effects after a lag phase of 12-16 h. In order to elucidate the mechanism of HDACIs action in HepG2 cells we have studied the effects of TSA, ITF2357 and SAHA on acetylation of p53 and histones H2A, H2B, H3 and H4.	Vorinostat	34-65	P53	Homo sapiens	302-305
18097557-2	2008	Trichostatin A (TSA), ITF2357 and suberoylanilide hydroxamic acid (SAHA), which were very effective agents, caused apoptotic effects after a lag phase of 12-16 h. In order to elucidate the mechanism of HDACIs action in HepG2 cells we have studied the effects of TSA, ITF2357 and SAHA on acetylation of p53 and histones H2A, H2B, H3 and H4.	Vorinostat	67-71	P53	Homo sapiens	302-305
18089819-9	2007	Therefore, functional p53 seems to stimulate the repair of CNU-induced cross-links and/or DSBs generated from CNU-induced lesions.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	90-94	P53	Homo sapiens	22-25
16333835-4	2007	This case along with a comprehensive review of the literature, illustrate the importance of both somatic and germline TP53 mutations in the pathogenesis MTT.	monooxyethylene trimethylolpropane tristearate	153-156	P53	Homo sapiens	118-122
18261311-5	2007	The effects of Ad-p53 on ADM mediated drug resistance were observed by MTT assay.	monooxyethylene trimethylolpropane tristearate	71-74	P53	Homo sapiens	18-21
17698841-8	2007	HDM2 was stabilized in the HCMV-infected cells by MG132, indicating a shift from p53 to HDM2 ubiquitination.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	P53	Homo sapiens	81-84
17515610-5	2007	p21CIP1 was found to be a critical p53 target for arrest induced by hydroxyurea or aphidicolin, but not etoposide, as judged by the ability of p21CIP1 suppression to mimic the effects of p53 disruption.	Aphidicolin	83-94	P53	Homo sapiens	35-38
17515610-5	2007	p21CIP1 was found to be a critical p53 target for arrest induced by hydroxyurea or aphidicolin, but not etoposide, as judged by the ability of p21CIP1 suppression to mimic the effects of p53 disruption.	Aphidicolin	83-94	P53	Homo sapiens	187-190
17602818-2	2007	Cells that acquire BaP/BPDE-induced DNA damage undergo S-phase arrest in a p53-independent manner.	bap/bpde	19-27	P53	Homo sapiens	75-78
17509529-1	2007	Using high-throughput screening with small-molecule libraries, we identified a compound, KCG165 [(2-(3-(2-(pyrrolidin-1-yl)ethoxy)-1,10b-dihydro-[1,2,4]triazolo[1,5-c]quinazolin-5(6H)-one)], which strongly activated p53-mediated transcriptional activity.	2-(3-(2-(pyrrolidin-1-yl)ethoxy)-1,10b-dihydro-[1,2,4]triazolo[1,5-c]quinazolin-5(6h)-one	98-187	P53	Homo sapiens	216-219
17718444-0	2007	[Real-time PCR used to detect p53 gene damage in workers exposed to arsenic].	Arsenic	68-75	P53	Homo sapiens	30-33
17718444-1	2007	OBJECTIVE: To evaluate the relationship between the metabolism of arsenic and the damage of exon 5 and 8 of p53 gene from workers in a arsenic mill, and with real-time PCR technique, to establish the method probing the gene-specific DNA damage in people.	Arsenic	66-73	P53	Homo sapiens	108-111
17718444-1	2007	OBJECTIVE: To evaluate the relationship between the metabolism of arsenic and the damage of exon 5 and 8 of p53 gene from workers in a arsenic mill, and with real-time PCR technique, to establish the method probing the gene-specific DNA damage in people.	Arsenic	135-142	P53	Homo sapiens	108-111
17718444-2	2007	METHODS: By real-time PCR, the damages of exon 5 and 8 of p53 gene were probed in 37 workers exposed highly to, 16 manager and logistic employees exposed less to an arsenic mill in Yunnan province, and also 25 local people who did not contact with any white arsenic in near past time.	Arsenic	165-172	P53	Homo sapiens	58-61
17718444-2	2007	METHODS: By real-time PCR, the damages of exon 5 and 8 of p53 gene were probed in 37 workers exposed highly to, 16 manager and logistic employees exposed less to an arsenic mill in Yunnan province, and also 25 local people who did not contact with any white arsenic in near past time.	Arsenic	258-265	P53	Homo sapiens	58-61
17718444-4	2007	The correlation between metabolism of arsenic and damage of p53 gene was evaluated.	Arsenic	38-45	P53	Homo sapiens	60-63
17718444-9	2007	The Ct relative value of exon 5 of p53 gene in high exposed group was higher than that in control male (P &lt; 0.05), and the increased tendency of Ct relative value of exon 5 of p53 gene was found in workers with organic arsenic concentration going up (r(s) = 0.355, P = 0.011).	Arsenic	222-229	P53	Homo sapiens	35-38
17718444-9	2007	The Ct relative value of exon 5 of p53 gene in high exposed group was higher than that in control male (P &lt; 0.05), and the increased tendency of Ct relative value of exon 5 of p53 gene was found in workers with organic arsenic concentration going up (r(s) = 0.355, P = 0.011).	Arsenic	222-229	P53	Homo sapiens	179-182
17718444-11	2007	CONCLUSION: The damages in exon 5 and 8 of p53 gene in workers exposed to arsenic may be induced.	Arsenic	74-81	P53	Homo sapiens	43-46
17585201-4	2007	A protease inhibitor N-Ac-Leu-Leu-norleucinal (ALLN) drastically increased the amount of p53 in HCT116 colon carcinoma cells, but it had no effect on the already high p53 level in a p21(-/-) derivative of this cell line.	n-ac-leu-leu	21-33	P53	Homo sapiens	89-92
16973168-5	2007	In addition, the high-arsenic exposure group with one or two variant genotypes of GSTP1 and p53 had 2.8- and 6.1-fold higher risks of carotid atherosclerosis, respectively, and showed a dose-dependent relationship.	Arsenic	22-29	P53	Homo sapiens	92-95
17146434-5	2007	Nutlin-3a also increased the cytotoxicity of both carboplatin and doxorubicin in a series of p53-mutant human tumor cell lines.	Carboplatin	50-61	P53	Homo sapiens	93-96
17371049-10	2007	At 20 degrees C, residual native-like structure was detected around Trp53 at high concentrations of denaturant.	denaturant	100-110	P53	Homo sapiens	68-73
17401425-5	2007	Chronic infection with HBV and HCV viruses, and oxyradical disorders including hemochromatosis, also generate reactive oxygen/nitrogen species that can both damage DNA and mutate cancer-related genes such as TP53.	reactive oxygen/nitrogen species	110-142	P53	Homo sapiens	208-212
17454128-2	2007	We demonstrated that UVA-irradiated NADH induced damage to (32)P-labeled DNA fragments obtained from the p53 gene in the presence of Cu(II).	Phosphorus-32	59-64	P53	Homo sapiens	105-108
17406801-0	2007	Radiosensitization dependent on p53 function in bronchial carcinoma cells by the isoflavone genistein and estradiol in vitro.	isoflavone genistein	81-101	P53	Homo sapiens	32-35
17226097-9	2007	Our findings also support the hypothesis that NF-kappaB- and/or p53-mediated neuronal cell death is prevented through decreasing oxidative stress by pitavastatin.	pitavastatin	149-161	P53	Homo sapiens	64-67
17158200-8	2007	In addition, cidofovir treatment of FGF2-T-MAE cells resulted in a pronounced up-regulation of the tumor suppressor protein p53.	Cidofovir	13-22	P53	Homo sapiens	124-127
17991682-5	2007	Long ADP-ribose chains (55-mer) promoted the formation of three specific complexes with p53.	Ribose	9-15	P53	Homo sapiens	88-91
17966099-7	2007	Therapy increased p53 expression and p53 phosphorylation at Ser392 and Ser20, and these changes correlated with poly-ADP-ribose levels and Ki-67 expression.	Ribose	121-127	P53	Homo sapiens	18-21
16849690-10	2006	During cisplatin incubation, VAD protected ATM and enhanced p53 phosphorylation.	VAD I protocol	29-32	P53	Homo sapiens	60-63
17032312-10	2006	Immunohistochemically, p53 protein expression in PG-Ca was significantly higher in loss of heterozygosity-positive cases with altered Chr.17 markers overall, especially the D17S796 marker, compared to cases without genetic instability.	pg-ca	49-54	P53	Homo sapiens	23-26
17029827-3	2006	The p53 protein activation appeared to have been a downstream response to the benzo[a]pyrene-induced DNA damage, suggesting p53 plays important roles in the defense against benzo[a]pyrene-induced genotoxicity.	benzo[a]	78-86	P53	Homo sapiens	4-7
17029827-3	2006	The p53 protein activation appeared to have been a downstream response to the benzo[a]pyrene-induced DNA damage, suggesting p53 plays important roles in the defense against benzo[a]pyrene-induced genotoxicity.	benzo[a]	78-86	P53	Homo sapiens	124-127
16930632-0	2006	Association of specific p53 polymorphisms with keratosis in individuals exposed to arsenic through drinking water in West Bengal, India.	Arsenic	83-90	P53	Homo sapiens	24-27
16930632-5	2006	This prompted us to study the association of three p53 polymorphisms with arsenic induced keratosis in a population exposed to arsenic through drinking water.	Arsenic	74-81	P53	Homo sapiens	51-54
16930632-5	2006	This prompted us to study the association of three p53 polymorphisms with arsenic induced keratosis in a population exposed to arsenic through drinking water.	Arsenic	127-134	P53	Homo sapiens	51-54
17109072-0	2006	Taurine chloramine inhibits proliferation of rheumatoid arthritis synoviocytes by triggering a p53-dependent pathway.	N-chlorotaurine	0-18	P53	Homo sapiens	95-98
17109072-7	2006	RESULTS: Treatment of RA FLS with Tau-Cl (200-500 microM) resulted in an early nuclear accumulation of p53 tumor suppressor protein.	N-chlorotaurine	34-40	P53	Homo sapiens	103-106
17109072-8	2006	Moreover, Tau-Cl inhibited PDGF-triggered cell proliferation (IC(50) value approximately 250-300 microM), accompanied by characteristic modulation of p53 transcriptional targets: down-regulation of proliferating cell nuclear antigen (PCNA) and survivin, and concomitant up-regulation of p21 mitotic inhibitor.	N-chlorotaurine	10-16	P53	Homo sapiens	150-153
17109072-9	2006	CONCLUSION: We propose that Tau-Cl inhibits proliferation of RA FLS by triggering a p53-dependent cell-cycle arrest and conclude that this compound suppresses pathways in FLS that are known to contribute to the pathology of RA.	N-chlorotaurine	28-34	P53	Homo sapiens	84-87
16682957-4	2006	Cooperation between p53 and NF-kappaB was required for activation of COX-2 promoter in response to daunomycin, a DNA-damaging agent.	Daunorubicin	99-109	P53	Homo sapiens	20-23
16682957-5	2006	Pharmacological inhibition of Cox-2 enhanced apoptosis in response to daunomycin, in particular in cells containing active p53.	Daunorubicin	70-80	P53	Homo sapiens	123-126
16807664-12	2006	These cellular abnormalities relate to the p53 dysfunction induced by arsenic.	Arsenic	70-77	P53	Homo sapiens	43-46
16518841-5	2006	Treatment with ginsenoside Rg1, which blocked the cell cycle in the G1-phase, induced a downregulation of cyclin D1 and an upregulation in the expression of p53, p21(WAF/CIP1), and p27(KIP1).	Ginsenosides	15-26	P53	Homo sapiens	157-160
16651519-4	2006	We show that the tumor suppressor p53 is selectively activated by imatinib in BCR-ABL-expressing cells as a result of BCR-ABL kinase inhibition.	Imatinib Mesylate	66-74	P53	Homo sapiens	34-37
16651519-5	2006	Inactivation of p53, which can accompany disease progression in human CML, impedes the response to imatinib in vitro and in vivo without preventing BCR-ABL kinase inhibition.	Imatinib Mesylate	99-107	P53	Homo sapiens	16-19
16651519-6	2006	Concordantly, p53 mutations are associated with progression to imatinib resistance in some human CMLs.	Imatinib Mesylate	63-71	P53	Homo sapiens	14-17
16510557-7	2006	The addition of wortmannin partially prevented cryptolepine-induced expression of p53 and p21(Cip1/WAF1) together with the S-phase block and sensitized cells to induction of cell death.	Wortmannin	16-26	P53	Homo sapiens	82-85
16337242-0	2006	Ellipticine induces apoptosis through p53-dependent pathway in human hepatocellular carcinoma HepG2 cells.	ellipticine	0-11	P53	Homo sapiens	38-41
16337242-5	2006	Ellipticine treatment was found to result in the upregulation of p53, Fas/APO-1 receptor and Fas ligand.	ellipticine	0-11	P53	Homo sapiens	65-68
16673057-0	2006	MG132 induced apoptosis is associated with p53-independent induction of pro-apoptotic Noxa and transcriptional activity of beta-catenin.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	P53	Homo sapiens	43-46
16673057-10	2006	In summary, our results demonstrate that MG132 induces the pro-apoptotic protein Noxa via a p53-independent mechanism that leads to caspase-dependent apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	41-46	P53	Homo sapiens	92-95
16506813-7	2006	Pretreatment with green tea polyphenol epigallocatechin-3-gallate (EGCG) effectively blocked peroxynitrite-induced glutathione depletion, p53 accumulation, and apoptosis in both normal and G6PD-deficient cells.	Peroxynitrous Acid	93-106	P53	Homo sapiens	138-141
16180010-8	2006	An inhibitor of phosphatidylinositol 3-kinase-related kinase (PIKK) pathway (wortmannin) suppressed the increase of p53 and its phosphorylation at Ser15.	Wortmannin	77-87	P53	Homo sapiens	116-119
16290060-7	2006	Moreover, proliferating cell nuclear antigen and p53 were expressed in 8-nitroguanine-positive epithelial cells in the basal layer.	8-nitroguanine	71-85	P53	Homo sapiens	49-52
16427050-2	2006	We found that LXR-mediated trans-activation was inhibited by 3-methylchoranthrene (MC) and doxorubicin (Dox) in HepG2 cells carrying wild-type p53, but not in Hep3B cells possessing mutant p53.	Methylcholanthrene	83-85	P53	Homo sapiens	189-192
16505117-9	2006	Furthermore, sanguinarine treatment was found to result in significant modulations in p53, p66Shc, MsrA, and superoxide dismutase levels.	sanguinarine	13-25	P53	Homo sapiens	86-89
16251483-4	2006	Significant DNA hypermethylation of promoter region of p53 gene was observed in DNA of arsenic-exposed people compared to control subjects.	Arsenic	87-94	P53	Homo sapiens	55-58
16251483-6	2006	Further, hypermethylation of p53 gene was also observed in arsenic-induced skin cancer patients compared to subjects having skin cancer unrelated to arsenic, though not at significant level.	Arsenic	59-66	P53	Homo sapiens	29-32
16251483-6	2006	Further, hypermethylation of p53 gene was also observed in arsenic-induced skin cancer patients compared to subjects having skin cancer unrelated to arsenic, though not at significant level.	Arsenic	149-156	P53	Homo sapiens	29-32
16251483-9	2006	In man, arsenic has the ability to alter DNA methylation patterns in gene p53 and p16, which are important in carcinogenesis.	Arsenic	8-15	P53	Homo sapiens	74-77
17135787-9	2006	The combination effect of rAAV-wt-p53 and cisplatin was measured by MTT assay.	monooxyethylene trimethylolpropane tristearate	68-71	P53	Homo sapiens	34-37
15887239-3	2005	We demonstrated that vitamin C inhibits DNA synthesis in HeLa cells and, mainly the form of dehydroascorbic acid (DHA), delays the entry of p53-deficient synchronized HeLa and T98G cancer cells into mitosis.	Dehydroascorbic Acid	92-112	P53	Homo sapiens	140-143
15887239-3	2005	We demonstrated that vitamin C inhibits DNA synthesis in HeLa cells and, mainly the form of dehydroascorbic acid (DHA), delays the entry of p53-deficient synchronized HeLa and T98G cancer cells into mitosis.	Dehydroascorbic Acid	114-117	P53	Homo sapiens	140-143
16273653-6	2005	RESULTS: The group transfected with pCMVp53 alone exhibited higher luciferase activity and higher apoptosis rate, otherwise, the p53 expression and reporter activity of PG13-CAT or P21-luc as well as cell apoptosis rate were obviously higher in the group cotransfected of pCMVp53 with pCMVHBVa, but not in the other cotransfected group.	pg13-cat	169-177	P53	Homo sapiens	40-43
16131836-5	2005	Global genomic DNA demethylation induced by 5-Aza-deoxycytidine activates the p53 signaling pathway and induces apoptosis, suggesting that DNA methylation mediated by Dnmts is associated with p53 signaling in maintaining genome stability.	Decitabine	44-63	P53	Homo sapiens	78-81
16131836-5	2005	Global genomic DNA demethylation induced by 5-Aza-deoxycytidine activates the p53 signaling pathway and induces apoptosis, suggesting that DNA methylation mediated by Dnmts is associated with p53 signaling in maintaining genome stability.	Decitabine	44-63	P53	Homo sapiens	192-195
16005638-5	2005	Inhibition of CXCR 4 by AMD 3100 abrogates the effect of gp120 on both p53 and Apaf-1.	plerixafor	24-32	P53	Homo sapiens	71-74
15967209-5	2005	Both mutation type and hot spots of p53 gene were significantly different in arsenic-induced and non-arsenic-induced TCCs.	Arsenic	77-84	P53	Homo sapiens	36-39
15967209-5	2005	Both mutation type and hot spots of p53 gene were significantly different in arsenic-induced and non-arsenic-induced TCCs.	Arsenic	101-108	P53	Homo sapiens	36-39
16025287-5	2005	Treatment with 5-aza-2"-deoxycytidine (5-aza-dC) led to up-regulated expression of TP53 mRNA and protein in U87MG and T98G cells, suggesting that promoter methylation is associated with reduced expression in some malignant glioma cells.	Decitabine	15-37	P53	Homo sapiens	83-87
16025287-5	2005	Treatment with 5-aza-2"-deoxycytidine (5-aza-dC) led to up-regulated expression of TP53 mRNA and protein in U87MG and T98G cells, suggesting that promoter methylation is associated with reduced expression in some malignant glioma cells.	Decitabine	39-47	P53	Homo sapiens	83-87
15961301-0	2005	Bitter gourd seed fatty acid rich in 9c,11t,13t-conjugated linolenic acid induces apoptosis and up-regulates the GADD45, p53 and PPARgamma in human colon cancer Caco-2 cells.	13t	44-47	P53	Homo sapiens	121-124
15738655-3	2005	In this study, we evaluated the effect of pioglitazone on p53 and p21 expression in various cancer cell lines with different p53 status.	Pioglitazone	42-54	P53	Homo sapiens	58-61
15727877-4	2005	3-(1-Piperazinyl)methyl and 3-(quinuclidin-3-yl)aminomethyl derivatives of 4,11-dihydroxynaphtho[2,3-f]indole-5,10-dione killed HCT116 colon carcinoma cells (carrying wild type p53) and their p53-null variant within the similar range of concentrations.	3-(1-piperazinyl)methyl	0-23	P53	Homo sapiens	192-195
15703812-0	2005	Microtubule inhibitor D-24851 induces p53-independent apoptotic cell death in malignant glioma cells through Bcl-2 phosphorylation and Bax translocation.	indibulin	22-29	P53	Homo sapiens	38-41
15703812-10	2005	Our results indicated that D-24851 effectively induces apoptosis through Bcl-2 phosphorylation and Bax translocation in human malignant glioma cells in a p53-independent manner.	indibulin	27-34	P53	Homo sapiens	154-157
15854392-12	2005	CONCLUSIONS: p53 mutation induced by cisplatin/carboplatin might play an important role in the development of acquired multi-drug resistance of lung cancer chemotherapy.	Carboplatin	47-58	P53	Homo sapiens	13-16
15533933-7	2005	Consistent with ATM or ATR activation, hyperoxia induced wortmannin-sensitive phosphorylation of Chk1, Chk2, and p53.	Wortmannin	57-67	P53	Homo sapiens	113-116
16196300-4	2005	MTT showed that p53 gene alone induced strong inhibitory effect on the growth of U251 cells (inhibition rate (IR), (79.60 +/- 5.69)%).	monooxyethylene trimethylolpropane tristearate	0-3	P53	Homo sapiens	16-19
15548818-8	2004	An increase in p53 expression was found in the 4 mg/ml trypan blue treated group at 10-30 minutes after trypan blue application.	Trypan Blue	55-66	P53	Homo sapiens	15-18
15548818-8	2004	An increase in p53 expression was found in the 4 mg/ml trypan blue treated group at 10-30 minutes after trypan blue application.	Trypan Blue	104-115	P53	Homo sapiens	15-18
15476743-0	2004	Extracellular signal-regulated kinase activation and Bcl-2 downregulation mediate apoptosis after gemcitabine treatment partly via a p53-independent pathway.	gemcitabine	98-109	P53	Homo sapiens	133-136
15476743-3	2004	We studied the molecular mechanisms of gemcitabine-induced apoptosis and determined the role of p53 function on the cytotoxic effects of gemcitabine in human nonsmall cell lung cancer (NSCLC) H1299 and H1299/p53 cells.	gemcitabine	137-148	P53	Homo sapiens	96-99
15453709-0	2004	Induction of apoptosis by shikonin through coordinative modulation of the Bcl-2 family, p27, and p53, release of cytochrome c, and sequential activation of caspases in human colorectal carcinoma cells.	shikonin	26-34	P53	Homo sapiens	97-100
15453709-6	2004	Here, we found that shikonin-induced apoptotic cell death was accompanied by upregulation of p27, p53, and Bad and down-regulation of Bcl-2 and Bcl-X(L), while shikonin had little effect on the levels of Bax protein.	shikonin	20-28	P53	Homo sapiens	98-101
15464472-13	2004	Combined gemcitabine and bortezomib enhanced p21 and p53 expression and induced S-phase and G2/M cell-cycle arrests, respectively.	gemcitabine	9-20	P53	Homo sapiens	53-56
16200870-6	2004	There was a significant correlation between p53 mutation with simultaneous expression of Pgp and MRP1 and drug-resistance to either vinorelbine or carboplatin.	Carboplatin	147-158	P53	Homo sapiens	44-47
15304255-6	2004	Using (32)P-labeled DNA fragments from the human p53 tumor suppressor gene, 4-HC was found to cause Cu(II)-mediated oxidative DNA damage, but CP did not.	Phosphorus-32	6-11	P53	Homo sapiens	49-52
15342409-5	2004	Functional analysis showed that p53 significantly enhanced the sequential activities of hOGG1 and APE in excising the 8-oxoG nucleotide from DNA in vitro.	8-oxog nucleotide	118-135	P53	Homo sapiens	32-35
15342418-1	2004	We have demonstrated previously that interferon (IFN)-gamma sensitizes human colon carcinoma cell lines to the cytotoxic effects of 5-fluorouracil combined with leucovorin and to the thymidylate synthase inhibitor, ZD9331, dependent on thymineless stress-induced DNA damage, independent of p53.	Leucovorin	161-171	P53	Homo sapiens	290-293
15254743-4	2004	Here, we show that SU5416 inhibited the expression of G1 cell cycle checkpoint regulators, p53, p21, p27 and MDM2 in ovarian carcinoma cells.	Semaxinib	19-25	P53	Homo sapiens	91-94
15147952-4	2004	Using the proteasome-specific inhibitors, MG132 and lactacystin, we show that the p53, the cdk inhibitors p21 and p27, and cyclin A are degraded by the ubiquitin-proteasome pathway in human osteosarcoma cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	42-47	P53	Homo sapiens	82-85
15069711-10	2004	The exoression patterns of p53+/p21-, and of p53-/p21+ were found in 5.0% and 82.5% of DP.	dp	87-89	P53	Homo sapiens	27-30
15069711-10	2004	The exoression patterns of p53+/p21-, and of p53-/p21+ were found in 5.0% and 82.5% of DP.	dp	87-89	P53	Homo sapiens	45-48
14722112-0	2004	5-aza-2"-deoxycytidine activates the p53/p21Waf1/Cip1 pathway to inhibit cell proliferation.	Decitabine	0-22	P53	Homo sapiens	37-40
15199526-2	2004	In breast cancer cell lines that expressed either wild-type p53 (MCF-7) or mutant p53 (MCF-7/Adr), sensitivity to the cytotoxic effects of gemcitabine during a 24-hour incubation was similar (IC(50) values 80 and 60 nmol/L in MCF-7 and MCF-7/Adr, respectively).	gemcitabine	139-150	P53	Homo sapiens	60-63
15199526-2	2004	In breast cancer cell lines that expressed either wild-type p53 (MCF-7) or mutant p53 (MCF-7/Adr), sensitivity to the cytotoxic effects of gemcitabine during a 24-hour incubation was similar (IC(50) values 80 and 60 nmol/L in MCF-7 and MCF-7/Adr, respectively).	gemcitabine	139-150	P53	Homo sapiens	82-85
14701864-5	2004	Specific glycosaminoglycan lyase digestions, followed by product analyses using fluorescence-assisted carbohydrate electrophoresis and immunoprecipitation experiments, showed that the p53 form is associated with syndecan-1 through both chondroitin sulfate and heparan sulfate.	Chondroitin Sulfates	236-255	P53	Homo sapiens	184-187
15035290-11	2004	The OSI-774 induced greater (p53-independent) apoptosis in more malignant GBM phenotypes and may be a promising therapeutic agent against secondary GBM.	Erlotinib Hydrochloride	4-11	P53	Homo sapiens	29-32
14700734-3	2004	The proteasome inhibitor, MG132, induced the accumulation of p53 in human dopaminergic neuroblastoma SH-SY5Y cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	26-31	P53	Homo sapiens	61-64
14637186-11	2003	The expression of p53, phospho-serine 15 of p53, and Bax, and inactivate form of CPP32 was suppressed by a pretreatment of a specific p38 MAPK inhibitor, SB203580.	SB 203580	154-162	P53	Homo sapiens	18-21
14637186-11	2003	The expression of p53, phospho-serine 15 of p53, and Bax, and inactivate form of CPP32 was suppressed by a pretreatment of a specific p38 MAPK inhibitor, SB203580.	SB 203580	154-162	P53	Homo sapiens	44-47
14695155-2	2003	Importantly, the cytotoxic effects of thymidine deprivation induced by 5-fluorouracil (FUra) combined with leucovorin (LV) was enhanced by IFN-gamma, and the synergism was shown to be dependent on Fas, FUra-induced DNA damage, and independent of p53.	Leucovorin	107-117	P53	Homo sapiens	246-249
14695155-2	2003	Importantly, the cytotoxic effects of thymidine deprivation induced by 5-fluorouracil (FUra) combined with leucovorin (LV) was enhanced by IFN-gamma, and the synergism was shown to be dependent on Fas, FUra-induced DNA damage, and independent of p53.	Leucovorin	119-121	P53	Homo sapiens	246-249
15198048-4	2003	The present study focused on patients with glottic T1a carcinoma treated with CO2 laser surgery in which correlation between histo-pathological aspects and expression of p53 protein on resection borders were confirmed by onset of local recurrence.	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	78-81	P53	Homo sapiens	170-173
14513366-9	2003	Wortmannin, a PI3-kinase (PI3-K) inhibitor, caused a dose-dependent inhibition of total p53 accumulation, Ser-15 phosphorylation and p21(WAF1/CIP1) transactivation in response to both CDDP and DACH-Ac-Pt, indicating that members of the PI3-K family are involved in phosphorylation of p53 and that transactivation of p21(WAF1/CIP1) is p53 dependent.	Wortmannin	0-10	P53	Homo sapiens	88-91
14513366-9	2003	Wortmannin, a PI3-kinase (PI3-K) inhibitor, caused a dose-dependent inhibition of total p53 accumulation, Ser-15 phosphorylation and p21(WAF1/CIP1) transactivation in response to both CDDP and DACH-Ac-Pt, indicating that members of the PI3-K family are involved in phosphorylation of p53 and that transactivation of p21(WAF1/CIP1) is p53 dependent.	Wortmannin	0-10	P53	Homo sapiens	284-287
14513366-9	2003	Wortmannin, a PI3-kinase (PI3-K) inhibitor, caused a dose-dependent inhibition of total p53 accumulation, Ser-15 phosphorylation and p21(WAF1/CIP1) transactivation in response to both CDDP and DACH-Ac-Pt, indicating that members of the PI3-K family are involved in phosphorylation of p53 and that transactivation of p21(WAF1/CIP1) is p53 dependent.	Wortmannin	0-10	P53	Homo sapiens	284-287
14595027-2	2003	To test whether the peptides could act as chaperones and rescue the tumor-suppressing function of oncogenic mutants of p53 in living cells, we treated human tumor cells with the fluorescein-labeled peptide Fl-CDB3 (fluorescent derivative of CDB3).	Fluorescein	178-189	P53	Homo sapiens	119-122
14602524-1	2003	We have recently demonstrated a significant dose-response relationship between vinyl chloride exposure and mutant p53 biomarkers in humans.	Vinyl Chloride	79-93	P53	Homo sapiens	114-117
14602524-2	2003	The aim of this study was to examine a common polymorphism in the DNA repair gene XRCC1 as a potential biomarker of susceptibility modifying this relationship, consistent with the known mechanism of production of p53 mutations via vinyl chloride-induced etheno-DNA adducts, which are repaired by XRCC1.	Vinyl Chloride	231-245	P53	Homo sapiens	213-216
14555708-0	2003	Amifostine impairs p53-mediated apoptosis of human myeloid leukemia cells.	Amifostine	0-10	P53	Homo sapiens	19-22
14555708-3	2003	As the apoptosis induced by many antitumoral agents is mediated by p53, we studied the effect of amifostine on p53-mediated apoptosis.	Amifostine	97-107	P53	Homo sapiens	111-114
14555708-6	2003	We found that amifostine dramatically reduced apoptosis by p53 in both cell lines, as assessed by cell morphology, annexin V binding, fraction of sub-G(1) cells, and DNA laddering.	Amifostine	14-24	P53	Homo sapiens	59-62
14555708-7	2003	To explore the mechanism responsible for this apoptosis protection, we tested the effect of amifostine on p53 transcriptional activity.	Amifostine	92-102	P53	Homo sapiens	106-109
14555708-8	2003	We found that amifostine reduced p53-mediated transactivation of target promoters in NB4 and K562.	Amifostine	14-24	P53	Homo sapiens	33-36
14555708-9	2003	Macroarray analysis confirmed that several p53 target genes as p21(Waf1), mdm2, gadd45, pig8, and pig3 were down-regulated at the mRNA level by amifostine in NB4 and K562.	Amifostine	144-154	P53	Homo sapiens	43-46
14555708-10	2003	Also, c-myc was up-regulated by amifostine in K562 in the presence of p53, consistently with the impairment of p53-mediated apoptosis exerted by c-Myc in these cells.	Amifostine	32-42	P53	Homo sapiens	70-73
14555708-11	2003	We conclude that amifostine impairs p53-dependent apoptosis of myeloid leukemia cells by reducing the activation of apoptosis-related genes.	Amifostine	17-27	P53	Homo sapiens	36-39
14555708-12	2003	Our results open the possibility that amifostine could reduce the effectiveness of antitumoral treatments when it is dependent on active p53.	Amifostine	38-48	P53	Homo sapiens	137-140
12960142-0	2003	Pyrazoloacridine is active in multidrug-resistant neuroblastoma cell lines with nonfunctional p53.	NSC 366140	0-16	P53	Homo sapiens	94-97
12960142-1	2003	PURPOSE: The purpose of this study was to determine the activity of pyrazoloacridine (PZA) in neuroblastomas that have acquired high-level resistance to multiple drugs (not associated with multidrug resistance-associated protein or P-glycoprotein) during therapy, including those with loss of p53 function.	NSC 366140	68-84	P53	Homo sapiens	293-296
12960142-1	2003	PURPOSE: The purpose of this study was to determine the activity of pyrazoloacridine (PZA) in neuroblastomas that have acquired high-level resistance to multiple drugs (not associated with multidrug resistance-associated protein or P-glycoprotein) during therapy, including those with loss of p53 function.	NSC 366140	86-89	P53	Homo sapiens	293-296
12907147-1	2003	This report describes the time-dependent biodistribution of human p53 plasmid delivered in aerosol with polyethyleneimine in mice compared to the distribution of this material following intravenous injection.	aziridine	104-121	P53	Homo sapiens	66-69
12837832-4	2003	p53 mutations were detected by direct dideoxynucleotide sequencing and p53 GeneChip analysis.	Dideoxynucleotides	38-55	P53	Homo sapiens	0-3
12883038-5	2003	In contrast, both low and high bizelesin concentrations enhanced p53 and p21 induction and triggered G(2)-M cell cycle arrest and eventual senescence without significant apoptotic cell death.	bizelesin	31-40	P53	Homo sapiens	65-68
12684687-4	2003	We report that Brca1-deficiency in p53-null cells was associated with increased sensitivity to the topoisomerase I poisons camptothecin and topotecan, the topoisomerase II poisons doxorubicin, mitoxantrone and etoposide, and to the platinum compounds carboplatin and oxaliplatin, but not to the antimetabolites 5-fluorouracil and gemcitabine and the taxanes docetaxel and paclitaxel.	Carboplatin	251-262	P53	Homo sapiens	35-38
12684687-4	2003	We report that Brca1-deficiency in p53-null cells was associated with increased sensitivity to the topoisomerase I poisons camptothecin and topotecan, the topoisomerase II poisons doxorubicin, mitoxantrone and etoposide, and to the platinum compounds carboplatin and oxaliplatin, but not to the antimetabolites 5-fluorouracil and gemcitabine and the taxanes docetaxel and paclitaxel.	gemcitabine	330-341	P53	Homo sapiens	35-38
12659945-9	2003	We demonstrated an antisense ODN of p53 delivered by PEI/DOTAP-Chol combination effectively inhibited the biosynthesis of p53 protein in HepG2 (68% inhibiton) and 2.2.15 cells (43% inhibition).	Polyethyleneimine	53-56	P53	Homo sapiens	36-39
12659945-9	2003	We demonstrated an antisense ODN of p53 delivered by PEI/DOTAP-Chol combination effectively inhibited the biosynthesis of p53 protein in HepG2 (68% inhibiton) and 2.2.15 cells (43% inhibition).	Polyethyleneimine	53-56	P53	Homo sapiens	122-125
12676607-8	2003	On the other hand, treatment with wortmannin, an inhibitor of DNA-activated protein kinase and ataxia-telangiectasia mutated, suppressed both chrysotile-induced Ser15 phosphorylation and accumulation of p53 protein.	Wortmannin	34-44	P53	Homo sapiens	203-206
12655090-7	2003	Both HTLV-I Tax and the proteasome-specific inhibitor MG132 inhibited p53-mediated TRX protein degradation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	54-59	P53	Homo sapiens	70-73
12640129-6	2003	Treatment of MCF10A cells with MG132, a 26S proteasome inhibitor, effectively stabilized monoubiquitinated p53 and rescued ADR-induced downregulation of Hdm2.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	P53	Homo sapiens	107-110
12733645-4	2003	DNA damage by these photosensitizers was examined using 32P-labeled DNA fragments obtained from the p53 tumor suppressor gene.	Phosphorus-32	56-59	P53	Homo sapiens	100-103
12618880-7	2003	Hypofractionated and accelerated radiotherapy supported with amifostine (HypoARC regimen) was significantly more effective than standard radiotherapy in cases with high cancer cell proliferation index, c-erbB-2 and p53 overexpression.	Amifostine	61-71	P53	Homo sapiens	215-218
12618886-0	2003	p53 protein regulates the effects of amifostine on apoptosis, cell cycle progression, and cytoprotection.	Amifostine	37-47	P53	Homo sapiens	0-3
12618886-1	2003	To determine the role of p53 protein on the cellular effects of amifostine, we used molecularly engineered HCT116 colon cancer cells in which the p53 gene was inactivated by targeted homologous recombination or p53 protein was degraded by high-level expression of papillomavirus E6 protein.	Amifostine	64-74	P53	Homo sapiens	25-28
12618886-2	2003	Amifostine induced a G1 arrest and protected against paclitaxel toxicity in p53-proficient but not in p53-deficient cells.	Amifostine	0-10	P53	Homo sapiens	76-79
13678314-9	2003	Because Caco-2 cells are lacking the wild allele of the P53 gene, the present results support the hypothesis that butyrate induces P21 gene expression by P53-independent mechanism.	Butyrates	114-122	P53	Homo sapiens	56-59
13678314-9	2003	Because Caco-2 cells are lacking the wild allele of the P53 gene, the present results support the hypothesis that butyrate induces P21 gene expression by P53-independent mechanism.	Butyrates	114-122	P53	Homo sapiens	154-157
12610816-10	2003	The expression of the p53 response proteins, MDM2 and p21, was elevated in MG132 treated chondrocytes.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	75-80	P53	Homo sapiens	22-25
12839645-3	2003	The recombinant plasmid pcDNA-p53/p21 was constructed by inserting the p53/p21 fusion gene into eukaryotic expression vector pcDNA3.1 and subsequently transfected into human oral squamous cell carcinoma cell line (Tca8113) with lipofectamine.	Lipofectamine	228-241	P53	Homo sapiens	30-33
12700649-6	2003	The p53-binding region in the first intron of the Fas gene was partially methylated in Caco(2), and 5-azadC potentiated Ad-wtp53-induced upregulation of Fas expression.	Decitabine	100-107	P53	Homo sapiens	4-7
14530614-7	2003	Using L-NAME (0.5 and 5.0 mM), the expression of p53 and Bax was increased, but Bcl-2 was unchanged.	NG-Nitroarginine Methyl Ester	6-12	P53	Homo sapiens	49-52
12624953-4	2003	Transcriptional activity and expression of p53 proved to depend on the proportion between p53 and GSE22.	gse22	98-103	P53	Homo sapiens	43-46
12624953-5	2003	The dominant-negative effect was observed only when GSE22 was in a multifold excess to p53.	gse22	52-57	P53	Homo sapiens	87-90
12624953-6	2003	GSE22 was shown to be suitable for complete reversible inactivation of p53.	gse22	0-5	P53	Homo sapiens	71-74
12858214-5	2003	P53 was assessed on AP-AAP stained sections.	ap-aap	20-26	P53	Homo sapiens	0-3
12499281-5	2002	Carboplatin and oxaliplatin treatment led also to stabilization of p53, whereas none of the platinums changed p73 levels.	Carboplatin	0-11	P53	Homo sapiens	67-70
12499281-8	2002	Clonogenic survival was enhanced by expressing a dominant negative p53 or ectopic HPV16 E6 in SiHa and HeLa cells treated with IR, carboplatin, or oxaliplatin or with a combination of IR + carboplatin or oxaliplatin.	Carboplatin	131-142	P53	Homo sapiens	67-70
12499281-8	2002	Clonogenic survival was enhanced by expressing a dominant negative p53 or ectopic HPV16 E6 in SiHa and HeLa cells treated with IR, carboplatin, or oxaliplatin or with a combination of IR + carboplatin or oxaliplatin.	Carboplatin	189-200	P53	Homo sapiens	67-70
12464677-0	2002	Induction of the Cdk inhibitor p21 by LY83583 inhibits tumor cell proliferation in a p53-independent manner.	6-anilino-5,8-quinolinedione	38-45	P53	Homo sapiens	85-88
12434295-2	2002	This study examines the effect of tumour suppressor protein p53 on metallothionein expression following CdCl2 treatment in eight human epithelial breast cancer cell lines differing in p53 and oestrogen-receptor status.	Cadmium Chloride	104-109	P53	Homo sapiens	60-63
12372430-2	2002	In this report, upon exposure of cells to ultraviolet (UV) or proteasome inhibitor MG132, ATF3 protein was induced more efficiently in cells with intact p53 allele than in those with null mutant p53 allele.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	P53	Homo sapiens	153-156
12372430-2	2002	In this report, upon exposure of cells to ultraviolet (UV) or proteasome inhibitor MG132, ATF3 protein was induced more efficiently in cells with intact p53 allele than in those with null mutant p53 allele.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	83-88	P53	Homo sapiens	195-198
12151395-5	2002	Moreover, the role of p53 in activation of this pathway was demonstrated by the fact that inhibition of p53 activity by pifithrin-alpha reduced the sensitivity of HCT116/p21(-/-) cells to daunomycin-induced apoptosis and restored a Bax/Bcl-2 ratio similar to that observed in HCT116p21(+/+) cells.	Daunorubicin	188-198	P53	Homo sapiens	22-25
12151395-5	2002	Moreover, the role of p53 in activation of this pathway was demonstrated by the fact that inhibition of p53 activity by pifithrin-alpha reduced the sensitivity of HCT116/p21(-/-) cells to daunomycin-induced apoptosis and restored a Bax/Bcl-2 ratio similar to that observed in HCT116p21(+/+) cells.	Daunorubicin	188-198	P53	Homo sapiens	104-107
12237923-9	2002	A significant difference in MC also was observed between regions of squamous metaplasia or dysplasia with projections of capillary loops into the bronchial mucosa and similar lesions without capillary loops (P &lt; 0.005); however, there was no difference in either the PI or the incidence of p53 overexpression between these groups.	Methylcholanthrene	28-30	P53	Homo sapiens	293-296
12185593-7	2002	After a transient treatment with replication inhibitors, we observed inhibition of the drug induced recombination by p53, particularly for the elongation inhibitor aphidicolin.	Aphidicolin	164-175	P53	Homo sapiens	117-120
12011072-4	2002	Clustering of the CD40 ligand is mediated by an association of the ligand with p53, a translocation of acid sphingomyelinase (ASM) to the cell membrane, an activation of the ASM, and a formation of ceramide.	Ceramides	198-206	P53	Homo sapiens	79-82
12160929-0	2002	Possible involvement of glutathione and p53 in trichloroethylene- and perchloroethylene-induced lipid peroxidation and apoptosis in human lung cancer cells.	Tetrachloroethylene	70-87	P53	Homo sapiens	40-43
12160929-2	2002	The aim of this study was to elucidate the role of glutathione (GSH) and p53 in TCE- and PERC-induced lung toxicity.	Tetrachloroethylene	89-93	P53	Homo sapiens	73-76
12160929-4	2002	The results showed that exposure to vapor TCE and PERC produced a dose-dependent and more pronounced accumulation of H(2)O(2) in p53-WT H460 than p53-null H1299 cells.	Tetrachloroethylene	50-54	P53	Homo sapiens	129-132
12160929-4	2002	The results showed that exposure to vapor TCE and PERC produced a dose-dependent and more pronounced accumulation of H(2)O(2) in p53-WT H460 than p53-null H1299 cells.	Tetrachloroethylene	50-54	P53	Homo sapiens	146-149
12160929-6	2002	Cotreatment of p53-WT H460 cells with free radical scavengers, such as D-mannitol, uric acid, and sodium selenite, significantly attenuated the TCE- or PERC-induced lipid peroxidation.	Tetrachloroethylene	152-156	P53	Homo sapiens	15-18
12160929-7	2002	In contrast, depletion of GSH in p53-null H1299 cells enhanced TCE- or PERC-induced lipid peroxidation.	Tetrachloroethylene	71-75	P53	Homo sapiens	33-36
12071847-9	2002	This phosphorylation was associated with an SB203580-sensitive accumulation of p53, even in the presence of a serine phosphatase inhibitor.	SB 203580	44-52	P53	Homo sapiens	79-82
12416024-11	2002	We also observed that p53 status influenced correlations between ENT1 transporter gene RNA levels and sensitivity to the drugs tiazafurin, AZQ and 3-deazauridine.	3-Deazauridine	147-161	P53	Homo sapiens	22-25
12067251-8	2002	Treatment of p53 cDNA with micromolar concentrations of (+/-)-anti-7,8-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydro-benzo[a]pyrene, (anti-BPDE, an ultimate carcinogen) or sub-micromolar concentrations of BP-7,8-dione in the presence of redox-cycling conditions (NADPH and CuCl(2)) also caused p53 mutations in a dose-dependent manner.	(+/-)-anti-7,8-dihydroxy-9alpha	56-87	P53	Homo sapiens	13-16
12067251-8	2002	Treatment of p53 cDNA with micromolar concentrations of (+/-)-anti-7,8-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydro-benzo[a]pyrene, (anti-BPDE, an ultimate carcinogen) or sub-micromolar concentrations of BP-7,8-dione in the presence of redox-cycling conditions (NADPH and CuCl(2)) also caused p53 mutations in a dose-dependent manner.	anti	62-66	P53	Homo sapiens	13-16
12067251-8	2002	Treatment of p53 cDNA with micromolar concentrations of (+/-)-anti-7,8-dihydroxy-9alpha,10alpha-epoxy-7,8,9,10-tetrahydro-benzo[a]pyrene, (anti-BPDE, an ultimate carcinogen) or sub-micromolar concentrations of BP-7,8-dione in the presence of redox-cycling conditions (NADPH and CuCl(2)) also caused p53 mutations in a dose-dependent manner.	anti	62-66	P53	Homo sapiens	299-302
12131661-5	2002	Butyrate reduced mutant p53 expression, whereas aspirin did not affect p53 expression.	Butyrates	0-8	P53	Homo sapiens	24-27
12048682-2	2002	METHODS: Recombinant eukaryotic expression vector pcDNA3 containing full-length human wild-type p53 cDNA was introduced by lipofectamine-mediated gene transfection into SKOV-3 cultured cells which were acted on by cisplatin of different concentrations.	Lipofectamine	123-136	P53	Homo sapiens	96-99
12010862-0	2002	XRCC1 and CYP2E1 polymorphisms as susceptibility factors of plasma mutant p53 protein and anti-p53 antibody expression in vinyl chloride monomer-exposed polyvinyl chloride workers.	Vinyl Chloride	122-136	P53	Homo sapiens	74-77
12010862-2	2002	Plasma mutant p53 protein and anti-p53 antibody have also been associated with vinyl chloride monomer (VCM) exposure, although the mechanism of VCM-related carcinogenesis remains unclear.	Vinyl Chloride	79-93	P53	Homo sapiens	14-17
12010862-2	2002	Plasma mutant p53 protein and anti-p53 antibody have also been associated with vinyl chloride monomer (VCM) exposure, although the mechanism of VCM-related carcinogenesis remains unclear.	Vinyl Chloride	79-93	P53	Homo sapiens	35-38
11960374-0	2002	P53 mediates ceramide-induced apoptosis in SKN-SH cells.	Ceramides	13-21	P53	Homo sapiens	0-3
11960374-4	2002	Ceramide-induced apoptosis is accompanied by accumulation of p53 followed by an increase of Bax and decrease of Bcl-2 levels.	Ceramides	0-8	P53	Homo sapiens	61-64
11960374-7	2002	These results suggest that p53 regulates the ratio Bcl-2/Bax and the expression/activation of caspases during ceramide-induced apoptosis in SKN-SH cells.	Ceramides	110-118	P53	Homo sapiens	27-30
11960374-9	2002	Thus ceramide-induced reduction in the Bcl-2/Bax ratio, increase in caspase activity, and apoptosis is dependent upon increases in cellular p53 levels which play a critical role in the regulation of apoptotic cell death.	Ceramides	5-13	P53	Homo sapiens	140-143
21315017-11	2002	Mutated p53 protein in parent cell line 801D was positive and in PEGFP-p53(AS)-801D was negative with immunochemical stain.	Arsenic	75-77	P53	Homo sapiens	71-74
11862428-5	2002	Functionality of the p53 pathway was evaluated by incubating cells with carboplatin or doxorubicin and monitoring the effects on the levels of the p53, p21(WAF1/CIP1), and MDM 2 proteins by Western blot analyses.	Carboplatin	72-83	P53	Homo sapiens	21-24
11802204-11	2002	This corresponded with suppression of Bcl-2 and Bcl-X/L expression in wt-p53 cells exposed to gemcitabine whereas Bcl-2 levels remained stable and Bcl-X/L levels increased in mut-p53 cells exposed to gemcitabine.	gemcitabine	94-105	P53	Homo sapiens	73-76
11802204-12	2002	We conclude that the p53 status of cancer cells influences their sensitivity to gemcitabine cytotoxicity.	gemcitabine	80-91	P53	Homo sapiens	21-24
11802204-13	2002	Our evidence suggests that loss of p53 function leads to loss of cell cycle control and alterations in the apoptotic cascade, conferring resistance to gemcitabine in cancer cell lines displaying a mut-p53.	gemcitabine	151-162	P53	Homo sapiens	35-38
11802204-13	2002	Our evidence suggests that loss of p53 function leads to loss of cell cycle control and alterations in the apoptotic cascade, conferring resistance to gemcitabine in cancer cell lines displaying a mut-p53.	gemcitabine	151-162	P53	Homo sapiens	201-204
11802206-0	2002	P53 overexpression predicts poor chemosensitivity to high-dose 5-fluorouracil plus leucovorin chemotherapy for stage IV colorectal cancers after palliative bowel resection.	Leucovorin	83-93	P53	Homo sapiens	0-3
11840331-4	2002	This p53wt diminution was dependent on proteasome activity, as inhibited by MG-132 inhibitor.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	76-82	P53	Homo sapiens	5-8
11782540-5	2002	The fluorescein-labeled peptide, FL-CDB3, binds wild-type p53 core domain with a dissociation constant of 0.5 microM, and raises the apparent melting temperatures of wild-type and a representative oncogenic mutant, R249S core domain.	Fluorescein	4-15	P53	Homo sapiens	58-61
11706017-0	2002	Mechanism of p53-dependent apoptosis induced by 3-methylcholanthrene: involvement of p53 phosphorylation and p38 MAPK.	Methylcholanthrene	48-68	P53	Homo sapiens	13-16
11706017-0	2002	Mechanism of p53-dependent apoptosis induced by 3-methylcholanthrene: involvement of p53 phosphorylation and p38 MAPK.	Methylcholanthrene	48-68	P53	Homo sapiens	85-88
11706017-3	2002	MC induced apoptosis, preceded by serine 15 phosphorylation and accumulation of p53.	Methylcholanthrene	0-2	P53	Homo sapiens	80-83
11706017-4	2002	MC failed to cause apoptosis in p53-deficient MG63 cells, whereas ectopic expression of p53 in MG63 cells restored the response to MC.	Methylcholanthrene	131-133	P53	Homo sapiens	88-91
11706017-5	2002	Therefore, MC-induced apoptosis was dependent on p53.	Methylcholanthrene	11-13	P53	Homo sapiens	49-52
11859874-4	2002	This study examined if mutations in the tumor suppressor gene p53 affected organochlorine exposure related breast cancer risk and survival.	Hydrocarbons, Chlorinated	75-89	P53	Homo sapiens	62-65
11859874-12	2002	These preliminary results suggest that p53 mutations may have a modifying effect on at least the breast cancer risk associated with exposures to organochlorines.	Hydrocarbons, Chlorinated	145-160	P53	Homo sapiens	39-42
12174820-1	2002	CP-31398, a styrylquinazoline, emerged from a screen for therapeutic agents that restore a wild-type DNA-binding conformation of mutant p53 to suppress tumors in-vivo (Science 286, 2507, 1999).	styrylquinazoline	12-29	P53	Homo sapiens	136-139
12599424-2	2002	METHODS: Recombinant eukaryotic expression vector pCB6.p53 containing human wild-type p53 cDNA was introduced by lipofectamine transfection regent into HeLa cell line.	Lipofectamine	113-126	P53	Homo sapiens	55-58
12658781-4	2002	MTT showed that p53 gene by itself induced strong inhibition effect on the growth of U251 cells [inhibition rate, IR (79.60 +/- 5.69)%].	monooxyethylene trimethylolpropane tristearate	0-3	P53	Homo sapiens	16-19
11594730-0	2001	Evidence for peroxynitrite-mediated modifications to p53 in human gliomas: possible functional consequences.	Peroxynitrous Acid	13-26	P53	Homo sapiens	53-56
11594730-3	2001	Furthermore, we show that p53, a key tumor suppressor protein, has evidence of peroxynitrite-mediated modifications in gliomas in vivo.	Peroxynitrous Acid	79-92	P53	Homo sapiens	26-29
11594730-4	2001	Experiments in vitro demonstrate that peroxynitrite treatment of recombinant wild-type p53 at physiological concentrations results in formation of higher molecular weight aggregates, tyrosine nitration, and loss of specific DNA binding.	Peroxynitrous Acid	38-51	P53	Homo sapiens	87-90
11594730-5	2001	Peroxynitrite treatment of human glioma cell lysates similarly resulted in selective tyrosine nitration of p53 and was also associated with loss of p53 DNA binding ability.	Peroxynitrous Acid	0-13	P53	Homo sapiens	107-110
11594730-5	2001	Peroxynitrite treatment of human glioma cell lysates similarly resulted in selective tyrosine nitration of p53 and was also associated with loss of p53 DNA binding ability.	Peroxynitrous Acid	0-13	P53	Homo sapiens	148-151
11594730-6	2001	These data indicate that tyrosine nitration of proteins occurs in human gliomas in vivo, that p53 may be a target of peroxynitrite in these tumors, and that physiological concentrations of peroxynitrite can result in a loss of p53 DNA binding ability in vitro.	Peroxynitrous Acid	117-130	P53	Homo sapiens	94-97
11594730-6	2001	These data indicate that tyrosine nitration of proteins occurs in human gliomas in vivo, that p53 may be a target of peroxynitrite in these tumors, and that physiological concentrations of peroxynitrite can result in a loss of p53 DNA binding ability in vitro.	Peroxynitrous Acid	189-202	P53	Homo sapiens	227-230
11594730-7	2001	These findings raise the possibility that peroxynitrite may contribute to loss of wild-type p53 functional activity in gliomas by posttranslational protein modifications.	Peroxynitrous Acid	42-55	P53	Homo sapiens	92-95
11498784-5	2001	Sucrose gradient experiments showed that p53 blocks translation initiation by preventing 80S ribosome formation on an mRNA bearing the FGF-2 mRNA leader sequence.	Sucrose	0-7	P53	Homo sapiens	41-44
11384212-6	2001	However, lung H441 adenocarcinoma cells, with a mutation in exon 5, codon 158 of p53, exhibited partial G1 arrest after the diol epoxides as well as actinomycin D, and H2030 adenocarcinoma cells did not show G1 arrest after any of the chemicals despite a normal p53.	diol epoxides	124-137	P53	Homo sapiens	81-84
11329373-4	2001	Immunocytochemistry of fixed human fibroblasts treated with either UV light, the kinase and transcription inhibitor DRB or the proteasome inhibitor MG132 revealed abundant p53 localized to the nucleus.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	148-153	P53	Homo sapiens	172-175
11329373-6	2001	However, in cells treated with MG132, residual p53 localized to distinct large foci.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	31-36	P53	Homo sapiens	47-50
11302731-5	2001	On the other hand, treatment with wortmannin or caffeine suppressed CdCl(2)-induced Ser 15 phosphorylation and accumulation of p53 protein.	Wortmannin	34-44	P53	Homo sapiens	127-130
11302731-5	2001	On the other hand, treatment with wortmannin or caffeine suppressed CdCl(2)-induced Ser 15 phosphorylation and accumulation of p53 protein.	Cadmium Chloride	68-75	P53	Homo sapiens	127-130
21044462-2	2001	METHODS: Vectors of three kinds of p53 minigene were transfected into p53-null H1299 cells through lipofectAMINE.	Lipofectamine	99-112	P53	Homo sapiens	35-38
21044462-2	2001	METHODS: Vectors of three kinds of p53 minigene were transfected into p53-null H1299 cells through lipofectAMINE.	Lipofectamine	99-112	P53	Homo sapiens	70-73
11287297-9	2001	Furthermore, a DNA damage- and oxidative stress-dependent protein, P53, could also been induced by CuQ treatments in a time-course and dose-dependent manners.	bis(8-quinolinolato)copper(II)	99-102	P53	Homo sapiens	67-70
11287297-11	2001	In conclusion, our current study strongly suggests that CuQ induces gene mutation, global DNA damage, and P53 expression through a ROS-dependent mechanism.	bis(8-quinolinolato)copper(II)	56-59	P53	Homo sapiens	106-109
11275476-2	2001	We investigated the ability of an aromatic amine, 4-aminobiphenyl (4-ABP) and its N-hydroxy metabolite (4-ABP(NHOH)) to cause oxidative DNA damage, using (32)P-labeled human DNA fragments from the p53 tumor suppressor gene and the c-Ha-ras-1 protooncogene.	aromatic amine	34-48	P53	Homo sapiens	197-200
11259619-0	2001	Activation of the p53 DNA damage response pathway after inhibition of DNA methyltransferase by 5-aza-2"-deoxycytidine.	Decitabine	95-117	P53	Homo sapiens	18-21
11313880-8	2001	Moreover, expression of functional p53 protein in glioma cells expressing mutant p53 using a temperature-sensitive human p53(Val138) induced ceramide accumulation by the activation of neutral sphingomyelinase which was dependent on the generation of O2-*.	Ceramides	141-149	P53	Homo sapiens	35-38
11313880-8	2001	Moreover, expression of functional p53 protein in glioma cells expressing mutant p53 using a temperature-sensitive human p53(Val138) induced ceramide accumulation by the activation of neutral sphingomyelinase which was dependent on the generation of O2-*.	Ceramides	141-149	P53	Homo sapiens	81-84
11313880-8	2001	Moreover, expression of functional p53 protein in glioma cells expressing mutant p53 using a temperature-sensitive human p53(Val138) induced ceramide accumulation by the activation of neutral sphingomyelinase which was dependent on the generation of O2-*.	Ceramides	141-149	P53	Homo sapiens	81-84
11313880-9	2001	Taken together, these results suggest that p53 may modulate ceramide generation by activation of neutral sphingomyelinase through the formation of O2-*, but not its downstream compounds H2O2 or * OH.	Ceramides	60-68	P53	Homo sapiens	43-46
12733349-5	2001	MTT colorimetric assay, TUNEL fluorenscence microscopy and flow cytometry showed that foreign bax or p53 gene inhibited the LCC growth and induced apoptosis (23.9% and 26.1% of inhibitory rate by bax gene and p53 plus bax genes respectively).	monooxyethylene trimethylolpropane tristearate	0-3	P53	Homo sapiens	101-104
11223405-2	2001	We have investigated sequence specificity of oxidative stress-mediated DNA damage by using 32P-labeled DNA fragments obtained from the human c-Ha-ras-1 and p53 genes.	Phosphorus-32	91-94	P53	Homo sapiens	156-159
11053443-0	2001	A role for the polyproline domain of p53 in its regulation by Mdm2.	polyproline	15-26	P53	Homo sapiens	37-40
11053443-3	2001	p53 protein lacking the polyproline region has impaired apoptotic activity and altered specificity for certain apoptotic target genes.	polyproline	24-35	P53	Homo sapiens	0-3
11053443-5	2001	p53 lacking the polyproline region was identified to be more susceptible to inhibition by Mdm2.	polyproline	16-27	P53	Homo sapiens	0-3
11053443-7	2001	This increased sensitivity to Mdm2 results from an enhanced affinity of Mdm2 toward p53 lacking the polyproline region.	polyproline	100-111	P53	Homo sapiens	84-87
11053443-9	2001	The polyproline region is proposed to be important in the modulation of the inhibitory effects of Mdm2 on p53 activities and stability.	polyproline	4-15	P53	Homo sapiens	106-109
11158590-2	2001	We have examined the response to p53 when DNA synthesis is blocked by hydroxyurea (HU) or aphidicolin or when DNA is damaged by gamma IR.	Aphidicolin	90-101	P53	Homo sapiens	33-36
11158590-5	2001	Moreover, the p53 response to gamma IR is inhibited by pretreatment of cells with HU or aphidicolin, suggesting that blocked DNA replication prevents p53 from being fully active as a transcription factor.	Aphidicolin	88-99	P53	Homo sapiens	14-17
11158590-5	2001	Moreover, the p53 response to gamma IR is inhibited by pretreatment of cells with HU or aphidicolin, suggesting that blocked DNA replication prevents p53 from being fully active as a transcription factor.	Aphidicolin	88-99	P53	Homo sapiens	150-153
11158615-6	2001	This reduction was prevented by the proteasome inhibitors MG132 and lactacystin, suggesting enhanced p53 degradation in the presence of dicoumarol.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	58-63	P53	Homo sapiens	101-104
11125034-7	2001	Notably, when MDM2 expression is inhibited in S-type cells, with a phosphorothioated antisense oligonucleotide (AS5), then p53 accumulates in the nucleus and the SH-EP1 cells undergo apoptosis.	phosphorothioated	67-84	P53	Homo sapiens	123-126
11106681-10	2000	CONCLUSIONS: Combinations of 4-HPR and modulators of ceramide metabolism may form the basis for a novel chemotherapy that is functional under hypoxic conditions (e.g., such as those within tumors) and is p53 independent and caspase independent.	Ceramides	53-61	P53	Homo sapiens	204-207
11082419-0	2000	Roles of nuclear factor-kappaB, p53, and p21/WAF1 in daunomycin-induced cell cycle arrest and apoptosis.	Daunorubicin	53-63	P53	Homo sapiens	32-35
11082419-1	2000	Daunomycin is a potent inducer of p53 and NF-kappaB transcription factors.	Daunorubicin	0-10	P53	Homo sapiens	34-37
11082419-5	2000	However, using different tumor cell lines where p53 or NF-kappaB was inactive, we showed that p21 activation and cell cycle arrest induced by daunomycin was p53-dependent and NF-kappaB-independent, whereas daunomycin-induced apoptosis was p53- and NF-kappaB-independent.	Daunorubicin	142-152	P53	Homo sapiens	48-51
11082419-5	2000	However, using different tumor cell lines where p53 or NF-kappaB was inactive, we showed that p21 activation and cell cycle arrest induced by daunomycin was p53-dependent and NF-kappaB-independent, whereas daunomycin-induced apoptosis was p53- and NF-kappaB-independent.	Daunorubicin	142-152	P53	Homo sapiens	157-160
11082419-5	2000	However, using different tumor cell lines where p53 or NF-kappaB was inactive, we showed that p21 activation and cell cycle arrest induced by daunomycin was p53-dependent and NF-kappaB-independent, whereas daunomycin-induced apoptosis was p53- and NF-kappaB-independent.	Daunorubicin	142-152	P53	Homo sapiens	157-160
11094173-14	2000	There could be a p53-dependent apoptotic pathway in butyrate-induced differentiated Y-79 cells due to the inability to regulate cell cycling.	Butyrates	52-60	P53	Homo sapiens	17-20
11798837-9	2000	CONCLUSION: After introduced into GLC-82 cells, Ad-p53 shows enhanced therapeutic efficiency for GLC-82 cells when combined with CDDP or As(2)O(3).	Arsenic	137-139	P53	Homo sapiens	51-54
10856831-6	2000	Exposure to AFB1-8, 9-epoxide alone induces a low frequency of AGG to AGT mutation in codon 249 of the p53 gene, as determined by an allele-specific polymerase chain reaction (AS-PCR) assay.	aflatoxin B1-2,3-oxide	12-29	P53	Homo sapiens	103-106
10845425-2	2000	A calpain inhibitor, n-acetyl-leu-leu-norleucinal (calpain inhibitor 1), was assessed for ability to enhance p53-dependent apoptosis in human tumor cell lines with endogenous wild-type p53 and in altered p53 cell lines with the replacement of wild-type p53 by a recombinant adenovirus (rAd-p53).	n-acetyl-leu-leu	21-37	P53	Homo sapiens	109-112
10866285-1	2000	PURPOSE: This study tests the hypothesis that p53 status, i.e. wild type versus mutant form, is a determinant in radiation protection of human glioma cells by WR-1065, the active thiol form of amifostine (WR-2721).	Amifostine	193-203	P53	Homo sapiens	46-49
10699891-0	2000	p53 mutation pattern in hepatocellular carcinoma in workers exposed to vinyl chloride.	Vinyl Chloride	71-85	P53	Homo sapiens	0-3
10779915-4	2000	Similar effects were observed upon transduction of the p53-GSE22 genetic suppressor element, known to reduce p53 transcriptional activity.	gse22	59-64	P53	Homo sapiens	55-58
10779915-4	2000	Similar effects were observed upon transduction of the p53-GSE22 genetic suppressor element, known to reduce p53 transcriptional activity.	gse22	59-64	P53	Homo sapiens	109-112
10874474-0	2000	Induction of p53-independent p21 during ceramide-induced G1 arrest in human hepatocarcinoma cells.	Ceramides	40-48	P53	Homo sapiens	13-16
10874474-6	2000	p21 induction was also observed in the Hep3B cells lacking a functional p53 after exposure to ceramide.	Ceramides	94-102	P53	Homo sapiens	72-75
10874474-11	2000	Together, these results suggest that p21, induced through p53-independent pathway, participates in the induction of pRb dephosphorylation by inhibiting cdk2 activity during ceramide-mediated G1 arrest in hepatocarcinoma cells.	Ceramides	173-181	P53	Homo sapiens	58-61
10585263-3	1999	Previously, we reported that p21 was induced in a p53-independent manner during ceramide-induced apoptosis in human hepatocarcinoma cell lines.	Ceramides	80-88	P53	Homo sapiens	50-53
10632350-2	1999	Overexpression of the p53 protein was present in 49% of the samples studied with CM1, 18% with PAb1801, 30% with DO7, and 44% with DO7.	[(2S,3S,4S,5R,6S)-6-methoxy-3,4,5-tris(oxidanyl)oxan-2-yl]methanesulfonic acid	113-116	P53	Homo sapiens	22-25
10632350-2	1999	Overexpression of the p53 protein was present in 49% of the samples studied with CM1, 18% with PAb1801, 30% with DO7, and 44% with DO7.	[(2S,3S,4S,5R,6S)-6-methoxy-3,4,5-tris(oxidanyl)oxan-2-yl]methanesulfonic acid	131-134	P53	Homo sapiens	22-25
10597302-0	1999	Induction of apoptosis in U937 human leukemia cells by suberoylanilide hydroxamic acid (SAHA) proceeds through pathways that are regulated by Bcl-2/Bcl-XL, c-Jun, and p21CIP1, but independent of p53.	Vorinostat	55-86	P53	Homo sapiens	195-198
10597302-0	1999	Induction of apoptosis in U937 human leukemia cells by suberoylanilide hydroxamic acid (SAHA) proceeds through pathways that are regulated by Bcl-2/Bcl-XL, c-Jun, and p21CIP1, but independent of p53.	Vorinostat	88-92	P53	Homo sapiens	195-198
10597302-9	1999	These findings indicate that SAHA potently induces apoptosis in human leukemia cells via a pathway that is p53-independent but at least partially regulated by Bcl-2/Bcl-XL, p21CIP1, and the c-Jun/AP-1 signaling cascade.	Vorinostat	29-33	P53	Homo sapiens	107-110
10544021-5	1999	Activation of p53 was accompanied by phosphorylation of p53 at Ser-15 and elevated p21 and MDM2, both of which were at least partly blocked by wortmannin, a kinase inhibitor against proteins with a PI3 kinase domain.	Wortmannin	143-153	P53	Homo sapiens	14-17
10544021-5	1999	Activation of p53 was accompanied by phosphorylation of p53 at Ser-15 and elevated p21 and MDM2, both of which were at least partly blocked by wortmannin, a kinase inhibitor against proteins with a PI3 kinase domain.	Wortmannin	143-153	P53	Homo sapiens	56-59
10576651-5	1999	Wortmannin-treated cultures display a diminished capacity for radiation-induced up-regulation of p53 protein and expression of p21WAF1, a p53-regulated gene involved in cell cycle arrest at the G1/S border; the treated cultures also exhibit decreased capacity for enhancement of CaMKII activity post-irradiation, known to be necessary for triggering the S phase checkpoint.	Wortmannin	0-10	P53	Homo sapiens	97-100
10576651-5	1999	Wortmannin-treated cultures display a diminished capacity for radiation-induced up-regulation of p53 protein and expression of p21WAF1, a p53-regulated gene involved in cell cycle arrest at the G1/S border; the treated cultures also exhibit decreased capacity for enhancement of CaMKII activity post-irradiation, known to be necessary for triggering the S phase checkpoint.	Wortmannin	0-10	P53	Homo sapiens	138-141
10473588-5	1999	We show that both recombinant and endogenous forms of p53 specifically interact with KIX.	kix	85-88	P53	Homo sapiens	54-57
10393722-14	1999	IMPLICATIONS: 4-HPR may form the basis for a novel, p53-independent chemotherapy that operates through increased intracellular levels of ceramide and that retains cytotoxicity under reduced oxygen conditions.	Ceramides	137-145	P53	Homo sapiens	52-55
10391688-3	1999	Not surprisingly, therefore, p53 has been intensively studied by 32P metabolic labelling.	Phosphorus-32	65-68	P53	Homo sapiens	29-32
10391688-5	1999	These data demonstrate for the first time that 32P labelling is sufficient to induce a biologically-significant, p53-mediated cellular response and strongly suggest that it perturbs the phosphorylation state of p53 which it is being used to measure.	Phosphorus-32	47-50	P53	Homo sapiens	113-116
10391688-5	1999	These data demonstrate for the first time that 32P labelling is sufficient to induce a biologically-significant, p53-mediated cellular response and strongly suggest that it perturbs the phosphorylation state of p53 which it is being used to measure.	Phosphorus-32	47-50	P53	Homo sapiens	211-214
10415582-2	1999	The cells were originally derived from a human liver biopsy and immortalized through lipofectamine-mediated transfection of albumin-promotor-regulated antisense constructions against the negative controlling cell cycle proteins Rb and p53 (pAlb asRb, pAIb asp53).	Lipofectamine	85-98	P53	Homo sapiens	235-238
10362106-6	1999	PNU 151807, like tallimustine, is able to induce an activation of p53, and consequently of p21 and BAX in a human ovarian cancer cell line (A2780) expressing wild-type p53.	tallimustine	17-29	P53	Homo sapiens	66-69
10341297-3	1999	In this study, we investigated the molecular mechanisms by which auristatin-PE, a newly developed experimental agent, and gemcitabine, a commercially available anti-cancer agent, exert their inhibitory effects on pancreatic cancer cell lines containing wild-type p53 (HPAC) and mutant p53 (PANC-1).	gemcitabine	122-133	P53	Homo sapiens	263-266
10390705-0	1999	Plasma p53 protein and anti-p53 antibody expression in vinyl chloride monomer workers in Taiwan.	Vinyl Chloride	55-69	P53	Homo sapiens	7-10
10472362-1	1999	Expression of mutant p53 in 19 patients with stage III moderately differentiated serous cystadenocarcinoma of the ovary, who all had optimal primary cytoreductive surgery and six cycles of cisplatin and cyclophosphamide was analyzed to determine its prognostic significance.	Cyclophosphamide	203-219	P53	Homo sapiens	21-24
10360645-0	1999	Ceramide triggers p53-dependent apoptosis in genetically defined fibrosarcoma tumour cells.	Ceramides	0-8	P53	Homo sapiens	18-21
10360645-8	1999	These results suggest that ceramide-induced apoptosis in tumour cells can be dependent on the status of p53 and imply that p53 is also important for stress-induced apoptotic signal transduction cascades generated at the plasma membrane.	Ceramides	27-35	P53	Homo sapiens	104-107
10360645-8	1999	These results suggest that ceramide-induced apoptosis in tumour cells can be dependent on the status of p53 and imply that p53 is also important for stress-induced apoptotic signal transduction cascades generated at the plasma membrane.	Ceramides	27-35	P53	Homo sapiens	123-126
10334203-5	1999	Using 32P-5"-end-labeled DNA fragments obtained from human p53 tumor suppressor gene and c-Ha-ras-1 protooncogene, we showed that PBQ plus NADH, and also PHQ, induced DNA damage frequently at thymine residues, in the presence of Cu(II).	phenylbenzoquinone	130-133	P53	Homo sapiens	59-62
10100719-0	1999	Expression of p53 in cisplatin-resistant ovarian cancer cell lines: modulation with the novel platinum analogue (1R, 2R-diaminocyclohexane)(trans-diacetato)(dichloro)-platinum(IV).	1R,2R-diaminocyclohexane	113-138	P53	Homo sapiens	14-17
10100719-0	1999	Expression of p53 in cisplatin-resistant ovarian cancer cell lines: modulation with the novel platinum analogue (1R, 2R-diaminocyclohexane)(trans-diacetato)(dichloro)-platinum(IV).	trans-diacetato)	140-156	P53	Homo sapiens	14-17
10190788-4	1999	Studies of the p53 gene sequence of ovarian tumors at diagnosis suggest that p53 mutations are a potent predictor of response to subsequent treatment with carboplatin.	Carboplatin	155-166	P53	Homo sapiens	15-18
10190788-4	1999	Studies of the p53 gene sequence of ovarian tumors at diagnosis suggest that p53 mutations are a potent predictor of response to subsequent treatment with carboplatin.	Carboplatin	155-166	P53	Homo sapiens	77-80
9879988-7	1998	Moreover, 3AB but not its analog inhibited irradiation-induced activation of sequence-specific DNA binding of wtp53 as detected using 32P-labeled or biotin-labeled p53 consensus sequence (p53CON).	Phosphorus-32	134-137	P53	Homo sapiens	112-115
9951689-4	1998	Chemosensitivity data, according to a short-term assay (FMCA), indicated that tumours with p53 mutation were more resistant to cisplatin and cyclophosphamide.	Cyclophosphamide	141-157	P53	Homo sapiens	91-94
9769393-6	1998	On the other hand, an A to G substitution at codon 170 in exon 5 of p53 gene resulting in glutamic acid (ACG) to glycine (GCG) was detected in the DNA of her tongue cancer.	gallocatechin gallate	122-125	P53	Homo sapiens	68-71
9683832-5	1998	The degree of DCsI of tumors with expression of p53 (19/mm2, n=50) was significantly lower than that of DCsI in 38 tumors without expression of p53 (27/mm2, P=0.0411).	dcsi	14-18	P53	Homo sapiens	48-51
9703286-0	1998	Therapy effect of either paclitaxel or cyclophosphamide combination treatment in patients with epithelial ovarian cancer and relation to TP53 gene status.	Cyclophosphamide	39-55	P53	Homo sapiens	137-141
9664074-0	1998	p53-dependent ceramide response to genotoxic stress.	Ceramides	14-22	P53	Homo sapiens	0-3
9664074-4	1998	In this study, we investigated the relationship between p53 and ceramide.	Ceramides	64-72	P53	Homo sapiens	56-59
9664074-6	1998	In these cells, p53 activation was followed by a dose- and time-dependent increase in endogenous ceramide levels which was not seen in cells lacking functional p53 and treated similarly.	Ceramides	97-105	P53	Homo sapiens	16-19
9664074-8	1998	However, in p53-independent systems, such as growth suppression induced by TNF-alpha or serum deprivation, ceramide accumulated irrespective of the upregulation of p53, indicating that p53 regulates ceramide accumulation in only a subset of growth-suppressive pathways.	Ceramides	107-115	P53	Homo sapiens	12-15
9664074-10	1998	Also, when cells lacking functional p53, either due to mutation or the expression of the E6 protein of human papilloma virus, were treated with exogenous ceramide, there was equal growth suppression, cell cycle arrest, and apoptosis as compared with cells expressing normal p53.	Ceramides	154-162	P53	Homo sapiens	36-39
9664074-10	1998	Also, when cells lacking functional p53, either due to mutation or the expression of the E6 protein of human papilloma virus, were treated with exogenous ceramide, there was equal growth suppression, cell cycle arrest, and apoptosis as compared with cells expressing normal p53.	Ceramides	154-162	P53	Homo sapiens	274-277
9664074-12	1998	Instead, they suggest that, in situations where p53 performs a critical regulatory role, such as the response to genotoxic stress, it functions "upstream" of ceramide.	Ceramides	158-166	P53	Homo sapiens	48-51
9661637-4	1998	BHT-101 and KAT-4 cells had mutant p53.	Butylated Hydroxytoluene	0-3	P53	Homo sapiens	35-38
9661637-10	1998	BHT-101 cells were most sensitive to killing by Ad-p53, with an IC50 of less than 2 multiplicity of infection; SW-1736 cells were intermediate in sensitivity; KAT-4 cells were resistant.	Butylated Hydroxytoluene	0-3	P53	Homo sapiens	51-54
9618491-4	1998	We show that concomitant with growth arrest, butyrate induces p21 mRNA expression in an immediate-early fashion, through transactivation of a promoter cis-element(s) located within 1.4 kb of the transcriptional start site, independent of p53 binding.	Butyrates	45-53	P53	Homo sapiens	238-241
9649136-2	1998	Here, we examined the effects of wild-type and mutated p53 (143 Val-Ala) on tumorigenic and metastatic potential of two human melanoma cell lines.	H-VAL-ALA-OH	64-71	P53	Homo sapiens	55-58
9636999-1	1998	We tested the hypothesis that the instability of the trinucleotide CTG at the myotonic dystrophy (DM) locus could be an intrinsic DNA damage recognisable by the p53 cell-cycle checkpoint system.	ctg	67-70	P53	Homo sapiens	161-164
9636999-4	1998	However, in the cells treated with adryamicin, p53 protein levels were comparable in DM and control cells.	adryamicin	35-45	P53	Homo sapiens	47-50
9677462-5	1998	Molecular analysis of the same specimen showed mutations of the p53 gene in 13.3% of OLs and 9, 6% of OSCCs.	N-biotin-C-Co4(mu3-O)4(Py)4(H2O)4-beta-alanine	85-88	P53	Homo sapiens	64-67
9610789-0	1998	p53 mutations in cyclophosphamide-associated bladder cancer.	Cyclophosphamide	17-33	P53	Homo sapiens	0-3
9610789-3	1998	We examined 19 cyclophosphamide-related bladder tumors to test the hypothesis that they might contain somatic mutations in the p53 tumor suppressor gene that could link a specific metabolite to the etiology of these cancers.	Cyclophosphamide	15-31	P53	Homo sapiens	127-130
9610789-5	1998	The p53 mutation spectrum of these cyclophosphamide-associated bladder cancers differed significantly from patterns reported for sporadic (P = 0.020), smoking-related (0.043), and schistosomiasis-linked (P = 0.002) tumors but not arylamine-associated neoplasms (P = 0.860).	Cyclophosphamide	35-51	P53	Homo sapiens	4-7
9635858-8	1998	Through a rigorous statistical test, the UV-induced p53 mutation spectrum appears to differ significantly (P &lt; 0.008) from the one induced by the antineoplastic drug chloroethyl-cyclohexyl-nitrosourea, and to be indistinguishable from the one observed in NMSC (P = 0.4).	Lomustine	169-203	P53	Homo sapiens	52-55
9548807-13	1998	Moreover, the induction of p53 by AZQ requires both the quinone and the aziridine moieties of the AZQ molecule.	aziridine	72-81	P53	Homo sapiens	27-30
9482505-0	1998	Molecular epidemiology of p53 protein mutations in workers exposed to vinyl chloride.	Vinyl Chloride	70-84	P53	Homo sapiens	26-29
9482505-3	1998	Workers exposed to vinyl chloride who are at risk for the development of the sentinel neoplasm angiosarcoma of the liver represent a model population for the study of such a mutant p53 biomarker, since vinyl chloride is known to cause specific p53 mutations in persons with angiosarcoma of the liver.	Vinyl Chloride	19-33	P53	Homo sapiens	181-184
9482505-3	1998	Workers exposed to vinyl chloride who are at risk for the development of the sentinel neoplasm angiosarcoma of the liver represent a model population for the study of such a mutant p53 biomarker, since vinyl chloride is known to cause specific p53 mutations in persons with angiosarcoma of the liver.	Vinyl Chloride	19-33	P53	Homo sapiens	244-247
9482505-3	1998	Workers exposed to vinyl chloride who are at risk for the development of the sentinel neoplasm angiosarcoma of the liver represent a model population for the study of such a mutant p53 biomarker, since vinyl chloride is known to cause specific p53 mutations in persons with angiosarcoma of the liver.	Vinyl Chloride	202-216	P53	Homo sapiens	181-184
9482505-3	1998	Workers exposed to vinyl chloride who are at risk for the development of the sentinel neoplasm angiosarcoma of the liver represent a model population for the study of such a mutant p53 biomarker, since vinyl chloride is known to cause specific p53 mutations in persons with angiosarcoma of the liver.	Vinyl Chloride	202-216	P53	Homo sapiens	244-247
9482505-4	1998	To determine the relation between vinyl chloride exposure and this p53 biomarker, the authors examined serum samples collected between 1987 and 1992 from a cohort of 225 French vinyl chloride workers and 111 unexposed controls (matched according to age, sex, race, smoking, and alcohol drinking) for the presence of mutant p53 protein, using an enzyme-linked immunosorbent assay.	Vinyl Chloride	34-48	P53	Homo sapiens	67-70
9482505-5	1998	Stratification of the exposed workers by quartile of vinyl chloride exposure (in estimated ppm-years) yielded a statistically significant trend of increasing odds ratios for p53 biomarker seropositivity with increasing exposure.	Vinyl Chloride	53-67	P53	Homo sapiens	174-177
9482505-6	1998	These results suggest that this serum biomarker for mutant p53 protein is related to vinyl chloride exposure and may be an early indicator of carcinogenic risk in exposed individuals.	Vinyl Chloride	85-99	P53	Homo sapiens	59-62
10223623-0	1998	Infrequent p53 mutations in arsenic-related skin lesions.	Arsenic	28-35	P53	Homo sapiens	11-14
10223623-6	1998	Accumulation of the p53 protein was detected (with a monoclonal DO-7 antibody) in 78% of the lesions from cases with arsenic exposure.	Arsenic	117-124	P53	Homo sapiens	20-23
10223623-7	1998	Two of the six (30%) arsenic-related premalignant lesions and in addition one UV related carcinoma in situ lesion were clearly and repeatedly positive when p53 exons 5 to 8 were screened by a nonradioactive single-strand conformation polymorphism (SSCP) analysis.	Arsenic	21-28	P53	Homo sapiens	156-159
10223623-10	1998	Our results suggest that the frequent accumulation of p53 protein in arsenic-related skin lesions is not due to p53 mutations.	Arsenic	69-76	P53	Homo sapiens	54-57
9398049-0	1997	Modulation of p53 expression in cultured colonic adenoma cell lines by the naturally occurring lumenal factors butyrate and deoxycholate.	Butyrates	111-119	P53	Homo sapiens	14-17
9398049-5	1997	We report that both butyrate and deoxycholate can down-regulate the expression of wild-type and mutant p53.	Butyrates	20-28	P53	Homo sapiens	103-106
9315628-7	1997	Using different chelators to interfere with copper transport by PDTC, we found that bathocuproinedisulfonic acid (BCS), a non-cell-permeable chelator of Cu1+, prevented both copper import and p53 down-regulation.	bathocuproine sulfonate	84-112	P53	Homo sapiens	192-195
9315628-7	1997	Using different chelators to interfere with copper transport by PDTC, we found that bathocuproinedisulfonic acid (BCS), a non-cell-permeable chelator of Cu1+, prevented both copper import and p53 down-regulation.	bathocuproine sulfonate	114-117	P53	Homo sapiens	192-195
9315628-8	1997	In contrast, 1,10-orthophenanthroline, a cell-permeable chelator of Cu2+, promoted the redox activity of copper and up-regulated p53 DNA-binding activity through a DNA damage-dependent pathway.	1,10-orthophenanthroline	13-37	P53	Homo sapiens	129-132
9315663-7	1997	Notably, the lack of pRB in these U937-derived clones renders these p53-null cells highly resistant to apoptosis induced by serum withdrawal, calphostin C, and ceramide.	Ceramides	160-168	P53	Homo sapiens	68-71
9374191-12	1997	In light of data suggesting that ALZ-50 recognizes a phosphorylated form of p53, we conclude that neuronal death in the developing nervous system involves the post-translational modification of an existing protein, p53.	alz-50	33-39	P53	Homo sapiens	76-79
9374191-12	1997	In light of data suggesting that ALZ-50 recognizes a phosphorylated form of p53, we conclude that neuronal death in the developing nervous system involves the post-translational modification of an existing protein, p53.	alz-50	33-39	P53	Homo sapiens	215-218
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	P53	Homo sapiens	112-115
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	P53	Homo sapiens	169-172
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	P53	Homo sapiens	169-172
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	P53	Homo sapiens	169-172
9266962-4	1997	Several observations indicate MG-132 alleviates squelching by influencing the conformation of newly synthesized p53 and E2F-1:MG-132 increased the fraction of wild type p53 bound by a monoclonal antibody which preferentially recognizes mutant conformers of p53, increased binding of hsp70 to p53 and inhibited nuclear accumulation of both p53 and E2F-1, but not the pocket protein p107.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	126-132	P53	Homo sapiens	169-172
9266962-6	1997	Because MG-132 and lactacycstin are highly specific inhibitors of the proteasome protease, our results suggest that the proteasome influences post-translational processes involved in proper folding and cytoplasmic clearing of E2F-1 and p53.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	8-14	P53	Homo sapiens	236-239
9224745-9	1997	This study showed that significant overexpression of p53 protein was higher in BD with chronic arsenic exposure.	Arsenic	95-102	P53	Homo sapiens	53-56
9136984-7	1997	In digitonin permeabilized cells IAF-p53 was imported into nuclei.	Digitonin	3-12	P53	Homo sapiens	37-40
9069316-2	1997	METHODS AND MATERIALS: p53 status in primary and SV40 T antigen-transformed AT cell lines was analyzed using immunocytochemistry and by sequencing with the dideoxynucleotide termination method.	Dideoxynucleotides	156-173	P53	Homo sapiens	23-26
9155049-6	1997	Interestingly, a strong statistical association was observed between p53 nuclear accumulation and MC (P = 0.0003).	Methylcholanthrene	98-100	P53	Homo sapiens	69-72
9155049-8	1997	When we analysed the concomitant influence of MC and p53 expression on overall survival, we were able to confirm a real predominant role of MC in comparison with p53.	Methylcholanthrene	140-142	P53	Homo sapiens	53-56
9155049-10	1997	These results underline the prognostic impact of MC and p53 protein accumulation in NSCLC and their reciprocal inter-relationship, supporting the hypothesis of a wild-type p53 regulation on the angiogenetic process through a VEGF up-regulation.	Methylcholanthrene	49-51	P53	Homo sapiens	172-175
9027627-0	1997	The inhibitory effect of UVB irradiation on the expression of p53 and Ki-67 proteins in arsenic-induced Bowen"s disease.	Arsenic	88-95	P53	Homo sapiens	62-65
9061063-12	1996	Further follow-up will be required to assess the value of p53 overexpression as a prognostic factor in invasive bladder cancer patients treated with neoadjuvant carboplatin-based chemotherapy.	Carboplatin	161-172	P53	Homo sapiens	58-61
8900110-2	1996	The present studies demonstrate that the antimetabolite 1-beta-D-arabinofuranosylcytosine (ara-C) induces binding of c-Abl and p53.	antimetabolite 1-beta-d-arabinofuranosylcytosine	41-89	P53	Homo sapiens	127-130
8651706-7	1996	The recombinant p53 isoforms were phosphorylated by 32P-labeling.	Phosphorus-32	52-55	P53	Homo sapiens	16-19
8639538-6	1996	Furthermore, topoisomerase I sediments at a higher molecular weight in the presence of p53 as revealed by sucrose density gradient analysis in the absence of DNA.	Sucrose	106-113	P53	Homo sapiens	87-90
8819013-2	1996	Vinyl chloride, a known human carcinogen that induces the rare sentinel neoplasm angiosarcoma of the liver, has been associated with specific A--&gt;T transversions at the first base of codons 249 and 255 of the p53 gene.	Vinyl Chloride	0-14	P53	Homo sapiens	212-215
8634092-0	1996	Preferential DNA damage in the p53 gene by benzo[a]pyrene metabolites in cytochrome P4501A1-expressing xeroderma pigmentosum group A cells.	benzo	43-48	P53	Homo sapiens	31-34
8829621-4	1996	When cells were cultured in the presence of phosphotyrosine, there was a marked decrease in p53 expression.	Phosphotyrosine	44-59	P53	Homo sapiens	92-95
8562931-4	1996	Whereas wild-type p53 activity per se induced maturation of certain cells, other underwent cell death judging from the reduced capability to exclude trypan blue and the appearance of fragmented DNA in flow cytometric analysis.	Trypan Blue	149-160	P53	Homo sapiens	18-21
9081399-20	1996	Several genes are involved in control of this process; these include the p53 gene, mutations of which have been linked to cisplatin resistance in our laboratory studies, as well as in clinical trials with carboplatin.	Carboplatin	205-216	P53	Homo sapiens	73-76
7658501-0	1995	Anti-p53 antibodies in sera of workers occupationally exposed to vinyl chloride.	Vinyl Chloride	65-79	P53	Homo sapiens	5-8
7658501-3	1995	PURPOSE: The objective of this study was to determine the prevalence and time of appearance of serum anti-p53 antibodies during the pathogenesis of ASL associated with occupational exposure to vinyl chloride.	Vinyl Chloride	193-207	P53	Homo sapiens	106-109
7658501-4	1995	METHODS: Enzyme-linked immunoassay (EIA) was used to detect anti-p53 antibodies in 148 serum samples from 92 individuals occupationally exposed (in France or in Kentucky) to vinyl chloride; 15 of these individuals (six from France and nine from Kentucky) had ASL.	Vinyl Chloride	174-188	P53	Homo sapiens	65-68
7658501-12	1995	Four of the 77 vinyl chloride-exposed workers without diagnosed ASL were positive for anti-p53 antibodies; two of the four had symptoms related to vinyl chloride toxicity.	Vinyl Chloride	15-29	P53	Homo sapiens	91-94
7658501-13	1995	Tumors from three of the six vinyl chloride-exposed workers from which sufficient DNA for analysis was obtained had A:T to T:A missense mutations of the p53 gene.	Vinyl Chloride	29-43	P53	Homo sapiens	153-156
7658501-16	1995	CONCLUSIONS AND IMPLICATIONS: Serum anti-p53 antibodies can predate clinical diagnosis of certain tumors, such as ASL, and may be useful in identifying individuals at high cancer risk, such as workers with occupational exposure to vinyl chloride.	Vinyl Chloride	231-245	P53	Homo sapiens	41-44
7670136-0	1995	The bcl-2 and p53 oncoproteins can be modulated by bryostatin 1 and dolastatins in human diffuse large cell lymphoma.	bryostatin 1	51-63	P53	Homo sapiens	14-17
7670136-0	1995	The bcl-2 and p53 oncoproteins can be modulated by bryostatin 1 and dolastatins in human diffuse large cell lymphoma.	dolastatins	68-79	P53	Homo sapiens	14-17
7727133-2	1995	A nuclear phosphoprotein, p53, was isolated by immunoprecipitation after biosynthetic labeling with 35S, 32P or 33P in cultured human cells.	Phosphorus-32	105-108	P53	Homo sapiens	26-29
7727133-7	1995	The relative phosphorylation of each p53 isoform was estimated by normalizing 33P or 32P isoform volumes with the corresponding 35S volume and showed progressive phosphorylation of acidic isoforms.	Phosphorus-32	85-88	P53	Homo sapiens	37-40
8187772-3	1994	In contrast to other systems, such as inhibition of GAL4 by GAL80 or of p53 by MDM2, where repression is mediated by direct interaction at regions overlapping the transcription activation domain, interaction with PHO80 involves two regions of PHO4 distinct from those involved in transcription activation or DNA-binding and dimerization.	pho80	213-218	P53	Homo sapiens	72-75
8247533-6	1993	Agents that produced double-strand breaks in DNA and/or inhibition of transcription caused an induction of p53 in the absence of radiation in control cells but not in ataxia-telangiectasia, but inhibitors of cell cycle progression such as mimosine and aphidicolin led to an increase in p53 in both cell types in the absence of radiation.	Aphidicolin	252-263	P53	Homo sapiens	107-110
1322917-5	1992	Furthermore, in control cells only 30% of the p53 was complexed with large-T antigen, whereas in butyrate-treated cells all the p53 was complexed with large-T antigen.	Butyrates	97-105	P53	Homo sapiens	128-131
1717923-2	1991	The presence of the mutant p53 was confirmed in the cell lines as substitutions in exon 7 (codon 238, TGT greater than AGT) and exon 5 (codon 152, CCG greater than CTG) respectively.	ctg	164-167	P53	Homo sapiens	27-30
33939887-10	2021	Breast tissue-occurring metabolites" antiproliferation was mainly exerted in p53-wild-type MCF-7 cells by curcuminoids through cell cycle arrest, senescence, and apoptosis induction via p53/p21 induction, while isoflavone-derived metabolites exerted estrogenic-like activity.	Diarylheptanoids	106-118	P53	Homo sapiens	186-189
33767588-6	2021	Delivery of the proteasome inhibitor, MG132, reversed the inhibitory effect of miR-26b on the level of p53 following doxorubicin treatment.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	38-43	P53	Homo sapiens	103-106
7703804-3	1994	Sequencing highly conserved open reading frames of the p53 gene of these cancer cells showed point mutations in the SCC-4 and Tu-177 cell lines, a base transition from CCC to TCC occurred at codon 151; and in the line FaDu, a mutation of CGG to CTG occurred at codon 248.	ctg	245-248	P53	Homo sapiens	55-58
34954595-0	2022	Discovery of phthalazino(1,2-b)-quinazolinone derivatives as multi-target HDAC inhibitors for the treatment of hepatocellular carcinoma via activating the p53 signal pathway.	phthalazino(1,2-b)-quinazolinone	13-45	P53	Homo sapiens	155-158
34800264-0	2022	Metoprolol Protects Against Arginine Vasopressin-Induced Cellular Senescence in H9C2 Cardiomyocytes by Regulating the Sirt1/p53/p21 Axis.	Metoprolol	0-10	P53	Homo sapiens	124-127
34800264-9	2022	Finally, Metoprolol was able to downregulate the AVP-induced expression of acetylated p53 and p21.	Metoprolol	9-19	P53	Homo sapiens	86-89
34380701-7	2022	The p53 signalling pathway was the most enriched signature in lung tissues and lung fibroblasts of SSc-ILD, and was significantly correlated with carbon monoxide diffusing capacity of lung, cellular senescence and apoptosis.	Carbon Monoxide	146-161	P53	Homo sapiens	4-7
34820006-0	2022	Tanshinone IIA potentiates the efficacy of imatinib by regulating the AKT-MDM2-P53 signaling pathway in Philadelphia chromosome-positive acute lymphoblastic leukemia.	Imatinib Mesylate	43-51	P53	Homo sapiens	79-82
34896434-6	2022	Ruthenium-phloretin complex could modulate p53 intervene apoptosis in the breast carcinoma, initiated by the trail of intrinsic apoptosis facilitated through Bcl2 and Bax and at the same time down regulating the PI3K/Akt/mTOR pathway coupled with MMP9 regulated tumor invasive pathways.	ruthenium-phloretin	0-19	P53	Homo sapiens	43-46
34781244-2	2021	Gemcitabine (GEM) is the first-line treatment for PDAC, but its efficacy is limited in most patients due to the GEM resistance from KRAS and P53 gene mutations.	gemcitabine	0-11	P53	Homo sapiens	141-144
34781244-2	2021	Gemcitabine (GEM) is the first-line treatment for PDAC, but its efficacy is limited in most patients due to the GEM resistance from KRAS and P53 gene mutations.	gemcitabine	13-16	P53	Homo sapiens	141-144
34797187-13	2021	CONCLUSION: High concentration of ZnO NP caused toxicity to HGF-1 cells and inhibited cell proliferation by regulating MDM2 and p53 expression.	zno np	34-40	P53	Homo sapiens	128-131
34180037-1	2021	Aim The oral MDM2 antagonist idasanutlin inhibits the p53-MDM2 interaction, enabling p53 activation, tumor growth inhibition, and increased survival in xenograft models.	RG7388	29-40	P53	Homo sapiens	54-57
34180037-1	2021	Aim The oral MDM2 antagonist idasanutlin inhibits the p53-MDM2 interaction, enabling p53 activation, tumor growth inhibition, and increased survival in xenograft models.	RG7388	29-40	P53	Homo sapiens	85-88
34180037-14	2021	Conclusions Idasanutlin demonstrated dose- and schedule-dependent p53 activation with durable disease stabilization in some patients.	RG7388	12-23	P53	Homo sapiens	66-69
34866972-9	2021	These chemotherapeutic and chemosensitising activities of hesperidin and hesperetin have been linked to several mechanisms, including the modulation of signalling pathways, glucose uptake, enzymes, miRNA expression, oxidative status, cell cycle regulatory proteins, tumour suppressor p53, plasma and liver lipid profiles as well as DNA repair mechanisms.	hesperetin	73-83	P53	Homo sapiens	284-287
34844492-6	2021	The BNE-PNP induced an early programmed necrotic (necroptosis) and late apoptotic death on the MCF7 cancer cells by up-regulating all the P53/TNF-alpha and Cas-3 gene expression, respectively.	bne-pnp	4-11	P53	Homo sapiens	138-141
34837558-9	2021	In vitro experiments showed that OST and lobaplatin could significantly induce apoptosis in the MDA-MB-231 cells (P < 0.05), as indicated by elevation in the translation level of p53/Bax/caspase-3 p17 and downregulation of the Bcl-2 protein.	osthol	33-36	P53	Homo sapiens	179-182
34837558-10	2021	Finally, combined treatment with OST and lobaplatin had an enhanced anti-tumor effect (P < 0.05) on proliferation and apoptosis, as well as more obvious effects on the related proteins (p53, Bax, Bcl-2, and caspase-3 p17).	osthol	33-36	P53	Homo sapiens	186-189
34832937-10	2021	Further analysis revealed that the hexane fraction-treated RMS cells upregulated the p53 gene twofold (2.72) compared to the p21 (0.77) gene, whereas in the MCF-7 cells, a 2.21-fold upregulation of p53 was observed compared to the p21 (0.64) gene.	Hexanes	35-41	P53	Homo sapiens	85-88
34832937-10	2021	Further analysis revealed that the hexane fraction-treated RMS cells upregulated the p53 gene twofold (2.72) compared to the p21 (0.77) gene, whereas in the MCF-7 cells, a 2.21-fold upregulation of p53 was observed compared to the p21 (0.64) gene.	Hexanes	35-41	P53	Homo sapiens	198-201
34832937-14	2021	The study"s findings highlighted that the non-polar compounds present in the hexane fraction of C. minima suppressed cell proliferation and induced apoptosis-mediated cell death in RMS and MCF-7 cells, mainly via the activation of the p53 gene.	Hexanes	77-83	P53	Homo sapiens	235-238
34835028-12	2021	These results suggest that AdBcl-xL plays negative roles in GSIV-induced mitochondrial apoptosis and virus replication by binding to AdBak and inhibiting p53 activation.	adbcl-xl	27-35	P53	Homo sapiens	154-157
34732786-5	2021	Transcriptomic analysis and gene set enrichment analyses revealed that p53 was one of the most significantly upregulated hallmarks in both LPS-primed and LPS-tolerant macrophages in the presence of carboplatin, while E2F and G2/M were the most negatively regulated hallmarks.	Carboplatin	198-209	P53	Homo sapiens	71-74
34170069-0	2021	A new diarylpentanoid with potential activation of the p53 pathway: combination of in silico screening studies, synthesis, and biological activity evaluation.	diarylpentanoid	6-21	P53	Homo sapiens	55-58
34226168-8	2021	Treatment response to CR or PR and TP53 mutation were 2 prognostic factor for OS and PFS in decitabine with CEG regimen.	Decitabine	92-102	P53	Homo sapiens	35-39
34390769-2	2021	In this study, the effects of ctHBx on HepG2 cells were investigated by measuring ctHBx-induced changes in the cell cycle-related target proteins cell division cycle 25C (cdc25C) and p53 downstream of the mitogen-activated protein kinase (MAPK) pathway.	cthbx	30-35	P53	Homo sapiens	183-186
34390769-2	2021	In this study, the effects of ctHBx on HepG2 cells were investigated by measuring ctHBx-induced changes in the cell cycle-related target proteins cell division cycle 25C (cdc25C) and p53 downstream of the mitogen-activated protein kinase (MAPK) pathway.	cthbx	82-87	P53	Homo sapiens	183-186
34390769-7	2021	In addition, ctHBx activated the ERK/JNK/p38 MAPK signaling pathway to regulate cell viability by affecting the expression of cyclin-related proteins, including cdc25C and p53.	cthbx	13-18	P53	Homo sapiens	172-175
34390769-8	2021	CONCLUSION: The present study demonstrates that ctHBx promote the formation and development of HCC via regulating MAPK/cdc25C and p53 axis.	cthbx	48-53	P53	Homo sapiens	130-133
34534222-6	2021	The aim of the present study is to test the effect of 5-AzaD on growth of human squamous cell carcinoma (FaDu), a HPV(-) and p53 mutated cells, in vitro and in vivo.	Decitabine	54-60	P53	Homo sapiens	125-128
34534222-11	2021	These findings may emphasis that 5-AzaD is effective in treatment of HPV(-) HNSCC tumours through TP53 independent pathway.	Decitabine	33-39	P53	Homo sapiens	98-102
34475054-9	2021	AITC increased p-ATMSer1981, p-ATRSer428, p53, p-p53Ser15, p-H2A.XSer139, BRCA1, and PARP at 10-30 muM at 24 and 48 h treatments.	allyl isothiocyanate	0-4	P53	Homo sapiens	42-45
34475054-9	2021	AITC increased p-ATMSer1981, p-ATRSer428, p53, p-p53Ser15, p-H2A.XSer139, BRCA1, and PARP at 10-30 muM at 24 and 48 h treatments.	allyl isothiocyanate	0-4	P53	Homo sapiens	49-52
34484411-14	2021	Molecular docking results showed that daucosterol, delusive, dioxin, and panthogenin-B had the highest affinity for TP53, RPS27A, and UBC.	Dioxins	61-67	P53	Homo sapiens	116-120
34296537-12	2021	It was also found that Ramelteon reduced the expressions of p21 and p53.	ramelteon	23-32	P53	Homo sapiens	68-71
34306307-4	2021	The indicated results showed that NAR suppresses free radical production (ROS and nitrite) and apoptosis-related molecule activation (caspase-3, p-p53, p-p38, and NF-kappaB p65) and secretion (TNF-alpha).	nar	34-37	P53	Homo sapiens	147-150
34084225-6	2021	ChiMDM2 and trametinib used in combination demonstrated a synergistic antitumor activity in HCT116 and LoVo colon cancer cells, and SNU-1 gastric cancer cells harboring wt TP53 and mt KRAS.	trametinib	12-22	P53	Homo sapiens	172-176
34108527-6	2021	M3814 synergistically sensitized p53 wild-type, but not p53-deficient, AML cells to killing by DSB-inducing agents via p53-dependent apoptosis involving both intrinsic and extrinsic effector pathways.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	95-98	P53	Homo sapiens	33-36
34108527-6	2021	M3814 synergistically sensitized p53 wild-type, but not p53-deficient, AML cells to killing by DSB-inducing agents via p53-dependent apoptosis involving both intrinsic and extrinsic effector pathways.	1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione	95-98	P53	Homo sapiens	119-122
34108527-8	2021	Further, combined with the fixed-ratio liposomal formulation of daunorubicin and cytarabine, CPX-351, M3814 enhanced the efficacy against leukemia cells in vitro and in vivo without increasing hematopoietic toxicity, suggesting that DNA-PK inhibition could offer a novel clinical strategy for harnessing the anticancer potential of p53 in AML therapy.	Daunorubicin	64-76	P53	Homo sapiens	332-335
34199777-5	2021	Carbon monoxide (CO) activated the ECE-1/endothelin-1 (ET-1) pathway, which could account for the protumoral effects of HO-1 in p53 wild-type cells, as demonstrated after treatment with bosentan (an antagonist of both ETRA and ETRB endothelin-1 receptors).	Carbon Monoxide	0-15	P53	Homo sapiens	128-131
35311459-1	2022	We examined the apoptotic response of two glioblastoma cells, p53 wild type U87 and p53 mutated T98G, to doxorubicin, bortezomib, and vorinostat, which respectively target DNA, 26S proteasome and histone deacetylase, to clarify p53"s function in apoptosis.	Vorinostat	134-144	P53	Homo sapiens	228-231
35311459-7	2022	In contrast, vorinostat promoted apoptosis in both U87 and T98G cells and reduced the basal level of p53 in U87 cells, indicating that p53 played no role in the vorinostat-induced apoptosis.	Vorinostat	13-23	P53	Homo sapiens	101-104
35461040-7	2022	MiR-377-3p downregulates transcription factor EGR1 expression to weaken the activation of p53.	mir-377-	0-8	P53	Homo sapiens	90-93
35512188-0	2022	Lenalidomide promotes the development of TP53-mutated therapy-related myeloid neoplasms.	Lenalidomide	0-12	P53	Homo sapiens	41-45
35512188-3	2022	In a systematic analysis of 416 patients with t-MN and detailed prior exposure history, we found that TP53 mutations were significantly associated with prior treatment with thalidomide analogs, specifically lenalidomide.	Lenalidomide	207-219	P53	Homo sapiens	102-106
35512188-4	2022	We demonstrated experimentally that lenalidomide treatment provides a selective advantage to Trp53-mutant hematopoietic stem and progenitor cells (HSPCs) in vitro and in vivo, the effect of which was specific to Trp53-mutant HSPCs and was not observed in HSPCs with other CH mutations.	Lenalidomide	36-48	P53	Homo sapiens	93-98
35512188-4	2022	We demonstrated experimentally that lenalidomide treatment provides a selective advantage to Trp53-mutant hematopoietic stem and progenitor cells (HSPCs) in vitro and in vivo, the effect of which was specific to Trp53-mutant HSPCs and was not observed in HSPCs with other CH mutations.	Lenalidomide	36-48	P53	Homo sapiens	212-217
35512188-6	2022	These findings highlight the role of lenalidomide treatment in promoting TP53-mutated t-MNs and offer a potential alternative strategy to mitigate the risk of t-MN development.	Lenalidomide	37-49	P53	Homo sapiens	73-77
35577753-6	2022	In the first case, a patient with CLL, complex karyotype, del 17p, and a mutation in TP53 experiences progression after ibrutinib, venetoclax, bendamustine, rituximab, and idelalisib.	venetoclax	131-141	P53	Homo sapiens	85-89
35368106-7	2022	Notably, 6 of 7 pts (86%) who received either allo-SCT3 or a combination therapy of DLIs, 5-azacytidine and venetoclax achieved CR despite poor cytogenetics post-allo-SCT2 (e.g. TP53).	venetoclax	108-118	P53	Homo sapiens	178-182
35359340-0	2022	Synergistic Effect of Erastin Combined with Nutlin-3 on Vestibular Schwannoma Cells as p53 Modulates Erastin-Induced Ferroptosis Response.	erastin	22-29	P53	Homo sapiens	87-90
35359340-0	2022	Synergistic Effect of Erastin Combined with Nutlin-3 on Vestibular Schwannoma Cells as p53 Modulates Erastin-Induced Ferroptosis Response.	erastin	101-108	P53	Homo sapiens	87-90
35328718-0	2022	p62 Promotes the Mitochondrial Localization of p53 through Its UBA Domain and Participates in Regulating the Sensitivity of Ovarian Cancer Cells to Cisplatin.	UBP 310	63-66	P53	Homo sapiens	47-50
35328718-5	2022	We found that the combined use of the proteasome inhibitor epoxomicin and cisplatin led to the accumulation of p53 and sequestosome1(p62) in the mitochondria, downregulated mitochondrial DNA (mtDNA) transcription, inhibited mitochondrial functions, and ultimately promoted apoptosis by enhancing cisplatin sensitivity in ovarian cancer cells.	epoxomicin	59-69	P53	Homo sapiens	111-114
35215995-0	2022	Ergosterol Peroxide Inhibits Porcine Epidemic Diarrhea Virus Infection in Vero Cells by Suppressing ROS Generation and p53 Activation.	ergosterol-5,8-peroxide	0-19	P53	Homo sapiens	119-122
35048531-0	2022	MUL1-RING recruits the substrate, p53-TAD as a complex with UBE2D2-UB conjugate.	BM	67-69	P53	Homo sapiens	34-37